Usmle Pathology

Front 1

Common congenital malformations: Name 7 common congenital malformations

Back 1

(1) Heart Defects (congenital rubella) (2) Hypospadias (3) Cleft lip with or without cleft palate (4) congenital hip dislocation (5) spina bifida (6) anencephaly (7) pyloric stenosis (associated with polyhydramnios & projectile vomiting)

Front 2

Common congenital malformations: Name 2 neural tube defects (NTDs)

Back 2

Spina bifida and anencephaly

Front 3

Common congenital malformations: Name 2 diagnostic associations with NTDs during gestation

Back 3

increased serum and amniotic fluid levels of a-fetoprotein

Front 4

Common congenital malformations: How can the incidence of NTDs be reduced?

Back 4

Folate ingestion during pregnancy

Front 5

Congenital Heart Disease: What kind of shunts cause early cyanosis?

Back 5

R-to-L "blue babies"

Front 6

Congenital Heart Disease: What kind of shunts cause late cyanosis?

Back 6

L-to-R "blue kids"

Front 7

Congenital Heart Disease: Name 3 common R-to-L shunts.

Back 7

The 3 T's: Tetralogy of Fallot (most common cause of early cyanosis), Transposition of the great vessels, truncus arteriosus

Front 8

Congenital Heart Disease: What might you see children with a R-to-L shunt do to relieve discomfort?

Back 8

Squat to increase venous return

Front 9

Congenital Heart Disease: Name 3 common L-to-R shunts.

Back 9

VSD, ASD, PDA

Front 10

Congenital Heart Disease: Rank them in order of frequency

Back 10

VSD > ASD > PDA

Front 11

Congenital Heart Disease: What are the auscultatory signs of an Atrial Septal Defect?

Back 11

Loud S1; wide, fixed split S2

Front 12

Congenital Heart Disease: How do you treat PDA?

Back 12

Indomethacin

Front 13

Congenital Heart Disease: Name 3 sequelae of L-to-R shunts.

Back 13

1) Increased pulmonary resistance due to arteriolar thickening. 2) Progressive pulmonary HTN 3) R-to-L shunt (Eisenmenger's)

Front 14

Eisenmenger's Syndrome: What are signs/symptoms of Eisenmenger's?

Back 14

Late cyanosis, clubbing, polycythemia

Front 15

Tetrology of Fallot: What is the Tetrology?

Back 15

(1) Pulmonary Stenosis (2) RVH (3) Overriding aorta (4) VSD (mnemonic: PROVe)

Front 16

Tetrology of Fallot: What is the direction of the shunt in the tetralogy?

Back 16

right-to-left across the VSD

Front 17

Tetrology of Fallot: What is the x-ray finding on the tetralogy?

Back 17

Boot-shaped heart due to RVH

Front 18

Tetrology of Fallot: What is the embryological cause of the tetralogy?

Back 18

Anterosuperior displacement of the infundibular septum.

Front 19

Transposition of great vessels: The transposition occurs because of a failure of the --------------- --------- to -------

Back 19

failure of the aorticopulmonary septum to spiral

Front 20

Transposition of great vessels: In transposition of the great vessels, the aorta leaves ------------ and the pulmonary trunk leaves the ------------

Back 20

aorta leaves the RV (anterior) and the pulmonary trunk leaves the LV (posterior)

Front 21

Transposition of great vessels: How might transposition of the great vessels, be compatible with life?

Back 21

If a shunt (e.g. VSD, PDA or patent foramen ovale) exists, blood from the systemic and pulmonary circulations can mix. Clinicians use PGE to keep PDA open.

Front 22

Transposition of great vessels: Transposition of the great vessels is a common congenital heart disease in offspring of mothers with what disease?

Back 22

Diabetes

Front 23

Coarctation of aorta: Where is the aortic stenosis in the infantile type of coarctation?

Back 23

Preductal (proximal to insertion of ductus arteriosus) - INfantile (in close to heart)

Front 24

Coarctation of aorta: Where is the aortic stenosis in the adult type of coarctation?

Back 24

Postductal (distal to ductus arteriosus). - ADult (Distal to Ductus)

Front 25

Coarctation of aorta: Name 3 symptoms in adult type coarctation?

Back 25

(1) Notching of the ribs (2) HTN in uper extremities (3) Weak pulses in uper extremities

Front 26

Coarctation of aorta: What is the Male-to-Female ratio in coarctation?

Back 26

3-to-1

Front 27

Coarctation of aorta: What pulses should you check on physical exam?

Back 27

Femoral

Front 28

Patent ductus arteriosus: Which direction is the shunt in a neonate with PDA?

Back 28

Left-to-right

Front 29

Patent ductus arteriosus: What change occurs to the heart in PDA?

Back 29

RVH and failure

Front 30

Patent ductus arteriosus: What is the auscultatory finding in PDA?

Back 30

Continuous, "machine-like" murmur.

Front 31

Patent ductus arteriosus: How is patency maintained in PDA?

Back 31

prostaglandin (PGE) synthesis and low Oxygen tension.

Front 32

Patent ductus arteriosus: What drug is used to close a PDA?

Back 32

Indomethacin

Front 33

Patent ductus arteriosus: How is a PDA kept open?

Back 33

porstaglandin--PGE

Front 34

Patent ductus arteriosus: Why would you want to keep a PDA open?

Back 34

To sustain life in conditions such as transposition of the great vessels.

Front 35

Autosomal trisomies: What is the most common chromosomal disorder and cause of congenital mental retardation?

Back 35

Down Syndrome (trisomy 21), 1:700

Front 36

Autosomal trisomies: In Down syndrome, 4% of cases are due to ------- translocation, and 1% are due to -------- mosaicism

Back 36

Robertsonian; Down

Front 37

Autosomal trisomies: 95% of Down syndrome cases occur because of --------- --------- of homologous chromosomes

Back 37

meiotic nondisjunction

Front 38

Autosomal trisomies: What is the type and cause of the most common congenital heart malformation in Down syndrome?

Back 38

Septum-primum-type ASD due to endocardial cushion defects

Front 39

Autosomal trisomies: Name 8 findings in trisomy 21

Back 39

(1) mental retardation (2) flat facial profile (3) prominent epicanthal folds (4) simian crease (5) duodenal atresia (6) congenital heart disease (7) Alzheimer's in affected >35 yrs old (8) Increased risk of ALL

Front 40

Autosomal trisomies: Name a risk factor for Down Syndrome

Back 40

Advanced maternal age (1:500 < 20 yo; 1:25 > 45 yo)

Front 41

Autosomal trisomies: What is the name of the syndrome associated with trisomy 18?

Back 41

Edwards' syndrome (Election age = 18)

Front 42

Autosomal trisomies: Name 7 findings in trisomy 18

Back 42

(1) severe mental retardation (2) rocker bottom feet (3) low-set ears (4) microngathia (5) congenital heart dz (6) clenched hands (flexion of fingers) (7) prominent occiput

Front 43

Autosomal trisomies: What is the life expectancy in trisomy 18?

Back 43

Death usually w/in 1 year of birth

Front 44

Autosomal trisomies: What chromosomal anomaly is found in Patau's syndrome?

Back 44

trisomy 13 (1:6000)

Front 45

Autosomal trisomies: Name 7 findings in Patau's

Back 45

(1) severe mental retardation (2) microphthamlia (3) microcephaly (4) cleft lip/palate (5) abnormal forebrain structures (6) polydactyly (7) congenital heart dz

Front 46

Autosomal trisomies: What is the life expectancy in Patau's?

Back 46

Death usually w/in 1 year of birth

Front 47

Genetic gender disorders: What is the chromosomal anomaly in Klinefelter's syndrome?

Back 47

XXY (1:850) - male

Front 48

Genetic gender disorders: Name 5 characteristics of Klinefelter's syndrome

Back 48

(1) Testicular atrophy (2) Enuchoid body shape (3) Tall, long extremities (4) Gynecomastia (5) Female hair distribution

Front 49

Genetic gender disorders: What is a Barr body and is it found kin Klinefelter's syndrome?

Back 49

It is the inactivated X chromosome. Yes.

Front 50

Genetic gender disorders: What is the chromosomal anomaly in Turner's syndrome?

Back 50

Female XO; (1:3000)

Front 51

Genetic gender disorders: Name 4 characteristics of Turner's syndrome

Back 51

(1) Short stature (2) Ovarian dysgenesis (streak ovary) (3) Webbing of next (4) Coarctation of the aorta

Front 52

Genetic gender disorders: Turner's syndrome is the most common cause of primary ------------

Back 52

amenorrhea

Front 53

Genetic gender disorders: Is there a Barr body in Turner's syndrome?

Back 53

No

Front 54

Genetic gender disorders: Double Y males have what genotype?

Back 54

XYY (1:1000) - male

Front 55

Genetic gender disorders: What is the double Y phenotype?

Back 55

Normal phenotype, very tall, severe acne, antisocial behavior (seein in 1-2% of XYY males; seen increasingly among prison inmates)

Front 56

Muscular dystrophies: How are muscular dystrophies diagnosed?

Back 56

Elevated CPK and muscle biopsy

Front 57

Muscular dystrophies: What is the gene involved in muscular dystrophy?

Back 57

Dystrophin

Front 58

Muscular dystrophies: What is the mutation in Duchenne's MD?

Back 58

Frame-shift mutation - deletion of dystrophin gene - accelerated muscle breakdown.

Front 59

Muscular dystrophies: What is the age of onset in Duchenne's MD?

Back 59

Before 5 years

Front 60

Muscular dystrophies: In what muscles does weakness begin with Duchenne's MD?

Back 60

Pelvic girdle muscles and progresses superiorly

Front 61

Muscular dystrophies: Name 3 diagnostic characteristics of Duchenne MD.

Back 61

(1) Pseduohypertrophy of calf muscles due to fibrofatty replacement of muscle (2) Cardiac myopathy (3) Use of Gowers' maneuver, requiring assistance of uper extremities to stand up - indicates proximal lower limb weakness

Front 62

Muscular dystrophies: What distinguishes Becker's from Duchenne's MD?

Back 62

Less severe mutation in Becker's. Less debilitating.

Front 63

Pseudohermaphroditism: What is pseudohermaphroditism?

Back 63

Disagreement between the phenotypic (external genitalia) and gonadal (testes vs. ovaries) sex.

Front 64

Pseudohermaphroditism: A female pseudohermaphrodite has ------- present, but external genitalia are -------- or -----------.

Back 64

ovaries; virilized or ambiguous

Front 65

Pseudohermaphroditism: What causes female pseudohermaphroditism?

Back 65

Excessive and inapropraite exposure to androgenic steroids during early gestation (i.e.,congenital adrenal hyperplasia or exogenous administration of androgens suring pregnancy).

Front 66

Pseudohermaphroditism: What are the phenotypes in female and male pseudohermaphroditism?

Back 66

female - XX; male - XY

Front 67

Pseudohermaphroditism: A male pseudohermaphrodite has ------- present, but external genitalia are --------- or ---------.

Back 67

testes; female or ambiguous

Front 68

Pseudohermaphroditism: What is the most common form of male pseudohermaphroditism?

Back 68

Testicular feminization (androgen insensitivity), which results from a mutation in the androgen receptor gene (x-linked); blind-end vagina

Front 69

Pseudohermaphroditism: What determines gender identity?

Back 69

External genitalia and sex of upbringing.

Front 70

True Hermaphrodite (46,XX or 47, XXY): What is a true hermaphrodite?

Back 70

Both ovary and testicular tissue present; ambiguous genitalia.

Front 71

True Hermaphrodite (46,XX or 47, XXY): What are the genotypic possibilities for a true hermaphrodite?

Back 71

46,XX or 47,XXY

Front 72

Testicular Feminization syndrome (46, XY): What is the molecular defect in testicular feminization syndrome?

Back 72

Defect in DHT receptor resulting in normal-apearing female

Front 73

Testicular Feminization syndrome (46, XY): What genitalia are present in testicular feminization syndrome?

Back 73

female genitalia with rudimentary vagina; uterus and uterine tubes generally absent; develop testes (often found in labia majora; surgically removed to prevent malignancy)

Front 74

Testicular Feminization syndrome (46, XY): What are the genotype and horomone levels in testicular feminization syndrome?

Back 74

46, XY; levels of testosterone, estrogen and LH are all high

Front 75

5a-reductase deficiency: What is the biochemical consequence of 5a-reductase deficiency

Back 75

Unable to convert testosterone to DHT.

Front 76

5a-reductase deficiency: Describe genital development in 5a-reductase deficiency.

Back 76

Ambiguous genitalia until puberty, when increased testosterone causes masculinization of genitalia.

Front 77

5a-reductase deficiency: What are the hormone levels in 5a-reductase deficiency.

Back 77

Testosterone/estrogen levels are normal; LH is normal or elevated.

Front 78

Cri-du-chat syndrome: What is the mutation in Cri-du-chat syndrome?

Back 78

Congenital deletion of short arm of chromosome 5 (46,XX or XY, 5p-)

Front 79

Cri-du-chat syndrome: What are the findings in Cri-du-chat

Back 79

Microcephaly, severe mental retardation, high-pitched crying/mewing, epicanthal folds, cardiac abnormalities.

Front 80

Cri-du-chat syndrome: What does Cri-du-chat mean in english, which might help remember the symptoms?

Back 80

Cry of the cat.

Front 81

Fragile X syndrome: What is the 2nd most common cause of genetic mental retardation?

Back 81

Fragile X syndrome

Front 82

Fragile X syndrome: What genetic change is involved in Fragile X syndrome?

Back 82

x-linked defect affecting the methylation and expression of the FMR1 gene.

Front 83

Fragile X syndrome: Name 4 physical features associated with Fragile X syndrome?

Back 83

(1) macro-orchidism (enlarged testes) (2) Long face with a large jaw (3) large everted ears (4) autism

Front 84

Cystic Fibrosis (CF): What is the genetic defect in cystic fibrosis?

Back 84

Autosomal-recessive defect in CFTR gene on chromosome 7

Front 85

Cystic Fibrosis (CF): What is the molecular defect in CF?

Back 85

Defective Cl- channel

Front 86

Cystic Fibrosis (CF): What are the consequences of the defect in CF?

Back 86

The defective chloride channel causes secretion of abnormally thick mucus that plugs lungs, pancreas and liver, which leads to recurrent pulmonary infections (pseudomonas species and S. aureus), chronic bronchitis, bronchiectasis, pancreatic insufficiency (malabsorption and steatorrhea), meconium ileus in newborns.

Front 87

Cystic Fibrosis (CF): Name a diagnostic test for CF.

Back 87

Increased concentration of Cl- ions in sweat test.

Front 88

Cystic Fibrosis (CF): Why does CF cause infertility in males?

Back 88

Absent vas deferens.

Front 89

Cystic Fibrosis (CF): What vitamins are often deficient in CF?

Back 89

Fat-soluble - A,D,E,K

Front 90

Most common lethal genetic disease of Caucasians.

Back 90

Cystic Fibrosis

Front 91

Cystic Fibrosis (CF): What is the treatment for CF?

Back 91

N-acetylcysteine to loosen mucous plugs.

Front 92

Autosomal-dominant diseases: A patient presents with flank pain, hematuria, hypertension, progressive renal failure and has a mutation in one of his copies of APKD1 (chromosome 16); what is the diagnosis?

Back 92

Adult polycystic kidney disease. N.B. the juvenile form is recessive.

Front 93

Autosomal-dominant diseases: Name 2 other characteristics of adult polycystic kidney disease.

Back 93

(1) always bilateral, (2) massive enlargement of the kidneys due to multiple large cysts.

Front 94

Autosomal-dominant diseases: What sequelae are associated with adult polycystic kidney disease?

Back 94

(1) polycystic liver disease (2) berry aneurysms (3) mitral valve prolapse

Front 95

Autosomal-dominant diseases: What disease involves elevated LDL owing to defective or absent LDL receptor?

Back 95

Familial hypercholesterolemia (type IIA)

Front 96

Autosomal-dominant diseases: What are the average cholesterol levels in heterozygotes and homozygotes with familial hypercholesterolemia (tyype IIA)?

Back 96

heterozygotes (1:500) - 300 mg/dL homozygotes - 700+ mg/dL

Front 97

Autosomal-dominant diseases: What are 3 sequelae of familial hypercholesterolemia (type IIA)?

Back 97

(1) severe atherosclerotic disease early in life (2) tendon xanthomas (classically in the Achilles tendon) (3) MI may develop before age 20

Front 98

Autosomal-dominant diseases: What is the genetic defect in Marfan's syndrome?

Back 98

Fibrillin gene mutation leads to connective tissue disorders.

Front 99

Autosomal-dominant diseases: What are the skeletal abnormalities in Marfan's?

Back 99

tall with long exteremities, hyperextensive joints, and long, tapering fingers and toes.

Front 100

Autosomal-dominant diseases: What are the cardiovascular risks in Marfan's?

Back 100

cystic medial necrosis of aorta leads to aortic incompetence and dissecting aortic aneurysms; flopy mitral valve.

Front 101

Autosomal-dominant diseases: What are the ocular risks in Marfan's?

Back 101

Subluxation of lenses.

Front 102

Autosomal-dominant diseases: What is another name for Neurofibromatosis type 1?

Back 102

von Recklinghausen's disease

Front 103

Autosomal-dominant diseases: What chromosome is affected in NF type 1?

Back 103

Long arm of chromosome 17 (17 letters in von Recklinghasen's)

Front 104

Autosomal-dominant diseases: What are 5 classic characteristics of people with NF type 1?

Back 104

(1) café-au-lait spots (2) neural tumors (3) Lisch nodules (pigmented iris hamartomas) (4) skeletal disorders (e.g., scoliosis) (5) Increased tumor susceptibility

Front 105

Autosomal-dominant diseases: What disease is associated with bilateral acoustic neuroma?

Back 105

Neurofibromatosis type 2

Front 106

Autosomal-dominant diseases: What gene is affected in neurofibromatosis type 2?

Back 106

NF2 gene on chromosome 22; (type 2 = 22)

Front 107

Autosomal-dominant diseases: What is the genetic mutation in Von-Hippel-Lindau disease?

Back 107

Deletion of VHL gene (tumor supressor) on chromosome 3p. (Von Hipel-Lindau = 3 words for chromosome 3)

Front 108

Autosomal-dominant diseases: What are the clinical findings in Von-Hippel-Lindau disease?

Back 108

hemiangioblastomas of retina/cerebellum/medulla; about half of affected individuals develop multiple bilateral renal cell carcinomas and other tumors.

Front 109

Autosomal-dominant diseases: What is the diagnosis in a 20-50 year old person who presents with depression, progressive dementia, choreiform movements, caudate atrophy, and decreased levels of GABA and Ach in the brain?

Back 109

Huntington's disease

Front 110

Autosomal-dominant diseases: What chromosome holds the gene involved in Huntington's?

Back 110

Chromosome 4; triplet repeat disorder ("Hunting 4 food")

Front 111

Autosomal-dominant diseases: What disease is responsible for a colon that ecomes covered with adenomatous polyps after puberty?

Back 111

Familial adenomatous polyposis (FAP)

Front 112

Autosomal-dominant diseases: What is the progression in Familial adenomatous polyposis if colon not resected?

Back 112

Colon cancer

Front 113

Autosomal-dominant diseases: What is the genetic defect in Familial adenomatous polyposise?

Back 113

deletion on chromosome 5 - 5 letters in polyp

Front 114

Autosomal-dominant diseases: What are 3 characteristics of hereditary spherocytosis?

Back 114

(1) spheroid erythrocytes (2) hemolytic anemia (3) increased MCHC

Front 115

Autosomal-dominant diseases: What is the cure for hereditary spherocytosis?

Back 115

splenectomy

Front 116

Autosomal-dominant diseases: What is the genetic defect in achondroplasia?

Back 116

Autosomal dominant cell-signaling defect of fibroblast growth factor (FGF) receptor 3.

Front 117

Autosomal-dominant diseases: What are the physical characteristics of achondroplasia?

Back 117

Dwarfism, short limbs, but head and trunk are normal size.

Front 118

X-linked or AR:: Cystic fibrosis

Back 118

AR

Front 119

X-linked or AR:: albinism

Back 119

AR

Front 120

X-linked or AR:: Fragile X

Back 120

X-linked

Front 121

X-linked or AR:: Duchenne's muscular dystrophy

Back 121

X-linked

Front 122

X-linked or AR:: hemophilia A and B

Back 122

X-linked

Front 123

X-linked or AR:: a1-antitrypsin deficiency

Back 123

AR

Front 124

X-linked or AR:: Fabry's

Back 124

X-linked

Front 125

X-linked or AR:: G6PD deficiency

Back 125

X-linked

Front 126

X-linked or AR:: Hunter's syndrome

Back 126

X-linked

Front 127

X-linked or AR:: Phenylketonuria (PKU)

Back 127

AR

Front 128

X-linked or AR:: thalassemias

Back 128

AR

Front 129

X-linked or AR:: sickle cell anemias

Back 129

AR

Front 130

X-linked or AR:: ocular albinism

Back 130

X-linked

Front 131

X-linked or AR:: glycogen storage diseases

Back 131

AR

Front 132

X-linked or AR:: mucopolysaccharidoses (except Hunter's)

Back 132

AR

Front 133

X-linked or AR:: sphingolipidoses (except Fabry's)

Back 133

AR

Front 134

X-linked or AR:: infant polycystic kidney

Back 134

AR

Front 135

X-linked or AR:: Lesch-Nyhan syndrome

Back 135

X-linked

Front 136

X-linked or AR:: Bruton's agammaglobulinemia

Back 136

X-linked

Front 137

X-linked or AR:: hemochromatosis

Back 137

AR

Front 138

X-linked or AR:: Wiskott-Aldrich syndrome

Back 138

X-linked

Front 139

X-linked or AR:: What are femal carriers of x-linked recessive disorders rarely affected?

Back 139

Inactivation of X chromosomes in each cell

Front 140

Neural Tube Defects (NTD): Name two associations with neural tube defects during pregnancy.

Back 140

(1) Low folic acid intake (2) Elevated a-fetoprotein in amniotic fluid

Front 141

Neural Tube Defects (NTD): What NTD is associated with failure of bony spinal canal to close, but no structural herniation?

Back 141

Spina bifida occulta

Front 142

Neural Tube Defects (NTD): Which NTD is involved with herniation of meninges through spinal canal defect?

Back 142

Meningocele

Front 143

Neural Tube Defects (NTD): What is the NTD that involves herniation of meninges AND spinal cord through spinal canal defect?

Back 143

Meningomyelocele

Front 144

Neural Tube Defects (NTD): Which NTD is usually seen at lower vertebral levels?

Back 144

Spina bifida occulta

Front 145

Neural Tube Defects (NTD): Take a look at the figures in the book for good visualization of the NTDs.

Back 145

0

Front 146

Fetal Alcohol Syndrome: Who is at greatest risk of FAS?

Back 146

Newborns of mothers who consumed significant amounts of alcohol (teratogen) during pregnancy (highest risk at 3-8 weeks).

Front 147

Fetal Alcohol Syndrome: Name 5 congenital abnormalities in FAS?

Back 147

(1) pre and postnatal developmental retardation (2) microcephaly (3) facial abnormalities (4) limb dislocation (5) heart and lung fistulas

Front 148

Fetal Alcohol Syndrome: How does FAS rank among congenital malformations in the U.S.?

Back 148

It's number 1

Front 149

Fetal Alcohol Syndrome: What is the presumed mechanism of FAS?

Back 149

Inhibition of cell migration?

Front 150

Fetal Alcohol Syndrome: AUTHOR

Back 150

Neha Pathak

Front 151

NEOPLASTIC PROGRESSION: when cells increase in number it is called?

Back 151

hyperplasia

Front 152

NEOPLASTIC PROGRESSION: what are two enzymes that allow neoplastic cells to invade th ebasement membrane?

Back 152

collagenase and hydrolase

Front 153

NEOPLASTIC PROGRESSION: when cells have an increased nulear to cytoplasmic ratio but have not invaded the basement membrane, it is called?

Back 153

carcinoma in situ

Front 154

_ -PLASIA DEFINITIONS: squamous _________ occurs in the trachea and bronchi of smokers

Back 154

metaplasia

Front 155

_ -PLASIA DEFINITIONS: what is it called when a cell has reversible preneoplastic changes with abnormal shape and size?

Back 155

dysplasia

Front 156

_ -PLASIA DEFINITIONS: abnormal cells that lack differentiation are called?

Back 156

anaplastic cells

Front 157

TUMOR STAGE VS. GRADE: staging of a tumor takes into account what factors?

Back 157

TMN size of tumor, node involvment, metastases

Front 158

TUMOR STAGE VS. GRADE: histolgy of a tumor is used to determine?

Back 158

grade

Front 159

TUMOR STAGE VS. GRADE: what has more prognostic value? Grade or stage?

Back 159

stage

Front 160

TUMOR NOMENCLATURE: the term _________ implies epithelial origin, whereas _________ implies mesenchymal origin

Back 160

carcinoma, sarcoma

Front 161

TUMOR NOMENCLATURE: a tumor of blood vessels is called what when it is benign? When it is malignant?

Back 161

hemangioma, angiosarcoma

Front 162

TUMOR NOMENCLATURE: what is a benign tumor of skeletal muscle called?

Back 162

rhabdomyoma

Front 163

DISEASES ASSOCIATED WITH NEOPLASMS: Kaposi's sarcoma and aggressive malignant lymphomas are associated with what disease

Back 163

AIDS

Front 164

DISEASES ASSOCIATED WITH NEOPLASMS: Actinic Keratosis predispose to what disease?

Back 164

squamous cell carcinoma of skin

Front 165

DISEASES ASSOCIATED WITH NEOPLASMS: down syndrome is associated with what neoplasm?

Back 165

ALL

Front 166

ONCOGENES: c-myc oncogenes are associated with what neoplasm?

Back 166

burkitt's lymphoma

Front 167

ONCOGENES: breast, ovarian, and gastic carcinomas all have this oncogene mutation in common?

Back 167

erb B2

Front 168

ONCOGENES: MEN II and III are associated with what oncogenic mutation?

Back 168

ret

Front 169

TUMOR SUPRESSOR GENES: Name the associated tumor witht the following tumor supressor gene mutations: Rb, APC, WT1

Back 169

retinoma blastoma, colorectal cancer, wilms tumor

Front 170

TUMOR SUPRESSOR GENES: p53 is on what chromosome

Back 170

17p

Front 171

TUMOR SUPRESSOR GENES: osteosarcoma is associated with what tumor supressor gene mutation

Back 171

Rb

Front 172

TUMOR MARKERS: TRAP is a tumor marker for what neoplasm

Back 172

hairy cell leukemia

Front 173

TUMOR MARKERS: what tumor marker is elevated in hyatidiform moles

Back 173

beta-HCG

Front 174

TUMOR MARKERS: ovarian tumors are associated with what tumor marker

Back 174

CA-125

Front 175

ONCOGENIC VIRUSES: the virus associated with burkitts and nasopharyngeal cancer is?

Back 175

ebv

Front 176

ONCOGENIC VIRUSES: hpv is responsible for what cancers?

Back 176

cervical, penile, and anal carcinoma

Front 177

ONCOGENIC VIRUSES: what virus is responsible for kaposis sarcoma?

Back 177

hhv8

Front 178

CHEMICAL CARCINOGENS: aflatoxin, vinyl chloride and ccl4 damage what organ?

Back 178

liver

Front 179

CHEMICAL CARCINOGENS: nitrosamines cause cancer in what organs?

Back 179

esophagus or stomach

Front 180

CHEMICAL CARCINOGENS: asbestos causes what types of cancer?

Back 180

bronchogenic and mesothelioma

Front 181

LOCAL EFFECTS OF TUMORS: When the following are obstructed, what can occur: bronchus? Biliary tree? Left colon?

Back 181

pneumonia, jaundice, constipation

Front 182

LOCAL EFFECTS OF TUMORS: tumor mass in the brain can cause the following

Back 182

seizure, increased intracranial pressure, mass effect and herniation

Front 183

LOCAL EFFECTS OF TUMORS: compression of the recurrent laryngeal nerve can cause what?

Back 183

hoarseness

Front 184

PROSTATIC ADENOCARCINOMA: what lobe/zone is most often involved in prostatic cancer?

Back 184

posterior lobe, peripheral zone

Front 185

PROSTATIC ADENOCARCINOMA: what is a common site of metastases for prostate cancer?

Back 185

bone

Front 186

PROSTATIC ADENOCARCINOMA: what are useful tumor markers for prostate CA

Back 186

psa, and prostatic acid phosphatase

Front 187

SKIN CANCER: this type of skin cancer has palisading nuclei

Back 187

basal cell carcinoma

Front 188

SKIN CANCER: dyplastic nevi are a precursor fot this type of cancer

Back 188

melanoma

Front 189

SKIN CANCER: this type of skin cancer is associated with keratin pearls

Back 189

squamous cell carcinoma of skin

Front 190

PRIMARY BONE TUMORS: the translocation 11;22 is associated with this cancer of the bone that occurs most commonly in young boys

Back 190

ewing's sarcoma

Front 191

PRIMARY BONE TUMORS: this tumor is characterized by a "double bubble" or "soap bubble" appearance

Back 191

benign giant cell tumor

Front 192

PRIMARY BONE TUMORS: this is the most common benign bone tumor, usually in men younger than 25, with a rare transformation to malignancy

Back 192

osteochondroma

Front 193

PRIMARY BONE TUMORS: AUTHOR

Back 193

Gabe Pitta

Front 194

Primary Brain Tumors-Adult peak incidence: Most common adult brain tumor?

Back 194

Glioblastoma multiforme (grade IV astrocytoma) See pseudopalisading tumor cells, central necrosis and hemorrhage.

Front 195

Primary Brain Tumors-Adult peak incidence: Second most common adult tumor?

Back 195

Meningioma, occurring in convexities of hemispheres and parasagittal region. See psammoma bodies.

Front 196

Primary Brain Tumors-Adult peak incidence: Benign, slow-growing tumor in frontal lobes?

Back 196

Oligodendroglioma, look for fried egg apearance, often calcified.

Front 197

Primary Brain Tumors-Adult peak incidence: Third most common tumor, often localized to CN8?

Back 197

Schwannoma, see it in acoustic Schwannoma. Antoni A (compact) and Antoni B (loose) patterns.

Front 198

Primary Brain Tumors-Adult peak incidence: Most common forms are prolactin-secreting?

Back 198

Pituitary Adenoma, which derives from Rathke's Pouch and can produce secondary bitemporal hemianopsia and hypopituitarism

Front 199

Primary Brain Tumors-Child Peak Incidence: Highly malignant cerebellar tumor?

Back 199

Medulloblastoma, can compress 4th ventricle and cause hydrocephalus. See rosettes or pseudorosettes.

Front 200

Primary Brain Tumors-Child Peak Incidence: Cerebellar tumor associated with von Hippel-Landau syndrome?

Back 200

Hemangioblastoma, see foamy cells and high vascularity, can produce excess EPO-->polycythemia.

Front 201

Primary Brain Tumors-Child Peak Incidence: Commonly found in fourth ventricle, causing hydrocephalus?

Back 201

Ependyomomas, which have perivascular rosettes and rod-shaped blepharoblasts near nucleus on exam.

Front 202

Primary Brain Tumors-Child Peak Incidence: Diffusely infiltrating glioma, usually found in posterior fossa?

Back 202

Low-grade Astrocytoma

Front 203

Primary Brain Tumors-Child Peak Incidence: Benign tumor often confused with pituitary adenoma?

Back 203

Craniopharyngioma, which also is derived from Rathke's pouch, also presents with bitemporal hemianopsia, also calcified.

Front 204

Common sites that receive metastatic tissue: To Brain?

Back 204

Lung, Breast, Skin (melanoma), Kidney (renal cell carcinoma), GI. Lots of Bad Stuff Kills Glia. 50% of brain tumors are due to metastases.

Front 205

Common sites that receive metastatic tissue: To liver?

Back 205

Colon>Stomach>Pancreas>Breast>Lung. Cancer Sometimes Penetrates Benign Liver. Metastases much more common than primary liver tumors.

Front 206

Common sites that receive metastatic tissue: To bone?

Back 206

Breast, lung, thyroid, testes, kidney, prostate.=> "BLT with a Kosher Pickle."

Front 207

Common sites that receive metastatic tissue: Most common organ receiving metastases?

Back 207

Adrenal medulla, then cortex.

Front 208

Common sites that receive metastatic tissue: Most common organ sending metastases?

Back 208

Lung>Breast/Stomach

Front 209

Paraneoplastic effects of tumors: Cushing's Syndrome

Back 209

ACTH/ACTH-like peptide from small-cell lung CA

Front 210

Paraneoplastic effects of tumors: SIADH

Back 210

ADH/ANP from small cell lung CA and intracranial neoplasms.

Front 211

Paraneoplastic effects of tumors: Hypercalcemia

Back 211

PTH-related peptide/TGF-alpha/TNF-Alpha/IL-2 from squamous cell lung CA, renal cell CA, Breast CA, multiple myeloma, bone metastasis.

Front 212

Paraneoplastic effects of tumors: Polycythemia

Back 212

EPO from renal cell CA.

Front 213

Paraneoplastic effects of tumors: Lambert-Eaton Syndrome

Back 213

Antibodies against presynaptic Ca2+ channels at NMJ, generated by Thymomas and bronchogenic CA.

Front 214

Paraneoplastic effects of tumors: Gout

Back 214

Hyperuricemia due to excess nucleic acid turnover, found in various neoplasms.

Front 215

Cancer Epidemiology: Male incidence?

Back 215

Prostate(32%)>Lung(16%)>Colon and Rectum (12%)

Front 216

Cancer Epidemiology: Male Mortality?

Back 216

Lung(33%)>Prostate(13%)

Front 217

Cancer Epidemiology: Female incidence?

Back 217

Breast (32%)>Lung(13%)>Colorectal(13%)

Front 218

Cancer Epidemiology: Female Mortality?

Back 218

Lung(23%)>Breast(18%)

Front 219

HEMATOLOGIC PATHOLOGY: Anemia

Back 219

0

Front 220

HEMATOLOGIC PATHOLOGY: Anemia presenting with increased TIBC, decreased ferritin, decreased serum iron.

Back 220

Mycrocytic, Hypochromic, usually secondary to iron deficiency. Also seen with Thalassemia, lead poisoning

Front 221

HEMATOLOGIC PATHOLOGY: Anemia in patients with B12/Folate deficiency

Back 221

Macrocytic (MCV>100), presents with PMN hypersegmentation on blood smear. B12 deficiency presents with neuro effects, folate deficiency much easily reached through bad diet. Also seen in patients taking drugs blocking DNA synthesis (sulfa drugs, AZT)

Front 222

HEMATOLOGIC PATHOLOGY: Anemia in patients with normocytic, normochromic smears?

Back 222

Hemorrhagic, autoimmune hemolytic, enzyme defects (G6PD), bone marrow dz, anemia of chronic dz. Decreased serum haptoglobin and increased LDH indicate RBC hemolysis. Direct Coomb's test can show an immune-mediated process.

Front 223

HEMATOLOGIC PATHOLOGY: Anemia in patients with a decreased TIBC, decreased serum iron, and decreased iron saturation?

Back 223

Anemia of chronic disease

Front 224

HEMATOLOGIC PATHOLOGY: Anemia in patients with an increased TIBC, decreased serum iron, and normal iron saturation?

Back 224

Iron-deficiency anemia.

Front 225

HEMATOLOGIC PATHOLOGY: Patient with normal TIBC, increased serum iron, and 100% iron saturation (normal is 20-50%)

Back 225

Iron overload (hemosiderosis)

Front 226

Aplastic Anemia: Patient presentation of Aplastic Anemia?

Back 226

Patients with pancytopenia characterized by severe anemia, neutropenia, and thrombocytopenia caused by failure or destruction of multipotent myeloid stem cells.

Front 227

Aplastic Anemia: What causes aplastic anemia?

Back 227

Radiation, benzene, chloramphenicol, alkylating agents, antimetabolites, viral agents, Fanconi's anemia, idiopathic causes.

Front 228

Aplastic Anemia: Common Sx?

Back 228

Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.

Front 229

Aplastic Anemia: How do the blood smear and bone marrow aspirate appear?

Back 229

Blood smear: pancytopenia with normal cell morphology. Aspirate:hypocellular marrow with fatty infiltration.

Front 230

Aplastic Anemia: What's the treatment of aplastic anemia?

Back 230

Withdraw offending agent, BMT, RBC/platelet transfusion, G-CSF or GM-CSF.

Front 231

Hereditary Spherocytosis: How do patients with hereditary psherocytosis present (smear and labs)?

Back 231

Smear shows microcytic RBCs that are small and round with no central pallor. The patients will have normal Hgb and MCV.

Front 232

Hereditary Spherocytosis: What's the cause of hereditary spherocytosis?

Back 232

Intravascular hemolysis due to spectrin defect.

Front 233

Hereditary Spherocytosis: How is it confirmed and tested?

Back 233

Will be Coombs' negative (unlike warm antibody hemolysis), can perform osmotic fragility test.

Front 234

Hereditary Spherocytosis: What are some associated diseases?

Back 234

Gallstones, splenomegaly, anemia, and jaundice.

Front 235

Blood Dyscrasias-Sickle Cell Anemia: What is the HbS mutation?

Back 235

Glutamate-->Valine in a Beta chain. Heterozygotes are usually malaria-resistant. *% of Af-Ams carry the HbS trait, 0.2% have the disease.

Front 236

Blood Dyscrasias-Sickle Cell Anemia: What can precipitate sickling?

Back 236

Low O2, dehydration.

Front 237

Blood Dyscrasias-Sickle Cell Anemia: What are the common complications of HbS homozygotes?

Back 237

aplastic crises from parvovirus infection, autosplenectomy, risk of encapsulated organism infection, salmonella osteomyelitis, vaso-occlusive pain crises, and splenic sequestration crises.

Front 238

Blood Dyscrasias-Sickle Cell Anemia: What is the HbC defect?

Back 238

Different Beta-chain mutation, the patients with HbC or HbSC have milder dz than HbSS patients.

Front 239

Blood Dyscrasias-Sickle Cell Anemia: What are the treatment options?

Back 239

Hydroxyurea (increased HbF) and bone marrow transplantation.

Front 240

Blood Dyscrasias-Alpha-Thalassemia: What populations have the most prevalence?

Back 240

Mediterranean populations. (thalaSEAmia)

Front 241

Blood Dyscrasias-Alpha-Thalassemia: What is the etiology?

Back 241

Underproduction of the alpha-globin chain, with no compensatory increase of any other chains. HbH has Beta-4 tetramers and lacks 3 alpha-globin genes.

Front 242

Blood Dyscrasias-Alpha-Thalassemia: What is the presentation of a patient lacking all four alpha-globin genes?

Back 242

hydrops fetalis and intrauterine fetal death.

Front 243

Blood Dyscrasias-Beta-Thalassemia: Patient Presentation of Beta-Thalassemia major?

Back 243

severe anemia requiring blood transfusion. Cardiac failure is often due to secondary hemochromatosis.

Front 244

Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-Thalassemia major?

Back 244

Beta chain is absent, fetal Hgb production is compensatorily increased but is inadequate.

Front 245

Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-thalassemia minor?

Back 245

The Beta chain is underproduced, again see fetal HgB compensatory increase. HbS/Beta-thalassemia heterozygote has mild to moderate disease.

Front 246

DIC: What is the definition of DIC?

Back 246

Activation of the coagulation cascade leading to microthrombi and global consumption of platelets, fibrin, and coagulation factors.

Front 247

DIC: What causes DIC?

Back 247

Obstetric complications (most common cause), gram-negative sepsis, transfusion, trauma, malignancy, acute pancreatitis, nephrotic syndrome.

Front 248

DIC: What are the lab findings in DIC?

Back 248

Increased PT, increased PTT, incrased fibrin split products (D-dimers), decreased platelet count.

Front 249

Bleeding Disorders: What disorder type presents with mucous membrane bleeding, petechiae, purpura, and prolonged bleeding time?

Back 249

Platelet abnormalities (microhemorrhages), which can be caused by ITP (antiplatelet antibodies and increased megakaryocytes), TTP (schistocytes), drugs, and DIC (increased fibrin split products).

Front 250

Bleeding Disorders: What disorder type presents with hemarthroses (bleeding into joints), easy brusing, prolonged PT and/or PTT?

Back 250

Coagulopathies (macrohemorrhages), which can be caused by Hemophilia A/B and von Willebrand's disease (most common)

Front 251

Bleeding Disorders: What is the deficiency in Hemophilia A?

Back 251

Factor VIII

Front 252

Bleeding Disorders: What is the deficiency in Hemophilia B?

Back 252

Factor IX

Front 253

Bleeding Disorders: What is the deficiency in vW dz?

Back 253

Deficiency of von Willebrand's antigen.

Front 254

Bleeding Disorders: Which factors does the PT measure?

Back 254

Extrinsic: Factors II, V, VII, and X.

Front 255

Bleeding Disorders: Which factors does the PTT measure?

Back 255

Intrinsic: All factors except VII and XIII.

Front 256

Hemorrhagic disorders: What presents with increased bleeding time, normal platelet count, and normal PT/PTT and platelet count?

Back 256

Qualitative platelet defects, can be Bernard Soulier disease (defect in adhesion) or Glanzmann's thrombasthenia (defect in aggregation). Can also see these labs in vascular bleeding.

Front 257

Hemorrhagic disorders: What presents with decreased platelet count, increased bleeding time, and normal PT/PTT?

Back 257

Thrombocytopenia

Front 258

Hemorrhagic disorders: Which diseases present with increased PTT and normal PT, platelet count, and bleeding time?

Back 258

Hemophilia A and B

Front 259

Hemorrhagic disorders: What presents with a high PTT, normal PT, normal platelets, and increased bleeding time?

Back 259

vW disease

Front 260

Hemorrhagic disorders: What presents with increased Bleeding time/Pt/PTT and decreased platelet count?

Back 260

DIC

Front 261

Lymphomas: Hodgkin's Versus NHL: Which one presents with Reed-Sternberg cells?

Back 261

Hodgkin's

Front 262

Lymphomas: Hodgkin's Versus NHL: Which one is associated with HIV and immunosuppression?

Back 262

NHL

Front 263

Lymphomas: Hodgkin's Versus NHL: Which one involves multiple, peripheral nodes, with common extranodal involvement?

Back 263

NHL

Front 264

Lymphomas: Hodgkin's Versus NHL: Which one is localized to a single group of nodes, with contiguous spread and rare extranodal involvement?

Back 264

HL

Front 265

Lymphomas: Hodgkin's Versus NHL: Which one presents with constitutional signs/symptoms: low-grade fever, night sweats, weight loss?

Back 265

HL (NHL has few signs/symptoms)

Front 266

Lymphomas: Hodgkin's Versus NHL: Which one presents with mediastinal lymphadenopathy?

Back 266

HL

Front 267

Lymphomas: Hodgkin's Versus NHL: Which one involves mostly the B cells (except lymphoblastic origin)?

Back 267

NHL

Front 268

Lymphomas: Hodgkin's Versus NHL: Which one has hypergammaglobulinemia?

Back 268

neither. Multiple Myeloma has hypergammaglobulinemia, where the excess B cells are in the resting state.

Front 269

Lymphomas: Hodgkin's Versus NHL: Which one has a 50% association with EBV?

Back 269

HL

Front 270

Lymphomas: Hodgkin's Versus NHL: Which one has bimodal age distribution?

Back 270

HL (NHL has peak incidence at 20-40 years old)

Front 271

Lymphomas: Hodgkin's Versus NHL: Which one has more common male presentation?

Back 271

HL

Front 272

Hodgkin's: What factors denote a good prognosis?

Back 272

Increased lymphocytes, decreased RS cells.

Front 273

Hodgkin's: Which HL type has the best prognosis?

Back 273

Nodular sclerosing (65-75%), which has least RS cells and lots of lymphocytes. Lymphocyte-predominant LH also has excellent prognosis.

Front 274

Hodgkin's: Which HL type is the most common?

Back 274

Nodular sclerosing, affecting women more than men and primarily young adults.

Front 275

Hodgkin's: What is the prognosis of mixed cellular HL?

Back 275

Intermediate. There are lots of lymphocytes but also lots of RS cells.

Front 276

Hodgkin's: Which HL type has the worst prognosis?

Back 276

Lymphocyte-depleted, which affects older males with disseminated disease.

Front 277

Hodgkin's: Which HL type has the most RS cells?

Back 277

Mixed cellular.

Front 278

NHL: Which NHL type has only B cells?

Back 278

Small Lymphocytic lymphoma, follicular lymphoma, Burkitt's

Front 279

NHL: Which NHL type has a mix of B cells and T cells?

Back 279

Diffuse large cell , occurring mostly in elderly but sometimes in children.

Front 280

NHL: Which NHL type has only T cells?

Back 280

Lymphoblastic Lymphoma, which has immature T cells. It is a very aggressive T-cell lymphoma.

Front 281

NHL: Which type is associated with a t(8;14) c-myc gene mutation?

Back 281

Burkitt's Lymphoma, occurring mostly in children. Has a high-grade "starry sky" apearance.

Front 282

NHL: Which type is associated with a t(14;18) mutation and overexpression of bcl-2?

Back 282

Follicular lymphoma, which is difficult to cure but has an indolent course.

Front 283

NHL: Which type is associated with EBV infection and is endemic in africa?

Back 283

Burkitt's

Front 284

NHL: Which is the most common childhood NHL?

Back 284

Lymphoblastic Lymphoma, which also presents with ALL and a mediastinal mass.

Front 285

NHL: Which is the most common adult version of NHL?

Back 285

Follicular lymphoma.

Front 286

NHL: Which types occur in adults?

Back 286

Small lymphocytic lymphoma, follicular lymphoma.

Front 287

NHL: Which types occur in children?

Back 287

Lymphoblastic lymphoma, Burkitt's lymphoma.

Front 288

NHL: Which one has a distribution of 80% adults and 20% children?

Back 288

Diffuse large cell lymphoma, which ALSO has an 80% B cells 20% T cell distribution.

Front 289

NHL: Which low-grade NHL type presents like CLL?

Back 289

Small Lymphocytic lymphoma.

Front 290

NHL: AUTHOR

Back 290

John Peoples

Front 291

Leukemias: Peripheral and bone marrow characteristics

Back 291

Increased circulating leukocytes, bone marrow infiltrates of leukemic cells

Front 292

Leukemias: Consequences of marrrow failure

Back 292

Anemia (dec. RBC's), infections (dec. WBC's), hemorrhage (dec. platelets)

Front 293

Leukemias: Common organs of infiltration

Back 293

Liver, spleen, lymph nodes

Front 294

Leukemias: Characteristics of acute leukemias

Back 294

Blasts predominate, children or elderly, short or drastic course

Front 295

Leukemias: ALL characteristics (4)

Back 295

Lympholasts (pre-B or pre-T), children, most responsive to therapy, associated with Down's Syndrome

Front 296

Leukemias: AML characteristics

Back 296

Myeloblasts, adults, auer rods

Front 297

Leukemias: Characteristics of chronic leukemias

Back 297

More mature cells, midlife age range, longer, less devastating course

Front 298

Leukemias: CLL characteristics - cells

Back 298

Lymphocytes, non-Ab producing B cells, increased smudge cells on peripheral blood smear

Front 299

Leukemias: CLL - population

Back 299

older adults

Front 300

Leukemias: CLL - presentation and course

Back 300

lymphadenopathy, hepatosplenomegaly, few sx., indolent course

Front 301

Leukemias: CLL is similar to?

Back 301

very similar to SLL (small lymphocytic lymphoma)

Front 302

Leukemias: CLL is associated with what type of anemia?

Back 302

warm antibody autoimmune hemolytic anemia

Front 303

Leukemias: CML cell characteristics

Back 303

Myeloid stem cells, increased neutrophils and metamyelocytes

Front 304

Leukemias: CML translocation?

Back 304

Ph Chromosome, t(9;22), bcr-abl

Front 305

Leukemias: CML acute complications?

Back 305

blast crisis (AML)

Front 306

Chromosomal translocations - the following disorder is associated with what translocation?: CML

Back 306

Ph chromosome, t(9;22), bcr-abl

Front 307

Chromosomal translocations - the following disorder is associated with what translocation?: Burkitt's lymphoma

Back 307

t(8;14), c-myc activation

Front 308

Chromosomal translocations - the following disorder is associated with what translocation?: Follicular lymphomas

Back 308

t(14;18), bcl-2 activation

Front 309

Chromosomal translocations - the following disorder is associated with what translocation?: AML- M3 type

Back 309

t(15;17), responsive to all-trans retinoic acid (ATRA)

Front 310

Chromosomal translocations - the following disorder is associated with what translocation?: Ewing's sarcoma

Back 310

t(11;22)

Front 311

Chromosomal translocations - the following disorder is associated with what translocation?: Mantle cell lymphoma

Back 311

t(11;14)

Front 312

Lymphomas and Leukemias: What are the chronic leukemias associated with T-lymphoblasts?

Back 312

Sezary Syndrome, CLL-T (both L2)

Front 313

Lymphomas and Leukemias: What are the acute leukemias associated with T-lymphoblasts?

Back 313

ALL-T (L2), ALL-null (L1), ALL-common(L1)

Front 314

Lymphomas and Leukemias: What are the chronic leukemias associated with B-lymphoblasts?

Back 314

CLL-B (L3)

Front 315

Lymphomas and Leukemias: What are the acute leukemias associated with B-lymphoblasts?

Back 315

ALL-B (L3)

Front 316

Lymphomas and Leukemias: What are the chronic leukemias associated with monoblasts?

Back 316

Chonic monocytic (M5), chronic myelomonocytic (M4)

Front 317

Lymphomas and Leukemias: What are the acute leukemias associated with monoblasts?

Back 317

Acute monocytic (M5), acute myelomonocytic (M5)

Front 318

Lymphomas and Leukemias: What are the chronic leukemias associated with myeloblasts?

Back 318

CML (M1, 2 and 3), Polycythemia rubra vera (M1), myelofibrosis (M1)

Front 319

Lymphomas and Leukemias: What are the acute leukemias associated with myeloblasts?

Back 319

AML (M2 and M1), Promyelocytic (M1)

Front 320

Lymphomas and Leukemias: What are the chronic leukemias associated with eos-myeloblasts?

Back 320

Eosinophilic (rare)

Front 321

Lymphomas and Leukemias: What are the chronic leukemias associated with normoblasts?

Back 321

Chronic erythroid (M6, rare)

Front 322

Lymphomas and Leukemias: What are the acute leukemias associated with normoblasts?

Back 322

acute erythroleukemia (M6)

Front 323

Lymphomas and Leukemias: What are the chronic leukemias associated with megakaryoblasts?

Back 323

Idiopathic thrombocytopenia (M7)

Front 324

Lymphomas and Leukemias: What are the acute leukemias associated wwith megakaryoblasts?

Back 324

acute megakaryocytic leukemias (M7)

Front 325

Multiple Myeloma: What type of cell proliferates in MM, and what is its histologic appearance

Back 325

Monoclonal plasma cell, fried egg apearance

Front 326

Multiple Myeloma: Where does MM arise?

Back 326

bone marrow

Front 327

Multiple Myeloma: The 2 most common ab's, in order, are:

Back 327

IgG (55%), IgA (25%)

Front 328

Multiple Myeloma: Common symptoms are:

Back 328

lytic bone lesions and hypercalcemia, renal insifficiency, increased suscpetibility to infection, anemia

Front 329

Multiple Myeloma: This disease is associated with:

Back 329

primary amyloidosis

Front 330

Multiple Myeloma: Ig light chains are also called:

Back 330

Bence Jones proteins

Front 331

Multiple Myeloma: 3 key diagnostic features:

Back 331

lytic bone lesions on x-ray, M-spike on serum protein electrophoresis, Bence-Jones proteins in urine

Front 332

Multiple Myeloma: Red blood cell appearance on peripheral smear:

Back 332

Rouleaux formation (poker chips)

Front 333

Multiple Myeloma: What 2 differences are seen in Waldenstrom's macroglobulinemia?

Back 333

M-spike is IgM, no lytic lesions

Front 334

Achalasia: Achalasia results from:

Back 334

failure of relaxation of lower esophogeal sphincter due to loss of the myenteric plexus (Aeurbach's). [A-chalasia = absence of relaxation]

Front 335

Achalasia: Achalasia causes:

Back 335

progressive dysphagia

Front 336

Achalasia: Diagnosis is made by:

Back 336

barium swallow showing "bird beak" dilated esophagus with distal stenosis.

Front 337

Achalasia: Secondary achalasia may result from this protozoan disease:

Back 337

Chagas disease (treponema cruzi)

Front 338

Achalasia: Associated with increased risk of:

Back 338

esophageal carcinoma

Front 339

Barrett's esophagus: The distal esophageal colummnar epithelium is replaced with….

Back 339

Gastric columnar epithelium

Front 340

Barrett's esophagus: Barrett's results from:

Back 340

Reflux

Front 341

Barrett's esophagus: Barrett's can progress to:

Back 341

adenocarcinoma

Front 342

Esophageal Cancer: Risk factors are (ABCDEF):

Back 342

achalasia, barrett's esophagus, corrosive esophagitis/cigarettes, diverticuli (e.g. zenker's), esophogeal web/EtOH, familial

Front 343

Esophageal Cancer: The most common esophageal cancer in the world is:

Back 343

squamous cell carcinoma

Front 344

Esophageal Cancer: The most common esophageal cancer in the US is:

Back 344

equal between squamous cell and adenocarcinoma (decreased cigarette use).

Front 345

Esophageal Cancer: Esophageal Adenocarcinoma is found where?

Back 345

lower third

Front 346

Esophageal Cancer: Esophageal squamous cell carcinoma is found where?

Back 346

uper 2/3

Front 347

Congenital Pyloric Stenosis: What does this cause in infant?

Back 347

Projectile vomiting at aproximately 2 weeks of age

Front 348

Congenital Pyloric Stenosis: Treatment entails:

Back 348

surgery

Front 349

Malabsorption syndromes: Autoantibodies are seen to what in Celiac Sprue?

Back 349

Gluten (gliaden) in wheat and other grains

Front 350

Malabsorption syndromes: The histologic appearance of celiac sprue:

Back 350

villous flattening, lymphocytic infiltrate

Front 351

Malabsorption syndromes: Tropical sprue is due to what type of agent?

Back 351

Infectious, treated with Antibiotics

Front 352

Malabsorption syndromes: What are you infected with if you have Whipple's Disease?

Back 352

Tropheryma whipelli

Front 353

Malabsorption syndromes: Histologic cell type seen in Whipple's disease:

Back 353

PAS+ macrophages

Front 354

Malabsorption syndromes: What is the most common disaccharide deficiency leading to malabsorption?

Back 354

lactase => milk intolerance

Front 355

Chronic Gastritis: Fundal gastritis (type A) is characterized by 4 A's, what are they?

Back 355

Autoimmune disorder with Autoantibodies to parietal cells, pernicious Anemia, Achlorydia

Front 356

Chronic Gastritis: Antral gastritis (Type B) is caused by:

Back 356

a Bug, H. Pylori infection

Front 357

Chronic Gastritis: Both forms of gastritis carry an increased risk of what?

Back 357

Gastric carinoma

Front 358

Peptic Ulcer Disease: 2 etiologic agents underlying gastric ulcers are:

Back 358

H. pylori (70%) and NSAID's

Front 359

Peptic Ulcer Disease: Degeneration of what leads to gastric ulcers?

Back 359

Gastric mucosal protection v. gastric acid

Front 360

Peptic Ulcer Disease: Does the pain of a gastric ulcer increase or decrease with meals?

Back 360

Increases => weight loss

Front 361

Peptic Ulcer Disease: One etiologic agent underlies duodenal ulcers - what is it?

Back 361

H. pylori (100%)

Front 362

Peptic Ulcer Disease: 2 pathogenic mechanisms are thought to lead to development of duodenal ulcer - what are they?

Back 362

Increased gastric acid secretion and decreased mucosal protection

Front 363

Peptic Ulcer Disease: What tends to hypertrophy with duodenal ulcers?

Back 363

Bruenner's glands

Front 364

Peptic Ulcer Disease: The margins of a doudenal ulcer are:

Back 364

clean and punched out

Front 365

Peptic Ulcer Disease: The 4 common complications of of duodenal ulcers are:

Back 365

bleeding, penetration, perforation, and obstruction (not necessarily pre-cancerous)

Front 366

Peptic Ulcer Disease: Does the pain of a duodenal ulcer increase or decrease with meals?

Back 366

Decreases => weight gain

Front 367

Peptic Ulcer Disease: How is H.pylori infection treated?

Back 367

triple therapy (metronidazole, bismuth salicylate, amoxocillin or tetracycline) with or without proton pump inhibitor

Front 368

Peptic Ulcer Disease: Does smoking effect peptic ulcer development?

Back 368

Yes, it is 2x as common in smokers

Front 369

IBD: The possible etiology of Crohn's disease is:

Back 369

Infectious

Front 370

IBD: The location and lesion type of Crohn's disease is:

Back 370

Skip lesions in any portion of GI tract, usually terminal ileum, SI, and colon. Rectal sparing.

Front 371

IBD: Gross Morphological features (6) of Crohn's disease are:

Back 371

Transmural inflammation, cobblestone mucosa, creeping fat, bowel wall tickening (string sign on x-ray), linear ulcers, and fissure. (FAT OLD CRONE SKIpING DOWN A COBBLESTONE ROAD)

Front 372

IBD: The microscopic morphological features of Crohn's disease are:

Back 372

non-caseating granulomas

Front 373

IBD: The four major complications of Crohn's disease are:

Back 373

Strictures, fistulas, perianal diease, malabsorption leading to nutritional depletion.

Front 374

IBD: Two major extraintestinal manifestations associated with Chron's disease are:

Back 374

migratory polyarthritis and erythema nodosum

Front 375

IBD: The possible etiology of UC is:

Back 375

autoimmune

Front 376

IBD: Location and lesion type of UC is:

Back 376

continuous lesions of colon with rectal involvement

Front 377

IBD: The two gross morphological features of UC are:

Back 377

mucosal inflammation, friable mucosal pseudopolyps with freely hanging mesentery.

Front 378

IBD: The microscopic morphological features of UC are:

Back 378

crypt abcesses, ulcers

Front 379

IBD: 3 severe complications of UC are:

Back 379

severe stenosis, toxic megacolon, and colorectal carcinoma

Front 380

IBD: Two major extraintestinal manifestations associated with UC are:

Back 380

pyoderma gangrenosum, sclerosing cholangitis

Front 381

Diverticular Disease: Diverticuli are blind pouches found in the:

Back 381

alimentary tract

Front 382

Diverticular Disease: Diverticuli are lined by (3 layers):

Back 382

Mucosa, muscularis, and serosa

Front 383

Diverticular Disease: The 4 GI tract locations of diverticuli are:

Back 383

esophagus, stomach, duodenum and colon

Front 384

Diverticular Disease: Why are most diverticuli termed false?

Back 384

They lack or have an attenuated muscularis mucosa.

Front 385

Diverticular Disease: Percent of older patients likely to get diverticulosis (many diverticula):

Back 385

50% of patients >60

Front 386

Diverticular Disease: The reasons for increasing number of diverticula with age are:

Back 386

Increased intraluminal pressure and focal weaknes in the colonic wall.

Front 387

Diverticular Disease: What type of diet is diverticulosis associated with?

Back 387

low-fiber

Front 388

Diverticular Disease: Sx of diverticulosis?

Back 388

usually asymptomatic, sometimes vague discomfort.

Front 389

Diverticular Disease: Diverticulitis commonly presents with pain where?

Back 389

LLQ

Front 390

Diverticular Disease: Complications of diverticulitis include:

Back 390

perforation, peritonitis, abcess formation, bowel stenosis

Front 391

Intussusception and Volvulus: What is intussuception?

Back 391

telecoping of 1 bowel segment into distal segment.

Front 392

Intussusception and Volvulus: Complication of intussusception is:

Back 392

compromised blood suply.

Front 393

Intussusception and Volvulus: What is volvulus?

Back 393

Twisting of portion of the bowel around its mesentery.

Front 394

Intussusception and Volvulus: What volvulus lead to?

Back 394

obstruction.

Front 395

Stomach Cancer: What is the most common type of stomach cancer?

Back 395

adenocarcinoma

Front 396

Stomach Cancer: Is this cancer aggresive?

Back 396

Yes, it has early aggressive local spread and node/liver mets

Front 397

Stomach Cancer: Stomach Cancer is associated with what 3 etiologic factors?

Back 397

dietary nitrosamines, achlorhydria, chronic gastritis

Front 398

Stomach Cancer: What is stomach cancer termed when it is diffusely infiltrative with thickened and rigid appearance?

Back 398

Linitis plastica

Front 399

Stomach Cancer: What does Virchow's node signify?

Back 399

involvement of supraclavicular node by stomach mets

Front 400

Stomach Cancer: What is Krukenberg's tumor?

Back 400

bilateral stomach cancer mets to the ovary

Front 401

Stomach Cancer: What are characteristics of Krukenberg's tumor?

Back 401

Abundant mucus, "signet ring" cells

Front 402

Hirschprung's Disease: What is Hirschprung's diease?

Back 402

congential megacolon

Front 403

Hirschprung's Disease: What is missing?

Back 403

enteric nerve plexus (both Auerbach's and Meissner's). Seen on biopsy

Front 404

Hirschprung's Disease: What is the cause of this disease?

Back 404

failure of neural crest migration.

Front 405

Hirschprung's Disease: How does this disease present?

Back 405

Chronic constipation early in life.

Front 406

Hirschprung's Disease: Which part of the colon is dilated?

Back 406

That part proximal to the aganglionic segment - aganglionic portion is constricted.

Front 407

Colorectal cancer risk factors: The risk factors are:

Back 407

colorectal villous adenoma, IBD, low-fiber diet, age, FAP, HNPCC, personal and family hx. of colon cancer.

Front 408

Colorectal cancer risk factors: What is Peutz-Jeghers, and does it lead to colorectal cancer?

Back 408

It is a benign polyposis syndrome which is not a risk factor.

Front 409

Colorectal cancer risk factors: Who schould be screened for colorectal cancer and how?

Back 409

People over age 50, screen with stool occult blood test.

Front 410

Cirrhosis/Portal HT: Cirrho in Greek means:

Back 410

tawny yellow

Front 411

Cirrhosis/Portal HT: Cirrhosis is:

Back 411

diffuse fibrosis of the liver with destruction of norml architecture, nodular regeneration.

Front 412

Cirrhosis/Portal HT: Cause of micronodular cirrhosis (nodules <3mm, uniform in size) is:

Back 412

metabolic insult

Front 413

Cirrhosis/Portal HT: Causes of macronodular cirrhosis (nodules >3mm, varied in size) are?

Back 413

Significant liver injury leading to hepatic necrosis (post-infectious, drug-induced hepatitis)

Front 414

Cirrhosis/Portal HT: Cirrhosis is assocated with what type of cancer?

Back 414

hepatocellular carcinoma

Front 415

Cirrhosis/Portal HT: The effects of portal hypertension are:

Back 415

esophageal varices (hemetemesis, melena), peptic ulceration (melena), splenomegaly, caput medusae, ascites, hemmorhoids, and testicular atrophy

Front 416

Cirrhosis/Portal HT: Portal hypertension may be relieved by what method?

Back 416

Portacaval shunt between splenic vein ad left renal vein.

Front 417

Cirrhosis/Portal HT: What are the effects of liver cell failure?

Back 417

Coma, scleral icterus, fetor hepaticus (breath smells like a freshly opened corpse), spider nevi, gynecomastia, jaundice, loss of sexual hair, asterixis, bleeding tendency, anemia, ankle edema

Front 418

Alcoholic Hepatitis: Hepatocytes in alcoholic hepatitis are:

Back 418

swollen and necrotic

Front 419

Alcoholic Hepatitis: Other histologic changes seen in aloholic hepatitis are:

Back 419

neutrophil infiltration, mallory bodies (hyaline), fatty change, and sclerosis areound central vein

Front 420

Alcoholic Hepatitis: SGOT (AST):SGPT (ALT) ratio is:

Back 420

usually more than 1.5 (A Scotch and Tonic: AST elevated)

Front 421

Budd Chiari Syndrome: What is Budd-Chiari Syndrome?

Back 421

Occlusion of the IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease

Front 422

Budd Chiari Syndrome: The features of congestive liver disease are:

Back 422

hepatomegaly, ascites, abdominal pain, and eventual liver failure

Front 423

Budd Chiari Syndrome: Budd-Chiari Syndrome is associated with what 3 conditions:

Back 423

polycythemia vera, pregnancy, hepatocellular carcinoma

Front 424

Wilson's Disease: Wilson's disease is?

Back 424

Coper accumulation, especially in liver, brain and cornea

Front 425

Wilson's Disease: It is due to what?

Back 425

failure of coper to enter circulation in the form of ceruloplasmin

Front 426

Wilson's Disease: What is another name for Wilson's Disease?

Back 426

Hepatolenticular degeneration

Front 427

Wilson's Disease: What are the symptoms of Wilson's Disease? (A,B,C-6,D)

Back 427

Asterixis, basal ganglia degeneration (parkinsonian symptoms), Ceruloplasmin decrease, cirrhosis, corneal deposits (kayser-fleischer rings), coper accumulation, carcinoma (hepatocellular), choreiform movements, Dementia

Front 428

Hemochromatosis: What is hemosiderosis?

Back 428

Deposit of iron (hemosiderin) - this causes hemochromatosis

Front 429

Hemochromatosis: The traid of sx. are?

Back 429

micronodular cirrhosis, pancreatic fibrosis, and skin pigmentation ("bronze" diabetes)

Front 430

Hemochromatosis: Possible complications include?

Back 430

CHF, increased risk of hepatocellular carcinoma

Front 431

Hemochromatosis: What is primary form?

Back 431

inherited, Autosomal recessive

Front 432

Hemochromatosis: What is secondary form due to?

Back 432

chronic transfusion therapy

Front 433

Hemochromatosis: What are ferritin, iron, TIBC and transferrin saturation levels?

Back 433

Ferritin increased, iron increased, TIBC decreased => transferrin saturation is increased

Front 434

Hemochromatosis: How much iron may the body contain?

Back 434

As much as 50g, enough to set off airport metal detectors

Front 435

Hemochromatosis: How is this condition treated?

Back 435

Phlebotomy, deferoxamine

Front 436

Hemochromatosis: AUTHOR

Back 436

Tzevan Poon

Front 437

Jaundice: bacteria convert conjugated bilirubin into what? what happens to some of this?

Back 437

urobilinogen --> some which is reabsorbed, some which is excreted. (urobilinogen that's reabsorbed is converted to urobilin= yellow pigment in urine)

Front 438

Jaundice: which is soluble in water/urine: conjugated or unconjugated bilirubin?

Back 438

conjugted of course!

Front 439

Jaundice: check out the 3 jaundice types: what are they? ***cover up the various parts of the chart in the text and test yourself.

Back 439

heptocellular vs. obstructive vs. hemolytic jaundice

Front 440

Heriditary hyper-bilirubinemias: What is the biochemical disorder in GILBERTS SYNDROME?

Back 440

mild ↓ in UDP-glucuronyl transferase (this is key enzyme in conjugation of bilirubin)

Front 441

Heriditary hyper-bilirubinemias: what are the symptoms?

Back 441

asymptomatic

Front 442

Heriditary hyper-bilirubinemias: what type of bilirubin is seen upon the lab findings? Do you have do you have major hemolysis?

Back 442

unconjugated bilirubin is elevated w/o overt hemolysis

Front 443

Heriditary hyper-bilirubinemias: What is the syndrome called when you have an ABSENCE of UDP-glc-ur-transferase?

Back 443

Crigler-Najjar (CN) syndrome type 1 (type 2 is LESS severe)

Front 444

Heriditary hyper-bilirubinemias: when does it present in life? What is the prognosis?

Back 444

presents early in life: pts die in a few years.

Front 445

Heriditary hyper-bilirubinemias: name 3 findings of C-N syndrome?

Back 445

jaundice, kernicterus, ↑ unconjugated bilirubin

Front 446

Heriditary hyper-bilirubinemias: type 2 is more sever or less severe? What do you treat it with?

Back 446

less severe than type 1; treat type 2 with phenobarbital.

Front 447

Heriditary hyper-bilirubinemias: what do you treat type 1 with (name 2)?

Back 447

plasmapheresis + phototherapy (breaks down unconj. Bilirubin)

Front 448

Heriditary hyper-bilirubinemias: What is Dubin Johnson syndrome?

Back 448

↑↑ hyperbilirubin (conjugated) due to defective liver EXCRETION

Front 449

Heriditary hyper-bilirubinemias: what does the liver look on gross exam?

Back 449

black liver grossly

Front 450

Heriditary hyper-bilirubinemias: what is the name of the less severe syndrome akin to Dubin Johnson?

Back 450

Rotor's syndrome: also no black liver.

Front 451

Heriditary hyper-bilirubinemias: see drawing: it's nice.

Back 451

0

Front 452

Primary sclerosing cholangitis: what is the pathophysiology

Back 452

segmental inflammation and fibrosis of bile ducts: unaffected parts are dilated.

Front 453

Primary sclerosing cholangitis: what test do you do to see this stricture/dilating/beading pattern?

Back 453

ERCP

Front 454

Primary sclerosing cholangitis: what disease is this associated with?

Back 454

Ulcerative Colitis

Front 455

Primary sclerosing cholangitis: What can prim. Scl. Cholangitis lead to?

Back 455

2° biliary cirrhosis/sclerosis

Front 456

Biliary sclerosis : what is the cause of Primary Biliary Sclerosis (PBS)? (compare the name/disease of PBS vs. PSC: primary sclerosing cholangitis)

Back 456

autoimmune disorder with antimitochondrial antibodies

Front 457

Biliary sclerosis : name 3 signs associated with PBS:

Back 457

1) severe obstructive jaundice 2) itching 3) hypercholesterolemia (xanthoma)

Front 458

Biliary sclerosis : What is the cause of SBS: secondary biliary sclerosis?

Back 458

EXTRA-hepatic biliary obstruction → ↑ pressure in INTRA-hepatic ducts → ↑ injury/sclerosis

Front 459

Biliary sclerosis : what is 2° biliary sclerosis associated with (name 3 things)?

Back 459

ascending cholangitis (bacterial infection), bile stasis, and bile lakes

Front 460

Heptocellular carcinoma = hepatoma: in liver cancers, is this common?

Back 460

yes, #1 most common!

Front 461

Heptocellular carcinoma = hepatoma: there is an ↑ incidence of hepatoma due to what diseases/exposures (name 7)

Back 461

1) hep B, 2) hep C, 3) Wilson's disease, 4) hemochromatosis, 5) a-antitrypsin def 6) EtOH cirrhosis 6) carcinogens (e.g. aflatoxin B1)

Front 462

Heptocellular carcinoma = hepatoma: How do hepatomas spread? How does this differ with renal cell ca. spread?

Back 462

They BOTH commonly spread hematogenously!

Front 463

Heptocellular carcinoma = hepatoma: What is major lab finding with hepatocelluar ca?

Back 463

↑ AFP (alpha fetoprotein)

Front 464

Reye's syndrome = rare!!! But…: What is this syndrome?

Back 464

Hepato-encephalopathy: fatal: occurs in childhood

Front 465

Reye's syndrome = rare!!! But…: name 3 findings:

Back 465

1) fatty liver w/ microvesicular fatty change 2) hypoglycemia, 3) coma

Front 466

Reye's syndrome = rare!!! But…: is this associated with any outside factors/triggering factors?

Back 466

yes: 1) viral infection (esp. VZV or influenza B) 2) salicylates!!!

Front 467

Reye's syndrome = rare!!! But…: if baby/child has fever what do you use in place of aspirin?

Back 467

use acetaminophen (but with caution): i.e. acetaminophen OD hepato-toxicity

Front 468

Gallstones: name 3 types of stones and tell me how they show up on CT scan:

Back 468

1) cholesterol stone (radiolucent but 10-20% opaque due to calcification) 2) mixed stone = cholesterol + pigment (radiolucent) 3) pigment stone (radio-opaque)

Front 469

Gallstones: Which is the most common type of gall stone?

Back 469

mixed stone

Front 470

Gallstones: name at least 5 out 9 risk factors for Cholesterol stones: is there a mnemonic?

Back 470

1) obesity 2) Crohn's D 3) Cystic fibrosis 4) elderly 5) clofibrate 6) estrogens 7) multiparity 8) rapid weight loss 9) native American origin mnemonic = 4 F's fat, female….

Front 471

Gallstones: name 4 risk factors for pigment stones:

Back 471

1) pts with chronic RBC hemolysis 2) alcoholic cirrhosis 3) elderly 4) biliary infection

Front 472

Gallstones: What is a good way to diagnosis stones?

Back 472

ultrasound

Front 473

Gallstones: What is CHARCOT'S TRIAD

Back 473

1) epigastric/RUQ pain 2)fever 3) jaundice

Front 474

Acute pancreatitis: this is what our US attorney general had. : pathophysiology mechanism?

Back 474

activation and thus autodigestion by pancreatic enzymes

Front 475

Acute pancreatitis: this is what our US attorney general had. : Causes? (good mnemonic)

Back 475

Get Smashed (EtOH will can lead to AP) = 1) Gallstones 2) EtOH 3) Trauma 4) Steroids 5) Mumps 6) autoimmune disease 7) scorpion sting of all things! 8) hyperlipidemia 9) drugs

Front 476

Acute pancreatitis: this is what our US attorney general had. : clinically presents with?

Back 476

intense epigastric pain radiating to back

Front 477

Acute pancreatitis: this is what our US attorney general had. : labs(name 2): which of the two has a higher specificity?

Back 477

↑ amylase + ↑lipase (higher specificity) "li is hi"

Front 478

Acute pancreatitis: this is what our US attorney general had. : Name 5 nasty complications that can result from AP?

Back 478

1) DIC 2) ARDS 3) diffuse fat necrosis 4) hypocalcemia 5) pseudocyst formation

Front 479

Acute pancreatitis: this is what our US attorney general had. : if you have CHRONIC pancreatitis: what do we think of your life habits?

Back 479

Chronic Pancr. Is strongly associated w/ alcoholism

Front 480

Pancreatic cancer: what is a common and fatal pancreatic cancer?

Back 480

pancreatic adenocarcinoma

Front 481

Pancreatic cancer: what is the prognosis?

Back 481

6 months: very aggressive: usually has mets when pt. presents

Front 482

Pancreatic cancer: where are tumors most commonly located? And what does this lead to?

Back 482

pancreatic head → obstructive jaundice.

Front 483

Pancreatic cancer: PATHOLOGY-RESPIRATORY SECTION

Back 483

0

Front 484

COPD = also known as OLD: obstructive lung disease: why is it called obstructive?

Back 484

obstruction of AIR FLOW → air traping in lungs

Front 485

COPD = also known as OLD: obstructive lung disease: what is the major PFT finding?

Back 485

FEV1 / FVC ration is ↓ (hallmark finding)

Front 486

COPD = also known as OLD: obstructive lung disease: name the 4 types of COPD

Back 486

1) Chronic Bronchitis (Blue Bloater) 2) emphysema (pink puffer) 3) asthma 4) bronchietasis

Front 487

COPD = also known as OLD: obstructive lung disease: what is the definition of Chronic Bronchitis

Back 487

productive cough for >3 consecutive months in two or more years.

Front 488

COPD = also known as OLD: obstructive lung disease: what do you expect on lung histology?

Back 488

hypertrophy of mucus-secreting glands in the bronchioles (Reid index of >50%)

Front 489

COPD = also known as OLD: obstructive lung disease: leading cause is smoking: what are the physical findings for Chronic Bronchitis? (name 3)

Back 489

1)cyanosis 2) wheezing 3) crackles

Front 490

COPD = also known as OLD: obstructive lung disease: what is the pathophysiological mechanism of EMPHYSEMA?

Back 490

destruction of fibrous septa/alveolar walls → enlargement of air space and ↓ total surface area for gas exchange

Front 491

COPD = also known as OLD: obstructive lung disease: if the cause is smoking, what kind of emphysema would you see on histo slide?

Back 491

centri-acinar emphysema

Front 492

COPD = also known as OLD: obstructive lung disease: what else can cause emphysema: (also may work synergistically with smoking): What kind of findings do you see in lung histo and name another organ affected?

Back 492

alpha 1-antitrypsin deficiency → panacinar emphysema + liver cirrhosis

Front 493

COPD = also known as OLD: obstructive lung disease: what causes the emphysema in this disorder?

Back 493

↑ elastase activity to damage lung tissue.

Front 494

COPD = also known as OLD: obstructive lung disease: name 4 findings of emphysema (in general)

Back 494

1) dyspnea; 2) ↓ breath sounds 3) tachycardia 4) ↓ I/E ratio

Front 495

COPD = also known as OLD: obstructive lung disease: What is mechanism of asthma

Back 495

BRONCHIAL hypersensitivity/hyperresponsiveness → REVERSIBLE bronchoconstriction

Front 496

COPD = also known as OLD: obstructive lung disease: name 3 common triggers

Back 496

1) viral URI 2) allergens 3) stress!!

Front 497

COPD = also known as OLD: obstructive lung disease: name 7 findings

Back 497

1) cough 2) wheezing 3) dyspnea 4) hypoxemia 5)↓ I/E ratio 6) tachypnea 7) pulsus paradoxus

Front 498

COPD = also known as OLD: obstructive lung disease: BRONCHIECTASIS: what is its mechanism??

Back 498

chronic necrotizing infection of BRONCHI → dilated airways, purulent sputum, recurrent infections, hemoptysis (see Robbins for a good discussion of this)

Front 499

COPD = also known as OLD: obstructive lung disease: what disorders is bronchietasis commonly associated with?

Back 499

1) bronchial obstruction 2) cystic fibrosis 3) poor ciliary motility

Front 500

Restrictive Lung Disease (RLD): What are classic PFT findings for RLD?

Back 500

↓ VC ↓TLC ; FEV1/FVC ration > 80%

Front 501

Restrictive Lung Disease (RLD): Name the two MAJOR types of RLD

Back 501

1) poor breathing mechanics (EXTRA-pulmonary) 2) Interstitial lung diseases

Front 502

Restrictive Lung Disease (RLD): cover up various parts of the text/table/outline to test yourself on the following: 1) 2 types of poor breathing mechanics 2) 8 types of interstitial disease that give you a restrictive picture.

Back 502

0

Front 503

Lung Physical Findings: cover up parts of the very good table to test yourself on various findings.

Back 503

0

Front 504

Lung Physical Findings: Obstructive vs. Restrictive findings

Back 504

0

Front 505

Lung Physical Findings: Name 3 lung volumes that are increased in COPD

Back 505

↑TLC, ↑FRC, ↑RV

Front 506

Lung Physical Findings: What 2 values are BOTH reduced in COPD and RLD?

Back 506

1) FEV1 and 2) FVC (think FEV1/FVC ratio) NOTE! in COPD, FEV1 is more dramatically reduced and thus the FEV1/FVC ratio is ↓

Front 507

Asbestosis = long latency = think shipbuilders and plumbers: what is the main pathology resulting from asbestosis?

Back 507

DIFFUSE, interstitial fibrosis caused by inhaled asbestos Fibers.

Front 508

Asbestosis = long latency = think shipbuilders and plumbers: What cancers are increased in pts with asbestosis?

Back 508

1) pleural mesothelioma 2) bronchogenic carcinoma (BC)

Front 509

Asbestosis = long latency = think shipbuilders and plumbers: Major finding in lung?

Back 509

Ferruginous bodies: asbestos fibers coated with hemosiderin also 2) ivory white pleural plaques

Front 510

Neonatal respiratory distress syndrome: What is the main cause

Back 510

surfactant deficiency --> to increased surface tension --> alveolar collapse

Front 511

Neonatal respiratory distress syndrome: surfactant is made by which cells? After when?

Back 511

type 2 pneumocytes after 35th gestational week

Front 512

Neonatal respiratory distress syndrome: what do you measure? Where do you get this fluid?

Back 512

lecithin-to-sphingomyelin ratio in the amniotic fluid = measure of lung maturation <1.5 in neonatal distress syndrome

Front 513

Neonatal respiratory distress syndrome: what is surfactant made of (chemical name)

Back 513

dipalmitoyl phosph-tidyl-choline (DP-PTC)

Front 514

Neonatal respiratory distress syndrome: treatment for poor maturation of lungs

Back 514

1) before birth = maternal steroids 2) after= artificial surfactant

Front 515

Karta-gener's syndrome: what is this?

Back 515

immotile cilia due to dynein arm defect

Front 516

Karta-gener's syndrome: results in what in female and male? (4 things)

Back 516

1) sterility (in male sperm also immotile) 2)bronchietasis 3)recurrent sinusitis (bacteria & particles not pushed out) 4) associated with situs inversus (e.g. dextro-cardia)

Front 517

Lung Cancer: name the 3 main classes of cancers that affect parts of the lung

Back 517

1) bronchogenic carcinoma (with different subtypes) 2) carcinoid tumor 3) metastasis

Front 518

Lung Cancer: list the 5 types of major bronchogenic carcinomas

Back 518

CENTRAL 1) squamous cell ca 2)small cell ca PERIPHERAL 3) adenocarcinoma 4) bronchoalveolar ca 5) large cell ca

Front 519

Lung Cancer: mnemonic: what is meant by SPHERE of symptoms?

Back 519

S= superior vena cava syndrome; P= pancoast tumor; H= Horner's syndrome; E= Endocrine (paraneoplastic); Recurrent laryngeal / hoarseness; E = Effusions (pleural OR pericardial)

Front 520

Lung Cancer: What can a CARCINOID tumor cause?

Back 520

Carcinoid Syndrome = flushing, diarrhea, wheezing, and salivation

Front 521

Lung Cancer: Metastases to lung is very common, LUNG cancer also prone to metastasize to what other parts?

Back 521

1) brain (epilepsy) 2) bone (fracture) 3)liver (jaundice + hepatomegaly)

Front 522

Pancoast tumor: What is it?

Back 522

it's a carcinoma of the apex of lung

Front 523

Pancoast tumor: what may it affect?

Back 523

may affect CSP= cervical sympathetic plexus causing Horner's syndrome

Front 524

Pancoast tumor: what is Horner's syndrome?

Back 524

P.A.M. is Horny = Ptosis, Anhydrosis, Miosis

Front 525

Pneumonia: 1st AID breaks it down into TYPE/ ORGANISM/ CHARACTERISTICS = cover parts of this table and fill in the blanks

Back 525

0

Front 526

Pneumonia: Lobar Pneumonia; Organism(s) and characteristics

Back 526

Pneumococcus; intraalveolar exudate -> consolidation, may involve entire lung

Front 527

Pneumonia: Bronchopneumonia: Organism and characteristics

Back 527

S aureus, H flu, Klebsiella, S pyogenes; Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving >= 1 lobes

Front 528

Pneumonia: Interstitial pneumonia; Organism(s) and characteristics

Back 528

Viruses, mycoplasma, legionella; diffuse patchy inflammation localized to interstitial areas at alvolar walls; distribution involving >= 1 lobes

Front 529

Pneumonia: PATHOLOGY - NEUROLOGIC

Back 529

0

Front 530

Degenerative diseases: name two diseases that affect the CEREBRAL CORTEX

Back 530

1) Alzheimer's disease 2) Pick's disease

Front 531

Degenerative diseases: name two diseases that affect BASAL GANGLIA & BRAIN STEM:

Back 531

1) Huntington's disease 2) Parkinson disease

Front 532

Degenerative diseases: name 5 diseases that affect SPINOCEREBELLAR MOTOR NEURON

Back 532

1) Olivo-ponto-cerebellar atrophy 2) Friedreich's ataxia 3)ALS = amyotrophic lateral sclerosis 4)Werdnig-Hoffmann disease 5) Polio

Front 533

Degenerative diseases: what is the most common cause of elderly dementia?

Back 533

Alzheimer's

Front 534

Degenerative diseases: name two pathological findings characteristic of Alzheimer's

Back 534

1) senile plaques = intracytoplasmic inclusion bodies 2) neurofibrillary tangles (abnormally phosphorylated tau protein)

Front 535

Degenerative diseases: what is the 2nd most common cause of dementia in elderly?

Back 535

multi-infarct dementia in elderly\\

Front 536

Degenerative diseases: How can Alzheimer also affect intracranial vasculature?

Back 536

amyloid angiopathy --> intracranial hemorrhage

Front 537

Degenerative diseases: The familial form of Alzheimer's is associated with what chromosomes (name 4) and (name the allele's name in 2 of the 4)

Back 537

chromosome 1, 14, 19 (APO-E4 allele), 21 (p-Ap gene)

Front 538

Degenerative diseases: What is pathognemomic with Pick's disease upon histology?

Back 538

Pick bodies = intra-cytoplasmic inclusion bodies

Front 539

Degenerative diseases: What cortical areas does Pick's disease affect

Back 539

Frontal and temporal lobes (remember; sharp, atrophic apearance of gross specimen)

Front 540

Degenerative diseases: What is the inheritance pattern of Huntington's

Back 540

Auto Dominant

Front 541

Degenerative diseases: What are some symptoms?

Back 541

1) chorea 2) dementia

Front 542

Degenerative diseases: Huntington's is due to atrophy of _____ what? Loss of ___ ergic neurons.

Back 542

atrophy of caudate nucleus = loss of GABA-nergic neurons

Front 543

Degenerative diseases: what is the genetic abnormality of Huntington's?

Back 543

1) Chr. 4 - expansion of CAG repeats

Front 544

Degenerative diseases: Parkinson disease is associated with what pathology findings?

Back 544

1) Lewy bodies 2) depigmentation of substantia nigra (loss of dopaminergic neurons)

Front 545

Degenerative diseases: rare cases of Parkinson's have been linked to what contaminant of certain illicit drugs?

Back 545

MPTP = contaminant to street drug

Front 546

Degenerative diseases: Parkinson's can make you feel in a "TRAP" = ?

Back 546

T = tremor at rest; R = cogwheel rigidity; A = akinesia ; Postural instability

Front 547

Degenerative diseases: ALS = Lou Gehrig's disease (the Iron Horse of the Yankees, hero of Joe DiMaggio) = what signs is ALS associated with?

Back 547

Both UMN and LMN deficits

Front 548

Degenerative diseases: Werdnig-Hoffman disease - presents as birth as?

Back 548

1) flopy baby syndrome 2) note tongue fasciculations as well (also seen in ALS)

Front 549

Degenerative diseases: for Polio, what kind of signs to you see?

Back 549

predominantly LMN deficits.

Front 550

Intracranial Hemorrhage/Hemotomas: name 4 types of cranial related hemorrhages (think of layers that could possibly be involved)

Back 550

1) epidural hemorrhage 2) subdural h 3) subarachnoid h 4) parenchymal h

Front 551

Intracranial Hemorrhage/Hemotomas: what is a common site of epidural hematoma/hemorrhage

Back 551

1) rupture of MMA: middle meningeal artery, often 2ndary to fracture of temporal bone

Front 552

Intracranial Hemorrhage/Hemotomas: what does CT show for epidural h?

Back 552

biconcave disc NOT crossing suture lines

Front 553

Intracranial Hemorrhage/Hemotomas: what else do you see?

Back 553

lucid interval

Front 554

Intracranial Hemorrhage/Hemotomas: How do subdural h. most often occur?

Back 554

rupture of bridging veins (think, elderly being jolted in roller coaster)

Front 555

Intracranial Hemorrhage/Hemotomas: this is venous bleeding so how would this influence symptomatic findings?

Back 555

venous = less pressure = delayed onset of symptoms

Front 556

Intracranial Hemorrhage/Hemotomas: what types of people do you see subdural h.?

Back 556

1) elderly, 2) alcoholics 3) blunt trauma/sudden change in velocity injuries

Front 557

Intracranial Hemorrhage/Hemotomas: for SUBDURALs what do you see upon CT?

Back 557

1) crescent-shaped hemorrhage instead 2) YES IT does cross the suture lines

Front 558

Intracranial Hemorrhage/Hemotomas: subarachnoid hemorrhage is often seen where (name 2 types

Back 558

rupture of 1) aneurysm (usually Berry aneurysm) or an 2)AVM

Front 559

Intracranial Hemorrhage/Hemotomas: symptoms?

Back 559

the worst headache of my life

Front 560

Intracranial Hemorrhage/Hemotomas: since its subarachnoid, what do you see on what test?

Back 560

bloody or xanthochromic CSF on spinal tap

Front 561

Intracranial Hemorrhage/Hemotomas: name 4 risk factors for parenchymal hematoma

Back 561

1) HTN 2) amyloid angiopathy 3) diabetes mellitus 4) tumor

Front 562

Intracranial Hemorrhage/Hemotomas: AUTHOR

Back 562

Hilcias Duran

Front 563

Berry aneurysms: most common site for Berry aneurysms

Back 563

bifurcation of the anterior communicating artery (Circle of Willis)

Front 564

Berry aneurysms: berry aneurysms are associated with

Back 564

adult polycystic disease, Ehlers-Danlos s., and marfan's

Front 565

Berry aneurysms: Classic triad of Multiple Sclerosis

Back 565

SIN: Scanning speech, intention tremor, nystagmus (affect woman 20-30s)

Front 566

Berry aneurysms: Prevalence of MS

Back 566

increase prevalence w/ increased distance from the equator

Front 567

Berry aneurysms: Clinical s/s of MS

Back 567

periventricular plaques, preservation of axons, loss of oligodentrocytes, reactive astrocystic gliosis, increased protein in csf(IgG) in CSF, relapsing course, optic neuritis, MLF syndrome, hemiparesis, bladder/bowel incontinence)

Front 568

Berry aneurysms: Progressive multifocal leukoencephalopathy (PML) is associated w/

Back 568

JC virus and seen in 2-4 % of AIDS pts (reactivation or latent infect)

Front 569

Berry aneurysms: pathogenesis of Guillian-Barre syndrome

Back 569

Inflammation and demyelination of peripheral nerves and motor fibers of the ventral roots (sensory effec less severe than motor)

Front 570

Berry aneurysms: s/s of Guillian-Barre syndrome

Back 570

symmetrical ascending muscle weakness beginning in the distal lower extremities. Autonomic fxn may be severely affected (eg. Cardiac irregularities, HTN, or hypoTN) Findings: inc. csf protein w/ normal cell count ("albumino-cytologic dissociation") elevated protein may lead to papilledema

Front 571

Berry aneurysms: association between G-B syndrome and…

Back 571

herpesvirus or camplobacter jejuni infection, inoculations, and stress but no definitive link to a pathogen

Front 572

Poliomyelitis: organism causing polio and mechanism of action

Back 572

poliovirus, transmitted via fecal oral route and enters blood stream then into CNS where it causes destruction of the anterior horn of S.C. leading in turn to LMN destruction

Front 573

Poliomyelitis: s/s of polio

Back 573

malaise, HA, fever, nausea, abd. Pain, sore throats, signs of LMN signs

Front 574

Poliomyelitis: finding of polio

Back 574

csf w/ lymphocytic pleocytosis w/ slight elevation of protein, virus recovered from stool or throat

Front 575

Aphasia : describe Broca's (expressive) aphasia

Back 575

confluent aphasia w/ intact comprehension broca's is broken speech

Front 576

Aphasia : describe Wernicke's (aphasia)

Back 576

Fluent aphasia w/ impaired concentration Wernick's ="What?" W area located in superior temperal gyrus

Front 577

seizures : describe two types of partial seizures

Back 577

1.simple partial (awareness is intact)--motor, sensory, autonomic, psychic 2.Complex partial (impaired awareness)

Front 578

seizures : describe types of Generalized seizure ( diffuse)

Back 578

1.absence- blank stare (petit mal) 2.myoclonic- quick repetitive jerks 3.tonic-clonic- alternating stiffening and mvmt (grand mal) 4. Tonic- stiffening 5.atonic-"drop" seizures

Front 579

seizures : what are the causes of seizures in children?

Back 579

genetic, infection, trauma, congenital, metabolic

Front 580

seizures : adults?

Back 580

tumors, trauma, stroke, infection

Front 581

seizures : elderly?

Back 581

stroke, tumor, trauma, metabolic, infection

Front 582

Horner's syndrome: what is Horner's syndrome?

Back 582

sympathectomy of face (lesion above T1) 1.Ptosis 2.anhidrosis and flushing of affected side 3.miosis [PAM is horny]

Front 583

Horner's syndrome: Horner's syndrome is associated w/ what type of tumor?

Back 583

pancoast tumor

Front 584

syringomyelia: what is syringomyelia?

Back 584

enlargement of the central canal of the S.C. Crossing fibers of spinothalamic tract are damaged.

Front 585

syringomyelia: what are the s/s of syringomyelia?

Back 585

b/l loss of pain and temp sensation in the uper extremities w/ the touch sensation. Most common at C8-T1

Front 586

syringomyelia: commonly seen in what pts?

Back 586

pts w/ Arnold-Chiari malformation

Front 587

Tabes dorsalis : what infection is tabes dorsalis associated w/?

Back 587

teriary syphilis

Front 588

Tabes dorsalis : what happens in the CNS?

Back 588

degeneration of dorsal columns and dorsal root

Front 589

Tabes dorsalis : dorsalis also is associated with what s/s?

Back 589

charcot's joint, shooting (lightning) pain, Argyll Robertson pupils, and absence of DTRs

Front 590

Osteoarthritis : what occurs in OA?

Back 590

mechanical wear and tear of the joints, leads to destruction of the articular cartilage, subchondral bone formation, sclerosis, osteophytes, eburnation, Herberden's nodes (DIP), and Bouchard's nodes (PIP)

Front 591

Osteoarthritis : classical presentation of OA?

Back 591

pain in weight bearing joints after use (worse at the end of the day0 improves w/ rest. No systemic symptoms

Front 592

Rheumatoid Arthritis : what happens in in RA?

Back 592

autoimmune inflammatory proccess which affects synovial joints, w/ pannus formation in joints (MCP, PIP), S-Q rheumatoid nodules, ulnar deviation,subluxation

Front 593

Rheumatoid Arthritis : classical presentation of RA?

Back 593

female, 80% pts Rf positive (anti-IgG Ab) morning stiffness improving w/ use, symmetrical joint involvement, and systemic symptoms (fever, fatigue, pleurtis, pericarditis)

Front 594

Rheumatoid Arthritis : AUTHOR

Back 594

Jason Portnof

Front 595

Sjogren's Syndrome: What is the classic triad of Sjogren’s syndrome?

Back 595

dry eyes (conjunctivitis, xeropthalmia), dry mouth (dysphagia, xerostomia), arthritis

Front 596

Sjogren's Syndrome: What is SICCA syndrome?

Back 596

dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis

Front 597

Sjogren's Syndrome: T/F Sjogren’s syndrome predominantly affects males between 40 and 60 years of age.

Back 597

False. Females between 40 and 60 y.o are predominantly affected in Sjogren’s syndrome.

Front 598

Gout: T/F Gout is the precipitation of monosodium urate crystals into joints due to hyperuricemia.

Back 598

TRUE

Front 599

Gout: What is the favored manifestation of gout?

Back 599

Podagra. (painful MTP joint)

Front 600

Gout: The crystals of gout are:

Back 600

needle shaped and negatively bifringent

Front 601

Pseudogout: T/F Pseudogout is the precipitation of calcium pyrophosphate crystals within the joint space.

Back 601

TRUE

Front 602

Pseudogout: The crystals of psuedogout are:

Back 602

basophilic, rhomboid crystals

Front 603

Pseudogout: Psudogout usually affects:

Back 603

Large joints (classically the knee)

Front 604

Pseudogout: T/F Both gout and psuedogout predominantly affect men.

Back 604

False. Gout is more common in men. Pseudogout affects both sexes equally, most pts are >50 years old.

Front 605

Pseudogout: T/F The treatment for both pseudogout and gout is allopurinol, probenecid, colchicines, and NSAIDS.

Back 605

False. That is the tx for gout. However, there is no tx for pseudogout.

Front 606

Celiac sprue: Celiac sprue is the autoimmune-mediated intolerance of what substance, leading to steatorrhea?

Back 606

gliadin (wheat)

Front 607

Celiac sprue: T/F Findings in Celiac sprue include blunting of villi, neutrophils in the lamina propria, and abnormal D-xylose test.

Back 607

False. lymphocytes, not neutrophils are found in the lamina propria.

Front 608

Systemic Lupus Erythematosus: What drugs can produce a SLE-like syndrome that is commonly reversible?

Back 608

HIp: Hydralazine, INH, Phenytoin, Procainamide

Front 609

Systemic Lupus Erythematosus: SLE causes LSE. What is LSE?

Back 609

Libman Sacks Endocarditis. Valvular vegetations found on both sides of valve (Mitral Valve Stenosis) and do not embolize.

Front 610

Systemic Lupus Erythematosus: T/F 90% Systemic lupus erythematousus pts are female between ages 14 and 45. SLE is most common and severe in black females.

Back 610

Both statements are true

Front 611

Systemic Lupus Erythematosus: What are 4 lab tests in SLE? Which test, when positive is predictive of a poor prognosis?

Back 611

1. ANA (antinuclear antibodies)- sensitive, not specific for SLE, 2. anti-ds DNA (antibodies to double stranded DNA)- very specific, poor prognosis, 3. Anti-Smith antibodies (anti-Sm)- very specific, but not prognostic, 4. Antihistone antibodies- drug induced lupus

Front 612

Systemic Lupus Erythematosus: In what organ are wire loop lesions found in SLE?

Back 612

kidney (with immune complex deposition and nephrotic syndrome)

Front 613

Systemic Lupus Erythematosus: What causes death commonly in SLE?

Back 613

Renal failures and infections

Front 614

Systemic Lupus Erythematosus: What are symptoms of SLE?

Back 614

fever, fatigue, wt loss, joint pain, malar rash, photosensitivity. Also: pleuritis, pericarditis, nonbacterial verrucous endocarditis, Raynaud’s phenomenon

Front 615

Sarcoidosis: What disease is characterized by gamaglobulinemia, rheumatoid arthritis, ace increase, interstitial fibrosis, and noncaseating granulomas?

Back 615

Sarcoidosis

Front 616

Seronegative spondyloarthropathies: Name 2 seronegative spondyloarthropathies.

Back 616

ankylosing spondylitis, reiters’ syndrome

Front 617

Seronegative spondyloarthropathies: What is a seronegative spondyloarthropathy?

Back 617

Arthritis without rheumatoid factor (no anti-IgG Ab). Strong association with HLA-B27 (gene that codes for HLA MHC1)

Front 618

Seronegative spondyloarthropathies: T/F seronegative spondyloarthropahties occur more often in males

Back 618

TRUE

Front 619

Seronegative spondyloarthropathies: What is the classic triad for Reiter’s syndrome?

Back 619

Urethritis, conjunctivitis and anterior uveitis, arthritis. “Can’t see, can’t pee, can’t climb a tree”

Front 620

Seronegative spondyloarthropathies: T/F reiter’s syndrome occurs commonly post respiratory or chlamydia infections.

Back 620

False. Post-GI or chlamydia infections

Front 621

Seronegative spondyloarthropathies: Describe ankylosing spondylitis

Back 621

Chronic inflammatory disease of spine and sacroiliac joints. Ankylosis (stiff spine), uveitis and aortic regurg.

Front 622

Scleroderma: T/F Crest syndrome is wider-spread than diffuse scleroderma.

Back 622

False. Diffuse scleroderma has widespread skin involvement, rapid progression, early visceral involvement. CREST syndrome has limited skin involvement, often confined to fingers and face. More benign clinical course.

Front 623

Scleroderma: T/F Crest syndrome occurs in male pts that have allergic rxn to toothpaste.

Back 623

False. CREST= calcinosis, raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia.

Front 624

Scleroderma: What antibodies are associated with scleroderma (progressive systemic sclerosis- PSS)?

Back 624

"diffuse scleroderma- anti-Scl-70 antibody, Crest syndrome- anticentromere antibody

Front 625

Skin disorders: T/F Pemphigus vulgaris is described as an autoimmune disorder with IgG antibody against epidural basement membrane (linear immunofluorescence). Affects skin but spares oral mucosa.

Back 625

False. That description is for Bullous pemphigoid (less severe disease than Pemphigus vulgaris). Pemphigus vulgaris is a potentially fatal autoimmune skin disorder. Intradermal bullae involve the oral mucosa and skin. Findings include acantholysis, IgG ab against epidermal cell surface.

Front 626

Skin disorders: T/F Dermatitis is a group of inflammatory pruritic skin disorders. The etiology is allergy (usually type IV hypersensitivity), chemical injury, or infection.

Back 626

TRUE

Front 627

Skin disorders: What HLA groups are associated with psoriasis?

Back 627

HLA-B27, HLA-13, HLA-17

Front 628

Skin disorders: What is psoriasis? Where is it most commonly found?

Back 628

Psoriasis is nonpruritic chronic inflammation of the skin, particularly on the knees and elbows.

Front 629

Goodpasture's: T/F Goodpasture’s syndrome affects the lungs and liver.

Back 629

False. Lungs and Kidneys. (Pulmonary hemorrhagesà hemoptysis, renal lesionsà hematuria, anemia, crescentic glomerulonephritis)

Front 630

Goodpasture's: What type of Abs are associated with Goodpastures?

Back 630

anti-glomerular basement membrane abs produce linear staining on immunofluorescence.

Front 631

Goodpasture's: Who commonly gets Goodpastures?

Back 631

Men between 20-40 years.

Front 632

Cushing's syndrome: What are etiologies of Cushing’s syndrome? Is ACTH always elevated?

Back 632

increased cortisol due to:, 1. Cushing’s disease (primary pituitary adenoma) increased ACTH, 2. Primary adrenal (hyperplasia/neoplasia) decreased ACTH, 3. Ectopic ACTH production (ie- small cell lung ca) increased ACTH, 4. Iatrogenic, decreased ACTH

Front 633

Cushing's syndrome: Describe the clinical picture of Cushings.

Back 633

HTN, wt gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin change (thinning, striae), osteoporosis, immune supression

Front 634

Hyperaldosteronism: T/F Conn’s syndrome is secondary hyperaldosteronism.

Back 634

False. Conn’s syndrome is primary hyperaldosteronism, caused by an aldosterone-secreting tumor. Results in HTN, hypokalemia, metabolic alkalosis, low plasma renin.

Front 635

Hyperaldosteronism: Which hyperaldosteronism is associated with high plasma renin?

Back 635

Secondary hyperaldosteronism. It is due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin-angiotensin sysem.

Front 636

Hyperaldosteronism: What is the tx for hyperaldosteronism?

Back 636

Spironolactone, a diuretic that works by acting as a aldosterone antagonist.

Front 637

Addison's Disease: What characterizes addison’s disease? (which hormones are elevated or deficient)? Is it associated with HTN or hypotension?

Back 637

Primary deficiency of aldosterone and cortisol due to adrenal atrophy, causing hypotension and skin hyperpigmentation. Adrenal atrophy, absence of hormone production, involves all 3 cortical divisions.

Front 638

Addison's Disease: T/F In primary insufficiency decreased pituitary ACTH production is characterized by skin hyperpigmentation.

Back 638

False: increased ACTH causes MSH activity & hyperpigmentation

Front 639

Tumors of adrenal medulla: T/F Neuroblastoma is the most common tumor of adrenal medulla in adults.

Back 639

False. Pheochromocytoma is the most common tumor of adrenal medulla in adults. It is derived from chromaffin cells (arise from neural crest). It is associated with neurofibromatosis MEN types II and III.

Front 640

Tumors of adrenal medulla: Where does neuroblastoma occur?

Back 640

Neuroblastoma is the most common tumor of adrenal medulla in children. It can occur anywhere along the sympathetic chain.

Front 641

Tumors of adrenal medulla: AUTHOR

Back 641

Jason Lee

Front 642

Pheochromocytoma: secrete combination of two molecules

Back 642

epinephrine and norepinephrine

Front 643

Pheochromocytoma: epidemiology (rule of 10's)

Back 643

10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids, 10% familial

Front 644

Pheochromocytoma: symptoms - 5 P's

Back 644

(elevated blood) Pressure, Pain (headache), Perspiration, Palpitations, Pallor/diaphoresis --> relapsing and remittant

Front 645

Pheochromocytoma: elevations in two lab values

Back 645

urinary VMA and serum catecholamines

Front 646

Pheochromocytoma: association with two other endocrine diseases

Back 646

MEN II and III

Front 647

Pheochromocytoma: treatment

Back 647

alpha-antagonists

Front 648

Multiple Endocrine Neoplasia: type I (Wermer's syndrome) - 3 P's

Back 648

Pancreas, Pituitary, and Parathyroid tumors

Front 649

Multiple Endocrine Neoplasia: type II (Sipple's syndrome)

Back 649

medullary carcinoma of thyroid, pheochromocytoma, parathyroid tumor, or adenoma

Front 650

Multiple Endocrine Neoplasia: type III

Back 650

medullary carcinoma of thyroid, pheochromocytoma, oral/intestinal ganglioneuromatosis

Front 651

Hypothyroidism and hyperthyroidism: myxedema is prominent in which one

Back 651

hypothyroidism

Front 652

Hypothyroidism and hyperthyroidism: chest pain, palpitations, arrhythmias

Back 652

hyperthyroidism

Front 653

Hypothyroidism and hyperthyroidism: TSH is (increased/decreased) in primary hyperthyroidism? In primary hypothyroidism?

Back 653

hyper - decreased, hypo - increased

Front 654

Hypothyroidism and hyperthyroidism: Graves' disease involves autoantibodies with what mechanism of action?

Back 654

stimulation of TSH receptors

Front 655

Hypothyroidism and hyperthyroidism: three symptoms of Graves'

Back 655

ophthalmopathy, pretibial myxedema, diffuse goiter

Front 656

Hypothyroidism and hyperthyroidism: Graves' is a type __ hypersensitivity

Back 656

type II

Front 657

Hashimoto's thyroiditis: thyroid is (enlarged/not enlarged) and (tender/nontender)

Back 657

enlarged, nontender

Front 658

Hashimoto's thyroiditis: autoimmune antibodies directed against ---

Back 658

microsomes

Front 659

Hashimoto's thyroiditis: histology shows (type of cell) infiltrate

Back 659

lymphocytes (with germinal centers)

Front 660

Subacute thyroiditis (de Quervain's): self-limited (hyper/hypo)thyroidism following ---

Back 660

hypothyroidism following flu-like illness

Front 661

Subacute thyroiditis (de Quervain's): symptoms include

Back 661

jaw pain, tender thyroid gland, early hyperthyroidism

Front 662

Thyroid cancer: most common, good prognosis, "ground glass" nuclei, psammoma bodies

Back 662

papillary carcinoma

Front 663

Thyroid cancer: poor prognosis, uniform follicles

Back 663

follicular carcinoma

Front 664

Thyroid cancer: calcitonin producing (C cells), sheets of cells

Back 664

medullary carcinoma (MEN II and III)

Front 665

Thyroid cancer: older patients, horrible prognosis

Back 665

undifferentiated/anaplastic

Front 666

Cretinism: caused by a lack of dietary --- or defect in --- formation

Back 666

iodine (endemic), T4 (sporadic)

Front 667

Cretinism: symptoms include

Back 667

pot-belly, paleness, puffy face, protuberant tongue, protruding umbilicus

Front 668

Acromegaly: caused by excess --- in adults

Back 668

growth hormone

Front 669

Acromegaly: symptoms include

Back 669

large furrowed tongue, deep voice, large hands and feet, coarse facial features

Front 670

Acromegaly: in children, leads to ---

Back 670

gigantism

Front 671

Diabetes mellitus: acute symptoms common to both types

Back 671

polydipsia, polyuria, polyphagia, weight loss

Front 672

Diabetes mellitus: match: (DKA/hyperosmolar coma) with (type I/type II)

Back 672

DKA=type I, hyperosmolar coma=type II

Front 673

Diabetes mellitus: effects (increased/decreased) of insulin deficiency and glucagon excess on 1) glucose uptake, 2) protein catabolism, 3) lipolysis

Back 673

1) decreased, 2) increased, 3) increased

Front 674

Diabetes mellitus: increased plasma free fatty acids leads to

Back 674

ketogenesis

Front 675

Diabetes mellitus: hyperglycemia has what effect on blood volume and electrolytes

Back 675

decreased volume (osmotic diuresis), electrolyte depletion

Front 676

Diabetes mellitus: three chronic manifestations

Back 676

retinopathy (hemorrhage, exudate, microaneurysm), nephropathy (nodular sclerosis), neuropathy (sensory, motor, autonomic)

Front 677

Diabetes mellitus: sorbitol accumulation leads to what sequelae in the eye

Back 677

cataracts, glaucoma

Front 678

Diabetes mellitus: three tests - what are they? which one measures long-term glucose control?

Back 678

fasting glucose, glucose tolerance test, HbA1c

Front 679

Diabetes mellitus: AUTHOR

Back 679

Jacob Pugsley

Front 680

Type 1 - juvenile onset: % of diabetes

Back 680

0.15

Front 681

Type 1 - juvenile onset: Insulin necessary in treatment

Back 681

Always

Front 682

Type 1 - juvenile onset: Age

Back 682

<30

Front 683

Type 1 - juvenile onset: Association with obesity

Back 683

No

Front 684

Type 1 - juvenile onset: Genetic predisposition

Back 684

weak, polygenic

Front 685

Type 1 - juvenile onset: Association with HLA system

Back 685

Yes (HLA-DR3 & 4)

Front 686

Type 1 - juvenile onset: Glucose intolerance

Back 686

Severe

Front 687

Type 1 - juvenile onset: Ketoacidosis

Back 687

Common

Front 688

Type 1 - juvenile onset: B-cell numbers in the islets

Back 688

decreased

Front 689

Type 1 - juvenile onset: Serum insulin levels

Back 689

decreased

Front 690

Type 1 - juvenile onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss

Back 690

Common

Front 691

Type 1 - juvenile onset: Theorized cause

Back 691

viral or immune destruction of B cells

Front 692

Type 2 - adult onset: % of diabetes

Back 692

0.85

Front 693

Type 2 - adult onset: Insulin necessary in treatment

Back 693

Sometimes

Front 694

Type 2 - adult onset: Age

Back 694

>40

Front 695

Type 2 - adult onset: Association with obesity

Back 695

Yes

Front 696

Type 2 - adult onset: Genetic predisposition

Back 696

Strong, polygenic

Front 697

Type 2 - adult onset: Association with HLA system

Back 697

No

Front 698

Type 2 - adult onset: Glucose intolerance

Back 698

mild to moderate

Front 699

Type 2 - adult onset: Ketoacidosis

Back 699

Rare

Front 700

Type 2 - adult onset: B-cell numbers in the islets

Back 700

Variable

Front 701

Type 2 - adult onset: Serum insulin levels

Back 701

Variable

Front 702

Type 2 - adult onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss

Back 702

Sometimes

Front 703

Type 2 - adult onset: Theorized cause

Back 703

increased resistance to insulin

Front 704

Diabetic Ketoacidosis (type 1): What precipitates this

Back 704

Increase in insulin requirements from increase in stress (e.g. infection)

Front 705

Diabetic Ketoacidosis (type 1): Ketone bodies from where

Back 705

Excess fat breakdown, increase ketogenesis from increased free fatty acids which are made into ketone bodies

Front 706

Diabetic Ketoacidosis (type 1): Signs/Symptoms

Back 706

Kussmaul respirations (rapid/deep breathing), hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration, fruity breath odor

Front 707

Diabetic Ketoacidosis (type 1): Labs

Back 707

Hyperglycemia, high H+, low HCO3- (anion gap metabolic acidosis), high blood ketone levels, leukocytosis

Front 708

Diabetic Ketoacidosis (type 1): Complications

Back 708

Life threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythimias, heart failure

Front 709

Diabetic Ketoacidosis (type 1): Treatment

Back 709

Fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia.

Front 710

Diabetes insipidus: summary

Back 710

intensive thirst, polyuria, inability to concentrate urine with fluid constriction owing to lack of ADH (central DI) or to lack of renal response to ADH (nephrogenic DI). Caused by lithium or demeclocycline

Front 711

Diabetes insipidus: Findings

Back 711

Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L

Front 712

Diabetes insipidus: Treatment

Back 712

adequate fluid intake; Central DI - intranasal desmopressin (ADH analog); nephrogenic DI - hydrochlorothiazide, indomethacin, or amiloride

Front 713

SIADH: what does it stand for

Back 713

Syndrome of inapropriate ADH

Front 714

SIADH: finds

Back 714

1) excess water retention 2) hyponatremia [may lead to seizures - correct slowly] 3) urine osmolarity > serum osmolarity

Front 715

SIADH: causes

Back 715

1) Ectopic ADH [small cell lung cancer] 2) CNS disorders/head trauma 3) pulmonary disease 4) Drugs

Front 716

Hyperparathyroidism: What causes primary hyperparathyroidism?

Back 716

Usually an adenoma

Front 717

Hyperparathyroidism: What are the findings of primary disease?

Back 717

hypercalcemia, hypercalciuria, hypophosphatemia, high parathyroid hormone, high cAMP in urine; often asymptomatic, may present with weakness and constipation

Front 718

Hyperparathyroidism: what is osteitis fibrosa cystica? (von Recklinghausen's syndrome)

Back 718

cystic bone spaces filled with non-neoplastic fibrous tissue

Front 719

Hyperparathyroidism: What causes secondary hyperparathyroidism?

Back 719

low serum Ca++, most often chronic renal disease.

Front 720

Hyperparathyroidism: What are the findings of secondary hyperparathyroidism?

Back 720

hypocalcemia, hyperphosphatemia, high parathyroid hormone

Front 721

Hypoparathyroidism: findings

Back 721

hypocalcemia, tetany.

Front 722

Hypoparathyroidism: causes

Back 722

accidental surgical excision (thyroid surgery) or DiGeorge syndrome

Front 723

Hypoparathyroidism: note: pseudohypoparathyroidism

Back 723

autosomal recessive kidney unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature

Front 724

Carcinoid syndrome: frequency

Back 724

rare

Front 725

Carcinoid syndrome: cause

Back 725

carcinoid tumors (neuroendocrine cells), especially those of the small bowel; they secrete high levels of serotonin (5-HT) that does not get metabolized by the liver due to liver metastases.

Front 726

Carcinoid syndrome: symptoms

Back 726

recurrent diarhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.

Front 727

Carcinoid syndrome: most common tumor of what?

Back 727

apendix

Front 728

Carcinoid syndrome: lab

Back 728

high 5-HIAA in urine

Front 729

Carcinoid syndrome: Rule of 1/3s:

Back 729

1/3 metastasize; 1/3 present with second malignancy; 1/3 multiple

Front 730

Carcinoid syndrome: Treatment?

Back 730

Octreotide

Front 731

Carcinoid syndrome: What is this medication?

Back 731

synthetic octapeptide analog of somatostatin (growth hormone-inhibiting hormone)

Front 732

Zollinger-Ellison syndrome: What kind of tumor causes this?

Back 732

Gastrin secreting tumor (usually) of the pancreas

Front 733

Zollinger-Ellison syndrome: what does it cause?

Back 733

recurrent ulcers

Front 734

Zollinger-Ellison syndrome: may be associated with what?

Back 734

MEN type I

Front 735

Osteoporosis: what is this?

Back 735

reduction in bone mass in spite of normal bone mineralization

Front 736

Osteoporosis: what characterizes type 1?

Back 736

Postmenopausal (10-15 years after menopause); increased bone reabsorption due to low estrogen levels. Treated with estrogen replacement

Front 737

Osteoporosis: what characterizes type 2?

Back 737

Senile osteoporosis - affects men and women > 70 y/o

Front 738

Osteoporosis: what races are affected most?

Back 738

whites>blacks>asians

Front 739

Osteoporosis: symptoms of vertebral crush fractures

Back 739

acute back pain, loss of height, kyphosis

Front 740

Osteoporosis: other

Back 740

distal radius (Colles') fracures, vertebral wedge fracures.

Front 741

Osteoporosis: see picure

Back 741

0

Front 742

Osteoporosis: PATHOLOGY - REPRODUCTIVE

Back 742

(end of endocrine)

Front 743

Benign prostatic hyperplasia: who gets BPH?

Back 743

common in men > 50 y/o

Front 744

Benign prostatic hyperplasia: what might cause it?

Back 744

may be due to age-related increase in estradiol with possible sensitization of the prostate to the growth promoting effects of DHT.

Front 745

Benign prostatic hyperplasia: findings

Back 745

nodular enlargement of the periurethral (lateral and middle) lobes of the prostate gland, compressing the urethra to a vertical slit.

Front 746

Benign prostatic hyperplasia: symptoms

Back 746

increased frequency of urination, nocturia, difficulty in starting and stoping the stream of urine, dysuria.

Front 747

Benign prostatic hyperplasia: complications

Back 747

may lead to distention and hypertrophy of the bladder, hydronephrosis, UTIs

Front 748

Benign prostatic hyperplasia: premalignant lesion?

Back 748

No

Front 749

Hydatidiform mole: What is it?

Back 749

pathologic ovum (empty egg - ovum with no DNA) resulting in a cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast).

Front 750

Hydatidiform mole: Most common precursor of what?

Back 750

choriocarcinoma

Front 751

Hydatidiform mole: what happens to B-hCG?

Back 751

elevated

Front 752

Hydatidiform mole: findings

Back 752

honeycombed uterus, cluster of grapes apearance

Front 753

Hydatidiform mole: genotype

Back 753

complete mole is 46,xx and is completely paternal in origin (no maternal chromosomes); no associated fetus. PARTial mole is made up of 3 or more PARTS (triploid or tetraploid)

Front 754

Pregnancy-induced hypertension (preeclampsia-eclampsia): what is the triad?

Back 754

hypertension, proteinuria, edema

Front 755

Pregnancy-induced hypertension (preeclampsia-eclampsia): what makes it eclampsia?

Back 755

addition of seizures to the triad

Front 756

Pregnancy-induced hypertension (preeclampsia-eclampsia): what % of pregnant women?

Back 756

0.07

Front 757

Pregnancy-induced hypertension (preeclampsia-eclampsia): when does it present?

Back 757

20 weeks gestation to 6 weeks postpartum

Front 758

Pregnancy-induced hypertension (preeclampsia-eclampsia): what increases the likelihood?

Back 758

preexisting hypertension, diabetes, chronic renal disease, autoimmune disorders

Front 759

Pregnancy-induced hypertension (preeclampsia-eclampsia): what is HELLP syndrome?

Back 759

Hemolysis, Elevated LFTs, Low Platelets

Front 760

Pregnancy-induced hypertension (preeclampsia-eclampsia): Clinical features

Back 760

headache, blurred vision, abdominal pain, edema of face and extremeties, altered mentation, hyperreflexia

Front 761

Pregnancy-induced hypertension (preeclampsia-eclampsia): Lab findings

Back 761

thrombocytopenia, hyperuricemia

Front 762

Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment

Back 762

Delivery of fetus as soon as viable. Otherwise, bedrest, salt restriction, monitoring and treatment of hypertension

Front 763

Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment for eclampsia (a medical emergency)

Back 763

IV Magnesium sulfate, diazepam

Front 764

Pregnancy complications: Abruptio placentae

Back 764

premature separation of the placenta. Painful uterine bleeding (usually 3rd trimester). Fetal death. May be associated with DIC

Front 765

Pregnancy complications: Placenta accreta

Back 765

defective decidual layer allows placenta to attach directly to myometrium. Predisposed by prior C-section or inflamation. May have massive hemorrhage after delivery.

Front 766

Pregnancy complications: Placenta previa

Back 766

attachment of the placenta to lower uterine segment. May occlude cervical os. Painless bleeding in any trimester.

Front 767

Pregnancy complications: Ectopic pregnancy

Back 767

most often in fallopian tubes, predisposed by salpingitis (PID).

Front 768

Cervical Pathology: Dysplasia and carcinoma in situ

Back 768

Disordered epithelial growth; begins at basal layer and extends outward. Classified as CIN 1, CIN 2, or CIN 3 (carcinoma in situ), depending on extent of dysplasia. Associated with HPV. May progress to invasive carcinoma.

Front 769

Cervical Pathology: Invasive carcinoma

Back 769

Often squamous cell carcinoma. Pap smears can catch cervical dysplasia (koilocytes) before it progresses to invasive carcinoma.

Front 770

Cervical Pathology: AUTHOR

Back 770

Gabi Rizzuto

Front 771

Uterine pathology: most common tumor in female (hint - has increased incidence in blacks)? Do they progress to malignancy?

Back 771

leiomyoma; no.

Front 772

Uterine pathology: endometriosis - most common site?

Back 772

ovary

Front 773

Uterine pathology: endometriosis in the myometrium = ?

Back 773

adenomyosis

Front 774

Uterine pathology: most common gyn malignancy? (hint - causes vaginal bleeding in a postmenopausal women)

Back 774

endometrial carcinoma

Front 775

Uterine pathology: Leiomyosarcoma: does it arise de novo or from leiomyoma?

Back 775

de novo

Front 776

PCOS (Stein-Leventhal syndrome): Major clinical manifestations include: amenorrhea, infertility, obesity, and ----?

Back 776

hirsutism

Front 777

Ovarian cysts: the four types of ovarian cysts

Back 777

follicular, corpus luteum, theca-lutein, chocolate

Front 778

Ovarian cysts: blood containing cyst from ovarian endometriosis

Back 778

chocolate cyst

Front 779

Ovarian cysts: cyst that is associated with choriocarcinoma and moles

Back 779

theca-lutein cyst

Front 780

Ovarian cysts: cyst defined by hemorrhage into persistent corpus luteum

Back 780

corpus luteum cyst

Front 781

Ovarian cysts: cyst defined by distention of unruptured graafian follicle

Back 781

follicular cyst

Front 782

Ovarian germ cell tumors : that which is analagous to male seminoma

Back 782

dysgerminoma

Front 783

Ovarian germ cell tumors : produces alpha-fetoprotein

Back 783

yolk sac tumor

Front 784

Ovarian germ cell tumors : associated with elevated hCG

Back 784

choriocarcinoma

Front 785

Ovarian germ cell tumors : monodermal teratoma made up of only thyroid tissue

Back 785

struma ovarii

Front 786

Ovarian germ cell tumors : most common germ cell tumor of ovary (90%)

Back 786

teratoma

Front 787

Ovarian germ cell tumors : True or False: immature teratomas are benign

Back 787

False. Mature ("dermoid cyst") ones are benign, immature ones are aggressively malignant

Front 788

Ovarian non-germ cell tumors: bilateral non germ cell tumor with fallopian tube like epithelium

Back 788

serous cystadenoma

Front 789

Ovarian non-germ cell tumors: Pseudomyxoma peritonei (intraperitoneal accumulation of mucinous material) may be a consequence of which ovarian non germ cell tumor?

Back 789

mucinous cystadenocarcinoma

Front 790

Ovarian non-germ cell tumors: tumor resembling bladder epithelium

Back 790

brenner tumor

Front 791

Ovarian non-germ cell tumors: triad of ovarian fibroma, ascites, and hydrothorax = ?

Back 791

Meigs' syndrome

Front 792

Ovarian non-germ cell tumors: Pathology term for the small follicles filled with eosinophilic secretions that are seen in granulosa cell tumors

Back 792

Call-Exner bodies

Front 793

Breast disease: Which one of the following does NOT put an individual at increased risk for breast disease? Gender, age, early 1st menarche, late 1st pregnancy, late menopause, family history, fibroadenoma/non-hyperplastic cysts

Back 793

fibroadenoma/hyperplastic cysts

Front 794

Breast disease: Eczematous patches on the nipple w/ corresponding large cell's with clear halo on histology are indicative of --?

Back 794

Paget's disease & most likely an underlying ductal carcinoma

Front 795

Breast disease: Fibrosis, cystic, sclerosing, & epithelial hyperplasia are all histologic subtypes of what breast disease?

Back 795

Fibrocystic disease (note: no increase risk of developing carcinoma)

Front 796

Breast disease: Most common breast tumor in women < 25 years of age? is it malignant or a precursor to malignancy?

Back 796

Fibroadenoma. No, no.

Front 797

Breast disease: A benign tumor of the breast that presents with nipple discharge

Back 797

Intraductal papilloma

Front 798

Breast disease: Are malignant breast tumors more common pre or post menopause

Back 798

post

Front 799

Hypertension: True of false: 50% is classified as secondary HTN (usually resulting from renal disease)

Back 799

false. (90% essential/primary, 10% secondary)

Front 800

Hypertension: "read the questioner's mind": HTN predisposes individuals to this disease (the one John Ritter died of)

Back 800

aortic dissection

Front 801

Hypertension: Pathology changes associated with HTN

Back 801

hyaline thickening & atherosclerosis

Front 802

Arteriosclerosis: This awful term refers to a stiffening of the arteries that invovles the media. Particularly likely to occur at the radial & ulnar arteries.

Back 802

Monckeberg arteriosclerosis

Front 803

Atherosclerosis: True or false: atherosclerosis is a disease of small sized arteries

Back 803

false. affects elastic, large & medium muscular arteries.

Front 804

Atherosclerosis: Earliest sign of atherosclerotic disease

Back 804

fatty streak

Front 805

Atherosclerosis: most likely location

Back 805

abdominal aorta. (then coronary artery, popliteal artery, and carotid artery)

Front 806

Ischemic heart disease: Type of angina resulting from coronary artery spasm

Back 806

Prinzmetal's variant

Front 807

Ischemic heart disease: This coronary artery branch is most commonly implicated in myocardial infarction

Back 807

LAD (left anterior descending)

Front 808

Ischemic heart disease: most common cause of sudden cardiac death

Back 808

(lethal) arrhythmia

Front 809

Infarcts: red vs. pale: Solid tissues like the heart, brain, kidney and spleen have only a single blood supply (not so good collaterals). Therefore infarcts are more likely to be --?

Back 809

pale

Front 810

Infarcts: red vs. pale: 2 instances where red infarct is likely

Back 810

(1) reperfusion (2) loose tissues with good collaterals - like the lungs or intestine

Front 811

Evolution of MI: Rank the following vessels from most to least commonly occluded: RCA, LAD, circumflex

Back 811

LAD>RCA>circumflex

Front 812

Evolution of MI: Histologic changes on day 1 of an MI?

Back 812

pallor of infarcted area; coagulative necrosis

Front 813

Evolution of MI: days 2-4?

Back 813

dilated vessels (hyperemia); neutrophil invasion; extensive coagulative necrosis

Front 814

Evolution of MI: days 5-10?

Back 814

yellow-brown softening of infarcted region; macrophages present; granulation tissue begins to grow in

Front 815

Evolution of MI: after 7 weeks?

Back 815

infarct is gray-white; scar complete

Front 816

Diagnosis of MI: True or false: ECG is not diagnostic during the first 6 hours following an MI

Back 816

False; it is the gold standard within this time period

Front 817

Diagnosis of MI: What is the test of choice within the first 24 hours?

Back 817

CK-MB

Front 818

Diagnosis of MI: This enzyme is elevated from 4 hours up to 10 days after an MI and is the most specific protein marker

Back 818

cardiac troponin I

Front 819

Diagnosis of MI: on ecg, transmural infarction causes ______

Back 819

ST elevation, Q wave changes

Front 820

MI complications: Most common (90% of patients)

Back 820

arryhthmias, esp. 2 days after infarct

Front 821

MI complications: automimmune phenomen several weeks post-MI that results in fibrinous pericarditis

Back 821

Dressler's syndrome

Front 822

MI complications: high risk of mortality

Back 822

cardiogenic shock (large infarcts)

Front 823

MI complications: seen about a week after the infarction

Back 823

rupture of ventricular wall, septum, or papillary muscle

Front 824

Cardiomyopathies: Most common

Back 824

dilated (congestive) cardiomyopathy; heart looks like a ballon on X-ray

Front 825

Cardiomyopathies: True or False: substance abuse is a common cause of dilated cardiomyopathy

Back 825

True; cocaine and alcohol especially

Front 826

Cardiomyopathies: These two infectious diseases are associated with dilated myopathy

Back 826

coxsackievirus B and Chagas' disease

Front 827

Cardiomyopathies: True or false: hypertrophic cardiomyopathy causes systolic dysfunction

Back 827

False; dilated myopathy causes systolic dysfunction, hypertrophic causes diastolic

Front 828

Cardiomyopathies: Half of hypertrophic myopathies are inherited as an _________ trait (x-linked, dominant, etc.)

Back 828

autosomal dominant; major cause of sudden death in young athletes

Front 829

Cardiomyopathies: On echo in hypertrophic disease, the LV thickens and the chamber looks how?

Back 829

like a banana

Front 830

Cardiomyopathies: These "-osis" diseases are major causes of restrictive/obliterative cardiomyopathy

Back 830

sarcoidosis, amyloidosis, hemochromatosis, endocardial fibroelastosis, endomyocardial (Loffler's) fibrosis….also, scleroderma but it's not an -osis

Front 831

Heart murmurs: Name two causes of holosystolic murmurs

Back 831

1) VSD, 2) mitral regurg, and 3) tricuspid regurg

Front 832

Heart murmurs: Widened pulse pressure seen with this diastolic murmur

Back 832

aortic regurg

Front 833

Heart murmurs: Describe the murmur associated with the most common valvular lesion

Back 833

Mitral prolapse; late systolic murmur following mid-systolic click

Front 834

Heart murmurs: True or false: aortic stenosis causes a decrescendo-crescendo murmur following an ejection click

Back 834

False; ejection click is followed by a crescendo-decrescendo systolic murmur

Front 835

Heart murmurs: cause of a continuous murmur loudest at time of S2?

Back 835

patent ductus artieriosis

Front 836

Heart murmurs: opening snap followed by late diastolic rumbling?

Back 836

mitral stenosis

Front 837

Cardiac tumors: most common heart tumor?

Back 837

metastasis

Front 838

Cardiac tumors: primary cardiac tumor in 1) adults and 2) children

Back 838

adults=myxoma (almost always in left atrium); children=rhabdomyoma

Front 839

CHF: fun gross pathologic term for changes in liver with CHF?

Back 839

nutmeg

Front 840

CHF: what are "heart failure cells"?

Back 840

hemosiderin-laden macrophages in lung

Front 841

CHF: dyspnea on exertion, pulmonary edema, and paroxysmal nocturnal dyspnea are symptoms of?

Back 841

left heart failure

Front 842

CHF: patient says "I have to sleep upright." the clinical term for this is?

Back 842

orthopnea

Front 843

embolus types: most pulmonary emboli arise from?

Back 843

DVT

Front 844

embolus types: True or false: Amniotic fluid can lead to DIC

Back 844

TRUE

Front 845

deep vein thrombosis: what are the component of virchow's triad?

Back 845

stasis, hypercoagulability, endothelial damage

Front 846

cardiac tamponade: what is pulsus paradoxus?

Back 846

greater than 10 mmHg drop in systolic on inspiration

Front 847

cardiac tamponade: what is electrical alternans?

Back 847

characteristic of tamponade on ECG in which QRS complex height varies beat-to-beat

Front 848

cardiac tamponade: AUTHOR

Back 848

James Rosoff / Flora Waples-Trefil

Front 849

Bacterial Endocarditis: What valve is usually involved in endocarditis?

Back 849

Mitral

Front 850

Bacterial Endocarditis: What valve indicated drug use if it is involved?

Back 850

Tricuspid

Front 851

Bacterial Endocarditis: Can endocarditis be non-bacterial?

Back 851

Yes. It can be secondary to metastasis, renal failure (maranctic or thrombotic), fungal

Front 852

Bacterial Endocarditis: What type of endocarditis does s. Aureus cause?

Back 852

rapid onset, high virulence, tends to occur secondary to infection elsewhere

Front 853

Bacterial Endocarditis: What do the vegetations look like

Back 853

Large.

Front 854

Bacterial Endocarditis: What type of endocarditis does s. viridians cause?

Back 854

subacute. Tends to have smaller vegetations.

Front 855

Bacterial Endocarditis: What predisposes you to s.viridins endocarditis?

Back 855

tends to occur on previously damaged valves, so rheumatic fever. It is commonly seen after dental work.

Front 856

Bacterial Endocarditis: What are the 8 sings of endocarditis?

Back 856

JR=NO FAME Janeway lesions, Roth's spots, Nail-bed hemorrhages, Osler's nodes, Fever, Anemia, Murmur (new), Emboli

Front 857

Bacterial Endocarditis: What do Janeway Lesions look like?

Back 857

multiple small flat erythematous lesions on palms and soles

Front 858

Bacterial Endocarditis: What are roth spots?

Back 858

round white spots on the retina surrounded by hemorrhage.

Front 859

Bacterial Endocarditis: What are osler's nodes?

Back 859

Tender raised lesions on the fingers and toes.

Front 860

Bacterial Endocarditis: What is the etiology of these lesions?

Back 860

Bacterial vegetations fliping off the heart valve and lodging in the periphery.

Front 861

Rheumatic Fever/Rheumatic Heart Disease: What type of bacteria causes rheumatic fever?

Back 861

Group A beta-hemolytic strep

Front 862

Rheumatic Fever/Rheumatic Heart Disease: when does it occur?

Back 862

Children 5-15 years, four weeks after a bacterial infection

Front 863

Rheumatic Fever/Rheumatic Heart Disease: Is the bacteria responsible for the symptoms?

Back 863

No. RF is an autoimmune reaction of a cross-reactive protein that is found in the initial bacterial infection.

Front 864

Rheumatic Fever/Rheumatic Heart Disease: What are the non cardiac clinical signs of rheumatic fever?

Back 864

FEVERSS - Fever, Erythema marginatum, valve damage, Elevated ESR, Red-hot joints (migratory polyarthritis), Subcutaneous nodules, and St. Vitus dance (chorea)

Front 865

Rheumatic Fever/Rheumatic Heart Disease: What hear valves are effected?

Back 865

Mitral (most frequent), Aortic, Tricuspid (5%) - high pressure valves mainly.

Front 866

Rheumatic Fever/Rheumatic Heart Disease: What is an Aschoff body?

Back 866

classic histological sign of RF, found in the myocardium, contained fibrinoid material, fragmented collages, surrounded by giant cells.

Front 867

Rheumatic Fever/Rheumatic Heart Disease: What are the cardiac signs of RF?

Back 867

Verrucious vegetations on the valve, pancarditis, possible pericardial effusions and myocarditis (most common cause of death)

Front 868

Pericarditis: Name four causes of serous pericarditis.

Back 868

RAIL - Rheumatic Arthritis, Infection, Lupus, and Uremia

Front 869

Pericarditis: What is serous pericarditis?

Back 869

straw colored, protein rich exudates - non-purulent, and acute

Front 870

Pericarditis: What are three causes of fibirnous exudates?

Back 870

MI, Rheumatic fever, and Uremia

Front 871

Pericarditis: Cloudy pericardial exudates indicated what?

Back 871

Bacterial infection

Front 872

Pericarditis: What are two causes of Hemorrhagic pericarditis?

Back 872

malignancy and TB

Front 873

Pericarditis: What is hemorrhagic pericarditis?

Back 873

Bloody and inflammatory exudates

Front 874

Pericarditis: What are the clinical signs of pericardial exudates?

Back 874

pericardial pain, friction rub, decreased heart sounds, ST elevation throughout, and pulses paradoxes (like cardiac tamponade)

Front 875

Pericarditis: What are the long term sequela of pericarditis?

Back 875

chronic adhesive or constrictive pericarditis

Front 876

Pericarditis: What is constiricit pericadritis

Back 876

Fibrous scarring in the pericardium obliterates the space and constrict the right side of the heart (because it is less able to withstand the pressure)

Front 877

Pericarditis: What types of pericaditis lead to this?

Back 877

TB and pyrogenic staph infections

Front 878

Syphilitic Heart Disease: What part of the heart does syphilis damage?

Back 878

The vaso vasorum of the aorta

Front 879

Syphilitic Heart Disease: What does this lead to?

Back 879

Dilation of the aorta and valve ring

Front 880

Syphilitic Heart Disease: What clinical results does this have?

Back 880

it can cause an aortic aneurysm or valvular incompetence

Front 881

Syphilitic Heart Disease: What parts of the aorta are effected

Back 881

ascending and arch

Front 882

Syphilitic Heart Disease: What is the appearance or the aorta?

Back 882

Called a "tree-bark" apearance.

Front 883

Buerger's Disease: Buerger's disease is also known as?

Back 883

smoker's disease, thromboangiitis obliterans

Front 884

Buerger's Disease: What are the Sx (5)?

Back 884

intermittent claudication, superficial nodular phlebitis, cold sensitivity, severe pain in affected part, may lead to gangrene

Front 885

Buerger's Disease: What is the Tx?

Back 885

Quit smokng

Front 886

Takayasu's arteritits: Also known as ?

Back 886

pulseless disease

Front 887

Takayasu's arteritits: What is it?

Back 887

thickening of aortic arch and/or proximal great vessels

Front 888

Takayasu's arteritits: ESR elevated?

Back 888

yes

Front 889

Takayasu's arteritits: Primarily affects whom?

Back 889

Young Asian Females

Front 890

Takayasu's arteritits: Mnemomic

Back 890

FAN MY SKIN On Wednesday

Front 891

Takayasu's arteritits: Sx (7)

Back 891

Fever, Arthritis, Night Sweats, Myalgia, Ocular Disturbances, Weak pulses in uper extremities (FAN MY SKIN On Wednesday)

Front 892

Temporal Arteritis: Also known as?

Back 892

Giant Cell Arteritis

Front 893

Temporal Arteritis: Affects what vessels?

Back 893

medium and small arteries (usually carotid branches)

Front 894

Temporal Arteritis: ESR elevated?

Back 894

yes

Front 895

Temporal Arteritis: Primarily affects whom?

Back 895

Elderly Females

Front 896

Temporal Arteritis: Sx (3)

Back 896

Unilateral Headache, Jaw claudication, impaired vision

Front 897

Temporal Arteritis: Many patients are also affected with this syndrome

Back 897

Polymalgia Rheumatica

Front 898

Temporal Arteritis: Tx (?)

Back 898

Steroids

Front 899

Polyarteritis Nodosa: How would you describe the inflammation in this disease?

Back 899

necrotizing, caused by immune complex deposition

Front 900

Polyarteritis Nodosa: In which vessels?

Back 900

small to medium-sized muscular arteries, renal and visceral vessels

Front 901

Polyarteritis Nodosa: ESR elevated?

Back 901

yes

Front 902

Polyarteritis Nodosa: Sx (7) … and they are SO specific

Back 902

fever,weight loss,malaise,abdominal pain,headache ,myalgia,hypertension

Front 903

Polyarteritis Nodosa: Other findings

Back 903

cotton-wool spots, microaneurysms, pericarditis, myocarditis, palpable purpura

Front 904

Polyarteritis Nodosa: What viral infection is found in 30% of PN patients?

Back 904

Hepatitis B

Front 905

Polyarteritis Nodosa: what antibody is associated with this disease?

Back 905

P-ANCA

Front 906

Polyarteritis Nodosa: What two ways can you remember the assoc Ab?

Back 906

P-ANCA --> PAN (PolyArteritis Nodosa)

Front 907

Polyarteritis Nodosa: What does P-ANCA refer to?

Back 907

Perinuclear pattern of Antineutrophil Cytoplasmic Antibodies

Front 908

Polyarteritis Nodosa: Primarily affects whom?

Back 908

Young males

Front 909

Polyarteritis Nodosa: Tx

Back 909

Corticosteroids, Azathioprine, Cyclophosphamide

Front 910

Wegener's Granulomatosis: What are three major findings (hint: they are necrotizing)

Back 910

Focal Necrotizing Vasculitis, Necrotizing granulomas of the lung and uper airway, Necrotizing glomerulonephritis

Front 911

Wegener's Granulomatosis: Sx (7)

Back 911

Perforated nasal septum, Chronic Sinusitis, Otitis Media, Mastoiditis, Cough , Dyspnea, Hemoptysis

Front 912

Wegener's Granulomatosis: What antibody is associated with this disease

Back 912

C-ANCA

Front 913

Wegener's Granulomatosis: What should you look for on CXR?

Back 913

large nodular densities

Front 914

Wegener's Granulomatosis: Tx

Back 914

Corticosteroids, Azathioprine, Methotrexate

Front 915

Kawasaki Disease: Who gets it?

Back 915

infants, kids

Front 916

Kawasaki Disease: What is the disease course?

Back 916

acute, self-limiting

Front 917

Kawasaki Disease: What vessels are involved?

Back 917

small and medium sized

Front 918

Kawasaki Disease: What does CRASH stand for

Back 918

Conjunctivitis, Rash (truncal), Aneurysms of Coronary Arteries, Strawberry tongue, changes in lips/oral mucosa, Hands and Feet show induration and desquamation

Front 919

Kawasaki Disease: Glomerular Pathology

Back 919

275

Front 920

Kawasaki Disease: What is prerenal azotemia?

Back 920

selective rise in BUN during early renal failure

Front 921

Kawasaki Disease: Define segmental.

Back 921

involving part of the glomerular tuft

Front 922

Kawasaki Disease: Nephritic Syndrome

Back 922

0

Front 923

Kawasaki Disease: hematuria, hypertension, oliguria, azotemia = ?

Back 923

Nephritic Syndrome, "I" = inflammation

Front 924

Kawasaki Disease: LM findings in post-strep glomerulonephritis?

Back 924

lumpy bumpy and hypercellular w/ neutrophils

Front 925

Kawasaki Disease: EM findings in post-strep glomerulonephritis?

Back 925

subepithelial humps (from deposition of cationic antigen)

Front 926

Kawasaki Disease: IF findings in post-strep glomerulonephritis?

Back 926

granular

Front 927

Kawasaki Disease: Goodpasture's is what type of hypersensistivity?

Back 927

type II (IgG binding directly to BM)

Front 928

Kawasaki Disease: Goodpasture's IF?

Back 928

linear

Front 929

Kawasaki Disease: Symptoms of Goodpasture's?

Back 929

hemoptysis, hematuria

Front 930

Kawasaki Disease: Membranoproliferative glomerulonephritis EM?

Back 930

subendothelial humps; "tram track"

Front 931

Kawasaki Disease: Course of crescentic glomerulonephritis?

Back 931

rapid (the Red Crescent is the Islamic Red Cross, an organization that provides relief during emergencies, like crescentic glomerulonephritis)

Front 932

Kawasaki Disease: Course of Membranoproliferative glomerulonephritis?

Back 932

slow

Front 933

Kawasaki Disease: IgA nephropathy IF and EM?

Back 933

mesangial deposits of IgA (Mes"A"ngium)

Front 934

Kawasaki Disease: Which can be post infectious, IgA nephropathy or Goodpasture's?

Back 934

IgA nephropathy

Front 935

Kawasaki Disease: Nephrotic Syndrome

Back 935

0

Front 936

Kawasaki Disease: Signs of nephrotic syndrome?

Back 936

massive proteinuria, hypoalbuminemia, generalized edema, hyperlipidemia (think "erotic" = an erection(edema) and ejaculate(massive proteinuria)

Front 937

Kawasaki Disease: LM of membranous glomerulonephritis?

Back 937

diffuse capillary and basement membrane thickening

Front 938

Kawasaki Disease: IF of membranous glomerulonephritis?

Back 938

granular

Front 939

Kawasaki Disease: EM of membranous glomerulonephritis?

Back 939

spike and dome ("if you have a spike in your dome, you must be insane in the "membran"e," -Chirag)

Front 940

Kawasaki Disease: Minimal change disease EM?

Back 940

foot process effacement

Front 941

Kawasaki Disease: Most common cause of childhood nephrotic syndrome?

Back 941

minimal change disease

Front 942

Kawasaki Disease: Focal segmental glomerular sclerosis LM?

Back 942

segmental sclerosis and hyalinosis

Front 943

Kawasaki Disease: Diabetic nephropathy LM?

Back 943

Kimmelstiel-Wilson lesions

Front 944

Kawasaki Disease: SLE (5 patterns of renal involvement) LM?

Back 944

wire-loop apearance w/ extensive granular BM depsits in membranous glomerulonephritis pattern

Front 945

Kidney Stones: What is the most common kidney stone?

Back 945

Calcium (with either oxalate of phosphate)

Front 946

Kidney Stones: What kidney stone is associated with a bacterial infection?

Back 946

Ammonium magnesium phosphate (struivte) stones are associated with urase positive bugs that make ammonium

Front 947

Kidney Stones: What are the two most common stone-forming bacteria?

Back 947

proteus vulgaris and Staph.

Front 948

Kidney Stones: What stones are associated with gout?

Back 948

Uric acid stones

Front 949

Kidney Stones: What else can cause uric acid stones?

Back 949

Any disease with high cell turnover (remember that uric acid is a by-product of DNA formation), so leukemia and myeloproliferative disease

Front 950

Kidney Stones: What stones are associated with cystineuria?

Back 950

cystine stones

Front 951

Kidney Stones: What two stones are radiolucent?

Back 951

Uric acid and cystine (the two purely metabolic causes)

Front 952

Kidney Stones: What are the complications of stones?

Back 952

Hydronephrosis and pyelonephritis

Front 953

Kidney Stones: What causes calcium stones?

Back 953

Anything that increases calcium in the blood, so high PTH, malignancy (bone breakdown, PTH production), vitamin D overdose.

Front 954

Renal Cell Carcinoma: Is this a common renal cancer?

Back 954

Yes, the most common

Front 955

Renal Cell Carcinoma: Who is prone to this?

Back 955

males, ages 50-70, smokers, gene deletions on chromosome 3

Front 956

Renal Cell Carcinoma: This is a cancer of what cell type?

Back 956

renal tubule cells, histologically they apear clear.

Front 957

Renal Cell Carcinoma: What are the clinical signs of this cancer?

Back 957

flank pain, fever, hematuria, palpable mass, secondary polycythemia

Front 958

Renal Cell Carcinoma: How does it spread?

Back 958

It invades the renal veins and IVC, to spread hematogenously

Front 959

Renal Cell Carcinoma: What hormones can it produce?

Back 959

ACTH, prolactin, Parathyroid-like hormone, gonadotropins and renin.

Front 960

Wilm's Tumor: Who gets this cancer?

Back 960

Children 2-4 years

Front 961

Wilm's Tumor: Is it common?

Back 961

The most common renal cancer in children

Front 962

Wilm's Tumor: What is the chromosomal abnormality that leads to this?

Back 962

deletion of tumor supressor gene WT1 on chromosome 11

Front 963

Wilm's Tumor: What tetrad is it associated with?

Back 963

WAGR - Wilm's, Anirida (lack of an iris), Genitourinary malformation, and Retardation

Front 964

Wilm's Tumor: How does it present?

Back 964

huge palpable mass and hemihypertrophy

Front 965

Wilm's Tumor: What is the histological appearance?

Back 965

mixed - with stromal, mesenchymal, tubular, glomerular and fibrous elements

Front 966

Transitional Cell Carcinoma: Where does this cancer occur?

Back 966

Urinary spaces (tract, calyces, pelvis, bladder)

Front 967

Transitional Cell Carcinoma: Does it recur?

Back 967

yes, often

Front 968

Transitional Cell Carcinoma: How does it spread?

Back 968

Local invasion

Front 969

Transitional Cell Carcinoma: What can predispose you to it?

Back 969

Pee SAC toxins - Phenacetin, Smoking, Aniline dye (benezenes), and Cyclophsophimide.

Front 970

Transitional Cell Carcinoma: How does it present?

Back 970

Hematuria

Front 971

Acid-Base Physiology: What is the primary disturbance in Metabolic acidosis?

Back 971

a decrease in bicarbonate

Front 972

Acid-Base Physiology: What is the compensation?

Back 972

A drop in CO2 by hyperventilation

Front 973

Acid-Base Physiology: What are common causes?

Back 973

diabetic ketoacidosis (production of ketone acids), diarrhea (loss of GI bicarb), salisylate overdose, acetazoleamide (diuretic) OD, lactic acidosis, renal failure (can't excrete organic acids), ethylene glycol ingestion

Front 974

Acid-Base Physiology: What is the primary disturbance in respiratory acidosis?

Back 974

A build-up in CO2

Front 975

Acid-Base Physiology: What is the compensation?

Back 975

Increased bicarb reabosrobtion from the kidney

Front 976

Acid-Base Physiology: What are some common causes?

Back 976

COPD, airway obstruction, opiates and sedatives, guillan-barr or ALS,

Front 977

Acid-Base Physiology: What is the primary disturbance in metabolic alkalosis?

Back 977

increased bicarbonate

Front 978

Acid-Base Physiology: What is the compensation?

Back 978

Increased CO2 by decreased respiration

Front 979

Acid-Base Physiology: What are some common causes?

Back 979

Vomiting, hyperaldosteronism (increased H+ secretion), loop or thiazide diuretics (volume contraction)

Front 980

Acid-Base Physiology: What is the primary disturbance in respiratory alkalosis?

Back 980

A drop in CO2

Front 981

Acid-Base Physiology: What is the compensation?

Back 981

increased excretion of bicarb by the kidney

Front 982

Acid-Base Physiology: What are some common causes?

Back 982

hyperventilation, high altitude, pneumonia and pulmonary embolus (hypoxemia causes hyperventilation_

Front 983

Acid-Base Physiology: What is the Henderson Haselbach equation?

Back 983

pH = pKa + Log (HCO3-)/(.03*pCO2)

Front 984

Acid Base Nomogram: Is there an awesome graph on page 277 that you should know?

Back 984

Yes

Front 985

Acid Base Nomogram: basically four cases

Back 985

0

Front 986

Acid Base Nomogram: Low pH, low pCO2 (low HCO3-)

Back 986

metabolic acidosis

Front 987

Acid Base Nomogram: Low pH, high pCO2 (high HCO3-)

Back 987

chronic respiratory acidosis

Front 988

Acid Base Nomogram: High pH, low pC02 (low HC03-)

Back 988

acute respiratory alkalosis

Front 989

Acid Base Nomogram: High pH, high pCO2 (high HCO3-)

Back 989

metabolic alkalosis

Front 990

Acidosis/Alkalosis: Check arterial pH

Back 990

0

Front 991

Acidosis/Alkalosis: pH < 7.4

Back 991

acidosis

Front 992

Acidosis/Alkalosis: pH > 7.4

Back 992

alkalosis

Front 993

acidosis: P (CO2) > 40

Back 993

Respiratory acidosis

Front 994

acidosis: P (CO2) > 40, Hypoventilation or Hyperventilation

Back 994

HYPO

Front 995

acidosis: Causes

Back 995

Acute lung disesae, chronic lung disease, Drugs (opioids, narcotics, sedatives), Weakening of Resp. muscles

Front 996

acidosis: P (CO2) < 40

Back 996

0

Front 997

acidosis: What should you do next?

Back 997

Check Anion Gap

Front 998

acidosis: What is the normal anion gap?

Back 998

8-12 mEq/L

Front 999

acidosis: Increased Anion Gap - 4 Causes

Back 999

Renal Failure, lactic acidosis, ketoacidosis, aspirin ingestions

Front 1000

acidosis: Normal anion gap metabolic acidosis (4)

Back 1000

Diarrhea, sniffin glue, renal tubular acidosis, hyperchloremia

Front 1001

acidosis: pH > 7.4

Back 1001

alkalosis

Front 1002

acidosis: pCO2 < 40

Back 1002

Respiratory alkalosis

Front 1003

acidosis: respiratory acidosis Causes (2)

Back 1003

HYPERventilation, aspirin ingestion (early)

Front 1004

acidosis: pCO2 > 40

Back 1004

metabolic alkalosis w/ compensation

Front 1005

acidosis: metabolic alkalosis Causes (4)

Back 1005

vomiting, diuretic use, antacids, hyperaldosteronism

Front 1006

Anion gap acidosis: How do you calculate it

Back 1006

Na - Cl - HCO3

Front 1007

Anion gap acidosis: What is normal?

Back 1007

8-12 mEq/L

Front 1008

Anion gap acidosis, MUDPILES: M

Back 1008

Methanol

Front 1009

Anion gap acidosis, MUDPILES: U

Back 1009

Uremia

Front 1010

Anion gap acidosis, MUDPILES: D

Back 1010

DKA

Front 1011

Anion gap acidosis, MUDPILES: P

Back 1011

Paraldehyde or Phenformin

Front 1012

Anion gap acidosis, MUDPILES: I

Back 1012

Iron tablets or INH

Front 1013

Anion gap acidosis, MUDPILES: L

Back 1013

Lactic Acidosis

Front 1014

Anion gap acidosis, MUDPILES: E

Back 1014

Ethanol, Ethylene Glycol

Front 1015

Anion gap acidosis, MUDPILES: S

Back 1015

Salicylates

Front 1016

Acid Base Compensations: Metabolic acidosis

Back 1016

pCO2 = 1.5(HCO3) + 8 +/- 2

Front 1017

Acid Base Compensations: Metabolic alkalosis

Back 1017

pCO2 increases 0.7 mm Hg per 1 mEq/L HCO3 increase

Front 1018

Acid Base Compensations: Respiratory acidosis (acute)

Back 1018

HCO3 increases by 1 mEq/L for every 10 mmHg increase of pCO2

Front 1019

Acid Base Compensations: Respiratory acidosis (chronic)

Back 1019

HCO3 increases by 3.5 mEq/L for every 10 mmHg increase of pCO2

Front 1020

Acid Base Compensations: Respiratory alkalosis (acute)

Back 1020

HCO3 decreases by 2 mEq/L for every 10 mmHg decrease of pCO2

Front 1021

Acid Base Compensations: Respiratory alkalosis (chronic)

Back 1021

HCO3 decreases by 5 mEq/L for every 10 mmHg decrease of pCO2

Front 1022

Acute Pyelonephritis: Affects _______ of kidney

Back 1022

cortex

Front 1023

Acute Pyelonephritis: Spares ____________

Back 1023

glomeruli/vessels

Front 1024

Acute Pyelonephritis: _______ _______ in urine are pathognomonic

Back 1024

WBC casts

Front 1025

Chronic Pyelonephritis: Tubules may contain __________ casts

Back 1025

Eosinophilic

Front 1026

Chronic Pyelonephritis: Coarse ________, _________ scarring

Back 1026

Asymmetric corticomedullary

Front 1027

Diffuse Cortical Necrosis: infarction of _________ of both kidneys

Back 1027

cortex (cortices)

Front 1028

Diffuse Cortical Necrosis: due to combination of _________ and _________

Back 1028

vasospasm and DIC

Front 1029

Diffuse Cortical Necrosis: associated with _________ and _________

Back 1029

obstetric catastrophes and septic shock

Front 1030

Acute Tubular Necrosis: Most common cause of

Back 1030

renal failure

Front 1031

Acute Tubular Necrosis: reversible or irreversible

Back 1031

reversible

Front 1032

Acute Tubular Necrosis: fatal or non-fatal

Back 1032

fatal, if left untreated

Front 1033

Acute Tubular Necrosis: associated with (3)

Back 1033

renal ischemia (shock), crush injury (myoglobulinuria), toxins

Front 1034

Acute Tubular Necrosis: Death occurs most often during initial oliguric phase; T or F

Back 1034

TRUE

Front 1035

Renal Papillary Necrosis: Associated with (3)

Back 1035

Diabetes mellitus, Acute pyelonephritis, Chronic phenacetin use

Front 1036

Acute Renal Failure: Definition

Back 1036

abrupt decline in renal function over a period of days

Front 1037

Acute Renal Failure: Will see increase in _______ & _______

Back 1037

BUN & Creatinine

Front 1038

Acute Renal Failure: Prerenal is due to decreased ______

Back 1038

RBF

Front 1039

Acute Renal Failure: Renal is due to

Back 1039

ATN, Ischemia, toxins

Front 1040

Acute Renal Failure: Post renal is due to

Back 1040

outflow obstruction

Front 1041

Acute Renal Failure: 3 causes of above

Back 1041

renal stones, BPH, neoplasia

Front 1042

Acute Renal Failure: bilateral or unilateral

Back 1042

bilateral

Front 1043

Pre or post renal failure: Urine osmolality > 500

Back 1043

prerenal

Front 1044

Pre or post renal failure: Urine osmolality < 350

Back 1044

renal or postrenal

Front 1045

Pre or post renal failure: urine Na < 10

Back 1045

prerenal

Front 1046

Pre or post renal failure: urine Na > 40

Back 1046

postrenal

Front 1047

Pre or post renal failure: urine Na > 20

Back 1047

renal

Front 1048

Pre or post renal failure: FE(Na) >4%

Back 1048

postrenal

Front 1049

Pre or post renal failure: FE(Na) <1%

Back 1049

prerenal

Front 1050

Pre or post renal failure: FE(Na) >2%

Back 1050

renal

Front 1051

Pre or post renal failure: BUN/Cr ratio <15

Back 1051

renal

Front 1052

Pre or post renal failure: BUN/Cr ratio >15

Back 1052

postrenal

Front 1053

Pre or post renal failure: BUN/Cr ratio > 20

Back 1053

prerenal

Front 1054

Pre or post renal failure: Chronic renal failure due to (2)

Back 1054

diabetes, hypertension

Front 1055

Pre or post renal failure: Consequences of Renal Failure (8) p.279

Back 1055

Why?

Front 1056

Pre or post renal failure: Anemia

Back 1056

lack of EPO

Front 1057

Pre or post renal failure: Renal osteodystrophy

Back 1057

lack of active Vit D

Front 1058

Pre or post renal failure: Arrythmia

Back 1058

hyperkalemia

Front 1059

Pre or post renal failure: Metabolic acidosis

Back 1059

decreased acid secretion

Front 1060

Pre or post renal failure: Uremia

Back 1060

increase in BUN and Cr

Front 1061

Pre or post renal failure: CHF/Pulmonary Edema

Back 1061

retention of Na and H20

Front 1062

Pre or post renal failure: Chronic Pyelonephritis

Back 1062

0

Front 1063

Pre or post renal failure: Hypertension

Back 1063

0

Front 1064

Pre or post renal failure: AUTHOR

Back 1064

Aaron Goldberg

Front 1065

Alcoholism: tremor, tachcardia, hypertension, malaise, nausea, delirium tremens are symtpoms of what?

Back 1065

alcohol withdrawal

Front 1066

Alcoholism: when do you get symptoms of alcohol withdrawal?

Back 1066

in case of physiological tolerance and dependence when intake is interrupted

Front 1067

Alcoholism: what is disulfiram and how does it work?

Back 1067

disulfiram is a pharmacological treatment of alcoholism - negatively conditions patient against EtOH

Front 1068

Alcoholism: a good possible referral to sustain EtOH abstinence in alcoholics

Back 1068

Alcoholics Anonymous and other peer groups

Front 1069

Alcoholism: 3 mechanisms of EtOH action

Back 1069

1) interpolates into membranes --> toxic effects, partic. in brain 2) alcohol dehydrogenase converts EtOH to acetaldehyde, forms adducts with proteins and nucleic acids, converted to acetate, Ac-CoA, FA synthesis, fatty liver 3) increased NADH/NAD ratio

Front 1070

Complications of alcoholism: Condition in which these are seen: hepatitis and cirrhosis, pancreatitis, dilated cardiomyopathy, peripheral neuropathy, cerebellar degeneration, Wernicke-Korsakoff syndrome, testicular atrophy and hyperestrinism, and Mallory-Weiss syndrome

Back 1070

alcoholism

Front 1071

Complications of alcoholism: name histological type of cirrhosis in alcoholism

Back 1071

micronodular cirrhosis

Front 1072

Complications of alcoholism: accompanying symptoms of alcoholic cirrhosis

Back 1072

jaundice, hypoalbuminemia, coagulation factor deficiences, portal hypertension

Front 1073

Complications of alcoholism: list clinical findings in alcoholic cirrhosis besides jaundice

Back 1073

peripheral edema and ascites, encephalopathy, neurologic manifestations (asterixis, flaping tremor of hands)

Front 1074

Complications of alcoholism: What is the cause of Wernicke-Korsakoff syndrome?

Back 1074

thiamine (B1) deficiency, particularly in alcoholics

Front 1075

Complications of alcoholism: what is the presenting triad of Wernicke's encephalopathy?

Back 1075

psychosis, ophthalmoplegia, and ataxia

Front 1076

Complications of alcoholism: distinguishing features of Korsakoff's from Wernicke's

Back 1076

in Korsakoff, also *memory loss*, confabulation,confusion.

Front 1077

Complications of alcoholism: is Korsakoff's syndrome reversible?

Back 1077

No.

Front 1078

Complications of alcoholism: Tx for Wernicke-Korsakoff syndrome

Back 1078

IV Vitamin B1 (thiamine)

Front 1079

Complications of alcoholism: What is Mallory-Weiss syndrome?

Back 1079

longitudinal lacerations at the gastroesophageal junction caused by excessive vomiting (for ex., in alcoholism) with failure of LES relaxation that could lead to fatal hematemesis

Front 1080

Argyll Robertson pupil: name for a pupil that constricts with accomodation but is not reactive to light, and what is it pathognomonic for?

Back 1080

Argyll Robertson pupil. Pathognomonic for 3' syphilis. "Prostitute's pupil" accomodates but does not react.

Front 1081

Amyloidosis: detect what using apple green biorefringence on Conco red stain?

Back 1081

amyloid

Front 1082

Amyloidosis: most common cause of amyloidosis?

Back 1082

primary light chain deposition seen with multiple myeloma.

Front 1083

Amyloidosis: another cause of primary amyloidosis?

Back 1083

Waldenstrom's macroglobulinemia.

Front 1084

Amyloidosis: Secondary amyloidosis can cause what in the kidney?

Back 1084

nephrotic syndrome

Front 1085

Amyloidosis: disease associated with beta amyloid deposition in cerebral cortex

Back 1085

Alzheimer's

Front 1086

Amyloidosis: islet cell amyloid deposition characteristic of what

Back 1086

diabetes mellitus type 2

Front 1087

Aschoff body: "-------- body" found in rheumatic heart disease

Back 1087

Aschoff body (granuloma with giant cells)

Front 1088

Aschoff body: "------- cells" found in rheumatic heart disease

Back 1088

Anitschkow's cells (activated histiocytes) "Aschoff and Anitschow" -- two RHussians with RHeumatic heart disease

Front 1089

Auer bodies (rods): peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts, name and primary association

Back 1089

Auer rods; primarily seen in acute promyelocytic leukemia (M3)

Front 1090

Auer bodies (rods): treatment of AML M3 can release what, leading to what?

Back 1090

release Auer rods, leading to DIC

Front 1091

Casts: RBC casts indicate

Back 1091

glomerular inflammation (nephritic syndromes), ischemia, or malignant hypertension

Front 1092

Casts: how to determine if hematuria/pyuria is of renal origin

Back 1092

presence of casts

Front 1093

Casts: WBC casts indicate

Back 1093

inflammation in renal interstitium, tubules, and glomeruli

Front 1094

Casts: casts often seen in normal urine

Back 1094

hyaline casts

Front 1095

Casts: casts seen in chronic renal failure

Back 1095

waxy casts

Front 1096

Erythrocyte sedimentation rate: ESR elevated in

Back 1096

dramatically in infection, malignancy, connective tissue disease; also in pregnancy, inflammatory disease, and anemia

Front 1097

Erythrocyte sedimentation rate: ESR lowered in

Back 1097

sickle cell anemia, CHF, and polycythemia

Front 1098

Erythrocyte sedimentation rate: Should ESR be used for asymptomatic screening

Back 1098

No

Front 1099

Erythrocyte sedimentation rate: ESR used to monitor course of -----

Back 1099

temporal arteritis and polymyalgia rheumatica

Front 1100

Erythrocyte sedimentation rate: ESR is expensive and specific. T/F

Back 1100

false. Cheap and nonspecific.

Front 1101

Ghon complex: indicates TB granulomas with lobar or perihilar lymph node involvement

Back 1101

Ghon focus and lymph node involvement, Ghon complex.

Front 1102

Ghon complex: Does a Ghon complex reflect primary or secondary TB?

Back 1102

primary.

Front 1103

Hyperlipidemia signs: plaque in blood vessel wall

Back 1103

atheromata

Front 1104

Hyperlipidemia signs: plaque or nodule composed of lipid-laden histiocytes in skin, especially eyelids

Back 1104

xanthoma

Front 1105

Hyperlipidemia signs: lipid deposit in tendon, especially Achilles

Back 1105

tendinous xanthoma

Front 1106

Hyperlipidemia signs: lipid deposit in cornea, nonspecific (arcus senilis)

Back 1106

corneal arcus

Front 1107

Psammoma bodies: laminated, concentric, calcific spherules in tumor

Back 1107

Psammoma bodies

Front 1108

Psammoma bodies: Psammoma bodies seen in:

Back 1108

1. papillary adenocarcinoma of thyroid 2. serous papillary cystadenoma of ovary 3. meningioma 4. malignant mesothelioma "PSaMMoma" Papillary (thyroid), Serous (ovary), Meningioma, Mesothelioma

Front 1109

RBC forms: Biconcave RBC

Back 1109

normal

Front 1110

RBC forms: Spherocytes

Back 1110

hereditary spherocytosis, autoimmmune hemolysis

Front 1111

RBC forms: Elliptocyte

Back 1111

hereditary elliptocytosis

Front 1112

RBC forms: Macro-ovalocyte

Back 1112

megaloblastic anemia, marrow failure

Front 1113

RBC forms: Helmet cell, schistocyte

Back 1113

DIC, traumatic hemolysis

Front 1114

RBC forms: Sickle cell

Back 1114

obviously sickle cell anemia

Front 1115

RBC forms: Teardrop cell

Back 1115

myeloid metaplasia with myelofibroblasts

Front 1116

RBC forms: Acanthocyte

Back 1116

spiny apearance in abetalipoproteinemia

Front 1117

RBC forms: Target cell

Back 1117

Thalassemia, liver disease, HbC

Front 1118

RBC forms: Poikilocyte

Back 1118

Nonuniform shapes in TTP/HUS, microvascular damage, DIC

Front 1119

RBC forms: Burr cell

Back 1119

TTP/HUS

Front 1120

HLA subtypes!: HLA B27

Back 1120

Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter's syndrome ("PAIR")

Front 1121

HLA subtypes!: HLA 13,17

Back 1121

Psoriasis

Front 1122

HLA subtypes!: HLA DR2

Back 1122

Multiple sclerosis, hay fever

Front 1123

HLA subtypes!: HLA DR3, DR4

Back 1123

Diabetes mellitus type I

Front 1124

HLA subtypes!: HLA DR5

Back 1124

Pernicious anemia -- B12 deficiency

Front 1125

HLA subtypes!: HLA DR7

Back 1125

Steroid-responsive nephrotic syndrome

Front 1126

Reed-Sternberg cells: Distinctive giant cell in blood; binucleate or bilobed with 2 halves as mirror images ("owl's eyes"); name and disease association

Back 1126

Reed-Sternberg cells, necessary but not sufficient for dx of Hodgkin's disease. Variants include lacunar cells in nodular sclerosis variant.

Front 1127

Reed-Sternberg cells: How many types of Hodgkin's disease?

Back 1127

4 - see also p. 241

Front 1128

Reed-Sternberg cells: Only variant of Hodgkin's seen more in women than men

Back 1128

nodular sclerosis

Front 1129

Reed-Sternberg cells: prognosis of nodular sclerosis variant of Hodgkin's

Back 1129

excellent

Front 1130

Virchow's (sentinel) node: firm supraclavicular lymph node, often on left side, easily palpable (ie, by medical students), also known as "jugular gland" - name and association

Back 1130

Virchow's node - presumptive evidence of malignant visceral neoplasm (classically stomach)

Front 1131

Peripheral blood smears: most common cause of microcytic hypochromic anemia

Back 1131

iron deficiency

Front 1132

Peripheral blood smears: ferritin levels in microcytic hypochromic anemia

Back 1132

low

Front 1133

Peripheral blood smears: serum iron-binding capacity in microcytic hypochromic anemia

Back 1133

elevated

Front 1134

Peripheral blood smears: lead poisoning gives what appearance on peripheral smear

Back 1134

microcytic hypochromic

Front 1135

Peripheral blood smears: causes of megaloblastic anemia

Back 1135

folate or B12 deficiency

Front 1136

Peripheral blood smears: 5-7 lobes (hypersegmented) PMNs in

Back 1136

megaloblastic anemia

Front 1137

Peripheral blood smears: large RBCs (MCV >100) in

Back 1137

megaloblastic anemia

Front 1138

Peripheral blood smears: do you give folate to pt. deficient in B12?

Back 1138

Never

Front 1139

Peripheral blood smears: autoimmune disease that causes B12 deficiency; what does it deplete?

Back 1139

pernicious anemia, depletes intrinsic factor

Front 1140

Peripheral blood smears: where is B12 absorbed in gut?

Back 1140

terminal ileum, with intrinsic factor from stomach

Front 1141

Peripheral blood smears: Target cells mnemonic

Back 1141

HALT (Hemoglobin C disease, Asplenia, Liver disease, Thalassemia)

Front 1142

Peripheral blood smears: Hemoglobin SS in what disease?

Back 1142

sickle cell anemia

Front 1143

Peripheral blood smears: molecular change B-globin GLU->VAL at #6

Back 1143

HbS

Front 1144

Peripheral blood smears: 8% of US african-americans carry what Hb

Back 1144

HbS

Front 1145

Peripheral blood smears: conditions in which HbSS cells sickle

Back 1145

hypoxia, dehydration, increased blood viscosity

Front 1146

Peripheral blood smears: vaso-occlusive crises with chest pain in young african-americanl; consider

Back 1146

sickle cell anemia

Front 1147

Peripheral blood smears: aplastic crises in sickle cell anemia associated with which virus

Back 1147

B19 virus

Front 1148

Peripheral blood smears: manifestation of sickle cell anemia in spleen

Back 1148

splenic sequestration crisis

Front 1149

Peripheral blood smears: increased risk of CVA in sickle cell anemia?

Back 1149

yes

Front 1150

Enzyme markers: AST or ALT used for MI?

Back 1150

AST only

Front 1151

Enzyme markers: AST or ALT more elevated in viral hepatitis

Back 1151

ALT>AST in viral hepatitis ("virALT")

Front 1152

Enzyme markers: AST or ALT more elevated in alcholic hepatitis

Back 1152

AST>ALT in alcoholic hepatitis ("ToAST")

Front 1153

Enzyme markers: Amylase elevation

Back 1153

acute pancreatitis, mumps

Front 1154

Enzyme markers: Low ceruloplasmin

Back 1154

Wilson's disease

Front 1155

Enzyme markers: Creatine phosphokinase elevated in

Back 1155

muscle disorders (Duchenne's muscular dystrophy), and MI

Front 1156

Enzyme markers: subtype of CPK elevated in MI

Back 1156

CPK-MB

Front 1157

Enzyme markers: GGT stands for and elevated in

Back 1157

gamma glutamyl transferase, various liver diseases

Front 1158

Enzyme markers: Lipase elevated in

Back 1158

acute pancreatitis

Front 1159

Enzyme markers: Alkaline phosphatase elevated in

Back 1159

Bone disease (Paget's disease of bone), obstructive liver disease (hepatocellular carcinoma)

Front 1160

Immunohistochemical stains: Vimentin stains what

Back 1160

connective tissue

Front 1161

Immunohistochemical stains: Desmin stains what

Back 1161

muscle

Front 1162

Immunohistochemical stains: Cytokeratin stains what

Back 1162

epithelial cells

Front 1163

Immunohistochemical stains: Glial fibrillary acid proteins (GFAP) stains what

Back 1163

neuroglia

Front 1164

Immunohistochemical stains: Neurofilament stains what

Back 1164

neurons

Front 1165

Immunohistochemical stains: AUTHOR

Back 1165

Shailen Sehgal

Front 1166

Enzyme Kinetics: _______ is elevated in a myocardial infarction. (AST, ALT, or both)

Back 1166

AST

Front 1167

Enzyme Kinetics: In viral hepatitis, is ALT or AST more elevated?

Back 1167

ALT

Front 1168

Enzyme Kinetics: In alcoholic hepatitis, is ALT or AST more elevated?

Back 1168

AST

Front 1169

Enzyme Kinetics: ________ can be elevated in mumps or acute pancreatitis, while _________ elevation is more specific for acute pancreatitis.

Back 1169

amylase, lipase

Front 1170

Enzyme Kinetics: What enzyme is elevated in Duchenne's muscular dystrophy, and after a myocardial infarction?

Back 1170

CPK

Front 1171

Enzyme Kinetics: _______ can be elevated in Paget's disease and hepatocellular carcinoma.

Back 1171

alkaline phosphatase

Front 1172

Enzyme Kinetics: Elevated GGT is seen in various diseases of which organ?

Back 1172

liver

Front 1173

Enzyme Kinetics: True or False? In a myocardial infarction, serum LDH-1>LDH-2

Back 1173

TRUE

Front 1174

Enzyme Kinetics: Decreased serum ceruloplasmin is seen in _______

Back 1174

Wilson's Disease

Front 1175

Immunohistochemical Stain Corresponding cell type: (Match the stain with the corresponding cell type)

Back 1175

0

Front 1176

Immunohistochemical Stain Corresponding cell type: Vimentin

Back 1176

connective tissue

Front 1177

Immunohistochemical Stain Corresponding cell type: Cytokeratin

Back 1177

Epithelial cells

Front 1178

Immunohistochemical Stain Corresponding cell type: Neurofilaments

Back 1178

neurons

Front 1179

Immunohistochemical Stain Corresponding cell type: Glial Fibrillary acid proteins (GFAP)

Back 1179

neuroglia

Front 1180

Immunohistochemical Stain Corresponding cell type: Desmin

Back 1180

muscle

Front 1181

Pharmacokinetics: amount of drug in body/_______ = Vd

Back 1181

plasma drug concentration (note: Vd is Volume of Distribution)

Front 1182

Pharmacokinetics: rate of elimination of drug/[plasma drug] = ?

Back 1182

CL (Clearance)

Front 1183

Pharmacokinetics: (.7)(Vd)/CL = ?

Back 1183

T 1/2

Front 1184

Pharmacokinetics: A drug infused at a constant rate reaches about 94% of steady state after _______ t 1/2s.

Back 1184

4

Front 1185

Dosage Calculations: A loading dose is calculated using this formula.

Back 1185

(Cp)(Vd)/F (note: Cp = target plasma concentration, and F = bioavailability)

Front 1186

Dosage Calculations: A maintenance dose is calculated using this formula.

Back 1186

(Cp)(CL)/F

Front 1187

Elimination of Drugs: Rate of elimination is proportional to _______ ______ in 1st order elimination.

Back 1187

drug concentration

Front 1188

Elimination of Drugs: In the case of EtOH, which is elimated by _____ order elimination, a constant amount of drug is eliminated per unit time.

Back 1188

zero

Front 1189

Phase I vs. Phase II metabolism: Phase ____ (I or II) reactions yield slightly polar metabolites that are often _____ (active or inactive)

Back 1189

I, active

Front 1190

Phase I vs. Phase II metabolism: Phase ____ (I or II) reactions yield very polar metabolites that are often _____ (active or inactive) and are excreted by the _______.

Back 1190

II, inactive, kidney

Front 1191

Phase I vs. Phase II metabolism: Phase II reactions are often of this type.

Back 1191

conjugation

Front 1192

Phase I vs. Phase II metabolism: Cytochrome P-450 is involved in _____ phase (I or II) reactions.

Back 1192

I

Front 1193

Drug Development: A patent lasts for _____ years after filing for application.

Back 1193

20

Front 1194

Drug Development: How many phases are there in drug development?

Back 1194

4

Front 1195

Drug Development: Drugs are first tested in patients in phase _____ of clinical testing, pharmacokinetic safety is determined in phase ______ of clinical testing, double blind tests are done in phase ____ and post-market surveillance is done in phase _____.

Back 1195

2,1,3,4

Front 1196

Pharmacodynamics: In a dose response curve, a competitive antagonist shifts the curve _____, while a non-competitive antagonist shifts the curve ______.

Back 1196

right, down

Front 1197

Pharmacodynamics: AUTHOR

Back 1197

HiralShah

Front 1198

Pharmacodynamics (continued): What pharmacologic relationship would determine the existence of spare receptors?

Back 1198

EC50 < Kd

Front 1199

Pharmacodynamics (continued): What does it mean if EC50 and Kd are equal?

Back 1199

The system does not have spare receptors

Front 1200

Pharmacodynamics (continued): A partial agonist acts on the same receptor system as a full agonist? T/F

Back 1200

TRUE

Front 1201

Pharmacodynamics (continued): What's the main difference between a partial agonist and a full agonist?

Back 1201

A partial agonist has a lower maximal efficacy.

Front 1202

Pharmacodynamics (continued): Is a partial agonist less potent than a full agonist?

Back 1202

Not necessarily. It can be less, more or equally potent as a full agonist.

Front 1203

Antimicrobial Tx -- Mechanism of Action: The penicillin type drugs work by blocking ------ synthesis, specifically by inhibiting this molecule from cross-linking?

Back 1203

blocks bacterial cell wall synthesis by inhibition of peptidoglycan synthesis.

Front 1204

Antimicrobial Tx -- Mechanism of Action: Which other drugs (aside from penicillin) have this same mechanism of action?

Back 1204

Imipenem, aztreonam and cephalosporins

Front 1205

Antimicrobial Tx -- Mechanism of Action: Bacitracin, vancomycin and cycloserine block the synthesis of this molecule, preventing cell wall synthesis

Back 1205

peptidoglycans

Front 1206

Antimicrobial Tx -- Mechanism of Action: These drugs block the 50s ribosomal subunit

Back 1206

clindamycin, chloramphenicol, erythromycin, lincomycin, linezolid, streptogramins "Buy AT 30, CELL at 50"

Front 1207

Antimicrobial Tx -- Mechanism of Action: These drugs block the 30s ribosomal subunit

Back 1207

Aminoglycosides and tetracyclines "Buy AT 30, CELL at 50"

Front 1208

Antimicrobial Tx -- Mechanism of Action: These drugs block nucleotide synthesis by interfering with the folate pathway

Back 1208

Sulfonamides (e.g. Bactrim), trimethoprim

Front 1209

Antimicrobial Tx -- Mechanism of Action: These drugs block DNA topoisomerases

Back 1209

Quinolones (e.g. Cipro)

Front 1210

Antimicrobial Tx -- Mechanism of Action: Which drug blocks mRNA synthesis

Back 1210

rifampin

Front 1211

Antimicrobial Tx -- Mechanism of Action: Which are the bacteriacidal Abx

Back 1211

Penicillin, cephalosporin, vancomycin, aminoglycosides, fluoroquinolones, metronidazole

Front 1212

Antimicrobial Tx -- Mechanism of Action: These drugs disrupt the bacterial/fungal cell membranes

Back 1212

polymyxins

Front 1213

Antimicrobial Tx -- Mechanism of Action: These specific disrupt fungal cell membranes

Back 1213

amphotericin B, nystatin, fluconazole/azoles (FAN the fungal cell membranes)

Front 1214

Antimicrobial Tx -- Mechanism of Action: What is the mechanism of action of Pentamidine

Back 1214

Unknown

Front 1215

Penicillin: Which is the IV form and which is the oral form

Back 1215

G = IV, V=oral

Front 1216

Penicillin: Which of these is not a mechanism of penicillin action: (1) binds penicillin-binding protein, (2) blocks peptidoglycan synthesis, (3) blocks transpeptidase catalyzed cross-linking of cell wall and (4) activates autolytic enzymes

Back 1216

Penicillin does not block peptioglycan synthesis, bacitracin, vancomycin and cycloserine do that

Front 1217

Penicillin: T or F: penicillin is effective against gram pos and gram neg rods

Back 1217

False: penicillin is used to treat common streptococci (but not staph), meningococci, gram pos bacilli and spirochetes (i.e. syphilis, treponema). Not used to treat gram neg rods.

Front 1218

Penicillin: What should you watch out for when giving penicillin?

Back 1218

Hypersensitivity rxn (urticaria,severe pruritus) and hemolytic anemia

Front 1219

Methicillin, nafcillin, dicloxacillin: These drugs are used mainly for what type of infection

Back 1219

Staphlococcal infection (hence very narrow spectrum)

Front 1220

Methicillin, nafcillin, dicloxacillin: T or F: these drugs have the same mechanism of action as penicillin

Back 1220

TRUE

Front 1221

Methicillin, nafcillin, dicloxacillin: Are these drugs penicillinase resistant? If so why?

Back 1221

Bulkier R group makes these drugs resistant to penicillinase

Front 1222

Methicillin, nafcillin, dicloxacillin: What should you watch out for when giving these drugs?

Back 1222

Hypersensitivity rxn (urticaria,severe pruritus); methicillin can cuase interstitial nephritis

Front 1223

Ampicillin and amoxicillin: T or F: these drugs have the same mechanism of action as penicillin

Back 1223

TRUE

Front 1224

Ampicillin and amoxicillin: Which has greater oral bioavailability?

Back 1224

amOxicillin (O for Oral)

Front 1225

Ampicillin and amoxicillin: What do you use these for?

Back 1225

Ampicillin/amoxicillin HELPS to kill enterococci (H. influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella)

Front 1226

Ampicillin and amoxicillin: Can penicillinase effect these drugs efficacy?

Back 1226

Yes, they are penicillinase sensitive

Front 1227

Ampicillin and amoxicillin: Why not give these drugs with a penicillinase inhibitor. Name one.

Back 1227

clavulanic acid

Front 1228

Ampicillin and amoxicillin: What should you watch out for when giving these drugs?

Back 1228

Hypersensitivity rxn (ampicillin rash), pseudomembranous colitis

Front 1229

Carbenicillin, piperacillin, ticarcillin: Why are these considered to have an extended spectrum?

Back 1229

Because they are effective against pseudomonas and other gram neg rods (enterobacter and some species of klebsiella)

Front 1230

Carbenicillin, piperacillin, ticarcillin: What should you watch out for when giving these drugs?

Back 1230

Hypersensitivity rxn

Front 1231

Carbenicillin, piperacillin, ticarcillin: Why does concomitant administration with clavulanic acid increase the efficacy of these drugs?

Back 1231

Because they are penicillinase sensitive. (only piperacillin and ticarcillin)

Front 1232

Cephalosporins: What is the mechanism of action of Cephalosporins?

Back 1232

inhibit cell wall synthesis

Front 1233

Cephalosporins: How are they similar/different from penicillin?

Back 1233

both have a beta-lactam ring structure but cephalosporins are less susceptible to penicillinases

Front 1234

Cephalosporins: What are the main similarities/difference between 1st and 2nd generation cephalosporins?

Back 1234

2nd gen has extensive gram neg coverage but weaker gram pos coverage

Front 1235

Cephalosporins: 1st gen covers what bugs?

Back 1235

gram positives (staph and strep), Proteus mirabilis, E. coli, Klebsiella (PEcK)

Front 1236

Cephalosporins: 2nd gen covers what bugs?

Back 1236

gram positives (staph and strep) though less so, H. influenzae, Enterobacter aerogenes, Neisseria, Proteus mirabilis, E. coli, Klebsiella (HEN PEcK)

Front 1237

Cephalosporins: What can 3rd generation drugs do that 1st and 2nd generation can't?

Back 1237

Cross the blood brain barrier

Front 1238

Cephalosporins: What are some other benefits of 3rd gen?

Back 1238

better activity against gram neg bugs resistant to beta-lactam drugs. Ceftazidime for Pseudomonas and ceftriaxone for N. gonorrhea

Front 1239

Cephalosporins: What are the benefits of 4th gen (e.g. Cefipime)?

Back 1239

increased activity against Pseudomonas, gram pos organisms and more beta-lactamase resistant (i.e. 4th gen combines 1st gen and 3rd gen characteristics into super drug)

Front 1240

Cephalosporins: What drugs should you avoid taking with cephalosporins?

Back 1240

Aminoglycosides (increases nephrotoxicity) and ethanol (causes a disulfiram-like rxn -- headache, nausea, flushing, hypotension)

Front 1241

Aztreonam: When would you use aztreonam?

Back 1241

Only to treat Klebsiella, Pseudomonas and Serratia sp.

Front 1242

Aztreonam: Is it beta-lactamase resistant?

Back 1242

Yes, this is one of the huge benefits of the drug, and it is not cross-reactive with PCN!

Front 1243

Aztreonam: Which population of pt. is this drug good for?

Back 1243

The PCN-allergic patient that can't take aminoglycosides b/c of renal insufficiency

Front 1244

Aztreonam: Are there any toxicity issues with this drug?

Back 1244

Not really. Generally well tolerated with occasional GI upset. Vertigo, Headache and rare hepatotoxicity have been reported.

Front 1245

Imipenem/cilastatin: What is imipenem?

Back 1245

broad spectrum beta-lactamase-resistant abx

Front 1246

Imipenem/cilastatin: What do you always administer it with and why?

Back 1246

cilastatin -- it decreases inactivation of imipenem in renal tubules

Front 1247

Imipenem/cilastatin: What do you use it for?

Back 1247

Gram pos cocci, gram neg rods and anaerobes (broad spectrum)

Front 1248

Imipenem/cilastatin: What bug is it the drug of choice for?

Back 1248

Enterobacter

Front 1249

Imipenem/cilastatin: What are its side-effects

Back 1249

GI distress, skin rash, seizures at high conc.

Front 1250

Vancomycin: Is it bactericidal or bacteriastatic and why?

Back 1250

Bactericidal because it blocks cross linkage and elongation of peptidoglycan by binding D-ala D-ala protion of cell wall.

Front 1251

Vancomycin: How does resistance to Vanco occur?

Back 1251

D-ala D-ala is replaced with D-ala D-lactate which vanco does not block

Front 1252

Vancomycin: What is it used for?

Back 1252

Used for serious infection that is resistant to other drugs (e.g. gram pos multi-drug resistant organisms like S. aureus and C. difficile, methicillin resistant staph (MRSA))

Front 1253

Vancomycin: What are the important toxicities of vanco?

Back 1253

generally NOT many problems except, Nephrotoxicity, Ototoxicity and Thrombophlebitis

Front 1254

Vancomycin: What can happen with rapid infusion of vanco?

Back 1254

Red man's syndrome. Diffuse flushing which can be controlled by pretreatment with anti-histamines and with slow infusion rate

Front 1255

Protein Synthesis Inhibitors: Which drugs target bacterial protein synthesis by blocking the 30S unit vs 50S unit?

Back 1255

Buy AT 30, CELL at 50

Front 1256

Protein Synthesis Inhibitors: What does AT stand for?

Back 1256

A = Aminoglycosides (streptomycin, gentamicin, tobramycin an damikacin. And T = Tetracyclines

Front 1257

Protein Synthesis Inhibitors: What does CELL stand for?

Back 1257

C = Chloramphenicol, E= Erythromycin, L= Lincomycin and L= cLindamycin

Front 1258

Protein Synthesis Inhibitors: Which of the above are bactericidal?

Back 1258

Only the aminoglycosides are, the rest are bacteriostatic

Front 1259

Aminoglycosides: Name some aminoglycosides?

Back 1259

Gentamicin, neomycin, amikacin, tobramycin and streptomycin

Front 1260

Aminoglycosides: How do these drugs work?

Back 1260

They inhibit formation of the initiation complex in mRNA translation

Front 1261

Aminoglycosides: Why are they ineffective against anaerobes?

Back 1261

They require oxygen for uptake into bacteria

Front 1262

Aminoglycosides: When would you use aminoglycosides?

Back 1262

against severe gram-negative rod infections

Front 1263

Aminoglycosides: What drugs can you use aminoglycosides with for synergy?

Back 1263

the drugs that inhibit cell wall synthesis (e.g. penicillin and cephalosporins -- the beta-lactam antibiotics). Presumably this allows the drug to get in with out reliance on oxygen transport

Front 1264

Aminoglycosides: What drug in this class is commonly used for bowel surgery?

Back 1264

Neomycin

Front 1265

Aminoglycosides: What are the two major toxicities?

Back 1265

Nephrotoxicity (esp. when used with cephalosporins) and Ototoxicity (esp. when used with loop diuretics). amiNOglycosides

Front 1266

Tetracyclines: Name some tetracylcines

Back 1266

Tetracycline, doxycycline, demeclocycline, minocycline

Front 1267

Tetracyclines: How does it work?

Back 1267

Blocks t-RNA attachment to 30S subunit

Front 1268

Tetracyclines: Which tetracycline can you use in patients with renal failure and why?

Back 1268

Can use doxycycline because its elimination is fecal

Front 1269

Tetracyclines: Should you take these drugs with a glass of milk?

Back 1269

NO, because it intereferes with absorption in the gut as does antacids and iron-containing preparations

Front 1270

Tetracyclines: What are tetracyclines used for?

Back 1270

VACUUM your Bed Room -- Vibrio cholerae, Acne, Chlamydia, Ureaplasma, Urealyticum, Mycoplasma pneumoniae, Borrelia burgdorferi, Rickettsia, tularemia

Front 1271

Tetracyclines: What are the common toxicities

Back 1271

GI distress, teeth discoloration, inhibition of bone growth in children, Fanconi's syndrome and photosensitivity

Front 1272

Macrolides: Name some macrolides?

Back 1272

Erythromycin, azithromycin, clarithromycin

Front 1273

Macrolides: How do these drugs work?

Back 1273

inhibit protein synthesis

Front 1274

Macrolides: What are they used for?

Back 1274

URIs, pneumonias, STDs -- gram pos cocci in patients that are allergic to PNC --- Mycoplasm, Legionella, Chlamydia, Neisseria.

Front 1275

Macrolides: Pneumonic for macrolide use?

Back 1275

Eryc's Niple is at his Mid Clavicular Line (Eryc is brand name for erythromycin). Mycoplasm, Legionella, Chlamydia, Neisseria.

Front 1276

Macrolides: What are the major toxicities?

Back 1276

GI discomfort, acute cholestatic hepatitis, eosinophilia, skin rashes

Front 1277

Macrolides: What is the most common cause for non-compliance to macrolides?

Back 1277

GI discomfort

Front 1278

Chloramphenicol: How does this drug work?

Back 1278

inhibits 50S peptidyltransferase

Front 1279

Chloramphenicol: Main use?

Back 1279

Meningitis (H. influenzae, N. meningitides, S. pneumo). Used conservatively b/c of toxicity

Front 1280

Chloramphenicol: What are the main toxicities?

Back 1280

Anemia and aplastic anemia (both dose dependent), gray baby syndrome (in premes b/c they lack UDP-glucoronyl transferase)

Front 1281

Clindamycin: How does it work?

Back 1281

blocks peptide bond formation at 50S

Front 1282

Clindamycin: When do you use it?

Back 1282

Anaerobic infections (e.g. Bacteroides fragilis and C.perfringens)

Front 1283

Clindamycin: Toxicities?

Back 1283

Pseudomembranous colitis, fever, diarrhea

Front 1284

Sulfonamides: Name some sulfonamides

Back 1284

Sulfamethoxazole (SMX), sulfisoxazole, triple sulfa and sulfadiazine

Front 1285

Sulfonamides: How does it work?

Back 1285

Inhibits bacterial folic acid synthesis from PABA by blocking dihydropteroate synthase.

Front 1286

Sulfonamides: What are its uses?

Back 1286

Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas and SMX for simple UTIs

Front 1287

Sulfonamides: Toxicities?

Back 1287

hypersensitivity rxn, hemolysis if G6PD deficient, nephorotoxicity (tubulointerstitial nephritis), kernicterus in infants, displace other drugs from albumin (e.g. warfarin)

Front 1288

Trimethoprim: How does it work?

Back 1288

inhibits folic acid pathway by blocking dihydrofolate reductase which humans have as well

Front 1289

Trimethoprim: What are its uses?

Back 1289

used in combo with Sulfamethoxazole (TMP-SMX) causing a sequential block of folate synthesis. Used for recurrent UTIs, Shigella, Salmonella, and prophylaxis for PCP in AIDS patients

Front 1290

Trimethoprim: Toxicities?

Back 1290

Megaloblastic anemia, pancytopenia (may be alleviated with suplemental folinic acid)

Front 1291

Fluoroquinolones: What the most famous floroquinolone?

Back 1291

Ciprfloxacin (treatment for Anthrax)

Front 1292

Fluoroquinolones: How does it work?

Back 1292

inhibits DNA gyrase (topoisomerase II)

Front 1293

Fluoroquinolones: What are its uses?

Back 1293

Gram neg rods or urinary and GI tract (incl. pseudomonas), Neisseria, some gram pos sp

Front 1294

Fluoroquinolones: What population is contraindicated for use?

Back 1294

pregnancy and children

Front 1295

Fluoroquinolones: What are its toxicities?

Back 1295

GI upset, superinfection, skin rashes, headache, dizziness and tendonitis and tendon rupture in adults. FluoroquinoLONES hurt attachment to BONES.

Front 1296

Metronidazole: How does it work?

Back 1296

forms toxic metabolites in the bacteria. Bactericidal.

Front 1297

Metronidazole: What are its uses?

Back 1297

anti-protozoal: Giardia, Entamoeba, Trichomonas, Gardnerella vaginalis, anaerobes (bacteroides, clostridium)

Front 1298

Metronidazole: What is the role of Metronidazole in H. pylori infection?

Back 1298

Used as part of triple therapy: bismuth, amoxicillin and metronidazole

Front 1299

Metronidazole: Main toxicity?

Back 1299

disulfiram-like (antabuse) reaction to alcohol and headache

Front 1300

Metronidazole: Which drug do you use to treat anaerobic infections above the diaphram and below the diaphram

Back 1300

anaerobes above diaphram: Clindamycin, and anaerobes below diaphram: metronidazole

Front 1301

Polymyxins: How does it work?

Back 1301

disrupts osmotic properties of bacteria, acts like a detergent

Front 1302

Polymyxins: What is it used for?

Back 1302

resistant gram negative infections

Front 1303

Polymyxins: Toxicities?

Back 1303

neurotoxicity, ATN

Front 1304

Isoniazid: How does it work?

Back 1304

decreases synthesis of mycolic acid

Front 1305

Isoniazid: What is it used for?

Back 1305

MTB (mycobacterium tuberculosis). The only agent used as solo prophylaxis against TB

Front 1306

Isoniazid: Toxicities?

Back 1306

Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicitiy, drug induced SLE. INH, Injures Neurons and Hepatocytes

Front 1307

Isoniazid: What vitamin prevents neurotoxicity

Back 1307

Vitamin B6 (pyridoxine)

Front 1308

Isoniazid: Why are toxicities particularly important to monitor in patients taking INH?

Back 1308

INH half-lives are different in fast versus slow acetylators!

Front 1309

Rifampin: How does it work?

Back 1309

inhibits DNA-dependent RNA polymerase

Front 1310

Rifampin: What is it used for?

Back 1310

MTB, meningococcal prophylaxis

Front 1311

Rifampin: Toxicities?

Back 1311

Minor hepatotoxicity and increases P-450

Front 1312

Rifampin: How can it be used for leprosy?

Back 1312

rifampin delays resistance to dapsone when used for leprosy

Front 1313

Rifampin: What would happen if you used rifampin alone?

Back 1313

get rapid resistance

Front 1314

Rifampin: What does it do to bodily fluids?

Back 1314

makes them red/orange in color

Front 1315

Rifampin: What are the 4 R's of Rifampin

Back 1315

RNA polymerase inhibitor, Revs up microsomal p-450, Red/Orange body fluids, Resistance is rapid

Front 1316

Anti-TB Drugs: What are the anti-TB drugs?

Back 1316

Rifampin, Ethambutol, Streptomycin, Pyrazinamide, Isoniazid (INH) -- RESPIre

Front 1317

Anti-TB Drugs: What do you use for TB prophylaxis?

Back 1317

INH

Front 1318

Anti-TB Drugs: What toxicity is common to all?

Back 1318

hepatotoxicity

Front 1319

Anti-TB Drugs: AUTHOR

Back 1319

Michael Shino

Front 1320

Resistance mechanisms for various antibiotics: Most common resistance mechanism for penicillins / cephalosporins.

Back 1320

Beta-lactamase cleavage of beta-lactam ring.

Front 1321

Resistance mechanisms for various antibiotics: Most common resistance mechanism for aminoglycosides.

Back 1321

Modification via acetylation, adenylation, or phosphorylation.

Front 1322

Resistance mechanisms for various antibiotics: Most common resistance mechanism for vancomycin.

Back 1322

Terminal D-ala of cell wall component replaced with D-lac; decrease affinity.

Front 1323

Resistance mechanisms for various antibiotics: Most common resistance mechanism for Chlorampenicol.

Back 1323

Modification via acetylation.

Front 1324

Resistance mechanisms for various antibiotics: Most common resistance mechanism for macrolides.

Back 1324

Methylation of rRNA near erythromycin's ribosome-binding site.

Front 1325

Resistance mechanisms for various antibiotics: Most common resistance mechanism for tetracycline.

Back 1325

Decrease uptake or increase transport out of cell.

Front 1326

Resistance mechanisms for various antibiotics: Most common resistance mechanism for sulfonamides.

Back 1326

Altered enzyme (bacterial dihydropteroate synthetase), decrease uptake, or increase PABA synthesis.

Front 1327

Nonsurgical antimicrobial prophylaxis: Drug of choice for meningococcal infection.

Back 1327

Rifampin (drug of choice), minocycline.

Front 1328

Nonsurgical antimicrobial prophylaxis: Drug of choice for gonorrhea.

Back 1328

Cefriaxone.

Front 1329

Nonsurgical antimicrobial prophylaxis: Drug of choice for syphilis.

Back 1329

Benzathine penicillin G.

Front 1330

Nonsurgical antimicrobial prophylaxis: Drug of choice for history of recurrent UTIs.

Back 1330

TMP-SMX.

Front 1331

Nonsurgical antimicrobial prophylaxis: Drug of choice for Pneumocystis carinii pneumonia.

Back 1331

TMP-SMX (drug of choice), aerosolized pentamindine.

Front 1332

Anti-fungal therapy: Mechanism of action of the anti-fungal therapy polyenes.

Back 1332

Form artificial pores in the cytoplasmic membrane.

Front 1333

Anti-fungal therapy: Mechanism of action of the anti-fungal therapies terbinafine and azoles.

Back 1333

Terbinafine blocks the conversion of squalene to lanosterol. Azoles block the conversion of lanosterol to ergosterol.

Front 1334

Anti-fungal therapy: Mechanism of action of the anti-fungal therapy flucytosine.

Back 1334

Blocks the production of purines from the precurors.

Front 1335

Anti-fungal therapy: Mechanism of action of the anti-fungal therapy griseofulvin.

Back 1335

Disrupts microtubles.

Front 1336

Amphotericin B: Mechanism of action of Amphotericin B.

Back 1336

Binds ergosterol (unique to fungi); forms membrane pores that allow leakage of electrolytes and disrupt homeostasis. "Amphotericin 'tears' holes in the fungal membrane by forming pores."

Front 1337

Amphotericin B: Clinical uses of Amphotericin B.

Back 1337

Used for a wide spectrum of sytemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.

Front 1338

Amphotericin B: Symptoms of Amphotericin B toxicity.

Back 1338

Fever/chills ("shake and bake"), hypotension, nephrotoxicity, arrhythmias ("amphoterrible").

Front 1339

Nystatin: Mechanism of action of Nystatin.

Back 1339

Binds to ergosterol, disrupting fungal membranes.

Front 1340

Nystatin: Clinical use of Nystatin.

Back 1340

Swish and swallow for oral candidiasis (thrush).

Front 1341

Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Mechanism of action for fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.

Back 1341

Inhibits fungal steroid (ergosterol) synthesis.

Front 1342

Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Clinical uses of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.

Back 1342

Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, coccidioides, Histoplasma, Candida albicans; hypercortisolism.

Front 1343

Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole.: Symptoms of fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole toxicity.

Back 1343

Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills.

Front 1344

Flucytosine: Mechanism of action of Flucytosine.

Back 1344

Inhibits DNA synthesis byconversion to fluorouracil, which competes with uracil.

Front 1345

Flucytosine: Clinical uses of Flucytosine.

Back 1345

Used in sytemic fungal infections (e.g. Candida, Cryptococcus).

Front 1346

Flucytosine: Symptoms of Flucytosine toxicity.

Back 1346

Nausea, vomitting, diarrhea, bone marrow supression.

Front 1347

Caspofungin: Mechanism of action for Caspofungin.

Back 1347

Inhibits cell wall synthesis.

Front 1348

Caspofungin: Clinical use of Caspofungin.

Back 1348

Invasive aepergillosis.

Front 1349

Caspofungin: Symptoms of Caspofungin toxicity.

Back 1349

GI upset, flushing.

Front 1350

Terbinafine: Mechanism of action of Terbinafine.

Back 1350

Inhibits the fungal enzyme squalene epoxidase.

Front 1351

Terbinafine: Clinical use of Terbinafinel.

Back 1351

Used to treat dermatophytoses (especially onychomycosis).

Front 1352

Griseofulvin: Mechanism of action of Griseofulvin.

Back 1352

Interfers with microtubule function; disrupts mitosis. Deposits in keratin-contianing tissues (e.g. nails).

Front 1353

Griseofulvin: Clinical use of Griseofulvin.

Back 1353

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm).

Front 1354

Griseofulvin: Symptoms of Griseofulvin toxicity.

Back 1354

Teratogenic, carcinogenic, confusion, headaches, increase warfarin metabolism.

Front 1355

Antiviral chemotherapy: Viral adsorption and penetration into the cell is blocked by ---------.

Back 1355

Gama-globulins (non-specific).

Front 1356

Antiviral chemotherapy: Uncoating of the virus after its penetration into the cell is blocked by --------.

Back 1356

Amantadine (influenza A).

Front 1357

Antiviral chemotherapy: Early viral protein synthesis is blocked by --------.

Back 1357

Fomivirsen (CMV).

Front 1358

Antiviral chemotherapy: Viral nuclei acid synthesis is blocked by --------.

Back 1358

Purine, pyrimidine analogs; reverse transcriptase inhibitors.

Front 1359

Antiviral chemotherapy: Late viral protein synthesis and processing is blocked by --------.

Back 1359

Methimazole (variola); protease inhibitors.

Front 1360

Antiviral chemotherapy: Packaging and assembly of new viron is blocked by --------.

Back 1360

Rifampin (vaccinia).

Front 1361

Amantadine: Mechanism of action of Amantadine.

Back 1361

Blocks viral penetration/uncoating; may buffer pH of endosome. Also causes the release of dopamine from intact nerve terminals. "Amantadine blocks influenza A and rubellA and causes problems with the cerebellA."

Front 1362

Amantadine: Clinical uses of Amantadine.

Back 1362

Prophylaxis for influenza A; Parkinson's disease.

Front 1363

Amantadine: Symptoms of Amantadine toxicity.

Back 1363

Ataxia, dizziness, slurred speech. (Rimantidine is a derivative with fewer CNS side effects.)

Front 1364

Zanamivir: Mechanism of action of Zanamivir.

Back 1364

Inhibits influenza neuraminidase.

Front 1365

Zanamivir: Clinical use of Zanamivir.

Back 1365

Both influenza A and B.

Front 1366

Ribavirin: Mechanism of action of Ribavirin.

Back 1366

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.

Front 1367

Ribavirin: Clinical use of Ribavirin.

Back 1367

RSV (respiratory syncytial virus).

Front 1368

Ribavirin: Symptoms of Ribavirin toxicity.

Back 1368

Hemolytic anemia. Severe teratogen.

Front 1369

Acyclovir: Mechanism of aciton of Acyclovir.

Back 1369

Perferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.

Front 1370

Acyclovir: Clinical use of Acyclovir.

Back 1370

HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in immunocompromised patients.

Front 1371

Acyclovir: Symptoms of Acyclovir toxicity.

Back 1371

Delirium, tremor, nephrotoxicity.

Front 1372

Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Mechanism of action of Ganciclovir.

Back 1372

Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.

Front 1373

Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Clinical use of Ganciclovir.

Back 1373

CMV, especially in immunocompromised patients.

Front 1374

Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine): Symptoms of Ganciclovir toxicity.

Back 1374

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

Front 1375

Foscarnet: Mechanism of action of Foscarnet.

Back 1375

Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."

Front 1376

Foscarnet: Clinical use of Foscarnet.

Back 1376

CMV retinitis in immunocompromised patients when ganciclovir fails.

Front 1377

Foscarnet: Symptoms of Foscarnet toxicity.

Back 1377

Nephrotoxicity.

Front 1378

HIV therapy: Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.

Back 1378

Protease inhibitor.

Front 1379

HIV therapy: Mechanism of action of protease inhibitors.

Back 1379

Inhibit assembly of new virus by blocking protease enzyme.

Front 1380

HIV therapy: Symptoms of protease inhibitor toxicity.

Back 1380

GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir).

Front 1381

HIV therapy: Reverse transcriptase inhibitors:

Back 1381

0

Front 1382

HIV therapy: Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), and abacavir are examples of --------- reverse transcriptase inhibitors.

Back 1382

Nucleoside.

Front 1383

HIV therapy: Nevirapine, delavirdine, and efavirenz are examples of --------- reverse transcriptase inhibitors.

Back 1383

Non-nucleoside.

Front 1384

HIV therapy: Mechanism of action of reverse transcriptase inhibitors.

Back 1384

Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of viral genome into host DNA.

Front 1385

HIV therapy: Symptoms of reverse transcriptase inhibitor toxicity.

Back 1385

Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).

Front 1386

HIV therapy: Highly active antiretroviral therapy (HAART) generally entails combination therapy with ---------- and -----------.

Back 1386

Protease inhibitors, reverse transcriptase inhibitors.

Front 1387

HIV therapy: When should HIV therapy be initiated?

Back 1387

When patients have low CD4 counts (<500 cells/mm3) or high viral load.

Front 1388

HIV therapy: -------- is used during pregnancy to reduce risk of fetal transmission.

Back 1388

AZT.

Front 1389

Interferons: Mechanism of action of Interferons.

Back 1389

Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.

Front 1390

Interferons: Clinical use of Interferons.

Back 1390

Chronic hepatitis B and C, Kaposi's sarcoma.

Front 1391

Interferons: Symptoms of Interferon toxicity.

Back 1391

Neutropenia.

Front 1392

Antiparasitic drugs: Clinical uses of Ivermectin.

Back 1392

Onchocerciasis "rIVER blindness treated with IVERmectin".

Front 1393

Antiparasitic drugs: Clinical uses of Mebendazole / thiabendazole.

Back 1393

Nematode/roundworm (e.g., pinworm, whipworm) infections.

Front 1394

Antiparasitic drugs: Clinical uses of Pyrantel pamoate.

Back 1394

Giant roundworm (Ascaris), hookworm (Necator/Ancylostoma), pinworm (Enterobius).

Front 1395

Antiparasitic drugs: Clinical uses of Praziquantel.

Back 1395

Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis) and cysticercosis.

Front 1396

Antiparasitic drugs: Clinical uss of Niclosamide

Back 1396

Cestode/tapeworm (e.g., Diphyllobothrium latum, Taenia species) infections except cysticercosis.

Front 1397

Antiparasitic drugs: Clinical uses of Pentavalent antimony.

Back 1397

Leishmaniasis.

Front 1398

Antiparasitic drugs: Clinical uses of Chloroquine, quinine, mefloquine, atovaquone, proguanil.

Back 1398

Malaria.

Front 1399

Antiparasitic drugs: Clinical uses of Primaquine.

Back 1399

Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P.ovale).

Front 1400

Antiparasitic drugs: Clinical uses of Metronidazole.

Back 1400

Giardiasis, amebic dysentery (Entamoeba histolytica), bacterial vaginitis (Gardnerella vaginalis), Trichomonas.

Front 1401

Antiparasitic drugs: Clinical uses of Pentamidine.

Back 1401

Pneumocystis carinii pneumonia prophylaxis.

Front 1402

Antiparasitic drugs: Clinical uses of Nifurtimox.

Back 1402

Chagas' disease, American trypanosomiasis (Trypanosoma cruzi).

Front 1403

Antiparasitic drugs: Clinical uses of Suramin.

Back 1403

African trypanosomiasis (sleeping sickness).

Front 1404

Pharmacology - CNS / Neurologic drugs: Parasympathetic preganglionic neurons release the neurotransmitter -------- which act on -------- receptors.

Back 1404

Ach, nicotinic.

Front 1405

Pharmacology - CNS / Neurologic drugs: Parasympathetic postganglionic neurons release the neurotransmitter -------- which act on ------- receptors.

Back 1405

Ach, muscarinic.

Front 1406

Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.

Back 1406

Ach, nicotinic.

Front 1407

Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.

Back 1407

Ach, muscarinic.

Front 1408

Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.

Back 1408

Ach, nicotinic.

Front 1409

Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.

Back 1409

NE, alpha and beta

Front 1410

Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.

Back 1410

Ach, nicotinic.

Front 1411

Pharmacology - CNS / Neurologic drugs: Sympathetic postganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.

Back 1411

Dopamine, D1

Front 1412

Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to the adrenal medulla release the neurotransmitter ------- which act on ------- receptors.

Back 1412

Ach, nicotinic.

Front 1413

Pharmacology - CNS / Neurologic drugs: Sympathetic preganglionic neurons to the adrenal medulla synapse directly on ------- cells of the adrenal medulla.

Back 1413

Chromaffin.

Front 1414

Pharmacology - CNS / Neurologic drugs: Somatic neurons synapse directly on -------- muscle and release the neurotransmitter ------- which act on ------- receptors.

Back 1414

skeletal muscle, Ach, nicotinic.

Front 1415

Autonomic drugs: Cholinergic:

Back 1415

0

Front 1416

Autonomic drugs: Ach is synthesized from acetyl-CoA and choline by the enzyme ---------.

Back 1416

Choline acetyltransferase.

Front 1417

Autonomic drugs: The transport of choline into the nerve terminal can be inhibited by --------.

Back 1417

Hemicholinium.

Front 1418

Autonomic drugs: The release of transmitter from vesicles in the nerve ending require the entry of ------ into the neuron.

Back 1418

Calcium.

Front 1419

Autonomic drugs: --------- inhibits the release of the stored Ach.

Back 1419

Botulinum toxin.

Front 1420

Autonomic drugs: The action of Ach in the synapse is terminated by its metabolism to acetate and choline by the enzyme ---------.

Back 1420

Acetylcholinesterase.

Front 1421

Noradrenergic:: In the noradrenergic nerve terminal, tyrosine is hydroxylated to -------, which is decarboxylated to --------, which is finally hydroxylated to NE.

Back 1421

DOPA, dopamine.

Front 1422

Noradrenergic:: Dopamine is transported into vesicles for hydroxylation to NE. This transport can be blocked by the drug --------.

Back 1422

Reserpine.

Front 1423

Noradrenergic:: The action of NE and DA is terminated by --------- and ----------.

Back 1423

Reuptake, diffusion (different than for Ach).

Front 1424

Noradrenergic:: --------- inhibits the release of the stored NE.

Back 1424

Guanethidine.

Front 1425

Noradrenergic:: The --------- drugs promote catecholamine release.

Back 1425

Amphetamine.

Front 1426

Noradrenergic:: The drugs --------- and ---------- inhibit the reuptake of NE.

Back 1426

Cocaine, TCA.

Front 1427

Noradrenergic:: The release of NE from a sympathetic nerve ending is modulated by ---------, --------- and ---------.

Back 1427

NE, Ach, angiotensin II.

Front 1428

Noradrenergic:: NE inhibits its own release at the noradrenergic nerve terminal through --------- receptors.

Back 1428

Alpha 2.

Front 1429

Noradrenergic:: Angiotensin II --------- (inhibits / stimulates) the release of NE from the noradrenergic nerve terminal.

Back 1429

Stimulates.

Front 1430

Noradrenergic:: Ach inhibits the release of NE from the noradrenergic nerve terminal by binding to --------- receptors.

Back 1430

M1.

Front 1431

Direct agonists:: Clinical application and action of Bethanechol.

Back 1431

Postoperative and neurogenic ileus and urinary retention. / Activates bowel and bladder smooth muscle.

Front 1432

Direct agonists:: Clinical application and action of Carbachol and Pilocarpine.

Back 1432

Glaucoma. / Activates ciliary muscle of eye (open angle), pupillary sphincter (narrow angle).

Front 1433

Indirect agonists (anticholinesterases):: Clinical application / action of Neostigmine.

Back 1433

Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative). / Increase endogenous Ach.

Front 1434

Indirect agonists (anticholinesterases):: Clinical application / action of Pyridostigmine.

Back 1434

Myasthenia gravis. / Increase Ach; increase strength.

Front 1435

Indirect agonists (anticholinesterases):: Clinical application / action of Edrophonium.

Back 1435

Diagnosis of myasthenia gravis (extremely short acting). / Increase endogenous Ach.

Front 1436

Indirect agonists (anticholinesterases):: Clinical application / action of Physostigmine.

Back 1436

Glaucoma (crosses blood-brain barrier) and atropine overdose. / Increase endogenous Ach.

Front 1437

Indirect agonists (anticholinesterases):: Clinical application / action of Echothiophate.

Back 1437

Glaucoma. / Increase endogenous Ach.

Front 1438

Indirect agonists (anticholinesterases):: Symptoms of cholinesterase inhibitor poisoning.

Back 1438

Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation (also abdominal cramping). "DUMBBELSS".

Front 1439

Indirect agonists (anticholinesterases):: Cholinesterase inhibitor poisoning may be caused by ---------.

Back 1439

Parathion and other organophosphates.

Front 1440

Indirect agonists (anticholinesterases):: The cholinesterase regenerator ------- can be used as an antidote for cholinesterase inhibitor poisoning.

Back 1440

Pralidoxime.

Front 1441

Indirect agonists (anticholinesterases):: Mechanism of action of Pralidoxime.

Back 1441

Regenerates active cholinesterase, chemical antagonist, used to treat organophosphate exposure.

Front 1442

Cholinoreceptor blockers:: Clinical uses of the muscarinic antagonist Atropine.

Back 1442

Dilate pupils, decrease acid secretion in peptic ulcer disease, decrease urgency in mild cystitis, decrease GI motility, reduce airway secretions, and treat organophosphate poisoning. "Blocks SLUD: Salivation, Lacrimation, Urination, Defecation."

Front 1443

Cholinoreceptor blockers:: Side effects of Atropine.

Back 1443

Increase body temp, rapid pulse, dry mouth, dry/flushed skin, disorientation, mydriasis with cycloplegia, and constipation. "Atropine parasympathetic block side effects: Blind as bat, Red as a beet, Mad as a hatter, Hot as a hare, Dry as a bone."

Front 1444

Cholinoreceptor blockers:: Hexamethonium (ganglionic blocker) blocks -------- receptors.

Back 1444

Nicotinic.

Front 1445

Cholinoreceptor blockers:: AUTHOR

Back 1445

Tzivia Moreen

Front 1446

antimuscarinic drugs: "tropi" are anti-muscarinic

Back 1446

while vacationing in the tropics you lie on a beach and your muscles waste away!

Front 1447

antimuscarinic drugs: benztropine is used to treat

Back 1447

Parkinson's disease

Front 1448

antimuscarinic drugs: scopolamine is used to treat

Back 1448

motion sickness

Front 1449

antimuscarinic drugs: scopolamine is an antimuscarinic that does not convert to the mnemonic!

Back 1449

0

Front 1450

antimuscarinic drugs: name 2 antimuscarinic drugs that act on the CNS

Back 1450

benztropine, scopolamine

Front 1451

antimuscarinic drugs: name a muscarinic used to treat motion sickness

Back 1451

scopolamine

Front 1452

antimuscarinic drugs: name a muscarinic used to treat Parkinson's disease

Back 1452

benztropine

Front 1453

antimuscarinic drugs: mechanism of action of benztropine

Back 1453

antimuscarinic

Front 1454

antimuscarinic drugs: mechanism of action of scopolamine

Back 1454

antimuscarinic

Front 1455

antimuscarinic drugs: name three antimuscarinics that act on eye

Back 1455

atropine, homatropine, tropicamide

Front 1456

antimuscarinic drugs: the action of atropine is ______

Back 1456

produce mydriasis, cycloplegia

Front 1457

antimuscarinic drugs: mechanism of atropine is

Back 1457

antimuscarinic

Front 1458

antimuscarinic drugs: the action of homatropine is ______

Back 1458

produce mydriasis, cycloplegia

Front 1459

antimuscarinic drugs: mechanism of homatropine is

Back 1459

antimuscarinic

Front 1460

antimuscarinic drugs: the action of tropicamide is

Back 1460

produce mydriasis, cycloplegia

Front 1461

antimuscarinic drugs: mechanism of tropicamide is

Back 1461

antimuscarinic

Front 1462

antimuscarinic drugs: ipatropium is used to treat

Back 1462

asthma, COPD

Front 1463

antimuscarinic drugs: mechanism of ipatropium is

Back 1463

antimuscarinic

Front 1464

antimuscarinic drugs: name an antimuscarinic used to treat asthma and COPD

Back 1464

ipatropium

Front 1465

neuromuscular blocking drugs: neuromuscular blocking drugs are used for

Back 1465

muscle paralysis in surgery or mechanical ventilation

Front 1466

neuromuscular blocking drugs: name a depolarising neurmuscular blocking drug

Back 1466

succinylcholine

Front 1467

neuromuscular blocking drugs: name 6 nondepolarizing neuromuscular blocking drugs

Back 1467

tubocurarine

Front 1468

neuromuscular blocking drugs: *mnemonic -- the "cur" drugs are nondepolarizing neuromuscular blocking agents

Back 1468

atracurium

Front 1469

neuromuscular blocking drugs: is succinylcholine depolarizing or nondepolarizing?

Back 1469

depolarizing

Front 1470

neuromuscular blocking drugs: is tubocurarine depolarizing or nondepolarizing?

Back 1470

nondepolarizing

Front 1471

neuromuscular blocking drugs: is atracurium depolarizing or nondepolarizing?

Back 1471

nondepolarizing

Front 1472

neuromuscular blocking drugs: is mivacurium depolarizing or nondepolarizing?

Back 1472

nondepolarizing

Front 1473

neuromuscular blocking drugs: is pancuronium depolarizing or nondepolarizing?

Back 1473

nondepolarizing

Front 1474

neuromuscular blocking drugs: is vacuronium depolarizing or nondepolarizing?

Back 1474

nondepolarizing

Front 1475

neuromuscular blocking drugs: is rapacuronium depolarizing or nondepolarizing?

Back 1475

nondepolarizing

Front 1476

neuromuscular blocking drugs: what is tubocurarine used for

Back 1476

nondepolarizing neuromuscular blockade

Front 1477

neuromuscular blocking drugs: what agents are used to reverse neuromuscular blockade by succinylcholine?

Back 1477

cholinesterase inhibitors in phase II (ex -- neostigmine)

Front 1478

neuromuscular blocking drugs: what phase of succinylcholine neuomuscular bloackade is reversible?

Back 1478

phase II (repolarized but blocked)

Front 1479

neuromuscular blocking drugs: what agents are used to reverse pahse I neuromuscular blockade by succinylcholine?

Back 1479

phase I Succinylcholine neuromuscular blockade cannot be reversed

Front 1480

neuromuscular blocking drugs: what phase of succinylcholine neuomuscular bloackade is irreversible?

Back 1480

phase I Succinylcholine neuromuscular blockade cannot be reversed

Front 1481

neuromuscular blocking drugs: what is atracurium used for

Back 1481

nondepolarizing neuromuscular blockade

Front 1482

neuromuscular blocking drugs: what is the effect of cholinesterase inhibitors on succinylcholine neuromuscular blockade?

Back 1482

phase I: cholinesterase inhibitors potentiates the blockade phase II: cholinesterase inhibitors reverse the blockade

Front 1483

neuromuscular blocking drugs: what cholinesterase inhibitor is used to reverse phase II of succinylcholine neuromuscular blockade?

Back 1483

neostigmine

Front 1484

neuromuscular blocking drugs: what is mivacurium used for

Back 1484

nondepolarizing neuromuscular blockade

Front 1485

Dantrolene: what is dantrolene used for

Back 1485

treat malignant hyperthermia

Front 1486

Dantrolene: what causes malignant hyperthermia

Back 1486

use inhalation anesthetics and succinylcholine together

Front 1487

Dantrolene: what inhalation anesthetic DOES NOT cause malignanat hyperthermia?

Back 1487

N2O

Front 1488

Dantrolene: what is dantrolene used for

Back 1488

neuroleptic malignant syndrome

Front 1489

Dantrolene: what is neuroleptic malignant syndrome

Back 1489

a toxicity of antipsychotic drugs

Front 1490

Dantrolene: what drug is used to treat malignant hyperthermia

Back 1490

dantrolene

Front 1491

Dantrolene: what is the mechanism of dantrolene

Back 1491

prevents release of Ca++ from saarcoplasmic reticulum of skeletal muscle

Front 1492

Sympathomimetics: epinephrine, NE, isoproterenol, dopamine, and dobutamine are all________________

Back 1492

catecholamines

Front 1493

Sympathomimetics: catecholamines are_____________________

Back 1493

sympathomimetics

Front 1494

Sympathomimetics: name 5 catecholamines

Back 1494

EPI, NE, Isoproterenol, dopamine, dobutamine

Front 1495

Sympathomimetics: what receptors does epinephrine act on?

Back 1495

alpha-1, alpha-2, beta-1, beta-2 adrenergics

Front 1496

Sympathomimetics: what receptors does NE work on?

Back 1496

alpha-1, alpha-2, beta-1 adrenergics

Front 1497

Sympathomimetics: what receptors does isoproterenol work on?

Back 1497

beta-1 = beta-2 adrenergics

Front 1498

Sympathomimetics: what receptors does dopamine work on?

Back 1498

D1 = D2, D1 and D2 more than beta, beta more than alpha

Front 1499

Sympathomimetics: what receptors does dobutamine work on?

Back 1499

beta-1 > beta-2

Front 1500

Sympathomimetics: which catecholamines are agonists to alpha-adrenergic receptors

Back 1500

EPI, NE > dopamine

Front 1501

Sympathomimetics: which catecholamines are agonists to beta-1 adrenergic receptors

Back 1501

EPI, NE, Isoproterenol, dopamine, dobutamine

Front 1502

Sympathomimetics: which catecholamines are agonists to beta-2 adrenergic receptors

Back 1502

EPI, isoproterenol, dopamine and dobutamine (less)

Front 1503

Sympathomimetics: what is epinephrine used to treat?

Back 1503

anaphylaxis, open-angle glaucoma, asthma, hypotension

Front 1504

Sympathomimetics: what is norepinephrine used to treat?

Back 1504

hypotension (but decreases renal perfusion)

Front 1505

Sympathomimetics: what is isoproterenol used to treat?

Back 1505

AV block

Front 1506

Sympathomimetics: what is dopamine used to treat

Back 1506

shock with renal failure, heart failure

Front 1507

Sympathomimetics: what is dobutamine used to treat

Back 1507

shock, heart failure

Front 1508

Sympathomimetics: what catecholamine is used to treat anaphylaxis

Back 1508

epinephrine ("EPI-pen")

Front 1509

Sympathomimetics: what catecholamines are used to treat hypotension

Back 1509

EPI, NE

Front 1510

Sympathomimetics: what catecholamine is used to treat asthma

Back 1510

epinephrine

Front 1511

Sympathomimetics: what catecholamine is used to treat AV block

Back 1511

isoproterenol

Front 1512

Sympathomimetics: what catecholamines are used to treat shock

Back 1512

doapmine, dobutamine

Front 1513

Sympathomimetics: what is the action of amphetamine

Back 1513

indirect general adrenergic agonist, releases stored catecholamines

Front 1514

Sympathomimetics: what is the action of ephedrine

Back 1514

indirect general adrenergic agonist, releases stored catecholamines

Front 1515

Sympathomimetics: what is amphetamine used to treat

Back 1515

narcolepsy, obesity, attention deficit disorder

Front 1516

Sympathomimetics: what is ephedrine used to treat

Back 1516

nasal decongestion, urinary incontinence, hypotension

Front 1517

Sympathomimetics: name three sympathomimetic drugs used to treat hypotension

Back 1517

epinephrine, norepinephrin, ephedrine

Front 1518

Sympathomimetics: what is the action of phenylephrine

Back 1518

adrenergic agonist, alpha-1 > alpha-2

Front 1519

Sympathomimetics: what is the action of albuterol

Back 1519

adrenergic agonist, beta-2 >beta-1

Front 1520

Sympathomimetics: what is the action of terbutaline

Back 1520

adrenergic agonist, beta-2 >beta-2

Front 1521

Sympathomimetics: what is phenylephrine used for?

Back 1521

pupil dilator, vasoconstriction, nasal decongestion

Front 1522

Sympathomimetics: what sympathomimetics are used to treat nasal congestion

Back 1522

ephedrine, phenylephrine

Front 1523

Sympathomimetics: what is the mechanism of cocaine

Back 1523

indirect general adrenergic agonist, catecholamine uptake inhibitor

Front 1524

Sympathomimetics: what is the action of cocaine

Back 1524

vasoconstriction, local anesthesia

Front 1525

Sympathomimetics: what is the mechanism of clonidine

Back 1525

centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow

Front 1526

Sympathomimetics: what drug has the same mechanism as amphetamine

Back 1526

ephedrine

Front 1527

Sympathomimetics: what is the mechanism of alpha-methyldopa

Back 1527

centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow

Front 1528

Sympathomimetics: what drug has the same mechanism as clonidine

Back 1528

alpha-methyldopa

Front 1529

Sympathomimetics: what are clonidine and alpha-methyldopa used to treat

Back 1529

hypertension, especially in renal disease because they do not decreased blood flow to the kidney

Front 1530

Sympathomimetics: what sympathomimetic is used to treat urinary incontinence

Back 1530

ephedrine

Front 1531

Sympathomimetics: what sympathomimetic is used to treat attention deficit disorder

Back 1531

amphetamine

Front 1532

Sympathomimetics: what sympathomimetic is used to treat narcolepsy

Back 1532

amphetamine

Front 1533

alpha-blockers: name a nonselective irreversible alpha blocker

Back 1533

phenoxybenzamine

Front 1534

alpha-blockers: name a nonselective reversible alpha blocker

Back 1534

phentolamine

Front 1535

alpha-blockers: what is the mechanism of phenoxybenzamine

Back 1535

nonselective irreversible alpha blocker

Front 1536

alpha-blockers: what is the mechanism of phentolamine

Back 1536

nonselective reversible alpha blocker

Front 1537

alpha-blockers: what are phenoxybenzamine and phentolamine used for

Back 1537

pheochromocytoma

Front 1538

alpha-blockers: what are the side effects of nonselective alpha blockers

Back 1538

orthostatic hypotension, reflex tachycardia

Front 1539

alpha-blockers: name 3 alpha-1 selective adrenergic blockers

Back 1539

prazosin, terazosin, doxazosin

Front 1540

alpha-blockers: what is the mechanism of prazosin

Back 1540

alpha-1 selective adrenergic blocker

Front 1541

alpha-blockers: what is the mechanism of terazosin

Back 1541

alpha-1 selective adrenergic blocker

Front 1542

alpha-blockers: what is the mechanism of doxazosin

Back 1542

alpha-1 selective adrenergic blocker

Front 1543

alpha-blockers: what are alpha-1 selective adrenergic alpha blockers used for

Back 1543

hypertension, urinary retention in BPH

Front 1544

alpha-blockers: what are the side effects of alpha-1 blockers

Back 1544

orthostatic hypotension, dizziness, headache

Front 1545

alpha-blockers: what is prazosin used for?

Back 1545

hypertension, urinary retention in BPH

Front 1546

alpha-blockers: what drugs have the same action as prazosin

Back 1546

terazosin, doxazosin

Front 1547

alpha-blockers: what are the side effects of terazosin?

Back 1547

orthostatic hypotension, dizziness, headache

Front 1548

alpha-blockers: what selective alpha blockers cause orthostatic hypotension

Back 1548

phenoxybenzamine, phentolamine, terazosin, prazosin, doxazosin

Front 1549

alpha-blockers: name an alpha-2 selective adrenergic blocker

Back 1549

yohimbine

Front 1550

alpha-blockers: what is yohimbine used for

Back 1550

impotence (effectiveness controversial)

Front 1551

alpha-blockers: what alpha blockers are used to treat pheochromocytoma

Back 1551

phenoxybenzamine, phentolamine

Front 1552

beta-blockers ("lol"s): name some beta-blockers

Back 1552

propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol

Front 1553

beta-blockers ("lol"s): what is the mechanism of propanolol

Back 1553

selective beta-adrenergic blocker

Front 1554

beta-blockers ("lol"s): what is the mechanism of metoprolol

Back 1554

selective beta-adrenergic blocker

Front 1555

beta-blockers ("lol"s): what is the mechanism of esmolol

Back 1555

selective beta-adrenergic blocker

Front 1556

beta-blockers ("lol"s): what is the mechanism of pindolol

Back 1556

selective beta-adrenergic blocker

Front 1557

beta-blockers ("lol"s): what are beta-blockers used to treat

Back 1557

hypertension, angina, MI, SVT, CHF, glaucoma

Front 1558

beta-blockers ("lol"s): how do beta blockers treat hypertension

Back 1558

decrease cardiac output, decrease renin secretion

Front 1559

beta-blockers ("lol"s): how do beta blockers treat angina

Back 1559

decrease heart rate, decrease cardiac contractility, decreased O2 consumption

Front 1560

beta-blockers ("lol"s): why are beta blockers used to treat MI

Back 1560

decrease MI mortality

Front 1561

beta-blockers ("lol"s): which beta blockers are used to treat SVT

Back 1561

propanolol, esmolol

Front 1562

beta-blockers ("lol"s): how do propanolol and esmolol treat SVT

Back 1562

decrease AV conduction velocity

Front 1563

beta-blockers ("lol"s): how do beta blockers treat CHF

Back 1563

slow progression of chronic failure

Front 1564

beta-blockers ("lol"s): which beta blocker is used to treat glaucoma

Back 1564

timolol

Front 1565

beta-blockers ("lol"s): what is timolol used to treat glaucoma

Back 1565

decrease secretion of aqueous humor

Front 1566

beta-blockers ("lol"s): what are the toxic effects of beta blockers

Back 1566

impotence, exacerbation of asthma, caution in diabetes

Front 1567

beta-blockers ("lol"s): what are the cardiovascular toxic effects of beta blockers

Back 1567

bradychardia, AV block, CHF

Front 1568

beta-blockers ("lol"s): what are the CNS adverse effects of beta blockers

Back 1568

sedation, sleep alterations

Front 1569

beta-blockers ("lol"s): which beta blockers are beta-1 selective

Back 1569

acebutolol, betaxolol, esmolol, atenolol, metaprolol (A BEAM of beta-1 blockers)

Front 1570

beta-blockers ("lol"s): which beta-1 blocker is short-acting

Back 1570

esmolol

Front 1571

beta-blockers ("lol"s): which beta blockers are non-selective

Back 1571

propanolol, timolol, pindolol, nadolol, labetalol

Front 1572

beta-blockers ("lol"s): which beta blocker also blocks alpha receptors

Back 1572

labetalol (all others are spelled "olol")

Front 1573

glaucoma drugs: which alpha agonists are used to treat glaucoma

Back 1573

epinephrine, brimonidine

Front 1574

glaucoma drugs: which beta blockers are used to treat glaucoma

Back 1574

timolol, betxolol, carteolol

Front 1575

glaucoma drugs: which cholinomimetics are used to treat glaucoma

Back 1575

pilocarpine, carbachol, physostigmine, echothiophate

Front 1576

glaucoma drugs: which diuretics are used to treat glaucoma

Back 1576

acetazolamide, dorzolamide, brinzolamide

Front 1577

glaucoma drugs: which prostaglandin is used to treat glaucoma

Back 1577

latanoprost

Front 1578

glaucoma drugs: what classes of drugs are used to treat glaucoma

Back 1578

alpha agonists, beta blockers, cholinomimetics, diuretics, prostaglandins (*mnemonic -- treating glaucoma is easy as ABCD)

Front 1579

glaucoma drugs: what is the effect of epinephrine in glaucoma

Back 1579

increase outflow of aqueous humor

Front 1580

glaucoma drugs: what are the side effects of epinephrine treatment in glaucoma

Back 1580

mydriasis, stinging

Front 1581

glaucoma drugs: what glaucoma should epinephrine NOT be used for

Back 1581

closed-angle glaucoma

Front 1582

glaucoma drugs: what is the effect of brimonidine in glaucoma

Back 1582

decreased aqueous humor synthesis

Front 1583

glaucoma drugs: what are the side effects of brimonidine treatment in glaucoma

Back 1583

no pupillary or vision changes

Front 1584

glaucoma drugs: what is the effect of beta-blocker treatment in glaucoma

Back 1584

decrease aqueous humor secretion

Front 1585

glaucoma drugs: what are the side effects of beta blocker treatment in glauzoma

Back 1585

no pupillary or vision changes

Front 1586

glaucoma drugs: what is the effect of cholinomimetics in glaucoma

Back 1586

ciliary muscle contraction, opening of trabecular meshwork, increase outflow of aqueous humor

Front 1587

glaucoma drugs: what are the side effects of cholinomimetics in glaucoma

Back 1587

miosis, cyclospasm

Front 1588

glaucoma drugs: what is the effect of diuretic treatment in glaucoma

Back 1588

inhibition of carbonic anhydrase --> decrease HCO3 secretion --> decrease aqueous humor secretion

Front 1589

glaucoma drugs: what are the side effects of diuretics in glaucoma

Back 1589

no pupillary or vision changes

Front 1590

glaucoma drugs: what is the effect of prostaglandin (latanoprost) treatment in glaucoma

Back 1590

increase outflow of aqueous humor

Front 1591

glaucoma drugs: what is the side effect of prostaglandin treatment in glaucoma

Back 1591

darkens color of iris (browning)

Front 1592

glaucoma drugs: which drugs used to treat glaucoma increase outflow of aqueous humor

Back 1592

cholinomimetics, prostaglandin, epinephrine

Front 1593

glaucoma drugs: can you use epinephrine in closed-angle glaucoma

Back 1593

NO

Front 1594

glaucoma drugs: brimonidine is used to treat what eye disease

Back 1594

glaucoma

Front 1595

glaucoma drugs: what kind of drug is latanoprost

Back 1595

prostaglandin

Front 1596

glaucoma drugs: latanoprost is used to treat what eye disease

Back 1596

glaucoma

Front 1597

glaucoma drugs: which glaucoma drugs decrease aqueous secretion

Back 1597

beta blockers, diuretics

Front 1598

L-dopa/carbidopa: what does L-dopa stand for

Back 1598

levodopa

Front 1599

L-dopa/carbidopa: what is the mechanism of action of L-dopa/carbidopa

Back 1599

increase dopamine level in brain

Front 1600

L-dopa/carbidopa: what is L-dopa/carbidopa used to treat

Back 1600

Parkinson's disease

Front 1601

L-dopa/carbidopa: how is L-dopa different from dopamine

Back 1601

L-dopa can cross the blood-brain barrier, dopamine cannot

Front 1602

L-dopa/carbidopa: what happens to L-dopa after it crosses the BBB

Back 1602

converted to dopamine by dopa decarboxylase

Front 1603

L-dopa/carbidopa: what enzyme convertes L-dopa to dopamine

Back 1603

dopa decarboxylase

Front 1604

L-dopa/carbidopa: what is the function of carbidopa

Back 1604

peripheral decarboxylase inhibitor

Front 1605

L-dopa/carbidopa: why is carbidopa given with L-dopa

Back 1605

increase L-dopa availability in CNS by inhibiting decarboxylase in periphery, also limits peripheral side effects

Front 1606

L-dopa/carbidopa: what are the side effects of L-dopa.carbidopa treatment

Back 1606

arrhythmias, dyskinesias

Front 1607

L-dopa/carbidopa: why do patients taking L-dopa get arrhythmias

Back 1607

peripheral effects of dopamine

Front 1608

L-dopa/carbidopa: why do patients taking L-dopa get dyskinesias

Back 1608

excess dopamine stimulation in CNS

Front 1609

Parkinson's disease drugs: what drugs are used to treat Parkinson's disease

Back 1609

dopamine agonists, MAO inhibitors, antimuscarinics

Front 1610

Parkinson's disease drugs: specifically, which drugs are used to treat Parkinson's

Back 1610

Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics (BALSA)

Front 1611

Parkinson's disease drugs: which dopamine agosts are used to treat Parkinson's

Back 1611

L-dopa/carbidopa, bromocriptine, pramipexole, ropinirole, amantadine

Front 1612

Parkinson's disease drugs: what is the action of bromocriptine in Parkinson's

Back 1612

ergot alkaloid, partial dopamine agonist

Front 1613

Parkinson's disease drugs: what is the action of amantadine in Parkinson's

Back 1613

enhances dopamine release

Front 1614

Parkinson's disease drugs: what MAOI is used to treat Parkinson's

Back 1614

selegiline

Front 1615

Parkinson's disease drugs: what is the mechanism of selegiline

Back 1615

selective MAO type B inhibitor

Front 1616

Parkinson's disease drugs: what antimuscarinic is used to treat Parkinson's

Back 1616

benztropine

Front 1617

Parkinson's disease drugs: what is the effect of benztropine in Parkinson's

Back 1617

improves tremor, rigidity, little effect on bradykinesia

Front 1618

Sumatriptan: what is sumatriptan used for

Back 1618

acute migraine, cluster headache attacks

Front 1619

Sumatriptan: what is the mechanism of sumatriptan

Back 1619

5-HT1D agonist

Front 1620

Sumatriptan: what is the half life of sumatriptan

Back 1620

less than 2 hours

Front 1621

Sumatriptan: what are the side effects of sumatriptan

Back 1621

chest discomfort, mild tingling

Front 1622

Sumatriptan: what are the contraindications for sumatriptan

Back 1622

patients with CAD or Prinzmetal's angina

Front 1623

Epilepsy drugs: which drugs are used for simple and complex partial seizures

Back 1623

phenytoin, carbamazapine, lamotrigine, gabapentin, topiramate, phenobarbital

Front 1624

Epilepsy drugs: what types of seizures is phenytoin indicated for

Back 1624

simple and complex partial, tonic-clonic, status epilepticus

Front 1625

Epilepsy drugs: what types of seizures is carbamazepine indicated for

Back 1625

simple and complex partial, tonic-clonic

Front 1626

Epilepsy drugs: what types of seizures is lamotrigine indicated for

Back 1626

simple and complex partial, tonic-clonic

Front 1627

Epilepsy drugs: what types of seizures is gabapentin indicated for

Back 1627

simple and complex partial, tonic-clonic

Front 1628

Epilepsy drugs: what types of seizures is topiramate indicated for

Back 1628

simple and complex partial

Front 1629

Epilepsy drugs: what types of seizures is phenobarbital indicated for

Back 1629

simple and complex partial, tonic-clonic

Front 1630

Epilepsy drugs: what drugs can be used for tonic-clonic seizures

Back 1630

phenytoin, carbamazapine, lamotrigine, gabapentin, phenobarbital, valproate

Front 1631

Epilepsy drugs: what drugs can be used for absence seizures

Back 1631

valproate, ethosuximide

Front 1632

Epilepsy drugs: what drugs can be used for status epilepticus

Back 1632

phenytoin, benzodiazapines (diazepam, lorazepam)

Front 1633

Epilepsy drugs: what types of seizure is valproate indicated for

Back 1633

tonic-clonic, absence

Front 1634

Epilepsy drugs: what types of seizure is ethosuximide inidcated for

Back 1634

absence

Front 1635

Epilepsy drugs: what type of seizure are benzodiazepines indicated for

Back 1635

status epilepticus

Front 1636

Epilepsy drugs: other than anti-seizure, what else is phenytoin used for

Back 1636

class 1B anti-arrhythmic

Front 1637

Epilepsy drugs: how should a patient taking carbamazepine be followed

Back 1637

monitor LFT's weekly

Front 1638

Epilepsy drugs: which seizure drugs have adjunct use

Back 1638

gabapentin, topiramate

Front 1639

Epilepsy drugs: which seizure drug is safest in pregnant women

Back 1639

phenobarbital

Front 1640

Epilepsy drugs: which seizure drug is used in Crigler-Najjar II

Back 1640

phenobarbital

Front 1641

Epilepsy drugs: what are the advantages of phenobarbital

Back 1641

can be used in pregnant women, Crigler Najjar II

Front 1642

Epilepsy drug toxicities: what are the side effects of benzodiazepines

Back 1642

sedation, tolerance, dependence

Front 1643

Epilepsy drug toxicities: what are the side effects of carbamazepine

Back 1643

diplopia, ataxia, CYP induction, blood dyscrasias, liver toxicity

Front 1644

Epilepsy drug toxicities: what are the side effects of ethosuximide

Back 1644

GI distress, lethargy, headache, urticaria, Stevens-Johnson syndrome

Front 1645

Epilepsy drug toxicities: what are the side effects of phenobarbital

Back 1645

sedation, CYP induction, tolerance, dependence

Front 1646

Epilepsy drug toxicities: what are the side effects of phenytoin

Back 1646

nystagmus, diplopia, ataxia, sedation, ginigival hyperplasia, hirsutism, anemias, teratogenic

Front 1647

Epilepsy drug toxicities: what are the side effects of valproate

Back 1647

GI distress, rare by fatal hepatotoxicity, neural tube defects (spina bifida)

Front 1648

Epilepsy drug toxicities: what are the side effects of lamotrigine

Back 1648

life-threatening rash, Stevens-Johnson syndrome

Front 1649

Epilepsy drug toxicities: what are the side effects of gabapentin

Back 1649

sedation, movement disorders

Front 1650

Epilepsy drug toxicities: what are the side effects of topiramate

Back 1650

sedation, mental dulling, kidney stones, weight loss

Front 1651

Epilepsy drug toxicities: which anti-epileptic drug is teratogenic

Back 1651

phenytoin

Front 1652

Epilepsy drug toxicities: which anti-epileptic drug can cause dependence

Back 1652

benzodiazepines, phenobarbital

Front 1653

Epilepsy drug toxicities: which anti-epileptic drug can cause neural tube defects

Back 1653

valproate

Front 1654

Epilepsy drug toxicities: which anti-epileptic drugs can cause GI distress

Back 1654

valproate, ethosuximide

Front 1655

Epilepsy drug toxicities: it is necessary to check LFT's with which anti-epileptic drugs

Back 1655

carbamazepine, valproate

Front 1656

Epilepsy drug toxicities: which anti-epileptic drugs cause CYP induction

Back 1656

phenobarbital, carbamazepine

Front 1657

Epilepsy drug toxicities: which anti-epileptic drugs can cause blood problems

Back 1657

carbamazepine, phenytoin

Front 1658

Epilepsy drug toxicities: which anti-epileptic drugs can cause Stevens-Johnson syndrome

Back 1658

lamotrigine, ethosuximide

Front 1659

Epilepsy drug toxicities: which anti-epileptic drugs can cause diplopia

Back 1659

carbamazepine, phenytoin

Front 1660

Phenytoin: what is the mechanism of phenytoin action

Back 1660

use-dependent blockade of Na+ channels

Front 1661

Phenytoin: what is the clinical application of phenytoin

Back 1661

grand mal seizures

Front 1662

Phenytoin: what are the toxicities of phenytoin

Back 1662

nystagmus, ataxia, diplopia, lethargy

Front 1663

Phenytoin: what are the chronic toxicities of phenytoin

Back 1663

gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia, malignant hyperthermia (rare)

Front 1664

Phenytoin: should pregnant women take phenytoin

Back 1664

NO -- teratogenic

Front 1665

Phenytoin: why does phenytoin cause megaloblastic anemia

Back 1665

causes decreased vitamin B-12

Front 1666

Barbiturates: name 4 barbiturates

Back 1666

phenobarbital, pentobarbital, thiopental, secobarbital

Front 1667

Barbiturates: what is the mechanism of barbiturate action

Back 1667

increase duration of Cl channel opening --> decreased neuron firing --> facilitate GABA-A action

Front 1668

Barbiturates: how do barbiturates facilitate GABA-A action

Back 1668

increase duration of Cl channel opening which decreases neuron firing (Barbidurate increases duration

Front 1669

Barbiturates: is barbiturate action on the CNS stimulatory or inhibitory

Back 1669

inhibitory

Front 1670

Barbiturates: what is the clinical application of barbiturates

Back 1670

sedative for anxiety, seizures, insomnia, anesthesia induction (thiopental)

Front 1671

Barbiturates: which barbiturate is used for anesthesia induction

Back 1671

thiopental

Front 1672

Barbiturates: what are the side effects of barbiturates

Back 1672

dependence, additive CNS depression effects with alcohol, respiratory or CV depression (death), drug interactions due to CYP induction

Front 1673

Barbiturates: what should you find out before giving a patient barbiturates

Back 1673

what other medications they take, because of CYP induction and many drug interactions

Front 1674

Barbiturates: what happens if you give barbiturates to a patient in alcohol-induced coma or DT's

Back 1674

they might DIE!! Because of additive effect of barbiturates and alcohol --> respiratory depression

Front 1675

Barbiturates: when are barbiturates contra-indicated

Back 1675

porphyria

Front 1676

Barbiturates: can barbiturates cause dependence

Back 1676

YES

Front 1677

Barbiturates: My friend Barb was very anxious so her doctor gave her barbiturates to increase the duration of the time she could speak in public without freaking out and having a seizure. She became so dependent on it that she recommended it to her friend Portia who couldn't take it because of porphyria. One day Barb drank too much alcohol and took her barbiturates and never woke up! THE END

Back 1677

clinical pharmacology made ridiculous. Period

Front 1678

Benzodiazepines: name a bunch of benzodiazepines

Back 1678

diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide (all have ZZZ in them)

Front 1679

Benzodiazepines: what is the mechanism of benzodiazepines

Back 1679

increase frequency of Cl channel opening --> facilitate GABA-A action (Frenzodiazepines increase frequency)

Front 1680

Benzodiazepines: which GABA receptors are facilitated by barbiturates and bezodiazepines

Back 1680

GABA-A

Front 1681

Benzodiazepines: what are the clinical applications of benzodiazepines

Back 1681

anxiety, spasticity, status epilepticus (diazepam), detoxification (alcohol withdrawal, DT's)

Front 1682

Benzodiazepines: which benzodiazepine can be used for status epilepticus

Back 1682

diazepam

Front 1683

Benzodiazepines: what drugs can be used to treat alcohol withdrawal

Back 1683

benzodiazepines

Front 1684

Benzodiazepines: which benzodiazepines are short-acting

Back 1684

TOM thumb: Triazolam, Oxazepam, Midazolam

Front 1685

Benzodiazepines: what are the toxic effects of benzos

Back 1685

dependence, additive CNS depression effects with alcohol

Front 1686

Benzodiazepines: how are benzos better than barbiturates

Back 1686

less respiratory depression and coma risk

Front 1687

Benzodiazepines: how do you treat benzo overdose

Back 1687

flumazenil

Front 1688

Benzodiazepines: what is flumzenil used for

Back 1688

benzo overdose

Front 1689

Benzodiazepines: how does flumazenil work

Back 1689

competitive antagonist at GABA receptor

Front 1690

Benzodiazepines: can a patient become benzodiazepine dependent

Back 1690

YES

Front 1691

Benzodiazepines: are barbiturates or benzodiazepines used for alcohol withdrawal

Back 1691

benzodiazepines

Front 1692

Antipsychotics (neuroleptics): what is another name for antipsychotics

Back 1692

neuroleptics

Front 1693

Antipsychotics (neuroleptics): name 4 antipsychotic drugs

Back 1693

thioridazine, haloperidol, fluphenazine, chlorpromazine

Front 1694

Antipsychotics (neuroleptics): how do you keep benzos straight from antipsychotics

Back 1694

Benzos help 3rd year Jon Kazam be less anxious around patients: Shazam Kazam! Without antipsychotics patients talk like a crazy 'zine (well, not perfect, but I'm working on it)

Front 1695

Antipsychotics (neuroleptics): what is the mechanism of most antipsychotics

Back 1695

block dopamine D2 receptors

Front 1696

Antipsychotics (neuroleptics): what is the clinical application of antipsychotics

Back 1696

schizophrenia, psychosis

Front 1697

Antipsychotics (neuroleptics): what are the side effects of antipsychotics

Back 1697

extrapyramidal side effects (EPS), sedation, endocrine, muscarinic blockade, alpha blockade, histamine blockade

Front 1698

Antipsychotics (neuroleptics): what is a long-term effect of antipsychotic use

Back 1698

tardive dyskinesia

Front 1699

Antipsychotics (neuroleptics): what is neuroleptic malignant syndrome

Back 1699

a side effect of antipsychotics; rigidity, autonomic instability, hyperpyrexia

Front 1700

Antipsychotics (neuroleptics): how do you treat neuroleptic malignant syndrome

Back 1700

dantrolene, dopamine agonists

Front 1701

Antipsychotics (neuroleptics): what is tardive dyskinesia

Back 1701

side effect of neuroleptics; stereotypic oral-facial movements, may be due to dopamine receptor sensitization

Front 1702

Antipsychotics (neuroleptics): what is the "rule of 4" with EPS side effects from antipsychotic drugs

Back 1702

evolution of EPS side effects: 4 hours -- acite dystonia, 4 days -- akinesia, 4 weeks -- akasthesia, 4 months -- tardvie dyskinesia

Front 1703

Antipsychotics (neuroleptics): is tardvie dyskinesia reversible

Back 1703

often irreversible

Front 1704

Antipsychotics (neuroleptics): what is fluphenazine used for

Back 1704

schizophrenia, psychosis

Front 1705

Atypical antipsychotics: name 3 atypical antipsychotics

Back 1705

clozapine, olanzapine, risperidone

Front 1706

Atypical antipsychotics: what type of antipsychotic is clozapine

Back 1706

atypical

Front 1707

Atypical antipsychotics: what type of antipsychotic is olanzapine

Back 1707

atypical

Front 1708

Atypical antipsychotics: what type of antipsychotic is risperidone

Back 1708

atypical

Front 1709

Atypical antipsychotics: what is the mechanism of atypical antipsychotics

Back 1709

block 5-HT2 and dopamine receptors

Front 1710

Atypical antipsychotics: what is the mechanism of clozapine

Back 1710

block 5-HT2 and dopamine receptors

Front 1711

Atypical antipsychotics: what is the mechanism of olanzapine

Back 1711

block 5-HT2 and dopamine receptors

Front 1712

Atypical antipsychotics: what is the mechanism of risperidone

Back 1712

block 5-HT2 and dopamine receptors

Front 1713

Atypical antipsychotics: what is the clinical application of clozapine

Back 1713

schizophrenia positive and negative symptoms

Front 1714

Atypical antipsychotics: what is the clinical application of olanzapine

Back 1714

schizophrenia positive and negative symptoms, OCD, anxiety disorder, depression

Front 1715

Atypical antipsychotics: what is the clinical application of risperidone

Back 1715

schizophrenia positive and negative symptoms

Front 1716

Atypical antipsychotics: how are atypical antipsychotics different from classic ones

Back 1716

atypicals treat positive and negative symptoms of schizophrenia, fewer extrapyramidal and anticholinergic side effects than classic antipsychotics

Front 1717

Atypical antipsychotics: which antipsychotics should be used to treat positive and negative symptoms of schizophrenia

Back 1717

atypical ones -- clozapine, olanzapine, risperidone

Front 1718

Atypical antipsychotics: which antipsychotics should be used for fewer side effects

Back 1718

atypical ones -- clozapine, olanzapine, risperidone

Front 1719

Atypical antipsychotics: what is a potential toxicity of clozapine

Back 1719

agranulocytosis

Front 1720

Atypical antipsychotics: which antipsychotic drug can cause agranulocytosis

Back 1720

clozapine

Front 1721

Atypical antipsychotics: what test must be done weekly on patients taking clozapine

Back 1721

WBC count because of potential agranulocytosis

Front 1722

Lithium: what is the mechanism of action of lithium

Back 1722

unknown; may be related to inhibition of phosphoinositol cascade

Front 1723

Lithium: what is the clinical application of lithium

Back 1723

mood stabilizer for bipolar disorder

Front 1724

Lithium: how does lithium help people with bipolar disorder

Back 1724

prevents relapse and acute manic episodes

Front 1725

Lithium: what are the side effects of lithium

Back 1725

tremor, hypothyroidism, polyuria, teratogenic

Front 1726

Lithium: is it OK for women taking lithium to get pregnant

Back 1726

NO -- teratogenic

Front 1727

Lithium: what does lithium cause polyuria

Back 1727

ADH antagonist --> nephrogenic diabetes insipidus

Front 1728

Lithium: AUTHOR

Back 1728

Hina Talib

Front 1729

Antidepressants: What do the following drugs inhibit: 1. MAO inhibitors, 2. Desipramine/maprotilline, 3. Mirtazapine and 4. Fluoxetine/trazodone?

Back 1729

1. MAO 2. NE reuptake 3. Alpha 2-R 4. 5HT reuptake

Front 1730

Antidepressants: All of the above actions are ------synaptic

Back 1730

PRE

Front 1731

List the Tricyclic Antidepressants: What are the three C's of their toxicity?

Back 1731

Convulsions, Coma, Cardiotoxicity (arrythmias). Also respiratory depression, hypyrexia.

Front 1732

List the Tricyclic Antidepressants: How about toxicity in the eldery?

Back 1732

confusion and hallucinations due to anticholinergic SE

Front 1733

List the Tricyclic Antidepressants: What is the mechanism of TCA?

Back 1733

block reuptake of NE and 5HT

Front 1734

List the Tricyclic Antidepressants: What is the clinical uses of TCAs?

Back 1734

Endogenous depresion. Bed wetting - imipramine. OCD- clomipramine.

Front 1735

List the Tricyclic Antidepressants: How are tertiary TCA's different than secondary in terms of side effects?

Back 1735

Amitriptyline (tertiary) has more anti-cholinergic effects than do secondary (nortriptyline). Desipramine is the least sedating.

Front 1736

List the Tricyclic Antidepressants: what are the SE of TCAs?

Back 1736

sedation, alpha blocking effects, atropine-like anti cholinergic side effects (tachycardia, urinary retention)

Front 1737

List the Tricyclic Antidepressants: Fluoxetine, sertraline, paroxetine, citalopram are what class of drugs?

Back 1737

pg 311 SSRI's for endogenous depression

Front 1738

List the Tricyclic Antidepressants: How long does it take an anti-depressant to have an effect?

Back 1738

2-3weeks

Front 1739

List the Tricyclic Antidepressants: How does the toxicity differ fromTCA's and what are they?

Back 1739

Fewer than TCA's. CNS stimulation - anxiety, insomnia, tremor, anorexia, nausea, and vomiting.

Front 1740

List the Tricyclic Antidepressants: What toxicity happens with SSRI's and MAO inhibitors given together?

Back 1740

Seratonin Syndrome! Hyperthermia, muscle rigidity, cardiovascular collapse

Front 1741

List the Tricyclic Antidepressants: What are heterocyclics?

Back 1741

pg 312 2nd and 3rd generation antidepressants with varied and mixed mechanisms of action. Used major depression.

Front 1742

List the Tricyclic Antidepressants: Examples of heterocyclics?

Back 1742

trazodone, buproprion, venlafaxine, mirtazapine, maprotiline

Front 1743

List the Tricyclic Antidepressants: Which one is used for smoking cessation?

Back 1743

Buproprion. Mechanism not known. Toxicity - stimulant effects, dry mouth, aggrevation of pyschosis

Front 1744

List the Tricyclic Antidepressants: Which one used in GAD?

Back 1744

Venlafaxine - inhibits 5HT and DA reuptake. Toxicity - stimulant effects

Front 1745

List the Tricyclic Antidepressants: which one blocks NE reuptake

Back 1745

maprotiline

Front 1746

List the Tricyclic Antidepressants: Which one increases release of NE and 5HT via alpha 2 antagonism?

Back 1746

mirtazapine. Also potent 5HT Rantagonist. Toxicity - sedation, increase serum cholesterol, increase apetite

Front 1747

List the Tricyclic Antidepressants: What is trazodone and it' SE?

Back 1747

primarily inhibits seratonin reuptake. Toxicity - sedation, nausea, priapism, postural hypotension

Front 1748

Give 2 examples of MAO: Mechanism and Clinical Uses?

Back 1748

non selevtive MAO inhibition. Atypical antidepressant, anxiety, hypochondriasis

Front 1749

Give 2 examples of MAO: What is the toxicity with tyramine ingestion (in foods) and meperidine?

Back 1749

Hypertensive crisis

Front 1750

Give 2 examples of MAO: Other toxicities?

Back 1750

CNS stimulation, contraindicated with SSRI's or B-agonists

Front 1751

What is the mechanims of selgiline (deprenyl)?: what is the clinical use and toxicity?

Back 1751

adjunctive agent to L-dopa for Parkinsons. May enhance adverse effects of L-dopa

Front 1752

General principles: What is the significance of drugs with decreased solubility in blood?

Back 1752

rapid induction and recovery times . Ie. N20

Front 1753

General principles: What is the significance of drugs with increased solubility in blood?

Back 1753

increased potency = I/ MAC. Ie. Halothane

Front 1754

Inhaled Anesthetics: list them

Back 1754

halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide

Front 1755

Inhaled Anesthetics: What is good about lower solubility?

Back 1755

the quicker the anesthetic response, and the quicker the recovery

Front 1756

Inhaled Anesthetics: What are these drug's effects?

Back 1756

myocardial depression, respiratory depression, nausea/emesis, increase cerebral blood flow

Front 1757

Inhaled Anesthetics: What toxicity mactches the following drugs 1. Halothane 2. Methoxyflurane 3. Enflurane 4. Rare

Back 1757

1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4. Malignant hyperthermia

Front 1758

IV anesthetics: What do barbituates, benzodiazepines, arylcyclohexylamines and narcotic analgesics have in common?

Back 1758

they are IV anesthetics

Front 1759

IV anesthetics: What the pharmacokinetics and uses of thiopental?

Back 1759

high lipid solubility, rapid entry into brain. Used for induction of anesthesia for short surgical procedures. Terminated by redistribution from brain. Decreased cerebral blood flow

Front 1760

IV anesthetics: Give an example of a benzo and what is this class's shortcoming?

Back 1760

midazolam used for endoscopy. Used with gaseous anesthetics and narcotics. May cause severe post-op respiratory depressio and amnesia

Front 1761

IV anesthetics: What does Ketamine (PCP analog and an arylcyclohexylamine) do?

Back 1761

dissociative anesthetic. Cardiovascular stimulant. Causes disorientation, hallucination, bad dreams. Increases cerebral blood flow.

Front 1762

IV anesthetics: How are narcotic analgesics used? Examples?

Back 1762

Morphone and fentanyl are used with CNS depressant during general anesthesia.

Front 1763

IV anesthetics: What is the advantage of propofol

Back 1763

used for rapid anesthesia induction and short procedures. Less post-op nausea than thiopental

Front 1764

Local anesthetics: Name some esters?

Back 1764

procaine, cocaine, tetracaine,

Front 1765

Local anesthetics: Name some amides?

Back 1765

lidocaine, bupivacaine, (amides have two I's in name!)

Front 1766

Local anesthetics: What is the mechanism and clinical use?

Back 1766

bind receptor and block Na channels. Tertiary amine local anesthetics penetrate membrane in uncharge form, then bind charged form. Use for minor surgical procedures, spinal anesthesia.

Front 1767

Local anesthetics: How do you decide to use ester or amides?

Back 1767

if allergic to esters, give amides

Front 1768

Local anesthetics: what is the toxicity

Back 1768

CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, arrhythmias (cocaine)

Front 1769

Local anesthetics: In infected ________ tissue, anesthetics are charged and cannot penetrate membrane. Therefore, ______ anesthetics are needed.

Back 1769

acidic; more

Front 1770

Local anesthetics: What is the order of nerve blockade for size and myelination? Which factor predominates?

Back 1770

small diameter> large diameter. Myelinated fibers> unmyelinated fibers. Size factor predominates

Front 1771

Local anesthetics: what is the order of loss of sensation?

Back 1771

pain first, then temp, then touch, then pressure

Front 1772

Local anesthetics: Why would you give these drugs with vasoconstrictors?

Back 1772

to enhance local action

Front 1773

Opiod analgesics: List as many as you can.

Back 1773

morphine, fentanyl, codeine, heroin, methadone, meperidine, dextromethorphan

Front 1774

Opiod analgesics: Mechanism: They act as _____ for opiod receptors to modulate synaptic transmission

Back 1774

agonists

Front 1775

Opiod analgesics: which drugs act at the mu, delta, kappa receptors?

Back 1775

morphine enkephalin, dynorphin

Front 1776

Opiod analgesics: Clinical use?

Back 1776

pain, cough supression (dex), diarrhea (loperamide), acute pulmonary edema, methadone maintenance programs

Front 1777

Opiod analgesics: What are the major toxicities?

Back 1777

addiction, respiratory depression, constipation, miosis, additive CNS depression wth other drugs

Front 1778

Opiod analgesics: Tolerance does not develop to __________and ______

Back 1778

miosis and constipation

Front 1779

Opiod analgesics: How would you treat toxicity?

Back 1779

naloxone, naltrexone (opiod R antagonist)

Front 1780

Other NSAIDS: List three NSAIDS?

Back 1780

ibuprofen, naproxen, indomethacin

Front 1781

Other NSAIDS: What is their mechanism?

Back 1781

reversibly inhibit COX 1 and 2. Blocks PG synthesis

Front 1782

Other NSAIDS: What is their clinical use (3As)?

Back 1782

Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.

Front 1783

Other NSAIDS: What are common toxicities?

Back 1783

renal damage, aplastic anemia, GI distress, ulcers

Front 1784

COX 2 Inhibitors: Where is cox2 found?

Back 1784

in inflammatory cells and mediates inflammation and pain

Front 1785

COX 2 Inhibitors: Why is cox2 inhibition better than cox1?

Back 1785

cox1 helps to maintain gastric mucosa, thus, should not have the corrosive effects of other NSAIDs on the GI lining (less incidence of ulcers and bleeding)

Front 1786

COX 2 Inhibitors: Clinical Use?

Back 1786

RA and osteoarthritis

Front 1787

Acetaminophen: What is its mechanism and where does it work?

Back 1787

reversibly inhibits cox, mostly in CNS. Inactivated peripherally.

Front 1788

Acetaminophen: What are its 2 As?

Back 1788

antipyretic, analgesic but NOT anti-inflammatory.

Front 1789

Acetaminophen: Overdose effects?

Back 1789

hepatic necrosis, acetaminophen metabolites depletes glutathine and forms toxic tissue adducts in the liver

Front 1790

cardiovascular therapy: Changes in CO affect two major pathways?

Back 1790

1. Carotid sinus firing, sympa discharge 2. Renal blood flow, renin-ang pathway

Front 1791

cardiovascular therapy: What is the effect of the following drugs: 1. Positive inotropic drugs 2. Beta blockers 3. Ace inhibitors 4. AII antagonists 5. Vasodilators and 6. Diuretics

Back 1791

1. Increases cardiac output. 2. Inhibit renin release. 3. Inhibit ACE 4. Inhibits effects of AngII including increasing the preload, increasing the afterload and remodelling. 5. Decrease the preload and afterload. 6. Decrease the preload and afterload

Front 1792

antihypertensive drugs: What are the adverse effects of these two diueretics: hydrochlorothiazide, loop diuretics

Back 1792

1. Hypokalemia, hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia 2. Hypokalemia, met alk, hypotension, ototoxicity

Front 1793

antihypertensive drugs: These are wahat class of drugs: clonidine, methyldopa, ganglionic blockers, reserpine, guanethidine, prazosin, beta blockers?

Back 1793

sympathoplegics

Front 1794

antihypertensive drugs: Adverse effects of clonidine?

Back 1794

dry mouth, sedation, severe rebound HTN

Front 1795

antihypertensive drugs: Adverse effects of methyldopa?

Back 1795

sedation, positive coombs test

Front 1796

antihypertensive drugs: Adverse effects of ganglionic blockers?

Back 1796

orthostatic HTN, blurred vision, constitpation, sexual dysfuncction

Front 1797

antihypertensive drugs: Adverse effects of reserpine?

Back 1797

sedation, depression, nasal stuffiness, diarrhea

Front 1798

antihypertensive drugs: adverse effects of beta blockers?

Back 1798

impotence, asthma, cardiovascular, cns

Front 1799

antihypertensive drugs: Adverse effects of guanethidine?

Back 1799

orthostatic and exercise Hypotension, sex dysfxn, diarrhea

Front 1800

antihypertensive drugs: Adverse effects of prazosin?

Back 1800

1st dose orthostatic hypotension, dizzy, headache

Front 1801

antihypertensive drugs: The following are what class: hydralazine, minoxidil, nifedipine, verapamil, nitroprusside

Back 1801

vasodilators

Front 1802

antihypertensive drugs: which one causes lupus like syndrome? Other toxicities?

Back 1802

hydralazine, nausea, headache, reflex tachycardia, angina, salt retention

Front 1803

antihypertensive drugs: adverse effets of minoxidil?

Back 1803

hypertrichosis (hair growth - think Rogaine with minoxidil!), pericardial effusion, reflex tachycardia, angina, salt retention

Front 1804

antihypertensive drugs: Side effects of nifedipine, verapamil?

Back 1804

dizziness, flushing, constipation, nausea

Front 1805

antihypertensive drugs: which one causes cynide toxicity?

Back 1805

nitroprusside

Front 1806

antihypertensive drugs: Adverse effects of ACE-I Captorpil? Think CAPTOPRIL

Back 1806

C: cough, A: angioedema, P: proteinuria, T: taste changes, O: hypOtension, P: pregnancy problems like fetal renal damage, R: rash, I: increased renin, L: lower angiotensin. Also hyperkalemia.

Front 1807

antihypertensive drugs: Losartan is a ----------- R-Inhibitor? With ____-toxicity and ____kalemia

Back 1807

angiotensin II, fetal renal, hyper

Front 1808

Hydralizine: Which two anti-htn drugs do you use with B blockers to prevent reflex tachycardia, diuretic to block salt retention?

Back 1808

hydralizine, minoxidil

Front 1809

Hydralizine: What is hydralizine's mechanims and clinical use?

Back 1809

increase cGMP --> smooth muscle relaxation. Vasodilates arteries > veins. Reduces afterload. Used for severe HTN or CHF

Front 1810

Calcium channel blockers, name three: Mechanism: block _____ chanels of cardiac and smooth muscles to reduce contractility

Back 1810

voltage dependednt L type Ca

Front 1811

Calcium channel blockers, name three: Rank their effects on vascular smooth muscle ad on the heart.

Back 1811

smooth muscle nifed> diltia > verapamil heart: vera> diltia> nifedepine

Front 1812

Calcium channel blockers, name three: What is the calcium channel blockers use?

Back 1812

HTN, angina, arrythmias (not nifedipine)

Front 1813

Calcium channel blockers, name three: ACE -I, name three

Back 1813

captopril, enalapril, lisinopril

Front 1814

Calcium channel blockers, name three: Mechanim considering bradykinin and renin release?

Back 1814

reduce lvels of ang II, prevent inactivation of bradykinin, renin release is increased to to loss of feedback inhibition

Front 1815

Calcium channel blockers, name three: what is the clinical use of these?

Back 1815

HTN, CHF, diabetic renal disease

Front 1816

Diuretics- site of action: What is the site of action of 1. Acetazolamide, 2. Osmotic agents, 3. Loop agents, 4. Thiazides, 5. Potassium sparing, 6. ADH antagonists

Back 1816

1. PCT 2. PCT, thin desc limb, CD 3. Thick ascending limb 4. Distal conv tubule 5. DCT a bit later 6. CD in inner medulla

Front 1817

Diuretics- site of action: How does mannitol an osmotic diuretic work?

Back 1817

increase tubular fluid osmolarity, producing increased urine flow

Front 1818

Diuretics- site of action: what is the use and toxicity?

Back 1818

Use: shock, drug overdose, decrease intracranial pressure. Toxicity - pulmonary edema, dehydration. Contraindicated in anuria, CHF

Front 1819

Acetazolamide: Is a ______inhibitor. Causes ______diuresis and _____ in total body HC03 stores.

Back 1819

Carbonic anhydrase, self-limited NaHCO3, reduction.

Front 1820

Acetazolamide: What electrolye disturbace does it treat? Does it cause?

Back 1820

treats met alk, causes in toxicity hyperchloremic met acidosis. ACIDazolamide caues ACIDosis.

Front 1821

Acetazolamide: Other toxicity?

Back 1821

neuropathy, NH3 toxicity, sulfa allergy

Front 1822

Acetazolamide: uses?

Back 1822

glaucoma, urinary alk, met alk, altitude sickeness

Front 1823

Furosemide: This sulfonamide loop diuretic inhibits _______cotransport

Back 1823

NA, K, 2CL

Front 1824

Furosemide: Furosemide also works by?

Back 1824

abolishes hypertonicit y of medulla, prevent concentration of urine. Increase Caexcertion. Loops Lose calcium

Front 1825

Furosemide: The three uses for this loop diuretic?

Back 1825

edematous states, htn, hypercalcemia

Front 1826

Furosemide: Toxicity using the OH DANG?

Back 1826

ototoxicity, hypokalemia, dehydration, allergy, nephritis interstitial, gout

Front 1827

Ethacrynic Acid: How is this drug different from furosemide? And how does that affect its use?

Back 1827

Although both have the same action, ethacrynic is a phenoxyacetic acid derivative not a sulfonamide. Therefore use this drug when you are allergic to sulfa.

Front 1828

Ethacrynic Acid: What drug can be used to treat acute gout?

Back 1828

ethacrynic acid

Front 1829

Ethacrynic Acid: AUTHOR

Back 1829

Stacy Ugras

Front 1830

Hydrochlorothiazide: Hydrochlorothiazide is a thiazide diuretic that inhibits the reabsorption of ----- in the ---- tubule

Back 1830

NaCl; early distal tubule

Front 1831

Hydrochlorothiazide: Does hydrochlorothiazide increase or decrease the excretion of calcium ion?

Back 1831

decrease

Front 1832

Hydrochlorothiazide: A toxic dose of hydrochlorathiazide will do what to the blood levels of these electrolites: potassium, sodium, glucose, lipid, uric acid, calcium

Back 1832

hypokalemic metabolic alkalosis, hyponatremia, hyperGlycemia, hyperLipidemia, hyperUricemia, hyperCalcemia (hyperGLUC)

Front 1833

K+-sparing diuretics: Spironolactone is a competitive antagonist to the --- receptor in the ---- tubule

Back 1833

aldosterone; cortical collecting tubule

Front 1834

K+-sparing diuretics: Name two K+-sparing diuretics that block Na+ channels in the cortical collecting duct

Back 1834

Triamterine and amiloride

Front 1835

K+-sparing diuretics: Besides causing hyperkalemia, a toxic dose of spironolactone will cause this endocrine effect

Back 1835

Gynecomastia (antiandrogen effect)

Front 1836

K+-sparing diuretics: Name three K+-sparing diuretics

Back 1836

Spironolactone, Triamterene, Amiloride (The K+ STAys.)

Front 1837

Diuretics: electrolye exchange: Diuretics are classified as carbonic anhydrase inhibitors, loop diuretics, thiazides, and K+-sparing diuretics. Which of these causes in increase in urine NaCl?

Back 1837

All of them!