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5243 Cards in this Set

  • Front
  • Back
Common congenital malformations: Name 7 common congenital malformations
(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)
Common congenital malformations: Name 2 neural tube defects (NTDs)
Spina bifida and anencephaly
Common congenital malformations: Name 2 diagnostic associations with NTDs during gestation
increased serum and amniotic fluid levels of a-fetoprotein
Common congenital malformations: How can the incidence of NTDs be reduced?
Folate ingestion during pregnancy
Congenital Heart Disease: What kind of shunts cause early cyanosis?
R-to-L "blue babies"
Congenital Heart Disease: What kind of shunts cause late cyanosis?
L-to-R "blue kids"
Congenital Heart Disease: Name 3 common R-to-L shunts.
The 3 T's: Tetralogy of Fallot (most common cause of early cyanosis), Transposition of the great vessels, truncus arteriosus
Congenital Heart Disease: What might you see children with a R-to-L shunt do to relieve discomfort?
Squat to increase venous return
Congenital Heart Disease: Name 3 common L-to-R shunts.
Congenital Heart Disease: Rank them in order of frequency
Congenital Heart Disease: What are the auscultatory signs of an Atrial Septal Defect?
Loud S1; wide, fixed split S2
Congenital Heart Disease: How do you treat PDA?
Congenital Heart Disease: Name 3 sequelae of L-to-R shunts.
1) Increased pulmonary resistance due to arteriolar thickening. 2) Progressive pulmonary HTN 3) R-to-L shunt (Eisenmenger's)
Eisenmenger's Syndrome: What are signs/symptoms of Eisenmenger's?
Late cyanosis, clubbing, polycythemia
Tetrology of Fallot: What is the Tetrology?
(1) Pulmonary Stenosis (2) RVH (3) Overriding aorta (4) VSD (mnemonic: PROVe)
Tetrology of Fallot: What is the direction of the shunt in the tetralogy?
right-to-left across the VSD
Tetrology of Fallot: What is the x-ray finding on the tetralogy?
Boot-shaped heart due to RVH
Tetrology of Fallot: What is the embryological cause of the tetralogy?
Anterosuperior displacement of the infundibular septum.
Transposition of great vessels: The transposition occurs because of a failure of the --------------- --------- to -------
failure of the aorticopulmonary septum to spiral
Transposition of great vessels: In transposition of the great vessels, the aorta leaves ------------ and the pulmonary trunk leaves the ------------
aorta leaves the RV (anterior) and the pulmonary trunk leaves the LV (posterior)
Transposition of great vessels: How might transposition of the great vessels, be compatible with life?
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.
Transposition of great vessels: Transposition of the great vessels is a common congenital heart disease in offspring of mothers with what disease?
Coarctation of aorta: Where is the aortic stenosis in the infantile type of coarctation?
Preductal (proximal to insertion of ductus arteriosus) - INfantile (in close to heart)
Coarctation of aorta: Where is the aortic stenosis in the adult type of coarctation?
Postductal (distal to ductus arteriosus). - ADult (Distal to Ductus)
Coarctation of aorta: Name 3 symptoms in adult type coarctation?
(1) Notching of the ribs (2) HTN in uper extremities (3) Weak pulses in uper extremities
Coarctation of aorta: What is the Male-to-Female ratio in coarctation?
Coarctation of aorta: What pulses should you check on physical exam?
Patent ductus arteriosus: Which direction is the shunt in a neonate with PDA?
Patent ductus arteriosus: What change occurs to the heart in PDA?
RVH and failure
Patent ductus arteriosus: What is the auscultatory finding in PDA?
Continuous, "machine-like" murmur.
Patent ductus arteriosus: How is patency maintained in PDA?
prostaglandin (PGE) synthesis and low Oxygen tension.
Patent ductus arteriosus: What drug is used to close a PDA?
Patent ductus arteriosus: How is a PDA kept open?
Patent ductus arteriosus: Why would you want to keep a PDA open?
To sustain life in conditions such as transposition of the great vessels.
Autosomal trisomies: What is the most common chromosomal disorder and cause of congenital mental retardation?
Down Syndrome (trisomy 21), 1:700
Autosomal trisomies: In Down syndrome, 4% of cases are due to ------- translocation, and 1% are due to -------- mosaicism
Robertsonian; Down
Autosomal trisomies: 95% of Down syndrome cases occur because of --------- --------- of homologous chromosomes
meiotic nondisjunction
Autosomal trisomies: What is the type and cause of the most common congenital heart malformation in Down syndrome?
Septum-primum-type ASD due to endocardial cushion defects
Autosomal trisomies: Name 8 findings in trisomy 21
(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
Autosomal trisomies: Name a risk factor for Down Syndrome
Advanced maternal age (1:500 < 20 yo; 1:25 > 45 yo)
Autosomal trisomies: What is the name of the syndrome associated with trisomy 18?
Edwards' syndrome (Election age = 18)
Autosomal trisomies: Name 7 findings in trisomy 18
(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
Autosomal trisomies: What is the life expectancy in trisomy 18?
Death usually w/in 1 year of birth
Autosomal trisomies: What chromosomal anomaly is found in Patau's syndrome?
trisomy 13 (1:6000)
Autosomal trisomies: Name 7 findings in Patau's
(1) severe mental retardation (2) microphthamlia (3) microcephaly (4) cleft lip/palate (5) abnormal forebrain structures (6) polydactyly (7) congenital heart dz
Autosomal trisomies: What is the life expectancy in Patau's?
Death usually w/in 1 year of birth
Genetic gender disorders: What is the chromosomal anomaly in Klinefelter's syndrome?
XXY (1:850) - male
Genetic gender disorders: Name 5 characteristics of Klinefelter's syndrome
(1) Testicular atrophy (2) Enuchoid body shape (3) Tall, long extremities (4) Gynecomastia (5) Female hair distribution
Genetic gender disorders: What is a Barr body and is it found kin Klinefelter's syndrome?
It is the inactivated X chromosome. Yes.
Genetic gender disorders: What is the chromosomal anomaly in Turner's syndrome?
Female XO; (1:3000)
Genetic gender disorders: Name 4 characteristics of Turner's syndrome
(1) Short stature (2) Ovarian dysgenesis (streak ovary) (3) Webbing of next (4) Coarctation of the aorta
Genetic gender disorders: Turner's syndrome is the most common cause of primary ------------
Genetic gender disorders: Is there a Barr body in Turner's syndrome?
Genetic gender disorders: Double Y males have what genotype?
XYY (1:1000) - male
Genetic gender disorders: What is the double Y phenotype?
Normal phenotype, very tall, severe acne, antisocial behavior (seein in 1-2% of XYY males; seen increasingly among prison inmates)
Muscular dystrophies: How are muscular dystrophies diagnosed?
Elevated CPK and muscle biopsy
Muscular dystrophies: What is the gene involved in muscular dystrophy?
Muscular dystrophies: What is the mutation in Duchenne's MD?
Frame-shift mutation - deletion of dystrophin gene - accelerated muscle breakdown.
Muscular dystrophies: What is the age of onset in Duchenne's MD?
Before 5 years
Muscular dystrophies: In what muscles does weakness begin with Duchenne's MD?
Pelvic girdle muscles and progresses superiorly
Muscular dystrophies: Name 3 diagnostic characteristics of Duchenne MD.
(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
Muscular dystrophies: What distinguishes Becker's from Duchenne's MD?
Less severe mutation in Becker's. Less debilitating.
Pseudohermaphroditism: What is pseudohermaphroditism?
Disagreement between the phenotypic (external genitalia) and gonadal (testes vs. ovaries) sex.
Pseudohermaphroditism: A female pseudohermaphrodite has ------- present, but external genitalia are -------- or -----------.
ovaries; virilized or ambiguous
Pseudohermaphroditism: What causes female pseudohermaphroditism?
Excessive and inapropraite exposure to androgenic steroids during early gestation (i.e.,congenital adrenal hyperplasia or exogenous administration of androgens suring pregnancy).
Pseudohermaphroditism: What are the phenotypes in female and male pseudohermaphroditism?
female - XX; male - XY
Pseudohermaphroditism: A male pseudohermaphrodite has ------- present, but external genitalia are --------- or ---------.
testes; female or ambiguous
Pseudohermaphroditism: What is the most common form of male pseudohermaphroditism?
Testicular feminization (androgen insensitivity), which results from a mutation in the androgen receptor gene (x-linked); blind-end vagina
Pseudohermaphroditism: What determines gender identity?
External genitalia and sex of upbringing.
True Hermaphrodite (46,XX or 47, XXY): What is a true hermaphrodite?
Both ovary and testicular tissue present; ambiguous genitalia.
True Hermaphrodite (46,XX or 47, XXY): What are the genotypic possibilities for a true hermaphrodite?
46,XX or 47,XXY
Testicular Feminization syndrome (46, XY): What is the molecular defect in testicular feminization syndrome?
Defect in DHT receptor resulting in normal-apearing female
Testicular Feminization syndrome (46, XY): What genitalia are present in testicular feminization syndrome?
female genitalia with rudimentary vagina; uterus and uterine tubes generally absent; develop testes (often found in labia majora; surgically removed to prevent malignancy)
Testicular Feminization syndrome (46, XY): What are the genotype and horomone levels in testicular feminization syndrome?
46, XY; levels of testosterone, estrogen and LH are all high
5a-reductase deficiency: What is the biochemical consequence of 5a-reductase deficiency
Unable to convert testosterone to DHT.
5a-reductase deficiency: Describe genital development in 5a-reductase deficiency.
Ambiguous genitalia until puberty, when increased testosterone causes masculinization of genitalia.
5a-reductase deficiency: What are the hormone levels in 5a-reductase deficiency.
Testosterone/estrogen levels are normal; LH is normal or elevated.
Cri-du-chat syndrome: What is the mutation in Cri-du-chat syndrome?
Congenital deletion of short arm of chromosome 5 (46,XX or XY, 5p-)
Cri-du-chat syndrome: What are the findings in Cri-du-chat
Microcephaly, severe mental retardation, high-pitched crying/mewing, epicanthal folds, cardiac abnormalities.
Cri-du-chat syndrome: What does Cri-du-chat mean in english, which might help remember the symptoms?
Cry of the cat.
Fragile X syndrome: What is the 2nd most common cause of genetic mental retardation?
Fragile X syndrome
Fragile X syndrome: What genetic change is involved in Fragile X syndrome?
x-linked defect affecting the methylation and expression of the FMR1 gene.
Fragile X syndrome: Name 4 physical features associated with Fragile X syndrome?
(1) macro-orchidism (enlarged testes) (2) Long face with a large jaw (3) large everted ears (4) autism
Cystic Fibrosis (CF): What is the genetic defect in cystic fibrosis?
Autosomal-recessive defect in CFTR gene on chromosome 7
Cystic Fibrosis (CF): What is the molecular defect in CF?
Defective Cl- channel
Cystic Fibrosis (CF): What are the consequences of the defect in CF?
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.
Cystic Fibrosis (CF): Name a diagnostic test for CF.
Increased concentration of Cl- ions in sweat test.
Cystic Fibrosis (CF): Why does CF cause infertility in males?
Absent vas deferens.
Cystic Fibrosis (CF): What vitamins are often deficient in CF?
Fat-soluble - A,D,E,K
Most common lethal genetic disease of Caucasians.
Cystic Fibrosis
Cystic Fibrosis (CF): What is the treatment for CF?
N-acetylcysteine to loosen mucous plugs.
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?
Adult polycystic kidney disease. N.B. the juvenile form is recessive.
Autosomal-dominant diseases: Name 2 other characteristics of adult polycystic kidney disease.
(1) always bilateral, (2) massive enlargement of the kidneys due to multiple large cysts.
Autosomal-dominant diseases: What sequelae are associated with adult polycystic kidney disease?
(1) polycystic liver disease (2) berry aneurysms (3) mitral valve prolapse
Autosomal-dominant diseases: What disease involves elevated LDL owing to defective or absent LDL receptor?
Familial hypercholesterolemia (type IIA)
Autosomal-dominant diseases: What are the average cholesterol levels in heterozygotes and homozygotes with familial hypercholesterolemia (tyype IIA)?
heterozygotes (1:500) - 300 mg/dL homozygotes - 700+ mg/dL
Autosomal-dominant diseases: What are 3 sequelae of familial hypercholesterolemia (type IIA)?
(1) severe atherosclerotic disease early in life (2) tendon xanthomas (classically in the Achilles tendon) (3) MI may develop before age 20
Autosomal-dominant diseases: What is the genetic defect in Marfan's syndrome?
Fibrillin gene mutation leads to connective tissue disorders.
Autosomal-dominant diseases: What are the skeletal abnormalities in Marfan's?
tall with long exteremities, hyperextensive joints, and long, tapering fingers and toes.
Autosomal-dominant diseases: What are the cardiovascular risks in Marfan's?
cystic medial necrosis of aorta leads to aortic incompetence and dissecting aortic aneurysms; flopy mitral valve.
Autosomal-dominant diseases: What are the ocular risks in Marfan's?
Subluxation of lenses.
Autosomal-dominant diseases: What is another name for Neurofibromatosis type 1?
von Recklinghausen's disease
Autosomal-dominant diseases: What chromosome is affected in NF type 1?
Long arm of chromosome 17 (17 letters in von Recklinghasen's)
Autosomal-dominant diseases: What are 5 classic characteristics of people with NF type 1?
(1) café-au-lait spots (2) neural tumors (3) Lisch nodules (pigmented iris hamartomas) (4) skeletal disorders (e.g., scoliosis) (5) Increased tumor susceptibility
Autosomal-dominant diseases: What disease is associated with bilateral acoustic neuroma?
Neurofibromatosis type 2
Autosomal-dominant diseases: What gene is affected in neurofibromatosis type 2?
NF2 gene on chromosome 22; (type 2 = 22)
Autosomal-dominant diseases: What is the genetic mutation in Von-Hippel-Lindau disease?
Deletion of VHL gene (tumor supressor) on chromosome 3p. (Von Hipel-Lindau = 3 words for chromosome 3)
Autosomal-dominant diseases: What are the clinical findings in Von-Hippel-Lindau disease?
hemiangioblastomas of retina/cerebellum/medulla; about half of affected individuals develop multiple bilateral renal cell carcinomas and other tumors.
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?
Huntington's disease
Autosomal-dominant diseases: What chromosome holds the gene involved in Huntington's?
Chromosome 4; triplet repeat disorder ("Hunting 4 food")
Autosomal-dominant diseases: What disease is responsible for a colon that ecomes covered with adenomatous polyps after puberty?
Familial adenomatous polyposis (FAP)
Autosomal-dominant diseases: What is the progression in Familial adenomatous polyposis if colon not resected?
Colon cancer
Autosomal-dominant diseases: What is the genetic defect in Familial adenomatous polyposise?
deletion on chromosome 5 - 5 letters in polyp
Autosomal-dominant diseases: What are 3 characteristics of hereditary spherocytosis?
(1) spheroid erythrocytes (2) hemolytic anemia (3) increased MCHC
Autosomal-dominant diseases: What is the cure for hereditary spherocytosis?
Autosomal-dominant diseases: What is the genetic defect in achondroplasia?
Autosomal dominant cell-signaling defect of fibroblast growth factor (FGF) receptor 3.
Autosomal-dominant diseases: What are the physical characteristics of achondroplasia?
Dwarfism, short limbs, but head and trunk are normal size.
X-linked or AR:: Cystic fibrosis
X-linked or AR:: albinism
X-linked or AR:: Fragile X
X-linked or AR:: Duchenne's muscular dystrophy
X-linked or AR:: hemophilia A and B
X-linked or AR:: a1-antitrypsin deficiency
X-linked or AR:: Fabry's
X-linked or AR:: G6PD deficiency
X-linked or AR:: Hunter's syndrome
X-linked or AR:: Phenylketonuria (PKU)
X-linked or AR:: thalassemias
X-linked or AR:: sickle cell anemias
X-linked or AR:: ocular albinism
X-linked or AR:: glycogen storage diseases
X-linked or AR:: mucopolysaccharidoses (except Hunter's)
X-linked or AR:: sphingolipidoses (except Fabry's)
X-linked or AR:: infant polycystic kidney
X-linked or AR:: Lesch-Nyhan syndrome
X-linked or AR:: Bruton's agammaglobulinemia
X-linked or AR:: hemochromatosis
X-linked or AR:: Wiskott-Aldrich syndrome
X-linked or AR:: What are femal carriers of x-linked recessive disorders rarely affected?
Inactivation of X chromosomes in each cell
Neural Tube Defects (NTD): Name two associations with neural tube defects during pregnancy.
(1) Low folic acid intake (2) Elevated a-fetoprotein in amniotic fluid
Neural Tube Defects (NTD): What NTD is associated with failure of bony spinal canal to close, but no structural herniation?
Spina bifida occulta
Neural Tube Defects (NTD): Which NTD is involved with herniation of meninges through spinal canal defect?
Neural Tube Defects (NTD): What is the NTD that involves herniation of meninges AND spinal cord through spinal canal defect?
Neural Tube Defects (NTD): Which NTD is usually seen at lower vertebral levels?
Spina bifida occulta
Neural Tube Defects (NTD): Take a look at the figures in the book for good visualization of the NTDs.
Fetal Alcohol Syndrome: Who is at greatest risk of FAS?
Newborns of mothers who consumed significant amounts of alcohol (teratogen) during pregnancy (highest risk at 3-8 weeks).
Fetal Alcohol Syndrome: Name 5 congenital abnormalities in FAS?
(1) pre and postnatal developmental retardation (2) microcephaly (3) facial abnormalities (4) limb dislocation (5) heart and lung fistulas
Fetal Alcohol Syndrome: How does FAS rank among congenital malformations in the U.S.?
It's number 1
Fetal Alcohol Syndrome: What is the presumed mechanism of FAS?
Inhibition of cell migration?
Fetal Alcohol Syndrome: AUTHOR
Neha Pathak
NEOPLASTIC PROGRESSION: when cells increase in number it is called?
NEOPLASTIC PROGRESSION: what are two enzymes that allow neoplastic cells to invade th ebasement membrane?
collagenase and hydrolase
NEOPLASTIC PROGRESSION: when cells have an increased nulear to cytoplasmic ratio but have not invaded the basement membrane, it is called?
carcinoma in situ
_ -PLASIA DEFINITIONS: squamous _________ occurs in the trachea and bronchi of smokers
_ -PLASIA DEFINITIONS: what is it called when a cell has reversible preneoplastic changes with abnormal shape and size?
_ -PLASIA DEFINITIONS: abnormal cells that lack differentiation are called?
anaplastic cells
TUMOR STAGE VS. GRADE: staging of a tumor takes into account what factors?
TMN size of tumor, node involvment, metastases
TUMOR STAGE VS. GRADE: histolgy of a tumor is used to determine?
TUMOR STAGE VS. GRADE: what has more prognostic value? Grade or stage?
TUMOR NOMENCLATURE: the term _________ implies epithelial origin, whereas _________ implies mesenchymal origin
carcinoma, sarcoma
TUMOR NOMENCLATURE: a tumor of blood vessels is called what when it is benign? When it is malignant?
hemangioma, angiosarcoma
TUMOR NOMENCLATURE: what is a benign tumor of skeletal muscle called?
DISEASES ASSOCIATED WITH NEOPLASMS: Kaposi's sarcoma and aggressive malignant lymphomas are associated with what disease
DISEASES ASSOCIATED WITH NEOPLASMS: Actinic Keratosis predispose to what disease?
squamous cell carcinoma of skin
DISEASES ASSOCIATED WITH NEOPLASMS: down syndrome is associated with what neoplasm?
ONCOGENES: c-myc oncogenes are associated with what neoplasm?
burkitt's lymphoma
ONCOGENES: breast, ovarian, and gastic carcinomas all have this oncogene mutation in common?
erb B2
ONCOGENES: MEN II and III are associated with what oncogenic mutation?
TUMOR SUPRESSOR GENES: Name the associated tumor witht the following tumor supressor gene mutations: Rb, APC, WT1
retinoma blastoma, colorectal cancer, wilms tumor
TUMOR SUPRESSOR GENES: p53 is on what chromosome
TUMOR SUPRESSOR GENES: osteosarcoma is associated with what tumor supressor gene mutation
TUMOR MARKERS: TRAP is a tumor marker for what neoplasm
hairy cell leukemia
TUMOR MARKERS: what tumor marker is elevated in hyatidiform moles
TUMOR MARKERS: ovarian tumors are associated with what tumor marker
ONCOGENIC VIRUSES: the virus associated with burkitts and nasopharyngeal cancer is?
ONCOGENIC VIRUSES: hpv is responsible for what cancers?
cervical, penile, and anal carcinoma
ONCOGENIC VIRUSES: what virus is responsible for kaposis sarcoma?
CHEMICAL CARCINOGENS: aflatoxin, vinyl chloride and ccl4 damage what organ?
CHEMICAL CARCINOGENS: nitrosamines cause cancer in what organs?
esophagus or stomach
CHEMICAL CARCINOGENS: asbestos causes what types of cancer?
bronchogenic and mesothelioma
LOCAL EFFECTS OF TUMORS: When the following are obstructed, what can occur: bronchus? Biliary tree? Left colon?
pneumonia, jaundice, constipation
LOCAL EFFECTS OF TUMORS: tumor mass in the brain can cause the following
seizure, increased intracranial pressure, mass effect and herniation
LOCAL EFFECTS OF TUMORS: compression of the recurrent laryngeal nerve can cause what?
PROSTATIC ADENOCARCINOMA: what lobe/zone is most often involved in prostatic cancer?
posterior lobe, peripheral zone
PROSTATIC ADENOCARCINOMA: what is a common site of metastases for prostate cancer?
PROSTATIC ADENOCARCINOMA: what are useful tumor markers for prostate CA
psa, and prostatic acid phosphatase
SKIN CANCER: this type of skin cancer has palisading nuclei
basal cell carcinoma
SKIN CANCER: dyplastic nevi are a precursor fot this type of cancer
SKIN CANCER: this type of skin cancer is associated with keratin pearls
squamous cell carcinoma of skin
PRIMARY BONE TUMORS: the translocation 11;22 is associated with this cancer of the bone that occurs most commonly in young boys
ewing's sarcoma
PRIMARY BONE TUMORS: this tumor is characterized by a "double bubble" or "soap bubble" appearance
benign giant cell tumor
PRIMARY BONE TUMORS: this is the most common benign bone tumor, usually in men younger than 25, with a rare transformation to malignancy
Gabe Pitta
Primary Brain Tumors-Adult peak incidence: Most common adult brain tumor?
Glioblastoma multiforme (grade IV astrocytoma) See pseudopalisading tumor cells, central necrosis and hemorrhage.
Primary Brain Tumors-Adult peak incidence: Second most common adult tumor?
Meningioma, occurring in convexities of hemispheres and parasagittal region. See psammoma bodies.
Primary Brain Tumors-Adult peak incidence: Benign, slow-growing tumor in frontal lobes?
Oligodendroglioma, look for fried egg apearance, often calcified.
Primary Brain Tumors-Adult peak incidence: Third most common tumor, often localized to CN8?
Schwannoma, see it in acoustic Schwannoma. Antoni A (compact) and Antoni B (loose) patterns.
Primary Brain Tumors-Adult peak incidence: Most common forms are prolactin-secreting?
Pituitary Adenoma, which derives from Rathke's Pouch and can produce secondary bitemporal hemianopsia and hypopituitarism
Primary Brain Tumors-Child Peak Incidence: Highly malignant cerebellar tumor?
Medulloblastoma, can compress 4th ventricle and cause hydrocephalus. See rosettes or pseudorosettes.
Primary Brain Tumors-Child Peak Incidence: Cerebellar tumor associated with von Hippel-Landau syndrome?
Hemangioblastoma, see foamy cells and high vascularity, can produce excess EPO-->polycythemia.
Primary Brain Tumors-Child Peak Incidence: Commonly found in fourth ventricle, causing hydrocephalus?
Ependyomomas, which have perivascular rosettes and rod-shaped blepharoblasts near nucleus on exam.
Primary Brain Tumors-Child Peak Incidence: Diffusely infiltrating glioma, usually found in posterior fossa?
Low-grade Astrocytoma
Primary Brain Tumors-Child Peak Incidence: Benign tumor often confused with pituitary adenoma?
Craniopharyngioma, which also is derived from Rathke's pouch, also presents with bitemporal hemianopsia, also calcified.
Common sites that receive metastatic tissue: To Brain?
Lung, Breast, Skin (melanoma), Kidney (renal cell carcinoma), GI. Lots of Bad Stuff Kills Glia. 50% of brain tumors are due to metastases.
Common sites that receive metastatic tissue: To liver?
Colon>Stomach>Pancreas>Breast>Lung. Cancer Sometimes Penetrates Benign Liver. Metastases much more common than primary liver tumors.
Common sites that receive metastatic tissue: To bone?
Breast, lung, thyroid, testes, kidney, prostate.=> "BLT with a Kosher Pickle."
Common sites that receive metastatic tissue: Most common organ receiving metastases?
Adrenal medulla, then cortex.
Common sites that receive metastatic tissue: Most common organ sending metastases?
Paraneoplastic effects of tumors: Cushing's Syndrome
ACTH/ACTH-like peptide from small-cell lung CA
Paraneoplastic effects of tumors: SIADH
ADH/ANP from small cell lung CA and intracranial neoplasms.
Paraneoplastic effects of tumors: Hypercalcemia
PTH-related peptide/TGF-alpha/TNF-Alpha/IL-2 from squamous cell lung CA, renal cell CA, Breast CA, multiple myeloma, bone metastasis.
Paraneoplastic effects of tumors: Polycythemia
EPO from renal cell CA.
Paraneoplastic effects of tumors: Lambert-Eaton Syndrome
Antibodies against presynaptic Ca2+ channels at NMJ, generated by Thymomas and bronchogenic CA.
Paraneoplastic effects of tumors: Gout
Hyperuricemia due to excess nucleic acid turnover, found in various neoplasms.
Cancer Epidemiology: Male incidence?
Prostate(32%)>Lung(16%)>Colon and Rectum (12%)
Cancer Epidemiology: Male Mortality?
Cancer Epidemiology: Female incidence?
Breast (32%)>Lung(13%)>Colorectal(13%)
Cancer Epidemiology: Female Mortality?
HEMATOLOGIC PATHOLOGY: Anemia presenting with increased TIBC, decreased ferritin, decreased serum iron.
Mycrocytic, Hypochromic, usually secondary to iron deficiency. Also seen with Thalassemia, lead poisoning
HEMATOLOGIC PATHOLOGY: Anemia in patients with B12/Folate deficiency
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)
HEMATOLOGIC PATHOLOGY: Anemia in patients with normocytic, normochromic smears?
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.
HEMATOLOGIC PATHOLOGY: Anemia in patients with a decreased TIBC, decreased serum iron, and decreased iron saturation?
Anemia of chronic disease
HEMATOLOGIC PATHOLOGY: Anemia in patients with an increased TIBC, decreased serum iron, and normal iron saturation?
Iron-deficiency anemia.
HEMATOLOGIC PATHOLOGY: Patient with normal TIBC, increased serum iron, and 100% iron saturation (normal is 20-50%)
Iron overload (hemosiderosis)
Aplastic Anemia: Patient presentation of Aplastic Anemia?
Patients with pancytopenia characterized by severe anemia, neutropenia, and thrombocytopenia caused by failure or destruction of multipotent myeloid stem cells.
Aplastic Anemia: What causes aplastic anemia?
Radiation, benzene, chloramphenicol, alkylating agents, antimetabolites, viral agents, Fanconi's anemia, idiopathic causes.
Aplastic Anemia: Common Sx?
Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.
Aplastic Anemia: How do the blood smear and bone marrow aspirate appear?
Blood smear: pancytopenia with normal cell morphology. Aspirate:hypocellular marrow with fatty infiltration.
Aplastic Anemia: What's the treatment of aplastic anemia?
Withdraw offending agent, BMT, RBC/platelet transfusion, G-CSF or GM-CSF.
Hereditary Spherocytosis: How do patients with hereditary psherocytosis present (smear and labs)?
Smear shows microcytic RBCs that are small and round with no central pallor. The patients will have normal Hgb and MCV.
Hereditary Spherocytosis: What's the cause of hereditary spherocytosis?
Intravascular hemolysis due to spectrin defect.
Hereditary Spherocytosis: How is it confirmed and tested?
Will be Coombs' negative (unlike warm antibody hemolysis), can perform osmotic fragility test.
Hereditary Spherocytosis: What are some associated diseases?
Gallstones, splenomegaly, anemia, and jaundice.
Blood Dyscrasias-Sickle Cell Anemia: What is the HbS mutation?
Glutamate-->Valine in a Beta chain. Heterozygotes are usually malaria-resistant. *% of Af-Ams carry the HbS trait, 0.2% have the disease.
Blood Dyscrasias-Sickle Cell Anemia: What can precipitate sickling?
Low O2, dehydration.
Blood Dyscrasias-Sickle Cell Anemia: What are the common complications of HbS homozygotes?
aplastic crises from parvovirus infection, autosplenectomy, risk of encapsulated organism infection, salmonella osteomyelitis, vaso-occlusive pain crises, and splenic sequestration crises.
Blood Dyscrasias-Sickle Cell Anemia: What is the HbC defect?
Different Beta-chain mutation, the patients with HbC or HbSC have milder dz than HbSS patients.
Blood Dyscrasias-Sickle Cell Anemia: What are the treatment options?
Hydroxyurea (increased HbF) and bone marrow transplantation.
Blood Dyscrasias-Alpha-Thalassemia: What populations have the most prevalence?
Mediterranean populations. (thalaSEAmia)
Blood Dyscrasias-Alpha-Thalassemia: What is the etiology?
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.
Blood Dyscrasias-Alpha-Thalassemia: What is the presentation of a patient lacking all four alpha-globin genes?
hydrops fetalis and intrauterine fetal death.
Blood Dyscrasias-Beta-Thalassemia: Patient Presentation of Beta-Thalassemia major?
severe anemia requiring blood transfusion. Cardiac failure is often due to secondary hemochromatosis.
Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-Thalassemia major?
Beta chain is absent, fetal Hgb production is compensatorily increased but is inadequate.
Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-thalassemia minor?
The Beta chain is underproduced, again see fetal HgB compensatory increase. HbS/Beta-thalassemia heterozygote has mild to moderate disease.
DIC: What is the definition of DIC?
Activation of the coagulation cascade leading to microthrombi and global consumption of platelets, fibrin, and coagulation factors.
DIC: What causes DIC?
Obstetric complications (most common cause), gram-negative sepsis, transfusion, trauma, malignancy, acute pancreatitis, nephrotic syndrome.
DIC: What are the lab findings in DIC?
Increased PT, increased PTT, incrased fibrin split products (D-dimers), decreased platelet count.
Bleeding Disorders: What disorder type presents with mucous membrane bleeding, petechiae, purpura, and prolonged bleeding time?
Platelet abnormalities (microhemorrhages), which can be caused by ITP (antiplatelet antibodies and increased megakaryocytes), TTP (schistocytes), drugs, and DIC (increased fibrin split products).
Bleeding Disorders: What disorder type presents with hemarthroses (bleeding into joints), easy brusing, prolonged PT and/or PTT?
Coagulopathies (macrohemorrhages), which can be caused by Hemophilia A/B and von Willebrand's disease (most common)
Bleeding Disorders: What is the deficiency in Hemophilia A?
Factor VIII
Bleeding Disorders: What is the deficiency in Hemophilia B?
Factor IX
Bleeding Disorders: What is the deficiency in vW dz?
Deficiency of von Willebrand's antigen.
Bleeding Disorders: Which factors does the PT measure?
Extrinsic: Factors II, V, VII, and X.
Bleeding Disorders: Which factors does the PTT measure?
Intrinsic: All factors except VII and XIII.
Hemorrhagic disorders: What presents with increased bleeding time, normal platelet count, and normal PT/PTT and platelet count?
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.
Hemorrhagic disorders: What presents with decreased platelet count, increased bleeding time, and normal PT/PTT?
Hemorrhagic disorders: Which diseases present with increased PTT and normal PT, platelet count, and bleeding time?
Hemophilia A and B
Hemorrhagic disorders: What presents with a high PTT, normal PT, normal platelets, and increased bleeding time?
vW disease
Hemorrhagic disorders: What presents with increased Bleeding time/Pt/PTT and decreased platelet count?
Lymphomas: Hodgkin's Versus NHL: Which one presents with Reed-Sternberg cells?
Lymphomas: Hodgkin's Versus NHL: Which one is associated with HIV and immunosuppression?
Lymphomas: Hodgkin's Versus NHL: Which one involves multiple, peripheral nodes, with common extranodal involvement?
Lymphomas: Hodgkin's Versus NHL: Which one is localized to a single group of nodes, with contiguous spread and rare extranodal involvement?
Lymphomas: Hodgkin's Versus NHL: Which one presents with constitutional signs/symptoms: low-grade fever, night sweats, weight loss?
HL (NHL has few signs/symptoms)
Lymphomas: Hodgkin's Versus NHL: Which one presents with mediastinal lymphadenopathy?
Lymphomas: Hodgkin's Versus NHL: Which one involves mostly the B cells (except lymphoblastic origin)?
Lymphomas: Hodgkin's Versus NHL: Which one has hypergammaglobulinemia?
neither. Multiple Myeloma has hypergammaglobulinemia, where the excess B cells are in the resting state.
Lymphomas: Hodgkin's Versus NHL: Which one has a 50% association with EBV?
Lymphomas: Hodgkin's Versus NHL: Which one has bimodal age distribution?
HL (NHL has peak incidence at 20-40 years old)
Lymphomas: Hodgkin's Versus NHL: Which one has more common male presentation?
Hodgkin's: What factors denote a good prognosis?
Increased lymphocytes, decreased RS cells.
Hodgkin's: Which HL type has the best prognosis?
Nodular sclerosing (65-75%), which has least RS cells and lots of lymphocytes. Lymphocyte-predominant LH also has excellent prognosis.
Hodgkin's: Which HL type is the most common?
Nodular sclerosing, affecting women more than men and primarily young adults.
Hodgkin's: What is the prognosis of mixed cellular HL?
Intermediate. There are lots of lymphocytes but also lots of RS cells.
Hodgkin's: Which HL type has the worst prognosis?
Lymphocyte-depleted, which affects older males with disseminated disease.
Hodgkin's: Which HL type has the most RS cells?
Mixed cellular.
NHL: Which NHL type has only B cells?
Small Lymphocytic lymphoma, follicular lymphoma, Burkitt's
NHL: Which NHL type has a mix of B cells and T cells?
Diffuse large cell , occurring mostly in elderly but sometimes in children.
NHL: Which NHL type has only T cells?
Lymphoblastic Lymphoma, which has immature T cells. It is a very aggressive T-cell lymphoma.
NHL: Which type is associated with a t(8;14) c-myc gene mutation?
Burkitt's Lymphoma, occurring mostly in children. Has a high-grade "starry sky" apearance.
NHL: Which type is associated with a t(14;18) mutation and overexpression of bcl-2?
Follicular lymphoma, which is difficult to cure but has an indolent course.
NHL: Which type is associated with EBV infection and is endemic in africa?
NHL: Which is the most common childhood NHL?
Lymphoblastic Lymphoma, which also presents with ALL and a mediastinal mass.
NHL: Which is the most common adult version of NHL?
Follicular lymphoma.
NHL: Which types occur in adults?
Small lymphocytic lymphoma, follicular lymphoma.
NHL: Which types occur in children?
Lymphoblastic lymphoma, Burkitt's lymphoma.
NHL: Which one has a distribution of 80% adults and 20% children?
Diffuse large cell lymphoma, which ALSO has an 80% B cells 20% T cell distribution.
NHL: Which low-grade NHL type presents like CLL?
Small Lymphocytic lymphoma.
John Peoples
Leukemias: Peripheral and bone marrow characteristics
Increased circulating leukocytes, bone marrow infiltrates of leukemic cells
Leukemias: Consequences of marrrow failure
Anemia (dec. RBC's), infections (dec. WBC's), hemorrhage (dec. platelets)
Leukemias: Common organs of infiltration
Liver, spleen, lymph nodes
Leukemias: Characteristics of acute leukemias
Blasts predominate, children or elderly, short or drastic course
Leukemias: ALL characteristics (4)
Lympholasts (pre-B or pre-T), children, most responsive to therapy, associated with Down's Syndrome
Leukemias: AML characteristics
Myeloblasts, adults, auer rods
Leukemias: Characteristics of chronic leukemias
More mature cells, midlife age range, longer, less devastating course
Leukemias: CLL characteristics - cells
Lymphocytes, non-Ab producing B cells, increased smudge cells on peripheral blood smear
Leukemias: CLL - population
older adults
Leukemias: CLL - presentation and course
lymphadenopathy, hepatosplenomegaly, few sx., indolent course
Leukemias: CLL is similar to?
very similar to SLL (small lymphocytic lymphoma)
Leukemias: CLL is associated with what type of anemia?
warm antibody autoimmune hemolytic anemia
Leukemias: CML cell characteristics
Myeloid stem cells, increased neutrophils and metamyelocytes
Leukemias: CML translocation?
Ph Chromosome, t(9;22), bcr-abl
Leukemias: CML acute complications?
blast crisis (AML)
Chromosomal translocations - the following disorder is associated with what translocation?: CML
Ph chromosome, t(9;22), bcr-abl
Chromosomal translocations - the following disorder is associated with what translocation?: Burkitt's lymphoma
t(8;14), c-myc activation
Chromosomal translocations - the following disorder is associated with what translocation?: Follicular lymphomas
t(14;18), bcl-2 activation
Chromosomal translocations - the following disorder is associated with what translocation?: AML- M3 type
t(15;17), responsive to all-trans retinoic acid (ATRA)
Chromosomal translocations - the following disorder is associated with what translocation?: Ewing's sarcoma
Chromosomal translocations - the following disorder is associated with what translocation?: Mantle cell lymphoma
Lymphomas and Leukemias: What are the chronic leukemias associated with T-lymphoblasts?
Sezary Syndrome, CLL-T (both L2)
Lymphomas and Leukemias: What are the acute leukemias associated with T-lymphoblasts?
ALL-T (L2), ALL-null (L1), ALL-common(L1)
Lymphomas and Leukemias: What are the chronic leukemias associated with B-lymphoblasts?
CLL-B (L3)
Lymphomas and Leukemias: What are the acute leukemias associated with B-lymphoblasts?
ALL-B (L3)
Lymphomas and Leukemias: What are the chronic leukemias associated with monoblasts?
Chonic monocytic (M5), chronic myelomonocytic (M4)
Lymphomas and Leukemias: What are the acute leukemias associated with monoblasts?
Acute monocytic (M5), acute myelomonocytic (M5)
Lymphomas and Leukemias: What are the chronic leukemias associated with myeloblasts?
CML (M1, 2 and 3), Polycythemia rubra vera (M1), myelofibrosis (M1)
Lymphomas and Leukemias: What are the acute leukemias associated with myeloblasts?
AML (M2 and M1), Promyelocytic (M1)
Lymphomas and Leukemias: What are the chronic leukemias associated with eos-myeloblasts?
Eosinophilic (rare)
Lymphomas and Leukemias: What are the chronic leukemias associated with normoblasts?
Chronic erythroid (M6, rare)
Lymphomas and Leukemias: What are the acute leukemias associated with normoblasts?
acute erythroleukemia (M6)
Lymphomas and Leukemias: What are the chronic leukemias associated with megakaryoblasts?
Idiopathic thrombocytopenia (M7)
Lymphomas and Leukemias: What are the acute leukemias associated wwith megakaryoblasts?
acute megakaryocytic leukemias (M7)
Multiple Myeloma: What type of cell proliferates in MM, and what is its histologic appearance
Monoclonal plasma cell, fried egg apearance
Multiple Myeloma: Where does MM arise?
bone marrow
Multiple Myeloma: The 2 most common ab's, in order, are:
IgG (55%), IgA (25%)
Multiple Myeloma: Common symptoms are:
lytic bone lesions and hypercalcemia, renal insifficiency, increased suscpetibility to infection, anemia
Multiple Myeloma: This disease is associated with:
primary amyloidosis
Multiple Myeloma: Ig light chains are also called:
Bence Jones proteins
Multiple Myeloma: 3 key diagnostic features:
lytic bone lesions on x-ray, M-spike on serum protein electrophoresis, Bence-Jones proteins in urine
Multiple Myeloma: Red blood cell appearance on peripheral smear:
Rouleaux formation (poker chips)
Multiple Myeloma: What 2 differences are seen in Waldenstrom's macroglobulinemia?
M-spike is IgM, no lytic lesions
Achalasia: Achalasia results from:
failure of relaxation of lower esophogeal sphincter due to loss of the myenteric plexus (Aeurbach's). [A-chalasia = absence of relaxation]
Achalasia: Achalasia causes:
progressive dysphagia
Achalasia: Diagnosis is made by:
barium swallow showing "bird beak" dilated esophagus with distal stenosis.
Achalasia: Secondary achalasia may result from this protozoan disease:
Chagas disease (treponema cruzi)
Achalasia: Associated with increased risk of:
esophageal carcinoma
Barrett's esophagus: The distal esophageal colummnar epithelium is replaced with….
Gastric columnar epithelium
Barrett's esophagus: Barrett's results from:
Barrett's esophagus: Barrett's can progress to:
Esophageal Cancer: Risk factors are (ABCDEF):
achalasia, barrett's esophagus, corrosive esophagitis/cigarettes, diverticuli (e.g. zenker's), esophogeal web/EtOH, familial
Esophageal Cancer: The most common esophageal cancer in the world is:
squamous cell carcinoma
Esophageal Cancer: The most common esophageal cancer in the US is:
equal between squamous cell and adenocarcinoma (decreased cigarette use).
Esophageal Cancer: Esophageal Adenocarcinoma is found where?
lower third
Esophageal Cancer: Esophageal squamous cell carcinoma is found where?
uper 2/3
Congenital Pyloric Stenosis: What does this cause in infant?
Projectile vomiting at aproximately 2 weeks of age
Congenital Pyloric Stenosis: Treatment entails:
Malabsorption syndromes: Autoantibodies are seen to what in Celiac Sprue?
Gluten (gliaden) in wheat and other grains
Malabsorption syndromes: The histologic appearance of celiac sprue:
villous flattening, lymphocytic infiltrate
Malabsorption syndromes: Tropical sprue is due to what type of agent?
Infectious, treated with Antibiotics
Malabsorption syndromes: What are you infected with if you have Whipple's Disease?
Tropheryma whipelli
Malabsorption syndromes: Histologic cell type seen in Whipple's disease:
PAS+ macrophages
Malabsorption syndromes: What is the most common disaccharide deficiency leading to malabsorption?
lactase => milk intolerance
Chronic Gastritis: Fundal gastritis (type A) is characterized by 4 A's, what are they?
Autoimmune disorder with Autoantibodies to parietal cells, pernicious Anemia, Achlorydia
Chronic Gastritis: Antral gastritis (Type B) is caused by:
a Bug, H. Pylori infection
Chronic Gastritis: Both forms of gastritis carry an increased risk of what?
Gastric carinoma
Peptic Ulcer Disease: 2 etiologic agents underlying gastric ulcers are:
H. pylori (70%) and NSAID's
Peptic Ulcer Disease: Degeneration of what leads to gastric ulcers?
Gastric mucosal protection v. gastric acid
Peptic Ulcer Disease: Does the pain of a gastric ulcer increase or decrease with meals?
Increases => weight loss
Peptic Ulcer Disease: One etiologic agent underlies duodenal ulcers - what is it?
H. pylori (100%)
Peptic Ulcer Disease: 2 pathogenic mechanisms are thought to lead to development of duodenal ulcer - what are they?
Increased gastric acid secretion and decreased mucosal protection
Peptic Ulcer Disease: What tends to hypertrophy with duodenal ulcers?
Bruenner's glands
Peptic Ulcer Disease: The margins of a doudenal ulcer are:
clean and punched out
Peptic Ulcer Disease: The 4 common complications of of duodenal ulcers are:
bleeding, penetration, perforation, and obstruction (not necessarily pre-cancerous)
Peptic Ulcer Disease: Does the pain of a duodenal ulcer increase or decrease with meals?
Decreases => weight gain
Peptic Ulcer Disease: How is H.pylori infection treated?
triple therapy (metronidazole, bismuth salicylate, amoxocillin or tetracycline) with or without proton pump inhibitor
Peptic Ulcer Disease: Does smoking effect peptic ulcer development?
Yes, it is 2x as common in smokers
IBD: The possible etiology of Crohn's disease is:
IBD: The location and lesion type of Crohn's disease is:
Skip lesions in any portion of GI tract, usually terminal ileum, SI, and colon. Rectal sparing.
IBD: Gross Morphological features (6) of Crohn's disease are:
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)
IBD: The microscopic morphological features of Crohn's disease are:
non-caseating granulomas
IBD: The four major complications of Crohn's disease are:
Strictures, fistulas, perianal diease, malabsorption leading to nutritional depletion.
IBD: Two major extraintestinal manifestations associated with Chron's disease are:
migratory polyarthritis and erythema nodosum
IBD: The possible etiology of UC is:
IBD: Location and lesion type of UC is:
continuous lesions of colon with rectal involvement
IBD: The two gross morphological features of UC are:
mucosal inflammation, friable mucosal pseudopolyps with freely hanging mesentery.
IBD: The microscopic morphological features of UC are:
crypt abcesses, ulcers
IBD: 3 severe complications of UC are:
severe stenosis, toxic megacolon, and colorectal carcinoma
IBD: Two major extraintestinal manifestations associated with UC are:
pyoderma gangrenosum, sclerosing cholangitis
Diverticular Disease: Diverticuli are blind pouches found in the:
alimentary tract
Diverticular Disease: Diverticuli are lined by (3 layers):
Mucosa, muscularis, and serosa
Diverticular Disease: The 4 GI tract locations of diverticuli are:
esophagus, stomach, duodenum and colon
Diverticular Disease: Why are most diverticuli termed false?
They lack or have an attenuated muscularis mucosa.
Diverticular Disease: Percent of older patients likely to get diverticulosis (many diverticula):
50% of patients >60
Diverticular Disease: The reasons for increasing number of diverticula with age are:
Increased intraluminal pressure and focal weaknes in the colonic wall.
Diverticular Disease: What type of diet is diverticulosis associated with?
Diverticular Disease: Sx of diverticulosis?
usually asymptomatic, sometimes vague discomfort.
Diverticular Disease: Diverticulitis commonly presents with pain where?
Diverticular Disease: Complications of diverticulitis include:
perforation, peritonitis, abcess formation, bowel stenosis
Intussusception and Volvulus: What is intussuception?
telecoping of 1 bowel segment into distal segment.
Intussusception and Volvulus: Complication of intussusception is:
compromised blood suply.
Intussusception and Volvulus: What is volvulus?
Twisting of portion of the bowel around its mesentery.
Intussusception and Volvulus: What volvulus lead to?
Stomach Cancer: What is the most common type of stomach cancer?
Stomach Cancer: Is this cancer aggresive?
Yes, it has early aggressive local spread and node/liver mets
Stomach Cancer: Stomach Cancer is associated with what 3 etiologic factors?
dietary nitrosamines, achlorhydria, chronic gastritis
Stomach Cancer: What is stomach cancer termed when it is diffusely infiltrative with thickened and rigid appearance?
Linitis plastica
Stomach Cancer: What does Virchow's node signify?
involvement of supraclavicular node by stomach mets
Stomach Cancer: What is Krukenberg's tumor?
bilateral stomach cancer mets to the ovary
Stomach Cancer: What are characteristics of Krukenberg's tumor?
Abundant mucus, "signet ring" cells
Hirschprung's Disease: What is Hirschprung's diease?
congential megacolon
Hirschprung's Disease: What is missing?
enteric nerve plexus (both Auerbach's and Meissner's). Seen on biopsy
Hirschprung's Disease: What is the cause of this disease?
failure of neural crest migration.
Hirschprung's Disease: How does this disease present?
Chronic constipation early in life.
Hirschprung's Disease: Which part of the colon is dilated?
That part proximal to the aganglionic segment - aganglionic portion is constricted.
Colorectal cancer risk factors: The risk factors are:
colorectal villous adenoma, IBD, low-fiber diet, age, FAP, HNPCC, personal and family hx. of colon cancer.
Colorectal cancer risk factors: What is Peutz-Jeghers, and does it lead to colorectal cancer?
It is a benign polyposis syndrome which is not a risk factor.
Colorectal cancer risk factors: Who schould be screened for colorectal cancer and how?
People over age 50, screen with stool occult blood test.
Cirrhosis/Portal HT: Cirrho in Greek means:
tawny yellow
Cirrhosis/Portal HT: Cirrhosis is:
diffuse fibrosis of the liver with destruction of norml architecture, nodular regeneration.
Cirrhosis/Portal HT: Cause of micronodular cirrhosis (nodules <3mm, uniform in size) is:
metabolic insult
Cirrhosis/Portal HT: Causes of macronodular cirrhosis (nodules >3mm, varied in size) are?
Significant liver injury leading to hepatic necrosis (post-infectious, drug-induced hepatitis)
Cirrhosis/Portal HT: Cirrhosis is assocated with what type of cancer?
hepatocellular carcinoma
Cirrhosis/Portal HT: The effects of portal hypertension are:
esophageal varices (hemetemesis, melena), peptic ulceration (melena), splenomegaly, caput medusae, ascites, hemmorhoids, and testicular atrophy
Cirrhosis/Portal HT: Portal hypertension may be relieved by what method?
Portacaval shunt between splenic vein ad left renal vein.
Cirrhosis/Portal HT: What are the effects of liver cell failure?
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
Alcoholic Hepatitis: Hepatocytes in alcoholic hepatitis are:
swollen and necrotic
Alcoholic Hepatitis: Other histologic changes seen in aloholic hepatitis are:
neutrophil infiltration, mallory bodies (hyaline), fatty change, and sclerosis areound central vein
Alcoholic Hepatitis: SGOT (AST):SGPT (ALT) ratio is:
usually more than 1.5 (A Scotch and Tonic: AST elevated)
Budd Chiari Syndrome: What is Budd-Chiari Syndrome?
Occlusion of the IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease
Budd Chiari Syndrome: The features of congestive liver disease are:
hepatomegaly, ascites, abdominal pain, and eventual liver failure
Budd Chiari Syndrome: Budd-Chiari Syndrome is associated with what 3 conditions:
polycythemia vera, pregnancy, hepatocellular carcinoma
Wilson's Disease: Wilson's disease is?
Coper accumulation, especially in liver, brain and cornea
Wilson's Disease: It is due to what?
failure of coper to enter circulation in the form of ceruloplasmin
Wilson's Disease: What is another name for Wilson's Disease?
Hepatolenticular degeneration
Wilson's Disease: What are the symptoms of Wilson's Disease? (A,B,C-6,D)
Asterixis, basal ganglia degeneration (parkinsonian symptoms), Ceruloplasmin decrease, cirrhosis, corneal deposits (kayser-fleischer rings), coper accumulation, carcinoma (hepatocellular), choreiform movements, Dementia
Hemochromatosis: What is hemosiderosis?
Deposit of iron (hemosiderin) - this causes hemochromatosis
Hemochromatosis: The traid of sx. are?
micronodular cirrhosis, pancreatic fibrosis, and skin pigmentation ("bronze" diabetes)
Hemochromatosis: Possible complications include?
CHF, increased risk of hepatocellular carcinoma
Hemochromatosis: What is primary form?
inherited, Autosomal recessive
Hemochromatosis: What is secondary form due to?
chronic transfusion therapy
Hemochromatosis: What are ferritin, iron, TIBC and transferrin saturation levels?
Ferritin increased, iron increased, TIBC decreased => transferrin saturation is increased
Hemochromatosis: How much iron may the body contain?
As much as 50g, enough to set off airport metal detectors
Hemochromatosis: How is this condition treated?
Phlebotomy, deferoxamine
Hemochromatosis: AUTHOR
Tzevan Poon
Jaundice: bacteria convert conjugated bilirubin into what? what happens to some of this?
urobilinogen --> some which is reabsorbed, some which is excreted. (urobilinogen that's reabsorbed is converted to urobilin= yellow pigment in urine)
Jaundice: which is soluble in water/urine: conjugated or unconjugated bilirubin?
conjugted of course!
Jaundice: check out the 3 jaundice types: what are they? ***cover up the various parts of the chart in the text and test yourself.
heptocellular vs. obstructive vs. hemolytic jaundice
Heriditary hyper-bilirubinemias: What is the biochemical disorder in GILBERTS SYNDROME?
mild ↓ in UDP-glucuronyl transferase (this is key enzyme in conjugation of bilirubin)
Heriditary hyper-bilirubinemias: what are the symptoms?
Heriditary hyper-bilirubinemias: what type of bilirubin is seen upon the lab findings? Do you have do you have major hemolysis?
unconjugated bilirubin is elevated w/o overt hemolysis
Heriditary hyper-bilirubinemias: What is the syndrome called when you have an ABSENCE of UDP-glc-ur-transferase?
Crigler-Najjar (CN) syndrome type 1 (type 2 is LESS severe)
Heriditary hyper-bilirubinemias: when does it present in life? What is the prognosis?
presents early in life: pts die in a few years.
Heriditary hyper-bilirubinemias: name 3 findings of C-N syndrome?
jaundice, kernicterus, ↑ unconjugated bilirubin
Heriditary hyper-bilirubinemias: type 2 is more sever or less severe? What do you treat it with?
less severe than type 1; treat type 2 with phenobarbital.
Heriditary hyper-bilirubinemias: what do you treat type 1 with (name 2)?
plasmapheresis + phototherapy (breaks down unconj. Bilirubin)
Heriditary hyper-bilirubinemias: What is Dubin Johnson syndrome?
↑↑ hyperbilirubin (conjugated) due to defective liver EXCRETION
Heriditary hyper-bilirubinemias: what does the liver look on gross exam?
black liver grossly
Heriditary hyper-bilirubinemias: what is the name of the less severe syndrome akin to Dubin Johnson?
Rotor's syndrome: also no black liver.
Heriditary hyper-bilirubinemias: see drawing: it's nice.
Primary sclerosing cholangitis: what is the pathophysiology
segmental inflammation and fibrosis of bile ducts: unaffected parts are dilated.
Primary sclerosing cholangitis: what test do you do to see this stricture/dilating/beading pattern?
Primary sclerosing cholangitis: what disease is this associated with?
Ulcerative Colitis
Primary sclerosing cholangitis: What can prim. Scl. Cholangitis lead to?
2° biliary cirrhosis/sclerosis
Biliary sclerosis : what is the cause of Primary Biliary Sclerosis (PBS)? (compare the name/disease of PBS vs. PSC: primary sclerosing cholangitis)
autoimmune disorder with antimitochondrial antibodies
Biliary sclerosis : name 3 signs associated with PBS:
1) severe obstructive jaundice 2) itching 3) hypercholesterolemia (xanthoma)
Biliary sclerosis : What is the cause of SBS: secondary biliary sclerosis?
EXTRA-hepatic biliary obstruction → ↑ pressure in INTRA-hepatic ducts → ↑ injury/sclerosis
Biliary sclerosis : what is 2° biliary sclerosis associated with (name 3 things)?
ascending cholangitis (bacterial infection), bile stasis, and bile lakes
Heptocellular carcinoma = hepatoma: in liver cancers, is this common?
yes, #1 most common!
Heptocellular carcinoma = hepatoma: there is an ↑ incidence of hepatoma due to what diseases/exposures (name 7)
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)
Heptocellular carcinoma = hepatoma: How do hepatomas spread? How does this differ with renal cell ca. spread?
They BOTH commonly spread hematogenously!
Heptocellular carcinoma = hepatoma: What is major lab finding with hepatocelluar ca?
↑ AFP (alpha fetoprotein)
Reye's syndrome = rare!!! But…: What is this syndrome?
Hepato-encephalopathy: fatal: occurs in childhood
Reye's syndrome = rare!!! But…: name 3 findings:
1) fatty liver w/ microvesicular fatty change 2) hypoglycemia, 3) coma
Reye's syndrome = rare!!! But…: is this associated with any outside factors/triggering factors?
yes: 1) viral infection (esp. VZV or influenza B) 2) salicylates!!!
Reye's syndrome = rare!!! But…: if baby/child has fever what do you use in place of aspirin?
use acetaminophen (but with caution): i.e. acetaminophen OD hepato-toxicity
Gallstones: name 3 types of stones and tell me how they show up on CT scan:
1) cholesterol stone (radiolucent but 10-20% opaque due to calcification) 2) mixed stone = cholesterol + pigment (radiolucent) 3) pigment stone (radio-opaque)
Gallstones: Which is the most common type of gall stone?
mixed stone
Gallstones: name at least 5 out 9 risk factors for Cholesterol stones: is there a mnemonic?
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….
Gallstones: name 4 risk factors for pigment stones:
1) pts with chronic RBC hemolysis 2) alcoholic cirrhosis 3) elderly 4) biliary infection
Gallstones: What is a good way to diagnosis stones?
Gallstones: What is CHARCOT'S TRIAD
1) epigastric/RUQ pain 2)fever 3) jaundice
Acute pancreatitis: this is what our US attorney general had. : pathophysiology mechanism?
activation and thus autodigestion by pancreatic enzymes
Acute pancreatitis: this is what our US attorney general had. : Causes? (good mnemonic)
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
Acute pancreatitis: this is what our US attorney general had. : clinically presents with?
intense epigastric pain radiating to back
Acute pancreatitis: this is what our US attorney general had. : labs(name 2): which of the two has a higher specificity?
↑ amylase + ↑lipase (higher specificity) "li is hi"
Acute pancreatitis: this is what our US attorney general had. : Name 5 nasty complications that can result from AP?
1) DIC 2) ARDS 3) diffuse fat necrosis 4) hypocalcemia 5) pseudocyst formation
Acute pancreatitis: this is what our US attorney general had. : if you have CHRONIC pancreatitis: what do we think of your life habits?
Chronic Pancr. Is strongly associated w/ alcoholism
Pancreatic cancer: what is a common and fatal pancreatic cancer?
pancreatic adenocarcinoma
Pancreatic cancer: what is the prognosis?
6 months: very aggressive: usually has mets when pt. presents
Pancreatic cancer: where are tumors most commonly located? And what does this lead to?
pancreatic head → obstructive jaundice.
COPD = also known as OLD: obstructive lung disease: why is it called obstructive?
obstruction of AIR FLOW → air traping in lungs
COPD = also known as OLD: obstructive lung disease: what is the major PFT finding?
FEV1 / FVC ration is ↓ (hallmark finding)
COPD = also known as OLD: obstructive lung disease: name the 4 types of COPD
1) Chronic Bronchitis (Blue Bloater) 2) emphysema (pink puffer) 3) asthma 4) bronchietasis
COPD = also known as OLD: obstructive lung disease: what is the definition of Chronic Bronchitis
productive cough for >3 consecutive months in two or more years.
COPD = also known as OLD: obstructive lung disease: what do you expect on lung histology?
hypertrophy of mucus-secreting glands in the bronchioles (Reid index of >50%)
COPD = also known as OLD: obstructive lung disease: leading cause is smoking: what are the physical findings for Chronic Bronchitis? (name 3)
1)cyanosis 2) wheezing 3) crackles
COPD = also known as OLD: obstructive lung disease: what is the pathophysiological mechanism of EMPHYSEMA?
destruction of fibrous septa/alveolar walls → enlargement of air space and ↓ total surface area for gas exchange
COPD = also known as OLD: obstructive lung disease: if the cause is smoking, what kind of emphysema would you see on histo slide?
centri-acinar emphysema
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?
alpha 1-antitrypsin deficiency → panacinar emphysema + liver cirrhosis
COPD = also known as OLD: obstructive lung disease: what causes the emphysema in this disorder?
↑ elastase activity to damage lung tissue.
COPD = also known as OLD: obstructive lung disease: name 4 findings of emphysema (in general)
1) dyspnea; 2) ↓ breath sounds 3) tachycardia 4) ↓ I/E ratio
COPD = also known as OLD: obstructive lung disease: What is mechanism of asthma
BRONCHIAL hypersensitivity/hyperresponsiveness → REVERSIBLE bronchoconstriction
COPD = also known as OLD: obstructive lung disease: name 3 common triggers
1) viral URI 2) allergens 3) stress!!
COPD = also known as OLD: obstructive lung disease: name 7 findings
1) cough 2) wheezing 3) dyspnea 4) hypoxemia 5)↓ I/E ratio 6) tachypnea 7) pulsus paradoxus
COPD = also known as OLD: obstructive lung disease: BRONCHIECTASIS: what is its mechanism??
chronic necrotizing infection of BRONCHI → dilated airways, purulent sputum, recurrent infections, hemoptysis (see Robbins for a good discussion of this)
COPD = also known as OLD: obstructive lung disease: what disorders is bronchietasis commonly associated with?
1) bronchial obstruction 2) cystic fibrosis 3) poor ciliary motility
Restrictive Lung Disease (RLD): What are classic PFT findings for RLD?
↓ VC ↓TLC ; FEV1/FVC ration > 80%
Restrictive Lung Disease (RLD): Name the two MAJOR types of RLD
1) poor breathing mechanics (EXTRA-pulmonary) 2) Interstitial lung diseases
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.
Lung Physical Findings: cover up parts of the very good table to test yourself on various findings.
Lung Physical Findings: Obstructive vs. Restrictive findings
Lung Physical Findings: Name 3 lung volumes that are increased in COPD
Lung Physical Findings: What 2 values are BOTH reduced in COPD and RLD?
1) FEV1 and 2) FVC (think FEV1/FVC ratio) NOTE! in COPD, FEV1 is more dramatically reduced and thus the FEV1/FVC ratio is ↓
Asbestosis = long latency = think shipbuilders and plumbers: what is the main pathology resulting from asbestosis?
DIFFUSE, interstitial fibrosis caused by inhaled asbestos Fibers.
Asbestosis = long latency = think shipbuilders and plumbers: What cancers are increased in pts with asbestosis?
1) pleural mesothelioma 2) bronchogenic carcinoma (BC)
Asbestosis = long latency = think shipbuilders and plumbers: Major finding in lung?
Ferruginous bodies: asbestos fibers coated with hemosiderin also 2) ivory white pleural plaques
Neonatal respiratory distress syndrome: What is the main cause
surfactant deficiency --> to increased surface tension --> alveolar collapse
Neonatal respiratory distress syndrome: surfactant is made by which cells? After when?
type 2 pneumocytes after 35th gestational week
Neonatal respiratory distress syndrome: what do you measure? Where do you get this fluid?
lecithin-to-sphingomyelin ratio in the amniotic fluid = measure of lung maturation <1.5 in neonatal distress syndrome
Neonatal respiratory distress syndrome: what is surfactant made of (chemical name)
dipalmitoyl phosph-tidyl-choline (DP-PTC)
Neonatal respiratory distress syndrome: treatment for poor maturation of lungs
1) before birth = maternal steroids 2) after= artificial surfactant
Karta-gener's syndrome: what is this?
immotile cilia due to dynein arm defect
Karta-gener's syndrome: results in what in female and male? (4 things)
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)
Lung Cancer: name the 3 main classes of cancers that affect parts of the lung
1) bronchogenic carcinoma (with different subtypes) 2) carcinoid tumor 3) metastasis
Lung Cancer: list the 5 types of major bronchogenic carcinomas
CENTRAL 1) squamous cell ca 2)small cell ca PERIPHERAL 3) adenocarcinoma 4) bronchoalveolar ca 5) large cell ca
Lung Cancer: mnemonic: what is meant by SPHERE of symptoms?
S= superior vena cava syndrome; P= pancoast tumor; H= Horner's syndrome; E= Endocrine (paraneoplastic); Recurrent laryngeal / hoarseness; E = Effusions (pleural OR pericardial)
Lung Cancer: What can a CARCINOID tumor cause?
Carcinoid Syndrome = flushing, diarrhea, wheezing, and salivation
Lung Cancer: Metastases to lung is very common, LUNG cancer also prone to metastasize to what other parts?
1) brain (epilepsy) 2) bone (fracture) 3)liver (jaundice + hepatomegaly)
Pancoast tumor: What is it?
it's a carcinoma of the apex of lung
Pancoast tumor: what may it affect?
may affect CSP= cervical sympathetic plexus causing Horner's syndrome
Pancoast tumor: what is Horner's syndrome?
P.A.M. is Horny = Ptosis, Anhydrosis, Miosis
Pneumonia: 1st AID breaks it down into TYPE/ ORGANISM/ CHARACTERISTICS = cover parts of this table and fill in the blanks
Pneumonia: Lobar Pneumonia; Organism(s) and characteristics
Pneumococcus; intraalveolar exudate -> consolidation, may involve entire lung
Pneumonia: Bronchopneumonia: Organism and characteristics
S aureus, H flu, Klebsiella, S pyogenes; Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving >= 1 lobes
Pneumonia: Interstitial pneumonia; Organism(s) and characteristics
Viruses, mycoplasma, legionella; diffuse patchy inflammation localized to interstitial areas at alvolar walls; distribution involving >= 1 lobes
Degenerative diseases: name two diseases that affect the CEREBRAL CORTEX
1) Alzheimer's disease 2) Pick's disease
Degenerative diseases: name two diseases that affect BASAL GANGLIA & BRAIN STEM:
1) Huntington's disease 2) Parkinson disease
Degenerative diseases: name 5 diseases that affect SPINOCEREBELLAR MOTOR NEURON
1) Olivo-ponto-cerebellar atrophy 2) Friedreich's ataxia 3)ALS = amyotrophic lateral sclerosis 4)Werdnig-Hoffmann disease 5) Polio
Degenerative diseases: what is the most common cause of elderly dementia?
Degenerative diseases: name two pathological findings characteristic of Alzheimer's
1) senile plaques = intracytoplasmic inclusion bodies 2) neurofibrillary tangles (abnormally phosphorylated tau protein)
Degenerative diseases: what is the 2nd most common cause of dementia in elderly?
multi-infarct dementia in elderly\
Degenerative diseases: How can Alzheimer also affect intracranial vasculature?
amyloid angiopathy --> intracranial hemorrhage
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)
chromosome 1, 14, 19 (APO-E4 allele), 21 (p-Ap gene)
Degenerative diseases: What is pathognemomic with Pick's disease upon histology?
Pick bodies = intra-cytoplasmic inclusion bodies
Degenerative diseases: What cortical areas does Pick's disease affect
Frontal and temporal lobes (remember; sharp, atrophic apearance of gross specimen)
Degenerative diseases: What is the inheritance pattern of Huntington's
Auto Dominant
Degenerative diseases: What are some symptoms?
1) chorea 2) dementia
Degenerative diseases: Huntington's is due to atrophy of _____ what? Loss of ___ ergic neurons.
atrophy of caudate nucleus = loss of GABA-nergic neurons
Degenerative diseases: what is the genetic abnormality of Huntington's?
1) Chr. 4 - expansion of CAG repeats
Degenerative diseases: Parkinson disease is associated with what pathology findings?
1) Lewy bodies 2) depigmentation of substantia nigra (loss of dopaminergic neurons)
Degenerative diseases: rare cases of Parkinson's have been linked to what contaminant of certain illicit drugs?
MPTP = contaminant to street drug
Degenerative diseases: Parkinson's can make you feel in a "TRAP" = ?
T = tremor at rest; R = cogwheel rigidity; A = akinesia ; Postural instability
Degenerative diseases: ALS = Lou Gehrig's disease (the Iron Horse of the Yankees, hero of Joe DiMaggio) = what signs is ALS associated with?
Both UMN and LMN deficits
Degenerative diseases: Werdnig-Hoffman disease - presents as birth as?
1) flopy baby syndrome 2) note tongue fasciculations as well (also seen in ALS)
Degenerative diseases: for Polio, what kind of signs to you see?
predominantly LMN deficits.
Intracranial Hemorrhage/Hemotomas: name 4 types of cranial related hemorrhages (think of layers that could possibly be involved)
1) epidural hemorrhage 2) subdural h 3) subarachnoid h 4) parenchymal h
Intracranial Hemorrhage/Hemotomas: what is a common site of epidural hematoma/hemorrhage
1) rupture of MMA: middle meningeal artery, often 2ndary to fracture of temporal bone
Intracranial Hemorrhage/Hemotomas: what does CT show for epidural h?
biconcave disc NOT crossing suture lines
Intracranial Hemorrhage/Hemotomas: what else do you see?
lucid interval
Intracranial Hemorrhage/Hemotomas: How do subdural h. most often occur?
rupture of bridging veins (think, elderly being jolted in roller coaster)
Intracranial Hemorrhage/Hemotomas: this is venous bleeding so how would this influence symptomatic findings?
venous = less pressure = delayed onset of symptoms
Intracranial Hemorrhage/Hemotomas: what types of people do you see subdural h.?
1) elderly, 2) alcoholics 3) blunt trauma/sudden change in velocity injuries
Intracranial Hemorrhage/Hemotomas: for SUBDURALs what do you see upon CT?
1) crescent-shaped hemorrhage instead 2) YES IT does cross the suture lines
Intracranial Hemorrhage/Hemotomas: subarachnoid hemorrhage is often seen where (name 2 types
rupture of 1) aneurysm (usually Berry aneurysm) or an 2)AVM
Intracranial Hemorrhage/Hemotomas: symptoms?
the worst headache of my life
Intracranial Hemorrhage/Hemotomas: since its subarachnoid, what do you see on what test?
bloody or xanthochromic CSF on spinal tap
Intracranial Hemorrhage/Hemotomas: name 4 risk factors for parenchymal hematoma
1) HTN 2) amyloid angiopathy 3) diabetes mellitus 4) tumor
Intracranial Hemorrhage/Hemotomas: AUTHOR
Hilcias Duran
Berry aneurysms: most common site for Berry aneurysms
bifurcation of the anterior communicating artery (Circle of Willis)
Berry aneurysms: berry aneurysms are associated with
adult polycystic disease, Ehlers-Danlos s., and marfan's
Berry aneurysms: Classic triad of Multiple Sclerosis
SIN: Scanning speech, intention tremor, nystagmus (affect woman 20-30s)
Berry aneurysms: Prevalence of MS
increase prevalence w/ increased distance from the equator
Berry aneurysms: Clinical s/s of MS
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)
Berry aneurysms: Progressive multifocal leukoencephalopathy (PML) is associated w/
JC virus and seen in 2-4 % of AIDS pts (reactivation or latent infect)
Berry aneurysms: pathogenesis of Guillian-Barre syndrome
Inflammation and demyelination of peripheral nerves and motor fibers of the ventral roots (sensory effec less severe than motor)
Berry aneurysms: s/s of Guillian-Barre syndrome
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
Berry aneurysms: association between G-B syndrome and…
herpesvirus or camplobacter jejuni infection, inoculations, and stress but no definitive link to a pathogen
Poliomyelitis: organism causing polio and mechanism of action
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
Poliomyelitis: s/s of polio
malaise, HA, fever, nausea, abd. Pain, sore throats, signs of LMN signs
Poliomyelitis: finding of polio
csf w/ lymphocytic pleocytosis w/ slight elevation of protein, virus recovered from stool or throat
Aphasia : describe Broca's (expressive) aphasia
confluent aphasia w/ intact comprehension broca's is broken speech
Aphasia : describe Wernicke's (aphasia)
Fluent aphasia w/ impaired concentration Wernick's ="What?" W area located in superior temperal gyrus
seizures : describe two types of partial seizures
1.simple partial (awareness is intact)--motor, sensory, autonomic, psychic 2.Complex partial (impaired awareness)
seizures : describe types of Generalized seizure ( diffuse)
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
seizures : what are the causes of seizures in children?
genetic, infection, trauma, congenital, metabolic
seizures : adults?
tumors, trauma, stroke, infection
seizures : elderly?
stroke, tumor, trauma, metabolic, infection
Horner's syndrome: what is Horner's syndrome?
sympathectomy of face (lesion above T1) 1.Ptosis 2.anhidrosis and flushing of affected side 3.miosis [PAM is horny]
Horner's syndrome: Horner's syndrome is associated w/ what type of tumor?
pancoast tumor
syringomyelia: what is syringomyelia?
enlargement of the central canal of the S.C. Crossing fibers of spinothalamic tract are damaged.
syringomyelia: what are the s/s of syringomyelia?
b/l loss of pain and temp sensation in the uper extremities w/ the touch sensation. Most common at C8-T1
syringomyelia: commonly seen in what pts?
pts w/ Arnold-Chiari malformation
Tabes dorsalis : what infection is tabes dorsalis associated w/?
teriary syphilis
Tabes dorsalis : what happens in the CNS?
degeneration of dorsal columns and dorsal root
Tabes dorsalis : dorsalis also is associated with what s/s?
charcot's joint, shooting (lightning) pain, Argyll Robertson pupils, and absence of DTRs
Osteoarthritis : what occurs in OA?
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)
Osteoarthritis : classical presentation of OA?
pain in weight bearing joints after use (worse at the end of the day0 improves w/ rest. No systemic symptoms
Rheumatoid Arthritis : what happens in in RA?
autoimmune inflammatory proccess which affects synovial joints, w/ pannus formation in joints (MCP, PIP), S-Q rheumatoid nodules, ulnar deviation,subluxation
Rheumatoid Arthritis : classical presentation of RA?
female, 80% pts Rf positive (anti-IgG Ab) morning stiffness improving w/ use, symmetrical joint involvement, and systemic symptoms (fever, fatigue, pleurtis, pericarditis)
Rheumatoid Arthritis : AUTHOR
Jason Portnof
Sjogren's Syndrome: What is the classic triad of Sjogren’s syndrome?
dry eyes (conjunctivitis, xeropthalmia), dry mouth (dysphagia, xerostomia), arthritis
Sjogren's Syndrome: What is SICCA syndrome?
dry eyes, dry mouth, nasal and vaginal dryness, chronic bronchitis, reflux esophagitis
Sjogren's Syndrome: T/F Sjogren’s syndrome predominantly affects males between 40 and 60 years of age.
False. Females between 40 and 60 y.o are predominantly affected in Sjogren’s syndrome.
Gout: T/F Gout is the precipitation of monosodium urate crystals into joints due to hyperuricemia.
Gout: What is the favored manifestation of gout?
Podagra. (painful MTP joint)
Gout: The crystals of gout are:
needle shaped and negatively bifringent
Pseudogout: T/F Pseudogout is the precipitation of calcium pyrophosphate crystals within the joint space.
Pseudogout: The crystals of psuedogout are:
basophilic, rhomboid crystals
Pseudogout: Psudogout usually affects:
Large joints (classically the knee)
Pseudogout: T/F Both gout and psuedogout predominantly affect men.
False. Gout is more common in men. Pseudogout affects both sexes equally, most pts are >50 years old.
Pseudogout: T/F The treatment for both pseudogout and gout is allopurinol, probenecid, colchicines, and NSAIDS.
False. That is the tx for gout. However, there is no tx for pseudogout.
Celiac sprue: Celiac sprue is the autoimmune-mediated intolerance of what substance, leading to steatorrhea?
gliadin (wheat)
Celiac sprue: T/F Findings in Celiac sprue include blunting of villi, neutrophils in the lamina propria, and abnormal D-xylose test.
False. lymphocytes, not neutrophils are found in the lamina propria.
Systemic Lupus Erythematosus: What drugs can produce a SLE-like syndrome that is commonly reversible?
HIp: Hydralazine, INH, Phenytoin, Procainamide
Systemic Lupus Erythematosus: SLE causes LSE. What is LSE?
Libman Sacks Endocarditis. Valvular vegetations found on both sides of valve (Mitral Valve Stenosis) and do not embolize.
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.
Both statements are true
Systemic Lupus Erythematosus: What are 4 lab tests in SLE? Which test, when positive is predictive of a poor prognosis?
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
Systemic Lupus Erythematosus: In what organ are wire loop lesions found in SLE?
kidney (with immune complex deposition and nephrotic syndrome)
Systemic Lupus Erythematosus: What causes death commonly in SLE?
Renal failures and infections
Systemic Lupus Erythematosus: What are symptoms of SLE?
fever, fatigue, wt loss, joint pain, malar rash, photosensitivity. Also: pleuritis, pericarditis, nonbacterial verrucous endocarditis, Raynaud’s phenomenon
Sarcoidosis: What disease is characterized by gamaglobulinemia, rheumatoid arthritis, ace increase, interstitial fibrosis, and noncaseating granulomas?
Seronegative spondyloarthropathies: Name 2 seronegative spondyloarthropathies.
ankylosing spondylitis, reiters’ syndrome
Seronegative spondyloarthropathies: What is a seronegative spondyloarthropathy?
Arthritis without rheumatoid factor (no anti-IgG Ab). Strong association with HLA-B27 (gene that codes for HLA MHC1)
Seronegative spondyloarthropathies: T/F seronegative spondyloarthropahties occur more often in males
Seronegative spondyloarthropathies: What is the classic triad for Reiter’s syndrome?
Urethritis, conjunctivitis and anterior uveitis, arthritis. “Can’t see, can’t pee, can’t climb a tree”
Seronegative spondyloarthropathies: T/F reiter’s syndrome occurs commonly post respiratory or chlamydia infections.
False. Post-GI or chlamydia infections
Seronegative spondyloarthropathies: Describe ankylosing spondylitis
Chronic inflammatory disease of spine and sacroiliac joints. Ankylosis (stiff spine), uveitis and aortic regurg.
Scleroderma: T/F Crest syndrome is wider-spread than diffuse scleroderma.
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.
Scleroderma: T/F Crest syndrome occurs in male pts that have allergic rxn to toothpaste.
False. CREST= calcinosis, raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia.
Scleroderma: What antibodies are associated with scleroderma (progressive systemic sclerosis- PSS)?
"diffuse scleroderma- anti-Scl-70 antibody, Crest syndrome- anticentromere antibody
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.
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.
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.
Skin disorders: What HLA groups are associated with psoriasis?
HLA-B27, HLA-13, HLA-17
Skin disorders: What is psoriasis? Where is it most commonly found?
Psoriasis is nonpruritic chronic inflammation of the skin, particularly on the knees and elbows.
Goodpasture's: T/F Goodpasture’s syndrome affects the lungs and liver.
False. Lungs and Kidneys. (Pulmonary hemorrhagesà hemoptysis, renal lesionsà hematuria, anemia, crescentic glomerulonephritis)
Goodpasture's: What type of Abs are associated with Goodpastures?
anti-glomerular basement membrane abs produce linear staining on immunofluorescence.
Goodpasture's: Who commonly gets Goodpastures?
Men between 20-40 years.
Cushing's syndrome: What are etiologies of Cushing’s syndrome? Is ACTH always elevated?
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
Cushing's syndrome: Describe the clinical picture of Cushings.
HTN, wt gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin change (thinning, striae), osteoporosis, immune supression
Hyperaldosteronism: T/F Conn’s syndrome is secondary hyperaldosteronism.
False. Conn’s syndrome is primary hyperaldosteronism, caused by an aldosterone-secreting tumor. Results in HTN, hypokalemia, metabolic alkalosis, low plasma renin.
Hyperaldosteronism: Which hyperaldosteronism is associated with high plasma renin?
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.
Hyperaldosteronism: What is the tx for hyperaldosteronism?
Spironolactone, a diuretic that works by acting as a aldosterone antagonist.
Addison's Disease: What characterizes addison’s disease? (which hormones are elevated or deficient)? Is it associated with HTN or hypotension?
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.
Addison's Disease: T/F In primary insufficiency decreased pituitary ACTH production is characterized by skin hyperpigmentation.
False: increased ACTH causes MSH activity & hyperpigmentation
Tumors of adrenal medulla: T/F Neuroblastoma is the most common tumor of adrenal medulla in adults.
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.
Tumors of adrenal medulla: Where does neuroblastoma occur?
Neuroblastoma is the most common tumor of adrenal medulla in children. It can occur anywhere along the sympathetic chain.
Tumors of adrenal medulla: AUTHOR
Jason Lee
Pheochromocytoma: secrete combination of two molecules
epinephrine and norepinephrine
Pheochromocytoma: epidemiology (rule of 10's)
10% malignant, 10% bilateral, 10% extra-adrenal, 10% calcify, 10% kids, 10% familial
Pheochromocytoma: symptoms - 5 P's
(elevated blood) Pressure, Pain (headache), Perspiration, Palpitations, Pallor/diaphoresis --> relapsing and remittant
Pheochromocytoma: elevations in two lab values
urinary VMA and serum catecholamines
Pheochromocytoma: association with two other endocrine diseases
Pheochromocytoma: treatment
Multiple Endocrine Neoplasia: type I (Wermer's syndrome) - 3 P's
Pancreas, Pituitary, and Parathyroid tumors
Multiple Endocrine Neoplasia: type II (Sipple's syndrome)
medullary carcinoma of thyroid, pheochromocytoma, parathyroid tumor, or adenoma
Multiple Endocrine Neoplasia: type III
medullary carcinoma of thyroid, pheochromocytoma, oral/intestinal ganglioneuromatosis
Hypothyroidism and hyperthyroidism: myxedema is prominent in which one
Hypothyroidism and hyperthyroidism: chest pain, palpitations, arrhythmias
Hypothyroidism and hyperthyroidism: TSH is (increased/decreased) in primary hyperthyroidism? In primary hypothyroidism?
hyper - decreased, hypo - increased
Hypothyroidism and hyperthyroidism: Graves' disease involves autoantibodies with what mechanism of action?
stimulation of TSH receptors
Hypothyroidism and hyperthyroidism: three symptoms of Graves'
ophthalmopathy, pretibial myxedema, diffuse goiter
Hypothyroidism and hyperthyroidism: Graves' is a type __ hypersensitivity
type II
Hashimoto's thyroiditis: thyroid is (enlarged/not enlarged) and (tender/nontender)
enlarged, nontender
Hashimoto's thyroiditis: autoimmune antibodies directed against ---
Hashimoto's thyroiditis: histology shows (type of cell) infiltrate
lymphocytes (with germinal centers)
Subacute thyroiditis (de Quervain's): self-limited (hyper/hypo)thyroidism following ---
hypothyroidism following flu-like illness
Subacute thyroiditis (de Quervain's): symptoms include
jaw pain, tender thyroid gland, early hyperthyroidism
Thyroid cancer: most common, good prognosis, "ground glass" nuclei, psammoma bodies
papillary carcinoma
Thyroid cancer: poor prognosis, uniform follicles
follicular carcinoma
Thyroid cancer: calcitonin producing (C cells), sheets of cells
medullary carcinoma (MEN II and III)
Thyroid cancer: older patients, horrible prognosis
Cretinism: caused by a lack of dietary --- or defect in --- formation
iodine (endemic), T4 (sporadic)
Cretinism: symptoms include
pot-belly, paleness, puffy face, protuberant tongue, protruding umbilicus
Acromegaly: caused by excess --- in adults
growth hormone
Acromegaly: symptoms include
large furrowed tongue, deep voice, large hands and feet, coarse facial features
Acromegaly: in children, leads to ---
Diabetes mellitus: acute symptoms common to both types
polydipsia, polyuria, polyphagia, weight loss
Diabetes mellitus: match: (DKA/hyperosmolar coma) with (type I/type II)
DKA=type I, hyperosmolar coma=type II
Diabetes mellitus: effects (increased/decreased) of insulin deficiency and glucagon excess on 1) glucose uptake, 2) protein catabolism, 3) lipolysis
1) decreased, 2) increased, 3) increased
Diabetes mellitus: increased plasma free fatty acids leads to
Diabetes mellitus: hyperglycemia has what effect on blood volume and electrolytes
decreased volume (osmotic diuresis), electrolyte depletion
Diabetes mellitus: three chronic manifestations
retinopathy (hemorrhage, exudate, microaneurysm), nephropathy (nodular sclerosis), neuropathy (sensory, motor, autonomic)
Diabetes mellitus: sorbitol accumulation leads to what sequelae in the eye
cataracts, glaucoma
Diabetes mellitus: three tests - what are they? which one measures long-term glucose control?
fasting glucose, glucose tolerance test, HbA1c
Diabetes mellitus: AUTHOR
Jacob Pugsley
Type 1 - juvenile onset: % of diabetes
Type 1 - juvenile onset: Insulin necessary in treatment
Type 1 - juvenile onset: Age
Type 1 - juvenile onset: Association with obesity
Type 1 - juvenile onset: Genetic predisposition
weak, polygenic
Type 1 - juvenile onset: Association with HLA system
Yes (HLA-DR3 & 4)
Type 1 - juvenile onset: Glucose intolerance
Type 1 - juvenile onset: Ketoacidosis
Type 1 - juvenile onset: B-cell numbers in the islets
Type 1 - juvenile onset: Serum insulin levels
Type 1 - juvenile onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss
Type 1 - juvenile onset: Theorized cause
viral or immune destruction of B cells
Type 2 - adult onset: % of diabetes
Type 2 - adult onset: Insulin necessary in treatment
Type 2 - adult onset: Age
Type 2 - adult onset: Association with obesity
Type 2 - adult onset: Genetic predisposition
Strong, polygenic
Type 2 - adult onset: Association with HLA system
Type 2 - adult onset: Glucose intolerance
mild to moderate
Type 2 - adult onset: Ketoacidosis
Type 2 - adult onset: B-cell numbers in the islets
Type 2 - adult onset: Serum insulin levels
Type 2 - adult onset: Classic symptoms of polyuria, polydipsia, thirst, weight loss
Type 2 - adult onset: Theorized cause
increased resistance to insulin
Diabetic Ketoacidosis (type 1): What precipitates this
Increase in insulin requirements from increase in stress (e.g. infection)
Diabetic Ketoacidosis (type 1): Ketone bodies from where
Excess fat breakdown, increase ketogenesis from increased free fatty acids which are made into ketone bodies
Diabetic Ketoacidosis (type 1): Signs/Symptoms
Kussmaul respirations (rapid/deep breathing), hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration, fruity breath odor
Diabetic Ketoacidosis (type 1): Labs
Hyperglycemia, high H+, low HCO3- (anion gap metabolic acidosis), high blood ketone levels, leukocytosis
Diabetic Ketoacidosis (type 1): Complications
Life threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythimias, heart failure
Diabetic Ketoacidosis (type 1): Treatment
Fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia.
Diabetes insipidus: summary
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
Diabetes insipidus: Findings
Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L
Diabetes insipidus: Treatment
adequate fluid intake; Central DI - intranasal desmopressin (ADH analog); nephrogenic DI - hydrochlorothiazide, indomethacin, or amiloride
SIADH: what does it stand for
Syndrome of inapropriate ADH
SIADH: finds
1) excess water retention 2) hyponatremia [may lead to seizures - correct slowly] 3) urine osmolarity > serum osmolarity
SIADH: causes
1) Ectopic ADH [small cell lung cancer] 2) CNS disorders/head trauma 3) pulmonary disease 4) Drugs
Hyperparathyroidism: What causes primary hyperparathyroidism?
Usually an adenoma
Hyperparathyroidism: What are the findings of primary disease?
hypercalcemia, hypercalciuria, hypophosphatemia, high parathyroid hormone, high cAMP in urine; often asymptomatic, may present with weakness and constipation
Hyperparathyroidism: what is osteitis fibrosa cystica? (von Recklinghausen's syndrome)
cystic bone spaces filled with non-neoplastic fibrous tissue
Hyperparathyroidism: What causes secondary hyperparathyroidism?
low serum Ca++, most often chronic renal disease.
Hyperparathyroidism: What are the findings of secondary hyperparathyroidism?
hypocalcemia, hyperphosphatemia, high parathyroid hormone
Hypoparathyroidism: findings
hypocalcemia, tetany.
Hypoparathyroidism: causes
accidental surgical excision (thyroid surgery) or DiGeorge syndrome
Hypoparathyroidism: note: pseudohypoparathyroidism
autosomal recessive kidney unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature
Carcinoid syndrome: frequency
Carcinoid syndrome: cause
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.
Carcinoid syndrome: symptoms
recurrent diarhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.
Carcinoid syndrome: most common tumor of what?
Carcinoid syndrome: lab
high 5-HIAA in urine
Carcinoid syndrome: Rule of 1/3s:
1/3 metastasize; 1/3 present with second malignancy; 1/3 multiple
Carcinoid syndrome: Treatment?
Carcinoid syndrome: What is this medication?
synthetic octapeptide analog of somatostatin (growth hormone-inhibiting hormone)
Zollinger-Ellison syndrome: What kind of tumor causes this?
Gastrin secreting tumor (usually) of the pancreas
Zollinger-Ellison syndrome: what does it cause?
recurrent ulcers
Zollinger-Ellison syndrome: may be associated with what?
MEN type I
Osteoporosis: what is this?
reduction in bone mass in spite of normal bone mineralization
Osteoporosis: what characterizes type 1?
Postmenopausal (10-15 years after menopause); increased bone reabsorption due to low estrogen levels. Treated with estrogen replacement
Osteoporosis: what characterizes type 2?
Senile osteoporosis - affects men and women > 70 y/o
Osteoporosis: what races are affected most?
Osteoporosis: symptoms of vertebral crush fractures
acute back pain, loss of height, kyphosis
Osteoporosis: other
distal radius (Colles') fracures, vertebral wedge fracures.
Osteoporosis: see picure
(end of endocrine)
Benign prostatic hyperplasia: who gets BPH?
common in men > 50 y/o
Benign prostatic hyperplasia: what might cause it?
may be due to age-related increase in estradiol with possible sensitization of the prostate to the growth promoting effects of DHT.
Benign prostatic hyperplasia: findings
nodular enlargement of the periurethral (lateral and middle) lobes of the prostate gland, compressing the urethra to a vertical slit.
Benign prostatic hyperplasia: symptoms
increased frequency of urination, nocturia, difficulty in starting and stoping the stream of urine, dysuria.
Benign prostatic hyperplasia: complications
may lead to distention and hypertrophy of the bladder, hydronephrosis, UTIs
Benign prostatic hyperplasia: premalignant lesion?
Hydatidiform mole: What is it?
pathologic ovum (empty egg - ovum with no DNA) resulting in a cystic swelling of chorionic villi and proliferation of chorionic epithelium (trophoblast).
Hydatidiform mole: Most common precursor of what?
Hydatidiform mole: what happens to B-hCG?
Hydatidiform mole: findings
honeycombed uterus, cluster of grapes apearance
Hydatidiform mole: genotype
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)
Pregnancy-induced hypertension (preeclampsia-eclampsia): what is the triad?
hypertension, proteinuria, edema
Pregnancy-induced hypertension (preeclampsia-eclampsia): what makes it eclampsia?
addition of seizures to the triad
Pregnancy-induced hypertension (preeclampsia-eclampsia): what % of pregnant women?
Pregnancy-induced hypertension (preeclampsia-eclampsia): when does it present?
20 weeks gestation to 6 weeks postpartum
Pregnancy-induced hypertension (preeclampsia-eclampsia): what increases the likelihood?
preexisting hypertension, diabetes, chronic renal disease, autoimmune disorders
Pregnancy-induced hypertension (preeclampsia-eclampsia): what is HELLP syndrome?
Hemolysis, Elevated LFTs, Low Platelets
Pregnancy-induced hypertension (preeclampsia-eclampsia): Clinical features
headache, blurred vision, abdominal pain, edema of face and extremeties, altered mentation, hyperreflexia
Pregnancy-induced hypertension (preeclampsia-eclampsia): Lab findings
thrombocytopenia, hyperuricemia
Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment
Delivery of fetus as soon as viable. Otherwise, bedrest, salt restriction, monitoring and treatment of hypertension
Pregnancy-induced hypertension (preeclampsia-eclampsia): Treatment for eclampsia (a medical emergency)
IV Magnesium sulfate, diazepam
Pregnancy complications: Abruptio placentae
premature separation of the placenta. Painful uterine bleeding (usually 3rd trimester). Fetal death. May be associated with DIC
Pregnancy complications: Placenta accreta
defective decidual layer allows placenta to attach directly to myometrium. Predisposed by prior C-section or inflamation. May have massive hemorrhage after delivery.
Pregnancy complications: Placenta previa
attachment of the placenta to lower uterine segment. May occlude cervical os. Painless bleeding in any trimester.
Pregnancy complications: Ectopic pregnancy
most often in fallopian tubes, predisposed by salpingitis (PID).
Cervical Pathology: Dysplasia and carcinoma in situ
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.
Cervical Pathology: Invasive carcinoma
Often squamous cell carcinoma. Pap smears can catch cervical dysplasia (koilocytes) before it progresses to invasive carcinoma.
Cervical Pathology: AUTHOR
Gabi Rizzuto
Uterine pathology: most common tumor in female (hint - has increased incidence in blacks)? Do they progress to malignancy?
leiomyoma; no.
Uterine pathology: endometriosis - most common site?
Uterine pathology: endometriosis in the myometrium = ?
Uterine pathology: most common gyn malignancy? (hint - causes vaginal bleeding in a postmenopausal women)
endometrial carcinoma
Uterine pathology: Leiomyosarcoma: does it arise de novo or from leiomyoma?
de novo
PCOS (Stein-Leventhal syndrome): Major clinical manifestations include: amenorrhea, infertility, obesity, and ----?
Ovarian cysts: the four types of ovarian cysts
follicular, corpus luteum, theca-lutein, chocolate
Ovarian cysts: blood containing cyst from ovarian endometriosis
chocolate cyst
Ovarian cysts: cyst that is associated with choriocarcinoma and moles
theca-lutein cyst
Ovarian cysts: cyst defined by hemorrhage into persistent corpus luteum
corpus luteum cyst
Ovarian cysts: cyst defined by distention of unruptured graafian follicle
follicular cyst
Ovarian germ cell tumors : that which is analagous to male seminoma
Ovarian germ cell tumors : produces alpha-fetoprotein
yolk sac tumor
Ovarian germ cell tumors : associated with elevated hCG
Ovarian germ cell tumors : monodermal teratoma made up of only thyroid tissue
struma ovarii
Ovarian germ cell tumors : most common germ cell tumor of ovary (90%)
Ovarian germ cell tumors : True or False: immature teratomas are benign
False. Mature ("dermoid cyst") ones are benign, immature ones are aggressively malignant
Ovarian non-germ cell tumors: bilateral non germ cell tumor with fallopian tube like epithelium
serous cystadenoma
Ovarian non-germ cell tumors: Pseudomyxoma peritonei (intraperitoneal accumulation of mucinous material) may be a consequence of which ovarian non germ cell tumor?
mucinous cystadenocarcinoma
Ovarian non-germ cell tumors: tumor resembling bladder epithelium
brenner tumor
Ovarian non-germ cell tumors: triad of ovarian fibroma, ascites, and hydrothorax = ?
Meigs' syndrome
Ovarian non-germ cell tumors: Pathology term for the small follicles filled with eosinophilic secretions that are seen in granulosa cell tumors
Call-Exner bodies
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
fibroadenoma/hyperplastic cysts
Breast disease: Eczematous patches on the nipple w/ corresponding large cell's with clear halo on histology are indicative of --?
Paget's disease & most likely an underlying ductal carcinoma
Breast disease: Fibrosis, cystic, sclerosing, & epithelial hyperplasia are all histologic subtypes of what breast disease?
Fibrocystic disease (note: no increase risk of developing carcinoma)
Breast disease: Most common breast tumor in women < 25 years of age? is it malignant or a precursor to malignancy?
Fibroadenoma. No, no.
Breast disease: A benign tumor of the breast that presents with nipple discharge
Intraductal papilloma
Breast disease: Are malignant breast tumors more common pre or post menopause
Hypertension: True of false: 50% is classified as secondary HTN (usually resulting from renal disease)
false. (90% essential/primary, 10% secondary)
Hypertension: "read the questioner's mind": HTN predisposes individuals to this disease (the one John Ritter died of)
aortic dissection
Hypertension: Pathology changes associated with HTN
hyaline thickening & atherosclerosis
Arteriosclerosis: This awful term refers to a stiffening of the arteries that invovles the media. Particularly likely to occur at the radial & ulnar arteries.
Monckeberg arteriosclerosis
Atherosclerosis: True or false: atherosclerosis is a disease of small sized arteries
false. affects elastic, large & medium muscular arteries.
Atherosclerosis: Earliest sign of atherosclerotic disease
fatty streak
Atherosclerosis: most likely location
abdominal aorta. (then coronary artery, popliteal artery, and carotid artery)
Ischemic heart disease: Type of angina resulting from coronary artery spasm
Prinzmetal's variant
Ischemic heart disease: This coronary artery branch is most commonly implicated in myocardial infarction
LAD (left anterior descending)
Ischemic heart disease: most common cause of sudden cardiac death
(lethal) arrhythmia
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 --?
Infarcts: red vs. pale: 2 instances where red infarct is likely
(1) reperfusion (2) loose tissues with good collaterals - like the lungs or intestine
Evolution of MI: Rank the following vessels from most to least commonly occluded: RCA, LAD, circumflex
Evolution of MI: Histologic changes on day 1 of an MI?
pallor of infarcted area; coagulative necrosis
Evolution of MI: days 2-4?
dilated vessels (hyperemia); neutrophil invasion; extensive coagulative necrosis
Evolution of MI: days 5-10?
yellow-brown softening of infarcted region; macrophages present; granulation tissue begins to grow in
Evolution of MI: after 7 weeks?
infarct is gray-white; scar complete
Diagnosis of MI: True or false: ECG is not diagnostic during the first 6 hours following an MI
False; it is the gold standard within this time period
Diagnosis of MI: What is the test of choice within the first 24 hours?
Diagnosis of MI: This enzyme is elevated from 4 hours up to 10 days after an MI and is the most specific protein marker
cardiac troponin I
Diagnosis of MI: on ecg, transmural infarction causes ______
ST elevation, Q wave changes
MI complications: Most common (90% of patients)
arryhthmias, esp. 2 days after infarct
MI complications: automimmune phenomen several weeks post-MI that results in fibrinous pericarditis
Dressler's syndrome
MI complications: high risk of mortality
cardiogenic shock (large infarcts)
MI complications: seen about a week after the infarction
rupture of ventricular wall, septum, or papillary muscle
Cardiomyopathies: Most common
dilated (congestive) cardiomyopathy; heart looks like a ballon on X-ray
Cardiomyopathies: True or False: substance abuse is a common cause of dilated cardiomyopathy
True; cocaine and alcohol especially
Cardiomyopathies: These two infectious diseases are associated with dilated myopathy
coxsackievirus B and Chagas' disease
Cardiomyopathies: True or false: hypertrophic cardiomyopathy causes systolic dysfunction
False; dilated myopathy causes systolic dysfunction, hypertrophic causes diastolic
Cardiomyopathies: Half of hypertrophic myopathies are inherited as an _________ trait (x-linked, dominant, etc.)
autosomal dominant; major cause of sudden death in young athletes
Cardiomyopathies: On echo in hypertrophic disease, the LV thickens and the chamber looks how?
like a banana
Cardiomyopathies: These "-osis" diseases are major causes of restrictive/obliterative cardiomyopathy
sarcoidosis, amyloidosis, hemochromatosis, endocardial fibroelastosis, endomyocardial (Loffler's) fibrosis….also, scleroderma but it's not an -osis
Heart murmurs: Name two causes of holosystolic murmurs
1) VSD, 2) mitral regurg, and 3) tricuspid regurg
Heart murmurs: Widened pulse pressure seen with this diastolic murmur
aortic regurg
Heart murmurs: Describe the murmur associated with the most common valvular lesion
Mitral prolapse; late systolic murmur following mid-systolic click
Heart murmurs: True or false: aortic stenosis causes a decrescendo-crescendo murmur following an ejection click
False; ejection click is followed by a crescendo-decrescendo systolic murmur
Heart murmurs: cause of a continuous murmur loudest at time of S2?
patent ductus artieriosis
Heart murmurs: opening snap followed by late diastolic rumbling?
mitral stenosis
Cardiac tumors: most common heart tumor?
Cardiac tumors: primary cardiac tumor in 1) adults and 2) children
adults=myxoma (almost always in left atrium); children=rhabdomyoma
CHF: fun gross pathologic term for changes in liver with CHF?
CHF: what are "heart failure cells"?
hemosiderin-laden macrophages in lung
CHF: dyspnea on exertion, pulmonary edema, and paroxysmal nocturnal dyspnea are symptoms of?
left heart failure
CHF: patient says "I have to sleep upright." the clinical term for this is?
embolus types: most pulmonary emboli arise from?
embolus types: True or false: Amniotic fluid can lead to DIC
deep vein thrombosis: what are the component of virchow's triad?
stasis, hypercoagulability, endothelial damage
cardiac tamponade: what is pulsus paradoxus?
greater than 10 mmHg drop in systolic on inspiration
cardiac tamponade: what is electrical alternans?
characteristic of tamponade on ECG in which QRS complex height varies beat-to-beat
cardiac tamponade: AUTHOR
James Rosoff / Flora Waples-Trefil
Bacterial Endocarditis: What valve is usually involved in endocarditis?
Bacterial Endocarditis: What valve indicated drug use if it is involved?
Bacterial Endocarditis: Can endocarditis be non-bacterial?
Yes. It can be secondary to metastasis, renal failure (maranctic or thrombotic), fungal
Bacterial Endocarditis: What type