Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
250 Cards in this Set
- Front
- Back
|
Bean shaped gram - cocci in pairs?
Lancet shaped gram + cocci in pairs? |
Neisseria meninigtidis
Strep pneumoniae (usually in strips but are in pairs sometimes) |
|
|
MCC of pneumonia in adults and immunocompetent patients
|
Strep pneumoniae (usually after a viral URI)
|
|
|
H. flu meningitis. Who gets this?
|
infants below 2 years of age (vaccine has eradicated it)
|
|
|
Neonate meningitis top 3
|
GBS>E.coli>listeria
|
|
|
Close quarters, meningitis, what bug?
People over 60 years old, meningitis, what bug? |
Both Neisseria meningitidis
|
|
|
MCC of osteomyelitis in SCA patients?
|
Salmonella
|
|
|
Persistent giardia infection with diarrhea
What disease? |
IgA deficiency
|
|
|
Anti apoptosis gene?
Pro apoptosis gene? |
Anti = Bcl-2 (Follicular lymphoma)
Pro = bax/bak/Bim ==> increases cyt c release and caspase activity leading to apoptosis |
|
|
Tennis racket intracytoplasmic granules on EM
What disease? What cell? |
Birbeck granules (langerhans cells) seen in HISTEOCYTOSIS X (leterer siwe or Hans shlskjdf)
|
|
|
Produces extracellular dextrans from sucrose
What bugs? |
Strep viridans (mutans and sanguis)
|
|
|
Golden crust skin lesion
What is this |
Impetigo = GAS
|
|
|
Immunocompromised patient showing symptoms of sepsis as well as cutaneous necrotic rash
What caused the rash? |
P. aeruginosa, invades vessels and causes destruction (exotoxin A = ADP ribosylates EF-2 to stop transcription
|
|
|
Main markers for NK cells?
What activates NK cells? (2) Do they require thymus for maturation? |
CD16 and CD56
IFN-y and IL-12 do NOT require thymus, thus are still present in digeorge patients |
|
|
What cells have Fas Ligand? Why?
|
CD8 T-cells, searching for cells expressing FAS receptor, crosslinking causes those cells to apoptosis via the extrinsic pathway
|
|
|
Hot tub + pustular rash
What is this? |
Hot tub folliculitis, pseudomonas infection of the hair follicle
|
|
|
Which viruses are the only ones that can be inserted into a cell and cause viral protein synthesis immediately?
|
NAKED, +ssRNA viruses
|
|
|
Sore throat, pneumonia like symptoms, diarrhea and conjunctivitis (+lymphadenopathy and crowded quarters)
What bug? |
Adenovirus (dsDNA)
|
|
|
Rheumatic fever follows what infection?
Post strep glomerulonephritis follows what infection? |
Rheumatic = GAS THROAT infection only
Post strep glom = throat AND skin infection |
|
|
What are the two treatments used for malaria and why are they used?
|
Chloroquine/Mefloquine used for merozoites in the blood, prevents hemolysis
Primaquine used for schizonts in the liver (P vivax/ovale) to prevent RECURRENCE |
|
|
How does neisseria get to the meninges? How does H flu B?
|
Neisseria = through the choroid plexus
H flu B = through lymphatics |
|
|
what type of bacteria are resistant to osmotic stress? What happened if they are suddenly sensitive to it?
|
Gram + bacteria
sensitivity can occur when they are given a beta lactam antibiotic that screwed up the PG cell layer (being placed in hypotonic solution causes swelling and blows em up) |
|
|
Which viruses are polycistronic and need proteases to cleave their transcripts?
|
Nonsegmented +ssRNA linear viruses
|
|
|
How does someone with GVHD present?
|
Desquamating rash, bloody diarrhea, ulcerations in intestinal mucosa
|
|
|
HCl and EtOH decolorization after staining with carbolfuchsin dye (aniline dye) = What test is this?
What does it mean if it fails to decolorize? What bugs? What do these bugs look like on gram stain and why? |
ACID FAST STAIN
If it fails to decolorize, means MYCOLIC ACID is present = TB or any mycobacterium, thus they are PINK on acid fast stain (counter stain all other bacteria are blue) On gram stain, mycobacterium may look gram + (slightly purple) by the mycolic acid waxy LCFAs prevents a good gram stain) Nocardia, MAC also stain acid fast |
|
|
Trouble walking, dilations of capillary vessels, repeated sinopulmonary infections and increased risk of cancer
What disease? Pathophysiology? |
Ataxia telangiectasia
Defective DNA repair enzymes leading to the cancer (hypersensitivity to ionizing radiation), as well as a COMBINED B and T CELL DEFICIENCY |
|
|
Hypersensitivity to ionizing radiation = what disease?
Hypersensitivity to UV radiation = what disease? Hypersensitivity to cross linking agents (alkylating agents) = What disease? Generalized chromosomal instability? Defective mismatch repair? |
Ionizing = Ataxia telangiectasia
UV = Xeroderma pigmentosum Cross linking agents = Fanconi's anemia generalized = Bloom syndrome, increased suceptiblity to neoplasms mismatch = MLH1/2 = dinucleotide mismatch instability = HNPCC |
|
|
No cell wall, sterols (need cholesterol to survive)
What bug? |
Mycoplasma species
|
|
|
What kind of bacteria are int he normal vaginal microflora?
|
Gram + lactobacilli
Lactobacillus, Sacchromyces, Bifidobacteria |
|
|
What signifies high infectivity in a hep B infection (not activity)
|
infectivity = HBeAg
|
|
|
Recurrent pulmonary infections, wide based gait, nests of distended capillaries on skin surface that blanch
What disease? Pathophysiology? Primary manifestation? |
Ataxia Telangiectasia
DNA is hypersensitive to ionizing radiation leads to B and T cell deficiency Primarily manifests as a IgA deficiency (sinopulmonary infections) |
|
|
Glutamate capsule (protein)
Which bacteria? |
Bacillus anthracis
|
|
|
Hemorrhagic mediastinitis (widened mediastinum), bloody pleural effusions, septic shock and death
What disease? Microscopy? |
Woolsorter's disease/animal contact leading to ANTHRAX
Microscopy will show serpentine like long chains or medusa head like (TB can also have serpentine chains) |
|
|
Inhibits GABA/Glycine
|
c. tetani, inhibits inhibitory NTs leading to spastic paralysis
|
|
|
Name the four toxins that increase cAMP
|
Cholera = increase Gs, increase AC, increase cAMP
Pertussis = decrease Gi, increase AC, increase cAMP ETEC labile toxin = increase AC, increase cAMP Anthrax Edema factor = AC, increases cAMP |
|
|
Episodic painless, nonpitting, well circumscribed edema of face, neck lips and tounge.
What disease is this? What predisposes you do it? Explain |
Angioedema
ACE + C1 esterase inhibitor deficiency C1 esterase inhibitor inactivates kallikrein normally which converts kininogen into BRADYKININ, ACE also inhibits the breakdown of Bradykinin Together leads to too much bradykninin and anaphylotoxins (C3a, C5a) leading to ANGIOEDEMA |
|
|
Why do APCs require acidified endosomes to function correctly?
|
When they make MHC Class II molecules, they must have an invariant chain taking up the antigen presentation site to prevent it from being broken down.
Acidified endosomes allow for breakdown of the invariant chain and allows for placement of carbohydrate antigen in the endosomes onto the MHC Class II molecule MHC Class 1 loading does NOT require this process |
|
|
Presentation of Chediak higashi?
|
recurrent pyogenic infections
Albinism peripheral neuropathy |
|
|
Two obligate intracellular organisms?
|
Chlamydia
Ricketssia |
|
|
What would an IL-12 receptor deficiency cause? What infections would occur?
|
Decreased Th1 cell mediated response
Decrease in IFN-y leading to increased chance for TB infection for example (requires delayed cell mediated hypersensitivity) |
|
|
What kind of patients will get recurrent giardia infections? Why?
|
B-cell deficiencies (Brutons, Hyper IgM, IgA def, CVID), due to no IgA which is required for clearance of giardia
|
|
|
Recurrent giardia infections, what are you thinking
|
B-cell deficiency disease
Brutons, Hyper IgM, igA def, CVID |
|
|
Mycoplasma and Ureaplasma require what kind of antibiotics to kill them? Why?
|
NON beta lactams (they don't have PG!) they have sterol membranes that need cholesterol
Use macrolides (no translocation, 50S) or Tetracyclines (no aminoacyl tRNA transferase, 30S) |
|
|
Cat/dog bites
What bug |
Pasturella multocida (gram -)
|
|
|
Repeated lower respiratory infections, persistent diarrhea from giardiasis, serum Ig levels are low, still have positive T-cell function
What disease? WHEN would they present? Pathophysiology? Lymphnode appearance? |
Bruton's agammaglobulinemia
6 months presentation Defect in bruton's tyrosine kinase leads to NO B-cell maturation Lymph node would have NO GERMINAL CENTERS/Follicles |
|
|
What happens in the germinal centers of a lymph node? paracortical zone?
|
Germinal center = B-cell hypermutation and class switching
Paracortex = T-cell/Dendritic cells hanging out, presenting antigen |
|
|
Gray discharge, fishy odor, squamous epithelial cells covered in bacteria
What bacteria? Tx? What if pruritic, white curd like discharge, pseudohyphae seen on KOH? What if yellow/green, foul smelling, wet mount positive? |
Garnerella vaginalis (Vaginosis)
Cure with metronidazole Candida (Miconazole or fluconazole) Trichimonas (metronidazole) |
|
|
HIV patient with esophagitis
Which organisms? (3) |
Candida, HSV, CMV
|
|
|
Red mucicarmine on BAL wash
What is this? Name two other tests that are positive |
Cryptococcus
India ink Latex agglutination Antigen in CSF Silver |
|
|
Disseminated vs. superficial candida infections
Which patients get which? |
Disseminated = neutropenic
Superficial = T-cell deficiency |
|
|
Toxin that inhibits 60S ribosome
|
Shiga toxin (EHEC also uses it)
|
|
|
Dimorphic fungi, list 4 of em
Explain what they change to at what temperature |
Histo, blasto, Coccidiodo, Sporothrix (thorn)
Body temp = yeast Colder = mold with hyphae |
|
|
Virulence factor of Strep pyogenes? What does it do
|
M protein, inhibits phagocytosis and activation of complement, cytotoxic for neutrophils (also responsible for molecular mimcry that causes rheumatic fever)
|
|
|
What 3 cells employ antibody dependent cytotoxicity? Talk about HOW they do this
|
NK cells = killing IgG tagged cells, released granzymes through porins made in the cells
Eosinophils = killing IgE tagged parasites, inserts MBP Macrophages do it too |
|
|
What two cells can cause type 1 hypersensitivity?
|
Mast cells = tissue
Eosinphils = blood IgE on cells cross link, histamine release |
|
|
Secretory diarrhea, explain the mechanism of action
|
Increased cAMP causes an efflux of sodium and chloride leading to a watery diarrhea, NO leukocytes (no invasion)
|
|
|
Curved rod shape/Comma shaped
Which two bacteria? What lab test discerns between the two |
Vibrio and Campylobacter
Vibrio survives in alkaline environment, Campylobacter cannot |
|
|
Diarrhea + leukocytes/neutrophils (what bacteria?)
Diarrhea + eosinphilia (what bug?) Diarrhea + RBCs |
Leukocytes/neutrophils = invading, salmonella or shiggela
Eosinophilia (parasites, ascaris, strongyloides, cryptosporidium) RBCs = Shigella, EHEC, campylobacter, Salmonella |
|
|
MCC of UTI?
What if they are immunocompromised/paraplegic? |
MCC = E. coli, klebsiella, staph or proteus (Indwelling catheter MC)
Immunocompromised/paraplegic = PSEUDOMONAS |
|
|
When does enterococci endocarditis occur? what tests do you use to confirm?
|
After GI/GU/Obstetrical surgeries
Survives hypertonic 6.5% saline as well as bile Gamma hemolytic |
|
|
Neisseira meningitidis virulence factor?
|
Pili (colonization of nasopharynx, also is antigenically varialble and escapes immune response)
|
|
|
UTIs with dysuria and hematuria = hemorrhagic cystitis
MC viral cause of this? |
Adenovirus
|
|
|
Nodules spreading along someone lymphatics
What bug? |
Sporothrix (dimorphic fungi, poked by a rose thorn)
|
|
|
graft vascular endothelium damage leading to obliterative intimal SM hypertophy and fibrosis
What kind of graft rejection? |
Chronic (B and T cell delayed response)
|
|
|
Vascular fibrinoid necrosis with neutrophil infiltration
What kind of graft rejection? |
Hyperacute (preformed antibodies)
|
|
|
Dense interstial infiltrate of lymphocytes in graft
What kind of graft rejection? |
Acute
|
|
|
Name the picornaviridae.
Which one stays in the URI and why? |
PERCH
Polio Echovirus Rhinovirus (stays URI, sensitive to acid) Coxsackie viruses Hep A |
|
|
Stabbing pain with dermatome localization of rash
What is this? |
VZV shingles with POST HERPETIC NEURALGIA (MC neurological complication of VZV infection)
|
|
|
Umbilical infection in africa that can be prevented by vaccination
What disease? |
Tetanus
Give tetanus vaccination at two months |
|
|
How can you measure if a fetal lung is mature by taking amniotic fluid?
|
Lecithin or phosphatidylcholine/Sphingomyelin ratio (L/S) is greater than 2
Lecithin = phosphatidylcholine = SURFACTANT |
|
|
Small Jaw, clenched hands with overlapping fingers
what disease? |
Edwards trisomy 18
|
|
|
Hydrocele is similar to what disease?
Explain the pathogenesis |
Indirect inguinal hernia (through the inguinal canal, peritoneum evagination)
Both are due to INCOMPLETE OBLITERATION OF PROCESSUS VAGINALIS (hydrocele is leakage of fluid while the hernia is protrusion of abdominal organs along inguinal canal) |
|
|
When do the neuropores close? Failure of closure of each = what disease?
|
Anterior neuropore = 25th day (failure to close = anencephaly/absence of brain or encephalocele/protrusion of neural tissue through cranial defect)
Posterior = 27th day (failure to close leads to spina bifida occulta, minigocele, miningomyelocele and rachischisis) |
|
|
Short palpebral fissures, smooth/long philtrum
What causes this? |
Fetal alcohol syndrome
|
|
|
MCC of MR in newborn?
|
Fetal alcohol syndrome
|
|
|
Lymphedema in hands and feet as well as the neck, horseshoe kidney
What disease is this? |
Turner's syndrome
45, XO Cystic hygroma of neck (webbed neck) Shield chest Streak ovaries |
|
|
What are the 3 MC brain metastases primary locations?
|
Lung
Breast Melanoma |
|
|
Name 6 disease that occur due to DNA repair defects
|
Ataxia Telangiectasia (increased suceptibility to ionizing radiation, decreased repair, combined B and T cell defect)
XP (mutation to endonuclease excision repair, Thymidine dimers, UV radiation suceptibility) Fanconi's anemia (suceptivility to DNA cross linking agents) Bloom syndrome (hypersensitivity to UV damage and chemo agents) HNPCC (DNA mismatch repair defects, dinucleotide defects) Breast cancer (BRCA, defective dsDNA break repair) |
|
|
What 2 things are increased in amniotic fluid in babies with NTDs?
|
Alpha fetoprotein (AFP)
Acetylcholinesterase |
|
|
Pathogenesis of Fragile X disease?
|
lots of CCG repeats leading to hypermethylation and decreased expression of the FMR1 gene
|
|
|
Voiding from the belly button.
What happened? What would cause recurrent infections at the belly button |
Patent allantois/urachus, connected to the bladder
Urachal CYST, failure of distal urachus to close near the umbilicus |
|
|
What is omphalocele? What is Gastroschisis?
|
Omphalocele = incomplete closure of anterior abdominal wall, protruding viscera is COVERED BY PERITONEUM
Gastroschisis = enlargment of fetal peritoneal cavity, Viscera protrude and are NOT COVERED BY PERITONEUM |
|
|
What causes abnormal kidney development?
What causes lower urinary tract formation defects? |
Bad contact between the ureteric buds (collecting system) and the metanpehric mesoderm (kidney structures) causes kidney defects since the bud causes the mesoderm to differentiate
bad bud development leads to lower urinary tract defects |
|
|
What becomes of the following:
Pronephros Mesonephros Metanephros |
Pro = first, regresses
Mesonephros = regresses by persists as epididymis and vas deferens (wolfian ducts) Metanephros = forms true kidney, splits into ureteric bud and metanephric mesoderm |
|
|
What is the triple test and when should it be performed for pregnant woman?
Explain what each one indicate |
AFP (produced by liver, high = NTDs, low = downs)
hCG (trophoblastic tissue makes it) estriol (placental and fetal function, low = placental insufficiency) 16-18 weeks |
|
|
Increased hCG
What two things are you thinking? |
Hydatiform mole
Choriocarcinoma |
|
|
Where do intestinal ganglia start/end their migration? What week in development?
Arrest of migration = what disease? How do they present? |
move DOWNward (caudally), reach the rectum by 12 weeks
Arrest = Hirschprung's disease, absence of ganglion cells, newborns fail to pass meconium, rectal vault is empty and may present with bilious vomiting and abdominal ditension |
|
|
Short episodes of myoclonic epilepsy and proximal muscle weakness. Muscles show blotchy red appearance.
What disease? Inheritence? |
Ragged red fibers (MERRF), Mitochondial inheritance, HETEROPLASMY
|
|
|
Encephalopahy with stroke like episodes, lactic acidosis and central blindness
What disease, Inheritance? |
Leber's optic neuropathy
Mitochondrial inheritance, heteroplasmy |
|
|
What is different between duodenal and jejunal atresia cause?
|
Duodenal = failure to recanalize
Jejunal and on = vascular accident (apple peel appearance) |
|
|
Main diseases associated with downs?
|
Hisrschprungs
Duodenal atresia VSD/ASDs Celiacs |
|
|
Where does the pancreas develop from? What parts of it are made from the ventral and dorsal heads?
|
Foregut duodenal portion buds off to make pancreatic buds
Ventral = part of head, uncinate process, main pancreatic duct Dorsal = most of the head, body, tail and small accesory pancreatic duct |
|
|
What pancreatic embryologic malformation can be clinically silent but can cause recurrent pancreatitis?
|
Pancreas divisum (failure of dorsal and ventral fusion)
TWO ducts (dorsal goes accesory to minor papilla, ventral goes main to major papilla) |
|
|
Floppy baby, lethargy, macroglossia, edema of skin/subQ fat, irreversible MR in a NEONATE
What is this? |
Hypothyroidism!
Need T3/T4 for brain development |
|
|
What is the difference between variable expression, pleiotropy and locus heterogeneity?
|
Variable expression = Nature/severity of one phenotype vary from 1 individual from another (NF, different severity, seen in AD diseases)
Pleiotropy = 1 gene has greater than 1 effect on phenotype Locus heterogeneity = mutations at different loc produce the SAME phenotype |
|
|
name 3 things that cause marfinoid habitus
What is a term that describes this |
Marfans syndrome
MEN IIB Homocystinuria Locus heterogeneity |
|
|
Gait ataxia, kyphoscoliosis, pes cavus and hammertoes
What disease is this? What areas in the body are defective? MCC of death? |
Friedrich's ataxia
CST and dorsal columns are getting hit, MCC of death = HOCM |
|
|
What is the molecular mechanism that causes CF?
|
POST-TRANSLATIONAL PROCESSING abnormality of the CFTR chloride channel, Phe deletion leads to degradation
|
|
|
Imperforate anus is associated with what other conditions? Presentation?
|
Urorectal, ureovesical and urovaginal fistuals leading to meconium discharge from urethra/vagina
Also associated with genitourinary malforamtions |
|
|
What stage are oocytes in before puberty? after?
|
before puberty = suspeneded in prophase 1
after puberty = follicle formation spits out an oocyte suspended in metaphase 2 (in response to FSH) |
|
|
Urethral folds fail to fuse, male? female?
|
Male = hypospadias, ventral surface of penis
Female = labia major (they don't fuse, NORMAL) |
|
|
Genital tubercule, male? female?
|
male = penis, defect = epispadias
female = clitoris |
|
|
What is 99 mm Pertechnetate scan detecting? What if it was localized to the RLQ?
|
Gastric mucosa
Meckel's diverticulum with some gastric tissue! (presents like appendicitis) |
|
|
Meckel's diverticulum can present like what? Predisposes you to what?
|
presents like appendicitis
Prediposes baby to INTUSSCEPTION |
|
|
Intracranial mass that is calcified and cystic, squamous keratin pearls filled with yellow viscous fluid
What is this? Derived from? Presentation? |
Craniopharyngioma
From Rathke's pouch HAs, growth failure, bitemporal hemianopsia |
|
|
Neonate born with agenesis of sacrum/lumbar spine, flaccid paralysis of the legs, dorsiflexed feet and urinary incontinence
What is this? What causes this? |
Caudal regression syndrome
Caused by maternal diabetes (more commonly just macrostomia) |
|
|
Cocaine during pregnancy leads to...? WHY?
|
Spontaneous abortion, IUGR, prematurity and placental abruption
due to vasoconstrictive effects |
|
|
What are the two types of hydatiform moles? Explain each of them. What is increased in the blood? Appearance? Malignancy risk?
|
Complete = 46, XX (all paternal, no fetal structures, choriocarinoma risk)
Partial = 69,XXY or XXX (fertilization of ovum by two or more sperm, fetal structures present, no choriocarcinoma risk) Grape clusters, uterus larger than it should be, hCG |
|
|
What 2 things increase risk for choriocarcinoma
Marker? |
Complete hydatiform mole
Spontanous abortion hCG |
|
|
MEN IIa and IIb tumors are caused by mutation to what gene? Where do these tumors arise from?
|
RET protooncogene
Neural crest cells! |
|
|
Neonate born with agenesis of sacrum/lumbar spine, flaccid paralysis of the legs, dorsiflexed feet and urinary incontinence
What is this? What causes this? |
Caudal regression syndrome
Caused by maternal diabetes (more commonly just macrostomia) |
|
|
Cocaine during pregnancy leads to...? WHY?
|
Spontaneous abortion, IUGR, prematurity and placental abruption
due to vasoconstrictive effects |
|
|
What are the two types of hydatiform moles? Explain each of them. What is increased in the blood? Appearance? Malignancy risk?
|
Complete = 46, XX (all paternal, no fetal structures, choriocarinoma risk)
Partial = 69,XXY or XXX (fertilization of ovum by two or more sperm, fetal structures present, no choriocarcinoma risk) Grape clusters, uterus larger than it should be, hCG |
|
|
What 2 things increase risk for choriocarcinoma
Marker? |
Complete hydatiform mole
Spontanous abortion hCG |
|
|
MEN IIa and IIb tumors are caused by mutation to what gene? Where do these tumors arise from?
|
RET protooncogene
Neural crest cells! |
|
|
Explain the pathogenesis of Klinfelter's disease
|
Semineferous tubules/Sertoli cells are progressively destroyed (No sperm or inhibin), Leydig cells are also decreased (less T)
Decreased inhibin (no negative feedback, usually made by tubules), Decreased testosterone (leydig cell destruction), leads to increased LH/FSH |
|
|
Congenital loss of GnRH secretion cells
|
Kallman's syndrome
|
|
|
MCC of neonatal hydronephrosis
|
Abnormal recanalization of uteropelvic junction
|
|
|
Meckel's diverticulum and a woman with increased hCG and no ultrasound visual of baby are both examples of?
|
ECTOPY
|
|
|
Baby presents with painless melena and acute episodes of appendicitis like pain
|
Meckel's! with gastric mucosa causing melena, band of tissue runs from ileum to the umbilicus
|
|
|
When are hCG levels increased after fertilization?
|
detectable 8-11 days after fertilization (implantation at day 6)
|
|
|
What do the paramesonephric ducts/Mullerian ducts become in women? men?
What happens when they are defective in women? |
Women = uterine tubes, uterus, cervix, superior 1/3 of the vagina
Defective = don't fuse right, BICORNATE uterus/vagina Men = vestigial appendicies of testes in men (woman mesonephric ducts/wolffian become gardner's ducts) |
|
|
Early onset alzheimer's genes?
Late onset? Protective? |
early = APP, Presnelin 1/2
Late = APO E4 protective = APO E2 |
|
|
Patient has normal secondary sexual characteristics, normal pituitary and presents with ammenorhea. What is the MC cause?
|
Imperforate hymen or other mullerian/paramesonephric duct anomalies
|
|
|
Pathogenesis of annular pancreas? Presentation?
|
ventral bud splits and forms a ring around the descending portion of the duodenum, leads to neonate with BILIOUS VOMITING recurrent
|
|
|
When does the midgut herniate through the umbilical ring?
When does it return into the abdomen. |
Herniates at 6 weeks
Returns at 10 weeks |
|
|
Intestinal malrotation leads to what findings? Presentation?
|
Cecum in the RUQ
Fibrous bands forming and causes intestinal obstruction Bilious vomiting |
|
|
Kidney bean on plain film of baby
Omega sign on plain film of adult What causes this? |
Midgut volvulus around the SMA
|
|
|
Name 3 tumors associated with von hippel lindau disease
|
Hemangioblastomas/Cavernous hemangiomas
Pheochromocytoma Bilateral renal cell carcinoma |
|
|
Delayed puberty in male + Anosmia
What disease? Pathophys? |
Kallman's syndrome
CENTRAL hypogonadism (no GnRH secreting cells, failure to migrate from the origin of the olfactory placode) |
|
|
What does FSH stimualate in men? females?
What does LH stimulate in men? females? |
FSH
Men = Proliferation of semineferous tubules, spermatogenesis, sertoli cells, inhibin feedback Females = Granulosa cells, aromatase converts androgens into estrogen LH Men = Leydig cells, testosterone Female = Theca cells, steroid to androsteinoinafd |
|
|
Heart embryology
Truncus arteriosus Bulbus cordis Primitive V Primitive A Left horn of sinus venosus Right horn of sinus venosus Right common cardinal vein and right anterior cardinal vein |
Truncus arteriosus = Ascending aorta/pulmonary artery
Bulbus cordis = RV, smooth parts (outflow tract) of L and R V Primitive V = portion of LV Primitive A = Trabeculated L and RA Left horn of sinus venosus = Coronary sinus Right horn of sinus venosus = smooth part of RA Right common cardinal vein and right anterior cardinal vein = SVC |
|
|
Endocardial cushion defects
Seen in which disease? What defects? |
Downs
Ostium primum ASD, regurgitant AV valves, VSDs |
|
|
Heart defects (2) seen in DiGeorge syndrome?
heart defects seen in diabetic mother's baby? Heart defect seen in tuberous sclerosis |
Tetralogy of Fallot, interrupted aortic arch
Transposition of great vessels Rhabdomyoma (functional MS? like a myxoma in adults) |
|
|
What two anti seizure drugs can lead to NTDs?
|
Phenytoin and Valproate (decreased folic acid absorption)
|
|
|
Fusion of heart leaflets, THickening/shortening of chordae tendinae
What is this? |
Chronic rheumatic fever (GAS pharyngitis) leading to mitral stenosis
|
|
|
SLE causes two heart sequelae. What are they? What causes them to occur?
|
Fibrinous pericarditis
Libman Sach's endocarditis (both sides of valves) Both occur due to UREMIA from renal failure |
|
|
MCC of hemorrhagic pericarditis? Fibrinous pericarditis?
|
Hemorrhagic = Pericardial tumors or TB
Fibrinous = Kidney failure/uremia |
|
|
When do you employ a T-test? ANOVA? ChiSquare test (X^2)?
|
T-test = Checking the difference between the MEANS of 2 groups
ANOVA = diference between means of 3 or more groups Chi Square test = comparing 2 or more percentages/proportions of categorical outcomes (NOT means) |
|
|
What are the three effects of dopamine?
|
Low dose = D1 receptors (renal vasculature, increases renal perfusion thus increasing GFR, RBF and sodium excretion, used in heart failure)
Medium dose = B1 receptors (increases HR, contractility and pulse pressure) High dose = a1 (vasoconstricts, decrease CO due to increased afterload) |
|
|
Why are BBs good for the heart AND the kidneys?
|
BBs block B1 receptors on renal vasculature and decreases renin release from JG cells, reduces AT1, AT2 and aldosterone
|
|
|
Statin with highest myopathy risk?
Taking statins with which other drug inreases myopathy risk big time? What other AE? Which two antilipidemics = big risk for gallstones? |
Simuvustatin (greatest myopathy risk)
Statins with FIBRATES increase risk for myopathy and hepatotox Fibrates + Bile acid resins = gallstones due to increased cholesterol concentration (decreased bile acid) in the bile |
|
|
Reproducible test = Give two terms that describe this
A test's ability to measure what its supposed to measure against a gold standard = two terms to describe this |
Reliable or Precise (precision)
Accurate, Validity |
|
|
How would a patient with aortic regurgitation maintain the same CO?
|
Increase preload to stretch the fibers more to try to eject more. Would cause ECCENTRIC hypertrophy
|
|
|
Which monoclonal antibody and what does it do?
1) Anti CD3 2) Anti CD20 3) Anti IgE |
1) Muromonab, binds to CD3 and inhibits T-cells, used for TRANSPLANTATION to prevent graft rejection
2) Rituximab, inhibits B-cells, used in treatment of RA or B-cell lymphomas 3) Omalizumab = for severe asthma to prevent mast cell degranulation |
|
|
What is the pathophysiology of Long QT syndrome? What are they predisposed to and how do you treat?
|
Decreased outward K+ current causes a prolonged phase 3 repolarization, increases the incidence of VTACH and TORSADES DE POINTS (treat with sotolol or quinidine
|
|
|
MCC of constrictive pericarditis? Signs?
|
TB! (radiation, cardiac surgery other causes)
Kussmauls (increase in JVP) Pericardial Knock Pulsus paradoxus |
|
|
name the proteins/peptides responsible for local amyloidosis in the following organs:
Heart Thyroid Pancreas Cerebrum/cerebral blood vessels Pituitary gland MULTIorgan |
Heart = ANP
Thyroid = Calcitonin (medullary carcinoma) Pancreas = Amylin, seen in DMII Cerebrum/cerebral blood vessels = Beta amyloid (alzheimers) Pituitary gland = Prolactin Multi organ = Immune globulin light chains (multiple myeloma), also found in urine as bence jones protein |
|
|
Name the 3 main peaks in an atrial pressure curve.
Which portion of the atrial waves changes in a patient with constrictive pericarditis? |
A wave = atrial kick
C wave = Ventricle contracting, pushing up into atria V wave = Maximal atrial filling Y dip = passive emptying of right atrium into the RV after V wave and before the A wave, this falls RAPIDLY in a patient with constrictive pericarditis |
|
|
What factor causes SM migration to the intima in endothelial injury? Who makes this factor?
|
PDGF, the endothelial cell that is injured releases/produces it
|
|
|
Biggest risk factor for aortic dissection? What is the primary event that starts it?
|
Hypertension!
Intimal tear |
|
|
Myxomatous changes in the media of large arteries
What is this? What disease? Risk factor for what? |
Cystic medial degeneration seen in MARFAN's and is a secondary risk factor for aortic dissection/dissecting hematomas
|
|
|
Treatment of choice for diabetic ketoacidosis? What does this do?
|
IV hydration + Insulin
Decreases serum glucose, osmolality and potassium Increases serum bicarb and sodium |
|
|
How do adenosine and ACh (vagal tone) decrease the HR?
|
activate K+ channels to prolong K+ efflux and hyperpolarize phase FOUR, elongates conduction time of nodal myocytes
ACh also decreases slow Ca2+ and Na+ influx in phase 4 |
|
|
What determines the HR in nodal myocytes?
|
Slope of phase 4 depolarization
|
|
|
Why do you coadminster BBs with nitrates?
|
Nitrates are vasodilators that can cause a reflex tachycardia that can potentially increase MVO2, block this reflex with BBs to prevent B1 receptors from being stimualted by catecholamines
|
|
|
Granulomatous inflammation of media of arteries
What disease? |
Temporal giant cell arteritis
Takayasu's |
|
|
Which vasculitis leads to differential cyanosis?
|
Takayasu's (affects aortic arch)
|
|
|
Transmural inflammation of arterial wall with fibrinoid necrosis
What vasculitis? |
Polyarteritis nodosa
|
|
|
Segmental thrombosing vasculitis extending into veins nerves leading to encasement of vessels in fibrous tissue
What disease is this? Which arteries in particular? |
Thromboangiitis obliterans (Buerger's disease)
SMokers, Tibial and radial arteries |
|
|
Medial band like calcifications of arteries
What disease? |
NOT a disease, Monckeberg's medial calcific sclerosis, seen with old age
|
|
|
First dose orthostatic hypotension
What drug? Uses? |
Alpha 1 blockers (-zosins)
BPH and HTN (vasodilate, loosen bladder neck) |
|
|
What drug would increase cardiac contractility while decreasing systemic vascular resistance in a dose dependent manner?
|
Isoproterenol (B1 and B2)
|
|
|
First dose orthostatic hypotension
What drug? Uses? |
Alpha 1 blockers (-zosins)
BPH and HTN (vasodilate, loosen bladder neck) |
|
|
What drug would increase cardiac contractility while decreasing systemic vascular resistance in a dose dependent manner?
|
Isoproterenol (B1 and B2)
|
|
|
Which Class 1 antiarrythmics Bind and release sodium channels extremely fast? What does this mean?
Which ones bind really bind and release SLOWLY? What does this mean? |
Class Ib (Lidocaine, mexilitine, tocainide)
This means that these antiarrythmics bind less avidly to channels and are dissociated quickly and thus are SELECTIVE for those that are rapidly depolarizing (ectopic pacemakers), Thus Class Ib are the best for post MI patients to prevent arrythmias Class Ic bind SLOWLY and tightly, thus they are contraindicated post MI |
|
|
Adult onset asthma, eosinophilia, polyneuropathies
What disease? What lab test? |
Churg Strauss
P-ANCA (anti myeloperoxidase) |
|
|
When the effect of a main exposure on an outcome is modified by another variable (Estrogen receptor agonist effecting a study on DVTs and smokers), What is this called?
Is this a bias? |
EFFECT MODIFICATION
NOT a bias |
|
|
What is the big side effect of patients using decongestants?
Name the drug that has a SIMILAR side effect |
Alpha agonists (phenylephrine or pseudoephedrine)
Cause tachyphylaxis due to depletion of NE from nerve terminals leading to REBOUND RINORRHEA (drugs don't work anymore, can't vasoconstrict) NITRO drugs also have tachyphylaxis, diminished release of NO from endothelial cells occurs leading to tachyphylaxis (need 8-10 hour drug free intervals) |
|
|
Explain why cells swell up in ischemic injury
|
When blood flow cannot meet cellular demands, cell switches to anaerobic metabolsim, ATP production can't keep up and ADP/AMP and adenosine (heart) builds up. Without ATP, the Na/K pumps fail and sodium and calcium build up in the cells leading to cellular and mitochondrial swelling
|
|
|
What drug can lead to calcium oxalate stones?
|
Furosemide! (causes hypercalciuria)
|
|
|
Why can ACEIs cause first dose hypotension?
Are ACEIs and BBs synergistic for treating HTN? Why or why not? |
ACEIs can cause first dose hypotension in people that are already on diuretics and volume contracted since they cause vasodilation
ACEIs and BBs are NOT synergistic because ACEIs are already blocking ATII production, thus there is no need to also block renin production with BBs |
|
|
How does COPD cause pulmonary HTN?
How does LV dysfunction cause pulmonary HTN? |
COPD = hypoxia leads to chronic vasoconstriction
LV dysfunction = increased pulmonary arterial pressure, reactive changes (endothelin/NO imbalance) leading to vasoconstriction |
|
|
1) Repetitive ischemia of cardiac myocytes or persistent hypoperfusion leading to a loss of contractile function. If this is reversible, what is this called?
2) Cardiac myocytes develop resistance to infarction due to prior reptitive non lethal ischemia, what is this called? 3) Brief ischemic episodes where contractile function decreases for hours/days, what is this called? |
1)HIBERNATION
2) Ischmia preconditioning 3) Myocardial stunning |
|
|
What is the earliest atherosclerotic lesion seen in arteries and at what age?
|
Fatty streaks (intimal lipid filled foam cells)
everyone about 10 y/o will have them |
|
|
Pink frothy sputum, orthopnea
what is this a sign for? |
LV failure, severe pulmonary edema, pink sputum from rupture of bronchial veins
|
|
|
Sudden standing
Vasalva maneuver Squatting Gripping Sitting Lying supine Which of these increase venous return? decrease? Explain how they affect HOCM murmur and AS murmur |
Sudden standing = decrease
Vasalva maneuver = decrease Squatting = increase Gripping = increase Sitting = increase Lying supine = increase Increasing venous return makes AS murmur louder and HOCM murmur softer Decreasing venous return makes AS murmur softer and HOCM murmur louder |
|
|
Why do CCBs NOT effect skeletal muscle?
|
DUH, skeletal muscle contraction is triggered via SODIUM voltage gated pumps that increase release of calcium from the SR, NOT the L-type calcium channels seen in smooth muscle or the heart that cause calcium release
|
|
|
How does the SM contraction cycle occur?
|
Calcium enters cell from EC space, binds calmodulin which activate myosin light chain kinase. THis phosphorylates myosin and allows it to bind to actin for contraction
|
|
|
Gold standard for PE diagnosis?
|
Angiography
|
|
|
What is the critical factor in determing the coronary blood flow?
|
Duration/length of DIASTOLE
|
|
|
What 2 drugs decrease the activity of platelet phosphodiesterase? Functions?
|
Dipyridamole
Cilastazole usually break down cAMP, increase in cAMP causes vasodilation and can be used for intermittent claudication |
|
|
Arterial vasodilators should be given with diuretics. Why?
|
They cause vasodilation and reflexive sympathetic activation elading to increased RAAS, this increases fluid retention. Sympatholytics are important too
|
|
|
Which antiHTN drug has both arterial and venodilatory effects?
What is the big side effect of this drug and how do you treat it? |
NITROPRUSSIDE
Cyanide tox, give em sodium thiocyanate or any other SULFUR compounds that can change the cyanide into thiocyanate to be excreted Nitrates can also be used, induce methemoglobinemia to bind CN- and prevent it from inhibiting cytochrome oxidase |
|
|
Chronic AV shunts in the body lead to what physiologic effects?
|
Increased cardiac output, and high output heart failure
Decreased TPR (from the shunts) lead to increased VR |
|
|
DOC for someone who ODed on BBs? MOA?
|
Glucagon, increases IC cAMP which increases IC calcium release and increases heart contractility and HR
|
|
|
4 main AEs of using Niacin and what you have to do to prevent them
|
Flushing/itching of skin (give aspirin prophylaxis to prevent PG release)
Postural hypotension in patients taking AntiHTN (lower dose) Glucose intolerance/Insulin resistance + Acanthosis nigricans (increase diabetes medications) Hyperuricemia (increase gout medication) |
|
|
Leads II, III and aVF show ST elevation, What artery?
Leads V1-V4 show ST elevation, What artery? Leads V5-V6 show ST elevation, What artery? Which one would cause bradycardia? |
II, III and aVF = posterior/inferior wall = RCA (would show bradycardia since it supplies AV/SA nodes)
V1-V4 = Anteroseptal wall = LAD V5-V6 = Lateral wall of LV = LCX |
|
|
Murmur that radiates to the carotids?
Murmur that radiates to the left axilla? Murmur that radiates to the left sternal border? |
AS
MR VSD |
|
|
MCC of aortic stenosis? What causes it to occur EARLY?
|
MCC is US = OLD AGE (calcified valve
EARLY = bicuspid aortic valve (calcifies early) |
|
|
Patient with a history of migraine headaches comes in with transient anginal chest pain during the nighttime with ST elevations.
What is the problem here? What 2 drugs can you use to treat the current issue? |
Patient has PRINZMETAL ANGINA (vasospasm) and is probably taking an ERGOT (DHT) that is exacerbating the prinzmetal angina.
Patient needs to be on CCBs or vasodilating nitrates for his prinzmetals angina |
|
|
Explain how endocarditis occurs and what the MCC of ACUTE endocarditis is.
|
Damage to valves, platelet and fibrin deposited on valve surface, bacteria can stick to it and be hidden by more fibrin and platelets.
MCC of ACUTe = staph aureus (seen more in IVDAs, pseudomonas and candida also) |
|
|
Explain the mechanism of how ANP is released and HOW it works
|
increased volume, increased release from atrial myocytes
ANP acts on afferent arterioles, increases cGMP and causes vasodialtion, this increases GFR and increases sodium and h20 excretion. It also inhibits renin secretion (leading to vasodilation |
|
|
Two best drugs for high LDLs?
Two best drugs for high TGs? Best drug for low HDL? |
High LDLs = Statin, then ezetimibe
High TGs = Fibrates then Niacin Low HDLs = Niacin |
|
|
What happens to your BP as you get older?
|
Isolated systolic HTN due to decrease in aortic compliance
|
|
|
Trace SA node to base of the ventricles.
Compare the velocity of Atria, ventricle, AV node and purkinje fiber conduction |
SA => AV => bundle of his => branches of bundle of his => purkinje fibers => ventricles (apex to base, endocardium to epicardium)
Velocity = Purkinje>Atria>Ventricle>AV node |
|
|
Absent p waves is a sign of what?
Prolonged QRS complexes is a sign of what? |
Absent p wave = SA node gone
Prolonged QRS = AV node gone, ventricular fibers are pacemakers |
|
|
Best indicator of severity of someones mitral regurgitation? mitral stenosis?
|
MR = Presence of S3 gallop (sign of dilation)
MS = Length between A2 (aortic valve closure) and the opening snap during diastole, the shorter the interval, the more sever the stenosis and the higher the left atrial pressure |
|
|
When would you use dobutamine? MOA?
|
ACute heart failure with decreased contractility
Dobutamine = B1 predominant agonist, increases cAMP and increases contractility, HR and MVO2 |
|
|
What is ebstein's anomaly? How does it occur?
|
Mom taking Lithium for bipolar during pregnancy
Tricuspid valve moves downwards, RV volume decreases, RA enlarges and must ATRIALIZE the top portion of the RV |
|
|
Which statin is the only renally excreted statin?
|
Pravastatin, everything else uses the p450 system
|
|
|
What do you prophylactically give to someone taking Niacin? Vancomycin? WHy?
|
Niacin = aspirin, prevent PG related flushing
Vancomycin = antihistamines, prevent histamine related red man syndrome |
|
|
Necrotizing ulcer in the nasopharynx. What disease?
|
Wegners, (positive C-ANCA, anti proteinase antibody)
|
|
|
Anti mitochondrial Ab?
Anti smooth muscle Ab? |
Anti mito = Primary biliary cirrhosis
Anti SM = Autoimmune hepatitis |
|
|
Name the heart defects associated with the following:
Down's Digeorge Friedrich's ataxia Marfan's Tuberous sclerosis Turner's Rubella |
Down's = Endocardial cushion defects (ostium primum ASD, regurgitant AV valves)
Digeorge = Aortic arch anomalies, Tetralogy of Fallot Friedrich's ataxia = HOCM Marfan's = Cystic medial necrosis of aorta, aortic dissection Tuberous sclerosis = cardiac rhabdomyomas (functional MS) Turner's = Coarctation Rubella = PDA |
|
|
Patient has sharp, pleuritic chest pain that decreases when the patient sits up and leans foward
What is this? what are some causes of this? |
Pericarditis (post MI, rheumatic fever, uremia and viral infection)
|
|
|
Name as many holosystolic murmurs as you can.
How are they affected by inspiration? |
MR, TR, VSD
TR will increase in intensity due to increased VR (heard at left sternal border) |
|
|
Segmental fibrinoid necrosis of small vessels.
What disease is this? |
Microscopic polyangitis aka Leukocytoplastic vasculitis
P-ANCA |
|
|
Strawberry and cherry hemangiomas
Who gets them? REgression? |
Strawberry = kids, intitally grows, then regresses
Cheery = adults, does not regress |
|
|
How will atrial fibrillation look on the EKG? Explain each finding (3)
|
Absent P waves (atrial depol is not organized)
Irregularly irregular (rate is crazy) Narrow QRS (ventricular conductance is fine so the wave is normal shaped but its narrow because of the tachycardia) |
|
|
Procollagen peptidase is deficient in what disease?
|
Ehlers danlos = problem in extracellular process (cross linking and peptidase cleaving of the procollogen triple helices that are secreted)
|
|
|
What part of the heart forms the diaphragmatic surface? Artery?
|
LV, inferior wall, supplied by PDA from the RCA
|
|
|
Name 3 things that you could do to abolish PSVTs. MOA?
|
Carotid massage
Vasalva maneuver Adenosine Slow AV nodal conduction to abolish the reentrant loop (prolongs AV nodal refractory period) |
|
|
Alcohol binging can cause what heart condition?
|
Holiday heart syndrome, can cause AFIB (absent P waves, narrow QRS complex, irregular irregular HR)
|
|
|
How does nitroprusside affect your stroke volume?
|
NO change (afterload and preload are decreased, preload = LVEDV)
|
|
|
MCC of mitral regurg?
|
MVP
|
|
|
Which antiarrythmics would cause a QT prolongation on EKG? why?
Which drug is the only one that would prolong QT AND the PR interval |
Class Ia, Class III
block potassium efflux, repolarization or phase three takes longer SOTALOL (BB and K+ blocking abilities) |
|
|
patient comes in with color vision changes (yellow), nausea and decreased appetite. What caused this and what is the biggest danger?
|
Digoxin tox
Ventricular arrythmias due to hyperkalemia, tx with management of hyperkalemia and anti-digoxin antibody fab fragmens. |
|
|
ANTI HTN drugs with gingival hyperplasia/constipation AE? Flushing?
|
Gingival hyperplasia and constipation = VERAPAMIL
Flushing = DILTIAZEM |
|
|
3 MCC of spontaneous intracranial hemorrhage?
|
AV malformations
Cerebral aneurysms Cocaine abuse (or anything that causes HTN) |
|
|
Risk factors for varicose veins?
Which veins are usually suspect? What is the big risk in a postpartum woman? |
Obesity, standing, age, multiple pregnancies
Superficial veins of the leg PHLEGMASIA ALBA DOLENS = peripartum women getting an iliofemoral venous thrombosos leading to a PAINFUL WHITE LEG, a type of varicose vein/DVT |
|
|
MCC of sudden cardiac death?
|
Arrythmia (Vfib)
|
|
|
MCC of sudden cardiac death?
|
Arrythmia (Vfib)
|
|
|
What kind of study:
What is happening? What happened? What will happen? |
What is happening = Cross sectional/Prevalence study
What happened = Case/Control (odds ratio) What will happen = Cohort (relative risk) |
|
|
Which Antiarrythmic has all four class properties?
Which Phase 3 elongating antiarrythmic has the LEAST risk for arrythmia risk? Which arrythmia is most oncerning |
All four class properties = Amiodarone
Amiodarone has the least risk for VTACH or TORSADES DE POINTES out of the Class III and Class Ia (phase 3 elongating) antiarrythmics |
|
|
How long until ischemia of the myocardium causes lactate accumulation?
When does it become irreversible? When does brain damage become irreversible? |
60 seconds until lactate accumulation occurs, 30 minutes or when ATP levels drop to 15% normal = irreversible
Brain damage ischmia = usually 5 minutes |
|
|
Small vascular bright red popular lesion in adult?
Bright red central papule surrounded by several outwardly radiating vessels? Soft blue compressible masses in skin, mucosa and viscera? |
1) Cherry hemangioma
2) Spider hemangioma (estrogen dependent) 3) Cavernous hemangioma (VHL disease in brain/viscera, liver ones are E dependent) |
|
|
MC CV symptom of someone with SLE? Describe presentation
|
Fibrinous pericarditis (can also have new onset murmur via libman sach's endocarditis presenting as a MS)
Fibrinous pericarditis = chest pain radiating to neck and shoulders that is relieved by sitting up, sharp in quality and increases with inspiration |
|
|
AV shunts/fistulas lead to what sequelae? Why?
What disease are these found in |
High output failure, due to bypassing capillaries and their high resistance beds, this leads to increased preload and bruits/thrills in the fistulas
Paget's disease of the bone |
|
|
Isolated systolic HTN is seen in what kind of patient?
What are the two first line drugs for this? What if they are diabetic? |
ELDERLY
1st line = HCTZ or DHPCCBs (nifedipine, amlodipine) Diabetic = ACE-I |
|
|
RPF equation?
RBF equation? |
RPF = PAH clearance = [U]PAH * V/[P]PAH
RBF = PAH clearance/(1-hematocrit) |
|
|
2 MC CV abnormalities in marfans'd disease? MCC of death?
|
MVP, Cystic medial necrosis
MCC death = aortic dissection |
|
|
What composes the majority of the anterior surface of the heart?
|
RV
|
|
|
MCC of death in acute rheumatic fever?
|
Myocarditis leading to a cardiac dilation and even functional MR (REPEATED episodes causes the mitral stenosis)
|
|
|
Are aspirin and clopidogrel synergestic?
|
YES
Asprin inhibits COX thus decreasing TXA2 levels leading to decreased platelet aggregation Clopidogrel (plavix) binds and blocks platelet ADP receptors that are also essential for platelet aggregation |
|
|
What is the triad of things seen on EKG in wolf parkinson white?
Explain why these are seen. |
Shortened PR
Delta wave (early hump on QRS) Widened QRS wave Bundle of kent exists that allows for sinus impulses to reach the ventricle first thus preexciting it before the AV impulse reaches the ventricular myocytes. |
|
|
When does a congenital bicuspid aortic valve present with disease? When does normal senile calcific aortic stenosis present with disease?
What condition do you see bicuspid aortic valves in? |
Bicuspid = stenosis in 50-60s
Senile = stenosis in 70s-80s Bicuspid valves are seen in TURNER's syndrome |
|
|
Severe aortic stenosis leads to what arrythmia? What happens as a result?
|
AFIB, you lose your atrial kick leading to severe hypotension (already occuring due to low LV volume due to hypertrophy)
|
|
|
Thyroid disease
Lung fibrosis Liver toxicity What drug? |
Amiodarone
Check LFTs, TFT, PFTs |
|
|
What is Cinchonism? What drug is this seen in?
|
Tinnitus, dizziness and fainting
Seen as an AE in people taking Quinidine (Class Ia antiarrythmic) |
|
|
Digoxin tox symptoms?
MCC of death with Digoxin? WHY? (what predisposes them to this?) Treatment? |
N/V, anorexia, confusion, VISION CHANGE (color perception)
MCC of death = vtach/vfib due to HYPERKALEMIA (inhibits Na/K pumps leading to increased EC potassium), Hypokalemia actually predisposes them to this Activated charcoal Insulin/Kayexlate/hemodialysisto manage to Hyperkalemia Anti-dig antibodies |
|
|
DOC for Vtach?
DOC for PSVT? DOC for Afib? |
Vtach = Amiodarone (used to be lidocaine, targets rapidly depolarizing and depolarized myocardial cells)
PSVT = Adenosine Afib = Cardioselective BBs/CCBs, Digoxin |
|
|
What kind of heart has a sigmoid septum? Why?
|
AGING heart due to decrease in LV chamber size, ventricular septum bulges into the LVOT
|
|
|
Hemochromatosis leads to what heart defect? Why?
|
Dilated cardiomyopathy, excess iron stores in cardiac myocytes
|
|
|
What is leaked into the serum as a marker for irreversible injury? What is the hallmark for reversible injurry?
|
Irreversible = CK release, fragmentation, dissolution and nuclear shrinkage
Reversible = cellular SWELLING (decreased ATP) |
|
|
Intrinsic ability for a drug to elicit an effect = ?
Dose of drug required to produce given effect = ? Affinity of drug effects which one of the above? |
Ability = Efficacy (maximal ceiling activity)
Dose = Potency (affinity of the drug) |
|
|
What are Aschoff bodies?
What are Anitschkow cells? Where are these found? |
Aschoff bodies = granulomas of inflammatory cells and large histeocytes
Anitschkow cells = plump macrophages with abundant cytoplasm and slender chromatin ribons Both are seen in Acute Rheumatic Bacterial carditis (jOnes), leads to Myocarditis, Pericarditis and endocaritis |
|
|
Lymphocytic interstitial inflammatory infiltrate with focal necrosis of myocytes = ?
|
Viral myocarditis
|
|
|
What is winter's formula and when would you use it?
|
PaCO2 = 1.5(HCO3-) + 8 +/- 2
Use this when someone has metabolic acidosis/alkalosis and must breathe off or hypoventilate |
|
|
What are kussmaul respirations and when do they occur?
|
Short fast shallow fast breaths to breathe off acid in DIABETIC KETOACIDOSIS
|
|
|
Relate white coat syndrome to classical conditioning and name the parts
what is OPERANT conditioning? |
Physician wearing the white coat = unconditioned stimulus
Sweating/increase BP = reflex response Any white coat = conditioned stimulus Operant = Positive reinforcement via a reward leading to conditioning for reptitive actions |
