bananas's version from 2015-05-20 02:56


Question Answer
machine like murmurPDA
opening snapMS
mid systolic clickMVP
Mitral stenosisfollows opening snap. delayed rumbling late diastolic murmur
follows opening snap. delayed rumbling late diastolic murmurMS
crescendo-decrescendo systolic ejection murmurAS
aortic stenosiscrescendo-decrescendo systolic ejection murmur loudest at heart base (R sternal border)
holosystolic high-pitched blowing murmurMR and TR
mitral regurgholosystolic high-pitched blowing murmur radiates toward axilla
tricuspid regurgitationholosystolic high-pitched blowing murmur radiates to R sternal border
late systolic crescendo murmur with mid systolic clickMVP
mitral valve prolapselate systolic crescendo murmur with mid systolic click
VSDholosystolic, harsh-sounding murmur
holosystolic harsh sounding murmurVSD
high-pitched blowing early diastolic decrescendo murmurAortic regurgitation
continuous machine-like murmur loudest at S2PDA
patent ductus arteriosuscontinuous machine-like murmur loudest at S2 (pulmonic area)
ASDloud S1 with wide, fixed split S2
loud S1 with wide, fixed split S2ASD

Valvular Disorders (other details)

Question Answer
loudest at heart baseAS
radiates to carotidsAS
pulses parvus et tardusAS (pulses are weak with delayed peak).
What can AS lead toCan lead to syncope, angina, and dyspnea on exertion.
where does aortic stenosis radiate to?carotids
which valvular defect is associated with pulsus parvus et tardus ?aortic stenosis
what is aortic stenosis often caused by?age related calcification or early onset calcification of bicuspid aortic valve
loudest at apex and radiates toward axillaMR
Often due to ischemic heart diseaseMR (post MI, MVP, LV dilatation)
can be caused by RF and infective endocarditisMR and TR
which murmur radiates to axilla?mitral regurg
what commonly causes tricuspid regurg?RV dilatation
which murmur radiates to R sternal border?tricuspid regurg, aortic stenosis
which murmurs can be caused by Rheumatic fever and infective endocarditistricuspid and mitral regurgitation
Due to sudden tensing of chord tendineaeMVP
best heard over apexMVP
loudest just before S2MVP
associated with chord ruptureMVP
most common valvular lesion?MVP
associated with marfan or Ehlers-danlos?MVP
Often due to aortic root dilation, bicuspid aortic valve, endocarditis, RFaortic regurgitation
Progresses to L Heart failureaortic regurg
when is aortic regurgitation severe and chroniclong diastolic murmur and signs of hyper dynamic pulse (widening PP, head bobbing, pulsatile nail beds
decreased interval between S2 and OS correlate with increased severitymitral stenosis
what can chronic MS result in?LA dilatation
best heard at L infraclavicular areaPDA
due to congenital rubella or prematurityPDA
what does inspiration do to heart sounds?increases venous return to RA so increases intensity of R heart sounds (Pulmonic and Tricuspid)
what does handgrip/rapid squat/passive leg raise/ alpha agonists do to heart sounds?increases afterload/preload. Increased intensity of MR, AR, AS, VSD murmurs, Decreased HCM, Later onset MVP click
what does valsalva/ sudden standing/ nitroglycerine admin do to heart sounds?decrease preload/afterload, decrease intensity of most murmurs (including AS), increase HCM intensity, MVP earlier onset of click
asymmetric hypertrophy of the septum compared to the free wallHCM


Question Answer
anterior surface of heartRV
posterior part of heartLA
atrial enlargement can causedysphagia due to compression of esophagus or hoarseness due to compression of laryngeal nerve (branch of vagus)
when does coronary blood flow peak?early diastole
what supplies SA and AV node?RCA --so infarct may cause bradycardia or heart block


Question Answer
Type I collagen high yieldbone
decreased production in osteogenesis imperfecta Itype I
Type II collagen high yieldcartilage
reticulintype III
defective in alport syndrome and targeted by autoantibodies in good pasture's syndrometype IV
corneatype I
tendontype I
late wound repairtype I
most common type of collagentype I
vitreous bodytype II
nucleus pulposustype II
cartilagetype II
skintype I and type III
blood vesselstype III
uterustype III
fetal tissuetype III
granulation tissuetype III
deficient in vascular type of ehlers danlostype III
basement membranetype IV
basal laminatype IV
lenstype IV
collagen in the eyecornea type I, vitreous body type II, lens type IV


Question Answer
3von Hippel-Lindau disease, renal cell carcinoma
4ADPKD with PKD2 defect, Huntington
5Cri-du-chat, FAP
7Williams syndrome, CF
9Friedreich ataxia
11Wilms tumor
13Patau syndrome, wilson disease
15prader-willie, angelman
16ADPKD with PKD2 defect
17 Neurofibromatosis I
18 Edwards syndrome
21Downs syndrome
22Neurofibromatosis 2, DiGeorge syndrome (22q11)
X Fragile X, X linked agammaglobulinemia, Klinefelters (XXY)


Question Answer
B1thiamine (TPP)
B2riboflavin (FAD, FMN)
B3Niacin (NAD+)
B5Pantothenic acid (CoA)
B6Pyridoxine (PLP)
Cascorbic acid
TPPthiamine B1 (thiamine pyrophosphate)
FADriboflavin B2
FMNriboflavin B2
NAD+Niacin B3
CoApantothenic acid B5
PLPpyridoxine B6 (pyridoxal 5 phosphate)
all wash out easily from body except...B12 and folate (stored in liver)


Question Answer
acidic amino acidsnegative charged. Aspartic acid, glutamic acid
basic amino acidspositive charged. arginine, lysine, histidine
most basic amino acidarginine
aa that are required during growth periodsarg and His
aa high in histonesArg and Lys. The bind negatively charged DNA
nonpolar hydrophobic aavaline, alanine, isoleucine, methionine, phenylalanine (shielded form direct contact to water and located interiorly on globular proteins)
essential AAglycogenic (methionine, valine histidine), glycogenic/ketogenic (isoleucine, phenylalanine, threonine, tryptophan), ketogenic (leucine, lysine)


Question Answer
B27Psoriatic arthritis, Ankylosing spondylitis, IBD, Reiter/Reactive arthritis
seronegative spondyloarthropathiesB27
hay feverDR2
SLEDR2 and DR3
Diabetes Mellitus 1DR3 and DR4
HashimotoDR3 and DR5
Pernicious anemiaDR5
MCH I loci(genes that code for MCH) HLA-A, B, C
DR2MS, hay fever, SLE, goodpastures
DR3DM1, SLE, graves, hashimoto
DR5pernicious anemia, hashimoto


Question Answer
delayed response to antigenIgG
most abundant in serumIgG
fixes complementIgG, IgM
crosses placentaIgG
passive immunity to infantIgG
opsonizes bacteriaIgG
neutralizes bacterial toxinsIgG
prevents attachment of bacteria and viruses to mucus membranesIgA
monomer in circulationIgA
dimer in secretionsIgA
crosses epithelial cells by transcytosisIgA
produced by peers patches in GI tractIgA
protects against gut infectionsIgA
most produced antibody overallIgA
released in secretionsIgA
what secretions can IgA be found in?tears, saliva, mucus, colostrum
where does IgA get its secretory component?epithelial cells
produced by immediate response to antigenIgM
antigen receptor on B cell surfaceIgM
pentamer when secretedIgM
what does the pentamer form allow for?in IgM--allows for binding to antigen while humoral response evolves
unclear functionIgD. Found on surface of many B cells and in serum
binds mast cells and basophilsIgE
cross links when exposed to allergensIgE
immediate type HSRIgE
releases histamineIgE
immunity to worms by activating eosinophilsIgE
lowest concentration in serumIgE


Question Answer
osteoclast activating factorIL1
fever, acute inflammationIL1
chemokine secretion to recruit WBCIL1
activates endothelium to express adhesion moleculesIL1
stimulates acute phase proteinsIL 6
recruits neutrophilsIL8
differentiation of T cells to Th1 cellsIL12
activates NK cellsIL12
septic shock mediatorTNF alpha
activates endotheliumTNF alpha
vascular leakTNF alpha
causes cachexia in malignancyTNF alpha
stimulates T cell growth (all T cells)IL2
stimulates bone marrowIL3
functions like GM-CSFIL3
secreted by NK cells in response to IL 12IFN gamma
stimulates macrophages to kill phagocytes pathogenIFN gamma
increases MHC expression and APC presentationIFN gamma
induces Th2 cell differentiationIL4
B cell growthIL4
growth of eosinophilsIL5
IgA productionIL5
B cell differentiationIL5
class switching to IgE and IgGIL4
inflammatory response modulatorIL10
attenuate immune responseIL10 and TGF beta
secreted by macrophagesIL1, 6, 8, 12, TNF alpha
secreted by T cellsIL2, 3
from Th1 cellsIFN gamma
from Th2 cellsIL4, 5, 10


Question Answer
T cellsTCR (binds antigen MHC complex), CD3 (TCR for signal transduction), CD28 (binds B7 on APC)
helper T cellsCD4, CD40L
cytotoxic T cellsCD8
T regsCD4, CD25
B cellsIg, CD19, CD20, CD21(EBV), CD40, MHC II, B7
MacrophagesCD14, CD40, MHC II, B7, Fc and C3b receptors for enhanced phagocytosis
NK cellsCD16 binds Fc of IgG, CD56
hematopoiteic stem cellCD34


Question Answer
Type Ifree antigen cross links IgE on presented mast cells and basophils triggering immediate release of histamine
anaphylactic and atopicType I
Type IIantibody mediated (IgM or IgG bind to fixed antigen on enemy cell and induce cellular destruction via opsonizaiton, compliment, antibody mediated cellular dysfunction)
antibody and compliment lead to MACType II
direct and indirect coombs testType II
Type IIIimmune complex mediated
attracts neutrophils that release lysosomal enzymestype III
serum sicknesstype III (most often caused by drugs acting as happens and occurs in membranes. Fever, urticaria, arthralgia, proteinuria, LAD)
arthus reactiontype III (on the skin due to injection causes edema, necrosis, compliment activation)
Type IVdelayed T cell mediated releases cytokines and leads to macrophage activation. No antibody involved
no antibody involvedType IV
cell mediatedType IV
delayedtype IV
not transferable by serumtype IV
transplant rejectionstype IV
PPDtype IV
contact dermatitistype IV
bee stingtype I
food/drug allergytype I
acute hemolytic transfusion reactiontype II
autoimmune hemolytic anemiatype II
bullous pemphigoidtype II
gravestype II
Guillain barretype II
ITPtype II
Myasthenia gravistype II
pephigus vulgaristype II
pernicious anemiatype II
Rheumatic Fevertype II
Polyarteritis nodosatype III
poison ivytype IV
nickel allergytype IV
MStype IV


Question Answer
anti-ACh receptorMyasthenia gravis
Anti-basement membraneGoodpasture
AnticardiolipinSLE, antiphospholipid syndrome
lupus anticoagulantSLE antiphospholipid
antidesmoglein (desmosome)pemphigus vulgaris
anti-glutamic acid decarboxylase (GAD-65)DM 1
antihemidesmosomebullous pemphigoid
anti-histoneDrug-induced lupus
anti-jo1, anti-SRP, anti MI2polymyositis, dermatomyositis
antimicrosomal, antithyroglobulinhashimotos
antimitochondrialprimary biliary cirrhosis
antinuclear antibodiesSLE nonspecific
anti parietal cellpernicious anemia
anti-Scl-70 (DNA topoisomerase I)Scleroderma
Anti-smooth muscleautoimmune hepatits
anti-SSA, SSB, Ro, LaSjogren
Anti-TSH receptorGraves
Anti-U1 RNP (ribonucleoprotein)mixed connective tissue disease
IgA anti-endomysial, transglutaminaseceliac
MPO-ANCA/P ANCAMicroscopic polyangiitis, eosinophilc granulomatosis with polyangiitis (Churg-Strauss) --associated with UC and PSC
PR3 - ANCA/C ANCAgranulomatosis with polyangiitis (wegener)
RFRA (nonspecific) IgM antibodies that target Fc portion of self IgG
anti-CCPRA (more specific)
anti-IFpernicious anemia


Question Answer
within minuteshyper acute
Donor specific antigen +hyper acute
type II HSR that activates complementhyper acute
widespread thrombosis of graft vessels and ischemic necrosishyper acute
how to treat hyper cute?graft must be removed
weeks to monthsacute
cellular or humorally mediatedacute
vasculitis of graft vessels with dense interstitial lymphocytic infiltrateacute
CD8 T cells activated against donor MHCscellular (T cell mediated) acute rejection
similar to hyper acute except antibodies develop after transplanthumoral acute rejection
treatment of acute rejection?prevent/reverse with immunosuppresnts (cyclosporin or tacrolimus --calcineurin inhibitors)
months to yearschronic
CD4 cells respond to recipient APCs presenting donor peptides including allogeneic MHCchronic
proliferation of vascular and smooth muscle and parenchymal fibrosisChronic
dominated by arteriosclerosischronic rejection
irreversible rejectionchronic
graft immunocompetent T cells proliferate in the immunocompromised host and reject host cells with foreign proteinsGVHD
severe organ dysfunctionGVHD
maculopapular rash, jaundice, diarrhea, hepatosplenomegalyGVHD
where is GVHD potentially beneficial?bone marrow transplant for leukemia (GV tumor effect)
oftne occurs in bone marrow and liver transplantsGVHD
autograftfrom self
syngeneic graftfrom identical twin or clone
isograftsame as syngeneic--from twin or clone
allograftfrom nonidentical individual of same species (cadaver)
xenograftfrom different species


Question Answer
PDGFsecreted by activated platelets and macrophages and induce vascular remodeling and smooth muscle cell migration --fibroblast growth for collagen synthesis
FGFstimulates angiogenesis
EGFstimulates cell growth by tyrosine kinases
TGF betaangiogenesis, fibrosis, cell cycle arrest (stops inflammation)
Metalloproteinasestissue remodelling
VEGFstimulates angiogenesis