Memorize This Stuff Flashcards
Stats for Case-Control Studies
Odds Ratio
ad/bc
Stats for Cohort Study
Relative Risk
(a/a+b) / (c/c+d)
with risk factor and disease / all with risk factor
without risk factor and disease / all without risk factor
Sensitivity
SNOUT
TP/ (TP + FN)
when neg, rules out disease
Specificity
SPIN
TN / (TN + FP)
when positive, rules in disease
PPV
varies directly with prevalence
low prevalence, low PPV
NPV
varies indirectly with prevalence
low prevalence, high NPV
Type 1 collagen
bone, tendon, skin, scars
Type 2 collagen
cartilage
car-two-lage
Type 3 collagen
Reticulin, blood vessels
vascular Ehlers Danlos
Type 4 collagen
basement membranes
Alport syndrome, Goodpastures
big testes, long face, jarge jaw, large ears, mitral valve prolapse
Fragile X
X linked FMR1 gene defect (CGG) repeats
Vitamin essential for maintenance of specialized spithelium, stored exclusively in the liver stellate cells
Vit A
Used to treat measles and AML-M3 (PML, auer rods)
Reactions using thiamine as a cofactor
Pyruvate dehydrogenase (PDH)
alphaketoglutarate dehydrogenase
transketolase (HMP shunt)
Branched Chain ketoacid dehydrogenase
TLCFN
Niacin deficiency
Pellagra
Diarrhea, dementia, dermatitis
Niacin is derived from tryptophan - Hartnup disease
Ethanol Metabolism
Uses up free NAD+
Increase NADH
Lactic Acidosis (pyruvate to lactate to regen NAD+)
Fasting hypoglycemia (prevents gluconeogenesis)
Fatty Change in liver
Strictly ketogenic AAs
Leucine and Lysine
Ketogenic and Glucogenic AAs
Trp, Phe, Tyr, Ile, Thr
Glucose 6 Phosphotase deficieny
Von Gierke
lysosomal alpha1,4glucosidase deficiency
Pompe
debranching enzyme deficiency
Cori disease
skeletal muscle glycogen phosphorylase deficiency
McArdle
alpha-galactosidase A deficiency
Fabry’s
Ceramide trihexoside
Glucocerebrosidase (beta-glucosidase) deficiency
Gaucher’s
glucocerebroside
Sphingomyelinase deficiency
Neimann-Pick
sphingomyelin
Hexosaminidase A deficiency
Tay-Sachs
GM2 ganglioside
Galactocerebrosidase deficiency
Krabbe
Arylsulfatase A deficiency
Metachromatic Leukodystrophy
alpha-L-iduronidase deficiency
Hurler
Heperan sulfate, dermatan sulfate
cataracts
iduronate sulfatase deficiency
Hunter
heparan sulfate, dermatan sulfate
NO cataracts
Encapsulated Organisms
Some Killers Have Pretty Nice Slimey Capsules
Strep pneumo and group B Klebs H flu Pseudomonas Neiserria m Salmonella Cryptococcus
Catalase Positive Organisms
Staph N Enterobacteriaceae Are Listed Catalase Postive
Staph Nocardia Entero Aspergillus Listeria Candida Pseudomonas
Urease positive organisms
K-PUNCHSS
Klebs Proteus Ureaplasma Nocardia Crytococcus H pylori Staph epi Staph sapro
Obligate aerboes
Nagging Pests Must Breathe
Nocardia
Pseudomonas
MycoBacterium
Obligate anaerobes
Can’t Breathe Air
Clostridium
Bacteroides
Actinomyces
Obligate Intracellular Bugs
rickettsia, chlamydia
can’t make any ATP
Facultative Intracellular Bugs
Some Nasty Bugs May Live FacultativeLY
Salmonella Neisseria Brucella Mycobacterium Listeria Francisella Legionella Yersina pestis
ToRCHeS
Toxo Rubella CMV HIV HSV Syphilis
Antibiotics to Avoid in Pregnancy
Sulfa - kernicterus Aminoglycosides - ototox FQs - tendons Clarithromycin - toxic Tetracyclines - bones, teeth Ribavirin - teratogen Griseofulvin - teratogen Chloramphenicol - gray baby
HLA A3
Hemochromatosis
HLA B27
seronegative arthropathies Psoriatic arthritis ankylosing spondylitis IBD reactive arthritis (Reiter)
HLA DQ2/DQ8
celiac disease
HLA DR2
MS, SLE, Goodpasture
HLA DR3
t1dm, SLE, Graves
HLA DR4
t1dm, RA
HLA DR5
pernicious anemia, hashimoto’s
Cytokines secreted by Macrophages
IL1,6,8,12, TNF-alpha
Cytokines secreted by T cells
IL2,3
cytokines secreted by Th1 cells
ifn-gamma
cytokines secreted by Th2 cells
IL4,5,10
IL-1
endogenous pyrogen
IL-2
stimulates t cells to divide
IL-3
bone marrow cell growth
IL-4
IgE class switching, Th2 growth and B cell growth
IL-5
IgA class switching, eosinophil growth
IL-6
endogenous pyrogen, acute phase proteins
IL-7
lymphoid differentiation
IL-8
major neutrophil chemotatic factor
IL-10
anti-inflamatory, inhibits Th1
IL-12
induces Th1 differentiation, activates NK cells
TNF-alpha
mediates septic shock, activates endothelium
IFN-gamma
antiviral, antitumor
increases killing of virally infected cells, increases MHC expression in all cells
responsible for forming granulomas
CD3
all T cells
CD 4
helper T cells
CD28
all t cells
binds B7 on the APC
CD40
b cells, needed for antibody class switching CD40L on Thelpers
CD8
killer t cells
CD19,20,21
B cell markers
21- receptor for EBV
B7
binds CD28 on t cells
on antigen presenting cells
CD14
macrophage specific
binds LPS
CD56
unique NK cell marker
Anergy
t cell gets MHCII stimulation, but no co-stimulatory signal
refractory to further signaling
auto-antibody: ACh receptor
myasthenia gravis
auto-antibody: basement membrane
goodpasture
auto-antibody: cardiolipin, lupus anticoagulant
SLE, antiphospholipid syndrome
auto-antibody: centromere
limited scleroderma, CREST syndrome
auto-antibody: desmoglein
pemphigus vulgaris (thin walled blisters)
auto-antibody: dsDNA, Smith
specific for SLE
auto-antibody: glutamate decarboxylase
t1dm
auto-antibody: hemidesmosome
bullous pemphigoid (tense blisters)
auto-antibody: Jo-1, SRP, Mi-2
polymyositis, dermatomyositis
auto-antibody: microsomal, thyroglobulin
hashimoto’s
auto-antibody: mitochondrial
primary biliary cirrhosis
auto-antibody: ANA
SLE, nonspecific
auto-antibody:SCl70 (DNA topo 1)
diffuse scleroderma
auto-antibody: smooth muscle
autoimmune hepatits
auto-antibody: SSA (Ro), SSB (La)
Sjogren
auto-antibody: TSH receptor
Graves
auto-antibody: U1 RNP (ribonucleoprotein)
Mixed connective tissue disease
auto-antibody: cANCA (PR3 ANCA)
granulomatosis with polyangitis (Wegner)
auto-antibody: IgA endomysial, IgA TTG
celiac
tissue trans glutaminase
auto-antibody: pANCA (MPO ANCA)
microscopic polyangitis, Churg-Strauss
auto-antibody: Rheumatoid factor, CCP
IgM anti IgG
RA
retroperitoneal structures
SAD PUCKER
Suprarenal (adrenals)
Aorta and IVC
Duodenum
Pancreas (except tail) Ureters Colon (up and down) Kidneys Esophagus (lower) Rectum
falciform ligament
fetal umbilical vein
hepatodoudenal ligament
holds the portal triad
layers of the gut wall
MSMS
Mucosa
Submucosa (Meissner plexus)
Muscularis (Myenteric / Auerbach plexus)
Serosa
Peyers patches
only in the illeum
SMA syndrome
transverse duodenum is entrapped between SMA and aorta, causing obstruction
Name six main collateral artery sets in the belly
Superior and inferior epigastric left and right gastric left and right gastroepiploic superior and inferior pancreaticoduodenal middle and left colic superior and middle/inferior rectal
Name three portosystemic anastomoses
left gastric - esophageal (to azygous) - varices
paraumbilical - small epigastric - caput medusa
superior rectal - mid/inf rectal - anorectal varices
Gut, Butt, Caput
cholecystokinin
I cells (duodenum)
increase panc/gall secretions (muscarinic), slow gastric emptying
increased by fat, amino acids
gastrin
G cells (stomach antrum)
increase H and motility
increased by food, vagal stimulation
ZE syndrome
Motilin
small bowel
produces migrating motor complexes
increased while fasting
Secretin
S cells (duodenum) increases panc bicarb secretion and bile secretion increased by fatty acids in the duodenum
Somatostatin
D cells (islets) D = down, slows everything down
stimulators of H release by parietal cells
Ach, vagus stim
Gastrin,
histamine, from enterochromaffin-like cells (most important)
uptake of glucose and galactose by gut lumen
SGLT1 (Na dependent) -> GLUT2 on bl
uptake of fructose by gut
GLUT5 (facilitated diffusion) -> GLUT2 on bl
iron absorption by the gut
duodenum, as Fe2 (2 goes in 2 the body)
folate absorption by the gut
jejunum and ileum
B12 absorption by the gut
terminal ileum, requires intrinsic factor
heme to biliverdin
heme oxygenase
makes bad bruises green
congenital defect of the bowel, may contain ectopic gastric mucosa or pancreatic tissue
Meckel diverticulum vitelline duct (omphalomesenteric duct)
Branced Amino Acids
Isoleucine, Leucine and Valine
Maple Syrup Urine Disease
normal S2 splitting
increases with inspiration
drops pressure, increases venous return, more blood through the right side, longer for the pulmonary valve to close
wide s2 splitting
conditions that delay RV emptying
pulm stenosis, RBBB
fixed s2 splitting
ASD
l->r shunt causes increased flow through pulmonic regardless of breathing
paradoxical s2 splitting
split with expiration, no split with inspiration
condtions that delay LV emptying
aortic stenosis, LBBB
cardiac auscultation: inspiration
increases venous return
increases intensity of right heart sounds
cardiac auscultation: hand grip
increases systemic vascular resistance
increase MR, AR, VSD
decreases AS
cardiac auscultation: valsava, standing
decreases venous return
decreases most mumurs
increases hypertrophic cardiomyopathy murmur
cardiac auscultation: rapid squatting
increases venous return, preload
increases AS
decreases HCM
cardiac auscultation: holosystolic blowing
MR or TR
cardiac auscultation: holosystolic harsh, loudest at tricuspid area, increased with hand grip
VSD
cardiac auscultation: late systolic crescendo with a midsystolic click, over the apex
MVP
cardiac auscultation: early diastolic snap and rumbling diastolic mumur
mitral stenosis
explain pulsus paradoxus
decrease in systolic BP of >10 with inspiration
increased venous return with little pericardial compliance will shove the ventricular septum over and compress the LV, resulting in decreased SV and BP
tamponade, pericarditis, obstructive pulmonary diseases (asthma), croup
Inulin CL
GFR
CR slightly overestimates
PAH CL
RPF
proteinuria leading to pellagra like symptoms
Hartnup disease
decreased absorption of neutral AAs, including tryptophan
B3 can be made from Trp, so get a decreased B3 lvl
Renal tubular defect: PCT
Fanconi
increased excretion of basically everything
AAs, glucose, phos, bicarb -> met acidosis
Wilson’s and toxins
causes type 2 RTA
Renal tubular defect: thick ascending loop[
Bartter - AR
Na/K/2CL defect
hypoK, met alk and hypercalicuria
Renal tubular defect: DCT
Gitelman - AR, not as severe as Bartter
NaCl resorbtive defect
hypoK, met alk, no hypercalciuria
Renal tubular defect: collecting duct
Liddle - AD
increased Na absorption (Enac)
hypoK, met alk, hypertension
Causes of extracellular K shift (hyper K)
digitalis hyperosmolarity Insulin deficiency cell lysis acidosis (H/K exchange) Beta block
Causes of intracellular K shift (hypoK)
hypo-osmolarity
insulin
alkalosis
Beta agonist
U waves on ECG
hypo K
Wide QRS and peaked T waves on ECG
hyper K
causes of anion gap met acidosis
MUDPILES Methanol Uremia DKA Propylene glycol Iron or INH Lactic acidosis Ethylene Glycol Salicylates
causes of non-gap met acidosis
HARD ASS hyperalimentation addison's RTA Diarrhea (increased Cl-) Acetazolamide Spironolactone Saline infusion
type 1 renal tubular acidosis
defect in alpha-intercalated cells (distal, ph > 5.5)
decreased secretion of H+
hypokalemia (decreased resorption)
caused by obstruction (mult myeloma), ampho B, analgelsic nephropathy
type 2 renal tubular acidosis
defect in PCT bicarb resorption (proximal, ph < 5.5)
increased bicarb secretion; acidified by intercalated cells
hypokalemia
caused by Fanconi syndrome, toxins (lead, aminoglycosides), CA inhibitors
type 3 renal tubular acidosis
hyper K, ph < 5.5
hypoaldo situations, K sparing diuretics
hyperK impairs ammonia generation in the PCT, decreased H excretion into the urine
urine cast: fatty (oval)
nephrotic syndrome
urine cast: granular, muddy brown
acute tubular necrosis
urine cast: waxy
chronic renal failure
AD kidney cysts in the medullary collecting ducts and shrunken kidneys
medullary cystic kidney disease
labs: pre-renal azotemia
serum BUN/Cr > 15-20 (due to fluid resorption)
UNa < 20
FENa < 1%
UOsm > 500
kidneys still work fine, can still concentrate the urine
nephrotic syndrome: kids
Minimal change disease
nml LM, neg IF, foot process effacement EM
damage mediated by cytokines (asso Hodgkin’s)
usually responds to steroids
nephrotic syndrome: hispanics, blacks, HIV patients
FSGS
also asso with sickle cell and heroin
foot process effacement like MCD, with findings on LM and neg IF
nephrotic syndrome: SLE and Caucasian adults
membranous nephropathy
diffuse membrane thickening LM, subepithelial (podocyte side) granular deposits, SPIKE AND DOME on EM
antibody to phospholipase A2
nephrotic syndrome: HBV, HCV and tram tracks
type 1 membranoproliferative subendothelial deposits (granular) split the GB membrane, causing the tram track appearance
nephrotic syndrome: C3 nephritic factor
type 2 MP
intramembranous deposits
low serum C3
C3 nephritic factor stabilizes C3 convertase
nephritic syndrome
hematuria, inflammed, hypercellular glomerulus
nephritic syndrome: after throat/skin infection
PSGN
about 2 weeks after infection
subepithelial deposits (granular)
nephritic syndrome: crescents
RPGN
crescents are comprised of macs and fibrin
get IF!!
linear - goodpasture’s
granular - PSGN or DPGN
neg - Wegners (cANCA), microscopic polyangitis or Churg-Strauss (p-ANCA)
nephritic syndrome: SLE
diffuse proliferative GN
subendothelial C3 deposits
wire-looping capillaries
most common cause of death in SLE
nephritic syndrome: IgA deposits
Berger’s (IgA) nephropathy
mesangial IgA deposits, mesangial proliferation
flares with URI/GI infection - 2-3 days after infection
renal tumor in tuberous sclerosis
angiomyolipoma
renal cell carcinoma paraneoplastic syndromes
EPO, renin, PTHrp, ACTH
wilms tumor defining cell type
blastema
mutations on chr11
WAGR syndrome
Wilms
Aniridia
Gential abnormality
Retardation
Denys-Drash Syndrome
Wilms, progressive glomerular disease, male pseudohermaphroditism
WT1 mutations
Beckwith-Wiedemann syndrome
wilms, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (esp tongue)
WT2 mutations