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164 Cards in this Set

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functions of thenar/hypothenar mm
OAF: oppose, aBduct, flex
changes in bloodflow / vascular resistance in compensated coarctation of aorta
decreased lower body SVR and increased upper body SVR (autoregulation --> vasodilation), allows blood flow to be normal in both upper and lower body
ostium primum vs ostium secundum
ASDs; primum is lower (septum primum grows cranial --> caudal), secundum is higher (represents the 'hole' formed in the septum primum to allow R-->L shunt during fetal life)
blood supply to head of femur
medial femoral circumflex (implicated in Legg-Calve-Perthes disease, aseptic necrosis if femur head)
progressively increasing chest pain
"crescendo" or unstable angina
monckeberg arteriosclerosis
"medial calcific sclerosis" -- dz of ELDERY, ring-like calcifications in MEDIA of MEDIUM-sized MUSCULAR arteries; no change in luminal diameter --> not clinically relevent
3 features of NF1
1) multiple neural tumors; 2) café-au-lait spots; 3) iris hamartomas (Lisch nodules)
course of common peroneal nerve, common site of injury
peroneal nerve courses by nec of the fibula (remember, fibula is lateral and superficial peroneal nerve innervates the lateral aspect of the foot -- SPooning from the side; also makes sense because peroneal nerve EVERTS the foot, so it must be lateral); neck of the fibula --> peroneal damage --> dropPED foot
bullous pemphigoid vs Staph scalded skin syndrome
staph in kids / infents; bullous pemphigoid is a dz of ELDERLY
cardiac tamponade vs constrictive pericarditis
both have: decreased CO, increased venous pressure (JVD); TAMPONADE: no kussmaul, yes pulsus paradoxus; PERICARDITIS: is opposite (yes kussmaul, no pulsus paradoxus - pressure not transmitted through rigid pericadrdial shell, but instead goes to jugular veins?? --> inc JVD with inspiration)
classic signs of tamponade
1) decreased arterial pressure (dec CO), 2) increased venous pressure (JVD), 3) small quiet heart
contents of carotid sheath
1) internal jugular vein; 2) common carotid artery; 3) vagus nerve
blood supply to inerventicular septum
anterior: LAD; posterior: posteriod descending artery (80% of time comes off of RCA, 20% off of L circumflex)
blood supply of SA and AV nodes
RCA
changes in cardiac function during exercise
1) increased CO because of inc stroke volume; 2) (later) increased heart rate --> inc CO
O2 and pH effects on contractility (and therefore stroke volume)
acidosis and hypoxia --> decreased contractility --> decreased SV
causes of increased blood volume
overtransfusion, sympathetic excitement
resistance as f(viscosity, length, and radius)
resistance = k * (viscosity * length / r^4)
what changes viscosity
viscosity ~= f(HCT); inc viscosity in: 1) polycythemia; 2) hyperproteinemic states, eg multiple myeloma; 3) hereditary spherocytosis (HS)
wenckebach block
mobitz type I; progressively increasing PR interval until dropped QRS, then reset
pulsus pardoxus
indicates cardiac tamponade; normally, decrease of thoracic pressure during inspiration --> increased venous return --> shift of septum --> slightly decreased L filling --> decreased pressure; in tamponade, fixed volume --> L ventricle compromised more --> exaggerated drop in BP
None
SA/AV node action potential
phase 4: slow Na leak current (no fast channels -- helps slow AV conduction), slope determines HR; phase 0: upstroke, mediated by Ca++ influx (no fast Na+ channels)
p wave represents
atrial depolarization
pr interval represents
conduction thru av node
qrs represents
ventricular depolarization
qt interval represents
mechanical contraction of ventricles
delta wave
wolff-parkinson-white syndrome; accessory pathway (bundle of kent) allows early depolarization of part of ventricles; can lead to reentry SVT
mobitz I vs mobitz II
mobitz I = wenckebach block, progressive lengthening of PR interval, asymptomatic; mobitz II: often n:1 block, can progress to 3rd degree --> BAD
peripheral chemoreceptors
aortic and carotid (~same loc as baroreceptors); respond to PO2 < 60, inc PCO2, and dec pH
central chemoreceptors
respond to CO2 and pH, NOT O2; cause CUSHING reaction (increased intracranial pressure --> hypertension, bradycardia, and irregular respirations)
cushing reaction
increased intracranial pressure --> cerebral hypoxia (vessels compressed) --> chemoreceptors --> inc BP until vessels patent --> hypoxia reversed, but inc BP detected by baroreceptors --> bradycardia
organ that gets largest share of cardiac output
liver
nl pressures:
RA: <5; RV: <25/5; PA: <25/10; LA: < 12; LV: <130/10; Ao: <130/90
3 congenital R-L shunts
early cyanosis, "blue babies" -- 1) Tetralogy of Fallot; 2) Transposition of the Great Vessels; 3) Truncus Arteriosus
3 congenital L-R shungs
late cyanosis (eisenmenger's), "blue kids" -- 1) VSD (harsh holosystolic murmur); 2) ASD (loud S1, wide fixed split S2); 3) PDA (close with indomethacin)
location of shunt in PDA
left pulmonary artery to aorta, derivative of branchial arch 6
eisenmenger syndrome
uncorrected L->R shunt --> PulmHTN --> shunt reverses --> late cyanosis, clubbing, polycythemia
defects in tetralogy of Fallot
PROVe: 1) Pulm Stenosis --> 2) RVH; 3) Overriding Aorta; 4) VSD; all caused by anterosuperior displacement of infundibular septum (unequal splitting of pulm trunk and AO
congenital cardiac defects a/w 22q11
Truncus arteriosus, Tetralogy of Fallot
congenital cardiac defects a/w Down syndrome
ASD (primum), VSD (endocardial cushion defect)
congenital cardiac defects a/w congenital rubella
Septal defects, PDA
congenital cardiac defects a/w Turner Syndrome
Infantile coarctation of the aorta (proximal to L. subclavian)
congenital cardiac defects a/w Marfan's Syndrome
AR
congenital cardiac defects a/w Child of diabetic mother
Transposition of the great vessels
progression of atherosclerosis
fatty streaks --> proliferative plaque --> complex atheroma
angina types and assoc pain
1) STABLE (pain with exertion); 2) PRINZMETAL'S (coronary spasm --> pain at rest); 3) UNSTABLE/CRESCENDO (worsening chest pain)
red infarcts
occur in organs with dual blood supply (eg lung, liver, intestines), or following reperfusion
most common coronary artery occluded
LAD > RCA > circumflex
ECG changes following MI
transmural: Q waves, ST elev; subendocardial: ST depression
dressler's syndrome
fibrinous pericarditis several weeks after MI (autoimmune)
causes of dilated (congestive) cardiomyopathy
(ABCCCDD): Alcohol, Beriberi, CoxsackiB, chronic Cocaine, Chagas, Doxorubicin tox, Diphtheria (exotoxin rockets); others: peripartum cardiomyopathy, hemochromatosis
types of ASD
ostium PRIMUM (5%): defect in lower atrial septum, can involve AV valves; ostium SECUNDUM (90%): center of atrial septum at foramen ovale, from abn of either setpum primum or secundum, AV valves nl;
effects of nitro on angina
helps with stable, doesn't help with prinzmetal or unstable
cardiac rhabdomyoma
most common primary cardiac tumor in KIDS; a/w TUBEROUS SCLEROSIS;
equilibration of pressures in all 4 heart chambers
seen in cardiac tamponade
electrical alternans
cardiac tamponade (heart axis shifts within fluid-filled pericardium from beat to beat)
signs of bacterial endocarditis
JANEWAY lesions (nontender, palms and soles); OSLER nodes (tender, fingers and toes); ROTH spots (retinal hemorrhages surrounding white spots); SPLINTER hemorrhages (nail bed)
vegetations on both sides of valve
libman-sacks endocarditis (a/w SLE); mitral stenosis, no embolic risk
findings in rheumatic fever
FEVERSS (Fever, Erythema marginatum, Valvular damage, Elevated ESR, Red-hot joints (polyarthritis), Subq nodules, Sydenham chorea)
causes of serious pericarditis
SLE, RA, infection, uremia (clear, straw colored exudate)
causes of fibrinous pericarditis
uremia, MI (dressler's), RF (fibrin-rich exudate)
causes of hemorrhagic pericarditis
TB, malignancy
findings in pericarditis
friction rub, ST elevations in all leads, "distant" heart sounds
near absence of muscle tone and peristalsis of esophagus
scleroderma -- replacement of muscle by dense connective tissue
hourglass-shaped stomach on barium swallow
hiatal hernia
tx for severe crohn's dz
corticosteroids (hydrocortisone suppositories for UC)
most imp predictor of Carcinoid tumor metastatic potential
site and size (carcinoid tumors in appendix / cecum, although most frequent, rarely met to liver; stomach/ileum/colon carcinoid tumors have high metastatic potential, esp if >2cm)
None
relevence of architecture / cell pleomorphism in neuroendocrine tumors
minimal
most common course of Hep B infection
60-65%: sublinical dz --> complete recovery; 20-25% acute hep (99% of these recover)
meconium ileus
retention of meconium in GI tract; often a manifestation of CYSTIC FIBROSIS (abormally visci pancreatic secretions --> gets stuck in small bowel);
1' presentation of diffuse esophageal spasm
midsternal pain, sometimes mis-dx as cardiac; caused by prolonged contraction of entier esophagus;
scleroderma vs achalasia
scleroderma has significant acid reflux with resultant esophagitis; achalasia has regurgitant food and heartburn
3 main components of free edge of lesser omentum
common bile duct, hepatic artery, portal vein (portal triad?)
connection between greater and lesser sacs
foarmen of winslow -- bounded by common bile duct, duodenum, stomach
time of presentation of ostium secundum ASD
late childhood -> 20s; systolic ejection murmur (increased RV volume) and wide fixed splitting of 2nd heart sound
embryo: what causes separation of the atria from ventricles
fusion of endocardial cushions
type of gallstones found in chronic hemolytic disorders
pigment (calcium bilirubinate)
white oral lesion with risk of malignancy
leukoplakia
bile duct obstruction a/w UC
PSC (primary sclerosing cholangitis), characterized by "beading" on ERCP
types of chronic gastritis
antral (Type B): a/w h.pylori; fundal (type A): a/w pernicious anemia
causes of hematemesis
duodenal ulcer, gastric ulcer, esophageal varices
common sites of ischemic bowel infarction
1) transverse colon near splenic flexure (switch from SMA to IMA); 2) rectosigmoidal junction (switch from IMA to Internal Iliac A.)
consequence of SMA aneurysm
compression of L. renal vein (passes anterior to aorta, just inferior to origin of SMA) --> can cause varicocele on the left along with renal and adrenal hypertension on the left
contents of saliva
mucin (lubricates food); alpha-amylase / ptyalin (breaks down starch); HCO3- (neutralizes oral bacterial acids, maintains dental health)
muscle of the esophagus
proximal 1/3 is skeletal, distal 1/3 is smooth (incl LES), middle 1/3 is mixed
dysphagia: diffulcty with solids vs liquids
just solids suggests mechanical disturbance, solids + liquids suggests motility disorder
odynophagia vs heartburn
odynophagia suggests esophageal spasm, heartburn suggests GERD
manifestation of congenital GI problems
manifest during neonatal period except for meckel diverticulum (can remain asymptomatic)
sharp stabbing pain vs burning epigastric pain
sharp stabbing usu pancreatitis, burning epigastric usu gastric/duodenal ulcer
precursor lesion to oral cancer
leukoplakia
virchow node
enlarged left-sided suprclavicular lymph node a/w gastric carcinoma
krukenberg tumor
metastatic dz to the ovaries from stomach; mucinous signet rign cells
achalsia
motility disorder, impaired relaxation of LES --> no liquids / solids can get through; tx w/ CCBs and nitrates
secretin
produced by duodenum in response to H+ --> increases pH by inhibiting gastric H+ secretion and increasing HCO3- secretion by pancreas, liver, gallbladder
duodenal vs gastric ulcer
DUODENAL: decreased pain after meals/antacids, a/w inc acid production; GASTRIC: pain persists, dec/nl acid production;
hiatal hernia
stomach thru diaphragm; can be caused by smoking or obesity; can cause GERD
small bowel vs large bowel obstructions
small bowel usu from adhesions; large bowel usu from neoplasms
rota vs norwalk vs adeno
rota usu in infants, adeno in kids, norwalk in older kids and adults
diverticulosis vs diverticulitis
diverticuLOSIS (MCC lower GI bleeding): bleeding, no pain; diverticuLITIS: PAIN (diverticuL-AIEEE-tis), bright red rectal bleeding, serious: perforation, peritonitis, abscess formation
protozoal causes of diarrhea
entamoeba (bloody), giardia (watery, foul-smelling), cryptosporidium (watery, large fluid loss, I/C pts)
pear-shaped trophozoite with four pairs of flagella and two nuclei resembling eyes
Giardia
which IBD a/w sclerosing cholangitis (PSC)
UC
abdominal pain disproportionate to physical findings (no guarding, distention, tenderness)
suggestive of mesenteric ischemia
abetalipoprotienemia
AR dz, lack of ApoB --> defective chylomicron formation, enterocytes stuffed with lipids; a/w acanthocytes ("burr" cells)
charcot triad
a/w acute cholangitis: 1) fever; 2) RUQ pain; 3) jaundice (obstructive --> conjugated bilirubinemia)
amylase/lipase levels in gallstone vs EtOH pancreatitis
much higher in gallstone-induced (thousands) vs hundreds in alcoholic pancreatitis
None
posterior duodenal ulcer -- what artery affected?
gastroduodenal
snRNPs
form spliceosomes in conjunction with proteins -- involved in removal of introns (RNA splicing)
killed vs live attenuated polio vaccines
killed (SalK) is given IM --> no GI IgA; live attenuated (Sabin) is given PO --> IgA
AZT (ziduvudine) mech
nucleoside RTI
gastrin
"food in stomach" hormone: secreted by G cells in antrum of stomach in response to distention, AA, peptides, or ACh; EFFECTS: increased HCl secretion by parietal cells in fundus of stomach, increased gastric motility, increased gastric mucosal growth (eg Zollinger-Ellison syndrome)
CCK
"fat in duod" hormone: secreted by I cells in duodenum in response to FA/AA; EFFECTS: decreased gastric motility, increased pancreatic enzyme secretion, increased gallbladder contraction, relaxtion of sphincter of oddi
Secretin
"acid in duod" hormone: secreted by S cells in duodenum in response to acid; EFFECTS: inhibits gastric HCl secretion, promotes pancreatic HCO3- secretion;
Somatostatin
"inhibitory hormone": secreted by delta cells of pancreas; EFFECTS: inhibits {GH, insulin, glucagon, CCK, gastrin} --> decreases acid and pepsinogen secretion, decreases pancreatic and intestinal fluid secretion, decreases gallbladder contraction
GIP
"gastric inhibitory peptide / glucose-dependent insulin peptide": secreted by K cells of duodenum in response to all three nutrient classes; EFFECTS: increased insulin release, decreased gastric H+ secretion;
trypsinogen
pro-protease secreted by pancreas into duodenum, acitvated to trypsin by enterokinase on duodenal brush border
trypsin
serine protease; activates other proenzymes (including trypsinogen)
age group affected by indirect hernias + anatomy
INfants, goes IN to INguinal canal (lateral to inferior epigastric vessels); occurs because of failure of processus vaginalis to close
anatomy of direct inguinal hernia
protrudes through Hesselbach's triangle (rectus m., inguinal ligament, inferior epigastric vessels)
palpable "olive mass" epigastrically
hypertrophic pylroic sphincter -- a/w vom, regurg in older kids (projectil vom at 2 weeks)
AST:ALT ratio
AST > ALT: alcoholic hep; ALT > AST: viral hep; AST only: MI
GERD
a/w hiatal hernia/incompetent LES, tobacco/EtOH; recumbent position increases discomfort
esophageal webs
mucosal folds above the aortic arch, a/w Plummer Vinson syndrome (Fe deficiency)
Esophageal Rings (Schatzki)
mucosal *rings* (vs folds) below aortic arch, near squamocolumnar junction; causes intermittent dysphagia
risk factors for esophageal cancer
ABCDEF (Alcohol, Barrett's, Cigarettes, Diverticuli (eg zenker's), Esophageal webs/Esophagitis, Familial)
celiac vs tropical sprue
celiac is AI, affects small bowel only; tropical is infectious, can affect entire small bowel
chronic gastritis TWO TYPES
Type A: fundal, Auto-antibodies to parietal cells --> pernicious Anemia, Achlorydia; Type B: antral, H.Pylori (type B = Bug); both inc risk of gastric carcinoma
menetriere's disease
enlarged gastric rugae --> loss of plasma proteins from altered mucosa --> protein losing enteropathy; inc risk of stomach cancer; gut looks like brain gyri
PUD and cancer
PUD does NOT predispose to cancer;
UC vs Crohns presentation
UC presents w/ bloody stool, a/w colon cancer, no fistulas; Crohns presents w/ nonbloody diarrhea and fistulae
acute necrotic pancreatitis vs bacterial peritonitis, grossly
acute necrotic pancreatitis can present w/ hemorrhage into necrotic areas, areas of white chalky fat necrosis on pancreas and other parts of abd cavity; bacterial peritonitis is characterized by a dull-appearing peritoneal surface w/ white-yellow supporative exudate
VIP
hormone produced by islet cells and neurons in GI mucosa; EFFECTS: relaxation of GI smooth muscle, dec H+ secretion, and stim of pancreatic HCO3- and Cl secretion
VIPoma
islet tumor --> PANCREATIC CHOLERA (WDHA: Watery Diarrhea, Hypokalemia, Achlorhydia); tx w/ somatostatin (octreotide)
histo presentation of Crohns vs UC
Crohns: intestinal inflam w/ scattered noncaseating granulomas; UC: collections of neutrophils within crypt lumina
characteristics of colonic diverticula
mech: pulsion (); structure: "false" -- only 2 layers;
adult vs fetal diverticula
diverticula acquired during adult life (eg Zenker) are usu false, while diverticula from fetal dev (eg Meckel) are true
traction vs pulsion diverticulum
TRACTION: due to inflam --> scarring; "true" structure; PULSION: pushed out by pressure (eg constipation --> straining); "false" structure
plemorphic adenoma
MC salivary gland tumor (usu parotid); BENIGN; contains myxoid/cartilage like elements + epithelial cells
adeno vs squamous cell carcinoma of esophagus
BOTH: dysphagia, anorexia, hematemesis; SQUAMOUS CELL: smoking, EtOH, upper and middle thirds of esoph; ADENO: barrett's, lower third
crohns vs UC epi
crohns: young jews;
complications of meckel diverticulum
intussusception (kids), volvulus (older)
PAS positive macrophages
Whipple disease (1' causes malabsorption; can affect any organ, a/w arthralgias, cardiac, and neuro sx)
carcinoid tumor
usu in appendix or SI; if met to liver, can become carcinoid syndrome --> vasoactive peptides --> flushing (5HT), watery diarrhea (VIP), right sided heart lesions (5-HT)
types of polyps
tubular (small, pedunculated MC, least malig potential) --> villous (large, sessile, velvety, many villi, HIGH malig protential)
None
congenital unconjugated hyperbilirubinemias
caused by defect in glucornyl-transferase; 1) GILBERT: 5% pop, usu asx; 2) CRIGLER-NAJJAR: Type I (dangerous, death/kernicterus), Type II (milder, tx w/ phenobarbital)
congenital conjugated hyperbilirubinemias
defect in bilirubin uptake; 1) DUBIN JOHNSON: black liver; 2) ROTOR: like DJ, but no liver discoloration
leptospirosis
Weil disease/ icterohemorrhagic fever: jaundice, renal failure, hemorrhage
alcoholic hepatitis: histo
fatty change, focal liver necrosis, neutrophilic infiltrates, and mallory bodies (intracytoplastmic eosinophilic hyaline inclusions)
alcoholic cirrhosis findings
micronodular hepatocelular damage, jaundice, hypoalbumin, coag factor deficiencies, Hyperestrinism
primary vs secondary biliary cirrhosis
BOTH: severe obstructive jaundice --> elev alk phos; PRIMARY: intrahepatic, autoimmune (AMA), mid aged women; SECONDARY: extrahepatic obstruction --> inflammation --> fibrous tissue formation, can lead to ascending cholangitis, histo: bile lakes
primary sclerosing cholangitis
PSC includes intra and extra hepatic bile ducts, is a/w UC, seen as "beading" on ERCP (alternating strictures and dilation; can lead to secondary biliary cirrhosis and cholangiocarcinoma; Charcot's triad of cholangitis: RUQ pain, fever, jaundice;
budd chiari syndrome
thrombotic occlusion of heptaic veins --> jaundice, hepatomegaly, liver failure; a/w polycythemia vera, HCC, abd neoplasms
hemangiosarcoma (angiosarcoma)
rare hepatic vascular tumor, a/w PVC, thorotrast, arsenic
cholangiosarcoma
bile duct carcinoma, a/w Clonorchis sinensis (liver fluke) and Thorotrast, NOT HBV/cirrhosis
types of gallstones
1) CHOLESTEROL: solitary, large, yellow; 2) PIGMENT: bilirubin, a/w HA and bacterial infection; 3) MIXED: MCC, cholesterol + calcium
clinical manifestations of pancreatic cancer
abd pain radiating to back, migratory thrombophlebitis (Trousseuau sign), obstructuve jaundice --> distended palpale gall bladder (Courvoisier law)
infiltrative gastric cancer
Linitis plastica (infiltration --> fibrosis --> thickened, rigid appearance)
most common location of diverticula (esp in elderly)
sigmoid colon, a/w low fiber diets
which part of bowel most likely to have volvulus
sigmoid colon (has redundant mesentary; ascending and descending are retroperitoneal, and transverse is stretched tight)
"apple core lesion"
CRC; left sided: obstructive, right sided: nonobstructive, but a/w anemia
micro vs macronodular cirrhosis
MICRO: metabolic insult (EtOH, hemochromatosis, wilson's); MACRO: significant liver injury (post-infec, drug-induced)
estrogen effects of cirrhosis
hyperestrinism (liver metabolizes estrogen)
alpha-1-antitrypsin deficiency
A1AT produced in liver, protects lungs from elastase; defienciency causes panacinar emphysema + liver cirrhosis (improperly secreted A1AT accumulates in liver)
cholesterol stones
big yellow gallstones; a/w obesity, Crohn disease, CF, old ppl, clofibrate, native americans