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;
164 Cards in this Set
- Front
- Back
- 3rd side (hint)
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
|
|