week 6- upper and lower GI Flashcards
1
Q
What is liver fibrosis? Causes? Ssx? Dx?
A
o excess CT scar dt chronic, repeated liver cell injury
o Causes: dos w hepatic effects, affecting hepatic blood flow, drugs, chemicals
o Ssx: asx, unless develop 2nd do
o Dx: bx
2
Q
• What is liver cirrhosis? Ssx? PE?
A
o late stage of hepatic fibrosis → widespread distortion of normal hepatic architecture
o ssx: often non-specific (anorexia, fatigue, weight loss); Late: portal HTN
o PE: Skin: Pallor, jaundice, petechiae, purpura; Abdomen: Ascites, SM; Extremities: nail clubbing
3
Q
• What is work-up for cirrhosis? Px?
A
o LFTs often normal, Albumin and bilirubin, more helpful
o PT (coag), CBC, Viral tests (to look for cause)
o Liver bx
o Px: irreversible
4
Q
• What is primary biliary cirrhosis? Ssx? PE? Work-up?
A
o AI liver do, progressive destruction of bile ducts →cholestasis, cirrhosis, liver failure
o Ssx: (insidious). Suspect in mid-age F w classic sxs: unexplained pruritis, fatigue, RUQ pn, jaundice, dry mouth
o PE: HM firm NNTP, mb SM
o Work-up: ↑GGT, ALP. abN AST and ALT. ↑ a-mito Abs. confirm w bx
5
Q
• How is blood supplied to liver?
A
o dual blood supply
o Portal v (2/3): rich nutrients, oxygen
o Hepatic a (1/3): O2 rich
o Hepatic veins: drain liver to IVC
6
Q
• How can the liver be injured?
A
o Ischemia: ischemic hepatitis, ischemic cholangiopathy
o Insufficient venous drainage: focal, diffuse, or → portal HTN
o Specific vascular lesions
7
Q
• What is ischemic hepatitis? Casues? Ssx? Work-up?
A
o diffuse liver damage dt inadequate blood, O2
o Causes: usu systemic, perfusion prob (HF, acute hypotension), Hypoxemia (resp failure, ↑CO2), ↑metabolic demand (sepsis)
o Ssx: N/V, tender HM
o Work-up: ↑aminotransferases (1000-3000IU/L), ↑bilirubin, ↑LDH (hrs). US, MRI, arteriography to identify obstructed vessel
8
Q
• What is ischemic cholangiopathy? Casues? Ssx? Work-up?
A
o focal damage to biliary tree dt disrupted flow from hepatic a via peribiliary arterial plexus
o Causes: procedure vascular injury: liver transplant, laparoscopic cholecystectomy, chemoembolization, radiation therapy→bile duct injury → cholestasis, cholangitis, biliary strictures
o SSX: Pruritis, pale stool
o Work-up: labs reveal cholestasis; UA (dark urine). US, MRCP, ERCP to r/o cholelithiasis, cholangiocarcinoma
9
Q
• What is congestive hepatopathy? Ssx? PE? Labs?
A
o RCHF →diffuse venous congestion in liver
o Ssx: usu asx, RUQ discomfort (liver capsule stretches), massive jaundice (severe)
o PE: ascites, HM, hepatojugular reflex (unlike in hepatic congestion dt Budd-Chiari syndrome)
o Lab: ↑ LFTs
10
Q
• What are the 2 hepatic artery dos? Causes, sxs, work-up?
A
o Hepatic a occlusion: dt thrombosis, emboli, iatrogenic, vasculitis, structural abn, eclampsia, cocaine, sickle cell crisis. Infarction mb asx, RUQ pain, fever, N/V, jaundice. US, angiography
o Aneurysm: uncommon. Usu saccular and multiple. Dt arteriosclerosis, trauma, vasculitis, infx. US, CT to confirm. Un-tx may → death
11
Q
• What are the 2 hepatic vein dos?
A
o Budd-chiari syndrome
o Veno-occlusice dz (Sinusoidal Obstruction Syndrome)
12
Q
• What is Budd-chiari syndrome?
A
o obstructed intra/extra-hepatic vessels → congested sinusoids, HM, portal HTN, ↓ portal blood flow, ascites, SM. Dt hypercoagulable state, clot of veins, IVC. Acute: fatigue, RUQ pn, n/v, mild jaundice, tender HM, ascites; ↑ aminotransferases. Chronic: wks-mos. Asx →fatigue, abdominal pain, HM lower extremity edema. Untx: die liver failure in 3 yrs
13
Q
• what is veno-occlusive dz?
A
o endothelial injury→non-thrombotic occlusion of terminal hepatic venules and sinusoids. dt irradiation, graft vs host disease, hepatotoxins. Suspect if unexplained liver dz AND matching hx (bone marrow transplant, irradiation, etc.). Sudden jaundice, Ascites, tender, smooth HM. ↑LFTs. US, liver bx
14
Q
• what are portal vein dos? Example?
A
o obstruct portal vein → portal HTN. Mb extra or intrahepatic
O Portal vein thrombosis: dt surgery, hypercoagulable states, CA, cirrhosis, trauma →GI bleeding from varices (usu esophagus, stomach). Usu asx unless assoc w another painful do (pancreatitis). ↑LFTs. US
15
Q
• What is peliosis hepatitis?
A
O Mult blood-filled cystic spaces randomly in liver, mm to 3 cm
O Usu dt damage to sinusoidal lining cells from hormones (OCPs, anabolic steroids), tamoxifen, vit A
O Usu asx. cysts rupture →hemorrhage, death. jaundice, HM, liver failure
O Often found incidentally on US, CT
16
Q
• What causes portal HTN? Ssx? PE?
A
O Cirrhosis (developed countries), Schistosomiasis (in endemic areas), hepatic vascular abn. →Esophageal varices, Portal-systemic encephalopathy O often asx, usu dt complications, acute variceal bleeding →sudden, painless upper GI bleeding O PE: ↓systolic BP, SM, ascites, peripheral edema, dilated abdominal wall veins, caput medusae (umbilicus), jaundice, spider angioma
17
Q
• What is work-up for portal HTN? Px?
A
O transjugular catheter (rare, invasive, to measure portal pressure). US, CT: dilated intra-abdominal collateral arteries
O Mortality >50% if acute variceal hemorrhage, depends w degree bleed and degree of hepatic reserve
18
Q
• What is portal-systemic encephalopathy? Causes? Pathophysiology?
A
O Aka hepatic encephalopathy: neuropsychiatric syndrome
O Causes: usu cirrhosis, portal HTN; fulminant hepatitis dt virus, drug, toxin
O Precipitators w liver dz: Metabolic stress (infx, electrolyte imbalance, dehydration, diuretics), dos that inc gut protein (GI bleeding, high protein diet), non-specific cerebral depressants (alcohol, sedatives, analgesics)
O Path: liver doesn’t detox →circulation →brain, mb toxic
19
Q
• What are ssx of portal-systemic encelpahlopathy? Work-up?
A
O Constructional apraxia. Uncommon: agitation and mania. Liver flap (asterixis) when arms outstretched, wrists dorsiflexed
O Wu: Psychometric eval. CMP: electrolytes, albumin, LFT. EEG: diffuse slow-wave activity
20
Q
• What is post-operative liver dysfunction?
A
O St after major surgery, even w/o of preexisting liver dos; usu dt hepatic ischemia, anesthesia
O Pts w well-compensated liver dz (eg, cirrhosis w normal LFTs) usu do well w surgery but may ↑severity of preexisting liver dos
21
Q
• What are the 3 types of post-op liver dysfunction?
A
O Jaundice: ↑bilirubin formation, ↓hepatic clearance, usu w multiple transfusions, worse few days post, clears gradually
O Hepatitis: dt insufficient liver profusion (not inflammation) → transient peri-op hypotension or hypoxia, ↑aminotransferases (>1000 units/L), mild ↑bili. only few days after, clears
O Cholestasis: extrahepatic biliary obstruction dt intra-abdominal complications, post-op drugs
22
Q
• What are the types of liver masses, CA, granulomas?
A
O Hepatic cysts O Benign liver tumors O Primary liver CA O Metastatic liver CA O Hematologic CAs O Hepatic granulomas
23
Q
• What are hepatic cysts?
A
O =fluid-filled, usu asx, no clinical significance
O incidentally on US, CT
O Rare polycystic liver assoc w polycystic kidneys, but good hepatocellular fxn, portal HTN rare
24
Q
• What are benign liver tumors?
A
o =solid, common, usu asx
o Types: Hepatocellualr adenoma, Focal nodular adenoma, Hemangiomas, lipomas, fibromas
o Ssx: HM, RUQ discomfort, IP hemorrhage
o LFTs usu normal to slightly abn; often incidental on US, CT; mb bx
25
• What is the major type of primary liver CA? ssx? Work-up? Px?
o Hepatocellular carcinoma: most common, esp East Asia and sub-Saharan Africa
o Usu w cirrhosis; common where HBV/HCV prevalent; also hemochromatosis, alcoholic cirrhosis
o Ssx: usu previously stable cirrhosis pt w RUQ pn/mass, weight loss, unexplained deterioration. St 1st sign is bloody ascites, shock, peritonitis, dt hemorrhage of tumor
o Work-up: a-Fetoprotein ↑ in40-65% (dedifferentiation of hepatocytes). CT, US, MRI. Liver bx if dx unclear
o Px: usu poor
26
• What are the other primary liver CAs?
o Fibrolamellar carcinoma, Cholangiocarcinoma, Hepatoblastoma, Angiosarcoma
o all uncommon
o Dx by liver bx, poor px
27
• What is metastatic liver CA? ssx? PE? Work-up?
o more common primary; from GI tract, breast, lung, pancreas
o asx early; non-specific: weight loss, anorexia, fever
o HM, hard, tender, palpable nodules (more severe=advanced), hepatic bruits rare, SM (esp if primary is pancreatic). Ascites from peritoneal seeding. mild jaundice
o Work-up: CT, MRI w contrast. Suspect in any pt w weight loss, HM, other primary tumor. LFTS non-specific. Dx liver bx
28
• What is the significance of the liver with hematologic cancers?
o Liver is commonly involved in advanced leukemia and blood related cancers
o Liver biopsy not needed
29
• What are hepatic granulomas? Causes? Ssx? Work-up?
o localized collections of chronic inflammatory, epithelioid, and giant multinucleated cells; not completely understood
o Causes: drugs, systemic do, infxs (TB and schistosomiasis worldwide)
o Ssx: usu asx, mb minor HM, mild jaundice; sxs reflect underlying cause (eg fever with infx)
o Work-up: LFTs; US, CT, MRI but not dx; dx by liver bx
30
• What are the inborn metabolic dos that cause hyperbilirubinemia?
o Unconj: gilbert syndrome, crigler-najjar syndrome, primary shunt hyperbilirubinemia
o Conj: dubin-johnson syndrome, rotor’s syndrome
31
• What is gilbert syndrome? Ssx? Labs?
o lifelong do, 5% of pop, dt defect in liver’s uptake of bilirubin, glucuronyl transferase activity is low, RBC destruction slightly accelerated
o usu asx
o Lab: mildly ↑ bilirubin, fluctuates 2-5mg/dL. normal LFTs, CBC. No urobilinogen
32
• What is crigler-najjar syndrome? 2 types?
o Rare inherited do, def glucuronyl transferase
o AR type I (complete) dz: Severe hyperbilirubinemia; usu die of kernicterus by 1 yr, may survive into adulthood; Tx: phototherapy, liver transplant
o AD type II (partial) dz: variable penetrance, less severe hyperbilirubinemia, live into adulthood, no neurologic damage
33
• What is primary shunt hyperbilirubinemia?
o Rare, familial, benign; overproduction of early-labeled bilirubin
34
• What are dubin-johnson and rotor syndromes?
o Conj hyperbilirubinemia wo cholestasis; only sx is jaundice
o DJ: rare, AR, impaired excretion of bilirubin glucuronides, dx liver bx, Liver is deeply pigmented dt melanin-like substance, histo normal
o R: rare, like DJ, but liver not pigmented
35
• What are the dos of the gall bladder?
```
o Cholelithiasis
o Cholecystitis: acute/chronic
o Acalculous biliary pain
o Postcholecystectomy syndrome (PCS)
o Choledocholithiasis
o Cholangitis
o Tumors of GB and bile ducts
```
36
• What is cholelithiasis? Prevalence? Risks?
o 1+ calculi (gallstones) in GB; most dos of biliary tract dt gallstones
o Prev: Developed countries: 10% adults, 20% ppl >65
o Risk: 5 F’s: female, fat, forty, fertile, FHx; American Indian ethnicity
37
• What is pathophysiology of cholelithiasis? 3 types?
o Biliary sludge, precursor to gallstones, develops during GB stasis
o Cholesterol stones: >85% in western world; bile supersaturated w cholesterol; dt excessive cholesterol secretion (obese, DM)
o Black pigment stones: small, hard; Ca2+ bilirubinate and inorganic salt
o Brown pigment stones: soft, greasy; Bilirubinate and fatty acids; dt infx, inflammation, parasites
38
• What are ssx of cholelithiasis? Work-up?
o 80% asx
o Biliary colic: RUQ pn may radiate to back, down R arm, sudden onset intense in 15-60 min, steady up to 12hr (usu <6), gradual disappear w dull ache
o n/v common w attacks
o Fever UNCOMMON unless cholecystitis has developed
o Work-up: labs unrevealing; dx abdominal US
39
• What is acute cholecystitis? Work-up?
o inflamed GB, develops over hrs, usu dt gallstone, obstructs cystic duct
o MC complication of cholelithiasis (≥95% w cholecystitis have cholelithiasis)
o Work-up: abdominal US; Cholescintigraphy if US equivocal or suspect acalculous cholecystitis; abdominal CT for complications like GB perforation (10%) → peritonitis, pancreatitis
40
• What are ssx of acute cholecystitis? PE?
o Ssx: pn like biliary colic but lasts longer (>6hr), subside 2-3 days, resolves 1 wk in 85%; Vomit common
o PE: R subcostal tenderness, (+) Murphy’s sign, Fever
41
• What is chronic cholecystitis? Ssx? PE? Work-up?
o > 1 wk, usu dt stones; range infiltrate of chronic inflam cells to fibrotic, shrunken GB; extensive calcification dt fibrosis = “porcelain gb”
o Ssx: Recurrent biliary colic; intensity not correlated to extent of damage
o PE: Upper abd tenderness, afebrile
o Work-up: abd US (Gallstones, st shrunken, fibrotic gb)
42
• What is acalculous biliary pain? Causes?
o biliary colic wo gallstones, dt structural or functional dos. Suspected when dx imaging can’t detect gallstones
o Causes: Microscopic stones, abn GB emptying, sensitive biliary tract, Sphincter of Oddi dysfunction, hypersensitive adjacent duodenum, mb gstones passed spontaneously
43
• What is work-up for acalculous biliary pan?
o Labs: abN biliary tract (↑ ALP, bilirubin, AST, ALT), or pancreatic abn (↑ lipase)
o abd US, mb endoscopic US (for small stones <1cm), ERCP w biliary manometry may reveal sphincter of Oddi dysfxn
44
• what is postcholecystectomy syndrome (PCS)? Sxs? Causes?
o abd sxs after cholecystectomy, 5-40%
o Ssx: Dyspepsia, Non-specific (not true colic), persistent pn
o altered bile flow dt loss of gb reservoir function
o Papillary stenosis (rare): fibrotic narrowing around sphincter dt trauma, inflammation dt pancreatitis, instrumentation (ERCP), prior stone passage
o retained stone
o Pancreatitis
o GERD
45
• What are consequences of PCS? Work-up?
o continuous ↑ bile flow into upper GI, may → esophagitis, gastritis
o lower GI: diarrhea, colic
o Work-up: Biliary manometry w ERCP (hi risk induce pancreatitis), ↑ P in biliary tract when pn is reproduced, ↓hepatic hilum-duodenal transit time suggests sphincter of Oddi dysfunction
46
• What is choledocholithiasis? Stone types?
o stones in bile ducts (stones can form in GB or ducts) →biliary colic, biliary obstruction, gallstone pancreatitis, cholangitis
o Primary: usu brown pigment, form in bile duct
o Secondary: usu cholesterol, form in GB and migrate to bile ducts; in developed countries >85%
o Residual: missed at cholecystectomy, seen 3yr. after surgery
47
• What are ssx of choledocholithiasis? Course?
o Ssx: may pass into duodenum asx, Biliary colic (duct partially obstructed)
o More complete obstruction: dust dilation, jaundice, eventual cholangitis (bacterial infx)
o obstruct ampulla of Vater → gallstone pancreatitis
48
• what is cholangitis? Types?
o bile duct infx/inflam, may →strictures, stasis choledocholithiasis
o acute= EMERGENCY!!!
o Recurrent pyogenic
o Sclerosing
49
• What is acute cholangitis? Ssx? PE?
o EMERGENCY!!! bile duct obstruction → bacteria ascend from duodenum
o 85% dt common bile duct stones, other dt tumors, etc
o Usu gram (-); other gram(+), mixed anaerobes
o Ssx: Charcot’s triad: abd pn, jaundice, fever/chills
o PE: RUQ TTP, HM TTP (abscesses), confusion and hypotension predict ~50% mortality rate, high morbidity
50
• What is recurrent pyogenic cholangitis? Cause?
o Intrahepatic brown stone →repeated obstruction, infx, inflame
o Stones = sludge, bacterial debris in bile ducts
o Occurs in SE Asia
o Undernutrition and parasitic infx ↑ susceptibility
51
• When should you suspect either cholangitis or choledocholithiasis?
o Both: common duct stone w jaundice and biliary colic
| o Acute Cholangitis: if fever and leukocytosis, w jaundice and biliary colic
52
• What is work-up for cholangitis (acute or recurrent)?
o suggest stone/extrahepatic obstruction: ↑bilirubin, ALP, ALT, GGT
o suggest acute: CBC and blood culture: leukocytosis, ↑AST, ALT (mb >1000IU/L) suggest hepatic necrosis dt microabscesses
o Abd US
53
• What is sclerosing cholangitis? 2 Types and causes?
```
o chronic cholestatic syndromes w patchy inflammation, fibrosis, strictures of intra/extrahepatic bile ducts
o primary: MC, unknown etio
o secondary (immune deficiencies, congenital in children, acquired in adults as AIDs cholangiopathy)
```
54
• what is assoc w primary sclerosing cholangitis? Ssx? Complications?
o 80% IBD, usu Ulcerative Colitis; unknown genetics, trigger (bacterial infx, duct injury?)
o Ssx: fatigue → pruritus →jaundice; Steatorrhea, def fat soluble vits; sx gstones, choledocholithiasis in 75%; some asx until late → HM, cirrhosis
o Comp: Cholangiocarcinoma in 10-15%
55
• What is work-up for primary sclerosing cholangitis?
o ↑ALP, GGT; ↑Gamma globulin and IgM; no anti-mito ab
o 1st US to r/o extrahepatic biliary obstruction
o MRCP: mult strictures in intrahepatic and extrahepatic bile ducts
o ERCP (2nd choice bc invasive)
o Liver bx: no need for dx, but show bile duct proliferation, periductal fibrosis, inflammation, loss of bile ducts
56
• What is AIDS cholangiopathy? Ssx? Work-up?
o Biliary obstruction 2nd to biliary tract strictures dt opportunist infxs
o Before ARV tx, cholangiopathy in 25% AIDs pts, esp w ↓CD4
o Ssx: RUQ, epigastric pn; severe pain usu indicate papillary stenosis; milder pain suggest sclerosing cholangitis; Diarrhea; few fever, jaundice
o Work-up: like cholestasis, ↑ ALP, GGT; ERCP and US
57
• What are the GB ad bile duct tumors?
o can cause extrahepatic biliary obstruction
o cholangiocarcinoma
o GB carcinoma
o GB polyps
58
• What is cholangiocarcinoma? Risk factors? Ssx? PE?
```
o Rare (1-2/100,000), usu malignant, usu in extrahepatic bile duct
o Risk: primary sclerosing cholangitis, 50-70, infestation with liver flukes, choledochal cyst
o Ssx: pruritis, pnless obstructive jaundice, abd pn, anorexia, weight loss
o PE: non-tender palpable mass (Courvoisier’s sign), HM
```
59
• What is GB carcinoma? Risk factors? Ssx? Px?
o rare (2.5/100,000 people)
o risk: Native American ethnicity, large gall stones (>3cm), GB calcification dt chronic cholecystitis (porcelain GB); 70-90% have gallstones
o ssx: varies w course, asx → biliary pain → advanced dz, constant pain, weight loss, abd mass, obstructive jaundice
o px: avg live 3 mo; cure possible if found early
60
• what are gb polyps?
o Usu asx, small, benign mucosal projections develop in lumen of GB
o found incidentally on US, require no tx
61
• What is the approach to a pt with lower GI conditions?
o Hx: Thorough questioning about sxs, bowel habits, stool characteristics
o PE : Abd exam; Peritonitis (Blumberg sign), Appendicitis (McBurney’s pt rebound/tenderness, Rovsing’s sign, Psoas/Obturator sign, Ascites (fluid wave and shifting dullness), Cholecystitis (Murphy’s sign), pyelonephritis (CVA tenderness)
o DRE, pelvic/gyn exam, male genitalia exam
o Lab: CBC, CMP, amylase/lipase, stool culture, CDSA (comp digestive stool analysis), GI health panel, O&P (ova and parasite exam for diarrhea), serology
o abd x-ray, US, endoscopy, sigmoidoscopy, colonoscopy, CT, MRI
62
• what are some stool characteristics found on hx, and indications?
o Ideal: large, soft, well-formed, no straining
o Alternating constipation and diarrhea: poor dietary habits, parasite infx, IBS, LV-GB dz
o Diarrhea: more severe irritation, malabsorption, infx
o Loose, not watery: mild intestinal irritation, malabsorption
o Difficult to pass: hemorrhoid, anal fissure, hypotonic bowel, ↓fiber, dehydration, pelvic muscle dysfunction
o Floating: fat malabsorption, ↓ transit time, ↑fiber
o Large and hard:dDehydration, hypotonic bowel
o Small and hard: ↓ fiber, ↓ transit time, dehydration, hypochlorhydria
o Pencil-shaped: spasm, IBS, colon stricture
o Ribbon-shaped: uterus mal-position, IBS, compression from mass
63
• What are stool odors and indications?
o Normal: little odor, good absorption and digestion
| o Offensive: malabsorption, food decay, dysbiosis
64
• What are stool colors and indications?
o Normal: medium brown, consistent
o Dark brown consistently: excessively alkaline colon, dysbiosis
o Very dark or black (melena)- blood loss from up high (ulcer, Crohn's, esophagitis, CA) pepto-bismol, iron
o Clay-colored: ↓ bile pigments, GB or LV obstruction
o Greenish/yellow: ↑ bile secretions
o Greasy, shiny: lipid malabsorption
o Blood visible (hematochezia): hemorrhoids, fissures, colitis, CA, diverticulitis, parasites
o Mucus: excessive production from irritation (colitis, food sensitivity, pancreatitis)
65
• What is ddx for abdominal pain in RUQ? LUQ? Epigastric?
o RUQ: Hepatitis, Cholecystitis/Cholelithiasis, Cholangitis, Biliary colic, Budd-Chiari syndrome, Pancreatitis, Pneumonia/pleurisy
o LUQ: Speen infarct, Splenic rupture, Gastritis, Gastric ulcer, Pancreatitis, Hiatal hernia (incarcerated)
o Epi: GERD, Gastritis, PUD, Pancreatitis, MI, Pericarditis, Ruptured aortic aneurism
66
• What is ddx of abdominal pain in right and left flank? Periumbilical? Suprapubic?
o R or L: Kidney inflm, Pyelonephritis
o Periumbilical: Early appendicitis, Gastroenteritis, Bowel obstruction, Peritonitis
o Suprapubic: Cystitis, Acute urinary retention, Female (uterine cramps, cervicitis, endometriosis, PID), Male (acute prostatitis)
67
• What is ddx for abdominal pain in RLQ? LLQ?
o RLQ: Appendicitis, IBD, Cecal diverticulitis, Inguinal hernia, Nephrolithiasis, Female (ovarian cyst rupture/torsion, salpingitis, endometriosis, ectopic pg), Male (testicular or epididymal inflame)
o LLQ: Diverticulitis, IBD, IBS, Nephrolithiasis, same female/male conditions
68
• What is ddx of diffuse abdominal pain?
o early appendicitis, gastroenteritis, intestinal obstruction, mesenteric ischemia, peritonitis, IBS
69
• what are some extra abdominal causes of abdominal pain?
```
o Abdominal wall (hematoma)
o Infectious (herpes zoster)
o Metabolic (DKA, porphyria, sickle cell dz)
o Thoracic (MI, PE, radiculitis)
o Toxic (spider bite, heavy metal poisoning, opioid withdrawal)
```
70
• What is diarrhea? Name the 4 major mechanism:
o >200g/d stool weight (norm: 100-200), ↑stool fluidity, or >3 BM/d
o Osmotic, secretory, exudative, motility
71
• What is osmotic diarrhea? Causes?
o too much water drawn into bowels, ↑ poorly absorbable solutes.
o maldigestion (pancreatic dz, celiac dz)
o osmotic laxatives, ions (MgSO4/epson salts), Mg, vit C
o undigested lactose (lactose intolerance)
o sugar alcohols (sorbitol)
72
• What is secretory diarrhea? Causes?
```
o ↑active secretion (Cl, water) or inhibed absorption (Na, water), little/no structural damage.
o enterotoxins (cholera, E. coli, staph)
o hormones (5HT, PGs)
o gastric hypersecretion (Zollinger-Ellison, short bowel)
o laxatives (castor oil, aloe, senna)
o bile salts: terminal ileal dz/resection, bile duct obstruct
o fatty acids: pancreatic insufficiency, SI mucosal dz
```
73
• What is exudative diarrhea? Causes?
o mucous, blood, protein from inflammation
o idiopathic: Crohn’s, UC
o infectious: shigella, salmonella, camphylobacter
o ischemic, vasculitis, radiation injury
74
• what is motility diarrhea?
o ↑ colonic motility: IBS
o Inc or dec contact bw GI contents and mucosal surface
o ↑: hyperthyroidism, postgastrectomy
o ↓: DM, hypothyroid, scleroderma
75
• What are red flags w diarrhea? Complications?
o blood, pus, fever, dehydration ssx, chronic, unintended wt loss, failure to thrive in kids
o comp: dehydration, electrolyte imbalance (Na, HCO3, K, Mg)
76
• what is constipation? Types? Red flags?
```
o =difficult to pass, infrequent, hard, incomplete feeling
o Acute (organic): Obstruction, adynamic ileus, meds (anticholinergics, opioids, etc)
o Chronic (functional or organic): Carcinoma, hypothyroid, CNS dos, slow transit, IBS
o RF: abdominal distention, vomiting, blood in stool, weight loss, severe or worsening symptom
```
77
• What is gas? Red flags? Common sxs w cause?
o colonic bacterial fermentation of nutrients, air swallowing (H2, CH4, CO2)
o RF: weight loss, blood in stool
o Belching: air swallowing, carbonated beverages, voluntary
o Bloating/distension: air swallow, IBS, gastroparesis, eating do, gynecologic
o Flatus: Diet, carb insufficiency (def dig), Celiac, pancreatic insufficiency
78
• What is GI bleeding? Causes of lower GI bleeding?
o gross or occult blood. Hematochezia: gross blood suggests lower GI bleed.
o SI: angioma, AV malformation, tumors, Meckel’s diverticulum
o Colon, anus: anal fissure, colitis (radiation, ischemic, infectious), carcinoma, polyps, diverticular dz, IBD, hemorrhoids
79
• What is dyschezia? Cause?
o difficulty evacuating: feel urge, but can’t defecate
| o often dt discoordination of rectal muscles and sphincter: hypotonia, prolapse
80
• what are some stool lab findings correlating w SI as source?
```
o Appearance: watery
o Vol: large
o Freq: ↑
o Blood: possible, never gross blood
o pH: possibly < 5.5
o WBC: < 5 /hpf (high power field)
```
81
• what are some stool lab findings correlating w LI as source?
```
o Appearance: mucoid and/or bloody
o Vol: small
o Freq: very hi ↑
o Blood: gross blood common
o pH: >5.5
o WBC: > 10/hpf common
```
82
• Why/how is an O&P done?
o x3 (3 samples)
o To find protozoa, worms, worm eggs, other parasites
o If one family member (+) usu tx. whole family (esp if food handler)
83
• What is commonly found on (+) O&P?
o Parasites: Entameba, Giardia, Cryptosporidium, Dientamoeba fragilis, Balantidium coli, Cyclospora cayetanensis
o Worms: Roundworms (Ascaris, Strongyloides), Hookworms, Tapeworms (Hymenolepis nana, Taenia solium, Diphyllobrithium), Flatworms and flukes (Fasciolopsis buski)
84
• When is a stool culture done?
o Immunocompromised
o Severe, inflammatory diarrhea
o IBD to distinguish bw flare and infx
85
• When is Fecal Occult Blood (Hemoccult) done? Fecal leukocytosis?
o to detect upper GI bleed
| o FL: w occult blood, can help confirm bacterial cause of diarrhea
86
• What is Fecal lactoferrin (latex agglutination assay)?
o marker for fecal WBCs
| o distinguish bw inflammatory diarrhea (bacterial infection, IBD) and non-inflammatory causes (viral infection, IBS)
87
• what is fecal lysozyme?
o N = absence of colonic inflammation and suggests irritation only
o marker to measure success of IBD tx
88
• what is a Comprehensive digestive stool analysis?
o Eg CDSA, GI Health Panel
| o Markers for digestion, absorption, metabolism, plus microbiology
89
• What is Salival secretory IgA (sIgA) significance in GI dos? Serology?
o ↓: celiac, IBD, allergy, chronic infx, chronic stress; more susceptible to GI Infx
o ↑: acute GI infx
o Sero: eg Celiac testing for antibodies
90
• What is bowel transit time? Retention time?
o B: variable, but usu start to see test substance at 12-14 hrs
o R: (N 36-48 hrs), sufficient mixing and normal tone in colon
o Short: spastic, tonic, no mixing, not enough time to digest, microflora imbalance
o long >72 hrs: atonic colon, poor muscle tone
91
• what are some procedures for lower GI work-up?
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o Anoscopy: in-office, to visualize hemorrhoids
o Sigmoidosopy, Colonoscopy: out-patient
o Endoscopy (upper GI): out-patient
o Abdominal plain film (xray)
o CT & MRI
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92
• What are visceral, parietal/somatic, and referred types of acute abdominal pn?
o V: ANS nerve fibers on viscera respond to distention and ms contraction; Sensations are vague, dull, nauseating, poorly localized
o P/S: somatic nerves in parietal peritoneum respond to irritation (infx, chem); Sensations are sharp and localized
o R: perceived pain (aching) distant from source, not reproducible at distant site
93
• What are possible causes of acute inflammation? Ischemia? Obstruction?
o Inflamm: appendicitis, cholecystitis, pancreatitis, diverticulitis, abscess, cystitis, regional enteritis, toxic megacolon
o Ischemia: Ischemic colitis (occlusive or non-), pulm embolism, MI
o Obstruct (pt restless): neoplasm, adhesions, intussusception, gallstone in duct
94
• How can a perforation/rupture cause acute abd pn?
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o Release of luminal contents
o Ulcers (esophagus, stomach), obstruction, ectopic pregnancy, cysts, appendicitis, cholecystitis
```
95
• What is peritonitis? Causes?
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o inflammation of peritoneal cavity (pt stays still)
o Perforation (chem inflam → bacterial infx), cholecystitis, pancreatitis, PID, toxic megacolon, diverticulitis, mesenteric ischemia
```
96
• How do you take hx for acute abd? PE?
o Hx: LMNOPQRST, concomitants, drugs, PMHx, surgery, pregnant? Recent travel
o PE: acute observations (anxious, pale, sweating, in obvious pain, restless/still), vitals, state of consciousness, Inspection, Auscultation, Percussion, Palpation; Special tests as needed
97
• What is appendicitis? Pathophysiology? Incidence?
o Acute inflammation of vermiform appendix
o Mc cause of acute abdominal pn, usu requires surgery
o Path: obstruction → appendiceal distention, bacterial overgrowth, ischemia; → possibly necrosis, gangrene (from E coli, Bacteriodes, Ppseumonas), perforation
o Incidence: gradually ↑ from birth, peaks 10-19, ↓ in geriatric years. M:F 1.4:1
98
• What can cause appendicitis?
```
o obstruction of appendiceal lumen from:
o lymphoid hyperplasia assoc w variety of inflammatory and infectious dos (Crohn’s, gastroenteritis, amoebiasis, respiratory infxs, measles, mononucleosis)
o fecaliths: Ca salts and fecal debris layered around a nidus of fecal material l in appendix
o parasites (Schistosomes, Strongyloides), foreign material (IUD, tongue stud, activated charcoal), TB, tumors (benign or malignant)
```
99
• what is the classic presentation of appendicitis?
o Periumbilical pain → N/V, anorexia. Pain then migrates to RLQ. Onset in < 48hrs (longer in elderly) ( “typical” in < motion, deep resp, coughing, sneezing) from periumbilical to RLQ (sn, sp ~80%)
o N/V can occur after onset pain. Vomiting that precedes pain suggests intestinal obstruction
o Anorexia common , St Constipation
o Concomitant: inflamed appendix near bladder/ureter → irritative voiding, hematuria, pyuria (ddx cystitis)
o male infant/kid st have inflamed hemiscrotum dt migration of inflamed appendix or pus thru a patent processus vaginalis (ddx testicular torsion)
100
• what PE is done for appendicitis?
o Low grade fever (101°) initially, may rise as inflammation worsens
o McBurney’s point tenderness
o Rebound tenderness, pain on percussion, rigidity, guarding
o Rovsing’s sign (+), Obturator sign (+), Psoas sign (+) esp in retrocecal appendix, Cough sign
o RLQ pn dt percussion of remote quadrant, or firm percussion of heel (suggests peritoneal inflammation)
o Markle sign: heel drop →pain at McBurney’s point
o DRE and pelvic exams needed to differentiate retrocecal appendix or adenexal mass
101
• What is work-up for appendicitis?
o CBC: 80-85% adults WBC > 10,000 w left shift (↑ w development of necrosis or perforation)
o Contrast-enhanced CT (esp for atypical presentations)
o Graded compression abd US
102
• What is ddx for appendicitis?
o Females: PID (r/o by hx, pelvic exam), ovarian pathology, endometriosis
o Males: epididymitis, testicular torsion
o Acute gastroenteritis or ileitis: N/V, pain more generalized, diarrhea
o Pancreatitis, Crohn’s, cholecystitis, pyelonephritis, IBS, renal colic
o Cecal diverticulitis, Meckel’s diverticulitis
o Children: volvulus (twisted bowel), intussusception (intestine slides into intestine)
103
• What is “chronic appendicitis?
o prolonged (>7 days) RLQ intermittent pain, normal WBC
o Histo: fibrosis/chronic inflamed appendix.
o Some may have a retained foreign body.
104
• What is acute mesenteris ischemia? Risk factors? Age?
o Emergency!
o ↓ mesenteric blood flow →bowel wall ischemia, inflammation, infarction (Sup mesenteric a, Inferior mesenteric a @ splenic flexure)
o risks: CAD, atrial fibrillation, hypercoaguable state, portal hypertension
o rare <60
105
• What are two mechanisms of etio of acute mesenteric ischemia?
o ↓ bowel perfusion dt ↓ CO, w cardiac dz (CHF), shock (MC),) drugs (vasopressors, cocaine)
o occlusive vascular dz of supply to bowel dt thrombosis, embolism; collateral circulation insufficient
106
• what are ssx of acute mesenteric ischemia? Imaging?
o Emergency! After infarct, mortality rate 70-90%
o ***Suspect if: >50, predisposing conditions, sudden onset severe abd pn
o severe abd pain w minimal physical findings (soft abd, little tenderness)
o Sudden onset pain suggests arterial embolism; gradual suggests venous thrombosis
o necrosis → peritoneal signs: abd tenderness, guarding, absent bowel sounds
o Hemoccult positive, shock sxs
o Imag: Mesenteric angiography, abd plain film or CT
107
• What is ischemic colitis?
o Episodic, transient ↓blood flow to bowel, dt small vessel atherosclerosis
o Milder, slower onset: LLQ pain, rectal bleeding
o Colonoscopy: mb mucosa and submucosa necrosis
108
• What is a hernia of the abdominal wall?
o emergency if strangulated!
o Acquired (surgical) or congenital weakness in abd wall (umbilical, epigastric)
o → protrusion of abd contents, asx unless strangulated → ↑pn, N/V, signs of peritonitis
o Surgical repair needed
109
• What is intestinal obstruction? Class? Path? Cause?
o emergency!
o Complete or partial blockage (mechanical) of S/L I
o Classifications: Complete or partial , Simple or strangulated, Location (high SI, low SI, LI), Onset: acute or gradual
o Path: Proximal bowel distends, distal bowel collapses. Walls edematous. Strangulation w ↓ blood flow → infarction/gangrene in <6h!
o Causes: adhesions, hernia, tumor, diverticulitis, foreign body, volvulus, intussusception, fecal impaction
110
• What are ssx of S/L I obstruction? Work-up?
o S: sudden onset Periumbilical/epigastric cramping, vomiting. Complete obstruction (obstipation); partial obstruction (diarrhea), NT abd if no strangulation, Severe constant pain if strangulation, mb palpable dilated loops of bowel
o L: gradual onset pain, obstipation, vomiting; NT abd distention, mb palpable mass, borborygmi
o Work-up: abd X-ray (bowel loops, fluid lines, distention), Volvulus: contrast enema w “bird-beak” deformity
111
• What is ileus? Causes? Ssx? PE? Work-up?
o Adynamic Ileus, Paresis, Paralytic Ileus
o Temporary arrest of intestinal peristalsis
o Causes: post-surgical, appendicitis, diverticulitis, perforation, AAA, hypokalemia, drugs (opiates, anticholinergics), lower lobe pneumonia, MI
o SSX: distention, vomiting, abd discomfort, colicky pain, watery stool
o PE: absent bowel sounds. NT abd (unless cause is inflammatory)
o Work-up: free air seen (usu colon) on abd x-ray or CT
