GI system Flashcards
Cirrhosis gen info
A. chronic liver dz d/t fibrosis, disruption of architecture, widespread nodules in the liver. There is hepatocellular injury that leads to replacement of dead or damaged cells with fibrous tissue
B. generally irreversible when advanced, can be reversible in early disease
C. distortion of liver anatomy causes two major events: (1) decr blood flow thru liver –> portal HTN –> ascites, peripheral edema, splenomegaly, varicosity of veins (gastric/esophageal varices, hemorrhoids) (2) hepatocellular failure –> impairment of biochemical fxns –> decr albumin and clotting factor synthesis
D. assessment of hepatic functional reserve –> child-pugh score estimates hepatic reserve, used to measure disease severity, predictor of morbidity and mortality. Class C = most severe dz, class A = mild dz
Cirrhosis causes
Alcoholic liver dz mc, chronic hep B and C 2nd mc, drugs, autoimmune hepatitis, PBC, PSC, inherited metabolic dz (hemochromatosis, wilson disease), hepatic congestion 2ry RHF, constrictive pericarditis. Alpha 1 antitrypsin deficiency, hepatic venoocclusive disease, NAFLD
Cirrhosis clinical features and complications
some asxs, may have sxs suggestive of one or more complications: AC 9H ascites, coagulopathy, hypoalbuminemia, hypoglycemia, portal HTN, hyperammonemia, hyperbilirubinemia, hyperestrinism, hepatic encephalopathy, hepatorenal syndrome, HCC (presents 10-25% of pts with cirrhosis)
varices, SBP
gen: anorexia, hepatosplenomegaly, gynecomastia, testicular atrophy, spider angioma, telangiectasias, hemorrhoids, caput medusa, muscle wasting, bleeding, palmar erythema, jaundice, dupuytren’s contractures, confusion, lethargy, asterixis
Cirrhosis diagnosis
liver biopsy is gold standard
classify severity of disease with child pugh or meld score
Cirrhosis comp vs decomp
development of complications of cirrhosis = decompensated disease with high morbidity and mortality
Cirrhosis comp: portal HTN
a. bleeding (hematemesis, melena, hematochezia), 2ry to esophagogastric varices = most life-threatening complicaiton
b. paracentesis can help dx
c. TIPs can be used to lower BP
Cirrhosis comp: varices
a. esophageal/gastric
- high mortality rate, screen, if present tx prophylactically with nonselective BB)
- sxs: massive hematemesis, melena, exacerbation of encephalopathy
- esophageal 90%, gastric 10%
- initially stabilize HD; fluids,
- IV abx prophylactically
- IV ocreotide (splanchnic vasoconstriction) > vasopressin (mesenteric vessels vasoconstriction) x 3-5 days
- emergent upper GI (once stabilized) for dx and to tx hemorrhage w variceal ligation > sclerotherapy (alt esophageal balloon tamponade temporarily, TIPs, surgical shunts, liver transplant)
- nonselective BB (propranolol, timolol, nadolol) long-term to prevent rebleeding.
b. rectal hemorrhoids
c. caput medusae (distention of abdominal wall veins)
Cirrhosis comp: ascites
ddx: CHF, chronic renal disease, massive fluid overload, TB peritonitis, malignancy, hypoalbuminemia, peripheral vasodilation 2ry endotoxin induced release of NO leading to incr renin secretion and 2ry hyperaldosteronism
a. accumulation of fluid in peritoneal cavity d/t portal HTN (incr hydrostatic pressure) and hypoalbuminemia (reduced oncotic pressure)
b. sxs - abdominal distension, shifting dullness, fluid wave
c. abd US (detects as little as 30 ml fluid)
d. diagnostic paracentesis - distinguishes from another process. Ind - new onset, worsening, or suss SBP. Examine cell count, albumin, gram stain, culture, serum ascites albumin gradient (>1.1 g/dL likely portal HTN, less than that is unlikely portal HTN,
e. tx - bed rest, low Na diet, and diuretics (furosemide, spironolactone), therapeutic paracentesis ind - tense ascites, SOB, early satiety; peritoneovenous shunt or TIPs to reduce portal HTN
Cirrhosis comp: hepatic encephalopathy
a. toxic metabolites (many but ammonia most important) that are normally detoxified or removed by the liver, accumulate and reach the brain
b. occurs in 50% of all cases with varying severity
c. precipitants - alkalosis, hypokalemia (diuretics), sedating drugs (narcotics, sleeping meds), GI bleeding, systemic infection, and hypovolemia
d. sxs - AMS, confusion, poor conc, stupor or coma, asterixis, rigidity, hyperreflexia, fector hepaticus (musty breath odor)
e. tx - lactulose prevents absorption of ammonia, metabolism
Cirrhosis comp: hepatic encephalopathy
a. toxic metabolites (many but ammonia most important) that are normally detoxified or removed by the liver, accumulate and reach the brain
b. occurs in 50% of all cases with varying severity
c. precipitants - alkalosis, hypokalemia (diuretics), sedating drugs (narcotics, sleeping meds), GI bleeding, systemic infection, and hypovolemia
d. sxs - AMS, confusion, poor conc, stupor or coma, asterixis, rigidity, hyperreflexia, fector hepaticus (musty breath odor)
e. tx - lactulose prevents absorption of ammonia (metabolism of lactulose by colon bacteria favors formation of NH4+ –> poorly absorbed from GI tract, promoting excretion of ammonia). Rifaximin (abx) kills bowel flora so decr ammonia production by intestinal bacteria. Limit protein to 30-40 g/day.
Cirrhosis comp: hepatorenal syndrome
indicates end-stage liver disease
progressive renal failure in advanced liver dz, 2ry to renal hypo-perfusion resulting from vasoconstriction of renal vessels
b. often precipitated by infection or diuretics
c. functional renal failure - kidneys are normal morphology and no specific causes of renal dysfunction are evident, condition does not respond to volume expansion
d. sxs- azotemia, oliguria, hyponatremia, hypotension, low urine sodium < 10 meq/L
e. tx- liver transplantation is only cure, prognosis very poor, condition usually fatal without liver transplantation
Cirrhosis comp: hepatorenal syndrome
indicates end-stage liver disease
a. vasoconstriction of renal vessels –> renal hypo-perfusion –> progressive renal failure in advanced liver dz
b. often precipitated by infection or diuretics
c. functional renal failure - kidneys are normal morphology and no specific causes of renal dysfunction are evident, but condition does not respond to volume expansion
d. sxs- azotemia, oliguria, hyponatremia, hypotension, low urine sodium < 10 meq/L
e. tx- liver transplantation is only cure, prognosis very poor, condition usually fatal without liver transplantation
Cirrhosis comp: SBP
infected ascitic fluid; occurs up to 20% of hospitalized patients; look for fever +- AMS in pt with known ascites.
a. usually in patients with ascites caused by ESLD, a/w high mortality rate 20-30%
b. has high recurrence rate (up to 70% in 1st yr)
c. etiologic agents - e coli mc, klebsiella, strep pneumoniae
d. sxs - abd pain, fever, vomiting, rebound tenderness, can lead to sepsis
e. dx established by paracentesis and exam of ascitic fluid for WBCs (esp PMNs), gram stain w culture and sensitivities. WBC> 500, PMN > 250, + culture (culture neg common as well!)
if not tx early mortality is high so have high index of suss (diagnostic paracentesis early on)
Cirrhosis comp: hyperestrinism
occurs d/t reduced hepatic catabolism of estrogens
a. spider angiomas - dilated cutaneous arterioles with central red spot and reddish extensions that radiate outward like spider web
b. palmar erythema
c. gynecomastia
d. testicular atrophy
Cirrhosis comp: coagulopathy
occurs 2ry decr synthesis of clotting factors
a. prolonged prothrombin time (PT), PTT may be prolonged with severe disease
b. vit K ineffective bc can’t be used by diseased liver
c. tx coagulopathy with FFP
Cirrhosis treatment
treat underlying cause; ETOH abstinence, interferons for hep B & C
avoid agents that may cause liver injury eg tylenol, etoh
once cirrhosis develops, aim tx to manage complications, most serious are varcieal bleeding, ascites, hepatic encephalopathy
liver transplant only definitive cure, no etoh for 6 mos prior required, decision depends on quality of life, severity of dz, absence of contraindications
Cirrhosis treatment
refer to hepatic specialist
treat underlying cause; ETOH abstinence, interferons for hep B & C
preventive; provide adequate nutrition (MVI, minerals)
vaccinate against hep a + b
screen for varices, HCC
pts w cirrhosis + GIB –> abx prophylaxis (ctx)
avoid agents that may cause liver injury eg tylenol, etoh
once cirrhosis develops, aim tx to manage complications, most serious are varcieal bleeding, ascites, hepatic encephalopathy
liver transplant only definitive cure, no etoh for 6 mos prior required, decision depends on quality of life, severity of dz, absence of contraindications
pentoxifylline may reduce complications but may not decr mortality in pts with advanced dz
moderate sodium restriction, free water < 1 L/day
no protein restriction
caution with pain medicine (no NSaids)
Signs of acute liver failure
any of the following coagulopathy jaundice hypoglycemia (liver stores glycogen) hepatic encephalopathy infection elevated LFTs any complication a/w cirrhosis
Acute mesenteric ischemia
results from a compromised blood supply, usually to the superior mesenteric vessels
4 types (3 d/t arterial dz, 1 to venous dz)
a. arterial embolism (50% cases), almost all cardiac origin (a-fib, MI, valvular dz)
b. arterial thrombosis (25%), most have atherosclerotic dz (CAD, PVD, stroke) at other sites. Acute occlusion occurs over preexisting atherosclerotic dz, acute event may be d/t decr in CO cardiac output (MI, CHF) or plaque rupture. Collateral circulation has usually developed.
c. nonocclusive mesenteric sichemia (20%) splanchnic vasoconstriction 2ry to low CO, seen in critically ill elderly patients
d. venous thrombosis
Acute mesenteric ischemia
results from a compromised blood supply, usually to the superior mesenteric vessels
4 types (3 d/t arterial dz, 1 to venous dz)
a. arterial embolism (50% cases), almost all cardiac origin (a-fib, MI, valvular dz)
b. arterial thrombosis (25%), most have atherosclerotic dz (CAD, PVD, stroke) at other sites. Acute occlusion occurs over preexisting atherosclerotic dz, acute event may be d/t decr in CO cardiac output (MI, CHF) or plaque rupture. Collateral circulation has usually developed.
c. nonocclusive mesenteric sichemia (20%) splanchnic vasoconstriction 2ry to low CO, seen in critically ill elderly patients
d. venous thrombosis (<10%) many predisposing factors; infection, hypercoagulable states, ocps, portal HTN, malignancy, pancreatitis
overall mortality for all types = 60-70%
with bowel infarction = >90% mortality rate
AMI much more common than chronic MI
*** pts often with pre-existing heart dz (CHF, CAD)
AMI different presentations based on types
embolic - sx more sudden and painful
thrombotic - sx more gradual and less severe
nonocclusive ischemia - with critically ill pts
venous thrombosis - sx for several days or even weeks with gradual worsening
AMI SXS
classically acute onset of severe abd pain disproportionate to physical findings, pain d/t ischemia =- infarction of intestines, analogous to MI in CAD
abd exam may appear benign even when there is severe ischemia
acuteness/severity of pain varies based on type
anorexia, vomiting, mild GI bleed, peritonitis, sepsis, shock
intestinal infarction sx- hypotension, tachypnea, lactic acidosis, fever, AMS, shock. Check lactate level if suss
AMI DX
mesenteric angiography definitive
obtain plain film of abd to exclude other causes
“thumbprinting” on barium enema d/t thickened edematous mucosal folds
