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GI/GU II Exam 2 > DSA 6: Chronic hepatitis, Chronic liver disease, Cirrhosis > Flashcards

DSA 6: Chronic hepatitis, Chronic liver disease, Cirrhosis Flashcards

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1
Q

what is the etiology of chronic hepatitis?

how does it present?

A

group of d/o’s chronic inflam rxn in the liver for at least 6 months

common sxs: fatigue, malaise, anorexia, low-grade fever, jaundice

some pts - complication of cirrhosis

HBV: polyarteritis nodosa

HCV: mixed cryoglobulinemia

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2
Q

what is diagnositic for chronic hepatitis

A

CBC (platelets), chem panel, coag studies

Bx: historic classification - grade-necrosis/inflam & stage- degree of fibrosis

identify presence/absence of fibrosis (cirrhosis) : serum fibrosure &/or US elastography

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3
Q

what is the etiology of chronic HBV

A

endemic: Asia & sub-saharan Africa (90% vertical transmission)

Asymp healthy carrier stat - 75% Asia & Pacific rim

younger the age of infection - higher the probablity of chronicity

Risk HCC & cirrhosis: M>F

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4
Q

What increases/decreases progression of HCV?

A

increase: Male, drink > 50g EtOH daily, acquire infection after 40 yo, immunocompromised, tobacco/cannibis/fatty liver promote fibrosis

high risk of cirrhosis & HCC in genotype 1b

decrease: coffee

HCV Ab + HCV RNA = chronic

most HCV is curable

normal AST/ALT

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5
Q

what is the presentation and PE of AIH

A

type 1 (MC): Anti-Sm M &/or ANA (F, 30-50)

type 2: anti-LKM Ab

progessive jaundice, epistaxis, amenorrhea

healthy young woman w/ stigmata of cirrhosis - multiple spider telangiectasias, cutaneous striae, acne, hirsutism and hepatomegaly

extrahepatic: AI sxs, UC

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6
Q

what is diagnostic of AIH

A

AST/ALT may be > 1000

increased total bili

serology:

type 1: hypergammaglobulinemia, SMA, ANA

type 2: anti-LKM Ab

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7
Q

what is Tx for AIH

A

glucocorticoids

indicated for sxs dz: Bx shows bridging necrosis, 5-10x AST/ALT, hypergammaglobuliemia

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8
Q

what are complications of AIH

A

leads to cirrhosis –> HCC

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9
Q

what is the etiology of alc liver dz (SAAD > 1.1)

A

excessive: >80g/day in males & 30-40g/day in females x 10 yrs

(often deny Hx of excess alc use)

fatty liver (steatosis) : asymp- hepatomegaly & mild elevation in biochem livers (reverse if stop EtOH)

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10
Q

what is the clinical presentation of alcohol liver dz

A

asymp –> severe dz w/ jaundice, ascites, GI bleeds and encephalopathy

anorexia, N/V, fever, jaundice, tender hepatomegaly & RUQ pain

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11
Q

what lab are diagnostic of alcoholic liver dz (SAAG > 1.1)

A

chem (CMP) - AST 2x > ALT; Bili >=10 mg/dL

CBC: leukocytosis (severe) and leukopenia (sometimes and resolve after drinking), anemia (macrocytic/megaloblastic); thrombocytopenia

PT/PTT/INR: marked prolongation of PT

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12
Q

what imaging diagnostics are found in alcohol liver dz

A

imaging: US- exclude biliary obstruction; CT w/ IV contrast/MRI: collateral vessels, space-occupying lesions; US elastography: fibrosis

liver Bx: mallory-denk bodies

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13
Q

what is the treatment for alcoholic liver dz

A

abstinence from alcohol

daily multivitamin, thiamine 100 mg, folic acid 1 mg, zinc: glucose administration increase thiamine requirement & can cause wernicke-korsakoff syndrome if thiamine not co-administered

severe alcoholic hepatitis = steroids, pentoxifylline

liver transplant - abstain from alc for 6 months

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14
Q

what is the prognosis and complications of alcoholic liver dz (SAAG >1.1)

A

MC precursor to cirrhosis in US –> risk of HCC

wernicke-encephalopathy- treat w/ thiamine

korsakoff (permanent)

adverse prognostic factors: poor prognosis -ascities, variceal hemorrhage, encephalopathy, hepatorenal syndrome. critically ill pt w/ alc hepatitis have 30 day mortality rate >50%

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15
Q

what is labs/symptoms present in severe alcoholic hepatitis

A

total bili > 8-10 and PTT > 6 = (50% mortality/susceptible to infxn, including invasive aspergilosis)

hypoalbuminemia, azotemia

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16
Q

what is

Maddrey’s discriminant fxn (DF)

Glasgow alc hepatitis score

A model for End-stage liver dz

A

Maddrey’s discriminant fxn (DF): >=32 - poor prognosis; may benefit from steroids

Glasgow alc hepatitis score: predict mortality based on multivariable model; >= 9 -higher survival rates

A model for End-stage liver dz: >21 significant mortality in alc hepatitis

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17
Q

what is hepatic steatosis and what is the etiology

A

fatty liver –> fatty liver that causes liver inflam = steatohepatitis –> cirrhosis

etiology: alc related or non-alc fatty liver dz (NAFLD) - < 20 g/day F and <30 g/day M

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18
Q

wha tis the etiology of NAFLD

A

MCC of chronic liver dz in USA

principal causes & increased risk for NAFLD - metabolic syndrome (obesity, DM, hypertriglyderigemia) - increased risk for CV disease, CKD, colorectal CA

protective: physical activity & coffee consumption

cirrhosis caused by NASH is UNCOMMON in african americans

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19
Q

what is the presentation and PE of NAFLD

what is the complication

A

asymp or mild RUQ

hepatomeg

complication - cirrhosis

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20
Q

what is diagnositic of NAFLD

A

labs: mild increase AST/ALT and ALP - may be normal =< 80% hepatic steatosis

imaging - US elastography- assess liver stiffness can be used to ESTIMATE hepatic fibrosis

Liver Bx = Diagnostic - histologic- local infiltration by PMN and mallory hylaine,indistinguishale from alc hepatitis, =NASH

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21
Q

what is the treatment/management of NAFLD

A

lifestyle modifications- wt loss, dietary fat restriction, exercise, vit E, gastric bypass

statins NOT contraindicated

in advanced cirrhosis –> liver transplant

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22
Q

What is the etiology of a1-antitrypsin def

A

AR

low level of a1-antitrypsin def –> build up in hepatocytes –> liver damage & decrease protease inhibitors

pulmonary emphysema

panacinar emphysema (at young age) - lower lobes; **smokers –> COPD/emphysema of upper lobe

liver dz

MC diagnosed inherited hepatic disorder in infants & children

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23
Q

what is diagnostic of a1-antitrypsin def

A

low a1-antitrypsin def level

check a1-antitrypsin def​ phenotype

PIZZ - homozygous (reduction in enzyme)

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24
Q

what are treatments of a1-antitrypsin def?

if not treated, what are complications?

A

smoking abstinence/cessation

liver transplant - MC genetic cause requiring liver transplant in kids

complication - emphysema at young age; cirrhosis –> HCC

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25
what is the etiology of PBC
**progressive non-suppurative destructive intrahepatic cholangitis** infxn w/ *Novosphingobium aromaticivorans or chlymagophilia _-_*_may trigger/cause it_ **= AI destruction of small intrahepatic bile ducts/cholestasis** **Female, median = 50 yo** **asymp _isolated_ elevation of ALP** or impaired bile excretion
26
what are the RF and clinical manifestation of PBC
RF: _UTI, smoking, use of hormone replacement therapy, hair dye_ clinical manifestation: **pruritus, progressive jaundice, xanthelasma,** osteoporsis, HSM, portal HTN associated w/ AI d/o's
27
what is diagnositic of PBC
**AMA, increasd IgM** _increased ALP, GGT (liver), bilirubin, cholesterol_
28
what is the treatment/management of PBC
**ursodeoxycholic acid** _liver transplantation for end stage dz_ Ca2+, vit D, bisphosphonate for osteoporosis
29
what complications may occur w/ PBC what is the prognosis
cirrhosis --\> liver failure prognosis --\> correlated w/ age, serum bili, serum albumin, PT, edema
30
what is the etiology of hemochromatosis
**HFE gene mutation -** increased Fe abs in **duodenum** ## Footnote **increase Fe saturation or ferritin or Fhx** **increased accumulation of Fe as gemosiderin in the liver, pancreas, heart, adrenals, testes, pituitary and kidneys**
31
what is the clinical manifestation of hemochromatosis
**tetrad: cirrhosis w/ hepatomegaly, abnormal skin pigment, DM, cardiac dysfxn** early sxs = nonspecifc late sxs= **skin pigmentation (bronze color), DM (bronze DM), erectile dysfxn (hypgonadism)**
32
what is diagnostic of hemochromatosis
_Labs:_ HFE gene mutation, mildly abnormal liver tests; _elevated plasma iron \> 45% transferring saturation; elevated serum ferritin_ _Imaging_: **MRI & CT** - iron overload of the liver; _MRI quantitate hepatic iron stores and hep assess the degress of hepatic fibrosis_ liver Bx: **homozygous - C282Y** - check for cirrhosis screening - test for HFE mutation for pt w/ **iron overload and all-first degree family members**
33
what is the treatment and mangement for hemochromatosis
**phlebotomy therapy:** goal - iron store depletion achieved **avoid foods rich in iron** _monitor HCT and serum iron_ **give PPI** **hemochromatosis and anemia/thalassemia** _(can't tolerate phlebotomy)_ use **deferoxamine** **liver transplantation**
34
what are risks for advanced fibrosis in hemochromatosis who is at increased risk for infxn
male, excess EtOH, DM increased risk for infxn - v. vulnificus, l. monocytogenes, y. enterocolitica and siderophilic organism (overall slight increase in mortality)
35
what is the etiology of wilsons dz
AR - _ATP7B;_ excess abs from SI or decreased excretion by liver **\< 40 yo** **impaired copper excretion into bile acid and failure to incorporate copper inot ceruloplasmin** accumulation of copper in **liver, brain and eyes ; also cause hemolytic anemia** **liver dz in teens & neuropsychiatric dz in young adults**
36
what is diagnostic for wilson dz
increased urinary copper excretion low serum ceruloplasmin hepatic copper concentration are high MRI of the brain molecular analysis - ATP7B
37
what is the clinical presentation and PE of wilson's dz
child/young adults: **_hepatitis, hemolytic anemia, neurologic/psychiatric abnormalities,_** _splenomegaly w/ hypersplenism, coombs-neg, portal HTN_ **kayser-fleischer ring -** fine pigmented granular deposits in sescemet membrane in cornea assocaited w/ renal canliculi, hemolytic anemia, subQ lipoma
38
what is the treatment of wilson dz
oral penicillamine (increases urinary excretion of chelated copper) liver transplant
39
what is the etiology of liver in HF
RHF --\> passive congestion of the liver (nutmeg liver) ischemic hepatitis - acute fall in CO statin therapy prior to admission may protect against ischemic hepatitis
40
what is the presentation of liver dx due to heart failure what are complications
hypotension absent or unwitnessed _hepatojugular reflux_ w/ tricuspid regurg _jaundice is associated w/ worse outcomes_ complications: **mortality rate due to underlying dz high**
41
what are diagnostics of liver dz due to heart failure
AST/ALT mildly elevated (_absence or superimposed ischemia_) **markedly elevated serum N-terminal-proBNP or BNP** hallmark = Shock Liver - rapid & striking **elevation of AST/ALT (\> 5000) & early rapid rise in serum LDH** MILD elevations inf ALP and bili
42
what is the epidemiology & RF of cirrhosis
peak incidence 40-60 RF: **alcohol, IV drug abuse, obesity, viral,** genetics, AI, meds life expectancy - markedly reduced
43
what is the pathophys of cirrhosis
**fibrosis** of liver --\> destroy the liver's vascular and lobular architecture --\> progressively deminish blood flow, decrease fxn, formation of **regenerative nodules** liver insufficiency **higher coffee and tea consumption -**_reduce_ risk of cirrhosis **MC: hep C, alcoholic liver dz, NAFLD**
44
what is historical info and clinical presentation of cirrhosis
hepatic cell dysfxn, portosystemic shunting, portal htn jaundice, ascites, encephalopathy RF = **viral, alc consumption, Hx of viral hep or jaundice**
45
what are PE findings of cirrhosis or liver dz
jaundice/icterus gynecomastia ascites testicular atrophy esophageal varices (splenomegaly) palmar erythema spider angioma caput medusae m. wasting asterixis dupuytran's contracture umbilical hernia hypoalbumin - muehrcke's lines & terry's nails
46
what are diagnostic labs for cirrhosis ?
**CBC -** decrease HBC, HgB, platelets **chem - CMP, cholesterol** decrease, **PTT/INR, ammonia, AFP** (last increased) (look at attached pic)
47
what are diagnostic imaging findings for cirrhosis
**ultrasonography + doppler** (RUQ/liver) **SAAG-** serum albumin - ascites albumin **(\>1.1 portal htn, \>250 PMNs/mL think SBP)** **several noninvasice predictive indicies for hepatic fibrosis** - imaging - _US elastography;_ more specific serum - _fibrosure_
48
what are possible complications of cirrhosis
HCC HIV co-infxn decompensated cirrhosis
49
what are treatments for cirrhosis
50
what are managements for cirrhosis
abstain from alcohol, recretaional drugs, smoking, liver toxic medicaitons/herbs stop nsaids endoscopy to screen for varices monitor labs AFP and US every 6 months to sceen for HCC immunizations
51
what are survival prognostic scores of cirrhosis
**MELD/MELD-Na** -order bilirubin, CK, Na, INR **Child-turcotte-pugh (CTP)** - order bilirubin, albumin, PT/INR, assess PE for encephalopathy and ascites always check these **liver transplant**
52
what is the etiology of ascities
pathologic of fluid in periotneal cavity MCC of ascites is portal HTN 2ndary to CLD
53
what is the hx/PE of ascities
Hx - increasing abd girth (+/-) abd pain PE: asterixis, shifting dullness, elevated jugualr venous pressure, large tender liver, signs of CLD, firm LN - think intraabd malignancy
54
what are diagnostic features of ascities
abd US (+ doppler)- Abd paracentesis CT: detect budd-chiari, LAD & masses Labs - SAAG, **WBC most important**, culture/gram stain
55
what is the tx for ascites
paracentesis: dx and tx treat the cause
56
draw out SAAG decision tree
57
what are sxs for esophageal varices what increases chances of bleed
acute GI hemorrhage - melena, hematochesia, hematoemesis can be serious/life threatenting - bleeding can lead to hypovolemia bleeding RF = size, red walte marking, severity of liver dz, active alcohol abuse (how do you tx and how do you prevent rebleed)
58
what is the etiology/pathophys of hepatic encephalopathy
alteration of mental status in presence of liver failure amonia levels are typically elevated in encephalopathy
59
what are precipitants of hepatic encephalopathy
**GI bleeding, constipation, sepsis** azotemia, high protein meal, hypoK alkolosis, CNS depressant drugs
60
what is diagnostics for hepatic encephalopathy how do you treat this
clincal diagnosis ammonia levels are typically elevated tx: Lactulose (nonabsorbable disaccharide) results in colonic acidification and diarrhea; goal = 2–3 soft stools/day
61
what is the presentation of encephalopathy what are the grades of overt encephalopathy
**asterixis (flapping temor)** confusion, slurred speech, change in personality, sleepy, difficult to arouse overt enceophalopathy: _mild confusion, droswy, stupor, coma_
62
what is primary peritonitis
63
what is secondary peritonitis
64
what is the etiology and clinical presentation/PE of HCC
male, 50-60s, high incidence Asia & Africa, Aflatoxin exposure cachexia, abd pain, fever, jaundice, asthenia, itching, tremors, disorientation, HSM, ascites, peripheral edema
65
how do you screen/prevent HCC and how do you dx
AFP and US every 6 months Dx: pt w/ known liver dz - abnormality on US or increase in AFP
66
how do you treat HCC
Surgical resection or liver transplantation (Tx, but rarely successful) Radiofrequency ablation Transcatheter arterial embolization (TACE)
67
when are liver transplants considered
irreversible, progressive CLD, acute liver failure, metabolic dz in which the metabolic defect if pt w/ alcoholism - _abstinent for 6 months_ consider in pts w/ worsening fxnal status - _based on MELD/MELD-Na score_ (MELD \>14) immnosuppresion needed after transplant

GI/GU II Exam 2 (19 decks)

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