Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

X Clin Med III Exam 2 > Alcoholic Liver Disease > Flashcards

Alcoholic Liver Disease Flashcards

1
Q

Leading cause of liver transplantation in US

A

Alcoholic liver disease (replaced HCV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Patterns of injury in alcoholic liver disease

A

Fatty liver (Simple steatosis)- present in almost all with chronic alcohol abuse
Alcoholic hepatitis
Chronic hepatitis with fibrosis or cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Progression of liver with ALD

A 
Normal liver
Steatosis
Steatohepatitis
Fibrosis
Cirrhosis
Hepatocellular carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When is there an increased risk of developing cirrhosis?

A

Men >3 drinks per day > 5 yrs

Women > 2 drinks per day> 5 yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Risk factors of ALD

A

Women are more sensitive to alcohol (develop more severe at lower doses with shorter duration)
African American>Hispanic>Caucasian males
Obesity
Genetic factors
Hep C leads to more rapid progression of liver disease
Smoking (risk of hepatocellular cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Recommendation for alcohol for HCV obese pt

A

No more than 1 drink per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Risk factors for ALD based on alcohol

A 
Amt ingested (most important)
Type maybe (beer or spirits more)
Pattern (drinking outside of meal time is worse)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathophysiology of fatty liver (hepatic steatosis)

A

Increased mobilization of free fatty acid from peripheral fat stores
Increased TAG formation
Decreased fatty acid oxidation
Reduced lipoprotein release by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Simple uncomplicated fatty liver

A

Usually asymptomatic and self limited (may be completely reversible with abstinence for 4-6 wks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is alcoholic hepatitis?

A

Inflammation of liver characterized by necrosis and fibrotic scarring (with history of chronic or current heavy alcoholic consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Presentation of alcoholic hepatitis

A

Can be asymptomatic, mild or severe
Severe with marked impairment of liver function:
Low fever, leukocytosis
Hepatic encephalopathy
Spider angiomas
Jaundice, hepatosplenomegaly with liver tenderness, edema, ascites, variceal bleeding!!!
Oliguria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is hepatic encephalopathy?

A

When liver can’t get rid of toxins like ammonia (due to hepatocellular dysfunction and portosystemic shunting) and they develop neuro sxs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Labs seen in alcoholic hepatitis

A 
Leukocytosis with left shift
Macrocytosis (MCV>100)
Thrombocytopena
AST/ALT ratio 2:1 (AST is 2-6x ULN) but both <300
ALP mildy elevated
Elevated bilirubin (more direct)
PT/INR elevated
Low albumin
Hyponatremia, hypokalemia
GTP elevated
Low folate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is seen on histology for alcoholic hepatitis?

A

Fatty infiltration
Neutrophil infiltration around clusters of necrotic hepatocytes
Clumps of intracellular material (Mallory bodies)
Fibrosis around hepatic venules (precursor to cirrhosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How to diagnose ALD

A

Liver biopsy required when unclear history of alcohol use and elevated liver tests and it is confounded by other risk factors for liver disease and we’re considering tx with steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tx of hepatic encephalopathy

A

Treat precipitating factors (GI bleeding, infection, sedating meds, lyte abnormalities, constipation and renal failure)
Lactulose for overt HE and secondary prophylaxis (also can use rifaximin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Signs of hepatic encephalopathy

A

EEG changes and flapping tremor (asterxisis-put hands out and back and they tremor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Grades of hepatic encephalopathy

A

I- changes in behaviors, mild confusion, slurred speech, disordered sleep (sublinical or covert encephalopath)
II- lethargy, moderate confusion (asterixsis)
III-marked confusion (Stupor), incoherent speech, sleeping but can arouse
IV-coma, unresponsive to pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Stroop test

A

For HE

Brief cognitive screening tool to evaluate psychomotor speed and cognitive flexibility (can diagnose minimal HE well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Management of alcoholic hepatitis

A

Hospitalize if high mortality rate (based on risk assessment calculators)
Discontinue all alcohol and complete abstinence is essential
If fluid overloaded, use diuretics (ascites etc)
Sodium restricted diet
Discontinue nonselective BBs b/c increased risk of AKI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Risk calculators for alcoholic hepatitis

A 
Model of End Stage Liver Disease (MELD)> 20 is severe with poor prognosis
Maddery discriminant factor (MDF) >32 is severe AH
Lillie score (labs over time) is used to determine if steroids should be continued!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Tx for severe alcoholic hepatitis

A

MDF>32 or MELD>20
Consider the steroid tx and discontinue if no effective on day 7 using Lillie score
Liver transplant in select population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is cirrhosis?

A

Widespread destruction and regeneration of liver tissue with marked increase in fibrotic connective tissue
Regenerated liver tissue forms nodules and permanently alters structure
Impaired liver function when increased connective tissue
Necrosis and fibrosis leads to deteriorration
Can have inflammatory cell infiltration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is compensated cirrhosis?

A

Portal pressure <10
Median survival about 12 yrs
May have splenomegaly (thrombocytopenia, leukopenia, anemia, AST elevation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is decompensated cirrhosis?

A

Increased portal pressure with decreased liver function
Median survival <2 yrs
Hepatic BF is bypassing vascular scars
Have portal HTN, porto-systemic shunting and impaired liver function

26
Q

Clinical manifestations of cirrhosis with increased portal HTN

A 
Ascites
Esophageal and rectal varices
Splenomegaly
Dilated abd veins
Encephalopathy
Jaundice
27
Q

Extra manifestations of decompensated cirrhosis

A

Fatigue, anorexia, weakness, palmar erythema, parotid enlargement, Dupuytrens contracture, jaundice, gynecomastia, testicular atrophy, spider nevi, muscle wasting, anemia
Signs of HE
Similar labs to alcoholic hepatitis

28
Q

Sites of obstruction in portal HTN

A

Prehepatic (portal vein thrombosis)
Intrahepatic (cirrhosis)
Posthepatic (CHF, constrictive pericarditis)

29
Q

What is the problem with portal HTN?

A 
Promotes collateral circulation:
Esophageal varices and rectal varices that can bleed
Splenomegaly
Ascites (caput medusa)
HE
30
Q

Labs in cirrhosis

A

Similar to alcoholic hepatitis
AST elevation (Can be normal in compensated)
Anemia
Thrombocytopenia
Coag abnormalities (not synthesize clotting factors)

31
Q

Tx of cirrhosis

A 
Prevent complications of portal HTN and cirrhosis:
Variceal surveillance (EGD) and banding
HCC surveillance (US q6mos and maybe AFP)
Non selective BB prophylaxis to prevent variceal bleeding (HR 55-60 and SBP<90) and wouldn't need to keep doing EGDs if so
32
Q

Tx of ascites

A

Adhere to less than 2g soidum
Diuretics
Fluid restriction ONLY if sodium <125
If refractory, stop BB, therapeutic paracentesis (with albumin if >5-6L drained)
Transjugular intrahepatic portosystemic shunt (TIPS)

33
Q

Complications of Transjugular intrahepatic portosystemic shunt (TIPS)

A

Stenosis or thrombosis

HE (b/c not filtering toxins)

34
Q

Liver transplant and cirrhosis

A

Refer for this with decompensated cirrhosis and MELD> or equal to 15
Must do 6 mos abstinence before considering (begin AA etc immediately)

35
Q

Prognosis of alcoholic fatty liver

A

Complete resolution may occur is STOP alcohol

36
Q

Prognosis of alcoholic hepatitis

A

Prognosis depends on severity
Mild is often reversible but need to d/b EtOH
If recurrent episodes, irreversible progressive liver disease and decompensated cirrhosis

37
Q

Prognosis of alcoholic cirrhosis

A

Worse

If continue to drink, 4 yr survival if have major complication is <20%

38
Q

Complications of cirrhosis

A

Portal HTN (dilated abd veins, ascites, congestive splenomegaly, esophageal varices and rectal varices)
Spontaneous bacterial peritonitis (infected ascetic fluid)
Hepatic encephalopathy
Hepatorenal syndrome

39
Q

What is hepatorenal syndrome?

A

Functional renal failure in setting of decompensated cirrhosis

40
Q

Types of hepatorenal syndrome

A

Type 1-rapidly and progressive renal failure with severe multi-organ failure (survival usually <4 wks)
Type 2: usually associated with refractory ascites (survival about 6 mos)

41
Q

Criteria to diagnose hepatorenal syndrome

A

Cirrhosis with ascites
Absence of shock
Renal impairment (rise in Cr of .3 mg/dL within 48 hr+ or 50% increase in baseline in 7 days)
No improvement with correction of volume status and albumin x 2 days (withdraw diuretics)
Absence of other causes of AKI (shock, infection, bleeding, sepsis, fluid losses etc)

42
Q

Presentation of hepatorenal syndrome

A 
Ascites
Serum Cr level >1.5 mg/dL
Azotemia (increased BUN)
Oliguria (urine vol <500 ml/d)
Hyponatremia (<130 mEq/L)
Hypotension
43
Q

How to prevent hepatorenal syndrome

A

Use albumin IV with large vol paracentesis (5L)
Protect GI bleeding with EGDs and BB use
Don’u use NSAIDs or supplements
Use SBP prophylaxis for pts that had previous dx of SBP, had variceal bleed for 3-7 days, pts with ascetic protein <1.5 g/dl

44
Q

What’s good to remember with alcoholics

A

Some will have a secondary or co-existing etiology of liver disease so must exclude other diseases with serological testing and maybe liver biopsy

45
Q

3 kinds of liver masses

A

Benign lesions that need no further intervention
Benign lesions that need investigation and therapy
Malignant lesions

46
Q

What benign liver lesions require no intervention?

A 
If IDed on imaging:
Cavernous hemangioma <4 cm
Focal nodular hyperplasia
Simple cyst < 4 cm and asymptomatic
Focal fatty change/sparing
47
Q

What benign liver lesions need management?

A

Adenoma (malignant potential and risk of bleeding-use of OCPs)
Liver abscess (pyogenic, amebic)
Inflammatory pseudotumor
Atypical/complex cysts and large symptomatic simple cysts
*refer to confirm and do management

48
Q

Malignant lesions of the liver

A

Metastases
Lymphoma (Great Masquerader)
Primary liver neoplasm (hepatocellular carcinoma, cholangiocarcinoma, other tumors like cystadenocarcinoma or angiosarcoma)

49
Q

What are hepatocellular carcinomas?

A

Neoplasms arising from parenchymal cells

50
Q

When should you be suspicious for hepatocellular carcinoma?

A

Cirrhotic pts or pts with non-cirrhotic hep B with liver lesion on imaging

51
Q

When do you see hepatocellular carcinoma more?

A

Male

Pts with chronic liver disease (hep C, autoimmune hep)

52
Q

What pts should have surveillance done for hepatocellular carcinoma?

A

All suspected cirrhotic pts from any liver disease (platelet <150,000 or US elastography with kPA>20)
Chronic Hep B non cirrhotic (asian females >50, asian males >40, any age with FH and person dx of hep B, Africans and African American black >20)

53
Q

What is the screening for hepatocellular carcinoma?

A

US q 6 mos and maybe AFP too

54
Q

Sxs of hepatocellular carcinoma

A

Cachexia, weakness, weight loss

Sudden appearance of ascites

55
Q

Labs in hepatocellular carcinoma

A

Elevated alk phos
Elevated AFP (not sensitive)
Tri-phasic CT first and if non-diagnostic due tri-phasic MRI (with gadolinium contrast)
Liver bx is not diagnositc (not needed if imaging is typical and AFP is elevated

56
Q

Why can you usually not resect a hepatocellular carcinoma?

A

Due to background cirrhosis
Non-cirrhotic HBV is usually resectable tho
Can do with cirrhotic HCC if bilirubin is normal and no portal HTN

57
Q

When can you do liver transplant with hepatocellular carcinoma?

A

1 lesion up to 5 cm or 3 lesions up to 3 cm AND no vascular invasion or distant spread

58
Q

What to do for hepatocellular carcinoma with small tumors in non-operative pts?

A

Radiofrequency ablation

59
Q

Another option for large tumors in hepatocellular carcinoma

A

Transarterial radioembolization or radiation if sufficient hepatic reserve

60
Q

End stage tx for hepatocellular carcinoma

A

Symptomatic (if just advance disease then systemic therapy for distant spread)

X Clin Med III Exam 2 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions