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Pathophysiology - Gastrointestinal > Introduction to Clinical Aspects of Liver Diseases > Flashcards

Introduction to Clinical Aspects of Liver Diseases Flashcards

1
Q

What are more specific symptoms of hepatocellular injury in adults?

A

Jaundice
Dark urine - bilirubin in urine
Light colored stools

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2
Q

What are symptoms which would indicate Hepatitis B vs EBV, vs drug-induced hepatitis?

A

Hep B - urticaria, arthritis, rash -> serum-sickness-like prsentation

EBV - lymphadenopathy

Drugs - rash

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3
Q

If the patient is not asymptomatic, what are some acute vs chronic signs of hepatitis? What will the consistency of the liver be?

A

Acute - scleral icterus, hepatomegaly, shrinking liver if fulminant necrosis, fever and lethargy

Chronic - firm liver (fibrosis), splenomegaly (portal HTN)

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4
Q

In hepatocellular injury with necrosis, will bilirubin be conjugated or unconjugated and why? What is the difference between these two?

A

Tends to still be conjugated -> liver has a remarkable capacity to compensate for bilirubin accumulation
-> Excretion of bilirubin is rate-limiting step

Unconjugated - not water soluble
Conjugated - has been glucuronidated -> water soluble

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5
Q

How will albumin change with hepatocellular injury?

A

Can be low if you have chronic disease -> albumin has a long halflife. Will take a while for effects of decreased liver production to be seen.

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6
Q

Is liver biopsy diagnostic of hepatocellular disease?

A

Sometimes, but often it is only suggestive or very nonspecific
-> need full clinical picture + serology to make a diagnosis

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7
Q

What is the treatment for hepatocellular injury?

A

Largely supportive, withdrawal of offending medication, until liver degenerates. Specific treatments depending on etiology.

Live transplant if it has progressed to hepatic failure / portal HTN / acute liver failure

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8
Q

What is the clinical definition of acute liver failure?

A

Severe hepatic dysfunction progressing to encephalopathy within 8-12 weeks from initial onset of liver disease (no history of pre-existing liver dz, otherwise acute on chronic)

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9
Q

How does severe liver injury affect the BBB?

A

Presence of toxins in blood damages the barrier and allows things to get it which normally wouldn’t
-> predisposes to encephalopathy

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10
Q

Other than icterus/jaundice, what are some physical signs which indicate acute liver failure?

A

Mental status changes progressing to coma, seizures

Hyperreflexia

Asterixis - flapping tremor (inability to hold a sustained muscle contraction) which may progress to decerebrate posturing and coma

Shrinking liver as necrosis progresses, ominous

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11
Q

Is low aminotransferases a good thing in acute liver failure?

A

Not necessarily. Aminotransferases are usually very high, indicating necrosis, but a decrease may indicate end-stage necrosis, a very ominous finding

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12
Q

Why does liver failure lead to cerebral edema?

A

Liver is responsible for converting ammonia waste into urea for excretion.

Increased ammonia -> uptake by astrocytes in brain -> increased glutamine content in brain cells -> cerebral edema

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13
Q

Does DIC occur in liver failure?

A

It can -> activated clotting factors not removed by liver.

Also, due to decreased production of clotting factors, liver failure can also present as bleeding with increased prothrombin time.

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14
Q

When is liver transplant done for acute liver failure? What prevents it from being done? How can you recover without it?

A

Done when regeneration won’t occur or won’t occur soon enough

LT is precluded by brain damage which could be caused by cerebral edema

Supportive treatment while waiting for regen -> manage glucose, prevent sepsis, prevent bleeding

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15
Q

Why is alkaline phosphatase elevated in cholestasis?

A

Overproduced by hepatocytes and biliary ductular cells during cholestasis
-> accounts for serum elevation without necrosis

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16
Q

What are the symptoms of cholestatic disorders?

A
  1. Jaundice
  2. Pruritis - itching, often bad enough to make patients suicidal
  3. Fat / fat-soluble vitamin malabsorption
  4. Coagulopathy - failure to absorb vitamin K
  5. Osteoporosis - failure to absorb vitamin D
  6. Xanthomas and xanthelasmas - cholesterol not excreted
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17
Q

What are physical signs of cholestasis disorders?

A 
Icterus
Skin excoriation - due to pruritis
Ecchymoses - coagulopathy (prolonged PT)
Xanthomas and xanthelasmas
Acholic (gray) stools
Gallbladder may be enlarged / palpable if obstructed
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18
Q

What is the usefulness of imaging for cholestasis and what is the most common modality used?

A

Can determine between a mechanical / “surgical” obstruction or a medical / “intrahepatic” obstruction

Most common modality is ultrasound, can also use MRI with contraast or CT scan

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19
Q

What are two special modalities used to check for hepatobiliary disease?

A
  1. ERCP - endoscopic retrograde cholangio-pancreatogram, inject dye into ampulla of vater
  2. PTC - percutaneous cholangiogram, find a bile duct through the skin and check for obstruction
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20
Q

Which cholestasis types are associated with the highest levels of AlkPhos?

A

PBC (primary biliary cholangitis)

Mechanical blockage by cancer; granulomas

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21
Q

What are the treatments for mechanical obstruction of the biliary tract?

A

Surgery -> traditional

Endoscopy -> therapeutic ERCP, with stenting, stone removal, and dilation of strictures

Percutaneous drain placement

22
Q

What are the treatments for medical jaundice / cholestasis?

A

Bile salt binding resins such as cholestyramine -> treat the pruritis

Ursodeoycholic acid - binds cholesterol and protects against gallstones

Vitamin K / Vitamin D supplementation

Medium chain triglycerides - can be absorbed without bile salts

23
Q

What fatal cholestatic diseases is liver transplant used to treat?

A

Primary sclerosing cholangitis and primary biliary cholangitis

24
Q

How can pregnancy cause acute liver failure and cholestasis?

A

Acute liver failure - acute fatty liver of pregnancy

Cholestasis - Intrahepatic cholestasis due to pregnancy and estrogens

25
Q

Is cirrhosis always symptomatic? Why mechanisms cause its symptoms?

A

No -> often asymptomatic and caught incidentally or not caught until after death

primary mechanisms:

  1. Hepatocellular dysfunction
  2. Portal hypertension
26
Q

How does hypersplenism of cirrhosis manifest itself in the CBC?

A

Congestion due to portal HTN leads to increased turnover of cells by splenic RES

Thrombocytopenia -> petechial bleeding

Leukopenia -> risk of infection

Anemia -> shortened RBC survival, precipitates gallstones

27
Q

What are the physical symptoms associated with cirrhosis?

A 
Ascites
Splenomegaly
Abdominal wall vascular accentuation -> caput medusae
Hematemesis -> esophageal varices
Gastric varices -> melena
28
Q

What are common physical signs of cirrhosis?

A

Muscle wasting, hepatomegaly, firm or shrunken liver with nodules,
Estrogen -> spider angiomata, palmar erythema
Mental status changes, asterixis
Bleeding problems -> petechiae, ecchymoses

29
Q

Give some examples of causes of pre-hepatic vs intrahepatic vs post-hepatic portal hypertension?

A

Pre-hepatic - portal vein thrombosis, splenic A-V fistula

Intrahepatic - cirrhosis, schistosomiasis, granulomas, veno-occlusive disease

Post-hepatic - hepatic vein thrombosis (Budd-Chiari syndrome), right sided HF, constrictive pericarditis, inferior vena cava web

30
Q

What are the treatments for portosystemic collaterals (varices)?

A
  1. Transfusion - for blood loss if bleeding
  2. Endoscopic injection - sclerose the vessels closed
  3. Rubber band ligation -> suck them closed
  4. Pharmacologic agents to lower portal pressure
  5. Decompression
31
Q

Why do we worry about varices? How can they contribute to hepatic encephalopathy?

A

Upper GI bleeding can be massive and often fatal.

Collaterals also contribute to infection and encephalopathy by bypassing the detoxification of the liver.

Furthermore, GI bleeding results in increased delivery of hemoglobin to the gut microbiome, which increases ammonia release by microbes and further exposes portal system to toxic levels of ammonia

32
Q

What pharmacologic agents are useful in reducing portal pressures and thus are useful in treating acute variceal bleeds?

A

Octreotide -> somatostatin analogy which decreases secretion of splanchnic vasodilators

Vasopressin -> constrictor of vascular beds

33
Q

What pharmacologic agents are used in the chronic treatment of varices?

A

Propranolol and nadolol, which prevent B2 vasodilation and B1 high output cardiac states from exacerbating varices

34
Q

How is surgical decompression of varices carried out and what is the risk?

A

Create a porto-systemic shunt via the TIPS procedure -> transjugular intrahepatic portosystemic shunt
-> bypass the fibrotic portion of the liver

Risk: Worsening of hepatic encephalopathy

35
Q

What are the three types of portosystemic encephalopathy? How do they differ broadly in terms of reversibility?

A

Acute type -> not due to portal HTN/ shunting, irreversible:

Type A - Acute - delirium + convulsions, commonly progress to coma -> BBB and cerebral edema

Chronic types -> usually due to shunting problem, usually reversible:

Type B - Bypasses -> Occurs in patients with portosystemic bypasses

Type C - Cirrhosis / Chronic liver disease - functional hepatocellular failure with large shunting / portal HTN component

36
Q

What factors are used to determine amount of hepatic encephalopathy?

A
  1. Mental status disturbances
  2. Hyper-reflexia
  3. EEG changes
  4. Asterixis / flapping tremor
37
Q

What is the pathogenesis of hepatic encephalopathy?

A

Nitrogenous / toxic substances from gut build up, often due to portal-systemic shunting

  1. Amino acid abnormalities upset brain neurotransmitter homeostasis
  2. GABA and benzos from endogenous or exogenous sources plays a role
    - > net result: neurotransmitter failure
38
Q

What factors precipitate worsening of hepatic encephalopathy?

A

Increased NH3 production or absorption:

  1. Excess oral protein intake -> ammonia builds
  2. GI bleed -> increased protein to gut microbes
  3. Constipation / infection

Decreased NH3 removal:

  1. Alkalosis / hypokalemia -> Increased K+ reabsorption stimulates H+ excretion via ammonia, but ammonia can make it back into blood
  2. Renal failure
  3. Diuretics -> hypokalemia
  4. TIPS procedure
  5. Benzos / sedatives
39
Q

What is the treatment for chronic encephalopathy?

A
  1. Lactulose -> increase NH4 generation by bacteria breaking down this sugar to produce lactic acid
  2. Rifaximin or neomycin -> kill urease-producing gut bacteria
  3. Benzodiazepine antagonists
40
Q

What are the factors which precipitate ascites in cirrhosis?

A

Portal hypetension and splanchnic / systemic vasodilation -> increased trans-sinusoidal pressure and fluid leakage

Loss of plasma volume and decreased effective flow due to vasodilation -> RAA activation, increasing salt and water, worsening ascities

Hypoalbuminemia further reduces oncotic pressure

41
Q

What are some other non-hepatic causes of ascites?

A 
Peritoneal infections, i.e. TB
Cancer - primary or metastatic to peritoneum
Nephrotic syndrome
Pancreatitis
CHF, constrictive pericarditis
42
Q

What lab tests are helpful in determining the etiology of the ascites fluid?

A
  1. Protein content
  2. WBC’s and type - monocytes elevated in TB, PMNs in bacterial peritonitis
  3. Malignant cells - diagnostic of cancer
  4. Amylase - elevated in pancreatitis
  5. Gram stain and culture - diagnostic of infection
43
Q

How does protein content help determine the etiology of ascites and what is the cutoff?

A

Protein content:

High in chronic infection and tumor (exudate)

Low in portal hypertension - transudate

If serum minus ascities albumin is greater than 1.1 g/dL -> portal HTN is very likely

44
Q

What are the problems associated with ascites?

A
  1. Spontaneous bacterial peritonitis
  2. Umbilical hernia with rupture -> Flood syndrome!
  3. Can lead to pleural effusions and generally diaphragm harder to move -> breathing difficulties
  4. Drug dilution due to increased volume of distribution
45
Q

What is the treatment for ascites?

A
  1. Na / H20 restriction
  2. Increase Na output - diuretics, paracentesis (kinda shit cuz albumin is removed too)
  3. TIPS
  4. Peritoneovenous shunts - high infection risk and breaks down quickly
  5. Liver transplant for cirrhotic ascites
46
Q

What is hepatorenal syndrome?

A

Renal failure or insufficiency in patients with advanced severe liver disease, presents with severe oliguria

-> not due to ATN because urine sediment is normal, there is no proteinuria, and renal ultrasound is normal

47
Q

What are the two types of hepatorenal syndrome?

A

Type 1 - rapid development of kidney failure in less than two weeks, worst prognosis

Type 2 - Slower onset -> diuretic resistant or unresponsive ascites

48
Q

What is the pathogenesis of hepatorenal syndrome? What will happen after liver transplant?

A

Unclear -> renal arteriolar vasoconstriction shifts cortical bloodflow to medullary portions of kidneys
-> leads to water retention and worsening of ascites, still prominent hypotension

-> kidney histology is normal, and kidneys will work after liver transplant

49
Q

How is hepatorenal syndrome diagnosed?

A

Must rule out pre-renal azotemia -> give trial of volume expansion with saline to see if this helps

There will be no evidence of acute renal failure by urine studies

50
Q

What is the treatment for hepatorenal syndrome?

A

Usually liver transplant is necessary, which is scary, since you just have to hope kidneys will work when you transplant liver

Can try albumin infusions and systemic vasoconstrictors to keep blood pressure up in meantime, and give dialysis to carry kidney function while waiting on transplant

Pathophysiology - Gastrointestinal (24 decks)

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