hepatitis Flashcards

1
Q

non alcoholic fatty liver disease

A

Risk factors are mainly those of metabolic syndrome, including obesity, type 2 DM, hypertension, and hyperlipidemia, steroids

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2
Q

Patients with NASH induced cirrhosis need US surveillance every 6 months due to what

A

increased risk of hepatocellular carcinoma

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3
Q

In non-alcoholic fatty liver disease ALT > AST. differentiate from what

A

alcoholic fatty liver disease where AST to ALT ratio is >2

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4
Q

Necrosis of liver cells followed by fibrosis and nodule formation.

A

cirhosis

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5
Q

what is end result of cirrhosis

A

End result is impairment of liver cell function and gross distortion of the liver architecture leading to portal hypertension

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6
Q

serum AFP if lvl higher than 200 suggest

A

HCC

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7
Q

hepatorenal syndrome

A

The development of acute kidney injury in a patient who usually has advanced liver disease, either cirrhosis or alcoholic hepatitis.

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8
Q

diagnosis of hepatorenal syndrome

A

o Oliguria
o Rising serum creatinine (over days to weeks)
o Low urine sodium (<10 mmol/L)

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9
Q

clinical features of ascites

A

• Fullness in the flanks with shifting dullness and fluid thrill. • Tense ascites is uncomfortable and produces respiratory distress.
• Pleural effusion (usually right sided) and peripheral edema may also be present.
• Meigs syndrome: triad of benign ovarian fibroma, ascites, and pleural effusion

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10
Q

what is SAAG ratio

A

Serum albumin – ascitic albumin (SAAG) ratio differentiates between different causes of ascites (Transudate vs Exudate). A high gradient (SAAG >11.1 g/L) indicates portal hypertension and suggests a nonperitoneal cause of ascites

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11
Q

what are causes of SAAG <11.1g/L (Exudate)

A

• Peritoneal carcinomatosis
• Peritoneal tuberculosis
• Pancreatitis
• Nephrotic syndrome
• Lymphatic obstruction (chylous)

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12
Q

causes of SAAG >11.1g/L (Transudate)

A

• Portal hypertension (cirrhosis)
• Heart failure
• Hepatic outflow obstruction (Budd-Chiari syndrome, venoocclusive disease)

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13
Q

what is asitic fluid protein

A

may be used to differentiate causes of ascites, esp. if ascitic albumin or serum albumin is not known

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14
Q

Ascitic T. Protein < 25

A

•Portal hypertension (cirrhosis)
•nephrotic syndrome

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15
Q

Ascitic T. Protein > 25

A

Heart failure

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16
Q

Spontaneous bacterial peritonitis (SBP)

A

-Most common infecting organism is Escherichia coli
-Suspect diagnosis in any patient with cirrhotic ascites who deteriorates

17
Q

Management of ascites due to portal hypertension/cirrhosis:

A

o Dietary sodium restriction 40 mmol/day and oral spironolactone daily
o Furosemide daily is added if the response is poor
o Aim of treatment: to lose about 0.5 kg of body weight each day
o Too rapid diuresis causes intravascular volume depletion & hypokalemia which can precipitate encephalopathy.
o A rising creatinine level or hyponatremia indicates inadequate renal perfusion and the need for temporary cessation of diuretic therapy

18
Q

portal vein formed by

A

union of superior mesenteric (from the gut) and
splenic vein (from the spleen) and transports blood to the liver.

19
Q

The normal portal pressure is 5–8 mmHg. >10mmHg indicates

A

portal htn

20
Q

Causes of Portal Hypertension Prehepatic
(due to blockage of the portal vein before the liver)

A

Portal vein thrombosis

21
Q

post hepatic causes of portal HtN

A

Budd-Chiari syndrome (thrombosis in hepatic veins)
Right heart failure
Constrictive pericarditis
Inferior vena cava obstruction

22
Q

what are most common causes of acute hepatic failure

A

Viral hepatitis and paracetamol overdose

23
Q

what is acute hepatic failure

A

Hepatic failure characterized by encephalopathy and coagulopathy

24
Q

hepatic encephalopathy

A

-Neuropsychiatric syndrome which occurs with advanced hepatocellular disease,
-Toxic substances normally detoxified by the liver bypass the liver via the collaterals and gain access to the brain.

25
what plays a major role in hepatic encephalopathy
Ammonia plays a major role and is produced from breakdown of dietary protein
26
symptoms and signs of hepatic encephalopathy
• Increasingly drowsiness, hypertonia and hyperreflexia. • Chronically, the patient may be irritable; confused; with slow, slurred speech and a reversal of the sleep pattern (sleeping during the day and restless at night) • Fetor hepaticus (a sweet smell to the breath) • Asterixis (flapping tremor of the outstretched hand) • Constructional apraxia (inability to draw a five-pointed star) • A prolonged trail-making test (ability to join numbers & letters in a certain time).
27
a1 antitripsin defecient in liver
• Normally, AAT is made in the liver and sent to the lungs to protect them. • In AATD, the abnormal protein accumulates in liver cells (hepatocytes).
28
How is AAT Deficiency Diagnosed?
1. Alpha-1 Antitrypsin Blood Test → Measures AAT levels (Low in AATD) 2. Genetic Testing (SERPINA1 Gene) → Identifies abnormal PiZZ or PiSZ mutations 3. Liver Function Tests (LFTs) → Detect liver damage (High ALT, AST, bilirubin) 4. Liver Biopsy → Shows AAT protein buildup in liver cells (PAS-positive globules) 5. Elastography or FibroScan → Measures liver stiffness (fibrosis/cirrhosis)
29
HEREDITARY HEMOCHROMATOSIS (HH)
-Autosomal recessive disorder due to a mutation in HFE on short arm of chromosome 6 -excessive iron deposition in various organs and eventually = fibrosis and functional organ failure
30
WILSON’S DISEASE
• Mutation in the ATP7B gene (affects the liver’s ability to remove copper). • Copper accumulates in the liver first, causing liver damage. • Over time, excess copper spills into the bloodstream and damages the brain, kidneys, and eyes.
31
where do u see greenish-brown rings called Kayser-Fleischer rings)
wilsons disease
32
diagnosis of wilsons
• Increased 24-hour urinary copper excretion due to proximal tubular dysfunction • Increased copper in a liver biopsy specimen (rhodanine stain) • Abnormally high copper in urine after giving penicillamine