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MBBS VI Medicine > Teaching clinic: 2 cases of cirrhosis HCV > Flashcards

Teaching clinic: 2 cases of cirrhosis HCV Flashcards

1
Q

Cause of black formed stool

A

Bismuth: forms bismuth sulphate which is black
Fe supplement

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2
Q

Tarry stool location

A

Upper GI to proximal colon

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3
Q

Haematemesis is from where?

A

Large volume blood loss above duodenal jejunal junction (ligament of treitz): esophageal varices

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4
Q

Cause of cirrhosis in HK

A

HBV > HCV (found in 1989) > alcoholic liver disease > NASH
* Cryptogenic cirrhosis (mostly HBV but lost surface antigen)
* autoimmune hepatitis
* PBC
* Wilsons disease (young <30)
* Haemochromatosis (in thal patients without transfusion: iron will still be elevated but not to haemochromatosis level)
* Cardiac cirrhosis

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5
Q
A
  • Pancytopenia due to hypersplenism
  • Hyperuricemia: GI bleeding and reabsorption of blood due to increase in protein
  • Subacute liver conditions: albumin may be low (25 days of half life)
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6
Q

Causes of high globulin in cirrhosis

A
  • Portosystemic shunting
  • Reduced antigen degradation by cirrhotic liver
  • Cirrhotic liver will produce antigens. Antigenemia: increased plasma cells (produce globulin)
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7
Q

Reversed de titis ratio 2 causes?

A

alcoholic hepatitis: megamitochondriac
liver malignancy (primary/secondary): large enough to cause secondary necrosis of liver

ALT in cytosol, AST in mitochondrial
ALT is liver specific

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8
Q

Cause of increased AST

A
  • Skeletal muscle
  • Myocardial muscle: MI
  • Hemolysis
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9
Q

Cause of elevated ALP

A

SOL such as Liver abscess
Cholestasis

polycystic liver: LFT normal

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10
Q

What enzyme inducers can cause increase in GGT?

A
  • Rifampicin
  • Antiepileptic drugs
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11
Q

Why is PT good for assessing liver function?

A

Relies on F5 and F7 which have short half life

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12
Q

Gardners line

A
  • RLQ
  • Umbilicus
  • Left anterior axillary line
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13
Q

What is the chance of becoming a chronic hep B and C carrier in an adult?

A

Hep B: 0-2%
Hep C: 50-85%

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14
Q

Which genotype of HCV most important?

A

Pangenotyopic agents. most important is genotype 1

HK 25% is genotype 6

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15
Q

Hep C transmission

A
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16
Q

Reason for high chronicity in hep C

A

Will become chronic carrier
* Rapid mutation esp in envelop protein –> quasispecies in the host simultaneously (suppress one quaispecies others rise up)
* Immune pressure on dominant stain: coexistent strain emerges to escape immune attack

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17
Q

Clinical course of hep C

A
  • Immune attack: neutralizing ab develop but are time limited and highly strain specific. Cell mediated responses cause liver damage.
  • The disease: viremia peaks at pre or early acute phase
  • Chronic hepatitis: fluctuating AST and ALT. Cirrhosis and HCC in 20-50 years
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18
Q

HBV time to HCC

A

55-60 years

19
Q

Changes in sustained virological response
AE of ribavirin

A

Ribavirin AE: Haemolysis

20
Q

3 main sites of action for direct acting antivirals

A
  • Protease inhibitor
  • RNA polymerase (NS5B) inhibitor
  • NS5A inhibitors
21
Q

Recommended agents

A

Harvoni: ledipasvir + sofosbuvir
Zapatier: grazoprevir (PI) + elbasvir (NS5A inhibitor)
Screening for resistance associated substitutions (RAS) recommended before treatment

22
Q

2 pangenotypic agents

A

Epclusa (sofosbuvir + velpatasvir)
Mavyret (glecaprevir and pibrentasvir)

23
Q

Who with HCV is treated?

A
  • ALL patients with chronic HCV, except those with short life expectancy due to non-HCV disease (s)
  • Patients with end-stage liver disease due to HCV should still be treated

Transplant patient first, then give HCV antivirals

24
Q

pretreatment assessment of HCV

A

proof of HCV replication: just need HCV RNA
Assess presence or absence of cirrhosis by non invasive methods e.g. fibroscan

25
Q

Recommended treatment for all genotypes

A
  • Epclusa (sofobuvir + velpatesvir): 12 weeks
  • Maviret (glecaprevir and pibrentasvir): 8-12 weeks

Ribavirin only needed for cirrhosis

26
Q

Which of the following is not for emergency first-line treatment? (1) Intravenous drip (2) X-match packed cell (3) Endoscopy sclerotherapy / band ligation (4) IV terlipressin (5) Sengstaken-Blakemore tube insertion

A

(5) Sengstaken-Blakemore tube insertion

27
Q

Mx of haematemesis

A
  • Nil by month except medication
  • IV drip (2D:1S): q6-8h
  • X match 2 units of packed cell
  • Syrup lactulose 20ml tds after endoscopy
  • Hourly BP, pulse
  • IV vit K1 only if warfarin overdose, cholestasis and cholestatic condition. Not given in liver parenchymal disease (just cannot produce sufficient PT). It is routinely given as not harmful

Prone to hepatic encephalopathy:
increased protein in gut due to blood digestion.
Increased blood supply to liver

28
Q

Cauases of haematemesis in cirrhotic patients

A
  • Varix (oesophageal & gastric (J scope and sclerosant glue: coagulates when comes into contact with oxygen))
  • Portal hypertensive gastropathy
  • Peptic ulceration (3x higher risk in cirrhosis)
  • Generalized bleeding tendency: prolonged PT and thrombocytopenia: Reduced clotting factors
  • Others, e.g., Mallory Weiss syndrome
29
Q

When does variceal bleeding occur?

A

Associated with vessel wall stress
Portal BP (unlikely to bleed if <10mmHg)
Large vessels with thin walls

30
Q

Mx of variceal bleeding

A
  • Treatment of shock
  • Monitor vital signs
  • Endoscopic diagnosis of source of bleeding
  • Prevention / treatment of hepatic encephalopathy
  • Vitamin K1 therapy & correction of clotting factor defects (in case there is any cholestatic element)
31
Q

Emergency mx of acute variceal bleeding

A

(I) Endoscopic treatment
- Band ligation
- Sclerotherapy
- Variceal obliteration by tissue adhesive
(II) Drug therapy
- Vasoconstrictors
- Vasodilators
(III) Balloon tamponade
- Sengstaken Blakemore tube
(IV) Esophageal stent
(V) Emergency surgery (rarely performed)

32
Q

Timing of band ligation/scleropathy

A
  • Immediate (effective but can be difficult)
  • Delay till initial bleeding stopped (or partially controlled) by drugs or balloon tamponade
  • All remaining vessels should be sclerosed in the weeks after stopping of haemorrhage
33
Q

Complications of band ligation/injection scleropathy

A
  • transient oesoph. Pain
  • oesophageal ulcers (rarely bleed)
  • sloughing of bands during subsequent endoscopies (wait 7-10 days in case 2nd OGD leads to sloughing off of band)
  • stricture (manage by dilatation)
  • mediastinitis (resolve by injections)
  • aspiration pneumonia
34
Q

Drugs for variceal bleeding

A

Terlipressin: reduction in hepatic arterial flow
Somatostatin/octreotide: decreased splanchnic blood flow

Vasoconstrictors
* Decrease sup mesenteric and splenic arterial flow –> decrease portal pressure
* Decrease blood flow to gut

Vasodilators: decrease intrahepatic vascular resistance (and portal pressure) without decrease in peripheral resistance

35
Q

Adv of terlipressin over pitressin

A
  • Adequate compensatory hepatic arterial blood flow to cover the decreased portal flow
  • No plasminogen activation –> no serious cardiac effect
  • Longer action (3-4 hours vs a few mins): can be used as bolus
  • Can be be used in acute peritonitis
  • Helps in preventing hepatorenal syndrome
36
Q

disadv of Sengstaken blakmore tube

A

gastric balloon, gastric aspiration, esophageal balloon (saliva), esophageal aspiration. Inflate to 25ml, can only use for 24 hours or else will cause esophageal necrosis.

  • Patient discomfort
  • Esophageal ulceration or necrosis
  • Asphyxia due to balloons
  • Aspiration pneumonia
37
Q

Q3. Which further treatment option is not indicated for this patient? (1) Propanolol (2) Monitor varices and sclerose them if recur (3) Direct acting antivirals if available at that time (4) Liver transplantation (5) None of the above

A

(5) none of the above

38
Q

Prevention of rebleeding from varices

A
  • Carvedilol (better than propranolol)

Decreased portal blood flow
* Effective in prevention of rebleeding
* Factors associated with recurrent blood: patients non compliance, abasence of persistent decrease in HR, HCC, continued ingestion of alcohol
* Can be combined with vasodilators e.g. isosorbide mononitrate

  • Long term band ligation
  • TIPS
  • Liver transplantation
39
Q

How is transjugular intrahepatic portosystemic stent shunt done?

A
  • Transjugular access to middle hepatic vein
  • Puncture and catheterization of R branch of portal vein (difficult)
  • Dilatation of needle tract (painful)
  • Implantation of stent joining hepatic and portal vein branch
40
Q

Indications for TIPS

A
  • Variceal bleeding
  • resistant and recurrent
  • acute uncontrolled
  • Refractory ascites
  • Refractory cirrhotic hydrothorax
  • Budd - Chiari syndrome
  • Prophylactic portal decompression prior to transplant
41
Q

Contraindincations to TIPS

A
  • Severe liver failure in patients not for transplant
  • HCC
  • Liver abscess/cholangitis
  • DIC
  • Cavernous formation of portal vein
  • Thrombosis of right and left internal jugular vein, SVC/IVC
42
Q

Acute complications of TIPS

A

Complication of procedure
* Severe/fatal intraabd bleed from perforation of liver capsule or stent at portal bifurcation: haemophilia, haematoma of liver

Acute complications
* Thromboembolism with clot in stent
* Volume overload with heart failure
* Renal failure (related to dye)
* DIC sepsis

43
Q

Chronic complications of TIPS

A
  • Hepatic encephalopathy: shunt flow proportional to stent diameter, incidence similar to distal splenorenal shunt
  • Recurrent bleeding either from non portal hypertensive bleed or from inadequate portal decompression
  • Stent stenosis/occlusion
44
Q

Mechanism of portal hypertensive gastropathy?
Possible ddx?

A

Congestive gastropathy: increased portal BP causes mucosal vascular ectasia (not due to H.pylori). More frequent in pts with large varices, poor liver function.
ddx: gastric antral vascular ectasia (GAVE) –> managed by argon plasma coagulopathy

In comparison to congestive gastropathy –> B blockers (carvedilol has better outcome)

MBBS VI Medicine (99 decks)

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