pt12 Flashcards

(50 cards)

1
Q

How is the severity of acute liver injury best assessed?

A

Prothrombin time and bilirubin levels (reflect synthetic dysfunction and excretory capacity).

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2
Q

Define chronic hepatitis.

A

Persistent hepatic inflammation > 6 months, due to viral, chemical (e.g., alcohol), or autoimmune causes.

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3
Q

How is hepatitis A virus transmitted and what is its typical outcome?

A

Fecal–oral spread; short incubation, self‐limiting, no chronic stage; rare fulminant hepatitis.

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4
Q

What prophylactic measures exist for hepatitis A?

A

Active immunization with inactivated vaccine; passive immunoglobulin for post‐exposure or short‐notice protection.

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5
Q

Describe the hepatitis B virus structure relevant to diagnostics and vaccination.

A

DNA virus with core antigen (HBcAg), e antigen (HBeAg) indicating infectivity, and surface antigen (HBsAg) used in vaccines.

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6
Q

What defines a chronic HBV carrier and their risks?

A

HBsAg persistence > 6 months; HBeAg or HBV DNA indicates high infectivity; risk of chronic hepatitis, cirrhosis, HCC.

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7
Q

Outline key features of hepatitis C infection.

A

RNA virus; blood‐borne/rare vertical transmission; short incubation; 60–90% become chronic carriers; high risk of cirrhosis and hepatocellular carcinoma; no vaccine.

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8
Q

How is acute HCV exposure in healthcare workers managed?

A

Immediate testing and early interferon‐based therapy post–needle‐stick to prevent chronic infection.

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9
Q

Which lab finding is true for haemolytic jaundice?

A

Increase in serum unconjugated bilirubin.

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10
Q

What is the principal transmission route for hepatitis A?

A

Faecal–oral route.

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11
Q

What are the three learning outcomes for this lecture?

A

Understand cirrhosis pathogenesis; describe liver tumour pathology; know alcoholic liver disease features.

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12
Q

How is cirrhosis defined histologically?

A

Diffuse, irreversible fibrosis and regenerative nodule formation following chronic hepatocyte necrosis.

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13
Q

What are the two main consequences of cirrhosis?

A

Impaired liver cell function and gross architectural distortion leading to portal hypertension and eventual liver failure.

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14
Q

List four major causes of cirrhosis.

A

Viral hepatitis (B, C, D), alcohol (Western world), autoimmune hepatitis, Wilson’s disease; plus drugs/NAFLD.

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15
Q

Describe the two histological patterns of nodules in cirrhosis.

A

Micronodular (small, uniform nodules) and macronodular (larger, variable nodules), often mixed.

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16
Q

What clinical signs arise from portal hypertension in cirrhosis?

A

Variceal haemorrhage (e.g., oesophageal varices), ascites, splenomegaly.

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17
Q

What features reflect decompensated cirrhosis?

A

Portal-systemic encephalopathy, hepatorenal syndrome, refractory ascites, coagulopathy.

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18
Q

Which primary malignancy arises almost exclusively on a background of cirrhosis?

A

Hepatocellular carcinoma (HCC).

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19
Q

Name three risk factors for HCC.

A

Chronic HBV/HCV infection, cirrhosis (especially viral), aflatoxin exposure; androgenic steroids & (weakly) OCPs.

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20
Q

Outline the stepwise progression to HCC.

A

Cirrhosis → dysplastic nodules → overt hepatocellular carcinoma.

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21
Q

How does well-differentiated HCC appear histologically?

A

Neoplastic hepatocyte cords, thicker than normal, with identifiable hepatocytic features.

22
Q

What distinguishes poorly-differentiated HCC microscopically?

A

Pleomorphic cells, giant nuclei, loss of normal hepatic architecture.

23
Q

What clinical presentation in a cirrhotic patient suggests HCC?

A

New weight loss, fever, anorexia, ascites or abdominal pain; or detection of a focal liver lesion.

24
Q

Which tumour marker is elevated in ~⅔ of HCC patients?

A

Alpha-fetoprotein (AFP).

25
What imaging findings support HCC diagnosis?
Ultrasound/CT showing filling defects; MRI or angiography if doubt remains.
26
When is liver biopsy indicated in suspected HCC?
Only if noninvasive tests (AFP + imaging) are inconclusive due to seeding risk.
27
What criteria confirm HCC non‐invasively in cirrhosis?
Cirrhosis plus a liver mass >2 cm on imaging.
28
What are the main treatment options for early HCC?
Surgical resection or liver transplantation; chemoembolisation in selected cases.
29
Why are chemotherapy and radiotherapy generally unhelpful for HCC?
HCC is relatively chemo- and radio-resistant.
30
What is the typical prognosis for advanced HCC?
Survival often <6 months without early intervention.
31
What are the three major pathological lesions of alcoholic liver disease?
Alcoholic fatty liver, alcoholic hepatitis, alcoholic cirrhosis.
32
How does alcoholic fatty liver present and reverse?
Asymptomatic hepatomegaly; ↑ MCV and γ-GT; reversible on alcohol cessation.
33
What histological feature is pathognomonic for alcoholic hepatitis?
Mallory (Mallory–Denk) bodies plus hepatocyte necrosis and neutrophilic infiltrate.
34
Which lab findings typify alcoholic hepatitis?
Leucocytosis, moderate ↑ AST/ALT (<500 IU/L, AST>ALT), ↑ bilirubin, ↓ albumin, prolonged PT.
35
What is the mainstay of treatment for severe alcoholic hepatitis?
Supportive care, nutritional support; corticosteroids in severe cases.
36
Describe the morphology of alcoholic cirrhosis.
Micronodular regeneration nodules surrounded by fibrous septa in a fatty liver background.
37
How does abstinence affect alcoholic cirrhosis outcome?
Lifelong alcohol cessation improves 5-year survival significantly.
38
Which statement is not true about cirrhosis?
That it is a localised (it’s diffuse) process; it is irreversible.
39
Which statement is correct regarding alcoholic liver disease?
All of the above: it’s the most common chronic liver disease in the West; more common in men; alcohol is hepatotoxic; major lesions include fatty liver and cirrhosis.
40
What are the main layers/components of the tracheal wall?
C-shaped cartilage plates, smooth muscle, pseudostratified ciliated epithelium, and submucosal glands.
41
How do bronchi differ from bronchioles histologically?
Bronchi have cartilage foci, a thicker smooth-muscle layer, respiratory epithelium and glands; bronchioles lack cartilage, have thinner muscle, simple ciliated epithelium and Clara cells.
42
What are the two pneumocyte types and their functions?
Type I for gas exchange; Type II secrete surfactant and serve as progenitors for Type I.
43
Describe the respiratory mucosa and its defence role.
Pseudostratified columnar ciliated epithelium with goblet cells; cilia beat ~1,000 times/min to move mucus—and trapped pathogens—up the airway.
44
What defines a catarrhal disorder of the upper respiratory tract?
Inflammation of nasal mucosa with abundant muco-purulent secretions (runny nose).
45
Which virus causes the common cold and why can’t we vaccinate against it?
Rhinoviruses (>100 strains in the picornavirus family); impractical to cover all strains.
46
What are the two key surface proteins of influenza and their roles?
Haemagglutinin (H) for cell attachment; Neuraminidase (N) for viral penetration and release.
47
Differentiate antigenic drift vs. antigenic shift in influenza.
Drift: minor genetic changes causing seasonal epidemics; Shift: major reassortment leading to pandemics.
48
What is the incubation period and main symptoms of influenza?
1–3 days; fever, shivering, generalized myalgia, severe headache, sore throat, dry cough.
49
Who should receive annual influenza vaccination and why?
Elderly (≥ 60 yrs) and immunocompromised patients, due to higher risk of severe disease and death (~10,000 UK deaths/yr).
50
Define lobar pneumonia vs. bronchopneumonia anatomically.
Lobar: consolidation of an entire lobe; Bronchopneumonia: patchy foci of exudate in bronchioles and adjacent alveoli.