Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Phase 2a > Liver and co. > Flashcards

Liver and co. Flashcards

(165 cards)

Start Studying
1
Q

What are the functions of the liver?

A
  • Glucose + fat metabolism.
  • Detoxification + excretion.
  • Protein synthesis (albumin, clotting factors).
  • Defence against infection.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do liver function tests measure?

A
  • Serum bilirubin, albumin + prothrombin time.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What enzyme raises in…

i) Cholestatic liver disease?
ii) Hepatocellular liver disease?

A
  • Alkaline phosphatase (ALP).

- Transaminases (AST, ALT).

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

What occurs in pre-hepatic jaundice? What are the urine + stools like?

A
  • Increased breakdown of erythrocytes results in increased levels of unconjugated bilirubin.
  • Urine + Stools normal, no itching, LFTs normal.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What occurs in cholestatic jaundice? What are the urine + stools like?

A
  • Can be due to liver disease (hepatic) or bile-duct obstruction (post-hepatic).
  • Raised conjugated bilirubin.
  • Dark urine + pale stools, itching, abnormal LFTs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the symptoms of jaundice?

A

Biliary pain, rigors (indicative of obstructive), weight loss.

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

PARACETAMOL OVERDOSE

What occurs in the therapeutic dose of paracetamol?

A
  • Mostly metabolised via sulfate/glucuronic acid conjugation pathway (Phase II).
  • If stores are low, undergoes phase I oxidation forming highly reactive toxic compound NAPQI which is immediately conjugated with glutathione + excreted.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PARACETAMOL OVERDOSE

What happens in paracetamol overdose?

A
  • Large amounts of paracetamol oxidised to NAPQI due to Phase II saturation.
  • Liver glutathione stores depleted, NAPQI persists > hepatotoxicity + kidney injury.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

PARACETAMOL OVERDOSE

What are the clinical features of paracetamol overdose?

A

Asymptomatic for first 24h.
Liver damage peaks 72h after…
- Jaundice, metabolic acidosis, hypoglycaemia.

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

PARACETAMOL OVERDOSE

What is the treatment for paracetamol overdose?

A
  • Gastric decontamination with activated charcoal.

- IV N-acetyl-cysteine (replenishes cellular glutathione stores).

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

LIVER FAILURE

What is the pathophysiology of liver failure?

A
  • Destruction of hepatocytes + development of fibrosis in response to chronic inflammation.
  • The destruction of the architecture of the nodules of the level removes the ability of the liver to adequately perform functions, repair + regenerate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

LIVER FAILURE

What is fulminant hepatic failure? How does it come about?

A
  • Massive necrosis of liver cells leading to severe impairment of liver function.
  • Can be acute or progress from a chronic liver disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

LIVER FAILURE

What is the aetiology of fulminant hepatic failure?

A
  • Infection (Hep B/C, CMV).
  • Induced (alcohol, drug toxicity).
  • Autoimmune hep, metabolic liver diseases.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

LIVER FAILURE

What is the clinical presentation of fulminant hepatic failure?

A
  • Jaundice.
  • Hepatic encephalopathy (drowsiness/confusion).
  • Clubbing.
  • Ascites.
  • Asterixis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

LIVER FAILURE

What is hepatic encephalopathy?

A
  • Liver unable to remove ammonia + so it’s able to cross BBB causing cerebral oedema.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

LIVER FAILURE

What are the investigations for fulminant liver failure?

A
  • Bloods – hepatitis, CMV + EBV serology, raised bilirubin, low glucose.
  • Abdominal USS.
  • Doppler flow studies of portal vein.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

LIVER FAILURE

What is the treatment for fulminant liver failure?

A
  • Nutrition + supplements.
  • Treat complications (lactulose, mannitol for hepatic encephalopathy)
  • Liver transplantation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ALCOHOLIC LIVER DISEASE

What are the three stages of alcoholic liver disease?

A
  • Fatty change.
  • Alcoholic hepatitis.
  • Alcoholic cirrhosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ALCOHOLIC LIVER DISEASE

Explain the fatty change stage.

A
  • Biopsy finding, hepatocytes contain macrovesicular droplets of triglycerides.
  • Fat disappears on cessation of alcohol intake.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ALCOHOLIC LIVER DISEASE

Explain the alcoholic hepatitis stage.

A
  • Ballooned hepatocytes that contain eosinophilic material called Mallory bodies, surrounding by neutrophils.
  • Fibrosis + foamy degeneration of hepatocytes possible, usually co-exists with cirrhosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ALCOHOLIC LIVER DISEASE

Explain the alcoholic cirrhosis stage.

A
  • Final stage of alcoholic liver disease where there’s destruction of liver architecture + fibrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ALCOHOLIC LIVER DISEASE

What are the clinical presentations of alcoholic hepatitis and alcoholic cirrhosis?

A 
Hepatitis...
- Rapid onset jaundice.
- Nausea, fever, ascites.
- Encephalopathy.
Cirrhosis...
- Spider naevi, loss of body hair.
- Clubbing, palmar erythema, white nails.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ALCOHOLIC LIVER DISEASE

What are the investigations for alcoholic liver disease?

A

Bloods = macrocytic anaemia.

Liver biochemistry = AST + ALT raised (AST>ALT ratio), GGT v raised.

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

ALCOHOLIC LIVER DISEASE

What is the treatment for alcoholic liver disease?

A
  • Alcohol cessation.

- Treat malnutrition from alcohol (thiamine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
CIRRHOSIS | What is the pathophysiology of cirrhosis?
- Cirrhosis results form necrosis of liver cells followed by fibrosis + nodule formation, the end result is impairment of liver cell function + gross distortion of the liver architecture leading to portal HTN.
26
CIRRHOSIS What is... i) compensated cirrhosis? ii) decompensated cirrhosis?
i) When the liver can still function effectively + there are no/few noticeable symptoms. ii) Liver is damaged to point it cannot function adequately + clinical complications present. Events causing this can be infection, portal vein thrombosis + surgery.
27
CIRRHOSIS | What is the aetiology of cirrhosis?
Chronic liver diseases... - Alcohol misuse (commonest in western world). - Hep B/C (commonest worldwide). - Obesity/T2DM.
28
CIRRHOSIS What is the clinical presentation of i) Chronic liver disease? ii) Secondary to portal HTN + liver failure?
i) Spider naevi + loss of body hair, clubbing, palmar erythema, white nails. ii) Ascites, abdominal pain, variceal haemorrhage, encephalopathy, jaundice.
29
CIRRHOSIS | What are the major complications with cirrhosis?
- MAJOR = hepatocellular carcinoma, screen for it every 6 months with ultrasound + serum alpha-fetoprotein, AFP. - Hepatic encephalopathy. - Abnormal bleeding (portal HTN > variceal haemorrhage). - Ascites.
30
CIRRHOSIS | What are the investigations for cirrhosis?
- Bloods, FBC = thrombocytopenia witih leukopenia + anaemia later. - Liver ultrasound + duplex. - Liver biopsy = diagnostic. - Ascitic tap.
31
CIRRHOSIS | What is the treatment for cirrhosis?
- Treat underlying. - Symptom relief = spironolactone for ascites, lactulose/mannitol for hepatic encephalopathy. - If ascites, prohylactic ciprofloxacin. - Liver transplant most effective.
32
PORTAL HYPERTENSION | What is the pathophysiology of portal HTN?
- Inflow of portal blood can be partially/completely obstructed leading to high pressure proximal to obstruction. - Endothelin-1 production is increased + NO production is decreased in cirrhosis so there's more vasoconstriction, increasing portal pressure.
33
PORTAL HYPERTENSION | What is the aetiology of portal HTN?
- Pre-hepatic (blockage of portal vein) = thrombosis or portal/splenic vein. - Intrahepatic (distortion of liver architecture) = cirrhosis (UK), schistosomiasis (worldwide). - Post-hepatic (venous blockage outside liver) = Budd-Chiari syndrome.
34
PORTAL HYPERTENSION | What is Budd-Chiari syndrome?
- Vascular disease associated with occlusion of hepatic veins that drain liver.
35
PORTAL HYPERTENSION | What are the complications tha can occur in portal HTN?
- Varices can occur due to diversion of blood into portosystemic collaterals (gastro-oesophageal junction) to relieve the pressure where they are superifical + liable to rupture, causing massive GI haemorrhage.
36
PORTAL HYPERTENSION | What is the clincial presentation of portal HTN?
Oesophago-gastric varcies... - Haematemesis. - Pallor. - Shock (hypotensive, tachycardic).
37
PORTAL HYPERTENSION | What are the investigations for portal HTN?
- Upper GI endoscopy.
38
PORTAL HYPERTENSION | What are the treatment for portal HTN?
``` Medical (reduce portal pressure)... - Beta blocker to reduce CO. - Nitrates + ADH analogue. Surgical... - Band ligation. - Trans-jugular intrahepatic portosystemic shunt (TIPSS). ```
39
ACUTE PANCREATITIS | What is the pathophysiology of acute pancreatitis?
- Inflammatory process with release of inflammatory cytokines (TNF-alpha, IL-6) + pancreatic enzymes (trypsin, lipase) which destroys the pancreas.
40
ACUTE PANCREATITIS | What are the three types of pancreatitis?
- Oedematous (acute fluid collection). - Necrotising. - Haemorrhagic.
41
ACUTE PANCREATITIS | What is the aetiology of acute pancreatitis?
I GET SMASHED... - Idiopathic. - Gallstones. - Ethanol (alcohol). - Trauma. - Steroids. - Mumps. - Autimmune. - Scorpion stings. - Hyperlipidaemia. - ERCP (endoscopic retrograde cholangiopancreatography). - Drugs.
42
ACUTE PANCREATITIS | What are the symptoms of acute pancreatitis?
- Severe epigastric abdominal pain (radiates to back, sitting forward may relieve). - May be gradual/sudden onset. - Vomiting.
43
ACUTE PANCREATITIS | What are the signs of acute pancreatitis?
- Periumbilical or flank bruising (Cullen's + Grey Turner's signs respectively) from blood vessel autodigestion + retroperitoneal haemorrhage. - Jaundice. - Shock.
44
ACUTE PANCREATITIS | What are the investigations for acute pancreatitis?
Diagnosis on 2/3... - Characteristic severe epigastric pain radiating to back. - Raised serum amylase (3-fold upper limit). - Abdominal CT scan pathology. - Serum lipase is more sensitive + specific.
45
ACUTE PANCREATITIS | What is criteria is used for predicting acute pancreatitis severity?
``` Modified Glasgow Criteria, PANCREAS ≥3 suggests severe... PaO2 < 8kPa. Age >55y/o Neutrophilia Calcium <2mmol/L. Raised urea >16mmol/L. Elevated enzymes. Albumin <32g/L. Sugar, blood glucose >10mmol/L. ```
46
ACUTE PANCREATITIS | What is the treatment for acute pancreatitis?
- Analgesia, IV fluids (maintian electrolyte balance). - Oxygen. - Treat cause. - Abx? Gallstone removal (progressive jaundice)? Drain oedematous fluid, surgery.
47
CHRONIC PANCREATITIS | What is the pathophysiology of chronic pancreatitis?
- Chronic inflammation of the pancreas leads to irreversible damage. - Pancreatic duct obstruction leads to activation of pancreatic enzymes leading to necrosis + subsequent fibrosis.
48
CHRONIC PANCREATITIS | What is the aetiology of chronic pancreatitis?
- Most excessive alcohol consumption as proteins precipitate in ductal lumen causing obstruction. - Smoking, autoimmune.
49
CHRONIC PANCREATITIS | What is the clinical presentation of chronic pancreatitis?
- Epigastric pain radiating to back (relieved sitting forward). - Weight loss. - Steatorrhoea (excretion of abnormal quantities of fat). - DM. - Nausea + vomiting.
50
CHRONIC PANCREATITIS | What are the investigations for chronic pancreatitis?
- Ultrasound ± CT shows pancreatic calcifications.
51
CHRONIC PANCREATITIS | What is the treatment for chronic pancreatitis?
``` Lifestyle = smoking + alcohol cessation, ?low fat diet. Drugs = analgesia, pancreatic enzyme replacement, steroids if autoimmune. Surgery = local resection. ```
52
BILIARY COLIC | What is the pathophysiology of biliary colic?
- RUQ pain due to gallstone blocking bile duct temporarily.
53
BILIARY COLIC | What is the aetiology of biliary colic?
Gallstones... | - Cholesterol, bile pigment + phospholipids are components seen.
54
BILIARY COLIC | What is the clinical presentation of biliary colic?
- Recurrent episodes of severe, persistent RUQ pain (back radiation). - Triggered by heavy, faty meal.
55
BILIARY COLIC | What are the investigations of biliary colic?
- Basis of history + ultrasound showing gallbladders. - Serum ALP + bilirubin increases during attack. - Absence of inflammatory features differentiates from acute cholecystitis.
56
BILIARY COLIC | What is the treatment for biliary colic?
- Analgesics + elective cholecystectomy.
57
ACUTE CHOLECYSTITIS | What is the pathophysiology of acute cholecystitis?
- Inflammation of the gallbladder following the impaction of a stone in the cystic duct/neck of gallbladder, obstruction to bile emptying.
58
ACUTE CHOLECYSTITIS | What is the aetiology + risk factors for acute cholecystitis?
- Gallstones. | - Fat, Forty, Female, Fertile.
59
ACUTE CHOLECYSTITIS | What is the clinical presentation of acute cholecystitis?
- Sever RUQ pain associated with fever, vomiting. - Gallbladder mass. - NO jaundice. - Murphy's sign (tenderness worse on inspiration when 2 fingers on RUQ).
60
ACUTE CHOLECYSTITIS | What are the complications of acute cholecystitis?
- Empyema (pus) + perforation with peritonitis.
61
ACUTE CHOLECYSTITIS | What are the investigations of acute cholecystitis?
- Bloods = FBC shows increased WCC. - Liver function tests to exclude liver/bile duct pathology. - Abdominal USS shows gallstones + distended gallbladder w/ thickened wall.
62
ACUTE CHOLECYSTITIS | What are the treatments for acute cholecystitis?
Supportive = nil-by-mouth, IV fluids, pain relief. | Laparoscopic cholecystectomy.
63
ASCENDING CHOLANGITIS | What is the pathophysiology of ascending cholangitis?
- Gallstone is stuck in the common bile duct + because flow of bile can no longer prevent intestinal bacteria from migrating up the biliary tree there is infection + inflammation.
64
ASCENDING CHOLANGITIS | What is the aetiology of ascending cholangitis?
- Gallstones. | - Infection (E. coli, klebsiella, enterococcos, group D strep).
65
ASCENDING CHOLANGITIS | What is the clinical presentation of ascending cholangitis?
- Charcot's triad = fever, RUQ pain + jaundice (cholestatic). - Reynold's pentad w/ hypotension + confusion.
66
ASCENDING CHOLANGITIS | What are the investigations for ascending cholangitis?
``` Bloods – WCC increased, blood cultures, positive, LFTs raised. MR cholangiopancreatography (MRCP) visualises site + Cause of obstruction. ```
67
ASCENDING CHOLANGITIS | What is the treatment for ascending cholangitis?
- Fluid resuscitation, Abx. | - ERCP for biliary drainage, stone removal + bile sample for culture.
68
PBC | What is the pathophysiology of primary biliary cholangitis (PBC)?
- Interlobular bile ducts (intrahepatic) are damaged by chronic autoimmune granulomatous inflammation causing cholestasis which can lead to fibrosis, cirrhosis + portal HTN.
69
PBC | What is the epidemiology + aetiology of PBC?
- F:M = 9:1, positive family Hx gives 10-fold risk. | - Unknown triggers, associated with other autoimmune diseases like coeliac.
70
PBC | What is the clinical presentation of PBC?
- Asymptomatic but may have pruritus, fatigue. | - Signs = jaundice, skin hyperpigmentation, hepatosplenomegaly.
71
PBC | What are the investigations for PBC?
Blood... - LFTs, increased ALP. - Serum autoantibodies, antimitochondrial antibodies (AMA, IgM). - Serum antibodies (IgM) increased.
72
PBC | What are the treatments for PBC?
- Colestyramine for pruritus. - Vitamin A, D, E + K supplementation. - Liver transplantation.
73
PSC | What is the pathophysiology of primary sclerosing cholangitis?
- Progressive cholestasis characterised by strictures + fibrosing inflammatory destruction of both intra + extrahepatic bile ducts.
74
PSC | What is the aetiology of PSC?
- Secodary to infection, thrombosis, trauma. - 75% association with ulcerative colitis. - Cancers more common.
75
PSC | What is the clinical presentation of PSC?
- Pruritus ± fatigue. | - Cirrhosis + hepatic failure if advanced (jaundice, fever).
76
PSC | What are the investigations for PSC?
- Serum autoantibodies like Anti-neutrophil cytoplasmic antibody (ANCA, not specific). - ERCP/MRCP show duct anatomy. - Liver biopsy.
77
PSC | What are the treatments for PSC?
- Colestyramine for pruritus. - Vitamin A, D, E + K supplementation. - Liver transplantation.
78
ASCITES | What is ascites?
- Accumulation of fluid in peritoneal cavity leading to abdominal distention.
79
ASCITES | Why does ascites occur in cirrhosis?
In cirrhosis, peripheral arterial vasodilation leads to reduction in effective blood volume, with activation of sympathetic nervous system + RAAS prompting renal salt + water retention. - Formation of oedema encouraged by hypoalbuminaemia + mainly localised to peritoneal cavity due to portal HTN.
80
ASCITES | What is the aetiology of ascites?
Exudative (cloudy)... - Local inflammation (peritonitis). Transudate (clear)... - Leaky vessels (imbalance between hydrostatic/oncotic pressures [H>O] Hp increased due to portal HTN + RAAS). - Low flow (cirrhosis, thrombosis, cardiac failure). - Low protein (hypoalbuminaemia decreases oncotic pressure).
81
ASCITES | What is the clinical presentation of ascites?
- Distended abdomen. - Shifting dullness. - Flank swelling. - Bulging flanks.
82
ASCITES | What is the major complication of ascites?
Spontaneous bacterial peritonitis... - Complication of ascites w/ cirrhosis. - Causes = E. coli, klebsiella, enterococcus. - Ascitic tap shows raised neutrophils. - Mange by cefotaxime, ciprofloxacin prophylaxis.
83
ASCITES | What are the investigations for ascites?
- Ultrasound/CT/MRI abdomen. - LFTs, serum albumin. - Ascitic tap.
84
ASCITES | What is the treatment fo ascites?
- Treat cause, limit dietary sodium + fluids. - Paracentesis (drainage). - Diuretics like spironolactone.
85
AUTOIMMUNE HEPATITIS | What is the pathophysiology of autoimmune hepatitis?
- Inflammatory liver disease characterised by abnormal T-cell function + autoantibodies directed against hepatocyte surface antigens.
86
AUTOIMMUNE HEPATITIS | What is the clinical presentation of autoimmune hepatitis?
- Insidious w/ anorexia, malaise, nausea, fatigue. | - Signs of chronic liver disease (spider naevi, jaundice etc).
87
AUTOIMMUNE HEPATITIS | What are the investigations for autoimmune hepatitis?
Circulating autoantibodies, IgG - Type 1 = antinuclear antibody (ANA), anti-smooth muscle antibody (ASMA). - Type 2 = anti-liver kidney microsome. Liver biopsy.
88
AUTOIMMUNE HEPATITIS | What are the treatments for autoimmune hepatitis?
- Immunosuppresion with prednisolone. | - Liver transplantation if failure of medical therapy.
89
VIRAL HEPATITIS | What are the pathological features of hepatitis? What is the difference between acute + chronic hepatitis?
- Liver cell necrosis + inflammatory cell infiltration. - Acute = most commonly hepatitis viruses, often self-limiting with return to normal structure + function. - Chronic = sustained inflammatory disease of liver lasting >6 months.
90
``` VIRAL HEPATITIS What is the aetiology of... i) Acute infective ii) Acute non-infective iii) Chronic ifnective ``` hepatitis?
i) Hepatitis A–E, EBV, CMV. ii) Alcohol, drugs, toxins, autoimmune. iii) Hepatitis B–D, E in immunocompromised.
91
VIRAL HEPATITIS A | What type of virus is hepatitis A? How is it spread? How long does it take to incubate?
- RNA virus, 100% acute w/ immunity after. - Faeco-oral, normally w/ travel history, contaminated food/water. - 2–6 weeks.
92
VIRAL HEPATITIS A | What are the symptoms of hepatitis A?
- Fever, malaise, anorexia, nausea then jaundice + hepatosplenomegaly.
93
VIRAL HEPATITIS A | What are the investigations for hepatitis A?
AST + ALT rise. Serology... - Anti-HAV IgM rises initially = recent infection. - Anti-HAV IgG detectable for life.
94
VIRAL HEPATITIS A | What is the treatment for hepatitis A?
- Preventative = vaccination for travellers. | - Supportive, avoid alcohol, manage close contacts.
95
VIRAL HEPATITIS B | What type of virus is hepatitis B? How is it spread?
- DNA virus (replicates in hepatocytes), acute. | - Blood-borne like IV drug users, sexual, needle-stick (highly infectious).
96
VIRAL HEPATITIS B | What is the first stage in the natural history of hepatitis B?
Immune tolerance phase = unimpeded viral replication leads to high HBV DNA levels.
97
VIRAL HEPATITIS B | What is the second stage in the natural history of hepatitis B?
Immune clearance phase = immune system stimulated by HBV proteins, liver inflammation + high ALT.
98
VIRAL HEPATITIS B | What is the third stage in the natural history of hepatitis B?
Inactive HBV carrier phase = HBV DNA levels low, ALT levels normal, no liver inflammation.
99
VIRAL HEPATITIS B | What is the last stage in the natural history of hepatitis B?
Reactivation phase = ALT + HBV DNA levels are intermitted + inflammation is seen on liver > fibrosis.
100
VIRAL HEPATITIS B | What are the symptoms of hepatitis B?
- Fever, malaise, arthralgia, then jaundice, hepatosplenomegaly.
101
VIRAL HEPATITIS B | What are the investigations for hepatitis B?
Viral serology... - HBV surface antigen detected 6w–3m. - Anti-HBV core IgM after 3m.
102
VIRAL HEPATITIS B | What is the treatment for hepatitis B?
- Supportive, monitor liver function, manage contacts. - Pegylated interferon alpha 2a (boosts immune system). - Follow up at 6m to see if HBV surface antigen cleared, if not chronic. - Prevention via vaccination (small amount of inactive HBsAg), HBVs IgG present in vaccinated.
103
VIRAL HEPATITIS B | What are the consequences of hepatitis B?
- Cirrhosis. - HCC. - Fulminant hepatic failure.
104
VIRAL HEPATITIS C | What type of virus is hepatitis C? How is it spread?
- RNA virus, 70% progress to chronic. | - Blood-borne like materno-foetal transmission.
105
VIRAL HEPATITIS C | What are the investigations for hepatitis C?
Viral serology... - Anti-HCV antibodies (IgM/G) confirms exposure. - HCV-PCR confirms ongoing infection.
106
VIRAL HEPATITIS C | What are the treatments for hepatitis C?
- Ribavirin + pegylated interferon alpha 2a.
107
VIRAL HEPATITIS D | What sort of virus is hepatitis D and how does it spread? What are the investigations for hepatitis D?
Defective RNA virus, needs HBV for assembly as it needs HBsAg for protection. Blood-borne transmission, esp. IVDU. Viral serology... - Anti-HDV antibody if HBsAg +ve also.
108
VIRAL HEPATITIS D | What is the treatment for hepatitis D?
- Complete prevention if HBV vaccination. | - Liver transplantation.
109
VIRAL HEPATITIS E | What type of virus is hepatitis E? How is it spread?
- Small RNA virus, acute but risk of chronic in immunocompromised. - Faeco-oral, contaminated food/water, undercooked pork in UK.
110
VIRAL HEPATITIS E | What are the investigations + treatment for hepatitis E?
Viral serology... - Anti-HEV IgM rises initially + means recent infection. - Anti-HEV IgG detectable for life. Vaccine, good food hygiene.
111
NAFLD | What is the pathophysiology of non-alcoholic fatty liver disease (NAFLD)? What is non-alcoholic steatohepatitis (NASH)?
- Represents increased fat in hepatocytes visualised that cannot be attributed to other causes like alcohol. - If inflammation is present = NASH.
112
NAFLD | What are the risk factors + investigations for NAFLD?
- Metabolic syndrome, T2DM. | - Rule out other causes of liver disease, enhanced liver fibrosis test (for advanced liver fibrosis).
113
NAFLD | What is the treatment for NAFLD?
- Control risk factors (lose weight, exercise more, avoid alcohol). - Address CV risk, monitor for complications.
114
LIVER ABSCESS | What is the pathophysiology of liver abscess?
- Pus-filled mas inside liver post-infection, appendicitis or haematogenous spread via portal vein.
115
LIVER ABSCESS | What is the aetiology of liver abscess?
- Elderly (biliary sepsis). - Trauma. - E. coli (most common), klebsielle pnuemoniae
116
LIVER ABSCESS | What is the clinical presentation, investigations + treatment of liver abscess?
- Fever, vomiting, RUQ pain. - Bloods = ALP, ESR/CRP raised, CT abdomen, ultrasound to detect + sample. - Aspiration under USS, anitbiotics like co-amoxiclav, metronidazole.
117
AMOEBIC ABSCESS | What is the pathophysiology of amoebic abscess?
- Entamoeba histolytica can be carried from bowel to liver in portal venous system leading to portal inflammation + development of abscesses.
118
AMOEBIC ABSCESS | What is the clinical presentation of amoebic abscess?
- Fever, abdominal pain, tender hepatomegaly, night sweats. | - Signs of effusion or consolidation.
119
AMOEBIC ABSCESS | What are the investigations + treatment of amoebic abscess?
- Serological test for amoeba (ELISA). - USS abdomen + cyst aspiration shows 'anchovy sauce' pus. - Metronidazole, aspiration.
120
DIARRHOEA | What is diarrhoea? What is acute + chronic diarrhoea?
- Abnormal passage of loose or liquid stool ≥3x daily. - Acute = usually due to infection/dietary indiscretion. - Chronic = defined as diarrhoea >14d.
121
DIARRHOEA | What three things leads to decreased stool consistency?
- Osmotic = large quantities of non-absorbed hypertonic substances in bowel draw fluid into intestine (malabsorption, laxatives). - Secretory = active intestinal secretion of fluid + electrolyes as well as decreased absorption. - Inflammatory = damage to intestinal mucosal cells leads to loss of fluid, blood + defective absorption of fluid + electrolytes.
122
DIARRHOEA | What is the aetiology of diarrhoeal infection?
- Traveller's diarrhoea, viral, bacterial, helminths. - Enterohaemorrhagic E.coli cause bloody diarrhoea + has shiga like toxin. - Enteropathogenic E. coli causes large volumes of watery diarrhoea.
123
DIARRHOEA | What are the aetiology of non-infectious diarrhoea and risk factors?
- Gastritis/peptic ulceration/acute cholecystitis/peritonitis. - Risks = food handlers, health care workers, children at nursery.
124
DIARRHOEA | What is the clinical presentation of infective, inflammatory + helminths diarrhoea?
- Sudden onset bowel frequency w/ crampy abdominal pains + fever = infective - Bowel frequency with loose, blood-stained stools = inflammatory. - Fever, eosinophilia, diarrhoea, cough, wheeze = helminths.
125
DIARRHOEA | What are the investigations for diarrhoea?
- Stool samples (culture + sensitivity), faecal calprotectin, faecal occult test. - Blood/mucous? - Family Hx? - Abdominal pain? - Foreign travel? - Bloating/weight loss?
126
DIARRHOEA | What are the preventative measures for diarrhoea?
- Access to clean water. - Good sanitation + hand hygiene. - Don't let food handlers go to work without negative stool sample - Close wards.
127
DIARRHOEA | What are the treatments for diarrhoea?
- Treat cause, oral rehydration ± electrolyte replacement. | - Anti-motility agents.
128
TRAVELLER'S DIARRHOEA | What is the pathophysiology + aetiology of traveller's diarrhoea?
- Increased secretion of Cl- into intestinal lumen, water follows down osmotic gradient. - Enterotoxigenic E. coli (ETEC), campylobactera jejuni, Giardia lamblia.
129
TRAVELLER'S DIARRHOEA | What are the varying clinical presentations for traveller's diarrhoea?
- ETEC = watery diarrhoea preceded by cramps + nausea. - Giardia = upper GI symptoms (bloating, belching). - C. jejuni = colitic symptoms, urgency, cramps.
130
TRAVELLER'S DIARRHOEA | what are the investigations + treatment for traveller's diarrhoea?
- >3 unformed stools/day + abdominal pain, cramps, nausea or vomiting. - Occurs within 3 days of arrival in new country, lasts week. - Oral rehydration + anti-motility agents.
131
INFECTIVE DIARRHOEA | What is the epidemiology of infective diarrhoea?
- 2nd leading cause of death in children <5y/o globally (after pneumonia).
132
INFECTIVE DIARRHOEA | What is the aetiology of infective diarrhoea?
``` Viral causes most... - Children = rotavirus. - Adults = norovirus (cruises, hospitals, restaurants). Bacterial causes... - C. jejuni (poultry association). - Children = E. coli, salmonella, shigella. - Anitbiotic association. - Parasitic (Giardia lamblia) ```
133
INFECTIVE DIARRHOEA | What antibiotics are associated with Costridium difficile diarrhoea?
Rule of Cs... - Clindamycin. - Ciprofloxacin (quinolones). - Co-amoxiclav (penicillins). - Cephalosporins.
134
INFECTIVE DIARRHOEA | What is C. diff? How does it present? What are the risk factors? How do you treat it?
- Gram +ve spore forming bacteria. - Pyrexia, colic, raised inflammatory markers. - Elderly, long hospital stay, acid suppression. - Metronidazole, oral vancomycin.
135
INFECTIVE DIARRHOEA | How does Giardia lamblia cause diarrhoea + how is it treated?
- Diarrhoea due to alteration of intestinal villi = decreased absorption. - Metronidazole.
136
INFECTIVE DIARRHOEA | What are the clinical presentations for infective diarrhoea?
- Blood indicates bacterial infection. - Vomiting, abdominal cramping. - Fever, fatigue, headache = virus.
137
INFECTIVE DIARRHOEA | What are the investigations of infective diarrhoea?
- Bloods = find alternative cause, raised WCC if parasitic, raised ESR/CRP indicate infection. - Stool culture. - Sigmoidoscopy with biops.y
138
INFECTIVE DIARRHOEA | What is the treatment of infective diarrhoea?
- Treay cause, oral rehydration, anti-emetics, anti-motility + Abx.
139
CHOLERA | What causes cholera + how do you investigate this?
- Infection from vibrio cholerae (gram-ve aerobic 'comma-shaped' rod) found in faecal contaminated water. - Stool culture sample.
140
CHOLERA | What is the clinical presentation + treatment of cholera?
- Rice-water stool (diarrhoea), vomiting + dehydration, metabolic acidosis. - Biggest preventer = safe-drinking water, oral rehydration salts, doxycycline.
141
HAEMOCHROMATOSIS | What is the pathophysiology of haemochromatosis?
Inherited disorder of iron metabolism in which an increase in intestinal iron absorption leads to iron accumulation/deposition in several places (joints, heart, pancreas).
142
HAEMOCHROMATOSIS | What is the aetiology of haemochromatosis?
- AR associated with HFE gene leading to deficiency in the iron regulatory hormone hepcidin.
143
HAEMOCHROMATOSIS | What is the clinical presentation of haemochromatosis?
- Slate-grey skin pigmentation. - DM ('bronze' diabetes from pancreatic iron deposition). - Cardiomyopathy.
144
HAEMOCHROMATOSIS | What are the investigations + treatment of haemochromatosis?
- Bloods = increased LFTs, ferritin, transferrin saturation ratio. - Confirm by HFE genotyping by PCR. - Excess tissue iron removed by venesection, desferrioxamine, may need insulin.
145
WILSON'S DISEASE | What is the pathophysiology of Wilson's disease? What is the aetiology?
- Disorder of copper metabolism where ther eis excessive deposition of copper in the liver + CNS. - AR disorder of a copper transporting ATPase.
146
WILSON'S DISEASE | What is the clinical presentation of Wilson's disease?
- Fayser-Fleischer rings = copper in iris. | - Neurological signs (tremor, dysphagia, dyskinesias) due to copper in CNS.
147
WILSON'S DISEASE | What are the investigations + treatment of Wilson's disease?
- Low total serum copper, increased 24h urinary copper. | - Lifetime penicillamine to excrete copper, reduce intake (shellfish, liver, chocolate).
148
ALPHA-1-ANTITRYPSIN DEF | What is the pathophysiology + aetiology of alpha-1-antitrypsin (A1AT) deficiency?
- Results in protein retention in the liver + eventually cirrhosis. - Deficiency of serine protease inhibitor A1AT (SERPINA1) gene), AR.
149
ALPHA-1-ANTITRYPSIN DEF | What is the clinical presentation of A1AT deficiency?
- COPD symptoms due to alveoli damage + emphysema. | - Jaundice, hepatitis, cirrhosis.
150
ALPHA-1-ANTITRYPSIN DEF | What are the investigations + treatment in A1AT deficiency?
- Serum A1AT levels. | - Manage COPD (stop smoking), liver transplantation is a cure.
151
LIVER CANCERS | What is the pathophysiology of liver cancers?
- Mostly secondary (90%) as they have metastasisted from the GI tract, breast + bronchus.
152
LIVER CANCERS | What are the two benign liver cancers?
- Haemangiomas = commonest, often incident on USS/CT, don't require treatment. - Adenomas = common, anabolic steroids, OCT, pregnancy, only treat if symptomatic.
153
LIVER CANCERS | What is the epidemiology of the two primary liver cancers?
- Hepatocellular carcinoma (HCC) = 90%, China/Africa. | - Cholangiocarcinoma = 10%.
154
LIVER CANCERS | What is the aetiology of liver cancers?
``` HCC... - Most occur in chronic liver disease, cirrhosis, viral hep B/C. - Alcohol + anabolic steroids. Cholangiocarcinoma... - Flukes biliary cysts, viral hep B + C. ```
155
LIVER CANCERS | What is the clinical presentation of liver cancers?
HCC... - Weight loss, fever, abdominal pain, ascites, hepatomegaly. Cholangiocarcinoma... - Fever, abdominal pain (± ascites).
156
LIVER CANCERS | What are the investigations for liver cancers?
HCC... - Bloods (serum AFR may be raised), USS/CT to identify lesions, biopsy. Cholangiocarcinoma... - Bloods = increased bilirubin, big incresaedin ALP. - ERCP for biopsies.
157
LIVER CANCERS | What is the treatment for liver cancers?
``` HCC... - Prevention with HBV vaccination. - Surgical resection, liver transplant. Cholagniocarcinoma... - Mostly inoperable, stent to relieve symptoms. ```
158
PANCREATIC CANCERS | What is the pathophysiology of pancreatic cancers?
- Mostly ductal adenocarcinoma (metastasise early, present late). - 60% arise from head, 25% body, 15% tail. - Some arise in ampulla of Vater (ampulllary tumour) or pancreatic islet cells (insulinoma, gastrinoma, glucagonomas etc).
159
PANCREATIC CANCERS | What is the aetiology of pancreatic cancers?
- Hereditary (dominant susceptibility gene) + environemtnal factors (smoking, obesity) contribute). - Chronic pancreatitis is pre-malignant.
160
PANCREATIC CANCERS | What is the clinical presentation of pancreatic cancers?
Male, >70y/o. Head/ampulla... - Painless obstructive jaundice, palpable gallbladder. Body + tail... - Epigastric pain (radiates to back, relieved by sitting forward), weight loss, anorexia.
161
PANCREATIC CANCERS | What are the investigations + treatment for pancreatic cancers?
- USS/CT scan to show pancreatic mass. - ERCP/MRCP. - Whipple's procedure for head of pancreas, laparoscopic excision for tail lesions, combined chemo/radiotherapy.
162
PERITONITIS | What is the difference between localised + generalised peritonitis?
- Localised = occurs with all acute inflammatory conditions of GI tract. - Generalised = occurs as a result of rupture of an abdominal viscus (duodenal ulcer, appendix).
163
PERITONITIS | What is the aetiology of peritonitis?
Bacterial... - Perforated organ, spontaneous bacterial peritonitis, secondary to peritoneal dialysis. Non-infective... - Bile leak, blood from ruptured ectopic.
164
PERITONITIS | What is the clinical presentation of peritonitis?
- Pain, tenderness, systemic symptoms (nausea, chills, rigor).
165
PERITONITIS | What are the investigations + treatment of peritonitis?
- Abdominal examination = guarding, rebound, rigidity, erect CXR = gas under diaphragm. - Localised = treat underlying cause, generalised = antibiotics, supportive measures.

Phase 2a (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions