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Phase 2 > Liver and Friends > Flashcards

Liver and Friends Flashcards

1
Q

What are the functions of the liver

A

Glucose and fat metabolism
Detoxification and excretion (Bilirubin, ammonia, drugs)
Protein synthesis (Albumin and clotting factors)
Defence against infection

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2
Q

What are the two types of liver injury

A

Acute - damage to and loss of cells with death occurring by necrosis or apoptosis <6months
Chronic - chronic damage leading to fibrosis (Cirrhosis)

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3
Q

What are the causes of acute liver injury

A 
Viral (Hep A, B and EBV)
Drugs 
Alcohol
Vascular 
Obstruction 
Congestion
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4
Q

What are the causes of chronic liver injury

A

Alcohol
Viral B and C
Autoimmune
Metabolic (iron, copper)

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5
Q

What is the presentation of acute liver injury

A 
Malaise 
Nausea 
Anorexia 
Jaundice 
Confusion - encephalopathy 
Bleeding - lack of clotting factors 
Liver Pain 
Hypoglycaemia
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6
Q

What is the presentation of chronic liver injury

A 
Ascites 
Oedema 
Haematemesis 
Malaise 
Weight loss 
Anorexia 
Wasting 
Easy bruising 
Itching 
Hepatomegaly 
Jaundice 
Confusion
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7
Q

Name three serum liver function tests

A

Serum bilirubin
Serum albumin
Prothrombin time

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8
Q

Do serum liver enzymes give an index of liver function

A

No

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9
Q

Name enzymes that increase in the serum in cholestatic liver disease (Duct and obstructive)

A

Alkaline Phosphate (Raised in both intrahepatic and extra hepatic cholestactic)

Gamma-GT (Microsomal liver enzyme)

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10
Q

What enzyme increases in serum hepatocellular liver disease

A

Transaminases (ALT and AST

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11
Q

What do elevated transaminases indicate

A

Enzymes are contained in hepatocytes and leak into the blood with liver cell damage

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12
Q

Anti-mitochondrial antibodies are seen in the serum with what condition

A

Primary billiary cirrhosis

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13
Q

Anti-nuclear cytoplasmic antibodies are fond in the serum of patients with what condition

A

Primary sclerosis cholangitis

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14
Q

What is a normal bilirubin concentration

A

3-17uM

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15
Q

At what bilirubin concentration does jaundice become visible

A

50uM

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16
Q

Describe the physiology of bile production

A
  1. Hb broken into globin and haem
  2. Haem broken down into biliverdin
  3. Biliverdin reduced by biliverdin reductase into unconjugated bilirubin which is transported to the liver bound to albumin
  4. Unconjugated bilirubin is converted to conjugated bilirubin by glucuronidation by uridine glucuronyl transferase in the liver
  5. Conjuagted bilirubin converted to urobilinogen which is reabsorbed and returned to the liver and re-excreted into the bile
  6. Some reabsorbed urobilinogen is excreted into the urine as urobilin
  7. Urobilinogen that remains in the GIT is converted to stercobilin and excreted
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17
Q

What are the pre-hepatic causes of jaundice?

A

Excess unconjugated bilirubin production due to haemolytic anaemia or ineffective erythropoiesis (Thalassaemia)

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18
Q

What are the unconjugated hepatic causes of jaundice

A
  1. Decreased bilirubin uptake due to drugs

2. Decreased bilirubin conjugation due to Gilberts syndrome or Crigler-Najjar or hypothyroidism

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19
Q

What is Gilbert’s disease

A

Autosomal dominant condition resulting in a partial deficiency in UDP-GT which increases unconjugated bilirubin

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20
Q

What is Crigler Najjar syndrome

A

Autosomal recessive condition resulting in a total UDP-GT deficiency

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21
Q

What are the conjugated hepatic causes of jaundice

A
  1. Hepatocellular dysfunction
    - Congenital (wilson’s, A1ATD)
    - Infection Hep A/B/C, CMV and EBV
    - Toxins (EtOH and drugs)
    - Autoimmune hepatitis
    - Hepatocellular carcinoma
  2. Decreased hepatic bilirubin excretion
    - Dubin-Johnson (MRP2 mutation)
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22
Q

What are the post hepatic causes of jaundice

A

Obstruction

  • Stones
  • Drugs
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
  • mirrizi
  • malignant
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23
Q

What colour is the urine in pre-hepatic jaundice

A

Normal

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24
Q

What colour is the urine in cholestatic (hepatic or post hepatic) jaundice

A

Dark

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25
Q

What colour are stools in pre hepatic jaundice

A

Normal

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26
Q

What colour are stools in cholestatic jaundice

A

Pale

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27
Q

Are liver tests normal or abnormal in prehepatic jaundice

A

Normal

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28
Q

Are liver tests normal or abnormal in cholestatic jaundice

A

Abnormal

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29
Q

What investigative tests would you carry out in a jaundiced patient

A
  • Very high AST/ALT
  • Dilated intrahepatic bile ducts on ultrasound
  • CT
  • MRI
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30
Q

Where do gall stones most commonly form

A

Gallbladder

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31
Q

Are gall stones more common in men or women

A

Women

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32
Q

Are gall stones normally symptomatic or asymptomatic

A

Asymptomatic

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33
Q

What are the risk factors for gall stones

A

Female
Fat
Fertile
Smoking

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34
Q

What are the two main types of gall stone

A 
Cholesterol stones (80%)
Bile pigment stones
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35
Q

Why do cholesterol gall stones form

A

Consequence of cholesterol crystallisation

  • Cholesterol supersaturation of bile
  • Deficiency of bile salts and phospholipids
  • Gall bladder stasis
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36
Q

Why do bile pigment stones form

A

Haemolysis - sickle cell

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37
Q

What are the two types of bile pigment stones

A
  1. Black pigment - calcium bilirubinate + Salts

2. Brown pigment - calcium salts and fatty acids

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38
Q

What is bilary colic

A

Pain associated with temporary obstruction of cystic or common bile duct by stone migrating from gall bladder

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39
Q

What are the symptoms of biliary colic

A

Pain is severe and constant with crescendo

initial site of pain is epigastrium but may be RUQ

Nausea and vomiting accompanying severe attacks

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40
Q

What is acute cholecystitis

A

Gall bladder inflammation due to obstruction to gall bladder emptying

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41
Q

What investigations would you carry out in someone with gall stones

A

Serum bilirubin/alkaline phosphatase and amintransferase are elevated

Abdominal ultrasound

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42
Q

What is the management of gall stones

A

Laproscopic cholecystectomy

Bile acid dissolution therapy = ursodeoxycholic acid

Extracorpeal shock wave lithotripsy

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43
Q

What are the three types of drug induced liver injury

A

Hepatocellular
Cholestatic
Mixed

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44
Q

What drugs most commonly cause drug induced liver injury

A
  1. Antibiotics (Flucoxacillin
  2. CNS drugs (Chlorpromazine)
  3. Analgesics (Diclofenac)
  4. Gastrointestinal drugs
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45
Q

What is paracetamol conjugated with in its phase II reaction

A

Glucuronic acid

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46
Q

What enzyme is responsible for mopping up reactive intermediates of paracetamol so prevents toxicity

A

Glutathione transferase

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47
Q

What is the highly reactive toxic intermediate in paracetamol metabolism

A

NAPQI

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48
Q

What is the clinical presentation of paracetamol poisoning

A

Asymptomatic for first 24 hr followed by anorexia, nausea, vomiting and RUQ pain

Jaundice and encephalopathy due to liver damage

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49
Q

What is the management of paracetamol toxicity

A

N acetyl cysteine which repletes glutathione stores

Supportive care to correct for coagulation defects, renal failure, hypoglycaemia

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50
Q

What is liver failure

A

When the liver loses ability to regenerate or repair as decompensation occurs

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51
Q

What are the three types of liver failure

A
  1. Acute = sudden liver failure with previously healthy liver
  2. Chronic = Liver failure on background of cirrhosis
  3. Fulminant = massive necrosis of liver cells
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52
Q

What are the causes of liver failure

A

Cirrhosis

Infection
- Hep A/B, CMV, EBV, Leptospirosis

Toxin
- EtOH, Paracetamol, isoniazid, halothane

Metabolic
- Wilsons, AIH, A1ATD, Haemochromatosis

Neoplastic = HCC

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53
Q

What are the signs of liver failure

A 
Jaundice 
oedema and ascites 
Bruising 
Encephalopathy 
 - Aterixis (Flapping tremor)
 - Apraxia
Fetor Hepaticus (Breath smells sweet)
Signs or cirrhosis
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54
Q

What investigations would you carry out in someone with liver failure

A

AST:ALT >2 = EtOH
AST:ALT <1 = viral
Albumin is decreased in chronic liver failure
Prothrombin time increase in acute liver failure

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55
Q

What is the management of liver failure

A

Treat the underlying cause
Good nutrition
Thiamine supplements

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56
Q

Give three causes of iron overload

A
  1. Genetic disorders (Haemochromatosis)
  2. Multiple blod transfusions
  3. Haemolysis
  4. Alcoholic liver disease
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57
Q

What is cirrhosis

A

A chronic disease of the liver resulting from necrosis of the liver cells followed by fibrosis - the end result is impairment of hepatocyte function and distortion of liver architecture

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58
Q

What are the two types of cirrhosis

A
  1. Micronodular - regenerating nodules <3mm all over liver

2. Macronodular - Nodules of variable size

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59
Q

What causes micro nodular cirrhosis

A

Chronic alcohol

Biliary tract disease

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60
Q

What causes macro nodular cirrhosis

A

Chronic hepatitis

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61
Q

What are the causes of cirrhosis

A 
Chronic alcohol 
Chronic hepatitis C and B
Genetic 
 - Wilson's/ a1ATD
Autoimmune
 - Autoimmune hepatitis 
 - Primary biliary cholangitis 
Drugs 
 - Methotrexate, Amiodarone, methyldopa
Neoplasm
 - HCC
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62
Q

What are the signs of cirrhosis in the hands

A 
Clubbing 
Leuconychia 
Terry's nails 
Palmar erythema 
Dupuytron's Contracture
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63
Q

What are the sings of cirrhosis in the face

A

Pallor

Xanthelasma

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64
Q

What are the signs of cirrhosis in the trunk

A

Spider naevi
Gynaecomastia
Loss of secondary sexual hair

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65
Q

What are the abdominal signs of cirrhosis

A 
Striae 
Hepatomegaly 
Splenomegaly 
Caput medusa 
Testicular atrophy
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66
Q

What are the complications of cirrhosis

A
  1. Decompensation = hepatic failure
    - Jaundice
    - Encephalopathy
    - Hypoalbuminaemia
    - Hypoglycaemia
    - Coagulopathy
  2. Spontaneous bacterial peritonitis
  3. Portal hypertension
  4. Increased risk of HCC
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67
Q

What investigations would you conduct in someone with cirrhosis

A

Decreased WCC
Increased LFTs
Decreased albumin and prolonged prothrombin time

Abdominal ultrasound showing small or largee liver with focal marginal nodularity

Liver biopsy to confirm the type and severity

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68
Q

What is the management for cirrhosis

A 
Good nutrition - decrease Na+
EtOH abstinence 
Colestyramine for pruritus 
Avoid NSAIDs and aspirin 
Screen for HCC with ultrasound 
Fluid restriction with spironolocatone
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69
Q

Portal vein is formed by the union of what veins

A

Superior mesenteric and splenic veins

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70
Q

Describe the pathophysiology of portal hypertension

A

Liver cirrhosis increases resistance of blood flow in the liver increasing pressure into the portal system. When the venous pressure increases to 10-12mmHg the venous system dilates and collaterals form

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71
Q

What are pre-hepatic causes of portal hypertension

A

Blockage of portal vein before the liver due to portal vein thrombosis (Pancreatitis)

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72
Q

What are the hepatic causes of portal hypertension

A

Distortion of the liver architecture due to cirrhosis and schistosomiasis and sarcoidosis

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73
Q

What are the post-hepatic causes of portal hypertension

A

Blockage of the portal vein outside the liver due to Budd chiari, constrictive pericarditis and RHF

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74
Q

Where do varices form following portal hypertension

A

Gastro-oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall

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75
Q

What are the symptoms of portal hypertension

A 
Splenomegaly 
Ascites 
Varices 
Encephalopathy 
Haematemesis 
Breathlessness
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76
Q

What investigations would you carry out in someone with portal hypertension

A

Portal vein blockage can be identified on ultrasound with Doppler imaging

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77
Q

What are the potential consequences of portal hypertension induced varices

A

If they rupture = haemorrhage

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78
Q

What is the treatment for varices

A

Endoscopic therapy = banding

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79
Q

Describe the pathophysiology of encephalopathy

A
  1. Decreased hepatic metabolic function
  2. Diversion of toxins from the liver directly into the systemic circulation due to collaterals around the liver
  3. Ammonia accumulates and passes to the brain where astrocytes Clear it causing glutamate conversion to glutamine
  4. Increased glutamine alters osmotic imbalance and causes cerebral oedema
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80
Q

What are the 4 classification stages of encephalopathy

A
  1. Confused (Irritable, confusion, sleep)
  2. Drowsy (Disorientated, slurred speech, asterixis)
  3. Stupor (rousable, incoherence)
  4. Coma (Unrousable)
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81
Q

What is the presentation of encephalopathy

A

Asterixis (Coarse flapping tremor when hands are outstretched)
Ataxia
Fetor Hepaticus = sweet breath
confusion
Dysarthia
Constructional apraxia (Unable to write or draw)
Seizures

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82
Q

What are the precipitants of encephalopathy (remember hepatics)

A 
Haemorrhage (Varicies)
Electrolytes (Decreased K+/Na+
Poisons (Diuretics, sedatives, anaesthetics)
Alcohol 
Tumour (HCC) 
Infection (SBP, Pneumonia)
Constipation 
Sugar decrease
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83
Q

What investigation result would you expect to see in someone with encephalopathy

A

Increased plasma ammonia

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84
Q

What is the treatment for encephalopathy

A

Correct precipitants
Lactulose (limits ammonia absorption) and PO4 enemas to decrease nitrogen forming bowel bacteria
Consider rifaximin to kill intestinal microflora

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85
Q

What is ascites

A

An accumulation of fluid in the peritoneal cavity leading to abdominal distension

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86
Q

What is the pathophysiology of ascites

A

Portal hypertension leads to fluid exudation leading to an effective drop in circulating volume - this leads to RAAS activation causing Na+ and H2O retention

In cirrhosis a decrease in albumin leads to decreased plasma oncotic pressure and aldosterone metabolism is impaired

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87
Q

What are the causes of ascites

A

Local inflammation - peritonitis

Leaky vessels - imbalance between hydrostatic and oncotic pressure

Low flow - cirrhosis, cardiac failure and thrombosis

Low protein - hypoalbuminaemia

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88
Q

What are the symptoms of ascites

A

Distension - abdominal discomfort, swelling and anorexia

Dyspnoea

Decreased venous return

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89
Q

How do you determine the cause of ascites

A

Serum ascites albumin gradient

  1. > 1.1g/dL = Portal HTN (Pre-hepatic and post and cirrhosis )
  2. <1.1g/dL = other causes
    (Neoplasia, inflammation (peritonitis), nephrotic syndrome, infection (TB peritonitis)
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90
Q

how do you determine the serum ascites albumin gradient

A

Serum albumin - Ascites albumin

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91
Q

What investigations would you Carry out in someone with suspected ascites

A

Bloods
Ultrasound
Ascitic tap
Liver biopsy

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92
Q

What is the treatment for ascites

A 
Weight reduction 
Fluid restriction <1.5L/d
Low Na+ diet 
Spironolatone (Aldosterone antagonist) 
Therapeutic paracentesis
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93
Q

What is spontaneous bacterial peritonitis

A

Ascites and peritonitis abdomen

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94
Q

What are the causes of spontaneous bacterial peritonitis

A

E.Coli, Klebsiella, Steps, Enterococci

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95
Q

What are the three phases of alcoholic liver disease

A
  1. Fatty change - hepatocytes contain triglycerides
  2. Alcohol hepatitis
  3. Cirrhosis - destruction of architecture and fibrosis
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96
Q

What might be seen histologically that indicates a diagnosis of alcoholic liver disease

A

Neutrophils and fat accumulation within hepatocytes

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97
Q

What are the effects of alcoholism on the GIT

A 
Gastritis
Peptic Ulcer Disease
Varices 
Pancreatitis 
Carcinoma
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98
Q

What are the effects of alcoholism on the CNS

A 
Poor memory 
Peripheral polyneuropathy 
Wernicke's Encephalopathy 
 - Confusion 
-  Ophthalmoplegia 
 - Ataxia 
Korsakoffs - amnesia
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99
Q

What are the effects of alcoholism on the heart

A

Arrhythmia ie AF
Dilated cardiomyopathy
Increased Bp

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100
Q

What are the effects of alcoholism on the blood

A

Increased mean corpuscular volume

Folate deficiency - anaemia

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101
Q

What are the CAGE questions for alcoholism

A

Do you think you should cut down
Are you annoyed by peoples criticism’s
Are you guilty about drinking
Do you need a drink to get up in the morning

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102
Q

What Is the treatment for alcoholism

A

Group therapy or self help
Baculofen and acamprosate to reduce cravings
Disulfiram = aversion therapy

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103
Q

What is the presentation of alcoholic hepatitis

A 
Anorexia 
Diarrhoea and vomiting 
Tender hepatomegaly 
Ascites 
Severe jaundice, bleeding, encephalopathy
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104
Q

What investigations and results would you see in alcoholic hepatitis

A

Bloods= increased MCV, increased GTT
AST:ALT >2 = EtOH
Ascititic Tap
Abdo ultrasound

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105
Q

What is the treatment for alcoholic hepatitis

A

Stop EtOH
High does B vitamins (Thiamine)
Optimise nutrition
Manage the complications of failure

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106
Q

What is non alcoholic fatty liver disease

A

Cryptogenic cause of hepatitis and cirrhosis associated with insulin resistance and metabolic syndrome

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107
Q

What is the most severe form of non alcoholic fatty liver disease

A

Non alcoholic steatohepatitis

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108
Q

What are the risk factors for NAFLD

A

Obesity
Hypertension
T2DM
Hyperlipidaemia

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109
Q

What is the presentation of NAFLD

A

Mostly asymptomatic

Hepatomegaly and RUQ discomfort

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110
Q

What investigations would you carry out in someone with NAFLD

A

BMI
Glucose
Increase transaminases AST:ALT <1
Liver biopsy to enable staging

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111
Q

What is the management of NAFLD

A

Lose weight
Control hypertension, diabetes mellitus and lipids
Exercise

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112
Q

What is budd-chiari syndrome

A

Hepatic vein obstruction –> Ischaemia and hepatocyte damage –> Liver failure

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113
Q

Give 4 reasons why liver patients are vulnerable to infection

A
  1. Have impaired reticule-endothelial function
  2. Reduced opsonic activity
  3. Leukocyte function is reduced
  4. Permeable gut wall
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114
Q

Name 3 metabolic disorders that can cause liver disease

A
  1. Haemochromatosis
  2. Alpha 1-antitrypsin deficiency
  3. Wilson’s disease
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115
Q

What is haemochromatosis

A

metabolic disorder resulting in excess Fe2+ deposits in organs leading to fibrosis and organ failure

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116
Q

What is the age of onset for haemochromatosis

A

40-60 years

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117
Q

What is the genetic cause of haemochromatosis

A

Autosomal recessive condition causing mutation in the Human haemochromatosis protein (HFE) –> C282Y

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118
Q

What is the pathophysiology of haemochromatosis

A

Increased intestinal Fe absorption resulting in deposition in liver heart joints endocrine, skin and pancreas leading to fibrosis and functional organ failure

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119
Q

What are the clinical features of haemochromatosis (Remember MEALS)

A

Myocardial

  • dilated cardiomyopathy
  • Arrhythmia

Endocrine

  • DM
  • Pituitary = hypogonadism
  • Parathyroid = hypocalcaemia, osteoporosis

Arthritis

Liver

  • Chronic liver disease leading to cirrhosis leading to HCC
  • Hepatomegaly

Skin

  • Slate grey discolouration
  • bronze skin pigmentation
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120
Q

How might you diagnose someone with haemochromatosis

A 
Raised ferritin 
increasing LFT
Increased Fe
Liver biopsy - pearls stain to quantify the FE 
MRI can estimate iron loading 
ECHO and ECG for cardiac complications 
X-ray shows chondrocalcinosis
HFE genotyping
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121
Q

What is the treatment for haemochromatosis

A

venesection - regular removal of blood to use up some excess iron to make new RBC’s

In patients who cant have venesection they can have chelation therapy (Desferrioxamine) which prevents iron absorption

Low iron Diet

Treat DM complication

Look for transplant in cirrhosis and screen 1st degree relatives

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122
Q

What is the pathophysiology of alpha 1 antitrypsin deficiency

A

a1AT is serine involved in control of inflammatory cascade by inhibiting neutrophil elastase

A1AT is synthesised by the liver and a deficiency results in lung damage

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123
Q

What is the presentation of alpha 1 anti-trypsin

A

Neonatal and childhood hepatitis
15% adults develop cirrhosis
75% have emphysema
5% die of liver disease

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124
Q

What investigations and results would you see in someone with alpha 1 antitrypsin deficiency

A

decreased a1AT levels
Liver biopsy = +ve periodic acid shift
Emphysematous changes on CXR
Obstructive defect on spirometry

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125
Q

What is the management of alpha 1 anti-trypsin deficiency

A

Quit smoking
Mostly supportive for pulmonary and hepatic complications
Consider a1AT therapy from donors
Patients with hepatic decompensation should get liver transplant

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126
Q

What is Wilson’s disease

A

Autosomal recessive disorder of copper metabolism where there is deposition of copper in the liver which can lead to fulminant hepatic failure and cirrhosis

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127
Q

When does Wilsons disease most commonly present

A

Between childhood and 30

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128
Q

What is the genetic cause of Wilsons disease

A

Autosomal recessive ATP7B gene on chromosome 13

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129
Q

Describe the pathophysiology of Wilson’s disease

A

Mutation of Cu transporting ATPase leading to impaired hepatocyte incorporation of Cu into caeruloplasmin and excretion into bile causingg Cu accumulation in liver and other organs

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130
Q

What are the clinical features of Wilson’s disease (Remember CLANKAH)

A

Cornea (Kayser-Fleischer rings)

Liver disease (Acute hepatitis in children and necrosis and cirrhosis in adults)

Arthritis
- Osteoporosis

Neurology
- Parkinsonism =bradykinesia, tremor, ataxia

Kidney
- Fanconi’s syndrome

Haemolytic anaemia

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131
Q

What are the investigative results in Wilson’s disease

A

Decreased copper and caeruloplasmin

increased urinay copper

Increased hepatic copper

MRI = basal ganglia degeneration

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132
Q

What is the management of Wilson’s disease

A

Diet = avoid high Cu foods ie. liver, chocolate, nuts

Penicillamine (Cu chelator)

Liver transplant If severe disease

133
Q

What are the side effects of penicillamine

A 
Nausea
Rash 
Decreased WCC
Decreased Hb 
Decreased platelets
134
Q

What is autoimmune hepatitis

A

Inflammatory disease of unknown cause characterised by Abs directed against hepatocyte surface antigens

135
Q

What age group is autoimmune hepatitis commonly seen in

A

Young and middle age women

136
Q

Describe the antibody classification of autoimmune hepatitis

A

T1 = Adult ( SMA+, ANA+ and IgG increase)

T2 = Young (LKM+)

T3 = Adult (SLA+)

137
Q

What is the presentation of autoimmune hepatitis

A 
Fatigue, fever, malaise 
Hirsute, acne, striae 
Hepatitis 
Hepatosplenomegaly 
Fever 
Amenorrhoea 
Polyarthritis 
Pulmonary infiltration
138
Q

What investigations would you carry out in autoimmune hepatitis

A 
Increased LFTs
Increased IgG
Auto Abs 
 - SMA
 - LKM
 - SLA
 - ANA 
Decreased WCC and platelets
Liver biopsy
139
Q

What is the management of autoimmune hepatitis

A

Immunosuppression
prednisolone
(Azithioprine as steroid sparer)
Liver transplant

140
Q

What age group does primary biliary cirrhosis most commonly affect

141
Q

What is the pathophysiology of primary biliary cirrhosis

A

Intrahepatic bile duct destruction by chronic granulomatous inflammation leading to cirrhosis

Lymphocyte mediated attack on bile duct epithelial, destruction of the bile ducts leading to cholestasis and cirrhosis

142
Q

What is the presentation of primary biliary cirrhosis

Remember BILE EXCESS

A 
Bone = osteoporosis 
Itch = pruritus 
Lethargy 
Eyes yellow due to jaundice
Eyes dry due to sicca 
Xanthelasma 
Cholesterol increase 
Enlarged liver 
Skin pigmentation 
Steatorrhoea
143
Q

Name three diseases associated with primary biliary cirrhosis

A 
Thyroiditis 
Rheumatoid arthritis 
Sjorgens syndrome 
Coeliac disease 
Renal tubular acidosis
144
Q

What is the investigations and results for primary biliary cirrhosis

A

LFTs
- Increased GGT
Increased AST and ALT

+ve for anti-mitochondiral antibodies

Increased cholesterol

increased IgM

Liver biopsy to show non-caseating granulomatous inflammation

145
Q

What is the treatment for symptomatic primary biliary cirrhosis

(Think about the symptoms)

A

Pruritus = colestyramine

Diarrhoea = codeine phosphate

Osteoporosis = bisphosphonates

Give vitamins ADEK

Ursodeoxcholic acid

Liver transplant

146
Q

What is primary sclerosing cholangitis

A

inflammation, fibrosis and stricture of both the intra and extra hepatic bile ducts leading to chronic biliary obstruction, secondary biliary cirrhosis and liver failure

147
Q

What is the pathogenesis of primary sclerosing cholangitis

A

Inflammation of the bile duct -> strictures and hardening -> progressive obliterating fibrosis of bile duct branches -> cirrhosis -> liver failure.

148
Q

What is the presentation of primary sclerosing cholangitis

A

Jaundice (Dark urine, pale stools)
Pruritus and fatigue
Hepatosplenomegaly
Abdominal pain

149
Q

What is primary sclerosing cholangitis associated with

A

Ulcerative colitis

Crohns

150
Q

What are the complications of primary sclerosing cholangitis

A

Bacterial cholangitis
Increased cholangiocarcinoma
Colorectal cancer

151
Q

What are the investigations for primary sclerosing cholangitis

A

LFTs increase in ALP
Abs pANCA, ANA and SMA
ERCP/MRCP
Biopsy

152
Q

What is the treatment for primary sclerosing cholangitis

A 
Symptomatic 
 - Pruritus = colestyramine 
- Diarrhoea = codeine phosphate
ADEK vitamins 
Ursodeoxycholic acid 
Liver transplant 
Screen for cholagniocarcinoma
153
Q

Where do 90% of liver tumours come from

A

2nd metastases from the stomach, lung and colon in men and breast, colon, stomach and uterus in women

154
Q

What are the symptoms of liver tumours

A 
Benign tumours are asymptomatic 
fever 
Malaise 
Weight loss
Anorexia 
RUQ pain 
Jaundice (late)
155
Q

What are the signs of liver cancer

A

Hepatomegaly
Abdominal mass
Hepatic bruit
Chronic liver disease signs

156
Q

What are the causes of hepatocellular carcinoma

A

Viral hepatitis B + C
Cirrhosis (EtOH)
Aflatoxins produced by apsergillus

157
Q

How do you investigate hepatocellular carcinoma

A

Imaging CT/MRI

Biopsy can be diagnostic

158
Q

What is the management of hepatocellular carcinoma

A

resection of solitary tumours

Chemo

159
Q

What is a cholangiocarcinoma

A

Biliary tree malignancy

160
Q

What are the causes of cholangiocarcinoma

A

Flukes
primary sclerosing cholangitis
HBV and HCV
Congenital biliary cysts

161
Q

What is the presentation of cholangiocarcinoma

A 
Fever
Malaise 
Abdomina pain
Ascites 
Jaundice
162
Q

What is the management of cholangiocarcinoma

A

Surgical resection is rarely possible

Liver transplant is contraindicated

163
Q

What is ascending cholangitis

A

Infection of the biliary tree normally ascending from duodenum

164
Q

What are the causes of ascending cholangitis

A 
Gallstones 
Primary infection
 - Klebsiella 
 - E.coli 
Pancreatic head malignancy
165
Q

What age group is ascending cholangitis most common in

A

50-60 with gall stone history

166
Q

What are the signs and symptoms of ascending cholangitis

A

Charcot’s triad

  • Fever and chills
  • RUQ pain
  • Obstructive jaundice (Dark urine and pale stools and pruritus)
167
Q

What are the investigations for ascending cholangitis

A

Blood test showing raised LFT
Imaging - ultrasound to look for blockage
ERCP

168
Q

What is the management of ascending cholangitis

A

Fluid resuscitation and treat infection with IV antibiotics such as cefotaxime and metronidazole

169
Q

What would be raised in the blood tests taken from someone with primary biliary cirrhosis?

A
  1. Raised IgM.
  2. Raised ALP.
  3. Positive AMA.
170
Q

What 4 features would you expect to see in the blood test results taken from someone who has overdosed on paracetamol.

A
  1. Metabolic acidosis.
  2. Prolonged pro-thrombin time (due to coagulability).
  3. Raised creatinine (renal failure).
  4. Raised ALT.
171
Q

What 3 symptoms make up the triad of Wernicke’s encephalopathy?

A
  1. Ataxia.
  2. Opthalmoplegia.
  3. Confusion.
172
Q

How can Wernicke’s encephalopathy be reversed?

A

Give IV thiamine.

173
Q

Where have most secondary liver cancers arisen from?

A
  1. The Gi tract.
  2. Breast.
  3. Bronchus.
174
Q

What investigations might you do on someone who you suspect has HCC?

A
  1. Bloods: serum AFP may be raised.
  2. US or CT to identify lesions.
  3. MRI.
  4. Biopsy if diagnostic doubt.
175
Q

Describe the treatment for HCC.

A
  1. Surgical resection of solitary tumours.
  2. Liver transplant.
  3. Percutaneous ablation.
176
Q

Name 3 diseases that lead to heamolytic anaemia and so a raised unconjugated bilirubin and pre-hepatic jaundice.

A

Causes of haemolytic anaemia:

  1. Sickle cell disease.
  2. Hereditary spherocytosis/elliptocytosis.
  3. GP6D deficiency.
  4. Hypersplenism.
177
Q

You do an ascitic tap in someone with ascites. The neutrophil count comes back as - Neutrophils > 250/mm3. What is the likely cause of the raised neutrophils?

A

Spontaneous bacterial peritonitis.

178
Q

Describe the treatment for spontaneous bacterial peritonitis.

A

Cefotaxime and metronidazole

179
Q

What distinctive feature is often seen on biopsy in people suffering from alcoholic liver disease?

A

Mallory bodies

180
Q

A patient’s oedema is caused solely by their liver disease. State one possible pathophysiological mechanism for their oedema.

A

Hypoalbuminaemia.

181
Q

What 2 products does haem break down in to?

A

Haem -> Fe2+ and biliverdin.

182
Q

What enzyme converts biliverdin to unconjugated bilirubin?

A

Biliverdin reductase.

183
Q

What is the function of glucuronosyltransferase?

A

It transfers glucuronic acid to unconjugated bilirubin to form conjugated bilirubin.

184
Q

What protein does unconjugated bilirubin bind to and why?

A

Albumin.

It isn’t H2O soluble therefore it binds to albumin so it can travel in the blood to the liver.

185
Q

What does conjugated bilirubin form?

A

Urobilinogen

186
Q

What is responsible for the conversion of conjugated bilirubin into urobilinogen?

A

Intestinal bacteria.

187
Q

What can urobilinogen form?

A
  1. It can go back to the liver via the enterohepatic system.
  2. It can go to the kidneys forming urinary urobilin.
  3. It can form stercobilin which is excreted in the faeces.
188
Q

Define hepatitis

A

Inflammation of the liver

189
Q

Define actue hepatitis

A

Hepatitis within 6 months of onset

190
Q

What are the symptoms of acute hepatitis

A

None or non specific
- malaise, lethargy, myalgia, fever
Gastrointestinal upset and stomach pain
Jaundice with pale stools and dark urine

191
Q

What are the signs of acute hepatitis

A

Tender hepatomegaly and jaundice

Signs of fulminant hepatitis

  • bleeding
  • Ascites
  • Encephalopathy
192
Q

What are the blood test results in acute hepatitis

A

raised transaminases (AST/ALT) and raised bilirubin
Raised or normal alkaline phosphatase
Raised or normal albumin

193
Q

What are the viral infective causes of acute hepatitis

A

Hep A, B+D, C+E
Human herpes virus
(HSV, VZV, CMV, EBV)

194
Q

What are the non-viral infective causes of acute hepatitis

A

Spirochetes (Leptospirosis, syphillis)

Mycobacteria (Tuberculosos)

Bacteria (Bartonella)

Parasites (Toxoplasma)

195
Q

What are the non-infective causes of acute hepatitis

A 
Drugs 
Alcohol 
Other toxins and poisons 
Pregnancy 
NAFLD 
Autoimmune hepatitis 
Hereditary metabolic causes
196
Q

Define chronic hepatitis

A

Hepatitis that lasts for 6 months or longer

197
Q

What are the symptoms of chronic hepatitis

A

Can be asymptomatic or may have non specific symptoms

May have signs of chronic liver disease

  • Clubbing
  • Palmar erythema
  • Dupuytren’s Contracture
  • Spider naevi
198
Q

What do blood results of someone with chronic hepatitis show

A

Transaminase can be normal

199
Q

What are the complications of chronic hepatitis

A

HCC

Portal hypertension

200
Q

What are the infective causes of chronic hepatitis

A

Viral Hep B+D and C+E

201
Q

What are the non-infective causes of chronic hepatitis

A 
Drugs 
Alcohol
Other toxins 
NAFLD 
Autoimmune hepatitis 
hereditary metabolic causes
202
Q

What disease commonly causes hepatitis A? is it an RNA or DNA virus

A

Picornavirus

RNA

203
Q

How is HAV transmitted

A

Faeco-oral transmission
- Contaminated food or water ingestion (Shellfish, traveller, infected food handlers)

Person to person contact
- Household
Sexual
Childcare

204
Q

Who is at risk of HAV

A

Travellers
Household contact
Sexual contact
Injecting drug use

205
Q

Is HAV acute or chronic

A

Acute, there is 100% immunity after infection

206
Q

What is the clinical presentation of HAV

A

Non specific = nausea, anorexia and distaste for cigarettes

After 1-2 weeks patients become jaundiced and urine dark and stools pale

207
Q

How might you diagnose someone with HAV infection

A

Viral serology

Initially anti-HAV IgM and then anti-HAV IgG

208
Q

What is the management of HAV

A

Supportive
Monitor liver function
Manage close contacts using human normal immunoglobulin to contacts within 14 days as well as vaccination

209
Q

What is the primary prevention of HAV

A

Vaccination - inactivated hepatitis A virus

210
Q

Is hepatitis E an RNA or DNA virus

A

HEV is a small RNA virus

211
Q

How is HEV transmitted

A

Faeco-orally

212
Q

Is HEV acute or chronic

A

usually acute but there is a risk of chronic disease in immunocompromised
(Transplant recipients, HIV patients,)

213
Q

What is the clinical presentation of HEV

A

95% are asymptomatic
Usually self limiting acute hepatitis
Extra-hepatic manifestations = neurological

214
Q

How might you diagnose someone with HEV infection

A

Viral serology - Initially anti-HEV IgM and then anti-HEV IgG

215
Q

Describe the primary prevention of HEV

A

Good food hygiene

Vaccine in development

216
Q

What is the management for acute HEV infection

A

Supportive

Monitor for fulminant hepatitis

217
Q

What is the management for chronic HEV infection

A

Reverse immunosuppression

If HEV persists treat with ribavirin

218
Q

Is HBV a RNA or DNA virus

A

HBV is caused by HEPADNAVIRUS and is a DNA virus which replicates in hepatocytes

219
Q

How is HBV transmitted

A 
Blood-borne virus 
 - Mother to child 
 -Sexual contact 
- Household contact 
Iatrogenic 
Injecting drug use 
Tattoos
220
Q

Describe the natural history of HBV in 4 phases.

A
  1. Immune tolerance phase: unimpeded viral replication -> high HBV DNA levels.
  2. Immune clearance phase: the immune system ‘wakes up’. There is liver inflammation and high ALT.
  3. Inactive HBV carrier phase: HBV DNA levels are low. ALT levels are normal. There is no liver inflammation.
  4. Reactivation phase: ALT and HBV DNA levels are intermittent and inflammation is seen on the liver -> fibrosis.
221
Q

What HBV protein triggers the initial immune response?

A

The core proteins.

222
Q

How might you diagnose someone with HBV?

A

Viral serology: HBV surface antigen can be detected from 6w – 3m or anti-HBV core IgM after 3 months.

223
Q

Describe the management of HBV infection.

A
  1. Supportive.
  2. Monitor liver function.
  3. Manage contacts.
  4. Follow up at 6 months to see if HBV surface Ag has cleared. If present -> chronic hepatitis.

Pegylated interferon alpha A2
Entecavir/tenofovir

224
Q

How would you know if someone had acute or chronic HBV infection?

A

You would do a follow up appointment at 6 months to see if HBV surface Ag had cleared. If it was still present then the person would have chronic hepatitis

225
Q

What are the potential consequences of chronic HBV infection?

A
  1. Cirrhosis.
  2. HCC.
  3. Decompensated cirrhosis.
226
Q

How can HBV infection be prevented?

A

Vaccination – injecting a small amount of inactivated HbsAg.

227
Q

Describe two treatment options for HBV infection.

A
  1. Alpha interferon – boosts immune system.

2. Antivirals e.g. tenofovir. They inhibit viral replications.

228
Q

HBV treatment: give 3 side effects of alpha interferon treatment.

A
  1. Myalgia.
  2. Malaise.
  3. Lethargy.
  4. Thyroiditis.
  5. Mental health problems.
229
Q

Is HDV a RNA or DNA virus?

A

It is a defective RNA virus. It required HbsAG to protect it.

230
Q

Infection with what virus is needed for HDV to survive?

A

HDV can’t exist without HBV infection! It needs HbsAg to protect it.

231
Q

How is HDV transmitted?

A

Blood-borne transmission, particularly IVDU.

232
Q

How do you test to see if someone has hepatitis D

A

Hepatitis D antibody

233
Q

What is the treatment for HDV

A

Pegylated interferon alpha

234
Q

Is HCV a RNA or DNA virus?

A

Flavivirus (RNA)

235
Q

How is HCV transmitted?

A 
Blood-borne 
o	IVDU 
o	Blood transfusion 
o	Tattoos/needlesticks 
o	Sexual 
o	Vertical
236
Q

What percentage of HCV patients develop acute hepatitis

237
Q

What percentage of HCV patients develop chronic hepatitis

238
Q

How might you diagnose someone with current HCV infection?

A

Viral serology – HCV RNA tells you if the infection is still present.

239
Q

You want to find out if someone has previously been infected with HCV. How could you do this?

A

Viral serology – anti-HCV IgM/IgG indicates that someone has either a current infection or a previous infection.

240
Q

Describe the treatment for HCV.

A

Lots of new drugs have been developed recently for HCV infection. Direct acting antivirals (DAA) are currently in use e.g. NS5A and NS5B.

241
Q

How can HCV infection be prevented.

A
  1. Screen blood products.
  2. Lifestyle modification.
  3. Needle exchange.
    There is currently no vaccination and previous infection does not confer immunity
242
Q

What types of viral hepatitis are capable of causing chronic infection?

A

Hepatitis B (+/-D); C and E in the immunosuppressed.

243
Q

Define diarrhoea

A

Abnormal passage of loose or liquid stool more than 3 times daily

244
Q

Define acute diarrhoea

A

Defined as lasting less than 2 weeks

245
Q

Define chronic diarrhoea

A

Lasting more than 2 weeks

246
Q

Define an infective cause of diarrhoea

A

Sudden onset of bowel frequency associated with crampy abdominal pains and fever

247
Q

Define an inflammatory cause of diarrhoea

A

Bowel frequency with loose and blood stained stools

248
Q

Name some diarrhoeal GI infections

A 
Traveller's diarrhoea 
Viral (Rotavirus and norovirus)
Bacterial (E.coli)
Parasite (Helminths, protozoa)
Nosocomial (C.diff and norovirus)
249
Q

Name some non diarrhoeal GIT infections

A 
Gastritis/peptic ulcer disease (H.pylori)
Acute cholecystitis 
Peritonitis 
Typhoid - salmonella 
Amoebic liver abscess
250
Q

What are the causes of diarrhoea

A 
Bacterial 
Viral 
Parasitic (Helminths and protozoa)
Nosocomial 
Hepatobiliary infections 
Travellers 
Whipple's disease 
Helicobacter pylori infection
251
Q

What is the leading cause of diarrhoeal illness in young children

252
Q

Define traveller’s diarrhoea

A

3 or more unformed stools per day and at least one abdominal pain/cramp/nausea/vomiting/dysentry which occurs within 2 weeks of arrival in a new country

253
Q

What are the causative organism of travellers diarrhoea

A

Enterotoxigenic E.coli
Campylobacter
Norovirus
Giardia

254
Q

Name the toxin producing E.coli and their mechanism of action

A
  1. Enterotoxigenic E.coli (ETEC)
    - heat labile and heat stable
    Activate intestinal adenylate or guanylate cyclase
  2. Enterohaemorrhagic E.coli (EHEC)
    - Shiga like toxin
255
Q

What sort of diarrhoea does enterotoxigenic E.coli produce

A

Travellers diarrhoea with watery diarrhoea

256
Q

What sort of diarrhoea does enterohaemorrhagic E.coli produce

A

Bloody diarrhoea and haemolytic uremic syndrome

257
Q

Name an invasive E.coli and what of disease does It cause

A

Enteroinvasive E.coli (EIEC)

Dysentery like illness

258
Q

Name the three types of adherent E.Coli and their mechanisms

A
  1. Enteropathogenic E.Coli (EPEC) - attach to epithelium
  2. Enteroaggregative E.Coli (EAEC) - Biofilms
  3. Diffusely adherent E.coli (DAEC) - afimbriate adhesion
259
Q

What type of diarrhoea does enteropatheogenic E.coli cause

A

Infantile diarrhoea

260
Q

What type of diarrhoea does enteroaggregative E.coli cause

A

Traveller’s Diarrhoea

261
Q

What type of diarrhoea does diffusely adherent E.coli cause

A

Persistent diarrhoea in children

262
Q

What parasites can cause diarrhoea

A

Protozoa

  • Entemoeba histolytica
  • Giardia
  • Cryptosporidium

Helminths

  • Schistosomiasis
  • Stronglyloides
263
Q

What are the symptoms of schistosomiasis

A 
Fever 
Eosinophilia 
Diarrhoea 
Hepato-splenomegaly 
Cough/wheeze
264
Q

Name an antibiotic associated cause of diarrhoea

A

Clostridium difficile

265
Q

Which antibiotics are associated with a clostridium difficile

A

Clindamycin
Ciprolfaxin (Quinolones)
Co-amoxiclav (Penicillins)
Cephalosporin

266
Q

What can contribute to antibiotics induced clostridium difficile

A

Acid suppression PPI (Lansoprazole and omeprazole)

H2 receptor antagonists

267
Q

What is the treatment for anti-biotic induced C.diff

A

Metronidazole
Oral vancomycin
Rifampicin/rifaximin

268
Q

Define peritonitis

A

Inflammation of the peritoneum

269
Q

What are the causes of peritonitis

A

Surgical - secondary bacterial peritonitis due to perforation or trauma

Spontaneous bacterial peritonitis

Paediatric in absence of ascites

Infection secondary to peritoneal dialysis

Pelvic inflammatory disease as complication of chlamydia

Tuberculosis

270
Q

What are 5 causes of diarrhoeal infection

A
  1. traveller’s diarrhoea
  2. Viral (Rotavirus)
  3. Bacterial (E.coli)
  4. Parasites (Helminths)
  5. Nosocomial (C.diff)
271
Q

What are 5 causes of non diarrhoeal infection

A 
Gastritis 
Acute cholecystitis 
Peritonitis 
Typhoid 
Ameobic liver disease
272
Q

Name three ways in which diarrhoea can be prevented

A
  1. Access to clean water
  2. Good sanitation
  3. Hand hygiene
273
Q

What are 3 causes of traveller’s diarrhoea

A
  1. Enterotoxigenic E.coli
  2. Campylobacter
  3. Norovirus
274
Q

Describe the pathophysiology of traveller’s diarrhoea

A

Heat table ETEC modifies Gs and it is in permanent lock on state - adenylate cyclase is activated and there is increased production of cAMP which leads to increased secretion of Cl- into the intestinal lumen with water following down an osmotic gradient = diarrhoea

275
Q

What type of E.coli can cause bloody diarrhoea and has shiga like toxin

A

Enterohaemorrhagic E.coli

276
Q

What is the leading cause of diarrhoeal illness in young children

277
Q

Give 5 symptoms of helminth infection

A 
Fever 
Eosinophilia 
Diarrhoea 
Cough 
Wheeze
278
Q

Briefly describe the reproductive cycle of schistosomiasis

A
  1. Fluke matures in blood vessels and reproduces sexually in host
  2. Eggs expelled in faeces and enter water source
  3. Asexual reproduction in an intermediate host
  4. Larvae expelled and penetrate back into human host
279
Q

Why is C.diff highly infectious

A

Spore forming bacteria (Gram positive)

280
Q

Give 5 risk factors for C.diff infection

A
  1. Increasing age
  2. Co-morbidities
  3. Antibiotic use
  4. PPI
  5. long hospital stays
281
Q

What can helicobacter pylori infection cause

A

H pylori produces urease –> Ammonia –> Damage gastric mucosa –> Neutrophil recruitment and inflammation = gastritis, peptic ulcer disease and gastric cancer

282
Q

What is acute pancreatitis?

A

An inflammatory process with release of inflammatory cytokines (TNF alpha, IL-6) and pancreatic enzymes (trypsin, lipase) resulting in auto-digestion of organ

283
Q

What are the 3 different types of acute pancreatitis?

A
  1. 70% are oedematous; acute fluid collection.
  2. 25% are necrotising.
  3. 5% are hemorrhagic.
284
Q

Give 5 causes of acute pancreatitis.

A
  1. Gallstones.
  2. Alcohol.
  3. Hyperlipidaemia.
  4. Direct damage e.g. trauma.
  5. Idiopathic.
  6. Toxic e.g. drugs, infection, venom
285
Q

Give 4 symptoms of acute pancreatitis.

A
  1. Severe epigastric pain that radiates to the back.
  2. Anorexia.
  3. Nausea, vomiting.
  4. Signs of septic shock e.g. fever, dehydration, hypotension
286
Q

How can acute pancreatitis be diagnosed?

A

Pancreatitis is diagnosed on the basis of 2 out of 3 of the following:

  1. Characteristic severe epigastric pain radiating to the back.
  2. Raised serum amylase.
  3. Abdominal CT scan pathology.
287
Q

Describe the treatment for acute pancreatitis

A
  1. ANALGESIA!
  2. Catheterise and ABC approach for shock patients.
  3. Drainage of oedematous fluid collections.
  4. Antibiotics.
  5. Nutrition.
  6. Bowel rest.
288
Q

Give 2 potential complications of acute pancreatitis.

A
  1. Systemic inflammatory response syndrome.

2. Multiple organ dysfunction.

289
Q

What is chronic pancreatitis?

A

Innapropriate activation of the pancreatic enzymes leading to protein plug and calcification leading to ductal hypertension and pancreatic damage and fibrosis

290
Q

Describe how alcohol can cause chronic pancreatitis

A

Alcohol -> proteins precipitate in the ductal structure of the pancreas (obstruction) -> pancreatic fibrosis.

291
Q

What immunoglobulin might be elevated in someone with autoimmune chronic pancreatitis?

292
Q

How is autoimmune chronic pancreatitis treated?

A

It is very steroid responsive.

293
Q

Give 5 symptoms of chronic pancreatitis.

A
  1. Severe abdominal pain.
  2. Epigastric pain radiating to the back.
  3. Nausea, vomiting.
  4. Decreased appetite.
  5. Exocrine/endocrine dysfunction.
  6. Diabetes mellutus
  7. Steatorrhoea
  8. Weight loss
294
Q

A sign of chronic pancreatitis is exocrine dysfunction. What can be a consequence of this?

A
  1. Malabsorption.
  2. Weight loss.
  3. Diarrhoea.
  4. Steatorrhoea.
295
Q

What is the treatment for chronic pancreatitis

A

Analgesics
No EtOH
Decrease fats and increase Carbs

Pancreatectomy

296
Q

What are the complications of chronic pancreatitis

A 
Pseudocyst 
DM 
Pancreatic Ca 
Biliary obstruction 
Splenic vein thrombosis
297
Q

Define peritonitis

A

Inflammation of the peritoneum

298
Q

What is the function of the peritoneum in health

A

Visceral lubrication

Fluid and particulate absorption

299
Q

What is the function of the peritoneum in disease

A

Pain perception
Inflammatory and immune responses
Fibrinolytic activity

300
Q

How can we classify peritonitis

A

Onset (Acute or chronic)
Origin (Primary/secondary)
Cause (Bacterial, chemical, traumatic, Ischaemic and miscellaneous)
Location (Localised or generalised)

301
Q

What are the primary causes of peritonitis

A 
Liver disease
Spontaneous bacterial peritonitis 
Ascites 
Immunocompromised
Females 
Peritoneal dialysis patient
302
Q

What are the secondary causes of peritonitis

A

Gastrointestinal perforation (Perforated ulcer, appendix)
Transmural translocation - No perforation (Pancreatitis, Ischaemic bowel, primary bacterial peritonitis)
Exogenous contamination (Drains, open surgery, trauama, peritoneal dialysis)
Female genital tract infection
Haematogenous spread (Septicaemia)

303
Q

What microorganisms from the GIT cause peritonitis

A

Escherichia coli
Streptococci
Enterococci

304
Q

What bacteria other than those from the GIT can cause peritonitis

A

Chlamydia trachomatis

Neisseria gonorrhoea

305
Q

What are the signs and symptoms of localised peritonitis

A 
Abdominal pain and nausea 
Guarding
Rebound 
Rigidity 
Pyrexia
Tachycardia 
Shoulder tip pain 
Tender rectal and vaginal exam
306
Q

What is guarding

A

Involuntary abdominal wall contraction to protect the viscus from examination

307
Q

What is rigidity

A

Involuntary constant contraction of the abdominal wall over inflamed site

308
Q

What are the signs and symptoms of EARLY diffuse peritonitis

A 
Abdominal pain Mae worse my moving or breathing 
Tenderness 
Generalised guarding 
Infrequent bowel sounds 
Fever 
Tachycardia
309
Q

What are the signs and symptoms of LATE diffuse peritonitis

A 
Generalised rigidity 
Distension 
Absent bowel sounds 
Circulatory failure 
Thready irregular pulse 
Loss of consciousness
310
Q

What are the signs and symptoms of end stage peritonitis

A 
Circulatory failure 
Cold and clammy extremities 
Sunken eyes 
Dry tongue 
Thready irregular pulse and anxious face
311
Q

What investigations would you conduct in someone with suspected peritonitis

A 
FBC, U+E and amylase and LFTs 
Blood/ascitic fluid culture (high lactate above 25mg/dL 
Plain X-ray of chest and abdo
CT scan abdomen 
urine dipstick for UTI
312
Q

What is the management for peritonitis

A

Resuscitate and antibiotics
Plasma volume needs to be restored and electrolyte concentrations corrected as patient is often hypovolaemic
Urinary catheterisation and GI decompression
Surgical repair of abdomen
- Repair perforated viscus
Excision of perforated organ

313
Q

What other forms of peritonitis exist

A

Bile peritonitis
Spontaneous bacterial peritonitis
Primary pneumococcal peritonitis
Tuberculosis peritonitis

314
Q

What is familial Mediterranean fever characterised by

A 
Abdominal pain
tenderness
Mild pyrexia
Polymorphonuclear leukocytosis 
Pain in thorax and joints
315
Q

What is spontaneous bacterial peritonitis

A

Acute bacterial infection of the ascitic fluid that is diagnosed by paracentesis

316
Q

How is familial Mediterranean fever treated

A

Colchicine therapy

317
Q

Define ascites

A

Effusion and accumulation of serous fluid in the peritoneal cavity

318
Q

Do men normally have fluid in the peritoneal cavity

319
Q

How much fluid do women normally have in the peritoneal cavity

320
Q

What is exudate

A

Fluid that leaks around cells due to inflammation (<25g/dl)

321
Q

What is transudate

A

Fluid that is pushed through due to blockage of venous drainage
>25g/dl)

322
Q

Describe the classification system for ascites

A

stage 1: detectable only after careful examination/US

Stage 2: Early detectable but of relatively small volume

Stage 3: Obvious but not tense

Stage 4: Tense ascites (Large)

323
Q

What are the causes of ascites

A 
Portal hypertension
Liver cirrhosis 
Malignancy
HF
TB 
Pancreatitis
324
Q

What are the symptoms of ascites

A 
Abdominal distension 
Nausea 
weight loss 
Anorexia 
Constipation 
Pain/discomfort = malignancy
Painless = non malignant
325
Q

What are the signs of ascites

A 
Signs of liver failure (Jaundice)
Shifting dullness on percussion
Puddle sign (150ml)
Shifting dullness (500ml)
Abdominal distension (1.5L)
Flank fullness (>1.5L)
326
Q

What are the investigations for someone with suspected ascites

A 
Ascitic fluid aspiration for culture and microbiology 
X-ray 
Ultrasound 
Biochemistry
 - Serum ascites albumin gradient 
(Serum albumin - ascites albumin)
327
Q

What does a serum ascites albumin gradient of <1.1g/dl suggest

A

Non portal hypertensive causes

328
Q

What does a serum ascites albumin gradient of >1.1g/dl suggest

A

Portal hypertensive causes

329
Q

What is the management of ascites

A

Portal high BP treatment (diuretics, fluid/salt restriction, albumin replacement)
Paracentesis (4-6L/day with colloid replacement)
- portosystemic shunt
- Peritoneovenous shunt

Phase 2 (16 decks)

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