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Phase 2a Lecture Notes > GI + Liver > Flashcards

GI + Liver Flashcards

1
Q

Role of liver

A

Glucose and fat metabolism
Protein synthesis e.g. albumin, clotting factors
Detoxification and excretion
Defence against infection: bilirubin, ammonia, drugs and hormone
reticuloendothelial system

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2
Q

Portal triad

A

Portal vein, hepatic A, bile duct

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3
Q

Acute liver injury results

A

Liver failure, recovery

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4
Q

Chronic liver injury results

A

Cirrhosis- scaring, can lead to liver failure
recovery
Liver failure (varices, hepatoma)

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5
Q

Causes of liver cell death

A

necrosis (associated with neutrophils), or apoptosis

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6
Q

Cirrhosis

A

Scarring of the liver, disturbs the portal triad

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7
Q

Causes of acute liver injury

A

viral (A,B, EBV)
drug
alcohol
Vascular
Obstruction
Congestion

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8
Q

Causes of chronic liver injury

A

alcohol
viral (B,C)
autoimmune
metabolic (iron, copper)

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9
Q

Presentation of acute liver injury

A

malaise, nausea, anorexia, jaundice
rarer (more common in failure): confusion, bleeding, liver pain, hypoglycaemia

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10
Q

Presentation of chronic liver injury

A

ascites, oedema, haematemesis (varices), malaise, anorexia, wasting easy bruising (clotting factors affected), itching, hepatomegaly, abnormal LFTs
rarer: jaundice (more related to acute), confusion

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11
Q

Chronic liver injury- management

A

Lifestyle changes and supportive treatment
Consider liver transplant

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11
Q

Acute liver injury- management

A

Identify and treat underlying cause
Monitor neurological status, blood tests
Consider liver transplant

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12
Q

Serum ‘liver function tests’

A

No one global test
Serum bilirubin, albumin, prothrombin time: (give some index of liver function)
Serum liver enzymes: -cholestatic: alkaline phosphatase, gamma-GT
-hepatocellular: transaminases (AST, ALT)- don’t give index of liver function

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13
Q

Jaundice

A

raised serum bilirubin

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14
Q

Pre-hepatic jaundice
Unconjugated bilirubin problems

A

Gilberts, Haemolysis

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15
Q

Hepatic jaundice
(conjugated bili) problems

A

Hepatitis: viral, drugs immune, alcohol
Ischaemia
Neoplasm
Congestion (CCF)

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16
Q

Post-hepatic jaundice
(conjugated) problems

A

Gallstone: bile duct, Mirizzi
Stricture: malignant, ischaemic, inflammatory

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17
Q

Prehepatic jaundice tests

A

Urine- normal
Stool- normal
Itching- no
Liver test- normal

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18
Q

Cholestatic jaundice tests

A

Urine- dark
Stool- may be pale
Itching- maybe
Liver test- abnormal

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19
Q

Jaundice history taking

A

Past history: biliary disease/intervention malignancy, heart failure blood products , autoimmune disease
Drug history (drugs/herbs started recently)
Social history- Alcohol, potential hepatitis contact (irregular sex, IVDU, exotic travel, certain foods)
Family Hx/ system review – rarely helpful

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20
Q

Jaundice investigations

A

Liver enzymes: Very high AST/ALT suggests liver disease, some exceptions
Biliary obstruction: 90% have dilated intrahepatic bile ducts on ultrasound
-no dilation means likely hepatic causes
Need further imaging: CT Magnetic resonance cholangioram MRCP Endoscopic retrograde cholangiogram ERCP

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21
Q

Gallstone

A

Most form in gallbladder- smaller stone more of a risk, than large stone that remain gallbladder
Very common: 1/3 women over 60
70% Cholesterol, 30% pigment+/- calcium

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22
Q

Gallstone risk factors

A

Risk factors: Female, fat, fertile (liver disease, ileal disease, TPN, clofibrate…)

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23
Q

Gallstone symptoms

A

Most asymptomatic
Weight loss, jaundice, referred in right shoulder

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24
Q

Gallstones presentation- in gallbladder

A

Biliary pain- yes
Cholecystitis- yes
Obstructive Jaunice- maybe (mirizzi)
Cholangitis- no
Pancreatitis- no

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25
Q

Gallstones presentation- in bile duct

A

Biliary pain- yes
Cholecystitis- no
Obstructive Jaunice- no
Cholangitis- yes
Pancreatitis- yes

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26
Q

Gallstones: management- gallbladder

A

Laparoscopic cholecystectomy
Bile acid dissolution therapy (<1/3 success)

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27
Q

Gallstones: management- bile duct stones

A

ERCP with sphincterotomy and:
removal (basket or balloon)
crushing (mechanical, laser..)
stent placement Surgery (large stones)

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28
Q

Are the ducts always dilated on ultrasound as result of gallstones

A

Ducts not always dilated on ultrasound (esp with “stone” jaundice)

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29
Q

Isoniazid complications

A

Acute liver injury

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30
Q

DRUG-INDUCED LIVER INJURY (DILI)

A

1/10000 patients/yr
30% of Acute Hepatitis
>65% of Acute Liver Failure - 50% Paracetamol
- 15% idiosyncratic- not due to ODs
Commonest reason for drug withdrawal from formulary

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31
Q

Types of DILI

A

Hepatocellular- ALT >2 ULN, ALT/Alk Phos ≥ 5
Cholestatic- Alk Phos >2 ULN or ratio ≤ 2
Mixed- Ratio > 2 but < 5
direct toxicity and idiosyncratic DILI

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32
Q

DILI: DIAGNOSTIC APPROACH

A

what did you start recently- usually 1-12 weeks of starting, onset may be weeks after stopping
resolution: 90% within 3 months of stopping
5-10%: prolonged- high mortality rate

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33
Q

DILI: “Usual Suspects”

A

32-45% Antibiotics
15% CNS Drugs-
5% Immunosuppressants
5-17% Analgesics/ musculoskeletal (Diclofenac…)
10% Gastrointestinal Drugs (PPIs…)
10% Dietary Supplements
20% Multiple drugs

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34
Q

Examples of drugs that commonly cause DILI- Antibiotics

A

Augmentin, Flucloxacillin, Erythromycin, Septrin, TB drugs

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35
Q

Examples of drugs that commonly cause DILI- CNS

A

Chlorpromazine, Carbamazepine Valproate, Paroxetin

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36
Q

Drugs unlikely to cause DILI

A

Low dose Aspirin
NSAIDs other than Diclofenac
Beta Blockers
HRT
ACE Inhibitors
Thiazides
Calcium channel blockers

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37
Q

Paracetamol metabolism

A

Acetaminophen> Stable
Metabolite > Excretion

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38
Q

Paracetamol OD

A

High doses of paracetamol produces liver cell necrosis. The toxic metabolite binds irreversibly to to liver cell membranes

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39
Q

Management of paracetamol induced fulminant hepatic failure

A

N acetyl Cysteine (NAC)
Supportive to correct
-coagulation defects, fluid electrolyte and acid base balance, renal failure, hypoglycaemia, encephalopathy

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40
Q

Paracetamol-induced liver failure: severity indicators

A

Late presentation (NAC less effective >24 hr)
Acidosis (pH <7.3)
Prothrommbin time > 70 sec
Serum creatinine ≥ 300 µmol/l
Consider emergency liver transplant- otherwise 80% mortality

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41
Q

Ascites- causes

A

Chronic liver disease (most) +/- Portal vein thrombosis, Hepatoma, TB
Neoplasia (ovary, uterus, pancreas…)
Pancreatitis, cardiac causes

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42
Q

Spider naevus

A

Vascular lesion characterized by anomalous dilatation of end vasculature found just beneath the skin surface- can be sign of cirrhosis, rheumatoid arthritis or hepatitis

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43
Q

Ascites- pathogenesis

A

Increased intrahepatic resistance + systemic vasodilation > secretion of Renin-angiotensin, Noradrenaline, Vasopressin + portal hypertension + low serum albumin
> fluid retention+ portal hypertension > ascites

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44
Q

Ascites- management

A

Fluid and salt restriction
Diuretics Spironolactone +/ Furosemide
Large-volume paracentesis + albumin
Trans-jugular intrahepatic portosystemic shunt (TIPS)

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45
Q

Alcohol liver disease and fat

A

Alcohol changes the way that hepatocytes metabolise and produce fat. Fat accumulation within hepatocytes is termed steatosis. It may be associated with acute liver injury, or as in the picture, chronic injury mediated by lymphocytes

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46
Q

Acute alcohol-related injury

A

causes hepatocyte ballooning and is mediated by neutrophils (acute alcoholic hepatitis)

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47
Q

Acute Decompensation

A

Fatty liver> alcohol hepatitis (90% of 1st episodes) or cirrhosis (more common later) +/ infection > acute decompensation

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48
Q

Alcoholic Liver Disease (ALD)

A

Main cause of liver death in UK
However, only 10-20% of heavy alcohol drinkers drinkers get serious ALD (unsure why)
Often not alcohol dependent
Poor outcome- 10 years survival 25%

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49
Q

Progression of Alcoholic Liver Disease (ALD)

A

Normal> Steatosis> Alcohol steatohepatitis/ fibrosis > Cirrhosis (or alcoholic hepatitis which can develop into cirrhosis) > Hepatocellular carcinoma

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50
Q

ALD management

A

Depends on type of liver disease
General- Stop drinking, Withdrawal symptoms treated with diazepam

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51
Q

Portal hypertension causes

A

cirrhosis, fibrosis, portal vein thrombosis

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52
Q

Portal hypertension- pathology

A

increased hepatic resistance, increased splanchnic blood flow

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53
Q

Portal hypertension complications

A

varices (oesophageal, gastric), splenomegaly

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54
Q

Liver transplantation for alcoholic liver disease?

A

Limited supply of liver, poor negative attitudes
However, post transplant survival similar to that for other liver diseases- did well
Drinking relapse –variable; recurrent ALD uncommon

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55
Q

Alcohol withdrawal treatment

A

Lorazepam

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56
Q

Causes of deterioration in chronic liver disease

A

Constipation
Drugs -sedatives, analgesics
NSAIDs, diuretics, ACE blockers
Gastrointestinal bleed
Infection (ascites, blood, skin, chest)
HYPO: natremia, kalaemia, glycaemia
Alcohol withdrawal (not typically)
Other (cardiac, intracranial)

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57
Q

Spontaneous bacterial peritonitis

A

Commonest serious infection in cirrhosis
based on neutrophils in ascitic fluid
Gram stain often neg; use blood culture bottles
After 1 episode:
-should have antibiotic prophylaxis
-consider liver transplantation

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58
Q

Renal failure in liver disease- causes

A

Drugs (diuretics, NSAIDS, ACEi, Aminoglycosides), Infection, GI bleeding, myoglobinuria, renal tract obstruction

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59
Q

Coma in patients with chronic liver disease

A

Hepatic encephalopathy (ammonia …) infection, GI bleed, constipation, hypokalaemia, drug (sedatives, analgesics)
Hyponatraemia / hypoglycaemia
Intracranial event

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60
Q

Encephalopathy

A

disease in which the functioning of the brain is affected by some agent or condition

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61
Q

Bedside tests for encephalopathy

A

Serial 7’s
WORLD backwards
Animal counting in 1 minute
Draw 5 point star
Number connection test

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62
Q

Other consequences of liver dysfunction

A

Malnutrition, coagulopathy, endocrine changes, hypoglycaemia

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63
Q

Drug prescribing in liver disease- Analgesia

A

sensitive to opiates
NSAIDs cause renal failure
paracetamol safest

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64
Q

Drug prescribing in liver disease- Sedation

A

use short-acting benzodiazepines- with care!!

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65
Q

Drug prescribing in liver disease- diuretics

A

excess weight loss hyponatraemia
hyperkalaemia
renal failure

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66
Q

Drug prescribing in liver disease- Antihypertensives

A

Can often stop, avoid ACEi

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67
Q

Drug prescribing in liver disease-
Aminoglycosides

A

Avoid!!!

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68
Q

Consequences of liver disease

A

Malnutrition
Variceal bleeding
Encephalopathy
Ascites / oedema
Infections- antibiotics

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69
Q

Treatment of consequences of liver disease- Malnutrition

A

Naso-gastric feeding

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70
Q

Treatment of consequences of liver disease- Variceal bleeding

A

Endoscopic banding, propranolol, terlipressin

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71
Q

Treatment of consequences of liver disease- Encephalopathy

A

lactulos

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72
Q

Treatment of consequences of liver disease- Ascites / oedema

A

salt / fluid restriction
diuretics, paracentesis

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73
Q

Liver patient ‘gone off’- what to do

A

ABC, look at chart (vital signs, O2, BM(glucose), drug chart), look at patient (focus of infection and bleeding)
Tests- FBC, U&E, blood cultures, ascitic fluid, clotting, LFTs

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74
Q

Causes of chronic liver disease

A

Alcohol
Non Alcoholic Steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune cholangitis
Metabolic
Vascular - Budd-Chiari

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75
Q

Causes of chronic liver disease- immune

A

[autoimmune hepatitis, primary biliary cirrhosis, sclerosing

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76
Q

Causes of chronic liver disease- metabolic

A

haemochromatosis, Wilson’s, alpha-1 antitrypsin deficiency

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77
Q

Chronic liver- history taking

A

Past history: -alcohol problems, biliary surgery, autoimmune disease, blood products
Social history: alcohol, sexual
Drug history (all drugs!!)
Family history

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78
Q

Investigation of chronic liver disease

A

Viral serology
Immunology
Biochemistry
Radiological investigations

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79
Q

Investigation of chronic liver disease- Viral serology

A

Hepatitis B surface antigen, hepatitis C antibody

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80
Q

Investigation of chronic liver disease- Immunology

A

autoantibodies- AMA, ANA, ASMA,
coeliac antibodies
immunoglobulins

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81
Q

Investigation of chronic liver disease- biochem

A

iron/ copper studies
caeruloplasmin
24 hr urine copper
alpha1-antitrypsin level
lipids, glucose

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82
Q

Investigation of chronic liver disease- radiology

A

Ultrasound (USS) / CT / MRI

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83
Q

Normal flora

A

the community of microorganisms that live on another living organism without causing disease

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84
Q

Role of normal flora

A

produces antimicrobial substances which discourage infection by:
Inhibiting overgrowth of endogenous pathogens
Preventing colonisation by exogenous pathogens

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85
Q

Disruption to normal flora

A

Antibiotics can disrupt this balance increasing susceptibility to infections such as C.Difficile.
Peritonitis can occur as if normal barriers are breached

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86
Q

C.Difficile

A

Gram positive spore forming bacteria
Up to 5% of population have c.diff as normal flora
Many are asymptomatic but can become a problem if the normal gut flora is altered, most notably is due to broad spectrum antibiotics- rule of C’s

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87
Q

Rule of C’s

A

associated with a higher risk of C. difficile infection
clindamycin, ciprofloxacin (quinolones), co-amoxiclav (penicillins) and cephalosporins (particularly 2nd and 3rd generation)

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88
Q

C diff treatment

A

metronidazole or oral vancomycin.
In refractory cases sometimes faecal transplant- aims to restore the normal flora

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89
Q

Diarrhoea causes

A

Infective, inflammatory, loss of absorptive area, pancreatic disease, drugs, colon cancer, systemic disease, IBS, gastrectomy

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90
Q

Infective causes of diarrhoea

A

Campylobacter, salmonella, HIV, bacterial, amoebic dysentery, cholera

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91
Q

Diarrhoea- history

A

Onset/duration
Characteristics of stool
Food/drink
Travel
Immunocompromised
Unwell contacts
Hobbies + fresh water
Animal contact
Medications

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92
Q

Diarrhoea characteristics

A

floating: fat content ?malabsorption/ Coeliac
blood or mucus: ?inflammatory/ invasive infection ?cancer
Watery small bowel infection

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93
Q

Food and drink diarrhoea

A

Dodgy take-aways – food poisoning (eating food contaminated with microorganisms or toxins)
Meat/BBQs: campylobacter
Rice: bacillus cereus
Poultry: salmonella
Shellfish: norovirus, v.parahaemolyticus

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94
Q

Watery diarrhoea

A

non-inflammatory, proximal small bowel, bacterial, viral (rotavirus, norovirus) and parasitic causes

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95
Q

Water diarrhoea- bacterial causes

A

E coli
Clostridium perfringens – cooked meats
Bacillus cereus – reheated rice (vomiting +++)
Staph. aureus enterotoxin has a direct effect on vomiting centre in brain! <6hr exposure

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96
Q

Water diarrhoea- parasitic causes

A

Giardia – offensive diarrhoea, chronic, bloating, flatulence, nurseries/old age facilities
Cryptosporidium – swimming pools

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97
Q

Blood, mucoid diarrhoea

A

Inflammatory, colon, bacterial and parasitic causes

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98
Q

Blood, mucoid diarrhoea- bacterial causes

A

Shigella 🡪 shiga toxin, causes gross injury to bowel surface; MSM at risk
Salmonella – poultry, eggs and dairy
E coli
Vibrio parahaemolyticus – shellfish
C.Diff – antibiotics
Campylobacter – meats, BBQ

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99
Q

Blood, mucoid diarrhoea- parasitic causes

A

Entamoeba histolytica- travel, MSM

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100
Q

Most common GI infections in the UK

A

Mainly viral, ie rotavirus, norovirus

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101
Q

Diarrhoea definition

A

3 or more unformed stool per day plus one of the following:
Abdo pain
Cramps
Nausea
Vomiting
Dysenty

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102
Q

Traveller’s diarrhoea

A

occurs within 10 days of arrival from a foreign country, most commonly Enterotoxigenic E. coli, be aware of cholera

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103
Q

E.coli

A

Most strains are harmless
Some serotypes are pathogenic

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104
Q

Types of E coli

A

ETEC: EnteroToxigenic
EHEC: EnteroHaemorrhagic
EIEC: EnteroInvasive
EPEC: EnteroPathogenic
EAEC: EnteroAggregative
DAEC: Diffusely Adherent

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105
Q

E coli ETEC

A

leading bacterial cause of diarrhoea in children in developing world and most common cause of travellers diarrhoea
380000 deaths- mostly children in developing world

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106
Q

E colic EHEC

A

Shiga-like toxin – intensive inflammatory response
Can cause Haemolytic uraemic syndrome

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107
Q

Haemolytic uraemic syndrome

A

Bloody diarrhoea, abdo pain, no fever
Haemolysis
Renal failure

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108
Q

E. coli EIEC

A

Enteroinvasive, dysentery like illness, similar to shigella

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109
Q

Cholera

A

Contaminated food/water
Cholera toxin
Profuse watery “rice water” diarrhoea upto 20L a day
Vomiting
Rapid dehydration

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110
Q

Cholera treatment

A

Doxycycline and fluids

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111
Q

Immunosuppressed- more at risk to

A

Bacterial- Cryptosporidium, Mycobacteria, Microsporidia
Viral- CMV, HSV
Overall risk increased

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112
Q

Diarrhoea- lab tests

A

Stool tests- Microscopy, Culture
Ova, cysts and parasites, Toxin detection
Blood tests- Blood culture, Inflammatory markers (FBC/CRP)

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113
Q

Diarrhoea Red flags

A

Dehydration
Electrolyte imbalance
Renal failure
Immunocompromise
Severe abdominal pain
Cancer risk factors
Over 50, Chronic diarrhoea, Weight loss, Blood in stool, FH cancer, change in bowel symptoms

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114
Q

Diarrhoea- Key management principles

A

Fluids, electrolytes
Antiemetics if long time? (effective against vomiting and nausea)
Infection control
Do public health need to be connected, PPE when treating patient, deep cleaning

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115
Q

Are antibiotics a treatment for bacterial diarrhoea

A

No, unless they are immunocompromised

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116
Q

RUQ pain infections

A

Biliary sepsis aka ascending cholangitis
Liver abscess
Pneumonia

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117
Q

Lower abdominal pain infections

A

PID- pelvic inflammatory disease

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118
Q

Peptic Ulcer Disease

A

Helicobacter pylori- commonest cause of ulcer
Lives within mucus layer overlying the gastric mucosa

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119
Q

Peptic Ulcer Disease- treatment

A

CAP = Clarithromycin, Amoxicillin, PPI eg omeprazole

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120
Q

Acute Cholecystitis

A

Gallbladder inflammation, cystic duct obstruction by gall stones
RUQ or epigastric pain, fever and leucocytosis

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121
Q

Acute Cholecystitis- treatment

A

Diagnosis: By ultrasound
Treatment: IV fluids, analgesia and antibiotics
Surgery: Cholecystectomy

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122
Q

Ascending Cholangitis

A

Obstruction of the CBD
fever, abdominal pain, and jaundice (Charcot’s triad)
High mortality

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123
Q

Ascending Cholangitis- management

A

Prompt admission and IV antibiotics
ERCP- endoscopic retrograde cholangiopancreatography
Cholecystectomy

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124
Q

Liver abscess causes

A

Bacterial : faecal flora eg E.coli, Klebsiella spp etc
Amoebic: Entamoeba histolytica
Hydatid: Echinococcus granulosus (dog tapeworm)

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125
Q

Peritonitis causes

A

Medical – SBP (spontaneous bacterial peritonitis), PID (pelvic inflammatory disease), dialysis related, TB
Surgical – perforation of GIT

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126
Q

Enteric fever

A

aka typhoid
Mortality 20% 🡪 < 1% with antibiotics!
2-3% become carriers

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127
Q

Enteric fever symptoms

A

Generalised / R lower quadrant pain
High fever
“Relative bradycardia”
Headache and myalgia
Rose spots
Constipation/green diarrhoea

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128
Q

Enteric fever- management

A

Diagnosis- blood culture
Antibiotic, ?emergency surgery for complications

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129
Q

Enteric fever- complications

A

GI bleed
Perforation / peritonitis
Myocarditis
Abscesses

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130
Q

Hepatitis

A

Inflammation of the liver

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131
Q

Hepatitis differential diagnosis

A

viral (A, B, C, CMV, EBV)
drug-induced
autoimmune
alcoholic

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132
Q

Autoimmune hepatitis (AIH)

A

Progressive inflammatory liver condition, mostly effects females (75%), pathogenesis not fully understood
type 1- Anti nuclear (ANA), anti-smooth muscle, (ASMA)
Type 2- anti- liver/ kidney microsomal

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133
Q

Autoimmune hepatitis (AIH) clinical features

A

40% present with acute hepatitis
30% have cirrhosis at presentation
Patients may be asymptomatic or present with fatigue, and abnormalities in liver bichem or present with liver disease on examination

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134
Q

Autoimmune hepatitis (AIH) investigations

A

Liver biochem- ALT high, IgG raised
Liver biopsy- AIH requires liver biopsy for diagnosis and evaluate disease progression

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135
Q

Autoimmune hepatitis (AIH) treatment

A

prednisolone +/- azathioprine

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136
Q

Cirrhosis

A

Liver architecture is diffusely abnormal and interferes with liver blood flow and function, leads to portal hypertension and liver failure

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137
Q

Primary Biliary Cirrhosis (PBC)

A

Progressive disease- progressive destruction of interlobular bile ducts
Pathogenesis unknown
Mostly woman effected (90%)

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138
Q

Primary Biliary Cirrhosis/Cholangitis (PBC) clinical features

A

Mainly itching +/ fatigue, can be asymptomatic with lab abnormalities
other presentations include- dry eyes, joint pain, variceal bleeding and liver failure

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139
Q

Primary Biliary Cirrhosis/Cholangitis (PBC) investigations

A

Serum IgM- high
Liver biochem- often high serum alkaline is the only liver abnormality
Liver biopsy- required for diagnosis, characteristic portal tract infiltrate

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140
Q

Primary Biliary Cirrhosis/Cholangitis (PBC) management

A

Ursodeoxycholic acid- improves bilirubin and ALT levels, should be given in early phase, no benefit in advanced disease
Liver transplant
treatment of cholestatic itch- cholestyramine, Rifampicin, opioid antagonist
treatment of fatigue- disabling, trials for Modafinil (narcolepsy drug)

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141
Q

Ductopenia

A

destruction of the bile duct branch as a result of serve immune damage

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142
Q

Primary Sclerosing Cholangitis (PSC)

A

chronic cholestatic liver disease characterised by fibrosing inflammatory destruction of intra/ extrahepatic bile ducts
50% have IBS
10% develop into cholangiocarcinoma (bile duct cancer)

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143
Q

Primary Sclerosing Cholangitis (PSC) clinical features

A

With IBS- often asymptomatic and picked up by screening with high serum ALP
Symptoms include itching, pain ± rigors, jaundice

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144
Q

Primary Sclerosing Cholangitis (PSC) investigations

A

Magnetic Resonance Cholangiopancreatography (MRCP)- biliary changes- irregularity of calibre of both intra and extrahepatic ducts

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145
Q

Primary Sclerosing Cholangitis (PSC) management

A

Liver transplant- only proven treatment
Ursodeoxycholic Acid: unclear benefits

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146
Q

Haemochromatosis

A

Inherited disease (mostly autosomal recessive)characterised by excess iron deposition in various organs, leading to eventual fibrosis and functional organ failure

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147
Q

Haemochromatosis pathology

A

total iron content is v high (20-40g) vs normal person (3-4g). Iron content is particularly increased in the liver and pancreas (50-100x higher), but still higher in other organs

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148
Q

Haemochromatosis investigation

A

Serum iron/ ferritin elevated
Liver biochem often normal
genetic testing

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149
Q

Haemochromatosis management

A

Venesection- prolongs life and may reverse tissue damage- many initially to reduce iron to normal level, then a few a year
Screening- first degree relative need screened

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150
Q

Alpha1-antitrypsin deficiency

A

Results in inability to export alpha1-antitrypsin from liver. Neonatal jaundice, chronic liver disease in adults
Can lead -to liver disease (protein retention in liver)
-emphysema (protein deficiency in blood)
no medical treatment

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151
Q

Hepatocellular carcinoma

A

Primary liver tumour
Adenocarcinoma formed of cells resembling normal hepatocyte
Most occur in patients with cirrhosis

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152
Q

Hepatocellular carcinoma risk factors

A

Risk: highest for hepatitis B,C, haemochromatosis
lower: cirrhosis from alcoholic, autoimmune disease
Males >Females

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153
Q

Hepatocellular carcinoma presentation

A

May presents with decompensation of liver disease, weight loss ascites, or abdominal pain

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154
Q

Hepatocellular carcinoma treatment

A

Limited- Transplantation, resection or local ablative therapies
Sorafenib recently shown to prolong life

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155
Q

Non-alcoholic liver disease (NAFLD)

A

Includes Non-alcoholic fatty liver (NAFL) and Non-alcoholic steatohepatitis (NASH)
Commonest cause of chronic liver disease

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156
Q

Non-alcoholic fatty liver (NAFL)

A

Too much fat around liver
commonest cause of mildly elevated LFTs

157
Q

Non-alcoholic steatohepatitis (NASH)

A

Fat around liver with inflammation, fibrosis
Important cause of cirrhosis(10-30% of patients develop cirrhosis)

158
Q

NAFLD risk factors

A

Obesity (70%), DM (35-75%), hyperlipidaemia (20-80%)

159
Q

NAFLD presentation

A

Usually asymptomatic, liver ache in 10%

160
Q

How to distinguish between NAFL and NASH

A

Liver biopsy- inflammation present in NASH

161
Q

NAFL treatment

A

Still no effective drug treatments
Weight loss works- the more the better

162
Q

Hepatic vein occlusion

A

prevents blood from flowing out of the liver and back to the heart
Congestion causes acute or chronic liver injury

163
Q

Hepatic vein occlusion causes

A

Thrombosis (Budd-Chiari syndrome)- may be underline thrombotic disorder
Membrane obstruction
Veno-occlusive disease (irradiation, antineoplastic drugs

164
Q

Hepatic vein occlusion presentation

A

abnormal liver test, ascites, acute liver failure

165
Q

Hepatic vein occlusion treatment

A

Anticoagulation
Transjugular intrahepatic portosystemic shunt
Liver transplantation

166
Q

Causes of chronic liver disease

A

Alcohol
Non alcoholic steatohepatitis (NASH)
Viral hepatitis (B, C)
Immune- autoimmune hepatitis, primary biliary cirrhosis, sclerosing cholangitis
Metabolic-haemochromatosis, Wilsons, 1 antitrypsin deficiency…
Vascular- Budd-Chiari

167
Q

Chronic liver disease- history taking

A

Past history: alcohol problems, biliary surgery, autoimmune disease, blood products
Social history: alcohol, sexual
Drug history (all drugs!!)
Family history

168
Q

upper GI bleeding

A

a very common medical emergency, 10% mortality risk

169
Q

Melena

A

Blood in stool, black and tary

170
Q

Haematemesis

A

Fresh blood in vomit

171
Q

Coffee ground vomiting

A

Old blood in vomit

172
Q

Common cause of upper GI bleeding

A

Peptic ulcer (most common), oesophageal varices

173
Q

Glasgow-Blatchford score

A

stratifies upper GI bleeding patients, uses BP, blood urea, haemoglobin levels, tachycardia, melaena, syncope, hepatic disease, cardiac failure

174
Q

Variceal bleed- suspect history

A

liver disease or alcohol excess

175
Q

Variceal bleed treatment

A

Antibiotics and Terlipressin (vasopressin agonist) reduce mortality.
Endoscopy within 12 hours

176
Q

Non-variceal bleed- suspect history

A

peptic ulcers, using certain medications; NSAIDs, anticoagulation or antiplatelets

177
Q

Non-variceal bleed
treatment

A

Consider proton pump inhibitors.
Endoscopy within 24 hours, longer than variceal

178
Q

What has a bigger impact on patient survival for upper Gi bleeds, initial management or endoscopy

A

Initial assessment and management is more important than endoscopy in most cases

179
Q

Difference in endoscopy treatment for variceal vs non variceal bleeding

A

Variceal- elastic band around bleed
Non-variceal- clipping bleed

180
Q

Intraluminal intestinal obstruction

A
  • tumour
    – carcinoma
    – lymphoma
  • diaphragm disease
  • meconium ileus
  • gallstone ileus
181
Q

Tumours obstructing GI lumen

A

Can form in wall and grow inwards/outwards, growth inwards leads to obstruction of gut

182
Q

Diaphragm disease

A

NSAIDs damage GI wall, mainly small bowel, fibrous ‘diaphragm’ scarring occludes the bowel lumen

183
Q

Diaphragm disease- difficult to diagnosis

A

Normally small bowel, can not use endoscopy or colonoscopy, need to use swallowable camera

184
Q

Gallstone ileus

A

mechanical intestinal obstruction due to impaction of one or more gallstones within the gastrointestinal tract

185
Q

intramural obstruction
of GI tract

A
  • inflammatory
    – Crohn’s disease
    – diverticulitis
  • tumours
  • neural
    – Hirschsprung’s disease
186
Q

Crohn’s disease obstruction

A

Characteristic ‘cobblestone’ appearance

187
Q

Diverticular disease

A

Infection in the tiny pouches in the colon. The pouches are called diverticula
Typically occurs in sigmoid colon
Can be asymptomatic, may need removal of sigmoid colon

188
Q

Diverticular disease- pathophysiology

A

Holes in muscularis (for blood vessels), points of weakness, lots pressure in colon, force mucosa into points of weakness, mucosa out pouches through muscularis, called diverticula

189
Q

Perpetrating Diverticulitis

A

Diverticulitis, breach of diverticula, contents spill into peritoneum, can lead to peritonitis

190
Q

intramural tumours

A

tumours grow outwards, compress bowel wall, leading to occulsion

191
Q

Hirschsprung’s disease

A

Congenital, due to missing nerve cells of muscle in colon
Part of bowel doesn’t move, causes obstruction

192
Q

extraluminal obstruction of intestinal wall

A
  • adhesions
  • volvulus
  • tumour
    – peritoneal deposits
193
Q

adhesions of intestine

A

Usually result of previous surgery, causes bands fibrous tissue between different parts of intestine
Can cause kink inn bowel

194
Q

volvulus- intestine obstruction

A

Sigmoid colon twists on itself, causing obstruction

195
Q

peritoneal tumour

A

Tumour growing in peritoneum compresses intestine, causing obstruction, problem in palliative care

196
Q

Small Bowel Obstruction (SBO)

A

Mechanical blockage of the small
intestine

197
Q

Small Bowel Obstruction (SBO)- expanded definition

A

a form of Intestinal failure (IF) is the inability of the gut to absorb
necessary water, macronutrients (carbohydrate, protein, and fat),
micronutrients, and electrolytes sufficient to sustain life and requiring
intravenous supplementation or replacement

198
Q

Small bowel obstruction (SBO) Aetiology

A

Compression- Adhesions (typically have episodes), hernia, tumour
Luminal- growth, foreign, stricture
Lack of peristalsis- Drugs (commonly opioids), electrolytes, neurological, serve Ileus/ postop

199
Q

Small bowel obstruction (SBO) symptoms

A

Colicky pain, absolute constipation (not passing of wind or stool), distension, vomiting

200
Q

Small bowel obstruction patient history

A

History of preventing compliant- onset, previous episodes (chronic suggests cancer)?
Previous surgery (suggests adhesions)
Medication (opioids= lack of peristalsis, or drugs that alter electrolytes)
Family history- cancer
Social history- functional status for surgery evaluation

201
Q

Small bowel obstruction (SBO)- clinical examination

A

Distended, tympanic, tender, hernias, bowel sounds (tinkling or absent), scars, PR

202
Q

Small bowel obstruction (SBO)- consequences

A

Perforation, nutrition, GI vitality (necrosis), Gut barrier/ translocation (bugs in bloodstream, leading to sepsis), fluid losses

203
Q

Small bowel obstruction (SBO)- investigation

A

CT scan, blood test (FBC, U+E, lactate- increases with poorly perfused gut, c-reactive protein)

204
Q

Small bowel obstruction (SBO)- treatment for all patients

A

Decompression- nasogastric tube
Fluid replacement/ maintenance, electrolyte replacement, Nutrition (>5 without intake may
need parenteral feed)
Surgery- remove bit obstructed, remove adhesion

205
Q

Barrett’s oesophagus

A

AKA CELLO- columnar lined lower oesophagus
Metaplasia due to presence of stomach acid in oesophagus destroying the squamous epithelium, leading to stem cells rising up from stomach producing glandular epithelium which is protected by mucin

206
Q

Metaplasia

A

change in differentiation of a cell from one fully-differentiated type to a different fully-differentiated type

207
Q

Barret’s oesophagus complications

A

Increase risk of oesophageal adenocarcinoma

208
Q

Oesophageal
squamous cancer- risk factor

A

Smoking, high alcohol intake, not result of Barret’s oesophagus

209
Q

Oesophageal symptoms that require urgent endoscopy

A

Acid reflux, pain, difficulty swallowing

210
Q

Gastric cancer global spread

A

Eastern Asia and eastern Europe high, linked to poor air quality, smoked and pickled food

211
Q

Helicobacter pylori and gastric cancer

A

Not always a cause, but can cause epithelium change in stomach to intestinal metaplasia, can lead to dysplasia and then carcinoma

212
Q

linitus plastica

A

Thicken wall, whole stomach infected by cancer

213
Q

Gastric cancer prognosis

A

Low survival rate (10-20% after 5 year), due to non-specific presentation

214
Q

Why is small intestine cancer uncommon

A

Fluidity and relative sterility of small bowel contents, and rapid transit time and of the relative sterility of the small bowel itself have been suggested as possible factors

215
Q

Colorectal cancer- risk factors

A

Most cancers arise from adenomas (dysplastic epithelium, most don’t turn into cancer), familial adenomatous polyposis (1% of colorectal cancer), hereditary nonpolyposis
colorectal cancer

216
Q

Familial adenomatous polyposis

A

Born in normal colons, in teenage years form thousands of polyps in cancer, due to inherited genetic mutation

217
Q

hereditary nonpolyposis colorectal cancer
(HNPCC)

A

a genetic disease of autosomal dominant inheritance. It is caused by a mutation in one of four genes of the DNA mismatch repair system

218
Q

hereditary nonpolyposis colorectal cancer
(HNPCC)- reasons for identifing

A

risk of further cancers in index patient and
relatives
* possible implications for therapy
– tolerance of 5-FU etc.
– do not recognise DNA damage
– apoptosis not activated

219
Q

macroscopic features
of colorectal cancer

A

38% of colorectal cancer (anus, rectum and rectosigmoid junction) can be felt on digital rectal examination

220
Q

What is the most common colorectal tumour

A

adenocarcinoma

221
Q

Treatment for colorectal cancer at each progression

A

Adenoma- endoscopic resection
Colorectal adenocarcinoma- surgical resection
Metastatic colorectal adenocarcinoma- chemo, palliative care

222
Q

Hepatitis

A

inflammation of the liver
(acute< 6 months, chronic persists beyond 6 months)

223
Q

Acute hepatitis- symptoms

A

None or non-specific, e.g. malaise, lethargy, myalgia
Gastrointestinal upset, abdominal pain
Jaundice + pale stools / dark urine

224
Q

Acute hepatitis- clinical signs

A

Tender hepatomegaly ± jaundice
± signs of fulminant hepatitis (acute liver failure), e.g. bleeding, ascites, encephalopathy
Blood tests- Raised transaminases (ALT/AST&raquo_space; GGT/ALP) ± raised bilirubin

225
Q

Causes of acute hepatitis- infectious viral

A

Hepatitis A, B ± D, C & E
Human herpes viruses, e.g. HSV, VZV, CMV, EBV
Other viruses

226
Q

Causes of acute hepatitis- infectious non- viral

A

Spirochaetes, e.g. leptospirosis, syphilis
Mycobacteria, e.g. M. tuberculosis
Bacteria, e.g. bartonella
Parasites, e.g. toxoplasma

227
Q

Causes of acute hepatitis- non-infection

A

Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Pregnancy
Autoimmune hepatitis
Hereditary metabolic causes

228
Q

Chronic hepatitis symptoms

A

Can be asymptomatic or have non-specific symptoms only

229
Q

chronic hepatitis- clinical signs

A

Clubbing, palmar erythema, Dupuytren’s contracture, spider naevi, etc
Transaminases (ALT/AST) can be normal

230
Q

chronic hepatitis- clinical signs compensated

A

liver function maintained

231
Q

chronic hepatitis- clinical signs decompensated

A

coagulopathy (↑PT, INR); jaundice (↑bilirubin); low albumin; ascites (± bacterial peritonitis); encephalopathy

232
Q

chronic hepatitis- complications

A

hepatocellular carcinoma (HCC); portal hypertension (varices, bleeding)

233
Q

chronic hepatitis- causes, infection

A

Hepatitis B ± D, C (& E)

234
Q

chronic hepatitis- causes, non- infection

A

Drugs
Alcohol
Other toxins / poisoning
Non-alcoholic fatty liver disease
Autoimmune hepatitis
Hereditary metabolic causes

235
Q

Most common form of viral hepatitis

A

chronic hepatitis B ≈ 257 million
then, chronic hepatitis C ≈ 71 million

236
Q

Hepatitis A (HAV)

A

Contaminated food & water
Linkage to access to safe drinking water & socioeconomic indicators
HICs- travel, MSM (men sex with men), IV drug use

237
Q

Hepatitis A: Clinical

A

Short incubation period (15-50 days), acute
Symptomatic
Rarely acute liver failure
100% immunity after infection

238
Q

Hepatitis A: symptoms

A

Symptomatic- Pre-icteric phase: constitutional symptoms + abdominal pain
Icteric phase (few days to 1 week after pre-icteric phase)

239
Q

Hepatitis A: serological response

A

anti- HAV IgM initially, anti-HAV IgG provide immunity

240
Q

Hepatitis A: Management

A

Supportive
Monitor liver function
Primary prevention- vaccines

241
Q

Liver function measures

A

INR, albumin, bilirubin

242
Q

hepatitis E

A

4 genotypes- affect different parts of world
G1+2- similar to HAV, transmission through food and water
G3+4- undercooked meat

243
Q

Hepatitis E: Clinical

A

> 95% cases asymptomatic
Usually self-limiting acute hepatitis
Extra-hepatic manifestations (neurological)

244
Q

Chronic Hepatitis E

A

Risk of chronic infection (GT3/4 only) in immunosuppressed patients
e.g. transplant recipients, HIV patients
rapid progression to cirrhosis

245
Q

Hepatitis E: serological response

A

anti-HEV IgM initially, partial immunity from anti-HEV IgG

246
Q

Hepatitis E: Management

A

Acute- supportive, monitor for acute-on-chronic liver failure
Chronic- Reverse immunosuppression (if possible)
If HEV RNA persists, treat with ribavirin ≥ 3 mths

247
Q

Hepatitis E: Prevention

A

Avoid eating undercooked meats (especially if immunocompromised)
Screening of blood donors
Vaccines in development

248
Q

hepatitis B

A

Blood-borne virus
Transmission via blood and body fluids

249
Q

Hepatitis B natural history adults !!!!!

A

Acute HBV infection
Symptomatic- Spontaneous resolution (rick of re-activation with immunosuppression
Chronic HBV infection- asymptomatic Cirrhosis> Hepatocellular carcinoma or Decompensated cirrhosis

250
Q

Hepatitis B natural history (neonates and infants)

A
251
Q

Hepatitis B: serological response

!!!

A

anti-HB core IgG- exposure to HBV infection
Hepatitis B surface antigen- Current HBV infection

252
Q

Acute Hepatitis B: presentation & management

A

Incubation period: 30 to 180 days (mean 75 days)
Supportive management
Monitor liver function (INR, albumin, bilirubin, etc.)
Rarely fulminant hepatitic failure: 0.1 to 0.5%
Oral nucleos(t)ide analogue (tenofovir, entecavir)
Liaise with hepatology / liver transplant centre
Management of close contacts (HBV vaccine if non-immune ± HBIG )

253
Q
A
254
Q

Hepatitis B: clearance in acute phase

A
255
Q
A
256
Q

Hepatitis B: failure to clear / chronic infection

A
257
Q

Chronic hepatitis B: who to treat?

!!!!!

A

e-antigen (eAg)- high viral load
e-antibody (eAb)- high immune response
Treat people in immune reactive and immune escape stage

258
Q

Chronic hepatitis B- treatment- pegylated interferon-α 2a

A

Immunomodulatory
stimulates immune response
Weekly subcutaneous injection
48 week long treatment course
Offers best chance of treatment-free control
Side effects & need for monitoring

259
Q

pegylated interferon-α 2a side effects

A
260
Q

Chronic hepatitis B- treatment- oral nucleos(t)ide analogues

A

Inhibit viral replication
HBV DNA polymerase
One tablet once a day
High barrier to resistance
Minimal side effects
Renal monitoring (TDF)
May be required lifelong

261
Q

Hepatitis B: Prevention

A

Antenatal screening (HBsAg testing) of pregnant mothers
Screening ± immunisation of sexual and household contacts
Childhood immunisation
Universal screening of blood products

262
Q

Hepatitis D

A

Defective RNA virus
Requires Hep B antigen presence to replicate
Blood-borne virus
Transmission via blood and body fluids

263
Q

Hepatitis B + D coinfection

A

Infected by hep B + D together, increased risk of fulminant hepatitis in acute infection

264
Q

Hepatitis B + D superinfetion

A

Infected by hep B, then hep D, acute on chronic hepatitis
accelerated progression to liver fibrosis

265
Q

Hepatitis B + D coinfection natural history

A
266
Q

Hepatitis D test

A

Hepatitis D antibody: if positive, test HDV RNA

267
Q

Hepatitis D treat

A

pegylated inteferon-α 48 weeks (2020: Myrcludex B)

268
Q

Hepatitis C

A

Blood-borne virus
Transmission via blood and body fluids- IV drug use, blood products

269
Q

Hepatitis C natural history (immunocompetent adults)
!!!

A
270
Q

Hepatitis C testing

A

HCV antibody
If +ive, HCV RNA (to see if infection is active)
If +ive, HCV genotype (to determine type of HCV)

271
Q

Hepatitis C treatment- Directly-acting antiviral (DAA) therapy

A

Combination of antivirals
Drugs have different effects on different genotypes (need to know genotype)

272
Q

Hepatitis C: Prevention

A

No vaccine
Previous infection does not confer immunity
Blood screening
Cure of ‘transmitters”, ie programs to reduce IV drug use

273
Q

Coeliac disease

A

Autoimmune entropy caused by ingestion of gluten
1/4 are genetically predisposed to disease

274
Q

Coeliac disease management

A

Gluten free diet- strict and lifelong
Dietitian review
Bone density score
Prescription of GF foods
Immunisation

275
Q

Coeliac disease symptoms

A

severe diarrhoea, excessive wind and/or constipation.
persistent or unexplained gastrointestinal symptoms.
iron, vitamin B12 or folic acid deficiency.
anaemia.
tiredness

276
Q

Coeliac disease associated diseases

A

Addison’s Disease
Arthritis
Autoimmune Hepatitis
Hashimoto’s Thyroiditis
Idiopathic Dilated Cardiomyopathy
IgA Nephropathy (Berger’s Disease)
Multiple Sclerosis (MS)
Sjogren’s Syndrome
Type 1 Diabetes Mellitus

277
Q

Mucosal Ischemia

A

Ischemia of blood vessels that supply mucosal layer of stomach, leads to reduce mucin layer and can lead to an ulcer
Common with people with in haemodynamic shock

278
Q

Mucosal Ischemia - treatment

A

Reverse the mucosal ischemia- cell revert back to normal
PPIs/ H2 blockers to remove acid

279
Q

Causes of gastric ulceration

A

NSAIDs, Helicobacter pylori (H. pylori), mucosal ischemia, bile reflux, alcohol (high percentage spirits)

280
Q

Helicobacter pylori (H. pylori)

A

Live in mucin layer in stomach, can lead to acute inflammation, long term helicobacter can cause intestinal metaplasia

281
Q

Causes of malabsorption

A

Insufficient intake, defective intraluminal digestion, insufficient absorptive areas, lack of digestive enzymes, defective epithelial transport, lymphatic obstruction

282
Q

Causes of malabsorption- Defective intraluminal digestion

A

Pancreatic insufficiency (CF, pancreatitis), Defective bile secretion (lack of fat solubility- biliary obstruction, ileal resection), Bacterial overgrowth

283
Q

Causes of malabsorption- Insufficient absorptive areas

A

Coeliacs disease, Crohn’s disease, extensive parasitic infection (giardia lamblia), small intestinal resection or bypass

284
Q

Causes of malabsorption- lack of digestive enzymes

A

disaccharidase deficiency (lactose intolerance- disaccharide broken down in small intestine, causes large release of CO2 and sugars causes diarrhoea), bacterial overgrowth

285
Q

Causes of malabsorption- defective epithelial transport,

A

Abetalipoproteinemia, primary bile acid malabsorption (mutations in bile acid transporter protein)

286
Q

Gallstones types

A

Cholesterol, pigment stones (bile acid, phosphate, Mg) + mixed stones

287
Q

Commonest type of gallstones

A

Cholesterol stones

288
Q

Biliary anatomy

A

Liver produces bile
Gallbladder stores bile
Responds to CCK
Biliary system drains into D2 (Ampulla of Vater)

289
Q

Gallstones- 5 Fs

A

fat, female, forty, fertile, fair (skin/ hair)

290
Q

Gallstones pathology

A

Biliary colic, jaundice, pancreatitis, cholecystitis (stone in stone bladder), choledocholithiasis (stones in bile duct), Cholangitis, Gallstone ileus, Mirizzi syndrome (stone in impacted in Hartman pouch)

291
Q

Biliary colic signs + symptoms

A

Post prandial colicky pain (worse with fats, RUQ), nausea/ vomiting,

292
Q

cholecystitis signs and symptoms

A

Constant pain, fever, rigours, tender as inflamed gallbladder contacting peritoneum

293
Q

choledocholithiasis signs and symptoms

A

jaundice

294
Q

Cholangitis signs and symptoms

A

Fever >39, jaundice

295
Q

Gallstones investigations

A

Ultrasounds (USS), FBC, LFTs (alkaline phosphates, ALT, bilirubin, albumin), Clotting factors, amylase (pancreatic damage), MRCP (MRI of bile system)

296
Q

Mirizzi syndrome

A
297
Q

Gallstone Ileus

A

a mechanical intestinal obstruction due to impaction of one or more gallstones within the gastrointestinal tract

298
Q

Gallstones treatment

A

Antibiotics, analgesia- NSAIDs with PPI cover, ECRP (to remove stone from bile duct), cholecystectomy, bile duct exploration/ reconstruction (surgical removal of stone)

299
Q

Pancreatitis- I GET SMASHED

A

Idiopathic, Gallstones, Ethanol, Trauma. Steroid use, Mumps, Autoimmune, Scorpion stings, Hypercalcemia + hypertriglyceridemia, ECRP, Drugs

300
Q

Most common cause of pancreatitis in England

A

Gallstones

301
Q

Pancreatitis- signs and symptoms

A

Abdominal pain that radiates to the back, Nauseas/ vomiting, Low BP, high HR/ RR, low SATS, high temp

302
Q

Pancreatitis complications

A

Auto digestion, SIRS

303
Q

Pancreatitis complications- Auto digestion

A

Haemorrhage, pseudoaneurysm, portal thrombosis, necrosis, infected necrosis, pseudocyst

304
Q

Pancreatitis complications- SIRS*****

A

ARDS,

305
Q

Pancreatitis- severity score

A

Modified Early Warning Score (MEWS), good history, response to resuscitation

306
Q

Modified Early Warning Score (MEWS)

A

HR, BP, RR, core body temp, mental status and urine output

307
Q

Pancreatitis treatment

A

Supportive (fluids, nutrition, antibiotics, critical care), ECRP (to remove stones from bile duct), Cyst drainage, treat pancreatic failure for both exocrine (replace enzymes) and endocrine (diabetic) function

308
Q

Chronic pancreatitis

A

Flares of pancreatitis with or without trigger, pain, malnutrition, pancreatic duct strictures, may need drainage procedure or total pancreatectomy

309
Q

Chronic idiopathic inflammatory bowel disease (CIIBD)

A

Crohn’s disease, Ulcerative colitis

310
Q

Crohn’s disease

A

Transmural, non continuous inflammation that can occur anywhere in the GI tract

311
Q

Characteristic Crohn’s disease appearance

A

Scarring causes ‘cobblestone’ appearance

312
Q

Main complications of Crohn’s disease

A

Mainly affects bowel, malabsorption, obstruction, perforation, fistula formation, neoplasia

313
Q

Ulcerative colitis

A

Only affects mucosa, starts at the rectum and is continuous inflammation, working up the bowel

314
Q

Ulcerative colitis complications

A

Affects many different parts of the body, Colon, joints, eyes, skin, liver

315
Q

CIIBD- aetiology

A

Currently unknown

316
Q

Function of Peritoneum- In health

A

Visceral lubrication
Fluid & particulate absorption

317
Q

Function of Peritoneum- In disease

A

Pain perception.
Inflammatory and immune responses
Fibrinolytic activity

318
Q

Which is more sensitive to pain (from pressure, temp and laceration) visceral or parietal peritoneum?

A

Parietal peritoneum

319
Q

Peritonitis

A

Inflammation of Peritoneum

320
Q

Peritonitis : Classification- onset

A

Acute : Sudden Onset. Eg Bacterial
Chronic : Gradual Onset . Eg TB

321
Q

Peritonitis : Classification- Source of origin

A

Primary : No documented Source
Secondary : Bowel Perforation, Appendicitis

322
Q

Peritonitis : Aetiology

A

Bacterial, gastrointestinal and non-gastrointestinal
Chemical, e.g. bile, barium
Traumatic, e.g. operative handling
Ischaemia, e.g. strangulated bowel, vascular occlusion
Miscellaneous, e.g. familial Mediterranean fever

323
Q

Paths to Peritoneal Infection

A

Gastrointestinal perforation
Transmural translocation (no perforation)
Exogenous contamination
Female genital tract infection, e.g. pelvic inflammatory disease
Haematogenous spread (rare), e.g. septicaemia

324
Q

Paths to Peritoneal Infection- Transmural translocation

A

Pancreatitis, ischaemic bowel, primary bacterial peritonitis

325
Q

Paths to Peritoneal Infection- Gastrointestinal perforation

A

Perforated ulcer, appendix, diverticulum

326
Q

Paths to Peritoneal Infection- Exogenous contamination

A

drains, open surgery, trauma, peritoneal dialysis

327
Q

Clinical feat. of localised peritonitis

A

Pain
Nausea and vomiting
Fever
Tachycardia
Localised guarding
Rebound tenderness
Shoulder tip pain ( subphrenic)
Tender rectal and / or vaginal examination (pelvic peritonitis).

328
Q

Diffuse (generalised) peritonitis- Early

A

Abdominal pain (worse by moving or breathing)
Tenderness
Generalised guarding
Infrequent bowel sounds (paralytic ileus)
Fever
Tachycardia

329
Q

Diffuse (generalised) peritonitis- Late

A

Generalised rigidity
Distension
Absent bowel sounds
Circulatory failure
Thready irregular pulse
(Hippocratic face)
Loss of consciousness

330
Q

Peritonitis- Investigations

A

Urine dipstix for urinary tract infection.
ECG if diagnostic doubt (as to cause of abdominal pain) or cardiac history.
Bloods I U&Es I Full blood count (WCC)
Serum amylase (acute pancreatitis/ others like perf duodenal ulcer)

331
Q

Medical management of peritonitis

A

Correction of Fluid Loss & Circulating Volume
Antibiotics
Urinary Catheterisation I Gastric Decompression
Analgesics

332
Q

Surgical treatment of peritonitis

A

Remove or divert cause:
Repair of perforated viscus – peptic ulcer
Excision of perforated organ
With or without drainage
With or without restoring continuity
Peritoneal lavage

333
Q

Ascites

A

Detectable collection of Fluid in the peritoneal cavity
Chronic accumulation of Fluid within the peritoneal cavity

334
Q

Ascites- Classification

A

Stage 1 detectable only after careful examination / Ultrasound scan (Mild)
Stage 2 easily detectable but of relatively small volume.
Stage 3 obvious, not tense ascites. (moderate)
Stage 4 tense ascites. (Large)

335
Q

Refractory ascites

A

not mobilised
or early recurrence (after therapeutic paracentesis) <4 weeks
Cannot be prevented by medical therapy

336
Q

Diuretic resistant ascites

A

refractory to dietary sodium restriction and intensive diuretic treatment

337
Q

Diuretic intractable ascites

A

ascites that is refractory to therapy due to the development of diuretic induced complications that preclude the use of an effective diuretic dosage

338
Q

Ascites - Causes

A

Cirrhosis- 75%, main cause
Malignancy- 10%
Heart failure, TB, pancreatitis

339
Q

Ascites malignancy causes

A

gynecologic neoplasms gastrointestinal malignancies
breast cancer

340
Q

Ascites - Portal Hypertension
- Pathophysiology

A

A state of sodium water imbalance
Interplay of various neurohormonal agents – renin, aldosterone, sympathetic nervous system, nitric oxide

341
Q

Ascites -Non Portal hypertension- Pathophysiology

A

Malignancy
Cardiac Failure
Nephrotic syndrome

342
Q

Ascitis in Liver Cirrhosis - Pathophysiology

A

Portal Hypertension
Shunting of Blood into the systemic Circulation
Splanchnic Vasodilation (release of vasodilators NO)
Systemic Blood Pressure falls due to vasodilation
Renal Hypoperfusion
Activation of RAAS
Increased Na & H20 Retention by kidney
Increased Plasma Hydrostatic Pressure
Increased Transudation of fluid in Peritoneal Cavity
Ascites

343
Q

Exudative Ascites

A

Occlusion / obstruction of lymphatic /venous drainage
Ascites Protein Concentration above 25 gm/l

344
Q

Transudative Ascites

A

passage of fluid through a membrane – osmotic pressure, hydrostatic pressure
Protein concentration below 25 gm/l

345
Q

Ascites- Exudate causes

A

Congestive cardiac failure
Constrictive pericarditis
Nephrotic syndrome
Myxoedma
Bud Chiari Syndrome – Hepatic venous thrombosis
Chylous ascites

346
Q

Ascites- Transudate causes

A

Cirrhosis
Hypoproteinemic states
-Protein losing enteropathy
-Malnutrition
-Tuberculosis ( minority)
-Malignancy ( minority)

347
Q

Ascites RF in history

A

Relating to liver disease- long term heavy alcohol consumption, infection (chronic viral hep, IV drug use, travel)
-Non-alcoholic steatohepatitis (Cirrhosis, DM type 2
Obesity, Hypercholesterolemia)
GI/ ovarian cancer
Cardiac
Renal- nephrotic syndrome
Malnutrition- selective protein deficiency

348
Q

Ascites- Clinical Presentation - Symptoms

A

Abdominal distension
Clothes getting tighter
? Gaining wait
Nausea, Loss of appetite
Constipation
Cachexia- wasting ? weight loss
Pain / Discomfort
Present – malignant
Absent – non malignant
Associated symptoms of underlying cause

349
Q

Ascites- Clinical Presentation - Signs

A

Abdominal distension
Fluid thrill
Jaundice and other stigmata of liver disease (If liver causse of disease)

350
Q

Ascites- diagnosis- analysis of ascitic fluid

A

Naked eye assessment
Chemistry
-Proteins
-Amylase
Microscopy
-Cytology
-Organisms
Culture

351
Q

Ascites- diagnosis- Naked eye assessment of ascitic fluid

A

Most ascitic fluid is transparent and tinged yellow
Pink/ blood tinged fluid implies trauma or malignancy
Cloudy fluid with a purulent consistency indicates infection

352
Q

Ascites- diagnosis- radiology

A

X-Ray ( 500ml)
Ultra sound scan ( at least 20ml)
CT abdomen (< v small amt)

353
Q

Ascites- diagnosis- Serum Ascites Albumin Gradient [SAAG]

A

Serum albumin - ascites albumin
Value 1.1 g/dl important cut off ( 97% accuracy)
>1.1 g/dl – Portal hypertension
<1.1 g/dl – non portal hypertensive cause

354
Q

Ascites treatment

A

*Treatment of underlying cause
*Portal hypertension- salt and fluid restrictions, diuretics, albumen/ colloid replacement
*Paracentesis
*Shunts
-Portosystemic shunts (liver cirrhosis)
-Peritoneovenous shunt- for patients with medically intractable ascites

355
Q

Ascites treatment- portal hypertension

A

Salt and Fluid restriction
Diuretics
Albumen / colloid replacement

356
Q

Paracentesis

A

procedure performed in patients with ascites, during which a needle is inserted into the peritoneal cavity to obtain ascitic fluid

357
Q

Crohn’s disease treatment- general

A

No curative treatment
Aims to induce/maintain clinical remission

358
Q

Crohn’s disease treatment- Induce remisson

A

Glucocorticosteroids- 1st line
Early Anti-TNF agents- for patients with poor prognosis
Management of extra-intestinal symptoms
Consider antibiotics

359
Q

Crohn’s disease treatment- Maintain remission

A

Azathioprine, mercaptopurine + methotrexate- conventional maintenance therapies
Anti- TNF agents + novel biological therapies

360
Q

Crohn’s disease treatment- surgical management

A

Indication for surgery- failure of medical therapy, complications, presence of perianal sepsis
Strictureplasty- to widen strictures
Subtotal Colectomy + Ileorectal anastomosis- if CD involves all of Colon and minimally rectum
Panproctocolectomy with an end ileostomy- if CD involves all of colon and rectum

361
Q

Crohn’s disease investigations

A

Blood tests (FBC, iron studies+ serum folate/B12, CRP and ESR)
Stool tests (Stool cultures including C. difficile toxin assay, faecal calprotectin- raised in active intestinal inflammation
Imaging (MR enterography > CT enterography)
Colonoscopy with biopsies (2 from 5 different locations)
Upper GI endoscopy for patients with relevant upper GI symptoms

362
Q

Crohn’s disease investigations- blood tests

A

FBC- Anaemia, leucocytosis, may be thrombocytosis: all signs of inflammation
Iron studies- may be normal, or may demonstrate changes consistent with iron deficiency due to malabsorption or GI bleeding
Raised C-reactive protein (CRP) + erythrocyte sedimentation rate (ESR)- Inflammatory markers

363
Q

Crohn’s disease investigations- colonoscopy

A

Aphthous ulcers, hyperaemia, oedema, skip lesions
Characteristic cobblestone appearance

364
Q

Ulcerative colitis investigations

A

Blood tests (FBC, ESR + CRP, comprehensive metabolic panel including LFTs)
Stool tests (Stool cultures including C. difficile toxin assay, faecal calprotectin- raised in active intestinal inflammation)
Endoscopy with mucosal biopsy is gold standard- flexible sigmoidoscopy/ colonoscopy
Abdominal X-ray- patients in acute severe UC attacks to exclude colonic dilation

365
Q

Ulcerative colitis investigations- blood tests

A

FBC- may show leukocytosis, thrombocytosis, and anaemia
Raised ESR + CRP- inflammatory markers
Comprehensive metabolic panel- should be checked every 6 to 12 months for surveillance of primary sclerosing cholangitis

366
Q

Ulcerative colitis investigations- flexible sigmoidoscopy/ colonoscopy

A

rectal involvement, continuous uniform involvement, loss of vascular marking, diffuse erythema, mucosal granularity, fistulas (rarely seen), normal terminal ileum (or mild ‘backwash’ ileitis in pancolitis)

367
Q

Ulcerative colitis treatment- medical management

A

Induce/ maintain remission
Aminosalicylate are mainstay treatment- effective at maintaining remission and inducing remission for mild to moderate active disease

368
Q

Ulcerative colitis treatment- refractory/ severe colitis

A

Investigated to confirm active colitis and exclude infection
Biological therapy with anti- TNF agent/ anti-integrin agent
Corticosteroids- initially oral prednisolone, if ineffective hospitalization with IV hydrocortisone and supportive treatment
If IV steroids ineffective after 3 days, either surgery or salvage medical therapy

369
Q

Ulcerative colitis treatment- surgery

A

Curative, but reduces QoL
Acute disease- Subtotal colectomy with end ileostomy, preservation of rectum is operative choice
More surgical options available at later date; proctectomy with a permeant ileostomy or ileo-anal pouch (1/3 of patients experience pouchitis)

370
Q

Functional Gastrointestinal Disorders (FGIDS)

A

Chronic GI symptoms in the absence of organic disease to explain the symptoms
Also termed “disorders of gut-brain interaction”
ie IBS, functional dyspepsia

371
Q

Disorders of Gut-Brain Interaction

A

A group of disorders, classified by GI symptoms, related to any combination of: visceral hypersensitivity, motility disturbances, altered CNS processing, gut microbiota, mucosal and immune function

372
Q

Irritable Bowel Syndrome (IBS)

A

Affects 10% of pop
Chronic frequent abdominal pain, Altered bowel habit, Bloating commonly associated

373
Q

Dyspepsia

A

affects 10% of the population
Functional dyspepsia (~80%)
Organic dyspepsia (~20%)

374
Q

Alarm features or Red Flags for GI disease

A
  • Age >45 years
  • Short history of symptoms
  • Documented unintentional weight loss
  • Nocturnal symptoms
  • Family history of GI cancer/IBD
  • GI Bleeding
  • Palpable abdominal mass or lymphadenopathy
  • Evidence of iron deficiency anaemia on blood testing
  • Evidence of inflammation on blood/stool testing
375
Q

Faecal Calprotectin

A

Marker of GI inflammation
Found in UC and CD, not in IBS

376
Q

Wernicke’s encephalopathy

A

Thiamine (vitamin B1) deficiency with classic triad of confusion, ataxia and ophthalmoplegia (nystagmus, lateral rectus or conjugate gaze palsies)

377
Q

Wernicke’s encephalopathy- causes

A

Chronic alcoholism, eating disorders, malnutrition, prolonged vomiting

378
Q

Wernicke’s encephalopathy- management

A

Diagnosis is primarily clinical
Urgent thiamine replacement via IV/IM then oral supplement until no longer at risk

379
Q

Gilbert’s syndrome

A

Common cause of unconjugated hyperbilirubinemia due to decrease UGT-1 activity (enzyme that conjugates bilirubin)

380
Q

Gilbert’s syndrome- diagnosis

A

Mild increased bilirubin, normal FBC and reticulocytes (normal haemolysis)

381
Q

Gilbert’s syndrome- presenation

A

May go unnoticed for years and usually presents in adolescence with intermittent jaundice occurring during illness, exercise or fasting

382
Q

Pancreatic cancer

A

Most common presentation is at 65-75 years of age with painless obstructive jaundice and weight loss. Generally presents late with advanced disease.

383
Q

Pancreatic cancer- pathology

A

Mostly ductal adenocarcinoma which metastasize early and present late
Ampullary or islet cell
tumours are rarer but better prognosis

384
Q

Pancreatic cancer- RFs

A

Smoking, alcohol, carcinogens, DM, chronic pancreatitis, high waist circumference, hight fat/red meat diet

385
Q

Pancreatic cancer- signs

A

Jaundice + palpable gallbladder, epigastric mass, hepato/ splenomegaly, lymphadenopathy, ascites, weight loss + anorexia

386
Q

Pancreatic cancer- Investigations

A

pancreatic protocol CT
abdominal ultrasound
LFTs (show degree of obstructive jaundice)

387
Q

Pancreatic cancer- Appearance on abdominal imaging

A

Pancreatic mass +/- dilated biliary tree +/- hepatic mets

388
Q

Pancreatic cancer- Management

A

Based on extent of disease, given most present late, a lot of treatment is palliative (ie surgery to relive symptoms, chemo to delay disease progression)

389
Q

Pancreatic cancer- prognosis

A

Mean survival <6 months
5 years survival is 3%
Prognosis better if clear margins during surgery, use of whipple procedure or if tumour is ampullary or islet cell

Phase 2a Lecture Notes (14 decks)

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