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Phase 2a > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is GORD?

A

Reflux of gastric acid, bile and duodenal contents back into the oesophagus

Lower oesophageal sphincter relaxes independently of a swallow, allowing gastric acid to flow back into oesophagus

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2
Q

Risk factors of GORD?

A

Male
Increased abdo pressure e.g. pregnancy
Smoking
Hitatus hernia

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3
Q

Clinical features of GORD?

A

Heartburn

Acidic taste in the mouth, often relieved by antacids

No investigations usually needed - diagnosis on clinical findings

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4
Q

Management of GORD?

A

Antacids e.g gaviscon

PPI e.g. lanzoprazole

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5
Q

Complications of GORD?

A

Peptic stricture

Barrets oesophagus = squamous to columnar

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6
Q

What are peptic ulcers? What types are there?

A

A break in epithelial cells which penetrate two to the mucosa, there are 2 types

Duodenal: worse at night (more common)
Gastric: worse on eating (lesser curve)

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7
Q

Causes of peptic ulcers?

A

Helicobacter pylori

NSAID use

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8
Q

If helicobacter causes peptic ulcer, Dx and Tx?

A

Diagnosis: urea breath test, serology, stool antigen test

Treatment: PPi and 2 antibiotics - clarithromycin and metronidazole

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9
Q

If NSAID use causes peptic ulcer, pathophysiology, Dx and Tx?

A

Pathophysiology: NSAIDs inhibit cox1 which inhibits the production of prostaglandins needed for mucous production

Dx: endoscopy

Tx: Stop NSAID, treat with PPi and use PPi prophylaxis if NSAID use again 6 months after

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10
Q

Describe coeliac disease?

A

Autoimmune disease characterised by abnormal jejunal mucosa, that improves when gluten is withdrawn from diet and relapses when it is reintroduced

SUSPECT IN: diarrhoea, weight loss and anaemia

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11
Q

Describe the pathophysiology of coeliac disease?

A
  1. Gliadin binds to secretory IgA in the mucosal membrane
  2. The gliadin IgA is transcytosed into the lamina propria
  3. Gliadin binds to tTG and is deaminated
  4. Deaminated gliadin is taken up by macrophages and expressed on MHC2
  5. T helper cells release inflammatory cytokines and stimulate B cells
  6. This causes gut damage
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12
Q

Diagnosis of coeliac disease?

A

IgA-tTG blood test

Duodenal biospy

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13
Q

Symptoms of coeliac?

A

Bloating
Failure to thrive
Diarrhoea
Dermatitis Herpetiformis

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14
Q

Management of coeliac?

A

Lifelong gluten free diet and correction of any vitamin deficiencies

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15
Q

Complications of coeliac?

A

There is an increased risk of malignancy, particularly intestinal T cell lymphoma, smlall bowel and oesophageal cancer

Incidence is reduced with GF diet

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16
Q

What would cause a suspicion of malabsorption?

A

Weight loss + steatorrhoea + anaemia = malabsorption

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17
Q

Causes of malabsorption?

A 
Poor intake 
Steatorrhoea
Reduced surface area 
Lack of digestive enzymes 
Defective epithelial transport 
Lymphatic obstruction
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18
Q

Symptoms of malasorption?

A 
Diarrhoea 
Weight loss 
Lethargy 
Steatorrhoea 
Bloating
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19
Q

Signs of malabsorption?

A 
Anaemia 
Bleeding disorders 
Oedema 
Metabolic bone disease 
Neurological features such as neuropathy
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20
Q

Tests for malabsorption?

A

FBC - low calcium, low ferritin, low B12 and folate, high INR, lipids and coeliac tests

Stool microscopy

Breath hydrogen test for bacteria

Endoscopy and small bowel biospy

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21
Q

What is Crohns disease?

A

type of IBD

Transmural granulomatous inflammation affecting any part of the gut

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22
Q

What would you see macroscopically and microscopically with Crohns?

A

MACROSCOPIC: skip lesions, cobblestone appearance, thickened and narrowed

MICROSCOPICA: transmural granulomas (non-caseating) goblet cells present

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23
Q

Symptoms of Crohns?

A

Diarrhoea
Abdominal pain in RLQ
Weight loss
Lethargy

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24
Q

Signs of Crohns?

A

Mouth ulcers

Tenderness in RIF

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25
Q

Risk factors for Crohn’s?

A

Smoking
Female
Mutation on NOD2 gene of chromosome 15
Chronic stress

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26
Q

Investigations of Crohn’s?

A

Diagnostic test - colonoscopy
Stool sample to rule out infectious causes
FBC - raised ESR/CRP often low Hb due to anaemia

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27
Q

Management of Crohns?

A

Oral corticosteroids
IV hydrocortisone in severe flare ups
Add antiTNF antibodies e.fg. infliximab if not improvement
Consider adding Azathioprine or methotrexate to remain in remission if frequent exacerbations

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28
Q

What is ulcerative colitis?

A

A type of IBD

Inflammatory condition of the colon mucosa

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29
Q

What would you see macroscopically and microscopically with ulcerative colitis?

A

MACROSCOPIC: continuous inflammation, no skip lesions, ulcers, pseudopolyps

MICROSCOPIC: mucosal inflammation, no granulomata, depleted goblet cells

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30
Q

Symptoms of ulcerative colitis?

A

Pain in the LOWER LEFT quadrant

Diarrhoea with blood and mucous

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31
Q

Signs of ulcerative colitis?

A

Fever, in acute UC
Clubbing
Erythema nodusum

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32
Q

Investigations of ulcerative colitis?

A

FBC - raised ESR and CRP
Testing for pANCA
Stool sample to rule out infectious cauess q

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33
Q

Management of ulcerative colitis?

A

Sulfasalazine, add oral prednisolone if no response

Colectomy indicated in patients with severe UC not responding to treatment

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34
Q

What is backwash ileitus?

A

In ulcerative colitis when proximal to the ileocecal valve is affected

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35
Q

What is irritable bowel syndrome?

A

A group of abdominal symptoms which no organic cause can be found

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36
Q

Risk factors for IBS?

A

Stress

Female gender

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37
Q

Symptoms of IBS?

A

Abdominal pain relieved by defacating
Bloating
Alternating bowel habits

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38
Q

Management of IBS?

A

Pain/bloating - buscopan
Constipation - laxative e.g. senna
Diarrhoea - antimotility e.g. loperamide

39
Q

Presentation of appendicitis?

A

ACUTE PAIN: 2/3 from umbilicus to RIF, McBurneys point

\+ Nausea 
\+ Vomiting 
\+ Fever 
\+ Pain on walking 
\+ Loss of appetite 
\+ Pyrexia
40
Q

Diagnosis of appendicitis?

A

Classic presentation + genetic inflammatory and infection markers

USS and CT

41
Q

Treatment for appendicitis?

A

Appendicectomy or IV antibiotics if cant undergo surgery

42
Q

What would you listen for in intestinal obstruction?

A

Tinkling or absent bowel sounds

43
Q

What can cause intestinal obstruction in the lumen of the bowel?

A
  • Tumours
  • Diaphragm disease: NSAIDS cause repeated ulceration and then fibrosis
  • Gallstone ileus: cholecystic enteric fistula
44
Q

What can cause intestinal obstruction in the wall of the bowel?

A
  • Tumours
  • Crohns: inflammation, fibrosis, contraction
  • Diverticulitis: outpouchings in the sigmoid
  • Hirschprungs: ganglion cells
45
Q

What can cause intestinal obstruction from the outside of the bowel?

A
  • Tumours: disseminated malignancy of the peritoneum
  • Adhesions: fibrosis after surgery
  • Volvulus: sigmoid colon has a floppy mesentery
46
Q

What is a hernia?

A

A protrusion of an organ or tissue out of the body cavity that it normally lies

47
Q

Causes of a hernia?

A

Muscle weakness = age, trauma

Body strain = constipation, heavy lifting, pregnancy, chronic cough

48
Q

Describe an inguinal hernia?

A

Protrusion of abdominal cavity through the inguinal canal, can be direct or indirect

49
Q

Describe a direct inguinal hernia?

A

Protrudes directly into the inguinal canal, MEDIAL to the inferior epigastric vessels

Behind superficial inguinal ring

50
Q

Describe an indirect inguinal hernia?

A

Protrudes through the inguinal ring LATERAL to the inferior epigastric vessels

Through deep inguinal ring

51
Q

Describe a hitatus hernia?

A

Part of the stomach herniates through the oesophageal hiatus of the diaphragm, two types: sliding and para-oesophageal

52
Q

Describe a sliding hiatus hernia?

A

Oesophageal-gastric junction slides through the hiatus and lies above the diaphragm

53
Q

Describe a paraoesophagheal hiatus hernia?

A

Uncommon - gastric fundus rolls up through hiatus alongside the oesophagus therefore gastro-oesophageal junction remains below the diaphragm

54
Q

What is ascites?

A

This is the presence of fluid in the peritoneal cavity - cirrhosis is the most common cause

55
Q

Aetiology of ascites?

A

In cirrhosis, peripheral arterial vasodilation, mediated by NO leads to a reduction in effective blood volume

RAAS activated promoting salt and water retention

Formation of oedema encouraged by hypalbuminaemia, mainly localised in peritoneum due to portal hypertension

56
Q

Causes of ascites?

A

Chronic liver disease +/- portal vein thrombosis, hepatoma, TB

Neoplasia

Hepatoma

57
Q

Clinical features of ascites?

A

Fullness in flanks with shifting dullness

Tense ascites is uncomfortable and produces respiratory distress

A pleural effusion and peripheral oedema may also be present

58
Q

Investigation of ascites?

A

A diagnostic aspiration of 10-20ml of ascitic fluid

+ albumin levels: >11g/L transduate <11g/L exudate
+ Neutrophil count of >250cells/mm3 indicates bacterial peritonitis
+ Gram stain and culture for bacteria and acid fast bacilli
+ Cytology for malignant cells

59
Q

Management of ascites?

A

Fluid and salt restriction

Diuretics: spironolactone +/- furosemide

Large volume paracentesis + albumin

Trans-jugular portosystemic shunt: TJPS

60
Q

Risk factors for infective diarrhoea?

A

Foreign travel
Poor hygiene
Overcrowding
New or different foods

61
Q

Causes of infective diarrhoea?

A

Usually viral: rotavirus, norovirus, adenovirus

Bacterial: campylobacter jejeni, e.coli, salmonella, shigella

Parasitic: Giardia lamblia, cryptosporidium

Abx associated (C.diff): clindamycin, ciprofloxacin, coamoxiclav, cephalosporins

62
Q

Investigations for infective diarrhoea?

A

Stool culture

Consider sigmoidoscopy and bloods

63
Q

Treatment for infective diarrhoea?

A

Rehydration
Antibiotics s
Antimotility
Maybe antiemetics

64
Q

What is peritonitis?

A

Inflammation of the peritoneum due to entry of blood, air, bacteria or GI contents

65
Q

Causes of peritonitis?

A

AEIOUP

Appendicitis 
Ectopic pregnancy 
Infection with TB 
Obstruction 
Peritoneal dialysis
66
Q

Symptoms of peritonitis?

A

Dull pain that becomes sharp
Pain that is worse on coughing or moving
Systemic symptoms of being generally unwell

67
Q

Investigations of peritonitis?

A

Clinical examination: rigid and guarding, laying still

AXR: dilated bowel, flat fluid level, gas under diaphragm

Bloods: FBC, U+E, LFT

Ascitic tap: high neutrophil count

68
Q

What is alpha 1 antitrypsin deficiency?

A

Accumulation of alpha-1 antitrypsin in the hepatocytes and lack of it in the serum causes a lack of protease inhibition in alveoli causing damage to alveoli and subsequent emphysema

COPD symptoms, liver transplant is curative

69
Q

What is wilsons?

A

Excess copper in the liver and CNS

kayser fletcher rings
Neurological signs as copper in brain and CNS

Mx: penicillamine to excrete copper, reduce copper intake - shellfish

70
Q

What is haemochromatosis?

A

Excess iron everywhere

Arthralgia from pseudogout
Serum ferritin is raised
Deferrioxamine to remove excess iron and reduce iron intake in the diet

Complications: restrictive cardiomyopathy due to iron deposition
Bronze diabetes

71
Q

Describe non alcoholic fatty liver disease?

A

Rf: metabolic syndrome, T2DM

Investigations: enhances liver fibrosis test

Mx: Lifestyle - loose weight

72
Q

How does alcoholic hepatitis progress?

A

alcoholic hepatitis > alcoholic steatosis > cirrhosis

73
Q

Describe the pathophysiology of alcoholic liver disease?

A

Reduced NAD+ >

Less oxidation of fat >

accumulation in the hepatocytes >

increased ROS damages the hepatocytes >

acetaldehyde damages the liver cell membranes

74
Q

Investigations for alcoholic liver disease?

A

GGT very raised
AST, ALT mildly raised

FBC = macrocytic anaemia

75
Q

Treatment for alcoholic liver disease?

A

Quit alcohol

Treat malnutrition from alcoholic - thiamine

76
Q

What are possible co-existing diseases due to alcoholism?

A
  • Acute/chronic pancreatitis
  • Mallory weiss tear
  • Alcohol withdrawal - delirium tremors
77
Q

Define jaundice?

A

Yellow discolouration of the sclerae and skin due to raised serum bilirubin

78
Q

Mechanism and causes of pre hepatic jaundice?

A

Increased breakdown of red blood cells leads to increased bilirubin

Haemolytic anaemia e.g. sickle cell and Gilbert’s syndrome

79
Q

Urine, stools and pruritus in pre hepatic jaundice?

A

Urine: normal
Stools: normal
Pruritus: no

80
Q

Liver test results in pre hepatic jaundice? UCB, CB. URB

A

UCB = normal/increased

CB = normal/increased

URB = normal/increased

81
Q

Mechanism and causes of intra hepatic jaundice?

A

Hepatocellular swelling in parnchymal liver disease or abnormalities at the cellular level of bile excretion

Viral hepatitis, drugs, alcohol, cirrhosis, autoimmune cholangitis, pregnancy

82
Q

Urine, stools and pruritus in intra hepatic jaundice?

A

Urine: Dark CB + URB
Stools: pale
Itching: maybe

83
Q

Liver test results in intra hepatic jaundice? UCB, CB, URB?

A

UCB: increased
CB: increased
URB: increased

84
Q

Mechanism and causes for post hepatic jaundice?

A

Extrahepatic cholestasis resulting in obstruction of bile flow at any point distal to the bile canaliculi

Common duct stones. carcinomas of duct/head of pancreas/ampulla, biliary stricture, sclerosing cholangitis

85
Q

Urine, stools and pruritus in post hepatic jaundice?

A

Urine: Dark CN
Stools: Pale
Pruritus: maybe

86
Q

Liver function test results in post hepatic jaundice? UCB + CB + URB

A

UCB: normal
CB: increased
URB: decreased

87
Q

What is cirrhosis?

A

Cirrhosis results from the necrosis of liver cells followed by fibrosis and nodule formation

The end result is impairment of liver function and gross distortion of the liver architecture leading to portal hypertension

88
Q

What is the most common cause of cirrhosis in the UK and worldwide?

A

UK: Alcohol
Worldwide: Hepatitis B and C

89
Q

Describe micronodular cirrhosis?

A

Uniform small nodules up to 3mm in diameter, often caused by ongoing alcohol

90
Q

Describe macronodular cirrhosis?

A

Nodules of variable size and normal acini may be seen within large nodules. This type is often seen following chronic viral hepatitis

91
Q

Clinical features of liver cirrhosis?

A

+ These are secondary to portal hypertension and liver cell failure

+ Cirrhosis with complications of encephalopathy, ascites or variceal haemorrhage and the damage is sufficient that it cannot function adequately = decompensated hepatic failure

+ without this complications = compensated

92
Q

Investigations in liver cirrhosis?

A

+ Liver biochemistry may be normal

+ FBC shows thrombocytopenia

+ Liver function: PTT and serum albumin

+ Low Na - severe disease secondary to either impaired free water clearance or excess diuretic

93
Q

Management of cirrhosis?

A

+ Cirrhosis is irreversible and frequently progresses - management is of complications seen in decompensated

+ correct underlying cause: venesection for haemochromatosis and alcohol abstinance for alcoholic cirrhosis

+ Hepatocellular carcinoma to identify tumours at an early stage

+ Transplantation for end stage cirrhosis

94
Q

What investigations would you carry out for jaundice?

A
  • Serum liver chemistry will confirm
  • Liver enzymes - very high ALT/AST suggests liver disease
  • PPT may be prolonged due to vitamin K malabsorption

Phase 2a (13 decks)

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