Issues with GIT

Question 1

Helicobacter pylori infection

Answer 1

Oral-oral or faecal-oral transmission
Chronic gastritis H. pylori becomes anchored - if Inflammation becomes persistent, peptic ulcer disease may result

Question 2

Peptic ulcer disease

Answer 2

Disruption of the balance between the secretion of gastric acid and the defence mechanisms located in the gastroduodenal

Question 3

Gastritis

Answer 3

May be acute or chronic,
Erosive (gut reaction) non-erosive (infective or fungal). Range of causes

Reduction in prostaglandin synthesis from use of painkillers is a key mechanism whereby protective mechanisms are reduced and so the stomach lining is more exposed to acid

Question 4

GORD – Gastro-oesophageal Reflux Disease

Answer 4

Poor mobility in the oesophagus, dysfunctional opening of oesophageal sphincter and delayed emptying causing intragastric pressure

Question 5

Hiatus Hernia

Answer 5

Reduced lower oesophageal sphincter pressure & relaxation times. Reduced oesophageal acid clearance, longer transient time

Muscle weakening and loss of elasticity

Question 6

Oesophagitis

Answer 6

Persistent acid exposure in reflux

Different types:
Reflux: infectious e.g. candida, herpes simplex; systemic-associated: e.g. inflammatory bowel disease, sarcoidosis; pharmacologic associated: e.g. antibiotics, NSAIDs, radiation. Risk factors differ by type
GORD risk factors apply for reflux

Question 7

Barrett’s Oesophagus

Answer 7

Secretion of bicarbonate

Hiatus hernia, reduced lower oesophageal sphincter pressure, delayed oesophageal clearance and gastro-oesophageal reflux

Often asymptomatic in itself, the usual symptoms associated are those of GORD heartburn, difficulty swallowing, regurgitation

Question 8

Constipation

Answer 8

Considerations are obstruction within the colon, impairment of motility and outlet obstruction (for example severe haemorrhoids). Can also be linked to liver function

Comfortable to pass – no pain, straining, uncomfortable looseness etc. dietary, systemic disease (e.g. hypothyroidism, Parkinsons, MS), neurological, certain medications, obstruction

Question 9

Diverticulitis

Answer 9

Single muscle layer in large intestine presents more vulnerability to herniation than the double muscle layer of the small intestine. Diverticula - small pouches in the large bowel wall. Pouches formed when inner layers of large bowel push through weak areas in the more superficial muscle layers. Most common in descending/sigmoid colon

Question 10

IBD Overview

Answer 10

Altered GI motility Hypersensitivity to pain and bowel movement, Microscopic inflammation Psychological disorder SIBO

Intestinal permeability, dietary intolerance, alterations in gut microbiome (and previous severe GIT infection), dysfunctional contractility and innervation, stress

Question 11

SIBO –Small intestinal bowel overgrowth

Answer 11

A slowing of flow and stagnation in the small intestine allowing bacteria to flourish (normally an area with lower bacterial populations)

Question 12

Coeliac

Answer 12

Pathophysiology
Exposure to gluten derived peptide GLIADIN: found in wheat, barley and rye; Human leukocyte antigen (HLA) presents gliadin to helper T cells; Helper T cells initiate inflammatory response; Autoantibodies develop within the immune response ; Lymphocyte infiltration and destruction of the intestinal lining.

Question 13

Hepatitis

Answer 13

Dependent on type
Immunological response to infection leads to Inflammation, leading to fibrosis (variable in Hep C) and Hepatocyte damage/necrosis

Question 14

Cirrhosis

Answer 14

Damage to liver tissue causing repeated fibrosis, which changes the normal structure within the liver to abnormal nodule. Irreversible process of scarring –inflammatory cytokines and elevated leukocytes are indicators of severity; fibrosis consists of excess deposition of collagen and other matrix substances in spaces between hepatocytes

Question 15

Acute pancreatitis

Answer 15

Inflammation of the pancreas caused by two key factors: alcohol and biliary stone impacting in the sphincter of Oddi (between pancreas and duodenum
High triglycerides and trauma to the abdomen are also causative
Less common factors drugs, infection, hypercalcaemia, hereditary, developmental abnormality

Question 16

Chronic pancreatitis

Answer 16

Fibrosis is the key response to the aetiological insult in chronic pancreatitis:

May be a result of blockage from biliary stone or more rarely, tumour-Fibrosis, necrosis and ischaemia may also contribute
May also occur in connection with autoimmune disease

Question 17

Gallstones - Cholelithiasis

Answer 17

May be either cholesterol or pigment ‘stone’. May form along biliary tract, most commonly within gallbladder

Key risk factors for cholesterol stone: ageing, female sex, obesity, pregnancy, metabolic syndrome, high fat/cholesterol diet, gallbladder stasis
Key risk factors for pigment stone: blood conditions causing high haem turnover e.g. sickle cell anaemia, leukaemia

Question 18

Acute cholecystitis

Answer 18

Calculous –obstruction of cystic duct, bile retention, reduced blood flow/lymph drainage, tissue ischaemia/necrosis-Acalculous –bile retention causing inflammation

Question 19

Microbiome

Answer 19

Diarrhoea
Constipation
Bloating
Halitosis (bad breath)
Nausea
A generally ‘upset stomach’
Joint pain and fatigue were also considered