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Year 2 - Excess > GI > Flashcards

GI Flashcards

1
Q

Describe the blood supply of the stomach

A

Fundus - short gastric arteries
Lesser curvature - left and right gastric arteries
Greater curvature- left and right gastro-omental arteries

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2
Q

Describe the function of haem oxygenase

A

Converts haem into bilverdin

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3
Q

Describe the function of biliverdin reductase

A

Converts bilverdin to unconjugated bilirubin

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4
Q

Describe the function of the interstitial cells of Cajal and relate this to the basic electrical rhythm (BER)

A

Pacemaker function - mediate enteric neurotransmission
Lie in the myenteric plexus
The Basic Electrical Rhythm (BER) controls how often an area of the gut can contract
Variations in BER determine directionality
E.g. higher BER in proximal intestine than distal intestine to move intestinal contents distally

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5
Q

Describe the function of enterochromaffin-like cells (ECL cells), including receptors

A

ECL cells secrete histamine, which acts on the H2 receptor on parietal cells, stimulating the release of acid via the H+/K+ pump

Histamine is released during the gastric phase

Histamine also acts on D cells via the H3 receptor to inhibit somatostatin production, inhibiting negative feedback and increasing acid secretion

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6
Q

Describe the function of G cells, including receptors

A

G cells are found in the antrum of the stomach and produce gastrin, which stimulates acid secretion via stimulation of ECL cells (acting on CCK2 receptor)

Also have a smaller effect on parietal cells (CCK2 receptor), stimulating acid secretion directly

Acetylcholine (ACh) also acts on G cells to increase gastrin secretion

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7
Q

Describe the function of D cells, including receptors

A

D cells produce somatostatin, which acts to decrease acid secretion
by inhibiting ECL cells and parietal cells

ACh also inhibits somatostatin secretion by acting on D cells

Somatostatin is released in response to low pH during the intestinal phase

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8
Q

Describe the function of parietal cells

A

Parietal cells secrete intrinsic factor (necessary for the digestion of cobalamin (vitamin B12) in the terminal ileum)

Parietal cells secrete hydrochloric acid via the H+/K+ pump (uses ATP)

ACh acts on M3 receptors on parietal cells during the cephalic phase to increase acid secretion

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9
Q

Causes of Acid-Peptic Disease: excess acid

A

Zollinger-Ellison syndrome:
Rare gastrin-secreting tumour
Helicobacter pylori antral gastritis:
Inflammation of antrum leads to decreased somatostatin production by D cells (decreased inhibition of acid secretion)

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10
Q

Causes of Acid-Peptic Disease: weakened defence

A

H.pylori corpus / pan gastritis:
Gastric lining becomes inflamed and ability to secrete mucus is impaired
NSAID/aspirin use
Inhibition of COX-1 (needed to produce prostaglandins which regulate gastric mucus secretion)
Stress ulceration:
Critically ill patients in the ICU e.g. shock, sepsis, trauma

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11
Q

Explain how H. pylori infection can be detected

A

Blood test: serology for antibodies
Stool test: for Helicobacter antigen in faeces
Test of urease activity:
Urea Breath Test
Patient ingests drink containing urea enriched with C13/C14 (radioisotope)
Urease within stomach breaks down urea into ammonium bicarbonate (ammonia + carbon dioxide)
Concentration of enriched carbon in exhaled carbon dioxide is measured as patient exhales
Rapid Urease Test
Using endoscopic biopsy tissue sample
Urea within a gel containing a coloured pH indicator
Urea broken down into ammonia in the presence of H. pylori leading to a rise in pH and a colour change

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12
Q

State the first-line treatment for H. pylori infection

A

1 proton pump inhibitor (PPI)
Omeprazole
2 antibiotics
Amoxycillin
Metronidazole

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13
Q

Which hormone is responsible for the relaxation of the gallbladder and the contraction of the sphincter of the hepatopancreatic ampulla?

A

Vasoactive intestinal polypeptide (VIP)

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14
Q

Define prebiotics, probiotics and faecal microbiota transplantation

A

Prebiotics are carbohydrates which selectively stimulate the growth of healthy bacteria in the gut

Probiotics are live microorganisms which provide health benefits to the host
- Lactobacilli
- Bifidobacteria
- Streptococcus S.
They are used in the prevention and treatment of diarrhoea

Faecal microbiota transplantation
The transfer of healthy faecal bacteria from one individual to another
Used to treat recurrent or refractory C. diff diarrhoea
Given orally or rectally

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15
Q

Describe the clinical algorithm associated with increased alkaline phosphatase (ALP)

A

Is GGT raised too?
No: bone disease
Yes: liver disease, perform ultrasound, CT or both
After performing utlrasound or CT:
- Are the ducts dilated?
Yes: space-occupying lesion, strictures or stones (diagnosis uncertain)
Perform percutaneous cholangiography to diagnose sclerosing cholangitis, strictures or stones

No: measure anti-mitochondrial antibody
If positive AMA: primary biliary cirrhosis (autoimmune)
If negative AMA: perform percutaneous cholangiography for diagnosis of sclerosing cholangitis, strictures or stones

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16
Q

Describe the 3 main types of gallstones

A

Cholesterol
Solitary, oval and large (up to 3cm)

Bile pigment
Multiple, irregular, hard
Associated with elevated haemolysis e.g. sickle cell

Mixed
Most common, multiple, multifaceted
Laminated appearance with layers of cholesterol, bile pigments and calcium salts

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17
Q

Define propulsion, retropulsion and grinding

A

Propulsion
Pushing food against an almost closed pyloric sphincter to force smaller particles into the duodenum

Retropulsion
Large food particles are forced back to the body of the stomach

Grinding
Muscle contractions trap food in the antrum and churn food via segmentation

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18
Q

Outline possible mechanisms and causes of hepatic jaundice

A

Impaired uptake of unconjugated bilirubin
Impaired conjugation of bilirubin (Gilbert’s syndrome: reduced UDP glucuronosyltransferase activity)
Impaired transport of bile into bile canaliculi (primary biliary cirrhosis: autoimmune destruction of small bile ducts)
Cirrhosis (e.g. alcohol-induced)
Hepatotoxic drugs (e.g. paracetamol overdose)
Viral hepatitis

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19
Q

Outline the histological features of alcoholic hepatitis

A

Fatty liver

Sublethal hepatocyte injury

Ballooning: increased fluid, swelling; cytoplasm appears granular
Mallory bodies: cytoskeleton aggregates; abnormal cytoskeleton leads to cell collapse
Necrosis

Neutrophil polymorph inflammation

Fibrosis
- Initially perivenular and pericellular, but eventually fibrous septa & cirrhosis

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20
Q

Describe the mechanism of motility in the stomach and small intestine during the interprandial period

A

The function of motility is to cleanse the gut in preparation for the next meal
Motility is controlled by the MMC (migrating motor complex)
This involves a cyclic contraction sequence occurring every 90 minutes
This is regulated by motilin, a polypeptide hormone produced by M cells in the small intestine
Motilin stimulates the contraction of the gastric fundus and gastric emptying

There are 4 phases
I: prolonged period of quiescence
II: increased frequency of contractility
III: a few minutes of peak electrical and mechanical activity
IV: declining activity merging to the next phase I

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21
Q

Outline the mechanisms through which alcohol toxicity can cause steatosis

A

Alcohol toxicity can cause fatty liver disease (steatosis) by:

Increased peripheral fat mobilisation
Altering hepatocyte fat metabolism
Lipid synthesis promoted and catabolism reduced
Cholesterol esters and fatty acids accumulate
Reduced lipoprotein synthesis

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22
Q

Describe the pathogenesis of gallstones

A

Cholesterol supersaturation
Normally cholesterol is soluble in bile but levels can become high in certain conditions, leading to the formation of cholesterol stones
These conditions include obesity, pregnancy, use of the oral contraceptive pill and liver disease
Can also occur when bile acid levels are low e.g. after a small bowel resection or in active Crohn’s (ineffective enterohepatic circulation)
Biliary stasis
Prolonged periods of fasting, starvation or parenteral nutrition can result in biliary stasis
Increased bilirubin secretion
Conjugated bilirubin is usually soluble in bile, but when production is high, stones can appear
Usually seen in conditions associated with elevated haemolysis, such as sickle cell anaemia, haemolytic anaemia and malaria
Could also be due to a failure of conjugation of bilirubin

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23
Q

Outline the complications of gallstones specifically affecting the gallbladder

A

Biliary colic
Gallstone impacted in GB neck/Hartmann’s pouch
Causes pain, especially after meals due to GB contraction
Pain resolved by gallstone moving back into body of GB
Presents without fever, normal LFTs, no jaundice
Commonly causes vomiting
If recurrent, treated via cholecystectomy
Cholecystitis
Infection of the gallbladder
Presents with abdominal tenderness, nausea, vomiting, fever, positive Murphy’s sign
Can lead to abnormal LFTs and jaundice
Treated with antibiotics and analgesia but if recurrent/severe then cholecystectomy
Mucocoele
Blockage of GB leads to accumulation of mucus
Empyema
GB fills with pus after cholecystitis
Cancer

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24
Q

Describe hepatic alcohol metabolism

A

2 main metabolic pathways, both of which produce acetaldehyde
Acetaldehyde is converted to acetate then acetyl-CoA, which enters TCA cycle to produce fatty acids
Reduces the hepatocytes’ capacity to oxidise other molecules

Cytoplasmic alcohol dehydrogenase (ADH)
Main route, not inducible
Polymorphisms result in differences between ethnic groups
Microsomal ethanol oxidising system (MEOS)
Found in the smooth endoplasmic reticulum, uses cytochrome P450:2E1
Inducible by excess alcohol consumption
Increases GGT
Generates toxic metabolites (acetaldehyde, free radicals, reactive oxygen species)
Affects metabolism of other drugs e.g. paracetamol

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25
Q

List the risk factors for gallstones

A

5 F’s: fat, forty, female, fertile, fair
Age
Family history
Caucasian
Low fibre diet
Inflammatory bowel disease

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26
Q

Celiac disease is associated with what genetic polymorphisms?

A

HLA-DQ2/8

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27
Q

What are the actions of CCK?

A

↑ secretion of enzyme-rich fluid from pancreas, contraction of gallbladder and relaxation of sphincter of Oddi,
↓ gastric emptying, trophic effect on pancreatic acinar cells, induces satiety

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28
Q

What are the actions of gastrin?

A

↑ acid secretion by gastric parietal cells, pepsinogen and IF secretion,
↑ gastric motility,
stimulates parietal cell maturation

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29
Q

What are the actions of secretin?

A

↑ secretion of bicarbonate-rich fluid from pancreas and hepatic duct cells,
↓ gastric acid secretion, trophic effect on pancreatic acinar cells

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30
Q

What features would be identified in the biopsy of celiac disease?

A

villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

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31
Q

What cell secretes intrinsic factor and what is the function of it?

A

Gastric parietal cells produce intrinsic factor. This binds to vitamin B12 enabling it to be absorbed by the small intestine.

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32
Q

What structures are supplied by coeliac trunk?

A

Foregut - stomach, spleen, liver, esophagus, and also parts of the pancreas and duodenum

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33
Q

What structures are supplied by superior mesenteric arteries?

A

midgut – which spans from the major duodenal papilla (of the duodenum) to the proximal 2/3 of the transverse colon.

34
Q

What structures are supplied by the inferior mesenteric artery?

A

Hindgut - i.e. distal 1/3 transverse colon, descending colon and sigmoid colon

35
Q

What is the spinal level of coeliac trunk?

A

T12

36
Q

What is Gilbert’s syndrome?

A

Gilbert’s syndrome is a condition that causes hepatic jaundice due to a genetic defect in uridine diphosphate glucuronosyltransferase (UGT)

This genetic defect affects chromosome 2, specifically the locus coding for the UGT-1A1 protein

This condition tends to be exacerbated by stress, fasting and acute illness

Confirm diagnosis by measuring unconjugated bilirubin

Stool and urine will be normal as this condition is characterised by unconjugated hyperbilirubinaemia

37
Q

Describe the liver’s role in plasma protein and enzyme synthesis

A

Most circulating proteins are synthesised by the liver and are used as a synthetic measure of liver function

The liver synthesises albumin, the most abundant plasma protein, as well as other glycoproteins due to its role in glycation of proteins

Also synthesises other transport and binding proteins e.g. transferrin, apoferritin

38
Q

List the causes of liver cirrhosis

A

Causes of hepatitis
Alcohol
Viral
Autoimmune
Drugs
Metabolic disease
Biliary disease
Drugs or toxins
Cryptogenic
Alcohol or metabolic
Biliary disease
Idiopathic
Haemochromatosi

39
Q

List the complications of liver cirrhosis

A

Liver failure
Portal hypertension
Hepatocellular cancer

40
Q

Outline the consequences of liver failure

A

Reduced albumin and other transport proteins
Reduced intermediary metabolism
Impaired synthesis of urea and glycogen (higher risk of hypoglycaemia)
Coagulopathy
Failure in the synthesis of clotting factors
Immunodeficiency
Lack of production of complement
Jaundice
Altered xenobiotic metabolism (reduced first-pass effect)
Circulatory and endocrine disturbances

41
Q

Outline the consequences of portal hypertension

A

Cirrhosis increases resistance to blood flow through the liver
Increases pressure in portal circulation causing:

Portal-systemic shunts and varices
There is a junction where the portal and systemic circulation meet
If pressure is high, portal circulation blood can go to systemic circulation
Examples
Gastroesophageal junction
Left gastric vein and tributaries to azygos vein
Anterior abdominal wall
Superficial veins of abdominal wall and paraumbilical veins (caput medusae)

Anus
Superior, middle and inferior rectal veins

Varices (vein enlargement) may rupture leading to massive haematemesis and precipitate hepatic failure & encephalopathy

Ascites
Increased fluid in abdominal cavity
Splenomegaly
Backpressure is exerted on spleen through portal circulation
Spleen is distensible so can accumulate more blood and become distended
More vulnerable to trauma
Consumption of platelets

42
Q

Briefly describe the types of hepatic lobules

A

Classical lobules
1-2mm hexagonal lobules centred on the terminal hepatic venule
Portal lobules
Triangular area formed by 3 central veins
Liver acinus
Ovoid area of liver tissue centred on the sides of the classical lobule between 2 central veins

43
Q

Describe the functions of the 3 zones of the liver acinus

A

Zone 1 - periportal
Closest to afferent arteriole, higher oxygen concentrations

Functions

Gluconeogenesis
Cholesterol synthesis
Oxidative energy metabolism e.g. TCA cycle
Amino acid utilisation
Bile acid synthesis
Urea synthesis
Hepatocytes actively synthesise plasma proteins and glycogen
Zone 2 - intermediate

Zone 3 - perivenular
Closes to terminal hepatic venule, low oxygen concentration
Susceptible to hypoxia
Alcoholic liver disease usually starts here

Functions

Xenobiotic metabolism
Glycolysis
Lipogenesis
Ketogenesis
Glutamine synthesis

44
Q

Explain the liver’s role in detoxification

A

Non-volatile and hydrophobic substances are made more hydrophilic by reactions in the liver to promote excretion in the urine or bile

Phase 1 reactions
Suitable when a polar group is available
Involve hydrolysis, oxidation and reduction
Occur in smooth endoplasmic reticulum utilising cytochrome P450 enzymes
These enzymes add an oxygen group to drug side-chains to make a reactive site
Produce hydroxylated or carboxylated compounds
Molecules produced are generally more reactive
Sometimes toxic or pharmacologically active molecules are produced
Precursor to phase 2 reactions
Phase 2 reactions
Subsequent conjugation with glucuronic acid, methyl/acetyl radicals, glycine/taurine or sulphate.
Tends to increase water solubility and potential for active transport to promote excretion

45
Q

Explain the role of the liver in carbohydrate metabolism

A

Stores carbohydrates as glycogen, releasing them during glycogenolysis

Carries out gluconeogenesis (synthesis of glucose from other sources such as lactate or pyruvate)

Utilises glucose as an energy substrate for glycolysis, TCA cycle

Converts fructose and galactose into glucose phosphate

46
Q

Explain the role of the liver in lipid metabolism

A

The liver synthesises cholesterol, fatty acids, triglycerides, phospholipids and lipoproteins

The liver carries out mitochondrial beta-oxidation of short-chain fatty acids

47
Q

Explain the role of the liver in amino acid metabolism

A

The liver performs deamination, removing an amino group from amino acids to form ammonia, while the carbon backbone is regenerated into glucose, fatty acids or Krebs cycle intermediates

Cells remove ammonia by converting it into urea, which is excreted by the kidneys

The liver performs transamination, transferring an amino group from an amino acid to a ketoacid and vice versa, producing a new amino acid and a new ketoacid

48
Q

Describe the anatomy of the biliary tree

A

Bile produced by hepatocytes drains into bile canaliculi
Bile canaliculi consist of the walls of two hepatocytes joined by tight junctions

Bile canaliculi drain into ducts (junction between these is known as the Canal of Hering)

> Interlobular ducts
Septal ducts
Intrahepatic ducts
Left and right hepatic ducts
Left hepatic duct drains left functional lobe
Right hepatic duct drains right functional lobe
Caudate lobe drained by both

Left and right hepatic ducts merge to form the common hepatic duct

The common hepatic duct merges with the cystic duct (drains the gallbladder) to form the common bile duct

The common bile duct merges with the pancreatic duct to form the hepatopancreatic ampulla of Vater

Enters the descending part of the duodenum via the greater duodenal papilla (controlled by the sphincter of Oddi)

49
Q

Describe the pathophysiology of liver cirrhosis

A

End-stage liver disease; a diffuse process (affecting the whole liver) characterised by nodule formation (micro or macronodular) and fibrosis.

Colour change (green) may result due to increased bile retention by liver and impaired secretory function

Cirrhosis is the result of chronic inflammation lasting for years due to persistence of the injury-causing agent

Hepatocyte injury leads to progressive liver cell loss

Fibrous scarring occurs, as well as hepatocyte regeneration, but hepatocytes may form hyperplastic nodules

Architecture becomes abnormal, pressing on portal tract, biliary and vascular structures, leading to ischaemia

Ischaemia worsens liver damage

50
Q

List the factors or conditions which could affect the metabolic function of the liver

A

Congenital enzyme deficiency
Nutritional deficiency/excess of substrate
Toxic/chemical damage to organelles
Hypoxic/ischaemic insult
Secondary to metabolic effects of disease
Inherited disease

51
Q

Describe the pathophysiology of duodenal ulcers and how they may be differentiated from gastric ulcers

A

Caused by H. Pylori infection

H. pylori produces urease, which converts urea and water into ammonium bicarbonate (dissociates into ammonia and carbon dioxide)

Ammonia is alkaline and allows the bacterium to survive in conditions of low pH

It disturbs the negative feedback mechanisms involving D cells, as they sense high pH levels, they do not secrete somatostatin to reduce gastric acid secretion

G cells continue to produce gastrin to stimulate acid secretion

Highly acidic secretions reach the duodenum causing ulceration

Duodenal ulcers are improved by milk/meals while gastric ulcers are worsened after a meal

52
Q

Name the parenchymal liver cells

A

Hepatocytes
Kupffer cells
Endothelial cells
Perisinusoidal (fat-storing) cells
Liver-associated lymphocytes

53
Q

List the components of bile

A

Bile salts
Conjugated bilirubin
Water
Electrolytes
Mucin
Bicarbonate
Cholesterol
Phospholipids

54
Q

Describe the changes undergone by bilirubin during its passage through the bowel

A

Conjugated bilirubin enters the duodenum and is converted into unconjugated bilirubin by beta-glucuronidase

Unconjugated bilirubin is acted upon by intestinal anaerobes, forming urobilinogen

Urobilinogen is mostly reabsorbed and returns to the liver via the enterohepatic circulation

Some urobilinogen is filtered by the kidneys and excreted in the urine

Urobilinogen which reaches the colon is converted to stercobilin, which is excreted in the faeces, giving them a brown colour

55
Q

Describe the anatomy of the hepatic recesses and why they are clinically important

A

Hepatic recesses form an extension of the peritoneal cavity

They form a potential space containing a small amount of fluid to allow smooth movement of internal organs

Subphrenic recess
Between superior anterior portions of liver and diaphragm
Separated into right and left by falciform ligament
Hepatorenal recess
Between right kidney and right suprarenal gland
Continuous with right subphrenic space anteriorly
Clinical importance:
Common site for abscesses
Pus can cause peritonitis

56
Q

Describe the complications of peptic ulcer disease

A

Bleeding
Due to drugs e.g. iron medication, gold, caffeine, cocaine
Can result in vomiting of blood (haematemesis) or passage of altered black blood to the rectum (melena)
Can lead to anaemia
Can erode an unusually large blood vessel (Dieulafoy’s lesion)
Perforation
Gastric or duodenal ulcer erodes through wall connecting peritoneal cavity with inner gastric lining
Presents acutely with severe abdominal pain

57
Q

Describe the pathophysiology of a hiatus hernia and how it is diagnosed

A

A hiatus hernia describes the protrusion of the stomach through the diaphragmatic hiatus from the abdominal cavity into the thoracic cavity

Results in a separation of the lower oesophageal sphincter from the phrenoesophageal ligament of the diaphragmatic crura

Predisposing factors which may weaken the phrenoesophageal ligament include obesity, pregnancy and age

The lack of separation between 2 high pressure zones leads to acid reflux

Diagnosis:
High resolution manometry
Endoscopy
Barium studies

58
Q

List the components of gastric juice

A

Hydrochloric acid
Mucin
Pepsin
Intrinsic factor

59
Q

Describe the symptoms and complications of gastro-esophageal reflux disease (GERD)

A

Regurgitation of food and fluid
Heartburn
Complications
- Columnar metaplasia
Barret’s oesophagus - risk of oesophageal adenocarcinoma

Benign stricture formation
Scarring causes oesophageal narrowing, leading to dysphagia
Treated through balloon dilation during endoscopy
Reflux oesophagitis
Ulceration
Can lead to bleeding/iron deficiency anaemia

60
Q

Describe the process of digestion & absorption of lipids

A

Mouth:
Small amounts of lingual lipase
Breaks down triglycerides into monoacylglycerols, diacylglycerols and fatty acids
Stomach:
Small amounts of gastric lipase
Duodenum:
Pancreatic lipase and co-lipase
Bile acids for emulsification of lipids & formation of micelles
Fatty acids diffuse to apical membrane in micelles, entering enterocyte
Short-chain fatty acids move directly into blood circulation
Long-chain fatty acids are packaged into chylomicrons and exit via basolateral membrane to enter lacteals
Eventually drain into blood circulation via thoracic duct

61
Q

Describe the process of absorption of glucose, galactose and fructose

A

Glucose and galactose are taken up by enterocytes via a sodium-glucose co-transporter (SGLT1)
Sodium is exchanged for potassium to maintain the electrochemical gradient

Fructose enters enterocytes via facilitated diffusion through a GLUT5 transporter

All 3 pass into the bloodstream by a GLUT2 transporter

62
Q

Describe the process of absorption of tripeptides, dipeptides and amino acids

A

The luminal plasma membrane contains sodium-dependent amino acid transporters

Amino acids are absorbed and enter the bloodstream via facilitated diffusion (selective uniporters)

Dipeptides and tripeptides are taken up by enterocytes via co-transport with hydrogen ions to undergo further breakdown, eventually entering the bloodstream as amino acids

63
Q

Describe the mechanism of action of antacids and alginates

A

Antacids:
Weak alkalis which neutralise acid and relieve symptoms of heartburn
Usually sodium hydroxide combined with a metal salt e.g. magnesium/aluminium hydroxide

Alginates:
Promote mucosal resistance
In presence of acid, form a gel-like raft which adheres to the top of the acid pocket in the proximal stomach
Release of CO2 makes gel float to proximal stomach and prevents acid reflux

64
Q

Describe the mechanism of action of H2 receptor antagonists and give examples

A

Acid suppressants which reversibly and competitively bind to the H2 receptor on parietal cells and prevent binding of histamine secreted by ECL cells
Reduced stimulation of parietal cells leads to reduced gastric acid secretion

Usually heals peptic ulcers but lower success rate with erosive oesophagitis

Examples
Cimetidine (Tagamet)
Ranitidine (Zantac)
Famotidine (Pepcid)

65
Q

Describe the mechanism of action of proton pump inhibitors (PPIs) and give examples

A

Acid suppressants which irreversibly bind to the H+/K+ pump on parietal cells, leading to reduced gastric acid secretion

Heals oesophagitis and peptic ulcers

Examples
Omeprazole (& esomeprazole)
Lansoprazole
Pantoprazole

66
Q

Describe the adverse effects associated with PPI use

A

Reduced micronutrient absorption (iron, calcium, vitamin B12)
Reduction in gastric acid output
Reduced gastric antimicrobial function
Increase in serum gastrin levels
Leads to hyperplastic mucosa in stomach
Fundic gland polyps can be found due to ECL cell hyperplasia
Rebound acid hypersecretion after discontinuation
Idiosyncratic
Diarrhoea due to lymphocytic colitis
Hypomagnesaemia (long-term)
Interstitial nephritis (rare)
Interaction w/ metabolism of other drugs

67
Q

State the total body content of iron as well as the daily nutritional need

A

Total: 4g

Daily need: 1-2mg/d

68
Q

Explain the mechanisms of cellular iron storage

A

Stored in 2 forms

Ferritin
Soluble, predominantly intracellular
Iron safe and readily available from reticuloendothelial system (RES)
Ferritin is an acute phase protein (can be increased due to tissue inflammation)
Haemosiderin
Insoluble conglomerates of ferritin
Iron slowly available

69
Q

Describe the process of digestion and absorption of iron

A

Haem iron: red meat
Easily absorbed
Non-haem iron: vegetables, white meat
Must be reduced from ferric (Fe3+) to ferrous (Fe2+) form by duodenal cytochrome b1 in the presence of vitamin C (vitamin C ferrireductase)
Iron is mainly absorbed in the duodenum & taken up by enterocytes via the divalent metal transporter (DMT1)

Iron is exported via the transmembrane protein ferroportin

Hepcidin degrades ferroportin

The interaction between hepcidin and ferroportin regulates GI iron absorption

70
Q

Describe the pathophysiology of Hereditary Haemochromatosis

A

Autosomal recessive disorder leading to iron overload as a result of abnormalities in HFE gene which regulates hepcidin
Homozygous for C282Y mutation or compound heterozygous (C282Y/H63D - less severe phenotype)
Males more at risk, females protected by menstruation and childbirth
Results in 100% transferrin saturation, so increased risk of metabolically active non-transferrin-bound iron
Can lead to tissue damage and lipid peroxidation

71
Q

Outline the symptoms and treatment of hereditary haemochromatosis

A

Symptoms
- Pancreas: diabetes

Heart: restrictive cardiomyopathy
Skin: bronzing (iron stimulates melanin production)
Liver: damage and cirrhosis
Joints: arthritis (affects 2nd and 3rd MPJ in hand)
Treatment
Venesection: take blood weekly until ferritin and transferrin saturation decrease

72
Q

Describe the pathophysiology of iron deficiency anaemia (IDA)

A

Causes:

Iron deficiency anaemia (IDA) in males and post-menopausal women is due to GI blood loss until proven otherwise
In young women it is usually due to menstruation/pregnancy
Exception: coeliac disease (iron malabsorption)

Presents with decreased transferrin saturation

Red blood cells are microcytic and hypochromic (small and light in colour)

73
Q

Explain the pathophysiology of Coeliac Disease

A

Gluten is digested by intestinal proteases but high proline content makes this difficult; undigested peptides appear
These need to be deamidated by tissue transglutamase (TTG) and presented to antigen-presenting cells (APCs) in intestinal mucosa
If the individual has HLA DQ2/8 APCs (genetically predisposed) presenting gluten peptides to CD4+ T cells, these will activate T cells and B cells to produce anti-gliadin antibodies
Cytokine cascade is initiated (interferon, interleukins…) which drives the inflammatory process

74
Q

Explain how coeliac disease is diagnosed

A

primary

75
Q

List the complications of coeliac disease

A

Osteoporosis
Dermatitis herpetiformis
IgA deficiency
Functional hyposplenism
Increased risk of cancer (especially T cell lymphoma and small bowel adenocarcinoma)
Increased overall mortality (secondary to increased autoimmune diseases)

76
Q

Describe the causes of osmotic diarrhoea

A

Increased water movement into gut, stops when patient fasts

2 causes

Non-absorbable solutes
Laxatives, antacids
Acarbose
Orlistat
- Failure to digest or absorb nutrients
Digestive enzyme deficiencies
Pancreatic insufficiency
Loss of enterocytes
Bacterial overgrowth
Lymphatic obstruction
Diabetes mellitus
Short bowel syndrome

77
Q

Describe the causes of secretory diarrhoea

A

Caused by acute infections; enterotoxins stimulate colonic enterocyte secretion (does not stop when patient is fasting)

  • Bacteria
    Vibrio cholerae
    Campylobacter
    Escherichia coli
    Salmonella
    Shigella
  • Viruses
    Norovirus
    Rotavirus
    Coronaviruses
    Sapovirus
    Adenoviruses
    Protozoa
    Cryptosporidium
    Giardia
  • Some endocrine syndromes
    Carcinoid syndrome (secretes hormones e.g. VIP)
    Zollinger-Ellison syndrome
    Drugs
    Some asthma medications, antidepressants, some cardiac drugs
    Certain metals, organic toxins, plant products (arsenic, insecticides, mushroom toxins)
78
Q

Describe the causes of inflammatory diarrhoea

A

Damage to intestinal transport system due to ongoing inflammation - destruction of the epithelium results in exudation of serum and blood into lumen and impairs absorption

Inflammatory bowel disease
- Crohn’s disease, ulcerative colitis

Irritable colon

Infectious disease

Shigella, salmonella

Types:
- Acute watery diarrhoea - dehydration e.g. E. coli, V. cholerae, rotavirus

Bloody diarrhoea - dysentery, intestinal damage, nutrient loss e.g. Shigella
Persistent diarrhoea - >14 days, undernourished children, concomitant disease

79
Q

Differentiate specificities of pancreatic endopeptidases trypsin and chymotrypsin & the structural basis for these specificities

A

Chymotrypsin acts on peptides where the carboxyl group is provided by tyrosine and phenylalanine (uncharged forms, aromatic amino acids)

Trypsin acts on peptides with lysine and arginine on C-terminal side (but not if there is a proline on the carboxyl side)

80
Q

Describe the lymphatic drainage of the GI tract

A

Lymphatic vessels drain into pre-aortic lymph nodes, which surround arteries

Coeliac nodes surround coeliac trunk
> collect lymph from organs derived from foregut
Superior mesenteric nodes surround SMA
> drain organs derived from midgut
Inferior mesenteric nodes surround IMA (hindgut)
Drainage of lymph: inferior > superior > coeliac
Coeliac nodes drain into cisterna chyli > thoracic duct > bloodstream

Year 2 - Excess (6 decks)

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