Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Medicine > 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the function of haem oxygenase

A

Converts haem into bilverdin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the function of biliverdin reductase

A

Converts bilverdin to unconjugated bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

State the first-line treatment for H. pylori infection

A
  • 1 proton pump inhibitor (PPI)
    Omeprazole
  • 2 antibiotics
    Amoxycillin
    Metronidazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Celiac disease is associated with what genetic polymorphisms?

A

HLA-DQ2/8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What structures are supplied by coeliac trunk?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
  • Hepatitis
Causes of hepatitis
    Alcohol
    Viral
    Autoimmune
    Drugs
    Metabolic disease
    Biliary disease
    Drugs or toxins
    Cryptogenic
  • Alcohol or metabolic
  • Biliary disease
  • Idiopathic
  • Haemochromatosis
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

Symptoms

  • 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
  • Duodenal biopsy
    Histology
    TTG +ve but biopsy -ve: inadequate biopsy or patchy/latent disease
    TTG -ve but biopsy +ve: consider other causes of villous atrophy
  • Serology: (antibody -ve coeliac disease is rare)
    anti-TTG
    IgA anti-endomysial
  • HLA typing
    HLA DQ2/8
  • Immunohistochemistry
  • Small bowel imaging
  • Response to gluten free diet
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 Medicine (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions