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Gastrointestinal > GI 2 > Flashcards

GI 2 Flashcards

1
Q

What are the physiological functions of mucosal tissue in the digestive system?

A
  • Gas exchange
  • Food absorption
  • Sensory activities
  • Reproduction
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2
Q

Where can M cells be found?

A

In the epithelial layer which covers Peyer’s patches; identified by characteristic membrane ruffles

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3
Q

How do M cells work?

A

1) They take up antigen by endocytosis and phagocytosis
2) Antigen transported across M cells in vesicles and released at the basal surface
3) Antigen is bound by dendritic cells which activate T cells

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4
Q

What is the composition of different antibodies in the intestine?

A
  • IgA is 80%/5g a day
  • IgM 15%
  • IgG 5%
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5
Q

How are T cells in the gut specialised?

A
  • 90% T cells with 80% CD8+ (=intraepithelial lymphocytes)
  • Activated appearance with restricted antigen receptor
  • Expression of a4:b7 integrin anchors them in the epithelium
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6
Q

How do intraepithelial lymphocytes (IELs) work?

A
  • Epithelial cells undergo stress (virus, infection, damage to toxic peptides)
  • Express/display signals which activate IELs
  • Activated IEL kills cell via perforin/granzyme pathway
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7
Q

What is the action of histamine in the digestive system?

A
  • Secreted by the enterochromaffin-like cells in the gastric glands in response to stimulation by acetylcholine
  • Binds to H2 receptors with subsequent activation of adenylyl cyclase
  • The increase in cAMP increases the number of proton pumps, increasing gastric acid secretion from parietal cells
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8
Q

What is the action of acetylcholine in the digestive system?

A
  • Released by parasympathetic cholinergic neurons
  • Binds to muscarinic (M3) ACh receptors on parietal cells with subsequent activation of PLC
  • The increase in intracellular Ca2+ evokes cell signalling pathways that increase the number of proton pumps, increasing gastric acid secretion from parietal cells
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9
Q

What is the action of gastrin in the digestive system?

A
  • Released by G cells
  • Binds to CCK2 receptors on parietal cells with subsequent activation of PLC
  • The increase in intracellular Ca2+ increases the number of proton pumps, increasing gastric acid secretion from parietal cells
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10
Q

What is the action of somatostatin in the digestive system?

A
  • Secreted by D cells in the gastric glands
  • Binds to SST2R receptors, inhibiting adenylyl cyclase
  • The decrease in cAMP results in decrease gastric acid secretion from parietal cells
  • Somatostatin binding to SST2R receptors on enterochromaffin cells results in reduced histamine release and decreased gastric acid secretion from parietal cells
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11
Q

What are the four different sections of the colon?

A

1) Ascending
2) Transverse
3) Descending
4) Sigmoid

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12
Q

What does the large intestine comprise of?

A
  • Caecum and appendix
  • Colon
  • Rectum
  • Anal canal and anus
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13
Q

Describe the longitudinal smooth muscle layer in the large intestine

A
  • Caecum and colon -> divided into 3 strands known as teniae coli
  • Rectum and anus -> encircled as normal
  • Internal anal sphincter -> markedly thickened
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14
Q

What is the haustra?

A

Sac-like bulges which very slowly change location due to the activity of the teniae coli and the circular muscle layers

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15
Q

Describe the action of the ileocaecal valve?

A
  • Maintains a positive resting pressure
  • Relaxes due to distension of the duodenum
  • Contracts due to distension of the ascending colon
  • Controlled by vagus nerve, sympathetic nerve, enteric neurones and hormonal signals
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16
Q

How does the caecum receive material from the terminal ileum?

A
  • The gastroileal reflex

- Entry permitted due to gastrin and CCK opening ileocaecal valve

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17
Q

What is the structure of the appendix?

A
  • Blind ended tube
  • Composed of lymphoid tissue
  • Connected to distal caecum via appendiceal orifice
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18
Q

What are the primary functions of the colon?

A

1) Absorption of Na+, Cl-, H2O and short chain fatty acids
2) Secretion of K+, HCO3- and mucus
3) Storage of colonic contents
4) Periodic secretion of faeces

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19
Q

What are the 3 patterns of motility in the large intestine?

A

1) Haustration (non-propulsive segmentation)
2) Peristaltic propulsive movements (mass movement)
3) Defaecation (periodic egestion)

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20
Q

What are the major functions of the liver?

A

1) Metabolism of carbohydrates, fats and proteins
2) Hormone activation/deactivation
3) Storage of vitamins, iron, copper and glycogen
4) Synthesis of proteins
5) Protection through Kupffer cells and immune factors
6) Detoxification
7) Bile secretion

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21
Q

What does neutral/slightly alike bile serve to assist?

A
  • Micelle formation
  • Neutralising acidic chyme
  • pH adjustment for digestive enzyme action
  • Protection of mucosa
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22
Q

What does the primary juice secreted by hepatocytes into the canaliculi contain?

A
  • IgA
  • Bile acids, mainly cholic and chenodeoxycholic acids
  • Water and electrolytes: Na+, K+, Ca2+, Cl- and HCO3-
  • Bilirubin
  • Lipids and phospholipids
  • Cholesterol
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23
Q

How does cholelithiasis or gallstones occur?

A

Concentration of bile in the gall bladder (caused by reabsorption of water) produces a supersaturated solution that is unstable; cholesterol may crystallise and over time grow into a gall stone

24
Q

What is enterohepatic recycling?

A

Most bile salts entering the duodenum are reabsorbed by active transport in the terminal ileum; a fraction of primary biliary acids are dehydroxylated by bacteria in the gut to form the secondary bile acids

25
Q

What are the two phases of drug metabolism?

A

1) Phase I (oxidation, reduction or hydrolysis) - makes drug more polar, adds a chemically reactive group to permit conjugation
2) Phase II (conjugation) - adds an endogenous compound increasing polarity

26
Q

What is the cytochrome P450 (CYP) family of monooxygenases?

A

Haem proteins located in the endoplasmic reticulum of liver hepatocytes (and elsewhere) mediating oxidation reactions (phase 1) of many lipid soluble drugs

27
Q

How does sodium absorption take place in the jejunum and duodenum?

A
  • Postprandial secondary active coupled cotransport of Na+/amino acid and Na+/glucose
  • Na+/H+ exchange at both apical (NHE2 and NHE3) and basolateral (NHE1) membranes
28
Q

How does sodium absorption take place in the ileum and proximal colon?

A

Na+/H+ and CI-/HCO3- exchange in parallel; Mainly in inter digestive period; Regulated by intracellular cAMP, cGMP and Ca2+, all reduce NaCl absorption

29
Q

How does sodium absorption take place in the distal colon?

A

Epithelial Na+ channels (ENaC) are highly efficient and important in Na+ absorption; Increased by aldosterone but not regulated by cAMP or cGMP

30
Q

What are the three actions of aldosterone regarding ENaC channels?

A

(i) Opens ENaC (seconds)
(ii) Inserts more ENaC into membrane from intracellular vesicle pool (minutes)
(iii) Increases synthesis of ENaC and Na+/K+-ATPase (hours)

31
Q

What are the cellular mechanisms of chloride absorption?

A
  • Passively via transcellular or paracellular routes
  • In the small and large intestine driving force provided by lumen negative potential
  • Cl–HCO3- exchange (ileum, proximal and distal colon)
  • Parallel Na+-H+ and Cl–HCO3- exchange (ileum and proximal colon)
32
Q

What are the cellular mechanisms of chloride secretion?

A
  • Occurs at basal rate at crypt cells but overshadowed by absorption
  • Three processes on the basolateral membrane:
    1) Na+/K+ATPase
    2) Na+/K+/2Cl- co-transporter (NKCC1)
    3) K+ channels (IK1 and BK)
33
Q

What can diarrhoea result in?

A

1) Dehydration (Na+ and H2O loss)
2) Metabolic acidosis (HCO3- loss)
3) Hypokalaemia (K+ loss)

34
Q

What are the causes of diarrhoea?

A

1) Impaired absorption of NaCl
2) Excessive secretion
3) Hypermotility
4) Non-absorbable or poorly absorbable solutes in the lumen

35
Q

What are transaminases?

A
  • Hepatic enzymes, usually intracellular but released from hepatocytes in context of hepatocellular injury
  • Catalyse gamma-amino group transfers
  • e.g. aspartate/alanine -> ketoglutarate
36
Q

Describe alanine aminotransferase (ALT).

A
  • More sensitive than AST
  • Predominantly cytosol-located
  • Predominantly Liver
  • Short Half-Life circa 47hrs
37
Q

Describe aspartate aminotransferase (AST).

A
  • In cytosol and mitochondria
  • Present in Liver, Heart, Pancreas, Skeletal muscle, Brain, Lungs, RBCs, WBCs
  • Half Life Circa 17hrs
38
Q

What are the modifiable risk factors for oesophageal cancers (adenocarcinoma and squamous cell carcinoma)?

A
  • Convincing -> body fatness and alcoholic drinks

- Probable -> drinking mate

39
Q

What are the modifiable risk factors for stomach cancer? (all convincing evidence)

A
  • Body fatness (cardia)
  • Alcoholic drinks (3/day)
  • Foods preserved by salting
40
Q

What are the modifiable risk factors for liver cancer?

A
  • Convincing -> aflatoxins (product of aspergillum fungus + contaminant of grains and peanuts), alcoholic drinks and body fatness
  • Probable -> coffee decreases risk
41
Q

What are the modifiable factors which increase risk of colon and rectum cancers?

A
  • Convincing -> processed meat, alcoholic drinks, body fatness, attained adult height
  • Probable -> red meat
42
Q

What are the modifiable risk factors which decrease risk of colon and rectum cancers?

A
  • Convincing -> physical activity (moderate and vigorous)

- Probable -> wholegrains, foods containing dietary fibre, calcium supplements, dairy products

43
Q

What are the guidelines on food consumption in line with cancer prevention?

A
  • Red meat -> if >90g/day reduce to 70g/day
  • Processed meat -> avoid completely as it is carcinogenic
  • 30g/day of dietary fibre
44
Q

What are the 5A’s of behaviour change counselling?

A

1) Ask
2) Assess
3) Advise
4) Agree
5) Assist

45
Q

What are aminotransferases?

A
  • Deranged in all pathologies
  • Marked increase in hepatocellular pathologies
  • Levels do not reflect extent or outcomes
  • <500 U/L in obstructive jaundice except acute phase with passage of obstruction into CBD
46
Q

What is alkaline phosphatase? (ALP)

A

Enzyme which catalyses the hydrolysis of a number of organic phosphate esters; half life of 1 week -> slow to rise, slow precipitation following resolution of pathology

47
Q

What are the origins of alkaline phosphatase (ALP)?

A
  • Biliary (epithelial cells of ducts) - cholestasis enhances synthesis and release of ALP
  • Bone
  • Placenta
  • Intestine
  • Kidney
48
Q

What is gamma-glutamyl transpeptidase? (GGT)

A
  • Enzyme involved in gluthionine metabolism, transfer of amino acids across cellular membranes and leukotriene metabolism
  • Diagnostic marker for liver or cholestatic diseases
  • Can determine whether ↑ALP is bone/liver origin
  • Levels can increase with consumption of alcohol
49
Q

Where is gamma glutamyl transpeptidase (GGT) found?

A

Cell membranes of:

  • Liver
  • Heart
  • Brain
  • Bile duct
  • Kidneys
  • Gallbladder
  • Pancreas
  • Spleen
  • Seminal vesicle
  • NOT BONE
50
Q

How can glutamylt transpeptidase (GGT) be “induced”?

A
  • Drugs: anticonvulsants, TCAs, paracetamol

- Diseases: diabetes mellitus, pancreatic disease, COPD, renal disease

51
Q

What is bilirubin?

A
  • Predominantly a product of heme breakdown
  • Transported to liver bound to albumin
  • Uptake into the hepatocytes
  • Undergoes conjugation
  • Excreted via urine/faeces (Urobilinogen/Stercobilinogen)
52
Q

What is prothrombin time? (PT)

A
  • Liver is responsible for synthesis of most clotting factors
  • Measure of time taken for prothrombin to be converted to thrombin
  • Elevated PT may reflect reduced synthetic functionality
53
Q

What are some causes of increased PT?

A
  • Liver pathology meaning not enough synthesis
  • Drugs (inc Warfarin)
  • Bile malabsorption causing relative vitamin K deficiency
  • Consumptive coagulopathies
  • Congenital coagulopathy
54
Q

What are some liver function patterns and probable causes?

A
  • ALT/AST > ALP; hepatocellular injury
  • ALT/AST < ALP; cholestasis
  • AST:ALT ratio > 2; alcohol
55
Q

What are the causes of unconjugated hyperbilirubinaemia?

A

1) Increased bilirubin production - extra/intravascular hemolysis; extravasation of blood into tissues
2) Impaired hepatic bilirubin uptake - heart failure; portosystemic shunts; drugs rifampicin, probenecid
3) Impaired bilirubin conjugation - hyperthyroidism; CN2; Gilberts; advanced liver disease

56
Q

What are the causes of conjugated hyperbilirubinaemia?

A

1) Extrahepatic Cholestasis (Biliary Obstruction) - cholelithiasis; primary sclerosing cholangitis; cholangiocarcinoma; head of pancreatic tumour; acute/chronic pancreatitis
2) Intrahepatic Cholestasis - sepsis/hypoperfusion states; cirrhosis; infiltrative diseases; acute hepatitis; TPN
3) Drugs - alkylated steroids; rifampicin; chlorpromazine; herbs

Gastrointestinal (8 decks)

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