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Years 1+2 > S4C2 > Flashcards

S4C2 Flashcards

1
Q

What must you consider before you accept a patients consent?

A

Whether they have been given the information they want or need, and how well they understand the details and implications of what is proposed

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2
Q

How do you test for Helicobacter Pylori infection?

A

Stool test - tests for foreign antigens associated with H.Pylori. PPI + Bismuth affects the results
Breath test - swallow 13C urea. If H.Pylori infection, it will it will be broken down and expelled in the breath. PPI + Bismuth affects the results
Blood test - cannot distinguish between active or previous infection
CLO test - biopsy during gastroscopy

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3
Q

Define shared-decision making

A

a collaborative process that allows patients, or their surrogates, and clinicians to make health care decisions together, taking into account the best scientific evidence available, as well as the patient’s values, goals, and preferences

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4
Q

Describe the mechanism of gastric emptying

A

Gastric emptying is biphasic
In thelag phase, the solids are redistributed from the gastric fundus and broken down to smaller particles (1–2mm) which then can pass through the pylorus during thelinear emptying phase

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5
Q

What is the adaptive relaxatory reflex? What happens after it?

A

Activates the proximal stomach to accommodate an increasing volume of contents with little change in luminal pressure. This is followed by a tonic contraction propelling gastric liquids and redistribution of solids to the distal stomach.

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6
Q

What is the action of ghrelin?

A

Stimulates gastric contractions and emptying

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7
Q

What is the action of glucagon-like peptide-1?

A

Inhibits the gastric emptying process

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8
Q

Where is pain from foregut structures felt? What spinal level is this?

A

Felt in the epigastric region

T7-T8

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9
Q

Where is pain from midgut structures felt? What spinal level is this?

A

Felt in the umbilical region
pain is usually colicky (intermittent with bowl contractions) in this area
T10

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10
Q

Where is pain from hindgut structures felt? What spinal level is this?

A

Felt in the hypogastric region

T12-L2

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11
Q

What is Helicobacter pylori?

A

A gram negative bacteria that causes inflammation of the stomach lining.
Found predominantly in the gastric antrum

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12
Q

How does H.Pylori cause inflammation?

A

Colonises antrum, the least acidic region
Burrows through mucus and adheres to epithelium - protection from acid
Metabolise urea (1-3 mM) - leads to a local increase of pH with NH3 and CO2 release
To control urea influx H. Pylori expresses a H+ gated urea channel

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13
Q

What are the virulence factors the H.Pylori possesses?

A

Flagella - bacterial mobility and chemotaxis to colonise under mucosa
Urease - neutralise gastric acid, causes gastric mucosal injury by ammonia
Lipopolysaccharides - adhere to host cells, inflammation
Type IV secretion system
Effectors - actin remodelling, IL-8 induction, host cell growth and apoptosis inhibition
Exotoxins - vacuolating toxin, gastric mucosal injury
Secretory enzymes - mucinase, protease, lipase gastric mucosal injury

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14
Q

How does H.Pylori cause ulcers?

A

Antrum is the site of gastrin release which is inhibited by somatostatin
Inflammation in the antrum inhibits somatostatin release
Therefore increase in H+ secretion Gastric metaplasia - cell transformation due to excessive acid exposure
Downregulation of defence factors - decrease in epidermal growth factor and bicarbonate production

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15
Q

What is triple therapy?

A

2 antibiotics and a proton pump inhibitor

70% effective

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16
Q

What is quadruple therapy?

A

Quadruple therapy includes bismuth compounds with the triple therapy which improve antibiotic effectiveness

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17
Q

What is the essential function of the stomach?

A

To synthesise intrinsic factors to absorb B12

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18
Q

What are the exocrine secretions of the stomach?

A

HCL - acidifies lumen, produces pepsin from pepsinogen
Controlled by:
Acetylcholine (Vagal input)
Gastrin
Histamine (from enterochromaffin cells)
Mucus - protects mucosal surface being damages by HCl
Pepsinogen - precursor of pepsin, an endopeptidase
Secreted by chief cells
Controlled by:
Acetylcholine (Vagal input)
Intrinsic factor - important in absorbing B12 and erythropoiesis (in terminal ileum)
Secreted parietal cells

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19
Q

What are the endocrine secretions of the stomach?

A

Gastrin - stimulates acid production

Somatostatin - inhibits release of gastrin

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20
Q

What is gastric acid secretion inhibited by?

A

Somatostatin (via decreased gastrin release)
Secretin (Via decreased gastrin secretion)
Gastric inhibitory peptide and other enterogastrones - Act directly on parietal cells

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21
Q

Name the types of cells and their function found in the stomach

A

Goblet cells - secrete alkaline mucus
Mucous cells - secrete mucus and pepsinogens
Parietal cells - secrete gastric acid and intrinsic factor
Chief cells - secrete pepsin and gastric lipase
G cells - gastrin
D cells (Found in the antrum) - somatostatin

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22
Q

What doe Cholecystokinin inhibit?

A

gastric emptying in response to high caloric value in the duodenum

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23
Q

What is the motor activity of the small intestine?

A

After meal, there are small irregular contractions of the small intestine
In the interdigestive state, the small intestine exhibits the migrating motor complex (MMC)
Can take 2 hours to pass along small intestine
Sweeps material through gut
Ingestion of food signals stop
This can be mimicked by gastrin and cholecystokinin (CCK) which are released from stomach and intestine respectively

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24
Q

What is the motor activity of the colon?

A

Almost continually active
Increased activity can be elicited by particular stimuli
2-3 day transit time
Transverse colon is the major component in terms of transit time (dehydration and storage)
Contractions of the circular muscle haustra (NOT LIKE PERISTALSIS)
As one haustrum fills and distends, contractions induced that push food into the next
Powerful propulsive contractions can be elicited by the introduction of food into the stomach - Gastrocolic reflex

25
Q

Describe glucose uptake in the SI

A

Couple transport process
Sodium Potassium ATPase pumps sodium out of the basolateral membrane
This drives the sodium-glucose symporter in the apical membrane

26
Q

Describe fat absorption in the SI

A

Large fat globules are emulsified by bile salts in the duodenum
Digestion of fat by the pancreatic enzyme lipase yields free fatty acids and monoglycerides which form micelles
Fatty acids and monoglycerides leave micelles and enter epithelial cells by diffusion
Chylomicrons containing fatty substances are transported out of the epithelial cells and into lacteals where they are carried away from the intestine by lymph

27
Q

Describe apical H+ secretion

A

Active transport of H+ by proton pump
K+ recycles via K+ ion channels
Cl- secreted via Cl- ion channels

28
Q

Describe basolateral HCO3- efflux

A

HCO3- leaves the cell passively by 1:1 exchange for Cl-
Exactly balances Cl- secretion at apical membrane
Basolateral Na+K+-ATPase maintains intracellular Na+ and K+

29
Q

Where is gastrin produced and what are its major actions?

A

G cells - antrum
Relax cardia
Increased antral activity
Increased gastric acid secretion

30
Q

Where is Motilin produced and what are its major actions?

A

Duodenum
Increased gastric acid secretion
Increased stomach activity

31
Q

Where is Gastric inhibitory peptide produced and what are its major actions?

A

Small intestine

Decreased gastric acid secretion

32
Q

Where is Cholecystokinin produced and what are its major actions?

A

Small intestine
Relaxes stomach
Increases pancreatic secretion
Contracts gallbladder

33
Q

Where is secretin produced and what are its major actions?

A

Small intestine
Relaxes stomach
Increases HCO3- secretion by pancreas

34
Q

Where is Vasoactive intestinal peptide produced and what are its major actions?

A

Glands and nerves

increased electrolyte secretion

35
Q

What regulates gastric acid?

A

Acetylcholine - released from neurones acts on muscarinic receptors
Prostagladins - released from local cells acts on EP3 receptors - increased cAMP
Histamine - released from enterochromaffin-like cells act on H2 receptors - increased cAMP
Gastrin - released from blood stream acts on cholecystokinin B receptors - increased Ca2+

36
Q

What is the gastric mechanism controlling acid?

A

If proteins are present, they act as buffers to keep luminal pH>3
As the stomach empties the luminal pH falls below 3
D cells release somatostatin to inhibit gastrin release and reduce acid secretion

37
Q

What is the duodenal mechanism controlling acid?

A

Acidification of the duodenal lumen releases secretin which inhibits gastrin secretion
Acidification of lumen with presence of fatty acids and salt
Duodenum release gastric inhibitory peptide, which acts directly on parietal cells to inhibit HCl secretion

38
Q

What are the complications of peptic ulceration?

A 
Pain
Heartburn
Reflux
Bleeding
Perforation
Stricture/obstruction
Malignancy
39
Q

What is mucus? What is it made up of?

A

A viscoelastic material - viscous behaviour of a liquid and the elastic properties of a sold
90% water and ions
5-10% glycoproteins
1-5% Mucins

40
Q

What are mucins?

A

extremely large glycoprotein polymers
dominated by sugars
repeated serine/threonine
essential component of epithelial protective barrier

41
Q

What are the 5 identified gel-forming mucins?

A 
MUC2
5AC
5B
6
19
42
Q

What does a knockout of Muc2 lead to?

A

Lack of mucus barrier
Tumours
Increased colitis susceptibility
Bacterial infection

43
Q

What are the role of Mucins?

A

Space filling - gel formation
Protease resistance
Pathogen binding/evasion/killing

44
Q

Describe pathogen subversion of the epithelial mucosal barrier

A

Most mucosal bacterial pathogens are flagellated - allows them to swim in mucus
Many mucosal pathogens produce enzymes to degrade the mucins and thereby disassemble the mucus barrier
Bacteria produce soluble toxins which can kill epithelial cells and/or arrest intestinal cell division
Many pathogen attach to the apical surface of epithelial cells and inject bacterial toxins
Many mucosal toxins disable tight junctions between adjacent epithelial cells

45
Q

What are the functions of mucins in defence against H.Pylori?

A

Muc5AC - binding
Muc6 - growth inhibition
Glycans inhibit cell wall synthesis

46
Q

What are the three phases of gastric secretion?

A

cephalic
gastric
intestinal

47
Q

Describe the cephalic phase.

A

Taste, smell, sensation and thoughts of food sends signals to the medulla oblongata
Parasympethic via Vagus nerve stimulates HCL and pepsin in stomach
Also results in gastrin production in lower part of stomach
Gastrin travels in blood causing more HCL and pepsin secretion
40% of gastric acid secretion occurs here

48
Q

Describe the gastric phase

A

Food has entered and distended the stomach
Distention activates Parasympethic reflex via medulla oblongata
Stimulate parietal cells and G cells
Result of increase of HCL and pepsin
Digested proteins also stimulate G cells
Has a direct stimulatory affect on gastric glands
50% of gastric acid secretion occurs here

49
Q

Describe the intestinal phase

A

Chyme entered duodenum
Chyme contains lipids and HCL
Brings pH <2 - gastric secretion is inhibited
Causes impulses to medulla oblongata to decrease parasympathetic innervation of the gastric glands
Release Secretin, gastric inhibitory peptide and cholecystokinin
Inhibit gastric gland secretion
Amino acids present in the bloodstream stimulate parietal cells
10% of gastric acid secretion occurs here

50
Q

What cells can be found in the gastric glands? What do they do?

A

Surface epithelial cells - HCO3- and mucus secretion
Mucous neck cells - mucus secretion
Parietal cells - HCl secretion
Chief cells - pepsinogen secretion

51
Q

What is the MOA of NSAIDs?

A

Inhibit COX-1 meaning a decrease in PGE2 in the mucosa of stomach and duodenum

52
Q

What does PGE2 do in the GI?

A

decreases H+ in parietal cells

increase mucosal protection

53
Q

What are the unwanted affect of NSAIDs on the GI tract?

A

Directly cytotoxic
Reduces mucus production
Increases likelihood of bleeding
Increased acidity - causing peptic ulcer

54
Q

How does the stomach digest proteins?

A

Pepsinogen, an inactive zymogen, is secreted into gastric juice from both mucous cells and chief cells. Once secreted, pepsinogen is activated by stomach acid into the active protease pepsin, which is largely responsible for the stomach’s ability to initiate digestion of proteins.

55
Q

How do PPIs work?

A

Block the gastric HK-ATPase
reduce acidity enhancing antibiotic action
Phosphate-competitive acid blockers may increase pH for longer

56
Q

How does Tetracycline work?

A

Protein synthesis inhibitors, inhibiting tRNA binding to mRNA

57
Q

How do H2 receptor antagonist work?

A

block H2 receptors in parietal cells which suppresses acid secretion

58
Q

How does Bismuth work?

A

blocks H+ influx into H. Pylori so enhance antibiotic action even as the effects of PPIs are diminishing with time

Years 1+2 (21 decks)

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