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Medicine 3 > GIM 2 > Flashcards

GIM 2 Flashcards

1
Q

What are the 3 regions of the pharynx?

A

Nasopharynx
Oropharynx
Laryngopharynx

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2
Q

What are the different types of oral epithelium?

A

Masticatory epithelium - keratinized stratified squamous epithelium found on structures involved in chewing

Lining epithelium - non-keratinzied stratified squamous epithelium found on all other surfaces

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3
Q

What are the different types of tongue papillae?

A

Filiform - mechanical
Fungiform - thermoregulatory
Circumvallate - sensory
Foliate - sensory

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4
Q

What are the 3 main layers of oral cavity mucosa?

A

Epithelium - stratified squamous non-keratinizing
Lamina propria- papillary layer, reticular layer
Submucosa - salivary gland, nerves, veins, bone

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5
Q

What are the different types of taste receptor cells?

A 
Type 1 - Epithelial sodium channel (ENaC) - salty
Type 2 - T1R/T2R - unami, sweet, bitter
Type 3 - TRP receptor - sour 
Type 4 - replace taste receptor cells
G-protein receptors in GI tract
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6
Q

What is the structure of a taste bud?

A

Open to surface via a taste pore
Sensory fibres penetrate base
Shielded by a selective barrier

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7
Q

What are the 3 paired large salivary glands in the oral cavity?

A

Sublingual - under tongue
Submandibular - under jaw
Parotid - cheeks

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8
Q

What is the histological appearance of salivary glands?

A

Irregular lobes divided by connective tissue strands called septa

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9
Q

What are the 2 parts of a salivary gland?

A

Acini

Duct

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10
Q

What is a myoepithelial cell?

A

Spider like contractile cell that mediates salivary expulsion

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11
Q

What is the function of acinar cells?

A

Produce primary saliva secretion (isotonic with plasma)

Secrete some salivary proteins

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12
Q

What is the functions of salivary ductal cells?

A

Modify salivary secretion:
Actively reabsorb Na+ and Cl-
Secrete K+ and HCO3-
Create a secretion that is hypotonic to plasma

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13
Q

How does and increase in salivary flow rate affect electrolyte concentration?

A

Na+, HCO3- and Cl- increase where K+ remains the same

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14
Q

How does parasympathetic stimulation of acinar cells affect salivation?

A

Production of large volumes of serous saliva (enzyme rich)

Vasodilation

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15
Q

How does sympathetic stimulation affect salivation?

A

Production of small volumes of thick saliva (mucous rich)

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16
Q

What are the functions of saliva?

A 
Digestion - enzymes
Mucous - aids swallowing 
Protection - IgA
Solvent for taste
Moisturiser - aids speech
Oral hygiene
Bicarbonate neutralises food acids - reduces dental cavities
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17
Q

Why is stomach food storage important?

A

Allows a delivery rate to small intestine appropriate for optimal digestion

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18
Q

What are the 3 layers of the alimentary canal?

A

Inner pipe - mucosa
Buffer space - submucosa
Outer pipe - muscularis

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19
Q

What are the 2 types of outermost layers of the alimentary canal?

A

Adventitia- lining of intraperitoneal surfaces

Serosa- parts attached to other body regions

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20
Q

How is a tumour staged in layered organs such as the alimentary canal?

A

By which layers are involved regardless of size

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21
Q

What epithelium is found in the oesophagus?

A

Non-keratinizing stratified squamous epithelium

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22
Q

What are the two main types of oesophageal cancer?

A

Squamous-cell carcinoma - tobacco, alcohol

Adenocarcinoma - long term acid reflux

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23
Q

What are the two types of stomach mucosa?

A

Non-oxyntic - mucus producing

Oxyntic - acid and pepsinogen producing

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24
Q

Describe the gastric mucosa

A

Hugh glandular mucosa forming gastric glands. Surface covered in thick mucus

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25
Q

What are the 4 different gastric epithelial cells?

A

Mucous - secrete mucus and bicarbonate

Parietal/oxyntic - secrete intrinsic factor and H+ ions

Enteroendocrine - secrete gut hormones

Chief/zymogenic - secrete pepsinogen

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26
Q

What is the purpose of mucus in the stomach?

A

Lubricant to prevent mechanical damage

Traps bicarbonate

Traps epidermal growth factor (EGF) which supports healing of gastric mucosal damage

27
Q

How is the gastric wall protected from the acidic environment in the stomach?

A

As more acid is secreted by parietal cells, more bicarbonate is created and delivered to mucosal cells as a protective barrier

28
Q

Why is surface folding in the GI tract so important?

A

Increased surface area for absorption of nutrients

29
Q

In the stomach, what cells produce HCl?

A

Parietal

30
Q

What is the role of secreted HCl in digestion in the stomach?

A

Activates pepsin and provides optimal pH

Aids breakdown of connective tissue and muscle fibres

Non-specific defence mechanism

31
Q

What is the role of intrinsic factor (IF) in digestion?

A

Binds vitamin B12 and allows its absorption in the ileum

Secreted by parietal cells

32
Q

What happens in the cephalic phase of gastric secretion?

What nerve is active?

A

Before food arrives, gastric secretion stimulated by expectation of food

Activity of vagus nerve

33
Q

What happens in the gastric phase of gastric secretion?

A

When food reaches the stomach.

Mechanical stimulation of food in antrum induces local vago-vagal reflexes

Peptide fragments stimulate gastrin release from G-cells

34
Q

What happens in the intestinal phase of gastric secretion?

A

Circulating amino-acids and gastrin act on parietal cells

35
Q

What is gastrin?

A

Peptide hormone that stimulates the release of HCl by parietal cells

36
Q

How is gastrin production regulated?

A

Somatostatin release inhibits gastrin secretion when pH drops below 2

37
Q

What is the function on bicarbonate in the duodenum?

A

Neutralise acid chyme for optimal digestion pH (neutral/slightly alkaline)

Micelle formation (fat absorption)

Protects duodenal mucosa

38
Q

What is the role of pancreatic amylase?

A

Digestion of carbohydrates (splits a-1,4 glycosidic links)

39
Q

How are monosaccharides transferred from gut lumen to vascular system?

A

Sodium co-transporters

40
Q

What are the 2 major classes of pancreatic proteolytic enzymes?

A

Endopeptidases - cleave interior peptide bonds

Exopeptidases - cleave external peptide bonds

41
Q

How are proteins broken down after the stomach?

A

Pancreatic proteolytic enzyme break down proteins into peptides

Peptides broken down into amino acids by peptidase on the brush border of epithelial cells.

42
Q

How is fat digested?

A

Bile acids emulsify lipid droplets to increase surface area and create micelles to enable absorption

43
Q

What happens to lipids after absorption?

A

Resynthesized into triglycerides and combine with protein, phospholipids and cholesterol to form a chylomicron

44
Q

How is pancreatic secretion stimulated?

A

Vagus nerve - cephalic and gastric phases

Secretin - stimulates HCO3- when acid in duodenum

Cholecystokinin (CCK) - stimulates enzyme rich secretion when fat and protein in duodenum

45
Q

How are pancreatic secretions reduced?

A

Sympathetic activation and somatostatin

46
Q

What is commensal flora?

A

Micro-organisms that are resident without damage to the host. Can be beneficial

47
Q

What are transient flora?

A

Micro-organisms that reside for a short time without damage to the host

48
Q

What are opportunist flora?

A

Only capable of invading or damaging host when immunity is compromised

49
Q

What is campylobacter?

A

Acquired from raw food with a 2-5 day incubation. Symptoms of diarrhoea, abdominal cramp and vomiting.

50
Q

What is Haemolytic Uraemic Syndrome (HUS)? What causes it?

A

Damage to the small blood vessels of the kidneys that lead to platelet destruction and anaemia. Caused by E. coli 0157 and increased risk with antibiotics

51
Q

How would you diagnose Helicobacter pylori infection?

A

Urease breath test:

Carbon-13 urea swallowed, H-pylori breaks down urea, carbon dioxide with carbon-13 is exhaled

52
Q

What does Helicobacter pylori infection cause?

A

Chronic gastritis

Duodenal ulcer disease

Inflammation

53
Q

What treatment method is used to eradicate H-pylori infection?

A

Triple therapy. Combination of 2 antibiotics from metronidazole, amoxicillin and clarithromycin and a PPI and/or H2 antagonist.

1 week then PPI alone

54
Q

What is gastro-oesophageal reflux disease (GORD) and what does it cause?

A

Reflux of gastric contents into oesophagus that leads to oesophagitis (heartburn)

55
Q

What is the main cause of peptic ulceration?

A

H-pylori infection

56
Q

How is gastric acid secretion increased?

A

Histamine (H2 receptors)
Gastrin
Acetylcholine ((M receptors)

57
Q

How is gastric acid secretion decreased?

A

Prostaglandins

Bicarbonate and mucus release

58
Q

What are the benefits of antacids with dyspepsia treatment?

What are some examples?

A

Rapid relief but not a cure. Raise pH

Sodium bicarbonate, magnesium hydroxide

59
Q

What are alginates and how do they work?

A

Alginic acid when combined with saliva forms a foam which floats on gastric contents and protects the oesophagus during reflux

60
Q

How do histamine receptor antagonists provide dyspepsia relief?

A

Prevent activation of histamine receptors which increase cAMP leading to H+ release from parietal cells. Provide short term symptomatic relief

61
Q

How do PPIs help treat dyspepsia?

A

Irreversible inhibition of proton pump inhibitor, inhibiting H+ secretion. Higher risk of campylobacter infection.

62
Q

What is an example of a PPI?

A

Omeprazole

63
Q

How do NSAIDs cause gastric ulceration?

A

NSAIDs inhibit cyclo-oxygenase. COX-1 is linked to gastric protection.

64
Q

How do you minimise GI damage from NSAIDs?

A

Prescribe with PPI and misoprostol (PGE1 analogue that acts on prostanoid receptors to inhibit gastric H+ secretion)

Medicine 3 (8 decks)

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