Week 2 - Peptic Ulceration Flashcards

(35 cards)

1
Q

What are the 4 types of salivary glands?

A

Parotid - in cheek - serous, watery secretion

Submandibular - under chin - mainly serous secretion

Sublingual - under tongue - mainly mucous secretion

Simple - random places - mainly mucous

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2
Q

What is the role of acinar cells?

A

Responsible for primary secretion, isotonic with plasma

Some salivary proteins secreted

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3
Q

What is the role of duct cells?

A

Modify secretion by acinar cells

Actively reabsorb Na+ and Cl- ions

Secrete K+ and HCO3- ions

Impermeable to water

Excess absorption = saliva is hypotonic to plasma

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4
Q

Lable the 4 cell types?

A
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5
Q

What are the functions of saliva?

A
  • Breakdon food components
  • Activate taste buds
  • Produce mucus for swallowing
  • Moisturiser to aid speech
  • Promotes oral hygeine
  • Contains bicarbonate –> neutralises acids in food reducing cavities
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6
Q

What happens to ion concentrations when high salivary flow rate?

A
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7
Q

What happens when acinar cells are parasympathetically vs sympathetically stimulated?

A

Para = + serous saliva is produced, rich in enzymes

Symp = small amount of thick saliva rich mucous produced

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8
Q

What role does bradykinin have in saliva production?

A

+ bradykinin = vasodilatation = increase in saliva secretion

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9
Q

What are the 2 phases of swallowing?

A

Oropharyngeal –> food bolus directed into oesophagus

Oesophageal –> oesophagus is protected from damage caused by passing food bolus via mucous secretion

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10
Q

What are the 2 regions of gastric mucosa?

Where are mucosal gland cells found?

A

Oxyntic mucosa = in fundus and body of stomach

Pyloric gland area = in antrum

In gastric pits

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11
Q

What is the role of parietal, cheif and surface epithelial cells in stomach?

A

Parietal = secrete HCl and intrinsic factor

Cheif = secrete pepsinogen

Surface epithelial = secrete mucous

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12
Q

How do parietal cells produce HCl?

A

P takes H+ in exchange for K+

A moves carbonate into blood and Cl- into cell

C transports Cl- and K+ into gastric lumen

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13
Q

What is the relationship between stomach HCl and pepsinogen?

A

HCl = provides acidic environment for pepsin to digest food

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14
Q

What is the cephalic phase of gastric secretion?

A
  • Gastric secretion stimulated prior to food arriving
  • Stimulated by thought of expectation
  • Contributes 30-50% gastric secretions
  • Is dependent upon vagus nerve activity
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15
Q

What is the gastric phase of gastric secretion?

A
  • When food reaches stomach
  • Contributes 50-60% gastric secretions
  • Occurs due to local vagal reflexes in response to mechanical stimulation
  • Gastrin release from G-cells stimulated by peptide fragments of partially digested proteins
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16
Q

What is the intestinal phase of gastric secretion?

A
  • Contributes 5% of gastric secretions
  • Due to circulating AAs or gastrin
17
Q

What effect does pH and enterogastrone have on gastrin release?

A

pH < 2 = inhibition of gastrin release from G cells via somatostatin release

Enterogastrone = released when duodenum distended or chyme = inhibits gastrin release

18
Q

How are gastric mucosa protected from autodigestion?

A

Luminal membranes = H+ impermeable = connected via tight junctions = no H+ between cells

Negative feedback = pH less than 2 inhibits G-cells via somatostatin from D-cells

Mucus = release from surface epithelial cells

Rapid repair of damaged mucosa

19
Q

What is the role of duct cells, centrocinar and acinar cells in the pancreas?

A

HCO3- exchange with Cl-

Bicarbonate secretion for neutralising acid chyme

Enzyme rich alkaline secretion

20
Q

What controls pancreatic secretions?

What is the role of acetylcholine in the pancreas?

A

Vagus nerve

Potentiates actions of secretin and cholecystokinin

21
Q

What are the functions of secretin and cholecystokinin?

A

Secretin = released in repsonse to acid in duodenum –> stimulates HCO3- production

Cholecystokinin = stimulates enzyme rich secretion released in response to fat and protein in duodenum

22
Q

Wjhat is the role of somatostatin in the pancreas?

A

Inhibits pancreatic secretions

23
Q

How are carbohydrates digested in the SI?

A
  • Digested as complex carb
  • Digestion ceases in acidic stomach environment
    • digestion from pancreatic alpha-amylase
  • Subsequent digestion by enzymes of SI brush border
  • Sodium dependent process
24
Q

How are proteins digested in the SI?

A
  • Digested in stomach by pepsin
  • Halted by alkaline pancreatic secretions
  • Endo and exopeptidases are pancreatic enzymes for digestion
  • Enzymes secreted in inactive form into duodenum
  • Further digestion by peptidases on brush border, fomring AAs
  • Absorbed via passive diffusion or facilitated transport
  • Intracellular peptidases breakdown peptides
25
How are lipids digested in the SI?
- Digested by pancreatic lipase (water soluble) - Fats emulsified by bile acids from liver, released by gall bladder - Monoglycerides and FFAs formed from pancreatic lipase action (absorbed by forming micelle) - Triglycerides reformed intracellularly, combined with phospholipids, cholesterol and protein - Forms chylomicron - Chylomicron is transported via lymphatic system
26
What are the main investigations for GI infection?
Grow bacteria in culture Look for specific toxins Look for parasites with microscope Attempt to detect specific antigens / antibodies
27
What are problems with C. diff infection?
- Vegetative cells produce toxin - Can colonise and not cause disease - Antibiotics kill other bacteria, allowing C. diff to thrive - Disease = diraahoea - toxic megacolon - perforation - Metronizadole for mild disease, vancomycin for severe
28
What are problems with H. pylori infection?
- Chronic gastritis - Bacterial - Duodenal ulcer disease = 80% - Inflammatory response - Association with gastric adenocarcinoma - Urea breath test, gastric biopsy, serology - 2 antibiotics + PPI for treatment
29
What are 4 anti-emetic drugs?
H1-receptor antagonists Anti-muscarinic agents Dopamine antagonists 5-hydroxytryptamine antagonists
30
What are 3 common causes of diarrhea?
Rotavirus - damages small bowel villi Invasive bacteria - damage epithelium Adhesive enterotoxigenic bacteria - adhere to brush border, + cAMP, Cl- and Na+ secretion followed by water
31
When are antibiotics, orlistat, misoprostol and PPIs used in diarrhoea?
Antibiotics = superinfection Orlistat = Pancreatic lipase inhibitor used for steatorrhea Misoprostol = used for inflammatory type response PPIs = used in infectionq
32
How do opioids help in diarrhoea?
Reduce tone and peristaltic movements of GI muscles Reduce ACh release + transit time + water reabsorption Symptomatic relief Can cause constipation
33
How can you treat constipation?
Osmotic laxatives: - Lactulose - Macrologs - Magnesium Bulking agents stimulating GI activity: - Stimulant laxatives - Prucalopride
34
Treatment for IBS?
Lactulose or loperamide Antispasmodics Amitriptyline
35
How do you treat IBD?
Anti-inflammatories and immunosupressants - 5-aminosalicylates - Corticosteroids - Immuniosupressants