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Medicine 2 > Week 2 - Peptic Ulceration > Flashcards

Week 2 - Peptic Ulceration Flashcards

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
Q

How are lipids digested in the SI?

A
  • 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
Q

What are the main investigations for GI infection?

A

Grow bacteria in culture

Look for specific toxins

Look for parasites with microscope

Attempt to detect specific antigens / antibodies

27
Q

What are problems with C. diff infection?

A
  • 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
Q

What are problems with H. pylori infection?

A
  • 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
Q

What are 4 anti-emetic drugs?

A

H1-receptor antagonists

Anti-muscarinic agents

Dopamine antagonists

5-hydroxytryptamine antagonists

30
Q

What are 3 common causes of diarrhea?

A

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
Q

When are antibiotics, orlistat, misoprostol and PPIs used in diarrhoea?

A

Antibiotics = superinfection

Orlistat = Pancreatic lipase inhibitor used for steatorrhea

Misoprostol = used for inflammatory type response

PPIs = used in infectionq

32
Q

How do opioids help in diarrhoea?

A

Reduce tone and peristaltic movements of GI muscles

Reduce ACh release

+ transit time

+ water reabsorption

Symptomatic relief

Can cause constipation

33
Q

How can you treat constipation?

A

Osmotic laxatives:

  • Lactulose
  • Macrologs
  • Magnesium

Bulking agents stimulating GI activity:

  • Stimulant laxatives
  • Prucalopride
34
Q

Treatment for IBS?

A

Lactulose or loperamide

Antispasmodics

Amitriptyline

35
Q

How do you treat IBD?

A

Anti-inflammatories and immunosupressants

  • 5-aminosalicylates
  • Corticosteroids
  • Immuniosupressants

Medicine 2 (29 decks)

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