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Digestive > Physiology > Flashcards

Physiology Flashcards

1
Q

Swallowing

A

Swallowing centre in medulla coordinates contraction of skeletal muscle (30-40 cm/s) causing rapid pharyngeal swallow of less than 1 second

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2
Q

Resting UOS pressure

A

30-200 mmHg

Decreases entry of air into oesophagus during tonic contraction

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3
Q

UOS relaxation

A

Only for 0.5 - 1 second

Occurs during swallowing, burping and vomiting

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4
Q

Peristalsis of oesophagus

A

Contraction above bolus and relaxation below bolus

Primary and secondary peristalsis

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5
Q

Primary peristalsis

A 
Initiated by swallowing
Continuation of pharyngeal contraction
3-5 cm/s
Lasts about 5 seconds
Pressure between 30-80 mmHg
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6
Q

Secondary peristalsis

A

Not induced by swallowing
Involuntary
Sensory receptors in oesophagus by retained bolus or gastric acid cause stimulation and contraction

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7
Q

Innervation of oesophageal peristalsis

A

Autonomic nervous system
Enteric nervous system: both submucosal and myenteric plexuses for reflex coordination
Systems communicate with each other

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8
Q

Lower oesophageal sphincter

A

Specialised segment of smooth muscle 2-4 cm long
Relaxes 1-2 s after swallowing. Relaxation lasts 5-10 s then hypercontracts
Can also relax transiently without swallowing when standing up to release air from stomach

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9
Q

Resting pressure of LOS

A

20-35 mmHg

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10
Q

3 phases of swallowing

A

Oral phase - voluntary
Pharyngeal phase - involuntary
Oesophageal phase - involuntary

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11
Q

Control of swallowing

A

Controlled by both cortex and brainstem
Swallowing centre in brainstem receives sensory input from receptors in posterior mouth and upper pharynx. Innervates swallowing muscles via cranial nerves

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12
Q

Oral phase of swallowing

A

Mastication
Saliva secretion
Transfer of bolus into pharynx
Tongue connects with hard palate, closes off anterior oral cavity to push bolus into back of mouth

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13
Q

Pharyngeal phase of swallowing

A

Lasts less than 1 second
Bolus enters pharynx from back of mouth and descends through pharynx by peristalsis at 30-40 cm/s
Tongue pushes against palate, sealing off the oropharynx. Soft palate elevates, sealing off nasopharynx. Epiglottis swings down, sealing off lower airway

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14
Q

Oesophageal phase of swallowing

A

UOS relaxes
Bolus enters oesophagus
Oesophageal peristalsis initiated

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15
Q

GORD

A

Gastro-oesophageal reflux disease
Gastric contents enter oesophagus which irritates stratified squamous epithelium
Most reflux episodes occur during transient relaxations of LOS

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16
Q

GORD risk factors

A

Disordered gastric motility
Hiatus hernia
Impaired oesophageal peristalsis
Hypotensive LOS (doesn’t contract enough)
Caffeine, alcohol, chocolate, fats, medications

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17
Q

Hiatus hernia

A

Oesophagus protrudes through hiatus, an opening in the diaphragm

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18
Q

GORD complications

A 
Reflux oesophagitis (ulceration)
Oesophageal structure (scarring leading to dysphagia)
Barretts oesophagus (metaplasia, potentially leading to cancer)
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19
Q

2 types of oesophageal cancer

A

Adenocarcinoma (likely to be in distal oesophagus/GO junction)
Squamous cell carcinoma (likely to be in proximal oesophagus)

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20
Q

Squamocolumnar junction

A

Junction between oesophagus and stomach forming a visible transition between stratified squamous and columnar epithelium

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21
Q

Causes of oesophageal ulceration

A

HSV
Cytomegalovirus
Doxycycline
Bisophosphonates

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22
Q

Eosinophilic oesophagitis

A

Eosinophils infiltrate the epithelium of oesophagus

Allergy mediated

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23
Q

Oesophageal ring/web

A

Used interchangeably

Thin mucosal membrane often associated with hiatus hernia

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24
Q

Adenocarcinoma likely causes

A

GORD, Barretts

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25
Q

Squamous cell carcinoma likely causes

A

Smoking, alcohol, diet

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26
Q

Oesophageal stricture

A

Narrowing of oesophagus
Can be peptic (due to stomach acid causing scarring)
Or caustic (due to ingestion of chemical agents)
Often occurs after radiotherapy and some surgeries
Malignant

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27
Q

Zenkers diverticulum

A

Pharyngeal pouch
UOS fails to relax
Excessive pressure causes weakest portion of pharynx to balloon out
Common in elderly

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28
Q

Diffuse oesophageal spasm (corkscrew oesophagus)

A

Non-peristaltic or simultaneous onset of contractions in the oesophagus
Chest pain, dysphagia, bolus obstruction

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29
Q

Achalasia

A

Degeneration of oesophageal nerves including ganglionic cells in myenteric plexus and inhibitory neurons in LOS that switch off tonic contraction
Prevents LOS relaxation and loss of peistalsis

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30
Q

Scleroderma

A

Connective tissue disorder causing fibrosis of submucosa and muscle layers
Absent peristalsis, weak contractions and loss of LOS tone
Dysphagia and reflux

31
Q

Functions of stomach

A 
Food reservoir
Adjusts osmolarity of contents
Grinding mill (fundus)
Particle size regulation (pylorus)
Acid secretion (among others)
32
Q

Gastric motility steps

A

Relaxation of fundus
Contraction of body and antrum
Pylorus contracts
Mixing by retropulsion

33
Q

Vagovagal reflex

A

Fundus relaxation

34
Q

Dumping syndrome

A

Food moves too quickly from stomach into duodenum, not completely digested
Hyperosmolar chyme
Rapid fluid shift into gut
Causes diarrhoea, pain, nausea, vomiting and cramping

35
Q

Prokinetics

A

Drugs that speed up gastric emptying e.g. metoclopramide which releases ACh at myenteric plexus

36
Q

Diabetic gastroparesis

A

Due to autonomic neuropathy
Variable rate of glucose absorption
Upper abdominal discomfort

37
Q

Gastric acid roles

A

Sterilisation
Protein denaturation
B12 and iron absorption
Achlorydia (absent or low gastric acid)

38
Q

Gastric pH

A

HCl produced at 160 nm = pH 0.8
pH in stomach lumen = 1.5 - 2
Buffers with meals to 5-6
Gradually falls during night

39
Q

Neurotransmitter

A

Molecule that transmits a signal from one neuron to another

40
Q

Autocrine

A

Molecule released by a cell that targets itself

41
Q

Paracrine

A

Molecule released by a cell that targets adjacent cells

42
Q

Endocrine

A

Molecule released by a cell that targets distant cells via bloodstream circulation

43
Q

ACh

A

Neurotransmitter
Released by vagus nerve and enteric neurons
Stimulates parietal cells to release HCl, ECL cells to release histamine (which stimulates parietal cells) and G cells to release gastrin (which stimulates parietal cells and ECL cells)

44
Q

ECL cells

A

Located in stomach body
Secrete histamine (molecule with paracrine activity)
Stimulates acid secretion directly by acting on adjacent parietal cells

45
Q

G cells

A

Located in stomach antrum
Secrete gastrin (hormone with endocrine activity)
Stimulates acid secretion indirectly via ECL cells which release histamine which stimulate parietal cells to secrete HCl

46
Q

D cells

A

Located in stomach antrum
Secrete somatostatin (hormone with endocrine and paracrine activity)
Inhibits acid secretion by inhibiting gastrin from adjacent G cells

47
Q

Cephalic phase mediation

A

Vagus nerve releases ACh which stimulates parietal cells

48
Q

Gastric phase mediation

A

Distension of body and antrum causes acid secretion by vagus nerve
Protein in antrum stimulates G cells which release gastrin

49
Q

Intestinal phase mediation

A

HCl in antrum causes somatostatin release from D cells. Gastrin inhibited.
HCl in duodenum stimulates secretin which inhibits gastric acid and stimulates bicarbonate secretion from pancreas
Partially digested fat and protein in duodenum stimulate CCK which inhibits gastric acid and emptying, also stimulating release of pancreatic enzymes and gallbladder contraction for bile release

50
Q

Causes of increased gastric acid secretion

A

H. pylori gastritis

Gastrinoma

51
Q

Causes of decreased gastric acid secretion

A

Loss of parietal cells e.g. pernicious anaemia
Vagotomy leading to less ACh
Drugs e.g. proton pump inhibitors and histamine 2 receptor antagonists
Gastric surgery

52
Q

Pepsinogen

A

Secreted from chief cells

Pro-enzymes of pepsin - cleaved in acid

53
Q

Pepsin

A

Degrades/hydrolyses proteins at aspartic amino acids

If pH less than 4 pepsin is inavtive

54
Q

Pepsinogen role in digestion

A

Cleaves to pepsin which hydrolyses proteins which are a stimulus for gastrin release

55
Q

Prostaglandins

A

Lipid molecules that protect and repair gastric mucosa

56
Q

Peptic ulcer disease

A

Pain, bleeding, perforation and obstruction
Can cause swelling and stricture
Treatment includes triple therapy antibiotics and in severe cases, gastrectomy, vagotomy and pyloroplasty

57
Q

H. pylori

A

Gastritis, ulcers, cancer, MALToma

58
Q

MALToma

A

Mucosa-associated lymphoid tissue lymphoma

59
Q

Triple therapy

A 
Omeprazole
Clarithromycin
Amoxycillin
14 day treatment
Low recurrence rate
60
Q

Other causes of peptic ulcer disease

A

Aspirin and NSAIDS

61
Q

Gastric adeocarcinoma

A

Intestinal: well-differentiated, cells arranged in a tubular/glandular pattern
Diffuse: poorly differentiated, lack glandular formation, linitis plastica

62
Q

Linitis plastica

A

Metastatic infiltration of the stomach

63
Q

H. pylori and gastric cancer link

A

Strong association for intestinal type adenocarcinoma
Widespread inflammation and destruction of parietal cells to reduce gastric acid secretion leading to achlorydia, bacterial overgrowth and carcinogens

64
Q

Osmotic diarrhoea

A

Macronutrient malabsorption retains osmotic pressure in lumen of intestines. Water also retained, increasing water content in stools

65
Q

Secretory diarrhoea

A

Increased second messengers increases anion secretion. To maintain charge balance in the cell cations stay or move in, bringing water along. No impact on sodium/glucose transporters.

66
Q

Solvent drag

A

Responsible for increased sodium and increased urea absorption in jejunum

67
Q

Transporters in intestinal epithelial cells

A

NaKATPases - mediate transcellular Na+ movement on the basolateral membrane
NaH exchanges
Na/glucose symporters on the apical membrane

68
Q

NK2Cl channel

A

K+, Na+ and 2 x Cl- transported into cell
2 x Cl- then transported out of cell through CFTR channel
Mediated by second messengers

69
Q

Absorption and secretion hormones

A

Enteric: ACh and secretagogues
Endocrine: Aldosterone
Paracrine: Serotonin

70
Q

Small intestine net absorption and secretion

A

Absorption of water, Na+, Cl-, K+

Secretor of HCO3-

71
Q

Hypovolemic shock

A

Decreased blood pressure due to water loss, heart rate rises to compensate BP and maintain cardiac output

72
Q

Cholera toxin

A

Activates CFTR channel which increases Cl- secretion

Na+ and water follow

73
Q

Oral rehydration therapy

A

Water and key ions to compensate extracellular fluid loss

During loss, body becomes acidotic. Oral rehydration therapy includes HCO3- to neutralise this effect

Digestive (9 decks)

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