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Physiology Flashcards

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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
Squamous cell carcinoma likely causes
Smoking, alcohol, diet
26
Oesophageal stricture
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
27
Zenkers diverticulum
Pharyngeal pouch UOS fails to relax Excessive pressure causes weakest portion of pharynx to balloon out Common in elderly
28
Diffuse oesophageal spasm (corkscrew oesophagus)
Non-peristaltic or simultaneous onset of contractions in the oesophagus Chest pain, dysphagia, bolus obstruction
29
Achalasia
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
30
Scleroderma
Connective tissue disorder causing fibrosis of submucosa and muscle layers Absent peristalsis, weak contractions and loss of LOS tone Dysphagia and reflux
31
Functions of stomach
``` Food reservoir Adjusts osmolarity of contents Grinding mill (fundus) Particle size regulation (pylorus) Acid secretion (among others) ```
32
Gastric motility steps
Relaxation of fundus Contraction of body and antrum Pylorus contracts Mixing by retropulsion
33
Vagovagal reflex
Fundus relaxation
34
Dumping syndrome
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
Prokinetics
Drugs that speed up gastric emptying e.g. metoclopramide which releases ACh at myenteric plexus
36
Diabetic gastroparesis
Due to autonomic neuropathy Variable rate of glucose absorption Upper abdominal discomfort
37
Gastric acid roles
Sterilisation Protein denaturation B12 and iron absorption Achlorydia (absent or low gastric acid)
38
Gastric pH
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
Neurotransmitter
Molecule that transmits a signal from one neuron to another
40
Autocrine
Molecule released by a cell that targets itself
41
Paracrine
Molecule released by a cell that targets adjacent cells
42
Endocrine
Molecule released by a cell that targets distant cells via bloodstream circulation
43
ACh
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
ECL cells
Located in stomach body Secrete histamine (molecule with paracrine activity) Stimulates acid secretion directly by acting on adjacent parietal cells
45
G cells
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
D cells
Located in stomach antrum Secrete somatostatin (hormone with endocrine and paracrine activity) Inhibits acid secretion by inhibiting gastrin from adjacent G cells
47
Cephalic phase mediation
Vagus nerve releases ACh which stimulates parietal cells
48
Gastric phase mediation
Distension of body and antrum causes acid secretion by vagus nerve Protein in antrum stimulates G cells which release gastrin
49
Intestinal phase mediation
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
Causes of increased gastric acid secretion
H. pylori gastritis | Gastrinoma
51
Causes of decreased gastric acid secretion
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
Pepsinogen
Secreted from chief cells | Pro-enzymes of pepsin - cleaved in acid
53
Pepsin
Degrades/hydrolyses proteins at aspartic amino acids | If pH less than 4 pepsin is inavtive
54
Pepsinogen role in digestion
Cleaves to pepsin which hydrolyses proteins which are a stimulus for gastrin release
55
Prostaglandins
Lipid molecules that protect and repair gastric mucosa
56
Peptic ulcer disease
Pain, bleeding, perforation and obstruction Can cause swelling and stricture Treatment includes triple therapy antibiotics and in severe cases, gastrectomy, vagotomy and pyloroplasty
57
H. pylori
Gastritis, ulcers, cancer, MALToma
58
MALToma
Mucosa-associated lymphoid tissue lymphoma
59
Triple therapy
``` Omeprazole Clarithromycin Amoxycillin 14 day treatment Low recurrence rate ```
60
Other causes of peptic ulcer disease
Aspirin and NSAIDS
61
Gastric adeocarcinoma
Intestinal: well-differentiated, cells arranged in a tubular/glandular pattern Diffuse: poorly differentiated, lack glandular formation, linitis plastica
62
Linitis plastica
Metastatic infiltration of the stomach
63
H. pylori and gastric cancer link
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
Osmotic diarrhoea
Macronutrient malabsorption retains osmotic pressure in lumen of intestines. Water also retained, increasing water content in stools
65
Secretory diarrhoea
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
Solvent drag
Responsible for increased sodium and increased urea absorption in jejunum
67
Transporters in intestinal epithelial cells
NaKATPases - mediate transcellular Na+ movement on the basolateral membrane NaH exchanges Na/glucose symporters on the apical membrane
68
NK2Cl channel
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
Absorption and secretion hormones
Enteric: ACh and secretagogues Endocrine: Aldosterone Paracrine: Serotonin
70
Small intestine net absorption and secretion
Absorption of water, Na+, Cl-, K+ | Secretor of HCO3-
71
Hypovolemic shock
Decreased blood pressure due to water loss, heart rate rises to compensate BP and maintain cardiac output
72
Cholera toxin
Activates CFTR channel which increases Cl- secretion | Na+ and water follow
73
Oral rehydration therapy
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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