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Physiology Flashcards

1
Q

What is oral to arboral

A

Tube running from mouth to anus

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2
Q

Where does carbohydrate digestion start

A

Mouth

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3
Q

Where does protein digestion start

A

Stomach

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4
Q

Parts of small intestine

A

Duodenum, Jejunum and Ileum

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5
Q

Accessory structures of digestive tract

A

Salivary gland, pancreas, liver and gall bladder

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6
Q

General structure of digestive tract wall

A

Mucosa
Submucosa
Muscularis externa
Serosa

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7
Q

What does contraction of circular muscle cause

A

Narrow and long lumen

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8
Q

What are adjacent smooth muscle cells joined by

A

Gap junctions to allow spread of electrical signal

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9
Q

What drives slow wave electrical activity in the heart

A

Interstitial cells of Cajal

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10
Q

Where are Interstitial Cells of Cajal located (ICC)

A

Between circular and longitudinal muscle layer and submucosa

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11
Q

Relation between force and action potential

A

Force is related to number of action potentials discharg

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12
Q

What does slow wave amplitude reaching threshold depend on

A

Neuronal, hormonal and mechanical stimuli

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13
Q

What determines basic electrical rhythm (BER)

A

Slow wave activity

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14
Q

Basic electrical rhythm (BER) in stomach

A

3 slow waves per minutes

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15
Q

Basic electrical rhythm in small intestine

A

12 and 8 waves/min in duodenum and ileum respective

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16
Q

Basic electrical rhythm in large intestine

A

8 and 16 waves/min proximal and distal colon

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17
Q

Where does the basic electrical rhythm tend to push small intestinal contents towards

A

Aboral direction

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18
Q

Where does the basic electrical rhythm tend to push large intestinal contents towards

A

Oral direction

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19
Q

Where do sympathetic fibres synapse in GI tract

A

Preganglionic fibres (ACh) synapse in prevertebral ganglia (release NA). Postganglionic fibres (NA) innervate enteric neurones but also other structures

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20
Q

Effect of sympathetic on GI tract

A

Decrease motility, secretion, blood flow and absorption. Increase sphincter tone

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21
Q

Where do parasympathetic fibres synapse

A

Preganglionic fibres (ACh) synapse with enteric neurones within ENS

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22
Q

Effect of parasympathetic on GI tract

A

Increase motility, secretion, blood flow and absorption

Decrease sphincter tone

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23
Q

Where do the pelvic nerves supply to

A

Distal third of large intestine

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24
Q

Two plexus found in ENS

A

Myenteric plexus - Regulate motility and sphincters

Submucous plexus - Modulate epithelia and blood flow

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25
Q

Another name for Myenteric and Submucous plexus

A

Auerbach’s and Meissner’s plexus

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26
Q

What can sensory neurones in ENS sense

A

Chemo, thermo or mechanoceptors

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27
Q

Example of local reflex

A

Peristalsis

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28
Q

Example of short reflex

A

Intestino-intestinal reflex

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29
Q

Examples of long reflex

A

Gastroileal reflex - Wanting to use toilet after breakfast

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30
Q

How does peristalsis come about in the GI tract

A

Bolus is pushed from oral to aboral.
Circular muscles relax aborally (release of NO and VIP from inhibitory interneuron/descending motorneurone)
Circular muscle contacts orally (release of ACh and substance P from excitatory/ascending motorneurone)
Longitudinal muscles are exact opposite

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31
Q

Major factors influencing obesity

A

Genetics, environment: energy dense food diet, cars, lack of exercise, less overall energy expenditure How

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32
Q

Consequences of obesity

A

Stroke, respiratory disease (sleep apnea), heart disease, osteoarthritis, cancer, dementia, NAFLD

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33
Q

How does long term obesity reprogramme the brain

A

The brain views the extra fat as normal and dieting as a threat to survival

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34
Q

Neural centre responsible for energy balance and body weight

A

Hypothalamus, lesioning ventromedial hypothalamus causes obesity and lateral causes leanness

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35
Q

What is satiation

A

Feeling of fullness between meals

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36
Q

What is satiety

A

Period of time between meals

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37
Q

How are meal sized limited

A

Satiation signals increase during meal to limit size

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38
Q

Name some satiation signals

A

Cholecystokinin, Peptide YY, Glucagon like peptide 1, Oxyntomodulin, Obestatin

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39
Q

Cholecystokinin (CKK)

A

Secreted from enteroendocrine cells in duodenum and jejunum. Released in proportion to lipids and proteins, signals via sensory nerves to hindbrain (nucleus of solitary tract) and stimulates this

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40
Q

Peptide YY

A

Secrete from endocrine mucosal L-cells of GI tract, levels increase postprandially. Inhibit gastric motility, slow emptying and reduce food intake

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41
Q

Glucagon like peptide 1 (GLP-1)

A

Secrete from L-cells of GI tract in response to food ingestion, inhibit gastric emptying and reduce intake

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42
Q

Oxyntomodulin (OXM)

A

Secreted by Oxyntic cells of small intestine postprandially. Suppresses apetite.

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43
Q

Satiation signals product of pro-glucagon gene

A

Glucagon-like protein 1 (GLP-1) and Oxyntomodulin OXN

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44
Q

Obestatin

A

Released from cells lining stomach/small intestine, peptide produced from gene encoding ghrelin. Actions unclear

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45
Q

What is a hunger signal

A

Ghrelin

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46
Q

What secretes Ghrelin

A

Oxyntic or Parietal cells in stomach

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47
Q

When do Ghrelin levels increase

A

Preprandial - Before meals, fasting and hypoglycaemia

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48
Q

What hormones report fat status to brain

A

Leptin ( From fat cells) and Insulin (Pancreatic cells)

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49
Q

Where are high levels of Insulin/Leptin receptors found

A

Hypothalamus

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50
Q

What does deletion of leptin/insulin receptor lead to

A

Obesity and maybe hyperglycemic/ insulinemic

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51
Q

Therapy for obesity

A

Leptin therapy, daily sc injections @ 10% predicted serum concentration. Given for 48 months.

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52
Q

Over the counter medication for obesity

A

Orlistat or Alli in UK - Inhibit pancreatic lipase thereby reducing triglyceride absorption and reducing calorie intake. Side effects of cramping + diarrhoea. Need vitamin supplement and not effective long term

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53
Q

Therapy for obesity with substantial weight loss

A

Bariatric surgery: gastric band, removal of portion of stomach or re-route small intestine to small stomach pouch. Reverse insulin resistance in most cases

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54
Q

Where is brown adipose tissue found

A

Neck, clavicle and spinal cord

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55
Q

Key function of uncoupling protein 1 (UCP-1)

A

Fatty acid activated protein, short circuits proton gradient in mitochondria and accelerates fuel oxidation, producing heat

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56
Q

Example of motility patterns in GI tract

A

Segmentation
Colonic mass movement
Migrating Motor Complex
Tonic contractions

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57
Q

Where do high pressure tonic contractions occur

A

Sphincters, low pressure in stomach (storage function)

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58
Q

Sphincters of GI tract

A

Upper/Lower Oesophageal Sphincter, Pyloric Sphincter, Illeocecal valve, Internal and external sphincter

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59
Q

Which part of the stomach is responsible for grinding

A

Antrum - Grinding, Body - Storage

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60
Q

What stimulation cause relaxation as food enter stomach

A

Vagal stimulation

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61
Q

Direction of mixing in stomach

A

Peristaltic contractions move retropulsively, from pylorus to fundus during mixing. Opposite way during emptying.

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62
Q

What is chyme

A

Food + gastric secretions to produce semi-liquid

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63
Q

What factors determine stomach emptying

A

Gastric and duodenal factors

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64
Q

How do gastric factors determine emptying

A

Rate of emptying proportional to volume of chyme in stomach. Distension increases motility. Emptying facilitated by thick liquid chyme.

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65
Q

Duodenal factors and stomach emptying

A

Neuronal - Decrease antral activity by signals from intrinsic nerve plexuses and ANS
Hormonal - Release of enterogastrones (Secretin and CCK) inhibits stomach contraction

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66
Q

What stimuli can drive duodenal factors

A

Fat - Delay gastric emptying
Acid - Neutralization of gastric acid by bicarbonate secreted from pancreas so pancreatic enzymes function
Hypertonicity - Products of carbohydrate and protein digestion osmotically active and draw water into small intestine, reduced plasma volume
Distension

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67
Q

Secretions of oxyntic mucosa (fundus and body) in stomach

A

Parietal cells - HCl, Intrinsic factor, Gastroferrin
Enterochromaffin like cell - Histamine
Chief cell - Pepsinogen

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68
Q

Secretions of pyloric gland area (antrum) in stomach

A

D cells - Somatostatin

G cell - Gastrin

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69
Q

Function of HCl secreted from oxyntic mucosa

A

Activates pepsinogen to pepsin
Denatures protein
Kills microbes taken in with food

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70
Q

Function of Pepsinogen secreted from oxyntic mucosa

A

Inactive precursor of pepsin. Formed pepsin activates more pepsinogen (autocatalytic)

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71
Q

Function of intrinsic factor, Gastroferrin oxyntic mucosa

A

Bind vitamin B12 and Fe2+ respectively, help absorb

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72
Q

Function of Histamine secreted from oxyntic mucosa

A

Stimulate HCl secretion

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73
Q

Function of mucus secreted from oxyntic mucosa

A

Protective

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74
Q

Function of gastrin secreted pyloric gland area

A

Stimulate HCl secretion

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75
Q

Function of Somatostatin secreted pyloric gland area

A

Inhibit HCl secretion

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76
Q

Function mucous secretion from pyloric gland area

A

Protective

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77
Q

How is HCl secretion form gastric parietal cells regulated

A

Direct and Indirect pathway
Direct - ACh, Gastrin and Histamine stimulate Parietal cells triggering secretion of H+ into the lumen
Indirect - ACh and Gastrin stimulate Enterochromaffin-like Cells (ECL cells) to secrete Histamine which acts on parietal cells causing H+ entry into lumen

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78
Q

What stimuli acts on the PLC-IP3 signalling pathway

A

Gastrin and ACh

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79
Q

What stimuli acts on the cAMP-PKA signalling pathway

A

Histamine (Secretory) and Somatostatin and Prostaglandin (Inhibitory)

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80
Q

Resting vs activated state of Parietal cells

A

In resting state of parietal cells, H+/K+ ATPase is within cytoplasmic tubulovescicles. Stimulated state of parietal cells, H+/K+ ATPase traffics to apical membrane (Canaliculus) taking residence in extended microvilli

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81
Q

3 phases of gastric acid secretion

A

Cephalic phase - Before food reaches stomach, driven by CNS and Vagus nerve
Gastric phase - Food is in stomach, physical and chemical mechanism
Intestinal phase - Food has left stomach
Neuronal and hormonal mechanisms

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82
Q

What can cause vagal activation to initiate gastric phase

A

Sight, smell, taste of food, chewing and swallowing

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83
Q

Eventual effect of enteric neurone stimulation by vagus nerve

A

ACh direct release activating Parietal cells
Release of GRP causing release of Gastrin from G cells into systemic circulation - Activates Parietal cell
Release of Histamine from Enterochromaffic-like cells (ECL) that activate local parietal cells
Inhibit Somatostatin decretion by D cells

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84
Q

3 phases of gastric acid inhibition

A

Cephalic phase - Cessation of eating and emptying of stomach leads to vagal activity cessation
Gastric phase - Food exiting stomach leads to a fall in Antrum pH.. This stimulates release of Somatostatin from D cells, inhibiting G cells Gastrin release. Prostaglandin E2 acts locally to reduce Histamine and Gastrin mediated HCl secretion
Intestinal phase - Neuronal and hormonal factors reducing gastric motility reduce gastric secretions

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85
Q

How is the mucosa protected from HCl and Pepsin

A

Locally produced prostaglandins -
Reduce acid secretion
Increase mucus and bicarbonate secretion
Increase mucosal blood flow

86
Q

Pathogen causing infection in gastric antrum, ulcer form

A

Helicobacter pylori

87
Q

How does Helicobacter pylori cause ulcers

A

It’s present in the mucus layer. It secretes agents that cause persistent inflammation weakening mucosal barrier until it eventually breaks down. This leaves the submucosa subject to attack by HCl and Pepsin

88
Q

How do Non-Steroidal Anti-Inflammatory Drugs cause peptic ulcers

A

NSAID inhibit cyclo-oxygenase, reducing prostaglandin formation. This eventually leads to the breakdown of the mucus membrane, exposing the mucosa to HCl and Pepsin. This triggers gastric ulcers and cause bleeding

89
Q

What can acid-reducing drugs be used for

A

Peptic ulcers, gastro-oesophageal reflux disease (GORD), acid hypersecretion and Cushings ulcers

90
Q

What is Zollinger-Ellison syndrome

A

Gastrin-producing tumour or hyperplasia of Islet cells of Pancreas. Leads to peptic ulcers

91
Q

What are Cushing’s ulcers

A

Peptic ulcers due to raised intracranial pressure which increases vagal tone.

92
Q

How do proton-pump inhibitors work

A

Inhibit H+/K+-dependant ATPase (proton pump)

93
Q

Where are proton-pump inhibitors activated

A

In strong acidic environment such as the Canaliculus

94
Q

Proton-pump inhibitor with longest plasma half life

A

Tenatoprazole

95
Q

Which HCl secretion receptor antagonists are not used clinically

A

Muscarinic ACh receptors antagonists (obsolete) and Gastrin Receptor Antagonists (used in experiments)

96
Q

What is used in combination with antibiotics and Histamine H2 antagonist (Ranitidine) to promote eradication of H.pylori and ulcer healing

A

Bismuth chelate, called Bismuth therapy

97
Q

How is Bismuth Chelate orally administered

A

In combination with Ranitidine

98
Q

What is succus entericus

A

Intestinal juice, clear to pale yellow in colour

99
Q

How is surface area increased in the small intestine

A

Circular folds (valves of Kerckring), villi and microvilli

100
Q

Secretions from small intestine

A

Gastrin - G cells of gastric antrum and duodenum
Cholecystokinin (CCK) - I cells of duodenum, jejunum
Secretin - S cells of duodenum
Motilin - M cells of duodenum, jejunum
Glucagon-like insulinotropic peptide (GIP) or Gastric Inhibitory Peptide - Incretin form K cells of duodenum and jejunum
Glucagon-like Peptide-1 (GLP1) - Incretin from L cells gut
Ghrelin - Gr cells of gastric antrum, SI and elsewhere

101
Q

What receptors do secretion from small intestine work

A

G-Protein Coupled Receptors

102
Q

What are Incretins

A

Incretins act upon Beta- cells of pancreas in feed-forward mechanism to stimulate release of Insulin

103
Q

What does the succus entericus contain

A

Mucus (protection/lubrication from goblet cells), aqueous salt (for enzymatic digestion, crypts of Lieberkuhn)

104
Q

Does the succus entericus have digestive juice

A

No

105
Q

Does fasting increase or decrease succus entericus

A

Decrease

106
Q

How does Na and Cl get into the lumen

A

Na/K/2Cl co transporter moves Cl into the cell along with Na and K. This Cl moves into the lumen via Cystic Fibrosis Transmembrane Conductance Regular (CFTR) which is a Ca channel. Na moves paracellularly along with water

107
Q

How does aboral movement in the small intestine occur

A

Duodenum has frequent segmentation contractions (12/min), Ileum has fewer (9/min). Net movement aboral

108
Q

What is segmentation in small intestine

A

Alternating contraction and relaxation of segments of circular muscle causing chopping of chyme back and forth. Initiated by small intestine pacemaker causing the basal electric rhythm

109
Q

What is the migrating motor complex

A

Distinct pattern of electrochemical activity 90-120 mins between meals which helps clear debris and mucus

110
Q

What triggers migrating motor complex

A

Motilin triggers this, Gastrin and CCK suppresses

111
Q

Exocrine pancreatic secretions

A

Digestive enzymes (Acinar cells), aqueous NaHCO3- solution (Duct cells) into pancreatic duct

112
Q

Function of Bicarbonate in the duodenum

A

Neutralize acidic chyme entering the duodenum

113
Q

Why do patients with cystic fibrosis have reduced pancreatic fluid secretion

A

Pancreatic duct cells use a Cystic FIbrosis Transmembrane Conductance Receptor (CFTR) to channel Cl into the lumen. This Cl comes back into the cell via Cl/HCO3- antiport. In cystic fibrosis, CFTR doesn’t function properly leading to less HCO3- production

114
Q

Why are acinar cell proteases stored in zymogen granule

A

These would digest digest cells in the pancreas if released before the duodenum. Thus, they are released in response to elevated Ca2+

115
Q

What activates pancreatic proteases

A

Enterokinase (Mucosal cells) in duodenum

116
Q

3 phases of intestinal secretion

A

Cephalic - Vagal stimulation of Acinar cells
Gastric - Gastric distention evokes a vasovagal reflex resulting in parasympathetic stimulation of acinar and duct cells
Intestinal - Neutralizes and digests

117
Q

Steps in neutralizing part of Intestinal control of pancreatic secretion

A

Acid in duodenal lumen
Increase Secretin release from S cells
Stimulation of pancreatic duct cells
Increase secretion of aqueous NaHCO3

118
Q

Steps in digesting part of Intestinal control of pancreatic secretion

A

Fat and protein in duodenal lumen
Increase Cholecystokinein from I cells
Stimulation of pancreatic acinar cells
Increase secretion of digestive enzymes

119
Q

Luminal vs membrane digestion

A

Luminal - Mediated by pancreatic enzymes secreted into the duodenum
Membrane - Enzymes situated at brush border of epithelial cells

120
Q

What is assimilation in GI tract

A

Process of digestion + absorption

121
Q

Amylose vs Amylopectin vs Glycogen

A

Amylose - alpha-1,4 linkage; branched chain
Amylopectin - alpha-1.4 and a-1,6 linkage; branched chain
Glycogen - Same as amylopectin but more branched

122
Q

What forms are carbohydrates absorbed

A

As monosaccharides; glucose, galactose and fructose

123
Q

What helps covert starch to oligosaccharides

A

Alpha-Amylase (From pancreas and salivary gland) in the lumen (intraluminal hydrolysis)

124
Q

What converts oligosaccharides to monosaccharides

A

4 oligosaccharidases - Lactase, maltase, sucrase-isomaltase at brush border (membrane digestion)

125
Q

alpha-Amylase can break a-1,4 linkages. Why can’t it produce glucose then?

A

a-Amylase can break internal a-1,4 linkages, not terminal ones. It also can’t cleave a-1,6 linkage at branch points or a-1,4 linkage adjacent to branch point

126
Q

Why is loss of lactase significant

A

Lactose - Glucose + Galactose can only be mediated by Lactase. Loss of lactase makes you lactose intolerant

127
Q

What can cleave terminal a-1,4 glycosidic bonds

A

Oligosaccharides and not a-Amylase

128
Q

What is sucrase responsible for

A

Sucrose - Glucose + Fructose

129
Q

Max length of monomers Maltase can degrade in oligomers

A

Maltase can degrade a-1,4 linkages in straight chain oligomers upto nine monomers in length

130
Q

Only enzyme split branching a-1,6 linkage in a-dextrins

A

Isomaltase

131
Q

Rate limiting for oligosaccharides

A

Lactase - Rate of hydrolysis is rate limiting in assimilation
For maltase, sucrase and isomaltase it is subsequent transport of released monomer

132
Q

What causes lactose intolerance

A

Lactase insufficiency, can’t digest lactose

133
Q

What can cause lactose intolerance

A

Primary lactase deficiency - Lack of lactase persistence (LP) allele, most common cause
Congenital lactase deficiency - Rare autosomal recessive disease, can’t digest lactose from birth
Secondary lactase deficiency - Acquired due to damage/infection of proximal small intestine

134
Q

Where do final products of carbohydrate digestion enter and exit enterocytes

A

Apical and basolateral membrane respectively

135
Q

What helps absorb glucose and galactose

A

Secondary active transport mediated by SGLT 1

136
Q

What helps absorb fructose

A

Facilitated diffusion by GLUT5

137
Q

How do monosaccharides exit the enterocyte

A

Facilitated diffusion by GLUT2

138
Q

How does SGLT - sodium glucose co-transporter work

A

2Na+ bind to the SGLT1. This increases affinity for glucose. Glucose binds; this along with Na+ translocate from extracellular to intracellular. 2Na+ dissociate and affinity for glucose falls, causing its dissociation

139
Q

How are proteins digested

A

Proteins - Oligopeptides - Amino acids

140
Q

Protein digestion in stomach

A

HCl starts to denature proteins. Pepsin cleaves proteins to peptides. It is an endopeptidase - preference for bonds between aromatic and larger neutral amino acids.

141
Q

Is pepsin essential for protein digestion?

A

No

142
Q

5 pancreatic proteases (proenzymes)

A

Trypsin, chymotrypsin, elastase, procarboxypeptidase A and procarboxypeptidase B

143
Q

Which enzymes have oligopeptides as end product

A

Trypsin, chymotrypsin and elastase (Endopeptidase)

144
Q

Which enzymes have single amino acid end products

A

Procarboxypeptidase A and B (Exopeptidase)

145
Q

Where are additional peptidases present

A

Brush border and cytoplasm of enterocytes

146
Q

How are amino acids absorbed

A

Brush border cells - 7 mechanisms, 5 are Na+ dependant co-transporters, 2 are Na+ independant
Basolateral membrane - 5 mechanisms, 3 mediates efflux of amino acids and 2 mediate influx

147
Q

How are bi, tri and tetrapeptides absorbed

A

H+-dependant mechanisms at brush border (co-transport). These are further hydrolysed to amino acids within enterocytes.

148
Q

Exit of amino acids via basolateral membrane is via Na+ independent transporters

A

True

149
Q

What is leptin

A

Satiety hormone released by fat cells, sends signals to the brain that tell us when to stop eating

150
Q

How doe excess fat impede satiety signals

A

Amount of leptin in the body depends on the number of fat cells. Higher the number of fat cells, more leptin in the body. However, the brain stops responding to these hormones causing them to overeat

151
Q

What waist circumference puts you at risk of heart disease and type 2 diabetes

A

Men > 40 inches and women > 35 inches

152
Q

Longitudinal smooth muscle layer in caecum and colon is divided into three strands called

A

Taeniae coli

153
Q

What type of muscles surround the internal anal sphincter

A

Internal anal sphincter is smooth muscles, surrounded by skeletal muscles of external anal sphincter

154
Q

Sac like bulges in the large intestine are called

A

Haustra

155
Q

Function of caecum and appendix

A

None in humans but cellulose metabolism in others

156
Q

What permits entry into the caecum

A

Ileocaecal valve via gastroileal reflex

157
Q

How does the gastroileal reflex work

A

Ileocaecal valve has a positive resting pressure. It relaxes in response to distention in duodenum. It contracts in response to distention of ascending colon

158
Q

What has potential to cause appendicitis

A

Faecalith - Hard stony mass of faeces in intestinal tract, may block appendiceal orifice

159
Q

Primary functions of colon

A

Absorption - Na, Cl and water to condense ileocaecal material
Absorption - Carbohydrates not absorbed by small intestine are broken into fatty acids by colonic flora. This farry acids are absorbed
Resovoir - Storage of colonic contents
Periodic elimination of faeces

160
Q

Does the colon absorb macronutrients

A

Nil except short chain fatty acids formed by colonic flora conversion of carbohydrates not absorbed in small intestine

161
Q

Does colon mucosa have villi

A

No but it has colonic folds, crypts and microvilli that increase surface area

162
Q

What helps with electrolyte absorption in colon

A

Colonocytes which are surface epithelial cells in colon

163
Q

How does water get absorbed into colon

A

Absorption of electrolytes drives absorption of water via osmosis

164
Q

What colonic cells mediate ion secretion

A

Crypt cells

165
Q

Function of goblet cells in colon

A

Secrete mucus containing glycosaminoglycans and trefoil proteins involved in host defence, stabilizing mucus layer and healing epithelium

166
Q

What is secretory diarrhoea

A

Diarrhoea when electrolyte absorption is impaired

167
Q

Significant loss of K in faeces may be due to

A

Secretory diarrhoea

168
Q

What causes haustration

A

Alternating contractions of circular muscles with low frequency contributing to long transit time

169
Q

What direction of movement does haustration cause

A

Orad - Towards the mouth

170
Q

Significance of haustration

A

Mixes contents and allows time for fluid and electrolyte reabsorption

171
Q

What patterns of motiity exist in large intestine

A

Haustration, peristaltic propulsive movement, defaecation

172
Q

What is mass movement in the colon

A

Simultaneous contractions of large sections circular muscles in ascending and transverse colon that drives faeces into distal regions

173
Q

What triggers mass movement or peristaltic propulsive movement

A

Gastrocolic response typically involving gastrin and extrinsic nerve plexus

174
Q

Does mass or peristaltic propulsive movement occur in the distal colon

A

Yes to propel faeces into the rectum and trigger the defaecation reflex in response to stretch

175
Q

Explain the defaecation reflex

A

If the passive distention of the rectum is large enough, it triggers an active contraction of rectal smooth muscles. This passive rectal distention also triggers the smooth internal anal sphincter muscles to relax (rectosphincteric reflex). If defaecatio isn’t desired, skeletal muscles of external anal sphincter contract involuntarily

176
Q

Main nerve of perineum that carries motor supply to external anal sphincter

A

Pudendal nerve

177
Q

Contraction of smooth muscle in sigmoid colon and rectum does what to internal anal sphincter

A

Relaxes it

178
Q

How is defaecation assisted

A

Straightening of anorectal angle, abdominal skeletal muscle contract and expiration against closed glottis

179
Q

What is defective in Hirschsprung disease

A

Rectosphincteric reflex

180
Q

What is the rectosphincteric reflex

A

Passive rectal distention if large enough can trigger smooth muscles of internal anal sphincter to relax

181
Q

Function of colonic flora

A

Increase intestinal immunity by competing with pathogens, promote motility, maintain mucosal integrity, synthesize vitamin K2 and free fatty acids (from carbohydrates), activate some drugs

182
Q

What is flatus

A

Intestinal gas

183
Q

What is a burp or belch known as

A

Eructation

184
Q

Causes of constipation

A

Ignoring or suppressing urge to defaecate, decreased colonic motility (age, improper diet, drugs), obstruction of faecal movement (cancer), paralytic ileus following abdominal surgery, impariment of motility/defaecation reflex (Hirschprung disease, absence of section of enteric nervous system)

185
Q

Symptoms of constipation

A

Headache, abdominal discomfort, loss of appetite, general malasie

186
Q

What causes feeling of malaise in constipation

A

Prolonged distention of large intestine not toxins absorbed from retained fecal matter

187
Q

What drives water absorption

A

Passive process driven by transport of solues (Na+)

188
Q

Where is the following transporter found -
Na+/glucose co-transport
Na+/amino acid co-transport

A

Throughout small intestine and most important in postprandial period
Found in colon in neonates

189
Q

Where are the following transported found -

Na+/H+ exchange

A

Duodenum and jejunum, stimulated by luminal HCO3-

190
Q

Where are the following transported found -

Parallel Na+/H+ and Cl-/HCO3- exchange

A

Ileum and colon most important in interdigestive period

191
Q

Where are the following transporters found -

Epithelial Na+ channels

A

Colon (distal particularly) and regulated by aldosterone

192
Q

Which Na channel is hormonal regulated

A

Epithelial Na+ channels found in distal colon, by Aldosterone

193
Q

Mechanism of Na+/glucose and Na+/amino acid co-transport

A

Secondary active transport, 2 Na+ move into the cell along with 1 glucose or 1 amino acid

194
Q

What generates a transepithelial potential (Vte)

A

Overall transport of Na in which lumen is negative. This drives parallel absorption of Cl-

195
Q

Where are NHE1 present

A

In basolateral membranes of entercoctyes whereas NHE2 and NHE3 are found at the apical surface of the enterocyte membrane

196
Q

What exchangers is known as cellular pH housekeeper

A

NHE1 at basolateral membrane of enterocytes

197
Q

What stimulates Na exchange at apical membrane in jejunum

A

Alkaline environment of lumen due to bicarbonate from pancreas

198
Q

What does cAMP, cGMP and Ca2+ regulate in Na absorption

A

Reduce NaCl absorption by Na/H and Cl/HCO3 exchange in parallel, causing diarrhoea

199
Q

How does Aldosterone regulate Na absorption

A

Opens Epithelial Na+ channels (ENaC), inserts more ENaC into membrane from intracellular vesicle pool and increase synthesis of ENaC and Na/K ATPase

200
Q

Passive Cl- absorption

A

Electrogenic movement of Na creates a negative potential in the lumen which allows passive movement of Na+ trans or paracellularly

201
Q

Non-electrogenic methods of Cl- absorption

A

Cl-HCO3 exchanger (Ileum and colon) and parallel Na/H and Cl/HCO3 exchange (Ileum and proximal colon)

202
Q

Cellular mechanism of Cl- secretion

A

Low intracellualr Na drives inward movement of Na/Cl and K via Na/K/2Cl cotransporter. Intracellular Cl increases providing an electrochemical gradient for Cl to exit cell via CFTR on apical membrane

203
Q

What activates CFTR mediated secretion of Cl

A

Bacterial exotoxins
Hormones and neurotransmitters
Immune cell products
Laxatives

204
Q

Secondary messengers that activate CFTR

A

cAMP, cGMP and Ca2+

205
Q

What can secretion of Cl-via apical CFTR cause

A

Secretory diarrhoea

206
Q

How can diarrhoea cause metabolic acidosis

A

Due to HCO3- loss

207
Q

Causes of diarrhoea

A

Impaired absorption - Congenital, inflammation, infection, excess bile in colon
Excessive secretion
Non-absorbale or poorly absorbale solute in intestinal luman - Lactase deficiency
Hypermotility- Not enough time to absorb water

208
Q

How can Cholera cause diarrhoea

A

Cholera toxin enters enterocyte and inhibits GTPase activity. This increases activity of adenylate cyclase. Increased concentration of cAMP stimulates CFTR. CFTR promotes secretion of Cl- with Na and water follows causing diarrhoea

209
Q

Why do sorbitol sweets cause diarrhoea

A

Sorbitol isnt well absorbed and hence causes diarrheoa

210
Q

How do oral rehydration salts work

A

Oral rehydration salts have glucose and sodium. When 2 sodium bind to SGLT1, affinity for glucose increases. These are transported intracellulary. 2Na dissociate and affinity for glucose decreases causing its dissociation. Water follows Na into the cell

211
Q

Action of opiods on alimentary tract

A

Inhibition of enteric neurones
Decrease peristalsis, increase segmentation
Increase fluid absorption
Constriction of pyloric, ileocaecal and anal sphincters
Increase tone of large intestine

212
Q

Major opiods in diarrhoea

A

Codeine - Converted to low dose morphine in liver
Diphenoxylate - Low CNS penetration, low solubility in water (decrease abuse potential)
Loperamide - Low CNS penetration, low solubility, undergoes enterohepatic cycling

GI (32 decks)

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