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Gastrointestinal Physiology Flashcards

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1
Q

What are the layers of muscle of the gi tract

A

Outer longitudinal
Middle circular
Inner submucosal

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2
Q

Where does the enteric nervous system sit in relation to gi muscles

A

Myenteric plexus between the circular and longitudinal layers
Submucosal plexus between submucosal and circular layers

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3
Q

What is the basal electrical rhythm of the gi tract.
Where does it effect
How is it controlled and transmitted

A

Effects gi tract beneath oesophagus.
Spontaneous variation of transmembrane potential from -70 to -40 in smooth muscle cells. On reaching -40 depolarise and contract. Determines maximum rate contraction can occur.
Controlled by interstitial cells of cajal
Transmitted through gap junctions.

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4
Q

What is the term for how the smooth muscle of the gi tract contracts in coordination joined by gap junctions

A

Syncytium l

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5
Q

What alters the frequency and amplitude of the basal electrical rhythm?

A

Location in the bowel
Modulation by the nervous system
Hormonal control
Drugs

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6
Q

What is the effect of acetylcholine on basal electrical rhythm of the gi tract
Adrenaline?

A

Ach Raises cell membrane potential stimulating contraction
Adrenaline hyperpolarises inhibiting contraction

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7
Q

What is peristalsis
Where does it occur
Type of reflex

A

Reflex response to gut wall stretch. When wall stretched causes a contraction behind that point and a relaxation in front.
Occurs throughout gi tract
Polysynaptic reflex - 2 interneurones, one triggering efferent contraction, the other relaxation

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8
Q

What areas of gi tract motility involve the somatic nervous system

A

Swallowing
External anal sphincter control (defication)

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9
Q

Where is swallowing controlled

A

Swallowing centre in the reticular system of medulla and lower pons

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10
Q

Inputs to the swallowing centre

A

Trigeminal
Glossopharyngeal
Superior laryngeal
Recurrent laryngeal
Vagus

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11
Q

Motor output from swallowing centre

A

Vagus

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12
Q

Stages of swallowing

A

Oral
Pharyngeal
Oesophageal

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13
Q

Events of oral stage of swallowing

A

Voluntary
Masticated food pushed into pharynx by upward backward pressure of tongue against hard palate

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14
Q

Events of pharyngeal stage of swallowing

A

Pressure detected on tonsillar pillars
Signal transmitted to swallowing centre
Soft palate elevates closing nasopharynx
Respiration halted
Vocal cords close and larynx moves anterior and cephalad with epiglottis covering glottis
upper oesophageal sphincter opens
Superior constrictor muscles of pharynx propel bolus into oesophagus

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15
Q

Events of oesophageal phase of swallowing

A

Primary peristaltic wave from pharynx moves bolus down oesophagus to lower oesophageal sphincter
Los relaxes allowing bolus into stomach.

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16
Q

What is the parasympathetic autonomic nerve supply to the gi tract
Effects

A

Vagus and sacral fibres
Increase motility, tone, force of contraction and gastric emptying, increase gastrin, salivary production and pancreatic/bile secretions

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17
Q

What is the sympathetic supply to the bowel
Effects

A

Spinal nerves via coeliac, mesentieric and pelvic ganglia
Increase salivary production, decrease motility and gastric emptying, vasoconstriction.

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18
Q

Length of oesophagus

A

30cm

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19
Q

What is the musculature of the upper oesophagus?
How does it differ from rest of gi tract

A

Upper 6cm striated skeletal with no autonomic activity

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20
Q

What forms the upper oesophageal sphincter
Innervation
Resting state

A

Cricopharyngeal and pharyngeal constrictor muscles
Vagus
Tonic contraction;

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21
Q

What forms the lower oesophageal sphincter

A

Functional zone of increased intralumnal pressure in distal 4cm of oesophagus from semicircular oesophageal muscle fibres on left and gastric sling fibres on right. Also crural fibres from diaphragm.

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22
Q

What is the barrier pressure of the lower oesophageal sphincter?

A

Pressure difference between los and intragastric pressure
Usually 15-25mmHg

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23
Q

What helps prevent reflux when intragastric pressure is raised?

A

Acute angle of los and encircling diaphragm creating a flutter valve

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24
Q

Types of muscle action in stomach?

A

When food enters stomach proximal stomach relaxes minimising increases in intergastric pressure.
When fed however, proximal stomach slowly contracts in sustained manner to fascilitate gastric emptying.
In antrum rhythmic contractions mix food with stomach contents (acid, pepsin etc) grinding it to chyme
Between meals strong synchronised contractions occur in bursts to open pyloric sphincter to eject indigestible material out of stomach.

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25
How does the stomach empty?
Pylorus doesn’t fully close so small volumes of chyme squirt out in each contraction
26
What reduces stomach emptying
Pain Anxiety Stress Medications Sns
27
What occurs on distension if the stomach?
Stimulation of vagus Increased acid secretion Increased peristaltic activity Increased gastric emptying
28
What happens if the stomach empties too quickly
Activation of duodena receptors (stretch, acid, osmolarity or fatty acid concentration) activating reflex to decrease gastric emptying
29
What’s is the implication of the decrease in gastric emptying caused by increased duodenal fatty or amino acid concentrations
Carb meals leave stomach fastest Then protein meals Then fatty meals the slowest
30
Length of small bowel
5m
31
What key vitamin is produced by large bowel bacteria
Vit k
32
Functions of large bowel
Water absorption Faeces storage Vitamin production Electrolyte absorption
33
How much saliva is produced per day
0.5 to 1.5L
34
Factors that decrease los tone
Antimuscarinics Dopamine Cholecystokinin Alpha blockade Beta stimulation Secretin Prostaglandin E1 Thiopental Alcohol
35
Functions of saliva
Lubrication Solvent for taste Buffering of irritants Antimicrobial Digestion of starch by amylase Digestion of fats by lipase
36
Volume of gastric juice secretions Ph
1.5 - 2.5L per day Ph 1 to 3.5
37
Function of gastric secretions
Protein digestion Activation of. Pepsinogen to pepsin Optimal ph for pepsin Improve solubility of dietary iron Antimicrobial Stimulate biliary and pancreatic secretions.
38
Glandular cell types in stomach - what do they release
Mucus - mucus and bicarb Parietal - hydrochloric acid and intrinsic factor Chief - pepsinogens and gastric lipase G - gastrin D - somatostatin Enterochromaffin like cells - histamine
39
How is gastric acid secreted Other ion changes in cell
From parietal cells via HKATPase pumps H out for k in H created in cells from breakdown of h2CO3 - bicarbonate then excreted into plasma Chloride enters cell from plasma and secreted along with the h
40
What stimulates gastric acid secretion via what receptors
Gastrin - gastrin receptor Ach - M1 muscarinic Histamine - H2
41
What is the effect of gastric acid production on bicarb and co2
Bicarb tide released at time of peak acid production causing alkali urine Co2 consumption high in stomach giving a negative respiratory quotient!
42
Enzyme pathway for breaking down proteins
Pepsinogen released by chief cells converted to pepsin in acid conditions Pepsinogen stored in secretory granules and released by same triggers for acid release
43
What is gastric mucus Release?
Glycoproteins, water, electrolytes and sloughed cells Released from mucus cells stimulated by vagus, gastrin, prostaglandins
44
What is secreted along with acid from parietal cells? What is it? Function
Intrinsic factor Glycoprotein B12 absorption in terminal ilium
45
Phases of gastric acid secretion
Cephalic - anticipation of food causes vagal stimulation to stomach increasing mobility, gastin and histamine release with increased gastric acid Gastric - stomach distension and luminal peptides promote local and vagal reflexes increasing gastrin secretion and thus acid. When pH reaches 2 acid secretion stopped by somatostatin Intestinal - chyme reaches duodenum feedback mechanisms including somatostatin inhibit gastric secretions. Stimulation from other factors also decreases.
46
How much pancreatic juice is produced per day? What does it contain
1500ml Proenzymes - trypsinogen (to trypsin), proelastase (to elastin) Enzymes - amylase, lipase Alkali
47
What stimulates pancreatic secretions? Where are they released from? Trigger?
Secretin (s cells of upper small intestine, released due to acid) - causes bicarb rich pancreatic fluid Cholecystokinin (duodenal mucosa, released due to amino acids, peptides and fat) - triggers pancreatic enzyme release Acetylcholine - vagus nerve - triggers Pancreatic enzyme release
48
Where are pancreatic enzymes stored
Zymogen granules
49
How much bile is produced per day? How much is stored in gallbladder?
500-1000ml 30-60ml
50
Composition of bile
Bile salts Pigments Inorganic compounds
51
What is the stored amount of bile salts? How is this managed
3.5g Recycled via enterohepatic circulation twice per meal!
52
Factors that control bile release? Location of release and trigger
Secretin - s cells in proximal small bowel, triggered by acid - create watery bicarb rich bile Cholecystokinin - duodenal mucosa in response to amino acids, fats and peptides, - stimulates gall bladder contraction and sphincter of oddi relaxation Acetylcholine - vagus nerve - gallbladder contraction Bile salts - from bile, if increased in portal circulation trigger increased bile secretion
53
Carbohydrate breakdown pathways to absorbable monomers
Lactose - [lactase] - galactose and glucose Starch - [amylase] - alpha dextrins, maltose - [alpha dextrinase, maltase] - glucose Sucrose - [sucrase] - fructose and glucose
54
How are carbohydrates absorbed
Small intestine only Galactose and glucose through SGLT-1 (sodium dependant glucose co- transporter-1) on luminal membrane then through GLUT-2 to plasma Fructose through GLUT-5 on luminal border and again into plasma
55
Maximal carbohydrate absorption rate
Glucose 100g/hr Fructose 50g/hr
56
Why can cellulose not be broken down
Beta glucose linkages
57
Breakdown of proteins in gi tract
Stomach = Protein - [pepsin] - polypeptides Duodenum = polypeptides [exopeptidase, trypsin, chemotrypsin, elastase] - free amino acids and mono/di/tripeptides Duodenum and epithelial cells = mono/di/tripeptides - [peptidases] - free amino acids
58
Absorption of amino acids and short peptides in gi tract Efficiency
Free amino acids in transporter with na Short peptides through pept-1 with hydrogen ions. Very efficient <5% protein escapes absorption
59
Absorption of lipids in gi tract
Triglycerides - [lipase] - free fatty acids and monoglycerides Fat soluble vitamins + fatty acids + cholesterol - [bile salts] - micelle Micelle fuses with epithelial cells leading to absorption and either fatty acids into portal vein or reform triglycerides then into chylomicrons into lymph
60
How much water per day is absorpbed in the intestine How much is lost in faeces Where is most water reabsorbed
10l 200ml Most in the small intestine, around 1.5 litres in the large
61
How much Na is absorbed in the intestine each day? Where does this come from?
35g Most reabsorbed from secretion, only about 5-8g from diet
62
Effect of aldosterone on gi tract
Increases na channels in epithelium and basolateral nak pumps resulting in increased sodium and thus increased water absorption.
63
How are fat soluble vitamins absorbed in the gi tract
In micelles with bile salts and fat
64
Examples of water soluble vitamins
Vit c Folic acid B12
65
How are Vit c and folic acid absorbed in the bowel
Active transport Vit c - passive transport Folic acid - na independent transport
66
How is Vit b12 absorbed
Intrinsic factor released in stomach then active sodium independent transport (Pinocytosis) in terminal iliu
67
How and where is iron absorbed in the bowel How much of dietary iron is absorbed
Pinocytosis in duodenum and jejunum 3-6%
68
How and where is calcium absorbed Controlling factors How much absorbed
Duodenum, active transport facilitated by proteins Regulated by 1.25 dihydroxycholcalciferol 30-80%
69
Where and how is magnesium absorbed in the bowel
Small and large active and passive transport, facilitated by protein
70
What is vomiting
Forceful expulsion of contents of the upper gi tract
71
Where is vomiting controlled
The vomiting centre - a number of interconnected areas in the brainstem
72
Phases of vomiting with description
Pre-ejection - nausea, sympathetic upregulation, reduced gastric acid secretion, reduced salivation, stomach relaxes, peristalsis of small bowel reverses, retrograde giant contraction begins in mid small bowel pushing contents back into stomach, deep inspriatory breath, closure of glottis Ejection - retching, contraction of abdominal wall and diaphragm producing increased abdominal pressure, perioesophageal diaphragm relaxes opening los, contents of stomach expelled from mouth. Respiration temporerally ceases to protect airway.
73
Areas involved in nausea and vomiting and links.
Chemoreceptor trigger zone activates nucleus tractus solitarius, and both CTZ and NTS activate brainstem vomiting centre triggering vomiting response.
74
Triggers to vomiting
Pain/ distress - higher centres - vomiting centre Motion/vertigo - labyrinth organs - cerebellum - vomiting centre Drugs and hormones - chemoreceptor trigger zone - vomiting centre Gastric irritants - vagus nerve - chemoreceptor trigger zone + nucleus tractus solitarius - vomiting center Pharyngeal irritation - glossopharyngeal nerve - nucleus tractus solitarius - vomiting centre

Primary Physiology (15 decks)

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