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Primary Physiology > Gastrointestinal Physiology > Flashcards

Gastrointestinal Physiology Flashcards

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
Q

How does the stomach empty?

A

Pylorus doesn’t fully close so small volumes of chyme squirt out in each contraction

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26
Q

What reduces stomach emptying

A

Pain
Anxiety
Stress
Medications
Sns

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27
Q

What occurs on distension if the stomach?

A

Stimulation of vagus
Increased acid secretion
Increased peristaltic activity
Increased gastric emptying

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28
Q

What happens if the stomach empties too quickly

A

Activation of duodena receptors (stretch, acid, osmolarity or fatty acid concentration) activating reflex to decrease gastric emptying

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29
Q

What’s is the implication of the decrease in gastric emptying caused by increased duodenal fatty or amino acid concentrations

A

Carb meals leave stomach fastest
Then protein meals
Then fatty meals the slowest

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30
Q

Length of small bowel

A

5m

31
Q

What key vitamin is produced by large bowel bacteria

A

Vit k

32
Q

Functions of large bowel

A

Water absorption
Faeces storage
Vitamin production
Electrolyte absorption

33
Q

How much saliva is produced per day

A

0.5 to 1.5L

34
Q

Factors that decrease los tone

A

Antimuscarinics
Dopamine
Cholecystokinin
Alpha blockade
Beta stimulation
Secretin
Prostaglandin E1
Thiopental
Alcohol

35
Q

Functions of saliva

A

Lubrication
Solvent for taste
Buffering of irritants
Antimicrobial
Digestion of starch by amylase
Digestion of fats by lipase

36
Q

Volume of gastric juice secretions
Ph

A

1.5 - 2.5L per day
Ph 1 to 3.5

37
Q

Function of gastric secretions

A

Protein digestion
Activation of. Pepsinogen to pepsin
Optimal ph for pepsin
Improve solubility of dietary iron
Antimicrobial
Stimulate biliary and pancreatic secretions.

38
Q

Glandular cell types in stomach - what do they release

A

Mucus - mucus and bicarb
Parietal - hydrochloric acid and intrinsic factor
Chief - pepsinogens and gastric lipase
G - gastrin
D - somatostatin
Enterochromaffin like cells - histamine

39
Q

How is gastric acid secreted
Other ion changes in cell

A

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
Q

What stimulates gastric acid secretion via what receptors

A

Gastrin - gastrin receptor
Ach - M1 muscarinic
Histamine - H2

41
Q

What is the effect of gastric acid production on bicarb and co2

A

Bicarb tide released at time of peak acid production causing alkali urine
Co2 consumption high in stomach giving a negative respiratory quotient!

42
Q

Enzyme pathway for breaking down proteins

A

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
Q

What is gastric mucus
Release?

A

Glycoproteins, water, electrolytes and sloughed cells
Released from mucus cells stimulated by vagus, gastrin, prostaglandins

44
Q

What is secreted along with acid from parietal cells? What is it? Function

A

Intrinsic factor
Glycoprotein
B12 absorption in terminal ilium

45
Q

Phases of gastric acid secretion

A

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
Q

How much pancreatic juice is produced per day?
What does it contain

A

1500ml
Proenzymes - trypsinogen (to trypsin), proelastase (to elastin)
Enzymes - amylase, lipase
Alkali

47
Q

What stimulates pancreatic secretions? Where are they released from? Trigger?

A

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
Q

Where are pancreatic enzymes stored

A

Zymogen granules

49
Q

How much bile is produced per day?
How much is stored in gallbladder?

A

500-1000ml
30-60ml

50
Q

Composition of bile

A

Bile salts
Pigments
Inorganic compounds

51
Q

What is the stored amount of bile salts?
How is this managed

A

3.5g
Recycled via enterohepatic circulation twice per meal!

52
Q

Factors that control bile release? Location of release and trigger

A

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
Q

Carbohydrate breakdown pathways to absorbable monomers

A

Lactose - [lactase] - galactose and glucose
Starch - [amylase] - alpha dextrins, maltose - [alpha dextrinase, maltase] - glucose
Sucrose - [sucrase] - fructose and glucose

54
Q

How are carbohydrates absorbed

A

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
Q

Maximal carbohydrate absorption rate

A

Glucose 100g/hr
Fructose 50g/hr

56
Q

Why can cellulose not be broken down

A

Beta glucose linkages

57
Q

Breakdown of proteins in gi tract

A

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
Q

Absorption of amino acids and short peptides in gi tract
Efficiency

A

Free amino acids in transporter with na
Short peptides through pept-1 with hydrogen ions.

Very efficient <5% protein escapes absorption

59
Q

Absorption of lipids in gi tract

A

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
Q

How much water per day is absorpbed in the intestine
How much is lost in faeces
Where is most water reabsorbed

A

10l
200ml
Most in the small intestine, around 1.5 litres in the large

61
Q

How much Na is absorbed in the intestine each day? Where does this come from?

A

35g
Most reabsorbed from secretion, only about 5-8g from diet

62
Q

Effect of aldosterone on gi tract

A

Increases na channels in epithelium and basolateral nak pumps resulting in increased sodium and thus increased water absorption.

63
Q

How are fat soluble vitamins absorbed in the gi tract

A

In micelles with bile salts and fat

64
Q

Examples of water soluble vitamins

A

Vit c
Folic acid
B12

65
Q

How are Vit c and folic acid absorbed in the bowel

A

Active transport

Vit c - passive transport
Folic acid - na independent transport

66
Q

How is Vit b12 absorbed

A

Intrinsic factor released in stomach then active sodium independent transport (Pinocytosis) in terminal iliu

67
Q

How and where is iron absorbed in the bowel
How much of dietary iron is absorbed

A

Pinocytosis in duodenum and jejunum
3-6%

68
Q

How and where is calcium absorbed
Controlling factors
How much absorbed

A

Duodenum, active transport facilitated by proteins
Regulated by 1.25 dihydroxycholcalciferol
30-80%

69
Q

Where and how is magnesium absorbed in the bowel

A

Small and large
active and passive transport, facilitated by protein

70
Q

What is vomiting

A

Forceful expulsion of contents of the upper gi tract

71
Q

Where is vomiting controlled

A

The vomiting centre - a number of interconnected areas in the brainstem

72
Q

Phases of vomiting with description

A

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
Q

Areas involved in nausea and vomiting and links.

A

Chemoreceptor trigger zone activates nucleus tractus solitarius, and both CTZ and NTS activate brainstem vomiting centre triggering vomiting response.

74
Q

Triggers to vomiting

A

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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