Physiology Flashcards

(37 cards)

1
Q

What 3 secretagogues induce HCl production?

How do they increase the HCl production?

What cell do they activate?

A

Think of witch melting in Wizard of Oz - like melting in acid - HCl = HAG
H = histamine
A = ACh
G = gastrin

Cause an increase in proton pumps

Parietal cells activated

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2
Q

Specifically where in the stomach is HCl produced and what enzyme is involved?

A

In gastric pit lumen outside parietal cells

H+/K+/ATPase pump

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3
Q

Name the 3 phases of gastrin secretion

A

Cephalic - before food has even reached stomach
Gastric - distension increases HCl production
Intestinal - once left stomach

CGI - think of a CGI stomach pumping out acids

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4
Q

During the cephalic phase of gastric secretion what causes an increase in HCl production?

A

Vagus nerve stimulates production of HAG
Histamine
ACh
Gastrin

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5
Q

Describe what happens to food when it enters the stomach in terms of movement through the stomach?

A

Tonic waves push food towards antrum

Slow antral waves move food towards pyloric sphincter where when it is too large - RETROPULSION

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6
Q

What part of brain controls appetite? What nerves stimulates appetite and what does it act on? Same for inhibits appetite?

A

Hypothalamus
Stimulates - orexigenic neurons - lateral hypothalamic
Inhibits - anorexiogenic neurons -ventromedial nuclei

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7
Q

What part of brain controls vomiting?

A

Medulla

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8
Q

What three secretagoues also have an impact on hunger. What cells produce them and where are these cells found?

A

Leptin inhibits - adipose cells - adipose tissue
Ghrelin stimulates - Gr cells - gastric antrum and small bowel (hungry work retropulsion)
CCK inhibits - I cells - duodenum and jejunum -

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9
Q

How does small intestine deal with highly acidic chyme?

A

Duodenum contains Brunner’s Glands which release an alkaline substance to neutralise

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10
Q

What is a TGA?

A

Triglcyeride - consumed from fat

Three glycerides = 3x glycerol + FA chains

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11
Q

What enzyme hydrolyses emulsions into free fatty acids? What releases it and what induces the organ to release it?

A

TGA-lipase

Released by panceras which is initated by release of CCK from I cells (duodenum and jejunum)

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12
Q

What is emulsion?

A

Combination of fat droplets and bile salts (produced by liver)

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13
Q

When a micelle reaches an enterocyte then what happens? How do lipids reach blood stream?

A

Release FAs
Small chain FAs - diffuse through enterocytes into capillaries
Large chain FAs - move via endocytosis into enterocytes and then become resynthesise into TGAs where they are incorprated into chylomicrons (lipoproteins) -> move into lymph via exocytosis

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14
Q

What transporters are involved in water balance in the small bowel and where are these found?

A

Na/glucose
Na/AA
Jejunum and ileum

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15
Q

When does removal of water take place in the small bowel?

A

Post-prandial (after food)

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16
Q

What vitamins are fat and water soluble?

A

Fat - ADEK

Water - BCH

17
Q

How does transport of a fat soluble and water soluble vitamin differ?

A

Fat soluble - passively diffuse having been incorprated into micelles then incorparated into chylomicrons
Water soluble - moved via active transporters

18
Q

What receptors do HAG work on?

A

Histamine - H2
ACh - M3
Gastrin - CCK2

19
Q

How role does CCK play in bile secretion and what signals its release?

A

30mins after food eaten it will enter as chyme into duodenum -> release of CCK
CCK causes gallbladder to contract and release bile
It also causes relaxation of the Sphincter of Oddi (allows bile to enter D2)

20
Q

How are bile salts created and where are they created?

A

In liver
Cholesterol broken down by hepatocytes into cholic acid (primary bile salt)
Travels to gallbladder for storage and concentration

21
Q

What is bile made of?

A
95% water
Cholesterol 
Bile salts
Bilirubin 
Alkaline in nature
22
Q

Why are bile salts amphiatic (hydrophobic on one end and hydrophillic on the other) nature important?

A

It allows the lipids to be formed into mixed micelles which allows TAG-lipase (from pancreas) to attack and further break down into monoglycerides and free FAs

23
Q

What is perastalsis?

A

Relaxation of GI wall followed by contraction triggered by gut wall distension

24
Q

What makes up the enteric nervous system?

A

ENS = brain of the gut
Submucosal plexus - submucosa
Myenteric plexus - muscularsis externa - in between circular and longitudinal layers of muscle

25
Describe the muscle wall during peristalsis?
Behind bolus of food - circular contract, longitudinal relax | Infront - circular relax, longitudinal contract
26
What cell is responsible for the slow wave contraction of gut wall and hence rate of perstalisis?
Intersital cells of Cajal AKA pacemaker cells
27
How does the ENS induce peristalsis
Causes depolarisation by opening Ca2+ channels
28
What chemicals cause relaxation and contraction of gut wall?
ACh - contraction | NO - relaxation (same as in blood vessels)
29
What do acinar cells produce?
Proteases
30
What do the following brush border enzymes act on and produce? Maltase Lactase Sucrase
Maltase - disaccharide = glucose and glucose Lactase - disaccharide = glucose and galactose Sucrase - sucrose = glucose and fructose
31
The loss of which enzyme is one of the key features in the development of steatorrhoea?
Lipase
32
What is the normal intragastric pH?
2
33
Pernicious anaemia is associated with other autoimmune conditions. True or false?
True
34
What do chief cells produce? | What does it become when hits gastric acid?
Pepsinogen -> pepsin
35
What cells produce HCl?
Parietal cells
36
What cells produce somatostatin?
D cells
37
What does enterochromaffin-like cells produce?
Histamine