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GI system > physiology/ pharmacology > Flashcards

physiology/ pharmacology Flashcards

1
Q

What is energy usually stored as?

A

primarily stored as fat

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2
Q

What is energy homeostasis?

A

process whereby energy is matched to energy expenditure over time

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3
Q

How do you calculate someone’s BMI?

what are the normal values?

A 
BMI = weight (kg) divided by square of height 
up to BMI of 25 = thin or normal 
25-30 = overweight 
30-39= obese 
40 or over = morbidly obese
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4
Q

What are the major factors contributing to obesity?

A

genetics - genes that make you susceptible to being fat

environment - unmask latent tendencies to develop obesity

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5
Q

Why is you are obese are you more susceptible to covid?

A

contain a lot of adipose tissue which contains the components for the virus to enter

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6
Q

Why is fat important? what does it do during prolonged illness?

A

energy storage, energy buffer during prolonged illness

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7
Q

Why is it sometimes difficult to lose weight?

A

your brain views the extra weight as normal and perceives dieting as a threat to the body’s survival

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8
Q

How does the CNS influence energy balance and body weight? behaviour, ANS and neuroendocrine

A

behaviour - feeding and physical activity
ANS activity - regulates energy expenditure
Neuroendocrine - secretion of hormones

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9
Q

where is the neural centre in the brain responsible for energy intake and body weight?

A

hypothalamus

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10
Q

What is the definition of satiation, satiety and adiposity

A

sensation of fullness during a meal, period of time between termination of one meal and initiation of next , the state of being obese

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11
Q

What are some satiation signals?

A

cholecystokinin = released in proportion to lipids and proteins in meal
glucagon like peptide - released in response to food ingestion

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12
Q

When does ghrelin increase and decrease

A

Ghrelin - increase before meals and decrease after meals

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13
Q

How is overall energy balance maintained?

A
  • feedback loops: signals are sent and sensed in the hypothalamus act accordingly
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14
Q

What are the two hormones that report fat status to the brain?

A 
leptin = made and released from fat cells
insulin = made and released form pancreatic beta cells
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15
Q

How does leptin cause weight loss?

A

inhibits food intake and decreases body weight (deletion of this receptor causes obesity)

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16
Q

how does the drug orlistat work?

What also needs supplemented?

A

inhibits pancreatic lipase decreasing triglyceride absorption
need to vitamin supplements along with it

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17
Q

What is liraglutide used for?

A

treatment of type 2 diabetes but also causes weight loss

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18
Q

what is gastric bypass surgery used for? (high level of what in diabetes)

A

produces substantial weight loss - high level of complete resolution of type 2 diabetes

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19
Q

How does 2,4-dinitrophenol work?

Side effects?

A

Work on adaptive thermogenesis - increase energy expenditure
Can cause severe hyperthermia

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20
Q

how is current transferred between smooth muscle cells?

How is a synchronous wave produced?

A
  • electrical gap junctions

- cells are depolarised at the same time causing a synchronous wave -

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21
Q

What are slow waves?

A

rhythmic patterns of membrane depolarisation that spread from cell to cell via gap junctions

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22
Q

What drives slow wave electrical activity?

Where are they located?

A

interstitial cells of Cajal - located between circular and longitudinal muscle layers (in a bridge like fashion)

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23
Q

When do slow waves cause contraction?

A
  • slow wave amplitude is enough to reach a threshold and trigger a smooth muscle cell action potential (spike)
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24
Q

What does the slow wave amplitude reaching threshold depend upon? (knock on effect)

A

depolarise muscle cells rather than influence slow waves directly - ie shifts slow wave peak to threshold

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25
Q

What is peristalsis?

A

peristalsis (wave of relaxation followed by contraction that proceeds a short distance along the gut

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26
Q

What is segmentation in the GI tract?

where does it occur?

A
  • (mixing) - rhythmic contractions of the circular muscle layer that mix and divide luminal contents
  • occurs in the small intestine
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27
Q

colonic mass movement ?

A

powerful sweeping contraction that forces faeces into rectum

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28
Q

What are sphincters?

A

one way valves by maintaining a positive resting pressure

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29
Q

What is the role of upper O sphincter, lower O, pyloric, ileocaecal

A

skeletal muscle - relaxes to allow swallowing and closes during inspiration
relaxes to allow entry of food, closed to prevent reflux
regulates gastric emptying, prevents duodenal gastric reflux
regulates flow from ileum to caecum

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30
Q

Why is the stomach important in the GI system?

how does it produce chyme?

A

Starting point for digestion of proteins (pepsin and HCL) and continues carbohydrate digestion (salivary amylase)

mixes food with gastric secretions to produce chyme

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31
Q

What are the two types of mechanical activity of the stomach? Orad and caudad

A

orad stomach - tonic (maintained) minimal mixing for amylase to work

caudad stomach - phasic (intermittent, slow waves - pump propels contents towards the pylorus

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32
Q

What is retropulsion of the caudad region?

A

velocity of contraction overtakes movement of chyme so it rebounds the food away from the antram to ensure proper mixing ensues

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33
Q

What are the gastric factors that determine the emptying of stomach?

A

Rate of emptying is proportional to volume of chyme in stomach:

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34
Q

What are the duodenal factors that determine the emptying of stomach?

A

neuronal response - decreased antral activity (enterogastric activity)

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35
Q

List some gastric secretions in the oxyntic mucosa (fundus and body) - HCL, pepsinogen and histamine - detail what they do

A

HCL - activates pepsinogen to pepsin and denatures proteins
Pepsinogen - inactive precursor to pepsin
histamine - stimulates HCL secretion

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36
Q

List some pyloric gland gastric secretions (gastrin, somatostatin)

A

Gastrin - stimulates HCL

somatostatin - inhibits HCL secretion

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37
Q

What is assimilation?

A

overall process of digestion and absorption

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38
Q

What is the definition of absorption?

A

absorbable products of digestion are transferred across both the apical and basolateral membranes of enterocytes

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39
Q

What are enterocytes

A

absorptive cells in the intestinal epithelium

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40
Q

What form must all dietary carbohydrates be in for absorption?

A

In the form of monosaccharides

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41
Q

What is produced when lactase is broken down?

A

breaks is down into glucose and galactose

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42
Q

Why is lactase rate limiting in assimilation?

A

The hydrolysis reactions dont occur at a faster rate than subsequent transport of the monomers produced

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43
Q

Where does the absorption of the monosaccharides take place? - What are glucose and galactose secondary active transport mediated by?

and how do they move across the membrane?

A

occurs in the duodenum and the jejunum

Glucose and galactose are absorbed by secondary active transport mediated by SGLT1

fructose by facilitated diffusion by GLUT2

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44
Q

How do the monosaccharides exit?

A

mediated by facilitated diffusion by glut2

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45
Q

How does the SGLT1 operate?

A

sodium binds to the channel which increases its affinity for glucose which means it is transported more readily

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46
Q

What is an example of a protein degradation reaction in order to release amino acids into the blood

A

Protein - peptides - amino acids - amino acids in enterocyte and then the amino acid gets released into the blood

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47
Q

Detail the process of the digestion of proteins in the stomach

A

HCL denatures proteins, pepsin cleaves proteins into peptides

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48
Q

How does digestion in the duodenum occur?

A

Five pancreatic proteases are secreted as pro enzymes from acing cells and converted to active form in the duodenum

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49
Q

Why are brush border peptidases numerous?

A

Each enzyme attacks a limited number of peptide bonds and oligopeptides have an extremely varied structure

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50
Q

How are amino acids transported out of enterocytes

A

brush border - sodium and non sodium dependant transporter

basolateral membrane - sodium dependant and independent transporters

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51
Q

How do di, tri and tetra peptides get absorbed?

A

via H+ dependant mechanism at brush border -

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52
Q

What is the role of the small intestine and what are the three parts of it?

A

Role = major site for digestion and absorption

three parts - duodenum, jejunum and ileum

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53
Q

What does the small intestine receive?

A

chyme from the stomach, pancreatic juice and bile from liver and gall bladder

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54
Q

What does motility cause in the small intestine?

A

Mixing of the chyme with digestive juices (segmentation), slow propulsion of the chyme (peristalsis) and removal of undigested residues (migrating motor complex)

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55
Q

How is segmentation initiaited

A

small intestine pacemaker cells causing the basal electrical rhythm

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56
Q

How is segmentation altered?

A

slowed down to allow time for absorption, strength is enhanced and decreased by parasympathetic activity

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57
Q

What is the migrating motor complex?

A

Strong peristaltic contraction slowly passing length of the intestine which clears stomach of debris, mucus and dead epithelial cells

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58
Q

What is the MMC inhibited by?

A

feeding and vagal activity - gastrin and CCK

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59
Q

What is the function of secreting gastrin?

A

stimulates hydrogen ion secretion and stimulates growth of gastric mucosa

60
Q

Secretin?

A

promotes secretion of pancreatic and biliary HCO3-

61
Q

Cholecystokinin?

A

inhibits gastric emptying, causes secretion of enzymes required for digestion, ejection of bile

62
Q

Why are gastric inhibitory peptides released?

A

stimulates release of insulin from pancreatic beta cells - inhibits gastric emptying

63
Q

Motilin?

A

Initiates MMC

64
Q

Ghrelin

A

stimulates appetite

65
Q

What are all peptide hormones?

A

they all act of G coupled receptors

66
Q

What are the juices called that the small intestine produces?

A

Succus entericus

67
Q

In the pancreas - What do the exocrine and endocrine parts secrete?

A

endocrine (islets of langerhans) - insulin, glucagon (to blood)

exocrine - digestive enzymes from acing cells, aqueous NaHCO3-, secreted to the duodenum collectively as pancreatic juice which neutralises acidic chyme entering the duodenum

68
Q

How is bicarbonate secreted?

A

co2 diffuses into cell and combines with water to form carbonic anhydrase, this then converted into carbonic acid which dissociates into hydrogen ions and bicarbonate which is secreted out of the cell and into the lumen

69
Q

How is is pancreatic secretion controlled?

A

cephalic - vagal stimulation

gastric - distension evokes a vasovagal reflex resulting in para stimulation

70
Q

What do mucus cells secrete in the gastric crypt?

A

mucus and bicarbonate

71
Q

Parietal cells

A

hydrochloric acid

72
Q

enterochromaffin-like cells

A

histamine

73
Q

G cells?

A

gastrin

74
Q

D cells

A

somatostatin

75
Q

chief cells?

A

Pepsinogen

76
Q

How is hydrochloric acid controlled in gastric parietal cells?

A

carbon dioxide and water from carbonic acid (with carbonic anhydrase) which then dissociates into bicarbonate to and Hydrogen ions

Bicarb is taken out of cell and replaced with chloride which is secreted out when hydrogen ions are exchanged for potassium ions

77
Q

What is the action of histamine?

A

secreted in response to acetyl choline

increases cAMP which increase number of proton pumps = more gastric acid secreted

78
Q

What is the action of acetylcholine in the gastric acid secretion?

A

Binds to muscarinic receptors, increases calcium release, increases no of proton pumps and so increases gastric acid secretion

79
Q

How does gastrin work?

A

binds to CCK2 receptors, which increases calcium and increases gastric acid secretion

80
Q

Somatostatin?

A

Inhibits cAMP and reduces histamine release which decreases the gastric acid secretion

81
Q

How does the vomiting centre work in the brain

A

recipes signals from:
higher cortical centres repulsive sights, smells etc

Chemo receptor trigger zone sends emetic signal to vomit centre

vagal afferents send signals from gut to brainstem

5Ht, dopamine and ACh are the main neurotransmitters involved in nausea and vomiting

82
Q

What do lipids comprise of?

A

triacylglycerols (fats/oils)
phospholipids
cholesterol
fatty acids

83
Q

Why is it important that droplets are emulsified?

A

increased surface area for digestive enzymes to work and are stabilised with an amphiphilic molecules (lipids)

84
Q

What must the structure of the lipid be if it is to be absorbed in the stomach?

A

Short and medium chain fatty acids are absorbed in stomach but long chains are not

85
Q

Where are pancreatic lipases secreted? - in response to what?

A

Acinar cells of pancreas in response to CCK which stimulates bile flow

86
Q

Where are bile salts released from? in response to what and what do they act are?

A

gall bladder in response to CCK and act as emulsifiers (big droplets to small)

87
Q

What structure do bile salts have?

A

Hydrophillic (projects from surface of droplet)

hydrophobic (adsorbs onto droplet)

88
Q

What are some consequences if bile salts are not secreted?

A

Lipid malabsorption - steatorrhea (fat in faeces)

secondary vitamin deficiency due to inability to absorb fat soluble vitamins

89
Q

Where are the final products of lipid digestion stored and released?

A

mixed micelles - as TAGs are hydrolysed they are replaced with TAGs which decrease droplet size until a mixed micelle is produced

90
Q

How do fatty acids and monoglycerides transport between cell membranes?

A

passive diffusion

91
Q

How are short and medium chain fatty acids absorbed?

A

diffuse through enterocyte, exit through basolateral membrane and enter villus capillaries

92
Q

long chain

A

resynthesied to triglycerides in the ER and incorporated into chylomicrons

93
Q

How is the chylomicron transported to the systemic circulation?

A

Carried in lymph vessels via the thoracic duct

94
Q

How is cholesterol absorbed?

Why is ezetimibe important in cholesterol absorption?

A

NPC1L1 transports biliary and dietary cholesterol from the intestinal lumen into the enterocyte to facilitate cholesterol absorption.

Prevents internalisation by binding to NPC1L1 so results in absorption of cholesterol (used with statins)

95
Q

Why is iron important?

A

important in the carrying of oxygen by haemoglobin

96
Q

What does the iron balance in the body depend upon

A

tightly regulated absorption of iron in the duodenum

97
Q

Where is dietary iron found?

A

mainly in the oxidised form (Fe3+)

98
Q

What are the consequences if iron isn’t tightly regulated?

A

deficiency - microcytic anemia

excess - toxic due to accumulation

99
Q

What is the purpose in iron absorption to have a molecular chaperone?

A

transport iron across the cell to the basolateral membrane

100
Q

What state must the iron be in to be absorbed?

A

reduced ferrous state (fe2+) and it occurs by the oxidised state accepting an electron

101
Q

What is the storage form of iron?

A

Ferratin - Fe2+

102
Q

How is the absorption of iron controlled?

A

Divalent metal transporter one is increased when there is blood loss occurring

decreased expression by human haemochromatosis protein (mutations can fuck with this)

103
Q

What are some fat soluble vitamins?

A

A D E and K (chylomicrons)

104
Q

Water soluble vitamins?

A

B complex vitamins (folic acid eg) , C (ascorbate) and H (biotin)

105
Q

What is the gross structure of the Large intestine?

A

Caecum and appendix, Colon - ascending, transverse, descending and sigmoid, rectum, anal canal and anus

106
Q

What is the taeniae coli?

A

longitudinal muscle that is split into three strands - encircles the rectum and anal canal

107
Q

When does smooth muscle become thickened at the end of the large intestine?

A

internal anal sphincter - surrounded by skeletal muscle of the external anal spinster

108
Q

What is the haustra?

A

sac like bulges caused by the activity of the taeniae coli and circular muscle layers in colon

109
Q

How does the ilecaecal valve work?

what is it controlled by?

A

maintaining positive resting pressure, relaxing in response to distension in duodenum, contrating in response to distension in the ascending colon - controlled by vagus nerves

110
Q

What is the appendix and when can appendicitis be triggered?

A

blind ended tube with lymphoid tissue connected to the distal caecum via the appendiceal orifice

appendicitis can occur when it is obstructed by a faecalith

111
Q

Detail the primary functions of the colon

A

absorption of Na+, Cl- and H2O condense ileocaecal material to solid or semisolid stool

Absorption of short chain fatty acids - carbs not absorbed by small intestine is fermented by colonic flora to short chain fatty acids

Periodic elimination of faeces - (voluntary control after childhood)

112
Q

What are faeces made up of?

A

water, cellulose, bacteria, bilirubin and small amounts of salt

113
Q

What increases the surface area of the colon?

A

Colonic folds, crypts and microvilli

114
Q

What is one of the main jobs of colonocytes?

A

mediate electrolyte absorption which drives absorption of water (osmosis)

115
Q

What are some transporters and ion channels involved in moving electrolytes

A

sodium ab and potassium secretion (ions) enhanced by aldosterone

116
Q

How does haustration work?

A

saccules of alternating contraction - similar to segmentation but is a much lower frequency

117
Q

When is mass movement important?

A

contraction of large section of muscle in colon to propel faeces to distal parts

118
Q

When is the defecation reflex triggered?

A

When faeces are propelled into the rectum

119
Q

Detail the nerves involved in when he rectum fills with matter

A

Activates stretch receptors that send signals to the brain + spinal cord which brings about an urge to defacate

120
Q

What is defective in Hirschsprung disease

A

the rectosphinteric reflex

121
Q

What are the consequences of holding in or relaxaing the skeletal muscle of external anal sphincter

A

relaxing - straightening of anorectal angle,

contraction - delayed defection - rectal wall will gradually relax

122
Q

Why is it good to have commensal bacteria in your colon?

A

increase immunity by competition with pathogenic microbes

maintain mucosal integrity and promote motility

123
Q

Why do we produce gas?

A 
swallowed air (eructation) enters small intestine - absorbed or passed to colon,
gas that is not absorbed is expelled through the anus -
124
Q

When is amitriptyline used?

A

for abdominal pain that is resistant to the other drugs (antispasmodic, laxatives etc)

125
Q

describe the homeostasis of gastrin in the stomach

A

Gastrin promotes parietal cells to secrete acid

feedback loop controlled in a negative fashion to inhibit gastrin secretion through G cells

126
Q

What is the definition of malabsorption?

A

Defective mucosal absorption

127
Q

what are some common causes of malabsorption?

A

Coeliac disease, chrons disease

128
Q

When should you suspect malabsorption?

A

Liver, pancreas or small bowel disease

129
Q

What can cause easy bruising?

A

vitamin K deficiency or vitamin C deficiency - scurvy

130
Q

What drives absorption of water? - does it require energy?

A

passive process driven by the transport of solutes from lumen into the blood stream - absorption of sodium provides the osmotic force for reabsorption of water

131
Q

What do faeces normally contain?

A

normally contain 100ml of water along with 50ml of cellulose, bilirubin and bacteria

132
Q

How does intestinal fluid and water move?

A

intestinal fluid - always coupled to solute movement

Water - transcellular or paracellular routes

133
Q

Where do epithelial sodium channels occur? - what is this regulated by?

A

occurs in colon and is regulated by aldosterone

134
Q

What drives the absorption of chlorine when Na+ is diffused into the cell

A

Net negative charge left so chlorine is repelled into the cell

135
Q

How do hydrogen ions help with sodium absorption?

A

high pH in lumen due to excreted of bicarbonate so it drives the diffusion of hydrogen ions out of the cell in exchange for sodium entering the cell

136
Q

How does the chlorine absorption occur?

A

It can occur passively going into the cell or through gap junctions - paracellular

137
Q

What is important in Cl- secretion?

A

important in many dihorreas, CFTR channel is used to secrete chlorine onto apical membrane

138
Q

How is the chlorine conductance mediated by CFTR?

A

opening of channels at apical membrane and insertion of new channels from intracellular vesicles into the membrane

139
Q

More chloride secreted than absorbed =

A

secretory diarrhoea

140
Q

If diarrhoea is present… what can it cause?

A

can involve small, large and intestine
dehydration, metabolic acidosis and hypokaelema
may be fatal - cholera

141
Q

How is diarrhoea treated?

A

fluid and electrolyte balance
anti infective agents (if appropriate)
Use of antidiarrhoeal agents - symptomatic

142
Q

Detail rehydration therapy involving SGLT1

A

sodium binds, increases affinity for glucose, then translocate from extra to intracellular, Sodium dissociates then glucose loses its affinity and dissociates. The cycle is then repeated

143
Q

What does low albumin cause in liver failure?

A

low plasma volume due to low albumin so AAAS is activated and because liver cant metabolise aldosterone there is high secondary levels

144
Q

What happens to the kidneys in liver failure?

A

Consequences for kidney – increased angiotensin 2, aldosterone, sympathetic nervous system and ADH results in (all vasoconstrictors) – potassium loss, sodium retention and water retention

Results in renal vasoconstrictors – renal prostaglandins(vaso dilate to protect from vasoconstrictors) – all these vasoconstrictors can lead to hepato-renal syndrome

145
Q

What is the livers drug metabolism?

A

Drug - Oxidation reduction hydrolysis - conjugate

Phase 1 ^ (P450) and affected early - fat soluble drugs

Phase 2 (conjugation) - affected late

146
Q

What is the mechanism of paracetamol toxicity in liver failure

A

Paracetamol toxicity – not have enough glutathione(in liver failure) – drugs have a longer half life, increased P450 in alcoholics and then can become toxic with normal doses
Alcohol can compete with paracetamol to reduce paracetamol toxicity

GI system (8 decks)

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