Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pharm phys intro > GI tract and blood glucose regulation > Flashcards

GI tract and blood glucose regulation Flashcards

1
Q

what are the layers, including the plexuses, of the GI tract walls from inner to outer?

A

mucosal layer
submucosal layer
submucosal/Meisner’s plexus
circular muscle
myenteric plexus
longitudinal muscle
serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe the structure of the mucosal and submucosal layers

A

mucosal:
epithelial cells for secretions/absorptions
lamina propria layer - connective tissue with blood an lymph vessels
muscularis mucosae - smooth muscle

submucosal -
collagen
elastin for recoil
glands
blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the effects of contraction of the circular and longitudinal muscles?

A

circular = reduces diameter
longitudinal = reduces length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the serosa?

A

outermost layer, made of connective tissue, can be surrounded my mesothelium to reduce friction in very active sections of tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the enteric nervous system? what is the difference between intrinsic and extrinsic control?

A

surrounds GI tract, more than 100 million neurons which is more than the spinal cord third division of the ANS and uses lots of NTs

intrinsic = enteric
extrinsic = sympathetic and parasympathetic (vagus nerve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

compare postganglionic neurons of the SNS and PNS

A

SNS = adrenergic
PNS = cholinergic (or peptidergic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does somatostatin do?

A

inhibits secretion of all GI hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

compare hormones, paracrines and neurocrines

A

hormones = endocrine cells, secreted into portal circulation of liver, for example GIP

Paracrines - from local endocrine cells, e.g. somatostatin
Neurocrines - released from neurons following an action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does smooth muscle work in the GI tract?

A

mostly unitary smooth muscle, couple by gap junctions for coordinated rapid response
works in phasic - 3-12 contractions/min
also has constant tonic activity

has a pacemaker - ICC interstitial cells of Cajal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how is tonic activity created in smooth muscle of GI tract?

A

uses the ICC
slow waves are caused by subthreshold depolarisation as a result of Ca2+ influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is backflow prevented along the GI tract?

A

sphincters of smooth muscle, use the increase volume, reduce pressure thing and vice versa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does the sphincter of Oddi do?

A

separates the gall bladder and pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does the mouth work in assisting GI tract?

A

teeth and tongue mechanically break down food, saliva is added from three salivary glands, end product = bolus

amylase - hydrolyses starch

chewing = mastication, due to innervation of mandibular muscles by CN V

next is swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what happens in the first two phases of swallowing?

A

1) oral = tongue forces bolus to the back of the mouth, something happens with the somatosensory receptors idk

2) pharyngeal = soft palette is pulled upwards (top of the mouth moves up)
epiglottis moves to cover the larynx
upper oesophageal sphincter relaxes

breathing is inhibited, peristaltic wave initiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

oesophagus - what is the lumen lined with?
what initiates the primary peristaltic wave?
what happens if the bolus gets a bit stuck?
what is the third stage of swallowing

A

oesophagus is lined with stratified squamous epithelia
primary peristaltic wave is initiated by closing of the upper oesophageal sphincter

distention of stuck bolus causes a secondary peristaltic wave at the site of the distention

third stage = oesophageal and involves all stuff mentioned above, plus opening of lower oesophageal sphincter by vagus nerve (CN 10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens in the three phases of the stomach?

A

1) receptive phase = thin wall of the orad (the upper stomach) relaxes, inc. volume dec. pressure, lower oesophageal sphincter closes to prevent backflow

2)lower region, the thick walled caudad, contracts strongly to mix food with gastric juices, now calling it the chyme
these contractions aren’t faster but stronger

3) gastric emptying = through pyloric sphincter to duodenum, is very slow to neutralise acid and allow for absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how long is the small intestine and what is it’s function?

A

6.5m long, main site for absorption of nutrients, water and ions with three sections - duodenum, jejunum and ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how is the pancreas stimulated in it’s three phases of secretion?

A

cephalic = smell and taste
gastric = a dull stomach
intestinal = chyme stimulates endocrine cells to secrete stimulatory hormones that act on the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do the liver and gallbladder assist?

A

hepatocytes secrete bile which the gallbladder stores
amphipathic bile salts emulsify and make lipids soluble by turning them into micelles

CCK - secreted when chyme reaches the small intestine - causes contraction of gall bladder and relaxing of the sphincter of Oddi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are segmentation contractions?

A

circular and longitudinal muscle work together to separate the chyme and expose it the the enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what do enterochromaffin cells do?

A

they secrete serotonin - part of the peristaltic reflex, anything not yet absorbed passes through the ileocecal sphincter into the caecum of the large intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the large intestine divided into?

A

first = caecum, then ascending, than transvers, then descending colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the three primary functions of the large intestine?

A

absorb water and electrolytes
produce and absorb vitamins like B and K (assisted by bacteria)
third = forming and propelling faeces to be excreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

structure and cells of the large intestine?

A

columnar epithelial cells to absorb
crypt cells that secrete mucus for protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what structure causes the bunches in the intestine?

A

three bands of longitudinal muscle - the taenia coli - are shorter than the intestine, forming these bunches known as haustra, allows for expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what volume of secretions is there daily?

A

8.5-10L with most of it being reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

which cells in the body of the stomach secrete what?

A

there are oxyntic glands in the body of the stomach
here, epithelial cells secrete bicarb and mucous cells secrete mucus
parietal cells - secrete HCl and intrinsic factor (required for vitamin B12 absorption)
chief cells secrete pepsinogen

28
Q

what cells in the antrum of the stomach secrete what?

A

has pyloric glands, similar to oxyntic but have no parietal cells so no HCl

they also have G cells to secrete gastrin
D cells to secrete somatostatin

29
Q

how do parietal cells produce HCl? how does this cause an alkaline surge in the blood?

A

Apical - K+/H+ ATPase moves H+ into lumen from the cells
Cl- secreted via chloride channel - making HCl

In cell carbonic anhydrase converts carbon dioxide and water to carbonic acid which dissociates in to bicarb and H+

Basolateral - Na+/K+ ATPase

bicarb/Cl- antiporter moves bicarb into blood and Cl- into cell (to be secreted into lumen), makes blood alkaline surge occur

30
Q

regulation of HCl secretion?

A

Secretagogues - vagus nerve - ACh - M3 receptor - Gq - IP3/Ca2+ = H+ secretion via the K+/H+ ATPase

G cells - gastrin - Gq - IP3/Ca2+ = H+ secretion
ECL (enterochromaffin) cells - histamine - H2 receptor - Gs - cAMP = H+ secretion

Inhibition caused by - low pH, somatostatin, prostaglandins

31
Q

how does the small intestine absorb hydrolysed food?

A

using luminal and brush border enzymes???

32
Q

what do the crypt epithelial cells of the intestines do?

A

secrete fluids and electrolytes in order to protect intestine from bacteria/toxins and flush them out

33
Q

describe transport in the intestines?

A

transcellular and paracellular (across and between cells)

34
Q

epithelial cells of the crypts -
what transporters are on the basolateral membrane and how are they useful?
what transporter on the apical and how is this effected by hormones/NTs?

A

on basolateral = Na+/K+ ATPase
NKCC2 - means sodium and chloride are moving from the blood into the cell so water follows (how fluid and electrolytes are secreted to flush out toxins

on the apical membrane there is a chloride channel where chlorine moves out of the cell into the lumen, this can be upregulated by NTs/hormones, using GPCRs that activate cAMP

*Na+ and water can move across gaps between cells too

35
Q

explain any absorption in the jejunum (SI)

A

Basolateral Na+/K+ ATPase lowers intracellular Na+ conc., allowing Na+ to be absorbed in from the lumen and bring glucose/amino acids with it via a cotransporter, required due to having conc. Gradient against absorption

In the cell CO2 and water form carbonic acid, carbonic anhydrase breaks it down to H+ and bicarb, bicarb moves across transport protein on basolateral into blood, H+ is secreted

36
Q

explain all the cellular transport in the ileum

A

in the SI as a whole net absorption of NA+ K+ and Cl- , secretion of bicarbonate

still has the basolateral Na+/K+ ATPase and glucose or amino acid facilitated diffusion protein

there’s a bicarb/Cl- exchange on apical for bicarb secretion and Cl- absorption
(H+ also secreted using a H+/Na+ exchange

37
Q

explain what happens with pancreatic secretions in terms of transport proteins

A

Ductal cells - secrete

Na+/K+ ATPase on basolateral
In cell carbonic acid forms and dissociates, bicarbonate is secreted across apical side while absorbing chloride,
Na+/H+ exchanger on basolateral to absorb H+ (Na+ moves in but the pump removes it again)

38
Q

absorption in the large intestine?

A

Na+ channel for absorption on apical side, aldosterone increases number of these channels
Na+ absorbed via the Na+/K+ ATPase on the basolateral

39
Q

how are carbohydrates absorbed?

A

glucose (and galactose) we know already

fructose just used facilitated diffusion using GLUT5 into cell and GLUT2 out

40
Q

how are proteins absorbed?

A

Na+/K+ ATPase pumps Na+ out to the blood as usual
amino acids/Na+ cotransporter is then used using Na+ conc. gradient

Dipeptides and tripeptides use H+ cotransporter (though this works because an apical H+/Na+ exchange protein moves H+ out so that it can come back in and bring dipeptides with it)

very similar to A level, same principles

41
Q

where are lipids absorbed and into what? what two things get lipid absorption started?
what are the products of lipid hydrolysis and what structure forms to make them soluble?

A

these are absorbed into lacteals within the villus, not into villus blood like carbohydrates or protein products

occurs in the duodenum and jejunum

bile salts emulsify, lipase does the complete lipid hydrolysis

the products of this hydrolysis - cholesterol, lysophospholipids, monoglycerides + fatty acids are made soluble in mixed micelles

42
Q

how are micelles absorbed, including all possible routes into the cell?

A

these micelles move into the enterocyte across it’s brush border (I think this is just the villi) - they can diffuse right across, incorporate into the membrane or use a transport protein

once in the cell, the products are modified into cholesterol esters, triglycerides and phospholipids

to leave the cell, these products join with apolicrase 3 to from a chylomicron which fuses with the membrane and releases it’s contents via exocytosis into the lymph

this fluid must be returned to the CV system to prevent shock and to get the lipid products to somewhere they can be used

43
Q

islets of Langerhans - there are 6 kinds of cells, what are they and ehat do they produce?

A

beta cells - insulin, proinsulin, and amylin

alpha cells - glucagon

delta cells - somatostatin

F cells - pancreatic polypeptide

epsilon cells - ghrelin

enterochromaffin cells - substance P

44
Q

what do somatostatin, amylin, pancreatic polypeptide and substance P do?

A

somatostatin downregulates hormones like glucagon and insulin and ghrelin

amylin is secreted with insulin to prevent glucagon release and slow gastric emptying

PP = stops exocrine function of pancreas (digestive enzymes)

substance P = also involved in regulating exocrine secretion

45
Q

how are islets of Langerhans perfused?

A

very good blood supply with a small artery going to the centre of the islet, small fenestrated capillaries distributing the blood from there

venous blood of one cell type bathes the others, encouraging paracrine function as well as endocrine

46
Q

how do cells in the islets communicate?

A

gap junctions between alpha and beta cells

delta cells have dendrite-like projections to beta cells

47
Q

basic neuronal control of islets?

A

adrenergic, cholinergic and peptidergic neurons, so both SNS and PNS, innervate the islets

48
Q

what is the biggest regulator of insulin secretion and how?

A

glucose

if high, it stimulates insulin secretion, entering B cells through GLUT 2 channels
glucose is metabolised and ATP increases, closing K+ channels, causing depolarisation

Ca2+ enters via voltage gated channels, causing exocytosis of insulin-containing vesicles

49
Q

what things upregulate insulin (aside from high glucose concentrations)?

A

ACh and CCK act on ZGPCR to upregulate insulin

B adrenergic agonsits act on GPCRs to increase insulin via adenylyl cyclase - cAMP - PKA
oddly enough glucagon also acts on GPCR and causes increase in insulin secretion the same way

50
Q

what things downregulate insulin?

A

somatostatin and alpha adrenergic agonists downregulate insulin by reducing adenylyl cyclase

51
Q

describe the structure of an insulin receptor

A

2 extracellular alpha chains
2 transmembrane beta chains
an intracellular tyrosine kinase

52
Q

B cells have insulin receptor - what does this mean?

A

insulin downregulates itself by the receptor using it’s tyrosine kinase to phosphorylate itself

53
Q

what two kinds of pathways can be triggered by insulin?

A

cell growth, proliferation and gene expression
or
synthesis of lipids, proteins, glycogen

54
Q

how does insulin cause the uptake of glucose from the blood to lower blood glucose concentration?

A

Binds to insulin receptors, causes signal transduction cascade (adenylyl cyclase, ATP to cyclic AMP, protein kinase C) causing vesicles to move to membrane and insert GLUT4 channels into it, allowing loads of glucose into cells form blood by facilitated diffusion

55
Q

what would be a huge issue if glucose blood concentration was too high?

A

it would effect osmosis

56
Q

describe all the ways in which insulin effects the liver

A

promotes glycogenesis by upregulating transcription of glucokinase/hexokinase and glycogen synthase, enzymes in the glycogenesis pathway

Insulin inhibits glycogenolysis and gluconeogenesis

Promotes metabolism of glucose

Promotes storage of glucose as fat - lipogenesis, forming triglycerides and lipid droplets for storage

Promotes protein synthesis

57
Q

is insulin required for glucose uptake?

A

no cells always need glucose really, they’ll still have something like the GLUT2 receptors

58
Q

what 4 effects does insulin have in muscle?

A

Promotes glucose uptake by recruiting GLUT4

Promotes glycogen synthesis by increasing transcription of glycogen synthase, glucokinase/hexokinase

Promotes glucose metabolism to make ATP

Promotes protein synthesis

59
Q

what effects does insulin have on the blood?

A

lowering of glucose concentration AND amino acid concentration as more amino acids are taken up as they are used in the promoted protein synthesis

60
Q

what 4 effects does insulin have on adipose tissue?

A

*Has loads of insulin receptors

Has the GLUT 4 thingy increasing glucose uptake

Then there’s lipogenesis - glucose converted to FAs, stored as triglycerides in lipid droplets

Also an increase in lipoprotein lipase - this liberates FAs so they can be turned into triglycerides

Inhibits mobilisation of fat stores - preventing breaking them down for energy

61
Q

what are the 2 wider acting effects of insulin?

A

promotion of K+ uptake via NA+/K+ ATPase (which is why hyperkalaemia is a symptom of diabetes mellitus)
directly affects the hypothalamus to cause feelings of satiety

62
Q

what happens in type I vs type II diabetes?

A

type I = destruction of islets of Langerhans often following a viral infection that causes an autoimmune response
this means B and A cells are destroyed, meaning insulin is not produced

type II = low insulin production + resistant insulin receptors

63
Q

what are the physiological effects of type I diabetes mellitus?

A

weight loss (glucose not taken up)
hyperglycaemia

increased blood fatty acid and ketoacid concentrations as a result of lipolysis

increased blood amino acid concentration as protein synthesis is not being promoted by insulin

polyuria, hypotension, hyperkalaemia

64
Q

what symptoms does type I diabetes mellitus cause?

A

Increased thirst and urination
Hunger
Weight loss
Fatigue
Irritability
Fruity smell on the breath (ketoacidosis)
Blurred vision due to osmotic effects on capillaries in eyes

65
Q

how are type I and type II diabetes treated?

A

type I = insulin therapy injections

type II = insulin therapy for the low insulin or insulin stimulating drugs
biguanide drugs to improve efficacy of the resistant receptors

type II - can be diagnosed as prediabetic and significant weight loss may prevent diabetes before it happens

66
Q

type II physiological effects and symptoms?

A

very similar to type I - insulin isn’t working

pharm phys intro (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions