W2: NUTRIENTS, STRUCT + FUNCTION, GASTRIC SECRETION, MOTILITY & GI ORGANS Flashcards

(38 cards)

1
Q

Describe the digestive processes for conversion of complex carbohydrates to monosaccharides

A

disacc.: breakdown by brush border enzymes

polysacch.: 
a-amylose starch => glucose chains
amylopectin => amylase: a-1,4
cellulose => unbranched linear glucose: B-1,4
glycogen: via pancreatic amylase: a-1,4
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2
Q

Describe the mechanisms whereby monosaccharides are absorbed across intestinal epithelial cells

A

GLUT 5 transporter (passive diffusion) - nil osmotic effect

SGLT1 (2º active transport); 1Na+glucose/galactose = change (Na gradient established by K-Na-ATPase
=>
GLUT2
=> osmotic gradient, H20 travels into small intestines

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3
Q

Describe the digestive processes for converting proteins to small peptides and amino acids.

A
endopeptidase = interior A.A
exopeptidase = terminal A.A
aminopeptidase = NH2 end of A.A
carboxypeptidase = COOH end of A.A
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4
Q

Describe the mechanisms of absorption for amino acids and small peptides.

A

Na-A.A transporter + Na independent carrier: Na gradient established by K-Na-ATPase =>osmotic gradient

PEPT1 (dipeptide/penicillin tripeptide) is H+ dependent. H+ microenvironment established by NHE3 (Na in; H+ out) d/t Na-K-ATP Na gradient in cell.

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5
Q

Describe the digestive processes for conversion of fats to triacylglycerols and monoglycerides.

A

smc contraction + emulsifying gent + bile => emulsification of lipid droplets (acidic environment d/t H+ balances FA charge)

pancreatic lipase = monoglyceride + 2 F.A

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6
Q

• Explain the requirement for emulsification of ingested fats.

A

Increases SA and accessibility of lipase action

  1. FA + monoclycerol enter sER = triacylglycerides reform
  2. emulsified by ampiphatic protein + vesicles transported to golgi
  3. exocytosed into ECF as CHYLOMICRONS
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7
Q

Describe the role of bile salts in the production of emulsification droplets and micelles

A

ampiphatic therefore binds to respective parts of lipids

=> repulsion and prevents reformation

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8
Q

• Describe the absorption of fat soluble and water soluble vitamins.

A

Vit B, C, Folic Acid (water soluble)
=> diffusion / carried-med transport

vit A, D, E, K
=> sER > Golgi > Chylomicrons (ECF) > thoracic Duct > Vena Cava

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9
Q

Describe the absorption of the important dietary minerals

A

B12: intrinsic factor in stomach = complex; absorbed in distal ileum

Fe: abs via DMT (duodenal enterocytes) > ferritin complex (intracellular store)
Vs
unbound fe via IREG1. bound to transferrin in blood.

  • Ferritin exp regulated via own Fe-levels
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10
Q

Describe the anatomy of the stomach and oesophagus and assign general physiological functions to each of its components

A

stomach is the site of intrinsic factor production essential for B12 abs.

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11
Q

Describe the features of the stomach and oseophagus canal wall structure

A
OESOPHAGUS WALL
mucosa: statified squamous
submucosa: glands for lubrication
muscularis ext: superior 1/3 skeletal; rest smc
adventitia
STOMACH WALL
lumenal mucus cells: gastric pits cont. glands
mucosa & submucosa: rugae
m. ext.: longitudinal, circular, oblique
serosa
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12
Q

What cells are found in the gastric glands

A

mucus neck
parietal: HCL + intrinsic factor
chief cells: pepsinogen

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13
Q

Describe the reflex control mechanism involved in swallowing.

A
  1. voluntary oral phase
  2. pharyngeal phase (medulla) d/t bolus presence
    propulsion to somach via peristalsis

receptive relaxation of stomach; vagal reflex: relaxation of thin elastic smc + fundus and body

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14
Q

Describe the structure and various functions of the stomach.

A

FUNDUS = storage

BODY = storage, mucus, HCl, pepsinogen, intrinsic factor

ANTRUM = mixing/grinding, gastrin (neuroendocrine Gcells)

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15
Q

Explain the importance of gastric acid and pepsin secretion and describe the hormonal and neural mechanisms responsible for their control

A
gastric acid  secr. (+)
cephalic phase (senses+thought)
1. CN. X
2. +ACh (parietal cells)
3. +Gastrin (G cells) > parietal cells
4. Gastrin/ACh (enterochromatin-like cells) > histamine > parietal

GASTRIC PHASE
+stomach distension = CN X => ACh (P cells)
+ peptides in lumen = Gastrin (g cells)
+ Gastrin/Ach (ECL) > Histamine > P Cells

PEPSINOGEN secr (chief cells) : zymogen; pH 3+lover; controlled by Gastrin | Histamine | ACh

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16
Q

HCl secretion in the stomach

A

Parietal cells

CO2 > carbonic acid > breakdown > H+ lumen; bicarb blood > Cl- enters and leaves cell to lumen > H20 drawn into lumen

HKATPase
(+) Gastrin via PKC
(+) Histamine via cAMP pkA
(+) ACh via CN X cholinergic M3 receptors > PKC
(-) Prostaglandin E3 receptor > Gi inhibits cAMP

17
Q

Explain the essential role of intrinsic factor in vitamin B12 absorption

A

IF secreted by parietal cells found in the gastric body

* IF/B12 complex absorbed in ILEUM

18
Q

Explain the functions of gastric mucus

A

(surface epith. and mucus neck)

*protective (pH7); lubricant;

19
Q

Inhibition of Gastric Acid secretion

A

(-) cephalic phase
(-) gastric phase

INTESTINAL PHASE: ENTEROGASTRIC SPLANCHNIC REFLEX
1. ACID in duodenum
=> SECRETIN (duodenal mucosal S cells)
bicarb secr.
=> ↓gastrin + ↓gastrin stimulation of P cells

  1. FAT + CHO in duodenum
    => GIP
    => ↓ gastric secr. + HCl secr.
20
Q

Role of enterogastrogens

A

protective and prevents acidic dmg to duodenum
inhibits: gastric acid section
and
↓↓gastric acid emptying via motility/pyloric sphincter

21
Q

Describe the organisation of the enteric nervous system & peristalsis

A

meissners plexus = submucosal
myenteric plexus = muscularis propria

pacemaker cells in LONGITUDINAL MUSCLE LAYER

slow wave; basic electrical rythm
conducted via gap junctions

gastrin(+) stim to threshold & AP
distension (+)
presence of producs/tonicity (-)

22
Q

Explain the mechanisms involved in the neutralisation of gastric acid in the duodenum, including control of bicarbonate secretion in the duodenum

A
BRUNNERS GLANDS (submucosal duodenal)
HCO3

(+) duodenal acid via CN X & ENS
(+) secretin (PANCREAS + LIVER)

-ve feedback; acid neutr. = inhibits secretin release + self-limiting

23
Q

Explain the functions of the pancreas

A

duct cells = bicarb
acinar cells = zymogen storage

sphincter of oddi @ hepatopancreatic ampulla = control of pancr. secr. and biliary output

24
Q

Describe the actions of secretin and cholecystokinin (CCK) on pancreatic and bile secretion and the stimuli which will cause their release

A

(+) SECRETIN (acid in duoden) => HCO3
(+) CCK (fat/A.A duoden) => zymogen stimulation
(+) Vagal/local (organic mol. presence)

25
Describe the control of pancreatic enzyme secretion and the role of zymogens
zymogens released from acinar cells; lobules connected to intercalated ducts via CCK zymogens are activated at the duoden brush border by ENTEROKINASE
26
Describe the structure of the exocrine pancreas
ACINAR LOBULES > INTERCALATED DUCT> INTERLOBULAR DUCT > PANCREATIC DUCT A + B CELLS > PANCREATIC ISLET > TO BLOODSTREAM
27
Describe the structure and function of the liver.
posta: connective tissue capsule allows branching + support portal triad: hepatic portal vein; hep art.; hepatic duct lobule: central hepatic vein => IVC
28
Hepatic blood flow
alimentary canal => hepatic portal vein => hepatic sinusoid Hepatic Arteries => hepatic sinusoid hepatocytes (bile synth, nutrient storage) ⇔ hepatic sinusoid Hepatic sinusoid => central vein => hepatic vein => RHS
29
Describe the composition and function of bile, the mechanisms controlling its storage and release from the gallbladder and the mechanism whereby it is reabsorbed.
Liver: prod and secr. of bile + bile components (bile acid from cholesterol) Bile is reabs and recycled @ileum via enterohepatic circulation/ excreted into urine / modified by bacteria
30
Falciform ligament significance
part of embryological foregut and forms a connection between the ventral abdominal wall and the liver.
31
Describe the structure and function of the small intestine
DUODENUM -acid neutr; digestion; Fe abs JEJENUM -abs ILEUM - NaCl/H20 abs => chryme dehydration
32
Describe the basic electrical rhythm and explain the difference between segmentation and peristalsis
segmentation: cicular muscles contraction - B.Elec.Rhythm determines frequency of segmentation - moves chyme up+down and brings into contact w/ abs surface and enzymes peristalsis: rythmic contraction of longitudinal muscles - pacemaker cycle through spontaneous depol->repol in longitudinal - sub-threshold > threshold => variable AP generated CN.X => ↑contraction VS Symp. ↓contraction
33
Describe the features which act to increase absorptive surface area along the alimentary canal
- PLICAE CIRCULARES: fold channels chyme follow - villi projections - lacteal core; peyer's; goblet cells - Crypt secretion of H20 via apical CFTR brings secretes Cl- => cell is -ve d/t 3Na pumped out for 2K (Na/K Cl co-transporter) -> Cl- gr builds up
34
State the structure and functions of the large intestine
simple columnar flat mucosa w/ large crypts + Goblets (stratified squamous epithleium @ anal canal - complete circular; incomplete longitudinal = TENIAE COLI = haustra pouches - COLON: active transport of Na from lumen->blood therefore abs of H20. Chyme dehydration.
35
Describe the importance of intestinal bacteria in the digestive process
Bacterial fermentation of undigested carbs • SCFA • Vitamin K synth • Flatulus
36
Describe the rectum, anal canal and rectal sphincters
Rectum: storage of stool until evacuation internal and external anal sphincters are rings of muscle at the opening of the anus. Keeps the anus closed as stool collects in the rectum. Increasing pressure on the rectum wall causes the internal anal sphincter to relax. external anal sphincter = skeletal muscle!
37
Describe the mechanisms controlling defecation
MASS MOVEMENT CONTRACTION => progressive distension of rectal wall (mechanoreceptors) Defection reflex (para. pelvic splanchnic nerves) - Rectal contraction - sphincters (int. relax ext constrict.) => descending pathways! - pressure on exp. sphincter
38
Describe the mechanisms which cause secretory diarrhoea and explain how this can be treated with simple salt/sugar solutions
enterotoxigenic bacteria (vibro cholerae; E. coli) activate Cl- secretion => H20 secretion ↑cAMP, cGMP, Calcium villus absorptive capacity hindered =>Na/Glucose solution drive H20 abs => reabs passive sodium-glucose cotransport (symporter)