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Physiology Block IV Flashcards

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1
Q

What is the class, origine, stimuli, and function of vasopressin/ADH

A

Vasopressin is a small peptide released from the hypothalamus. Its stimuli are hyperosmolality and hypotension. It increases distal nephrone water uptake and is a vasoconstrictor

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2
Q

What is the class, origin, stimuli, and function of aldosterone?

A

aldosterone is a steroid released from the zona glomerulosa of the adrenal cortex in response to hypotension and hyperkalemia. it increases renal Na uptake and K excretion.

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3
Q

What is the class, origin, stimuli and function of renin?

A

Renin is a proteolytic enzyme released by vascular smooth muscle in response to hypotension, decrease of Cl delivery to the macula densa, and renal sympathetics. It increases renal Na uptake, and aldosterone synthesis. It is a vasoconstrictor.

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4
Q

What is the class, origin, stimuli, and function of atriopeptin?

A

It is a small peptid released by atrial myosites in response to hypervolemia. It increases GFR, decreases aldosterone production ,adn decreases prox. tubular uptake of Na and water.

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5
Q

Which receptor has the higher affinity for CCK as compared with gastrin? What mediates this effect?

A

CCK-1 receptors have a much higher affinity for sulfonated CCk than for gastrin (sulfonated tyrosyl)

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6
Q

what effects are mediated by CCK binding to cck1 receptors?

A

strongly- gall bladder contraction and pancreatic secretion

weakly- gastric acid secretion

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7
Q

what affects are mediated by gastrin?

A

strongly- cck2 receptors- gastric acid secrtion

weakly- cck1 receptors- gall bladder conctraction and pancreatic secretions

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8
Q

where are cck1 and cck 2 receptors located?

A

cck1- gall bladder and pancreas

cck2- stomach

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9
Q

what three factors determine the specificity of gastrin and CCK for their given receptors?

A

concentration (gastrin much much higher than cck after a meal), affinity (cck has a much higher affinity for cck1 receptors than gastrin when it is sulfonated), and location (cck1 in gall bladder/pancrease; cck2 in stomach

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10
Q

which part of secretin ins needed for its activity?

A

all 27 aas necessary

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11
Q

what are the trophic effects of gastrin and cck?

A

growth of gastric secreting cells (gastrin)

cck- growth of exocrine pancreas

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12
Q

what enteric nervous system plexus is responsible for controlling motility throughout the gut? between what two layers is it found?

A

aurbach’s plexus/myenteric plexus between the outer longitudinal and inner circular layers of the digestive tract?

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13
Q

What plexus controls most of epithelial cells secretion and blood flow in the gi tract? where is it located?

A

meissner’s plexus/ submucosa. located in the submucosa

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14
Q

What is the important symporter and two important antiporters of the salivary gland?

A

Na-2Cl-K cotransporter and the Na/H and Cl/HCO3 exchangers (Na and Cl in; h and HCO3 out into blood. HCO3 can also leak into the lumen through the Cl channels).

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15
Q

Which part of the salivary gland is relatively impermeable to water?

A

the duct.

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16
Q

What are the roles of gastric acid?

A
  1. convert pesinogen to pepsin, which promotes further conversion since the initial pepsins can autocaltylyze to make more pepsin from pepsinogen.
  2. provide a good environment for pepsin action
  3. antibacterial stuff
  4. break down digested food.
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17
Q

Describe/draw the ion channels, transporters, and pumps of the parietal cell.

A

parietal cells border the blood and the stomach lumen.
there is an NaKATPase on the blood side. There is an KH pump on the lumen side. H is pumped into the lumen and K is pumped into the cell. this is an active process
There is a luminal K channel to prevent excessive K buildup from both pumps.
The H for the pumps/secretion comes from the break down of water and its interaction with CO2 to form HCO32.
The HCO3 is secretedinto the blood in an HCO3/Cl exchanger (no energy required). Cl is secreted into the lumen via luminal Cl channels.

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18
Q

What is the alkaline tide?

A

alkaline tide refers to the way you can roughly estimate HCl secretion intothe stomach lumen based on how much HCO3 has been secreted into the blood through the HCO3/Cl exchanger

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19
Q

What happens to the Na concentration in the stomach as gastric secretion goes up?

A

Na concentration goes down- it is diluted by HCl solution!

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20
Q

Describe control of gastric acid secretion in the resting state.

A

parietal cells secrete acid constitutively. Low pH stimulates D cells. D cells secrete somatostatin. Somatostatin inhibits gastrin secretion by G cells.

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21
Q

What are the three components of the gastric mucosal barrier?

A
  1. alkaline mucus
  2. tightness of gastric epithelium
  3. continuous, rapid cellular renewal.
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22
Q

What are the three treatments for ulcers?

A
  1. inorganic antacids
  2. H2 histamine blockers
  3. H/K ATPase blocers
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23
Q

What cells do most bile secretion?

A

hepatocytes

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24
Q

where and by what are primary and secondary bile acids made?

A

primary made in hepatocytes; secondary made from primary by bacteria in the intestinal lumen, esp. the ileum

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25
What is enterohepatic circulation?
bile salts are reabsorbed in the ileum, circulate through the blood until they get to the liver, and then are resabsorbed by the hepatocytes.
26
To where is the bile secreted by the hepatocytes between meals?
the gall bladder
27
What regulates the secretion rate of bile by the hepatocytes and gall bladder.
the conc. of returning bile salts in the portal blood- the more bile salts returning to the liver, the more secretion. Also secretin. gall bladder: CCK in a meal causes contraction of gall bladder and dilates the sphincter of Oddi. vagal release of ACh is similar in effect to CCK
28
What are the two main taypes of digestive activity in the gut?
cavital- takes place in the lumen of the gut as a result of secreted digestive enzymes membrane/contact digestion- takes place directly at the apical surface of the small intestine via enzymes anchored in the wall of the intestinal epithelial cells.
29
which enzyme that digests carbs can cleave 1,6 glycolytic bonds? What is the most important luminal enzyme for carb digestion?
1,6 bonds is isomaltase | luminal is amylase
30
what monosaccharides are absorbed by intestinal epithelial cells?
glucose galactose and fructose
31
What are the two groups of pancreatic peptidases?
enteropeptidases (trypsin, chymotrypsin, elastase)- act on a specific sequence within a peptide chaine exopeptidases (carboxypeptidases A and B)- hydrolyse the carboxyterminal peptide bonds in sequence along the peptide chain
32
What happens to the small peptide products of secreted peptidases/proteases?
further broken down by brush border membrane anchored proteins
33
what cells contain renin?
juxtaglomerular cells
34
What are the two main things that renin/antiotensin does? (very broad)
defends bp and blood vol. causes vasoconstriction and retains sodium
35
What are three major stimuli for renin release? what inhibits renin release? Where are these stimuli sensed?
stimuli: decreased bp in afferent arterioles, decreased NaCl delivery to early distal convoluted tubule/very late TAL, increased renal sympathetic nerve activity (beta 1 receptors mediate this effect directly) inhibition: angiotensin II
36
Where are juxtaglomerular cells located? Where are macula densa cells located?
JG cells in afferent arteriole. macula densa in early distal tubule.
37
Congestive heart failure is a pathology that often leads to the release of what hormone? through what mechanism
renin/angiotensin (aldo) through increased rneal sympathetic nerve activity
38
What receptors mediate angiotensin vascular smooth muscle vasoconstriction?
AT1 receptors
39
By what THREE mechanisms does angiotensin II promote sodium retention?
1. directly: increased early prox. tubutlar Na reabsorption by increasing activity of NaH exchanger 2. preferentially constricts efferent arterioles more than afferents (decreases blood flow, increases filtration fxn, decreases cap pressure and increases osmotic pressure, which promotes reabsorption) 3. stimulates aldo synthesis and release
40
What are the two MAJOR stimuli for aldosterone release?
angiotensin II (and anything that causes sustained release of angiotensin II), and high K concentration in the ECF.
41
What are the two major (general) actions of aldosterone? Any specifics? What is an important indirect effect?
1. increase renal K secretion (ENaC and NaK pump) 2. increase renal Na reabsorption- ENaC and Na/K pump in CCT princpal cells. 3. Acid secretion- increase K in lumen, gets involved w KH exchanger in alpha cells.
42
What is aldosterone escape?
describes the phenomenon where continued high aldo is ineffective in maintaining high rates of sodium retention. this is because increased vol. leads to atripeptin release and pressure natriuresis
43
What are the main stimuli for vasopressin release (2 MAIN stimuli)
INCREASES in ECF osmolality | changes in blood vol or blood pressure
44
What kind of diuretics are used to treat SIADH? Why?
loop diuretics to prevent concentration of urine. (SIDAH pts retain water but lose sodium normally so they are hyponatremic- we want to prevent them from concentrating their urine so that they don't loose so much sodium)
45
What kind of diuretics can be used to treat diabetes insipidis? Why?
thiazide diuretics (these patients don't retain enough water, so they are hypernatremic. we want them to loose sodium, so thiazides should do the trick!)
46
What four factors contribute to thirst?
angiotensin II, increased ECF osmolality, and decreased blood vol./pressure as detected by baroreceptors
47
What stimulates ANP release?
increased blood vol in atrium
48
What are the effects of ANP
Increase GFR, decrease Na reabsorption, inhibit vasopressin-induced reabsorption decrease renin inhibit angiotenisn decrease aldo secretion vaso dilate increase vascular permability inhibit thirst
49
How is fructose absorbed from the small intestine?
via facilitated diffusion
50
how are glucose and galactose absorbed from the small intestine? How are they taken into the blood?
absorbed via Na-coupled secondarily active transport. secreted in blood via carrier mediated facilitated diffusion
51
how are di and tripeptides absorbed by intestinal epithelial?
proton coupled cotransporter
52
how are free amino acids absorbed by intestinal epithelium?
sodim coupled secondarily active transport
53
how are amino acids tranported into blood from intestinal epithelial cells?
non-sodium coupled transporters
54
What five factors increase K uptake by Na/KATPases to allow for potassium buffering by the ICF
increased extracellular K conc. insulin, beta 2 agonist receptors incresed pH, aldo
55
what factors increase k secretion in the principle cells?
increased Na delivery distally (ie. lots of Na in the collecting duct area. this causes membrane apical membrane depolarization as sodium enters the cell, increased NaK pump activity, and therefore increased K secretion. increased flow rate- washes secreted K away, so we see incr. K secretion to make up for that. reduced urinary Cl concentrations- sodium reabsorbtion must be balanced by K secretion from a charge perspective. aldo- increased Na reabsorption, leading to membrane depol, leading to K secretion. A
56
What are the two biggest stimulators of ADH
incr. osmolality and hypovolemia
57
what is the effect of ADH on the glomerulus?
vasoconstriction and a decrease in filering surface area of glomerulus
58
what are the effects of ADH on the collecting ducts?
cortical collecting duct- water reabsorption and K secretion | medullary- water reabsorption and urea reabsorbtion (for recycling!)
59
which part of the collecting tubules is permeable to urea?
the innermost medullary collecting ducts
60
how does urea recycling work?
in the presence of ADH, water is reabsorbed in the cortical collecting tubules and the outer medullary collecting tubules.
61
what is the key reason that we don't see hyponatremia with loop diuretics?
loop diuretics prevent the establishment of a significant gradient in the medulla around the LOH. therefore, even when ADH adds water channels in the CCT in response to vol. depletion, there is less drive for water to be reabsorbed in the CCT, so water and sodium are lost proportionately and there isn't hyponatremia.
62
What do we see with diarrhea in terms of acid base?
normal anion gap with negative urine anion gaps. we see loss of K and bicarb, both through diarrhea and through aldo to correct for vol. depletion
63
what do we see in renal tubular acidosis?
normal anion gap in the serum but positive urinary anion gap
64
what happens in type II renal tubular acidosis?
decreased acidification in the proximal tubule.- we aren't getting bicarb regeneration. also some hypokalemia.
65
what happens in type I renal tubular acidosis?
it is hypokalemic distal tubular problem. little HCO3 reclamation and, importantly, impaired proton secretion.
66
what happens in type IV renal tubular acidosis?
decreased distal H and K secretion, so hyperkalemic. ex. is insensitivity to aldo
67
do we see normal or increased anion gap with renal failure (serum)
increased anion gap

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