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princip, pharm, phys, regional > phys-renal III > Flashcards

phys-renal III Flashcards

1
Q

what is the difference between pressure diuresis and pressure naturesis?

A
  1. pressure diuresis is when excess water pressure causes fluid to be excreted into filtrate
  2. pressure naturesis is when excess salt is excreted and water follows
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2
Q
  1. what makes sodium a “slow leaker”?

2. why is that good?

A
  1. in the potassium leak channels, potassium leaks 100:1, sodium is charged as well but it needs a protein carrier to move thru (i.e. cotransporter).
  2. the caveat is, that when sodium moves, water moves right behind it
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3
Q
  1. how many intra renal mechanisms do we have?

2. what are they?

A
  1. 2

2. glumerular tubular & macula densa

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4
Q

what does the glumerular tubules do to

A

use paracrine hormones to increase the GFR (vasoconstrict the EFFERENT arterioles- this slows down the outflow) and affect the tubule reabsorption rate by giving it more time to reabsorb.

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5
Q

name the paracrine hormones

A

bradykinin, prostaglandins (F etc.)

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6
Q

how does the macula densa (which is part of the JGA) affect filtration?

A

The macula densa monitors sodium level in filtrate. if the sodium is LOW, the macula densa will allow the granular cells to secrete renin which vasoconstricts the afferent tubule. this decreases the bloodflow coming IN and DECREASES the reabsorption time (allowing more sodium to be excreted in filtrate).
macula densa and renin increase secretion

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7
Q

what is an extra renal mechanism

A

maintain homeostatis using neural and hormonal means.

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8
Q

what hormonal mechanisms maintain the kidneys

A
  1. respond to low pressure
  2. renin/angiotensin/aldosterone
  3. ADH
  4. ANP (atrial naturetic peptide)-
  5. ANP responds to high pressure, the rest are secreted during low pressure.
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9
Q

extrarenal: neural mechanism-

what neurotransmitters work on the kidneys?

A

sympathetic system (NE, epi)

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10
Q

glumerulus and macula densa work in conjunction how?

A

take turns opposing each other to maintain self regulation

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11
Q
  1. what is ANP
  2. what does it do?
  3. how does ANP work?
A
  1. a hormone secreted by the atrial walls (endocrine glands)
  2. decreases intravascular fluids; stimulated by stretch on heart (atrium)
  3. causes an increase in GFR which decreases sodium (pressure naturesis) which decreases fluid (tries to reduce BP).
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12
Q

with the pressure/ filtrate model; what are the nornal parameters:

  1. map?
  2. liters/day u/o
A
  1. map=96

2. u/0=1L/day average

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13
Q
  1. whit the u/o/ pressure curve; what happens if you have acute changes in pressure (MAP)?
  2. what does a slight but chronic increase in presure cause?
A
  1. acute increase in pressure causes a slight increase in urine output
  2. a chronic increase in pressure causes a significant increase in urine output
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14
Q

what happens with chronic HTN to increase urine output?

A

HTN over time supresses renin/angiotensin system. without renin/angio, no sodium is reabsorbed so you pee it all out

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15
Q

what can help to buffer some of the blood pressures effect on urine output?
1-what happens with increased pressure?
2-what happens with decreased pressure?

A

starlings hypothesis: blood hydrostatic
1-increased pressure increases filtration. this increases filtration which dereases venous return and causes edema.
2-decreased pressure decreases filtration which increases venous return

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16
Q

what happens with extra venous blood ?

A

shunted back to the heart

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17
Q

why does blocking renin cause alot of diuresing in chronic HTN?

A

–eventually the high blood hydrostatic stretches the podocytes which causes osmotically active protein to leak into the filtrate. ——this draws even more water

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18
Q

How does the extrensic system work?

A

uses sympathetic postganglionic nerve fibers: nor epi and epi stimulate B receptor in JGA. this secretes renin/angiotensin and/ aldosterone. this causes increased reabsorption in the PCT. the arterioles vasoconstrict to decrease GFR. (slow down production line and work harder to pull out nutrients).

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19
Q

how does the kidney respond to low Na+ or low BP?

A
  1. angiotensinogen produced in liver (affected by scirrosis)
  2. renin released by granular cells
  3. renin cleaves angiotensinogen to angiotensin 1
  4. angotensin 1 goes to lungs and is converted to angio2 by ACE
  5. angiotentin 2 : constricts systemic vessels and efferent arteriole; increases thirst (to increase volume), increases reabsorption in PCT; and stimulates release of aldosterone from adrenal medulla.
20
Q

where des aldosterone work>

A
  1. cortical duct
  2. late distal convoluted tubule

cause increase in sodium reabsorption & K+ or H+ secretion

21
Q
  1. 65% of gross adjusting is done by ___?
  2. what causes it to increase?
  3. what can it increase to?
A
  1. PCT
  2. angiotensin II
  3. 75%
22
Q

how does the body ion trap phosphate ion?

A
  1. HPO4– is able to cross membrane easily (2 negative charges)
  2. it joins with H+ ions outside of apical & basolateral membrane
  3. becomes H2PO4 which is non lipid soluble, cannot re-enter
23
Q

ion traping of ammonia?

A
  1. glutamate (amino acid) in cell gets broken down
  2. the acetyl group is taken to krebs
  3. leaving a NH3 (ammonia) component
  4. ammonia diffuses thru membrane and joins with H+
  5. this forms lipid insoluble ammonium ion NH4+
24
Q

which one does more reabsorption of the vessels; Peritubular capillaries or vasa recta?

A

peritubular capillaries (98%)

25
Q

what happens in the proximal convoluted tubule (PCT), interstitial fluid, and peritubular capillaries (PTC)?

A
  1. sodium, K+, chloride, amino acids, glucose and bicarb are drawn from filtrate into interstitial fluid
  2. blood oncotic (32mmhg pull)and tissue hydrostatic (6 mmhg push) gets nutrients into blood. (38 total into blood vessel)
  3. blood hydrostatic pushes 13mmhg and tissue oncotic pulls 15 mmhg (28 going out)
  4. 38-28=+10 going into vessel (peritubular capillary)
26
Q

on a graph, how does an acute change in bp differ from a chronic elevated bp as far as urine out put (what degree angle does each one repersent)

A

chronic=90 degree angle (|) of increased urine

acute=45 degree (/) with of increased urine

27
Q

at the PCT: describe the fxn of angiotensin II graph
blockage of angiotensin
normal angiotensin
high angiotensin

A
  1. blockage of angio II = low pressure naturesis (45 degree from 40-90mmhg)
  2. normal angiotensin =90 degree angle at map of 96 mmhg
  3. high angiotensin II= pure naturesis (45 degree from 96 to 180mmhg)
28
Q

osmoreceptors in the hypothalamus do what in ersponse to:
1.hyperosmotic or
2. hypoosmotic fluid?
( what hapens to them, and how do they respond?)
3. what type of hormone is ADH

A
  1. hypo osmotic=swell-will decreas ADH release (expell more water)
  2. hyper osmotic=shrink- will increase ADH release (retain more water)
  3. neuropeptide
29
Q

what happens in DI

A

UNDERsecretion of ADH, which allows for copious amounts of urine and loss of sodium.

30
Q

what about GFR seems counterintuitive?

A

to increase re-absorpion you must decrease the GFR
GFR means how fast you pass fluids through

to increase filtration, you increase the GFR

31
Q

what hormone has the highest control over BP and renal sodium?

A

angio II (90%)

aldosterone ony does 5-10%

32
Q

what can cause the release of aldosterone?

A

high potassium or low sodium

sodium exchangers pull Na+ in and kick out K+ or H+

33
Q

if angiotensin level is high, what will happen?

A

you will have a high reabsorption rate (you pull in alot of Na+ which increases your BP and makes your GFR go up).

34
Q

what is cushing’s disease?

A

adrenal hyperplasia…

  1. the number of adrenal cells increases.
  2. This in turn causes increase in aldostorone production
  3. this causes increase in Na+ reabsorption (hypernatremia)
  4. causing high pressure naturesis causing excess K+ secretion (hypokalemia)
  5. this lowers resting potential below threshold (now it takes more to reach action potential)
  6. aldosterone also exchanges sodium for H+ (& K+), loss of H+ leads to metabolic alkalosis
35
Q

what is addison’s disease?

A
  1. autoimmune cells destroy adrenal glands
  2. inability to produce aldosterone decreases Na+ reabsorptin (hyponatremia)
  3. this pulls more fluid into the urine to dilute the excess Ns+
  4. dehydration and hyperkalemia with excess H+ (acidosis) due to lack of Na+/K+;H+ exchange.
  5. resting potential is increased by hyperkalemia- easir to reach action potential (hyper excitable).
36
Q
  1. normal K+ levels
  2. what is lethal?
  3. small changes in K+ make ___ changes in ____?
A
  1. 3.5-4.5
  2. > 8
  3. large changes in resting membrane potential
37
Q

causes of

  1. hyperkalemia:
  2. hypokalemia:
A
  1. hyperkalemia: cell lysis, acidosis (DKA etc), strenuous exercise
  2. hypokalemia: hyperaldosteronemia, hyperinsulinemia, alkalosis, sympathetic stimulation (only slight)
38
Q

what controls calcium levels?

A

parathyroid hormone (which is active in PCT)

39
Q

how much of CO2 is transported as bicarb?

A

75%

40
Q

since H+ and K+ trade places, what does alkalosis cause and acidosis cause
(remember, it’s inside the cell that we speak of in terms of acidosis or alkalosis)

A

alkalosis=hypokalemia

acidosis=hyperkalemia

41
Q

what is the action of the principal cell?

A
  1. to trade Na+ for K+/H+ at the anterolateral membrane and allow 3:2 exchange of Na+ out/ K+in respectively.
    ( in essence it gets rid of excess K+ or H+)
42
Q

what do intercalated cells do?

A

pretty much get rid of excess acid (H+) using carbonic anhydrase

43
Q

central chemoreceptors read what?

A

co2 levels (by seeing how many H+ ions are made)

44
Q

periphreal chemoreceptors read what?

A

CO2, but also O2 and H+

45
Q

name the kidneys 2 capillary beds:

A

glumerulus

peritubuar capillaries

46
Q

cells of thick ascending loop????

A
  1. has a triple co-transporter that pulls in Na+, K+, and 2 Cl- in the anterolateral membrane
  2. exchanges 2K+ (in) for 3Na+(out) at the basolateral membrane
  3. potassium leaks out side leak channels and up thru tight leaky junctions into filtrate
  4. this repels calcium pushing it thru tight-leaky jxn into interstitial space.

princip, pharm, phys, regional (18 decks)

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