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Renal - Zachow > Zachow - renal > Flashcards

Zachow - renal Flashcards

1
Q

Is there more intracellular fluid or extracellular fluid in our bodies?

A

Intracellular

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2
Q

What is an example where you might be euvolemic but the intravascular pressure is low?

A

Cardiac failure. The pump (heart) isn’t working properly, so it doesn’t adequately perfume the tissues, so the baroreceptors tell the brain to retain more water. Now there is too much fluid so you are at risk of edema.

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3
Q

What is an effective osmol?

- examples?

A

A solute which can not traverse cell. Membranes easily so they are sequestered somewhere.
Na+ and Glucose

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4
Q

What is one example of an ineffective osmol?

A

Blood Urea Nitrogen (BUN) - it readily traverses the plasma membrane.

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5
Q

Equation for effective osmolality? Range?

A

Effective osmolality = 2(Na+) + Glucose/18

285-295

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6
Q

Does glucose get filtered? Does it get reabsorbed? What is it’s clearance?

A

Glucose gets completely filtered and then completely reabsorbed. It’s clearance is zero because all of the glucose should be put back into the body and not peed out.

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7
Q

Is protein filtered? Reabsorbed? What is the clearance of protein?

A

Proteins are not filtered, so there will be the same amount of protein in the renal artery and renal veins. It is not reabsorbed because it is not filtered. It should also have a clearance of zero because there should be none in our urine.

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8
Q

Is creatinine filtered? Reabsorbed? What is the clearance of creatinine?

A

Creatinine is filtered into the roaming urine. It is not reabsorbed. The clearance of creatinine is an indicator of GFR.

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9
Q

Is there a Difference in GFR between sexes? At different ages?

A

Men have higher GFRs, and as you get older your GFR will go down.

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10
Q

What would you like your GR to be above?

A
  1. If it is below 15 you have kidney failure. ANything in between is varying levels of kidney damage. But again, remember, as you get older your GFR will just gradually decrease.
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11
Q

Who will have elevated creatinine?

A

People with kidney damage
People who we would generally consider more muscular
People who eat a lot of meat

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12
Q

As GFR Decreases what happens to BUN and plasma creatinine levels?

A

Increase

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13
Q

What is a filtered load? Fractional Excretion?

A

Filtered Load - amount of something filtered per unit time.

Fractional Excretion - Ratio of amount of substance excreted in urine divided by filtered load

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14
Q

What forces Are pushing water out of the glomerulus into bowman so capsule? What forces are going from bowman so capsule into the glomerular capillary? Who wins?

A

The hydrostatic force of the glomerular capillary is pushing liquid out as well as the oncotic pressure of bowman so capsule.
Things that are trying to bring liquid into the glomerular capillary from bowman so capsule is the hydrostatic pressure of bowman so capsule as the oncotic pressure of the glomerular capillary.
Of course The first set of conditions wins because it causes filtration.

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15
Q

Where are the two biggest drops in pressure in the nephron?

A

Afferents and Efferent arteriole

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16
Q

WHat is the difference between the peritubular capillaries and the vasa recta?

A

Peritubular capillaries surround the proximal and distal convoluted tubules. The vasa recta surround the loop of henle.

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17
Q

Why is reabsorption generally favored by the peritubular capillaries?

A

Essentially, there is a great amount of hydrolic pressure in the forming urine in the PCT so fluid will want to flow to the peritubular capillary. In addition, there is great oncotic pressure in the peritubular capillary because most things were left in the blood flow, so the fluid will want to flow it as well.

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18
Q

TGF Mechanism of blood pressure regulation

A

Essentially, there are these things called macula densa cells in the macula densa in the thick ascending limb that can sense NaCl concentrations. In BP goes up, then GFR goes up, and there is more NaCl in the forming urine. The macula densa cells recognize this and are activate. They then secrete vasoconstricters into the afferents arteriole such as aldosterone are thromboxane. Remember that the TAL and the afferents arteriole are right next to each other.

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19
Q

What does renin do? Where is it secreted from?
What does ACE do?
What receptors does AII bind to?

A

1) it converts angiotensinogen to AI and it is secreted from juxtaglomerular cells
2) ACE converts AI–>AII
3) AII binds to AT1-R and AT2-R

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20
Q

In what. Way does. The kidney control renal BP?

A

It was renin being secreted from juxtaglomerular cells, which are triggered to activate by SNS fibers. Then, in the peritubular epithelial cells there is both ACE and angiotensinogen.
So, in the effect of low BP, the system is activated and the efferent arteriole is constricted so that the GFR increases, which largely favors reabsorption because it increases the gradient.

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21
Q

Why does the RAS system activate when we are low in BP? Why would we want to vasoconstrict? Less blood will get to the efferent arteriole and to systemic circulation?

A

This is because when we have low BP, the RAS system is being activated systemically as well in order to increase conservation. Additionally, if we decrease t he amount of liquid going through the efferent arteriole to the peritubular capillaries, then there will be a gradient for reabsorption of Na+ and water to occur. Reabsorption occurs optimally at specific GFR ranges. If BP is low, then GFR is reduced, so we vasoconstrict for GFR to go back up.

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22
Q

What are two thing That effect intrarenal BP?

A

TGF mechanism - macula densa cells

RAS - SNS activated

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23
Q

What does AT1-R do? AT2-R?

A

1 - Conservation - Intrarenally, it causes vasoconstriction, Na+ reabsorption, SNS tone. Impairs renin secretion because of negative feedback mechanism. Outside of the kidney it causes the same things but also aldosterone secretion.
2 - excretion - Essentially the opposite of AT-1R. NO, cGMP, Bradykynins

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24
Q

What will an ARB Do?

A

Angiotensin receptor blocker. Exampled is losartan. They selectively block AT-1R so we will see vasodilation and so decreased GFR. Also, the AT-R1 can sometimes cause some bad consequences so we will sometimes shunt some of the AII over to the AT-R2

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25
Q

How can it be that you can give an ARB and ACEI and still not have a drop in BP?

A

When we do this, our renin levels will continue to rise and rise with nowhere to go (partially because AII can’t provide negative feedback). So, there are these things called ACE-independent Chymases, which, as the name implies, can convert AI into AII independently of ACE and then can bind to AT-R1 that can’t be blocked by ARB.

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26
Q

What happens WheN We have pathophysiologically low BP?

A

So normally when we have low BP, there is vasoconstriction of the efferent arteriole and vasodilation of the afferent arteriole. This increases GFR and results in good reabsorption. When BP is reaaaaaly low, then the afferent arteriole constricts as well and we start to see inadequate renal perfusion, which leads to renal ischemia.

27
Q

Name all relevant transporters in the proximal tubule

A 
SGLT
NHE-3
GLUT
Na+/HCO3- transporter
Na+/K+ ATPase
28
Q

SGLT

A

Found in the proximal convoluted tubule, it reabsorbs Na+ and glucose from the forming urine back into the peritubular cells so that these things can eventually be reabsorbed into the circulation.

29
Q

NHE-3

A

Found in the Proximal convoluted tubule as well as the TAL, the NHE-3 reabsorbs Na+ from the forming while kicking out H+ From the peritubular epithelial cell to the forming urine. This allows the Na+ to eventually be reabsorbed into circulation. It is activated by AII binding at AT-R1. Keep in mind that this means that NHE-3 plays a role in acid-base

30
Q

GLUT

A

Found in the proximal convoluted tubule, it reabsorbed glucose from the peritubular epithelial cell to circulation.

31
Q

Na+/K+ ATPase

A

Found in the proximal convoluted tubule, it reabsorbs Sodium from the peritubular epithelial cells to circulation and moves K+ from circulation to the peritubular epithelial cells.

32
Q

Na+/HCO3- cotransporter

A

Found in the proximal convoluted tubule, it Reabsorbs both sodium and bicarbonate from the peritubular epithelial cells to circulation.

33
Q

What important transporters are there in the Thick Ascending Limb (TAL)?

A

NKCC
ROMK
NHE-3
Cl-/HCO3- exchanger

34
Q

NKCC

A

Found in the TAL, it reabsorbs Na+, K+, and 2 chlorides into the peritubular epithelial cell from the forming urine. It is activated by AII meeting the AT-1R

35
Q

ROMK

A

FOund in the TAL, it excreted K+ from the peritubular epithelial cells to the forming urine.

36
Q

What transporters are found in the distal convoluted Tubule??

A

NCC
ENaC
Calcium transporter
NaCl transporter on basolateral side

37
Q

NCC

A

Found in the Distal convoluted tubule, it reabsorbs Na+ and 2 Cl- from the forming urine back into the peritubular epithelial cells. It is activated by AII meeting with AT1-R. It is the target for thiazide diuretics.

38
Q

ENaC

A

Sodium transporter found in the DCT that just brings sodium back into the peritubular epithelial cell from forming Urine. Activated by AII

39
Q

What does Furosemide act on?

A

NKCC, be very careful bout Ca+ levels when you. Do this because it Will lower them a lot.

40
Q

What does HCTZ (thiazides in general) act on?

A

NCC

41
Q

What does aldosterone do?

A

Na+ reabsorption and K+ secretion

42
Q

What are the two types of cells in the cortical collecting tubule (CCT) and what do they do? How does aldosterone play a role?

A

Principal cells - responsible for Na+/K+ balance
Intercalating cells - Responsible for proton (bicarbonate) and K+

Aldosterone activates ENaC here and ROMK and a Na+/K+ ATPase in the principal cells. Aldosterone also activates an K+/H+ ATPase as well as an H+ ATPase in the intercalating cells in order to excrete H+ into the forming urine.

43
Q

Where is aldosterone made?

A

ZOna glomerulosa in the adrenal cortex

44
Q

So, we said that aldosterone trades sodium for potassium, but wouldn’t that make us hyperkalemic?

A

So we said that aldosterone is Responsible for activating Many transporters. One of them was ROMK, which essentially just excretes potassium. So aldosterone still does activate all of those other transporters (NCC, ENaC), but in the case of ROMK, it only activates ROMK when we are hyperkalemic, in which case it is coupled with other things to excrete potassium. In the case where we are hyperkalemic, aldosterone activates ROMK but in activates NCC, so we have blunted sodium resorption so we are not hypervolemic but still excrete potassium.

45
Q

Salt-sensitive vs. salt-insensitive

A

If you are salt-sensitive, then when you ingest sodium you all have an increase in MAP, that Is accompanied with the excretion Of sodium. However, if you are salt-insensitive, then when you ingest salt, you won’t have a proportional increase in sodium excretion, so your BP rises.

46
Q

Can the brain sense BP?

A

Well, the Bain has sodium sensors, so if you are high in NaCl, the Na concentration in your CSF will go up. This is a stimulus to upregulate AII in the brain, and eventually aldosterone. This causes systemic Na resorption, but it is also coupled to the production of Ouabain, which will upregulate the aldosterone secretion from AT-1R. Ouabain also causes systemic vasoconstriction by disrupting NCX. So, Ouabain will essentially be secreted in high sodium environments in the Brain and will cause systemic vasoconstriction due to blocking the NCX transporter. This will elevate blood pressure.
- if you think about it, usually the RAAS system is activated in low sodium environments, but here it is being activated in a high sodium environment.

47
Q

Mineralocorticoid Hypertension

A

Essentially there is too much aldosterone being secreted. It can either be primary or secondary. Essentially the reason for this is that aldosterone would be really activating ENaC so there would be a lot of sodium reabsorption, but at the same time though we would be losing a lot of potassium from ROMK so they might be hypokalemic.

48
Q

Pseudohypoaldosteronism

A

Essentially not enough aldosterone is being made. These people might be hyperkalemic. You might also see metabolic acidosis because aldosterone is coupled to H+ secretion. Of course, expect hypotension. The reason for this is that there is a Mutation in the ENaC transporter, so not enough Na+ can be reabsorbed and so we tone down the aldosterone levels.

49
Q

What are the receptors that respond to ADH/AVP/Vasopressin?

A

V1aR, V1bR, V2R.

The one that we are concerned with here is V2R. V2R will higher BP by holding on to water.

50
Q

What does AVP///ADH/ Vasopressin do?

A

In the last part of the nephron, the pressure inside is much higher than the pressure outside do things will want to leave. However, it can’t unless AVP///ADH/Vasopressin is present, because it activates aquaporins to let’s water out.
So, it causes antidiuresis and vasoconstriction.

51
Q

ANP

A

It is Secreted From the right atrium when the right atrium is distended. It becomes distended when the blood volume goes up (also BP goes up). It causes vasodilation, increased GFR, and natriuresis. It also inhibits renin.

52
Q

Diabetes Insipidus

A

Basically the AVP system isn’t working. If it is neurogenic then not enough AVP is being made. If it is nephrogenic, then plenty of AVP is being made but it is not being responded to. Therefore, the person will be peeing a lot, have too much blood volume. Also, as opposed to diabetes mellitus, the urine will not be sweet. She would also be hyperosmolar because if you remember. The mechanism of action of AVP, if it doesn’t work then you wouldn’t have water reabsorption, so there would be more Na+ per water.

53
Q

SIADH

A

Again, it can Be neurogenic or nephrogenic but essentially you will have too much AVP. Because of this, the person might have a high BP, concentrated urine, infrequent urination. They would be nyponatremic.

54
Q

Where is AVP excreted from?

A

Posterior pituitary gland

55
Q

Renal Tubule Acidosis (RTA)

A

Renal pathologies where the kidney can no longer buffer like they should. You will see a metabolic acidosis with no AG and hypercalemia. There is Type 2 (proximal) or type 1 and 4 (distal)

56
Q

Type 2 RTA

A

In the PCT, you would see a hyperchloremia, problems in their Vitamin D and Calcium levels, and they would have glucose in their urine but not have high glucose levels in the plasma.

57
Q

WHat would a UAG look like in a person with an RTA?

A

It would be positive. If you remember, the equation is UNa + UK - UCl. So, in an RTA there is often problems forming NH4+, which is one of the cations that is not measured, so there would be more detectable cations than there should be, and because NH4+ usually combines with Cl- to be excreted, the amount of Cl- will be lower in the urine too, so UAG will largely positive.

58
Q

WHy will increased aldosterone cause hypokalemic metabolic alkalosis?

A

So, if you remember, in the distal nephron, aldosterone is responsible for activating many transporters that are involved in H+ secretion. So, pH would rise because of the loss of all of these protons. In order to combat this, they do a K+/H+ swap to bring pH back to normal. This would cause excretion of K+ and hypokalemia. Keep in mind HCO3 levels will rise because the excreted protons will also largely combine to form HCO3-.

59
Q

What does insulin do? Where is it made?

A

Insulin lowers blood glucose in the liver, adipocytes, and skeletal muscle. It halts the breakdown of glucagon into glucose and causes the uptake of FFA and glucose and their conversion into fatty AIDS, triglycerides, and lipids. It is made in the beta cells of the islets of langerhans in the pancreas.

60
Q

What role do the kidneys play with regard to insulin?

A

They break down insulin. So, if you have renal failure, then you will be unable to break down insulin and that will cause you to have a really low blood sugar level.

61
Q

what happens to the kidneys of people with diabetes mellitus?

A

Because there will be so much glucose in the blood it eventually it will end up in the urine. Because of this, the SGLT transporters become saturated as well as the GLUT. AFter a while, Due to hyperfiltration, the slit pores will get larger and you will get albumin in your urine. Your BP will also creep up. Of course, GFR will decrease and BUN and creatinine will increase.

62
Q

What ion/s do you lose when you have diarrhea?

A

HCO3-

K+

63
Q

What are some BP sensors and what do they sense?

A

Baroreceptors in the aortic and carotid bodies
Osmoreceptors in the hypothalamus sense osmolality
Macula densa cells sense amount of NaCl

Renal - Zachow (7 decks)

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