Renal Physiology Review Flashcards

1
Q

A patient with essential HTN has vasoconstriction/dilation at afferent arterioles and vasoconstriction/dilation at efferent arterioles?

What controls this?

A

Vasoconstriction at afferent.
Vasodilation at efferent.

High pressure at juxtaglomerular apparatus leads to DECREASED RENIN secretion&raquo_space; low Ang II&raquo_space; VASODILATION at efferent arterioles

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

A patient with renal artery stenosis has vasoconstriction/dilation at afferent arterioles and vasoconstriction/dilation at efferent arterioles?

Why?

A

Vasodilation at afferent arterioles.
Vasoconstriction at efferent arterioles.

Low pressure at afferents. INCREASED RENIN SECRETION&raquo_space; increased Ang II&raquo_space; vasoconstriction of efferent arteriole

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

A patient comes in with diarrhea, vomiting, or hemorrhaging. What is important to conserve?
What is one way to do this?

A

Extracellular volume by increasing reabsorption of fluid and electrolytes at PROXIMAL TUBULES.

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

What is not working in nephrogenic DI? What is not possible to do?

A

ADH receptors. Not possible to increase reabsorption at CD.

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

How do you treat nephrogenic DI?

What does this correct?

A

Tx - thiazide diuretic reduces extracellular volume, which increases peritubular oncotic pressure&raquo_space; increasing water reabsorption in PT.

The increased water reabsorption and sodium loss in urine (action of thazide duretic) corrects hypernatriemia.

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

What helps preserve GRF and volume in a volume depleted state?

A

Ang II

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

What happens in a 25yoM dehydrated person in the desert?

A

Volume status depleted&raquo_space; high Ang II&raquo_space; vasconstriction of efferent arteriole&raquo_space; increase of GFR and decrease in RPF&raquo_space; increase in FF&raquo_space; more palsma filtered in glom&raquo_space; higher albumin concentration and higher oncotic pressure in glom capillaries&raquo_space; increase in peritubular reabsorption&raquo_space; increased FF&raquo_space; increased reabsorption in PT.

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

What happens if you give NSAIDS to a 75yoM who is hemorrhaging?

A

Function of NSAIDS is to inhibit PG synthesis.
In this case, PGs are protective because….
Increase in sympathetic tone due the stressed state causes vasoconstriction of afferent arterioles and local production of PGs.
PGs&raquo_space; vasodilation of afferent arterioles&raquo_space; modulating vasoconstriction of afferent by SNS.
This vasoconstriction from SNS and Ang II lead to PROFOUND REDUCTION IN RPF AND GFR&raquo_space; could cause RENAL FAILURE.

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

85yoF is confused, on hydrochlorothiazide, bicarbonate is 34mEq/L (normal is 23mEq/L). What is the cause of metabolic alkalosis?

What other states could cause this?

A

This is contraction alkalosis.
THIAZIDE diuretic causes decrease in intravascular volume (same as what vomitting or dehydration/sweating would do - but NOT diarrhea). Decreased volume increases renin secretion&raquo_space; increasing Ang II&raquo_space; activate sodium/hydrogen exchanger&raquo_space; increases reabsorption of bicarbonate&raquo_space; maintains metabolic alkalosis.

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

What does administration of mannitol do?

A

Freely filtered, but not resorbed, so prevents/reduces normal reabsorption of solute that results in osmotic pull of water into lumen and DIURESIS occurs.
Glucose exceeding the TM in an important example from the standpoint of PT.

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

65yoM presents with hyponatremia. Serum osmolarity is low, urine osmolarity is high. Dx of SIADH. Started on fluid restriction, but is not compliant. What do you give him? What increases? Why?

A

Loop Diuretic given and plasma sodium increases. Loops decrease reabsorption of sodium and water in Loop, removing concentrating effect of the Loop, decreasing osmolar gradient. This decreases reabsorption for free water from the CD.

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

55yoF hx of ESRF confused after missing dialysis. Her potassium is elevated. She is treated with injection of bicarbonate and insulin with dextrose while waiting for dialysis. Why?

A

Bicarbonate gives her alkalosis. Causes protons to leave intracellular space down concentration gradient. Potassium maintains electroneutrality by shifting INTO cells, which decreases EC potassium concentration.
Insulin activates the NA/K ATPase that increases shift of K into the cell as well.

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

What do loop diuretics block?

A

Loops block Na+, K+, 2Cl- tranporter in ATL&raquo_space; reducing their reabsorption.
By blocking this transporter, Mg and Ca++ reabsorption also diminished&raquo_space; DIURESIS

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

What do thiazide diuretics block?

In addition to being a diuretic, when else are they used?

A

Block NaCl sympoter in distal tubule, which enhances Ca++ reabsorption in DT and can result in hypercalcemia.
Also used to increase plasma calcium.

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

What do potassium sparing diuretics block?

A
Block ENaC (i.e. amiloride) or block aldosterone receptors (i.e. spirolactone) or block aldosterone production (blockers of RAAS system).  
Because Na+ reabsorption is reduced, potassium secretion is diminished.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Signs of nephrotic syndrome (5).

Syndrome is associated with what?

A

Associated with disruption of filtrating membrane, typically associated with non-inflammatory injury to glom membrane system.

(1) Marked proteinuria (more than 3.5g/day).
(2) Edema (loss of plasma oncotic pressure).
(3) Hypoalbuminemia (albumin lost in urine).
(4) Lipiduria (disrupted membrane system and proteins in urine).
(5) Hyperlipidemia (increased lipid synthesis in liver).

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

Signs of nephritis syndrome (5).

Syndrome associated with what?

A

Associated with inflammatory disruption of glom membrane system. Allows proteins and cells to cross filtering membrane.

(1) Proteinuria (less than 3.5g/day)&raquo_space; evidence of disrupted membrane.
(2) Hematuria (distrupted membrane).
(3) Oliguria (inflam infiltrates reduce fluid movement across membrane).
(4) HTN (inability of kidney to regulate the EC volume).
(5) Azotemia (inability to filter and excrete urea).

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

What is Gitelman’s syndrome? Caused and result.

A

A genetic disorder resulting in a mutated NaCl transporter with REDUCED function. Patient presents with hypokalemia, alkalosis, and low urine Ca++.

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

Patient presents with hypokalemia, alkalosis, and low urine Ca++. What does he/she possibly have?

A

Gitelman’s Syndrome

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

Major extracellular constituent

Major intracellular constituent

A

Extracellular - Na+ and Cl-

Intracellular - K+ and PO4-

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

When does edema become apparent?

What compensatory mechanism for renal retention of Na+and water is done to maintain plasma volume?

A

When interstitial volume is increased by 2.5 to 3L.

RESPONSE TO EDEMA IS UNDERFILLING OF VASCULATURE.

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

Non pitting edema is due to increased ___.

Does it respond to diuretics?

A

ICF volume.

No.

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

Pitting edema is due to increased ____.
Does it respond to diuretics?
Examples.

A

Interstitial volume.
Yes.
nephrotic syndrome, CHF, pregnancy, cirrhosis

24
Q

1st cap network: GLOMERULAR CAPILLARIES do what? High or low hydrostatic pressure?
2nd cap network: PERITUBULAR CAPILLARIES do what? High or low hydrostatic pressure?

A

Large fluid volume filtered OUT into Bowman’s. High hydrostatic pressure.

Large amounts of water and solute reabsorbed. LOW hydrostatic pressure.

25
Q

What does sympathetic activation do to the afferent arteriole (2 things).

A

(1) FAST ARTERIOLAR CONSTRICTION via smooth muscle

(2) SLOW Increase in RENIN SECRETION from granular cells

26
Q

Endothelium is highly permeable to what?
Glom BM contains what charge? (collagen and proteoglycans).
Podocyte epithelium restricts what with slit pores?

A

Water and dissolved solutes.
negative charge
Restricts large molecules.

27
Q

GFR=?

A

(Kf) x (P uf)
K f = (Lp (hydraulic conductivity)) (SA for filtration)
P uf = capillary ultrafiltration pressure

28
Q

Primary glomerular disease lowers GFR by doing what?

A

decreases SA available for filtration due to damage to glom erularmembrane

29
Q

(P uf) = differnce of what 3 pressures?

A

glom hydrostatic pressure - Bowman capsule pressure - Glomerular oncotic pressure

30
Q

how do you change Kf?

A

mesangial cell contraction, which shortens cap loops, which lowers Kf, which LOWERS GFR

31
Q

Increased systemic arterial pressure does what to:
Glom cap Hydrostatic pressure
RBF
GFR

A

Glom cap Hydrostatic pressure - increased
RBF - increased
GFR - increased

32
Q

Afferent arteriolar constriction does what to:
Glom cap Hydrostatic pressure
RBF
GFR

A

Glom cap Hydrostatic pressure - decreased
RBF - decreased
GFR - decreased

33
Q

Moderate efferent arteriolar constriction
Glom cap Hydrostatic pressure
RBF
GFR

A

Glom cap Hydrostatic pressure - increased
RBF - decreased
GFR - increased

34
Q

Angiotesin 2 does what?

A

Efferent arteriole constriction

Stimulates Na+ reabsorption

35
Q

Clearance - definition and units

A

Volume of plasma from which substance is completely removed by kidneys in a given period of time.
Units in vol/time

36
Q

What approximates GFR?

A

Creatinine clearance!

37
Q

Clearance equation

A

((concentration of solute in urine)(urine volume)) / (concentration of solute in plasma)

38
Q

What is the relationship between plasma creatinine concentration and GFR?

A

If GFR falls 50% of normal, plasma creatinine concentration should increase x2.

39
Q

Filtration fraction and equation.

What’s normal?

A

Filtration Fraction is the proportion of fluid reaching the kidneys which pass into the renal tubules.
FF=GFR/RPF=0.2 (about 20% passes into tubules)

40
Q

What factors could change blood flow to the kidney (RPF)?

A

Hemorrhage, renal artery stenosis, etc.

41
Q

PcT:
reabsorbs what?
secretes what?

Pwwered by what transporter?

A

Reabsoribs most filtered water, Na+, K+, Cl-, bicarbonate, Ca2+, phosphate.
Reabsorbs ALL GLUCOSE.
Secretes some organic anions and cations (i.e. drugs, drug metabolites, creatinine, urate)

Na/K ATPase

42
Q

What do SGLT-2 inhibitors do?

What is normal Tmax for glucose?

A

Lowers Tmax for glucose excretion, resulting in increased glucose reabsorption. ORAL ANTI-HYPERGLYCEMICS.
Normal Tmax for glucose is 375mg/min.

43
Q

If a person overdose on aspirin or acetylsalicylate or any organic acid, what is the best treatment?

A

Alkalization of urine through HCO3 administration. It promotes urinary excretion by trapping acid in tubular lumen (because it remains charged&raquo_space; and will be excreted).

44
Q

What two area are the MAJOR PHYSIOLOGICAL CONTROL SITES OF SALT AND WATER?

A

LATE DCT AND CD.

45
Q

What does aldosterone stimulate? What segment?

A

LATE DCT AND CD.
Na reabsorption
K secretion
H secretion

46
Q

What does ANP do? What segment?

A

Medullary CD:

Inhibit Na reabsorption

47
Q

ADH does what?

A

Stimulates water reasorption

48
Q

What does Aldosterone do? What segment?

A

Late DCT and CD principal cells.

Increases Na reabsorption, POTASSIUM and H secretion

49
Q

What does lack of insulin and/or B-adrenergic blockers do?

What setting is this possible?

A

Both increase K pulled into cells, decrease its secretion!

Lack of insulin (diabetic person) compromises K+ tolerance, predisposing for hyperK. Results in inability to bring K out of cell, resulting in possible hyperK.
B-blockers (i.e. tx HTN or epinephrine) impair sequestration of acute K+ load - decrease getting rid of K.

50
Q

Increased Na in CD will cause what to happen to K?
A person on a low sodium diet at risk for what?
How can hyperK be treated?

A

Increased secretion.
At risk for hyperK.
Increase Na delivery to CD to increase Na reabsorption and K secretion.

51
Q

ADH does what?

A

Increases water and urea permeability (reabsorption) in teh Late DCT and CD.

52
Q

SIADH results in what?

Diabetes insipidus resutls in what?

A

SIADH results in high levels of ADH = low volume, highly concentrated urine.
DI results in low ADH, so very hgih volume of dilute urine excreted. LOWER SOLUTE CONCENTRATIONS IN MEDULLARY INTERSTITUM.

53
Q

What is free water clearance?
When positive, means what?
When negative, means what?

A

Excretion of solute free water by the kidneys.
Positive means pure water excreted. Urine osm less than plasma osm. Well hydrated.
Negative means that pure water is retained. Urine osm is greater than plasma osm. Dehydrated.

54
Q

What is hyperchloremic acidosis?

A

When A.G. is unchanged, but person will have gain of Cl- matched by loss of HCO3.

55
Q

What is high anion gap acidosis?

Caused by what? MUDPILES

A

HCO3- is replaced by unmeasured anion. A.G. increases.

Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.

56
Q

DAVENPORTS!

A

look at ppt