Renal Physiology Review Flashcards
A patient with essential HTN has vasoconstriction/dilation at afferent arterioles and vasoconstriction/dilation at efferent arterioles?
What controls this?
Vasoconstriction at afferent.
Vasodilation at efferent.
High pressure at juxtaglomerular apparatus leads to DECREASED RENIN secretion»_space; low Ang II»_space; VASODILATION at efferent arterioles
A patient with renal artery stenosis has vasoconstriction/dilation at afferent arterioles and vasoconstriction/dilation at efferent arterioles?
Why?
Vasodilation at afferent arterioles.
Vasoconstriction at efferent arterioles.
Low pressure at afferents. INCREASED RENIN SECRETION»_space; increased Ang II»_space; vasoconstriction of efferent arteriole
A patient comes in with diarrhea, vomiting, or hemorrhaging. What is important to conserve?
What is one way to do this?
Extracellular volume by increasing reabsorption of fluid and electrolytes at PROXIMAL TUBULES.
What is not working in nephrogenic DI? What is not possible to do?
ADH receptors. Not possible to increase reabsorption at CD.
How do you treat nephrogenic DI?
What does this correct?
Tx - thiazide diuretic reduces extracellular volume, which increases peritubular oncotic pressure»_space; increasing water reabsorption in PT.
The increased water reabsorption and sodium loss in urine (action of thazide duretic) corrects hypernatriemia.
What helps preserve GRF and volume in a volume depleted state?
Ang II
What happens in a 25yoM dehydrated person in the desert?
Volume status depleted»_space; high Ang II»_space; vasconstriction of efferent arteriole»_space; increase of GFR and decrease in RPF»_space; increase in FF»_space; more palsma filtered in glom»_space; higher albumin concentration and higher oncotic pressure in glom capillaries»_space; increase in peritubular reabsorption»_space; increased FF»_space; increased reabsorption in PT.
What happens if you give NSAIDS to a 75yoM who is hemorrhaging?
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»_space; vasodilation of afferent arterioles»_space; modulating vasoconstriction of afferent by SNS.
This vasoconstriction from SNS and Ang II lead to PROFOUND REDUCTION IN RPF AND GFR»_space; could cause RENAL FAILURE.
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?
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»_space; increasing Ang II»_space; activate sodium/hydrogen exchanger»_space; increases reabsorption of bicarbonate»_space; maintains metabolic alkalosis.
What does administration of mannitol do?
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.
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?
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.
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?
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.
What do loop diuretics block?
Loops block Na+, K+, 2Cl- tranporter in ATL»_space; reducing their reabsorption.
By blocking this transporter, Mg and Ca++ reabsorption also diminished»_space; DIURESIS
What do thiazide diuretics block?
In addition to being a diuretic, when else are they used?
Block NaCl sympoter in distal tubule, which enhances Ca++ reabsorption in DT and can result in hypercalcemia.
Also used to increase plasma calcium.
What do potassium sparing diuretics block?
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.
Signs of nephrotic syndrome (5).
Syndrome is associated with what?
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).
Signs of nephritis syndrome (5).
Syndrome associated with what?
Associated with inflammatory disruption of glom membrane system. Allows proteins and cells to cross filtering membrane.
(1) Proteinuria (less than 3.5g/day)»_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).
What is Gitelman’s syndrome? Caused and result.
A genetic disorder resulting in a mutated NaCl transporter with REDUCED function. Patient presents with hypokalemia, alkalosis, and low urine Ca++.
Patient presents with hypokalemia, alkalosis, and low urine Ca++. What does he/she possibly have?
Gitelman’s Syndrome
Major extracellular constituent
Major intracellular constituent
Extracellular - Na+ and Cl-
Intracellular - K+ and PO4-
When does edema become apparent?
What compensatory mechanism for renal retention of Na+and water is done to maintain plasma volume?
When interstitial volume is increased by 2.5 to 3L.
RESPONSE TO EDEMA IS UNDERFILLING OF VASCULATURE.
Non pitting edema is due to increased ___.
Does it respond to diuretics?
ICF volume.
No.