Renal Physio 2 Flashcards Preview

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Flashcards in Renal Physio 2 Deck (16):

Where is the counter current system

The entire Loop of Henle all 3 parts


Purpose of the vasa recta?

Part of the countercurrent mechanism. They preserve the hyperosmolar gradient of the renal medulla while reclaiming the solutes and water from the interstitial space back into circulation


Discuss EPO

90% made in the kidneys. Released in response to hypoxia. and stimulates RBC production by the bone marrow by activating proerythroblasts in the bone marrow, accelerating their growth


Vitamin D is stored how? When is it released? What about PTH?

In the liver as 25-OH-Cholecalciferol. Decreased plasma Ca2+ levels stimulate PTH secretion, which activates 1alpha-hydroxylase in the kidneys . This in turn enables the hydroxylation of 25-OH to 1,25-OH which is the active form, and which increases the intestinal absorption of Ca2+ and decreases renal Ca2+ and phosphate excretion.

PTH by itself is a little different. It reabsorbs Ca2+ but rejects Phosphate...awww...


Vitamin D resistance has two etiologies

1. Genetic = Bad 1 alpha-hydroxylase
2. Chronic kidney disease (your kidneys are just too damaged)



ANF causes vasodilation of the afferent arterioles, vasoconstriction of the efferent, and decreased Na reabsorption in the late DCT and CDs when the heart starts to stress from hypervolemia

BNP is released from the ventricles when they get distended and is often more connected to the respiratory pathway due to its presence with CHF and dyspnea


What are the four things that stimulate renin and where is it stored?

Renin is stored as pro-renin in the juxtaglomerular cells of the kidney, which if you remember, is that part between the glomerulus and the afferent arteriole.

1. Hypotension which leads to decreased renal perfusion and a sensing juxtaglomerular cell
2. Increased renal parasympathetic activity
3. Beta 1 adrenergic stimulation
4. Decreased Na+ load/ Na+ delivery to the macula densa


When renin is in the blood stream, now active and ready to go, what happens?

Finds angiotensinogen and cleaves it to make angiotensin I. Angiotensin 1 goes to the lung vasculature and/or the kidneys, finds ACE, turns to 2.


3 Methods by Angiotensin II to elevate arterial BP

1. Direct action on the kidneys - Stimulates Na+-H+ exchange at the level of the PCT, thereby increasing resorption of Na+ and HCO3-.

2.Fast response - Direct vasoconstriction of the arterioles to increase TPR and the veins to promote increased venous return to the heart. Both of these increase BP.

3. Slow response - Deceased excretion of Na and water to preserve volume via stimulation of aldosterone in the adrenals.


2 effects of aldosterone and where these occur.

1. Late DCT - Stimulates mineralcorticoid receptors in the alpha cells to make a bunch more pumps to get that K out and that Na and water into the blood.

2. Collecting Duct - Stimulates alpha cells to excrete more H+ so that water gets absorbed. This has the dual effect of getting water and keeping acid base balance by regulating H and HCO3-


We know about ADH already but what happens when there is a lot of it?

High levels of ADH gives them a new function, stimulating V1 receptors in arterioles to constrict. This happens due to extreme volume loss like in hemorrhage.


What causes ADH release and where is it released from?

RAAs system releases it.

Also, systemic baroreceptors in the carotid sinus sense decreased BP which causes ADH release from the posterior pituitary gland.


High anion gap conditions

Diabetic ketoacidosis
Isoniazid, Infection, Iron
Lactic acidosis
Ethylene Glycol, Ethanol


Non anion gap conditions (Hyperchloremic)

Hyperalimentation - IV nutrition patients
Renal Tubular Acidosis
Ureteroenteric Shunt
Pancreatic Fistula


Acid Base Cards from Week 6

Do them next.


Fanconi Syndrome

Damage to the proximal tubules compromises reabsorption of glucose, amino acids, phosphate, and bicarb.