RAAS. Dialysis Flashcards

(28 cards)

1
Q

What are the triggers for Renin release?

A

Low blood pressure, sympathetic nervous cell, low Na in the distal convulted tubule

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2
Q

Where is renin released

A

Relased from the JuxtaGlomerular cells (smooth muscle cells)

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3
Q

How is the macula densa involved in renin release?

A

In distal tubule of nephron, senses low Na (low bp leads to less Na). Stimulated via local PGs

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4
Q

Where is angiotensinogen made

A

Liver cells. Not active.

Combines with renin

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5
Q

Where is ACE found?

A

Blood vessels and lungs

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6
Q

List the sites of angiotensin II active

A

Smooth muscle of blood vessels- constriction
Kidney- water rention, increase GFR by vasconstriction of efferent
Pituitary Gland ADH release
Adrenal Gland- Aldosterone release

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7
Q

How are volume and osmolarity affected with aldosterone versus ADH

A

Aldosterone: Increase in volume with no change in osmolarity as porportional change
ADH: Inverserly related if volume increased Osmolarity decreases

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8
Q

Where is aldosterone made and why

A

Made from cholesterol in the adrenal cortex. Stimulated by Angiotensin II and increased K+

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9
Q

Where does aldosterone have it’s action

A

Principal cells in the late distal convulted tubule and collecting duct

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10
Q

What are the affects of aldosterone locally and in the blood

A

Makes Na/K atpase pump work harder; K+ channels in apical membrane (efflux); Na channels in apical membrane (influx)
Blood: Loose K+; Na + increases; Water increase

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11
Q

Where does ADH have its affect and how

A

Collecting duct cells that are impermeable to water. Aquaporins are placed in the cells to allow water to move through.

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12
Q

How does Aldosterone alter pH

A

Alpha interculated cells. When too acidic will give HCO3- (exchange with Cl-) to blood to form H20/CO2
Cl-goes to blood through channel
H+ leaves through transporter through apical membrane; channel exchange for Na+

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13
Q

What is renal replacement therapy

A

Blood circulated in an extracorpeal circuit its composition is modified by a mass transfer of solute and water by diffusive/convective forces accros an interfacing semipermebale membrane

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14
Q

Define diffusion in dialysis

A

Movement down concentration gradient or thermodynamic potenetial

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15
Q

What are the determinates for diffusion

A
Molecular weight (inverse)
molecular charge, protien binding, volume of distribution; celluar seclusion
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16
Q

Define Convection in dialysis

A

water driven through membrane by hydrostatic pressure gradients, solutes disolved in water move through by solvent drag

17
Q

What are the determinates for convection

A

hydrostatic pressure gradient, hydralic pressure and membrane surface area / seiving coefficent

18
Q

Define adsorption

A

molecular attachement of a solute to a material surface. Hemoperfusion

19
Q

What is the primary mechanism for Intermitent hemodialysis, CRRT, CVVHDF

A

IHD: Diffusion (some convection, adsorption)
CRRT: Convection (some diffusion adsoprtion)
CVVHDF: Both diffusion convection

20
Q

What is dialysis disequilibrium syndrome and how to avoid

A

Removal of solutes results in gradient, plasma water moves from vascular to intracellular space. When solutes are removed with small volume relative to the efficiency
Avoid reduce urea <5% /hr for > 300 mg/dl and <10% for <300 mg/dl BUN

21
Q

What are characteristics to use RRT for toxicity

A

Low molecular weight (< 1500 Da)
Small volume of distribution
Minimal protien binding
Add hemoperfusion if don’t meet.

22
Q

What is peritoneal dialysis

A

Removal of metabolites and water by the administration of a large amount of dialysate solution into the peritoneal cavity.

23
Q

What is the primary mechanisms for peritoneal dialysis

A

Membrane is the peritoneal membrane.
Diffusion, convection, osmosis (ultrafiltration)
Osmosis- water movement

24
Q

List complications of RRT

A

Hemorrhage- heparization

HypoCa - citrate anticoagulation

25
What is the difference in aphresis and TPE
Aphresis: Blood removed and seperated into its componenets then one or more is processed/removed and returned to patient TPE is aphresis of the plasma
26
What determines the success of TPE
Volume of distribution rapiditiy substance equilibrates between body compartments ability to remove adequate amounts
27
Disease process in which TPE may be used to treat
Myasthenia Gravis, IMHA, Multiple myeloma, IMpolyradiculoneuritis
28
Complications of TPE
plasma rxns, hypocalcemia/alkalsosis- citrate; blood loss- clot in circuti; hypotension, hypoprotienemia