RAAS. Dialysis Flashcards

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
Q

What is the difference in aphresis and TPE

A

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
Q

What determines the success of TPE

A

Volume of distribution
rapiditiy substance equilibrates between body compartments
ability to remove adequate amounts

27
Q

Disease process in which TPE may be used to treat

A

Myasthenia Gravis, IMHA, Multiple myeloma, IMpolyradiculoneuritis

28
Q

Complications of TPE

A

plasma rxns, hypocalcemia/alkalsosis- citrate; blood loss- clot in circuti; hypotension, hypoprotienemia