2 Renal Physiology refresher and Mendelian forms of HTN Flashcards Preview

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Flashcards in 2 Renal Physiology refresher and Mendelian forms of HTN Deck (32):
0

Fluid distribution

2/3 intracellular.
280-300 mOsm/l

1

Effects of adding fluids

Hypotonic NaCl - Increases intracellular fluid more than extracellular
Isotonic NaCl- Increases extracellular fluid only
Hypertonic NaCl- increases extracellular shrinks intracellular compartmments

2

Net filtration pressure

usually 10mmHg = 60(glomerular hydrostatic) - 18(bowmans capsule pressure) - 32 (glomerular oncotic pressure)

3

Normal GFR

125 ml

4

GFR

GFR= ultrafiltration coefficient (net filtration force)

5

Relationship between GFR and MAP

No change in GFR with higher BP because of autoregulation.
*myogenic
*tubuloglomerular feedback

6

Hormones that decrease GFR

NE, Epinephrine, Endothelin (all by increasing constriction)

7

Hormone with no change in GFR/ prevention of decreasing GFR

ANGII (preferentially constricts efferent arteriole)

8

Hormones/substances that increase GFR

Endothelal derived NO
Prostaglandins

9

Filtration barrier

Fenestrations = 700 angstroms
Basement membrane= IV collagen, laminin, fibronectin (neg proteins)
Podocyte slit pores = 40-140 angstroms

10

Solubility of proteins

Myoglobin (17kDa) .75
Albumin (69 kDa) .005

11

Thin descending loop function

passive resorption of water 2/2 cortical medullary osmotic gradient

12

Thin ascending limb function

Passive resorption of sodium and excretion of urea to dilute tubular fluid

13

Thick ascending limb

*25%sodium resorbed by NA/K/CL transporter
* Na resorbed in exchange for H+
*Sodium potassium ATP pump on interstitial side
*Chloride pore on interstitial side
*positive luminal fluid also pushes K, Na, MG, and Ca into interstitium via paracellular diffusion

14

Furoseminde

Blocks NA, K, CL cotransporter

15

Early distal tubule

*Paracellular Mg, Ca resorption
*NaCl cotransporter resption
*Na/K ATPase on interstitial side
* Cl channel on interstitial side

16

Late distal tubule and collecting duct

*Resorbs Na, secretes K (via interstitial NA/K atpase and KC and ENaC on luminal side)
*aldosterone dependant
*ADH causes aquoporin translocation

17

Medullary collecting duct

*Na resorption via NaK atpase and ENaC
*ADH aquoporin translocation
*Urea resorption in medullary collecting duct

18

Aldosterone

^ NaK atpase activity

19

ANP

Decreases NaCL resorption in distal tubule and collecting tubule and duct.

20

ANGII

*Increases Na and H20 resorption in proximal tubule through NaK atpase on intertitial side and NaHCO3- cotransporter
* increases H secretion through NaH exchanger

MOST IMPORTANT FOR SODIUM RETENTION

21

ADH

Increases H2O resorption from late distal tubule on

22

PTH

Decreases proximal PO4 resorption
Increases CA++resorption in thick ascending and early distal tubule.

23

AME (Apparent Mineralocorticoid Excess)

*Presentation: Low weight, FTT, early childhood severe hypotension, organ damage, renal failure
*Clinical S/S: Hypertension, hypokalemia, metabolic alkylosis, low plasma renin activity, low plasma aldosterone

24

AME cause

*Deficiency in 11B HSD2 - converts cortisol into cortisone (resulting in high active cortisol concentrations and binding of cortisol to MR)
Common on consanguineous relationships (kissing cousins)

25

Liddle synddrome

*HTN, Hypokalemia, Metaboolic alkylosis, Low plasma renin activity, LOW PLASMA AND URINARY ALDOSTERONE.

26

Liddle syndrome cause

*constituatively open ENaC
SCNN1G or SCNN1B gene mutations

27

AME treatment

Condition usually recognized too late for treatment to be effective.

Amiloride and Triamterene (block sodium channel)
Spironolactone and Eplerenone (block MR)
Dexamethasone (Block ACTH)

28

Liddle Syndrome treatment

Amiloride and Triamterene (block sodium channel)
(good prognosis with treatment)

29

Bartter syndrome

Early childhood presentation
*Growth and mental retardation, polyuria, polydipsia,
*HYPERCALCEMIA, hypokalemia, hyperreninemia,hyperaldosteronism, metabolic alkylosis, HYPOTENSION

30

Gitelman Syndrome

Adolescent or adult presentation
*cramping, fatigue, plyuria,noctura
*HYPOMAGNESEMIA
HYPOtension

31

Barter and Gitelman causes

Autosomal recessive
*NaCl resorption problems
*RAS activation and hyperaldosteronism
Bartter is NA/K/CL transporter in thick ascending
Gitelman is NaCl transporter in distal tubule