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01 Renal Respiratory > 2 Renal Physiology refresher and Mendelian forms of HTN > Flashcards

2 Renal Physiology refresher and Mendelian forms of HTN Flashcards

0
Q

Effects of adding fluids

A

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

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1
Q

Fluid distribution

A

2/3 intracellular.

280-300 mOsm/l

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2
Q

Net filtration pressure

A

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

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3
Q

Normal GFR

A

125 ml

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4
Q

GFR

A

GFR= ultrafiltration coefficient (net filtration force)

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5
Q

Relationship between GFR and MAP

A

No change in GFR with higher BP because of autoregulation.

  • myogenic
  • tubuloglomerular feedback
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6
Q

Hormones that decrease GFR

A

NE, Epinephrine, Endothelin (all by increasing constriction)

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7
Q

Hormone with no change in GFR/ prevention of decreasing GFR

A

ANGII (preferentially constricts efferent arteriole)

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8
Q

Hormones/substances that increase GFR

A

Endothelal derived NO

Prostaglandins

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9
Q

Filtration barrier

A

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

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10
Q

Solubility of proteins

A

Myoglobin (17kDa) .75

Albumin (69 kDa) .005

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11
Q

Thin descending loop function

A

passive resorption of water 2/2 cortical medullary osmotic gradient

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12
Q

Thin ascending limb function

A

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

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13
Q

Thick ascending limb

A
  • 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
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14
Q

Furoseminde

A

Blocks NA, K, CL cotransporter

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15
Q

Early distal tubule

A
  • Paracellular Mg, Ca resorption
  • NaCl cotransporter resption
  • Na/K ATPase on interstitial side
  • Cl channel on interstitial side
16
Q

Late distal tubule and collecting duct

A
  • Resorbs Na, secretes K (via interstitial NA/K atpase and KC and ENaC on luminal side)
  • aldosterone dependant
  • ADH causes aquoporin translocation
17
Q

Medullary collecting duct

A
  • Na resorption via NaK atpase and ENaC
  • ADH aquoporin translocation
  • Urea resorption in medullary collecting duct
18
Q

Aldosterone

A

^ NaK atpase activity

19
Q

ANP

A

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

20
Q

ANGII

A
  • 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
Q

ADH

A

Increases H2O resorption from late distal tubule on

22
Q

PTH

A

Decreases proximal PO4 resorption

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

23
Q

AME (Apparent Mineralocorticoid Excess)

A
  • 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
Q

AME cause

A

*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
Q

Liddle synddrome

A

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

26
Q

Liddle syndrome cause

A

*constituatively open ENaC

SCNN1G or SCNN1B gene mutations

27
Q

AME treatment

A

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
Q

Liddle Syndrome treatment

A

Amiloride and Triamterene (block sodium channel)

good prognosis with treatment

29
Q

Bartter syndrome

A

Early childhood presentation

  • Growth and mental retardation, polyuria, polydipsia,
  • HYPERCALCEMIA, hypokalemia, hyperreninemia,hyperaldosteronism, metabolic alkylosis, HYPOTENSION
30
Q

Gitelman Syndrome

A

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

31
Q

Barter and Gitelman causes

A

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

01 Renal Respiratory (34 decks)

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