Renal - Exam 4 Flashcards

1
Q

Kidneys regulate body fluid

A

osmolarity and electorlytes

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2
Q

sodium salts are what % of osmolarity?

A

90%

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3
Q

Normal osm =

A

300 mOsm/kg

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4
Q

kidneys reabsorb what?

A
  • water
  • glucose
  • Proteins
  • vitamins
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5
Q

Production of renin in response to

A
  • decreased renal blood flow

- Increased sympathetic discharge (beta 1 effect)

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6
Q

**This area of the kidney is most vulnerable to ischemia secondary to hypotension:

A

Inner stripe of outer zone (in medulla)

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7
Q

** What structures are within the inner zone of the Medulla?

A

Collecting duct
duct of bellini
Thin loop of Henle

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8
Q

This structure is important in countercurrent mechanism:

A

Vasa Recta

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9
Q

Juxtaglumerular (JG) apparatus is made up of these two structures:

A
  1. ) Macula Densa (sensor)

2. ) Juxtaglomerular cells (Secrete)

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10
Q

Role of juxtaglomerular apparatus?

A

sodium control

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11
Q

JG cells secrete:

A

RENIN

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12
Q

Afferent arterioles protrude into bownman’s capsule doing what?

A

bringing blood IN arriving

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13
Q

Efferent arterioles do what?

A

EXIT bowmans capslule and take blood out

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14
Q

Vasa recta is a capillary bed along the

A

loop of Henle

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15
Q

the sum of filtration, reabsorption and secretion =

A

excretion

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16
Q

Net filtration pressure needed for glomerular filtration to occur?

A

10mmHg

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17
Q

glomerular fluid each day results in production of,

out of which how many liters is reabsorbed

A

180 liters

179 liters

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18
Q

normal GFR =

A

125ml/min

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19
Q

Factors governing filtration rate at cap. bed:

A
  1. net filtration rate
  2. total surface area availalbe for filtration
  3. filtration membrane permeability
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20
Q

GFR is directly proportional to the

A

net filtration pressure

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21
Q

changes in GFR results from changes in

A

glomerular blood pressure

decreae bp, decrease filtration, decrease urine

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22
Q

if GFR is too high

A

substances can’t be reabsorbed fast enough

lost in urine

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23
Q

if GFR is too low

A

everything is reabsorbed

-including toxins/waste that normally are disposed

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24
Q

BUN and CRT increase when

A

GFR decreases

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25
Q

GFR decreases with

A

age

26
Q

vasoconstriction of afferent arteriole =

A

decrease GFR

blocking entry

27
Q

vasoconstriction of efferent arteriole =

A

increased GFR

blocking outlet
Angiotensin II

28
Q

Ureteral stone impact on RBF and GFR:

A

RBF - no change

GFR - decreases

29
Q

Ace inhibitors do what to arterioles?

results in?

A

dilate efferent arterioles

  • decreased Glomerular pressure
  • decrease GFR

**leads to renal insufficiency

30
Q

avoid ace inhibitors in what patients?

A

those with bilateral renal artery stenosis

*will make GFR worse

31
Q

avoid ace inhibitors in what patients?

A

those with bilateral renal artery stenosis

*will make GFR worse

32
Q

what level is all glucose reabsorbed?

A

<250 mg/dl (or 200?)

33
Q

glucose >350 mg/dl means?

A

all carriers are saturated
no reabsorption occurs above 350 mg/dl

it’s excreted

34
Q

plasma threshold at which glucose first appears in urine:

A

200 mg/dl

35
Q

where is glucose reabsorbed?

A

Prox. Tubule

36
Q

ADH is synthesized in

A

hypothalamus

by supraoptic and paraventricular nuclei

37
Q

increase serum osm stimulates

A

ADH release

and vis versa: decrease: inhibits

38
Q

actions of ADH

A
  1. increase H2O reabsorption from LDT and CD’s via V2 receptor (cAMP)
  2. Vasoconstrictor via V1 receptor (IP3 )
39
Q

**where does the osmotic gradient occur?

A

**loop of henli

40
Q

**why do we need osmotic gradient?

A

to make concentrated urine

41
Q

dehydration results in:

A

increase serum osm

ADH release

42
Q

in the presence of ADH what happens to the nephron?

A

the collecting duct changes and becomes completely impermeable to water so increase water absorption

this happens when dehydrated!

43
Q

Affect of ADH on Urine vol and osmolarity

A

with ADH: Low vol/ High osm

without ADH: High Vol, low osm

44
Q

countercurrent exchange occurs where?

A

in the vasa recta

45
Q

NA exchange and transport with?

A

exchange: acid (H+)
transport : Glucose

b/c of Na/K pump

46
Q

Na reabsorption occurs where?

A

early Prox tubule

47
Q

na absorption in the PCT % and effect of aldosterone:

A

in the presence or not of Aldosterone

PCT will absorb 67% of sodium

48
Q

** Aldosterone saves:

A

saves sodium

Gets rid of K+ and H+

49
Q

MCC of hyponatremia

A

hospitalized pt

and SIADH

50
Q

tx for symptomatic hyponatremia:

A

3%NaCl

*symptomatic with seizures delirium

51
Q

Hyper and hyponatremia both have a profound effect on the brain. Examples:

A
  1. altered neuro function
  2. rapid shrinking can tear vessels and lead to HEMORRHAGE
  3. rapid swelling can cause HERNIATION
52
Q

the brain cannot increase its vol by more than what % before herniation?

A

10%

53
Q

K handling in the presence or absence of aldosterone:

A
  • increase aldosterone: increase K secretion

- decrease aldosterone : decreases K secretion

54
Q

alkalosis effect on K+

A

HYPOKALEMIA

exchange of IC H+ for EC K+

55
Q

Acidosis effect on K+

A

HYPERKALEMIA

56
Q

why does hypokalemia cause weak skeletal muscles?

A

hyperpolarization

57
Q

Magnesium deficiency will make what worse?

A

hypokalemia

replace the Mg first and the K will “stick”

58
Q

in presence of hypokalemia, dose of muscle relaxant should be:

A

reduced

59
Q

with hypokalemia, avoid

A

hyperventilation

60
Q

hyperventilation does what to K?

A

each reduction 10mmHg of PCO2 =

0.5 mEq/L reduction in K+

61
Q

Things we can do to treat hyperkalemia:

A
  • Calcium gluconate (protect cardiac membrane)
  • Sodium bicarb
  • Hyperventilation
  • Loop Diuretics
  • Insulin, D50
  • Kayexalate
  • Beta 2 agonist
  • Dialysis in RF
62
Q

best forms of fluid replacement for hypovolemia?

A

NS
LR
Blood loss: crystalloid 3:1