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renal section Flashcards

1
Q

what type of bio transformations is the kidney capable of

A

phase 1 and 2

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2
Q

lungs excrete _______ acids and kidneys excrete ________ acids

A

lungs: volatile
kidneys: non volatile

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3
Q

when is EPO released via the kidney

A

when theres inadequate O2 delivery to kidney (anemia, reduced intravascular volume, hypoxia)

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4
Q

what stimulates erythrocyte production

A

EPO stimulates stem cells in bone marrow

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5
Q

what effect does PGE1 and PGE2 have on renal arterioles

A

vasodilation

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6
Q

what effect does thromboxane A2 have on renal arterioles

A

constriction

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7
Q

role of calcitrol with kidneys

A
  1. stimulates absorption of calcium from food
  2. instructs kidneys to reduce calcium and phosphate excretion
  3. increase deposition of calcium into bone
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8
Q

increased PTH _____’s calcitrol

A

increases

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9
Q

kidneys can synthesize _______ from amino acids

A

glucose

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10
Q

the kidneys receive _____ of CO (________mL/min_

A

20-25% (1000-1250mL/min)

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11
Q

How much of blood is filtered at glomerulus

A

20%

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12
Q

how much blood is reabsorbed in peritubular capillaries

A

99%

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13
Q

renal blood flow equation =

A

(MAP - renal venous pressure) / renal vascular resistance

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14
Q

how does blood flow through the kidney?

A

renal arteries -> renal segmental artery -> interlobular artery -> articulate artery -> interlobular artery -> afferent arterioles -> glomerular capillary bed -> efferent arterioles -> peritubular capillaries (reabsorption and secretion) -> venues -> interlobular vein ->arcuate vein -> interloper vein -> renal segmental vein

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15
Q

renal autoregulation includes

A

myogenic mechanism
JG apparatus
tubuloglomerular feedback
RAAS
prostaglandins
ANS
SNS

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16
Q

lower chloride concentration in ultrafiltrate does what

A

triggers renin release to activate RAAS

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17
Q

role of A2 and increase in GFR

A

constricts efferent arterioles

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18
Q

go over RAAS pathway

A

angiotensin–>(renin) angiotensin 1–> (ACE) angiotensin 2

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19
Q

5 roles of angiotensin 2

A

vasoconstriction (peripheral vessels and efferent arteriole)
increased aldosterone release from adrenal gland
SNS activation
increased ADH release from posterior ptuitary
increased thirst

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20
Q

where is aldosterone produced

A

zona glomerulosa of adrenal gland

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21
Q

what does aldosterone stimulate in kidney

A

Na/K/ATPase in principal cells of distal tubules and collecting ducts. H2O reabsorption and K/H excretion occurs

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22
Q

what two electrolyte changes increase aldosterone release

A

increased K or decreased Na

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23
Q

what is addisons

A

adrenocortical insufficiency (destruction of all cortical zones)

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24
Q

what stimulates ADH release

A

increased osmolarity of ECF. increased sodium shrinks osmoreceptors in hypothalamus. initiates transport of ADH from hypothalamus to posterior pituitary.
increased BV via unloading of baroreceptors in carotid sinuses, transverse aortic arch, great veins, right atrium

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25
Q

how doe ADH restore BP

A

stimulates V1 (vasoconstriction, increase in IP3, DAG, Ca2+), increases SVR
stimulates V2 in collecting duct (increased cAMP), aquaporin 1 channels inserted into walls of collecting ducts, H2O reabsorption, decreased plasma osmolarity, increased urine osmolarity.
net result= expansion in plasma volume

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26
Q

where are prostaglandins produced

A

afferent arterioles

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27
Q

arachidonic acid is liberated from cell membrane in response to

A

ischemia, HoTN, NE, AT2

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28
Q

how does NSAIDs decrease RBF

A

inhibiting production of vasodilation prostaglandins

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29
Q

endotoxins release ________, which leads to renal vasoconstriction

A

leukotriene production

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30
Q

what does the myocardium release in response to distention

A

ANP and BNP

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31
Q

what is the role of natriuretic peptides

A

inhibit renin release (negative feedback for RAAS) vasodilation and decreased BP.
promotes Na/H2O excretion into collecting ducts

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32
Q

where are dopamine 1 receptors found

A

kidneys and splanchnic circulation

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33
Q

second messenger and function of DA1 receptors

A

cAMP (increased),
vasodilator, increase RBF, increases GFR, diuresis, Na excretion

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34
Q

where are dopamine 2 receptors found

A

present on presynaptic adrenergic nerve terminal

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35
Q

second messenger and function of DA2 receptors

A

cAMP (decreased),
function, decreases NE release

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36
Q

what is freely filtered at the glomerulus

A

water, electrolytes, glucose

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37
Q

what determines glomerular hydrostatic pressure

A
  1. arterial BP
  2. afferent arteriole resistance
  3. efferent arteriole resistance
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38
Q

reabsorption in kidneys

A

substance transferred from tubule to peritubular capillaries

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39
Q

secretion in the kidneys

A

substance transferred from peritubular capillaries to tubule

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40
Q

what is excretion in the kidneys

A

substance removed from body in urine

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41
Q

what is the proximal convoluted tubule responsible for

A

bulk reabsorption of solutes and water
-water follows Na here via osmosis
-K/Cl/HCO3- follow Na in direct proportion
-organic bases, acids, and hydrogen ions are secreted into proximal tubule via Na counter transport mechanism

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42
Q

what percent of ions are absorbed in proximal tubule

A

65%

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43
Q

what is the primary role of the descending loop of henle

A

countercurrent mechanisms and high permeability to H2O
-primary function is to form concentrated or dilute urine.
-separates handling of Na/H2O
- theres an osmotic gradient, highly permeable to H2O and moderately permeable to ions

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44
Q

vasa recta

A

peritubular capillaries that run parallel to the loop of hence. returns reabsorbed water to the blood allowing osmolarity in peritubular insterstitium to remain high

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45
Q

what is the primary role of the ascending loop of henle

A

countercurrent mechanisms and no H2O permeability
- unlike descending LOH, thin and thick segments are not permeable to H2O
-ions pumped from tubular fluid into peritubular interstitium. Na/K/Cl co transporter is most important pump.
-since H2O cannot follow Na into peritubular interstitium, tubular fluid becomes more dilute and peritubular interstitium becomes concentrated

46
Q

primary role of distal convoluted tubule

A

fine tune solute concentration
-Na(5%) is reabsorbed and Na/K/HCO3- follow via sodium co transport mechanism
-late distal tubule is impermeable to H2O except in the presence of aldosterone or ADH
-home to juxtaglomerular apparatus
-adjusts urea concentration

47
Q

primary role of collecting duct

A

regulates final concentration of urine
-reabsorbs Na
-ADH and aldosterone also work in collecting duct
-ANP inhibits Na/H2O reabsorption
-adjusts hydration concentration

48
Q

what is the function of carbonic anhydrase in the proximal tubule? (5 steps)

A
  1. CO2 and H2O diffuse into proximal convoluted tubule cells
  2. carbonic anhydrase facilitates production of H2CO3
  3. H2CO3 dissociates into H and HCO3-
  4. HCO3- diffuses into interstitium then blood
  5. H+ is returned to tubal lumen
49
Q

carbonic anhydrase inhibitors noncompetitively inhibit

A

carbonic anhydrase in the cells that make up the proximal tubule.

50
Q

what do carbonic anhydrase inhibitors reduce the reabsorption of?

A

HCO3, NA, H2O

51
Q

examples of carbonic anhydrase inhibitors

A

acetazolamide 250-500mg

52
Q

side effect and ultimate uses for carbonic anhydrase inhibitors

A

mild metabolic acidosis. used to treat high altitude sickness and central sleep apnea since it increases respiratory drive

53
Q

what are osmotic diuretics (make up)

A

sugars that undergo filtration but not reabsorption

54
Q

role of osmotic diuretics

A

inhibit water reabsorption in the proximal tubule (primary site). transiently increases plasma osmolarity

55
Q

how loop diuretics exert their effect

A

disrupt the Na/K/2Cl transporter in the medullar region of the thick portion of the ascending loop of henle (primary site).
the amount of sodium that remains in the tubule overwhelms the distal tubules’ reabsorption capability so the patient eliminates large volumes of dilute urine

56
Q

examples of loop diuretics

A

furosemide, bumetanide, ethacrynic acid

57
Q

clinical uses of loop diuretics

A

acute pulmonary edema, AKI, CHF, increased Ca2+, HTN, anion DO, ICH, mobilization of edema fluid

58
Q

key complication of loop diuretic

A

hypochloremic metabolic alkalosis

59
Q

thiazides inhibit

A

Na/Cl co transporter in distal tubule. increases Ca reabsorption and serum calcium

60
Q

SE of thazides

A

hyperglycemia, increased Ca, hyperuricemia (gout patients), hypokalemic hypochlorremic metabolic alkalosis, hypovolemia, HLD sexual dysfunction

61
Q

meds that can increase risk of hyperkalemia

A

NSAIDS (decreases renin and atII mediated aldosterone release)
BB (suppression of aldosterone secretion at adrenal cortex and reduction in K uptake)
ACEI

62
Q

tests and normal values of glomerular function include

A

BUN 10-20mg/dL
serum creatinine .7-1.5mg/dL
creatinine clearance 110-150mL/min

63
Q

tests and normal values of tubular function (concentrating ability) include

A

fractional exertion of sodium 1-3%
urine osmolality 65-1400mOsm/L
urine sodium concentration 130-260mEq/day
urine specific gravity 1.003-1.030

64
Q

100% increase in creatinine = ___________ in GFR

A

50% decrease

65
Q

what is fractional exertion of sodium Fe(na)

A

relates to Na clearance to creatinine clearance.

66
Q

if FeNa is less than 1%

A

more Na is conserved relative to the amount of creatinine cleared. this suggests pre renal axotemia

67
Q

If FeNa is greater than 3%

A

more Na is excreted relative to the amount of creatinine cleared. suggests impaired tubular function

68
Q

pre renal oliguria
FeNa
Urinary Na
urine osmolality
BUN:creatinine ratio
sediment

A

FeNa <1
Urinary Na <20
urine osmolality >500
BUN:creatinine ratio >20:1
sediment: normal, possible hyaline cysts

69
Q

acute tubular necrosis
FeNa
Urinary Na
urine osmolality
BUN:creatinine ratio
sediment

A

FeNa >3%
Urinary Na >20
urine osmolality <400
BUN:creatinine ratio 10-20:1
sediment: tubular epithelial cells, granular casts

70
Q

three systems used to classify AKI

A
  1. RIFLE (risk, injury, failure, loss, end stage)
  2. AKIN (acute kidney injury network)
  3. KDIGO: kidney disease improving global outcomes
71
Q

causes of pre renal injury

A

hypo perfusion, decreased CO, systemic vasodilation, renal vasoconstriction, increased intra abdominal pressure

72
Q

treatment of pre renal injury

A

IVF, hemodynamic support, PRBC’s, renal prostaglandins mediate vasodilation. avoid NSAIDS.
improvement in UOP after IVF confirms pre renal azotemia

73
Q

causes of intra renal injury

A

ATN, ishemia, nephrotoxic drugs, parenchymal dysfunction

74
Q

treatment of intra renal injury

A

restore renal perfusion, supportive

75
Q

excessive use of .9% NaCl can cause

A

hyperchloremic metabolic acidosis

76
Q

vasopressin constricts what in the kidney

A

efferent arteriole

77
Q

do not use the following to prevent or treat AKI

A

low dose dopa, fenoldopam, ANP, recombinant human (Rh) IGF 1

78
Q

avoid which abx

A

ahminoglycosides, amphotericin B (IV)

79
Q

stages of chronic kidney disease (5)

A
  1. GFR >90
  2. GFR 60-89
  3. GFR 30-59
  4. GFR 15-29
  5. GFR < or = 15
80
Q

s/sx of uremia

A

anemia, fatigue, n/v, anorexia, coagulopathy

81
Q

1st line tx for uremia

A

desmopressin

82
Q

2 ways CKD increases anemia

A

decreased production of EPO via kidneys, normochromic normocytic anemia
excess PTH replaces bone marrow with fibrotic tissue which increases anemia.

83
Q

CKD shifts oxyhgb dissociation curve

A

to the right to help with metabolic acidosis

84
Q

how does osteodystrophy happen in CKD

A

caused by decreased vitamin D production, secondary to hyperparathyroidism. PTH demineralizes bone to restore serum calcium conentration

85
Q

5 indications for HD

A
  1. volume overload
  2. increased K (over 6)
  3. severe metabolic acidosis
  4. symptomatic uremia
  5. OD with a drug
86
Q

FDA recommend that sevoflurane be administered at a rate of __L/min for no more than ___ MAC hours

A

1L/min for more than 2 MAC hours.

87
Q

best nondepolarizing NMB’s for CKD

A

cisatracurium and atracurium

88
Q

do you need an increased or decreased dosage of propofol in CKD patients?

A

increased related to hyper dynamic circulation and disruption of BBB secondary to azotemia

89
Q

better opioid analgesics for CKD patients (that dont have metabolites that can accumulate) include

A

fentanyl, sufentanyl, alfentanil

90
Q

radiographic contrast media causes nephrotoxicity by

A

ischemic injury due to vasoconstriction in renal medulla, direct cytotoxic effect

91
Q

use what kind of contrast with CKD?

A

non ionic iso or low osmolar contrast instead of hyperosmolar

92
Q

strategies to prevent injury from free myoglobin include

A

maintenance of RBF and tubular flow with IV hydration, osmotic diuresis with mannitol, keep UOP >100-150mL/h, administer NaHCO3 or acetazolamide to alkalinize the urine

93
Q

two ways sevo can theoretically impair renal functoin

A
  1. compound A
  2. free fluoride ions
94
Q

calcineuron inhibitors

A

are immunosuppressant agents that prevent the rejection of transplanted organs. sirolumus is a non cal

95
Q

sirolumus

A

non calcineurin inhibitor that carries a much lower risk of nephrotoxity

96
Q

most common approach to TURP (anesthetic)

A

spinal (T10 level necessary)

97
Q

distilled H2O irrigation solution for TURP
osmolarity
pros
cons

A

0 mOsm/L
good surgical visibility
increases risk of TURP syndrome, hyponatramia, hemolysis, hemoglobinuria, renal failure

98
Q

glycine irrigation solution for TURP
osmolarity
pros
cons

A

200 mOsm/L
decrease risk of TURP syndrome
increased ammonia, decreased LOC, transient post visual syndrome, blind/blurry vision for 24-48h, glycine is inhibitory transmitter in eye

99
Q

sorbitol 3.3% irrigation solution for TURP
osmolarity
pros
cons

A

165 mOsm/L
decreased risk of TURP syndrome
increased BG, osmotic diuresis, lactic acidosis

100
Q

mannitol 5% irrigation solution for TURP
osmolarity
pros
cons

A

275 mOsm/L
osmolarity similar to plasma, renal filtration and excretion (no metabolism)
cons: osmotic diuresis, transient plasma expansion

101
Q

NaCl .9% irrigation solution for TURP
osmolarity
pros
cons

A

303 mOsm/L
osmolarity just a bit higher than plasma. absent of many SE’s associated with other solutons
cons: can only be used with bipolar electrocautery. do not use with monopoly.

102
Q

presentation of TURP syndrome

A

triad: HTN, bradycardia, change in mental status

103
Q

treatment of TURP syndrome

A

support with O2/CV. labs: lytes, HCT, creatinine, glucose
12 lead,
if Na >120 then restrict fluids and give furosemide
if <120 then give 3% NaCl at <100mL/h

104
Q

bladder perf presentation and tx

A

abdominal and shoulder pain, decrease in irrigation fluid return
tx: supportive. serial H/H, emergent suprabupic cystotomy or even exlap

105
Q

absolute contraindications to lithotripsy

A

pregnancy and risk of bleeding

106
Q

relative contraindications to lithotripsy

A

Pacer/ICD. calcified aneurysm of aorta or renal artery, URI, obstruction, morbid obesity

107
Q

anesthesia considerations for percutaneous lithotripsy

A

used when ESWL ineffective
stents placed
GETA and in prone
irrigation used
pneumothorax is a complicaton

108
Q

anesthesia considerations for laser litho

A

breaks up stone, irrigation used, pts are usually in lithotomy.

109
Q

how to calculate creatinine clearance (men)

A

(140- age) * (weight in kg) / (serum creatinine /72)

110
Q

how to calculate creatinine clearance (men)

A

(140-age)* (kg) / (serum creat*72)

111
Q

how to calculate creatinine clearance (women)

A

.85 (140-age)*(kg)/ (serum creat *72)

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