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Pharmacology II - Emily Britton > Nephrology drugs > Flashcards

Nephrology drugs Flashcards

1
Q

Review the nephron on slide

A

2

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2
Q

About ___% of plasma that arrives at the bowman’s capsuel passes through the filtration barrier to become filtrate

A

25%

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3
Q

What is reabsorbed in the PT?

A

NaCl (majority), glucose, potassium, amino acids, bicarb, phosphate, protein, urea, water (follows NaCl)

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4
Q

What is secreted in the PT?

A

Hydrogen, foreign substances, organic anions and cations

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5
Q

What diuretics exert their effect at the PT?

A

Carbonic Anyhrdrase Inhibitors and osmotic diuretics

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6
Q

The LOH _________ urine

A

concentrates

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7
Q

In the descending LOH ______ is reabsorbed and ______ diffuses in

A

Water / NaCl

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8
Q

In the ascending LOH ________ is actively reabsorbed and ________ stays in

A

Sodium / water

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9
Q

Loop diuretics exert their effect at the

A

LOH

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10
Q

In the DT what is reabsorbed?

A

NaCl, water (ADH required), bicarb

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11
Q

In the DT what is secreted

A

Potassium, urea, hydrogen, NH3, some medications

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12
Q

What drugs exert their effect at the DT?

A

thiazaides

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13
Q

The collecting duct is responsible for final _____________. Water is reabsorbed and ______ is required for this. ________ is also reabsorbed. In the collecting duct, Na, K, H, NH3 can be either _____ or ____.

A

concentration / ADH / NaCl / reabsorption or secretion

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14
Q

CKD is defined as kidney damage for > 3 months defined by structural or functional abnormalities with or without decreased _______

A

GFR

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15
Q

GFR < 60 ml/min for > 3months with or without kidney damage

A

CKD

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16
Q

Damage with nml or increased GFR: GFR >90 ml/min

A

CKD 1

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17
Q

Damage with mild decreased GFR: GFR 60-89

A

CKD 2

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18
Q

Moderate decreased GFR: GFR 30-59

A

CKD 3

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19
Q

Severe decrease in GFR: GFR 15-29

A

CKD 4 ( this is where you start thinking about adjusting drug doses)

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20
Q

Kidney failure: GFR < 15 ml/min

A

CKD 5

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21
Q

Dialysis

A

CKD 6

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22
Q

RIFLE criteria looks at what?

A

ACUTE KIDNEY DZ: Risk, Injjury, Failure, Loss, ESRD

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23
Q

Review slides 8 and 9

A

8 and 9

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24
Q

Review slide 10

A

where in the nephron diuretics work

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25
Q

Carbonic Anyhdrase Inhibitors

A

Acetazolamide, Methazolamide, Dichlorophenamine

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26
Q

Carbonic Anyhdrase Inhibitors MOA: Inhibit CA which inhibits _____ SECRETION in the _____. Bicarb and sodium are blocked from _______. Effect is short lived due to compensation at _______.

A

H+ / PT / reabsorption / LOH

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27
Q

CA inhibitors cause a loss of _______ and which results in what metabolic disorder.

A

NaHCO3 / hypokalemic metabolic acidosis

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28
Q

Tolerance to CA inhibitors develops in __ to __ days

A

2 to 3

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29
Q

With CA inhibitors, an enhanced Na delivery results in ____ loss in the collecting duct

A

Potassium

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30
Q

Common side effects from CA inhibitors

A

blurred vision, changes in taste, constipation, diarrhea, drowsiness, frequent urination, loss of appetite, N/V

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31
Q

CA Inhibitos sides effects side note

A

don’t cause significant fluid shifts, would be worried about PONV with these

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32
Q

Examples of osmotic diuretics

A

mannitol and urea

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33
Q

MOA for osmotic diuretics: Non-reabsorbable solute filtered freely in the __________. Uncouples _____ and water _______ by increasing the somotic gradient in the PT. Sodium reabsorption initially, but water is not, leading to decreased sodium reabsorption distally.

A

glomerulus / Na / reabsorption

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34
Q

Mannitol causes _____ of water, ________ intracellular volume, and _______ risk

A

loss / reduced / hypernatremia

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35
Q

Main effect of mannitol is at the ___________ tubule

A

proximal

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36
Q

Osmotic diuretics can be administered in large quantities to alter the ________ of plasma, glomerular filtrate, and renal tubular fluid resulting in _______ diuresis

A

osmolarity/ osmotic

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37
Q

With osmotic diuretics, Osmotic effect in the renal tubules results in an osmosmotic diuretic effect with urinary excretion of what 4 things

A

water, sodium, chloride, bicarbonate ion

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38
Q

_______pH is not altered by mannitol-induced osmotic diuresis

A

urinary

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39
Q

IV mannitol ________ plasma osmolarity and acutely ___________ the intravascular volume

A

increases / expands

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40
Q

Redistribtution of fluid from mannitol _________ brain bulk, may preferentially increase renal blood flow to the ________, but detrimental effecets of redistribution include ________ in patients with poor myocardial function.

A

decreases / medulla / CHF

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41
Q

Clincial uses for mannitol

A

prophylaxis against ARF, diffferential diagnosis of acute oliguria, treatment of increase in ICP, decreasing IOP

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42
Q

T/F Mannitol is no better than plain saline for pre-radiocontrast dye

A

TRUE

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43
Q

Mannitol really has no use in ARF prophylaxis except in _______ ___________ surgery

A

renal transplant

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44
Q

Using mannitol for differntial diagnosis of acute oliguria

A

Mannitol 0.25 g/kg IV: UOP is increased when the cause of acute oliguria is decreased intravascular volume. If glomerular or rena tubular function severely compromised, mannitol will not increase urine output

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45
Q

Mannitol 0.25 g to 1G/kg IV is used for increased ICP. By administering this, the plasma osmolarity is ____________ which draws water from tissues, including the brain, along an osmotic gradient. It also decreases ____ volume by decreasing the rate of ____ formation

A

increased / CSF / CSF

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46
Q

T/F The more mannitol is used (chronic) the less effective it becomes

A

TRUE

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47
Q

T/F Mannitol use for ICP reduction requires an intact BBB

A

TRUE

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48
Q

Mannitol can cause ___________ of vascular smooth muscle which depends on dose and rate of administration.

A

vasodilation

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49
Q

Vasodilation from mannitol affects intracranial and extracranial vessels and can simultaneously __________ cerebral blood volume and ICP while ________ systemic BP

A

increase / decrease

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50
Q

Since mannitol may initially increase ICP what treatments can be done that decrease intracranial volume?

A

corticoseteroids and hyperventilation

51
Q

Mannitol use in eye surgery will decrease IOP by increasing _______ ________ that causes fluid to leave the eye

A

plasma osmolarity

52
Q

Mannitol side effects

A

precipitates pulmonary edema, hypovolemia, electrolyte disturbances, plasma hyperosmolarity due to water and NaCl secretion

53
Q

T/F It is possible you may have to run fluids while administering mannitol due to fluid shifts

A

TRUE

54
Q

Urea is another effective _______ diuretic. It is ________ in molecular size, so it will eventually penetrate cells and cross the ______. Greater rebound increase in _______________ than after mannitol.

A

osmotic / small / BBB / ICP

55
Q

High incidence of ________ _______ and tissue necrosis after extravasation with urea (not seen with mannitol)

A

venous thrombosis

56
Q

Increased _______ after urea administration should NOT be confused with ARF

A

BUN

57
Q

Loop diuretics

A

lasix, bumex, demedex, ethacrynic acid

58
Q

Loop diuretics are __________ based with the exception of ________

A

sulfa / ethacrynic acid

59
Q

MOA for loop diuretics: Inhibits ___ and ____ reabsorption in the ______ LOH and to a lesser extent the PT

A

Na and Cl / Ascending

60
Q

Loop diuretics cause a loss of ___ and _____. There is also an increased ____ loss.

A

Na and water / Ca++

61
Q

What metabolic disorder can result from loop diurectics?

A

hypokalemic metaoblic alkalosis

62
Q

Which diuretic has the highest risk of electrolyte disturbances?

A

Lasix

63
Q

Renovascular effect: Furosemide induced production of __________ results in renal VASODILATION and increased RBF. This redistributes RBF from the inner to the outer renal ___________ and contributes to the diruetic effect of furosemide.

A

prostaglandins / cortex

64
Q

Furosemide induced increases in RBF are inhibited by _______

A

NSAIDS

65
Q

Loop diuretics are used to mobilize edema fluid due to renal, hepatic or cardiac dysfunction. It can also be used to treat increased ___________ and ____________. Also used in differential diagnosis of acute _________.

A

ICP / hypercalcemia / oliguria

66
Q

T/F Lasix will increase lymph flow through the thoracic duct

A

TRUE

67
Q

With lasix, ICP is decreased by _______ diuresis. It also decreases CSF production by interfering with _____ transport in glial tissue which resolves cerebral edema by improving cellular ______ transport.

A

systemic / Na / water

68
Q

Decreased ICP from lasix is not accompanies by changes in ________ or changes in _______ ______

A

CBF / plasma osmolarity

69
Q

Which is better at treating increased ICP, mannitol of lasix

A

mannitol

70
Q

Mannitol may produce a rebound intracranial HTN if disrupted ______ allows mannitol to enter the CNS

A

BBB

71
Q

Combination of _______ and ______________ is more efffective in decreasing ICP then either drug alone; however, there is an increased risk of _______ and ________

A

mannitol and lasix / dehydration and electrolyte imbalance

72
Q

Loop diuretic side efffects

A

hypokalemia, hypochloremia, hyponatremia, hypomagnesemia, metabolic alkalosis

73
Q

Acute tolerance from loop diuretics characterized by loss of effectiveness from not replacing electrolytes is termed the _________ _________

A

braking phenomenon

74
Q

With loop diuretics, ________ occur with prolonged increases in the plasma conentrations of these drugs in the presence of other ototoxic drugs. The possible mechanism for this is drug-induced changes in the electrolyte composition of the __________________. Transient of permanent deafness is a rare and dose__________.

A

deafness / endolymph / dependent

75
Q

What cross-sensitivity reactions should be concerned for loop diuretics

A

sulfa antibotics, sulfonylureas, thiazaide diuretics

76
Q

Aminoglyocides and loop diuretics can increase renal tissue concentrations of aminoglycosids and enhances the possibility of __________

A

nephrotoxicity

77
Q

Cephalasporins and loop diuretics together can cause ____________

A

nephrotoxicity

78
Q

PCN and furosemide is associated with allergic ____________ neprhritis, similar to that seen occasionally with PCN

A

interstitial

79
Q

Thiazide diuretics

A

chlorothiazide, HCTZ, indapamide, metolazone, chlorthalidone

80
Q

MOA for thiazaide diuretics: Compete for the _______ cotransporter in the _____ to inhibit reabsorption. Inhibit only urinary diluting capacity, not _________ capacity.

A

Na-Cl / DT / concentrating

81
Q

Thiazide diuretics result in a loss of ____ and _____. Increased ____ reabsorption which can cause ___________.

A

Na and water / Ca++ / hypercalcemia

82
Q

What metabolic disorder can result from thiazide diurectics

A

hypokalemic metaoblic alkalosis

83
Q

Thiazide clincial uses

A

HTN and mobilization of edema

84
Q

Treatment for HTN with thiazaide diuretics initially results in a _________ extracellular volume and often a decreased ______. Sustained treatment with thiazaide results in peripheral _____________which takes weeks to develop.

A

decreased / CO / vasodilation

85
Q

Metabolic and electrolyte side effects from thiazides

A

hypokalemia, hypochloremia, HYPERCALCEMIA, metabolic alkalosis with chronic admin. Sodium and magnesium depletion may accompany kaliuresis

86
Q

Cardiac side effects from thiazide diuretics result from diuretic induced ________ and ________

A

hypokalemia and hypomagnesemia

87
Q

**Other side effects of thiazides

A

skeletal muscle weakness, GI ileus, increased likelihood of developing dig toxicity, potentiation of NDNMBs

88
Q

Side effects of thiazide diuretics include decreased ___________ volume, HYPERGLYCEMIA, HYPERURICEMIA (GOUT), and decreased renal or hepatic function

A

intravascular

89
Q

Difference between loops and thiazides is that thiazides can cause ______________ and do not lose _____________- as severe as loops

A

hypercalemia / potassium

90
Q

Potassium sparing diuretics

A

amiloride / Triamterene / Spironolactone / Eplerenone

91
Q

MOA for Amiloride and Triamteren

A

Inhibit Na reabsorption induced by aldosterone. Inhibit active counter transport of Na and K in the colecting duct

92
Q

MOA for spironolactone and Eplerenone

A

competes for aldosterone receptor sites in the DT to block Na reabsoprtion and K secretion

93
Q

Aldosterone antagonisits (K sparing diuretics) result in what 3 things?

A

loss of Na and water, Hyperkalemia, some risk for acidosis

94
Q

K sparing diuretics are less effective at diuresis alone but better when used in combination with something else. Used for treatment of ___________ edematous states due to CHF and cirrhosis of liver. Works in these situations because decreaed hepatic function and metabolism lead to increased plasma concentration of ___________

A

refractory / aldosterone

95
Q

Principle side effect from K+ sparing diuretics is ______________

A

Hyperkalemia

96
Q

What other drugs if taking K+ sparing diuretics put them at increased riks of hyperkalemia

A

NSAIDS, ACE-I, beta blockers

97
Q

Unlike thiazides, K+ sparing diuretics doe not produce _____________ or _____________

A

hyperuricemia or hyperglycemia

98
Q

Review slide 46

A

summary of side effects by class

99
Q

Mannitol can give you ________

A

hypernatremia

100
Q

Hyperkalemia can result from what?

A

renal failure, hypoaldosteronism, potassium supplements, ACEi/ARB, heparin, NSAIDS, K-sparing diurectics and digoxin

101
Q

Hypokalemia can result from what?

A

loop diurectics, thiazides, osmotics, hyperaldosteronism, mineralcorticoids, fluid loss (vomit/diarrhea)

102
Q

Emergent treatment of Hyperkalemia is indicated when?

A

Tall peaked T waves, loss of P wave, wide QRS, rapid rise of serum potassium to greater than 6, decreased renal function, presence of significant acidosis

103
Q

Presentation of hyperkalemia

A

usually asymptomatic, weakness, fatigue, GI hypermotility,

104
Q

Review slide 50

A

treatment of hyperkalemia

105
Q

Treatment of hyperkalemia with IV calcium

A

protects myocardium, EKG improvments within 2-3 minutes, caution for patients on digoxin, no effects on potassium level, could use magnesium as an alternative to stabilize the myocardium

106
Q

Fastest way to bring down potassium

A

insulin and dextrose

107
Q

Is sodium bicarb recommended to lower potassium

A

no

108
Q

_____________ is an oral GI potassium binder to increase fecal excretion. Not for emergency use d/t delayed onset of action. Should not be taken with othe meds and should be separated by 3 hrs.

A

patiromer (veltassa)

109
Q

A new agent called _____________________ is better suited for acute therapy. IT is an oral GI potassium binder to increase fecal excretion with an onset of 1 hr resulting in normal K within 2.2 hrs with sustained action up to ___ months

A

sodium zirconium cyclosilicate / 12 months

110
Q

Hypernatremia can be from:

A

increase via food intake, pure water loss (DI), ADH abnormalities, osmotic diuretics

111
Q

Hyponatremia can be from:

A

loss of body fluid, thiazides, loops, CHF, carbamazepine, lithium, liver dz

112
Q

Sodium disorders present as what?

A

nuerologic depression, seizures, respiratory depression, coma

113
Q

Correction rates for severe symptomatic hyponatremia

A

6-12 mEq/L in the first 24 H and 18 mEq/L or less in 48 hr

114
Q

Correction rate for chronic hypernatremia

A

0.5 mEq/L/hr with max change of 8-10 mEq/L in a 24H period

115
Q

VAPTANs (vasopressin receptor blockers) are for ___________ and _____________ HYPONATREMIA

A

euvolemic and hypervolemic

116
Q

V1A/V2

A

conivaptan

117
Q

V1A selective (V1RA)

A

Relcovaptan

118
Q

V1B selective (V3RA)

A

Nelivaptan

119
Q

V2 selective (V2RA)

A

Lixivaptan, Mozavaptan, Satavaptan, Tolvapatan

120
Q

Calcium level is dependent upon _________.

A

albumin

121
Q

Hypercalcemia is most often caused by what

A

hyperparathyroidism, cancer, thiazides

122
Q

Hypocalcemia is most often caused by what

A

hypoparathyroidism, renal disease, loop diuretics

123
Q

Clincial manifestations of Hypercalcemia (highlights, review slide 60 for complete list)

A

nephrogenic DI, nephrolithiaisiis, bone pain, osteoporosis, N/V, abdominal pain, HTN, short QT interval, itching

124
Q

Review slides 61 and 62

A

more on calcium too much to type. Have a nice day :)

Pharmacology II - Emily Britton (5 decks)

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