Nephrology drugs Flashcards
1
Q
Review the nephron on slide
A
2
2
Q
About ___% of plasma that arrives at the bowman’s capsuel passes through the filtration barrier to become filtrate
A
25%
3
Q
What is reabsorbed in the PT?
A
NaCl (majority), glucose, potassium, amino acids, bicarb, phosphate, protein, urea, water (follows NaCl)
4
Q
What is secreted in the PT?
A
Hydrogen, foreign substances, organic anions and cations
5
Q
What diuretics exert their effect at the PT?
A
Carbonic Anyhrdrase Inhibitors and osmotic diuretics
6
Q
The LOH _________ urine
A
concentrates
7
Q
In the descending LOH ______ is reabsorbed and ______ diffuses in
A
Water / NaCl
8
Q
In the ascending LOH ________ is actively reabsorbed and ________ stays in
A
Sodium / water
9
Q
Loop diuretics exert their effect at the
A
LOH
10
Q
In the DT what is reabsorbed?
A
NaCl, water (ADH required), bicarb
11
Q
In the DT what is secreted
A
Potassium, urea, hydrogen, NH3, some medications
12
Q
What drugs exert their effect at the DT?
A
thiazaides
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
14
Q
CKD is defined as kidney damage for > 3 months defined by structural or functional abnormalities with or without decreased _______
A
GFR
15
Q
GFR < 60 ml/min for > 3months with or without kidney damage
A
CKD
16
Q
Damage with nml or increased GFR: GFR >90 ml/min
A
CKD 1
17
Q
Damage with mild decreased GFR: GFR 60-89
A
CKD 2
18
Q
Moderate decreased GFR: GFR 30-59
A
CKD 3
19
Q
Severe decrease in GFR: GFR 15-29
A
CKD 4 ( this is where you start thinking about adjusting drug doses)
20
Q
Kidney failure: GFR < 15 ml/min
A
CKD 5
21
Q
Dialysis
A
CKD 6
22
Q
RIFLE criteria looks at what?
A
ACUTE KIDNEY DZ: Risk, Injjury, Failure, Loss, ESRD
23
Q
Review slides 8 and 9
A
8 and 9
24
Q
Review slide 10
A
where in the nephron diuretics work
25
Carbonic Anyhdrase Inhibitors
Acetazolamide, Methazolamide, Dichlorophenamine
26
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 _______.
H+ / PT / reabsorption / LOH
27
CA inhibitors cause a loss of _______ and which results in what metabolic disorder.
NaHCO3 / hypokalemic metabolic acidosis
28
Tolerance to CA inhibitors develops in __ to __ days
2 to 3
29
With CA inhibitors, an enhanced Na delivery results in ____ loss in the collecting duct
Potassium
30
Common side effects from CA inhibitors
blurred vision, changes in taste, constipation, diarrhea, drowsiness, frequent urination, loss of appetite, N/V
31
CA Inhibitos sides effects side note
don’t cause significant fluid shifts, would be worried about PONV with these
32
Examples of osmotic diuretics
mannitol and urea
33
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.
glomerulus / Na / reabsorption
34
Mannitol causes _____ of water, ________ intracellular volume, and _______ risk
loss / reduced / hypernatremia
35
Main effect of mannitol is at the ___________ tubule
proximal
36
Osmotic diuretics can be administered in large quantities to alter the ________ of plasma, glomerular filtrate, and renal tubular fluid resulting in _______ diuresis
osmolarity/ osmotic
37
With osmotic diuretics, Osmotic effect in the renal tubules results in an osmosmotic diuretic effect with urinary excretion of what 4 things
water, sodium, chloride, bicarbonate ion
38
_______pH is not altered by mannitol-induced osmotic diuresis
urinary
39
IV mannitol ________ plasma osmolarity and acutely ___________ the intravascular volume
increases / expands
40
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.
decreases / medulla / CHF
41
Clincial uses for mannitol
prophylaxis against ARF, diffferential diagnosis of acute oliguria, treatment of increase in ICP, decreasing IOP
42
T/F Mannitol is no better than plain saline for pre-radiocontrast dye
TRUE
43
Mannitol really has no use in ARF prophylaxis except in _______ ___________ surgery
renal transplant
44
Using mannitol for differntial diagnosis of acute oliguria
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
45
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
increased / CSF / CSF
46
T/F The more mannitol is used (chronic) the less effective it becomes
TRUE
47
T/F Mannitol use for ICP reduction requires an intact BBB
TRUE
48
Mannitol can cause ___________ of vascular smooth muscle which depends on dose and rate of administration.
vasodilation
49
Vasodilation from mannitol affects intracranial and extracranial vessels and can simultaneously __________ cerebral blood volume and ICP while ________ systemic BP
increase / decrease
50
Since mannitol may initially increase ICP what treatments can be done that decrease intracranial volume?
corticoseteroids and hyperventilation
51
Mannitol use in eye surgery will decrease IOP by increasing _______ ________ that causes fluid to leave the eye
plasma osmolarity
52
Mannitol side effects
precipitates pulmonary edema, hypovolemia, electrolyte disturbances, plasma hyperosmolarity due to water and NaCl secretion
53
T/F It is possible you may have to run fluids while administering mannitol due to fluid shifts
TRUE
54
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.
osmotic / small / BBB / ICP
55
High incidence of ________ _______ and tissue necrosis after extravasation with urea (not seen with mannitol)
venous thrombosis
56
Increased _______ after urea administration should NOT be confused with ARF
BUN
57
Loop diuretics
lasix, bumex, demedex, ethacrynic acid
58
Loop diuretics are __________ based with the exception of ________
sulfa / ethacrynic acid
59
MOA for loop diuretics: Inhibits ___ and ____ reabsorption in the ______ LOH and to a lesser extent the PT
Na and Cl / Ascending
60
Loop diuretics cause a loss of ___ and _____. There is also an increased ____ loss.
Na and water / Ca++
61
What metabolic disorder can result from loop diurectics?
hypokalemic metaoblic alkalosis
62
Which diuretic has the highest risk of electrolyte disturbances?
Lasix
63
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.
prostaglandins / cortex
64
Furosemide induced increases in RBF are inhibited by _______
NSAIDS
65
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 _________.
ICP / hypercalcemia / oliguria
66
T/F Lasix will increase lymph flow through the thoracic duct
TRUE
67
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.
systemic / Na / water
68
Decreased ICP from lasix is not accompanies by changes in ________ or changes in _______ ______
CBF / plasma osmolarity
69
Which is better at treating increased ICP, mannitol of lasix
mannitol
70
Mannitol may produce a rebound intracranial HTN if disrupted ______ allows mannitol to enter the CNS
BBB
71
Combination of _______ and ______________ is more efffective in decreasing ICP then either drug alone; however, there is an increased risk of _______ and ________
mannitol and lasix / dehydration and electrolyte imbalance
72
Loop diuretic side efffects
hypokalemia, hypochloremia, hyponatremia, hypomagnesemia, metabolic alkalosis
73
Acute tolerance from loop diuretics characterized by loss of effectiveness from not replacing electrolytes is termed the _________ _________
braking phenomenon
74
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__________.
deafness / endolymph / dependent
75
What cross-sensitivity reactions should be concerned for loop diuretics
sulfa antibotics, sulfonylureas, thiazaide diuretics
76
Aminoglyocides and loop diuretics can increase renal tissue concentrations of aminoglycosids and enhances the possibility of __________
nephrotoxicity
77
Cephalasporins and loop diuretics together can cause ____________
nephrotoxicity
78
PCN and furosemide is associated with allergic ____________ neprhritis, similar to that seen occasionally with PCN
interstitial
79
Thiazide diuretics
chlorothiazide, HCTZ, indapamide, metolazone, chlorthalidone
80
MOA for thiazaide diuretics: Compete for the _______ cotransporter in the _____ to inhibit reabsorption. Inhibit only urinary diluting capacity, not _________ capacity.
Na-Cl / DT / concentrating
81
Thiazide diuretics result in a loss of ____ and _____. Increased ____ reabsorption which can cause ___________.
Na and water / Ca++ / hypercalcemia
82
What metabolic disorder can result from thiazide diurectics
hypokalemic metaoblic alkalosis
83
Thiazide clincial uses
HTN and mobilization of edema
84
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.
decreased / CO / vasodilation
85
Metabolic and electrolyte side effects from thiazides
hypokalemia, hypochloremia, HYPERCALCEMIA, metabolic alkalosis with chronic admin. Sodium and magnesium depletion may accompany kaliuresis
86
Cardiac side effects from thiazide diuretics result from diuretic induced ________ and ________
hypokalemia and hypomagnesemia
87
**Other side effects of thiazides
skeletal muscle weakness, GI ileus, increased likelihood of developing dig toxicity, potentiation of NDNMBs
88
Side effects of thiazide diuretics include decreased ___________ volume, HYPERGLYCEMIA, HYPERURICEMIA (GOUT), and decreased renal or hepatic function
intravascular
89
Difference between loops and thiazides is that thiazides can cause ______________ and do not lose _____________- as severe as loops
hypercalemia / potassium
90
Potassium sparing diuretics
amiloride / Triamterene / Spironolactone / Eplerenone
91
MOA for Amiloride and Triamteren
Inhibit Na reabsorption induced by aldosterone. Inhibit active counter transport of Na and K in the colecting duct
92
MOA for spironolactone and Eplerenone
competes for aldosterone receptor sites in the DT to block Na reabsoprtion and K secretion
93
Aldosterone antagonisits (K sparing diuretics) result in what 3 things?
loss of Na and water, Hyperkalemia, some risk for acidosis
94
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 ___________
refractory / aldosterone
95
Principle side effect from K+ sparing diuretics is ______________
Hyperkalemia
96
What other drugs if taking K+ sparing diuretics put them at increased riks of hyperkalemia
NSAIDS, ACE-I, beta blockers
97
Unlike thiazides, K+ sparing diuretics doe not produce _____________ or _____________
hyperuricemia or hyperglycemia
98
Review slide 46
summary of side effects by class
99
Mannitol can give you ________
hypernatremia
100
Hyperkalemia can result from what?
renal failure, hypoaldosteronism, potassium supplements, ACEi/ARB, heparin, NSAIDS, K-sparing diurectics and digoxin
101
Hypokalemia can result from what?
loop diurectics, thiazides, osmotics, hyperaldosteronism, mineralcorticoids, fluid loss (vomit/diarrhea)
102
Emergent treatment of Hyperkalemia is indicated when?
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
Presentation of hyperkalemia
usually asymptomatic, weakness, fatigue, GI hypermotility,
104
Review slide 50
treatment of hyperkalemia
105
Treatment of hyperkalemia with IV calcium
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
Fastest way to bring down potassium
insulin and dextrose
107
Is sodium bicarb recommended to lower potassium
no
108
_____________ 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.
patiromer (veltassa)
109
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
sodium zirconium cyclosilicate / 12 months
110
Hypernatremia can be from:
increase via food intake, pure water loss (DI), ADH abnormalities, osmotic diuretics
111
Hyponatremia can be from:
loss of body fluid, thiazides, loops, CHF, carbamazepine, lithium, liver dz
112
Sodium disorders present as what?
nuerologic depression, seizures, respiratory depression, coma
113
Correction rates for severe symptomatic hyponatremia
6-12 mEq/L in the first 24 H and 18 mEq/L or less in 48 hr
114
Correction rate for chronic hypernatremia
0.5 mEq/L/hr with max change of 8-10 mEq/L in a 24H period
115
VAPTANs (vasopressin receptor blockers) are for ___________ and _____________ HYPONATREMIA
euvolemic and hypervolemic
116
V1A/V2
conivaptan
117
V1A selective (V1RA)
Relcovaptan
118
V1B selective (V3RA)
Nelivaptan
119
V2 selective (V2RA)
Lixivaptan, Mozavaptan, Satavaptan, Tolvapatan
120
Calcium level is dependent upon _________.
albumin
121
Hypercalcemia is most often caused by what
hyperparathyroidism, cancer, thiazides
122
Hypocalcemia is most often caused by what
hypoparathyroidism, renal disease, loop diuretics
123
Clincial manifestations of Hypercalcemia (highlights, review slide 60 for complete list)
nephrogenic DI, nephrolithiaisiis, bone pain, osteoporosis, N/V, abdominal pain, HTN, short QT interval, itching
124
Review slides 61 and 62
more on calcium too much to type. Have a nice day :)
