Diuretics, Renal meds, and Lytes Flashcards

(112 cards)

1
Q

Where does NaCl reabsorption primarily occur?

A

Proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What diuretics work primarily on the proximal tubule?

A

CAI’s and Osmotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the role of the loop of henle?

A

Concentration of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the difference b/w the descending and ascending loop of henle?

A

Descending: water is reabsorbed and NaCl diffuses in

Ascending: water stays in and NaCl ACTIVELY reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What diuretics work primarily on the loop of henle?

A

Loop diurectics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the role of distal convoluted tubule?

A

Reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What diuretics work primarily on the DCT?

A

Thiazides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the role of the collecting duct?

A

Final concentraient of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What meds work on the collecting duct?

A

Potassium-sparing diuretics

Vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

2 definitions of Chronic kidney disease

A

Kidney damage > 3 months defined by structural or functional abnormalities with or without decreased GFR

Or

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

difference b/w acute and chronic kidney damage

A

Acute is < 3 months

Chronic is > 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Stage I kidney disease

A

GRF > 90ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Stage II Kidney disease

A

GFR 60-89 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stage III Kidney disease

A

GFR 30-59 ml/min (Moderate)

Its less than 60, so its where CKD begins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stage IV kidney disease

A

GFR 15-29 ml/min (severe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Stage V kidney disease

A

GFR < 15 ml/min (Kidney failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Stage VI kidney disease

A

Dialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

At what stage of CKD are meds starting to be renally adjusted?

A

Stage 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What criteria is use to diagnose acute kidney disease

A

RIFLE criteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

RIFLE criteria is based on ___

A

GFR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pre-renal injury is usually due to ____

A

dehydration (occurs before the kidney)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Intrinisic renal injury is usually due to ___

A

medications (large molecules)

causes damage along the nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Post-renal injury is usually due to ____

A

obstruction (kidney stone, growth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is FENa?

A

Fractional Excretion of Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
FENa levels for pre-renal, intrinsic, and post-renal
Pre-renal: <1% Instrinic: <1.3% Post-renal: <1.5%
26
What is the most common carbonic anhydrase inhibitor?
Diamox (Acetazolamide)
27
What are carbonic anhydrase inhibitors primarily used for?
Glaucoma and altitude sickness
28
MOA of carbonic anhydrase inhibitors?
Inhibit CA, which inhibits H+ secretion in the proximal tubule. Bicarb and sodium are blocked from reabsorption. Effect is short lived due to compensation at loop of Henle.
29
CAI's cause a loss of Bicarb, which leads to ____
*Hypokalemic metabolic ACIDOSIS*
30
Tolerance to CAI's usually develops after ____
2-3days
31
Main SE's of CAI's
1. PONV/GI upset 2. Blurred vision leading to confusion and agaitation Not too worried about fluid shifts
32
Examples of osmotic diuretics
Mannitol | Urea
33
MOA of osmotic diuretics
large molecules result it movement of water through osmosis
34
What major electrolyte abnormality can occur with osmotic diuretics?
*hypernatremia* due to loss of water an reduced intracellular volume
35
Giving mannitol to a a patient with poor myocardial function can results in ___
CHF
36
What diuretics can be given to for differential diagnosis of acute oliguria?
Mannitol | Loops
37
Mannitol is only nephroprotective for which patients?
*Renal transplant surgery*, less incidence of ARF no evidence it prevents ARF in other cases (CV surgery, trauma, other transplants, surgery in the presence of liver dz/jaundice)
38
T/F Mannitol requires the presence of intact BBB
true
39
T/F Mannitol can initially increase ICP if given too rapidly
True | due to vasodilation of intracranial and extra cranial vessels simutaneously
40
How long should Mannitol be administered to decrease ICP?
Over 10 mins
41
SE's of mannitol
*pulmonary edema* hypovolemia electrolyte disturbances plasma hyperosmolarity
42
Is urea small/large molecule size
small
43
T/F urea can cross BBB
True
44
What has a greater rebound increase in ICP after administration, mannitol or urea?
Urea
45
What are two major drawbacks to urea?
*high incidence of VTE* Tissue necrosis (not seen with mannitol)
46
What lab value will change when giving urea?
Increase BUN (due to fluid shifts, NOT ARF)
47
T/F Compared to mannitol, urea has more SE and is less effective
True
48
Examples of Loop diuretics
* Furosemide (Lasix) * Bumetanide (Bumex) * Torsemide (Demedex) * Ethacrynic acid (Edecrin)
49
MOA of loop diurectics
Inhibits Na and Cl reabsorption in the ascending loop and to a lesser extent in the proximal tubule.
50
T/F loop diuretics are the best meds for chronic edema (form CHF and liver dz)
True
51
DOA of loop diuretics
6-12hrs
52
what loop diuretic has the worst oral bioavailability?
lasix
53
Loop diuretics are contraindicated in patients with ___ allergy
sulfa except Ethacrynic acid (Edecrin)
54
The only difference b/w loop diuretics is _____
oral bioavailability (no difference IV)
55
Which loop diuretic is safe in patients with a sulfa allergy?
Ethacrynic acid (Edecrin)
56
Loop diuretics can lead to what 3 things
Loss of Na and water Hypokalemic metabolic alkalosis divalent loss (both K+ and Mg+) Hypocalcemia
57
carbonic anhydrase inhibitors can cause hypokalemic metabolic _____, loop diuretics can cause hypokalemic metabolic _____
acidosis | alkalosis
58
What other med should be ordered along with loop diuretics?
potassium
59
Which loop diuretic has the highest risk of electrolyte abnormalities?
Lasix
60
Clinical uses of loop diuretics
1. mobilizaiton of edema fluid due to renal, hepatic, or cardiac dysfunction. 2. Treatment of increased ICP. 3. Treatment of hypercalcemia. 4. Differential diagnosis of acute oliguria.
61
Lasix produces diuresis within __
2-10 mins
62
Furosemide induced production of prostaglandins (E4) results in renal vaso____ and increased ____.
renal vasodilation and increased RBF
63
What med can inhibit Furosemide-induced increases in RBF?
NSAID's
64
What 3 classes of antibiotics can interact with lasix?
Cephlasporins (nephrotoxicity) Aminoglycosides (nephrotoxicity) PCN (higher risk of allergic interstitial nephritis)
65
T/F Combination of Furosemide and Mannitol is more effective in decreasing ICP then either drug alone.
True
66
T/F Effects of lasix on ICP is affected by intact BBB
FALSE not affected by alterations in BBB. Mannitol requires a intact BBB
67
What is more effective in decreasing ICP, mannitol or lasix?
mannitol
68
What effect is seen if mannitol is given to someone with a disruption in BBB?
rebound intracranial HTN
69
SE's of loop diuretics
1. fluid/electroly abnormalities (can cause arrhythmias and seizures) 2. Acute tolerance (braking phenomenon) 3. Deafness/Tinnitus (esp if used with ASA) 4. cross-sensitivity with sulfa allergies 5. Drug interactions
70
use caution if giving loop diuretic with what 2 other nephrotoxic drugs
NSAID's and ACE inhibitors (eps if already hypotensive)
71
What 5 electrolyte abnormalities can occur with loop diuretics?
``` Hypokalemia Hypochloremia Hyponatremia Hypomagnesemia Metabolic alkalosis ```
72
What is the "braking phenomenon"?
Once the electrolytes get depleted so far, the fluid will stop following the electrolytes (because it would than cause a reverse osmosis) urine is less concentrated because your peeing everything out, the fluid will start going back into the body because it is so electrolyte dependent
73
Examples of thiazide diuretics
``` Chlorothiazide (Diuril) Hydorchlorothiazide (Hydrodiuril) Indapamide (Lozol) Metolazone (Zaroxolyn) Chlorthalidone (Hygroton) ```
74
MOA of thiazide diuretics
Compete for the Na-Cl cotransporter in the distal tubule to inhibit reabsorption. Inhibit only urinary diluting capacity, not concentrating capacity.
75
Thiazide diuretics lead to what 3 things
1. Loss of Na and water 2. Hypokalemic metabolic alkalosis 3. Increased Ca reabsorption (Hypercalcemia)
76
What is the difference b/w loop diuretics an thiazide diuretics in regards to calcium?
Thiazides = hypercalcemia loops = hypocalcemia
77
What class of diuretics is 1st line treatment for HTN?
Thiazides loops have too many electrolyte abnormalities
78
2 specific SE's seen with thiazide diuretics
Hyperglycemia and hyperuricemia (gout)
79
Examples of potassium-sparing diuretics
K+ sparing: Amiloride (Midamor) Triamterene (Dyrenium) Aldosterone antagonist: Spironolactone (Aldactone) Eplerenone (Inspra)
80
MOA of K+ sparing potassium diuretics
Amiloride and Triamterene: | Inhibit Na reabsoprtion induced by aldosterone. Inhibit active counter transport of Na and K in the collecting duct
81
MOA of aldosterone antagonist potassium spring diuretics
Spironolactone and Eplerenone: C Competes for aldosterone receptor sites in the distal tubule to block Na reabsorption and K secretion can cause HYPERKALEMIA (esp with spironolactone)
82
Clinical uses of potassium sparing diuretics
Used for the treatment of refractory edematous states due to: CHF and Cirrhosis of the liver.
83
Main SE of potassium-sparing diuretics
Hyperkalemia (esp if used in combo with NSAID's, ACE inhibitors, and beta blockers) does not produce hyperglycemia and hyperuremias like thiazides
84
What form of calcium is preferred to treat hyperkalmia, gluconate or chloride?
Gluconate chloride is an option if central line is in place
85
What combo of meds is the quickest way to treat hyperkalmia?
Insulin and dextrose (works in 15-30mins, last 2-6hrs)
86
When treating hyperkalemia with insulin, when would you not need to dextrose along with it?
If BG >200/250
87
What is drawback to using kayexalate for hyperkalemia?
takes 4 to 6 hrs to reach the colon where it exerts its actions
88
Patiromer (Veltassa) and Sodium zirconium cyclosilicate (Lokelma) are newer agents to treat hyperkalemia. Which one is used for acute treatment?
Sodium zirconium cyclosilicate (Lokelma) onset = 1hr, but takes 48 to mainly see a benefit
89
What is a draw back to Patiromer (Veltassa)?
give separate from other meds by 3 hours (before and after)
90
What is a draw back to Sodium zirconium cyclosilicate (Lokelma)?
sustained action up to 12 months
91
What other med be given to stabilize the cardiac membrane besides calcium?
Magnesium caution using calcium in patients who are also on dig....can worsen dig toxicity
92
Calcium levels are dependent on ____
albumin if low albumin, ca+ will look falsely low
93
what is a drawback to using albuterol to treat hyperkamlemia?
absorbs systemically
94
Thiazide diuretics increase the likelihood of ___ toxicity
digoxin think increased Ca+
95
Thiazide diuretics can potentiate the effects of ___
non-depolarizing NMB's
96
What electrolyte also needs to be corrected along with potassium?
Magnesium
97
IV calcium lowers/increases the threshold potential of the myocardium
lowers
98
Should you give bicarb to treat hyperkalemia?
No. Unless they are severely acidotic
99
What can occur if you treat hyponatremia too quickly?
central pontine demylinosis | permanent
100
What meds are assoc. with hyponatremia?
``` Thiazides diuretics Loop diuretics Carbamazepine lithium SSRI's ```
101
Hyponatremia should be corrected no faster than ___ in the 1st 24 hours and _____ in 48 hours
6-12 mEq/L 18 mEq/L or less
102
Presentation of hyponatremia
1. Neurologic depression 2. Seizures 3. Respiratory depression 4. Coma
103
VAPTAN's (vasopressin receptor blockers) are indicated for ___ and ___ hyponatremia
euvolemic and hypervolemic
104
When would not want to give a VAPTAN to treat hyponatremia?
If hypovolemic, don’t have the fluid volume to remove....would do more harm remember vasopressin causes you to hold onto water.
105
Treatment for hypernatremia
D5
106
causes of hypercalcemia
Hyperparathyroidism, cancer, thiazides
107
causes of hypocalcemia
Hypoparathyroidism, renal disease, loop diuretics
108
If someone has low albumin, how do you calculate their corrected calcium level
Normal albumin level (4) - current albumin level (ex. 2.5) = 1.5 take 80% of that and add it to the Ca+ value that is measured on your BMP and that will give you the corrected calcium level
109
T/F If a patient has liver or renal disease, you want to measure their calcium level of the BMP
FALSE need to use ionized calcium levels (free form of calcium)
110
Treatment for hypercalcemia
Give fluids to try and dilute out, you can use diuretics (NOT a thiazide diuretic) you can use a loop diuretic can used meds to treat to osteoporosis (Zoledronic acid, Denosumab and Myocalcin ).....slow down osteoblasts and start holding more Ca+ in the bones Nasal myocalcin or IV Zoledronic acid à to store it away and get it out of the blood stream Corticosteroids if start to get symptomatic
111
Antihypertensive effects from Thiazides is from ______
*vasodilation* Emily harped on that is not from fluid movement. Initially there is decreased ECF and decreased CO, but the sustained antihypertensive effect is from vasodilation (takes weeks to months to develop)
112
T/F Thiazide diuretics inhibit only urinary diluting capacity, not concentrating capacity
True be careful bc its easy to think to affects the concentrating capacity bc its site of action is the DCT