Diurectics Flashcards
1
Q
What do you need for heparin to work?
A
Antithrombin
2
Q
What do diuretics block?
A
These drugs block sodium & chloride reabsorption at different sites in the nephron
3
Q
What do diuretics increase?
A
Increases urinary sodium and water loss
4
Q
What are diuretics used to treat? (6)
A
Used in treatment of HTN, heart failure, edematous states, hypercalcemia, renal dysfunction, & glaucoma
5
Q
Review diuretics action at the nephron.
A
6
Q
Where do Carbonic Anhydrase Inhibitors bind?
A
drugs bind to carbonic anhydrase in the proximal renal tubule
7
Q
What do Carbonic Anhydrase Inhibitors result in?
A
results in decreased reabsorption of sodium, bicarbonate, & water (water & bicarbonate ion loss)
8
Q
What is the functional unit of the kidney?
A
Nephron
9
Q
What drugs are Carbonic Anhydrase Inhibitors?
A
acetazolamide
10
Q
What are the clinical uses for Carbonic Anhydrase Inhibitors?
A
acetazolamide
- decrease intraocular pressure in tx of glaucoma (decreases formation of aqueous humor
- tx of idiopathic intracranial HTN (inhibits formation of CSF)
- altitude sickness
11
Q
What is the amount of sodium reabsorbed?
A
- 2/3 at the proximal convoluted tubule
12
Q
What are side effects of Carbonic Anhydrase Inhibitors?
A
Acetazolamide
- metabolic acidosis (loss of bicarbonate ions)
13
Q
What is the action of Loop Diuretics?
A
Acts by impairing the activity of the Na-K-2Cl transport protein in the ascending loop of Henle
14
Q
How much of sodium is ascending reabsorbed at the loop of henle?
A
where 20% - 30% of Na is normally reabsorbed
15
Q
What are we inhibiting with Loop Diuretics?
A
Inhibit reabsorption of sodium, potassium, & chloride
16
Q
Loop diuretics are the most _____ diuretics
A
potent
17
Q
What are the drugs of loop diuretics?
A
furosemide, torsemide, bumetanide, ethacrynic acid, azosemide
18
Q
What is the formularies for Furosemide?
A
Oral or IV
19
Q
What is the onset of Furosemide?
A
Fast onset of action; produces diuresis within 5-10 minutes
20
Q
When is the peak effect of Furosemide?
A
peak effect 30 minutes
21
Q
What is the duration of Furosemide?
A
duration of action 2 – 6 hours
22
Q
What is the dose Furosemide in normal renal function?
A
With normal renal function, 40mg IV will produce maximal diuresis
23
Q
What is the dose Furosemide in renal dysfunction?
A
With chronic renal insufficiency, 160mg – 200mg slow IV produces maximal diuresis, continuous infusion can also be considered instead of repeat bolus doses
24
Q
What is the formularies of Bumetanide?
A
Can be given oral, IM, or IV
25
What is the potency of Bumetanide?
40 times more potent than furosemide
26
What is the clinical use of Loop Diuretics?
first-line therapy in patients w/fluid retention from heart failure; HTN; pulmonary edema; intracranial pressure
27
What is the most common side effect of Loop Diuretics?
hypokalemia
28
What are other side effects of Loop Diuretics?
* Hypovolemia
* Increase tissue concentrations of aminoglycosides enhancing nephrotoxicity
* Potentiate nondepolarizing NMBDs
29
Patients allergic to ______ may exhibit cross-sensitivity to furosemide
sulfonamide drugs
30
Plasma concentrations of ____ may be acutely increased w/IV furosemide
lithium
31
Define components of hypokalemia and loop diuretics.
increases likelihood of digoxin toxicity
32
Define components of hypovolemia and loop diuretics.
* should only be administered to patients w/normal or increased intravascular fluid volume
* resulting hypotension can exacerbate renal ischemic injury
33
What do Thiazide Diuretics produce?
These drugs produce diuresis & Na loss by inhibiting reabsorption of Na & chloride ions in distal convoluted tubule; block Na-chloride cotransporter/water
34
What is urinary excretion of Thiazide Diuretics?
Urinary excretion of Na, chloride, & K ions; also stimulate reabsorption of Ca in distal convoluted tubule
35
What are drugs of Thiazide Diuretics?
HCTZ, chlorthalidone, metolazone
36
What is the first line use of Thiazide Diuretics?
* First-line therapy for essential HTN by decreasing extracellular fluid volume & peripheral vasodilation
* tx of calcium-containing renal calculi (stimulate Ca reabsorption)
37
What is the components of Chlorthalidone?
longer acting, reduces risk of major cardiovascular events
38
What are side effects of Thiazide Diuretics?
* Hypokalemia, hypochloremia, metabolic alkalosis
* cardiac arrhythmias d/t hypokalemia or hypomagnesemia, hypercalcemia (esp in pts receiving Ca or Vit. D supp)
39
hypokalemia may predispose pts to \_\_\_\_\_\_
dig toxicity
40
What are side effects of Thiazide Diuretics?
* Potentiation of nondepolarizing NMBDs
* Potentiate lithium toxicity (promote lithium reabsorption)
* Hyperglycemia in diabetic pts
* Hyperlipidemia
41
Must consider _________ status in patients receiving thiazide diuretics & scheduled for surgery
fluid volume
42
Patients w/ ________ may demonstrate cross-reactivity to thiazide & loop diuretics
Patients w/sulfa allergy may demonstrate cross-reactivity to thiazide & loop diuretics
43
What is the relationship of thiazide diuretics and diabetic patients?
Hyperglycemia in diabetic pts (esp when used in combo w/beta blockers)
44
What do Osmotic Diuretics result in?
* Osmotic diuretics result in increased plasma & renal tubular fluid osmolality which results in osmotic diuresis
45
Where do Osmotic Diuretics act?
Act primarily at proximal renal tubules & loop of Henle
46
What is the osmotic drugs in clinical use?
mannitol
47
What is the cellular effects of Osmotic Diuretic: Mannitol?
Increases plasma osmolarity & draws fluid from intracellular to extracellular spaces
48
What does Osmotic Diuretic: Mannitol expand?
Acute expansion of intravascular fluid volume
49
What pt population is Osmotic Diuretic: Mannitol poorly tolerated?
may be poorly tolerated in patients w/borderline cardiac function
50
What are the clinical uses of Osmotic Diuretic: Mannitol?
* Acute management of elevated ICP
* tx of glaucoma
* used during cardiac & major vascular surgery for renal protection
51
What are the renal protection effects of mannitol?
* Renal protection effects:
* osmotic diuresis that forces casts & necrotic debris out of renal tubules
* vasodilation of renal vasculature by release of prostaglandins which improves renal blood flow/protect kidneys from acute failure following renal tubular necrosis
* oxygen-free radical scavenger property may prevent cellular injury
52
What are side effects of Osmotic Diuretic: Mannitol?
* May cause hypernatremia from water diuresis
* May cause pulmonary edema
* May cause hypovolemia, hypokalemia, plasma hyperosmolarity
53
increased intravascular volume with Osmotic Diuretic: Mannitol in pts w/\_\_\_\_\_\_\_\_\_\_
poor LV function
* increase risk of pulmonary edema
54
Where do Potassium-Sparing Diuretics act?
Act on the renal collecting ducts
55
NSAIDs block what?
Prostaglandins and this can be bad for the kidneys
56
What are the two groups off Potassium-Sparing Diuretics?
pteridine analogues & aldosterone receptor blockers
57
What are the effects of pteridine anaglogues Potassium-Sparing Diuretics?
prevent Na reabsorption
58
What are pteridine anaglogues Potassium-Sparing Diuretics drugs?
triamterene & amiloride
59
What is the MOA of Aldosterone antagonists Potassium-Sparing Diuretics?
prevent synthesis & activation of aldosterone-dependent Na-K-ATPase pump which decrease Na reabsorption without increased K excretion
60
What are the drugs of Aldosterone antagonists Potassium-Sparing Diuretics?
* spironolactone
* eplerenone
* used w/thiazide diuretic
61
What are the clinical uses of Potassium-Sparing Diuretics??
* tx of essential HTN (in combo w/thiazides) – prevents thiazide-induced hypokalemia & hypomagnesemia
* promotes diuresis in patients w/edema & fluid overload asso/w hyperaldosteronism such as liver cirrhosis, nephrotic syndrome, & heart failure
62
What is the effect of spironolactone with ACE-I?
spironolactone w/ ACE-I in tx of heart failure decreases CV morbidity & mortality
63
What are the side effects of Potassium-Sparing Diuretics?
hyperkalemia (especially when combined w/ACE-Is or ARBs or w/NSAIDS)
64
What do Dopamine Receptor Agonists result in?
These drugs result in natriuresis & increased renal blood flow via action on renal tubular dopamine-1 (D1) receptors
65
Where is the activation of Dopamine Receptor Agonists? What does it cause?
Activation of D1 receptors in proximal renal tubule & loop of Henle increases cyclic AMP production resulting in inhibition of the Na-H exchange & Na-K-ATPase pump
66
What do D1 receptors also mediate?
increased renal blood flow & increased GFR
67
What is an example of D receptor agonists?
**fenoldopam**
* fast-acting IV antihypertensive used in short-term treatment of severe HTN
* administration results in increased renal blood flow & decreased SVR
68
What is the metabolism divisions of lipoprootein?
exogenous & endogenous pathways
69
What are the exogenous pathway of Lipidoprotein metabolism?
Exogenous pathway: processing of dietary fats, cholesterol, & lipid-soluble vitamins
70
What are the endogenous pathway of Lipidoprotein metabolism?
hepatic cholesterol synthesis & its distribution to peripheral tissues
71
What lipoproteins increased risk of cardiovascular disease?
Increased plasma concentration of total & LDL cholesterol
72
What lipoproteins reduce the risk of atherosclerosis & CV events?
Higher HDL cholesterol levels
73
What is the characteristics of lipoproteins and CAD?
Lowering plasma concentrations of total & LDL cholesterol w/ drugs decreases risk of cardiac events in patients with and without CAD
74
Lipid-lowering agents are used to treat \_\_\_\_\_\_\_\_\_\_\_
hyperlipidemia
75
What is an example of Lipid-Lowering Agents?
Statins
76
What are statins MOA?
Statins are competitive inhibitors of HMG-CoA reductase, the enzyme that catalyzes cholesterol biosynthesis within the liver
77
What do Lipid-Lowering Agents: Statins cause?
* Cause decreased cholesterol synthesis and increased LDL uptake by liver resulting in decreased LDL concentration
* also cause increase in HDL
78
What is the metabolism of Lipid-Lowering Agents: statins?
Hepatic metabolism – CYP3A4
79
What drugs are Lipid-Lowering Agents: statins?
atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin
80
What do Lipid-Lowering Agents: Statins stabilize?
Stabilize atherosclerotic plaques
81
What is the properties of Lipid-Lowering Agents: Statins?
Antiinflammatory, antioxidant, & vasodilatory properties
82
What are the skeletal muscle effects of Statins?
* Statin-related myotoxicity (skeletal muscles)
* myalgia
* myositis
* CPK can range between mild and extreme elevations
* rhabdomyolysis
83
Severe statin muscle-related adverse events secondary to \_\_\_\_\_\_\_
drug interactions
84
What are the drug interactions that cause statin-Statin-related myotoxicity (skeletal muscles)?
Drug interactions with agents that are also metabolized by hepatic CYP450 system
85
What drugs are most frequently associated with Myopathy?
most frequent w/ atorvastatin, simvastatin, lovastatin
86
What are the CYP3A4 inhibitors that can effect statin levels?
CYP3A4 inhibitors (warfarin, protease inhibitors, macrolide antibiotics, azole antifungals) may increase concentration of statins & lead to myopathy
87
\_\_\_\_\_\_\_\_\_\_\_ does not increase incidence of statin-induced myopathy
Succinylcholine
88
What does hepatic dysgunctioon with statins manifest as?
manifests as plasma aminotransferase elevation
89
What are the two primary side effects of Statins?
* Statin-related myotoxicity (skeletal muscles)
* Hepatic dysfunction
