Renal and Reproduction Pharm Flashcards
1
Q
What organism causes UTI
A
- E. Coli (gram - rod)
2
Q
How do we treat UTI?
A
- Many different antibiotics
- Nitrofurantoin
- Trimethoprim/Sulfamethoxazole
3
Q
Inhibitors of Metabolism
A
- Interfere with folate synthesis and reduction
- Sulfamethoxazole inhibits folate synthesis
- Trimethoprim inhibits folate reduction
4
Q
How does Sulfamethoxazol/Trimethoprim work
A
- Sulfamethoxazol competes with PABA and blocks synthesis of dihydrofolic acid
- Trimethoprim prevents synthesis of tetrahydrofolic acid
- Example of synergistic effect
- Gram + and Gram - activity (UTIs, Pneumocystis carinii, bronchitis, otitis media, MRSA)
5
Q
Sulfamethoxazol/Trimethoprim
A
- Sulfonamide Antibiotic
- Classification: metabolism inhibitor, inhibits folic acid, bacteriostatic broad spectrum
- Dosing: in terms of TMP component (single strength vs double strength tab)
- Drug interactions: Warfarin (increases levels of warfarin = bleeding)
- AE: hyperkalemia, thrombocytopenia, neutropenia, megaloblastic anemia, Kernicterus = bilirubin issue (avoid in pregnant women near term, nursing moms, peds over 2 months), renal dysfunction, hypersensitivity reaction (Stevens-Johnson syndrome) = vomiting, hives, dehydration
6
Q
How does Nitrofurantoin work
A
- Generally considered bacteriostatic but bactericidal at high concentrations
- Only therapeutic concentrations in the urine
- MOA: damages bacterial cell DNA (reduced by bacterial flavoproteins to reactive intermediates)
7
Q
Nitrofurantoin
A
- Nitrofuran antibiotics
- Spectrum of activity: some g+ and some g-
- Only used for UTI (used a lot in pregnancy for UTI bc safe)
- 3 salt forms
- Avoid in pts with low creatinine clearance = less than 40 (kidney function) because has to get to the urine to work
- AE: can turn urine brown; GI disturbances (anorexia, n/v/d); pulmonary rxns (acute and subacute), agranulocytosis, peripheral neuropathy, hepatotoxicity
8
Q
Alpha blockers
A
- Alpha 1 adrenergic receptors Located in vasculature
- Stimulate alpha 1 = release catecholamines and have vasoconstriction
- To vasodilate, block Alpha 1
9
Q
Calcium channel blockers
A
- Calcium channels in smooth muscle
- Stimulate calcium channels = constrict
- To dilate Ca++ channels, block channels
- 2 types: dihydropyridines and non-dihydropyridines
- Dihydropyridines = for HTN
- Non-dihydropyridines = focus on calcium channels in heart, used to slow heart rate (a fib)
10
Q
Beta blockers
A
- B1 receptors in heart
- Stimulate B1 = increased HR and contractility
- B2 receptors in lungs and smooth muscle
- Stimulate B2 = dilate, open up bronchioles
- Block B1 = decrease HR and contractility (Metoprolol)
- Block B2 = constrict bronchioles
11
Q
Other drugs for HTN
A
- Vasodilate vascular smooth muscle (Hydralazine, Amlodipine)
- Block central alpha 2 (brainstem)
- Drugs on kidneys and RAAS
- Combo A and B blocker: labetalol
12
Q
Metoprolol
A
Beta-adrenergic blockers (specific to B1)
- Actions: decreased CO, suppress reflex tachycardia caused by vasodilators, reduces release of renin, long term use reduces PVR
- AE: bradycardia, heart block, bronchoconstriction (trouble breathing)
13
Q
Hydralazine
A
- DIrect acting vasodilator
- Causes arterial vasodilation
- AE: reflex tachycardia
- Can give PO and IV
- Hydralazine can cause a systemic lupus erythematosus-like reaction (rash, blotchy-looking)
14
Q
Amlodipine (Dihydropyridines)
A
- Calcium channel blocker
- causes vasodilation
- Can cause reflexive tachycardia
- AE: peripheral edema
- Safe, most people respond well
15
Q
RAAS Drug targets
A
- ACE inhibitors
- Angiotensin Receptor blockers
