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Pharmacology > Renal > Flashcards

Renal Flashcards

1
Q

Degarelix

A

Hormonal treatment for prostate cancer

GnRH antagonist: Directly blocks the binding of GnRH to its receptor directly

Do not get initial androgen flare like you do with the GnRH agonists (leuprolide and goserelin)

This drug lacks the initial androgen flare that is seen with the agonists

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2
Q

Leuprolide

A

Decapeptide hormonal treatment for prostate cancer

GnRH normally released in pulsatile fashion, but the synthetic agonists are given so that they simulate a sustained release of GnRH, after 2-4 weeks of treatment, you down regulate the testosterone levels

GnRH agonist: MOA is to desensitize/downregulate the GnRH receptors on the pituitary

Modified to lengthen half-life and minimize break down

Used in combination with androgen receptor antagonists to avoid the androgen flare associated with these drugs

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3
Q

Goserelin

A

Decapeptide hormonal treatment for prostate cancer

GnRH normally released in pulsatile fashion, but the synthetic agonists are given so that they simulate a sustained release of GnRH, after 2-4 weeks of treatment, you down regulate the testosterone levels

GnRH agonist: MOA is to desensitize/downregulate the GnRH receptors on the pituitary

Modified to lengthen half-life and minimize break down

Used in combination with androgen receptor antagonists to avoid the androgen flare associated with these drugs

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4
Q

Flutamide, Nilutamide, Bicalutamide, Cyproterone, Spironolactone

A

Hormonal treatment of prostate cancer

Androgen receptor antagonists: Bind to steroid receptor intracellularly and prevent its translocation into the nucleus

Used in conjunction with GnRH agonists

Flutamide: has diarrhea nausea and vomiting for toxicity

Bicalutamide: less side effects and most used

Cyproterone: also has slight agonist activity. Have to watch out for this

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5
Q

Abiraterone

A

Irreversible inhibitor of 17-hydroxylase and C-17,20-lyase (CYP17) activity that blocks testosterone biosynthesis

Used with prednisone. It is better than ketoconazole

Use if patient isn’t responding well to leuprolide and androgen blocking agents or in conjunction with them

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6
Q

Mitoxanthrone

A

Used for hormone-refractory prostate cancer

Doxorubicin analog with less cardiotoxicity

Sometimes used with prednisone

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7
Q

Docetaxel and cabazitaxel

A

Used for hormone-refractory prostate cancer

Inhibits microtubule disassembly

Cabazitaxel used with prednisone, most widely used today

Toxicity is neutropenia and neurotoxicity

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8
Q

Sipuleucel-T (PROVENGE)

A

Autologous cellular immunotherapy for the treatment of asymptomatic or minimally symptomatic, metastatic, hormone refractory prostate cancer

Toxicity is infusion reactions

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9
Q

Bladder cancer chemotherapy

A

Intravesicular agents (given as a catheter in the bladder in conjunction with transurethral resection)- bacillus calmette-guerin, thiotepa, mitomycin, valrubicin, agents are very toxic if given systemically** **

Bacillus calmette-guerin: it is an attenuated organism, causes a granulomatous reaction that kills the cancer

Thiotepa: activated by CYP450 and is an alkylator and damages DNA, absorbed a little and causes myelosuppression

Mitomycin: Alkylator that is not absorbed at all

Valrubicin: Synthetic analog of doxirubicin for BCG resistant bladder cancer

MVAC for advanced cases (methotrexate, vinblastine, doxorubicin, cisplatin-more renal damage than carboplatin)

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10
Q

MVAC

A

Systemic agents for advanced cases of bladder cancer

Methotrexate, vinblastine, doxorubicin, cisplatin

Renal damage from cisplatin is reduced by hydration/saline diuresis, can use carboplatin in combo with paclitaxel in patients with renal dysfunction

Can also use gemcitabine with cisplatin or carboplatin

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11
Q

IL-2

A

Differs from native IL-2 in that it is not glycosylated, so it is more stable

Stimulates proliferation and activities of tumor-attacking lymphokine-activated killer cells and CTLs

Toxicities: inflammation/capillary leak, hypertension, arrythmias, peripheral edema, nausea, diarrhea, vomitting, and fever

Used to treat patients with cancers that are refractory to conventional treatment, such as renal cell carcinoma and melanoma

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12
Q

Sunitinib

A

Renal cell carcinoma treatment

Inhibitor of receptor tyrosine kinases (VEGF-R2, PDGF-R, c-KIT, and other tyrosine kinases)

Reduces proliferation and angiogenesis

Resistance is through receptor tyrosine kinase mutation

Toxicity: bleeding, hypertension, proteinuria, thromboembolism, intestinal perforation, and myelosuppression

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13
Q

Sorafenib

A

Renal cell carcinoma treatment

Oral inhibitor of VEGF-R1,2,3 tyrosine kinases within tumor cells to reduce proliferation and angiogenesis

Toxicity: bleeding, hypertension, proteinuria, thromboembolism, intestinal perforation, and myelosuppression

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14
Q

Bevacizumab

A

Renal cell carcinoma treatment

Humanized mAb against VEGF

Inhibits interaction with VEGF receptors which inhibits angiogenesis in tumors

Often given with interferon-alpha

Toxicity: CNS hemorrhage, severe hypertension, congestive heart failure, gastric perforation, and proteinuria

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15
Q

Pazopanib

A

Renal cell carcinoma treatment

Inhibits tyrosine kinase activity of VEGF-R2

Toxicity: bleeding, hypertension, proteinuria, thromboembolism, intestinal perforation, and myelosuppression

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16
Q

Temsirolimus, Everolimus, Sirolimus

A

Rapamycins

mTOR forms the mTORC1 complex with the FK506-binding protein family, FKBP12. mTORC1 phosphorylates S6 kinase and relieves inhibitory effect of 4EBP on initiation factor elf-4E thereby increasing protein synthesis and metabolism

Antitumor actions result from binding FKBP12 and inhibition of mTORC1

Temsirolimus is metabolized to sirolimus

Inhibit cell-cycle progression and angiogenesis, promote apoptosis

Resistance: mTORC2 can take over for mTORC1 complex

Toxicity is mild: rash, small chance of leukopenia, inhibit CYP450s

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17
Q

Treatment of UTI’s

A

Main outpatient pathogens are E. coli, then Klebsiella and Proteus, then Staph. saprophyticus

Pseudomonas is rare in outpatient but common in hospital setting

Treat cystitis with TMP-SMX, ciprofloxacin/levofloxacin (resistance is increasing to fluoroquinolones), cefpodoxime proxetil

Treat pyelonephritis with fluoroquinolones (high doses to overcome resistance), treat susceptible strains with TMP-SMX

Treat suspected bacteremia with IV antibiotics (third generation cephaolsporins, ciprofloxacin, gentamycin, aztreonam)

Extremely sick treat with IV cefepime, ciprofloxacin, carbepenem

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18
Q

Mineralocorticoids

A

Aldosterone is the naturally occurring mineralocorticoid (because it is protected from 11B-HSD2 deactivation)

Increase Na+ reabsorption in distal nephron/collecting duct (mainly through prinicipal cells)

Leads to increase H20 reabsorption, K+ secretion (worry about hypokalemia if we over-do it), H+ secretion, and bicarb generation (can create alkalosis if we secrete too much H+ and generate too much bicarb)

Side effects: HTN, edema via sodium and water retention

Glucocorticoids are more abundant than Mineralocorticoids and bind GR and MR however: 11B-HSD2 oxidizes -OH (Carbon11) to =O (C11) that cannot bind to the mineralocorticoid receptor*** - We can flood this system and the glucocorticoids can eventually bind to the MR and lead to aldosterone-like effects

Component in licorice that inhibits 11B-HSD2 and allows these glucocorticoids to remain capable of binding MR

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19
Q

Fludrocortisone

A

Binds very well to mineralocorticoid receptor***

Binds POTENTLY to GR and MR

Both a glucocorticoid and a mineralcorticoid

NEVER use as an anti-inflammatory as it will cause severe edema, water-retention, HTN

Use when Pts cannot make aldosterone themselves

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20
Q

Triamcinolone

A

A glucocorticoid that has ABSOLUTELY NO activity at the mineralocorticoid receptor (thus no aldosterone-like activity)

Useful treatment if you need to switch a patient to an anti-inflammatory without water retention/due to their HTN with the other glucocorticoids (such as prednisone, which has a slight affinity for the MR)

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21
Q

Mineralocorticoid Receptor Antagonists

A

Aldosterone antagonists***

Spironolactone (gynocomastia, impotence for this one too) - Eplerenone

Can cause hyperkalemia and metabolic acidosis as they are no longer allowing K+ secretion, H+ secretion, or HCO3- creation

Can treat aldosterone or cortisol excess

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22
Q

Calcitriol

A

People who are in renal failure do not make active vitamin D (Calcitriol, AKA 1,25-dihydroxy-cholecalciferol)

Hyperphosphatemic and Hypocalcemic- PTH is released because of hypocalcemia which leads to bone resorption, calcium reabsorption in kidney, and phosphate excretion in kidney

However, if the kidney is damaged we don’t see this but we end up seeing secondary hyperparathyroidism - Will see renal osteodystrophy with this excessive resorption***

Calcitriol is already active and will help Ca2+ absorption in the gut, increase Ca2+ in the blood, and STOP PTH production/bone resorption

Don’t give ergocalciferol or other calcitriol analogs lacking the 1-hydroxylation

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23
Q

DHT - Dihydrotachysterol

A

Synthetic Vitamin D

No 1-OH needed for activation so no renal activation needed to be active Vitamin D

Could also give 1-apha-hydroxycalciferol, but this one needs liver function to be activated

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24
Q

Paricalcitol and 22-oxacalcitriol

A

Calcitriol analog

Reduces PTH without hypercalcemia and used in chronic renal failure

22-oxacalcitriol is basically the same thing

These drugs are used AFTER you get the calcium, phosphate, etc. back in check but PTH is still elevated for whatever fucking reason

25
Q

Sevelamer

A

Phosphate binding polymer for elimination in the gut

Eliminates phosphate to prevent phosphate binding up all the calcium and creating bone damage in renal failure

26
Q

Cinacalcet

A

“Calcimimetic”; inhibits PTH be making CaSR more sensitive

Treatment of secondary hyperparathyroidism due to chronic renal failure

Another drug used AFTER levels of calcium and phosphate have been corrected

27
Q

Colchicine

A

ACUTE Gout Drug (nothing to do with Uric Acid production or reabsorption)

Get inflammation under control first so you don’t spread it around (NSAIDs first!!!)

NSAIDs: Naproxen, Indomethacin, Sulindac (the big-Gunns)

Interferes with mitotic spindle function - Inhibits migration and phagocytic actions of granulocytes - Inhibits neutrophil elaboration of inflammatory glycoprotein - Side effects: Nausea, vomiting, affects rapidly proliferating epithelial cells in GI tract

28
Q

Acute Gout Drugs

A

FIRST LINE = NSAIDs (Naproxen, Indomethacin, Sulindac)

AFTER NSAIDs don’t work = Colchicine

29
Q

Chronic Gout Drugs

A

Keeping uric acid levels low to prevent further gout attacks

Allopurinol: Xanthine oxidase inhibitor (metabolite alloxanthine) to decrease uric acid synthesis (can be used with impaired renal function). Inhibits metabolism of some purine chemotherapeutics, like azothioprine or 6-MP, so you have to watch dosages.

Febuxostat: Nonpurine xanthine oxidase inhibitor (liver function abnormalities, diarrhea, nausea but less drug interactions)

Probenecid: Uricosuric agent, inhibits uric acid renal tubular reabsorption (originally developed to inhibit renal tubular secretion of penicillin and multiple drug interactions) DO NOT GIVE IF PATIENT IS PRONE TO DEVELOPING URATE STONES AS YOU ARE INCREASING CONCENTRATION OF URATE IN THE TUBULES***

Rasburicase: Recombinant urate oxidase that oxidizes uric acid into soluble and inactive metabolite allantoin; used to manage plasma uric acid levels in PEDIATRIC patients receiving chemotherapy

30
Q

Immunosuppressive agents

A

Used to reduce immune system for kidney transplants

Cyclosporine/tacrolimus: targeting specific pathway for T-cells. Inhibits calcineurin phosphatase activity, which prevents activation of NFAT (via dephosphorylation) acting as transcription factor of IL-2 gene, and thus prevents chemokine production. They are AWESOME because we preserve neutrophil production, platelet production, blood cell production, B-cell production, etc. Cyclosporine can have renal toxic effects, tacrolimus can have a hyperglycemic effect (watch for this in diabetics).

Sirolimus: Doesn’t decrease IL-2 production, but leads to less response to IL-2 by T-cells (lessens mTOR pathway). Has hyperlipidemia as an adverse effect

Everolimus: same as sirolimus, but with a shorter half life (faster steady state)

Azothioprine, methotrexate, cyclophosphamide, and mycophenalate mofetil are all big guns brought in to non-specifically depress the immune system in acute rejection via decreased DNA synthesis. They also suppress the bone marrow

31
Q

Muromonab CD3

A

Used to get someone through an acute reaction to kidney transplant

Expensive and IV infusion

Antibody blocks binding of APC to T-cell, which blocks T-cell function and decreases functional T-cell number because new populations arise that don’t have CD3 to prevent inhibition… but they suck because they don’t have CD3… jokes on them

Initial stimulation of cytokine release syndrome (feels like the worst case of the flu they have ever had because of all the IL-2). This can be avoided by pretreatment with prednisone

32
Q

Daclizumab, Basiliximab

A

Used to prevent acute reactions to kidney transplants

Monoclonal antibodies against IL-2 receptor

Blocks IL-2 mediated T-cell activation

33
Q

Adrenergics in the kidney

A

B2: Relaxes bladder smooth muscle

A1: Contracts bladder at base, urethral sphincter, prostate

B1: Increases renin release

Side note: M3 agonists stimulate voiding

34
Q

Cholinergic activating agents

A

Bethanacol, neostigmine

Stimulates bladder emptying

Treatment of urinary retention problems POST-SURGERY

ONLY use when NO OBSTRUCTION present… or very painful

35
Q

Anti-cholinergics

A

Tolterodine, oxybutynin, darifenacin, solifenacin

Relaxes the bladder to counteract bladder spasms because of infection or post-surgery

Used to treat leaking urine here/urinary incontinence due to a hyperactive bladder

36
Q

Alpha-1-agonists

A

Ephedrine, pseudoephedrine

Treatment of urinary incontinence

Promote retention/sphincter contraction

Watch for hypertension, but try to keep doses low

37
Q

Alpha-1-Antagonists

A

Prazosin, terazosin, doxazosin, tamsulosin

Treatment of symptoms of urinary obstruction (BPH), so typically seen/used in older men

Tamsulosin (Flomax) has greater potency in inhibiting contraction in prostate smooth muscle vs vascular smooth muscle. This means you more selectively hit prostate muscle rather than the vasculature muscle that prevents orthostatic hypotension upon sudden-standing

38
Q

Carbonic Anhydrase Inhibitors (Diuretics)

A

Acetazolamide, Methazolamide, Dichlorphenamide

Act in proximal tubule

Prevents carbonic anhydrase (lumen) from combining H+ and HCO- from combining and creating CO2 and H2O that will freely travel into the cell and be reformed via CA (cytosolic) into H+ and HCO3- internally. This prevents H+ formation that will be exchanged for Na+ across the apical membrane (NHE3 exchanger). Na+ isn’t reabsorbed and thus water stays in the lumen

**THESE ARE WEAK AS SHIT. **You can reabsorb Na+ elsewhere in greater quantities and thus you don’t really lose much Na+ or H2O. These also trigger tubuloglomerular feedback via the macula densa (sensing a high load of NaCl). This triggers a constrictor signal to drop GFR and thus are self-limited diuretics

Increased bicarb secretion/urinary alkalinization. This is a good way to treat renal stones that form in acidic conditions, get rid of an acidic drug, treat metabolic alkalosis, etc. Can also be used for glaucoma.

Toxicity: metabolic acidosis, renal stone formation (from alkaline conditions), hypokalemia, and allergic sulfur reactions

39
Q

Osmotic Agents (Diuretics)

A

Mannitol, Isorbide, Urea

Limit Na+ and H2O reabsorption, expand ECF leading to decrease in renin release and increase in RBF

Increase urinary excretion of nearly all electrolytes including Na+, K+, Ca2+, Mg2+, Cl-, Phosphate

Treatment of acute renal failure (runner in our cases), dialysis disequilibrium syndrome, and reduction of intracranial and intraocular pressure

Trying to increase blood flow and increase pressure to unblock whatever is blocked

Don’t want to dose more than once if it doesn’t work as it will suck all the water out of the brain and will create loads of pressure

Side-effects: Increased ECF that will kill patients with CHF or pulmonary edema, as well as electrolyte loss

40
Q

Loop diuretics (Diuretics)

A

Furosemide, Bumetanide, Ethacrynic acid, Torsemide

Act on Loop of Henle in the TAL

Inhibits the NKCC2 from moving Na+, 2Cl-, and K+ into the cell. Potassium typically back-leaks to make the lumen positively charged. This positive lumen charge (+70mV) is higher than the interstitial positive charge (+60mV) which drives positive ions paracellularly into the interstitial space. SO, if you block this transporter you block Na+, Cl-, K+, Ca2+, and Mg2+ reabsorption. This also decreases osmolar gradient in medulla, decreasing concentrated urine production

Loop diuretics block the SENSING MECHANISM that prevent the macula densa from responding to the increased solute loads. In fact, it actually doesn’t sense anything so it increases blood flow and GFR even more, which leads to even more loss of fluids and electrolytes.

Also in the TAL you’re moving solutes without water movement (gap junctions are impermeable to H2O) and therefore you typically set up the concentrated interstitial gradient of the medulla. Without this gradient, you cannot reabsorb water later on like you typically would

STRONG MUTHAFUCKAS - Use in pulmonary edema, CHF, acute renal failure, and HTN (use thiazides first)

Side Effects: Electrolyte loss, ototoxicity, metabolic alkalosis, sulfer hypersensitivity (except Ethacrynic acid)

41
Q

Thiazide diuretics (Diuretics)

A

Chlorothiazide, Hydrocholothiazide, Chlorthalidone, Indapamide, Metolazone, Quinethazone, etc.

Past the macula densa, so we don’t worry about if it will provide the macula densa with a greater solute load to affect GFR through TGM feedback.

Inhibits NCC in the DCT and thus also blocks H2O reabsorption

Can cause hypokalemia like all the others (save for potassium sparing diuretics) because you increase sodium presentation to the principal cells which excrete potassium after uptaking sodium

DECREASE Ca2+ excretion (increase Ca2+ absorption), so prevents calcium stones in those who are prone to them

Treats HTN, edema, calcium nephrolithiasis, hypocalcemia

Side effects: hyponatremia, hypokalemia, metabolic acidosis, hypercalcemia, allergic sulfur reaction

42
Q

Potassium Sparing Diuretics

A

Amiloride and Triamterene (Na+ channel inhibitors)

Spironolactone, Eplerenone (Aldosterone receptor inhibitors)

Increase urinary excretion of Na+, decrease urinary excretion of K+ and H+ (because you aren’t bringing in Na+ to push out K+ and H+). Not extremely strong diuretics but are used in combination with thiazides/loops to prevent the hypokalemia.

Treat HTN and edema (spironolactone and eplerenone can treat hyperaldosterone)

Side effects: Hyperkalemia, metabolic acidosis, gynecomastia, impotence (spironolactone)

43
Q

Nesiritide

A

Brain natriuretic peptide

Binds to specific receptors all along the nephron (mainly MCD) via c-GMP signaling, which inhibits Na+ reabsorption in the IMCD and thus increase Na+ excretion Also inhibits renin-AngII-aldosterone pathway

Peptide so given IV

New drug used to acutely decompensated CHF

44
Q

Imipenem

A

Carbapenem that is resistant to chromosomal beta-lactamases

Always administered with cilastatin (inhibitor of dehydropeptidase in proximal tubule brush border that breaks down imipenem)

Toxicity: Hypersensitivity, causes nausea, vomitting, and seizures in high doses. Only give when you have an extremly ill patient that needs IV antibiotics

45
Q

Aztreonam

A

Resistant to plasmid extended spectrum beta-lactamases (not as resistant as imipenem)

Effective against enterobacteriaceae and pseudomonas aeruginosa (like imipenem) in pyelonephritis

Has no pencillin hypersensitivity reaction!

Toxicity: well-tolerated, lacks hypersensitivity

46
Q

Aminoglycosides

A

Gentamicin, neomycin, streptomycin, tobramycin, amikacin (most resistant to resistance development), netilmicin

Great for Gram Negatives!

Used to treat urinary catheter associated UTI usually caused by Enterobacteriaceae (gram negative bacilli)

Treat with aminoglycoside plus fluoroquinolone, third-generation cephalosporin, or piperacillin/tazobactam

MOA- binds to 30S ribosomal subunit–> blocks the initiation of protein synthesis, blocks translation and elicits premature terminatin of translation with detachment of ribosomal complex, and causes incorporation of incorrect amino acids resulting in protduction of abnormal/nonfuctional proteins

Renal toxicity- (all reversible to a point) accumulation and retention of aminoglycoside in proximal tubular cells, impaired renal concentration ability, proteinuria, and appearance of hyaline and granular casts, GFR is reduced after several days, reduced sensitivity of collecting-duct epithelium to endogenous antidiuretic hormone, severe acute tubular necrosis is rare but may occur, most commonly there is a mild rise in plasma creatinine, reduced exretion of drug (itself/renal damage) predisposes to ototoxicity which is irreversible

Other toxicities- ototoxicity (irreversible damage to vestibular and cochlear sensory cells, irreversible), produces neuromuscular blockade by inhibiting ACh release via competition with Ca2+ (important for anesthesia administration, as you can lower dosages)

47
Q

Tetracyclines and macrolides

A

UTI’s in women with risk factors for sexually transmitted diseases, give doxycycline twice daily for 7 days or azithromycin 1 gram single dose

Tetracycline- can produce renal tubnular acidosis, azotemia, and Fanconi’s syndrome (expired drugs), excreted as nephrotoxic metabolites by kidney except for doxycycline (feces)

Tigecycline- it is a glycycycline, not absorbed orally so it is given IM, can overcome tetracycline resistance (can avoid efflux pump and ribosomal protection proteins)

Macrolides- azithromycin, clarithromycin, erythromycin

48
Q

Trimethoprim-sulfamethoxazole

A

Sulfonamides inhibit dihydropteroate synthase (folate synthesis in bacteria, not mammals)

Trimethoprim inhibits bacterial dihydrofolate reductase

Mammals cannot convert aminobenzoic acid to dihydrofolic acid which makes this drug bacteria specific, very affective drug

Adverse affects due to the sulfonamide group in hypersensitive patients, causes fever and rash, hives, nausea, vomitting

Can be given prophylactically in patients prone to UTIs

Primary treatment for UTIs

49
Q

Quinolones and Fluoroquinolones

A

DNA gyrase inhibitors in gram-negative bacteria

Topoisomerase IV inhibitors in gram-positive bacteria

Quinolones- Nalidixic acid and cinoxacin have limited usefulness bc of narrow antibacterial spectrum (gram-negative only). They also required high doses, as they induce mutations in DNA gyrase.

Fluoroquinolones- ciprofloxacin, ofloxacin, levofloxacin, norfloxacin. Widely used, but now have begun to show increased resistance.

50
Q

Methenamine

A

Not used as much anymore

Prophylaxis of chronic UTI

Metabolized to formaldehyde spontaneously at low urine pH but not in plasma at pH 7.4, formaldehyde is what kills the bacteria

51
Q

Nitrofurantion

A

Widely used for lower UTI uncomplicated cystitis

Effective against gram-positive enterococci and gram negative E.coli, but proteus, pseudomonas, enterobacter, and klebsiella are resistant

Not activated by low pH (but low pH does make it more effective), activated by bacteria only, bc of this it can be given prophyllactically, if patient does not have infection the drug will be excreted unchanged/unactivated in the urine

Can be given orally and prophyllactically to patients prone to UTIs with sulfonaide allergy, as it will be eliminated unchanged in these scenarios

40% of drug is excreted into urine unchanged where bacteria reduce nitrofurantoin to form highly reactive intermediates that damage DNA

52
Q

Praziquantel

A

First-choice against all strains of Schistosoma

Causes muscular contraction and paralysis and at higher drug levels can cause tegumental damage by influx of Ca+

Toxicity is abdominal distress mostly from the drug but also from the killing of the parasites. This can be dose limiting

53
Q

Metrifonate

A

Second line antischistosomal

Only effective against Schistosoma haematobium

Must be activated to dichlorovos which inhibits AChE in the worm

54
Q

Oxamniquine

A

Second line antischistosomal

Not effective against S. haematobium or S. japonicum, only used for S.mansoni

An enzyme converts oxamniquine into an ester, the ester spontaneously dissociates and the resulting electrophilic reactant alkylates schistosome DNA

55
Q

Finasteride

A

5-alpha-hydroxylase inhibitor used to treat benign prostate hyperplasia

This blocks synthesis of dihydrotestosterone, and is therefore not as effective at treating prostate cancer as it does not affect synthesis of testosterone

56
Q

Treatment of Prostatitis

A

Same bacteria that cause UTIs cause Prostatitis

Usually gram-negative enteric organisms

Causes a tender prostate (which you can jam your finger on to elciit screaming)

Treat acute with TMP-SMX, chronic with long bouts of TMP-SMX or ciprofloxacin

Difficult to get drugs into the prostate. TMP-SMX and ciprofloxacin are both lipid soluble so can actually reach the prostate

57
Q

Prostaglandin Effects on the Kidney

A

PGE2 and PGI2 are main players (made by COX-2, so COX-2 selective inhibitors have same side effects), they:

1) Increase renal blood flow by dilating the afferent arteriole
2) Decrease/antagonize ADH induced blood flow
3) Increase chloride reabsorption in loop of Henle
4) Increase renin release

NSAIDs block these effects, important to keep in mind for patients with compromised renal function

58
Q

Aspirin Side Effects

A

At high range of therapeutic index, can initially lead to respiratory alkalosis by direct stimulation of respiratory centers in the CNS (more so in adults than children)

At toxic levels, can then lead to metabolic acidosis by uncoupling oxidative phosphorylation and by direct presence of an acid in the plasma

At highest toxic levels, you can get a combined respiratory and metabolic acidosis as respiratory centers are depressed

Pharmacology (12 decks)

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