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Gout, BPH, Stable IHD - Coggle Diagram
Gout
Pharmacologic Treatment
Oral Colchicine
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- Begin within first 24-h of an acute attack - response in 2/3 of pts
- If initiation is delayed, probability of success diminishes substaintially
- Start within 36 hours of attack onset
ADEs
- Dose-dependent GI AEs (nausea, vomiting, and diarrhea)
- Dose:
- 1.2 mg initially, followed by a single 0.6 mg dose 1h later
- 0.6 mg once or twice daily can be started 12 hours following the initial 1.2-mg dose
and continued until the acute attack resolves.
- CYP3A4 inhibitors increase colchicine concentration
- Dose adjustment in pt with impaired kidney and hepatic function
Interleukin-1 Inhibitors
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Rilonacept
Dose: 160 mg subQ loading dose followed by 80 mg subQ once weekly for 16 weeks OR 320 mg subQ loading dose followed by 160 mg subQ once weekly for 16 weeks
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Uricosurics
Probenecid
Dose: 250 mg BID for 1 week; may increase to 500 mg BID; maximum 2 g/day
- If serum uric acid levels are within normal limits and gout attacks have been absent for 6 months, daily dosage may be reduced by 500 mg every 6 months.
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Sulfinpyrazone
Dose: 200-400 mg daily in 2 divided doses, increase gradually over 1 week up to 400-800 mg/day to reach desired urate blood level
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Corticosteroids
Prednisone
Dose: 30 to 40 mg/day given once daily or in 2 divided doses until symptom improvement, followed by a 7- to 10-day taper (or 14- to 21-day taper in patients with multiple prior flares)
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- 1-2 joints are involved: oral or intra-articular injection
- Polyarticular: systemic
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Clinical Presenations
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Warmth, swelling, and inflammation of involved joints
elevated serum uric acid concentrations, leukocytosis
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Diagnosis
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for long-standing gout, radiographs can show asymmetric swelling within a joint or subcortical cysts without erosisons
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Etiology
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many conditions are associated with hyperuricemia and decreased kidney clearance/or an overproduction of uric acid
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Monitoring
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Presence of ADEs (eg, diarrhea [colchicine], agitation [corticosteroids], allopurinol hypersensitivity syndrome [allopurinol])
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Risk factors
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diabetes, alcohol abuse, advanced age increase likelihood of septic arthritis
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BPH
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Complications
avoid testosterone replacement regimens, alpha-adrenergic agonists, oral decogestiants. - also avoid antihistamines, phenothiazines, TCAs, anticholinergic drugs
acute, painful urinary retention --> acute renal failure
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bladder diverticula, bladder stones, chronic renal failure from long-standing bladder outlet obstruction
Pharmacologic Treatment
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PDE-5 Inhibitors
MOA: inhibits PDE-5 in prostate, urethra, bladder, and pelvic blood vessels to relax smooth muscle of prostate and bladder neck
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Tadalafil: 5mg PO QD; if CrCl is 30-50 mL, use 2.5mg; do not use in CrCl <30mL
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Monitor for: headache, myalgia, hearing loss, vision changes
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B3-agonist
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Monitor for: HTN, tachycardia, headache, and bowel habits
Etiology
- age ≥ 40yo: prostate experiences a second growth spurt and continues to grow for the rest of his life (when BPE develops_
- stimulatory effect of androgens: estrogen is believed to stimulate the growth of the stroll portion of the prestige gland. the ratio of testosterone to estrogen decreases as men age due to decreased testosterone production, contributing to the enlargement of the prostate
- increased alpha adrenergic tone in smooth muscle: a1A receptors are found in this area of the body,
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Clinical Presentations
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symptoms
obstructive sx
slow urinary stream, intermittency, hesitancy, straining to urinate, incomplete emptying, dribbling
Irritative sx
urgency, frequency, nocturia
signs: digital rectal exam revelas enlarged prostate (>20 g) with no nodules or indurations; prostate is soft, symmetric, and mobile
Goals of Therapy
Reduction of LUTS by: improvement of AUA Symptom Score by at least 3 points, an increase in peak urinary flow rate, and normalization of PVR to less than 50mL
Stable IHD
Risk Factor Modification
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Diet low in saturated and trans-fats, and more carbohydrates and unsaturated fatty acids
Pharmacologic Treatment
Oral Nitrates
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MOA: turns to nitroc oxide in the body, causing increase of cGMP in the vascular endothelium leading to reduction in cytoplasmic calcium and vasodilation
ADE: headache, flushing, nausea, orthostatic hypotension, syncope
Available as sublingual which provides relief in 2-5 minutes, transdermal is longer-acting (use in AM not PM), isosorbide mononitrate is BID
May cause tolerance, fix with nitrate-free interval for 12 to 14 hours a day
Antiplatelets
Aspirin
MOA: irreversibly blocks COX-1 activity for the life of the platelet, thereby inhibiting TXA2 production, reducing platelet activation and aggregation
dosing: 30 mg can provide effecacy, and 75-100mg provides little additional antiplateley activity
concomitant use of naproxen or ibuprofen can interfere with aspirin's anti platelet effect due to competing for the COX-1 active site.
Aspirin non-responsiveness is a risk, so be sure to monitor its effectiveness
Clopidogrel
significantly reduces the incidence of stroke, MI, or vascular death in patients with ASCVD compared to aspirin.
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pt responsiveness is highly variable. Any variation in CYP2C19 may lead to clopidogrent non-responsiveness.
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Beta Blockers
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MOA: competetively inhibits effects of catecholamines on B1-adrenoreceptors resulting in decreased chronotropy, inotropy, and BP------> decreased myocardial demand
ADE: bradycardia, hypotension, heart block, impaired glucose metabolism, and altered serum lipids, fatigue
Contraindications: pre-existing bradycardia, 2nd/3rd degree AV heart block, uncontrolled airway disease, decompensated HF
B1 selective: atenolol, metoprolol, bisoprolol, nebivolol
B1/B2 nonselective: propranolol, carvedilol, labetalol
CCBs
Adjunctve therapy, first line for vasospastic disease
Non-DHP
MOA: block calcium entry into the myocardium with little effect on vascular smooth muscle, reducing HR and contractility
ADE: bradycardia, hypotension, AV block, LV depression, avoid in HFrEF
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DHP
MOA: modulate calcium entry into the vascular smooth muscle cells, lowering arterial blood pressure with little effect on myocardium
ADE: reflex tachycardia (especially with short-acting agents), hypotension, headache, gingival hyperplasia, peripheral edema
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ACE Inhibitors
In ASCVD, ACEi stabilize coronary plaque, provide restoration or improvement in endothelial function, inhibit vascular smooth muscle cell growth, decrease macrophage migration, and possibly prevent oxidative stress
lowers risk of primary endpoints: CV death, MI, or stroke
Per ACC/AHA guidelines, class I recommendation to use ACEi in pat with SIHD who have HTN, DM, HErEF, CKD
ARBS
recommended if for same population as ACEi, if intolerant to ACEi
Diagnosis
Physical examination: tachycardia, diaphoresis, SOB, N/V, lightheadedness, increased BP, pulmonary crackles
ECG conducted during an exercise or pharmacologically-induced stress test. Use adenosine or dobutamine.
Coronary angiography is GOLD STANDARD but invasive, requires arterial access and contrast to view blood flow and pressure through the heart
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Monitoring
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surrogate endpoints to monitor efficacy of medication and stability of SIHD:
- BP goal attainment, use of high-intensity statin, A1c goal attainment, smoking cessation, and achieving healthy weight
- follow up required every 1-2 months until goals are achieved.
- follow up every 6-12 months therafter
Frequency and severity of chest discomfort, SL NTG use, exercise tolerance, presence/control of SIHD risk factors, presence/control of SIHD-related complications
Clinical Presenation
Exertional chest pain
precipitated by exertion such as walking, gardening, sexual activity, or activities of daily living (showering, cleaning the house, doing laundry)
Cardiac chest pain described as squeezing, heaviness, or tightness
Typical angina
(1) substernal chest discomfort with characteristic quality and duration
(2) provoked by exertion or emotional stress
(3) relieved by rest or NTG
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Non-cardiac chest pain
sharp, increases with inspiration and expiration, reproducible with palpation
Etiology
Obstructive artheroslerotic plaques in the coronary arteries cause decreased oxygen supply to the heart during periods of increased oxygen demand --->myocardial ischemia
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Risk factors: smoking, dyslipidemia, HTN, DM, and genetics
Goals of Therapy
Reducing the number of ischemic episodes, enabling pt to perform ADLs, and prevent mortality associated with the following complications: MI, HF, stroke