Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
23 Cards in this Set
- Front
- Back
|
What is ambulatory blood pressure monitoring? |
Uses a device that is continuously worn, that can be programmed to measure BP q15-20 minutes during the day, q30-60 minutes at night. Compensates for white coat HTN, reveals resistant HTN, masked HTN and suspected episodic HTN - Good BP is < 140/90 during day, nightitime < 125/75, with 24 hour average being 135/85 - Dipping is normal (15% decrease compared to daytime values) -failure to nighttime dip is associated w/ increasd LVH and increased risk of cardiovascular death |
|
|
When should HTN be diagnosed? |
Should only be made in the office setting when threshold BP has been documented on at least 3 visits over 1 week or longer - Should use ambulatory monitoring to avoid over diagnosis |
|
|
What medications elevate BP |
Black licorice, alcohol, NSAIDs, sympathomimetics, appetite suppressants, decongestants, amphetamines SSRIs/SNRIs Erythrocyte stimuattion agents HAART VEGF antagonists Steroids OCPs COcoaine |
|
|
When should plasma renin/aldo level be measured in newly diagnosed HTN? |
Recommended for patients with hypokalemia and HTN, and patients w/ moderate and severe HTN or resistant HTN |
|
|
What is the JNC 8 definition of HTN? |
140/90 In elderly > 60 goal 150> 90 In CKD goal treat 140/90; The kidney disease - impoving global outcomes suggests a lower BP goal of < 130/80 in apteints w/ proteinuria > 500mg/g Diabetes |
|
|
What are the genetic etiologies to HTN? |
20-30% of patients have genetic reasin Best described mtuations are those directly affecting sodium channels in the distal renal tubule and collecting duct There are also mtuations that lead to excessive mineralocorticoid effect |
|
|
What are the preferred anti-HTN agents in blacks and nonblacks |
Blacks: thiazide or CCB; in general black patients have less BP reduction with ACE, blacks initially treated with ACE rather than CCB have a 50% or higher rate of stroke For all other patients, including those with diabetes, treat with thiazide, CCB, ACE or ARB as first line For patients with CKD --> ACE/ARB |
|
|
What anti-HTN medicaitons are most useful for preventing HF? |
THiazides have a slight advantage over CCB/ACE with ACEs better than CCB - but differences were not found by JNC 8 to be compeeling |
|
|
How do thiazide medications work? |
They inhibit the Na+ Cl- cotransporter int he distal renal tubule THey lose potency when patients hve stage III or stage IV CKD |
|
|
When should potassium sparing meds be used? |
Use inresistant HTN or aldosterone mediated HTN - Use with caution in patients already on ACEs/ARBs |
|
|
WHat is the interaction ebtween statins and calcium channel blockers? |
Simva at 10 and above and lova at 20 and above is contraindicated with verapamil or dilt Simva at 20 and above is contraindicated with amlodipine due to increased risk of myopathy |
|
|
What is the general rule of thumb regarding doses of meds? |
50% of the max dose achieves 75% of the overall effect Sometimes two different medications in combination can be used to greater effect, on minimal dose |
|
|
What is resistant HTN? |
Uncontroleld HTN despite 3 agents of different classes, one of which is a diuretic At this point, should identify an underlying cause of HTN; CKD, coarctation of teha orta, cushing's, drug induced, pheno, renovascular , hyperaldo Thyroid disease Primary hyperPTH OSA |
|
|
How should patients with CKD be treated? |
First line: ACE/ARB Thiazide --> with decreasing GFR, the effectiveness decreases Loop diuretics should be used Also recommend that one medication be placed at night to restore normal fall in BP at night |
|
|
What are the clinical manifestations of renovascular disease? How is it managed? |
Recurrent episodes of flash pulmoanry edema A marked increase in BP, esp with use of ACE/ARB There is no evidence that angioplasty or stenting improves blood flow to the stenotic kidney, --> medical management |
|
|
What is the differential of primary hyperaldo? |
Liddle's syndrome, syndrome of apparent mineralocorticoid excess, and familial hyperalodsteronoism - These are mutations of sodium channels in the distal nephron and other disorders of adrenal steroid synthesis - Renin and aldo levels are suppressed |
|
|
How should diabetics HTN be treated? |
140/90, the ACCORD trial showed no signifciant cardiovascular benefit w/ increased risk of SEs in patients treated to 120/80 KDIGO suggests BP < 130/80 in patiets with proteinuria > 500mg/g |
|
|
What autoimmune diseases cause chronic tubulointerstitial disease?? |
1. Sjogren's syndrome: plasmacytic and lymphocytic infiltration of the parotid, salivary and lacrimal glands; --> biopsy shows granuloma formation 2. Sarcoidosis - presets at diagnosis of sarcoid - presence of noncaseating granuloms and interstitial nephritis. Other causes includes hypercalcemia, nephrocalcionosis, kidney stones, RP fibrosis and direct ureteral invovlement 3. IgG4 related disease: infiltration of lymphoplasmacytic infiltrates of IgG4 positive plasma cells with resultant fibrosis --> can result in membranous and membranoproliferative glomerulonephritis 4.. SLE - poor prognostic sign - concurrent with nephritis |
|
|
What malignancies can cause tubulointerstitial disease? |
Kidney infiltration by lymphoma and leukemia, MM can cause proteinuria, pyuria and enlarged kidneys |
|
|
What medications can cause tubulointerstitial disease? |
Calcineurin inhibitors: cyclosporine and tac: can cause reversible AKI and a usually irreversible chronic tubulointerstitial disease - RFs are duration of exposure and cumulative dose - Can result in hyperkalemia, hypophosphatemia, hypomag, hyperuricemiam and type IV RTA - Ktidy biopsy shows tubular atrophy and interstitial fibrosis 2) Lithium: chronic litium therapy can cause chornic TI disease, CKD and ND. RFs: dosea nd duration, serum lithium levels do not correlate well - DI - polyuria and polydipsia, nocturia, can also manifest as type I (distal hypokalemia) RTA 3) Lead - Kidney biopsy shows a nonspecific chronic interstitial nephritis - |
|
|
How is lithium induced tubulointerstitl disease treated? |
STOP lithium If this is not possible, treat with amiloride which prevents entry of lithium into tubular studies |
|
|
What are the major causes of tubulointerstitial disease? |
Medications Malignancy Infection Connective TIssue Disease Hyperuricemia --> inflammatory resposne results in interstitial fibrosis Obstruction --> can result in type 4 hyperkalemic distal RTA consistent with tubular atrophy and injury |
|
|
What is the management of tubulointerstitial disease? |
BP control Use of ACE and ARBs when significant proteinuria is presents Metabolic control of calcium/phos |
