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43 Cards in this Set
- Front
- Back
What do we look for when we do medical evaluation for HTN?
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-look medical (family) history
-PE -Lab/diagnostic testing |
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-When evaluating an individual, what do we need to assess?
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-target organ damage
-identify CVD risk factors -rule-out secondary forms of HTN |
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T/F: primary HTN is the second most reason for physician's office visit.
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True
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What organs can possibly be damaged by uncontrolled HTN?
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-cardiac: hypertrophy, failure, infarction
-large vessel: aneurysm, dissection -cerebral: ischemia, thrombosis, hemorrhage -renal: nephrosclerosis, ESRD -Urgency/emergency: accelerated malignant |
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What is the leading causes of death in 2007?
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Heart Disease (1st)
Cerebrovascular diseases (3rd) Hypertension and hypertensive renal disease (13th) |
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HTN prevalence: age, sex, and ethnicity
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age: >60 YO
sex: male ethnicity: non-hispanic black |
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What are the non-modifiable stroke prevention factors?
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-increasing age
-gender (m>w) -family hx -prior stroke or TIA |
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What are the modifiable stroke prevention factors?
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-htn
-diabetes -CAD -atrial fibriallation -hyperlipidemia -tobacco -inactivity -EtOH and drug abuse |
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Starting at _____ mmHg, CVD risk doubles with each increments of 20/10 mmHg throughout the BP range.
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115/75 mmHg
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Reduction of sodium intake to less than 2.4 g a day is equivalent to a single drug therapy for HTN. T/F
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True, in JNC7
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ACE inhibitors will increase or decrease bradykinin?
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Increase; ACE increase the breakdown of bradykinin; therefore ACEI will decrease the metabolism of bradykinin. Bradykinin is a vasodilator
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Angiotension I ---> Angiotension II by what enzyme?
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ACE; blocking
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Aldosterone inhibitors increase or decrease BP?
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decrease; in the RAAS, angiotension II will increase the release of aldosterone and it acts to increase the reabsorption of sodium and water; increase volume.
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Angiotensinogen ---> Angiotensin I is catalyzed by which enzyme? And what drug class block this enzyme?
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Renin; BB and renin inhibitors will block this process
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Volume or V hyptension is predominately renin-angiotensin mediated. T/F
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False, predominately sodium-volume mediated
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Drug class that are effective in tx V HTN.
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-reduce sodium-volume factor
-diuretics, CCB, sprironolactone, alpha1-blockers |
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R hypertension characteristics
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-plasma renin activity > .65 ng/ml/hr
-direct renin > 5uU/mL -progressively more renin-angiotension mediated |
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Drug class for R HTN.
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-block plasma renin-angiotensin system
-ACEI, ARB, DRI, BB |
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Blood pressure = cardiac output x ________
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Peripheral resistnace
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MAP = CO x ________
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total peripheral resistance (TPR)
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high blood pressure are due to:
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-increase CO
-and or increase PR |
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sympathetic overactivity is the common pathway that connects obesity and hypertension. T/F
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true; glucose, high leptin, and insulin can increase sympathetic tone
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Overall effectiveness of anti-HTN monotherapies.
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thiazide: 50-55%
ACEI (ARB): 50-60 BB: 45-50 CCB: 40-45 alpha 1 blocker: 35-40 alpha 2 agonist: 30-35 |
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When using a diuretic and ACE inhibitors, racial differences in respondents disappear. T/F
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True, when use diuretic and ACE inhibitor, all pt respond similarly. This can be the best combination to treat HBP
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When choosing a combination anti-htn drug, they need to be:
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In different drug class, drugs with complementary MOA
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What time of the day pt BP most elevated?
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most elevated at noon and morning upon waking up. Decrease when sleep called dipping. non-dipping pts have more chance of CVD.
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Describe systolic and diastolic pressure as we age.
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Systolic increases as age increases; diastolic increases until 50-60 years old, then plateau and decrease. So if patients are HTN before 50 yo, it may be cause by diastolic hypertension. Above 50, more likely it is systolic hypertension.
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Describe the blood pressure and CHD death rates relating to differences in diastolic and systolic pressure.
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The greater the diff in systolic and diastolic, the more risk of CHD deaths. Ex. systolic 160 and distolic 70.
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Describe the arterial pressure waves
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In older adults the arterial pressure wave travels faster than normal and is quickly reflected off the peripheral resistance.
The reflected wave returns to the central aorta in systole rather than diastole where it augments the systolic pressure, increases cardiac work, and reduces diastolic pressure upon which coronary flow is dependent. |
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Arterial stiffness is the major cause of HF, stroke and myocardial ischemia
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Fact
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T/F: treating stage 1 systolic hypertension 140-159 mmHg) should be withheld if pt is under 30 yo b/c there is no benefit.
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False: JNC 7 conclusively proven the benefits of treating individuals with stage 1 sysolic htn; therapy should not be withheld on the basis of age; unless DBP is lovered to 55 or 60 mmHg by treatment.
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“Are newer types of antihypertensive agents, which are currently more costly, as good or better than diuretics in reducing CHD incidence and progression?”
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no...new drugs and old drugs have similar results
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ALLHAT trial: why is doxazosin did not complete study?
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Increase hospitalization due to HF
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in the ALLHAT study: which medication seems to be more effective in treating HTN: chlorthalidone, amlodipine, lisinopril
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Chlorthalidone: systolic control are best and diastolic better than amlodipine.
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in the ALLHAT study: describe the results of primary outcome in chlorthalidone, amlodipine, and lisinopril.
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All 3 treatment has no significant difference in primary outcome (fatal CHD and nonfatal MI)
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Lisinopril group had a 15% higher risk for stroke compare to chlorthalidone.
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True. There is no difference with amlodipine.
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The ALLHAT trial summary:
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thiazide-type diuretics should be considered first for pharmacologic therapy in patients with hypertension. They are unsurpassed (i.e., they are equal) in lowering BP, reducing clinical events, and tolerability, and they are less costly
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Furosemdie
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-not as effective for lowering bp
-used if GFR is below 25-3o ml/min -most potent, but short duration of action ~6 hours |
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HCTZ
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-most commonly prescribed, but not as effective as chlorthalidone
-shorter duration compare to chlrothalidone |
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Chlorthalidone
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diuretic-like
-used in most major clinical trials -long t1/2 and duration -work during sleep so provide dipping bp |
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what non-metabolic side effects of chlorthalidone?
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dizziness, lightheadedness, weakness, fatigue, nausea, male impotence
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What are metabolic side effects of chlorthalidone?
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hypokalemia, hypomagnesemia, hyperglycemia, hyperuricemia, hypercholesterolemia.
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hypokalemia caused by chlorthalidone ca be minimized by:
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using loser dose and combine with low salt diet.
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