Antihypertensives Flashcards
1
Q
What is the leading RF for CVD?
A
- HTN
83% of people with CVD - cause was HTN - 25% of adults over 18 have HTN
2
Q
HTN is more common in what ethnicities?
A
- african americans
- native americans
- hispanics
- more common in younger men than women, no difference after age of 55
3
Q
HTN is a major contributing factor in the development of and death from?
A
- CVD
- stroke
- heart failure
- renal failure
4
Q
What factors effect BP in the body?
A
- arterial BP is product of CO and PVR
- other factors:
SNS activity
kidney fxn (Na and water retention)
electrolyte composition of ICF and ECF
cell membrane transport mech
alterations in vascular endothelium: caused by HTN, insulin resistance, smoking
Hyperinsulinemia (increased Na retention)
dietary Na intake, excessive Na retention - humoral influences: RAA mechanism
5
Q
2 categories of HTN?
A
- essential (primary) HTN: chronic elevation in BP occurs without evidence of other disease
- secondary: elevation in BP results from some other disorder (kidney disease, pheochromocytoma, OCPs, Cushings)
6
Q
How many pts have essential HTN
A
- 90-95% of pts - no identifiable cause of HTN is found
- familial patterns are common
- enviro factors plat a role:
obesity, alcohol consumption, sedentary lifestyle, and salt intake (huge factor)
7
Q
When is Essential HTN usually detected?
A
- during screening procedures or when person seeks medical care for another reason
- typically asx
8
Q
Possible sxs of Essential HTN?
A
- HA: occurs most frequently on awakening, usually felt in the back of head or neck
- common end organ damage in long term undx and untx HTN: common early sx which indicates the kidneys are losing ability to concentrate urine - elevated BUN/Creat and CVD disease
9
Q
How does family hx contribute to HTN likelihood?
A
- 2 or more first degree relatives with HTN before age 55, you have 3.8x greater risk for development of HTN before 50
- persons from high risk families should participate in regular HTN screening
10
Q
How are age and gender major risk factors for HTN?
A
- blood pressure increases with age in both men and women. Lifetime risk for HTN is nearly 90%
- 2/3 of Americans over 60 have HTN
- older women (60 and older) currently have highest rates of HTN, and mortality rates from HTN are higher in women than men
- HTN is also becoming more common in children and teens
- BP increass from 78 mm Hg at 10 days of age to 120 at end of adolescence
- systolic BP continues a slow rate of increase throughout adult life
- diastolic BP increases until age 50, then declines from 60 on up
11
Q
How is race a factor in HTN
A
- more prevalent in Blacks
- occurs earlier
- tend to experience greater cardiovascular and renal damage at any level of pressure:
compared to caucasians, Blacks have 1.8x the rate of fatal stroke, 1.5x risk of fatal heart disease, and 4.2x the rates of end stage kidney disease. In general about 34% of Black men and women have HTN. It may account for over 40% of all deaths in this group - they are often not tx early enough nor aggressive enough
- have higher prevelance of RFs that are associated with HTN
12
Q
How does salt intake and obesity increase rates of HTN?
A
- high salt intake: known as a risk factor because of findings of decreased incidence of HTN among primitive, unacculturated people from widely different parts of the world.
- obesity: wt reduction as little as 10 lbs can produce a sig decrease
- fat distribution may be more of an indicator than actual overweight - central obesity
- sedentary lifestyle plays a part in HTN also
13
Q
How does diabetes, hyperinsulinemia factor into HTN?
A
- up to 75% of CV problems in diabetics may be due to HTN
- activation of smypathetic nervous system and its effects on CO, PVR, and renal Na retention
- insulin stimulated changes in growth of vascular smooth muscle that result in an increased PVR
- the effect of insulin on salt and water retention by the kidney
- changes in Na and Ca transport across cell membrane of vascular smooth muscle
14
Q
How does excess alcohol contribute to HTN?
A
- regular consumption of 3 or more drinks/day increase risk of HTN, mechanism is unknown, suggested correlation with lifestyle factors
15
Q
How do cigarettes and coffee contribute to HTN?
A
- stimulate SNS
- smoking damages vasculature
16
Q
How does low birth wt correlate with HTN?
A
- particularly in girls
- high levels of stress hormones
- LBW is assoc with subsequent obesity
17
Q
How does stress contribute to HTN?
A
- mental stress: in 20 yr study men who had high stress were 2x as likely to have high BP as those with normal stress. The effects of stress on blood pressure in women were less clear. Job stress and lack of career success specifically linked to high BP in both men and women
- anxiety: anxiety rf for HTN, particulary in women
- depression: depression has physiological effects that impair the heart an dthat it contributes to destructive behaviors, such as wt gain, smoking, alcohol abuse. Link particularly strong in African Americans, depression was the strongest RF in this group
18
Q
How does time and seasonal factors contribute to HTN?
A
- BP levels tend to be lowest during the morning and midday hours and highest at end of the day
- seasonal changes also affect BP, with HTN increasing during cold months and declining though the summer, blood pressure readings can vary by as much as 40% depending on time of day and season
19
Q
How do OCPs contribute to HTN?
A
- unknown MOA
- perhaps constant estrogen and progesterone are responsible
- usually disappears with d/c, may take as long as 6 months
20
Q
What are complications of HTN?
A
- target organ damage
- TIA, stroke, dementia
- angina, MI
- PVD
- diabetic retinopathy: fundal hemorrhages or exudates (neovascularization, AV nicking, silver wiring)
- renal impairment, proteinuria (microalbumineria first early sign)
- arteriosclerosis
21
Q
What is isolated systolic HTN? Why is it so bad?
A
- may pose sig danger for heart events and stroke events even when the diastolic is normal
- most common form of HTN in people 50 and older. Favors the development of LVH
- increased myocardial O2 demands
- eventual left heart failure
22
Q
What is a elevated pulse pressure?
A
- diff between systolic and diastolic BP
- produces greater stretch of arteries
- causing damage to elastic elements of the vessel
- predisposing to aneurysms and development of intimal damage that leads to atherosclerosis
23
Q
What are the 2 causes of renovascular HTN?
A
- renal artery stenosis: (atherosclerotic renal artery disease) - usually affect the proximal aspect of renal artery, most common in older men, is often bilateral
- fibromuscular dysplasia: fibrosis and aneurysm formation in middle and distal renal arteries
- most common in younger women
24
Q
What are the 2 adrenal causes of HTN?
A
- hyperaldosteronism
- pheochromocytoma
25
Q
What % of pts are there that a secondary cause of HTN can be found?
A
- 5%
- think secondary in pts with new onset HTN that are younger than 30, older than 55
- had previously well controlled HTN that develps sudden increase in BP
- pts with poorly controlled BP despite mult. antiHTN meds
26
Q
What conditions increase CO?
A
- Hypervolemia: renal artery stenosis renal disease hyperaldosteronism hypersecretion of ADH aortic coarction pregnancy (preeclampsia) - stress: sympathetic activation - pheochromocytoma: increased catecholamines
27
Q
What conditions increase systemic vascular resistance?
A
- stress: sympathetic activation - atherosclerosis - renal artery disease (increased AII) - pheochromocytoma: increased catecholamines sympathetic - thyroid dysfunction - diabetes - cerebral ischemia
28
Q
What do you want to R/O before looking for secondary HTN?
A
- increase Na+ intake
- non-compliance with meds
- drugs that may interfere with antihtn meds, or meds that cause HTN:
OCPs
corticosteroids (symp stim)
NSAIDs: cox cause kidneys to retain Na and water - OTC cold remedies containing ephedrine or sympathomimetics
29
Q
How common is renovascular HTN?
A
- 1-2% of cases of HTN
- most common cause of secondary HTN
- stenosis of renal artery - kidney isn’t getting adequate blood flow and senses low O2 - so JG cells send out renin to lungs and this stimulates conversion of AI to AII and this than causes vasoconstriction in periphery and stimulates adrenals to release aldosterone to retain Na and water - this causes increase PVR and increased volume leading to icnrease in BP
30
Q
What are some clinical clues that HTN is due to renovascular HTN?
A
- sudden development of HTN in a pt with no family hx
- drug resistant HTN
- abdominal bruit
- renal insufficiency
- worsening renal fxn after ACEI** (check BUN, creatinine and K+)
31
Q
Diagnostic tests for renovascular HTN?
A
- renal fxns, BUN, creatinine
- plasma renin levels (high because O2 deprived)
- angiography is definitive
32
Q
Why should ACEIs be avoided in renovascular HTN?
A
- kidney is receiving inadequate blood supply so it activates RAAS system. Therefore a single dose of this ACEI will abruptly reduce renal fxn in the ischemic kidney
- this is why ACEI are CI in renal artery stenosis/ Although they are good at controlling BP, they exacerbate renal failure in already compromised (ischemic) kidney
33
Q
Tx of renovascular HTN?
A
- eliminating stenosis: percutaneous technique (balloon angioplasty)
surgery with stent placement: this will stabilize or improve renal fxn, assoc with small but significant decrease in BP, may need antiHTN for life (b/c of damage done to kidney)
34
Q
What hyperaldosteronism conditions are more common in men? women?
A
- unilateral adrenal adenoma: more common in women
- bilateral adrenal hyperplasia: more common in men: secreting aldosterone so increased retention of Na and increased volume so leads to HTN and excreting more K+
35
Q
How does primary hyperaldosteronism cause HTN?
A
- increase aldosterone stimulates excessive renal Na+ retention with resultant volume expansion and HTN
- increase intravascular volume augments renal perfusion, thereby renin secretion is suppressed
- increases Na+ retention and increases K+ excretion
(will have low serum renin since there is increased intravascular volume
36
Q
Dx tests for primary hyperaldosteronism?
A
- serum renin will be low
- urine aldosterone levels
- increased sreum aldosterone level that doesn’t suppress after saline-induced volume expansion
- CT to diff b/t adrenal adenomas and hyperplasia
37
Q
How is primary hyperaldosteronism tx?
A
- adrenal tumors are resected, resolved HTN 50% of the time
- adrenal hyperplasia: spironolactone (diuretiic, K+ sparing, aldosterone antagonist)
additional diuretics
38
Q
Tx of pheochromocytoma?
A
- surgical resection: alpha and beta blockage and volume expansion before surgery
- unresectable tumors: chronic therapy with phenoxybenzimine (alpha adrenergic blocker)
39
Q
Sxs of episodic pheochromocytoma?
A
- HA
- sweating
- palpitations, tachycardia
- chest pain
- anxiety, fear of impending death
- tremor
- fatigue or exhaustion
- nausea, vomiting
- abdominal pain
- visual disturbances
- sxs b/t paroxysms:
- increased sweating
- cold hands and feet
- wt loss
- constipation
40
Q
What is an aortic coarctation?
A
- narrowing of the aorta (typically just distal to left subclavian artery), congenital defect that obstructs aortic outflow leading to elevated pressures proximal to coarction (head and arms). Distal pressures, however, are not necessarily reduced as would be expected from hemodynamics assocd with stenosis
- reason for this is that reduced systemic blood flow, and in particular reduced renal blood flow, leads to an increase in release of renin and activation of RAAS system - this in turns elevates blood volume and arterial pressure. ALthough the aortic arch and carotid sinus baroreceptors are exposed to higher than normal pressures, the baroreceptor reflex is blunted due to structural changes in the walls of vessels where baroreceptors are located
- also, baroreceptors become desensitized to chronic elevation in pressure and become “reset” to the higher pressure
41
Q
How is proper BP measurement taken?
A
- pt should be seated with back supported, arm bared and supported
- pts should refrain from smoking or caffeine for 30 min prior
- pts should rest at least 5 min prior
- appropriate size cuff and calibrated equipment should be used
- 2 or more readings should be averaged
42
Q
According to JNC 8, what is considered HTN?
A
- in everyone younger than 60, all ages with diabetes, all ages with CKD w/ or w/o diabetes: 140/90
60 and older: 150/90
43
Q
Pts have how much of a risk becoming HTN if already pre-hypertensive?
A
- those in 130-139/80-89 BP range are at twice the risk to develop HTN as those with lower values
44
Q
What should be included in eval of pt with HTN?
A
- thorough hx and physical
- goals of eval:
assess for presence and extent of HTN target organ damage - ID clinical factors that may influence choice of therapy (heart failure, renal failure)
- determine presence of CVD RFs
- recognize occasional pt with secondary HTN
45
Q
HTN’s sxs?
A
- rarely symptomatic
- occipital HAs
- blurred vision
- fatigue
- dizziness
- epistaxis
- dyspnea
- chest pain
46
Q
Sxs of end organ damage?
A
- CHF
- CVD
- Cerebrovascular disease
- uremia
- microalbuminemia
- aortic dissection
47
Q
Historical features in person with HTN?
A
- family hx
- dietary Na + intake
- exercise
- alcohol use
- Rx and non-Rx drug use: OCPs, anabolic steroids, NSAIDs
48
Q
What should you focus on after confirming the presence of HTN?
A
- should focus on recognizing evidence of end organ damage on PE
(eyes, heart, Peripheral artery disease)
49
Q
PE of pt with HTN?
A
- BP in both arms and compared with pressure in legs
- funduscopic exam: look for retinal changes, AV nicking, copper wire changes, retinal hemorrhages and exudates
- heart: S4 gallop (decreased ventricular compliance), S3- CHF
- vascular exam: carotid bruits. PVD, abdominal bruits
- neuro exam: evidence of prior strokes
50
Q
dx lab work up of pt with HTN?
A
- initial lab screening and dx:
CMP: renal function, serum glucose, electrolytes - fasting lipids
- U/A
- CBC: hematocrit (hemachromotosis)
- EKG: LVH, prior MI (large Q wave)
- echo; evidence of left ventricular enlargement or failure should be noted
51
Q
Tx goal of primary HTN?
A
- to prevent long term mobirdity and mortality assocd with prolonged elevations in BP
- method of aggressiveness depends on these several factors:
absolute level of BP
presence of end organ damage
coexisting medical conditions
overall cardiac risk
52
Q
Lifestyle changes?
A
- exercise at least 40 min/day
- maintain normal wt
- reduce NaCl intake
- increase K+ intake
- DASH diet: consume a diet rich in fruits, veggies, and low fat dairy products
- reduce total and sat fat intake
- limit alcohol consumption: mod alcohol consumption: 1-2 glasses a day may actually lower risk of heart attack among men with HTN
- stop smoking
- good sleep habits
- stress reduction
- psychological considerations
53
Q
What are causes of secondary HTN?
A
- renal pathology: stenosis, or fibromuscular dysplasia
- endocrinal: pheo or hyperaldosteronism
- drugs: OCPs, NSAIDs, steroids
- neurogenic, psychogenic (anxiety)
- co-arction of aorta
- pregnancy
- OSA (most common): decrease O2 - sympathetic stimulation - HR and BP rises
54
Q
What is short term goal of antiHTN therapy? long term?
A
- short term: reduce BP
- long term: controlling all of pts modifiable CV risk factors, want to reduce mortality due to HTN induced disease:
stroke, CHF, CAD (beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg
nephropathy, PAD, retinopathy
55
Q
When should you tx patient?
A
- in absence of end-organ damage, a pt shouldn’t be labeled as having HTN unless BP is persistently elevated after 3-6 visits over a several month period
- antiHTN meds should begin if the systolic pressure is persistently over or = to 140 and/or the diastolic pressure is persistently greater or equal to 90 in office and at home despite attempted nonpharmacologic therapy
56
Q
BP = ?
A
BP = COx PVR
57
Q
Where are the sites of regulation of CO and PVR?
A
- arterioles
- postcapillary venules
- heart
- kidneys
58
Q
Tx choices for primary HTN? secondary htn tx?
A
drugs that:
1) reduce blood volume (which reduces central venous pressure, and CO)
2) reduce systemic vascular resistance
3) reduce CO by depressing HR and SV
secondary htn tx:
best tx by controlling or removing underlying disease or patholgoy, although they still may require antihypertensive drugs
59
Q
What are the major classes of antihypertensives used for initial therapy?
A
- diuretics
- B -blockers
- ACEIs
- ARBs
- CCBs
- Alpha blockers
- alpha agonists
- vasodilators
- direct renin inhibitors
