Antihypertensives Lecture 1 Flashcards
(75 cards)
1
Q
HTN is a major contributing factor in the development of, and death from?
4
A
- Cardiovascular disease
- Stroke
- Heart failure (MI)
- Renal failure (fibrotic)
2
Q
What is arterial blood pressure the product of?
A
cardiac output and peripheral vascular resistance.
3
Q
WHat other factors affect aterial blood pressure?
8
A
- Sympathetic nervous system activity
- Kidney function in terms of salt and water retention
- Electrolyte composition of the intracellular and extracellular fluids-
- Cell membrane transport mechanisms- CA blockers
- Alterations in vascular endothelium
- Hyperinsulinemia- proinflammatory, prothrombotic, causing problems in your pipes
- Dietary Na+ intake, excessive sodium retention- causes an increase in blood volume.
- Humoral influences- EF start to come up
Renin-angiotensin-aldosterone mechanism
4
Q
How does the sympathetic nervous system affect afterload?
A
decrease afterload
5
Q
How does Ca channel blockers affect preload?
A
CA blocker increases preload.
Alpha agonists
Ca- SM relaxation.
6
Q
What are alterations in vascular endothelium caused by?
How to treat?
A
Caused by
- HTN,
- insulin resistance,
- smoking-
Nitric Oxide treatment/opens things up
7
Q
What are the two categories of hypertension and describe them?
A
Essential (Primary) Hypertension
Chronic elevation in blood pressure occurs without evidence of other disease
Secondary Hypertension
Elevation in blood pressure results from some other disorder (i.e. kidney disease)
8
Q
What kind of patterns are common in primary HTN pts?
Environmental factors that play a role?
4
A
Familial patterns
1, Obesity
- Alcohol consumption
- Sedentary lifestyle
- Salt intake!!!!!!
9
Q
How is primary hypertension often detected?
A
- -Typically asymptomatic
- -Often detected during screening procedures or when person seeks medical care for another reason.
10
Q
Possible symtpoms of primary hypertension?
When does it occur most frequently and where is it felt?
A
Headache
Occurs most frequently on awakening
Usually felt in the back of the head or neck
11
Q
What is the most common finding of undiagnosed and untreated hypertension?
Common early symptom which indicates the kidneys are losing their ability to ________ _____.
What two things will we see to support our this diagnosis? 2
A
Common end organ damage in long term
concentrate urine
- Elevated BUN/Creat
- Cardiovascular disease
12
Q
What is our systolic value at 10 days of life and our systolic valie at the end of adolescence?
Systolic and Diastolic pressures change how as we age?
A
78mmHg
120mmHg
Systolic B/P continues a slow rate of increase throughout adult life. (Atherloscleritic/less elastic)
Diastolic B/P increases until age 50, then declines from the sixth decade onward.
13
Q
Weight reduction as little as __lbs can produce a significant decrease in B/P
Fat distribution may be more of an indicator than actual overweight. What kind of weight are we worried about?
A
10
Central obesity
14
Q
How does hyperinsulinemia cause HTN?
acts on what and this has effects on what? 3
A
Activation of the sympathetic nervous system and its effects on
- cardiac output,
- PVR and
- renal sodium retention.
15
Q
Why does insulin increase PVR?
A
Insulin stimulated changes in GROWTH of VASCULAR SMOOTH MUSCLE that result in an increased PVR.
16
Q
How do cigarettes and coffee increase BP?
A
Stimulate the sympathetic nervous system
Smoking damages vasculature
17
Q
Why does low birth weight a risk factor for increased blood pressure? 2
A
Particularly in girls
- High level of stress hormones
- LBW is associated with subsequent obesity
18
Q
At what time of the day does blood pressure tend to be lower?
higher?
BP increases during what seasons?
Decreases?
A
Blood pressure levels tend to be lowest during the morning and midday hours and highest at the end of the day.
Seasonal changes also affect blood pressure, with hypertension increasing during cold months and declining during the summer.
19
Q
Why are oral contraceptives a risk factors for HTN?
How can you deal with this?
A
Perhaps constant estrogen and progesterone are responsible for the effect.
Usually disappears with discontinuation, although it may take as long as 6 months.
20
Q
Complications - Target Organ Damage for undiagnosed, long term HTN: Neuro? 3 Cardio? 5 Optho? 1 Nephro? 1
A
- TIA,
- Stroke,
- Dementia
2.
- Heart Failure,
- Left ventricular hypertrophy
- Angina,
- Myocardial infarct
- Peripheral vascular disease
- Diabetic Retinopathy
- Fundal hemorrhages or exudates
- Renal impairment, proteinuria (leaking protein)-once they get to macro its usually too late
21
Q
Describe isolated systolic hypertension?
What does it favor the development of?
3
A
Elevated systolic pressure may pose a significant danger for heart events and stroke events even when diastolic is normal
- left ventricular hypertrophy
- Increased myocardial 02 demands.
- Eventual left heart failure.
22
Q
Why is the systolic HTN worse than diastolic?
A
- -not as elastic as they used to be
- -wide pulse pressure is systolic hypertension is worse
more left ventriclular hypertrophy
23
Q
What is pulse pressure?
What does this cause?
3
A
the difference between the systolic and diastolic blood pressure
- Produces greater stretch of the arteries.
- Causing damage to the elastic elements of the vessel.
- Predisposing to aneurysms and development of intimal damage that leads to atherosclerosis.
24
Q
What are the clinical manifestation of diabetic retinopathy?
4
A
- Flame hemorrhage
- Cotton wool spots
- Hard exudates
- Neovascularization
25
What are the two most common causes of secondary hypertension?
Renovascular Hypertension
| Adrenal causes of Hypertension
26
What causes renovascular HTN? 2
What causes adrenal HTN? 2
Renal artery stenosis
Fibromuscular dysplasia- young women
Hyperaldosteronism
Pheochromocytoma
27
What things would we see that would cause us to look for a secondary cause of HTN?
3
1. Patients with new-onset hypertension
- Less than age 30- doesnt make sense
- Greater than age 55- more complex pts
2. Previously well controlled HTN develops sudden increase in BP.!!
3. Patients with poorly controlled B/P despite multiple antihypertensive medications.
28
What things would cause hypervolemia leading to increased cardiac output and eventually HTN?
Causes of Stress that would increase cardiac output?
How would pheochromocytoma increase cardiac output?
1. renal artery stenosis
2. renal disease
3. hyperaldosteronism
4. hypersecretion of ADH
5. aortic coarctation
6. preeclampsia
1. Sympathetic activation
1. increased catecholamines
29
1. What things would cause stress that could lead to increased systemic vascular resistance?
2. Vascular issues that could cause SVR?
3. Renal disease that could cause SVR?
4. Pheochromocytoma?
5. Endrocrine problems? 2
6. Neuro issues?
1. Sympathetic activation
2. Atherosclerosis
3. Renal artery disease causing increased angiotensin II
4. increased catecholamines
5. Thyroid dysfunction and diabetes
6. cerebral ischemia
30
We have to R/O any of the following factors before we start to seach for secondary HTN causes. What are they?
3
1. Increase in Na+ intake
2. Non-compliance with meds
3. Drugs that may interfere with antihypertensive meds, or meds that may cause HTN
31
Drugs that may interfere with antihypertensive meds, or meds that may cause HTN include?
4
1. Oral contraceptives
2. Corticosteroids- increase symtpathetic nervous system
3. NSAIDS (Why?)- cause kidneys to retain sodium and also water (increase in intracellular volume)
4. Over the counter cold remedies containing ephedrine or sympathomimetics.
32
What is the most common cause of secondary HTN?
Why?
Renovascular Hypertension
Stenosis of the renal artery
33
Describe how stenosis of the renal artery would cause HTN?
1. kidney senses decrese O2 (blood flow)
2. releases renin from JG cells into the blood stream to
3. lungs which secrete angiotensin converting enzyme and make angiotnesin II,
4. which signals secretion of adrenal aldosterone,
5. Aldosterone increases NA+ retention which equals more water and more volume.
34
How would an ACE inhibitor make the renal artery stenosis worse?
ACE inhibitors- stop ace in its tracks and drops blood pressure. slowing killing kidneys.
contraindicated in renal artery stenosis. how do we fix it? stent it
35
RENOVASCULAR HTN
1. ________ in renal blood flow stimulates an increase in renin release with subsequent ________ production of angiotensin II.
2. Angiotensin II in turn ________ the release of aldosterone resulting in Na+ and water ________ and________ intravascular volume.
1. Decrease
increased
2. stimulates
retention
increased
36
Atherosclerotic renal artery disease usually affects what part of the renal artery?
Who is it most common in?
Bilateral or unilateral?
Usually affects the proximal aspect of the renal artery
Most common in older men
Is often bilateral
37
Fibrosis and aneurysm formation usually occur in which part of the renal arteries? 2
Most common in who?
Fibromuscular dysplasia
Fibrosis and aneurysm formation in the
1. middle and 2. distal renal arteries
(going to want to do some kidney protective things ahead of time)
Most common in younger women
38
Clinical clues to Renovascular Hypertension? 5
What should we check on a followup with someone who we just put on an ACE I or ARB? 3
And why?
1. Sudden development of hypertension in a patient with no family history
2. Drug resistant hypertension
3. Abdominal bruit
4. Renal insufficiency
5. Worsening renal function after ACE inhibitor
check BUN, creatitine and potassium on followup
(if these go up the may have stenosis)
39
Diagnostic tests for renovascular HTN? 5
| whats the definitive test?
1. Renal functions,
2. BUN,
3. Creatinine
4. Plasma renin levels (can skip and just order angio most times)-renin would be high if you checked it
5. Angiography is definitive
40
Based on the fact that a kidney that is receiving an _______ ______ ______ will activate the RAAS system. Therefore, a single dose of this ____ ________will abruptly reduce renal function in the ischemic kidney.
This is why ____ _______ should not be used in the treatment of Renal Artery Stenosis. Although they do a good job of controlling B/P, they exacerbate renal failure in an already compromised (ischemic) kidney.
inadequate blood supply
ACE inhibitor
ACE Inhibitors
41
Treatment for renovascular HTN?
(what two ways can we accomplish this?)
What medication might you need for life after this?
Eliminating the stenosis
- -Percutaneous technique (balloon angioplasty)
- -Surgery with stent placement
antihypertensives
42
Primary Hyperaldosteronism
What are the two kinds and who are they more common in?
Are these usually benign or malignant?
Why do these lead to high blood pressure?
Unilateral adrenal adenoma
More common in women
Bilateral adrenal hyperplasia
More common in men
Benign
LOTS Of fluid retention
43
Primary Hyperaldosteronism
Increase aldosterone stimulates 1. WHAT with resultant 2. WHAT (2)?
Increase 1. _______ ________ augments renal perfusion, thereby renin secretion is 2. _______.
1. Increase __ retention?
2. Increase __ excretion?
1. excessive renal Na+ retention
2. volume expansion and hypertension.
1. intravascular volume
2. suppressed
1. Na+
2. K+
44
Primary Hyperaldosteronism
Diagnostics?
4
1. Serum renin level (low)
2. Urine aldosterone levels
3. Increased serum aldosterone level that does not suppress after saline-induced volume expansion
4. CT
45
Why would we want to do a CT on a Primary Hyperaldosteronism pt?
3
1. to differentiate between adrenal adenomas and hyperplasia.
2. unilateral or bilateral,
3. whether its coming from adrenal or pituitary)
46
How would we treat an adrenal tumor causing Primary Hyperaldosteronism and HTN?
2
1. Adrenal tumors are resected
Resolution of hypertension 50% of the time
2. Adrenal hyperplasia
Spironolactone (diuretic, K sparing)
Aldosterone antagonist
Additional diuretics
47
Pheochromocytoma
1. What are the signs and symptoms of a Pheo??
2. How can we diagnose it?
3. How can we treat it? 2
1. Tumor of the adrenal medulla- too much epi and nor epi. This is episodic. Will be activating sympathetic nervous system!
2. 24 hour urine for catecholamines, and metanephrines (byproducts of epi and norepi)
3. Surgical resection
Alpha and beta blockage and volume expansion before surgery
Unresectable tumors
Chronic therapy with phenoxybenzmine (alpha adrenergic blocker)
gotta find it and get rid of it. perioperatively can spill out epi and norepi. have to be careful.
48
What is Aortic Coarctation?
Why does it cause this?
Coarctation, or narrowing of the aorta , is a congenital defect that obstructs aortic outflow leading to elevated pressures proximal to the coarctation
The reason for this is that reduced systemic blood flow, and in particular reduced renal blood flow, leads to an increase in the release of renin and an activation of the renin-angiotension-aldosterone system.
49
Where does the narrowing occur in aortic coarctation?
Where are the elevated pressures usually found?
(typically just distal to the left subclavian artery)
(i.e., elevated arterial pressures in the head and arms). Distal pressures, however, are not necessarily reduced as would be expected from the hemodynamics associated with a stenosis.
50
What would help us diagnose aortic coarctation?
| 2
Big difference in an arm and a leg or side to side. IN A CHILD
51
When there is an increased activation of renin-angiotension-aldosterone system in aortic coarctation what happens?
elevates blood volume and arterial pressure even though the aortic arch and carotid sinus barorecptors are exposed to higher than normal pressures.
52
Aortic Coarctation
Why are the baroreceptors blunted?
2
1. the baroreceptor reflex is blunted due to structural changes in the walls of vessels where the baroreceptors are located.
2. Also, baroreceptors become desensitized to chronic elevation in pressure and become "reset" to the higher pressure.
53
What should our blood pressure goal be in a pt 60 and older?
SBP less than 150
| DBP less than 90
54
What should our blood pressure goal be in a patient less than 60?
SBP less than 140
| DBP less than 90
55
WHat should our blood pressure goal be in all ages of pts with diabetes and no CKD?
SBP less than 140
| DBP less than 90
56
All ages with CKD present with ot without diabetes?
SBP less than 140
| DBP less than 90
57
Evaluation of Patient with Hypertension: Goals?
| 4
1. Assess for presence and extent of hypertensive target organ damage.
2. Identify clinical factors that may influence choice of therapy (renal failure, heart failure).
3. Determine presence of cardiovascular risk factors.
4. Recognize occasional patient with secondary hypertension.
58
Hypertension itself is rarely symptomatic but may include?
7
1. Occipital headaches
2. Blurred vision
3. Fatigue
4. Dizziness
5. Epistaxis
6. Dyspnea
7. Chest pain
59
Symptoms of end organ damage
due to HTN?
6
1. CHF
2. Cardiovascular disease
3. Cerebrovascular disease
4. Uremia
5. Microalbuminemia
6. Aortic dissection
60
Evaluation of Patient with Hypertension: Historical features we should talk about?
1. Family history
2. Dietary sodium intake
3. Exercise
4. Alcohol use
5. Prescription and non-prescription drug use
61
Prescription drugs we should be aware of that may cause HTN?
| 3
Oral contraceptives
Anabolic steroids
NSAIDs
62
What should we look for in the fundoscopic exam for a pt with HTN?
4
1. Retinal changes
2. AV nicking
3. Copper wire changes
4. Retinal hemorrhages and exudates
63
Heart exam on a HTN pt might show us what (and what would these findings tell us)?
2
Vascular exam? 3
Neuro exam? 1
Heart Exam
1. S-4 gallop – decreased ventricular compliance
2. S-3 gallop – associated with CHF
Vascular exam
1. Carotid bruits
2. PVD
3. Abdominal bruits
Neuro exam
1. Search for evidence of prior strokes
64
Evaluation of Patient with Hypertension:
Initial lab screening and diagnostics?
6
1. Comprehensive metabolic panel
2. Fasting lipids
3. U/A
4. CBC
5. EKG
6. Echo
65
What are we looking for specifically on the CMP? 3
How about on the CBC? 1
EKG? 1
Echo? 1
1. Renal function
2. Serum glucose
3. Electrolyes
1. hematocrit (hemochromotosis)
1. (LVH, prior MI)- big Q
1. Evidence of left ventricular enlargement or failure should be noted.
66
Treatment of Primary Hypertension Goal?
The method of aggressiveness depends on what?
4
To prevent the long-term morbidity and mortality associated with prolonged elevations in blood pressure.
1. Absolute level of blood pressure
2. Presence of end-organ damage
3. Coexisting medical conditions
4. Overall cardiac risk
67
Lifestyles changes for pts with HTN?
| 10
1. Exercise at least 40 minutes/day
2. Maintain normal weight
3. Reduce salt intake
4. Increase potassium intake
5. DASH diet (Dietary Approaches to Stop HTN)
Consume a diet rich in fruits, veggies and low-fat dairy products
Reduce total and saturated fat intake
6. Limit alcohol consumption
Moderate alcohol consumption (1-2) glasses/day may actually lower the risk of heart attack among men with HTN.
7. Stop Smoking
8. Good sleep habits
9. Stress reduction
10. Psychological Considerations
68
Definition Of Hypertension
Can be caused by:
1. Renal pathology 3
2. Endocrinal 5
3. Drugs 4
4. Neurogenic, psychogenic
5. Co-arctation of aorta
6. Pregnancy 2
7. Obstructive sleep apnea
8. Fibromuscular dysplasia
Elevation of arterial blood pressure above 140/90 mm Hg.
1.
renin artery stenosis,
electrolyte balance
Fibromuscular dysplasia
2.
adrenal gland problems (pheocytochromtosis, Hyperaldosteronism, Unilateral adrenal adenoma, Bilateral adrenal hyperplasia),
hyperinsulemia
```
3.
NSAIDS,
steriods,
BC,
cyclosporin
```
5
6. - preeclampsia, HELP syndrome
7. - not getting oxygen. constant sympathetic stimulation- HP
8. - renal artery that block blood - young females
69
Short term goal of HTN therapy?
| Long Term Goal of antihypertensive therapy?
Reduce blood pressure
Therapy should be directed at controlling all of the patient’s modifiable CV risk factors
70
Long-term goal of antihypertensive therapy?
Reduce mortality due to hypertension-induced disease
6
1. Stroke
2. Congestive heart failure
3. Coronary artery disease
- --Beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg
4. Nephropathy
5. Peripheral artery disease
6. Retinopathy
71
In the absence of end-organ damage, a patient shouldn’t be labeled as having HTN unless what?
Antihypertensive medications should begin if the systolic pressure is persistently _____and/or the diastolic pressure is persistently________in the office and at home despite attempted nonpharmacologic therapy.
the BP is persistently elevated after three to six visits over a several month period
> or = to 140
> or = 90
72
Arterial blood pressure is directly proportional to the product of the ________ _________and the ____________________ through _____________ _________- peripheral vascular resistance. (PVR).
3
1. blood flow (cardiac output)
2. resistance to the passage of blood
3. pre-capillary arterioles
B/P = CO X PVR
73
Sites and Regulation of CO and PVR?
| 4
1. Arterioles
2. Postcapillary venules
3. Heart
4. Kidneys
74
Patients with primary hypertension are generally treated with drugs that:
3
Patients with secondary hypertension are best treated by what?
1) reduce blood volume (which reduces central venous pressure and cardiac output)
2) reduce systemic vascular resistance
3) reduce cardiac output by depressing heart rate and stroke volume.
controlling or removing the underlying disease or pathology, although they may still require antihypertensive drugs.
75
Major Classes of Antihypertensives For Initial Therapy
| 9
1. Diuretics (lasiks, HCTZ (thiazide group))
2. Beta-Blockers
3. ACE Inhibitors (ACEIs)
4. Angiotensin II Receptor Blockers (ARBs)
5. Calcium Channel Blockers (CCBs)
6. Alpha blockers
7. Alpha agonists
8. Vasodilators
9. Direct Renin Inhibitors
