Hypertension and Diseases of Peripheral Vasculature Flashcards Preview

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Flashcards in Hypertension and Diseases of Peripheral Vasculature Deck (65):

What are the three layers of aorta?

  • luminal surface - intima (endothelial cells)
  • middle - media (smooth muscle cells, collagen, elastic fibers)
    • collagen - tensile strength to deal with high pressure
    • elastin - stretching up to 250%, ability to recoil under pressure
  • outer - adventitia (collagen, perivascular nerves, vasa vasorum = network that supplies O2 blood to aorta itself


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What happens to aortic layers as you age?

Why does systolic pressure tend to rise with age?

Media layer of the aorta in young age has 1collagen (tensile) :2 elastin (stretch and recoil). With age, elastin wears off and collagen become predominant - arteries stiffen.

With less elastin, aorta is not stretching as much during systole and most energy from myocardial contraction is spent pushing blood through stiffer aortic walls.


What is an aneurysm?

An aneurysm is an abnormal localized dilatation of an artery. 


What is an aortic aneurysm? How is it different from diffuse ectasia?

aortic aneurism - dilatation of a portion of the aorta by at least 50%. true aneurysm - dilatation of all three layers of the aorta - large bulge.

diffuse ectasia - generalized (vs localized) dilatation of the aortic diameter, tends to be lesser than aneurism. 


What are the two types of true aortic aneurisms?

a fusiform aneurysm - symmetrical dilation of the entire circumference of a segment of the aorta, more common

a saccular aneurysm is a localized outpouching involving only a portion of a circumference

memory aid : think "fuse" for double sided and "sac (bag)" for one sided

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What is the difference between true and false aneurysm?

true aneurysm -  dilation of all three layers of the aorta (intima, media and adventitia), caused by degenerative changes in the aortic wall.

false aneurysm or pseudoaneurysm - contained hole (rupture) of the vessel wall that develops when blood leaks out of intimal and medial layers, but is contained by adventitia or perivascular clot (not all of 3 layers are affected). false anneurysms are unstable and can rupture completely. 


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What is cystic medial degeneration or cystic medial necrosis?

cystic medial degeneration = cystic medial necrosis

degeneration changes in media with destruction of elastic and muscular tissues. associated with aging, genetic conditions (like Marfan syndrome) and hypertension.  cystic b/c sometimes can form cyst-like shapes. characteristic of an aneurysms.

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What conditionals are associated with true aortic aneurysms?

1. cystic medial necrosis (usually for ascending aortic aneurysms)

2. atherosclerosis (usually for descending and abdo aneurysms)

3. infection of the arterial wall

4. vasculitis



What is atherosclerosis?

condition in which an artery wall thickens as a result of the accumulation of calcium and fatty materials such as cholesterol and triglyceride -> reduced elasticity, less blood flow, higher bp.


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How is atherosclerosis different from arterosclerosis and arteriolosclerosis?

arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (from Greek ἀρτηρία (artēria), meaning "artery", and σκλήρωσις (sklerosis), meaning "hardening"); arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries); atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque.


What are risk factors for atherosclerosis?

  • smoking
  • hypertension
  • dyslipidemia (abnormal amount of lipids = cholesterol and fats in the blood)
  • male gender
  • advanced age


Clinical presentation of aortic aneurysms?

Most aneurysms are asymptomatic

Symptoms may be related to compression of nearby-structures. Thoracic aortic aneurysms may compress the trachea or bronchus = cough, dyspnea (shortness of breath), pneumonia

compression of the esophagus can lead to dysphagia (difficulty swallowing), involvement of recurrent laryngeal nerve - voice hoarseness.

abdominal aortic aneurysms  can cause abdo or back pain or non-specific GI symptoms.

most worried about rupture (risk related to size), which can be fatal. 


Optional: aortic aneurysm

risk of rupture vs surgical risk

thoracic aneurysms rupture (annual rates)

2% for

3% for 5-5.9 cm

7% for > 6 cm

mortality due to surgical repair = 3-5%


abdo aneurysm rupture (annual risk)

0.3% for < 4 cm

1.5% for 4-4.9 cm

6.5% for 5-5.9 cm

mortality due to surgical removal of abdo eneurysms = 1-2%


What is the management of aortic aneurysms?

Repeated imaging every 6-12 months

surgical treatment for ascending aneurysms >5.5-6 cm, less if Marfan

surgical treatment for descending aneurysms >6.5-7 cm,

abdo > 5.5 or those that enlarge at >1.0 cm/year



thoracic aneurysms rupture (annual rates)

2% for

3% for 5-5.9 cm

7% for > 6 cm

mortality due to surgical repair = 3-5%


abdo aneurysm rupture (annual risk)

0.3% for < 4 cm

1.5% for 4-4.9 cm

6.5% for 5-5.9 cm

mortality due to surgical removal of abdo eneurysms = 1-2%


How are aortic aneurysms surgically repaired?

thoracic: bypass -> aneurysm resected -> replaced with a prosthetic Dacron graft

multiple segments done in stages if necessary

in some cases, endovascular stent is possible across aneurysm via transluminal placement


abdo: prosthetic graft



What are some steps towards management of aortic aneurysms?

medical management: lifestyle (smoking reduction, diet, exercise)

beta-blockers for Marfan syndrome

surgery considered


What is aortic dissection?

blood from the aortic lumen goes through a tear in the intima and spreads in medial layer. can be due to advanced age, hypertension, other causes (cystic medial necrosis,...)


What are the two types of aortic dissection?

Stanford type A - ascending aorta is involved, regardless of site of primary tear

Stanford type B - does not involve ascending aorta or arch, only descending thoracic and abdo aorta


ascending thoracic aorta (65%)

descending thoracic aorta (20%)

aortic arch (10%)

abdo (5%)

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What is the treatment for Stanford Type A aortic dissection and Stanford Type B aortic dissection?

reduce systolic blood pressure -> 100-120 mm Hg

decrease force of ventricular contraction to minimize aortic wall stress -> beta blockers (to reduce force of contraction and heart rate), vasodilators (sodium nitroprusside, etc)

Type A dissection -  more serious because of risk of spread to coronary and arch vessels (2/3 or all dissections). In this type, early surgical intervention is shown to improve outcomes (repairing tear, suturing the edges +/- insrting a synthetic aortic graft)

Type B dissection - if uncomplicated, can be managed with meds alone.  Surgery is indicated in rare cases (if spreading, compromises major branches of aorta, etc)





What do grafts do in aortic dissection?

they "seal" the entry site of dissection, so that false lumen can thrombose and close



What is the clinical presentation of aortic dissections?

sudden, severe pain with "rearing" or "ripping" quality in the anterior chest (typical type A dissection) or between the scapulae (type B dissections). the pain travels as dissection spreads and can radiate anywhere in thorax and abdomen. painless dissections rare (6.4%)

some physical findings:

hypertension (either as cause or secondary to severe pain (sympa response) or decreased renal vascular flow (renin-angiotensin activated)

if dissection occludes one of the subclavian arteries, there may be a difference in systolic bp between arms

neurologic deficits may accompany dissection into the carotid vessels. 

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What is peripheral artery disease (PAD)?

Peripheral artery disease (PAD) is an occlusion or stenosis (narrowing) of an artery that provides blood to the limbs. 


List causes of peripheral artery disease (PAD)?






What is the most common cause of PAD?



What are major risk factors for atherosclerotic PAD?


diabetes mellitus




about 40% of PAD patients also have CAD

=> 2x increase in cardiovascular death if diagnosed with PAD



What is the relationship between blood flow, vessel radius and length?

Poiseuille's equation:

delta P = pressure drop across stenosis

r = vessel radius

n = blood viscosity

L= length of stenosis

the degree of vessel narrowing by the stenosis (change in r) has the gratest impact on flow

also for stenoses of same radius and legth, the greater the pressure drop, the greater the flow

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Compare normal physiology of arteries during exercise to that of peripheral artery disease due to atherosclerosis?

exercise -> muscle metabolism -> adenosine, etc released -> act locally to dilate arterioles -> decrease in vascular resistance -> increase in blood flow to active muscle -> increased flow stimulates healthy arterial endothelium to release more vasodilating factors (ex. NO) -> increased radii of upstream vessels


PAD -> obstructed artery -> cannot respond to vasodilating muscle stimuli -> flow does not increase accordingly + atherosclerotic endothelium does not release normal amounts of vasodilating substances -> lack of adequate blood flow to distal tissues -> ischemia


What are characteristics of peripheral artery disease due to atherosclerosis?

reduced blood flow to extremities

=> changes in muscle fiber metabolism + atrophy to adapt to intermittent ischemia -> changes in muscle structure and function (weak limbs)

dramatic reduction in exercise capacity 

severe peripheral atherosclerosis may reduce limb flow so that it cannot even provide enough blood for resting state -> worry about tissue necrosis and gangrene -> risk of limb amputation


What is the clinical presentation of PAD?

most frequently affects lower limbs

starts with buttock, thigh or calf discomfort after exercise/walking, disappears after rest

exertional limb fatigue and pain is called claudication

location of claudication is the location of diseased artery

in severe PAD, patients may experience pain at rest, usually of feet and toes.

lack of blood flow increaes chances of ulcers, infection and skin necrosis, especially for patients who smoke or who have diabetes mellitus

physical exam generally shows loss of pulse below arterial obsturction. bruits (swishing soungs auscultaged over a region of turbulent blood flow) may be heard 

in patients with chronic severe ischemia, lack of blood flow -> muscle atrophy, pallor, cyanotic discoloration, hair loss at site, occasionally gangrene and necrosis of foot and digits

ischemic ulcers possible - small wounds in areas of increased pressure or regions prone to injury, especially in diabetic patients



What do you look for on a physical if peripheral artery disease is suspected?


measure ratio of blood pressure in the ankles to that in the arms (ankle-brachial index (ABI); normal ABI >=1.0 (ankle pressure is equal to or slightly greater than, that in the arms). An index

lack of blood flow increaes chances of ulcers, infection and skin necrosis, especially for patients who smoke or who have diabetes mellitus => this is why we look at feet during cardiac exam

physical exam generally shows loss of pulse below arterial obsturction. bruits (swishing soungs auscultaged over a region of turbulent blood flow) may be heard

in patients with chronic severe ischemia, lack of blood flow -> muscle atrophy, pallor, cyanotic discoloration, hair loss at site, occasionally gangrene and necrosis of foot and digits

ischemic ulcers possible - small wounds in areas of increased pressure or regions prone to injury, especially in diabetic patients



What is ankle-brachial index (ABI)?

used in the evaluation of peripheral artery disease

measure ratio of blood pressure in the ankles to that in the arms (ankle-brachial index (ABI); normal ABI >=1.0 (ankle pressure is equal to or slightly greater than, that in the arms). An index


what is claudication?

claudication = pain and discomfort that happens during exercise/walking, which disappears at rest

suspect peripheral artery disease


What are treatment options for peripheral artery disease?

- antiplatelet therapy (Aspirin have been shown to reduce CV morbidity and mortality in patients with PAD)

- risk factor modification (smoking cessation, lipid lowering, control of diabetes and hypertension)

- supportive care of the feet to prevent trauma or restriction of blood flow - exercise, esp walking is recommended: formal exercise program is considered first-line therapy

-cilostazol is drug that increases cyclic adenosine monophosphate and has vasolidating and platelet inhibiting proerties, also shown to increase exercise capacity for patients with PAD

- most vasodilator drugs not helpful in relieving claudication

- mechanical revascularization is indicated when conventional therapy failed in patients with disabling claudication and as first-line therapy in cases of severe limb ischemia

- stents and bypass operations to bypass occluded arteries are also possibilities

- amputations may be necessary if blood flow cannot be reestablished


What is essential hypertension?

essential hypertension - cause of high bp unknown, 90% of patients


What is secondary hypertension?

secondary hypertension - high bp attributed to a specific cause  - treat cause


What is hypertension?

definitions vary,  Lilly uses

diastolic >= 90 mm Hg consistently


systolic >= 140 mm Hg consistently



What is prehypertension?

systolic pressure of 120-139 mm Hg

diastolic of 80-99 mm Hg



What are the formulas for BP and CO?


where CO - cardiac output

TPR - total peripheral resistance


CO = SV x HR

SV - stroke volume

HR - heart rate



What systems are responsible for blood pressure regulation?

the heart, which supplies the pumping pressure

blood vessel tone - systematic resistance

kidney* - regulates intravascular volume of blood

hormones - regulate the function of the three above



* high BP is not just cardiovascular problem. no matter how high BP is, kidneys can return blood pressure to normal by reducing intravascular volume. kidney implant from normotensive to hypertensive typically improves bp.


What is a baroreceptor reflex?

The baroreflex or baroreceptor reflex is one of the body's homeostatic mechanisms for maintaining blood pressure.

System relies on specialized neurons, known as baroreceptors, located primarily in the aortic arch and carotid sinuses.  Baroreceptors monitor changes in bp by sensing the stretch and deformation of repsective arteries. If bp rises, the baroreceptors are stimulated, they increase transmission of nerve impulses to medulla (CNS). 



How do baroreceptors regulate BP?

The higher the rise in bp, the more baroreceptors are engaged in firing, the greater the impulse transmission rate to medulla. Carotid sinus sends signals via glossopharyngeal nerve (cranial nerve IX), aortic arch receptors communicate thorugh vagus nerve (cranial nerve X). Glossopharyngeal and vagus meet at tractus solitarius int eh medulla, where the baroreceptor impusles inhibit sympathetic nervous system and excite parasympathetic nervous system. Net result is:

1) decline in peripheral vascular resistance (vasodilation)

2) reduction in CO (because of lower HR and reduced force of cardiac contraction)

if fall in bp is sensed, fever impulses sent ot medulla, leading to increase in bp. 

baroreceptors only regulate short-term bp, as they constantly reset themselves to new values.


What are some clues that hypertension is secondary (non-essential)? Why should we care?

Secondary hypertension is often curable and may require different therapy from EH. 


  • if patient develops hypertension btwn ages 20 and 50
  • secondary hypertension often causes bp to rise dramatically, EH tends to be mild to moderate
  • often presents abruptly in a patient who was previously normotensive
  • process that leads to secondary hypertension may lead to other symptoms that can be seen on physical exam
  • lack of family history of hypertension more likely


Optional: hypertension during pregnancy

difference between gestational hypertension and pre-eclampsia

Table 34-1. Diagnosis of Hypertensive Disorders Complicating Pregnancy
Gestational Hypertension:

Systolic BP ≥140 or diastolic BP ≥90 mm Hg for first time during pregnancy
No proteinuria
BP returns to normal before 12 weeks postpartum
Final diagnosis made only postpartum
May have other signs or symptoms of preeclampsia, for example, epigastric discomfort or thrombocytopenia

Minimum criteria:

BP ≥140/90 mm Hg after 20 weeks' gestation
Proteinuria ≥300 mg/24 hours or ≥ 1+ dipstick
Increased certainty of preeclampsia:

BP ≥160/110 mm Hg
Proteinuria 2.0 g/24 hours or ≥ 2+ dipstick
Serum creatinine >1.2 mg/dL unless known to be previously elevated
Platelets < 100,000/μL
Microangiopathic hemolysis—increased LDH
Elevated serum transaminase levels—ALT or AST
Persistent headache or other cerebral or visual disturbance
Persistent epigastric pain

Seizures that cannot be attributed to other causes in a woman with preeclampsia
Superimposed Preeclampsia On Chronic Hypertension:

New-onset proteinuria ≥ 300 mg/24 hours in hypertensive women but no proteinuria before 20 weeks' gestation
A sudden increase in proteinuria or blood pressure or platelet count < 100,000/μL in women with hypertension and proteinuria before 20 weeks' gestation
Chronic Hypertension:

BP ≥ 140/90 mm Hg before pregnancy or diagnosed before 20 weeks' gestation not attributable to gestational trophoblastic disease

Hypertension first diagnosed after 20 weeks' gestation and persistent after 12 weeks postpartum

ALT = alanine aminotransferase; AST = aspartate aminotransferase; BP = blood pressure; LDH = lactate dehydrogenase.

National High Blood Pressure Education Program Working Group Report on High Blood Pressure in Pregnancy (2000).


OPTIONAL: gestational hypertension and pre-eclampsia : more info

Gestational Hypertension
The diagnosis of gestational hypertension is made in women whose blood pressure reaches 140/90 mm Hg or greater for the first time after midpregnancy, but in whom proteinuria is not identified. Almost half of these women subsequently develop preeclampsia syndrome, which includes signs such as proteinuria and thrombocytopenia or symptoms such as headaches or epigastric pain. Gestational hypertension is reclassified as transient hypertension if evidence for preeclampsia does not develop, and the blood pressure returns to normal by 12 weeks postpartum.


Proteinuria is the surrogate objective marker that defines the system wide endothelial leak, which characterizes the preeclampsia syndrome. Even so, when blood pressure increases appreciably, it is dangerous to both mother and fetus to ignore this rise because proteinuria has not yet developed. As Chesley (1985) emphasized, 10 percent of eclamptic seizures develop before overt proteinuria is identified.

As shown throughout this chapter, preeclampsia is best described as a pregnancy-specific syndrome that can affect virtually every organ system. As discussed, although preeclampsia is much more than simply gestational hypertension with proteinuria, appearance of proteinuria remains an important objective diagnostic criterion. Proteinuria is defined by 24-hour urinary protein excretion exceeding 300 mg, a urine protein:creatinine ratio of ≥ 0.3, or persistent 30 mg/dL (1+ dipstick) protein in random urine samples (Lindheimer and colleagues, 2008a). None of these values are sacrosanct. 

 Abnormal laboratory findings in tests of renal, hepatic, and hematological function increase the certainty of preeclampsia. Persistent premonitory symptoms of eclampsia, such as headache and epigastric pain, also increase the certainty. That said, some women may have atypical preeclampsia with all aspects of the syndrome, but without hypertension or proteinuria, or both (Sibai and Stella, 2009).


Headaches or visual disturbances such as scotomata can be premonitory symptoms of eclampsia. Epigastric or right upper quadrant pain frequently accompanies hepatocellular necrosis, ischemia, and edema that stretch Glisson capsule. This characteristic pain is frequently accompanied by elevated serum hepatic transaminase levels. Thrombocytopenia is also characteristic of worsening preeclampsia. It probably is caused by platelet activation and aggregation as well as microangiopathic hemolysis induced by severe vasospasm. Other factors indicative of severe preeclampsia include renal or cardiac involvement as well as obvious fetal-growth restriction, which attest to its duration.

The more profound these signs and symptoms, the less likely it is that they can be temporized, and the more likely it is that delivery will be indicated. The differentiation between nonsevere and severe gestational hypertension or preeclampsia can be misleading because what might be apparently mild disease may progress rapidly to severe disease.


The onset of convulsions in a woman with preeclampsia that cannot be attributed to other causes is termed eclampsia. The seizures are generalized and may appear before, during, or after labor. In older reports, up to 10 percent of eclamptic women, especially nulliparas, did not develop seizures until after 48 hours postpartum (Sibai, 2005). Others have reported that up to a fourth of eclamptic seizures developed beyond 48 hours postpartum (Chames and co-workers, 2002). 


What tests should be ordered to investigate cause of hypertension?

screen for secondary causes:

1) urinalysis and measurement of serum concentration of creatinine and blood urea nitrogen to evaluate for renal abnormalities

2) serum potassium level (abnormlaly low in renovascular hypertension  or aldosteronism)

3) blood glucose level (elevated in diabetes, which is strongly associated with hypertension and renal disease)

4) serum cholesterol, HDL cholesterol, and triglyceride levels, as part of the global vascular risk screen

5) electrocardiogram (for evidence of left ventricular hypertrophy caused by chronic hypertension)



What organs are damaged by hypertension?

Heart Cerebrovascular system Kidney Retina


What are examples of nonpharmacologic treatment in hypertension?

weight reduction exercise diet sodium levels potassium levels alcohol other smoking cessation relaxation therapy


Why should weight loss be considered during hypertension?

obesity and hypertension correlated, especially if fat is of central (belly) distribution. blood pressure reduction follows weight loss in a large portion of hypertensive patients who are more than 10% above their ideal weights. Each 10 kg weight loss - 5-20 mm Hg fall in systolic pressure.


Why should exercise be considered in treatment of hypertension?

sedentary people have a 20-50% higher risk of developing hypertension


What are dietary considerations in hypertension?

salt restriction - sodium controversial issue, as salt should be simply excreted by kidneys, but in 50% of patients with essential hypertension, BP varies with sodium intake sensitivity to salt is more common in African Americans and elderly patients. low-salt diets tend to increase the effectiveness of antihypertensive meds in general, current recommendation is to limit salt to


What is the effect of smoking on hypertension?

smoking transiently increases BP, likely because nicotine stimulates autonomic NS smoking also a risk factor for sustained hypertension atherogenic effect of smoking may contribute to the development of renovascular hypertension


What is the effect of relaxation therapy on hypertension?

BP often rises under conditions of stress essential hypertensive patients and their relatives show higher than normal basal sympathetic tone and exaggerated autonomic response to mental stress.


What are the main classes of antihypertensive drugs?

  • diuretics
  • sympatholytic agents (alpha and beta blockers)
  • vasodilators: Calcium channel blockers, direct vasodilators
  • renin-angiotensin-aldosterone system antagonists (angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, direct renin inhibitors)


What drugs are commonly linked to hypertension?

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What drugs are commonly linked to hypertension?

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What are diuretics? How do they treat hypertension?

Diuretics reduce circulatory volume, CO, and mean arterial pressure and are most effective in patients with mild to moderate hypertension who have normal renal function.



What are thiazide diuretics. When should they be used?

Thiazide diuretics (hydrochlorothiazide) and potassium-sparing diuretics (eg. spironolactone) promote Na+ excretion in the distal nephron, with water following it, reducing circulatory volume -> reducing CO

best used in patients with normal kidney function


What are potassium-sparing diuretics?

Similarly to thiazide diuretics, potassium-sparing diuretics promote Na+ excretion in the distal nephron, with water following it, reducing circulatory volume -> reducing CO (ex. spironolactone), but spare potassium to prevent hypokalemia (common with loop diuretics)


What are loop  diuretics? When should they be used?

Loop diuretics are drugs that act on ascending loop of Henle (ex. furosemide), leading to Na+ excretion -> water follows -> urine production increases while circulatory volume decreases. They are generally too strong and their effect too short to be used in otherwise healthy hypertensive patients, but are used to lower BP in patients with renal disease, who usually do not respond to other diuretics.  

they act on Na+/K+/Cl- symporter and may lead to K+ deficiency, so that is why sometimes K+ sparing diuretics are used in combo with loops.


What are sympatholytic agents? 

Describe function of beta blockers and alpha agonists?

Sympatholytic agents include

1) beta blockers

2) central alpha-adrenergic agonists

3) systemic alpha-adrenergic-blocking drugs (alpha 1 antagonists)

beta blockers lower BP by:

  decreased HR -> reduction in CO  (CO = HR+SV)  &  mild decrease in contractility 

 decreasing secretion of renin -> angiotensin II decreases -> decrease in total peripheral resistance

less effective then diuretics in elderly and African-American

worry about bronchospasms (since beta 2 receptors blocked, which cause bronchodilation), fatigue, impotence and hyperglycemia.

centrally acting alpha 2 adrenergic agonists lower BP by:

reducing sympathetic stimulation to heart, blood vessels and kidneys

but not well liked because of sedation (think blocked sympathetic - really parasympathetic) - dry mouth, sedation, etc

systemic alpha 1- antagonists 

cause a decrease in TPR thorugh relaxation of vascular smooth muscle, useful in older men also because they also improve symptoms of prosthetic enlargement in men (alpha 1 vasoconstricts sphincters and makes it more difficult to pee, antagonist reverses it)

not greatly recommended in general population as a big trial showed that they are more risky then diuretics (more cardiovascular events) 


What are vasodilators? How do they reduce hypertension?

Vasodilators consist of direct vasodilators (hydralazine, minoxidil) and calcium channel blockers. Both reduce BP by decreasing peripheral vascular resistance.

Ca ++ blockers reduce influx of calcium, cardiac and vascular smooth muscles require Ca for contraction, so Ca++ blockers reduce cardiac contractility  and TPR. 

Studies show that Ca++ blockers reduce the chance of myocardial infarction and stroke. 

Direct vasodilators (hydralazine, minoxidil) reduce BP by directly relaxing vascular smooth muscle of pre-capillaries, but it can result in reflex increase in HR, so beta blockers are often necessary in combo. 


What are ACE inhibitors? How do they reduce blood pressure?

renin-angiotensin-aldosterone system antagonists

ACE inhibitors decrease BP by blocking the conversion of angiotensin I to angiotensin II, reducing the vasoconstricting effect that angiotensin II would have had, as well as reducing production of aldosterone angiotensin II would have stimulated.

ACE inhibitors -> peripheral vascular resistance decreases & sodium retention by kidney declines (aldosterone decreased)

ACE inhibitor also increases the concentration of vasodilator bradykinin. 


What do Angiotensin II receptor blockers do? (dah!)

renin-angiotensin-aldosterone system antagonists

block binding of angiotensin II to its receptors  -> vasodilation and reduced secretion of aldosterone -> BP falls

efficacy similar to ACE inhibitors, but generally better tolerated


What do direct renin inhibitors do?

renin-angiotensin-aldosterone system antagonists

"newly introduced class of anti-hypertensive drugs. It reduces levels of angiotensin I and II by binding to the proteolytic site of renin, thus inhibiting cleavage of angiotensinogen. Antihypertensive effectiveness is no greater than other drugs from renin-angiotensin family"


What effect do birth control pills have on blood pressure?

Estrogen in birth control pills can lead to secondary hypertension in some women. This is because estrogen stimulates liver to produce angiotensinogen, which later gets cleaved into angiotensin I (via renin) and angiotensin II (via ACE). Angiotensin II, in turn, causes vascular constriction and production of aldosterone, which causes water reabsorption in kidneys and increase in circulation volume.