Overview of HTN: Epidemiology and Consequences AND Pathology of HTN

Question 1

T/F Hypertension encompasses a large group of disorders.

Answer 1

T

Question 2

Two broad groups of htn

Answer 2

1. primary/essential: resistance or compliance htn

2. secondary

Question 3

What is the underlying abnormal regulation that contributes to htn?

Answer 3

drysregulated svr supplemented by abnormal regulation of sodium/fluid and abnormal fibrosis of tissues

Question 4

Consequences of htn: left ventricle

Answer 4

higher systolic pressure, higher systolic wall stress, hypertrophy, fibrosis of myocardium leading to impaired diastolic relaxation

Question 5

Consequences of htn: arterial system

Answer 5

increased wall stress, arterial vascular disease (aneurysms, atherosclerosis), arteriolar disease (obliterative destruction of systemic arterioles) leading to even more increased SVR

Question 6

Consequences of htn: kidney

Answer 6

destruction of kidney due to arteriolar destruction leading to even more reduced ability to excrete sodium –> nephroarteriolosclerosis

Question 7

Why is htn regarded the “silent killer”?

Answer 7

leads to conditions that actually have lots of symptoms and damage

1. cardiac dysfunction secondary to progressive lvh and myocardial fibrosis –> increased frequency of systolic/diastolic chf
2. accelerated atherosclerotic disease in large/small arteries –> MI, stroke, aneurysm
3. renal dysnfucntion secondary to progressive renal destruction –> chronic renal failure

Question 8

What is secondary htn and how common is it?

Answer 8

5-10% of pts –> due to underlying disease process, most often renal or adrenal

Question 9

What is primary htn?

Answer 9

multigene controlled plus environmental factors leading to htn syndrome

Question 10

What is benign htn?

Answer 10

adaptive: any most people have this: diastolic bp>90 or systolic > 140 –> clinically silent until later in course

Question 11

What is malignant htn?

Answer 11

5% of pts –> usually follows benign ht –> diastolic bp>120, systolic>210 w/clinical symptoms that will be lethal if not treated rapidly

Question 12

What vascular diseases can be accelerated by htn but may exist otherwise?

Answer 12

1. atherosclerosis

2. hyaline arteriolosclerosis

Question 13

What vascular disease are the consequence of htn?

Answer 13

1. adaptive: vasoconstriction, hypertrophy, fibroelastic intimal hyperplasia
   destructive: fibrinioid necrosis, hyperplastic arteriolitis, microangiopathic hemolytic anemia

Question 14

What is the difference between adaptive and destructive htn w/regards to their according causative htn?

Answer 14

adaptive: any htn
destructive: only malignant htn

Question 15

What kinds of vascular changes are irreversible?

Answer 15

arterial fibroelastic intimal hyperplasia, hyalin arteriosclerosis, advanced atherosclerosis

vs reversible vasoconstriction, medial hypertrophy

Question 16

What is hte consequence of irreversible change

Answer 16

fixed increase in vascular resistance causing difficulty to treat

Question 17

What hypothesis explains destructive vascular changes w/htn?

Answer 17

upregulation of RAAS –> toxic effects on blood vessels as in fibrinoid necrosis or hyperplastic intimal arteriolitis

Question 18

Consequences of htn: cardiac (not just left ventricle)

Answer 18

coronary atherosclerosis leading to CHF, angina, MI

Question 19

Consequences of htn: cerebral

Answer 19

microaneurysms, rupture of berry, lacunae, charcot-bourchard aneurysms leading to intracerebral hemorrhage, white infarcts from ischemia due to emboli from larger cerebral vessels

Question 20

Which effects of nephroarteriolosclerosis are aggravators of htn?

Answer 20

1. decreased GFR, decreased Na excretion
2. activation of RAA
3. loss of urodilatin/natriuretic peptides from kidney

loss of renal excretory function produces chronic renal failure

Question 21

Risk factors for malignant htn?

Answer 21

men, smokers, African Americans, low SES status

Question 22

Mortality associated with malignant htn?

Answer 22

90% in 1 year untreated

75% in 5 years if treated

Question 23

Clinical presentation of malignant htn

Answer 23

headache, nausea, vomiting, visual, papilledema, retinal flame-shaped hemorrhage, hematuria, proteinuria, MAHA, activation of RAAS, azotemia

Question 24

Causes of death in malignant htn

Answer 24

1. acute renal failure
2. stroke
3. acute congestive heart failure w/wo MI

Question 25

Causes of renal artery stenosis

Answer 25

1. atherosclerosis (eccentric narrowing in older patients) –> proximal artery
2. fibromuscular dysplasia (concentric narrowing in younger patients, women) –> distal to middle renal artery

Question 26

3 adrenal causes of htn

Answer 26

1. adrenal cortical adenoma
2. adrenal cortical hyperplasia
3. adrenal medullary pheochromocytoma

Question 27

Mechanisms that should prevent development of htn

Answer 27

1. baroreceptor reflex
2. pressure natriuresis
3. RAAS

Question 28

intrinsic phenomenon whereby the rate at which kidney puts out sodium in urine is determined by input blood pressure

Answer 28

pressure natriuresis

Question 29

What kind of htn? abnormality is abnormal regulation of vascular resistance

Answer 29

resistance: svr is elevated, systolic, diastolic, map elevated, pulse pressure elevated –> 150/100 typical

Question 30

What kind of htn? decreased vessel compliance/stiff pipes

Answer 30

compliance –> older people, moderately incr/normal svr, elevated systolic, modestly elevated map, pulse pressure elevated –> 170/60 typical

Question 31

What do we think renal natriuretic hormone does?

Answer 31

Na/K inhibitor –> drives up Na/Ca exchanger –> increase svr

Question 32

What happens to renal sympathetic function in those with htn?

Answer 32

increase afferent and efferent sympathetic nerve activity –> if these pathways can be calmed down, maybe therapeutic

Question 33

Receptor role on kidney: alpha-1b

Answer 33

reduce renal blood flow, reduce glomerular filtration

-renal arteriole cells

Question 34

Receptor role on kidney: alpha 1 a

Answer 34

activate Na/K atapse, increase na/h2o reabsorption

-renal tubule cells

Question 35

Receptor role on kidney: b1

Answer 35

increase renin

-jg cells

Question 36

localized dilation of blood vessel

Answer 36

aneurysm

1. saccular vs fusiform
2. berry, atherosclerotic, syphilitic
3. dissecting hematoma

Question 37

saccular vs fusiform aneurysm

Answer 37

saccular = bulges out
fusiform = involves whole circumference of blood vessel

Question 38

At what level do AAAs tend to arise?

Answer 38

below renal artery and above iliacs

Question 39

What is the etiology of AAAs?

Answer 39

1. atherosclerosis leading to ischemic injury to the media –> weakening and dilation
2. inflammatory mediators
3. htn can promote growth

Question 40

How does laplace relate to aneurysms?

Answer 40

wall pressure = P*R/W –> r, p goes up and thickness go down so increase wall stress –> tendency to grow and rupture

Question 41

What is a dissecting hematoma?

Answer 41

underlying medial necrosis leading to dilation to thoracic aortic aneurysm (ascending), sometimes cystic, accelerated by atherosclerosis, htn, marfan’s syndrome –> aortic valve insufficiency, dissection and loss of blood from vasa vasorum which rupture as aorta dilates