Pathology of Hypertension

Question 0

Major vascular changes with all HTN?

Answer 0

Acceleration of other diseases: esp. atherosclerosis and hyalin arteriosclerosis.
Adaptive changes: vasoconstriction, medial hypertrophy, fibroelastic intimal hyperplasia.

Question 1

What’s the threshold BPs for malignant hypertension? How bad is it?

Answer 1

Diastolic > 120 mmHg or Systolic > 210 mmHg.
It’s really bad, often lethal within 2 years.
Also, it’s probably symptomatic (unlike regular HTN).

Question 2

What changes do you really only see in malignant hypertension?

Answer 2

Destructive changes: e.g. fibrinoid necrosis, hyperplastic arteriolitis.

Question 3

Where does hyalin arteriolitis come from? What’s one organ where it’s a big problem?

Answer 3

High BP -> leaky endothelium -> deposition of plasma proteins and ECM.
Often a problem in renal arterioles.
Not reversible.

Question 4

What can proliferate in HTN that will occlude renal arterioles?

Answer 4

Fibroblastic intimal hyperplasia happens, reduces lumen diameter greatly.
(This is not reversible.)

Question 5

What’s the problem with irreversible changes such as fibroblastic intimal proliferation and hyalin arteriolitis?

Answer 5

They cause a permanent increase in SVR, making treatment of HTN very difficult.

Question 6

When does hyperplastic intimal arteriolitis happen? What does it look like?

Answer 6

This happens in malignant hypertension.

It is concentric proliferation of vascular smooth muscle that looks like “onion skinning.”

Question 7

What should you think if you see a bunch of schistocytes (RBC fragments) on a blood smear? (in the context of a HTN lecture)

Answer 7

Blood is being forced through fibrin clots at high pressures.
This is seen in malignant hypertension, and called microangiopathic hemolytic anemia.

Question 8

5 outcomes of “benign” hypertension?

Answer 8

CHF
Stroke
MI
Renal failure
Malignant hypertension

Question 9

Cardiac effects of HTN?

Answer 9

LV hypertrophy -> CHF, coronary atherosclerosis -> MI/angina/CHF.

Question 10

Cerebral effects of HTN?

Answer 10

Microaneurysms

Berry aneurysms

Question 11

Why does reduced blood flow to kidney (caused by atherosclerosis / hyalin arteriolitis) worsen HTN?

Answer 11

Lower GFR -> less Na+ and H2O excretion.

But also: Juxtaglomerular apparatus thinks that low blood flow is because of low BP -> activation of RAAS.

Question 12

Does HTN fuck up your eyes?

Answer 12

Yeah. Retinal microaneurysms.

Question 13

Can HTN cause intracerebral hemorrhage?

Answer 13

Yeah, it can make your brain bleed. Like these lectures.

Question 14

Neuro review: Should you place a clip on the middle cerebral artery when trying to clamp off a big old berry aneurysm?

Answer 14

Nope, unless you’re really trying to get nice example of a berry aneurysm from the autopsy.

Question 15

Even if malignant hypertension is adequately treated, what’s the 5 year mortality?

Answer 15

75%

Question 16

Symptoms of malignant hypertension?

Answer 16

Visual changes, headache, hematuria.

Question 17

P.E. findings in malignant hypertension? (other than high BP, of course)

Answer 17

Papilledema, retinal hemorrhages, “exudates”

Question 18

Lab findings in malignant HTN?

Answer 18

Azotemia (lots of nitrogen) with proteinuria and hematuria, microangiopathic hemolytic anemia, RAAS activation

Question 19

Effect of malig. HTN on kidneys?

Answer 19

Acute cortical necrosis (grossly, this looks like alternating infarct and hemorrhage)

Question 20

Cerebral effect of malig. HTN?

Answer 20

Edema with increased ICP

Question 21

What do you see in retinas with malig. HTN?

Answer 21

Papilledema

Flame shaped hemorrhages (ruptured aneurysms)

Question 22

4 organs/processes ultimately responsible for secondary HTN (not necessarily the root cause, though)?

Answer 22

Renal - increased renin, decreased Na+ excretion.
Adrenal - too much aldosterone, cortisol, or catecholamines.
Pregnancy - pre-eclampsia.
Increased ICP - vasomotor control in brainstem?

Question 23

What in the kidney senses Na+ levels?

Answer 23

The macula densa of the distal tubule.

Question 24

How does renal artery stenosis cause secondary HTN?

Answer 24

Mainly activation of RAAS. (assuming just one artery is blocked, GFR probably isn't the limiting step)

Question 25

2 main cause of renal artery stenosis?

Answer 25

``` Atherosclerosis Fibromuscular dysplasia (concentric narrowing - affects mainly younger women - it's rare) ```

Question 26

3 adrenal causes of secondary hypertension?

Answer 26

Cortical adenoma -> aldosterone Cushing's -> cortical hyperplasia -> glucocorticoids Pheochromocytoma -> catecholamines

Question 27

2 morphological classifications of aneurysms?

Answer 27

Saccular (it's a bulging sack) Fusiform (literally, "tapering at both ends" or "spindle shaped" - the vessel increases in diameter over part of its length)

Question 28

3 ways aneurysms cause symptoms?

Answer 28

Mass effect Thromboembolus generation Rupture

Question 30

What does LaPlace tell you about aneurysms?

Answer 30

As radius increases, pressure increases, and/or wall thickness decreases, the wall tension increases,making rupture more likely. (this... is pretty intuitive)

Question 31

What actually happens in a dissecting aneurysm / hematoma?

Answer 31

Weakness ("degeneration") in the media combined with a ruptured vasa vasorum leads a hematoma to form between the media and adventitia... which then extends in either direction. Usually an "exit site" forms that connects the hematoma to the lumen. Sometimes there's a site of reentry into the lumen. This can lead to hemorrhage if it breaks through the adventitia.

Question 32

When there's a exit site (lumen -> hematoma) in a dissecting hematoma of the aorta, where is it usually located?

Answer 32

Usually in ascending aorta just above the aortic valve.

Question 33

Treatment for dissecting (aortic) hematoma?

Answer 33

Replace involved portion of aorta with a vascular prosthesis. Meds to decrease BP and LV contractile force.

Question 34

Signs/symptoms of dissecting hematoma? (3 things)

Answer 34

Pain - migrating anterior chest-> back -> abdomen. Blocked aortic branches -> loss of pulses depending on which blocked. Rupture - exsanguination symptoms, cardiac tamponade (if inferior to the pericardial reflection - see slide 76).