Pathology of Hypertension Flashcards
Major vascular changes with all HTN?
Acceleration of other diseases: esp. atherosclerosis and hyalin arteriosclerosis.
Adaptive changes: vasoconstriction, medial hypertrophy, fibroelastic intimal hyperplasia.
What’s the threshold BPs for malignant hypertension? How bad is it?
Diastolic > 120 mmHg or Systolic > 210 mmHg.
It’s really bad, often lethal within 2 years.
Also, it’s probably symptomatic (unlike regular HTN).
What changes do you really only see in malignant hypertension?
Destructive changes: e.g. fibrinoid necrosis, hyperplastic arteriolitis.
Where does hyalin arteriolitis come from? What’s one organ where it’s a big problem?
High BP -> leaky endothelium -> deposition of plasma proteins and ECM.
Often a problem in renal arterioles.
Not reversible.
What can proliferate in HTN that will occlude renal arterioles?
Fibroblastic intimal hyperplasia happens, reduces lumen diameter greatly.
(This is not reversible.)
What’s the problem with irreversible changes such as fibroblastic intimal proliferation and hyalin arteriolitis?
They cause a permanent increase in SVR, making treatment of HTN very difficult.
When does hyperplastic intimal arteriolitis happen? What does it look like?
This happens in malignant hypertension.
It is concentric proliferation of vascular smooth muscle that looks like “onion skinning.”
What should you think if you see a bunch of schistocytes (RBC fragments) on a blood smear? (in the context of a HTN lecture)
Blood is being forced through fibrin clots at high pressures.
This is seen in malignant hypertension, and called microangiopathic hemolytic anemia.
5 outcomes of “benign” hypertension?
CHF Stroke MI Renal failure Malignant hypertension
Cardiac effects of HTN?
LV hypertrophy -> CHF, coronary atherosclerosis -> MI/angina/CHF.
Cerebral effects of HTN?
Microaneurysms
Berry aneurysms
Why does reduced blood flow to kidney (caused by atherosclerosis / hyalin arteriolitis) worsen HTN?
Lower GFR -> less Na+ and H2O excretion.
But also: Juxtaglomerular apparatus thinks that low blood flow is because of low BP -> activation of RAAS.
Does HTN fuck up your eyes?
Yeah. Retinal microaneurysms.
Can HTN cause intracerebral hemorrhage?
Yeah, it can make your brain bleed. Like these lectures.
Neuro review: Should you place a clip on the middle cerebral artery when trying to clamp off a big old berry aneurysm?
Nope, unless you’re really trying to get nice example of a berry aneurysm from the autopsy.
Even if malignant hypertension is adequately treated, what’s the 5 year mortality?
75%
Symptoms of malignant hypertension?
Visual changes, headache, hematuria.
P.E. findings in malignant hypertension? (other than high BP, of course)
Papilledema, retinal hemorrhages, “exudates”
Lab findings in malignant HTN?
Azotemia (lots of nitrogen) with proteinuria and hematuria, microangiopathic hemolytic anemia, RAAS activation
Effect of malig. HTN on kidneys?
Acute cortical necrosis (grossly, this looks like alternating infarct and hemorrhage)
Cerebral effect of malig. HTN?
Edema with increased ICP
What do you see in retinas with malig. HTN?
Papilledema
Flame shaped hemorrhages (ruptured aneurysms)
4 organs/processes ultimately responsible for secondary HTN (not necessarily the root cause, though)?
Renal - increased renin, decreased Na+ excretion.
Adrenal - too much aldosterone, cortisol, or catecholamines.
Pregnancy - pre-eclampsia.
Increased ICP - vasomotor control in brainstem?
What in the kidney senses Na+ levels?
The macula densa of the distal tubule.
How does renal artery stenosis cause secondary HTN?
Mainly activation of RAAS. (assuming just one artery is blocked, GFR probably isn’t the limiting step)
2 main cause of renal artery stenosis?
Atherosclerosis Fibromuscular dysplasia (concentric narrowing - affects mainly younger women - it's rare)
3 adrenal causes of secondary hypertension?
Cortical adenoma -> aldosterone
Cushing’s -> cortical hyperplasia -> glucocorticoids
Pheochromocytoma -> catecholamines
2 morphological classifications of aneurysms?
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)
3 ways aneurysms cause symptoms?
Mass effect
Thromboembolus generation
Rupture
What does LaPlace tell you about aneurysms?
As radius increases, pressure increases, and/or wall thickness decreases, the wall tension increases,making rupture more likely.
(this… is pretty intuitive)
What actually happens in a dissecting aneurysm / hematoma?
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.
When there’s a exit site (lumen -> hematoma) in a dissecting hematoma of the aorta, where is it usually located?
Usually in ascending aorta just above the aortic valve.
Treatment for dissecting (aortic) hematoma?
Replace involved portion of aorta with a vascular prosthesis.
Meds to decrease BP and LV contractile force.
Signs/symptoms of dissecting hematoma? (3 things)
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).
