Cardiology > HTN Pathology > Flashcards

HTN Pathology Flashcards

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1
Q

secondary vs primary HTN

A

-secondary: 5-10%; with some identified underlying disease most often renal or adrenal -primary: 90-95%; no identified underlying single cause; probably multigene controlled plus environment

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2
Q

Benign vs Malignant HTN

A

-benign: 95%; diastolic>90 or systolic >140; clinically silent until late in the course -malignant: 5% usually follows benign HTN after 8 years but can rarely be de novo; diastolic >120, systolic >210; likely clinically symptomatic; LETHAL if not treated rapidly and adequately; usually in patients with secondary HTN

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3
Q

Vascular changes in HTN that are not unique to HTN

A

-acceleration of other vascular diseases like atherosclerosis, hyalin arteriolosclerosis; seen with any HTN

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4
Q

Vascular changes unique to HTN

A

-1. adaptive: vasoconstriction of arterioles, medial hypertrophy of large/medium arteries, fibroelastic intimal hyperplasia of small arteries; seen with any HTN 2. destructive: fibrinoid necrosis, hyperplastic arteriolitis (concentric proliferation of SMCs and interstitial PGs), microangiopathic hemolytic anemia; SEEN WITH MALIGNANT HTN ONLY!

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5
Q
A

fatty streaks in aorta (the early lesion of atherosclerosis)

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6
Q
A

hyaline arteriolosclerosis (within kidney)

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7
Q
A

intimal fibroelastic hyperplasia in small renal artery

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8
Q

Examples of reversible vs irreversible changes in vascular resistance and what the consequences are

A
  • function and some structural changes are reversible: vasoconstriction, medial hypertrophy
  • some structural changes are irreversible: arterial fibroelastic intimal hyperplasia, hyalin arteriolosclerosis, advanced atherosclerosis
  • irreversible changes lead to a fixed increase in vascular resistance, making rx more difficult
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9
Q

3 destructive changes of malignant HTN

A
  • fibrinoid necrosis
  • hyperplastic intimal arteriolitis
  • microangiopathic hemolytic anemia
  • all of these occuring in arterioles
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10
Q
A

fibrinoid necrosis in malignant HTN; a destructive change occuring due to deposition of fibrin and other plasma proteins in the walls of arterioles, associated with the necrosis of endothelial cells and medial smooth muscle

-top arrow is fibrinoid necrosis; bottom is lumen

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11
Q
A

hyperplastic intimal arteriolitis (destructive changes in malignant HTN): concentric proliferation of SMCs and interstitial PG deposition in small arteries and arterioles

  • onion skinning appearance
  • due to healing of fibrinoid necrosis acute lesions and probably driven by PDGF
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12
Q
A

Microangiopathic Hemolytic anemia (MAHA): shearing off of red cell fragments resulting in schistocytes by passage through fibrin mesh at increased pressures within the lumen of arterioles

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13
Q

Clinical manifestations of benign HTN :The silent killer

A
  • benign HTN is silent until…
    1. CHF
    2. MI
    3. Stroke
    4. chronic renal failure
    5. subsequent malignant HTN
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14
Q

Cardiac lesions due to effects of HTN

A

-concentric LVH, accelerated coronary atherosclerosis (leading to angina, MI, CHF): increased demand but decreased O2 supply

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15
Q

Renal lesions due to effects of HTN

A

-nephroarteriolosclerosis= microvascular disease with glomerlar scarring and tubular atrophy –> chronic renal failure

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16
Q

cerebral effects due to HTN

A

-microaneurysms ( –> intracerebral hemorrhage), lacunae, rupture of berry aneurysm (SAH), accelerated atherosclerosis leading to possible ischemic infarction

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17
Q
A

hypertrophied myocytes in HTN

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18
Q

3 effects of cLVH

A
  • increased myofibrils, increases energy requirements, less efficient function
  • as myocardial arteries compromised, decreased peak myocardial blood flow leading to ischemia, atrophy, fibrosis
  • decreased compliance of LV with impaired diastolic filling and impaired systolic contractility
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19
Q
A

hyaline arteriolosclerosis with glomerular sclerosis and tubular atrophy due to HTN

-benign nephrosclerosis

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20
Q

5 components of renal benign nephrosclerosis

A
  1. bilateral symmetrical moderate decrease in size with decrease in cortical thickness
  2. granular surface
  3. vascular changes: hyaline arteriolosclerosis
  4. gradual fibrosis replacement of glomeruli (glomerulosclerosis) and associated tubular atrophy due to chronic ischemia
  5. possible progression to chronic renal failure
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21
Q

Nephroarteriolosclerosis is a microvascular disease with glomerular scarring and tubular atrophy which can lead to chronic renal failure. What are effects of this process that make HTN even worse?

A
  • decreased GFR and decreased Na secretion
  • activation of RAAS
  • loss of urodilatin *or some naturetic factor of renal origin)
  • general loss of renal excretory function to produce chronic renal failure
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22
Q
A

microaneurysms in retina due to HTN

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23
Q

Who gets malignant hypertension?

A
  • usually preceded by benign HTN for avg of 8 years
  • 35-50 years old
  • more frequent in men, smokers, AAs, pts of lower SES
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24
Q

Mortality of malignant HTN if treated vs untreated

A
  • 90% mortality within 1 year if untreated
  • 75% 5 year survival if treated properly
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25
Symptoms, phyisical exam and lab findings of malignant HTN
- sxs: visual impairment (scotoma), headache, nausea, vomiting (collectively called HTN encephalopathy), hematuria - PE: papilledema, retinal hemorrhage and exudates - lab: azotemia with proteinuria and hematuria, MAHA, RAAS activation
26
Organ effects of malignant HTN
1. renal: destructive vascular changes (malignant nephrosclerosis), acute cortical necrosis, hemorrhage and infarcts 2. adrenal: cortical hyperplasia 3. cerebral: edema, increased intracranial pressure
27
retinal flame shaped hemorrhages and papilledema in malignant HTN
28
acute cortical necrosis of the kidney in malignant HTN: extensive areas of hemorrage and infarction with little preserved parenchyma
29
top: hemorrhage, bottom: infarct - renal cortical necrosis in malignant HTN
30
Causes of death in malignant HTN
- acute renal failure (acute cortical necrosis) - stroke - acute congestive heart failure +/- acute MI
31
Causes of death from HTN over all
- CHF (acute or chronic) 26% - CVA (acute) 15% - renal failure (usually chronic): 20% - coronary artery disease (acute): 10%
32
4 causes of secondary HTN
1. renal: increase RAAS, decrease Na excretion, GFR and naturesis, renoprival (medullary destruction) ex urodilatin 2. adrenal: increase aldosterone, GCs from cortex, or catechols from medulla 3. pregnancy: pre-eclampsia (increase due to placental anti-angiogenic substance like sFLT-1) 4. increased intracranial pressure though to directly act on vasomotor center in brainstem
33
red box: top is afferent arteriole, bottom is juxtaglomerular cells containing renin granules - green box left is distal tubule and right is macula densa yellow: JG apparatus
34
1. proximal tubular 2. JG cells (blue with renin granules) 3. Afferent arteriole 4. macula densa 5. distal tubule
35
2 main causes of renal artery stenosis and their differences
- atherosclerosis: proximary renal artery, eccentric narrowing, older patients, usually unilateral - fibromuscular dysplasia: middle to distal renal artery, concentric narrowing usually of the media, younger patients, often women, rare; can be bilateral
36
Conn's Syndrome vs Cushing's Syndrome
- conn's: excess aldosterone production usually due to adrenal cortical adenoma, rarely hyperplasia - cushing's: due to agrenal cortical hyperplasia, adenoma, or rarely carcinoma, also iatrogenic steroid treatment
37
Pheochromocytoma
- adrenal medullary neoplasm - episodic HTN
38
adrenal coritical adenoma: Conn's syndrome
39
adrenal cortical hyperplasia: Cushing's syndrome
40
pheochromocytoma: note its not yellow like cortical adenoma or hyperplasia bc doesn't make steroids and thus use lipid
41
Define aneurysm and their morphology/implications
- localized dilation of a blood vessel, usually an artery. - saccular vs fusiform - saccular is eccentric, spherical, and lumen is out of mainstream of blood flow and therefore is more likely to experience stasis and fill with thrombus - fusiform: circumferential and lumen is traversed by mainstream of flow
42
3 examples of true aneurysms and the category that is historically, yet incorrectly, included
- true: berry, atherosclerotic, syphilitic - dissecting hematoma is misnomer
43
left is saccular vs right fusiform aneurysm
44
Berry Aneurysm
saccular aneurysms of cerebral arteries, usually in or near Circle of Willis at branch points (ICA/MCA junction), usu. related to congenital weakness in arterial wall, with slow enlargement over years, perhaps aggravated by systemic hypertension in some patients; cause symptoms by mass effect within the cranium or by rupture (subarachnoid hemorrhage)
45
Atherosclerotic aneurysms
occur because of acquired weakening of arterial wall by atherosclerosis (destruction of internal elastica and media by ischemic injury, due to thickening of intima by atherosclerosis and/or by direct medial injury by activation of inflammation with breakdown of matrix and smooth muscle by matrix metalloproteinases activated by angiotensin II and cyclophilin A – see reference 6- new information). 1. Most frequent cause of aortic aneurysms, especially abdominal, usually below renal arteries and above iliac bifurcation 2. Can be fusiform or saccular
46
What is the most frequent cause of aortic aneurysms?
-atherosclerosis
47
3 ways aneurysms cause symptoms by:
- mass effect: large size impinging on other structures - distal embolization from contained thrombus - rupture with extravascular hemorrhage
48
LaPlace and aneurysm rupture
-Hence, as the vessel dilates due to aneurysm formation, the increasing radius increases wall stress; if the wall is thinned in the aneurysm, this further increases wall stress. Since wall stress is a measure of the net forces attempting to tear the vessel wall, it is not surprising that as aneurysms enlarge, the likelihood of rupture increases. The likelihood of rupture is further aggravated if there is hypertension
49
Dissecting hematoma usually involves \_\_\_\_\_\_\_\_\_\_.
-thoracic aorta, abdominal aorta, and branches of aorta
50
Pathology of dissecting hematomas
Pathologically characterized by focal destruction of elastica and accumulation of extracellular mucopolysacchride, sometimes in cystic spaces (cystic medial necrosis). This results in structural weakening of the arterial media, which can result in: a. dilation (ectasia) of the arteries, e.g. widening of the aortic root and valve ring, leading to aortic regurgitation b. disruption of vasa vasorum, allowing hemorrhage in the media which can then spread or dissect along the plane of the weakened media. 2. Present in many cases of dissecting hematoma, but also in some elderly patients without dissecting hematoma. 3. Morphologically similar changes, including dissecting aneurysms, seen at earlier age in patient’s with Marfan syndrome,
51
-elastic fiber degeneration in media of aorta with dissecting hematoma
52
Symptoms of dissecting aortic hematoma
pain: tearing, migratory (anterior to posterior chest to back to abdomen) - blocked aortic branches: loss of pulse on one side if subclavian, stroke is carotid, angina/MI if coronary - rupture: exsanguination into body cavity, cardiac tamponage into pericardium
53
Type A vs Type B dissections
- type A: involves ascending aorta - B: does not involve ascending aorta
54
note rupture is inferior to the pericardial reflection and therefore into the pericardial sac -causes tamponade
55
Dissecting hematoma initiation
- initiated by rupture of the vasa vasorum - can extend in either direction along media - exit site usually present, more often above aortic valve, possible reentry site distally (double barrelled aorta)
56
Pathogenesis of dissecting hematoma
- abnormally weak aterial media fails to provide good support for delicate vasa vasorum entering media from adventitia - shear forces in aortic wall from LV contractions rupture vasa vasorum, leading to intramural hemorrhage, which dissects along the plane of least resistance (ie weakened media) - this can spread antegrade or retrograde (toward heart)
57
Dissection can occur without an intimal tear, but often there is one (exit tear) in the aorta, most often \_\_\_\_\_\_\_\_\_\_\_\_\_. They may relate to high shear stress affecting the underlying weak media above the aortic valve. Once there is an intima tear, the propulsive force of LV contraction can \_\_\_\_\_\_\_\_\_\_\_\_.
- short distance above the aortic valve - promote further spread of the dissection
58
Sometimes in aortic dissections, there is a downstream second tear in the intima, allowing \_\_\_\_\_\_\_\_\_\_, which can help to limit further spread of the dissection.
-allowing reentry of blood from the false lumen back into the true lumen creating a double barrel aorta
59
Definitive treatment of dissecting aortic hematoma
replace the involved portion of aorta(and branches if necessary) withvascular prosthesis. Medical treatment is to ↓ BP and LV force of contractionwith drugs, (and↓TGF-βactivity with Losartan -experimental and used more for prophylaxis against future dissection)
60
Natural history of dissecting hematomas
- 35% fatal in 15 minutes - 75% fatal in 1 week if untreated - 2/3 survive at least 2 years with best therapy
Cardiology
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