Tag Archives: hypertension

Malignant Hypertension

Malignant Hypertension and Accelerated Nephrosclerosis

Gross Appearance:size dependent on duration of hypertension. Pinpoint hemorrhages “flea bitten”

Histology

1. arterioles: fibrinoid necrosis
2. arteries and arterioles: fibroelastic hyperplasia (onion-skinning)
3. glomeruli: necrotizing glomerulitis

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Endometrial Carcinoma

Endometrial Carcinoma

Features of Endometrial Carcinoma

1. glands back to back
2. desmoplastic reaction
3. endometrial stromal foam cells (seen in hyperplasia too)

Risk Factors for Endometrial Carcinoma

- estrogen use, tamoxifen
- obesity, Diabetes, Hypertension, Polycystic ovarian syndrome,
- functioning granulosa cell and thecoma tumours
- gonadal dysgenesis (Turner syndrome)

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Pheochromocytoma Tumor

Pheochromocytoma

Familial syndromes associated with Pheochromocytoma:
- MEN IIa
- MEN IIb
- VHL
- NF1
- Sturge Weber

Clinical presentation: Hypertension

Gross: variable size, hemorrhage,

Microscopy:

- zellballen pattern (small nests of polygonal cells) “often a bit spindly” and rich vascular network
- atypia often present
- can get capsular invasion with benign, so need metastases to call pheochromocytoma malignant

Immunohistochemistry: chromogranin, synaptophysin, S-100 positive sustentacular cells
Electron microscopy: dense core membrane bound neurosecretory granules
Laboratory and biochemistry: metanephrines, VMA (vanillyl mandelic acid)
Note: extra-adrenal pheochromocytomas more often malignant than adrenal

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Pulmonary hypertension

Pulmonary hypertension

Causes of Pulmonary Hypertension

•    Chronic obstructive or interstitial lung disease (eg. UIP)

•    Antecedent congenital or acquired heart disease (eg. mitral stenosis)

•    Recurrent thromboemboli

•    Autoimmune disease (eg. systemic sclerosis)

•    Idiopathic (primary) pulmonary hypertension

Microscopic features seen with increasing severity

•    Grade 1 = medial hypertrophy of arteries and muscularisation of arterioles

•    Grade 2 = intimal proliferation in arteries

•    Grade 3 = intimal concentric laminar fibrosis prominent in muscular arteries

•    Grade 4 = dilatation of small arteries with development of plexiform lesions

•    Grade 5 = plexiform and angiomatoid lesions prominent; hemosiderin deposition

•    Grade 6 = necrotising arteritis

Pulmonary hypertension complications

•    Cor pulmonale

•    Thromboembolism

•    Pneumonia

•    Pulmonary artery atherosclerosis

•    Sudden death

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Berry Aneurysm

Berry  Aneurysm

Most common locations of Berry Aneurysms:

·         Anterior cerebral artery (anterior communicating artery)

·         Middle cerebral artery

·         Internal carotid artery

Associated systemic conditions for Berry Aneurysms:

·         ADPCKD

·         Ehlers-Danlos syndrome (type IV)

·         Neurofibromatosis type 1

·         Marfan syndrome

·         Coarctation of aorta

·         Fibromuscular dysplasia of extracranial arteries

Predisposing factors for Berry Aneurysms:

-   Cigarette smoking and hypertension are

Berry Aneurysm Gross Features

Unruptured aneurysms are a thin-walled arterial outpouchings at branch points of the circle of Willis or a major vessel just beyond. Measure 2-3 mm and are shiny, bright red surface with thin, translucent wall. Atheromatous plaques, thrombosis, or calcification may be found in wall or lumen of aneurysm. Brownish discolouration of brain/meninges indicates previous hemorrhage. Rupture occurs at apex of sac with extravasation of blood to subarachnoid space, substance of brain, or both.

Histological Features of Berry Aneurysms:

Arterial wall adjacent to aneurysm shows intimal thickening and attenuation of media as it approaches the neck of the aneurysm. At the neck of the aneurysm the muscular wall and intimal elastic lamina stop short and are absent from the aneurysmal wall itself. The sac is made up of thickened, hyalinised intima. The adventitia covering the sac is continuous with that of the parent artery

References:

Robbins Basic Pathology 7th ed, edited by Vinay Kumar, Ramzi S. Cotran, and Stanley J. Robbins, 873 pp, Philadelphia, Pa, Sounders, 2003.

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