L29- CVS Pathology VII Flashcards
HTN levels and Classifications
- Normal: <120/80
- Elevated: SBP 120-129, DBP <80
- Stage 1: SBP 130-139, DBP 80-89
- Stage 2: SBP >140, DBP >90
- Crisis: SBP >180, DBP >120
- (1)% of people have HTN
- (2) are the leading risk factors
- (3) are the chronic complications
1- 25%
2- DM, smoking, hyperlipidemia
3- end organ damage, vascular damage —- ‘silent killer’ b/c only Dx when Sxs appear
BP = (1)
2) list the 4 factors affecting and regulating BP/(1
1- BP = CO * PVR 2: -endocrine: RAAS, ANP, ADH, aldosterone -neural: SNS, PSNS -blood volume: Na, mineralcorticoids, ANP -cardiac: HR, contractility
most HTN is (primary/secondary)
primary / essential, 95%
what are the secondary causes of HTN (disease)
(5-10% of all HTN)
- Renal: glomerulonephritis, RAS
- Endocrine: Cushing’s, phemochromocytoma, OCP, myxedema, acromegaly, etc.
- Vascular: coarctation of aorta, aortic insufficiency, polyarteritis nodosa
- Neurogenic: psychogenic, polyneuritis, intracranial pressure
list the 3 main end organ damages caused by HTN
- renal failure
- LV failure
- hypertensive encephalopathy
what are the 2 pathological features seen on small blood vessels due to HTN
- hyaline arteriolosclerosis
- hyperplastic arteriolosclerosis
describe hyaline arteriolosclerosis
- homogenous, pink, hyaline thickening of Arteriole walls + loss of structural details and lumen narrowing
- plasma leakage across endothelium + inc ECM production via SM cells
- chronic hemodynamic stress via HTN OR metabolic stress via DM accentuates endothelial injury
describe hyperplastic arteriolosclerosis
- related to acute and or severe BP elevations
- ‘onion-skin’, concentric, laminated Arteriole walls thickening + lumen narrowing
- Necrotizing Arteriolitis: fibrinoid deposition and acute vessel wall necrosis
what are the HTN complications in:
(1) small BVs
(2) large BVs
(3) brain
(4) eyes
(5) heart
(6) kidney
1- hyaline and hyperplastic arteriolosclerosis
2- atherosclerosis (foam cells, SM cells)
3- cerebral hemorrhage, infarction
4- HTN retinopathy
5- LVH, HTN CM => IHD, MI
6- nephrosclerosis (benign, malignant)
Vasculitis is defined as (1), involving (2). Classification of vasculitis is based on (3) and (4). Symptoms of vasculitis include (5).
1- inflammation, necrosis 2- arteries, veins, capillaries 3- vessel type 4- etiology 5- local Sxs + constitutional Sxs: fever, myalgia, arthralgia, malaise
what are the possible etiologies of vasculitis
1) immunological
2) direct infection (bacterial, rickettsial, spirochetal, fungal)
3) unknown
what are examples of vasculitis with ‘unknown’ causes (etiology)
- Giant Cell (temporal) arteritis
- Takayasu arteritis
- Polyarteritis nodosa
what are the 4 immunological mechanisms of vasculitis
- IC mediated: HBC/HCV, SLE/RA, drug induced
- ANCA (antineutrophil cytoplasmic Ab mediated): Wegener’s granulomatosis, Churg-Strauss syndrome
- direct Ab attack mediated: Kawasaki disease (anti-endothelial cell Abs)
- cell mediated: allograft organ rejection
ANCA, aka (1), comes in type (2) and (3). It is defined as a group of (4) targeted against (5) found in (6) cells.
1- anti-neutrophilic cytoplasmic antibodies
2- Anti-Proteinase-3 (PR3-ANCA, c-ANCA)
3- Anti-Myeloperoxidase (MPO-ANCA, p-ANCA)
4- auto-Abs
5- enzymes
6- primary granules in neutrophils, lysosomes of monocytes, endothelial cells
Note- neutrophil degeneration/degranulation –> release of CKs –> BV inflammation
(1) is the most common vasculitis that mainly affects the following vessels: (2). Its pathogenesis mainly involves (3).
1- Giant Cell Arteritis (GCA, aka temporal arteritis)
2- arteries in the head: Aorta (giant cell aortitis), temporal artery, vertebral artery, ophthalmic artery (=> blindness)
3- unknown // possibly due to T-cell rxn against elastin
GCA mainly affects people of (1) age and affects (males/females) more. General symptoms include (3). If localized to ophthalmic artery, (4) symptoms are evident.
(giant cell / temporal arteritis)
1- >50 y/o
2- equal M=F
3- fever, weight loss, fatigue, facial pain, HA
4- diplopia, progressive hazy vision, vision loss
list and describe the critical pathological features of GCA
(giant cell / temporal arteritis)
- focal, nodular thickening + lumen narrowing
- granulomatous inflammation of intima and media
- giant cell, mononuclear infiltration
- fragmentation of internal elastic lamina
Diagnosis of GCA requires (1) and (2), in addition to its association with (3). It is treated with (4) and has a (good/bad) prognosis.
1- elevated ESR 2- temporal artery biopsy: 2-3 cm segment / multiple sections with elastic trichrome stain 3- polymyalgia rheumatica 4- steroids, analgesics 5- good
(1) is a granulomatous vasculitis of medium and large arteries leading to (2). It will commonly infect (3) vessel with (2) at (4) of the associated vessels of (3). Other common arteries involved are (5). It has a (6) etiopathogenesis.
1- Takayasu arteritis 2- narrowing and obliteration of lumen 3- aortic arch 4- origin of great vessels branching from arch 5- pulmonary, coronary, renal arteries 6- unknown
Takayasu most affects (1- age*, sex) people. It has the following:
- ocular changes, (2)
- upper limb changes, (3)
- neurological changes, (4)
1- <40* y/o females
2- visual disturbances, retinal hemorrhages, blindness
3- low BP + progressive diminution of UL pulses w/ coldness or numbness of fingers —- ‘pulseless disease’
4- dizziness, focal weakness, complete hemiparesis
describe the gross and histological changes seen in Takayasu disease
Gross: irregular thickening of aorta / branch vessel wall w/ intimal wrinkling and lumen narrowing
Histo:
- mononuclear media inflammation w/ granulomatous change –> patchy necrosis
- collagenous fibrosis in all vessel wall layers
(1) is a systemic vasculitis involving (2) type vessels and sparing (3) type vessels. Typically it involves (2) type vessels in (4) areas, and importantly spares (5).
1- PAN, polyarteritis nodosa 2- small, medium muscular arteries (transmural necrotizing inflammation) 3- arterioles, capillaries, venules 4- renal, visceral arteries 5- pulmonary circulation
PAN mostly affects (1) people in a (acute/chronic) course. 30% of patients will have evidence of (3) infection. Constitutional symptoms include (4) and localized symptoms can be evident in (5), where (6) are importantly spared.
(polyarteritis nodosa)
1- young adults
2- acute, subacute, chronic and often remittent
3- HBV Ag in serum
4- aches/pains, HTN, peripheral nerve damage
5- infarctions: MI, hepatic infarcts, gangrene, bowel infarcts, renal infarcts
6- lungs
