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
(gross appearance), PAN will affect the arteries in the following areas, (1- in order of descending frequency) particularly in (2) parts of the vessels.
PAN will show (3) in the acute stage histologically and (4) in the chronic stage.
(polyarteritis nodosa)
1- kidney, heart, liver, GIT
2- branching points
3- transmural inflammation, fibrinoid necrosis of inner half of vessel wall
4- fibrous tissue replacing inflammation –> thickening vessel wall
Note- 3/4 can co-exist in different or even the same vessel — characteristic feature
what are the complications of PAN
(polyarteritis nodosa)
-weak arterial wall due to inflammatory process –> aneurysmal dilatation, localized rupture
-perfusion impairment –> ulcerations, infarcts, ischemic atrophy, hemorrhages in supplied areas
Kawasaki disease, aka (1), involves (2) type vessels, mostly in (3) people.
1- mucocutaneous lymph node syndrome (MCLNS)
2- large, medium, small arteries (often coronary arteries)
3- young children (80% <4y/o)
Note- epidemic in Japan, leading cause of acquired heart disease in children in US
describe the pathogenesis of Kawasaki disease
- UNKNOWN
- possibly: autoantibodies against endothelium, smooth muscle cells => acute vasculitis
describe symptoms and treatment for MCLNS
(Kawasaki disease- mucocutaneous lymph node syndrome)
- fever
- conjunctival / oral erythema
- edema of hands/feet
- skin rash w/ desquamation
- enlarged cervical lymph nodes
Tx: high dose ASA, IV Igs
describe the vessel morphology of MCLNS (+ critical complication)
(Kawasaki disease- mucocutaneous lymph node syndrome)
Lesion ranges:
-mild changes limited to intima
TO
-severe destruction of all vessel wall layers by segmental necrosis + moderate fibrinoid changes + dense inflammatory cell infiltration
-acute vasculitis can => coronary aneurysm formation + associated thrombosis with MI
Buerger disease, aka (1), is characterized by the (2) of (3) type vessels. The main (3) type vessels involved are (4) with (5) also evident. It mainly affects (6- age, gender) people.
1- thromboangitis obliterans
2- segmental, thrombosing, acute and chronic inflammation
3- medium, small arteries
4- tibial or radial arteries
5- secondary extension to veins, nerves of extremities
6- males <35 y/o
what are the predisposing factors for Buerger disease
- cigarette smoking + hypersensitivity rxn to tobacco –> directly injuring endothelium
- genetics: seen in India, Israel, Japan
list the clinical features of Buerger disease
-superficial nodular phlebitis
-cold sensitivity
-claudication pain on instep
-severe progressive pain (due to neural involvement) on exercise and at rest (atherosclerosis)
-chronic ulcerations of toes, feet, fingers — followed by gangrene
(Reynaud’s phenomenon)
describe the morphology of Buerger disease
- segmental acute/chronic vasculitis of medium and small arteries of extremities
- acute/chronic inflammation permeates arterial wall + accompanied thrombosis in lumen
- thrombus has micro-abscesses with central focal neutrophils surrounded by granulomatous tissue
- thrombus with evidence of organization and recanalization
- inflammation extends to contigous nerves and veins (all encased in fibrous tissue)
