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Pathology > Exam IV: Hypertension & Vessel Diseases I > Flashcards

Exam IV: Hypertension & Vessel Diseases I Flashcards

1
Q

Essential Hypertension

A

Also known as Primary Hypertension
95% of cases and idiopathic/unknown cause
Multifactorial: enetic polymorphisms and environmental factors
Usually does not cause short-term problems
If controlled: compatible with long life and asymptomatic

Mechanisms:
Genetic factors
Reduced renal sodium excretion
Vasoconstrictive influences
Environmental factors
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2
Q

Primary vs. Secondary Hypertension

A

Essential = Primary Hypertension: means that it is the initial presentation of any disease
Secondary: developed from a disease that the patient had first

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3
Q

Primary/Essential Hypertension

A

Primary 90-95% of patients
Environmental, Lifestyle, Genetic
No single gene identified, but substantial genetic component - 32-57%
Western diet lifestyle increases risk

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4
Q

Secondary Hypertension

A

Secondary = 2-5% of patients
Renovascular
Other Renal
Endocrine: endogenous or exogenous (OCP/oral contraceptive pill, 5% develop hypertension)

Renal Artery Stenosis- #1 cause
90% - Atherosclerotic in aorta blocks the renal arteries
Usually > 50 of age and smoke
10% Fibromuscular dysplasia- usually young women

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5
Q

Secondary Hypertension: Fibromuscular Dysplasia

A

Fibromuscular Dysplasia -tends to affect young women (20s and 30s)

Pathology
Intimal and medial layers affected (most common) with adventitial subtypes
Distal arterial segmental stenosis

String of beads sign – intimal thickening in certain areas and not in other areas causing the beads formation
Just change in vasculature

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6
Q

Secondary Hypertension: Endocrine

A

Hyper or hypothyroidism

Adrenal Adenoma/Hyperplasia:

  1. Aldosteronoma
  2. Cushings syndrome
  3. Pheochromocytoma

Primary disease in endocrine organs leading to secondary hypertension

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7
Q

Secondary Hypertension: Vascular

A

Coarctation of the aorta
Narrowing just distal to subclavian- causes damage to surface
Typically upper limb hypertension with lower extremity gradient

Occurs in Turner’s syndrome

Key clinical point- hypertension in upper extremities, but lower extremities are normal

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8
Q

Myocardial and Renal Effects of Hypertension

A

Myocardial– cardiac hypertrophy, ischemic injury because pushing against high pressure, compensation for overloading/high volume

Vascular and Renal:

  1. Hyaline arteriolosclerosis and arterial sclerosis (benign nephrosclerosis)
  2. Proliferative arteriolosclerosis (onion-skinning) and fibrinoid necrosis (malignant nephrosclerosis/hypertension)
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9
Q

Hypertensive Emergency(Malignant Hypertension)

A

Severe hypertension causing acute organ impairment
CNS, KIDNEY, HEART
Pathologically with more severe vessel damage, often thrombus (thrombotic microangiopathy) and fibrinoid necrosis of vessel wall
Since turbulence in vessels = clot formation
Fibrinoid necrosis of vessel wall = start to see a lot of problems like ischemia, thrombosis, etc.

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10
Q

Accelerated (Malignant) Hypertension

A

~5% of hypertensives
Rapidly rising blood pressure
Untreated: death within a year or two because continuous under perfusion of organs

Severe hypertension:
Systolic >200 mm Hg
Diastolic >120 mm Hg)

Renal failure
Retinal hemorrhages and exudates with or without papilledema
Superimposed on pre-existing benign hypertension

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11
Q

Malignant Hypertension: Kidneys and Thrombotic Microangiopathy

A

Flea – bitten kidney in malignant hypertension; petechial hemorrhages due to areas of fibrinoid necrosis of vessels

Thrombotic microangiopathy may be seen microscopically:
No more nice vessel wall- broken down
Clot formation in lumen

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12
Q

Hypertension in the Retina

A

Retina: narrowing of vessels causing hemorrhages within the eyes

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13
Q

Hypertension in the Brain

A

Intracerebral Hemorrhage
Mid to late life – peak in 60s
Rupture of small intraparenchymal vessel
Hypertension accounts for >50%

Charcot- Bouchard Microaneurysms- small aneurysms of small vessels usually in the basal ganglia

Just one vessel to cause a big hemorrhage
Bleeding in the brain- drill holes to release pressure and bleeding

Lacunar Infarcts: lake-like spaces (not more than 15 mm)

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14
Q

Hypertensive Encephalopathy

A

Hypertensive Encephalopathy: presentation of hypertensive emergency

Clinical pathologic entity: severe cerebral dysfunction and pathologic correlates of cerebral edema and fibrinoid necrosis of arterioles

Fibrinoid necrosis: deposition of Ab-Ag complexes in the vessel walls (antibody antigen complexes)

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15
Q

Regulation of Normal Blood Pressure

A

Blood pressure: function of cardiac output and peripheral vascular resistance

Influenced by multiple genetic, environmental, and demographic factors

Major factors that determine blood pressure variation:
BMI and diet = modifiable
Age and gender = cannot modify

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16
Q

Hypertension: Small Blood Vessel Disease

A

Hypertension: associated with 2 forms of small blood vessel disease

  1. Hyaline arteriolosclerosis
  2. Hyperplastic arteriolosclerosis
17
Q

Hyaline Arteriolosclerosis

A

Morphology:
Homogeneous, pink hyaline thickening
Luminal narrowing
Generalized and severe in individuals with hypertension
Common feature of diabetic microangiopathy

Deposition of hyaline (pink stuff) with nice nuclei, but in fibrinoid necrosis you won’t see nice nuclei

18
Q

Hyperplastic Arteriolosclerosis

A

Morphology:
“Onion-skin” lesions- concentric laminated thickening of walls and luminal narrowing
Smooth muscle cells and reduplicated basement membranes

Occurs in severe (malignant) hypertension (kidney)
“Onion-skin” lesion plus fibrinoid deposits
Vessel wall necrosis (necrotizing arteriolitis)

19
Q

Aneurysm

A

Aneurysm: atherosclerotic plaque in intima layer pushes on media layer and starts to die because prevents blood and nutrients from getting through as well as the waste material from exiting
Causes necrosis of media/breakdown of media and wall gets weak and thin so bulges out

Most common in abdominal aorta

20
Q

Classifications of Aneurysms

A

True – contains all layers of the vessel wall
False (pseudo) – contained rupture

Fusiform – circumferential and symmetric
Saccular – asymmetric bulging of a portion of the wall (one sided)

Dissection

21
Q

Aortic Dissection

A

Intramural blood between inner 2/3 and outer 1/3 of aorta
Between the intima and media: because small break in intima and zipper stars to spread out
May or may not be associated with aortic dilation

22
Q

Cystic Medial Degeneration

A

Pooling of mucosubstances, elastic fragmentation with disruption of elastic lamellar structure, fibrosis and loss of smooth muscle cell nuclei
Media degenerates and breaks down
Seen in Marfan’s syndrome

23
Q

Aortic Aneurysm

A

Localized permanent pathologic dilatation of a vessel at least 50% >normal

What is normal?
Relates to age, location, body habitus and daily workload
Increase age = increase diameter
Ascending normal <3.0 cm

24
Q

Complications of Aortic Dissection

A
  1. Rupture or tear of vessel and can get into the pericardium
  2. Within pericardium, only supposed to be 15mL fluid in there, but the blood leaking in causes blood all around the heart in the pericardium and will clot and cause cardiac temponade so heart cannot beat and stops beating
  3. Causing collapse of coronary arteries

Either way you cut it… not a good thing to have

25
Q

Marfan’s Syndrome

A

Tend to see aortic dissections in Marfan’s syndrome because mucosubstance build up in the media layer
Fibrillin gene mutation causes breaks/disruptions in elastic bands (stars in photo A)
Mucopolysubstances – get intima damage/tears, separate and then aortic dissection

26
Q

Peripheral Arterial Diseases

A

Large vessels: aorta; diseases include granulomatous disease with giant cell arteritis and Takayasu arteritis

Medium: branches off of aorta and arteries; diseases include immune complex mediated such as polyarteritis nodosa, and anti-endothelial cell Ab such as Kawasaki disease

Small: arterioles, capillaries, venules, and veins

27
Q

Giant Cell (Temporal) Arteritis

A

Most common form of vasculitis among elderly individuals in the United States and Europe

Chronic, granulomatous inflammation of large to small-sized arteries:
Arteries in the head, temporal arteries, and vertebral and ophthalmic arteries

Nodular intimal thickening: see altering/skip lesions (makes bead formation) to reduce diameter and blood flow isn’t going where is needs to causing transient ischemic changes

Classic lesions: see granulomatous inflammation (giant cells), but if you don’t see this stain the elastic lamina and if fragmentation present then know it is temporal arteritis

28
Q

Takayasu Arteritis

A

Also known as granulomatous vasculitis of medium and larger arteries
Ocular disturbances
Marked weakening of the pulses in the upper extremities AKA pulseless disease
Transmural fibrous thickening of the aorta
Severe luminal narrowing of the major branch vessels
Adventitial mononuclear infiltrates are perivascular, so cuffing of the vasa vasorum
Intense mononuclear inflammation in the media
Granulomatous inflammation: giant cells and patchy medial necrosis

29
Q

Polyarteritis Nodosa

A

Systemic vasculitis of small or medium-sized muscular arteries
Not arterioles, capillaries, or venules
Involving renal and visceral vessels but sparing the pulmonary circulation, thus it DOES NOT AFFECT THE LUNGS

Microscopically: Areas of un-involved tissue aka has segmental involvement
Fibrinoid necrosis

30
Q

Kawasaki Disease

A

Leading cause of acquired heart disease in children
Acute febrile, self-limited illness
Associated with an arteritis: affects large to medium-sized and small vessels
Predilection for coronary artery involvement
Pronounced inflammation affecting the entire thickness of the vessel wall

The child is ill or just recovered from an illness… have fever if ill

31
Q

Microscopic Polyangiitis

A

Necrotizing vasculitis
Affects capillaries, arterioles and veins
AKA hypersensitivity vasculitis or leukocytoclastic vasculitis
Necrotizing glomerulonephritis and pulmonary capillaritis–particularly common
Segmental fibrinoid necrosis of the media with focal transmural necrotizing lesions
INVOLVEMENT OF THE LUNGS

32
Q

Churg-Strauss Syndrome

A

AKA allergic granulomatosis and angiitis
Relatively rare
Small-vessel necrotizing vasculitis

Associations: asthma, allergic rhinitis, lung infiltrates, peripheral hypereosinophilia, extravascular necrotizing granulomas

Vascular lesions:
Similar to polyarteritis nodosa or microscopic polyangiitis
Accompanied by granulomas and eosinophils

Other clinical findings:
Palpable purpura
Gastrointestinal tract bleeding
Renal disease (focal and segmental glomerulosclerosis)

33
Q

Wegener Granulomatosis

A

New name: Granulomatosis with polyangiitis
Necrotizing vasculitis: vessel walls fall apart and blood surround tissue and alveolar hemorrhage

Triad:

  1. Acute necrotizing granulomas of the URT or LRT or both
  2. Necrotizing or granulomatous vasculitis affects small to medium-sized vessels
  3. Renal disease: focal necrotizing, often crescentic, glomerulonephritis
34
Q

Wegener Granulomatosis: Lesions

A

Lung lesions:
Granulomas with geographic patterns of central necrosis = caseous
Vasculitis
Alveolar hemorrhage

Renal lesions:
Focal and segmental necrotizing glomerulonephritis
Crescentic glomerulonephritis

Middle aged person without eosinophils = Wegener’s case
Intermittent coughing up blood

35
Q

Thromboangiitis Obliterans

A

AKA Buerger’s disease
Almost exclusive to heavy cigarette smokers
Before the age of 35
Medium-sized and small arteries: tibial and radial arteries
Segmental and thrombosing
Acute and chronic inflammation
Luminal thrombosis: small microabscesses
Claudication symptoms or cramping in lower legs because reduction in lumen in lower extremities and the blood flow isn’t adequate
Sometimes patients must have amputation of fingers or legs

36
Q

Raynaud Phenomenon

A

Exaggerated vasoconstriction of digital arteries and arterioles
Characteristic changes: digits show red, white, and blue color changes; most proximal to most distal

37
Q

Secondary Raynaud Phenomenon

A

Secondary Raynaud phenomenon
Vascular insufficiency of the extremities secondary to arterial disease caused by other entities including:
SLE, scleroderma, Buerger disease, or atherosclerosis

Pathology (14 decks)

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