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Pathology > Cardio 2 > Flashcards

Cardio 2 Flashcards

1
Q

Vasculitis

A

Inflammation of vessels

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2
Q

Clinical vascultis

A

Depends on vascular bed affected (CNS vs heart vs small bowel)
-constitutional sx: fever, malaise, arthralgias, myalgia

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3
Q

Any vessel may have vascultis. Which are affect most

A

Arterioles, capillaries and venues (a few vasculitides tend to affect only one vessel type or location)

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4
Q

Form of vascultis

A

Immune mediated

Infectious

Physical and chemical

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5
Q

Immune mediated inflammation

A

Immunosuppressive Tx for immune mediated vascultis

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6
Q

Infectious vascultis

A

Direct or indirect induced a noninfectious vascultis

-generating immune complexes or trigggering cross reactive immune response

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7
Q

Physical and chemical injury vascultis

A

Injury can also cause vascultis

-irradiation, mechanical trauma, toxins

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8
Q

Non infectious vascultis major cause

A

Immune response (local or systemic)

  • immune complex associated vasculitis
  • antineutrophil cytoplasmic antiboeise
  • antiendothelial cell antibodies
  • gaint cell antibodies
  • giant cell temporal arteritis
  • takayasu arteritis
  • polyarthritis nodose
  • kawasaki disease
  • microscopic poly angiitis
  • churg Strauss syndrome
  • behcet disease
  • granulomatous is with poly angiitis
  • thrombi angiitis obliterates
  • vascultis associated with other NONINFECIOUS DOS
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9
Q

The granulomas of giant cell arteritis are found with int he vessel wall as part of the inflammation comprising the vasculitis, but need not be preset to render the diagnosis. The granulomas if granulomatous with polyangitis are longer, spanning between vessels and associated with areas of tissue necrosis

A

Ok

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10
Q

Giant cell arteritis

A 
Aorta
Rare
Lymphocytes and macrophages
Sometimes giant cells
Over forty and polymyalgia rheumatica
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11
Q

Granulomatous is with polyangitis

A

Granulomas

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12
Q

Churg Strauss syndrome

A

Eosinophils *, lymphocytes, macrophages, neutrophils

Asthma atopy

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13
Q

Polyarthritis nodosa

A

Ok

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14
Q

Leukocytociastic vascultis

A

Ok

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15
Q

Burger disease

A

Thrombosis

Young male smoker

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16
Q

Bechet disease

A

Neutrophils

Orogenital ulcers

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17
Q

Noninfectious vascultis immune complex vascultis

A

Autoantibody production and formation of immune complexes

Deposition of antigen antibody complexes in vascular walls

  • incites an inflammatory reaction within the wall
  • antigen is often unidentified
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18
Q

Who has immune complex vascultis

A

SLE

Drug hypersensitivity
-PCN acts as a hapten binding to serum proteins of vessel wall
—streptokinase acts as a foreign protein

Cl

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19
Q

Clinical immune complex vasculitis

A

Mild to fatal; skin lesions most common

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20
Q

What always consider with immune complex vascultis

A

Drug hypersensitivity. Stop drug! Get resolution of vascultisi

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21
Q

Secondary immune complex vascultisi

A

Secondary to exposure of infectious agent

-ab to microbial constituents form immune complexes that deposit in vascular lesions

Polyarthritis nodose: 30% associated with HBsAg and anti-HBsAg

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22
Q

Antineutrophil cytoplasmic antibodies ANCA

A

A heterozygous group of antibodies reactant with cytoplasmic enzymes found in neutrophil granules, monocytes and endothelial cells

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23
Q

PR3-ANCA

A

Anti-proteinase 3 associated with polyangitis

Previously c-ANCA

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24
Q

MPO-ANCA

A

Anti-myeloperoxidase
Previously pANCA

Induced by Rex: propylthiouracil

Assoc with microscopic polyangitis and churg Strauss syndrome

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25
Q

ANCA titres generally follow disease __

A

Severity

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26
Q

What do ANCA activate

A

Neutrophils, which then renease ROS

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27
Q

Pauci immune

A

Due to ANCA Ab directed against cellular constituents and do not form circulating immune complexes
-vascular lesions do not typically contain Ab and cimplement

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28
Q

Non infectious vascultis * Giant cell (temporal arteritis and aortitis

A

Most common vascultis among older patients, may present with constitutional symptoms (fever, fatigue, weight loss); facial pain, headache

Chronic (T cell mediated CD4>CD8) inflammation of arteries int he head espicially the temporal arteries

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29
Q

Giant cell (temporal arteritis and aortitis

A

Medial granulomatous inflammation, often with multinucleated giant cells

Fragmentation of the elastic lamina and intima thickening

Sites of involvement within an artery may be patchy and focal (at least 1 cm)

Healed sites of inflammation show scarring of the media and intima thickening

Double vision of involvement of the ophthalmic artery may lead to vision loss

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30
Q

Giant cell temporal arteritis and aortitis

A

Rare before 50

If. Granulomas,have to have macrophages

Medical emergency due to possible loss of vision when ophthalmic artery is involved

Temporal artery may be painful to palpating

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31
Q

Non infectious vascultis: takayasu arteritis

A

Characterized by ocular disturbances and marked weakening of pulses of the UE (pulseless disease)
-may present with weak pulse and low blood pressure in the UE

Granulomatous vascultis of medium and larger arteries

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32
Q

Takayasu has similar histological findings to giant cell arteritis except

A

Involves the aortic arch (aortitis) and major branch vessels
-occ aortitis causes dilation and aortic valve insuffiency

Pulmonary artery (involved 1/2 of cases), coronary and renal arteries may be involved

Younger age group <50

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33
Q

Takayasu arteritis

A

Transmural fibrous thickening of the aorta, espicially aortic arch and great vessels; producing narrowing of the major branch vessels

Historically associated with Japanese population, now global distribution

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34
Q

Marked intima thickening in takayasu arteritis

A

Due to intima thickening

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35
Q

Takayasu arteritis morph

A

Narrowing of brachiocephalic, carotid and subclavian arts

Increase intima thickening
Decrease lumen

Giant cells

Destruction and fibrosis of the arterial media associated with mononuclear infiltrates and inflammatory giant cells

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36
Q

Non infectious vasculitis : polyarthritis nodosa

A

Systemic vascultis, likely immune complex mediated

Involves
Renal vessels, heart, liver, GI tract
Pulsars vessels are spared

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37
Q

Who gest PAn

A

Any age group, but classically young adult

Almost 1/3 have chronic hepatitis B
-HBsAg-HBsAb complexes are found in the involved vessels

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38
Q

Treat PAN

A

Immunosuppressive therapy is usually effective

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39
Q

Morph PAN

A

Segmental transmural necrotizing inflammation (neutrophils , eosinophils, lymphocytes and macrophages) predilection for branch points

Ulcerations, infarcts, ischemic atrophy or hemorrhage may be first sign of dz
Sites of inflammation are typically not circumferential

Inflamed vessel wall susceptible to..

  • thrombus formation/occlusion
  • aneurysm
  • rupture
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40
Q

All stages of PAN may coexist in different vessels of even same vessel, suggesting what

A

Ongoing or recurrent insults

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41
Q

Kawasaki disease

A

Acute arteritis of infants and small children (80% <4 years)

Often involves the coronary arteries
-affected sites may form aneurysms->thrombus or rupture->acute MI

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42
Q

Presentation Kawasaki disease

A

Erythema of the conjunctiva, oral mucosa, palms and soles, desquamative rash
-cervical lymphnode enlargement “mucocutaneous lymph node syndrome”

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43
Q

Treat Kawasaki

A

Usually self limited but IVIg ANS asprin are indicated to lower the risk of a coronary event

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44
Q

What causes Kawasaki disesase

A

Infectious agents (mainly viral) have been implicated in triggering the disease in genetically susceptible individuals. The vascular damage is primary mediated by activated T cells and monocytes/macrophages

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45
Q

Microscopic polyangitis

A

Necrotizing vasculitis involving arterioles capillaries and venues
-henoch-schonlein purpura, essential mixed cryoglobinemia, vascultis Association with CT DOS

Affect vessels of many organ systems
-renal glomeruli and lung capillaries most common (90% necrotizing glomerulonephritis)

Most cases associated with MPO-ANCA

Segmental necrotizing inflammation with fibrinoid necrosis

  • many apoptotic neutrophils are usually sen
  • leukocytoclastic vascultiis or hypersensitivity vascultiis

Immunosuppression induces remission, markedly improves long term survival

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46
Q

Churg Strauss syndrome non infectious vascultisi

A

Small vessel necrotizing vascultiis , associated with
-asthma, allergic rhinitis, hypereosinophihlia, lung infiltrates, extravascular granulomas

The inflammation may resemble PAN or microscopic polyangitis, with the addition of eosinophils and granulomas

Less than 1/2 show ANCA positivity (MPO-ANCA mostly)

May organ systems may be involved
-multisystem diseases with cutaneous involvement (palpable purpura), GI tract bleeding, and renal disease (primarily as focal and segmental glomerulosclerosis)

Myocardial involvement may give rise to cardiomyopathy; heart involved in 605 of patients and accounts for almost half of the deaths in the syndrome

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47
Q

Bechet disease

A

Vascultiis of small-medium vessels with classic triad

Aphthous ulcers of the oral cavity
Genital ulcers
Uveitis
-also GI pulmonary manifestations

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48
Q

Bechet disease gene

A

HLA-B51

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49
Q

Morph bechet disease

A

Vessel inflammation is neutrophilic and morpholgically nonspecific, may involve visceral organ systems with subsequent aneurysm formation

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50
Q

Prognosis bechet disease

A

Mortality related to severe neurologic involvement or rupture of aneurysms

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51
Q

Treat bechet

A

Immunosuppression with steroid or TNF antagonists tax effective

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52
Q

*granulomatosis with polyangitis: non infectious polyangitis

A

Necrotizing vascultis featuring:

  • necrotizing granulomas of the upper and/or lower respiratory tracts
  • necrotizing or granulomatous vasculitis , most prominently in the respiratory tract
  • focal necrotizing, often cresenteric glomerulonephritis
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53
Q

Granulomatosis with polyangitis (formerly wegener granulomatosis) associated

A

PR3-ANCA (up to 95%)

A form of T cell mediated hypersensitivity response to normally innocuous inhaled microbial or other environmental agents

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54
Q

Clinical features granulomatosis with polyangitis (wegener)

A

M>F, avg age 40

Most patients have persistent pneumonitis and sinusitis, renal disease, and nasopharyngeal ulceration
-rashes, myalgias , articular involvement, neural inflammation and fever

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55
Q

What happens if granulomatosis with polyangitis is not treated

A

Rapidly fatal, 80% mortality at one year

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56
Q

Treat granulomatosis with polyangitis

A

Steroids, cyclophosphamide, TNF antagonists

Once fatal, now chronic relapsing and remitting

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57
Q

Morphology granulomatosis with polyangitis

A

Upper respiratory tract: sinonasal and pharyngeal inflammation with granulomas and vascultiis (granulomas with geographic patterns of central encrosis* and accompanying vascultisi)

Lower respiratory tract: multiple necrotizing granulomas, which may coalesce and cavitation

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58
Q

Thrombi angiitis obliterates (Berger disease)

A

Segmental thrombosis , acute chronic vascultis of small and medium vessels, espicially
—tibial arteries and radial arteries
—occ secondary extension to veins and nerves of extremities (leading to pain

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59
Q

What does thrombi angiitis obliterates lead to

A

Vascular insuffiency of the extremities

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60
Q

Who gets thrombi angiitis obliterates (Berger)

A

Heavy smoker<35
-most have hypersensitivity to intraderamlly injected tobacco products
—associated with HLA HaplotypE of certain ethnic groups: Israeli, Indian subcontinent and Japanese

Chronic ulcerations, which may lead to gangrene

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61
Q

The strong relationship between Berger and smoking

A

May stem from either a direct idiosyncratic endothelial cell toxicity caused by some component of tobacco, or an immune response to components of tobacco smoke that modify host vascular wall proteins . Most patients have hypersensitivity to intradermally injected tobacco extracts, and their vessel exhibit impaired endothelium dependent vasodilation when challenged with acetylcholine

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62
Q

Histology Berger

A

Acute and chronic inflammation, accompanied by luminal thrombosis. Thrombus can contain small microabscesses composed of neutrophils surrounded by granulomatous inflammation

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63
Q

The thrombus in buerger

A

May eventually organize and recanalize. The inflammatory process extends into contiguous veins and nerves (rare with other forms of vascultiis) and with time all three structures can be encased in fibrous tissue

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64
Q

Infectious vascultisi

A

Direct invasion of infectious agents

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65
Q

What agents cause infectious vascultiis

A

Pseudomonas

Aspergilllus

Mucor

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66
Q

Vascular invasion of infectious vascultiis

A

As part of a localized tissue infection, or less commonly hematogenous spread
-septicemia or embolization from infective endocarditis

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67
Q

Mycotic aneurysms

A

Vascular infections weaken arterial walls

-or induce thrombosis or infarction

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68
Q

Raynaud phenomenon

A

Excessive vasospasm of small arteries and arterioles, espicially fingers and toes
-red white and blue-proximal vasodilation, central vasoconstriction and distal cyanosis

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69
Q

Primary raynaud phenomenon

A

Induced by cold or emotion; symmetric involvement of the digits
Estimated 3-5% general population; young women

Benign course

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70
Q

Secondary raynaud

A

A component of another arterial disease such as SLE, *scleroderma, or thrombi angiitis obliterates;asymmetric involvement of digits

Worsens with time

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71
Q

Raynaud fingers

A

Sharply demarcated pallor of distal fingers resulting from spasm of the digital arteries

and cyanosis
Of fingertips

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72
Q

Myocardial vessel vasospasm

A

Excessive vasoconstriction of myocardial arteries or arterioles (cardiac raynaud) may cause ischemia or infarct

High levels of vasoactive mediators can precipitate prolonged myocardial vessel contraction
-usually caused by circulation vasoactive agents, which may be endogenous (epinephrine, pheochromocytoma) or exogenous (cocaine)

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73
Q

Outcome of myocardial vessel vasospasm

A

Sudden cardiac death or

Takotsubo cardiomyopathy: broken heart syndrome associated with emotional duress

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74
Q

Thyroid hormone myocardial vessel vasospasm

A

Elevated thyroid hormone causes a similar effect by increasing the sensitivity of vessels to circulating catecholamines, while autoantibodies and T cells in scleroderma can cause vascular instability and vasospasm. In some individuals, extreme psychological stress and the attendant release of catecholamines can lead to atholgic vasospasm

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75
Q

Varicose veins*

A

Abnormal dilation of veins with valvular incompetence, secondary to sustained intraluminal pressure
-stasis, congestion, thrombus, edema, and ischemia of overlying skin (stasis dermatitis)

Embolism from thrombi of superficial lower extremity veins is rare
-as opposed to DVT

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76
Q

Esophageal varices

A

Portal HTN (often due to cirrhosis) opens portosystemic shunts which direct blood to veins at the gatroesophageal junction

  • esophageal varices (clinically important bc they may fatally rupture)
  • the rectum (hemorrhoids)
  • and periumbilicus (Capet Medusa)
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77
Q

Superior vena cava syndrome *

A

Neoplasms compress or invade the SVC
-bronchogenic carcinoma, mediastinal lymphoma, or aortic aneurysm

Obstruction produces a characteristic clinical complex

  • marked dilation of the veins of the head, neck, and arms with cyanosis
  • pulmonary vessels can also be compressed ->respiratory distress
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78
Q

Inferior vena cava syndrome

A

Neoplasms that compress or invade the IVC ; or thrombosis of the hepatic, renal or lower extremity veins that propagates cephalic

Hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC); tend to grow within veins, can ultimately occlude the IVC and extend into the right atrium

IVC obstruction induces marked lower extremity edema, distention of the superficial collateral veins of the lower abdomen
-renal vein involvement ->massive proteinuria

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79
Q

Hemorrhoids

A

Dilation of the venous plexus at the anorectal junction

-extremely common, and cause pain, bleeding and may ulcerate

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80
Q

Thrombophlebitis

A

Venous thrombosis and inflammation

Almost always involves deep veins in the legs, and can be completely asymptomatic

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81
Q

Risk factor for thrombophlebitis

A

in LE is prolonged inactivity/immobilization

Maybe systemic hypercoagulability

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82
Q

Serious complication of thrombophlebitis

A

Pulmonary embolism is most serious

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83
Q

Migratory thrombophlebitis (trousseau sign)

A

Patients with cancer may experience hypercoagulability as a paraneoplastic syndrome

Particularly seen with mucin producing adenocarcinoma (mucin is though to be thrombogenic)

In the classic case, venous thrombosis appear at one site, disappear and reappear at a different site

Associated with adenocarcinoma of the LUNG, OVARY,PANCREAS

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84
Q

Benign neoplasms

A

Hemangioma

Lymphangioma

Gloms tumors

Vascular ecstasia

Reactive vascular proliferation’s

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85
Q

Hemangioma

A

Capillary hemangioma

Cavernous hemangioma

Pyogenic granuloma

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86
Q

Lymphangioma

A

Simple(capillary) lymphangioma

Cavernous lymphangioma (systolic hygrometer)

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87
Q

Vascular ecstasia

A

Nexus flammeus

Spider telangiectasia (arterial spider)

Hereditary hemorrhagic telangiectasia (Oiler-Weber-tendu disease)

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88
Q

Reactive vascular proliferation’s

A

Bacillary angiomatosis

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89
Q

Intermediate grade neoplasms

A

Kaposi sarcoma

Hemangioendothelioma

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90
Q

Malignant neoplasm

A

Angiosarcoma

Hemangiopericytoma

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91
Q

Hemangioma

A

Common; localized increase in neoplastic blood vessels

  • common in skin and mucosa membranes of the head and neck and in the liver
  • congenital (juvenile or strawberry) hemangiomas often regress
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92
Q

Capillary hemangioma

A

Most common

Thin walled capillaries; tightly packed together

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93
Q

Cavernous hemangioma

A

Irregular, dilated vascular channels making a lesion with an indistinct border

More likely to involve deep tissue, more likely to bleed

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94
Q

Pyogenic granuloma (lobular capillary hemangioma)

A

A type of capillary hemangioma (not pyogenic, not a granuloma)

Rapidly growing , often in oral mucosa (where they may ulcerate)

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95
Q

Lymphangioma: simple lymphangioma

A

Simple lymphangioma
-appear very similar to capillary hemangiomas but without RBC

Subcutis of head/neck and axilla

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96
Q

Lymphangioma: cavernous lymphangioma (cystic hygrometer)

A

Neck or axilla of kids

Can be large (up to 15 cm)

Large cavernous lymphangiomas of the neck are often seen in Turner syndrome

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97
Q

Glomus tumor (gloms glioma, paraganglioma)

A

Benign tumors arising from glomus bodies, and most often appear in distal fingers

Of smooth muscle origin rather than endothelial

Painful

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98
Q

Glomus are benign but painful

A

Arising from modified smooth muscle cells of the glomus bodies, arteriovenous structures involved in thermoregulation. Although they may superficially resemble hemangiomas (may be blue), glioma gliomas arise from smooth msucle cells rather than endothelial cells. They are most commonly found in the distal portion of the digits espicially under the fingernales.

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99
Q

Treat glomus

A

Excision is curative

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100
Q

Turner

A

Missing X on 23 pair

Results from complete or partial monosomy of the X chromosome and is characterized primarily by hypogonadism in phenotypic females. Bilateral neck webbing and persistent looseness of skin not he back of the neck. Congenital heart disease is also common. Left sided cardiovascular abnormalities , particularly predictable coarctation of the aorta and bicuspid aortic valve, are seen most frequently. Cardiovascular abnormalities are the most important cause of increased mortality in children with turner

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101
Q

*bacillary angiomatosis

A

A vascular proliferation in response to gram negative bartonella bacilla

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102
Q

Who gets bacillary angiomatosis

A

Skin of immunocompromised patients

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103
Q

Describe lesions of bacillary angiomatosis

A

Localized, forming red papules

Micro: proliferation of capillaries with plump endothelial cells

The bacteria can be identified with PCR or visualized with a warthin starry stain*

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104
Q

Treat bacillary angiomatosis

A

Macrolides antibiotics effective

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105
Q

Epithelial hemangioendothelioma

A

Neoplastic endothelial cells are plump and cuboidal , resembling epithelium. Vascular channels may be difficult to recognize

Variable clinical behavior with metastasis in 20-30%

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106
Q

Kaposi sarcoma cause by what

A

HHV8

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107
Q

What are the four forms of kaposi sarcoma

A

AIDS associated KS

Classic KS

Endemic african KS

Transplant associated KS

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108
Q

AIDS associated KS

A

The most common form seen int he US. Most common AIDS related malignant tumor. May spread to lymph nodes and viscera

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109
Q

Classic kaposi sarcoma

A

Older men from middle eastern, Mediterranean or Eastern European descent, NOT associated with HIV,

Tumors localized to skin

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110
Q

Endemic african kaposi

A

Not associated with HIV, patients <40. Can involve lymph nodes

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111
Q

Transplant associated KS

A

Not associate with HIV

But with T cell immunosuppression. Can spread to lymph nodes and viscera

112
Q

Kaposi sarcoma morph

A

Sheets of plump, proliferating spindle cells

Coalescent red purple macules and plaques of the skin

113
Q

Angiosarcoma

A

Malignant endothelial tumor

M=F

114
Q

What causes angiosarcoma

A

Can be induced by radiation exposure can arise ins eating of lymphedema (UE after radical mastectomy)
-hepatic angiosarcoma associated with arsenic, pesticides, thorotrast (contrast agent), polyvinyl chloride)

115
Q

Where get angiosarcoma

A

Skin
Soft tissue
Breast
Liver

116
Q

Angiosarcoma prognosis

A

Locally invasive and may metastasize

5 year survival around 30%

117
Q

Pathology of vascular intervention

A

Therapeutic intervention that injures the endothelium also tends to induce intima thickening by recruiting smooth msucle cells promoting extracellular matrix deposition, analogous to atherosclerosis

118
Q

Endovascular stenting

A

Balloon angioplasty

Coronary stents

Drug elating stents

119
Q

Balloon angioplasty

A

Rupture of occluding plaque and limited dissection produced

-abrupt reclosure can result frmoextensive dissection thus 90% angioplasties followed by stent placement

120
Q

Coronary stents

A

Expandable tubes of metallic mesh

  • due to endothelial injury may induce thrombosis
  • long term: proliferative in stent restenosis (1/3 of patients within 6-12 mo)
121
Q

Drug elating stents: leach antiproliferative drugs to block sm m activation

A

Decrease restensois at 1 year by 50-80%

Paclitaxel sorilimus

122
Q

Vascular replacement

A
  • synthetic or autologous vascular grafts
  • synthetic large bore works for aorta, but small bore fail due to thrombosis or intima hyperplasia at junction of the graft with the native vasculature

Thus utilize saphenous vein or left internal mammary arteries for small bore grafts (coronary arteries)

Saphenous vein 50% potency at 10 years

Internal mammary arteries: 90% at 10 years

123
Q

Intima hyperplasia histology

A

Angiogram constriction

Gore Tex graft

Photomicrograph demonstrating gore Tex graft with prominent intima proliferation and very small residual lumen

124
Q

28 yo male presented to ED because of repeated episodes of acute vertigo that occurred after chiropractic neck manipulations for chronic neck pain. The first PE was normal and the patient was discharged. However, the following day, besides vertigo the patient also had loss of balance , blurred vision and mild numbness and weakness of the left extremities, with cerebellar signs on the right side. Angiography revealed dissection of the vertebral artery

A

Vertebral artery dissection

125
Q

What are the three concentric layers of vascular

A

Intima

Media

Adventitia

126
Q

Intima

A

Single layer of endothelial cells

-internal elastic lamina demarcates intima from media

127
Q

Media

A

Arteries well organized concentric layers of smooth muscle, veins haphazard

Different in elastic arteries, muscular arteries and arterioles

128
Q

Media elastic arteries

A

High elastin content allows expansion during systole, recoil during diastole

  • propels blood towards organs
  • less compliant with increased age-> increased systolic BO
129
Q

Media muscular arteries

A

Circumferential oriented smooth msucle

-arteriolar sm m contraction=vasoconstriction, or relaxation=vasodilation

130
Q

Arterioles media

A

Principal point of physiologic resistance to blood flow

  • resistance to fluid flow is inversely proportional to the fourth power of the diameter
  • halving the diameter increases resistance 16 fold (small changes in vasoconstriction has profound effects on BP_
131
Q

Adventitia

A

External to media , often separated from media by wide external elastic lamina

Vasa vasorum=vessels of hte vessels, small arterioles supply I2 to outer media or large arteries

132
Q

Three types of arteries

A

Large elastic arteries-aorta and its major branches (common carotid, iliac pulm art)
Medium sized muscular arteries-smaller branches of the aorta (coronary and renal)

Arterioles-within tissues and organs

133
Q

Capillaries

A

Diameter of an RBC, no media, pericytes (resembles sm m cells)

134
Q

Veins

A

Most inflammatory reactions, vascular leakage and leukocyte exudation
-large lumens, thinner less organized walls; contains about 2/3 of the total blood vol

  • less rigid-susceptible to dilation and compression, as well as infiltration by tumors and inflammatory process
  • reverse flow dueto gravity prevented in extremities by venous valves
135
Q

Lymphatics

A

Thin walled, lined by specialized endothelium
-return intestinal tissue and fluid and inflammatory cells too the blood stream

-transplant bacteria and tumor cells-pathway for disease dissemination

136
Q

Although the basic organization of the vasculature is constant, the thickness and composition of the various layers differ according to hemodynamics forces and tissue requirements. The aorta has substantial elastic tissue to accommodate high pulsating forces, with the capacity to recoil and transmit energy into forward blood flow. The muscular arteries and arterioles have concentric rings of medial smooth muscle cells whose contractile state regulates vessel caliber and, thereby, blood flow and blood pressure. The venous system has relatively poorly developed medial layers that permit greater capacitance. The capillary wall permits ready diffusion of oxygen and nutrients bc it is comprised only of an ndothelial cell and spares encircling pericytes. The differing structural and functional attributes leave the various parts of the vascular tree vulnerable to particular disorders. This , loss of aortic elastic tissue in a large artery may result in aneurysm, while statsis in a dilated venous bed may produce a thrombus

A

Ok

137
Q

Vascular anomalies

A

Berry aneurysms

Arteriovenous malformations

Fibromuscular dysplasia

138
Q

Berry aneurysm

A

Circle of Willis, ADPKD

139
Q

Arteriovenous malformations

A

Reviewed in CNS (artery->vein, no capillaries)

  • usually developmental defect, but can arise from trauma etc
  • large or multiple AVMs may shunt blood from arterial to venous circulation, forces heart to pump additional volume leading to high output cardiac failure
140
Q

Fibromusclar dysplasia

A

Focal irregular thickening in medium and large muscular arteries (renal, carotid, splanchnic, and vertebral vessels)

141
Q

What causes fibromuscular dysplasia

A

Unknown, probably developmental

First degree relatives have increased incidence; young women*

142
Q

Medial and intima hyperplasia->

A

Luminal stenosis

143
Q

Renovascular HTN

A

Due to fibromuscular dysplasia of renal arteries

144
Q

Fibromuscular dysplasia morphology

A

String of beads on angiography due to making attenuation of adjacent media

145
Q

Problem with fibromuscular dysplasia

A

Can develop aneurysms that may rupture

146
Q

Is fibromuscular dysplasia asssoacited with oral contraception or increased estrogen

A

No

147
Q

Endothelial cells

A

Distinct gene expression profiles, behaviors and morph in different portions of the vascular tree

  • nonthrombogenic surface=maintains blood in a fluid state
  • modulate medial sm m tone (influence vasc resistance)
  • metabolize hormones (angiotensin), regulate inflammation, affect growth of other cells ypes (esp sm m cells)
148
Q

Endothelial activation figure 11-2

A

Ok

149
Q

Endothelial dysfunction

A

Alteration in phenotype->proinflammatory and prothrombogenic

-initiation of thrombus formation, atherosclerosis and vascular lesions of HTN

150
Q

Vascular smooth muscle cells

A

NL vasc repair and atherosclerosis

  • ability to proliferate
  • synthesize collagen , elastin and proteoglycans
  • elaborate growth factors and cytokines
  • vasoconstriction and/or dilation
151
Q

Intima thickening

A

Stereotypical responses of a vessel wall to any insult

  • associated with endothelial cell dysfunction or loss , stimulates sm m cell recruitment and proliferationa nd associated matric synthesis->intima thickening
  • neointimal response

Neointimal sm m cells are motile, undergo cell division, acquire new biosynthetic capabilities

  • sm m cells can return to nonproliferative state with normalization of endothelial layer
  • however, the healing response results in intima thickening that may impede blood flow
152
Q

Basal and activated endothelial cell states. Normal blood pressure, laminar flow, and low growth factor levels promotes a basal endothelial cell state that maintains a nonthrombotic, nonadhesive surface with appropriate vascular wall smooth msucle tone. Injury or exposure to certain mediators results in endothelial activaiton, a state where endothelial cells develop a procoagulatn surface that can be adhesive for inflammatory cells, and also express factors that cause smooth muscle contraction and/or proliferation and matrix synthetisis. VEGF, vascular endothelial growth factor

A

Ok

153
Q

Basal endothelial state

A

normotension, laminar flow and growth factors (VEGF)

->Non adhesive, non thrombogenic surface

154
Q

Initial event following vascular injury ?

A

Endothelial cell activation

155
Q

Activated state

A

Turbulent flow, HTN, cytokines, complement, bacterial products, lipid products, lipid products, advanced glycation end products, hypoxia, acidosis, viruses, cigarette smoke
->

Increased expression of *procoagulants, *adhesion molecules, and proinflammatory factors

Altered expression of chemokine, cytokines, and *growth factors

156
Q

Response to vascular injury

A

Intima thickening, emphasizing intima smooth msucle cell migrationa Nd proliferationa ssociated with extracellular matrix synthesis. The new intima cells are shown in a different color to emphasize that they have a proliferative, synthetic, and noncontractile phenotype distinct from medial smooth msucle cells

157
Q

Response to vascular injury steps

A
  1. Recruitment of smooth msucle cells or smooth msucle precursor cells to the intima
  2. Smooth msucle cell mitosis
  3. Elaboration of extracellular matrix
158
Q

Hypertensive vascular disease

A

High BP->end organ damage and major risk factor in atherosclerosis

159
Q

Sustained diastolic >89mmHg or sustained systolic >139 mmHg associated with what

A

Increased risk of atherosclerosis

-295 OF POPULATIONA RE HYPERTENSIVE BASED ONT HESE NUMBERS

160
Q

Secondary HTN

A

Underlying renal or adrenal disease 5% of pop

Primary aldosteronism, Cushing, pheochromacytoma

Hypertension secondary to renal artery stenosis is caused by increased production of renin from the ischemic kidney; a bruit can be heard on auscultation of the affected kidneys

161
Q

Essential HTN

A

Idiopathic 90-95% of population

Prevelance and vulnerability increase with age: african American high risk

Cardiac hypertrophy and heart failure (hypertensive heart disease), multi infarct failure, another third die of stroke

162
Q

Malignant htn

A

5% rapid increase BP lead to death in 1-2 years

Systolic>200, diastolic >120 mmHg

Severe HTN, renal failure, reitinal hemorrhages and exudates with or without papilledema

Often superimposed on pre existing benign HTN

163
Q

Cause of HTN in most individuals is

A

Unknown

Multifactorial genetic, environmental

164
Q

Essential HTN

A

95% of cases

165
Q

Secondary HTN renal

A

Acute glomerulonephritis

Chronic renal disease
Polycystic disease

Renal artery stenosis
Renal vasculitis

Renin producing tumors

166
Q

Secondary htn endocrine

A

Adrenocortical hyperfunction (Cushing, aldosteronism, congenital adrenal hyperplasia)
-exogenous hormones
Pheochromacytoma
Acromegaly

167
Q

Cardiovascular cause of secondary htn

A

Coarctation of aorta

Polyarthritis nodosa

Increased intravascular volume

168
Q

Neurologic causes secondary htn

A

Psychogenic

Increased intracranial pressure

Sleep apnea

Acute stress, including surgery

169
Q

BP is a function of what

A

Cardiac output and peripheral vascular resistance, both are influenced by multiple genetic and environmental factors

170
Q

Cardiac output

A

Heart rate and stroke volume (which is strongly influenced by blood volume which is regulated by renal sodium excretion or resorption)

171
Q

Vascular resistance

A

Regulated at level of arterioles; influenced by neural and hormonal inputs

172
Q

Cardiac output is a function of what

A

Stroke volume and heart rate

173
Q

Blood pressure=

A

COx peripheral resistance

174
Q

What effects CO

A

Blood volume-Na, mineralocorticoids, ANP

Cardiac features-HR and contractility

175
Q

What effects peripheral resistance

A

Humoral constrictors-angiotensin II, catecholamines, thromboxane, leukotrienes, endothelin1

Humoral dilators-prostagladin, kinins, NO

Constricting -a adrenergic

Dilators -b adrenergic

Autoregulaton pH , hypoxia

176
Q

A and b adrenergic systems

A

Regulate fill pressure and heart rate/contractility (also vascular tone)

177
Q

Filling pressure

A

Most impt determinate of stroke vol

178
Q

Heart rate and myocardial contractility (2nd factor affecting stroke volume)

A

Ok

179
Q

CO

A

A and b adrenergic

Filling pressure

Heart and myocardial contractility (2nd factor affecting stroke vol)

180
Q

Peripheral resistance

A

Neural and hormonal input regulates at arterioles

Vascular tone=balance between vasoconstrictors and vasodilator

Vasoconstriction-angiotensin II, catecholamines, endothelin1

Vasodilator: kinin, prostagladin, nitric acid

Resistance vessels also exhibit autoregulation; increased blood flow->vasoconstriction to protect tissue against hyperperfusion BP fine tuned by tissue pH and hypoxia to accommodate local metabolic demands

181
Q

Blood volume and vascular tone modified and maintained by

A

Renin angiotensin aldosterone system

182
Q

In states of low volume or low peripheral resistance, or a decreased glomerular filtration rate, __ is released by juxtaglomerular cells in the afferent arterioles in the kidney

A

Renin

183
Q

What does renin do

A

Cleaves circulationg angiotensinogen from angiotensin I

Angiotensin I is cleaved to form angiotensin II by ACE

184
Q

Angiotensin II

A

Potent but short lived vasoconstrictor

Stimulated adrenal cortex to release aldosterone, causing renal reabsorption of Na and water
Resistance and voincreased raising bp

185
Q

The volume expansion induces myocardial release of ___, leading to Na excretiona dn diuresis as well as vasodilation thus lowering bp

A

ANP

186
Q

ANP and RAAS

A

Maintains bp homeostasis

187
Q

HTN

A

30% adults

Major risk factor for atherosclerosis, CHF and renal failure

188
Q

Essential HTN

A

90-95% of cases see figures 11-4 11-5

189
Q

Sustained HTN

A

Requires participation of the kidney

190
Q

HTN controlled by

A

A single gene DO or is secondary to renal disease, adrenal disease or other endocrine DO

191
Q

What does HTN cause

A

Degenerative vegetative changes in the walls of large and medium arteries, that can lead to aortic dissection and/or cerebrovascular hemorrhage

192
Q

What are two forms of blood vessel disease

A

Hyaline arteriosclerosis

Hyperplastic arteriosclerosis

193
Q

Hyaline arteriosclerosis

A

Increased smooth muscles matric synthesis

Plasma protein leakage across damaged endothelium
HOMOGENOUS PINK HYALINE THICKENING of the vessel wall, with associated luminal narrowing

194
Q

Hyperplastic arteriosclerosis

A

Occurs in SEVERE HTN

Smooth msucle cells form CONCENTRIC LAMELLATIONS (INION SKINNING) with resultant luminal narrowing

195
Q

Morphology vascular HTN

A

Hyalinized vessel wall-> narrow lumen
-the arteriolar wall is thickened with increased protein deposition (hyalinized) and the lumen is markedly narrowed

Hyperplastic arteriosclerosis
-onion skinning causing luminal obliteration PAS stain

196
Q

Benign HTN

A

Mild to moderate increase of bp and an asymptomatic period of several years before the inevitable onset of symptoms and end organ damage (hence the condition is not truly benign)

197
Q

Malignant HTN

A

Marked increase of bp and rapid progression over a few weeks to end organ failure. Most patients with essential HTN follow the benign pattern, although it may accelerate to malignant HTN. The characteristic vascular lesion of benign essential HTN is widespread hyaline arteriosclerosis manifest by thickening of the walls of the smalla rteries and arterioles by amorphous eosinophilic material composed of degenerated smooth cells and deposited plasma proteins

198
Q

Hyaline arteriosclerosis

A

With associated small cortical scare (hyaline arteriolonephrosclerosis) is commonly seen in the kidneys . Hyperplastic arteriosclerosis, marked luminal narrowing by cellular intima proliferation in a lamellar, onionskin pattern , is the characteristic lesion of malignant HTN. In severe malignant HTN, fibrinoid necrosis of the glomerular arterioles occur. As associated ischemic injury develops rapidly, leading to petechial hemorrhages in multiple organs, including the kidneys (hyperplastic arteriolonephrosclerosis)

199
Q

Arteriosclerosis

A

Hardening of the arteries, generic term

-arterial wall thickening and loss of elasticity

200
Q

Arteriosclerosis

A

Sm arterioles and arterioles, may cause downstream ischemic injury (see previous hyaline vs hyperplastic_

201
Q

Monckenberg medial sclerosis

A

> 50

Calcification of muscular arteries, internal elastic membrane involved, NO narrowing of lumen, NO clinical significance

202
Q

Atherosclerosis

A

Gruel and hardening , most frequent and clinically important pattern

203
Q

Atherosclerosisunderlies pathogensis of what

A

Coronary, cerebral and peripheral vascular disease

204
Q

Atherosclerosis demographics

A

Common espicially in the developed world

  • causes more morbidity and mortality (roughly half of all deaths) in the western world than any other disorder
  • myocardial infarction responsible for almost 1/4 of all deaths in US
  • soviet union highest ischemic heart disease mortality 3-5x US 7-12 x japan
205
Q

Atheroma=atheromatous-atherosclerotic plaque

A

Raised lesion with a soft rumors core of lipid covered by a fibrous cap

206
Q

Describe atherosclerotic plaque. INTIMAL BASED PROCESS**

A

Fibrous cap-smooth msucle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovasculaturization)

Necrotic center -cell debris, cholesterol crystals, foam cells, calcium

Media

207
Q

What is prevelance and extend or atherosclerosis related to

A

Multiple risk factors, which have synergistic (rather than additive) effect

40-60yo incidence up 5x

208
Q

Death rates from ischemic heart disease increase each __

A

Decade

209
Q

Premenopausal women are somewhat protected from atherosclerosis

A

Atheroprotective effect of estrogen if started early postmenopausal, otherwise no benefit

210
Q

Hypercholestermia

A

Major risk factor even in absence of other factors, it is sufficient to initiate lesion development

211
Q

Metabolic syndrome

A

Associated with central obesity

Insulin resistance, HTN, dyslipidemia (increase LDL decrease HDL), hypercoagulability, and proinflammatory state may contribute to endothelial dysfunction andor thrombosis

212
Q

Nonmodifiable factors of atherosclerosis

A

Genetic abnormalities

Family history

Increasing age

Male gender

213
Q

Modifiable risk factors of atherosclerosis

A

Hyperlipidemia

HTN

Cigarette

Diabetes

Inflammation

214
Q

See table 11-2

A

Ok

215
Q

10year rate of coronary artery disease in 55 year old men and women as function of established risk factors (hyperlipidemia, HTN, smoking and diabetes)

A

Increase

216
Q

CRP predicts cardiovascular risk

A

Increase@

217
Q

Response to injury model for atherosclerosis

A

Chronic injury and/or dysfunction of endothelium, leading to chronic inflammation and attempts to repair the tissue

218
Q

Endothelial injury and dysfunction : hemodynamics turbulence

A

Atherosclerosis does not occur. Randomly in vessels, nor does it occur everywhere uniformly

Mostlesions tend to occur at openings of exciting vessels, branch points, posterior abdominal aorta-due to flow disturbances ormally seen in these locations

219
Q

Andothelial injury and dysfunctionL Circulating lipids

A

Lipids in atheromatous plaques are predominantly cholesterol and cholesterol esters

Accumulate in the intima, are taken up by macrophages and partially oxidized
This modified LDL further accumulates within macrophages and smooth msucle cells, forming foam cells and a lesion known as a fatty streak

This stimulates an inflammatory response to accumulation of this toxic form of LDL

220
Q

Arterial wall response to injury

A

Chronic endothelial injury

Endothelial dysfunction

Macrophages activation, smooth msucle recruitment

Macrophage and smooth msucle cells engulf lipids

Smooth msucle proliferation, collagen and other extracellular matrix deposition, extracellular lipid

221
Q

Chronic endothelial injury

A 
Hyperlipidemia
HTN
Smoking
Homocysteine
Hemodynamics factors
Toxins
Viruses
Immune reactions
222
Q

Endothelial dysfunction

A

Increased permeability leukocyte adhesion

Monocytes adhesion and emigration

223
Q

Macrophage activation, smooth msucle recruitment

A

See smooth msucle cells

224
Q

Macrophages and smooth muscle cells engulf ___

A

Lipid

See fatty streak and T cells

225
Q

Smooth msucle proliferation, collagen and other extracellular matrix deposition, extracellular lipid

A

Lipid debris, T cell and collagen

226
Q

Evolution of arterial wall changes in the response to injury

A
  1. Normal
  2. Endothelial injury with monocyte and platelet adhesion
  3. Monocyte and smooth msucle cell migration into the intima with macrophage activation
  4. Macrophage and smooth muscle cell uptake of modified lipids, with further activation and recruitment of T cells
  5. INTIMAL smooth msucle cell proliferation with extracellular matrix production, forming a well developed plaque
227
Q

Inflammation atherosclerosis pathogenesis

A

Accumulation of cholesterol crystals within macrophages is recognized by the inflammasome which leads to IL1 secretion

More macrophages and T cells are recruited and activated

Inflammatory cytokines further activate endothelial cells, and growth factors stimulate smooth muscle cells to migrate to the intima and proliferate

228
Q

Smooth muscle proliferation and matrix deposition pathogenesis atherosclerosis

A

Several growth factors are implicated in smooth msucle cell proliferation, including PDGF as well as macrophages, endothelial cells and smooth msucle cells, fibroblast growth factor and transforming growth factor TGF-a

Proliferating smooth msucle cells synthesize extracellular matric including collagen

Due to the INTIMAL expansion from foam cells and extracellular lipid recruited inflammatory and smooth msucle cells and increased ECM, an atheromatous plaque is formed

Over time a soft fibrofatty plaque becomes covered with a fibrous cap (dense collagen fibers). The center of the plaque is necrotic, containing lipid debris, foam cells and thrombus, surrounded by a zone of inflammatory and smooth msucle cells

229
Q

What happens when have hyperlipidemia, hyperglycemia, HTN, and endothelial injury

A

Platelet adhesion and recruitment of circulating monocytes and T cells, with subsequent smooth msucle cell migration and proliferation as well as further macrophage activation. Foam cells in atheromatous plaques derive from macrophages and smooth msucle cells that have accumulated modified lipids via scavenger and LDL receptor related proteins. Extracellular lipid is derived from insulation fromt he vessel lumen, particularly in the presence of hypercholesterolemia, as well as from degenerating foam cells. Cholesterol accumulation inthe plaque reflects an imbalance between influx and EF flux; HDL likely helps clear cholesterol fromthese accumulations. In response to the elaborated cytokines and chemokine, smooth msucle cells migrate to the intima, proliferate and produce extracellular matrix, including collagena dn proteoglycans

230
Q

Common sites of atherosclerosis

A 
Abdominal aorta
Coronary arteries
Popliteal arteries
Internal carotid arteries
Circle of Willis
231
Q

Complications of atherosclerotic plaques

A

Rupture and ulceration
-may lead to thrombosis

Hemorrhage
-may follow plaque rupture

Embolism

  • may follow plaque rupture
  • aneurysm formation
232
Q

Histology fatty streak

A

Collection of foamy macrophages in the intima

233
Q

Mild vs severe atherosclerosis aorta histology

A

Mild-fibrous plaques

Severe-diffuse and complicated lesions including an ulcerated plaque and lesion overlying thrombus

234
Q

Stenosis of the atrial lumen from atherosclerosis

A

Plaques tend to continually grow bc of repeated cycling through the injury healing process

The lumen of the affected vessel gradually shrinks, eventually leading to ischemia downstream (a point known as critical stenosis-approximately 70% occluded)

This may lead to chronic ischemia of myocardium, bowel and brain , the extremities

235
Q

Acute plaque change atherosclerosis

A

An acute Thrombus may form over the plaque, occluding the artery. This may occur secondary to:

  • Rupture of the plaque
  • erosion or ulceration of the plaque surface

Hemorrhage into the plaque may acutely expand its volume

236
Q

Some plaques are more prone to rupture than others

A

The fibrous cap is continually being degraded and resynthesized (remodeled

Increased inflammation int he plaque can accelerate fibrous cap degradation and inhibit its resynthesis, Thur reducing the amount of collagen in the cap and weakening it

Physical stresses can cause plaque rupture
-changes in blood pressure
Vasoconstriction

237
Q

Aneurysms

A

Localized abnormal dilation of a blood vessel, or the heart, that may be congenital or acquired

238
Q

True aneurysm

A

An intact (but thinned) muscular wall at the site of dilation

239
Q

False aneurysm

A

Defect through the wall of the vessel, or heart, communicating with an extravascular hematoma

240
Q

An aneurysm can occur whenever the connective tissue of the vascular wall is weakened, whether by acquired or congenital conditions

A

Defective vascular wall CT
-marfan (defective fibrillin synthesis)

Net degradation of vascular wall CT
-inflammatory conditions (such as atherosclerosis)->increased matric metalloprotease

Weakening of the vascular wall by ischemia

  • atherosclerosis->ischemia of inner media
  • HTN->ischemia of outer media
  • tertiary syphilis->ischemia of outer media (thoracic aorta)
241
Q

Tertiary syphilic and aneurysm

A

Obliterating endarteritis (characteristic of late stage syphilic) shows a predilection for small vessels, including those of the vasa vasorum of the thoaracic aorta. This elads to ischemic injury of the aortic media and aneurysmal dilation. Which sometimes involves the aortic valve annulus (aortic valve regurgitation)

242
Q

Cystic medial degeneration aneurysm

A

Loss of vascular wall elastic tissue, or ineffective elastin synthesis, leads to cystic medial degeneration, which disrupted and disorganized elastin filaments and increased ground substance (proteoglycans)

Final common result of different conditions, including ischemic medial damage and marfans

243
Q

Two most important causes of aortic aneurysms are

A

Atherosclerosis and HTN

244
Q

Mycotic aneurysms

A

Can originate from:

Septic emboli (usually complication of infective endocarditis)

Extension of an adjacent suppurative process

Circulating organisms directly infecting the arterial wall

245
Q

Cystic medial degeneration

A

Marfan

Elastin fragmentation and areas devoid of elastin that resemble cystic spaces but are actually filled with proteoglycans

Normal media for comparison, showing the regular layered pattern of elastic tissue

246
Q

AAA

A

Abdominal aortic aneurysm

Usually from atherosclerosis

Occur in abdominal area, usually below the renal arteries, and often involve the common iliac arteries

247
Q

Who gets aaa

A

Men smokers 6th decade

248
Q

Characterization aaa

A

Severe atherosclerosis of the aorta, covered with mural thrombus

May be detected as a pulsating mass in the abdomen

249
Q

Complications aaa

A

Rupture and hemorrhage

Occlusion of branching arteries and downstream ischemia

Embolism

Impingement on another structure

250
Q

Morph aaa

A

Lines of Shan-alternating light pink bands (fibrin and platelets) with dark pink bands RBC

251
Q

Thoracic aortic aneurysm

A

Often due to HTN or less commonly congenital defect in CT Marfan

252
Q

Marfan

A

AD genetic disorder resulting in defective synthesis of fibrillin that leads to aberrant TGF-B activity that weakens elastic tissue

253
Q

Clinical presentation thoracic aortic aneurysm

A

Impingement

  • lower respiratory tree
  • esophagus
  • recurrent laryngeal nerves

Aortic valvular insuffiency

Rupture

254
Q

Aortic dissection

A

Occurs when blood enters a defect in the intima and travels through a tissue plane within layers of the aortic media

255
Q

Who gets aortic dissection

A

HTN males 40-60

Younger patents with disorders of vessel CT (marfan)

256
Q

Primary risk factor aortic dissection

A

HTN

257
Q

Classic presentation of aortic dissection

A

Sudden onset of severe chest pain (usually beginning in anterior chest) radiating to the back between the scapulae, and moving downward as the dissection progresses
-can be confused with AMI

258
Q

Aortic dissection pathogensis

A

Blood enters aortic wall via an INTIMAL tear forming an intramural hematoma

Usually in hypertensive patients, there is some degree of cystic medial degeneration

259
Q

Where are most aortic dissection

A

Most dissections arise in the ascending aorta, within 10cm of the aortic valve

260
Q

What happens when dissections rupture through the adventitia

A

Massive hemorrhage (into the thoracic or abdominal cavities) or cardiac tamponade (hemorrhage into the pericardial sac)

261
Q

If the dissecting hematoma renters the lumen of the aorta through a second distal INTIMAL tear

A

A new false vascular channel (double barreled aorta) is created
-this averts a fatal extraaortic hemorrhage, and over time, such false channels can be enotheliazed to become recognizable chronic dissections

262
Q

Type A dissection (involving the ascending aorta)

A

Are more common and associated with higher morbidity and mortality

263
Q

Most common cause of death in both dissections

A

Rupture

Dissection may also extend along arterial branches of the aorta, causing potential occlusion of those vessels

264
Q

Treat type a dissection

A

Antihypertensive therapy and an attempt to surgically reprair the INTIMAL tear

265
Q

Type B

A

Distal debarked III arise after the take off of the great vessels

266
Q

What dissection has most serious complications and mortality

A

Type A

267
Q

The effects of HTN with excessive hemodynamics trauma on a weakened aortic wall can lead to the formation of a ___ in the media

A

Hematoma

268
Q

The hematoma dissects longitudinally to split the media, which creates a dissecting hematoma or a __ __, a double barreled aorta with true and false lumens. In most cases, a proximal INTIMAL tear allows blood to enter the false lumen under systemic pressure

A

Dissecting aneurysmtype A dissections

269
Q

The proximal INTIMAL tear is inthe ascending thoracic aorta

A

Type a

270
Q

Type b dissection

A

The proximal INTIMAL tear is int he aortic arch or the descending thoracic aorta

271
Q

What are type a dissections prone to

A

External rupture intothe mediastunmin or pericardial cavity, necessitate surgical intervention. Some dissections develop distal tears and become chronic with the potential for late rupture. Blood pressure control is key in the treatment of any aortic dissection

272
Q

Severe diseases give rise to annuloaortic ecstasia

A

A progressive aneurysmal dilation of the aortic root with accompanying aortic valvular incompetence.

273
Q

Atherosclerotic aneurysms of the iliofemoral arteries

A

Fills with unorganized mural thrombus and the expanding aneurysms become susceptible to rupture

274
Q

Aortic root and ascending aorta atherosclerotic aneurysms

A

Secondary to end arterioles is of the vasa vasorum produced years previously by systemic infection of trep pallidumm=

275
Q

The entire abdominal aorta and the descending thoracic aorta form a

A

Thoracoabdominal atherosclerotic aortic aneurysm

Pathology (36 decks)

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