Cardiology Blood Vessel Pathology-large

7/28/2019 Cardiology Blood Vessel Pathology-large

1/38

Flashcard Set Title: "Cardiology: blood vessel pathology"Study this set online at: http://www.flashcardexchange.com/cards/cardiology-blood-vessel-pathology-727120

Name the types of vessels

that lack medial layer. (3)

- capillaries- post-capillary venules

- lymphatics

Which type of vessel is this?

- thick medial layer

- rich in elastic fibers separated by

alternating smooth muscle cells

large elastic arteries


- elastin in internal and external elastic lamina

- circulatory or spirally arranged smooth muscle

cells

medium sized muscular

arteries


- no medial layer

- one cell layer endothelium

- no valves

capillaries

page 1 / 38


2/38



- no medial layer

- one cell layer endothelium

- one way valves

lymphatic vessel


- 1-2 layers of smooth muscle cells

- resistance vessels

- internal elastic lamina

arterioles


- thin medial layer

- no internal elastic lamina

- one way valves

- large capacitance

veins


- no medial layer

- site of vascular leakage and leukocyte

emigration

post-capillary venules

page 2 / 38


3/38


Atherosclerosis usually takes

place in which type of vessels?

What about HTN?

Atheroclerosis

- large elastic arteries

- medium sized muscular arteries

HTN

- small size muscular arteries

- arterioles

Which type of capillaries are in

these organs?

- endocrine glands, renal

glomeruli, some digestive tract

capillaries

fenestrated


these organs?

- heart, lung, skin, muscle, CNS

continuous


these organs?

- liver, spleen, marrow

sinusoids

page 3 / 38


4/38


What are some antigensexpressed on endothelial cells

under normal condition?

- CD31(PECAM1) at inter-endothelial

junction: leukocyte transmigration- CD34 on endothelial cells in lymph

nodes: bind to naive T cell

- vWF

Ultrastructure

near endothelial

cell membrane.pinocytic vesicles

Ultrastructure of

endothelial cells

with

neighbouring

cells.

junctional complexes: eg

tight junctions, etc.

Intracellular

ultrastructure of

endothelial cells.

(hint: storage site

for vWF)

Weibel-Palade bodies

page 4 / 38


5/38


Endothelial cell functions.

(6)

- transfer of molecules

- produce ECM- regulate blood flow

- regulate stasis

- regulate cell growth

- regulate inflammation, immuniry.

How does endothelial cells

regulate blood flow?

- synthesis of vasoconstrictors:

endothelin, ACE

- synthesis of vasodilators: NO,

prostacyclin


regulate stasis?

- synthesis of pro-thrombotic factors: vWF, TF,

plasminogen activator inhobitor

- synthesis of anti-thrombotic factors:

prostacyclin, thrombomodulin, plasminogen

activator, heparin like molecules


regulate cell growth?

- synthesis of growth stimulators:

PDGF, FGF, CSF

- synthesis of growth inhibitors:

TGF-beta, heparin

page 5 / 38


6/38


How does endothelial cellsregulate inflammation and

immunity?

- make cytokines: IL1,6,8- make surface molecules: VCAM1,

ICAM, E-selectin, P-selectin, CD31, HLA

antigens.

Which of the following is faster?

- endothelial stimulation

- endothelial activation

- endothelial stimulation:

seconds to minutes

Endothelial stimulation or activation?

- rapid, reversible

- induced by histamine to increase permeability, inhibit

NO synthesis

- redistribute P-selectin from Weibel-Palade bodies to

cell surface

endothelial stimulation:

histamine,

thrombin, PAF,

cytokines by

activated

macrophages

Endothelial stimulation or activation?

- slow, hours to days

- express newly acquired properties:

altered gene expression and synthesis of

new proteins

endothelial activation:

- activators: cytokines, lipid products,

hemodynamic forces, viruses, complement

products, hypoxia, advanced glycosylation end

products.

- induced genes: adhesion molecules,

cytokines, GF, vasoactive mediators,

coagulation proteins, MHC molecules.

page 6 / 38


7/38


What are some normalfunctions of smooth muscle

cells in blood vessels? (3)

- vasoconstriction, vasodilation- synthesize collagen, elastin,

proteoglycans

- synthesize GF, cytokines

Minor or major vascular injury?

- proliferation of endothelial cells to repair

the injury

- smooth muscle minimally stinulated and

stay in the medial layer

minor vascular injury

Minor or major vascular injury?

- stimulation of smooth muscle cells: migrate to

intimal layer and increase in proliferation and

synthesis of ECM, lost ability to contract.

Major/chronic vascular

injury

- results in intimal thickening

-> stenosis, thrombotic

occlusion

Causes of intimal

thickening. (3)

- progressive atherosclerosis (most

common)

- post-angioplasty: restenosis

- post-organ transplant: stenosis

page 7 / 38


8/38


What is the cause of thelargest morbidity of all US

diseases?

atherosclerosis

What is the age onset of

atheroscleosis?

teens, usually becomes

symptomatic in middle age.

Describe the progression of

atherosclerosis from normal artery

to clinical evident diseases.

- normal artery

- fatty streak

- fibrofatty plaque

- vulnerable plaque

- aneurysm, rupture,

thrombosis, stenosis.

What is this disease?

- hardening of large arteries

atherosclerosis

page 8 / 38


9/38



- hardening of small arteries and

arterioles

ateriolosclerosis


- thickened arterial walls

- calcium deposits in medial layer of medium

muscular arteries

- do not cause stenosis alone

Monckeberg medial calcific

sclerosis

What is the "foot print" of

atherosclerosis?

atheromatous plaque:

yellowish-gray,slightly

elevated.

What are these

called? Compare

these 2 pictures.

left: atheromatous plaque, class IV

or V lesion

right: ulcerated athreroatous

plaque, class VI lesion.

page 9 / 38


10/38


What are the components of

atheromatous plaque?

What is this

disease?

coronary artery plaque

- fibrosis in intima: fibrous cap

- weak,thin media

- lipid core of cholesterol clefts

- 65% stenosis of lumen

Which class of atherosclerosis is

this?

- isolated macrophage foam cells

with lipid

class I


this?

- fatty streak

class II

page 10 / 38


11/38


Which class of atherosclerosis is this?

- fatty streak

- small extracellular lipid pool

class III

Which class of atherosclerosis isthis?

- atheroma: core of extracellular

lipid

class IV


this?

- fibroatheroma: lipid core and

fibrotic layer

class V

Which class of atherosclerosis is this?

- lesion with surface defect (ulceration)

- hematoma or thrombosis

- accompanied by dystrophic calcification

class VI

page 11 / 38


12/38


Which classes ofatherosclerosis are clinically

significant?

class V and VI

Class VI atherosclerotic lesion:

What is the cause of hemorrhage?

- rupture of neovascular

vessels or fibrous cap

Class VI atherosclerotic lesion:

What is the cause of thrombosis (most

serious complicaiton)?

- exposure of

thrombogenic

substance ->

secondary acute

occlusion of lumen

-> acute ischemic

infarction

What are the top 5

manifestations of

atherosclerosis in the US?

- coronary arteries: angina, MI

- cerebral arteries: TIA, infarction, multi-infarct dementia

- aorta: aneurysm, embolism

- lower extremity arteries: ischemia (claudication), stasis

ulcers, gangrenous necrosis

- mesenteric arteries: ischemic enteritis, acute infarction.

page 12 / 38


13/38


What happens to the mediallayer of medium/large

arteries in atherosclerosis?

aneurysm

- variable atrophy- loss of elastic fibers

- dystrophic

calcification

What are the components of

fatty streak?

- lipid filled foam cells(macrophages)

- small amounts of T cells

- extracellular lipids

- not raised

Phases of atherosclerosis:

- chronic endothelial injury

Phase I- hyperlipidemia

- HTN

- smoking

- homocysteine

- hemodynamic factors

- toxins

- viruses

- immune reactions

How does hyperlipidemia

cause chronic endothelial

injury?

- LDL-cholesterol oxidized at sites of

fatty streak -> chemotactic for

monocytes, toxic to endothelial cells

- ingested by macrophages

page 13 / 38


14/38



- increased endothelial permeability

- leukocyte adhesion via VCAM1

- monocyte adhesion via VCAM1 and

emigration

Phase II:

endothelial

dysfunction


- smooth muscle emigrate into intimal layer: change from

contractile phenotype to sythetic phenotype

- macrophage activation: secrete IL1,TNF, monocyte

chemoattractant protein-1, smooth muscle cell growth

factor (PDGF, FGF, TGF-alpha)

Phase III:

smooth muscle

cell emograion


- macrophages and smooth muscle cells engulf

lipid: oxidzed LDL-cholesterol

- T cells augment inflammation and secrete

cytokines

Phase IV: lipid

phagocytosis


- smooth muscle cell proliferation

- collagen, ECM deposition

- extracellular lipid

Phase V:

collagen and

extracellular lipid

deposition and

smooth muscle

cell proliferation

page 14 / 38


15/38


T/F: Risk factors foratherosclerosis are more

than additive.

T.

Non-modefiable risks for

atherosclerosis.

- aging

- male

- family history

- genetic abnormality

Modefiable risks for

atherosclerosis.

- hyperlipidemia

- HTN

- smoking

- diabetes

- lack of exercise

Which genetic lipoprotein disorder

is this?

- defeciency of LDL receptor

heterozygous familial

hypercholesterolemia

page 15 / 38


16/38


Which genetic lipoprotein disorder

is this?

- apo B-100 problem

- familial defectiveapoprotein B

- hypobetalipoproteinemia

Give four common lipoprotein

disorders that put people at risk for

atherosclerosis

- familial combined hyperlipidemia: 1:200

- heterozygous familial hypercholesterolemia

and familial hypertriglyceridemia: 1:500

- familial defective apoprotein B: 1:700

- hypobetalipoproteinemia: 1:1000

Name the three biochemical

risk factors for

atherosclerosis.

- CRP: reflect chronic component of

atherosclerosis

- homocycteine: risk for ischemic heart disease

- Lp(a): apoB-100 of LDL linked to apoA,

particularly for men.

Two congenital vascular

anomalies.

- berry (saccular) aneurysms of

cerebral arteries

- arteriovenous fistula

page 16 / 38


17/38


Where is a common location

of berry aneurysms?

ACA and MCA near branch

points

What increases the risk for

berry aneurysm to rupture?

- inherited disease: marfan, Ehlers-

Danlos, NF-1

- smoking

- HTN

What is consequence when

berry aneurysms rupture?subarachnoid hemorrhage

What are some causes of

AV fistula?

- trauma

- inflammation

- surgery created fistula for

vascular access during

hemodialysis

page 17 / 38


18/38


What are AVM or AV fistula

at risks for?

- high output heart failure: more blood on

venous side

- inadequate exchange of O2, CO2, and

nutrients: bypass capillaries

- rupture with hemorrhage

What is this

disease?

cerebral AVM

- gross: soft, spongy, red-brown mass

- histo: haphazard arrangement of

variably-sized vessels, most larger than

capillaries.

What are the two most likely

cause of essential HTN?

- retention of

excess Na

- vasoconstriction

and vascular

hypertrophy

What are hypertensive

people most likely at risk

for? (6)

- heart failure: cardiac hypertrophy

- atherosclerosis

- renal failure: renal vascular arteriolosclerosis

- cerebral hemorrhage and infarction

- aortic dissection

- ruptured berry and atherosclerotic aneurysms

page 18 / 38


19/38


Which of the following seconday cause of

HTN is most common?

- renal

- cardiovascular

- endocrine

- neurologic

- renal

What are hypertensive

people most likely at risk

for? (6)

- heart failure: cardiac hypertrophy

- atherosclerosis

- renal failure: renal vascular arteriolosclerosis

- cerebral hemorrhage and infarction

- aortic dissection (CMD)

- ruptured berry and atherosclerotic aneurysms

Which of the following seconday cause of

HTN is most common?

- renal

- cardiovascular

- endocrine

- neurologic

- renal

What is the most common

lesion associated with HTN?

Hyaline

arterioloscleosis

- thickening of media

by pink hyaline

material

page 19 / 38


20/38


What is the pathogenesis of

hyaline arteriolosclerosis?

HTN -> endothelial damage ->

leakage of plasma to media ->

stimulation of smooth muscle to

synthesize ECM

Sequelae of hyaline

arteriolosclerosis (HTN)

Progressive arteriolar stenosis:

- diffuse renal ischemia -> atrophy of glomeruli

-> nephrosclerosis -> renal insufficiency ->

worsen HTN (increased TPR)

What lesion is associated

with malignant HTN?

Hyperplastic

arteriolosclerosis

- "onion-skin"

thickening of

arteriolar media and

intima

What type of HTN is this?

- diastolic pressure >

110-120

malignant HTN

page 20 / 38


21/38


True or False aneurysm?

- vascular wall contains all components of

arterial wall

- blood ramains within normal circulation

- true

True or False aneurysm?

- extravascular hematoma

communicating with vascular space

- false

What are the two causes of

true aneurysm?

- atherosclerosis

- cystic medial degeneration


false aneurysm?

- trauma

- surgery

page 21 / 38


22/38



mycotic aneurysm?

- infection induced

- any infectious agent

What is the most common site to

find atherosclerotic aortic

aneurysm?

- abdominal aorta > common iliac > aortic

arch > descending thoracic aorta

- most develop between renal arteries

ans aortic bifurcation

Pathogenesis of

atherosclerotic aortic

aneurysm (AAA). (4)

- media layer gradually thinned and weakened

by intimal plaques.

- connective tissue defects

- HTN and atherosclerosis

- complicated grade VI atherosclerosis

What is this?

AAA of abdominal aorta

- layered fibrin

- unorganized thrombus in lumen

page 22 / 38


23/38


These are associated with which disease?

- pulsatile mass (palpable in thin people)- impingement on ureter

- atherosmbolism

- ischemia due to occlusion od ostium of major

aortic branch

-

AAA

What is this

disease?

syphilic aneurysm- obliterative endarteritis of vasa vasorum

-> ischemic injury to media -> aneurysm

-> aortic valvular insufficiency

(regurgitation) with left ventricular

hypertrophy

What do you think of when a

patient presents with sudden

onset or acutely worsening chest

or back pain?

aortic dissection (an

emergency)

What people are at risk for

aortic dissection?

- HTN patients

- Marfan syndrome

- pregnant women

- patients undergoing invasive

vascular procedures

page 23 / 38


24/38


Where in the media does

aortic dissection happen?

between middle and outer

1/3 of media

What is the

cause of death

of this person?

aortic dissection- proximal spread -> weakened

aortic valve annulus -> ruptured

aortic root with resulting massive

hemopericardium

Name some complications

of aortic dissection.

- compression/occlusion of aotic

branches -> ischemia of areas

supplied by these branches

What disease is

this?

aortic dissection

- double shadow sign: column of

blood on medial layer creates the

sedcond line peripheral to the

aortic lumen

page 24 / 38


25/38


What is this?Type A aortic dissection

- hemopericardium

What is this?

Type A aortic disseciton

- extending around coronary

arteries into peridcardial sac

What is this?

and what can

this cause?

Cystic medial degeneration

(always present in Marfan

syndrome)

- aneurysm

- aortic dissection

Raynaud disease or phenomenon?

- younger women

- proxysmal and reversibe

- due to exaggerated vasomotor response to

cold or emotion

- no underlying disease

Raynaud disease

page 25 / 38


26/38


Raynaud disease or phenomenon?

- older adults

- intermittent and chronic cyanosis and coldness of samearea

- due to persistent arterial ischemia

- cause arterial stenosis

- due to exaggerated vasomotor response to cold or

emotion

- associated with atherosclerosis, SLE, Buerger disease.

Raynaud phenomenon

What are the two pathogenic

mechanisms of vasculitis?

- immune-mediated

- direct invasion by

infectious agent

What is the most common

vasculitis in the US?

giant cell arteritis (temporal

arteritis)

Two patterns of active giant

cell arteritis.

- granulomatous inflammation od inner

media with giant cells

- nonspecific panarteritis without giant

cells

page 26 / 38


27/38


What is this

disease?

giant cell arteritis

- intimal fibrosis- scattered giant cells

- patchy, transmural infiltrate of

lymphocytes, plasma cells and

macrophages

Where are the major

arteries affected by giant

cell arteritis?

- temporal

- vertebral

- ophthalmic


- younger women, under age 40

- weaker pulses and lower pressure in arms

than legs

- see giant cell miscroscopically

Takayasu arteritis (pulseless

disease)

- intimal thickening -> narrowed

arotic orifice of major arteries to

upper body

What is this

disease?

Takayasu arteritis (puseless disease)

- multiple stenosis of aortic arch vessels

- severe fibrosis with stenosis

- lymphocytic infiltrate with multinucleated

giant cells

page 27 / 38


28/38


What is this

disease?

PAN

- destruction of medial smooth muscle cell- fibrinoid necrosis of intima and media

- obliteration/stenosis of lumen

- transmural neutrophils (necrotizing

inflammation)

Name a segmental disease. PAN


- systemic vasculitis with transmural necrotizing

inflammation if medium/small arteries in any

organ except lungs.

PAN

What is the most frequently

affect artery in PAN?

Kiney

- heart

- liver

- GI tract

- pancreas

- testes

- skeletal muscle

- nervous system- skin

page 28 / 38


29/38


The following are sequelae of what disease?

- microaneurysms- obstruction

- ischemia with ulceration

- hemorrhage

- necrosis

- infarction

PAN


- vasculitis in medium sized vessels in

young children

- cardiac sequelae

Kawasaki syndrome


- sinusitis by necrotizing granulomatous

inflammation

- necrotizing capillaritis in lungs

- acute focal glomerulitis

Wegener granulomatosis

- upper respiratory

tract lesion

- lung

- kidney

What is this?

necrotizing capullaritis of lung

- neutrophils infiltrating alveolar

septae

- wegener granulomatosis

page 29 / 38


30/38


What is this?transmural necrosis and obliteratio

of lumen in medium sized artery

- wegener granuloamtosis

What type of arteritis is this?

- pneumonitis -> secondary

pulmonary vasculitis

infectious arteritis


- meningitis -> vasculitis in adjacent

superficial cerebral arteries



- endicarditis -> embolization to

arteries


page 30 / 38


31/38


Pathogenesis of varicose

veins in the leg.

venous stasis -> incompetent

venous valves -> congestion,

thrombosis ->

edema/dermatitis/ulcers

T/F: Pulmonary emboli are

often from superficial

venous varices.

F.

Pathogenesis of esophageal

varices.

cirrhosis -> portal hypertension ->

progressively enlarging varices

Pathogenesis of

hemorrhoids.

prolonged pelvic venous

congestion caused by pregnancy,

chronic constipation, straining at

stool, pants too tight.

page 31 / 38


32/38


Thrombosis in veins is

called ___.

thrombophlebitis /

phlebothrombosis

Where does phlebothrombosis

most likely originate from?deep leg veins

What are some risk factors

for phlebothrombosis?

- prolonged bed rest

- cardiac failure

- neoplasia

- pregnancy

- post operative state

- obesity

- genetic hypercoagulable state


- leg edema, redness, swelling

- + homan sign

phlebothrombosis

page 32 / 38


33/38


What is usually the firstmanefestation of

phlebothrombosis?

embolic event

What is the #1 cause of

sudden death in post-op

patients?

pulmonary thrmobiembolism

(saddle)

Which patients are at risk

for pulmonary

thromboembolism?

- cancer

- post-operative

- cardiac failure

What are some sequelae of

pulmonary thromboembolism?

- acute ischemia of lung

- impaired filling of left atrium and

ventricle, may lead to

cardiovascular collapse

page 33 / 38


34/38



- dusky cyanosis

- dilated veins of head, neck, arms

- respiratory disress

Superior vena cacal syndrome- obstruction of SVC by neoplasm

(lung cancer mostly)

What ist his disease?

- leg edema

- distension of superficial abdominal

collateral veins

- massive proteinuria

inferior vena caval syndrome- neoplasm compress or envade

vein

- mostly hepatocellular carcinoma,

renal cell carcinoma


- dilated lymphatics up to the point of

obstruction

- big body parts

- secondary induration and ulaceration of

skin

primary lymphedemas (rare)

Name a hereditary familial

lymphedema syndromeMilroy disease

page 34 / 38


35/38



- female, 10-25 age

- edema in feet, progress upward

lymphedema praecox


- painful red subcutaneous streaks

- regional llymphadenopathy

lymphangitis

- bacterial infection: group A

strep most common

What is this

disease?

hemangioma (begnine)

- red-purple spongy mass

- +/- thrombosis

What is this

disease?

hemangioma (benign)

- proliferating blood vessels

- irregular vessels lined by uniform

endothelial cells

page 35 / 38


36/38


What is this

disease?

vascular ectasia (benign)

- dilation of preformed vessels- telangiectasia

- nevus flammeus

- spider telangiectasia of skin: cirrhosis,

pregnancy

What is this

disease?

osler-weber-rendu disease

- spontaneous epistaxis

- diffuse telangiectasia

- death from intestinal bleeding

What is the

cause of this?

bacillary angiomatosis

- bartonella henselae (cat-scratch)

- bartonella quintana

tumor like growth capillary growth with

cellular atypia and mitoses

Name 2 malignant vascular

tumors.

- angiosarcoma

- hemagiopericytoma

page 36 / 38


37/38


Which type of kaposisarcoma do europeans

have?

chronic

Which type of kaposi

sarcoma do Africans have?lymphadenopathic

Which type of kaposi

sarcoma do transplant

patients have?

immunosuppression

associated

Which virus is associated

with kaposi sarcoma?HHV8

page 37 / 38


38/38


Describe the stages of skin

lesions in kaposi sarcoma.

- patch- plaque

- nodule

What is this

disease?

kaposi sarcoma

- patches and plaque

Documents

Cardiology Blood Vessel Pathology-large