Lec 2- Blood Vessels

8/3/2019 Lec 2- Blood Vessels

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Characteristics Structures Involved Clinical Features Lab Diagnosis Treatment

Giant Cell

Arteritis

- Age >50 yrs

Def: An acute and

chronic granulomatous

inflammation

- nodular thickenings

affected artery develop

these nodular

thickenings and may

become thrombosed

ischemia

(palpably firm andpainful)

Vasculitis produces this

b/c thrombus Ischemia

- Temporal artery (pain,

head ache),

- Ophthalmic artery-

blindness, diplopia

- Branches of external

carotid arteries: TIA (

episodes last< 24 hours).

Stroke (>24 hours)

- Polymyalgia

rheumatica (joint &

muscle pain), jaw pain

(caludication), abrupt

headaches, weight loss,

anorexia, loss of vision

and tenderness*.

- Temporal headache,

sudden diplopia.

Cannot see a thrombus

here…maybe it is gone

- ↑ ESR

Characteristics Structures Involved Clinical Features Lab Diagnosis Treatment

Takayasu

Arteritis

- Age <40 yrs

- Female

- pulseless

disease

- Granulomatous vasculitis

- branches of aortic arch,

renal, pulmonary and

Ophthalmic artery.

- Renal artery

Sec. hypertension (

↑Renin level)

1. aneurysm

2. narrowing

3. Occlusion

- BP and weaker

pulses in the upper

extremities ( carotid,

radial, ulnar) than in

the lower= pulseless

disease*.

- Ocular disturbances.

Giant Cell



Characteristics Structures Involved Clinical Features Lab Diagnosis

Wegner

Granulomastosis

- aka…

Necrotizing

(granulomatous)

vasculitis

Triangle of death

1. Hole in the hard palate

(eroding the bone) systemic

involvement

2. Giant cell granuloma

3. Renal and Respiratory

system involved

- affects capillaries,

venules, arterioles, and

arteries.

- Giant cells is the blood vessels in

lung, kidney

- Death within 1 year if

untreated (malignant course).

- Nasopharynx:

- Mucosal ulceration,

sinusitis*, rupture of nasal

septum/ bleeding.

- Lung:

Pneumonitis/condolidation=

Hemoptysis*.

1. Mucosal ulcer in the

nose

2. Sinusitis

3. Bleeding from nasal

septum

- Kidney:

- Crescentic

Glomerulonephritis → acute

renal failure (hematuria*+

elevated BUN, creatinine).

- 20

Hypertension.

- c-ANCA* is positive in the serum in

95% & is used to monitor disease

activity.

dd TB bcz see caseous necrosis

- giant cell seen in both but in this case

it is found around the blood vessels

NOT tissue

It’s a quick course….2-3 months



Characteristics Structures Involved Clinical Features Lab Diagnosis

Polyarteritis

Nodosa (PAN)

•It is a Systemic vasculitis.

–Hepatitis B surface

antigen present (HBsAg)*.

–Typically ANCA negative

PAN produces aneurysm

of the renal artery! Similar

to that seen in the

Wegenar.

- Involves Kidney, skin

and other organs….

Except the lungs***

Age: all age group

Course: E pisodic illness*.

Others:-

1.Malaise, fever of unknown cause, and

weight loss;

2.Hypertension, Abdominal pain and

melena (bloody stool)

3.*Skin: Palpable skin Purpura ( but this is

more common in leukocytoclastic vascuitis)

Morphology: : Patchy fibrinoid

necrosis (bright pink, fibrin-like,

refractile intimal deposit)* of intima

and adventitia with thrombosis.



Characteristics Structures Involved Clinical

Features

Lab Diagnosis

Churg- Strauss

Syndrome

(variant of PAN)

•Features:

Involve pulmonary vasculature

Eosinophilia

Asthma

Morphologically is similar to PAN

pANCA is positive

MORPHOLOGY similar to PAN

PAN Churg- Strauss

Syndrome

No

Eosinophilia

Eosinophilia

Kidney inv. No Kidney inv

NO Lung Involves LUNG

pANCA neg. pANCA pos.

-



Characteristics/ Etiology Structures Involved Clinical Features Lab Diagnosis

Immune Complex

Vasculitis:

AKA (Microscopic

polyarteritis,

Hypersensitivity,

OR

Leukocytoclastic

Vasculitis.)

•Etiology: reaction to an antigen

such as –Drugs (e.g., penicillin),

–Microorganisms (e.g.,

streptococci) or

–Malignancy

- pANCA is positive

•Affects arterioles, capillaries, andvenules-vessels. (venules… like in

Wegners)

•Deposition of antigen-antibody

complex in vessels wall.

•Skin: Palpable skin Purpura ( this

is more common than PAN),

hemoptysis, arthralgia, muscle painor weakness.

•Morphology: neutrophilic

vasculitis*.




Henoch-

Schonlein

Purpura

- Type of Leukocytoclastic vasculitis

-

•IgA mediated Skin purpura (vasculitis).

•Dermal IgA deposit: Dermatitis

herpetiformis.

•IgA deposition in kidney= recurrenthematuria.

•Abdominal manifestations:

–Pain, vomiting, and intestinal bleeding;

nonmigratory arthralgia. Negative for p-

anca.




Thromboangiitis

Obliterance

- AKA (Buerger

Disease)

•Thrombus and abscess in the

artery.

•Age & sex: middle aged(

before 35 years)

•Men > women

•There is a very close

association with smoking*. Tx

Stop smoking!

•Site: tibial and radial arteries.

- Early: Fingers show Raynaud

phenomenon and feet show

claudication.

- Late: Gangrene in some

In upper limbs: Raynaud

Phenomenon

In lower limbs: Claudication

Raynaud Phenomenon:

Paroxysmal color change:

whitebluered

Two types: –Primary = Vasoconstriction due

to cold, stress etc= neurological.

–Secondary: due to pathological

obstruction of artery as seen in

Buerger disease, scleroderma,

SLE etc.

Pathophysiology: Smoking Nicotine endothelial injury

thrombus. --> ischemia

gangreene (tibial/radial)

Arrow is showing ABSCESS!

(puss)

- Lumen occluded by a

thrombus with two

microabscesses (arrow)




Kawasaki Disease •Age: young children •Location: coronary artery →

AneurysmMyocardial infarction

•Clinical: conjunctivitis +

maculopapular skin rash +

lympadenopathy.

Looks like viral infection

Coronary artery aneurysm may

occur.

Characteristics/ Etiology Structures

Involved

Clinical Features Lab Diagnosis

Systemic Lupus

Erythematosus •Fibrinoid necrosis is present. Like PAN.

•Antibodies in SLE: –Anticardiolipin Ab.→ deep VENOUS thrombosis

(aka- Antiphospholipid syndrome) present.

–ds-DNA ANA, anti-smith ANA- not involved in DVT.

Antiphospholipin syndrome of DVT

1. SLE, 2. DVT 3. Anticardiolipin Ab.

- Fibrinoid necrosis seen here.

IT is an exudate made out of

fibrinogen.




Varicose Veins Abnormally dilated, tortuous veins

produced by

1.Prolonged, increased intraluminal

pressure (valve incompetence).2.Loss of vessel wall support-

muscle weakness- paralysis.

3.Weak valve or genetic

•Esophageal varices: seen in

patients who have cirrhosis of the

liver and its attendant portalhypertension.

•Hemorrhoids:

–varicose dilation of the

hemorrhoidal plexus of veins at

the anorectal junction: produce

fresh blood during defecation.

–Caused by repeated

pregnancies, straining at stools

(by cocaine).

Clinically silent (NO PAIN)

Varicos veine: without

THROMBUS and is NOT

painful/tender OF SUPERFICIAL

VEINS (i.e great saphenus).

Thrombophlebitis: vericose vein

with THROMBUS and has

Inflmmation and is TENDER and

PAINFUL.




Deep Vein

Thrombosis

•Cause: these veins usually don’t

form thrombus b/c of the fast flow.

Viscocity of the blood is elevated

due to: hypercoagulable states: – Adenocarcinoma , pregnancy,

immobilization, bone fracture* and

others.

- Viscosity of the blood is elevated

due to the

- Iliac, femoral, popliteal veins. - All 3 veins: asymptomatic, leg

swelling, erythema in some

cases.

Complications: Thrombus

acute cor pulmonale (RHF).

Also: Pulmonary infarction

which is acute and quick death.

Note: thrombus. Infarcted

area becomes RED.




Angiosarcoma

Tumor of the

blood vessel

• Age: often in older adults

• Marker: CD31, CD34, or vWF, FVIII• Carcinogen: Arsenic, polyvinyl

chloride (plastic factory),

Thorotrast.

- Most commonly in the SKIN and

LIVER (others: soft tissue, breast).

-

•Morphology: proliferatingvascular channels,

hyperchromatic spindle cells

(cancerous) and RBC.

Characteristics/ Etiology Structures

Involved

Clinical Features Lab Diagnosis

Kaposi’s

Sarcoma

Agent: HIV and KSHV-8

-If it occurs in the SKIN= Kaposi’s sarcoma. It is

basically an angiosarcoma, of the skin.

- HIV infectionImmune system is depressed

herpes virus comes in to produce this sarcoma- Vimentin is a nonspecific marker here.

Pathogenesis: KSHV proteins Incorporate in host

genome and:

1.May disrupt the control of cellular proliferation

(cell cycle S PHASE) by inactivating Rb gene , and

2.Prevent apoptosis of endothelial cells, through

the production of p53 inhibitors.

- It is a dermal

angiosarcoma.

•Clinical : Multiple growing red

to purple skin plaques or

nodules or on the hard palate

(Kaposi’s does not look like a

cancer clinically (despite itbeing cancer)…it looks like a

skin rash!!!.

In perineal, lower limbs and

oral cavity.

NON-painful and does not look

like cancer. Covers your whole

skin very rapidly.

•Morphology: sheets of plump,

proliferating hyper chromatic spindle

cells & RBC (CD31, CD34 and vWF,

Factor 4 and 8, Vimentin…) and slit like

spaces

Note: white slit

like spaces. Lots

of spaces & RBCs



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Lec 2- Blood Vessels