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8/12/2019 Bloods Vessel

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BLOODS VESSEL

In general vascular abnormalities cause clinical disease

by:

1. Progressively narrowing the lumina of vessel &

producing ischemia of the tissue perfused by that

vessel.

2.Provoking intravascular thrombosis, causing acute

obstruction or embolism or both!.

".#eakening the walls of vessels there by leading to

dilatation or rupture.

I.Congenital anomaly:

1.$erry aneurisma.

2.%rteriovenous fistula.


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II.Atherosclerosis & other forms of

arteriosclerosis.

A.Atherosclerosis:

haracteri'ed by intimal thickening & lipid deposition.

(he basic lesion, the atheroma, or fibrofatty pla)ue

consists of a raised focal pla)ue within the intima,

having a core of lipid mainly cholesterol & cholesterol

ester! and a covering fibrous cap.

*eath from cardiovascular disease in +.. rose from 1-

of all deaths in 1/"0 to - in 1/3.

4isk factors for atherosclerosis :

Major:

5iperlipidemia hypercholesterolemia,

hypertriglycerimia!.


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Minor:

6besity, physical inactivity, male gender, increasing

age, family history, stress, oral contraceptives, high

carbohidrat intake.

%therosclerotic pla)ue have three principalcomponents:

1. ell, including smooth muscle cell, macrophages

and other leucocytes.

2. onnective tissue e7tracellular matri7, including

collagen, elastic fibers & proteoglycans.

". Intracellular & e7tracellular lipid deposits.

(he complicated lesion of atherosclerosis:

1. alcification.

2. 8ocal rupture or gross ulceration.

". (hrombosis.


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-. 5emorrhage.

B.MOC!EBE"#$S Arteriosclerosis.

9edial calcific sclerosis!.

haracteri'ed by ring like calcifications within the

media of medium si'ed to small muscular arteri.

(he calcification is not associated with anyinflammatory reaction, and the intima and adventitia

are largely un affected.

(he calcific deposit do not narrow the lumen.

C.A"%E"IOLOSCLE"OSIS.

9arked by proliferation or hyaline thickening of the

walls of small arteries & arteriol.

III.ILAMMA%O"' DISEASE( %)E

VASC*LI%IDES.

+.#iants cell ,tem-oral arteritis.


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(he most common of the vasculitides, is a focal

granulomatous inflammation of arteries of medium si'e

and small si'e that affects principally the cranialvessel, especially the temporal arteries in older

individuals rare before age !, but also the

vertebrae and ophthalmic arteries!.

(he histologic change:

1. ;ranulomatous lesion with giant cell.

2.


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virtual obliteration of the great vessels arising in the

arch.

(he cause and pathogenesis are unknown.

0.1OL'A"%E"I%IS ODOSA #"O*1 ,1A.

P%< is manifested by necroti'ing inflammation of

small or medium si'ed muscular arteries.(ypically involving renal and visceral vessel & sparing

the pulmonary circulation.


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9ucocutaneous lymph node syndrome!.

Is an arteritis involving large, medium si'e & small

arteries of the coronary arteries! that is associatedwith the mucocutaneus lymph node syndrome usually in

young children & infant 3 yonger then four years

old!.

(he acute illness is manifested by fever, con=unctival &

oral erythema & erosion, edema of the hands & feet,

erytheme of the palm & soles, a skin rash often with

des)uamation & enlargement of cervical lymph node it

is usually self limited.

4.Microsco-ic -olyangitis.

9icroscopic polyarteritis , hypersentivity!.

(his type of necroti'ing vasculitis generally affects

smaller vessel than P%< arteriols, capillaries, &

venules!.


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intermediate & small arteries & sometimes vein of the

e7tremities.

(he condition had accured almost e7clusively in menwho were heavy cigarret smoker.

IV.Ane6risma & Dissection.

A.An ane6risma is a locali'ed abnormal dilatation ofany vessel.

6ccur in any artery or vein of the body, most commonly

the aorta.

%therosclerosis, the most fre)uent etiology of

aneurysm causes arterial wall thinning through medial

destruction secondary to pla)ue that originates in the

intima.

>):?%bdominal aortic aneurysm.

?yphilitic luetic! aneurysm.

B.AO"%IC DISSEC%IO:


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Is an catastrophic illness characteri'ed by dissection

of blood along the luminar planes of the aortic media,

with formation of blood filled channel within the aorticwall & that often rupture, causing massive hemorrhage.

In contrast to atherosclerotic and syphilitic aneurysm,

aortic dissection is not usually associated with marked

dilatation of the aorta.

ome dissection are related to the inheritedconnective tissue disorder marfan syndrome, an

autosomal dominant disease of connective tissue

fibrillin, characteri'ed by skeletal, cardiovascular &

ocular manifestation.

(he serious cardiovascular complication is dilatation ofthe aortic rootannuloaortic ectasia! and mitral valve

prolapsed.

V.VEI & L'M1)A%ICS.

A.Varicose 9eins.

%re abnormali dilated, turtous veins produced by

prolonged, increased intraluminal pressure.


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(he superficial veins of the legs are the preponderant

site of involvement.

Portal hypertention cirrhosis of the liver! leads tovarices in the esophageal & hemorhoidal veins!.

B.Lym-hangitis.

C.Lym-eema:

(he most common causes:

1. pread of malignant tumor.

2. 4adical surgical procedure.

". Post irradiation fibrosis.

-. 8ilariasis.

. Post inflammatory thrombosis & scarring of

lymph channel!.

VI.%*MO".


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+.)emangioma:

apillary hemangioma:

%re composed of blood vessels that resemble

capillaries, narrow, thin walled & lined by relatively thin

endothelium. +sually occurring in the skin,

subcutaneous tissue & mucous membrane of the oral

cavities & lips, they may occur in internal vicera, such

as liver, spleen & kidney.

avernous hemangioma:

*istinguished by the formation of large cavernous

vascular channels.

6ften occurring in childhood, they have predilection

for the skin of the head & neck & mucosal surface of

the body, also found in many viscera, particulary the

liver, spleen, pancreas, & occasionally the brain.

/.#"A*LOMA 1'O#EIC*M;ranulation tissue

type hemangioma!.


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6f uncertain neoplastic nature & currently considered

a plypoid form of capillary hemangioma, these masses

appear as e7ophytic red nodule on the skin & gingival ororal mucosa & are often ulserated.

0.#LOM*S %*MO".,#lomangioma.

% benign but e)uisitely painful tumor that arise from

the modified smooth muscle cell of the glomus body.

% neuromyoarterial receptor that is sensitive to

variation in temperature & regulates arterial flow.

2.VASC*LA" EC%ASIA ,%elangiectasia.

*esignates a group of abnormally prominent capillaries,

venules & arteriol that created a small focal red lesion,

usually in the skin or mucous membrane.

4.)EMA#IOEDO%)ELIOMAintermediate

malignancy!.


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% true neoplasma of vascular origin composed

predominantly of masses of endothelial cell growing in

and about vascular lumina.

5.A#IOSA"COMA ,)EMA#IOSA"COMA.

Is a malignant neoplasma of vascular origin,

characteri'ed by masses of endothelial cell displaying

the celluler atypia & anaplasia characteristic of

malignancy.

7.)EMA#IO1E"IC'%OMA ,malignant

(he origin of these tumors to pericyte most of these

neoplasms are small.

(hey consist of numerous capillary channel surrounded

by & enclosed within nest & masses of spindle shaped

cells. (hat these cell are outside the basement

membrane of the endothelium.

;.!A1OSI$S SA"COMA.


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onsist spindle shaped stromal cell containing irregular,

angulated, slit like spaces filled with red cells & lined

by recogni'able endothelium, interwined with normalvascular channels.

B.L'M1)A#IOMA:

+.SIM1LE ,ca-illary lym-hangioma.

(hese masses composed of small lymphatic channels

tend to occur subcutaneously in the head & neck region

& in the a7illa.

/.CAVE"O*S L'M1)A#IOMA ,cystic hygroma.

omposed of cavernous lymphatic spaces and therefore

are analogous to cavernous hemangioma.

0.L'M1)A#IOSA"COMA.

(he tumor is composed of channels lined by anaplastic

endothelial cells.


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%)E )EA"%

auses of cardiovascular dysfunction:

1. @oss of blood.

2. Iregular heart beat.

". 6bstructed flow.

-. 4egurgitant flow.

. Pump failure.

?ontractile dysfunction systole failure!.

?Inade)uate filling diastolic failure!.

I.CO#ES%IVE )EA"% AIL*"E ,C).

#hen sufficiently severe or advanced, may ultimately

impair cardiac function and render the heart unable to

maintain an output sufficient for the metabolicre)uirements of the tissues & organs of the body,

producing congestive heart disease.


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%s stated 58, occurs either because of a decreased

myocardial capacity to contract or because of an

inability to fill the cardiac chambers with blood.

CA"DIAC )'1E"%"O1)'.

(he compensatory response of the myocardium to

increased work.

9yocardial hyperfunction induces increased myocite

si'e cellular hypertrophy! that increase in the overall

mass and si'e of the hearts.

aused the cardiac hypertrophy:

1. 5ypertension.

Pressure overload.

2. Aalvular disease.

Pressure andBor volume overload.

". 9yocardial infarction.

4egional dysfunction with volume overload.


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II.ISC)EMIC )EA"% DISEASE ,I)D.

Is the generic designation for a group of closely

related syndrome resulting from ischemia.

*epending on the rate of development and ultimate

severity of the arterial narrowing and the myocardial

response, four ischemiac syndrome may result.

+.Angina -ectoris.

Is a symptom comple7 of I5* characteri'ed by

paro7ysmal attacks of substernal or precordial chest

discomfort variously described as constricting,

s)uee'ing, choking or knife like! caused by transient

1 secons to 1 minutes!.

(here are three pattern of angina pectoris

?table or typical angina.

?Prin'mental.


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?+nstable or crescendo angina.

/.Myocarial Infarction.

9yocardial ischemia that falls short of inducing the

cellular necrosis that difines infarction.

(here are two types of myocardial infarction each

having differing morphology & clinical significance.

%ransm6ral infarct:

In which the ischemic necrosis involve the full

thickness of the ventricular wall.

(his pattern of infarction is usually associated with

coronary atherosclerosis, pla)ue rupture &

superimposed thrombosi

S68enocarial infarct:

onstitutes an area of ischemic necrosis limited to the

inner one?third or at most one?half of the ventricular

wall.


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(he clinical diagnosis of acut myocardial infarction is

mainly based on :

?ymptoms.

?>lectrocardiographic >;!.

?>levation of specific serum en'yme creatine

phosphokinase PC! & @actate dehidrogenase @*5!.

0.C)"OIC ISC)EMIC )EA"% DISEASE.

Is used here for the hearts in patients often but not

e7clusively elderly, insidiously develop 58, some times

fatal, as a conse)uences of ischemic myocardial

damage.

Its must instances there has been a history of angina &

usually prior episodes of myocardial infarction, often asremote as to 1 year before the onset of the 58.


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2.S*DDE CA"DIAC DEA%)

9ost commonly sudden cardia death *! is defined

as une7pected death from cardiac causes early usuallywithin 1 hour!. %fter or without the onset of symtoms.

III.)'1E"%ESIVE )EA"% DISEASE.Is the response of the heart to the increased demands

induced by systemic or pulmonary hypertension.

A.Systemic ,left(sie hy-ertensi9e heart isease.

(he minimal criteria for diagnosis:

1. @eft ventricular hypertrophy usually concentric!

in the absence of other cardiovascular pathology

that might have induced it.

2. % history of hypertension.


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B.16lmonary ,right(sie hy-ertensi9e heart

isease.

,CO" 1*LMOALE.

ontitutes the rights ventricular enlargement,

secondary to pulmonary hypertention caused by

disorder that affect the lung or pulmonary vasculature.

*isorders predisposing to cor pulmonale:

1. *iseases of the lung.

2. *iseases of pulmonary vessels.

". *isorders affecting chest movement

-. *isorder inducing pulmonary arteriolar

constriction

IV.CO#EI%AL )EA"% DISEASE.

%.@eft to?right shunts? late cyanosis.

+.Atrial se-tal efect ,ASD.


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%n abnormal opening in the atrial septum that allows

free communication of blood between the right & left

atria.

(he three ma=or types of %*:

?ecundum type %*.

?Primum anomaly?sinus venosus.

/.Ventric6lar se-tal efect ,VSD.

%n abnormal opening in the ventricular septum thatallows free communication between right & left

ventricles.

0.1atent 6ct6s arterios6s ,1DA.


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4esuts when ductus arteriosus, a normal

aortopulmonary vascular channel during intra uterine

life remain open after birth.

2.Atrio9entric6lar se-tal efect.

4esult from abnormal development of the embryologic

atrioventricular canal, which the superior & inferior

endocardial cushion fail to fuse ade)uately, resulting in

complete closure of the %A septum & inade)uate

formation of the septal tricuspid & anterior mitral

leaflefts.

B."ight to left sh6nts( early cyanosis.

+.%etralogy of fallot:

(he four features , the most common form of cyanotic

congenital heart disease are:

a. A*.


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b. 6bstruction to the right ventricular outflow

tract subpulmonary stenosis!.

c. %n aorta that overrides the A*.

d. 4ight ventricular hypertrophy.

/.%rans-osision of great anomaly.

(ransposision implies ventriculoarterial discordancesuch that the aorta arise from the right ventricle and

the pulmonary artery emanates from the left ventricle.

0.%r6nc6s arterios6s.

(he persistent truncus arteriosus anomaly arises from

a developmental failure of separation of the

embryologic truncus arteriosus into aorta & pulmonary

artery.


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2.%ric6s-i atresia:

omplete occlusion of the tricuspid valve orifice is

know as tricuspid atresia. It results embryologicallyfrom une)ual division of the %A canal, thus the mitral

valve is large than normal.

C.O8str6cti9e congenital anomaly.

1.oarctatio aorta narrowing, constriction!.

6f the aorta ranks, high in fre)uency among the

common structural anomalies.

2.Pulmonary stenosis or atresia with intact ventricular

septum.

".%ortic stenosis & atresia.


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V.VALV*LA" )EA"% DISEASE

1.*egenerative calcific aortic valve stenosis.

#ith either tricuspid or bicuspid valve is heaped up

calcifified masses within the aortic cusps that

ultimately protrude through the outflow surface into

the sinuses of valsava.

2.ongenitally bicuspid aortic valve.

".9itral annular calcification.

In elderly individuals, especially women, degenerative

calcific deposit can develop in the ring annulus! of the

mitral valve!.

-.9itral valve prolapse.

9y7omatous degeneration of the mitral valve!.

In this valvular abnormality, one or both mitral leaflets

are enlarged, redundant or DfloppyE & prolapse or

balloon back into the left atrium during systole.

.4heumatic fever & 4heumatic heart disease.


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Is an acute, often recurrent, inflammatory disease

principally of children ?1 year! that generally

follows a pharyngeal but not skin! infection with group% beta hemolytic streptococcus.

48 is the result of an immune response to

streptococcal antigen inciting either a cross reaction

to tissue antigens or streptococcal inducedautoimmune reaction to normal tissue antigens.

48 is characteri'ed by fever, anthralgia & a

constellation of findings that includes.

%.9a=or manifestations:

1. 9igratory polyarthritis of the large =oints.

2.arditis, .

".ubcutaneus nodules

-.>rythema marginatum of the skin.

.yndenhamFs chorea


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% neurologic disorder with involuntary purpose,

rapid movementFs.

$.9inor manifestation:

8ever, athralgia , or elevated acute phase reactant.

(he diagnosis is established by the Gones criteria.

>vidence of a preceding group % streptococcalinfection with the presence of two ma=or manifestation

or of one ma=or and one minor manifestation.

5.Infecti9e enocaritis.

Is characteri'ed by coloni'ation or invasion of the

heart valves or the mural endocardium by a

microbiologic agent.

omplication:

Aalvular insufficiency, myocardial ring abcess, emboli,

infarction renal, glomerulonephritis.


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7.on 8acterial throm8otic enocaritis.

Is a form of vegetative endocarditis most often

encountered in debilitated patients, such as those with

cancer or sepsis.

;.Enocaritis of systemic l6-6s erythematos6s.

In @> mitral & tricuspidal valvulitis is occasionallyencountered & leads to the development of small

sterile vegetation.


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Idiophatic * is characteri'ed by the gradual chamber

hypertrophy & dilatation of the heart of unknow cause.

/.)y-ertro-hic cariomyo-athy.

Idiopathic hyperthrophic subaortic stenosis,

obstructive cardiomyopathy!.

Its characteri'ed by a heavy muscularhypercontracting heart.

0."estricti9e cariomyo-athy.

(he ventricles are appro7imately normal si'e or slightly

enlarged.

(he cavities are not dilated & the myocardium is firm.

$iaterial dilatation is commonly observed.

9icroscopically: (here is patchy or difuse interstitial

fibrosis which can vary from minimal to e7tensive. $ut

the cause is unknown.


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2.Myocaritis:

Is best defined as an inflammatory involvement of the

heart muscle, characteri'ed by a leucocyte infiltrate &resultant non ischemic necrosis or degeneration of

myocytes.

VII.1E"ICA"DIAC DISEASE.

%.%ccumulation of fluids in the pericardium normally

therenis "? ml of thin, clear,strow?collored,

translucent fluid in the pericardial space.

5emopericardium, is the accumulation of pure blood in

tpericardial sac, distint from hemorrhagic pericarditis,

a condition in which there is an inflammatory e7udates

containing blood mi7ed with pus.

B.1ericaritis.

Inflammation of the pericardium are usually secondary

to systemic disorder or to metastases from neoplasms

arising in remote site.


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C."he6matoi heart isease.

(he most common finding is a fibrinous pericarditis

that may progress to fibrous thickening of visceral &

parietal pericardium with dense adhesions.

4heumatoid inflammatory granulomatous noduleresembling those that occur subcutaneously may be

identifiable deep to the pericardial surface.

VII.EO1LAS%IC )EA"% DISEASE.

+.My=oma:

%re the most common primary tumor of the heart in

adults. %bout / are located in the atria.

/.Li-oma:

9ay occur in the subendocardium, subepicardium or

within the myocardium.

".Papillary fibroelastoma.


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2."ha8omyoma.

4.Sarcoma.