Download Cardiovascular System

Cardiovascular System
By
Prof. Maha Abuhashim
2013-2014
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Diseases of the heart (ILOs)
Congenital cardiovascular malformations
Rheumatic fever
Endocarditis
Ischaemic heart diseases
Cardiomyopathy
Pericardial diseases
Tumors of heart and pericardium
Heart failure
Congenital Heart Diseases
Incidence:- 50% Of all congenital anomalies of the body.
- 1-2% of all heart diseases. - 10% of heart diseases in children.
Causes:1- Hereditary
2- Teratogenic effects of infections (G. measles or syphilis) or drugs during the
first 3 months of pregnancy.
Congenital Heart Diseases
Acyanotic group
1- Venticular septal defect (VSD)
2- Atrial Septal Defect (ASD)
3- Patent ductus arteriosus
Hemodynamics
- Blood passes from the left to right side and no cyanosis is produced.
- Right side overload …..failure……increased pressure … reversal of the shunt from
right to left……cyanosis
ASD
VSD
PDA
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4- Coarcitation of the aorta
Aortic narrowing between the origin of the left subclavian artery and ductus
arteriosus leading to
1- Stronger pulse in the upper half of the body.
2- Hypertension in the upper half of the body.
3- Left ventricular failure (due to hypertension
Cyanotic group
1- Falott’s tetralogy
2- Falott’s triology
3- Eisenmenger disease.
1- Falott’s tetralogy
It includes
a. pulmonary stenosis
b. VSD
c. Rt vent. failure
d. Dextroposition of aorta…it receives blood from both ventricles
 2- Falott’s triology
a.Pulm.stenosis
b.Rt.vent.failure
c.ASD
 3- Eisenmenger disease.
a. Rt.vent.failure
b.VSD
c.Dextro-position of the aorta
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Rheumatic fever
- An autoimmune disease affecting mainly the heart, joints, subcutaneous tissue and
CNS.(multi-system autoimmune disease)
Incidence:- Children between 5-15 years.
- Developing countries.
- Low socioeconomic standards
Pathogenesis:- Rheumatic fever is an immune disorder that follows an upper respiratory tract
infection (1-4 wks after) in children by certain strains of streptococci (group A β
hemolytic streptococci).
- Streptococcal antigen stimulate antibody production in certain susceptible
individuals which cross-react with host cardiac antigen evoking the disease.
- An elevated anti-streptolysin O (ASO) is evidence of recent streptococcal
infection
Aschoff’s nodule
Grossly:- Aschoff’s nodules
appear as pale, lemon shaped foci. They heal by fibrosis
Unit lesion is called Aschoff’s nodule which is a granuloma formed of central fibrinoid
necrosis, chronic inflammatory cells and Aschoff’s type giant cell.
Rheumatic fever
Pancarditis
- Rheumatic fever produce inflammation of three heart layers
1- Pericardium
2- Myocardium
3- Endocardium
i.e. it is Pancarditis
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Rheumatic pericarditis
- Aschoff’s nodules form in the pericardium associated with acute pericarditis.
- It produces serofibrinous pericarditis especially at the base of the heart.
- Pericarditis heals by organization (fibrosis) which can result in……
Rheumatic pericarditis
1- White patches of fibrosis at the surface of the heart (milk patches).
2- Adhesions between the visceral and parietal pericardium (bread and butter
appearance)
3- Adhesions between the parietal pericardium and adjacent mediastinal structures
(adherent mediastino-pericarditis) …interferes with cardiac contractions
Serofibrinous pricarditis, rough surface
Rheumatic Myocarditis
- Aschoff’s nodules developing in the myocardium are associated with interstitial
edema and mild inflammation, sometimes with muscle fiber necrosis.
- The condition is usually mild, but may rarely produce left ventricular failure
Rheumatic endocarditis
1- Mural endocardium
…… Inflammation and Aschoff’s nodules especially at the Mc Callum’s patch on the
posterior wall of left atrium…..healing by fibrosis…rough surface…..thrombosis
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2- Valvular endocarditis
- Inflammation of the cardiac cusps especially the mitral and aortic valves.
- Aschoff’s nodules with edema results in swelling of the leaflets of the cusps,
friction of their free borders….injury of the endothelium……thrombosis
(vegetations)
Rheumatic vegetations
- Small adherent valvular thrombi
- Found on the free border of the valve mainly mitral and aortic.
Why??
- Later on they are organized by fibrous tissue
 N/E:
Chronic valvular endocarditis
Fibrosed, thick cusps. Fibrous retraction produces deformities:
a) Stenosis b) Incompetence
c) Combined
Calcification can occur in any form.
 M/E:
- Valve cusps are fibrosed; contain thick walled
vessels and some lymphocytes. Patches of
calcification may be seen.
- Vegetations are fibrosed
Normal aortic valve
Normal Valve
Calcific Stenosis
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Valvular complications of rheumatic fever
Aortic stenosis
- Healing of acute valvular lesion by fibrosis with fusion of the cusps result in
inability of the valve to open properly…….
stenosis
Aortic incompetence
- Healing of acute valvular lesion by fibrosis with contraction of the cusps result in
inability of the valve to close properly…….
incompetence
Mitral stenosis
The valve has a fish-mouth appearance.
- Mitral stenosis ……. Pulmonary hypertension…….. Right sided heart failure
(Cor pulmonal)
Mitral stenosis results in chronic venous congestion of the lung
Complications of rheumatic fever
 Cardiac arrhythmias especially atrial fibrillation.
 Valvular lesions.
 Sub-acute bacterial endocarditis
Non Cardiac Manifestations of Rheumatic Fever
1- Fever, malaise and increased ESR.
2- Joint involvement …arthralgia, arthritis and migratory polyarthritis that usually
heals without residual effect due to sparing of the articular cartilage.
3- Subcutaneous nodules especially over bony prominences.
4- Sydenham’s chorea …involuntary purposeless muscular movements and emotional
lability
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Diagnosis of Rheumatic Fever
Jones criteria
Major criteria
- Carditis
- Polyarthritis
- Chorea
-Dermatologic affection.
- Subcutaneous nodules
Minor criteria
- Fever
- Arthralgia
- increased ESR or CRP
-Raised ASO titre.
- ECG changes
- Leucocytosis
At least
-Two major or
- One major +two minors
 Types of endocarditis
Endocarditis
1- Non infective endocarditis
a. Rheumatic fever
b. Systemic lupus erythematosus
c. Endocarditis of carcinoid syndrome
d. Marantic endocarditis …mitral and aortic valves in patients died from wasting
diseases
2- Infective….TB, S, typhoid
Viral, fungal, histoplasma capsulatum
Most commonly seen is Infective bacterial endocarditis
I. Non infective endocarditis
 A.Libman-Sacks endocarditis
Occurs in systemic lupus erythematosus (SLE)
- Affects mainly the mitral valve.
- They are multiple , small, near the valve ring.
- Result from immune complex mediated endocardial injury followed by thrombus
formation
 B. Endocarditis of Carcinoid syndrome
Intestinal carcinoid tumors with metastases to the liver…. Secretion of vasoactive
amines (mainly serotonin)….secreted to the hepatic vein….IVC to the right side of
the heart….damage of the endocardium which heals by fibrosis especially of the
tricuspid valve
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 Non-bacterial thrombotic endocarditis (NBTE)
Known as marantic endocarditis.
- Occurs in debilitated patients as those with advanced metastaic cancer.
- Pathogenesis is not exactly known.
- They are sterile vegetations on cardiac valves, that may be infected.
II-Infective endocarditis
Bacterial endocarditis
1. Acute bacterial endocarditis
2. Subacute bacterial endocarditis
3. Endocarditis on prosthetic valve
Effects of Infective Endocarditis
 Result from 4 main sets of events:1- Valve destruction
2- Dissemination of bacteria.
3- Embolization.
4- Immune complexes
*Acute infective endocarditis
- Virulent microorganism + normal valve.
Causative organism …Staph.Aureus (50% of cases)
- Valves affected…. Mostly mitral and aortic. Right side valve affection in drug
addicts.
- Lab. Diagnosis…..Blood culture
- Acute suppurative inflammation.
-Severe valve destruction
- Vegetations are large polypoid yellow and friable
-When detached they cause PYAEMIA
- Myocardium shows abscesses
- Severe toxemia, rapidly fatal
Acute Infective endocarditis
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 * Sub acute infective endocarditis:- Low virulence organism + diseased valve.
- Causative organism Streptococcal viridans (more then 50% of cases)
- Non suppurative inflammation.
- Less severe valve destruction
- Vegetations are smaller,less valve destruction.
- When detached they cause infarctions or mycotic aneurysm.
-Chronic toxemia leads to toxic capillaritis in the skin &kidney
Endocarditis on prosthetic valves
 - Staphylococcal infection (more than 50% of cases).
- Occurs 2 months after surgery.
- It is due to intra-operative contamination with drug resistant pathogens (staph.gram negative bacteria or fungus)
Ischemic Heart Diseases
- A group of diseases due to insufficient arterial blood flow to the myocardium.
- Chronic ischemia results in angina pectoris which may be stable or unstable.
- Acute ischemia results in myocardial infarction.
 Angina pectoris
An episode of pain in the substernal area of the chest precipitated by exercise or
excitement and relieved by rest.
 Causes :
– Coronary atherosclerosis.
– Coronary spasm.
– Aortivc valve stenosis or incompetence
 Types:-
Angina pectoris
1- Stable angina…evoked by exercise and relieved by rest.
2- Unstable angina…sever pain precipitated by less and less effort (preinfarction angina)
3- Prinzmetal (vasospastic) angina…occurs at rest, due to coronary spasm,
relieved by vasodilator (nitroglycerine) therapy.
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Myocardial infarction
 It is anoxic necrosis of myocardial cells caused by ischemia.
It may be:* Transmural…involving the whole thickness of the heart in certain anatomical
area supplied by certain coronary artery.
* Circumferential subendocardial….involving the subendocardium of left and less
commonly right ventricles.
Caused by hypo perfusion not actual coronary artery occlusion.
Acute ischemia (myocardial infarction)
 Causes and risk factors:
A- Complicated atheroma of coronary vessel. (Thrombosis, rupture of
the plaque or heamorrhage into the plaque).
B- Unusual causes include:
1- Embolism due to vegetations of bacterial endocarditis of aortic valve.
2- Polyarteritis nodosa
3- Occlusion of coronary ostia in dissecting aneurysms and syphilis
4- Coronary spasm
Thrombosis of the coronary artery
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Sites of myocardial infarction
 Aorta….Left and right coronary arteries.
- Left coronary
*Lt ant descending artery.…anterior part of left ventricle and interventricular
septum
* Lt. circumflex artery ….lateral wall of left ventricle.
- Right coronary …right ventricle, posterior wall of left ventricle and
interventricular septum.
Pathology Of Myocardial Infarction
 Before 6 hours of the occurrence of the infarction, no gross or microscopic
changes are detected on the myocardium.
12-24 hours
Grossly:- Infarct area is pale opaque and dry. It is slightly swollen
M/E
-Cytoplasm becomes more acidophilic
- Striations lost.
- Nuclei disappear
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24 -72 hours
Grossly :- Infarct area more pale, well circumscribed
M/E - Coagulative necrosis of myocytes.
- Neutrophil infiltration
- Contraction bands. - Affected myocytes show contraction bands which
represent condensation of contractile protein. They run perpendicular to the
direction of myocytes.
3-10 days
Grossly - Infarct area is yellow, surrounded by a zone of hyperemia.
-Red granulation tissue invades the infarct area from outside inwards.
M/E :- -Replacement of neurophils by macrophages which engulf necrotic debris.
- Starting invasion of the infarct by young granulation tissue from the periphery to
the center
Weeks -months
Grossly :- -Increasing pallor of the infarct due to progressive fibrosis till a well
developed grey-white scar is formed.
M/E :- - Progressive maturation of granulation tissue with collagenization
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- After 4-6 weeks granulation tissue invades the area of infarction till at last it is
completely replaced by fibrous tissue
Complications of myocardial infarction
 1- Arrhythmia…..most common cause of death in the first few hours following
infarction
2- Myocardial (pump) failure…can lead to congestive heart failure and/or cardiogenic
shock
3- Myocardial Rupture
- Occurs within 4-7 days after Infarction (due to neutrophilic liquifactive enzymes).
- Can lead to cardiac temponade and compression of the heart by hemorrhage into
the pericardial space.
4- Myocardial aneurysm with thrombosis inside.
5- Rupture of papillary muscle…..mitral incompetence.
6- Dressler’s syndrome….an autoimmune disorder resulting from damage of the
myocardium……release of auto-antigens ……..autoimmune pericarditis and pleurisy.
7- Chronic heart failure.
8- Acute pericarditis.
9- Prolonged confinement to bed +wk cardiac action….leg thrombosis &pulmonary
embolism
Diagnosis of myocardial infarction
 1- ECG and echocardiography
2 - Laboratory diagnosis
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CK-MB troponin LDH
6-h
Wk +
WK +
12-16 St +++
St+++
24 h
peaks
peaks
2day
persists persists
3day
---
persists
peaks
4-7d
---
persists
persists
Myocarditis
Causes:1- Toxic……e.g. diphtheria
2- Infective
bacterial (pyemia and septicemia), TB, S Viral….. Coxacki v
3- Immunological Rheumatic fever & SLE
Effects :- …Arrhthmias & heart failure
Cardiomyopathy
- It is heart muscle disease that is non-inflammatory and not associated with
hypertension, congenital, valvular or coronary heart disease.
- May be primary (idiopathic) or secondary to toxic or metabolic diseases.
 - Primary type may be either
1- Hypertrophic
2- Congestive
3- Restrictive…endocardial fibroelastosis or cardiac amyloidosis.
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Hypertrophic
Hypertrophy of 4 cardiac chambers especially interventricular septum
Congestive
- Most common type.
- may be related to alcoholism
Fibro-elastosis
Infiltration of the myocardium by fibrous tissue or amyloid interferes with the
pumping action of the heart
Tumors of the heart
 A.Primary
1- Myxoma of the left atrium
- Most common cardiac tumor.
- Found most commonly in adults.
2- Rhabdomyoma
- Found mostly in infants and young children.
-Associated with tuberous sclerosis
 B.Metastatic
- More common than primary.
Diseases of the pericardium
A .Pericardial effusion
 1- Hydropericardium…
- Is an accumulation of serous transudate in the pericardial space.
- It may result from any condition causing systemic edema. e.g. congestive heart
failure, hypoproteinemia, nephrotic syndrome or chronic liver disease.
 2- Hemopericardium…
- Is an accumulation of blood in the pericardial space.
- it is usually caused by traumatic perforation of the heart, aorta or myocardial
rupture associated with acute myocardial infarction
Acute pericarditis
1- Serous pericarditis …
- Associated with SLE, rheumatic fever and viral infections.
-The pericardium accumulates a clear, straw colored , protein rich exudate with small
number of inflammatory cells.
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2-Fibrinous pericarditis
- Characterized by fibrin rich exudate.
* Found in cases of uremia, myocardial infarction , or acute rheumatic fever
3-Purulent pericarditis
Characterized by cloudy or frankly purulent inflammatory exudate.
- Caused by bacterial infection.
4- Hemorrhagic pericarditis… characteized by bloody inflammatory exudate.
- Cause by tumor invasion of the pericardium.
- Can result from TB or other bacterial infections
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Pericarditis (Tuberculous)
- Common with pulmonary TB.
Route of infection..lymphatic or direct from the pleura.
Exudate is turbid or blood stained.
Tubercles may be seen grossly.
M/E… excess lymphocytes & no mesothelial cells
Chronic (constrictive) pericarditis
 Usually complicates TB or pyogenic infection.
 There is thickening and scarring of the pericardium with proliferation of fibrous
tissue and occasional foci of small calcification….loss of elasticity….interferes with
cardiac action and venous return…heart failure.
Heart failure
 Insufficient cardiac output to meet the body needs in spite of adequate venous
filling pressure.
 It may be acute or chronic
 Chronic may be right or left sided or total heart failure.
Chronic left sided failure
Causes
 Ischemic heart disease
 Hypertension
 Aortic and mitral valve diseases
 Myocardial diseases
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Chronic right sided failure
Causes
- Left sided heart failure
 Pulmonary hypertension
 Myocardial diseases
 Tricusped and pulmonary valve diseases
Diseases Of Blood Vessels
These include
1- Inflammation
Infective
a. Bacterial sepsis.
b. Bacterial thrombophlibitis.
c. Syphilis.
d. Fungal vasculitis.
Non infective
a.Polyarteritis nodosa
b.SLE
c.Burger’s disease
d.Giant cell arteritis
2- Vasospastic disorders
3- Degenerative:a. Atherosclerosis
b.Arteriolosclerosis of hypertension
c. Medial calcification
4- Aneurysms
5- Tumors
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Vasculitis (inflammation of blood vessels)
 Infective
a. Bacterial sepsis.
b. Bacterial thrombophlibitis.
c. Syphilis.
d. Fungal vasculitis.
 Non infective
a. Polyarteritis nodosa
b. SLE
c. Burger’s disease
d. Giant cell (Temporal) arteritis
e. Wegner granulomatosis
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a.Polyarteritis Nodosa
Systemic autoimmune vasculitis. Type III hypersensitivity reaction
More common in males.
Cause is mostly unknown-30%have chronic viral hepatitis B.
Small and medium sized arteries of the kidney, heart, liver, GIT and skeletal
muscle are affected.
Blood vessels of the lung are spared
 Type III hypersensitivity with characteristic Anti- Neutrophil Cytoplasmic
Antibodies (ANCA).
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Segmental affection of arterial vessel wall
Fibrinoid necrosis and perivascular inflammatory infiltrate
Complicated by fibrosis,ischemia, thrombosis, rupture, aneurysmal dilatation.
Good response to corticosteroids
b. Lupus Erythematosus
- It is an auto-immune immune complex (type III) reaction
- Due to formation of anti-nuclear antibodies (ANA). (anti double stranded DNA
antibodies).
- May be discoid which appear as mculopapular skin rash affecting the butterfly
area of the face or systemic affecting many organs.
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Systemic Lupus Erythematosus
- Middle aged females.
- Small arteries and arterioles
are affected diffusely.
- - Any organ can be affected including the lungs.
- Organs most seriously affected
heart and kidneys
- Cardiac vegetations (Libman sacs endocarditis), myocarditis and serous
pericarditis.
- Wire loop glomerulonephritis is characteristic.
- - Causes of death
- Heart failure
- Renal failure
c.Thromboangiitis obliterans
Burger’s disease
- Hypersensitivity to tobacco protein, hereditary predisposition (more in Jewish,
Japanese and Indians).
- Males 20-35 years of age.
- Acute inflammation of small and medium sized arteries of the extremities
followed by thrombosis , chronic inflammation and fibrosis.
- Results in ischemia and gangrene.
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d. Giant cell (temporal) arteritis
An old age disease, rare before 50 years.
There’s granulomatous arteritis with giant
cells involving mainly temporal vessels,.
Temporal vessels are tortuous and nodular.
Clinically, there’s headache and visual symptoms.
The disease is self limiting.
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e. Wegener Granulomatosis
It is necrotizing arteritis involving respiratory tract and kidney.
There is ulceration of respiratory mucosa and pulmonary necrosis.
Renal failure develops due to crescntic glomerulonephritis.
Good response to cyclophosphamide.
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3- Degenerative diseases of arteries
 Arteriosclerosis
General term for 3 types of vascular diseases all characterized by rigidity
(sclerosis) and thickening of arteries and arterioles.
 It includes
1- Atherosclerosis.
2- Arteriolosclerosis of hypertension.
3- Monckeberg arteriosclerosis (medial calcific sclerosis)
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Atherosclerosis
- The commonest arterial disease characterized by formation of fibro fatty plaques,
formed of a deeper soft part and a hard sclerotic fibrous cap
Epidemiology….
a. Most common cause of morbidity caused by vascular disease.
b. Highest incidence in Finland, Western Europe, USA and Canada.
c. Increased incidence with advanced age.
d. More in males than females up to the age of menopause.
Risk factors
- Constitutional risk factors.
- Hard risk factors
- Soft risk factors
Constitutional risk factors
Age…The number and severity of atheromatous lesions increase with age.
- Sex…more common in males than females up to the age of 55 years. Estrogen has
a protective effect ??
- Familial predisposition
Hard risk factors
- Hyperlipidemia…Increased level of cholesterol and LDL is associated with increased
risk of atherosclerosis.
-Increased LDL may be dietary or due to familial hyperlipidemia.
- On the contrary, HDL has a protective effect against atherosclerosis.
- Hypertension
- Diabetes mellitus …due to associated hyperlipidemia
- Cigarette smoking
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Soft risk factors
- Exercise… Reduces the incidence of atherosclerosis and death from ischemic heart
diseases
- Overweight….atherogenic diet high in animal saturated fatty acids and cholesterol.
- High complex sugars in diet.
- Low vegetables and fish.
- Stress and personality…Personality A
Pathogenesis of Atherosclerosis
 Current concept…..
Reaction to injury formulation
Injury (or dysfunction) of arterial endothelium
leads to…
a. Entry of monocytes and lipids to subendothelim.
b. Platelet adhesion and aggregation.
c. Release of mitogenic factors from platelets and macrophages…..proliferation
and migration of smooth muscle fibers.
d. Monocytes and smooth muscle cells engulf lipid and cause lipid deposition into
the lesion.
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Pathology of atherosclerosis
Sites….
* Aorta, especially descending
* Coronaries and cerebrals
* Femoral , renal, superior mesenteric and internal carotids.
Grossly….
- Multiple irregular patches more around ostea of branches.
- Color ranges from yellow to white according to relative amount of fat and fibrous
tissue.
- Covered by glistening intima (if not complicated)
M/E:- The plaques are formed of
1- Central core of cholesterol and cholesterol esters, lipid laden macrophages (foam
cells), necrotic debris and calcification.
2- Subendothelial fibrous cap formed of proliferated smooth muscle cells, foam
cells and extra cellular matrix
Complications of atherosclerosis
1- Narrowing of vascular lumen…chronic ischemia.
2- Superimposed thrombosis…acute ischemia.
3- Ulceration with liberation of fatty core … acute ischemia, fat emboli, DIC.
4- Pressure atrophy of the media with fibrosis….weakening of the wall …. Aneurysmal
dilatation.
5- Dystrophic calcification.
 Aorta: Aneurysm, stenosis of the ostia, thrombosis and embolization.
 Coronaries and cerebrals: Gradual ischemia (angina, cerebral atrophy), Sudden
ischemia (myocardial or cerebral infarct), and aneurysm (cerebral only)
 Medium sized arteries:
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Lower limb: intermittent claudicating or gangrene.
Intestine: malabsorption and gangrene.
Renal: renal ischemia with renal hypertension, renal failure
Hypertension
It is persistent elevation of blood pressure above 140/90
-It may be primary (essential) or secondary.
- Each type may be benign or malignant (according to severity).
- Each type can affect many organs the most important of which are…heart, blood
vessels, kidney, brain and retina
Secondary hypertension
Secondary to….
1- Renal…renal diseases, renal ischemia.
2- Endocrine… hyperaldosteronism, pheochromocytoma, hyperthyroidism.
3- Toxemia of pregnancy, contraceptive pills.
4- Coarctation of the aorta.
5- Stress, psychogenic, post-operative.
6- Polycythemia rubra vera
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Primary (essential) hypertension
Represent about 90% of cases of hypertension.
Patients usually above 40 years.
Pressure rises gradually not exceeding 180/100.
Course of disease is prolonged
Primary (essential) hypertension
It is hypertension of unknown etiology but there are certain predisposing (risk) factors
a. Familial predisposition (75% of hypertensive patients )
b. High salt intake
c. Cigarette smoking, alcoholism.
d. Emotional stress.
e. Lack of exercise.
Pathogenesis of hypertension
Mean arterial blood pressure = Cardiac output X Total peripheral resistance
BP= C.O X TPR
Effects of hypertension
Heart changes.
Brain changes.
Vascular changes
Retinal lesions.
Renal changes.
Causes of death ???
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Character
- Incidence
Benign hypertension
- 90% of cases
Malignant hypertension
5 – 10 %
- age
- starts after 40 ys
-30-40 years.
- onset
- pressure rises gradually to 180/100
- pressure rises suddenly to 200/110
- course
- prolonged for many years
- course is short for months or few years
(unless it is on top of benign)
Heart lesions Concentric left ventricular hypertrophy
with bulge of the interventricular
septum.
Followed by decompansated stage (Left
ventricular failure)
- These cardiac changes are minimal (no time
to occur).
Blood vessels 1- Benign arteriolosclerosis:
This is manifested as
lesions
a- Hyaline arteriolosclerosis.
1-Malignant arteriolosclerosis:
b- Elastosis.
This is manifested as
a- Necrotising arteriolitis (fibrinoid necrosis)
b- Cellular hyperplasia
2- Hypertension arteriosclerosis
3- Atheroma tends to be more severe.
Renal lesions Benign nephrosclerosis:
2-Hypertension arteriosclerosis as in benign
but less severe.
3- Atheroma less severe.
Malignant nephrosclerosis:
N/E:
- Size
 The kidney are small contracted
(primary contracted kidney)
 Kidneys are normal or enlarged.
- Capsule
 The capsule is adherent
 The capsule strips easily and shows patches
of subcapsular heamorrhages
- Shape
 The cut section shows reduced cortex
and medulla which are not demarcated
from each other, arteries at the base of
the pyramids are thick and dilated.
1- Blood vessels: hyaline
arteriolosclerosis.
 The cut section shows haemorrhagic patches
and arteries at the base of pyramids are thick
and dilated.
M/E
1- Necrotizing arteriolitis
2- Non-functioning nephrons:
Atrophic, fibrosed and hyalinised.
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2- Necrosis followed by fibrosis.
3- Functioning nephrons: show
compensatory hypertrophy.
3- Compensatory dilatation (not marked)
 Hyaline droplets and hemorrhage.
Lesion in the
brain
Lesion in
retina
Complication
and causes of
death
4- Interstitial Tissue: fibrosis and few
4- Minimal fibrosis + heamorrhage.
lymphocytes.
 Benign hypertensive encephalopathy Malignant Hypertensive encephalopathy:
With cerebral oedema, papilledema,
with microaneurysms.
encephalomalcia, liquafactive necrosis due
to ischaemia and spontaneous massive
cerebral haemorrhage.
Benign hypertensive retinopathy
retinal haemorrhages and exudate
- Left ventricular failure
- cerebral heamorrhage
Malignant hypertensive retinopathy: Odema,
heamorrhage, necrosis may lead to blindness
- progressive ureamia
- left ventricular failure
- cerebral heamorrhage
- chronic uremia
3- Monkeberg medial calcification
 Involves the media of muscular , medium sized arteries typically of the lower
extremities
 Affects ages above 50 years.
 Medial degeneration followed by calcification and may be ossification.
 Lumen is not affected because intima is not affected.
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Aneurysm
 It is localized dilatation of the wall of an artery due to weakening of the wall
and/or increase of blood pressure.
 - It may be either true in which the wall is part of arterial wall or false in which
the wall is formed of fibrous tissue.
1- False aneurysm
 In which the wall is formed of fibrous tissue
1- Simple pulsating aneurysm (pulsating hematoma).
2- Arteriovenous fistula…due to traumatic injury joining two adjacent vessels.
2- True aneurysm
 ***According to its cause they can be classified
A- Weak wall
1- Congenital weakening of the wall
a. Berry aneurysm in the circle of Wills at the base of the brain.
b. Medionecrosis (Marfan's syndrome)…dissecting aortic aneurysm.
2- Inflammatory weakening of the wall:a. Mycotic aneurysm of subacute bacterial endocarditis, polyarteritis nodosa, TB.
b. Syphilitic aortic aneurysm of thoracic aorta.
3- Degenerative.. Atheroma and hypertensive changes.
B- Increased intravascular pressure
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*** According to the site , aneurysm are classified into
1- Aortic aneurysm
a. Atheromatous…..abdominal aorta….may be complicated by thrombosis
b. Syphilitic…thoracic aorta.
c. Dissecting….blood passes inside the wall of the aorta. It may be due to
medionecrosis of Marfan's syndrome or blood passes in a crack of atheromatous
plaque.
Aortic aneurysm
Dissecting
II- Cerebral aneurysm
 a. Berry aneurysm (CONGENITAL)
- Small, multiple, saccular.
- Occur in the circle of Willis at sites of medial weakness at the bifurcations.
- They are the most common cause of subarachnoid hemorrhage.
 b. Mycotic aneurysm (SBE).
 c.Hypertensive microaneurysm (benign hypertension
 d. Atheromatous
Berry aneurysm
Cerebral aneurysm
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Complications of aneurysms
1) Rupture leading to fatal hemorrhage
2) Pressure on the surrounding structures.
3) Thrombosis and embolization
Varicose veins
 It is dilatation, elongation, thickening and tourtousity of veins
 Causes of varicose veins:a. Weakening of the wall of the vein
b. Rupture of the valves.
c. Increased venous pressure due to
- Prolonged standing
- Venous obstruction e.g. by thrombus, heart failure, liver cirrhosis.
- Compression of the vein from the outside… pregnant uterus, nearby tumor.
Sites
 1- Superficial veins of the lower limbs….found in persons who spend much of their
time standing.
May be complicated by varicose ulcer
 2- Varices of the esophagus…found in portal hypertension as in liver cirrhosis or
bilharzial fibrosis.
 3- Hemorrhoids …varices of the internal or external hemorrhoidal plexus of the
rectum (piles )
 4- Varicocele …….varices of the pampiniform plexus of the spermatic cord.
Complications
1.
2.
3.
4.
5.
Local chronic venous congestion and edema.
Hemorrhage e.g. esophageal varicese.
Thrombosis and embolization.
Varicose ulcer is premalignant (Sq.C.C)
Inflammation leading to septic thrombophlibitis
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 Benign:
1- Hemangioma: a) Capillary
Tumours of blood vessels
b) cavernous
2- Glomangioma: tumor of glomus body under the nail, it is painful.
 Malignant:
1- Hemangiopericytoma.
2- Hemangioendothelioma.
3- Kaposi’s sarcoma: it is related to cytomegalovirus and complicates
immunodeficiency as in AIDS and transplanted persons. It is a vascular sarcoma
which may involve the skin only or skin and internal organs.
Kaposi sarcoma

-M/E… The tumor consists of sheets of malignant spindle-shaped cells with
vascular slits, endothelial lined vascular channels with micro-hemorrhages and
hemosidrin deposition.
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