Infectious Heart Diseases

8/13/2019 Infectious Heart Diseases

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Infectious

Heart

Diseases


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PREDISPOSINGFACTORSPRECIPITATINGFACTORS

Non-Modifiable Factors:Age (5 15 years old)Genetic PredispositionModifiable

Environmental Conditions(overcrowding)Economic Factors

(malnutrition and poor access tohealth care)Immunodeficiency

Exposure to GABS

Entry of themicroorganismsUpper airway organs are affectedpharynx tonsils

Local inflammatoryresponse


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pharynx tonsils

Local inflammatory response

PAIN

Inadequate

intake (loss of

weight)

Increase WBC on to the site in order toretard GABS and prevent it from

entering the systemic circulation

Increase in WBC WBC vs M.O.

Release of pyrogens

Fever

Breakage of the

endotheliallining

Absorption of

GABS via thelymphatic veins

Entry of GABS in

the bloodstream

bacteremia

The foreign body will

stimulate the production of

antibodies

GABS travel in the entire body

via the circulatory and

lymphatics system


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bacteremia

The foreign body will stimulate the

production of antibodiesGABS travel in the entire body via the

circulatory and lymphatic system

The body codes theantigens

STREPTOLYSIN-O

The body codes theantigens CHON

located in their cell

membraneFormation of ANTI-

STREPTOLYSIN-O

(ASO) antibodies

Formation of

MCHON

antibodies

Increase in ASO

titer Increase in M-

CHON titer

ANTIASO vs

GABS

Failure of the anti-

ASO to retard

GABS

Increased hemolyisis of

the RBCs

Elevated ESR and

decrease in hgband hct

A

JOINTS SKIN CNS HEART

B C D E


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B

JOINTS

Vascular changes occur in the blood vessel

Permeability of the capillaries supplying the synovial

membrane of the joints

Extravasation of plasma from the capillaries to the synovial

fluid (prostaglandin and arachidonic acid)

Local inflammatory reaction in the synovial membrane

ARTHRITIS

(POLYARTHRITIS)


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C

By way of the stratum germinativum, GABSreach the skin surface

Local inflammation

Formation of inflammatory

lesions

Erythema

Marginatum

Inflammation of the

tendon sheaths

Formation of

inflammatory nodules

Subcutaneous

Nodules


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D

Entry via the midcerebral artery

Affects the upper motor neuron (caudate nucleus)

Firing of impulses

Afferent neuron to the anterior motor horn of the

spinal cord

Reception of the lower motor neuron

Chorea (Sydenhams Chorea or St. Vitus Dance)


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E

Venous return (carries GABS)

Comes in contact with the

endocardium

Follows the normal flow

of blood

Inflammation of the

endocardium

ENDOCARDITIS

Infected blood enters the

lungsPulmonary Infections

Infected deoxygenatedblood exits the left

ventricle

Damage and

shortening of the

chordae tendinae

Formation of tiny

translucent

vegetations

around the valve

leaflets

Calcifications of the valves and partial

opening (stenosed)

VALVULAR DISORDERS(Mitral Valve Stenosis)

Infected blood enters the coronary arteries

Inflammation of theMYOCARDIUM Inflammation of thePERICARDIUM

MYOCARDITIS PERICARDITIS

A

MURMURS


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MYOCARDITIS PERICARDITIS

Restrictions to Contraction

Decrease in stroke volume

Decrease in cardiac output

Baroreceptor reflex

Increased SNS stimulation

Tachycardia and vasoconstriction

Left ventricle has to increase preload in order to resist

increase afterload (but with decrease volume)

Restrictions to contraction progresses

Further decrease in cardiac output

HEART FAILURE (LEFT or RIGHT SIDE)

ASCHOFFS

BODIES


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Infective Endocarditis

NON MODIFIABLEMODIFIABLE

dental proceduresupper respiratorytract infection andurinary tract infectionintravenous drugusers (2-5 )

age (47-64years old)

reproductiveconditionpre-existing heart

diseases

Microbial infection of the endothelial surface of

the heart, especially the valves.


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NON-MODIFIABLE FATORS MODIFIABLE FACTORS

AGE: 4764 year sold Dental procedures, URTI, UTI,

intravenous drug users,

reproductive condition, pre-existing heat condition

Entry of the microorganisms via the various routes

Incorporation in the bloodstreamSystemic affectation

WBC vs M.O.

Release of the

chemical pyrogen

FEVER

Contaminated blood

enters the heart via the

venous return

Damage on the

endocardium

ENDOCARDITIS

Colonization of the other endothelial structures

Formation of bacterial colonies on the edges of

the heart valves

Irregularly shaped bacterial colonies would

attract platelet aggregates

Formation of vegetations


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Damage and

shortening of the

chordae tendinae

Formation of tiny

translucent

vegetationsaround the valve

leaflets

Calcifications of the valves and partial

opening (stenosed)

VALVULAR DISORDERS

(Mitral Valve Stenosis)

ENDOCARDITIS Formation of vegetations

Growth of the

vegetations by

further attraction

of more platelet

aggregates

Further damage

to the valves

Platelet

aggregates are

loosely attachedon the valvular

lining

Dislodgement of

clots/thrombi

Embolism

A

Vegetations

continue to

release infectious

substances

SYSTEMIC

INFECTION

Travels to theskin via the

stratum

germinativum

Inflammatory

lesions (rashes)/nodules on the

fingertips (Oslers

nodes)

Decreased preload

Decrease stroke volume

Decrease cardiac output

Baroreceptor reflex

Increase SNS activity

Tachycardia,

vasoconstriction

Marked increase in

preload and increase in

afterload

Marked decrease in

stroke volume and

cardiac output Heart failure


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A

Abdominal aorta

Abdominal pain

Renal Artery

Renalparenchymal

damage

Flank pain Proteinuria,

hematuria,

casts,acidosis,

electrolyte

imbalance

MCA

TIA, CVA,ataxia,

aphasia

Retinal artery

Retinal damage

Loss of

vision

Formation of

round

necrotic

tissues

around the

retina

Roths Spots

Coronary artery

AnginaPectoris/Myocar

dial infarction

Pulmonary artery

Difficulty of

breathing and

pulmonary

vasculature

damage

Radial/ulnar artery

koilonychia


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MYOCARDITIS


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Entry of the microorganisms via the respiratory system Toxic effects of exogenous substance

Local inflammatoryprocess

FLU-LIKE SYMPTOMS

Release of endogenous

toxins of the

microorganisms

Damage of the myocytes (myocardium)

Decrease contractile state of the myocardium

Decrease in preload

hypotension

Baroreceptor reflex

Increase in SNS stimulation

Tachycardia, tachypnea,

vasoconstriction


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Tachycardia, tachypnea, vasoconstriction

Decrease in ventricular filling

Preload decreases

Further decrease in stroke

volume

Further decrease in cardiac

output

Further stimulation of

adrenergic system (SNS)

Decrease in pressure in the

ventricles

Faint heart sounds

Pooling of

blood inthe

atria

Left atrial

enlargement

Increase SA

node activity

Atrial tachycardia/ atrial

fibrillationleading to

mural thrombi formation

Further damage inthe myocardium

(elevation of the cardiac enzymes)

serum creatinine kinase

troponin Ttroponin I

ECG Changes: ST segment elevation,

T wave inversion, transient Q waves

Loss of ventricular compliance

S3gallop


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Pooling of blood in the atria Further damage in the

myocardium

Portions that are

damaged

regenerate and are

replaced by non

pliable fibrous

tissues

Compensation of

the other heart

muscles

Hypertrophy of the myocardium

Conduction system defects

(dysrhythmias)

Myofibril damage and

stretching of the remaining

functional fibers

HEART FAILURE

CHEST PAIN

PULMONARY

HYPERTENSION


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PERICARDITIS


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Entry of the microorganisms via the respiratory system

Local inflammatoryprocess

FLU-LIKE SYMPTOMS

Damage on the

endothelial surface

Reaches the alveolar

capillary membranes

Incorporation of the microorganism in the systemic circulationBACTEREMIA

Vascular changes take place in response to the microorganism/s

Hydrostatic pressure increases

Increase in capillary permeability

(particularly of the capillaries

supplying the serous membrane ofthe heart)

Edema on the dependent

parts of the body

Synovial membrane of the

joints (ARTHRITIS)

extravasation of fluids, together with the microorganisms, fibrin

deposits and the chemical mediators of inflammation


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extravasation of fluids, together with the microorganisms, fibrin

deposits and the chemical mediators of inflammation

Formation of fibrous

exudates in thepericardial space

Inflammation of the

visceral and parietalpericardium

Formation of fibrous

exudates in the

pericardial space

ACUTEPERICARDITIS

Slow filling

Decrease amount of

serous fluid in the

pericardial space

PERICARDIAL with

EFFUSION

Rubbing of the

inflamed layers

PERICARDIAL

FRICTION RUBMuffled heart

sounds

Pressure of the inflamed pericardium over the intercostal muscles

Chest Pain

Impaired contraction of

the ventricles

Decrease in stroke volume

Decrease in cardiac output

Hypotension

Baroreceptor reflex

Adrenergic receptor

stimulation (increased SNS

activity)

Tachycardia, tachypnea,

vasoconstriction


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Tachycardia, tachypnea, vasoconstriction

Decrease in ventricular filling

Preload decreases

Further decrease in stroke

volume

Further decrease in cardiac

output

Further stimulation of

adrenergic system (SNS)

Decrease in pressure in the

ventricles

Faint heart sounds

Increase in left

ventricular diastolicvolume and pressure

Decrease ventricular

filling

Further decrease in

cardiac output

Pooling of blood in the left atrium

Pulmonary HPN Mitral valve

damage

Rise in pulmonaryartery pressure

Rise in right

ventricular

pressureHypertrophy


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Inflammation of the pericardium and thickening of the exudate causes fusion of the two layers

CHRONIC CONSTRICTIVE

PERICARDITIS

Entire pericardium restricts myocardial contraction

Contraction of the heart increases but becomes inefficient

Hypertrophy of the heart muscles

Conduction system defects

Right Sided Heart

Failure

Left Sided Heart

Failure


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cute PericarditisEXUDATIVE PERICARDITIS

Agents/ processes causingpericardial inflammation

Formation of exudate:fibrin, WBC, endothelialcells

Exudate covers pericardium

Further inflam. of serous

pleura & tses.

CO

Restricts heart filling& emptying

Cardiac tamponade

Exudates

accumulates inpleural sac

Localization of

fibrinous exudate


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DRY PERICARDITIS

Delicate adhesions from within the pericardialspace along with serous fibrin deposits, hge

& calcification

Adhesion obliterate the pericardial sac

Inflammation of the pericardium

Penetration to the myocardium

myopericarditis


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Chronic Constrictive Pericarditis

Repeated cases of acute pericarditis

Formation of thick, fibrous band of tse

Encircles, encases, and compresses the heart

Prevents proper ventricular filling and emptying

CO/ heart failure

Chronic inflammatory condition in which the pericardium

changes into a thick, fibrous band of tissue.


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Pericardial Effusion

Rapid FluidAccumulation

Compression of heart

Ventricular filling

CO

Sudden FluidAccumulation

Stretching ofpericardium

Loss of elasticity ofpericardium

Fibrosis of pericardium

Infectious Heart Diseases

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