2011-08-patho-hemodynamics 1

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I.Edema

accumulation of abnormal amounts of fluid in the

interstitial tissue spaces or body cavities

*Effusion = edema in body cavities

Two Major Types of Edema

1. Inflammatory Edema due to increased

vascular permeability (exudate)

*TUMOR in inflammation

2. Non-inflammatory Edema (Hemodynamic

Edema) due to hemodynamic alterations

(transudate)

Factors that Maintain Normal Fluid Exchange

1. Plasma important factors; major

y Hydrostatic Pressure

y Colloid osmotic Pressure

2. Interstitial Tissue minor role in

maintaining fluid balance

y Interstitial Colloid Osmotic Pressure

y Interstitial Tissue Hydrostatic

Pressure

3. Lymphatic Drainage important since it

drains any accumulation of fluid in the

interstitial tissue and drains it into the

Thoracic Duct

DIAGRAM ABOVE:

*Microcirculation arterioles, capillaries and

venules.

*In the arteriolar end:

y Hydrostatic pressure is 32mmHg

y Interstitial Pressure is 12mmHg

*In the venular end:y Osmotic Pressure is 20mmHg

*Whatever fluid that comes out from the arteriolar

end is absorbed in the venular end; it is almost zero.

Pathophysiologic Classification of Hemodynamic

Edema

A. Increased hydrostatic pressure

y CHF

y Liver cirrhosis

B. Reduced plasma osmotic pressurey Nephrotic syndrome

y Liver cirrhosis

y Malnutrition

C. Sodium retention

y Excess salt intake with reduced

renal function

y Increased tubular reabsorption of

sodium

Reduced renal perfusion

Increased renin

angiotensin-aldosterone

secretion

D. Lymphatic obstruction Localized edema

y Inflammatory disease

Filariasis

y Post-mastectomy

*A, B, and C = GENERALIZED EDEMA

Subject: PathologyTopic: Hemodynamics 1Lecturer: Dr. Ignacio De GuzmanDate of Lecture: 08/02/2011Transcriptionist: BellasPages: 12 S

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2011-2012


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Difference between Exudate and Transudate

*Malignant Effusion

y Exudate

y Bloody, high SG, high protein concetration

Ascites accumulation of fluid in the peritoneal

cavity

*OVARIAN Cancer *

Hydrothorax pleural effusion; fluid accumulation

in the pleural cavity

Hydropericardium pericardial effusion

*if clear and yellowish = hemodynamic cause

*bloody and cloudy = inflammation or malignancy

Anasarca (Generalized Edema)

*maybe due to Rh incompatibility


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Periorbital Edema (in renal disease)

Bipedal Edema (in CHF)

Localized Edema (Filariasis)

*due to obstruction of the lymphatics secondary to

infectious agent

Lymphedema (Post-Mastectomy)

Pulmonary Edema - fatal


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*fluids in the alveolar spaces

*causes: Left Ventricular Failure, Infection,

Hypersensitivity Reaction, Renal Failure, etc.

Cerebral Edema fatal due to brain herniation that

can compression of the vital center of the brain

*bubbles or holes indicating edema

Cerebral Edema with Herniation

*affected side RIGHT (bigger)

*Tonsilar Herniation due to edema

*Tx/Prevention = DIURETICS

II. Hyperemia and Congestion

- Increased volume of blood in affected

tissues

Hyperemia

- arterial and arteriolar dilation with

increased capillary blood flow due to

sympathetic-neurogenic factors- ACTIVE process

- e.g: muscular exercise, febrile state, early

acute inflammation

- Color: Bright red (oxygenated blood)

Congestion

- Due to impaired venous outflow

- PASSIVE process

- Related to edema

- e.g: CHF, cirrhosis (portal hypertension)- Color: Blue-red (unoxygenated blood)


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*LUNGS

-induration/firmness due to fibrosis of the

interstitium

-brown due to hemosiderin

*Hemosiderin particles

*LIVER

-centrilobular congetion

-mottled appearance

*CARDIACCIRRHOSIS

-due to fibrosis in severe and long-standing

congestion

-liver is cirrhotic, not the heart

III.Hemorrhage

rupture of blood vessels due to trauma, surgery,

vascular disease or diseases of the blood factors

Types of Hemorrhages

1. Hematoma collection of blood in the skin

or subcutaneous tissues or even within

visceral organs

2. Ecchymoses collection of blood within

subcutaneous tissues

3. Petechiae capillary bleeding

4. Purpura larger petechiae

5. Hemothorax

6. Hemopericardium

7. Hemoperitoneum

Three Factors that Determine the Significance of

Any Type of Hemorrhage

1. Amount of blood loss

2. Rate of blood loss sudden or slow

3. Site of haemorrhage brain, pericardial,

external

Hematoma


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Ecchymoses

Petechiae

Purpura

Hemothorax

Hemopericardium


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Hemoperitoneum

*ruptured ectopic pregnancy

Hemorrhage

*most likely cause is hypertensive hemorrhage

IV. Hemostasisand Thrombosis

Hemostasis

factors that control excessive bleeding by forming

a solid plug of blood to close ruptured blood vessels

(physiologic)

Three Factors involved in Hemostasis1. Vascular wall

2. Platelets

3. Coagulation system

Events in the Formation of Hemostatic Plug

1. vessel injury vasoconstriction (transcient)

2. adherence of platelets to subendothelial

collagen activation of platelets release

of ADP, thromboxane A2 recruit

additional platelets platelet aggregation hemostatic plug (primary hemostasis)

3. release of tissue factors and platelet factors

activates plasma coagulation thrombin

converts fibrinogen to fibrin and induces

further platelet release and aggregation

(secondary hemostasis)

4. polymerized fibrin and platelets aggregate

to form solid mass (permanent plug)

Thrombosis

pathologic process characterized by formation of

a clotted mass of blood within intact vascular

system

Pathogenesis

1. Endothelial Injury

y Platelets gain access to the

subendothelial collagen

y Mural thrombi overlying areas of

myocardial infarction

y Ulcerated plaques of

atherosclerotic aorta

y Inflamed heart valves

2. Alterations in normal blood flow (stasis or

turbulence)

y Atrial fibrillation in RHD

y Aneurysms

y Sites of myocardial infarction

y Varicose veins

3. Alterations in the blood inducing

hypercoagulability

y Genetic

Common: mutations in

Factor V gene, prothrombin

gene,


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methyltetrahydrofolate

gene

Rare: antithrombin

deficiency, protein C

deficiency, protein S

deficiency, fibrinolysis

defects

y Acquired Prolonged immobilization,

DIC, APAS, contraceptive

pill, postpartum state, NS,

severe burns, disseminated

cancer

AtheroscletoricPlaque

Aortic Aneurysm

Morphology

1. Mural thrombi thrombi applied to one

wall of a capacious underlying structure

(heart, aorta)


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2. Vegetations thrombi deposited in heart

valves (infective and non-infective

endocarditis)

3. Arterial thrombi occlusive thrombi in

coronary, cerebral and femoral artery

*important factor = ENDOTHELIAL INJURY

4. Venous thrombi (phlebothrombosis)

invariably occlusive; most affect lowerextremities (90%), deep calf; femoral,

popliteal; ileal

*important factor = STASIS

Mural thrombi

(Left Ventricle)

*INFARCTION

- potential area for thrombosis due to:

a. endothelial injury

b. stasis

(Left Atrium)

*Rheumatic Heart Disease (RHD)

-most commonly affected valve is MITRAL VALVE

resulting in fibrosis of the valve, causing dilation of

the Left Atrium resulting to atrial fibrillation

Vegetations

(Infective Endocarditis)

-gross: large and bulky

Mitral Valve


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Aortic and Pulmonic Valves

(Non-Infective Endocarditis)

-gross: small and uniform in size

(Non-Infective Libman-Sacks Endocarditis in SLE)

Arterial Thrombi

(Coronary Artery Thrombosis)

(Cerebral Artery Thrombosis)


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Venous thrombi

(Femoral Vein Thrombosis)

Fate of Thrombosis

1. Propagation

-enlarge depending on the site

-arterial = retrograde

-venous = towards the blood flow

2. Embolization

- Fragmentation of the thrombus

- Depend on the localition

- If in the lower ex = LUNGS

- If in the heart/valves = depending on the

blood flow

3.

Dissolution (Resolution)-if the thrombus is small

4. Organization and Recanalization

-organization invasion by capillaries,

fibroblast, endothelial cell and smooth

muscles

-recanalization - channels are formed by

the capillaries which can retain some

degree of blood flow

Propagation

Embolization


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Organization

Recanalization

Clinical Significance of Thrombosis

1. Obstruction of arteries (INFARCTION)

2. Obstruction of veins

y Congestion and edema

y Will NOT cause Infarction except for

organs that have a single VENOUS

DRAINAGE such as TESTES and

OVARIES3. Provide possible source of emboli if

fragmented

--------------- END OF TRANSCRIPTION--------------

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Note:This is based solely on the ppt and lecture

recordings. Please read your books for additional

explanation and information. Thanks.

2011-08-patho-hemodynamics 1

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