Anda di halaman 1dari 100

DE PEDRO PALER BSPHIII

Contents
Edema Thrombosis Hemostasis Embolism Infarction Hemorrhage Shock

Edema

abnormal increase in interstitial fluid within tissues caused by either increased capillary pressure or diminished colloid osmotic pressure mostly seen in subcutaneous tissues, lungs and brain. Type of edema: exudate in inflammatory and transudate in non inflammatory conditions

Edema - Pathogenesis

PATHOPHYSIOLOGIC CATEGORIES OF EDEMA

I. Increased Hydrostatic Pressure


results to focal impairment in venous return. Most common cause - Congestive heart failure, others DVT

Congestive Heart Failure

Constrictive Pericarditis

Venous Obstruction

II. Reduced Plasma Osmotic Pressure


occurs when albumin is not synthesized in adequate amounts or is lost from the circulation results to a net movement of fluid into the interstitial tissues with subsequent plasma volume contraction
Nephrotic syndrome, Cirrhosis, Malnutrition

Ascites (Liver Cirrhosis)

III. Sodium and Water Retention


causes both increased hydrostatic pressure and diminished vascular colloid osmotic pressure. occurs whenever renal function is compromised Renal failure, Renin- Angiotensin - Aldosterone

IV. Lymphatic Obstruction


causes chronic inflammation with fibrosis, invasive malignant tumors, physical disruption, radiation damage and infectious agents

Hyperemia & Congestion

Hyperemia
Locally increased blood volumes Active Process
Arteriolar dilation leads to increased blood flow

Redness due to engorgement with oxygenated blood Erythema

Erythema

Congestion
locally increased blood volumes Passive process
resulting from reduced outflow of blood from a tissue. can be systemic or local

blue-red color (Cyanosis) Commonly leads to Edema

Cyanosis

Chronic Passive Congestion


Lack of blood flow
Leads to: - chronic hypoxia - ischemic tissue injury and scarring

Capillary rupture

Acute Pulmonary Congestion


Engorged alveolar capillaries Alveolar septal edema Focal intra-alveolar hemorrhage

Chronic Pulmonary Congestion


Thick and fibrotic septa Heart failure cells
Hemosiderin - laden macrophages in alveoli

Acute Hepatic Congestion


Distended central vein and sinusoids Centrilobular hepatocytes can be ischemic Periportal hepatocytes may only develop fatty change.

Chronic Passive Hepatic Congestion


The centrilobular regions are grossly red - brown and slightly depressed.
centrolobular necrosis + hemorrhage periportal fatty change cardiac fibrosis

Microscopically:
Central vein is congested as well as the hepatic sinusoids centrilobular hemorrhage hemosiderin-laden macrophages degeneration of hepatocytes

Chronic Passive Splenic Congestion


Gross:
Enlarged, firm with deep red to grey red cut surface Thickened capsule

Microscopically:
Sinusoids of red pulp are dilated and engorged with blood Hemorrhage may occur

Hemostasis

Hemostasis and Thrombosis


Three general components:
Vascular wall (endothelium) Platelets Coagulation cascade

SEQUENCE of EVENTS following VASCULAR INJURY

Vasoconstriction
Reflex neurogenic mechanism; endothelin

Primary hemostasis
Platelet adhesion and aggregation

Secondary hemostasis
Thrombin activation; fibrinogen to fibrin; fibrin deposition

Thrombus and antithrombotic events


Fibrin polymerizes TPA limits plug

Hemorrhage

Hemorrhage
Extravasation of blood into the extravascular space. Hemorrhagic Diathesis
increased tendency to hemorrhage that occurs in a variety of clinical disorders

within tissue hematoma

Petechiae - 1 - 2 mm; skin + mucosa


Intravascular pressure, platelets

Purpura - 3 mm trauma, vasculitis, vascular fragility Ecchymoses - > 1 to 2 cm


B ruise; R B C phagocytosis by macrophages: Hb (red blue) bilirubin (blue-green) hemosiderin (golden brown)

Accumulation of blood in the Cavity


Hemothorax Hemopericardium Hemoperitoneum Hemarthrosis

Hemorrhage sequelae
Loss volume
>20% - hemorrhagic shock

Loss rate
Acute - hemorrhagic shock Chronic - peptic ulcer, menstrual bleeding
Iron deficiency anemia

Site of hemorrhage
Subcutaneous tissues - fatal in brain

Thrombosis

Thrombosis
The formation of a blood clot (thrombus) in an uninjured vessel after an injury. The THROMBUS is formed of blood elements essentially platelets.

3 Primary abnormalities
Virchows triad
Endothelial injury Stasis or turbulence of blood flow Blood hypercoagulability

Types of Thrombi
Pale Thrombus
In a flowing blood as in cardiac chambers or in arteries. Formed mainly of platelets FIRM PALE REDDISH G RE Y

Red Thrombus
In a stagnant blood adjacent to complete vascular occlusion Formed of fibrin platelets SOFT DARK RED & G ELATI N O U S

Mixed Thrombus
In a slowly flowing blood usually in veins & arteries. Formed of alternating layers of platelets and fibrin ALTER N ATI N G RED & PALE LAY ERS

Pale Thrombus
Site: heart valve, artery Component: Platelet, fibrin

Red Thrombus

Mixed Thrombus
Site: heart chamber, vein Component: Platelet, fibrin, R B C

Mural thrombosis
Thrombi occurring in heart chambers or in the aortic lumen.

Mural thrombosis

hyaline thrombi in a glomerulus


Fibrinous thrombi are visible within parts of capi. of the glomerulus

Pathogenesis

Pathogenesis

Iliac artery aneurysm with laminated thrombus

Left atrial mural thrombus in a case of rheumatic mitral stenosis

Pathogenesis

Fate of Thrombus
Propagation
Thrombi accumulate additional platelets and fibrin.

Embolization
Thrombi dislodge and travel to other sites in the vasculature

Dissolution
the result of fibrinolysis, which can lead to the rapid shrinkage and total disappearance of recent thrombi.

Organization and recanalization


Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts

Morphology
Thrombi may develop anywhere inside the C V S. They are variable in size and shape depending on its site of origin and the causes of their development. Thrombi are significant because they cause obstruction of arteries and veins, and are sources of emboli.

Arterial or Cardiac Thrombi

Venous Thrombi

Arterial/Cardiac Thrombosis
Atherosclerosis major cause.
Loss of endothelial integrity with abnormal vascular flow

Acute Myocardial infarction = old atherosclerosis + fresh thrombosis

Occlusive arterial thrombus

Venous Thrombosis (Phlebothrombosis)


Occlusive
occur in the superficial or deep veins of the leg.

Superficially,
venous thrombi typically occur in the saphenous veins in the setting of varicosities.

Gross: firm, red, attached to wall Microscopically: RBC + fibrin known as red, or stasis.

Deep Venous Thrombosis (DVT)


In the larger veins (at or above the knee) more serious because thrombi embolize to the lungs.

Disseminated Intravascular Coagulation (DIC)


the sudden or insidious onset of widespread fibrin thrombi in the microcirculation.
Obstetric complications Advanced Malignancy Shock

Not a primary disease but rather a potential complication.

Embolism

Embolus
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin. Coined by Rudolf Virchow in 1848.
fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or even foreign bodies.

Types of Embolism
Pulmonary embolism
95% venous emboli from deep leg veins Depending on the size may lodge pulmonary artery bifurcation (saddle embolus) or in the small arterioles. Most pulmonary emboli are clinically silent (small) Sudden death, right heart failure (cor pulmonale) occurs when more 60% or more of the pulmonary circulation is obstructed by emboli

Types of Embolism
Systemic thromboembolism
Emboli traveling in arterial circulation 80% from intracardiac mural thrombi Aortic aneurysm, thrombi, atherosclerotic plaques, paradoxical thrombi Lower extremities (75%); brain (10%)

Types of Embolism
Fat embolism
Microscopic fat globules seen in circulation 90% with severe skeletal injuries Pulmonary insufficiency, neurologic symptoms, anemia and thrombocytopenia (1-3 days after injury)

Types of Embolism
Air embolism
Excess of more than 100cc is required to have clinical effect Decompression sickness- sudden change in atmospheric pressure Bends (gas bubbles within skeletal muscles) (caissons disease)

Types of Embolism
Amniotic fluid embolism
1 in 50,000 deliveries Infusion of amniotic fluid or fetal tissue into the maternal circulation via tear in the placenta or rupture of uterine veins.

Infarction

Infarction
Ischemic necrosis caused by occlusion of either arterial supply or the venous drainage 99% of all infarcts results from thrombotic episodes Almost all result from arterial occlusion

Infarction
Red infarct venous occlusion, loose tissues, tissue with dual circulation White infarct arterial occlusions solid organs Mostly ischemic coagulative necrosis Brain-liquefactive necrosis

Infarction Factors
NATURE of VASCULAR SUPPLY RATE of DEVELOPMENT
SLOW (BETTER) FAST (WORSE)

VULNERABILITY to HYPOXIA
MYOCYTE vs. FIBROBLAST

BLOOD OXYGEN CONTENT

Morphology
1. red infarcts
venous occlusion loose tissue (lung) blood collection dual circulation lung + bowel previously congested organs reperfusion (angioplasty, drug-induced thrombolysis)

2. white infarcts
arterial occlusion solid organs heart (yellow), spleen, kidney

RED VS. WHITE

Morphology
wedge shape
apex to occluded artery base to organ periphery + fibrinous exsudate (pleuritis, pericarditis epistenocardiaca)

onset poorly defined, hemorrhagic in time sharper margins + hyperemic rim

WEDGE SHAPED SCARRED INFARCT following the distribution of an end artery branch of the renal artery. FIBROSIS implies that it is old (months to years)

ischemic coagulative necrosis 3 zones


dominant histologic characteristic of infarction

1. total necrosis - centre


loss of nuclei, eosinophilia architecture is preserved of cytoplasm,

2. partial necrosis
some cells survive inflammation (neutrophils) 1-2 days degradation of dead tissue

healing
granulation tissue (5-7 day) fibrous scar (6-8 weeks) In brain liquefactive necrosis pseudocyst

Septic infarctions
occur when infected cardiac valve vegetations embolize or when microbes seed necrotic tissue. the infarct is converted into an abscess, with a correspondingly greater inflammatory response.

Shock

Shock
characterized by systemic hypotension due either to reduced cardiac output or to reduced effective circulating blood volume. Consequences:
impaired tissue perfusion cellular hypoxia

Shock
the final common pathway for several potentially lethal clinical events:
severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis.

Shock
Features:
hypotension, tachycardia, tachypnea, cool cyanotic skin

Causes:
Cardiogenic Septic Hypovolemic

Cardiogenic Shock
results from low cardiac output due to myocardial pump failure. This can be due to intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression, or outflow obstruction.
MI Ventricular rupture Arrythmia Cardiac tamponade Pulmonary embolism

Hypovolemic Shock
results from low cardiac output due to the loss of blood or plasma volume
Hemorrhage Fluid loss (e.g. vomiting, diarrhea, burns)

Septic Shock
results from vasodilation and peripheral pooling of blood as part of a systemic immune reaction to bacterial or fungal infection.
Overwhelming microbial infection Endotoxic shock Gram positive septicemia Fungal sepsis Superantigens

Shock
Neurogenic Shock
loss of vascular tone e.g. spinal cord injury

Shock
Anaphylactic Shock
denotes systemic vasodilation and increased vascular permeability caused by an IgEmediated hypersensitivity reaction. acute widespread vasodilation results in tissue hypoperfusion and hypoxia.

Clinical Stages

Nonprogressive

Progressive

Irreversible

Morphology
brain - ischemic encephalopathy
tiny ischemic infarctions (border zones)

heart
subendocardial hemorrhage + necroses, contr. bands

kidney - acute tubular necrosis (shock kidney)


pale, edematous tubular epithelium necroses casts

lung diffuse alveolar damage (shock lung)


heavy, wet congestion + edema + hyaline membranes

Morphology
adrenal gland
lipid depletion

GIT hemorrhagic enteropathy


mucosal hemorrhages + necroses

liver
fatty change, central necrosis

Clinical Stages
1. nonprogressive
Compensatory mechanism (neurohumoral) activation centralization of blood circulation

2. progressive
tissue hypoperfussion metabolic dysbalancies

3. irreversible
incurred cellular damage + tissue injury

Clinical Progression of Symptoms


Hypotension

Tachycardia
Tachypnea

Warm skin Cool skin Cyanosis


Renal insufficiency

Obtundance
Death