Hemodynamic Disorders Flashcards
Accumulation of fluid in tissues or body cavities
EDEMA - tissues
EFFUSIONS - body cavities
Increased blood volume w/n tissues
hyperemia
congestion
Pathologic counterpart of hemostasis
Thrombosis
A detached intravascular solid, liquid or gaseous mass that is carried by the blood from its point of origin to a distant site where it often causes tissue dysfunction or infarction
Embolus
Area of ischemic necrosis caused by occlusion of either arterial supply or venous drainage
Infarct
State in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion — cellular hypoxia
Shock
4 main mechanisms of edema formation
- INCREASED hydrostatic pressure
- DECREASED oncotic pressure
- INCREASED vascular permeability
- Lymphatic OBSTRUCTION
General morphologic appearance of edema
- Clearing and separation of ECM
- Subtle cell swelling
58/M w/ hx of MI presented w/ paroxysmal noctunal dyspnea (PND)
CXR - bilateral pleural effusion
diagnosis, mechanism of edema, kind of effusion
Congestive Heart Failure
Increased Hydrostatic Pressure
Transudate
32/M, hx of remittent fever and productive cough, developed dyspnea
CXR -R pleural effusion w/ L parenchymal infiltrates
diagnosis, mechanism of edema, kind of effusion
Parapneumonic effusion; CAP MR
Increased vascular permeability
Exudate
57/M chronic alcoholic, increase in abdominal girth. Chem showed low serum albumin and elevated ALT and AST. Abdominal UTZ showed moderate ascites
diagnosis, mechanism of edema, kind of effusion
Decreased oncotic pressure
34/F, known case of breast cancer stage 2 (T2N0M0), s/p MRM, developed left arm swelling
mechanism of edema
Lymphatic obstruction
Transudate
abnormalities in Starling forces
normal vascular permeability
absent plasma protein leak
low protein content of fluid
<1.012
absent fibrin
absent inflammatory cells
Exudative
increased vascular permeability
presence of plasma protein leak
high protein content in fluid
>1.012
present fibrin
present inflammatory cells
It is an ACTIVE process d.t. augmented blood flow from ARTERIOLAR DILATION of increased O2 demand; affected tissue is REDDER than normal because of engorgement w/ OXYGENATED blood
Hyperemia
It is a PASSIVE process d.t. IMPAIRED VENOUS RETURN out of a tissue, has BLUE-RED color d.t. accumulation of DEOXYGENATED blood in the affected tissue
Congestion
24/F w/ large left atrial myxoma that obstructed flow of blood into the left atrium. Autopsy of the lung showed engorged alveolar capillaries, alveolar septal edema and focal intraalveolar hemorrhage.
Diagnosis
Acute pulmonary congestion
34/F died from acute R sided HF sec to saddle embolus. Autopsy of the liver showed distended central vein and sinusoids, centrilobular ischemic necrosis and periportal fatty change
Diagnosis
Acute Hepatic Congestion
55/M died of complications from congestive heart failue. Autopsy of the lung showed thickened and fibrotic alveolar septa and hemosiderin laden macrophases.
Diagnosis
Chronic Passive Congestion, Lung
60/M died of complications from HF. On autopsy, liver is heavier than normal and has nutmeg like appearance. Sections show centrilobular hemorrhage, hemosiderin laden macrophages and hepatocyte loss of variable degrees.
Diagnosis
Chronic Passive Congestion, liver
Components of Virchow Triad
Endothelial Injury
Stasis
Hypercoagulability
Major contributor to the development of ARTERIAL thrombi
Turbulence or Endothelial injury
Major contributor to the development of VENOUS thrombi
Stasis
Any alteration of the COAGULATION pathway that predisposes to thrombosis
Can be primary (Factor V Leiden, Protein C and S deficiency), or secondary (cancer, atrial fibrillation and prolonged immobilization)
Hypercoagulability
Lamination composed of PALE PLATELETand FIBRIN deposits alternating w/ DARKER RED cell rich layers signify formation of thrombus in flowing blood
Present in ANTEMORTEM THROMBOSIS
Lines of Zahn
MC siteof ARTERIAL THROMBOSIS
Coronary > Cerebral > Femoral
MC site of VENOUS thrombosis
Superficial or deep veins of the leg
thrombi - superficial leg veins - RARELY embolize
thrombi - deep leg veins - MC source of venous emboli
Fates of Thrombus
PROPAGATION - thrombi accumulate additional platelets and fibrin
EMBOLIZATION - thromb dislodge and travel to other sites in the vasculature
DISSOLUTION - rapid shrinkage and total disappearance of recent thrombi
ORGANIZATION AND RECANALIZATION -thrombi becomes incorporated in the vessel wall w/ formation of new capillary channels that restore blood flow
MC and most dreaded sequelae of DVT
Pulmonary Embolism
Embolus occluding the bifurcation of the pulmonary trunk
Associated w/ sudden death d.t. acute R sided HF
Saddle embolus
65/F, known case of DVT came from a 17 hr flight, developed respiratory dstress w/ R ventricular wall dysfunction on 2D echo.
Diagnosis
Pulmonary Embolism
45/F, known case of thyrotoxic heart disease and chronic atrial fibrillation developed sudden L sided weakness and loss of sensation.
Type of Embolism
Systemic thromboembolism (from mural thrombus)
38/M, known case of Non Hodgkin Lymphoma, developed sudden R sided weakness. Has had a recent admission for a month and has a history of cardiac pathology.
Phenomenon observed in the patient
Paradoxical Embolism (Cardiac pathology is PFO)
32/M involved in a motorcycle accident and sustained mid-shaft right femoral fracture w/o any blunt or penetrating head and chest trauma.
Developed progressive respiratory distress and died. Autopsy shows fat globules in pulmonary vasculature.
Diagnosis
Fat Embolism
25 G1P1 (1001) developed respiratory distress, seizures and refractory bleeding post partum and died. Autopsy showed fetal skin and lanugo in pulmonary vasculature.
Diagnosis
Amniotic Fluid Embolism
30/M diver, developed respiratory distress and joint pain after rapid ascent. Work up showed gas bubbles in pulmonary vasculature and joints.
Diagnosis
Air Embolism (Decompression sickness)
Infarcts that tend to occur in LOOSE tissues and in those w/ DUAL CIRCULATIONS previously congested tissues or when FLOW IS REETABLISHED AFTER AN INFARCTION (i.e. angioplasty of obtructed artery
Red(Hemorrhagic) Infarct
*pulmonary and bowel infarcts
Infarct that tend to occur in SOLID ORGANS w/ END ARTERIAL circulations
White (Anemic) Infarct
*Myocardial and Splenic Infarcts
55/M known case of MASSIVE MI, developed VENTRICULAR FIBRILLATION and died.
Kind of Shock
Cardiogenic Shock
65/M with RUPTURED ABDOMINAL AORTIC ANEURYSM, died.
Kind of Shock
Hypovolemic Shock
23/M, college student and doremr, developed COUGH and COLDS for 2 days followed by REMITTENT HIGH GRADE FEVER w/ DUSKY ECCHYMOSES on the lower extremities. At ER, px was STUPUROUS w/ BP = 50 palpatory.
Diagnosis andKind of Shock
Meningococcemia
Septic Shock
25/F, suffered from a BEE STING, developed GENERALIZED WHEALS, PERIORBITAL EDEMA and RESPIRATORY DISTRESS. BP = 70/50 .
Kind of Shock
Anaphylactic Shock
28/F, suffered from a BLUNT TRAUMA of the BACK after a vehicular accident, was HYPOTENSIVE for several days and was started on VASOPRESSORS for management.
Kind of Shock
Neurogenic Shock
Antiphospholipid Antibody Syndrome (APAS)
one or more antiphospholipid (aPL) autoantibodies
*anti-cardiolipin
*lupus anticoagulant
*anti-B2 glycoprotein
AND
recurrent thrombosis or pregnancy complications
thrombocytopenia
Antiphospholipid Antibody Syndrome (APAS)
one or more antiphospholipid (aPL) autoantibodies
*anti-cardiolipin
*lupus anticoagulant
*anti-B2 glycoprotein
AND
recurrent thrombosis or pregnancy complications
thrombocytopenia
Paradox of APAS
thrombosis
thrombocytopenia
prolonged aPTT
