CHAPTER 7--HEMODYNAMIC DYSFUNCTION = 2 Q'S Flashcards
CELLS & TISSUES are dependant on
- Normal Fluid Environment = increase edema and decrease dehydration
- Adequate Blood supply
- Thrombosis
- Embolism
- Infarction
- Hemorrhage
know
______–Accumulation of excess fluid (transudate, exudate, lymph) in the intercellular (interstitial) tissue spaces and body cavities:
Body cavities are:
- pleural cavity (hydrothorax)
- peritoneal cavity (ascites )
- pericardial cavity (hydropericardium)
**Edema can be local or generalized
EDEMA
Pitting edema of the leg
reflects the “________” of the fluid- filled tissue
in-elasticity
Pathogenesis of Edema
- INCREASE capillary hydrostatic pressure (hemodynamic edema): protein-poor transudate
- INCREASE capillary permeability (inflammatory edema):protein-rich exudate
- DECREASE collodial osmotic pressure of plasma proteins: liver (dec. protein synthesis), kidney (nephrotic syndrome)
- INCREASE tissue osmotic pressure (sodium retention)
- obstruction of lymphatics (lymphedema): in malignancy, surgery, radiation therapy, or filariasis
KNOW
Causes of generalized edema
1. Cardiac = Left ventricular failure + Right ventricular failure
2. Renal–Acute glomerulonephritis & Nephrotic syndrome
3. Hepatic:–decreased protein synthesis & portal hypertension
4. 4. Nutritional: protein malnutrition
(kwashiorker or starvation)
KNOW
Causes of localized edema
1. Inflammatory edema
-INCREASE vascular permeability
-__________ hydrostatic pressure to arteriolar dilation
(= exudate)
2. Edema due to localized ________ obstruction
-thrombosis, varicose veins, compression
-hydrostatic pressure (= transudate)
3. Edema due to____________ obstruction
-surgery, cancer, parasites
-in early stage, edema is pitting ( = lymph)
-later, edematous tissue becomes fibrosed, thickened & non-pitting (elephantiasis)
INCREASE
venous
lymphatic
_________: INCREASE of blood due to active arterial dilation:
a. Physiologic : muscles during exercise
b. Pathologic: inflammation
__________: passive INCREASE of blood due to impaired venous drainage:
- –localized as due to venous obstruction, or
- -generalized as with right heart failure
Hyperemia
Congestion
Pulmonary congestion—Etiology: _____ ventricular failure (hypertension, myocardial infarction, rheumatic heart)
Alveolar capillaries: engorged, dilated, tortuous:
-edema of interstitial tissue
-transudate in alveoli
-hemorrhage
Left
Chronic passive congestion of the lungs
.
Increased venous pressure leads to extra vasation of
red blood cells into the alveoli and alveolar edema.
The hemosiderin formed from hemoglobin released from hemolyzed red blood cells is taken up by intraalveolar macrophages. These macrophages are
sometimes called “_____ _____ ______” because of
their association with pulmonary congestion with
congestive heart failure
.
“heart failure cells”
Liver congestion
Etiology—_______ side heart failure, pulmonary fibrosis, tricuspid stenosis, & thrombosis of hepatic vein or inferior vena cava
Right
Chronic passive congestion (nutmeg liver), gross. a “nutmeg” liver seen with chronic______ ________ of
the liver
.
passive congestion
__________— (blood clot):
A solid mass formed from blood constituents within heart and blood vessels during life. It is composed of layers of aggregated platelets and fibrin
Thrombus
Thrombosis is a normal hemostatic mechanism that stops _____-_____
bleeding:
Thrombosis is a normal hemostatic mechanism that stops bleeding.
- Formation of platelet plug:
-injury of __________ exposes subendothelial collagen
-adhesion of platelets to exposed collagen
-platelet release reaction: secretion of ADP platelet
aggregation (they aggregate on top of each other)
endothelium
Thrombosis is a normal hemostatic mechanism that stops bleeding.
- Coagulation of blood:
-activation of ________________ activates intrinsic pathway
-tissue thromboplastin released by injury activates
extrinsic pathway
3._________:—-prevents excess thrombus formation
Hageman factor (XII)
Fibrinolysis
Three important factors are involved in hemostasis
- Endothelial cells
- Blood platelet
- Coagulation factors
know
ENDOTHELI AL CELLS-Releasing antithrombotic or
thrombotic factors
A—-intact endothelial cells prevent thrombosis through;
1. Anti-platelet properties
2. Anti -coagulant properties
3. Fibrinolytic properties
B-Injured endothelial cells = initiate thrombosis
—Synthesize von WILLIBRANDS FACTOR–binds platelets to exposed subendothelial collagen (platelet adhesion)
-Release tissue factor (thromboplastin) = activates
__________ clotting pathway
:
extrinsic
PLATELETS—-Derived from cytoplasmic fragmentation of megakaryocytes
- platelet ________ to subendothelial collagen mediated by von W factor
adhesion
COAGULATION SYSTEM x 2
Intrinsic Pathway = Activation of XII
Extrinsic Pathway = Release of tissue thromboplastin
- **Coagulation is confined to site of injury through:
- natural anti-thrombin
- removal of activated factors (liver & phagocytic cells)
- dilution
know
THROMBOGENESIS Predisposing factors (VIRCHOW'S TRIAD)
- Endothelial injury
- Alteration of normal blood flow
- Hyper-coagulability of blood
know
Morphology of Thrombi
1. Arterial thrombi:
“ _______ ___ _____ “ which are the alternating pale pink bands of platelets with fibrin and red bands
of RBC’s forming true thrombus
- Venous thrombi—commonly (90% ) in veins of
lower limbs—almost always occlusive
lines of Zahn
________ veins of the legs = Severe varicosities of
the superficial leg veins have led to stasis dermatitis
and secondary ulcerations
Varicose
Fate of Thrombi x 5
- _______: accumulate more platelets & fibrin to obstruct a critical vessel
- Fibrinolysis: re-establishment of lumen (fibrinolytic
Activity) - Thromboembolism: partial or complete detachment
- ___________: inward growth of granulation
tissue - Recanalization: capillaries of granulation tissues form
anastomosing channels
Propagation
Organization (fibrosis)
EMBOLISM
______:–an insoluble mass (solid, liquid, gaseous)
circulating in the blood
.
________:–occlusion or obstruction of a blood vessel by an embolus.
Embolus
Embolism
