Exam 1 Edema, Thrombosis, and Shock Flashcards
1
Q
What is edema?
A
increased fluid in extravascular (interstitial) space
2
Q
How does increased hydrostatic pressure contribute to edema?
A
Impaired venous return -congestive heart failure (CHF) -constrictive pericarditis -cirrhosis -venous obstruction (thrombosis, external pressure, lower extremity inactivity) Arteriolar dilation (adding more blood will increase hydrostatic pressure) -heat -neurohormonal regulation
3
Q
How does reduced plasma oncotic pressure (hypoproteinemia) contribute to edema?
A
Loss of plasma proteins -through urine (nephrotic syndrome) -protein-losing gastroenteropathy Reduced synthesis of plasma proteins -hepatic insufficiency -protein malnutrition
4
Q
How does lymphatic obstruction contribute to edema?
A
Impaired lymphatic drainage results in lymphedema Causes: -inflammation -neoplastic (abnormal growth) -post surgical -post irradiation
5
Q
How does sodium and water retention contribute to edema?
A
-Increased vascular hydrostatic pressure and decreased plasma oncotic pressure Causes: -acute reduction in renal function -renal hypo perfusion -renin-angiotensin-aldosterone secretion
6
Q
What is anasarca?
A
Extreme generalized edema, is a medical condition characterized by widespread swelling of the skin due to effusion of fluid into the extracellular space
-subcutaneous edema
7
Q
What type of edema:
- can be severe but not life threatening
- distribution depends on cause (dependent areas or generalized)
- signals underlying disease (heart failure, renal dysfunction)
- can impair wound healing
A
Subcutaneous edema
8
Q
What type of edema:
- impairs ventilatory function-may cause acute respiratory failure
- increased susceptibility for bacterial infection
- life threatening
A
Pulmonary edema
9
Q
What type of edema:
- life threatening
- can lead to herniation
- there are only so many places this fluid can go in this area
A
Cerebral Edema
- Uncal herniation: uncut squeezed through, dilated eye
- Cerebral tonsil herniation-tonsils of cerebella herniate through foramen
10
Q
What are some pharmacologic intervention of acute edema? (pulmonary, cerebral)
A
- osmotic agents (mannitol, glycerol)
- steroids (decadron-reduces inflammatory response)
- morphine (anti-anxiety–>reduces effects of pulmonary edema
- loop diuretics
11
Q
What are some pharmacologic intervention of chronic edema? (subcutaneous)
A
Diuretics
12
Q
What is this version of local increase in volume of blood in particular tissue:
- active process
- increased inflow of blood due to arteriolar dilation
- erythema due to engorgement with OXYGENATED blood
A
Hyperemia
13
Q
What is this version of local increase in volume of blood in particular tissue:
- passive process
- decreased outflow of blood
- cyanotic due to accumulate of DEOXYGENATED blood
- often associated with edema
- can lead to tissue hypoxia, cell death, and hemorrhage
A
Congestion
14
Q
What is hemostasis?
A
- Maintenance of blood in a fluid state in normal vessels
- Ability to induce rapid and localized hemostatic plug at site of vascular injury
- Dysregulation of the process= hemorrhage diathesis (blood too thin) , hypercoagulability (if blood is too thick)
15
Q
What are the four stages of normal hemostasis?
A
1) vasoconstriction
- reflex, secrete factors like endothelin
2) primary hemostasis (platelet plug formation)
3) secondary hemostasis
- coagulation cascade
- fibrin deposition and polymerization
4) antithrombiotic mechanisms
- limit hemostatic plug to site of injury
16
Q
What is the role of platelets in hemostasis?
A
- Platelets adhere to site of injury
- Von Willebrand Factor (vWF) is a chemical bridge between platelet glycoprotein Ib and exposed collagen
- Secretes granular contents
- Primary hemostatic plug = platelets
- -driven by ADP and thromboxane A2; inhibited by aspirin and antiplatelet agents (Plavix)
- Secondary hemostatic plug= platelets and fibrin
- -driven by coagulation cascade
17
Q
Whats the role of coagulation cascade in hemostasis?
A
Culminates in the formation of thrombin, which then converts soluble fibrinogen into insoluble fibrin
-cant occur without Ca2+
18
Q
What is the dominant pathway in coagulation cascade?
A
Extrinsic
19
Q
What are the common factors between extrinsic and intrinsic?
A
X, V, II, I
20
Q
What are the prothrombotic properties of endothelium?
A
*most important Platelet effects (disrupted endothelium) -von WIllebrand factor (vWF) Procoagulant effects -tissue factor Antifibrinolytics -inhibitors of plasminogen activator
21
Q
What are the antithrombotic properties of endothelium?
A
Antiplatelet effects (intact endothelium)
-prevention of platelet aggregation to underlying extracellular matrix
-prostacyclin (PGI2), NO, ADPase
Anticoagulante effects
-heparin-like molecules
-thrombomodulin
-tissue factor pathway inhibitor
Fibrinolytic effects
-tissue-type plasminogen activator (t-PA)
22
Q
the extravasation of blood due to vessel rupture
A
Hemorrhage
-Hemorrhagic diathesis: increased tendency to hemorrhage from insignificant injury
23
Q
increased tendency to hemorrhage from insignificant injury
A
-Hemorrhagic diathesis
24
Q
Type of hemorrhage:
-Accumulation of blood within a tissue
A
Hematoma
25
Type of hemorrhage:
| 1-2 mm hemorrhages in skin, mucous membranes, or serial surfaces
Petechiae
26
Type of hemorrhage:
Slightly larger than petechia
3mm
Purpura
27
Type of hemorrhage:
| Larger 1 to 2 cm subcutaneous hematoma
Ecchymoses
28
What are the types of hemorrhage that accumulate in body cavities
hemothorax, hemoperricardium, hemoperitoneum, hemarthrosis
29
What is the clinical significance of hemorrhage?
Depends on volume and rate of bleeding:
-rapid loss of up to 20% of blood volume or slow losses may have little impact
-greater losses can result in hemorrhagic (hypovolemic) shock
Site of hemorrhage is important
Iron deficiency anemia can develop in chronic or recurrent blood loss
30
Inappropriate activation of a normal hemostatic process
Thrombosis
31
What is the importance of endothelial injury in Virchow Triad? (predisposes to thrombosis)
Physical injury of endothelium
-myocardial infarction (mural thrombosis in cardiac chambers)
-ulcerated atherosclerotic plaques
-inflammatory vascular injury (vasculitis)
Disruption of the pro- and antithrombotic effects of endothelium in absence of endothelial cell loss
-hypertension
-valvular disease
-bacterial endotoxins
-other causes of endothelial injury (homocystinuria, hypercholesterolemia, cigarette smoke)
32
What is the importance of abnormal blood flow in Virchow Triad? (predisposes to thrombosis)
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Clinical examples:
-aneurysms
-cardiac valve disease/artifical valves
-artrial fibrillation
-hyperviscosity (polycythemia, sickle cell disease)
Pathogenesis:
-disruption of laminar blood flow
-prevent dilution of coagulation factors
-slow inflow of plasma anticoagulants
-promote procoagulant endothelial properties
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33
What is the importance of hypercoagulability in Virchow Triad? (predisposes to thrombosis)
- any alteration of the coagulation pathways that predisposes to thrombosis
- inherited (primary)
- acquired (secondary)
- both endothelial injury and abnormal blood flow lead to hypercoagulability
34
What is disseminated intravascular coagulation? (DIC)
- sudden or insidious onset of widespread fibrin thrombi in the microcirculation
- diffuse circulatory insufficiency especially in the brain, heart, lungs, and kidneys
- rapid consumption of platelets and coagulation proteins (consumption coagulopathy)
- activation of fibrinolytic mechanisms with evolution into a bleeding disorder
- NOT a primary disease but a potential complication of any condition associated with widespread activation of thrombin
35
what are the 4 fates of a thrombus?
- propagation
- embolization
- dissolution
- organize and recanalize (re-establish channels)
36
What is an embolus?
- detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin
- almost all represent some part of a dislodged thrombus (thromboembolism)
37
What are some examples of nonthrombotic emboli?
```
Fat
air
nitrogen
atherosclerotic debris (cholesterol)
tumor fragments
bone marrow
amniotic
foreign body
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38
- 95% originate from deep leg vein
- carried to right side of heart to lungs
- can be clinically silents or result in sudden death
- Multiple: can cause pulmonary hypertension and right heart failure
Pulmonary thromboembolism
| Sites: main pulmonary artery, bifurcation of the pulmonary artery, pass into smaller arterioles
39
-refers to emboli traveling within arteries
-most from intracardiac mural thrombi (left A or Left V)
-remainder originate from thrombi associated with ulcerated atherosclerotic plaques
lower extremities 75%
brain 10%
kidneys, spleen, and upper extremities
Systemic Thromboembolism
40
Type of nonthrombotic emboli:
- Trauma fracture of long bone or rarely soft tissue trauma
- this syndrome is characterized by pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia
Fat embolism
41
Type of nonthrombotic emboli:
- obstetric procedures, chest wall injury
- decompression sickness
Air embolism
42
Type of nonthrombotic emboli:
sudden severe dyspnea, cyanosis, hypotensive shock
-mortality 20-40%
Amniotic fluid
43
What is ischemic necrosis caused by occlusion of arterial supply or venous drainage?
Infarct
44
What do nearly all infarcts result from?
```
Thromboembolic disease
Other mechanisms:
-local vasospasm
-hemorrhage within an atherosclerotic plaque
-extrinsic compression of a vessel
-twisting of the vessels
-compression of blood supply by edema
-entrapment in a hernia sac
-traumatic rupture of blood supply
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45
What are the factors that influence development of an infarct?
- Nature of the vascular supply
- Rate of development of the occlusion
- vulnerability to hypoxia
- blood oxygen content
* heart, spleen, kidney, where you have one source of blood supple
* liver and lungs have multiple blood supplies so hardly ever have infarct
46
A constellation of clinical signs and symptoms caused by impaired tissue perfusion
-effects mediated by some combination of reduced cardiac output and reduced effective blood volume
shock
47
What is a cardiac clinical sign of shock?
hypotension
48
Etiology: pump failure
myocardial damage (infarction, cardiomyopathy)
-extrinisic compression (tamponade)
-outflow obstruction (pulmonary embolism, coarctation)
-other (ventricular arrhythmia, ventricular rupture)
Cariogenic shock
49
Etiology: loss of intravascular volume
- internal or external hemorrhage
- fluid loss (large burns, massive diarrhea)
Hypovolemic shock
50
Etiology: sudden denervation causing systemic vasodilation
- spinal cord injury
- anesthetic accidents
Neurogenic shock
| *uncommon
51
Etiology: immunological IgE hypersensitivity
- systemic vasodialation
- peanut allergies
Anaphylactic shock
| *uncommon
52
Etiology: microbial infection
-gram-negative causes the majority
Pathogenesis: release of high levels of microbial lipopolysaccharide (LPS; endotoxin)
-activation of macrophages, neutrophils, complement
-endothelial damage with activation of coagulation cascade
-release of cytokines and other factors
-not necessarily accompanied by bacteremia
Septic shock
53
What is the non progressive stage of shock?
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Initially compensatory mechanisms maintain tissue perfusion
-catecholamine release
-renin-angiotensin axis
-autonomic sympathetic stimulation
Clinical effects
-tachycardia, tackypnea
-renal fluid conservation
-peripheral vasoconstriction (cool, clammy skin-except with septic)
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54
What is the progressive stage of shock?
Decreased perfusion leads to tissue hypoxia
-glycolysis and lactic acidosis
-decreased vasomotor function, vasodilation
-endothelial damage
Clinical signs:
-renal insufficiency/decreased urine output
-confusion
-metabolic acidosis
-electrolyte imbalance
55
What is the irreversible stage of shock?
```
Severe, generalized hypoxic damage
-lysosomal enzyme effects
-superimposed sepsis due to ischemic bowl
-renal shutdown due to tubular necrosis
High mortality rate
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