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Pathology > Exam 1 Edema, Thrombosis, and Shock > Flashcards

Exam 1 Edema, Thrombosis, and Shock Flashcards

1
Q

What is edema?

A

increased fluid in extravascular (interstitial) space

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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
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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
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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
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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
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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

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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

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8
Q

What type of edema:

  • impairs ventilatory function-may cause acute respiratory failure
  • increased susceptibility for bacterial infection
  • life threatening
A

Pulmonary edema

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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
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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
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11
Q

What are some pharmacologic intervention of chronic edema? (subcutaneous)

A

Diuretics

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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

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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

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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)
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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

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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
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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+

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18
Q

What is the dominant pathway in coagulation cascade?

A

Extrinsic

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19
Q

What are the common factors between extrinsic and intrinsic?

A

X, V, II, I

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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
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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)

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22
Q

the extravasation of blood due to vessel rupture

A

Hemorrhage

-Hemorrhagic diathesis: increased tendency to hemorrhage from insignificant injury

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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
Q

Type of hemorrhage:

1-2 mm hemorrhages in skin, mucous membranes, or serial surfaces

A

Petechiae

26
Q

Type of hemorrhage:
Slightly larger than petechia
3mm

A

Purpura

27
Q

Type of hemorrhage:

Larger 1 to 2 cm subcutaneous hematoma

A

Ecchymoses

28
Q

What are the types of hemorrhage that accumulate in body cavities

A

hemothorax, hemoperricardium, hemoperitoneum, hemarthrosis

29
Q

What is the clinical significance of hemorrhage?

A

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
Q

Inappropriate activation of a normal hemostatic process

A

Thrombosis

31
Q

What is the importance of endothelial injury in Virchow Triad? (predisposes to thrombosis)

A

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
Q

What is the importance of abnormal blood flow in Virchow Triad? (predisposes to thrombosis)

A 
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
33
Q

What is the importance of hypercoagulability in Virchow Triad? (predisposes to thrombosis)

A
  • 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
Q

What is disseminated intravascular coagulation? (DIC)

A
  • 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
Q

what are the 4 fates of a thrombus?

A
  • propagation
  • embolization
  • dissolution
  • organize and recanalize (re-establish channels)
36
Q

What is an embolus?

A
  • 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
Q

What are some examples of nonthrombotic emboli?

A 
Fat
air
nitrogen
atherosclerotic debris (cholesterol)
tumor fragments 
bone marrow
amniotic 
foreign body
38
Q
  • 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
A

Pulmonary thromboembolism

Sites: main pulmonary artery, bifurcation of the pulmonary artery, pass into smaller arterioles

39
Q

-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

A

Systemic Thromboembolism

40
Q

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
A

Fat embolism

41
Q

Type of nonthrombotic emboli:

  • obstetric procedures, chest wall injury
  • decompression sickness
A

Air embolism

42
Q

Type of nonthrombotic emboli:
sudden severe dyspnea, cyanosis, hypotensive shock
-mortality 20-40%

A

Amniotic fluid

43
Q

What is ischemic necrosis caused by occlusion of arterial supply or venous drainage?

A

Infarct

44
Q

What do nearly all infarcts result from?

A 
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
45
Q

What are the factors that influence development of an infarct?

A
  • 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
Q

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

A

shock

47
Q

What is a cardiac clinical sign of shock?

A

hypotension

48
Q

Etiology: pump failure
myocardial damage (infarction, cardiomyopathy)
-extrinisic compression (tamponade)
-outflow obstruction (pulmonary embolism, coarctation)
-other (ventricular arrhythmia, ventricular rupture)

A

Cariogenic shock

49
Q

Etiology: loss of intravascular volume

  • internal or external hemorrhage
  • fluid loss (large burns, massive diarrhea)
A

Hypovolemic shock

50
Q

Etiology: sudden denervation causing systemic vasodilation

  • spinal cord injury
  • anesthetic accidents
A

Neurogenic shock

*uncommon

51
Q

Etiology: immunological IgE hypersensitivity

  • systemic vasodialation
  • peanut allergies
A

Anaphylactic shock

*uncommon

52
Q

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

A

Septic shock

53
Q

What is the non progressive stage of shock?

A 
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)
54
Q

What is the progressive stage of shock?

A

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
Q

What is the irreversible stage of shock?

A 
Severe, generalized hypoxic damage
-lysosomal enzyme effects
-superimposed sepsis due to ischemic bowl
-renal shutdown due to tubular necrosis
High mortality rate

Pathology (4 decks)

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