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Pathophysiology > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

What is the mechanism behind the equilibrium of interstitial fluid?

A

Outflow of fluid by capillary hydrostatic pressure (HP) is balanced by inflow of fluid by blood colloid osmotic pressure (BCOP).

HP fluid out = BCOP fluid in

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2
Q

What pathways lead to development of systemic edema?

A
  1. Increased hydrostatic pressure (CHF).
  2. Reduce osmotic pressure (hypoproteinemia, malnutrition).
  3. Lymphatic obstruction (inflammatory/neoplastic condition).
  4. Sodium retention (renal failure).
  5. Increased vascular permeability (inflammation).
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3
Q

What are the hormones involved in the development of systemic edema?

A
  1. Angiotensin II

2. Aldosterone

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4
Q

What is the sequence of normal hemostasis at site of vascular injury?

A
  1. Transient arteriolar vasoconstriction.
  2. Formation of platelet plug (injured endothelium reveals von Willebrand Factor which activates platelet adhesion).
    - - platelet changes shape
  3. Deposition of fibrin.
    - - factor VII –> thrombin –> fibrinogen into fibrin
  4. Clot stabilization and resorption.
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5
Q

What are the 2 types of platelet granules?

A

Alpha-granules.

  • P-selectin
  • Fibrinogen
  • Factor V & IV

Dense granules.

  • ADP, ATP
  • Ionized Ca2+
  • serotonin, epinephrine
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6
Q

What are the functions of alpha-granules and dense granules?

A

Activate and recruit platelets in the context of formation of hemostatic plug.

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7
Q

Describe the role of Vitamin K in the coagulation cascade.

A

Vitamin K is a key cofactor to activating enzymatic activities such as for Factors II, VII, IX and X.

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8
Q

What is role of thrombin and its activities in hemostasis?

A

Thrombin activates and aggregates platelets via proteolytic cleavage of protease-activated
receptor (G-protein).

Converts fibrinogen to fibrin creating secondary hemostatic plug.

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9
Q

What is the role of plasminogen in the fibrinolytic cascade?

A

Plasminogen is the precursor to plasmin.

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10
Q

What is the role of plasminogen ACTIVATORS in the fibrinolytic cascade?

A

Plasminogen ACTIVATORS conversion plasminogen to plasmin; notably t-PA (tissue plasminogen factor).

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11
Q

What is the role of plasmin in the fibrinolytic cascade?

A

Plasmin breaks down fibrin and interferes with polymerization (which controls the size of clot and contribute to its dissolution).

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12
Q

What are the classes of anti-thrombotic properties of normal epithelium?

A
  1. Platelet inhibitory effect. (prostacyclin, nitric oxide, adenosine phosphatase)
  2. Anticoagulation effect. (thrombomodulin, enothelial protein C receptor, heparin-like receptor, tissue factor pathway inhibitor)
  3. Fibrinolytic effect. (t-PA; tissue plasminogen factor)
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13
Q

What are the three (3) primary abnormalities that lead to thrombus formation?

A
  1. Endothelial injury.
    (Procoagulant and anti-fibrinolytic changes)
  2. Stasis or turbulent blood flow.
    (Allow contact of endothelium and prevent washout)
  3. Hypercoagulability of blood (Virchow’s Triad).
    (Primary v. Secondary; aka inherited v. acquired)
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14
Q

Distinguish between the primary and secondary hypercoagulable states. What are the most common causes for each?

A

1° - inherited; gene alterations of factor V and prothrombin

2° - acquired; HIT, cancer, oral contraceptives, tissue injury, immobilization

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15
Q

Distinguish between mural thrombi, arterial thrombi and venous thrombi.

A

Mural: occuring in heart chambers or in aortic lumen

Arterial: occlusive, rich in platelets

Venous: invariably occlusive, enmeshed red cells, stasis thrombi

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16
Q

What are the four (4) possible outcomes of thrombosis?

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and recanalization
17
Q

What are the consequences of embolization of systemic circulation v. pulmonary circulations?

A

Systemic:
- embolization and presence/absence of collateral circulation, tissue infarction

Pulmonary:

  • from LE DVT
  • right-sided heart failure, pulmonary hemorrhage/infarction, death
18
Q

What is the origin and most common risk factors for development of pulmonary emboli?

A

Origin: DVT

Risk factors: prolonged bed rest, surgery, trauma, CHF, contraceptives, disseminated cancer.

19
Q

What is origin and underlying conditions predisposing to development of systemic emboli?

A

Origin: intracardiac mural thrombi (from infarcts)

Predisposing factors: L. ventricular infarcts, dilated L. atria, aneurysms, valvular vegetation

20
Q

What are the predisposing factors for and pathgenesis of fat emboli?

A

Predisposing factors: Skeletal injuries, soft tissue injuries, rupture of marrow sinusoids.

Pathogenesis: injuries release microscopic fat globules into circulation

21
Q

Describe the underlying mechanism of amniotic fluid emboli.

A

Entry of amniotic fluid via tears in maternal circulation in the placental membrane or uterine vein rupture.

22
Q

What is the mechanisms of the development of air emboli and its ability to damage tissues?

A

Gas bubbles coalesce, obstruct vascular flow and cause ischemic injury.

Can cause hypoxia, edema, hemorrhages, focal atelectasis, emphysema, coma and death (depending on location).

23
Q

What are the classifications of infarcts and the common necrotic findings?

A

Classification:

  1. Color (red v white)
    - -> coagulative, liquefactive
  2. Microbial infection (septic or bland)
    - -> abscess
24
Q

What are the three (3) variables that dictate the outcome of infarct?

A
  1. Presence/absence of alternative blood supply.
  2. Rate of occlusion.
  3. Tissue vulnerability to hypoxia.
25
Q

What are the 3 major categories of shock and their underlying pathogenic mechanisms?

A
  1. Myogenic - inadequate blood or plasma volume, decreased CO (hemorrhage)
  2. Cardiogenic - heart failure (myocardial damage)
  3. Septic - microbial infections, SIRS
    * Neurogenic - anesthesia or spinal cord injury.
    * Anaphylactic - IgE hypersentivity.
26
Q

What are the factors playing a role in development of septic shock and major pathogenic pathways?

A
  1. Inflammatory and counterinflammatory responses. (microbial cell wall engage TLR)
  2. Endothelial activation and injury. (vascular leakage, edema, decreased perfusion)
  3. Induction of procoagulant state. (thrombin activation decrease perfusion)
  4. Metabolic abnormalities. (hyperglycemia decreases neutrophil function, lactate acidosis)
  5. Organ dysfunction. (decreased tissue perfusion, decreased CO, ARDS, organ failure)
27
Q

What are the three (3) stages of shock and mechanisms behind their features?

A
  1. Non-progressive; reflex compensatory mechanisms are activated and vital organ perfusion is maintained. (baroreceptor reflex, ADH maintain perfusion)
  2. Progressive; tissue hypoperfusion, worsening circulatory and metabolic derangement (anaerobic, lactic acidosis)
  3. Irreversible; cellular and tissue injury is severe that survival is not possible. (lysosomal enzyme leakage, intestinal flora enters circulation)

Pathophysiology (9 decks)

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