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Pathology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

Decribe the process of heart failure that results in edema

A

(-) arterial blood vol. –> (-) renal perfusion –> Pooling of blood in vein

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2
Q

Causes of albumin loss and influence on vascular pressure

A

Causes:

Nephrotic syndrome

Result: Decreased plasma osmotic pressure

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3
Q

Causes of reduced plasma protein lvls and influence on vascular pressure

A

Causes:

  1. Nephrotic syndrome (membranous Glomerulonephritis)
  2. Malnutrition
  3. Cirrhosis - reduced protien synthesis

Result:

  • Decreased plasma osmotic pressure and reabsorption of water
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4
Q

Causes of sodium and water retention and influence on vascular pressure

A

Causes:

  1. Glomerulonephritis (GN)
  2. acute renal failure

Result:

  • Decreased osmotic pressure
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5
Q

What is anascara

A

Generalized edema of Subcutaneous tissue

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6
Q

What is dependent edema?

A

when edema distribution is influenced by gravity (goes to legs after standing for long periods)

Also characteristic of CHF edema

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7
Q

Causes of pulmonary edema

A

Causes:

  1. L ventricular failure (blood not pumped out of the lungs
  2. Renal failure
  3. Pulmonary infections
  4. Acute respiratory distress syndrome
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8
Q

Hyperemia vs Congestion

A

Hyperemia:

  • Increased inflow of blood into tissues due to arteriolar dilation
  • Ex: inflammation
  • Ex: skeletal mm during exercise

Congestion:

  • Decreased or blocked outflow of blood
  • Ex: Cardiac failure (systemic)
  • Ex: Venous obstruction (local)
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9
Q

What disease process is occuring in this liver?

A

Chronic passive congestion (results in focal hemorrhage)

Called a “nutmeg liver”

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10
Q

What is a hematoma?

A

Hemorrhage enclosed within tissue or an organ

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11
Q

What are the size differences between petechiae, purpura, and ecchymoses

A

petechiae: 1-2mm
purpura: >3mm
ecchymoses: 1-2cm

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12
Q

Amount of blood loss needed to induce hemorrhagic shock

A

>20%

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13
Q
A
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14
Q

What is secreted by endothelial cells to inhibit platelet adherence?

A
  1. NO
  2. Prostacyclin
  3. ADPas
    • ADP promotes platelet aggregation
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15
Q

What anticoagulants are secreted by endothelial cells?

A
  1. Heparin-like molecules
    • activate antithrombin
    • Inhibit IXa, Xa, XIa, XIIa, and thrombin
  2. Thrombomodulin
    • Hydrolysis of Va and VIIIa
  3. Tissue Factor Pathway inhibitor
    • Inhibits extrinsic pathway of coagulation
  4. tPA
    • Stimulates plasmin production, which degrades fibrin
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16
Q

What is secreted by endothelial cells to stimulate platelet adherence?

A

von Willebrand factor: Platelet adherence to ECM via glycoprotein 1b (G1b)

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17
Q

What is secreted by endothelial cells to stimulate the clotting cascade?

A
  1. Tissue Factor
    • Stimulates extrinsic factor
  2. Plasminogen activator inhibitor-1
    • inhibits tPA, (-) plasmin, so no degradation of fibrin
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18
Q

Primary hemostatic plug

A

Platelets adhere to damaged endothelium to form platelet plug

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19
Q

Secondary hemostatic plug

A

conversion of fibrinogen to fibrin and its addition to the platelet plug, causing contraction of platelets

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20
Q

What factors stimulate platelet aggregation (formation of primary hemostatic plug)?

A
  1. ADP
  2. TxA2
  3. thrombin
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21
Q

In which type of platelet granule are ADP and Ca carried? What are their functions?

A

Delta granules

Functions:

  • ADP: stimulate platelet aggregation
  • Ca: cofactor in coagulation pathway
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22
Q

Coagulation Cascade

A
23
Q

Functions of Thrombin

A
  1. Fibrin –> fibrinogen
  2. formation of Va, VIIIa, XIIIa
  3. Induces production of TxA2
  4. Induces platelet aggregation
24
Q

Factors that convert plasminogen to plasmin

A
  1. Kalikrein
  2. Urokinase-like plasminogen activator
  3. Tissue-type plasminogen activator (tPA)
25
Q

Why can DIC rapidly become a bleeding disorder?

A

There are many clots, which use up all of the clotting factors

26
Q

What causes Heparin-induced thrombocytopenia? What is the result?

A

Cause:

  • development of Abs to heparin-platelet factor 4, which forms immune complexes which bind platelets and activate them

Result:

  • Thromboses and thrombocytopenia (low number of platelets) due to aggregations
27
Q

What is the cause of antiphospholipid antibody syndrome? What is the result?

A

Cause:

  • Abs to cardiolipin induce a hypercoagulable state

Result:

  • Thrombocytopenia
  • Recurrent thrombi
  • Frequent miscarriages
28
Q

What is the result of a Factor V gene mutation?

A

Hypercoagulability due to resistance of Factor V to inactivation by protein C

29
Q

What is the result of Prothrombin gene mutation?

A

Elevated levels of prothrombin and hypercoagulability

30
Q

Arterial vs Venous thrombi:

  1. Cause
  2. Direction of growth
  3. Composition of Thrombi
  4. Vessels most affected
A

Arterial:

  1. Cause:
    • Endothelial damage
    • Turbulence
  2. Direction of growth
    • Against flow (toward heart)
  3. Composition of Thrombi: N/A
  4. Vessels most affected
    • Coronary, cerebral, and femoral

Venous:

  1. Cause
    • Stasis
  2. Direction of growth
    • With flow (direction of heart)
  3. Composition of Thrombi
    • RED THROMBI: more RBCs due to stasis
  4. Vessels most affected
    • veins of the legs
31
Q

What are lines of Zahn? Where are they located?

A

Laminations associated with thrombi of heart or aorta.

Pale layer = platelets and fibrin

Dark layer = RBCs

32
Q

What are mural thrombi? Where are they located? What are some causes?

A

Thrombi that form in the cardiac chambers or aortic lumen.

Causes:

  • Cardiac: MI or abnormal contraction (fibrillation)
  • Aortic: ulceration of a plaque or aneurysm
33
Q

Superficial vs Deep Venous Thrombi

Where are they found? What is the result?

A

Superficial:

  • saphenous veins where there are varicosities
  • Result: varicose ulcers, rarely embolize

Deep:

  • Femoral and iliac veins
  • Result: potential embolism (to lungs)
34
Q

Cause of pulmonary thromboembolizm

A

Deep leg vein thrombi

35
Q

Systemic thromboembolism

  1. What are possible causes?
  2. What are likely sites of embolism?
A

Causes:

  1. Left ventricular wall infarct
  2. fibrillating left atria
  3. aortic aneurysm
  4. Fragmentation of valvular vegetations
  5. Paradoxical (from vein - thru art-ven communication)

Sites of embolism:

  1. Legs (femoral artery)
  2. Brain (Middle cerebral artery)
  3. Intestines
  4. Kidney
  5. Spleen
36
Q

What causes fat embolisms? What tissues are most affected?

A

Cause:

  • fat globules from bone marrow following fracture of long bones

Tissues most affected:

  1. Lungs
  2. Brain
37
Q

What are the symptoms of fat embolism syndrome?

A
  1. Pulmonary distress
  2. anemia
  3. thrombocytopenia
  4. petechiae
  5. neurological manifestations
38
Q

What causes decompression sickness? What are the symptoms? What is another name for this?

A

Cause:

  • air embolism following sudden change in atmospheric pressure

Symptoms:

  • Musculoskeletal pain (aka the bends)
39
Q

When is venous thrombosis more likely to cause infarction?

A

When there is only oneoutflow channel

Ex: Testes and Ovaries

40
Q

Red Infarcts

  1. Occlusion of what vessel type causes this?
  2. What type of tissue?
  3. Why is it red?
A
  1. Venous occlusions
  2. Loose tissue that allows blood to collect (with dual circulation)
  3. Red color is due to collection of blood
  4. Causes
    • tissues that were previously congested
    • re-establishment of blood flow to a necrotic site
41
Q

White Infarcts

  1. Occlusion of what vessel type causes this?
  2. What type of tissue?
A
  1. Arterial occlusion (blood not brought in)
  2. Solid organs with end-arterial circulation
    • Heart, spleen, kidney
42
Q

Septic Infarcts

  1. What are the causes?
  2. What are the results?
A
  1. Causes
    • valve endocarditis vegetations break off
    • bugs seed necrotic tissue
  2. Results
    • Abcess
    • Fibrosis
43
Q

Tissues with dual blood supply and resulting decreased sensitivity to infarction

A
  1. Lungs (pulmonary and bronchial arterial supply)
  2. Liver (hepatic and portal circulation)
  3. Hand/Forearm (radial and ulnar circulation)
  4. Small Intestine
44
Q

Types of shock, causes, and symptoms

  1. Cardiogenic
  2. Hypovolemic
  3. Septic
  4. Anaphylactic
  5. Neurogenic
A
45
Q

What is the Cytokine cascade associated with Septic Shock?

A
46
Q

Pathogenesis of Septic Shock

A
47
Q

What is the cytokine cascade associated with Septic Shock and what are the consequence?

A
48
Q

Lungs are resistant to the effects of which type of shock?

A

Hypovolemic shock

(resistant to hypoxic injury)

49
Q

Difference in initial septic shock vs other forms of shock (skin)

A

Most forms: skin is cool and cyanotic

Septic: skin is red and warm

50
Q

Describe the following phases of shock:

  1. Nonprogressive
  2. Progressive
  3. Irreversible
A
  1. Nonprogressive
    • reflex compensatory mechanisms maintain perfusion
    • tachycardia, vasoconstriction, retention of fluid by kidney
  2. Progressive
    • Tissue hypoperfusion w/circulatory and metabolic imbalance
    • anaerobic glycolysis lowers pH and inhibits vasomotor response (vasodilation)
  3. Irreversible
    • Severe cell injury and death
51
Q

What is pictured?

A

Acute tubular necrosis associated with shock

52
Q

What is pictured?

A

Contraction band necrosis

53
Q

Clinical presentation of shock

A
  1. hypotension
  2. weak, rapid pulse
  3. Tachypnea
  4. cool, cyanotic skin (warm and red in septic shock)

Pathology (27 decks)

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