Pathology > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

(53 cards)

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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

23
Q

Functions of Thrombin

Study These Flashcards
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

Study These Flashcards
A
  1. Kalikrein
  2. Urokinase-like plasminogen activator
  3. Tissue-type plasminogen activator (tPA)
25
Why can DIC rapidly become a bleeding disorder?
There are many clots, which use up all of the clotting factors
26
What causes Heparin-induced thrombocytopenia? What is the result?
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
What is the cause of antiphospholipid antibody syndrome? What is the result?
Cause: * Abs to cardiolipin induce a hypercoagulable state Result: * Thrombocytopenia * Recurrent thrombi * Frequent miscarriages
28
What is the result of a Factor V gene mutation?
Hypercoagulability due to resistance of Factor V to inactivation by protein C
29
What is the result of Prothrombin gene mutation?
Elevated levels of prothrombin and hypercoagulability
30
Arterial vs Venous thrombi: 1. Cause 2. Direction of growth 3. Composition of Thrombi 4. Vessels most affected
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
What are lines of Zahn? Where are they located?
Laminations associated with thrombi of heart or aorta. Pale layer = platelets and fibrin Dark layer = RBCs
32
What are mural thrombi? Where are they located? What are some causes?
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
Superficial vs Deep Venous Thrombi Where are they found? What is the result?
Superficial: * saphenous veins where there are varicosities * Result: varicose ulcers, rarely embolize Deep: * Femoral and iliac veins * Result: potential embolism (to lungs)
34
Cause of pulmonary thromboembolizm
Deep leg vein thrombi
35
Systemic thromboembolism 1. What are possible causes? 2. What are likely sites of embolism?
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
What causes fat embolisms? What tissues are most affected?
Cause: * fat globules from bone marrow following fracture of long bones Tissues most affected: 1. Lungs 2. Brain
37
What are the symptoms of fat embolism syndrome?
1. Pulmonary distress 2. anemia 3. thrombocytopenia 4. petechiae 5. neurological manifestations
38
What causes decompression sickness? What are the symptoms? What is another name for this?
Cause: * air embolism following sudden change in atmospheric pressure Symptoms: * Musculoskeletal pain (aka the bends)
39
When is venous thrombosis more likely to cause infarction?
When there is only oneoutflow channel Ex: Testes and Ovaries
40
Red Infarcts 1. Occlusion of what vessel type causes this? 2. What type of tissue? 3. Why is it red?
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
White Infarcts 1. Occlusion of what vessel type causes this? 2. What type of tissue?
1. Arterial occlusion (blood not brought in) 2. Solid organs with end-arterial circulation * Heart, spleen, kidney
42
Septic Infarcts 1. What are the causes? 2. What are the results?
1. Causes * valve endocarditis vegetations break off * bugs seed necrotic tissue 2. Results * Abcess * Fibrosis
43
Tissues with dual blood supply and resulting decreased sensitivity to infarction
1. Lungs (pulmonary and bronchial arterial supply) 2. Liver (hepatic and portal circulation) 3. Hand/Forearm (radial and ulnar circulation) 4. Small Intestine
44
Types of shock, causes, and symptoms 1. Cardiogenic 2. Hypovolemic 3. Septic 4. Anaphylactic 5. Neurogenic
45
What is the Cytokine cascade associated with Septic Shock?
46
Pathogenesis of Septic Shock
47
What is the cytokine cascade associated with Septic Shock and what are the consequence?
48
Lungs are resistant to the effects of which type of shock?
Hypovolemic shock | (resistant to hypoxic injury)
49
Difference in initial septic shock vs other forms of shock (skin)
Most forms: skin is cool and cyanotic Septic: skin is red and warm
50
Describe the following phases of shock: 1. Nonprogressive 2. Progressive 3. Irreversible
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
What is pictured?
Acute tubular necrosis associated with shock
52
What is pictured?
Contraction band necrosis
53
Clinical presentation of shock
1. hypotension 2. weak, rapid pulse 3. Tachypnea 4. cool, cyanotic skin (warm and red in septic shock)
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