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MOD Exam 1 > Ch. 4 Hemodynamics > Flashcards

Ch. 4 Hemodynamics Flashcards

1
Q

Edema

A

Accumulation of fluid in Tissues

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2
Q

Effusions

A

Accumulation of fluid in body cavities:

  • Pleural
  • Pericardial
  • Peritoneal
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3
Q

2 primary causes of fluid accumulation

A
  1. Increased hydrostatic pressure

2. Decreased plasma oncotic pressure

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4
Q

Under normal conditions, what system removes the fluid that naturally accumulates in tissue?

A

Lymphatics

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5
Q

Describe the fluid that accumulates in a non-inflammatory state of edema

A

Protein-poor (Transudate)

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6
Q

Examples of Pathologies caused by increased hydrostatic pressure causing edema/effusion

A

CHF
Ascites
Thrombosis

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7
Q

Examples of pathologies caused by reduced oncotic pressure (hypoproteinemia)

A

Nephrotic syndrome

Malnutrition

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8
Q

Nephrotic Syndrome

A

Loss of protein in urine due to abnormally permeable glomerular capillaries

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9
Q

Factors that can cause lymphedema

A

Trauma
Fibrosis
Tumors
Infections

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10
Q

Patient presents with edema of the external genitalia and lower limbs bilaterally. What is the name of this presentation and what is caused by?

A

Elephantiasis caused by parasitic filariasis

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11
Q

Dependent Edema

A

Edema that is influenced by gravity

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12
Q

Periorbital edema is a common characteristic of disease affecting what organ system?

A

Severe Renal Disease

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13
Q

Chylous Effusion

A

milky peritoneal effusion caused by lymphatic blockage

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14
Q

Hyperemia

A

arteriolar dilation leads to increased blood flow resulting in erythema.

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15
Q

Congestion

A

Passive process resulting from reduced outflow of blood from tissue. (Venous block)
- Caused primarily by increased hydrostatic pressure

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16
Q

Morphology of chronic pulmonary congestion

A

Septa of alveoli are thickened and fibrotic with hemosiderin-laden macrophages called heart failure cells

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17
Q

Describe nutmeg liver

A

Acute hepatic congestion causes the central vein and sinusoids to be distended. Centrilobular hepatocytes that are distal from the hepatic arteries undergo ischemic necrosis.

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18
Q

Hemostasis

A

process by which blood clots form at sites of vascular injury

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19
Q

Hemorrhagic disorders

A

excessive bleeding caused by insufficient hemostatic mechanisms to control blood loss

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20
Q

Thrombotic disorders

A

Abnormal clotting within intact blood vessels

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21
Q

Hemostasis steps

A
  1. Arteriolar Vasoconstriction by endothelin
  2. Primary Hemostasis by exposure of vWF and collagen that promotes platelet adherence
  3. Secondary Hemostasis (deposition of fibrin)
  4. Clot resorption
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22
Q

Tissue factor

A

Binds and activates factor VII

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23
Q

Function of ADP and TxA2 in hemostasis

A

Induce platelet aggregation via GpIIb-IIIa binding to fibrinogen

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24
Q

a-granules of platelets

A

contain P-selectin, fibrinogen, Factor V, and vWF

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25
Q

d-granules of platelets

A

contain ADP, ATP, Ca, Serotonin, and epinephrine

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26
Q

How does Aspirin cause a mild bleeding defect?

A

Inhibits platelet aggregation by inhibiting cyclooxygenase which reduces TxA2 production

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27
Q

Glanzmann Thrombasthenia

A

Defect in GpIIb-IIIa leads to decreased binding of platelets to fibrinogen.

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28
Q

Define the Intrinsic Pathway of clotting

A

XII–> XI–> IX + VIII–> X + V –> Thrombin–> Fibrin

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29
Q

Define the Extrinsic Pathway of clotting

A

VII–> VII + TF–> IX–> X + V–> Thrombin–> Fibrin + XI
* Factor XI then activates Factor IX
Figure 4-6

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30
Q

What role to platelets play in the clotting cascade?

A

Provide negatively charged phospholipid surface for the assembly of coagulation factors

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31
Q

What factors are affected by Vit K antagonists?

A

II, VII, IX, and X

Protein C and S

32
Q

Prothrombin Time

A

assesses the extrinsic pathway of coagulation

Factors II, V, VII, X, Fibrinogen

33
Q

Partial thromboplastin time

A

Assesses intrinsic pathway

Factors II, V, VIII, IX, X, XI, XII, Fibrinogen

34
Q

Factor XII deficiency

A

susceptibility to thrombosis

35
Q

Which factors are implicated in moderate to severe bleeding disorders?

A

V, VII, VIII, IX, X

36
Q

Thrombin functions

A
  1. Conversion of fibrinogen
  2. Platelet Activation
  3. Pro-inflammatory effect
  4. Anti-coagulant effect in the presence of normal endothelium (PGI2, tPA, NO)
37
Q

Plasmin

A

Most important enzyme of fibrolysis

Breaks down fibrin

38
Q

t-PA

A

tissue plasminogen activator- activates plasmin to break down clots
*Important for stroke patients within 6 hours of onset

39
Q

What regulates plasmin activity?

A

a2-plasmin inhibitor

40
Q

Endothelium factors that are antithrombotic towards platelets

A
  1. PGI2
  2. NO
  3. ADPase
41
Q

Antithrombotic factors produced by endothelium that interfere with coagulation

A

Thrombomodulin
Protein C Receptor
heparin-like molecules
tissue factor pathway inhibitor

42
Q

Protein C/S complex

A

inhibits Factors V and VIII

43
Q

Heparin-like molecules

A

bind and activate antithrombin III

Complex inhibits thrombin and Factors IX-XII

44
Q

Primary hemostasis bleeding disorders

A

vWF disease

  • causes small bleeds in skin or mucus membranes
  • presents with petechiae and/or purpura
45
Q

Secondary hemostasis bleeding disorders

A

Coag factor deficiencies

- bleeding into soft tissues and joints (hemarthrosis)

46
Q

Virchow’s Triad

A

Primary abnormalities that lead to thrombosis

  1. Endothelial Injury
  2. Hypercoagulability
  3. Abnormal blood flow
47
Q

How do stasis and turbulent blood flow contribute to thrombosis?

A

Promote endothelial activation
Platelets come into contact with endothelium
Prevent washout of clotting factors (stasis)

48
Q

Primary hypercoagulability

A

Genetic disorders such as Factor V Leiden disease

  • Arg to Glu substitution
  • Cannot be inactivated by Protein C
49
Q

Prothrombin mutation

A

3’UTR SNP that leads to increased prothrombin

50
Q

Secondary Hypercoagulability

A

Prolonged bed rest (say a flight)
MI
Disseminated Intravascular Coagulation (DIC)

51
Q

When should hypercoagulability disorders be considered in a patient?

A

Patients <50 who present with thrombosis

52
Q

Heparin-Induced Thrombocytopenia (HIT)

A

Appearance of ab’s against heparin complexes and platelet factor 4
- Ab binds to complex and inactivates it, which consumes the anti-coagulants and create a pro-thrombotic state

53
Q

A female patient presents with recurrent thromboses, miscarriages, and thrombocytopenia. What disease encompasses these presentations?

A

Antiphospholipid Antibody Syndrome

54
Q

Arterial Thrombi grow in what direction compared to venous thrombi?

A

Arterial- Retrograde
Venous- direction of blood flow
* Both are towards heart

55
Q

Lines of Zahn

A

platelet/fibrin deposits that signify thrombus has formed in flowing blood (antemortem clots)

56
Q

Mural Thrombi

A

Occur in heart chambers or aortic lumen

57
Q

Arteries primarily affected by arterial thrombi (greatest to least)

A

Coronary>Cerebral>Femoral Aa

58
Q

Vegetations

A

thrombi of heart valves that bacteria/fungi can adhere to

59
Q

4 fates of a Thrombosis

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and Recanalization
60
Q

Which vein thrombosis usually embolisms more: superficial or deep?

A

Deep (popliteal, femoral, Iliac veins)

61
Q

Disseminated Intravascular Coagulation (DIC)

A

Widespread formation of thrombi in the microcirculation

62
Q

Paradoxical Embolism

A

Embolus that enters systemic arterial circulation

63
Q

Systemic Thromboembolisms

A

Usually arise from mural thrombi, aortic aneurysms, vegetations.
- Most travel to lower extremity

64
Q

Fat Embolism

A

Release of bone marrow fat from fractured long bones that embolisms in the lung
* Diffuse petechial rash can be seen diagnostically

65
Q

Decompression Sickness

A

Rapid changes in atmospheric pressure that cause gases to become insoluble in blood and lead to embolism

66
Q

Amniotic Fluid Embolism

A

Introduction of amniotic fluid or fetal tissue into maternal circulation via a tear in placental membranes or rupture of uterine veins
Presents with sudden onset of dyspnea, cyanosis, and shock

67
Q

Infarction

A

Ischemic Necrosis caused by occlusion of either arterial supply or venous drainage

68
Q

Types of infarcts

A

Red (Hemorrhagic)
White (anemic)

Septic or bland

69
Q

White infarcts occur mainly in what type of organs/tissues

A

Organs/tissues with one blood supply and where tissue density limits pooling of blood (heart, kidney, spleen)

70
Q

Shock

A

State of diminished cardiac output or reduced effective circulation that leads to cellular hypoxia

71
Q

Cardiogenic shock

A

low CO due to pump failure

72
Q

Hypovolemic Shock

A

Low blood volume

73
Q

Septic Shock

A

triggered by gram (+) infection followed by gram (-) and fungi infection
Figure 4-20

74
Q

Factors of Septic shock

A

Everything that can go wrong does so read up page 132-133

75
Q

Stages of Shock

A
  1. Nonprogressive- compensating with reflexes (RAAS, ADH, etc)
  2. Progressive- tissue hypoperfusion, lactic acidosis
  3. Irreversible- you dead

MOD Exam 1 (5 decks)

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