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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
d-granules of platelets
contain ADP, ATP, Ca, Serotonin, and epinephrine
26
How does Aspirin cause a mild bleeding defect?
Inhibits platelet aggregation by inhibiting cyclooxygenase which reduces TxA2 production
27
Glanzmann Thrombasthenia
Defect in GpIIb-IIIa leads to decreased binding of platelets to fibrinogen.
28
Define the Intrinsic Pathway of clotting
XII--> XI--> IX + VIII--> X + V --> Thrombin--> Fibrin
29
Define the Extrinsic Pathway of clotting
VII--> VII + TF--> IX--> X + V--> Thrombin--> Fibrin + XI * Factor XI then activates Factor IX Figure 4-6
30
What role to platelets play in the clotting cascade?
Provide negatively charged phospholipid surface for the assembly of coagulation factors
31
What factors are affected by Vit K antagonists?
II, VII, IX, and X | Protein C and S
32
Prothrombin Time
assesses the extrinsic pathway of coagulation | Factors II, V, VII, X, Fibrinogen
33
Partial thromboplastin time
Assesses intrinsic pathway | Factors II, V, VIII, IX, X, XI, XII, Fibrinogen
34
Factor XII deficiency
susceptibility to thrombosis
35
Which factors are implicated in moderate to severe bleeding disorders?
V, VII, VIII, IX, X
36
Thrombin functions
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
Plasmin
Most important enzyme of fibrolysis | Breaks down fibrin
38
t-PA
tissue plasminogen activator- activates plasmin to break down clots *Important for stroke patients within 6 hours of onset
39
What regulates plasmin activity?
a2-plasmin inhibitor
40
Endothelium factors that are antithrombotic towards platelets
1. PGI2 2. NO 3. ADPase
41
Antithrombotic factors produced by endothelium that interfere with coagulation
Thrombomodulin Protein C Receptor heparin-like molecules tissue factor pathway inhibitor
42
Protein C/S complex
inhibits Factors V and VIII
43
Heparin-like molecules
bind and activate antithrombin III | Complex inhibits thrombin and Factors IX-XII
44
Primary hemostasis bleeding disorders
vWF disease - causes small bleeds in skin or mucus membranes - presents with petechiae and/or purpura
45
Secondary hemostasis bleeding disorders
Coag factor deficiencies | - bleeding into soft tissues and joints (hemarthrosis)
46
Virchow's Triad
Primary abnormalities that lead to thrombosis 1. Endothelial Injury 2. Hypercoagulability 3. Abnormal blood flow
47
How do stasis and turbulent blood flow contribute to thrombosis?
Promote endothelial activation Platelets come into contact with endothelium Prevent washout of clotting factors (stasis)
48
Primary hypercoagulability
Genetic disorders such as Factor V Leiden disease - Arg to Glu substitution - Cannot be inactivated by Protein C
49
Prothrombin mutation
3'UTR SNP that leads to increased prothrombin
50
Secondary Hypercoagulability
Prolonged bed rest (say a flight) MI Disseminated Intravascular Coagulation (DIC)
51
When should hypercoagulability disorders be considered in a patient?
Patients <50 who present with thrombosis
52
Heparin-Induced Thrombocytopenia (HIT)
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
A female patient presents with recurrent thromboses, miscarriages, and thrombocytopenia. What disease encompasses these presentations?
Antiphospholipid Antibody Syndrome
54
Arterial Thrombi grow in what direction compared to venous thrombi?
Arterial- Retrograde Venous- direction of blood flow * Both are towards heart
55
Lines of Zahn
platelet/fibrin deposits that signify thrombus has formed in flowing blood (antemortem clots)
56
Mural Thrombi
Occur in heart chambers or aortic lumen
57
Arteries primarily affected by arterial thrombi (greatest to least)
Coronary>Cerebral>Femoral Aa
58
Vegetations
thrombi of heart valves that bacteria/fungi can adhere to
59
4 fates of a Thrombosis
1. Propagation 2. Embolization 3. Dissolution 4. Organization and Recanalization
60
Which vein thrombosis usually embolisms more: superficial or deep?
Deep (popliteal, femoral, Iliac veins)
61
Disseminated Intravascular Coagulation (DIC)
Widespread formation of thrombi in the microcirculation
62
Paradoxical Embolism
Embolus that enters systemic arterial circulation
63
Systemic Thromboembolisms
Usually arise from mural thrombi, aortic aneurysms, vegetations. - Most travel to lower extremity
64
Fat Embolism
Release of bone marrow fat from fractured long bones that embolisms in the lung * Diffuse petechial rash can be seen diagnostically
65
Decompression Sickness
Rapid changes in atmospheric pressure that cause gases to become insoluble in blood and lead to embolism
66
Amniotic Fluid Embolism
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
Infarction
Ischemic Necrosis caused by occlusion of either arterial supply or venous drainage
68
Types of infarcts
Red (Hemorrhagic) White (anemic) Septic or bland
69
White infarcts occur mainly in what type of organs/tissues
Organs/tissues with one blood supply and where tissue density limits pooling of blood (heart, kidney, spleen)
70
Shock
State of diminished cardiac output or reduced effective circulation that leads to cellular hypoxia
71
Cardiogenic shock
low CO due to pump failure
72
Hypovolemic Shock
Low blood volume
73
Septic Shock
triggered by gram (+) infection followed by gram (-) and fungi infection Figure 4-20
74
Factors of Septic shock
Everything that can go wrong does so read up page 132-133
75
Stages of Shock
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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