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M3 Path Block 2 > 7 - Hemodynamics (1st Half) > Flashcards

7 - Hemodynamics (1st Half) Flashcards

1
Q

Normal Homeostasis of Blood (4)

A

Integrity of vessel, hydrostatic pressure, colloidal osmotic presure, blood as a fluid

Fluid exits vessel because of hydrostatic pressure (e.g. blood pressure) pushing it out

Fluid returns to vessel because of oncotic (osmotic) pressure pulling it back in

At the capillary level, the pushing forces are about equal to the pulling forces

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2
Q

Events due to failure of homeostasis (6)

A

Interstitial water accumulation (edema)

Clotting at inappropriate sites (thrombosis)

Migration of clots (embolism)

Blood flow obstruction to tissues –> cell death (infarction)

Inability to clot after vascular injury (hemorrhage)

Extensive hemorrhage –> hypotension (shock)

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3
Q

Edema (2)

A

Increased accumulation of fluid in interstitial space

Generalized edema is known as anasarca

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4
Q

Edema: Transudate (4)

A

Noninflammatory

Low protein

Low SG: <1.020

E.g. CHF, renal disorder, malnutrition

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5
Q

Edema: Exudate (Pus) (4)

A

Inflammatory

High protein

High SG: >1.020

E.g. DIC

Inflammatory edema by acute inflammation caused with help of: histamine, PAF, C3a and C5a, and leukotrienes

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6
Q

Possibilities of Edema (4)

A

Increased hydrostatic pressure

Reduced oncotic pressure

Lymphatic obstruction

Sodium/Water Retention (where sodium goes, fluid goes)

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7
Q

Increased hydrostatic pressure problems (5)

A
  1. CHF
  2. Ascites
  3. Pericarditis
  4. Venous Thrombosis
  5. Lower limb inactivity
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8
Q

Problems with reduced plasma oncotic pressure (4)

A
  1. Nephrotic syndrome
  2. Protein losing enteropathy
  3. Malnutrition
  4. Liver cirrhosis
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9
Q

Lymphatic obstruction

A
  1. Inflammatory
  2. Neoplastic
  3. Postsurgical
  4. Irradiation
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10
Q

Sodium retention (3)

A

High salt intake

Increased renin-angiotensin mechanism

Reduced renal perfusion

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11
Q

Term for cardiac edema and cause

A

Pulmonary edema

Cause: L/R heart failure due to various reasons

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12
Q

Term for renal edema and cause

A

Associated with Nephrotic syndrome

Cause: trauma, infections, anasarca

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13
Q

Term for brain edema and cause

A

Cerebral edema

Cause: Trauma, infections, tumors

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14
Q

Features of lymphatic obstruction and cause

A

Peu-d’-orange appearance of breast in breast carcinoma

Cause: Filiariasis, any surgical procedures that impede the lymphatic channels, including radiation

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15
Q

Hyperemia and Congestion

A

Increased blood volumes within tissues, but have DIFFERENT underlying MECHANISMS and CONSEQUENCES

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16
Q

Hyperemia (5)

A

Def: Increased blood volume within tissue

Active process

Arteriolar dilatation

Red in color

E.g. skeletal muscle exercise or inflammation

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17
Q

Congestion (5)

A

Increased blood volume within tissue

Passive process

Reduced outflow from tissue

Dusky red in color

E.g. chronic venous congestion of lung, liver

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18
Q

Venous congestion of Lung: Chronic (3)

A

Septa are thickened and fibrotic

Lumen contains hemosidern laden macrophages called ‘heart failure cells’

Changes in chronic venous congestion of lung also known as brown induration of the lungs

19
Q

Venous Congestion of Liver: Chronic (2)

A

Red brown, slightly depressed area with accentuated uncongested area - ‘nutmeg area’

Hepatocyte necrosis

CHF

20
Q

Hemostasis

A

An orchestrated process involving platelets, clotting factors, and endothelium

Occurs at the site of vascular injury and culminates in the formation of a clot to prevent or limit the bleeding

21
Q

Blood is always in a homeostasis between, and just like bone always is?

A

Hemostasis and thrombosis. Just like bone always is between ossification and resorption.

22
Q

Hemostatic sequence at the injured vessel: Primary hemostasis (steps) (5)

A
  1. Arteriolar vasoconstriction: Neurogenic, endothelin
  2. Primary hemostasis: formation of platelet plug
  3. von Willebrand fact (vWF) and collagen binds to subendothelial collagen
    • vWf is glue between platelets and exposed ECM
  4. Activation of platelets + release of secretory granules
  5. Platelet aggregation to form a primary hemostatic plug
23
Q

Hemostatic sequence at the injured vessel: Secondary Hemostasis (steps) (4)

A
  1. Tissue factor binds and activates factor VII
  2. Activation of coagulation cascade
  3. Formation of fibrin meshwork
  4. Clot stabilization and resolution
24
Q

Role of endothelial cells: Antithrombotic Properties (4)

A

Antiplatelet effects: prostacyclin (PGI2) and nitric oxide, adenosine, diphosphatase

Thrombomodulin is tissue factor pathway inhibitor

Protein C and protein S inhibit factors Va and VIIIa

Fibrinolytic effects: t-PA

25
Q

Role of endothelial cells: Pro-thrombotic properties (3)

A

Platelet effects: von Willebrand factor (vWF)

Procoagulant effects: tissue factor

Antifibrinolytic effects: inhibitors of plasminogen activator (PAIs)

26
Q

Platelet release (4)

A

Thromboxane A2

ADP

vWF and other clotting factors

Platelet derived growth factor

27
Q

Platelet aggregation (4)

A

Thromboxane A2 and ADP set up autocatalytic reaction

ADP causes platelet aggregation and change in GpIIb-IIIa configuration for fibrinogen bridging

GP1B deficiency = bernard soulier

GP2B deficiency –> Glanzmann’s thrombasthenia

28
Q

Thrombin Functions: Conversion of fibrinogen to fibrin

A

Activates factors V, VII, XI, XIII

29
Q

Thrombin Functions: Platelet activation

A

By activating platelet activating receptor (PAR)

30
Q

Thrombin Functions: Pro-inflammatory effects

A

PAR’s expressed on neutrophils and lymphocytes that helps in tissue repair and angiogenesis

31
Q

Thrombin Functions: Anticoagulant effects

A

Thrombin stimulates production of tissue repair and angiogenesis

32
Q

Lab: Prothrombin Time (PT)

A

Measures extrinsic pathway (7)

10-15 seconds

33
Q

Lab: Partial Thromboplastin Time (PTT)

A

Measures only intrinsic pathway

25-30 seconds

34
Q

Fibrinolytic Cascade (3)

A

Moderates the size of the ultimate clot

Accomplished through the enzymatic activity of plasmin

Plasmin breaks down fibrin

35
Q

Fibrinolytic Substances (3)

A

Tissue plasminogen activator - most important plasminogen activator. Plasminogen becomes plasmin and than induces FIBRINOLYSIS

Urokinase-like PA (u-PA)

Streptokinase

36
Q

Fibrinolytic Substances: Regulation of plasmin activity (2)

A

alpha 2 - plasmin inhibitor

Plasminogen activator inhibitor (PAI)

37
Q

Hemorrhagic Disorders: Hemostasis (assoicated with bleeding) (3)

A

Defect in vessel wall

Platelets

Coagulation factors

38
Q

Hemorrhagic Disorders: Sudden massive bleeding disorders

A

Aortic dissection in Marfan’s syndrome

39
Q

Hemorrhagic Disorders: Mild bleeding disorders (2)

A

von Willebrand’s Disease: epistaxis, surgical bleedings, menstruation

Coagulation factor deficiencies

40
Q

Defects of primary hemostasis (8)

A
  1. Platelet of VWD
  2. Small bleeds in skin and mucous membranes
  3. Petechiae (1-3 mm) - pinpoint hemorrhages under skin
  4. Purpura (3 mm)
  5. Bleeding in mucus membranes
  6. Menorrhagia
  7. Epistaxis
  8. Intracranial and GI bleeding
41
Q

Defects of secondary hemostasis (4)

A

Coagulation factor deficiencies

Bleeding into soft tissues and joints

Hemarthrosis - bleeding into soft tissues and joints

Intracranial hemorrhage

42
Q

Generalized defects involve blood vessels (4)

A

Ecchymosis –> large palpable masses (> 3 mm)

Palpable purpura

Hematoma

Vasculitidis

43
Q

Thombosis: 3 parts

A

Endothelial injury: can lead to abnormal blood flow

Stasis of turbulent blood flow

Hypercoagulability of the blood

M3 Path Block 2 (10 decks)

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