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Pathophysiology > Ch. 6 & 7 (abnormalities of blood coagulation, circulatory disturbances) > Flashcards

Ch. 6 & 7 (abnormalities of blood coagulation, circulatory disturbances) Flashcards

1
Q

Hemostasis

A

Arrest of bleeding caused by activation of the blood coagulation mechanism

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2
Q

Factors contributing to hemostasis: (5)

A
  • Integrity of small blood vessels
  • Adequate numbers of platelets
  • Normal amounts of coagulation factors
  • Normal amounts of coagulation inhibitors
  • Adequate amounts of calcium ions in the blood
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3
Q

What roles do small vessels play in hemostasis (3)?

A
  • Small vessels are first line of defense in the body
  • Constrict on injury to facilitate closure by a clot
  • Exposure of underlying connective tissue of the endothelium causes platelet adhesion and activates coagulation mechanism
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4
Q

3 functions platelets play in hemostasis

A
  • PLUG defect in the vessel wall
  • Liberate vasoconstrictors and compounds causing platelets to AGGREGATE
  • Release substances that INITIATE coagulation
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5
Q

What are the three phases of blood coagulation

A

Phase I: prothrombin activator generated

Phase 2: Conversion of prothrombin into thrombin

Phase 3: Thrombin converts fibrinogen into fibrin

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6
Q

Phase 1 of blood coagulation

A

prothrombin activator generated

  • Intrinsic system
  • Extrinsic system
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7
Q

Phase 1 of blood coagulation: intrinsic system

A

components derived from blood

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8
Q

Phase 1 of blood coagulation: extrinsic system

A

tissue injury yields tissue thromboplastin

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9
Q

Phase 3 of blood coagulation: what happens?

A

Conversion of fibrinogen into fibrin by thrombin

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10
Q

blood clot

A

end stage of clotting process

Made up of an interlacing meshwork of fibrin threads with plasma, red cells, white cells, and platelets

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11
Q

coagulation inhibitors / how they regulate blood coagulation

A
  • Coagulation factors are counterbalanced by coagulation inhibitors
  • Restrict clotting process to limited area
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12
Q

antithrombin / how it regulates blood coagulation

A
  • Inhibits thrombin

- Inhibits other activated coagulation factors generated in clotting process

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13
Q

plasmin / how it regulates blood coagulation

A
  • Important control system
  • dissolves fibrin after formed
  • Fibrinolytic system activated at same time coagulation process initiated
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14
Q

What are the four classes of disturbances of blood coagulation?

A
  1. Abnormalities of small blood vessels
  2. Abnormality of platelet formation
  3. Deficiency of one or more plasma coagulation factors
  4. Liberation of thromboplastic material into circulation
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15
Q

what causes abnormalities of small blood vessels?

A
  • Abnormal bleeding resulting from failure of small blood vessels to
    contract after tissue injury
  • Abnormality of blood vessel formation
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16
Q

Thrombocytopenia

A

platelet deficiency

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17
Q

what causes thrombocytopenia (4)?

A
  1. Injury or disease of bone marrow damaging the megakaryocytes (precursors of platelets)
  2. Infiltration of bone marrow by leukemic cells or cancer cells, crowding out the megakaryocytes
  3. Antiplatelet antibodies destroy platelets in peripheral blood (autoimmune disease)
  4. Abnormal function of platelets despite normal count
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18
Q

What are petechiae and what causes them?

A
  • Small red or red-blue spots about 1-5 mm
  • Pinpoint-sized hemorrhages of small capillaries in skin or mucous membranes
  • Indicative of defective or inadequate platelets or a capillary defect
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19
Q

Petechial hemorrhages are indicative of

A

thrombocytopenia or defective platelet function

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20
Q

what are some causes of disturbances of phase 1 of blood coagulation cascade?

A

usually hereditary / rare except:

  • hemophelia (most common and best understood)
  • von Willebrand disease
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21
Q

what are some causes of disturbances of phase 2 of blood coagulation cascade?

A

deficiency of prothrombin or factors required for the conversion of prothrombin into thrombin

  • Factors produced in liver
  • Vitamin K required for synthesis of most factors
  • Vitamin K synthesized by intestinal bacteria or obtained from food
  • Bile required for its absorption
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22
Q

Hemophilia and common symptom

A

X-linked hereditary disease affecting males

hemorrhage in joints and internal organs after minor injury

A & B

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23
Q

Hemophilia A

A

classic hemophilia = Factor VIII (anti-hemophilic factor)

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24
Q

Hemophilia B

A

Christmas disease (after affected patient) = Factor IX (Christmas factor)

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25
Q

von Willebrand factor

A
  • Autosomal dominant disease
  • Large protein molecule produced by endothelial cells required for platelets to adhere to vessel wall at site of injury
  • vWF adheres to the damaged vessel wall, forms a framework that allows platelets and coagulation factors to adhere, interact, form clot
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26
Q

Disturbance of blood coagulation caused by prothrombin deficiency or related factors suggests:

A
  • Administration of anticoagulant drugs
  • inadequate synthesis of vitamin K
  • inadequate absorption of vitamin K
  • severe liver disease
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27
Q

inadequate synthesis of vitamin K occurs if…

A

the intestinal bacteria have been eradicated with prolonged use of antibiotics

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28
Q

Inadequate absorption of vitamin K occurs if…

A

there is a blockage of common bile duct by a gallstone or tumor, preventing bile from entering the intestine to promote absorption of vitamin

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29
Q

severe liver disease impairs…

A

synthesis of adequate amounts of coagulation factors

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30
Q

Administration of anticoagulant drugs inhibits

A

synthesis of biochemically active clotting factors

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31
Q

What are some causes of thromboplastin being released into the circulation? (3)

A
  1. Diseases associated with shock
  2. bacterial infections
  3. tissue necrosis
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32
Q

Disseminated intravascular coagulation syndrome

A

widespread release of thromboplastin substances throughout the body in circulation

  • Causes widespread intravascular clotting
  • Activation of fibrinolytic system
  • Clots are dissolved
  • end result = abnormal bleeding
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33
Q

pathogenesis of disseminated intravascular coagulation syndrome (DIC)

A
  • activation of clotting mechanism
  • thrombosis
  • clot lysis
  • consumption of platelets and clotting factor OR formation of fibrinogen and fibrin degradation products
  • hemorrhage
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34
Q

? What are some signs and symptoms of DIC syndrome

A
  • Bleeding, from many sites in the body
  • Blood clots
  • Bruising
  • Drop in blood pressure
  • Shortness of breath
  • Confusion, memory loss or change of behavior
  • Fever
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35
Q

What are the 3 factors involved in the pathogenesis of intravascular clotting (Virchow’s Triad)?

A
  1. Slowing or stasis of blood flow
  2. Blood vessel wall damage
  3. Increased coagulability of blood
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36
Q

Doe blood normally clot within the vascular system?

A

no

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37
Q

Thrombus

A

an intravascular clot; can occur in any vessel or within the heart; stays in one place

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38
Q

Embolus

A

a detached clot (or other material) carried into pulmonary or systemic circulation; plugs vessel of smaller caliber than diameter of clot, blocking blood flow and causing necrosis

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39
Q

Infarct

A

tissue necrosis caused by interruption in blood flow

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40
Q

What is the relationship between the following: a thrombus, an embolus, and an infarct?

A

thrombus –> embolus –> infarct

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41
Q

What are the predisposing factors for venous thromboses?

A
  • Prolonged bed rest
  • Cramped position for an extended period
  • Impaired “milking action” of leg musculature that normally promotes venous return resulting in stasis of blood in veins
  • Varicose veins or any condition preventing normal emptying of veins
  • Increased blood coagulability
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42
Q

Where do the majority of venous thromboses form?

A

The majority of thrombi form in the deep veins of the legs

Deep Venous Thrombosis (DVT)

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43
Q

What are possible outcomes of venous thromboses?

A
  • Leg swelling from partial blockage of venous return in leg

- Pulmonary embolism
Clot detaches and lodges in pulmonary artery or one of its branches

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44
Q

Pulmonary Embolism

A

clinical manifestations depend on size of embolus and where it lodges in the pulmonary artery; commonly from the leg, always coming back to the heart

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45
Q

Large pulmonary emboli characteristics

A
  • May completely block main pulmonary artery or major branches obstructing blood flow to lungs
  • Lung not infarcted due to collateral blood flow from bronchial arteries (from descending aorta) that interconnect with pulmonary arteries via collateral channels
46
Q

Large pulmonary emboli signs and symptoms

A
  • dyspnea (severe)
  • Cyanosis
  • Shock
  • Sudden death
47
Q

Small pulmonary emboli characteristics

A
  • Small emboli may pass through main pulmonary arteries, becoming impacted in peripheral arteries supplying lower lobes of the lungs
  • Inadequate collateral circulation
  • Affected lung segment undergoes necrosis; wedge-shaped pulmonary infarct
48
Q

Small pulmonary emboli signs and symptoms

A
  • Dyspnea
  • Pleuritic chest pain
  • Cough
  • Hemoptysis
49
Q

How are pulmonary emboli diagnosed? (golden standard and most common)

A
  • chest x ray
  • radioisotope lung scans
  • pulmonary angiogram (GOLD STANDARD)
  • spiral CT scan (most common)
50
Q

How are pulmonary emboli treated?

A
  • general supportive care
  • anticoagulation
  • thrombolytic drugs
  • surgery
  • PREVENTION
  • IVC filter for those with recurrent PE for prevention
51
Q

chest x ray diagnosis of pulmonary embolism

A

detects infarct but not the embolus

52
Q

radioisotope lung scans diagnosis of pulmonary embolism

A

(Ventilation/Perfusion P/Q Scan)

detects abnormal pulmonary blood flow caused by embolus

53
Q

pulmonary angiogram diagnosis of pulmonary embolism

A

(Gold Standard)
detects blocked pulmonary artery
BUT: Invasive, time consuming, expensive, rarely done

54
Q

spiral CT diagnosis of pulmonary embolism

A

detects pulmonary embolus indicated by obstructed flow of contrast medium, information comparable to pulmonary angiography without requiring insertion of catheter in pulmonary artery

Cheaper, less invasive, often used

55
Q

What is the main cause of an arterial thrombus?

A

injury to vessel wall from arteriosclerosis, causing ulceration, roughening of arterial lining with thrombi formation

56
Q

blocked flow of coronary artery causes

A

myocardial infarction

57
Q

blocked flow of major leg artery causes

A

gangrene

58
Q

blocked flow of cerebral artery causes

A

stroke

59
Q

gangrene

A

death of body tissue due to either a lack of blood flow or a serious bacterial infection (usually in extremities)

60
Q

What are causes of intracardiac thrombi?

A

anything involving the hematic stasis or the slackening of the blood flow

(e.g., acute myocardial infarction, left ventricular [LV] aneurysms, cardiomyopathies and myocarditis, valve disease and/or prosthesis, atrial fibrillation)

61
Q 
What may result from the formation of intracardiac thrombi?
Within atrial appendages: 
Surfaces of heart valves: 
Wall of left ventricle:
Left side:
Spleen/kidney/brain:
A

Within atrial appendages: heart failure or arrhythmia

Surfaces of heart valves: valve injury

Wall of left ventricle: myocardial infarction

May dislodge into systemic circulation and cause infarction: spleen, kidneys, brain

left side of heart = big problem (systemic)

62
Q

What are the factors that lead to thrombosis by increased coagulability?

A
  1. surgery or injury
  2. Estrogen in contraceptive pills
  3. Hereditary gene mutations
  4. Thrombosis in patients with cancer
63
Q

Rise in coagulation factors following surgery or injury is due to

A

release of thromboplastin

64
Q

Hereditary gene mutations that lead to thrombosis by increased coagulability

A
  • mutation of gene that codes for factor V results in abnormal factor V Leiden
  • mutation of gene regulating prothrombin syntheses
65
Q

as prothrombin level rises… risk for _____ increases

A

venous thrombosis

66
Q

abnormal factor V Leiden

A
  • caused by mutation of gene that codes for factor V

- more resistant to inactivation, prolonged activity, increased coagulability

67
Q

Thrombosis in patients with cancer by increased coagulability

A

Tumors slowly leak/release extra thromboplastic material continuously; production of coagulation factors exceeds destruction leading to hypercoagulability

68
Q

Edema

A
  • Accumulation of fluid in tissues
  • Often first noted in ankles and legs (due to gravity)
  • Results from disturbance / imbalance of extracellular fluid circulation between capillaries and interstitial fluid
69
Q

What are the factors regulating fluid flow between capillaries and interstitial tissue?

A
  1. Capillary hydrostatic pressure
  2. Capillary permeability
  3. Osmotic pressure
  4. Open lymphatic channels
70
Q

Capillary hydrostatic pressure

A

force pushing fluid from capillaries into extracellular space

71
Q

Capillary permeability

A

determines ease of fluid flow through capillary endothelium; how leaky the vessel; bigger openings in capillary walls allows more fluid to leave

72
Q

Osmotic pressure

A

water-attracting property of a solution; exerted by proteins (albumin = most popular) in the blood (colloid osmotic pressure) that attract fluid from interstitial space back into the capillaries

73
Q

Open lymphatic channels

A

collect fluid forced out of the capillaries by the hydrostatic pressure and return fluid into circulation

74
Q

Pitting edema

A

pit or indentation formed when edematous tissue is compressed with the fingertips; takes a while for the fluid to refill the area (+1 is mild, +4 is the worse)

75
Q

Pleural effusion (Hydrothorax)

A

fluid accumulates in pleural cavity

76
Q

Ascites

A

fluid accumulates in peritoneal cavity; in and amongst organs

77
Q

What are the four causes of edema?

A
  1. Increased capillary permeability
  2. Low plasma proteins
  3. Increased hydrostatic pressure
  4. Lymphatic obstruction
78
Q

Increased capillary permeability

A
  • Causes swelling of tissues with acute inflammation
79
Q

Low plasma proteins can lead to

A

Excess protein loss (kidney disease)
malnutrition
liver failure

80
Q

Increased hydrostatic pressure can cause

A
  • Heart failure (backing up of blood in venous circulation -> edema)
  • Localized venous obstruction
81
Q

Lymphatic obstruction

A

Blocks return of fluid from the interstitial space to the circulation

82
Q

Shock

A

condition in which the circulatory system is not providing enough blood to all parts of the body, causing the body’s organs to fail to function properly

ALWAYS life threatening with one exception (Neurogenic (vascular) shock)

83
Q

Categories of shock (CASH)

A

Cariogenic shock
Anaphylactic shock
Septic shock
Hypovolemic shock

84
Q

Hypovolemic shock

A

low blood volume leading to low blood pressure

causes: hemorrhage and dehydration (severe burns, vomiting/diarrhea, diuretic meds)

85
Q

Cardiogenic shock and 3 causes

A

inadequate cardiac output of blood by the heart when it fails to pump effectively

causes:
1. myocardial infarction
2. pericardial effusion
3. valvular disease

86
Q

Septic shock

A

excessive vasodilatation secondary to release of microbial toxins and inflammatory mediators (infection)

87
Q

Anaphylactic shock

A

excessive vasodilatation from release of inflammatory mediators due to severe allergic reaction

88
Q

Neurogenic (vascular) shock

A

massive parasympathetic output –> dilation of vessels –> unconsciousness –> fall –> when horizontal the person wakes back up

(ex. passing out when getting blood drawn)

89
Q

Signs and symptoms of shock

A
  • Skin is cool, clammy, and pale
  • Weakness, dizziness, thirst, or nausea
  • Breathing may be shallow and rapid
  • Pulse is weak and rapid (thready pulse)
  • BP is low
  • Lips and fingernail beds may be cyanotic
  • Pt may be confused or suddenly become unconscious
90
Q

Prognosis of shock

A

depends on early recognition and rapid appropriate treatment

  • Drugs that promote vasoconstriction
  • Use of intravenous fluids or blood to restore blood volume secondary to fluid loss or hemorrhage (breaking death spiral until you find out the real problem)
  • Treat underlying cause
91
Q

low blood plasma leads to

A

kidney disease
malnutrition / liver disease
edema

92
Q

most serious consequence of deep vein thrombosis DVT

A

pulmonary embolism

93
Q

May completely block main pulmonary artery of major branches obstructing blood flow to lungs:

  1. Deep Venous Thrombosis (DVT)
  2. Large Pulmonary Embolism
  3. Small Pulmonary Embolism
  4. Arterial Thrombosis
  5. Intracardiac Thrombosis
A
  1. Large Pulmonary Embolism
94
Q

Injury to vessel wall from arteriosclerosis, causing ulceration, roughening of arterial lining with thrombi formation

  1. Deep Venous Thrombosis (DVT)
  2. Large Pulmonary Embolism
  3. Small Pulmonary Embolism
  4. Arterial Thrombosis
  5. Intracardiac Thrombosis
A
  1. Arterial Thrombosis
95
Q

The majority of thrombi

  1. Deep Venous Thrombosis (DVT)
  2. Large Pulmonary Embolism
  3. Small Pulmonary Embolism
  4. Arterial Thrombosis
  5. Intracardiac Thrombosis
A
  1. Deep Venous Thrombosis (DVT)
96
Q

Clot forms inside chambers of the heart

  1. Deep Venous Thrombosis (DVT)
  2. Large Pulmonary Embolism
  3. Small Pulmonary Embolism
  4. Arterial Thrombosis
  5. Intracardiac Thrombosis
A
  1. Intracardiac Thrombosis
97
Q

May pass through main pulmonary arteries, becoming impacted in peripheral arteries supplying lower lobes of the lungs

  1. Deep Venous Thrombosis (DVT)
  2. Large Pulmonary Embolism
  3. Small Pulmonary Embolism
  4. Arterial Thrombosis
  5. Intracardiac Thrombosis
A
  1. Small Pulmonary Embolism
98
Q

Low blood volume leading to low blood pressure

  1. Anaphylactic Shock
  2. Cardiogenic Shock
  3. Hypovolemic Shock
  4. Neurogenic Shock
  5. Septic Shock
A
  1. Hypovolemic Shock
99
Q

Excessive vasodilation from release of inflammatory mediators due to severe allergic reaction

  1. Anaphylactic Shock
  2. Cardiogenic Shock
  3. Hypovolemic Shock
  4. Neurogenic Shock
  5. Septic Shock
A
  1. Anaphylactic Shock
100
Q

Excessive vasodilation secondary to release of microbial toxins and inflammatory mediators

  1. Anaphylactic Shock
  2. Cardiogenic Shock
  3. Hypovolemic Shock
  4. Neurogenic Shock
  5. Septic Shock
A
  1. Septic Shock
101
Q

Inadequate cardiac output of blood by the heart when it fails to pump effectively

  1. Anaphylactic Shock
  2. Cardiogenic Shock
  3. Hypovolemic Shock
  4. Neurogenic Shock
  5. Septic Shock
A
  1. Cardiogenic Shock
102
Q

Only non life-threatening type of shock

  1. Anaphylactic Shock
  2. Cardiogenic Shock
  3. Hypovolemic Shock
  4. Neurogenic Shock
  5. Septic Shock
A
  1. Neurogenic Shock
103
Q

A patient presents with a regular rhythm & a heart rate of less than 60 bpm.

  • What is would this be noted in a chart as?
  • Should the physicians be concerned with this patient?
A

Sinus bradycardia

No - sinus is good

A normal sinus rhythm is an ECG w/in normal limits w/ a HR b/w 60-100bpm
Sinus bradycardia is a HR that is slightly below normal but is still considered okay - this may be common in athletes or runners

104
Q

Causes include lack of sleep, caffeine, nicotine, alcohol, & anxiety/stress & is one of the most common but least harmful.

Atrial Fibrillation (A-fib)
Cardiac Arrest
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation (V-fib)
Ventricular Tachycardia (V-tach)
A

Premature Ventricular Contractions (PVCs)

105
Q

Rapid & uncoordinated ventricular beat & is totally ineffective for pumping blood & will quickly lead to death if not corrected.

Atrial Fibrillation (A-fib)
Cardiac Arrest
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation (V-fib)
Ventricular Tachycardia (V-tach)
A

Ventricular Fibrillation (V-fib)

106
Q

Seen in patients with cardiac disease & is characterized 3 or more PVCs.

Atrial Fibrillation (A-fib)
Cardiac Arrest
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation (V-fib)
Ventricular Tachycardia (V-tach)
A

Ventricular Tachycardia (V-tach)

107
Q

Typically seen in older adults with multiple areas of depolarization & only some of the impulses reach the ventricles.

Atrial Fibrillation (A-fib)
Cardiac Arrest
Premature Ventricular Contractions (PVCs)
Ventricular Fibrillation (V-fib)
Ventricular Tachycardia (V-tach)
A

Atrial Fibrillation (A-fib)

108
Q

What is the disease that impairs the passage of blood from the left atrium to the left ventricle? cause of disease?

A

Mitral stenosis
(Mitral valve is not able to fully open)
cause: rheumatic heart disease

109
Q

What is infective endocarditis? difference between subacute and acute?

A

When the heart valve becomes infected w/ vegetations which are a build up of large, easily fragmented infective masses

subacute: only affects damaged valves
acute: affects normal heart valves

110
Q

Put in ascending (correct) order:

  1. Formation of an atheroma
  2. Initial endothelial injury
  3. Macrophages invade the area
  4. Cholesterol precipitates as crystals causing necrosis.
  5. Unstable plaques formed
A
  1. Initial endothelial injury
  2. Macrophages invade the area
  3. Unstable plaques formed (due to lipid invasion of cytoplasm)
  4. Cholesterol precipitates as crystals causing necrosis
  5. Formation of an atheroma
111
Q

What are the six complications of a myocardial infarction?

A
  1. Arrhythmias
  2. Heart failure
  3. Intracardiac thrombi
  4. Papillary muscle dysfunction
  5. Cardiac rupture
  6. Ventricular aneurysm
112
Q

does blood clot within the vascular system?

A

not normally

Pathophysiology (3 decks)

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