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Histopathology and Cytologic Techniques (Lecture) > Circulatory and Hemodynamic Disorders (M) > Flashcards

Circulatory and Hemodynamic Disorders (M) Flashcards

1
Q

True or False

Capillary hydrostatic and osmotic forces are normally balanced so that there is no net loss or gain of fluid across the capillary bed

A

True

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2
Q

What will cause extravascular fluid to accumulate?

A

Increased hydrostatic pressure / diminished plasma oncotic pressure

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3
Q

What is the action of tissue lymphatics and what is its mechanism?

A

To remove much of the excess volume, eventually returning it to the circulation via the thoracic duct

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4
Q

What is the result if the capacity for lymphatic drainage is exceeded?

A

It results to tissue edema

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5
Q

What are the components (/ formula) for BP?

A

BP = CO X TPR

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6
Q

What is the meaning of BP?

A

Blood pressure

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7
Q

What is the meaning of CO?

A

Cardiac output

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8
Q

What is the meaning of TPR?

A

Total peripheral resistance

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9
Q

What are the components (/ formula) of CO?

A

CO = BV X HR

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10
Q

What is the meaning of BV?

A

Blood volume

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11
Q

What is the meaning of HR?

A

Heart rate

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12
Q

What is present in the arterial end in the capillary bed that results to edema?

A

Increased hydrostatic pressure

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13
Q

What is present in the venous end in the capillary bed that results to edema?

A

Decreased plasma colloid osmotic pressure

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14
Q

What are the pathophysiologic categories (/ causes) of edema?

A

1) Increased hydrostatic pressure
2) Reduced plasma oncotic pressure (w/c results to hypoproteinemia)
3) Lymphatic obstruction
4) Sodium retention
5) Inflammation

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15
Q

What are the causes of increased hydrostatic pressure?

A

1) Impaired venous return
2) Congestive heart failure
3) Constrictive pericarditis
4) Ascites (liver cirrhosis)
5) Venous obstruction or compression
a. Thrombosis
b. External pressure (ex. mass)
c. Lower extremity inactivity w/ prolonged dependency
6) Arteriolar dilation
a. Heat
b. Neurohumoral dysregulation

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16
Q

What are the causes of reduced plasma osmotic pressure?

A

1) Protein-losing glomerulopathies (nephrotic syndrome)
2) Liver cirrhosis (ascites)
3) Malnutrition
4) Protein-losing gastroenteropathy

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17
Q

What are the causes of lymphatic obstruction?

A

1) Inflammatory
2) Neoplastic
3) Postsurgical
4) Postirradiation

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18
Q

What are the causes of Na retention?

A

1) Excessive salt intake w/ renal insufficiency
2) Increased tubular reabsorption of Na
a. Renal hypoperfusion
b. Increased renin-angiotensin-aldosterone secretion

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19
Q

What are the causes of inflammation?

A

1) Acute inflammation
2) Chronic inflammation
3) Angiogenesis

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20
Q

How (/ what is the pathway) can elderly pts w/ cardiac conditions (in the bg of heart and renal failure) have edema?

A

Heart failure -> a. increased capillary hydrostatic pressure & b. decreased renal flow -> b. leads to activation of the renin-angiotensin system -> retention of Na^(+) and H2O whereas renal failure occurs -> increased blood volume -> then a. and b. leads to edema

Malnutrition, decreased hepatic synthesis, and nephrotic syndrome -> decreased plasma albumin -> decreased plasma osmotic pressure -> leading to edema

Pathways leading to systemic edema from primary heart failure, primary renal failure, / reduced plasma osmotic pressure (ex. from malnutrition, diminished hepatic synthesis, / protein loss from nephrotic syndrome)

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21
Q

What should be done in pleural fluid analysis (whereas pleural effusion in CHF is used)?

A

1) Identify if the fluid is a transudate / exudate (transudative / exudative)
2) To identify if the fluid is a transudate / exudate, identify the protein and glucose lvls of the pt
3) Identify if there’s presence of inflammatory cells and/or malignant cells
4) Identify if there’s presence of infectious microorganisms

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22
Q

What is the meaning of CHF?

A

Congestive heart failure

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23
Q

In pleural fluid analysis, the sx is placed in how many containers?

A

4

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24
Q

The sx (for pleural fluid analysis) present in 4 containers are for what tests?

A

1st: for clinical microscopy
2nd: for qualitative analysis (clinical chemistry)
3rd: for microbiologic studies
4th: for cytology

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25
Q

What is the difference between transudate and exudate in terms of the ff:

1) Appearance
2) Pleural fluid:serum protein
3) Pleural fluid:serum LD
4) Pleural fluid:serum bili
5) Pleural fluid chole
6) Pleural fluid:serum chole
7) Cell cts (WBC)

A

Transudate

1) Clear, pale yellow
2) < 0.5
3) < 0.6
4) < 0.6
5) < 60 mg/dL
6) < 0.3
7) < 1,000/uL

Exudate

1) Cloudy, turbid, purulent, or bloody
2) 0.5 >
3) 0.6 >
4) 0.6 >
5) 60 mg/dL >
6) 0.3 >
7) 1,000/uL >

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26
Q

What is the fxn of von Willebrand factor (VWF)?

A

It fxns as an adhesion bridge between subendothelial collagen and the glycoprotein Ib (GpIb) PLT receptor

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27
Q

How is aggregation accomplished?

A

It is accomplished by fibrinogen bridging GpIIb-IIIa receptors on diff PLTs

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28
Q

Congenital deficiencies in the various receptors or bridging molecules lead to what?

A

It leads to the diseases indicated in the colored boxes

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29
Q

What is the meaning of ADP?

A

Adenosine diphosphate

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30
Q

How can the coagulation pathway be assessed?

A

1) Prothrombin time (PT)

2) Partial thromboplastin time (PTT) (/ activated partial thromboplastin time / APTT)

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31
Q

What is the fxn of PT?

A

It assesses the fxn of the proteins in the extrinsic pathway

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32
Q

What are the proteins (/ clotting factors) present in the extrinsic pathway?

A

Factors:

1) VII
2) X
3) II
4) V
5) I (fibrinogen)

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33
Q

How is PT accomplished / done?

A

It is accomplished by adding tissue factor (TF) and phospholipids to citrated plasma

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34
Q

What are the fxns of Na citrate?

A

1) It chelates Ca

2) It prevents spontaneous clotting

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35
Q

Coagulation in PT is initiated by what?

A

It is initiated by the addition of exogenous Ca and the time for a fibrin clot to form is recorded

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36
Q

What is the fxn of PTT?

A

It screens for the fxn of the proteins in the intrinsic pathway

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37
Q

What are the clotting factors present in intrinsic pathway?

A

Factors:

1) XII
2) XI
3) IX
4) VIII
5) X
6) V
7) II
8) I (fibrinogen)

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38
Q

How is clotting initiated in PTT?

A

It is initiated through the addition of (-) charged particles

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39
Q

What are the exs of (-) charged particles that are added to initiate clotting in PTT?

A

1) Ground glass

2) Beads

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40
Q

What are the fxns of (-) charged particles (that are added in PTT)?

A

Activates:

1) Factor XII (Hageman factor)
2) Phospholipids
3) Ca

The time to fibrin clot formation is recorded

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41
Q

What are the roles of thrombin?

A

1) It can activate monocyte
2) It can activate lymphocyte
3) For endothelial activation to produce NO, PGI2, and tPA
4) It can promote PLT aggregation
5) It can present a fxn in PLT plug formation and fibrin clot formation
6) For neutrophil adhesion

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42
Q

What are present in the fibrinolytic system?

A

Various:

1) Plasminogen activators; and
2) Inhibitors

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43
Q

What is thrombosis?

A

It is an inappropriate activation of normal hemostatic process

It is an area of attachment to underlying vessel / heart wall

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44
Q

The presence of thrombosis results to what?

A

It results to the formation of a blood clot (thrombus) in an uninjured vasculature / occlusion of a vessel after a relatively minor injury

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45
Q

What are the factors that bring about thrombosis?

A

Virchow’s triad

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46
Q

What are the components of Virchow’s triad?

A

1) Endothelial injury
2) Stasis / turbulence of blood flow (/ abnormal blood flow)
3) Blood hypercoagulability

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47
Q

What are the causes of hypercoagulable states?

A

1) Primary (genetic)
a. Common
b. Rare
c. Very rare
2) Secondary (acquired)
a. High risk for thrombosis
b. Lower risk for thrombosisWa

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47
Q

What are the conditions / disorders hypercoagulable states are present?

A

1) Primary (genetic)
a. Common
b. Rare
c. Very rare
2) Secondary (acquired)
a. High risk for thrombosis
b. Lower risk for thrombosis

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48
Q

What are the common primary (genetic) conditions / disorders where hypercoagulable states are present?

A

1) Factor V mutation (G1691A mutation; factor V Leiden)
2) PT mutation (G20210A variant)
3) 5, 10-Methylenetetrahydrofolate reductase (homozygous C677T mutation)
4) Increased lvls of factors VIII, IX, XI, / fibrinogen

49
Q

What are the rare primary (genetic) conditions / disorders where hypercoagulable states are present?

A

1) Antithrombin III deficiency
2) Protein C deficiency
3) Protein S deficiency

50
Q

What are the very rare primary (genetic) conditions / disorders where hypercoagulable states are present?

A

1) Fibrinolysis defects

2) Homozygous homocystinuria (deficiency of cystathione β-synthetase)

51
Q

What are the conditions / disorders that are whereas high risk for thrombosis is present w/c are secondary (acquired)?

A

1) Prolonged bedrest / immobilization
2) Atrial fibrillation
3) Cancer
4) Heparin-induced thrombocytopenia
5) Tissue injury (surgery, fracture, burn)
6) MI
7) DIC
8) Prosthetic cardiac valves
9) APAS

52
Q

What are the conditions / disorders that are whereas lower risk for thrombosis is present w/c are secondary (acquired)?

A

1) Nephrotic syndrome
2) Sickle cell anemia
3) Hyperestrogenic states (pregnancy and postpartum)
4) Cardiomyopathy
5) Oral contraceptive use
6) Smoking

53
Q

What is the characteristic of all thromboses?

A

All are firmest at the point of origin

54
Q

What are the fates of thrombus?

A

1) Propagation
2) Dissolution
3) Organization / Recanalization
4) Embolization

55
Q

What is the meaning of DIC?

A

Disseminated Intravascular Coagulopathy

56
Q

What is DIC?

A

It is the sudden / insidious onset of widespread fibrin thrombi in the microcirculation

57
Q

What are the characteristics of DIC?

A

1) It is not grossly visible
2) These are readily apparent microscopically
3) It can cause diffuse circulatory insufficiency, particularly in the brain, lungs, heart, and kidneys

58
Q

The widespread microvascular thrombosis results in what?

A

PLT and coagulation protein consumption (hence the synonym consumption coagulopathy), and at the same time, fibrinolytic mechanisms are activated

59
Q

True or False

It should be emphasized that DIC is not a primary disease but rather a potential complication of any condition associated w/ widespread activation of thrombin

A

True

60
Q

What is an embolus (how does embolism occur)?

A

It is a detached intravascular solid, liquid, / gaseous mass that is carried by the blood to a site distant from its point of origin

61
Q

The diff types of embolism depends on what?

A

These depends on the nature of the emboli

62
Q

What are the diff types of embolism?

A

1) Fat embolism
2) Bone marrow embolism
3) Air (nitrogen) embolism
4) Amniotic fluid embolism
5) Tumor embolism
6) Foreign bodies (bullets) embolism
7) Thromboembolism

63
Q

True or False

All emboli represent part of a dislodged thrombus, hence the term thromboembolism

A

False, because almost all emboli represent part of a dislodged thrombus, hence the term thromboembolism

64
Q

True or False

Unless otherwise specified, an embolism should be considered to be thrombotic in origin

A

True

65
Q

What is pulmonary thromboembolism?

A

These are blood clots that occlude large pulmonary arteries

66
Q

What is the characteristic of pulmonary thromboembolism?

A

These are almost always embolic in origin

67
Q

What are the characteristics of in-situ thromboses?

A

1) These are rare

2) These develop only in the presence of pulmonary hypertension, pulmonary atherosclerosis, and heart failure

68
Q

Where is pulmonary thromboembolism usually present?

A

In deep leg veins

69
Q

What are the exs of deep leg veins where pulmonary thromboembolism is usually present?

A

1) Iliac veins
2) Femoral veins
3) Popliteal veins

70
Q

What is the percentage of occurrence of pulmonary thromboembolism in deep leg veins?

A

95% > of the cases

71
Q

The remaining 5% of the cases of pulmonary thromboembolism occurs where?

A

1) Pelvic veins
2) Vena cava
3) Right atrium
4) Tricuspid and pulmonary valves
5) Left ventricle

72
Q

What are the clinical presentations (/ clinical manifestations) of pulmonary thromboembolism (PTE)?

A

1) Massive pulmonary thromboembolism
2) Acute embolism w/out infarction
3) Acute pulmonary infarction
4) Multiple (small vessel) PTE

73
Q

The morphological classification and consequences of PTE depend on what?

A

1) Size of the embolic mass

2) General state of the circulation (large, medium, and small)

74
Q

What is saddle embolus?

A

It is a large thromboemboli involving the pulmonary bifurcation

75
Q

*At what state of pt does acute pulmonary infarction occur? (slide 42)

A

In pts w/ inadequate cardiovascular fxn

76
Q

*Thromboembolism affects what sites?

A

Multiple (small vessel)

77
Q

*If 60% > is obstructed, pts may present what condition / disorder?

A

Pulmonary hypertension (HPN) / Cor Pulmonale

78
Q

What is systemic thromboembolism?

A

It is the emboli present in the arterial circulation

79
Q

Systemic thromboembolism arises from where (/ what sites)?

A

From:

  • 1) Intracardiac mural thrombi (80% of cases)
    2) Aortic aneurysms
    3) Thrombi on ulcerated atherosclerotic plaques
    4) Fragmentation of a valvular vegetation w/ a small fraction due to paradoxical emboli
    5) 10 - 15% are of unknown origin
80
Q

What is the difference (/ comparison) between venous emboli and arterial emboli?

A

Venous emboli: tend to lodge in 1 vascular bed (the lung)

Arterial emboli: can travel to a wide variety of tissues

81
Q

The point of arrest for systemic thromboembolism depends on what?

A

Depends on the source and the relative amt of blood flow that downstream tissues receive

82
Q

What are the major sites for arterial embolization?

A

1) Lower extremities (75%)
2) Brain (10%)
3) Intestines, kidneys, spleen, and upper extremities involved to a lesser extent

83
Q

The consequences of embolization in a tissue depends on what?

A

1) Its vulnerability to ischemia
2) The caliber of the occluded vessel
3) Whether there is a collateral blood supply

84
Q

In general, arterial emboli causes what?

A

It causes infarction of the affected tissues

85
Q

What is arteriosclerosis?

A

It literally means the “hardening of the arteries”

86
Q

What are the general clinical presentations (/ clinical manifestation) of arteriosclerosis?

A

1) Arterial wall thickening

2) Loss of elasticity

87
Q

What is arteriolosclerosis?

A

It affects small arteries and arterioles

88
Q

Arteriolosclerosis may cause what?

A

Downstream ischemic injury

89
Q

Atherosclerosis came from what Greek root words?

A

1) “gruel”

2) “hardening”

90
Q

*What is atherosclerosis?

A

It is the most frequent and clinically impt…

91
Q

*What is the mechanism of the pathogenesis of atherosclerosis?

A

“Response-to-injury hypothesis”

92
Q

What is the pathogenesis of atherosclerosis?

A

1) Views atherosclerosis as a chronic inflammatory and healing response of the arterial wall to endothelial injury
2) Lesion progression occurs through the interaction of modified lipoproteins, monocyte-derived macrophages, and T lymphocytes w/ the normal cellular constituents of the arterial wall

93
Q

*What is the process (/ steps) of evolution of arterial wall changes in the response to injury hypothesis?

A

1) Normal
2) Endothelial injury w/ adhesion of monocytes and PLTs (the latter to sites where endothelium has been lost)
3) Migration of monocytes and smooth muscle into the intima
4) Smooth muscle cell proliferation in the intima w/ ECM production
5) Well-developed plaque

94
Q

What is the characteristic of atherosclerosis?

A

It is characterized as by having intimal lesions called atheromas

95
Q

Atheromas is also called as what?

A

Atheromatous / atherosclerotic plaques

96
Q

What is the component of atheromatous plaque?

A

It consists of a raised lesion w/ a soft, yellow, grumous core of lipid (mainly chole and chole esters covered by a white fibrous cap)

97
Q

In connection to atherosclerosis, the precipitating lesion for pts who develop myocardial infarction (MI) and other acute coronary syndromes is what?

A

It is not necessarily a severely stenotic and hemodynamically significant lesion before its acute change

98
Q

What is an infarct?

A

It is an area of ischemic necrosis

99
Q

What is the cause of the occurrence of an infarct?

A

It is caused by occlusion of either the arterial supply or the venous drainage

100
Q

What are the characteristics of tissue infarction?

A

1) It is common

2) It is an extremely impt cause of clinical illness

101
Q

*Tissue infarction (/ infarction) can cause what disorders / conditions?

A

1) MI (/ heart attack)
2) Cerebral infarction (stroke)
3) Pulmonary infarction
4) Bowel infarction
5) Necrosis of extremities (gangrene) in diabetics

102
Q

True or False

All infarcts result from thrombotic / embolic arterial occlusions

A

False, because nearly all infarcts result from thrombotic / embolic arterial occlusions

103
Q

*What are the other mechanisms w/c are presented by infarcts?

A

1) Local vasospasm
2) Hemorrhage into an atheromatous plaque
3) Extrinsic vessel compression (by a tumor)
4) Torsion of vessel
5) Traumatic
6) Vascular compromise due to edema
7) Entrapment in a hernial sac

104
Q

*What is shock?

A

It is the final common pathway for several potentially lethal clinic events

105
Q

*What are the potentially lethal clinic events (in connection to shock)?

A

1) Severe hemorrhage
2) Extensive trauma or burns
3) Large MI
4) Massive pulmonary thromboembolism
5) Microbial sepsis

106
Q

What is the characteristic of shock?

A

It is characterized by systemic hypotension

107
Q

Systemic hypotension (w/c is the characteristic of shock) is caused by what?

A

It is due either to reduced cardiac output or due to reduced effective circulating blood volume

108
Q

Reduced effective circulating blood volume (w/c may be the cause of systemic hypotension) leads to what?

A

1) Impaired tissue perfusion

2) Cellular hypoxia

109
Q

What are the 3 major types of shock?

A

1) Cardiogenic
a. Cardiac tamponade
b. Pulmonary embolism
2) Hypovolemic
3) Septic

110
Q

Provide clinical exs of cardiogenic type of shock

A

1) MI
2) Ventricular rupture
3) Arrhythmia

111
Q

What are the principal mechanisms of the clinical exs of cardiogenic type of shock?

A

Failure to myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow

112
Q

Provide a clinical ex of hypovolemic type of shock

A

Fluid loss (hemorrhage, vomiting, diarrhea, burns, / trauma)

113
Q

What is the principal mechanism of fluid loss?

A

Inadequate blood or plasma volume

114
Q

Provide a clinical ex of septic type of shock

A

Overwhelming microbial infections (bacterial and fungal)

115
Q

What are the principal mechanisms of overwhelming microbial infections?

A

Peripheral vasodilation and pooling of blood; endothelial activation / injury; leukocyte-induced damage, disseminated intravascular coagulation; activation of cytokine cascades

116
Q

What are the stages of shock?

A

1) Nonprogressive phase
2) Progressive stage
3) Irreversible stage

117
Q

What are the events that occur in the initial nonprogressive phase?

A

1) The reflex compensatory mechanisms are activated

2) Perfusion of vital organs is maintained

118
Q

What are the characteristics of progressive stage?

A

It is characterized by:

1) Tissue perfusion
2) Onset of worsening circulatory and metabolic imbalances, including acidosis

119
Q

When does irreversible stage takes place (explain its principle)?

A

It sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defects are corrected, survival is not possible

120
Q

What are the clinical consequences (/ clinical manifestations) of hypovolemic and cardiogenic shock?

A

1) Hypotension
2) A weak, rapid pulse
3) Tachypnea
4) Cool, clammy, and cyanotic skin

121
Q

What are the clinical consequences (/ clinical manifestations) of septic shock?

A

The skin of the pt may initially be warm and flushed because of peripheral vasodilation

Histopathology and Cytologic Techniques (Lecture) (17 decks)

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