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MOD Exam 1 > Hemodynamics and Shock > Flashcards

Hemodynamics and Shock Flashcards

1
Q

Hemostasis

A

formation of blood clot at the site of injury

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2
Q

Conditions that lead to an increase in hydrostatic pressure

A

Venous obstruction (DVT)

Cirrhosis

CHF

CKD

Pregnancy

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3
Q

Most systemic emboli arise from what type of thrombus?

A

mural thrombi

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4
Q

An increase in salt retention leads to an increase in water retention; how does this effect the pressures across a blood vessel?

A

Leads to an increase in hydrostatic pressure and a decrease in oncotic pressure

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5
Q

What is the main goal of the coagulation cascade?

A

Production of fibrin to solidify the platelet plug

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6
Q

What occurs when there is a derrangement in the balance between hydrostatic and oncotic pressure?

A

Increased fluid movement out of the vessels and into the tissues

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7
Q

What are the possible mechanisms of edema?

A

Increased hydrostatic pressure

Decreased oncotic pressure

Increased vascular permeability

Lymphatic obstruction

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8
Q

When does edema occur?

A

When rate of fluid leakage from vessel exceeds rate of lymph drainage, fluid accumulates in tissues (interstitial space)

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9
Q

Alias for factor IIa?

A

Thrombin

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10
Q

In the coagulation cascade, thrombin is responsible for?

A

Converting fibrinogen into fibrin monomers

Activating factor V into factor Va

Activating factor VIII into factor VIIIa

Activates factor XIII to stabilize fibrin

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11
Q

What is the main concern when platelet counts drop to less than 2000/μL

A

Intracranial bleeding

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12
Q

Diseases associated with sudden massive hemorrhage

A

Aortic dissection in the setting of Marfan syndrome

AAA

MI

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13
Q

What are possible reasons for a decrease in albumin levels?

A

Malnutrition

Liver disease

Nephrotic syndrome

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14
Q

Transudates represent what type of edema?

A

Non-inflammatory edema

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15
Q

What is the goal of primary hemostasis?

A

To form a weak platelet plug at the site of injury

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16
Q

Where do mural thrombi form?

A

In the heart chambers

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17
Q

What is the main cause of increased hydrostatic pressure?

A

Impaired venous return

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18
Q

Pathogenesis of septic shock

A

TLRs recognize PAMPs

Release of inflammatory mediators (INF-γ, TNF, IL-1, IL-12, IL-18)

Activation of complement

Endothelial cell activation leading to vasodilation and edema

Endothelial dysfunction leading to release of procoagulant factors

Results in HoTN, hypovolemia, thrombosis and decreased tissue oxygenation

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19
Q

What are the high risk secondary or acquired causes of hypercoagulability?

A

prolonged bed rest or immobilization

MI

A-fib

tissue injury

CA

prosthetic cardiac valves

disseminated intravascular coagulation

heparin induced thrombocytopenia (HIT)

Antiphospholipid Ab syndrome

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20
Q

What cofactor does protein C require in order to inhibit factors Va and VIIIa and thus function as an anticoagulant?

A

protein S

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21
Q

Signs and symptoms of a DVT

A

unilateral swelling

pain

warmth and redness

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22
Q

In what direction do venous thrombi tend to grow?

A

in the direction of blood flow, toward the heart

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23
Q

What underlies the most serious and most common forms of cardiovascular disease?

A

Thrombosis

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24
Q

Libman-Sacks Endocarditis

A

A sterile verrucous endocarditis that occurs in the setting of systemic lupus erythematous

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25
Q

A deficiency in factor VIII results in what disease?

A

Hemophilia A

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26
Q

In what circumstances would there be an alteration in blood flow, from laminar to turbulent?

A

Normal arterial bifurcation

Dilated vessels (aneurysm, hemorrhoid)

Internal obstruction (atherosclerotic plaque)

External compression

Inadequate heart chamber function (Afib)

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27
Q

Alias for factor II

A

Prothrombin

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28
Q

Fate of a thrombus

A

Propagation

Embolization

Dissolution

Organize/recanalize

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29
Q

What factors are responsible for platelet adhesion to the subendothelial surface?

Where are these factors located?

A

Von Willebrand Factor (released from endothelial cells)

Gp1b (receptor located on platelet)

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30
Q

What is the morphology of a transudative effusion?

A

Protein poor

Translucent

Straw colored

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31
Q

Manifestations of hypoxic tissue injury

A

heart failure

HoTN

Renal failure

Lung failure

Coma

Death

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32
Q

Where do arterial thrombi usually occur?

A

coronary aa

cerebral aa

femoral aa

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33
Q

Chronic congestion can lead to what condition?

A

Hemosiderosis

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34
Q

How does endothelial activation cause prothrombic events?

A

Damage to the endothelium exposes vWF and tissue factor which will trigger coagulation

Downregulates thrombomodulin and protein C

Release plasminogen activator inhibitors (to inhibit tPA)

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35
Q

What conditions predispose a patient to formation of mural thrombi?

A

Arrhythmias

Dilated cardiomyopathy

MI

Myocarditis

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36
Q

Endothelial cells release von willebrand factor, where is this factor located within the cells?

A

Weibel Palade bodies

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37
Q

Three stages of shock

A

Nonprogressive phase: perfusion remains

Progressive stage: hypoperfusion of organs

irreversible stage: severe tissue injury

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38
Q

What morphological changes are seen with edema?

A

Clearing and separation of the ECM and subtle cell swelling

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39
Q

Most common trigger of septic shock

A

Gram-positive bacterial infection

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40
Q

Fibrinolysis limits the size of a clot through the activity of what enzyme?

A

Plasmin

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41
Q

Endothelial activation is believed to have an important role in triggering what type of event?

A

Arterial thrombotic event

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42
Q

Hemosiderin-laden macrophages are often termed what because of the condition that causes this?

A

Heart failure cells

(CHF leads to chronic congestion which leads to hemosiderin-laden macrophages)

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43
Q

Plasmin is tightly controlled by what inhibitory factor?

A

α2-plasmin

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44
Q

What clinical manifestation can lead a physician to a defect in primary hemostasis?

A

Mucocutaneous bleeding

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45
Q

Antiphospholipid antibody syndrome

A

An acquired hypercoagulable condition resulting from Abs against plasma proteins that bind to phospholipids, leading to a prothrombic state

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46
Q

After injury, what is the first thing to occur prior to onset of primary hemostasis? What is the mechanism behind this?

A

Vasoconstriction

A neurogenic reflex and endothelin

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47
Q

A majority of emboli are

A

dislodged thrombi

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48
Q

Most common pathogenic feature of shock associated with systemic inflammation is?

A

Massive outpouring of inflammatory mediators from cells of the innate and adaptive immune system, producing arterial vasodilation, vascular leakage, and venous blood pooling

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49
Q

What type of thrombus underlies the majority of infarctions?

A

arterial

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50
Q

Septic infarctions are often converted into

A

Abscesses

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51
Q

Development of DVT is common where?

A

Lower extremity

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52
Q

What type of edema signals potential underlying cardiac or renal disease?

A

Subcutaneous edema

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53
Q

What protein is key to maintaining plasma osmotic pressure?

A

Albumin

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54
Q

Why are amniotic emboli lethal?

A

Squamous cells, hair, fat and mucin from the fetus enter maternal circulation; mother has an anaphylactic rxn to the material

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55
Q

Purpura and ecchymoses are characteristic of what kinds of disorders?

A

Systemic disorders that disrupt small blood vessels

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56
Q

Alias for factor VIII

A

Antihemophilic A factor (AHF)

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57
Q

Dependent edema

A

The distribution of subcutaneous edema shifts with changes in gravity

i.e. in the legs when standing, in the sacrum when laying recumbent

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58
Q

What typically leads to salt retention?

A

Kidney disease

Kidney hypoperfusion 2/2 cardiovascular disease

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59
Q

What are common consequences of a PE?

A

right sided heart failure

pulmonary hemorrhage

pulmonary infarction

sudden death

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60
Q

What is the most common form of thromboembolic disease?

A

Pulmonary emboli

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61
Q

Chronic congestion differs from acute congestion in that

A

a chronic increase in blood volume can lead to capillary rupture, releasing blood cells in addition to fluid

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62
Q

Transudate fluid contains

A

low protein content, few cells

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63
Q

What is the significance of the lines of zahn to a pathologist?

A

Shows that the clot formed antemortem in flowing blood, rather than postmortem

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64
Q

Types of shock

A

Cardiogenic

Hypovolemic

Septic

Neurogenic

Anaphylactic

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65
Q

Plasmin is activated from its zymogen form, plasminogen, by what factor?

A

t-PA

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66
Q

What is the purpose of secondary hemostasis?

A

Production of fibrin to stabilize the weak clot produced by primary hemostasis

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67
Q

Common effects of a venous thrombus?

A

Painful congestion and edema distal to obstruction

Can embolize to the lungs

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68
Q

Common location of a superficial venous thrombosis?

A

Saphenous Vs

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69
Q

What are the characteristics of a postmortem clot?

A

Gelatinous

Dark red dependent portion of settled RBCs

Yellow fatty upper portion

Not attached to underlying vessel wall

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70
Q

A prothrombin time (PT) assesses the function of what proteins in what pathway?

A

Factors VII, X, V, II and fibrinogen in the extrinsic pathway

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71
Q

Liver failure results in edema and ascites, what is ascites?

A

Fluid accumulation in the abdomen

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72
Q

What type of edema typically results from renal dysfunction

A

Periorbital edema

(edema in areas containing loose CT)

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73
Q

What are the peripheral manifestations of endocarditis?

A

Purpura (Janeway lesions)

Roth spots in the retina

Splinter hemorrhages in nail bed

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74
Q

What is the dominant histologic characteristic of infarction?

A

Ischemic coagulative necrosis

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75
Q

Standard of care for treating septic shock?

A

Abx to treat the underlying infection

Pressors and supplemental O2

IV fluids

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76
Q

What factors help to maintain CO and BP in the nonprogressive phase of septic shock?

What does this result in?

A

Baroreceptors, catecholamines, RAAS, ADH

Results in tachycardia, peripheral vasoconstriction, renal conservation of fluid

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77
Q

What is a major cause of arterial thromboses?

A

Atherosclerosis

78
Q

Pulmonary edema occurs 2/2

A

Left ventricular failure (mainly)

Renal failure

ARDS

79
Q

Functional role of thrombin im primary hemostasis?

A

initiation of the release factors from platelet granules

80
Q

What conditions predispose a patient to formation of aortic thrombi?

A

Ulcerated atherosclerotic plaques

Dilated aneurysms

81
Q

What are the two types of platelet adhesion disorders discussed in the lecture?

A

Von Willebrand disease

Bernard Soulier syndrome

82
Q

What occurs in Kwashiorkor?

A

Malnutrition leads to protein deficiency which then leads to development of edema

83
Q

What clinical manifestation is seen with thrombocytopenia but not usually seen with qualitative disorders?

A

Petechiae

84
Q

In what condition are septic emboli common?

A

Endocarditis

85
Q

Main effect of an arterial thrombus?

A

Occlusion of a critical vessel (coronary or cerebral A)

86
Q

IWhat renal condition leads to a loss of albumin into the urine, leading to a decrease in oncotic pressure and thus edema?

A

Nephrotic syndrome

87
Q

What are the most common inherited causes of hypercoagulability (thrombophilia)?

A

Point mutation in factor V (most common)

Prothrombin gene mutation

88
Q

Common cause of fat emboli seen postmortem?

A

CPR

89
Q

What do venous thrombi contain that distinguish them from postmortem clots?

A

Lines of Zahn

90
Q

How does Renal failure contribute to the production of edema?

A

Renal failure leads to the retention of salt and water, increasing blood volume and leading to edema

91
Q

What is the most common cause of renal hypoperfusion?

A

CHF

92
Q

Bleeding time was often a method used by physicians to determine if there was a defect in platelets, what is the normal bleeding time?

A

2-7 minutes

93
Q

What steps are involved in platelet aggregation?

A

The conformational change in the GpIIb-IIIa receptor complex allows for fibrinogen to bind with higher affinity, these fibrinogen molecules cross-link to form aggregates

94
Q

The nutmeg appearance of the liver results from what condition?

A

CHF or local thrombus which results in chronic passive congestion of the central vein

95
Q

Types of granules within platelets

A

α-granules

δ-granulse (dense)

96
Q

Factor XI deficiency

A

Leads to mild bleeding due to thrombin’s ability to positively feedback on XI to amplify the cascade.

97
Q

What factors are dependent on vitamin K?

A

Factors II, VII, IX, X

Protein C and protein S

98
Q

When do arterial thrombi usually occur?

A

When there is turbulent blood flow or endothelial injury

99
Q

What is the major contributor to the formation of venous thrombi?

A

Stasis

100
Q

Venous thrombi are termed stasis thrombi for what reason?

A

Thet form in the sluggish venous circulation and contain more enmeshed RBCs

101
Q

Effusion

A

When rate of fluid leakage from vessel exceeds rate of lymph drainage, fluid accumulates in body cavities

102
Q

What type of infarct occurs when there is collateral supply to an organ, like the lung?

A

Red infarct

103
Q

What disorder is characterized by the loss or impaired production of platelets?

A

Thrombocytopenia

104
Q

Vitamin K is antagonized by what drug?

A

Coumadin

105
Q

Hyperemia

A

increase blood volumes arriving to a tissue; a physiologic process that occurs 2/2 arterial dilation during exercise

106
Q

what factors influence the development of an infarct?

A

Anatomy of vascular supply (one vs dual)

Rate of occlusion

Tissue vulnerability to hypoxia

107
Q

What leads to ascites?

A

Decreased production of albumin 2/2 liver failure

Portal HTN leading to congestion

108
Q

Cardiogenic shock

A

Low cardiac output 2/2 inability of the heart to pump properly

109
Q

What do hyperemia and congestion have in common? What differentiates them?

A

They both involve an increase in blood volume within tissues, but they differ in the mechanism for which this occurs

110
Q

Morphology of acute pulmonary congestion

A

Engorged alveolar capillaries, alveolar septal edema and focal intraalveolar hemorrhage

111
Q

In what direction do arterial thrombi tend to grow?

A

Retrograde, toward the heart

112
Q

Pulmonary emboli typically originate from?

A

DVTs

113
Q

What obstetric thrombotic complications occur with antiphospholipid antibody sydrome?

A

unexplained miscarriage or stillbirth

114
Q

Characteristics of an amniotic embolism

A

sudden severe dyspnea

cyanosis

shock

If patient survives: pulmonary edema develops

115
Q

What conditions lead to an increase in capillary permeability?

A

Sepsis

Inflammation

Burns

116
Q

Glanzmann thrombasthenia results from a defect in what factor of hemostasis?

A

The GpIIb-IIIa receptor complex

117
Q

Common causes of air emboli

A

Cardiac catheterization

Decompression sickness (the bends, caisson dz)

118
Q

What must be considered in patients < 50 y/o who present with thrombosis, even if acquired risk factors are present?

A

Inherited causes of hypercoagulability

119
Q

Bernard Soulier syndrome involves a defect in what factor?

A

Gp1b receptor on platelets

120
Q

Exudative fluid components?

What is an exudate indicative of?

A

High protein, some RBC or WBC

Inflammation

121
Q

Shock

A

A state in which dimished cardiac output or reduced efective circulating blood vlume impairs tissue perfusion and leads to cellular hypoxia

122
Q

Edema is most commonly seen in what tissues?

A

Subcutaneous tissues

Lungs

Brain

123
Q

Mutations in prothrombin gene leads to increased risk of thrombus formation how?

What mutation occurs?

A

Leads to elevated prothrombin levels

Single nucleotide change in the 3’ untranslated region (G20210A)

124
Q

What vascular thrombotic complications occur with antiphospholipid antibody sydrome?

A

arterial or venous thrombosis

125
Q

Where does fluid accumulate in pulmonary edema?

A

Within the alveolar spaces

126
Q

Do the disorders involved in platelet adhesion, Von Willebrand and Bernard Soulier, have a defect in platelet aggregation as well?

A

No

127
Q

What are the primary abnormalities that lead to thrombosis?

what are these termed?

A

Endothelial injury

Abnormal blood flow

Hypercoagulability

(Virchow Triad)

128
Q

What are the other genetic causes of hypercoagulability, that are less common?

A

Antithrombin III deficiency

Protein C deficiency

Protein S deficiency

129
Q

What type of embolism is a major cause of maternal mortality?

A

Amniotic fluid embolism

130
Q

Air embolism

A

introduction of air into closed circulation

131
Q

What is the most common cause of morbidity and mortality in Western society?

A

Cardiovascular disease

132
Q

What factors are released from endothelial cells that inhibit platelet activation and aggregation?

A

PGI2

NO

ADPase

133
Q

In septic shock, disseminated intravascular coagulation leads to a widespread deposition of what substances?

In what locations?

A

Fibrin-rich microthrombi

Brain, heart, lungs, kidney, adreanl glands and GI tract

134
Q

Septic emboli result from

A

bloodborne infective material

135
Q

What test is performed clinically to assess markers of thrombotic states?

A

D-dimer

136
Q

alias for factor I

A

fibrinogen

137
Q

Fat emboli result from

A

fracture or soft tissue trauma that leads to bone marrow being introduced into circulation

138
Q

Filariasis

A

A parasitic infection (Wuchereria) in which the organism induces obstructive fibrosis of lymphatic channels and lymph nodes, leading to lymphedema

139
Q

Fat embolism syndrome is characterized by

A

respiratory distress

mental status change

anemia

thrombocytopenia

(can be fatal)

140
Q

What is the mechanism that leads to hepatic congestion

A

Obstruction of the central vein

141
Q

A patient with breast CA that had lymph nodes removed would develop what type of fluid accumulation:

edema, effusion, lymphedema?

A

lymphedema

142
Q

What complex is the most important activator of factor IX?

A

factor VIIa/Tissue factor complex

143
Q

What are the steps involved in primary hemostasis?

A
  1. Adhesion
  2. Activation
  3. Aggregation
144
Q

Hemosiderosis

A

abnormal accumulation of iron as hemosiderin in alveolar macrophages

145
Q

Thromboxane A2 is a potent promoter of platelet aggregation, what inhibits formation of TxA2?

A

Aspirin

146
Q

Lymphedema results from

A

a disruption in the lymphatic vessels causing an impairment in the clearance of interstitial fluid

147
Q

What bacterial proteins are the underlying cause of toxic shock syndrome?

A

Superantigens

148
Q

What triggers platelet activation?

A

ADP and Thrombin

149
Q

Platelet activation occurs after platelets have adhered to the subendothelial layer, what steps occur during activation?

A

A conformational change in the platelets increasing the surface area

Negatively charge phospholipids translocate to the surface to bind calcium

Conformational change in the GpIIb-IIIa receptor complex to increase it’s affinity for fibringoen

Release of granular contents (ADP and TxA2)

150
Q

Endothelial cells express multiple factors that oppose coagulation, these factors include

A

thrombomodulin

endothelial protein C receptor

151
Q

How is the definitive secondary hemostatic plug formed?

A

Thrombin converts fibrinogen into fibrin, cementing the aggregated platelets from primary hemostasis in place

152
Q

Explain the nutmeg liver appearance

A

Alterations of light and dark areas, dark areas are dying hepatocytes

153
Q

An exudate represents what type of edema?

A

Inflammatory edema, caused by an increase in vascular permeability 2/2 release of inflammatory mediators

154
Q

What type of infarct results when the organ is dependent on one vessel, like the spleen?

A

White infarct

155
Q

What disorder is commonly associated with hemophilia?

A

hemarthrosis, bleeding into the joints

156
Q

What are the low risk secondary or acquired causes of hypercoagulability?

A

Cardiomyopathy

Nephrotic syndrome

Hyperestrogenic states (pregnancy, postpartum)

OCP

sickle cell anemia

smoking

157
Q

Morphology of an exudative effusion

A

Protein rich

Cloudy d/t presence of WBCs

158
Q

what cells produce tPA?

A

Endothelial cells

159
Q

Thrombi often contain lines of Zahn, what defines this?

A

pale platelet and fibrin deposits alternating with darker red cell-rich laters

160
Q

Septic infarctions result when?

A

Cardiac valve vegetations embolize or when microbes seed necrotic tissue

161
Q

What normally balances the fluid and solutes within blood?

A

Hydrostatic pressure pushing water and salts out

Colloid osmotic pressure pulling water and salts in

162
Q

What differentiates transudate from exudate in terms of endothelial changes?

A

Exudate results from inflammation and inflammation leads to an increased interendothelial space, which does not occur in fluid leakage of a transudate

163
Q

What are the dermatologic manifestations of defects in homeostasis, most commonly platelet dysfunctions?

A

Petechiae (small, < 3 mm)

Purpura (larger)

Ecchymosis (palpable)

164
Q

What things contribute endothelial activation?

A

physical injury

infectious agents

abnormal blood flow

inflammatory mediators

toxins

metabolic abnormalities

165
Q

What complex is the most important activator of factor X?

A

factor IXa/factor VIIIa complex

166
Q

Localized edema 2/2 infection, inflammation, trauma, tumors, surgery or malformations is characterized as?

A

Lymphedema

167
Q

Hypovolemic shock

A

Low cardiac output d/t low blood volume, likely resulting for massive hemorrhage

168
Q

Coagulation involves the assembly of reaction complexes that depend on Calcium binding to what on factors II, VII, IX and X?

A

γ-carboxylated glutamic acid

169
Q

How does turbulent blood flow contribute to the prothrombotic state?

A

Activates endothelium

Pushes platelets toward the periphery, in closer contact to the endothelium

Prevents washout of clotting factors which typically occurs with laminar blood flow

170
Q

Of the coagulation factors, which is the most important due to its various roles in hemostasis?

A

Thrombin

171
Q

What is the most common cause of hepatic congestion

A

Right heart failure

172
Q

Infarcts are classified according to color and the presense or absence of infarction, what are the classifications?

A

White infarct: arterial, platelet-rich infarcts occurring in high shear stress

Red infarct: venous, red cell rich, occur in stasis typically in LE

173
Q

Factor V Leiden

A

Mutation leading to a glutamine for arginine substitution that renders factor V resistent to inactivation by protein C, increasing risk of developing a thrombus

174
Q

what occurs with the organization of a thrombus?

A

There is ingrowth of endothelial cells, smooth muscle cells, and fibroblasts

175
Q

Histologically, one can determine Bernard Soulier syndrome based on what changes in the platelets?

A

They appear larger

176
Q

Reactions that produce γ-carboxylated glutamic acide are dependent on what co-factor?

A

Vitamin K

177
Q

A saddle emolism results in instantaneous death for what reason?

A

emolism leads to right heart failure

178
Q

Conditions that lead to decreased oncotic pressure

A

Malabsorption

Nephrotic Syndrome

Liver failure

Malnutrition

179
Q

A partial thromboplastin time (PTT) assesses the function of what proteins in what pathway?

A

Factors XII, XI, IX, VIII, X, V, II, fibrinogen in the intrinsic pathway

180
Q

Most common cause of mild bleeding tendencies

A

inherited defects in vWF

Aspirin

Uremia

181
Q

Congestion

A

Reduced flow of blood from a tissue often pathologic in origin

182
Q

why do patients in septic shock exhibit insulin resistence and hyperglycemia?

A

IL-1 and TNF drive gluconeogenesis and impair the surface expression of GLUT4 transporters

183
Q

What is the mechanism behind Heparin-induced Thrombocytopenia (HIT) syndrome?

A

Occurs after administration of unfractionated heparin, which causes Ab production against platelet factor 4-heparin complexes, leads to a prothrombic state 2/2 activation and aggregation of platelets

184
Q

The clinical significance of hemorrhage depends on what?

A

Volume of blood loss

Rate

Location

185
Q

Due to the decrease in outflow of blood from congestion, what typically develops?

A

Edema

186
Q

Secondary antiphospholipid antibody syndrome occurs in what type of individual?

A

One with a well-defined autoimmune disease, often systemic lupus erythematosus

187
Q

In patients with thrombocytopenia, are the functions of the platelets intact?

A

Yes

188
Q

Heparin-like molecules are present on the surface of endothelial cells, these molecules bind and activate what molecule that in turn inhibits factors IXa, Xa, thrombin

A

Antithrombin III

189
Q

What factors limit coagulation?

A

Blood flow by washing away the factors that activate clotting

Loss of factors on platelet d/t fibrin coat

Plasmin

190
Q

Most common cause of DVT formation

A

Immobilization

MOD Exam 1 (5 decks)

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