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HistoPathology > [P] Week 3: HEMODYNAMIC DISORDERS, THROMBOEMBOLIC DISEASES, AND SHOCK [AI generated] > Flashcards

[P] Week 3: HEMODYNAMIC DISORDERS, THROMBOEMBOLIC DISEASES, AND SHOCK [AI generated] Flashcards

1
Q

What is hemostasis?

A

The process by which we activate the clotting mechanism that prevents excessive bleeding after blood vessel damage.

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2
Q

What can inadequate hemostasis result in?

A

Hemorrhage, thrombosis, or embolism.

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3
Q

What is edema?

A

The increased amount of fluid in the interstitial tissue spaces.

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4
Q

What are the two main opposing forces in edema?

A
  • Hydrostatic pressure
  • Plasma colloid osmotic pressure (oncotic pressure of plasma protein)
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5
Q

What happens under normal conditions regarding fluid movement?

A

Proteins in the plasma are retained within the vasculature, leading to little net movement of water and electrolytes into the tissues.

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6
Q

What is the role of lymphatic vessels in fluid accumulation?

A

They drain a small amount of fluid to prevent accumulation in the interstitial tissue space.

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7
Q

What causes fluid accumulation?

A
  • Increased hydrostatic pressure
  • Decreased plasma colloid osmotic pressure
  • Blockade in lymphatic flow
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8
Q

What is the role of RMTs when fluid is aspirated?

A

Perform assays requested by clinicians, including Chemistry Analysis, Cell Count Analysis, and Culture & Sensitivity.

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9
Q

What distinguishes inflammatory-related edema from non-inflammatory-related edema?

A

Inflammatory-related edema is protein-rich, while non-inflammatory-related edema is protein-poor (transudate).

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10
Q

What are common clinical correlations of edema?

A
  • Deep Venous Thrombosis
  • Congestive Heart Failure
  • Periorbital Swelling in Nephrotic Syndrome
  • Low Serum Protein
  • Lymphedema
  • Parasitic Filariasis (Elephantiasis)
  • Pulmonary Edema
  • Brain Edema
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11
Q

What is Deep Venous Thrombosis (DVT)?

A

Localized increase in hydrostatic pressure due to disorders that impair venous return, typically seen in the lower extremities.

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12
Q

What is Congestive Heart Failure (CHF) associated with?

A

Systemic increases in venous pressure leading to widespread edema.

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13
Q

What is pitting edema?

A

A type of edema where pressing on the skin leaves a depression corresponding to the size of your thumb.

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14
Q

What causes periorbital swelling in Nephrotic Syndrome?

A

Decreased oncotic pressure due to massive amounts of proteins excreted in the urine.

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15
Q

What are the causes of low serum protein leading to edema?

A
  • Severe liver diseases (e.g., liver cirrhosis)
  • Decreased protein intake (e.g., malnutrition)
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16
Q

How does sodium and water retention affect hydrostatic pressure?

A

It increases hydrostatic pressure due to intravascular fluid volume expansion and diminishes vascular colloid osmotic pressure due to dilution.

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17
Q

What is lymphedema?

A

Edema associated with chronic inflammation, malignancy, physical disruption, radiation damage, and certain infections due to lymphatic obstruction.

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18
Q

What is parasitic filariasis and its effect on lymphatics?

A

A condition where an organism induces obstructive fibrosis of the lymphatic channels, resulting in edema, often referred to as elephantiasis.

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19
Q

What is pulmonary edema characterized by?

A

Fluid-filled lungs, with frothy fluid material exuding when cut, and alveoli filled with pinkish, eosinophilic material.

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20
Q

What is brain edema and its consequences?

A

Swelling of the brain causing narrowed sulci and distended gyri, potentially leading to herniation and compression of vital centers.

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21
Q

What is hyperemia?

A

An active process resulting from arteriolar dilation, usually occurring at sites of inflammation.

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22
Q

What is congestion?

A

A passive process resulting from reduced outflow of blood from a tissue, leading to a blue-red or cyanotic appearance.

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23
Q

What is the difference between acute and chronic pulmonary congestion?

A

Acute pulmonary congestion is marked by engorged capillaries and edema within alveoli, while chronic leads to heart failure cells (hemosiderin-laden macrophages).

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24
Q

What are heart failure cells?

A

Hemosiderin-laden macrophages formed from engulfed red cells in chronic pulmonary congestion

These cells are indicative of chronic conditions such as congestive heart failure.

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25
Q

What is the difference in septa between acute and chronic pulmonary congestion?

A

In chronic pulmonary congestion, the septa are thicker and fibrotic

In acute pulmonary congestion, the septa are not as thick.

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26
Q

What happens to centrilobular hepatocytes during acute hepatic congestion?

A

They may undergo ischemic necrosis

This occurs because they are farthest from the blood supply.

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27
Q

What is ‘nutmeg liver’ indicative of?

A

Chronic passive congestion of the liver

It is characterized by grossly red-brown centrilobular regions undergoing necrosis.

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28
Q

What are the histomorphologic findings in chronic passive congestion of the liver?

A

Centrilobular necrosis, hemorrhage, and abundance of hemosiderin-laden macrophages

Degeneration of hepatocytes is most marked around the central vein.

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29
Q

What is hemostasis?

A

The process by which blood clots form at sites of vascular injury

It is crucial for preventing hemorrhagic disorders.

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30
Q

What types of hemorrhages can occur in tissues?

A

Petechiae, purpura, ecchymoses

Hemorrhage can vary in size from small to large.

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31
Q

What is the goal of hemostasis?

A

To maintain blood in a fluid, clot-free state while forming a hemostatic plug at injury sites

This prevents or limits bleeding.

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32
Q

What are the three major components of hemostasis?

A
  • Vascular Wall (endothelium)
  • Platelets
  • Coagulation Cascade
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33
Q

What induces vasoconstriction after vascular injury?

A

Endothelin

This is a neurohumoral factor that causes blood vessels to constrict.

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34
Q

What is the endpoint of primary hemostasis?

A

Formation of the platelet plug

This occurs after platelet activation and aggregation.

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35
Q

What triggers platelet adhesion in primary hemostasis?

A

Exposure of subendothelial collagen and the von Willebrand factor

This leads to platelet activation.

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36
Q

List the five steps in primary hemostasis.

A
  • Platelet Adhesion
  • Shape Change
  • Granule Release (ADP, TXA2)
  • Recruitment
  • Aggregation (Hemostatic Plug)
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37
Q

What is the endpoint of secondary hemostasis?

A

Deposition of fibrin

This occurs as fibrin forms a meshwork among platelets.

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38
Q

What activates tissue factor in secondary hemostasis?

A

Exposure at the site of vascular injury

Tissue factor activates Factor VII, initiating the coagulation cascade.

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39
Q

What is clot stabilization?

A

Contraction of fibrin and platelets forms a solid permanent plug

This aims to prevent further hemorrhage.

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40
Q

What are the antithrombotic properties of the endothelium?

A
  • Anticoagulant factors
  • Inhibition of platelet aggregation
  • Promotion of fibrinolysis
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41
Q

What role does t-PA play in hemostasis?

A

t-PA cleaves plasminogen to form plasmin which degrades thrombi

This is part of the fibrinolytic process.

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42
Q

What is the clinical significance of von Willebrand factor?

A

Essential for platelet binding to collagen; absence leads to defects in primary hemostasis

vWF disease can cause small bleeds in skin or mucosal membranes.

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43
Q

What is the role of thrombomodulin in hemostasis?

A

Converts thrombin from a procoagulant to an anticoagulant

It activates protein C, which inhibits clotting.

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44
Q

What are the procoagulant properties of the endothelium?

A
  • Production of vWF
  • Induction by endotoxins/cytokines
  • Antifibrinolytic effects
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45
Q

What is the primary cause of mucosal bleeding associated with defects in primary hemostasis?

A

Deficiency of von Willebrand Factor (vWF)

Mucosal bleeding can manifest as epistaxis, GI bleeding, or menorrhagia.

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46
Q

What is the clinical significance of tissue factor?

A

Tissue factor is regarded as a procoagulant essential for thrombin formation

Thrombin facilitates the conversion of fibrinogen to fibrin.

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47
Q

What is hemarthrosis?

A

Bleeding in the joints, often following minor trauma

This is particularly characteristic of hemophilia.

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48
Q

What are the manifestations of defects in von Willebrand Factor and tissue factor?

A

Petechiae, purpura, ecchymoses, hemarthrosis, hematoma

These are examples of bleeding manifestations.

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49
Q

What are plasminogen activator inhibitors (PAIs)?

A

PAIs are counter-regulatory factors that inhibit fibrinolysis

They act against tissue plasminogen activator (t-PA), which promotes fibrinolysis.

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50
Q

What is the role of intact endothelial cells in hemostasis?

A

Intact endothelial cells inhibit platelet adhesion and blood clotting

They prevent platelets from binding to non-injured endothelium.

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51
Q

List the components that define anticoagulants.

A
  • Prostacyclin (PGI2)
  • Nitric Oxide (NO)
  • ADPase
  • Heparin-Like Molecules
  • Thrombomodulin
  • Protein C
  • Protein S
  • Tissue Factor Pathway Inhibitor
  • t-PA
  • Plasmin

These substances help to regulate and prevent excessive coagulation.

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52
Q

What is the primary role of platelets in hemostasis?

A

Platelets form the primary hemostatic plug

This plug limits bleeding at the site of vascular injury.

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53
Q

What are the two types of granules found in platelets?

A
  • Alpha granules
  • Dense bodies

Alpha granules contain proteins for coagulation and wound healing, while dense bodies contain ADP and other substances.

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54
Q

What is the receptor involved in platelet adhesion to von Willebrand Factor?

A

GpIb (glycoprotein Ib)

GpIb binds to vWF for platelet adhesion.

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55
Q

What happens during the platelet shape change step?

A

Platelets undergo a conformational change, developing a spiky appearance

This step is crucial for increasing their surface area and promoting aggregation.

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56
Q

What triggers the release reaction in platelets?

A

Activation by thrombin and ADP

This leads to the release of granules from the platelets.

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57
Q

What is the significance of thromboxane A2 (TXA2) in platelet function?

A

TXA2 promotes platelet aggregation and attracts other platelets

It is an important factor in the recruitment of platelets.

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58
Q

What does GpIIb/IIIa receptor do during platelet aggregation?

A

It allows binding of fibrinogen, stabilizing the platelet plug

Fibrinogen is converted to fibrin, which helps to consolidate the clot.

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59
Q

What is Glanzmann Thrombastenia?

A

A bleeding disorder caused by inherited deficiency of GpIIb/IIIa

This condition affects platelet aggregation.

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60
Q

What are the two primary assays for evaluating coagulation factors?

A
  • Prothrombin Time (PT)
  • Partial Thromboplastin Time (PTT)

PT assesses the extrinsic pathway, while PTT assesses the intrinsic pathway.

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61
Q

What is the most important activity of thrombin?

A

Conversion of fibrinogen into cross-linked fibrin

Thrombin also activates platelets and has proinflammatory and anticoagulant effects.

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62
Q

What are natural anticoagulants?

A
  • Antithrombin III
  • Protein C & S
  • Tissue Factor Pathway Inhibitor (TFPI)

These factors help limit coagulation and prevent excessive clotting.

63
Q

What is fibrinolysis?

A

The process of breaking down fibrin to dissolve clots

It is primarily mediated by plasmin.

64
Q

Which is the most important plasminogen activator?

A

t-PA (tissue-type plasminogen activator)

t-PA is synthesized by endothelial cells and is most active when bound to fibrin.

65
Q

What is thrombosis?

A

Formation of a clot within a vessel

It is associated with endothelial injury, stasis, and hypercoagulability.

66
Q

What are the primary abnormalities leading to thrombosis?

A
  • Endothelial injury
  • Stasis or turbulent blood flow
  • Hypercoagulability of the blood

Each factor contributes to the likelihood of clot formation.

67
Q

What are the three components of Virchow’s triad in thrombosis?

A

Endothelial injury, stasis or turbulent blood flow, hypercoagulability

Among these, endothelial integrity is the most important factor.

68
Q

What does stasis refer to in the context of thrombus formation?

A

Atrial fibrillation, immobilization, non-ambulatory state

69
Q

What is hypercoagulability?

A

An abnormally high tendency of the blood to clot, often caused by alterations in coagulation factors

70
Q

What is the significance of endothelial injury in thrombosis?

A

It is the single most important factor influencing thrombus formation

71
Q

True or False: Endothelial cells must be physically disrupted to contribute to thrombosis.

A

False

72
Q

What are procoagulant changes associated with activated endothelial cells?

A

Downregulation of thrombomodulin, protein C, and tissue factor protein inhibitor

73
Q

What do activated endothelial cells secrete that limits fibrinolysis?

A

Plasminogen activator inhibitors (PAIs)

74
Q

Fill in the blank: The normal blood flow is said to be _______ where platelets flow centrally in the vessel lumen.

A

laminar

75
Q

What are the effects of turbulence and stasis on thrombus formation?

A
  • Promote endothelial activation * Disrupt laminar flow * Prevent washout of activated clotting factors
76
Q

What clinical conditions can altered blood flow contribute to?

A
  • Ulcerated atherosclerotic plaques * Aortic and arterial dilations (aneurysms) * Rheumatic mitral valve stenosis
77
Q

What mutation is most commonly associated with inherited hypercoagulability?

A

Factor V Leiden mutation

78
Q

What is the inheritance pattern of Factor V Leiden?

A

Autosomal Dominant

79
Q

What is the prothrombin gene mutation associated with?

A

Elevated prothrombin levels and increased risk of thrombosis

80
Q

What are common acquired causes of thrombotic diathesis?

A
  • Oral contraceptive use * Hyperestrogenic state of pregnancy * Smoking * Obesity * Disseminated cancers
81
Q

What is Heparin-Induced Thrombocytopenia (HIT)?

A

A serious disorder following the administration of unfractionated heparin

82
Q

What characterizes Antiphospholipid Antibody Syndrome (APS)?

A
  • High titer of circulating Ab against anionic phospholipid * Venous or arterial thromboses * Pregnancy complications
83
Q

Differentiate between primary and secondary antiphospholipid syndrome.

A
  • Primary: Hypercoagulable state without other autoimmune disorders * Secondary: Associated with a well-defined autoimmune disease
84
Q

Where can thrombi develop in the cardiovascular system?

A

Cardiac chambers, valve cusps, arteries, veins, and capillaries

85
Q

What are lines of Zahn?

A

Laminations in thrombi indicating formation in flowing blood

86
Q

What are mural thrombi?

A

Arterial thrombi occurring in heart chambers or aortic lumen

87
Q

What are the most common sites for arterial thrombi?

A
  • Coronary * Cerebral * Femoral
88
Q

What are characteristics of venous thrombi?

A
  • Form in sluggish venous circulation * Contain more enmeshed erythrocytes * Firm and focally attached to the wall
89
Q

What distinguishes postmortem clots from antemortem venous thrombi?

A
  • Gelatinous consistency * Dark-red dependent portion * Yellow ‘chicken fat’ upper portion
90
Q

What is the fate of a thrombus?

A
  • Propagation * Embolization * Dissolution * Organization & Recanalization
91
Q

What happens during the propagation of a thrombus?

A

Thrombi accumulate additional platelets and fibrin

92
Q

What occurs during the dissolution of a thrombus?

A

Fibrinolysis leading to rapid shrinkage and total disappearance

93
Q

What is involved in the organization and recanalization of older thrombi?

A
  • Ingrowth of endothelial cells, smooth muscle cells, and fibroblasts * Formation of capillary channels reestablishing original lumen continuity
94
Q

What is dissolution in relation to thrombi?

A

The result of fibrinolysis, leading to rapid shrinkage and total disappearance of recent thrombi

Fibrinolysis is also known as resolution.

95
Q

What occurs during the organization of thrombi?

A

Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts

96
Q

What is recanalization?

A

The formation of capillary channels that reestablish the continuity of the original lumen, albeit to a variable degree

97
Q

What is Virchow’s Triad?

A

Endothelial injury, abnormal blood flow, and hypercoagulability

98
Q

What is disseminated intravascular coagulation (DIC)?

A

Widespread fibrin thrombi in the microcirculation causing circulatory insufficiency and consumption coagulopathy

DIC is a complication of various conditions associated with systemic activation of thrombin.

99
Q

What is an embolus?

A

A detached intravascular solid, liquid, or gaseous mass carried by blood to a distant site, causing tissue dysfunction or infarction

100
Q

What are the most common types of embolism?

A

Pulmonary thromboembolism and systemic thromboembolism

101
Q

What is pulmonary thromboembolism?

A

Pulmonary emboli that originate from deep vein thrombosis (DVT) and are the most common form of thromboembolic disease

102
Q

What percentage of pulmonary emboli are clinically silent?

A

60% to 80%

103
Q

What are the functional consequences of pulmonary emboli?

A

Sudden death, acute right heart failure, pulmonary hemorrhage, and pulmonary hypertension

104
Q

What is systemic thromboembolism?

A

Thrombi that originate from the heart and are thrown into systemic circulation

105
Q

Where do most systemic emboli originate from?

A

Intracardiac mural thrombi (80%)

106
Q

What is fat embolism?

A

Presence of microscopic fat globules in the vasculature after fractures of long bones or soft tissue trauma

107
Q

What are the clinical symptoms of fat embolism?

A

Pulmonary insufficiency, neurologic symptoms, anemia, and thrombocytopenia

108
Q

What is the pathogenesis of fat embolism?

A

Mechanical obstruction and biochemical injury caused by fat microemboli and free fatty acids

109
Q

What is air embolism?

A

Gas bubbles within circulation that obstruct vascular flow and cause distal ischemic injury

110
Q

What is decompression sickness?

A

A form of gas embolism occurring when individuals experience sudden decreases in atmospheric pressure

111
Q

What are the bends?

A

Painful condition caused by rapid formation of gas bubbles within skeletal muscles and supporting tissues

112
Q

What are the chokes?

A

Respiratory distress caused by gas bubbles in the lungs leading to edema and hemorrhage

113
Q

What is caisson disease?

A

Chronic form of decompression sickness characterized by persistence of gas emboli leading to ischemic necrosis

114
Q

What characterizes infarction?

A

Area of ischemic necrosis caused by occlusion of arterial supply or venous drainage

115
Q

What are the factors influencing infarct development?

A

Nature of the vascular supply, rate of development, vulnerability of tissue, blood oxygen content

116
Q

What are the two types of infarction?

A

Red (hemorrhagic) and white (anemic) infarcts

117
Q

What is a hemorrhagic (red) infarction?

A

Occurs with venous occlusion, in loose tissue, or when flow is reestablished to a site of previous arterial occlusion

118
Q

What is anemic infarction?

A

Occurs with arterial occlusions in solid organs with end-arterial circulation

119
Q

What is the classic morphology of infarcts?

A

Wedge-shaped, with the occluded vessel at the apex and the periphery of the organ forming the base

120
Q

What is coagulation necrosis?

A

The dominant histologic characteristic of infarction, indicating ischemic coagulative necrosis

121
Q

What histologic changes may be absent shortly before death?

A

Histologic changes may be absent shortly (minutes to hours) before the death of the person.

It takes 4 to 12 hours for the dead tissue to show microscopic evidence of necrosis.

122
Q

When does acute inflammation typically become well defined in infarcts?

A

Acute inflammation is usually well defined within 1 to 2 days.

Acute inflammation is present along the margins of infarcts within a few hours.

123
Q

What does the absence of a nucleus in coagulated fiber indicate?

A

The absence of a nucleus indicates an area of necrosis.

124
Q

What is the exception to the generalization regarding infarcts and tissue regeneration?

A

The brain is an exception, as central nervous system infarction results in liquefactive necrosis.

125
Q

What are septic infarctions?

A

Septic infarctions occur when infected cardiac valve vegetations embolize or when microbes seed necrotic tissue, converting the infarct to an abscess.

This leads to a greater inflammatory response.

126
Q

What is shock in a medical context?

A

Shock is a state of circulatory failure that impairs tissue perfusion and leads to cellular hypoxia.

127
Q

What are the primary categories of shock?

A

Categories of shock include:
* Cardiogenic Shock
* Hypovolemic Shock
* Septic Shock

Each category has different underlying causes.

128
Q

What defines sepsis?

A

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.

129
Q

What is septic shock?

A

Septic shock is a subset of sepsis characterized by profound circulatory, cellular, and metabolic abnormalities with a greater risk of mortality.

130
Q

What is Systemic Inflammatory Response Syndrome (SIRS)?

A

SIRS is a sepsis-like condition associated with systemic inflammation triggered by non-microbial insults such as burns, trauma, and pancreatitis.

131
Q

True or False: Septic shock is most frequently triggered by gram-negative bacterial infections.

A

False.

Septic shock is most frequently triggered by gram-positive bacterial infections.

132
Q

What initiates pro-inflammatory responses in sepsis?

A

Pro-inflammatory responses are initiated by microbial cell wall constituents engaging receptors on cells of the innate immune system.

133
Q

What are Pathogen-associated molecular patterns (PAMPs)?

A

PAMPs are substances recognized by Toll-like receptors (TLRs) that trigger inflammatory responses.

134
Q

What role do cytokines play in sepsis?

A

Cytokines such as TNF, IL-1, and others are released, contributing to inflammation and endothelial activation.

135
Q

What is the effect of inflammatory cytokines on endothelial cells?

A

Inflammatory cytokines loosen endothelial cell tight junctions, causing vascular leakage and tissue edema.

136
Q

What metabolic abnormalities are observed in septic patients?

A

Septic patients exhibit insulin resistance and hyperglycemia.

137
Q

What are the proposed mechanisms for immune suppression in sepsis?

A

Proposed mechanisms include:
* Shift from pro-inflammatory (Th1) to anti-inflammatory (Th2) cytokines
* Production of anti-inflammatory mediators
* Lymphocyte apoptosis
* Immunosuppressive effects of apoptotic cells

These mechanisms contribute to oscillation between hyperinflammatory and immunosuppressed states.

138
Q

What leads to multiple organ dysfunction in shock?

A

Multiple organ dysfunction results from systemic hypotension, interstitial edema, and small vessel thrombosis that decrease oxygen and nutrient delivery.

139
Q

What characterizes the initial non-progressive stage of shock?

A

Reflex compensatory mechanisms maintain cardiac output and blood pressure, resulting in tachycardia and peripheral vasoconstriction.

140
Q

What occurs during the progressive stage of shock?

A

The progressive stage is characterized by widespread tissue hypoxia and worsening circulatory and metabolic derangement.

141
Q

What is the irreversible stage of shock?

A

In the irreversible stage, cellular and tissue injury is so severe that survival is not possible, even if hemodynamic defects are corrected.

142
Q

Fill in the blank: The pro-inflammatory state and endothelial cell activation in sepsis lead to widespread vascular _______.

A

leakage.

143
Q

What is the clinical significance of Waterhouse-Friderichsen Syndrome?

A

It is associated with adrenal insufficiency and can occur due to disseminated intravascular coagulation (DIC).

144
Q

What is the endpoint of shock?

A

Multiorgan Failure

Main organs involved include the heart, lungs, kidneys, and gastrointestinal tract.

145
Q

What are the main organs involved in multiorgan failure due to shock?

A
  • Heart
  • Lungs
  • Kidneys
  • GIT

GIT stands for gastrointestinal tract.

146
Q

What characterizes the Non-Progressive Phase of shock?

A

Reflex neurohumoral mechanisms to maintain cardiac output and blood pressure

Includes tachycardia, peripheral vasoconstriction, and renal conservation of fluid.

147
Q

What occurs during the Progressive Stage of shock?

A
  • Widespread tissue hypoxia
  • Anaerobic glycolysis with production of lactic acid
  • Arterioles dilate & blood pools in microcirculation
  • Subsequent DIC

DIC stands for Disseminated Intravascular Coagulation.

148
Q

What happens during the Irreversible Stage of shock?

A
  • Lysosomal enzyme leakage
  • Worsening myocardial contractile function due to nitric oxide synthesis
  • Superimposed bacteremia
  • Complete renal shutdown (Acute Tubular Necrosis)

Acute Tubular Necrosis is a condition that can lead to complete renal failure.

149
Q

True or False: The Non-Progressive Phase of shock is characterized by widespread tissue hypoxia.

A

False

The Non-Progressive Phase is about maintaining cardiac output and blood pressure, not widespread tissue hypoxia.

150
Q

Fill in the blank: In the Progressive Stage of shock, intracellular aerobic respiration is replaced by _______.

A

anaerobic glycolysis

This shift leads to the production of lactic acid.

151
Q

What is a consequence of lysosomal enzyme leakage in the Irreversible Stage of shock?

A

Worsening myocardial contractile function

This is due to nitric oxide synthesis.

152
Q

What is the role of neurohumoral mechanisms in the Non-Progressive Phase of shock?

A

To maintain cardiac output and blood pressure

This phase involves tachycardia and peripheral vasoconstriction.

153
Q
A

HistoPathology (10 decks)

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