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Block 5 > Pathology > Flashcards

Pathology Flashcards

1
Q

What causes inflammation?

A
  1. Infections
  2. Tissue Necrosis
  3. Foreign Bodies
  4. Immune Reactions (Hypersensitivity)
    1. Allergies
    2. Autoimmune Diseases
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2
Q

Major components of acute inflammation?

A
  1. Dilation of small vessels leading to increase blood flow
  2. Increased permeability of the vessels enabling plasma proteins and leukocytes to leave the circulation
  3. Emigration of the leukocytes from the microcirculation, accumulation, and activation to eliminate the agent
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3
Q

What is exudation?

A

The escape of fluid, proteins, and blood cells from the vascular system into the interstitial tissue or body cativities.

(Indicative of some sort of tissue injury and ongoing inflammatory response)

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4
Q

What is transudate?

A

Fluid with low protein content, little or no cellular material, and low specific gravity

(Produced as a result of osmotic or hydrostatic imbalance across the vessel wall without increase in vascular permeability)

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5
Q

What is edema?

A

Excess fluid in the interstitial tissue or serous cavities

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6
Q

What induces vasodilation?

A
  • Action of several mediators (Notably Histamine) on vascular smooth muscle
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7
Q

What follows vasodilation?

A

Increased permeability, resulting in engorgemnet of small vessels with slowly moving red cells (stasis) and blood leukocytes accumulate along the outside of the vessel along the vascular endothelium

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8
Q

What is VEGF?

A

A factor the promotes vascular leakage

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9
Q

What are the phases of leukocyte transcytosis?

A
  1. Margination, Rolling, and Adhesion to the Endothelium
  2. Migration across the endothelium and vessel wall
  3. Migration in the tissues toward a chemotactic stimulus
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10
Q

What is chemotaxis?

A

Locomotion along a chemical gradient

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11
Q

What can act as chemoattractants?

A
  1. Exogenous
    1. Bacterial Products (Peptides/Lipids)
  2. Endogenous
    1. Cytokines (IL-8)
    2. Complement (C5a)
    3. Arachadonic Acid Metabolites (Leukotriene B4)
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12
Q

The components of inflammatory infiltrate change over the lifetime of the inflammatory response, what cells predominate the early stage and the later stage?

A

Early Stage = Neutrophils

Later Stage = Monocytes

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13
Q

What are the steps of phagocytosis?

A
  1. Recognition and attachment of the particle
  2. Engulfment
  3. Killing or Degradation
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14
Q

What is the intracellular destruction of microbes and debris caused by?

A
  1. Reactive Oxygen Species
  2. Reactive Nitrogen Species
  3. Lysosomal Enzymes
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15
Q

What are the chemical mediators of inflammation and what do they do?

A
  • Histamine
    • Vasodilation
  • Serotonin
    • Similar to histamine, released from platelets as they aggregate
  • Complement
    • Increase vascular permeability; C5a also aids in chemotaxis
  • Activated Hageman Factor (Factor XIIa)
    • Initiates clotting system
  • Prostaglandins
    • Contribute to pain and fever
  • Cytokines
    • Modulate a variety of immune pathways
  • Free Radicals
    • Account for much of tissue injury
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16
Q

Serous inflammation forms what?

A

Effusions

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17
Q

Fibronous inflammation forms what?

A

Fibronous exudates

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18
Q

Suppurative (purulent) inflammation forms what?

A

Pus

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19
Q

Ulcerations are made up of what 4 parts?

A
  1. Necrosis
  2. Acute and/or Chronic Inflammation
  3. Granulation Tissue
  4. Scar
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20
Q

What is chronic inflammation?

A

A response of prolonged duration (weeks or months) in which inflammation, tissue injury, and attempts to repair coexist, in varying combinations

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21
Q

What are the general causes of chronic inflammation?

A
  1. Persistent infections
  2. Hypersensitivity diseases
  3. Prolonged exposure to toxic agents
    1. Exogenous or endogenous
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22
Q

What are the morphological features of chronic inflammation?

A
  1. Mononuclear cells in inflammatory infiltrate
  2. Tissue destruction
  3. Healing/scarring
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23
Q

What are the dominant cells in most chronic inflammatory?

A

Macrophages

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24
Q

What is granulomatous inflammation?

A

A form of chronic inflammation chacterized by collections of activated macrophages, often with T lymphocytes, and sometimes associated with central necrosis

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25
Q

What are the two major types of granulomatous inflammation?

A
  1. Foreign Body
    1. Incited by relatively inert foreign bodies, in the absence of T cell-mediated immune responses
  2. Immune
    1. Agents capable of inducing a persistent T-cell mediated immune response
    2. Produces granulomas usually
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26
Q

What is the morphology of necrotizing (caseating) granulomas?

A
  1. Amorphous
  2. Structurless
  3. Eosinophilic
  4. Granular debris
  5. Complete loss of cellular details
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27
Q

Whatj are the systemic effects of inflammation?

A
  1. Fever
    1. Cytokines (TNF, IL-1) stimulate production of prostaglandins in hypothalamus
  2. Production of acute-phase proteins
    1. C-reactive protein, others; synthesis stimulated by cytokines (mainly IL-6) acting on liver cells
  3. Leukocytosis
    1. Cytokines stimulate production of leukocytes from precursors in the bone marrow
  4. Septic shock
    1. Fall in blood pressure, disseminated intravascule coagulation, metabolic abnormalites; induced by high levels of TNF and other cytokines
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28
Q

What are hemodynamics?

A

Factors that influence how blood moves

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29
Q

What is hemostasis?

A

Factors that influence how blood clots

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30
Q

What is edema caused by?

A

Increased hydrostatic pressure or reduced plasma protein

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31
Q

What physiologic events can cause edema?

A
  • Increased Hydrostatic Pressure
    • Heart failure, Ascites, Venous Obstructions
  • Hypoproteinemia
    • Nephrotic syndrome, Liver cirrhosis, Malnutrition, Gastroenteropathy
  • Lymphatic Obstruction
    • Inflammation, Neoplasia, Post-surgiucal, Post-radiation
  • Hypernatremia
    • Excessive sal intake w/ renal insufficiency, Increased renal reabsorption of sodium
  • Inflammation
    • Infection
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32
Q

What is hyperemia?

A

Engorgement of tissue with oxygenated blood → red tissue caused by arterial dilation

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33
Q

What is congestion?

A

Engorgement of tissue with deoxygenated blood → dusky reddish-blue tissue caused by reduced outflow from tissue

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34
Q

A hemorrhage contained within tissue

A

Hematoma

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35
Q

A 1-2 mm hemorrhage

A

Petechiae

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36
Q

> or = 3mm hemorrhage

A

Purpura

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37
Q

Pathologic compression of an organ

A

Tamponade

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38
Q

What is primary hemostasis?

A

The formation of a platelet plug

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39
Q

What is secondary hemostasis?

A

Deposition of fibrin creating fibrin meshwork

40
Q

What is tertiary hemostasis?

A

Clot stabalization and resorption by t-PA to limit clotting to the site of injury

41
Q

What are the steps of hemostasis?

A
  1. Vasoconstriction
  2. Primary Hemostasis
  3. Secondary Hemostasis
  4. Tertiary Hemostasis
42
Q

What is the purpose of vasoconstriction in hemostasis?

A

It produces laminar flow that slams cellular components (platelets) into the endothelial cells

43
Q

During primary hemostasis what do platelets specifically bind to?

A

vWF and Collagen

44
Q

What happens to platelets once they bind to vWF or collagen?

A

They undergo a conformational change that is accompanied by alterations in the GpIIb-IIIa receptor, increasing its affinity for fibrinogen, and translocation of negatively charged phospholipids to the platelet surface

45
Q

What factors are involved in the common clotting pathway?

A

I, II, V, X (Paper Bills)

46
Q

What factors are involved in the intrinsic pathway?

A

VIII, IX, XI, XII

47
Q

Where does the coagulation cascade happen?

A

Cell surfaces

48
Q

What the the vitamin K-dependent factors?

A

X, IX, VII, II, Protein C, and Protein S (1972)

49
Q

Where are vitamin K dependent factors made?

A

Liver

50
Q

What do Vitamin K-Dependent factors need in order to bind phospholipids on endothelial cells?

A

Glutamic acid

51
Q

How does warfarin work?

A

Blocks a Vitamin K Reductase

  • Reduces the amount of Vitamin K available for the carboxylation of glutamic acid
52
Q

What is Disseminated Intravascular Coagulation?

A

An acute, subacute, or chronic thrombohemorrhagic disorder characterized by the excessive activation of coagulation forming a thrombi

53
Q

What two major mechanisms trigger disseminated intravascular coagulation?

A
  1. Release of tissue factor or other, poorly characterized procoagulants, into circulation
  2. Widspread injury to endothelial cells
54
Q

What is plasmin?

A

A product of the cleavage of plasminogen by Factor XII and Plasminogne that breaks down fibrin, interfering with polymerization of platelets forming the clot

55
Q

What are lines of Zahn?

A

Alternating layers of RBCs and pale platelet/fibrin deposits

Indicates thrombus has formed in flowing blood

56
Q

What is hypercoagulability also known as?

A

Thrombophilia

  • Primary is genetic
    • Most common are point mutations in Factor V (Leiden mutation) and prothrombin (prothrombin mutation) genes
  • Secondary is acquired
57
Q

Unfractionated heparin may cause what?

A

Thrombocytopenia

58
Q

What is an embolus?

A

A detached intravascular solid, liquid, or gaseous mass carried by the blood to a distant site

59
Q

What is a saddle embolus?

A

A large embolus that occludes the main pulmonary artery, straddling the bifurcation

60
Q

What are the common embolic diseases?

A
  1. Pulmonary embolism
  2. Fat embolism
  3. Bone Marrow embolism
  4. Air embolism (Decompression sickness)
  5. Amniotic Fluid embolism
61
Q

What primary abnormalities lead to thrombosis?

A
  1. Endothelial injury
  2. Stasis or Turbulent Blood Flow
  3. Hypercoagulability
62
Q

What is an infarct?

A

An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage

63
Q

What is shock?

A

A state in which (1) diminished cardiac output or (2) reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia

64
Q

What are the general categories of shock?

A
  • Cardiogenic
    • MI, arrythmias, tamponade, PE
  • Hypovolemic
  • Septic
    • Overwhelming infections
    • Superantigens
65
Q

What are the stages of shock?

A
  1. Initial (Compensated)
    1. Tachycardia, cool clammy skin
  2. Progressive
    1. Tissue hypoperfusion
    2. Acidosis
  3. Irreversible
66
Q

What is hypertrophy?

A

Increase in cell size → increase in organ size

67
Q

What is hyperplasia?

A

Increase in number of cells → increase in organ size

68
Q

What is atrophy?

A

Cell shrinkage due to decreased protein synthesis or degradation

69
Q

What is metaplasia?

A

Conversion of one differentiated cell type to another, often due to repetitive injury (may lead to dysplasia and neoplasia)

70
Q

What are the different types of hyperplasia?

A
  1. Phyiologic
    1. Hormonal
    2. Compensatory - Liver regeneration
  2. Pathologic
    1. Excess estrogen
    2. Viral infections (HPV)
71
Q

What is necrosis?

A

Cell death due to irreversible cell injury denoted by cell membrane damage, swelling, and rupture of plasma membrane

Invokes an inflammatory response

72
Q

What is apoptosis?

A

Programmed cell death denoted by intact cell membranes and shrinkage

Does NOT invoke an inflammatory response

73
Q

What is the fundamental cause of cell necrosis and death?

A

Reduction of ATP levels

74
Q

What is the importance of the rupture of plasma membrane in necrosis?

A

Leakage of markers (Troponin, CK-MB in MI or AST/ALT in hepatocyte necrosis)

May elicit inflammatory reaction

75
Q

What are the types of tissue necrosis?

A
  1. Coagulative
    1. Ischemia/Infarct
  2. Liquefactive
    1. Abscess/bacterial infections
  3. Fat
    1. Acute pancreatitis
  4. Caseous
    1. TB
  5. Gangenous
  6. Fibrinoid
76
Q

What is the typical morphology of necrosis?

A
  • Hypereosinophilia (bright pink/red cytoplasm)
  • Pyknosis (shrunken dark nucleus)
  • Karyorrhexis (fragmentation of the nucleus)
  • Karyolysis (disintegration of the nucleus)
77
Q

What is liquefactive necrosis?

A

Enzymatic digestion of necrotic cells and removal, rather than scar formation

78
Q

Fat necrosis

A

Denoted by chalky white deposits (calcium soaps) in the tissue and amorphous, basophilic/purple deposits at the periphery of necrotic adipocytes

79
Q

Caseous Necrosis

A

Typical leasion of tuberculosis in which dead tissue persists indefinitely as amorphous, coarsely granular debris (Combo of coagulative and liquefactive)

80
Q

Gangrenous Necrosis

A

Cell death involving an entire region and multiple tissue planes

Loss of blood supply (coagulative)

Termed “wet gangrene” when complicated with infection (liquefactive necrosis)

81
Q

Fibrinoid Necrosis

A

Ag-Ab complexes combine with leaked fibrin from injured vessels

82
Q

Intrinsic (Mitochondrial) Pathway of Apoptosis

A
  • Caspase 9
  • Under tight control by Bcl2 family of proteins
  • Release of cytochrome c from mitochondrial membrane
83
Q

Extrinsic (Death Receptor) Pathway of Apoptosis

A
  • Caspase 8/10
  • Fas receptor mediated
  • Converges with mitochondrial pathway
84
Q

What is Oil Red-O Stain used for?

A

Stains steatosis/fatty change

85
Q

Hyaline Change

A

Descriptive histological term seen in the accumulation of extracellular and intracellular proteins

Appears glassy

86
Q

What is amyloidosis?

A

Extracellular deposition of amyloid, a substance formed by various types of protein

Can be: abnormal amount of normal protein or a normal amount of mutant protein

Creates a cross-ß-pleated sheet conformation

87
Q

Congo Red Stain

A

Used to stain amyloids, of which stain pink-red under LM and “green birefringence” under polarized light

88
Q

Histologically, what is the distinction between lipids and intracellular accumulations of glycogen?

A

Lipids appear very round and glycogen accumulations have rough edges

89
Q

Prussian Blue Stain

A

Used to stain iron in accumulations of hemosiderin

90
Q

Histologically what does calcification look like?

A

Calcium looks blueish under microscope

91
Q

What is cellular aging?

A

Progressive decline in viability and function due to accumulation of damage from exogenous insults and genetic abnormalities

92
Q

Red Top Test Tube

A

No Additive

Used for serology, blood bank, chemistry tests

93
Q

Blue Top Test Tube

A

Sodium Citrate

Used for coagulation tests

94
Q

Purple Top Test Tube

A

EDTA

Used for CBC, ammonia

95
Q

Green Top Test Tube

A

Heparin

Used for blood gases, chemistry tests

Block 5 (4 decks)

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