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Fundamentals > Pathology > Flashcards

Pathology Flashcards

1
Q

what is hypertrophy?

A

an increase in cell size

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2
Q

what is hyperplasia?

A

increase in cell number

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3
Q

what is atrophy?

A

decrease in cell size and/or number; survival is maintained by decrease in function

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4
Q

what is metaplasia?

A

replacement of one cell type by another

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5
Q

important characteristics of necrosis?

A
  • always pathologic
  • have nuclear degradation
  • disruption of plasma membrane
  • digestive enzyme leakage
  • cellular swelling
  • inflammation
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6
Q

important characteristics of apoptosis?

A
  • can be normal or pathologic
  • nuclear shrinkage and fragmentation into nucleosome size paritcles
  • plasma membrane stays intact
  • no leakage of enzymes and no inflammation
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7
Q

what is coagulative necrosis?

A

protein denaturation but the cell and tissue framework remains

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8
Q

when do you often see coagulative necrosis?

A

in hypoxia or ischemia

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9
Q

what is liquefactive necrosis?

A

complete digestion of tissue - becomes liquid mass

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10
Q

when do you often see liquefactive necrosis?

A

in bacterial infections and hypoxia of CNS

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11
Q

what is gangrenous necrosis?

A

when coagulative necrosis occurs in the extremities, called wet gangrene when accompanied with bacterial infection

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12
Q

what is caseous necrosis?

A

a type of necrosis where it looks cheesy - it is friable and proteinaceous

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13
Q

when do you see caseous necrosis?

A

tuberculosis

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14
Q

what is fat necrosis?

A

when lipases spill out into adipose tissue and the fat cells are liquefied - the fatty acids are released and combine with calcium to produce chalky areas

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15
Q

what is fibrinoid necrosis?

A

when proteins (ab/antigens often) are deposited in blood vessels

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16
Q

what are the two pathways for apoptosis?

A

mitochondrial and death receptor pathways

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17
Q

describe the mitochondrial pathway for apoptosis.

A

cellular stress causes BCL proteins to be activated, they activate Bax and Bak which insert into mitochondrial membrane and create pores, cytochrome C is released and activates caspases which cause apoptosis

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18
Q

describe the death receptor pathway of apoptosis.

A

the plasma membrane death receptor binds with its ligand (TNF, Fas receptors) and this binding signals caspases that control apoptosis

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19
Q

what are some morphological features of reversible cell injury?

A

fatty change (lipid vacuoles in cytoplasm) and cellular swelling

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20
Q

what can fatty change be a sign of?

A

alcohol abuse, diabetes

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21
Q

what is lipofuscin?

A

it is the “wear and tear” pigment common in aging - it is a sign of free-radical injury and lipid peroxidation; it’s yellow-brown

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22
Q

what is hemosiderin?

A

it’s a golden yellow-brown pigment that is a storage form of iron

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23
Q

what is dystrophic calcification?

A

calcium deposition when there is necrosis, can occur in normal calcium metabolic situations)

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24
Q

what is metastic calcification?

A

this occurs when calcium metabolism is out of balance - usually with hypercalcemia (no necrosis)

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25
Q

what are the key events of acute inflammation?

A

vascular dilation, exudation, leukocyte migration and accumulation

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26
Q

describe histamine’s function as a mediator of acute inflammation.

A

histamine is made in mast cells, platelets, and basophils; it causes increased vascular permeability, vasodilation, and it activates endothelial cells to prep for leukocyte migration

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27
Q

describe serotonin’s function as a mediator of acute inflammation.

A

serotonin is made in platelets and it functions to increase vascular permeability and vasodilate

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28
Q

describe thromboxane’s function as a mediator of acute inflammation.

A

thromboxane is made by the cyclooxygenase pathway and it functions to vasoconstrict and cause platelet aggregation

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29
Q

describe prostacyclin’s function as a mediator of acute inflammation.

A

prostacyclin is made by the cyclooxygenase pathway and it funcitons to vasodilate and inhibit platelet aggegation.

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30
Q

describe prostaglandin’s function as a mediator in acute inflammation.

A

prostaglandin is made by the cyclooxygenase pathway and it functions to increase vascular permeability, vasodilate, cause fever.

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31
Q

describe leukotriene B’s function as a mediator of acute inflammation

A

a product of the lipoxygenase pathway (5-LO)and it functions as a chemotactic susbtance for neutrophils (and can also activate them)

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32
Q

describe the functions of leukotrienes C, D, E in acute inflammation

A

these are products of the lipoxygenase pathway (5-LO) and their function is to cause neutrophil activation and adhesion as well as bronchospasm and increased vascular permeability and vasodilation

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33
Q

describe the funciton of lipoxin in acute inflammation

A

this is a product of the lipoxygenase pathway (12-LO) and it functions to inhibit neutrophil adhesion and chemotaxis (anti-inflammatory)

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34
Q

describe the function of platelet activating factor in acute inflammation

A

made by platelets, mast cells, endothelial cells, and leukocytes; functions to

  • bronchoconstriction
  • oxidative burst
  • vascular permeability and vasodilation
  • leukocytes adhesion
  • chemotaxis
  • platelet aggregation
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35
Q

what do TNF/IL-1 do locally?

A

they increase endothelial adhesion molecule expression, they increase vascular permeability and vasodilation, they activate leukocytes, and cause production of chemokines, cause fibroblast proliferation and collagen synthesis

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36
Q

what do TNF/IL-1 do systemically?

A

cause fever, leukocytosis, acute phase response, decrease appetite, increase sleep need

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37
Q

what cells do CXC chemokines act on?

A

neutrophils

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38
Q

what cells do CC chemokines act on?

A

basophils, eosinophils, lymphocytes, and monocytes

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39
Q

what cells do C chemokines act on?

A

lymphocytes

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40
Q

what cells do CX3C chemokines act on

A

mononuclear cells

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41
Q

describe the function of reactive oxygen species in inflammation.

A

they are made by NADPH oxidase in leukocytes (among other cells) and they function to destroy microbes and can even cause endothelial injury to increase vascular permeability

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42
Q

what antioxidants can take care of ROSs?

A

glutathione, SOD, and catalase

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43
Q

what is the role of nitric oxide in acute inflammation?

A

NO is made in neural cells (nNOS), endothelial cell (eNOS) where it is constituitively being made and in macrophages (iNOS) where it is induced by IL-1, TNF, IFN-gamma, and endotoxin
it is made by NO synthase from L-arginine

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44
Q

what mediators stimulate the production of NO is macrophages?

A

IL-1, TNF, IFN-gamma, and endotoxin

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45
Q

what are the three types of proteases present in the large azurpohilic granules of neutrophils

A

acid proteases, neutral proteases, anti-proteases

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46
Q

what are three complement inhibitors?

A

C1 inhibitor, decay accelerating factor and CD59 which prevent formation of C3 convertase

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47
Q

how is bradykinin made and what does it do?

A

kininogen is cleaved by kallikrein to make bradykinin which functions to increase vascular permeability, cause smooth muscle contraction and vasodilation

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48
Q

what are three ways to increase vascular permeability?

A
  • intracellular gaps form when endothelial cells are signalled
  • cell injury from external
  • intential cell injury from ROS/NO
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49
Q

what are the protein interactions responsible for leukocyte rolling?

A

the sialyated-lewis glycoproteins on the leukocytes bind to E and P selectins on endothelial cells

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50
Q

what stimulates expression of E selectins on leukoctyes?

A

TNF and IL-1 from macrophages

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51
Q

what stimulates expression of P selectins on leukocytes?

A

histamine!

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52
Q

what are the protein interactions that are responsible for tight adhesion?

A

integrins on the leukocyte bind to ICAM-1 and VCAM-1 which are induced by TNF

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53
Q

what protein is responsible for diapedesis?

A

PECAM-1 driven by chemokines

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54
Q

what are the four ways leukocytes are activated?

A
  1. chemokines binding to GPCRs
  2. microbes binding to toll-like receptors
  3. cytokines binding to receptors
  4. microbes binding to phagocytic receptors
55
Q

what are the hallmarks of chronic inflammation?

A

prolonged duration, lymphocytes, macrophages abundant, healing and inflammation occurring in unison, fewer local and systemic signs

56
Q

what are the two ways that macrophages can become activated?

A 
classical pathways (pro-inflammatory) via IFN-gamma
 and the alternative pathway (anti-inflammatory) via IL-14, 3
57
Q

which interleukins activate T lymphocytes

A

IL12, IL6, and IL23 from macrophages

58
Q

what are eosinophils activated by?

A

eotaxin - a CC chemokine

59
Q

how do eosionophils combat their targets?

A

they participate in allergic rxns and are activated by parasites - they use MBP (major basic proteins) that are toxic to parasites (but also lyses mammalian cells)

60
Q

what is serous inflammation?

A

characterized by transudate (protein poor fluid) building up in spaces created by cell injury or in body cavities lined by thin layers of tissue

61
Q

what is fibrinous inflammation

A

when vascular permeability is so great that fibrinogen gets though and fibrin is deposited in the tissues (exudate obvs); can lead to scarring

62
Q

what is suppurative inflammation?

A

characteristics include protein rich exudate that often has dead leukocytes and cell debris in it - PUS

63
Q

what is the most common cause of suppurative inflammation?

A

bacterial infections that cause liquefactive necrosis

64
Q

what is an abscess?

A

it is a type of suppurative inflammation in which the pus is in a localized area like a tissue, organ, or confined space

65
Q

what is an ulceration?

A

removal of the overlying epithelium of a tissue by necrosis and sloughing off of dead tissue - this happens when necrosis occurs near the surface of a tissue

66
Q

what is granulomatous inflammation?

A

characterized by focal accumulations of epitheliod macrophages that often fuse to form giant cells; have a lymphocyte collar around accumulation, can have CASEOUS necrosis in the center

67
Q

what kind of necrosis is typically seen with granulomatous inflammation?

A

caseous necrosis

68
Q

what is fibrosis?

A

deposition of collagen as a consequence of chronic inflammation - provides structural strength and allows function

69
Q

what are periendothelial cells?

A

aka pericytes, these are contractile cells that surround the blood vessels - they migrate in at the end of angiogenesis

70
Q

what are MMPs?

A

these are matrix metallo-proteins and they are involved in ECM changes after scar formation

71
Q

what are some characteristics of granulation tissue?

A

proliferating fibroblasts and endothelium, highly vascularized loos connective tissue - edema; some leukocytes can remain

72
Q

what cell is most important in scar formation?

A

the macrophage - this cell directs angiogenesis and ECM deposition

73
Q

viral infections see the increase in which wbc?

A

lymphocytes!

74
Q

bacterial infections see the increase in which wbc?

A

neutrophils

75
Q

parasitic infections see the increase of which wbc?

A

eosinophils!

76
Q

what are some acute phase reaction proteins?

A

CRP, SAA, and fibrinogen

77
Q

what do CRP and SAA do int he acute phase response?

A

they acts as opsonins and help fix the complment

78
Q

what does fibrinogen do in the acute phase response?

A

it causes RBCs to aggregate, which increases the erythrocyte sedimentation rate

79
Q

how do we get a fever?

A

pyrogens stimulate prostaglandin which increases cAMP

80
Q

what is the epidermal growth factor (EGF)?

A

it stimulates mitosis for keratinocytes and fibroblasts, important in granulation tissue

81
Q

what is the vascular endothelial growth factor?

A

mitogenic for endothelial cells and causes increased vascular permeability

82
Q

what is the platelet derived growth factor?

A

many function but it is chemotactic for many cells, it acitvates lots of cell, stimulates production of ECM components (MMPs, fibronectin, and HA) and it stimulates angiogenesis

83
Q

what are the two ways fluid dynamics can cause edema?

A

increased hydrostatic pressure on the arterial side of capillaries and blockage of blood outflow on the venous side of capillaries

84
Q

what is hyperemia?

A

it is an active process due to augmented blood flow from arteriolar dilation (like in exercise or inflammation)

85
Q

what is congestion?

A

it is a passive process caused by impaired outflow and subsequent capillary engorgement

86
Q

what is acute congestion?

A

vessels simply become distended and organs become hyperemic

87
Q

what is chronic congestion?

A

it is when capillaries may rupture, may get a hemorrhage and may get hemosiderin-laden macrophages; this can happen in the lungs and liver (nutmeg liver) causing organ atrophy or death with fibrosis

88
Q

what is transudate?

A

low protein content fluid; specific gravity <1.020

89
Q

what is exudate?

A

high protein content fluid; specific gravity >1.020

90
Q

what are three types of exudate?

A

suppurative (pus), serosanguinous (blood-tinged), hemorrhagic (bloody)

91
Q

what is pleural effusion?

A

edema between the lungs and the chest cavity (aka hydrothorax, pyothorax is pus, hemothorax is bloody)

92
Q

what is anasarca?

A

whole body edema (characteristic of renal disease)

93
Q

what is ascites?

A

fluid in the peritoneal cavity

94
Q

what are petechiae?

A

small, 1-2mm hemorrhages in the skin, mucous membranes or serosal surfaces

95
Q

what are purpura?

A

hemorrhages greater than 2mm (due to trauma, local vascular inflammation)

96
Q

what are ecchymoses?

A

1-2cm subcutaneous hematoma associated with trauma or bleeding disorders

97
Q

what does endothelin do?

A

it works with the “reflex neurogenic mechanisms” to cause transient vasoconstriction after endothelial injury

98
Q

what does vWF do and where is it made?

A

vWF allows platelets to bind to it via the GPIb receptor to begin to lay them over an injured area; it is made by endothelial cells

99
Q

what is in the alpha granules of platelets?

A

P-selectin so that more platelets can attach, growth factors, and coagulation factors

100
Q

what is in the delta (dense) granules of platelets?

A

ADP, Ca2+, and vasoactive amines

101
Q

what does ADP do in coagulation?

A

ADP causes receptors on the platelets to change conformation (GPIIb-IIa) which allows fibrinogen to attach to the platelets

102
Q

what does the phospholipid complex on platelets do?

A

it acts as a location for calcium and coagulation factors to go in order to start the coagulation cascade

103
Q

how is the intrinsic pathway of the coagulation cascade initiated?

A

using Hageman factor (XII)

104
Q

how is the extrinsic pathway of the coagulation pathway initiated?

A

tissue factor that is released by endothelial cells (stimulated to be made by TNF/IL-1 or endotoxin)

105
Q

in the extrinsic pathway what factor does tissue factor activate?

A

factor VII

106
Q

what do both the intrinsic and extrinsic pathways activate as they converge?

A

thrombin

107
Q

what does thrombin do?

A

thrombin converts the soluble fibrinogen to the insoluble fibrin - forming the secondary platelet plug

108
Q

name the anti-coagulation factors (there are 11!)

A

antithrombin, heparin, protein C, protein S, thrombomodulin, tissue factor pathway inhibitor, tissue plasminogen activator, urokinase, plasmin, prostacyclin, NO, adenosine phosphatase

109
Q

what does antithrombin do?

A

inhibits thrombin (so you don;t get fibrin production)

110
Q

what does heparin do?

A

activates antithrombin

111
Q

what do protein C and protein S do?

A

inactivate cascade factors

112
Q

what does thrombomodulin do?

A

binds to and changes thrombin which then activates protein C (get inactivation of cascade factors)

113
Q

what does tissue factor pathway inhibitor do?

A

it inactivates Xa and VIIa (tissue factor)

114
Q

what do tissue plasminogen activator and urokinase do?

A

make plasminogen into plasmin

115
Q

what does plasmin do?

A

breaks down fibrin

116
Q

what do prostacyclin and NO do?

A

inhibit platelet aggregation

117
Q

what does adenosine phosphatase do?

A

degrades ADP

118
Q

what type of environment do venous thrombi occur?

A

they occur at sites of stasis and are occlusive; most commonly they affect the lower extremity veins

119
Q

what type of environment do arterial thrombi occur in?

A

they occur at sites of endothelial injury or turbulence, they are nonocclusive (aka mural)

120
Q

what are the lines of Zahn?

A

pale layers of platelets and fibrin alternative with darker, erythrocyte-rich layers present in arterial thrombi

121
Q

where does venous thrombosis occur? and what does it lead to?

A

occurs in deep or superficial leg veins and can cause congestion and swelling (edema)

122
Q

what are two possible causes of arterial/cardiac thrombosis?

A

atherosclerosis and myocardial infarction

123
Q

what are consequences of arterial/cardiac thrombosis?

A

loss of blood supply/ischemic necrosis (coagulative)

124
Q

what are some heritable hypercoagulable states?

A

factor V gene mutations, deficiencies in antithrombin III, protein C, and protein S

125
Q

what is the factor V gene mutation?

A

it causes a hypercoagulability state in which factor V is resistant to being inactivated by protein C

126
Q

what are some acquired hypercoagulable states?

A

prolonged bed rest, tissue injury, cancer, HITS (heparin-induced thrombocytopenia), antiphospholipid antibody syndrome, drugs (estrogen), smoking

127
Q

what are some clinical warning signs to hypercoagulable states?

A

repeated miscarriages, stroke in young person, recurrent thrombosis/emboli, resistance to anticoagulation

128
Q

what is infarction?

A

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

129
Q

what is a red infarct?

A

it occurs in venous occlusion, loose tissues, tissues with dual blood supply, the gut, and sites of previous occlusion and necrosis where flow has been reestablish

130
Q

what is a white infarct?

A

it occurs in solid organs with end arterial blood

131
Q

what are factors that affect whether an infarction occurs?

A

what the vascular supply is like (dual supply is better), rate of occlusion development (slow is better), vulnerability of tissue to hypoxia (tissues that can last longer without oxygen are better - fibroblasts vs. neurons), and oxygen content of blood (higher is better)

132
Q

what is a pulmonary thromboembolism?

A

it is when one or more pulmonary arteries are blocked; often come from thromboses in the lower extremities

133
Q

what is disseminated intravascular coagulation?

A

this is when coagulative proteins become overactive; manifested by bleeding and thrombosis concurrently

Fundamentals (11 decks)

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