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D&D > Unit 2 Lectures > Flashcards

Unit 2 Lectures Flashcards

1
Q

What are the four cellular adaptations to stress?

A
  • hypertrophy (increased size of cells)
  • hyperplasia (increased number of cells)
  • atrophy (decreased size and functional capacity)
  • metaplasia (one cell type replaced by another)
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2
Q

What is the mechanism of atrophy?

A

decreased protein synthesis, increased protein degradation (ubiquitin-proteasome pathway)

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3
Q

What are the two types of reversible cell injury?

A
  • swelling: failure of energy-dependent ion pumps

- fatty changes: accumulation of lipid vacuoles due to increased synthesis of fatty acids

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4
Q

Accumulation of lipid in hepatocytes is a sign of (reversible/irreversible) injury and is (specific/non-specific)

A

reversible, non-specific

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5
Q

intracellular changes associated with reversible cell injury

A
  • plasma membrane alterations
  • mitochondrial changes
  • dilation of ER with detachment of ribosomes
  • chromatin clumping
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6
Q

What are two types of irreversible cell injury?

A
  • apoptosis

- necrosis

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7
Q

During irreversible cell injury, there are increased ____________ and decreased ___________ in the cytoplasm (cell types)

A

eosinophilia, basophils

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8
Q

pyknosis

A
  • nuclear shrinkage (DNA condenses)

- increased basophilia

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9
Q

karyorrhexis

A

pyknotic nucleus fragments

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10
Q

karyolysis

A

dissolution of nucleus (basophils fade, breakdown of denatured chromatin)

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11
Q

In an H&E stain, nucleic acids stain _________ using a ______ dye and ____________ stain _________

A
  • blue, basic (nucleic acids are acidic)

- eosinophils, pink (eosinophils are basic)

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12
Q

coagulative necrosis

A
  • tissue architecture preserved for several days (due to structural damage)
  • tissue appears pale
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13
Q

___________ necrosis is typically seen in hearts following MI (characteristic of infarcts)

A

coagulative

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14
Q

Bacterial infections and hypoxia in the CNS often lead to ____________

A

liquefactive necrosis

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15
Q

In liquefactive necrosis, microbes (bacterial, fungal) stimulate the accumulation of __________ cells and ___________ digest the tissue

A

inflammatory, leukocyte enzymes

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16
Q

What type of necrosis is characteristic of TB?

A

caseous

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17
Q

_____________ is characteristic of caseous necrosis

A

granulomatous inflammation

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18
Q

What is a histiocyte?

A

a macrophage (giant cell with lots of nuclei)

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19
Q

Fat necrosis is typically seen following what events?

A

acute pancreatitis, trauma

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20
Q

____________ is an immune reaction in which complexes of antigens and antibodies are deposited in the walls of arteries

A

fibrinoid necrosis

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21
Q

What type of necrosis is seen in vasculitis?

A

fibrinoid

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22
Q

If you disrupt the Ca2+ gradient, you get a(n) (influx/efflux) of Ca2+, leading to ____________

A

influx, decreased ATP (nuclear damage)

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23
Q

What are the two major pathways for cell injury by free radicals?

A
  • redox reactions during mitochondrial respiration (normal)

- phagocytic leukocytes

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24
Q

What can assist with removal of ROS? (3)

A
  • SOD
  • glutathione peroxidase
  • catalase
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25
Q

What are caspases?

A

cysteine proteases that cleave proteins after aspartic residue (in apoptosis)

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26
Q

What are the two main pathways of apoptosis?

A
  • mitochondrial (intrinsic)

- death receptor (extrinsic)

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27
Q

The initiator caspase for the mitochondrial pathway is caspase ___ and the caspase for the death receptor pathway is ___

A

9, 8

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28
Q

What is autophagy?

A

cell eats its own contents

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29
Q

What are the 4 main pathways of intracellular accumulation?

A
  • inadequate removal
  • failure to degrade
  • accumulation of abnormal endogenous substance
  • accumulation of abnormal exogenous substance
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30
Q

Describe the difference in cellular infiltrate between acute and chronic inflammation

A

acute: neutrophils
chronic: monocytes, macrophages, lymphocytes

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31
Q

stimuli for acute inflammation

A

infection, trauma, foreign material, immune reaction

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32
Q

What is an inflammasome?

A

a complex of proteins that mediates cellular responses (especially to dead/damaged cells but also microbes)

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33
Q

A drop in _________ can stimulate the inflammasome.

A

intracellular K+

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34
Q

Inflammasomes activate _______, which cleaves ________ to its active conformation, which leads to inflammation

A

caspase 1, IL-1B

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35
Q

Two vascular changes during acute inflammation are _________ and _________

A
  • increased vessel permeability

- increased blood flow

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36
Q

Endothelial cells _________ as a response to mediators

A

contract

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37
Q

What are some early and late mediators that affect acute inflammation?

A

early: histamine, bradykinin
late: IL-1, TNF

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38
Q 
Exudate vs. transudate:
common cause:
protein content: (increased/decreased)
cell content: (increased/decreased)
specific gravity: (high/low)
A 
Exudate vs. transudate:
common cause: increased vascular perm; altered intravascular pressure
protein content: increased; decreased
cell content: increased; decreased
specific gravity: high; low
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39
Q

In leukocyte recruitment, the endothelium is induced to move adhesion molecules to the surface by ________ and _________ (chemical mediators)

A

histamine (p-selectin)

IL-1 (E-selectin)

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40
Q

What are the two general ways for leukocytes to bind foreign material?

A
  • receptors for specific products of microbes or necrotic cells
  • receptors for opsonins
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41
Q

What are opsonins?

A

host proteins in the blood or produced locally that coat microbes (i.e.: IgG, C3b)

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42
Q

What types of cells are involved in chronic inflammation?

A
  • mononuclear cell infiltrate:
  • plasma cells
  • lymphocytes
  • monocytes
  • macrophages
  • eosinophils
  • mast cells
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43
Q

Settings characterized by chronic inflammation (3)

A
  • persistant infection
  • immune-mediated disease (autoimmune, allergy)
  • prolonged exposure to toxins
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44
Q

What is the main phagocyte in the adaptive immune response?

A

macrophages

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45
Q

What activates M1 macrophages?

A
  • endotoxin
  • INFgamma
  • foreign material
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46
Q

What activates M2 macrophages?

A
  • IL-4

- IL-13

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47
Q

What do M1 macrophages produce?

A
  • ROS
  • NO
  • lysosomal enzymes
  • proinflammatory cytokines
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48
Q

What do M2 macrophages produce?

A

Growth factors for…

  • new vessel growth
  • fibroblast activation
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49
Q

What are the main functions of M1 macrophages?

A
  • killing microbes

- chronic inflammation

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50
Q

What are the main functions of M2 macrophages?

A
  • tissue repair

- fibrosis

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51
Q

Th1 CD4+ T lymphocytes secrete _______, which activates the _________ pathway for macrophages

A

INFgamma, classical

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52
Q

Th2 CD4+ T lymphocytes secrete ________, which activates the _________ pathway for macrophages

A

IL-4, IL-5, IL-13, alternative (and activates eosinophils)

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53
Q

Th17 CD4+ T lymphocytes secrete ________, which recruits _________ and _________

A

IL-17, neutrophils, monocytes

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54
Q

Eosinophils are involved in ________ inflammation

A

chronic

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55
Q

What is granulomatous inflammation and when does it occur?

A
  • enlarged macrophages form a nodule, which is often surrounded by lymphocytes
  • chronic inflammation
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56
Q

What (3) mediators are responsible for the systemic effects of inflammation?

A

TNF, IL-1, IL-6

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57
Q

Vascular cells in the _______ are stimulated by _______ to produce __________ that lead to __________

A

hypothalamus, pyrogens, prostaglandins, fever (pyrexia)

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58
Q

What two proteins adhere to cell walls and act as opsonins?

A
  • C-reactive protein (CRP)

- serum amyloid A (SAA)

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59
Q

More leukocytes get released from the bone marrow during inflammation under the influence of ______ and _______

A

IL-1, TNF

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60
Q

Continued inflammation leads to increased production of __________ that increases bone marrow production of leukocytes

A

colony-stimulating factor

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61
Q

What is suggested by an increase in …?

  • neutrophils
  • lymphocytes
  • eosinophils
  • decreased leukocytes
A
  • neutrophils: bacterial
  • lymphocytes: viral
  • eosinophils: asthma, parasitic infection
  • decreased leukocytes: specific infection (i.e.: Typhoid)
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62
Q

Vasoactive amines are (cell-derived/plasma protein derived) mediators and include __________ and ____________

A

cell-derived; histamine and serotonin

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63
Q

What type of cells release histamine?

A

mast cells

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64
Q

Serotonin is found in _________ and is important in (vasodilation/vasoconstriction)

A

platelets, vasoconstriction

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65
Q

What are some sources of arachidonic acid?

A

leukocytes, mast cells, endothelium, platelets

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66
Q

What are the two pathways along which arachidonic acid is produced?

A

cyclooxygenase: prostaglandins, thromboxanes
lipoxygenase: leukotrienes, lipoxins

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67
Q

NSAIDs block _______________

A

cyclooxygenase

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68
Q

Glucocorticoids block ___________

A

phospholipase A2

69
Q

Leukotrienes mediate ___________

A

inflammation

70
Q

Lipoxins antagonize ___________ and are ___________

A

leukotrienes, anti-inflammatory

71
Q

What are some functions of platelet-activating factors?

A
  • platelet aggregation
  • vasodilation
  • vascular permeability
  • bronchoconstriction
72
Q

TNF and IL-1 are examples of ___________

A

cytokines

73
Q

TNF and IL-1 cause _____________

A

endothelial activation (leukocyte binding and recruitment)

74
Q

INFgamma stimulates…

A

classical M1 macrophage activation

75
Q

IL-12 stimulates…

A

growth and function of T cells

76
Q

ROS are released from … (2)

A
  • activated neutrophils

- macrophages

77
Q

What are some of the roles of NO?

A
  • free radical that kills microbes
  • mediates vasodilation
  • antagonizes platelet activation
  • reduces leukocyte recruitment
78
Q

alpha-1-antitrypsin

A

-protease inhibitor (neutralizes proteases that are active outside the cell, limits damage to host tissue)

79
Q

Neuropeptides can initiate __________

A

inflammation

80
Q

Substance P is an example of a ____________

A

neuropeptide (initiates inflammation)

81
Q

T/F: Complement is systemically in circulation

A

true

82
Q

What are the results of activated complement…?

  • C3a, C5a
  • C5a
  • C3a, C4a, C5a
  • C3b
  • the MAC
A
  • C3a, C5a: increase vascular permeability (histamine release)
  • C5a: AA metabolism
  • C3a, C4a, C5a: activate leukocytes
  • C3b: enhanced phagocytosis
  • the MAC: creates pores that violate bacterial membrane
83
Q

Factor ___ is an important clotting factor that activates the _______ system

A

XII, clotting

84
Q

What are some anti-inflammatory mediators?

A
  • lipoxins (antagonize leukotrienes)
  • C1 inhibitor (complement)
  • IL-10 (downregulates macrophages)
  • TGFbeta (promotes fibrosis)
85
Q

What are labile tissues?

A

tissues that are continuously dividing

86
Q

What are the two characteristics of stem cells?

A
  • self-renewal

- asymmetric replication

87
Q

Are adult stem cells more or less undifferentiated than embryonic stem cells?

A

less undifferentiated

88
Q

What are some roles of the ECM in tissue repair?

A
  • proliferation
  • differentiation and movement of cells
  • substrate for cell adhesion and migration
  • reservoir for growth factors
89
Q

What are the 3 components of the ECM?

A
  • fibrous structural proteins (collagen, elastins)
  • water-hydrated gels (proteoglycans, hyaluronan)
  • adhesive glycoproteins
90
Q

T/F: If the ECM is damaged, repair can only be accomplished by tissue regeneration

A

true

91
Q

What organ has the most robust regenerative capacity?

A

liver

92
Q

_______% of the liver can be removed in living-donor transplant

A

40-60%

93
Q

In angiogenesis, increased permeability is induced by ________

A

VEGF

94
Q

What are some steps in angiogenesis?

A
  • periocytes detach
  • degradation of basement membrane
  • recruitment of periendothelial cells to form mature vessels
95
Q

What are the main growth factors that orchestrate deposition of ECM proteins during tissue repair?

A

PDGF, FGF2, TGFbeta (come from M2 macrophages)

96
Q

____________ accomplish the degradation of collagens and other ECM components (remodeling)

A

matrix metalloproteases

97
Q

What are some systemic factors that influence tissue repair?

A
  • nutritional: impair collagen synthesis
  • metabolic: delay repair
  • vascular: ischemia, venous drainage
98
Q

A ___________ is a hypertrophic scar that does not regress

A

keloid

99
Q

What is first intention (the principle mechanism of tissue repair)?

A

epithelial regeneration

100
Q

Suture wound strength is ____% of normal skin. When sutures are removed, strength is _____%. After 3+ months, strength is _____%

A

70%, 10%, 70-80%

101
Q

A transudate has __________ hydrostatic pressure and __________ oncotic pressure

A

increased, reduced

102
Q

An exudate has _________ vascular permeability

A

increased

103
Q

The specific gravity of a transudate is (higher/lower) than that of an exudate

A

lower

104
Q

The total protein concentration of a transudate is (higher/lower) than that of an exudate

A

lower

105
Q

The protein: fluid/serum ratio of a transudate is (higher/lower) than that of an exudate

A

lower

106
Q

The LDH: fluid/serum ratio of a transudate is (higher/lower) than that of an exudate

A

lower

107
Q

The glucose: fluid/serum ratio of a transudate is (higher/lower) than that of an exudate

A

higher

108
Q

There are (more/less) WBCs in a transudate compared to an exudate

A

less

109
Q

What is Virchow’s triad?

A
  • endothelial injury (hypercholesterolemia, inflammation)
  • abnormal blood flow (stasis, turbulence)
  • hypercoagulability (inherited, acquired)
110
Q

The most common type of embolus is __________

A

Deep Vein Thrombosis (affects lungs)

111
Q

Fat/bone marrow emboli come from __________ and affect ___________

A

long bone fractures, lungs

112
Q

10% of maternal deaths occur due to ____________

A

amniotic fluid emboli

113
Q

Atheroemboli are caused by __________

A

atherosclerotic plaque

114
Q

What is a DIC?

A

disseminated intravascular coagulation (thrombosis and hemorrhage occurring simultaneously)

115
Q

What is an infarction?

A

tissue death (necrosis) caused by vessel occlusion

116
Q

organs with “white” infarction

A

heart, kidney, spleen

117
Q

organs with “red” infarction

A

lung, liver, intestine

118
Q

What is cardiogenic shock?

A

myocardial pump failure (myocardial damage, extrinsic compression, outflow obstruction)

119
Q

What is hypovolemic shock?

A

low blood volume (severe dehydration, burns, hemorrhage)

120
Q

What is the difference between a carcinoma and adenocarcinoma?

A

carcinoma: epithelial tissue
adenocarcinoma: glandular structure

121
Q

characteristics of cancer pathobiology

A
  • evading apoptosis
  • self-sufficiency in growth signals
  • insensitivity to anti-growth signals
  • sustained angiogenesis
  • limitless replicative potential
  • tissue invasion and metastasis
122
Q

What are the physiologic effects of cortisol?

  • carbohydrates:
  • protein:
  • fat:
A
  • carbohydrates: gluconeogenesis - increased blood glucose
  • protein: decreased protein synthesis - increased AA to glucose
  • fat: lipolysis - increased free fatty acids
123
Q

Aldosterone is a __________ that leads to ________

A

mineralocorticoid, increased Na+ resorption (increased BP)

124
Q

Cortisol needs a _____ group at the 11 position

A

-OH

125
Q

Why do prednisone and cortisone have no topical activity?

A

they have to go through the liver to convert ketone to hydroxyl

126
Q

Where does cortisone get activated to cortisol (or prednisone to prednisolone)?

A

liver

127
Q

Where does cortisol (or prednisolone) get inactivated?

A

kidney

128
Q

How can you treat a mother with GCs without an effect on the fetus?

A

placental enzyme converts active drug to prodrug

129
Q

Ratio of glucocorticoid: mineralocorticoid action:

  • cortisol:
  • prednisone:
  • methylprednisolone:
A
  • cortisol: [1:1]
  • prednisone: [5:1]
  • methylprednisolone: minimal mineralocorticoid action
130
Q

What is the most potent anti-inflammatory agent?

A

dexamethasone

131
Q

T/F: glucocorticoid side effects are unavoidable

A

true

132
Q

The risk of osteoporosis from using large cumulative doses of GCs can be decreased by using __________

A

bisphosphonates

133
Q

The use of ___________ can reduce peptic ulcers resulting from large cumulative doses of GCs

A

antacids

134
Q

Substance P mediates __________ and causes ____________

A

inflammation, pain

135
Q

Platelet-activating factor has (local/systemic) effects

A

local (platelet activating, vasoconstriction, bronchospasms, chemotaxis

136
Q

Bradykinin is synthesized by the ________ and activated at its site of action

A

liver

137
Q

Rheumatoid arthritis: transudate or exudate?

A

exudate

138
Q

INFgamma is associated with (acute/chronic) inflammation

A

chronic (M1 activation)

139
Q

IL-13 and IL-4 increase production of ______

A

TGFbeta

140
Q

Two examples of acute inflammatory cytokines are…

A

TNF, IL-2

141
Q

Two examples of chronic inflammatory cytokines are…

A

INFgamma, IL-12

142
Q

Delay-activating factor and factor H limit _____ in the complement system

A

C3/C5 convertase formation

143
Q

Initial scars are made of type ____ collagen and scar remodeling consists of type ____ collagen

A

III, I

144
Q

COX__ is constitutively expressed almost anywhere and COX__ is induced by inflammatory cytokines

A

1, 2

145
Q

At low doses, aspirin is COX__ selective and can exert a _________________ effect.

A

COX-1 selective; anti-thrombotic, cardioprotective

146
Q

Aspirin has no effect if taken after ____________

A

ibuprofen (ibuprofen preferentially binds the COX’s, making aspirin incapable of binding them)

147
Q

What is hyperemia?

A

an active increase in blood flow due to arteriolar dilation

148
Q

Examples of transudates include…

A
  • heart failure
  • fluid overload
  • liver disease
  • venous obstruction
149
Q

Examples of exudates include…

A
  • inflammation
  • toxins
  • burns
150
Q

_____________ cells are responsible for vasodilation

A

endothelial cells (contraction)

151
Q

Chololithiasis vs. cholecystitis

A

chololithiasis: hardened deposit within the fluid of the gall bladder
cholecystitis: inflammation of the gall bladder

152
Q

What are hemorrhoids?

A

swollen and inflamed veins in the rectum and anus that cause discomfort and bleed

153
Q

Bronchus undergoes a _________ to __________ metaplasia and the esophagus undergoes a ____________ to __________ metaplasia

A

columnar, squamous

squamous, columnar

154
Q

(arterial/venous) emboli affect the lungs

A

venous

155
Q

A type of carcinoma with central necrosis and keratin pearls is _______________

A

squamous cell carcinoma

156
Q

What types of carcinoma attempts to form glands and occurs in never smokers?

A

adenocarcinoma

157
Q

Substance P is associated with … (3)

A
  • pain
  • fever
  • acute phase reaction
158
Q

C5 is associated with activation of coagulation factor ____

A

XII

159
Q

Rheumatoid arthritis manifests with a ____________

A

an exudate

160
Q

Are lipoxins chemotactic?

A

no

161
Q

IL-4 and IL-13 associating with macrophages is likely to induce increased _________ production

A

TGFbeta

162
Q

Neovascularization, fibroblast proliferation, and macrophages constitute _________ tissue response

A

granulation

163
Q

What are some common causes for defective leukocyte function?

A
  • acquired: chemo, diabetes

- inborn genetic defect

164
Q

What do macrophages do during chronic inflammation?

A
  • ingest microbes
  • initiate tissue repair
  • secrete inflammatory mediators
  • present antigens to adaptive immune system
165
Q

Aspirin is COX__ selective at low doses

A

COX1 (cardioprotective)

166
Q

effusion

A

extravasation of fluid into (usually natural) spaces

167
Q

Can a red or white infarct be re-perfused?

A

red

168
Q

cavitary

A

direct seeding of body cavities or surface (i.e.: ovarian cancer)

D&D (3 decks)

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