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Preventive And Social Medicine II > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the mechanism by wc the lesions are produced?

A

Pathogenesis

‘HOW’ of dse

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2
Q

What is the increase in cell SIZE that occurs in tissues incapable of cell division?

A

Hypertrophy

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3
Q

What can be the stimulus for hypertrophy?

A

Increase in fxnal demand

Increase in hormonal stimulation

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4
Q

Mechanism for hypertrophy

A

Increase cellular protein production

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5
Q

Hypertrophy examples in physiologic & pathologic

A

Physiologic: Gravid uterus, muscle of body builders
Pathologic: LVH

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6
Q

What is the increase in NUMBER of cells that occurs in tissues capable of cell division?

A

Hyperplasia

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7
Q

Stimulus of Hyperplasia

A

Hormonal or compensatory mechanism

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8
Q

Mechanism of Hyperplasia

A
  • Growth factor driven proliferation of mature cells

- Increase output of new cells from tissue stem

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9
Q

Examples of physiologic and pathologic hyperplasia

A

Physiologic: pubertal breast changes, liver regeneration
Pathologic: endometrial hyperplasia

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10
Q

What is the decrease in cells SIZE and NUMBER?

A

Atrophy

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11
Q

Stimulus of Atrophy

A
  • Decrease workload, denervation
  • Ischemia
  • Malnutrition
  • Loss of endocrine stimulation
  • Pressure
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12
Q

Mechanism of Atrophy

A
  • Decrease protein synthesis
  • Increase protein degradation
  • Autophagy
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13
Q

Examples of physiologic and pathologic atrophy

A

Physiologic: embryonal atrophy (notochord & thyroglossal duct)
Pathologic: senile atrophy of brain

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14
Q

What is a differentiated cell type replaced by another cell type?

A

Metaplasia

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15
Q

Stimulus and mechanism of metaplasia

A

Stress that leads to reprogramming of stem cells

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16
Q

Examples of metaplasia

A
  • Columnar to squamous: Vit A deficiency

- Squamous to columnar: Barrett’s esophagus

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17
Q

What happens during atrophy or loss of brain substance?

A

Narrow gyrus and widen sulci

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18
Q

What is defined as the effect of a variety of stresses d/t etiologic agents a cell encounters, wc result in changes in its internal and external environment?

A

Cell injury

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19
Q

What causes cell injury?

A

1) O2 deprivation (hypoxia) and Ischemia
2) Physical agents
3) Chemicals and drugs
4) Infectious/Microbial agents
5) Immunologic
6) Genetic derangements (mutate)
7) Nutritional derangements/imbalances

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20
Q

What are morphologic alterations in reversible cell injury?

A 
Cell swelling (eosinophilic)
Fatty change
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21
Q

Ultrastructure changes

A
  • Plasma mem alterations (bleb, blunt, loss microvilli)
  • Mitochondrial changes (swell, amorphous densities)
  • Dilation of ER (form myelin figures)
  • Nuclear alterations (disaggregation of granular & fibrillar)
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22
Q

What are the two processes underlying changes in necrosis?

A

Denaturation of proteins

Enzymatic digestion

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23
Q

Necrotic cells are more eosinophilic (pink) than

A

viable cells

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24
Q

What appears “glassy” homogenous, vacuolated cell membranes, fragmented?

A

Necrotic cell - it is mainly as a result of the loss of glycogen

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25
Q

What are dead cells that may be replaced by large, whorled phospholipid masses?

A

Myelin figures (seen in reversible injury)

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26
Q

What nuclear change is a small dense nucleus?

A

Pyknosis

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27
Q

What nuclear change is a faint dissolved nucleus?

A

Karyolysis

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28
Q

What nuclear change is a fragmented nucleus?

A

Karyorrhexis

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29
Q

What is the most common tissue pattern of necrosis?

A

Coagulative necrosis

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30
Q

Protein denaturation with preservation of cell & tissue framework

A

Coagulative necrosis

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31
Q

A. wedge-shaped kidney infarct (yellow)
B. loss of nuclei and an inflammatory infiltrate

“tombstone” appearance

A

Coagulative necrosis

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32
Q

Digestion of dead cells, resulting in the transformation of the tissue into a liquid viscous mass (pus)

A

Liquefactive necrosis

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33
Q

Localized bacterial infection (abscesses) and in the brian

A

Liquefactive necrosis

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34
Q

Autolysis or heterolysis predominates over protein denaturation

A

Liquefactive necrosis

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35
Q

What isn’t a pattern of cell death but a term commonly used in clinical practice?

A

Gangrenous necrosis

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36
Q

What type of gangrene is predominantly coagulative?

A

Dry gangrene

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37
Q

What type of gangrene is more liquefactive (w abscess)?

A

Wet gangrene

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38
Q

Tuberculous lesions

Soft, friable, cheese-like

A

Caseous necrosis

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39
Q

Microscopic: amorphous eosinophilic material w cell debris (fragments of nucleus and inflammatory cells)

Like homogeneous pink substance

A

Caseous necrosis

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40
Q

In fat necrosis, how does release of FA (wc attract Ca salts)then complex w Ca soaps (saponification) happen?

A

Lipase activation

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41
Q

What can be seen in pancreatitis?

A

Fat necrosis

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42
Q

Gross: white chalky areas (fat saponification)
Microscopic: vague cell outlines, Ca deposition

A

Fat necrosis

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43
Q

Necrosis: Immune rxns involving BV

A

Fibrinoid necrosis

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44
Q

Brain

A

Liquefactive

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45
Q

Heart, kidneys

A

Coagulative

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46
Q

Limb

A

Gangrenous

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47
Q

TB

A

Caseous

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48
Q

Vasculitis

A

Fibrinoid

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49
Q

What is the fundamental cause of necrotic cell death?

A

ATP depletion

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50
Q

What is the consequence of ischemic & toxic injury?

A

ATP depletion

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51
Q

In ATP depletion, what will reduced Na pump activity (dt hypoxia) then increase influx of Na, H2O and Ca cause?

A

Cell swelling

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52
Q

What happens when there is hypoxia?

A

Increase glycolysis then glycogen depletes, lactic acid increases and there’ll be intracellular acidosis

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53
Q

What is the consequence of increased cytosolic Ca, ROS and O2 deprivation?

A

Mitochondrial damage

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54
Q

Abn oxidative phosphorylation then formation of ROS leads to necrosis

A

Mitochondrial damage

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55
Q

What happens when Ischemia/toxins –> Ca influx + release of Ca from mitochondria and ER?

A
  • activates phospholipases –> degrades mem phospholipids (wc inc mem perm that leads to cell swelling or leakage of caspases)
  • activates proteases –> brks down mem and cytoske CHONs
  • activates ATPases –> ATP depletion
  • activates endonucleases –> chromatin fragmentation
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56
Q

What are important mediators of cell injury?

A

Ca ions

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57
Q

What is the most common type of injury?

A

Ischemic and hypoxic injury

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58
Q

What happens when there’s mechanical obstruction in the arteries?

A

Ischemia then reduce venous drainage, compromised delivery of substrates for glycolysis

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59
Q

What are the mechanisms of ischemic cell injury?

A

Sequence of events:

1Decreased O2 tension
2Loss of oxidative phosphorylation
3Decreasee prodxn of ATP
4Failure of Na pump –> loss of K –> influx of Na and water –> cell swell
5Ca influx
6Progressive glycogen loss, decreased CHON synthesis

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60
Q

What is the death of cells after bld flow resumes and is also associated w neutrophilic infiltration?

A

Ischemia-reperfusion injury

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61
Q

What are the mechanisms of ischemia-reperfusion injury?

A
  • inc generation of O2-derived free radicals
  • resulting inflammation and recruitment of PMNs
  • activation of complement
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62
Q

What is the difference between direct and indirect chemical injury?

A

Direct - bind to critical molecular component

Indirect - conversion to reactive toxic metabolites

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63
Q

Anti-apoptotic

A

BCL2
BCL-XL
MCL1

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64
Q

Pro-apoptotic

A

BAX

BAK

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65
Q

Sensors

A

BAD, BIM, BID, Puma, and Noxa

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66
Q

What is the activation of death receptors on the cell membrane (TNFR1 and Fas) called?

A

Extrinsic (Death Receptor) Pathway

- caspases 8 & 10

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67
Q

Initiator caspases –> executioner caspases –> nuclear fragmentation; endonuclease activation; brkdwn of cytoskeleton

A

Execution Phase

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68
Q

What are examples of apoptosis?

A 
Growth factor deprivation
DNA damage 
Protein misfolding
TNF family receptors
Cytotoxic T lymphocytes
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69
Q

What does necroptosis resemble?

A

Necrosis morphologically

Apoptosis mechanistically

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70
Q

What is the cause of necroptosis?

A

TNF and viral proteins

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71
Q

Necroptosis is caspase-independent and it activates

A

RIP1 and RIP3 (Receptor Interacting Proteins) complexes –> increases ROS and decreases mitochondrial ATP prodxn –> necrosis

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72
Q

What is the most common lipid?

A

TAGs

Other lipids: CHOL, CHOL esters, phospholipids

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73
Q

What occurs when a normal constituent (tags) accumulates, leading to increase in intracellular lipids?

A

Steatosis - most common in liver

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74
Q

True or False. Is steatosis reversible?

A

True. Though it may lead to cirrhosis if in excess.

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75
Q

What is the reabsorption droplets in proximal renal tubules?

A

Nephrotic syndrome

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76
Q

What is the excess of normally-secreted proteins?

A

Plasma cells actively producing Igs (Russell Bodies)

Seen in MM

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77
Q

What is the defective intracellular transport and secretion?

A

a1-antitrypsin deficiency

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78
Q

What is the accumulation of cytoskeletal proteins?

A

Alzheimer’s dse (neurofibrillary tangles)

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79
Q

What is the aggregation of abn proteins?

A

Amyloidosis

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80
Q

Intracellular hyaline

A

a1-antitrypsin deficiency

81
Q

Extracellular hyaline

A

Hyaline arteriosclerosis in HPN and DM

82
Q

Examples of exogenous pigments

A

Carbon or coal dust (anthracosis)

Tattooing

83
Q

Examples of endogenous pigments

A

Lipofuscin
Melanin
Homogentisic acid
Hemosiderin

84
Q

Sign of lipid peroxidation

Lipids + phospholipids in complex w protein

A

Lipofuscin

85
Q

Alkaptonuria (ochronosis)

A

Homogentisic acid

86
Q

What is dystrophic tissue type?

87
Q

What is the metastatic tissue type?

88
Q

Where is serum Ca increased? Dystrophic or Metastatic?

A

Metastatic

Causes: excess PTH, bone resorption, vit D dis, renal failure

89
Q

Clinical importance of Dystrophic

A

Psamomma bodies- sand-like lamellated concretions

P Papillary thyroid CA
S Serous cystadenoCA of ovaries
M Meningioma
M Mesothelioma

90
Q

Clinical importance of Metastatic

A

Lung involvement

Nephrocalcinosis

91
Q

What are the mechanisms that counteract aging?

A

Decreased IGF-1 signaling

Increased sirtuins

92
Q

What are proteins that fxn in response to food deprivation and DNA damage and are found in red wine?

A

Sirtuins - promote longevity eyyy tara laklak jk minimal

93
Q

What is due to vascular dilatation and congestion?

94
Q

What is dt vascular dilatation?

95
Q

What is dt mediator release?

96
Q

What is due to increased vascular permeability?

97
Q

What is dt pain, edema, tissue injury?

A

Functio laesa

98
Q

What elicits inflammation regardless of the cause of cell death, wc may include ischemia (reduced bld flow, cause of MI), trauma, and physical and chemical injury?

A

Tissue necrosis

99
Q

What elicits inflam by themselves or bcs they cause traumatic tissue injury or carry microbes? Necrotic cells also trigger

A

Foreign bodies

100
Q

What are the 5 steps in inflammatory rxn?

A 
1 Recognition of the infectious agents
2 Recruitment of leukocytes
3 Removal of the agent
4 Regulation (ctrl) of the response
5 Resolution (repair)
101
Q

In sensors of cell damage, what happens when molecules that are recognized, result from injury s/a UA, ATP, reduced K, DNA

A

They activate inflammasome (multiprotein cytosolic complex) –> IL-1 prodxn –> leukocyte recruitment –> inflammation

102
Q

For the Fc tails of antibodies and complement proteins

A

Leukocyte receptors

103
Q

What recognize microbes coated (opsonized) w Ab and complement?

A

Leukocyte receptors

104
Q

Complement
MBL
Collectins

A

Circulating proteins

105
Q

What recognizes microbial sugars and promotes ingestion of microbes and the activation of complement system?

106
Q

What can bind to and combat microbes?

A

Collectins

107
Q

Increase blood flow

A

Dilation of small vessels

108
Q

What happens when there’s increase microvascular permeability?

A

Plasma proteins and leukocytes leave the circulation

109
Q

What is an extravascular fluid has a high protein conc and contains cellular debris?

110
Q

What implies increase in the permeability of small BV triggered by tissue injury and an ongoing inflammatory rxn?

111
Q

What is a fluid w low protein content, little or no cellular material, and low SG?

A

Transudate

112
Q

What is an ultrafiltrate of plasma that is produced as a result of osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability?

A

Transudate

113
Q

What is an accumulation of leukocytes along the endothelium?

A

Stasis
- activation of endothelial cells and expression of increased levels of adhesion molecules –> adhere to endothelium–> migrate to interstitial

1 arterioles
2 capillary beds

114
Q

Heat and redness

115
Q

Slowly moving red cells; seen as vascular congestion and localized redness of involved tissue

116
Q

What is the hallmark of acute inflammation?

A

Increased vascular permeability

117
Q

What happens when there is endothelial injury?

A

Endothelial cell necrosis and detachment –> immediate and sustained endothelial peakage

118
Q

What occurs rapidly after injury and is reversible and transient (15-30mins)?

A

Endothelial cell contraction or “immediate transient response”

119
Q

Vessel lumen to tissue interstitium

A

Margination, rolling, adhesion to the endothelium, transmigration across endothelium, migration in interstitial tissues

120
Q

Necrosis response

A

1° neutrophils during first 6 to 24 hrs

Then replaced by monocytes after 24-48 hrs

121
Q

Rolling in Endothelial cell vs Leukocytes

A

Endothelial cell: E and P selectins

Leukocytes: Sialyl Lewis

122
Q

Firm adhesion in Endothelial cell vs Leukocytes

A

Endothelial cell: ICAM and VCAM

Leukocytes: Integrins

123
Q

Transmigration (diapedesis) in Endothelial cell vs Leukocytes

A

Both PECAM 1

124
Q

Migration (Chemotaxis) in Endothelial cell vs Leukocytes

A

Endothelial cell: Bacterial products (C5a, IL-8, LT b4, Kallikrein)

Leukocytes: Leukocyte surface G protein-coupled receptors

125
Q

What are synthesized from arg, molecular O2 and NADPH?

A

Nitric oxide

126
Q

What can kill microbes by increasing mem perm?

A

Leukocyte granules

127
Q

What contains MPO, bactericidal factors (lysozymes), acid hydrolases and neutral proteases?

A

Azurophilic (1°) granules

128
Q

What contains lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator and histaminase?

A

Specific (2°) granules

129
Q

What inflam mediators are either preformed and released by granules exocytosis or synthesized de novo following a stimulus?

A

Cell-derived mediators

130
Q

What inflam med are typically synthesized in the liver and circulate as inactive precursors wc are activated by proteolysis?

A

Plasma-derived mediators

131
Q

Its release is triggered by physical injury, immune-mediated (allergies), anaphylatoxins (C3a and C5a), cytokines (IL-1 and IL-8), and neuropeptidases (substance P)

A

Histamine (dilator) - inc perm of venules

132
Q

Sources: plts and neuroendocrine cells

A

Serotonin (constrictor)

133
Q

Primary fxn is as a neurotransmitter in the GI tract

A

Serotonin (constrictor)

134
Q

What eicosanoid can cause vasodilation?

A

PG PGI2 (prostacyclin), PGE1, PGE2, PGD2

135
Q

What eicosanoid can cause vasoconstriction?

A

Thromboxane A2, leukotrienes C4, D4, E4

136
Q

What eicosanoids can inc vascular permeability?

A

Leukotrienes, C4, D4, E4

137
Q

What eicosanoids can undergo chemotaxis, leukocyte adhesion?

A

Leukotrienes B4, HETE

138
Q

Act primarily as chemoattractants and activators

A

Chemokines

139
Q

Ig-Ag complex

Activated by MBL w bacterial surface proteins

140
Q

What are the anaphylatoxins?

A

C3a, C5a, and C4a

141
Q

What promotes histamine release –> vasodilation and inc vasc perm?

A

Anaphylatoxins

142
Q

Chemoattractant to neutrophils, monocytes, eo and baso

Activates lecithin-type oxidized receptors in PMNs and monocytes –> inflamm mediators

143
Q

Plt-Activating Factor in various concs

A

High: ikaw jk vaso- and bronchoconstriction
Low: histamine-like effects

144
Q

Products of coagulation

A

Protease-activated receptors

145
Q

Distinctive form of chronic inflammation

A

Granulomatous inflammation

146
Q

What is composed of neoplastic cells?

- based on classification of tumors and their behavior

A

Parenchyma

147
Q

What is composed of CT, BV, and variable numbers of cells of adaptive and innate IS?

A

Reactive stroma

148
Q

Soft and fleshy tumor that has scant CT

Desmoplasia

A

Reactive stroma

149
Q

What are tumors forming gross or microscopic finger like projections?

150
Q

What is a tumor projecting macroscopically above mucose?

151
Q

Derived from neoplastic clone of a single germ layer that differentiates into more than one cell type

  • mixed saliv gland tumors cont epi cells
  • myxoid stroma that may contain islands of cartilage or bone
A

Mixed tumors

152
Q

Various parenchymal cell types representative of more than one germ cell layer

  • arise from totipotential cells capable of forming endodermal, ecto, and mesenchymal tissues
  • can be benign or malignant
    Typicla: testis, ovary, rare in midline embryonic rsts
153
Q

Ectopic rests of nontranformed tissues

  • pancreatic cells under the small bowel mucosa
A

Choristoma

154
Q

Masses of disorganized tissue indigenous to a particular site

  • many are clonal w char acquired chromosomal abn
A

Hamartoma

- lung hamartomas exhibit cartilage, bronchi, and BV

155
Q

What is the hallmark of malignancy?

“To form backward”

156
Q

Variation in size and shape
Cells within the same tumor arent uniform, but range from small cells w an undifferentiated appearance, to tumor giant cells

A

Pleomorphism

157
Q

Malignancy: large, irreg, hyperchromatic nuclei w coarsely clumped chromatin sometimes w large nucleoli

Inc N:C ratio 1:1 vs normal of 1:4 or 1:6

A

Abn nuclear morphology

158
Q

Nuclear pleomorphism, hyperchromatic, nuclei, and tumor giant cells

A

Rhabdomyo sarcoma

159
Q

What is always found in association w tissue damage, repair, and regeneration?

A

Metaplasia

- stratified sq epi replacing respi epi in bronchioles of smokers

160
Q

What is the disordered growth char by a constellation of changes that includes a loss in the uniformity of the individual cells and loss in archi orientation? Mild to severe

A

Dysplasia

- can occur adjacent to frank malignancy

161
Q

When dysplastic changes are marked and involves the full thickness of epi but lesion doesn’t penetrate the basement mem, it is considered a preinvasive neoplasm and is referred to as

A

Carcinoma in situ

162
Q

Exudates

High protein content

A

Inflammatory

163
Q

Transudates

Low protein content

A

Non-inflammatory

164
Q

How does heart failure lead to edema?

A

Either

  • Increase capillary hydrostatic pressure
  • Reduced bld flow –> RAAS activation –> retention of Na and H2O (renal failure) –> increase BV –> EDEMA
165
Q

How does malnutrition, decrease hepatic synthesis, and nephrotic syndrome lead to edema?

A

Decrease plasma albumin then decreased plasma osmotic pressure

166
Q

What appears in tissues w loose CT matrix s/a the eyelids (periorbital edema)?

A

Edema from renal dysfxn

167
Q

What is the appearance of sulci and gyri in brain edema?

A

Narrowed sulci and distended gyri

168
Q

What is the active process in wc arteriolar dilation leads to increased bld flow?

169
Q

Affected tissues turn red (erythema) dt engorgement of vessels w oxygenated bld

170
Q

What os the passive process resulting from reduced outflow of bld from a tissue?

A

Congestion

171
Q

What os the passive process resulting from reduced outflow of bld from a tissue?

A

Congestion

172
Q

Dusky reddish-blue (cyanosis) dt red cell stasis and accumulation of deoxygenated Hb

A

Congested tissues

173
Q

Engorged alveolar capillaries w alveolar septal edema and focal intra-alveolar hemorrhage

A

Acute pulmonary congestion

174
Q

Septa are thickened and fibrotic

Capillary rupture may cause focal hemorrhage; and subsequent brkdwn results in Hemosiderin-laden macrophages

A

Chronic pulmonary congestion

175
Q

Distended central vein and sinusoids

Ischemic necrosis of centrilobular hepatocytes w periportal steatosis

A

Acute hepatic congestion

176
Q

Hemorrhagic centrilobular hepatocytes accentuated against uncongested tan liver (nutmeg)

Hemosiderin-laden macro; variable degrees of hepatocyte dropout and necrosis

A

Chronic passive hepatic congestion

177
Q

Difference of turbulence and stasis in abn bld flow

A

Turbulence: arterial and cardiac thrombi
Stasis: venous thrombi

178
Q

What are laminations composed of pale plt and fibrin deposits alternating w darker red cell-rich layer?

A

Lines of Zahn

  • signifies thrombus has formed in flowing bld
  • distinguish antemortem clots from nonlaminated clots in postmortem
179
Q

Thrombi occuring in the heart chambers or in aortic lumen

A

Mural thrombi

180
Q

Usually begins at sites of turbulence or endothelial injury

A

Arterial thrombi

  • frequently occlusive
  • friable meshwork of plt, fibrin, rbc, and degenerating leukocytes
181
Q

What are the most common sites of arterial thrombi?

A

Coronary arteries
Cerebral arteries
Femoral arteries

182
Q

What usually begins at sites of stasis?

A

Venous thrombosis

  • almost invariably occlusive
  • firm, attached to vessel wall and cont lines of Zahn
183
Q

What is the most common site of venous thrombosis?

A

Calf vein

- resp of DVT

184
Q

What are the 4 fates of thrombus?

A

1 Propagation
2 Embolization
3 Dissolution
4 Organization and Recanalization

185
Q

Where does superficial venous thrombi occur in the setting of varicosities?

A

Saphenous veins

186
Q

Sx of venous thrombosis

A

Local congestion
Swelling
Pain and tenderness
Rarely embolize

187
Q

DVT involves one of the large leg veins - at or above the knee

A

Popliteal
Iliac
Femoral veins

188
Q

Sx of DVT

A

Local pain and edema dt venous obstruction

189
Q

What can give rise to pulmonary infarction?

190
Q

Originate from DVT and are most common form of thromboembolic disease

A

Pulmonary embolism

191
Q

Ischemic necrosis of femoral heads, tibia, and humerus

A

Caisson dse

192
Q

What is the 5th most common cause of maternal mortality worldwide?

A

Amniotic fluid embolism

193
Q

Areas of ischemic necrosis c/b occlusion of either the arterial supply (most common) or venous drainage (less frequent)

A

Infarction

194
Q

What is the most common cause of infarction?

A

Arterial thrombosis or arterial embolism

195
Q

Its etiology includes:

  • local vasospasm, hemorrhage into atheromatous plaque, or extrinsic vessel compression (tumor)
  • torsion of a vessel, traumatic vascular rupture, or vascular compromise by edema or by entrapment in a hernia sac
A

Infarction

196
Q

Morphology: wedge, w occluded vessel at apex and periphery of organ at base
Histo: ischemic coagulative necrosis

Replaced by scar tissue

A

Infarction

197
Q

Venous occlusion
Loose tissue
Dual circ (eg lung and smol int)

A

Hemorrhagic (red) infarction

198
Q

What occurs in solid organs w end-arterial circulation (heart, spleen, kidneys)?

A

Pale (white) infarction

199
Q

What occurs in solid organs w end-arterial circulation (heart, spleen, kidneys)?

A

Pale (white) infarction

Preventive And Social Medicine II (32 decks)

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