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PATHOLOGY > M1: Cellular Adaptation > Flashcards

M1: Cellular Adaptation Flashcards

0
Q

Type of Pathology that pertains to alterations in specialized organs and organ system

A

Specific

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1
Q

Study of structural changes that underlies disease. Uses molecular, microbiological, immunological and. Morphologic technique.

A

Pathology

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2
Q

Type of Pathology that pertains to basic reactions of cells and tissues to abnormal stimuli

A

General

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3
Q

Backbone in which diagnosis are made. Cause of the disease (genetic/acquired) A disease can be understood or a treatment plan to be developed.

A

Etiology

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4
Q

Etiology: due to bacteria, virus & parasites

A

Infectious

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5
Q

Etiology: due to deficiency or overproduction

A

Nutritional

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6
Q

Etiology: due to mutations or gene variants

A

Genetic

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7
Q

Etiology: due to UV rays

A

Chemical/Physical

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8
Q

Etiology: underlying causes such as multimutagenic factors and environmental factors (cance/atherosclerosis)

A

Multifactorial

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9
Q

Stars from initial to ultimate expression of disease. Sequence of events in response to etiological agent. A link between the specific molecular abnormalities to the specific clinical manifestations, to design new therepaeutic approaches.

A

Pathogenesis

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10
Q

Biochemical & Structural alterations in cells that are either characteristic or diagnostic of the etiological process

A

Molecular & Morphological Changes

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11
Q

Identify the nature and progression of disease by studying morphologic and chemical alterations but has limitations. Molecular, biological & immunologic process in analyzing disease states.

A

Diagnostic Pathology

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12
Q

Functional consequences. Progress of signs and symptoms and includes prognosis.

A

Functional Derangement and Clinical Manifestations

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13
Q

Father of Modern Pathology. All forms of disease start with a molecular or structural alterations in cells.

A

Rudolf Virchow

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14
Q

Normal cell with narrow range of structure and function caused by

A

Genetic program of Metabolism, Differentiation & Specialization “MDS”

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15
Q

Are more malignant than specialized cells

A

Undifferentiated cells

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16
Q

Altered physiologic state

A

Cellular Adaptation (reversible)

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17
Q

Reduced oxygen supply; chemical injury (ischemia) and microbiological infection.

A

Cellular injury & Cell death

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18
Q

Metabolic alterations. Can be genetic or acquired.

A

Intracellular accumulations & calcifications

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19
Q

Prolonged life span with cumulative sublethal injury but not enough to cause cell injury

A

Cellular aging

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20
Q

Cell injury can be reverted back to normal if the stimulus is

A

Removed

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21
Q

Chronic & Progressive stimuli. Downhill.

A

Irreversible Injury

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22
Q

Two types of Cell Injury

A

Fatty change & Cellular swelling “FC”

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23
Q

First manifestation. Hydrophobic degeneration.

A

Cellular swelling

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24
Q

Reversible changes in size, number, phenotype, metabolic activity or functions of cells. New but altered steady state are achieved fpr cell to survive or continue.

A

Cellular Adaptation

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25
Q

Examples of Reversible Injuries

A

Hypertrophy, Hyperplasia, Atrophy & Metaplasia “HHAM”

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26
Q

Increase in cell size & organ size. Occurs in both dividing & non-dividing cells. Can be physiologic or pathologic. Synthesis of more structural components of the cells. Caused by increased functional demand or by stimulation of hormones and growth factors.

A

Hypertrophy

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27
Q

Stimulus for Hypertrophy

A

Increased work load

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28
Q

Abnormal levels of hormones. Enlargement of thyroid gland (excess t3/t4, goiter) Increase functional demand. Chronic hemodynamic overload in left ventricular hypertrophy (hypertension & valvular disease)

A

Pathologic Hypertrophy

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29
Q

Hormonal increase in uterine size during pregnancy, breast and organs during puberty & breast during lactation. Functional demand increases like skeletal muscles during exercise.

A

Physiologic Hypertrophy

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30
Q

Hypertrophy results from increased production of

A

Cellular proteins

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31
Q

Hypertrophy is induced by

A

Growth factors, Vasoactive agents & Mechanical sensors “GVM”

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32
Q

Two biochemical pathways in Hypertrophy

A

Phosphoinositide 3-kinase/Akt pathway & Signaling downstream of G protein-coupled receptors “PS”

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33
Q

Among the two biochemical pathways of hypertrophy which one is pathologic

A

Signaling downstream of G protein-coupled receptors

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34
Q

Among the two biochemical pathways of hypertrophy which one is physiologic

A

Phosphoinositide 3-kinase/Akt pathway

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35
Q

Switch of this occurs during adult fetal transition

A

Contractile proteins

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36
Q

Some genes are expressed in _______ development and re-expressed in hypertrophic cells.

A

Early

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37
Q

It reaches a limit when enlargement of muscle mass can no longer compensate at regressive changes resulting to

A

Lysis & Loss of contractile elements

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38
Q

Dies by apoptosis or necrosis

A

Myocyte

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39
Q

Increase in number of cells & organ mass in cell population capable of dividing. A normal metabolic reaction.

A

Hyperplasia

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40
Q

Two types if Hyperplasia

A

Physiologic & Pathologic

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41
Q

A type of hyperplasia in which there is an increase in tissue mass after damage (after hepatectomy since liver is capable of regenerating)

A

Physiologic Compensatory Hyperplasia

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42
Q

Excess of hormones (endometrial atypical cancerous hyperplasia & benign prostatic hyperplasia due to the increase number of prostate gland) or growth factors (keloid from excessive collagen/skin deposition & papilloviruses such as warts in the skin)

A

Pathologic Hyperplasia

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43
Q

A type of hyperplasia in which there is an increase functional capacity of tissue when needed (breast when pregnant or puberty, uterus im pregnancy & proliferative endometrium)

A

Physiologic Hormonal Hyperplasia

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44
Q

Mechanism of Hyperplasia: Increase of _________.

A

Growth factor

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45
Q

Mechanism of Hyperplasia: Increase of growth factor _________.

A

Receptors

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46
Q

Mechanism of Hyperplasia: Activation of cellular __________.

A

Signalling pathways

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47
Q

Mechanism of Hyperplasia: Result of __________ driven proliferation of mature cells.

A

Growth-factor

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48
Q

Mechanism of Hyperplasia: Increased output of new cells from ____________.

A

Tissue stem cells

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49
Q

Reduced size of organ or tissue from decrease in cell size and number. Reduction of metabolic needs for cell survival. Fewer mitochondria, RER & cytoskeleton. Cells may have diminished function, but not yet dead.

A

Atrophy

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50
Q

Atrophied cells usually die by

A

Apoptosis

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51
Q

Type of Atrophy which is common during early development. Uterus after parturition.

A

Physiologic Atrophy

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52
Q

Due to diminished blood supply & irreversible injury. Inadequate nutrition, pressure & loss of endocrine stimulation.

A

Pathologic Atrophy

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53
Q

Pathologic atrophy due to decreased workload

A

Atrophy of disuse

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54
Q

Pathologic atrophy due to loss of innervation

A

Denervation atrophy

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55
Q

Atrophy is due from decreased ___________ (reduced metabolic activity) and increased ____________.

A

Protein synthesis. Protein degradation.

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56
Q

Mechanism of Atrophy: Pathway activated by nutrient deficiency and disuse. Cancer cachexia and responsible for accelerated proteolysis.

A

Ubiquitin-proteosome pathway

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57
Q

Mechanism of Atrophy: starved cells eat up its own components. Vacuoles fuse with lysosomes.

A

Increased Autophagy (Autophagic vacuoles)

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58
Q

Mechanism of Atrophy: Increased ___________. (Chronic renal disease with presence of scarring)

A

Residual bodies

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59
Q

Brown atrophy of the heart

A

Lipofuscin pigment

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60
Q

Reversible change from one differentiated cell type to another. May initiate malignant transformation in metaplastic epithelium. Reprogramming of stem cells or undifferentiated mesenchymal cells.

A

Metaplasia

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61
Q

Type of Metaplasia: Columnar to squamous (most common) & Squamous to columnar.

A

Epithelial Metaplasia

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62
Q

Epithelial Metaplasia examples are respiratory tract/ Vitamin A deficiency, Excretory ducts of glands-stones, Endocervix & chronic cervicitis.

A

Squamous to columnar

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63
Q

An example of Epithelial metaplasia that has a squamous to columnar transition in which if it persist may initiate malignant transformation

A

Barret Esophagus

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64
Q

Metaplasia is basically a result of

A

Stem cell reprogramming

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65
Q

Can undergo both hypertrophy & hyperplasia at the same time

A

Uterus during Pregnancy

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66
Q

Medical term for the specific symptom or landmark of a disease

A

Pathognomonic

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67
Q

Normal ventricular thickness

A

1.3-1.5cm

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68
Q

Occurs in both epithelial & mesenchymal tissues

A

Metaplasia

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69
Q

Type of Metaplasia from muscle to bone. Formation of cartilage, bone or adipose in places that do not contain these elements.

A

Connective tissue metaplasia

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70
Q

Example of a connective tissue metaplasia

A

Myositia Ossificans

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71
Q

Limits of adaptive responses are exceeded or cells are exposed to injurious agents, deprived of nutrients or by mutations. Suffers irreversible injury if stimulus persists or is severe.

A

Cell Injury

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72
Q

Causes of Cell Injury

A

Chemical agents & drugs, Oxygen deprivation, Physical agents, Infectious agents, Immunologic reactions, Nutritional imbalances & Genetic derangements “COPIING”

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73
Q

Reduced aerobic oxidative respiration due to Oxygen deprivation

A

Hypoxia

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74
Q

Hallmark of Reversible Injury

A

Depletion of ATP & Cellular swelling

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75
Q

In early stages or mild forms of injury. Reduced oxidative phosphorylation with depletion of ATP & cellular swelling. Mitochondria & Cytoskeletom have alterations.

A

Reversible Injury

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76
Q

With continuing damage. Irreversible. Necrosis & Apoptosis. End result of Autophagy.

A

Cell death

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77
Q

Digestion of cell. Mainly pathologic.

A

Necrosis

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78
Q

Cell kills itself

A

Apoptosis

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79
Q

Cellular swelling, fatty change, blebbing of plasma membrane, detachment of ribosomes from ER and clumping of nuclear chromatin.

A

Reversible Injury

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80
Q

During hypoxic injury there is appearance of liquid vacuoles (toxin & metabolic injury)

A

Fatty change

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81
Q

Cells are incapable of maintaining homeostasis. Failure of energy-dependent ion pumps.

A

Cellular swelling

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82
Q

Mechanism of Cell Injury: response depends on ________, _______ and _______ of injury.

A

Nature, Duration & Severity “NDS”

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83
Q

Mechanism of Cell Injury: Consequences depend on _______, _______ and ________ of the cell.

A

Type. State. Adaptability.

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84
Q

Mechanism of Cell Injury: Results from different __________ mechanisms acting on several essential cellular components.

A

Biomechanical

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85
Q

Mechanism of Cell Injury: May simultaneously trigger _____________ systems.

A

Multiple interconnected

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86
Q

Mechanism of Cell Injury: Associated with hypoxic & toxic injury. Reduced supply of oxygen and nutrients, mitochondrial damage & actions of some toxins.

A

Depletion of ATP

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87
Q

Depletion of ATP: If depletion of 5-10%, Na K ATPase _________(causing swellling), Increase in ________ glycolysis & Influx of ______.

A

Reduce. Anaerobic. Calcium.

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88
Q

Depletion of ATP: If depletion of 5-10%, Reduction of ________ synthesis, _______ protein response and Irreversible damage to _______ & ________ enzymes.

A

Protein. Unfolded. Mitochondrial & Lysosomal.

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89
Q

Increase in cytosolic Ca, ROS & O2 deprivation.

A

Mitochondrial Damage

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90
Q

Mitochondrial Damage: high conductance channel & loss of membrane potential (cyclophilin D)

A

Mitochondrial Permeability Transition Pore

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91
Q

Mitochondrial Damage: Activation of apoptotic pathways

A

Cytochrome C & Caspases

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92
Q

Opening of the mitochondrial permeability transition pore. Failuer to generate ATP. Activates phospholipases, proteases, endonucleases and ATPases. Induces apoptosis by activiating caspases and increasing mitochondrial permeability.

A

Influx of Intracellular Ca & Loss of Ca Homeostasis

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93
Q

Initiate autocatalytic reactions. Disruption of organelles. Mutations and loss of enzymatic activity.

A

Accumulation of Oxygen-Derived Free Radicals

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94
Q

Are produced normally but are degraded and removed by cellular defense systems. When this increases or when scavenging systems are ineffective, there would be an excess which leads to oxidative stress.

A

ROS

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95
Q

ROS are produced by

A

Neutrophils & Leukocytes

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96
Q

Molecular oxygen is reduced by transferring 4 electrons to H+ to generate 2 H20 Molecules.

A

Redox Reaction

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97
Q

Products of Redox Reaction

A

Superoxide anion, Hydrogen peroxide & Hydroxyl ions “SHH”

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98
Q

Redox Reaction: Absorption of radiant energy. _________ water to OH and H+.

A

Hydrolyze

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99
Q

Redox Reaction: __________ of ROS during Inflammation.

A

Rapid burst

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100
Q

Redox Reaction: __________ of exogenous chemicals or drugs.

A

Enzymatic metabolism

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101
Q

Redox Reaction: Transition metals like

A

Copper & Iron

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102
Q

Redox Reaction: As free radical or converted to ONOO

A

Nitric Oxide

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103
Q

Removal of Free Radicals: block formation or inactivate free radicals

A

Antioxidants (Vit. E & A)

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104
Q

Removal of Free Radicals: minimized by bonding to storage and transport proteins

A

Iron & Copper Bonding

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105
Q

Removal of Free Radicals: breakdown H202 and O2

A

Free radical scavenging systems

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106
Q

Free radical scavenging system: H202 to H2O +O2

A

Catalase

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107
Q

Free radical scavenging system: O2 to H2O2

A

Superoxide Dismutase

108
Q

Free radical scavenging system: OH to H2O2 to H20 plus O2

A

Glutathione Peroxidise

109
Q

Pathologic Effects of Free Radicals: Lipid _______ in membranes.

A

Peroxidation

110
Q

Pathologic Effects of Free Radicals: _________ modification of proteins.

A

Oxidative

111
Q

Pathologic Effects of Free Radicals: Lesions in ______.

A

DNA

112
Q

Mechanisms of Membrane Damage: Results of ________ & ____ mediated activation of phospholipases also by toxins or agents.

A

ATP depletion & Calcium

113
Q

Mechanisms of Membrane Damage: ROS through _________.

A

Lipid peroxidation

114
Q

Mechanisms of Membrane Damage: Decreased phospholipid ________.

A

Synthesis

115
Q

Mechanisms of Membrane Damage: Increased phospholipid _________. Accumulation of lipid breakdown products.

A

Breakdown

116
Q

Mechanisms of Membrane Damage: _________ abnormalities.

A

Cytoskeletal

117
Q

Consequences: opening of permeability transition pore

A

Mitochondrial damage

118
Q

Consequences: Loss of osmotic balance and influx of fluid and ions

A

Plasma membrane damage

119
Q

Consequences: Leakage of enzymes

A

Lysosomal membrane damage

120
Q

Damage to DNA and proteins

A

Improper folding

121
Q

End result of progressive cell injury. Irreversible. Caused by ischemia, infection and toxins. Normal and essential in embryogenesis. Two pathways would be necrosis and apoptosis. Autophagy and cells can no longer recover from injury.

A

Irreversible Injury/Cell Death

122
Q

Due to nutrient deprivation

A

Autophagy

123
Q

Spectrum of morphologic changes that follow cell death in living tissue due to denaturation of proteins and progressive enzymatic digestion. Unable to maintain integrity resulting to its contents leaking out and eliciting inflammation. Take hours to develop. Enzymes derived from lysosomes. Gross appearance depends on the appearance.

A

Necrosis/Cell Death

124
Q

Microbiologic features of Necrosis: Increased eosinophilia due to loss of

A

Cytoplasmic RNA

125
Q

Microbiologic features of Necrosis: More ______, homogenous appearance (loss of glycogen)

A

Glassy

126
Q

Microbiologic features of Necrosis: presence of _______ figures. Become ________.

A

Myelin. Calcified.

127
Q

Microbiologic features of Necrosis: Nuclear changes are noted like

A

Pyknosis, Karyorrhexis & Karyolysis “PKK”

128
Q

Nuclear changes: fragmentation

A

Karyorrhexis

129
Q

Nuclear changes: nuclear shrinkage and increased basophilia

A

Pyknosis

130
Q

Nuclear changes: chromatin fades

A

Karyolysis

131
Q

Most common except in the brain. Basic cellular outline preserved. Firm texture & Nuclear changes. Intracellular acidosis block proteolysis. Hypoxic death. Preserved architecture but cannot precipitate the cellular details, no nucleus. Localized area (infarct) wedge shaped.

A

Coagulative

132
Q

Loss of blood supply. Has undergone coagulative necrosis. Mostly in the limbs.

A

Gangrenous

133
Q

Focal bacteria or occasionally fungal infections. Hypoxia & CNS affectations. Complete digestion of dead cells and presence of pus. Transformation into liquid viscous mass. Accumulation of leukocytes. Wet gangrene. Initiated by Inflammation.

A

Liquefactive

134
Q

Liquefactive necrosis usually occurs in the

A

Brain

135
Q

Cheeselike, white appearance in area. Amorphous granular debris enclosed by granulomatous wall. Architecture completely obliterated. Granuloma. Foci of TB which may undergo non-caseation necrosis; hard or soft tubercle.

A

Caseous

136
Q

Examples of Granulomas

A

Langhans fibrosis, Epitheloid cells & Lymphocytes “LEL”

137
Q

Important in caseous cells/necrosis granulomatous walls which is activated by macrophages

A

Epitheloid cells

138
Q

Multinucleated; horseshoe-shaped. Nucleus peripherally found.

A

Langhan’s type Giant Cell

139
Q

Centrally located nucleus. Considered as haphazards.

A

Foreign Body Giant Cell

140
Q

Focal area of fat destruction from release of pancreatic lipases. Visble chalky-white areas. Nonspecific pattern of cell death. Shadowing outlines. Lipase liquefy cell membranes-triglycerides-FFA+Ca-saponified fats. In acute pancreatitis.

A

Fat/Enzymatic

141
Q

Breakdown fats to TG FFA then combines to calcium which is a process called sapofonication

A

Pancreatic lipases

142
Q

Immune reaction involving blood vessels and vascular channels. Ag & Ab deposited in arterial walls. Renal problem like malignant nephrosclerosis. Chemical or toxic injury like cyanide, carbon tetrachloride and acetaminophen.

A

Fibrinoid

143
Q

Most common type of cell injury. Restoration of blood flow exacerbates and accelerates cell injury. Additional cell loss. Hypoxia and Ischemia.

A

Ischemic and Hypoxic Injury

144
Q

Reduced oxygen availability

A

Hypoxia

145
Q

Reduced blood flow leading to a decreased supply of oxygen and nutrients which the cause more severe injury.

A

Ischemia

146
Q

Example of Ischemic & hypoxic Injury

A

Anemia & CO poisoning

147
Q

Mechanisms of Ischemic Cell Injury: oxygen ________ decrease. Then loss of ______. Results to decrease ______ generation.

A

Tension. OP. ATP.

148
Q

Mechanisms of Ischemic Cell Injury: Failure of ________ (loss of K, influx of Na & H2O) and cell ________.

A

Na-K pump. Swelling.

149
Q

Mechanisms of Ischemic Cell Injury: Influx of ____.

A

Calcium

150
Q

Mechanisms of Ischemic Cell Injury: Loss of _______ and decrease _______ synthesis.

A

Glycogen. Protein.

151
Q

Mechanisms of Ischemic Cell Injury: Presence of ________ figures.

A

Myelin

152
Q

Mechanisms of Ischemic Cell Injury: Cytoskeleton disperses with loss of its structural features

A

Blebs

153
Q

Mechanisms of Ischemic Cell Injury: ________ mitochondria and ______ ER.

A

Swollen. Dilated.

154
Q

Mechanisms of Ischemic Cell Injury: May become irreversible. _______ of fatty acid residues.

A

Calcifications

155
Q

Protective response promotes new BV formation, cell survival pathways and anaerobic glycolysis.

A

Hypoxia-inducible factor 1

156
Q

Reperfusion after loss of blood supply may still pose danger. Reperfused tissues may sustain loss of cells in addition to the cells that are irreversibly damaged at the end of ischemia. Restoration of blood flow exacerbates and accelerates cell injury. E

A

Ischemia-Reperfusion Injury

157
Q

Mechanisms of Ischemia-Reperfusion Injury: Increased generation of _____, _______ and ________ pathways.

A

ROS, RNS & Activation.

158
Q

Mechanisms of Ischemia-Reperfusion Injury: Ischemia associated with inflammation and hypoxia due to

A

Cytokine production

159
Q

Mechanisms of Ischemia-Reperfusion Injury: Activation of the

A

Complement system (IgM)

160
Q

Injure cells directly by combining with critical molecular components. Most toxic chemicals must be converted to reactive toxic metabolites which act on target cells (CP450) examples are cyanide, CCL4 & Acetaminophen.

A

Chemical (Toxic Injury)

161
Q

Programmed cell death. Induced by tightly regulated intracellular program. Chromatic condensation d/t nuclear changes. Formation of apoptotic bodies. Membrane remains intact. Structure alteration which leads to break up into apoptotic bodies. Does not elicit an inflammatory response. No nuclear changes.

A

Apoptosis

162
Q

Tightly regulated suicide program in which cells are destined to die activate enzymes that degrade the cell’s own nuclear DNA and nuclear & cytoplasmic proteins.

A

Apoptosis

163
Q

Physiologic/Pathologic Apoptosis: eliminate cells that are no longer needed to maintain the number of cell population

A

Physiologic

164
Q

Physiologic/Pathologic Apoptosis: Embryogenesis- implantation, organogenesis, developmental involution and metamorphosis involution of hormone-dependent tissue upon hormone withdrawal.

A

Physiologic

165
Q

Physiologic/Pathologic Apoptosis: Eliminate cells that are injured beyond repair

A

Pathologic

166
Q

Physiologic/Pathologic Apoptosis: Involution of hormone-dependent tissues

A

Physiologic

167
Q

Physiologic/Pathologic Apoptosis: DNA damage directly or via free radical production

A

Pathologic

168
Q

Physiologic/Pathologic Apoptosis: Accumulation of misfolded protein (ER stress)

A

Pathologic

169
Q

Physiologic/Pathologic Apoptosis: Elimination of harmful lymphocytes

A

Physiologic

170
Q

Physiologic/Pathologic Apoptosis: Cell loss in proliferating cell populations

A

Physiologic

171
Q

Physiologic/Pathologic Apoptosis: Elimination of harmful lymphocytes

A

Physiologic

172
Q

Physiologic/Pathologic Apoptosis: Cell deaths in certain infections

A

Pathologic

173
Q

Physiologic/Pathologic Apoptosis: Elimination of cells that are not needed anymore or in excess

A

Physiologic

174
Q

Physiologic/Pathologic Apoptosis: Death of host cell

A

Physiologic

175
Q

Physiologic/Pathologic Apoptosis: Atrophy in parenchymal organs

A

Pathologic

176
Q

Morphologic Changes: cell shrinkage

A

Apoptosis

177
Q

Morphologic Changes: cell swelling

A

Necrosis

178
Q

Morphologic Changes: nuclear changes

A

Necrosis

179
Q

Morphologic Changes: chromatin condensation (peripheral aggregates)

A

Apoptosis

180
Q

Morphologic Changes: cytoplasmic blebs and apoptotic bodies

A

Apoptosis

181
Q

Morphologic Changes: phagocytosis by macrophage

A

Apoptosis

182
Q

Morphologic Changes: inflammation and engulfment of necrotic debris

A

Necrosis

183
Q

Morphologic Changes: membrane blebs and destruction

A

Necrosis

184
Q

Morphologic Changes: plasma membrane is intact until the last stages

A

Apoptosis

185
Q

Biochemical Features: Activation of ________. Cysteine proteases. Must undergo enzymatic cleavage to become active.

A

Caspases

186
Q

Biochemical Features: Initiator caspases

A

Caspases 8, 9 & 10

187
Q

Biochemical Features: Executioner caspases

A

Caspases 3 & 6

188
Q

Biochemical Features: DNA & Protein breakdown by _____ & _____ dependent endonucleases.

A

Ca2+ & Mg2+

189
Q

Biochemical Features: Membrane alterations and recognition by ________. Movement of phosphatidylserine by _________.

A

Phagocytes. Annexin V.

190
Q

Major mechanism. Result of increased mitochondrial permeability and release of pro-apoptotic molecules.

A

Intrinsic/Mitochondrial Pathway

191
Q

Mitochondrial Pathway: initiates a suicide program

A

Cytochrome C

192
Q

Mitochondrial Pathway: regulate apoptosis

A

BCl-2 proteins (Bcl-2, Bcl-x & Mcl-1)

193
Q

Mitochondrial Pathway: allow proteins to leak out to the cytoplasm. Block Bcl-2 and Bcl-x.

A

Bax & Bak

194
Q

Mitochondrial Pathway: Cytochrome C binds to Apag-1 to form _______ to bind to _______.

A

Apoptosome. Caspase 9.

195
Q

Mitochondrial Pathway: block the activation of caspases

A

IAPs

196
Q

Initiated by engagement of plasma membrane death receptors (TNF receptor family) Death Receptor Initiated Pathway.

A

Extrinsic Pathway

197
Q

Extrinsic Pathway: delivery of apoptotic signals

A

Death domain

198
Q

Extrinsic Pathway: example of death receptors

A

TNFR1 & FAS

199
Q

Extrinsic Pathway: expressed on cytotoxic T cells

A

FasL

200
Q

Extrinsic Pathway: form caspase 8 & 10

A

FADD

201
Q

Extrinsic Pathway: form a binding site for FADD

A

3 Fas molecules

202
Q

Extrinsic Pathway: inhibits apoptotic pathway but cannot cleave and activate caspase due to lack of protease domain

A

FLIP

203
Q

Execution Phase: caspases involved. Cleaves a cytoplasmic DNAse inhibitor to make it active. Promote fragmentation.

A

3 & 6

204
Q

Removal of Dead cells: is on the outer layer of the membrane

A

Phosphatidylserine

205
Q

Removal of Dead cells: target dead cells for engulfment

A

Thrombospondin

206
Q

Triggered by intrinsic pathway. Decrease synthesis of Bcl-2 and Bcl-x.

A

Growth factor deprivation

207
Q

Arrests the cell cycle (G1 phase) Triggers apoptosis if damage is great. If absent it is incapable of apoptosis. DNA damage.

A

Gene p53

208
Q

Due to ER stress

A

Protein misfolding

209
Q

Activates NF-KB to promote cell survival

A

TNF

210
Q

Promote entry of granzymes to activate caspases

A

Perforin

211
Q

Secretes perforin. Medicated Apoptosis.

A

Cytotoxic T-Lymphocyte

212
Q

Defective apoptosis and increase cell survival is due to

A

Mutation of p53

213
Q

Increased apoptosis and excessive cell death results to

A

Neurodegenerative disease, Ischemic injury & Death of virus infected cells “NID”

214
Q

Cell eats its own content. Intracellular organelles and cytosol portions are first sequestered to an autophagic vacuole and fuses to form a autophagolysosome to be digested by lysosomal enzymes.

A

Autophagy

215
Q

Autophagy is regulated by

A

Atgs

216
Q

Normal cellular constituent. Normally produced by cell but will synthesize in abnormal amounts. Abnormal substance can be endogenous or exogenous. Can be transient or permanent, harmless or toxic, intracytoplasmic or intranuclear and produced in cell or just stored in cell.

A

Intracellular accumulations

217
Q

Four Abnormalities leading to intracellular accumulations

A

Lack of enzyme, Abnormal metabolism, Ingestion of indigestible materials and Defect in protein folding & transport “LAID”

218
Q

Reversible. Fatty change. Abnormal accumulations of TGs within parenchymal cells. Seen in liver, heart, kidney & muscle. Causes are alcohol abuse, toxins, protein malnutrition, DM, obesity & anoxia. Excess accumulation results from excessive entry of defective metabolism and export of lipids.

A

Steatosis

219
Q

Morphology of Steatosis: yellow, soft, greasy & tigered effect.

A

Macro

220
Q

Morphology of Steatosis: clear vacuoles. (+) Sudan IV, (+) Oil Red O & fatty cyst.

A

Micro

221
Q

Cholesterol & Cholesteryl Esters: smooth muscle cells and macrophage within the intima layer filled with lipid vacuoles.

A

Atherosclerosis

222
Q

Cholesterol & Cholesteryl Esters: accumulation of cholesterol within macrophages

A

Xanthomas

223
Q

Cholesterol & Cholesteryl Esters: focal accumulations in lamina propia of gallbladder

A

Cholesterolosis

224
Q

Neimann-Pick disease & type C lysosomal storage disease

A

Cholesterol & Cholesteryl Esters

225
Q

Normal Protein: reabsorption of droplets is proximal renal tubules

A

Proteinuria

226
Q

Normal Protein: large, homogenous eosinophilic inclusions in the ER. Immunoglobulins.

A

Russel bodies

227
Q

Rounded, eosinophilic droplets, vacuoles or aggregates in the cytoplasm.

A

Abnormal Protein

228
Q

Abnormal Protein: defective intracellular transport and secretion of critical proteins.

A

ã1-antitrypsin deficiency

229
Q

Abnormal Protein: accumulation of cytoskeletal proteins

A

Neurofibrillary tangles

230
Q

Abnormal Protein: aggregation of abnormal proteins

A

Amyloidosis & Proteinopathies

231
Q

Homogenous, glassy pink appearance on H&E stain. Example is ARDS.

A

Hyaline Change

232
Q

Hyaline Change: extravasated plasma proteins and deposition of basement membrane material-collagenous tissue in old scar, hyalinated arterial walls, DM and long standing HPN.

A

Extracellular

233
Q

Hyaline Change: Reabsorption of droplets, russel bodies and alcoholic hyaline.

A

Intracellular

234
Q

Defect in synthesis of breakdown of glycogen; glycogen storage disease.

A

Glycogenoses

235
Q

(+) Periodic Acid Shift & best Carmine

A

DM

236
Q

Pigments: from outside of the body

A

Exogenous pigments

237
Q

Pigments: Synthesized within the body. Do not evoke inflammatory response. Tattoo.

A

Endogenous pigment

238
Q

Exogenous Pigments: associated with pneumoconiosis & anthracosis.

A

Carbon (coal dust)

239
Q

Exogenous Pigments: deposition of black pigment in lungs

A

Anthracosis

240
Q

Exogenous Pigments: coal miner disease

A

Pneumoconiosis

241
Q

Endogenous Pigments: from the free radical damage and lipid peroxidation. Seen in aging, malnutrition & cancer. Micro yellow brown with perinuclear granules.

A

Lipofuscin

242
Q

Endogenous Pigments: produced in melanocytes. Breakdown of tyrosine. Micro is black brown granules.

A

Melanin

243
Q

Endogenous Pigments: alkaptonuria or ochronosis. Micro black granules.

A

Homogentisic acid

244
Q

Endogenous Pigments: Hematin & Bilirubin. Hgb-derived. In liver, heart & endocrine organs. Hemosiderosis & Hemochromatosis. Micro gold brown granules and (+) Prussian blue.

A

Hemosiderin

245
Q

Hematin is for

A

Malaria

246
Q

Bilirubin is for

A

Jaundice

247
Q

Abnormal tissue deposition of calcium and salts

A

Pathologic Calcification

248
Q

Abnormal deposition of calcium salts in non-viable tissue. In areas of necrosis and occurs locally and in the absence of derangement in Ca2+ metabolism. Calcium levels not elevated.

A

Dystrophic Calcification

249
Q

Dystrophic Calcification: Two process

A

Initiation & Propagation

250
Q

Dystrophic Calcification: fine white granules

A

Macro

251
Q

Dystrophic Calcification: Intracellular or extracellular basophilic granules. Psammoma bodies.

A

Micro

252
Q

Dystrophic Calcification: medial calcifisclerosis. Calcification in Tunica Intima

A

Monckeberg’s

253
Q

Abnormal deposition of Calcium salts in normal tissue in hypercalcemia. Found in interstitial tissue of gastric mucosa, kidney, lungs, arteries and pulmonary veins (internal alkaline compartments). Excretion of acid to have an internal alkaline compartment that predisposes them to this.

A

Metastatic Calcification

254
Q

Causes of Metastatic Calcification: Increased PTH secretion

A

Hyperparathyroidism

255
Q

Causes of Metastatic Calcification: destruction of _________.

A

Bone tissue

256
Q

Causes of Metastatic Calcification: ________ related disorders.

A

Vit. D

257
Q

Causes of Metastatic Calcification: ______ failure.

A

Renal

258
Q

Result from progressive decline of cellular function and viability. Caused by genetic abnormalities and accumulation of cellular and molecular damage due to effects of exposure to exogenous influences.

A

Cellular Aging

259
Q

Rare disease characterized by premature aging. Defective DNA helicase. Rapid accumulation of chromosomal damage.

A

Werner Syndrome

260
Q

Most effective way of prolonging lifespan. Increase insulin activity and glucose metabolism.

A

Caloric restriction

261
Q

Family of proteins with histone deactylase activity. Promote the expression of several genes whose products increase metabolic activity, reduce apoptosis, stimulate protein folding to and inhibit harmful effects of oxygen free radicals.

A

Sirtuins

262
Q

Increase in cell size resulting in increased size of organs

A

Hypertrophy

263
Q

Restoration of blood flow to ischemic but otherwise viable tissue paradoxically results in exacerbated and accelerated injury.

A

Ischemia-Reperfusion Injury

264
Q

Refers to any abnormal accumulation of TAGs within parenchymal cells. Most often seen in the liver but can also occur in the heart, skeletal muscle and kidneys.

A

Steatosis

265
Q

Most common cause of cell injury

A

Ischemia

266
Q

Presence of cholesterol-filled macrophages in subepithelial connective tissue of skin or tendons

A

Xanthomas

267
Q

Irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis

A

Pyknosis

PATHOLOGY (2 decks)

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