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Pathology > Exam 1 Terminology > Flashcards

Exam 1 Terminology Flashcards

1
Q

Pathology

A

Study of disease

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2
Q

Disease

A

any deviation from the normal structure or function

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3
Q

Pathogenesis

A

sequence of events from initial stimulus to ultimate expression of a disease

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4
Q

Molecular and morphologic changes

A

biochemical and structural alterations induced in cells and organs of the body

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5
Q

Clinical manifestations

A

clinical signs resulting from functional abnormalities of affected tissues

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6
Q

Diagnosis

A

concise statement or conclusion concerning the nature, cause, or name of a disease

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7
Q

Prognosis

A

outcome

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8
Q

Lesion

A

any morphological change in tissues during disease

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9
Q

Morphologic diagnosis (MDx)

A

includes pathological process, location, distribution, duration and severity

This is a summary of the lesion, but generally does not describe what is causing the lesion

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10
Q

Etiologic diagnosis (EDx)

A

includes pathological process, location and cause

This type of diagnosis is restricted to two words only -the causative agent and the site of the lesion

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11
Q

Pathognomonic lesions

A

characteristic of a specific disease

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12
Q

5 Pathological Processes

A
  1. Degeneration & necrosis
  2. Inflammation & repair
  3. Circulatory & Disorders
  4. Disorders of growth
  5. Deposits & Pigmentations
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13
Q

Etiology

A

This is the causative agent only - it may also be stated as cause, causative agent, or etiologic agent. It does not ask for the organ, distribution, or any other type of information

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14
Q

General Pathology

A

The main pathological processes incited by various injurious stimuli and applies to all cells & tissues

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15
Q

Systemic Pathology

A

Systemic-specific disease processes that are build on main pathological processes but takes into account: unique response to injury of each tissue and specific diseases for each system

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16
Q

10:1 ratio

A

formalin:tissue ratio for fixing samples

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17
Q

Autolysis

A

(Post Mortem Change) Self-digestion or degradation of cells and tissues by hydrolytic enzymes normally present in tissues. Occurs after somatic death due to total diffuse hypoxia. Cells degenerate as for hypoxic injury.

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18
Q

Putrefaction

A

(Post Mortem Change) Process by which post mortem bacteria break down tissues. Gives color, texture changes, gas production, odor

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19
Q

Rigor Mortis

A

(Post Mortem Change) Contraction of the muscles after death. Due to the depletion of ATP and inability of myosin to detach from actin binding site.

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20
Q

Livor Mortis (Hypostatic congestion)

A

(Post Mortem Change)

Gravity pulls blood to one side PM. Typically easily seen in bilateral organs

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21
Q

Chicken fat clot appearance

A

(Post Mortem Change)
Due to separation of RBCs and clotted serum (yellowish white components found dorsally because RBCs migrate to the bottom)

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22
Q

Antemortem Clot

A

Attached to vessel walls, dry and dull, lamellated, and friable

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23
Q

Postmortem Clot

A

Unattached, shiny and wet, elastic, and perfect cast of vessel lumen

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24
Q

Hemoglobin imbibition

A

(Post Mortem Change)

Red staining of tissue, especially the intima of heart, arteries and veins

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25
Q

Bile imbibition

A

(Post Mortem Change)
Yellowish to greenish brown tissues stained due to the bile in the gallbladder penetrating the wall. Organs affected are gallbladder, liver, and intestines

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26
Q

Bloat

A

(Late Post Mortem Change)

Results from bacterial gas formation in the lumen of the GIT. Heat can make this worse.

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27
Q

Associated changes from bloat

A

Rectal/vaginal prolapse; froth in trachea; ruptured viscera

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28
Q

PM eye changes

A

(Post Mortem Change)

Corneal opacity due to dehydration of cornea, “cold cataracts”

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29
Q

Pseudomelanosis

A

(Post Mortem Changes)
Decomposition of blood by bacterial action forming hydrogen sulfide with iron. Typically green-black color of tissues in contact with the gut.

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30
Q

Features of a description

A 
Number
Size
Location
Distribution
Shape
Color
Consistency
Margins/Surface
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31
Q

Focal

A

Type of distribution; one isolated lesion

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32
Q

Multifocal

A

Type of distribution; numerous similar lesions that can be of variable size

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33
Q

Diffuse

A

Type of distribution; throughout a large portion of the affected tissue, spread out over a large area; not concentrated

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34
Q

Extensive

A

Type of distribution; covering or affecting a large area

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35
Q

Coalescing

A

Type of distribution; come together and form one mass or whole

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36
Q

Features of a MDx

A

Organ, pathologic process, distribution, chronicity, severity

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37
Q

Two major classes of factors causing disease

A

Genetic & Acquired

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38
Q

Principal responses of adaption are:

A

Atrophy, Metaplasia, Hypertrophy, Hyperplasia, and Dysplasia

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39
Q

Homeostasis

A

Tendency to stability in the normal body states of the organs; it is the ability to maintain internal equilibrium by adjusting its physiological processes

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40
Q

Atrophy

A

Decrease in size and/or number of the cells and their metabolic activity after normal growth has been reached

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41
Q

Hypertrophy

A

Increased size of cells and their function. Bigger cells. Typically cells with little replication

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42
Q

Three triggers that induce hypertrophy

A

Mechanical stress, hormones, and growth

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43
Q

Concentric hypertrophy

A

All the walls of the heart is increased in a similar amount and the chambers are reduced in size. Walls go to the inside. Thick walls.

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44
Q

Eccentric hypertrophy

A

Goes towards the outside

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45
Q

Hypertrophy cardiomyopathy (HCM) is caused by mutation of what gene?

A

MYBPC3 gene that is inherited autosomal dominant. Results in bilateral cardiac concentric hypertrophy

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46
Q

Hyperplasia

A

Increase in the number of cells of an organ. Typically happens with cells capable of replication

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47
Q

Metaplasia

A

Change in phenotype of a differentiated cell. May result in decrease function or increase propensity for malignant transformation. Last possibility of a reversible change.

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48
Q

Neoplasia

A

the formation or presence of a new, abnormal growth of tissue.

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49
Q

Dysplasia

A

Abnormal development typically of epithelial cells.

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50
Q

Acute Cell Swelling

A

Reversible cell injury. Hydropic degeneration. Early, sub-lethal manifestation of cell damage, characterized y increased cell size and volume due to H2O overload. Most common cell injury.

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51
Q

Acute Cell Swelling Etiology

A

Loss of ionic and fluid homeostasis. Failure of cell energy production, cell membrane damage, and injury to enzymes regulating ion channels of membranes

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52
Q

Acute Cell Swelling Pathogenesis

A

A cell doesn’t get enough oxygen and gets hypoxia. So ATP production decreases and Na+ and H2O move in the cell and K+ moves out of the cell. Water follows Na+. Osmotic pressure increases. Cisternae of endoplasmic reticulum distend, rupture, and form vacuoles. Excessive vacuolation. Hydropic degeneration.

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53
Q

Acute Cell Swelling Gross Appearance

A

Slightly swollen organ with rounded edges. Pallor when compared to normal. Cut surface: tissue bulges & cannot be easily put in correct apposition. Slightly heavy “wet organ”.

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54
Q

Acute Cell Swelling Histological Appearance

A

H2O uptake dilutes the cytoplasm. Cells are enlarged with pale cytoplasm. May show increased cytoplasmic eosinophila. Nucleus position, with no morphological changes (comparing nuclei they look alike).

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55
Q

Acute Cell Swelling Ultrastructural Features

A

Plasma membrane alterations, such as blebbing, blunting and loss of microvilli. Mitochondrial change, including swelling and the appearance of small amorphois densities. Dilation of the ER, with detachment of polysomes; intracytoplasmic myelin figures may be present. Nuclear alterations with disaggregation of granular and fibrillar elements.

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56
Q

Hydropic

A

Fatty change (cell swelling): due to increase uptake of H2O and then to diffuse disintegration of organelles and cytoplasmic proteins.

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57
Q

Hypertrophy

A

Cell enlargement: the cell enlargement is caused by increase of normal organelles

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58
Q

Acute Cell Swelling Prognosis

A

Depends on the number of cells affected and importance of cells. Good (if O2 is restored before the “point of no return”)

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59
Q

Fatty Change

A

Reversible cell injury. Sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation. May be preceded or accompanied by cell swelling.

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60
Q

Fatty Change Pathogenesis

A

Impaired metabolism of fatty acids. Accumulation of triglycerides. Formation of intracytoplasmic fat vacuoles.

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61
Q

Fatty Change Etiology

A

Hypoxia, toxicity, metabolic disorders. Seen in abnormalities of synthesis, utilization and or mobilization of fat.

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62
Q

Fatty Change Gross Appearance

A

Enhanced reticular pattern in specific zones, edges are rounded and will bulge on section, tissue soft and often friable, cuts easily and has a greasy texture.

Typically seen in the liver.

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63
Q

Fatty Change Histologic Appearance

A

Well delineated, lipid-filled vacuoles in the cytoplasm, vacuoles are single to multiple, either small or large, vacuoles may displace the cell nucleus to periphery

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64
Q

Necrosis

A

An irreversible cell injury. Outcome can be inflammation. Oncosis, oncotic necrosis

65
Q

Necrosis Etiology

A

Cell death after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury

66
Q

Necrosis Morphology

A

Due to denaturation of proteins, enzymatic digestion of the cell

67
Q

Necrosis Ultrastructurally

A

Changes for coagulative necrosis, nuclei will become smaller and shrink, more condensed, hyperchromatic, and darker in color, or undergo kayrolysis or karyorrhexis

68
Q

Karyolysis

A

Nuclear Fading Necrosis

69
Q

Pykinosis

A

Nuclear shrinkage Necrosis

70
Q

Karyorrhexis

A

Nuclear Fragmentation Necrosis

71
Q

Coagulative (coagulation) Necrosis

A

Architecture of dead tissues is preserved (days). Ultimately the necrotic cells are removed by phagocytosis by WBC, digestion by the action of lysosomal enzymes of the WBCs. Common cause: Ischemia

72
Q

Liquefactive Necrosis

A

Necrotic architecture is “liquefied”. Dead cells are digested and transformation of the tissue into a liquid viscous mass.

73
Q

Abscess

A

A localized collection of pus (liquefied tissue) in a cavity formed by disintegration of tissues surrounded by fibrous connective tissue

74
Q

Septic Abscess

A

Infection, release of enzymes from WBCs and infectious agent

75
Q

Sterile Abscess

A

process caused by non-living irritants such as drugs

76
Q

Gangrenous Necrosis

A

Not a specific pattern of cell death but begins mostly as coagulative necrosis. Likely due to ischemia.

77
Q

Dry Gangrene

A

Necrosis, no bacterial superinfections; tissue appears dry

78
Q

Wet Gangrene

A

Necrosis, bacterial superinfections has occurred - tissue looks wet and liquefactive. By actions of degradative enzymes in the bacteria and the attracted WBCs

79
Q

Caseous Necrosis

A

Friable (crumble) white: area of necrosis. Necrotic debris represents dead WBCs. A chronic necrosis. Often associated with poorly degradable lipids of bacterial origin

80
Q

Enzymatic Necrosis

A

A type of fat necrosis; aka pancreatic necrosis of fat.

81
Q

Traumatic Necrosis

A

A type of fat necrosis; Dystocia, subcutaneously in inter-muscular fat at sternum

82
Q

Necrosis of Abdominal Fat

A

A type of fat necrosis

83
Q

Fibrinoid Necrosis

A

A special form of necrosis usually seen in immune reaction involving blood vessels. Occurs when Ag-Ab complexes are desposited in the walls of arteries.

84
Q

Two examples of Liquefactive Necrosis

A

Leukoencephalomalacia = white matter

Polioencephalomalacia = grey matter

85
Q

Apoptosis

A

Irreversible cell injury. Programmed cell death

86
Q

Apoptosis Etiology

A

It is genetically regulated and sometimes referred to as programmed cell death.

87
Q

Apoptosis Physiologic

A

Programmed cell death during embryogenesis. Hormone dependent involutions or organs in the adult (e.g. thymus, uterus-post-parturition). Cell deletion in proliferating cell populations (intestinal epithelial turnover). Deletion of auto-reactive T cells in the thymus (by cytotoxic T cells)

88
Q

Apoptosis Pathologic

A

Tumor Necrosis Factor (TNF) or Fas Ligand (FasL) infuction of apoptosis in many cells. DNA damage. Accumulation of misfolded proteins. Cell injury in certain infections: viral. Pathologic atrophy in parenchymal organs after duct obstruction.

89
Q

Apoptosis Morphology

A

Cell shrinkage with increase cytoplasmic density. Chromatin condensation (pyknosis). Formation of cytoplasmic blebs and apoptotic bodies (fragmentation). Phagocytosis of apoptotic cells by adjacent healthy cells.

90
Q

Intrinsic Pathway

A

Mitochondrial pathway. Result of increase mitochondrial permeability & release of pro-apoptotic molecules (death inducers) into the cytoplasm.

91
Q

Cytochrome C

A

Essential for life; released into cytoplasm and initiates suicide program of apoptosis

92
Q

Extrinsic Pathway

A

Death receptor initiated pathway.

93
Q

Fas-L

A

Expressed on T-cells that identify self Ag & some cytotoxic T-cells (perforin, granzymes)

94
Q

Apoptotic bodies

A

Edible for phagocytes, expressed phospholipids in the outer layer of the membrane. May become coated with natural Ab and proteins of the complement system.

95
Q

Apoptotic cells

A

Secrete soluble factors that recruit phagocytes. Some express thrombospondin

96
Q

Phosphatidylserine

A

A type of phospholipid that carries a negative charge. Located on the inner membrane. Involved in electrostatic protein interactions. When it flips to the outer membrane it either signal for phagocytes or is a cofactor in blood clotting

97
Q

Spingomyeline & Glycolipids

A

A type of phospholipid. Preferentially expressed on the outer face and is important in cell-to-cell interaction or cell-to-matrix interactions. Ion and metabolite transport.

98
Q

Lipid Rafts

A

Horizontal associated of sphingomyeline and cholesterol

99
Q

Passive Transport

A

Molecules move down a concentration or electrical gradient

100
Q

Active Transport

A

Molecules move against a gradient, required ATP.

101
Q

Channels

A

Create hydrophilic pores and permit rapid movement of solutes

102
Q

Carriers

A

Bind a specific solute, undergo conformational changes to transport the solute across the membrane. Slower movement of solutes

103
Q

Potocytosis

A

A form of endocytosis, non-coated vesicles, implicated in regulation of transmembrane signaling and or cell adhesion via internalization of receptors and integrins

104
Q

Pinocytosis

A

Membrane pinches off to form a clathrin coated vesicle. It will recycle contents back to the plasma membrane via exocytosis OR remove the clathrin and fuses with a lysosome.

105
Q

Cell Polarity

A

Maintained by the cytoskeleton, refers to the spatial differences in shape, structure, and function of cells.

106
Q

Actin Microfilaments Structure

A

Thinnest of the filaments. Comprised of globular protein subunits. G protein subunits polymerize into a polarized double-stranded helix (F-actin)

107
Q

Actin Microfilaments Function

A

In muscle cells: muscle contraction via association with myosin.

In non-muscle cells: control shape and movement. Various actin-binding proteins facilitate assembly of F-actin into well organized bundles.

108
Q

Intermediate Filaments Structure

A

10nm, large and individual types are tissue specific

109
Q

Cytokeratin

A

Intermediate filament for epithelial cells

110
Q

Vimentin

A

Intermediate filament for mesenchymal cells

111
Q

Desmin

A

Intermediate filament for muscle cells

112
Q

Intermediate Filament Function

A

Tensile strength, cell shape, cytoskeletal cross talk, signal transduction, adhesion, motility, tethering and positioning of organelles, regulation of nuclear transcription

113
Q

Microtubules Structure

A

25 nm, Non-covalently polymerized dimers. Arrayed in hollow tubes, constantly elongating or shrinking, defined polarity.

114
Q

Microtubules Negative End

A

Embedded in the microtuble organizing center (MTOC)

115
Q

Microtubules Positive End

A

Elongates or recedes as needed

116
Q

Microtubules Function

A

Connecting cables for molecular motor proteins. Molecular motor proteins use ATP to move vesicles, organelles, or other molecules around cells. Participate in sister chromatid separation during mitosis. Adapted to form motile cilia or flagella

117
Q

Kinesins

A

Moves along the microtubules from positive to negative (antegrade)

118
Q

Dyneins

A

Moves along the microtubules from negative to positive (retrograde)

119
Q

Endoplasmic Reticulum

A

Site of synthesis of all transmembrane proteins and lipids

120
Q

Ribosomes

A

Translate mRNA into proteins

121
Q

Proteins within the ER

A

Oligomerize, form disulfide bonds and have sugar moieties attached

122
Q

Oligomerize

A

chemical process that converts monomers to macromolecular complexes through a finite degree of polymerization

123
Q

Chaperone molecules

A

Retain proteins in the ER until all modifications are complete and the protein is properly folded.

124
Q

Smooth ER

A

Responsible for sequestering intracellular calcium

125
Q

Golgi apparatus

A

Shuttle proteins and lipids destined for other organelles or extracellular exports

126
Q

Mannose-6-Phosphate

A

An example of a golgi apparatus that directs enzymes to lysosomes

127
Q

Lysosomes

A

Waste management system that contain numerous hydrolases. Digest macromolecules.

128
Q

Pinocytosis

A

Fluid phase. Material passes from the plasma membrane to the early endosome to the late endosome and into the lysosome.

129
Q

Endocytosis

A

Receptor mediated. Material passes from the plasma membrane to the early endosome to the late endosome and into the lysosome.

130
Q

Autophagy

A

Senescent organelles and large denatured proteins moved into a double membrane derived from the ER. Progressively expands to form an autophagosome. The autophagosome fuses with lysosomes and contents are catabolized.

131
Q

Phagocytosis

A

Microorganisms, large fragments of matrix or debris. Material engulfed to form a phagosome. Phagosome fuses with lysosome.

132
Q

Proteasomes

A

Degrade cytosolic proteins, denatured, or misfolded proteins and other macromolecules. Identified when proteins bind to a marker (ubiquitin). Digest proteins into 6-12 AA fragments.

133
Q

Ubiquitin

A

is a small protein that is found in almost all cellular tissues, which helps to regulate the processes of other proteins in the body

134
Q

Mitochondrial Function

A

Aerobic metabolism, Warburb Effect, Source of ROS, and Apoptosis

135
Q

Aerobic Metabolism

A

TCA/Kreb’s Cycle or ETC

136
Q

TCA/Kreb’s Cycle

A

oxidize substrates to CO2. Transfers high energy electrons from glucose to molecular oxygen

137
Q

Electron Transport Chain

A

Oxidation drives the H+ pump. Transfer H+ from core matrix into the intermembrane space. As H+ flow down the electrochemical gradient, energy is released as ATP.

138
Q

The Warburg Effect

A

Occurs in rapidly growing cells. Uses the TCA cycle and for building blocks of lipids, nucleic acid proteins needed for cell growth.

Uses glucose and instead of making ATP they make these building blocks.

Decrease production of ATP/glucose molecule.

139
Q

Chromatin organization

A

DNA is organized around histones into nucleosomes. Nucleosomes are wound into a helix to form chromatin. Chromatin wound again into a supercoiled chromosomes.

140
Q

Chromatin

A

DNA complex to protein

141
Q

Euchromatin

A

Uncoiled, transcriptionally active

142
Q

Heterochromatin

A

Coiled, transcriptionally inactive

143
Q

Nucleolus

A

Organelle of the nucleus, composed of RNA protein chromatin, functions in synthesis of rRNA. Prominence is a subjective measure of a cell’s synthetic activity.

144
Q

6 Major Mechanism of Cell Injury

A
  1. Depletion of ATP
  2. Mitchondrial damage
  3. Calcium influx and loss of calcium homeostasis
  4. Oxidative stress
  5. Defects in membrane permeability
  6. Damage to DNA and Proteins
145
Q

Hypoxia

A

An oxygen deficiency. Partial reduction in O2 delivery to a tissue.

146
Q

Anoxia

A

An oxygen deficiency. No O2 delivery to a tissue.

147
Q

Ischemia

A

Reduction in blood supply that can cause oxygen deficiency

148
Q

Depletion of ATP

A

Fundamental cause of necrotic cell death.

Na/K ATPase pump failure leads to cell swelling, ER swelling, plasma membrane damage.

Altered cell metabolism, use of anaerobic glycolysis which leads to depletion glycogen stores, increase lactic acid, decreased pH and loss of enzyme function.

Lastly ribosome detachment which leads to decreased protein synthesis.

149
Q

Mitochondrial damage leads to three consquences

A
  1. Formation of the Mitochondrial Permeability Transition Pore (MPTP) which leads to cell necrosis
  2. Increased production of ROS
  3. Activation of apoptotic pathways
150
Q

Loss of Ca homeostasis - accumulation

A

Either from cell damage (extrinsic) or released from SER & mitochondria (intrinsic). Leads to membrane damage, nuclear damage, ATP depletion.

151
Q

Reactive Oxygen Species

A

Type of oxygen derived free radical, well established role in cell injury. Normally produced during mitochondrial respiration. Degraded and removed by cell scavenging defense systems.

152
Q

ROS Mechanisms

A

Initiated autocatalyic reactions

153
Q

Formation of ROS

A 
Normal metabolic processes
Absorption of radiant energy
Inflammation
Transition metals
Nitric Oxide (NO)
154
Q

Removal of ROS

A

Spontaneous decay
Antioxidants - will block initiation
Storage and Transport proteins
Enzymes

155
Q

Pathologic effects of ROS

A

Lipid peroxidation in membrane
Oxidative modification of proteins
Lesions in DNA

156
Q

Membrane Damage Mechanisms

A

Reactive Oxygen Species
Decreased Phospholipid synthesis
Increased phospholipid breakdown
Cytoskeletal abnormalities

157
Q

Alanine Aminotransferase (ALT)

A

Located in the cytoplasm of hepatocytes and convert alanine into pyruvate which is used for gluconeogenesis. Used for clinical pathology correlation. When hepatocytes are injured they release ALT.

158
Q

Protein Damage

A

Accumulation of misfolded proteins from either genetics or ROS

159
Q

DNA Damage

A

Radiation, cytotoxic anticancer drugs, hypoxia from eithe rdirect damage or ROS

Pathology (3 decks)

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