Unit 1 General Concept Review Flashcards
(129 cards)
1
Q
Nucleus
A
Contains DNA and RNA arranged into chromatids.
Present in all cells except RBCs and platelets
Main overseer of cytoplasmic events
2
Q
Cytoplasm
A
Cellular contents between cellular membrane and nucleus
Contains organelles and cytosol
3
Q
Mitochondria
A
Organelle involved primarily in the (aerobic) production of ATP
4
Q
Ribosomes
A
Small granules of rRNA
Either free or attached to RER
Protein synthesis (free => for internal use; RER => for export. Ish)
5
Q
Cytosol
A
Fluid portion of cytoplasm
AKA intracellular fluid (ICF)
H2O, dissolved solutes, suspended particles
Hyaloplasm + microtubules and microfilaments
6
Q
Smooth Endoplasmic Reticulum
A
Extends from RER
In liver, catabolism of drugs, hormones, carcinogens
Synthesis of steroids and fatty acids
In liver, kidneys and intestines, releases glucose into bloodstream
In muscles release Ca+
7
Q
Rough Endoplasmic Reticulum
A
Protein production
8
Q
Golgi Apparatus
A
Create secretory granules and lysosomes
Modify and package cellular products
9
Q
Lysosomes
A
Membrane-bound digestive cytoplasmic organelles
Rich in lytic enzymes
Created by golgi apparatus
10
Q
Hyaloplasm
A
Ground substance of cytoplasm;
Fluid portion of cytosl
11
Q
Cytoskeleton
A
Composed of microfilaments (actin and myosin), microtubles, and intermediate filaments
Maintains cell shape; enables cell to adapt to external mechanical pressure.
12
Q
Plasma membrane
A
Outer surface of cell.
Selectively permeable
Phosolipid bilayer
Hydrophobic inside, hydrophilic outside
13
Q
Reversible cellular damage
A
Within range of homeostasis Cellular swelling and temporary loss of function: - reduced energy production - decreased protein synthesis - increased autophagy Membrane intact.
14
Q
Irreversible Cell Damage
A
Overwhelming insult, toxins, anoxia –> nuclear changes and loss of membrane integrity
15
Q
Atrophy
A
Decrease in the size of cells –> reduced tissue mass
Possible causes include age, poor nutrition, immobility
16
Q
Hypertrophy
A
Increase in the size of individual cells –> increased tissue mass
17
Q
Dysplasia
A
Inconsistent cell size and shape within a tissue.
Large nuclei, increased mitotic rate.
May indicate precancerous state
18
Q
Hyperplasia
A
Increased number of cells –> increased tissue mass
19
Q
Metaplasia
A
One mature cell type replaced by a different mature cell type
20
Q
Apoptosis
A
Regulated, programmed cell death
Result of a series of molecular signals within cell
Cancer often involves impaired apoptosis
21
Q
Autolysis
A
Death of cells and tissues in a dead organism
22
Q
Necrosis
A
Exogenously induced cell death
23
Q
Forms of necrosis
A
- coagulative
- liquefactive
- caseous
- enzymatic fat
24
Q
Coagulative necrosis
A
Most common form of necrosis, most often caused by anoxia, most often in solid internal organs
Rapid inactivation of cytoplasmic hydrolytic enzymes –> prevents lysis of tissues
Tissues retain form and consistency
25
Liquefactive necrosis
Characterized by tissue dissolution.
Leukocytes invade necrotic tissue, release lytic enzymes, which transform solid tissue into liquid pus
Occurs most often in the brain
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Secondary liquefaction
Tissue that have undergone coagulative necrosis may attract leukocytes and undergo liquefaction later on.
27
Caseous necrosis
Typically found in TB, as well as with some fungal infections
Coagulative necrosis with limited liquefaction
28
Enzymatic fat necrosis
Special form of liquefactive necrosis caused by action of LIPOlytic enzymes
Limited to fat tissue, usually around the pancreas. Usually digestive enzymes from damaged pancreas invade surrounding fatty tissue
Appears like liquified fat with whitish specks of calcium soap
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Pancreatic enzymes degrade fat into ________. _______ react with _____ to create _______.
Glycerol and free fatty acids
Free fatty acids
Ca+
calcium soaps
30
Wet Gangrene
Bacterial infection of coagulated tissue, leading to secondary liquifaction
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Dry Gangrene
Necrotic tissue dries out and becomes black and mummified.
Most often extremities, related to peripheral vascular disease
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TB is associated with what sort of necrosis
caseous
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Brains tend to undergo what sort of necrosis
liquefactive
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Solid organs tend to undergo what sort of necrosis
coagulative
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Fat surrounding the pancreas is prone to what sort of necrosis
enzymatic fat
36
Inflammation
The body's nonspecific response to tissue injury
37
Cardinal signs of inflammation
```
Redness
Swelling
Heat
Pain
Loss of function
```
38
Pathogenesis of inflammation involves what four steps?
1. changes in circulation of blood
2. changes in vessel wall permeability
3. release of soluble mediators of inflammation
4. cellular actions
39
Inflammation: changes in circulation
First response to injury
- Vasoconstriction followed by vasodilation --> hyperemia
- blood flow slows -->congestion --> erythrocytes form rouleaux --> further impeding circulation
- WBC's attach to endothelium (pavementing)
40
Inflammation: changes in vascular permeability
Second step
- increased pressure inside blood vessels and soluble mediators of inflammation cause endothelial cells to contract --> leaky endothelium
41
Difference between cell derived and plasma derived soluble mediators of inflammation
Plasma-derived must be activated
| Cell-derived either prefab and stored in platelets and leukocytes, or created de novo
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Histamine
Preformed SMI
Released by platelets and mast cells
=> immediate transient reaction
Increases endothelial leakiness
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Bradykinin
Cell derived SMI, created de novo so takes longer to take effect.
Formed in plasma by activation of Coagulation Factory XII
Increases endothelial leakiness and incites pain.
44
Complement System
Cascade of protein activation following three paths (classical, alternative, lectin), all leading to formation of the Membrane Attack Complex (MAC)
Also causes histamine release, vasodilation, and promotes chemotaxis
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Arachidonic Acid Derivatives
Cell membrane derived amino acids metabolized through two pathways:
1. lipoxygenase
2. cyclo-oxygenase
46
Lipoxygenase pathway
One of the Arachidonic Acid pathways
Creates:
1. leukotrienes (promote chemotaxis, increase vascular permeability)
2. lipoxins (inhibit chemotaxis)
47
Cyclo-oxygenase pathway
One of the arachidonic acid pathways
Produces
1. prostaglandins (vasodilation, vascular permeability, mediation of pain and fever)
2. thromboxane (platelet aggregation, thrombosis, vasoconstriction)
48
Soluble Mediators of Inflammation (SMIs)
Histamine
Bradykinin
Complement System
Arachidonic Acid Derivatives (Lipoxygenase and Cyclo-oxygenase pathways)
49
Cellular events associated with inflammation
Emigration of leukocytes
Phagocytosis
Chemotaxis
50
Leukocytes involved in inflammation
Polymorphonuclear neutrophils
Eosinophils
Basophils
Macrophages
51
Chemotaxis
Active movement of WBCs in respond to the release of chemical mediators
WBCs move up concentration gradient
52
Edema
Excess fluid in tissue
Local or systemic
53
Transudate
Fluid that filters through a membrane.
Contains very few proteins, cells
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Exudate
Fluid with high concentration of cells and proteins.
In inflammation, formed by emigration of cells across vascular walls
Pus is a purulent exudate.
55
Polymorphonuclear neutrophils
Most numerous circulating WBC
Multi segmented nucleus
First to arrive.
Bactericidal, phagocytitic, releases cytokines
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Eosinophils
2-3% of circulating WBCs
Segmented nucleus
Prominent in allergic reactions and inflammatory responses to parasites
57
Basophils
Less than 1% of circulating WBCs
Most prominent in IgE reactions
Precursor of mast cells
58
Macrophages
Derived from blood monocytes
Late to party (3-4 days), but long lived. Involved in chronic inflammation.
Phagocytitic and bactericidal
59
Acute inflammation
Removal of stimuli stops acute response
Possible outcomes: resolution, abscess formation, chronic inflammation.
60
Chronic inflammation
Either prolonged acute or persistent causative agents.
May not demonstrate classic cardinal signs
Secretory products of inflammatory cells cause fibrosis and more inflammation.
Outcomes: tissue destruction, fibrosis
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7 kinds of inflammation
1. Serous
2. Fibrinous
3. Purulent
4. Ulcerative
5. Pseudomembranous
6. Chronic
7. Granulomatous
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Serous inflammation
Mild, occurs in early stages
Self limiting
Characterized by clear fluid
Viral infections, burns, arthritis
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Fibrinous inflammation
Fibrin-rich exudate
More severe than serous.
Doesn't resolve easily
Bacterial infections (strep throat, bacterial pneumonia, pericarditis)
Leads to fibrosis in parenchyma --> loss of function
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Purulent inflammation
Caused by pus-forming bacteria such as staph and strep.
Pus can accumulate in mucosa, skin, internal organs
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Abscess
Localized collection of pus
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Pyrogenic cytokines
Interleukin 1
| Tumour necrosis factor
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Leukocytosis
Increase in circulating WBC
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Loss of continuously dividing cells
AKA mitotic or labor cells
Continuously replacing
Resolution- minimal tissue damage; rapid recovery
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Loss of quiescent cells
AKA facultative mitotic or stable cells
Don't divide regularly but can be stimulated to divide by damage (or hepatocytes)
Regeneration: damaged tissue replace by identical tissue from proliferation by nearby cells.
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Loss of non-dividing cells
AKA post-mitotic or permanent cells
Repair -- damaged parenchymal tissue replaced with connective tissue
Functional capacity lost
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Healing by first intention
Wound is clean, free of foreign material, non-necrotic, and edges are close together.
72
Delayed primary healing
Wound is left open, allowing debridement and cleaning before closure attempted
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Healing by second intention
Large break in tissue, more inflammation
Longer healing times
Scar tissue (granulation tissue allowed to build instead of closing wound immediately)
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Keloid scar
Excessive collagen
Scar overgrowth beyond limits of wound
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Contraction
Fixation and deformity of joint
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Adhesion
Bands of scar tissue that join two normally separated surfaces.
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Hypersensitivity reaction
Allergic or autoimmune disorders
Abnormal immune response to exogenous antigen or endogenous anti-antigen
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Ab-Ag reaction
The complex formed when antibodies and antigens bond to each other
79
Agglutination
Antibodies to insoluble antigens (like to RBCs) clump and separate from serum
Complement cascade --> cell lysis
Occurs in all IgM and IgG complexes
80
Type I Hypersensitivity
Anaphylactic or atopic
IgE and mast cells or basophils.
First exposure --> plasma cells produce specific IgE
Reexposure --> AgAb complex --> histamine.
81
Hay fever
Type 1 hypersensivity
82
Atopic dermatitis
Type 1 hypersensivity
83
Bronchial asthma
Type 1 hypersensivity
84
Anaphylactic shock
Type 1 hypersensivity
85
Type 2 hypersensivity
Cytotoxic Antibody-Mediated Reaction
Mediated by IgG or IgM
Often autoimmune
Reexposure activates complement --> cell lysis
Can be triggered by extrinsic or intrinsic factors.
86
Goodpastures
Type 2 hypersensivity
Autoimmune response to collagen type IV on basement membranes --> severe renal and pulmonary damage
87
Graves' disease
Type 2 hypersensivity
Ab to TSH --> overproduction of thyroid hormone
88
Myasthenia gravis
Type 2 hypersensivity
Ab to ACh receptors --> muscle weakness and paralysis
89
Type 3 hypersensivity
Immune-complex mediated reaction
Overproduction of IgG and IgM -->Deposition of AgAb complexes in tissues
- triggers complement -> damage to tissues
Acute or chronic; local or systemic
90
SLE
Lupus
| Systemic Type 3 hypersensitivity
91
Poststreptococcal Glomerulonephritis
Type 3 hypersensitivity
Follows strep throat --> AgAb complex sticks in glomerular basement membrane.
92
Polyarteritis nodosa
Type 3 hypersensitivity
Localized in small to medium sized arteries
Acute focal fibrinoid necrosis -->chronic destruction of blood vessel wall
93
Type 4 hypersensitivity
Cell-mediated Delayed-type reaction
T lymphocyte and macrophages aggregate and form granulomas
94
M tuberculosis
Type 4 hypersensitivity
95
Mycobacterium leprae
Type 4 hypersensivity
96
Sarcoidosis
Type 4 hypersensitivity
Idiopathic granulomatous disease
97
Contact dermatitis
Most common Type 4 hypersensitivity
No granulomas
98
5 classes of antibodies
```
IgG
IgM
IgA
IgE
IgD
```
99
IgM
Largest immunoglobulin
Neutralizes microorganisms.
May mediate Type 2 Hypersensitivity
First on scene
ABO antibody
100
IgG
Smallest and most numerous
Can mediate Type II Hypersensitivity
Can cross placenta
Acts as opsonin (makes bacteria tasty for phagocytes)
101
IgA
Mucus, breast milk, nasal secretions, tears.
102
IgE
Found in trace amounts in serum.
Created by mast cells
Mediates type I hypersensitivity
103
IgD
Bound to cell membranes on B cells.
Participates in B cell activation
104
Neoplasia
Uncontrolled, unregulated cell growth
Autonomous
Excessive
Disorganized
105
Benign vs malignant tumours: macroscopic
Benign: demarcated, often encapsulated.
Malignant: Unencapsulated, infiltrative
106
Benign vs malignant tumours: microscopic
Benign: resemble original tissue. Differentiated.
Malignant: anaplasic, undifferentiated
107
Anaplasia
Cells (often malignant) showing features not present in original tissue
108
Benign vs malignant tumours: cellular
Benign: uniform, similar features. Regular shaped nuclei
Malignant: nuclear pleomorphism. Large nuclei; aneuploid
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Pleomorphism
Variability in size, shape, staining properties of tumour cell nuclei.
110
Aneuploid
Chromosomal abnormalities seem in malignant cells.
111
Metastatic spread can occur along what three pathways
Lymphatics
Blood
Body cavities/surfaces
112
~oma
Usually denote benign tumours of mesenchymal cells
113
Malignant ~Oma exceptions
Lymphoma
Glioma
Seminoma
114
~sarcoma
Denotes malignant tumour of mesenchymal cells
115
~blastoma
Malignant tumour of embryonic cells
116
Benign tumours from germ cells
Teratoma
117
Malignant tumours of germ cells
Teratocarcinoma
118
Cancer staging
Extent of tumour spread
Has better predictive value than grading
Size (T) , lymph node involvement (N), distant metastasis (M) -- each assigned number in TNM system
Also I-IV and A-D scales
119
Cancer grading
I. Well differentiated
II. Moderately well differentiated.
III. Undifferentiated
120
Steps of carcinogenesis
1. Ingestion of (pro)carcinogen
2. initiation (genetic changes)
3. Promotion (proliferation of affected cells)
4. Conversion (to new cell type)
5. Progression (acquisition of new features)
6. Clonal expansion.
121
Proto-Oncogenes converted to oncogenes by:
1. Point mutation
2. Gene amplification
3. Chromosomal rearrangement
4. Insertion of viral genome. (HBV inserted in liver cancer genome)
122
Clinical manifestation of cancer
CAUTION
```
Change in bowel/bladder habit
A sore that won't heal
Unusual bleeding or discharge
Thickening or lump in breast or elsewhere
Indigestion of difficulty swallowing
Obvious change in wart or mole
Nagging cough or hoarseness
```
123
Cachexia
Wasting despite normal food intake
124
Paraneoplastic syndrome
Symptoms caused by cancer secretions, but not by local presence of cancer cells.
125
Incidence
Number of new cases in a specific time period in a specific population
126
Prevalence
Number of all cases in a specific population at a given time
127
Cancer incidence: men
Men
1. Prostate
2. Lung/bronchial
3. Colorectal
128
Cancer incidence: women
1. Breast
2. Lung/bronchial
3. Colorectal
129
Cancer mortality
1. Lung/bronchus
2. Prostate/breast
3. Colorectal.
