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All Path Review 700 > Unit 1 General Concept Review > Flashcards

Unit 1 General Concept Review Flashcards

1
Q

Nucleus

A

Contains DNA and RNA arranged into chromatids.
Present in all cells except RBCs and platelets
Main overseer of cytoplasmic events

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2
Q

Cytoplasm

A

Cellular contents between cellular membrane and nucleus

Contains organelles and cytosol

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3
Q

Mitochondria

A

Organelle involved primarily in the (aerobic) production of ATP

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4
Q

Ribosomes

A

Small granules of rRNA
Either free or attached to RER
Protein synthesis (free => for internal use; RER => for export. Ish)

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5
Q

Cytosol

A

Fluid portion of cytoplasm
AKA intracellular fluid (ICF)
H2O, dissolved solutes, suspended particles

Hyaloplasm + microtubules and microfilaments

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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+

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7
Q

Rough Endoplasmic Reticulum

A

Protein production

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8
Q

Golgi Apparatus

A

Create secretory granules and lysosomes

Modify and package cellular products

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9
Q

Lysosomes

A

Membrane-bound digestive cytoplasmic organelles
Rich in lytic enzymes
Created by golgi apparatus

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10
Q

Hyaloplasm

A

Ground substance of cytoplasm;

Fluid portion of cytosl

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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.

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12
Q

Plasma membrane

A

Outer surface of cell.
Selectively permeable
Phosolipid bilayer
Hydrophobic inside, hydrophilic outside

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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.
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14
Q

Irreversible Cell Damage

A

Overwhelming insult, toxins, anoxia –> nuclear changes and loss of membrane integrity

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15
Q

Atrophy

A

Decrease in the size of cells –> reduced tissue mass

Possible causes include age, poor nutrition, immobility

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16
Q

Hypertrophy

A

Increase in the size of individual cells –> increased tissue mass

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17
Q

Dysplasia

A

Inconsistent cell size and shape within a tissue.
Large nuclei, increased mitotic rate.
May indicate precancerous state

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18
Q

Hyperplasia

A

Increased number of cells –> increased tissue mass

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19
Q

Metaplasia

A

One mature cell type replaced by a different mature cell type

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20
Q

Apoptosis

A

Regulated, programmed cell death
Result of a series of molecular signals within cell

Cancer often involves impaired apoptosis

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21
Q

Autolysis

A

Death of cells and tissues in a dead organism

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22
Q

Necrosis

A

Exogenously induced cell death

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23
Q

Forms of necrosis

A
  1. coagulative
  2. liquefactive
  3. caseous
  4. enzymatic fat
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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

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25
Q

Liquefactive necrosis

A

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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26
Q

Secondary liquefaction

A

Tissue that have undergone coagulative necrosis may attract leukocytes and undergo liquefaction later on.

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27
Q

Caseous necrosis

A

Typically found in TB, as well as with some fungal infections
Coagulative necrosis with limited liquefaction

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28
Q

Enzymatic fat necrosis

A

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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29
Q

Pancreatic enzymes degrade fat into ________. _______ react with _____ to create _______.

A

Glycerol and free fatty acids

Free fatty acids
Ca+
calcium soaps

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30
Q

Wet Gangrene

A

Bacterial infection of coagulated tissue, leading to secondary liquifaction

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31
Q

Dry Gangrene

A

Necrotic tissue dries out and becomes black and mummified.

Most often extremities, related to peripheral vascular disease

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32
Q

TB is associated with what sort of necrosis

A

caseous

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33
Q

Brains tend to undergo what sort of necrosis

A

liquefactive

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34
Q

Solid organs tend to undergo what sort of necrosis

A

coagulative

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35
Q

Fat surrounding the pancreas is prone to what sort of necrosis

A

enzymatic fat

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36
Q

Inflammation

A

The body’s nonspecific response to tissue injury

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37
Q

Cardinal signs of inflammation

A 
Redness
Swelling
Heat
Pain 
Loss of function
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38
Q

Pathogenesis of inflammation involves what four steps?

A
  1. changes in circulation of blood
  2. changes in vessel wall permeability
  3. release of soluble mediators of inflammation
  4. cellular actions
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39
Q

Inflammation: changes in circulation

A

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)
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40
Q

Inflammation: changes in vascular permeability

A

Second step
- increased pressure inside blood vessels and soluble mediators of inflammation cause endothelial cells to contract –> leaky endothelium

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41
Q

Difference between cell derived and plasma derived soluble mediators of inflammation

A

Plasma-derived must be activated

Cell-derived either prefab and stored in platelets and leukocytes, or created de novo

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42
Q

Histamine

A

Preformed SMI
Released by platelets and mast cells
=> immediate transient reaction

Increases endothelial leakiness

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43
Q

Bradykinin

A

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.

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44
Q

Complement System

A

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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45
Q

Arachidonic Acid Derivatives

A

Cell membrane derived amino acids metabolized through two pathways:

  1. lipoxygenase
  2. cyclo-oxygenase
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46
Q

Lipoxygenase pathway

A

One of the Arachidonic Acid pathways
Creates:
1. leukotrienes (promote chemotaxis, increase vascular permeability)
2. lipoxins (inhibit chemotaxis)

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47
Q

Cyclo-oxygenase pathway

A

One of the arachidonic acid pathways
Produces
1. prostaglandins (vasodilation, vascular permeability, mediation of pain and fever)
2. thromboxane (platelet aggregation, thrombosis, vasoconstriction)

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48
Q

Soluble Mediators of Inflammation (SMIs)

A

Histamine
Bradykinin
Complement System
Arachidonic Acid Derivatives (Lipoxygenase and Cyclo-oxygenase pathways)

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49
Q

Cellular events associated with inflammation

A

Emigration of leukocytes
Phagocytosis
Chemotaxis

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50
Q

Leukocytes involved in inflammation

A

Polymorphonuclear neutrophils
Eosinophils
Basophils
Macrophages

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51
Q

Chemotaxis

A

Active movement of WBCs in respond to the release of chemical mediators

WBCs move up concentration gradient

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52
Q

Edema

A

Excess fluid in tissue

Local or systemic

53
Q

Transudate

A

Fluid that filters through a membrane.

Contains very few proteins, cells

54
Q

Exudate

A

Fluid with high concentration of cells and proteins.

In inflammation, formed by emigration of cells across vascular walls

Pus is a purulent exudate.

55
Q

Polymorphonuclear neutrophils

A

Most numerous circulating WBC

Multi segmented nucleus

First to arrive.

Bactericidal, phagocytitic, releases cytokines

56
Q

Eosinophils

A

2-3% of circulating WBCs

Segmented nucleus

Prominent in allergic reactions and inflammatory responses to parasites

57
Q

Basophils

A

Less than 1% of circulating WBCs

Most prominent in IgE reactions

Precursor of mast cells

58
Q

Macrophages

A

Derived from blood monocytes

Late to party (3-4 days), but long lived. Involved in chronic inflammation.

Phagocytitic and bactericidal

59
Q

Acute inflammation

A

Removal of stimuli stops acute response

Possible outcomes: resolution, abscess formation, chronic inflammation.

60
Q

Chronic inflammation

A

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

61
Q

7 kinds of inflammation

A
  1. Serous
  2. Fibrinous
  3. Purulent
  4. Ulcerative
  5. Pseudomembranous
  6. Chronic
  7. Granulomatous
62
Q

Serous inflammation

A

Mild, occurs in early stages
Self limiting
Characterized by clear fluid

Viral infections, burns, arthritis

63
Q

Fibrinous inflammation

A

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

64
Q

Purulent inflammation

A

Caused by pus-forming bacteria such as staph and strep.

Pus can accumulate in mucosa, skin, internal organs

65
Q

Abscess

A

Localized collection of pus

66
Q

Pyrogenic cytokines

A

Interleukin 1

Tumour necrosis factor

67
Q

Leukocytosis

A

Increase in circulating WBC

68
Q

Loss of continuously dividing cells

A

AKA mitotic or labor cells

Continuously replacing

Resolution- minimal tissue damage; rapid recovery

69
Q

Loss of quiescent cells

A

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.

70
Q

Loss of non-dividing cells

A

AKA post-mitotic or permanent cells

Repair – damaged parenchymal tissue replaced with connective tissue
Functional capacity lost

71
Q

Healing by first intention

A

Wound is clean, free of foreign material, non-necrotic, and edges are close together.

72
Q

Delayed primary healing

A

Wound is left open, allowing debridement and cleaning before closure attempted

73
Q

Healing by second intention

A

Large break in tissue, more inflammation

Longer healing times

Scar tissue (granulation tissue allowed to build instead of closing wound immediately)

74
Q

Keloid scar

A

Excessive collagen

Scar overgrowth beyond limits of wound

75
Q

Contraction

A

Fixation and deformity of joint

76
Q

Adhesion

A

Bands of scar tissue that join two normally separated surfaces.

77
Q

Hypersensitivity reaction

A

Allergic or autoimmune disorders

Abnormal immune response to exogenous antigen or endogenous anti-antigen

78
Q

Ab-Ag reaction

A

The complex formed when antibodies and antigens bond to each other

79
Q

Agglutination

A

Antibodies to insoluble antigens (like to RBCs) clump and separate from serum

Complement cascade –> cell lysis
Occurs in all IgM and IgG complexes

80
Q

Type I Hypersensitivity

A

Anaphylactic or atopic

IgE and mast cells or basophils.

First exposure –> plasma cells produce specific IgE

Reexposure –> AgAb complex –> histamine.

81
Q

Hay fever

A

Type 1 hypersensivity

82
Q

Atopic dermatitis

A

Type 1 hypersensivity

83
Q

Bronchial asthma

A

Type 1 hypersensivity

84
Q

Anaphylactic shock

A

Type 1 hypersensivity

85
Q

Type 2 hypersensivity

A

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
Q

Goodpastures

A

Type 2 hypersensivity

Autoimmune response to collagen type IV on basement membranes –> severe renal and pulmonary damage

87
Q

Graves’ disease

A

Type 2 hypersensivity

Ab to TSH –> overproduction of thyroid hormone

88
Q

Myasthenia gravis

A

Type 2 hypersensivity

Ab to ACh receptors –> muscle weakness and paralysis

89
Q

Type 3 hypersensivity

A

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
Q

SLE

A

Lupus

Systemic Type 3 hypersensitivity

91
Q

Poststreptococcal Glomerulonephritis

A

Type 3 hypersensitivity

Follows strep throat –> AgAb complex sticks in glomerular basement membrane.

92
Q

Polyarteritis nodosa

A

Type 3 hypersensitivity

Localized in small to medium sized arteries

Acute focal fibrinoid necrosis –>chronic destruction of blood vessel wall

93
Q

Type 4 hypersensitivity

A

Cell-mediated Delayed-type reaction

T lymphocyte and macrophages aggregate and form granulomas

94
Q

M tuberculosis

A

Type 4 hypersensitivity

95
Q

Mycobacterium leprae

A

Type 4 hypersensivity

96
Q

Sarcoidosis

A

Type 4 hypersensitivity

Idiopathic granulomatous disease

97
Q

Contact dermatitis

A

Most common Type 4 hypersensitivity

No granulomas

98
Q

5 classes of antibodies

A 
IgG
IgM
IgA
IgE
IgD
99
Q

IgM

A

Largest immunoglobulin

Neutralizes microorganisms.

May mediate Type 2 Hypersensitivity

First on scene
ABO antibody

100
Q

IgG

A

Smallest and most numerous

Can mediate Type II Hypersensitivity

Can cross placenta

Acts as opsonin (makes bacteria tasty for phagocytes)

101
Q

IgA

A

Mucus, breast milk, nasal secretions, tears.

102
Q

IgE

A

Found in trace amounts in serum.

Created by mast cells

Mediates type I hypersensitivity

103
Q

IgD

A

Bound to cell membranes on B cells.

Participates in B cell activation

104
Q

Neoplasia

A

Uncontrolled, unregulated cell growth

Autonomous
Excessive
Disorganized

105
Q

Benign vs malignant tumours: macroscopic

A

Benign: demarcated, often encapsulated.

Malignant: Unencapsulated, infiltrative

106
Q

Benign vs malignant tumours: microscopic

A

Benign: resemble original tissue. Differentiated.

Malignant: anaplasic, undifferentiated

107
Q

Anaplasia

A

Cells (often malignant) showing features not present in original tissue

108
Q

Benign vs malignant tumours: cellular

A

Benign: uniform, similar features. Regular shaped nuclei

Malignant: nuclear pleomorphism. Large nuclei; aneuploid

109
Q

Pleomorphism

A

Variability in size, shape, staining properties of tumour cell nuclei.

110
Q

Aneuploid

A

Chromosomal abnormalities seem in malignant cells.

111
Q

Metastatic spread can occur along what three pathways

A

Lymphatics
Blood
Body cavities/surfaces

112
Q

~oma

A

Usually denote benign tumours of mesenchymal cells

113
Q

Malignant ~Oma exceptions

A

Lymphoma
Glioma
Seminoma

114
Q

~sarcoma

A

Denotes malignant tumour of mesenchymal cells

115
Q

~blastoma

A

Malignant tumour of embryonic cells

116
Q

Benign tumours from germ cells

A

Teratoma

117
Q

Malignant tumours of germ cells

A

Teratocarcinoma

118
Q

Cancer staging

A

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
Q

Cancer grading

A

I. Well differentiated
II. Moderately well differentiated.
III. Undifferentiated

120
Q

Steps of carcinogenesis

A
  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
Q

Proto-Oncogenes converted to oncogenes by:

A
  1. Point mutation
  2. Gene amplification
  3. Chromosomal rearrangement
  4. Insertion of viral genome. (HBV inserted in liver cancer genome)
122
Q

Clinical manifestation of cancer

A

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
Q

Cachexia

A

Wasting despite normal food intake

124
Q

Paraneoplastic syndrome

A

Symptoms caused by cancer secretions, but not by local presence of cancer cells.

125
Q

Incidence

A

Number of new cases in a specific time period in a specific population

126
Q

Prevalence

A

Number of all cases in a specific population at a given time

127
Q

Cancer incidence: men

A

Men

  1. Prostate
  2. Lung/bronchial
  3. Colorectal
128
Q

Cancer incidence: women

A
  1. Breast
  2. Lung/bronchial
  3. Colorectal
129
Q

Cancer mortality

A
  1. Lung/bronchus
  2. Prostate/breast
  3. Colorectal.

All Path Review 700 (7 decks)

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