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Gen Path 300 > Classes 1-2 > Flashcards

Classes 1-2 Flashcards

0
Q

Symptoms

A

Subjective indicator

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1
Q

Sign

A

Objective indicator of pathology

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2
Q

Nucleocytoplasmic ratio

A

Ratio of nucleus to cytoplasm

Higher in undifferentiated adult cells, fetal cells, tumour cells.

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3
Q

Mitochondria

A

Double membrane involved in cellular energy production

Higher energy demands –>
More mitochondria

Undifferentiated cells have fewer mitochondria.

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4
Q

Ribosomes

A

Small RNA granules involved in protein synthesis.

Free floating (internal purposes) or attached to RER (for export)

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5
Q

Endoplasmic reticulum

A

Mesh work of membranes continuous with nuclear and plasma membranes.

Rough – have ribosomes – protein synthesis
Smooth – catabolism of drugs, hormones, nutrients.

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6
Q

Golgi apparatus

A

Adjacent to nucleus
Composed of membrane-blind cisterns

Modified, sorts and packages macromolecules

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7
Q

Lysosomes

A

Membrane bound digestive organelles
Lytic enzymes
Fuse with vesicles to digest materials.

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8
Q

Passive cell projections

A

Microvilli

Serve to increase surface area for absorption, but not involved in locomotion etc

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9
Q

Active cell projections

A

Require energy

Cilia
Flagella.

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10
Q

Three Forms of integration

A

Autocrine
Paracrine
Endocrine

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11
Q

Autocrine stimulation

A

Cell secretes substance that stimulates itself

Simplest

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12
Q

Paracrine Stimulation

A

Cell secretes substance that stimulates a nearby cell

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13
Q

Endocrine stimulation

A

Cell releases substance into bloodstream that stimulates structure far away

Always hormones

Can involve anatomically distinct organs

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14
Q

Atrophy

A

Decrease in size of cells resulting in reduced tissue mass

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15
Q

Hypertrophy

A

Increase in size of individual cells resulting in enlarged tissue mass.

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16
Q

Hyperplasia

A

Increased number of cells resulting in increased tissue mass

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17
Q

Metaplasia

A

When one mature cell is replaced by a different mature cell type.

Ex. In smokers ciliates columnar epithelia replaced by stratified squamous.

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18
Q

Dysplasia

A

Cells vary in size and shape.
Large nuclei.
Rate of mitosis increases

Possibly precancerous.

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19
Q

Intracellular accumulations

A

May occur as a result of overload of metabolites or exogenous material, or prevention of excretion.

Ex. Black lung or fatty liver.

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20
Q

Apoptosis

A

Endogenously programmed cell death

Active. Can by triggered by external or internal events.
Typically affects single cells.

Cell divides into smaller apoptic bodies which are phagocytized by macrophages or adjacent cells. (In necrosis the fragments are phagocytized by neutrophils).

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21
Q

Necrosis

A

Exogenously induced cell death

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22
Q

Four types of necrosis

A

1 coagulative
2 liquifactive
3 caseous
4 fat

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23
Q

Coagulative necrosis

A

Most common form.
Occurs when cell proteins altered/destroyed, mostly due to anoxia (ex heart attack)

Rapid inactivation of cytoplasmic hydrolytic enzymes, thus preventing cell lysis

Tissues retain regular form and consistency.

Most common in solid internal organs.

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24
Q

Liquifactive necrosis

A

Dead cells liquify, tissue becomes soft and diffluent.

Mostly brain. Typical of brain infarct

May be secondary to coagulative.

25
Q

Caseous necrosis

A

Typical of TB and some fungal infections.

Coagulative necrosis with limited liquifaction.

Centre becomes yellow and cheesy.

26
Q

Enzymatic Fat Necrosis

A

A form of liquifactive necrosis caused by lipolytic enzymes, usually around the pancreas.

Pancreatic enzymes released into fat dissolve tissue into glycerol and free fatty acids (which bind with Ca+ and become soapy)

27
Q

Gangrene

A

Dead tissue.

Wet (liquifaction) or dry (mummification)

Can undergo secondary change, such as calcification.

28
Q

What is a telltale sign of necrosis?

A

Ruptured cell membrane

29
Q

Pathological apoptosis

A

Example. Muscular dystrophy, and the excessive death of muscle cells.

Also, rejected transplanted organs.

30
Q

Pathological lack of apoptosis

A

Syndactyly

Chronic lymphomatic leukaemia.

31
Q

Inflammation

A

Body’s nonspecific response to injury

Necessary part of healing.

32
Q

Signs of inflammation

A 
Swelling
Heat 
Altered function
Redness
Pain
33
Q

Four components of acute inflammation

A
  1. Circulatory changes
  2. Changes in vessel wall permeability
  3. Release of SMIs
  4. Cellular events.
34
Q

Inflammation: change in blood circulation

A

First response.
Mechanical stimulus –> constriction followed by relaxation of sphincters –> blood rushes into capillaries –> hyperaemia.

Congestion caused by slowing blood, RBCs forming rouleaux, and WBC’s pavementing along endothelium.

35
Q

Inflammation: changes in vessel wall permeability

A

Increased permeability due to:
1 increased pressure (due to congestion),
2 reduced O2 and nutrient supply,
3 adhesion of platelets and WBC to vessel wall
4 release of SMIs

36
Q

Histamine

A

SMI. Biogenic amine.

Preformed. Released from mast cells and platelets

Contraction of epithelial cells –> gaps –> increased permeability.

Rapidly deactivated by histaminase

Immediate transient reaction.

37
Q

Bradykinin

A

SMI.
Created de novo through activation of Factor 12 (Hageman Factor)

Similar effect as histamines, but slower acting. Also incites pain.

38
Q

Hageman Factor

A

AKA Coagulation Factor 12.

In intrinsic pathway, combines with calcium –> activated Factor 10 –> fibrin

Also creates plasmin, which breaks fibrin apart.

And also involved in creation of bradykinin.

39
Q

Complement system

A

Circulating proteins, produced by liver, actives in inflammatory response.

Three pathways (classical, lectin and alternative).

40
Q

Result of the complement system

A
  1. Opsonin (make bacteria tasty for phages)
  2. Anaphylatoxins (mediate release of histamines from mast cells –> increased vascular permeability)
  3. Chemotaxis.(Attracting leukocytes)
  4. Membrane Attack Complex (MAC) –> cell lysis.
41
Q

Arachidonic Acid Derivatives

A

Mediators of inflammation derived from phospholipids of cell membrane (through action of phospholipase)

42
Q

What are the two pathways for arachidonic acid?

A

Lipoxygenase Pathway

Cyclooxygenase Pathway

43
Q

Lipoxygenase Pathway

A 
From arachidonic acid, forms:
1 leukotrienes (promotes chemotaxis and increases vascular permeability)
2. Lipoxins. (Inhibit chemotaxis)
44
Q

Cyclooxygenase Pathway

A

One way arachidonic acid is metabolized.

Creates:

  1. Prostaglandins (vasodilation, vascular permeability, mediates pain and fever)
  2. Thromboxane. (Platelet aggregation, thrombosis, vasoconstriction)
  3. Prostacyclin (counteracts effects of thromboxane).
45
Q

How do anti-inflammatory drugs work on the arachidonic acid system?

A

Corticosteroids: interrupt phospholipase, so arachidonic acid is never produced, and entire pathway is aborted.

Cox inhibitors (aspirin, ibuprofen, etc) block cyclooxygenase (first step of cyclooxygenase pathway) so thromboxane, prostaglandins and prostacyclin not produced.

46
Q

Prostaglandins

A

Eicosanoids produced in the cyclooxygenase pathway of arachidonic acid metabolism.

Stimulate vasodilation and vascular permeability, and mediate pain and fever (antipyretic)

47
Q

Thromboxane

A

Produced by the cyclooxygenase pathway of arachidonic acid metabolism.

Involved in vasoconstriction, platelet aggregation and thrombosis.

48
Q

Prostacyclin

A

Eicosanoid. Produced by the cyclooxygenase pathway of arachidonic acid metabolism.

Counters effect of thromboxane.

Inhibits platelet aggregation. Vasodilator.

49
Q

Leukotrienes

A

Eicosanoid. Produced by the lipoxygenase pathway of arachidonic acid metabolism.

Promote chemotaxis and increase vascular permeability.

50
Q

Lipoxin

A

Eicosanoid. Produced by the lipoxygenase pathway of arachidonic acid metabolism.

Inhibit chemotaxis.

51
Q

Emigration of Leukocytes

A

Increased permeability of vessel walls, lasting hours to days, allows for leakage of fluid into the institial space.

52
Q

Transudate

A

Leakage of fluid into interstitial spaces due to increased hydrostatic pressure.

Mostly fluid; very few proteins or large solutes

53
Q

Exudate

A

Fluid that emigrates across vessel walls during inflammation. Increased permeability of walls means that exudate contains many proteins and large solutes.

Acute stages mostly PMNs

H2O. Fibrinogen. Other coagulative proteins. Immunoglobulin. Complement factors. Macroglobulins. Microglobulin.

54
Q

Steps in emigration of plasmamorphonuclear neutrophils/Leukocytes (PMNs).

A
  1. Adhesion
  2. Pseudopods inserted between endothelial cells
  3. Passage through basement membrane
  4. Movement toward source of inflammation.
55
Q

Cells of inflammation

A 
Neutrophils
Eosinophils
Basophils
Macrophages
Platelets
56
Q

Polymorphonuclear Neutrophils

A

PMNs

Most numerous of the circulating WBCs

Multisegmented nuclei

Properties: mobility; bactericidal; phagocytosis; produce and release cytokines

57
Q

Eosinophils

A

2-3% of circulating WBCs

Slower mobility, reactivity

Segmented nucleus

Allergic reactions and response to parasites.

58
Q

Basophils

A

Less than 1% circulating WBCs

Precursor to mast cells

Important in inflammatory reactions mediated by IgE

Single nucleus.

59
Q

Macrophages

A

Tissue cells derived from monocytes

Phagocytic and bactericidal

Appear 3-4 days after onset of inflammation.

60
Q

Platelets

A

Contain membrane bound granules that contain histamine, coagulative proteins, cytokines, growth factors etc.

Gen Path 300 (8 decks)

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