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Flashcards in Classes 1-2 Deck (61):
0

Sign

Objective indicator of pathology

1

Symptoms

Subjective indicator

2

Nucleocytoplasmic ratio

Ratio of nucleus to cytoplasm

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

3

Mitochondria

Double membrane involved in cellular energy production

Higher energy demands -->
More mitochondria

Undifferentiated cells have fewer mitochondria.

4

Ribosomes

Small RNA granules involved in protein synthesis.

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

5

Endoplasmic reticulum

Mesh work of membranes continuous with nuclear and plasma membranes.

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

6

Golgi apparatus

Adjacent to nucleus
Composed of membrane-blind cisterns

Modified, sorts and packages macromolecules

7

Lysosomes

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

8

Passive cell projections

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

9

Active cell projections

Require energy

Cilia
Flagella.

10

Three Forms of integration

Autocrine
Paracrine
Endocrine

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Autocrine stimulation

Cell secretes substance that stimulates itself

Simplest

12

Paracrine Stimulation

Cell secretes substance that stimulates a nearby cell

13

Endocrine stimulation

Cell releases substance into bloodstream that stimulates structure far away

Always hormones

Can involve anatomically distinct organs

14

Atrophy

Decrease in size of cells resulting in reduced tissue mass

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Hypertrophy

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

16

Hyperplasia

Increased number of cells resulting in increased tissue mass

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Metaplasia

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

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

18

Dysplasia

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

Possibly precancerous.

19

Intracellular accumulations

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

Ex. Black lung or fatty liver.

20

Apoptosis

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).

21

Necrosis

Exogenously induced cell death

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Four types of necrosis

1 coagulative
2 liquifactive
3 caseous
4 fat

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Coagulative necrosis

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.

24

Liquifactive necrosis

Dead cells liquify, tissue becomes soft and diffluent.

Mostly brain. Typical of brain infarct

May be secondary to coagulative.

25

Caseous necrosis

Typical of TB and some fungal infections.

Coagulative necrosis with limited liquifaction.

Centre becomes yellow and cheesy.

26

Enzymatic Fat Necrosis

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

Gangrene

Dead tissue.

Wet (liquifaction) or dry (mummification)

Can undergo secondary change, such as calcification.

28

What is a telltale sign of necrosis?

Ruptured cell membrane

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Pathological apoptosis

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

Also, rejected transplanted organs.

30

Pathological lack of apoptosis

Syndactyly

Chronic lymphomatic leukaemia.

31

Inflammation

Body's nonspecific response to injury

Necessary part of healing.

32

Signs of inflammation

Swelling
Heat
Altered function
Redness
Pain

33

Four components of acute inflammation

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

34

Inflammation: change in blood circulation

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

Inflammation: changes in vessel wall permeability

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

Histamine

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

Bradykinin

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

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

38

Hageman Factor

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

Complement system

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

Three pathways (classical, lectin and alternative).

40

Result of the complement system

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

Arachidonic Acid Derivatives

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

42

What are the two pathways for arachidonic acid?

Lipoxygenase Pathway

Cyclooxygenase Pathway

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Lipoxygenase Pathway

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

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Cyclooxygenase Pathway

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

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

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

Prostaglandins

Eicosanoids produced in the cyclooxygenase pathway of arachidonic acid metabolism.

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

47

Thromboxane

Produced by the cyclooxygenase pathway of arachidonic acid metabolism.

Involved in vasoconstriction, platelet aggregation and thrombosis.

48

Prostacyclin

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

Counters effect of thromboxane.

Inhibits platelet aggregation. Vasodilator.

49

Leukotrienes

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

Promote chemotaxis and increase vascular permeability.

50

Lipoxin

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

Inhibit chemotaxis.

51

Emigration of Leukocytes

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

52

Transudate

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

Mostly fluid; very few proteins or large solutes

53

Exudate

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

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

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

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Cells of inflammation

Neutrophils
Eosinophils
Basophils
Macrophages
Platelets

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Polymorphonuclear Neutrophils

PMNs

Most numerous of the circulating WBCs

Multisegmented nuclei

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

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Eosinophils

2-3% of circulating WBCs

Slower mobility, reactivity

Segmented nucleus

Allergic reactions and response to parasites.

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Basophils

Less than 1% circulating WBCs

Precursor to mast cells

Important in inflammatory reactions mediated by IgE

Single nucleus.

59

Macrophages

Tissue cells derived from monocytes

Phagocytic and bactericidal

Appear 3-4 days after onset of inflammation.

60

Platelets

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