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Semester 3 > General Pathology 1-2 (terminology, cell review / cell death and inflammation) > Flashcards

General Pathology 1-2 (terminology, cell review / cell death and inflammation) Flashcards

1
Q

what is pathology

A

study of nature/cause of disease

changes in structure/function

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2
Q

disease

A

subjective SYMPTOMS/complaints

objective/clinical SIGNS

lab/radiography findings

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3
Q

pathogenic

A

VECTOR/environment causing disease/pathology

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4
Q

vector

A

“an organism, typically a biting insect or tick, that transmits a pathogen, disease, or parasite from one animal or plant to another.”

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5
Q

terminology

A

A- , an-: without
Acro-: extremity
Adeno-: glandular
-Algia: pain
Angio-: blood or lymph vessels
Arthr-: joint
Brady-: slow
Carcin-: crab (cancer)
Cardio-: heart
Cervi-, cervico- : neck
-Cele: swelling, hernia

Cep-, Ceph-: head, brain
Chole: bile
Com-, con-: with, together
Contra-: against
Cyst: hollow organ
Demo-: people
Derm-: skin
Dia-: through
Dys-: difficulty
Ecto-, -ectomy: outside, removal
-Emia: blood

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6
Q

terminology 2

A

Endo-: inside
Epi- upon
Erythr-: red
Ex-: out of
-Gen: beginning, producing
Glyco-: relating to sugar
-Graphy: recording, writing
Hemo-: blood
Hemi-: one-half
Hepat-: liver
Hydro-: water

Hyper-: above, too much.
Hypo-: below, too little
-itis: inflammation
-Lepsis: seizure (lepsy, leptic)
Leuko-: white
Lipo-: fat
Litho-: rock
-Logy: study
-Lysis, -lyso: destruction
Mega-: large
Meno-: month

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7
Q

terminology 3

A

Metr-: mother (uterus)
Micro-: small
Myco-: fungus
Mye-: marrow or spinal cord
Myo-: muscle
Narco-: stupor
Necro-: death
Neo-: new
Nephro-: kidney
Neuro-: nerve
-Oid: resembles
-Oma: tumor

Onco-: tumor
Orchi-: testes
-Osis: pathologic condition
Osteo-: bone
Para-: alongside, near
Peri-: around
Phagia-: eating
-Philia: affinity
Phleb-: vein
Phyto-: plants
-Plasia: growth
-Plasm, -plasma: formed

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8
Q

terminology 4

A

Patho-: disease state
Physio-: nature
Pseudo-: false
Psych-: the mind, mental
Ren-: kidney
-Rrhagia, -rrhea: flowing
Rhino-: nose
Sarco-: flesh
Sclero-: hardness, scarring

Spondy-: spine
-Stasis: stagnation, standing still
Stoma-: an opening; mouth
Syn-, Sym-: with
Thrombo-: clot
Therm-: temperature
-Trophy, -trophic: nutrition, growth
Vaso-: blood vessel

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9
Q

e.g. of prefixes/suffixes put together

A

Angiogenesis
Metrorrhagia
Hemophilia
Rhinitis
Arthralgia
Hydrocephalus
Macrophages - phagocytosis

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10
Q

diagnosis

A

id of disease via evaluation of:

signs/symptoms
lab findings

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11
Q

etiology

A

causative factors

e.g.
congenital
virus
“malignancy”

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12
Q

idiopathic

A

unknown cause

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13
Q

iatrogenic

A

iatro = medical treatment

iatrogenic = caused by treatment, and/or procedure/error

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14
Q

pathogenesis

A

development of disease

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15
Q

terms relating to onset

A

acute:
sudden/obvious
short term (?)
develops quickly

gradual:
milder condition (?)
developing gradually

insidious:
gradual progression
vague/mild signs

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16
Q

insidious

A

“proceeding in a gradual, subtle way, but with harmful effects.”

“a gradual progression with vague or mild signs”

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17
Q

manifestations

A

clinical evidence or effects

e.g.
signs/symptoms

signs = objective indicators=
(e.g. fever)

symptoms = subjective indicators =
(e.g. pain/nausea)

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18
Q

syndrome

A

collection of signs/symptoms

usually occurs together

in response to certain condition

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19
Q

complications

A

secondary/additional problems pathological events

arise via/after original disease/pathology

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20
Q

prognosis

A

outcome of disease

the probable outcome(s) of a disease

“probability or likelihood for recovery”
better definition:
“the likely course of a disease or ailment.”

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21
Q

communicable/contagious

A

infections that can be spread between people

“Communicable diseases are illnesses caused by viruses or bacteria that people spread to one another through contact with contaminated surfaces, bodily fluids, blood products, insect bites, or through the air.”

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22
Q

cell structure/function

A

Plasma membrane

Nucleus

Cytoplasm (Cytosol & Organelles)

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23
Q

plasma membrane

A

recall:

Membrane proteins functions as =
channels,
carriers,
receptors,
ligands,
enzymes,
linkers,
identity markers

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24
Q

cytoplasm

A

recall:

Consists of cytosol, organelles, cytoskeleton

cytoplasm volume can vary

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25
Q

Nucleocytoplasmic ratio

A

ratio of nucleus (volume?size?) vs cytoplasm “

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26
Q

Nucleocytoplasmic ratio is higher in

A

Higher in:

a) undifferentiated adult cells,
b) fetal cells,
c) tumour cells

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27
Q

organelles of cytoplasm

A

Nucleus
Mitochondria
Ribosomes
Endoplasmic reticulum
Golgi complex
Lysosomes

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28
Q

nucleus?

A

Separated from the rest of the cell by nuclear membrane

Consists of DNA organized into chromatin

Condenses into chromosomes during cell division

Blueprint for protein synthesis

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29
Q

mitochondria?

A

Double membrane involved in cellular energy production (internal cristae?)

Energy demanding cells are mitochondrial rich
(liver, nerve, red muscle)

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30
Q

few mitochondria which cells?

A

undifferentiated cells

many malignant tumor cells

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31
Q

ribosomes

A

small RNA granules

can be:
a) free floating
b) on RER

involved in protein synthesis

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32
Q

free ribosomes vs RER ribosomes

A

free ribosomes = proteins for internal cell environment use

RER ribosomes = for “export”
(note “LUXARY proteins”)

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33
Q

luxary proteins

A

“A protein that is produced only in specialized cells and is not necessary for general cell maintenance, unlike the so-called housekeeping proteins.”

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34
Q

endoplasmic reticulum

A

membranes continuous with plasma membrane (?) and nuclear membrane

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35
Q

rough ER

A

involved in protein synthesis; studded with ribosomes

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36
Q

smooth ER

A

involved in catabolism of drugs, hormones, nutrients

no ribosomes

“associated with the production and metabolism of fats and steroid hormones.”

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37
Q

golgi apparatus

A

Adjacent to nucleus

membrane bound cisternae

modifies, sorts and packages macromolecules such as proteins and lipids before their secretion

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38
Q

golgi body and proteins before secretion

A

“The Golgi complex plays a central role in protein secretion by regulating cargo sorting and trafficking”

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39
Q

lysosome?

A

digestive organelle

lytic enzymes

Fuse with vesicles to digest material

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40
Q

what does lysosome digest?

A

E.g. worn out structures, bacteria, etc.

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41
Q

lyososomes and lysis

A

Can release its contents into the cell to lyse cell

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42
Q

why lysis?

A

(worn out, damaged, too many, infected, etc.)

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43
Q

cell projection types (PASSIVE PROJECTIONS)

A

microvilli

(no energy required)

FUNCTION??
Increase cell SA

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44
Q

cell projections (ACTIVE PROJECTIONS)

A

require energy

Cilia
Flagella (flagellum)

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45
Q

cilia

A

Cilia:
numerous, short, hairlike projections

move substances across the surface of the cell

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46
Q

flagella (flagellum)

A

single, long projection

functions to move the cell (sperm)

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47
Q

integration

A

for homeostasis

bringing together various parts –> FUNCTION AS WHOLE

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48
Q

three types of integration

A

Autocrine

Paracrine

endocrine

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49
Q

Autocrine stimulation (type of integration)

A

secretes substance that stimulate itself

SIMPLEST

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50
Q

Paracrine stimulation (type of integration)

A

secretes a substance that stimulates a nearby cell

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51
Q

endocrine stimulation (type of integration)

A

release substance into the bloodstream

then stimulate distant cell

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52
Q

Highest form of integration?

A

endocrine stimulation

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53
Q

endocrine stimulation can involve cells of _____

A

cells of anatomically distinct organs

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54
Q

causes of cell injury?

A

Hypoxia / ischemia / anoxia

Physical agents (temp/vibration/radiation)
Mechanical damage (trauma)

Abnormal metabolite accumulation

Fluid or electrolyte imbalance

pH imbalance

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55
Q

other causes of cell injury

A

Chemicals (heavy metals/drugs)

Microbiological agents (bacteria/viruses)

Immunological reactions (autoimmune/host cells)

Genetic defects

Nutritional imbalances

Aging

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56
Q

reversible cell damage

A

Within range of homeostasis

Membrane left relatively intact (pumps)

Mitochondria able to sustain energy demands

Mild and/or short-lived

Cell returns to its original state

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57
Q

pumps intact?

A

No Na+K+ pumps puming Na+ out?

= cell swells, and membrane ruptures = lysis

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58
Q

irreversible cell damage?

Structure/function of cell

A

Decrease energy production

Decrease metabolism

Decrease in pH

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59
Q

irreversible cell damage?

nucleus

A

Shrinking, fragmentation, lysis (nucleus)

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60
Q

irreversible cell damage?

lysosomes

A

Can burst releasing degrading enzymes and increase cell damage

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61
Q

irreversible cell damage?

plasma membrane

A

Extensive plasma membrane damage

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62
Q

irreversible cell damage?

A

Accumulation of amorphous, Ca-rich densities in the mitochondrial matrix

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63
Q

cellular adaption

A

cells adapt their growth/differentiation

e.g. normal adaptations
breast/uterine growth during pregnancy

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64
Q

when tissue modify?

A

modified frequently in response to hormonal stimulation, environmental changes, irritation

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65
Q

atrophy

A

decrease in the size of cells

resulting in reduced tissue mass

caused by poor nutrition, aging, immobility

i.e.
whole organ, or cellular (?)

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66
Q

atrophy e.g.

A

Decreased demand, oxygen, nutrients, nerve innervation. Persistent cell injury

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67
Q

hypertrophy

A

increase in the size of individual cells

resulting in enlarged tissue mass

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68
Q

hypertrophy e.g.

A

eg.
Striated muscle cells – working out.

Cardiac muscle – cardiovascular disease

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69
Q

hypertrophic cardiomyopathy

A

.

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70
Q

hyperplasia

A

increased number of cells

resulting in enlarged tissue mass

can occur in conjunction with hypertrophy

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71
Q

hyperplasia e.g.

A

e.g. endometrial thickening of the uterus

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72
Q

metaplasia

A

when one mature cell type is replaced by a different mature cell type

(can be pathological or occur under regular circumstances)

e.g. ciliated columnar epithelia of the respiratory tract changes to stratified squamous epithelia
(IN SMOKERS)

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73
Q

endometrial hyperplasia

A

Endometrial hyperplasia develops when a woman has an imbalance of estrogen and progesterone.

There are a number of reasons this can occur: Having irregular menstrual periods, being obese, or having polycystic ovary syndrome (PCOS) may interfere with ovulation, which reduces progestin exposure.

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74
Q

benign prostate hyperplasia

A

.

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75
Q

dysplasia

A

“cells of a tissue vary in size and shape, large nuclei are present and the rate of mitosis increases; may indicate a precancerous state”

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76
Q

intracellular accumulations

A

overload of various metabolites/exogenous material

OR

prevention of excretion of metabolic byproducts

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77
Q

intracellular accumulations via ____

A

overload,
underutilization,
underexcretion

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78
Q

intracellular accumulations e.g.

A

Black Lung (anthracosis) – accumulation of coal particles

Fatty liver disease (alcoholics or nonalcoholics “) – damage to liver cells, cause decrease in lipoprotein production, therefore an increase in lipid storage

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79
Q

aging

A

complex adaptations and irreversible cellular events

associated with impaired wound healing (?)

Over 300 theories
E.g.
wear-and-tear, genetic hypotheses, telomere aging clock theory and free radical theory

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80
Q

PHARMACOLOGY LECTURE 1 ***

A

..

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81
Q

language of pharmacology

A

how are drugs named?

drug classificaitons, uses, side effects

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82
Q

pharmacokinetics and pharmacodynamics

A

…

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83
Q

how are drugs administered?

how are drugs processed in body?

A

…

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84
Q

why do massage therapists need to know how medications work?

A

.

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85
Q

allopathy?

A

“the treatment of disease by conventional means, i.e., with drugs having opposite effects to the symptoms.”

“Also called biomedicine, conventional medicine, mainstream medicine, orthodox medicine, and Western medicine.”

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86
Q

why MT familiar with pharmacology?

A

1) clients combine allopathic therapy with Complementary therapy (alternative “ ?)

2) drugs can interfere with physiological response of Massage & hydrotherapy

3) some medication is contraindication of massage and/or hydrotherapy

4) minor changes in Tx depending on drug / drug delivery (?)

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87
Q

pharmacology define

A

study of action of chemicals on living organisms

produce biological effects

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88
Q

pharmacology includes

A

pharmacokinetics

pharmacodynamics

pharmacy

toxicology

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89
Q

pharmacokinetics

A

What the body does to the drug

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90
Q

pharmacodynamics

A

What the drug does to the body

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91
Q

pharmacy

A

“the science or practice of the preparation and dispensing of medicinal drugs.”

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92
Q

toxicology

A

noun: toxicology
1.
the branch of science concerned with the nature, effects, and detection of poisons.

2.
the measurement and analysis of potential toxins, intoxicating or banned substances, and prescription medications present in a person’s body.

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93
Q

what is pharmacokinetics

A

“what the body does to the drug”

How the body absorbs, distributes, metabolizes, and eliminate the drug

How long the body takes to accomplish this process, and the drug levels the body is exposed to as a result of this process

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94
Q

what is pharmacodynamics

A

“what the drug does to the body”

Does the drug mimic normal physiological processes or inhibit processes

This is defined in the “mechanism of action” of the drug

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95
Q

mechanism of action of drug

A

“In medicine, a term used to describe how a drug or other substance produces an effect in the body.”

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96
Q

E.g. of why RMT needs to know effects of drugs when relevent

A

client taking pain medication

asks for deep work

is bruised and in more pain the next day

therefore, therapist should know what medication is and what it does to body
E.g.
how effects soft tissue, recovery, or sensory feedback

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97
Q

what should massage therapists know?

A

a basic understanding of the actions and effects of commonly used drugs

ability to research the effects of other medications encountered

knowledge of how massage affects the body’s physiology

ability to apply this knowledge to varying clients

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98
Q

Common pharmaceutical terms and concepts

A

…

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99
Q

Drug names

Drug classifications

Uses or indications

pharmacodynamic terms (effects of medications, “Mechanism of action”)

pharmacokinetic terms (half-life, onset of action, bioavailability)

A

..

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100
Q

how are drugs named?

A

via:

generic name
or
brand (trade) name

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101
Q

generic name

A

term that refects chemical structure of drug

assigned by international committee

same around the world

E.g.
Diazepam
= generic name for…
7 chloro-1,3-dihydro-1-methyl-5-phenyl-2H-1,4-benziodiazepin-2-one (C16 H13 CIN2 )

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102
Q

brand (trade) name

A

formulation is assigned a brand name by manufacturing company

doesn’t reflect chemistry of drug

drug is developed, researched, tested, and produced for sale

i.e. drug manufacturing company

E.g.
Ibuprofen = generic name
brand name = Advil, Motrin, etc

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103
Q

generic medications

A

generic drug companies produce the medication

cheaper than brand name version

meet FDA requirements

concerns about effectiveness vs brand name (?)

possibly not as effective as “original” (?)

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104
Q

when generic medication?

A

After a patent expires on a drug, generic drug companies may produce it

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105
Q

drug classifications

A

non-prescription drugs

prescription drugs

restricted and controlled drugs

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106
Q

other drug classifications

A

therapeutic properties (action/effect on body)

action or effect on body system

chemical structure

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107
Q

therapeutic properties

A

describes the effect that the drug has on the body

E.g.
anti-hypertensive to reduce blood pressure

108
Q

action or effect on specific body system

A

describes the body system that the drug affects

E.g.
central nervous system stimulant

109
Q

chemical structure

A

escribes basic chemical or pharmacologic properties of the drug

E.g.
beta-blocker

110
Q

what if client does not remember name of drug?

A

they will know what the drug is used for

can use knowledge of general class of drugs to alter treatment
or
further research drug

111
Q

Uses/indications for drug

A

list of diseases/disorders drug is officially recommended for
by
Health Canada

112
Q

what if a drug helps a condition, but Health Canada has not approved the use for “

A

There may be some conditions that the drug has shown benefit for

ut Health Canada has not approved use of the drug for “

E.g.
insufficient trial data

113
Q

contraindications for a drug

A

disease/disorder that the drug has a negative effect on

should not be prescribed to a client with that condition

114
Q

(Pharmacodynamics) effects of medication based on

A

1) Therapeutic effects

2) side effects or adverse effects

3) unpredictable effects

115
Q

Factors that influence Effects

A

dosage,
age,
gender,
lifestyle,
pathologies

116
Q

1) Therapeutic effects

A

desired effect which is intended to help the user get better

117
Q

2) side effects or adverse effects

A

undesirable reactions:

can be b/c of “too much” of therapeutic effect
E.g.
hypotension for hypertension drugs

can be unrelated to therapeutic effect
E.g.
stomach ulcers, GI irritation via Aspirin

can also be via interaction of multiple drugs

118
Q

side effects or adverse effects via

A

1) too much therapeutic effect

2) unrelated effect

3) via interaction of multiple drugs

119
Q

3) unpredictable effects

A

two types:
a) allergic/hypersensitive reactions

b) idiosyncratic reactions

120
Q

a) allergic / hypersensitive reactions

A

can be mild
E.g.
(hives, joint pain, fever)

can be severe
E.g.
anaphylaxis

121
Q

b) idiosyncratic reactions

A

unexpected or highly unusual effects

occur in small number of people

122
Q

important note

A

client’s primary complaint might be as a result of a drug side effect

should monitor patient symptoms
be alert for unusual
be alert for changes
vs.
massage tx

123
Q

pharmacodynamics (Mechanism of action)

A

..

124
Q

how do drugs create changes?

A

DRUGS DO NOT create new functions

drugs alter existing cellular activities

125
Q

Mechanism of action occurs via

A

one or a combination of the following:

a) Combining with specific cellular receptors

b) Chemically altering body fluids

c) Chemically altering cell membranes

d) Interacting with extracellular enzyme systems

126
Q

a) Combining with specific cellular receptors

A

binding to receptor can alter cellular function

E.g.
benzodiazepines binds to a neurotransmitter receptor

127
Q

b) Chemically altering body fluids

A

E.g.
antacid to neutralize excess stomach acidity and reduce or prevent digestive discomfort

128
Q

c) Chemically altering cell membranes

A

E.g.
alter electrical stability
alter responsiveness to stimuli

can influence the cell’s permeability
I.e.
speeding up / slowing down of ions into/out of cell

129
Q

d) Interacting with extracellular enzyme systems

A

enzyme?
protein molecule that facilitate/catalyze chemical reactions of all cells

E.g.
NSAIDs alter pain by blocking the activity of enzymes in the inflammatory response

130
Q

(Pharmacokinetics) Half-life

A

time it takes body to reduce concentration of drug to 50%

via metabolism/elimination

E.g. 100mg dose of drug with 20 minute half-life
3.125mg after 100 minutes

131
Q

(Phamarcokinetics) onset of action

A

duration of time it takes for drug to become effective

132
Q

onset of action can be determined by

A

how was the drug administered/taken?

E.g.
IV versus orally

133
Q

why onset of action important to know?

A

can help determine schedule of Massage therapy

134
Q

(pharmacokinetics) bioavailability

A

amount of drug that enters systemic circulation

amount available to produce effects

***also determined via how drug is administered/taken

E.g.
50mg of a drug taken orally and bioavailability is approximately 50%,
if 50mg administered via injection, bioavailability is 100%

135
Q

other things that determine bioavailability

A

doseage/frequency

age

general health

136
Q

blood thinners, blood thinning and bruising

A

“Bruises happen when the smallest blood vessels under the skin (capillaries) break and start to leak, causing discolouration. Blood thinners are designed to slow down the blood clotting, so the broken blood vessels take longer to stop leaking, which can lead to a worse bruise or bruising more easily.”

137
Q

**General Pathology 300 — Class 2 **

A

.

138
Q

Cell death 2 types

A

1) apoptosis

2) necrosis

139
Q

inflammation?

A

will discuss:

signs symptoms

pathogenesis

cellular events in inflammation

cells of inflammation

140
Q

apoptosis

A

endogenously programmed (mechanism)

initiating event can be endogenous OR exogenous

141
Q

endogenous vs exogenous

A

growing or originating from within an organism.

growing or originating from outside an organism.

142
Q

necrosis

A

exogenously induced

via irreversible cell injury

E.g.
toxins, anoxia, etc.

143
Q

4 types of necrosis

A

coagulative, liquefactive, caseous, fat

144
Q

1) coagulative necrosis

A

most common type of necrosis

mechanism?
Cell proteins are altered or denatured

Via inactivation of hydrolytic enzymes in CYTOPLASM –> these prevent lysis of tissue
–>
Note: cytoplasmic hydrolytic enzymes

145
Q

most common necrosis type?

A

coagulative necrosis

146
Q

which cell proteins denature or are altered in coagulative necrosis?

A

cytoplasmic hydrolytic enzymes that prevent lysis of tissue

147
Q

characteristic of tissue during coagulative necrosis

A

tissues retains original form

firm consistency

148
Q

where is coagulative necrosis typical?

A

solid internal organs

149
Q

common cause of coagulative necrosis

A

anoxia

E.g.
heart attack

150
Q

2) liquefactive necrosis

A

dead cells liquefy

via influence of certain enzymes

dissolution of tissues

SOFT/DIFFLUENT tissue

151
Q

liquefactive necrosis – where most often?

A

brain

brain cells liquefied

brain becomes soft, fluid-filled cavity

152
Q

note secondary liquefaction

A

tissue may undergo LIQUEFACTIVE necrosis after undergoing COAGULATIVE necrosis

“Coagulative necrosis may liquefy”

153
Q

3) caseous necrosis

A

special type of COAGULATIVE NECROSIS

w/ limited LIQUEFACTIVE necrosis

hybrid of two types

tissue becomes “CHEESE-like” and yellow-white

153
Q

Caseous necrosis where?

A

TUBERCULOSIS

(almost unique to tuberculosis)

154
Q

caseous necrosis also where?

A

Some FUNGAL INFECTIONS

155
Q

caseous necrosis and tuberculosis

A

Center of a tuberculous granuloma becomes necrotic and the cells fall apart

156
Q

“granuloma”

A

“What is a granuloma? A granuloma is a tiny cluster of white blood cells and other tissue. It can appear in your lungs, skin or other parts of your body. Granulomas aren’t cancerous. They form as a reaction to infections, inflammation, irritants or foreign objects.”

157
Q

granuloma and tuberculosis

A

“Tuberculosis is the formation of an organized structure called granuloma. It consists mainly in the recruitment at the infectious stage of macrophages, highly differentiated cells such as multinucleated giant cells, epithelioid cells and Foamy cells, all these cells being surrounded by a rim of lymphocytes.”

158
Q

4) Fat necrosis

A

special type of LIQUEFACTIVE necrosis

via?
action of LIPOLYTIC enzymes

where?
limited to fat tissue
Esp around pancreas

159
Q

which necrosis is special type of liquefactive necrosis

A

fat necrosis

160
Q

which necrosis type is a special type combining liquefactive and coagulative necrosis

A

caseous necrosis

161
Q

mechanism of fat necrosis

A

pancreatic enzymes

release into fat tissue

degrade fat into:
GLYCEROL
FREE FAs
I.e.
from Triglyceride?

162
Q

necrosis – miscellaneous term

A

Gangrene

163
Q

gangrene

A

dead tissue

164
Q

necrotic tissue and secondary changes E.g.

A

Necrotic tissue can undergo secondary changes such as
E.g.
CALCIFICATION

Also note:
secondary liquefaction
E.g.
liquefactive necrosis after undergoing coagulative necrosis

165
Q

note frostbite, dry gangrene, and coagulative necrosis – also note ischemic necrosis

A

ischemic necrosis is a type of coagulative necrosis

“preservation of cellular architecture and protein coagulation”

“Severe frostbite injuries can lead to dry gangrene”

(“lack in blood supply and oxygen”)

“Frostbite is a cold-induced injury of tissue characterized by freezing and ischemic necrosis.”

166
Q

apoptosis

A

programmed cell death

under normal conditions

may occur when:
A) abnormal cell development

B) excessive cell numbers

C) injured cells

D) aged cells

167
Q

apoptosis – what happens?

A

cells “self-destruct”

appear to digest itself

disintegrate

I.e.
LYSIS

168
Q

which cell death type is active

A

apoptosis

169
Q

apoptosis important facts

A

active

requires energy

regulated

requires specific genes/enzymes

mechanism is endogenous (endogenously programmed)

intiating event can be endogenous/exogenous

affects single cells
I.e.
mechanism that operates at a single cellular level

170
Q

apoptosis is normal development (e.g. formation of digits)

A

lack of apoptosis can cause pathology

E.g.
important in formation of digits

171
Q

syndactyly

A

occurs when digits fused together (e.g. in hands/feet)

172
Q

inflammation 5 signs

A

swelling

heat

redness

pain

(occasionally) loss of function

173
Q

inflammation

A

“to set on fire”

body’s nonspecific response to tissue injury

E.g.
Appendicitis, laryngitis, pancreatitis, mastitis, etc.

174
Q

inflammation, facts

A

biological response of vascular tissues to harmful stimuli
E.g.
pathogens, damaged cells or irritants

175
Q

inflammation function

A

protective attempt by the organism to remove/localize the injurious stimuli

initiate the healing process for the tissue

176
Q

why inflammation important?

A

Without inflammation wounds and infections would not heal and further destruction of tissue would compromise survival of organism.

177
Q

when inflammation occur?

A

cut, allergy, bite, infection, burn, etc.

178
Q

infection and inflammation

A

With infection, a microorganism is present

179
Q

signs and symptoms of inflammation

A

symptoms:
pain/tenderness

signs:
redness, swelling, heat, loss of function

180
Q

non-specific symptoms of inflammation

(ESP w/ SYSTEMIC INFLAMMATION – possibly when not visible?)

A

fatigue

weakness

decreased appetite

aching

181
Q

PATHOGENESIS OF INFLAMMATION

A

1) changes in circulation of blood

2) changes in vessel wall permeability

3) release of SOLUBLE MEDIATORS OF INFLAMMATION (SMIs)

4) cellular events

182
Q

1) changes in circulation of blood

A

body’s first response to injury

“Mechanical stimulus stimulates nerves that transmit signals to smooth muscle cells on arterioles”

“Constriction followed by relaxation of sphincter”

Blood rushes into capillaries leading to redness, swelling, warmth… (hyperemia)

Blood flow in dilated capillaries is slow leading to congestion

Sludged erythrocytes form stacks (rouleaux) impeding circulation

WBCs are marginalized and become attached to endothelium (pavementing)

183
Q

what happens when blood rushes into capillaries

A

redness, swelling, warmth… (hyperemia)

184
Q

why congestion in capillaries?

A

Blood flow in dilated capillaries is slow leading to congestion

185
Q

what do red blood cells form in dilated capillaries?

A

Sludged erythrocytes form stacks (rouleaux) impeding circulation

“ROULEAUX”

186
Q

what happens in WBC in dilated capillaries?

A

WBCs are marginalized and become attached to endothelium
(PAVEMENTING)

187
Q

2) changes in vessel wall permeability

A

due to:

Increased pressure inside the congested blood vessels

Slowing of circulation

Adhesion of leukocytes and platelets to endothelial cells (PAVEMENTING)

Release of soluble mediators of inflammation (SMIs)

188
Q

3) release of SOLUBLE MEDIATORS OF INFLAMMATION (SMIs)

A

Plasma derived and cell derived

Plasma derived must be activated

Biochemically heterogeneous

Multifunctional and thus have numerous effects on blood vessels, inflammatory cells, etc.

189
Q

SMIs list

A

a) Histamine

b) Bradykinin

c) Complement system

d) Arachidonic Acid Derivatives

190
Q

a) histamine

A

BIOGENIC AMINE

Released from platelets and mast cells

Provokes contraction of endothelial cells of blood vessels

Leads to formation of gaps

Increases blood vessel permeability

Allows fluids to exit into interstitial spaces

Occurs quickly

Histamine is rapidly inactivated by histaminase

Immediate transient reaction

191
Q

what does histamine do to BC permeability

A

increases

“formation of gaps” (??)

allows fluid to go to interstitial spaces

192
Q

histamine timing

A

occurs quickly

rapidly inactivated
via
HISTAMINASE

“IMMEDIATE TRANSIENT REACTION”

193
Q

where histamine released from?

A

Released from platelets and mast cells

194
Q

b) Bradykinin

A

Plasma protein

Similar effects as histamine but occurs at a slower pace

Formed in the plasma through activation of Hageman factor or coagulation factor XII

Incites pain

NOTE THAT CLOTTING FACTOR xii IS ACTIVATED VIA PLATELETS VIA INTRINSIC PATHWAY OF BLOOD CLOTTING – COAGULATION PHASE (STEP IN HEMOSTASIS)
I.e.
inflammation when clotting is needed

195
Q

Bradykinin vs Histamine timing

A

Bradykinin effects occur at slower rate

196
Q

which SMI incites pain?

A

Bradykinin

197
Q

which plasma protein activates Bradykinin?

A

AKA Hageman factor

COAGULATION FACTOR XII (clotting factor 12)

plasma protein

198
Q

c) Complement system (SMI)

A

group of plasma proteins

released via LIVER

circulate in INACTIVE form

activate in cascade (activate one another)

Numbered C1 to C9

occuring via 3 pathways:
Classical pathway
Alternative pathway
Lectin pathway

activation leads to formation of active fragments
(e.g. C3a)

activation leads to formation of intermediate complexes
(e.g. C567)

activation leads to terminal membrane attack complexes
(e.g. MAC)

199
Q

where are complement system plasma proteins created?

A

produced by LIVER

200
Q

how to complement system plasma proteins circulate?

A

in INACTIVE form

201
Q

how are they numbered?

A

C1 to C9

202
Q

which three pathways activate complement system proteins?

A

Classical pathway

Alternative pathway

Lectin pathway

203
Q

what are three ways complement system proteins can activate?

A

formation of biologically active fragments (E.g. C3a)

formation of intermediate COMPLEXES (E.g. C567)

formation of terminal MEMBRANE ATTACK COMPLEXES (E.g. MAC)

204
Q

MAC mechanism (membrane attack complex)

A

“MAC destroys cells by boring holes in plasma membrane”

205
Q

MAIN FUNCTION OF ACTIVATED COMPLEMENT DERIVATIVES

A

OPSONIZATION

ANAPHYLAXIS

CHEMOTAXIS

CELL LYSIS

206
Q

opsonization

A

“Antibody opsonization is a process by which a pathogen is marked for phagocytosis.”

207
Q

opsonin

A

“any of various proteins (as complement or antibodies) that bind to foreign particles and microorganisms (as bacteria) making them more susceptible to the action of phagocytes.”

208
Q

anaphylaxis

A

histamine release with increased vessel wall permeability

“an acute allergic reaction to an antigen (e.g. a bee sting) to which the body has become hypersensitive.”

209
Q

anaphylactic shock

A

“an extreme, often life-threatening allergic reaction to an antigen to which the body has become hypersensitive.”

210
Q

chemotaxis – general definition

A

“Chemotaxis is the movement of a cell or organism in response to a chemical stimulus. This phenomenon is commonly seen in bacteria and other single-celled organisms, which use chemotaxis to navigate towards nutrients or away from harmful substances in their environment. Chemotaxis is an important mechanism for the survival and behavior of many organisms.” (AI)

“movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.”

211
Q

chemotaxis

A

migration of leukocytes

212
Q

cell lysis

A

via MAC

213
Q

d) ARACHIDONIC ACID DERIVATIVES (SMI)

A

Arachidonic acid

derived from phospholipids of cell membranes

via 2 pathways:
LIPOXYGENASE PATHWAY
&
CYCLOOXYGENASE PATHWAY

214
Q

2 pathways for metabolism of arachidonic acid (derivatives)

A

LIPOXYGENASE PATHWAY
&
CYCLOOXYGENASE PATHWAY

215
Q

lipoxygenase pathway

A

formation of:

Leukotrienes
– promote chemotaxis and incr. vasc. permeability

Lipoxins
– inhibit chemotaxis

216
Q

cyclooxygenase pathway

A

formation of:

Prostaglandins
– cause vasodilation, vascular permeability, mediate pain and fever

–> Prostacyclin
– counteracts thromboxane

Thromboxane
– platelet aggregation, thrombosis, vasoconstriction

217
Q

thrombosis

A

“Thrombosis is a blood clot within blood vessels that limits the flow of blood.”

218
Q

4) CELLULAR EVENTS (FINAL POINT IN “PATHOGENESIS OF INFLAMMATION”

A

emigration of leukocytes

NOTE:
Increased permeability of vessel wall lasts up to several hours

Accompanied by leakage of fluid into interstitial spaces

Leads to formation of edema

Emigration of cells across vascular wall leads to formation of exudate

219
Q

4) CELLULAR EVENTS (phagocytosis)

A

PMNs (polymorphonuclear neutrophils)
—> Lose their mobility —> act as scavengers

Active uptake of bacteria/cellular debris

often PMNs die in their fight with bacteria

220
Q

The cells of inflammation****

A

1) Neutrophil (most common)

2) Eosinophils (2-3%)

3) Basophils (1%)

4) Macrophages

5) Platlets

221
Q

1) Neutrophils (Polymorphonuclear neutrophils –> PMNs)

A

most numerous (of circulating WBCs)

“Multi-segmented” nucleus (up to 5)

They are first to appear in acute inflammation

characteristics:
mobility, bactericidal activity, phagocytosis, produce and release cytokines

222
Q

cytokine

A

“any of a number of substances, such as interferon, interleukin, and growth factors, which are secreted by certain cells of the immune system and have an effect on other cells.”

“From the Greek cyto (cavity or cell) and kine (movement), cytokines are proteins involved in cell signaling and function as immunomodulating agents.”

223
Q

which cell most numerous circulating WBC?

A

PMNs (polymorphonuclear neutrophils)

224
Q

which cell first to appear in acute inflammation?

A

PMNs

225
Q

which cell mutliple nuclei (“multi-segmented”) – up to 5

A

PMNs

226
Q

2) EOSINOPHIL

A

2-3% of circulating WBCs

characteristics:
slower mobility

slower to react to “chemotactic” stimuli
–>
see “chemotaxis”

ALSO SEGMENTED NUCLEUS (2)

prominent in:
allegic reaction
inflammatory response to parasites

227
Q

eosinophil percentage

A

2-3% of circulating WBC

228
Q

eosinophil rate of action

A

slower mobility

slower reaction to chemotactic stimuli

229
Q

eosinophil # of nuclei

A

2 (multi-segmented)

230
Q

eosinophil common in

A

allergic reactions

inflammatory response to PARASITES

231
Q

PMNs common in

A

acute inflammation (first to appear)

232
Q

3) BASOPHILS

A

less than 1% of ciruclating WBC

present in inflammatory reactions

prominent in allergic reactions mediated by immunoglobulin E (IgE)

Non-segmented nucleus

CYTOPLASMIC GRANULES

LARGER THAN PMNS (big basophils)

structurally related to Mast Cells

233
Q

immunoglobulin define

A

“any of a class of proteins present in the serum and cells of the immune system, which function as antibodies.”

234
Q

globulin

A

“Globulins are a group of proteins in your blood. They are made in your liver by your immune system.”

235
Q

which WBC less than 1% circulating WBC

A

Basophil

236
Q

which WBC larger than PMNs

A

slides say larger than PMNs

google says slightly smaller than PMNs

Type Approx. % in adults Diameter (μm)

Neutrophil 62% 12–15

Eosinophil 2.3% 12–15 (slightly bigger than neutrophils)

Basophil 0.4% 12–15 (slightly smaller than neutrophils)

237
Q

largest WBC

A

monocyte

238
Q

which WBC related to mast cells

A

Basophil.

239
Q

basophil segmented or non-segmented nucleus?

A

non-segmented

240
Q

basophil cytoplasm

A

cytoplasm has granules

241
Q

where are basophils MOST COMMON

A

Most common in allergic reactions mediated by immunoglobulin E (IgE)

242
Q

IgE most common allergies (Immunoglobulin E)

A

Peanut allergy: Peanut allergy is one of the most common and severe food allergies, and it is mediated by IgE antibodies.

Tree nut allergy: Similar to peanut allergy, tree nut allergy is also mediated by IgE antibodies and can cause severe reactions.

Wheat allergy: Wheat allergy is another common food allergy that is caused by an IgE-mediated response to wheat proteins.

Milk allergy: Milk allergy is a common allergy in infants and young children, and it is caused by an IgE-mediated response to milk proteins.

Egg allergy: Egg allergy is another common food allergy that is caused by an IgE-mediated response to egg proteins.

Fish and shellfish allergy: Fish and shellfish allergy are also common food allergies that are mediated by IgE antibodies.

Insect sting allergy: Insect sting allergy is a severe allergic reaction that occurs when an individual is stung by an insect, such as a bee or wasp, and is caused by an IgE-mediated response to the insect venom.

Hymenoptera venom allergy: Hymenoptera venom allergy refers to an allergic reaction to the venom of insects such as bees, wasps, hornets, and yellow jackets.

Mold allergy: Mold allergy is a common respiratory allergy that is caused by an IgE-mediated response to mold spores.

Dust mite allergy: Dust mite allergy is another common respiratory allergy that is caused by an IgE-mediated response to dust mite allergens.

243
Q

4) MACROPHAGE

A

tissue cells
derived from blood MONOCYTES

“are produced by the differentiation of monocytes in tissues.”

BEANSHAPED nucleus

larger than PMN

“Macrophages are generally larger than typical monocytes.”
–> Recall:
Monocyte/macrophage = biggest – but differentiated macrophage = bigger

244
Q

when macrophage appear at inflammation site?

A

3-4 days after onset

live long

typical in chronic inflammation

phagocytic/bactericidal

245
Q

which WBC slowest/quickest?

A

macrophage slowest & live longest

PMNs quickest reaction

eosinophils slower reaction

246
Q

which WBC derived from monocytes

A

macrophage

247
Q

which WBC bean shaped nucleus

A

macrophage

248
Q

which WBC long lived – appear @ infl site after 3-4 days –> typical in chronic inflammation?

A

Macrophage

249
Q

5) PLATELETS

A

what?
fragments of cytoplasm released from MEGAKARYOCYTES in bone marrow

NO NUCLEUS

membrane-bound granules which contain HISTAMINE, coagulative proteins, cytokines, growth factors, etc

250
Q

OTHER WBCs

A

LYMPHOCYTES

PLASMA CELLS

251
Q

are platelets technically considered to be White blood cells?

A

no nucleus, no genes

Not generally considered to be a white blood “Cell”

cell fragment

252
Q

what are MEGAKARYOCYTES

A

A megakaryocyte (mega- + karyo- + -cyte, “large-nucleus cell”)

“LARGE NUCLEUS CELLS”

“a large cell that has a lobulated nucleus, is found especially in the bone marrow, and is the source of blood platelets.”

253
Q

no nucleus?

A

platelets

254
Q

what do platelets contain?

A

membrane-bound granules –> contain:

HISTAMINE

COAGULATIVE PROTEINS

CYTOKINES

GROWTH FACTORS

255
Q
A
256
Q

other important terminology

A

EDEMA

transudate

exudate

chemotaxis

Pus

purulent/suppurative

257
Q

edema

A

“a localized or generalized condition in which the body tissues contain excessive fluid”

258
Q

Transudate

A

the fluid that passes through a membrane; compared to exudate has fewer cells

259
Q

Exudate

A

a fluid released from the body with a high concentration of cells and protein

260
Q

exudate vs transudate

A

EXUDATE:
“Exudate is fluid that leaks out of blood vessels into nearby tissues. The fluid is made of cells, proteins, and solid materials. Exudate may ooze from cuts or from areas of infection or inflammation.”

TRANSUDATE:
“Transudates are fluids that pass through a membrane or squeeze through tissue or into the EXTRACELLULAR SPACE of TISSUES. Transudates are thin and watery and contain few cells or PROTEINS.”

261
Q

chemotaxis (see above)

A

The movement of WBCs in response to the release of chemical mediators

WBCs move up or along the concentration gradient

Requires energy

Active

262
Q

pus

A

“protein rich fluid contain WBCs and cellular debris produced during inflammation”

“a thick yellowish or greenish opaque liquid produced in infected tissue, consisting of dead white blood cells and bacteria with tissue debris and serum.”

263
Q

purulent/suppurative

A

“forming or containing pus”

264
Q

purulent vs suppurative

A

“Not knowing any official difference, I think of purulent as ‘stinky’ and suppurative as ‘oozing’.”

purulent etymology:
“festering” “pus”

265
Q
A

Semester 3 (32 decks)

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