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
Nucleocytoplasmic ratio
ratio of nucleus (volume?size?) vs cytoplasm "
26
Nucleocytoplasmic ratio is higher in
Higher in: a) undifferentiated adult cells, b) fetal cells, c) tumour cells
27
organelles of cytoplasm
Nucleus Mitochondria Ribosomes Endoplasmic reticulum Golgi complex Lysosomes
28
nucleus?
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
29
mitochondria?
Double membrane involved in cellular energy production (internal cristae?) Energy demanding cells are mitochondrial rich (liver, nerve, red muscle)
30
few mitochondria which cells?
undifferentiated cells many malignant tumor cells
31
ribosomes
small RNA granules can be: a) free floating b) on RER involved in protein synthesis
32
free ribosomes vs RER ribosomes
free ribosomes = proteins for internal cell environment use RER ribosomes = for "export" (note "LUXARY proteins")
33
luxary proteins
"A protein that is produced only in specialized cells and is not necessary for general cell maintenance, unlike the so-called housekeeping proteins."
34
endoplasmic reticulum
membranes continuous with plasma membrane (?) and nuclear membrane
35
rough ER
involved in protein synthesis; studded with ribosomes
36
smooth ER
involved in catabolism of drugs, hormones, nutrients no ribosomes "associated with the production and metabolism of fats and steroid hormones."
37
golgi apparatus
Adjacent to nucleus membrane bound cisternae modifies, sorts and packages macromolecules such as proteins and lipids before their secretion
38
golgi body and proteins before secretion
"The Golgi complex plays a central role in protein secretion by regulating cargo sorting and trafficking"
39
lysosome?
digestive organelle lytic enzymes Fuse with vesicles to digest material
40
what does lysosome digest?
E.g. worn out structures, bacteria, etc.
41
lyososomes and lysis
Can release its contents into the cell to lyse cell
42
why lysis?
(worn out, damaged, too many, infected, etc.)
43
cell projection types (PASSIVE PROJECTIONS)
microvilli (no energy required) FUNCTION?? Increase cell SA
44
cell projections (ACTIVE PROJECTIONS)
require energy Cilia Flagella (flagellum)
45
cilia
Cilia: numerous, short, hairlike projections move substances across the surface of the cell
46
flagella (flagellum)
single, long projection functions to move the cell (sperm)
47
integration
for homeostasis bringing together various parts --> FUNCTION AS WHOLE
48
three types of integration
Autocrine Paracrine endocrine
49
Autocrine stimulation (type of integration)
secretes substance that stimulate itself SIMPLEST
50
Paracrine stimulation (type of integration)
secretes a substance that stimulates a nearby cell
51
endocrine stimulation (type of integration)
release substance into the bloodstream then stimulate distant cell
52
Highest form of integration?
endocrine stimulation
53
endocrine stimulation can involve cells of _____
cells of anatomically distinct organs
54
causes of cell injury?
Hypoxia / ischemia / anoxia Physical agents (temp/vibration/radiation) Mechanical damage (trauma) Abnormal metabolite accumulation Fluid or electrolyte imbalance pH imbalance
55
other causes of cell injury
Chemicals (heavy metals/drugs) Microbiological agents (bacteria/viruses) Immunological reactions (autoimmune/host cells) Genetic defects Nutritional imbalances Aging
56
reversible cell damage
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
57
pumps intact?
No Na+K+ pumps puming Na+ out? = cell swells, and membrane ruptures = lysis
58
irreversible cell damage? Structure/function of cell
Decrease energy production Decrease metabolism Decrease in pH
59
irreversible cell damage? nucleus
Shrinking, fragmentation, lysis (nucleus)
60
irreversible cell damage? lysosomes
Can burst releasing degrading enzymes and increase cell damage
61
irreversible cell damage? plasma membrane
Extensive plasma membrane damage
62
irreversible cell damage?
Accumulation of amorphous, Ca-rich densities in the mitochondrial matrix
63
cellular adaption
cells adapt their growth/differentiation e.g. normal adaptations breast/uterine growth during pregnancy
64
when tissue modify?
modified frequently in response to hormonal stimulation, environmental changes, irritation
65
atrophy
decrease in the size of cells resulting in reduced tissue mass caused by poor nutrition, aging, immobility i.e. whole organ, or cellular (?)
66
atrophy e.g.
Decreased demand, oxygen, nutrients, nerve innervation. Persistent cell injury
67
hypertrophy
increase in the size of individual cells resulting in enlarged tissue mass
68
hypertrophy e.g.
eg. Striated muscle cells – working out. Cardiac muscle – cardiovascular disease
69
hypertrophic cardiomyopathy
.
70
hyperplasia
increased number of cells resulting in enlarged tissue mass can occur in conjunction with hypertrophy
71
hyperplasia e.g.
e.g. endometrial thickening of the uterus
72
metaplasia
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)
73
endometrial hyperplasia
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.
74
benign prostate hyperplasia
.
75
dysplasia
"cells of a tissue vary in size and shape, large nuclei are present and the rate of mitosis increases; may indicate a precancerous state"
76
intracellular accumulations
overload of various metabolites/exogenous material OR prevention of excretion of metabolic byproducts
77
intracellular accumulations via ____
overload, underutilization, underexcretion
78
intracellular accumulations e.g.
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
79
aging
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
80
PHARMACOLOGY LECTURE 1 ***
..
81
language of pharmacology
how are drugs named? drug classificaitons, uses, side effects
82
pharmacokinetics and pharmacodynamics
...
83
how are drugs administered? how are drugs processed in body?
...
84
why do massage therapists need to know how medications work?
.
85
allopathy?
"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."
86
why MT familiar with pharmacology?
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 (?)
87
pharmacology define
study of action of chemicals on living organisms produce biological effects
88
pharmacology includes
pharmacokinetics pharmacodynamics pharmacy toxicology
89
pharmacokinetics
What the body does to the drug
90
pharmacodynamics
What the drug does to the body
91
pharmacy
"the science or practice of the preparation and dispensing of medicinal drugs."
92
toxicology
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.
93
what is pharmacokinetics
“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
94
what is pharmacodynamics
“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
95
mechanism of action of drug
"In medicine, a term used to describe how a drug or other substance produces an effect in the body."
96
E.g. of why RMT needs to know effects of drugs when relevent
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
97
what should massage therapists know?
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
98
Common pharmaceutical terms and concepts
...
99
Drug names Drug classifications Uses or indications pharmacodynamic terms (effects of medications, "Mechanism of action") pharmacokinetic terms (half-life, onset of action, bioavailability)
..
100
how are drugs named?
via: generic name or brand (trade) name
101
generic name
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 )
102
brand (trade) name
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
103
generic medications
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" (?)
104
when generic medication?
After a patent expires on a drug, generic drug companies may produce it
105
drug classifications
non-prescription drugs prescription drugs restricted and controlled drugs
106
other drug classifications
therapeutic properties (action/effect on body) action or effect on body system chemical structure
107
therapeutic properties
describes the effect that the drug has on the body E.g. anti-hypertensive to reduce blood pressure
108
action or effect on specific body system
describes the body system that the drug affects E.g. central nervous system stimulant
109
chemical structure
escribes basic chemical or pharmacologic properties of the drug E.g. beta-blocker
110
what if client does not remember name of drug?
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
Uses/indications for drug
list of diseases/disorders drug is officially recommended for by Health Canada
112
what if a drug helps a condition, but Health Canada has not approved the use for "
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
contraindications for a drug
disease/disorder that the drug has a negative effect on should not be prescribed to a client with that condition
114
(Pharmacodynamics) effects of medication based on
1) Therapeutic effects 2) side effects or adverse effects 3) unpredictable effects
115
Factors that influence Effects
dosage, age, gender, lifestyle, pathologies
116
1) Therapeutic effects
desired effect which is intended to help the user get better
117
2) side effects or adverse effects
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
side effects or adverse effects via
1) too much therapeutic effect 2) unrelated effect 3) via interaction of multiple drugs
119
3) unpredictable effects
two types: a) allergic/hypersensitive reactions b) idiosyncratic reactions
120
a) allergic / hypersensitive reactions
can be mild E.g. (hives, joint pain, fever) can be severe E.g. anaphylaxis
121
b) idiosyncratic reactions
unexpected or highly unusual effects occur in small number of people
122
important note
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
pharmacodynamics (Mechanism of action)
..
124
how do drugs create changes?
DRUGS DO NOT create new functions drugs alter existing cellular activities
125
Mechanism of action occurs via
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
a) Combining with specific cellular receptors
binding to receptor can alter cellular function E.g. benzodiazepines binds to a neurotransmitter receptor
127
b) Chemically altering body fluids
E.g. antacid to neutralize excess stomach acidity and reduce or prevent digestive discomfort
128
c) Chemically altering cell membranes
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
d) Interacting with extracellular enzyme systems
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
(Pharmacokinetics) Half-life
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
(Phamarcokinetics) onset of action
duration of time it takes for drug to become effective
132
onset of action can be determined by
how was the drug administered/taken? E.g. IV versus orally
133
why onset of action important to know?
can help determine schedule of Massage therapy
134
(pharmacokinetics) bioavailability
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
other things that determine bioavailability
doseage/frequency age general health
136
blood thinners, blood thinning and bruising
"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
******General Pathology 300 --- Class 2 ******
.
138
Cell death 2 types
1) apoptosis 2) necrosis
139
inflammation?
will discuss: signs symptoms pathogenesis cellular events in inflammation cells of inflammation
140
apoptosis
endogenously programmed (mechanism) initiating event can be endogenous OR exogenous
141
endogenous vs exogenous
growing or originating from within an organism. growing or originating from outside an organism.
142
necrosis
exogenously induced via irreversible cell injury E.g. toxins, anoxia, etc.
143
4 types of necrosis
coagulative, liquefactive, caseous, fat
144
1) coagulative necrosis
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
most common necrosis type?
coagulative necrosis
146
which cell proteins denature or are altered in coagulative necrosis?
cytoplasmic hydrolytic enzymes that prevent lysis of tissue
147
characteristic of tissue during coagulative necrosis
tissues retains original form firm consistency
148
where is coagulative necrosis typical?
solid internal organs
149
common cause of coagulative necrosis
anoxia E.g. heart attack
150
2) liquefactive necrosis
dead cells liquefy via influence of certain enzymes dissolution of tissues SOFT/DIFFLUENT tissue
151
liquefactive necrosis -- where most often?
brain brain cells liquefied brain becomes soft, fluid-filled cavity
152
note secondary liquefaction
tissue may undergo LIQUEFACTIVE necrosis after undergoing COAGULATIVE necrosis "Coagulative necrosis may liquefy"
153
3) caseous necrosis
special type of COAGULATIVE NECROSIS w/ limited LIQUEFACTIVE necrosis hybrid of two types tissue becomes "CHEESE-like" and yellow-white
153
Caseous necrosis where?
TUBERCULOSIS (almost unique to tuberculosis)
154
caseous necrosis also where?
Some FUNGAL INFECTIONS
155
caseous necrosis and tuberculosis
Center of a tuberculous granuloma becomes necrotic and the cells fall apart
156
"granuloma"
"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
granuloma and tuberculosis
"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
4) Fat necrosis
special type of LIQUEFACTIVE necrosis via? action of LIPOLYTIC enzymes where? limited to fat tissue Esp around pancreas
159
which necrosis is special type of liquefactive necrosis
fat necrosis
160
which necrosis type is a special type combining liquefactive and coagulative necrosis
caseous necrosis
161
mechanism of fat necrosis
pancreatic enzymes release into fat tissue degrade fat into: GLYCEROL FREE FAs I.e. from Triglyceride?
162
necrosis -- miscellaneous term
Gangrene
163
gangrene
dead tissue
164
necrotic tissue and secondary changes E.g.
Necrotic tissue can undergo secondary changes such as E.g. CALCIFICATION Also note: secondary liquefaction E.g. liquefactive necrosis after undergoing coagulative necrosis
165
note frostbite, dry gangrene, and coagulative necrosis -- also note ischemic necrosis
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
apoptosis
programmed cell death under normal conditions may occur when: A) abnormal cell development B) excessive cell numbers C) injured cells D) aged cells
167
apoptosis -- what happens?
cells "self-destruct" appear to digest itself disintegrate I.e. LYSIS
168
which cell death type is active
apoptosis
169
apoptosis important facts
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
apoptosis is normal development (e.g. formation of digits)
lack of apoptosis can cause pathology E.g. important in formation of digits
171
syndactyly
occurs when digits fused together (e.g. in hands/feet)
172
inflammation 5 signs
swelling heat redness pain (occasionally) loss of function
173
inflammation
"to set on fire" body's nonspecific response to tissue injury E.g. Appendicitis, laryngitis, pancreatitis, mastitis, etc.
174
inflammation, facts
biological response of vascular tissues to harmful stimuli E.g. pathogens, damaged cells or irritants
175
inflammation function
protective attempt by the organism to remove/localize the injurious stimuli initiate the healing process for the tissue
176
why inflammation important?
Without inflammation wounds and infections would not heal and further destruction of tissue would compromise survival of organism.
177
when inflammation occur?
cut, allergy, bite, infection, burn, etc.
178
infection and inflammation
With infection, a microorganism is present
179
signs and symptoms of inflammation
symptoms: pain/tenderness signs: redness, swelling, heat, loss of function
180
non-specific symptoms of inflammation (ESP w/ SYSTEMIC INFLAMMATION -- possibly when not visible?)
fatigue weakness decreased appetite aching
181
PATHOGENESIS OF INFLAMMATION
1) changes in circulation of blood 2) changes in vessel wall permeability 3) release of SOLUBLE MEDIATORS OF INFLAMMATION (SMIs) 4) cellular events
182
1) changes in circulation of blood
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
what happens when blood rushes into capillaries
redness, swelling, warmth... (hyperemia)
184
why congestion in capillaries?
Blood flow in dilated capillaries is slow leading to congestion
185
what do red blood cells form in dilated capillaries?
Sludged erythrocytes form stacks (rouleaux) impeding circulation "ROULEAUX"
186
what happens in WBC in dilated capillaries?
WBCs are marginalized and become attached to endothelium (PAVEMENTING)
187
2) changes in vessel wall permeability
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
3) release of SOLUBLE MEDIATORS OF INFLAMMATION (SMIs)
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
SMIs list
a) Histamine b) Bradykinin c) Complement system d) Arachidonic Acid Derivatives
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a) histamine
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
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what does histamine do to BC permeability
increases "formation of gaps" (??) allows fluid to go to interstitial spaces
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histamine timing
occurs quickly rapidly inactivated via HISTAMINASE "IMMEDIATE TRANSIENT REACTION"
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where histamine released from?
Released from platelets and mast cells
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b) Bradykinin
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
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Bradykinin vs Histamine timing
Bradykinin effects occur at slower rate
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which SMI incites pain?
Bradykinin
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which plasma protein activates Bradykinin?
COAGULATION FACTOR XII (clotting factor 12) AKA Hageman factor = plasma protein
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c) Complement system (SMI)
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)
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where are complement system plasma proteins created?
produced by LIVER
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how to complement system plasma proteins circulate?
in INACTIVE form
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how are they numbered?
C1 to C9
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which three pathways activate complement system proteins?
Classical pathway Alternative pathway Lectin pathway
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what are three ways complement system proteins can activate?
formation of biologically active fragments (E.g. C3a) formation of intermediate COMPLEXES (E.g. C567) formation of terminal MEMBRANE ATTACK COMPLEXES (E.g. MAC)
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MAC mechanism (membrane attack complex)
"MAC destroys cells by boring holes in plasma membrane"
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MAIN FUNCTION OF ACTIVATED COMPLEMENT DERIVATIVES
OPSONIZATION ANAPHYLAXIS CHEMOTAXIS CELL LYSIS
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opsonization
"Antibody opsonization is a process by which a pathogen is marked for phagocytosis."
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opsonin
"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."
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anaphylaxis
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."
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anaphylactic shock
"an extreme, often life-threatening allergic reaction to an antigen to which the body has become hypersensitive."
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chemotaxis -- general definition
"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."
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chemotaxis
migration of leukocytes
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cell lysis
via MAC
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d) ARACHIDONIC ACID DERIVATIVES (SMI)
Arachidonic acid derived from phospholipids of cell membranes via 2 pathways: LIPOXYGENASE PATHWAY & CYCLOOXYGENASE PATHWAY
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2 pathways for metabolism of arachidonic acid (derivatives)
LIPOXYGENASE PATHWAY & CYCLOOXYGENASE PATHWAY
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lipoxygenase pathway
formation of: Leukotrienes – promote chemotaxis and incr. vasc. permeability Lipoxins – inhibit chemotaxis
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cyclooxygenase pathway
formation of: Prostaglandins – cause vasodilation, vascular permeability, mediate pain and fever --> Prostacyclin – counteracts thromboxane Thromboxane – platelet aggregation, thrombosis, vasoconstriction
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thrombosis
"Thrombosis is a blood clot within blood vessels that limits the flow of blood."
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4) CELLULAR EVENTS (FINAL POINT IN "PATHOGENESIS OF INFLAMMATION"
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
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4) CELLULAR EVENTS (phagocytosis)
PMNs (polymorphonuclear neutrophils) ---> Lose their mobility ---> act as scavengers Active uptake of bacteria/cellular debris often PMNs die in their fight with bacteria
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The cells of inflammation******
1) Neutrophil (most common) 2) Eosinophils (2-3%) 3) Basophils (1%) 4) Macrophages 5) Platlets
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1) Neutrophils (Polymorphonuclear neutrophils --> PMNs)
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
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cytokine
"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."
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which cell most numerous circulating WBC?
PMNs (polymorphonuclear neutrophils)
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which cell first to appear in acute inflammation?
PMNs
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which cell mutliple nuclei ("multi-segmented") -- up to 5
PMNs
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2) EOSINOPHIL
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
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eosinophil percentage
2-3% of circulating WBC
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eosinophil rate of action
slower mobility slower reaction to chemotactic stimuli
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eosinophil # of nuclei
2 (multi-segmented)
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eosinophil common in
allergic reactions inflammatory response to PARASITES
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PMNs common in
acute inflammation (first to appear)
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3) BASOPHILS
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
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immunoglobulin define
"any of a class of proteins present in the serum and cells of the immune system, which function as antibodies."
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globulin
"Globulins are a group of proteins in your blood. They are made in your liver by your immune system."
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which WBC less than 1% circulating WBC
Basophil
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which WBC larger than PMNs
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)
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largest WBC
monocyte
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which WBC related to mast cells
Basophil.
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basophil segmented or non-segmented nucleus?
non-segmented
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basophil cytoplasm
cytoplasm has granules
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where are basophils MOST COMMON
Most common in allergic reactions mediated by immunoglobulin E (IgE)
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IgE most common allergies (Immunoglobulin E)
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.
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4) MACROPHAGE
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
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when macrophage appear at inflammation site?
3-4 days after onset live long typical in chronic inflammation phagocytic/bactericidal
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which WBC slowest/quickest?
macrophage slowest & live longest PMNs quickest reaction eosinophils slower reaction
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which WBC derived from monocytes
macrophage
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which WBC bean shaped nucleus
macrophage
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which WBC long lived -- appear @ infl site after 3-4 days --> typical in chronic inflammation?
Macrophage
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5) PLATELETS
what? fragments of cytoplasm released from MEGAKARYOCYTES in bone marrow NO NUCLEUS membrane-bound granules which contain HISTAMINE, coagulative proteins, cytokines, growth factors, etc
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OTHER WBCs
LYMPHOCYTES PLASMA CELLS
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are platelets technically considered to be White blood cells?
no nucleus, no genes Not generally considered to be a white blood "Cell" cell fragment
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what are MEGAKARYOCYTES
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."
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no nucleus?
platelets
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what do platelets contain?
membrane-bound granules --> contain: HISTAMINE COAGULATIVE PROTEINS CYTOKINES GROWTH FACTORS
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****
****
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other important terminology
EDEMA transudate exudate chemotaxis Pus purulent/suppurative
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edema
"a localized or generalized condition in which the body tissues contain excessive fluid"
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Transudate
the fluid that passes through a membrane; compared to exudate has fewer cells
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Exudate
a fluid released from the body with a high concentration of cells and protein
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exudate vs transudate
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."
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chemotaxis (see above)
The movement of WBCs in response to the release of chemical mediators WBCs move up or along the concentration gradient Requires energy Active
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pus
"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."
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purulent/suppurative
"forming or containing pus"
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purulent vs suppurative
"Not knowing any official difference, I think of purulent as 'stinky' and suppurative as 'oozing'." purulent etymology: "festering" "pus"
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