Midterm 1 Flashcards
(420 cards)
1
Q
Pathophysiology
A
study of the physiological changes in the body as a result of disease or injury
2
Q
leading causes of death in canada
A
- cancer
3
Q
Males life expectancy at birth
A
79 years
4
Q
Females life expectancy at birth
A
84 years
5
Q
Health adjusted life expectancy males
A
69 years
6
Q
Health adjusted life expectancy females
A
70 years
7
Q
ethology definition
A
the study of the causes of disease
8
Q
common etiological factors
A
Genetics
- Congenital defects
- Microorganisms (viruses, bacteria)
- Immune dysfunction
- Metabolic dysfunction
- Degenerative changes
- Burns, radiation, other trauma, inflammation
- Other environmental factors
- Nutritional deficiencies or excess
9
Q
Idiopathic
A
cause of disease is unkown
10
Q
iatrogenic
A
treatment, procedure/ error that caused the disease
11
Q
predisposing factors
A
risk factors/behaviours that promote the development of disease
12
Q
prophylaxis
A
measures taken to preserve health and prevent onset or progression of disease
13
Q
Disease onset can be _ or _
A
acute or insidious (gradual)
14
Q
disease itself can be _ or _
A
acute or chronic
15
Q
diseases can be classified by
A
stages, states, and periods
16
Q
incubation period
A
time between infection and onset of symptoms
17
Q
subclinical state
A
disease in it’s earliest stages
18
Q
prodromal period
A
feels mild symptoms but infection not yet progressed to fullest
19
Q
Clinical manifestations of disease
A
signs/symptoms
20
Q
disease can be classified based on
A
remissions and exacerbations
21
Q
Some diseases have symptoms triggered by
A
precipitating factors
22
Q
disease prognosis
A
probability of recovery vs other outcomes
23
Q
prevalence
A
all cases (new and pre-existing)
24
Q
Incidence
A
limited to new cases only
25
Morbidity
state of being unhealthy
26
mortality
number of deaths that occur
27
NCD
not spread from person to person
28
Communicable diseases
infections that can be spread from person to person
29
epidemic
higher than normal (or expected) number of cases of an infection disease within a given area
30
pandemic
higher numbers around the world
31
endemic
disease regularly found among particular population or in certain area
32
cellular changes can be
temporary or permanent
33
examples of how cellular changes can happen
- hormones, environment
34
what can changes in DNA lead to
- permanent changes in structure and function, tissue damage, tumors
- damage due to changes in metabolic processes, ATP production, pH
35
atrophy cell changes caused by
not enough use of cells
- cells get squashed and small
36
hypertrophy cell changes caused by
overuse of cells
- large cells
37
hyperplasia cell changes caused by
increase in cell division
- increased number of cells in a tissue
38
metaplasia
one mature cell type replaced by a different mature cell type
39
dysplasia
cells vary in size, shape (mitotic rate)
40
Neoplasia
uncontrolled/abnormal growth
41
benign neoplasm
noncancerous uncontrolled cell growth
42
malignant neoplasm
cancerous uncontrolled cell growth
43
what are the two ways in which cell death occurs
1. apoptosis
2. Necrosis
44
apoptosis
Programmed cell death
- self-destruction by enzymatic digestion
- debris engulfed by phagocytes
45
what are the steps of apotosis
1. elimination of unwanted cells
2. cell shrinks
3. nuclear fragmentation (units leave cell)
4. apoptotic bodies (dead fragments)
5. phagocytosis of apoptotic bodies (no inflammation)
46
Necrosis
Injury or disease lead to cell death
47
steps of necrosis
1. always pathological
2. cell enlargement
3. loss of membrane integrity
4. leakage of content
5. inflammation
6. nuclear degeneration
48
pharmacology
study of medications or chemical compounds that interact with some part of the body (molecules, cells, tissues, systems) in order to produce a certain effect
- examining a drugs action, dosage, therapeutic use, and adverse effects
49
drug terminology
- each drug has at least 3 names
(chemical name based on its chemical structure)
- generic name= usually shortened chemical name used by health professionals
- brand/trade names given by pharmaceutical companies
50
drug dose
precise amount of active ingredient in the medication
51
How can we make a drug more convenient to use and improve its effectiveness at getting to its target in the body
combining it with inactive substances that help fill out the medication
52
3 phases of drug action
1. pharmaceutical
2. pharmacokinetic
3. pharmacodynamic
53
goal of drug action
get the drug from its point of entry to target tissue
54
pharmaceutical phase
how the drug progresses from the state in which its being administered to being dishevel in solution
55
two type of routes drug is administered through
Enteral and Parenternal
56
Enteral routes of drug administration
oral, sublingual, rectal
57
Paranteral routes of drug administration
Injections (intravenous (iv), subcutaneous (sc), intramuscular),
Inhalation (lungs and nasal), Transdermal
58
4 subphrases of the movement of drug through the body in the Pharmacokinetic phases
1. Absorption
2. Distribution
3. Metabolism
4. Elimination
59
Pharmacokinetics: Absorption
Passive diffusion vs active transport vs pinocytosis
*oral drugs must first past thought the metabolism
60
Administration routes of drugs
- IV is the most effective
- intramuscular vs subcutaneous
- oral: GI contents, drug coating, blood supply
61
Pharmacokinetic: distribution phase-factors that could effect distribution
- concentration absorbed
- blood flow to tissue
- % drug bound to plasma protein
62
Pharmacokinetic: metabolism
- primarily in the liver
* inactivation by enzymes
*prepares for excretion
- determines the half life of a drug
63
what determines the half life of a drug
metabolism
64
pharmacokinetic phases:
- Elimination
Primarily done by kidneys
- bile, feces, saliva, sweat, respiration
65
aerobic exercise effects on pharmacokinetics
- decrease the absorption after oral administration and increases absorption after intramuscular and subcutaneous administration
66
therapeutic action:
stimulation or inhibition of function
67
graph of drug effect vs dose
68
drug potency
strength of a drug at a particular dose
- concentration needed to produce 50% of the maximum effect
69
Drug efficacy
maximum effect that can be achieved by a drug
(the affect of the drug on the receptor once its bound
70
potency axis
x axis
71
efficacy axis
Y axis
72
Pharmacodynamics graph
the concentration of drugs effect
73
pharmacokinetics graph
the time it takes to be concentrated
74
pharmacokinetics/pharmacodynamics
the time it takes to have an effect
75
drug indications
approved uses for which the drug has been proven effective
76
off-label uses=
uses for which the drug has shown some effectiveness but originally approved purpose
77
contraindications
circumstances which the drug should not be taken
78
side effects
unwanted or intended actions, usually mild
79
adverse effects
serious side effects
80
adverse side effects examples
hypersensitivity
idiosyncratic reaction
iatrogenic effect
teratogenic effect
interactions
81
iatrogenic effect
state of ill health caused by medical treatment
82
teratogenic effect
drugs that can cause birth defects
83
idiosyncratic reaction
drug reactions that are adverse and cannot be explained by known mechanisms of action of the drug
84
therapeutic index
ration between toxic dose and minimum effective dose
85
toxicity is drug specific meaning:
- chemical properties
- routes and rates of administration
- rates of absorption, biotransformation and excretion
86
how do we avoid drug toxicity
need to determine the minimum effective dose, the amount that will produce the desired effect and minimize potential toxic effects
87
importance of regular dosing
- maintain desirable blood level
- reach effective blood levels quickly
88
factors influencing blood levels of a drug
- age
- genetic factors
- food and fluid intake
- health status, presence of other diseases, chronic or acute
- liver and kidney function
(absorption, metabolism, excretion)
- circulation and cardiovascular function
- body weight and proportion of fat tissue
- activity level and exercise
89
3 phases of drug action
pharmaceutical, pharmacokinetic, pharmacodynamic
90
Dose vs Concentration vs Time (half life graph) explained
it takes half the time too reach it's maximum concentration?
91
concentration effect: potency and efficacy effects
potency: amount of drug needed to produce and effect
efficacy: drugs capacity to produce and effect
92
iatrogenic effect is due to
an error in dosage
93
antagonistic interactions of a drug
one substance blocks or reduce the effect of another drug
94
potentiating drug interactions
one substance can increase the effects of another
95
synergistic drug interactions
two substances work together to produce a stronger effect
96
therapeutic index
ratio between toxic dose and minimum effective dose
97
fluid balance in the body (fluid gained or lost)
2.2 intake + 0.3 metabolic production - 2.5 L/day=0
98
electrolyte balance explained
- electrolytes are kept at a specific concentration inside and outside cells
- maintenance of homeostasis (rather than equilibrium) is essential for normal function
99
osmolarity
measure of solute
100
Blood plasma contains
- Proteins (albumin)
- Na+
- Ca2+
- Cl-
- HCO3-
101
Interstitial fluid contains
- Ca2+
- Na+
- Cl-
- HCO3-
- Proteins (K+, K+, Mg2+, intracellular fluid)
102
how are water and electrolyte levels regulated
- thirst
- kidneys
(hormones and direct regulation)
103
thirst components
- osmoreceptors in the hypothalamus (measure blood osmolarity)
104
kidney fluid and electrolyte regulation explained
varying the amounts that are excreted and reabsorbed
- direct + hormone
105
hormones that act on kidneys
- ADH
- aldosterone
- atrial natriuretic peptide
106
ADH effect
regulates water level
107
aldosterone
regulates NA+ and water level
108
Atrial Natriuretic Peptide
regulates Na+ and water levels
109
how does water move between compartments
filtration and osmosis
110
what drives filtration at capillaries
hydrostatic pressure
111
what drives osmosis across cells
osmotic pressure
112
osmotic pressure causes water to move from
low solute to high solute
113
Largest method of water gain
Food and drink 2.2 L/day
114
Largest method of water loss
Urine 1.5L/day
115
body weight water found in
2/3rds fluid inside cells
1/3rd fluid outside cells
blood plasma
116
extracellular fluid
interstitial fluid + blood plasma
117
sodium is found in high concentration,
outside or cells
118
sodium is found in low concentration
inside our cells
119
potassium high amounts
inside cell
120
potassium low amounts found
outside cell
121
most important electrolyte
sodium
122
To keep our electrolyte charge, that means that
maintenance of homeostasis is more important than equilibrium
123
difference between blood plasma and fluid around cells is
protein content
124
osmolarity
measure of solute concentration
125
Hydrostatic pressure
forces fluid out : Net filtration
126
Osmotic pressure
draws water in to area of higher solute
127
why is total blood solute higher than solute in cells
due to the amount of proteins
128
where is fluid excess located edema
fluid in the interstitial compartment
129
edema types
- isotonic : rention of isotonic fluid (same osmolarity)
- hypotonic: retention of hypotonic fluid (low osmolarity)
- hypertonic: retention of hypertonic fluid (high osmolarity)
*depending on the cause of edema
130
edema consequences
swelling within the tissues (localized or generalized)
- functional impairment
- pain
- impaired circulation
131
4 causes of edema
1. high local blood pressure
2. decreased osmotic pressure in the blood
3. blocked or missing lymphatic vessels;l
4. increased capillary permeability
132
high local blood pressure: edema cause
increase hydrostatic pressure
- increased net fluid movement into interstitial space
phatalogiclal states:
- severe hypertesion
- increased blood volume
133
decreased osmotic pressure in the blood
- increased net fluid movement into interstitial space
due to lowered plasma concentration
pathalogical states:
- kidney disease: excess protein excretion
- malnutrition or malabsorption
134
blocked missing lymphatic vessel
fluid and protein not filtered out into lymphatic vessel of drainage- causes localized edema
- pathological states:
tumor blocking
lymphatic drainage
135
isotonic dehydration
water and electrolyte loss
136
hypertonic dehydration
more water lost than electrolyte
136
hypotonic dehydration
more electrolytes lost than water
137
how can you test for dehydration
skin turgor test
138
acute pain
fast, localized,
- from injury: can be mechanical and thermal
- travels along pathway of A-delta myelinated fibres
139
chronic pain general overview
- slow, diffuse, prolonged
- existing stimuli, chemical
- pathway is the slow unmyelinated C fibres
140
chronic pain details
- lasting more than 3 months
- may become a nerve hypersensitivity issue
- may be localized within the CNS (no peripheral stimulus input)
- may be a mix of excitatory and inhibitory systems
141
chronic pain pathology involves not on the foot stuck on the accelerator
but also a dysfunction with the brake
142
current research about chronic pain
chronic inflammation of the nervous system due to malfunctioning glial cells as a cause of chronic pain
143
chronic pain ideal combo treatment
- exercise
- fish oil
- neuromodulation
144
pain management types of treatment
- pharmacological treatment (medication)
* analgesics
* anesthetics
- non pharmacological treatment
145
analgesics
decreased pain perception
146
anesthetics
don't block the pathway but block out ability to sense it: block the pain sensation
147
pain management is
multidisciplinary
- prevention
- psychological
- physical
- pharmaceutical
148
neuromodulation
transcranial magnetic stimulation
- uses electromagnetic coil to deliver a magnetic pulse that stimulates nerve cells in specific regions of the brain
- shown to be effective treatment for chronic depression and chronic neuropathic pain
149
what type of exercise can help with chronic pain
- exercise that helps desensitize the sensitized nervous system
- exercise is anti-inflammatory
- helps visualize the movement first
- find enjoyable exercise
150
two types of defence mechanisms in the body
1. innate immunity :
2. adaptive immunity :
151
adaptive immunity
specific diseases -> immune response
*all defences overcome injury or disease
152
innate immunity
nonspecific defences-
* fluids
*barriers like skin and mucous in the membrane
*phagocytosis: cellular elimination
153
inflammation
important defence mechanism of the body
- immunovascular responsec
154
how is inflammation caused
by a stimulus
- pathogen
- physical damage
155
how do we respond to inflammation stimuli
restore the balance by removing the cause, remove the damage, repair tissue
156
5 cardinal signs of acute inflammation
1. pain: due to chemical mediators
2. heat: increased
3. redness
4. swelling
5. loss of function
* can be localized vs systemic
157
Acute inflammation response overview
1. initiation and amplification
- chemical mediators released into the blood and at site of injury by resident immune cells, immune cells recruited to area
2. destruction
- neutralization of the injury and debris removal by chemical mediators and immune cells that were just released
3. termination
cytokines and chemokine will end the inflammatory process (anti-inflammatories)
158
local action of chemical mediators
- pain response
- vascular reposes: vasodilation and increased capillary permeability
- cellular response: attract immune cells to site of injury
159
cytokines:
immune cell proteins that coordinate the immune response: some are pro- inflammatory and some are antiinflammatory
160
chemical mediators
Cause pain response, allow blood flow, chemical mediator release, draw the immune cells to site of injury
161
cells involved in the inflammatory response
platelets- release blood-clotting proteins at wound site
mast cells- secrete chemical mediators
neutrophils- migrate to the site and secrete factors that kill pathogens, phagocytosis to remove
macrophages- secrete cytokines, phagocytosis to remove pathogens and debris
162
when are platelets cells involved
if there a physical tear
163
resident immune cells
live and wait for wounds
164
neutrophils,
first responders in the blood
165
macrophages
contribute to chemical mediator release
166
chemical mediators in the inflammatory response
- mast cells
- macrophages
- platelets
- plasma proteins
167
histamine
vasodilation and increased capillary permeability
168
prostaglandins
vasodilation and increased capillary permeability, pain, fever
169
leukotrienes
vasodilation and increased capillary permeability, chemo taxis
169
cytokines
fever, chemotaxis, recruit more WBC
170
platelets
activating factor: clotting and blood vessel repair
171
plasma proteins
bradykin- vasodilation
complement system- vasodilation and increased permeability
C-reactive proteins (CRP)- scretion of more cytokines, complement system, chemotaxis
prothrombin and fibrinogen - blood clotting
172
exudate
interstitial fluid collected in the area of inflammation
173
types of exudate
- serous:classic white fluid
- fibrinous: thick and sticky, higher cell fibrin content
- purulent: thick yellow and green colour, higher WBC and debris, microrganisms: suggest bacterial infection
- hemorrhagic: blood vessels damaged
174
abscess
pocket of prudent exudate in a solid tissue
175
how is Advil used to treat inflammation
it inhibits the enzymes involved with the inflammatory response
176
how is prednisone used to treat inflammation
suppresses the immune response, inhibiting inflammation
177
non-pharmaceutical treatments to inflammation
- compression
- cold: causes vasoconstriction to reduce sensory nerve transmission
- hot: promotes circulation in order to promote healing
- elevation
- rest: avoid further trauma
178
elements of healing (3 r’s)
- resolution: damaged cells recover
- regeneration: damaged cells are a type that can divide by mitosis and can be replaced by identical cell type
- replacement: damaged cells replaced by connective tissue, loss of function in this area
179
scar tissue=
cross linking of collagen
180
steps of from injury to healing
1. injury 2. acute inflammation 3. release of chemical mediators : causing
- increased BF, vasodilation, chemotaxis, nerve ending irritation, capillary permeability (edema) 4. prep for healing 5. healing
- scar tissue firbrosis
- regeneration
- resolution
181
acute inflammation: what type of immune cells infiltrate
neutrophils
182
chronic inflammation: what type of immune cells inflitrate
monocytes, macrophages, lymphocytes
183
pro-inflammatory cytokines
CRP: c-reactive peptide
IL-6: interleukin 6
184
chronic inflammation is typically
low grade
185
chronic inflammation can result from
- acute inflammation that is unable to resolve
- low level exposure to an irritant or foreign material
- autoimmune disorders
- inflammatory and biochemical inducers causing oxidative stress and dysfunction
186
non pharmacologic treatment of chronic inflammation
- nutrition :avoid sugar, refined carbs, trans fats, hydrogenated oils. avoid alcohol consumption, consume grains, whole foods, veg and fish
- aerobic & resistance exercise:
promotes meetabolically healthy tissues
anti-inflammatory benefits
- sleep quality & quantity
- stress reduction
187
how is the acid-base balance regulated- 3 methods
1) buffer systems in the blood
2) respiratory system: regulate CO2 level
3) kidneys: variable excretion/reabsorption of H+ and HCO3-
188
hypokalemia:
decreased K+ in the blood(increased pH)
- caused by alkalosis
- causes muscle cramping and weakness
189
hyperkalemia
increased K+ in blood
- caused by acidosis
- causes tingling and numbness
190
hyponatremia
losing more water Na+ than water or gaining more water than Na+
- muscle cramps, weakness
191
hypernatremia
increased Na+ in the blood
- increased thirst, decreased urine
192
acidosis
- respiratory acidosis: increased CO2
- metabolic acidosis: decrease in HCO3- (excess acid present)
193
alkalosis
- respiratory alkalosis: decreased CO2
- metabolic alkalosis: increased HCO3- (excess acid loss from the blood)
194
respiratory acidosis compensation (too much CO2)
metabolic: kidneys reabsorb HCO3- and excrete H+
respiratory: increase rate and depth of breathing
195
metabolic acidosis (too much HCO3) compensation
respiratory: hyperventilation to expel more CO2
metabolic: kidneys reabsorb HCO3- and excrete H+
196
respiratory alkalosis (decreased PCO2) compensation
Metabolic: kidneys excrete HCO3- and reabsorb H+
Respiratory: rebreathing= paper bag
197
metabolic alkalosis (increased HCO3- out)
Respiratory: hypoventilation to increase CO2 level in blood
Metabolic: kidneys excrete HCO3- and reabsorb H+
198
ROME acronym
Respiratory Opposite
- increase in PCO2=decrease pH
- decrease in PCO2=increase in pH
Metabolic Equal
- increase in HCO3-=increase in pH
- decrees in HCO3-= decrease in pH
199
our experience of pain can be described by what two components
1. sensory component
2. affective & cognitive component
200
Nociceptive pain
arises from an identifiable tissue, causing tissue damage
- thermal, mechanical, chemical
* somatic pain: with the skin or deeper
* within or around organs: sympathetic nervous system fibres, detect pain stimulus
201
neuropathic pain
caused by dysfunction of the nervous system
- often no indentifiable tissue damage
- can present in many different ways
202
pain threshold:
level of stimulation needed to activate the pain pathway and achieve a perceivable signal to the brain
203
pain tolerance
ability to withstand pain- intensity and Time
*70% of pain tolerance is due to genetics
- modulated by endorphins (increased with pain tolerance)
- modulated by fatigue, stress, mental health (decreased pain tolerance)
204
pain perception and response
- affected by age, culture, family traditions, prior experience, fear or anxiety , personality
205
enorphin
neurotransmitters that help reduce pain (increase the pain threshold)
- endogenous opioids
206
is pain cut and dry
no
207
3 key points for reconceptualizing pain
1. pain level is not proportionate to tissue injury
2. pain is modulated by many factors
(somatic, psychological, social domains)
3. the relationship between pain and the state of the tissue becomes less predictable as pain persists
208
Pain receptor: nociceptor
responds to extreme thermal, mechanical, or chemical stimuli
209
what type of fibres are the pain stimuluses carried by
1. A-delta fibers
2. C fibers
210
C fibers
(small unmyelinated
- high threshold thermo, mechano, chemo receptors (dull, throbbing, aching, burning pain, poorly localized)
211
A- delta fibers
(larger, myelinated)
- low threshold pain (mechanical and thermal)
- transmits sharp well localized pain sensations
212
pain stimuli can be inhibited by
- afferent touch stimuli coming into the spinal cord at the same time as pain stimuli: stimulates interneurons that inhibit the nociceptor 1st order afferent neuron
- descending signals from the brain: release endorphins directly onto nociceptor 1st order afferent neutrons or indirectly via interneurons
213
endogenous opioids also known as
endorphins
214
Gate Control Theory: Pain control : gate open
1. painful stimulus
2. substance p release
3. pain stimulus sent to brain
4. RAS alert
5. Pain is percieved
215
Gate control: Gate closed
painful stimulus inhibited!
* activates an interneuron releasing endorphin >enkephalin< which is an endogenous opioid. this causes an inhibition of release of substance P
Block the release of substance P
1. put pressure on muscle: to distract the brain with mechanical stimuli in area of painful stimuli
2. allow endorphins to block the pain
216
enkephalin
blocks substance P, allows for serotonin to kick in
217
reticular formation
can directly inhibit nociceptor
- activates interneuron
through serotonin inhibiting substance P
-> reducing the amount of neurotransmitter released and reducing the firing rate of second order afferent
218
Referred pain
brain interprets organ pain in the skin of the area of the organ
219
acute pain
fast, localized
A-delta myelinated fibers
short term
220
chronic pain
slow, diffused, prolonged
slow unmyelinated C fibers
221
chronic pain
- last no more than 3 months
- may become an issue of nerve hypersensitivity
- may be localized within the CNS
- mix of excitatory and inhibitory systems
222
chronic pain pharmacological treatments
- analgesics
- anesthetics
223
chronic pain management non pharmacological treatments
multidisciplinary
- prevention, psychological, physical, pharmaceutical
224
neuromodulation
- transcranial magnetic solution
uses a coil to deliver magnetic pulses stimulating nerve cells in specific regions of the brain to help with chronic pain
225
chemotaxis
migration of cells in response to a chemical stimulus
226
Possible threats on our body
- microorganisms
- toxins
allergens
- our own cells that have turned into tumour
227
immune system is designed to protect us from threats in which 3 steps
1. prevent entry
2. prevent spread/growth
3. removal of threat
228
infectious disease caused by
pathogens (microorganisms that invade, multiply, and cause damage)
- this includes bacteria, viruses,protozoa, prions
229
infection
a pathogen has reproduced in the hosts body
230
bacteria
prokaryotic single cell organisms, rigid cell wall
- contain DNA, RNA
- survive and divide outside living host
- named based on their shape and characteristics
231
viruses
small intracellular parasite
a protein coats with a core that contains DNA or RNA
requires a living hosts to replicated
231
fungi
found everywhere in the environment
- eukaryotic (single celled yeast) or chains of cells (mold)
- can produce bigger spores that become airborne (inhalation=allergic reaction_
- only certain fungi are pathogenic
worse for people who are immunocompromised
232
protozoa
parasites (pathogenic protozoa)
complex eukaryotic organisms
- unicellular motile
ex. pin worms, tape worms, amoebas, malaria
233
234
235
236
prions
infection transmitted by protein particles that are able to self-propagate
(induces protein into brain, misfiled, non functional, neurodegeneration)
-do not contain genetic material
- symptoms cause death (neuro-degenerative)
236
reservoir
source carrying the infection
236
infection modes of transmission
direct contact
indirect contact
droplets
aerosol
vector-borne
236
infection steps
reservoir, portal of exit, mode of transmission, portal of entry, susceptible victim
237
physiology of infection, PERIODS
incubation period. prodromal period, acute period
237
8 steps of infection
1. pathogen enters host
2. pathogen colonizes to appropriate site
3. pathogen reproduces rapidly
4. prodromal signs appear
5. acute signs present
6. decreased reproduction and death of pathogens
7. recovery- signs subside
*can have chronic infection : mild signs but destructive
8. total recovery
237
components of the immune system
- organs and tissues
- cells
- molecules / chemical mediators
237
organs and tissues of the immune system
bone marrow, slpeen, thymus glands, tonsils, lymph nodes and vessels
237
immune system cells
leukocytes (WBCs)
237
molecules/chemical mediators of the immune system
cytokines
- complement system
- anti bodies
- chemical mediators: histamine, bradykinin, prostaglandin, leukotrienes
238
what is the compliment system
group of small proteins in the blood. that complement the immune response
238
innate immune response
defence mechanism:
- physical & chemical barriers, inflammatory response
*FAST
*NO MEMORY
immune cells: non-specific
*distinguish between what should and shouldn't be in the body
molecular components: non-specific, chemical mediators involved in an inflammatory response
239
Adaptive immune response
defence mechanism: Kill compromised cells (antibody tags antigen)
*Initial response takes a few weeks
*immunologic memory: stronger and faster response each time the pathogen is present
- immune cells are specific for each invader
certain cells have antigens- ID
- molecular components: antibodies and chemical mediators
240
Leukocytes involved in the INNATE immune response: explained
all cells differentiated from myeloid progenitor:
- found circulating the in the blood within tissues at all times
- natural killer cells also part of the innate immune response: target cells infected with virus + cancer cells
----> TRIGGERING APOTOSIS
241
which cells are the link between the innate and adaptive immune repsonse
dendritic cells
242
types of leukocytes involved in the adaptive immune response
- antigen presenting cells: dendric cells
- B lymphocytes
- T lymphocytes
243
what do B lymphocytes do
recognize specific antigens that have invaded the body before *AKA MEMORY
and
secrete antibodies
244
what do T lymphocytes do
recognize specific antigen that is presented by the dendritic cells
turn into:
- helper T cells: secreting cytokines to help coordinate the immune response
- cytotoxic T cells: kill target cells that present a specific antigen
245
during an innate immune response,
local neutrophils & macrophages:
- do phagocytosis
secrete chemical mediators that
- trigger inflammatory response
- trigger release of other chemical mediators
- recruit more immune cells
(basophils, eosinophils, neutrophils, macrophages, dendritic cells)
+ natural killer cells
(if the pathogen is a virus or tumour)
- apoptosis of viral-infected abnormal cells
246
initiation of the adaptive immune response
1. dendritic cell pahgocytizes a pathogen for the first time
2. breaks up the pathogen in to small peptides
3. travels to lymph node and presents an antigen to T cells
4. T cells mature and reproduce
5. antigen- specific B cells develop and reproduce, target specific pathogen: turn into plasma cells once exposed to antigen : plasma cells secrete antibodies
*memory B cells reproduce for next time
*antibodies attach to the pathogen to mark it for destruction
247
Acute exercise effect on immune response
- leukocytes: higher number of natural killer cells, T cells, immature B cells
- increased antipathoden activity
- enhanced blood redistribution to target tissues
- increased activity of antioxidant enxymes
248
chronic exercise effect on immune system
- increase T cell proliferative capacity
- increased phagocytosis and cytotoxic activity
- increased production of anti-inflammatory mediators
- increased cell energy production
249
hypersensitivity reactions
immune system overreacts to damage instead of protection
- ex allergic reactions
chronic inflammation in the airways
- trigger
- dendritic cells
- helper T cells
- cytokines
- mast cells & eosinophils
-- more cytokines & leukotrienes
RESULT:
- local inflammatory response
- bronchospasm (smooth bronchioles contract) increased mucus secretion
250
autoimmune conditions
immune system can't distinguish between certain self and non self antigens
- it forms antibodies
- autoantibodies attack self-antigens and immune complexes
- inflammation and tissue damage occur
251
immunodeficiency
consequence of a defect in one or more components of the immune sytesm
- primary
INHERITED defect in the immune system
- secondary (acquired)
induced as a consequence of disease, treatment, or malnutrtion
* when immune cell is activated it produces more virus that leaves the cell, infects more immune cells
252
immunocompromised condition
any condition that leaves your body vulnerable to an infection, because of an issue with the normal functioning of the immune system,
253
ethology of autoimmune disorders is
unknown
- likely genetics, environmental
254
autoimmune disorders steps
- trigger
- cell damage or death
- immune system reacts and forms antibodies
- inflammation
255
how to keep an infection live HIV chronic
anti-retroviral therapy:
256
exercise considerations for people living with immunodeficiencies like HIV
exercise can improve risk,
257
how does age related decline contribute to osteoporosis
- decline in stem cells that produce osteoblasts
- decline in growth factors involved in promotion of bone formation
258
considerations of modifiable factors
- diet
- physical inactivity
- alcohol intake
- medication
259
OPG
osteoprotergerin (secreted by osteoblasts and other tissues)
- A decoy receptor: blocks the action of RANKL by binding to it. Causes RANK L to not be able to bind to its receptor on osteoclast precursor cell so osteoclast differentiation is inhibited
260
control of bone remodeling
RANKL binds to it's receptor->osteoclast differentiation and activation
261
estrogen role in control of bone remodelling
inhibits expression of RANK-L
increases production of OPG
- inhibits osteoclast formation
262
secondary osteoporosis can be caused by (etiologies)
-disease: endocrine or high cortisol
- excessive alcohol use: inhibits OB, increased pro-inflammatory cytokines, impaired vitamin absorption
- prolonged steroid use
- female athlete triad: intense training, poor nutrition, low estrogen/menstrual dysfunction
263
are pro inflammatory cytokines good or bad
bad
264
An osteoporotic bone has
- lower trabecular number and thickness
- increased trabecular spacing and cortical thinning + expansion of bone marrow cavity
265
an osteoporotic can be caused by
- increased bone resorption
- decreased bone formation
- increase osteoclasts
266
signs and symptoms of osteoporosis
spontaneous fractures
back pain (from compression fractures of vertebrae)
abnormal curvatures of spine with loss of height (stooped posture)
267
treatment of osteoporosis
- dietary supplements : Vitamin D, Ca 2+
- pharmaceuticals : promote bone formation/inhibit resorption
- estrogen replacement therapy for post-menopausal females
268
how does physical activity help with osteoporosis prevention
1. anti-inflammatory effects
2. mechanical loading of bone
(stimulates osteoblast differentiation and promotes osteocyte survival)
269
how much of a bones mass and improved fracture risk does PA have
- 5-10% difference in peak bone mass
- 25-50% difference in hip fractiure risk
270
therapeutic goal
prevents bone loss and prevents falls: preventing fractures
271
272
synovial joints
move freely within their ROM
- lined with articular cartilage and chondrocytes and extracellular matrix, synovial membrane, outer fibrous joints
272
ACSM and Osteoporosis canada exercise recommendations
- at least 150mins/week mod-big aerobic exercise
- emphasis on weight-bearing activities, not high impact
Progressive resistance training for all major muscle groups:
- at least 2d/week
- exercise intensity at 8-12 RM
- spine sparing strategies : posture, strength and flexibility in core muscles and spinal extensors
273
chondrocytes
maintain the cartilage
- secrete different enzymes to balance breakdown of old and production of new cartilage
274
extracellular matrix
collagen- structure support
proteoglycans - provide elasticity and high tensile strength
275
276
synovial membrane contents
inner lining of joint
- forms loose connective tissue
- blood vessels
- cells that clear debris and cells that secrete synovial fluid
277
outgrows fibrous joint capsule
attaches to bone
reinforces with ligaments
278
menisci
pads of fibrocartilage which helps stabliize and is a extra shock absorber
279
bursae
between tendons and ligaments
- fluid filled sacs providing extra cushioning
280
osteiarthritis
considered a disease of mechanical degeneration + inflammation within a synovial joint
- degeneration of articular cartilage, friction and damage, inflammation, pain
*localized to the affected joint
- result of something that causes increased release degradative enzymes by chondrocytes
- favours cartilage breakdown
281
osteoarthritis risk factors
age
genetics
obesity
join injury
inflammation
282
osteoarthritis steps
- chondrocytes triggered to release degradative enzymes
- breakdown of cartilage
- small cartilage pieces break of into joint space
- synovium cells remove debris, immune cells recruited, cytokine secretion, inflammation of synovium
- cracks form, synovial fluid enters and cracks widen
(no longer have smooth even surface)
- bone is exposed and rubs against articulating bone
- bone eburnation (looks polished)
- osteophytes and cysts develop
283
osteoarthritis results with
narrowed joint space with decreased ROM
inflammation in and around the join and surrounding tissues
284
osteoarthritis signs and symptoms
- asymmetric joints, often weight bearing
- beginning and end of day stiffness, increases with activity
- pain with movement/weight bearing
- limited ROM
- localized inflammation
- enlarged joint: can harden as osteophytes develop
285
osteoarthritis treatment
- exercise physiotherapy
- pharmacological: anti inflammatories
- hyaluronic acid or corticosteroid injections
- survey
286
rheumatoid arthritis
- chronic inflammatory disease: autoimmune
characterize by exacerbations and remissions : progressive joint damage
287
describe the onset of inflammatory disease
slow onset, usually with symmetric (bilateral join involvement)
* often begins in small joints of fingers
288
describe the severity of rheumatoid arthritis
severity varies based on # of joints implicated, degree of inflammation, rapidity of progression
289
rheumatoid arthritis risk factors
genetics:
sex: 3:1
environmental hazards
infections
autoimmune
290
rheumatoid athritis - pathophysiology
autoimmune response
- inflammation of the synovial membrane: vasodilation, capillary permeability, immune cells recruited, cytokine release
- cytokines trigger synovial cells to proliferate
- forms panes (thickened and inflamed synovial membrane with granulation scar tissue)
- panes releases proteolytic enzymes and cytokines
- destruction of cartilage
291
with inflammation , ___ usually comes along
vasodilation
increased capillary permeability
immune cells recruited
cytokine release
292
what happens when immune cells fail to recognize self
produce autoantibodies
293
rheumatoid arthritis signs and symptoms
3+ joints affected often symmetrically.
- often begins in the fingers
- chronic morning stiffness lasts for at least an hour (stiffness improves throughout the day)
- limited range of motion, pain with movement
- joint deformities with disease progression
- blood markers: elevated blood CRP and rheumatoid factor
- possibility of systemic symptoms: fever, fatigue, loss of appetite
294
308
309
fracture
complete or partial break in bone
310
types of fractures
- complete or incomplete
- open or closed
- number of fracture lines
- direction of fracture lines
311
complete fracture
bone is broken in two pieces
312
incomplete fracture
bone is partially severed
- more common break in children because of their softer bone
313
greenstick fracture
incomplete fractureo
314
open fracture/compound
skin is broke
bone fragments may protrude through skin
usually more damage to soft tissue surrounding bone
higher risk of infectionc
315
closed fracture
skin is not broken through
316
number of fracture lines: simple
single break, bone ends maintain alignment and position
317
comminuted fracture
multiple fracture lines and bone fragments
318
compression fracture
bone is crushed into smaller pieces and collapses
319
transverse fracture line
across the bone
320
spiral fracture line
angles around the bone
321
longitudinal fracture line
along the axis of the bone
322
oblique fracture line
at an angle with respect to diaphysis
323
impacted fracture
one end force into the other at the location of the break
-><-
324
stress fracture
repeated excessive stress
325
pathologic bone
weakness in bone structure due to other conditions
326
coles fracture
distal radius fracture
with dorsal angulation(upwards)
- like a dinner for
327
fractures treatment
- immediate immobilization
- survey if needed
(insertion of rods, plates, pins, realignment)
- exercise to maintain range of motion, muscle mass, and circulation
328
broken bone healing process 4 steps
1. hematoma formation
2. inflammatory phase
3. reparative phase
4. remodelling phase
329
hematoma formation
- bone break
- bleeding from the blood vessels in and around/bone and surrounding tissues
- clot forms in the medullary cavity, under periosteum and between bone fragments
- fibrin mesh forms, seal off fracture site and act as scaffolding in steps
330
inflammatory response and reparative phase
inflammatory response due to cell damage/necrosis and presence of debris at the cite (infiltration of immune cells)
- growth of new tissue within the fibrin mesh network
- new capillaries infiltrate the area
- fibroblasts and chondroblast migrate here, form the pro callus (3 weeks post injury)
331
reparative phase of bone healing
osteoblasts generate new bone over the fibrocartilage model (pro callus)
- the procallus is replaced by bone (bony callus)
332
Bone healing remodeling
during the following months in response to mechanical stress on the bone, repaired bone is remodelled by osteoblasts and osteoclast activity
- excessive callus removed and more compact bone laid down
*osteoclasts chisel to make a perfectly shaped bone remodel
333
factors that affect bone healing
age:
- kids 1-2 months
- adults 2+ months
extend of damage:
- prolonged inflammation
- complicated breaks
systemic factors:
- aging
- circulatory issues
- anemia
- diabetes
- nutritional deficits
- drugs
- smoking
334
fractures possible complications
- broken ends of the bone damaging surrounding structures
- compartment syndrome (bleeding)
- fractures of long bones
(rare but potential for release of adipose from fracture area to enter the bloodstream)
- ischemia
- infection
335
compartment syndrome
- bleeding or edema
- increased pressure inside limb
- impaired blood supply
336
what happens when adipose tissue from fractured area enters the bloostream
obstruction of blood flow
- in lungs: pulmonary embolism
- in Brain: stroke
337
ischemia in fracture
- due to cast compression
- due to edema within casted area
- monitor distal portion of limb for colour temp and feel
338
infection in fractures
most common with compound fractures or those that require surgical interventions
- osteomyelitis
bacteria entering the bone
local and systemic manifestations
* can cause pain
339
heal abnormalities : long term fracture complication
- malunion
- delayed union
- nonunion
340
malunion
healing outside of alignment: causes deformity
341
delayed union
more time to heal
342
nonunion
failed to heal
343
mobility complications in fracture long term complications
- joint stiffness
- instability
- contractures (muscular) limited ROM
344
side effects of long term immobilization in fractures
pressure injury
blood clots (deep vein thrombosis)
345
can smoking effect bone healing, how?
Yes, smoking causes decreased circulation contributing to non-union
346
lumbar lordosis
spine curves inwards at lower back
- common risk, poor posture, pregnancy, central obesity
347
kyphosis
"hunchback"
- rounded upper back
- risk of poor postures
348
scoliosis
S or C shaped sideways curvature of the spine
- risk factor genetics
349
lumbar lordosis exercise treatment
- build strength in hip extensors and stretch hip flexors
- build strength in abdominals
350
concussion
mild traumatic brain injury induced by biomechanics forces
- direct blow to head or transmitted
- no obvious brain trauma on imaging
351
most common causes of concussions
- motor vehicle accident
- contact sport
- falling down stairs
- domestic violence
352
two main types of concussion
- coup-contrecoup injury
- torque (rotational) injury
353
coup-contrecoup injury
movement of brain hitting one side of skull to other side of skull
[contusion from impact (coup) causes movement of brain to impact opposite side of skull (countrecoup)]
- results in stretching and shearing of neurone
354
torque rotational injury
head and neck twists causing brain to rotate
- results in stretching and shearing of neuronc
355
concussion pathophysiology
1. neuron injured due to stretching and shearing
2. axons leak: resulting in spontaneous AP firing
3. excess glutamate (excitatory neurotransmitter release)
4. neurons stimulated EPSP
5. increase in metabolic activity
4. increased glucose demand in blood, but decrease in blood to brain
5. imbalance of nutrient supply and demand (hours to days)
6. neurons damaged and enter a low metabolic state for short period of time (up to 30 days)
356
356
357
357
357
358
359
glutamate
excitatory post synaptic potential
360
GABA
inhibitory post synaptic potential
361
concussion symptoms
diagnosis based on description and symptoms
362
4 domains of concussion symptoms
somatic: nausea, pain, vomitting, vision, sound
cognitive: concentration and memory
mood: emotion
sleep: too much or too little
363
acute concussion symptoms
- confusion
- memory loss
- loss of consciousness
364
chronic symptoms
- headache
- dizziness
- nausea
- sensitivity to light noise
- fatigue
- vision
- emotional
- sleep
365
concussion treatment
- early mild-mod PA can reduce time-to-symptom-free
- avoid activity that could cause excess brain movement
366
what can repeated concussion lead to
- damage and misfolding of a structural protein: Tau protein (clustering and buildup around blood vessels in brain)
- neuronal death
- brain atrophy
- dementia
367
spinal cord injury (SCI)
- obstructs transmission of neural messages through spinal cord
--->
loss of somatic and autonomic control of the trunk, limbs, viscera below the site of injury
368
complete spinal cord injury
loss of all sensory and motor function at and below the level of injury
369
incomplete spinal cord injury
some function remains
370
somatic nervous system disruption
motor and sensory pathways
371
autonomic nervous system disruption
SNS&PNS
- won't pass info from brain and won't be able to receive feedback
372
tetraplegia
C4 Injury and C6 injury
373
paraplegia
T6 injury L1 injury
374
primary SCI injury
1. sudden trauma to the spine
2. acute spinal cord compression: shear, stress, severing and pulling on spinal cord
3. acute impact to neurons, glial cells and neural parenchyma
375
SCI secondary injury
* primary injury triggers a secondary injury
- involves cascade of biochemical and metabolic changes within the neural tissues
- secondary injury is the consequence of these downstream effects (haemorrhage and inflammation)
376
3 phases of a secondary injury
- acute phase
: hemorrahage, inflammation, ischemia, cell death begins
- sub acute phase
: further neurotoxicity, scar tissue formation, undamaged tracts begin to resume function
- chronic phase:
continued cell death and scar tissue
cyst development
377
378
asia scale Acomplete
no sensory or motor function is preserved in the sacral segments S4-S5
379
380
asia scale incomplete B
sensory but no motor function is preserved below the neurological level and include sacral segments S4-S5
381
asia scale incomplete C
motor function is preserved below neurological level and more than half the key muscles below neurological level have a muscle grade greater than or equal to 3
382
asia scale incomplete D
motor function is preserved below the neurological level, at least half of key muscles below the neurological level have a muscle grade greater or haul to 3
383
asia scale Normal E
sensory and motor functions are norma
384
side effect of SCI
- cardiovascular:: HR BP issues loss of NS signals
- pulmonary: ventilation impaired with injuries abouve C5
- bowel and bladder function: sexual function all likely affected
- thermoregualation : harder to regulate below level of SCI
- hyperreflexia (spasticity) : due to central disinhibition of spinal reflex arcs: leads to inappropriate activation of stretch reflex muscle
- autonomic dysreflexia
385
autonomic dysreflexia
uncontrolled SNS response to an afferent stimulus below SCI level
- widespread vasoconstriction below level of injury
*can be life threatening: sudden acute hypertension along with Bradycardia
386
PA guidelines for adults with SCI
STARTING LEVEL
20 mins 2x of aerobic activity
3sets 10reps 2x week strength training activity
ADVANCED LEVEL
30mins 3x week aerobic activity
3sets10reps2xweek strength training activity
387
muscular dystrophies
genetic
- progressive degeneration of skeletal muscle fibers (necrosis)
- muscle fibers replaced by adipose and connective tissue
387
skeletal muscle disorders examples
- disuse atrophy
- muscular dystrophies
- myasthenia graves
- amyotrophic lateral sclerosis (lou Gehrig)
388
neuromuscular junction disorders can be
drug/toxin induced or genetic
389
gravis
- autoimmune
- attack on the nicotinic acetylcholine receptors
390
Amyotrophic lateral sclerosis (Lou Gehrig)
- genetic or unknown ethology
(genetics and environment?)
- rapidly progressive
- degeneration of motor neuron's
(protein misfolding, neuronal death, neuronal degeneration)
- affects upper and/or lower MNs,
(muscle weakness, spasticity, impaired fine motor control, hyporeflexia, brainstem involvement, dysphagia, dysarthria, dysphonia
- end stage is paralysis, respiratory failure and multiple sclerosis
391
multiple sclerosis
- inflammatory autoimmune disease that effects the conduction of neural impulses
* chronic degenerative disease
demyelination of the neuron's(from interneurons 1A and 1B) within the CNS, scar tissue forms
392
what results from multiple sclerosis
- clumsiness and muscle weakness
393
what ages is onset of multiple sclerosis
onset between 15 and 50 years od age
394
Multiple sclerosis etiology
unknown
- links to genetics, environment, virus
395
multiple sclerosis symptom details
- demyelination can occur anywhere, in patches within the CNS
- usually characterized by exacerbations and remissions
- 80% of diagnoses begin as relapsing-remitting
- degeneration can be progressive
*myelin can be repaired
- variable severity (mild and slow vs fast and progressive)
395
in MS, location of demyelination will determine
the symptom type
396
MS- extent of demyelination will determine the
symptom severity
396
MS- cerebellum demyelination symptoms
loss of balance and ataxia and tremor
397
MS- cranial nerve demyelination symptoms
diplopia and loss of vision
398
MS-motor nerve tracts demyelination
weakness and paralysis
399
MS- damage to sensory nerve tracts
paresthesia, prickling burning sensation
400
multiple sclerosis pathophysiology
1. unknown tigger
2. activated T cells cross the blood brain barrier
3. secretes cytokines
4. immune cells recruited, macrophages
5. attack oligodendrocytes(cells that form the myelin sheath with CNS)
6. myelin damaged and breaks down
7. scar tissue formation, axonal destruction
401
multiple sclerosis diagnosis and treatment
Diagnosis: of exclusion
treatment:
- disease modifying drugs, slow down progressions
- pharmaceuticals to treat complications
- physio and exercise to maintain strength and mobility
- occupational therapy to support ADL
- adaptive equipment
402
exercise prescriptions in those with MS
shown to improve muscle weakness, bladder and bowel function, fatigue, psychological health, quality of life
considerations for exercise prescription
- physical limitations
- supportive equipment
- variable strength levels
403
cerebral palsy(neuromuscular disorder originating from the brain)
- neurodevelopment condition: something happens during development (pre or post natal)
- muscles affected depends on what part of the brain is affected
spastic: upper motor neurons are damaged
dyskinetic: involuntary movements if basal ganglia is damaged
ataxic: damage to cerebellum
404
parkinsons disease
disease of synaptic transmission
- dopamine is released and reduced via destruction of neurons of the nigrostrital pathway
* progressive and degenerative
* average age of diagnosis: mid 502
405
Parkinson's disease progression
cardinal symptoms-> dementia (sometimes)-> death due to complications
406
in parkinsons patients dopamine neurons in the ____ degenerate
nigro-stratial pathway
407
dopaminergic neurons of the substantial nigra normally responsible for
1. allowing signals to be sent to cerebral cortex for movement initiation
2. fine tuning of signals to prevent unwanted movement
408
explain how the dopamine release is reduced in Parkinson's disease
destruction of neurons of the nigrostriatal pathway (neurons that project from substantial nigra to stratum within basal ganglia)
409
parkinsons disease pathophysiology
1. unknown trigger
2. degeneration of neurons of the substantial nigra that produce and release dopamine
3. less dopamine released onto neurons of striatum
4. imbalance of excitatory and inhibitory neurotransmitters released in striatum
5. result= not enough voluntary initiation of movement and too much involuntary movement
410
dopamine job
neurotransmitter that produces an inhibitory or excitatory stimulus on postsynaptic neurons
> dopamine plays key role in control and fine tuning
411
parkinsons 4 cardinal symptoms
- bradykinesia (slow movement)
- muscle rigidity (spastic movement)
- resting tremor
- postural instability
412
how is Parkinson's diagnosed
diagnosed based on symptoms
413
parkinsons treatment
Pharmaceutical treatment:
- dopamine replacement therapy
dopamine cannot cross blood-brain-barrier so, L-dopa (levodopa) given; it's a precursor so it will be converted to dopamine in the brain
- drugs that inhibit dopamine breakdown so that dopamine that is produced will last longer
Exercise, PT, OT:
- maintain mobility, stability, and posture to delay disability
- exercise to maintain strength, balance, and flexibility
- safe exercise
414
