Studied by 39 people
how do antibodies trigger the inflammatory immune response
antibodies start with unique pathogens. highly specific antibodies recognize uniqueness which triggers inflammatory immune response.
what are cytokines
-major form of communication between all cells of the body to coordinate/balance various functions
-essential for regulating the body’s healing steps
cytokines are similar to —- but aren’t limited to —-
-hormones
-excretion by glands
if cytokines are imbalanced, that may lead to autoimmune disorders and chronic inflammation, which are known as
pro-inflammatory cytokines
how do free radicals damage tissue
-change cell structures
-mitate cellular DNA
-result: dead or non-functioning cells which cause inflammation that can turn chronic
macrophages
when inflammation is chronic, there is a an increased number of these (aka SBCs) when compared to acute
cardiovascular disease
the structural changes affecting any part of the body’s entire circulatory system (CVD)
two physiological descriptions of coronary artery disease
-structural changes in the arteries that supply nutrients/O2 to the heart
-chronic ischemic disease of the heart muscle tissue with a predictable pathophysiology.
the goal of circulatory system and what dysfunction causes.
-goal: deviler needed blood to keep tissues alive
-disease= decreased ablity to deliever
ischemia is the imbalance of two things:
-demand of tissue (needs change based upon activity)
-ability to supply blood through diseased circulation (continuum of ability based upon the mix of damage and needs)
most common pathology of CAD
atherosclerosis
atheroma is the ——— comprised of
-atypical inflammatory mass embedded within vessel wall/smooth muscle cells
-lipids, WBCs, blood clotting proteins, pro-inflammatory cytokines, calcium deposits, scar tissue
sclerosis =
non-functioning tissue (scar tissue)
etiology of CAD
-age = over 65
-family history
-natal sex (male before 55, females b65)
-ethnicity
Common comorbidities that cause inefficiency in CAD
-diabetes
-smoking/alcohol/substance abuse
-BMI
-sedentary lifestyle
-hypertension
-dyslipidemia
-BASICALLY ALL ABOUT WEAR AND TEAR FROM INFLAMMATION
AHA/ACC optimal lipidemia numbers (CRP, HDL, LDL, triglycerides, total cholesterol, ratio of total and HDL)
-CRP = less than 1
-HDL over 60 mg/dL
-LDL under 100 mg/dL
-trig = under 150 mg/dL
-total = under 200 mg/dL
-ratio = 4:1 or lower
Common autonomic measure of dysfunction of CAD
-inefficiency in the balance between sympathetic and para systems
-heart rate variability
-heart rate recovery
-blood pressure
CAD predicitable pathophysiology
endothelial dysfunction → chronic vascular inflammation → decreased lumen size
how does CAD cause endothetlial dysfunction
can’t: balance between blood clot/thin, balance fluid volume, vessel healing, formation of nrer circulation and vasoconstriction/dilation.
how does exercise help with CAD and endothelial dysfunction
-increasing the number and activity of endothelial cells, rebalancing the dysfunction
-increasing activity of cells and enzymes in endothelial layer that grow new blood vessels, diminishing ischemia
chronic vascular inflammation pathophysiology step by step
-dysfunctional endothelial results in the development of chronic inflammation which causes LDL irritation which is oxidized creating free radicals starting an atheroma.
-atheroma causes continued inflammatory response, where macrophage arrive to destroy LDL. LDl is neutralized but the particles remain, triggering more inflammation.
-the cycle continues til atheroma grow, which decreased lumen sie, resulting in heart muscle ischemia.
routines of —- can decrease inflammation for chronic inflammation
aerobic endurance
common factors that influence prognosis (increased severity = risk of myocardial infraction)
-type 1 or 2 atheroma
-hypertension
-length of artery that has atheroma
type 1 vs type 2 atheroma
-stable atheromas = low active inflammation
-active and complicated atheromas = immune cells trigger beginning of plaque formation = bigger size of atheroma
effects of exercise training on balanced clotting in relation to clotting factors and a more active endothelial layer
-clotting = less risk of blood clot forming accidentally
-more active layer = thicker, more proteice cap on surface of atheroma that won’t cause a clot
dose-response warnings. more severe increase in proinflammatory cytokines have been seen with exercise in certain populations. what happens when too much happens at lower volume of exercise for:
-55 and older
-children classified as obese
-type 1 diabetes
-autoimmune conditions
-55 and older = vascular diseases
-children classified as obese = resistance training
-type 1 diabetes = chronic fatigue syndrome
-autoimmune conditions =COPD
CAD prognosis
-every 1 in 4 deaths in the US
-leading cause of death
Peripheral artery disease (PAD) definition
atherosclerosis of the extremities resulting in ischemia
ischemia is the lack of
blood supply to tissue/organ
the risk of stretching of PAD
-pathophysiology of atherosclerosis (artieresies aren’t flexible because of scaring)
-instinctive action when cramping sensations occur
-main symptom of ischemia
special considerations for PAD from medical concerns. can you do upper body strength training or a 6 min walk test
-lack of blood supply can cause difference in skin quality
-upper = no, ask permission
-6 min = provider needs to be performed you are pushing to max effort
special considerations for PAD.
-warm-up should be non weight bearing, why?
-long warm up, why?
-expectations of symtoms?
-warm up = because want to challenge calves during warm up because it will be challenging during progression
-long warm up = longer for extremities to get warmer because of arteries
-expectations = diminished of symptoms in 8 weeks
what is angina pectoris
painful chest pain due to ischemia in heart muscle
cladication
extremities discomfort from ischemia
prognosis after MI. survivor’s mortality risk is calculated using
-the extent of muscle damage measured by ejection fraction
-degree of ischemia
-level of cardiorespiratory fitness
what is infraction
complete blockage of blood supply
what is the most common barrier to exercise in the MI popoulation?
PTSD + mental
exercise prescription for all CVD conditions (warm up, aerobic endurance, strength, flexiblity)
-low intensity, longer warm up and cool down
-aerobic endurance → intensity (below 120 bpm or 6 RPE), frequency (3 days a week), duration (20-60 minutes)
-strength → avoid valsalva maneuver
-flexibility → get MD ok due to vessel sclerosis
essential hypertension (HTN), what is healthy bp
-systemic and/or diastolic arterial blood pressure is elevation
-less than 130 and less than 80
stop exercise if systolic or diastolic reaches —- resting or ——- exercising and decrease intensity but exercise if ——
-200 s or 110 d
-250 s or 115 d
-180/110
with hypertension, after acture 30-45 min aerobic reduced BP may persist —- later. BP response to exercise returns to baseline without continuation of exercise program.
22 hours
special considerations of hypertension.
-watch for hypotension by…
watching body positioning, going gradual, post-exertional hypotension also a concern, AND valsalva rule
chronic obstructive pulmonary disease
irreversible disorders that decrease the ability to inflate lungs, due to mechanical, neurological, muscular dysfunction, or fibrous scarring
hyperpnea
need muscle work to exhale die to decreased elasticity
dyspnea
subjective measure of breathlessness
tachycardia and tachypnea
-cardia = increased heart rate
-pnea - more than 20 breaths per minute
COPD umbrella has unifying symptoms =
inefficiency
general etiology for umbrella of COPD
-toxins
chronic bronchitis diagnosis (all 3 have to be present)
-persistent cough that produces sputum
-at least three months
-in two consecutive years
chronic bronchitis signs
-cyanotic/pale coloring from hypoxis
-fluid retention
-wheezing
-worsens when supine
pathophysiology of chronic bronchitis
starts with oxidative stress from toxin → inflammation changes secondary/tertiary bronchi to bronchioles
emphysema
enlargement of the air spaces distal to the terminal bronchioles due to destruction of the delicate membrane walls of alveoli
emphysema signs and symtoms
-flushed, possibly thineer
-rales (crackles during breathing)
-pursed lip breathing
-barrel chest
COPD prognosis: BODE index
B: body index, <21 = rapid decline
O: airflow obstruction: scar tissue, inflammation
D: dyspnea
E: exercise capacity
asthma signs and symptoms
-chronic cough
-acute wheezing, chest tightness, coughing, after activity or irritant exposure
-seasonal changes in symptom severity
-illness tend to be extended and increased symptoms
-relief possible when medication is used
asthma irritants
-allergen triggers
-indoor irritants
effects of exercise for asthma
-improve ventilatory efficiency
-reduced hyperinflation
-desentized to dyspnea
-decreased inflammation
how to reduce risk of causing asthma attack
-decrease exposure ti triggers
-time of day (mid-morning)
-prolonged warm up and cool down
-check for illness, stress, lack of sleep
peak flow meter
objectively measures max speed of exhalation (PEF)
where does exercise induced asthma defined as a fall in PED
20% from baseline (individualized) number
modified borg dyspnea scale
correlates the measured values of PEF with the subjective perceptions of the clients breathlessness, giving them more self-awareness.
with a new client with asthma, must have a ——— program of —— aerobic endurance
-six week steady program
-60% max intensity
exercise induced asthma (EIA)
episode of asthma brought on by physical activity 10-15 minutes after initiation of exercise. symptoms start at about 75% intensity, for up to 30 minutes after exercise
describe metabolic disease
the system for processing/utilizing energy is not working properly somewhere along the line
type 1 vs type 2 diabetes
type 1 = insulin dependent diabetes
type 2 = insulin resistant diabetes
possible diabetes if numbers are above —- for blood glucose and —- for hemoglobin Alc over ——
-125 ml/dl
=6.5%
hyperglycemia vs hypOglycemia
if someone is undiagnosed what end will they be?
hyper - blood glucose is higher than it should be for optimal metabolic efficiency
hpo- lower
-undiagnosed = hyper
GLUT 1 vs GLUT 4
Glut 1: always open, not that many, only enough to surve, doesn’t adapt
Glut 4: opens with insulin, depends how many, as many as the body says to adapt to, it adapts but still needs insulin to adapt
glycation definition
accidental binding of a glucose to a lipid or protein
hbA1c defintion
concentration of hemoglobin molecules that have glycated with a glucose molecule
peripheral neuropathy - how does it happen?
-nerve becomes ischemia (from capillary damge)
-myelin sheath of free nerve endings susceptible to free radical damage)
small vessel damage creates multiple reasons why foot checks are a rule
-risk (tissue quality is different = ^ risk of tissue damage
-heal (if you get the damage, it’s harder to heal)
-feel (don’t know when damage has occured and don’t protect themselves as much)
probably should add more but
I AM DONE FOR NOW!
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