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WEEK 2 - MECHANISM OF DISEASE Pain - unpleasant sensory and emotional experience

Roles of genetics and cellular injury disease: associated with actual/potential damage
Cancer in Canada: Males - 45% ; Females - 42% Learning someone’s pain: location, severity, alleviating factors,
Proliferation - Uncontrolled cell growth and division; they are not aggravating factors, descriptive quality, duration, functional impact
specialized cells Acute pain - sudden onset, resolves with healing of underlying
- Cancer cells are the body’s own cells that are growing out of cause
control. As more abnormal cells grow and divide, they form tumors Chronic pain - persistent, >3 months, resistant to treatments
(neoplasms) w/c are growths of tissue that serve no purpose. Types of pain:
- Cancer cells ignore signals that normally tell cells to stop dividing - Nociceptive: somatic - injury to skin, ms, bones, jt, connective
or begin the process of programmed cell death (apoptosis); result tissue
of acquired gene mutations (is a permanent alteration in the visceral - internal organs/ tissues
DNA sequence that makes up a gene, such that the sequence - Neuropathic - nervous system that sustain pain even after an injury
differs from what is found in most people. heals
- Gene mutation is a change of genetic sequence in the cell. - Psychogenic - psychological disturbance
Happen when: Pain Management
1. Born with a mutated gene that is either inherited from a parent or Gate control Theory - built into normal pain pathways that can
that develops in an embryo modify the entry of pain stimuli into the spinal cord and brain;
2. Exposed to something around us that damages our genes stimulation of A-beta fibers (non-nociceptive)
3. Age Ex. deep pressure, ES, compression, traction
- Breast Cancer Gene 1 (BRCA1) - normally found in the body and Mirror therapy, desensitization, exercise (ROM, Stretching,
is considered a tumor suppressing gene. endurance)
Bacterial Infections Non-opioid analgesics - reduce production of prostaglandins
Pathogens - disease causing microbes (acetaminophen, ibuprofen) s/e: constipation, liver damage,
- bacteria : replicate at various rates; lead to bacterial infections >bleeding risk
- Virus : tend to mutate during replication; may alter host cell Opioid - work in the brain to change how the body feels &
chromosomes -> cancer; lead to viral infections responds to pain (morphine, fentanyl) s/e: drowsiness, nausea,
Main routes of Transmissions: constipation, addiction
1. Contact - direct (people-people), indirect (object), droplet WEEK 4 - DISEASES OF MSK SYSTEM
2. Vehicle - blood through contaminated items Hip Fracture - 1 in 3 women & 1 in 5 men, osteoporosis, 2 Mil
3. Airborne - droplet particles, dust canadians, 80% overall fx, 1 in 3 pt re-fracture in 1 yr, mid 30s,
Nosocomial Infections - (Hospital Acquired Infection) 28% - women, 37% - men will die
- Patient must be admitted for reasons other than the infection Occurs in: intertrochanteric, subtrochanteric, shaft, extracapsular,
- Risk factors: ICU stay, compromised immune system, elderly and intracapsular, femoral neck, subcapital, femoral head
young, hospital staff not following proper infection control Risk factors:
procedure aging - dec bone density, dec strength, flexibility, balance, vision,
Antimicrobial Resistance - resistant to infection cognition, meds
- Not necessary to use drugs to treat Falls - high risk of incidence of falls
- Increased use of antimicrobials pelvis /hip Fx- 90% of fx assoc. With falls
- New emerging disease and superbugs Mortality usually due to respiratory failure
Antibiotic Resistance - the resistant bacteria proliferate Falls:
Factors: overprescribing, incorrect prescription/dosage, not Environmental r/f: poor bldg design, slippery floors & stairs, looser
specific to bacterial infection, failure to follow dosage/reducing rugs, insufficient lighting, cracked or uneven sidewalks
treatment, antibiotics in food, antibacterial agents sprayed on socioeconomic : low income & edu level, inadequate housing, lack
fruits/veg social interaction, limited access to health & social services, lack of
Stages of Tissue Healing: community resources
1. Acute stage - inflammatory reaction ( up to 6 days) Behavioral : multiple med use, excess alcohol intake, lack of
2. Subacute - proliferation (3-21+ days) exercise, inappropriate footwear
3. Chronic - Maturation ( end of proliferation up to 1+ year) Biological : age, gender, race, chronic illness, physical, cognitive
WEEK 3 - MECHANISM OF HEALING AND RECOVERY capacities
The Immune System Open reduction internal fixation - intramedullary nail fixation,
skin - protective barrier secretes antimicrobial proteins dynamic hip screw
Thymus - small organ in upper chest where T cells mature OTA - ms activation PTA - strengthening
Bone Marrow - produces most white blood cells (leukocytes) Osteoporosis (bone porous) - dec mineral content, weak
Bloodstream - immune cells circulate, patrolling for antigens bone, no symptoms
Lymphatic system - network of vessels and tissues; includes lymph T-score bone mineral density scan, high risk for fx (wrist, hips,
nodes that filter lymph looking for antigens spine)
innate /Natural Immunity: built-in present at birth; non-specific & Osteopenia - low bone density
nonadaptive Primary - not related to other med condition
Phagocytes - go into tissues in w/c infection has developed and r/f: age, postmenopausal, caucasian, fam hx, sedentary, low in
consume any foreign substances/ pathogens; digest the calcium & vit D
pathogens, antigenic material appears on their surface to identify Degenerative Disc Disease & Spinal Stenosis
them as foreign invaders. End plate - flattened appearance,allows the disc to migrate in to
T-cells - type of lymphocyte the vertebral body
Macrophages - type of phagocytes Annulus Fibrosus - resists rotation, develops clefts or fissures w/c
Antigens - foreign substances on the surfaces of pathogens and allows the nucles to migrate outward, less able to withstand load
other foreign substances Nucleus polposus - dehydrates & thins, becomes more fibrous and
acquired /Adaptive Immunity: specific and adaptive (has stiff, less able to withstand load
memory) Neural foramen - narrowing due to flattening of discs and boney
B- cell - secretes antibodies that directly destroys the antigen overgrowth
Antibodies - proteins that recognize and bind to antigens and Central canal - narrowing due to intrusion of the disc or other
destroy them. spinal structures.
Active: naturally from environmental exposure or artificially by Spinal stenosis: (1) central canal stenosis - narrowing of space
vaccination around spinal cord; put pressure on spinal cord. (2) foramen
Passive: transfer of antigen (mother to baby, medication) stenosis - narrowing of the foramen; pressure on the nerve roots.
Both result in back & leg pain, numbness, weakness in legs.
Herniated Discs. (1) Herniation - nucleus polpusus extends Week 9 - Respiratory Disease
through the outer rings of the annulus fibrosis (2) Bulge - Nucleus COPD - lung d/o charac by long-term airway obstruction, making it
buges difficult to breathe
Most common forms: Emphysema & Chronic Bronchitis
CB - a chronic productive cough for 3 mos in each of two
successive yrs in whom other causes of chronic cough have been
excluded. // charac by obstructed airway d/t inflammation of the
bronchi & excessive mucus production// Pathophysio: lining of
bronchial tubes is constantly irritated and inflamed, causing a long
term cough with excessive mucus
Emphysema - abn & permanent enlargement of the airspaces
(alveoli) distal to terminal bronchioles that is accompanied by
destruction of the airspace walls w/out obvious fibrosis// elastin
gets destroyed which affects the recoil of alveoli (elastin makes
walls of alveoli snap - recoil)
COPD
Cardinal signs: Dyspnea, chronic cough, mucus production
Ssx: wheezing, cachexia, pursed lip breathing, accessory ms use,
tripod position
Modified borg scale://RF: smoking, smoke from factory,
genetics//Single best variable for airflow obstruction - hx of >40
pack yrs of smoking//MM: bronchodilators (short&long acting- relax
ms in airways, clear mucus),anti inflamm(steroids)-reduce
inflamm,vaccination(reduce risk of flu and pneumonia)// PTA mgt:
pursed lipped, diaphragmatic, rollator walke//OTAmgt: energy
conservation, pacing strat, use of AD

Week 11 - Respiratory system


Virus - infective agent that cannot reproduce by itself
Week 8 - Autoimmune diseases Common cold, influenza, COVID-19: RNA virus
Rheumatoid Arthritis - A systematic, inflammatory, autoimmune, Common cold: rhinovirus, respiratory synctial virus, coronavirus;
disease that results in pain, swelling, stiffness and loss of function infect nose & throat
in the joints (attacks frequently wrist, hands, elbows, knees, and Influenza: caused by influenza A&B virus(MC);infect
ankles) nose,throat&lungs
Risk factors: F, 40-60 yo, Genetics, Pathogens, Smoker COVID-19:novel 2019 coronavirus,called severe acute respiratory
Hallmark Characteristics of RA:Inflammation, Cartilage destruction, syndrome coronavirus 2, or SARS-CoV-2, affect
Bone erosion nose,throat,lungs,organs,tissues
Pathophysiology All 3 result in nasal congestion, sore throat,cough (nose&throat
Inflammation results from abn activation of WBC (T & B cells) affected)
which release cytokines (cell signaling molecules that aid cell to Influenza&COVID-19: systemic ssx: fever,body aches,fatigue//can
cell communication). Cytokines cause synovial cells to release be mild,severe,fatal: lung injury is common in COVID-19
destructive substances and synovial membrane to grow new blood Prognosis: recover few days to <2weeks. Some develop
vessels (angiogenesis). New blood vessels & inflammatory cells pneumonia, lung infections can be life threatening and result in
facilitates growth of pannus (thickened synovium) -> invades & death. RF:old age, compromised immune sys, multiple comorbidit
destroys areas of cartilage and bone. Increased chondrocyte (main Transmission: contact of infected surfaces & droplets in air
cellular component of cartilage) activity -> further cartilage COVID-19: also spread through airborne
destruction & inc. osteoclast activity -> contributes to bone erosion. Transmission is less likely D & A when >6ft from source
Ssx: Hallmark characteristics leads to jt swelling, damage, Stopping: PPE,handwashing,>6ft/2m,meds
deformity and ankyloses in some cases which contributes to pain Pneumonia: infection in one or both lungs (specifically alveoli) that
and motion loss develops in response to a pathogen (bacteria, virus, fungi)
Other ssx: Tenosynovitis, peripheral neuropathy, periarticular Types:
osteoporosis, fatigue, occasional fevers, loss of energy, sjogren’s Bacterial: caused by streptococcus (MC), staphylococcus, bacteria
syndrome, rheumatoid nodules, pericarditis, pleuritis already present in the body or enters body, tx: antibiotics
MM: NSAIDS - inhibit enzymes that are active in the inflammatory Viral: caused by virus (eg influenza A, respiratory syncytial virus
process, Corticosteroids - immunosuppresive and inflammatory (RSV), SARS-CoV-2, resolves on its own but some may take
effects antivirals, may be complicated by bacterial pneumonia
DMARDS: suppress overactive immune system Types:
Biologics: Target cytokines Community-acquired: MC type, caused by bacteria or develops
Jt replacement, tendon reconstruction, arthrodesis (fusion), after cold/flu
synovectomy Nosocomial (hospital-acquired): acquired in hospitals or other hc
Rehab Mgt: jt protection techniques and devices, ROM, stretching, facilities within a specific timeframe, higher risk: on ventilator &
strengthening, ms endurance ex. after surgery
Fibromyalgia - a chronic syndrome of unknown cause charac. By Aspiration pneumonia: after inhaling particles into lungs; higher
widespread pain and other symptoms risk: swallowing issues or vomiting
Ssx: ms and jt pain (radiating & diffuse), Opportunistic pneumonia: affects people with weak immune sys
Tender points, poor sleep, chronic fatigue, fibro fog (impairment in (HIV,COPD,organ transplant)
memory & thinking) Ssx & Why
Pathophysio: research suggests FB is a d/o of abn central Dyspnea - decreased gas exchange
processing of nociceptive pain input Chest pain- inflammation of the alveoli
Chronic pain: activation of glial cells -> neuroinflammation, cellular Cough- reflex mechanism to rid of body secretions
destruction, inc activation of SNS & hypothalamic-pituitary complex Fever- inc temp to decrease viral replication
How diagnosed? Specific score range on widespread pain index X-ray findings:
and symptom severity, symptoms present at a similar level atleast Consolidation- area of inc opacity (whiteness) indicating lung is
for 3 mos, exclusion of other d/o that may be source of pain. filled w/ dense material (pus in pneumonia) or other fluid
Tx:medication, cognitive&behavioral therapy, exercise (blood/cell
Pleural effusion-a collection of fluid in the pleural space, reducing Sinuses - Rhinosinusitis
ability to expand lungs Pancreas - Diabetes
- Indicator of an underlying dse (heart failure, Skin - Salty sweat
malignancy, pulmonary embolism,pneumonia) Reproductive organs - male infertility
- Tx: tx of underlying condition or surgery Small intestine - malnutrition
Pneumonia tx: Large intestine - intestinal impaction & obstruction (abdomen pain,
Percussion: alternately clapping with both hands on pt’s chest wall distention, nausea)
with a cup hand Lung - Pneumonia, Hemoptysis
Vibration: shaking motion with a flat hand firmly against the pt’s Ms weakness, high risk for osteoporosis
chest wall Meds: Mucolytic (pulmozyne), antibiotics, bronchodilators,
Acute Respiratory Distress Syndrome (ARDS) hydrators, CFTR modulators (correct defective protein CFTR)
Acute, diffuse, inflammatory lung injury charac by pulmonary Airway/mucus clearance: Postural drainage (use gravity
edema (fluid build up in alveoli), inflammatory molecules cause the dependent position to drain mucus from lungs), Percussion
capillaries to leak fluid which goes into the alveoli, making it (tapping in certain areas in diff positions), vibration
difficult for gas exchange, caused by trauma/damage to the alveoli Pulmonary fibrosis: an interstitial lung dse in which lung
by factors such as: sepsis, smoke inhalation, near drowning tissue becomes scarred, over time thickens and becomes
Hallmark: hypoxemia (low oxygen), bilat. Radiographic opacities, widespread
diffuse alveolar damage Pathophysiology: repeated injury to alveoli -> stimulates
What happens: Fluid filled alveoli results in: inflammatory response ->normal healing becomes uncontrolled &
Hypoxemia unregulated -> fibrotic tissue is formed
Inc lung stiffness- difficult for lungs to inflate Ssx: gradual onset
Inc work of breathing - difficult to get air into lungs SOB during or after physical activity
Can’t carry work of breathing & low oxygen -> respiratory failure Spasmodic, dry cough
Ssx of Pulmonary edema in ARDS: Gradual, unintended weight loss
● Coughing up blood or bloody froth Fatigue and weakness
● Diff breathing when lying down (orthopnea) Chest discomfort
● Feeling of “air hunger” or “drowning” (paroxysmal Clubbing d/t buildup of tissue
nocturnal dyspnea) that often causes client to wake up Prognosis: progressive, survival rate: 3-5 yrs after diagnosis
and try to catch breath MM: lifestyle changes, RF management, supplemental O2,
● Grunting, gurgling, or wheezing sounds with breathing medications (anti-fibrotics,steroids), vaccinations
● Problems speaking in full sentences because of SOB Lung transplantation: surgical procedure in which lungs are
Some pts will develop a pneumothorax replaced w/ healthy lungs from a donor
Pneumothorax: presence of air/gas in the pleural cavity causing PF- leading indication for lung transplant
collapse of the lung, commonly result of a tear on the surface of Risk of LT: Organ rejection, infections, airway problems, disease
the lung or existing dse. Pulmonary Rehabilitation: an exercise & educational program
Tx: Chest tubes: designed for people with lung dse goal of improving symptoms,
● Drains fluid and air from pleural space and helps re- restoring fxn and QOL.
expand the lung Asthma: chronic inflammatory d/o of the airways that is charac. By
● Avoid tube kinks, pinching beneath patient or b/w bed bronchial hyperresponsiveness and variable airflow obstruction.
rails Types:
● Collection chamber must always be kept below chest Allergic: young age of onset, respond better to tx
level for proper drainage Nonallergic: adult onset,assoc w/other comorb,less responsiveto tx
● Watch for bubbling in the tube (leak) Ssx: recurrent episodes of chest tightness, wheezing, coughing,
Tx: dyspnea (night or morning)
Diuretics - inc urination to get rid of fluid Meds:
Mechanical ventilation - pushes air into lungs and forces some of Long term (corticosteroids/LABAs) - taken regularly to control
the fluid out of the alveoli chronic symptoms and prevent asthma attcks, reduce inflammation
Antibiotics- treats underlying infection Quick relief (Short acting beta agonists) - taken as needed for
OTAPTA tx for critically ill: ROM, ambulation, pedal ergometer, rapid,short term relief of symptoms - used to prevent or treat an
deep breathing asthma attack, relax bronchial tubes (dilate)
Prognosis for ARDS:
30-50% will die from resp failure, underlying med problems Week 13 - Integumentary system
(pneumonia, kidney failure) or complications (sepsis, multiorgan Cellulitis - serious bacterial infection (streptococcus &
failure, blood clots) staphylococcus) enter through a crack/break in the skin, common
Prolonged hospital stay in lower legs//ssx: red area that tends to expand, swelling,
Prolonged recovery w/ inc morbidity tenderness, pain, warmth, fever, blisters, skin dimpling//RF: skin
People who survive - memory loss or QOL problems d/t brain not injury (cut/burn), skin cond. (eczema,shingles), chronic swelling of
getting enough O2 arms&legs that causes skin to crack, IV drug use, weak immune
s.// MM: antibiotics, wash wound daily w/ soap&water, protective
Week 12 - Respiratory cream&ointment, protect wound w/ bandage, monitor signs of
Cystic Fibrosis - an inherited, incurable, chronic dse charac by worsening infection
buildup of thin, sticky mucus that can damage many of the body’s Burns- permanent destruction of tissue cause by released of
organs//MC fatal genetic dse among canadian children&adults energy from an external agent//thermal injuries caused by:
Etiology: mutation in the cystic fibrosis transmembrane flames,steam,hot liquids,hot
conductance regulator (CFTR) gene results in CF. metals,electricity,radiation,toxicchemicals,extereme cold
CFTR gene- provides instructions for making a protein called Extent of burns = %TBSA
CFTR, protein fxn as channel across the membrane of cells that Burn depth: superficial (E), partial thickness (E&D), full thickness
produce mucus, sweat, saliva, tears and digestive enzymes, (E,D,all underlying structures)
transports chloride ions into and out of the cell Burn rehab: compression sleeves(reduce edema and manage scar
Chloride- helps control movt of water which is necessary for tissue formation), splints (red. Contracture formation), use of AD to
production of thin, freely flowing mucus improve fxn, PROM (early phase), self stretching, ms endurance,
Pathophysio: mutation-> chloride ions cannot move freely -> organ strengthening ex.
produce mucus that is thick and sticky -> obstructs airways and Surgical wounds - Surgical sites
glands Hydrocholloid technology - comfort & flexility
Ssx:
Hydrofiber tech- micro contours to wound bed, eliminating voids
where bacteria grow, locks in wound exudate and removes it from
wound bed
Ionic silver infusion - sustained antimicrobial activity for 7 days
Polyurethane film - waterproof barrier that helps viral and bacterial
infection
Ssx:
Care: handwashing, dont scrub/rub infection, dont remove tape
strips or dressing unless instructed to, avoid use of lotions or
power on unhealed incisions, avoid prolonged exposure to
sunlight, prevent incision from getting wet
Normal ssx: soreness,tenderness, redness, warmth,tingli
ng/numbness,mild oozing, numbness
Other types: avulsion (sharp pointy object),abrasion(skin partially
or completely torn away),puncture(superficial scraping or wearing
away), laceration(tearing or cutting of tissue)//Woundhealing:
Hemostatis: body’s reaction to injury to stop bleeding,
Inflammation: WBC protect body from pathogens,
Proliferation:fibroblast form new collagen in 2-3days, angiogenesis
(blood vessels start to regrow)
Remodeling: granulation tissue matures into scar and tissue
strength is inc.

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