OT412 Rehab Medicine

What caused the disease

Events that occur in a disease (development of it)

What you see in someone with a certain disease

Signs: objective, measurable parts of a disease

Symptoms: what the patient complains about (subjective)

outcome/sequence of a disease

Secondarily arises as a result of the disease

inherited from chromosomes/genes

Ex: Huntington's Disease, Krabbe, Tai Sachs

• present @ birth
• -not all congenital diseases are inherited
• -not all inherited diseases are congenital

Ex: Down syndrome, FAS, spina bifida

ingestion of poison

Ex: salmonilla, carbon monoxide poisoning

invasion by a pathogen

Ex: Encephalitis, flu, mono

caused by physical injury/trauma

Ex: TBI, car accident, burn, concussion

degeneration of a part of the body

Ex: dementia, muscular dystrophy, multiple sclerosis, arthritis

3 types:

• 1. hypersensitivity (allergy): latex, drug, food, indoor, seasonal
• 2. autoimmunity: rheumatoid arthritis, lupus, celiac disease
• 3. immunodeficiency: AIDS

cancer

Ex: Melanoma

deficiency of proteins, calories, vitamins, minerals

Ex: anorexia, anemia, rickets, obesity, scurvy

disturbance in some metabolic process

Ex: hypothyroidism, diabetes, Cushing's disease

a defect in a single molecule

Ex: sickle cell anemia

originating in the brain

Ex: schizophrenia, depression, ADHD

produced inadvertantly by medical treatment

Ex: staph infection, depression

cause is unknown

Ex: schizophrenia, autism, SIDS

concentrations that fall between the minimum theraputic concentration and toxic concentrations

Food, Drug and Cosmetic Act (FDCA): regulates quality, purity, potency, effectiveness, safety, labeling and packaging of food, drug and cosmetic products

responsible for enforcing FDCA

• Phase I: animal studies
• Phase II: small number of healthy volunteers
• Phase III: small number of people with the disease
• Phase IV: large number of people with the disease in controlled studies

Drug Enforcement Agency: concerned with drugs that have the potential of being abused and of causing physical and psychological dependence

Drugs that have the potential of being abused and of causing physical and psychological dependence

• I: high potential for abuse with no recognized medical use (LSD, heroin, marijuana, psilocybin)
• II: high potential for abuse and addiction; some recognized medical use (cocaine, Ritalin, Demerol, opium, Morphine, amphetamines)

movement of drugs through the body

getting the drug into the systemic circulation to the target tissue

Drugs given orally (PO): 'first pass effect' - some of the drug is metabolized before entering circulation (reduced bioavailability due to acid in the GI tract)

enteral: oral (PO), sublingual (SL), buccal, rectal

parenteral: intravenous (IV), subcutaneous (SQ, SC) injection, intramuscular (IM) injection, intrathecal injection, inhalation, transdermal

some of the drug is metabolized before entering circulation

location: the liver is primarily responsible for metabolizing drugs

general steps: 2 step process- enzymes inactivate and enzymes transform to water soluble form

• cause of drug interactions: some drugs stimulate the production of enzymes and some drugs inhibit metabolic enzymes
• - e.g. phenobarbitol stimulates enzymes with warfarin (take more warfarin)
• - e.g. cimetidine inhibits enzymes with theophylline (take less theophylline)

volume fo blood (cc) cleared of drug / minute

time it takes for drug concentration to be reduced bt 1/2

how the drug acts in the body at the cellular and physiological levels (mechanism of action)

agonists (morphine): has the same effect as endrogenous (our own) substances

antagonists (naloxne): binds to receptors but has no effect (good antidote)

potency: how much of a drug is needed to produce a theraputic effect

theraputic efficacy: at the optimal dose, how well does the drug work

side effects: predictable from pharmacology; occur at theraputic doses ('context dependent')

idiosyncratic reaction: anaphyllaxis

tolerance & dependence: resistance over time and withdrawl

persistent elevation of systolic and/or diastolic blood pressure

normal: systolic = <120 and diastolic = <80

prehypertensive: systolic = 120-139 or diastolic = 80-89

stage I hypertension: systolic = 140-159 or diastolic = 90-99

stage II hypertension: systolic = >(or equal) 160 or diastolic >(or equal) 11

BP = CO(->HR) x TPR(->SV) --> (P=QxR)

• BP= blood pressure
• CO= cardiac output
• TPR= total peripheral resistance
• HR= heart rate
• SV= stroke volume

heart rate and stroke volume

Increased sympathetic cardiac nn. --> decreased activity of parasympathetic nn. --> increased heart rate and contractility --> higher cardiac output --> increased blood pressure

Increased activity of parasympathetic n (vagus n.) --> decreased activity of sympathetic nn. --> reduction of heart rate --> lower cardiac output --> lower blookd pressure

It raises blood pressure if it should fall (like when we stand up)

It converts angiotensin I into angiotensin II to raise blood pressure

25% of American adults are hypertensive (twice as prevalent in African Americans than any other race)

Only 18% of people are at target blood pressure levels with their medical management

• Cigarette smoking/second hand smoke
• Diabetes
• Family history of hypertension
• Being obese/overweight
• Sedentary lifestyle
• Men over the age of 45
• Elevated cholesterol levels
• Frequently consuming alcoholic beverages
• Being African American

• 1. ACEI - angiotensin-converting enzyme inhibitor
• 2. ARB - angiotensin receptor blocker
• 3. BB - beta-blocker
• 4. CCB - calcium channel blocker

• Weight reduction
• Adopt DASH eating plan
• Dietary sodium reduction
• Physical activity
• Moderation of alcohol consumption

endothelial damage (atherosclerosis, stroke)

cardiac damage (cardiomyopathy, heart failure)

renal damage (renal failure)

increased urinary calcium excretion (osteoporosis)

• hypertension
• obesity
• dyslipidemia
• diabetes mellitus
• cigarette smoking
• physical inactivity
• microalbuminuria
• age (>55 for men, >65 for women)
• family history of premature CAD (men <55, women <65)

• Lowers HDL and raises LDL
• Increases blood pressure and heart rate
• Nicotine and carbon monoxide damage endothelium and increases liklihood of clots
• Damage to the endothelium triggers atherosclerosis

• Causes direct trauma to the endothelium
• Inflammation promotes clot formation

• High blood lvls of LDL result in an increase in lipoproteins sticking to the damaged endothelium
• They bind to the artery wall and are internalized
• Attract macrophages - causing foam cell formation
• Formation of plaque occurs

• LDL: <100
• HDL: <40
• Total: <200

hyperglycemia causes an increase in LDL cholesterol

• Raises HDL cholesterol
• Lowers LDL cholesterol
• Lowers blood pressure
• Lowers heart rate
• Prevents osteoporosis

• lack of oxygen to myocardium
• tight or crushing sensation in chest
• nausea, vomitting, diaphoresis (sweat), dyspnea, fatigue, pallor, syncope
• often relieved with rest
• can be constant
• does not change with breathing

Screening for abnormalities in EKG that result from ischemia

Detects plaque and blood flow to the heart

• Balloon: surgical procedure to dilate a narrowed vessel and improve circulation where a balloon is inserted and inflated in a vessel
• Stent: a metal or wire mesh "scaffolding" is inserted to maintain vessel opening; reduces risk of restenosis
• Drug-Eluding Stent: a stent that slowly releases a drug to prevent tissue regrowth ad restenosis

Stent

• W/stent: 17% restenosis after 1 year
• W/o stent: 35% restenosis after 6 months

• Due to atheroscleroticplaques
• As oxygen demand of heart increases with exertion, ischemic pain results

• stable: Repeating pattern, predictable
• Lasts 5 – 15 minutes
• Provoked by exertion, relieved by rest
• Unchanged over several weeks
• Appears gradually
• Increased risk for MI
• unstable: Variable intensity and frequency
• Presents as a severe episode of pain
• Stable angina can progress to unstable
• Angina at rest

• Acute Coronary Syndrome:
• any group of clinical symptoms compatible with acute myocardial ischemia:
• angina
• shortness of breath
• diaphoresis
• nausea
• lightheadedness

• Myocardial Infarction:
• Ischemia with myocardial damage

• zone of infarction: tissue necrosis
• zone of hypoxic injury: tissue may or may not survive
• zone of ischemia: reversible tissue damage

• Transient ST segment elevations
• Dynamic T wave changes
• ST segment depressions
• Q waves

• STEMI: Complete obstruction of a coronary artery
• Damage includes full thickness of the myocardium

• Non-STEMI: Incomplete obstruction of a coronary artery
• Damage does not involve full thickness of the myocardium

• 6-24 hrs: Inflammatory response; intracellularrelease; tissue necrosis; no healing
• 2-4 days: Tissue necrosis; recovery starts
• 4-10 days: Debris cleared; collagen matrix laiddown
• 10-14 days: Weak scar; revascularizationbeginning; area vulnerable to stress
• 6 weeks: Scarring complete

• Troponin I Peaks at 12 hrs
• CK-MB Peaks at 18 - 24 hrs (Creatine Kinase)

• ASA (decreases platelet aggregation)
• beta-blockers (decrease preload and afterload)
• IV started
• Supplemental oxygen provided
• Appropriate labs including lipids
• Pain control
• REPERFUSION STRATEGY: PTCI or Thrombolytics

• associated with:
• decreased stroke
• decreased reinfarction
• increased infarcted artery patency
• increased short term/long term survival

"clot buster"

Healthy blood vessels are used to create a detouraround a blocked coronary artery

• Procedure:
• 4-6 hour surgery under general anesthesia
• Median sternotomy
• Heart stabilized (on-pump/off-pump)
• Graft harvested, sutured distal to the occlusion
• Sternum wired shut
• Tissues stitched/stapled/glued

Can be on right or left side of chest

Also can be combined with automatic interna lcardiac defibrillator(AICD)

PTCI: more effective if symptom onset is >3 hours

thrombolytics: more effective if symptom onset is less than 2 hours

A clinical syndrome resulting from a cardiac disease which compromises ventricular systolic or diastolic function o rboth

Results when the heart is unable to generate a cardiac output sufficient to meet the demands of the body.

A clinical syndrome caused by heart disease, characterized by breathlessness and abnormal sodium and water retention, and resulting in edema

Ejection fraction: Amount of blood that is pumped out of the ventricle with each myocardial contraction

Normal EF is ~55% -65%

• 1. hypertension
• 2. coronary artery disease
• 3. MI
• 4. cardiomyopathy

• Systolic heart failure: Left ventricle ejects <40% of its contents per beat
• Diastolic heart failure: Left ventricle does not relax properly and therefore fills under pressure
• Cardiothoracic ratio: >0.50

• Heart failure: People with heart failure may feel excessively short of breath when doing things that are normally easy, such as climbing stairs. As heart failure gets worse, a person becomes completely disabled, unable to walk or even to move around the house.
• CHF: One of the first signs of heart failure is sudden weight gain due to the accumulation of fluid in the feet, ankles, and legs.
• May have jugular vein distension and/or ankle and foot edema
• Fluids may accumulate in the lungs and abdomen causing shortness of breath. If this happens at night the patient may wake up with a choking feeling.
• People suffering from heart failure usually have difficulty lying flat in bed. They need to sleep with their head raised on pillows.(orthopnea)
• As fluid accumulates in the lungs, patients with CHF typically develop a persisten tcough that may include mucus or blood.
• As fluid continues to accumulate in the lungs, the chances of having a heart attack also increase due to ischemia

• Non-compliance with care
• Myocardial ischemia
• Myocardial Infarction
• Brady- or tachy- arrhythmias
• COPD exacerbation
• Anemia
• Hyperthyroidism

• 1. Assess LV systolic function
• 2. ACE-I or ARB therapy if LVEF <40%
• 3.Anticoagulant for HF and atrial fibrillation
• 4. Discharge instructions provided
• 5. Smoking cessation information provided

• Stenosis: Calcification of heart valve. Increases preload
• Regurgitation: Valve is not closing properly (leaky)

• 3 types:
• 1. porcine valve
• 2. Mechanical Valve Replacement –Ball and Cage
• 3. Mechanical Valve Replacement –St Jude Valve

• Long term care:
• Must be on anticoagulants for the rest of their life if they have a mechanical valve– 3 months for tissue valves Must be aware of risk for bacterialendocarditis - Take antibiotics prophylactically

• Collection of chronic diseases that affect movement of air into and out of the lungs, particularly
• within the small airways.
• Conditions that cause irreversible damage to the lungs and affect the ability to function independently

• 1. emphysema
• 2. bronchitis
• 3. asthma

• 1. mucous
• 2. constriction
• 3. surrounding tissue destroyed-can't hold airway open

Clinical: Pathological accumulation of air in tissue, particularly in the lungs

Anatomical: Characterized by enlargement of the airspaces distal to the terminal bronchiole, with destruction of their walls

• Lung shape/volume: larger volume
• Diapragm: flat

• 1. Excessive cough
• 2.Dyspnea during exercise and then rest
• 3.Wheezing
• 4.Hyperinflation
• 5.Accessory use of muscles (inspiration)
• 6.Fatigue
• 7.Anorexia

loss of alveolar walls, increase alveolar diameter and decrease gas exchange surface area

• Genetic abnormality (dec. in alpha1-antitrypsin) or Excessive amount of enzymes released that destroy elastin (proteases, elastase) -->
• Loss of elasticity causes narrowing or collapse of the bronchioles. Increased ventilatory dead space, hyperinflation (pink puffer) -->
• Reduced capillaries -->
• Altered ventilation perfusion matching (VA/Q), hypoxic, hypercapnic -->
• Increased risk for infection and edema (R sided heart failure)

Any patient who has persistent cough with sputum production for at least 3 months per year for 2 consecutive years.

• •Excessive cough
• •Expectoration
• •Wheezing
• •SOB, especially on exercise

• •Chronic exposure to irritants (i.e. air pollution), SMOKING, dust
• •Prolonged irritation, inflammation of bronchial lining

• Hypersecretion and hypertrophy of mucous-secreting glands in bronchi
• Mucosa is inflamed and swollen
• Swollen glands obstruct airways and alveoli
• Loss of ciliary function reduces mucus clearance
• Chronic inflammation
• Low oxygen
• Dyspnea
• Pulmonary hypertension
• Dyspnea and fatigue

negative

Periods of reversible obstructive disease that are caused by hypersensitivity of the airways to various stimuli resulting in airway constriction

• Extrinsic: (allergic)
• - Inhaled allergens, ex. hay fever, pet dander, dust
• - More common in children

• Intrinsic: (non-allergic)
• - Infections, cold, exercise, stress, meds
• - More common in adults

• •Smooth muscle contracts causing bronchoconstriction
• •Hypertrophy of mucous glands
• •Edema of the bronchiole wall
• •Infiltration of inflammatory mediators and extensive activation of the immune system
• •Thick, slow moving mucus plugs block alveoli
• •Chronic asthma – fibrosis of alveoli

• Hyper-reactivity of airway in response to smoke, cold air, exercise, irritants
• Medical history
• Abnormal PFTs - acutely
• Exposing patient to increased inhaled concentrations of methacholine

• Therapy:
• Control inflammation
• Reverse bronchoconstriction
• Avoid triggers
• Treat underlying allergy

• Drugs:
• 1.Beta two Agonists
• 2.Corticosteroids

See notes/graph

Chronic progressive disorder that affects the body’s digestive and respiratory systems

Cause: Defect in CF gene

• Diagnostic factors:
• •Family history
• •Poor digestion, abdominal distention
• •Failure to meet growth milestones
• •Recurrent pulmonary infection
• •Chronic cough
• •Sweat test (pos)
• •Chronic infection/Inflammation
• •X-ray
• •Abnormal pulmonary function tests

Lungs: Impaired mucociliary transport --> Increased secretions, Mucus plugs=air trapping, Bacterial growth=infections --> Permanent structural damage --> Respiratory failure or Cor Pulmonale

Digestive tract: Small intestine blocked --> Mucus plugs exocrine glands in the pancreas and reduces digestive enzymes --> Malabsorption/malnutrition --> Liver damage

Affects all systems of the body

• Abnormally thick,
• sticky mucus, which clogs the lungs and leads to recurring lung and sinus infections as well as difficulty breathing. Reduced oxygen in the blood also leads to a characteristic rounding and enlargement of the nail bed in the fingers and toes, called clubbing. Those with the disease may also develop a barrel-shaped chest as a result of their increased work to breathe. Repeated infections often lead to fleshy growths inside the nose, called nasal polyps.

The thick mucus also obstructs the ducts of the pancreas, preventing digestive enzymes from reaching the intestines. So those with CF do not absorb nutrients from their food well, and they eliminate nondigested food through the bowel, resulting in very large, smelly stools. Because so little food is absorbed, children with CF have difficulty gaining and maintaining weight, despite a healthy appetite and diet.

CF also affects the reproductive systems of both males and females. Although females with CF have normal fallopian tubes and ovaries, their thick cervical secretions may block sperm entry and prevent them from getting pregnant. Males with CF are almost always sterile because they produce relatively few or no sperm. Abnormally thick secretions may block the ducts that carry sperm, or the ducts may not develop properly.

positive (air trapping)

A major category of lung disease including any condition that limits lung expansion

Physiologically defined by reduced total lung capacity, vital capacity, functional residual capacity with preserved airflow

• 1.Reduction in lung volume
• 2.Excessive/increased elastic recoil
• 3.Arterial hypoxemia from VA/Q abnormalities
• 4.Impaired diffusion = exercise-induced desaturation
• 5.Excessive reflexive stimulation = hyperventilation

• Lung Parenchyma:
• •Diffuse Interstitial Pulmonary Fibrosis
• •Sarcoidosis
• •Collagen diseases

• Disease of chest wall:
• • Scoliosis
• • Ankylosing Spondylitis
• • Broken ribs

• Diseases of Pleura:
• •Pneumothorax (i.e. air)
• •Pleural effusion (i.e. fluid)
• •Pleural thickening

• Neuromuscular disease:
• • Poliomyelitis, Guillain-Barre, ALS, Myasthenia gravis, Multiple Sclerosis, Muscular Dystrophy

• •Thickening of the alveolar wall
• •Alveolar destroyed and scarring
• •Alteration in lung parenchyma
• •Decrease in lung compliance
• •Lung volumes are decreased

• •Inflammation
• •Early - Infiltration with lymphocytes
• •Later – Fibroblasts lay down collagen
• •Irregular pattern gives honeycomb effect

• •Etiology unknown – inflammation?
• •Uncommon – late middle age
• •Diagnosis – suggested by history – biopsy
• •Dyspnea during exercise and rest (later stage)
• •Nonproductive cough
• •Finger clubbing, crackles
• •Treatment – corticosteroids, anti-fibrotics
• Progression insidious, can be terminal in 4-6 years

• Starts as tiny, grain-like lumps called granulomas, which most often appear in your lungs or lymph nodes. They can
• clump together and form larger lumps that attack other organs. Sarcoidosis often affects your skin, eyes or liver

Lungs: Cough, SOB, Chest pressure/pain

Eyes: Dryness, blurred vision/floaters, pain

Lymph: Enlarged

• Joints: Painful/swollen, Stiff
• General: Fatigue/weakness, Night sweats, Low grade fever, Weight loss, Trouble sleeping, “Something just isn’t right”, Tender reddish bumps or patches on skin, Enlarged liver, Kidney stones, Arrhythmias, pericarditis, heart failure, Nasal stiffness and hoarse voice

• •Medical history
• •X-ray
• •CT scan
• •PFT’s
• •Bronchoscopy with biopsy to remove granulomas and rule out infection
• •Blood
• •Biopsy of bumps around body and organs

• Inflammatory disease
• Insidious

"allergic" reaction to inhalent

• Acute:
• •Influenza-like syndrome
• •Resp. distress/dyspnea/dry cough/fever chills/myalgias 4-48 hrs. post exposure
• •Rapid resolution after exposure ends

• Chronic:
• •Insidious onset exertional dyspnea
• •Fatigue
• •Cough, dyspnea, sputum, wt. loss,
• •Few initial sx.
• •Interspersed with acute exacerbation possible
• •Progress to fibrosis

• 1.Lung volumes
• –spirometry
• –body plethysmograph
• 2.Exp. and Insp. flow rates
• 3.Airway resistance
• 4.Flow-volume curves
• 5.Arterial blood gases and pH

• •Evaluate impairment of function
• –severity
• –type
• –demonstrate unsuspected disease
• •Evaluate effectiveness of treatment
• •Follow-up and prognosis
• •Pre-surgery evaluation
• •Research and drug testing
• •Education

• •Make a specific clinical diagnosis
• •Make specific bacteriological diagnosis
• •Make specific regional diagnosis except with specialized equipment

increased TLC, increased RV (always forcefully exhaling), increased time to expire, decreased vital capacity, FEV% decreased

decreased TLC, decreased residual volume (so much elastic recoil), forced expiratory volume could be normal, FEV% could be normal