OT412 Rehab Medicine

  1. etiology
    What caused the disease
  2. pathogenesis
    Events that occur in a disease (development of it)
  3. manifestations
    What you see in someone with a certain disease
  4. signs and symptoms
    Signs: objective, measurable parts of a disease

    Symptoms: what the patient complains about (subjective)
  5. sequelae
    outcome/sequence of a disease
  6. complication
    Secondarily arises as a result of the disease
  7. familial disease
    inherited from chromosomes/genes

    Ex: Huntington's Disease, Krabbe, Tai Sachs
  8. congenital disease
    • present @ birth
    • -not all congenital diseases are inherited
    • -not all inherited diseases are congenital

    Ex: Down syndrome, FAS, spina bifida
  9. toxic disease
    ingestion of poison

    Ex: salmonilla, carbon monoxide poisoning
  10. Infectious disease
    invasion by a pathogen

    Ex: Encephalitis, flu, mono
  11. traumatic disease
    caused by physical injury/trauma

    Ex: TBI, car accident, burn, concussion
  12. degenerative disease
    degeneration of a part of the body

    Ex: dementia, muscular dystrophy, multiple sclerosis, arthritis
  13. immunologic disease
    3 types:

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

    Ex: Melanoma
  15. nutritional disease
    deficiency of proteins, calories, vitamins, minerals

    Ex: anorexia, anemia, rickets, obesity, scurvy
  16. metobolic disease
    disturbance in some metabolic process

    Ex: hypothyroidism, diabetes, Cushing's disease
  17. molecular disease
    a defect in a single molecule

    Ex: sickle cell anemia
  18. psychiatric disease
    originating in the brain

    Ex: schizophrenia, depression, ADHD
  19. iatrogenic disease
    produced inadvertantly by medical treatment

    Ex: staph infection, depression
  20. idiopathic disease
    cause is unknown

    Ex: schizophrenia, autism, SIDS
  21. theraputic window
    concentrations that fall between the minimum theraputic concentration and toxic concentrations
  22. What is the major law related to drug safety and market standards?
    Food, Drug and Cosmetic Act (FDCA): regulates quality, purity, potency, effectiveness, safety, labeling and packaging of food, drug and cosmetic products
  23. What is the role of the Food and Drug Administration (FDA)?
    responsible for enforcing FDCA
  24. What are the 4 stages of drug development?
    • 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
  25. What is the DEA?
    Drug Enforcement Agency: concerned with drugs that have the potential of being abused and of causing physical and psychological dependence
  26. What is meant by 'controlled' substances?
    Drugs that have the potential of being abused and of causing physical and psychological dependence
  27. What are some examples of drugs in schedule I and II?
    • 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)
  28. pharmacokinetics
    movement of drugs through the body
  29. absorption
    getting the drug into the systemic circulation to the target tissue
  30. What is one factor that affects bioavailability?
    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)
  31. What are the major enteral and parenteral routes of administration?
    enteral: oral (PO), sublingual (SL), buccal, rectal

    parenteral: intravenous (IV), subcutaneous (SQ, SC) injection, intramuscular (IM) injection, intrathecal injection, inhalation, transdermal
  32. What is meant by 'first pass effect'?
    some of the drug is metabolized before entering circulation
  33. Metabolism: location, general steps, cause of drug interactions
    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)
  34. clearance
    volume fo blood (cc) cleared of drug / minute
  35. elimination half-life
    time it takes for drug concentration to be reduced bt 1/2
  36. pharmacodynamics
    how the drug acts in the body at the cellular and physiological levels (mechanism of action)
  37. actions of agonists vs. antagonists
    agonists (morphine): has the same effect as endrogenous (our own) substances

    antagonists (naloxne): binds to receptors but has no effect (good antidote)
  38. potency vs. theraputic efficacy
    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
  39. adverse reactions
    side effects: predictable from pharmacology; occur at theraputic doses ('context dependent')

    idiosyncratic reaction: anaphyllaxis

    tolerance & dependence: resistance over time and withdrawl
  40. hypertension
    persistent elevation of systolic and/or diastolic blood pressure
  41. normal, prehypertensive, stage I, stage II hypertensive blood pressure values
    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
  42. blood pressure determinants
    BP = CO(->HR) x TPR(->SV) --> (P=QxR)

    • BP= blood pressure
    • CO= cardiac output
    • TPR= total peripheral resistance
    • HR= heart rate
    • SV= stroke volume
  43. Cardiac output factors
    heart rate and stroke volume
  44. Effect of sympathetic and parasympathetic activity on heart and blood pressure
    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
  45. What is the role of the renin-angiotensin system in blood pressure regulation?
    It raises blood pressure if it should fall (like when we stand up)
  46. What is angiotensin converting enzyme (ACE)?
    It converts angiotensin I into angiotensin II to raise blood pressure
  47. What is the prevalence of hypertension?
    25% of American adults are hypertensive (twice as prevalent in African Americans than any other race)
  48. How effective is pharmacological treatment for managing hypertension?
    Only 18% of people are at target blood pressure levels with their medical management
  49. What are some major risk factors associated with hypertension?
    • 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
  50. Name 4 drug classes used to manage hypertension
    • 1. ACEI - angiotensin-converting enzyme inhibitor
    • 2. ARB - angiotensin receptor blocker
    • 3. BB - beta-blocker
    • 4. CCB - calcium channel blocker
  51. What are the recommended lifestyle modifications for hypertension?
    • Weight reduction
    • Adopt DASH eating plan
    • Dietary sodium reduction
    • Physical activity
    • Moderation of alcohol consumption
  52. What are the effects of hypertension on arteriole endothelium, heart, kidneys, urinary calcium excretion (and secondarily, bone)?
    endothelial damage (atherosclerosis, stroke)

    cardiac damage (cardiomyopathy, heart failure)

    renal damage (renal failure)

    increased urinary calcium excretion (osteoporosis)
  53. What are the major risk factors of CAD?
    • 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)
  54. What is the pathogenesis of CAD due to smoking?
    • 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
  55. What is the patogenesis of CAD due to hypertension?
    • Causes direct trauma to the endothelium
    • Inflammation promotes clot formation
  56. What is the pathogenesis of CAD due to dyslipidemia?
    • 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
  57. Cholesterol guidelines: normal values for LDL, HDL and total cholesterol
    • LDL: <100
    • HDL: <40
    • Total: <200
  58. Relationship of hyperglycemia and LDL cholesterol
    hyperglycemia causes an increase in LDL cholesterol
  59. Effect of exercise on risk factors for CAD
    • Raises HDL cholesterol
    • Lowers LDL cholesterol
    • Lowers blood pressure
    • Lowers heart rate
    • Prevents osteoporosis
  60. Signs/symptoms & manifestations of angina
    • 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
  61. What is a stress test?
    Screening for abnormalities in EKG that result from ischemia
  62. What information does angiography provide?
    Detects plaque and blood flow to the heart
  63. Describe procedures known as PTCA (Percutaneous Transluminal Coronary Angioplasty)
    • 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
  64. Which PTCA is most effective for preventing restenosis-balloon or stent?

    • W/stent: 17% restenosis after 1 year
    • W/o stent: 35% restenosis after 6 months
  65. Myocardial ischemia (acute coronary syndrome)
    • Due to atheroscleroticplaques
    • As oxygen demand of heart increases with exertion, ischemic pain results
  66. stable vs. unstable angina
    • 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
  67. acute coronary syndrome vs myocardial infarction
    • 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
  68. cardiac tissue responses due to ischemia
    • zone of infarction: tissue necrosis
    • zone of hypoxic injury: tissue may or may not survive
    • zone of ischemia: reversible tissue damage
  69. EKG changes due to myocardial ischemia (acute coronary syndrome)
    • Transient ST segment elevations
    • Dynamic T wave changes
    • ST segment depressions
    • Q waves
  70. STEMI (ST Elevation MI) vs Non-STEMI
    • 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
  71. Pathogenesis of tissue over time following MI
    • 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
  72. What are the enzyme changes with MI?
    • Troponin I Peaks at 12 hrs
    • CK-MB Peaks at 18 - 24 hrs (Creatine Kinase)
  73. What are the AHA hospital admission guidelines for suspected acute MI?
    • 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
  74. PTCI
    • associated with:
    • decreased stroke
    • decreased reinfarction
    • increased infarcted artery patency
    • increased short term/long term survival
  75. thrombolytics
    "clot buster"
  76. CABG (Coronary Artery Bypass Grafting)
    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
  77. pacemaker implantation
    Can be on right or left side of chest

    Also can be combined with automatic interna lcardiac defibrillator(AICD)
  78. What are the time considerations of PTCI vs. thrombolytics?
    PTCI: more effective if symptom onset is >3 hours

    thrombolytics: more effective if symptom onset is less than 2 hours
  79. heart failure
    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.
  80. congestive heart failure
    A clinical syndrome caused by heart disease, characterized by breathlessness and abnormal sodium and water retention, and resulting in edema
  81. What is the ejection fraction and what is a normal value?
    Ejection fraction: Amount of blood that is pumped out of the ventricle with each myocardial contraction

    Normal EF is ~55% -65%
  82. 4 causes of congestive heart failure
    • 1. hypertension
    • 2. coronary artery disease
    • 3. MI
    • 4. cardiomyopathy
  83. Diagnosis: Systolic vs.diastolic& cardiothoracic ratio
    • 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
  84. Signs/symptoms & related disability (including those related to fluid accumulation)
    • 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
  85. Precipitating factors in the transition from heart failure to congestive heart failure
    • Non-compliance with care
    • Myocardial ischemia
    • Myocardial Infarction
    • Brady- or tachy- arrhythmias
    • COPD exacerbation
    • Anemia
    • Hyperthyroidism
  86. Hospital treatment guidelines for heart failure
    • 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
  87. Valve dysfunction: stenosis vs. regurgitation
    • Stenosis: Calcification of heart valve. Increases preload
    • Regurgitation: Valve is not closing properly (leaky)
  88. Valve dysfunction treatment: 3 types of valve replacement and long term care following treatment
    • 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
  89. Chronic Obstructive Pulmonary Disease (COPD)
    • 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
  90. 3 examples of COPD
    • 1. emphysema
    • 2. bronchitis
    • 3. asthma
  91. 3 mechanisms of airway obstruction in COPD
    • 1. mucous
    • 2. constriction
    • 3. surrounding tissue destroyed-can't hold airway open
  92. Emphysema: clinical and anatomical definition
    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
  93. Emphysema: raidiologic signs
    • Lung shape/volume: larger volume
    • Diapragm: flat
  94. Emphysema: clinical symptoms
    • 1. Excessive cough
    • 2.Dyspnea during exercise and then rest
    • 3.Wheezing
    • 4.Hyperinflation
    • 5.Accessory use of muscles (inspiration)
    • 6.Fatigue
    • 7.Anorexia
  95. Emphysema: pathology
    loss of alveolar walls, increase alveolar diameter and decrease gas exchange surface area
  96. Emphysema: pathogenesis
    • 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)
  97. Chronic bronchitis
    Any patient who has persistent cough with sputum production for at least 3 months per year for 2 consecutive years.
  98. Chronic bronchitis: symptoms
    • •Excessive cough
    • •Expectoration
    • •Wheezing
    • •SOB, especially on exercise
  99. Chronic bronchitis: Causes
    • •Chronic exposure to irritants (i.e. air pollution), SMOKING, dust
    • •Prolonged irritation, inflammation of bronchial lining
  100. Chronic bronchitis: pathology
    • 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
  101. Chronic bronchitis: X-ray findings
  102. Asthma
    Periods of reversible obstructive disease that are caused by hypersensitivity of the airways to various stimuli resulting in airway constriction
  103. Asthma: intrinsic vs. extrinsic
    • 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
  104. Asthma: Pathology
    • •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
  105. Asthma: diagnosis
    • 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
  106. Asthma: therapy/drugs
    • Therapy:
    • Control inflammation
    • Reverse bronchoconstriction
    • Avoid triggers
    • Treat underlying allergy

    • Drugs:
    • 1.Beta two Agonists
    • 2.Corticosteroids
  107. COPD as a function of smoking cessation and age
    See notes/graph
  108. Cystic fibrosis
    Chronic progressive disorder that affects the body’s digestive and respiratory systems
  109. Cystic fibrosis: cause and diagnosis factors
    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
  110. Cystic fibrosis: Pathophysiology - lungs and digestive tract
    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
  111. Cystic fibrosis: symptoms and pathology
    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.
  112. Cystic fibrosis: x-ray findings
    positive (air trapping)
  113. Restrictive lung disease
    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
  114. Restrictive lung disease: general pathology
    • 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
  115. General types of restrictive lung disease
    • 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
  116. Fibrotic diseases: pathology
    • •Thickening of the alveolar wall
    • •Alveolar destroyed and scarring
    • •Alteration in lung parenchyma
    • •Decrease in lung compliance
    • •Lung volumes are decreased
  117. Fibrotic Diseases: pathogenesis
    • •Inflammation
    • •Early - Infiltration with lymphocytes
    • •Later – Fibroblasts lay down collagen
    • •Irregular pattern gives honeycomb effect
  118. Fibrotic diseases: clinical signs/symptoms
    • •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
  119. Sarcoidosis: pathology
    • 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
  120. Sarcoidosis: signs/symptoms
    Lungs: Cough, SOB, Chest pressure/pain

    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

  121. Sarcoidosis: diagnosis
    • •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
  122. Sarcoidosis: etiology
    • Inflammatory disease
    • Insidious
  123. Hypersensitivity pneumonitis: etiology
    "allergic" reaction to inhalent
  124. Hypersensitivity pneumonitis: acute vs. chronic characteristics
    • 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
  125. Pulmonary Function Tests: What do they measure?
    • 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
  126. Pulmonary Function Tests: Information they provide
    • •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
  127. Pulmonary Function Tests: What they cannot do
    • •Make a specific clinical diagnosis
    • •Make specific bacteriological diagnosis
    • •Make specific regional diagnosis except with specialized equipment
  128. Obstructive profiles
    increased TLC, increased RV (always forcefully exhaling), increased time to expire, decreased vital capacity, FEV% decreased
  129. Restrictive profiles
    decreased TLC, decreased residual volume (so much elastic recoil), forced expiratory volume could be normal, FEV% could be normal
Card Set
OT412 Rehab Medicine
Midterm Review