Pathophys final

  1. Leading cause of death in the US. _____ ______ _____. also known as ischemic heart disease.
    coronary artery disease
  2. Most all CAD involve ______ (defined as a condition in which fatty material collects along the walls of the arteries. Fatty material thickens, hardens, and may eventually block the arteries.
  3. -LDL, "____" transports cholesterol ___ cells encouraging plaques.
    -HDL"____" transports cholesterol _____ from cells.
    • bad, to
    • good, away
  4. _____ ____: decreased oxygen to myocardium as a result of obstructed arteries and decreased blood flow. 3 types: stable, unstable, variant.
    angina pectoris
  5. Non Modifiable causes of cardiac conditions (3)

    Modifiable causes of cardiac conditions (7)
    • 1. age >40, genetics, gender
    • 2. obesity, high fat diets, smoking, sedentary lifestyle, diabetes, hypertension, and heavy alcohol consumption
  6. 3 types of angina pectoris: stable variant unstable
    ______: chest pains with physical exertion or emotional stress. most common. predictable.
    _____: unexpected. usually occurs at rest. can be severe and prolonged. may precede myocardial infarction.
    _____: spontaneous and nearly always occurs at rest. due to vasospasm at rest.
    stable, unstable, variant
  7. _______ ______: total obstruction of a coronary artery leading to ischemia and cell death.
    ______: primary cause
    • myocardial infarction
    • atherosclerosis (thrombus, vasospasm, emobolus)
  8. ______ ______: deviations from the heart's typical beat cycle. Caused by interference in heart's conduction system. Bradycardia, tachycardia, irregular are all examples.
    cardiac dysrhythmias
  9. ______= standstill or "cardiac arrest". No activity in the heart.
  10. ________: may develop as primary infection in lungs or may be secondary. Organisms enter lungs via inhalation (virus), bacteria, fungi, parasites, aspiration. 1/2 of cases are believed to be viral.
  11. _______ Pneumonia: inflammation of alveolar wall and leakage of cells, fibrin, and fluid into alveoli causing consolidation.
    _______: inflammation and purulent exudate in alveoli often arising from prior pooled secretions or irritation.
    ______ pneumonia: interstitial inflammation around alveoli.
    • lobar
    • bronchopneumonia
    • interstitial pneumonia
  12. ________: transmitted by oral droplets of myobacteria from a person with active infections that are inhaled into lungs. Insidious onset, cough becomes increasingly severe and more productive. 2nd leading cause of death worldwide.
  13. _____ _____: genetic disease. Caused by a mutated CFTR gene on the 7th chromosome, transmitted as autosomal recessive disorder. Large proportion of population is carriers with no symptoms.
    cystic fibrosis
  14. ______: exact cause is unknown. Family history of hay fever and eczema is common. Children living sedentary lifestyles which leads to exposure to allergens due to poor ventilation. Attacks cause reversible bronchial obstruction and most children grow out of it.
  15. _______ ______: persistent severe attack, may be fatal due to severe hypoxia and respiratory acidosis leading to cardiac arrhythmias or CNS depression.
    status asthmaticus
  16. Asthma:
    _____: typically childhood onset and involves acute episodes triggered by typeI hypersensitivity reactions to an inhaled agtigen.
    _____: adult onset and acute attacks triggered by stimuli such as repiratory infections; exposure to cold, exercise, aspirin, stress, and inhalation of iiritants.
    • extrinsic
    • intrinsic
  17. ____ ____ ____ ____: long term exposure to lung irritants. most common is cigarrette smoking. rarely genetic component (alpha-1 antitrypsin deficiency). Causes irreversible and progressive damage to the lungs. Eventually respiratory failure may result due to hypoxia, or right sided congestive heart failure my result due to lung disease.
    Chronic Obstructive Pulmonary Disease
  18. _________: alveolar walls and septae are destroyed leading to permanently inflated alveolar spaces. The alveoli can be destroyed by a genetic deficiency of alpha1 antitrypsin, cigarette smoking, and certain bacterial infections.
  19. ______ _____: fibrosis and thickening of the bronchial wall occures from constant irritation from smoking or exposure to industrial pollution. Oxygen levels are low during coughing episodes cyanosis may occur.
    chronic bronchitis
  20. ________: an irreversible abnormal dilataion of bronchi caused by recurrent inflammation and infection in the airways. In dilated areas, large amounts of fluid constantly collect and become infected.
  21. ________: onset is gradual. Dyspnea first noted on exertion, then is present during rest. Hyperventilation leading to development of "barrel chest". Anorexia and fatigue lead to weight loss. Clubbed fingers and secondary polycythemia.
  22. Rule of Nines for burns:

    Head and each arm: ___%
    Each leg:___%
    Anterior & posterior surface of trunk:___%
    Groin: ___%
    • 9
    • 18
    • 18
    • 1
  23. ______ ______ ______ ______: Formerly known as 1st degree burns; damage to _________ and possibly some of upper ________. Ex: mild sunburn, mild scald.
    Superficial Partial Thickness Burns


  24. ______ ______ _______ _______: formerly known as 2nd degree burns; damage to the _________ and part of _______. Appears red, edematous, blistered and waxy. Some burns may appear _____ and irregular.
    Deep Partial Thickness Burns



  25. ______ ______ ______: formerly known as 3rd and 4th degree burns; causes destruction of ____ & _____ fully. Appears ______ due to nerve destruction. Usually require _____ because of lack of cells available to produce new skin.
    Full Thickness Burns

    epidermis & dermis

    skin grafts
  26. _____: account for about 70% of burns in children and common in elderly.

    _____: cause about 50% of adult burns; usually deep partial or full thickness.

  27. Treatment for Superficial Partial Thickness Burns:

    apply ____ _____, take meds for pain and swelling; do not apply _____ or _____ as these may lead to infection

    Usually heals within ____ week.
    cold compress; ointments or butter; one week
  28. Deep Partial Thickness Burns usually heal within ___ weeks if kept clean and protected.
  29. Burns co-morbidities: (5)
    inability to sweat, need for skin rehydration, change in skin color, change in skin strength, change in skin sensation
  30. Inflammatory response results in major shift of water, proteins and electrolytes into the tissues which then causes edema associated with burns is:
  31. Common problems associated with burns include all of the following except:

    Respiratory issues
  32. Degenerative joint disease resulting in pain, stiffness, loss of ROM and function.
  33. Is OA a systemic disorder?
    No, does not affect other organs of the body
  34. OA
    The primary form is the (most/least) common and due to _____ and _____.

    The secondary form is due to ____ or ______. Common with participation in sports and certain occupations.
    • most common, obesity and aging
    • injury or abuse
  35. Genetic factor of OA
    ________ cartilage has accelerated breakdown.
    Once damaged, it further degenerates causing uneven stress to other part of the ______ resulting in OA
    • Articular
    • Joint
  36. T/F: One in 3 adults in the US has some degree of OA.
    T/F: Women affected greater than men
    T/F: Incidence rate decreases with age, leveling off at about 80.
    • True
    • False, men > women
    • False, increases
  37. The course of OA is usually (regressive/progressive). Loss of cartilage decreases its ability to act as a shock absorber and eventually causes friction between bones leading to _____ and loss of _______.
    • Progressive
    • Pain and loss of mobility
  38. Which joints are most commonly affected by mechanical stress leading to erosion or unknown breakdown in OA?
    knees and hips (weight bearing joints)
  39. Tissue damage in OA causes release of enzymes from cells, which (accelerates/slows) the disentegration of the cartilage.
  40. T/F:
    In OA, subchondral bone may be exposed and damaged leading to development of cysts and osteophytes, whcihc can break off into the synovial cavity, causing further damage.
  41. 3 ways to diagnose OA
    Xray, MRI and blood tests (rules out other diseases that mimic OA)
  42. For OA, is pain reliable?
  43. OA
    Joint appears large and hard as ______ develop.
  44. What term refers to grinding/grating of joints?
  45. OA
    Bony enlargement of distal interphalangeal joints
    Heberden's nodes
  46. Subtypes of OA
    _______ OA: Typically in middle-aged women. RA like syptoms, predominantly affects PIPs and DIPs and treated with NSAIDs
    ________ OA: erosion of cartilage, especially in hands. Symptoms are pain, tenderness & swelling.
    • Inflammatory OA
    • Erosive OA
  47. Subtypes of OA
    ________: Idiopathic, older adults, caused by wear and tear
    _______: degenerative disease of synovial joints caused by previous condition. Often in younger population
    • Primary
    • Secondary
  48. OA treatment goal is to reduce joint pain and inflammation while maximizing function. Treatments include: (5)
    • Rest
    • Diet control
    • Amb. aids
    • Min stress on joint
    • Orthotic inserts (reduce risk of deformity and help maintain function)
  49. 4 drugs used in treatment of OA
    Glucosamine, intraarticular injection, glucocorticoids, NSAIDs
  50. Cause of diabetes is a deficiency of insulin secretion from ___ cells in the ______ of ______ in the pancreas.
    • beta
    • Islets of Langerhans
  51. Type __ diabetes: immune system destroys insulin producing cells which leads to little or no insulin creating a buildup of sugar in the blood stream.
    Type __ diabetes: cells become resistant to the action of insulin, and your pancrease is unable to make enough to overcome this resistance.
    • type 1
    • type 2
  52. _______ diabetes: hormones produced by placenta buildup a resistance to insulin.
    gestational diabetes
  53. ________: excess of insulin causes a deficit of glucose in the blood.
    _____ ____: results from low insulin levels, which leads to high blood glucose levels and mobilization of lipids.
    • hypoglycemia
    • diabetic ketoacidosis
  54. _______: obstruction or rupture of capillaries and small arteries, resulting in neuropathy and loss of function.
    _______: obstruction of large arteries, leading to heart attacks, strokes, and peripheral vascular disease in diabetics.
    • microangiopathy
    • macroangiopathy
  55. How many stages are there in diabetes?
    • 2
    • initial stage (insulin deficit)
    • progressive stage (insulin deficit is severe or prolonged)
  56. initial stage of diabetes
    _______: casued by the rising glucose levels that exceed the limit to be reabsorbed which spills into the urine.
    _______: glucose in the urine creates an osmotic pressure which is present in the filtrate, leading to a large volume of urine to be excreted.
    _______: dehydration causes excessive thirst.
    _______: limited amount of nutrients entering the cells stimulates excessive appetite.
    • glucosuria
    • polyuria
    • polydipsia
    • polyphagia
  57. progressive phase of diabetes
    _____: ketoacids are excreted in the urine
    _____ ____: as dehydration develops, the excretion of acids is more limited, which leads to decompensated metabolic acidosis.
    • ketonuria
    • diabetic coma
  58. Risk factors of type I diabetes
    -low vitamin __ consumption or some cereals consumed before 4 months and after 7 months.
  59. diabetes _____: occurs because of body's inability of regulating fluids. Due to innefficiency of production/regulation of anti-diuretic hormone.
  60. _______ diabetes insipidus: damage to pituitary gland which creates problems in production and storage of ADH.
    _____ diabetes insipidus: problem with kidney tubules that do not respond well to ADH.
    _____ diabetes insipidus: excessive fluid intake suppress ADH, affects hypothalamus.
    • central
    • nephrogenic
    • dispogenic
  61. 3 p's of diabetes:
    polydipsia, polyuria, polyphagia
  62. Normal fasting glucose: ___-___ mg/dl
    greater than ___ mg/dl on 2 or more different test days =diabetes or if one random BGT without fasting is ___ mg/dl or higher= diabetes
    • 70-100
    • 126
    • 200
  63. ____ ____ ___: 100-126 mg/dl, not diagnosed with diabetes, but at high risk for progressing to it.
    impaired glucose test
  64. _____ ____ tolerance test: gold standard in diagnosing type 2 diabetes. pt. fasts overnight, fasting plasma glucose is tested first, then pt. receives 75 g of glucose and blood glucose is tested in intervals. (standard= __ times in a period of __ hrs.)
    • oral glucose tolerance test
    • 5 in 3
  65. Reasons for why a joint might be replaced: Hip: (3)
    • §Arthritis – most
    • common


    §Hip fracture
  66. (3) Reasons why a joint may be replaced Knee:
    • Osteoarthritis – most common
    • Rheumatoid arthritis
    • Post-traumatic arthritis
  67. Flexion can increase following TJR __-__ degrees per day depending on patient tolerance>
    5-10 d
  68. Following TJR, complete recovery is usually within __ weeks.
  69. ______ Approach: Most commonly used
    approach- 70% ;“Moore” or “Southern”
    Approach; Goes through deep hip rotators.
    _______ Approach: Goes through Glute Medius and Minimus.
    _______ Approach:Goes between TFL and Glute Medius.
    _______ Approach: Goes between
    Sartorius and TFL
    posterior, lateral, antero-lateral, anterior
  70. General hip precautions following TJR: (3)
    • -Do not bend past 90degrees
    • -Do not bring the operated leg past midline position (cross legs)
    • -Avoid any hip rotation
  71. General knee precautions following TJR: (2)
    • -Weight bearing status: know the doctors orders
    • -Do not cross legs
  72. Precautions for PT/OT following TJR: (4)
    • ▪High temperature
    • ▪Nausea and Vomiting
    • ▪Confusion
    • ▪Dizziness or Light-headedness
  73. Clinical features of FAS: (5)
    • elongated midface
    • thin upper lip
    • flattened maxilla
    • microencephaly
    • small palpebral fissures
  74. Children with ____ are prone to a variety of developmental delays, like ADHD, memory and abstraction difficulties.
    Fetal Alcohol Syndrome
  75. Co-morbidities of FAS: (6)
    • ADHD
    • Vision/Hearing problems
    • Heart defects
    • Lung defects
    • Kidney defects
    • Statis Encephalopathy
  76. T/F: There is no known safe amount or time to drink alcohol during pregnancy.
  77. ______ ______ _______: alcohol is consumed by mother, enters the bloodstream and crosses the placenta; fetus is unable to metabolize alcohol as fast causing increase BAC; interferes with delivery of oxygen and nutrients leading to ____ ______.
    Fetal Alcohol Syndrome

    Developmental deficits
  78. Birth Defects of FAS:

    Head circumference at or below the ___th percentile.

    Poor _____-_____ coordination or nystagmus

  79. ______, ______, _____ and _____ drugs are used to treat FAS.
    stimulants, antidepressant, neuroleptics, and anti-anxiety drugs
Card Set
Pathophys final
pathophys final