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2012-04-27 18:42:52
Patho Final Exam

Flash Cards for Patho Final Exam
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  1. Osmolarity
    • concentration of the blood
    • Normal 270-295
  2. Normal sodium levels
  3. Nomal Hematocrit
  4. Normal BUN
  5. Diabetes Insipidus "Tasteless diabetes"
    • insufficiency of ADH, leading to polyuria and polydipsia
    • hx of head injury, pituitary tmor, craniotomy
  6. Types of Diabetes Insipidus
    • Neurogenic (central)
    • Nephrogenic
  7. Neurogenic Diabetes Insipidus
    • insufficient ADH
    • may follow head injury or surgery near the lesion area
  8. Nephrogenic Diabetes Insipidus
    • End organ failure
    • insensitivity of the renal tubule to ADH
    • drugs and disorders damage the renal tubule
  9. Pathophysiology of Diabetes Insipidus
    • Partial or total inabilty to concentrate urine. Insufficient ADH secretion causes secretion of large volumes of dilute urine, leading to an increase in plasma osmolatity
    • urine out put 3 to >12 L/day
    • Specific Gravity 1.00-1.005
    • Dehydration can develop rapidly
  10. Specific Gravity
    • measure of concentration of urine
    • Normal 1.010 - 1.020
  11. Nursing Care for Diabetes Insipidus
    • Monitor fluids
    • Replace Fluids
    • Check neuro states
    • Check vital signs
    • check muccous membranes
  12. Clinical Manifestations of Diabetes Insipidus
    • Polyuria, nocturia, thirst, polydipsia
    • increase plasma osmolality
    • decrease urine spenific gravity
    • decreased urine osmolality
    • hypovolemia, tachycardia, decreased b/p
  13. Hyperthyroidism (Thyrotoxicosis)
    condition that results from increased levels of thyroid hormone. could be due to graves disease, adenomas, carcinomas, pituitary issue
  14. Most common cause of hyperthyroidism
    Graves disease
  15. Clinical Manifestations of Hyperthyroidism (Thyrotoxicosis)
    • result of increased circulating thyroid hormones
    • increased T3, T4, decreased TSH
    • clubing fingers, Tremors, increaed diarrhea, Menstrual changes (amenorrhea), intolerance to heat, fine straight hair, bulging eyes, facial flushing, enlarged thyroid, tachycardia, increase systolic BP, breast enlargement, weight loss, muscle wasting, nervousness, increased appetite
  16. Graves Disease
    • more common in women, Familial tendency, autoimmune disease
    • Thyroid autoantibodies are found in more than 95% of clients
  17. The hyperfunction of the thyroid gland leads to
    suppression of TSH and TRH, increased iodine uptake, increaed thyroid gland metabolism, lead to enlargment of the gland
  18. Goiter
    • enlarged thyroid gland
    • can be seen ini both hypo and hyperthyroidism
  19. Myxedema
    subcutaneous swelling legs and hands
  20. Ocular Manifestations of Grave's Disease
    Exophthalmos (Bulging eyes), Edema of the orbital contents, protrusion of the globe can occur which can lead to visual disturbances, irritation, pain
  21. Thyroid Storm
    • excerbation of hyperthyroidism
    • worsened thyrotoxic state that can be fatal if not treated
    • death can occur w/i 48hrs
    • most frequently occurs in undiagnosed, partially treated and stressed individuals
  22. Whos at risk for Thyroid Storm?
    infections, cardiopulmonary disorders, emotional distress, poor preparation for thyroid surgery
  23. Systoms of Thyroid storm
    Hyperthermia, tachycardia, high-output heart failure, agitation, NVD
  24. Hypothyroidism
    most common throid disorder due to deficient productoin of thyroid hormone by the throid gland
  25. Primary Hypothyrodism
    • loss of functional throid tissue
    • leads to decreased production of TH
    • that leads to increased production od TSH
    • that may lead to goiter
  26. Secondary Hypothyrodism
    • due to problem w/ pituitary gland and insufficient TSH
    • pituitary tumors
    • Decreased TSH, decreased TH
  27. Subacute thyroiditis
    nonbacterial inflammation preceded by a virus
  28. Autoimmune Thyroiditis
    • destruction of thyroid tissue
    • ex-Hashimoto disease
  29. Clinical Manifestations of Hypothyroidism
    hair loss, apathy, lethargy, dry skin (coarse & Scaly), muscle aches and weakness, constipation, intolerance to cold, receding hairline, facial & eyelid edema, Dull-blank expression, extreme fatigue, thick tongue, slow speech, anorexia, brittle nails and hair, menstrual disturbances
  30. late: subnormal temp, bradycardia, weight gain, decresed LOC, thickened skin, cardiac complications
  31. Myxedema in Hypothroidism result from
    • alteration in the composition of the dermis and other tissues
    • protein-mucopolysaccharide complex binds w/ water
  32. Myxedema Coma
    • excerbation of Hypothroidism
    • decreased LOC, hypothermia, hypoventilation, hypoglycemia,
  33. Congenital Hypothyroidism
    occurs in infants as a result of absent thyroid tissue and hereditary defects in thyroid hormone synthesis
  34. Cretinism
    due to untreated congenital hypothyroidism
  35. Thyroid Carcinoma
    • most common cause is exposure to ionizing radiation during childhood. Small thyroid nodule or metastatic tumor in lungs, brain, bone
    • s/s due to pressure on surrounding tissue
  36. Cushing Syndrome
    • manifestation of hypercortisolism from any cause
    • Cushing disease
    • Benign or Malignant adrenal tumor
    • Ectopic Cushing
    • Iatrogenic Cushing
  37. To Diagnosis Diabetes Mallitus
    • 1. more than one fasting plasma glucose level >or = 126 mg/dl
    • 2. plasma glucose value in the 2 hr sample of OGTT > 200 mg/dl
    • 3. Casual plasma glucose level > or = 200mg/dl with symptoms
    • 4. HgbA1C= normal <7%
  38. HgbA1C
    shows overal status of a person BS for the past few months
  39. Classifications of Diabetes Mellitus
    • Type 1
    • Type 1.5
    • type 2
    • Gestational
  40. 1A Immune Mediated Diabetes Mellitusenvironmental-genetic factors result in Bcell destruction
    • autoantibbodies detected of pancreas and B cells
    • 95%
    • peakage 11-13 years
  41. 1B Idiopathic Diabetes Mellitus
    • cause unknown
    • no evidence of autoimmunity
  42. Clincal Manistations of Type 1
    Polyuria, polydipsia, polyphagia, weight loss, fatigue, increase frequency of infection, rapid onset, insulin dependent, familial tendency, peak incidence from 10-15 years
  43. In Type 1 Diabetes Mellitus hyperglycemia due to
    lack of insulin
  44. In Type 1 Diabetes Mellitus polydipsia is due
    to elevated glucose levels pull water from cells which results in intracellular dehydration
  45. In Type 1 Diabetes Mellitus polyuria is due to
    the effects of hyperglycemia as an osmotic diuretic renal threshold for glucose excreded
  46. In Type 1 Diabetes Mellitus Polyphagia is due to
    depletion of cellular stores of CHO, fats, proteins, resulting in cellular starvation
  47. In Type 1 Diabetes Mellitus weight loss is due to
    fluid loss w/ osmotic diuresis, loss of body tissue
  48. In Type 1 Diabetes Mellitus fatigue is due to
    metabolic changes
  49. Pathophysiology of Type 2 Diabetes
    • 1. Peripheral insulin resistance
    • 2. Deranged secrections of insulin by pancreatic cells
    • 3. increased glucose production by the liver
  50. The biggest risk factor for type 2 diabetes
    obesity, diabesity, visceral fat
  51. Syndrome X (Metabolic Syndrome, Insulin Resistance syndrome)
    • 1. hyperglycemia
    • 2. hypertension
    • 3. hyperlipidemia-High triglycerides (>150
    • 4. Abdominal obsesity
  52. Normal FSBS
  53. Clinical Manifestations of Type 2 Diabetes
    genital pruritus, visual changes, parethesias, fatigue
  54. Impaired fasting Glucose (Borderline/Previsional Diabetics)
    Fasting glucose >100 and <126 mg/dl
  55. Impaired Glucose Tolerance (IGT)
    2 hour postload glucose level greater than or equal to 140 but less that 200 mg/dl
  56. Gestational Diabetes mellitus (GND)
    glucose intolerance first recognized during pregnacy, most likely in the third trimester. Following pregnancy glucose may normalize remaini impaired or progress to Diabetes Mellitus.
  57. Hypoglycemia
    • lowered plasma glucose 45-60 mg/dl
    • occcurs more frequently in individuals treated w/ insulin
  58. Symptoms of hypoglycemia
    • tachycardia, diaphoresis, pallor, tremors, dizziness, headahcem visual changes
    • Adrengic-pallor, sweating, tachycardia, sweating, palpitations, hunger, restlesness, anxiety, tremors, clammy skin
    • Neurogenic- Fatigue, irritabilty, headache, visual changes, dizziness, convulsions
  59. Diabetic Ketoacidosis
    • most commonly occurs in Type 1 diabetics
    • develops when ther is an absolute or relative deficiency of insulini and an increase in insulin counterregulatory hormones. Hepatic glucose production increases. peripheral glucose usage decreases, fat mobiliaztion increase and ketogenesis is simulated
  60. ounterregulatory Hormones
    • catecholamines, cortisol, glucagon, growth hormon
    • are realses during a stress responce
  61. Precipitating Factors of DKA
    type 1, illness, infection, trama, surgery, mi, stress evernt
  62. Metabolic Components of DKA
    • Hyperglycemia (BG 300-750)
    • Ketosis (Ketones come from fat metabolism)
    • Metabolc Acidosis (ketones acid) ,low bicarb <15, low pH <7.3
  63. Clinical Manifestations of DKA
    polyuria, polydipsia, N/V, Fatigue, hypotension, tachycardia, stupor leads to coma, abdominal pain, fruity breath, kussmauls respirations
  64. Kussmauls Respirations
    • Hyperventilation
    • rapid , deep
  65. why is a person woth DKA at risk for dehydration?
    fluid loss from osmotic diuresis due to hyperglycemia
  66. What metabolic changes are seen in DKA
    K+ normal or elevated (Met Acid= high K+), shift of H20 and K+ from EC due to hyperosmolarity of ECF due to hyperglycemia, NA normal or decreased
  67. herniation or saclike outpouching of mucosa thru muscle layers
    • diverticula
    • asymptomatic diverticular disease
    • diverticulosis
    • inflammation of pouchings
    • diverticulitis
    • most frequent site for diverticulitis
    • sigmoid colon
  68. patho for diverticula
    form at weak points in colon wall, usually where arteries penetrate tunica mucularis to nourish mucosal layer. colonic mucosa herniates through smooth muscle layers. muscle hypertrophy and contraction occurs
  69. risk factors of diverticula
    • age
    • diet of refined foods
  70. clinical manifestations of diverticula
    • may be vague or absent
    • cramping
    • diarrhea, constipation, distention, flatulence
    • inflammation and abcesses may occur
    • fever, leukocytosis tenderness, LLQ
    • Mass that protrudes into lumen of gut. benign neosplasm
    • adenomatous polyp
    • raised mucosal nodules of adenomatous polyp
    • sessile
    • attached by stalk of adenomatous polyp
    • pedunculated
    • most common site of adenomatous polyp
    • rectosigmoid colon
    • 3rd most common cause of cancer and cancer death in us for men and women most begin with adenomatous polyp > 50 years of age
    • colorectal cancer
    • risk factors of colorectal cancer
    • family hx
    • ulcerative colitis
    • high fat, lowfiber diet
    • alcohol
    • sedentary lifestyle
    • smoking
  71. clinical manifestations of colorectal cancer
    • depends on site
    • bleeding
    • change in bowel habits
    • pain is late sign
  72. abnormally high accumulation of bilirubin billi > 2.5-3.0
    • jaundice (icterus)
    • may see 1st in sclera
  73. abnormally high pressure in portal venous system > 10 mm Hg
    • portal hypertension
    • normal is 3 mm Hg
    • d/t obstruction, thrombosis, inflammation, cirrhosis
    • Altered immunologic response to antigen that results in disease or damage to host
    • hypersensitivity
  74. Four types of hypersensitivity reactions
    • Type I: IgE mediated
    • Type II: Tissue-specific reactions
    • Type III: Immmune complex mediated
    • Type IV: Cell Mediated
    • Seasonal allergic rhinitis and asthma are examples of:
    • IgE mediated reaction
    • Rate of development-Immediate
    • Antibody involved-IgE
    • Effector cells involved-Mast cells
    • Participation of complement-NO
    • Autoimmune thrombocytopenic purpura, Graves disease, autoimmune hemolytic anemia are examples of:
    • Tissue specific reaction
    • Rate of development-Immediate
    • Antibody involved- IgG and IgM
    • Effector cells involved-Macrophages in tissues
    • Participation of complement-Frequently
    • Systemic lupu erythematosus is an example of:
    • Immune complex mediated reaction
    • Rate of development-Immediate
    • Antibody involved-IgG and IgM
    • Effector cells involved- Neutrophils
    • Participation of complement-Yes
    • Contact sensitivity to poison ivy and metals (jewelry) are examples of:
    • Cell-mediated reaction
    • Rate of development-Delayed
    • Antibody involved-None
    • Effector cells involved-lymphocytes and macrophages
    • Participation of complement-No
  75. Type I hypersensitivity reaction
    • IgE mediated-result of excessive or inappropriate production of IgE antibodies after exposure to some type of environmental antigen.
    • With initial exposure to antigen, IgE (immunoglobulin)binds to Fc receptor on surface of mast cell. Individual now sensitized to antigen. Antigens cause allergic responses called allergens. With subsequent exposure to antigen, tiny sacs in mast cells called granules break open and release histamine, which then triggers inflammatory response
    • Most potent mediator of Type I reaction
    • Histamine
    • Contracts Bronchial smooth muscles
    • Increases Vascular permeability
    • Increases blood flow to affected area
    • Increased gastric acid secreation (N/V)
    • Examples of Type I
    • Hay fever
    • Food and drug allergies
    • Bee stings
    • Asthma
    • Anaphylaxis
  76. Clinical manifestations of Type I:
    • Sudden onset
    • GI symptoms
    • Urticaria-hives
    • ENT and respiratory symptoms
    • Anaphylaxis-rapid onset, urticaria, cramps, difficulty breathing. Caused by bronchospasm, angioedema, hypotension, shock. Can be Lethal
  77. Who are atopic individuals?
    • Predisposition to develop allergies
    • Genetic tendency
    • Higher quantities of IgE
    • More Fc receptors on mast cells which connect IgE
  78. Type II:Tissue-specific Reactions
    • Blood transfusions-red blood cell reaction
    • Specific cell or tissue (tissue specific antigens) is target of immune response. Direct interaction b/t IgG and IgM class antibodies and tissue or cell surface antigens.
  79. Five mechanisms of Type II
    • Cell is destroyed by antibodies and complement
    • Antibody may cause cell destruction through phagocytosis
    • Toxic products produced by neutrophils
    • Antibody dependent cell mediated cytotoxicity (ADCC)
    • Cell malfunctions
  80. Examples of Type II
    • Erythroblastosis Fetalis-Rh or Abo incompatibility b/t blood of mother and fetus
    • Hemolytic anemia-antibodies produced against red blood cells could be drug induced
    • Transfusion reaction-Antibodies produced against donor cells
  81. Type III:Immune complex mediated
    • Abnormal creation that forms. ex-autoimmune disorder
    • caused by antigen antibody immune complexes formed in circulation and deposited later in vessel walls and other tissue.
    • Size influences whether remain in plasma or lodge in tissues where they result in tissue damage.
    • Complement activated and neutrophils degranulate enzymes damage tissue. can damage and destroy healthy tissue
  82. Examples of Type III
    • Serum sickness
    • Systemic lupus erythematosus
    • arthus reaction-local reaction
    • Acute glomerulonephritis that follows strept infection
  83. Type IV Hypersensitivity Reaction
    • Mediated by Sensitized T lymphocytes
    • Don't involve antibody
    • Reaction delayed-24-72 hours after exposure
  84. Examples of Type IV reaction
    • Graft rejection
    • Skin test for TB
    • Allergic contact dermatitis- poison ivy and metals
  85. Autoimmunity
    • Breakdown of tolerance to own antigens
    • SLE
    • Chronic multisystem inflammatory disease-abnormal antibodies attack RBC's
    • Autoantibodies against nucleic acids, erythrocytes, Coagulation porteins, platelets
    • Deposition of circulating immune complexes containing antibody against host DNA
    • More common in females
    • Clinical manifestation-Butterfly rash, Lupus
  86. Common Findings of SLE-serial or simultaneous presence of at least four
    • Not just localized-can become systemic
    • facial rash
    • discoid rash
    • photosensitivity
    • Oral or nasophyaryngeal ulcers
    • arthritis
    • serositis
    • renal disorders
    • neurologic dis
    • hematologic disorder
    • immunologic disorder
    • Presence of antinuclear antibody-blood test of ANA-titer. some reaction going on in body if ANA is elevated
  87. Syndrome caused by viral disease-Human Immunodeficiency virus (HIV).
    • Acquired Immunodeficiency Syndrome (AIDS)
    • Blood borne pathogen. Increasing faster in women than men.
    • Depletes CD4 Th cells
    • Incidence:Worldwide 5 mill/yr
    • US 31K/yr
  88. Pathogenesis of AIDS
    • Retrovirus
    • Genetic information stored in RNA rather than DNA
    • Contains reverse transcriptase to convert RNA into double stranded DNA
    • Integrase inserts new DNA into infected cells genetic material
    • Structure:GP 120 proteins bind to CD$ molecule found on surface of CD4 Th cells
  89. Normal CD4 count
    800-1000 cells/mm3
  90. Clinical manifestations of AIDS
    • Antibody 4-7 wks after blood products
    • Antibody 6-14 mo after sexual transmission
    • Window period
    • Can still be infectious
    • Early signs-flu symptoms, swollen lymph glands, diarrhea, fatigue
  91. Opportunistic infections (pg 201, Box 7-2)
    Organisms produce infection in persons w/impaired immune function
  92. Neurologic Complications of AIDS
    • Encephalopathy
    • Myelopathy
    • Neuropathy
    • Viral meningitis
    • Opportunistic infections
    • Neoplasms
    • Bleeding
  93. Benign Tumors
    • Tumors of the skin are normally associated with aging
    • Seborrheic Keratosis
    • Actinic Keratosis
  94. Seborrheic Keratosis
    • Benign proliferation of the basal cells that produce smooth or waxy elevated lesions
    • more common in older adults
    • on chest, back, face
    • Shades of tan, yellow, flesh colored, brown-black lesions
  95. Actinic Keratosis
    • precancerous tumors associated with exposure to UV radiation of the sun
    • risk=individuals w/ unprotected light skin
    • pigments patchese of rough skin
  96. Nevi
    • Mole
    • pigments and nonpigmented
    • Flat and elevated
    • watch for malignant transformation
  97. Risk Factor for skin cancer
    fair complexion, excessive exposure to the sun, tanning salons, or ultraviolet radiation predisposes a person
  98. Basal Cell Carcinoma
    • caused by sunlight exposure
    • on face, neck
    • slow growth
    • metastatic spread rate
    • more common in men then women
  99. Basal cell lesions..
    • start as nodule
    • Pearly/Ivory
    • Depressed Center and rolled borders
    • progressess to ulceration with waxy borders
  100. Squamous Cell Carcinoma
    • A tumor of the epidermis
    • Malignant potential
    • sun exposure and fair complexion
    • Red, scaly, elevated, irregular borders
    • shallow chronic ulcer
  101. Malignant Melanoma
    • A tumor originating from the melanocytes
    • Rapidly progressive, metastatic
    • intermittent intense sun exposure
    • Raised, black, brown most from Nevi or moles shades of red, blue or white
  102. Melanocytes
    cells that synthesize the pigment melanin
  103. Cancer ACDE
    • A=Asymmetry
    • B=Border Irregularity
    • C=Color variation
    • D= diameter >6mm
    • E=Evolving Change
  104. Kaposi Sarcoma
    • Vascular Malignancy
    • Endothelial Cell
    • Purplish brown macules-develop into plaques and nodules
    • Immunosuppression, transplant recipient, AIDS, African middle aged blacks, Jewish descent