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Pathophysiology
Exam 3
| Question | Answer |
|---|---|
| How to stimulate an immune response | -Become exposed to antigens |
| Dendritic cell | -Antigen presenting cells -Act as messengers between innate and adaptive immunity |
| T Helper Cells | -CD4 -Necessary for normal immune function -Recognize foreign antigens -Help activate antibody-producing B lymphocytes -Orchestrate cell-mediated immunity -Influence the phagocytic function of monocytes and macrophages |
| T Cytotoxic Cells | -CD8 -Kill cells infected with viruses |
| Hummoral Immune Response | -Generated by B lymphocytes -Mediated by antibodies -Is the principal defense against extracellular microbes and toxins |
| B Lymphocytes | -Memory Cells -When an antigen comes back the body will remember it and can fight it off easier |
| Allergy to Latex | -Exposure:Cutaneous,Mucous membrane,Most severe reactions mouth, vagina, urethra, or rectum, Inhalation,Internal tissue,Intravascular -Reaction types type I(less common, more serious) and type IV(more common) |
| Types of Hypersensitivity Reactions | -Type I, Ig-E–mediated disorders -Type II, antibody-mediated disorders -Type III, complement-mediated immune disorders -Type IV, T-cell–mediated disorders |
| Histocompatibility Complex | -Set of molecules displayed on cell surfaces -Lymphocyte recognition -Antigen presentation -Control the immune response through recognition of self and nonself |
| Type I Hypersensitivity Reactions | Atopic -Hereditary predisposition -Urticaria (hives), allergic rhinitis (hay fever), atopic dermatitis, food allergies, some forms of asthma Nonatopic disorders -Lack the genetic component and organ specificity of the atopic disorders |
| Type II Hypersensitivity Reactions | -Action Mediated by IgG or IgM directed against target antigens on the surface of cells -Endogenous antigens:on the membranes -Exogenous antigens: absorbed Ex: Mismatched blood transfusion reactions,Hemolytic disease of the newborn,drug reactions |
| Type III Hypersensitivity Reactions | -Systemic immune complex disorders Serum sickness -Localized immune complex reactions Arthus reaction |
| Type IV Hypersensitivity Reactions | -Cell-mediated immune response -Basic types -Direct cell-mediated cytoxicity Hepatitis -Delayed-type hypersensitivity Allergic contact dermatitis Hypersensitivity pneumonitis |
| HIV Transmission | -Blood, semen, vaginal fluids, and breast milk |
| Opportunistic Infection | -Involve common organisms that do not produce infection unless there is an impaired immune function, after the first serious illness and as the immune system fails, opportunistic illnesses become progressively more severe and difficult to treat |
| Allergic Rhinitis | -Inflammation of the Nasal Muscosa |
| Influenza Vaccine | -Trivalent inactivated influenza vaccine (TIIV) Developed in the 1940s Administered by injection -Live, attenuated influenza vaccine (LAIV) Approved for use in 2003 Administered intranasally |
| TIIV | -Mainstay for prevention -Inexpensive,effective -recommended for high risk group and those unable to cope w/infection -Effectiveness of the vaccine depend on age&immunocompetence and match btw virus strains in vaccine and those during flu season |
| LAIV | -cold adapted viruses that replicate efficiently in the 25*C temps of the nasopharynx, but replicate inefficiently at the 38 degree C temperature of the lower airways It is an option for the 2-29 yo of healthy non-pregnant persons |
| Tuberculosis | -Caused by mycobacterium, -Infects any organ, lungs most frequent -Bovine or human strain -Cough/Sneeze spread infected droplets -Cell Mediated Immune Response -Hematogenous Dissemination |
| Manifestations of Hypothyroidism | -Mental and physical sluggishness -Myxedema -Somnolence -Decreased cardiac output, bradycardia -Constipation -Decreased appetite -Hypoventilation -Cold intolerance -Coarse, dry skin and hair -Weight gain |
| Signs and Symptoms of Cushing's Disease | -Altered fat metabolism -Muscle weakness -Muscle wasting -Purple striae -Osteoporosis -Derangements in glucose metabolism -Hypokalemia -Gastric acid secretion -Hirsutism, mild acne, and menstrual irregularities |
| Thyrotoxic Crisis | -Acute exaggerated manifestation of of thyrotoxicosis -Happens when the tissues have been exposed to too much TH -Most common cause - Grave's Disease |
| Hyperthyroidism | -Thyroid storm -Restlessness, irritability, anxiety -Wakefulness -Increased cardiac output -Tachycardia and palpitations -Diarrhea, increased appetite -Dyspnea -Heat intolerance, increased sweating -Thin and silky skin and hair -Weight loss |
| Hyponatremia | -Can be a result of adrenal insufficiency |
| Causes of Hypothyroidism | -Can be congenital or acquired -Congenital - develop prenatally and present at birth -Acquired - primary disease of the thyroid gland or secondary to disorders of hypothalmic or pituitary origin. |
| Causes of Acromegaly | -Most common:Somatotrope adenoma -Other causes:Excess secretion of GHRH by hypothalamic tumors, Ectopic GHRH secretion by nonendocrine tumors such as carcinoid tumors or small-cell lung cancers, Ectopic secretion of GH by nonendocrine tumors |
| Hypothalamic pituitary adrenal system | - |
| Pathophysiology of Asthma | -Genetic Atopy (allergic hypersensitivity not in direct contact with an allergen) Early vs. late phase -Environmental:Viruses,Allergens, Occupational exposure |
| Factors contributing to an Asthma Attack | -Allergens -Respiratory tract infections -Exercise- vasoconstriction -Drugs and chemicals -Hormonal changes and emotional upsets -Airborne pollutants -Gastroesophageal reflux |
| Asthma Severity | -Mild intermittent- don’t have to be treated; perfume irritation -Mild persistent- always there; doesn’t cause exacerbated symptoms -Moderate persistent- need medication; inhaler; nasal spray -Severe persistent- find out what’s causing it |
| Parainfluenza Virus | -Viral Infection of Upper Respiratory Disease |
| Bronchopulmonary Dysplasia | -Develops in premature infants who were treated with a mechanical ventilator from RDS -Symptoms: persistent hypoxemia, reduced lung compliance,increased airway resistance -Mismatch V&P -Pul. hypertension and Pul. resistance increase |
| Signs of BPD | -Barrel chest -Tachycardia -Shallow,rapid breathing -Chest retractions -Poor weight gain -Coughing -Clubbing of fingers |
| Rhinosinusitis | -develops when a viral upper respiratory tract infection or allergic rhinitis obstructs the ostia and impairs the mucociliary clearance mechanism. |
| Classifications of Rhinosinusitis | -Acute rhinosinusitis May be of viral, bacterial, or mixed viral-bacterial origin May last from 5 to 7 days up to 4 weeks -Subacute rhinosinusitis Lasts from 4 weeks to less than 12 weeks -Chronic rhinosinusitis Lasts beyond 12 weeks |
| Allergic Rhinosinusitis | -Occurrence with allergic rhinitis,Mucosal changes same Symptoms:Nasal stuffiness, itching&burning of the nose, sneezing, recurrent frontal headache, watery nasal discharge Treatment:Oral antihistamines, nasal decongestants, and intranasal cromolyn |
| Signs and Symptoms of AIDS | -Fever -Fatigue -Rash -Headache -Lymphadenopathy -Pharyngitis -Arthralgia -Myalgia -Night sweats -Gastrointestinal problems -Aseptic meningitis -Oral or genital ulcers |
| Prevention of AIDS | -Personalized risk assessment -Prevention plan -Education -Behavioral intervention |
| Life Cycle of HIV: Part 1 | 1)Attachment of HIV to CD4+ 2)Internalization&uncoating of virus w/ viral RNA and reverse transcriptase 3)Reverse transcription produces mirror image of viral RNA& double-stranded DNA 4)Integration of viral DNA into host DNA using the integrase enzyme |
| Life Cycle of HIV: Part 2 | 5)Transcription of inserted viral DNA to produce viral messenger RNA 6)Translation of viral messenger to create viral polyprotein 7)Cleavage of viral polyprotein into indiv viral proteins that make up new virus 8)Assembly&release of new virus from host |
| Phases of HIV | 1)Primary infection phase 2)Chronic asymptomatic or latency phase 3)Overt AIDS phase These happen over a period of 8 -12 years |
| Primary infection phase | -This may include fever,fatigue, myalgias,sore throat,night sweats,GIproblem,lymphadenopathy, and maculopapular rash&HA -Increase in viral replication -Symptoms appear 1-4 wks after exposure,last 7-10d -Try to start Tx in this stage |
| Chronic Asymptomatic/Latency Phase | -No signs or symptoms -Lasts about 10 years -Cell count falls from normal (800-1000) to 200 -Can develop lymphadenopathy |
| Overt AIDS phase | -CD4 cell count less than 200 -Without Tx can lead to death in 2-3 years -Greater increase for opportunistic infection and death |
| CDC HIV/AIDS classification | -Category 1: >500 cells/μL -Category 2: 200 to 499 cells/μL -Category 3: <200 cells/μL |
| Clinical Course of AIDS | -Typical:60–70% acquire AIDS 10–11y after inf -Rapid:10–20% progress rapidly&get AIDS in <5y -Slow:5–15% dont progress to AIDS for>15 years. -Longterm non:1% have been infected at least 8y,are antiretroviral naive,high CD4+&usually very low viral load |
| Consequences of CD4 Death | -Opportunistic infections -Malignant tumors -Nervous system manifestations -Wasting syndrome -Metabolic disorders |
| Most Common Opportunistic Infections | -Pneumocystis jiroveci pneumonia -CMV (cytomegalovirus) -Oropharyngeal or esophageal candidiasis (thrush) -Infections caused by MAC |
| Nervous System Manifestations | -late stages -AIDS Dementia Complex -HAND cog w/motor dys or behav/psychosocial s -HAD-impaired attention& concentration,slowing mental speed&agility,motor speed& apathetic behav -Toxoplasmosis-fever,HA, neurologic dys,confusion&lethargy, visual |
| Diagnostic Tests | -HIV antibody-least expensive, Pos=color -Western Blot-more specific, uses viral antigens, pos=# of bands -OraSure test -Polymerase Chain Reaction-detect presence of virus rather then antibody to virus - |
| Criteria for HIV Intervention | -Determined by the level of disease activity based on -Viral load -Degree of immunodeficiency based on the CD4+ cell count -Appearance of specific opportunistic infections |
| Medications for HIV | -Nucleoside reverse transcriptase inhibitors -Nucleotide analog reverse transcriptase inhibitors -Non-nucleoside reverse transcriptase inhibitors -Protease inhibitors -Fusion inhibitors |
| Reverse transcriptase inhibitors | -Inhibit HIV replication by acting on enzyme reverse transcriptase by blocking elongation of DNA chain by stopping more nucelotides from being added |
| Protease Inhibitors | -Bind to protease enzyme which prevents the cleavage of the polyprotein chain to individual proteins which would be used to construct new virus |
| Fusion Inhibitors | -Prohibit HIV from entering or fusing with the CD4 cell thus blocking the virus from inserting its genetic information into the CD4T cell |
| Graves Disease | -Caused by overstimulation of TSH |
| Atopic Dermatitis | -Itchy,inflammatory skin disorder that is characterized by poorly defined erythema w/edema,vesicles,weeping at acute stage&skin thickening at chronic stage -IG-E hypersensitivity -Presents differently in dif ages/races -Topical Steroids for acute |
| Transplantation Rejection | -Only requires T lymphocytes -Induced by:destruction of graft cells by CD8 and delayed hypersensitivity reactions triggered by CD4 -Types: Hyperacute, Acute, Chronic Host vs. Graft |
| Hyperacute Rejection | -Occurs almost immediately after transplantation -Produced by existing recipient antibodies to graft antigens initiating a type III, Arthus-type hypersensitivity reaction |
| Acute Rejection | -Occurs within first few months after transplantation with signs of organ failure; may occur months or years after immunosuppression has been terminated -T lymphocytes respond to antigens in the graft tissue. |
| Chronic Host vs. Graft Rejection | -Occurs over a prolonged period -Manifests with dense intimal fibrosis of blood vessels of the transplanted organ -The actual mechanism is unclear but may include release of cytokines that stimulate fibrosis. |
| Parainfluenza Virus | -Group of Lower Respiratory Tract Virus but manifested by the URT such as a cold |
| Squamous Cell Lung Carcinoma | -Closely related to smoking |
| Adenocarcinoma | -Most common in North America -More common in women and nonsmokers -Origin in bronchiolar or alveolar tissues -More peripherally located -Associated with scarring -Poor stage to stage progression |
| Small Cell Carcinoma | -Small round, to oval cells -Highly malignant -Strongest association with cigarette smoking -Infiltrate widely, disseminate early, rarely resectable |
| Large Cell Carcinoma | -Large polygonal cells -Spread early in development -Occur in periphery of lung -Invade bronchi and larger airway -Poor prognosis because of early spread |
Created by:
prettyinpink7
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