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101 Cards in this Set
- Front
- Back
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Idiopathic |
Cause of infection is unknown |
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Iatrogenic infection |
infection caused by medical treatment |
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Acute infection |
short term infection
many times is more severe but with sudeen onset and short duration |
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Nosocomial infection |
infection obtained while in healthcare setting |
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Communicable disease |
contagious |
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Insidious disease and give example |
disease with no sysmtoms until opportunity presents itself
ex) AIDS |
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Epidemiology |
Study of the disease in the population |
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Mortality |
death rate |
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Morbidity |
How the disease affects the individual |
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Prevalence |
rate of disease in population |
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Incidence |
the occurrence, rate or frequency of a disease |
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Hypertrophy and give example |
overgrowth of a muscle cells
ventricular hypertrophy |
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Hyperplasia |
overgrowth of cells |
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Metaplasia and who does this happen to? |
change from one cell type to another cell type
Smokers will see this due to chronic irritation of the airway, this eventually leads to cancer |
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Dysplasia |
Deformed cells, precursor to cancer |
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Atrophy |
Loss of growth |
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Benign Vs Malignant |
Benign: slow growing encapsulated mass of differentiated cells. similar to normal cells with fairly normal mitosis. remains localized and life threatening if in brain. Malignant: rapidly growing anaplastic cells that invade nearby tissue and spread through blood and lymph system. |
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Anaplasia |
undifferentiated and overgrowing cells without form aka CANCER |
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Hypoxia |
low levels of oxygen to an area -usually, but not always, due to ischemia
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Ischemia and what are its affects |
overall lack of blood flow to an are -can cause cardiac ischemia, mesenteric ischemia, stroke -Infarcted: when cells have been deprived of oxygen for too long and there is cell death -huge problem in heat and CNS because those cells don't recover |
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What is Apoptosis? |
Programmed cell death |
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What is Necrosis and what are the different types (6)? |
Cell death 1. Liquefaction: liquified tissue from enzymes 2. Coagulative: dead tissue retains form 3. Fat: broken down fatty acids (induce inflammation) 4. Caseous: cheesy 5. Infarction: cell death from hypoxia 6. Gangrene: bacterial infected necrotic tissue |
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What are the 6 types of Exudate? |
1. Serous: clear yellow fluid 2. Fibrinous: fibrin (clotting factor) 3. Purulent: "Pus" - many dead WBCs 4. Abcess: "walled off" to protect health areas. Ucusually needs to be I&D 5. Hemorrhagic: compromised artery/vein resulting in blood collection 6. Necrotizing Faciitis: skin eating disease |
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What are 4 types of healing? |
1. Keloid: hypertrophic scar tissue formation 2. Contracture: joints and visceral organs not properly sliding 3. 1st intention healing: sutured, small scar 4. 2nd intention healing: open, bigger scar |
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Acute vs Chronic Inflammation |
Acute: massive swelling and exudate Chronic: more lymphocytes and marcophages, potential for larger scar |
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What are 2 medications for inflammation? |
1. NSAIDs: block inflammatory process by blocking COX2 inhibitor ex) Aprin, ibuprogen, naproxen, Celebrex 2. Coricosteroids - more potent than NSAIDs, block immune response by decresing cap perm, leukocytes, histamine Adverse: osteoporosis, catacracts, skin thinning, increased risk of infection Nurse imp: patients with diabetes Seen in: back injury's, COPD, asthma
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What are the steps in innate (non-specific) Immunity? |
1. Injury 2. Cells release histamine 3. Histamine increases vasodilation and ICP 4. Leukocytes move to site of injury due to chemotaxis 5. Phagocytosis occurs - removal of debris in preparation for healing -Specifically: Macrophages engulf debris thus initiating specific immunity
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Major players in Non-specific (innate) immunity? |
-Inflammation: -Complement: -Phagocytosis: |
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Players in specific (adaptive) immunity? |
Humoral: B-cells (mature in bone marrow) - Plasma cell: Ig producing B-cell - B-lymphocyte: Effective against bacteria/viruses outside of cell - B-memory cell: activate Ig production Cell-mediated: T-cells (mature in thymus) -seek out and destroy antigen infected cells -T-lymphocytes: effective against virus, fungal, protozoal, cancer and transplanted tissue |
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What are the 5 different types of Antibodies (aka Ig's aka Immunoglobulins)? |
1. IgG: Most abundant. Important in 2nd reponse. large activator of complement. 2. IgM: large protein bound to B-cells. "first responder". large activator of complement. Important in 1st response. 3. IgA: tears, secretions, colostrum 4. IgE: Mast cells, release of histamine (allergic reactions) 5. IgD: bound to B-cells |
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What are the 4 different types of T-cells? |
1. T-helper: coordinate specific immunity crucial in B, T and macrophage activation 2. T-killer: destroy infected cells (cytotoxic) 3. T-memory: activated with second response 4. Natural Killer: destroy foreign cells (cancer) wtihout activation
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The 3 lines of Immunity Defense? |
1. Phagocytosis: Marcophages engulf antigen and present to bone marrow where specific immunity is activated. 2. Complement system: activates inflammatory response 3. Specific immunity: Macrophages, B-cells, T-cells |
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What are the different types of Immunity? |
Active: body undergoes immune response and makes B and T-memory cells -Natural: acquired through illness -artificial: vaccination Passive: "borrowing" someone else's Ig's. body does not make antibodies. -Natural: placenta or breast milk -antivenin, rabies shot, RhoGham (expt. mom)
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Name the 4 different types of Immune reponse |
1. Type I: Allergic reaction 2. Type II: Cytotoxic (ABO incompatibility) 3. Type III: Ag-Ab complex (immune complex) 4. Type IV: Cell mediated/delayed hypersensititivy |
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Type I: Allergic reaction |
-IgE mediated mast cell reaction (histamine) -Results in: VD (causing low BP), cap perm, edema, airway obstruction, hypoxia. allergies, anaphylaxis -Caused by: stings, nuts, shellfish, antibiotics, anesthetics -Nursing Imp: Anaphylaxis due to low BP and bronchial edema (swelling) can both be life threatening early signs/Sx: pruritus, tingling, soughing, SOB Late signs/sx: dizziness, fainting, low bp, hives, edema |
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Treatments for Type 1 Allergic reactions |
Epinephrine = vasoconstrictor
Diphenhydramine = antihistamine
Glucocorticoids = decrease immune response
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Type II: Cytotoxic (ABO incompatibility) |
-Blood typing - the type of antigen (or lack of) on RBCs determines your blood type - If incompatible blood is transfused then hemolysis occurs -Signs/sx: SOB, CP, diaphoresis, Jandice -Can result in death |
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Type III: Ag-Ab complex (immune complex) |
-Occurs when Ag-ab complex fails to be removed after phagocytosis and debris is deposited into tissue, this then results in complement activation causing damage to host tissue/organ -Causes: Serum sickness, post-strep, rheumatic fever -Rheumatic fever: when strep isnt properly treated and heart tissue is damaged causing lifelong heart murmurs. -Autoimmune disorder: Lupus, Rheumatoid arthritis, MS |
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Type IV: Cell Mediated/delayed hypersensitivity |
-Mediated by T-cells when they become sensitized to antigens causing cell destruction through cytokines -Causes: contact dermatitis (latex, nickel, poison ivy), Graft host reaction (transplant rejection), positive TB test -Chest X-ray ordered if + TB test |
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Patho and treatment of burns: |
-Hypovolemia shock: fluid loss in one part of body due to massive fluid shift to injured area causing BP to drop. Respiratory: always look at patient airway to see if they inhaled burn Pain: immense due to skin nerve endings Infection: Beware due to 2nd intention healing Metabolic needs: patient needs high calorie/protein diet Nurse Implication: kidney failure possible due to increased protein in blood, need to check heart in the case of electrical burn, if hands/face affected >5% then patient transferred to burn unit
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What are the 3 classifications of Burns? |
1. Superficial thickness (1st degree): doesn't penetrate past epidermis, no blisters, resolves quickly (ex = sunburn) 2. Partial thickness (2nd degree): complete epidermis penetration and partial dermis penetration resulting in blistering (may leave scar and may mean increased risk of cancer) 3. Full thickness (3rd degree): damage all the way through dermis and going into connective tissue (result in permanent disability) |
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parkland formula |
determines how much fluid to give patient to prevent hypovolemia - uses the "rule of nines" |
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Local vs Systemic infection |
Local: redness, warmth, swelling, edema, pain, loss of function Systemic: pyrexia (fever), malaisa, fatigue, HA, anorexia |
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Gram + vs Gram - treatment |
Broad Spectrum: antibiotic effective against both Gram + and - bacteria Narrow spectrum: effective against either gram + or - bacteria |
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What immune cell is Primarily affected, why does this cause such a huge problem and can HIV be destoryed? |
-Infect T-helper (CD4) cell of host -Problem because once there is T-cell proliferation Killer T-cells start destroying T-helper cells resulting in severe immunodeficiency leaving door open for opporunistic infections -HIV can't be destroyed but AntiVIrals can be given to control viral reproduction |
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Spreading of cancer |
Invasion: local spread where tumor grows into adjacent tissues and destroys normal cells Metatasis: spreading via blood/lymph -"hot nodes" = cancer containing nodes Seeding: movement of neoplastic cells in body fluids or along membranes usually in cavity. -can also occur iatrogenically |
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Cancer risk factors: |
genetics, viruses, radiation, chemicals, biological, age, diet, hormones
These can be modifiable vs. nonmodfiable |
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TNM Cancer staging |
-determines extent of disease and is monitored through out the course of the disease. -basis for treatment and prognosis T: size of primary Tumor N: extent of regional Node involvement M: signs of Metatasis |
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What does "CNC with Diff" mean and what should the normal total be? |
Complete blood count with White Blood Count differential
4,500-10,500/mm^3 |
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What is a Neutrophil and what should normal differential % be? |
-Type of granulocyte (WBC) - usually in response to bacteria
-57-70% |
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What is a lymphocyte and what should normal differential % be? |
-type of agranulocyte (WBC) examples) B and T-cells
-20-25% |
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What is a Eosinophil and what should normal differential % be? |
-type of granulocyte involved in allergic reactions
-2-4% |
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What is a Monocyte and what should normal differential % be? |
-Agranulocyte that floats around in blood but once diapedesis occurs they are then called macrophages
-suggest infection recovery
-3-8% |
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What is a basophil and what should normal differential % be? |
-Granulocyte: histamine releasing phagocyte involved in allergic reactions
-0.5% -1% |
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What are the 2 types of WBC's? |
Granulocytes: -Neutrophil -Basophil -Eosinophil
Agranulocytes: -Lymphocytes -Monocytes |
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Negative vs Positive feedback loop (give example for positive) |
Negative: output of system acts to keep homeostasis Positive: output unable to keep homeostasis ex) heart failure
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Diagnosis |
what we do when some presents: Signs -things we see and symptoms- things patient tells us |
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Etiology |
what caused the disease |
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Pathogenesis |
the process of the disease |
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Syndrome and give example |
compilation of signs and symptoms ex) AIDS |
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Brain and heart death |
Brain (aka somatic death) = 5 mins -important for organ procurement Heart =30 mins |
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What is pyrexia (fever) caused by? |
Pyrogens |
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Leukocytosis |
Elevated WBCs (especially neutrophils) |
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Differential Count |
Proportion of WBCs altered |
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What does an elevated ESR suggest? |
An elevated rate means sedimentation is slower |
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Presence of ALT |
isoenzymes suggesting liver damage |
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Presence of AST |
isoenzymes suggesting something is damaged but usually either liver or cardiac |
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Presence of CK-MB |
Isoenzymes suggest cardiac damage |
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Explain why there would be more lymphocytes than macrophages in chronic inflammation? |
There isnt a need for macrophages because the antigen has already been identified and now the B and T-cells are taking over. |
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The three "R"s of cellular healing and what are the exceptions |
1. Resolution - heals quick with minimal damage 2. Regeneration - tissue regenerated with new cells 3. Replacement - original cells can't regenerate resulting in scar tissue - Cardiac, Nerve and burn tissue |
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which important chemical mediators do macrophages secrete and what do they do? |
Interleukins and monokines - stimulate lymphocyte production, communicate between cells |
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Titer |
level and functionality of Ig's in serum |
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Autoantibodies |
Antibodies against own tissue |
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Explain Systemic Lupus erythromatosis |
-Autoimmune disorder resulting in "wolf skin" -butterfly rash on face -ischemia results in tissue/organ destruction Nurse imp: treated with steroids -Can be tested by taking Anti-DNA titer or ESR |
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ANA diagonostic test |
Tests for autoimmune disease -Anti-nuclear antibody -not good indicator b/c 40% of people come up + |
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You become HIV positive when: |
body has detected HIV and made antibodies to virus |
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Primary vs secondary immunodeficiency and give examples |
Primary: basic development failure Ex) Hypogammaglobulinemia - not enough proteins to produce Ig's Secondary: acquired through lifespan ex) splenectomy, malnutrition, liver disease, immunosuppresive drugs, stress, HIV, HPV |
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HIV tests |
PCR - Polymerase chain reaction blood testing - if that is + then western blot test done |
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When is there an AIDS diagnosis |
HIV with the presence of opportunistic infection |
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Prokaryotic |
bacteria lacking nucleus |
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Name 3 different kinds of Cocci bacteria and infection they cause |
1. Staph (clusters) - staph 2. Strep (chains) - ears, nose, throat 3. Diplo (pairs) - pneumonia |
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Capsule/slime layer |
protection against immune recognition |
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Cilia |
hair like structures for mobility |
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Pili/fembriae |
-hair like structures to cling to other bacterium -sex pili: used to transfer DNA (often used for transferring antibiotic resistance) |
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2 types of bacteria toxins |
-Exotoxins: secreted by bacteria during metabolim -Endotoxins: in cell wall and released upon bacteriums death |
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Viron |
what a virus is called when its outside of host cell |
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Treatment of viral infections |
Antivirals and Interferons |
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Fungi (yeast/mold) |
-Eukaryotic -Nurse imp: seen a lot on diabetics -Can be beneficial: yogurt, penicillin |
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Protozoa aka parasites cause: |
trichamoniasis, malaria, dysentery |
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Vent protocol |
patient taking prophylactic to prevent nosocomial infection |
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What is host resistance what is very important in defense against viruses? |
-ability of patient to resist invader -interferons |
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Pathogenesis |
capacity of microbe to cause disease |
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Virulence |
Degree of pathogencity based on: 1. invasive quality 2. Toxic quality 3. Adherence to tissue 4. Ability to avoid host |
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What does a gram stain/culture tell us? |
tells us what microbe |
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Sensitivity testing |
tells us how to treat |
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What are the 7 chemical mediators of tissue injury and what do they do? |
1. Histamine 2. Chemotactic factor 3. Kinins 4. Cytokines 5. Leukotrienes 6. Prostaglandins 7. Complement system they all increase fluid to area |
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Histamine |
-"early bird" - causes: vasodialation, increased IVP |
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Chemotactic factors |
-attract WBC/leukocytes to area |
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kinins |
-cause pain, chemotaxis, vasodilation, Increased IVP |
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Cytokine |
-released from T-cells -cause: fever |
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2 delayed mast cells that are made from arachidonic acid |
Leukotrienes and Prostaglandins |
