Exam 2 Flashcards
classification of hyper sensitivity reactions
source of antigen, time (immediate or delayed), immunological mechanism causing tissue injury
types 1 2 and 3 sensitivities are
immediate, humoral immunity, and mediated by antibodies
type 4 sensitivity is
delayed, cell mediated immunity, and are mediated by T-cells and don’t involve antibodies
type 1 immune responce
IgE mediated reaction, from exposure to allergen, person becomes sensitized to allergen, IgE attaches to mast cells and basophils (chemical mediators of inflammation are released on second exposure), plasma cells produce the antibodies
type 1 reactions local
skin wheal localized (pale w/ fluid surrounded by reddened area) ex. mosquito bite
type 1 reactions systemic
anaphylaxis, occurs in minutes, can lead to airway obstruction and vascular collapse, initial itching and edema at site of exposure
manifestations of anaphylaxis
watery red eyes, bronchial edema (wheezing), dilated pupils, weak thread pulse, angioedema, cyanosis (first in finger tips and lips) shortness of breath
treatment of anaphylaxis
epinephrine, diphenhydramine (Benadryl), hydrocortisone, O2, IV fluids, H2 receptor blocker
type 1 atopic reactions
inherited tendency to become sensitized to environmental allergens, ex. allergic rhinitis asthma urticaria (hives) angioedema, atopic dermatitis
allergic rhinitis
hay fever, can be year round (dust mold animal dander), can be seasonal (pollen from grass weeds or trees), affects the eyes and respiratory tract (rhinorrhea= runny nose, lacrimation, mucosal swelling w/ airway obstruction, pruritus= itching)
atopic dermatitis
chronic skin disorder, increase IgE levels, skin lesions more generalized then wheal, blood vessels dilate and cause tissue edema
urticaria
cutaneous reaction to allergens, wheals (pink raised edematous pruritic), vary in shape/size, spread over body, after exposure to allergen, may last minutes or hours, hives
angioedema
localized skin lesions, like hives but deeper, effects eyelids lips tongue larynx hands/feet GI tract and genitalia
lab tests for type 1
eosinophil level elevated, eosinophils in sputum nasal and bronchial secretions, elevated IgE levels, ELISA test for IgE antibodies to allergens when skin cant be tested
type 2 immune response (examples and categories)
cytotoxic (cell toxic) and cytolytic (cell breakdown), Examples: hemolytic transfusion reaction, goodpasture syndrome, immune thrombocytopenic purpura, graves disease, RH incompatibility reaction, autoimmune and drug related hemolytic anemia
type 2 reactions (how it works)
tissue specific IgG/ IgM mediated, immunoglobulins attach to antigen on cell surface, mistakenly identifies normal cell as foreign and destroys target cell (normally WBC RBC or platelets), this antigen-antibody complex activates the complement system (results in cytolysis or phagocytosis)
type A blood is compatible with
type A or O
type B blood is compatible with
type B or O
type AB blood is compatible with
type A, B, AB, or O
type O blood is compatible with
only type O
Type O is the
universal donor
Type AB is the
Universal recipient
Incompatibility reaction (acute hemolytic reaction)
antibodies coat the foreign blood cells causing agglutination, this causes small blood vessels to be blocked which uses up clotting factors which can cause bleeding, within hours neutrophils and macrophages phagocytize the clumped cells
hemolytic transfusion reactions
as the cell dies it releases hemoglobin into the urine and plasma
manifestations of transfusion reaction
chills/fever, backache/ headache, flushing, apprehension, chest pain, increased pulse and RR, dyspnea, hypotension, hemoglobinuria, jaundice, dark urine, bleeding, acute kidney injury (increase BUN creatinine), shock, cardiac arrest
delayed hemolytic reaction
more than 24 hours after transfusion to 14 days after, fever chills mild jaundice and decreased hemoglobin, no acute treatment needed, may need another transfusion
febrile blood transfusion reaction
leucocytes incompatibility, occurs in minutes to hours, fever chills Nausea flushing tachycardia anxiety
bacterial infection from blood transfusion
caused by contaminated blood products, occurs in minutes to less than 24 hours, tachycardia hypotension fever chills and shock
allergic reaction from blood transfusion
hypersensitivity to plasma proteins in donors blood, occurs immediately or within 24 hours, mild urticaria itching flushing, can progress to anaphylaxis (hypotension, dyspnea, decreased O2 sat, flushing)
transfusion related acute lung injury TRALI reaction
reaction between transfused anti-leukocyte antibodies and recipients leukocytes leading to pulmonary inflammation and edema, can cause fever hypotension tachypnea dyspnea decreased O2 sat and frothy pinky sputum
circulatory overload reaction
fluid given faster than pt can tolerate, slow administration to pts at risk, administer furosemide (lasixs) between units, signs & symptoms include: cough dyspnea adventitious breath sounds, h/a, HPTN, increased HR and JVD
type 3 immune complex reactions
antigens combine w/ antibodies that are deposited in tissue or small blood vessels, they cause release of chemotactic factors that lead to inflammation and destruction of the involved tissues, can be local or systemic (immediate or delayed), common sites are kidneys skin joints blood vessels and lungs, associated with acute glomerular nephritis SLE and RA
type 4 hypersensitivity reaction
delayed reaction (contact dermatitis-tb test, microbial hypersensitivity reactions, transplant rejection), cell-mediated immune response, sensitized t lymphocytes attack antigens and release cytokines, 24- 48 hours for response to occur
signs and symptoms of contact dermatitis
inflamed red vascular lesions, itching, burning, stinging, scratching causes spread
latex allergies
can come into contact directly or through air, cross sensitivity to some foods (bananas kiwi avocados chestnuts potatoes tomatoes grapes hazelnuts peaches apricots), can be either type 1 or type 4 reaction, greater risk with multiple exposure family history hay fever asthma
autoimmunity
immune response against self, could be inherited tendency, typically starts with a trigger, if a person has one autoimmune disease they are more likely to have another
Microorganisms and Human Relationships
Mutual (Normal flora, relationship can be breeched by injury) and Opportunistic microorganisms
Pathogens cause disease in human host cells by:
Direct destruction of host cell by pathogen, interference with the host cell’s metabolic function, and rendering a cell dysfunctional by accumulation of pathogenic substances and toxins
Infection
A state of tissue destruction resulting from invasion of microorganisms
Pathogenicity
Virulence, Infectivity, Toxigenicity, Antigenicity, Antigenic Variability, Pathogenic Defense Mechanism, Coinfection, Superinfection
Type of Pathogens
Obligate- requires the host for metabolism and reproduction
Faculative- live on the host, but can survive independently EX: worms
Classes of Infectious Microorganisms
Bacteria, Viruses, Rickettsiae, Micoplasms, chlamydiae, Fungi, and Protozoa
Bacteria Class
Cocci, Bacilli, Spirochetes, Gram Stain
Positive Gram Stain
No decolorization with alcohol, infection of respiratory tract and soft tissues Ex: Steptococcus Pneumoniae
Negative Gram Stain
Decolorization with alcohol, infections of Genitourinary and GI tract Ex: E. Coli
Bacterial Resistance to Lines of Defense
Production of thick capsules of carbs or proteins, Exotoxins (proteins released during bacterial growth), and Endotoxins (released during lysis or destruction of the bacteria)
Complications of Infection
Septicemia (when microoganisms gain access to the blood and circulate throughout the body), Bacteremia (when septicemia is caused by bacteria), Septic Shock (process of systematic vasodilation due to severe infection, usually gram -, decreased BP, decreased O2 delivery)
Viral Disease
Requires a host cell, 6 phase of replication, latency (cold sores), not sensitive to antibiotics or normal defense mechanisms
Fungal Disease
large thick walled microoganisms, yeast/mold, mycoses-(diseases caused by fungi), Dermatophytes- (fungi that invades skin, hair, or nails)
Yeast- opportunistic, candida albicans
Modes of Transmission
direct contact, droplet transmission, airborne transmission, vector transmission
Local Manifestations of Infection
heat, incapacitation, pain, edema, redness, lymphadenitis, purulent exudate
Systemic Manifestations of Infection
Fever, weakness, headache, malaise, anorexia, nausea
Counter measures against Pathogenic Defenses
Live Virus (attenuated), Inactivated (killed), toxoid- purified toxins that have been chemically detoxified w/o loss of immunogenicity
Community-associated infections
An infection that is acquired by a person who has not been hospitalized or had a medical procedure within the past year
Healthcare-associated infections
Contracted in a hospital or institutional setting, were not present or incubating in the pt on admission, more difficult to treat because is often drug resistant, MRSA most common, prevent by using disinfectants and antiseptics
Pneumonia types
can be community required pneumonia, hospital acquired pneumonia, pneumococcal pneumonia, and viral pneumonia
pneumonia pathophysiology
infectious process, respiratory droplet spread, causes inflammation in the lungs, occurs commonly in the bronchioles interstitial lung tissues and/or the alveoli
pneumonia clinical manifestations
fever, chills, cough, sputum production, fatigue, loss of appetite, hemoptysis (cough up blood), dyspnea, tachypnea tachycardia, pleuritic pain, crackles in lungs
acute bronchitis
acute infection or inflammation of airways or bronchi, commonly follows viral illness, can hear wheezes or crackles in upper airways
treatment: aspirin humidity and cough suppression
anti-infective
any medication effective against pathogens, classified by susceptible organisms chemical structure and mechanism of action
empirically
to treat known or suspected infection by a particular organism
prophylactically
to prevent infection (ex. before surgery)
list beta lactam antibiotics
penicillins, cephalosporins, carbapenems, monobactams
list non-beta lactam antibiotics
macrolides, quinolones, aminoglycosides, tetracyclines, sulfonamides
drugs that inhibit cell wall synthesis
Penicillin, Cephalosporins, Carbapenems, Monobactams, and Vancomycin
drugs that inhibit protein synthesis
Macrolides, Ketolides, Tetracyclines, Aminoglycosides
drugs that inhibit bacterial DNA replication
Fluroquinolones and miscellaneous antibacterials (bacitracin, metronidazole (Flagyl), polylmyxin, rifampin, telithromycin)
drugs that inhibit folic acid production
sulfonamides
drugs that disrupt the fungal cell membrane
azoles
Methicillin-resistant Staphylococcus aureus (MRSA)
Resistant to certain antibiotics, At least 60% of MRSA infections resistant to penicillin, Most often acquired in hospital, Usually occurs in patients with weakened immune systems, Still sensitive to vancomycin, Ones that are resistant to vancomycin may have susceptibility to linezolid (Zyvox)
Vancomycin-resistant Enterococci (VRE)
Enterococci found in GI tract female genital tract wounds and pressure ulcers,Therapy options are limited: vancomycin is only antibiotic effective against multidrug-resistant VRE strains, Newer antibiotics are being used when resistant to vancomycin
natural penicillins
penicillin G (IM or IV) and penicillin V (PO use)
subgroups of penicillins
Aminopenicillins (amoxicillin, ampicillin), Extended-spectrum (eg. Ticarcillin IM or IV, piperacillin, ticarcillin, carbenicillin), Penicillinase-Resistant (cloxacillin, dicloxacillin, nafcillin, oxacillin)
chemicals that inhibit beta-lactamase
Clavulanic acid, Tazobactam, Sulbactam
These chemicals bind with beta-lactamase and prevent the enzyme from breaking down the penicillin, thus making the drug more effective
Penicillin–beta-lactamase inhibitor combination drugs
Ampicillin + sulbactam = Unasyn
Amoxicillin + clavulanic acid = Augmentin
Ticarcillin + clavulanic acid = Timentin
Piperacillin + tazobactam = Zosyn
penicillin indications
used to treat or prevent infections from gram + bacteria
penicillin adverse effects
risk for allergic reaction, cross sensitivity to other beta lactams, can cause N/v diarrhea bone marrow suppression and abdominal pain
penicillin interactions
NSAIDS, Oral contraceptives, warfarin
Cephalosporins
Similar to penicillin, Assess if there is an allergy to penicillin (cross-sensitivity), Five groups or generations,Well absorbed from the GI tract Metabolized in the liver excreted in the urine, Adverse Effects:
mild diarrhea abdominal cramps rash pruritus redness edema, Drug-to-Drug Interactions: Aminoglycosides oral anticoagulants ETOH (alcohol)
Cephalosporins: First generation
Good gram-positive coverage
Parenteral and PO forms
Examples: Cefazolin (Ancef), Cephalexin (Keflex)
Cephalosporins: Second generation
Good gram-positive coverage, Better gram-negative coverage than first generation
Examples: cefaclor – (Ceclor)
Cephalosporins: Third generation
Most potent group against gram-negative bacteria, Less active against gram-positive bacteria
Examples: Ceftriaxone (Rocephin) IV and IM, long half-life, once-a-day dosing, Can cross BBB
Cephalosporins: Forth generation
Broader spectrum than third generation,Uncomplicated and complicated UTI
Example: cefepime (Maxipime)
IM or IV only, Can cross BBB
Cephalosporins: Fifth generation
Example: Ceftaroline (Telfaro)
Broader spectrum of antibacterial activity, Effective against MRSA
Carbapenems
broad-spectrum, Reserved for complicated body cavity and connective tissue infections, *May cause drug-induced seizure activity, All given parenterally, Cross sensitivity reaction if client is allergic to PCN or cephalosporins
Examples: imipenem/cilastatin (Primaxin), Cilastatin inhibits an enzyme that breaks down imipenem, meropenem (Merrem), ertapenem (Invanz), doripenem (Doribax)
Imipenem-Cilastin (Primaxin)
Indications: gram positive and negative microbes, aerobic and anaerobic, some strains of MRSA, Route: IM and IV, Half Life: short requires dosing every 6 hours. Adverse Effects: nausea, vomiting diarrhea and rash. Confusion and seizures rare but serious.
Monobactam
Example: aztreonam (Azactam)
Primarily active against aerobic gram-negative bacteria (E. coli, Klebsiella spp., Pseudomonas spp.) Bactericidal, Parenteral use only, Used for moderately severe systemic infections and UTIs
Tetracyclines
Affect Bacterial Protein Synthesis
Examples: tetracycline, doxycycline (Doryx, Vibramycin)
Indications
Interaction with milk, antacids, iron salts and calcium, oral contraceptives, Avoid in pregnancy and lactation and pediatric clients (due to effect on bones and teeth, Alteration in intestinal flora may result in: Superinfection (overgrowth of nonsusceptible organisms such as Candida), Diarrhea, Pseudomembranous colitis
*Caution patients about photosensitivity
Macrolides
Affect Bacterial Protein Synthesis
Examples: erythromycin (E-mycin, E.E.S, others) and azithromycin (Zithromax)
Considered bacteriostatic, Used to treat: Strep infections Mild to moderate URI and LRI Haemophilus influenzae Spirochetal infections Syphilis and Lyme disease Gonorrhea, Chlamydia, Mycoplasma, Will cause increased serum level of digoxin,Taken on an empty stomach, Adverse Effects: N/v diarrhea hepatotoxicity jaundice anorexia
Ketolide
Affect bacterial protein synthesis, Example: telithromycin (Ketek)
Better antibacterial coverage than macrolides, Active against gram-positive bacteria, Associated with severe liver disease, Use is limited
Aminoglycosides
affect bacterial protein synthesis, Examples:gentamicin (Garamycin), neomycin (Neo-fradin), tobramycin (Nebcin), amikacin (Amikin)
Bactericidal, against gram-negative aerobic bacteria causing cell death, Given IM or IV Exception: neomycin which is given orally to decontaminate the GI tract before surgical procedures, Can cause Nephrotoxicity or
Ototoxicity- need to do peak and trough to monitor toxicity, Drug-to-Drug Interactions: Diuretics neuromuscular blockers
Fluroquinolones
Inhibit bacterial DNA replication (don’t effect human cells), Examples: ciprofloxacin (Cipro), levofloxacin (Levaquin), moxifloxacin (Avelox)
against gram - bacteria, respiratory infections and STDs, Adverse effects: Headache fatigue N/V diarrhea thrush Prolonged QT interval arrthymias, Black box warning: increased risk of tendonitis and tendon rupture
QT say no to OB
Quinolones and tetracyclines can’t be used in pregnancy
Ketolides
Lincosamides
Metranidazole
(Example: telithromycin (Ketek))
(Example: clindamycin); more toxic
(Flagyl)
Oxazolidinones
Example: Linezolid (Zyvox)
Inhibit bacterial protein synthesis
Indications: Hospital Aquired Pneumonia, VRE (vancomycin resistant enterococus), MRSA of skin, Community aquired Pneumonia
Adverse Effects: Headach, N/v, diarrhea, decreased platelet count
*May cause hypotension, serotonin syndrome if taken with SSRIs, and reactions if taken with tyramine-containing foods
Lipopeptide
Daptomycin (Preg. Cat. B)
Effective for Methicillin Resistant Staph Aureus (MRSA), VRSA,VRE
Bacteriocidal
Streptogramins
Quinupristin/dalfopristin ( Synercid)
30: 70 combination (work synergistically), Used for bacteremia and infections caused by vancomycin-resistant Enterococcus (VRE) and other complicated skin infections, May cause arthralgias, myalgias
- Preg. Cat. B
Sulfonamides
inhibit the formation of bacterial folic acid/Bacteriostatic,
Combination with non sulfonamide=Sulfamethoxazole/ Trimethoprim (Bactrim, Septra, SMX-TMP - to treat UTI)
Sulfasalazine – ulcerative colitis and rheumatoid arthritis, Allergic reactions fairly common, Can’t use when pregnant
Adverse effects: Hemolytic and aplastic anemia, Photosensitivity, exfoliative dermatitis, Stevens-Johnson syndrome, epidermal necrolysis, crystalluria
Vancomycin
PO or IV, treat MRSA and gram +, may need peak and trough, should be infused over an hour, Adverse Effects:
Ototoxicity Nephrotoxicity fever chills hypotension erythema of neck and back (Red man syndrome)
Pregnancy Category B for PO; C for injection
Urinary Antiseptics
Examples: Nitrofurantoin(Furadamtom), Nitrofurantoin Macrocrystals (Macrobid, Macrodantin)
Encourage hydration, May change urine to a brown color
Disease that respond to antiviral meds
Influenza A and some respiratory viruses, herpes virus, cytomegalovirus, Ebstein-Barr, varicella zoster, HIV AIDS, hepatitis B
HSV type one, HSV type 2, CMV, varicella zoster, Epstein Barr virus
Oral herpes, genital herpes, activates when immune system is down, shingles, mono
Drugs used to treat herpes
Systemic: acyclovir, famciclovir, ganciclovir, and valacyclovir
Topical: docosanol
Acyclovir
Suppresses HSV 1 and 2, IV PO or topical, adverse effects IV: nephrotoxicity and neurotoxicity, valacyclovir is the prodrug
Ganciclovir
Treat CMV, given prophylactically (organ transplant pts), toxicity is bone marrow suppression, adverse effects: GI effects headache parenthesis neuropathy, can be toxic to kidneys, avoid in pregnancy and location
why give antiviral medications for the flu
Prevention and decreases severity of the flu
Drugs used for influenza
Amantadine, oseltmavir, ribavirin(category x), rimantidine, zanamivir (inhaled)
Amantadine
Adverse effects: CNS effects like insomnia dizziness and confusion, excreted by kidneys, avoid alcohol, also used to treat Parkinson’s, ramantidine has a longer half life
Oseltmavir
Active against influenza A and B, must be started within 48 hrs of symptoms, can shorten duration of illness, should not be used within two weeks of live attenuated vaccine, side effects: n/v and diarrhea
Adverse effects and contraindications of systemic antifungals
Hepatotoxicity, nephrotoxicity, bone marrow suppression, rash GI distress, phlebitis
Pregnancy, lactation, hepatic dysfunction or failure, bone marrow suppression, prolonged QT interval
oral candidiasis is also called
thrush
Amphotericin B
given IV topical or oral, adverse effects: fever chills vomiting headache phlebitis ototoxicity nephrotoxicity hypokalemia hypomagnesaemia, need to pretreat to prevent adverse effects, used for systemic fungal infection
fluconazole
inhibits cell replication, can cause increase AST and ALT, interacts with many drugs due to hepatic enzyme metabolism but also hypoglycemic agents
onochomycosis
toe or nail fungus, treated with terbinafine itraconazole fluconazole
grizeofulvin
prevents reproduction of fungi, 2-4 week treatment, avoid during pregnancy, can cause neutropenia
terbinafine
used topically to treat superficial infections, used orally to treat fungal infections of nails
nursing considerations when giving antifungals
baseline blood counts, baseline liver and renal function tests
Premedicate monitor VS during infusion and monitor for adverse reactions when giving amphotericin B
Metronidazole
antiprotozoal, used for dysentery venereal disease peritonitis bacterial septicemia H. pylori, given PO IV and topical, monitor liver document stools take with meals avoid alcohol inform client of dark red/brown urine
Nystatin
Works by causing altered fungal cellular metabolism, Used topically for candida diaper rash, Used orally to prevent candidal infections in the immunocompromised population, Used for treatment of oral candidiasis
_______is released in response to cell injury and is metabolized by ______ or _____ leading to _______
Arachidonic acid,Leukotriene or Prostaglandin Pathway, Both lead to inflammation
Inflammation is mediated by endogenous compounds such as
Proteins of the complement system, Histamine, Serotonin, Bradykinin, Leukotrienes, Prostaglandins
anti-pyretic
drug that reduces fever
analgesic
drug that reduces mild to moderate pain, non-opioid or opioid
Anti-inflammatory drugs
NSAIDS- treat moderate pain fever and inflammation (inhibits Leukotriene and Prostaglandin Pathways), Corticosteroids
NSAIDS inhibition of COX
Reduces pain and inflammation, Reduces the gastro-protection of prostaglandins in the stomach, Decreases platelet aggregation ( and therefore increases the risk of bleeding), Reduces temperature by causing peripheral vasodilation and sweating
nonsteroidal anti-inflammatory drugs (NSAIDs)
Aspirin is a first-generation salicylate, Originally derived from willow bark, is an Analgesic anti-inflammatory antipyretic and anticoagulant, Works by suppressing synthesis of prostaglandins by inhibiting cyclooxygenase (COX), Has adverse effects on GI mucosa
Aspirin
Class: salicylate, MOA: blocks or inactivates cyclooxygenase which inhibits prostaglandin synthesis in CNS & peripheral tissues, Uses: mild to moderate pain, fever, inflammatory conditions (arthritis), prophylaxis of stroke and heart attack (suppression of platelet aggregation), Adverse effects: Nausea heartburn bleeding tinnitus nephrotoxicity hepatotoxicity
Aspirin contraindications and overdose
Contraindications: Can’t be given to children under 19 b/c risk of Reye syndrome renal impairment pregnancy within one week of surgery or vitamin K deficiency, Overdose can cause: Tinnitus Metabolic acidosis Hyperventilation Respiratory alkalosis Dehydration Agitation N/v
Salsalate (Argesic, Disalcid)
Treatment of pain (in OA or RA) fever and inflammation in adults, less GI adverse effects, Adverse effects: N/v GI bleeding heartburn rash, Take with food or milk to decrease GI upset, Toxicity: may cause liver, kidney or ear dysfunction
List of Ibuprofen like drugs
ibuprofen (Advil, Motrin), naproxen (Naprosyn, Aleve),
diclofenac (Voltaren), meloxicam (Mobic), Indomethacin(Indocin), ketorolac (Toradol)
what to know about ibuprofen like drugs
Therapeutic uses include OA, RA (anti-inflammatory), mild to moderate pain (analgesic), fever reduction (antipyretic), myalgia, dental pain, dysmenorrhea
Can inhibit platelet aggregation, Can be nephrotoxic, Can be irritating to the gastric mucosa, Not cardio-protective like aspirin, MOA: Inhibition of prostaglandins
Metabolized in the liver, excreted via the kidney, Drug interactions: anticoagulants NSAIDs alcohol and corticosteroids
contraindications of NSAIDs
Cardiac Disorders & HTN, Gastric ulcers or other bleeding disorders, Pregnancy, lactation, Caution with renal or hepatic disease, Should not be given with corticosteroids
Celecoxib (Celebrex)
COX-2 inhibitor, Analgesic, anti-inflammatory, anti-pyretic without causing platelet aggregation or GI irritation, Treatment of RA, OA, dysmenorrhea, dental procedures, HA, some indication that it decreases risk of colon cancer, Metabolized by the liver, excreted in the feces and some in the urine
Nursing considerations with NSAIDs patient teaching
No smoking, Wear sunblock and protective clothing, avoid prolonged exposure to sunlight, Notify HCP if suspected pregnancy (pregnancy category depends on trimester-third trimester category D), Teach patient to report bleeding, Notify HCP if symptoms do not improve within a few days, Increased risk of bleeding with garlic, ginkgo, ginger
Anti Gout medications
first line is NSAIDs, then Allopurinol Colchicine Probenecid
Allopurinol (Lopurin, Zyloprim)
Prevents: nephrolithiasis due to calcium oxate stones in pts with elevated uric acid levels, Precautions: Hepatic or renal impairment Peptic ulcers Lower GI tract disease Bone marrow depression Pregnancy, Adverse effects: rash n/v Toxic epidermal necrosis Stevens–Johnson syndrome Bone marrow depression Retinopathy Thrombocytopenia, Need to Obtain serum and urinary acid levels to monitor, MOA: inhibits action of xanthine oxidase (enzyme for formation of uric acid)
Colchicine (Colcrys)
Anti-gout, Adverse effects: n/v diarrhea anorexia bone marrow toxicity hepatotoxicity and nephrotoxicity, need to increase fluids to 3-4 L, take drug on an empty stomach
Probenecid
Inhibits reabsorption of uric acid, Also used to delay excretion of penicillin, Contraindications: peptic ulcer and blood dyscrasias, Ineffective in patients with renal impairment, Pregnancy category B
DMARDS
Disease Modifying Antirheumatic Arthritis Drugs, Medications that slow the degenerative effects of the disorder, Usually prescribed secondary to NSAIDS, slower onset, contraindications: active bacterial infections active herpes zoster TB acute or chronic hepatitis
List Non-biologic DMARDS
methotrexate, Lefunomide, Hydroxycholorquine, Sulfasalazine
List Biologic DMARDS
Adalimumab, Anakinra, Etanercept, Abatacept
Anakinra
DMARD, given subQ injection, Adverse effects: monitor injection site for rash pain redness and pruritus
Adalimumab (Humara)
DMARD, adverse effects: injection site reaction neurological injury (numbness tingling visual disturbance), avoid in pts with heart failure
Etanercept
DMARD, can cause bone marrow suppression, given subcutaneously 2X per week, Adverse Effects: Injection site reactions Risk for heart failure CNS demylenating disorders Hematological disorders
Methotrexate
Indication: RA, once a week, Adverse effects: bone marrow suppression hepatotoxicity, avoid with pregnancy, onset of action in 3-6 weeks, patients instructed to take folic acid while taking
Hydroxychloroquine (Plaquenil)
DMARD, Pregnancy category C, Therapeutic uses: RA SLE second line drug in the treatment of malaria, Often taken concurrently with NSAIDS and corticosteroids, Adverse Reactions: Retinal damage Anorexia N/V Blurred vision photophobia Bone marrow depression renal and liver toxicity (but less than other DMARDS)
Infiximab
Adverse effects: infusion reactions hepatotoxicity, given IV infusion over several hours followed by subcutaneous injections in 2 weeks and then 6 weeks later Maintenance dose is given every 8 weeks, Often given with methotrexate
Sulfasalazine (Azulfidine)
Used for: RA Chron’s disease ulcerative colitis, Enteric coated tablet 3-4 X per day, Should see results in 4 weeks, Adverse Effects:GI and Dermatologic reactions Bone marrow suppression hepatitis Steven Johnson syndrome
Gold Salts/Aurothioglucose (Solganal)
Reduce the progression of joint damage caused by arthritic process, Aurothioglucose (Solganal)-Gold Compound, Used for RA, Gold compounds can be toxic, Adverse effects: Puritus rash metalic taste stomatitis diarrhea, Treatment of toxicity: Dimercaprol – enhances gold excretion, With advent of newer and less toxic drugs not used as much
Cancerous cells do not have
Growth control mechanisms, Positive physiologic function
Cancer cells can either
Grow and invade adjacent tissues, or Break away from original tumor mass and travel by means of blood or lymphatic system to distant sites
steps of cancer
Primary lesion- Original site of growth, Metastasis-Uncontrolled cell growth (Secondary lesion in a new and remote part of the body), Neoplasm (“new tissue”)- Mass of new cells, Tumor- Benign or Malignant (cancer)
Paraneoplastic Syndromes
Various group of symptoms that cannot be directly linked to a cancerous tumor, May be the first sign of malignancy(Cachexia- uncontrolled weight loss, Fatigue, fever)
Normal cell cycle
the number of cells produced = the number of cells that die (due to apoptosis), The total number of cells in the body remains constant
Proto-oncogenes
The normal genes that direct synthesis of proteins that regulate cell division
Neoplasia
occurs when Cells do not wait to multiply, Apoptosis should be a normal stimulus for the development of new cells, Cancer cells do not exhibit apoptosis, Cells do not exhibit contact inhibition (go straight to where they want)Cells ignore signals to stop dividing
Cancer cells are poorly
differentiated
Oncogenes
mutated pro-oncogenes (from radiation tobacco ect.), are tumor inducing, lead to abnormalities
initiation, promotion and progression of oncogenes
initiation- DNA damage, Promotion- division, progression- malignant tumor
Benign Tumors
Contain cells that look like normal tissue cells, Well differentiated, May perform the normal function of the tissue (like secreting hormones), This may lead to over-secretion, Usually have a capsule around them, Usually do not invade neighboring tissues, Slow growing (low mitotic index)
Malignant tumors
Tumor cells do not look like normal adult cells, Poorly differentiated (anaplasia), Autonomous (cancer cells are independent of normal cellular control), These cells divide rapidly (mitosis), Tumors grow quickly (faster growing than benign), The tumor does not have clear boundaries (not encapsulated) and sends “legs” out into surrounding tissue; can invade blood vessels and lymphatics
Routes of metastasis
Local Seeding – distribution of shed cancer cells occurs in the local area of the primary tumor, Blood Borne metastasis – tumor cells ender the blood (most common), Lymphatic Spread
the metastasize tumor can establish its own
Establish blood supply (angiogenesis)
classification of cancer
Anatomic site, Solid, Hematologic (Leukemia, Lymphoma, Myeloma), Histology (grading), Extent of disease (staging)
naming tumors
-Benign tumors: tissue name + “-oma”
-Malignant tumors (cancers) Epithelial tissue: tissue name + “carcinoma” Ductal or glandular epithelial tissue: tissue name + “adenocarcinoma” Connective (mesenchymal) tissue: tissue name + “sarcoma” Lymph tissue: lymphoma
Cancer of blood forming cells: leukemias
TNM classification system
used to determine the anatomic extent of the disease involvement according to 3 parameters:
(T) tumor size & invasiveness
(N) presence or absence of regional spread to the lymph nodes
(M) metastasis to distant organ sites
Chemotherapy
Using nonselective cytotoxic drugs, Affect normal (especially those that rapidly divide) and malignant cells, Goal is to destroy enough of the cancer cells so the body can take over and to spare normal cell, Single agent chemotherapy- Can see positive effects decrease over time, Combination chemotherapy- Decreases the risk of drug resistance Can use lower doses which may decrease harmful effects to normal cells
nursing implications with chemotherapy
Encourage Hydration, Administer antiemetics several hours before chemotherapy, Chemotherapeutic agents may cause hyperuricemia – consider allopurinol, Pregnant nurses should avoid rooms with chemotheapy, Monitor for phlebitis or extravasation, Monitor for signs of anaphylactic reactions
Negative Feedback and the endocrine system
Most common type of endocrine feedback, Gland responds by increasing or decreasing secretion of hormone based on other factors- Insulin secretion increased BG stimulates insulin secretion, As BG decreases the stimulus for insulin secretion decreases
alpha cells =
glucagon
beta cells =
insulin (allows glucose into cells) and amylin -both lower blood glucose
gut =
incretin effect
Counter-regulatory hormones increase blood glucose
Glucagon, Epinephrine (stress hormone), Growth Hormone (GH), Glucocorticoids (steroids)
incretin hormones
secreted from the gut that causes release of insulin from the beta cells prior to an elevation of blood glucose levels. Release of incretin hormones stimulated by food in the gut
Insulin
Release is stimulated primarily by presence of glucose in the blood, Insulin stimulates transport of glucose into cells to be used as energy, Primary purpose is to decrease blood sugar, It is the storage hormone (stores glucose as glycogen), Inhibits the breakdown of fat and glycogen, Increases protein synthesis and inhibits gluconeogenesis
Glucagon
Release is stimulated by low blood glucose levels, Inhibited by increased glucose levels, Causes increased BG via glycogenolysis, Onset within minutes, Encourages Gluconeogenesis
High blood glucose causes
pancreas to release insulin=cells take up glucose from the blood and the liver produces glycogen
Low blood glucose causes
pancreas to release glucagon- liver breaks down the glycogen- blood glucose rises
Glucocorticoids (adrenal gland)
Stimulate gluconeogenesis, Physical or emotional stress causes: increase of ACTH (results in release of cortisol from adrenal gland) and Decreased BG results in increased cortisol secretion
Type 1 diabetes mellitus
“Juvenile Diabetes” often diagnosed < 18, Absolute lack of insulin= Pancreatic beta cell destruction predominantly by an autoimmune process
3 P’s of diabetes (more common in type 1) and other clinical manifestations
Polyuria Polydipsia Polyphagia (cells aren’t getting sugar, no insulin), glycosuria (overwhelms renal system), weight loss (no food to cells, typicallt type 1), fast BG over 126 mg/dl
Type 2 diabetes mellitus
Non insulin dependent diabetes mellitus (NIDDM), Most common type, Insulin resistance (= less glucose uptake into cells), Hyperglycemia in the presence of relative insulin deficiency , Insulin release insufficient to meet the demand of increased BG, Resistance of the cells to the function of insulin (increased insulin resistance or decreased cellular sensitivity)
Oral glucose tolerance test OGTT
Measures body’s ability to remove glucose from the blood, Client drinks concentrated glucose solution (75 GRAMS), Serum glucose concentrations measured at 1 and 2 hours, Normal: glucose levels return to NL 2-3 hours after glucose load ingested
Glycosylated Hemoglobin HbA1C
Based on 120-day life cycle of RBC, Measures BG levels over past 2-3 months, Normal is 4-6%, Goal for a diabetic: less than 6.5 - 7%
Disadvantages: anemia, other blood disorders
Prediabetes
impaired glucose tolerance or impaired fasting glucose, Fasting glucose levels higher than normal (>100 mg/dl, but <126 mg/dl), IGT: 2-hour plasma glucose higher than normal (between 140 and 199 mg/dl), HgA1C 5.7 to 6.4%
Diagnosis of diabetes
A1C >6.5 %, fasting glucose >126, 2hr plasma glucose >200 during OGTT, or random plasma glucose > 200
Metabolic syndrome
is a risk factor for many things, manifestations include: Increased abdominal adiposity, Elevated triglycerides, Reduced HDL, Increased blood pressure, Hyperglycemia
3/5 are needed to diagnose
medications to raise BG
Can give IV IM subq oral, Examples: 1) Glucagon- given IV for emergency patient unable to take PO(normal causes vomiting, take precautions)
2) “BD Glucose” – OTC tablet form 3) 50% IV dextrose
%
Adverse effects: nausea, vomiting, hypotension or hypertension (both are transient), tachycardia
Cautious use: pregnancy/lactation, impaired renal, hepatic, or cardiovascular function
Basal insulin
typically delayed onset and longer duration of action, normal only once a day, Examples: NPH, glargine (Lantus) insulin, detemir (Levemir)
Prandial insulin
quick onset but shorter duration of action, Categorized as “short-acting” or “rapid-acting”, normally at meal times and sometimes at HS, Based on sliding scale
Examples: insulin aspart, lispro or glulisine (all rapid acting insulin) OR Regular insulin (short acting)
Do not mix ____ and _____ insulin in the same syringe
Rapid and long
Rapid acting insulin
Insulin lispro-Humalog, Insulin aspart-Novolog, Insulin glulisine (Apidra)
Clear in solution, Compatible with Regular, NPH
Short acting insulin
Regular, clear in solution
Intermediate acting insulin
NPH, Less frequent dosing required, Cloudy in solution
Fixed combination insulin
50/50 or 70/30, Mixture of short acting and intermediate acting, Most used is 70/30 which is 70% NPH and 30% regular, Do not mix with other insulins
Glargine (Lantus)
Basal insulin, Mimics the basal level of insulin in the body, Used with rapid acting and should not be mixed with any other insulin, Rapid acting insulin is given before meals to handle the increase in glucose postprandially
Amylinomimetic agent
Pramlintide (Symlin), used in types 1 and 2, given with meal insulin, acts like amylin (decreases gastric emptying, suppresses glucagon regulates food intake) given subq, black box warning severe hypoglycemia
Insulin methods
SubQ, pens, pumps, regular insulin can be given IV
Somogyi effect
hypoglycemia occurs typically at 2-3 am. The body compensates by increasing catecholamines, glucagon, cortisol and GH
Compensatory mechanisms cause increased BG levels by morning, Morning BG level is elevated, Diagnosis is the blood glucose test 2-3am, Treatment is by lowering the evening insulin dose or by giving an hs snack
Dawn Phenomenon
High fasting BG level, Typically occurs in the morning, 5-9 AM, Thought to be related to release of growth hormone (and possibly cortisol), Pre-dawn BG level is elevated, Common in adolescents and young adults, Treatment is to increase the insulin dose
