-If not receiving correct dose, can be LIFE THREATENING
-Cause Circulatory collapse, hypotension, bloody diarrhea, shock, and cardiac arrest.
-Abdominal cramps, salivation, flushing of the skin, nausea and vomiting, transient syncope, transient complete heart block, dyspnea, and orthostatic hypotension
Indications: (do give these to pt in hospital) preoperatively to reduce salivation and excessive secretions in the respiratory and GI tracts
Contraindications: hypersensitivity, angle-closure glaucoma, myasthenia gravis, GI or GU tract obstruction, tachycardia, myocardial ischemia, hepatic disease, ulcerative colitis, and toxic and megacolon
S/E: H/A, drowsiness, nasal congestion, blurred vision, dry mouth, tachycardia, flushing
Localized protective response stimulated by injury to tissues, which serves to destroy dilute, or wall off (sequester) both the injurious agent and the injured tissue
-pain, fever, loss of function, redness, and s welling
-Endogenous compounds (coming internally from the body), including proteins of the complement system, histamine, serotonin, bradykinin, leukotrienes, and prostaglandins
-Increased heart rate
-Tinnitus, hearing loss, dimness of vision, headache, dizziness, mental confusion, drowsiness
-Nausea, vomiting, diarrhea
-Sweating, thirst, hyperventilation (due to acid to blow off CO2), hypoglycemia or hyperglycemia
-Aspirin is a salicylate
Acetic Acid Derivative
-Analgesic, anti-inflammatory, anti-rheumatic, and antipyretic properties
-Uses: RA, OA, acute bursitis or tendonitis, ankylosing spondylitis (inflammation of the spine/vertebrae), acute gouty arthritis, PDA, and treatment of preterm labor
-Oral, rectal, intravenous use
-First and only remaining COX-2 inhibitor
-Indicated for OA, RA, acute pain symptoms, ankylosing spondylitis, and primary dysmenorrhea, is an analgesia
-Adverse effects include headache, sinus irritation, diarrhea, fatigue, dizziness, lower extremity edema, and hypertension
-Little effect on platelet function
-Celecoxib is not to be used in patients with a known sulfa allergy
-Only works on cox-2 so less of GI effects as a lot of the other NSAIDs
-Black box warning: it can lead to some of the cardiovascular events usually leading to clotting, that is why others of these drugs FDA banned from market
Caused by oversecretion of corticosteroids
S/S: Moonface, buffalo hump, thin , emotionally unstable, HTN, Low K+ , high cortisol levels, Fractures, GERD, PUD (peptic ulcer disease), DM (diabetes)
Nursing Care: Monitor electolytes, BG, VS
Can be caused by a tumor or a mass. On the adrenals that's causing it to Overstimulate, but it can also be Caused by glucocorticoid therapy
Even topical steroids for diseases such as ecsema can be systemically absorbed when overused and used for a very long time
Encourage patients to take measures that promote a generally good state of health so as to prevent, relieve, or decrease symptoms of COPD
-Avoid exposure to conditions that precipitate bronchospasm (Allergens, smoking, stress, air pollutants).
-Adequate fluid intake
-Compliance with medical treatment
-Avoid excessive fatigue, heat, extremes in temperature, and caffeine
Teach Patients to gargle and rinse the mouth with lukewarm water afterward to prevent the development of oral fungal infections. (can also use mouthwash)
If a beta-agonist bronchodilator and corticosteroid inhaler are both ordered, the bronchodilator should be used several minutes before administration of the corticosteroid to help decrease the inflammation.
(bronchodilator used first -open up airway first, then corticosteroid)
Interferes with production of vitamin K dependent clotting factors.
-1/2 life 42 hours (fairly long)
-INR must be monitored (given orally at the same exact time every day; almost always at 6pm unless following home regimen)
-Category X (it really heightens the risk of bleeding because it has such a narrow therapeutic index, the risks outweigh the benefits. We do not want to make pregnant women bleed out that significantly for that long. If she had complication with pregnancy she could bleed out and die.)
-Antidote: Vitamin K FFP (works on vitamin K clotting factors, sometimes that takes awhile to work. Another thing we can give in the hospital, pt. comes in car accident which is trauma and they are wearing medication bracelet that says they're on Coumadin, we need to make sure to reverse the Coumadin. We would administer orally if awake or IV cause faster. We could give FFP (fresh frozen plasma) to help the blood to clot and the INR level to go down)
-Blood tests Q. 2-3 weeks (at home need to be monitored. First once a week blood test, than 2-3, than a month but this is a life long medication, they need to be monitored that closely)
Control intake of dietary vitamin K (dark green leafy veggies like kale; if pt. generally eat lots of salad and kale they should maintain same diet so the blood test can be consistent to get correct dose, but if the patient does not eat a lot of vitamin k they shouldn't get nothing but vitamin K because then they will alter the blood tests and it will affect how the warfarin will work and make them have an increase chance for clots)
EtOH intake (vitamin K clotting factors formed in liver, if we start overloading liver with alcohol you could have issues with making the clotting factors and INR levels woul go up pretty high)
Very narrow therapeutic index, amount of drug we give patients is a fine balance. Sometimes they will take a certain dose on Mondays, smaller dose on Tuesdays and Wednesdays they will take the same dose as Monday so that we can get the patient to that therapeutic level of either INR 2-3 or INR 21/2 -3/1/2 depending on why they are taking Coumadin
Break down, or lyse, preformed clots
Reestablish blood flow to the heart muscle via coronary arteries, preventing tissue destruction (it works as well for stroke; clot buster medications we heard about when patients are having strokes, we have to give it in very short period of time, generally it is less than 3 hours, if you have clot that has formed you are not getting oxygenation or circulation to that tissue and eventually that tissue will die, once it dies we can't do anything to bring it back, if tissue just is lacking oxygen and it is a short amount of time we might be able to bring back the function)
This medication would be given within that short window for both MI and strokes; window is so short because if it passed short window the tissue has probably died and we can't bring it back. This puts the patient at high bleeding, so the risks outweigh the benefits at this time.
None of those meds aspirin, Clopidogrel (Plavix), Cilostazol (pletal) break down clots, they all help clots to not form but none can break down fibrin)
These thrombolytic meds can do that. We are breaking down clots.
How fibrinolytics work.. fibrin will convert to plasminogen and the plasmin helps to work with the clot breakdown, so plasminogen transforms to plasmin to help with breakdown
Tx of anemia associated with ESRD (End Stage renal disease(, chemotherapy-induced anemia
Ineffective without adequate body iron stores and bone marrow function (then Epogen will not work, monitor these)
S/E: HTN (most common we would see with this med), fever, headache, pruritus, rash, nausea, vomiting, arthralgia, and injection site reaction
Given as SQ
Darbepoetin (Aranesp) (similar drug) --> Longer lasting
Hemoglobin level assessed as lab result we don't want to give if a 10 or above for cancer patient & 12 or above for renal patients. If give when hemoglobin really high you are putting them at risk for getting thrombosis (Clot)
Untreated hypothyroidism (reasons why we would need to medicate patients with our thyroid hormones)
-State of untreated hypothyroid
-Triggered by illness or trauma
S and S:
-Metabolic: hyponatremia, hypoglycemia, lactic acidosis, hypothermia (no thermoregulation)
-Systemic: CV (cardiovascular) collapse, coma
-Nursing ABC's, LOC, IV Hydrocortisone, IV Levothyroxine; maintain airway and breathing and circulation of your patient.
(Typically occurs durinng adulthood when they're having that hypersecretion of the thyroid hormone, and it can be either primary or secondary cause
Early signs include depression, decreased cognition, lethargy, somnolence, hypothermia.
We would give hydrocortisone until coexisting adrenal insufficiency is ruled out. Can be precipitated by infection and sedatives given during surgery.
A patient that has hyperthyroidism might have a goiter (big enlargement of the thyroid gland); typically should be small able to palpate thyroid for normal finding but not with this condition.
Goiter can be very large, cause of over-stimulation of thyroid gland, typically because thyroid stimulating hormones are continuing to be released because they want more thyroid floating around in the system but is not working because the thyroid is not working)
-Replace what the thyroid gland itself cannot produce to achieve euthyroid (Normally functioning thyroid) condition
-Adverse effects: CARDIAC DYSRHYTHMIA
Tachycardia, palpitations, angina, hypertension, insomnia, tremors, headache, aniety, nausea, diarrhea, menstrual irregularities, weight loss, sweating, heat, intolerance, fever, others
(Cardiac dysrhythmia the most concerning and deadly.
Thyroid medication can also have a diuretic effect on the patients, because of the stimulation of the beta receptors it increases the sensitivity to catecholamines (epi/norepi which constrict blood vessels and increase CO by increasing BP) when CO is increased, kidneys get better blood flow. With good kidney better blood flow and circulation it increases the glomerular filtration rate, which produces a diuretic effect