NURS 3537 Week 2 Meds PDF

How do we help patients achieve glycemic control? enabling patient and their family to become more active in their care nutritional therapy exercise maintenance of desired body weight self monitoring of blood glucose encouraging adherence to medication therapy 1 Medication Therap...

How do we help patients achieve glycemic control? enabling patient and their family to become more active in their care nutritional therapy exercise maintenance of desired body weight self monitoring of blood glucose encouraging adherence to medication therapy 1 Medication Therapy Oral Hypoglycemic Agents Non-insulin Injectable Agents Insulin 2 Insulin Example Onset of Action Adverse Effects/Nursing Classification Implications Rapid-acting Lispro (Humalog) Approx. 10 – 15 min Hypoglycemia Aspart (NovoRapid) (aspart can be a Meal time insulin little as 4 min) Administer 10 – 15 min before meals Can be given up to 15 min post meal Short-acting Regular (Humulin R) 30 – 60 min Hypoglycemia Meal time insulin Administer 30 – 45 min before meals Intermediate- NPH (Humulin N) 2 – 4 hrs Peak 4– 10 hrs, can lead to acting hypoglycemia Long-acting Glargine (Lantus) Steadily and No peak of action Degludec (Tresiba) continuously over Administered usually once 24 hrs (onset 2 – 4 daily at bedtime hrs) Premixed (short or Regular/NPH (30/70) Decreased potential for rapid acting mixed (Humulin 30/70) adequate glucose control due with 3 intermediate) Aspart/Aspart Protamine to inflexible dosing (30/70) 4 Sliding Scales Hypoglycemia Protocol Call MD unit units units units units 5 Question for the class What are some contraindications to insulin administration? 6 Nursing Implications for Insulin Administration Check CBG Do no administer if blood glucose level < 4.0 mmol/L (follow agency hypoglycemia protocol) Independent double check with another nurse Ensure meal is available and patient is able to eat not NPO not experiencing NV Rotate injection sites 7 Oral Example Mechanism of Action Contraindicatio Adverse Effects Hypoglycemic ns Agents Drug Class Biguanide Metformin Inhibits hepatic Kidney disease GI upset (NVD) (Glucophage glucose production Creatinine Less weight gain ) increases peripheral clearance < Unlikely and liver sensitivity to 30ml/min hypoglycemia insulin Potential lactic Caution with acidosis May decrease contrast CTs Renal or hepatic intestinal absorption of impairment glucose and improve Has to be held for insulin receptor 48hrs prior to or sensitivity following IV contrast dye Insulin Gliclazide Stimulates release of Hypoglycemia Weight gain Secretagogues (Diamicron) insulin from B-cells, NPO Hypoglycemia Sulfonylureas decreases secretion of ETOH use Nausea glucagon and Epigastric burning gluconeogenesis 8 Oral Example Mechanism of Contraindicatio Adverse Effects Hypoglycemic Action ns Agents Drug Class Dipeptidyl Sitagliptin Enhance the Known drug URTI Peptidase-4 (DPP- (Januvia) incretin system, allergy Sore throat 4) Inhibitor Linagliptin stimulate release Diarrhea (Trajenta) of insulin from Headache pancreatic B cells, and inhibit hepatic glucose production Sodium-Glucose Canagliflozi Enhance urinary Known drug Genital infections Cotransporter n glucose secretion allergy UTIs Type 2 (SGLT2) (Invokana) Kidney disease Diarrhea Inhibitors Empaglifloz Blocks tubular Constipation in reabsorption of Nausea (Jardiance) glucose in the Hypotension 9 kidneys Increased lipids Type Example Mechanism of Contraindicatio Adverse Effects Action ns Noninsulin Semaglutid Stimulate release of Known drug NVD Injectable Agents: e insulin; decrease allergy Weight loss GLP-1 Receptor (Ozempic) glucagon secretion, Kidney disease Hypoglycemia Agonists increase satiety, Headache Liraglutide decrease gastric (Victoza) emptying 10 11  Pituitary Drugs 12  Anterior Pituitary Gland Hormone Medicatio Used to Mechanism of Action Contraindicati Adverse n(s) Treat ons Effects Adrenocorticotr Cosyntropin Adrenocorti Targets adrenal cortex Asthma Edema opic Hormone (synthetic cal and stimulates the Infectious HTN (ACTH) ACTH) insufficienc secretion of disease Rash y mineralocorticoid cortisol Follicle- Menotropin Typically Simulates oogenesis and Untreated or HA stimulating s female follicular growth in uncontrolled AP Hormone (FSH) infertility females & endocrine Bloating spermatogenesis in disorder Breast males soreness Pain at injection site 13  Anterior Pituitary Gland Hormone Medication( Used to Mechanism of Contraindicat Adverse s) Treat Action ions Effects Growth Somatropin Hypopituitary Promotes skeletal HIV Pain at Hormone Dwarfism and muscle growth (wasting) injection site (GH) Increases protein Pregnancy HA synthesis, liver Acute illness glycogenolysis and fat mobilization Octreotide Acromegaly Reduces growth Diarrhea Acetate GI Bleeds hormone & insulin Caution in Hypotension Carcinoid like growth factor patients with Conduction Tumors Reduces blood flow renal abnormalitie to GI tract impairment s Reduces diarrhea in Caution in Hypo/hyper vasoactive intestinal diabetic glycemia polypeptide VIP patients tumor pts 14  Anterior Pituitary Gland Hormone Medicatio Used to Mechanism of Action Contraindicati Adverse n(s) Treat ons Effects Luteinizing Clomiphene Typically Stimulates ovulation Untreated or HA Hormone (LH) Citrate female and uncontrolled Bloating infertility estrogen release by endocrine Breast ovaries disorder soreness Stimulates Unexplained Intermenstr spermatogenesis and heavy ual testosterone secretion vaginal bleeding Increases LH levels bleeding and chance of Liver disease pregnancy 15  Posterior Pituitary Gland Hormone Medication Used to Treat Mechanism of Contraindicat Adverse (s) Action ions Effects Antidiuretic Vasopressin Diabetes Increases water Renal Increase in Hormone (synthetic Insipidus reabsorption in impairment BP (can also (ADH) ADH) (polydipsia distal tubules Hyponatremi be desired and Concentrates a effect) Desmopressi polyuria) urine HA n Acetate Von Anti-diuretic Vertigo (synthetic Willenbrand’ action Nausea vasopressin) s disease Potent Epigastric Mild vasoconstrictio burning hemophilia n (vasopressin) A Hypotension of various causes (vasopressin ) Oxytocin Oxytocin Induction of Contraction of Predispositio Uterine 16 labour uterine smooth n for uterine rupture Abuse of Growth Hormone Does not increase muscle mass or strength greater than seen with exercise alone Not indicated for anti-aging formula Adverse effects include—acromegaly, diabetes, hypertension, increased risk of cardiovascular disease, tumor growth & cancer 17  Thyroid & Anti-Thyroid Drugs 18 Endogenous Thyroid Thyroid produces three hormones: Thyroxine (T4) Triidothyronine (T3) Calcitonin T3 more potent but with a shorter duration of action Production of thyroid hormones is dependent on iodine & tyrosine (needed to form thyroglobulin) Control rate of cellular metabolism, linear growth, brain function, dentition, bone development & neural development 19 Hypothyroidism Hypothyroidism occurs when the thyroid is no longer able to produce sufficient thyroxine Possible causes: Lymphocytic thyoiditis (Hashimoto’s thyroiditis or autoimmune thyrioiditis) Following treatment for hyperthyroidism Thyroid Surgery Failure of Pituitary gland to releases TSH to stimulate production of thyroxine Iodine deficiency 20  Thyroid Replacement Drugs Management of hypothyroidism involves life-long treatment with synthetic thyroxine hormones. Goal of thyroid replacement therapy to provide adequate amount of thyroid hormone to compensate for lack of supply by the thyroid gland  Thyroid Replacement Drugs Hormo Medication Used to Mechanism of Contraindications Adverse ne (s) Treat Action Effects T4 Levothyroxin Hypothyroidis 100% Synthetic T4 Known drug Arrhythmia e m induce changes in allergy (usually metabolic rate, Adrenal with OD) cellular growth and insufficiency increases oxygen Hyperthyroidism consumption Careful consideration with celiac patients T3 Cytomel Hypothyroidis replaces Adrenal Adverse m endogenous thyroid insufficiency interaction hormone s with controls DNA other ***Dosingtranscription is in and drugs such MCG*** protein synthesis as 22 antidiabeti c drugs Assessment for Hypothyroidism Drugs Monitor for signs of ENDOCRINE & METABOLIC hyperthyroidism  Monitor diabetic clients for development of hyperglycaemia CVS  Diaphoretic (Sweating) Apical pulse (tachycardia) if resting pulse rate > 100  Increased temperature (Fever) beats/min (in adult) notify  Hyperactivity MD BP Chest pain GI Heart rhythm (dysrhythmia)  Weight loss  Abdominal cramping CNS  Diarrhea or constipation Nervousness (anxiety)  Increased appetite Administration of Hypothyroidism Drugs Administration & Patient Teaching Administer early in the day to avoid insomnia Best taken every morning empty stomach to obtain best absorption Antacid, iron supplement & sucralfate should be taken about 2 hours after avoid these agents due to weakening of thyroid medication effects Missed dose should be taken ASAP if two or more missed dose occur call on health care professional Hyperthyroidism Hyperthyroidism (a.k.a. thyrotoxicosis) is a condition in which the thyroid gland is overactive produces too much thyroxine characterized by excessive thyroxine & enlarged glands, can affect all the body systems causing increase in metabolism Possible causes: Autoimmune disease (Graves' disease) Single benign tumour of the thyroid (toxic nodular disease) May follow from a viral infection Multimodal disease Thyroiditis Pituitary tumour & thyroid cancer 25 Hyperthyroidism Drugs Reduce TH production to normal level to relieve symptoms Possibly remove the cause of the condition Destruction of the gland There are two approaches to reduce the effect of hyper-secretion by the glands. 1) treat primary cause vs 2) treat symptoms of disease: 1. Reduce level of circulating thyroid hormone by blocking synthesis of the hormone (anti-thyroid meds) - these are anti-thyroid meds. that inhibits thyroid hormone synthesis by blocking the incorporation of iodine into tyrosine & blocks the coupling of iodotyrosines 26 2. Reduce the eff ect of the hyper-secretion by producing relieve of symptoms (beta Blockers)  Antithyroid Drugs Medication( Used to Treat Mechanism of Action Contraindication Adverse Effects s) s Methimazole Hyperthyroidis Inhibits Hepatic Drowsiness m thyroperoxidase and patients HA in turn decreases the Myelosuppressi NVD synthesis of thyroid on (decreased Rash hormones (T3 and T4) bone marrow Hematological activity) (leukopenia, Hypersensitivity thrombocytope Allergy nia) Liver and bone marrow toxicity Propylthioura Hyperthyroidis blocks the inclusion of Same as above Same as above cil (PTU) m iodine in the peptide Grave’s structure of the disease hormone, thus Thyroid Storm preventing synthesis of the hormone 27  Antithyroid Drugs Medication( Used to Treat Mechanism of Action Contraindication Adverse Effects s) s Lugol’s Hyperthyroidi Inhibits the release of TB Anaphylaxis Solution sm (short thyroxine when given Sensitivity to (Iodine term) in high doses. Effect iodine solution) Thyroid lasts only for a few storm days Can be used in preparation for surgery ***Thyroid Storm: life-threatening health condition that is associated with untreated or undertreated hyperthyroidism. During thyroid storm, an individual's heart rate, blood pressure, and body temperature can soar to dangerously high levels. Can cause extreme 28 agitation. Without prompt, aggressive treatment, thyroid storm is often fatal *** Hyperthyroidism Treatment AGENTS TO TREAT THYROID Adverse Effects - Na I131 Na I131  May lead to hypothyroidism Radioactive destruction of thyroid tissues/cells  Isolation of client required It has a 8-day half-life & 99% of  Radiation protections radiation effect; dissipates by the 56th measures required day following administration It is administered orally or IV it is rapidly taken up by the thyroid gland. It reduces hormone secretion & destroys the functional thyroid tissue. It can lead to destruction of the entire gland  Antithyroid Drugs (Approach II) AGENTS TO TREAT THYROID Adverse Effects - Beta- Adrenergic Blocking Agents Beta-Adrenergic Blocking Agents (BB) (BB) BB have no effect on thyroid hormone secretion or circulating blood levels; they CVS  Bradycardia only block symptoms.  Cardiac failure propranolol, metoprolol & nadolol  Hypotension propranolol in addition to blocking Respiratory symptoms also blocks the conversion of  Bronchospasm thyroxine into T3 GI used as adjuvant therapy before surgery to  Constipation remove thyroid gland ENOCRINE & METABOLIC suppress signs & symptoms of  cold extremities hyperthyroidism e.g., tachycardia, tremor,  Fatigue anxiety CNS  sleep disturbance Special Populations Thyroid disorders change metabolism of other drugs Children w/congenital hypothyroidism, tx should be started within 6 weeks of birth If untreated for several months after birth, severe congenital hypothyroidism can lead to growth failure and permanent intellectual disability Drug of choice is levothyroxine Monitor ht. & wt. If hyperthyroid, can use Propylthiouracil (PTU) or methimazole, radioactive iodine in children is discouraged Thyrotoxicosis manage in intensive care Special Populations s/s of thyroid disorders may mimic other disorders in older adults Thorough Physical Exam & diagnostic workup Levothyroxine is appropriate Start with small doses, may increase in small increments monthly Monitor vitals closely For hyperthyroidism, use PTU or methimazole. May use radioactive iodine. Thyrotoxicosis manage in intensive care  Adrenal Drugs 33 Endogenous Corticosteroids Steroid hormones are collectively called corticosteroids Synthesized from cholesterol Corticosteroids are produced ON DEMAND by the adrenal cortex in response to stimuli low plasma levels of steroids pain, anxiety, trauma, illness, anesthesia Bound to plasma proteins = lipids Corticosteroids are metabolized by liver & excreted in bile or urine Endogenous Corticosteroids Negative feedback system maintain normal plasma levels: The corticosteroids comprise 1. Glucocorticoids (activate immune system) 2. Mineralocorticoids (regulate blood vol / pressure) 3. Gonado-corticoids (testosterone / estrogens) Endogenous Corticosteroids Glucocorticoids Cortisol (a.k.a. hydrocortisone) is the major glucocorticoid (~95%) corticosterone & cortisone Approx. 15-20 mg of glucocorticoids, & 1.5 mg corticosterone secreted daily. Glucocorticoid secretion is cyclical largest amount being produced in the early morning small amount in the evening This rhythm is affected by acute stress Stress  Cortisol  levels of glucose, fatty acids  Role of Endogenous Corticosteroids 4. Respiratory: Keeps airways open 1. CVS: help to regulate arterial but does not have direct BP by modifying smooth muscle bronchodilation effect tone of blood vessels 2. CNS:  nerve excitability & slow 5. Inflammatory Response: activity in the cerebral cortex Stabilize mast cells & other cells to inhibit the release of broncho- 3. MSK:  bone formation & constrictive & inflammatory increase breakdown of bone substances such as histamine. 6. GI:  gastric mucus thus  stomach protection  peptic ulcers  Role of Endogenous Corticosteroids Mineralocorticoids Aldosterone accounts for 95% & is the most potent mineralocorticoid Gonadocorticoids (Sex hormones) Most are weak androgens which are converted to testosterone in males or estrogen in females.  EXOGENOUS CORTICOSTERIODS DRUGS Indications for corticosteroid use Any illness with an inflammation or immunologic component  Allergic or hypersensitivity Asthma & COPD disorders  Collagen disorders - lupus, scleroderma & periarteritis Arthritis—if three or fewer  Dermatologic joint, can give joint injections;  Endocrine disorders no more than three per year  Inflammatory bowel disorders  Neoplastic disease - suppress Chemotherapy induced emesis lymphocytes  —strong anti-emetic effect, Neurologic disorders-cerebral edema, myasthenia gravis mechanism unknown. Usually give dose with serotonin antagonist & Reglan Systemic Corticosteroids Betamethasone & Dexamethasone (orally, parenteral) Prevents respiratory distress syndrome in premature infants administered 48 hr. to 72 hr. Preferred for cerebral edema because it crosses the blood brain barrier & reaches high concentrations in the CSF BRAIN TUMOUR NEUROSURGERY MENINGITIS Dexamethasone is the choice for cerebral edema associated with brain tumour, craniotomy & head injury. SYSTEMIC CORTICOSTEROIDS Hydrocortisone & cortisone choice to treat adrenocortical insufficiency (Addison’s disease). requires replacement of glucocorticoids & mineralocorticoids Prednisone glucocorticoid of choice for inflammation, allergy, stress & as immunosuppressive therapy. Methylprednisolone, hydrocortisone & dexamethasone acute life-saving situation that requires a corticosteroid Anaphylaxis Spinal Shock  Adverse Effects of Long-Term Use of SYSTEMIC CORTICOSTEROIDS Endocrine GI Suppression of hypothalamic– Peptic ulcer pituitary–adrenal (HPA) axis Abdominal distension loss of adrenocortical function Skin Mood change Hirsutism Moon face Thin fragile skin Elevate serum glucose Acne Reduce effect of insulin Bruising MSK CVS Muscle wasting Increase BP & fluid Fat deposits (Buffalo hump) retention Osteoporosis Weight gain SYSTEMIC CORTICOSTEROIDS Contraindications Systemic fungal infection Hypersensitivity Use with caution in patients = increased monitoring At risk for infection Masks symptoms of infection Diabetics Peptic ulcer Inflammatory bowel disease CHF Renal insufficiency NURSING ASSESSMENT PRE-ADMINISTRATION Activity level Appetite Caution Weight Daily administration of 15- POST-ADMINISTRATION 20mg of hydrocortisone or Signs of Infection its equivalent for 2 weeks Fever suppresses the HPA axis Sore throat MUST taper down Weight gain ≥ 5lb/week Activity level Appetite Hypertension PATIENT TEACHING For patients on long term treatment Increase Ca+, & Vit. D PREVENT OSTEOPOROSIS Increase protein intake PREVENT MUSCLE WASTING Increase Vit C PREVENT EXCESSIVE BRUISING Decrease Na+ & increase K+ PREVENT HYPOKALEMIA Should carry a medical alter or warning card RESPONSE TO SHOCK IS ALTERED NURSING ADMINISTRATION Nursing Implementation Preferred systemic route of administration is oral Acute treatment is usually in larger doses over 48-72 hrs. & then tapers off as condition improves Steroid Flare from injection post injection flare (similar to infection: pain, redness warmth) treat with rest, analgesics and local application of ice  Questions? 48