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118 Cards in this Set
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- Back
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What is Rheumatoid Arthritis (RA) |
systemic inflammatory disease, not limited to joints- affects all age groups & autoimmune- primary characteristic = symmetric polyarticular inflammation |
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Ideal RA therapy |
Help w/ pain, inflammation, stiffness Maintain joint function & ROM Non-drug: PT, surgery |
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Antiarthritic drugs |
NSAID, DMARDS (Disease-modifiying antirheumatic drugs), Glucocorticoids Start with NSAIDS, then DMARDS, then Glucocorticoids until DMARDS take effect |
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DMARDS- Methotrexate (Rheumatrex) |
capapble of arresting progression of RA and may induce remission |
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Sulfasalazine treats? |
Treat IBD & now for RA as well Helps with anti-inflammatory & inmmunomodulatory actions Slow progression of joint deterioration |
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DMARDS II: name of major biologic DMARDs |
Tumor necrosis factor inhibitors Supress immune function, risk for infection, neutraize tumor necrosis factor (TNF) ex: Etanercept (Enbrel) Infliximab (Remicade) Adalimumab (Humira) |
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What does Etanercept help |
Therapy: helps manage RA Kinetics: weekly subq injections- slow onset & uncertain duration Dynamics: binds to circulating TNF, prevents TNF from binding to cells & stops further response Contra: hypersenstivity Adverse: blood dyscrasias, infetion, TB, HF, cancer, injection site reactions, headache, N, rhinitis |
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Etanercept edu max/min |
max therapy: weekly, rotate injection sites min: aseptic technique, no live virus vaccines, do not give if discolored/ cloudy/ has particles Edu: symptoms, preparation & administer, avoid ill people **as young as 4 years old*** Assess: improved ROM, less stiff/pain/swollen joints, CVC, ESR, C-reactive protein levels/ tests |
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What is Gout: |
recurrent inflammatory disorder, mainly men
Hyperuricemia- uric acid levels greater than 7 mg/dl men & greater than 6 mg/dl in women Uric acid crystals deposit in joints Severe joint pain (due to up made or low excrete) Diagnosis: analysis of synovial fluid |
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Gout short term vs long term therapy |
Short: relieve symptoms of attack Infrequent flare-ups (fewer than 3 per year) NSAIDS first then glucocorticoids Long term to lower blood uric acid 3+ flare ups= uricosuric drugs |
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Gouty Arthritis- NSAIDS |
First choice- better tolerated & more predictable than colchicine; releif in 24 hours & swelling lessens over a few days Adverse: GI ulcers, decrease renal function, fluid retention, increased CV events Drugs: Indomethacin (indocin) Naproxen (Naprosyn) Diclofenac (Voltaren) |
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Gout- Glucocorticoids |
Highly effective in relieving pain Useful to people who cannot have NSAIDS Avoid in hyperglycemic patients Does not reduce uric acid levels |
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What is Colchicine |
Anit-inflammatory agent- no longer first line; reserved for patients who dont tolerate safer agents Use: acute gouty attack, reduce attack incidents, abort impending attack Inhibits leukocyte migration= interrupts cyclic inflammatory process- does not inhibit phagocytosis of uric acid crystals= does not affect uric acid clearance |
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Colchicine adverse |
GI most common- 80% N/V/D/ pain/ paralytic ileus Long term= bone marrow depression & myopathy |
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Goals of hyperuricemia therapy |
Promote dissolution of uric crystals, prevent formation, prevent progression, improve life quality, reduce attack freq. Not useful in acute gouty attack b/c no analgesic or anti-inflammatory properties |
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Drugs for Hyperuricemia
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Allopurinol (Zyloprim) inhibit uric acid formation Febuxostat (Uloric) inhibit uric acid formation Probenecid (Benemid) increase uric acid excretion Sulfinpyrazone (Anturane) incruse uric acid excretion |
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Methotrexate therapy & pharm |
Therapy: folate antimetabolite used in treated malignancies & RA; most rapid acting DMARD, effect 3-6 wks Kinetics: PO or parenteral; metabolized liver; excreted kidneys Dynamics: immunosuppressive effects by stopping replication & function of T lymphocytes that stimulate production of cytokines |
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Methotrexate precautions, adverse |
contra: immunosuppression, blood dyscrasia, pregnancy, lactation Adverse: rash, hepatic fibrosis, GI ulcer, bone marrow suppression, pneumonitis, stomatis, V/D/N Interacts with many things |
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Methotrexate factors |
Health status: assess for co-morbidity Life span/ gender: caution to young & elderly Lifestyle, diet, habits: alcohol or illicit drugs Environment: routinely given at home Max: administer med as ordered; drink many water to stop nephrotoxicity Min: folic acid interferes with drug effectiveness, cause photosensitivity Edu: prevent infection, adverse effects, med as prescribed Assess: effective treatment, monitor for blood dyspepsia, suppressed bone marrow, pulmonary changes, hepatic/renal dysfunction |
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What is/ what does Allopurinol |
Manage chronic gout, recurrent Ca renal stones, & hyperuricemai Given: PO, IV- metabolized in liver, decrease production of uric acid by inhibiting xanthine oxidase action Adverse: pruitus, maculopapular rash, N/V, elevated LFTs, acute gout symptoms Teaching: develop meal plans, limit uric acid production, fluid intake between 2.5-3 L/day Titrate drug based on uric acid levels |
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Probenecid (Benemid) action |
Acts on renal tubules to inhibit reabsorption of uric acid May exacerbate acute episodes of gout; add indomethacin for relief Adverse: well tolerated, mild GI, take with food |
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Ca Physiology |
Functions & daily: critical function of the skeletal, nervous, muscular, & CV systems |
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Ca Body Stores |
More than 98% stored in bones Total serum Ca= 10 mg/dL Ab: small intestine, increased by parathyroid hormone & vitamin D; glucocorticoids decreased absorption Excretion: calcitonin augments calcium elimination |
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Hypercalcemia symptoms, cause, drugs to treat |
usually asymptomatic; symptoms usually involve kidneys Cause: cancer, hyperparathyroidism Treat: promote urinary excretion, decrease mobilize from bone & intestinal absorption, IV saline Drugs: Furosemide (Lasix)- Glucocorticoids Others- calcoitonin, bisphosphonates, inorganic phosphates, gallium nitrate |
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Hypocalcemia presentation & treatment |
Increase neuromuscular excitability Presentation- tetany, convulsions, spasm of pharynx Cause: deficiency of PTH, vitamin D, Ca Treat: Ca supplementation (Ca gluconate), Vitamin D |
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drugs for Disorders involving Ca |
Ca salts, Vitamin D, Calcitonin-salmon (Calcimar, Miacalcin, Fortical) Bisphosphonates (Alendronate, risedronate, ibandronate, tiludronate, etidronate, zoledronate, pamidronate) |
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What is Teriparatide (Forteo) |
Form of PTH, produced by recombinant DNA, increase bone formation, generally well tolerated (N, headache, back pain, leg cramps) |
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What is Osteoporosis & how to diagnosis |
Most common disorder of Ca metabolism Low bone mass & increased bone fragility Primary Prevention: Ca, Vitamin D, lifestyle Diagnosis: bone mineral density, dual energy x-ray absorptiometry |
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Osteoporosis in Women |
--Antireorptive therapy- drugs that reduce bome resorption --Estrogen (Premarin(, Raloxifene (Evista), --Bisphonsphonates [Alendronate (Fosamax) most common] Risedronate (Actonel), Ibandronate (Boniva) --Calcitonin-salmon nasal spray (Miacalcin) Drugs to promote bone formation: Teriparatide (Forteo) |
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Osteoporosis in Men |
Antiresorptive therapy- reduce bone absorption Not much research avaiable for men Four Drugs: Bisphosphonates--> Alendronate (Fosamax) Risedronate (Actonel) Teriparatide (Forteo) Zoledronate (Reclast) |
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Bisophosphonate contraindications |
Contraindications: esophageal disorders that impede swallowing or delay esophageal emptying Not able to stand or sit upright for at least 30 minutes Hypoglycemia, hypersensitvity Pregnancy: C |
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What is Alendronate (Fosamax) (action & adverse) |
Kinetics: PO, excreted kidneys Dynamics: inhibits normal & abnormal bone resorption & increase bone mineral density Adverse: musculoskeletal pain, flatulence, acid regurgitation, esophageal ulcer, gastritis, headache, erythemia Interactions: wait 30 minutes after taking alendronate before another drug |
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Alendronate (Fosamax) edu & assessment |
Edu: 30 mins before eating, swallow with 6-8 ounces of water, not lie down for 30 mins after Assess: verify throughout therapy that patient is not experiencing hypocalcemia or other adverse effects |
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Allopurinol for chronic tophaceous gout - rash |
give Benadryl/ anti-allergy drug & monitor for other reaction & tell primary provider |
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Thyroid- 2 active hormone Regulation |
2 active hormones: T3- triiodothyronine T4- thyroxin, tetraiodothyronine Regulation- Hypothalamus (TRH)- anterior Pituitary (TSH)- Thyroid (T3, T4)- Biologic effects |
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Thyroid actions/ pathology |
Actions: metabolism: stimulation of energy Stimulation of heart Promotion of growth & development Patho: hypo & hyper -thyroidism |
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Thyroid function tests--> 3 types |
Serum thyroid-stimulating hormone (TSH) screen & diagnose hypo/ elevated TSH indicates hypo T4: can cause total T4 or free T4 T3: can measure total T3 or free T3 |
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Levothyroxine (Synthroid) treats/ what is it |
Synthetic prep T4 & drug of choice for hypothyroidism-- > Conversion to T3 Half life: 7 days All forms of hypothyroidism Therapy- hypo, pituitary suppression of TSH & prevent euthroid goiter, manage secondary to thyroid cancer, treatment for myxedema coma***Life long |
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Levothyroxine actions, adverse |
Kinetics: PO, IV- myxedma coma Highly protein bound (7 day half life)- liver metabolizes, excreted via bile Contra: hypersensitivity, thyrotoxicosis Adverse: HTN, up HR, angina, hyperreflexima, tremor, anxiety Interactions: antacid, Ir & Ca supplements, Warfarin increased Eval- reversal of deficiency, TFT, skin color, temp, texture, vitals |
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What is Liothyronine (T3) |
Synthetic prep of T3 Effects same as Levothyroxin Rapid onset, short half-life, short duration of action More expensive |
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Hyperthyroidism (Graves) medications |
Antithyroid drugs: Thionamides Methimazole Propylthiouracil (PTU) Radioactive Iodine |
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Use of Methimazole (Tapazole) |
First line for hyperthyroidism Action: Block synthesis of thyroid hormones (3-12 weeks for therapeutic effects) 4 applications: -sole therapy for Graves -Adjunct to radiation until effects of radiation manifest -Suppress thyroid hormone synthesis in prep for thyroid gland surgery Patients experience thyrotoxic crisis (PTU preferred) |
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Methimazole (Tapazole) action & adverse |
Kinetics- PO, GI tract, liver metabolized, GI tract, give with food to reduce GI discomfort Contraindi- Pregnancy & lactation: D Adverse: Agranulocytosis, hypothyroidism, skin rash, pruritis, vertigo, drowsy, GI N/V |
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Propylthiouracil (PTU) action & drug info |
Anti-thyroid compound (Suppress T3, T4) Kinetics: PO, well absorbed/ liver met. & renal ex Second line to graves 90 min half life Full benefits take 6-12 months Therapeutic: graves, adjunct to radiation, thyrotoxic crisis, prep for thyroid surgery Adverse: Agranulocytsis, preg. lactaion, hypo, severe liver damage |
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PTU vs Methimazole |
PTU- severe liver damage, shorter half-life, crosses placenta less readily & lower in breast milk, blocks T4 to T3 conversion in periphery Methimazole- no liver damage, 2-3 daily doses, crosses placenta more easily, does not block in periphery Respons: baseline & coordinate testing --> skin color, temp, texture, LFT & RFT, CBC, TFT |
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Iodine -131 (Radioactive Iodine) info |
Radioactive isotope of stable iodine Emits gamma & beta rays Half life: 8 days 2-3 months for full effect treat hypertyroidism; effective in treating thyroid cancer All thyroid tissue to radiation; eliminate probs of surgery, outpatient treatment, induce hypothyroidism |
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Nonradioactive Iodine |
Strong Iodine (Lugol's Solution) suppress thyroid function in prep for thyroidectomy Adverse: brassy taste, burning sensation, soreness of teeth & gums, frontal headache, coryza, salvation, various skin eruptions -2-6 drops 3x daily for 10 days mixed w/ juice to mask the taste |
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Beta Blockers action |
suppress tachycardia & other graves symptoms benefits from beta-adrenergic blockade, not from reducing levels of T3 or T4 Beneficial in thyrotoxic crisis |
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part of brain controlling vomiting of GI contents |
vomiting center in medulla of the brain gastric secretions parasympathetic NS |
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Peptic Ulcer |
Cause: H. pylori, latrogenic: NSAID, sterioids, Hypersecretion of acid (Zollinger-Ellison syndrome) Antiulcer drugs- antibiotics, antacids, anti-secretary agents, mucosal protectants |
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H. Pylori Agents |
many drugs required to eradicate H. pylori Antimicrobials- two minimum or 3 used Amoxicillin, clarithromycin, metronidazole, tetracycline, tinidazole Bismuth salicylate (Pepto-bismol) Proton pump inhibitor or H2 antagonist--> suppression of gastric acid |
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Proton Pump Inhibitor --> omeprazole (Prilosec) |
Therapy- H. pylori w/ antibiotics, symptomatic treatment of heartburn & GERD, short term treatment of gastric & duodenal ulcers Dynamics- potent HCL inhibiotr prevents release gastric acid into stomach Kinetics: PO, 3-5 days, rapid absorption after leaving stomach, enteric coated prep destroyed in acid Contra: hypersensitvity, preg. C Adverse: headache, diarrhea, rebound hypersecretion, C. dificle infection-- low Mg Teach: 1 hr before meals, not crush or chew, entire time prescribed |
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Histamine-2 receptor antagonist drugs |
all equally effective: Ranitidine (Zantac) Cimetidine (Tagamet) Famotididne (Pepcid) Nizatidine (Axil AR) |
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Histamine-2 receptor antagonists--> Ranitidine (Zantac) |
Therapy: active/ benign duodenal gastric ulcers treat hyper-secretory conditions & erosive esophagitis Dynamics: Block H2 action at parietal cells, inhibit gastric acid secretion Kinetics: PO, IV, IM; absorb w & w/o food, liver & renal excretion Contra: hypersensitivity / Pre: hepatic or renal impairment Adverse: headache, blood count, GI Interactions: no inhibition of cytochrome P-450 Implications: trough levels in patients w/ renal or liver impairment, IV slowly to prevent hypotension, arrhythmia, long term= blood |
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Antacids |
Substances that neutralize acids, raise pH of gastric environment, & inhibit conversion of pepsinogin to pepsin |
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Antacid classification |
Aluminum compounds: amphogel/ constipates/ no diarrhea/ hypophosphatemia Magnesium compounds: milk of magnesia/ no constipation/ diarrhea/ mg toxicity Calcium compounds: Ca carbonate (tums, tetralac)/ constipation/ no diarrhea/ acid rebound, Co2 Sodium compounds: Sodium biocarb (alka-seltzer, baking soda)/ no constipation or diarrhea/ Na loading, Co2 |
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Aluminum Hydroxide w/ Mg Hydroxide Aluminum hydroxide w/ magnesium hydroxide (Maalox) |
Therapy: relieve hyperacidity, GERD, pain of duodenal ulcers Kinetics: minimal GI absorption, rapid onset, duration 20-60 mins on empty stomach Dynamic: raise pH about 4= stop pepsin= increase lower esophageal sphincter Contra: low phosphate, renal probs, massive GI bleed, renal failure, pregnancy/ lactation Adverse: constipation, diarrhea, high Mg, low phosphate Interac: many others; 2 hrs after other drugs, monitor OTC drugs |
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What is Sucralfate (Carafate) |
Barrier drug Combines with ulcer exudates to make protective barrier Speeds ulcer healing Not absorbed systemically |
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What is Prostaglandin & action |
Produced in mucosal cells of duodenum & stomach prevent ulcers in patients on NSAIDs increase mucosal blood flow & mucus production only short term--> stimulates uterine contractions in pregnant patients |
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Prostaglandin ex of drug |
Misoprostol (Cytotec)
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Antiflatulents--> simethicone (Mylicon) |
changes surface tension of gas bubbles so they can be passed more easily Not systemically absorbed Give after meals; tablets chewed well |
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Laxative action on body |
Soften, increase volume, hasten fecal passage, facilitate evacuation of stool Indication: fresh stool sample, expelling dead parasites, pregnancy or opioids, preventing impactation in bedridden, removing poisons Contra: ab. pain, N/C, UC, bowel obstruction, habitual use, fecal impactation, other bowel disorders |
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4 laxative classifications |
Bulk forming- Psyllium (Metamucil) Surfactant- Docusate sodium (Colace) Stimulant- Bisacodyl (Dulcolax) Osmotic- Milk of Magnesia (MOM) |
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Bulk forming Laxatives |
similar to fiber- swell with water= gel like & soften Most natural temporary constipation- diverticulosis & IBS Adverse: esophageal obstruction Drink many fluids |
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Surfactant Laxatives |
Two effects: stimulate motility & increase quantities of water & electrolyte in intestinal lumen Widely used & abused Legit: opioid induced & slow intestinal transit |
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Stimulant Laxative info |
direct effect on intestinal mucosa & stimulate peristalsis Bisacodyl (Fleet, Modane, Correctol, Dulcolax) Cascara sagrada (Cascara Aromatic) Sennosides (Senexon, Ex-lax, Senokot, Senna-Gen) Castor Oil (purge, Emulsoil, Neoloid) |
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Osmotic Laxative info |
Lax salts: Mg & Na= poorly absorbed draw water into intestines- softens fecal mass, enlarges, stimulates peristalsis Low: 6-12 hrs High: 2-6 hrs Adverse: dehydration, renal decline/ toxicity, Na retention= htn, edema, exacerbate HF |
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Other Laxatives |
Lubiprostone- selective chloride channel activators Glycerin suppository Mineral Oil |
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Lubricant Laxatives --> mineral oil |
Coats walls of intestine= easier passage chronic use= decrease absorption of fat soluble vitamins |
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Bowel-cleansing products for colonoscopy |
Allow for good visualization of bowel two kinds: Sodium phosphate: hypertonic w/ body fluids; cause dehydration & electrolyte disturbances; possibility of renal damage Polyethylene glycol (PEG) plus electrolytes (ELS) Isotonic w/ body fluids; require large volume of bad tasting liquids |
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GI drugs |
Antiemetics, antidiarrheals, IBS drugs, IBD drugs |
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Antiemetic info/ action |
Given to suppress N/V Emetic= reflex after activating vomiting center in medulla oblongata Several receptors in emetic response: dopamine, acetylcholine, histamine, serotonin, glucocorticoids -Possibly interacts |
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Antiemetics= serotonin receptor antagonists |
Granisetron, dolasetron, palonosetron Ondansetron (Zofran)- first for chemo induced N/V Blocks type 3 serotonin receptors on vagal nerve More effective w/ dexamethasone Give 30 mins before |
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Ondansetron (Zofran) actions & info |
blocks stimulation of special serotonin receptors in chemoreceptor trigger zone (CTZ) Treat N/V: chemotherapy, postoperatively Should be given 30 mins before chemo or anesthesia Adverse: headache, constipation, malaise, arrhythmias, hypotension, extrapyramidal effect |
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Types of Antiemetics |
Dopamine antagonists (Phenothiazines), Antihistamines, Benzodiazepines, Prokinetic agents, |
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Dopamine antagonists--> Phenothiazine |
Block dopamine2 receptors in CTZ Surgery, cancer, chemo, & toxins Adverse: extrapyramidal reactions, anticholinergic effects, hypotenison, sedation |
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Prokinetic Agent actions |
Increase GI tone & motility= more peristalsis, increased gastric emptying Therapy: GERD, chemo (N/V), diabetic gastroparesis Metoclopramide (Reglan, Maxolon, Octamide) -blocks dopamine & serotonin in CTZ -Increase upper GI Y suppress emesis |
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Motion sickness drugs |
Scopolamine- muscarinic antagonist/ adverse: dry mouth, blurred vision, drowsy Antihistamines- dimenhydrinate (Dramamine); considered anticholinergics- block receptors for acetylcholine & histamine Adverse: sedation, dry mouth, blurred vision, urinary retention, constipation |
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Diarrhea manage |
Diagnose/ treat underlying disease; replace water & salts; cramping; reduce passage of unformed stool 2 major groups- specific anti-diarrheal drugs nonspecific anti-diarrheal drugs |
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Nonspecific Antidiarrheal Agents |
Opioids- most effective anti-diarrheal agents activate opioid receptors in GI tract >> decrease intestinal motility, slow intestinal transit, allow more fluid to be absorbed, decrease secretion of fluid in sm. intestine |
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Nonspecific Antidiarrheal Agents |
Diphenoxylate (Lomotil)- may create euphoria (abuse & liperamide (Imodium) -formulated w/ atropine to discourage abuse; opioid used only diarrhea; high dose= morphine like Loperamide (Imodium)- structural analog of meperidine, no abuse |
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Manage infectious diarrhea |
general: variety of bacterial & protozoa, self-limiting infections, no treatment, antibiotics only when clearly indicated Travelers diarrhea |
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IBS- 4 groups of drugs |
Antispasmodics, bulk forming agents, anti-diarrheals, tricyclic antidepressants Antibiotics or an acid suppressant may be effective for some patients |
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What are: Crohns disease Ulcerative colitis |
C- transmural inflammation Affects terminal ileum (impact all parts of GI tract) UC- Inflammation of the mucosa & submucosa of colon & rectum/ may cause rectal bleeding/ may need hospitalization |
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Drugs for IBD |
IBD: caused by exaggerated immune response against normal bowel flora Not curative: control disease process –Aminosalicylates(sulfasalazine) –Glucocorticoids (hydrocortisone) –Immunosuppressants(azathioprine) –Immunomodulators (infliximab) –Antibiotics (metronidazole)conom |
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Digestive Enzymes--> Pancrelipase (Pancrease) Alseton (Lotronex) |
Replacement for bodys intrinsic enzymes when body produces insufficient quantity: Cystic fibrosis, chronic pancreatitis, post pancreatectomy --Should be give w/ meals Aleston (Lotronex)- serotonin type 3 blocker to reduce diarrhea in IBS, mostly works in women, not men |
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Antiobesity Agents--> orlistat (Xenical) |
Inhibit digestive enzyme lipase to decrease absorption of dietary fats Used w/ weight loss diet to manage obesity GI adverse effects common; take with every meal containing fat Teach to skip if meal has no fat/ skipped meal |
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Anorectal Preparations |
Symptomatic relief of hemorrhoids & other anorectal disorders -- local anesthetics, hydrocortisone, emollients, astringents many forms |
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Adrenal Cortex Hormones |
Affect many processes: Maintenance of glucose availability Regulate of water & electrolyte balance Develop of sex characteristics Life-preserving responses to stress |
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The endocrine system |
Adrenal glands--> adrenal medulla & adrenal cortex--> synthesize & secretes==>catecholamines (epi & norepi) & glucocorticoids/ mineralocorticoids/ androgens |
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Adrenocortical hormones- 3 classes |
steroid hormones: glucocorticoids, mineralocorticoids, androgens |
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Physiology of Adrenal corticoids |
Effect almost every organ; metabolize carbs, proteins, fats, electrolytes, water Play role in CV function & immune effects Zona reticularis region of adrenal cortex= important in production & secretion of other steroid hormones (adrenal androgens/ progesterones/ estrogens) |
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Glucocorticoids: physiologic effects |
carb, protein, fat metabolism; CV system; skeletal system; CNS system; stress; respiratory system in neonates |
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Glucocorticoids--> metabolism & effects |
Role in glucose metabolism- increase blood glucose, hepatic sensitivity, proteolysis, decrease protein synthesis in muscles Effects: gluconeogenesis, mobilize AA form protein striated muscle, protein catabolism, fat synthesis & lipolysis |
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Mineralocorticoid actions |
Influence renal processing of Na, K, & H Aldosterone- promote Na & K hemostasis, maintain IV volume, harmful CV effects w/ high levels, RAAS |
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Patho of the Adrenocortical Hormones |
Two most familiar forms of adrenocortical dysfunction: 1- Adrenal hormone excess (Cushings syndrome) 2- Adrenal hormone deficiency (Addisons disease) |
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Patho of cushing Adrenal insufficiency (1 &2) |
Cushing- rare disorder from increased adrenocortical secretion of cortisol, resulting in chronic elevation in glucocorticoids & adrenal androgen hormones AI- Primary: Addisons disease results from destruction of the adrenal cortex caused by infection or hemorrhage Secondary: adrenal insufficiency, deficiency of cortisol secretion secondary to insufficient secretion of ACTH by anterior pituitary |
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Adrenal Hormone Excess Cushing |
Cushing: cause> high ACTH, glucocorticoids, give glucocorticoids in large doses Present: obese, hyperglycemia, glycosuria, HTN, fluid & electrolyte disturbance Treat: carcinoma/ adenoma: surgical removal of adrenal gland// replace glucocorticoids & mineralocorticoids for bilateral adrenalectomy/ drugs w/ surgical treatment |
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Primary hyperaldosteronism |
Excessive secretion of aldosterone Cause: low K, metabolic acidosis, HTN Treat: underlying cause, surgery or aldosterone antagonist (spironolactone) |
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Adrenal hormone insufficiency |
Replace w/ glucocorticoids -mimic normal patterns of corticosteroid secretion -2/3 in morning & 1/3 in afternoon -increase dose in times of stress -doses for endocrine disorders much smaller than nonendocrine disorders |
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Primary adrenocortical insufficiency |
Addisons disease Present: weakness, hypotension, emaciation, hypoglycemia, high K, low Na, increased pigmentation of skin & mucus membranes Treat: replace therapy w/ adrenocorticoids, hydrocortisone is the drug of choice (glucocorticoid & mineralocorticoid) |
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Secondary Adrenal Hormone Insufficiency |
Secondary adrenocortical insufficiency from decreased secretion of ACTH Tertiary insufficiency from low CRH Both cases, adrenal secretion of glucocorticoids is diminished where mineralcorticioids is usually normal Treatment: replace therapy with glucococorticoid (hydorcortisone) |
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Acute Adrenal insufficiency (adrenal crisis) |
Can lead to death Present: weak, dehydration, lethargy, GI symptoms, hypotension Cause: adrenal, pituitary failure; inadequate doses of corticoidsteroids or abrupt withdrawal Treat: rapid replacement of fluid, salt, glucocorticoids// glucose: NS w/ dextrose |
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Congenital adrenal hyperplasia |
Treatment: glucocorticoids employed-- hydrocortisone, dexamethasone, prednisone Screening |
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Replacemetn therapy for adrenocortical insufficiency |
Require replacement therapy w/ corticosteroids Glucocorticoid always required Some patients require mineralocorticoid Principle glucocorticoids employed are: hydrocortisone, dexamethasone, prednisone Fludrocortisone only mineralocorticoid |
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Hydrocortisone actions & adverse |
Synthetic steroid w/ structure identical to cortisol Therapeutic: adrenal insufficiency, cancer, allergic reactions Adverse of high dose: Adrenal suppression, cushings syndrome (never stop replacement therapy) |
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Dexamethasone action & test |
Syntheticsteroid –Primarily glucocorticoid properties; verylittle mineralocorticoid activity Overnight dexamethasone test to diagnose Cushing’s syndrome Prolonged examethasone suppression test |
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Corticosteroid use in body |
Used in replacement therapy to maintain adequate levels of hormones in patients with inadequate adrenal function Used as: anti-inflammatory, anti-allergic, immuno-suppresive |
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Glucocorticoid drugs low vs high doses |
Corticosteriods & nearly identical to one made by body (low doses)–Modulation of glucose metabolism inadrenocortical insufficiency (high doses)–Suppress inflammation |
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Pharmacology of glucocorticoids |
Anti-inflammatory & inmmunosuppressant effects Therapeuticuses in nonendocrinedisorders–RA, Systemic lupus erythematosus, IBD, Miscellaneous inflammatory disorders, Neoplasms, suppress allograft rejection, asthma, skin disorders, allergic conditions, prevent respiratory distress syndrome in neonates |
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Molecular mechanics of glucocorticoids |
Gluco- molecular mechanisms different: receptors inside cell Y modulate the production of regulatory proteins vs signaling pathways effect metabolism & electrolytes// abrupt stop= acute adrenal insufficiency |
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Adverse Effects of glucocorticoids |
CNS:stimulation, anxiety, mood swings, insomnia, headache GI:N/V, increased appetite, weight gain, dyspepsia, peptic ulcerdisease Endocrine: hyperglycemia, suppress pituitary ACTH release, menstrualirregularities Increasedsusceptibility to infection w/long-term use Acuteadrenal insufficiency (with drug withdrawal) Cushingoidcharacteristics Fluidand electrolyte disturbances Cataracts, glaucoma, Myopathy(Muscle injury resulting in weakness) Hyperlipidemia& thrombus formation–Delayedwound healing Osteoporosis;calcium loss; and resultant fractures Growthretardation in children (asthma) |
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Glucocorticoid interactions & contraindications |
I: K loss, NSAID, vaccines, insulin, oral hypoglycemics C- systemic fungal infections, live virus vaccines, caution w/ peds & preg/ breast feeding |
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Adrenal suppression occurs: 3 |
Adrenal suppression Physiologic stress Glucocorticoid withdrawal: Taper over 7 days, switch from many to single drug, taper dose to 50% of physiologic value, monitor insufficiency |
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Glucocorticoid Routes & difference |
PO, parenteral (IV, IM, subQ), topical (page 916; table 72-2) Difference in 3 ways: Biologic half life: time required for leaving body tissues is slower than blood Mineralcorticoid & glucocorticoid potency |
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Dosage of glucocorticoid |
individualized, through trial & error No immediate threat: start low and slow–Immediate threat—start high & decrease aspossible Long-time: smallest effective amount Long high doses only if disorder is life-threatening or has potentialto cause permanent disability More when stressed & slow stopping Alternate-daytherapy |
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Glucocorticoid therapy (min & max) |
Max: daily or alternate-day dose of gluco. early in morning before 9am Min: monitor surgical patient for infection, PUD, do not stop quickly, adhere to regimen, reduce gastric irritation, oral hygiene, avoid caffeine/ alcohol/ aspirin products |
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Glucocorticoid edu & assessment |
Edu; take as prescribed, notify all providers about glucocorticoid therapy, medical identifiers, adverse effects & measure relief, diet & exercise, infection prevention Assess: therapeutic response, adverse, toxicity indications |
