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Pharmacology Exam 2 Study Guide 2023Pharmacology Exam 2 Study Guide 2023, Exams of Nursing

Pharmacology Exam 2 Study Guide 2023

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2022/2023

Available from 07/14/2023

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Download Pharmacology Exam 2 Study Guide 2023Pharmacology Exam 2 Study Guide 2023 and more Exams Nursing in PDF only on Docsity! Pharmacology Exam 2 Study Guide  Liver failure o Tea colored urine  Opioids o Decrease RR, decrease GI tract o Antidote: Narcan/ narlaxone o Administer when decrease RR Chapter 15 Miscellaneous Central nervous system medications  Dantrolene (Dantrium) o Antidote for malignant hyperthermia o Muscle relaxants and antispasmodics o MOA: stops muscle contraction o Peripherally acting muscle relaxant that acts directly on spastic muscles and inhibits muscle contraction by preventing release of calcium in skeletal muscles o Relief of spasticity related to cerebral palsy, spinal cord injury and multiple sclerosis o Treatment of malignant hyperthermia o Can cause CNS depression: sleepiness, lightheadedness, fatigue o Hepatic toxicity: o Anorexia, nausea, vomiting, abdominal pain, jaundice o Nurse: obtain baseline liver function test, observe for indications of toxicity, and notify provider if they occur, and start at a low dose o Muscle weakness: o Nurse: Monitor for effectiveness of medication o Contradictions: Baclofen and dantrolene o Pregnancy risk category C o Use both meds cautiously in patients who have impaired liver and renal function o Interactions: CNS depressants (alcohol, opioids, antihistamines) have additive CNS depressant effects. Advise patient to avoid concurrent use o Nursing administration: Provide assistance as needed in self-administration of medication and performance of ADLs. Advise to not stop med abruptly to avoid withdraw reaction o Nursing evaluation: increased ability to preform ADLs, absence of pain, muscle rigidity, spasms and good range of motion o Relation to calcium:  Cyclobenzaprine, tizanidine o Goes back to muscle; muscle spasticity; working in central nervous system (CNS) o Acts in the CNS to enhance GABA and produce sedative effects and depress spasticity of muscles. They have no direct muscle relaxant action and do not decrease muscle strength. Therapeutic uses: Relief of muscle spasm related to muscle injury.  Diazepam o Acts in the CNS to enhance GABA and produce sedative effects and depress spasticity of muscules o Valium o 5- 30mg max o Therapeutic uses: Pharmacology Exam 2 Study Guide  Muscle spasms related to muscle injury and spasticity  Anxiety and panic disorders  Insomnia  Status epilepticus  Alcohol withdrawal  Anesthesia induction  Baclofen o Lorazepam (Ativan) first choice for seizures o Acts in the CNS to enhance GABA, produce sedative effects, and depress hyperactive spasticity of muscle. There are no direct effects on skeletal muscles o Therapeutic uses: Relief of spasticity related to cerebral palsy, spinal cord injury, and multiple sclerosis Chapter 33 Connective tissue disorders  Systemic lupus erythematous o An autoimmune condition that can cause damage to joints, skin, blood vessels, and organs  Fibromyalgia o A syndrome characterized by muscle pain and fatigue  Gout o A painful type of arthritis caused by eleveated levels of uric acid, they accumulate and cause localized inflammation in synovial areas  Antigout o Medications work by either reducing inflammation or decreasing serum uric acid levels. o Allopurinol -Agents for hyperuricemia; select prototype medication; oral, IV -Chronic gout or frequent gout attacks Nursing considerations: Hypersensitivity reaction, fever, rash, and kidney liver damage: If administering IV, stop infusion, severe reaction can require hemodialysis or glucocorticoids Kidney injuries: Alkalinize the urine and encourage intake of 2 to 3 L of fluids/daily. Monitor I&O, BUN, and Creatinine Hepatitis: Monitor liver enzymes GI distress (n/v): Administer with food Increase in gout attacks: During first months of treatment; instruct client to report increased gout attacks to provider. Colchicine or an NSAID can be prescribed along with allopurinol to prevent this Contraindications: -Pregnancy risk category C -Contraindicated in patients who have medication hypersensitivity or idiopathic hemochromatosis -Rhabdomyolysis is most likely with long-term use. Risk is higher in clients taking statins for high cholesterol and those who have impaired kidneys or liver Pharmacology Exam 2 Study Guide  Prenisone o Steroid o Used for Rheumatoid Arthritis o Increase glucose levels o Increase risk for infection o Increase blood sugar o Increase fluid o Increase sodium o Increase HTN o Decrease bone density: causing osteoporosis o Decrease potassium o Take calcium, vitamin D and bisphosphonate (etidronate) supplements  Autoimmune condition, administer steroid in exacerbation period, put PT in remission you have to wing them off/taper down to avoid rebound effect o Not all the way because it develops Cushings Syndrome, hypertension, and poor wound healing  Calcitonin: o Prototype: Calcitonin- salmon o Expected pharmacological action: o Decreases bone resorption by inhibiting the activity of osteoclast in osteoporosis o Increase renal calcium excretion by inhibiting tubular resorption o Therapeutic uses: Treats (but does not prevent) post menopausal osteoporosis, moderate to severe Paget’s disease, hypercalcemia caused by hyperparathyroidism, and cancer o Complications: o Nausea: Advice patient that nausea is usually self limiting o Nasal dryness and irritation with intranasal route: instruct patient to alternate nostrils daily, and inspect nasal mucosa periodically for ulcerations o Interactions: Concurrent use with lithium can decrease serum lithium levels; monitor lithium levels o Calcitonin- salmon is mostly commonly given by nasal spray. It can also be given IM or SQ. Rotate injection site to prevent inflammation o Medication effectiveness: Increase bone density, serum calcium level within the expected reference range of 9 to 10.5 mg/dL  Hypocalcemia o S/S: decrease blood sugar o Trousseaus: apply BP cuff and hand will curve o Chovtek : jaw joint, then 2 fingers towards the nose; use cotton ball o Meds: (salts, carbonate) IV drugs Pharmacology Exam 2 Study Guide  Hypercalcemia o S/S: cardiac dysrhythmias, decreased blood sugar *Vitamin D enhances calcium levels  Hypokalemia o S/S:  Hyperkalemia o S/S:  Diuretics o Loop : loss of potassium, decrease sodium, H2O, decrease BP (you get rid of fluid), increase glucose (more concentration), increase blood sugar, increase phosphate, increase LDL; most potent  Loop of henle: conducts urine with in each nephron of kidney; recover of H2O and sodium chloride from urine (you will lose Na+ and K, decrease sodium)  Block Na+ and CL –  Prevents reabsorption of Na+  Fluid change can make vascular system collapse  Increase of blood sugar because volume decreases making there more concentration in the blood  Increase contractibility of the heart: creates a positive inotropic effect  Vacuum loop diuretic  Cardiac aminoglycosides  Digoxin, lanoxin (treats HF, a.fib, and heart rhythm problems)  Meds: -Furosemide: IV push straight into vein; check BP -Torsemide: *Bumex:  Foods: o K+ Sparing: keeps K+ because it is at the collecting duct; Shock  Contraindicated: foods high in potassium, digoxin (ACE inhibitor) because inhibiting enzyme, doesn’t allow A2 to excrete. *Renin converts to ACE  A1 (mild vasoconstriction), PT in shock  decrease BP, we need vasoconstriction to get out of it so A1 converts to A2 (moderate to severe vasoconstriction) then converts to aldosterone (retains water and Na+) now potassium drops  Give ACE inhibitors because PT has hypotension, so it blocks renin, called ARB (angiotensin renin blocker) so it blocks at A2, causing K+ to increase o Give to heart failure, hypotension, and less fluid PTs  If you inhibit the process of angiotensin; you inhibit sodium, so potassium will increase *DON’T give potassium sparing diuretics  Med: Spironolactone *When do you not take potassium diuretics? o ACE inhibitors o ARB- Angiotensin Receptor Blockers o Complete renin Pharmacology Exam 2 Study Guide o Thiazides :  Med: Chlorotyiside  Mild and moderate hypertension  Less potent  Distal  Tubule o Osmotic :  Proximal tubules  Creates osmotic pressure by pulling H2O into nephron  Increase excretion of electrolytes  Dexamethasone (decadron)- steroid- treats inflammation  Oliguric phase (acture kidney disease)  Vancomycin- ototoxic and nephrotoxic *** check for urination  Mannitol: treats hypervolemic shock (Inhibits reabsorption of water and sodium (Na+) Increases the osmolality of blood and renal failure Creatine level 0.6-1.35  Dehydration o Urine output o Electrolytes o HCT o Mucus membranes o LOC o Weight loss  Heart Failure or Renal Failure o PTs fluid accumulates in lungs (life threatening; use ABC’s)  Albumin o Use for: malnutrition, hypovolemic shock, liver failure, cirrhosis (liver isn’t producing albumin)  Brings back into intracellular and extracellular space o The liver produces albumin o Pulls fluid o Expands level of plasma for ascites  Myasthenia Gravis o Autoimmune o We need to block the receptors o Block // Nerve o Muscle weakness #1 (at diaphragm level) o Slurred speech, ptosis, swallowing, diplopia, stop breathing- tell them to breathe through mechanical ventilation Pharmacology Exam 2 Study Guide o When can we administer these expanders? o Prevent hypovolemic shock  Steroids o Everything  Antiheumatic drugs DMARDs I: major non-biologic o Immunomodulation medications: methotrexate, lefluomide (modulates immune, inflammation wont continue, and it slows down) o Antimalarial agent: hydroxychloroquine o Anti-inflammatory medication: sulfasalazine o Tetracycline antibiotic: minocycline *They can cause less side of effects DMARDs II: major biologic o Tumor necrosis factor antagonist o Etanercept o Infliximab o Adalimbumab o B-lymphocyte-depleting agent: Rituximab o Interleukin- 1 receptor antagonist: Abatacept DMARDs III: o Minor nonbiologic and nonbiologic o Slow degration of bones o Gold salts: Auranofin o Penicillamine o Immunosuppressant medications: -Azathioprime -Cyclosporine o Glucocorticoids -Prednisone -Prednisolone NSAIDs: o Aspirin o Ibuprofen o Diclofenac o Indomethacin o Meloxicam o Naproxen o Celecoxib Chapter 15 Miscellaneous Central Nervous System Medications Pharmacology Exam 2 Study Guide  Neuromuscular blocking agents cause muscle relaxation during general anesthesia, control of seizures, during electroconvulsive therapy, and suppression of gag reflex during endotracheal intubation. Meds: succinylcholine and vecuronium  Muscle relaxants and antispasmodic agents affect both the central and peripheral nervous system. These are used for spasticity related to muscle injury, cerebral palsy, spinal cord injury and multiple sclerosis. o Muscarinic agonist is used for urinary retention o Oxybutynin is a muscarinic antagonist used for neurogenic bladder  Neuromuscular blocking agents  Prototype medication: o Depolarizing neuromuscular blockers: Succinylcholine o Nondepolarizing neuromuscular blockers: Pancuronium  Other meds: Nondepolarizing neuromuscular blockers -Atracurium Cisatracurium Rocuronium Vecuronium  Pharmalogical action o Nondepolarizing neuromuscular blocking agents block acetylcholine (ACh) at the neuromuscular junction, resulting in muscle relaxation and hypotension. They do not cross the blood‐brain barrier, so complete paralysis is achieved without loss of consciousness or decreased pain sensation.  Succinylcholine o Mimics ACh by binding with cholinergic receptors at the neuromuscular junction. This agent fills the cholinergic receptors, preventing ACh from binding with them, and causes sustained depolarization of the muscle, resulting in muscle paralysis. o Short duration of action because of degradation by the plasma enzyme pseudocholinesterase. o Once constituted put in fridge o Anesthesia o ECT electricity to brain o Endoscopic o Melth venti  Pancuronium, atracurium, vecuronium o Block Ach from binding with cholinergic receptors at the motor end plate. Muscle paralysis occurs because of inhibited nerve depolarization and skeletal muscle contraction o Reversal agent: neostigmine ANTIDOTE for: succinylcholine it binds with E. Cholingeric receptors  Respiratory arrest: from paralyzed respiratory muscles  Prolonged apnea: low pseudocholinesterase activity can lead to prolonged apnea  Malignant hyperthermia: antidote dentrolene: manifestations include muscle rigidity accompanied by increased temperature as high as 43 C (109.4F) –from general anesthesia  Muscle relaxants o Flexophil o Baclophil Pharmacology Exam 2 Study Guide  Menopause o Duavee o Benzedoxifene o Decrease in estrogen production o S/S:  Post menopause o Meds: help with pain/dryness o Ospemiphen (osphema)
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