CNUR 202 - Pharmacology – Cheat Sheet PDF

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main points you will need to know to get you through clinical and this course...

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Pharmacology – Cheat Sheet

10 Rights of Medication Administration 1. Right Dose 2. Right Person 3. Right Route 4. Right Time 5. Right Documentation 6. Right Education 7. Right Evaluation 8. Right Drug 9. Right to Refuse 10. Right Reason

CNS Drugs: Neurotransmitters System: 1. Cholinergic System: NT: Acetylcholine. Found in the ANS and peripheral NMJ’s 2. Dopaminergic System: NT: Dopamine 3. GABAergic System: NT: GABA. Inhibitory (mostly) in CNS 4. Noradrenergic System: NT: norepinephrine. Excitatory (mainly), stimulates brain to increase activity 5. NE Receptor System: Alpha & Beta adrenergic 6. Serotonergic System: NT: Serotonin. Widely distributed in CNS. Synthesize from amino acids. Normally Inhibitory 7. Amino Acid System: NT: Aspartate (excitatory), glycine (inhibitory) and glutamate (excitatory) Depressants for Pain: Endogenous Analgesic System: Body’s own ability to supress transmission of pain. It has a similar response like morphine. Peptides interact with opiate receptors = inhabitation of transmission of pain Ex: Endorphins 1. Opioid Analgesics: Used for moderate to severe pain. Inhibits release of substance P. Metabolized in the liver and excreted in urine. Mechanism of action: Binds with opioid receptors in the body, block transmission of pain and activates Endogenous analgesic system. Prototype: morphine. 30% bound to plasma proteins, other 70% is available to the body to use. Commonly used opioids:  Acetaminophen with codeine  Codeine  Fentanyl  Hydromorphone  Meperidine- Demerol  Morphine  Methadone  Oxycodone  Tramadol Systemic effects:  Analgesia- helps any other pain too  CNS depression

o Drowsiness, sleep, unconscious, resp. depression, decreased mental activity, pupil constriction  GI- decreased motility = constipation o Smooth muscle spasms = cramping (bowel and biliary tract) Sedation & Resp. depression major side effects*** Contradictions:  Resp. depression  Chronic lung disease  Liver/Kidney disease b/c they have problems metabolizing and excreting  Prostatic hypertrophy  Increased ICP 2. Opioid Antagonists: Reserve/ block analgesia, respiratory/ CNS depression. Competes for opioid receptors. Narcan (Naloxone). If chronic opioid use, Narcan can cause withdrawal  Opioid Withdrawal: anxiety, aggression, restless, body aches, insomnia, dilated pupils, increased RR/temp/BP  *Narcan makes withdrawal short but intense but only a week long give or take. If you slowly wean them off, withdrawal is not as intense. 3. Analgesics, Anti-Pyretics, & Anti-Inflammatory: Also known as AntiProstaglandins. Mechanism of action: Inhibit prostaglandin synthesis in CNS and peripherally, also inactivate the COX enzyme = no prostaglandin production. This can cause gastric irritation and GI bleeding b/c prostaglandins are protective in the stomach. Also have anti-platelet effects, which inhibit platelet aggregation by preventing the synthesis of thromboxane (derivative of prostaglandins). Commonly used drugs: (low to moderate pain)  ASA (Aspirin)- Nonsteroidal anti-inflammatory drugs, anti-platelet effect. Children should never have this b/c of Reye’s syndrome. Used for inflammatory disorders (arthritis), headaches, muscle aches and fever  NSAID’s (Advil, Toradol, Naproxen) - Nonsteroidal anti-inflammatory drugs, anti-platelet effect. Used for anti-inflammatory, analgesic, antipyretic and Toradol effect similar to opioid.  Tylenol – choice of drug for children with fever and elderly with renal failure. Commonly the best choice for children with fever and elderly with decreased renal fx, pregnancy b/c there is no risk for bleeding. o Pain & Prostaglandins: work with bradykinin and histamine to increase pain associated with immunity and inflammation response o Fever & Prostaglandins: are stimulated by these processes therefore prostaglandins (along with bacterial toxins, etc.) function as pyrogens (substances that cause fever) o Inflammation & Prostaglandins: initiate pain along with heat, edema, pressure, etc. during inflammation Anxiety/Insomnia: 1. Benzodiazepines: Considered a controlled substance. CNS depressant. Binds with receptors in the brain and GABA receptors (inhibitory). Muscle relaxant, hypnotic, anti-convulsants, anti-panic, pre-operative sedation. Relief of anxiety, tension and nervousness = ability to sleep. Metabolize in the liver and excreted form the kidneys. Commonly given with anti-depressant. Abrupt withdrawal = hyperarousal and CNS stimulation. Antidote is flumazenil Anti-depressants & Mood Stabilizers:

1. SSRI (Selective Serotonin Reuptake Inhibitors), TCA (Tricyclic Antidepressant) & MAOI’s (Monoamine Oxidase Inhibitors): Undergo 1st pass metabolism through the liver before reaching systemic circulation = increase doses orally d/t this. Alter the amount of NT and number/sensitivity of receptors in the brain. Prevent the reuptake, so the NT will stay in the cleft = increase sensitivity or number of receptors. Indications include depressive symptoms persisting for 2 weeks or longer. If toxicity or OD occurs may have to perform dialysis to remove the drug. Commonly used drugs:  Amitriptyline – TCA  Prozac – SSRI Anti-Seizure Drugs 1. Anti-Seizure (AED) : used to control not cure. Medication should be tapered off not stopped abruptly. Exact mechanism is unknown. Thought to: decrease movement of ions into nerve cells = altering activity of NTs. Goal is decrease excitability and increase inhibitory NTs = stabilize neuronal membranes and decrease neuronal firing in response to stimuli. Metabolized in the liver and eliminated via the kidneys. Prevention/Treatment of seizures – drug of choice depends on type and severity Ex: IV benzodiazepine - there will be times when it does work and when it doesn’t work at all Anti-Parkinson’s Disease 1. Anti-Parkinson’s disease: drug will either increase dopamine levels or decrease acetylcholine levels.

ANS Drugs: SNS: Adrenergic Drugs Alpha1: Vasoconstriction = increase BP and decrease nasal congestion, CNS stimulation, decrease insulin release and pupil dilation Beta1: Cardiac stimulation = increase myocardial contraction, increased HR and increase conduction though AV node Beta2: Vasodilation, bronchodilation, relaxation of uterus and GI, increased gylcogenolysis and increased renal secretion 1. Epinephrine (Adrenaline): Prototype. 1st line drug often used in a code. Naturally produced. Potent mix of alpha and beta-adrenergic drugs. It causes vasoconstriction; increase BP, cardiac stimulation, and dilation of bronchioles. Used in tx of respiratory distress d/t bronchospasm and anaphylaxis 2. Salbutamol (Ventolin): Beta2 adrenergic bronchodilator. Should be used for breakthrough asthma symptoms. If used more then 3x a week then an antiinflammatory should be added. People can build a tolerance to this med 3. Salmeterol: Beta2 adrenergic. Used for long-term maintenance of asthma, prevention of bronchospasm, and prevention of exercise induced bronchospasms. Not used for acute management 4. Salbutamol & Salmeterol: Stimulate Beta2 adrenergic, this activation causes the bronchi to dilate. This is bronchodilator of choice b/c produce fever cardiac related side effects such as tachycardia 5. Pseudoephedrine: Stimulate both alpha1 and both beta-receptors. Used as bronchodilator and nasal decongestant. Alpha causes vasoconstriction in the nasal mucosa. Main ingredient in crystal meth.

Adrenergic Blocking Drugs Inhibit/block the stimulation of the SNS including endogenous catecholamine and adrenergic drugs. Lyse or inhibit sympathetic NT’s such as epinephrine and norepinephrine 1. Alpha Blockers: acts primarily on skin, mucosa, intestines, lungs and kidneys to block or prevent alpha mediated vasoconstriction. Dilate arterioles, constriction of pupils, increase GI motility. Examples: Tamsulosin: Used for tx of BPH- relaxes smooth muscle in the prostate gland and urinary bladder neck, decreases urinary resistance to outflow Phentolamine (regitine): quickly reverses the potent vasoconstriction effects of extravasated vasopressor. If any meds ever go interstitial you would inject this drug, restores blood flow and prevents tissue necrosis. 2. Alpha2 Agonists: Prevent release of norepinephrine from terminal endings. Example: Clonidine: use as breakthrough drug, reduces BP within an hour, used in tx of HTN. Methyldopa: Older drug, works within 2-4 hours, drugs of choice for HTN in pregnancy 3. Nonselective Blockers: Occupy peripheral alpha1 receptors, causes vasodilation 4. Beta Blockers: occupy beta-receptor sites and prevent the receptors from responding to sympathetic stimulation. Metabolized by liver and excreted through the kidneys 5. Beta1 Blockers: Decrease HR, SNS stimulation of the heart, Prolongs SA node recovery, slow conduction rate through AV node, decrease myocardial contractility, decreased myocardial oxygen demand Example: Metoprolol 6. Beta2 Blockers: 7. Nonselective Beta Blockers: heart effects, bronchioles constrict and increase SOB, vasodilation, decrease demand for myocardial oxygen, inhibits stimulation from circulating catecholamines, anti-dysrhythmias, impairs secretion of insulin Example: Propranolol 8. Alpha1, Beta1 & Beta2 Blockers: block Alpha1, Beta1 & Beta2 to contribute to Anti-hypertensive effects. May cause less bradycardia but more postural hypotension. May cause less reflex tachycardia Examples: Labetalol & Carvedilol (showing use in management of Heart failure) PNS: Cholinergic Drugs 1. Cholinergic Agents: drugs that stimulate the PNS and mimic the effects of Ach. Mechanism of these drugs: Salivation, Lacrimation, Urinary incontinence, Diarrhea, GI cramps and Emesis. Also used for the tx of Alzheimer’s Disease helps increase or maintain memory and learning capabilities -> not a cure Example: Bethanechol- urinary tract stimulate Donezapil – Alzheimer’s disease tx 2. Direct Acting cholinergics: bind directly to the receptor on the organ. Highly resistance on the enzyme that breaks down Ach. Decrease HR, changes in BP, increase tone and contractility of GI smooth muscles, relaxes sphincters;

increase salivary glands and GI secretions. Constriction of pupils and contraction of ciliary muscles = accommodation for near vision 3. Indirect Acting cholinergics: make the endogenous Ach more available, allowing it to bind and stimulate receptors more easily Anticholinergic Drugs 1. Anticholinergics: occupy the receptor site on target organs. Blocking the PNS allows SNS to dominate. Anti-histamines, TCA, MAOI’s result in increase effects. Example: Atropine (anti-cholinergic): antidote for cholinergic OD. Only reverse the effects on muscarinic receptors, doesn’t reverse nicotinic effects of skeletal muscle weakness or paralysis

Endocrine Drugs: 1. Exogenous Corticosteroids: inhabitation of a.a. metabolism = decrease inflammation. Strengthening biological membrane = decrease edema and decrease fluid leakage. Impairs phagocytosis and lymphocytes. Reduce symptoms, not cure. Suppression of symptoms requires ++ dosing Example: Prednisone- non-endocrine disorders requiring anti-inflammatory/anti-allergic effects Dexamethasone- brain tumours- can penetrate BBB to help decrease cerebral edema. Hypoglycaemia Drugs 1. Exogenous Insulin: replaces endogenous insulin and elicits the same response. Effective in Type 1 and type 2 if needed. Used in times of stress, acute pancreatitis, sx removal of pancreas, other drugs and pregnancy. Increase temp = decrease potency of insulin (must be stored in fridge) Oral Hypoglycaemic Drugs 1. Sulfonylureas: oldest oral agent. Increases secretion of insulin. Increases peripheral use of glucose and decreases glucose production in liver. Metabolized in the liver, excreted via kidneys and bile. May not be effective during periods of stress. Contraindicated in sulfa allergies. 3rd choice of oral hypoglycaemia d/t risk of CV event 2. Alpha-Glucosidase Inhibitor: inhibit enzyme that digest carbs, and other simple sugars= slowed glucose. Take with 1st bite of meal. Works well with combination of other meds- ex: acarbose 3. Biguanide’s: increase use of glucose by muscle and fat cells. Decreases hepatic glucose production, decreases intestinal absorption of glucose. Normally does not cause hypoglycaemia. Not metabolized therefore excreted unchanged in the urine. Works well with other meds. Renal fx needs to be assessed Examples: Metformin

Respiratory System Drugs General Drug Therapy 1. Bronchodilators: prevent and tx of constriction, decrease smooth muscle tone, improve expiratory flow, decrease air trapping 2. Anti-Inflammatories: prevent and tx of inflammation, decrease constriction by decreasing airway, hyper-reactivity 3. Adrenergics: mimics SNS. Stimulates Beta2 adrenergic receptors of smooth muscle of bronchi and bronchioles, CV stimulation (increase HR and contraction = adverse effects)

4. Epinephrine: Nonselective beta-adrenergic agonists. SNS effects on all body system. Used for ACUTE bronchospasm 5. Inhaled Selective Beta2 Adrenergics Agonist: prevention and tx of bronchospasm, selective to beta2 receptors for prolonged tx, these will not be used b/c they will become tolerant to them 6. Anti-cholinergic: Anti-PNS. Maintenance rather then emergent. Blocks Ach effects of bronchial smooth muscle. Chronic inflammation increases vagal tone = Ach stimulation = increase PNS response = bronchoconstriction and increase mucous secretions so this drug prevents this from happening 7. Xanthines: thought to inhibit Ca+ movement into smooth muscle (decrease muscle constriction). Inhibit prostaglandin synthesis and release, pulmonary edema. Strengthen diaphragm contraction and decreasing inflammation. Theophylline consider 2nd line agent 8. Corticosteroids: suppresses airway inflammation, decrease mucous secretion, decreases airway edema, repair damaged epithelium; enhance effectiveness of Beta2 adrenergic bronchodilators. Short term effects. Normally given with bronchodilator Common Drugs: Pulmicort Solu-Cortef 9. Leukotriene Receptor Antagonists (LTRA’s): Blocks the action of Leukotrienes causing bronchodilation. Needs other meds to be effective. Less effective compared to steroids. Not effective for ACUTE tx. Example: Singulair (Montelukast) 10. Mast Cell Stabilizers: found in mucous, coated in IgE cells, release mediators which cause hypersensitivity= prevent the release of bronchoconstriction and inflammatory substances. Not effective in ACUTE bronchospasm. Used in combination with other meds 11. IgE Neutralizing Antibody: binds to IgE and inhibits the action of mast cells and basophils. Prevents inflammatory response to allergens. Immunosuppressive - not a 1st line drug b/c its suppresses the immunity Anti-Histamines & Allergic Drugs 1. Anti-Histamines: block the action of histamines by occupying histamine receptor sites. Inhibit smooth muscle contraction, decrease capillary permeability, decrease salivation and formation of tears 2. First Generation Anti-Histamines (H1 receptor Antagonist): Nonselective or sedating agents. Bind to both central and peripheral H1 receptors. CNS depression or stimulation, dry mouth, urinary retention, constipation and blurred vision Common Drugs: Diphenhydramine (Benadryl)- hypersensitivity to ex, motion sickness, insomnia Dimetapp & Chlor-Tripolon- cause less drowsiness Hydroxine & Promethazine- Anti-emetic 3. 2nd Generation Anit-histamine: developed to produce less sedation. Do not cross BBB. Can be given to young children. More expensive then 1st generation Common Drugs: Reactine – metabolite of hydroxyzine but causes less drowsiness. Anti-emetic Claritin Allegra

Gastrointestinal System Drugs Antacids: Alkaline, inorganic compounds that help neutralize stomach acids. Used for the treatment of mild GERD but usually aren’t used alone when treating PUD. Commonly used in a mixture with hydroxide preparations including: 1. Aluminum Compounds: Require larger dose, slower onset of action, can cause constipation, prolonged ingestion can lead to hypophosphatemia & osteomalacia, rarely used alone for peptic ulcer disease 2. Magnesium Compounds: High neutralizing capacity, quick onset of action, can cause diarrhea and hypermagnesemia, avoid in patients with renal failure b/c they can’t get rid of this compound. 3. Calcium Compounds: Rapid onset of action, can cause hypercalcemia and hyper-secretion of gastric acids, used less frequently in PUD Common Drugs Include: Dioval, Maalox, Tums, Gravol Nursing Considerations: Teach about the use – occasional use is fine but everyday, several times a day likely requires something different Shake liquid preparations well H2 Receptor Antagonists (H2 RA): Block the histamine2 receptors in the stomach (b/c they increase acid secretions), which in turn suppresses the volume and acidity of the stomach Common adverse effects: infrequent in normal administration and confusion Use cautiously in: children, pregnant women, older adults, and impaired hepatic or renal function Common drugs: Ranitidine (Zantac), Famotidine (Pepcid- which has antacid with it) Proton Pump Inhibitors (PPI’s): reduce acid secretions by binding to parietal cells; this inhibits both daytime and nocturnal acid secretions. More effective then H2RAs because it heals stomach ulcers in 2 weeks compared to 4 weeks and has a longer duration. Metabolize in the liver and excreted in urine. Effects last 48-72 hours after last dose. Common adverse effect: nausea, diarrhea, and headache Administer: 30 minutes before meals Common drugs: Omeprazole (Losec), Esomeprazole (Nexium), Lansoprazole (Prevacid), Pantoprazole (Pantoloc- only IV), Raberprazole (Pariet) Prostaglandin: 1. Misprotol (Cytotec): used in conjunction with NSAIDs to prevent GI irritation. Not for use in pregnant women b/c it can cause abortion. Causes diarrhea 2. Sucrlfate (Sulcrate): binds to normal and ulcerated GI mucosa. Used in IBS and Chrones Treatment for H.Pylori (Gram Negative): therapy for 7-14 days  Treatment of ulcers – PPI’s  Treatment of infection with 2 antibiotics – usually amoxicillin, clarithromycin, metronidazole, and tetracycline (but it has a lot of dietary restrictions)  Occasionally use bismuth salicylate (Helps inhibit bacterial growth by preventing H.Pylori from adhering to gastric mucosa) for added protection of the GI Anti-emetics: most act by inhibiting dopamine or serotonin receptors in the brain. Eight Different classes:

1. Anti-cholinergics – ex: scopolamine for motion sickness 2. Anti-histamines – ex: dimenhydrinate (Gravol) 3. Benzodiazepines – ex: diazepam (Valium) 4. Cannaboids – ex: cannabidiol (Sativex) 5. Glucocorticoids – ex: dexamethasone (Decadron) 6. Phenothiazines – ex: prochlorperazin (Stemetil) 7. Prokinetic – ex: metocloperamide (Maxeran) 8. Serotonin Receptors Antagonists – ex: ondasetron Dimenhydrinate (Gravol): Anti-histamine  Thought to relieve N&V by blocking action of acetylcholine in the brain  Side effects: drowsiness  Metabolized in liver and excreted via kidneys  IM Gravol burns when its injected Metocloperamide: Prokinetic  Increases GI motility  Treats N&V associated with gastroparesis  Side effects include: sedation, restlessness, extra pyramidal reactions (Akathisia dystonia)  Not used in patients with Parkinson’s Disease Ondasetron (Zofran): Serotonin Receptor Antagonist or 5 Hydroxytriptamine3  Useful in treating N&V associated with chemotherapy treatments, post-op nausea or moderate to severe nausea  Antagonize serotonin receptors before the noxious stimuli can activate them Prochloperazine (Stemetil): Phenothiazines  CNS depressant helpful in treating psychoses  Ability to block dopamine from receptors in the brain and chemoreceptors trigger zone  Not used as front line agent d/t numerous side effects such as sedation, cognitive impairment, extra pyramidal effects Nursing Considerations:  Based on severity of symptoms: o Chemotherapy induced N&V – ondasetron with glucocorticoid might be chose first o Motion sickness – drugs with anti-cholinergic and anti-histamine properties – dimenhydrinate or scopalamine o Will sedation be a problem – if so try to avoid agents that have high sedative properties – might opt for metocloperamide (Maxeran)  Teaching about medication adverse effects: drowsiness  Pediatrics are used cautiously with anti-emetics d/t increased risk of s...