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138 Cards in this Set
- Front
- Back
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PROSTAGLANDINS:
What type of effects do they produce... |
-Promote inflammation, pain, pyresis (fever)
-Broncho and Vasoactive effects (constriction or dilation) -Regulate platelet fxn -Stimulate GI motility, uterine contraction -Maintenance of renal bld flow -Protect the stomach from gastric acid |
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NSAIDs:
Can be used to treat what.... Action of NSAIDs... Salicylates are derived from what... ASA is... Another form of salicylates is... |
-Inflammation
-Mild to moderate pain -HA's and fever -Arthritis -Menstrual cramps -Inhibit the cyclooxygenase (COX) enzymes I and II -Salicin, which is a chemical from willow bark -Acetylsalicylic acid (aspirin) -Diflunisal (Dolobid) |
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ASPIRIN:
Mech of action... Type of effects... |
-Irreversible inhibition of COX I and II (non-selective)
-Antipyretic -Analgesic -Anti-inflammatory -Antiplatelet -Prophylaxis of MI and stroke |
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ASPIRIN DOSES:
Dose for antipyretic effect... Dose for analgesic effect... Dose for stroke prevention... Dose for prophylaxis of MI... Dose for anti-inflamm effect... |
-Oral, rectal 325-650mg Q4-6hrs (max 4g/d)
-Same dose as antipyretic effect -75-325 mg/d (Bayer aspirin) -Lower dose for pts on ACE-i's -30-325 mg/d (Bayer) -Oral, initial 2.4-3.6 g/d in divided doses -Maintenance dose 3.6-5.4 g/d |
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ASPIRIN:
Preparations availiable... Well absorbed where... Duration of action... Bound to what... Type of elimination... |
-Caplet, enteric-coated aspirin, buffered tablets, chewable, controlled release, gelcap, rectal suppositories
-Across stomach wall (95% 1st pass clearance) -4-6 hrs -highly bound to plasma albumin -Dose dependent (low doses are 1st order; high doses are zero order) |
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Metabolism of Aspirin:
Parent compound is converted into salicylate by... Salicylate is metabolized where... Parent compounds and metabolites are eliminated by... Dependent on... |
-Esterases in the gut, RBC, and synovial fluid
-In the liver by conjugation -Tubular secretion and glomerular filtration -pH dependent |
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ARTHRITIS:
1st line of Tx is... DMARDS stands for... Action of these compard to NSAIDs... Example of these... |
-NSAIDS
-Disease Modifying Anti-Rheumatic Drugs -Much slower acting (6wk-6mo) -Methotrexate |
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METHOTREXATE:
Clinical use... Mechanism of action... Types of administration... Onset... Protein binding... How much is absorbed w/ PO... Type of metabolism/excretion... |
-Drug of choice for RA
-Inhibits aminoimidazolecarboxamide ribonucleotide (AICAR) transformylase and thymidylate synthetase. These enzymes are import for PMN chemotaxis and leukocyte proliferation during inflammation -Also inhibits dihydrofolate reductase, which inhibits DNA synthesis -SC, IM,IV, IT and oral -3-6 wks -50% -70% -Hepatic/renal |
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METHOTREXATE:
Dose... Side effects... Contraindications... |
-100-500 mg/m^2
-Nausea -Musocal ulcers -Dose-dependent hepatotoxicity -Leukopenia -Thrombocytopenia -Hepatic impairment -Bone marrow suppression -Pre-existing blood dyscrasis |
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Examples of TNF Alpha Blocking Agents...
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-Adalimumab
-Infliximab -Etanercept |
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GOUT:
How does it form... Examples of the drugs used to Tx gout... |
-Immune disorder where urate crystals build up and cause mechanical damage to cartilage and tissue damage
-Colchicine -Allopurinol -Probenecid -NSAIDS -Corticosteroids |
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COLCHICINE:
Clinical use... Mechanism of action... Onset of action... Protein binding... |
-Prophylaxis of gouty arthritis
-Binds to the protein tubulin and inhibits leukocyte migration and phagocytosis -Also inhibits the formation of LTB4, which induces inflamm -12 hrs -10-31% |
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COLCHICINE:
Metabolized... Excretion... Dosing... Side effects... |
-Partially by the liver
-Feces and urine -1-2 mg daily -Prophylaxis of attacks, 0.6 mg, 2X daily -Diarrhea, N/V, abd pain -Usually dose dependent |
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ALLOPURINOL:
Clinical uses... It is an isomer of... Mech of action... Initially administered how... Onset of action... Protein binding... |
-Preferred treatment for Gout
-Hypoxanthine -Reduces total uric acid in body by inhibiting xanthine oxidase (the enzyme that converts xanthine to urate) -Co-admin w/ Colchicine to stabilize serum uric acid - 1-2 wks - <1% |
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ALLOPURINOL:
Metabolism/excretion... Dosing... Side effects... |
-Hepatic/renal
-Initial dose: 100mg/d -Mild: 200-300 mg -Severe 400-600mg -GI intolerance -N/V -Diarrhea -Peripheral neuritis -Necrotizing vasculitis -Depression of bone marrow elements -Allergic reaction |
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PROBENECID:
Clinical use... Mech of action... Onset of action... Half life... Metabolism/excretion... |
-Gouty attacks when Allpurinol is contraindicated
-Inhibits reabsorption of uric acid in renal proximal tubules, which dec urate pool and plasma concen -2 hrs -6-12 hrs -Hepatic/renal |
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PROBENECID:
Dosing... Side effects... Caution to remember when taking... |
-0.5 mg tablets or 250mg 2X daily
-GI irritation -Nephrotic syndrome -Rash -Must maintain large urine volume to minimize urate stone formation |
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FEBUXOSTAT:
Type of drug... Important why... Effectiveness compared to others... |
-Uricosuric drug
-First non-purine inhibitor of xanthine oxidase -More effective than allopurinol at an 80 or 120mg dose (so better efficacy) |
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ANTI-INFLAMMATORY STERIODS:
The hypothalamus sends nerves to the posterior pituitary, causing... Hypothalamus secretes what to the anterior pituitary... This causes the ant pit to secrete... |
-Post pituitary to secrete Oxytocin and Vasopressin into the bld stream
-CRF (corticotrophin releasing factor) -ACTH (adrenocorticotrophic hormone) -GH (growth hor) -TSH (thyroid stimulating hor) -LH (luteinizing hor) -FSH (follicle stimulating hor) |
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Explain how glucocorticoids are secreted...
Biosynthesis of Glucocorticoids: Include... 90% are... Type of release... |
-CRH stimulates secretion of ACTH
-ACTH stimulates adrenal cortex to secrete corticosteroids. 2 types: glucocorticoids (EX: cortisol), mineralocorticoids (EX: aldosterone) -Glucocorticoids provide (-)feedback on pituitary -Cortisol (95%) -Corticostrone -Cortisone -Bound to plasma proteins -Circadian release (highest in the early morning, lowest in the evening) |
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PRIMARY ADRENOCORTICAL INSUFFICIENCY:
Syndrome is called... What is the problem... Examples of causes... |
-Addison's Disease
-Destruction or atrophy of the adrenal cortex leads to inadequate production of cortisol and aldosterone -TB, cancer, hemorrhage -Autoimmune dz -Prolonged corticosteroid tx (long term admin) -Surgical excision of adrenal glands |
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SECONDARY ADRENOCORTICAL INSUFFICIENCY:
What is the problem... Examples of causes... What is not altered... CONGENITAL ADRENOGENITAL SYNDROMES AND ADRENAL HYPERPLASIA: What is the problem... Type of deficiency... |
-Inadequate secretion of corticosteroid (mainly a GC deficiency)
-Prolonged tx w/ corticosteroids (early effects) -Mineralocorticoid secretion -Abnormally low cortisol levels results in excessive ACTH secretion, excessive adrenal secretion of androgens and hyperplasia -Synthetic enzyme |
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ADRENOCORTICAL HYPERFUNCTION:
Syndrome is called... What is the problem... Example of causes... |
-Cushing's Disease
-Excessive ACTH secretion -Abnormally high corticosteroid levels -Adrenal tumor (benign or malignant) |
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Mechanism of Action for Anti-Inflammatory Steroids...
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-Suppress T-cell activation & cytokine production
-Suppress mast cell degranulation -Decrease capillary permeability indirectly by inhibiting mast cells and basophils -Reduce the expression of COX II and prostaglandin synthesis -Reduce prostaglandin, leukotriene and platelet activating factor levels by altering phospholipase A2 activity |
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Examples of Routes of Admin for GC...
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Local (preferred):
-Intra articular (IA) -Intrabursal (IB) -Intralesional (IL) -Intrasynovial (IS) -Soft tissue (ST) -Intrarectal (IR) -Topical, Nasal, Inhaled Systemic: -PO, IM, IV, SubQ (SC) |
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Pharmacokinetics of GC:
Daily admin of corticosteroids at physiological concen for at least 2 wks does what... Recovery may take how long... The liver is the primary site of... GC are metabolized by... How are GCs excreted... |
-Suppresses the HPA axis, resulting in decreased production of endogenous hormones
-up to 9-12 months -GC inactivation -Cytochrome P450 3A4 enzymes -25% are excreted in bile and feces -75% of GC metabolites are excreted in urine |
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The differences in individual corticosteroids have to do with...
Examples of short acting GCs... Intermediate acting GCs... Long acting GCs... |
-Biological Half life
-Mineralocorticoid potency -GC(anti-inflammatory) potency -Hydrocortisone and Cortisone -Prednisone -Prednisolone -Methylprednisolone -Triamcinolone -Betamethasone -Dexamethasone -Paramethasone |
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HYDROCORTISONE:
Type of action... Clinical uses... Relative anti-inflamm potency... Plasma half life... Biological half life... |
-Short acting GC (8-12hrs)
-Localized inflammatory conditions (EX: ulcerative colitis) -Dermatitis -1 -30 mins -8-12 hrs |
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HYDROCORTISONE:
Types of admin... Contraindications to IR admin... |
-Oral
-Injectable -Topical (creams and ointments) -IR (foam) -Systemic fungal infection -Recent ileocolostomy -Intestinal anatomoses and abscess |
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PREDNISONE:
Type of action... Clinical uses.... Relative anti-inflamm potency is... Metabolized how... Plasma half life... Biological half life... Administered how... |
-Intermediate acting GC
-Adjunct therapy for arthritis (short term admin), asthma, COPD -UC and Crohn’s disease -Rheumatic and dermatologic disorders -4 (so its 4x more potent than cortisol) -In the liver to become an active metabolite -60min -18-36hrs -PO only! 1mg/kg/d |
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PREDNISOLONE:
Type of action... Clinical uses.. Plasma half life... Biological half life... Type of admin... |
-Intermediate acting GC
-Opthalmic disorders, respiratory diseases -60 min -18-36 hrs -Oral, injectable (systemic and local) |
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METHYLPREDNISOLONE:
Type of action... Clinical uses... Plasma half life... Biological half life... Type of admin... Adverse effects... |
-Intermediate acting GC
-RA, intra articular injections, UC, severe alcoholic hepatitis -60 min -18-36 hrs -Oral, injectable (systemic and local) -Vertigo -HA -Wt gain, Na/H20 retention -Impaired wound healing |
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TRIAMCINOLONE:
Type of action... Clinical uses... Plasma half life... Biological half life... Type of admin... |
-Intermediate acting GC
-Opthalmic disorders, respiratory diseases (Similar to prednisolone) -60 min -18-36 hrs -Oral, injectable (systemic and local) |
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Inhaled Glucocorticoids:
Used how... Mechanisms of action... Side effects... |
-For long term control of chronic asthmatic symptoms
-Reduce bronchial hyperreactivity -Decrease synthesis and release of inflammatory mediators (leukotrienes, prostaglandins, histamine) -Decrease infiltration and activity of inflammatory cells (eosinophils, leukocytes) -Decrease edema of the airway mucosa and mucus production -Increase responsiveness to B2-agonists -Oropharyngeal candidiasis (Thrush) -Dysphonia (hoarseness) -Adrenal suppression -Bone loss -Retarded growth |
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Examples of Inhaled GC's used for Long term control of Chronic Asthma...
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-Beclomethasone
-Budesonide -Flunisolide -Fluticasone propionate -Triamcinolone acetonide |
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BETAMETHASONE:
Type of action... Clinical uses... Relative anti-inflamm potency is... Plasma half life... Biological half life... Type of admin... |
-Long acting GC (36-54 hrs)
-Respiratory dz's or distress syndrome, local inflammatory conditions (similar to prednisone). Life threatening or disabling condition -25 -300+ min (~5hrs) -36-54 hrs -Oral, topical, injectable (systemic or local) |
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DEXAMETHASONE:
Type of action... Clinical uses... Type of anti-inflam action... Relative anti-inflam potency... Plasma half life... Biological half life... Type of admin... |
-Long acting GC
-Lupus and RA; Life threatening or disabling conditions -MAXIMAL anti-inflamm action -25 -110-210 min (~1.5-3.5 hrs) -36-54 hrs -Oral, topical, injectable (systemic or local) |
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Adverse Effects of GCs:
Adrenocortical insufficiency leads to suppression of... Adrenocortical excess leads to... CNS effects... Musculoskeletal effects... Cardiovascular effects... Other effects... GC withdrawl should be done how... Withdrawal symptoms... |
-HPA axis
-Cushing's disease (moon face, buffalo hump) -Psychological and behavioral changes, aggravation of pre-existing psychiatric disorders -Osteoporosis, muscle weakness and atrophy -Fluid retention, edema, HTN -Diabetes mellitus -Impaired wound healing -Slowly! -Hypotension, hypoglycemia, myalgia and fatigue |
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Drugs that Enhance Corticosteroid Effects include...
What do all of these agents have in common? Drugs that reduce their effects include... what do these drugs have in common? |
-Estrogens
-Oral contraceptives -Antifungal agents -Antibiotics -They all inhibit cytochrome P450 enyzymes -Antacids -Cholestyramine *these drugs decrease the absorption of corticosteroids -Phenytoin (induces cytochrome P450 enyzymes) |
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PARKINSON'S DISEASE:
What kind of disorder is it... What is the pathophysiology behind it... DA is a precursor to... |
-An idopathic neurological disorder of the extrapyramidal system which regulates movement
-Normally, dopamine (DA) neurons, orginating in the substantia nigra, inhibit the GABAergic output from the corpus striatum. Cholinergic neurons exert an excitatory effect on them. In Parkinson's, there is a degeneration of DA inhibitory neurons. Ach then stimulates GABA neurons unopposed, resulting in abnormal movements -Epi and NorEpi (NE) |
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What are the goals of therapy...
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-Restore dopaminergic activity (Levodopa + DA agonist)
-Restore normal balance of cholinergic and dopaminergic control of the basal ganglia (anticholinergic drugs) |
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LEVODOPA:
Clinical use... Can be combined with... It is a precursor to... Mech of action of levodopa... Mech of action of Carbidopa... Absorbed where... Absorption depends on... How much enters the brain... |
-1st line drug or supplement to DA agonist
-Levodopa/carbidopa is the most effective -Precursor to DA -It crosses the BBB and is decarboxylated to DA. It activates the DA receptors and restores fxn -Blocks the degradation of levodopa in the periphery, increasing the amount that reaches the brain -In small intestine -Depends on gastric emptying -1-3% |
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LEVODOPA:
Levodopa/Carbidopa combo (Sinimet) administered how... Onset of action... Duration of action... Metabolized by... into what... Excretion... Dosing tips... What can be done to improve response and alleviate adverse effects... |
-Orally to prolong half life
- 1hr -1-3 hrs -Liver into homovanillic acid and dihydroxyphenylacetic acid -Renal -Take 30 mins before meals -May be used in combo with DA agonist to keep levels constant -Drug holidays of 3-21 days |
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Adverse Effects of LEVODOPA:
GI effects... Cardiovascular effects... Dyskinesias... CNS effects... Other effects... |
-When given alone, N/V and anorexia
-Tachycardia, ventricular extrasystoles (increased catecholamines); postural hypotension; HTN with high doses -Choreoathetosis of face and distal extremities is most common -Depression, anxiety, agitation, insomnia, somnolence, confusion, delusions, hallucinations and nightmares -Mydriasis (excessive pupil dilation)- may precipitate an acute glaucoma attack |
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LEVODOPA:
Contraindications include... Drug Interactions: Drugs that decrease effect of Levodopa... Drugs that increase effect of Levodopa... |
-Hypersensitivity to Levopdopa or carbidopa
-Narrow angle glaucoma -CV (MI dysrhythmia) -Psychotic pt: exacerbate mental disturbance -Malignant melanoma: DA is precursor for skin melanin -Peptic Ulcer disease: GI bleeding -Antipsychotics, benzodiazepines -Phenytoin -High protein diet -Iron binds levodopa -Phenothiazine -Nonselective MAOI's (they cause hypersensitive rxns b/c they incr the storage and release of DA, leading to a hypertensive crisis |
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Dopamine Agonists:
Clinical uses... Mechanism of action... Examples of DA agonists... |
-1st line drug or supplement to Levodopa
-Direct stimulation of DA receptors; lower incidence of the response to fluctuations -Bromocriptine or Pergolide (Old drugs) -Pramipexole and Ropinirole (newer drugs) -Apomorphine (Only used to rescue pts from disabling response to fluctuations to levodpa |
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BROMOCRIPTINE:
Type of drug... Type of admin... Onset of action... Duration of action... Protein binding... Metabolism/excretion... How to dose... |
-D2 receptor agonist
-Oral -1-2 hrs -6-8 hrs -90-95% -Hepatic/ bile and feces -Lower doses initially, then gradual increase over 2-3 months. This is to minimize ADE's |
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BROMOCRIPTINE:
Contraindications include... Which drugs decrease its effect... Which drugs increase its effect... |
-Hypersensitivity to bromocriptine
-Uncontrolled HTN -Severe ischemic heart disease -Pregnancy -Antipsychotics and metaclopramide --Alpha agonists, anti-fungals, MAOI's |
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PERGOLIDE:
Type of drug... Type of admin... Half life... Protein binding... Metabolism/excretion... Type of dosing... Contraindications include... Which drugs decrease its effect... Which drugs increase its effect... |
-D1 and D2 receptor agonist
-Oral -27hrs -90% -Hepatic/renal -VERY low (.05mg for 2 days), then increase gradually -Hypersensitivity to pergolide -Pts on azole antifungals and some macrolide antibiotics -Antipsychotics, metoclopramide -Levodopa and MAOI's |
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PRAMIPEXOLE:
Type of drug... Type of admin... Duration of action... Protein binding... Metabolism/excretion... Contraindications include... Which drugs decrease its effect... Which drugs increase its effect... |
-D3 receptor agonist
-Oral -~8 hrs -15% -Hepatic/renal -Hypersensitivity to Pramipexole -Renal insuffciency (adjust the dose) -Preexisting dyskinesias -DA antagonists (antipsychotics and metaclopramide) -Cimetidine |
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ROPINIROLE:
Type of drug... Onset... Duration of action... Metabolism/excretion... Can be effective when... Contraindications include... What drugs decrease its effects... What drugs increase its effects... |
-D2 receptor agonist
-1 hr -6 hrs -Hepatic/renal -In mild states as a monotherapy -Hypersensitivity to ropinirole -Pts at risk for hypotension (drug may cause postural hypotension) -Preexisting dyskinesias -Antipsychotics, cigarette smoking, metaclopramide -Ciprofloxacin (abx); Refecoxib (COXII inhibitor); estrogens |
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What are the similar adverse effects that all DA receptor agonists cause....
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-Anorexia
-N/V -Constipation -Dyspepsia -Postural hypotension -Dyskinesia -Confusion -Hallucinations -Delusions -Headaches |
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COMT Inhibitors:
Clinical uses... How do they work... |
-Used to offset increase in COMT degradation of Levodopa following carbidopa (decarboxylase inhibitor) activity
-Carbidopa is a dopa decarboxylase (DDC) inhibitor. When DDC is inhibited, other compensatory pathways activate, like the COMT. -COMT increases levels of 3OMD, which competes w/ Levodopa to be transported across the BBB. -So inhibit COMT, inhibit 3OMD, less competition for levodopa, more crosses BBB |
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Examples of COMT Inhibitors...
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-Entacapone (has peripheral effects only)
-Tolcapone (has both peripheral and central effects; more potent) -Stalevo is combo of levodopa, carbidopa and entacapone |
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TOLCAPONE:
Type of admin... Onset of action... Half life... Protein binding... Metabolism/excretion... Important things to remember about dosing... Contraindications... |
-Oral
-1 hr -2-3 hrs - >99% -Hepatic/renal -Decrease levodopa levels 30% initially (first 48 hrs) to prevent overshoot -If Tx isn’t effective w/in 3 wks, discontinue use -Hypersensitivity to Talcapone -H/O liver disease -Hyperpyrexia -Preexisting dyskinesias |
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TOLCAPONE:
Side effects include... What drugs increase its effects... Concomitant use w/ MAOI's increase... |
-Diarrhea, abd pain
-Liver injury -Orthostatic hypotension -Sleep disturbances(insomnia) -Orange discoloration of urine -Additive effects with CNS depressants (barbiturates and benzodiazepines) -Increase risk of cardiovascular effects |
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DOPAMINE RELEASERS:
Clinical uses... Mech of action... Examples... |
-Reduce tremors and rigidity associated with Parkinson’s disease (advanced stage)
-Antiviral agent -Mode of action is unknown, may potentiate DA synthesis, release and uptake -Amantadine |
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AMANTADINE:
Type of admin... Onset of action... Protein binding... Half life... Metabolism/excretion... Beneficial effects of dosing... Contraindications... |
-Oral
-48 hrs -67% -16 hrs -Hepatic/renal -Effects are short lived, only a few wks -Not as potent as Levodopa -Liver dz -History of dermatitis -Uncontrolled psychosis -Pts on CNS stimulant drugs |
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AMANTADINE:
Side effects include... What drugs decrease its effects... What drugs increase its effects... |
-Restlessness, insomnia, excitement
-Depression, irritability -Hallucinations, confusion -Peripheral edema -Headache -Heart failure -Postural hypotension -Urinary retention -Antipsychotics -Anticholinergics potentiate CNS effects |
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MAO-B Inhibitors:
2 types of monoamine oxidases... Clincal uses... Mech of action... Examples... |
-MAO-A metabolizes NE and 5HT
-MAO-B metabolizes DA -Parkinson’s disease as an adjunct to levodopa -Irreversible inhibitor of MAO-B; decreases breakdown of DA; enhances the effects of levodopa -Selegiline -Rasagiline (more potent in preventing MPTP-induced Parkinson’s dz) |
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SELEGILINE:
Type of drug... Type of admin... Onset of action... Duration of action... Protein binding... Metabolism/excretion... Take dose when... Contraindications... |
-MAO-B inhibitor
-Oral -1 hr -24-72 hrs -90% -Hepatic/renal -w/ breakfast or lunch -Hypersensitivity to selegiline -Pheochromocytoma -Concomitant use of SSRIs, St. John’s Wort, or other MAOI's. |
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SELEGILINE:
Side effects include... What drugs decrease its effects... What drugs increase its effects... |
-Headaches
-Dizziness -Nausea -Hypotension -Chest pain -Phenytoin, Carbamazepine, Phenobarbital -Amphetamines, Methyphenidate, Meperidine |
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Centrally Acting Anticholinergic Drugs:
Clinical uses... Mech of action... Examples... |
-Improves tremors and rigidity associated w/ Parkinson’s
-Decrease effects of acetylcholine -Improves balance between DA and Ach in the basal ganglia -Trihexyphenidyl -Benztropine |
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TRIHEXYPHENIDYL:
Type of drug... Type of admin... Onset of action... Half life... Metabolism/excretion... Side effects include... |
-Anticholinergic drug
-Oral -1 hr -3-4 hrs -Hepatic/renal -Tachycardia -Confusion -Agitation -Constipation -Headaches -Euphoria |
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TRIHEXYPHENIDYL:
Contraindications include... Drug interactions include... |
-Narrow angle glaucoma
-Duodenal obstruction -Peptic ulcers -Increases gastric degradation of levodopa and amount absorbed |
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MAC:
Stands for... What is it... When is anesthesia achieved... How does MAC relate to potency... Importance of a MAC of 1.3 of any inhalation anesthesia... |
-Minimum Alveolar Concentration
-the measure of the potency of inhalation anesthesia. The concentration of anesthetic that prevents skeletal muscle movement in response to a supramaximal painful stimulus in 50% of pts. -When all of the partial pressures are in equilibrium (PA of anesthesia, Pa in bld, Pbr in brain) -High MAC = low potency -Low MAC = high potency -Prevents movement in approximately 95% of pts |
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Solubility:
How does it affect time to induction of anesthesia... Type of relationship btwn solubility and rate of rise of arterial tension... |
-If a drug has a low solubility (EX: nitrous oxide), few molecules are required to raise partial pressure, and concen of drug in the brain rises quickly
-A drug with high solubility has more of its molecules dissolve before the partial pressures change significantly, so induction to anesthesia rises slowly (EX: halothane) -INVERSE RELATIONSHIP between bld solubility and rate of rise of arterial tension (induction of anesthesia) |
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FACTORS THAT ALTER MAC:
Factors that produce NO change in MAC... Factors that increase MAC... |
-Duration of anesthesia
-Gender -Anesthetic metabolism -Thyroid gland dysfunction -Hyperkalemia or hypokalemia -PaCO2 15- 95 mmHg -PaO2 >38 mmHg -Hyperthermia -Drugs that increase CNS catecholamines -Infants -Hypernatremia -Chronic ethanol abuse (?) |
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Factors that decrease MAC...
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-Hypothermia
-Preop meds -IV anesthetics -Neonates -Elderly -Pregnancy -Postpartum -alpha-2 agonists -Acute ethanol ingestion -Lithium -Hyponatremia -Cardiopulmonary bypass -Systemic blood pressure <40mmHg -PaO2 <38 mmHg |
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Objectives of Anesthesia:
In most situations, the objectives of general anesthesia include the triad of... |
-Movement (muscular relaxation)
-Pain (Suppression of reflex responses to noxious surgical stimuli) -Unconsciousness (amnesia, sedation) |
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INHALED ANESTHETICS:
Example of gases... Examples of volatile liquids... |
-Nitrous oxide
-Methoxyflurane -Enflurane -Isoflurane -Desflurane -Sevoflurane |
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General Anesthetics:
Overall goal is... They also cause what... Relationship btwn induction rates and recovery rates... |
-Unconsciousness
-Depression of CV and respiratory systems -Drugs with rapid induction rates have quicker recovery rates |
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Nitrous Oxide:
Induction rate... Anesthesia... Eliminate reflex to pain... Muscle paralysis... Effect on BP... Ventilation... Sevoflurane... |
-3-5 min
-Incomplete -Yes -No -No change -No change -3-5mins -yes -Some -Some -Decrease -Decrease |
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Desflurane:
Induction rate... Anesthesia... Eliminate reflex to pain... Muscle paralysis... Effect on BP... Ventilation... Enflurane... |
-3-5min
-Yes -Some -Some -Decrease -Decrease -10-30 min -Yes -Some -Some -Decrease -Decrease |
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Isoflurane:
Induction rate... Anesthesia... Eliminate reflex to pain... Muscle paralysis... Effect on BP... Ventilation... Methoxyflurane... |
-10-30mins
-Yes -Some -Some -Decrease -Decrease ->60 mins -Yes -Some -Minimal -Decrease -Decrease |
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Ether:
Induction rate... Anesthesia... Eliminate reflex to pain... Muscle paralysis... Effect on BP... Ventilation... |
->60 min
-Yes -Some -Yes -Increase -Increase |
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NITROUS OXIDE:
Color and odor... Flammable... Mech of action... Clinical uses... |
-Colorless and odorless
-Nonexplosive and nonflammable -CNS depressant; suppresses action potentials in CNS neurons -General anesthesia, sedation, and analgesia, adjunct to other inhalation and IV anesthetics |
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EFFECTS OF NITROUS OXIDE:
CV effects... Respiratory sys effects... Brain effects.. Kidney effects... Liver effects... Eliminated how... |
-None
-Decreases tidal volume -Increases respiratory rate -Increases cerebral bld flow, intracranial pressure and cerebral metabolic rate -Reduces seizures -Reduces renal blood flow, GFR and urinary output -Reduces blood flow -ALL eliminated by exhalation. Less tha 0.01% is metabolized by the liver |
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NITROUS OXIDE:
Dosing... Contraindications... Toxicity effects if toxic levels reached... Drug interactions.. |
-25%-50% w/ O2 (sedation and analgesia)
-40%-70% w/ O2 (general anesthesia) via a mask -Air embolism -Pneumothorax -Acute intestinal obstruction -Intracranial air -Pulmonary air cysts -Intraocular air bubbles -BM depression -Neurological deficiencies -Attenuates the circulatory and respiratory effects of volatile anesthetics -Potentiates neuromuscular blockade |
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Reticular Activating System:
Located where... Controls what... |
-In the brain stem
-Maintains a state of consciousness, controls respirations and cardiac rhythms |
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Mechanism of Action for Inhalation Anesthetics loss of consciousness:
GABA stands for... What is it... Found where... What does it do... What responds to GABA... How do inhalation anesthetics affect GABA... |
-Gamma AminoButyric Acid
-An inhibitory neurotransmitter within the Reticular Activating System which depresses CNS neural activity -1/3 of all CNS neurons -Enhance the binding of GABA to its receptor -Augment chloride conductance through the GABA A receptor -Alter nicotinic receptor activity (fast excitatory transmission) |
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ISOFLURANE:
Chemical isomer of... Clinical uses... Type of solubility... Type of induction and recovery... Onset... Duration of action... Metabolize/excretion... Dosing... |
-Enflurane
-Induction and maintenance of general anesthesia -Low solubility -Rapid -7-10mins -Depends on drug concen in bld -0.2% metabolized in liver/exhalation -Induction 1.5-3% in adults |
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Effects of Isoflurane:
CV effects... Respiratory effects... Brain effects... Kidney effects... Liver effects... |
-Decreases BP and systemic vascular resistance
-Increases HR without altering CO -Reduces tidal volume -Increases PaCO2 -Increases cerebral bld flow and intracranial pressure -Reduces cerebral metabolic rate and seizures -Reduces renal blood flow, GFR, and urinary output -Reduces hepatic bld flow |
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ISOFLURANE:
Contraindications... Adverse effects... Drug Interactions... |
-None
-Respiratory acidosis with deeper levels of anesthesia -PaCO2 increases but doesn’t return back to normal ventilation -Potentiates nondepolarizing neuromuscular blockers -Increases the arrhythmogenic effects of epinephrine -Opioids reduce the MAC for isoflurane |
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SEVOFLURANE:
Clinical uses... Type of solubility... Type of induction and recovery... Onset... Duration of action... Metabolism/excretion... |
-Induction and maintenance of anesthesia
-Low (low bld:gas partition coeff) -Rapid -2 min -Depends on bld concen -3-5% by liver/exhalation |
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Effects of Sevoflurane:
CV effects... Respiratory effects... Brain effects... Kidney effects... Liver effects... |
-Reduces BP, HR, systemic vascular resistance and CO
-Decreases tidal volume -Increases PaCO2 -Increase cerebral bld flow and Intracranial pressure -Decreases cerebral metabolic rate and seizures -Reduces renal blood flow, GFR and urinary output -Reduces hepatic blood flow |
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SEVOFLURANE:
Contraindications... Drug interactions... |
-Hypersensitivity to Sevoflurane
-Pts with renal insufficiency, hepatic conditions -Malignant Hyperthermia -Aminoglycosides increase the risk of nephrotoxicity -Benzodiazepines and opioids reduce its MAC -Potentiate the effects of nondepolarizing NMB |
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Malignant Hyperthermia:
Type of disorder... What is abnormal... What is the treatment for this... There are mutations in what... This causes adverse rxns to... |
-Inherited genetic disorder
-Skeletal muscle is abnormal -Ryanodine receptor, an intracellular Ca channel that regulates release of intracelluar Ca from internal stores -Inhalation anesthetics and succinylcholine -Dantrolene sodium injection -Works by inhibiting the ryanodine receptors to prevent increases in intracellular calcium and excitation-contraction coupling |
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What are some of the effects that malignant hyperthermia causes...
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-Excessive calcium release
-Increased intracellular calcium -Sustained contraction -Increased energy utilization -Increased heat production -Hypermetabolism -Fever -Hyperkalemia -Cardiac Arrhythmias |
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Balanced Anesthesia:
Induction is done using... What else can be given... what is given to facilitate intubation... What is given for maintenance of anesthesia... |
-IV agent (EX: Thiopental, Propofol, Etomidate or Ketamine) which causes unconsciousness long enough to establish anesthetic brain tension
-Supplemental analgesic agent (EX: opioid or N2O) -Neuromuscular blocking (NMB)agent (EX: succinylcholine or curariform drugs) -Halogenated hydrocarbon anesthetic (EX: Sevoflurane, desflurane, enflurane and isoflurane; sometimes with N2O) |
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Rapid-Sequence Induction of Anesthesia:
What is the standard method... Advantages... |
-Thiopental + opioid followed by succinylcholine
-Propofol + opioid followed by succinylcholine -Minimizes time during which the trachea is unprotected Quick onset of anesthesia (w/in 30sec) -Trachea may be intubated w/in 60-90sec (assist with an oxygen mask) |
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Inhalation Induction of Anesthesia:
What is given... Onset of induction is... Advantages... Disadvantages... |
-N2O + (sevoflurane or desflurane or isoflurane) + NMB agent, IV
-3-5 mins -Can be titrated according to pt’s needs; minimize risk of overdose -Slower induction time and longer period of time without protection of the airway |
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Combined Intravenous-Inhalation Induction Anesthesia:
What is given... Onset of induction... Advantages... |
-Thiopental, propofol or midazolam given IV before inhalation of a volatile anesthetic
-Induced rapidly -Anesthetic dose may be titrated according to the pts needs |
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Factors That Speed Induction of Anesthesia....
These factors also speed up what... IV Induction agents distribute to what parts of the body first... |
-Elimination of rebreathing
-High fresh gas flows -Low anesthetic-circuit volume -Low absorption by the anesthetic circuit -Decreased solubility -High cerebral blood flow -Increased ventilation -Recovery from anesthetics -Brain, heart, liver, and kidneys. Then skeletal muscle and skin. Then adipose, bone, and conn tissue |
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THIOPENTAL:
Clinical use... MOA... Solubility... Routes of admin... Protein binding... Half life of distribution... Elimination half life... Metabolism/excretion... |
-Induction anesthetic; supplement to anesthesia (long term surgical procedure); maintenance hypnotic for short term surgical procedure.
-Depress neuronal activity by stimulating chloride conduction through GABA channels -Enhance the binding of benzodiazepines and GABA -Increases cerebral vascular resistance which reduces intracranial pressure -Highly lipid soluble -IV and rectal -80% -Rapid -3-12 hrs -Liver/renal |
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THIOPENTAL:
Side effects include... |
-Drowsiness
-Cardiovascular depression (decreases myocardial contractility and dilates capacitance vessels, which reduces venous return) -Respiratory depression |
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ETOMIDATE:
Clinical uses... MOA... Type of admin... Type of solubility... At physiological pH, what state is it in... Metabolism/excretion... Side effects... |
-Induction of anesthesia (it is a hypnotic with no analgesic activity)
-IV -High lipid solubility -Largely unionized -Hepatic/renal -Minimal CV & respiratory depressant effects -More N/V than with barbituates -Long-term infusion induces adrenocortical suppression |
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KETAMINE:
Clinical uses... MOA... Type of admin... Solubility... Protein binding... Type of uptake and redistribution... |
-Induction of anesthesia; dissociative (trance-like and cataleptic) anesthesia
-Relays sensory info to cerebral cortex from reticular activating system from the limbic cortex -Some NMDA antagonist activity -Analgesic effects -Increases cerebral bld flow and CO -IV and IM -Lipid soluble -Less protein binding than Thiopental -Rapid |
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KETAMINE:
Side effects... |
-Serious, excitatory and hallucinatory activity (cry, hallucinate, scream)
-Cardiostimulatory effects -Vomiting, salivation, lacrimation, shivering, skin rash -Increases intracranial pressure and pulmonary vascular resistance |
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PROPOFOL:
Clinical uses... MOA... Type of admin... Metabolism/excretion... |
-Hypnotic with moderate to deep sedation
-Induction of anesthesia -Anti-emetic properties (preferred outpt anesthetic) -Facilitates inhibitory neurotransmission by GABA -IV -Also available as oil-in-water emulsion (may cause allergic rxn and pain on injection) -Hepatic -Clearance rate is 10X that of Thiopental -Renal excretion |
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PROPOFOL:
Side effects... |
Cardiorespiratory depressant activity:
-Decreased ABP -Hypotension is greater than with thiopental -Impairs baroreflex resonse to hypotension -Apnea -Inhibits hypxic ventilatory drive -Reduces cerebral blood flow -Hiccups -Twitching may accompany anesthesia |
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MIDAZOLAM:
Type of drug... Clinical use... MOA... Type of admin... Solubility... Metabolism/excretion... Side effects... |
-Benzodiazepine
-Premedication -Induction of anesthesia; hypnotics/sedation -Facilitates GABA receptor binding (Slower loss of consciousness and a longer recovery than Thiopental) -IM, IV, intranasal, buccal and sublingual -Water soluble at low pH -Hepatic/renal -Minimal CV depressant effects -IV admin produces respiratory depression -Reduced cerebral bld flow (less than barbituates) |
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Intravenous Anesthetics in Ambulatory Anesthesia:
Methohex: Dose... Recovery... SE's... Propofol... Thiopental |
-1.5 – 3.0 mg/kg
-Rapid -Pain, Excitation -1.5 – 2.5 -Rapid -Pain, CV Depression -3.0 – 6.0 -Immediate -Drowsiness |
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Intravenous Anesthetics in Ambulatory Anesthesia:
Etomidate: Dose... Recovery... SE's... Ketamine... Eltanolone... |
-0.15 – 3.0 mg/kg
-Immediate -Pain, myoclonus, N&V -0.75 – 1.5 -Immediate -CV stimulation, Hallucinations -0.5 – 1.0 -Immediate (?) -Myoclonus, Drowsiness? |
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Midazolam:
Dose... Recovery... SE's... |
-0.1 – 0.2 mg/kg
-Slow -Sedation, amnesia |
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LOCAL ANESTHETICS:
LAs are either... How do LAs work... Voltage gated Na channels are found where... Na channel is composed of what... When do Na channels open and there is Na influx... |
-Amino amides or esters
-Prevent conduction of nerve impulse by inhibiting influx of Na ions across cell membrane -In the nerve axon only -One major glyco-protein and differing number of sub-units -When MP moves from resting (-65mV) to -55mg, the Na channel opens and there is Na influx -Na permeability increases 500-5000 fold -Channel closes and cant open until it returns to RMP |
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LA Mechanism of Action:
LAs work how... LAs promote what... |
-By preventing generation of AP. They bind to Na channels and prevent the membrane from achieving threshold
-The inactive state of the channel |
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Structure-Activity Relationship:
The speed of onset of a drug is determined by... How does a LA cross the membrane... Comparing speed of onset of action of Mepivicaine (with pKa-7.6 and %RN at pH 7.4 of 40) to Bupivicaine (with pKa 8.1 and %RN of 18)... |
-pKa of the LA
-It has to be in UNIONIZED form. Once in the neuron, it becomes more acidic, causing LA to become ionized -Mepivicaine crosses the membrane quicker b/c more of it is in an unionized form, so its onset of action will be quicker -Bupivicaine has a slower onset of action and will last longer |
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Structure-Activity Relationship:
The potency of a LA is directly related to... The duration of action is determined by... |
-The lipid solubility of a LA
-More lipid soluble, the less of that drug it takes to produce the same effect. -Increase lipid solubility, increase potency -Protein binding (Na channel) and lipid solubility of the LA |
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Summary:
LA with a high lipid solubility will have what type of onset of action, potency, and duration of action... Drug with a decreased lipid solubility will have... |
-Slower onset of action
-Increased potency -Longer duration of action -Quick onset of action -Decreased potency -Shorter duration of action |
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Examples of drugs with low anesthetic potency and short duration of action...
Examples of drugs with intermediate anesthetic potency and duration of action... Exmaples of drugs with high anesthetic potency and long duration of action... |
-Procaine, chloroprocaine
-Lidocaine, Mepivacaine, Prilocaine -Bupivacaine, Etidocaine, Tetracaine |
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LAs and Fetal Circulation:
What kind of pH does a fetus have... What kind of anesthetic do you want to use... Example.... |
-It is more acidic than the mothers
-One that is not as lipid soluble -Chloroprocaine used for obstetric epidurals b/c it is rapidly metabolized, so there is a lower chance of it entering the fetus |
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METABOLISM OF LAs:
Ester LAs are metabolized by... The ester metabolite is... This metabolite is important why... Amide LAs are metabolized by... Prilocaine is metabolized to what... Why is this metabolite important... |
-Plasma pseudocholinesterases (which do NOT accumulate in the bld)
-P-aminoBenzoic Acid (PABA) -It evokes allergic hypersensitivity rxns in some pts -Cytochrome P450 system -O-toluidine derivative -It converts normal HgB to Met-HgB, which cannot carry O2 (b/c it contains ferric Fe+++ instead of ferrous Fe++) |
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Blood Concentration of LA:
You can reduce the chance of toxicity by... To do this, what is administered w/ the LA... |
-Minimizing the spread of LA into the bld stream
-Vasoconstrictor (Epi), it decreases tissue bld flow and the LA will remain at the site |
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Blood Flow in Tissues:
Examples of tissues with high bld flow to low bld flow... So there is a greater chance of toxicity in which tissues... |
-Intravenous
-Tracheal -Intercostal -Caudal -Paracervical -Epidural -Brachial Plexus -Subarachnoid, Sciatic, Femoral -Subcutaneous -At the top (intravenous) |
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Steps to Preventing Toxicity...
Treatment of Toxicity... |
-Use recommended dose
-Aspirate before injecting -Use 5 mcg/cc of Epi and monitor HR -Always inject slowly and talk to pt, who can report minor symptoms (EX: start to speak or act irrationally -Stop the injection -Give O2 -Convulsions are generally self-limited. If they last longer than 15-20 seconds, use an anticonvulsant: Thiopental 100-200mg Diazepam 5-20mg -Supportive therapy |
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Anesthetic Duration and Toxicity of Local Anesthetic Isomers:
If an LA produces toxicity, it is due to... Etidocaine: Duration... Toxicity... Mepivacaine... Bupivacaine... Ropivacaine... |
-Racemic configuration. It has 2 isomers (R and S) and depending on the drug, either R or S will produce longer actions
-S=R -S=R -S>R -S=R -S>R -S<R -S>R -S<R |
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Neuromuscular Blockade (NMB):
Clinical Indications for NMBs... Acetylcholine: What is it... Nicotinic effects... |
-Facilitates intubation
-Provides muscular relaxation during surgery -Facilitates artificial ventilation -The primary NT at the neuromuscular junction -Stimulates autonomic ganglia Stimulates skeletal muscle |
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SUCCINYLCHOLINE:
What is it... Composed of... How does it alter each phase... Type of onset... Type of duration... Type of solubility... Metabolized by... How is it reversed... |
-Only clinically used depolarizer muscle relaxer
-Diacetylcholine or suxamethonium (two joined Ach molecules) -Phase I: depolarization block Phase II: desensitization block -30-60sec -<10 mins -Low lipid solubility -Pseudocholinersterase in the circulation -Effects are not reversed as it is rapidly hydrolyzed in the plasma by cholinesterase enzyme |
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Complications of Succinylcholine include...
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-Fasciculations (initial muscle contractions)
-Low levels of plasma pseudocholinesterase (EX: pregnancy, liver disease) -Raised intraocular pressure (caution in pts w/ glaucoma) -Bradycardia -Increase in serum potassium (so hyperkalemia could be a problem) -Triggering agent in Malignant Hyperthermia -Any type of neuromuscular disorder (EX: MS), don’t want to give this to them! |
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Nondepolarizers:
Bind to what... What do they do... How can you overcome a NMB... Examples of NDNMB... How are they reversed... |
-Bind to post-synaptic cholinergic receptor of the motor endplate
-Competitively prevent Ach transfer to Ach receptor -Increase the amount of Ach -Vecuronium -Pancuronium -Rocuronium -With a combination of Acetylcholinesterase inhibiteracetylcholinesterase inhibitor (EX: neostigmine) and an antimuscarinic (EX: atropine or glycopyrrolate) |
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Factors Affecting Selection of NMBs include...
Steroid NDNMBs are... Benzylisoquinoline NDNMBs release... What are some characteristics of NDBMBs... |
-Cardiovascular effects
-Duration of action -Pharmacokinetic Profile -Class of muscle relaxant -Onset of time -Reversal of neuromuscular block -Vagolytic, so they can block muscarinic receptors -Histamine -Facilitate intubation -Prevent fasciculations -Maintains relaxation |
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NMB Duration of Action:
Succinylcholine: Type of duration of action... Mivacurium... Atracurium... Cisatracurium... Vecuronium... Rocuronium... Pancuronium... Pipecuronium... Doxacuronium... |
-Very short
-Short -Intermediate -Intermediate -Intermediate -Intermediate -Long -Long -Long |
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What is an example of a new non-depolarizer...
What is important about it... |
-Cis-Atracurium (NIMBEX)
-There is a reduction in histamine release -More cardiac stability |
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What accounts for the differences in their duration of action?
Succinylcholine: Type of metabolism... Type of Excretion... Atracuronium... Cisatracuronium... Mivacuronium... |
-All based on route of elimination
-Very rapid -Insignificant -Rapid -Insignificant -Rapid -Insignificant -Rapid -Renal |
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Doxacuronium...
Pancuronium... Pipecuronium... Vecuronium... Rocuronium... |
-Insignificant
-Renal -Slow -Renal -Slow -Renal -Slow -Biliary -Insignificant -Biliary |
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NMB Metabolism:
Succinylcholine and Mivacurium are both metabolized by... Rate of metabolism... Pancuronium and Vecuronium are metabolized to what... Rate of metabolism... Atracuronium is metabolized by what... Rate of metabolism... Type of elimination... |
-Pseudocholinesterases
-Rapid -Active metabolites by the liver -Slow -Nonspecific esterases and spontaneous nonenzymatic chemical degradation -Rapid -Hofmann elim |
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NMB Metabolism:
Cisatracurium is metabolized by what... Rate of metabolism... Type of elimination... Doxacurium and Pipecurium are metabolized by... Rate of metabolism... Rocuronium is metabolized how... |
-Nonenzymatic chemical degradation
-Rapid -Hoffmann elim -Minor degree of metabolism by plasma cholinesterases -Slow rate -It is not metabolized -It is excreteed unchanged |
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NMB Side Effects:
Which NMBs have a slight effect on histamine release... Which NMBs have NO effect on histamine release... |
-Succinylcholine
-Mivacurium -Atracurium -Cisatracurium -Vecuronium -Rocuronium -Pancuronium -Pipecuronium -Doxacuronium |
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NMB Side Effects:
Which NMBs cause a negligible or NO effect on heart rate and a slight effect on arterial BP... Which NMBs cause bradycardia and a decreased arterial BP... Which NMBs cause modest tachycardia and a small increase in arterial BP... |
-Mivacurium
-Atracurium -Cisatracurium (no effect) -Vercuronium -Rocuronium -Pipecuronium -Doxacuronium -Succinylcholine -Pancuronium |
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Effects of NMBs on HR:
Succinylcholine causes bradycardia how... Pancuronium causes tachycardia how... |
-By stimulating muscarinic receptors on the SA node and reducing electrical conduction
-By blocking vagal muscarinic receptors in the SA node. Ventricular dysrhythmia by increasing AV conduction and catecholamine release |
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Effect of NMBs on Arterial BP:
Succinylcholine causes hypotension how... Mivacurium and Atracurium produce hypotension how... Pancuronium produces a variety of effects including... |
-By stimulating muscarinic receptors on vascular endothelial cells to produce vasodilation and the heart which causes bradycardia
-By stimulating the release of histamine, which produces vasodilation which lowers TPR -Antimuscarinic activity, ganglionic stimulation, catecholamine release from adrenergic nerves and reduced catecholamine uptake |
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NMB Side Effects:
Atracuronium produces what type of effects... Should be avoided in what type of pts... high doses, both Atracurium and Cisatracurium are metabolized to... This has been shown to produce what... |
-Bronchospasms and anaphylactoid rxns (rare)
-Should be avoided in asthmatic pts -Laudanosine -Produce CNS excitation, increases MAC (less potent) and may precipitate seizures |
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Effect on D-NMBs...
Effect on ND-NMBs... Antibiotics Anticonvulsants Cholinesterase Inhibitors Dantrolene Inhalational Anesthetics |
-Potentiate
-Potentiate -? -Reduce -Potentiate -Reduce -? -Potentiate -Potentiate -Potentiate |
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Effect on D-NMBs...
Effect on ND-NMBs... Ketamine Local Anesthetics Lithium Carbonate Antiarrhythmics Magnesium Sulfate |
-?
-Potentiate -Potentiate -Potentiate -Potentiate -? -Potentiate -Potentiate -Potentiate -Potentiate |
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How do you determine whether the NMB is effective in producing muscle relaxation or whether the patient is recovering from neuromuscular blockade?
Disappearance of the 4th twitch indicates how much of a blockade... 3rd twitch... 2nd twitch... Clinical relaxation requires what... |
-Monitor neuromuscular function during administration of NMB using a nerve stimulator
-75% -80% -90% -75-95% NMB |
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Recovery from NMB:
Depends on what... Order in which muscles recover from NMB... |
-Type of NMB used and intensity of blockade
-Diaphragm -Intercostal muscles -Muscles of the trunk and abdomen -Small, rapidly moving muscles |
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NEOSTIGMINE:
Clinical uses... Neostigmine methylsulfate is used to treat... MOA... Types of admin... |
-Reversal of NMB
-Myasthenia gravis -Competes with Ach for its binding site on Ach-esterase -Potentiates the action of ACh at the NMJ and GI tract -Inhibits both pseudo-ChE and true AChE -Termination by AChE |
