non-opioid analgesic techniques lack respiratory depression, physical dependence and abuse not regulated under controlled substances act multimodal adjuvants: NSAID magnesium lidocaine lyrica

NSAIDS are weak:

acids

NSAIDS: low or high volume of distribution:

low with minimal tissue binding

metabolizes NSAIDS:

liver

NSAIDS and hepatic or renal disease:

alter binding and metabolism more unbound drug more side effects

reduced renal function and NSAIDS:

prolongs half life lower dose

irreversible binding NSAID

aspirin

COX2 selective:

celecoxib

NSAID recommended for cardiovascular disease:

naproxen

COX2 major concerns:

cardiovascular risks: MI HTN stroke HF

COX 1 inhibition causes: 1 2 3

1. inhibit platelet aggregation 2. decrease renal blood flow 3. loss of gastric mucosa secretion - GI bleed, peptic ulcers

COX2 inhibition causes: 1 2 3

1. anti inflammatory 2. antipyretic 2. analgesic

Ketorolac dose:

30mg

Cox 2 have less _______ toxicity than non selective NSAID

which NSAID may be safter in perioperative setting:

COX 2- celecoxib

major 4 adverse effects of NSAIDS

1. cardiovascular risk- htn, hf, mi (more likely with cox 2) 2. respiratory- bronchospaspm, nasal polyps, dysnpnea, asthma 3. GI- peptic ulcer 4. hematologic- inhibits platelet aggregation- bleeding risk

symptoms of hypothyroidism

fatigue weight gain myxedema depression

hyperthyroidism symptoms - Graves’ disease:

muscle wasting weight loss hot exopathlamos

hypothyroidism treatment

levothyroxine

levothyroxine vs liothyronine

liothyronine has multiple dosing intervals, more potent, requires frequent lab work levothyroxine- once a day

levothyroxine MOA:

T4 is converted to T3 intracellulary

when to take Levothyroxine

empty stomach gel form available if intolerant

half life and steady state of levothyroxine

7 day half life 4-6 weeks to steady state

4 categories to treat hyperthyroid

1. antithryoid: interfere with synthesis of TH 2. ionic inhibitors: block iodide transport mechanism 3. high concentration iodine: decrease release of TH from gland and decrease synthesis 4. radioactive iodine: ionizing radiation to damage gland

adjuvant therapy for thryotoxicosis

beta blockers CCB

hyperthyroidism: radioiodine medications: 1 2 3

carbimazole methimazole porpylthiouracil PTU

beta blockers for hyperthyroidism

propranolol nadolol

antithryoid drugs that categorized:

thiourylenes

thiourylene prototype

propylthioruracil

MOA of propylthioruracil

bind and inhibit peroxidase enzyme preventing iodine organification (iodine reaction with tyrosyl residue of thyroglobulin) inhibiting formation of thyroid horomones

propylthioruracil vs methimazole

propylthioruracil inhibits peripheral deiodination of T4 to T3 and methimazole does not

2 adverse effects of antithryoid drugs: propylthioruracil and methimazole:

1. agranulocytosis 2. liver function

iodide MOA:

quantity of bound iodine increases iodide has the capacity to limit its own transport: negative feedback inhibits release of TH- rapid and effective in severe thyrotoxicosis thyroid gland becomes less vascular, cells become smaller and firmer reaccumulates in the follicles

radioactive iodine MOA

rapidly and efficiently trapped by thyroid and deposited into the colloid of the follicles beta particles are emitted that destroy parenchymal cells of the thyroid

treat thyroid storm:

propylthioruracil radioactive dyes BB or CCB for tachydysththmias dexamethasone 10mg supportive measures: cooling or sedation

radiographic contrast: iopanoic acid and sodium ipodate MOA

block thyroid hormone release as a result of the iodide released from the dyes inhibit T4 to T3 conversion

dexamethasone MOA for thyroid storm:

inhibit conversion of T4 to T3

adverse effects of corticosteroids

suppression of the hypothalamic pituitary adrenal axis weight gain skeletal muscle wasting

corticosteroids produce:

anti-inflammatory effects

corticosteroid with more anti-inflammatory potency:

dexamethasone least: cortisol

corticosteroids MAO

cortisol attached to cytoplasmic receptors to enhance or suppress changes in the transcription of DNA and protein synthesis 2 receptors: mineralocorticoid: sodium and water retention: aldosterone -distal renal tubules, colon, salivary glands, hippocampus glucocorticoid: cortisol -widely distributed

clinical uses of corticosteroids

allergy asthma antiemetic replacement therapy for deficient state: Addison anti-inflammatory acute adrenal insufficiency analgesia cerebral edema aspiration pneumonitis (laryngospasm) immunosuppression post intubation laryngeal edema- to de-swell or prevent myasthenia gravis arthritis