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ADV PHARM TEST 3 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the thyroid?

A
  • A butterfly-shaped gland located in the neck inferior to the larynx
  • Synthesizes and secretes thyroid hormones (T4, T3) and calcitonin
    • release 90% in T4, 10% T3
    • T3 active form
    • T4 changed peripherally to T3
  • Responsible for growth and development of nervous system in infants
  • Regulates metabolism and body temperature
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2
Q

What is thyroid hormone made of?

Difference between T4 and T3?

A
  • Thryoid hormones are made up of two tyrosine molecules iodinated and connected by an ether linkage
  • Iodine is an essential component of thyroid hormones
  • Orientation and position of the iodine molecules determines the type of thyroid hormone produced
  • T4: 4 iodines attached to tyrosine backbone
  • T3: 3 iodines (more active form)
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3
Q

Process of thyroid hormone release?

A
  • Hypothalamus releases Thyrotropin-releasing hormone (TRH)
  • TRH causes release of Thyroid-stimulating hormone (TSH) from the anterior pituitary
  • TSH acts on the thyroid, controlling all aspects of thyroid hormone synthesis and release
  • Thyroid gland secretes more T4 than T3
  • T4 is converted into T3 in the periphery (PRN)
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4
Q

Cuase of hyperthryoidism?

A
  • Graves’ Disease
    • IgG Ab specific for TSH receptor acts as an agonist activating TSH receptor- overstimulate thyroid gland to produce and release T3/T4
    • Stimulates synthesis and release of thyroid hormone
  • Toxic Multi-Nodular Goiter
    • Nodules over-secrete thyroid hormone
  • Iatrogenic - excess via exogenous administration of iodine or thyroid
  • Rare
    • Pituitary Tumor (Overproducting TSH)
    • Thyroid Cancer,
    • Testicular Cancer (HCG levels go up, HCG very similar to TSH and high enough concentrations can stimulate the thyroid gland like TSH)
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5
Q

Treatment of hyperthyroidism/graves’ disease?

A
  • Anti-thyroid Drugs (Thioamides/Thioureylenes)
    • Propylthiouracil (PTU) - no brand
    • Methimazole (Tapazole)
  • Blocks organification (integration of iodine into globulin) process by competing with thyroglobulin for oxidized iodide
  • Reduces synthesis of thyroid hormones
  • Onset of action 1-2 weeks due to thyroid gland stores
  • Only useful in overproduction of thyroid hormones
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6
Q

Most concerning adverse effect with PRU and Methimazole?

A

Can result in formation of goiter

  • Inhibition of thyroid hormone production leads to an up-regulation of TSH release
  • Increased plasma TSH not able to increase thyroid hormone levels due to medication
  • Elevated TSH levels stimulates thyroid gland hypertrophy in an attempt to increase thyroid hormone synthesis
  • Leads to eventual goiter development
    • ​need good airway assessment and assess for goiters because this can impair our ability to secure airway
    • usually will have awake fiberoptic intubation

Other adverse effects of both agents

  • Pruritic rash early in treatment - usually resolves
  • Arthralgias - common reason for discontinuation
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7
Q

Rare s/e of PTU and metimazole?

A
  • Agranulocytosis (<0.1%)- get CBC when start and follow first 90 days. let PCP know if develop fever/sore throat
    • Usually within 1st 90 days of treatment
    • Monitor WBC at baseline and if patient develops fever or sore throat
  • Hepatotoxicity
    • May be associated with an allergic reaction
  • Vasculitis
    • Can manifest as drug-induced lupus
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8
Q

Why is methimazole preferred to treat hyperthryoidism compared to PTU?

A
  • Preferred agent in clinical practice for most cases of hyperthyroidism
  • Longer half-life allows for once daily dosing
  • More potent than PTU (lower dose required)
    • Less dose = less side effects
  • Serious adverse effects less frequent than with PTU
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9
Q

Why, in certain cases, might PTU be a better treatment for hyperthyroidism?

Concern with PTU around surgery?

Daily frequency?

A
  • Also inhibits conversion of T4 to T3 in the periphery
    • good for if patient in acute hyperthyroid state ie thyroid storm
  • Short half-life requires TID dosing
  • Serious adverse effects more frequent compared to methimazole
  • Preferred agent in pregnancy- crosses placenta less than methamazole
  • Preferred in acute management of hyperthyroidism (thyroid storm) due to inhibition of T4 to T3 peripheral conversion
  • No IV version so have to give NG for intra-operative thyroid storm
  • Can deplete levels of prothrombin leading to increased bleeding tendency

remember, PTU Preferred in Pregancy and stopping Peripheral conversion (thyroid storm). causes decreased Prothrombin (LOTS OF Ps)

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10
Q

What is radioactive iodine and role in hyperthyroidism treatment?

A
  • Large percentage of patient respond to thioamides within 6-12 months
  • If hyperthyroidism persists, additional therapy includes:
    • Radioactive Iodine - I131 - Thyroid Gland Ablation patients often hypothyroid afterwards
      • thyroid takes up the radioactive iodine, emit destructive beta rays (that only affect thyroid gland), destorying thyroid tissue.
      • sometimes too much gland can be destroyed and now pt needs synthroid after med.
    • Surgical removal of thyroid gland followed by thyroid replacement
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11
Q

Role of B blockers in hyperthyroidism treatment?

A

b-blockers – symptomatic therapy

  • Use while waiting for thioamides to work- helpful short term but not definitive treatment
  • Blocks hyperadrenergic effects of thyroid excess (tachycardia, tremor, nervousness)
  • Blocks peripheral conversion of T4 to T3
  • Use esmolol for thyroid storm due to quick onset of action and short half-life (9 min)
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12
Q

Corticosteroids role in hyperthyroidism?

A
  • Symptomatic treatment
  • Blocks peripheral conversion of T4 to T3
  • Suppresses thyroid receptor Ab and inflammation
    • most common cause hyperthyroidism is grave’s disease which is immune mediated
    • suppress immune system and suppress response
  • Prednisone or methylprednisolone
    • prescribed while waiting for thioamides to take full effect
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13
Q

Iodide salts role in hyperthyroisidm treatment?

A

Iodide - Iodide salts (Lugol’s Solution)

  • Blocks peripheral conversion of T4 to T3
  • Decreases vascularity of thyroid gland
  • Promptly but temporarily blocks thyroid hormone release from the thyroid gland
  • Gland is so busy trying to uptake it that is cannot make/release thyroid hormone
    • shift thyroid gland to taking up iodine instead of making hormone
  • After Iodide is all taken up, will have lots of T3/T4 to release so this only a temporary treatment
    • if going past 2/3 week period before surgery, can find it makes everything much worse.
    • long-term problematic, only temporary treatment
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14
Q

Summary of all meds/treatments used for hyperthryoidism?

A
  • Anti-thyroid drug (thioamides/thioureylenes)
    • Propylthiouracil (PTU)
    • Methimazole (Tapazole)
  • Radioactive Iodine (I 131)
  • Surgical removal of thyroid
  • Beta bockers- symptomatic therapy
  • Coritcosteroids- helpful in graves’ disease
  • Iodide salts- reduce T3/T4 immediately before sx. also reduces vascularity
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15
Q

Main causes of hypothyroidism?

A
  • Primary Hypothyroidism (Hashimoto’s Thyroiditis)
    • Autoimmune disorder similar to Graves’ in that Ab’s are produced – this time against many thyroid gland proteins
    • It blocks production of thyroid hormone via gradual inflammatory destruction of the thyroid gland
  • Iatrogenic
    • Thyroid gland ablation or surgery
    • Drugs than contain large amounts of Iodine, which can suppress the thyroid gland
    • Pituitary - not producing as much TSH, especialyl space-occupying pituitary tumors. Compress pituitary and piuitary inable to secrete TRH
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16
Q

What is levothyroxine?

A

Levothyroxine (Synthroid, Levoxyl, Levothyroid)- treatment of hypothyroidism

  • Drug of choice
  • Chemically synthesized T4
  • Body converts it to T3 as needed
  • Long half-life (7 days) allows for once daily dosing
  • Wide availability of strengths - ease of titration
  • Monitor TSH, free T4- monitor for effectiveness of therapy. Once TSH returns to normal, then patient has adequate synthroid
  • Monitor for signs and symptoms of hyperthyroidism indicative of too high dose
  • Allergic rash possible secondary to dye or excipients
  • PO preferred but IV form acceptable in emergency/OR situation
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17
Q

Why don’t we just give T3 (Liothyronine (cytomel)) to hypothyroid patients?

A

Why not give T3 Liothyronine(Cytomel)?

  • Better to have a reservoir of T4 (prodrug) to normalize metabolism over a wide range of conditions
    • more physiologic. We convert T4–> T3 just as needed
  • Half-life of T3 is shorter (1 day)
  • DO use in life-threatening hypothyroidism (myxedema coma) where faster onset of T3 is more useful
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18
Q

Levothyroxine drug interactions?

A
  • Increases levothyroxine metabolism
    • Phenobarbital, phenytoin, rifampin, carbamazepine
  • Decreases T4 to T3 conversion
    • PTU, b-blockers, amiodarone, glucocorticoids
  • Decreases absorption from gut
    • Cholestyramine, FeSO4, Al(OH)3, sucralfate, sodium polystyrene sulfonate (Kayexelate)
    • Administer at different times
  • Increases Thyroid Binding Globulin (binds T3, T4)
    • Pregnancy, estrogen (OC’s, HRT)
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19
Q

Drugs that alter thyroid status?

A
  • Amiodarone
    • Structurally resembles thyroid hormone, contains large amounts of iodine
    • Can result in hypothyroidism or hyperthyroidism
  • Lithium
    • Actively concentrated in the thyroid gland
    • Body thinks it is iodine
    • Can inhibit thyroid synthesis leading to hypothyroidism
  • Metoclopramide (Reglan)
    • Increases TSH production/release
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20
Q

Different categories for corticosteroids?

A

Can divide by natural/synthetic structure

  • Natural Forms
    • Examples: cortisol (hydrocortisone), cortisone, & aldosterone
  • Synthetic Forms- alteration in structure to provide different PK/PD effects
    • Examples: Prednisolone, Prednisone, Methyprednisolone, and Dexamethasone

Can also divide steroids by type of effect it has:

  • Mineralocorticoid effects
    • Reabsorption of Na and excretion of K in renal distal tubule of (aka aldosterone)
  • Glucocorticoid effects
    • Antiinflammatory effect
    • Augmentation of sustained SNS activity during periods of emotional or physical stress

some meds have both mineralocorticoid and some have more glucocorticoid effects. Mineralo vs gluco is more clinically relevant in practice

  • ie, someone in addison’s crisis, we need balance of mineralocorticoid and glucocorticoid. give cortisol since that’s what we’re deficient in
  • someone who needs anti inflammatory, give decadron because we don’t need the mineralocorticoid effect, we only need glucocorticoid effect
21
Q

Structure of corticosteroids?

A
  • All have same “steroid nucleus” as part of their molecular structure
  • Molecular substitutions and/or alterations to this basic nucleus accounts for variable
    • Potency
    • Absorption
    • PB
    • Metabolism
22
Q

MOA/effects Corticosteroids?

A
  1. Corticosteroids enter cells bind to steroid receptors in cytoplasm- remember, steroids are able to pass through phospholipid membrane without binding to external receptor
    • Mineralocorticoid receptors found “organs of exretion” colon, salivary glands, sweat glands,kidney and hippocampus
    • Glucocorticoid receptors more wide spread
  2. Steroid + receptor enters nucleus where it influences DNA transcription = protein synthesis regulation (either enhances or inhibits expression of specific genes).
    • generally enhances antiinflammatory protein and decrease proteins that are proinflammatory
    • also promotes catabolic state to mobiliz glucose, AA, FA to increase energy to brain/body
    • Metabolic enzymes and inflammatory response greatly influenced
  3. Metabolic effects are to increase nutrient availability by raising:
    • blood glucose- Antagnoizes insulin action and promoting gluconeogenesis
    • amino acid- catabolism of muscle protein and AA used by liver for gluconeogesis
    • triglyceride levels.- increase release FFA
      • ​**metabolic effects are GREAT short term, but harmful long term!
  4. Inflammatory response inhibited
    • The enzyme phospholipase A2 inhibited by a steroid generated protein = arachidonic acid formation greatly decreased.–> therefore less COX 1/COX2–> decrease in inflammation but also decrease in beneficial prostaglandins that maintain GI health–> increase ulcer risk
    • Cytokine and chemokine release is decreased.
  5. Cell membrane permeability to ions altered (mineralocorticoid receptors)- aldosterone altered
  6. Neurohormone production altered
23
Q

Cortisol pharmacokinetic info, PB, Metabolized, e 1/2 T?

How much cortisol do we make a day? when we’re stressed?

A
  • Many routes of administration
  • Cortisol Succinate (Solu-Cortef) IV form of cortisol
  • Endogenous cortisol secreted: circadian pattern (normal pattern)
    • 10-20mg a day average
    • 50-150 mg a day during extreme physiological stress
      • when thinking of giving stress dose, think of how stressful sx is
      • minor sx, not much stress, major sx, need more
  • 90% PB (corticosteroid binding globulin)
  • 70% metabolized conjugated in liver (to minimally active H2O soluble metabolites)
    • The rest eliminated unchanged via urine
  • E1/2 t 1.5-3.0 hrs – clinical effects seen for much longer
24
Q
A
25
Q

Which corticosteroids are equal glucocoritcoid and mineralocorticoid effect? which have more glucosoticoid?

A
  • Equal glucocoritocid and mineralocorticoid:
    • cortisol
    • cortisone
  • More glucocorticoid:
    • dexamethasone
    • prednisone
    • methylprednisolone
    • betamethasone

  • Remember that as you’re giving glucocorticoids, will have negative feedback loop on further cortiosl release. Therefore, you want a little mineralocorticoid effect with the glucocortioicds.*
    • also, DOA of corticosteroids are more important than 1/2 life!*
26
Q

Highlights of various synthetic corticosteroids?

A
  • Methylprednisolone (intraarticular/IV) intense glucocorticoid effect; often used of HPA axis depression replacement
  • Betamethasone (PO/IV) lacks mineralocorticoid effects
  • Dexamethasone (PO/IV) used for cerebral edema (specifically brain tumors), antiemetic and airway edema control Peri-op
  • Triamcinolone (intraarticularly, IV, PO) often used for epidural injections LBP
  • Prednisolone (PO/ IV) mineralocorticoid & glucocorticoid effects
  • Prednisone is also PO or IV converted to prednisolone after absorption
27
Q

Clinical uses of corticosteroids?

A
  • Replacement therapy for deficiency related to adrenal or pituitary disease
  • Antiinflammatory (i.e. temporary “palliative” therapy for life-threatening inflammation) underlying problem must be addressed with other therapies
    • only short term use
    • use to get pt through acute exacerbations while altering other drugs to treat dx process
28
Q

Corticosteroid use for adrenal insufficiency?

A
  • Acute adrenal insufficiency – cortisol 100mg q8 hours
    • Fluid and electrolyte imbalances must be evaluated and treated as well
  • Chronic adrenal insufficiency cortisone PO 25 mg q AM and 12.5 q afternoon
    • In addition patient usually needs specific mineralocorticoid added fludrocortisone for example
29
Q

Corticosteroid use in allergies/asthma?

A
  • Acute Therapy = IV glucocorticoids
    • 1 hour beta adrenergic agonist enhancement-cortisol makes epi work better!!! therefore get cortisol on board early!
    • 4-6 hours antiinflammatory benefits seen
    • So…. If giving pre-op or during acute bronchospasm/anaphylaxis will need to consider delayed onset in planning/manage symptoms of acute anaphylaxis w/ epinephrine etc. for acute relief
  • Chronic Therapy = Inhaled glucocorticoids via MDI (beclomethasone, triamcinolone, flunisolide)1st line prevention of bronchospasm in asthmatics
    • 80-90% MDI dose swallowed at risk for dysphonia (laryngeal muscle myopathy)
    • axiUsually do not see HPA- s disturbance until daily doses > 1500mcg adults, >400mcg pediatrics
30
Q

Use of corticosteroids as anti-emetic?

A
  • Dexamethasone (Decadron) 8-10mg IV useful if given shortly after induction of anesthesia- not as effective if given at end of case. Particularly effective when given with zofran
  • MOA unclear: theories include reduction in prostaglandin synthesis, enhanced endorphin release, improved appetite
  • E1/2t = 3 hrs; antiemetic effect may persist for 24 hours
  • Inhibition of the cyclooxygenase & lipoxygenase pathway may also result in post-op analgesic effect w/glucocorticoids
31
Q

Other miscellaneous uses of corticosteroids…

A
  • Intracranial tumors= ICP & cerebral edema control NOT helpful with CHI, global ischemia related ICP↑
  • Aspiration pneumonitis = no evidence strongly supports effectiveness
  • Immunosuppression in transplant patients
  • Lumbar Disc Herniation = epidural injection to reduce edema & inflammation at the nerve root (usually temporary treatment of sciatic related pain/sensory loss)
    • 25-50 mg triamcinolone or 40-80 mg methylprednisolone w/lidocaine
    • HPA axis suppressed 1-3 months after injection
32
Q

Continued other clinical uses of corticosteroids…

A
  • Rheumatoid arthritis – last resort….
  • SLE, sarcoidosis, and other collagen related diseases
  • Ocular and cutaneous inflammation (topical to the eye or skin – avoid if abrasions present)
  • Ulcerative colitis
  • Myasthenia gravis
  • Prevention of RDS in premature neonates (given to mothers threatening labor <37 wks GA)- speeds maturation of neonate lungs and increase amt surfactant in neontal lungs. prevents respiraotry distress syndrome
  • Leukemia (antilymphocytic effects)
33
Q

S/E Corticosteroids?

A
  • HPA axis suppression – CV collapse intra-op!
    • flimsy evidence but widely accepted in practice
  • Fluid and electrolyte imbalances/ metabolic derangements
  • Increased risk for infection- suppressing arachidonic acid formation predisposes pt to oppportunistic infection and decreased ability to fight infection
  • Osteoporosis – fractures w/positioning!- increase osteoclasts &decrease osteoblasts
  • Peptic ulcer disease- blocking beneficial prostaglandin (inhibit phospholipase A2 and therefore COX pathway)
  • Skeletal muscle weakness- protein catabolism
  • Psychiatric disorders- high doses
  • CBC changes
  • Growth retardation in children
  • Decreases anticoagulant effectiveness
34
Q

Who will need periop steroid coverage?

A
  • Clinical findigns of Addison disease
  • Otherwise unexplained findings consistent with adreno-cortical insufficiency, such as hypotension, hyponatremia, hyperkalemia, and eosinophilia
  • Risk for hypothalamic pituitary adrenal axis suppression and adrenal insufficiency based on the course of therapy
    • amount of time not exact– 1 month therapy in last 6-12 months is candidate
35
Q

Recommendations for stress dose needed based on degree of surgical stress?

A
  • Minor- preop corticosteroid dose plus hydrocortison 25 mg or equivalent
  • Moderate (lower extremity revascularizaiton, Total joint)- hydrocortison 50-75mg
  • Major- cardiac sx, aortic aneurysm- hydrocoritson 100-150 mg q 8 h for 48-72 h

Dr. B plays it by ear. If someone has RA and has been taking coritcosteroids for 2 years, will definitely need stress dose. Someone who had a 2 week course 4 months ago, may not need the extra stress dose. She has the dose drawn up just in case, but may or may not give it. If pt has consistent hypotension, will treat with steroid to assist BP.

36
Q

What is glucagon?

A
  • Polypeptide Hormone of ~20 amino acids
  • “The hyperglycemic hormone” - the anti insulin
    • Produced by alpha cells pancreas and upper GI tract in response to hypoglycemia or ↑plasma proteins
    • Secretion is decreased with hyperglycemia
    • major physiologic purpose is to regulate BG levels
  • Other effects caused by glucagon are at supra-physiologic concentrations- this doesn’t happen with normal physiologic concentrations
37
Q

Glucagon MOA?

A
  • Enhances the formation of cAMP- major reason we give this is when someone is beta blocked, and unable to react to sympathomimetics, can give glucagon at supraphysiologic doses to help relieve symptoms d/t beta blockade
    • Increases myocardial contractility (stroke volume) and HR- can get to extreme tachycardia
    • Decreases gastric motility
    • Increases renal blood flow
    • Increased insulin secretion- rise in glucose
    • Increased hepatic gluconeogenesis and glycogenolysis
    • Relaxation of smooth muscle (biliary sphincters)- given in endo suite during biliary procedures
  • Enhances the systemic release of catecholamines (secondary)
  • Vasodilator (one of many reasons for decreased SVR in hepatic disease)- think this is why cirrhotic patients are hyperdynamic because cirrhotic livers don’t metabolize glucagon
38
Q

Glucagon clinical uses?

A
  • 1-5 mg IV or 5mcg/kg/min (20mg/hr)- gives us cardiac effect
  • Increased CO ( w/Beta Adrenergic Blockade)
    • given with beta blocker OD
  • Biliary dilation- placement of biliary stents
    • dose 0.3 mg at a time
    • can cause nausea/tachycardia
  • Improves low CO (s/p MI or CPB)
  • Improves CHF symptoms- enhancing CO and SVR decrease
  • Enhanced AV nodal conduction- digitalis toxicity
  • Diagnosis of pheochromocytoma
39
Q

S/E Glucagon?

A
  • Hyperglycemia
  • Hypoglycemia (paradoxical)- more rare. when they don’t have adequate stores of glucose, stimulating too much insulin release and get hypoglycemia
  • Hypokalemia- increase glucose, insulin and K uptake
  • Nausea and vomiting
  • Abrupt HR increase in patients with atrial fibrillation (AV node enhanced conduction)
  • Only useful in acute situations - cardiac contractility and heart rate are not increased for prolonged periods of time
40
Q

What is octreotide/somatostatin?

A
  • Somatostatin is a GI regulatory peptide secreted by pancreatic delta cells
  • Octreotide is a Somatostatin analogue - Both inhibit the production and release of hormones from the GI tract and pancreas
    • inhibit growth hormone release
    • Inhibit the secretion of insulin (hyperglycemia possible during treatment)
    • Inhibits the release of glucagon (vasodilator) and vasoactive intestinal peptide
      • again, hyperdynamic circulation in cirrhotic patients is r/t all vasodilatory activity. If you give octreotide, you can reduce variceal bleeding by reducing vasodilatory`` activity in splanchnic circulation, improving variceal bleedgin
41
Q

Clinical uses of octreotide?

A
  • Somatostatin E1/2 life is 3 min
  • Octreotide E1/2 life is 2.5 hrs

Used to treat

  • Carcinoid crisis - decreases the release of vasoactive amines (especially serotonin)- s/s carcinoid flushing, bronchospasm, hypo/hypertension
    • Bradycardia/2nd and 3rd degree heart block possible with bolus- give slow!!
    • Octreotide dosing for carcinoid crisis:
      • 50-100mcg/hr + PRN bolus of 25-100mcg
      • prevent release vasocative amines (esp 5-HT) and prevent crisis
  • Hepatorenal syndrome- massive vasodilation decreases blood volume to kidneys. get decrease RBF and GFR. octreotide helps to improve hemodynamics
  • Control of esophageal variceal bleeding
    • Octreotide 50mcg/hr
42
Q

What is arignine vasopressin?

A

aka ADH

  • Three receptor classes for vasopressin
    • V1- arterial vasoconstriction
    • V2- collecting ducts to increase H2O
    • V3 (↑ ACTH release)
  • Action at V2= collecting ducts in nephron - increased H2O permeability/reabsorption back into circulation
  • Action at V1= arterial smooth muscle to cause profound vasoconstriction (lg. doses)
  • E1/2 t = 10-20 minutes
43
Q

Clinical uses vasopressin?

A
  • Diabetes insipidus (central origin only)
  • Esophageal varices r/t hemorrhage
    • preferentially vasoconstricts splanchnic circulation
    • if less blood flow going through circulation, then less blood flow through portal vein, and therefore less blood flow varices
  • Hemorrhagic or septic shock- redistributes blood flow to brain, heart, lungs. not best for peripheral circulation
  • Cardiac arrest resuscitation agent
44
Q

Vasopressin s/e?

A
  • Increased BP (larger doses) (V1)
    • Depends on baroreceptor tone
  • Coronary artery vasoconstriction
    • Angina, ischemia, MI, EKG changes, arrhythmia
  • Gastrointestinal Hyperperistalsis
    • Nausea and vomiting, abdominal pain
45
Q

What is DDAVP?

A

Synthetic analogue of AVP with E1/2 t = 2.5-4.4 hours

  • More selective for V2 receptors (antidiuretic) than V1 receptors (vasoconstriction)
  • Better choice for diabetes insipidus secondary to SE profile (V2 specificity)
  • Stimulates endothelial cells to increase secretion of von Willebrand factor, tissue type plasminogen activator and prostaglandins
    • ​pt with renal failure have issue with quality of PLT. DDAVP can be used to improve platelet function in renal pt
  • Intranasal preparation: chronic AVP replacement
    • Pituitary sx/tumor
46
Q

What is synthetic oxytocin?

A
  • Acts on uterus to cause contraction (mimics spontaneous labor)
    • Induction of labor
    • ↑uterine tone post partum particularly after C-section
    • ↓ post partum or post D&C hemorrhage
  • Dosed in units which describes potency
    • Labor Induction - 1-2 mU/min gtt increase q 15-30 minutes by 1-2mU/min until contractions 2-3 minutes apart<– don’t need to memorize dosing numbers
    • For post partum uterine atony - up to 40 mU/min
47
Q

Effects of oxytocin?

A
  • In high doses SVR can be decreased reducing SBP and DBP
    • Usually not seen in doses used for labor induction
    • Hypovolemic patients and those with blunted compensatory responses (under GA) may have more profound hypotension with oxytocin
  • In high doses can have weak AVP activity with H2O retention
  • Concerns of vasoconstriction no longer an issue - current preparations = pure oxytocin
48
Q

How do OC work? Anesthetic considerations with ovarian hormones?

A
  • Oral Contraceptives - Usually combination estrogen & progestin that inhibits ovulation
    • Estrogen - prevents release of FSH
    • Progesterone - prevents release of LH
  • Side Effects
    • Thromboembolism (increased plt aggregation and clotting factors by estrogen)
    • MI and stroke - increased risk
    • HTN - increased risk
  • Suggamaddex will also encapsulate OC. Make sure pt is told to use backup method if given suggamaddex

ADV PHARM TEST 3 (5 decks)

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