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Pharmacology > Endo Pharm 1 > Flashcards

Endo Pharm 1 Flashcards

1
Q

Somatropin

A

GH Preparation

identical to full-length Human GH (191-aa) Pituitary Hormone

Given IM/SC/Depot

MOA: activate the human GH receptor (cell-surface R). Coupled to JAK-STAT pathway - effects in nucleus

**Therapy: **replacement therapy in children with GH deficiency prior to epiphyseal closure

  • Increased linear growth until epiphyseal closure
  • increased muscle/bone formation, decreased fat, maintenance of physiology in adults
  • Turner & Prader-Willi Syndromes (short stature of unk cause)
  • poor growth due to renal insufficiency, AIDS achexia, wound healing in cutaneous burns
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2
Q

Somatropin Adverse

A

Increased Mortality vs general population

Abuse for anabolic purposes (athletes, bodybuilders)

Laron Dwarfism - pts with GH-receptor defect, not responsive to GH agonist, need IGF (end organ hormone)

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3
Q

Sermorelin

A

Synthetic GHRH analog (shorter version), minimum residues for activity. Hypothalamic Hormone

  • Admin daily (IV/SC/nasal)

**MOA: **activates GHRH-R on pituitary cells (cell surface GCPR)

  • Stimulates release of endogenous GH –> IGF-1 release

**Therapy: **Approved for GH deficiency (GH analogs preferred in most cases)

Ineffective in pts with pituitary defect (require GH or IGF)

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4
Q

Octreotide

A
  • Syntehtic analog of human **somatostatin, **hypothal. hormone
    • ​​​Shortened and stabilized compared to endog. SST
    • Longer half-life
    • ​Less effect on insulin than SST
  • ​2-3 SC inj/day, monthly depot inj
  • **MOA: **activates SST receptors (GPCR)
    • ​selectivity for SST-2 & -5 receptors (hormone-secreting tumors)
  • ​**Therapy: **for acromegaly due to GH-secreting adenoma
    • ​hormone-secreting tumors w/ SST-Rs (metastatic carcinoid (5HT-secreting), adenomas secreting VIP, TSH, glucagon
  • ​**Adverse: **inhibition of GI motility and secretions (loose stools, nausea, malabsorption, flatulence)
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5
Q

Cabergoline

A
  • DA Agonist to inhibit PRL release
    • ​NOT a peptide (orally effective)
    • 1-2/wk dosing
  • ​**MOA: **PRL inhibition via D2 dopamine receptors (D2-selective)
  • **Therapy: **to treat hyperprolactinemia / resulting infertility
    • ​prolactinoma
    • suppression of lactation
    • to inhibit GH release in acromegaly (PRL inhibits GH secretion only in acromegaly, same p-way as SST)
  • ​**Adverse: **nausea, dizziness, hypotension
    • ​mostly due to D2 receptors
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6
Q

Arginine vasopressin

A
  • ​​Synthetic peptide identical to human hormone
  • Short-acting, IV/IM/SC/nasal admin
  • Both V1 & V2 effects
  • **MOA: **agent of choice for V1 receptor effects & for short duration of action
  • **Therapy: **treatment of temporary Diabetes Insipidus after pituitary surgery
    • ​(V2 use, but AVP used for short action)
    • CVA use: V1 receptor action. Local admin for constriction of bleeding artery, preventing/treating various hemorrahge, resusc. of V-fib/tach
  • ​**Adverse: **Increased blood pressure
    • ​GI / uterine contractions / cramps
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7
Q

Desmopressin acetate

A
  • Modified synthetic peptide **analog **of vasopressin
    • ​much longer-acting, V2>>>>V1 effects
    • IV/SC, inhaled nasal prep is widely used
  • ​**MOA: **selective activation of V2 vasopressin receptor
  • **Therapy: **First choice drug for Diabetes Insipidus (replacement therapy)
    • ​Hemophilia, von Willebrand’s (Increase clotting factor synthesis)
    • Nocturnal enuresis (to concentrate urine) (associated w/ hyponatremia)
  • ​**Adverse: **minimal V1-side effects, no major V2 side effects
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8
Q

Levothyroxine

A
  • Pure T4
  • Slow onset, long duration (converted to T3 in body)
    • Less potent than T3, more protein-bound, longer half-life
  • ​Primary Drug used in replacement therapy (for longer duration of action)
  • Used in Myxedema coma -> IV bolus to fill plasma binding sites, continued as maintenance therapy
    • ​more predictable than liothyronine
  • ​Use in pregnancy –> TH requirements increase in pregnancy
    • Slow onset (days-weeks) & long duration of effects (slow reversibility)
  • ​Adverse: minimal, generally due to over-dosage (similar to hyperthyroidism)
    • ​many drug interactions
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9
Q

Liothyronine

A
  • ​Pure T3
  • Rapid onset, short half-life (4x more potent than levothyroxine)
    • ​less protein-bound, shorter half-life
  • ​**Therapy: **rarely used in chronic therapy
    • ​very rapid onset, sudden physiologic changes
    • safer to let body convert levothyroxine to T3
    • Some use in surgery for thyroid cancer
      • ​maintain TSH suppression while pts are tapered off of levothyroxine prior to surgery & rapid onset after surgery
    • ​Short-term support after radio-iodine for hyperthyroid
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10
Q

Propanolol

A
  • ß-blocker
  • Symptomatic relief for HYPERthyroidism
    • primarily due to sympathetic stimulation
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11
Q

Methimazole

A
  • Thioamide prototype - antithyroid drug for hyperthyroidism
    • ​Inhibitor of peroxidase and TH synthesis (iodination, cuopling, TH synthesis)
    • do not inhibit release of preformed TH (latent period 1-2 weeks)
  • ​**Therapy: **First-line therapy, non-destructive. For iniital ‘rapid’ control of TH production
    • ​Avg. therapy of 1 year, useful in 30% of pts
  • ​PK: oral, concentrated in thyroid (duration of action longer than plasma half-life) Met. by conjugation -> excretion in urine
  • **Adverse: **agranulocytosis
    • ​w/ both thioamide drugs, first few months of therapy
    • Sore throat, fever (immediately discontinue, treat infection, dont use thioamides in pt again)
    • ​​also skin rash, drug fever, hypothyroidism, goiter if over-dosage
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12
Q

Propylthiouracil (PTU)

A
  • Thioamide
  • Less potent and shorter half-life than MMI (MMI has increased compliance with 1/d)
  • **Therapy: **decrease conversion T4–>T3
    • ​more rapid effect in thyroid storm
    • PTU safer during pregancy and breast-feeding (MMI has fetal toxicity). Used to treat to mild hyperthyroidism in mother (therapy prior to pregnancy is best)
  • **Adverse: **PTU can cause liver toxicity or failure (not seen with MMI)
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13
Q

Potassium Iodide

A
  • **MOA: **acute inhibition of synthesis and release of THs
    • ​No Effect on converstion of T4–>T3
    • Rapid effects, short duration
  • ​**Therapy: **decrease size and vascularity of thyroid
    • ​vasoconstrictor effect (firm up)
    • easier surgical removal (pre-op last 10 days before thyroidectomy)
  • Beneficial in thyroid storm –> prevent release of preformed THs (only drugs that do this​)
  • Used in radiation release emergencies –> decrease uptake of radioactive iodine into thyroid
    • ​do not use prior to radioactive iodine therapy (decrease uptake)
  • ​**Adverse: **sore throat, burning mouth, rash, diarrhea
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14
Q

Radioactive Iodine

A
  • 131I isotope
  • 8-day half-life, 15% gamma radiation
    • ​thyroid diagnostic & imaging uses
  • ​85% weak beta radiation
    • ​travels 1-2mm in tissue (localized destruction
  • ​**Therapy: **Large does for non-surgical destruction of thyroid tissue
    • ​over course of several weeks
    • ​​give thioamides prior, decrease TH, increase TSH —> promote uptake of radioiodine (and reduce risk of treatment-induced thyroid storm
  • ​**Adverse: **contraindicated in pregnancy, breast feeding, young children (damage rapidly growing/developing tissues)
    • ​Permanent hypothyroidism
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15
Q

Regular Insulin (injection)

A
  • Traditional insulin preparation
    • ​rapid-acting / short-acting
    • physiological level of zinc
    • readily soluble and absorbed
  • ​Onset 1/2-1 hr, peak 2-4 hr, duration 5-8 hr, can be given IV
  • Therapy: glucose control after meal (rapid / short duration)
    • ​injected 1/2-1hr before meal (active during meal)
  • ​Available without prescription
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16
Q

Isophane insulin suspension

(NPH)

A
  • Traditional long-acting insulin preparation
    • ​complexed with protamine at neutral pH
    • slower absorption, longer action than regular
  • ​Onset 1-2 hr, peak 6-12 hr, duration 18-24 hr
  • Cloudy suspension, NOT given IV
  • **Therapy: **glucose control between meals and overnight
    • ​slower onset, action - sustained effefct
17
Q

Insulin Lispro

A
  • First ultra-rapid insulin
    • ​aggregrates less, more rapid effect (shorter duration)
  • **Therapy: **injected immediately before meal, less hypoglycemia risk
    • ​Better control of glucose load
    • Less post-prandial hypoglycemia__​
  • ​Can be given IV like regular
18
Q

Insulin aspart

A
  • Second synthetic rapid insulin
  • Somewhat l_onger duration_ than lispro, faster and shorter than regular insulin
  • **Therapy: **Injected SC before meal (can be IV)
19
Q

Insulin glulisine

A
  • Third synthetic rapid insulin
  • **Therapy: **Injected before immediately After Meal
20
Q

Isophane Synthetics (Mixes)

A
  • Formulations of synthetic rapid insulins with protamine
    • ​slows and prolongs action
    • Kinetics similar to isophane insulin
    • for between-meal support
  • ​Premix combos
    • ​Lispro 75:25 (NPL Insulin) - 75% protamine-complexed
    • Lispro 50:50 (**NPL Insulin) - **50% protamine-complexed
    • Aspart 70:30 (NPA Insulin)
21
Q

Insulin Glargine

A
  • New ultra-LONG synthetic insulin
    • ​altered solubility properties (slow absorption, increase duration
  • ​**MOA: **extra zinc and acidic (pH-4) –> decreases aggregation
    • ​Absorption: Precipitates when injected SC, slow dissolution from injection site (low, constant action)
    • Given 1/day, at bedtime
  • ​PK: ‘peakless’ or ‘flat’ PK (opposite from lispro, aspart, glulisine)
    • ​Should NOT be mixed with other pH-7 rapid insulins
    • Can both be used, injected separately
22
Q

Insulin detemir

A
  • Ultra-LONG synthetic insulin
  • Modifications that slow release and prolong action
    • ​Fatty acid chain binds to albumin to prolong action
  • ​Formulated at neutral pH (not acidic like glargine)
  • Better & less variable than glargine
    • ​Should NOT be mixed with rapid insulin
  • ​Combinations
    • ​Synthetic ultra-long + synthetic rapid analogs
    • Basal-plus-bolus
      • ​short-acting bolus-boost with meals
23
Q

Pramlintide

A
  • Amylin analog peptide
    • ​analog of amylin -> released with insulin from beta cells
  • ​**MOA: **decreases post-prandial glucose, decreases liver glucose formation, slows gastric emptying, increases satiety
  • **Therapy: **diabetics on insulin and not controlled by insulin alone
    • ​injected SC before meals, along with insulin
    • works and reduces weight
  • ​Adverse: mild nausea, headache
    • ​risk of hypoglycemia (reduce rapid insulin dose)
    • avoid drugs that decrease GI motility
24
Q

Glucagon

A
  • Hyperglycemic Agent (treating HYPOglycemia)
  • IM or SC
  • If patient becomes unconscious
  • Counteracts insulin by multiple mechanisms
25
Q

Diazoxide

A
  • HYPERglycemic agent
  • Inhibits insulin secretion
    • ​Binds & activates ATP-sensitive K+ channel, (normally inhibited by glucose to increase insulin release)
    • Diazoxide activates channel -> decreases insulin release, less hypoglycemia
26
Q

Glimepiride

A
  • SULFONYLUREA
    • ​**increase insulin secretion **(block ATP K+ channel)
    • increase tissue sensitivity
    • decrease glucagon sensitivity
  • ​**PK: **30 min. prior to each meal. Oral, protein-bound, excreted in urine and bile
  • **Adverse: **hypoglycemia (esp. with insulin)
    • ​often cause weight gain
    • risk with liver / kidney disease
    • glyburie risk inelderly (falls)
27
Q

Repaglinide

A
  • ​MEGLITINIDE prototype
    • ​similar mechanism and use as SUs
    • increase insulin secretion
  • ​Lowest effciacy of all oral agents
  • Faster & shorter action than SUs (30 min before meal)
  • May be safer than SUs
    • ​less concern of hypoglycemia
    • safer in kidney disease
  • ​Still cause weight gain
28
Q

Metformin

A
  • BIGUANIDE prototype
  • **MOA: **primarily effects in liver
    • ​decreases glucose production and increases glucose uptake
    • increases insulin effectiveness, not insulin secretion
    • activates AMP-protein kinase (AMP-K)
      • ​central rose in glucose regulation
  • ​​**Therapy: **together with insulin in insulin resistance, also together with SUs
    • ​First-line drug
    • Does not cause hypoglycemia or weight gain
  • ​**PK: **oral, 2-4 times/day. well absorped (not protein-bound)
    • ​renal excretion without metabolism (dangerous in kidney disease)
  • ​**Adverse: **risk of lactic acidosis (inhibits lactic acid metabolism)
  • dangerous even in mild kidney disease
    • _​_danger with alcohol
    • unpleasant GI side effects
29
Q

Acarbose / Miglitol

A
  • Decrease glucose absorption from the gut
    • ​inhibit a-glucosidase & amylase
    • block hydrolysis of complex sugars in GI tract
    • enzyme inhibitors, not direct inhibitors of uptake
  • ​**Use: **30 min before meal, post-prandial glucose control
    • ​used in mild disease or w/ other agents
  • ​**PK: **Acarbose poorly absorbed, remains in gut
    • ​Miglitol gets absorbed
  • ​**Adverse: **do not cause hypglycemia on their own
    • ​risk of hypoglycemia with insulin or SU
    • GI: flatulence, cramps, diarrhea
30
Q

Pioglitazone / Rosiglitazone

A
  • Thiazolidenediones
    • ​Rosiglitazone had limitations on use b/c CV Risk
  • ​**MOA: **activate PPAR-y (peroxisome proliferator-activated R)
    • ​nuclear receptors / transcription factor
    • enhances transcription of insulin-responsive genes
    • (lipid, glucose-handling enzymes, transporters)
  • ​**Therapy: **increase responsiveness to insulin
    • ​liver: decrease glucose & TG synth & release
    • muscle: increase glucose uptake
    • adipose: increased glucose uptake
    • in patients with insulin resistance (insulin sensitizers)
  • ​**Adverse: **Liver toxicity (liver function tests every 2 months)
    • ​rosiglitazone had clear CV toxicity
    • no major hypoglycemia risk
31
Q

Exenatide

A
  • GLP-1 analog
  • **MOA: **​’incretin’ - potentiate insulin secretion
    • decrease glucagon secretion
    • slow gastric emptying, promote satiety
      • ​decrease in fasting Glc, no weight gain
  • ​​**PK: **peptide, require injection (pen)
  • **Adverse: **increased hypoglycemia risk (esp w/ SUs)
    • ​nausea, thyroid C-cell tumors & pancreatitis
    • decrease absorption of some drugs
    • avoid in kidney disease
32
Q

Sitagliptin

A
  • ​DDP-IV inhibitor
  • **MOA: **di-peptidyl-peptidase-4 inhibitors
    • ​similar to exenatide
    • prevent degradation of endogenous incretins
  • ​**PK: **oral, 1/day (not a peptide drug, peptidase inhibitor)
    • ​increase conc. endogenous incretins is preferable
  • ​**Therapy: **approved for use as monotherapy or fixed dose with metformin
    • ​(GLP-1 agonists are not)
    • Not used for Type 1 DM
  • ​**Adverse: **No weight gain OR weight loss
    • ​increased hypoglycemia risk in combos
    • increased risk of respiratory infections
33
Q

Canaglifozin

A
  • SGLT2- inhibitor
  • **MOA: **Sodium/glucose co-transporter 2 in kidney
    • ​reduce glucose reabsorption, increase Glc excretion
  • ​**PK: **orally effective, small molecule inhibitors
  • **Adverse: **No effects on insulin (No hypoglycemia risk)
    • ​increased risk of genital and UTIs
    • Diuretic effect can cause problems
34
Q

Hydrocortisone / Cortisone

A
  • Drug name for cortisol
    • **​cortisone - **prodrug form of hydrocortisone
  • ​Activty at both the GC and **MC **receptors
  • **PK: **8-12 hr duration, doesd multiple times/day
  • **Therapy: **Adequate for most endocrine replacement therapy uses
    • ​it IS the endogenous hormone
35
Q

Prednisolone / Prednisone

A
  • Minor modifications from cortisol / hydrocortisone
  • **PK: **Oral effective, 18-36 hr duration (once / day)
    • ​more convenient
  • ​**Therapy: **partially selective for GC vs. MC receptor
    • ​mainly impt for anti-inflammatory uses
    • stronger anti-inflammatory effects without MC side effects
      *
36
Q

Dexamethasone / Betamethasone

A
  • **Highly GC-selective **(30-fold)
  • Minimal MC action even at strong GC dose
  • **PK: **Very Long duration of action (36-54 hr)
    • ​Very potent - works at low doses
    • Low protein-binding & slow metabolism
  • ​**Therapy: **when very strong anti-inflammatory effects are needed (with no MC action)
37
Q

Fludorocortisone

A
  • Modifications to increase MC receptor potency and selectivity
    • ​still retains strong GC receptor potency
  • ​PK: oral, 1/day
  • **Therapy: **when MC replacement is the Goal
    • ​adrenal failure
    • 21-hydroxylase deficiency (make some cortisol but not aldosterone)

Pharmacology (2 decks)

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