endo pharm moa, class, usage, adverse

Somatropin class

growth hormone

Somatropin moa

Stimulates IGF-1 from liver and other tissues to promote growth rate/height

Somatropin use

Used to treat hormone growth deficiency, such as girls with turners syndrome

Somatropin adverse

• Hyperglycemia

• May cause antibody formation from long term usage, that can neutrailze desired effect.

Desmopressin class

ADH replacement

Desmopressin MOA

causes water reabsorption, as opposed to excretion → decreases the urine volume

Desmopressin usage

treats diabetes insipidus (involves water imbalance instead of blood sugar imbalance), usually when body produces weird amount of ADH hormone, causing too much H2O secretion.

Desmopressin adverse

• Hyponatremia (occurs because there is too much water, so sodium becomes diluted)

• Siezures (from fluid overload)

Levothyroxine Class

Thyroid hormone replacement (T4)

Levothyroxine MOA

Coverts T4 to T3, which then restores metabolism

Levothyroxine Usage

Used for hypothyroidism (lifelong therapy)

• Myxedema coma (IV)

Levothyroxine adverse (think too much metabolis/ Hyper)

• Hyperthyroidism

• tachycardia

• angina

• insomnia

• hyperthermia

• sweating/nervousness

Propylthiouracil class

antithyroid drug

Propylthiouracil moa

blocks synthesis of thyroid hormone by blocking iodine from being integrated into tyrosine→ thus blocking conversion from T4 to T3

Can T4 and T3 be made from salt only?

No, Iodine is needed.

Propylthiouracil usage

Hyperthyroidism (graves disease)

• can be used alone ir also with radiation iodine

Propylthiouracil adverse (think less, so low WBC, hypo)

• Hypotheyroidism

• agranulcytosis

• rash

• joint/muscle pain

Glipizide class

sulfonylureas

Glipizide MOA

Release insulin from beta islet cells, requires that patient have functioning pancreas (specifically, working beta cells) for this to work

Glipizide use

Type 2 Diabates mellitus

Glipizide adverse

• hypoglycemia (can trigger hunger due to low BG→ more eating→ weight gain)

• weight gain

• kidney or liver malfunctioning

Metformin class

biguanide

Metformin MOA

• Decreases absorption of glucose from intestine

• Decreases synthesis of glucose by liver

• Increases sensitivity of insulin receptors in tissues→ decreases insulin resistance

Metformin use

Treats type 2 Diabetes mellitus (first line of drug for DM 2)

Metformin adverse

• GI (N/V/D)

• Metallic taste (think “MET” formin)

• lactic acidosis due to oxidation

• B12 and folic acid deficiency

Pioglitazone class

thiazolidinediones

Pioglitazone moa

Reduce insulin resistance in tissues → insulin must be available, either endogenous or may need exogenous (injected)

Pioglitazone usage

used for type 2 DM (usually combined with metformin), insulin must be available.

Pioglitazone adverse

• fluid retention (edema, weight gain, HF)

• livery injury

• bladder cancer

• Increased fracture in women taking it for a long period of time

• Elevated HDL/LDL/TG

• URI

Sitagliptin class

gliptin

Sitagliptin moa

blocks the DPP-4 enzyme from breaking down natural incretin hormones. This keeps incretin levels high, which signals the pancreas to release more insulin and the liver to produce less glucagon.

Sitagliptin use

Type 2 DM (oral only)

Sitagliptin Adverse

• Pancreatitis

• Stevens johnson syndrome

• URI

Ozempic class

semaglutide

Ozempic MOA

Works by mimicking the incretin glucagon (GLP-1), enhancing pancreatic cell growth to increase insulin production

Inhibits production of glucagon, which increases glycogenelysis (release of carbs stored in liver) and gluconogenesis (making of new glucose)

Slows down digestion in stomach, decreasing appetite

Ozempic use

Type 2 DM

• Obesity/ weight loss

Ozempic adverse

• Hypoglycemia

• N/V

• dehydration

• pancreatities

• vision changes

• liver/gallbladder disease

• depression

Glucagon class

hyperglycemic

Glucagon moa

Activates liver to convert glycogen to glucose

Glucagon use

Hypoglycemia when PT is unconscious

• also used for beta blocker overdose

Glucagon adverse

• headache

• N/V

• rebound hypoglycemia

Hydrocortisone class

glucorticoid

Hydrocortisone moa

synthesis of cortisol→ replaces the bad glucocorticoids

Hydrocortisone usage

Addisons disease (main drug)

Hydrocortisone adverse

• Low reactions at low dosage

• Cushings syndrome (at higher dose)

• adrenal suppression (high dose)

Fludrocortisone class

mineralocorticoids

Fludrocortisone moa

Synthetic aldosterone→ stimulates RAAS→ promotes sodium and water retention, and K+ excretion

Fludrocortisone Use

addisons disease (used with hydrocortisone)

• primary hypoaldosteronism

• Congenital adrenal herplesia (CAH)
  

Fludrocortisone adverse

• Same as hydrocortisone where low dosage→ low side effects

• High dose effects are:

Fluid retention (edema)

HTN

Hypokalemia

Weight gain

Insulin rapid acting name

lispro

Insulin rapid acting onset

15-30 mins

Insulin rapid acting peak

30 mins - 2.5 hours

Insulin rapid acting duration

3-6 hours

insulin short acting name

regular insulin

insulin short acting onset

30 min to 1 hour

insulin short acting peak

1-5 hour

insulin short acting duration

6-10 hours

insulin intermediate acting name

NPH

insulin intermediate acting onset

1-2 hour

insulin intermediate acting peak

6-14 hours

insulin intermediate acting duration

16-24 hours

insulin long acting name

glargine

insulin long acting onset

70 mins

insulin long acting peak

none (basal insulin only)

insulin long acting duration

18-24 hours