Pharmacology Exam 1 Diseases

primary pathology

• the problem lies within the target organ system

• due to intolerance of a hormone rather than hormone deficiency

secondary pathology

• problem lies within the anterior pituitary

tertiary pathology

problem lies within the hypothalamus

GH deficiency

• tertiary pathology (the problem is with the hypothalamus)

• treated with semorelin or tesamorelin (GHRH alternatives)

• also treated with somatropin (GH agonist)

laron dwarfism

• primary GH deficiency (the problem is with the target organ system/intolerance to GH)

• treated with mecasemin (recombinant IGF-1)

gigantism

• extra GH BEFORE puberty (before bone plates close)

• caused by anterior pituitary tumors

acromegaly

• extra GH AFTER puberty

• can be caused by anterior pituitary tumors

prolactinomas

• benign tumors that secrete prolactin

• usually silent and due to pituitary tumors

• can be treated using dopamine agonists since dopamine antagonizes prolactin

neurogenic diabetes

• caused by insufficient ADH

• treated with desmopressin

nephrogenic diabetes

• there’s enough ADH, but the kidneys aren’t responding to it

• usually caused by another drug, find that drug and discontinue

• we can use thiazide diuretics until we find the culprit

SIADH

• excessive ADH

• too much kidney receptor activation → too much water reabsorbed → blood becomes diluted (hypoatremia) and there’s decreased plasma osmolarity

• pee will become more concentrated since your kidneys are holding onto water and not letting it pass into pee

• can be treated with tolvaptan and conivaptan

cushing’s syndrome

• different pathologies that can increase cortisol production

1. Tumors

• ectopic small cell carcinomas

• pituitary adenomas

• adrenal cortex adenomas

2. excessive glucocorticoid therapy

• can cause weird skin pigmentation since too much ACTH means more melanin since they are both cleaved from POMC

• can be treated with mifepristone to inhibit steroidogenesis or surgery to the adrenal gland, somatostatin analogs and dopamine agonist to inhibit anterior pituitary ACTH secretion

chrousos syndrome

• glucocorticoid resistance syndrome

• familial

• mutation/deletion of NR3C1 causes nonfunctioning glucocorticoid receptors → even if they have normal cortisol levels

• it looks like a deficiency in cortisol activity

• symptoms:

• hypertension

• hypokalemia

• menstrual irregularities

Addison’s disease

• there is NO negative feedback on ACTH (adrenocorticotropic hormone)

• can cause increased skin pigmentation if it’s a secondary dysfunction

• patients can be deficient in both corticosteroids and mineralocorticoids

• can affect salt/water balance and blood pressure