Pcol 2 Exam 4 Flashcards
Insulin Lispro
Rapid acting insulin
Recombinant DNA by swapping Proline 29 and Lysine30 –> To Lysine 29 and Proline 30 –> giving LysineProline (Enhence LisPro)
Duration of action is 15-20mins
Humalog, admelog, Lyumev
Insulin Aspart
Rapid acting insulin
Novolong, Fiasp
Glulisine
Rapid acting insulin
Apidra
Novalin N
Intermediate insulin
In NPH with phosphate buffer
Insulin + Protamine + Zinc –> has large crystals of Zinc
Humalin N
Intermediate insulin
NPH –> Insulin + Protamine + Zinc –> has large crystals of zinc in phosphate buffer
Insulin Glargine
Long acting insulin
Non crystallized recombinat DNA water soluble insulin long acting
Duration is 24 hr
Lantus, Basaglar, toujeo
Insulin Detemir
leve
Recombinant DNA to produce non crystallized water soluble insulin
Duration of action is 24 hrs and given once a day subcu injection
Levemir
Insulin Degludec
Long acting insulin
Tresiba
Glargine yfgn
Long ancting insulin
semglee
Pralintide
Exogenous administration of amylin
-Has Proline in position 25,28,29 –> therefore prevents polymerization
MOA:
-Pranlintide exogenous administration of amylin –> amylin receptor contains calcitonin receptor that associate with RAMP and get a GCPR –> can supress the release of glucagon and delay gastric emptying–> therefore slowing the gastric emptying will cause less glucose to be absorb from the GIT
Thera;
-Treat type 1 DM and Type 2 DM
Symlin
Metformin
For type 2 DM
MOA
-Will activate the AMPK enzyme in the liver which results in a change in gene transcription –> Resulting in reduction og gluconeogenesis so less glucose produce
-Decrease gene expression of lipogenic enzymes
-Increase fatty acid oxidation –> So fat breakdown so less fatty acid in the liver which leads to increase insulin sensitivity because decrease fatty acids in liver –> Improve insulin sensitivity
Thera:
-For type 2 dm –> because metformin will make them more sensitive to their own insulin so more glucose transporter inserted to their membrane also improve insulin sensitivity in their muscle
-No risk of hypoglycemia –> because no increase in endogenous insulin release
AE:
-Metallic taste
-Anorexia–> Decrease appetitie
-Diarrhea –> ER formulation is better to use
-High levels of metformin can cause metabolic acidosis–> because metformin is excreted unchange and if the patient has poor renal function (kidney function) they will not be able to excrete the metformin and it builds up in the blood
-Pt should stop metformin if is going to get a GI Scan because is going to be put on constrat media –> and the contrast media will cause the kidney to stop working so cannot excrete the metformin
Glucophage
Pioglitazone
ac
-Glitazone
MOA:
Works by activating the PPARy a nuclear hormone receptor and will increase gene transcription and will increase insulin sensitivity
-And cause reduction in free fatty acids in the liver –> so improve insulin sensitivity
-No risk of hypoglycemia
-If administer will insulin need to half the dose of insulin
Thera:
-For type 2 DM
AE:
-Anemia –> Decrease RBC
-Edema–> Weight gain]
-Peripheral edema
-Pulmonary edema
-Can cause HF because of all the fluid acumulation –> CI if pt has HF
-Increase myocardiac infarction
Actos
Rosiglitazone
Ava
-Glitazone
MOA:
Works by activating the PPARy a nuclear hormone receptor and will increase gene transcription and will increase insulin sensitivity
-And cause reduction in free fatty acids in the liver –> so improve insulin sensitivity
-No risk of hypoglycemia
-If administer will insulin need to half the dose of insulin
Thera:
-For type 2 DM
AE:
-Anemia –> Decrease RBC
-Edema–> Weight gain]
-Peripheral edema
-Pulmonary edema
-Can cause HF because of all the fluid acumulation –> CI if pt has HF
-Increase myocardiac infarction
Avandia
Acarbose
pre-
Alpha glucosidase inhibitor
MOA:
Works only in the GIT and inhibits alpha glucosidase –> therefore slows down the breakdown of the polymers of carbohydrates such as mannitol, dextrin and starch –> prevents the hydrolysis at alpha 1-4 glucosidic bonds so no release of glucose
Thera:
-For type 2 dm
-no risk of hypoglycemia
AE:
-Bloating
-Flatulence
Prelose
Miglitol
gly-
Alpha glucosidase inhibitor
MOA:
Works only in the GIT and inhibits alpha glucosidase –> therefore slows down the breakdown of the polymers of carbohydrates such as mannitol, dextrin and starch –> prevents the hydrolysis at alpha 1-4 glucosidic bonds so no release of glucose
Thera:
-For type 2 dm
-no risk of hypoglycemia
AE:
-Bloating
-Flatulence
Glyset
Glyburide
Micro
Sulfonylureas insulin secretagogues
MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
-Has active metabolites so need to check kidney function –> because if poor kidney function –> the active metabolites will not be excreted and accumulates causing toxicity
Thera:
-For type 2 DM
AE:
-Gain weight
-Hypoglycemia (Hyperinsulemia)
-Fetal abnormalities –> avoid in preg
Micronase, Dibeta
Glipizide
Gluco
Sulfonylureas insulin secretagogues
MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
AE:
-Gain weight
-Hypoglycemia (Hyperinsulemia)
-Fetal abnormalities –> avoid in preg
Glucotrol
Glimepride
Ama-
Sulfonylureas insulin secretagogues
MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
AE:
-Gain weight
-Hypoglycemia (Hyperinsulemia)
-Fetal abnormalities –> avoid in preg
Amaryl
Repaglinide
pra-
Meglitide - insulin secretagogues
-MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
Prandin
Nateglinide
Meglitide - insulin secretagogues
-MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
Starlix
Exenatide
by-
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-In the N-terminal has His-Gly (replacing Alanine to glycine ) which prevent de activation from DPP-IV
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Byetta
Liraglutide
Vict-
Sax
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-Has a Palmitic acid conjugated in one of the glutamic acid residues
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Victoza ,Saxenda
Dulaglutide
tru-
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-In the N-terminal has His-Gly (replacing Alanine to glycine ) which prevent de activation from DPP-IV
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Trulicity
Ozempic
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-Supress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
semiglutide
Rybelsus
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Taken PO is a coated tablet that sticks to the gastric mucosa -> so need to take it on a empty stomach, with minimal water and separate from other meds
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Tirzapetide
Zep-, Moun-
GLP-1/GIP agonist
MOA:
-GIP –> is secreted by K-type cells in the intestine, duodenum and upper intestine .
-GIP –> Gastric-inhibitory peptide –> will cause inhibition of gastric secretion from parietal cells in the stomach –> therefore it causes indigestion
-GIP –> has dual activity and can activate GLP-1 receptors in the pancreas beta cells and cause the release of insulin in response to high levels of blood glucose
Thera:
-Weight loss
-Type 2 DM
AE:
-Fetal abnormalities
-Nausea–>because slow GE and things can back up from the stomach
Zepbound, mounjaro
Sitagliptin
jan-
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Januvia
Vidagliptin
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Galvus
Sixagliptin
Ongly-
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Onglyza
Linagliptin
trad-
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Tradgenta
Empagliflozin
Jar
-gliflozin -SGLT2 inhibitor
Inhibit Glucose reabsorption
Works in the proximal renal tubule –> inhibits glucose reabsorption now stays in the nephron to be excreted
Thera:
-Treat DM
-have cardiovascular benefits
AE:
-Hyperkalemia –> avoid drugs that can increase K+ levels
-UTI
-Polyuria
Jardiance
Canagliflozin
Inv-
SGLT2 inhibitor
Use PO
MOA:
Inhibits SGLT2 in the proximal renal tubule –> prevent glucose reabsorption –> glucose stay in the nephron to be excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-UTI
-Polyureia
-Hyperkalemia –> Avoid drugs that can cause hyperkalemia
Invonkana
Dapagliflozin
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Farxiga
Sotagliflozin
in-
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Inpefa
Bexagliflozin
bren-
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Brenzavvy
Ertugliflozin
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Steglatro
depo testosterone
androgel
testin
Jantezo(po )
Kyzatrex (po)
Tlando (po)
testosterones
thera:
male hypogonodism- during puberty see that the boy is not growing and is unable to make endogenous testosterone so receive exogenous for life time
Low T- as the male ages the levels of testosterone drop and can suffer from low sex drive, low energy, and muscle loss —- so give testosterone expgenous to treat it
AE:
-high cholesterol
high LDL
low HDL
increase BP
methyl testosterone
use for hormone replacement therapy in post menopause women but give low dose
AE
increase BP
danocrine
is a testosterone analog
thera
for endometriosis- high levels of estrogen will cause enlargement of the uterus so give androgens and will cause feedback inhibition so no LH and FSH release onto the ovaries therefore causing no estrogen to be produced
AE
increase BP
increase intracranial hypertension
increase LDL
decrease HDL
Fluoxymesterone
Halo-
Anabolic steroid
MOA:
-Is a poor substrate of aromatase so less estrogen produced
Thera:
-Use for erythropoeisis –> to raise RBC production
But athletes abuse it because can increase bone mineral density
AE:
-Increase LDL
-Increase cholesterol
-Decrease HDL
-Infertility
-Hepatic tumors (bening and malignant)
-Peliosisw hepatitis –. cause hepatocytes to die
Halotestin
Oxyandrolone
anav-
Anabolic steroid
MOA:
-Is a poor substrate of aromatase so less estrogen produced
Thera:
-Use for erythropoeisis –> to raise RBC production
But athletes abuse it because can increase bone mineral density
AE:
-Increase LDL
-Increase cholesterol
-Decrease HDL
-Infertility
-Hepatic tumors (bening and malignant)
-Peliosisw hepatitis –. cause hepatocytes to die
Anavar
Oxymetholone
Anad-
MOA:
-Is a poor substrate of aromatase so less estrogen produced
Thera:
-Use for erythropoeisis –> to raise RBC production
But athletes abuse it because can increase bone mineral density
AE:
-Increase LDL
-Increase cholesterol
-Decrease HDL
-Infertility
-Hepatic tumors (bening and malignant)
-Peliosisw hepatitis –. cause hepatocytes to die
anadrol
Dergarelix
Firma
GNRH receptor antagonist -relix
MOA:
-Block GNRH receptors so no LH or FSH release
Thera:
-For prostate cancer but need to co admin androgen antagonist
-For endometriosis in female
-For androgen deprevation
AE:
-Decrase bone mineral density
-Hot flashes in female
-Decrease sex libido
Firmagon
Elagolix
Ori-
-GNRH receptor antagonist -lix
MOA:
-Block GNRH so no GNRH release no FHS and no LH
Thera:
-For prostate cancer when co admin with androgen antagonist
-For endometriosis in female
-Androgen deprevation
AE:
-Decrease bone mineral density
-Hot flashes in female
-Decrease sex libido
orilisa
Relugolix
Orgo-
GNRH receptor antagonist -lix
MOA:
-Block GNRH receptor so no GNRH release no LH and no FSH
Thera:
-For endometriosis in female
-Androgen deprevation
-For prostate cancer but need to coadmin androgen antagonist
AE:
-Decrease sex libido
-Hot flashes in female
Decrease bone mineral density
Orgovyx
Leuprolide
Lu-
GNRH receptor agonist
MOA:
-GNRH receptor is a GCPR and at the begining its active and the symptoms worsen. But constant stimulation of the receptor will cause receptor down regulation and the receptor shuts down –> therefore no release of GNRH onto pituitary gland so no LH and FSH release
Thera:
-Breast cancer
-Prostate cancer
-Endometriosis
-Precocius –. when the kid puberty is very early in age early than normal so want to stop LH and FHS release
AE:
-Hot flashes –> in woman
-Decrease bone mineral density
-Osteoporosis
Lupron
Nafarelin
Syn-
GNRH receptor agonist -relin
MOA:
-At the begining the activation of GNRH receptor a GCPR will cause the symptoms to worsen –> but then constant stimulation of the receptor will cause receptor down regulation so stops working –> so no GNRH release –> no LH and FSH release
Thera:
-Endometriosis
-Breast cancer
-Prostate cancer
-Precocius –> early puberty than normal –> so to treat want to reduce levels of FSH and LH
AE:
-Hot flashes –> in women
-Decrease bone mineral density
-Osteoporosis
Synerel
Goserelin
Zola-
GNRH receptor agonist -relin
MOA:
-Activation of GNRH receptor (a GCPR) at the begining the symptoms worsens but then constant stimulation of the receptor will cause receptor down regulation so no release of GNRH –> no LH and FSH release
Thera:
-Breast cancer
-Endometriosis
-Prostate cancer
-Precocius –> early puberty –> so to treat want to stop release of LH and FSH
AE:
-Oseteoporosis
-Decrease bone mineral density
-Hot flashes in women
Zoladex
Buserelin
Supre-
GNRH receptor agonist (-relin)
MOA:
-Activation of the GNRH reptor (a GCPR) at the begining will cause the symptoms to worsen –> but then constant stimulation of the receptor will cause receptor down regulation –> so no release of GNRH no LH and FSH
Thera:
-Prostate cancer
-Endometriosis
-Breast cancer
-Precocius –> early puberty so want to decrease and stop release of LH and FSH
AE:
-Hot flashes in women
-Decrease bone mineral density
-Osteoporosis
Suprefact
Histerelin
Van-
GNRH receptor agonist (-relin)
MOA:
-GNRH receptor agonist (is a GCPR) and activation of GNRH receptor at the begining it will cause the symptoms to get worse –> but eventually constant stimulation of the receptor will cause receptor down regulation and no release of GNTH and FSH and LH
Thera:
-Prostate cancer
-Breast cancer
-Endometriosis
-Precocius –> early puberty –> want to decrease levels of LH and FSH
AE:
-Hot flashes in women
-Decrease bone mineral density
-Osteoporosis
Vantas
Triptorelin
GNRH receptor agonist (-relin)
MOA:
-GNRH receptor is a GCPR –> at the begining the activation of GNRH receptor will cause the symptoms to get worse –> but then constant stimulation of the receptor will cause receptor down regulation so no release of GNRH, LH and FSH
Thera:
-Prostate cancer
-Breast cancer
-Endometriosis
-Pecocius –> early puberty and to treat you want to decrease levels of FSH and LH
AE:
-Hot flashes in women
-Decrease bone mineral density
-Osteoporosis
Bicalutamide
Caso-
Androgen receptor antagonist (-lutamide)
MOA:
-Block androgen receptors so prevent endogenous androgens from binding (testosterone)
Thera:
-Treat primary prostate cancer –> androgen dependent cancer –> the cancer causes the prostate to grow in response to androgens –. but because Bicalutamide (Casodex) blocks the androgen receptors –> it will cause to stop growing
Harmful effects of androgen receptor antagonist:
-The hypothalamus will think there is low testosterone so will release more FSH and LH from the pituitary gland –>FSH and LH bind to receptors on the testes and cause the production of testosterone –> so to prevent need to co-admin GNRH receptor antagonist Degarelix (Firmagon), Elagolix (Orilisa), Resugolix (Orgovyx)
Casodex
Apalutamide
Er-
Androgen receptor antagonist (-lutamide)
thera:
-Treat primary prostate cancer – androgen dependent cancer –> that grows in response to androgens stimulating the receptors –> but apalutamide (erleada) block androgen receptors so stop from growing
Harmful effects of androgen receptors antagonist:
-The hypothalamus will think there is low testosterone and will stimulate the release of LH and FSH from the pituitary gland –> LH and FSH bind to receptors in the testes and cause production of testosterone –> so to prevent need to co-admin GNRH receptor antagonis: Degarelix (Firmagon), Elagolix (Orilisa), Relugolix (Orgovyx)
Erleada
Enzalutamide
Xtan-
Androgen recepto antagonist (-lutamide)
Thera:
-Treat primary prostate cancer –> androgen dependent cancer –> that grows in response to androgens –> but enzalutamide (Xtandi) will block androgen receptors so cancer stops growing
Harmful effects of androgen receptor antagonist:
-The hypothalamus will think there is low testosterone –> so will stimulate the release of FSH and LH from the pituitary gland and FSH and LH act on the testes and produces testosterone –> to prevent need to coadmin GNRH antagonist Degarelix (Firmagon), Elagolix (Orilisa), Resugolix (Orgovyx)
Xtandi
Darolutamide
nube-
Androgen recepto antagonist (-lutamide)
Thera:
-Treat primary prostate cancer –> androgen dependent cancer –> that grows in response to androgens –> but darolutamide (Nubeqa) will block androgen receptors so cancer stops growing
Harmful effects of androgen receptor antagonist:
-The hypothalamus will think there is low testosterone –> so will stimulate the release of FSH and LH from the pituitary gland and FSH and LH act on the testes and produces testosterone –> to prevent need to coadmin GNRH antagonist Degarelix (Firmagon), Elagolix (Orilisa), Resugolix (Orgovyx)
Nubeqa
Clascoterone
Win-
Androgen receptor antagonist use topically to treat acne
Winlevi
Somatorelin
Somatrem
Somatrogon
Somapacitan
Human recombinant growth hormones (Soma-)
Thera:
-Growth hormone are administer to pt that have deficiency on growth hormones –> measure the levels of growth hormones and if the levels are low then decide to supplement the child with exogenous growth hormone injection and allow them to grow in a normal rate and reach their expected heigh
-Idiopathic short stature –> no known cause for it –> measure the pt heigh and they are lower than what they are expected to grow and when do the growth hormone level check the levels are normal –> idiopathic height means that they are in the lowest 1.2% for their sex and age and can be treated with growth hormones
AE:
-Administrating growth hormones can increase cell division, cell differentiation, cell growth and when you increase cell growh –> increase risk of malignant transformation and increase risk of cancer
CI:
-Leukemia
Sermorelin
Tesamorelin
Peptides that mimic GHRH
Thera:
-To test the pituitary gland to find out if is working –> give sermorelin and tesamorelin and measure the growth hormone levels
-Can increase the levels of growth hormones –> so can increase IGF-1
Recombinant human IGF-1
Some pt suffer from mutation in their growth hormone receptor and the growth hormone is unable to activate the receptor and is unable to cause the tissue to grow
and is unable to cause IGF-1 secretion –> so give exogenous IGF-1
Ocreotide
Lanreotide
Pasireotide
SST5 receptor agonist (-reotide)
MOA:
-activate somatostatin 5-receptor in the pituitary gland –> so will cause decrease release of growth hormone
Thera:
-For acromegaly / gigantism –> a condition where there is a tumor in the pituitary gland causing excess release of growth hormone. To treat want to surgically remove it or radiation for shrinking of the tumor. But can give Ocreotide, lanreotide, pasireotide until the pt gets surgery or radiation
Mechanism based AE:
-Can also activate SST5 receptors in the GIT –> causing abdominal pain, and reduce fat absorption
Off target AE:
-Due to poor selectivity can also activate SST3 receptor in the pancrease beta cells –> and causes decrease release of insulin –> causing hyperglycemia
Bromocriptine
Par
D2 receptor agonist ergot derivative
-It was used to treat parkinson but not anymore
-Activation of D2 receptors on the pituitary gland will cause decrease prolactin release –> and is useful to treat breast cancer
-Activation of D2 receptors on the pituitary gland will cause decrease growth hormone release –> and is useful to treat acromegaly/gigantism
Pardolel , cycloset
Pardolel, Cycloset
Pegvisomat
Soma-
Growth hormone receptor antagonist
MOA:
-Pegvisomat (Somavert) will block growth hormone receptors –> therefore blocking growth hormones from binding to its receptors in the tissues
Thera:
-For acromegaly/gigantism –> can use pegvisomat (somavert) until the pt is going for surgery to remove the tumor in the pituitary gland or radiation for shrinking of the tumor
Somavert
Alendronate (Fosa-
Risedronel (Acto-
Ibandronate (Boni-
Pamidronate
Zoledronate
Alendronate (Fosamax)
Risedronel (Actonel)
Ibandronate (Boniva)
Biphosphonates (-dronate) Antiresorptive drugs
MOA:
-Biphosphonates will bind to the calcium in the bloodstream
When bone remodeling is occuring the osteoblast will take Calcium and Phosphate –> and forms hydroxyapetite that is a inorganic bone matrix that the osteoblast will use to fill the resorptive area
Biphosphonates because they are bound to calcium –> they will be on the surfacr of the bone and when osteoclast come in for resorption they will take the biphosphonate –> and then the biphosphonate will cause apoptosis of the osteoclast
-So a pt that is taking biphosphonates will have reduce number of osteoclas –> so less bone destruction
Thera:
-Treat osteoporosis
Counseling:
-Biphosphonates have poor oral bioavailability therefore it should be taken on a empty stomach with full glass of water
-Pt should avoid taking calcium suplements and milk while taking biphosphonates because want to prevent biphosphonates from binding to calcium in the GIT
-Biphosphonates are very acidic –> so pt should take the medication standing up during the day –> avoid laying down because if the pt lays down–> the biphosphonates will cause the stomach contents to back up causing damage to the esophagus leading to erosive esophagitis and can further lead to esophageal cancer
-Is a weekly dose not a daily dose
AE:
-Muscle ache
-Osteonecrosis of jaw–> bone in the jaw becomes more suceptible for fracture and breaking due to a change in bone architecture. So pt on biphosphonates should always inform dentist
-Fluoride –> it is use in kids becaus it hardens the tooth. It was used in adults to decrease osteoporosis because fluoride can increase bone mineral density but it causes a change in bone architecture therefore leading to increase risk of bone fractures
Denosumab (Pro-
Monoclonal antibody against RANKL (Rank Ligand) is a anti-resorptive drug
MOA:
-Denosumab (Prolia) binds to RANKL and reduces the ability of RANKL to bind RANK receptors on the surface of immature osteoclast –> therefore it reduces # of osteoclast and reduces osteoporosis
Thera:
-For osteoporosis –> denosumab (Prolia)
AE:
-Muscle and joint pain
-Lower back pain
-Hypocalcemia –> low levels of calcium in the blood because bone is not being broken down so no release of Ca2+ into the bloodstream
Prolia
Romosozumab (Eve-
Monoclonal antibody against Sclerostin –> is a anti-resorptive drug
MOA:
-Normally WNT protein will bind to the complex and activates it receptors and increase gene transcription and increase osteoblast activity
-But when Sclerostin (a endogenous inhibitor) come it will bind to the complex and prevent WNT from binding –> so no gene transcription
-So Romosozumab (Evenity) will directly bind to sclerostin and prevent it from binding to the complex –> so allow WNT protein to bind –> increases osteoblast activity and decreases osteoclast activity
Thera:
-Osteoporosis
AE:
-Muscle and joint pain
-Increase risk of cardiovascular events –> increase risk of MI
Evenity
Calcitonin
Endogenous peptide released by the thyroid gland in response to high levels of calcium in the blood
-Calcitonin will bind to receptors in the bone and will inhibit osteoclast activity –> so less digestion of bobne layer , less release of Ca2+ into the bloodstream
-Calcitonin will also cause to reduce Calcium reabsorbtion in the kidney and increase calcium excretion
-Is given as a salmon nasal spray –> because salmon calcitonin has better affinity
Thera:
-Treat osteoporosis
AE:
-Salty taste
-Paresthesia –> tingenling in fingers and toes
-Fluid retention
Calcium
Give calcium supplement to prevent the release of parathyroid hormone from the thyroid gland ( parathyroid hormone is release in response to low levels of calcium but because pt is on supplement it will not be release)
So prevent the effects of parathyroid hormone –> so no activation of osteoclast in the bone (no resorption so no release of calcium to blood), no activation of parthyroid receptors in the kidney, no activation of parathyroid receptors in the GIT ( so no absorption of Ca2+ in GIT)
AE:
-Constipation
-Increase BP –> too much Ca2+ causes blood vessels to constrict
-Arrythmia –> too much Ca2+ can cause arrythmia
-Increase risk of kidney nephrolithiasis (kidney stones) –> so pt should maintain hydration
Vitamin D
Vitamin D2 (ergocalciferol)
Vitamin D3 (cholecalciterol)
Calcitriol
Vitamin D is taken from our diet or from sun exposure to our skin
Vitamin D will bind to its receptor a nuclear hormone receptor and will increase gene transcription and protein synthesis
Increases transcription of Ca2+ transporters in the GIT and in the kidney –> so increases Ca2+ to move from the GIT and kidney into the blood stream
So prevents osteoporosis
Teriparatide (For
Abaloparatide (Tym-
Teriparatide (Forteo)
Abaloparatide (Tymlos)
Anabolic bone drugs (-paratide)
MOA:
-Teriparatide (Forteo), Abaloparatide (Tymlos) will increase the activity of osteoblast –> so increase hydroaxiapetite (inorganic bone matrix) to be put onto the surface of new bone, increase bone mineral density
Thera:
-They are use for severe cases of osteoporosis - osteopenia –> and they are peptide so need to give by injection
AE:
-Increase growth of bone can cause osteosarcoma –> bone cancer –> so the pt has a limit dose of only 2 yrs –> if they pt already took teriparatide (Forteo), Abaloparatide (Tymlos) for 2 yrs then the pt should be switch to antiresorptive drugs
-Orthostatic hypotension –> drop in BP after injection so pt should stay sitted
-Hyperurecimia
Cinacalcet (Sensi
Cinacalcet (Sensipar)
Drug for hyperparathyrodism
MOA:
-Is a calcimimetic at the calcium receptors in the parathyroid gland
-Cinacalcet (Sensipar) will bind to the calcium receptor via allosteric modulation –> meaning it binds to a different portion of the receptor. And the parathyroid gland will think there is high levels of calcium so it wont release parathyroid hormone –> so no activation of osteoclast
Thera:
-For hyperparathyrodism
Etelcalcitide (Par
Etelcalcitide (Parsabiv)
Drug for hyperthyrodism
MOA:
-Is a calcimimetic at the calcium receptors on the parathyroid gland
-It will bind to the calcium receptors via allosteric binding –> meaning it binds to a different area of the receptor –. and the parathyroid gland senses “high calcium” so it wont release parathyroid hormones so no activation of osteoclast
Thera:
-For hyperparathyrodism
Natpara
Natpara PaloYor
Exogenous version of parathyroid hormone
Use for hypoparathyrodism
Palopegteriparatide
NATPAR PaloYor
Exogenous version of parathyroid hormone
Use for hypoparathyroidism
Yorvipath
T4: Levothyroid, Synthyroid, Levoxyl, Unithroid
T4
-Can remove a iodine by using the enzyme 5’di iodinase that is also in the bloodstream and get T3 (triidothyronine)
-T4 has T1/2 of 7 days –> so only weekly dose
-Undergoe entero hepatic circulation and is excreted in bile and reabsoberd again
-Need to be taken on empty stomach because has amphotetic structure –> always exist as charged and uses active transporter requires ATP and if taken with food or Ca, Mg it will saturate the transporters
-Pt should take it in the morning
-50% oral bioavailability and if pt takes IV need to decrease the dose by half
AE:
-Palpitations
-Increase HR
T3 Liothyronine , cytomel
Has t1/2 half life of one day
-Is less ionized at phisiological pH so the thyroid receptors love that
-Less PPB
-pKA 8.3 because the OH only has one electron withdrawing group
-Take it on empty stomach , withiout Mg, Ca
-Take it AM dosing
AE:
-Palpitation
-Increase HR
T3 and T4 combo
lio-, thy-
T3 and T4 combo (liotrix, Thyrolar)
Take it on a empty stomach
AM
AE:
-Palpitations
-Increase HR
Liotrix, thyrolar
Dessicated thyroid
Armo-
Extract the thyroid glands from animals and extract out the T3 and T4
-For hypothyrodism
-take on empty stomach and without Ca, Mg
-take it AM
AE:
-palpitations
-Increase HR
Armour thyroid
Propylthiouracil (PTU)
Thioperoxidase inhibitor
MOA:
-inhibit thioperoxidase in the thyro globulin –> so prevent oxidation rxn of iodide to iodine. also prevent iodination rxn and prevent incorporation of iodine to tyrosine ring –> so decrease production of T3 and T4
Thera:
-Graves disease
-Hyperthyrodism –> pt suffer from palpitations, too hot, weight loss
AE:
-allopecia
-Hepatotoxicity–> monitor LFT
-Agranularcytosis –> decrease WBC
-Skin rash
-Joint pain
Methimazole
Tapa-
Thioperoxidase inhibitor
–> So preven oxidation of idodide to iodine , prevent idonization rxn so no incorporation of idodine to tyrosine rings
Thera:
-For graves disease –> hyperthyrodism
AE:
-Hepatotoxicity
-Allopecia
-Skin rash
-Agranularcytosis –> decrease WBC
-Joint pain
Tapazole
Iodide
High levels of iodide will shut down the iodide symporter –>so no iodide taken up from the bloodstream .
-And also block the iodide symporter in theother right end so prevent the release of T3 and T4
-See the drop in T3 and T4 immediately
-Also use to protect against radioactive iodide
Cortisol (Hydrocortisone)
Prednisone (Deltasone)
Prednisolone
Cortisone
Methylprednisolone
GC>MR
glucorticoid receptor agonist
Thera:
-Primary adrenal insuficiency –> pt cannot produce adequate levels of cortisol
-Secondary adrenal insuficiency –> pt dont produce cortisol –> addison deisease so need to coadmin fludrocortisone (Florinef)
Betamethasone
Dexamethasone (decadron)
triamcinolone
GC»>MR
glucorticoid receptor agonist
Thera:
-Primary adrenal insuficiency –> pt cannot produce adequate levels of cortisol
-Secondary adrenal insuficiency –> pt dont produce cortisol –> addison deisease so need to coadmin fludrocortisone (Florinef)
Fludrocortisone
Is a mineralcorticoid receptor agonist
-it will release aldosterone when angiotensin activate the receptor
–> causes Na+ reabsorbtion and H2O follows –> so increase blood volume –> increases BP
-Can also cause constriction of the blood vessels
Thera:
-For adrennal insuficiency (addison disease) –> give glucocorticoids along with fludrocortisone
-For hypotension
Florinef
Conotropin Releasing Factor (CRF)
AchoCosy
Achthrel
Exogenous CRF –> use to measure if the pituitary gland is working –> measure the levels of CRF and the ACTH and hydrocortisone (cortisol) –> to see if the pituitary gland is working
Adrenocorticotropin hormone (ACTH)
ACHoCosy
Cosyn-
exogenous ACTH (cosyntropin)
to see if the pituitary gland is working
So measure the levels of ACTH and CRF and hydrocortisone (cortisol)
Cosyntropin
