Pcol 2 Exam 4 Flashcards

Question

Rybelsus

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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

Answer 6

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

Answer 7

-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

Answer 8

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

Answer 9

-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

Answer 10

-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

Answer 11

-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

Answer 12

-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

Answer 13

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

Answer 14

use for hormone replacement therapy in post menopause women but give low dose AE increase BP

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

-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

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

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

Answer 25

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

Answer 26

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

Answer 27

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

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

Androgen receptor antagonist use topically to treat acne | Winlevi

Answer 33

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

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

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

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

Exogenous version of parathyroid hormone Use for hypoparathyrodism

Answer 49

Exogenous version of parathyroid hormone Use for hypoparathyroidism | Yorvipath

Answer 50

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

Answer 51

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

Answer 52

T3 and T4 combo (liotrix, Thyrolar) Take it on a empty stomach AM AE: -Palpitations -Increase HR | Liotrix, thyrolar

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

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

Answer 57

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)

Answer 58

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)

Answer 59

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

Answer 60

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

Answer 61

exogenous ACTH (cosyntropin) to see if the pituitary gland is working So measure the levels of ACTH and CRF and hydrocortisone (cortisol) | Cosyntropin

Pcol 2 Exam 4 Flashcards

(85 cards)