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Pharmacology Exam 3 > ENDOCRINE > Flashcards

ENDOCRINE Flashcards

1
Q

How do we treat hypopituitarism?

What are the hormones we are going to be replacing?

A
  • Replacing missing hormones

- Growth hormone (somatropin) and Vasopressin (AVP, AKA: antidiuretic hormone)

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2
Q

Growth Hormone (somatotropin):

  • Growth hormone (somatropin) is a weight based ___________ _________.
  • The MOA for GH is that it has a role in bone, ______ muscle and organ growth; increased ___ mass; and transport of ______, electrolytes, and fluid
  • The AE of GH is that it can cause _______ ________/edema, and ________ and joint pain
A
  • subcutaneous injection
  • skeletal, RBC, water
  • fluid retention, muscle
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3
Q

Vasopressin (AVP) AKA ADH:

  • Vasopressin has a role of ________ water excretion by _________ urine concentration.
  • A deficiency in AVP can cause what?
  • In order to treat a lack of vasopressin what do we give someone?
  • DDAVP (desmopressin) is given _________, PO, or intranasal
  • The MOA for DDAVP (desmopressin) is that it binds to __ receptors which causes an increase in ____ water channels on the cell membrane to make it more permeable; water enters in and then is released back into body by AQP_ and _ channels
  • DDAVP is also used for ________
  • What are the AE of DDAVP?
A
  • decreased, increasing
  • Diabetes insipidus (large production of urine)
  • Synthetic pharmacological product= desmopressin (DDAVP)
  • subcutaneous
  • V2, AQP2, 3 and 4
  • Nocturia
  • dry mouth, hyponatremia
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4
Q

When we have a AVP or DDAVP binding to the V2 receptors this results in water _________, meaning ____ urine.

A

reabsorption, less

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5
Q
  • For hyperpituitarism, ________ is in adults while _________ is in children.
  • It is often characterized by _______ bone and soft tissue growth;_____glycemia due to insulin resistance; _______ is greatest concern due to CV risk
  • What is the treatment for acromegaly?
A
  • acromegaly, gigantism
  • excessive, hyperglycemia, cardiomegaly
  • surgery
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6
Q

Therapeutic concerns with pituitary treatment:

  • Drug treatment accuracy is _______ meaning that there could be altered hormone levels exceeding normal ranges (or low).
  • Low GH levels will result in low _____ _______ which could cause bone fractures and slipped capital femoral epiphyses (ice cream falling off cone in hip joint)
A
  • difficult

- bone density

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7
Q

ADRENOCORTICOIDS

A

ADRENOCORTICOIDS

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8
Q

-Adrenocortical hypofunction can result in _______ disease. This is an insufficient production of _______ and ________
Adrenocortical hyperfunction can result in _______ disease. This is an excessive glucocorticoids from ________ production and _______ intake

A

Addison’s disease
-corticol and aldosterone
Cushing’s disease
-endogenous, exogenous

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9
Q
  • Adrenocorticosteroid is a steroid produced in the ______ _______.
  • This is further subdivided into whether it has more effect on ____/___ metabolism or _______/____ balance.
  • The one that has a more metabolic effect is a ____corticoid while the one with an electrolyte effect is a _____corticoid.
A
  • Adrenal medulla
  • carb/fat metabolism, electrolyte/water balance
  • glucocorticoid (hydrocortisone, cortisol), mineralocorticoid (aldosterone)
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10
Q
  • Excessive glucocorticoids can cause _______ syndrome.
  • This is due to an excess ________ glucocorticoid administration or an excessive ________ production from the adrenal gland.
  • The overall problem with this is hyper_________.
  • The first line treatment for excessive glucocorticoids is ________ but they may need pre or post-op medication such as __________ inhibitors which block cortisol synthesis or ___________ antagonist which blocks cortisol binding to receptor
A
  • Cushing’s
  • exogenous, endogenous
  • hypercorticolism
  • surgery, steroidogenesis inhibitors or glucocorticoid antagonists
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11
Q

-Glucocorticoid deficiency can be divided into a _______ and _______ adrenal insufficiency.
-If it is a primary insufficiency it can cause _______ disease. This disease is usually _______, destroying all regions of adrenal cortex.
-Secondary insufficiency is most often due to _______ corticosteroid administration, our body becomes reliant to the outside administration causing a decrease in ____ release.
Why is it important to taper off of steroids?

A
  • primary and secondary
  • Addison’s, autoimmune
  • exogenous, ACTH
  • Body isn’t making it, will cause a deficiency if taken off instantly.
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12
Q
  • What is the treatment for glucocorticoid deficiency?
  • The short term AE are _______ glucose levels, mood or appetite changes, fluid retention (edema).
  • Long term AE can include _________, thinning of skin, infection, poor would healing.
A
  • replace glucocorticoids = hydrocortisone, cortisone, or prednisone
  • increased
  • osteoporosis
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13
Q
  • Since primary adrenal insufficiency (Addison’s disease) is causing a destruction of the adrenal cortex we have to replace glucocorticoids as well as the ___________ with __________ to decrease hyperkalemia.
  • In times of acute stress, they may require significantly _____ med doses because stress increases adrenal requirements.
  • They may also require additional hydrocortisone before ________
A
  • mineralocorticoids with fludrocortisone
  • increased
  • strenuous exercise
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14
Q
  • Mineralocorticoid excess (hyper_________) can be caused by adrenal tumor (_____ syndrome) or adrenal hyperplasia.
  • The S/Sx or hyperaldosteronism includes ______ weakness, _______, paresthesias, headache, polydipsia, nocturnal polyuria, ___
  • If pharm treatment is needed we use ________ receptor antagonist (AKA: _______ _________ diuretic)
  • What are the two drugs we would use for hyperaldosteronism? Are they selective or nonselective for aldosterone receptors?
  • Which of these has less AE? What other disease states are these meds used for?
A
  • hyperaldosteronism, Conn’s syndrome
  • muscle weakness, fatigue, HTN
  • aldosterone, potassium sparing diuretic
  • Spironolactone (nonselective for aldosterone receptors), Eplerenone (selective for aldosterone receptors)
  • eplerenone, also used for HTN and heart failure
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15
Q

-Mineralocorticoid deficiency (hypo_________) is related to _______ disease and is treated with ____________.

A

-hypoaldosteronism, Addison’s disease, fludrocortisone

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16
Q

Therapeutic concerns about Adrenal Steroids;

  • ______ effect on supporting tissues, bone density which can lead to what?
  • Glucocorticoids and mineralocorticoids may cause ___ due to Na+ retention
  • Can cause an increased susceptibility to _______
  • Drug toxicity can lead to ____ ______, phychosis
A
  • Catabolic effects which can lead to weakness and osteoporosis
  • HTN
  • infection
  • mood changes
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17
Q

MALE AND FEMALE HORMONES

A

MALE AND FEMALE HORMONES

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18
Q
  • Testes produce testosterone which is regulated by which hormones?
  • ___ and testosterone produce masculinizing effects
  • Testosterone in puberty increases size of _____ and _____
A
  • LH and FSH
  • DHT
  • muscle and bone
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19
Q
  • Androgen defeciency can be either primary or secondary. Primary involves ________ failure while secondary involves decreased _____.
  • An excess in women can lead to ______ and acne
A
  • testicular, GnRH

- hirsutism

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20
Q
  • If there is an androgen deficiency we must weight the benefits of treating symptoms vs the ___ risk associated.
  • There are no __ options due to hepatotoxicity.
A
  • CV

- PO

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21
Q
  • The reason we only use testosterone if its truly indicated is because its increased risks of __, stroke, or CV death.
  • Prolonged use could result in _____ toxicity
  • Large doses can suppress spermatogenesis resulting in ________.
A
  • MI
  • hepatic
  • infertility
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22
Q

AAS stands for what?
-Potential risks of anabolic-androgenic steroids includes derm, __, cancer, infection, endocrine, musculoskeletal, and psych issues.

A
  • Anabolic-adrogenic steroids

- CV

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23
Q

-Ovaries produce ______ and _________

A

-estrogen and progestins

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24
Q
  • The menstrual cycle is __ days and is regulated by an interaction between pituitary (__ and ___) and ovarian (______ and _______) hormones
  • Altering normal control between pituitary and ovarian hormones provides ________ control
A
  • 28 days
  • LH and FSH, estrogen and progesterone
  • contraceptive
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25
Q
  • What is the main use of estrogen and progesterone?
  • Which hormone functions to suppress FSH and LH surge?
  • What are the AE associated with taking estrogen and progesterone?
  • What are the rare but serious AE?
  • What is another option for contraception?
A
  • Contraception (COC)
  • estrogen (ethinyl estradoil)
  • increase BP, N/V, weight gain, depression
  • DVT and PE (more common if obese or immobile), stroke, MI
  • Long-acting intrauterine device (IUD)
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26
Q
  • Another estrogen and progesteron use includes post-menopausal ____.
  • This will cause a _______ in menopausal sx, an ________ in BMD, and a _______ fracture risk
  • Estrogen can be taken in a variety of ways and includes AE of _______, ___, breast tenderness, and vaginal bleeding
  • Progesterone can be take __ and by patch and includes AE of ______,___, weight gain, and irritability
  • The known risks of these products are ___, PE, gallbladder disease, and breast/endometrial cancer.
A
  • HRT (hormone replacement therapy)
  • decrease, increase, decrease
  • nausea, HA
  • PO, bloating, HA
  • DVT
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27
Q
  • BPH stands for what?
  • What are the 4 main drug classes used to treat BPH?
  • Alpha-adrenergic antagonists MOA is to relax smooth muscle in prostate and bladder neck. What is the AE?
  • 5a-reductase inhibitors MOA is to interfere with stimulatory effects of testosterone. This can result in what AE?
  • Anticholinergic agents includes what drug? MOA is to have an antispasmodic effect on smooth muscle; blocks Ach on smooth muscle. What are the AE?
  • B3-adrenergic agonists includes what drug? The MOA is to relax detrusor muscle to decrease voiding symptoms. What is the AE of this?
A
  • Benign prostatic hypertrophy
  • Alpha-adrenergic antagonists; 5a reductase inhibitors; anticholinergic agents; B3-adrenergic agonist
  • Hypotension
  • Hypotension
  • oxybutynin/Cant see, spit, pee, or poop
  • mirabegron (Myrbetriq)/ may increase BP
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28
Q

Gender transition can take _____ to achieve the full effect.
M to F would take what?
F to M would take what?
When looking at risks associated we have to look at both their ___ at birth and their ______ after transition.

A
  • years
  • estrogen w/ or w/out progesterone, spironolactone (T blockade), finasteride (T blockade)
  • testosteronoe
  • sex, gender
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29
Q

Therapeutic Concerns about Sex Hormones:

  • Monitor BP since these hormones promote ___ and ______ retention.
  • ______ abuse in athletes
A
  • Na+ and water

- androgen, be sure they know the risks associated

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30
Q

PARATHYROID DYSFUNCTION

A

PARATHYROID DYSFUNCTION

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31
Q
  • Hyperparathyroidism can be divided into ______ and ________.
  • Primary is due to parathyroid ______ (benign tumor), hyperplasia, or carcinoma. This is typically treated by ______.
  • Secondary can be caused by things such as CKD (chronic kidney disease) in which calcium levels become low which prompts increased levels of ___
  • Hyperparathyroidism is a common cause of _________
  • One way to treat this is through ____mimetics which interact with calcium-sensing receptor (CaSR) so it has greater affinity for calcium resulting in a decrease ____
  • What is the most common AE associated with calcimimetics?
  • What other drug class may be used for hyperparathyroidism? Why is it used?
A
  • primary and secondary
  • adenoma, surgery
  • PTH
  • hypercalcemia
  • calci, PTH
  • N/V
  • Bisphosphonates/ prevents calcium loss from bone
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32
Q
  • Hypoparathyroidism is often due to injury to ________.

- This will cause ____calcemia and we will treat it with what?

A
  • parathyroid glands

- hypocalcemia, will treat with Ca+ (1-3g/day) and vitamin D

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33
Q

HYPOTHYROIDISM

A

HYPOTHYROIDISM

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34
Q

-Hypothyroidism can be _______ or _________
-Primary is often from autoimmune destruction of the gland: ______
-Secondary hypothyroidism is from a reduction in secretion of ___ from pituitary or reduced ___ from hypothalamus
-Symptoms of hypothyroidism include _______, anemia, _______, weight gain, cold intolerance, menstrual irregularities, _____ weakness
What can also occur due to hypothyroidism?

A
  • primary or secondary
  • Hashimoto’s thyroiditis
  • TSH, TRH
  • bradycardia, lethargy, muscle
  • goiter
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35
Q
  • What is the most common drug used to treat hypothyroidism?
  • Its MOA is it is the synthetic version of _______ (__) that is converted to T3 which has its usual effects.
  • Is it a NTI?
  • Requires monitoring initially every - weeks, then every - months when stable.
  • Levothyroxine is typically ___ _______ unless overtreated. The signs of overtreatment can include _______, heat intolerance, tachycardia, diarrhea, nervousness, menstrual irregularities, increase basal metabolic rate
A
  • Levothyroxine
  • thyroxine (T4)
  • Yes
  • Requires monitoring every 4-8 weeks, then 6-12 months when stable
  • well tolerated, sweating
36
Q
  • It is ideal to take levothyroxine on a ______ ________ __-__ minutes before AM meal or - hours after PM meal and seperate from other medications (iron, calcium, magnesium, and aluminum containing products)
  • Chronic hypothyroidism has an increased risk of __ disease.
  • This is more likely in people with baseline risk factors such as angina, tachycardia, abnormal heartbeat
A
  • empty stomach, 30-60 minutes before AM, 3-4 hours after PM

- CV

37
Q

-What are the rarely used meds used for hypothyroidism?

A

-Thyroid USP, Liothyronine, Liotrix

38
Q

Long term overtreatment of hypothyroidism can lead to decreased ____________ and increased _______________
-Make sure to maintain the _______ effective dose, especially in postmenopausal women

A
  • bone density, risk of fractures

- least

39
Q

HYPERTHYROIDISM

A

HYPERTHYROIDISM

40
Q
  • A hyper active thyroid can lead to _______ disease which is identified by _______ eyes.
  • If graves disease gets severe it can cause a _______ storm which can be fatal. Thyroid storm can be identified by dehydration, ________, delirium, fever, etc.
A
  • Graves, bulging

- thyroid storm, tachycardia

41
Q

What are the three treatment options for hyperthyroidism?

A
  • Antithyroid meds (thioamides)- sometimes 1st line
  • Radioactive iodine- sometimes 1st line or after failing antithyroid meds
  • Thyoidectomy- surgery
42
Q
  • The two antithyroid meds include what two drugs?
  • They may be given as a monotherapy for ~1 year to induce remission (only effective in __%)
  • These are usually given if ____ hyperthyroidism, elderly, small goiter, or need to avoid radioactive iodine
  • The MOA of these drugs is they block formation of __ and __ by inhibiting oxidation of _____.
  • The common AE of these medications are rash, _______, arthralgia (refer to provider due to risk of more rare but serious polyarthritis)
  • The rare AE of these medications include ________ and ________.
  • Treatment can cause ___________
A
  • Methimazole and Propylthiouracil (PTU)
  • 50%
  • mild
  • T4 and T3, iodine
  • GI upset
  • agranulocytosis, hepatotoxicity
43
Q
  • What drug is typically preferred to treat hyperthyroidism unless in the first trimester of pregnancy? Why?
  • What is the black box warning for PTU (propylthiouracil)?
A
  • methimazole, only needs to be dosed 1x or 2x a day as opposed to PTU being 4x/day
  • hepatotoxicity
44
Q
  • Other treatments for hyperthyroidism include what?
  • What is unique about radioactive iodine?
  • Propranolol is used to treat _______ until thyroid levels normalize.
A
  • radioactive iodine, propranalol
  • causes destruction of thyoid which will result in hypothyroidism (requires lifelong treatment)
  • symptoms
45
Q

OSTEOPOROSIS

A

OSTEOPOROSIS

46
Q
  • Osteoporosis is a decreased ___ _____ occuring when formation of new bone doesn’t keep up with bone resorption.
  • With osteoporosis we have a decline in _______ function and increase in ________ function.
  • Who is most at risk for this?
A
  • bone density
  • osteoblast (formation), osteoclast (resorption)
  • women, especially postmenopausal
47
Q
  • Osteoporosis can be _______ and ________.
  • Primary osteoporosis is ______ (cause unknown) while secondary onset is relates to another _________ ________,_________, __________.
A
  • primary and secondary
  • idiopathic
  • medical condition, use of certain meds, or disease processes
48
Q

Bone mass peaks between the ages of __ and __, after this time, bone reabsorption begins to ______ bone formation.

A
  • 25 and 35

- exceed

49
Q
  • Osteoporosis can result in what fracture?
  • Osteoporis is generally “______”
  • Osteoporosis results in increased kyphosis of the _______ spine
A
  • compression (most common)
  • silent
  • thoracic
50
Q
  • Typically we will use medication for osteoporosis for men and women above the age of __ if: hip or vertebral fracture, osteoporosis, osteopenia
  • Also used for patients taking long-term _________ and men receiving androgen-deprivation therapy for ________ cancer and have high fracture risk
  • Antiresorptive therapy acts to block the _____________. This includes what drugs?
  • Anabolic therapy is used to increase _____________. This includes the drug ________.
A
  • 50
  • steroids, prostate
  • breakdown of bone; includes drugs bisphosphonates, denosumabs, SERMs, estrogen, and calcitonin
  • formation of bone, teriparatide
51
Q
  • What supplements will they take if they aren’t getting enough in their diets?
  • Generally speaking, the calcium dosage will be ____mg in younger patients and _____mg in older patients.
  • Generally speaking, the vitamin D dosage will be _____ international units daily for younger patients and _____ international units daily for older patients
A
  • Calcium and vitamin D
  • 1000, 1200
  • 600, 800
52
Q
  • Bisphosphonates end in what?
  • How often are these drugs taken?
  • Bisphosphonates are the ______ and most common treatment
  • Bisphosphonates MOA is to bind to a key enzyme to _______ natural bone turnover pathways which results in increased _______ apoptosis which decreases bone turnover.
  • Ultimately we are decreasing the number of osteoclasts resulting in less ____ breakdown.
A
  • end in -dronate
  • 1st line
  • inhibit, osteoclast
  • bone
53
Q
  • Bisphosphonates are taken with plain water __-__ minutes before any food or medication.
  • Food and meds can decrease absorption up to __%.
  • When are GI AE increased?
  • What are the contraindications for taking bisphosphonates?
A
  • 30-60 minutes
  • 90%
  • GI AE are increased when not upright
  • hypocalcemia, PO only if esophageal abnormalities, inability to remain upright for necessary time
54
Q

What is a rare but serious risk associated with bisphosphonates?

A

-Atypical femur fracture (usually benefit>risk)

55
Q

What is another rare but serious risk associated with bisphosphonates?
What population is this more common in?

A
  • osteonecrosis of jaw (ONJ)

- cancer patients

56
Q
  • What is the only drug associated with Anti-RANKL class?
  • Denosumab (Prolia) has evidence to decrease risk of ________, non-__________ and hip _________ in postmenopausal women
  • This drug is taken __________ every _ months in the provider’s office
  • Typically RANKL is excreted by ________, which binds to RANK on osteoclast surfaces and activates action to promote resorption.
  • Denosumab binds to ______ which ultimately inhibits bone resorption.
A
  • denosumab (Prolia)
  • vertebral, non-vertebral, hip fracture
  • subcutaneously every 6m
  • osteoblasts
  • RANKL
57
Q
  • Denosumab (Prolia) AE include ______, limb pain, derm reactions and less commonly ________ edema and hypocalcemia.
  • Denosumab, like biphosphonates, has the rare but serious risk of what?
  • What rare side effect is specific to denosumab?
A
  • arthralgia
  • peripheral
  • atypical femur fracture and ONJ
  • increased risk of infections because RANKL is also on T-cells
58
Q
  • Sclerostin Inhibitors drug is ______(Evenity).
  • This drug is two injections taken ____ a month for __ months.
  • This drug class MOA is to inhibit sclerostin which is a regulatory factor in bone metabolism which results in ___________
  • What is the most common AE associated?
  • The rare risks are hypocalcemia, ________ fractures, ___, increase risk of CV death if an event in the past year
A
  • Romosozumab
  • once a month for 12 months
  • increased bone formation
  • arthralgia
  • atypical, ONJ
59
Q

-What is teraparatide (Forteo)?
-This drug is taken _________ daily for 2 years.
-This drugs MOA is that it stimulates ________ function, increases GI calcium absorption, and increases renal tubular reabsorption of calcium. This all results in an increase in ___.
The AE related to this is transiest _______________ (within 4hrs of dose)

A
  • synthetic version of PTH
  • subcutaneously
  • osteoblast, BMD
  • orthostatic hypotension
60
Q

Therapeutic Concerns about Thyroid and Parathyroid drugs:

  • Excessive doses of drugs used to treat can produce symptoms of the _________ disorder.
  • Avoid overexertion in patients with decreased CO and hypotension caused by ___________
  • Excessive doses of calcium supplements for parathyroid dysfunction can alter CV function resulting in ________
  • Take advantage of weight bearing activities to stimulate __________ AND be aware when high impact activities should be avoided (_______)
A
  • opposite
  • hypothyroidism
  • arrhythmias
  • bone formation, osteoporosis
61
Q

DIABETES MELLITUS

A

DIABETES MELLITUS

62
Q

-Type I diabetes mellitus is characterized by selective _____ cell destruction, beta cells are important because they are what produces _______.
Type I is due to a severe or _______ insulin deficiency
-Type I is typically diagnosed before age __
-The cause of Type I ______, _______, and possibly a _____ trigger. These patients ________ insulin.

A
  • beta, insulin
  • absolute
  • 30
  • autoimmune, genetics, require
63
Q
  • Type II diabetes mellitus is characterized by insulin _________.
  • These patients have a ________ beta cell destruction that can progress to a more severe.
  • This is usually diagnosed in _______, but we are seeing a growing incidence in youth.
  • The cause for Type II is ________
  • This can be treated with just ____, non-_______ medications, or insulin
A
  • resistance
  • moderate
  • adults
  • multifaceted
  • diet, non-insulin meds,
64
Q

The symptoms of diabetes include:

  • ______
  • increased _________ and hunger
  • _______ dysfunction
  • sudden weight loss (type I)
  • ____ would healing
  • vaginal infections
  • ________ in hands or feet
  • increased thirst
  • blurry vision
A
  • fatigue
  • urination
  • poor
  • numbness/tingling
65
Q
  • What measurement is used to measure diabetes control?
  • What are the levels associated with:
    • diabetes
    • prediabetes
    • normal
A
  • A1C
  • diabetes=6.5 or above
  • prediabetes=5.7-6.4
  • normal=about 5
66
Q

Type II Diabetes Pathophys S71

  • Incretic hormones play a role in ____________ and _______
  • The kidney increases glucose ________ meaning we are getting rid of less through our urine.
A
  • insulin release and satiety

- reabsorption

67
Q

What are two other forms of diabetes mellitus?

A
  • gestational diabetes (diagnosed during pregnancy)

- LADA (type 1.5)- slower beta cell destruction

68
Q
  • People with Type II and Type I diabetes are at risk for ____glycemia. What level is considered ____glycemia?
  • Symptoms of hypoglycemia are _____, sweaty, nervous or upset.
  • ____-blockers may mask symptoms except for ______.
  • Hypoglycemia is treated with quick-acting ________
  • _________ is given in an emergency.
A
  • hypo, blood glucose <70
  • shaky
  • Beta-blockers, sweating
  • glucose
  • glucagon
69
Q

-What is the most common drug used for Type II diabetes? What class is this drug?
-The MOA isn’t fully known but it does inhibit production of _______, inhibits _________ absorption of glucose and increases ________ sensitivity in muscle and fat
-This drug has a ____ risk of hypoglycemia
The common AE of this drug is ______ (N/D/abdominal cramping)
-This drug also has a risk of vitamin ____ deficiency that usually results after long term use. A deficiency in this is often misdiagnosed as peripheral neuropathy (numbness/tingling in hands or feet)
-What is the boxed warning associated with this drug?

A
  • metformin (Glucophage), Biguanide
  • glucose, intestinal, insulin
  • low
  • diarrrhea, GI issues
  • B12
  • lactic acidosis
70
Q
  • Sulfonylureas MOA is to bind to sulfonylurea receptor in the ________ which results in depolarization triggering ______ release
  • This has AE of _________ (especially in elderly and renal dysfunction) and weight gain.
  • This is typically taken before _________; immediate release must be __ minutes before meal, if not taken correctly it can increase _________ risk
  • Some of these drugs are associated with the ______ List because of the hypoglycemia risk
A
  • pancreas, insulin
  • hypoglycemia
  • breakfast,30 minutes, hypoglycemia
  • Beers
71
Q
  • Thiazolidinedione (TZDs) MOA is increasing _______ sensitivity in muscle and fat by agonizing peroxisoe proliferator-activated receptor-gamma (PRARgamma) which ________ gene responses that influence glucose metabolism.
  • This is sometimes referred to as an “______________”
  • This class of drugs has a ____ hypoglycemia risk.
  • The AE of this class includes edema, long term increased risk of ____________ (especially in females)
A
  • insulin
  • insulin sensitizer
  • low
  • bone fracture
72
Q
  • DPP-4 Inhibitors end in what?
  • The MOA of this class of drugs is that it inhibits DPP-4 that typically breaks down incretin hormones (GLP-1 and GIP) which causes an ________ in insulin synthesis and release and also _________ glucagon secretion (which decreases hepatic glucose production)
  • This class has a ____ risk of hypoglycemia
  • These are generally well tolerated but there have been case reports of _______ occuring at any point during treatment
A
  • end in -gliptin
  • increase, decrease
  • arthralgia
73
Q
  • SGLT2 inhibitors end in what?
  • The MOA of this class is that they block glucose reabsorption in the ______ at SGLT2 in proximal renule tubules thus __________ urinary glucose excretion
  • Common AE associated with this class are ________-depletion related AE, genitourinary infections, renal insufficiency
  • This class also has the rare risk of euglycemic _______ __________
  • What drug increases the risk of bone fracture and lower limb amputations (boxed warning- watch for signs of foot infection!)
A
  • end in flozin
  • kidney, increasing
  • volume
  • diabetic ketoacidosis (DKA, more if dehydrated)
  • canagliflozin
74
Q
  • GLP1 rreceptor agonists are taken either ________ or PO either daily or _________.
  • This class of drugs is used as an analog of endogenous GLP1 (incretin hormone) to ________ insulin secretion in presence of elevated glucose, ________ glucagon secretion, _____ gastric emptying
  • What is the common AE associated with this drug class?
  • A good way to remember this is GLP (gut, liver, pancreas)
    • gut- gastric emptying
    • liver- decrease hepatic glucose production
    • pancreas- increase insulin secretion
A
  • injectable, daily or weekly
  • increase, decrease, slow
  • GI (N/D, bloating)
75
Q
  • Insulin is used in people with more ________ type II diabetes or in type I.
  • The MOA is that insulin binds to ______ ________ receptors in most tissues which triggers an increase expression of _____ receptor on muscle and fat cell surfaces to ______ glucose uptake; inhibits production of glucose
  • Common AE associated with this are _________! and weight gain
  • This is the only FDA approved treatment for _____
  • The two types of insulin are ____ and _____
  • Insulin is delivered as a _________ injection
A
  • severe
  • tyrosine kinase, GLUT4, increase
  • hypoglycemia
  • T1DM
  • basal and bolus
  • subcutaneous
76
Q

Why are multiple insulins used?

A
  • We are trying to mimic what the body is actually doing.

- Some work all day long as our base and some work as the peak insulin like we have after we eat.

77
Q

Basal insulin think “____” meaning what?

This is generally though of as a __ hour insulin.

A
  • Base, always working in the background.

- 24

78
Q

-Bolus insulin think of “____” of food.
-There are two types, ____ or _______
-Rapid has an onset of around __ minutes, and a duration of - hours.
-Regular has an onset of around __ minutes, and has a duration lasting around - hours.
-Bolus insulin is typically given __________
-This can also be given to correct _________
Which is used more commonly?

A
  • bowl
  • rapid or regular
  • 10-30 minutes, 3-5 hours
  • ~30 minutes, 4-12 hours
  • before a meal
  • hyperglycemia
  • Rapid bolus insulin
79
Q
  • Other insulin injections includes intermediate (___).
  • This is injected - times daily
  • Mixed insulin is also an example and is a combination of an ___________ with a rapid or regular acting
  • This is usually injected before a meal
  • This is given as a _, with the first number being the longer-acting and the second number being the shorter-acting (Ex: 70% intermediate and 30% regular acting / 70/30)
A
  • NPH
  • 1-2
  • intermediate
  • %`
80
Q
  • What are three other examples of insulin?
  • U-500 is ____ concentrated
  • U-500 is used for both ______ and _____ purposes
  • Inhaled regular insulin is the only __________ product
  • The most common AE associated with inhaled insulin is what?
A
  • Concentrated insulin, U-500, Inhaled regular insulin
  • ultra (hypoglycemia)
  • basal and bolus
  • non-injected
81
Q

There are 3 miscellaneous drugs for diabetes, what are they?

A

-Pramlintide (Symlin), Alpha-glucosidase inhibitors, and Meglitidines

82
Q

The first line treatment for diabetes is ________, and our 2nd line is ______________.

A

-metformin, patient specific

83
Q

S93 OVERVIEW

A

S93 OVERVIEW

84
Q

Therapeutic considerations for DM?

A

Does the patient have diabetic associated comorbities?

  • diabetic retinopathy
  • diabetic nephropathy
  • diabetic neuropathy
  • peripheral vascular disease
  • CV disease
Beneficial effects of exercise?
-increased carbohydrate metabolism (which lowers blood glucose)
-body weight
-increased HDL
-decreased triglycerides
-decreased BP
=decreased stress and tension

Monitor blood glucose level

  • below 100mg/dL: eat a snack before activity
  • > 300mg/dL NO PHYSICAL THERAPY
  • monitor 6-12 hours after exercise
  • know the symptoms of hypo and hyperglycemia
85
Q

What is the leading cause of blindness in adults?

A

diabetes

Pharmacology Exam 3 (10 decks)

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