Pharmacology Test 3 Flashcards

1
Q

Cause of hypopituitarism

A

deficiency in any hormones

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2
Q

Anterior Pituitary hypopituitarism

A

deficiency in GH = dwarfism

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3
Q

Tx for dwarfism

A

replace GH with synthetic form somatropin

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4
Q

MOA of somatropin

A

increase bone, skeletal and organ growth, RBC mass, transport of water, electrolytes and fluid

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5
Q

AE of somatropin

A
  1. fluid retention/edema 2. muscle and joint pain
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6
Q

Posterior pituitary hypopituitarism

A

decreased ADH = Diabetes Insipidus

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7
Q

what is ADH also called?

A

Vasopressin

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8
Q

What does ADH normally do?

A

decrease water excretion by increasing urine concentration

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9
Q

Tx of Diabetes Insipidus

A

Desmopressin (DDAVP)

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10
Q

what is desmopressin?

A

synthetic form of Vasopressin (ADH)

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11
Q

administration route for Desmopressin?

A

1). subcut. 2). PO 3). intranasal

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12
Q

MOA of desmopressin

A

increase water reabsorption @ kidney by increasing aquaporin 2 channel permeability

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13
Q

other indications for Desmopressin?

A

nocturia

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14
Q

Desmopressin AE

A

1). dry mouth 2). hyponatremia

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15
Q

What hormones does the Anterior Pituitary normally secrete?

A

1). GH 2). LH and FSH 3). TSH 4). ACTH 5). Pr

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16
Q

What hormones do the posterior pituitary normally secrete?

A

1). oxytocin 2). ADH

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17
Q

Hyperpituitarism

A

excessive production of hormones from pituitary (typically anterior)

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18
Q

Hyperpituitarism results in which disease(s)?

A

1). Gigantism 2). Acromegaly

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19
Q

T/F: Gigantism occurs in children not adults

A

TRUE

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20
Q

what is gigantism in adults called?

A

Acromegaly

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21
Q

What causes acromegaly?

A

excessive GH

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22
Q

physiologic effects of acromegaly

A

1). affects bone and soft tissue growth 2). hyperglycemia 3). cardiomeglia (increase risk for HTN and arrhythmias)

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23
Q

T/F: individuals with acromegaly have an increased risk for HTN and arrhythmias?

A

TRUE

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24
Q

TX for acromegaly

A

1). surgery is 1st line - typically remove a tumor that is the cause 2). medications follow surgery

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25
Q

Medications used in Tx of acromegaly

A

1). somatostatin analogue 2). GH receptor anatagonist

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26
Q

Therapeutic Concerns with Hypopituitarism Tx

A

1). easy to over treat 2). watch for AE of increased hormone levels 3). communicate with endocrinologist any changes 4). decreased GH = decreased BMD

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27
Q

T/F: there is an increased risk of bone fractures in individuals with dwarfism?

A

TRUE

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28
Q

what is slipped capital femoral epiphyses and who is at greater risk for it?

A

essentially a hip condition that causes hip dislocations. Hypopituitarism has increased risk for it

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29
Q

Suffix for synthetic GHs

A

-trope/tropin

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30
Q

Various brand names for synthetic GHs

A

1). Humatrope 2). Genotropin 3). Norditropin

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31
Q

Hyperthyroidism disease

A

Graves disease

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32
Q

S/sx of Graves disease

A

goiter, expothalmos, increased metabolism, nervousness, weight loss despite increased appetite

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33
Q

T/F: graves disease can result in thyroid storm

A

TRUE

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34
Q

what is thyroid storm

A

fatal symptoms of dehydration, tachycardia, delirium and fever

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35
Q

TX for graves disease

A

1). anti-thyroid meds 2). Radioactive Iodine 3). Thyroidectomy

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36
Q

Antithyroid meds

A

1). Methimazole 2). Propylthirouracil (PTU)

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37
Q

Which antithryoid med is the preferred option?

A

Methimazole - smaller dose needed and no black box warning

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38
Q

PTU black box warning

A

heptatoxicity

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39
Q

MOA of antithyroid meds

A

blocks formation of T4 to T3 by inhibiting iodine oxidation

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40
Q

When are antithyroid meds used?

A

1). mild cases 2). older 3). avoid radioactive iodine

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41
Q

AE of antithyroid meds

A

1). rash 2). GI upset 3). arthralgia

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42
Q

how often is methimazole dosed?

A

one or 2x daily

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43
Q

how often is propylthirouracil dosed?

A

initially dosed 4x/day

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44
Q

T/F: methimazole can cause birth defects in 1st trimester of pregnancy?

A

TRUE

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45
Q

When is PTU preferred over methimazole

A

1). during 1st trimester of pregnancy 2). while breastfeeding

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46
Q

Rare AE of antithyroid meds

A

1). agrunulocytosis 2). heptotoxicity

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47
Q

s/sxs of agrunlocytosis

A

1). fever 2). sore throat 3). mouth ulcers

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48
Q

what is radioactive iodine?

A

radioactive destruction of thyroid

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49
Q

AE for radioactive iodine?

A

hypothyroidism (will require life long treatment)

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50
Q

What other med can be used in trx of hyperthyroidism?

A

Propanolol >> used to trx symptoms

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51
Q

Types of Hypothyroidism

A

1). primary 2). secondary

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52
Q

What is primary hypothryoidism?

A

autoimmune destruction of thyroid gland

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53
Q

What is secondary hypothryoidism?

A

1). reduced secretion of TRH (hypothalamus) 2). reduced secretion of TSH (pituitary)

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54
Q

S/Sxs of hypothyroidism (8)

A

1). bradycardia 2). anemia 3). lethargy 4). wt gain 5). cold intolerance 6). menstrual irregularities 7). general muscle weakness 8). Goiter is possible

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55
Q

Tx for hypothyroidism

A

Levothyroxine (Synthroid)

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56
Q

What is levothyroxine

A

synthetic T4 > it is the DOC for hypothyroidism b/c it is cheap

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57
Q

MOA of Levothyroxine

A

synthetic T4 is converted to T3

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58
Q

T/F: Levothyroxine is an NTI drug?

A

TRUE >> requires monitoring and dose adjustments

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59
Q

AE of Levothyroxine (Synthroid)?

A

overall well tolerated unless overtreated: 1). sweating 2). heat intolerance 3). tachycardia 4). diarrhea 5). nervousness 6). menstrual irregularities 7). increased BMR

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60
Q

Special considerations for Levothyroxine (2)

A

1). take on empty stomach 2). don’t take along with Fe, Ca, Mg, Al containing products

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61
Q

T/F: chronic hypothyroidism can increase your risk of CV disease?

A

TRUE

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62
Q

Types of hyperparathyroidism

A

1). primary 2). seconday

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63
Q

Cause of primary hyperparathyroidism

A

1). parathyroid adenoma 2). hyperplasia or carcinoma

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64
Q

Causes of secondary hyperparathyroidism

A

underlying conditions such as chronic kidney disease > Ca lvls become low triggering release of PTH

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65
Q

TX options of primary hyperparathyroidism

A

1). surgery 2). medications

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66
Q

Medications used to trx hyperparathyroidism

A

1). Calcimimetics 2). Bisphosphonates

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67
Q

MOA of calcimimetics

A

competitive antagonist of Ca receptors >> decreases PTH secretion

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68
Q

AE of calcimimetics

A

1). most common: N/V 2). monitor for hypocalcemia

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69
Q

TX options for secondary hyperparathyroidism

A

treat underlying condition

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70
Q

Causes of Hypoparathyroidism

A

All result in hypocalcemia1). injury during surgery 2). autoimmune disease 3). congenital defect

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71
Q

TX for hypoparathyoidism

A

1). Calcium 1-3 grams/day 2). Vitamin D

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72
Q

Over treatment of hypoparathyroidism can cause _________

A

1). hypercalcemia 2). hypercalciuria >> leading to nephrolithiasis

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73
Q

The adrenal glands secrete from what regions?

A

1). Cortex 2). medulla

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74
Q

What is secreted from the medulla of the adrenal glands?

A

1). NE 2). epinephrine

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75
Q

What is secreted from the cortex of the adrenal glands?

A

1). mineralocorticoids 2). glucorticooids 3). some sex steroid

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76
Q

What is an example of a mineralocorticoid?

A

Aldosterone

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77
Q

What do mineralocorticoids do?

A

effects electrolyte/water balance

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78
Q

What do glucocorticoids do?

A

effect carb/fat metabolism

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79
Q

What are some examples of glucocorticoids?

A

1). hydrocortisone 2). cortisol

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80
Q

A deficiency of mineralocorticoids is called _____

A

Hypoaldosteronism

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81
Q

What disease is primarily associated with hypoaldosteronism?

A

Addison’s Disease

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82
Q

What causes Addison’s disease?

A

1). general adrenocoticoid insufficiency >> autoimmune system destroys adrenal cortex (main cause)2). defective aldosterone producing enzyme (rare)

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83
Q

TX for Addison’s disease

A

Fludrocortisone (synthetic aldosterone)

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84
Q

What is excessive production of aldosterone called?

A

hyperaldosteronism

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85
Q

causes of Hyperaldosteronism?

A

1). Adrenal tumor (Conn’s syndrome) 2). Adrenal hyperplasia

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86
Q

Tx for Conn’s syndrome

A

Surgery

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87
Q

Tx for adrenal hyperplasia

A

1). Spironolactone 2). Eplerenone

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88
Q

why are diuretics used to treat hyperaldosteronism

A

they are aldosterone receptor antagonists

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89
Q

which diuretic tx for hyperaldosteronism have less AE?

A

Eplerenon (selective for aldosterone receptors, Spironolactone is nonselective)

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90
Q

S/Sxs of Hyperaldosteronism (7)

A

1). muscle weakness 2). fatigue 3). paresthesias 4). headache 5). polydipsia 6). nocturnal polyuria 7). HTN

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91
Q

What is excessive production of glucocorticoids called?

A

1). Cushing’s syndrome

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92
Q

What is Cushing’s syndrome due to?

A

Hypercortisolism

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93
Q

what can lead to hypercortisolism?

A

1). take too much 2). make too much 3). tumor on pancreas/thyroid telling adrenal gland to make too much

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94
Q

TX options for Cushing’s syndrome?

A

1). surgery (1st line)2). meds surrounding surgery

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95
Q

Medications used as adjunct TX in Cushing’s syndrome?

A

1). Steroidogenesis inhibitors 2). Glucocorticoid-antagonist

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96
Q

Glucocortioid deficiency types

A

1). primary adrenal insufficiency 2). secondary adrenal insufficiency

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97
Q

What is primary adrenal insufficiency?

A

Addison’s Disease >> autoimmune destruction of adrenal cortex

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98
Q

Primary adrenal insufficiency results in what ______?

A

deficiency of both mineralcorticoids and glucocorticoids

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99
Q

What causes secondary adrenal insufficiency?

A

Too much exogenous corticosteroid admin >> suppresses hypothalamic-pituitary-adrenal axis >> decreased ACTH release

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100
Q

What does secondary adrenal insufficiency tell us about steroid dosages?

A

It is important to taper off of steroids

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101
Q

TX for primary and secondary adrenal insufficiency

A

1). Both = replace glucocorticoids (hydrocortisone, prednisone, cortisone) 2). primary = fludrocortisone as well (replace aldosterone)

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102
Q

Short term AE of primary/secondary adrenal insufficiency TX

A

1). increased blood glucose 2). mood changes 3). fluid retention

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103
Q

Long term AE of primary/secondary adrenal insufficiency TX

A

1). osteoporosis (increased fracture risk) 2). thin skin 3). muscle wasting 4). poor wound healing 5). Adrenal suppresion 6). Cushing’s syndrome 7). increased risk of infection

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104
Q

T/F: exercise and increased stress will require higher med dosing for glucocortioid deficiencies?

A

TRUE

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105
Q

Therapeutic Concerns of Adrenal Steroids

A

1). lots of pts w/dif disorder use them (RA, lupus, bursitis, etc.)2). catabolic effect on supporting tissue >> fall risk ! do not overload 3). can cause HTN 4). immunosupressive = increase infection risk 5). drug toxicity >> mood changes, psychoses

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106
Q

Stimulation cascade for sex hormones

A

Hypothalamus releases GnRH –> Ant. pituitary gland releases LH and FSH –> stimulates gonads to release sex hormones

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107
Q

Effects of testosterone (6)

A

1). masculinizing effects 2). development of male genitals in embryo 3). increase muscle/bone size 4). stimulates synthesis of clotting factors in liver 5). stimulates production of erythropietin in kidneys 6). regulates LH production from ant pituitary

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108
Q

Types of testosterone deficiency

A

1). primary 2). secondary

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109
Q

what causes primary testosterone deficiency?

A

testicular failure

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110
Q

what cause secondary testosterone deficiency?

A

decreased GnRh

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111
Q

S/Sxs of testosterone deficiency? (8)

A

1). delay in puberty 2). low energy 3). decreased libido 4). ED 5). decreased pubic hair6). anemia 7). osteoporosis 8). muscle atrophy

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112
Q

TX for testosterone deficiency

A

exogenous admin of testosterone (IM or topical)

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113
Q

T/F: perfectly safe to administer testosterone PO?

A

FALSE >> risk of heptatoxicity

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114
Q

IM admin of testosterone considerations

A

1). variable symptom relief (cycle between high to low)2). mood changes 3). can cause hepatic adenomas

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115
Q

topical admin of testosterone considerations

A

keep it covered so no contact

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116
Q

Risks/AE with testosterone administration

A

1). increased risk of MI, stroke, CV death 2). hepatotoxicity (long-term) 3). large doses may cause infertility

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117
Q

AE of testosterone in Athletic populations (11)

A

1). acne 2). MI, CV death, VTE3). PE 4). Cancer (testicular or prostate) 5). injection site infections 6). feminization 7). menstrual irregularities (in women) 8). tendon/ligament rupture 9). insomnia 10) mood disorder 11). aggressiveness

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118
Q

Therapeutic concerns with testosterone TX

A

1). monitor BP 2). athletic use of androgens

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119
Q

Role of estrogen (4)

A

1). develops female genitals in embryo 2). causes puberty and female specific changes 3). deposition of subcutaneous fat stores 4). widens pelvic girdle

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120
Q

What is the menstrual cycle?

A

28 day cycle. regulated by interaction between pituitary and ovarian hormones

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121
Q

Positive feedback loop in Menstrual cycle

A

1). low estrogen levels increase LH release 2). LH release further increases estrogen

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122
Q

Negative feedback loop in Menstrual cycle

A

LH and FSH are inhibited during second half of cycle from high estrogen and progesterone levels

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123
Q

What does the altering normal control between pituitary and ovarian hormones provide?

A

contraceptive control

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124
Q

Estrogen and Progesterone Medical uses

A

1). Contraceptives 2). Post-menopausal hormone replacement therapy (HRT)

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125
Q

Types of Contraceptives

A

1). Combination Oral contraceptive (COC)2). Long-acting intrauterine device (IUD)

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126
Q

common COC AEs (6)

A

1). increased BO2). N/V 3). weight gain 4). acne 5). depression 6). topical rxn

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127
Q

Rare COC AEs (3)

A

1). DVT/PE 2). Stroke 3). MI

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128
Q

T/F: the risk for MI from contraceptive use increases after 35 years of age?

A

TRUE, also if uncontrolled smoker and diabetic

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129
Q

T/F: AE of N/V from COC generally improve after 2-3 cycles?

A

TRUE

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130
Q

Complications from IUDs?

A

pelvic inflammatory disease

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131
Q

Goals of HRT?

A

1). decrease menopausal symptoms 2). increase BMD 3). decrease fracture risk

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132
Q

TX for HRT

A

1). estrogen only (if no uterus) 2). estrogen + progestogens

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133
Q

Route of admin for estrogen (4)

A

1). PO 2). transdermal patch/spray 3). topical gel/solution 4). vaginal ring/cream

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134
Q

Estrogen AE (4)

A

1). nausea 2). HA 3). breast tenderness 4). vaginal bleeding

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135
Q

Progestogens admin

A

1). PO 2). patch

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136
Q

Progestogens AE (4)

A

1). bloating 2). headache 3). weight gain 4). irritability

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137
Q

Known risks with HRT TXs

A

1). DVT 2). PE 3). gallbladder disease 4). breast cancer (with combo) 5). endometrial cancer (with estrogen alone)

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138
Q

General Men’s health disorder

A

Benign prostatic hypertrophy (BPH)

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139
Q

TX options for BPH

A

1). Alpha-adrenergic antagonists 2). 5a-reductase inhibitors 3). anticholinergic agents 4). B3-adrenergic agonsit

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140
Q

Alpha-adrenergic antagonist used for BPH

A

Tamsulosin

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141
Q

MOA of tamsulosin

A

relax smooth muscle in prostate and bladder neck

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142
Q

5a-reductase inhibitor used for BPH

A

finasteride

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143
Q

MOA of finasteride

A

interfere with stimulatory effects of testosterone

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144
Q

AE of tamsulosin and finasteride

A

Hypotension

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145
Q

Anticholinergic agents used to treat BPH

A

oxybutynin

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146
Q

MOA of oxybutynin

A

antispasmodic effect on smooth muscle >> blocks acetylcholine on smooth muscle

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147
Q

AE of oxybutynin

A

ABCDs

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148
Q

B3-adrenergic agonist used to treat BPH

A

mirabegron (Myrbetriq)

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149
Q

MOA of mirabegron (Myrbetriq)

A

relaxes detrusor muscle to decrease voiding symptoms

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150
Q

AE of mirabegron (Myrbetriq)

A

may increase BP

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151
Q

Other indication for mirabegron (Myrbetriq)

A

OAB

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152
Q

Male to Female gender transition meds

A

1). Estrogen and Progesterone 2). Spironolactone (testosterone blocker) 3). Finasteride (testosterone blocker)

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153
Q

Female to Male gender transition meds

A

testosterone

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154
Q

T/F: sex at birth still defines some risks for individuals undergoing gender transition?

A

TRUE

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155
Q

What causes Osteoporosis?

A

decreased osteoblast function

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156
Q

T/F: osteoporosis is more common in post-menopausal women?

A

TRUE

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157
Q

Types of Osteoporosis

A

1). primary 2). seconday

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158
Q

What causes primary osteoporosis?

A

1). idiopathic (unknown 2). increased age

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159
Q

what causes secondary osteoporosis?

A

1). underlying diseases2). medications

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160
Q

Clinical manifestations for osteoporosis

A

1). sudden back pain (compression fx of vertebral body) 2). increased kyphosis of T spine 3). decreased height

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161
Q

Risk factors for developing osteoporosis (9)

A

1). decreased bone mass after 35 years old 2). female hormone changes 3). genetics 4). Caucasian 5). low physical activity 6). tobacco/alcohol use 7). medications 8). depression 9). diet/nutrition deficits

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162
Q

TX for osteoporosis?

A

1). calcium and Vitamin D2). Bisphosphonates (most common tx) 3). Denosumab 4). Sclerostin Inhibitor 5). Teriparatide

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163
Q

AEs of calcium?

A

Consitipation

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164
Q

suffix for Bisphosphonates

A

-dronate

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165
Q

MOA of Bisphosphonates

A

binds key enzyme to inhibit natural bone turnover pathway >> increases osteoclast apoptosis which decreases bone turnover

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166
Q

Bisphosphoantes considerations

A

1). stay upright 2). take w/water 30-60 minutes before food

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167
Q

Bisphosphonates common AE

A

GI issues (increased if not upright)

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168
Q

Rare Bisphosphoantes AE

A

1). atypical femur fx 2). osteonecrosis of jaw (ONJ) - from IV use or long-term trx

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169
Q

Bisphosphonates contraindications

A

1). hypocalcemia 2). esophageal abnormalities 3). inability to remain upright

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170
Q

what type of drug is denosumab (Prolia)

A

Anti-RANKL

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171
Q

denosumab (Prolia) AEs

A

same as bisphospnates

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172
Q

denosumab (Prolia) considerations

A

administered in provider’s office

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173
Q

Sclerostin inhibitors MOA

A

increase bone formation

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174
Q

Sclerostin inhibitors common AE

A

arthraligia

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175
Q

Sclerostin inhibitors rare AEs

A

1). hypocalcemia (atypical) 2). femur fx3). ONJ 4). increased risk of MI, stroke, or CV death

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176
Q

Synthetic PTH MOA

A

1). stimulate osteoblast function 2). increases GI calcium absorption 3). increase renal calcium absorption all this increases BMD

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177
Q

Synthetic PTH AEs

A

transient OH within 4 hours of dose

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178
Q

Drug name for Synthetic PTH

A

Teriparatide (Forteo)

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179
Q

Osteoporosis medication considerations

A

also given to pts with longterm steroid use and men receiving androgen deprivation therapy

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180
Q

Osteoporosis meds Therapeutic Concerns

A

1). excessive doses of Ca supplements can cause arrhythmias 2). utilize weight bearing activities to promote bone growth 3). avoid high impact activities for pts with osteroporosis

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181
Q

Types of Diabetes

A

Type 1Type 2

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182
Q

Pathophysiology T1DM

A

selective beta cell destruction in the pancreas >> can’t produce insulin

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183
Q

what causes T1DM?

A

Autoimmune dysfunction, genetic, viral infections

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184
Q

What is T2DM?

A

1). moderate beta cell destruction that can become more severe 2). Insulin resistance

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185
Q

Which type of diabetes is more prevalent in youth?

A

T1DM

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186
Q

what is LADA?

A

latent autoimmune diabetes in adults (Type 1.5 >> requires insulin)

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187
Q

What type of diabetes can only be treated with insulin?

A

T1DM

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188
Q

Pathophysiology of T2DM?

A

Egregious Eleven

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189
Q

what is the overall result of the egregious eleven?

A

Hyperglycemia

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190
Q

TX options for T2DM?

A

1). diet 2). exercise 3). non-insulin meds 4). insulin

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191
Q

what are non-insulin meds that treat T2DM also called?

A

Antihyperglycemic Drug

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192
Q

List the classes of Antihyperglycemic Drugs (6)

A

1). Biguanide 2). Sulfonylureas 3). Thiazolidinedione (TZDs) 4). DPP-4 inhibitor 5). SGLT2 Inhibitor 6). GLP1 Receptor agonist

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193
Q

MOA for Biguanide

A

unclear, but it stops: 1). production of glucose 2). intestinal absorption of glucose also 3). increases insulin sensitivity in muscle and fat

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194
Q

AE of Biguanide

A

1). GI (N/V/cramps) 2). Vitamin B12 deficiency

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195
Q

how is vitamin B12 deficiency from Biguanide important?

A

it can be misdiagnosed as peripheral neuropathy

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196
Q

Biguanide boxed warnings

A

lactic acidosis

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197
Q

Sulfonylureas MOA

A

increase insulin release

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198
Q

Sulfonylureas AE

A

1). hypoglycemia 2). weight gain

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199
Q

AE from Sulfonylureas are increased in which populations?

A

1). elderly 2). individuals with renal dysfunction

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200
Q

T/F: some Sulfonylureas are on the Beer’s List?

A

TRUE

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201
Q

Thiazolidinedione (TZDs) MOA

A

increase insulin sensitivity in muscle and fat

202
Q

Thiazolidinedione (TZDs) AE

A

1). edema 2). long-term increased risk of bone fractures

203
Q

Thiazolidinedione (TZDs) boxed warnings

A

HF

204
Q

What does DPP-4 inhibitor stand for?

A

Dipeptidyl peptidase 4 inhibitor

205
Q

DPP-4 inhibitor MOA

A

inhibit breakdown of incretin => 1). increases insulin sensitivity and release 2). decreases glucagon secretion 3). decreases liver glucose production

206
Q

DPP-4 inhibitor AE

A

very well tolerated

207
Q

rare AE of DPP-4 inhibitor

A

1). arthraliga 2). increased risk of HF

208
Q

SGLT-2 Inhibitor MOA

A

blocks glucose reabsorption in kidneys => increases urinary glucose excretion

209
Q

SGLT2 inhibitor AE

A

1). volume depletion related 2). genitourinary infections 3). renal insufficiency

210
Q

Rare SGLT2 inhibitors AE

A

euglycemic diabetic ketoacidosis

211
Q

SGLT2 inhibitor boxed warnings

A

increased risk of bone fractures and lower limb amputations

212
Q

GLP1 receptor agonist MOA

A

1). increase insulin secretion 2). decrease glucagon secretion 3). decrease gastric emptying (incretin hormones)

213
Q

GLP1 receptor agonist AE

A

GI (nausea, bloating, diarrhea)

214
Q

Sulfonylureas suffix

A

-ide

215
Q

DPP-4 inhibitor suffix

A

-gliptin

216
Q

SGLT2 inhibitor suffix

A

-flozin

217
Q

GLP1 receptor agonist suffix

A

-tide

218
Q

What are the symptoms of Diabetes? (10)

A

1). tired 2). always hungry 3). frequent urination 4). always thirsty 5). blurry vision 6). numb/tingling hands or feet 7). sexual problems 8). sudden weight loss 9). wounds that won’t heal 10). vaginal infections

219
Q

MOA of Insulin

A

1). increase glucose uptake 2). inhibit glucose production

220
Q

Types of Insulin

A

1). basal 2). bolus 3). Other

221
Q

What are the “Other” types of insulin?

A

1). intermediate (NPH) 2). mixed 3). concentrated 4). U-500 5). inhaled regular insulin (afrezza)

222
Q

how often is basal insulin injected?

A

normally only once daily, sometimes twice

223
Q

types of bolus insulin

A

1). rapid 2). regular

224
Q

onset for rapid bolus insulin

A

10-30 minlasts for 3-5 hours

225
Q

onset for regular bolus insulin

A

~30 minlasts 4-12 hours

226
Q

what type of insulin can be given as correction insulin?

A

rapid bolus insulin

227
Q

Therapeutic considerations for DM?

A

1). exercise = good 2). monitor blood glucose 3). avoid heat/massage @ injection site 4). need good footwear 5). exercise after meals

228
Q

if blood glucose is <100 mg/dL then _______

A

eat a snak

229
Q

if blood glucose is >300 mg/dL then _______-

A

No PT

230
Q

what are the signs of hypoglycemia?

A

1). shaky 2). sweaty 3). dizzy 4). confusion 5). difficulty speaking 6). weak/tired 7). HA 8). nervous/upset

231
Q

_______ masks all the symptoms of hypoglycemia except ______

A

1). Beta blockers 2). sweating

232
Q

Which Antihyperglycemic Drugs reduce the risk for hypoglycemia?

A

1). Biguanide 2). Thiazolidinedione (TZDs) 3). DPP-4 inhibitors

233
Q

what is ADHD?

A

a series of behavioral disorders

234
Q

what are the subtypes of ADHD?

A

1). inattentive 2). hyperactive-impulsive 3). combined

235
Q

what is the etiology of ADHD?

A

multi-factorial: environmental, genetic and biological factors

236
Q

what increases the risk of developing ADHD?

A

pre/perinatal expsoure to cigarettes/alcohol

237
Q

TX options of ADHD?

A

1). stimulants 2). Atomoxetine (Strattera) 3). Other

238
Q

How do stimulants work?

A

block NE and dopamine reuptake

239
Q

boxed warnings with stimulants?

A

1). increase CV risk 2). abuse potential

240
Q

common AE for stimulants?

A

1). decreased appetite/weight loss 2). stomach ache 3). insomnia 4). HA 5). irritability/jitteriness

241
Q

Rare/uncommon AE for stimulants?

A

1). dysphoria 2). “spacey”/zombie-like state 3). tics/abnormal movements 4). HTN, HR fluctuations 5). hallucinations 6). discolorations from patch

242
Q

Atomoxetine (strattera) MOA

A

selective NE re-uptake inhibitor (SNRI)

243
Q

Pro/Con of Atomoxetine (Strattera)?

A

less effective than stimulants but also less abuse potential

244
Q

AE of Atomoxetine (Strattera)

A

more fatigue, sedation and dizziness than stimulants

245
Q

boxed warnings for Atomoxetine (Strattera)

A

increased risk of suicide

246
Q

Other ADHD drugs

A

1). alpha-2 adrenergic agonists 2). Bupropion 3). Lithium 4). Anti-psychotics

247
Q

What is epilespy?

A

a chronic condition characterized by recurrent seizures

248
Q

what is a seizure?

A

a finite event resulting from excessive discharge of cerebral neurons causing transient impairments or loss of consciousness

249
Q

what can cause a seizure?

A

1). too little GABA 2). too much Glutamate 3). CNS inflammation

250
Q

what is GABA?

A

main CNS inhibitory neurotransmitter > normally inhibits depolarization

251
Q

what is Glutamate?

A

an excitatory neurotransmitter

252
Q

What are the types of seizures?

A

1). partial 2). generalized

253
Q

what occurs in a partial seizure?

A

one cerebral hemisphere with no loss of consciousness

254
Q

what is a a generalized seizure?

A

effects both hemispheres and results in loss of consciousness

255
Q

Types of generalized seizures?

A

1). Tonic/Clonic 2). only Tonic 3). only Clonic

256
Q

What is the most common type of generalized seizure?

A

Tonic/Clonic

257
Q

how long does an only tonic seizure last?

A

a few seconds

258
Q

how long does an only clonic seizure last?

A

a few seconds

259
Q

What occurs during a tonic/clonic seizure?

A

1). rigid extensor spasm 1st 10-30 seconds 2). rhythmic flexor spasm 2-4 minutes

260
Q

during the rigid extensor spasm what can happen?

A

stopped respiration, poop, pee and salivate

261
Q

during the rhythmic flexor spasm what can happen?

A

continued loss of consciousness >> alertness will slowly return after

262
Q

what are the two types of epilepsy?

A

1). Primary 2). Seconday

263
Q

What causes primary epilepsy?

A

it is idiopathic and accounts of 50% of cases

264
Q

what causes secondary epilepsy?

A

1). in children: injury @ birth or metabolic disease 2). in adults: TBI

265
Q

TX for epilepsy

A

excitatory or inhibitory:1). antiepileptic drug (AED) 2). antiseizure drug (SD) 3). anti-convulsant

266
Q

drug TX for epilepsy depends on ____

A

1). patient specific factors 2). type of seizure 3). response to previous meds

267
Q

goals for epilepsy TX

A

1). eliminate seizures 2). experience no AEs 3). improve QOL

268
Q

AE of Epileptic drugs

A

1). rash (Steven Johnson’s Syndrome)2). neurotoxicity 3). hypothyroidism

269
Q

At risk populations for Epilepsy

A

1). Women 2). pregnant women 3). children 4). elderly

270
Q

Therapeutic considerations for Epilepsy

A

1). some drugs are NTI 2). watch for sedation, dizziness and ataxia 3). rashes 4). bone marrow depression 5). vitamin K deficiency 6). ask about seizure activity 7). know how to respond appropriately to a seizure

271
Q

therapeutic considerations for women and AEDs

A

1). decreased ovarian function 2). infertility 3). PCOD 4). weight gain

272
Q

what is PCOD?

A

polycystic ovarian disease

273
Q

what is multiple sclerosis (MS)?

A

a chronic, progressive disease of CNS - axonal damage and demyelination

274
Q

what is the etiology of MS

A
  1. autoimmune process
  2. genetic predisposition
  3. environmental exposure
275
Q

what are the clinical symptoms of MS?

A
  1. weakness, poor endurance
  2. sensory impairments
  3. balance impairments
  4. ataxia
  5. UMN signs
  6. blurred vision, nystagmus
  7. dysarthria
  8. autonomic dysfunction
276
Q

what are UMN signs in MS?

A
  1. spasticity
  2. hyperreflexia
277
Q

What are some outcome measures used to determine trx effectiveness in MS?

A
  1. MRI - visualize lesion
  2. relapse rate
  3. expanded disability severity scale (EDSS)
278
Q

how is the Kurtzke EDSS scored?

A

0-10 (0 = normal, 10 = death)

279
Q

what are the major aspects of MS treatment?

A
  1. Disease modifying therapies
  2. symptom management
280
Q

what do DMTs lessen?

A
  1. # of new lesions that form/keep existing from getting larger
  2. lessen # of relapses
281
Q

name 5 DMT drugs

A
  1. Interferon B
  2. Glatiramer acetate
  3. Sphingosine 1-Phosphate Receptor Modulator
  4. Dimethyl fumarate
  5. Monoclonal antibodies
282
Q

MOA for Interferon-B

A

exact MOA is unknown. Impacts immune function

283
Q

Administration route for Interferon-B

A

subcut or IM

284
Q

Indications for Interferon-B

A
  1. relapsing MS 2. decrease exacerbations and delay accumulation of physical disability
285
Q

AE for >50% Interferon-B

A
  1. flu-like symptoms
  2. HA
  3. injection site rxn
286
Q

AE for >20% Interferon-B

A
  1. fatigue
  2. depression
  3. pain
  4. abdominal pain
  5. nausea
  6. leukopenia
  7. increase LFTs
  8. myalgia
  9. back pain
  10. weakness, fever
287
Q

*monitor Interferon-B for __________

A
  1. Neuropsychiatric changes
  2. drug-induced hypothyroidism
  3. worsening cardiac function in HF
288
Q

MOA of Glatiramer acetate

A

reduce autoimmune response to myelin by reducing T-cell response against myelin

289
Q

Administration route for Glatiramer acetate

A

subcut or IM

290
Q

Indication for Glatiramer acetate

A

relapsing MS, decreasing exacerbation and lesion on MRI

291
Q

Most common AE for Glatiramer acetate

A

injection site rxs

292
Q

other common AE for Glatiramer acetate

A
  1. rash
  2. VD
  3. dyspnea
  4. chest pain
293
Q

what drug is a S1P receptor modulator?

A

Fingolimod

294
Q

Fingolimod MOA

A

coverts to active metabolite which blocks release of lymphocytes into CNS = decrease in inflammation

295
Q

Fingolimod use

A

PO daily to decrease exacerbation and overall disease severity

296
Q

Fingolimod >15% AE

A

headache, increased LFTs

297
Q

Rare Fingolimod AEs

A
  1. macular edema (report vision changes immediately),
  2. infection
298
Q

What AE warrants an immediate referral for somone on an S1P receptor modulator?

A

vision changes

299
Q

Dimethyl fumarate Use

A

PO 2x/day to decrease exacerbations and disease severity

300
Q

MOA of dimethyl fumarate

A

unknown in MS; may have anti-inflammatory properties

301
Q

AEs of dimethyl fumarate

A
  1. GI (N/V/D, abdominal pain in 12-18%)
  2. flushing (up to 40%)
302
Q

Rare AE for dimethyl fumarate

A

hepatoxicity

303
Q

Monoclonal Antibodies drugs suffix

A

-mab

304
Q

general MOA for monoclonal antibodies

A

decrease inflammation in CNS and autoantibody formation

305
Q

Use of Monoclonal antibodies

A
  1. may decrease exacerbations
  2. decrease lesions on MRI and slow progression
306
Q

Common AEs for monoclonal antibodies

A
  1. infusion related rxns
  2. HA
  3. fatigue
  4. arthralgia
307
Q

What is PML?

A

Progressive Multifocal Leukoencephalopathy

demyelinating CNS disorder caused by reactivation of JCV

308
Q

Patients on which meds are at a higher risk of developing PML?

A
  1. Monoclonal Antibodies
  2. Dimethyl Fumarate
  3. SP1 receptor modulators
309
Q

Signs and Symptoms of PML?

A
  1. altered mental status (AMS)
  2. aphasia
  3. ataxia
  4. hemiparesis
  5. hemiplegia
  6. visual field disturbances (double vision, partial blindness)
  7. seizures
310
Q

Off-label trxs for relapsing/progressive MS

A
  1. Azathioprine
  2. Methotrexate
311
Q

Symptom trx for MS

A
  1. Spasticity – baclofen
  2. ambulation and mobility impairments – dalfampridine
  3. Upper extremity tremor – botulinum toxin type A
  4. Central neuropathic pain – gabapentin
  5. Psudobulbar dysfunction – combo dextromethorphan/quinidine sulfate
  6. Urinary symptoms – oxybutynin
  7. depression/anxiety – antidepressants
312
Q

Drug Concerns for MS patients

A
  1. Fatigue
  2. Corticosteroid drug treatment
  3. DMT drugs can have substantial AEs influcing flu-like symptpoms to immunosuppression
313
Q

Key features of Alzheimer’s Disease

A
  1. Progressive neurodegenerative disease
  2. Gradual loss of memory and function leading to total dependence on caregivers
  3. Eventual inability to recognize family/friends/self
314
Q

What neurotransmitters are depleted in AD?

A
  1. Acetylcholine
  2. serotonin
  3. somatostatin
  4. NE
315
Q

General trx approach for AD

A
  1. Mild case
    1. cholinesterase inhibitor
  2. Moderate case
    1. cholinesterase inhibitor + memantine (delays progression)
    2. address behavioral and pyschological symptoms
  3. Severe case
    1. consider if meds will be beneficial
    2. may continue cholinesterase inhibitor
316
Q

Cholinesterase Inhibitor Drug

A

Donepezil (Aricept)

317
Q

Cholinesterase Inhibitors pros

A

modest improvements in cognition and ADLs

benefits last ~3-24 months

318
Q

Cholinesterase Inhibitors MOA

A

inhibit acetylcholinesterase from breaking down acetylcholine =

increased ACh helps correct ACh deficiency in AD

319
Q

Primary AEs for Cholinesterase Inhibitors

A

SLUDGE

DUMBELLS

320
Q

T/F: Cholinesterase Inhibitors can exacerbate UTOs, asthma, and COPD

A

TRUE

321
Q

T/F: Cholinesterase Inhibitors are on the Beers List?

A

TRUE

322
Q

what class of drug is Memantine (namenda)

A

NMDA antagonist

323
Q

NMDA antagonist MOA

A

antagonise NMDA receptor = stops excessive receptor activation by glutamate = decreases excitation and neuronal death

324
Q

When are NMDA antagonists used?

A
  1. monotherapy for moderate cases
  2. in conjunction with cholinesterase inhibitor in moderate cases
  3. Not FDA approved for mild cases
325
Q

NMDA Antagonists AE

A
  1. usually well tolerated
  2. monitor for falls
326
Q

Individuals with AD should not be taking what?

A
  1. Anticholinergic Drugs
  2. OTC antihistamines (Benadryl)
327
Q

AD drug concerns

A
  1. Cholinergic meds: GI issues (NVD) most common
  2. Memantine may cause dizziness, watch for falls
  3. Communicate behavioral issues to healthcare providers
328
Q

What should be taken into consideration when scheduling PT for patients with AD?

A
  1. lots of structure to help reduce behavioral issues
  2. reduce behavioral issues related to sundowning
  3. utilize time of day when pateint most alert
329
Q

Characterizations of Parkinson’s Disease

A
  1. Akinesia
  2. Bradykinesia
  3. Postrual instability
  4. Rigidity (freezing episode)
  5. Tremor (pill-roll)
330
Q

Pathophysiology of PD

A
  1. progressive death of dopamine-producing neurons in basal gangali
  2. reduced communication with Thalamus
  3. results in loss of voluntary movement, especially automatic movements
331
Q

Etiology of basal ganglia neurotransmitter imbalance

A

Overall unknown, possible impact of

  1. genetics
  2. environmental factors
332
Q

Medical management of PD

A
  1. Dopamine replacement
  2. Dopamine agonist therapy
  3. Anticholinergic therapy
333
Q

Overall goal of pharmacologic treatment Parkinson’s Disease

A

Restore neurochemical balance

334
Q

Name of Parkinson’s Disease Scales

A
  1. Unified Parkinson’s Disease Rating Scale (UPDRS)
  2. Hoehn & Yahr Scale
335
Q

PD, dopamine replacement therapy drugs

A

Levodopa-carbidopa (L-dopa)

MAO-B inhibitors

COMT Inhibitor

Amantadine (both agonist and replacement therapy)

336
Q

PD, dopamine agonist therapy

A

Amantadine

Ropinirole (Requip)

337
Q

Anticholinergic Therapy Drugs for PD

A
  1. Benztropine (Cogentin)
  2. Trihexyphenidyl
338
Q

benefits of Levodopa-carbidopa

A
  1. improves movement velocity
  2. may reduce tremor
  3. reduce rigidity
  4. improves force production & coordination of anticipatory postural task
339
Q

What are the long-term effects of dopamine replacement therapy

A
  1. Movement-related complications
  2. Dyskinesia
  3. Motor Fluctuations
340
Q

how does dopamine impact cholinergic response?

A

without dopamine the cholinergic response is uninhibited

341
Q

what is the 1st line trx and most effective treatment for PD patients?

A

Levodopa-carbidopa (Sinemet)

342
Q

carbidopa MOA (why is it combined with l-dopa)?

A

stops breakdown of l-dopa to dopamine in periphery so more l-dopa crosses BBB

343
Q

AE of Levodopa-carbidopa (Sinemet)

A
  1. End of dose “wearing of”
  2. “Delayed on” or “no on”
  3. Freezing
  4. “on” period dyskinesia
344
Q

MOA for MAO-B inhibitors

A

inhibit monoamine oxidase (MAO) B which breaks down dopamine = increased dopamine levels in CNS

345
Q

what PD treatment has a risk for serotonin syndrome?

A

Selegiline (a type of MAO-B inhibitor) when combined with serotonergic meds

346
Q

MOA of COMT inhibitors

A

Inhibit COMT which in turn decreases breakdown of l-dopa

347
Q

when are COMT inhibitors used?

A

Adjunct

used to reduce end of dose wearing off with l-dopa

348
Q

AE of COMT Inhibitors

A

>10% = involuntary movements, nausea

349
Q

what has Amantadine been used to treat in the past?

A

Influenze

350
Q

MOA of Amantidine

A

Unknown

possibly increases dopamine release

351
Q

Amantadine AE

A
  1. confusion
  2. hallucinations
  3. dizziness
  4. dry mouth
  5. constipation
  6. livedo retiularis
352
Q

T/F: Dopamine agonists can be a 1st line option for trx PD?

A

TRUE

353
Q

Dopamine Agonist Drug

A

ropinirole (Requip)

354
Q

ropinirole (Requip) AE

A
  1. nausea
  2. drowsinee
  3. dizziness
  4. syncope
355
Q

what to monitor for on a pt on ropinirole?

A
  1. light-headedness
  2. postural hypotension
  3. hallucinations
  4. lower-extremity edema
356
Q

less common AE of ropinirole

A
  1. impulsive behavior
  2. sleep attacks
357
Q

when might ropinirole be used?

A

as a monotherapy

adjunt therapy to reduce end of dose wearing off with l-dopa

358
Q

Anticholinergic Therapy for PD MOA

A

antagonzie muscarinc receptors to prevent acetylcholine binding

359
Q

PD Drug concerns

A
  1. Timing of PT session with delivery of meds
  2. Effects of exercsie on med absorption, utilization, and motor effects
  3. Long-term meds use and disease progression
360
Q

What is spasticity?

A

caused by a lesion on the spine or brain which leads to reduced neural innervation and increased tone

361
Q

Spasticity is synonymous with _________

A

hypertonicity

362
Q

What is muscle tone?

A

continuous tension in muscle

  • normal tone enables motor function
  • low tone = flaccid
  • high tone = excessive muscle tension
363
Q

spasticity is ___________ resistance to ________ stretch

A

velocity-dependent

passive

364
Q

What scale measures spasticity?

A

Ashworth Scale (0-4)

365
Q

Hypertonicity can lead to impairment with:

A
  1. ROM
  2. coordination
  3. skin hygiene
  4. pain
  5. functional mobility
  6. ADLs
366
Q

What are muscle spasms?

A

increased muscle tension following musculoskeletal injury and inflammation

no damage to brain or spinal cord

367
Q

What overall drug class is used to treat spasticity and muscle spasms?

A

Muscle Relaxants

and

Antispasticity meds

368
Q

Drug list for treating muscle spasms and spasticity

A
  1. Tizanadine
  2. Cyclobenzaprine (Flexaril)
  3. Diazepam (Valium)
  4. Botox (botulinum toxin)
  5. Baclofen (Lioresal)
  6. ITB pump (intrathecal baclofen)
369
Q

What type of drug is tizandine?

A

alpha-2 agonist

370
Q

MOA of tizanadine

A

bind to alpha-2 receptors to decrease excitatory NTs which decrease excitability to post synaptic neurons

371
Q

tizanadine instructions for use

A

2-3x/day

PO at night

must tritate to find correct dosage

372
Q

tizanadine AEs

A
  1. drowsiness
  2. dizziness
  3. asthenia
  4. sedation (within 30 min, peaks 1.5 hrs after dose)
  5. hypotension (within 1 hr, peaks 2-3 hrs after dose)
373
Q

what type of drug is cyclobenzaprine (Flexaril ) and diazepam (Valium)?

A

Centrally acting antispasmodic

374
Q

MOA of centrally acting antispasmodics

A

Unknown

might inhibit polysnaptic reflex in spinal cord

possible GABA and serotonin effects

375
Q

instructions for use of cyclobenzaprine (Flexaril)

A

onset: 1 hr
peak: 3-8 hrs
duration: 12-24 hr

376
Q

AEs of cyclobenzaprine (Flexaril)

A
  1. sedation
  2. dizziness
  3. **on the Beers list
377
Q

Note on Benzodiazepines (aka Valium)

A

Schedule IV drug

Sedation and respiratory depression when used with opiods

378
Q

how does botox work?

A

works at the neuromuscular junction to block the release of ACh

379
Q

T/F: botox has decreased efficacy with longterm use

A

TRUE

380
Q

instructions for Botox use

A

onset: 1-3 days

duration 3-6 months

381
Q

Botox (botulinum toxin) AEs

A

Boxed warnings!

may spread to distal tissues causing issues = distant paralysis

382
Q

what type of drug is Baclofen (Lioresal)?

A

Ethyl Alcohol and Phenol Direct Acting Agent

383
Q

Baclofen MOA

A

inhibits excitatory neurons = decreased NT release and K+ influx to increase inhibition

384
Q

Use of Baclofen (Lioresal)

A

PO

intrathecal pump (ITB)

385
Q

baclofen (Lioresal) AEs

A
  1. CNS depression
  2. muscle weakness
  3. memory and cognitive impairments in adults with TBI
386
Q

why would someone use an ITB?

A

better results with less AEs

generally need smaller doses

387
Q

PT notes for post-implantation of ITB?

A
  1. assess changes in motor skills due to muscle tone changes
  2. equipment modifications
  3. no modalities near pump site
  4. refill is needed every 3 months
  5. battery must be replaced every 4-5 years
388
Q

Complications of an ITB pump

A
  1. infection
  2. dislodgement
  3. kinking and blocking
  4. failure
  5. observe for signs of withdrawl or overdose
389
Q

Boxed warnings for ITB

A

abruptly stopping meds can cause:

  1. fever
  2. altered mental status (AMS)
  3. exaggerated rebound spasticity/rigidity
  4. in extreme cases
    1. rhabdomyolysis
    2. organ failure
390
Q

Therapeutic concerns for pts on muscle relaxants and antispastic meds

A
  1. sedation and weakness are biggest AEs
    1. can result in limited participation in PT
  2. requires intensive PT to develop new motor patterns and functional abilities
  3. must assess equipment
  4. be aware of ITB pump malfunctions
391
Q

what is depression?

A

mood disorder described as having the presence of 2 or more symptoms effecting:

  1. energy level
  2. sleep
  3. appetite
  4. self-esteem
  5. concentration
  6. decision-making
392
Q

what are the 2 major categories of depression?

A
  1. major depressive disoder
  2. dysthymic disorder
393
Q

what is major depression disorder?

A

symptoms for 2+ weeks

classified as mild, moderate, or severe

394
Q

what is dysthymic disorder?

A

mild chronic depression

symptoms for 2+ months

can still have major depressive episodes

395
Q

what are the symptoms typically for dysthymic disoder?

A

more cognitive features (low self-esteem)

affective (low mood)

social dysfuncction (social withdrawal)

396
Q

what are the overall symptoms of depression?

A
  1. low mood
  2. lost of interest
  3. loss of motivation
  4. loss of libio
  5. feelings of helplessness, hopelessness
  6. sleep distrubances
  7. suicidal thoughts
  8. eating disturbance
  9. pessimism
397
Q

Depression can increase your risk for what other diseases?

A
  1. reduced cardiovascular health (MI)
  2. osteoporosis, PUD, DM
  3. increased cortisol levels
398
Q

Pathophysiology of Depression

A

exact pathogenesis not completely understood

Possible factors:

  1. Monoamine hypothesis
  2. receptor downregulation and changes in sensitivity
  3. Neuroplasticity hypothesis
399
Q

what is the monoamine hypothesis?

A

deficiency or imbalance of monoamines leading to receptor downregulation and changes in sensitivity

400
Q

what is neuroplasticity hypothesis?

A

neurohistological changes lead to changes in the hardwiring of the brain

Antidepressants reverse these changes

401
Q

General MOA of antidepressants

A

inhibit reuptake of monoamines (5-HT or NE)

desensitizationof autoreceptors

enhance NE release

402
Q

What is a risk in treatment of depression?

A

Serotonin Syndrom

403
Q

Individuals undergoing Antidepressant therapy should be monitored for what?

A
  1. DDIs (cyp enzymes)
  2. BP/HR
  3. worsening depression (**red flag statement)
  4. serotonin syndrome
  5. boxed warnings
    • increased suicidal thoughts
404
Q

What is Serotonin Syndrome?

A

accumulation of high levels of serotonin

classified as mild, moderate, severe, and life threatening

405
Q

what are the symptoms of mild Serotonin Syndrome?

A
  1. HTN
  2. tachycardia
  3. tremor
406
Q

what are the symptoms of moderate Serotonin Syndrome?

A

same as mild in addition to:

  1. hyperthermia (1040)
  2. hyperactive bowels
  3. mild agitation
407
Q

what are the symptoms of severe Serotonin Syndrome?

A

all of the mild/moderate symptoms

hyperthermia (106 degrees)

408
Q

what medication puts you at the highest risk of Serotonin Syndrome?

A

MAO Inhbitors

409
Q

treatment for Serotonin Syndrome?

A
  1. Benzodiazepines
  2. Serotonin antagonist
  3. discontinuing serotonergic agents
  4. cardiac monitoring
410
Q

what is the goal of Antidepressant Therapy (treating depression)?

A
  1. reduce acute symptoms
  2. return to baseline level of function
  3. prevent further episodes
  4. prevent suicide attempts
411
Q

how long does it take after starting meds to see improvements in physical symptoms of depression ?

A

usually 2 weeks

412
Q

how long does it take after starting meds to see improvements in emotional symptoms of depression?

A

usually 6-8 weeks

413
Q

Drug Classes for Depression

A
  1. Selective Serotonin Reuptake Inhibitors (SSRI)
  2. Seretonin/NE Reuptake Inhibitors (SNRI)
  3. Atypical agents
  4. Tricyclic Antidepressants
  5. MAO Inhibitors
  6. Other
414
Q

SSRI suffix

A

-pram

415
Q

SSRI Drugs

A
  1. citalopram (Celexa)
  2. escitalopram (Lexapro)
416
Q

SSRI MOA

A

selectively inhibit 5-HT reuptake

417
Q

SSRI AE

A
  1. HA
  2. N/V/D
  3. insomnia
  4. sexual side effects

*Rare = hyponatremia, bleeding

418
Q

SSRI Indications

A
  1. Depression
  2. eating disorders
  3. PTSD
  4. anxiety
  5. OCD
  6. bipolar disorder
  7. vasomotor menopausal symptoms
419
Q

SNRI suffix

A

-ine

420
Q

SNRI drugs

A
  1. venlafaxine (Effexor)
  2. duloxetine (Cymbalta)
421
Q

SNRI MOA

A

inhibits 5-HT and NE reuptake

422
Q

SNRI AE

A
  1. HA
  2. nausea
  3. dry mouth
  4. sweating
  5. sexual dysfunction
  6. insomnia
423
Q

SNRI indications

A
  1. depression
  2. anxiety
  3. OCD
  4. panic disorder
  5. PTSD
  6. vasomotor menopausal symptoms
  7. fibromyalgia
  8. neuropathic pain
424
Q

Atypical Agents used to treat Depression

A

Buproprion (Wellbutrin)

425
Q

what is buproprion (Wellbutrin) used to treat in depression?

A

used as adjunct therapy to reduce sexual dysfunction

426
Q

buproprion (Wellbutrin) MOA

A

inhibits reuptake of DA and NE

427
Q

buproprion (Wellbutrin) AE

A
  1. HA
  2. nausea
  3. insomnia
  4. tremor
  5. dry mouth
  6. decreased appetite

**risks of seizures

428
Q

buproprion (Wellbutrin) Indications

A
  1. depression
  2. ADHD
  3. smoking cessation
  4. weight loss
429
Q

T/F: Tricyclic Antidepressants are cholinergic?

A

FALSE -> they are anticholinergic

430
Q

Tricyclic Antidepressants MOA

A

inhibits reuptake of 5-HT and NE. Creates receptor blockades for other NTs

431
Q

Tricyclic Antidepressants AE

A
  1. weight gain
  2. sexual dysfunction
  3. sedation
  4. anticholinergic effects (ABCDs)

**risks = overdose (cardiac)

432
Q

Tricyclic Antidepressants Indications

A
  1. Depression
  2. Neuropathic pain
  3. migraine prevention
  4. insomnia
433
Q

MAO Inhibitors MOA

A

inhibits MAO enzyme = more monoamines

434
Q

MAO Inhibitors AEs

A
  1. OH
  2. weight gain
  3. sexual dysfunction
435
Q

MAO Inhibitors Risks

A

Serotonin Sydrome

Hypertenisve crisis

436
Q

someone on an MAO Inhibitor should avoid what things to reduce their risk of hypertensive crisis?

A
  1. tyramine containing foods (wine, beer, cheese)
  2. sympathomimetic agents
437
Q

MAO Inhibitors Indications

A
  1. depression
  2. Parkinson’s Disease
438
Q

Other agents used to treat depression?

A
  1. alpha 2 antagonists
  2. 2nd generation antipsychotics
  3. Katamine (for highly trx resistant depression)
    • admin in providers office
  4. Trazodone
  5. Nefazodone
439
Q

What medication is 1st line in treating depression?

A

SSRI

due to efficacy and tolerability

440
Q

what drug is 1st line for fibromyalgia and neuropathic pain?

A

SNRIs

441
Q

Therapeutic Concerns for Antidepressant therapy

A
  1. intermittent tx may diminish drug efficacy
  2. monitor BP/HR
  3. tremor and sedation will impact participation in PT
442
Q

what is anxiety?

A

an appropriate response that becomes pathologic when out of proportionto the siutation

443
Q

Somatic symptoms of anxiety?

A
  1. muscle ache
  2. GI issues
  3. fatigue
  4. restlessness
444
Q

Psychological symptoms of anxiety

A
  1. sleep disturbances
  2. excessive worrying
  3. poor concentration
445
Q

Pathophysiology of anxiety

A

impacts the following regions of the brain

  1. periaqueductal gray matter (PAG)
  2. locus coeruleus
  3. hypothalamus
  4. limbic system
    • amygdala
    • hippocampus
446
Q

what does stimulation of the PAG cause?

A

vascular effects of anxiety

447
Q

what does stimulation of the locus coeruleus cause?

A

anxious behavior and panic

448
Q

how is the hypothalamus involved in anxiety?

A

central to anxiety response (hypothalmus-pituitary-adrenal axis)

secretes hormones involved in stress reaction

449
Q

describe the limbic system’s role in anxiety

A
  1. amygdala is connected to area involved in anxiety
  2. chronic stress (cortisol) reduces hippocampal volume
450
Q

Neurochemistry of Anxiety

A
  1. Monoamines = alpha 2 decrease sympathetic outflow to decrease anxiety
  2. serotonergic system = releases serotonin
  3. GABAergic system = inhibits release of GABA
451
Q

drugs used to treat anxiety act where?

A
  1. Serotonergic system
  2. GABAergic system
452
Q

Treatment of Anxiety

A
  1. SSRIs
  2. SNRI
  3. Tricyclic Antidepressants
  4. MAO Inhibitors
  5. Propranolol
  6. Benzodiazepines
  7. buspirone (Buspar)
453
Q

what is the 1st line treatment for anxiety?

A

SSRIs and SNRIs

454
Q

what is used in maintenace treatment for anxiety?

A

Tricyclic antidepressants and MAO inhibitors

455
Q

what is used for long-term treatment of anxiety?

A

propranolol = for panic attacks

456
Q

how are benzodiazepine used to treat anxiety?

A

only for acute treatment

457
Q

how is buspirone used to treat anxiety?

A

maintenance in generalized anxiety

458
Q

Benzodiazepines drug

A

alprazolam (Xanax)

459
Q

alprazolam (Xanax) MOA

A

binds BZD receptors ot enhance GABA inhibitory effects

460
Q

alprazolam (Xanax) AEs

A
  1. sedation
  2. ataxia
  3. memory problems

**high abuse potential

461
Q

alprazolam (Xanax) Indications

A
  1. spasticity
  2. muscle spasms
  3. acute anxiety
  4. serotonin syndrome
462
Q

buspirone (Buspar) MOA

A

unknown

binds to 5-HT and DA receptors

463
Q

buspirone (Buspar) AEs

A
  1. dizziness
  2. paradoxical anxiety (potentially)
464
Q

buspirone (Buspar) indications

A
  1. anxiety
  2. panic disorders (less useful)
465
Q

what are the advantages to using buspirone (Buspar)?

A
  1. no abuse risk
  2. no dependence
  3. no withdrawal
466
Q

what are the disadvantages of using buspirone (Buspar)?

A
  1. DDIs (cyp enzymes)
  2. onset = 3 weeks
467
Q

Therapeutic concerns with drugs that treat anxiety

A
  1. caution in elderly -> BZDs increase fall risk
  2. BZDs can interfere with sleep cycle (REM)
  3. overall sedation will
    • limit PT participation
    • increase fall risk
468
Q

what is Schizophrenia?

A

psychotic illness w/periods of psychosis

chronic dysfunction of mood, cognition, and social behavior

469
Q

Etiology of Schizophrenia

A

Unknown

possible genetic disposition and birth complications

470
Q

Possible pathophysiology of Schizophrenia

A

Possible cause

reduced prefrontal blood flow during cognitive tasks along with dopamin “dysregulation” (imbalance with overactivity and underactivity in various brain regions)

471
Q

what are the types of symptoms (categories) that Schizophrenic patients can have?

A
  1. Positive - presence of behaviors
  2. Negative - diminished/absent behaviors
  3. Cognitive - impaired behaviors
472
Q

what are some positive symptoms of schizophrenia?

A
  1. hallucinations
  2. disturbed reality
  3. abnormal motor behaviors
473
Q

What are some negative symptoms of schizophrenia?

A
  1. diminished speech
  2. flattened emotions
  3. social withdrawal
474
Q

what are some cognitive symptoms of schizophrenia?

A
  1. reduced attention
  2. decreased executive function
475
Q

what is the overall goal for treatment in schizophrenia?

A

reduce symptoms and mediate AE while improving function and QOL

476
Q

what schizophrenic symptoms are easier/harder to treat?

A

easier = positive symptoms

harder = negative symptoms

477
Q

what types of medications are typically used to treat schizophrenia?

A

antipsychotics

at a min takes 4-6 weeks to observe changes

478
Q

what are the classifications of antipsychotics?

A
  1. First generation (FGA) = older, more AE
  2. Second generation (SGA) = newer, less EPS and TD AEs
479
Q

what is the 1st line trx for schizophrenia and why?

A

SGA = there are less extrapyramidal symptoms and tardive dyskinesia

480
Q

what are extrapyramidal symptoms?

A

collection of symptoms that are drug induced movement disorders. include:

  1. actue dystonia
  2. akathesia
  3. delayed tardive dyskinesia
  4. acute parkinsonism
481
Q

what is tardive dyskinesia?

A

repetitive and involuntary movements such as grimicing and eye blinking

*orofacial dyskinesia

482
Q

T/F: tardive dyskinesia can be irreversible if left untreated and unnoticed?

A

TRUE

483
Q

what is acute dystonia?

A

spasm of muscles of tongue, face, neck and back

484
Q

what is akathesia?

A

restlessness and inability to stay still, manifests with finger-tapping, pacing

485
Q

MOA of first generation antipsychotics?

A

block dopamine receptors in mesolimbic tract where excess dopamine may contribute to postive symptoms

486
Q

SGA drugs on our list

A

quetiapine (Seroquel)

487
Q

quetiapine (Seroquel) MOA

A

block D2 receptors but less than FGA; more affinity for 5-HT receptors

*variable effect on histamine, muscarinic and alpha receptors = more variable AE

488
Q

SGA binding to D2 receptors AEs

A
  1. Motor = bradykinesia, and possible EPS
  2. Endocrine (higher risk for metabolic syndromes)
  3. Neuroleptic malignant syndrome
489
Q

if SGAs bind to other receptors what possible AEs can occur?

A
  1. H1 receptors
    • sedation and wt gain
  2. Muscarinic receptors
    1. ABCDs
  3. a1 receptors
    1. hypotension, dizziness
490
Q

Rehab concerns for FGAs

A
  1. CV risks
  2. caution with UV exposure
  3. imapired thermoregulation = caution with overexertion
  4. monitor for EPS
491
Q

Rehab concerns for SGAs

A
  1. wt gain, hyperglycemia, and lipid abnormalities
  2. CV abnormalities risk
  3. risk for heat intolerance
492
Q

what are the types of Bipolar Disorder?

A
  1. Bipolar I disorder
  2. Bipolar II disoder
493
Q

what is Bipolar I disorder (aka manic-depression illness)

A

one manic episode accompanied by history of one or more major depressive episodes

494
Q

what is Bipolar II disoder?

A

major depressive disorder accompanied by at least one hypomanic or milder manic phases

495
Q

what is hypomania?

A

at least 4 days of elevated/irritable mood combined with over-activity

496
Q

Pathogenesis of Bipolar Disoder?

A

Unknown

appears to be dysregulation in dopamine and serotonin systems

497
Q

what regions of the brain are altered in Bipolar disoder and how?

A
  1. limbic-cortical dysfunction
    • hippocampus and prefrontal cortex have diminished acitivty w/smaller volumes
    • amygdala is hyperactivity leading to emotional sensitivity
498
Q

how is Bipolar disorder treated?

A
  1. acute depressive episode = SSRI, bupropion
  2. acute manic episode = lithium
  3. maintenance trx = lithium
499
Q

what is the role of Lithium in treatment of Bipolar Disorder?

A
  1. Management of acute manic or hypomanic episode
  2. prevention of further manic and depressive episodes
500
Q

If lithium is so effective in lots of patients what is the drawback?

A

Lots of AEs