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DPT Semester 1 > Pharmacology Test 3 cont > Flashcards

Pharmacology Test 3 cont Flashcards

1
Q

Somatropin indication

A

Hypotituitarism (dwarfism)

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2
Q

Somatropin MOA

A

synthetic GH

has a role in bone, skeletal muscle, and organ growth.

Increases RBC mass, water transport, and electrolyte transport

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3
Q

Somatropin AE

A
  1. fluid retention/edema
  2. muscle and joint pain
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4
Q

Somatropin PT Specific Considerations

A
  1. drug accuracy is difficult
  2. altered hormone levels exceeding normal ranges
  3. report abnormal ailments to endocrinologist
  4. Low GH = low BMD = fracture risk
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5
Q

What is DDAVP?

A

synthetic ADH (Vasopressin)

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6
Q

Desmopressin (DDAVP) indication?

A
  1. hypopituitarism
  2. nocturia
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7
Q

Desmopressin (DDAVP) MOA

A

decreases water exceretion, increasing urine concentration

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8
Q

Desmopressin (DDAVP) AE

A
  1. dry mouth
  2. hyponatremia
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9
Q

Drug class for spironolactone

A

Diuretic (K+ sparring)

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10
Q

Spironolactone indication

A
  1. Hyperaldosteronism (mineralocorticoid excess)
  2. HTN
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11
Q

Spironolactone MOA

A

nonselective for aldosterone receptors

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12
Q

Spironolactone AE

A
  1. hyperkalemia
  2. lethargy
  3. mental confusion
  4. produces gynecomastia in males
  5. irregualrity in females
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13
Q

Spironolactone notes

A

used in testosterone blockade for gender transition (male to female)

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14
Q

Eplerenone drug class

A

Diuretic

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15
Q

Eplerenone Indication

A

Hyperaldosteronism (mineralocorticoid excess)

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16
Q

Eplerenone MOA

A

aldosterone receptor blocker

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17
Q

Eplerenone AE

A
  1. hyperkalemia
  2. lethargy
  3. mental confusion
  4. produces gynecomastia in males
  5. irregualrity in females
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18
Q

Eplerenone Notes

A

more selective than spironolactone

more sought out

more expensive

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19
Q

Drug Classes that treat Muscle Spasticity

A
  1. Alpha 2 adrenergic agonist
  2. centrally acting antispasmodics
  3. DAA
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20
Q

Muscle spasticity drugs

A
  1. Tizanidine (Zanaflex)
  2. cyclobenzaprine (Flexeril)
  3. baclofen
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21
Q

Alpha 2 adrenergic agonist drug that treats muscle spasticity

A

tizanidine (Zanaflex)

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22
Q

Centrally acting antispasmodic drug that treats muscle spasticity

A

cyclobenzaprine (Flexeril)

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23
Q

DDA drug that treats muscle spasticity

A

baclofen

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24
Q

tizanidine (Zanaglex) MOA

A

selectively binds to alpha 2 receptors in CNS to decrease release of excitatory NT from presynaptic terminals and decrease excitability of postsynaptic neurons

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25
Q

tizanidine (Zanaflex) AE

A
  1. dizziness
  2. drowsiness
  3. asthenia
  4. hypotension up to 33% within 1 hr,
    • peaks 2-3 hrs after doses
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26
Q

tizanidine (Zanaflex) PK/PD considerations

A

sedation: within 30 minutes of dose

peak 1.5 hours after dose

may take with or w/o food but be consistent due to variable absorption

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27
Q

cyclobenzaprine (Flexeril) MOA

A

unknown

may inhibit polysnaptic reflex in SC

also possible GABA and serotonin effects, varies by drug

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28
Q

cyclobenzaprine (Flexeril) AE

A
  1. sedation
  2. dizziness
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29
Q

Notes on cyclobenzaprine (Flexeril)

A
  1. Beer’s list
  2. increased risk of fractures
  3. some anticholinergic effects
  4. may have limited efficacy at tolerable doses
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30
Q

baclofen MOA

A

inhibitory effects on alpha motor neuron through inhibition of excitatory neurons (blocks Ca2+ influx into presynaptic terminal = decreases NT release)

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31
Q

baclofen AE

A
  1. CNS depressant
    • sedation, ataxia, cardiac/resp depression
  2. Muscle weakness
  3. In older adults and TBI -> impaired memory and cognition
  4. transient drowsiness usually disappears within a few days
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32
Q

baclofen PK/PD considerations

A

increased drug effectiveness with smaller doses

usually intrathecal method

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33
Q

baclofen PT specific considerations

A

DO NOT abruptly stop meds = can lead to:

  1. high fever
  2. AMS
  3. exaggerated rebound spasiticity and muscle rigidity
  4. rhabdomyolysis
  5. system failure
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34
Q

Testosterone Indication

A

Androgen deficiency

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35
Q

Testosterone administration route

A
  1. Topical
  2. subcutaneous
  3. patch
  4. gel
  5. nasal spray
  6. buccal
  7. NO PO option = hepatotoxicity
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36
Q

Testosterone AE

A
  1. increase risk of MI, stroke, CV death
  2. Prolonged use
    • hepatic toxicitiy
    • hepatitis
    • jaundice
  3. IM
    • hepatic adeomas
    • infertility with large doses
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37
Q

Testosteron PK/PD considerations

A

IM –> large swings from trough to peak = variable symptoms relief and mood changes

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38
Q

Testosterone PT specific considerations

A
  1. avoid contact with path/gel areas
  2. monitor BP
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39
Q

B3 adrenergic agonist drug

A

Mirabegron (Myrebetriq)

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40
Q

mirabegron (Myrbetriq) indication

A

Men’s BPH (begnin prostatic hypertrophy)

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41
Q

mirabegron (Myrbetriq) MOA

A

relaxes detrusor muscle = decreases voiding symptoms

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42
Q

mirabegron (Myrbetriq) AE

A

increases BP

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43
Q

oxybutynin drug class

A

anticholinergic

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44
Q

oxybutynin indication

A

Men’s BPH (benign prostatic hypertrophy)

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45
Q

oxybutynin MOA

A

antispasmodic effect on smooth musce = blocks acetylcholine on smooth muscle

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46
Q

oxybutynin AEs

A

ABCDs

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47
Q

levothyroxine (Synthroid) indication

A

hypothyroidism

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48
Q

levothyroxine MOA

A

synthetic thyroxine (T4), converted to T3, has usual effects

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49
Q

levothyroxine AE

A

well tolerated unless overtreated

  1. sweating
  2. heat sensitivity
  3. tachycardia
  4. dirrhea
  5. nervousness
  6. menstrual irregularities
  7. increase BMR
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50
Q

levothyroxine PK/PD considerations

A
  1. take on empty stomach
  2. take 30-60 mins before meal or 3-4 hours after
  3. do not take with Ca, Mg, Fe, and Al products
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51
Q

levothyroxine PT specific considerations

A
  1. requires monitoring/close adjustments
  2. monitor for cardiac symptoms
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52
Q

levothyroxine Notes

A

highest risk: baseline CAD, HF

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53
Q

methimazole indication

A

hyperthyroidism

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54
Q

methimazole MOA

A

used a monotherapy for 1st year to induce remission

blocks formation of T3, T4 by inhibiting oxidation of iodine

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55
Q

methimazole AE

A

Common

  1. rash
  2. GI upset
  3. arthralgia (can develop into polyarthritis)

Rare AE

  1. agranulocytosis
  2. hepatotoxicitiy
  3. can cause hypothyroidism
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56
Q

methimazole PT specific considerations

A

refer if pt develops fever, sore throat, mouth ulcers (possible agranulocytosis)

*hepatotoxicity: increased risk with PTU

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57
Q

methimazole NOTES

A

can cause birth defects in 1st trimester of pregnancy

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58
Q

what is used to treat hypoparathyroidism?

A

calcium

vitamin D

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59
Q

MOA of vitamin D

A

stimualtes hematoporeisis

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60
Q

AE for calcium trx of of hypoparathyroidism

A

overtreatment can cause:

  1. hypercalcemia
  2. hypercalciuria = leading to nephrolithiasis
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61
Q

what class of drug is metformin (Glucophage)?

A

Biguanide

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62
Q

metformin (Glucophage) indication

A

Diabetes Type II

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63
Q

metformin (Glucophage) MOA

A

not fully known

  1. inhibits production of glucose
  2. inhibits intestinal absorption of glucose
  3. increases insulin sensitivity to muscle and fat
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64
Q

metformin (Glucophage) AE

A
  1. GI cramping
  2. N/V/D
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65
Q

metformin (Glucophage) PT specific considerations

A

boxed warnings: lactic acidosis

more common if:

  1. renal impairment
  2. dehydration
  3. elderly
  4. acute decompensated HF
  5. excess alcohol
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66
Q

metformin (Glucophage) Notes

A

Vitamin B12 deficiency can be misdiagnosed as peripheral neuropathy

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67
Q

what class of drug is glipizide?

A

Sulfonylureas

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68
Q

glipizide indication

A

Diabetes Type II

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69
Q

glipizide MOA

A

binds sulfonurea receptor in pancreas –> depolarization causes insulin release

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70
Q

glipizide AE

A
  1. hypoglycemia (especially in elder and renal dysfunction)
  2. weight gain
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71
Q

glipizide PK/PD considerations

A

take before breakfast

immediate release must be 30 mins before meal

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72
Q

glipizide PT specific considerations

A

if not taken correctly can increase hypoglycemia risk

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73
Q

glipizide Notes

A

on ther Beer’s List

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74
Q

Stimulant drugs

A
  1. mixed amphetamine salts (Adderall)
  2. methyphenidate (Concerta, Ritalin)
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75
Q

mixed amphetamine salts drug class

A

Stimulants

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76
Q

Mixed amphetamine salts brand name

A

Adderall

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77
Q

Adderall indication

A

ADHD

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78
Q

Adderall MOA

A

block dopamine and NE reuptake, increase dopamine and NE release

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79
Q

AE for:

Adderall

methylphenidate (Concerta, Ritalin)

A
  1. decrease appetite
  2. wt. loss
  3. stomach ache
  4. insomnia
  5. HA
  6. irritabililty/jitteriness
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80
Q

Rare AE for:

Adderall

methylphenidate (Concerta, Ritalin)

A
  1. dysphoria
  2. spacey state
  3. Tics
  4. HTN and HR fluctuations
  5. hallucinations
  6. chemical leukoderma (white skin from patch)
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81
Q

PK/PD considerations for:

mixed amphetamine salts (Adderall)

methylphenidate (Concerta, Ritalin)

A

if taken with food, slower onset and may decrease absorption and some AE

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82
Q

PT Specific considerations for:

mixed amphetamine salts (Adderall)

methylphenidate (Concerta, Ritalin)

A

report concerns about dependence or non therapeutic use

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83
Q

Boxed warnings for:

mixed amphetamine salts (Adderall)

methylphenidate (Concerta, Ritalin)

A
  1. CV risk – misuse can cause death or CV AE
  2. use w/caution w/CV disease present
  3. abuse potential (especially illictly)
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84
Q

atomoxetine (Strattera) indication

A

ADHD

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85
Q

atomoxetine (Strattera) MOA

A

selective NE reuptake ihibitor (SNRI)

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86
Q

atomoxetine (Stratter) AE

A

similar to other stimulants but more fatigue, sedation, and dizziness

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87
Q

atomextine (Strattera) PK/PD considerations

A
  1. onset: 2-4 weeks
  2. 6-12 weeks when reaching full benefit (must build up)
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88
Q

PT specific considerations atomoxetine (Strattera)

A

Boxed warnings:

monitor for suicidal ideation in adolescents/children

monitor mood changes

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89
Q

T/F: atomoxetine (Strattera) can be used as a monotherapy +/- stimulant

A

TRUE

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90
Q

Drug classes used to in treatment of Parkinson’s Disease

A
  1. Dopamine replacement therapy
  2. Dopamine agonist therapy
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91
Q

levodopa-carbidopa (Sinemet) drug class

A

dopamine replacement therapy

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92
Q

levodopa-carbidopa (Sinemet) MOA

A
  1. L-dopa is a precursor to dopamine that can cross the BBB and be converted to have CNS action
  2. carbidopa stops the breakdown of l-dopa to dopamine in periphery so that more l-dopa crosses BBB
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93
Q

levodopa-carbidopa (Sinemet) AE

A
  1. motor disturbances
  2. end of dose “wearing off”
  3. delayed or “no on” effect
  4. freezing
  5. “on” perioid dyskinesia
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94
Q

levodopa-carbidopa (Sinemet)

“wearing off” AE

A

stiffness returns (short 1/2 life of l-dopa)

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95
Q

what is freezing from levodopa-carbidopa (Sinemet)?

A

sudden inhibition of LE function

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96
Q

what is levodopa-carbidopa (Sinemet) “on” period dyskinesia?

A

involuntary mvmt of neck, trunk, extremities

due to peak drug levels causing increase dopamine response

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97
Q

PK/PD considerations of levodopa-carbidopa (Sinemet)

A

L-dopa has a short 1/2 life.

have consistent meal routine (high protein meal decreases absorption)

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98
Q

PT specific considerations for levodopa-carbidopa (Sinemet)?

A

ask them if they are taking the med regularly

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99
Q

ropinirole (Requip) drug class

A

Dopamine Agonist Therapy

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100
Q

what is ropinirole (Requip) indicated for?

A

PD

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101
Q

ropinirole (Requip) MOA

A

Binds to and agonizes dopamine receptors - helps with restless leg syndrome

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102
Q

ropinirole (Requip) AE

A
  1. Nausea
  2. drowsiness
  3. dizziness
  4. syncope
  5. light headedness
  6. postural hypotension
  7. hallucinations
  8. lower extremity edema
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103
Q

less common AE for ropinirole (Requip)

A
  1. impulsive behavior
  2. sleep attacks
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104
Q

when would ropinirole (Requip) be used as a monotherapy?

A

in younger pts.

normally be used as adjunct to reduce end of dose wearing off of l-dopa

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105
Q

Drugs used to treat MS

A
  1. Interferon beta
  2. glatiramer acetate
  3. fingolimod (Gilenya)
  4. dimethyl fumarate (Tecfidera)
  5. natalizumab (Tysabri)
  6. ocrelizumab (Ocrevus)
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106
Q

Drug class of interferon Beta

A

Interferon

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107
Q

interferon beta MOA

A

exact is unknown in MS

IFN-B is a protein produced by fibroblasts and has impact on immune function

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108
Q

interferon beta AE

A
  1. >50% – flu like symptoms
  2. >20%
    1. fatigue
    2. depression
    3. pain
    4. abdominal pain
    5. nausea
    6. leukopenia
    7. increased LFTs
    8. myalgia
    9. back pain
    10. weakness
    11. fever
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109
Q

PT specific considerations fo interferon B?

A
  1. monitorr for neuropyschic changes
  2. drug induced hyperthyroidism
  3. worsening cardiac function in HF
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110
Q

glatiramer acetate MOA

A

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

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111
Q

glatiramer acetate common AE

A
  1. ***injection site rxns (most common)
  2. rash
  3. dyspnea
  4. chest pain
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112
Q

S1P receptor modulator drug

A

fingolimod (gilenya)

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113
Q

fingolimod (Gilenya) MOA

A

converted to active metabolites which blocks release of lymphocytes into CNS = reduces inflammation

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114
Q

fingolimod (Gilenya) AE

A
  1. >15% = HA, increased LFTs
  2. rare = macular edema, infection
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115
Q

dimethyl fumarate brand name

A

Tecfidera

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116
Q

dimethyl fumarate (Tecfidera) MOA

A

may have anti-inflammatory properties

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117
Q

dimethyl fumarate (Tecfidera) AE

A
  1. GI (N/V/D, abdominal pain in 12-18%)
  2. flushing (40%)
  3. ***Rare = hepatoxicity
118
Q

monoclonal antibodies AE

A
  1. infusion related rxns
  2. HA
  3. fatigue
  4. arthalgia
  5. monitor for infection (respiratory, skin, herpes related)
119
Q

donepezil (Atricept) drug class

A

acetylcholinesterase inhibitor

120
Q

donepezil (Atricept) indication

A

AD

121
Q

donepezil (Atricept) MOA

A

inhibit acetylcholinesterase which breaks down ACh = increased ACh, corrects for ACh deficiency in AD

122
Q

donepezil (Atricept) AE

A

SLUDGE

DUMBELLS

123
Q

donepezil (Atricept) PK/PD considerations

A

taper if discontinuing and monitor for worsening cognitive function

124
Q

donepezil (Atricept) Other

A
  1. Beer’s list for bradycardia
  2. avoid if history of syncope that may be related to bradycardia
125
Q

memantine (Namenda) drug class

A

NMDA antagonist

126
Q

memantine (Namenda) indication

A

AD

127
Q

memantine (Nameda) MOA

A

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

128
Q

memantine (Namenda) AE

A

usually well tolerated

monitor for falls

129
Q

tizanidine brand name

A

Zanaflex

130
Q

tizanidine (Zanaflex) drug class

A

Alpha 2 adrenergic agonist

131
Q

tizanidine (Zanaflex) MOA

A

selectively bind to alpha 2 receptors in CNS to decrease release of excitatory NTs from presynaptic terminals = decreased excitability of postsynaptic neurons

132
Q

tizanidine (Zanaflex) AE

A
  1. dizziness
  2. drowsiness
  3. asthenia
  4. HTN up to 33% within 1 hr (peaks 2-3 hrs after dose)
133
Q

tizanidine (Zanaflex) PK/PD Considerations

A

sedation can occur within 30 minutes of dose

peaks ~1.5 hrs after dose

may take with or w/o food but be consistent due to variable absorption

134
Q

cyclobenzaprine brand name

A

Flexeril

135
Q

cyclobenzaprine (Flexeril) drug class

A

Centrally Acting Antispasmodics

136
Q

cyclobenzaprine (Flexeril) MOA

A

unclear

may inhibit polysnaptic reflex in spinal cord

also possible GABA and serotonin effects

137
Q

cyclobenzaprine (Flexeril) AE

A
  1. sedation
  2. dizziness
138
Q

cyclobenzaprine (Flexeril) Notes

A

on Beer’s list = increased risk for

  1. fractures
  2. some anticholinergic effects
  3. may have limited efficacy at tolerable doses
139
Q

baclofen drug class

A

DAA

140
Q

baclofen MOA

A

inhibitory effect on alpha motor neuron through inhibition of excitatory neurons (blocks Ca influx into presynaptic terminal) = decreases NT release

141
Q

baclofen AE

A
  1. CNS depression
  2. muscle weakness
  3. impaired memory and cognition in older adults and TBI
142
Q

baclofen PK/PD Considerations

A

increased drug effectiveness with smaller doses using intrathecal method (ITB)

143
Q

baclofen specific concerns

A

Do not abruptly stop med >> can lead to:

  1. altered mental state (AMS)
  2. fever
  3. exaggerated rebound spasticity
  4. rhabdomylosis
  5. organ failure
144
Q

what is Schizophrenia?

A

psychotic illness w/periods of psychosis

chronic dysfunction of mood, cognition, and social behavior

145
Q

Etiology of Schizophrenia

A

Unknown

possible genetic disposition and birth complications

146
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)

147
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
148
Q

what are some positive symptoms of schizophrenia?

A
  1. hallucinations
  2. disturbed reality
  3. abnormal motor behaviors
149
Q

What are some negative symptoms of schizophrenia?

A
  1. diminished speech
  2. flattened emotions
  3. social withdrawal
150
Q

what are some cognitive symptoms of schizophrenia?

A
  1. reduced attention
  2. decreased executive function
151
Q

what is the overall goal for treatment in schizophrenia?

A

reduce symptoms and mediate AE while improving function and QOL

152
Q

what schizophrenic symptoms are easier/harder to treat?

A

easier = positive symptoms

harder = negative symptoms

153
Q

what types of medications are typically used to treat schizophrenia?

A

antipsychotics

at a min takes 4-6 weeks to observe changes

154
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
155
Q

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

A

SGA = there are less extrapyramidal symptoms and tardive dyskinesia

156
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
157
Q

what is tardive dyskinesia?

A

repetitive and involuntary movements such as grimicing and eye blinking

*orofacial dyskinesia

158
Q

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

A

TRUE

159
Q

what is acute dystonia?

A

spasm of muscles of tongue, face, neck and back

160
Q

what is akathesia?

A

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

161
Q

MOA of first generation antipsychotics?

A

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

162
Q

SGA drugs on our list

A

quetiapine (Seroquel)

163
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

164
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
165
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
166
Q

Rehab concerns for FGAs

A
  1. CV risks
  2. caution with UV exposure
  3. imapired thermoregulation = caution with overexertion
  4. monitor for EPS
167
Q

Rehab concerns for SGAs

A
  1. wt gain, hyperglycemia, and lipid abnormalities
  2. CV abnormalities risk
  3. risk for heat intolerance
168
Q

what are the types of Bipolar Disorder?

A
  1. Bipolar I disorder
  2. Bipolar II disoder
169
Q

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

A

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

170
Q

what is Bipolar II disoder?

A

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

171
Q

what is hypomania?

A

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

172
Q

Pathogenesis of Bipolar Disoder?

A

Unknown

appears to be dysregulation in dopamine and serotonin systems

173
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
174
Q

how is Bipolar disorder treated?

A
  1. acute depressive episode = SSRI, bupropion
  2. acute manic episode = lithium
  3. maintenance trx = lithium
175
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
176
Q

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

A

Lots of AEs

177
Q

Common AEs of Lithium?

A
  1. GI
  2. weight gain
  3. polydipsia and polyuria
  4. CNS issues
    • mental dullness, decreased memory and concentration, fine hand tremor, fatigue and muscle weakness
178
Q

why does lithium require plasma concentration monitoring?

A

can be toxic and toxicity can occur at doses close to therapeutic levels

179
Q

what are signs of Lithium toxicity?

A
  1. persitent diarrhea
  2. vomiting
  3. coarse tremor
  4. mild ataxia
  5. drowsiness
  6. muscular weakness
180
Q

what circumstances can alter lithium concentrations and increase the risk of toxicity?

A
  1. medial illness
  2. crash diets and Na+ restriction diets
  3. strenuous exercise
  4. very hot climate
  5. surgery
  6. advanced age
  7. prenancy and delivery
181
Q

T/F: Lithium is assocaited with many DDIs?

A

TRUE

182
Q

What other medication class can be used in the treatment of Bipolar Disorder?

A

Anticonvulsant medications

  1. Valproic acid (VPA
  2. Carbamazepine
183
Q

what boxed warnings are there for anticonvulsants meds used to treat Bipolar Disorder?

A
  1. Valproix acid = hepatotoxicity
  2. Carbamazepine = Stevens-Johnson Syndrome and toxi epidermal necrolysis (TEN)
184
Q

how do Beta-blockers impact the heart during rest and exercise?

A

decrease HR, CO, and BP

185
Q

Beta-blockers impact on thermoregulation

A

increase sweating by 10% during exercise

186
Q

Beta-blockers +exercise consideration

A

beware of premature fatigue – espeically around 90 min after meds are taken

187
Q

how should you gauge exercise tolerance in a patient on beta-blockers?

A

BORG RPE

188
Q

Calcium channel blockers suffix

A

-dipine

189
Q

Calcium channel blockers drugs

A
  1. Dihydropyridines
  2. Benzothiazepines
190
Q

impact of Dihydrpyridines (amlodipine) on cardiac function?

A
  1. increased HR at rest and during exercise
  2. can leadto angina due to increased myocardial O2 consumption
  3. coronary steal phenomenon
191
Q

what is coronary steal phenomenon?

A

shunting of blood from ischemic to normally perfused areas of myocardium

all the vessels are dilated reducing any gradient that would drive blood towards ischemic regions

192
Q

Benzothiazepine (diltiazem) cardiac effects

A
  1. reduce HR at rest and during exercise
  2. more effective for treating exertional angina
  3. less likely to cause reflex tachycardia
193
Q

if a patient is on CCB or beta-blockers medication should be readily available to them?

A

nitroglycerin (Nitrates) if they were prescribed to them, make sure it is available during PT

194
Q

general guidelines for CCBs and Beta-Blockers and exercise prescription

A
  1. 3-5 days/week, 20-60 min duration
  2. limit HR increases to 20 bpm above RHR when pt. misses dose or has a dose adjustment
195
Q

all antithromotics have a risk of _______

A

causing bleeding –> so monitor/prevent for falls!

196
Q

antithrombotics we covered

A
  1. Heparin
  2. Warfarin
  3. LMWH
197
Q

how does Heparin work?

A

prevents conversion of fibrinogen to fibrin

198
Q

Heparin risks/notes

A
  1. increased risk for HIT
  2. increased risk for osteoporosis
  3. requires monotoring of aPTT
199
Q

how does Warfarin work?

A

decreaes Vitamin K stores which stops production of coagulation factors

200
Q

Warfarin Notes

A
  1. monitor INR (increased INR = less clotting factors = increased risk of bleeding)
  2. many drug & food inreactions
201
Q

how does LMWH work?

A

increases inhibition of FXa (more specific than Heparin)

202
Q

LMWH notes

A
  1. simpler dosing than Heparin and requires no lab monitoring
  2. decreased risk of HIT and osteoporosis
203
Q

PT notes for Antithrombotics

A
  1. avoid soft tissue mobilization
  2. avoid pressure
  3. avoid cutting ot tissue (sharp debridement)
204
Q

what are Nitrates used to treat?

A

Angina (exertional, variant, and unstable)

*may be used in conjunction with CCB and BB

205
Q

how do Nitrates work?

A
  1. decrease intracellular Ca to work directly on heart smooth muscle
  2. this decresaes preload/afterload and decreases O2 demand
206
Q

how are Nitrates administered?

A

IV

sublingual (used for acute attacks, tingle means its working)

topical (transderm patches)

207
Q

Nitrates dosing/storage info

A

up to 3 doses in 15 minutes

store in dark, brown glass bottle

good for 6 months unopened and only 3 months once opened

208
Q

Goal of Antiarrhythmic Drugs

A

restore normal rhythm or control abnormal

209
Q

how are antiarrhythmic drugs classified?

A
  1. origin = ventricular/atrial (supraventricular)
  2. pattern/rhythm = fibrillation or flutter
  3. speed/rate = brady or tachycardia
210
Q

Classes of Antiarrhythmic drugs

A

Class II

Class III

Class IV

211
Q

Antiarrhythmic Drug

Class II

A

beta-blocker

try to control rate

212
Q

Antiarrhythmic Drug

Class III

A

Amiodarone

controls rhythm (works by blocking K+ channles to lengthening AP)

**remember blue man

213
Q

what would Amidoarone be used to treat?

A

recurrent V-tachycardia

214
Q

Antiarrhythmic Drugs

Class IV

A

verapril and diltiazem (CCBs) - used for atria

*used to control origin

NOT for pts w/HFrEF

215
Q

what are 2 types of non-pharmacological trxs that increase survival from COPD?

A
  1. smoking cessation
  2. long-term O2 therapy
216
Q

main pharmacology trx for COPD

A

Bronchodilators

217
Q

how are bronchodilators helpful in pts with COPD?

A

increased exercise capacity which can improve QOL

218
Q

Types of Bronchodilators

A
  1. beta 2 agonists
  2. muscarinic antagonists
219
Q

Beta 2 Agonists types

A

SABA

LABA

220
Q

SABA info

A

drug = albuterol

used for acute exacerbations

onset 5 min

duration 4-6 hrs

221
Q

LABA info

A

drug = salmeterol

used to maintenance, daily use

duration = 12-24 hrs

222
Q

what do both SABAs and LABAs treat?

A

bronchospasms

223
Q

Common AE for Beta 2 agonists?

A
  1. tremor
  2. tachycardia
  3. hypokalemia (when taken w/thiazide)
224
Q

types of muscarinic antagonists (antimuscarinics)

A

SAMA
LAMA

225
Q

SAMA info

A

drug = ipratropium

used w/nebulizer

onset = 15-20 min

duration = 6-8 hrs

226
Q

LAMA info

A

drug = tiotropium

used for maintenance, daily use

duration = 12-24 hrs

227
Q

Common muscarinic antagonists AE

A

ABCDs

*specifically dry mouth

228
Q

what is used to treat severe COPD?

A

PDE-4 Inhibitors

229
Q

how do PDE-4 inhibitors work?

A

decrease cyclic AMP breakdown = decreased inflammation

230
Q

PDE-4 Inhibitors AE

A
  1. nausea
  2. diarrrhea
  3. weight loss
231
Q

Treatments for Cystic Fibrosis

A
  1. CFTR Modulators
  2. Bronchodilators
  3. Mucolytics
232
Q

how do CFTR Modulators work?

A

increase chloride transport = increased regulation of Na+ and water = mucous thinning

233
Q

CFTR Modulators AE

A
  1. GI
  2. HA
  3. *Orkambi = hypotension
234
Q

which mucolytics are primarily used in treating CF?

A

hypertonic saline

dornase alfa

235
Q

Hypertonic Saline notes

A

2-4x daily

almost all pts use them

work by increases salt which increases water in airway = water down mucus = increased function of mucociliary elevator

236
Q

Dornase alfa notes

A

1-2x daily

amost all pts

work by cleveing DNA = decreased viscosity of mucus

AE: chest pain

237
Q

Pulmonary medications Exercise Consideration

A
  1. time PT w/meds
  2. watch for paradoxial breathing
  3. B-agonists and methylxanthines = Increase RHR
  4. watch for R vent failure
  5. pts should always carrier rescue inhaler (especially during PT sessions)
238
Q

what is the most serious complication that can occur from Diabetes?

A

Diabetic Autonomic Neuropathy

239
Q

what are the signs of Diabetic Autonomic Neuropathy?

A
  1. exercise intolerance (BP and HR response blunted)
  2. orthostatic hypotension
  3. Silent MI
  4. hypoglycemima unawareness
240
Q

what is silent MI?

A

delay in recognizing angina

unexplained fatigue, condusion, dyspnes, N/V, hemoptysis, diaphoresis, dysrrhthmias, edema

241
Q

T1DM Exercise Considerations

A

exercise does not increase glucose uptake, possibly due to increased free fatty acids

242
Q

T1DM + insulin

Exercise Consideration

A
  1. monitor blood glucose with exercise
    • before
    • during
    • after (2 hrs after, possibly middle of night)
  2. make changes in insulin and carb consumption
243
Q

Overall Diabetes Exercise Considerations

A
  1. Proper footwear is essential
  2. avoid high impact activitees for older adults
  3. keep fast acting CHO nearby
  4. no exercise if glucose >300 mg/dL
  5. injest CHO if glucose <70 mg/dL prior to activity
  6. avoid insuling injection sites
  7. illness can increase glucose levels
244
Q

Treatments for Cystic Fibrosis

A
  1. CFTR Modulators
  2. Bronchodilators
  3. Mucolytics
245
Q

PDE-4 Inhibitors AE

A
  1. nausea
  2. diarrrhea
  3. weight loss
246
Q

how do PDE-4 inhibitors work?

A

decrease cyclic AMP breakdown = decreased inflammation

247
Q

what is used to treat severe COPD?

A

PDE-4 Inhibitors

248
Q

Common muscarinic antagonists AE

A

ABCDs

*specifically dry mouth

249
Q

LAMA info

A

drug = tiotropium

used for maintenance, daily use

duration = 12-24 hrs

250
Q

SAMA info

A

drug = ipratropium

used w/nebulizer

onset = 15-20 min

duration = 6-8 hrs

251
Q

types of muscarinic antagonists (antimuscarinics)

A

SAMA
LAMA

252
Q

Common AE for Beta 2 agonists?

A
  1. tremor
  2. tachycardia
  3. hypokalemia (when taken w/thiazide)
253
Q

what do both SABAs and LABAs treat?

A

bronchospasms

254
Q

LABA info

A

drug = salmeterol

used to maintenance, daily use

duration = 12-24 hrs

255
Q

SABA info

A

drug = albuterol

used for acute exacerbations

onset 5 min

duration 4-6 hrs

256
Q

Beta 2 Agonists types

A

SABA

LABA

257
Q

Types of Bronchodilators

A
  1. beta 2 agonists
  2. muscarinic antagonists
258
Q

how are bronchodilators helpful in pts with COPD?

A

increased exercise capacity which can improve QOL

259
Q

main pharmacology trx for COPD

A

Bronchodilators

260
Q

what are 2 types of non-pharmacological trxs that increase survival from COPD?

A
  1. smoking cessation
  2. long-term O2 therapy
261
Q

Antiarrhythmic Drugs

Class IV

A

verapril and diltiazem (CCBs) - used for atria

*used to control origin

NOT for pts w/HFrEF

262
Q

what would Amidoarone be used to treat?

A

recurrent V-tachycardia

263
Q

Antiarrhythmic Drug

Class III

A

Amiodarone

controls rhythm (works by blocking K+ channles to lengthening AP)

**remember blue man

264
Q

Antiarrhythmic Drug

Class II

A

beta-blocker

try to control rate

265
Q

Classes of Antiarrhythmic drugs

A

Class II

Class III

Class IV

266
Q

how are antiarrhythmic drugs classified?

A
  1. origin = ventricular/atrial (supraventricular)
  2. pattern/rhythm = fibrillation or flutter
  3. speed/rate = brady or tachycardia
267
Q

Goal of Antiarrhythmic Drugs

A

restore normal rhythm or control abnormal

268
Q

Nitrates dosing/storage info

A

up to 3 doses in 15 minutes

store in dark, brown glass bottle

good for 6 months unopened and only 3 months once opened

269
Q

how are Nitrates administered?

A

IV

sublingual (used for acute attacks, tingle means its working)

topical (transderm patches)

270
Q

how do Nitrates work?

A
  1. decrease intracellular Ca to work directly on heart smooth muscle
  2. this decresaes preload/afterload and decreases O2 demand
271
Q

what are Nitrates used to treat?

A

Angina (exertional, variant, and unstable)

*may be used in conjunction with CCB and BB

272
Q

PT notes for Antithrombotics

A
  1. avoid soft tissue mobilization
  2. avoid pressure
  3. avoid cutting ot tissue (sharp debridement)
273
Q

LMWH notes

A
  1. simpler dosing than Heparin and requires no lab monitoring
  2. decreased risk of HIT and osteoporosis
274
Q

how does LMWH work?

A

increases inhibition of FXa (more specific than Heparin)

275
Q

Warfarin Notes

A
  1. monitor INR (increased INR = less clotting factors = increased risk of bleeding)
  2. many drug & food inreactions
276
Q

how does Warfarin work?

A

decreaes Vitamin K stores which stops production of coagulation factors

277
Q

Heparin risks/notes

A
  1. increased risk for HIT
  2. increased risk for osteoporosis
  3. requires monotoring of aPTT
278
Q

how does Heparin work?

A

prevents conversion of fibrinogen to fibrin

279
Q

antithrombotics we covered

A
  1. Heparin
  2. Warfarin
  3. LMWH
280
Q

all antithromotics have a risk of _______

A

causing bleeding –> so monitor/prevent for falls!

281
Q

general guidelines for CCBs and Beta-Blockers and exercise prescription

A
  1. 3-5 days/week, 20-60 min duration
  2. limit HR increases to 20 bpm above RHR when pt. misses dose or has a dose adjustment
282
Q

if a patient is on CCB or beta-blockers medication should be readily available to them?

A

nitroglycerin (Nitrates) if they were prescribed to them, make sure it is available during PT

283
Q

Benzothiazepine (diltiazem) cardiac effects

A
  1. reduce HR at rest and during exercise
  2. more effective for treating exertional angina
  3. less likely to cause reflex tachycardia
284
Q

what is coronary steal phenomenon?

A

shunting of blood from ischemic to normally perfused areas of myocardium

all the vessels are dilated reducing any gradient that would drive blood towards ischemic regions

285
Q

impact of Dihydrpyridines (amlodipine) on cardiac function?

A
  1. increased HR at rest and during exercise
  2. can leadto angina due to increased myocardial O2 consumption
  3. coronary steal phenomenon
286
Q

Calcium channel blockers drugs

A
  1. Dihydropyridines
  2. Benzothiazepines
287
Q

Calcium channel blockers suffix

A

-dipine

288
Q

how should you gauge exercise tolerance in a patient on beta-blockers?

A

BORG RPE

289
Q

Beta-blockers +exercise consideration

A

beware of premature fatigue – espeically around 90 min after meds are taken

290
Q

Beta-blockers impact on thermoregulation

A

increase sweating by 10% during exercise

291
Q

how do Beta-blockers impact the heart during rest and exercise?

A

decrease HR, CO, and BP

DPT Semester 1 (12 decks)

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