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PHARMACOLOGY > EXAMS 4 (FINALS) > Flashcards

EXAMS 4 (FINALS) Flashcards

1
Q

advantages of inhalation route for asthma and COPD drugs

A
  • enhanced therapeutic effect
  • minimal systemic effects
  • rapid relief for acute attacks
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2
Q

metered dose inhalers

A
  • requires hand breath coordination

- spacers

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3
Q

inhaled corticosteroids / glucocorticoids

A
  • beclomethaSONE
  • fluticaSONE
  • mometaSONE
  • BudeSONIDE
  • cicleSONIDE

ADVERSE EFFECTS ARE MINIMAL

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4
Q

oral glucocorticoids

A

prednisone
prednisolone
methylprednisolone

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5
Q

adverse effect of inhaled glucocorticoids

A

oropharyngeal candidiasis
dysphonia
slow growth ( DOES NOT AFFECT OVERALL HEIGHT)

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6
Q

adverse effect of oral glucocorticoids

A

osteoporosis
adrenal suppression
hyperglycemia
peptic ulcers

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7
Q

counseling point for inhaled glucocorticoids (BUDESONIDE)

A

solution for nebulizer

  • rinse mouth and gargle with water after use
  • use daily as directed for preventing of exacerbations
  • chronic inhaled steroids can decrease the rate of growth in children does not limit overall height
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8
Q

leukotriene modifiers drugs

A
  • ziLEUton
  • zafirLUKAST
  • monteLUKAST (2nd line therapy for asthma. can be used for allergic riginits and exercise induced bronchospasm)
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9
Q

cromolyn mechanism of action

A
  • mast cell stabilizer
  • prevents relapse of histamine and other mediators
  • reduce inflammation

CONSDERATION: less effective than glucocorticoids

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10
Q

beta 2 agonists (first line drugs for asthma and copd)

A

SHORT ACTING (PRN for ongoing attacks)

  • albuterol
  • levalbuterol

LONG ACTING BETA 2 AGONISTS

  • arformoterol
  • formorerol
  • salmeterol
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11
Q

adverse effect of short acting beta 2 agonist

A

tachycardia
angina
tremor

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12
Q

adverse effects of long acting beta 2 agonist

A
  • increase risk of severe asthma and asthma related death
  • only use in combination with another long term control medication
  • NEVER USE ALONE
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13
Q

Long acting Beta 2 agonist role

A

ASTHMA

  • 2nd line therapy
  • use with glucocorticoids

COPD

  • 1st line therapy
  • given on schedule not PRN
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14
Q

methylxanthines (theoPHYLLINE and aminoPHYLLINE) physiologic effects

A

INDICATIONS: last line therapy in asthma and COPD

bronchodilation

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15
Q

anticholinergic drugs for asthma/COPD

A

ipraTROPIUM ( can be used with ALBUTEROL)
tioTROPIUM
aCLIDINIUM
umeCLIDINIUM

ADVERSE EFFECTS: dry mouth

besides ipraTROPIUM, DO NOT USE FOR IMMEDIATE RELIEF

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16
Q

treatment goals for asthma

A

REDUCING IMPAIRMENT

  • prevent chronic symptoms
  • reduce SABA use to less than 3 days per week
  • maintain normal pulmonary function
  • maintain normal activity levels
  • meet patient and family expectations for care

REDUCING RISK

  • prevent recurrent exacerbations
  • minimize need for ED visits
  • prevent loss of lung function
  • maximal benefits with minimal ADEs
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17
Q

severe exacerbations of asthma and COPD

A
  • given oxygen
  • systemic glucocorticoid (PO/IM/IV)
  • high dose of nebulized SABA
  • nebulized ipratropium
  • consider magnesium IV
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18
Q

COPD treatment goals (CONSIDER ANTIBIOTIC)

A

REDUCE IMPAIRMENT

  • reduce symptoms
  • improve patients health status
  • increase exercise tolerance

REDUCING RISK

  • reduce mortality
  • prevent progression
  • prevent exacerbations
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19
Q

role of glucocorticoids (steroids) in metabolism

A

CARBOHYDRATES

  • stimulates gluconeogenesis
  • decrease peripheral glucose utilization and glucose update by muscles and adipose cells
  • promotes glucose storage

PROTEIN
- break down protein allow amino acids for production of glucose

FAT
- breakdown fat

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20
Q

role of glucocorticoids (steroids) CNS

A

affect mood
CNS excitation
euphoria

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21
Q

role of glucocorticoids (steroids) Cardiovascular system

A
  • maintain functional integrity of the vascular system
  • increase RBC and hemoglobin levels
  • increase neutrophil counts
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22
Q

role of glucocorticoids (steroids) STRESS RESPONSE

A

increase level of glucocorticoids released in order to maintain blood pressure and glucose levels

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23
Q

role of glucocorticoids (steroids) respiratory system in neonates

A

necessary for lung maturation in preterm infants

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24
Q

drug of choice for mineralocorticoid replacement

A

fludrocortisone

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25
Q

drug of choice for glucocorticoids

A

hydrocortisone
prednisone
dexamethasone

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26
Q

what changes should be made to dose in event of stress or illness (GOUCOCORTICOID REPLACEMENT)

A

dose should be increased according to the 3 by 3 rule

3 by 3 rule = take 3 times the patients normal dosage for 3 days

27
Q

glucocorticoids replacement

A

it’s a lifelong therapy

  • replacement therapy should mimic normal patterns of glucocorticoids secretion
  • take entire daily dose upon waking up
  • take 2/3 of the dose in morning and 1/3 in afternoon
28
Q

drug interactions of glucocorticoids

A

NSAIDS - increase risk of peptic ulcer disease
INSULIN and oral anti diabetic agents - increase glucose release (may require higher doses of anti diabetic agents)
VACCINES - may decrease efficacy of vaccines

CONTRAINDICATIONS

  • systemic fungal infections
  • lice virus vaccines due to risk of developing infection
29
Q

adverse effects of glucocorticoids

A
  • adrenal suppression
  • osteoporosis
  • glucocorticoids intolerance
  • infection
  • psychological disturbances (CAN ALSO BE MINIMIZED) (insomnia agitation anxiety = can also be minimized by administering glucocorticoids in the morning
  • peptic ulcer disease
  • myopathy
30
Q

what is cosyntropin test

A

synthetic analog of ACTH used to test adrenal function and diagnose adrenal insufficiency

31
Q

what test is preferred to diagnose hypothyroidism

A

serum THS

  • diagnose hypothyroid
  • monitor treatment of hypothyroid
  • differentiate primary and secondary hypothyroid
  • serum T4 (but TSH IS PREFERRED)
32
Q

what tree at is preferred for hyperthyroidism

A

serum t3

  • measures total t3 bound and unbound

USED TO DIAGNOSE HYPERTHYROIDISM

33
Q

why is management of hypothyroidism in infants and pregnant women especially important

A

PREGNANCY
- can be difficult to identify due to non specific symptoms, decreases IQ Oof fetus, impairment of other neurological functions MOST DETRIMENTAL IN 1st TRISEMESTER

INFANTS
- fetus cannot produced their own thyroid hormone yet

34
Q

MEDICATIONS USED TO TREAT HYPOTHYROIDISM

A

levothyroxine (keep by bed, take when wake up on empty stomach)
liothronine
liotrix
armour thyroid

35
Q

counseling points for levothyroxine

A
  • take on empty stomach 30 to 6 mins before eating
  • monitor TSH 6 to 8 weeks after initiation or dose change
  • IV dose is ~ 50% less than PO dose (ORAL IS BETTER)

50 mcg IV = 100 PO

30 PO = 15 IV

IV is half of PO

36
Q

drug classes for hyperthyroidism

A
  • thionamides
  • radioactive iodine
  • beta blockers
  • non radioactive iodine ( lugol’s solution )
37
Q

thionamides ( methimazole, porpylthiouracil (PTU) ) mechanism of action

A
  • inhibits the peroxidase enzyme
  • prevents oxidation of iodine to iodine
  • prevents copping of iodinated tyrosines

PTU has extra mechanism= blocks conversion of t4 or t3 in the periphery (in acute crisis, this is not gonna work alone)

THIONAMIDES DO NOT DESTROY THYROID HORMONE that has already been produced

38
Q

thionamides adverse effects

A
  • well tolerated
  • symptoms of hypothyroid
  • agranulocytosis = severe dangerously low WBC count
  • hepatotoxicity (PTU)

METHIMAZOLE= considered hazardous agents wear gloves

39
Q

THIONAMIDES COMPARISON

A

methimazole = generally 1st line therapy but PRU preferred in pregnancy

  • hazardous agent
  • long highlife
  • use once daily
  • cause

PolyThioUracil (PTU) = patient experiencing thyroid storm

  • preferred in pregnancy
  • short half life so require frequent dosing
  • blocks coversion of T4 to t3
40
Q

RADIOACTIVE IODINE MECHANISM OF ACTION

A
  • isotope 131-I is concentrated in the thyroid gland
  • beta particles destroy thyroid tissue but do not leave thyroid gland
  • MAXIMAL EFFECTS SEEN IN 2 to 3 MONTHS
41
Q

ADVANTAGES OF RADIOACTIVE IODINE

A
  • low cost
  • avoidance of thyroid surgery
  • rare adverse effects
  • no damage to non thyroid tissues
42
Q

NON RADIOACTIVE IODINE ( LUGOL SOLUTION)

- DOES NOT DESTROY TISSUE LIKE RADIOACTIVE IODINE

A
  • iodine is converted to IODIDE in the GI tract before absorption
  • IODIDE decreases uptake of iodine into the thyroid gland
  • IODIDE suppresses iodination of tyrosine coupling of tyrosine residues

HIGH CONCENTRATIONS INHIBITS RELEASE OF THYROID HORMONE

43
Q

beta blockers for hyperthyroidism

A

MOA: used for symptomatic management. dosing is individualized (titration to effect)

PREFERRED BETA BLOCKER FOR HYPERTHYROIDISM
- also prevent conversion t4 to t3 in the periphery

IV - give slowly to avoid hypotension

44
Q

how are insulins differentiated from one another

A

tight glycemic control ~ HIGH RATES OF HYPOGLYCEMIA (avoid in patients at high risk for hypoglycemia)
- INTENSIVE THERAPY= glucose levels are maintained in a specific range around the clock

loose glycemic control
- less intensive monitoring

45
Q

MONITORING TREATMENT of DIABETES MELLITUS

A

self monitoring blood glucose

  • recommended for all patients with DM receiving insulin
  • finger stick
HEMOGLOBIN A1c (HgbA1c)
- long term management of DM
46
Q

ONSET AND DURATION OF EACH TYPE OF INSULIN

A
  • short duration ( aspart, lispro )= peak 15-30 mins, short duration of few hours

intermediate duration
long duration = do not display a significant peak and last up to 24 hours

47
Q

short duration insulin

A

FAST ACTING

  • insulin aspart
  • insulin lispro

GIVEN WITH MEALS TO CONTROL POST-
PRANDINAL RISE IN GLUCOSE
GIVE WITH MEALS OR SNACKS

SLOWER ACTING

  • insulin regular
  • before meals to control post-prandial rise in blood glucose
  • IV infusion for management of diabetic ketoacidosis
  • duration 6-10 hours
48
Q

intermediate duration insulin

A

NPH ( neutral protamine hagedorn) insulin

  • cloudy in color can be mixed with short acting
  • glucose between meals and overnight
  • cannot be used to control mealtime increases in blood glucose
  • CONTROL OF BG BETWEEN MEALS AND OVERNIGHT
49
Q

LONG DURATION INSULIN ( glargine U-100 and U-300, detemir, degludec )

A
  • insulin glargine ( U-100 )
  • insulin detemir

between meals and overnight
some time each day
DO NOT EXHIBIT PEAK like NPH does

DECREASES RISK OF HYPOGLYCEMIA

ULTRA LONG (glargine U 300 and degludec)

U-300 is 3 times more concentrated than U-100 formation.

be careful when dealing with these preparations as it can be easy to make an error when dosing

50
Q

MIXING INSULIN

A
  • short acting should be drawn into the vial first

- draw NPH insulin unit the vial second

51
Q

INSULIN STORAGE

A

unopened vials should be kept refrigerated
- vials should never be frozen, IF FROZEN, DISCARD

  • opened vials can be kept at a room temperature for 28 days
  • avoid shaking insulin vial as this destroys the insulin molecules
52
Q

INSULIN THERAPY

A

required for all with TYPE 1

  • optional for type 2 diabetes
  • drug of choice for gestational DM

more carbs= higher doses

53
Q

adverse effects of insulin

A

hypoglycemia
weight gain
hypokalemia
allergic reaction

54
Q

COUNSELING POINTS INSULIN

A
  • signs and symptoms of hypoglycemia

- use of GLUCAGON if necessary for hypoglycemia

55
Q

BIGUANIDES DRUG

A

metformin = drug of choice for initial management of type 2 diabetes

56
Q

metformin mechanism of action

A
  • inhibits glucose production in the liver
  • sensitizes insulin receptors in skeletal and adipose tissue
  • reduces glucose absorption in the gut

DOES NOT STIMULATE INSULIN RELASE = LOW RISK OF HYPOGLYCEMIA

57
Q

METFORMIN adverse effects

A
  • diarrhea
  • nausea
  • decreased appetite vitamin B12 and folic acid deficiency
  • lactic acidosis ( avoid use in patients with significant renal impairment )
58
Q

monitoring of metformin

A
  • hemoglobin A1c
  • GI adverse effects
  • Renal functions
59
Q

COUNSELING POINTS METFORMIN

A
  • do not crush ER tablets
  • take with food
  • start low doses and titrate up
  • GI adverse effects are common but will resolve with continued use
60
Q

Thiazolidinediones (TZDs) drugs

A

MOA= cells become more responsive to insulin and therefore blood glucose levels will decrease. insulin must be present for these drugs to work

pioGLITAZONE = preferred in clinical experience 
rosaGLITAZONE = biggest concern

evaluated by FDA for possible increase in CV including myocardial infarction

61
Q

Thiazolidinediones adverse effect

A

do not typically cause hypoglycemia on their own
- monitor liver function tests

ADVERSE EFFECT:

  • upper respiratory tract infection
  • exacerbation of existing heart failure (DO NOT USE IN PATIENTS WITH SEVERE HF
  • hepatotoxicity
62
Q

Alpha glucose inhibitors (acarbose, miglitol) ADVERSE EFFECT

A

GI ADVERSE EFFECTS

flatulence
cramps
abdominal distention and bloating
diarrhea

DO NOT CAUSE HYPOGLYCEMIA WHEN USED ALONE

63
Q

DIPEPTIDYL PEPTIDASE-4 (DPP-4) inhibitors (-GLIPTIN)

A
  • inhinits dipstidyl peptidase (DPP-4) enzyme
  • DPP 4 enzymes normally inactivates incretin hormones, by doing such, incretin hormones have a longer duration of action

INCRETIN: stimulates release of insulin and suppresses glucagon secretion. these actions prevent blood glucose levels from rising too high

ADVERSE EFFECT: pancreatitis

COUNSELING

  • monitor blood glucose when used with sylfonylurea
  • sign and symptoms of pancreatitis

PHARMACOLOGY (7 decks)

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