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Pharm Final review > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What percent of inhaled meds actually get to the lungs?

A

12%

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2
Q

What order do you give inhaled meds?

A

Give bronchodilators, then anything with a steroid second. Open up lung field to increase surface area

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3
Q

What muscarinic receptors act where?

A

M3 – primary in lungs.
M2 in heart.
M4 CNS

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4
Q

Is glycopyrrolate used for acute management?

A

NO

Probably for long-term COPD

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5
Q

Which agent is most effective in treating bronchospasm due to beta antagonists?

A

Ipratropium (atrovent)

More effective than beta-agonists in chronic bronchitis or emphysema

Duoneb/Combivent ®- in combo with albuterol

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6
Q

What are the two main side-effects of inhaled anticholinergics?

A

Narrow angle glaucoma
Urinary retention

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7
Q

Are beta-2 agonists metabolized by COMT and MAO?

A

Non-catecholamine structure makes them resistant to COMT. MAO only

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8
Q

What are the uses for inhaled beta 2 agonists?

A

Preferred treatment for acute episodes of asthma.

Prevention of exercise-induced asthma.

Improve airflow and exercise tolerance in patients with COPD.

Tocolytic to stop premature uterine contractions.

Treatment of hyperkalemia

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9
Q

What is the preferred treatment for acute episodes of asthma?

A

Inhaled beta 2 agonists

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10
Q

Which med is inhaled epinephrine?

A

Primatene Mist

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11
Q

Isoproterenol

A

Non-selective sympathomimetic
Act at Beta1 and Beta2 receptors.

Highly pro-arrhythmic.

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12
Q

What is the preferred Beta2 agonist for acute bronchospasm?

A

Albuterol

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13
Q

Why were short acting beta agonists made? Meds like levoalbuterol and metaproterenol?

A

Made because of “less cardiostimulatory effects”…for people with a-fib, etc…

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14
Q

What is terbutaline and ritodrine?

A

Tocolytic- reduces contractions to postpone labor for hours to days – used in O.B

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15
Q

What are beta-2 agonists also used for?

A

Treating hyperkalemia….they cause hypokalemia

They also CAUSE hyperglycemia

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16
Q

Which class of medication is unsafe to use as monotherapy due to an increased risk of asthma related death?

A

Long acting beta agonist (LABA)

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17
Q

Which class of med is used in prophylactic treatment of bronchial asthma and has
no role in the treatment of established (acute) bronchoconstriction?

A

Membrane Stabilizers like cromolyn sodium

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18
Q

What are methylxanthines?

A

Theophylline/Aminophylline
Caffeine
Theobromine

They are non-selective Phosphodiesterase Inhibitors and inhibit all fractions of PDE isoenzymes

Stimulate the CNS.

Inc BP

Increase myocardial contractility and heart rate
PDE3

Relax smooth muscle (airways). PDE4

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19
Q

Which methylxhanthine is used for treatment of bronchospasm due to acute exacerbation of asthma and has various toxicity levels associated with v-tach and seizures?

A

Theophylline

15-25 mcg/ml: GI upset, N/V, tremor
25-35: Tachycardia, PVCs
> 35: VTach, seizures

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20
Q

Caffeine

A

Adenosine releases Gaba leading to drowsiness. Caffeine blocks adenosine leading to less GABA.

Vasoconstriction from adenosine A1 effects…helps headaches by constricting..

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21
Q

Histamine receptors

A

4 types, but drugs typically target H1 and H2

Benadryl plus Pepcid to combat the H1 AND H2 receptors..have to give both

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22
Q

H-1 Receptors

A

Evoke smooth muscle contraction in the respiratory and G.I. tracts.

Cause pruritus and sneezing by sensory nerve stimulation.

Causes nitric oxide mediated vasodilitation.

Slow the heart rate by decreasing A-V nodal conduction.

Mediate epicardial coronary vasoconstriction.

23
Q

H-2 Receptors

A

Activates adenyl cyclase and increases intracellular cAMP.
Activates proton pump of gastric parietal cells to secrete hydrogen ion.

Increase myocardial contractility and heart rate.
Vasodilating effects on coronary vasculature opposes the vasoconstricting effects of H1 receptors.

With H1 receptors increase capillary permeability and vasodilitation.

23
Q

H-2 Receptors

A

Activates adenyl cyclase and increases intracellular cAMP.
Activates proton pump of gastric parietal cells to secrete hydrogen ion.

Increase myocardial contractility and heart rate.
Vasodilating effects on coronary vasculature opposes the vasoconstricting effects of H1 receptors.

With H1 receptors increase capillary permeability and vasodilitation.

24
Q

Which histamine receptors do you need to completely block to block the vasodilatory effects?

A

Need H1 and H2 blockers

25
Q

What is the triple response (wheel and flare)?

A

Edema due to increased permeability.

Dilated arteries around the edema (Flare).
Due to histamine stimulating nerve endings.

Pruritus due to histamine in the superficial layers of the skin.

26
Q

H1 vs H2 on airway

A

H1 constricts, H2 relaxes

27
Q

What is the difference between the two generations of H1 receptor antagonists?

A

The first generation is more sedating and have anticholinergic effects and have more QT prolongation

28
Q

What are H1 clinical uses?

A

prevent allergic rhinitis, antipruritic, sedative, antiemetic, some protection against bronchospasm

29
Q

What are H1 clinical uses?

A

prevent allergic rhinitis, antipruritic, sedative, antiemetic, some protection against bronchospasm

30
Q

Does having Benadryl on board make for a difficult reversal with naloxone?

A

YEP

31
Q

What is Dimenhydrinate (Dramamine®) used for?

A

Used to treat motion sickness and PONV.

32
Q

What are some 2nd generation antihistamines?

A

Zyrtec/Xyzal = Cetirizine/Levocetirizine

Claritin= Loratidine

Allegra: Fexofenadine

33
Q

What is the closest thing we have to cortisol?

A

Hydrocortisone

34
Q

Tell me about aldosterone..

A

Secreted secondary to inc K, dec Na, dec BP/fluid volume

Renin -> AG1 -> AG2 -> Aldosterone

Effects:
K excretion
Na retention
Increase water retention, increase blood volume

renin released from the kidney, angiotensinogen released from the liver…renin acts on angiotensinogen to make angiotensin 1…ACE acts on angiotensin 1 to make angiotensin 2…angiotensin 2 acts on the adrenal gland to make aldosterone..aldosterone acts on the kidney to absorb NA and water! yay! go fuck yaself!

35
Q

What is another name for primary adrenal insufficiency, and what is happening with it?

A

Addison’s Disease

Adrenals do not secrete cortisol or aldosterone

Replacement therapy must include glucocorticoid and mineralocorticoid (must include both)

36
Q

What is secondary adrenal insufficiency?

A

Due to chronic steroid use and suppression of the H-P-A axis.

Aldosterone secretion maintained

Replacement usually requires only glucocorticoid (anti-inflammatory)

37
Q

Glucocorticoids have a _____ effect while mineralocorticoids have a _____ effect

A

glucocorticoids are anti-inflammatory

mineralocorticoids reabsorb NA for K excretion

38
Q

Which steroids are naturally occurring?

A

Cortisol (hydrocortisone)
Cortisone
Corticosterone
Desoxycorticosterone
Aldosterone

39
Q

Which steroids are synthetic?

A

Glucocorticoids:
Prednisolone
Prednisone
Methylprednisolone
Betamethasone
Dexamethasone
Triamcinolone

Mineralocorticoids:
fludrocortisone

40
Q

What is the antiinflammatory:NA absorbent (glucocorticoid:mineralcorticoid) relationship for cortisol?

A

Cortisol (hydrocortisone) has 1:1 effect

41
Q

Anti-inflammatory alone AND mixed

A

anti-inflammatory only:
dexamethasone, betamethasone, triamcinolone

Both:
cortisol, cortisone, prednisolone, prednisone, methylprednisolone

fludrocortisone does both but WAY more sodium retaining

42
Q

Which of the following has both anti-inflammatory and mineralocorticoid effects?

A

Methylprednisolone

Also, cortisol, hydrocortisone, prednisone, prednisolone, methylprednisone

43
Q

Which corticosteroid has WAYYYYY more NA retaining (mineralocorticoid) properties than anti-inflammatory (glucocorticoid)?

A

FLUDRACORTISONE

10:125

44
Q

Do we need to taper steroids?

A

YES we need to stop steroids SLOWLY or they will go into an adrenal crisis

45
Q

Which is an absolute contraindication for corticosteroid use?

A

None of the above!!

Answers:
A.
Hyperglycemia

B.
Edema

C.
Infection

CorrectD.
None of the above

46
Q

What are the electrolyte changes with corticosteroids?

Hint: this also happens with thiazides and loop diuretics

A

Hypokalemic Metabolic Alkalosis:
Mineralocorticoid effect of cortisol on distal renal tubules leading to enhanced absorption of Na+ and loss of K+

47
Q

What do corticosteroids do regarding blood sugar?

A

Promote hepatic gluconeogenesis

Resultant hyperglycemia may require diet, insulin, or both to manage

48
Q

What does taking too may steroids do to the body?

A

CUSHINGS DISEASE YUCK

Redistribution of body fat:
Deposition on back (buffalo hump), supraclavicular, and face (moon facies)
Loss of fat from the extremities

49
Q

What can happen if you give even small doses of glucocorticoids to children?

A

Arrest of growth can result from the administration of relatively small doses of glucocorticoids to children

50
Q

Why do surgeons care about giving steroids intraoperatively?

A

Masking infection or further complicating surgery intended to treat infection

Altering glucose control in diabetics

Aseptic necrosis of the femoral head

Failure of bone fusion

51
Q

HPA suppression

A

Therapies unlikely to suppress H-P-A Axis:

Prednisone 5mg/day or less or 10 mg QOD
Long term every other day dosing associated with less suppression
Glucocorticoids, any dose < 3 weeks does not clinically suppress the H-P-A Axis

Prednisone or Dexamethasone (even physiologic doses) given as a single daily dose at bedtime is associated more commonly with H-P-A Axis suppression
Bedtime dosing more commonly associated

Therapies assumed to suppress H-P-A Axis (absolutely yes it will):

Prednisone 20mg/day (or equivalent) for > 3 weeks within the previous year

Patient with clinical signs of Cushing Syndrome from any steroid dose

No need to test the H-P-A Axis in these patients, just supplement with stress dose steroids

Therapies that may or may not suppress H-P-A Axis:
> 5mg/day but < 20mg/day of prednisone (or equivalent) for > 3 weeks the previous year
May have suppression of the H-P-A function depending on:
Dose
Duration
Individual patient
*After cessation of steroid therapy, recovery of the H-P-A function can take 12 months or longer
H-P function returns to normal before adrenal function
Options:
Test for responsiveness of the adrenals if time permits
Cosyntropin (ACTH) stimulation test
Give stress doses of glucocorticoids prophylactically (assume suppressed)

52
Q

Do burns or sepsis increase the need for steroids?

A

YES they surely do

53
Q

Signs and Symptoms of Acute Adrenal Crisis

A

Hypotension unresponsive to vasopressors
Hypoglycemia
Hyponatremia
Hypovolemia

Hyperdynamic circulation
Hyperkalemia

Metabolic acidosis
Decreased level of consciousness

Pharm Final review (24 decks)

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