Respiratory Meds Flashcards

1
Q

Inhalation Technique

A

deep breath in, blow all out
MDI over 5-6 sec slow inhale
hold breathe x10 sec
repeat

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2
Q

How much is delivered to lungs with inhalation?

A

12%

ETT - less delivered unless mechanically ventilated

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3
Q

How much delivered by nebulizer vs MDI for same degree of bronchodilation?

A

need 6-10x amount for neb compared to MDI

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4
Q

T/F: Admin bronchodilators before corticosteroids?

A

TRUE

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5
Q

M1 Muscarinic Receptors

A

Location: endocrine glands, autonomic ganglia, salivary glands, stomach

Function: arousal, attention, REM, emotional response

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6
Q

M2 Muscarinic Receptors

A

Location: atria, conducting heart tissues

Function: cardiac inhibition

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7
Q

M3 Muscarinic Receptors

A

Location: exocrine glands, smooth muscle, lungs, GI tract

Function: lacrimal, salivary, mostly stimulatory

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8
Q

M4 Muscarinic Receptors

A

Location: CNS

Function: direct regulatory action on K and Ca channels

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9
Q

M5 Muscarinic Receptors

A

Location: substantia nigra, CNS

Function: may regulate dopamine release

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10
Q

Metabolic response of beta 2 agonism?

A

hyperglycemia
hypokalemia
hypomagnesemia

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11
Q

Black Box warning of LABA’s

A

increased risk of asthma related death, should not be used alone

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12
Q

Histamine…

A

naturally occurring, low molecular weight, hydrophillic endogenous amine.

produces variety of responses

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13
Q

Histamine acts..

A

through G-protein coupled membrane receptors

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14
Q

What is an example of a chemical mediator of inflammation in allergic reaction?

A

Histamine

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15
Q

Which cells contain large amounts of histamine and where are they located

A

mast cells, located in skin, lungs, GI and circulating basophils

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16
Q

What is histamine released in response to?

A

certain drugs
AG-AB reactions

*histamine does not easily cross the BBB

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17
Q

H1 Receptors

A
  1. evoke smooth muscle contraction in resp and GI tract
  2. pruritis, sneezing
  3. NO mediated vasodilation
  4. slow HR (decreased AV nodal conduction)
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18
Q

Through H1 and H2 receptors, histamine causes…

A

increased capillary permeability**, HoTN, tachycardia, flushing, headache

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19
Q

H2 Receptors

A
  1. activates adenyl cyclase and increase intracellular cAMP
  2. activates proton pump of gastric parietal cells - secrete hydrogen ion
  3. Increase HR - vasodilating effects at coronary vasc contradicts H1 actions
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20
Q

Histamine: CV

A

dilation - flushing, decreased SVR, HoTN, edema

inotropic, chronotropic, coronary vasodilation (H2) and vasocontriction (H1)

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21
Q

T/F: Need H1 and H2 blockers to competitively block the vasodilatory effects

A

TRUE

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22
Q

Triple Response: Wheal and Flare

A
  1. edema - d/t increased permeability
  2. Dilated arteries around edema (flare)
  3. pruritis - histamine at superficial layers
23
Q

Histamine: Respiratory

A

H1 - contricts bronchioles - usually ok but not if asthmatic

H2- relaxes bronchiol smooth muscle

24
Q

Gastric Hydrogen Ion Secretion

A
  • can increase even if not enough to cause HoTN, due to H2 stim
  • vagal stim alsto increases H+ secretion
25
Q

Histamine Receptor Antagonists

A

-competitive, reversible antagonists of histamine receptors

**does not inhibit release, blocks receptors

26
Q

Adrenal Cortex Layers and secretions

A
  1. Outermost - Zona Glomerulosa - Minralocorticoid
  2. Middle - Zona Fascicula - Glucocorticoids
  3. Inner - Zona Reticularis - Weak androgens
27
Q

Cortisol

A

hormone - released d/t stim of HPA axis by stress

28
Q

Cortisol metabolic effects

A

carb, protein, fat metab
fluid and electrolyte balance
multiple organ system stability
inhibition of allergic/inflam rspons

29
Q

Circadian Rhythm

A

secretory rates are high in early morning and low in late evening

30
Q

Primary Adrenocortical Insufficiency

A

addison’s disease - adrenals do not secrete cortisol or aldosterone

replacement therapy must include glucocorticoid and mineralocorticoid

31
Q

Secondary Adrenocortical Insufficiency

A

d/t chronic steroid use and suppression of HPA axis

  • aldosterone secretion is maintained
  • replacement must include glucocorticoid
32
Q

Physiological effects of cortisone

A

increased CO, RR, gluconeogenesis, analgesia

decreased inflammation

inhibition of digestion

redistribution of CNS blood flow

33
Q

Glucocorticoid effect

A

anti-inflammatory response

34
Q

Mineralocorticoid effect

A

evoke distal renal tubular re-absorption of Na in exchange for K

35
Q

Naturally Occurring Corticosteroids

A
cortisol (hydrocortisone)
cortisone
corticosterone
desoxycorticosterone
aldosterone
36
Q

Synthetic Corticosteroids

A
Glucocorticoids:
prednisolone
prednisone
methylprednisolone
betamethasone
dexamethasone
triamcinolone

Mineralocorticoids:
fludrocortisone

37
Q

Inhaled Corticosteroids

A
end in -sone or -ide
fluticasone
budesonide
beclometasone
mometasone
cicleonide
triple combos
38
Q

PK of corticosteroids

A

effective orally, water soluble forms can be given IV, prolonged effects IM

39
Q

Are corticosteroids able to cross the placenta?

A

yes

40
Q

Side Effects of Corticosteroids

A

tons, stimulatory
adrenal atrophy, cushing’s syndrome, diabetes, HTN, psychosis, immunosuppression, Na dn water retention, K and H loss, skin atrophy

41
Q

Hypokalemic Metabolic Alkalosis

A

mineralocorticoid effect of cortisol on distal renal tubules leading to enhanced absorption of Na and loss of K

also leads to edema and weigh gain

42
Q

T/F: corticosteroids inhibit glucose use in peripheral tissues and promote hepatic gluconeogenesis

A

TRUE, may require diet and insulin

43
Q

Catabolic corticosteroid effects

A

peripherally, amino acids mobilize in tissues - decreased skeletal muscle mass, oseoporosis, thin skin

44
Q

How will long term corticosteroids effect hct and WBC counts?

A

increase Hct

increase WBC counts

45
Q

Fear going into surgery with patient who is on steroid therapy?

A

HPA Axis suppression –> hypotensive shock

46
Q

Therapies unlikely to suppress HPA axis

A

prednisone 5 mg/day or 10 mg QOD
every other day
dose < 3 wks

47
Q

T/F: Prednisone and dexamethasone (even physiologic doses) given as a single daily dose at bedtime is associated with HPA axis suppression

A

TRUE

48
Q

Therapies assumed to suppress HPA axis (high risk)

A
  • prednisone 20 mg/day > 3 wks within previous year
  • pt with cushings presentation
  • dont test, just supplement
49
Q

Therapies that we don’t really know how they effect HPA Axis

A
  • > 5 mg/day, < 20 mg/day of prednisone >3 wks

- test ACTH if possible, assume suppression and dose glucocorticoid

50
Q

Pts to supplement..

A
  • diagnosed secondary adrenal insufficiency

- high risk pts

51
Q

How do burns/sepsis effect corticosteroid need?

A

may exaggerate need for exogenous corticosteroid supplementation

52
Q

S/S of Acute Adrenal Crisis

A
HoTn, unresponsive to tx
hypoglycemia
high K
low Na
hypovolemia
metabolic acidosis
decreased LOC
53
Q

What causes release of aldosterone?

A

increased K
decreased Na
decreased BP

54
Q

Effects of aldosterone?

A

increased excretion of K
retention of Na
retention of water