Respiratory Flashcards
What percent of inhaled meds actually get to the lungs?
12%
What order do you give inhaled meds?
Give bronchodilators, then anything with a steroid second. Open up lung field to increase surface area
What muscarinic receptors act where?
M3 – primary in lungs.
M2 in heart.
M4 CNS
Is glycopyrrolate used for acute management?
NO
Probably for long-term COPD
Which agent is most effective in treating bronchospasm due to beta antagonists?
Ipratropium (atrovent)
More effective than beta-agonists in chronic bronchitis or emphysema
Duoneb/Combivent ®- in combo with albuterol
What are the two main side-effects of inhaled anticholinergics?
Narrow angle glaucoma
Urinary retention
Are beta-2 agonists metabolized by COMT and MAO?
Non-catecholamine structure makes them resistant to COMT. MAO only
What are the uses for inhaled beta 2 agonists?
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
What is the preferred treatment for acute episodes of asthma?
Inhaled beta 2 agonists
Which med is inhaled epinephrine?
Primatene Mist
Isoproterenol
Non-selective sympathomimetic
Act at Beta1 and Beta2 receptors.
Highly pro-arrhythmic.
What is the preferred Beta2 agonist for acute bronchospasm?
Albuterol
Why were short acting beta agonists made? Meds like levoalbuterol and metaproterenol?
Made because of “less cardiostimulatory effects”…for people with a-fib, etc…
What is terbutaline and ritodrine?
Tocolytic- reduces contractions to postpone labor for hours to days – used in O.B
What are beta-2 agonists also used for?
Treating hyperkalemia….they cause hypokalemia
They also CAUSE hyperglycemia
Which class of medication is unsafe to use as monotherapy due to an increased risk of asthma related death?
Long acting beta agonist (LABA)
Which class of med is used in prophylactic treatment of bronchial asthma and has
no role in the treatment of established (acute) bronchoconstriction?
Membrane Stabilizers like cromolyn sodium
What are methylxanthines?
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
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?
Theophylline
15-25 mcg/ml: GI upset, N/V, tremor
25-35: Tachycardia, PVCs
> 35: VTach, seizures
Caffeine
Adenosine releases Gaba leading to drowsiness. Caffeine blocks adenosine leading to less GABA.
Vasoconstriction from adenosine A1 effects…helps headaches by constricting..
Histamine receptors
4 types, but drugs typically target H1 and H2
Benadryl plus Pepcid to combat the H1 AND H2 receptors..have to give both
H-1 Receptors
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.
H-2 Receptors
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.
H-2 Receptors
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.
Which histamine receptors do you need to completely block to block the vasodilatory effects?
Need H1 and H2 blockers
What is the triple response (wheel and flare)?
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.
H1 vs H2 on airway
H1 constricts, H2 relaxes
What is the difference between the two generations of H1 receptor antagonists?
The first generation is more sedating and have anticholinergic effects and have more QT prolongation
What are H1 clinical uses?
prevent allergic rhinitis, antipruritic, sedative, antiemetic, some protection against bronchospasm
What are H1 clinical uses?
prevent allergic rhinitis, antipruritic, sedative, antiemetic, some protection against bronchospasm
Does having Benadryl on board make for a difficult reversal with naloxone?
YEP
What is Dimenhydrinate (Dramamine®) used for?
Used to treat motion sickness and PONV.
What are some 2nd generation antihistamines?
Zyrtec/Xyzal = Cetirizine/Levocetirizine
Claritin= Loratidine
Allegra: Fexofenadine
What is the closest thing we have to cortisol?
Hydrocortisone
Tell me about aldosterone..
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!
What is another name for primary adrenal insufficiency, and what is happening with it?
Addison’s Disease
Adrenals do not secrete cortisol or aldosterone
Replacement therapy must include glucocorticoid and mineralocorticoid (must include both)
What is secondary adrenal insufficiency?
Due to chronic steroid use and suppression of the H-P-A axis.
Aldosterone secretion maintained
Replacement usually requires only glucocorticoid (anti-inflammatory)
Glucocorticoids have a _____ effect while mineralocorticoids have a _____ effect
glucocorticoids are anti-inflammatory
mineralocorticoids reabsorb NA for K excretion
Which steroids are naturally occurring?
Cortisol (hydrocortisone)
Cortisone
Corticosterone
Desoxycorticosterone
Aldosterone
Which steroids are synthetic?
Glucocorticoids:
Prednisolone
Prednisone
Methylprednisolone
Betamethasone
Dexamethasone
Triamcinolone
Mineralocorticoids:
fludrocortisone
What is the antiinflammatory:NA absorbent (glucocorticoid:mineralcorticoid) relationship for cortisol?
Cortisol (hydrocortisone) has 1:1 effect
Anti-inflammatory alone AND mixed
anti-inflammatory only:
dexamethasone, betamethasone, triamcinolone
Both:
cortisol, cortisone, prednisolone, prednisone, methylprednisolone
fludrocortisone does both but WAY more sodium retaining
Which of the following has both anti-inflammatory and mineralocorticoid effects?
Methylprednisolone
Also, cortisol, hydrocortisone, prednisone, prednisolone, methylprednisone
Which corticosteroid has WAYYYYY more NA retaining (mineralocorticoid) properties than anti-inflammatory (glucocorticoid)?
FLUDRACORTISONE
10:125
Do we need to taper steroids?
YES we need to stop steroids SLOWLY or they will go into an adrenal crisis
Which is an absolute contraindication for corticosteroid use?
None of the above!!
Answers:
A.
Hyperglycemia
B.
Edema
C.
Infection
CorrectD.
None of the above
What are the electrolyte changes with corticosteroids?
Hint: this also happens with thiazides and loop diuretics
Hypokalemic Metabolic Alkalosis:
Mineralocorticoid effect of cortisol on distal renal tubules leading to enhanced absorption of Na+ and loss of K+
What do corticosteroids do regarding blood sugar?
Promote hepatic gluconeogenesis
Resultant hyperglycemia may require diet, insulin, or both to manage
What does taking too may steroids do to the body?
CUSHINGS DISEASE YUCK
Redistribution of body fat:
Deposition on back (buffalo hump), supraclavicular, and face (moon facies)
Loss of fat from the extremities
What can happen if you give even small doses of glucocorticoids to children?
Arrest of growth can result from the administration of relatively small doses of glucocorticoids to children
Why do surgeons care about giving steroids intraoperatively?
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
HPA suppression
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)
Do burns or sepsis increase the need for steroids?
YES they surely do
Signs and Symptoms of Acute Adrenal Crisis
Hypotension unresponsive to vasopressors
Hypoglycemia
Hyponatremia
Hypovolemia
Hyperdynamic circulation
Hyperkalemia
Metabolic acidosis
Decreased level of consciousness
