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78 Cards in this Set
- Front
- Back
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what is VLS
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vascular leak syndrom
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describe the process behind allergic rhinitus
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pollen/antigen sits on mast cells which release histamines, proaglandins, and leukotrienes, all of which are vasoactive amines which cause increased vascular permeability. which causes fluid release from the vessels = SNOT
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in the vascular system histamines produce
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dilation of blood vessels and increased capillary permeability
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in the bronchi, histamines produce
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constriction
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in the stomach, histamine does what
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stimulates gastric acid secretion
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in the cns, histamine does what?
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acts as a neurotransmitter
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in the periphery, histamine is synthesized and stored in what two types of cells
how are is stored? |
mast cells and basophils
in structures called secretory granules |
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what is the initial requirement for the allergic release of histamine?
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the production of antibodies of the IgE class, generated in response to exposure to specific allergens.
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after the initial exposure, how is histamine released
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after syntheses of the IgE antibodies, the antibodies become attached to the outer surface of mast cells and basophils. When the individual is re-exposed to the allergen, the allergen becomes bound by the antibodies. Binding of allergen to adjacent antibodies creates a bridge btw those antibodies. The bridging process mobilizes intracellualr calcium in the mast and basophil cells. The calcium causes the secretory granules to fuse with the cell membrane and disgorge their contents into the extracellular space.
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what are the two types of receptors that histamine acts through?
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H1 and H2
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what are the effects of H1 receptor stimulation by histamine?
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1.dilation of small blood vessels (arterioles and venules).
2. increased capillary permeability 3.bronchoconstriction 4.CNS effects 5. itching and pain 6. secretion of mucus |
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describe the vasodilation effects of H1 receptor activation by histamine
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Vasodilation is prominent in the skin of the face and upper body, causing warmth and flushness. If extensive vasodilation occurs, total peripheral resistance declines and blood pressure falls.
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describe the vasodilation effects of H1 receptor activation by histamine
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activated H1 receptors cause capillary endothelial cells to contract, which creates openings between these cells through which fluid, protein, and platelets can escape. escape of fluid and protein into the interstitial space produces edema. if loss of intravascular fluid is substantial, blood pressure may fall
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why are antihistamines not helpful in treating asthma?
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because histamine is not the cause of bronchoconstriction that occurs during a spontaneous asthma attack
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what are the responses to activation of H2 receptors by histamine?
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secretion of gastric acid
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describe the gastric acid secretion effects of H2 receptor activation by histamine
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histamine acts directly on parietal cells of the stomach to promote acid release
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why are antihistamines not useful during anaphylactic shock
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because although histamine is involved in anaphylazis, it plays a minor role. Leukotriienes and other subs are the principal mediators.
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what is the classic RAD scenario for asthma
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Exposure to an allergen
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what is the principal characteristic of astma and the three resulting processes?
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an increased reactivity of the
trachea and bronchi to various stimuli which results in: Constriction of the bronchioles |
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describe the early phase of asthma
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Early phase actions combined to restrict the
diameter of the airway, producing shortness of breath, cough, and wheeze |
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describe late phase asthma
what do both early and late phase responses create? |
the late phase actions demonstrate the inflammatory nature of asthma.
t cells and mast cells secrete vasoactive amines which add to the problem of bronchial hyper-responsiveness, inflammation, and infiltration by various WBC classes both responses can produce hypoxemia and respiratory acidosis |
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what is MDI?
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metered dose inhaler
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how much drug gets to site of action when taken by MDI?
By dry powder inhalers/diskus inhalers? |
10%
20% |
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what is the best administration option for most drug getting to site of action
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nebulization
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what are the two types of antihistamines?
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H1 antagonists: produce selective blockade of H1 receptors
H2 antagonists: produce selective blockade of H2 receptors |
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what is the principal use of H1 antagonists?
H2 antagonists? |
treatment of mild allergic disorders
treatment of gastric and duodenal ulcers |
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what are the two classifications of antihistamines?
what is the principal difference btw the two? |
1st generation
2nd generation first gen are highly sedating and can cross the blood brain barrier, wherease 2nd gen cannot and are not sedating for the most part |
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what is the mechanism of action for histamine receptor antagonists?
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bind selectively to H1 histaminic receptors, thereby blocking the actions of histamine at these sites. they are blockers, they do not prevent the release of histamine from mast or basophil cells, they just block the binding of the histamine to the receptor by competing for the receptor.
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what are the adverse effects of antihistamines (mostly first gen) on the CNS?
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at therapeutic doses, causes CNS depression: reaction time is slowed, alertness is diminished, and drowsiness is likely
Overdose can produce CNS stimulation, convulsions are frequent. (young children sensitive to this) |
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what other receptor types do H1 antagonistic antihistamines bind to and block besides H1 receptors? What effect does this have?
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muscarinic receptors - causes anti cholinergic effects.
mucus membrane drying (mouth, nasal passages, throat) urinary hesitancy and constipation heart palpatations |
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dermatographism
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one of the most common types of urticaria,[1] in which the skin becomes raised and inflamed when stroked, scratched, rubbed, and sometimes even slapped
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what is a wheal?
what are wheals and flares caused by? |
raised bump, localized edema
caused by VLS into the skin, often with severe itching |
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what is angioedema?
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the rapid swelling (edema) of the dermis, subcutaneous tissue,[1] mucosa and submucosal tissues. It is very similar to urticaria, but urticaria, commonly known as hives, occurs in the upper dermis
Should be treated as a MEDICAL EMERGENCY when involving the lips - leads to swelling of larynx = intubation |
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what is rhinitis?
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Inflammation of the nasal mucosa, VLS, edema, nasal congestion
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what is a good antihistamine to use for motion sickness?
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promethazine
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what are the advantages of loratadine/claritin over diphenhdramine/benedryl
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even though claritin is much more expensive it is desirable because it has less side effects (non drowsy) and its dosing schedule is less frequent (1/day compared to one every 6 hours)
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list the uses of antihistamines
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(aka… no see, no pee, tachyee, no spit, no shit)
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how are 1st gen vs 2nd gen antihistamines metabolized?
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1st: liver met., renal elim
2nd: mix of liver met. and renal/fecal elim of active and inactive metabolites. |
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antihistamines are not useful in what cases?
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nonallergic rhinitis or colds
TheThey just dry out mucous membranes, which is good for colds, but bad for asthma… be careful |
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in full blown anaphylaxis, which should you use first, epinephrine or antihistamine
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epi! Far more important as first agent on board
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what conditions should you be very careful with when giving antihistamines? Why
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glaucoma, hyperthyroidism (tachycardia), CV disease, HTN, BPH (benign prostatic hyperplasia) or other urinary problems.
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what is always contraindicated with 1st gen antihistamines?
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alcohol (EtOh)
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what types of drugs should you be cautious with antihistamines?
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EtOh, hypnotics, anti-psychotics, anxiolytics, narcotic analgesics;
increased anticholinergic side effects: antipsychotics, TCAs, atropine, other parasympathomimetics |
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how often should glucocorticoids be used?
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on a fixed schedule, NOT PRN
2 puffs BID after B2 agonist(albuterol/bronchodilator) |
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what would you give if you wanted to prevent mast cell degranulation
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cromolyn/Intal or nedocromil/Tilade
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what is Churg-Strauss syndrome and which drug would it be associated with?
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Churg–Strauss syndrome (also known as "Allergic granulomatosis"[1]) is a medium and small vessel autoimmune vasculitis, leading to necrosis. It involves mainly the blood vessels of the lungs (it begins as a severe type of asthma), gastrointestinal system, and peripheral nerves, but also affects the heart, skin and kidneys
fluticasone |
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intranasal glucocortidoids are effective for what symtoms?
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all are
equally effective in suppression of nasal symptoms only, rhinorrhea, sneezing, nasal itching… will do nothing for eyes, bronchioles |
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intranasal glucocortidoids will take how long to give benefits?
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1 week
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intranasal glucocortidoids when given by MDI can cause what side effect and why?
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Given by MDI, the steroid is carried in a vehicle,
generally alcohol, which can dry out the mucosa and cause bleeding |
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what is the first choice medication for allergic rhinitis?
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antihistamines
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how do glucocortidoids work?
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they inhibit PGs and LTs which decreases edema and inflammation.
Need three days to get the benefits |
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how do decongestants work (which receptors?)
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Decongestants belong to the alpha-1 agonist class, meaning they seek
out the alpha-1 receptor, and as a result of stimulation, will cause vasoconstriction in the nasal mucosa, which will dramatically reduce VLS and edema, decreasing symptoms by opening up the airway and making breathing through the nose more easy |
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what is the grand-daddy decongestant?
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pseudoephedrine/sudafed
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what is a big side effect of alpha1 agonists decongestants?
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causes vasoconstriction everywhere, not just in the nose. Causes hypertension, if someone is already hypertensive, that's a problem.
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what is a good nasal decongestant and what is its side effect?
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oxymetazoline/afrin
after 4 days, your alpha1 receptors are down regulated and you need more and more, because you are decreasing the number and sensitivity to the drug. |
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rhinitis medicinotoba
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addicted to afrin/oxymetazoline = can't breath/decongested without using it every 10 minutes
Takes 1 month to get normalized |
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what is Claritin-D?
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120mg long acting psuedoephedrine (decongestant) combined with antihistamine Loratidine/claritin. Great for congestion only moderately relieved by claritin.
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why use nasal washes?
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removes mucous before taking medication to prevent medicine from staying in the mucous layer on top of the membrane.
It also takes cold viruses 12-18 hours to take hold, so if you wash it out, prevent colds. Also good for allergic rhinitis to remove allergens. |
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cough is caused by
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pharyngeal irritation
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how long does it take to make antibodies?
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7-14 days
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topical alpha 1s are not absorbed:
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systemically
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PO alpha1s do not cause:
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rhinitis medicamentosa
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when you have a cough, you must:
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drink lots of water to thin out the mucus to better bring it up
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how do you stop a dry hacking cough
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antitussives
ie.Robitussin AC |
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all narcotics are great
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antitussives
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what is a great narcotic to reduce coughing?
what is a side effect? |
codeine
causes constipation caution around kids!!! b/c of respiratory depression |
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what is poor man's robitussin AC?
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tylenol with codeine
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how do antitussives work?
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An antitussive suppresses a cough by acting within the
CNS, or more peripherally by decreasing pharyngeal irritation, or both |
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What does Robitussin DM contain to reduce cough?
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DM=dextromethorphan, the D-isomer of
morphine… no analgesic properties but a good antitussive |
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what is the big drug reaction that you have to watch out for when giving dextromethorphan?
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monoamine oxidase inhibitors (MAOIs) (anti-depressants)
Causes big drug interaction by an unknown mechanism = apnea, muscular rigidity, hyperpyrexia, laryngospasm |
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cromolyns are what?
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mast cell stabilizers
great alternative to flonase |
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a cold virus that has taken up residence in the Upper respiratory tract will cause:
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inflammation, and release of vasoactive amines:
histamine, PG and LT |
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what is the mechanism of action for decongestants?
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Decongestants belong to the alpha-1 agonist class, meaning they seek
out the alpha-1 receptor, and as a result of stimulation, will cause vasoconstriction in the nasal mucosa, which will dramatically reduce VLS and edema, decreasing symptoms by opening up the airway and making breathing through the nose more easy |
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what are the two primary decongestants to know
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psuedoephedrine/Sudafed PO
Oxymetazoline/Afrin Nasal inhalant (topical) much faster acting than PO |
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what is the big side effect to watch for when using PO decongestants (i.e. pseudoephedrine)
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hypertension - watch for in people with uncontrolled HTN and CV disease
But 60/TID should not produce any CV effects |
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if you are congested due to:
Allergic rhinitus, you need a: rhinovirus, you need a |
antihistamine
decongestant |
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what is the limiting factor with cromolyns?
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short half life means increase dosing frequency, 3-6 times per day, limits compliance
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what are some side effects of alpha1 agonists (decongestants) if taken PO?
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If taken PO can over-stimulate the CNS by increasing
HR and BP, nervousness, palpitations, possibly HTN, urinary retention |
