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Low molecular weight endogenous amine that is found in low concentrations in most tissue except for the brain:
What enxyme plays a role in histamine degradation that, if inhibited, will cause an increase in histamine response?
g protein receptors
When histamine binds to a receptor, what causes the physiologic and pathologic responses?
- bronchial smooth muscle contraction
- separation of endothelial cells
- pain and itching due to insect stings
Five things that h1 activation causes:
Which histamine receptor has presynaptic regulation of neurotransmitter release (dopamine, GABA, glutamate, ACH, NE, and 5ht)?
The effects of these receptors on smooth muscles is rapid and transient, they are sensitive to lower histamine concentrations, they cause constriction and increased GI motility:
- hypotension from vasodilation
- reflex tachycardia
- increased capillary permeability
- decreased peripheral resistance
What are the 4 combined receptor responses of h1 and h2 on smooth muscle?
If a pt is on a beta blocker and they experience hypotension, will there be any reflex tachycardia?
- increased capillary permeability causes total body edema and depleted intravascular volume
What is one of the major treatments of anaphylaxis and why?
if they've ever had a vascetomy becuase they will be sensitive to the protamine that is given
What do we have to ask male pts before having cabg and why?
Which substance causes a predominant histamine response but is more responsive to histamine receptor antagonism?
edema and pruritis
The variable effect of histamines in human is seen when they are blocked by a h antagonist with:
hypotension and bradycardia
The variable effect of histamines in human is seen when they are not completely blocked by a h antagonist with:
surface of the mast cell and inhibits histamine release
Where does cromolyn work and what does it do?
You're in the OR, the pts PAP and PIP both increase rapidly and the PAOP falls, what is occuring?
- circulatory collapse
- bronchial artery vasoconstriction
6 clinical manifestations of anaphylaxis:
angioedema can still persist that you cannot see
Why should you let the cuff down a few minutes before pulling the ETT?
When the IgE antigen stimulates histamine, tryptase, prostaglandins, leukotrienes, kinins, and nitric oxide, what occurs?
Which antigen's mechanism is via cellular signaling via phospholipase C and what are the inflammatory cells?
Which antigen's mechanism is via complement activation and anaphylatoxin generation and what are the inflammatory cells?
Anaphylaxis or anaphylactiod:
No sensitization required and may occur at first drug exposure.
What technique does Dr. Nolan suggest when trying to get around an anaphylactoid reaction?
rocuronium, atracurium, succinylcholine
What are the alleged 3 most common NMBs associated with anaphylaxis?
- stone fruits
5 fruits that are associated with latex allergy:
multiple operations and other incidences of frequent contact with latex
What other situations place people at risk for developing latex allergy?
speed of administration
What is important in drugs that are known histamine releasers, but not for anaphylaxis, since small doses may trigger reactions?
Can pretreated patients for anaphylaxis with antihistamines or steroids still have anaphylaxis?
How many minutes before the initial loading dose of a drug should the test dose be administered?
1) Discontinuation of drug that caused it
2) 100% o2
4) IV epinephrine
6) rantidine or cimetidine
What are the steps in managing anaphylaxis?
relax the bronchial smooth muscle
Why do we give albuterol and ipratropium in anaphylactic reaction?
- to prevent late or delayed symptoms
- early hours of the resuscitation period
Why do we give corticosteroids in anaphylaxis? When do we give them?
milrinone, inhaled NO, inhaled prostacyclin
What are 4 pulmonary vasodilating drugs that can treat pulmonary HTN if blood pressure is stable?
they prevent binding of the histamine to the receptor thus preventing the response
How do h blockers work?
- Sedative and anticholinergic effects:
- Antiemetic effects:
4 to 24 hours
- Sedative effects:
- Anticholinergic and antiemetic effects:
Which second generation h1 antagonists have no sedative effects, anticholinergic activity, or antiemetic effects?
first generation h1 blockers
These h blockers are lipid soluble and can cross the BBB, they are well absorbed, and metabolized:
constipation or diarrhea
Adverse reactions of 1st gen h1 blockers (8):
H1 receptor blockers are prescribed for (4) in addition to conjunctivitis and urticaria:
H1 antihistamine overdose
Fever, excitement, pupil dilation, hallucinations, and convulsions are all signs of what?
hot as a stove
red as a beet
dry as a bone
mad as a hatter
Way to remember the S&Ss of H1 antihistamine overdose:
2nd gen h1 antihistamines
Lipid soluble with highly ionized functional group resulting in less CNS penetration, well absorbed, metabolized in the liver, and the half life is 5-6 hours:
Diphenhydramine actions (4) as a h1 antagonist (1st gen):
- allergenic and allergic reactions
- prevention of motion sickness
Indications of duphenhydramine (4):
adverse effects of diphenhydramine
Hypotension, tachycardia, dizziness, urinary retention, seizures, sedation, delirium are all adverse effects of what drug?
they are considered non-drowsy
2nd gen h1 blockers have what main difference from 1st gen h1 blockers?
This 2nd gen h1 blocker shouldn't be given with fruit juice as it decreases the efficacy and is used to treat seasonal allergies like hay fever and chronic urticaria:
peripheral h1 receptors
Which receptor do histamine blockers work on to relieve chronic urticaria?
Which 2nd gen h1 blocker has adverse reactions of somnolence, fatigue, dry mouth, pharyngitis, and dizziness?
the risk vs the benefit
Some pts that take 2nd gen h1 blockers may benefit from higher than recommended doses but what needs to be considered?
Which histamine receptors are responsible for the important stimulation of hcl acid release by the parietal cells?
- indirect parasymapthetic activation
- direct ACETYLCHOLINE parasympathetic activation on M3 receptor
2 ways in which activation of parietal cells occurs:
Indirect parasympathetic activation of the enterochromaffin cells causes what to be released?
H2 blockers prevent ____ from stimulating the ____ pump thus inhibiting the release of hcl into the stomach.
gastrin and ach
Even though h2 blockers inhibit the release of hcl, what two substances are still actively at work?
H2 blockers exhibit what kind of inhibition at the parietal cell h2 receptor?
H2 blockers suppress ____ and ____ stimulated acid secretion in a linear, dose dependent manner.
H2 receptor blockers also reduce the volume of gastric secretion and the concentration of what?
When given in usual prescription doses, h2 blockers inhibit acid what percentage of the total 24 hour acid secretion?
Are h2 blockers more effective on nocturnal acid secretion or meal stimulated acid secretion?
smelling food and chewing gum
Despite being given h2 blockers to increase the acid ph in the stomach, what two things can cause the acid to go back down preoperatively?
Is the impact of the h2 blockers on daytime and meal-stimulated acid production more or less than nocturnal and fasting intragastric ph?
- liver metabolism
- renal filtration
- renal tubular secretion
Clearance of h2 blockers is dependent on what 3 things?
The dose of h2 blockers should be decreased in renal dysfunction, hepatic dysfunction, or both?
Antagonism of the cerebral h2 receptors causes what side effects of h2 blockers?
warfarin and midazolam
Cimetidine and rantidine interfere with the cyp 450 system and can prolong what 2 drugs (Dr. Nolan mentioned)?
H2 blockers produce ____ inhibition of histamine at h2 receptors of the gastric parietal cells resulting in reduced gastric acid secretion, gastric ____, and ____ ion concentration.
- pulmonary aspiration prophylaxis
- gastric acid hypersecretion
- anaphylaxis prophylaxis (not a good idea per Dr. Nolan)
Indications for h2 blockers:
- inhibit coronary vasodilation
- inhibit increased cardiac contractility
H2 blockers may cause what 3 side effects?
So blocking the h2 receptors not only blocks their responses, but allows uninhibited responses of __ receptors.
Inhibiting the CYP 450 system causes an ____ in plasma drug levels and ____ their clearance.
bone marrow suppression
elevated LFTs (d/c drug)
Both cimetidine and rantidine have what similar adverse effects?
- high skeletal muscle contraction (myalgia)
- SJS, epidermal necrolysis, erythema multiform
Side effects of cimetidine that are absent with rantidine:
low skeletal muscle contraction (no myalgia) and no gynecomastia
What two side effects does rantidine have that differs from cimetidine?
Which of 3 h2 blockers (cimetidine, rantidine, or famotidine) has a higher renal elimination percentage of the IV dose?
decrease the clearance
What do cimetidine and rantidine do to the clearance of warfarin, phenytoin, and meperidine?
Do h2 blockers decrease the amount of acid or increase the ph of acid that is in the stomach before giving the drug?
- Nonuclear dyspepsia
- prevention of stress ulcers
- gastrinoma or other hypersecretory conditions
- preop med
PPI clinical uses:
increase gastric pH and decrease gastric volume
The goal of preop therapy of PPIs is to achieve what 2 things?
mechanism of action
PPIs are substituted benzimidazoles that resemble h2 blockers in structure but have a completely different what?
True of False:
PPIs can block both fasting and meal stimulated acid secretion whereas h2 blockers only block fasting secretion.
the proton pump
PPIs can block 90-98% of all acid secretion because they block the final common pathway of acid secretion which is what?
H/K/ATPase pump (AKA proton pump)
No matter what source of gastric acid stimulation (histamine, gastrin, or ach), there is only one way it goes from the parietal cell to the gastric lumen- what is it?
inhibit the pump
In order to stop the secretion of all gastric acid, you have to inhibit the last step in the acid secretion process which is what?
Unlike h2 blockers that competitively and reversibly bind to the h2 receptor, PPIs form a ____ disulfide bond with the ATPase enzyme, leading to an ____ inhibition of the pump.
The covalent disulfide bond that PPIs form with the ATPase pumps do not produce an ____ action, but the action is ____.
SO when the drug is stopped, what does the body have to do in regards to the ATPase pumps?
20mg night before AND
no < 3 hours before surgery
What is the ideal way to administer omeprazole as a preop dose?
UGI bleeds and h-pylori
Aside from the usual GERD, hypersecretory conditions, and preop treatments, pantoprazole is also used to treat what?
40mg IV and rantidine 50mg IV
What combination of drugs decreases gastric acid volume and increases gastric acid ph and should be given 1 hour prior to surgery?
Cromolyn can be like clonidine in respect to that it cannot be abruptly discontinued, it must be:
It prevents release of histamine, leukotrienes, prostaglandins, and platelet activating factors of what cells ONLY?
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