·
Geriatric patients loose PHASE 1 of metabolism first.
·
Iodine allergies reflect primarily the hyperosmolarity of the contrast agent with resultant non-IgE mediated
mast cell degranulation.
Although
shellfish may be rich in iodine, the reaction to shellfish is usually caused by
IgE antibodies to the proteins in the fish and not the iodine.and they are not
interrelated.
·
The warfarin
dose should be decreased by half when amiodarone is started,
with close monitoring of the INR owing to amiodarone's inhibition of warfarin
metabolism.
·
Effects on thyroid function does interferon alpha-2B for
hepatitis C infection haveBoth hypothyroidism
and hyperthyroidism may be observed, and in most patients these
abnormalities are transient, requiring treatment if symptomatic.
·
Drugs that have been associated with thrombocytopenia:
Abciximab, ticlopidine, linezolid, heparin, isotretinoin, H2Ras, and
trimethoprim.
·
In patients with hyperphosphatemia, calcium carbonate be taken with or directly before
meals (calcium carbonate is more soluble at a lower gastric pH).
What calcium-containing product
should not be used as a phosphate binder in patients with renal failure is
Calcium citrate because it increases the risk of aluminum toxicity by
increasing gastric absorption of aluminum.
·
Intravenous iron products do not require test dose before
treatment are Iron sucrose and sodium ferric gluconate.
·
Diltiazem is often
used in transplant patients to achieve desired cyclosporine levels with lower cyclosporine doses because it inhibits
the hepatic elimination of cyclosporine and allows lower doses of cyclosporine
to be used.
·
SULFONAMIDE
CONTAINING DRUGS: Carbonic anhydrase inhibitors, all loop diuretics
except ethacrynic acid, thiazides, sulfa antibiotics, celecoxib,
phenothiazines, propylthiouracil, sulfonylureas,white wine
·
Concomitant use of linezolid and SSRIs may increase the
risk of serotonin syndrome. The literature supports discontinuation
of the serotonergic agent 2 weeks before starting linezolid.
Linezolid has monoamine oxidase
inhibitory activity (albeit relatively weak compared with traditional MAO
inhibitors).
·
Cholestyramine given 8 g
three times a day for 11 days is recommended for all childbearing women
stopping leflunomide, since up to 2 years may be required to reach undetectable
levels of the active metabolite.
·
Methotrexate must be used in combination with infliximab
for rheumatoid arthritis to minimize the formation of antibodies to infliximab.
·
ACE inhibitors increase the risk of Stevens-Johnson
syndrome when given with allopurinol.
·
Activated charcoal, a fine, black powder with
a high adsorptive capacity, is considered to be a highly valuable agent in the
treatment of many kinds of drug poisoning. Drugs that are well adsorbed by
activated charcoal include primaquine, propoxyphene, dextroamphetamine,
chlorpheniramine, phenobarbital, carbamazepine, digoxin, and aspirin.
Mineral acids, alkalines,
tolbutamide, and other drugs that are insoluble in acidic aqueous solution are
not well adsorbed. Charcoal also does not bind Ca, lithium (Li), or Fe.
·
We manage cyanide
poisoning first by dealing with the high reactivity of CN-with
Fe(II) in hemoglobin and the subsequent formation of Fe(III) hemoglobin. We do
that by first administering sodium nitrite
(intravenously) to regenerate active cytochromes and convert hemoglobin to the
more cyanide-reactive methemoglobin. Then we administer sodium thiosulfate to form the somewhat less
toxic and more readily excreted thiocyanate.
·
Disodium EDTA
(edetate sodium), a calcium chelator that is used to treat severe, acute
hypercalcemia, causes hypocalcemic tetany on
rapid IV administration. This effect is not observed on slow
infusion (15 mg/min) because extracirculatory calcium stores are available and
drawn upon to prevent a significant reduction in plasma calcium levels. When
Ca-Na2EDTA is given IV (it is sometimes used to diagnose or treat lead
poisoning), hypocalcemia does not develop, even when large doses are required.
·
Arsenic
is a constituent of fungicides, herbicides, and
pesticides. Symptoms of acute toxicity include tightness in the
throat, difficulty in swallowing, and stomach pains. Projectile vomiting and
severe diarrhea can lead to hypovolemic shock, significant electrolyte
derangements, and death. Chronic poisoning may cause peripheral neuritis,
anemia, skin keratosis, and capillary dilation leading to hypotension. Dimercaprol (British anti-Lewisite [BAL]) is
the main antidote used for arsenic poisoning.
·
Most of the adverse
responses to nerve gases (irreversible ACh esterase inhibitors such
as soman and sarin) are due to a buildup of ACh
at muscarinic receptors (i.e., ACh released from postganglionic
parasympathetic nerves or sympathetic/cholinergic nerves innervating sweat
glands). Those responses will be attenuated by atropine, because it is a highly
specific competitive muscarinic antagonist. However, skeletal muscle
stimulation (or eventual paralysis) involves nicotinic receptor activation.
That will not be affected by atropine, and unless other
supportive measures are provided, the patient is likely to die from ventilatory
arrest/apnea.
·
Succimer
(a more polar salt of dimercaprol; British anti-Lewisite; BAL)
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