adverse reactions

autoimmune diseases lupus

Lupus: drugs inducing itHIP:
Hydralazine
INH
Procanimide
relating to neurotransmitter
antidopaminerg
extrapyramidal
tardive dyskinesa
may persist after withdrawal
involuntary movements of jaw, tongue and face
after long term use
acute dystonic reactons (slow, prolonged muscle spasms of tongue, neck and face)
parkinsonian syndrome (bradykinic rigidity, tremor)
akathisia (motor restlessness)
prolactin elevation endocrine alteration: galactorrhea, amenorrhea, infertility, decreased libido
alpha-blockade
reflex tachycardia
orthostatic hypotension
ani-serotoninerg weight gain
antihistaminic
weight gain
sedation
anticholinergic
tachycardia
dry mouth, constipation, urinary retention, blurry vision
CNS sedation cognitive impairment
GENERAL
Type A (Augmented) Type B (Bizarre) Predictable Unpredictable Dose-dependent Dose-independent
High incidence Low incidence (90% ADRs) Often serious May respond to Generally need dose
adjustment to stop drug
endocrinal effects
thyroid
hyperthyrodism
hypothyrodism
interferon
decreases absorption of T4
raloxifene
calcium
ciprofloxacin
lithium
amiodarone
medication can alter TSH levels
somatostatin and analogs minimal effect
dopamine
agonists and antagonists
minimal effect
corticosteroids minimal effect
insulin
hyperglycaemia
furosemide
thiazides
isoniazide
pentamidine (long-term effect)
nicotinic acid
protease inhibitors
phenytoin
oestrogen
diuretics
corticosteroids
ciclosporin
beta agonist, sympathomimetics
atypical antipsychotics
hypoglycaemia
pentamidine (initial effect)
fenfluramine
fluoxetine
MAO
salicylates (large doses)
sulphonamides
beta-blockers (prolonged hypo-and masking of symptoms)
alcohol
ACE inhibitors
endocrinal effects
prolactin levels
decreasing
ergot alkaloids
L-dopa
increasing
phenothiazines
haloperidol
methyldopa
syndrome of inappropriate antidiuretic hormone secretion (SIADH)
SIADH-inducing drugs ABCD:
Analgesics: opioids, NSAIDs
Barbiturates
Cyclophosphamide/ Chlorpromazine/ Carbamazepine
Diuretic (thiazide)

Gynaecomastia-causing drugs DISCOS:
Digoxin
Isoniazid
Spironolactone
Cimetidine
Oestrogens
Stilboestrol
relating to metabolism uric acid
hyperuricemia are renal dysfunction, metabolic acidosis, tumor lysis syndrome,
purine-rich diet, and use of furosemide, thiazide diuretics, and niacin.2,15
Hyperuricemia may be associated with the development of gouty arthri-
tis, nephrolithiasis, and gouty tophi.2
Decreased Uric Acid
Decreased uric acid levels (hypouricemia) are usually of little clinical signifi-
cance but may occur with a low-protein diet, deficiency of xanthine oxidase,
or use of allopurinol, probenecid, or high doses of aspirin or vitamin C.2,1
decrease
increase nateglinide
relating to blood
There are two types of the Coombs' test:
The indirect Coombs' test looks for free-flowing antibodies against certain red blood cells. It is is most
often done to determine if you may have a reaction to a blood transfusion.
The direct Coombs' test is used to detect antibodies that are stuck to the surface of red blood cells.
Many diseases and drugs (including quinidine, methyldopa, and procainamide) can cause this. These
antibodies sometimes destroy red blood cells and cause anemia. Your doctor may order this test if you
have signs or symptoms of anemia or jaundice.
decreased platelet count
acetazolamide, acetohexamide, antimony, antineoplastic drugs, brompheniramine maleate,
carbamazepine, chloramphenicol, furosemide, gold salts, isoniazid, mephentoin, methyldopa,
sulfonamides, thiazide, heparin, valproic acid and many others.
G6PD deficiency
Glucose-6-phosphate dehydrogenase deficiency is an X-linked recessive hereditary disease
characterized by abnormally low levels of glucose-6-phosphate dehydrogenase, a metabolic enzyme
involved in the pentose phosphate pathway, especially important in red blood cell metabolism. G6PD
deficiency is the most common human enzyme defect.Individuals with the disease may exhibit
nonimmune hemolytic anemia in response to a number of causes, most commonly infection or
exposure to certain medications or fava beans. G6PD deficiency is closely linked to favism, a disorder
characterized by a hemolytic reaction to consumption of fava or broad beans, with a name derived
from the Italian name of the broad bean (fava). The name favism is sometimes used to refer to the
enzyme deficiency as a whole, although this is misleading as not all people with G6PD deficiency or
Favism will manifest physically observable symptoms to the consumption of broad beans. Symptomatic
patient are all almost exclusively males.
G6PD: oxidant drugs inducing hemolytic anemia AAA: Antibiotic (eg: sufamethoxazole)

Antimalarial (eg: primaquine)

Antipyietics (eg: acetaniliu, but not aspiiin oi acetaminophen
hemolytic anemia
isosorbid dinitrate
quinidin
phenacetin
aspirin
primaquinine
nitrofurantoin
sulfonamide
quinine
Porphyrias: acute intermittent porphyria symptoms 5 P's:

Pain in abdomen
Polyneuropathy
Psychologial abnormalities
Pink urine
Precipitated by drugs (eg barbiturates, oral contraceptives, sulpha drugs)

relating to electrolytes
Cl-levels use of acid suppressants (H2 blockers and proton pump inhibitors [PPIs])
Na-level
decreasing
2,10 Sodium depletion
may also be seen in SIADH, cystic fibrosis, mineralocorticoid deficiency, or
fluid replacement with solutions that do not contain sodium.10
SIADH may be associated with disease states such as cancer or the use of
medications, including chlorpropamide, thiazide diuretics, and carbamazepine.2
increasing
Phosphat-level
decreasing
increasing
Ca-level
decreasing loop diuretics
increasing lithiium and thiazides
K-level
decreasing and use of amphotericin B or thiazide, loop, or osmotic diuretics
increasing
2,10 Medications such as angiotensin enzyme
converting (ACE) inhibitors, angiotensin receptor blockers (ARBs), potassium
supplements, potassium-sparing diuretics, and oral contraceptives containing
drospirenone are also contributing factors to hyperkalemia.1,10
K+ increasing agents K-BANK:
K-sparing diuretic
Beta blocker
ACEI
NSAID
K supplement
CNS reaction
seizures antibiotics penicillin G, imipenem, amphotericin B, metronidazole
disulfiram like reactions
sulfonylureas
metronidazole
depression
5 drugs causing it PROMS:
Propranolol
Reserpine
Oral contraceptives
Methyldopa
Steroids
delirium
Delerium-causing drugsACUTE CHANGE IN MS:
Antibiotics (biaxin, penicillin, ciprofloxacin)
Cardiac drugs (digoxin, lidocaine)
Urinary incontinence drugs (anticholinergics)
Theophylline
Ethanol
Corticosteroids
H2 blockers
Antiparkinsonian drugs
Narcotics (esp. mepridine)
Geriatric psychiatric drugs
ENT drugs
Insomnia drugs
NSAIBs (eg inuomethacin, napioxin
Muscle relaxants
Seizuie meuicines
medicine groups
Sulfonamide side effects:
Steven-Johnson syndrome
Skin rash
Solubility low (causes crystalluria)
Serum albumin displaced (causes newborn kernicterus and potentiation of other serum
albumin-binders like warfarin)
teratogenic drugs

Antibiotics contraindicated during pregnancy MCAT:
Metronidazole
Chloramphenicol
Aminoglycoside
Tetracycline
Teratogenic drugs"W/ TERATOgenic":
Warfarin
Thalidomide
Epileptic drugs: phenytoin, valproate, carbamazepine
Retinoid
ACE inhibitor
Third element: lithium
OCP and other hormones (eg danazol)
TAP CAP Thalidomide Androgens Progestins Corticosteroids Aspirin & indomethacinPhenytoin
organ toxicity
kidney
mouth taste disturbances
Other Antihistamines, antineoplastics, bronchodilators, anti-inflammatories, smoking cessation
aids, antifungals, antivirals
acetazolamide
clacitriol
phenindione
chlorhexidine
griseofulvin
metformin
gold salts
penicillamine
aspirin
Psychotropics Most tricyclic antidepressants, some antipsychotics, anxiolytics, mood stabilizers,
hypnotics
imipramine
Endocrine medications Most thyroid medications carbimazole
Cardiac medications Many antihypertensives, diuretics, statins, antiarrhythmics
clofibrate
captopril
Neurologic medications Antiparkinsonians, CNS stimulants, migraine medications, muscle relaxants
lithium carbonate
levodopa
Antibiotics Ampicillin, macrolides, quinolones, sulfamethoxazole, trimethoprim, tetracycline,
metronidazole
metronidazole
heart
BP influenced by drugs
decreased a1 blocker effect
neuroleptics
clozapin
thioridazine
TCA
increased
erythropoetin
immunosuppressiva: ciclosporin and tacrolismus
NSAIDs
decreased GFR
decreased synthesis of prostacyclin in afferent arteries to glomeruli
estrogens increased angiotensinogen synthesis in liver
glucocorticoids, hydrocortison+prednisolon over mineralocorticoid receptors
psychostimulans
ephedrin
cocain
amphetamin
methylphenidate
noradrenalin reuptake increases
appetit inhbitiors, amfepramon or sibutramin
duloxetin
venlafaxin
reboxetin
MAO A or B antagonists
a-agonisten
torsades de pointes
TEQ Tricyclic antidepressants, Erythromycin, Quinidine
APACHE A miodarone, Procainamide, Arsenium, Cisapride, Haloperidol, Eritromycin
eye ocular toxicity
corticosteroids
phenothiazines
chlorpromazine
amiodarone
chloroquine, hydroxy-
lungs
Respiratory depression inducing drugs"STOP breathing":
Sedatives and hypnotics
Trimethoprim
Opiates Polymyxins
pulmonary toxicity
"uo BAN Ne!":
Gold Bleomycin/ Busulphan/ BCNU
Amiodarone/ Acyclovir/ Azathioprine
Nitrofurantoin
Melphalan/ Methotrexate/ Methysergide
bromocriptine
nitrofurantoin
amiodarone
bleomycine
liver
Hepatic necrosis: drugs causing focal to massive necrosis
"Very Angry Hepatocytes":
Valproic acid
Acetaminophen
Halothane
cholestatic jaundice
methyldopa
sulindac
certain TCA
trazodone
chlorpropamide
erythromycin estolate
chlorpromazine
ear
ringing in the ear quinidine
ototoxicity
loop diuretics
minocycline
animoglycosides
salicylates
hypersensitivy reactions
Pseudoallergic reactions(anaphylactoid)
They are, however, mediated pharmacologically and not immunologically (e.g. aspirin and NSAIDs in
asthma). The fact that they do not occur in everyone indicates some predisposition (e.g. genetic). This
is why this type of reaction is considered to be type B rather than type A. Cross-sensitivity occurs with
drugs which have the same action, but not structure, cf. true allergy.
Most drugs have small molecular weights (often ~300 D) and are too small to be antigenic in
themselves. They act as haptens, binding to endogenous proteins to form antigenic complexes that
incite antibody production. This process usually takes 12 weeks. Reexposure to the chemical results
in an antigenantibody interaction that provokes the typical manifestations of allergy a release of
mediators (e.g. histamine) cell damage or cell death.
see under IMMUNOLOGY
type V
Grave's disease
autoimmune disorders ???
type IV cell mediated
e.g. contact dermatitisby poison ivy)
infections (tuberculosis, leprosis,listeria)
acute graf rejection
contact dermatitis
T-cells
type III immune complex
Serum sickness (urticaria, arthralgia, lymphadenopathy and fever), is a classical presentation (e.g.
serum sickness due to sulphonamides or penicillins). Extreme form a StevensJohnson syndrome
non-organic autoimmune diseases
sjogren syndrome
rheumatoid arthritis
SLE
type II cytotoxic
(e.g. penicillinhaemolytic anaemia, quinidine thrombocytopenia,sulphonamide neutropenia).
organic autoimmune diseases
thrombocytopenia
Hashimoto
myasthenia gravis
pencillin, cephalosporin, quinidine, methyldopa may result in hemolytic anemia
Rh disease
IgM and IgG
type I immediate/anaphylactic
(e.g. anaphylaxis,urticaria and bronchospasm due to penicillin
certain vaccines
hormones
penicillin, cephalosporin
pollens
IgE
URINE CHANGES red colour
vitamin B
chlorpromazine
daunomycin / daunorubicin
warfarin
rifampicin
prochlorperazine
senna (anthrachinone)