Nutrisi Dan Toksikologi Flashcards
Obat , toksik, antidotum
marijuana (Cannabis) withdrawal syndrome
marijuana (Cannabis) withdrawal syndrome has been debated.
The World Health Organization’s International Classification of
Diseases-10th Revision does recognize a cannabis withdrawal
syndrome. This withdrawal syndrome was not previously
recognized in the DSM-IV but included in the DSM-V. Symptoms of
cannabis withdrawal syndrome may include nervousness or
anxiety, decreased appetite or weight loss, insomnia, restlessness,
irritability, anger or aggression, depressed mood, and physical
symptoms such as headache, fever, chills, sweating, tremors and/or
abdominal pain. Marijuana is typically smoked, although it is also
ingested orally when added to other foods or drinks. One of the
most studied cannabinoids in cannabis is δ-9-tetrahydrocannabinol
(THC), and this accounts for its psychoactive effects. This is in contrast to cannabidiol (CBD), which has no psychoactive effects
and accounts for many of the medicinal properties of cannabis.
Common side effects include increased appetite (THC is sometimes
used for anorexia and as an antiemetic in cancer and AIDS
patients), tachycardia, dry mouth, conjunctival injection, excessive
laughter, memory impairment, poor attention span, sedation,
paranoia, anxiety, delusions, impaired coordination, and poor
insight and judgment. Chronic use may cause flat affect, apathy,
lack of motivation, and neurocognitive and memory impairments,
especially when used in adolescence. THC is active in the ventral
tegmental area, nucleus accumbens, hippocampus, caudate nucleus,
and cerebellum. THC’s effects on the hippocampus may help
explain the memory problems that can develop with the use of
cannabis, and those on the cerebellum may help explain the loss of
coordination and imbalance sometimes seen.
Opiat intoxication
Opiate use and intoxication classically are associated with miosis,
or pinpoint pupils, not mydriasis. Of note, this must be
differentiated from pontine lesions, which can also cause pinpoint pupils. All of the other options can be seen with opiate
intoxication, including decreased body temperature and coma. In
addition to these findings, common side effects include euphoria,
drowsiness, analgesia, and constipation (hence the use of opiates
and opiate derivatives as antidiarrheals). Opiate toxicity/overdose
creates a “silent gut”, which can help in the diagnosis. Because of
its cough suppressant effects, codeine is sometimes used in cough
medicines.
Treatment opiate overdose
Treatment of suspected opiate overdose includes the opioid
antagonist naloxone at 0.4 to 2 mg intravenously every 2 to 3
minutes. The diagnosis should be questioned if there is no response
even after administration of 10 mg.
Tatalaksana jangka panjang ketergantungan opiat Dan alkohol
Naltrexone is also an opioid
antagonist, but used in longer-term treatment of opioid and alcohol
dependence
Opiate withdrawal
Opiate withdrawal occurs within hours to several days of
cessation. Withdrawal symptoms are often quite severe and cause
significant functional impairment. They include dysphoria,
myalgias, nausea, vomiting, rhinorrhea, lacrimation, piloerection,
diaphoresis, diarrhea, mydriasis, fever, and insomnia. Difficulty
often exists in differentiating opiate from sedative (e.g., alcohol,
benzodiazepines) withdrawal. Hyperactive deep tendon reflexes
(DTRs) can help in this differentiation because increased DTRs are
typical in alcohol or sedative withdrawal but not opioid
withdrawal. Therefore, if you see increased DTRs and give more
opioids for suspected opioid withdrawal in the setting of actual
sedative withdrawal, benzodiazepine or alcohol withdrawal
seizures will be a likely complication.
Mekanisme aksi opiat
Opiates are one of multiple euphoria-producing drugs. All
euphoria-producing drugs cause release of dopamine from the
midbrain to the forebrain in the reward circuit (ventral tegmental
area and the nucleus accumbens). The caudate nucleus is included
in this pathway. These areas contain especially high concentrations
of dopaminergic synapses. The opiates also interact with other
structures modulated by endorphins, including the amygdala, locus
coeruleus, arcuate nucleus, thalamus, and the periaqueductal gray
matter, which influence dopaminergic pathways indirectly. There
are natural and synthetic forms of opiates. Opioid receptors are a
group of G-protein coupled receptors, with opioids acting as
ligands. The endogenous opioids are dynorphins, enkephalins,
endorphins, and endomorphins. There are four major subtypes of
opioid receptors. The first is δ, including subtypes δ1 and δ2. They
are involved with analgesia, antidepressant effects, and physical
dependence. The second is κ and includes κ1, κ2, and κ3. These are
involved in spinal analgesia, sedation, miosis, and inhibition of
antidiuretic hormone release. The third is μ and includes μ1, μ2, and
μ3. The subtype μ1 is involved in supraspinal analgesia and physical
dependence; μ2 is involved in respiratory depression, miosis,
euphoria, reduced gastrointestinal motility, and physical
dependence. The actions of μ3 are not clear. The fourth is
ORL1/orphanin (or nociceptin receptor), which is involved in
anxiety, depression, appetite, and development of tolerance to μ
agonists.
Mekanisme aksi amphetamine
Amphetamines work by causing direct release of dopamine and
norepinephrine and inhibiting their reuptake.
Mekanisme aksi cocain
Cocaine works by
primarily inhibiting presynaptic reuptake of dopamine (as well as
serotonin and norepinephrine).
Klinis penggunaan Amphetamine and cocaine
Amphetamine and cocaine use
present with similar findings, which include mydriasis (as opposed
to opiates, which cause miosis), euphoria, tachycardia, cardiac
arrhythmias, hypertension, nausea/vomiting, weight loss,
diaphoresis, agitation, anxiety, respiratory depression, seizures,
psychosis, formication (sensation of crawling bugs on skin),
dyskinesias, and dystonia. Stroke and myocardial infarction can
occur
alcohol intoxication.
Symptoms include
confusion, somnolence, ataxia, dysarthria, hypotension (later
hypertension), impaired judgment, and tachycardia
Wernicke’s encephalopathy
Wernicke’s encephalopathy is characterized by confusion/mental
status changes, ataxia, ophthalmoplegia, and nystagmus. The
chronic phase of Wernicke’s encephalopathy, known as Korsakoff
syndrome, is associated with anterograde amnesia, although there
are components also of retrograde amnesia. MRI findings in
Wernicke’s encephalopathy may include petechial hemorrhages
classically in the mammillary bodies, but also in hypothalamus,
medial thalami, and periaqueductal gray matter, sometimes even
extending into the medulla, with atrophy seen in chronic stages.
Acute thiamine deficiency does not typically lead to changes in the
caudate nucleus.
Korsakoff
syndrome
The
chronic phase of Wernicke’s encephalopathy, known as Korsakoff
syndrome, is associated with anterograde amnesia, although there
are components also of retrograde amnesia.
Mekanisme aksi alkohol
Alcohol and other sedative-hypnotic drugs affect not only the
basic structures of the reward circuit but also several other
structures that use GABA as a neurotransmitter. GABA is one of the
most widespread neurotransmitters in several parts of the brain,
including the cortex, the cerebellum, hippocampus, amygdala, and
superior and inferior colliculi. Alcohol exerts its effects by
stimulation of the GABAA receptor, similar to the mechanism of
action of benzodiazepines. This is why benzodiazepines are used to
prevent withdrawal symptoms. Alcohol also inhibits glutamateinduced excitation, which leads to additive CNS-depressant effects.
Alkohol withdrawal
Alcohol withdrawal can be quite severe and can even lead to death
if not treated appropriately. Minor withdrawal symptoms begin
within 6 to 36 hours from the last drink and include headache,
tremors, diaphoresis, palpitations, insomnia, gastrointestinal upset,
diarrhea, anorexia, agitation, and anxiety. Mentation is preserved
during this period. Seizures can occur generally 6 to 48 hours after
the last drink. Alcoholic hallucinosis begins at 12 to 48 hours and
includes hallucinations (mostly visual but can also be auditory and
tactile), intact orientation, and stable vital signs. Delirium tremens
occurs at 48 to 96 hours if adequate prophylaxis is not initiated and
is characterized by delirium, hallucinations, disorientation,
agitation, encephalopathy, hypertension, tachycardia, arrhythmias,
low-grade fever, and diaphoresis. In severe cases, delirium tremens
can be fatal. β-Blockers and calcium channel blockers can be used
for hypertension and tachycardia, although these will merely mask
symptoms.
Mekanisme aksi nikotin
Nicotine is an agonist at nicotinic acetylcholine receptors. Nicotine
leads to increased levels of several neurotransmitters, especially
dopamine, in the reward circuits of the brain. This leads to
euphoria, relaxation, and addiction. Nicotine in tobacco stimulates
several areas in the reward circuit and its connections, such as the
noradrenergic neurons of the locus coeruleus. Several other areas
in the brain that secrete acetylcholine, such as the hippocampus
and cortex, also appear to be affected by nicotine, and this may
explain the increased attentiveness that smokers often describe
after nicotine ingestion.
Mekanisme efek stimulasi kafein
Adenosine is a purine nucleotide that is released in the brain,
primarily from astrocytes. Adenosine normally inhibits release of
excitatory neurotransmitters, leading to reduced neuronal firing
rate and decreased cortical excitability. Caffeine competitively
antagonizes the adenosine A1 and A2A G-protein–coupled receptor
subtypes. The resulting decreased activity of adenosine by caffeine
leads to increased release of excitatory neurotransmitters, and thus
the stimulating effects noted with caffeine.
phenylcyclohexyl piperidine / phencyclidine (PCP)
phenylcyclohexyl piperidine, more commonly known as
phencyclidine (PCP). This was a drug developed initially as a
dissociative anesthetic, primarily used in animals. It is structurally
similar to ketamine, which is used for medical anesthesia.
Hypertension, tachycardia, nystagmus (vertical, lateral, horizontal,
Mekanisme aksi PCP
PCP is used by oral, intravenous, or intranasal routes. It acts as a
noncompetitive antagonist at the glutamate NMDA receptor. PCP
has been shown to affect biogenic amine (dopamine,
norepinephrine, serotonin) release and reuptake. These actions
probably account for the sympathomimetic effects of PCP.
PCP is structurally similar to ketamine, but it differs from
ketamine in that it is longer acting, is more likely to cause seizures,
and tends to cause more emergent confusion and delirium.
Ketamine also acts as a noncompetitive antagonist of the NMDA
receptor. It also has interactions with muscarinic, nicotinic, and
cholinergic receptors and inhibits reuptake of norepinephrine,
dopamine, and serotonin.
Keracunan arsenic
Arsenic is a naturally occurring element most commonly
incorporated into organic or inorganic compounds, both of which
are very toxic. It can also occur in gas form. With acute exposure,
symptoms may develop within minutes to hours and usually begin
with gastrointestinal symptoms such as abdominal pain, nausea,
vomiting, and diarrhea. A garlic odor on the breath is
characteristic. These symptoms can be followed by hypotension,
dehydration, and cardiac and respiratory instability. Delirium,
encephalopathy, coma, and seizures may occur. Other acute
manifestations include proteinuria, hematuria, and acute tubular
necrosis. If patients survive, within 1 to 3 weeks, they can develop
hepatitis, pancytopenia, and a symmetric sensorimotor peripheral
neuropathy, which typically begins with distal paresthesias,
followed rapidly by an ascending sensory loss and weakness, which
mimics Guillain–Barré syndrome. The neuropathy can progress to
intense burning pain, especially in the soles. In addition,
dermatologic lesions can occur and may include alopecia, oral
mucosal ulcerations, diffuse pruritic macular rash, and scaly rash
on the palms and soles. A dry hacking cough and Mees lines
(horizontal 1 to 2 mm white lines on the nails) may also occur. In
chronic poisoning, the peripheral neuropathy and dermatologic
symptoms are usually more prominent than the gastrointestinal
symptoms. Cancers of the liver, bladder, kidney, skin, lung, nasal
mucosa, and prostate have been reported with chronic exposure.
Diagnosis Dan tatalaksana keracunan arsenic
After a suspected acute ingestion of arsenic, abdominal
radiographs may reveal gastrointestinal radiopaque material. Urine
arsenic levels are preferable to blood arsenic levels, but both can
be used. Fish or shellfish intake within the previous 48 to 72 hours
can cause falsely elevated levels of arsenic. For chronic exposure,
hair and nail samples can be analyzed for the presence of arsenic,
and 24-hour urine arsenic or spot urine arsenic and creatinine
levels can be checked. Additional evaluations should include renal
and liver function tests, complete blood cell count, urinalysis, and
electrodiagnostic testing if there are symptoms of peripheral
neuropathy. A distal sensorimotor axonopathy is the typical
finding.
Acute treatment includes fluid and electrolyte replacement,
cardiac monitoring, activated charcoal, and chelation therapy.
Chelation agents typically used include dimercaprol (British AntiLewisite) and meso-2,3-dimercaptosuccinic acid (succimer).
Keracunan sianida
In
industrialized countries, the most common cause of cyanide
poisoning are domestic fires due to combustion of products
containing carbon and nitrogen, such as wool, silk, polyurethane
(insulation/upholstery), and plastics. There are many industrial
causes, such as electroplating in this case. There are also dietary
causes, especially from ingestion of plant products from the family
Rosaceae, including the seeds and pits of the plum, peach, pear,
bitter almond, cherry laurel, apricot, and apple.
Cyanide is a rapidly lethal mitochondrial toxin that can cause
death within minutes to hours of exposure. Cyanide competes with
oxygen and binds to the ferric ion (Fe3+) of cytochrome oxidase
a3, which inhibits this final enzyme in the mitochondrial
cytochrome complex, resulting in cessation of oxidative
phosphorylation. As a result, cells cannot use oxygen in their
electron transport chain and must switch to anaerobic metabolism.
Because of the decreased utilization of oxygen by tissues, venous
oxyhemoglobin concentration will be high, making venous blood
appear bright red and thus, the bright red coloration of skin,
similar to the effects of carbon monoxide. Cyanide also causes toxic
oxygen free radicals, release of glutamate, and inhibition of
glutamic acid decarboxylase (the enzyme that helps form the
inhibitory neurotransmitter GABA).
CNS symptoms include headache, anxiety, abnormal taste,
encephalopathy, vertigo, and seizures. Cardiovascular symptoms
include chest pain, initial tachycardia, and hypertension, then
bradycardia and hypotension, atrioventricular block, and
arrhythmias. Respiratory symptoms include initial tachypnea, then
bradypnea and pulmonary edema. Gastrointestinal symptoms
include nausea, vomiting, and abdominal pain. Skin symptoms
include flushing, cherry-red color. Cyanosis may occur late. Renal
and hepatic failure may also occur.
Diagnosis Dan tatalaksana keracunan sianida
Laboratory evaluation reveals severe metabolic acidosis with
increased anion gap, elevated lactate level, and elevated blood
cyanide level. Levels of more than 3.0 mg/L are fatal. Treatment
must be initiated quickly, and includes removal of the cyanide
source (such as from the skin) and activated charcoal. The Taylor
Cyanide Antidote Package may be used. This includes amyl nitrite,
sodium nitrite, and sodium thiosulfate. Hydroxocobalamin is also
used to directly bind and neutralize cyanide and is often combined
with sodium thiosulfate.
Keracunan merkuri
The organic
forms of mercury are the most toxic, such as dimethylmercury and
methylmercury. Some fish and shellfish concentrate mercury in the
form of methylmercury. However, inorganic forms of mercury,
such as cinnabar, are also highly toxic by ingestion or inhalation of
the dust. Besides mining, other occupational exposures to mercury
include dentistry, chloralkali industries, and thermometer factories.
It was called “mad hatter’s disease” in the past because hat makers
frequently worked with mercury to set and shape hats. If inhaled, a
fatal interstitial pneumonitis may occur. It can be absorbed through
the skin and orally ingested. Other symptoms include severe
intention tremor, cerebellar ataxia, paresthesias, tender and
inflamed gums, excessive salivation, swollen salivary glands,
change in personality, and psychiatric symptoms such as anxiety,
irritability, fearfulness, memory loss, depression, and fatigue.
Treatment includes chelation therapy with British Anti-Lewisite,
penicillamine, 2,3 dimercaptopropane-1-sulfonate, and
dimercaptosuccinic acid.
Tatalaksana keracunan merkuri
Treatment includes chelation therapy with British Anti-Lewisite,
penicillamine, 2,3 dimercaptopropane-1-sulfonate, and
dimercaptosuccinic acid
