Nutrisi Dan Toksikologi

Question 1

marijuana (Cannabis) withdrawal syndrome

Answer 1

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.

Question 2

Opiat intoxication

Answer 2

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.

Question 3

Treatment opiate overdose

Answer 3

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.

Question 4

Tatalaksana jangka panjang ketergantungan opiat Dan alkohol

Answer 4

Naltrexone is also an opioid
antagonist, but used in longer-term treatment of opioid and alcohol
dependence

Question 5

Opiate withdrawal

Answer 5

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.

Question 6

Mekanisme aksi opiat

Answer 6

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.

Question 7

Mekanisme aksi amphetamine

Answer 7

Amphetamines work by causing direct release of dopamine and

norepinephrine and inhibiting their reuptake.

Question 8

Mekanisme aksi cocain

Answer 8

Cocaine works by
primarily inhibiting presynaptic reuptake of dopamine (as well as
serotonin and norepinephrine).

Question 9

Klinis penggunaan Amphetamine and cocaine

Answer 9

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

Question 10

alcohol intoxication.

Answer 10

Symptoms include
confusion, somnolence, ataxia, dysarthria, hypotension (later
hypertension), impaired judgment, and tachycardia

Question 11

Wernicke’s encephalopathy

Answer 11

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.

Question 12

Korsakoff
syndrome

Answer 12

The
chronic phase of Wernicke’s encephalopathy, known as Korsakoff
syndrome, is associated with anterograde amnesia, although there
are components also of retrograde amnesia.

Question 13

Mekanisme aksi alkohol

Answer 13

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.

Question 14

Alkohol withdrawal

Answer 14

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.

Question 15

Mekanisme aksi nikotin

Answer 15

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.

Question 16

Mekanisme efek stimulasi kafein

Answer 16

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.

Question 17

phenylcyclohexyl piperidine / phencyclidine (PCP)

Answer 17

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,

Question 18

Mekanisme aksi PCP

Answer 18

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.

Question 19

Keracunan arsenic

Answer 19

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.

Question 20

Diagnosis Dan tatalaksana keracunan arsenic

Answer 20

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).

Question 21

Keracunan sianida

Answer 21

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.

Question 22

Diagnosis Dan tatalaksana keracunan sianida

Answer 22

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.

Question 23

Keracunan merkuri

Answer 23

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.

Question 24

Tatalaksana keracunan merkuri

Answer 24

Treatment includes chelation therapy with British Anti-Lewisite,
penicillamine, 2,3 dimercaptopropane-1-sulfonate, and
dimercaptosuccinic acid

Question 25

Keracunan CO

Answer 25

CO is an odorless, tasteless, colorless gas. It binds to the
iron moiety of heme in hemoglobin with much higher affinity than
does oxygen, forming carboxyhemoglobin, which results in
impaired oxygen transport and utilization. It competes with oxygen
in binding hemoglobin. This binding leads to a structural change,
which limits the ability of the other three oxygen binding sites to
release oxygen to peripheral tissues and hence the cherry-red
flushed coloration. It can also lead to CNS lipid peroxidation and
delayed neurologic sequelae. Some sources include poorly
functioning heating systems and improperly vented fuel-burning
devices such as kerosene heaters, charcoal grills, camping stoves,
gasoline-powered generators, and motor vehicles. Symptoms most
commonly include headache, nausea, malaise, dizziness, and
cherry-red skin coloration. Severe toxicity can cause seizures,
encephalopathy, coma, and cardiovascular instability.

Question 26

Diagnosis Dan tatalaksana keracunan CO

Answer 26

Diagnosis is
based on clinical history and elevated carboxyhemoglobin levels
(which may be normally elevated to an extent in smokers).
Other family members in the same
household may have similar symptoms, which gives a clue to
diagnosis.
Treatment should include high-flow 100% oxygen via a
nonrebreather mask. In severe cases, histopathology in chronic
stages reveals necrosis in the globus pallidus and confluent areas of
necrosis in subcortical white matter.

Question 27

Lead poisoning

Answer 27

lead intoxication as lead-based paint in old houses has been a
frequent etiology, especially in children. Many other occupational
exposures are possible but would be seen more in adults. Lead
inhibits the sulfhydryl-dependent enzymes such as γ-aminolevulinic
acid dehydratase and ferrochelatase in heme synthesis, which
causes disruption of hemoglobin synthesis and leads to the
production of free erythrocyte protoporphyrins. Lead also
competes with calcium in several biologic systems and processes,
such as mitochondrial respiration and nerve functions, and has
been implicated as contributing mechanisms in neurotoxicity.
Common symptoms of lead toxicity include abdominal pain (lead
colic), constipation, myalgias, arthralgias, seizures, psychomotor
slowing, headache, and anorexia. Basophilic stippling of red blood
cells and microcytic hypochromic anemia are often seen. In
addition, a bluish pigmentation at the gum-tooth line is sometimes
seen. A peripheral neuropathy classically with extensor weakness
or “wrist/ankle drop” is associated with lead toxicity and is due to
an axonal degeneration that primarily affects motor nerves.
Generally, removal from the lead source is the only treatment
needed, although chelation therapy with 2,3-dimercaptosuccinic
acid (succimer), and calcium disodium ethylenediaminetetraacetate
are also available

Question 28

manganese toxicity.

Answer 28

manganese toxicity most
commonly seen in those with chronic liver disease (impaired
biliary excretion), those receiving total parenteral nutrition containing manganese, and those in the welding and steel
industries. Symptoms include parkinsonian features, tremors,
incoordination, confusion, personality changes, hallucinations,
agitation, psychosis (manganese madness), memory disturbances,
headache, and aggression. Brain MRI may show high T1 signal
predominantly in the globus pallidus. Chelation therapy with
ethylenediaminetetraacetate has been used as treatment.

Question 29

Keracunan methanol

Answer 29

Methanol and
ethylene glycol are found in automotive antifreeze, de-icing
solutions, antifreeze, and windshield wiper fluid and solvents,
among others. Symptoms include nausea, headache, visual
complaints, blindness, dizziness and encephalopathy, inebriation,
and sedation. Findings classically include necrosis of optic nerves
and the putamen on neuroimaging. Toxicity occurs when methanol
is oxidized by alcohol dehydrogenase and aldehyde dehydrogenase,
forming the metabolite formate. Formate causes retinal injury and
permanent blindness and injury to the basal ganglia (especially
putamen).

Question 30

Tatalaksana keracunan methanol

Answer 30

Fomepizole can be used as treatment, which acts as an
alcohol dehydrogenase inhibitor. Ethanol can also be used to
competitively bind to alcohol dehydrogenase, preventing breakdown of methanol into its toxic metabolites. Treatment also
consists of correction of systemic acidosis.

Question 31

Intoksikasi lem / cat

Answer 31

Hexacarbon solvents are found in paints, glues (glue
sniffing), and solvents, and they also cause peripheral neuropathy,
euphoria, hallucinations, and headache.

Question 32

Keracunan pestisida / baygon

Answer 32

Organophosphates and carbamates are potent cholinesterase
inhibitors leading to severe cholinergic toxicity. Toxicity can result
from ingestion, cutaneous exposure, or inhalation. Some
organophosphates are also used as terrorist nerve agents and
include tabun, sarin, and soman.
Two common mnemonics used to remember the
cholinergic/muscarinic crisis signs are as follows:
SLUDGE: Salivation, Lacrimation, Urination, Defecation, Gastric
Emesis.
DUMBELS: Defecation, Urination, Miosis,
Bronchorrhea/Bronchospasm/Bradycardia, Emesis,
Lacrimation, Salivation.
Often these patients will develop the “intermediate syndrome,”
approximately 12 to 96 hours after exposure that consists of
weakness, fasciculations, tachycardia, hypertension, decreased
deep tendon reflexes, cranial nerve abnormalities, proximal muscle
weakness, and respiratory insufficiency. In addition, some
organophosphates can cause organophosphorus-induced delayed
neuropathy, occurring 2 to 3 weeks after exposure. Symptoms
include painful but transient “stocking-glove” paresthesias followed
by a symmetrical motor polyneuropathy with flaccid weakness of
the lower extremities, which ascends to the upper extremities.
Neurobehavioral symptoms may also occur as chronic sequelae.

Question 33

Tatalaksana keracunan pestisida / baygon

Answer 33

Atropine competes with acetylcholine at muscarinic receptors to
help prevent cholinergic activation. Since atropine does not bind to
nicotinic receptors, it is ineffective in treating neuromuscular
dysfunction, so the cholinesterase-reactivating agent pralidoxime is
typically given concurrently with atropine and is effective in
treating manifestations resulting from activation of both
muscarinic and nicotinic receptors. Benzodiazepines are used for
organophosphate-related seizures and sometimes for seizure
prophylaxis. Activated charcoal is recommended if presentation is
within 1 hour of ingestion. Gastric lavage is not recommended

Question 34

Tetanus

Answer 34

Botulism is
a potentially life-threatening neuroparalytic syndrome resulting
from exposure to botulinum toxin, produced by Clostridium
botulinum. There are at least eight distinct types of botulinum
toxin, although the most commonly involved is botulinum toxin A.
There are multiple forms of botulism including foodborne botulism
(ingestion of food contaminated by botulinum toxin), wound
botulism (infection of a wound by C. botulinum, with subsequent
production of neurotoxin), infantile botulism (ingestion of
clostridial spores that then colonize the gastrointestinal tract and
release toxin), adult enteric infectious botulism (toxin produced in
the gastrointestinal tract), and inhalational botulism (aerosolized
toxin related to acts of bioterrorism).
Botulinum toxin binds to the synaptotagmin II receptor on
presynaptic cholinergic synapses and neuromuscular junctions.
After the heavy chain of the toxin binds to the receptors, the light
chain translocates into the nerve cell via endocytosis. Upon
entering the cytoplasm, the toxin irreversibly inhibits acetylcholine
release by cleaving various proteins involved in neuroexocytosis of
acetylcholine. Botulinum toxin A and E cleave SNAP-25; botulinum
toxin C cleaves SNAP-25 and syntaxin; and botulinum B, D, F, and
G cleave synaptobrevin. Reversal of this inhibition requires
sprouting of a new presynaptic terminal and formation of a new
synapse. This generally takes 3 to 6 months. Although the toxin can
be quite harmful, these effects are used for therapeutic purposes,
such as for the treatment of dystonia, spasticity, and other
neurologic disorders.
Symptoms related to foodborne botulism may begin within 12 to
36 hours after ingestion of the toxin but may be delayed for
several days. Symptoms include acute onset of multiple cranial
neuropathies, blurred vision (due to fixed pupillary dilation),
symmetric descending weakness, urinary retention, and
constipation. Gastrointestinal symptoms such as diarrhea,
abdominal pain, nausea, and vomiting often precede neurologic
symptoms in foodborne botulism