6 - Nutritional, Toxic Disorders

Question 1

Thiamine (B1) deficiency

• function
• derived from
• in USA

Answer 1

Facilitates multiple biochemical rxns

• essential for energy production
• plays role in peripheral nerve conduction

May foods
-little in milled rice/grains = bigger problem in developing countries (rice as staple food)

Usually due to alcoholism or chronic illness (cancer)

Question 2

Thiamine (B1) deficiency
-symptoms
—early
—prolonged
—CNS

Answer 2

Non-specific irritability, decr short-term memory

Beriberi

• CV symptoms = wet
• peripheral neuropathy = dry

CNS esp with alcoholics
-Wernicke’s encephalopathy
—triad: mental impairment, ataxia, eye stuff (nystagmus, ophthalmoplegia)
-can progress to Wernicke-Korsakoff syndrome (add’l memory loss, confabulatory psychosis)

Question 3

Thiamine (B1) deficiency

• dx
• tx
• prognosis

Answer 3

Functional enzymatic assay

IV and/or oral supplementation

CV/ophthalmic improvement within 24 hours
Others gradually clear
Psychosis can be permanent

Question 4

Nutritional optic neuropathy

• misnomer
• main issue

Answer 4

Tobacco-alcohol amblyopia
-whether either susbstance has a direct effect on ON remains unclear

Nutrition - esp decr B 12, 9, 1
-esp for mitochondrial function (highly metabolically active)

Question 5

Nutritional optic neuropathy
-characterized by __
—why
—type of VF loss

Answer 5

Damage to papillomacular bundle

Most highly metabolically active = one of first things to go when nutrition is lacking

Central/centrocecal defect

Question 6

Nutritional optic neuropathy

-tx

Answer 6

Supplementation may reverse some loss, prevent progression

Question 7

Chronic toxicity
-heavy metal poisoning
—significant threat to health due to
—ex metals (4)
—pathophysiology

Answer 7

Low-level environmental and occupational exposures

Lead, mercury, arsenic, cadmium

Absorbed -> blood transfers it to bone, liver, kidney

Question 8

Chronic toxicity
-heavy metal poisoning
—problems with higher levels
—subclinical exposure
—dx
—tx

Answer 8

Acute convulsions, coma, death

Neurodegenerative delays (children), cognitive dysfunction and HTN (adults)

Blood levels

ID/eliminate exposure
Chelation as indicated (oral, IV, IM)
-formation of formic acid disrupts mitochondria (similar to nutritional)

Question 9

Acute poisoning and drug overdose
-basics of dx
—physical exam: stimulated, depressed, discordant, normal

Answer 9

Stim: pupillary mydriasis, incr pulse, BP, respiration, temp, etc.

Dep: miosis, decr vitals

Dis: mixed vital signs and neuromuscular abnormalities

Normal status may exist initially with “toxic time bombs”

Question 10

Acute poisoning and drug overdose
-methanol toxicity
—common sources
—adverse effects result from
—presentation
—dx
—tx

Answer 10

Household cleaning products, poorly distilled moonshine, industrial solvents

Metabolic acidosis (formic acid)

Symptoms generally w/in 24-48 hrs

• neurologic
• visual dysfunction: swollen/hyperemic ON

Primarily from history

Supportive, bicarb, antidote, hemodialysis
-ethanol can be used to bind methanol so it will be excreted

Question 11

Acute poisoning and drug overdose
-carbon monoxide poisoning
—what it is, does
—presentation
—dx
—tx

Answer 11

Colorless, odorless gas produced when burning fuels
Replaces O2 in RBCs (displaces, binds 200x more strongly)

Blurred vision, HA/dizzy, nausea/vomiting, dispnea, confusion, death

• may go unnoticed if sleeping/intoxicated
• vision affected bc occipital (postchiasmal) is affected

Hx, blood sample

Pure or hyperbaric O2