Blood Poisonings Flashcards
hemoglobin binding disorders
- carbon monoxide poisoning
- methemoglobinemia
carbon monoxide poisoning - overview
*exposure to CO that leads to hypoxia (low tissue oxygen)
*leading cause of death due to unintentional poisoning
*risks:
-exposure to methylene chloride (paint thinner)
-vehicle exhaust exposure
-smoke inhalation
-exposure to wood-burning heaters, charcoal, gas, or petroleum
carbon monoxide poisoning - clinical presentateion
*headache, lightheadedness, nausea/vomiting
*physical exam:
-NORMAL PULSE OX
-dyspnea
-chest pain
-tachycardia
-altered mental status
-CHERRY-RED SKIN
carbon monoxide poisoning - pathogenesis
*CO displaces O2 from Hg via COMPETITIVE INHIBITION:
-causes a LEFT SHIFT in the O2-hemoglobin curve (decreased O2 delivery to tissues)
*binds to cytochrome oxidase (disrupts electron transport chain)
carbon monoxide poisoning - diagnosis
*NORMAL O2 saturation, BUT tissue hypoxia is present (elevated lactic acid)
*ABG (low pH, metabolic acidosis) or portable CO monitor
*carboxyhemoglobin levels normal (< 3% for non-smokers, < 10% for smokers)
*elevated LACTIC ACID
*elevated TROPONIN due to myocardial injury; check EKG
carbon monoxide poisoning - treatment
*remove CO source
*RESPONDS to 100% oxygen:
-displaces CO from Hb
-decreases half-life of CO
*hyperbaric oxygen:
-second line treatment
-reserved for children, pregnant, persistent mental status changes
methemoglobinemia - overview
*a disease of reduced oxygen-carrying capacity of hemoglobin in which some or all reduced (ferrous) Fe2+ iron in Hb are OXIDIZED (ferric) to Fe3+
*congenital:
-defect in cytochrome b5 reductase or defect in Hb M (genetic mutation in globulin)
*acquired (most common):
-exposure to oxidizing: direct oxidizing agents (benzocaine), indirect oxidizing agents (nitrates), or metabolic activation (dapsone)
methemoglobinemia - symptoms
*symptoms are based on % of Met-Hb:
-asymptomatic
-lightheaded, headache
-cyanosis, tachypnea
-altered cardiac arrhythmias
-seizure
-death
note - does NOT improve with supplemental O2
methemoglobinemia - diagnosis
*REFRACTORY (non-responsive) to supplemental oxygen
*ABG diagnosis for % methemoglobinemia, ABG sat is inaccurate
*pulse ox is inaccurate
methemoglobinemia - pathophysiology
*forms when iron is oxidized Fe3+
*shifts the O2-dissociation curve to the LEFT (decreased O2 delivery to tissue)
*REFRACTORY to supplemental oxygen treatment
*associated with G6PD, but NOT due to G6PD deficiency
methemoglobinemia - treatment
*remove from inciting agent
*methylene blue -> activates methemoglobin reduction (side effect: turns urine blue/green)
*supplemental oxygen
electron transport chain-mediated blood poisonings
- cyanide poisoning
- arsenic poisoning
cyanide poisoning - overview
*toxic salt
*exposure through inhalation, ingestion, direct contact
*sources:
-fires (carpets and textiles)
-occupational exposure: plastic, rubber, pesticides
-medical: sodium nitroprusside (prevented by adding thiosulfate)
-diet: stone fruits (cherries, apricots, plums, peaches), apple seeds
*serum levels of cyanide 2.5x higher in smokers
cyanide poisoning - clinical presentation
*hypoxia NOT RESPONSIVE to supplemental O2
*headache, confusion, vertigo
*physical exam:
-CHERRY-RED SKIN
-ALMOND SMELL (esp. breath and skin)
-cyanosis
-nausea/vomiting
-tachycardia/HTN followed by bradycardia and hypotension
cyanide poisoning - pathogenesis
*cyanide binds to Fe3+ in the mitochondrial CYTOCHROME COMPLEX IV → NO ATP PRODUCTION
*cells can’t utilize O2
*cells convert to anaerobic metabolism → accumulation of lactic acid + METABOLIC ACIDOSIS
*results in functional hypoxia (cells unable to use O2)
cyanide poisoning - diagnosis
*elevated lactic acid → anaerobic metabolism
*ABG: METABOLIC ACIDOSIS with anion gap
*cyanide concentration
cyanide poisoning - treatment
*remove from exposure (consider clothing as a source)
*supplemental O2 not helpful but started regardless
*HYROXOCOBALAMIN - combines with cyanide to form cyanocobalamin, which is renally excreted
*sodium thiosulfate - converts cyanide to thiocyanide, which is renally secreted
*activated charcoal if oral ingestion
arsenic poisoning - overview
*naturally occurring element in Earth’s crust
*found in crustaceans
*tasteless, odorless
*exposure through:
-rock, mining
-semiconductors
-fossil fuel combustion
-moonshine
-inhalation
arsenic poisoning - clinical presentation
*symptoms are organ-specific
*acute poisoning: nausea/vomiting, abdominal pain and watery diarrhea, GARLIC ODOR to breath and stool
*chronic exposure: skin lesions, peripheral neuropathy
arsenic poisoning - pathogenesis
*RBCs absorb arsenic and distribute to tissues
*inhibits pyruvate dehydrogenase and acetyl-CoA formation
*INHIBITS ATP FORMATION and therefore depletion of ATP stores
arsenic poisoning - diagnosis
*24 hour urine collection = GOLD STANDARD
*abdominal x-ray: radiopaque metallic flecks
*CBC - anemia 2/2 hemolysis
*CMP - renal & liver function
*UA for proteinuria
*EKG for QTc or arrhythmias
arsenic poisoning - treatment
*don’t delay treatment for confirmatory test results
*CHELATION THERAPY (binds the arsenic and helps eliminate from the body)
*treat cardiac arrhythmias
