“Cherry red cyanosis”
Carbon monoxide poisoning
Oxidizing agents - Nitrogen oxide poisoning
“Chocolate cyanosis”
Carbon monoxide competes with O2 in heme binding site to form
Carboxy-hemoglobin
Nitrogen oxides oxidize Heme Fe2+ to Heme Fe3+, AKA
Methemoglobin
Strong acids interacting with flesh results in
Precipitative necrosis (coagulative necrosis)
Strong bases interacting with flesh results in
Dissolution necrosis (liquefactive necrosis)
Salicylates inhibit
COX enzymes;
causes decreased Prostaglandin synthesis
Salicylate toxicity can cause acid-base imbalance by
stimulating medullary respiratory nuclei -> hyperventilation -> Respiratory Alkalosis and
Metabolic Acidosis
Hydrocortisone
Steroidal Anti-inflammatory meds
SAIDs inhibit
Phospholipase A2 enzyme -> prevent formation of arachidonic acid -> decrease Prostaglandin synthesis
Adverse effects of SAIDs
Hyperglycemia
Cushing’s disease (thin extremities, trunk obesity, moon face, buffalo hump)
Immunosuppression
Increase protein catabolism (for GNG)- muscle wasting and poor wound healing
Decreased ACTH secretion
Narcotic analgesics cause
CNS depression;
Medullary depression -> CV and resp nuclei depression;
Cheyne-Stokes breathing;
overactive Vagus -> spastic GI tract - vomiting and constipation, sinus bradycardia, stim E-W nucleus - pupillary constriction (miosis)
Narcotic analgesics include
morphine, codeine, oxycontin
Non-narcotic analgesics include
acetaminophen/Tylenol
Non-narcotic analgesics cause
Inhibition of PG synthesis in brain
Chronic overdose of NNAs can cause
kidney failure
Acute overdose of NNAs can cause
Centrilobar hepatic necrosis
MAO inhibitors include
Tranylcypromine
MAO inhibitors cause
Increased activity at aminergic synapses- NE, serotonin;
used as an anti-depressant
Tricyclic antidepressants include
Imipramine
Tricyclic antidepressants cause
Prolonged QT interval on ECG;
Block muscarinic ACh receptors on smooth m.s, exocrine glands, and SA node -> intestinal stasis, pupillary dilation, decreased secretions- dry mucous membranes
SSRIs include
Prozac and Zoloft
(Di-)Ethylene glycol is the main component of
antifreeze
Ethylene glycol causes
CNS depression; hypocalcemia - tetany, decreased myocardial contractility and peristalsis
Ethylene glycol forms
Oxalic acid in the liver and
Calcium Oxalate stones in soft tissue**
The preferred substrate for Alcohol Dehydrogenase is
Ethyl alcohol
Hypocalcemia from ethylene glycol poisoning causes tetany by acting on the
Axon Hillock
Methanol consumption will result in
Metabolic acidosis and an
Increase in Anion Gap acidosis
Metabolism of ALL lower alcohols (few carbons) can result in
ATP synthesis
Alcohol is oxidized by the enzyme
Alcohol Dehydrogenase
alchohol dehydrogenase removes a H+ via the coenzyme
NAD+
Alcohol is oxidized to form an
aldehyde
Aldehyde is oxidized to form
a weak acid (proton donor)
The weak acid resulting from alcohol metabolism
ionizes to form an Anion and H+
Chronic alcoholism can cause
Fatty liver, cirrhosis, portal hypertension, and esophageal varices
Acute overdose of alcohol can cause
CNS depression, Hypoglycemia, and Metabolic acidosis
Subacute overdose of alcohol can cause
Decreased LES (cardiac sphincter) tone -> heartburn -> GERD; Increased HCl secretions -> gastritis
The most common type of metabolic acidosis
Lactate acidosis (forms acetic acid and acetate)
Management of alcohol overdose
D5W infusion (5% dextrose/water) and Thiamine (vitamin B1)
Alcohol Aversion Therapy (Disulfiran)
Increases blood concentration of Acetaldehyde (by inhibiting Aldehyde dehydrogenase)
Formate anion is the product of methanol metabolism, which causes
Destruction of ganglion cells at the retina, leading to blindness
Methanol and ethylene glycol poisoning are treated by
Titrated doses of Ethyl alcohol/Ethanol, the preferred substrate for Alcohol DH - gives the kidneys time to filter out MetOH/EG