1. BY: KATRINA APODACA

2.  Daily Vitamin › Used as a supplemental intake of iron and other essential vitamins in order to increase overall health benefits  Prenatal Vitamin › Used during pregnancy.

3.  It is a nutritional deficiency › Children & pre-menopausal woman are the most prone to developing this deficiency  Affects about 1/3 of the world population › About 1 billion people suffer with iron deficiency anemia, the most severe stage of iron deficiency

4.  Adults › Have less energy and less ability to work  Pregnant Women › Have poorer short-term memory and attention span  Adolescents › Have poorer verbal learning and memory  Infants › Have more respiratory infections

5.  Stage 1—Depletion of Iron Stores  Stage 2—Iron Deficiency without Anemia  Stage 3—Iron Deficiency Anemia (IDA) › All three deficiencies require an additional supplemental intake of iron

6. Stage 1  Iron is normally stored in the liver, spleen, and bone as ferritin. › Ferritin is the main intracellular iron protein › Ferritin levels are measured and have a direct correlation with the amount of iron stored in the body.  In this stage blood measures of hemoglobin and hematocrit usually remain in the normal range.

7. Stage 2  Iron transport through the body decreases  Hemoglobin concentration and hematocrit remain in the normal range › However ranges may be closer to the low end of the normal range

8. Stage 3  Advanced stage of iron deficiency  The absorption of iron is insignificant  Hemoglobin synthesis is impaired › Subnormal hemoglobin concentrations and hematocrits are the indications of anemia

9.  Formation of hemoglobin & certain enzymes  Essential for many enzymes that sustain good health  Transport oxygen in the blood to all parts of the body,

10.  Regulate cell growth and differentiation  Regulate immune activity  Essential for proper functioning of the liver  Protects against the actions of free radicals.

11. PharmacologyManifestations Cellular effects of Iron Target organ damage GI irritation  Vomitting, Bloody diarrhea Damage to mucosal cells  Leukocytosis & fever Venous pooling & Increase blood viscosity Hypotension Decrease brain perfusion/direct effect of iron Lethary Direct action of iron/ferritinVasodilation  Shock Complications of liver failureHypoglycemia Fatty degeneration of renal cells Renal impairment Ferrous mediated peroxidation Pulmonary hemorrhage/edema

12.  Young children are the most common hospitalized for iron poisoning › Minimum that has been reported is a total of only 200mg of iron that has killed a child  Equivalent to 7-prenatal vitamins  Children with infant siblings are at greater risk › Due to perinatal iron therapy of postpartum mothers

13.  Corrosive  Uncouples Oxidative Phosphorylation  Free Radical Production  Metabolic Acidosis  Disruption of Coagulation Proteins

14.  It is a disturbance of acid-base balance › Results in excessive acidity of the blood  Directly related symptoms include rapid breathing, confusion and lethargy  Can lead to shock or death

15.  Occurs in Phases › Phase I: Gastric › Phase II: Latency › Phase III: Shock & Cyanosis › Phase IV: Hepatic Necrosis › Phase V: GI Scarring

16. a a  Phase I : Gastric › 0-6 hrs post › Vomiting, lethargy, explosive diarrhea, asympotomatic, coma/semi-coma, irritability, seizures and hypovolemic shock  Phase II: Latency › 6-24 hrs post › Stabilization and subjective improvement › Complete recovery if mild to moderate ingestion  Phase III: Shock & Cyanosis › 12-48 hrs post › Distributive shock, vascular collapse, refractory acidosis with cyanosis and fever  Phase IV: Hepatic Necrosis › 48-96 hrs post  Cardiogenic shock and hepatic failure  Complications of liver failure  Phase V: Scarring › Pyloric scarring and gastrointestinal obstruction

17.  Deferoxamine › Mechanism of Action  Chelating agent that removes excess iron  Binds free iron to form ferrioxamine which leads to prevention of absorption and thus enhancing elimination via urine › Dose / Administration Technique  Intravenous - ≤15 mg/kg/hr  Max - 6 grams per day

18.  Hypotension due to rapid injection  Anaphylactoid reaction with rapid injection  Hypotension associated with ferrioxamine accumulation in patients with renal impairment

19.  Fever, dysuria, leg cramps, rashes and puritis  Acute respiratory distress syndrome (ARDS) with infusion durations greater than 24 hrs › Severe lung disease › characterized by a diffuse inflammation of lung parenchyma

20. When to call Signs/ Symptoms Suspect Overdose

21.  Anderson AC. Iron poisoning in children. Curr Opin Pediatr 1994;6(3): 289-94.  Tenenbein M, Rodgers GC. The four A's of decreasing the toll of childhood iron poisoning deaths. Arch Fam Med 1994;3:754-5.  Reynolds LG, Klein M. Iron poisoning — a preventable hazard of childhood. S Afr Med J 1985;67(17):680-3.  Fine JS. Iron poisoning. Curr Probl Pediatr 2000;30(3):71-90.  Shannon M. Ingestion of toxic substances by children. N Engl J Med 2000; 342 (3): 186-91.  Litovitz TL, Felberg L, White S, Klein-Schwartz W. 1995 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 1996;14(5):487-537.  Litovitz TL, Smilkstein M, Felberg L, Klein-Schwartz W, Berlin R, Morgan JL. 1996 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 1997;15(5):447-500.  Litovitz TL, Klein-Schwartz W, Dyer KS, Shannon M, Lee S, Powers M. 1997 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 1998;16(5):443-97.