2. Fe formation of Hb → carry O 2 (Fe 2+ ) 65% erythrocytes 17.5% stored as Ferritin (soluble) hemosiderin (Insoluble) (Fe 3+ ) (in Macrophages) Cyt oxidase Myoglobin

3. Fe 2+ blood Fe 3+ Types of Fe 2+ salts FerrousElemental iron Fe 2+ gluconate12% Fe 2+ ferrochlorinate13% Fe 2+ Sulfate20% Fe 2+ chloride28% Fe 2+ fumarate33% Fe 2+ Bind with mucoprotein Become Fe 3+ & bind with transferrin

4.  < 20 mg/kg → mild (asymptomatic).  20 – 60 mg/kg → moderate.  60 – 180 mg/kg → severe.  200 – 250 mg/kg → lethal. E.g:patient (55 kg) ingested 60 tablets of FeSO 4 325mg each. E.g: patient (55 kg) ingested 60 tablets of FeSO 4 325mg each. 60 tab x 325 mg = 19500 mg. 20% …..i.e 100 mg FeSO 4 → 20 mg elemental Fe. 19500 mg → X so X = 3900 mg. 3900 mg → 55 kg. X ← 1kg so X = 70 mg/kg so severe.

5.  Patients who remains asymptomatic 6 or more hrs after ingestion are unlikely to develop symptoms later. 4 stages.  Iron poisoning can be divided into 4 stages. Stage I: 1 -6 hrs. Stage II: 6 – 14 hrs. Stage III: 14 – 48 hrs. Stage IV: 4 – 6 weeks.

6. Diarrhoea Vomiting Fe Bloody diarrhoea (Melena) Bloody vomitus (Hematemesis) Irritation Corrosion Irritation Corrosion GIT

7. CVS Reflex tachycardia GIT Released from damaged GIT tissue

8.  ↓ B.P  hypoperfusion  hypoxemia  anaerobic  lactic à.  Fe →uncoupling oxidation phosphorylation →↓ ATP production. CNS Lethargy, severe coma or seizures. Lactic acidosis Glucose not consumed  Hyperglycemia (at early stage). RS ↑ Medullary respiratory center ↑ R.R Tachypnea

9. Stage of recovery (Signs & symptoms of GIT subsides, patient feel normal). If patients treated early in right way  cure at this stage

10. Fe Fe Fe Fe Fe Fe Fe Fe Fe Transferrin Fe Fe Fe Fe Ferritin Hepatic Necrosis Fe in GIT (erosion) carrier (part of iron) + Free iron blood Fe Fe Fe Fe deposition in soft tissue.

11. Uncoupling oxidative phosphorylation  Excretion of HCO 3 - Metabolic Acidosis Fe ↓

12. Invasion of damaged intestinal mucosa by bacteria Passed into blood

13. Hepatic cirrhosis. Pyloric stricture (pyloric stenosis) → corrosive action.

16. a.Emetics: (. a.Emetics: as Ipeca syrup (if no hypotension or vomiting (hematemesis)). b. Gastric lavage: b. Gastric lavage: by NaHCO 3 2-3% NaHCO 3 + Fe 2+ → ferrous carbonate (insoluble salt, thus prevent absorption to blood)

17. Activated charcoal: Not used (has no affinity). c. Activated charcoal: Not used (has no affinity). d. Cathartics: used if no diarrhea & some iron reach intestine.

18.  Used when?  Serum iron > 500  g/dl, ↑ blood glucose, ↑ WBCs, ↓ B.P, seizures.  Bind what? Deferoxamine + free iron ( Fe 3+ )→ Ferrioxamine (sol coloured). Also bind with  transferrin, ferritin, hemosiderin Not bind with  iron in Hb or in cyt P 450.

19. Dose:Dose: Provocative dose: 25 – 50 mg/kg I.M if vin rose colour of urine excessive iron in blood. Dose: 50 mg/kg I.M every 4-6hrs. In Severe case: 15 mg/kg/hr I.V infusion. If ↑ rate: hypotension, erythema & urticaria. Antidote must be tapered on 24hrs to prevent pulmonary edema. Endpoint of ttt is the disappearance of vin rose colour.

20. N.B: Deferoxamine is not contraindicated in pregnancy. Deferoxamine may be transported across the placenta, chelating iron in utero so making iron therapy necessary at birth.

21.  Hypotension: Patients should be placed in Trendlenburg position. Normal saline (I.V, 1-2 liter)- not ↑ to avoid cerebral & pulmonary oedema) Dopamine (2-5  g/kg/min). NE (0.1 – 0.2  g/kg/min, if ↑ dose tissue ischemia).  Seizures: diazepam.  Exchange transfusion: may be attempted in patients who remain oliguric.

22. A 5 year old girl, weighing 25 kg, was brought 5 hours to hospital after ingesting 25 tablets of her mother’s ferrous chloride medicament. The girl was lethargic, with abdominal pain, diarrhea and hemotemesis. Her vital signs were B.P 70/50mmHg, R.R 30/min. Blood analysis revealed elevated level of lactic acidosis, and a serum iron level of 400µg/dl.

23.  Was this a toxic dose, CALCULATE in details.  If this was a toxic dose, what is the degree of toxicity, WHY?  In which stage is this girl?, rationalize your answer.  What is the cause of her low blood pressure?

24. A 16 year old boy, weighing 60 kg, committed suicide by ingesting 70 tablets of ferrous sulfate. He was brought to the E.D 6 hours after ingestion. The boy was lethargic and complained of homotemesis and abdominal pain. Upon examination he was found hypotensive, with increased level of lactic acid; testing his serum iron level it was 400µg/dl. In the department they started giving him an antidote, and shortly after his urine turned vin-rose.

25.  Was this a toxic dose, CALCULATE in details  If this was a toxic dose, what is the degree of toxicity, WHY?  Explain WHY was the urine color turned vin-rose? What does this color indicate?  What is the cause of his elevated lactic acid level?

26. C. B. is a 35-year-old 55 kg female who ingested sixty 325 mg tablets of ferrous sulfate six hours before coming to the hospital. On admission, she was diaphoretic, lethargic, and complained of abdominal pain, nausea, and vomiting. Emesis in the emergency department was guaiac positive. Vital signs were BP 85/60 mm Hg, pulse 135/minute, respirations 34/minute, and temperature 98.6° F.

27.  Assess the potential severity of this ingestion.  What additional laboratory information would be useful?  A flat plate x-ray of the abdomen revealed a clump of undissolved tablets in C. B.’s stomach. What measures can be taken to decrease iron absorption?

28.  C. B.’s serum iron concentration (on admission was 680 mcg/dL (70 to 170); her TIBC was 400 mcg of iron/dL (300 to 400). Is chelation therapy with deferoxamine indicated?  How should deferoxamine be administered? What side effects are associated with its use? What are the endpoints of treatment?  What general treatment measures are necessary in C. B.’s case?