Done early tomorrow or today

Question 1

Late causes of death in wounds

Answer 1

1. SEPSIS: Generalized infection (septicemial/ pyemia) causing septic shock or Localized infection which may be transmitted to vital organs as the lungs resulting in fatal pneumonia Tetanus caused by Cholistridium Tetanii
2. DISSEMINATED INTRAVASCULAR COAGULATION (DIC): Trauma can trigger thromboplastin-initiated coagulation. Stasis of blood flow can precipitate intravascular coagulation.
   .
3. SUPRA-RENAL HEMORRHAGE: It occurs few days after trauma. Bilateral adrenal hemorrhage leads to catastrophic adrenal insufficiency. Bilateral adrenal hemorrhage is rarely due to trauma. When unilateral, it is often clinically silent.
4. ADULT RESPIRATORY DISTRESS SYNDROME (ARDS): This lung condition is a complication of traumatic and stressful incidents including aspiration of gastric contents, inhalation of irritant gazes, sepsis , drug overdose .near drowning .
5. CRUSH SYNDROME: In case of crushing of a whole limb, as in car accidents, there will be release of myoglobin from the crushed muscles which will reach the circulation and cause irritation of the renal tubules leading to their swelling and obstruction and finally causing renal failure and death.
6. ACUTE RENAL FAILURE: Shock and decrease renal blood flow. DIC due to micro-thrombi formation. Crush syndrome.
7. SURGICAL INTERFERENCE:
   The assailant is responsible for the result of the operation so long it was indicated and skillfully done.

Question 2

MOA of CO poisoning

Answer 2

CO bind to Hb:
carboxyhemoglobin → Red coloration (Red asphyxia)
↓ association of O2 and Hb → anemic anoxia
↓ dissociation of O2 and Hb → shifting O2-dissociation curve to the left

CO bind to other iron containing protein:

Myoglobin → myocardial and Skeletal muscle dysfunction
Cytochrome oxidase (allow cells to utilize O2)
Brain lipid peroxidation → neuronal dysfunction

Question 3

Clinical picture of CO poisoning

Answer 3

Mild (↓20% COHb): headache and vomiting.

Moderate (↓40% COHb) : tachycardia, tachypnea, dyspnea, weakness, Rhabdomyolysis

Severe (↓60% COHb) coma convulsions hypotension, myocardial ischemia, hypoxia, metabolic acidosis

Fatal (↑60% COHb)

Question 4

Treatment of CO

Answer 4

Prophylactic: CO detector for workers

Curative: O2

COHb ↓ 15% → fresh air)
COHb ↑15% → 100% O2)
COHb ↑40% → Hyperbaric O2)

*Hyperbaric O2 → ↑ dissociation CO, ↑ O2 transport

Bed rest: ↓ O2 utilize

Question 5

Complications of CO poisoning

Answer 5

Amnesia.
Parkinsonism & paralysis.
changes in personalities.
depression
Encephalopathy
hearing and Visual impairment

Question 6

MOA of Cyanide

Answer 6

Blocks Cytochrome oxidase enzyme → paralysis No utilize O2→ O2 in artery = O2 in vein→ (cellular, Red asphyxia) histotoxic anoxia

Anaerobic metabolism → ↑ lactic acid → metabolic acidosis

Reduced ATP stores

Question 7

Manifestations of cyanide in face

Answer 7

Ch= characteristic smell

Question 8

Cyanide manifestations

Answer 8

Large dose: sudden death within 1 minute

Small dose:

CNS: headache, coma

CVS: bradycardia and hypertension followed by tachycardia and hypotension Res.: tachypnea followed by tachypnea and pulmonary edema metabolic acidosis

Question 9

Cyanide antidote

Answer 9

Antidote:

A) Cyanide Kit

B) Kelocyanor 300-600 mg (IV) → chelates cyanide in blood only.

C) Vitamin B12 → bind to cyanide

D) Methyl aminophenol (MAP) → rapid met-hemoglobinemia

Care of respiration: Using 100% O2
GIT decontamination: Gastric lavage (if ingested) by H2O2

Question 10

Action of kerosene (used in fuel and can be drunk by suicidal female)

Answer 10

1. Local:
   - Skin irritation.
   - Mucus membranes irritation.
2. Remote:

• CNS depression due to:
  *Direct effect (large amount).
  ·Hypoxia due to chemical pneumonitis.
  *Acidosis

Question 11

Clinical picture of a suicidal female that drank fuel? (kerosene)

Answer 11

• G.l.T irritation: nausea, vomiting, colic and diarrhea.
• C.N.S. depression: coma with cyanosis, death in 24 hours.
• Lung: aspiration pneumonitis due to its aspiration during vomiting or ingestion.

Question 12

Treatment of a suicidal female that drank fuel? (kerosene)

Answer 12

1) Supportive measures: ABC

2) GIT decontamination:
- Gastric lavage (with cuffed endotracheal tube) is indicated in: Ingestion of large amounts.

3)Decontamination of skin and eyes:
1. Remove contaminated clothes.
2. Wash skin with soap and water.
3. Irrigate exposed eyes with copious water.

4) Symptomatic: (aspiration pneumonitis)
1. Antipyretics for fever.
2. Antibiotics for bronchopneumonia.
3. Bronchodilators for bronchospasm.

Question 13

Discuss the 4 clinical phases of Paracetamol (Acetaminophen)

Answer 13

@ 24h: Asymptomatic then becomes pain, nausea and vomiting

@24-48 h: Past symptoms cease but there is elevation if bilirubin and transaminase—> upper right quadrant tenderness

@ 48-72: Fulminant hepatic failure, pancreatitis, acute renal failure, hepatic encephalopathy, hypoglycemia, metabolic acidosis

Treatment is NAC (mucomyst or parvolex)

Question 14

MOA of Paracetamol antidote

Answer 14

It is metabolized by the hepatocytes to a glutathione precursor ( cysteine) that provides protective levels of glutathione to detoxify the hepatotoxic metabolite NAPQI by providing (-SH) group (minor pathway).

Enhances sulphation conjugation by providing Sulfur

Question 15

Discuss the stages of iron toxicity and its antidote

Answer 15

6h: pain, nausea, vomiting, melena, hematemesis and dehydration and shock

6-24h: latent period; apparent recovery as there is no symptoms because iron redistributed from blood to RES cells

24-48h: Fever and leukocytosis, lethargy and coma and metabolic acidosis

Deferoxamine, deferasirox, deferiprone

Question 16

Treatment of iron toxicity

Answer 16

1. Supportive: ABC
2. GIT Decontamination: Gastric lavage using the local antidote: Na Hco3 to convert free ferrous salt into ferrous carbonate, which is poorly absorbable.

• Deferoxamine orally: binds with iron in the gut and reduces its absorption.

*Whole bowel irrigation.

3. Physiological antidote:
   Deferrioxamine: It binds free iron only. It does not bind iron in hemogiobin or myoglobin.

Administration is either l.M: in mild toxicity or l.V. infusion in severe toxicity.

Question 17

Give the acid base abnormalities that occur in aspirin toxicity

Answer 17

 Metabolic acidosis———> Metabolic alkalosis (dt : accumulation of organic acids) (dt : vomiting)

 Respiratory alkalosis ———> Respiratory acidosis
(dt : hyperventilation) (in later stages)

 Hyperglycemia ——————–> Hypoglycemia
(dt : increased glycolysis) (dt : depletion of glycogen stores)

Question 18

Give the treatment of aspirin toxicity

Answer 18

1. Supportive: ABCs
2. GIT decontamination:
   -Gastric lavage using sodium bicarbonate.
   -MDAC appears to be superior to single doses.
   -Whole bowel irrigation: helpful with sustained-release preparations and enteric-coated forms.
3. No Specific antidotes.
4. Elimination of the poison from the blood:
   -Forced alkaline diuresis: Effective in moderate toxicity (>40mg/dL in acute toxicity).
   -Hemodialysis:
   -Effective in salicylate poisoning

5.Symptomatic treatment: (See General Toxicology) Treatment of convulsion, coma, hypokalemia, hypoglycemia, cerebral edema, pulmonary edema, hyperthermia and hypotension, dehydration, metabolic acidosis & bleeding tendencies

Question 19

Discuss the MOA of digoxin and its early manifestations

Answer 19

• Slows conduction through the atrioventricular (AV) node.
• It inhibits Na+-Ka+ ATPase in the cardiac muscle fibers

1) GIT: Nausea,Vomiting,colic and diarrhea
2) Visual: Blurring and Halos (yellow/green)
3) CNS: Headache,drowsiness and disorientation
4) Hyperkalemia

Question 20

Treatment of digoxin poisoning

Answer 20

1. Supportive measures: ABC
2. G. I. T. decontamination: Gastric lavage. Activated charcoal. and
   - Multiple dose activated charcoal (MDAC) due to enterohepatic circulation.
3. Antidote: Digi-bind
   a. It is antibodies that bind to digoxin molecules that are excreted by the kidney.
4. Elimination of the poison from blood: Ineffective because of its large volume of distribution (in digoxin toxicity) & because of high protein binding (in digitoxin toxicity).
5. Symptomatic: Treatment of hypokalemia & arrhythmia. Hyperkalemia:
   * insulin in 5% glucose.
   *Avoid the use of calcium as it may increase digitalis toxicity