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A collection of menonics in forensic medicine & Toxicology (Metals) to help easily memorize important points
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ForensicMnemonics
***
Metals
***
Lead (Pb)
***
As All Metals, it has Mixed action:
- Local : G.I.T- Remote : Target Organs can be coded by its chemical symbol:
Pb
Peripheral Nerves
Proximal Tubules of the Kidney
blood
brain
bone
A Target organ I always 4get is Kidney, so to remember :)
The main use of Pb when came up was Water pipes.
So, do u remember the organ with the Largest Water channel systemin the Body?
Yes, it’s the Kidney, so don’t 4get to mention the Kidney as a targetorgan in Both Acute & Chronic Lead poisoning, producing
(Fanconi – Like syndrome) (Reveraible) ;
-Due to Proximal Tubule affection; Glucosuria, Aminoaciduria,Phosphaturia, Albumin, Blood & Casts in Urine.
***Occupational Exposure to Lead can also be coded by its Chemical
Symbol:
Pb
Plumbers
Painters
Petroleum Industry Workers (exposed to: TEL “Organo lead”)
(N.B. Tetra Ethyl Lead (TEL) is the Most LEThal & rapidly producesEncephalopathy).
battery & bullet (Missile) Industries
***
Special Features of PLumbism
- LOCal: GIT
Don’t 4get to talk about
3 CO
COLors
COLic
COnstipation
ColorsOral: Blue line at gingival Line (PbS)
Intestinal: Black Offensive stool (PbS)
Colic:
Paroxysmal & relieved byPressure.
Constipation:With Black offensive stool (PbS)
***Blood & Vascular System
A, B, C
A nemia (Microcytic Hypochromic), due to:
Haemo-lysis (++ Fragility of RBC’s _ interferes with Na\K Pump & attachesto the membrane >> ++ Fragility)
Heme-Synthesis (inhibition of several Enzymes in Heme Synthesis Pathwaythrough binding to their SH- group)
- With subsequent Compensatory Release of Immature RBC’s(Reticulocytes) Reticulocytosis.
***
Basophilic stippling (Punctate Basophilia), due to:
Inhibition of Pyridine –5- Nucleotidase (Responsible for Breakdown ofRNA) Clumping of Ribosomal RNA.
***
Circum Oral Pallor, due to VC.
***Peripheral Nerves
Lead Palsy (Wrist & Foot Drop)
PlumbuM produces
Purely Motor Peripheral Neuritis, esp. affecting Extensors.
***
Proximal Tubules of the Kidney: Fanconi-Like Syndrome.
***Brain:
Encephalopathy.
Esp. in Children (Immature BBB)Esp. with TEL.
***Bone:
Bone aches & Arthritic pain (Lead esp. deposits near Joints)
***
Others:
- Plumbum affects Parents
♀ Abortion (ecboilc)
♂ Sterility & Impotence
- PlumbUM affects MyocardiUM (Miocarditis)
***
Regarding Investigations:
- One of the important investigations in Lead poisoning, is
detection of
Amino-Levulinic Acid in urine (++ ALA, due to inhibition of ALA
Dehydratase enzyme in Heme synthesis pathway).***
Regarding TTT
PROphylaxis through:
PROmote adequate supply of Ca, Zn & Fe. (-- Pb absorption)
PROper Ventilation
PROtective clothing, Masks, gloves & boots.
PERiOdic Medical Examination of exposed workers.
***Regarding the Chelator
(BAL)
-It’s excreted in BiLe, so the chelator of choice in RenalCompromise
-It’s contraindicated in 4 F
- Concurrent administration or toxicity of Fe Fe-BAL Complex is
toxic.
- Favism (G6PD Deficiency) Haemolysis.
- Liver Failure (excreted in Bile).
- Fetal Gestation (Pregnancy).
***Arsenic
***
Acute ARsEniC***
As all Metals, mixed action:
Local: G.I.T
- Nausea, vomiting, colic, Diarrhea with RiCE stools
- DD : Cholera,
- To remember the points of Differentiation, ask yourself this Qu:
How To Verify it’s ChOLera or ArSENIc Toxicity ?
Temperature
Vomiting
COLic
ANALYsIsTenesmus
***
Remote: ArsENic
- ParENchymatous organs (Liver, Kidney & Heart)
***
Chronic Arsenic:
-Local: G.I.T: Anorexia, diarrhea Alternating with Constipation.
- Remote: As acute +
Aplastic Anemia
Skin & MM.
Peripheral Neuritis; Mainly Sensory
***
Iron
***
Acute Iron Toxicity
Condition of Poisoning:
Mainly Accidental, esp. in Children as Iron Preparations are:
- Attractive, similar to candies.
- Available at home.
Mechanism of Action:
- Local:
- GIT: Corrosive effect; may cause Hemorrhagic Necrosis &Perforation.
- To remember this Hemorrhagic action, remember that the Chief Role ofIron in the Body is incorporation in Hemoglobin of RBC’s (Blood cell
Synthesis), in contrast, when in excess, it causes (Blood Loss), HemorrhagicNecrosis.
- Remote:
- To Remember all Systems affected, Remember these actions coded by
3 P
Peri-portal Necrosis (Liver)
Blood Pressure (Hypotension) (Cardiovascular)
Blood PH (Metabolic Acidosis) (Metabolism)
***To Remember what causes stage I & II in acute Iron Toxicity,
Stage I.
G.i.T
- Due to irritant Corrosive effect of Iron.
***Stage II.
Apparent Recovery
- Due to Redistribution of Iron from Blood to Reticulo-
endothelial system.
***
N.B.
The 2 Main Toxins during our study, targeting the Liver are
Iron & Paracetamol; They share some distinct characters:
1- Both are originally handled by liver in Therapeutic doses
Iron (Stored in the Liver)Paracetamol (Metabolized in the Liver)
2- When ingested in excess, they Target it, passing Through 4stages
Note that
LIVer IV 4
The 4 Stages are in order:
I. GITII. Apparent Recovery & Altered Blood Chemistry
III. Liver Failure & Overt symptomsIV. Prognosis
See the following Table :)
N.B. Pay attention to timing of Stages in each, as a stage may beasked using the time & not the name or symptoms.
Iron (Fe) (1-6 hrs) ( 6-24 hrs) ( 12-48 hrs) ( 2-6 Wks)To remember: F is the 6th Letter, so 1st stage lasts for 6 hours,
then complete the sequence :)
Paracetamol: (1\2 – 24 hrs) (24-72 hrs) (72-96 hrs) (7-10 days)
dr R.M
Stage
• Stage I•G.I.T
• Stage II•Apparent
Recovery (Both)•Altered Blood
Chemistry(Paracetamol).
• Stage III• Liver Failure
• Stage IV• Prognosis
• Abdominal pain.
• Nausea, Vomiting,Hematemesis & Melena.
• Shock & Dehydrationfrom Fluid Loss.
• ـــــــــــــــــــ
• The patient appearsfalsely stable for a time.
• ـــــــــــــــــــ
• Hepatic Necrosis & Livercell failure .
• Lethargy & Coma.•(But don't 4get that iron in
addition has a corrosiveeffect & targets CVS &
Metabolism, so add:
• Recurrence of G.I.TSymptoms.
• Shock, Hypotension &Metabolic acidosis.
• ـــــــــــــــــــ• G.I.T Scarring & Narrowing
• with or withoutObstruction
(Pylorostenosis, GastricFibrosis or small bowel
stricture).
dr R.M
Iron
• Abdominal pain.
• Nausea, Vomiting,Hematemesis & Melena.
• Shock & Dehydrationfrom Fluid Loss.
• ـــــــــــــــــــ
• The patient appearsfalsely stable for a time.
• ـــــــــــــــــــ
• Hepatic Necrosis & Livercell failure .
• Lethargy & Coma.•(But don't 4get that iron in
addition has a corrosiveeffect & targets CVS &
Metabolism, so add:
• Recurrence of G.I.TSymptoms.
• Shock, Hypotension &Metabolic acidosis.
• ـــــــــــــــــــ• G.I.T Scarring & Narrowing
• with or withoutObstruction
(Pylorostenosis, GastricFibrosis or small bowel
stricture).
Paracetamol
• Malaise & Diaphoresis.
• Nausea & Vomiting.
• Drowsiness (No loss ofconsciousness)• ـــــــــــــــــــ
• Pain & Tenderness in Rt.Hypochondrium.
• Altered Liver FunctionTests.
• ـــــــــــــــــــ
• Liver failure
• (Jaundice, Coagulationdefects, encephalopathy& Altered concious level)
• ـــــــــــــــــــ
• Recovery: Resolution ofhepatic dysfunction &
complete hepaticrecovery within 3 - 6
months.
• Death: In severe casesdue to Multi-organ
failure.
dr R.M
Paracetamol
• Malaise & Diaphoresis.
• Nausea & Vomiting.
• Drowsiness (No loss ofconsciousness)• ـــــــــــــــــــ
• Pain & Tenderness in Rt.Hypochondrium.
• Altered Liver FunctionTests.
• ـــــــــــــــــــ
• Liver failure
• (Jaundice, Coagulationdefects, encephalopathy& Altered concious level)
• ـــــــــــــــــــ
• Recovery: Resolution ofhepatic dysfunction &
complete hepaticrecovery within 3 - 6
months.
• Death: In severe casesdue to Multi-organ
failure.