Forensic Mnemonics - Metals 4h1de

Forensic Mnemonics *** 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 :) The main use of Pb when came up was Water pipes.

So, do u the organ with the Largest Water channel system in the Body? Yes, it’s the Kidney, so don’t 4get to mention the Kidney as a target organ 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 (N.B. Tetra Ethyl Lead (

(exposed to: TEL “Organo lead”)

TEL) is the Most LEThal & rapidly produces Encephalopathy).

battery & bullet (Missile) Industries ***

Special Features of PLumbism

-

LOCal: GIT

Don’t 4get to talk about 3

CO

COLors COLic COnstipation Colors Oral: Blue line at gingival Line (PbS) Intestinal: Black Offensive stool (PbS) Colic:

Paroxysmal & relieved by Pressure. 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 & attaches to the membrane >> ++ Fragility)

Heme-Synthesis (inhibition of several Enzymes in Heme Synthesis Pathway through 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 of RNA)

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 ts) *** Others:

-

Plumbum affects Parents ♀ Abortion (ecboilc) ♂ Sterility & Impotence

-

Plumb

UM 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

B L

( A )

-It’s excreted in

BiLe, so the chelator of choice in Renal Compromise

-It’s contraindicated in

-

Concurrent istration or toxicity of

4F

Fe

Fe-BAL Complex is

toxic.

-

Favism (G6PD Deficiency) Haemolysis. - Liver Failure (excreted in Bile). - Fetal Gestation (Pregnancy). *** Arsenic ***

Acute A

RsEniC ***

As all Metals, mixed action: Local: G.I.T -

Nausea, vomiting, colic, Diarrhea with -

-

RiCE stools

DD : Cholera,

To the points of Differentiation, ask yourself this Qu:

How

To it’s ChOLera or ArSENIc Toxicity ?

Temperature Vomiting COLic ANALYsIs Tenesmus ***

ENic

Remote: Ars

-

Par

ENchymatous organs (Liver, Kidney & Heart) *** Chronic

-Local: G.I.T:

Arsenic:

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 this Hemorrhagic action, that the Chief Role of Iron in the Body is incorporation in Hemoglobin of RBC’s (Blood cell Synthesis), in contrast, when in excess, it causes (Blood Loss), Hemorrhagic Necrosis. -

-

Remote:

To all Systems affected, these actions coded by

3

P

Peri-portal Blood

Necrosis (Liver)

Pressure (Hypotension) (Cardiovascular)

Blood

PH (Metabolic Acidosis) (Metabolism) ***

To what causes stage I & II in acute Iron Toxicity, Stage I. G -

i

.i . T

Due to rritant Corrosive effect of Iron. *** Stage II. Apparent

-

Due to

Recovery

Redistribution of Iron from Blood to Reticuloendothelial 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, ing Through 4 stages Note that L

IVer

IV 4

The 4 Stages are in order: I. II.

GIT

Apparent Recovery & Altered Blood Chemistry III. Liver Failure & Overt symptoms IV.

Prognosis

See the following Table :) N.B. Pay attention to timing of Stages in each, as a stage may be asked using the time & not the name or symptoms. Iron (Fe) (1-6 hrs) ( 6-24 hrs) ( 12-48 hrs) ( 2-6 Wks) To : 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)

Stage

• Stage I •G.I.T

• Stage II •Apparent Recovery (Both) •Altered Blood Chemistry (Paracetamol).

• Stage III

• Liver Failure

Iron

Paracetamol

• Abdominal pain.

• Malaise & Diaphoresis.

• Nausea, Vomiting,

• Nausea & Vomiting.

• Shock & Dehydration from Fluid Loss. • ‫ـــــــــــــــــــ‬

• Drowsiness (No loss of consciousness) • ‫ـــــــــــــــــــ‬

Hematemesis & Melena.

• The patient appears falsely stable for a time. • ‫ـــــــــــــــــــ‬ • Hepatic Necrosis & Liver cell failure . • Lethargy & Coma.

• Liver failure

•(But don't 4get that iron in addition has a corrosive effect & targets CVS & Metabolism, so add:

• (Jaundice, Coagulation defects, encephalopathy & Altered concious level)

• Recurrence of G.I.T Symptoms. • Shock, Hypotension & Metabolic acidosis.

• Stage IV • Prognosis

• Pain & Tenderness in Rt. Hypochondrium. • Altered Liver Function Tests. • ‫ـــــــــــــــــــ‬

• ‫ـــــــــــــــــــ‬ • G.I.T Scarring & Narrowing • with or without Obstruction (Pylorostenosis, Gastric Fibrosis or small bowel stricture).

• ‫ـــــــــــــــــــ‬ • Recovery: Resolution of hepatic dysfunction & complete hepatic recovery within 3 - 6 months. • Death: In severe cases due to Multi-organ failure.

dr R.M