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Forensic Mnemonics

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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 system
in the Body?
Yes, its the Kidney, so dont 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

Dont 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 RBCs _ 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 RBCs


(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 Joints)
***
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 )

-Its excreted in

BiLe, so the chelator of choice in Renal


Compromise

-Its contraindicated in

Concurrent administration 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 remember the points of Differentiation, ask yourself this Qu:

How

To Verify its 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 remember this Hemorrhagic action, remember that the Chief Role of


Iron in the Body is incorporation in Hemoglobin of RBCs (Blood cell
Synthesis), in contrast, when in excess, it causes (Blood Loss), Hemorrhagic
Necrosis.
-

Remote:

To Remember all Systems affected, Remember these actions coded by

Peri-portal
Blood

Necrosis (Liver)

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 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, passing 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 remember: F is the

6th

Letter, so 1st stage lasts for

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.

Drowsiness (No loss of


consciousness)

Hematemesis & Melena.

The patient appears


falsely stable for a time.

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.


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


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

dr R.M

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