Methanol

Formaldehyde

Formic Acid

Metabolic Acidosis

Renal Toxicity

Distributed in the tissues having

high water content, high conc. Is

found in vitreous body and optic

nerve, hence causes optic neuritis.

General signs of poisoning

Odour present in breath.

Effects on CNS is well marked

Urine is strongly acidic and containacetone and trace of albumin. Metabolic acidosis: Due to excessof lactic acid and respiratorydepression

Retinal ganglion cells and optic disc

shows degenerative changes.

In fatal cases: Convulsions

Death may occur from respiratory

depression

Cause of death:

Death is mainly due to metabolic

acidosis resulting from production of

organic acids mainly, Formic Acid.

CNS depression leading to respiratory

depression.

Also known as alcohol or ethyl

alcohol

Considered the same whether

beverage is wine, beer or hard liquor

Classified as a food but contains

empty calories

Not digested like other foods

It can go directly into the

bloodstream

Alcohol absorption throughout the GI

tract

It is quickly distributed throughout the

body

Can be absorbed into the

bloodstream at:

• Mouth

• Esophagus

• Stomach

• Small Intestine

About 20% to 25% is absorbed

Factors that influence absorption:

the rate of intake

presence of food

the rate of gastric emptying

75-80% is absorbed.

This absorption is extremely rapid.

Alcohol Dehydrogenase (ADH)

• Stomach

• Liver

Microsomal Ethanol Oxidizing System

(MEOS)

› Liver

In the cytoplasm, ADH converts

ethanol to acetaldehyde

CH3-CH2-OH + NAD+ CH3-CHO + NADH + H+

Ethanol ADH Acetaldehyde

In the mitochondria, acetaldehyde is

converted to acetate and in turn acetate is

converted to acetyl CoA which leads the

two-carbon molecule into the TCA cycle

CH3-CHO + NAD+ CH3-COOH + NADH + H+

Acetaldehyde ADH Acetate

Alternate pathway used, in addition to

ADH, when alcohol intake is excessive

End products include:

• Ethanol acetaldehyde

• NADPH + H+ NADP+

No ATP formation = Energy Wasteful

LIVER

Fatty liver

Cirrhosis

Hypoglycemia (low blood sugar)

Central Nervous System

When intoxication occurs it affects emotional

and sensory function, judgment, memory and

learning ability

Smell and taste are dulled

Ability to withstand pain increases

Long term effects include tolerance,

dependency and irreversible damage

Brain is most affected

Blood

Blood-Sludging

Anemia

Weakness of bone structure

Decrease resistance to infection and

inability to fight off infections

Muscles

Reduced blood flow. Causing muscle weakness

and deterioration

Irregular heartbeat, sluggish heart, and muscle

aches

Endocrine

Sedates glands

Sexual functioning

-Low doses decrease

inhibitions

-High doses decrease

sexual functioning for

men and women

Acetyl salicylate

Acetylsalicylate inhibits prostaglandin

and thromboxane production by human

platelets suspended in plasma or buffer.

Acetylsalicylate inhibits arachidonate-

induced aggregation of human platelets

suspended in plasma

This compound belongs to the

phenol esters. These are aromatic

compounds containing a benzene ring

substituted by an hydroxyl group and an

ester group.

Absorption

Absorption is generally rapid and

complete following oral administration but may

vary according to specific salicylate used,

dosage form, and other factors such as tablet

dissolution rate and gastric or intraluminal pH.

Mechanism of action

Acetylsalicylic acid's antirheumatic ( anti-

inflammatory) actions are a result of its analgesic

and anti-inflammatory mechanisms.

the therapeutic effects are not due to

pituitary-adrenal stimulation.

The platelet aggregation-inhibiting effect of

acetylsalicylic acid specifically involves the

compound's ability to act as an acetyl donor to

cyclooxygenase.

the nonacetylated salicylates have no

clinically significant effect on platelet aggregation.

Effects of overdose

abdominal pain,

hypokalemia,

hypoglycemia,

pyrexia,

hyperventilation,

dysrhythmia,

hypotension,

hallucination,

renal failure,

confusion,

seizure,

coma,

death.