Cooked Inflation

Can inflation be cooked, engineered, doctored or tailored?

The answer is yes.

As we look in hindsight, major causes of inflation were famines, destroyed crops, deficient irrigation, absence of proper storage and processing facilities of food articles.

Now, that all of the above problems have been solved, majority of food is being stashed in advanced storage facilities, armed with the plan to sell them in the wake of shortage in market. Hence, in effect, this theory arises that this process may aid to an artificial shortage, and finally money making by unscrupulous entities. So, whoever has got the capability to stall the normal flow of the market i.e, whoever has got the money, makes the most of it.

How to get rid of it?

Answer is again, whoever has got the capability in terms of money, storage facility, production capacity and a higher shock-absorbing abilty, can take on it.

In today's world,barring only a lucky few, most people don't have the above mentioned economic capabilities.Those who have it, and are genuinely not unscrupulous, combat it effectively

Glaucoma

Chronic progressive optic neuropathy caused by a group of ocular conditions leading to damage of optic nerve and loss of visual function.Most common risk factor being a raised intraocular pressure.

A sustained increase in IOP may be due to

-increased formation of aqueous humour (rare)

-difficulty in its exit (most common)

-raised pressure in episcleral veins (rare)

Raised IOP is essentially due to an increased resistance to the circulation of aqueous humour at the pupil &/or to its drainage through the angle of the anterior chamber.

If trabecular meshwork is blocked, some drainage does occur through the uveoscleral outflow, but these alternative channels are not efficient & they are icapable of dealing with sudden changes of IOP.

Mechanical Changes:

The coats of the eye can withstand fairly high IOPs except at the lamina cribrosa, the fenestrated region through which optic nerve fibres enter the eye. Here, nerve fibres are supported by glial tissue & have to bend over the edge of the disc. A raised IOP causes mechanical pressure on the lamina cribrosa altering capillary blood flow & decreasing axoplasmic flows in the initial stages.Later, significant backward displacement & compaction of the laminar plates narrows the openings through which the axons pass, directly damaging the nerve fibre bundles.

Vascular Perfusion:

The perfusion of the optic nerve head may be affected because of a lack of an adequate autoregulatory mechanism. A substantial rise in IOP can also decrease the capillary blood flow due to mechanical compression of vessels at lamina cribrosa or a decreased flow at the annulus of Zinn, which supplies nutrition to the laminar & post laminar optic nerve head. A fall in perfusion pressure at optic disc can also be caused by systemic factors such as hypotension, vasospasm & acute blood loss.

Other Factors:

Patients with Primary Open Angle Glaucoma have a susceptibility to damage, in some part, because of the presence of larger openings in the lamina cribrosa that allows for greater mechanical displacement of the nerve fibres coursing through.

Dysfunctional axoplasmic transport, because of these mechanical or vascular changes, lead to fewer trophic factors reaching the ganglion cells-damage & eventual death of ganglion cells-triggers apoptosis of adjacent cells. As the loss of nerve fibres extends beyond the normal physiological overlap of functional zones, visual field defects become apparent.initially & predominantly @ superior & inferior poles.The normal distribution of nerve fibres in retina is such that polar loss of nerve fibres translates into an arch above & below the macular area, ending in a horizontal line nasally, with neither crossing it.


Diagnosis:
-charactaristic changes in optic nerve head
-abnormalities in the visual field
-rise in IOP

-type of glaucoma is determined by clinical features & status of anterior chamber determined by gonioscopy
-primary open angle glaucoma is diagnosed if at least two of the three abnormalities are detected
-in acute & subacute primary angle closure glaucoma & the secondary glaucomas- the presence of raised IOP is enough to make a diagnosis

Vascular:

Pupil

usual size -ranges from 2-5 mm, determined by pupillary light reflex pathways (afferent & efferent), function of sphincter & dilator pupillae muscles

miosis- decrease in pupillary size (organophosphorous poisoning)

mydriasis- increase in pupillary size (atropine action)

cycloplegia- loss in accommodation reflex (atropine action)

Subconscious Ambitions

When we gain knowledge of the world around us, or as it is shown or told to us: we develop our own method of observation, judgement, opinion and the drive to change something or to achieve something to balance the arena. Nobody tells us,teaches us to do these things or to nurture habits fulfilling these necessities.These are wise, gentle, usually bear some philosophy, achievable and helpful to many and most of the people around us.

Outer world makes us learn things, take decisions, earn money, fame and name, may be throughout our life, preoccupied by their effects and hence a rush sets in,if we fail a step in achieving them, we start missing the effects also.It's a continuous process.

Sometimes our outer world ambitions and subconscious may be in conflict.There is a chance that they may antagonize each other & hence the net result becomes feeble, lands us in the no man's land of indecisiveness: origin of a personality disorder

Acid Base Balance

pH<7.35 => acidosis

pH>7.45 => alkalosis

major extracellular buffering system of body HCO3-/H2CO3

H2O + CO2 << H2CO3 << H+ + HCO3-

le Chatelier's principle usually followed.

1. PaCO2 controlled by changes in ventilation (normal value 35-45 mm Hg) 40 is usual value.

acidosis compensated by hyperventilation (lt shift), alkalosis by hypoventilation (rt shift).

2.HCO3- (22-30 meq/L) 24 is usual value

acidosis compensated by renal reabsorption of bicarbonates by tubular cells from tubular fluid,collecting duct cells secrete more hydrogen and generate more bicarbonate, and ammoniagenesis leads to increased formation of the NH₃ buffer, alkalosis compensated by excretion of more bicarbonate from kidney, by decreasing hydrogen ion secretion from the tubular epithelial cells, and lowering rates of glutamine metabolism and ammonia excretion

major extracellular buffer- bicarbonate & ammonia

major intracellular buffer- proteins & phosphates

For usual calculation, look for the primary defect in terms of acidosis or alkalosis by pH value.

Next is identifying the primary defect in terms of metabolic or respiratory acidosis or alkalosis, both the reason and effect being in the same direction in terms of change in hydrogen ion concentration.

Third is to identify the compensatory mechanism, if any

Organophosphorous Poisoning

Setting: Agricultural poison, often accidental due to contact,inhalation or ingestion

Victim: Agricultural workers, handlers of organophosphorous compounds

Clinical features: Often smell of organophosphorous compounds

Cholinergic effects: miosis+bradycardia+parasympathetic activation+increased secretion of glands+muscular contraction+urinary incontinence most often

Diagnosis: Cholinesterase activity Plasma vs Red cell If that in plasma decreases,and red cell constant,implies exposure mild. If both affected southwards,severe form of exposure. In tissue samples at room temperature,cholinesterase activity can be assessed till 1-2 days,at temp 4-8 degrees,can be assessed even after months.

Clinical diagnosis: iv injection of 2 ml atropine relieves most symptoms,whereas in normal subjects it causes atropinization (mydriasis+cycloplegia+abolition of light reflex+tachycardia+sympathetic activation+decreased secretion of glands+voluntary muscle relaxation+sphincter tone rise+body temperature rise)

Treatment: Atropine 2-4 mg iv repeat every 10-15 minutes till patient stabilizes usual maint dose 40 mg/day max 1000 mg/day

Oximes: Pralidoxime