Hypernatremia

Hypernatremia is a greater than normal concentration of sodium in the blood. Sodium is an electrolyte that helps with nerve and muscle function, and also helps to maintain blood pressure.
Hypernatremia occurs when the body loses too much water in relation to the amount of sodium in the blood. Excessive water loss can occur if the kidneys excrete too much urine.
Hypernatremia can cause neurological damage due to shrinkage of brain cells. Hypernatremia is the condition of drinking a tremendously large amount of h2o in a short period. It is important to learn about this condition so that you don't overload you're system with water. Hypernatremia is defined as a plasma sodium concentration greater than 150 meq/L and is less common than hyponatremia. Hypernatremia – Seen in infants with dehydration, renal disease or diabetes insipidus. Severe hypernatremia can lead to confusion, muscle twitching, seizures, coma, and death.
Patients with hypernatremia may also have evidence of ECF volume expansion. Hypernatremic dehydration can occur when a child with diarrhoea receives fluids that contain high quantities of sodium. The tendency to hypernatremia is aggravated when PD is initiated with frequent exchanges of small volumes of hypertonic solution. Most patients with hypernatremia secondary to water loss appear euvolemic with normal total body sodium, because loss of water without sodium does not lead to overt volume contraction. So someone with severe hypernatremia, you still give them normal saline.
Similarly, a patient with hypernatremia must have lost more water than he was able to drink.
We present three neonates with severe hypernatremia secondary to inadequate exclusive breast-feed, two of whom developed intracranial hemorrhage during hospital stay with review of literature.
Although hyponatremia may be present, hypernatremia is not unusual because of the relatively high sodium administration in the various solutions because of the greater perspiration (higher respiration rate, relatively higher body surface area, thinner skin, artificial heating lamp) and especially because of the correction of acidosis with sodium bicarbonate. This listing is a sample listing of patents related to Hypernatremia for is only meant as a recent sample of applications filed, not a comprehensive history. If the body does not maintain salt balance then it may lead to hypernatremia with heart attack and even death.
Hyperchloremia, excess sodium OR deficit of bicarb. Can be expected with hypernatremia or metabolic acidosis. Hypernatremia reflects a deficiency of water relative to total body sodium content and is actually a disorder of water balance rather than a disorder of sodium balance.

Primary angle closure glaucoma

Primary angle closure glaucoma medical terminology is a type of primary glaucoma (wherein there is no obvious systemic or ocular cause) in which rise in intraocular pressure occurs due to blockage of the aqueous humour outflow by closure of a narrower angle of the anterior chamber.
ETIOLOGY
(A) Predisposing risk factors. These can be divided into anatomical and general factors:
I. Anatomical factors. Eyes anatomically predisposed to develop primary angle-closure glaucoma (PACG) include:
Hypermetropic eyes with shallow anterior chamber.
Eyes in which iris-lens diaphragm is placed anteriorly.
Eyes with narrow angle of anterior chamber, which may be due to: small eyeball, relatively large size of the lens and smaller diameter of the cornea or bigger size of the ciliary body.
Plateau iris configuration.
II. General factors include:
Age. PACG is comparatively more common in 5th decade of life.
Sex. Females are more prone to get PACG than males (male to female ratio is 1:4)
Type of personality. It is more common in nervous individuals with unstable vasomotor system.
Season. Peak incidence is reported in rainy season.
Family history. The potential for PACG is generally believed to be inherited.
Race. In caucasians, PACG accounts for about 6% of all glaucomas and presents in sixth to seventh decade. It is more common in South-East Asians, Chinese and Eskimos but uncommon in Blacks. In Asians it presents in the 5th to 6th decade and accounts for 50% of primary adult glaucomas in this ethnic group.

(B) Precipitating factors. In an eye that is predisposed to develop angle closure glaucoma, any of the following factors may precipitate an attack:
Dim illumination, Emotional stress, Use of mydriatic drugs like atropine, cyclopentolate, tropicamide and phenylephrine.
(C) Mechanism of rise in IOP. The probable sequence of events resulting in rise of IOP in an anatomically predisposed eye is as follows:
First of all due to the effect of precipitating factors there occurs mid dilatation of the pupil which increases the amount of apposition between iris and anteriorly placed lens with a considerable pressure resulting in relative pupil block. Consequently the aqueous collects in the posterior chamber and pushes the peripheral flaccid iris anteriorly (Iris bombe), resulting in appositional angle closure due to iridocorneal contact.
Eventually there occurs rise in IOP which is transient to begin with. But slowly the appositional angle closure is converted into synechial angle closure (due to formation of peripheral anterior synechiae) and an attack of rise in IOP may last long.
In some cases a mechanical occlusion of the angle by the iris is sufficient to block the drainage of aqueous. For this reason the instillation of atropine in an eye with a narrow angle is dangerous, since it may precipitate an attack of raised IOP.

Herpes Zoster Ophthalmicus Medical Terminology

Medical terminology course explain about Herpes zoster ophthalmicus is an acute infection of Gasserian ganglion of the fifth cranial nerve by the varicella-zoster virus (VZV).
It constitutes approximately 10 percent of all cases of herpes zoster.

Etiology

Varicella zoster virus. It is a DNA virus and produces acidophilic intranuclear inclusion bodies. It is neurotropic in nature.

Comprehensive OPHTHALMOLOGY

Mode of infection. The infection is contracted in childhood, which manifests as chickenpox and the child develops immunity. The virus then remains dormant in the sensory ganglion of trigeminal nerve.
It is thought that, usually in elderly people (can occur at any age) with depressed cellular immunity, the virus reactivates, replicates and travels down along one or more of the branches of the ophthalmic division of the fifth nerve.

Clinical features

In herpes zoster ophthalmicus, frontal nerve is more frequently affected than the lacrimal and nasociliary nerves.
About 50 percent cases of herpes zoster ophthalmicus get ocular complications.
The Hutchinson's rule, which implies that ocular involvement is frequent if the side or tip of nose presents vesicles (cutaneous involvement of nasociliary nerve), is useful but not infallible.
Lesions of herpes zoster are strictly limited to one side of the midline of head.
Clinical phases of H. zoster ophthalmicus are :
1. Acute, which may totally resolve.
2. Chronic, which may persist for years.
3. Relapsing, where the acute or chronic lesions reappear sometimes years later.

Inflammations Of The Cornea Medical Terminology

Medical terminology online course explain about Inflammation of the cornea (keratitis) is characterised by corneal oedema, cellular infiltration and ciliary congestion.

Classification

It is difficult to classify and assign a group to each and every case of keratitis; as overlapping or concurrent findings tend to obscure the picture.
However, the following simplified topographical and etiological classifications provide a workable knowledge.

Topographical (morphological) classification:
(A) Ulcerative keratitis (corneal ulcer) Corneal ulcer can be further classified variously.
1. Depending on location:
(a) Central corneal ulcer
(b) Peripheral corneal ulcer
2. Depending on purulence:
(a) Purulent corneal ulcer or suppurative corneal
ulcer (most bacterial and fungal corneal ulcers
are suppurative).
(b) Non-purulent corneal ulcers (most of viral, chlamydial and allergic corneal ulcers are non-suppurative).
3. Depending upon association of hypopyon:
(a) Simple corneal ulcer (without hypopyon).
(b) Hypopyon corneal ulcer.
4. Depending upon depth of ulcer:
(a) Superficial corneal ulcer
(b) Deep corneal ulcer
(c) Corneal ulcer with impending perforation
(d) Perforated corneal ulcer.
5. Depending upon slough formation:
(a) Non-sloughing corneal ulcer
(b) Sloughing corneal ulcer
(B) Non-ulcerative keratitis.

1. Superficial keratitis:
(a) Diffuse superficial keratitis
(b) Superficial punctate keratitis (SPK)
2. Deep keratitis:
(a) Non-suppurative
(i) Interstitial keratitis
(ii) Disciform keratitis
(iii) Keratitis profunda
(iv) Sclerosing keratitis
(b) Suppurative deep keratitis
(i) Central corneal abscess
(ii) Posterior corneal abscess.

Etiological classification:
1. Infective keratitis:
(a) Bacterial
(b) Viral
(c) Fungal
(d) Chlamydial
(e) Protozoal
(f) Spirochaetal
2. Allergic keratitis
(a) Phlyctenular keratitis
(b) Vernal keratitis
(c) Atopic keratitis
3. Trophic keratitis
(a) Exposure keratitis
(b) Neuroparalytic keratitis
(c) Keratomalacia
(d) Atheromatous ulcer
4. Keratitis associated with diseases of skin and mucous membrane.
5. Keratitis associated with systemic collagen vascular disorders.
6. Traumatic keratitis, which may be due to mechanical trauma, chemical trauma, thermal burns, radiations.
7. Idiopathic keratitis e.g:
(a) Mooren's corneal ulcer
(b) Superior limbic keratoconjunctivitis
(c) Superficial punctate keratitis of Thygeson.