BHMS Final Professional Result 2020 Under Dhaka University

BHMS Final Prof Result 2020 Under Dhaka University 

BHMS Final Prof Result 2020 Under Dhaka University 

BHMS Final Prof Result 2020 Under Dhaka University 

 

Golden rule-

     When definite improvement sets in, discontinue the administration of the remedy and do not repeat until the patient fails to show further reaction to the dose.

     Continue with the same potency as long as it gives a reaction.

     If the remedy be well chosen do not be in a hurry to change. In cases of apparent failure first try another potency (higher or lower) of the same drug.

     When in doubt as to the advisiability of repeating or changing wait.

     High potencies often cause a preliminary aggravation.

ü  Low potencies- 1x to 12x. Chiefly used in acute conditions & frequent doses.

ü  Medium potencies- 12 to 30, useful at the beginning of either acute or chronic cases and especially when deep, organic changes are suspected.

ü  High potencies- 200 up, mostly used in chronic conditions and in infrequent doses.

N.B.: Many drugs appear to be inert between 3x and 8x.

 

🔻

 Aconitum napellus

 Monkshood.
 Ranunculaceae.

- Is generally indicated in acute or recent cases occurring in young persons, especially girls of a full, plethoric habit who lead a sedentary life; persons easily affected by atmospheric changes; dark hair and eyes, rigid muscular fibre.
 - Complaints caused by exposure to dry cold air, dry north or west winds,  or exposure to draughts of cold air while in a perspiration; bad effects of checked perspiration.
 - Great fear and anxiety of mind,  with great nervous excitability; afraid to go out, to go into a crowd where there is any excitement or many people; to cross the street.
 - The countenance is expressive of fear; the life is rendered miserable by fear; is sure his disease will prove fatal; predicts the day he will die; fear of death during pregnancy.
 - Restless, anxious, does everything in great haste; must change position often; everything startles him.
 - Pains : are intolerable, they drive him crazy; he becomes very restless; at night.
 - Hahnemann says : "Whenever Aconite is chosen homoeopathically, you must, above all, observe the moral symptoms, and be careful that it closely resembles them; the anguish of mind and body; the restlessness; the disquiet not to be allayed."
 - This mental anxiety, worry, fear accompanies the most trivial ailment.
 - Music is unbearable, makes her sad (Sab.-during menses, Nat. c.).
 - On rising from a recumbent position the red face becomes deathly pale, or he becomes faint or giddy and falls, and he fears to rise again; often accompanied by vanishing of sight and unconsciousness.
 - Amenorrhoea in plethoric young girls; after fright,  to prevent suppression of menses.
 - For the congestive stage of inflammation before localization takes place.
 - Fever : skin dry and hot; face red, or pale and red alternately; burning thirst for large quantities of cold water; intense nervous restlessness, tossing about in agony; becomes intolerable towards evening and on going to sleep.
 - Convulsions : of teething children; heat, jerks and twitches of single muscles; child gnaws its fist, frets and screams; skin hot and dry; high fever.
 - Cough, croup; dry, hoarse, suffocating; loud, rough, croaking; hard, ringing, whistling; on expiration (Caust.-on inhalation, Spong.); from dry, cold winds or drafts of air.
 - Aconite should never be given simply to control the fever, never alternated with other drugs for that purpose. If it be a case requiring Aconite no other drug is needed; Aconite will cure the case.
 - Unless indicated by the exciting cause, is nearly always injurious in first stages of typhoid fever.
 - Aggravation. Evening and night, pains are insupportable; in a warm room; when rising from bed; lying on affected side (Hep., Nux. m.).
 - Amelioration. In the open air (Alum., Mag. c., Puls., Sab.).
 - Relation. Complementary : to Coffea in fever sleeplessness, intolerance of pain; to Arnica in traumatism; to Sulphur in all cases. Rarely indicated in fevers which bring out eruptions.
 - Aconite is the acute of Sulphur, and both precedes and follows it in acute inflammatory conditions.

The Renin-Angiotensin-Aldosterone System (RAAS)

The smaller system that controls blood pressure is the tubuloglomerular feedback system.

Your body has a huge system involved in the sensation and control of blood pressure, not only within the kidneys, but all over the body - especially in times of great need. This is in contrast to a smaller system called tubuloglomerular feedback, which you can think of as the system that senses and controls blood pressure and glomerular filtration rate within the kidneys on a moment-by-moment basis. When called upon, this smaller system can also rev up the really big system I'm about to get into. So, what is this really big system?
Could I get a drumroll? The most important system involved in the regulation of systemic blood pressure, renal blood flow and glomerular filtration rate is called the renin-angiotensin-aldosterone system, or (RAAS) for short.

The Release of Renin

When systemic hypotension, or low blood pressure throughout the body, occurs, receptors in your blood vessels called baroreceptors sense this change. Cells of the kidney's juxtaglomerular apparatus get involved as well. Detection by one or both of these mechanisms leads juxtaglomerular cells in the kidneys to release an enzyme called renin. Renin is an enzyme released by the juxtaglomerular cells of the kidneys in response to low blood pressure, causing the transformation of angiotensinogen to angiotensin I.

Angiotensinogen & Angiotensin I

Angiotensinogen is a precursor protein made in the liver for a hormone called angiotensin I. Essentially, renin catalyzes a reaction that converts the angiotensinogen protein into angiotensin I, which is a precursor hormone that is converted to an active hormone called angiotensin II by an enzyme known as angiotensin-converting enzyme in the lungs. Wow, that was a mouthful! Let's break this down.
Here's how to remember what becomes what. Angiotensinogen's purpose is to serve as a precursor to angiotensin I. Angiotensinogen is cleaved, or broken apart, by renin. Since it's broken apart, it gets smaller and becomes shorter in name as well. Therefore, it's now called plain old angiotensin I. Angiotensin I decides to have a little kid and name it after itself. Therefore, when angiotensin I is converted in the lungs by an enzyme called ACE, it becomes angiotensin junior - or more technically, angiotensin II.

Angiotensin I is converted into angiotensin II in the lungs by the enzyme ACE.

Angiotensin-Converting Enzyme (ACE) & Angiotensin II

It bears repeating that the angiotensin-converting enzyme, or ACE for short, is an enzyme located mainly in the lungs that converts angiotensin I into angiotensin II. Once angiotensin II is made, it can have a big effect on the body. Namely, angiotensin II is a vasoconstrictive hormone that increases systemic blood pressure, renal perfusion pressure and the glomerular filtration rate.
Angiotensin II not only constricts blood vessels all over the body in order to increase systemic blood pressure, it also works in the kidneys in order to maintain blood pressure in the glomerulus so that the glomerular filtration rate stays normal even in the face of low blood pressure.

Control of the Glomerular Filtration Rate (GFR) by the RAAS

Let's see how this works with a familiar example. If you connect a hose to a faucet and turn the faucet on, a certain pressure will be exerted by the water on the walls of the hose. Likewise, blood running through the glomerulus (our hose) does the same thing. If the faucet is turned down a bit due to hypotension, there is less water running through the hose and therefore less pressure being exerted on the hose. If this were to happen in our glomerulus due to hypotension, this would be very bad. We need to maintain pressure in the glomerulus at a certain level if we want to filter our blood enough to stay alive.
To maintain pressure in the glomerulus and therefore keep the glomerular filtration rate steady, angiotensin II constricts both the efferent and afferent arteriole, but with a much greater effect on the efferent arteriole. Remember, the effect of angiotensin II is greater on the efferent arteriole. This means that the blood entering the glomerulus has a much harder time leaving it because the exit is far smaller than the entrance. This causes a backup of blood in the glomerulus, increases the pressure within it and, therefore, keeps the GFR at an appropriate rate.

Angiotensin II constricts the afferent and efferent arterioles.

In addition, angiotensin II increases the absorption of sodium in the renal tubule. Since water follows sodium, it increases the amount of fluid in the blood vessels, further causing an increase in blood pressure in addition to the vasoconstriction that already occurred.

Aldosterone

Angiotensin does some other important things that you must remember. It causes the release of a hormone called aldosterone from the adrenal glands. Aldosterone is a hormone that increases the absorption of water from the distal convoluted tubule and collecting duct of the kidney's nephrons.
Aldosterone has many other functions, including the secretion of potassium into urine. However, for this lesson, you should understand that aldosterone causes the absorption of sodium out of the renal tubule's filtrate and into the blood. Since water follows sodium, more water is reabsorbed back into the blood in order to increase the blood pressure.

Anti-Diuretic Hormone (ADH)

As if constricting blood vessels and releasing aldosterone to retain water and sodium weren't enough, angiotensin II also causes the release of a hormone called anti-diuretic hormone, commonly called vasopressin, or ADH for short.
ADH is a hormone released from the posterior pituitary gland that causes an increase in blood pressure. ADH vasoconstricts our blood vessels, which causes increased blood pressure. It also increases water absorption from the distal tubule and collecting ducts. Now that you know what it does, it's easy to remember this because 'anti' in 'anti-diuretic' means 'against,' and 'diuretic' means 'excess urine production' that occurs thanks to water loss. Hence, ADH is against the loss of water in urine from your body!

Vasopressin raises blood pressure by vasoconstricting blood vessels and increasing water absorption.

Negative Feedback Mechanisms & Loops on the RAAS

Finally, you must understand that if the RAAS system was to run wild without any inhibitory control, it would actually kill you. This is why there are several mechanisms in place that try to control the RAAS system so that it doesn't go into overdrive. We'll go over some of the most important aspects of this inhibitory feedback system.
First off, increasing levels of angiotensin II are sensed by your body, and this by itself suppresses renin release. This is called an inhibitory feedback loop. As angiotensin II increases, renin decreases, which means angiotensin II also decreases since it depends on renin for its production.
Secondly, as blood pressure is restored back to normal thanks to vasoconstriction and water retention, baroreceptors in your body's blood vessels sense the increased pressure and send signals to the juxtaglomerular cells to stop secreting renin. This signaling eventually stops the entire RAAS cascade. No renin means no angiotensin II and therefore no aldosterone or ADH either.

“I dreamt that you were mine, and then I woke up smiling because I realized it was not a dream. You are already mine!”
Love you Srabon

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