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Goosebumps Medical Term Meaning

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Ever had your hairs on skin suddenly stand up? Of course you had. But all you know about it is either “Oh I’m getting chills” or “OMG that’s hilarious”. Walk through our blog that explains the minutes of Goosebumps or the Piloerection. Featuring Trivia also that will really answer some weird question of yours.

Definition

Definition What are Goose bumps
Having Violin in your hair?

Goose bumps (Goosebumps) or medical term “Cutis anserine” is a physiological process of human body in response to cold (hypothermia) or strong emotions which causes involuntary erection of hairs. Goosebumps are also referred as Goose flesh or Goose pimples.

Origin of word

Origin of word “Goose bumps”
Goose + Bumps, simple, isn’t it?

It’s not like someone plucked feathers from the goose, and the goose skin got protrusions exactly where the feathers were, but hey, it’s exactly is! The word “Goose bumps” originates from the goose protrusions on goose skin after a feather had been plucked from it. Human skin is just like that goose who faced the feather plucking, and hence the term “Goose bumps” for the humans too.

Causes

The reflex of producing goose bumps is known as horripilation, piloerection, or the pilomotor reflex. This reflex can be initiated by stimuli like Cold (hypothermia) or strong emotions like fear, nostalgia, pleasure, euphoria, awe, admiration, and sexual arousal.

Causes of Goose bumps
Maybe the Goose did bump?

Apart from this, weird causes involve when hearing plastic or metal being scratched. Indeed weird! But hey, we got explanation for that too

An important point to add is that Goose bumps can occur only in mammals, since other animals do not have hair. The term “goose bumps” is therefore misleading: the bumps on the skin of a plucked goose technically do not qualify as piloerection. Birds do however have a similar reflex of raising their feathers in order to keep warm.

Diseases

Diseases in which Goose bumps can occur
As a Doctor, you should know everything

Rarely, Goose bumps may be included as symptom of some diseases, such as temporal lobe epilepsy, some brain tumors, and autonomic hyper-reflexia. Goose bumps can also be caused by heroin withdrawal. A skin condition that mimics goose bumps in appearance is keratosis pilaris.

Mechanism

Mechanism of Goose bumps
Arrector Pili causes erection of hairs

In response to the stimuli explained in the section Causes of Goose bumps, the basics of piloerection can be better understood by the following:

Somatomotor and Sympathetic Nervous System
Somatomotor and Sympathetic Nervous System

Stimulus initiates pilomotor reflex through sympathetic nervous system and hence causing tiny muscles at the base of each hair, known as arrector pili muscles, to contract and pull the hair erect.

Detailed Diagram of Goosbumps cause
Detailed Diagram of Goosbumps Cause

Sites

Where goose bumps occur
Goosbumps occuring on thigh and legs

In humans, goose bumps are strongest on the forearms, but also occur on the legs, back, and other areas of the skin that have hair. In some people, they even occur in the face or on the head.

In animals, these can occur throughout parts of skin covered by hair. Most important example may include Porcupines! Have a look what they look after goose bumps-

porcupine goosebumps
Exaggerated response perhaps

Advantages

Piloerection as a response to cold or fear is vestigial in humans; as humans retain only very little body hair, the reflex (in humans) now serves no known purpose.

In animals, this may serve as heat preservation (more hairs=more insulation) or for defense as in porcupine or maybe some else.

goosebumps
Goosebumps on kitties can definitely be scary sometimes

Trivia

Q1- Why not on face?

Ans- Piloerection (the muscular reflex that causes goosebumps) is found throughout the animal kingdom and is usually put to use by angry or scared animals. The piloerection causes hair to stand on its end making animals appear larger to predators and rivals.

goose bumps human body
You don’t get goosebumps on beard, do you?

Humans, through the course of evolution have retained comparatively very little body hair, so piloerection no longer serves much of a purpose. As such, it functions to varying degrees among people; a genetic variation similar to hair color or nose length. That’s the long way of saying, while most people do not get goosebumps on their face as it has not assisted in human evolutionary survival for quite some time, some people still do.

Q2- Why Goosebumps in scratching sounds?

Ans- The mechanism of piloerection (Goosebumps) has to do with your natural reflexes to external stimuli.

Fear and temperature both have strong effects on piloerection (Goosebumps) through autonomic nervous systems feedback systems. These are mediated like other emotion-linked autonomic reflexes by routing through the limbic system. These other emotion-linked autonomic reflexes include blushing, blanching, butterflies in the stomach.

The limbic system is the site of primitive drives: sex, fear, rage, aggression and hunger. Anatomical sites for the limbic system include amygdala, parahippocampal gyrus, uncus, subcallosal gyrus, cingulate gyrus, fornix, dentate gyrus, hypothalamus and hippocampus. These are found around a major structure called the thalamus which receives virtually all sensory input. The medial forebrain bundle is a bidirectional communication with the brainstem which then directly mediates autonomic reflexes. A second method of invoking the autonomic reflexes is through the hypothalamus which also sends nerve projections to the brainstem.

Specifically, direct stimulation of the amygdala and hypothalamus evokes the piloerection pathway. It’s in these physical structures that emotional stimulation by music or the reading of poetry, etc. can result in piloerection. So also non-pleasant and/or unexpected sounds may elicit a fight or flight reaction, which may include piloerection (goosebumps).

Q3- Can it be controlled?

Ans- Medical term clearly says- “Involuntary action”, so indeed no. But news has been that some people do control it!

Indian Penal Code 233 IPC

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Indian Penal Code 233 or IPC 233 became viral as news messages started to spread across social media. According to news, the new law passed will grant women the right to kill or injure the sex organs of attacker. However, the truth about it is totally different.

A latest news went viral on social media about a new Anti-rape law being passed named Indian penal code 233 or IPC 233 which stated as the following :-

“A new law has been passed and under section Indian penal code 233, if a girl is suspected to be raped or getting raped, she has a right to kill the man, injure his sexual organ or harm the person within ipc 233. In such a situation, the girl would not be charged with murder.”

And the original message was:-

“If a girl is suspected to be raped or gettin raped , then she has the supreme ryt to kill the man, injure his sexual part or harm that person as dangerously under ipc 233 by modi govt.. that girl wont be blamed fr murder ……..tell as many as u can .. its your power .. create awareness …. Finally…”

This clearly doesn’t sound like a statement from Supreme Court, right? To add, one of the Supreme Court lawyer stated the following about Indian Penal Code 233:

“The act of rape is punishable under the IPC section 376, not under IPC 233 and punishment starts from 10 years to life imprisonment. There is no bill in the parliament about any amendments to the laws relating to rape currently. However, in certain cases judges have increased life imprisonment and have ordered that the accused will live and die in jail.”

There is no word of IPC 233! Adding to the following, he also said-

“The existing laws in the country are good enough if the prosecution can establish that there was a case of rape. We just need an active and efficient investigation agency, a brilliant prosecution and a dispassionate judge to decide based on facts presented. Further, under the current judicial system and based on the various statutes of the IPC, judges have the power to order that the sentence cannot be reduced and there will be no commutation of imprisonment.”

Answer to Hoax or Truth about Indian Penal Code 233

So this has been declared a False statement being viral all around on social media like WhatsApp and Facebook. So far, the real accused of the false statement is out of reach, but the main question is, “What is IPC 233 or Indian Penal Code 233” and “What is the anti-rape law then?”

We have got all answers as you go through this article. Just make sure you spread to your friends that this is indeed a hoax. But before that, have a look at something really interesting!

Gun For Indian Women

Nirbheek (Nirbhaya) – A 500gm Gun worth 1.22 lakhs for Women is out now! India has launched a new handgun for women, named after a student who was gang-raped in Delhi in December 2012 and later died of her injuries. Officials say it will help women defend themselves, but critics say it’s an insult to the victim’s memory. Let’s see how far it can beat IPC 233 then?

Coming back to the original topic, let’s have a look at the answers-

What is IPC 233 or the Indian penal code 233?

Central Government Act,
Section 233 in the Indian Penal Code

Real Indian Penal Code 233 states as:

“Making or selling instrument for counterfeiting coin.—Whoever makes or mends, or performs any part of the process of making or mending, or buys, sells or disposes of, any die or instrument, for the purpose of being used, or knowing or having reason to believe that it is intended to be used, for the purpose of counterfeiting coin, shall be punished with imprisonment of either description for a term which may extend to three years, and shall also be liable to fine.”

So now you know what exactly is Indian Penal Code 233. If IPC 233 is not anti-rape, then what is? Let’s have a look at it.

The Real Anti-Rape laws

IPC Section 375

It states definition of Rape and IPC Section 376 states the Punishment of rape. IPC 233 is completely irrelevant.

IPC Section 375

It states definition of Rape. The new definition of rape was amended on Jan 1, 2013.

Old Rape Definition

“Sexual intercourse with a woman against her will is called rape.”

New definition as per January 1, 2013

“Penetration, no matter how slight, of the vagina or anus with any body part or object, or oral penetration by a sex organ of another person, without the consent of the victim.”

IPC Section 376

It states punishment for rape as follows

The punishment for committing rape is generally decided under rape laws – IPC section 376, punishing with a maximum sentence of life imprisonment and a minimum of seven years, where the rape accused is also liable to fine unless the woman raped is his wife and is not under twelve years of age. So, you see, no IPC 233 yet!

Additional Laws of Self defense

There are other laws as well which explains the Private Defense. But an important requirement goes as follows for the laws below:

“The right of private defense is only available when there is a reasonable apprehension of receiving injury/sexual assault. Also, the victim needs to provide the necessary evidence of sexual assault/rape either by herself or from the witnesses.”

IPC Section 79

Nothing is an offense which is done by any person who is justified by law, or who by reason of a mistake of fact and not by reason of a mistake of law in good faith, believes himself to be justified by law, in doing it.

IPC Section 96

Things done in private defense.—Nothing is an offense which is done in the exercise of the right of private defense.

IPC Section 97

Right of private defense of the body and of property.—Every person has a right, subject to the restrictions contained in section 99.

IPC Section 100

When the right of private defense of the body extends to causing death.

But wait, there’s another law that explains when the Right of self defense is not applicable!

IPC Section 99

There is no right of private defense against an act which does not reasonably cause the apprehension of death or of grievous hurt.

Summary of Additional laws applicable to Woman

According to the IPC section 100, about Private Defense, a person/woman has a right to defend his/her body when there is a physical assault, with the intention of committing rape or gratifying unnatural lust. And according to section 96, nothing is an offense which is done in the exercise of the right of private defense. In cases of sexual assault, the right of private defense of one’s body can extend to the voluntary causing of death or of any other harm to the assailant. But it is important to note that:

The right of private defence is only available when there is a reasonable apprehension of receiving injury/sexual assault. Also, the victim needs to provide the necessary evidence of sexual assault/rape either by herself or from the witnesses.

The conclusion is that when a woman is attacked and physically assaulted by a man with an intention of rape or lust, the woman has every right to defend herself (not under IPC 233 ofcourse). She can go to any extent to protect herself from the danger, she won’t be blamed or accused for murder – she will only need to prove the sexual assault. Moreover, according to IPC section 97, during the assault, any person associated with the woman also has the legal right to defend her body and fight/kill the assailant.

So next time someone passes the message of new anti-rape law IPC 233 , or says Indian Penal Code 233 has arrived as the savior, slap him with all the LAWS! Share the info now to let everyone know.

Snakes: Difference between Poisonous and Non-Poisonous

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Have you seen in movies the sucking of venom by mouth? And you wonder that’s suicide, right? Well, medically, that’s POSSIBLE! Let us find out what this blog has got about snakes. This blog will explain you everything about snakes, that is, Types of snakes, Common snakes in India, How to find if snake is poisonous, General management for snake bite and the Treatment.

Almost everyone faces a snake, at least once in the lifetime, so why not just get some basics of snakes in short? A simple read can save someone’s life someday, and worth value for the doctors.

Snakes – An overview

Snakes are cylindrical, long, limbless, cold-blooded reptiles. There are about 3500 species of snakes known among which about 350 species are venomous. In India, about 216 species are found and among them, about 52 are poisonous.

The body of snake is divided into:

  1. Head
  2. Trunk
  3. Tail

Types of Poisonous snakes

Poisonous snakes are divided into 5 families:

Types of Poisonous snakes
Fig: Fangs in different snake families
  1. Colubridae: e.g. African boomslanag snake, twig snakes.
  2. Alractaspididae: e.g. mole vipers or adders.
  3. Elapidae: e.g. cobra, krait, coral snake.
  4. Viperidae: e.g. Russell’s viper, saw-scaled viper.
  5. Hydrophidae: e.g. Sea snakes.

Difference between Poisonous and Non-Poisonous Snakes

The following image will just clear out all doubts as to how you are going to quickly find out if the snake is venomous:

Difference between Poisonous and Non-Poisonous Snakes
Figure- A to H: Important features of poisonous and non-poisonous snakes: (A) Poison apparatus and fangs (canalised and grooved), (B) Ventral shields (belly scales) and vertebrals, (C) Head scales, (D) Cobra (note the hood and spectacle mark) (E) Cobra – Third supralabial touching eye and nasal shield, (F) Krait — four infralabials (note the large fourth one), (G) Krait — enlarged vertebrals on the back, and (H) Pit viper — a pit between eye and nostril

Common Non-Poisonous Snakes in India

  1. Rat snake (Dhaman Snake)
  2. Vine snake
  3. Bronze back tree snake
  4. Banded kukri
  5. Sand boa

Dhaman Snake is the most common non-poisonous snake found in India and also known as Rat Snake. Non-poisonous snakes, at times, may resemble poisonous snakes and create confusion.

Features of Common Poisonous Snakes in India

Common cobra

Common cobra
Fig: Common cobra

Zoological name: Naja naja
Common names: Common cobra, nag

Features:

Common cobra features
Fig: Dorsal aspect of cobra with marks
  • Common cobras are usually brown or black in color
  • Head is covered with shields. The third supra-labial shield touches the eye and nose
  • A small wedge shaped scale called as cuneate is present between 4th and 5th infra-labials
  • Pupils are round
  • Hood is present. Dorsal aspect of hood may have monocellate (monocele) or binocellate (spectacle) mark. Ventral surface of hood have two dark spots
  • Fangs are short, grooved and situated anteriorly
  • Tail is cylindrical. Caudal scales (scales on undersurface of tail) are divided and double
  • Venom — neurotoxic

Common Krait

Common Krait
Fig: Common krait

Zoological name: Bungarus caeruleus
Common name: Indian krait, common krait, Maniyar, Kawadya

Features:

Common Krait features
Fig: Common krait head
  • Usually steel blue or black in color with single or paired white bands on back. The bands are more distinct towards the tail
  • Pupils are round
  • Large hexagonal scale presents over back
  • The 4th infra-labial scale is the largest scale of other infra-labial scales
  • The subcaudal (ventral scales distal to vent) are undivided and entire
  • Fangs are short, grooved and situated anteriorly
  • Venom — neurotoxic

Banded Krait

Banded Krait
Fig: Banded krait

Zoological name: Bungarus fasciatus
Common name: Banded krait

Features:

  • Inverted “V” shaped mark on head
  • Broad black and yellow glistening bands encircle the body. On cross-section, the bands are triangular in shape
  • As per habitat, the snake is shy in nature often seen basking near water bodies usually in morning hours
  • Venom — neurotoxic

Saw Scaled Viper

Saw Scaled Viper
Fig: Saw scaled viper

Zoological name: Echis carinatus
Common name: Carpet viper, phoorsa, afai

Features:

  • Aggressive snake
  • Viviparous
  • Usually brown in color and grows up to 1.5 to 2 feet
  • Head triangular with small scale. White “arrow mark” or “spear mark” may present on head
  • Pupils are vertical
  • Wavy white line (zig-zag pattern) may present on each flank
  • Diamond shaped markings over back
  • Belly scales are broad and cover entire width
  • The scales of viper are serrated, saw like thus name sawscale viper
  • Fangs are long, curved, hollow, channelised and hinged
  • Venom — vasculotoxic and hemotoxic
  •  (Can also be remembered as 5 V’s; V= viper, V=viviparous, V=vertical pupil, V=v shaped head (triangular), V=vasculotoxic venom)

Russell’s Viper

Russell’s Viper
Fig: Russell’s viper

Zoological name: Vipera russelli
Common name: Kander, ghonas

Features:

  • Head is large, flat and triangular with small scales. White V shaped mark present on head
  • Pupils are vertical
  • Large nostrils
  • Body is stout and fatty with brown or yellowish color
  • Body scales are semi-elliptical
  • Three rows of chained dark spots present on back
  • Tail is narrow and short. Scales are divided into two rows
  • Fang are long, curved, hollow, channelized and hinged
  • When disturbed, makes a loud and hissing sound
  • Venom — Vasculotoxic and hemotoxic

Sea Snakes

  • Sea snakes are usually bluish, grayish or greenish in color. They have prominent nostrils and are situated on the top of snout
  • Body is flat and belly scales are not broad
  • Tail is flattened and paddle shaped
  • Venom — myotoxic

Venom

Basically snake venom are of three types, namely neurotoxic, haemotoxic and myotoxic venom.

Types of venom are:

Neurotoxic Venom

  • Origin—Common in Elapidae snakes, e.g. krait, cobra, etc.
  • Action—Acts like Curare, mainly on the motor nerve cells and results in muscular paralysis, the muscles are affected in following order:
  • >Firstly—Muscles of the mouth
  • >Secondly—Muscles of the throat
  • >Finally—Muscles of respiration
  • Symptoms at bite site—Local manifestations are least with neurotoxic venom snake bite
  • Other symptoms—Convulsions may be seen with Cobra venom (Krait venom produces only paralysis)

Haemotoxic Venom

  • Origin—Common in Viperidae snakes, e.g. Pit viper (Crotalidae); Pit-less viper (Russell’s viper, Saw scaled viper/Phoorsa/Echis/Echis Carinata), and Bamboo snake (Common green pit viper)
  • Action—Acts by cytolysis of endothelium of blood vessels, lysis of red cells and other tissue cells and coagulation disorders. All these can lead to:
  • >Severe swelling with oozing of blood and spreading cellulitis at bite site. Blood from such patients fails to clot even on adding thrombin, because of very low level of fibrin.
  • >Necrosis of renal tubules, and
  • >Functional disturbances like convulsions, due to intracerebral haemorrhage.

Myotoxic Venom

  • Origin—Common in hydrophidae or sea snakes
  • Action—Produces generalized muscular pain, followed by:
  • >Myoglobinuria within 3 to 5 hours
  • >Death usually occurs due to respiratory failure

Fatal Dosage for Venom?

Depending upon snake type, some common snake venoms with dosage toxicity are:-

Clinical Features

The signs and symptoms of snake bite vary depending on the snake that bites:

Non-Poisonous Snake

  1. Fear and apprehension
  2. Sweating
  3. Patient may be in state of shock with feeble pulse, hypotension, syncope, rapid and shallow breathing
  4. Bite area — may show multiple teeth marks

Poisonous snake

Elapid Bite

Local Features:

Elapid Bite Local Features
Fig: Bite area in elapid bite
  • Fang marks
  • Burning pain
  • Swelling and discoloration sometimes associated with some blisters
  • Serosanguinous discharge from bite site
  • In comparison with viper bite, local manifestations are milder in elapid bite

Systemic features:

Elapid Bite Systemic Features
Fig: Flow chart showing clinical features in elapid bite
  • Pre-paralytic stage — characterized by vomiting, headache, giddiness, weakness, lethargy
  • Paralytic stage — characterized by spreading paralytic features with ptosis, ophthalmoplegia, drowsiness, dysartheria, convulsions, bulbar paralysis, respiratory failure and death

Viperid bite

Local features:

Local features in Viperid bite
Fig: Local features in Viperid bite
Local features in Viperid bite 2
Fig: Local features in Viperid bite
  • Rapid swelling of the bite site
  • Discoloration
  • Blister formation — may extend to entire limb and even spread to trunk
  • Bleeding from bite site
  • Pain

Systemic features:

  • Generalized bleeding—epistaxis, hemoptysis, hemetemesis, bleeding gums, hematuria, melaena, hemorrhagic areas over skin and mucosa
  • Shock
  • Renal failure

Hydrophid bite

Local features:

  • Local swelling
  • Pain

Systemic features:

  • Myalgia
  • Muscle stiffness
  • Myoglobinuria
  • Renal failure

Diagnosis

Diagnosis depends on:

  1. Identification of fang marks
  2. Identification of snake—vide supra
  3. Laboratory methods

Fang marks

Multiple Bite mark in poisonous snake
Fig: Multiple bite marks in poisonous snake
Multiple Fang mark in poisonous snake
Fig: Fang marks in poisonous snake

Usually, two fang marks in form of puncture wound can be noticed. The puncture wounds are usually separated from each other by a distance varying from 8 mm to 4 cm depending up on the type of poisonous snake. At times, due to sideswipe, a single mark may be produced or if the area is bitten at multiple times, it may result in more fang marks.

Laboratory methods

  • Complete blood count—leucocytosis may be evident with thrombocytopenia
  • Smear — hemolysed and fragmented RBCs
  • Increased prothrombin time and increased partial thromboplastin time
  • Immunodiagnosis — consists of:
  1. Immunodiffusion
  2. Counter-current immunoelectrophoresis
  3. ELISA
  4. Radioimmunoassay

Management

General Measures

Non-poisonous snakebite:

  • Allay the anxiety and fear
  • Reassure the patients that all snakes are not poisonous
  • Avoid alcohol or morphine, for these can increase the rate of absorption of venom

First aid and field management

First aid in snakebite
Fig: First aid in snakebite
  • Reassurance
  • Limit systemic spread of venom by immobilizing the affected part (e.g. limb)
  • For Viperid bites, the bitten limb should be splinted if possible and kept at approximately heart level
  • For elapid or sea snakebites, the Australian pressure immobilization technique is beneficial. In this method, the entire bitten limb is wrapped with an elastic or crepe bandage and then splinted
  • Tourniquet—a proximal lymphatic-occlusion constriction band or torniquet may limit the spread of venom if applied within 30 minutes. The tourniquet should be applied such that it does not prevent arterial flow of blood and the distal pulsation should be appreciated

Hospital Management

  • Monitor vital signs, cardiac rhythm, oxygen saturation and urine output
  • The level of local edema/swelling/erythema in the bitten limb should be marked and the circumference should be measured every 15 minutes until swelling has stabilized
  • Intravenous access with fluid resuscitation. If needed, vasopressors (e.g. dopamine) should be administered
  • Blood and urine should be collected for laboratory evaluation
  • Care of bite site — apply dry sterile dressings. Splint may be applied
  • Tetanus immunization should be updated as appropriate
  • If the swelling in the affected limb continues and impending tissue perfusion causing muscle compartment syndrome, intracompartmental pressure should be checked. If pressure is elevated prompt surgical consultation should be obtained while antivenin continues
  • Antivenin therapy—antivenin should be administered only when indicated. Antivenins are available as monovalent (i.e. species specific) or polyvalent. In India, polyvalent antivenin is available that is effective against common cobra, common krait, Russell’s viper and sawscaled viper. The antivenin should be administered with caution. Usually the antivenins are of equine origin and carry risk of anaphylaxis or delayed-hypersensitivity type of reactions. Prior to administration of antivenin infusion, the patient should receive appropriate loading doses of intravenous antihistamines. The antivenin should be administered as intravenous infusion. It should be dissolved in 500 ml of normal saline or Ringer’s lactate or 5% dextrose for adults and 20 ml/kg for children
  • Severe hemorrhage or bleeding may require blood or fresh frozen plasma
  • If there are features of neurotoxicity, neostigmine may be required. Every injection of neostigmine should be preceded with atropine
  • Oxygen, ventilatory support
  • Management of renal failure on usual line

Adverse reactions to antivenin

  • Anaphylaxis
  • Delayed type of hypersensitivity reaction

Chronic Kidney Disease – An Occasion of CKD Day

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On the very special day for the beany kidneys, we are going to stir you up about the disease of kidney, especially the chronic kidney disease, with our latest blog.

Overview

Kidney, being one the most vital organ (of course all organs are vital but Kidney is close to topping the chart) most often gets neglected by common people. By the time patients realize the complications it can yield, the disease would have reached an advanced stage. March 12th -World Kidney Day did not get the attention it most certainly requires among the masses. So let’s get to know more about Chronic Kidney Diseases (CKD).

What is CKD?

Chronic Kidney Disease PathologyChronic Kidney Disease is defined as persistent kidney damage accompanied by a reduction in the glomerular filtration rate (GFR) and the presence of albuminuria.

Statistics and Etiology

According to World Health Organization (WHO) Global Burden of Disease Project, disease of the kidney and urinary tract contribute to approximately 8,50,000 deaths every year of which Chronic Kidney Disease (CKD) is the 12th leading cause of death and 17th leading cause of disability in the world.

The global increase in CKD is due to diabetes mellitus, hypertension, obesity, and aging. The two most common causes of kidney disease are diabetes and high blood pressure. People with a family history of any kind of kidney disease are also at high risk.

Diabetic Nephropathy

It is a progressive disease characterized by nephrotic syndrome and diffuse glomerulosclerosis. Initially it causes glomerular hyperfiltration which progresses to BM (Basement membrane)thickening which leads to microalbuminuria .This is the earliest detectable change in the course of diabetic nephropathy.

Proliferation of mesangium follows and finally nodular sclerosis occurs. The Armanni-Ebstein change or Armanni-Ebstein cells which are deposits of glycogen in the tubular epithelial cells are seen in the end stages of this disease.

Hypertension and CKD

The relationship between HTN and CKD is cyclic in nature. Uncontrolled HTN is a risk factor for developing CKD and is also associated with a more rapid progression of CKD. Primarily, there is impairment in the glomerular filtration causing microalbuminuria.

Other Causes

Autoimmune diseases (such as systemic lupus erythematosus and scleroderma),infection-related diseases, and sclerotic diseases may also cause CKD. Irrational use of NSAID’s can also lead to CKD by causing interstitial nephritis.

Signs and Symptoms

The patient usually presents with the following symptoms:-

  • Edema
  • Persistent fatigue or shortness of breath
  • Loss of appetite
  • Increasing blood pressure
  • Pale, itchy, dry skin
  • Odoor in breath

Staging

  • Staging can be done by the following investigations:
  • Glomerular filtration rate (GFR)
  • Urine albumin:

Staging of Chronic Kidney Disease

  • Blood Urea Nitrogen (BUN)
  • Kidney imaging
  • Kidney Biopsy

Complications

The kidneys make and release hormones and balance the minerals in the blood. When the kidneys stop working, most people develop conditions that affect the blood, bones, nerves, and skin. These complications can range from uncomfortable to damaging and potentially even life-threatening. Managing these complications may help prevent or slow further damage to your kidneys and help you stay as healthy as possible.

The following image may shortly explain the complications of chronic kidney disease:-
Complications of Chronic Kidney Disease

Treatment

For stages I- IV, the first line therapy is to not only lower BP, but also to reduce proteinuria. Such drugs are:

  • ACE Inhibitors
  • ARB’s
  • Thiazide/Loop diuretics
  • Aldosterone antagonists
  • Renin inhibitors
  • Calcium Channel Blockers
  • Beta blocker

Lifestyle modifications are also suggested:

Increase physical activity, weight loss, and dietary modifications. Patient should be advised not to smoke/consume alcohol, explaining his situation.

For Vth stage of the disease, RTT (Renal Replacement Therapy) is advised.
Renal replacement therapy includes kidney transplant, peritoneal dialysis & Hemodialysis. Renal replacement therapy is usually indicated in end stage renal disease.

MBBS Third Year Books and Syllabus

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Third year MBBS consists of one year which includes the Subjects– Ophthalmology, ENT and Community medicine. Ophthalmology refers to Eye, ENT is based on Ear Nose and Throat while Community Medicine is somewhat branch of Medicine but with detailed Epidemiology. Following are the best MBBS Books for Third Year and the syllabus for each subject. Don’t forget to check our Downloads Section to get the books in PDF Format.

If you are in other year, you can jump to the below sections:

Ophthalmology

Ophthalmology in Third Year MBBS deals with primary eye care and study of related diseases.

Syllabus

The Syllabus for Ophthalmology for Third Year MBBS has been listed below:

1. COMMON DISEASE OF EYE

A) Conjunctiva

  • Symptomatic conditions: – Hyperemia, Sub conjunctival Haemorrhage
  • Diseases: – Classification of Conjunctivitis
  • > Mucopurulant Conjunctivitis
  • > Membranous Conjunctivitis Spring Catarrh
  • > Degenerations :- Pinguecula and Pterigium

B) Cornea

  • Corneal Ulcers: Bacterial, Fungal, Viral, Hypopyon
  • Interstitial Keratitis
  • Keratoconus
  • Pannus
  • Corneal Opacities
  • Keratoplasty

C) Sclera

  • Episcleritis
  • Scleritis
  • Staphyloma

D) Uvea

  • Classification of Uveitis
  • Gen. Etiology, Investigation and Principles Management of Uveitis
  • Acute & Chronic Iridocyclitis
  • Panophthalmitis
  • End Ophthalmitis
  • Choriditis

E) Lens

  • Cataract – Classification & surgical management of cataract
  • Including Preoperative Investigation
  • Aphakia
  • IOL Implant

F) Glaucoma

  • Aqueous Humor Dynamics
  • Tonometry
  • Factors controlling Normal I.O.P
  • Provocative Tests
  • Classifications of Glaucoma
  • Congenital Glaucoma
  • Angle closure Glaucoma
  • Open Angle Glaucoma
  • Secondary Glaucoma

G) Vitreous

  • Vitreous. Opacities
  • Vitreous. Haemorrhage

H) Intraocular Tumours

  • Retinoblastoma
  • Malignant Melanoma

I) Retina

  • Retinopathies : Diabetic, Hypertensive Toxaemia of Pregnancy
  • Retinal Detachment
  • Retinitis Pigmentosa, Retinoblastoma

J) Optic nerve

  • Optic Neuritis
  • Papilloedema
  • Optic Atrophy

K) Optics

  • Principles : V.A. testing Retinoscopy, Ophthalmoscopy
  • Refraction Errors
  • Refractive Keratoplasty
  • Contact lens, Spectacles

L) Orbit

  • Proptosis – Aetiology, Clinical Evaluation, Investigations & Principles of Management
  • Endocrinal Exophthalmos
  • Orbital Haemorrhage

M) Lids

  • Inflammations of Glands
  • Blepharitis
  • Trichiasis, Entropion
  • Ectropion
  • Symblepharon
  • Ptosis

N) Lacrimal System

  • Wet Eye
  • Dry Eye
  • Naso Lacrimal Duct Obstruction
  • Dacryocystitis

O) Ocular Mobility

  • Extrinsic Muscles
  • Movements of Eye Ball
  • Squint : Gen. Aetiology, Diagnosis and principles of Management
  • Paralytic and Non Paralytic Squint
  • Heterophoria
  • Diplopia

P) Miscellaneous

  • Color Blindness
  • Lasers in Ophthalmology – Principles

Q) Ocular Trauma

  • Blunt Trauma
  • Perforating Trauma
  • Chemical Burns
  • Sympathetic Ophthalmitis

2) Principles of Management of Major Opthalmic Emergencies

  • Acute Congestive Glaucoma
  • C. Ulcer
  • Intraocular Trauma
  • Chemical Burns
  • Sudden Loss of vision
  • Acute Iridocyclitis
  • Secondary Glaucomas

3) Main Systemic Diseases Affecting the Eye

  • Tuberculosis
  • Syphilis
  • Leprosy
  • Aids
  • Diabetes
  • Hypertension

4) Drugs

  • Antibiotics
  • Steroids
  • Glaucoma Drugs
  • Mydriatics
  • Visco elastics
  • Fluoresceue

5) Community Ophthalmology

  • Blindness : Definition Causes & Magnitude
  • N.P.C.B. – Integration of N.P.C.B. with other health
  • Preventable Blindness
  • Eye care
  • Role of PHC’s in Eye Camps
  • Eye Banking

6) Nutritional

  • Vitamin A Deficiency

Best Books

Following MBBS Books are recommended for Ophthalmology in Third year MBBS:



  1. BASAK – OPHTHALMOLOGY ORAL & PRACTICAL
  2. BASAK – ESSENTIALS OF OPHTHALMOLOGY
  3. CHATTERJEE -HANDBOOK OF OPHTHALMOLOGY
  4. D.K. (SAMANT) – OPHTHALMOLOGY: THEORY PRECTICAL WITH MCQ’S
  5. AK KHURANA – OPHTHALMOLOGY
  6. NEMA – TEXTBOOK OF OPHTHALMOLOGY
  7. PARSON’S – DISEASES OF THE EYE
  8. SEETHARAMAN – PRACTICAL OPHTHALMOLOGY
  9. SHEKHAR – MCQ’S IN OPHTHALMOLOGY

ENT (Ear Nose Throat)

ENT in Third Year MBBS deals with common disorders, emergencies in ENT, and basic principles of impaired hearing and rehabilitation.

Syllabus

The Syllabus for ENT for Third Year MBBS has been listed below:

Throat

  • Anatomy/physiology
  • Diseases of buccal cavity
  • Diseases of pharynx
  • Tonsils and adenoids
  • Pharyngeal tumours and related topics (trismus, Plummer .Vinson Syndrome etc.)
  • Anatomy /physiology/examination
  • Methods/symptomatology of larynx
  • Stridor /tracheostomy
  • Laryngitis /laryngeal trauma/ Laryngeal paralysis/ foreign body larynx/Bronchus, etc.
  • Laryngeal tumours

Nose and Paranasal sinuses

  • Anatomy /physiology/ exam.
  • Methods /symptomatology
  • Diseases of ext. nose/cong.
  • Conditions
  • • Trauma to nose/p.n.s/Foreign Body. / Rhinolith
  • • Epistaxis
  • • Diseases of nasal septum
  • • Rhinitis
  • • Nasal polyps/nasal allergy
  • • Sinusitis and its complications
  • • Tumours of nose and Para nasal sinuses

Ear

Study of Ear, including the basic anatomy, physiology and diseases related to ear.

Syllabus
  • Anatomy / Physiology
  • Methods / methods of examination
  • Congenital diseases / ext.ear /middle ear
  • Acute/chronic supp. otitis media – Aetiology, clinical features and its management/complications
  • Serous/adhesive otitis media
  • Mastoid/middle ear surgery
  • Otosclerosis/tumours of ear
  • Facial paralysis/Meniere’s disease
  • Tinnitus /ototoxicity
  • Deafness/hearing aids/rehabilitation
  • Audiometry

Best Books

Following MBBS Books are recommended for ENT in Third Year MBBS:

  1. BHARGAVA – A SHORT TEXTBOOK OF E.N.T. DISEASE
  2. DHINGRA- DISEASE OF EAR, NOSE AND THROAT
  3. HATHIRAM- E.N.T. SIMPLIFIED
  4. LOGAN TURNER’S – DISEASE OF THROAT, NOSE AND EAR
  5. PRABHAT- PRACTICAL ENT

Community Medicine

Community Medicine in Third Year MBBS deals with Teachings of the community and general understanding.

Syllabus

The Syllabus for Community Medicine for Third Year MBBS has been listed below:

  • Basic concept of Health and disease
  • Sociology and health
  • Epidemiology
  • Communicable disease epidemiology
  • Non-communicable disease epidemiology
  • National Health Programmes of India
  • Environment and impact on health
  • Entomology
  • Occupational Medicine / occupational health
  • Genetics and health
  • Nutrition and health
  • Health care management India and International
  • Primary Health care
  • International Health and travelers health

Best Books

Following MBBS Books are recommended for Community Medicine in Third year MBBS:

  1. Text book of Community Medicine, Kulkarni A.P. and Baride J.P
  2. Park’s Textbook of Preventive and Social Medicine, Park
  3. Principles of Preventive and Social Medicine, K. Mahajan
  4. Textbook of Community Medicine, B. Shridhar Rao
  5. Essentials of Community Medicine, Suresh Chandra
  6. Textbook of Biostatistics, B. K. Mahajan
  7. Review in Community Medicine, V.R. Sheshu Babu
  8. Sociology and Health Niraj Pandit
  9. National Health Programme, J Kishor

Further Reading

  1. Epidemiology and Management for health care for all P.V. Sathe and A.P. Sathe
  2. Essentials of Preventive Medicine O.P. Ghai and Piyush Gupta

MBBS Second Year Books and Syllabus

2

Second Year MBBS consists of one and a half year comprising of three semesters which includes the Subjects – Pathology, Pharmacology, Microbiology and Forensic medicine. There are many MBBS Books you can read in Second year, but the best ones are always textbooks. About the MBBS Syllabus for Second year, it is given as such to help you understand more deeply. Don’t forget to check our Downloads Section for latest books in PDF Format.

If you are in other year, you can jump to the below sections:

Pathology

Pathology in Second Year MBBS deals with causes and mechanisms of diseases.

Syllabus

The Syllabus for Pathology for Second Year MBBS has been listed below:

A. General Pathology
B. Hematology
C. Systemic Pathology
D. Clinical Pathology

These are detailed as follows:

A) GENERAL PATHOLOGY

  • Microscopy and tissue processing
  • Identify the common types of cells by light microscopy
  • Intracellular accumulation
  • Acute inflammation
  • Chronic inflammation and Repair
  • Thrombosis, embolism, infarction and gangrene
  • Edema and congestion
  • Disturbances of pigment metabolism
  • Tuberculosis
  • Leprosy
  • Amyloidosis
  • Disturbances of growth (Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, hypoplasia)

B) HEMATOLOGY

  • Collection of specimen, anticoagulants and common hematological tests (Hb)
  • Common Haematological Counts (TLC, DLC) & Interpretation of ESR
  • Haemopoiesis
  • Investigations in Anemia
  • Investigations in Leukemia
  • Investigations in hemorrhagic disorders
  • Blood Banking

C) SYSTEMIC PATHOLOGY

  • Diseases of blood vessels (Atherosclerosis, syphilitic aortitis)
  • Diseases of Heart (IHD & RHD)
  • Pneumonia
  • Tumors of lung
  • Diseases of kidney
  • Gross and Microscopic features of peptic ulcer and duodenal ulcer
  • Gross and Microscopic features of other intestinal ulcers
  • Tumors of GIT
  • Diseases of Liver
  • Lymphomas
  • Diseases of male and female genital system
  • Tumors of breast
  • Tumors of skin (Pigmented)
  • Tumors of skin (non-pigmented)
  • Soft tissue tumors
  • Tumors of bone
  • Diseases of thyroid

D) CLINICAL PATHOLOGY

  • Urine RE – Carryout a bedside routine urine examination and interpret the results.
  • Pregnancy test and Semen Analysis – (Practical demonstration).
  • Common cytological preparations (lecture demonstration).
  • CSF examination.
  • Serous effusion examination.

Best Books

Following MBBS Books are recommended for Pathology in Second year MBBS:

  1. Text book of Pathology by Robbins
  2. Text book of General Pathology Part I & II by Bhende and Deodhare
  3. Clinical Pathology by Talib
  4. Textbook of Pathology by Harsh Mohan
  5. Textbook of Pathology by Muir
  6. Hematology De Gruchi
  7. IAPM text book of Pathology

Reference books

  1. Anderson’s text book of Pathology Vol I & II
  2. Oxford text book of Pathology Vol. I, II & III
  3. Pathology by Rubin and Farber
  4. Pathological basis of Disease Robbins

Pharmacology

Pharmacology in Second Year MBBS deals with Rational and scientific basis of therapeutics.

Syllabus

The Syllabus for Pharmacology for Second Year MBBS has been listed below:

A) INTRODUCTION

  • Pharmacology – a foundation to clinical practice
  • Development of the branch of pharmacology; Scope of the subject; role of drugs as one of the modalities to treat diseases, definition of drug; nature and sources of drugs; subdivisions of pharmacology rational pharmacotherapy

B) GENERAL PHARMACOLOGY

  • Pharmacokinetics
  • Application to pharmacotherapeutics
  • Adverse Drug Reactions

C) AUTONOMIC PHARMACOLOGY

D) CARDIOVASCULAR SYSEM INCLUDING DRUGS AFFECTING
COAGULATION AND THOSE ACTING ON KIDNEYS

  • General Considerations and Overview of anti-hypertensive therapy
  • Diuretics
  • Angiotensin Converting Enzyme (ACE) inhibitors
  • Sympatholytic & vasodilators
  • Management of hypertension
  • Antianginal: Nitrates & others
  • Calcium channel blockers
  • Pharmacotherapy of chest pain
  • Anticoagulants & Coagulants
  • Thrombolytic & Antiplatelet Agents
  • Drugs for CCF: Digitalis glycosides, other agents
  • Management of CCF
  • Antiarrhythmic Agents
  • Agents used for the management of shock
  • Hypolipidaemic drugs
  • Role of Nitric oxide and endothelin to be covered in CVS

E) HAEMATINICS AND HAEMATOPOIETIC FACTORS

  • Agents used in therapy of iron deficiency anemia and megaloblastic anemia; Erythropoietin
  • Management of anemia

F) NEUROPSYCHIATRIC PHARMACOLOGY INCLUDING INFLAMMATON,
PAIN & SUBSTANCE ABUSE

  • General Considerations
  • Sedative-Hypnotics
  • Psychopharmacology: Antianxiety; Antipsychotics; Antidepressants
  • Anti-epileptics
  • Therapy of neurodegenerative disorders:
  • Anti-Parkinsonian agents; cerebral vasodilators/nootropics
  • Local anesthetics
  • Analgesics: Opioids; NSAIDs
  • Pharmacotherapy of pain including migraine
  • Pharmacotherapy of rheumatoid arthritis and gout
  • Substance abuse: Management of opioid, alcohol and tobacco Addictions

G) MISCELLANEOUS TOPICS – I

  • Autocoids (to be covered before pain lectures)
  • Antiallergics: Antihistaminic
  • Drugs used for bronchial asthma
  • Pharmacotherapy of cough
  • Drugs acting on immune system: Immunostimulants, immunosuppressants; pharmacology of vaccines & sera
  • Drugs acting on the uterus

H) CHEMOTHERAPY INCLUDING CANCER CHEMOTHERAPY

  • General considerations
  • Antimicrobial agents:
  • • Sulphonamides & Cotrimoxazole
  • • Quinoline derivatives
  • • Penicillins, Cephalosporins & Other? Lactams
  • • Aminoglycosides
  • • Macrolides
  • • Tetracyclines & Chloramphenicol
  • Pharmacotherapy of UTI
  • General principles of Antimicrobial use
  • Antimycobacterial therapy: Anti-Kochs agents; Anti-leprotic agents
  • Pharmacotherapy of tuberculosis
  • Antiprotozoal agents: Antiamoebic, Antimalarials and Anti Kala azar, Pharmacotherapy of malaria
  • Antihelminthics (against intestinal Nematodes and Cestodes; extra intestinal Nematodes and Trematodes)
  • Antifungal agents
  • Antiviral agents including antiretroviral agents
  • Pharmacotherapy of STDs
  • Principles of cancer chemotherapy and their adverse drug reactions (individual agents and regimes need not be taught)

I) ENDOCRINOLOGY

  • Introduction to endocrinology (including Hypothalamic and Anterior Pituitary hormones)
  • Steroids
  • Glucocorticoids: Use and Misuse
  • Oestrogens & antagonists
  • Progestins & antagonists
  • Oral contraceptives & pro-fertility agents
  • Testosterone & anabolic steroids
  • Fertility control
  • Thyroxine and anti-thyroid agents
  • Agents affecting calcification
  • Antidiabetic agents: Insulin; Oral antidiabetic drugs
  • Pharmacotherapy of Diabetes Mellitus

J) AGENTS USED IN GASTROINTESTINAL DISORDERS

  • Pharmacotherapy of nausea & vomiting
  • Pharmacotherapy of peptic ulcer
  • Management of dyspepsia
  • Management of diarrhoea and constipation

K) PERI-OPERATIVE MANAGEMENT: to be covered as a case study

  • Pre-anesthetic medication
  • Preparation of surgical site: antiseptics etc.
  • Local Anesthetics
  • Skeletal muscle relaxants
  • Drugs used in post-operative period: analgesics, anti-emetics etc.

L) MISCELLANEOUS TOPICS – II

  • Drug-Drug Interactions
  • Drug use at extremes of age, in pregnancy & in organ dysfunction
  • Use of chelating agents in heavy metal poisonings; Environmental &
  • Occupational toxicants and principles of management (particularly cyanide and CO)
  • Ocular pharmacology
  • Dermatopharmacology
  • General Anesthetics
  • Pharmacotherapy of glaucoma and conjunctivitis

M) RATIONAL PHARMACOTHERAPY

  • Prescription writing and P-drug concept
  • Rational Drug Use; Essential Drug List (EDL)
  • Criticism with reference to Fixed Drug Combinations (FDCs)
  • Use and misuse of commonly used preparations: vitamins, antioxidants, enzymes etc.

Best Books

Following MBBS Books are recommended for Pharmacology in Second year MBBS:



  1. Basic & Clinical Pharmacology. Katzung BG (Ed), Publisher: Prentice Hall International Ltd., London
  2. Pharmacology & Pharmacotherapeutics. Satoskar RS, Bhandarkar SD (Ed), Publisher: Popular Prakashan, Bombay
  3. Essentials of Medical Pharmacology. Tripathi KD (Ed), Jaypee Brothers, publisher:Medical Publishers (P) Ltd
  4. Clinical Pharmacology. Laurence DR, Bennet PN, Brown MJ (Ed). Publisher: Churchill Livingstone
  5. Shanbagh Pharmacology

Reference books

  1. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. Hardman JG & Limbird LE (Ed), Publisher: McGraw-Hill, New York.
  2. A Textbook of Clinical Pharmacology. Roger HJ, Spector RG, Trounce JR (Ed), Publisher: Hodder and Stoughton Publishers.

Microbiology

Microbiology in Second Year MBBS deals with Etiology, pathogenesis, pathogenicity, laboratory diagnosis, treatment, control and prevention of infections and infectious diseases.

Syllabus

The Syllabus for Microbiology for Second Year MBBS has been listed below:

A) GENERAL MICROBIOLOGY

  • Introduction and Historical background
  • Morphology of bacteria and Classification
  • Physiology of bacteria including growth requirements & metabolism
  • Sterilization
  • Disinfectants
  • Waste disposal
  • Bacterial genetics and drug resistance to antimicrobial agents.
  • Host parasite relationship and bacterial infections
  • Normal flora
  • Methods of identification of bacteria. Diagnosis of infectious diseases (direct and indirect)

B) IMMUNOLOGY

  • Introduction
  • Antigens, HLA
  • Antibodies
  • Serological reactions
  • Immune response
  • Complement
  • Hypersensitivity
  • Autoimmunity
  • Transplantation & tumor immunology
  • Immuno-Deficiency

C) SYSTEMIC BACTERIOLOGY

  • Pathogenesis includes:
  • Infectious agent
  • Habitat
  • Source / reservoir
  • Mode
  • Infective dose
  • Multiplication, spread
  • Clinical features, pathology
  • Complications
  • Virulence factors
  • Immunological response

Laboratory diagnosis:

  • Specimen selection
  • Collection
  • Transport
  • Primary smear, hanging drop
  • Selection of media
  • Pathogenicity testing
  • Anti microbial drug susceptibility testing
  • Serological interpretation

D) MYCOLOGY

  • Introduction to Mycology
  • Agents of Superficial mycosis
  • Subcutaneous mycosis
  • Systemic mycosis & Opportunistic fungal infections

E) VIROLOGY

  • Morphology, pathogenesis, laboratory diagnosis, prevention and control for all viruses.
  • General Virology
  • Laboratory diagnosis of viral infections
  • Viral immunity
  • Pox viruses
  • DNA viruses
  • Respiratory viruses
  • Picornaviruses
  • Hepatitis viruses
  • Arboviruses
  • Rhabdoviruses
  • Slow and Oncogenic viruses
  • Retroviruses

F) PARASITOLOGY

  • Geographical distribution
  • Habitat
  • Morphology (different stages) found in human beings
  • Life cycle
  • Pathogenesis
  • Laboratory diagnosis
  • Treatment
  • Control
  • Immunoprophylaxis of E. histolytica, Free living amoebae and flagellates, Hemoflagellates, Malaria, Toxoplasma, Taenia saginata & solium, Echinococcusgranulosus, Schistosomiasis, A.duodenale, A. lumbricoides, E. vermicularis, T. tritura, W. bancrofti, D. medinensis, T. spiralis

Best Books

Following MBBS Books are recommended for Microbiology in Second year MBBS:

  1. Textbook of Microbiology – R. Ananthanarayan
  2. A Textbook of Microbiology – P. Chakraborty
  3. Textbook of Medical Microbiology – Rajesh Bhatia & Itchpujani
  4. Textbook of Medical Microbiology – Arora and Arora
  5. Textbook of Medical Parasitology – C. K. Jayaram Panikar
  6. Textbook of Medical Parasitology – Arora and Arora
  7. Textbook of Medical Parasitology – S.C.Parija
  8. Microbiology in clinical practice – D. C. Shanson

Reference books:

  1. Mackie McCartney practical Medical Microbiology- Colle JG, Fraser AG
  2. Principles of Bacteriology, Virology & Immunology vol. 1, 2, 3, 4, 5- Topley Wilsons
  3. Medical Mycology (Emmons) – Kwon – Chung
  4. Review of Medical Microbiology (Lange) – Jawetz
  5. Immunology- Weir DM
  6. Medical Microbiology- David Greenwood, Richard Stack, John Pentherer
  7. Parasitology- KD Chatterjee
  8. Medical virology- Timbury MC
  9. Mackie McCartney Medical, Microbiology vol.1- Duguid JP
  10. Microbial infections- Marmion BP, Swain RHA

Forensic Medicine and Medical Jurisprudence and Toxicology

FMT in Second Year MBBS deals with the medico-legal sciences.

Syllabus

The Syllabus for Forensic Medicine for Second Year MBBS has been listed below:




A) DEFINITION, SCOPE RELEVANT TO SUBJECT

  • History of Forensic Medicine
  • Need, Scope, Importance and probative value of Medical evidence in Crime Investigation

B) PERSONAL IDENTITY NEED AND ITS IMPORTANCE

  • Data useful for Identification of Living and Dead
  • Age estimation and its medico-legal Importance
  • Sex determination and its medico-legal importance
  • Other methods of establishing identity: Corpus Delicti, Dactylography, Tattoo marks, Deformities, Scars and other relevant factors
  • Identification of decomposed, mutilated bodies and skeletal remains
  • Medico legal aspect of *DNA fingerprinting – a brief introduction
  • Medico – legal aspect of blood and blood stains Collection, Preservation and Dispatch of Specimen for Blood and other ancillary material for identification and Medico-legal examination

C) MECHANICAL INJURIES AND BURNS

  • Definition and classification of injuries: Abrasions, Contusions, Lacerations, Incised and Stab injury, Firearm and Explosion injury, Fabricated and Defense injury
  • Medico-legal aspect of injury/hurt, simple and grievous hurts, murder, Ante -mortem, Postmortem Wounds, Age of the injury, cause of death and relevant sections of I.P.C., Cr.P.C.
  • Causative Weapon and appearance of Suicidal, Accidental and Homicidal injuries
  • Physical methods of Torture and their identification
  • Reporting on Medico-legal cases of Hurts
  • Regional injuries: Head injury, cut throat injuries and Road traffic accident injuries
  • Thermal injuries: Injuries due to heat and cold, Frostbite, Burns, Scalds and Bride burning
  • Injuries due to Electricity, Lightening Collection, Preservation and Dispatch of Specimen for Blood and other ancillary material for Medico-legal examination

D) MEDICO-LEGAL ASPECTS OF SEX, MARRIAGE AND INFANT DEATH

  • Sexual Offenses and perversions: Natural (Rape, Adultery, and Incest), Unnatural (Sodomy, Bestiality and Buccal coitus) Lesbianism, perversions and relevant sections of I.P.C. and Cr.P.C.
  • Fertility, Impotence, Sterility, Virginity, and Nullity of marriage and divorce on Medical ground
  • Pregnancy, Delivery, Paternity, Legitimacy, Artificial Insemination,Fertilisation in Vitro, Sterilization (Family Planning Measures)
  • Abortions, Medical Termination of pregnancy, criminal abortions, Battered Baby Syndrome, Cot deaths and relevant sections of I.P.C. and Cr.P.C., M.T.P. Act of 1971 and fetal sex determination act
  • Infant death (Infanticide)
  • Definition Causes, Manners and Autopsy features:
  • ii. Determination of age of Fetus and Infant
  • iii. Signs of live-born, stillborn and dead born child
  • Collection, Preservation and Dispatch of Specimen: Hair, seminal fluid/stains and other ancillary material for medico-legal examination, examination of seminal stains and vaginal swabs

E) MEDICO-LEGAL ASPECTS OF DEATH

  • Definition and concept of death, stages, modes, Signs of death and its importance
  • Changes after death, Cooling, Hypostasis, Changes in eye, Muscle changes, Putrefaction, Saponification, Mummification, Estimation of time since death
  • Death Certification, Proximate causes of death, causes of sudden deaths, Natural deaths. Presumption of death and survivor-ship, disposal and preservation of dead
  • Introduction to *The Anatomy Act, *The Human organ transplantation Act. 1994
  • Medico-legal aspects and findings of post-mortem examination in cases of death due to common unnatural conditions
  • Sudden unexpected death, deaths from starvation, cold and heat and their medico-legal importance
  • Medico-legal aspects of death from Asphyxia, Hanging, Strangulation, Suffocation and Drowning

F) MEDICO-LEGAL AUTOPSY

  • Autopsy: Objectives, Facilities, Rules and Basic techniques, Proforma for reporting medico-legal autopsy
  • Exhumation, examination of mutilated remains, Obscure autopsy and post-mortem artifacts
  • Collection, preservation and dispatch of material for various investigations to Forensic Science Laboratory

G) FORENSIC PSYCHIATRY

  • Definition, General terminology and Basic concept of normality and abnormality of human behavior, Civil and Criminal responsibility
  • Examination, Certification, restraint and admission to Mental Hospital
  • Mental Health Act – Principles and Objectives

Part – 2 Toxicology

A) POISONS AND THEIR MEDICO-LEGAL ASPECTS

  • Definition of poison, General consideration and Laws in relation to poisonsNarcotic drugs and psychotropic substances Act, Schedules H and L drugs, *Pharmacy Act, Duties and responsibilities of attending physician
  • Common poisons and their classification, Identification of common poisons, Routes of administration, Actions of poisons and factors modifying them, Diagnosis of poisoning (Clinical and Confirmatory) , Treatment/ Management of cases of acute and chronic poisonings
  • Addiction and Habit forming drugs, drug dependence
  • Occupational and environmental poisoning, prevention and Epidemiology of common poisoning and their legal aspects particularly pertaining to Workmen’s Compensation Act
  • Medico-Legal aspects and findings of postmortem examination in cases of death due to poisonings

B) POISONS TO BE STUDIED

  • Corrosive: Euphoric Acid, Nitric Acid, Hydrochloric Acid, Carbolic Acid and Oxalic Acid, Sodium and Potassium and Ammonium Hydro-Oxide
  • Non-metallic, Metallic Poisons and Industrial hazards: Phosphorus and compounds of Lead, Arsenic, and Mercury, Copper, and Glass powder
  • Plant Poisons: Castor, Croton, Capsicum, Semicarpus Anacardium (Bhilawa), Calatropis Gigantea, Abrus Precatorius (Ratti), Dhatura,
  • Cannabis Indica, Cocaine, Opium, Aconite, Yellow Oleander, Strychnine
  • Animal and Bacterial Poisons: Snakes, Scorpion and Food poisoning
  • Alcohol (Drunkenness) Ethyl Alcohol, Methyl Alcohol, Kerosene, Barbiturates
  • Asphyxiant & Gaseous Poisons: Carbon Monoxide, War gases, Hydrocyanic acid, and Cyanides
  • Insecticides, pesticides and Miscellaneous poisons: Organo- Phosphorus Compounds, Organo-Chloro Compounds, Carbamates (Carbaryl) and Rodenticides (Phosphides) Collection, Preservation and forwarding of evidence, remains of poison, body discharges and viscera etc. to Forensic Science Laboratory in cases of poisoning

C) FORENSIC SCIENCE LABORATORY: (BRIEF)

  • Aims, objects, general knowledge about Forensic Science Laboratory
  • General principles of analytical toxicology

Part – 3 Medical Jurisprudence

A) LEGAL AND ETHICAL ASPECTS OF PRACTICE OF MEDICINE

  • The Indian Medical Council, the Act, Formation and Functions; State Medical Council: Formation, Functions, and Registration
  • Rights and obligations of Registered Medical Practitioners and patient, Duties of physicians and patients, Euthanasia
  • Infamous conduct, Professional secrecy and privileged communications
  • Codes of Medical Ethics, medical etiquette, Medical Negligence and contributory negligence, Precautionary measures and defences for Medical Practitioners against legal actions, Medical/Doctors indemnity insurance, Consumer Protection Act relevant to medical practice
  • Medical Ethics and prohibition of Torture & care of Torture Victims

B) DEFINITION OF HEALTH AND ITEMS TO CERTIFY ABOUT HEALTH

  • Common medico-legal problems in Hospital practice, Consent in Medical Examination and treatment, under treatment/ Sickness and
  • Fitness certificate, maintenance of medical records
  • Social, Medical, Legal and Ethical problems in relation to AIDS

C) ACTS AND SCHEMES RELATED TO MEDICAL PROFESSION IN BRIEF:

  • Workmen compensation Act, * Mental Health Act, Medical Practitioner Act, Protection of human rights Act, 1993, * National Human Rights Commission, * Human Organ Transplantation Act and other relevant sections of I.P.C., Cr.P.C. and I.E. Act. Maharashtra civil medical code, Hospital administration manual

Part – 4 Legal procedures in medico-legal cases: (N=8)

  • Medico-Legal Investigations of death in suspicious circumstances, different Inquest, type of offenses
  • Types of Criminal courts and their powers, punishments prescribed by law, kinds of witnesses, Evidence, Documentary Medical evidence, Dying declaration and Dying deposition
  • The Trial of criminal cases, Rules and Conventions to be followed by Medical Witness at Medical evidence, subpoena, conduct money
  • Relevant Sections from the Indian Evidence Act, Indian Penal code and Criminal Procedure code

Best Books

Following MBBS Books are recommended for Forensic Medicine in Second year MBBS:

  1. Modi’s Textbook of Medical Jurisprudence and Toxicology Ed. 22, 1999, by B.V. Subramanyam, Butterworth
  2. The Essentials of Forensic Medicine & Toxicology by K.S. Narayan Reddy
  3. Parikh’s Textbook of Medical Jurisprudence and Toxicology
  4. Nagesh Kumar Forensic Medicine
  5. Text Book of Forensic Medicine – J.B. Mukherjii VOL 1 & 2
  6. Principles of Forensic Medicine – A. Nandy
  7. Toxicology at a Glance by Dr S.K. Singhal
  8. Bernard Knight ET. All: Cox’s Medical Jurisprudence & Toxicology

Reference books:

  1. Russell S. Fisher & Charles S.Petty: Forensic Pathology
  2. Keith Simpson: Forensic Medicine
  3. Jurgen Ludwig: Current Methods of autopsy practice.
  4. Gradwohl – Legal Medicine
  5. A Doctors Guide to Court – Simpson
  6. Polson C.J.: The essentials of Forensic Medicine
  7. Adelson, L.: The Pathology of Homicide.
  8. Atlas of Legal Medicine (Tomro Watonbe)
  9. Sptiz, W.U. & Fisher, R.S.: Medico-legal Investigation of Death.
  10. A Hand Book of Legal Pathology (Director of Publicity)
  11. Taylor’s Principles & Practice of Medical Jurisprudence. Edited by A.Keith Mant, Churchill Livingstone.
  12. Ratanlal & Dhirajlal, the Indian Penal Code; Justice Hidayatullah & V.R. Manohar
  13. Ratanlal & Dhirajlal, the Code of Criminal procedure; Justice Hidayatullah & S.P. Sathe
  14. Ratanlal & Dhirajlal, the Law of Evidence; Justice Hidayatullah & V.R. Manohar
  15. Medical Law & Ethic in India – H.S. Mehta
  16. Bernard Knight: Forensic Pathology
  17. Code of medical ethics : Medical Council of India, approved by Central Government, U/S 33 (m) of IMC Act, 1956 (Oct 1970)
  18. Krogman, W.M.: The human skeleton in legal medicine.
  19. FE Camps, JM Cameren, David Lanham: Practical Forensic Medicine
  20. V.V. Pillay: Modern Medical Toxicology

MBBS Books and Syllabus : First Year

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First year of MBBS consists of one year teaching basic science which includes the Subjects – Anatomy, Physiology and Biochemistry with some learning of Community Medicine. We will guide you with every aspect of 1st year MBBS with detailed list of best & recommended MBBS Books and Syllabus. Additionally, you can check our Download Section to get the eBooks in PDF format.

If you are in other semester, do check out the following:

MBBS Books List

Subject

Book Name

Description

Anatomy

BD Chaurasia Human Anatomy: 3 Volumes

Handbook of Anatomy

Osteology

Inderbir Singh Essentials of Osteology
A.K Dutta Textbook of Osteology

Embryology

Langman’s Medical Embryology
Kadasne Medical Embryology

Physiology

Sembuligam Essential of Physiology
Guyton Textbook of Physiology
Ganongs Review of Medical Physiology
A.K Jain Textbook of Physiology: 2 Volumes
Indu Khurana Textbook of Physiology

Biochemistry

Satyanarayana Textbook of Biochemistry
Harpers Illustrated Biochemistry
Lippincott Illustrated Reviews of Biochemistry

Anatomy

Anatomy may be one of the toughest subjects to handle in first year of MBBS. The subject deals with the structure of human body.

It is suggested to stick to B.D Chaurasia anatomy book, as it is still considered the bible of anatomy. Following mbbs books and curriculum will help you further through 1st year :

Syllabus

The Syllabus for Anatomy for First Year MBBS has been listed below:

1. General Anatomy

2. Regional Anatomy
a. – Upper limb
b. – Lower limb
c. – Abdomen
d. – Thorax
e. – Head Face Neck
f. – Spinal Cord & Brain

3. Micro-Anatomy
I – General Histology
II – Systemic Histology

4. Developmental Anatomy
I – General Embryology
II – Systemic Embryology

5. Genetics

6. Radiological Anatomy, USG, CT, MRI

7. Surface Anatomy, Living & Marking

Best Books

Following MBBS Books are recommended for Anatomy in First year MBBS:

  1. B.D Chaurasia Human Anatomy 3 volumes
  2. Cunningham manual of Practical Anatomy
  3. Gray’s Anatomy
  4. Sahana’s Human Anatomy
  5. Regional Anatomy by R. J. Last
  6. Human Histology by Inderbir Singh
  7. Atlas of Human Histology- DIFORE
  8. Surgical Anatomy- McGregor
  9. Histology- by ham
  10. Human Embryology – Inderbir Singh
  11. Human Embryology- Kadasne
  12. Medical Embryology – Langman
  13. Surface Anatomy & Radiology – Halim Das
  14. General Anatomy by – Chowrisia
  15. Text book of Neuroanatomy – Inderbir Singh
  16. Central Nervous System – Podar Bhagat
  17. Clinical anatomy for medical students – Richard Snell

Physiology

Physiology is quite easy to understand as it is relatively easy and less to mug up. However, don’t lose focus or you are going to lose a whole year of mbbs. Comprehensive knowledge of the normal functions of the organ systems of the body to facilitate an understanding of the physiological basis of health and diseases.

Following physiology books of mbbs are recommended (Ak Jain physiology being on top of the list) along with the syllabus of physiology :-

Syllabus

The Syllabus for Physiology for First Year MBBS has been listed below:

  1. General Physiology
  2. Hematology
  3. Nerve
  4. Muscle
  5. Respiratory Physiology
  6. Cardiovascular Physiology
  7. Renal Physiology
  8. Body Temperature Regulation
  9. Alimentary System
  10. Nutrition
  11. Endocrine System
  12. Reproductive Physiology
  13. Special Senses: Eye, Ear, Taste, Smell
  14. Central Nervous System

Best Books





Following MBBS Books are recommended for Physiology in First year MBBS:

Textbooks of Physiology

  1. A.K Jain – Textbook of Physiology
  2. K Sembulingam- Textbook of Physiology
  3. Guyton – Textbook of Physiology
  4. Ganong – Review of Medical Physiology
  5. S. Wright – Applied Physiology

Reference Books

  1. Best and Taylor – Physiological basis of medical practice
  2. Berne & levy. – Principles of Physiology

Biochemistry

As far as i gave my biochemistry exam, all i remember is mugging up things and it was still the best thing. This subject very few worthy topics for an mbbs student, unless you plan to go for post-graduation or diploma in biochemistry.

Biochemistry is all about scientific basis of the life processes at the molecular level. Following mbbs books are recommended for biochemistry, U Satyanarayan being the preferred choice along with the mbbs syllabus for biochemistry as follows :-

Syllabus

The Syllabus for Biochemistry for First Year MBBS has been listed below:

  1. Molecular and functional organization of a cell and its sub-cellular components
  2. Chemistry of enzymes and their clinical applications
  3. Chemistry and metabolism of proteins and related disorders
  4. Chemistry and metabolism of purines and pyrimidines and related disorders
  5. Chemistry and functions of DNA and RNA , Genetic code ; Protein biosynthesis & regulation (Lac-operon)
  6. The principles of genetic engineering and their applications in medicine
  7. Chemistry and Metabolism of hemoglobin
  8. Biological oxidation
  9. Molecular concept of body defense and their applications in medicine
  10. Vitamins and Nutrition
  11. Chemistry and metabolism of carbohydrates and related disorders
  12. Chemistry and metabolism of lipids and related disorders
  13. Mineral metabolism: Water and electrolyte balance & imbalance
  14. Acid base balance and imbalance
  15. Integration of various aspects of metabolism and their regulatory pathways with Starvation metabolism
  16. Mechanism of hormone action
  17. Environmental biochemistry
  18. Liver function tests, Kidney function tests, Thyroid function tests
  19. Detoxification mechanisms
  20. Biochemical basis of cancer and carcinogenesis
  21. Radioisotopes
  22. Investigation techniques : (LCD-Topics ) Colorimeter, Electrophoresis, Chromatography & Flame photometer

Best Books

Following MBBS Books are recommended for Biochemistry in First year MBBS:

Textbooks of Biochemistry

  1. Medical Biochemistry – U.Satyanarayan
  2. Lippincott Illustrated Reviews of Biochemistry
  3. Biochemistry for Medical students by D.M.Vasudevan & Shree Kumari
  4. Medical Biochemistry by M.N. Chatterjea and Rana Shinde
  5. Text Book of Medical Biochemistry by Ramakrishnan, Prasannan & Rajan
  6. Medical Biochemistry by Debajyoti Das
  7. Biochemistry by A.C.Deb

Reference Books

  1. Harper’s Illustrated Biochemistry
  2. Medical Biochemistry by N.V.Bhagwan
  3. Biochemistry by L.Stryer
  4. Biochemistry by Orten & Neuhans

If we have missed any MBBS Books or any part of syllabus, feel free to mention them in comments and keep the list updated.

Blood Test Interpretation with Normal values

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We’ve just prepared the best Blood Test Interpretation guide for you with normal values and ranges. It’s definitely going to help you a lot, if you like it, do save it in bookmarks for future reference. About the four ominous signs of blood work, just read below.

Before we proceed, what are Four Ominous Signs in Blood work?

Four Ominous Signs of Blood Work

  1. Albumin 3.5 or below with a 1500 or less lymphocyte count is one of the four OMINOUS signs
  2. Calcium levels higher than 2.7 is one of the four OMINOUS signs
  3. A/G ratio less than 1.0 is one of the four OMINOUS signs
  4. Cholesterol values below 140 are considered one of the four OMINOUS signs

GLUCOSE

Glucose: This is the chief source of energy for all living organisms. A level greater than 105 in someone who has fasted for 12 hours suggests a diabetic tendency. If this level is elevated even in a non-fasting setting one must be concerned that there is a risk for developing diabetes. This is an incredibly powerful test and can predict diabetes ten years or more before one develops the strict definition of diabetes which is levels greater than 120.

Clinical Adult Range: 70-115 mg/dL
Optimal Adult Range: 85-100 mg/dL
Red Flag Range <50 or >250 mg/dL

Common Causes of Glucose Increase: Diabetes, poor carbohydrate utilization, syndrome X
Less Common Causes of Glucose Increase: Cerebral lesions, uremia, pregnancy, intracranial pressure, cushing’s disease, hyperthyroidism, chronic nephritis, infections, first 24 hours after a severe burn, pancreatitis, cerebral lesions, uremia, early hyperpituitaris.

Common Causes of Glucose Decrease: Fasting Hypoglycemia

Clinical Note: LDH will frequently be decreased or in the low normal with Fasting Hypoglycemia, however, LDH will almost ALWAYS be decreased with Reactive Hypoglycemia
Less Common Causes of Glucose Decrease: liver damage, pancreatic adenoma, addison’s disease (adrenal insufficiency), starvation, late hypopituitarism Carcinoma of islet tissue
Clinical Notes: Order Glycohemoglobin (HGB A1C) with serum glucose values above 160 and to monitor diabetics under therapy

Nutrition Tip: Thiamine Deficiency has been linked to increase in glucose levels

SODIUM

Sodium: This element plays an important role in salt and water balance in your body. A low level in the blood can be caused by too much water intake, heart failure, or kidney failure. A low level can also be caused by loss of sodium in diarrhea, fluid or vomiting. A high level can be caused by too much intake of salt or by not enough intake of water.

Clinical Adult Range: 135-145
Optimal Adult Range: 140-144
Red Flag Range <125 or >155 mmol/L

Common Causes of Sodium Increase: Nephritis (kidney problems), dehydration, hyper-cortico-adrenalism (increased adrenal function)
Clinical Notes: Water Softeners have been linked to cause an increase in sodium
Common Causes of Sodium Decrease: Reduced kidney filtration, diarrhea, Addison’s disease, adrenal hypo-function

POTASSIUM

Potassium: This element is found primarily inside the cells of the body. Low levels in the blood may indicate severe diarrhea, alcoholism, or excessive use of water pills. Low potassium levels can cause muscle weakness and heart problems.

Clinical Adult Range: 3.5-5.0
Optimal Adult Range: 4.0-4.6
Red Flag Range <3.0 or >6.0 mmol/L

Common Causes of Potassium Increase: Adrenal hypo-function, cortisol resistance, acidosis, ongoing tissue destruction
Common Causes of Potassium Decrease: Diarrhea, diuretic use, kidney problems, adrenal hyper function
Less Common Causes of Potassium Decrease: Anemia, over dosage of testosterone, hereditary periodic paralysis, and hypertension

Nutrition Tip: Excessive licorice consumption has been linked to lower potassium levels

MAGNESIUM

Magnesium: This important element is found in the arteries, heart, bone, muscles, nerves, teeth.

Clinical Adult Range: 1.7-2.4
Optimal Adult Range: 2.2-2.6
Red Flag Range <1.2 mg/dL

Common Causes of Magnesium Increase: Kidney problems

Common Symptoms of Magnesium Deficiency: Anxiety, aching muscles, disorientation, low body temperature, easily angered, hyperactivity, insomnia, muscle tremors, nervousness, rapid pulse, sensitivity to noise and loud sounds, epilepsy

Clinical Note: Magnesium should be evaluated on all patients suffering with heart disease.
Clinical Note: Patient suffering with fibromyalgia may have a low serum magnesium accompanied with a low C02 and an increased anion gap

Nutrition Tip: Excessive use of antacids containing magnesium may increase magnesium levels

Clinical Note: If your magnesium is less than 2.0, it is strongly recommended to have an erythrocyte magnesium test or a magnesium loading test

CHLORIDE

Chloride: Is an electrolyte controlled by the kidneys and can sometimes be affected by diet. An electrolyte is involved in maintaining acid-base balance and helps to regulate blood volume and artery pressure. Elevated levels are related to acidosis as well as too much water crossing the cell membrane.

Clinical Adult Range: 96-110 mmol/L
Optimal Adult Range: 100-106 mmol/L
Red Flag Range <90 or >115 mmol/L

Common Causes of Chloride Increase: Renal (kidney) problems, metabolic acidosis
Common Causes of Chloride Decrease: Kidney problems, metabolic alkalosis, hypochlorhydria (too little acid in the stomach)
Less Common Causes of Chloride Increase: Hyperventilation, anemia, prostate problems, and salicylate poisoning, excess intake of salt, dehydration
Less Common Causes of Chloride Decrease: Diabetes, pneumonia, intestinal obstruction, pyloric spasm. Adrenal hypo-function

Clinical Note: Suspect hypochlorhydria if chloride is below 100, the total globulin is less than 2.4 and serum phosphorus is less than 3.0
Clinical Note: Chloride is required for the production of HCL by the chief cells of the stomach

BLOOD UREA NITROGEN

BUN (Blood Urea Nitrogen): BUN is a waste product derived from protein breakdown in the liver. Increases can be caused by excessive protein intake, kidney damage, certain drugs, low fluid intake, intestinal bleeding, exercise, heart failure or decreased digestive enzyme production by the pancreas. Decreased levels are most commonly due to inadequate protein intake, malabsorption, or liver damage
.
Clinical Adult Range: 10-26 mg/dL
Optimal Adult Range: 13-18 mg/dL
Red Flag Range <5 or >50 mg/dL

Common Causes of BUN Increase: Renal disease, gout, drug diuretics
Common Causes of BUN Decrease: Pregnancy, protein malnutrition
Less Common Causes of BUN Increase: Metallic poisoning, pneumonia, ulcers, Addison’s disease, increased protein catabolism, dysbiosis, congestive heart failure
Less Common Causes of BUN Decrease: Acute liver destruction, dysbiosis, celiac sprue

Clinical Note: Decreased BUN less than 8 with a decreased urinary specific gravity may indicate posterior pituitary dysfunction
Clinical Note: Increased BUN above 25 usually indicates kidney disease. However, if Creatinine is not above 1.1, then kidney disease may not be the problem. Instead consider anterior pituitary dysfunction, dehydration or hypochlorhydria.

Nutrition Tip: Increased BUN may indicate a Boron deficiency

CREATININE

Creatinine: Creatinine is also a protein breakdown product. Its level is a reflection of the bodies muscle mass. Low levels are commonly seen in inadequate protein intake, liver disease, kidney damage or pregnancy. Elevated levels are generally reflective of kidney damage and need to be monitored very carefully.

Clinical Adult Range: 0.7-1.5 mg/dL
Optimal Adult Range: 0.7-1.0 mg/dL
Red Flag Range >1.6 mg/dL

Common Causes of Creatinine Increase: Kidney Problems, Gout
Clinical Note: If Creatinine is 1.2 or higher in a male over the age of 40, Prostate Hypertrophy MUST be ruled out

Less Common Causes of Creatinine Increase: Renal Hypertension, uncontrolled diabetes, congestive heart failure, urinary tract infection, dehydration
Clinical Note: Suspect early nephritis ( kidney disease) if creatinine is between 2-4 mg/dL. Suspect severe nephritis is creatinine is between 4-35 mg/dL

Common Causes of Creatinine Decrease: Amyotonia congenital

BUN/CREATININE RATIO

BUN/Creatinine Ratio: increased values may indicate catabolic states, dehydration, circulatory failure leading to fall in renal blood flow, congestive heart failure, acute and chronic renal (kidney) failure, urinary tract obstruction, prostatic enlargement, high protein diet. Decreased values may indicate overhydration, low protein/high carbohydrate diet, pregnancy

Clinical Adult Range: 6-10
Optimal Adult Range: 10-16
Red Flag Range <5 or >30

Common Causes of BUN/Creatinine Ratio Increase: Kidney problems
Less Common Causes of BUN/Creatinine Ratio Increase: Catabolic states, prostatic hypertrophy, high protein diet, dehydration, shock
Common Causes of BUN/Creatinine Ratio Decrease: Low protein/high carbohydrate diet, pregnancy

URIC ACID

Uric Acid: Uric acid is the end product purine metabolism. High levels are seen in gout, infections, high protein diets, and kidney disease. Low levels generally indicate protein and molybdenum (trace mineral) deficiency, liver damage or an overly acid kidney.

Clinical Female Range: 2.4-6.0 mg/dL
Clinical Male Range: 3.4-7.0 mg/dL
Optimal Female Range: 3.0-5.5 mg/dL
Optimal Male Adult Range: 3.5-5.9 mg/dL
Red Flag Range <2 mg/dL or >9.0 mg/dL

Common Causes of Uric Acid Increase: Gout, kidney problems, arteriosclerosis, arthritis Less Common Causes of Uric Acid Increase: Metallic poisoning (mercury, lead), intestinal obstruction, leukemia, polycythemia, malignant tumors, drug diuretics Common Causes of Uric Acid Decrease: Chronic B-12 or folate anemia, pregnancy
Less Common Causes of Uric Acid Increase: Salicylate and atrophine therapy

Nutrition Tip: If the uric acid is low with a normal MCV and MCH, a molybdenum deficiency may be present

PHOSPHORUS

Phosphorus: Phosphorus is closely associated with calcium in bone development. Therefore most of the phosphate in the body is found in the bones. But the phosphorus level in the blood is very important for muscle and nerve function. Very low levels of phosphorus in the blood can be associated with starvation or malnutrition and this can lead to muscle weakness. High levels in the blood are usually associated with kidney disease. However the blood must be drawn carefully as improper handling may falsely increase the reading.

Clinical Adult Range: 2.5-4.5
Optimal Adult Range: 3.2-3.9
Red Flag Range <2.0 mg/dL or >5.0 mg/dL

Common Causes of Phosphorus Increase: Parathyroid dysfunction, kidney dysfunction, excessive phosphoric acid in soft drinks.

Important Fact: Children will have an increase in Phosphorus due to normal bone growth. In addition, people with fractures will usually reveal an increase.

Less Common Causes of Phosphorus Increase: Bone tumors, edema, ovarian hyper-function, diabetes, excess intake of vitamin D
Common Causes of Phosphorus Decrease: Parathyroid Hyper-function, osteomalacia, rickets
Less Common Causes of Phosphorus Decrease: Diabetes, liver dysfunction, protein malnutrition, neurofibromatosis, myxedema

Nutrition Tip: Phosphorus is frequently decreased with diets high in refined sugars

Clinical Note: Suspect Vitamin D deficiency with low levels of calcium, phosphorus and increased levels of alkaline phosphorus
Clinical Note: Phosphorus is a general indicator of digestive function. Consider hypochlorhydria when phosphorus is below 3.0 and total serum globulin is greater than 3.0 or less than 2.4

CALCIUM

Calcium: Calcium is the most abundant mineral in the body. It is involved in bone metabolism, protein absorption, fat transfer, muscular contraction, transmission of nerve impulses, blood clotting, and heart function. It is highly sensitive to elements such as magnesium, iron, and phosphorous as well as hormonal activity, vitamin D levels, CO2 levels and many drugs. Diet, or even the presence of calcium in the diet has a lot to do with “calcium balance” – how much calcium you take in and how much you lose from your body.

Clinical Adult Range: 8.5-10.8
Optimal Adult Range: 9.7-10.1
Red Flag Range <7.0 mg/dL or >12.0 mg/Dl

Common Causes of Calcium Increase: Hyperparathyroidism
Less Common Causes of Calcium Increase: Tumor of the thyroid, hypervitaminosis (excess Vitamin D), multiple myeloma, neurfibromatosis, osteoporosis, ovarian hypo-function, adrenal hypo-function
Clinical Note: Serum protein influences calcium levels. Calcium goes up with increased protein and goes down with decreased protein

Common Causes of Calcium Decrease: Hypoparathyroidism, pregnancy, hypochlorhydria, kidney dysfunction
Less Common Causes of Calcium Decrease: Vitamin D deficiency, diarrhea, celiac disease, protein malnutrition, chemical/heavy metal toxicity, HPA-axis dysfunction

Clinical Fact: Poor intestinal fat absorption may be suspected with low levels of calcium, bilirubin and phosphorus

Nutrition Note: Pancreatic enzyme deficiency may be suspected with low levels of calcium, triglycerides and increased levels of LDH

Clinical Note: Circadin rhythm abnormality should be a primary consideration with calcium levels either above or below normal

ALBUMIN

Albumin: The most abundant protein in the blood, it is made in the liver and is an antioxidant that protects your tissues from free radicals. It binds waste products, toxins and dangerous drugs that might damage the body. Is also is a major buffer in the body and plays a role in controlling the precise amount of water in our tissues. It serves to transport vitamins, minerals and hormones. Lower levels are seen in poor diets, diarrhea, fever, infections, liver disease, kidney disease, third-degree burns, edemas or hypocalcemia.

Clinical Adult Range: 3.0-5.5
Optimal Adult Range: 4.0-4.4
Red Flag Range <4.0 g/dL

Common Causes of Albumin Increase: Dehydration
Less Common Causes of Albumin Increase: Thyroid and adrenal hypo-function
Common Causes of Albumin Decrease: Liver Disease
Less Common Causes of Albumin Decrease: Acute Nephritis, malnutrition, acute cholecysitis (gall bladder), multiple sclerosis, vitamin B-12 or folic acid anemia

Clinical Note: Albumin 3.5 or below with a 1500 or less lymphocyte count is one of the four OMINOUS signs

Nutrition Tip: Decreased albumin with decreased serum phosphorus may indicate digestive inflammation

Calcium/Albumin Ratio: elevated in malnutrition or visceral protein loss.
Levels higher than 2.7 is one of the four OMINOUS signs

GLOBULIN

Globulin: Globulins have many diverse functions such as, the carrier of some hormones, lipids, metals, and antibodies. High levels are found in chronic infections, liver disease, rheumatoid arthritis, myelomas and lupus. Lower levels may be seen in immune compromised patients, poor dietary habits, malabsorption, liver and kidney disease.

Clinical Adult Range: 2.0-4.0
Optimal Adult Range: 2.8-3.5
Red Flag Range <2.0 g/dL or >3.5 g/100ml

Common Causes of Globulin Increase: Hypochlorhydria, liver disease (infection)
Less Common Causes of Globulin Increase: liver parasites, multiple myeloma, rheumatoid arthritis, typhoid fever
Common Causes of Globulin Decrease: Anemia, hemorrhage

Clinical Note: Anytime the total globulin is less than 2.0 or greater than 3.5 a Serum Protein Electrophoresis

A/G RATIO

A/G Ratio: is an important indicator of disease states. Low ratio suggests ulcerative colitis, burns, kidney disease, cirrhosis, multiple myeloma. A/G ratio less than 1.0 is one of the four OMINOUS signs
Clinical Adult Range: 1.1-2.5 Optimal Adult Range:1.2-1.5
Red Flag Range <1.0

Nutrition Note: Elevated A/G ratio, elevated protein and an elevated cholesterol may indicate too high protein consumption

ALKALINE PHOSPHATASE

Alkaline Phosphatase: Alkaline phosphatase is an enzyme that is found in all body tissue, but the most important sites are bone, liver, bile ducts and the gut. A high level of alkaline phosphatase in your blood may indicate bone, liver or bile duct disease. Certain drugs may also cause high levels. Growing children, because of bone growth, normally have a higher level than adults do. Low levels indicate low functioning adrenal glands, protein deficiency, malnutrition or more commonly, a deficiency in zinc.

Clinical Adult Range: 30-115
Optimal Adult Range: 60-80
Red Flag Range <30U/L or >Laboratory range

Common Causes of Alkaline Phosphatase Increase: Primary bone lesion, invasive liver lesion, biliary duct (liver) obstruction, osteomalacia, paget’s disease, rheumatoid arthritis
Less Common Causes of Alkaline Phosphatase Increase: Excess ingestion of Vitamin D, rickets, Cirrhosis of liver, adrenal hyper-function, shingles, hodgkin’s disease, osteogenic sarcoma, alcoholism, multiple myeloma, jaundice
Common Causes of Alkaline Phosphatase Decrease: Anemia, Hypothyroidism, celiac disease
Less Common Causes of Alkaline Phosphatase Decrease: Adrenal hypo-function, vitamin C deficiency, progesterone deficiency

Nutrition Note: Alkaline Phosphatase levels below 70 U/L may indicate a Zinc Deficiency

Clinical Note: Any patient having a significant increase in Alkaline Phosphatase should have a ALP isoenzyme
Clinical Note: It is considered “NORMAL” for Alkaline Phosphatase to be elevated in children under 18 and people with bone fractures.

SGPT/ALT & SGOT/AST

Transaminases (SGPT/ALT) & (SGOT/AST): These are enzymes that are primarily found in the liver. Drinking too much alcohol, certain drugs, liver disease and bile duct disease can cause high levels in the blood. Hepatitis is another problem that can raise these levels. Low levels of GGT may indicate a magnesium deficiency. Low levels of SGPT and SGOT may indicate deficiency of vitamin B6.

Clinical Adult Range: 0-41
Optimal Adult Range: 18-26
Red Flag Range >100 U/L

SGOT/AST is found in the heart, skeletal muscles, brain, liver and kidneys

Clinical Note: In acute congestive heart failure and/or myocardial infarction, the SGOT/AST will significant increase. However, these values will slowly return to normal. SGPT/ALT will also increase in these cardiac heart emergencies, however, SGOT/AST normally will not return to normal as quick as SGPT

Common Causes of SGOT/AST Increase: Myocardial Infarction, pulmonary embolism, congestive heart failure, myocarditis
Other Common Causes of SGOT/AST Increase: Hepatitis, liver cirrhosis, liver disease, pancreatitis
Less Common Causes of SGOT/AST Increase: liver neoplasm

Nutrition Note: Low levels of SGOT/AST and SGPT/ALT may indicate a B-6 deficiency
SGPT/ALT is found in the liver, kidneys, heart and skeletal muscles.

Common Causes of SGPT/ALT Increase: Acute hepatitis, cirrhosis of liver, mononucleosis
Less Common Causes of SGPT/ALT Increase: Pancreatitis, biliary dysfunction, diabetes

Clinical Note: SGPT values are greater than SGOT in liver obstruction, toxic hepatitis. SGOT values are greater than SGPT in cirrhosis of the liver, liver neoplasms and jaundice

GGT (Gamma-Glutamyl transerase)

Gamma-Glutamyl transerase (GGT): Believed to be involved in the transport of amino acids into cells as well as glutathione metabolism. Found in the liver and will rise with alcohol use, liver disease, or excess magnesium.

Clinical Adult Range: 0-55U/L
Optimal Adult Range: 10-30U/L
Red Flag Range >90U/L

Common Causes of GGT Increase: Biliary obstruction, alcoholism, cholangitis/cholecystitis (bile duct and gall bladder inflammation)

Clinical Note: If GGT is greater than 150 U/L with a serum bilirubin of over 2.8 mg/dL, strongly suspect biliary obstruction. Seek immediate medical attention
Clinical Note: If GGT values are five times higher than the clinical range suspect pancreatitis
Less Common Causes of GGT Increase: Brucellosis, hepatitis, mononucleosis, bacterial and viral infection, malignancy, congestive heart failure biliary.

Nutrition Note: Low levels of GGT may indicate a B-6 deficiency.

Additional Clinical Notes: Food allergy/sensitivity is a very common finding with biliary dysfunction

LDH

Lactate Dehydrogenase (LDH): LDH is an enzyme found in all tissues in the body. A high level in the blood can result from a number of different diseases such as hepatitis, anemia etc. Also, slightly elevated levels in the blood are common and usually do not indicate disease. The most common sources of LDH are the heart, liver, muscles, and red blood cells.

Clinical Adult Range: 60-225U/L
Optimal Adult Range: 140-200U/L
Red Flag Range >250U/L

Common Causes of LDH Increase: Liver/biliary dysfunction, pulmonary embolism, myocardial infarction, tissue inflammation, tissue destruction, malignancy anywhere in the body, several types of anemias

Clinical Note: LDH will frequently increase with low thyroid function
Clinical Note: LDH is frequently increased with birth control usage
Nutrition Note: Decrease LDH may indicate reactive hypoglycemia. (Check glucose)

TOTAL PROTEIN

Total Protein: This is a measure of the total amount of protein in your blood. Total protein is the combination of albumin and total globulin and is affected by the albumin and total globulin. A low or high total protein does not indicate a specific disease, but it does indicate that some additional tests may be required to determine if there is a problem.

Clinical Adult Range: 6.0-8.5g/dL
Optimal Adult Range: 7.1-7.6g/dL
Red Flag Range <5.9g/dL or > 8.5g/dL

Common Causes of Protein Increase: Dehydration, “early” carcinoma, multiple myeloma (should be correlated with serum protein electrophoresis)
Less Common Causes of Protein Increase: malignancy, diabetes, rheumatoid arthritis
Common Causes of Protein Decrease: Protein malnutrition, digestive inflammation (colitis, gastritis)
Less Common Causes of Protein Decrease: hypothyroidism, leukemia, adrenal hyper-function, congestive heart failure

Nutrition Note: If protein and calcium are found to be on the low side of the Optimal range suspect poor protein absorption.

Additional Nutrition Notes: Decreased protein, cholesterol and SGPT may indicate fatty liver congestion

IRON

Iron: The body must have iron to make hemoglobin and to help transfer oxygen to the muscle. If the body is low in iron, all body cells, particularly muscles in adults and brain cells in children, do not function up to par. If this test is low you should consider getting a Ferritin test, especially if you are a female who still has menstrual cycles.

Clinical Adult Range: 40-150ug/ml
Optimal Adult Range: 50-100ug/ml
Red Flag Range <25ug/ml or >200ug/ml

Common Causes of Iron Increase: Hemochromomatosis, liver dysfunction, iron therapy, pernicious and hemolytic anemia
Less Common Causes of Iron Increase: cooking with iron utensils
Common Causes of Iron Decrease: Pathologic bleeding (especially in geriatric population), iron deficiency anemia
Less Common Causes of Protein Decrease: chronic infections, kidney and liver problems

Nutrition Note: Increased iron with decreased hemocrit (HCT) suggests intrinsic factor deficiency

Clinical Notes: An iron evaluation is not complete without ordering Ferritin (see below)

FERRITIN

Ferritin: This test is considered the “gold standard” in documenting iron deficiency anemia. Low levels below 25 indicate a need for iron. High levels may an inflammatory disorder, infections, rheumatoid arthritis, and chronic kidney disease.

Clinical Male Adult Range: 33-236ng/mL
Clinical Female Adult Range (before menopause): 11-122ng/mL
Clinical Female Adult Range (after menopause): 12-263ng/mL
Optimal Male Adult Range: 20-200ng/mL
Optimal Female Adult Range (before menopause): 10-110ng/mL
Optimal Female Adult Range(after menopause): 20-200ng/mL
Red Flag Range <8ng/mL or >500ng/mL

Common Causes of Ferritin Increase: Iron overload, hemochromatosis
Less Common Causes of Ferritin Increase: inflammation, liver disease, rheumatoid arthritis
Common Causes of Ferritin Decrease: Iron deficiency anemia
Less Common Causes of Ferritin Decrease: Free radical pathology

Clinical Notes: Serum ferritin greater than 1000 suspect hemochromatosis
Clinical Notes: Iron overload and/or hemochromatosis are silent and can result in cirrhosis of the liver, bacterial infections, dementia, arteriosclerosis, diabetes and stroke
Nutrition Note: Doctors specializing in chelation have found a correlation with increased iron and arteriosclerosis.

TRIGLYCERIDES

Triglycerides: These are fats used as fuel by the body, and as an energy source for metabolism. Increased levels are almost always a sign of too much carbohydrate intake and hyperlipidism. Decreased levels are seen in hyperthyroidism, malnutrition and malabsorption.

Clinical Adult Range: 50-150mg/dL
Optimal Adult Range: 70-110mg/dL
Red Flag Range <35mg/dL or >350mg/dL

Common Causes of Triglycerides Increase: Hyperlipidism, diabetes, alcoholism
Less Common Causes of Triglycerides Increase: Hypothyroidism, early stages of fatty liver
Common Causes of Triglycerides Decrease: chemical/heavy metal overload, liver dysfunction, hyper thyroid function

Clinical Notes: Resistive exercise training has been found to be effective in lowering elevated triglycerides

CHOLESTEROL

Cholesterol: Group of fats vital to cell membranes, nerve fibers and bile salts, and a necessary precursor for the sex hormones. High levels indicate diet high in carbohydrates/sugars. Low levels indicate low fat diet, malabsorption, anemia, liver disorders, carbohydrate sensitivity. Cholesterol values below 140 are considered one of the four OMINOUS signs.

Clinical Adult Range: 120-200mg/dL
Optimal Adult Range: 150-180mg/dL
Red Flag Range <50mg/dL or >400mg/dL

Common Causes of Cholesterol Increase: Early stages of diabetes, fatty liver, arteriosclerosis, hypothyroidism
Less Common Causes of Cholesterol Increase: biliary obstruction, multiple sclerosis, pregnancy
Common Causes of Cholesterol Decrease: Liver dysfunction, chemical/heavy metal overload, hyperthyroidism, viral hepatitis, free radical pathology

Nutrition Note: Increased cholesterol levels have been found to be lowered by the amino acid methionine

Clinical Notes: Cholesterol level below 130 is considered one of Four Ominous signs
Clinical Notes: If cholesterol is above 220 with a SGPT below 10 suspect liver congestion/fatty liver

LDL CHOLESTEROL

LDL Cholesterol: LDL is the cholesterol rich remnants of the lipid transport vehicle VLDL (very-low density lipoproteins) there have been many studies to correlate the association between high levels of LDL and arterial arteriosclerosis.

Clinical Adult Range: <130mg/dL
Optimal Adult Range: <120mg/dL
Red Flag Range >180mg/dL

Common Causes of Cholesterol LDL Increase: Arteriosclerosis, diabetes, Syndrome X

Nutrition Note: Increased cholesterol levels have been found to be lowered by the amino acid methionine

HDL

HDL (High Density Lipoprotein): HDL or High-density lipoprotein is the cholesterol carried by the alpha lipoproteins. A high level of HDL is an indication of a healthy metabolic system if there is no sign of liver disease or intoxication. the two mechanisms that explain how HDL offers protection against chronic heart disease are that HDL inhibits cellular uptake of LDL and serves as a carrier that removes cholesterol from the peripheral tissues and transports it back to the liver for catabolism.

Clinical Adult Males Range: >50mg/dL
Clinical Adult Female Range: >55mg/dL
Optimal Adult Male Range: >55mg/dL
Optimal Adult Male Range: >60mg/dL
Red Flag Range <35mg/dL

Common Causes of HDL Cholesterol Decrease: Arteriosclerosis, diabetes, Syndrome X
Less Common Causes of HDL Cholesterol Decrease: Cigarette smoking, steroids, beta-blockers

Nutrition Note: Diets high in refined carbohydrates, lack of exercise and genetic predisposition have been found to lower HDL

Clinical Notes: If HDL is decreased, triglycerides are greater than 50% of the cholesterol value, LDL is increased and uric acid is increased rule out arteriosclerosis.

CHOLESTEROL/HDL RATIO

Cholesterol/HDL ratio: this ratio is an important marker for cardiovascular health. A ratio <4.0 is considered adequate. A ratio <3.1 is ideal.

Carbon Dioxide (CO2)

CO2: The CO2 level is related to the respiratory exchange of carbon dioxide in the lungs and is part of the bodies buffering system. Generally, when used with the other electrolytes, carbon dioxide levels indicate pH or acid/alkaline balance in the tissues. This is one of the most important tests that we measure. Most people have too much acid in their body. If you garden you will know that it is very difficult to grow plants in soil where the pH is incorrect. Our blood is similar to soil in many respects and it will be difficult to be healthy if our body’s pH is not well balanced.

Clinical Adult Range: 24-32mmol/L
Optimal Adult Range: 26-30mmol/L
Red Flag Range <18mmol/L or >38mmol/L

Common Causes of CO2 Increase: Alkalosis, hypochlorhydria
Less Common Causes of CO2 Increase: acute vomiting, fever, adrenal hyper-function, emphysema (respiratory distress)
Common Causes of CO2 Decrease: Acidosis
Less Common Causes of CO2 Decrease: Diabetes, sleep apnea, severe diarrhea

Nutrition Note: Low levels of CO2 may indicate a need for thiamine (a B-vitamin)

Clinical Notes: If CO2 is above 32mmol/L, a Pulmonary Function Test should is warranted.

WHITE BLOOD CELLS

White Blood Cell (WBC): White blood count measures the total number of white blood cells in a given volume of blood. Since WBCs kill bacteria, this count is a measure of the body’s response to infection.

Clinical Adult Range: 4,500-11,000cu.mm
Optimal Adult Range: 5,000-8,000cu.mm
Red Flag Range <3,000cu.mm or >13,000cu.mm

Common Causes of WBC Increase: Active Infections, Leukemia, Childhood diseases (measles, mumps, chicken-pox, rubella, etc.
Less Common Causes of WBC Increase: asthma, emphysema, adrenal dysfunction, intestinal parasites, severe emotional stress
Common Causes of WBC Decrease: Chronic Viral or Bacterial Infections, Lupus (SLE)
Less Common Causes of WBC Decrease: Hepatitis, Immune dysfunction, Chemical/Heavy metal toxicity

Nutrition Note: Decreased WBC may indicate a need for Vitamin B-12, B-6 and folic acid.

Clinical Notes: An increase or decrease in total WBC in conjunction with a lymphocyte count below 20 and serum albumin below 4.0 is a pattern frequently seen in a developing neoplasm (tumor)

NEUTROPHILS

Neutrophils: elevated in acute infection

Clinical Adult Range: 35-65 percent of total WBC
Optimal Adult Range: 40-60 percent of total WBC
Red Flag Range <30 percent of total WBC or >80 percent of total WBC

Common Causes of Neutrophils Increase: see WBC
Common Causes of WBC Decrease: see WBC

Clinical Notes: Neutrophils tend to increase with chronic bacterial infections and decrease with chronic viral infections

MONOCYTES

Monocytes: elevated in bacterial infections, protozoal infections

Clinical Adult Range: 0-10 percent of total WBC
Optimal Adult Range: <7 percent of total WBC
Red Flag Range >15 percent of total WBC

Common Causes of Monocytes Increase: Bacterial Infections, parasitic infections
Common Causes of WBC Decrease: high doses of corticosteroids will depress monocytes

Clinical Notes: Increased monocytes are frequently present with prostate hypertrophy, ovarian and uterine dysfunction
Clinical Notes: An increase in monocytes with an increase in the basophils (>1.0) and a mild increase of eosinophils (>3.0) may indicate intestinal parasites

LYMPHOCYTES

Lymphocytes: elevated in acute and chronic infections. Decreased in viral infection and immune deficiency

Clinical Adult Range: 20-40 percent of total WBC
Optimal Adult Range: 25-40 percent of total WBC
Red Flag Range <20 percent of total WBC or >55 percent of total WBC

Common Causes of Lymphocytes Increase: Chronic viral or bacterial infection, Childhood diseases (measles, mumps, chicken-pox, rubella, etc.), HIV, Hepatitis
Less Common Causes of Lymphocytes Increase: Chemical/heavy metal toxicity
Common Causes of Lymphocytes Decrease: Active infections

Clinical Notes: Suspect a viral infections when the lymphocytes increase to a point that either equal or exceeds the neutrophil level.

EOSINOPHILS

Eosinophils: Elevated in allergic conditions, skin diseases, parasitic diseases

Clinical Adult Range: 0-7 percent of total WBC
Optimal Adult Range: 0-3 percent of total WBC
Red Flag Range <20 percent of total WBC or >55 percent of total WBC

Common Causes of Eosinophils Increase: Allergic condition (asthma), food sensitivities, parasitic infection
Less Common Causes of Eosinophils Increase: Chemical/heavy metal toxicity, Hodgkin’s disease, ovarian and bone tumors

BASOPHILS

Basophils: Elevated in Infections

Clinical Adult Range: 0-2 percent of total WBC
Optimal Adult Range: 0-1 percent of total WBC
Red Flag Range <5 percent of total WBC

Common Causes of Basophils Increase: Inflammation, Childhood diseases (measles, mumps, chicken-pox, rubella, etc.), acute trauma and parasites
Less Common Causes of Basophils Increase: Chemical/heavy metal toxicity

Clinical Notes: Symptoms of inflammation in the absence of trauma may indicate a need to order C-Reactive Protein and/or a Sed rate
Clinical Notes: Consider ordering a comprehensive stool and digestive test to rule out intestinal parasites if the basophils are increased with no sign of inflammation

RED BLOOD CELLS

RBC (Red Blood Cells): made in the spleen. Reveals the oxygen carrying ability of the blood.

Clinical Adult Male Range: 4.60-6.0 million cu/mm
Clinical Adult Female Range: 3.90-5.50 million cu/mm
Optimal Adult Male Range: 4.20-4.90 million cu/mm
Optimal Adult Female Range: 3.90-4.50 million cu/mm
Red Flag Range for Men <3.90 or >6.00 million cu/mm
Red Flag Range for Women <3.50 or >5.00 million cu/mm

Common Causes of RBC Increase: Polycythemia, dehydration, Respiratory Distress (asthma, emphysema)
Less Common Causes of RBC Increase: acute poisoning, cystic fibrosis, adrenal hyperfunction
Common Causes of RBC Decrease: Iron deficiency anemia, internal bleeding
Less Common Causes of RBC Decrease: Excessive exercise, salicylate toxicity, lead poisoning

Nutrition Tip: Low levels of RBC may indicate a need for B-12, B-6 and folic acid

Clinical Notes: Consider checking iron and ferritin levels with low levels of RBC

HEMOGLOBIN

Hemoglobin: Hemoglobin provides the main transport of oxygen and carbon in the blood. It is composed of “globin”, a group of amino acids that form a protein and “heme”, which contains iron. It is an important determinant of anemia (decreased hemoglobin) or poor diet/nutrition or malabsorption.

Clinical Adult Male Range: 13.5-18.0g/dL
Clinical Adult Female Range: 12.5-16.0g/dL
Optimal Adult Male Range: 14.0-15.0g/dL
Optimal Adult Female Range: 13.5-14.5g/dL
Red Flag Range <10.0 or >17g/dL

Common Causes of Hemoglobin Increase: Polycythemia, dehydration, emphysema, asthma
Common Causes of Hemoglobin Decrease: Anemia, internal bleeding, digestive inflammation

Nutrition Tip: Low levels of Hemoglobin may indicate a need for B-12, folic acid and thiamine

Clinical Notes: Consider checking iron and ferritin levels with low levels of Hemoglobin

HEMATOCRIT

Hematocrit: Hematocrit is the measurement of the percentage of red blood cells in whole blood. It is an important determinant of anemia (decreased), dehydration (elevated) or possible over hydration (decreased).

Clinical Adult Male Range: 40.0-52.0 percent
Clinical Adult Female Range: 36.0-47.0 percent
Optimal Adult Male Range: 40.0-48.0 percent
Optimal Adult Female Range: 37.0-44.0 percent
Red Flag Range <32.0 or >55 percent

Common Causes of Hematocrit Increase: same as hemoglobin
Common Causes of Hematocrit Decrease: same as hemoglobin

Clinical Notes:
Suspect Iron anemia if serum iron, hemoglobin and hemocrit are all low
Suspect B-6 anemia if MCT, hemocrit and iron are low (also look for a low SGOT)
Suspect B12/folic acid anemia if you have a low hemocrit with a high MCH, MCV and iron

Clinical Notes: Consider getting a ferritin test

PLATELETS

Platelets: Platelets are concerned with the clotting of the blood.

Clinical Adult Range: 150,000-450,000cu.mm
Optimal Adult Range: 200,000-300,000cu.mm
Red Flag Range <50,000 or >600,000cu.mm

Common Causes of Platelets Increase: Polycythemia, inflammatory arthritis, several types of anemia, arteriosclerosis, and acute blood loss
Common Causes of Platelets Decrease: Leukemia, liver dysfunction
Less Common Causes of Platelets Decrease: Chemical/heavy metal toxicity

Nutrition Tip: Low levels of Platelets may indicate a B12, folic, selenium and iron deficiency

Clinical Notes: The following drugs have been found to lower Platelets: quinidine, heparin, gold salts, sulfas, digitoxin

RETICULOCYTE COUNT

Reticulocyte Count: This is an excellent test to confirm chronic microscopic bleeding

Clinical Adult Range: 0.5-1.5%
Optimal Adult Range: same as clinical range
Red Flag Range >2.0%

Common Causes of Reticulocyte Count Increase: Internal bleeding
Common Causes of Reticulocyte Count Decrease: Vitamin b-12, B-6 and folic acid anemia

MCV

Mean Corpuscular Volume (MCV) The MCV indicates the volume occupied by the average red blood cell.

Clinical Adult Range: 81.0-99.0cu.microns
Optimal Adult Range: 82.0-89.9cu.microns
Red Flag Range <78.0 or >95.0cu.microns

Common Causes of MCV Count Increase: Vitamin B-12/Folic Acid Anemia
Common Causes of MCV Count Decrease: Iron anemia, internal bleeding

Clinical Notes: If the MCV is >89.9 and the MCH is >31.9, suspect Vitamin B-12 or folic anemia. This should be confirmed with a serum or urinary methylmalonic (vitamin B-12) and a serum or urinary homocysteine (folic acid and vitamin B-6)
Clinical Notes: If iron, ferritin are normal and MCV, MCH, Hemoglobin and Hematocrit are all decreased, suspect a toxic metal body burden.

MCH

Mean Corpuscular Hemoglobin (MCH) The MCV indicates the volume occupied by the average red blood cell

Clinical Adult Range: 26.0-33.0micro-micro grams
Optimal Adult Range: 27.0-31.9micro-micro grams
Red Flag Range <24.0 or >34.0micro-micro grams

Common Causes of MCV Count Increase: Vitamin B-12/Folic Acid Anemia
Common Causes of MCV Count Decrease: Iron anemia, internal bleeding

Clinical Notes: If the MCV is >89.9 and the MCH is >31.9, suspect Vitamin B-12 or folic anemia. This should be confirmed with a serum or urinary methylmalonic (vitamin B-12) and a serum or urinary homocysteine (folic acid and vitamin B-6)
Clinical Notes: If iron, ferritin are normal and MCV, MCH, Hemoglobin and Hematocrit are all decreased, suspect a toxic metal body burden

T3

T3 (Tri-Iodothyronine): T-3 is a thyroid hormone produced mainly from the peripheral conversion of thyroxine (T-4)

Clinical Adult Range: 22-33%
Optimal Adult Range: 26-30%

Common Causes of T3 Increase: Hyperthyroidism
Common Causes of T3 Decrease: Hypothyroidism

T4

T-4 (Tetra-Iodothyronine): T-4 is the major hormone secreted by the thyroid gland.

Clinical Adult Range: 4.0-12.0mcg/dL
Optimal Adult Range: 7.0-8.5mcg/dL

Common Causes of T4 Increase: Hyperthyroidism
Common Causes of T3 Decrease: Hypothyroidism, anterior pituitary hypo-function

T7

T7 (FTI-Free Thyroxine Index) FTI is an estimate, calculated from T-4 and T-3 uptake.

Clinical Adult Range: 4.0-12.0mcg/dL
Optimal Adult Range: 7.0-8.5mcg/dL

Common Causes of T7 Increase: See T-3 uptake
Common Causes of T3 Decrease: See T-3 uptake

T-3 UPTAKE

T-3 Uptake T-3 uptake measures the unsaturated binding sites on the thyroid bindng proteins

Clinical Adult Range: 22-36%
Optimal Adult Range: 27-37%
Red Flag Range <20 percent of uptake or >39 percent of uptake
Common Causes of T-3 Uptake Increase: Thyroid hyperfunction
Less Common Causes of T-3 Uptake Increase: Kidney dysfunction, salicylates toxicity and protein malnutrition
Common Causes of T3 Decrease: Thyroid hypo-function

TSH

TSH (Thyroid Stimulating Hormone): is used to confirm or rule out suspected hypothyroidism when T3, T4, T7 are essentially normal and clinical signs suggest hypothyroidism

Clinical Adult Range: 0.4-4.4mlU/L
Optimal Adult Range: 2.0-4.0mlU/L
Red Flag Range <0.3mlU/L or >10.0mlU/L

Common Causes of TSH Increase: Thyroid hypofunction
Less Common Causes of TSH Increase: liver dysfunction
Common Causes of TSH Decrease: Thyroid hyper-function, anterior hypo-function

Clinical Notes: The axillary temperature (underarm) will frequently be <97.8 with thyroid hypo-function. The axillary temperature should be taken for 10 minutes before leaving bed and ideally should be taken for five days in a row and averaged. Reduced axillary temperature is common with adrenal stress, thiamine deficiency, diets low in essential fatty acids and protein malnutrition
Clinical Notes: Difficulty losing weight, fatigue, lack of motivation, sensitivity to cold, dry or scaly skin, ringing in ears, low blood pressure, impaired hearing, constipation, difficulty working under pressure and headaches that start in the morning but improve during the day.

ESR (Erythrocyte Sedimentation Rate)

ESR (Erythrocyte Sedimentation Rate): documents if organic disease is truly present in patients with vague symptoms. Monitors the course of chronic inflammatory conditions. Elevated in patients with breakdown of tissue

Clinical Adult Male <50 Range: 0-15mm/hour
Clinical Adult Male >50 Range: 0-20mm/hour
Clinical Adult Male <50 Range: 0-25mm/hour
Clinical Adult Female >50 Range: 0-30mm/hour
Optimal Adult Male Range: <5mm/hour
Optimal Adult Female Range: <10mm/hour
Red Flag Range >45 mm/hour

Common Causes of ESR Increase: Tissue Inflammation

Coffee with Paracetamol for Fever?

0

Fever and Pain? And you want to get rid of it within minutes?? Go through what we have here and share the information with people. We will give you clinical experimental information performed on how efficacious this miraculous combination can be. Indeed, sometime we want to get over with fever to face most worthy and precious moments of our life.

Getting Started

“Increased intensity of action of drugs that are activated by metabolism. Acute paracetamol toxicity is due to one of its metabolites-toxicity occurs at lower doses in patients receiving enzyme inducers.”- K.D tripathi pharmacology

Mechanism of Combination therapy

Paracetamol metabolism is increased 2-4 folds by microsomal enzyme induction through cytochrome p450.

Effect of Combination

Increased Anti-pyretic and Analgesic effect (Mainly nociceptive). Inappropriate or higher dosages may cause paracetamol toxicity.

What doses can I take?

500mg of paracetamol+100mg of caffeine
100mg= roughly one mug of coffee

Box 1. Caffeine content of commonly consumed items compared with paracetamol with caffeine tablets.

Beverage/item Container/size Typical caffeine content
Coffee
— Instant
— Percolated
250 mL cup 60–80 mg
60–120 mg
Tea 250 mL cup 10–50 mg
Coca Cola 375 mL can 48.75 mg
Energy drink 250 mL can 80 mg
Chocolate bar 100 g bar 20 mg
Paracetamol with caffeine 1 dose (= 2 tablets) 130 mg

Adverse effects

Most problematic can be Paracetamol toxicity, though it is rare (occurs with genetic or overdose).

Treatment of Overuse

It includes headache as the most prominent sign of withdrawal.

Contraindicated in Pregnant and Breast

Feeding women and pregnant women should not consume more than 200 mg caffeine per day, as this may increase the risk of spontaneous miscarriage. Consuming > 300 mg per day may also increase the risk of preterm delivery and fetal growth retardation.
Caffeine is readily transferred to breast milk and young infants are poor metabolizers of caffeine. Infants who are breastfed by mothers consuming > 300 mg caffeine per day may become jittery and restless, and may experience sleep difficulties.

References

K.D Tripathi: Page 27-28

The Original Trial

So does caffeine added to painkillers make them work better?

In the light of a new Cochrane review, the simple answer seems to be yes. The reviewers looked for studies comparing the pain-relieving effect of common painkillers with and without added caffeine. As well as searching key databases the authors contacted drug companies known to have carried out trials that have not been published.

19 randomized controlled trials (RCTs) of 7238 people were included, assessing several acute pain conditions including headache, post-dental pain, postoperative pain following childbirth, and period pain. Most studies used paracetamol (500 mg to 1500 mg) or ibuprofen (100 mg to 400 mg), with two using aspirin (650 mg and 800 mg), one aspirin (500 mg) plus paracetamol (400 mg), one diclofenac (100 mg), and one tolfenamic acid (200 mg). Caffeine was added at doses of 50 mg to 260 mg, with most studies using between 100 mg and 200 mg. In most studies participants were not allowed to have any caffeine in food, drink or other medicines for a specified time within the trial.

Results

There was a small but statistically significant benefit with caffeine used at doses of 100 mg or more for all pain conditions and painkillers. About 5% to 10% more people achieve a good level of pain relief with the addition of caffeine.

There was only one serious health event in one person treated with caffeine plus painkiller and this was not considered related to the study medication.

Most of the studies were old, with only three (in headache) published since 2000, but they were generally of good methodological quality.

There are 20 more studies with over 9000 participants for which data for analysis were not obtainable. However, even if all the missing data showed no effect of caffeine, the additional effect of caffeine would still be statistically significant.

The authors concluded that the existing evidence is probably sufficient to support the use of caffeine with analgesics, with the addition of ≥ 100 mg caffeine to a standard dose of commonly used analgesics providing a small but important increase in the proportion of people who experience a good level of pain relief.

100mg of caffeine is roughly equivalent to the caffeine in a mug of coffee. So if you’ve got a headache and have standard painkillers in the cupboard, you may do well to wash them down with a coffee.

Summary

Swallow down the PCM with coffee and feel the effects much faster than taking paracetamol with water.

This was all about the Paracetamol-Caffeine Combination for Fever.

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