HLA system

Areas in brain

Human Herpes Virus

Human Herpes Virus 1-8

HHV I————-HSV-I

HHV-II———–HSVII

HHVIII———–Herpes Zoster Virus

HHV IV———–Ebstein Barr Virus

HHV V————CMV

HHV VI VII—–Febrile illness in children

HHV VIII——-Karposi Sarcoma

Visualize the canal as a cylinder, stretching from the deep inguinal ring to the superficial inguinal ring.^[1]

To help define the boundaries, the canal is often further approximated as a box with six sides. Not including the two rings, the remaining four sides are usually called the “anterior wall”, “posterior wall”, “roof”, and “floor”. These consist of the following:

mnemonic “MALT”, starting at the top and going counterclockwise:

• M – muscles
• A – aponeuroses (The A in MALT coincides with the position of the wall – Anterior. Hence, it is impossible to mix up whether the direction of the mnemonic is clockwise or anticlockwise)
• L – ligaments
• T – transversalis/tendon

Contents

• in males : the spermatic cord and its coverings + the ilioinguinal nerve.
• in females : the round ligament of the uterus + the ilioinguinal nerve.

The classic description of the contents of spermatic cord in the male are: 3 arteries: artery to vas, testicular artery, cremasteric artery 3 fascial layers: external spermatic,internal spermatic,cremastic 3 other vessels: pampiniform plexus, vas deferens, lymphatics 1 nerve: genital branch of the genitofemoral nerve (L1/2)

The ilioinguinal nerve passes through the superficial ring to descend into the scrotum, but does not formally run through the canal.

Gonads (ovaries or testes) descend from their starting point on the posterior abdominal wall (para-aortically) and near the kidneys down the abdomen and through the inguinal canal to reach the scrotum. The testis then descends through the abdominal wall into the scrotum, behind the processus vaginalis (which later obliterates). Thus lymphatic spread from a testicular tumour is to the para-aortic nodes first, and not the inguinal nodes.

Source:Wikipedia

PDA,TOF,TGA,TAPVC

In the developing fetus, the ductus arteriosus (DA) is the vascular connection between the pulmonary artery and the aortic arch that allows most of the blood from the right ventricle to bypass the fetus’ fluid-filled compressed lungs. During fetal development, this shunt protects the right ventricle from pumping against the high resistance in the lungs, which can lead to right ventricular failure if the DA closes in-utero.
When the newborn takes its first breath, the lungs open and pulmonary vascular resistance decreases. After birth, the lungs release bradykinin to constrict the smooth muscle  wall of the DA and reduce bloodflow through the DA as it narrows and completely closes, usually within the first few weeks of life. In most newborns with a patent ductus arteriosus the blood flow is reversed from that of in utero flow, i.e. the blood flow is from the higher pressure aorta to the now lower pressure pulmonary arteries.
A patent ductus arteriosus allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs. This uses more calories than normal and often interferes with feeding in infancy. This condition, as a constellation of findings, is called congestive heart failure. In some cases, such as in transposition of the great vessels (the pulmonary artery and the aorta), a PDA may need to remain open. In this cardiovascular condition, the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the patent ductus arteriosus open.Without treatments, the disease may progress from left-to-right (noncyanotic heart) shunt to right-to-left shunt (cyanotic heart) called Eisenmenger syndrome.

TOF

Tetralogy of Fallot results in low oxygenation of blood due to the mixing of oxygenated and deoxygenated blood in the left ventricle via the VSD and preferential flow of the mixed blood from both ventricles through the aorta because of the obstruction to flow through the pulmonary valve. This is known as a right-to-left shunt. The primary symptom is low blood oxygen saturation with or without cyanosis from birth or developing in the first year of life. If the baby is not cyanotic then it is sometimes referred to as a “pink tet”.Other symptoms include a heart murmur which may range from almost imperceptible to very loud, difficulty in feeding, failure to gain weight, retarded growth and physical development, dyspnea on exertion, clubbing of the fingers and toes, and polycythemia.

Children with tetralogy of Fallot may develop “tet spells”. The precise mechanism of these episodes is in doubt, but presumably results from a transient increase in resistance to blood flow to the lungs with increased preferential flow of desaturated blood to the body. Tet spells are characterized by a sudden, marked increase in cyanosis followed by syncope, and may result in hypoxic brain injury and death. Older children will often squat during a tet spell, which increases systemic vascular resistance and allows for a temporary reversal of the shunt.Oxygen is effective in treating spells because it is a potent pulmonary vasodilator and systemic vasoconstrictor. This allows more blood flow to the lungs.

Squatting

There are also simple procedures such as squatting and the knee chest position which increases aortic wave reflection, increasing pressure on the left side of the heart, decreasing the right to left shunt thus decreasing the amount of deoxygenated blood entering the systemic circulation.

The abnormal “coeur-en-sabot” (boot-like) appearance of a heart with tetralogy of Fallot is easily visible via chest x-ray

The Blalock-Taussig shunt (also referred to as a Blalock-Thomas-Taussig shunt) is a surgical procedure to give palliation to cyanotic heart defects which are common causes of blue baby syndrome. In modern surgery, this procedure is temporarily used to direct blood flow to the lungs and relieve cyanosis while the infant is waiting for corrective or palliative surgery.

One branch of the subclavian artery or carotid artery is separated and connected with the pulmonary artery. The lung receives more blood with low oxygenation from the body. The first area of application was tetralogy of Fallot.

TGA

Total Anomalous Pulmonary venous connection

Total anomalous pulmonary venous connection (TAPVC) consists of an abnormality of blood flow in which all 4 pulmonary veins drain into systemic veins or the right atrium with or without pulmonary venous obstruction. Systemic and pulmonary venous blood mix in the right atrium. An atrial defect or foramen ovale (part of the complex) is important in left ventricular output both in fetal and in newborn circulation.

Eisenmenger Syndrome

Eisenmenger’s syndrome (or Eisenmenger’s reaction) is defined as the process in which a left-to-right shunt caused by a ventricular septal defect in the heart causes increased flow through the pulmonary vasculature, causing pulmonary hypertension, which in turn, causes increased pressures in the right side of the heart and reversal of the shunt into a right-to-left shunt. Eisenmenger’s syndrome specifically refers to the combination of systemic-to-pulmonary communication, pulmonary vascular disease and cyanosis.

The left side of the heart supplies blood to the whole body, and as a result has higher pressures than the right side, which supplies only deoxygenated blood to the lungs. If a large anatomic defect exists between the sides of the heart, blood will flow from the left side to the right side. This results in high blood flow and pressure travelling through the lungs. The increased pressure causes damage to delicate capillaries, which then are replaced with scar tissue. Scar tissue does not contribute to oxygen transfer, therefore decreasing the useful volume of the pulmonary vasculature. The scar tissue also provides less flexibility than normal lung tissue, causing further increases in blood pressure, and the heart must pump harder to continue supplying the lungs, leading to damage of more capillaries.

The reduction in oxygen transfer reduces oxygen saturation in the blood, leading to increased production of red blood cells in an attempt to bring the oxygen saturation up. The excess of red blood cells is called polycythemia. Desperate for enough circulating oxygen, the body begins to dump immature red cells into the blood stream. Immature red cells are not as efficient at carrying oxygen as mature red cells, and they are less flexible, less able to easily squeeze through tiny capillaries in the lungs, and so contribute to death of pulmonary capillary beds. The increase in red blood cells also causes hyperviscosity syndrome.

A person with Eisenmenger’s Syndrome is paradoxically subject to the possibility of both uncontrolled bleeding due to damaged capillaries and high pressure, and random clots due to hyperviscosity and stasis of blood.

Eventually, due to increased resistance, pulmonary pressures may increase sufficiently to cause a reversal of blood flow, so blood begins to travel from the right side of the heart to the left side, and the body is supplied with deoxygenated blood, leading to cyanosis and resultant organ damage.

Cor Pulmonale

Cor pulmonale (Latin cor, heart + New Latin pulmōnāle, of the lungs) or pulmonary heart disease is enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs.

Chronic cor pulmonale usually results in right ventricular hypertrophy (RVH), whereas acute cor pulmonale usually results in dilation.

Hypertrophy is an adaptive response to a long-term increase in pressure. Individual muscle cells grow larger and change to drive the increased contractile force required to move the blood against greater resistance.

Dilation is a stretching of the ventricle in response to acute increased pressure.

To be classified as cor pulmonale, the cause must originate in the pulmonary circulation system.

Nutmeg liver may result…

The House Of Aminoacids

A house of Aminoacids, the thought itself may seem immature, but there are many things on the surface of earth which exists. This House is believed to exist in the outskirts of Amsterdam.

The purpose of this house may seem silly, but people do many things just for fun. This house was built just to learn more about amino acids and their classification.I became so interested and went through this house on a visit there, so that a topic which has been so confusing through out my life could be learnt so easily.

The house of Amino Acids is built based on the memory principles, Peg system of memory and the loci system of memory.Doors and rooms are designed so as to make a lasting memory of Amino acids and their classification.

Usually tourist places have an entry fee, just for the maintenance, but the people who managed this House was so reluctant to accept any entry fee.I was welcomed with a warm shakehand, and they explained what to expect there and gave a classification of essential and non essential amino acids.

Just to mention

Essential:Isoleucne,Leucine,threonine,lysine,methionine,phenylalanine,tryptophan,valine

Semi essential:Arginine and histidine

Simple Aa:glycine,alanine

Only optically inactive amino acid:Glycine

There was a Big Gate welcoming visitors, it was painted Silver and THE HOUSE OF AMINOACIDS was inscribed on it with RED.

The front door was beautifully furnished, the name Isoleucine was printed on with, I wonder why some ice cubes were drawn on the front door. ICE=ISO?, there was a big hallway in front of me, rooms on either side with doors.The amino acids in the first room were Non polar and they were 8 in number 6 were essential and 2 were non essential.

I first decided to take a count of number of rooms, total 9 rooms, and 10 doors including the front door, I understood that the doors were meant to memorize the amino acids and rooms were meant to memorize the different properties of amino acids.There were 3 rooms on the left and 4 rooms on the right.

2.second door was meant for Leucine, on entering this room I got the smell of burnt charcoal( Keto aminoacid)

3. The third door was an extension of the first room, and Threonine was written on it, threonine had some friends inside too,these friends were drinking water( polar).

4. The fourth door was meant for Lysine, it felt just like a bedroom and since bed room is meant for a basic need(sleep ) I thought some other basic aminoacids will be present too.I was right I saw Arginine and Histidine sleeping on the bed!

5. Fifth door Methionine. I also remembered that methionine and cysteine were sulfur containing amino acids.

6.Phenylalanine. Also that Phenylalanine and tyrosine are Aromatic Amino acids

7.Tryptophan.Histidine and tryptophan are heterocyclic

8.Valine.Along with Valine,leucine and isoleucine are branched Amino acids

As you can see doors 1 to 8 were meant for essential amino acids.Now you can place whatever in these rooms to fit in the other classifications ie polar and non polar, Simple, branched,Ketogenic glucogenic etc etc.

Any Help In Learning These Little Molecules Proves Truly Valuable

9 and 10 were on the other side of the building for Arginine and Histidine Both semiessential amino acids

Mind Map-Upperlimb muscle innervation

Pathological Bodies and diseases concerned

Aschoff Bodies – rheumatic fever

Asteroid body – sporotrichosis

BABES – ERNST Bodies – metachromatic granules

BALBIANI’S Bodies – yolk nucleus

Bamboo bodies – asbestosis

Bodies OF ARANTIUS – aortic valve nodules

BODY OF HIGHMORE – mediastinum testis

Bollinger bodies – fowlpox
Brassy body – dark shrunken blood corpuscle found in malaria

Call exners bodies – granulosa theca cell tumour

Chromatid bodies – entamoeba histolytica precyst

Citron bodies – cl. Septicum

Civatte bodies – lichen planus

Councilman bodies – hepatitis B

Coccoid X bodies – psittacosis
Creola bodies – asthma
Cystoid bodies – in degenerated retinal nerve fibers ( seen in Cotton wool spots)
Donnes bodies – colostrums corpuscles

Donovan bodies – granulose inguinale (LGV)

Ferruginous bodies – asbestosis

Gamma gandy bodies – congestive splenomegaly

Guarnieri bodies – inclusion bodies of vaccinia

Henderson Peterson bodies – molluscum contagiosum

Harting bodies – calcospheritis in the cerebral capillaries

Heinz bodies – G 6 PD deficiency

Herring bodies – neurohypophysis

Heterophil antibodies – infectious mononucleosis

Hirano bodies – alzheimer’s disease

Lewy bodies – parkinsonism

Levinthal coles lille bodies – psittacosis

Mallory bodies – alcoholic hepatitis

Masson bodies – rheumatic pneumonia

Michelis guttman bodies – malakoplakia

Mooser bodies – endemic typhus
Moot bodies – multiple myeloma
Negri bodies – rabies
Odland body – keratinosome
Oken’s body – mesonephros

Paschen bodies – vaccinia / variola

Pick bodies – picks disease

Psamomma bodies –

• 1. papillary carcinoma of thyroid
• 2. serous papillary carcinoma of ovary
• 3. meningioma
• 4. mesothelioma

Reilly bodies – hurler’s syndrome

Rokitansky bodies – teratoma

Ross’s bodies – syphilis
Rushton bodies – odontogenic cyst
Sclerotic bodies – chromoblastomycosis
Sandstorm bodies – parathyroid glands

Schillar dual bodies – yolk sac tumour

Schaumann bodies – sarcoidosis
Verocay bodies – schwanoma
Winkler bodies – syphilis

Zebra bodies – metachromatic leukodystrophy