Also known as Mucopolysaccharidosis Type 2.
Enzyme Deficient : Iduronate 2 sulfatase
Accumulated Sunstance : Heparan Sulfate And Dermatan Sulfate.
Inheritance : X Linked Recessive
History : Named After Charles A. Hunter ( 1873-1955) Described In 1917.
Gene Affected : On X Chromosome Xq28 Location.
 
Sign And Symptoms :

These are used to control spastic muscle tone. These drugs include diazepam (which binds to GABA receptors), dantrolene (which acts directly on muscles by interfering with the release of calcium from the sarcoplasmic reticulum) and baclofen (which probably acts at GABA receptors in the CNS.
Actions: The benzodiazepines relax the spasticity of skeletal muscle, probably by increasing presynaptic inhibition in the spinal cord.
Therapeutic Uses: Diazepam is useful in the treatment of skeletal muscle spasms such as occur in muscle strain, and in treating spasticity from degenerative disorders, such as multiple sclerosis and cerebral palsy.

These include drugs that block cholinergic transmission between motor nerve endings and the nicotinic receptors on the neuromuscular end-plate of skeletal muscle. These neuromuscular blockers are structural analogs of acetylcholine and act either as antagonists (nondepolarising type) or agonists (depolarising type) at the receptors on the end-plate of the neuromuscular junction. Neuromuscular blockers are clinically useful during surgery to produce complete muscle relaxation.
a) Nondepolarising (competitive) blockers: These agents constitute the majority of the clinically-relevant neuromuscular blockers. They act by blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors

Today I'm gonna talk about nephrotic and nephritic syndrome, and how to differentiate between the two. To do that I will assume that we have five persons, but before that I think I should talk about the anatomy of the glomerulus (you should know that each kidney contains 1.2 million nephron, and the two kidneys combined can have up to 2 - 2.5 million nephron).
First the blood enters through the afferent arteriole and leaves through the efferent arteriole and the arteriole is surrounded by the bowman's capsule. Between the bowman's capsule and the arteriole we have the glomerular basement membrane (GBM). The arteriole wall got endothelial cells which are fenestrated (which means they have pores) and the bowman's capsule is lined with cells called podocytes, and these cells are lined in a fashion that they leave slits between them, now the pores size in the endothelial cells in the arteriole are about 70-100 nanometer, and the slits between the podocytes are about 20-30 nanometer, and if the molecules want to pass through these three layers first they have to be small (for example, the WBC, the RBC are large and can't pass through), the second thing is that negative charges can't pass through these membranes because the three membranes are themselves negatively charged (for example, albumin is small enough to pass through, but because its also negatively charged it can't pass through), is simple words any molecule which have to pass, it has to face the size barrier and the charge barrier.

The reason I mentioned the botulism poisoning and black widow spider bites is the same sentence because these two condition effect the body in the opposite way. I mean in botulism poisoning which is a poisoning produced by the Clostridium botulinum bacterial toxins - mainly food borne - that will enter your body and your nerve cell endings. They will then attack the proteins which are responsible for fusing the vesicle which contains acetylcholine with the nerve ending membrane and subsequently DECREASE the release of acetylcholine to the synapse. So in these patient there is no acetylcholine release and they will be flaccid and in most of the cases die because of respiratory failure. While the black widow spider venom which is called latrotoxin, works by increasing the binding of the acetylcholine vesicle to the nerve ending membrane and subsequently INCREASE the release of acetylcholine to the synapse, and these patients will suffer from cholinergic crisis and they will present with lacrimation, salivation, abdominal cramps and bradycardia... blah blah etc.

In this post I'll talk about one side effect, which is allergic reaction, now you should know that penicillin can cause type I, type II, and even type III allergic reaction, to differentiate between the three, you should know that type I is "immediate reaction" and it's caused after the body metabolizes penicillin and produce penicilloic acid.  
In some people penicilloic acid binds to the human proteins, now this combination of the penicilloic acid with the human proteins makes the immune system produce antibodies against it and produce IgE. This IgE will activate the mast cells and basophils, and the mast cell will start secreting prostaglandin and leukotrienes, and the granules will release histamine and proteolytic enzymes. On prolonged activation they will start releasing IL-1 and TNF which will cause the skin rashes, bronchoconstriction and the other signs and symptoms of allergic reaction, but this happens after minutes to penicillin administration, and in some RARE cases they may cause anaphylactic shock.