Blood Groups

Blood groups are created by molecules present on the surface of red blood cells (and often on other cells as well).

The ABO Blood Groups

The ABO blood groups are the most important in assuring safe blood transfusions.

When red blood cells carrying one or both antigens are exposed to the corresponding antibodies, they agglutinate; that is, clump together. People usually have antibodies against those red cell antigens that they lack.

The critical principle to be followed is that transfused blood must not contain red cells that the recipient's antibodies can clump. Although theoretically it is possible to transfuse group O blood into any recipient, the antibodies in the donated plasma can damage the recipient's red cells. Thus all transfusions should be done with exactly-matched blood.

The Rh System

Rh antigens are transmembrane proteins with loops exposed at the surface of red blood cells. They appear to be used for the transport of carbon dioxide and/or ammonia across the plasma membrane. They are named for the rhesus monkey in which they were first discovered.

There are a number of Rh antigens. Red cells that are "Rh positive" express the one designated D. About 15% of the population have no RhD antigens and thus are "Rh negative".

The major importance of the Rh system for human health is to avoid the danger of RhD incompatibility between mother and fetus.

During birth, there is often a leakage of the baby's red blood cells into the mother's circulation. If the baby is Rh positive (having inherited the trait from its father) and the mother Rh-negative, these red cells will cause her to develop antibodies against the RhD antigen. The antibodies, usually of the IgG class, do not cause any problems for that child, but can cross the placenta and attack the red cells of a subsequent Rh⁺ fetus. This destroys the red cells producing anemia and jaundice. The disease, called erythroblastosis fetalis or hemolytic disease of the newborn, may be so severe as to kill the fetus or even the newborn infant. It is an example of an antibody-mediated cytotoxicity disorder.

Although certain other red cell antigens (in addition to Rh) sometimes cause problems for a fetus, an ABO incompatibility does not. Rh incompatibility so dangerous when ABO incompatibility is not

It turns out that most anti-A or anti-B antibodies are of the IgM class and these do not cross the placenta. In fact, an Rh⁻/type O mother carrying an Rh⁺/type A, B, or AB fetus is resistant to sensitization to the Rh antigen. Presumably her anti-A and anti-B antibodies destroy any fetal cells that enter her blood before they can elicit anti-Rh antibodies in her.

This phenomenon has led to an extremely effective preventive measure to avoid Rh sensitization. Shortly after each birth of an Rh⁺ baby, the mother is given an injection of anti-Rh antibodies. The preparation is called Rh immune globulin (RhIG) or Rhogam. These passively acquired antibodies destroy any fetal cells that got into her circulation before they can elicit an active immune response in her.

Rh immune globulin came into common use in the United States in 1968, and within a decade the incidence of Rh hemolytic disease became very low.

 Pain, Temperature, and Crude Touch and Pressure

General somatic nociceptors, thermoreceptors, and mechanoreceptors sensitive to crude touch and pressure from the face conduct signals to the brainstem over GSA fibers of cranial nerves V, VII, IX, and X.

The afferent fibers involved are processes of monopolar neurons with cell bodies in the semilunar, geniculate, petrosal, and nodose ganglia, respectively.

The central processes of these neurons enter the spinal tract of V, where they descend through the brainstem for a short distance before terminating in the spinal nucleus of V.

Second-order neurons then cross over the opposite side of the brainstem at various levels to enter the ventral trigeminothalamic tract, where they ascend to the VPM of the thalamus.

Finally, third-order neurons project to the "face" area of the cerebral cortex in areas 3, 1, and 2 .

Discriminating Touch and Pressure

Signals are conducted from general somatic mechanoreceptors over GSA fibers of the trigeminal nerve into the principal sensory nucleus of V, located in the middle pons.

Second-order neurons then conduct the signals to the opposite side of the brainstem, where they ascend in the medial lemniscus to the VPM of the thalamus.

 Thalamic neurons then project to the "face" region of areas 3, I, and 2 of the cerebral cortex.

 Kinesthesia and Subconscious Proprioception

Proprioceptive input from the face is primarily conducted over GSA fibers of the trigeminal nerve.

The peripheral endings of these neurons are the general somatic mechanoreceptors sensitive to both conscious (kinesthetic) and subconscious proprioceptive input.

Their central processes extend from the mesencephalic nucleus to the principal sensory nucleus of V in the pons

The subconscious component is conducted to the cerebellum, while the conscious component travels to the cerebral cortex.

Certain second-order neurons from the principal sensory nucleus relay proprioceptive information concerning subconscious evaluation and integration into the ipsilateral cerebellum.

Other second-order neurons project to the opposite side of the pons and ascend to the VPM of the thalamus as the dorsal trigeminothalamic tract.

Thalamic projections terminate in the face area of the cerebral cortex.

Respiratory system plays important role in maintaining homeostasis . Other than its major function , which is supplying the cells with needed oxygen to produce energy and getting rid of carbon dioxide , it has other functions :

1 Vocalization , or sound production.
2 Participation in acid base balance .
3 Participation in fluid balance by insensible water elimination (vapors ).
4 Facilitating venous return .
5 Participation in blood pressure regulation : Lungs produce Angiotensin converting enzyme ( ACE ) .
6 Immune function : Lungs produce mucous that trap foreign particles , and have ciliae that move foreign particles away from the lung. They also produce alpha 1 antitrepsin that protect the lungs themselves from the effect of elastase and other proteolytic  enzymes

Factors , affecting glomerular filtration rate :

 Factors that may influence the different pressure forces , or the filtration coefficient will affect the glomerular filtration rate . 
 
1. Dehydration : Causes decrease hydrostatic pressure , and thus decreases GFR
2- Liver diseases that may decrease the plasma proteins and decrease the oncotic pressure , and thus increases glomerular filtration rate .
3- Sympathetic stimulation : will decrease the diameter of afferent arteriole and thus decreases glomerular filtration rate.
4- Renal diseases : Nephrotic syndrome for example decreases the number of working nephrons and thus decreases the filtration coefficient and thus decreases the glomerular filtration rate.
Glomerulonephritis will causes thickening of the glomerular basement membrane and thus decreases the glomerular filtration rate by decreasing the filtration coefficient too.

Contractility : Means ability of cardiac muscle to convert electrical energy of action potential into mechanical energy ( work).
The excitation- contraction coupling of cardiac muscle is similar to that of skeletal muscle , except the lack of motor nerve stimulation. 

Cardiac muscle is a self-excited muscle , but the principles of contraction are the same . There are many rules that control the contractility of the cardiac muscles, which are:

1. All or none rule: due to the syncytial nature of the cardiac muscle.There are atrial syncytium and ventricular syncytium . This rule makes the heart an efficient pump.

2. Staircase phenomenon : means gradual increase in muscle contraction following rapidly repeated stimulation..

3. Starling`s law of the heart: The greater the initial length of cardiac muscle fiber , the greater the force of contraction. The initial length is determined by the degree of diastolic filling .The pericardium prevents overstretching of heart , and allows optimal increase in diastolic volume.

Thankful to this law , the heart is able to pump any amount of blood that it receives. But overstretching of cardiac muscle fibers may cause heart failure.

Factors affecting  contractility ( inotropism)

I. Positive inotropic factors:

1. sympathetic stimulation: by increasing the permeability of sarcolemma to calcium.
2. moderate increase in temperature . This due to increase metabolism to increase ATP , decrease viscosity of myocardial structures, and increasing calcium influx.
3. Catecholamines , thyroid hormone, and glucagon hormones.
4. mild alkalosis
5. digitalis
6. Xanthines ( caffeine and theophylline )

II. Negative inotropic factors:

1. Parasympathetic stimulation : ( limited to atrial contraction)
2. Acidosis
3. Severe alkalosis
4. excessive warming and cooling .
5. Drugs ;like : Quinidine , Procainamide , and barbiturates .
6. Diphtheria and typhoid toxins.

Proteinuria—Protein content in urine, often due to leaky or damaged glomeruli.

Oliguria—An abnormally small amount of urine, often due to shock or kidney damage.

Polyuria—An abnormally large amount of urine, often caused by diabetes.

Dysuria—Painful or uncomfortable urination, often from urinary tract infections.

Hematuria—Red blood cells in urine, from infection or injury.

Glycosuria—Glucose in urine, due to excess plasma glucose in diabetes, beyond the amount able to be reabsorbed in the proximal convoluted tubule.