NEET MDS Lessons
Physiology
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.
|
Blood Group |
Antigens on RBCs |
Antibodies in Serum |
Genotypes |
|
A |
A |
Anti-B |
AA or AO |
|
B |
B |
Anti-A |
BB or BO |
|
AB |
A and B |
Neither |
AB |
|
O |
Neither |
Anti-A and anti-B |
OO |
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.
Structure and function of skeletal muscle.
Skeletal muscles have a belly which contains the cells and which attaches by means of tendons or aponeuroses to a bone or other tissue. An aponeurosis is a broad, flat, tendinous attachment, usually along the edge of a muscle. A muscle attaches to an origin and an insertion. The origin is the more fixed attachment, the insertion is the more movable attachment. A muscle acts to shorten, pulling the insertion toward the origin. A muscle can only pull, it cannot push.
Muscles usually come in pairs of antagonistic muscles. The muscle performing the prime movement is the agonist, the opposite acting muscle is the antagonist. When the movement reverses, the names reverse. For example, in flexing the elbow the biceps brachii is the agonist, the triceps brachii is the antagonist. When the movement changes to extension of the elbow, the triceps becomes the agonist and the biceps the antagonist. An antagonist is never totally relaxed. Its function is to provide control and damping of movement by maintaining tone against the agonist. This is called eccentric movement.
Muscles can also act as synergists, working together to perform a movement. This movement can be different from that performed when the muscles work independently. For example, the sternocleidomastoid muscles each rotate the head in a different direction. But as synergists they flex the neck.
Fixators act to keep a part from moving. For example fixators act as postural muscles to keep the spine erect and the leg and vertebral column extended when standing. Fixators such as the rhomboids and levator scapulae keep the scapula from moving during actions such as lifting with the arms.
The hepatic portal system
The capillary beds of most tissues drain into veins that lead directly back to the heart. But blood draining the intestines is an exception. The veins draining the intestine lead to a second set of capillary beds in the liver. Here the liver removes many of the materials that were absorbed by the intestine:
- Glucose is removed and converted into glycogen.
- Other monosaccharides are removed and converted into glucose.
- Excess amino acids are removed and deaminated.
- The amino group is converted into urea.
- The residue can then enter the pathways of cellular respiration and be oxidized for energy.
- Many nonnutritive molecules, such as ingested drugs, are removed by the liver and, often, detoxified.
The liver serves as a gatekeeper between the intestines and the general circulation. It screens blood reaching it in the hepatic portal system so that its composition when it leaves will be close to normal for the body.
Furthermore, this homeostatic mechanism works both ways. When, for example, the concentration of glucose in the blood drops between meals, the liver releases more to the blood by
- converting its glycogen stores to glucose (glycogenolysis)
- converting certain amino acids into glucose (gluconeogenesis).
1. Automatic control (sensory) of respiration is in - brainstem (midbrain)
2. Behavioral/voluntary control is in - the cortex
3. Alveolar ventilation -the amount of atmospheric air that actually reaches the alveolar per breath and that can participate in the exchange of gasses between alveoli and blood
4. Only way to increase gas exchange in alveolar capillaries - perfusion-limited gas exchange
5. Pulmonary ventiliation not effected by - concentration of bicarbonate ions
6. Central chemoreceptors - medulla - CO2, O2 and H+ concentrations
7. Peripheral chemoreceptors - carotid and aortic bodies- PO2, PCO2 and pH
8. Major stimulus for respiratory centers - arterial PCO2
9. Rhythmic breathing depends on
1. continuous (tonic) inspiratory drive from DRG (dorsal respiratory group)
2. intermittent (phasic) expiratory input from cerebrum, thalamus, cranial nerves and ascending spinal cord sensory tracts
10. Primary site for gas exchange - type I epithelial cells for alveoli
1 - Passive processes - require no expenditure of energy by a cell:
- Simple diffusion = net movement of a substance from an area of high concentration to an area of low concentration. The rate of diffusion is influenced by:
- concentration gradient
- cross-sectional area through which diffusion occurs
- temperature
- molecular weight of a substance
- distance through which diffusion occurs
- Osmosis = diffusion of water across a semi permeable membrane (like a cell membrane) from an area of low solute concentration to an area of high solute concentration
- Facilitated diffusion = movement of a substance across a cell membrane from an area of high concentration to an area of low concentration. This process requires the use of 'carriers' (membrane proteins). In the example below, a ligand molecule (e.g., acetylcholine) binds to the membrane protein. This causes a conformational change or, in other words, an 'opening' in the protein through which a substance (e.g., sodium ions) can pass.
2 - Active processes - require the expenditure of energy by cells:
- Active transport = movement of a substance across a cell membrane from an area of low concentration to an area of high concentration using a carrier molecule
- Endo- & exocytosis - moving material into (endo-) or out of (exo-) cell in bulk form
Events in gastric function:
1) Signals from vagus nerve begin gastric secretion in cephalic phase.
2) Physical contact by food triggers release of pepsinogen and H+ in gastric phase.
3) Muscle contraction churns and liquefies chyme and builds pressure toward pyloric sphincter.
4) Gastrin is released into the blood by cells in the pylorus. Gastrin reinforces the other stimuli and acts as a positive feedback mechanism for secretion and motility.
5) The intestinal phase begins when acid chyme enters the duodenum. First more gastrin secretion causes more acid secretion and motility in the stomach.
6) Low pH inhibits gastrin secretion and causes the release of enterogastrones such as GIP into the blood, and causes the enterogastric reflex. These events stop stomach emptying and allow time for digestion in the duodenum before gastrin release again stimulates the stomach.
The Nerve Impulse
When a nerve is stimulated the resting potential changes. Examples of such stimuli are pressure, electricity, chemicals, etc. Different neurons are sensitive to different stimuli(although most can register pain). The stimulus causes sodium ion channels to open. The rapid change in polarity that moves along the nerve fiber is called the "action potential." In order for an action potential to occur, it must reach threshold. If threshold does not occur, then no action potential can occur. This moving change in polarity has several stages:
Depolarization
The upswing is caused when positively charged sodium ions (Na+) suddenly rush through open sodium gates into a nerve cell. The membrane potential of the stimulated cell undergoes a localized change from -55 millivolts to 0 in a limited area. As additional sodium rushes in, the membrane potential actually reverses its polarity so that the outside of the membrane is negative relative to the inside. During this change of polarity the membrane actually develops a positive value for a moment(+30 millivolts). The change in voltage stimulates the opening of additional sodium channels (called a voltage-gated ion channel). This is an example of a positive feedback loop.
Repolarization
The downswing is caused by the closing of sodium ion channels and the opening of potassium ion channels. Release of positively charged potassium ions (K+) from the nerve cell when potassium gates open. Again, these are opened in response to the positive voltage--they are voltage gated. This expulsion acts to restore the localized negative membrane potential of the cell (about -65 or -70 mV is typical for nerves).
Hyperpolarization
When the potassium ions are below resting potential (-90 mV). Since the cell is hyper polarized, it goes to a refractory phrase.
Refractory phase
The refractory period is a short period of time after the depolarization stage. Shortly after the sodium gates open, they close and go into an inactive conformation. The sodium gates cannot be opened again until the membrane is repolarized to its normal resting potential. The sodium-potassium pump returns sodium ions to the outside and potassium ions to the inside. During the refractory phase this particular area of the nerve cell membrane cannot be depolarized. This refractory area explains why action potentials can only move forward from the point of stimulation.
Factors that affect sensitivity and speed
Sensitivity
Increased permeability of the sodium channel occurs when there is a deficit of calcium ions. When there is a deficit of calcium ions (Ca+2) in the interstitial fluid, the sodium channels are activated (opened) by very little increase of the membrane potential above the normal resting level. The nerve fiber can therefore fire off action potentials spontaneously, resulting in tetany. This could be caused by the lack of hormone from parathyroid glands. It could also be caused by hyperventilation, which leads to a higher pH, which causes calcium to bind and become unavailable.
Speed of Conduction
This area of depolarization/repolarization/recovery moves along a nerve fiber like a very fast wave. In myelinated fibers, conduction is hundreds of times faster because the action potential only occurs at the nodes of Ranvier (pictured below in 'types of neurons') by jumping from node to node. This is called "saltatory" conduction. Damage to the myelin sheath by the disease can cause severe impairment of nerve cell function. Some poisons and drugs interfere with nerve impulses by blocking sodium channels in nerves. See discussion on drug at the end of this outline.