NEET MDS Lessons
Physiology
Platelets
Platelets are cell fragments produced from megakaryocytes.
Blood normally contains 150,000 to 350,000 per microliter (µl). If this value should drop much below 50,000/µl, there is a danger of uncontrolled bleeding. This is because of the essential role that platelets have in blood clotting.
When blood vessels are damaged, fibrils of collagen are exposed.
- von Willebrand factor links the collagen to platelets forming a plug of platelets there.
- The bound platelets release ADP and thromboxane A2 which recruit and activate still more platelets circulating in the blood.
- (This role of thromboxane accounts for the beneficial effect of low doses of aspirin a cyclooxygenase inhibitor in avoiding heart attacks.)
ReoPro is a monoclonal antibody directed against platelet receptors. It inhibits platelet aggregation and appears to reduce the risk that "reamed out" coronary arteries (after coronary angioplasty) will plug up again.
Respiration involves several components:
Ventilation - the exchange of respiratory gases (O2 and CO2) between the atmosphere and the lungs. This involves gas pressures and muscle contractions.
External respiration - the exchange of gases between the lungs and the blood. This involves partial pressures of gases, diffusion, and the chemical reactions involved in transport of O2and CO2.
Internal respiration - the exchange of gases between the blood and the systemic tissues. This involves the same processes as external respiration.
Cellular respiration - the includes the metabolic pathways which utilize oxygen and produce carbon dioxide, which will not be included in this unit.
Ventilation is composed of two parts: inspiration and expiration. Each of these can be described as being either quiet, the process at rest, or forced, the process when active such as when exercising.
Quiet inspiration:
The diaphragm contracts, this causes an increase in volume of the thorax and the lungs, which causes a decrease in pressure of the thorax and lungs, which causes air to enter the lungs, moving down its pressure gradient. Air moves into the lungs to fill the partial vacuum created by the increase in volume.
Forced inspiration:
Other muscles aid in the increase in thoracic and lung volumes.
The scalenes - pull up on the first and second ribs.
The sternocleidomastoid muscles pull up on the clavicle and sternum.
The pectoralis minor pulls forward on the ribs.
The external intercostals are especially important because they spread the ribs apart, thus increasing thoracic volume. It's these muscles whose contraction produces the "costal breathing" during rapid respirations.
Quiet expiration:
The diaphragm relaxes. The elasticity of the muscle tissue and of the lung stroma causes recoil which returns the lungs to their volume before inspiration. The reduced volume causes the pressure in the lungs to increase thus causing air to leave the lungs due to the pressure gradient.
Forced Expiration:
The following muscles aid in reducing the volume of the thorax and lungs:
The internal intercostals - these compress the ribs together
The abdominus rectus and abdominal obliques: internal obliques, external obliques- these muscles push the diaphragm up by compressing the abdomen.
Respiratory output is determined by the minute volume, calculated by multiplying the respiratory rate time the tidal volume.
Minute Volume = Rate (breaths per minute) X Tidal Volume (ml/breath)
Rate of respiration at rest varies from about 12 to 15 . Tidal volume averages 500 ml Assuming a rate of 12 breaths per minute and a tidal volume of 500, the restful minute volume is 6000 ml. Rates can, with strenuous exercise, increase to 30 to 40 and volumes can increase to around half the vital capacity.
Not all of this air ventilates the alveoli, even under maximal conditions. The conducting zone volume is about 150 ml and of each breath this amount does not extend into the respiratory zone. The Alveolar Ventilation Rate, AVR, is the volume per minute ventilating the alveoli and is calculated by multiplying the rate times the (tidal volume-less the conducting zone volume).
AVR = Rate X (Tidal Volume - 150 ml)
For a calculation using the same restful rate and volume as above this yields 4200 ml.
Since each breath sacrifices 150 ml to the conducting zone, more alveolar ventilation occurs when the volume is increased rather than the rate.
During inspiration the pressure inside the lungs (the intrapulmonary pressure) decreases to -1 to -3 mmHg compared to the atmosphere. The variation is related to the forcefulness and depth of inspiration. During expiration the intrapulmonary pressure increases to +1 to +3 mmHg compared to the atmosphere. The pressure oscillates around zero or atmospheric pressure.
The intrapleural pressure is always negative compared to the atmosphere. This is necessary in order to exert a pulling action on the lungs. The pressure varies from about -4 mmHg at the end of expiration, to -8 mmHg and the end of inspiration.
The tendency of the lungs to expand, called compliance or distensibility, is due to the pulling action exerted by the pleural membranes. Expansion is also facilitated by the action of surfactant in preventing the collapse of the alveoli.
The opposite tendency is called elasticity or recoil, and is the process by which the lungs return to their original or resting volume. Recoil is due to the elastic stroma of the lungs and the series elastic elements of the respiratory muscles, particularly the diaphragm.
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
Oxygen Uptake in the Lungs is Increased About 70X by Hemoglobin in the Red Cells
- In the lungs oxygen must enter the blood
- A small amount of oxygen dissolves directly in the serum, but 98.5% of the oxygen is carried by hemoglobin
- All of the hemoglobin is found within the red blood cells (RBCs or erythrocytes)
- The hemoglobin content of the blood is about 15 gm/deciliter (deciliter = 100 mL)
- Red cell count is about 5 million per microliter
Each Hemoglobin Can Bind Four O2 Molecules (100% Saturation)
- Hemoglobin is a protein molecule with 4 protein sub-units (2 alphas and 2 betas)
- Each of the 4 sub-units contains a heme group which gives the protein a red color
- Each heme has an iron atom in the center which can bind an oxygen molecule (O2)
- The 4 hemes in a hemoglobin can carry a maximum of 4 oxygen molecules
- When hemoglobin is saturated with oxygen it has a bright red color; as it loses oxygen it becomes bluish (cyanosis)
The Normal Blood Hematocrit is Just Below 50%
- Blood consists of cells suspended in serum
- More than 99% of the cells in the blood are red blood cells designed to carry oxygen
- 25% of all the cells in the body are RBCs
- The volume percentage of cells in the blood is called the hematocrit
- Normal hematocrits are about 40% for women and 45% for men
At Sea Level the Partial Pressure of O2 is High Enough to Give Nearly 100% Saturation of Hemoglobin
- As the partial pressure of oxygen in the alveoli increases the hemoglobin in the red cells passing through the lungs rises until the hemoglobin is 100% saturated with oxygen
- At 100% saturation each hemoglobin carries 4 O2 molecules
- This is equal to 1.33 mL O2 per gram of hemoglobin
- A person with 15 gm Hb/deciliter can carry:
- Max O2 carriage = 1.33 mL O2/gm X 15 gm/deciliter = 20 mL O2/deciliter
- A plot of % saturation vs pO2 gives an S-shaped "hemoglobin dissociation curve"
- At 100% saturation each hemoglobin binds 4 oxygen molecules
At High Altitudes Hemoglobin Saturation May be Well Below 100%
- At the alveolar pO2 of 105 mm Hg at sea level the hemoglobin will be about 97% saturated, but the saturation will fall at high altitudes
- At 12,000 feet altitude alveolar pO2 will be about 60 mm Hg and the hemoglobin will be 90% saturated
- At 29,000 feet (Mt. Everest) alveolar pO2 is about 24 mm Hg and the hemoglobin will be only 42% saturated
- At very high altitudes most climbers must breath pure oxygen from tanks
- During acclimatization to high altitude the hematocrit can rise to about 60%- this increases the amount of oxygen that can be carried
- Hematocrits above 60% are not useful because the blood viscosity will increase to the point where it impairs circulation
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.
Control of processes in the stomach:
The stomach, like the rest of the GI tract, receives input from the autonomic nervous system. Positive stimuli come from the parasympathetic division through the vagus nerve. This stimulates normal secretion and motility of the stomach. Control occurs in several phases:
Cephalic phase stimulates secretion in anticipation of eating to prepare the stomach for reception of food. The secretions from cephalic stimulation are watery and contain little enzyme or acid.
Gastric phase of control begins with a direct response to the contact of food in the stomach and is due to stimulation of pressoreceptors in the stomach lining which result in ACh and histamine release triggered by the vagus nerve. The secretion and motility which result begin to churn and liquefy the chyme and build up pressure in the stomach. Chyme surges forward as a result of muscle contraction but is blocked from entering the duodenum by the pyloric sphincter. A phenomenon call retropulsion occurs in which the chyme surges backward only to be pushed forward once again into the pylorus. The presence of this acid chyme in the pylorus causes the release of a hormone called gastrin into the bloodstream. Gastrin has a positive feedback effect on the motility and acid secretion of the stomach. This causes more churning, more pressure, and eventually some chyme enters the duodenum.
Intestinal phase of stomach control occurs. At first this involves more gastrin secretion from duodenal cells which acts as a "go" signal to enhance the stomach action already occurring. But as more acid chyme enters the duodenum the decreasing pH inhibits gastrin secretion and causes the release of negative or "stop" signals from the duodenum.
These take the form of chemicals called enterogastrones which include GIP (gastric inhibitory peptide). GIP inhibits stomach secretion and motility and allows time for the digestive process to proceed in the duodenum before it receives more chyme. The enterogastric reflex also reduces motility and forcefully closes the pyloric sphincter. Eventually as the chyme is removed, the pH increases and gastrin and the "go" signal resumes and the process occurs all over again. This series of "go" and "stop" signals continues until stomach emptying is complete.
(RDS) Respiratory distress of Newborn
1. hyaline membrane disease of the new born
2. decrease in surfactant, Weak, Abnormal complience of chest wall
3. Small alveoli, difficult to inflate, Alveoli tent to collapse, many of varied sizes
4. decrease in O2 diffusion area, lung difficult to expand, in compliance