NEET MDS Lessons
Physiology
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.
AdenosineTriphosphate (ATP)
- Animal cells cannot directly use most forms of energy
- Most cellular processes require energy stored in the bonds of a molecule, adenosine triphosphate (ATP)
- ATP is referred to as the energy currency of the cell
It is a nucleotide, formed from:
- the base adenine (the structure with 2 rings),
- the 5 carbon sugar deoxyribose (one ring)
- 3 phosphates
Energy is stored in the bonds between the phosphates and is released when the bonds are broken
Red Blood Cells (erythrocytes)
- Women average about 4.8 million of these cells per cubic millimeter (mm3; which is the same as a microliter [µl]) of blood.
- Men average about 5.4 x 106 per µl.
- These values can vary over quite a range depending on such factors as health and altitude.
- RBC precursors mature in the bone marrow closely attached to a macrophage.
- They manufacture hemoglobin until it accounts for some 90% of the dry weight of the cell.
- The nucleus is squeezed out of the cell and is ingested by the macrophage.
RBC have characteristic biconcave shape
Thus RBCs are terminally differentiated; that is, they can never divide. They live about 120 days and then are ingested by phagocytic cells in the liver and spleen. Most of the iron in their hemoglobin is reclaimed for reuse. The remainder of the heme portion of the molecule is degraded into bile pigments and excreted by the liver. Some 3 million RBCs die and are scavenged by the liver each second.
Red blood cells are responsible for the transport of oxygen and carbon dioxide.
HEART DISORDERS
- Pump failure => Alters pressure (flow) =>alters oxygen carrying capacity.
- Renin release (Juxtaglomerular cells) Kidney
- Converts Angiotensinogen => Angiotensin I
- In lungs Angiotensin I Converted => Angiotensin II
- Angiotensin II = powerful vasoconstrictor (raises pressure, increases afterload)
- stimulates thirst
- stimulates adrenal cortex to release Aldosterone
(Sodium retention, potassium loss) - stimulates kidney directly to reabsorb Sodium
- releases ADH from Posterior Pituitary
- Myocardial Infarction
- Myocardial Cells die from lack of Oxygen
- Adjacent vessels (collateral) dilate to compensate
- Intracellular Enzymes leak from dying cells (Necrosis)
- Creatine Kinase CK (Creatine Phosphokinase) 3 forms
- One isoenzyme = exclusively Heart (MB)
- CK-MB blood levels found 2-5 hrs, peak in 24 hrs
- Lactic Dehydrogenase found 6-10 hours after. points less clearly to infarction
- Serum glutamic oxaloacetic transaminase (SGOT)
- Found 6 hrs after infarction, peaks 24-48 hrs at 2 to 15 times normal,
- SGOT returns to normal after 3-4 days
- Creatine Kinase CK (Creatine Phosphokinase) 3 forms
- Myocardium weakens = Decreased CO & SV (severe - death)
- Infarct heal by fibrous repair
- Hypertrophy of undamaged myocardial cells
- Increased contractility to restore normal CO
- Improved by exercise program
- Prognosis
- 10% uncomplicated recovery
- 20% Suddenly fatal
- Rest MI not fatal immediately, 15% will die from related causes
- Congenital heart disease (Affect oxygenation of blood)
- Septal defects
- Ductus arteriosus
- Valvular heart disease
- Stenosis = cusps, fibrotic & thickened, Sometimes fused, can not open
- Regurgitation = cusps, retracted, Do not close, blood moves backwards
Clinical Physiology
Heart Failure : Heart failure is inability of the heart to pump the enough amount of blood needed to sustain the needs of organism .
It is usually called congestive heart failure ( CHF) .
To understand the pathophysiology of the heart failure , lets compare it with the physiology of the cardiac output :
Cardiac output =Heart rate X stroke volume
Stroke volume is determined by three determinants : Preload ( venous return ) , contractility , and afterload (peripheral resistance ) . Any disorder of these factors will reduce the ability of the heart to pump blood .
Preload : Any factor that decrease the venous return , either by decreasing the intravenous pressure or increasing the intraatrial pressure will lead to heart failure .
Contractility : Reducing the power of contraction such as in myocarditis , cardiomyopathy , preicardial tamponade ..etc , will lead to heart failure .
Afterload : Any factor that may increase the peripheral resistance such as hypertension , valvular diseases of the heart may cause heart failure.
Pathophysiology : When the heart needs to contract more to meet the increased demand , compensatory mechanisms start to develope to enhance the power of contractility . One of these mechanism is increasing heart rate , which will worsen the situation because this will increase the demands of the myocardial cells themselves . The other one is hypertrophy of the cardiac muscle which may compensate the failure temporarily but then the hypertrophy will be an additional load as the fibers became stiff .
The stroke volume will be reduced , the intraventricular pressure will increase and consequently the intraatrial pressure and then the venous pressure . This will lead to decrease reabsorption of water from the interstitium ( see microcirculation) and then leads to developing of edema ( Pulmonary edema if the failure is left , and systemic edema if the failure is right) .
Bile contains:
- bile acids. These amphiphilic steroids emulsify ingested fat. The hydrophobic portion of the steroid dissolves in the fat while the negatively-charged side chain interacts with water molecules. The mutual repulsion of these negatively-charged droplets keeps them from coalescing. Thus large globules of fat (liquid at body temperature) are emulsified into tiny droplets (about 1 µm in diameter) that can be more easily digested and absorbed.
- bile pigments. These are the products of the breakdown of hemoglobin removed by the liver from old red blood cells. The brownish color of the bile pigments imparts the characteristic brown color of the feces.
Ingestion: Food taken in the mouth is
- ground into finer particles by the teeth,
- moistened and lubricated by saliva (secreted by three pairs of salivary glands)
- small amounts of starch are digested by the amylase present in saliva
- the resulting bolus of food is swallowed into the esophagus and
- carried by peristalsis to the stomach.