NEET MDS Lessons
Physiology
Urine is a waste byproduct formed from excess water and metabolic waste molecules during the process of renal system filtration. The primary function of the renal system is to regulate blood volume and plasma osmolarity, and waste removal via urine is essentially a convenient way that the body performs many functions using one process. Urine formation occurs during three processes:
Filtration
Reabsorption
Secretion
Filtration
During filtration, blood enters the afferent arteriole and flows into the glomerulus where filterable blood components, such as water and nitrogenous waste, will move towards the inside of the glomerulus, and nonfilterable components, such as cells and serum albumins, will exit via the efferent arteriole. These filterable components accumulate in the glomerulus to form the glomerular filtrate.
Normally, about 20% of the total blood pumped by the heart each minute will enter the kidneys to undergo filtration; this is called the filtration fraction. The remaining 80% of the blood flows through the rest of the body to facilitate tissue perfusion and gas exchange.
Reabsorption
The next step is reabsorption, during which molecules and ions will be reabsorbed into the circulatory system. The fluid passes through the components of the nephron (the proximal/distal convoluted tubules, loop of Henle, the collecting duct) as water and ions are removed as the fluid osmolarity (ion concentration) changes. In the collecting duct, secretion will occur before the fluid leaves the ureter in the form of urine.
Secretion
During secretion some substances±such as hydrogen ions, creatinine, and drugs—will be removed from the blood through the peritubular capillary network into the collecting duct. The end product of all these processes is urine, which is essentially a collection of substances that has not been reabsorbed during glomerular filtration or tubular reabsorbtion.
A rise in blood pressure stretches the atria of the heart. This triggers the release of atrial natriuretic peptide (ANP). ANP is a peptide of 28 amino acids. ANP lowers blood pressure by:
- relaxing arterioles
- inhibiting the secretion of renin and aldosterone
- inhibiting the reabsorption of sodium ions in the collecting ducts of the kidneys.
The effects on the kidney reduce the reabsorption of water by them thus increasing the flow of urine and the amount of sodium excreted in it (These actions give ANP its name: natrium = sodium; uresis = urinate). The net effect of these actions is to reduce blood pressure by reducing the volume of blood volume in the system.
The Heartbeat
During rest, the heart beats about 70 times a minute in the adult male, while pumping about 5 liters of blood.
The stimulus that maintains this rhythm is self-contained. Embedded in the wall of the right atrium is a mass of specialized heart tissue called the sino-atrial (S-A) node. The S-A node is also called the pacemaker because it establishes the basic frequency at which the heart beats.
The interior of the fibers of heart muscle, like all cells, is negatively charged with respect to the exterior. In the cells of the pacemaker, this charge breaks down spontaneously about 70 times each minute. This, in turn, initiates a similar discharge of the nearby muscle fibers of the atrium. A tiny wave of current sweeps over the atria, causing them to contract.
When this current reaches the region of insulating connective tissue between the atria and the ventricles, it is picked up by the A-V node (atrio-ventricular node). This leads to a system of branching fibers that carries the current to all parts of the ventricles.
The contraction of the heart in response to this electrical activity creates systole.
A period of recovery follows called diastole.
- The heart muscle and S-A node become recharged.
- The heart muscle relaxes.
- The atria refill.
The Electrocardiogram
The electrical activity of the heart can be detected by electrodes placed at the surface of the body. Analysis of an electrocardiogram (ECG or EKG) aids in determining, for example, the extent of damage following a heart attack. This is because death of a portion of the heart muscle blocks electrical transmission through that area and alters the appearance of the ECG
Control of the Heart
Although the A-V node sets the basic rhythm of the heart, the rate and strength of its beating can be modified by two auxiliary control centers located in the medulla oblongata of the brain.
- One sends nerve impulses down accelerator nerves.
- The other sends nerve impulses down a pair of vagus nerves
Accelerator Nerves
The accelerator nerves are part of the sympathetic branch of the autonomic nervous system, and like all post-ganglionic sympathetic neurons release noradrenaline at their endings on the heart.
They increase the rate and strength of the heartbeat and thus increase the flow of blood. Their activation usually arises from some stress such as fear or violent exertion. The heartbeat may increase to 180 beats per minute. The strength of contraction increases as well so the amount of blood pumped may increase to as much as 25-30 liters/minute.
Vigorous exercise accelerates heartbeat in two ways;
- As cellular respiration increases, so does the carbon dioxide level in the blood. This stimulates receptors in the carotid arteries and aorta, and these transmit impulses to the medulla for relay by the accelerator nerves to the heart.
- As muscular activity increases, the muscle pump drives more blood back to the right atrium. The atrium becomes distended with blood, thus stimulating stretch receptors in its wall. These, too, send impulses to the medulla for relay to the heart.
Distention of the wall of the right atrium also triggers the release of atrial natriuretic peptide (ANP) which initiates a set of responses leading to a lowering of blood pressure
The Vagus Nerves
The vagus nerves are part of the parasympathetic branch of the autonomic nervous system. They, too, run from the medulla oblongata to the heart. Their activity slows the heartbeat.
Pressure receptors in the aorta and carotid arteries send impulses to the medulla which relays these by way of the vagus nerves to the heart. Heartbeat and blood pressure diminish.
Excitability ( Bathmotropism ) : Excitability means the ability of cardiac muscle to respond to signals. Here we are talking about contractile muscle cells that are excited by the excitatory conductive system and generate an action potential.
Cardiac action potential is similar to action potential in nerve and skeletal muscle tissue , with one difference , which is the presence of plateau phase . Plateau phase is unique for cardiac muscle cells .
The resting membrane potential for cardiac muscle is about -80 mV.
When the cardiac muscle is stimulated an action potential is generated . The action potential in cardiac muscle is composed of four phases , which are :
1. Depolarization phase (Phase 0 ) :
A result of opening of sodium channels , which increase the permeability to sodium , which will lead to a rapid sodium influx into the cardiac muscle cell.
2. Repolarization : Repolarization in cardiac muscle is slow and triphasic :
a. Phase 1 (early partial repolarization ) : A small fast repolarization , results from potassium eflux and chloride influx.
b. Phase 2 ( Plateau ) : After the early partial depolarization , the membrane remains depolarized , exhibiting a plateau , which is a unique phase for the cardiac muscle cell. Plateau is due to opening of slow calcium-sodium channels , delay closure of sodium channels , and to decreased potassium eflux.
c. Phase 3 ( Rapid repolarization) : opening of potassium channels and rapid eflux of potassium.
d. Phase 4 ( Returning to resting level) in other words : The phase of complete repolarization. This due to the work of sodium-potassium pump.
Absolute refractory period:
Coincides wit phase 0,phase1 , and phase 2 . During this period , excitability of the heart is totally abolished . This prevents tetanization of the cardiac muscle and enables the heart to contract and relax to be filled by blood ..
Relative refractory period :
Coincides with the rapid repolarization and allows the excitability to be gradually recovered .
Excitation contraction relationship : Contraction of cardiac muscle starts after depolarization and continues about 1.5 time as long as the duration of the action potential and reaches its maximum at the end of the plateau. Relaxation of the muscle starts with the early partial repolarization.
Factors , affecting excitability of cardiac muscle:
I. Positive bathmotropic effect :
1. Sympathetic stimulation : It increase the heart , and thus reduces the duration of the action potentia; . This will shorten the duration of the absolute refractory period , and thus increase the excitability .
2. Drugs : Catecholamines and xanthines derivatives .
3. Mild hypoxia and mild ischemia
4. Mild hyperkalemia as it decreases the K+ efflux and opens excess Na+ channels .
5. Hypocalcemia
II. Negative bathmotropic effect :
1. Parasympathetic stimulation: The negative bathmotropic effect is limited to the atrial muscle excitability , because there is no parasympathetic innervation for the ventricles. Parasympathetic stimulation decreases the heart rate , and thus increases the duration of cardiac action potential and thus increases the duration of the absolute refractory period.
2. moderate to severe hypoxia
3. hyponatremia , hypercalcemia , and severe hyperkalemia.
Clinical Physiology : Extrasystole is a pathological situation , due to abnormal impulses , arising from ectopic focus .It is expressed as an abnormal systole that occur during the early diastole .
Extrasystole is due to a rising of excitability above the normal , which usually occurs after the end of the relative refractory period ( read about staircase phenomenon of Treppe)
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.
Reflexes
A reflex is a direct connection between stimulus and response, which does not require conscious thought. There are voluntary and involuntary reflexes.
The Stretch Reflex:
The stretch reflex in its simplest form involves only 2 neurons, and is therefore sometimes called a 2-neuron reflex. The two neurons are a sensory and a motor neuron. The sensory neuron is stimulated by stretch (extension) of a muscle. Stretch of a muscle normally happens when its antagonist contracts, or artificially when its tendon is stretched, as in the knee jerk reflex. Muscles contain receptors called muscle spindles. These receptors respond to the muscles's stretch. They send stimuli back to the spinal cord through a sensory neuron which connects directly to a motor neuron serving the same muscle. This causes the muscle to contract, reversing the stretch. The stretch reflex is important in helping to coordinate normal movements in which antagonistic muscles are contracted and relaxed in sequence, and in keeping the muscle from overstretching.
Since at the time of the muscle stretch its antagonist was contracting, in order to avoid damage it must be inhibited or tuned off in the reflex. So an additional connection through an interneuron sends an inhibitory pathway to the antagonist of the stretched muscle - this is called reciprocal inhibition.
The Deep Tendon Reflex:
Tendon receptors respond to the contraction of a muscle. Their function, like that of stretch reflexes, is the coordination of muscles and body movements. The deep tendon reflex involves sensory neurons, interneurons, and motor neurons. The response reverses the original stimulus therefore causing relaxation of the muscle stimulated. In order to facilitate that the reflex sends excitatory stimuli to the antagonists causing them to contract - reciprocal activation.
The stretch and tendon reflexes complement one another. When one muscle is stretching and stimulating the stretch reflex, its antagonist is contracting and stimulating the tendon reflex. The two reflexes cause the same responses thus enhancing one another.
The Crossed Extensor Reflex -
The crossed extensor reflex is just a withdrawal reflex on one side with the addition of inhibitory pathways needed to maintain balance and coordination. For example, you step on a nail with your right foot as you are walking along. This will initiate a withdrawal of your right leg. Since your quadriceps muscles, the extensors, were contracting to place your foot forward, they will now be inhibited and the flexors, the hamstrings will now be excited on your right leg. But in order to maintain your balance and not fall down your left leg, which was flexing, will now be extended to plant your left foot (e.g. crossed extensor). So on the left leg the flexor muscles which were contracting will be inhibited, and the extensor muscles will be excited
Damage to Spinal Nerves and Spinal Cord |
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Damage |
Possible cause of damage |
Symptoms associated with innervated area |
Peripheral nerve |
Mechanical injury |
Loss of muscle tone. Loss of reflexes. Flaccid paralysis. Denervation atrophy. Loss of sensation |
Posterior root |
Tabes dorsalis |
Paresthesia. Intermittent sharp pains. Decreased sensitivity to pain. Loss of reflexes. Loss of sensation. Positive Romberg sign. High stepping and slapping of feet. |
Anterior Horn |
Poliomyelitis |
Loss of muscle tone. Loss of reflexes. Flaccid paralysis. Denervation atrophy |
Lamina X (gray matter) |
Syringomyelia |
Bilateral loss of pain and temperature sense only at afflicted cord level. Sensory dissociation. No sensory impairment below afflicted level |
Anterior horn and lateral corticospinal tract |
Amyotrophic lateral sclerosis |
Muscle weakness. Muscle atrophy. Fasciculations of hand and arm muscles. Spastic paralysis |
Posterior and lateral funiculi |
Subacute combined degeneration |
Loss of position sense. Loss of vibratory sense. Positive Romberg sign. Muscle weakness. Spasticity. Hyperactive tendon reflexes. Positive Babinski sign. |
Hemisection of the spinal cord |
Mechanical injury |
Brown-Sequard syndrome |
Below cord level on injured side |
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Flaccid paralysis. Hyperactive tendon reflexes. Loss of position sense. Loss of vibratory sense. Tactile impairment |
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Below cord level on opposite side beginning one or two segments below injury |
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Loss of pain and temperature |
Each hormone in the body is unique. Each one is different in it's chemical composition, structure, and action. With respect to their chemical structure, hormones may be classified into three groups: amines, proteins, and steroids.
Amines- these simple hormones are structural variation of the amino acid tyrosine. This group includes thyroxine from the thyroid gland and epinephrine and norepinephrine from the adrenal medulla.
Proteins- these hormones are chains of amino acids. Insulin from the pancreas, growth hormone from the anterior pituitary gland, and calcitonin from the thyroid gland are all proteins. Short chains of amino acids are called peptides. Antidiuretic hormone and oxytocin, synthesized by the hypothalamus, are peptide hormones.
Steroids- cholesterol is the precursor for the steroid hormones, which include cortisol and aldosterone from the adrenal cortex, estrogen and progesterone from the ovaries, and testosterone from the testes.