NEET MDS Lessons
Physiology
Graded Contractions and Muscle Metabolism
The muscle twitch is a single response to a single stimulus. Muscle twitches vary in length according to the type of muscle cells involved. .
Fast twitch muscles such as those which move the eyeball have twitches which reach maximum contraction in 3 to 5 ms (milliseconds). [superior eye] and [lateral eye] These muscles were mentioned earlier as also having small numbers of cells in their motor units for precise control.
The cells in slow twitch muscles like the postural muscles (e.g. back muscles, soleus) have twitches which reach maximum tension in 40 ms or so.
The muscles which exhibit most of our body movements have intermediate twitch lengths of 10 to 20 ms.
The latent period, the period of a few ms encompassing the chemical and physical events preceding actual contraction.
This is not the same as the absolute refractory period, the even briefer period when the sarcolemma is depolarized and cannot be stimulated. The relative refractory period occurs after this when the sarcolemma is briefly hyperpolarized and requires a greater than normal stimulus
Following the latent period is the contraction phase in which the shortening of the sarcomeres and cells occurs. Then comes the relaxation phase, a longer period because it is passive, the result of recoil due to the series elastic elements of the muscle.
We do not use the muscle twitch as part of our normal muscle responses. Instead we use graded contractions, contractions of whole muscles which can vary in terms of their strength and degree of contraction. In fact, even relaxed muscles are constantly being stimulated to produce muscle tone, the minimal graded contraction possible.
Muscles exhibit graded contractions in two ways:
1) Quantal Summation or Recruitment - this refers to increasing the number of cells contracting. This is done experimentally by increasing the voltage used to stimulate a muscle, thus reaching the thresholds of more and more cells. In the human body quantal summation is accomplished by the nervous system, stimulating increasing numbers of cells or motor units to increase the force of contraction.
2) Wave Summation ( frequency summation) and Tetanization- this results from stimulating a muscle cell before it has relaxed from a previous stimulus. This is possible because the contraction and relaxation phases are much longer than the refractory period. This causes the contractions to build on one another producing a wave pattern or, if the stimuli are high frequency, a sustained contraction called tetany or tetanus. (The term tetanus is also used for an illness caused by a bacterial toxin which causes contracture of the skeletal muscles.) This form of tetanus is perfectly normal and in fact is the way you maintain a sustained contraction.
Treppe is not a way muscles exhibit graded contractions. It is a warmup phenomenon in which when muscle cells are initially stimulated when cold, they will exhibit gradually increasing responses until they have warmed up. The phenomenon is due to the increasing efficiency of the ion gates as they are repeatedly stimulated. Treppe can be differentiated from quantal summation because the strength of stimulus remains the same in treppe, but increases in quantal summation
Length-Tension Relationship: Another way in which the tension of a muscle can vary is due to the length-tension relationship. This relationship expresses the characteristic that within about 10% the resting length of the muscle, the tension the muscle exerts is maximum. At lengths above or below this optimum length the tension decreases.
Regulation of Blood Pressure by Hormones
The Kidney
One of the functions of the kidney is to monitor blood pressure and take corrective action if it should drop. The kidney does this by secreting the proteolytic enzyme renin.
- Renin acts on angiotensinogen, a plasma peptide, splitting off a fragment containing 10 amino acids called angiotensin I.
- angiotensin I is cleaved by a peptidase secreted by blood vessels called angiotensin converting enzyme (ACE) — producing angiotensin II, which contains 8 amino acids.
- angiotensin II
- constricts the walls of arterioles closing down capillary beds;
- stimulates the proximal tubules in the kidney to reabsorb sodium ions;
- stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reclaim still more sodium and thus water.
- increases the strength of the heartbeat;
- stimulates the pituitary to release the antidiuretic hormone (ADH, also known as arginine vasopressin).
All of these actions, which are mediated by its binding to G-protein-coupled receptors on the target cells, lead to an increase in blood pressure.
1.Rhythmicity ( Chronotropism ) : means the ability of heart to beat regularly ( due to repetitive and stable depolarization and repolarization ) . Rhythmicity of heart is a myogenic in origin , because cardiac muscles are automatically excited muscles and does not depend on the nervous stimulus to initiate excitation and then contraction . The role of nerves is limited to the regulation of the heart rate and not to initiate the beat.
There are many evidences that approve the myogenic and not neurogenic origin of the rhythmicity of cardiac muscle . For example :
- transplanted heart continues to beat regularly without any nerve supply.
- Embryologically the heart starts to beat before reaching any nerves to them.
- Some drugs that paralyze the nerves ( such as cocaine ) do not stop the heart in given doses.
Spontaneous rhythmicity of the cardiac muscle due to the existence of excitatory - conductive system , which is composed of self- exciting non-contractile cardiac muscle cells . The SA node of the mentioned system excites in a rate , that is the most rapid among the other components of the system ( 110 beats /minute ) , which makes it the controller or ( the pacemaker ) of the cardiac rhythm of the entire heart.
Mechanism , responsible for self- excitation in the SA node and the excitatory conductive system is due to the following properties of the cell membrane of theses cells :
1- Non-gated sodium channels
2- Decreased permeability to potassium
3- existence of slow and fast calcium channels.
These properties enable the cations ( sodium through the none-gated sodium voltage channels , calcium through calcium slow channels) to enter the cell and depolarize the cell membrane without need for external stimulus.
The resting membrane potential of non-contractile cardiac cell is -55 - -60 millivolts ( less than that of excitable nerve cells (-70) ) .
The threshold is also less negative than that of nerve cells ( -40 millivolts ).
The decreased permeability to potassium from its side decrease the eflux of potassium during the repolarization phase of the pacemaker potential . All of these factors give the pacemaker potential its characteristic shape
Repeating of the pacemaker potential between the action potentials of contractile muscle cells is the cause of spontaneous rhythmicity of cardiac muscle cells.
Factors , affecting the rhythmicity of the cardiac muscle :
I. Factors that increase the rate ( positive chronotropic factors) :
1. sympathetic stimulation : as its neurotransmitter norepinephrine increases the membrane permeability to sodium and calcium.
2. moderate warming : moderate warming increases temperature by 10 beats for each 1 Fahrenheit degree increase in body temperature, this due to decrease in permeability to potassium ions in pacemaker membrane by moderate increase in temperature.
3. Catecholaminic drugs have positive chronotropic effect.
4. Thyroid hormones : have positive chronotropic effect , due to the fact that these drugs increase the sensitivity of adrenergic receptors to adrenaline and noreadrenaline .
5. mild hypoxia.
6. mild alkalemia : mild alkalemia decreases the negativity of the resting potential.
7. hypocalcemia.
8. mild hypokalemia
II. Factors that decrease rhythmicity ( negative chronotropic):
1.Vagal stimulation : the basal level of vagal stimulation inhibits the sinus rhythm and decrease it from 110-75 beats/ minute. This effect due to increasing the permeability of the cardiac muscle cell to potassium , which causes rapid potassium eflux , which increases the negativity inside the cardiac cells (hyperpolarization ).
2. moderate cooling
3. severe warming : due to cardiac damage , as a result of intercellular protein denaturation. Excessive cooling on the other hand decrease metabolism and stops rhythmicity.
4. Cholenergic drugs ( such as methacholine , pilocarpine..etc) have negative chronotropic effect.
5. Digitalis : these drugs causes hyperpolarization . This effect is similar to that of vagal stimulation.
6. Hypercapnia ( excessive CO2 production )
7. Acidemia.
8. hyper- and hyponatremia .
9. hyperkalemia
10. hypercalcemia
11. Typhoid or diphteria toxins.
There are three types of muscle tissue, all of which share some common properties:
- Excitability or responsiveness - muscle tissue can be stimulated by electrical, physical, or chemical means.
- contractility - the response of muscle tissue to stimulation is contraction, or shortening.
- elasticity or recoil - muscles have elastic elements (later we will call these their series elastic elements) which cause them to recoil to their original size.
- stretchability or extensibility - muscles can also stretch and extend to a longer-than-resting length.
The three types of muscle: skeletal, cardiac, and visceral (smooth) muscle.
Skeletal muscle
It is found attached to the bones for movement.
cells are long multi-nucleated cylinders.
The cells may be many inches long but vary in diameter, averaging between 100 and 150 microns.
All the cells innervated by branches from the same neuron will contract at the same time and are referred to as a motor unit.
Skeletal muscle is voluntary because the neurons which innervate it come from the somatic or voluntary branch of the nervous system.
That means you have willful control over your skeletal muscles.
Skeletal muscles have distinct stripes or striations which identify them and are related to the organization of protein myofilaments inside the cell.
Cardiac muscle
This muscle found in the heart.
It is composed of much shorter cells than skeletal muscle which branch to connect to one another.
These connections are by means of gap junctions called intercalated disks which allow an electrochemical impulse to pass to all the connected cells.
This causes the cells to form a functional network called a syncytium in which the cells work as a unit. Many cardiac muscle cells are myogenic which means that the impulse arises from the muscle, not from the nervous system. This causes the heart muscle and the heart itself to beat with its own natural rhythm.
But the autonomic nervous system controls the rate of the heart and allows it to respond to stress and other demands. As such the heart is said to be involuntary.
Visceral muscle is found in the body's internal organs and blood vessels.
It is usually called smooth muscle because it has no striations and is therefore smooth in appearance. It is found as layers in the mucous membranes of the respiratory and digestive systems.
It is found as distinct bands in the walls of blood vessels and as sphincter muscles.
Single unit smooth muscle is also connected into a syncytium similar to cardiac muscle and is also partly myogenic. As such it causes continual rhythmic contractions in the stomach and intestine. There and in blood vessels smooth muscle also forms multiunit muscle which is stimulated by the autonomic nervous system. So smooth muscle is involuntary as well
Gonadotropin-releasing hormone (GnRH)
GnRH is a peptide of 10 amino acids. Its secretion at the onset of puberty triggers sexual development.
Primary Effects
FSH and LH Relaese
Secondary Effects
Increases estrogen and progesterone (in females)
testosterone Relaese (in males)
Growth hormone-releasing hormone (GHRH)
GHRH is a mixture of two peptides, one containing 40 amino acids, the other 44. GHRH stimulates cells in the anterior lobe of the pituitary to secrete growth hormone (GH).
Corticotropin-releasing hormone (CRH)
CRH is a peptide of 41 amino acids. Its acts on cells in the anterior lobe of the pituitary to release adrenocorticotropic hormone (ACTH) CRH is also synthesized by the placenta and seems to determine the duration of pregnancy. It may also play a role in keeping the T cells of the mother from mounting an immune attack against the fetus
Somatostatin
Somatostatin is a mixture of two peptides, one of 14 amino acids, the other of 28. Somatostatin acts on the anterior lobe of the pituitary to
- inhibit the release of growth hormone (GH)
- inhibit the release of thyroid-stimulating hormone (TSH)
Somatostatin is also secreted by cells in the pancreas and in the intestine where it inhibits the secretion of a variety of other hormones.
Antidiuretic hormone (ADH) and Oxytocin
These peptides are released from the posterior lobe of the pituitary
Asthma = Reversible Bronchioconstruction 4%-5% of population
Extrinsic / Atopic = Allergic, inherited (familia), chromosome 11
IgE, Chemical Mediators of inflammation
a. Intrinsic = Negative for Allergy, Normal IgE, Negative Allergic Tests
Nucleotide Imbalance cAMP/cGMP: cAMP = Inhibits mediator release, cGMP = Facilitates mediator release
b. Intolerance to Asprin (Triad Asthma)
c. Nasal Polyps & Asthma
d. Treatment cause, Symptoms in Acute Asthma
1. Bronchial dilators
2. steroids edema from Inflamation
3. Bronchiohygene to prevent Secondary Infection, (Remove Excess Mucus)
4. Education
An anti-diruetic is a substance that decreases urine volume, and ADH is the primary example of it within the body. ADH is a hormone secreted from the posterior pituitary gland in response to increased plasma osmolarity (i.e., increased ion concentration in the blood), which is generally due to an increased concentration of ions relative to the volume of plasma, or decreased plasma volume.
The increased plasma osmolarity is sensed by osmoreceptors in the hypothalamus, which will stimulate the posterior pituitary gland to release ADH. ADH will then act on the nephrons of the kidneys to cause a decrease in plasma osmolarity and an increase in urine osmolarity.
ADH increases the permeability to water of the distal convoluted tubule and collecting duct, which are normally impermeable to water. This effect causes increased water reabsorption and retention and decreases the volume of urine produced relative to its ion content.
After ADH acts on the nephron to decrease plasma osmolarity (and leads to increased blood volume) and increase urine osmolarity, the osmoreceptors in the hypothalamus will inactivate, and ADH secretion will end. Due to this response, ADH secretion is considered to be a form of negative feedback.