NEET MDS Lessons
Physiology
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.
- it's the individual pressure exerted independently by a particular gas within a mixture of gasses. The air we breath is a mixture of gasses: primarily nitrogen, oxygen, & carbon dioxide. So, the air you blow into a balloon creates pressure that causes the balloon to expand (& this pressure is generated as all the molecules of nitrogen, oxygen, & carbon dioxide move about & collide with the walls of the balloon). However, the total pressure generated by the air is due in part to nitrogen, in part to oxygen, & in part to carbon dioxide. That part of the total pressure generated by oxygen is the 'partial pressure' of oxygen, while that generated by carbon dioxide is the 'partial pressure' of carbon dioxide. A gas's partial pressure, therefore, is a measure of how much of that gas is present (e.g., in the blood or alveoli).
- the partial pressure exerted by each gas in a mixture equals the total pressure times the fractional composition of the gas in the mixture. So, given that total atmospheric pressure (at sea level) is about 760 mm Hg and, further, that air is about 21% oxygen, then the partial pressure of oxygen in the air is 0.21 times 760 mm Hg or 160 mm Hg.
Membrane Structure & Function
Cell Membranes
- Cell membranes are phospholipid bilayers (2 layers)
- Bilayer forms a barrier to passage of molecules in an out of cell
- Phospholipids = glycerol + 2 fatty acids + polar molecule (i.e., choline) + phosphate
- Cholesterol (another lipid) stabilizes cell membranes
- the hydrophobic tails of the phospholipids (fatty acids) are together in the center of the bilayer. This keeps them out of the water
Membranes Also Contain Proteins
- Proteins that penetrate the membrane have hydrophobic sections ~25 amino acids long
- Hydrophobic = doesn't like water = likes lipids
- Membrane proteins have many functions:
- receptors for hormones
- pumps for transporting materials across the membrane
- ion channels
- adhesion molecules for holding cells to extracellular matrix
cell recognition antigens
Bronchitis = Irreversible Bronchioconstriction
. Causes - Infection, Air polution, cigarette smoke
a. Primary Defect = Enlargement & Over Activity of Mucous Glands, Secretions very viscous
b. Hypertrophy & hyperplasia, Narrows & Blocks bronchi, Lumen of airway, significantly narrow
c. Impaired Clearance by mucocillary elevator
d. Microorganism retension in lower airways,Prone to Infectious Bronchitis, Pneumonia
e. Permanent Inflamatory Changes IN epithelium, Narrows walls, Symptoms, Excessive sputum, coughing
f. CAN CAUSE EMPHYSEMA
Characteristics of Facilitated Diffusion & Active Transport - both require the use of carriers that are specific to particular substances (that is, each type of carrier can 'carry' one type of substance) and both can exhibit saturation (movement across a membrane is limited by number of carriers & the speed with which they move materials
Cardiac Output:
Minute Volume = Heart Rate X Stroke Volume
Heart rate, HR at rest = 65 to 85 bpm
Each heartbeat at rest takes about .8 sec. of which .4 sec. is quiescent period.
Stroke volume, SV at rest = 60 to 70 ml.
Heart can increase both rate and volume with exercise. Rate increase is limited due to necessity of minimum ventricular diastolic period for filling. Upper limit is usually put at about 220 bpm. Maximum heart rate calculations are usually below 200. Target heart rates for anaerobic threshold are about 85 to 95% of maximum.
Terms:
End Diastolic Volume, EDV - the maximum volume of the ventricles achieved at the end of ventricular diastole. This is the amount of blood the heart has available to pump. If this volume increases the cardiac output increases in a healthy heart.
End Systolic Volume, ESV - the minimum volume remaining in the ventricle after its systole. If this volume increases it means less blood has been pumped and the cardiac output is less.
EDV - ESV = SV
SV / EDV = Ejection Fraction The ejection fraction is normally around 50% at rest and will increase during strenuous exercise in a healthy heart. Well trained athletes may have ejection fractions approaching 70% in the most strenuous exercise.
Isovolumetric Contraction Phase - a brief period at the beginning of ventricular systole when all valves are closed and ventricular volume remains constant. Pressure has risen enough in the ventricle to close the AV valves but not enough to open the semilunar valves and cause ejection of blood.
Isovolumetric Relaxation Phase - a brief period at the beginning of ventricular diastole when all valves are closed and ventricular volume is constant. Pressure in the ventricle has lowered producing closure of the semilunar valves but not opening the AV valves to begin pulling blood into the ventricle.
Dicrotic Notch - the small increase in pressure of the aorta or other artery seen when recording a pulse wave. This occurs as blood is briefly pulled back toward the ventricle at the beginning of diastole thus closing the semilunar valves.
Preload - This is the pressure at the end of ventricular diastole, at the beginning of ventricular systole. It is proportional to the End Diastolic Volume (EDV), i.e. as the EDV increases so does the preload of the heart. Factors which increase the preload are: increased total blood volume, increased venous tone and venous return, increased atrial contraction, and the skeletal muscular pump.
Afterload - This is the impedence against which the left ventricle must eject blood, and it is roughly proportional to the End Systolic Volume (ESV). When the peripheral resistance increases so does the ESV and the afterload of the heart.
The importance of these parameters are as a measure of efficiency of the heart, which increases as the difference between preload and afterload increases
The Adrenal Glands
The adrenal glands are two small structures situated one at top each kidney. Both in anatomy and in function, they consist of two distinct regions:
- an outer layer, the adrenal cortex, which surrounds
- the adrenal medulla.
The Adrenal Cortex
cells of the adrenal cortex secrete a variety of steroid hormones.
- glucocorticoids (e.g., cortisol)
- mineralocorticoids (e.g., aldosterone)
- androgens (e.g., testosterone)
- Production of all three classes is triggered by the secretion of ACTH from the anterior lobe of the pituitary.
Glucocorticoids
They Effect by raising the level of blood sugar (glucose). One way they do this is by stimulating gluconeogenesis in the liver: the conversion of fat and protein into intermediate metabolites that are ultimately converted into glucose.
The most abundant glucocorticoid is cortisol (also called hydrocortisone).
Cortisol and the other glucocorticoids also have a potent anti-inflammatory effect on the body. They depress the immune response, especially cell-mediated immune responses.
Mineralocorticoids
The most important of them is the steroid aldosterone. Aldosterone acts on the kidney promoting the reabsorption of sodium ions (Na+) into the blood. Water follows the salt and this helps maintain normal blood pressure.
Aldosterone also
- acts on sweat glands to reduce the loss of sodium in perspiration;
- acts on taste cells to increase the sensitivity of the taste buds to sources of sodium.
The secretion of aldosterone is stimulated by:
- a drop in the level of sodium ions in the blood;
- a rise in the level of potassium ions in the blood;
- angiotensin II
- ACTH (as is that of cortisol)
Androgens
The adrenal cortex secretes precursors to androgens such as testosterone.
Excessive production of adrenal androgens can cause premature puberty in young boys.
In females, the adrenal cortex is a major source of androgens. Their hypersecretion may produce a masculine pattern of body hair and cessation of menstruation.
Addison's Disease: Hyposecretion of the adrenal cortices
Addison's disease has many causes, such as
- destruction of the adrenal glands by infection;
- their destruction by an autoimmune attack;
- an inherited mutation in the ACTH receptor on adrenal cells.
Cushing's Syndrome: Excessive levels of glucocorticoids
In Cushing's syndrome, the level of adrenal hormones, especially of the glucocorticoids, is too high.It can be caused by:
- excessive production of ACTH by the anterior lobe of the pituitary;
- excessive production of adrenal hormones themselves (e.g., because of a tumor), or (quite commonly)
- as a result of glucocorticoid therapy for some other disorder such as
- rheumatoid arthritis or
- preventing the rejection of an organ transplant.
The Adrenal Medulla
The adrenal medulla consists of masses of neurons that are part of the sympathetic branch of the autonomic nervous system. Instead of releasing their neurotransmitters at a synapse, these neurons release them into the blood. Thus, although part of the nervous system, the adrenal medulla functions as an endocrine gland.The adrenal medulla releases:
- adrenaline (also called epinephrine) and
- noradrenaline (also called norepinephrine)
Both are derived from the amino acid tyrosine.
Release of adrenaline and noradrenaline is triggered by nervous stimulation in response to physical or mental stress. The hormones bind to adrenergic receptors transmembrane proteins in the plasma membrane of many cell types.
Some of the effects are:
- increase in the rate and strength of the heartbeat resulting in increased blood pressure;
- blood shunted from the skin and viscera to the skeletal muscles, coronary arteries, liver, and brain;
- rise in blood sugar;
- increased metabolic rate;
- bronchi dilate;
- pupils dilate;
- hair stands on end (gooseflesh in humans);
- clotting time of the blood is reduced;
- increased ACTH secretion from the anterior lobe of the pituitary.
All of these effects prepare the body to take immediate and vigorous action.