NEET MDS Lessons
Physiology
The Kidneys
The kidneys are the primary functional organ of the renal system.
They are essential in homeostatic functions such as the regulation of electrolytes, maintenance of acid–base balance, and the regulation of blood pressure (by maintaining salt and water balance).
They serve the body as a natural filter of the blood and remove wastes that are excreted through the urine.
They are also responsible for the reabsorption of water, glucose, and amino acids, and will maintain the balance of these molecules in the body.
In addition, the kidneys produce hormones including calcitriol, erythropoietin, and the enzyme renin, which are involved in renal and hemotological physiological processes.
Anatomical Location
The kidneys are a pair of bean-shaped, brown organs about the size of your fist. They are covered by the renal capsule, which is a tough capsule of fibrous connective tissue.
Right kidney being slightly lower than the left, and left kidney being located slightly more medial than the right.
The right kidneys lie just below the diaphragm and posterior to the liver, the left below the diaphragm and posterior to the spleen.
Resting on top of each kidney is an adrenal gland (adrenal meaning on top of renal), which are involved in some renal system processes despite being a primarily endocrine organ.
They are considered retroperitoneal, which means that they lie behind the peritoneum, the membrane lining of the abdominal cavity.
The renal artery branches off from the lower part of the aorta and provides the blood supply to the kidneys.
Renal veins take blood away from the kidneys into the inferior vena cava.
The ureters are structures that come out of the kidneys, bringing urine downward into the bladder.
Internal Anatomy of the Kidneys
There are three major regions of the kidney:
1. Renal cortex
2. Renal medulla
3. Renal pelvis
The renal cortex is a space between the medulla and the outer capsule.
The renal medulla contains the majority of the length of nephrons, the main functional component of the kidney that filters fluid from blood.
The renal pelvis connects the kidney with the circulatory and nervous systems from the rest of the body.
Renal Cortex
The kidneys are surrounded by a renal cortex
The cortex provides a space for arterioles and venules from the renal artery and vein, as well as the glomerular capillaries, to perfuse the nephrons of the kidney. Erythropotein, a hormone necessary for the synthesis of new red blood cells, is also produced in the renal cortex.
Renal Medulla
The medulla is the inner region of the parenchyma of the kidney. The medulla consists of multiple pyramidal tissue masses, called the renal pyramids, which are triangle structures that contain a dense network of nephrons.
At one end of each nephron, in the cortex of the kidney, is a cup-shaped structure called the Bowman's capsule. It surrounds a tuft of capillaries called the glomerulus that carries blood from the renal arteries into the nephron, where plasma is filtered through the capsule.
After entering the capsule, the filtered fluid flows along the proximal convoluted tubule to the loop of Henle and then to the distal convoluted tubule and the collecting ducts, which flow into the ureter. Each of the different components of the nephrons are selectively permeable to different molecules, and enable the complex regulation of water and ion concentrations in the body.
Renal Pelvis
The renal pelvis contains the hilium. The hilum is the concave part of the bean-shape where blood vessels and nerves enter and exit the kidney; it is also the point of exit for the ureters—the urine-bearing tubes that exit the kidney and empty into the urinary bladder. The renal pelvis connects the kidney to the rest of the body.
Supply of Blood and Nerves to the Kidneys
• The renal arteries branch off of the abdominal aorta and supply the kidneys with blood. The arterial supply of the kidneys varies from person to person, and there may be one or more renal arteries to supply each kidney.
• The renal veins are the veins that drain the kidneys and connect them to the inferior vena cava.
• The kidney and the nervous system communicate via the renal plexus. The sympathetic nervous system will trigger vasoconstriction and reduce renal blood flow, while parasympathetic nervous stimulation will trigger vasodilation and increased blood flow.
• Afferent arterioles branch into the glomerular capillaries, while efferent arterioles take blood away from the glomerular capillaries and into the interlobular capillaries that provide oxygen to the kidney.
• renal vein
The veins that drain the kidney and connect the kidney to the inferior vena cava.
• renal artery
These arise off the side of the abdominal aorta, immediately below the superior mesenteric artery, and supply the kidneys with blood.
Contractility : Means ability of cardiac muscle to convert electrical energy of action potential into mechanical energy ( work).
The excitation- contraction coupling of cardiac muscle is similar to that of skeletal muscle , except the lack of motor nerve stimulation.
Cardiac muscle is a self-excited muscle , but the principles of contraction are the same . There are many rules that control the contractility of the cardiac muscles, which are:
1. All or none rule: due to the syncytial nature of the cardiac muscle.There are atrial syncytium and ventricular syncytium . This rule makes the heart an efficient pump.
2. Staircase phenomenon : means gradual increase in muscle contraction following rapidly repeated stimulation..
3. Starling`s law of the heart: The greater the initial length of cardiac muscle fiber , the greater the force of contraction. The initial length is determined by the degree of diastolic filling .The pericardium prevents overstretching of heart , and allows optimal increase in diastolic volume.
Thankful to this law , the heart is able to pump any amount of blood that it receives. But overstretching of cardiac muscle fibers may cause heart failure.
Factors affecting contractility ( inotropism)
I. Positive inotropic factors:
1. sympathetic stimulation: by increasing the permeability of sarcolemma to calcium.
2. moderate increase in temperature . This due to increase metabolism to increase ATP , decrease viscosity of myocardial structures, and increasing calcium influx.
3. Catecholamines , thyroid hormone, and glucagon hormones.
4. mild alkalosis
5. digitalis
6. Xanthines ( caffeine and theophylline )
II. Negative inotropic factors:
1. Parasympathetic stimulation : ( limited to atrial contraction)
2. Acidosis
3. Severe alkalosis
4. excessive warming and cooling .
5. Drugs ;like : Quinidine , Procainamide , and barbiturates .
6. Diphtheria and typhoid toxins.
Exchange of gases takes place in Lungs
- A person with an average ventilation rate of 7.5 L/min will breathe in and out 10,800 liters of gas each day
- From this gas the person will take in about 420 liters of oxygen (19 moles/day) and will give out about 340 liters of carbon dioxide (15 moles/day)
- The ratio of CO2 expired/O2 inspired is called the respiratory quotient (RQ)
- RQ = CO2 out/O2 in = 340/420 = 0.81
- In cellular respiration of glucose CO2 out = O2 in; RQ = 1
- The overall RQ is less than 1 because our diet is a mixture of carbohydrates and fat; the RQ for metabolizing fat is only 0.7
- All of the exchange of gas takes place in the lungs
- The lungs also give off large amounts of heat and water vapor
1. Automatic control (sensory) of respiration is in - brainstem (midbrain)
2. Behavioral/voluntary control is in - the cortex
3. Alveolar ventilation -the amount of atmospheric air that actually reaches the alveolar per breath and that can participate in the exchange of gasses between alveoli and blood
4. Only way to increase gas exchange in alveolar capillaries - perfusion-limited gas exchange
5. Pulmonary ventiliation not effected by - concentration of bicarbonate ions
6. Central chemoreceptors - medulla - CO2, O2 and H+ concentrations
7. Peripheral chemoreceptors - carotid and aortic bodies- PO2, PCO2 and pH
8. Major stimulus for respiratory centers - arterial PCO2
9. Rhythmic breathing depends on
1. continuous (tonic) inspiratory drive from DRG (dorsal respiratory group)
2. intermittent (phasic) expiratory input from cerebrum, thalamus, cranial nerves and ascending spinal cord sensory tracts
10. Primary site for gas exchange - type I epithelial cells for alveoli
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.
The Nerve Impulse
When a nerve is stimulated the resting potential changes. Examples of such stimuli are pressure, electricity, chemicals, etc. Different neurons are sensitive to different stimuli(although most can register pain). The stimulus causes sodium ion channels to open. The rapid change in polarity that moves along the nerve fiber is called the "action potential." In order for an action potential to occur, it must reach threshold. If threshold does not occur, then no action potential can occur. This moving change in polarity has several stages:
Depolarization
The upswing is caused when positively charged sodium ions (Na+) suddenly rush through open sodium gates into a nerve cell. The membrane potential of the stimulated cell undergoes a localized change from -55 millivolts to 0 in a limited area. As additional sodium rushes in, the membrane potential actually reverses its polarity so that the outside of the membrane is negative relative to the inside. During this change of polarity the membrane actually develops a positive value for a moment(+30 millivolts). The change in voltage stimulates the opening of additional sodium channels (called a voltage-gated ion channel). This is an example of a positive feedback loop.
Repolarization
The downswing is caused by the closing of sodium ion channels and the opening of potassium ion channels. Release of positively charged potassium ions (K+) from the nerve cell when potassium gates open. Again, these are opened in response to the positive voltage--they are voltage gated. This expulsion acts to restore the localized negative membrane potential of the cell (about -65 or -70 mV is typical for nerves).
Hyperpolarization
When the potassium ions are below resting potential (-90 mV). Since the cell is hyper polarized, it goes to a refractory phrase.
Refractory phase
The refractory period is a short period of time after the depolarization stage. Shortly after the sodium gates open, they close and go into an inactive conformation. The sodium gates cannot be opened again until the membrane is repolarized to its normal resting potential. The sodium-potassium pump returns sodium ions to the outside and potassium ions to the inside. During the refractory phase this particular area of the nerve cell membrane cannot be depolarized. This refractory area explains why action potentials can only move forward from the point of stimulation.
Factors that affect sensitivity and speed
Sensitivity
Increased permeability of the sodium channel occurs when there is a deficit of calcium ions. When there is a deficit of calcium ions (Ca+2) in the interstitial fluid, the sodium channels are activated (opened) by very little increase of the membrane potential above the normal resting level. The nerve fiber can therefore fire off action potentials spontaneously, resulting in tetany. This could be caused by the lack of hormone from parathyroid glands. It could also be caused by hyperventilation, which leads to a higher pH, which causes calcium to bind and become unavailable.
Speed of Conduction
This area of depolarization/repolarization/recovery moves along a nerve fiber like a very fast wave. In myelinated fibers, conduction is hundreds of times faster because the action potential only occurs at the nodes of Ranvier (pictured below in 'types of neurons') by jumping from node to node. This is called "saltatory" conduction. Damage to the myelin sheath by the disease can cause severe impairment of nerve cell function. Some poisons and drugs interfere with nerve impulses by blocking sodium channels in nerves. See discussion on drug at the end of this outline.
The bulk of the pancreas is an exocrine gland secreting pancreatic fluid into the duodenum after a meal. However, scattered through the pancreas are several hundred thousand clusters of cells called islets of Langerhans. The islets are endocrine tissue containing four types of cells. In order of abundance, they are the:
- beta cells, which secrete insulin and amylin;
- alpha cells, which secrete glucagon;
- delta cells, which secrete somatostatin, and
- gamma cells, which secrete a polypeptide of unknown function.
Beta Cells
Beta cells secrete insulin in response to a rising level of blood sugar
Insulin affects many organs. It
- stimulates skeletal muscle fibers to
- take up glucose and convert it into glycogen;
- take up amino acids from the blood and convert them into protein.
- acts on liver cells
- stimulating them to take up glucose from the blood and convert it into glycogen while
- inhibiting production of the enzymes involved in breaking glycogen back down (glycogenolysis) and
- inhibiting gluconeogenesis; that is, the conversion of fats and proteins into glucose.
- acts on fat (adipose) cells to stimulate the uptake of glucose and the synthesis of fat.
- acts on cells in the hypothalamus to reduce appetite.
Diabetes Mellitus
Diabetes mellitus is an endocrine disorder characterized by many signs and symptoms. Primary among these are:
- a failure of the kidney to retain glucose .
- a resulting increase in the volume of urine because of the osmotic effect of this glucose (it reduces the return of water to the blood).
There are three categories of diabetes mellitus:
- Insulin-Dependent Diabetes Mellitus (IDDM) (Type 1) and
- Non Insulin-Dependent Diabetes Mellitus (NIDDM)(Type 2)
- Inherited Forms of Diabetes Mellitus
Insulin-Dependent Diabetes Mellitus (IDDM)
IDDM ( Type 1 diabetes)
- is characterized by little or no circulating insulin;
- most commonly appears in childhood.
- It results from destruction of the beta cells of the islets.
- The destruction results from a cell-mediated autoimmune attack against the beta cells.
- What triggers this attack is still a mystery, although a prior viral infection may be the culprit.
Non Insulin-Dependent Diabetes Mellitus (NIDDM)
Many people develop diabetes mellitus without an accompanying drop in insulin levels In many cases, the problem appears to be a failure to express a sufficient number of glucose transporters in the plasma membrane (and T-system) of their skeletal muscles. Normally when insulin binds to its receptor on the cell surface, it initiates a chain of events that leads to the insertion in the plasma membrane of increased numbers of a transmembrane glucose transporter. This transporter forms a channel that permits the facilitated diffusion of glucose into the cell. Skeletal muscle is the major "sink" for removing excess glucose from the blood (and converting it into glycogen). In NIDDM, the patient's ability to remove glucose from the blood and convert it into glycogen is reduced. This is called insulin resistance. NIDDM (also called Type 2 diabetes mellitus) usually occurs in adults and, particularly often, in overweight people.
Alpha Cells
The alpha cells of the islets secrete glucagon, a polypeptide of 29 amino acids. Glucagon acts principally on the liver where it stimulates the conversion of glycogen into glucose (glycogenolysis) which is deposited in the blood.
Glucagon secretion is
- stimulated by low levels of glucose in the blood;
- inhibited by high levels, and
- inhibited by amylin.
The physiological significance of this is that glucagon functions to maintain a steady level of blood sugar level between meals.
Delta Cells
The delta cells secrete somatostatin. Somatostatin has a variety of functions. Taken together, they work to reduce the rate at which food is absorbed from the contents of the intestine. Somatostatin is also secreted by the hypothalamus and by the intestine.
Gamma Cells
The gamma cells of the islets secrete pancreatic polypeptide. No function has yet been found for this peptide of 36 amino acids.