NEET MDS Lessons
Physiology
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.
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
Surface Tension
1. Maintains stability of alveolus, preventing collapse
2. Surfactant (Type II pneumocytes) = dipalmityl lecithin
3. Type II pneumocyte appears at 24 weeks of gestation;
1. Surfactant production, 28-32 weeks;
2. Surfactant in amniotic fluid, 35 weeks.
3. Laplace equation for thin walled spheres P = 2T
a. P = alveolar internal pressure r
b. T = tension in the walls r = radius of alveolus
4. During normal tidal respiration
1. Some alveoli do collapse (Tidal pressure can't open)
2. Higher than normal pressure needed (Coughing)
3. Deep breaths & sighs promote re-expansion
4. After surgery/Other conditions, Coughing, deep breathing, sustained maximal respiration
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.
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.
Respiratory system plays important role in maintaining homeostasis . Other than its major function , which is supplying the cells with needed oxygen to produce energy and getting rid of carbon dioxide , it has other functions :
1 Vocalization , or sound production.
2 Participation in acid base balance .
3 Participation in fluid balance by insensible water elimination (vapors ).
4 Facilitating venous return .
5 Participation in blood pressure regulation : Lungs produce Angiotensin converting enzyme ( ACE ) .
6 Immune function : Lungs produce mucous that trap foreign particles , and have ciliae that move foreign particles away from the lung. They also produce alpha 1 antitrepsin that protect the lungs themselves from the effect of elastase and other proteolytic enzymes
Bleeding Disorders
A deficiency of a clotting factor can lead to uncontrolled bleeding.
The deficiency may arise because
- not enough of the factor is produced or
- a mutant version of the factor fails to perform properly.
Examples:
- von Willebrand disease (the most common)
- hemophilia A for factor 8 deficiency
- hemophilia B for factor 9 deficiency.
- hemophilia C for factor 11 deficiency
In some cases of von Willebrand disease, either a deficient level or a mutant version of the factor eliminates its protective effect on factor 8. The resulting low level of factor 8 mimics hemophilia A.