NEET MDS Lessons
Physiology
The Sliding Filament mechanism of muscle contraction.
When a muscle contracts the light I bands disappear and the dark A bands move closer together. This is due to the sliding of the actin and myosin myofilaments against one another. The Z-lines pull together and the sarcomere shortens
The thick myosin bands are not single myosin proteins but are made of multiple myosin molecules. Each myosin molecule is composed of two parts: the globular "head" and the elongated "tail". They are arranged to form the thick bands.
It is the myosin heads which form crossbridges that attach to binding sites on the actin molecules and then swivel to bring the Z-lines together
Likewise the thin bands are not single actin molecules. Actin is composed of globular proteins (G actin units) arranged to form a double coil (double alpha helix) which produces the thin filament. Each thin myofilament is wrapped by a tropomyosin protein, which in turn is connected to the troponin complex.
The tropomyosin-troponin combination blocks the active sites on the actin molecules preventing crossbridge formation. The troponin complex consists of three components: TnT, the part which attaches to tropomyosin, TnI, an inhibitory portion which attaches to actin, and TnC which binds calcium ions. When excess calcium ions are released they bind to the TnC causing the troponin-tropomyosin complex to move, releasing the blockage on the active sites. As soon as this happens the myosin heads bind to these active sites.
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
Phases of cardiac cycle :
1. Early diastole ( also called the atrial diastole , or complete heart diastole) : During this phase :
- Atria are relaxed
- Ventricles are relaxed
- Semilunar valves are closed
- Atrioventricular valves are open
During this phase the blood moves passively from the venous system into the ventricles ( about 80 % of blood fills the ventricles during this phase.
2. Atrial systole : During this phase :
- Atria are contracting
- Ventricles are relaxed
- AV valves are open
- Semilunar valves are closed
- Atrial pressure increases.the a wave of atrial pressure appears here.
- P wave of ECG starts here
- intraventricular pressure increases due to the rush of blood then decrease due to continuous relaxation of ventricles.
The remaining 20% of blood is moved to fill the ventricles during this phase , due to atrial contraction.
3. Isovolumetric contraction : During this phase :
- Atria are relaxed
- Ventricles are contracting
- AV valves are closed
- Semilunar valves are closed
- First heart sound
- QRS complex.
The ventricular fibers start to contract during this phase , and the intraventricular pressure increases. This result in closing the AV valves , but the pressure is not yet enough to open the semilunar valves , so the blood volume remain unchanged , and the muscle fibers length also remain unchanged , so we call this phase as isovolumetric contraction ( iso : the same , volu= volume , metric= length).
4. Ejection phase : Blood is ejected from the ventricles into the aorta and pulmonary artery .
During this phase :
- Ventricles are contracting
- Atria are relaxed
- AV valves are closed
- Semilunar valves are open
- First heart sound
- Intraventricular pressure is increased , due to continuous contraction
- increased aortic pressure .
- T wave starts.
5. Isovolumetric relaxation: This phase due to backflow of blood in aorta and pulmonary system after the ventricular contraction is up and the ventricles relax . This backflow closes the semilunar valves .
During this phase :
- Ventricles are relaxed
- Atrial are relaxed
- Semilunar valves are closed .
- AV valves are closed.
- Ventricular pressure fails rapidly
- Atrial pressure increases due to to continuous venous return. the v wave appears here.
- Aortic pressure : initial sharp decrease due to sudden closure of the semilunar valve ( diacrotic notch) , followed by secondary rise in pressure , due to elastic recoil of the aorta ( diacrotic wave) .
- T wave ends in this phase
Ingestion: Food taken in the mouth is
- ground into finer particles by the teeth,
- moistened and lubricated by saliva (secreted by three pairs of salivary glands)
- small amounts of starch are digested by the amylase present in saliva
- the resulting bolus of food is swallowed into the esophagus and
- carried by peristalsis to the stomach.
Structure and function of skeletal muscle.
Skeletal muscles have a belly which contains the cells and which attaches by means of tendons or aponeuroses to a bone or other tissue. An aponeurosis is a broad, flat, tendinous attachment, usually along the edge of a muscle. A muscle attaches to an origin and an insertion. The origin is the more fixed attachment, the insertion is the more movable attachment. A muscle acts to shorten, pulling the insertion toward the origin. A muscle can only pull, it cannot push.
Muscles usually come in pairs of antagonistic muscles. The muscle performing the prime movement is the agonist, the opposite acting muscle is the antagonist. When the movement reverses, the names reverse. For example, in flexing the elbow the biceps brachii is the agonist, the triceps brachii is the antagonist. When the movement changes to extension of the elbow, the triceps becomes the agonist and the biceps the antagonist. An antagonist is never totally relaxed. Its function is to provide control and damping of movement by maintaining tone against the agonist. This is called eccentric movement.
Muscles can also act as synergists, working together to perform a movement. This movement can be different from that performed when the muscles work independently. For example, the sternocleidomastoid muscles each rotate the head in a different direction. But as synergists they flex the neck.
Fixators act to keep a part from moving. For example fixators act as postural muscles to keep the spine erect and the leg and vertebral column extended when standing. Fixators such as the rhomboids and levator scapulae keep the scapula from moving during actions such as lifting with the arms.
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 |
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.