NEET MDS Lessons
Physiology
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.
The defecation reflex:
As a result of the mass movements, pressure is exerted on the rectum and on the internal anal sphincter, which is smooth muscle, resulting in its involuntary relaxation. Afferent impulses are sent to the brain indicating the need to defecate. The external sphincter is voluntary muscle and is controlled by the voluntary nervous system. This sphincter is relaxed along with contraction of the rectal and abdominal muscles in the defecation reflex
Vital Capacity: The vital capacity (VC) is the maximum volume which can be ventilated in a single breath. VC= IRV+TV+ERV. VC varies with gender, age, and body build. Measuring VC gives a device for diagnosis of respiratory disorder, and a benchmark for judging the effectiveness of treatment. (4600 ml)
Vital Capacity is reduced in restrictive disorders, but not in disorders which are purely obstructive.
The FEV1 is the % of the vital capacity which is expelled in the first second. It should be at least 75%. The FEV1 is reduced in obstructive disorders.
Both VC and the FEV1 are reduced in disorders which are both restrictive and obstructive
Oxygen is present at nearly 21% of ambient air. Multiplying .21 times 760 mmHg (standard pressure at sea level) yields a pO2 of about 160. Carbon dioxide is .04% of air and its partial pressure, pCO2, is .3.
With alveolar air having a pO2 of 104 and a pCO2 of 40. So oxygen diffuses into the alveoli from inspired air and carbon dioxide diffuses from the alveoli into air which will be expired. This causes the levels of oxygen and carbon dioxide to be intermediate in expired air when compared to inspired air and alveolar air. Some oxygen has been lost to the alveolus, lowering its level to 120, carbon dioxide has been gained from the alveolus raising its level to 27.
Likewise a concentration gradient causes oxygen to diffuse into the blood from the alveoli and carbon dioxide to leave the blood. This produces the levels seen in oxygenated blood in the body. When this blood reaches the systemic tissues the reverse process occurs restoring levels seen in deoxygenated blood.
The Cardiac Cycle: the sequence of events in one heartbeat.
systole - the contraction phase; unless otherwise specified refers to left ventricle, but each chamber has its own systole.
diastole - the relaxation phase; unless otherwise specified refers to left ventricle, but each chamber has its own diastole.
1) quiescent period - period when all chambers are at rest and filling. 70% of ventricular filling occurs during this period. The AV valves are open, the semilunar valves are closed.
2) atrial systole - pushes the last 30% of blood into the ventricle.
3) atrial diastole - atria begin filling.
4) ventricular systole - First the AV valves close causing the first heart sound, then after the isovolumetric contraction phase the semilunar valves open permitting ventricular ejection of blood into the arteries.
5) ventricular diastole - As the ventricles relax the semilunar valves close first producing the second heart sound, then after the isovolumetric relaxation phase the AV valves open allowing ventricular filling.
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
Lung volumes and capacities:
I. Lung`s volumes
1. Tidal volume (TV) : is the volume of air m which is inspired and expired during one quiet breathing . It equals to 500 ml.
2. Inspiratory reserve volume (IRV) : The volume of air that could be inspired over and beyond the tidal volume. It equals to 3000 ml of air.
3. Expiratory reserve volume (ERV) : A volume of air that could be forcefully expired after the end of quiet tidal volume. It is about 1100 ml of air.
4. Residual volume (RV) : the extra volume of air that may remain in the lung after the forceful expiration . It is about 1200 ml of air.
5. Minute volume : the volume of air that is inspired or expired within one minute. It is equal to multiplying of respiratory rate by tidal volume = 12X500= 6000 ml.
It is in female lesser than that in male.
II. Lung`s capacities :
1. Inspiratory capacity: TV + IRV
2. Vital capacity : TV+IRV+ERV
3. Total lung capacity : TV+IRV+ERV+RV
Platelets
Platelets are cell fragments produced from megakaryocytes.
Blood normally contains 150,000 to 350,000 per microliter (µl). If this value should drop much below 50,000/µl, there is a danger of uncontrolled bleeding. This is because of the essential role that platelets have in blood clotting.
When blood vessels are damaged, fibrils of collagen are exposed.
- von Willebrand factor links the collagen to platelets forming a plug of platelets there.
- The bound platelets release ADP and thromboxane A2 which recruit and activate still more platelets circulating in the blood.
- (This role of thromboxane accounts for the beneficial effect of low doses of aspirin a cyclooxygenase inhibitor in avoiding heart attacks.)
ReoPro is a monoclonal antibody directed against platelet receptors. It inhibits platelet aggregation and appears to reduce the risk that "reamed out" coronary arteries (after coronary angioplasty) will plug up again.