Talk to us?

- NEETMDS- courses
NEET MDS Lessons
Physiology

Alveolar Ventilation: is the volume of air of new air , entering the alveoli and adjacent gas exchange areas each minute . It equals to multiplying of respiratory rate by ( tidal volume - dead space).
Va = R rate X (TV- DsV)
     = 12 X ( 500-150)
     = 4200 ml of air.

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.

Functional Divisions of the Nervous System:

1) The Voluntary Nervous System - (ie. somatic division) control of willful control of effectors (skeletal muscles) and conscious perception. Mediates voluntary reflexes.

2) The Autonomic Nervous System - control of autonomic effectors - smooth muscles, cardiac muscle, glands. Responsible for "visceral" reflexes

Tubular secretion:

Involves transfer of substances from peritubular capillaries into the tubular lumen. It  involves transepithelial transport in a direction opposite to that of tubular absorption.

Renal tubules can selectively add some substances that have not been filtered to the substances that already have been filtered via tubular secretion.

Tubular secretion mostly function to eliminate foreign  organic ions, hydrogen ions ( as a contribution to acid base balance ), potassium ions ( as a contribution to maintaining optimal plasma K+ level to assure normal proceeding of neural and muscular functions), and urea.
Here we will focus on K+ secretion and will later discuss H+ secretion in acid base balance, while urea secretion will be discussed in water balance.

K+ is filtered in glomerular capillaries and then reabsorbed in proximal convoluted tubules as well as in thick ascending limb of loop of Henley ( Na-2Cl-K symporter)

K+ secretion takes place in collecting tubules (distal nephron) . There are two types of cells in distal nephron:

- Principal cells that reabsorb sodium and secrete K+ .
- Intercalated cells that reabsorb K+ in exchange with H+.


Mechanism of secretion of K+ in principal cells : Two steps


- K+ enters tubular cells by Na/K ATPase on the basolateral membrane.
- K+ leaves the tubular cells via K+ channels in apical membrane.


Aldosterone is a necessary regulatory factor.

If there is increased level of K+ in plasma,excessive K+ is secreted , some of which is reabsorbed back to the plasma in exchange with H+ via the intercalated cells.        

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

Typical Concentration Gradients and Membrane Potentials in Excitable Cells

The Na Pump is Particularly Important in the Kidney and Brain

  • All cells have Na pumps in their membranes, but some cells have more than others
  • Over-all Na pump activity may account for a third of your resting energy expenditure!
  • In the kidney the Na pump activity is very high because it is used to regulate body salt and water concentrations
    • Kidneys use enormous amounts of energy: 0.5% of body weight, but use 7% of the oxygen supply
  • Pump activity is also high in the brain because Na and K gradients are essential for nerves
    • The brain is another high energy organ; it is 2% of body weight, but uses 18% of the oxygen supply

In the Resting State Potassium Controls the Membrane Potential of Most Cells

  • Resting cells have more open K channels than other types
  • More K+ passes through membrane than other ions- therefore K+ controls the potential
  • Blood K+ must be closely controlled because small changes will produce large changes in the membrane potentials of cells
    • Raising K will make the membrane potential less negative (depolarization)
  • High blood K+ can cause the heart to stop beating (it goes into permanent contraction)

During an Action Potential Na Channels Open, and Na Controls the Membrane Potential

  • Whichever ion has the most open channels controls the membrane potential
  • Excitable cells have Na channels that open when stimulated
  • When large numbers of these channels open Na controls the membrane potential

Blood Groups

Blood groups are created by molecules present on the surface of red blood cells (and often on other cells as well).

The ABO Blood Groups

The ABO blood groups are the most important in assuring safe blood transfusions.

Blood Group

Antigens on RBCs

Antibodies in Serum

Genotypes

A

A

Anti-B

AA or AO

B

B

Anti-A

BB or BO

AB

A and B

Neither

AB

O

Neither

Anti-A and anti-B

OO

When red blood cells carrying one or both antigens are exposed to the corresponding antibodies, they agglutinate; that is, clump together. People usually have antibodies against those red cell antigens that they lack.

The critical principle to be followed is that transfused blood must not contain red cells that the recipient's antibodies can clump. Although theoretically it is possible to transfuse group O blood into any recipient, the antibodies in the donated plasma can damage the recipient's red cells. Thus all transfusions should be done with exactly-matched blood.

The Rh System

Rh antigens are transmembrane proteins with loops exposed at the surface of red blood cells. They appear to be used for the transport of carbon dioxide and/or ammonia across the plasma membrane. They are named for the rhesus monkey in which they were first discovered.

There are a number of Rh antigens. Red cells that are "Rh positive" express the one designated D. About 15% of the population have no RhD antigens and thus are "Rh negative".

The major importance of the Rh system for human health is to avoid the danger of RhD incompatibility between mother and fetus.

During birth, there is often a leakage of the baby's red blood cells into the mother's circulation. If the baby is Rh positive (having inherited the trait from its father) and the mother Rh-negative, these red cells will cause her to develop antibodies against the RhD antigen. The antibodies, usually of the IgG class, do not cause any problems for that child, but can cross the placenta and attack the red cells of a subsequent Rh+ fetus. This destroys the red cells producing anemia and jaundice. The disease, called erythroblastosis fetalis or hemolytic disease of the newborn, may be so severe as to kill the fetus or even the newborn infant. It is an example of an antibody-mediated cytotoxicity disorder.

Although certain other red cell antigens (in addition to Rh) sometimes cause problems for a fetus, an ABO incompatibility does not. Rh incompatibility so dangerous when ABO incompatibility is not

It turns out that most anti-A or anti-B antibodies are of the IgM class and these do not cross the placenta. In fact, an Rh/type O mother carrying an Rh+/type A, B, or AB fetus is resistant to sensitization to the Rh antigen. Presumably her anti-A and anti-B antibodies destroy any fetal cells that enter her blood before they can elicit anti-Rh antibodies in her.

This phenomenon has led to an extremely effective preventive measure to avoid Rh sensitization. Shortly after each birth of an Rh+ baby, the mother is given an injection of anti-Rh antibodies. The preparation is called Rh immune globulin (RhIG) or Rhogam. These passively acquired antibodies destroy any fetal cells that got into her circulation before they can elicit an active immune response in her.

Rh immune globulin came into common use in the United States in 1968, and within a decade the incidence of Rh hemolytic disease became very low.

Explore by Exams