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Physiology

Abnormalities of Salt, Water or pH

  • Examples:
    • Hyperkalemia: caused by kidney disease & medical malpractice
      • High K+ in blood- can stop the heart in contraction (systole)
    • Dehydration: walking in desert- can lose 1-2 liters/hour through sweat
      • Blood becomes too viscous to circulate well -> loss of temperature regulation -> hyperthermia, death
    • Acidosis: many causes including diabetes mellitus and respiratory problems; can cause coma, death

A rise in blood pressure stretches the atria of the heart. This triggers the release of atrial natriuretic peptide (ANP). ANP is a peptide of 28 amino acids. ANP lowers blood pressure by:

  • relaxing arterioles
  • inhibiting the secretion of renin and aldosterone
  • inhibiting the reabsorption of sodium ions in the collecting ducts of the kidneys.

The effects on the kidney reduce the reabsorption of water by them thus increasing the flow of urine and the amount of sodium excreted in it (These actions give ANP its name: natrium = sodium; uresis = urinate). The net effect of these actions is to reduce blood pressure by reducing the volume of blood volume in the system.

The Heartbeat

During rest, the heart beats about 70 times a minute in the adult male, while pumping about 5 liters of blood.

The stimulus that maintains this rhythm is self-contained. Embedded in the wall of the right atrium is a mass of specialized heart tissue called the sino-atrial (S-A) node. The S-A node is also called the pacemaker because it establishes the basic frequency at which the heart beats.

The interior of the fibers of heart muscle, like all cells, is negatively charged with respect to the exterior. In the cells of the pacemaker, this charge breaks down spontaneously about 70 times each minute. This, in turn, initiates a similar discharge of the nearby muscle fibers of the atrium. A tiny wave of current sweeps over the atria, causing them to contract.

When this current reaches the region of insulating connective tissue between the atria and the ventricles, it is picked up by the A-V node (atrio-ventricular node). This leads to a system of branching fibers that carries the current to all parts of the ventricles.

The contraction of the heart in response to this electrical activity creates systole.

A period of recovery follows called diastole.

  • The heart muscle and S-A node become recharged.
  • The heart muscle relaxes.
  • The atria refill. 

The Electrocardiogram

The electrical activity of the heart can be detected by electrodes placed at the surface of the body. Analysis of an electrocardiogram (ECG or EKG) aids in determining, for example, the extent of damage following a heart attack. This is because death of a portion of the heart muscle blocks electrical transmission through that area and alters the appearance of the ECG

Control of the Heart

Although the A-V node sets the basic rhythm of the heart, the rate and strength of its beating can be modified by two auxiliary control centers located in the medulla oblongata of the brain.

  • One sends nerve impulses down accelerator nerves.
  • The other sends nerve impulses down a pair of vagus nerves

Accelerator Nerves

The accelerator nerves are part of the sympathetic branch of the autonomic nervous system, and  like all post-ganglionic sympathetic neurons  release noradrenaline at their endings on the heart.

They increase the rate and strength of the heartbeat and thus increase the flow of blood. Their activation usually arises from some stress such as fear or violent exertion. The heartbeat may increase to 180 beats per minute. The strength of contraction increases as well so the amount of blood pumped may increase to as much as 25-30 liters/minute.


Vigorous exercise accelerates heartbeat in two ways;

  • As cellular respiration increases, so does the carbon dioxide level in the blood. This stimulates receptors in the carotid arteries and aorta, and these transmit impulses to the medulla for relay  by the accelerator nerves  to the heart.
  • As muscular activity increases, the muscle pump drives more blood back to the right atrium. The atrium becomes distended with blood, thus stimulating stretch receptors in its wall. These, too, send impulses to the medulla for relay to the heart.

Distention of the wall of the right atrium also triggers the release of atrial natriuretic peptide (ANP) which initiates a set of responses leading to a lowering of blood pressure

The Vagus Nerves

The vagus nerves are part of the parasympathetic branch of the autonomic nervous system. They, too, run from the medulla oblongata to the heart. Their activity slows the heartbeat.

Pressure receptors in the aorta and carotid arteries send impulses to the medulla which relays these  by way of the vagus nerves  to the heart. Heartbeat and blood pressure diminish.

Proteinuria—Protein content in urine, often due to leaky or damaged glomeruli.

Oliguria—An abnormally small amount of urine, often due to shock or kidney damage.

Polyuria—An abnormally large amount of urine, often caused by diabetes.

Dysuria—Painful or uncomfortable urination, often from urinary tract infections.

Hematuria—Red blood cells in urine, from infection or injury.

Glycosuria—Glucose in urine, due to excess plasma glucose in diabetes, beyond the amount able to be reabsorbed in the proximal convoluted tubule.

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.

White Blood Cells (leukocytes)

White blood cells

  • are much less numerous than red (the ratio between the two is around 1:700),
  • have nuclei,
  • participate in protecting the body from infection,
  • consist of lymphocytes and monocytes with relatively clear cytoplasm, and three types of granulocytes, whose cytoplasm is filled with granules.

Lymphocytes: There are several kinds of lymphocytes, each with different functions to perform , 25% of wbc The most common types of lymphocytes are

  • B lymphocytes ("B cells"). These are responsible for making antibodies.
  • T lymphocytes ("T cells"). There are several subsets of these:
    • inflammatory T cells that recruit macrophages and neutrophils to the site of infection or other tissue damage
    • cytotoxic T lymphocytes (CTLs) that kill virus-infected and, perhaps, tumor cells
    • helper T cells that enhance the production of antibodies by B cells

Although bone marrow is the ultimate source of lymphocytes, the lymphocytes that will become T cells migrate from the bone marrow to the thymus where they mature. Both B cells and T cells also take up residence in lymph nodes, the spleen and other tissues where they

  • encounter antigens;
  • continue to divide by mitosis;
  • mature into fully functional cells.

Monocytes : also originate in marrow, spend up to 20 days in the circulation, then travel to the tissues where they become macrophages. Macrophages are the most important phagocyte outside the circulation. Monocytes are about 9% of normal wbc count

Macrophages are large, phagocytic cells that engulf

  • foreign material (antigens) that enter the body
  • dead and dying cells of the body.

Neutrophils

The most abundant of the WBCs. about 65% of normal white count  These cells spend 8 to 10 days in the circulation making their way to sites of infection etc  Neutrophils squeeze through the capillary walls and into infected tissue where they kill the invaders (e.g., bacteria) and then engulf the remnants by phagocytosis. They have two types of granules: the most numerous are specific granules which contain bactericidal agents such as lysozyme; the azurophilic granules are lysosomes containing peroxidase and other enzymes

Eosinophils : The number of eosinophils in the blood is normally quite low (0–450/µl). However, their numbers increase sharply in certain diseases, especially infections by parasitic worms. Eosinophils are cytotoxic, releasing the contents of their granules on the invader.

Basophils : rare except during infections where these cells mediate inflammation by secreting histamine and heparan sulfate (related to the anticoagulant heparin). Histamine makes blood vessels permeable and heparin inhibits blood clotting. Basophils are functionally related to mast cells.  . The mediators released by basophils also play an important part in some allergic responses such as hay fever and an anaphylactic response to insect stings.

Thrombocytes (platelets):

Thrombocytes are cellular derivatives from megakaryocytes which contain factors responsible for the intrinsic clotting mechanism. They represent fragmented cells  which contain residual organelles including rough endoplasmic reticulum and Golgi apparati. They are only 2-microns in diameter, are seen in peripheral blood either singly or, often, in clusters, and have a lifespan of 10 days.

HEART DISORDERS

  1. Pump failure => Alters pressure (flow) =>alters oxygen carrying capacity.
    1. Renin release (Juxtaglomerular cells) Kidney
    2. Converts Angiotensinogen => Angiotensin I
    3. In lungs Angiotensin I Converted => Angiotensin II
    4. Angiotensin II = powerful vasoconstrictor (raises pressure, increases afterload)
      1. stimulates thirst
      2. stimulates adrenal cortex to release Aldosterone
        (Sodium retention, potassium loss)
      3. stimulates kidney directly to reabsorb Sodium
      4. releases ADH from Posterior Pituitary
  2. Myocardial Infarction

     

    1. Myocardial Cells die from lack of Oxygen
    2. Adjacent vessels (collateral) dilate to compensate
    3. Intracellular Enzymes leak from dying cells (Necrosis)
      1. Creatine Kinase CK (Creatine Phosphokinase) 3 forms
        1. One isoenzyme = exclusively Heart (MB)
        2. CK-MB blood levels found 2-5 hrs, peak in 24 hrs
        3. Lactic Dehydrogenase found 6-10 hours after. points less clearly to infarction
      2. Serum glutamic oxaloacetic transaminase (SGOT)
        1. Found 6 hrs after infarction, peaks 24-48 hrs at 2 to 15 times normal,
        2. SGOT returns to normal after 3-4 days
    4. Myocardium weakens = Decreased CO & SV (severe - death)
    5. Infarct heal by fibrous repair
    6. Hypertrophy of undamaged myocardial cells
      1. Increased contractility to restore normal CO
      2. Improved by exercise program
    7. Prognosis
      1. 10% uncomplicated recovery
      2. 20% Suddenly fatal
      3. Rest MI not fatal immediately, 15% will die from related causes
  3. Congenital heart disease (Affect oxygenation of blood)
    1. Septal defects
    2. Ductus arteriosus
    3. Valvular heart disease
      1. Stenosis = cusps, fibrotic & thickened, Sometimes fused, can not open
      2. Regurgitation = cusps, retracted, Do not close, blood moves backwards

The Parathyroid Glands

The parathyroid glands are 4 tiny structures embedded in the rear surface of the thyroid gland. They secrete parathyroid hormone (PTH) a polypeptide of 84 amino acids. PTH increases the concentration of Ca2+ in the blood in three ways. PTH promotes

  • release of Ca2+ from the huge reservoir in the bones. (99% of the calcium in the body is incorporated in our bones.)
  • reabsorption of Ca2+ from the fluid in the tubules in the kidneys
  • absorption of Ca2+ from the contents of the intestine (this action is mediated by calcitriol, the active form of vitamin D.)

PTH also regulates the level of phosphate in the blood. Secretion of PTH reduces the efficiency with which phosphate is reclaimed in the proximal tubules of the kidney causing a drop in the phosphate concentration of the blood.

Hyperparathyroidism

Elevate the level of PTH causing a rise in the level of blood Ca2+ .Calcium may be withdrawn from the bones that they become brittle and break.

 Patients with this disorder have high levels of Ca2+ in their blood and excrete small amounts of Ca2+ in their urine. This causes hyperparathyroidism.

Hypoparathyroidism

This disorder have low levels of Ca2+ in their blood and excrete large amounts of Ca2+ in their urine.

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