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 endocrine system along with the nervous system functions in the regulation of body activities.  The nervous system acts through electrical impulses and neurotransmitters to cause muscle contraction and glandular secretion and interpretation of impulses.  The endocrine system acts through chemical messengers called hormones that influence growth, development, and metabolic activities

The small intestine

Digestion within the small intestine produces a mixture of disaccharides, peptides, fatty acids, and monoglycerides. The final digestion and absorption of these substances occurs in the villi, which line the inner surface of the small intestine.

This scanning electron micrograph (courtesy of Keith R. Porter) shows the villi carpeting the inner surface of the small intestine.

The crypts at the base of the villi contain stem cells that continuously divide by mitosis producing

• more stem cells
• cells that migrate up the surface of the villus while differentiating into
  1. columnar epithelial cells (the majority). They are responsible for digestion and absorption.
  2. goblet cells, which secrete mucus;
  3. endocrine cells, which secrete a variety of hormones;
• Paneth cells, which secrete antimicrobial peptides that sterilize the contents of the intestine.

All of these cells replace older cells that continuously die by apoptosis.

The villi increase the surface area of the small intestine to many times what it would be if it were simply a tube with smooth walls. In addition, the apical (exposed) surface of the epithelial cells of each villus is covered with microvilli (also known as a "brush border"). Thanks largely to these, the total surface area of the intestine is almost 200 square meters, about the size of the singles area of a tennis court and some 100 times the surface area of the exterior of the body.

Incorporated in the plasma membrane of the microvilli are a number of enzymes that complete digestion:

• aminopeptidases attack the amino terminal (N-terminal) of peptides producing amino acids.
• disaccharidasesThese enzymes convert disaccharides into their monosaccharide subunits.
  • maltase hydrolyzes maltose into glucose.
  • sucrase hydrolyzes sucrose (common table sugar) into glucose and fructose.
  • lactase hydrolyzes lactose (milk sugar) into glucose and galactose.

Fructose simply diffuses into the villi, but both glucose and galactose are absorbed by active transport.

• fatty acids and monoglycerides. These become resynthesized into fats as they enter the cells of the villus. The resulting small droplets of fat are then discharged by exocytosis into the lymph vessels, called lacteals, draining the villi.

• it's the individual pressure exerted independently by a particular gas within a mixture of gasses. The air we breath is a mixture of gasses: primarily nitrogen, oxygen, & carbon dioxide. So, the air you blow into a balloon creates pressure that causes the balloon to expand (& this pressure is generated as all the molecules of nitrogen, oxygen, & carbon dioxide move about & collide with the walls of the balloon). However, the total pressure generated by the air is due in part to nitrogen, in part to oxygen, & in part to carbon dioxide. That part of the total pressure generated by oxygen is the 'partial pressure' of oxygen, while that generated by carbon dioxide is the 'partial pressure' of carbon dioxide. A gas's partial pressure, therefore, is a measure of how much of that gas is present (e.g., in the blood or alveoli). 
   
• the partial pressure exerted by each gas in a mixture equals the total pressure times the fractional composition of the gas in the mixture. So, given that total atmospheric pressure (at sea level) is about 760 mm Hg and, further, that air is about 21% oxygen, then the partial pressure of oxygen in the air is 0.21 times 760 mm Hg or 160 mm Hg.

1.Rhythmicity ( Chronotropism ) :  means the ability of heart to beat regularly ( due to repetitive and stable depolarization and repolarization )  . Rhythmicity of heart is a myogenic in origin , because cardiac muscles are automatically excited muscles and does not depend on the nervous stimulus to initiate excitation and then contraction . The role of nerves is limited to the regulation of the heart rate and not to initiate the beat.

There are many evidences that approve the myogenic and not neurogenic origin of the rhythmicity of cardiac muscle . For example :
-  transplanted heart continues to beat regularly without any nerve supply.
-  Embryologically the heart starts to beat before reaching any nerves to them.
-  Some drugs that paralyze the nerves ( such as cocaine ) do not stop the heart in given doses.

Spontaneous rhythmicity of the cardiac muscle due to the existence of excitatory - conductive system , which is composed of self- exciting non-contractile cardiac muscle cells . The SA node of the mentioned system excites in a rate , that is the most rapid among the other components of the system ( 110 beats /minute ) , which makes it the controller or ( the pacemaker ) of the cardiac rhythm of the entire heart.

Mechanism , responsible for self- excitation in the SA node and the excitatory conductive system  is due to the following properties of the cell membrane of theses cells :
1- Non-gated sodium channels
2- Decreased permeability to potassium
3- existence of slow and fast calcium channels.

These properties enable the cations ( sodium through the none-gated sodium voltage channels , calcium through calcium slow channels) to enter the cell and depolarize the cell membrane without need for external stimulus.

The resting membrane potential of non-contractile cardiac cell is -55 - -60 millivolts ( less than that of excitable nerve cells (-70) ) . 

The threshold is also less negative than that of nerve cells ( -40 millivolts ).

The decreased permeability to potassium from its side decrease the eflux  of potassium during the repolarization phase of the pacemaker potential . All of these factors give the pacemaker potential its characteristic shape

Repeating of the pacemaker potential between the action potentials of contractile muscle cells is the cause of spontaneous rhythmicity of cardiac muscle cells.

Factors , affecting the rhythmicity of the cardiac muscle :

I. Factors that increase the rate ( positive chronotropic factors) :
1. sympathetic stimulation : as its neurotransmitter norepinephrine increases the membrane permeability to sodium and calcium.
2. moderate warming : moderate warming increases temperature by 10 beats for each 1 Fahrenheit degree increase in body temperature, this due to decrease in permeability to potassium ions in pacemaker membrane by moderate increase in temperature.
3. Catecholaminic drugs have positive chronotropic effect.
4. Thyroid hormones : have positive chronotropic effect , due to the fact that these drugs increase the sensitivity of adrenergic receptors to adrenaline and noreadrenaline .
5. mild hypoxia.
6. mild alkalemia : mild alkalemia decreases the negativity of the resting potential.
7. hypocalcemia.
8. mild hypokalemia

II. Factors that decrease rhythmicity ( negative chronotropic):

1.Vagal stimulation : the basal level of vagal stimulation inhibits the sinus rhythm and decrease it from 110-75 beats/ minute. This effect due to increasing the permeability of the cardiac muscle cell to potassium , which causes rapid potassium eflux , which increases the negativity inside the cardiac cells (hyperpolarization ).
2. moderate cooling
3. severe warming : due to cardiac damage , as a result of intercellular protein denaturation. Excessive cooling on the other hand decrease metabolism and stops rhythmicity.
4. Cholenergic drugs ( such as methacholine , pilocarpine..etc) have negative chronotropic effect.
5. Digitalis : these drugs causes hyperpolarization . This effect is similar to that of vagal stimulation.
6. Hypercapnia ( excessive CO2 production )
7. Acidemia.
8. hyper- and hyponatremia .
9. hyperkalemia
10. hypercalcemia
11. Typhoid or diphteria toxins.

GENERAL SOMATIC AFFERENT (GSA) PATHWAYS FROM THE BODY

Pain and Temperature

Pain and temperature information from general somatic receptors is conducted over small-diameter (type A delta and type C) GSA fibers of the spinal nerves into the posterior horn of the spinal cord gray matter .

Fast and Slow Pain

Fast pain, often called sharp or pricking pain, is usually conducted to the CNS over type A delta fibers.

Slow pain, often called burning pain, is conducted to the CNS over smaller-diameter type C fibers.

Touch and Pressure

Touch can be subjectively described as discriminating or crude.

Discriminating (epicritic) touch implies an awareness of an object's shape, texture, three-dimensional qualities, and other fine points. Ability to recognize familiar objects simply by tactile manipulation.

The conscious awareness of body position and movement is called the kinesthetic sens

Crude (protopathic) touch,  lacks the fine discrimination described above and doesn't generally give enough information to the brain to enable it to recognize a familiar object by touch alone.

Subconscious Proprioception

Most of the subconscious proprioceptive input is shunted to the cerebellum.

Posterior Funiculus Injury

Certain clinical signs are associated with injury to the dorsal columns.

 As might be expected, these are generally caused by impairment to the kinesthetic sense and discriminating touch and pressure pathways.

 They include

 (1) the inability to recognize limb position,

 (2) as­tereognosis,

 (3) loss of two-point discrimination,

 (4) loss of vibratory sense, and

 (5) a positive Romberg sign.

Astereognosis is the inability to recognize familiar objects by touch alone. When asked to stand erect with feet together and eyes closed, a person with dorsal column damage may sway and fall. This is a posi­tive Romberg sign.