Events in gastric function:

1) Signals from vagus nerve begin gastric secretion in cephalic phase.

2) Physical contact by food triggers release of pepsinogen and H⁺ in gastric phase.

3) Muscle contraction churns and liquefies chyme and builds pressure toward pyloric sphincter.

4) Gastrin is released into the blood by cells in the pylorus. Gastrin reinforces the other stimuli and acts as a positive feedback mechanism for secretion and motility.

5) The intestinal phase begins when acid chyme enters the duodenum. First more gastrin secretion causes more acid secretion and motility in the stomach.

6) Low pH inhibits gastrin secretion and causes the release of enterogastrones such as GIP into the blood, and causes the enterogastric reflex. These events stop stomach emptying and allow time for digestion in the duodenum before gastrin release again stimulates the stomach.

Excitability ( Bathmotropism ) : Excitability means the ability of cardiac muscle to respond to signals. Here we are talking about contractile muscle cells that are excited by the excitatory conductive system and generate an action potential.

Cardiac action potential is similar to action potential in nerve and skeletal muscle tissue , with one difference , which is the presence of plateau phase . Plateau phase is unique for cardiac muscle cells .
The  resting membrane potential for cardiac muscle is about -80 mV.
When the cardiac muscle is stimulated an action potential is generated . The action potential in cardiac muscle is composed of four phases , which are :

1. Depolarization phase (Phase 0 ) :

A result of opening of sodium channels , which increase the permeability to sodium , which will lead to a rapid sodium influx into the cardiac muscle cell.

2. Repolarization : Repolarization in cardiac muscle is slow and triphasic :

a. Phase 1 (early partial repolarization ) : A small fast repolarization , results from potassium eflux and chloride influx.
b. Phase 2 ( Plateau ) : After the early partial depolarization , the membrane remains  depolarized , exhibiting a plateau , which is a unique phase for the cardiac muscle cell. Plateau is due to opening of slow calcium-sodium channels , delay closure of sodium channels , and to decreased potassium eflux.
c. Phase 3  ( Rapid repolarization) :  opening of potassium channels and rapid eflux of potassium.
d. Phase 4 ( Returning to resting level) in other words : The phase of complete repolarization. This due to the work of sodium-potassium pump.

Absolute refractory period:

Coincides wit phase 0,phase1 , and phase 2 . During this period , excitability of the heart is totally abolished . This prevents tetanization of the cardiac muscle and enables the heart to contract and  relax to be filled by blood ..

Relative refractory period : 

Coincides with the rapid repolarization and allows the excitability to be gradually recovered .
Excitation contraction relationship : Contraction of cardiac muscle starts after depolarization and continues about 1.5 time as long as the duration of the action potential and reaches its maximum at the end of the plateau. Relaxation of the muscle starts with the early partial repolarization.

Factors , affecting excitability of cardiac muscle:

I. Positive bathmotropic effect :

1. Sympathetic stimulation : It increase the heart , and thus reduces the duration of the action potentia; . This will shorten the duration of the absolute refractory period , and thus increase the excitability .
2.  Drugs : Catecholamines and  xanthines derivatives .
3. Mild hypoxia and mild ischemia
4. Mild hyperkalemia as it decreases the K+ efflux and opens excess Na+ channels .
5. Hypocalcemia

II. Negative bathmotropic effect :

1. Parasympathetic stimulation: The negative bathmotropic effect is limited to the atrial muscle excitability , because there is no parasympathetic innervation for the ventricles. Parasympathetic stimulation decreases the heart rate , and thus increases the duration of cardiac action potential and thus increases the duration of the absolute refractory period.
2. moderate to severe hypoxia
3. hyponatremia , hypercalcemia , and severe hyperkalemia.

Clinical Physiology : Extrasystole is a pathological situation , due to abnormal impulses , arising from ectopic focus .It is expressed as an abnormal systole that occur during the early diastole .
Extrasystole  is due to a rising of excitability above the normal , which usually occurs after the end of the relative refractory period ( read about staircase phenomenon of Treppe)

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

Oxygen Transport in Blood: Hemoglobin

A.    Association & Dissociation of Oxygen + Hemoglobin

1.    oxyhemoglobin (HbO₂) - oxygen molecule bound
2.    deoxyhemoglobin (HHb) - oxygen unbound
    
H-Hb     +    O₂  <= === => HbO₂ + H+

3.    binding gets more efficient as each O₂ binds
4.    release gets easier as each O₂ is released

5.    Several factors regulate AFFINITY of O₂

a.    Partial Pressure of O₂
b.    temperature
c.    blood pH (acidity)
d.    concentration of “diphosphoglycerate” (DPG)

B.    Effects of Partial Pressure of O₂

1.  oxygen-hemoglobin dissociation curve

a.    104 mm (lungs) - 100% saturation (20 ml/100 ml)
b.    40 mm (tissues) - 75% saturation (15 ml/100 ml)
c.    right shift - Decreased Affinity, more O2 unloaded
d.     left shift- Increased Affinity, less O₂ unloaded

C.    Effects of Temperature
    
1.    HIGHER Temperature    --> Decreased Affinity (right)
2.    LOWER Temperature        --> Increased Affinity (left)

D.    Effects of pH (Acidity) 

1.    HIGHER pH    --> Increased Affinity (left)
2.    LOWER pH    --> Decreased Affinity (right) "Bohr Effect"
a.    more Carbon Dioxide, lower pH (more H+), more O2 release

E.    Effects of Diphosphoglycerate (DPG)

1.    DPG - produced by anaerobic processes in RBCs
2.    HIGHER DPG    > Decreased Affinity (right)
3.    thyroxine, testosterone, epinephrine, NE - increase RBC metabolism and DPG production, cause RIGHT shift

F.    Oxygen Transport Problems

1.    hypoxia - below normal delivery of Oxygen

a.    anemic hypoxia - low RBC or hemoglobin
b.    stagnant hypoxia - impaired/blocked blood flow
c.    hypoxemic hypoxia - poor lung gas exchange

2.    carbon monoxide poisoning - CO has greater Affinity than Oxygen or Carbon Dioxide 
 

SPECIAL VISCERAL AFFERENT (SVA) PATHWAYS

Taste

Special visceral afferent (SVA) fibers of cranial nerves VII, IX, and X conduct signals into the solitary tract of the brainstem, ultimately terminating in the nucleus of the solitary tract on the ipsilateral side.

Second-order neurons cross over and ascend through the brainstem in the medial lemniscus to the VPM of the thalamus.

Thalamic projections to area 43 (the primary taste area) of the postcentral gyrus complete the relay.

SVA VII fibers conduct from the chemoreceptors of taste buds on the anterior twothirds of the tongue, while SVA IX fibers conduct taste information from buds on the posterior one-third of the tongue.

SVA X fibers conduct taste signals from those taste cells located throughout the fauces.

Smell

The smell-sensitive cells (olfactory cells) of the olfactory epithelium project their central processes through the cribiform plate of the ethmoid bone, where they synapse with mitral cells. The central processes of the mitral cells pass from the olfactory bulb through the olfactory tract, which divides into a medial and lateral portion The lateral olfactory tract terminates in the prepyriform cortex and parts of the amygdala of the temporal lobe.

These areas represent the primary olfactory cortex. Fibers then project from here to area 28, the secondary olfactory area, for sensory evaluation. The medial olfactory tract projects to the anterior perforated sub­stance, the septum pellucidum, the subcallosal area, and even the contralateral olfactory tract.

Both the medial and lateral olfactory tracts contribute to the visceral reflex pathways, causing the viscerosomatic and viscerovisceral responses.

• There Are 12 Pairs of Cranial Nerves

• The 12 pairs of cranial nerves emerge mainly from the ventral surface of the brain
• Most attach to the medulla, pons or midbrain
• They leave the brain through various fissures and foramina of the skull

• Nerve	Name	Sensory	Motor	Autonomic Parasympathetic
  I	Olfactory	Smell
  II	Optic	Vision
  III	Oculomotor	Proprioception	4 Extrinsic eye muscles	Pupil constriction Accomodation Focusing
  IV	Trochlear	Proprioception	1 Extrinsic eye muscle (Sup.oblique)
  V	Trigeminal	Somatic senses (Face, tongue)	Chewing
  VI	Abducens	Proprioception	1 Extrinsic eye muscle (Lat. rectus)
  VII	Facial	Taste Proprioception	Muscles of facial expression	Salivary glands Tear glands
  VIII	Auditory (Vestibulocochlear)	Hearing, Balance
  IX	Glossopharyngeal	Taste Blood gases	Swallowing Gagging	Salivary glands
  X	Vagus	Blood pressure Blood gases  Taste	Speech Swallowing Gagging	Many visceral organs (heart, gut, lungs)
  XI	Spinal acessory	Proprioception	Neck muscles: Sternocleidomastoid Trapezius
  XII	Hypoglossal	Proprioception	Tongue muscles Speech

   

• Many of the functions that make us distinctly human are controlled by cranial nerves: special senses, facial expression, speech.

• Cranial Nerves Contain Sensory, Motor and Parasympathetic Fibers