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.

The hepatic portal system

The capillary beds of most tissues drain into veins that lead directly back to the heart. But blood draining the intestines is an exception. The veins draining the intestine lead to a second set of capillary beds in the liver. Here the liver removes many of the materials that were absorbed by the intestine:

• Glucose is removed and converted into glycogen.
• Other monosaccharides are removed and converted into glucose.
• Excess amino acids are removed and deaminated.
  • The amino group is converted into urea.
  • The residue can then enter the pathways of cellular respiration and be oxidized for energy.
• Many nonnutritive molecules, such as ingested drugs, are removed by the liver and, often, detoxified.

The liver serves as a gatekeeper between the intestines and the general circulation. It screens blood reaching it in the hepatic portal system so that its composition when it leaves will be close to normal for the body.

Furthermore, this homeostatic mechanism works both ways. When, for example, the concentration of glucose in the blood drops between meals, the liver releases more to the blood by

• converting its glycogen stores to glucose (glycogenolysis)
• converting certain amino acids into glucose (gluconeogenesis).

Cystic Fibrosis
→ Thick mucus coagulates in ducts, produces obstruction, Too thick for cilia to move
 
→ Major Systems Affected: Respiratory System, G. I. Tract,Reproductive Tract

→ Inherited, autosomal recessive gene, most common fatal genetic disorder

→    Major characteristic, Altered electrolyte composition (Saliva & sweat Na+, K+, Cl-)

→    Family history of Cystic Fibrosis
→    Respiratory Infections & G.I.Tract malabsorption
→    Predisposes lung to Secondary infection (Staphylococcus, Pseudomonas)
→    Damages Respiratory Bronchioles and Alveolar ducts, Produces Fibrosis of Lungs, Large cystic dilations)

Physiology - science that describes how organisms FUNCTION and survive in continually changing environments  

Chemical Controls of Respiration

A.    Chemoreceptors (CO2, O2, H+)

1.    central chemoreceptors - located in the medulla
2.    peripheral chemoreceptors - large vessels of neck

B.    Carbon Dioxide Effects

1.    a powerful chemical regulator of breathing by increasing H+ (lowering pH)
    
a. hypercapnia            Carbon Dioxide increases -> 
                        Carbonic Acid increases ->
                        pH of CSF decreases (higher H+)- >
                        
DEPTH & RATE increase (hyperventilation)

b. hypocapnia - abnormally low Carbon Dioxide levels which can be produced by excessive hyperventilation; breathing into paper bag increases blood Carbon Dioxide levels

C.     Oxygen Effects

1.    aortic and carotid bodies - oxygen chemoreceptors

2.    slight Ox decrease - modulate Carb Diox receptors
3.    large Ox decrease - stimulate increase ventilation
4.    hypoxic drive - chronic elevation of Carb Diox (due to disease) causes Oxygen levels to have greater effect on regulation of breathing

D.    pH Effects (H+ ion)

1.    acidosis - acid buildup (H+) in blood, leads to increased RATE and DEPTH (lactic acid)

E.    Overview of Chemical Effects

 Chemical                             Breathing Effect

increased Carbon Dioxide (more H+)     increase
decreased Carbon Dioxide (less H+)     decrease

slight decrease in Oxygen             effect CO2 system
large decrease in Oxygen             increase ventilation

decreased pH (more H+)                 increase
increased pH (less H+)                 decrease

Principal heart sounds

1. S1: closure of AV valves;typically auscultated as a single sound 

Clinical note: In certain circumstances, S1 may be accentuated. This occurs when the valve leaflets are “slammed” shut in early systole from a greater than normal distance because they have not had time to drift closer together. Three conditions that can result in an accentuated S1 are a shortened PR interval, mild mitral stenosis, and high cardiac-output states or tachycardia.

2. S2: closure of semilunar valves in early diastole , normally “split” during inspiration . S2: best appreciated in the 2nd or 3rd left intercostal space

Clinical note: Paradoxical or “reversed” splitting occurs when S2 splitting occurs with expiration and disappears on inspiration. Moreover, in paradoxical splitting, the pulmonic valve closes before the aortic valve, such that P2 precedes A2. The most common cause is left bundle branch block (LBBB). In LBBB, depolarization of the left ventricle is impaired, resulting in delayed left ventricular contraction and aortic valve closure.

3. S3: ventricular gallop, presence reflects volume-overloaded state 
 
 Clinical note: An S3 is usually caused by volume overload in congestive heart failure. It can also be associated with valvular disease, such as advanced mitral regurgitation, in which the “regurgitated” blood increases the rate of ventricular filling during early diastole.
 
4. S4: atrial gallop, S4: atrial contraction against a stiff ventricle, often heard after an acute myocardial infarction.

Clinical note: An S4 usually indicates decreased ventricular compliance (i.e., the ventricle does not relax as easily), which is commonly associated with ventricular hypertrophy or myocardial ischemia. An S4 is almost always present after an acute myocardial infarction. It is loudest at the apex with the patient in the left lateral decubitus position (lying on their left side).