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Physiology

Regulation of glomerular filtration :

1. Extrinsic regulation : 

- Neural regulation : sympathetic and parasympathetic nervous system which causes vasoconstriction or vasodilation respectively .
- Humoral regulation : Vasoactive substances may affect the GFR , vasoconstrictive substances like endothelin ,Angiotensin II , Norepinephrine , prostaglandine F2 may constrict the afferent arteriole and thus decrease GFR , while the vasodilative agents like dopamine , NO , ANP , Prostaglandines E2 may dilate the afferent arteriole and thus increase the filtration rate .

2. Intrinsic regulation : 

- Myogenic theory ( as in the intrinsic regulation of cardiac output) .
- Tubuloglomerular feedback: occurs by cells of the juxtaglomerular apparatus that is composed of specific cells of the distal tubules when it passes between afferent and efferent arterioles ( macula densa cells ) , these cells sense changes in flow inside the tubules and inform specific cells in the afferent arteriole (granular cells ) , the later secrete vasoactive substances that affect the diameter of the afferent arteriole.

Heart Failure : Heart failure is inability of the heart to pump the enough amount of blood needed to sustain the needs of organism .
It is usually called congestive heart failure ( CHF) .

To understand the pathophysiology  of the heart failure ,  lets compare it with the physiology of the cardiac output :
Cardiac output =Heart rate X stroke volume

Stroke volume is determined by three determinants : Preload ( venous return ) , contractility , and afterload    (peripheral resistance ) . Any disorder of these factors will reduce the ability of the heart to pump blood .

Preload : Any factor that decrease the venous return , either by decreasing the intravenous pressure or increasing the intraatrial pressure will lead to heart failure .

Contractility : Reducing the power of contraction such as in  myocarditis , cardiomyopathy , preicardial tamponade ..etc , will lead to heart failure .

Afterload : Any factor that may increase the peripheral resistance such as hypertension , valvular diseases of the heart may cause heart failure.

Pathophysiology : When the heart needs to contract more to meet the increased demand , compensatory mechanisms start to develope to enhance the power of contractility  . One of these mechanism is increasing heart rate , which will worsen the situation because this will increase the demands of the myocardial cells themselves . The other one is hypertrophy of the cardiac muscle which may compensate the failure temporarily but then the hypertrophy will be an additional load as the fibers became stiff  .

The stroke volume will be reduced , the intraventricular pressure will increase and consequently the intraatrial pressure and then the venous pressure . This will lead to decrease reabsorption of water from the interstitium ( see microcirculation) and then leads to developing of edema ( Pulmonary edema if the failure is left , and systemic edema if the failure is right) .
 

 Acute Obstructive Disorders
 1.    Heimlich maneuver
 2.    Bypass, tracheostomy w/catheter to suck up secretion

Membrane Structure & Function

Cell Membranes

  • Cell membranes are phospholipid bilayers (2 layers)
  • Bilayer forms a barrier to passage of molecules in an out of cell
  • Phospholipids = glycerol + 2 fatty acids + polar molecule (i.e., choline) + phosphate
  • Cholesterol (another lipid) stabilizes cell membranes
  • the hydrophobic tails of the phospholipids (fatty acids) are together in the center of the bilayer. This keeps them out of the water

Membranes Also Contain Proteins

  • Proteins that penetrate the membrane have hydrophobic sections ~25 amino acids long
  • Hydrophobic = doesn't like water = likes lipids
  • Membrane proteins have many functions:
    • receptors for hormones
    • pumps for transporting materials across the membrane
    • ion channels
    • adhesion molecules for holding cells to extracellular matrix

cell recognition antigens

1. Automatic control (sensory) of respiration is in - brainstem (midbrain) 

2. Behavioral/voluntary control is in - the cortex

3. Alveolar ventilation -the amount of atmospheric air that actually reaches the alveolar per breath and that can participate in the exchange of gasses between alveoli and blood

4. Only way to increase gas exchange in alveolar capillaries - perfusion-limited gas exchange 

5. Pulmonary ventiliation not effected by - concentration of bicarbonate ions

6. Central chemoreceptors - medulla -  CO2, O2 and H+ concentrations

7. Peripheral chemoreceptors - carotid and aortic bodies- PO2, PCO2 and pH 

8. Major stimulus for respiratory centers - arterial PCO2 

9. Rhythmic breathing depends on 
1. continuous (tonic) inspiratory drive from DRG (dorsal respiratory group)
2. intermittent (phasic) expiratory input from cerebrum, thalamus, cranial nerves and ascending spinal cord sensory tracts

10. Primary site for gas exchange - type I epithelial cells for alveoli

 

Properties of cardiac muscle

Cardiac muscle is a striated muscle like the skeletal muscle , but it is different from the skeletal muscle in being involuntary and syncytial .

Syncytium means that cardiac muscle cells are able to excite and contract together due to the presence of gap junctions between adjacent cardiac cells.

Cardiac muscle has four properties , due to which the heart is able to fulfill its function as a pumping organ. Studying and understanding these properties is essential for students to understand the cardiac physiology as a whole.

1. Rhythmicity ( Chronotropism )
2. Excitability ( Bathmotropism ) 
3. Conductivity
4. Contractility

Heart sounds


Heart sounds are a result of beating heart and resultant blood flow . that could be detected by a stethoscope during auscultation . Auscultation is a part of physical examination that doctors have to practice them perfectly.
Before discussion the origin and nature of the heart sounds we have to distinguish between the heart sounds and hurt murmurs. Heart murmurs are pathological noises that results from abnormal blood flow in the heart or blood vessels.
Physiologically , blood flow has a laminar pattern , which means that blood flows in form of layers , where the central layer is the most rapid . Laminar blood flow could be turned into turbulent one .

Turbulent blood flow is a result of stenotic ( narrowed ) valves or blood vessels , insufficient valves , roughened vessels` wall or endocardium ,  and many diseases . The turbulent blood flow causes noisy murmurs inside or outside the heart.

Heart sounds ( especially first and second sounds ) are mainly a result of closure of the valves of the heart . While the third sound is a result of vibration of ventricular wall and the leaflets of the opened AV valves after rapid inflow of blood from the atria to ventricles . 

Third heart sound is physiologic in children but pathological in adults.

The four heart sound is a result of the atrial systole and vibration of the AV valves , due to blood rush during atrial systole . It is inaudible neither in adults nor in children . It is just detectable by the phonocardiogram .


Characteristic of heart sounds :

1. First heart sound  (S1 , lub ) : a soft and low pitch sound, caused by closure of AV valves.Usually has two components ( M1( mitral ) and T1 ( tricuspid ). Normally M1 preceads T1.

2. Second heart sound ( S2 , dub) : sharp and high pitch sound . caused by closure of semilunar valves. It also has two components A2 ( aortic) and P2 ( pulmonary) . A2 preceads P2.

3. Third heart sound (S3) : low pitched sound.

4. Fourth heart sound ( S4) very low pitched sound.

As we notice : the first three sounds are related to ventricular activity , while the fourth heart sound is related to atrial activity.
Closure of valves is not the direct cause for heart sounds , but sharp blocking of blood of backward returning of blood by the closing valve is the direct cause.
 

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