NEET MDS Lessons
Physiology
CNS PROTECTION
- Bones of the Skull Frontal, Temporal, Parietal, Sphenoid, Occipital
- Cranial Meninges Dura mater, Arachnoid Space, Pia mater
- Cerebrospinal Fluid
Secreted by Chroid Plexi in Ventricles
Circulation through ventricles and central canal
Lateral and Median apertures from the 4th ventricle into the subarachnoid space
Arachnoid villi of the superior sagittal sinus return CSF to the venous circulation
Hydrocephalic Condition, blockage of the mesencephalic aqueduct, backup of CSF, Insertion of a shunt to drain the excess CSF
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) .
Regulation of Blood Pressure by Hormones
The Kidney
One of the functions of the kidney is to monitor blood pressure and take corrective action if it should drop. The kidney does this by secreting the proteolytic enzyme renin.
- Renin acts on angiotensinogen, a plasma peptide, splitting off a fragment containing 10 amino acids called angiotensin I.
- angiotensin I is cleaved by a peptidase secreted by blood vessels called angiotensin converting enzyme (ACE) — producing angiotensin II, which contains 8 amino acids.
- angiotensin II
- constricts the walls of arterioles closing down capillary beds;
- stimulates the proximal tubules in the kidney to reabsorb sodium ions;
- stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reclaim still more sodium and thus water.
- increases the strength of the heartbeat;
- stimulates the pituitary to release the antidiuretic hormone (ADH, also known as arginine vasopressin).
All of these actions, which are mediated by its binding to G-protein-coupled receptors on the target cells, lead to an increase in blood pressure.
Control of processes in the stomach:
The stomach, like the rest of the GI tract, receives input from the autonomic nervous system. Positive stimuli come from the parasympathetic division through the vagus nerve. This stimulates normal secretion and motility of the stomach. Control occurs in several phases:
Cephalic phase stimulates secretion in anticipation of eating to prepare the stomach for reception of food. The secretions from cephalic stimulation are watery and contain little enzyme or acid.
Gastric phase of control begins with a direct response to the contact of food in the stomach and is due to stimulation of pressoreceptors in the stomach lining which result in ACh and histamine release triggered by the vagus nerve. The secretion and motility which result begin to churn and liquefy the chyme and build up pressure in the stomach. Chyme surges forward as a result of muscle contraction but is blocked from entering the duodenum by the pyloric sphincter. A phenomenon call retropulsion occurs in which the chyme surges backward only to be pushed forward once again into the pylorus. The presence of this acid chyme in the pylorus causes the release of a hormone called gastrin into the bloodstream. Gastrin has a positive feedback effect on the motility and acid secretion of the stomach. This causes more churning, more pressure, and eventually some chyme enters the duodenum.
Intestinal phase of stomach control occurs. At first this involves more gastrin secretion from duodenal cells which acts as a "go" signal to enhance the stomach action already occurring. But as more acid chyme enters the duodenum the decreasing pH inhibits gastrin secretion and causes the release of negative or "stop" signals from the duodenum.
These take the form of chemicals called enterogastrones which include GIP (gastric inhibitory peptide). GIP inhibits stomach secretion and motility and allows time for the digestive process to proceed in the duodenum before it receives more chyme. The enterogastric reflex also reduces motility and forcefully closes the pyloric sphincter. Eventually as the chyme is removed, the pH increases and gastrin and the "go" signal resumes and the process occurs all over again. This series of "go" and "stop" signals continues until stomach emptying is complete.
Water: comprises 60 - 90% of most living organisms (and cells) important because it serves as an excellent solvent & enters into many metabolic reactions
- Intracellular (inside cells) = ~ 34 liters
- Interstitial (outside cells) = ~ 13 liters
- Blood plasma = ~3 liters
40% of blood is red blood cells (RBCs)
plasma is similar to interstitial fluid, but contains plasma proteins
serum = plasma with clotting proteins removed
intracellular fluid is very different from interstitial fluid (high K concentration instead of high Na concentration, for example)
- Capillary walls (1 cell thick) separate blood from interstitial fluid
- Cell membranes separate intracellular and interstitial fluids
- Loss of about 30% of body water is fatal
Ions = atoms or molecules with unequal numbers of electrons and protons:
- found in both intra- & extracellular fluid
- examples of important ions include sodium, potassium, calcium, and chloride
Ions (Charged Atoms or Molecules) Can Conduct Electricity
- Giving up electron leaves a + charge (cation)
- Taking on electron produces a - charge (anion)
- Ions conduct electricity
- Without ions there can be no nerves or excitability
- Na+ and K+ cations
- Ca2+ and Mg2+ cations control metabolism and trigger muscle contraction and secretion of hormones and transmitters
Na+ & K+ are the Major Cations in Biological Fluids
- High K+ in cells, high Na+ outside
- Ion gradients maintained by Na pump (1/3 of basal metabolism)
- Think of Na+ gradient as a Na+ battery- stored electrical energy
- K+ gradient forms a K+ battery
- Energy stored in Na+ and K+ batteries can be tapped when ions flow
- Na+ and K+ produce action potential of excitable cells
Acute Obstructive Disorders
1. Heimlich maneuver
2. Bypass, tracheostomy w/catheter to suck up secretion
4. Emphysema
1. Permanent enlargement of airways with distension of alveolar walls
Thickened Bronchial Submucosa, Edema & Cellular Infiltration (loss of elasticity), Dilation of Air spaces, due to destruction of alveolar walls (Air trapped by obstruction)
2. Lower Respiratory tree destruction
Respiratory Bronchioles, Alveolar ducts, & Alveolar sacs
Types of Emphysema:
1. Centrilobular (Centriacinar) = Respiratory Bronchioles
Rarely seen in non Smokers, More in Men than Women, Found in Smokers with Bronchitis
2. Panlobular (Panacinar)
Hereditary, Single autosomal recessive gene. Deficient in 1-globulin (1-antitrypsin), Protects respiratory tract from neutrophil elastase (Enzyme that distroys lung connective tissue) , Aged persons, Results from Bronchi or Bronchiolar constriction
NOTE: Smoking = Leading cause of Bronchitis, Emphysema