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NEET MDS Synopsis - Lecture Notes
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📖 Physiology

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Characteristics of Facilitated Diffusion & Active Transport
Physiology

Characteristics of Facilitated Diffusion & Active Transport - both require the use of carriers that are specific to particular substances (that is, each type of carrier can 'carry' one type of substance) and both can exhibit saturation (movement across a membrane is limited by number of carriers & the speed with which they move materials

Glomerular filtration

Physiology

Glomerular filtration

Kidneys receive about 20% of cardiac output , this is called Renal Blood Flow (RBF) which is approximatley 1.1 L of blood. Plasma in this flow is about 625 ml . It is called Renal Plasma Flow (RPF) .
About 20 % of Plasma entering the glomerular capillaries is filtered into the Bowman`s capsule .
Glomerular filtration rate is about 125 ml/min ( which means 7.5 L/hr and thus 180 L/day) This means that the kidney filters about 180 liters of plasma every day.

The urine flow is about 1ml/min ( about 1.5 liter /day) This means that kidney reabsorbs about 178.5 liters every day .

Filtration occurs through the filtration unit , which includes :

1- endothelial cells of glomerular capillaries , which are fenestrated . Fenestrae are quite small so they prevent filtration of blood cells and most of plasma proteins .

2- Glomerular basement membrane : contains proteoglycan that is negatively charged and repels the negatively charged plasma proteins that may pass the fenestrae due to their small molecular weight like albumin . so the membrane plays an important role in impairing filtration of albumin .

3- Epithelial cells of Bowman`s capsule that have podocytes , which interdigitate to form slits .


Many forces drive the glomerular filtration , which are :

1- Hydrostatic pressure of the capillary blood , which favours filtration . It is about 55 mmHg .

2- Oncotic pressure of the plasma proteins in the glomerular capillary ( opposes filtration ) . It is about 30 mm Hg .

3- Hydrostatic pressure of the Bowman`s capsule , which also opposes filtration. It is about 15 mmHg .

The net pressure is as follows :

Hydrostatic pressure of glomerular capillaries - ( Oncotic pressure of glomerular capillaries + Hydrostatic pressure of the Bowman capsule):
55-(35+10)
=55-45
=10 mmHg .

Te glomerular filtration rate does not depend only on the net pressure , but also on an other value , known as filtration coefficient ( Kf) . The later depends on the surface area of the glomerular capillaries and the hydraulic conductivity of the glomerular capillaries.
 

HEART DISORDERS

Physiology

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

Factors Affecting Heart Rate

Physiology

A heart rate that is persistently greater than 100bpm is termed tachycardia. A heart rate that is persistantly lower than 60 pulse per min  is termed bradycardia. Let's examine some factors that could cause a change in heart rate:

  • Increased heart rate can be caused by:
    • Increased output of the cardioacceleratory center. In other words, greater activity of sympathetic nerves running to the heart and a greater release of norepinephrine on the heart.
    • Decreased output of the cardioinhibitory center. In other words, less vagus nerve activity and a decrease in the release of acetylcholine on the heart.
    • Increased release of the hormone epinephrine by the adrenal glands.
    • Nicotine.
    • Caffeine.
    • Hyperthyroidism - i.e., an overactive thyroid gland. This would lead to an increased amount of the hormone thyroxine in the blood.
  • Decreased heart rate can be caused by:
    • Decreased activity of the cardioacceleratory center.
    • Increased activity of the cardioinhibitory center.
    • Many others.