“Cardiac output refers to the volume of blood pumped out per ventricle per minute.”
Cardiac output is the function of heart rate and stroke volume.
STROKE VOLUME:
The amount of blood pumped by the left ventricle in one compression is called the stroke volume.
Heart Rate
The cardiac output increases with the increase in heart rate.
LOCATION: WALL OF GUT
NEURONS: 100 MILLIONS
GIT MOVEMENTS AND SECRETIONS
COMPOSED: TWO PLEXUSES
OUTER PLEXUS (MYENTERIC AND AUERBACH'S PLEXUS)
INNER PLEXUS (MEISSNER'S PLEXUS AND SUBMUCOSAL PLEXUS)
MYENTERIC PLEXUS
GI MOVEMENTS
SUBMUCOSAL PLEXUS
SECRETION AND LOCAL BLOOD FLOW
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
“Cardiac output refers to the volume of blood pumped out per ventricle per minute.”
Cardiac output is the function of heart rate and stroke volume.
STROKE VOLUME:
The amount of blood pumped by the left ventricle in one compression is called the stroke volume.
Heart Rate
The cardiac output increases with the increase in heart rate.
LOCATION: WALL OF GUT
NEURONS: 100 MILLIONS
GIT MOVEMENTS AND SECRETIONS
COMPOSED: TWO PLEXUSES
OUTER PLEXUS (MYENTERIC AND AUERBACH'S PLEXUS)
INNER PLEXUS (MEISSNER'S PLEXUS AND SUBMUCOSAL PLEXUS)
MYENTERIC PLEXUS
GI MOVEMENTS
SUBMUCOSAL PLEXUS
SECRETION AND LOCAL BLOOD FLOW
Regulation of arterial blood pressure (The Guyton and Hall Physiology)Maryam Fida
BLOOD PRESSURE
The pressure exerted by the blood on vessel wall is known as blood pressure.
SYSTOLIC BLOOD PRESSURE
The maximum pressure exerted in the arteries during systole of heart.
Normal systolic pressure: 120 mm Hg.
DIASTOLIC BLOOD PRESSURE
The minimum pressure exerted in the arteries during diastole of heart.
Normal diastolic pressure: 80 mm Hg.
PULSE PRESSURE
The difference between the systolic pressure and diastolic pressure.
Normal pulse pressure: 40 mm Hg (120 – 80 = 40).
MEAN ARTERIAL BLOOD PRESSURE
The average pressure existing in the arteries.
Mean Arterial Blood Pressure = Diastolic Pressure + 1/3 Pulse Pressure
Pulse Pressure = (Systolic – Diastolic)
Mean Arterial Blood Pressure =Diastolic Pressure+1/3(Systolic – Diastolic)
Pharmacokinetics - drug absorption, drug distribution, drug metabolism, drug ...http://neigrihms.gov.in/
A power point presentation on general aspects of Pharmacokinetics suitable for undergraduate medical students beginning to study Pharmacology. Also suitable for Post Graduate students of Pharmacology and Pharmaceutical Sciences.
HORMONAL CONTROL OF TUBULAR REABSORPTION (The Guyton and Hall physiology)Maryam Fida
REGULATION OF SODIUM AND WATER BALANCE
by hormones
• Aldosterone
• Angiotensin II
• Atrial natriuretic Peptide
• Parathyroid Hormone
• Antidiuretic hormone (ADH) or vasopressin
ALDOSTERONE
Release: Aldosterone is secreted by the zona glomerulosa cells of the adrenal cortex in response to
Increased extracellular potassium concentration
Increased angiotensin II levels in conditions associated with sodium and volume depletion or low blood pressure.
Site of Action: Major renal tubular site of aldosterone action is on the principal cells of the cortical collecting tubule.
Effects on the Renal Tubules
Aldosterone increases sodium reabsorption and potassium secretion by stimulating the sodium-potassium ATPase pump on the basolateral side of the cortical collecting tubule membrane.
Aldosterone also increases the sodium permeability of the luminal side of the membrane.
physiology of the renal system
that explains how the renal system works...................................................................................................................................................................................................................................................................................................................................................................................................................................................................................
Renal blood flow (The Guyton and Hall physiology)Maryam Fida
In an average 70-kilogram man, the combined blood flow through both kidneys is about 1100 ml/min, or about 22 per cent of the cardiac output. Two kidneys makes about 0.4 % of total body weight but receive very high blood flow as compared with other body organ. The purpose of additional blood flow is to supply sufficient plasma for high rates of GF which is essential for regulating body fluid volumes & solute concentrations.
Characteristics of the renal blood flow:
1, High blood flow. 1100 ml/min, or 22 percent of the cardiac output. 94% to the cortex.
2, Two capillary beds
High hydrostatic pressure in glomerular capillary (about 60 mmHg) and low hydrostatic pressure in peritubular capillaries (about 13 mmHg)
Blood flow to renal medulla is supplied by vasa recta.
Blood flow in vasa recta of medulla is very low as compared to blood flow in cortex.
Blood flow in renal medulla is 1-2 % of total renal blood flow.
Vasa recta are important to form concentrated urine.
Forensic medicine medical negligence 2-bolam principle
Lec47
1. Control of Renal Calcium Excretion and Extracellular Calcium Ion Concentration The total calcium in the plasma 5 mEq/L Ca ion activates the sliding filament mechanism and essential factor in blood clotting About 50 per cent of the plasma calcium is ionized, with the remainder being bound to the plasma proteins or complexed with anions such as phosphate About 50 per cent of the plasma calcium can be filtered at the glomerulus
2. When calcium ion concentration falls to low levels (hypocalcemia), the excitability of nerve and muscle cells increases markedly and can in extreme cases result in hypocalcemic tetany Hypercalcemia depresses neuromuscular excitability and can lead to cardiac arrhythmias
3. One of the most important regulators of bone uptake and release of calcium is PTH The parathyroid glands are directly stimulated by the low calcium levels to promote increased secretion of PTH PTH regulates plasma calcium concentration through (1) by stimulating bone resorption (2) by stimulating activation of vitamin D in the kidneys (3) by directly increasing renal tubular calcium reabsorption
4. Compensatory responses to decreased plasma ionized calcium concentration mediated by parathyroid hormone and vitamin D
6. Phosphate excretion by the kidneys Plasma phosphate concentration is usually maintained at about 4 mEq/L The renal tubules have a normal transport maximum for reabsorbing phosphate of about 0.1 mM/min Parathyroid hormone regulate phosphate concentration through: (1) PTH promotes bone resorption, thus dumping large amounts of phosphate ions into the extracellular fluid from the bone salts (2) PTH decreases the transport maximum for phosphate by the renal tubules, so that a greater proportion of the tubular phosphate is lost in the urine
7. Integration of Renal Mechanisms for Control of Extracellular Fluid Extracellular fluid volume is determined mainly by the balance between intake and output of water and salt When ADH-Thirst mechanisms are functioning normally a change in the amount of sodium chloride in the extracellular fluid is matched by a similar change in the amount of extracellular water, so that osmolarity and sodium concentration are maintained constant
8. Sodium Excretion Is Controlled by Altering Glomerular Filtration or Tubular Sodium Reabsorption Rates The two variables that influence sodium and water excretion are the rates of filtration and the rates of reabsorption: Excretion = Glomerular filtration – tubular reabsorptionGFR normally is about 180 L/day, tubular reabsorption is 178.5 L/day, and urine excretion is 1.5 L/day Tubular reabsorption and GFR usually are regulated precisely, so that excretion by the kidneys can be exactly matched to intake of water and electrolytes
9. If the kidneys become greatly vasodilated and GFR increases, this raises sodium chloride delivery to the tubules, which in turn leads to (1) increased tubular reabsorption of much of the extra sodium chloride filtered, called glomerulotubular balance (2) macula densa feedback, in which increased sodium chloride delivery to the distal tubule causes afferent arteriolar constriction and return of GFR toward normal
10. Neither of these two mechanisms operates perfectly to restore distal sodium chloride delivery back to normal When this happens other feedback mechanisms such as changes in blood pressure and changes in various hormones, that eventually return sodium excretion to equal sodium intake
11. Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance One of the mechanisms for control of blood volume and extracellular fluid volume, as well as for the maintenance of sodium and fluid balance, is the effect of blood pressure on sodium and water excretion-called the pressure natriuresisand pressure diuresismechanisms, respectively.
12. Pressure diuresis refers to the effect of increased blood pressure to raise urinary volume excretion Pressure natriuresis refers to the rise in sodium excretion that occurs with elevated blood pressure
13. Pressure Natriuresis and Diuresis Are Key Components of a Renal-Body Fluid Feedback for Regulating Body Fluid Volumes and Arterial Pressure The extracellular fluid volume, blood volume, cardiac output, arterial pressure, and urine output are all controlled at the same time as separate parts of this basic feedback mechanism This feedback mechanism helps to maintain fluid balance and to minimize changes in blood volume, extracellular fluid volume, and arterial pressure as follows:
14. An increase in fluid intake above the level of urine output causes a temporary accumulation of fluid in the body As long as fluid intake exceeds urine output, fluid accumulates in the blood and interstitial spaces, causing parallel increases in blood volume and extracellular fluid volume An increase in blood volume raises mean circulatory filling pressure An increase in mean circulatory filling pressure raises the pressure gradient for venous return
15. An increased pressure gradient for venous return elevates cardiac output An increased cardiac output raises arterial pressure An increased arterial pressure increases urine output by way of pressure diuresis The increased fluid excretion balances the increased intake, and further accumulation of fluid is prevented
16.
17. The renal-body fluid feedback mechanism operates to prevent continuous accumulation of salt and water in the body during increased salt and water intake As long as kidney function is normal and the pressure diuresis mechanism is operating effectively, large changes in salt and water intake can be accommodated with only slight changes in blood volume, extracellular fluid volume, cardiac output, and arterial pressure
18. Sympathetic Nervous System Control of Renal Excretion Changes in sympathetic activity can alter renal sodium and water excretion as well as regulation of extracellular fluid volume under some conditions When blood volume is reduced by hemorrhage, the pressures in the pulmonary blood vessels decrease causing activation of the sympathetic nervous system
19. Effects of increases renal sympathetic nerve activity (1) constriction of the renal arterioles, with resultant decreased GFR (2) increased tubular reabsorption of salt and water (3) stimulation of renin release and increased angiotensin II and aldosterone formation, both of which further increase tubular reabsorption Sympathetic Nervous System Control of Renal Excretion
20. Role of Angiotensin II In Controlling Renal Excretion When sodium intake is elevated above normal, renin secretion is decreased, causing decreased angiotensin II formation, thus increasing the kidneys' excretion of sodium and water The net result is to minimize the rise in extracellular fluid volume and arterial pressure that would otherwise occur when sodium intake increases Changes in activity of the renin-angiotensin system act as a powerful amplifier of the pressure natriuresis mechanism for maintaining stable blood pressures and body fluid volumes.
21. Role of Aldosterone in Controlling Renal Excretion Aldosterone increases sodium reabsorption, especially in the cortical collecting tubules The increased sodium reabsorption is also associated with increased water reabsorption and potassium secretion The net effect of aldosterone is to make the kidneys retain sodium and water but to increase potassium excretion in the urine
22. The function of aldosterone in regulating sodium balance is closely related to that of angiotensin II Reduction in sodium intake, the increased angiotensin II levels that occur stimulate aldosterone secretion, which in turn contributes to the reduction in urinary sodium excretion and, therefore, to the maintenance of sodium balance Role of Aldosterone in Controlling Renal Excretion
23. Role of ADH in Controlling Renal Water Excretion High levels of ADH increase water reabsorption by the kidneys and help to minimize the decreases in extracellular fluid volume and arterial pressure that would otherwise occur
24. Water deprivation for 24 to 48 hours normally causes only a small decrease in extracellular fluid volume and arterial pressure. If the effects of ADH are blocked with a drug that antagonizes the action of ADH, the same period of water deprivation causes a substantial fall in both extracellular fluid volume and arterial pressure Role of ADH in Controlling Renal Water Excretion
25. Role of Atrial Natriuretic Peptide in Controlling Renal Excretion Atrial natriuretic peptide (ANP), released by the cardiac atrial muscle fibers The stimulus for release of this peptide is overstretch of the atria, which can result from excess blood volume
26. ANP cause small increases in GFR and decreases in sodium reabsorption by the collecting ducts These combined actions of ANP lead to increased excretion of salt and water, which helps to compensate for the excess blood volume Role of Atrial Natriuretic Peptide in Controlling Renal Excretion