Physiology 🫁 Flashcards

Question

What is the value of Purkinje fibers conduction?

Answer 1

Velocity: 4 m/sec

Answer 2

large fibers & high permeability of gap junctions.

Answer 3

immediate transmission of cardiac impulse in the ventricles.

Answer 4

The ability of the muscle to do mechanical work (contraction & relaxation).

Answer 5

Action potentials pass over the muscle fiber membrane → spread to the interior along the transverse (T) tubules → open Ca++ channels → inc. entry of Ca++ into the sarcoplasm → act on the longitudinal sarcoplasmic reticulum (SR) → inc. release of Ca++ into the sarcoplasm → Ca++ bind to troponin → sliding between actin & myosin filaments → muscle shortening (contraction).

Answer 6

ECF: via Ca channels in the cell membrane & down the T tubules S.R: via calcium-induced calcium-release.

Answer 7

the concentration of Ca++ in extracellular fluids

Answer 8

Stoppage of Ca++ influx & pumping back of Ca++ from the sarcoplasm into SR & ECF via Ca++ pumps & Na+ Ca++ exchangers.

Answer 9

“Within limit, the greater the initial length of the cardiac muscle fiber, the greater the force of contraction”.

Answer 10

diastolic filling (end-diastolic volume = EDV).

Answer 11

Inc. venous return (e.g., muscle exercise) → inc EDV (filling) → stretch of the muscle → inc the force of contraction

Answer 12

prevents stagnation of blood in the CVS.

Answer 13

Dec. Contractility

Answer 14

1.5 times as long as AP.

Answer 15

just after the start of depolarization

Answer 16

BY the end of plateau.

Answer 17

AT the end of plateau.

Answer 18

When RP is complete

Answer 19

Absolute refractory period (ARP) Relative refractory period (RRP) Supernormal phase

Answer 20

Zero Gradually increase Above normal

Answer 21

No response, whatever the strength of the 2nd stimulus Strong stimulus → weak contraction Weak stimulus → Strong contraction

Answer 22

Rapid depolarization & plateau = Contraction Rapid repolarization = 1st half of relaxation At the end of AP = 2nd half of relaxation

Answer 23

Prevents tetanus (continuous contraction) Null May cause extrasystole

Answer 24

1- Nervous: Sympatyhaeic, Parasympathetic 2- Physical: Warming, Cooling, and Excessive warming/cooling 3- Chemical: Drugs and Hormones, Blood gases, Ions and typhoid/bacteria toxins

Answer 25

- Sympathetic → noradrenaline → inc Na influx → rapid depolarization → inc rhythmicity, excitability & conductivity. - Sympathetic → B1 adrenergic receptors → inc Ca influx → inc contractility of all cardiac muscles.

Answer 26

- Basal parasympathetic discharge (vagal tone) to atrial structures only → acetylcholine → inc K efflux → hyperpolarization (inhibition)→ dec rhythmicity (of SAN from 120 → 70 /min), excitability & conductivity. - Strong vagal stimulation can stop rhythmicity, excitability & conductivity in atrial structures only. "Like in shocks" - Parasympathetic stimulation → muscarinic receptors → dec Ca influx → dec contractility of atrial muscle only.

Answer 27

- Moderate warming (fever) → inc ionic fluxes across the membrane → inc rhythmicity (10 beats/1°F), excitability, conductivity, and inc contractility (due to Increased metabolic reactions, Ca influx, and decreased viscosity).

Answer 28

- Moderate cooling: opposite effects to moderate warming.

Answer 29

- Excessive warming or cooling → cardiac damage → stop the heart.

Answer 30

- Catecholamines, Thyroxine, xanthene-derivatives (theophylline & caffeine) → inc all cardiac properties. - Cholinergic → dec all cardiac properties.

Answer 31

Decreased O2: Mild hypoxia → inc rhythmicity, excitability, conductivity, and dec contractility "due to fatigue" Increased CO2 (hypercapnia) → inc H+ (acidosis = dec pH) → dec rhythmicity, excitability, conductivity, and contractility (dec affinity of troponin to Ca)

Answer 32

- increased K+ (hyperkalemia) → dec K efflux → prolong repolarization → dec all cardiac properties. Marked K increase → stop the heart in diastole (irreversible relaxation) - increased Ca++ (hypercalcemia) → increases K efflux → hyperpolarization → dec rhythmicity, excitability, conductivity, and inc contractility. Marked Ca increase → stop the heart in systole (calcium rigor = irreversible contraction).

Answer 33

Dec rhythmicity, excitability, conductivity, and contractility (direct inhibition). "However other organisms that cause fever increase cardiac properties due to warming"

Answer 34

The cardiac events that occur from the beginning of one heartbeat to the beginning of the next.

Answer 35

A period of contraction (systole) and a period of relaxation (diastole) occur during the cardiac cycle

Answer 36

``` Valves. Heart sounds (ECG) Atrial pressure Ventricular pressure Ventricular volume Aortic pressure ```

Answer 37

Atrial systole (0.1 sec) Ventricular systole (0.3 sec) - Isometric contraction phase - Maximum ejection phase. - Reduced ejection phase Ventricular diastole /0.5 sec) - Isometric relaxation phase - Rapid filling phase. - Reduced filling phase

Answer 38

AV opened Semi-lunar closed

Answer 39

Yes, 4th heart sound Normally inaudible but can be recorded by the phonocardiogram.

Answer 40

P wave (atrial depolarization) starts 0.02 second before systole.

Answer 41

Increase from zero -› 2 mmHg (due to atrial contraction), Then, pressure returns zero due to evacuation into the ventricles. "Inc then dec"

Answer 42

Inc slightly (due to rush of blood from the atria), then dec again as the ventricles are still relaxed. "Inc then dec"

Answer 43

slightly (30%) due to rush of blood from the atria. “It was already passively filled with 70%"

Answer 44

Dec gradually, due to flow of blood to the peripheral vessels.

Answer 45

AV close Semilunar closed

Answer 46

QRS complex, starts 0.02 second before this phase

Answer 47

Slight sharp increase, due to sudden closure of AV valve and ballooning of its cusps towards the cavity of the atrium by the sudden rise of ventricular pressure.

Answer 48

The ventricle contracts so ventricular pr > atrial pr so sudden closure of the AV valves. - All valves are closed, and the ventricle becomes a closed chamber full of blood which is incompressible, so the ventricle contracts isometrically (without change in the length of fibers)

Answer 49

Early part of the 1st sound due to closure of AV valves

Answer 50

No change. (a closed chamber)

Answer 51

Dec gradually, due to flow of blood to the peripheral vessels.

Answer 52

AV closed Semilunar open

Answer 53

1st heart sound continues, due to flow of blood from ventricles to the aorta and pulmonary arteries.

Answer 54

Early part The T wave starts in the late of this phase.

Answer 55

sharp dec (due to pulling down the AV ring) Then gradual inc (due to Accumulation of venous blood in the atria and Upward displacement of AV ring to its normal position.) "Dec then inc"

Answer 56

Marked inc (due to continuous contraction of the ventricles). Ventricular pressure is higher than aortic or pulmonary pressure.

Answer 57

Dec rapidly, due to ejection of blood into the aorta or pulmonary artery.

Answer 58

Inc rapidly, due to ejection of blood from the left ventricle but remains ‹ ventricular pressure.

Answer 59

AV closed. Semilunar opened

Answer 60

The top of T wave.

Answer 61

Gradual inc (due to venous return)

Answer 62

Slightly decrease

Answer 63

Still decreasing

Answer 64

Slightly decrease, because the blood leaving the aorta is greater than the blood pumped into the aorta

Answer 65

It is the lateral force exerted by the blood on the arterial wall.

Answer 66

- Pulsatile. - It is not constant during a cardiac cycle. - The systolic BP is caused by the sudden ejection of blood into the aorta during systole. - The diastolic BP is caused by the passive elastic recoiling of the arteries (elastic recoil or windkessel effect)

Answer 67

It is the highest arterial pressure during a cardiac cycle, It is measured after the heart contracts (systole) and blood is ejected into the arterial system.

Answer 68

It is the lowest arterial pressure during a cardiac cycle, It is measured when the heart is relaxed (diastole) and blood is returned to the heart via the veins.

Answer 69

is the difference between the systolic and diastolic pressures.

Answer 70

It is the average arterial pressure with respect to time.

Answer 71

Can be calculated approximately as diastolic pressure plus one-third of pulse pressure.

Answer 72

1) It maintains sufficient pressure to keep the blood flowing. 2) It provides enough hydrostatic pressure inside the capillaries essential for the formation of interstitial fluid, urine, etc. "The pressure in the capillaries causes the ejection of nutrients and vitamins to the cells, it also allows the absorbance of wastes from them"

Answer 73

- The ABP is about 50/30 mmHg. - After birth, Increase of age will increase ABP till adulthood where it is 120/80. - After the age of 50 years it increases gradually due to normal gradual loss of arterial elasticity. - It may become normally 140/90

Answer 74

- ABP is generally slightly higher in adult males than in females. - However, it becomes slightly higher in females after menopause.

Answer 75

ABP is higher in obese persons

Answer 76

Exposure to cold increases both Systolic and systolic pressures due to cutaneous vasoconstriction.

Answer 77

Increase the ABP considerably

Answer 78

Systolic ABP increases while the diastolic is often not changed or decreases due to arteriolar vasodilatation.

Answer 79

The ABP increases slightly after meals due to VD of the splanchnic area which increases both VR and COP.

Answer 80

On standing, the force of gravity increases the mean ABP below a reference point in the heart and decreases it above that point by about 0.77 mm/cm height.

Answer 81

- Cardiac output - Peripheral resistance - Elasticity of the arterial wall - The total blood volume in relation to the capacity of the circulatory system

Answer 82

Changes in the stroke volume with the HR constant affect the systolic more than the diastolic pressure.

Answer 83

Changes in the HR with constant SV affect the diastolic more than the systolic blood pressure.

Answer 84

PR = VL/r4 a) Viscosity of blood (V): It is the property by which a fluid resists a change in shape, It represents the force with which the fluid particles adhere to each other and resists their separation b) Length of the blood vessels (L) c) The diameters of arterioles (r)

Answer 85

there is a marked increase in systolic “pushing of blood" and a decrease in diastolic blood "decrease in elasticity" pressure resulting in higher pulse pressure.

Answer 86

Changes in blood volume:- - Mild to moderate - Severe Changes in the capacity of the circulatory system: - Increase - Decrease

Answer 87

1- Fast, neurally mediated baroreceptor mechanism 2- Slower, hormonally regulated renin-angiotensin–aldosterone mechanism

Answer 88

fast, neural mechanisms.

Answer 89

- It is a negative feedback system that is responsible for the minute-to-minute regulation of arterial blood pressure - Baroreceptors are stretch receptors located within the walls of the carotid sinus near the bifurcation of the common carotid arteries.

Answer 90

1) A decrease in arterial pressure decreases stretch on the walls of the carotid sinus and aortic arch. 2) Decreased stretch decreases the firing rate of the baroreceptors (which send information to the vasomotor center in the brain stem). 3) The vasomotor center responds to the decrease in mean arterial blood pressure by decreasing parasympathetic outflow to the heart and increasing sympathetic outflow to the heart and blood vessels to increase mean arterial pressure to 100mmHg

Answer 91

↑ heart rate ↑ contractility and stroke volume ↑ vasoconstriction of arterioles ↑ vasoconstriction of veins (venoconstriction)

Answer 92

resulting from the decreased parasympathetic tone and increased sympathetic tone to the SA node of the heart.

Answer 93

resulting from increased sympathetic tone to the heart.

Answer 94

They produce an increase in cardiac output that increases arterial pressure.

Answer 95

resulting from the increased sympathetic outflow.

Answer 96

TPR and arterial pressure will increase.

Answer 97

resulting from the increased sympathetic outflow.

Answer 98

causes a decrease in unstressed volume and an increase in venous return to the heart.

Answer 99

- slow, hormonal mechanism. | - used in long-term blood pressure regulation by adjustment of blood volume.

Answer 100

- Renin is an enzyme. - Angiotensin I is inactive. - Angiotensin II is physiologically active. - Angiotensin II is degraded by angiotensinase. - One of the peptide fragments, angiotensin III, has some of the biologic activity of angiotensin II.

Answer 101

1) A decrease in renal perfusion pressure causes the juxtaglomerular cells of the afferent arteriole to secrete renin. 2) Renin is an enzyme that catalyzes the conversion of angiotensinogen to angiotensin I in plasma. 3) Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II, primarily in the lungs. 4) angiotensin II has many effects

Answer 102

a) It stimulates the synthesis and secretion of aldosterone by the adrenal cortex. b) It increases Na+–H+ exchange in the proximal convoluted tubule. c) It increases thirst and therefore water intake. d) It causes vasoconstriction of the arterioles, thereby increasing TPR and arterial pressure.

Answer 103

- Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid (ECF) volume, blood volume, and arterial pressure.

Answer 104

because it requires new protein synthesis.

Answer 105

- This action of angiotensin II directly increases Na+ reabsorption, complementing the indirect stimulation of Na+ reabsorption via aldosterone. - This action of angiotensin II leads to contraction alkalosis.

Answer 106

1) Cerebral ischemia 2) Chemoreceptors in the carotid and aortic bodies 3) Vasopressin [antidiuretic hormone (ADH)] 4) Atrial natriuretic peptide (ANP)

Answer 107

- When the brain is ischemic, the partial pressure of carbon dioxide (PCO2) in brain tissue increases. - Chemoreceptors in the vasomotor center respond by increasing sympathetic outflow to the heart and blood vessels. - Constriction of arterioles causes intense peripheral vasoconstriction and increased TPR. - Blood flow to other organs (e.g., kidneys) is significantly reduced in an attempt to preserve blood flow to the brain.

Answer 108

- The Cushing reaction is an example of the response to cerebral ischemia. Increases in intracranial pressure cause compression of the cerebral blood vessels, leading to cerebral ischemia and increased cerebral PCO2. - The vasomotor center directs an increase in sympathetic outflow to the heart and blood vessels, which causes a profound increase in arterial pressure.

Answer 109

located near the bifurcation of the common carotid arteries and along the aortic arch.

Answer 110

have very high rates of O2 consumption and are very sensitive to decreases in the partial pressure of oxygen (Po2).

Answer 111

Decreases in PO2 activate vasomotor centers that produce vasoconstriction, an increase in TPR, and an increase in arterial pressure.

Answer 112

It is involved in the regulation of blood pressure in response to hemorrhage, but not in minute-to-minute regulation of normal blood pressure.

Answer 113

Atrial receptors respond to a decrease in blood volume (or blood pressure) and cause the release of vasopressin from the posterior pituitary.

Answer 114

Vasopressin has two effects that tend to increase blood pressure toward normal: - It is a potent vasoconstrictor that increases TPR by activating V1 receptors on the arterioles. - It increases water reabsorption by the renal distal tubule and collecting ducts by activating V2 receptors.

Answer 115

from the atria in response to an increase in blood volume and atrial pressure.

Answer 116

- ANP causes relaxation of vascular smooth muscle, dilation of arterioles, and decreased TPR. - causes increased excretion of Na+ and water by the kidney, which reduces blood volume and attempts to bring arterial pressure down to normal. - inhibits renin secretion.

Answer 117

The is the volume of blood pumped by each ventricle per minute, It is also called minute volume.

Answer 118

Normally, it is about 5 liters/minute during rest and is equal for both ventricles.

Answer 119

Is the volume of blood in the ventricle at the end of diastole, it is about (110-130 ml).

Answer 120

Is the volume of blood in the ventricle at the end of the systole, is about (40-60 ml).

Answer 121

- It is the volume of blood pumped by each ventricle per beat. - SV = EDV (130) – ESV (60) = 70 ml.

Answer 122

The COP = SV x HR. = 70 x 70 = 4900 ml/minute, at rest.

Answer 123

Is the volume of blood pumped by each ventricle/square meter of body surface area/minute.

Answer 124

about 3.2 litres/m2/min.

Answer 125

It is used to compare the COP between the different individuals.

Answer 126

Is the percentage ratio of the SV to the EDV.

Answer 127

- EF = SV / EDV x 100 | - Normally, it is about 65%.

Answer 128

It is a sensitive indicator of myocardial contractility.

Answer 129

ventricular contractility, in Heart failure

Answer 130

by echocardiography.

Answer 131

Venous return (preload) Arterial blood pressure (afterload) Heart rate (HR) Strength of ventricular contraction

Answer 132

- the volume of blood returned by the veins from the tissues i.e. by the metabolic activity of the tissues, particularly the voluntary muscles. - So, VR → ↑COP

Answer 133

1) The pumping action of the heart (most important) 2) Pressure gradient 3) Respiratory movements 4) Gravity 5) Vascular system 6) Skeletal muscle contraction (a muscular pump) 7) Blood volume

Answer 134

forcing blood into the blood vessels.

Answer 135

- The pressure gradient for venous return is the difference between the mean circulatory pressure (MCP) and the right atrial pressure (RAP). - In the recumbent position, (MCP ) is 7-8 mm Hg and (RAP) is 2 mm Hg, this leads to a venous return of about 5 liters/minute.

Answer 136

Is the blood pressure in peripheral venules and veins in the recumbent position and is normally about 7-8 mm Hg.

Answer 137

It is the pressure in the right atrium, In the recumbent "patients are carried in this position" position it is 2 mmHg.

Answer 138

Venous return increases with inspiration and decreases with expiration.

Answer 139

Normal inspiration makes the intrathoracic pressure more negative and the intraabdominal pressure more positive → blood is sucked from extra to intrathoracic veins → VR. “Breathe to let blood in”

Answer 140

During normal expiration, the negativity inside the thorax is decreased, and so the VR is less than during inspiration.

Answer 141

- Gravity influences VR in a mechanical way. - In the recumbent position, gravity has no effect on VR. - In the erect position, gravity helps the VR from parts above the level of the heart but reduces it from parts below the level of the heart.

Answer 142

- Normally, the tone of the arterioles leads to partial VC. | - VD of arterioles →↑VR.

Answer 143

- If all the capillaries of the body are widely dilated, as by injection of histamine, the whole blood volume will be retained in them → no VR, no COP, ➔shock and death i.e., “Histamine shock”. “No use of vasodilators in case of decreased cardiac output” - Thus, VD of capillaries → ↓VR →↓ COP.

Answer 144

- About 10% only of the capillaries are opened and the other 90% are collapsed during the rest.

Answer 145

- Venous tone prevents full distension of veins with blood, So, it maintains VR. - VD of veins → stagnation blood into veins →↓ VR and COP and vice versa.

Answer 146

- During muscular contraction, the muscle fibers compress the blood vessels lying in between them, squeezing the blood into veins towards the heart, so increasing the VR and COP. - During muscular relaxation, the blood does not regurgitate back to the muscles because the veins possess very efficient valves which direct the bloodstream towards the thoracic veins.

Answer 147

- Increased blood volume (e.g. during muscular exercise due to contraction of blood reservoirs →↑VR and COP. - Decreased blood volume →↓VR, COP.

Answer 148

Changes in ABP have no effect on the COP provided the VR is kept constant. 1) When the blood pressure rises suddenly, the first systole will not be strong enough to pump all the blood received during diastole and some blood remains in the ventricle, This residual blood is added to the diastolic filling→↑EDV of the next systole→↑force of myocardial contraction (according to Starling's law). 2) When the ABP is lowered the opposite occurs, The first few beats expel more blood than that received during diastole→↓ ESV→↓EDV→↓force of myocardial contraction (according to Starling's law).

Answer 149

both the amount of VR and the extent of changes in heart rate.

Answer 150

- If the venous return is kept constant, moderate changes in HR have no effect on COP, it affects only the SV. - The SV increases when the heart slows (as it has enough time to fill with more blood) and decreases when the heart accelerates, So, the COP remains constant in both instances

Answer 151

If the venous return is kept constant marked acceleration or slowing of the heart decreases the COP.

Answer 152

In paroxysmal tachycardia: (HR 200 beats/min or more). - The diastolic period will be greatly shortened with no sufficient time for filing of the heart and so the COP decreases. ▪ e.g. COP = SV x HR = 20 x 200 = 4000 ml/min. In complete heart block: COP= SV x HR = 130 x 30 = 3900 ml/min

Answer 153

- When the VR is increased, the acceleration of the heart becomes of fundamental importance in increasing the COP.

Answer 154

This is because: - Increased EDV  With an enhanced rate of blood flow, the heart can be filled to a maximum in a short diastolic period leading to an increase in the EDV. - Decreased ESV  Also, sympathetic stimulation during exercise → forced ventricular contraction →↓ESV. - These factors lead to a marked increase of the SV and so the COP increases 7-8 folds.

Answer 155

- when the ventricles contract more strongly, they pump more blood. - Starling's law of the heart represents an important mechanism of cardiac reserve power. - In a normal heart within limits, when the VR increases as in muscular exercise, → the ventricle dilates i.e. increases the initial length of the cardiac muscle fiber during diastole →↑force of ventricular contraction →↑SV and COP.

Answer 156

1) The direct Fick's principle | 2) Echocardiography

Answer 157

This principle states that: The amount of a substance taken up by an organ or by the whole body/min = arterial content – venous content X blood flow/min.

Answer 158

- The O2 consumption/min - The O2 content in the mixed venous blood (from the pulmonary trunk by a cardiac catheter). - The O2 content in the arterial blood - Therefore, the COP = 250/ (190-140) = 250/ 50 = 5 liters/min.

Answer 159

Is the ability of the cardiac muscle to change its COP to meet the body requirements under different situations. - COP may be changed by changing the SV or HR or both.

Answer 160

Studied by the heart-lung preparation that allows the study of the cardiac muscle independent of nervous or hormonal factors in experimental animals.

Answer 161

Heterometric and homeometric

Answer 162

``` Definition Nature Cause Starts Lasts EDV ESV SV Explained by ```

Answer 163

- Is the regulation of COP with the change of the initial length. - Intrinsic - ↑Preload (VR) - Within 30 sec. - Few minutes (Transient mechanism) - Marked ↑↑ “sudden return of blood” - Slight ↑ - ↑ - Is the regulation of COP without change of the initial length. - Intrinsic - ↑Afterload (ABP) - Within 5 min. - Continues as long as after-load is ↑ (Steady-state mechanism). - returns to normal "blood is pumped" - ↓below normal "due to better contraction" - ↑ "due to better contraction"

Answer 164

↑ the initial length of the ventricle (EDV) | i.e starling‘s law.

Answer 165

1) The preceding heterometric stage ➔ better metabolic state i.e. More warmth and Ca++ etc. ▪ This leads to forceful contraction. 2) Pressure-induced regulation: The rise in the aortic pressure will increase the coronary blood flow that will provide more O2 to the contracting myocardium. 3) Release of myocardial catecholamines.

Answer 166

Physiologically, the heterometric autoregulation is observed when a person goes from the standing position to the recumbent position, a relatively large volume of blood shifts from the veins of the lower limbs to the heart →↑ EDV →↑SV → ↑COP.

Answer 167

The autonomic nerve supply of the heart and the circulating blood hormones regulate the COP by adjusting both the heart rate and the stroke volume.

Answer 168

Sympathetic stimulation increases the COP by: 1) +ve chronotropic effect, it increases the heart rate. 2) It increases the strength of ventricular contraction, by: ✓ The increased forces of ventricular contraction, decrease the ESV –> increase SV ✓ Also forceful ventricular contraction →rapid relaxation acts as suction force ↑ filling of the ventricles at the short diastole. 3) It increases the mean circulatory pressure ➔ increases the pressure gradient of VR ➔ increase VR and increases COP. Parasympathetic stimulation decreases the COP by slowing the heart. (HR)

Answer 169

Inc COP by Inc Both: Catecholamines, Thyroxine Inc COP by Inc SV "force of contraction": Digitalis, Xanthine derivatives e.g. caffeine, theobromine, and theophylline, Glucagon, and corticosteroids Dec COP by dec HR "chronotropic effect": Acetylcholine and other parasympathomimetic drugs such as methacholine, carbachol, and pilocarpine

Answer 170

❖ Blood is a complex reddish fluid that circulates within the cardiovascular system ❖ Blood consists of a yellowish fluid (plasma) (55% of blood volume) in which cellular elements (45% of blood volume) are suspended. Plasma:- consists of: - 90% Water - 0.9% Inorganic substance (Na+, K+, Cl-, HCO3, PO4, SO4) - 9.1% Organic substances (plasma proteins, lipids, others) Cellular elements:- Include: - Red blood cells (RBCs) - White blood cells (WBCs) - Platelets

Answer 171

Its volume is about 8% of the bodyweight i.e. 5600 ml in a 70 kg man. “ One litter must be lost to show effect”

Answer 172

1) Major transport medium: - Blood transports many substances like glucose, O2, CO2, end products of metabolism as urea, and hormones 2) Hemostatic function: - Stoppage of bleeding from injured blood vessel by platelets and clotting 3) Homeostatic function: - Keeping the composition (pH, electrolytes, and water) of the internal environment (ECF) constant. - This is done by continuous exchange of substances between the interstitial fluid (ECF) and blood then between the blood and the external environment through the gastrointestinal tract, lungs, kidneys, and skin. 4) Defensive function: - WBCs provide the main defense mechanisms against a wide variety of micro-organisms through phagocytosis and the formation of antibodies

Answer 173

- Its diameter → 7.5 um. - Its thickness → at the thickest point is about 2.5 um. - Its average volume → 90 to 95 u3.

Answer 174

RBCs are not true cells, because they have no nuclei, so called corpuscles. 1) The cell membrane: - They are surrounded by a plastic semipermeable membrane and has a large surface area, so RBCs are biconcave 2) Its contents: - Hb is the main constituent of RBCs "carry o2" (34% of their weight). "Third!" - K ion is the chief intracellular cation. - Carbonic anhydrase enzyme, which is important for CO2 transport. - NO Mitochondria in the RBCs, so they obtain their energy from anaerobic glycolysis. “For ion balance for example”

Answer 175

- It is an iron-containing red pigment that is present inside RBCs. ``` - contents:  in adult males→ 14-18 gm/dl "more RBCs"  in adult females→ 12-16 gm/dl  in newborn → 18 gm/dl  in children → 12 gm/dl ```

Answer 176

1) Functions of cell membrane: ❖ It has a large surface area than the actual cell volume: - It gives RBCs its biconcave shape. - It allows easy diffusion of gases through the cell membrane. ❖ It is plastic, so it enhances cell flexibility to allow RBCs to be squeezed in small capillaries without rupture of it. ❖ It keeps Hb inside RBCs, so prevent its loss in urine: - Filtration of Hb into glomeruli causes its precipitation in renal tubules and acute renal failure. 2) Functions of Hb: ❖ It transports CO2 "with carbonic anhydrase enzyme" and O2 between lungs and tissues. ❖ It is an excellent acid-base buffer. "Maintains pH" 3) Functions of carbonic anhydrase enzyme: ❖ It helps in the transport of CO2. "In the form of HCO3" 4) Blood viscosity: ❖ RBCs share in the production of blood viscosity, which maintains arterial blood pressure (ABP).

Answer 177

8- 12 days "Short"

Answer 178

Have a role in hemostasis: - Release of V.C. substances such as serotonin and thromboxane A2. - Formation of a primary hemostatic plug. - Release of platelet phospholipids (PF3) which is essential for blood clotting. - Stabilization of the blood clot and induction of clot retraction. - Help repair the damaged vessel wall.

Answer 179

Formed in the bone marrow

Answer 180

 60-70% (neutrophils) “ as they are continuously lost”  1-5% (eosinophils)  0.0-1.0% (basophils)

Answer 181

The first line of defense against bacterial infection by phagocytosis

Answer 182

- Defense against parasitic infection e.g. schistosomiasis | - Prevent the spread of the local inflammatory during an allergic reaction

Answer 183

- Synthesize and liberates heparin (anticoagulant) into the blood. - Releases histamine, serotonin, and bradykinin during allergic reactions.

Answer 184

Formed in the lymphoid tissues. 20-30%

Answer 185

Formed in bone marrow 3-8%

Answer 186

months or even years “Very long”

Answer 187

 T lymphocytes for cell-mediated immunity |  B lymphocytes secrete antibodies

Answer 188

Phagocytosis "100 and doesn't dye" of bacteria and old cells such as RBCs by forming tissue (fixed) macrophage system or reticuloendothelial system (RES)

Answer 189

It is the process of formation of blood cells

Answer 190

In the early few weeks of embryonic life  blood cells are produced in the yolk sac. In the middle trimester of gestation  blood cells are produced in the liver, spleen, and lymph nodes. (RES) In the last trimester and after birth  hematopoiesis is restricted to the red bone marrow (bone marrow of all bones). After the age of 20 years  the bone marrow of all long bones becomes fatty and the RBCs are produced only by the membranous (flat) bones, such as the vertebrae, sternum, ribs, and ilia.

Answer 191

All blood cells originate from pluripotential hematopoietic stem cells (PHSCs), which divide and differentiate into 2 cells lines by hemopoietic growth factors: 1) Lymphoid stem cells: gives rise to lymphocytes, which include the T cells, B cells, and natural killer (NK) cells. These cells quickly migrate from the bone marrow to lymphatic tissues e.g. lymph nodes, spleen, and thymus. 2) Myeloid stem cells: gives rise to all the other formed elements, including the RBCs; megakaryocytes that produce platelets; and a myeloblast lineage that gives rise to monocytes and granular leukocytes: neutrophils, eosinophils, and basophils

Answer 192

``` Hemopoietic growth factors Healthy bone marrow. Healthy liver Hormones Nutritional factors ```

Answer 193

- It is a glycoprotein hormone secreted in the adults by the kidney (90%) and liver (10%) and during fetal life, is formed mainly by the liver.

Answer 194

Its secretion is stimulated mainly by hypoxia "Low o2 due to low RBCs", cobalt and androgens.

Answer 195

It acts on stem cells to differentiate them into proerythroblasts and on proerythroblasts to differentiate them into mature RBCs.

Answer 196

Is a glycoprotein hormone, is produced by the liver and kidneys.

Answer 197

Stimulates the production of megakaryoblasts and the development of megakaryocytes into platelets

Answer 198

60-75% of platelets are released in the blood and 25% are trapped in the spleen, so splenectomy rises the platelets levels in the blood (thrombocytosis)

Answer 199

Are glycoproteins secreted by a wide variety of cells, including red bone marrow, leukocytes, macrophages, fibroblasts, and endothelial cells. It includes 2 groups:

Answer 200

a) Colony-stimulating factors (CSFs): 1) Granulocyte CSFs: trigger the differentiation of myeloblasts into granular leukocytes (neutrophils, eosinophils, and basophils). 2) Monocyte CSF: induces the production of monocytes 3) GM-CSF: induce the production of both granulocytes and monocytes 4) granulocytes, monocytes, platelets, and erythrocytes are stimulated by multi-CSF. b) Interleukins: interleukin 3, promotes the growth and reproduction of virtually all the different types of committed stem cells. "First step"

Answer 201

 Healthy bone marrow is essential to produce RBCs and other blood cells  Destruction of bone marrow by irradiation or chemicals, drugs leads to deficiency of all blood cells (aplastic anemia).

Answer 202

A healthy liver is essential for normal RBC formation and Platelets because it is the site for secretion of erythropoietin and thrombopoietin and stores iron and Vit B12

Answer 203

Most hormones including thyroid hormones, androgens "testosterone, that's why males have more RBCs" and glucocorticoids are essential for hematopoiesis, as they promote tissue metabolism in general.

Answer 204

1) Proteins: ❖ Animal proteins (high biological value proteins) that present in the liver, kidney, and muscles are superior in the production of RBCs to other proteins 2) Minerals: ❖ Copper and cobalt act as cofactors in hemoglobin synthesis. ❖ Iron is essential for heme synthesis 3) Vitamins: ❖ All vitamins are needed for hematopoiesis especially vitamin B12 and folic acid ❖ Vitamin B12 and folic acid are important for the final maturation of the blood cells because they are essential for the synthesis of DNA ❖ Deficiency of either vitamin B12 or folic acid causes megaloblastic anemia, Leukopenia, and thrombocytopenia.

Answer 205

is a ↓ in O2 carrying capacity of blood due to deficiency of Hb which can be caused by either ↓ed number of RBCs or too little Hb in the cells.

Answer 206

1) Blood loss anemia: due to blood loss as in hemorrhage, 2) aplastic “ALL BLOOD CELLS” anemia: due to failure of functions of bone marrow 3) megaloblastic anemia: due to lack of Vit B12 and folic acid and "causes rupture" 4) hemolytic anemia: due to excessive RBCs destructions as in thalassemia "disturbance in HB synthesis"

Answer 207

is a bleeding disorder (manifested by red spots in the skin) due to deficiency in platelets count (thrombocytopenia) or functions (non-thrombocytopenic purpura)

Answer 208

include: 1) Leucopenia means WBCs count is less than 4000/mm3 2) Leukocytosis means WBCs count is more than 11000/ mm3 3) Leukemia means an abnormal increase in the number of WBCs (cells are immature and undifferentiated cells)

Answer 209

Synthetic forms of CSF and interleukin hormones are often administered to patients, with various forms of cancer who are receiving chemotherapy, to revive their WBC counts.

Answer 210

Prevention of blood loss after injury.

Answer 211

- Vascular spasm: occurs immediately after the blood vessel has been cut - Formation of a platelet plug (temporary hemostatic plug). - Formation of a blood clot (definitive hemostatic plug). - Fibrosis of the blood clot to close the hole in the vessel permanently.

Answer 212

- Nervous reflexes are initiated by the pain from the traumatized vessel. - Local myogenic contraction due to direct damage. - Local vasoconstrictor factors as serotonin and thromboxane A2 (from platelets).

Answer 213

Transverse cut & traumatized vessels "nervous reflex"

Answer 214

The vascular spasm reduces the flow of blood from the vessel rupture.

Answer 215

☺ It is extensively invaginated membrane with a complex canalicular system that allow contact with the ECF. ☺ Contain a coat of glycoprotein • Repulses adherence to normal endothelium • Allow adherence to the injured vessel wall. ☺ Contains large amounts of phospholipids • Play several roles in the process of blood clotting.

Answer 216

Contains many active structures as: - Contractile proteins for platelet contraction as actin, myosin, and thrombosthenin - Residual of both endoplasmic reticulum and Golgi apparatus for synthesis of enzymes and storage of Ca2+. - Mitochondria • Can form ATP & ADP. - Enzyme system • Can synthesize prostaglandins - Clotting factors as fibrin-stabilizing & von Willebrand factors - A growth factor that helps repair damaged vessel walls.

Answer 217

Platelet adhesion Platelet activation Platelet aggregation

Answer 218

Such adhesion is potentiated by the von Willebrand factor (a glycoprotein presents in the plasma and subendothelial tissue) and the platelets membrane glycoprotein

Answer 219

When a blood vessel is injured, the platelets adhere to the exposed subendothelial collagen.

Answer 220

Initiated by platelet adhesion.

Answer 221

- The activated platelets swell, develop pseudopodia, become sticky, and discharge their granules mainly ADP. - Also, its enzyme system is activated to form thromboxane A2. "VC"

Answer 222

- The released ADP and thromboxane –A2 activate the nearby platelets, Making them stickier and adhere to the originally activated platelets and release ADP and thromboxane – A2 which, in turn, activates more and more platelets. - Thus, a vicious circle of platelets activation and aggregation is elicited leading to the formation of a loose platelet plug. "Purpura is due to non-formation or non-function of platelets"

Answer 223

Salicylates (aspirin) can inhibit the thromboxane –A2 formation and so inhibits platelets activation and aggregation.

Answer 224

Platelet plugs are extremely important for closing the minute ruptures occurring in the wall of vessels many thousand times daily

Answer 225

The active process occurs within 3-6 minutes.

Answer 226

- The clotting process is initiated by active substances from the traumatized vascular wall, platelets, and coagulation factors. - The clotting process to occur, certain factors named clotting factors (plasma protein of beta globulin type) must be activated.

Answer 227

- Plasma proteins of beta globulin type, are proteolytic enzymes present in an inactive form

Answer 228

Factor I: Fibrinogen Factor II: Prothrombin Factor III: Tissue thromboplastin Factor IV: Calcium ions (Ca++) Factor V: Proaccelerin or labile factor - ------- Prekallikrein - ------- HMW kininogen - ------- Platelets F3 Factor VII: Proconvertin or stable factor Factor VIII: Antihaemophilic factor Factor IX: Christmas factor Factor X: Stuart prewar factor Factor XI: Plasma thromboplastin antecedent Factor XII: Hegeman factor Factor XIII: Fibrin stabilizing factor

Answer 229

 Formation of prothrombin activator  Conversion of prothrombin into thrombin  Conversion of fibrinogen into fibrin

Answer 230

It is initiated by contact of blood with traumatized vascular walls or extra-vascular tissues.

Answer 231

It is a rapid process and occurs according to the following steps: - Traumatized tissues release a complex of several factors called tissue thromboplastin (composed of phospholipids and lipoprotein that functions as a proteolytic enzyme). - The lipoprotein of tissue thromboplastin activates factor VII and then complexes with it. • This complex in the presence of Ca2+ and tissue phospholipids act on factor X to form activated factor X - Formation of the prothrombin activator. • The activated factor X complexes immediately with the tissue phospholipids, Ca2+and with activated factor V to form the complex called prothrombin activator.

Answer 232

It begins with trauma to the blood itself or exposure of the blood to collagen from a traumatized vessel wall or contact of the blood with water – wettable surface e.g., glass.

Answer 233

It continues through the following series of cascading reactions: 1) Trauma to the blood or exposure of the blood to vascular wall collagen "slow blood flow, roughy intima" 2) leads to 2 effects; first, activation of factor XII; second, the release of platelet phospholipids (platelet factor 3 or PF3). 3) The activated factor XII activates factor XI. • This reaction requires high molecular weight kininogen (HMW) and is accelerated by prekallikrein 4) The activated XI acts on factor IX to activate it. 5) The activated factor IX together with factor VIIIa and platelet phospholipids (PF3) activate factor X. 6) The activated factor X combines with activated factor V, Ca2+, and platelets phospholipids to form the prothrombin activator

Answer 234

In vivo, 15-20 sec In vivo and vitro, 3-6 min

Answer 235

After the prothrombin activator has been formed, it causes the conversion of prothrombin to thrombin in the presence of sufficient amounts of Ca2+.

Answer 236

- Formed thrombin removes 4 low-molecular-weight peptides from each molecule of fibrinogen, forming a molecule of fibrin monomer. - Many fibrin monomer molecules polymerize within seconds into long fibrin threads that constitute the meshwork of the clot. - Within a few minutes after the clot is formed a substance called fibrin stabilizing factor, released from the platelets, strengthens the fibrin meshwork by adding more and more bonds between the fibrin monomer molecules and formation of multiple cross-linkages between the fibrin thread. - Finally, the firm blood clot is formed which is composed of a meshwork of fibrin threads running in all directions and entrapping blood cells, platelets, and plasma.

Answer 237

- It can become invaded by fibroblasts, which subsequently form connective tissue till the clot is completely organized into fibrous tissue within about 1 to 2 weeks. "Permanent healing" • This course usually happened with the clot that is formed in a small hole in the vessel wall. - It can dissolve: • This usually occurs with the clots formed in the tissues.

Answer 238

- Except for the first two steps in the intrinsic pathway, Ca2+ is required for acceleration of all the blood clotting reactions. - Therefore, in the absence of Ca2+, blood clotting by either pathway does not occur.

Answer 239

either by de-ionizing the calcium by addition of citrates or by precipitating the calcium by oxalates.

Answer 240

Vitamin K "from the colon" is necessary for the liver formation of five important clotting factors, prothrombin, factor VII, Factor IX, Factor X, and protein C. "1972"

Answer 241

In the absence of vitamin K, deficiency of these coagulation factors results in serious bleeding tendencies (so it is called antihemorrhagic vitamin).

Answer 242

- They become attached to the fibrin threads in a way that they bind different threads together. - Platelets secrete fibrin stabilizing factor (factor XII) which causes more cross-linking bonds between the fibrin threads. - Activation of the platelet contractile proteins by thrombin and Ca2+ cause strong contraction of the platelet attached to the fibrin.

Answer 243

the edges of the broken blood vessels are pulled together, thus contributing to the ultimate state of hemostasis.

Answer 244

After a clot is formed, it begins to contract & a clear yellowish fluid is squeezed called serum

Answer 245

1) Induces vascular spasm (serotonin & thromboxane A2) 2) Formation of primary platelet plug 3) Release of platelets phospholipid (Pf 3) which is essential for clotting mechanism. 4) Stabilization of blood clot (fibrin – stabilizing factor) 5) Clot retraction (Ca2+). 6) Repair of damaged vessels wall (platelet-derived -growth factor)

Answer 246

Endothelial surface factors and blood factors

Answer 247

"Smooth glycocalyx and thrombomodulin" 1) The smoothness of the endothelial surface: prevent contact activation of the intrinsic system. 2) Presence of a layer of glycocalyx (mucopolysaccharide) on the endothelium: repels clotting factors and platelets, thereby preventing activation of clotting process. 3) Presence of Thrombomodulin: - a protein bound with the endothelial membrane which binds thrombin. - the thrombomodulin thrombin complex activates a plasma protein called Protein-C, that inactivates activated factor V and VIII.

Answer 248

"Adsorption of antithrombin III and heparin to the fibrinolytic system" 1) Adsorption of about 85 to 90% of the thrombin formed from prothrombin to the fibrin threads this prevents excess spread of the clot. 2) Antithrombin III: The thrombin that does not adsorb to the fibrin "the remaining 15%" threads soon combines with antithrombin III, which further blocks the effects of thrombin, then inactivates it. 3) Heparin: - A powerful anticoagulant that produced mainly by mast cells and small amounts formed by blood basophil cells. - The heparin secreting mast cells are abundant in tissues surrounding lungs & liver. 4) The presence of fibrinolytic system that continuously removes small clots

Answer 249

- Heparin by itself, has little or no anticoagulant property. - It acts as cofactor for anti-thrombin III. When it combines with antithrombin III, the effectiveness of anti-thrombin III in removing thrombin increases about 100-1000 times. - Also, the heparin–antithrombin complex removes several other activated coagulation factors e.g., factor XII, XI, IX and X.

Answer 250

is one of plasma proteins present in an inactive form and when activated it is converted to plasmin (or fibrinolysin).

Answer 251

- A proteolytic enzyme that digests the fibrin threads as well as other coagulant factors as fibrinogen, factor V, factor VIII, prothrombin, and factor XII. - Plasmin can cause complete lysis of the blood clot.

Answer 252

This occurs via a group of substances called plasminogen activators. They include: 1) Tissue plasminogen activator (t-PA) 2) Other plasminogen activators

Answer 253

- When a clot is formed, a large amount of plasminogen is trapped in the clot along with other plasma proteins. - The injured tissues and vascular endothelium very slowly release a powerful activator called tissue plasminogen activator that eventually converts plasminogen to plasmin few days after the clot has stopped the bleeding. "Unlike tissue thromboplastin which is secreted quicker" - The formed plasmin in turn removes the remaining blood clot.

Answer 254

- Thrombin and active factor XII. - Urokinase: it prevents the formation of blood clots in the urinary tract. - Streptokinase: derived from certain types of bacteria known as haemolytic streptococci and is used for treatment of early acute myocardial infarction to dissolve the clot.

Answer 255

- The liver produces a t-PA inhibitor called antiplasmin that inhibit the t- PA and delays the fibrinolysis. - The protein-C inactivates this inhibitor and consequently stimulates fibrinolysis. "As well as inactivation of factor five and factor eight'

Answer 256

“SUMIIIII” S: Many Small blood vessels in which the blood flow has been blocked by clots are reopened by fibrinolysis. U: It prevents the blood clotting inside the Urinary tract "urokinase" and prevents clotting of the menstrual blood. MI: The stimulation of fibrinolysis is used clinically in early management of acute Myocardial Infarction. This is accomplished either by intravenous injection of t-PA or injection of Streptokinase or urokinase locally in the clot via a cardiac catheter.

Answer 257

These are the substances used to prevent blood clotting.

Answer 258

A) In vitro anticoagulants “prevent intrinsic” | B) In vivo anticoagulants

Answer 259

1) Collecting blood in smooth bags lined with silicone. 2) Precipitation of calcium by citrate. 3) Addition of heparin. 4) Addition of EDTA (ethylene – diamine tetra-acetic acid). It chelates the Ca2+ in the blood.

Answer 260

Are used to prevent clotting outside the body.

Answer 261

Are used to prevent clotting inside the body.

Answer 262

Heparin Coumarin derivatives as dicumaroul & warfarin

Answer 263

It is a naturally occurring anticoagulant used in the treatment of intra-vascular thrombosis, It is formed by mast cells and basophil leucocytes.

Answer 264

The action of heparin (acidic) can be neutralized by adding protamine (basic protein) which forms an irreversible complex with heparin.

Answer 265

They inhibit the action of vitamin K in the liver through competitive inhibition with subsequent decreased synthesis of factors II, VII, IX, and X as well as protein C.

Answer 266

Origin: Mast cells and basophils - Plant Mode of action: -Activates antithrombin III thereby inactivating thrombin, factors IX, X and XI -Competitive inhibition with vit. K in liver, so it inhibits the formation of prothrombin, factors VII, IX & X. Site of action: in vivo and in vitro - only in vivo Route of administration: I.V or I.M. "May cause hematoma" - oral Onset: Rapid - slow Duration: short "should be repeated" - long Antidote: Protamine sulphate 1% + Fresh blood transfusion - Vit K

Answer 267

In vitro anticoagulants : • Ca++ → deionization by citrate. → Precipitation by oxalate. → Chelation of Ca++ by EDTA * Collecting of blood in ''unwettable'' silicone coated tubes , that prevent activation of factor XII. * Addition of heparin.

Answer 268

A) Conditions that cause excessive bleeding. 1. Purpura 2. Vitamin K deficiency 3. Hemophilia: deficiency of factors VIII, IX, or X B) Conditions that cause excessive intra vascular clotting.

Answer 269

- It is a congenital sex linked; recessive disease carried on X chromosome. - It is carried by females and manifested always in males.

Answer 270

Deficiency of factor VIII, IX, or XI. So, there are three types of hemophilia.

Answer 271

-Hemophilia A:  Is the classic hemophilia.  It is caused by deficiency of factor VIII and represents 85% of cases of hemophilia. -Hemophilia B:  Is due to absence of factor IX. -Hemophilia C:  Is due to absence of factor XI.

Answer 272

-Hemophilia is characterized by:  Excessive bleeding after mild trauma.  Whole blood coagulation is prolonged.

Answer 273

- Capillaries are the smallest blood vessels in the body, connecting the smallest arteries to the smallest veins. These vessels are often referred to as the "microcirculation."

Answer 274

- They are responsible for facilitating the transport and exchange of gases, fluids, and nutrients in the body.

Answer 275

- Metarterioles branch into the capillary beds. At the junction of the arterioles and capillaries is a smooth muscle band called the precapillary sphincter.

Answer 276

- True capillaries "those of nutritional benefit" do not have smooth muscle; they consist of a single layer of endothelial cells surrounded by a basement membrane.

Answer 277

- Clefts (pores) between the endothelial cells allow passage of water- soluble substances. The clefts represent a very small fraction of the surface area.

Answer 278

1. Lipid-soluble substances: include O2 and CO2; cross the membranes of the capillary endothelial cells by simple diffusion. 2. Small water-soluble substances: include water, glucose, and amino acids; cross via the water-filled clefts between the endothelial cells. - Generally, protein molecules are too large to pass freely through the clefts. - In the brain, the clefts between endothelial cells are exceptionally tight (blood–brain barrier). - In the liver and intestine, the clefts are exceptionally wide and allow passage of protein. These capillaries are called sinusoids. 3. Large water-soluble substances: can cross by pinocytosis.

Answer 279

- Blood usually does not flow at a continuous rate through capillaries, but it flows intermittently. The cause of this intermittency is the phenomenon called vasomotion.

Answer 280

- is intermittent contraction of the metarterioles and precapillary sphincters➔alternating cycle of constriction and relaxation for 5-10 times/minute so that only 10-20% of cap are opened at a time.

Answer 281

it is controlled mainly by O2 concentration in the tissues. -Decrease O2 concentration leads to: ✓ Increase intermittent periods of BF. ✓ Increase duration of each period. "To supply more o2" Which Allows blood to carry increased quantities of O2 to tissues.

Answer 282

- At the arterial end, the pressure is about 30-35 mmHg. - At the venous end it is about 10-15 mmHg. - At the middle of the capillary is 25 mmHg.

Answer 283

The capillary BP may be influenced passively by extracapillary factors, and actively by the contraction of the capillaries themselves.

Answer 284

a. The diameter of arterioles: Arteriolar VD→ Inc. capillary BF and--->capillary BP and vice versa. b. The venous pressure:the venous pressure→ Inc. capillary BP and dec. capillary BF. "Due to the closure of the Venous outflow and continuous flow from arterioles" c. Gravity: in areas above the heart→ Dec. capillary BP, however in areas below the heart→ Inc. capillary BP by antagonizing venous return.

Answer 285

The actual cause of capillary contraction is not yet known, but it may be due to: a. Contraction of the precapillary sphincter. b. Contraction of smooth muscle fibers in the wall of the metarterioles.

Answer 286

-Fluid flux across the capillary is governed by the 2 fundamental forces that cause water flow: ➢ Hydrostatic force, which is simply the pressure of the fluid. ➢ Osmotic (oncotic) force, which represents the osmotic force created by solutes that do not cross the membrane. - Each force exists on both sides of the membrane. Filtration is the movement of fluid from the plasma into the interstitium, while absorption is movement of fluid from the interstitium into the plasma.

Answer 287

- About 20 liters of fluid are filtered every day at the arterial ends of capillaries, 18 liters of them are reabsorbed back at the venous ends, and the remaining 2 liters are drained by the lymphatic system.

Answer 288

1. The capillary hydrostatic pressure (Pc). "The main filtering force" 2. The interstitial fluid hydrostatic pressure (Pi). 3. The plasma colloid osmotic pressure (πc). 4. The interstitial fluid colloid osmotic pressure (πi). Starling 's principle states that: " the rate & direction of fluid movement is proprotional to the algabric sum of hydrostatic and osmotic forces"

Answer 289

An increase in Pc favors filtration out of the capillary.

Answer 290

■ Pc is determined by arterial and venous pressures and resistances. ■ An increase in either arterial or venous pressure produces an increase in Pc; increases in venous pressure have a greater effect on Pc.

Answer 291

■ It is 30 mmHg in the arterial end, 10 mmHg in the venous end. The functional mean capillary pressure is about 17.3 mmHg (i.e. it is the average effective pressure).

Answer 292

An increase in πi favors filtration out of the capillary.

Answer 293

- is determined by the concentration of protein in the interstitial fluid. Normally the small amount of protein that leaks to the interstitium is minor and is removed by the lymphatics. Under most conditions, this is not an important factor influencing the exchange of fluid.

Answer 294

- The average protein concentration of the interstitial fluid is about 3 gm/100 ml. - resulting in average colloid osmotic pressure of about 8 mmHg. "Small effect"

Answer 295

An increase in πc opposes filtration out of the capillary.

Answer 296

■ πc is increased by increases in the protein concentration in the blood (e.g., dehydration). ■ πc is decreased by decreases in the protein concentration in the blood (e.g., nephrotic syndrome, protein malnutrition, liver failure). ■ Small solutes do not contribute to πc.

Answer 297

■ Albumin is the most abundant plasma protein and thus the biggest contributor to this force.

Answer 298

■ The colloidal osmotic pressure or the oncotic pressure of normal human plasma average about 28 mmHg.

Answer 299

■ An increase in Pi opposes filtration out of the capillary.

Answer 300

■ It is about -3 mmHg "causes suction as it is connected to lymphatics that drain fluids" and is called negative interstitial fluid pressure.

Answer 301

A. Forces moving the fluid outward: - Capillary pressure 30 - Negative interstitial fluid pressure 3 - Interstitial fluid colloid osmotic pressure 8 Total outward force 41 B. Forces moving the fluid inward - Plasma colloid osmotic pressure 28 Summation of the forces: Outward force 41 Inward force 28 Net outward force: 13 Thus 13 mmHg filtration pressure occurs at the arterial ends of the capillaries.

Answer 302

At the venous end of the capillary: A. Forces tending to move fluid outward: - Capillary pressure 10 - Negative interstitial fluid pressure 3 - Interstitial fluid colloid osmotic pressure 8 Total outward force 21 B. Forces tending to move fluid inward: - Plasma colloid osmotic pressure 28 Summation of forces: Outward force 21 Inward force 28 Net inward force: 7 -Thus 7 mmHg is the reabsorbing pressure at the venous ends of the capillaries.

Answer 303

the venous capillaries are more numerous and more permeable so it reabsorbs about 9/10 of the fluid, the remainder flows into the lymph vessels.

Answer 304

- The veins conduct the blood from the tissues to the heart. They accommodate the main bulk of blood volume (about 60%)

Answer 305

1. Drainage of blood from all parts of the body to the heart. Also the lymph drainage opens into the venous system. 2. They act as blood reservoirs; they contain about 3 liters of blood. 3. By means of venous pump, it aids in propelling the blood forward (towards the heart) and helps to regulate the cardiac output.

Answer 306

- It is a point in the circulation, lies 5-7 cm below the diaphragm, at which the venous pressure (VP) is kept constant at 10-11 mmHg, independent of the body posture. - VP below this point increases and above this point decreases.

Answer 307

- It is the venous pressure in big veins at their entrance with the right atrium, or the intrathoracic portions of vena cavae. - It averages 4.6 mmHg in recumbancy and 2 mmHg on standing It is 2 mmHg during inspiration and 6 mmHg during expiration.

Answer 308

- Positive intrathoracic pressure like straining - Congestive heart failure "Due to fullness with blood” - hypervolemia (blood transfusion) - Sympathomimetics due to venoconstriction and increasing the venous return

Answer 309

- Negative intrathoracic pressure during respiration - Standing (CVP decreases to 2 mm mercury) - Hypovolemia (hemorrhage) - Sympatholytics due to venodilation and decreasing the venous return

Answer 310

``` 1- Gravity or posture 2- Rate of blood inflow into veins 3- Rate of blood outflow from veins 4- Venomotor tone 5- Blood volume 6- Muscular exercise 7- Respiratory movement ```

Answer 311

- In recumbent position gravity has no effect on circulation. - On standing, PVP is increased in lower limbs to 90 mmHg in feet veins and CVP is decreased from 4.6 mmHg to 2 mmHg→ Dec. venous return→ Dec COP → decABP (postural hypotension) in prolonged standing.

Answer 312

- Vasodilatation of arterioles without capillary dilatation→Inc CVP and PVP and vice versa. - If the capillaries are dilated, they accommodate blood and decrease the blood inflow to veins→ Dec CVP and PVP.

Answer 313

- Normally, the rate of blood inflow into veins equals the rate of its outflow. “Due to venous congestion or due to inc in intrathoracic pressure” - If the outflow is less than the inflow→ Dec the venous return→Inc CVP and PVP

Answer 314

- Tonic contraction in veins maintains normal VP. | - inc venous tone due to sympathetic stimulation or noradrenaline→ Inc CVP and PVP are vice versa.

Answer 315

- CVP and PVP are increased in hypervolaemia (blood transfusion). - CVP and PVP are decreased in hypovolaemia (haemorraghe).

Answer 316

- Contracting skeletal muscle press on veins, increasing the VP. - Arteriolar dilatation of active muscle, increasing the VP. - However VP is not much increased in exercise, due to increase the outflow from veins because the heart rate and the stroke volume are increased during exercise.

Answer 317

- Inspiration: The diaphragm descends → inc VP in abdominal veins and dec VP in intrathoracic veins→ Inc VR. - Expiration: the opposite effect occurs.

Answer 318

■ One-way flap valves permit interstitial fluid to enter, but not leave, the lymph vessels. ■ Flow through larger lymphatic vessels is also unidirectional.

Answer 319

1. Drainage of excess interstitial fluid filtered from capillaries back to blood. 2. Drainage of filtered proteins. 3. Absorption of fat from the intestine. 4. The lymph nodes have the following functions: - Filtration of lymph (i.e. by removing foreign substances from it). - Formation of lymphocytes. - Take part in the formation of immune bodies.

Answer 320

Normally, the lymph flows towards the thorax; it is maintained by the following factors: 1. Rhythmic contraction of smooth muscles in the wall of the lymphatic vessels. "Like veins and arteries" 2. Skeletal muscle contraction compresses the lymph vessels → inc lymph flow. 3. Arterial pulsations are mechanically conducted to lymph vessels, which may help lymph flow. 4. Gravity helps the lymph flow from parts above the level of the heart, but antagonizes it from parts below the level of the heart. 5. The hydrostatic pressure of the interstitial fluid is normally negative (- 3 mmHg), this helps the lymph flow. "Suction force"

Answer 321

The lymph flow increases as a result of increased rate of tissue fluid formation. This occurs in the following conditions: 1. Dilatation of the capillaries and arterioles ➔ increase capillary filtration and increase lymph flow. 2. Venoconstriction➔increase capillary pressure➔increase filtration and lymph flow. 3. Increased tissue activity→accumulation of metabolites→dilatation of the arterioles and precapilalry sphincters. 4. Lymphagogues: These are substances that increase the lymph flow. They act mainly by increasing fluid filtration into the tissue spaces as histamine and bradykinin.

Answer 322

Edema is the accumulation of fluid in the interstitial space

Answer 323

Intracellular non-pitting and extracellular fitting

Answer 324

Means edema due to increased intracellular fluid (i.e. intracellular swelling). It results from disturbance of the membrane permeability. "May be Due to a problem in sodium potassium pump"

Answer 325

Occurs when there is excess fluid accumulation in the extracellular spaces i.e. increased interstitial fluid.

Answer 326

Significant alterations in the Starling forces, which then tip the balance toward filtration, increase capillary permeability and/or interrupt lymphatic function, resulting in edema.

Answer 327

▪ Arteriolar dilatation as in fever. ▪ Increased venous pressure as in congestive heart failure, venous obstruction and pregnancy. "Due to enlarged uterus" ▪ Extracellular volume expansion.

Answer 328

Decreased plasma protein concentration to 5 gm% as in: ▪ Severe liver disease (failure to synthesize proteins). ▪ Protein malnutrition. ▪ Nephrotic syndrome (loss of protein in urine).

Answer 329

It leads to excessive fluid and protein filtration, so edema develops as in: ▪ Burn ▪ Inflammation (release of histamine; cytokines) ▪ Allergy (allergic edema) due to histamine release ▪ Vitamin C deficiency. ▪ Bacterial toxins.

Answer 330

Accumulation of tissue fluid and protein in tissue spaces produces edema as in: ▪ Infections (e.g. filaria) produce edema called elephantiasis and it is non pitting. ▪ Cancer produces cancer edema and it is non pitting. ▪ Surgical: due to interruption of lymphatic vessels. ▪ Congenital absence of lymphatics.