Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSL205 Basic Human Physiology > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

Cardiac Cycle

A
  • Events associated with the flow of blood through the heart during a single complete heartbeat - systole (contraction) + diastole (relaxation)
  • Valves open passively due to pressure gradients
    • AV valves open when pressure in the atria > ventricles
    • Semilunar valves open when pressure in the ventricles > arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Phases of the Cardiac Cycle

A
  1. F - Ventricular Filling
  2. C - Isovolumetric Ventricular Contraction
  3. E - Ventricular Ejection
  4. R - Isovolumetric Ventricular Relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Phases of the Cardiac Cycle: Ventricular Filling

A

DIASTOLE

  • Pressure in atria > ventricles -AV valves open
  • Passive phase: No atria or ventricular contraction
  • Active phase: Atria contracts
  • End of the phase has the atrial contraction that has a little squeeze to fill the rest of the ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Phases of the Cardiac Cycle: Isovolumetric Ventricular Contraction

A

SYSTOLE

  • Ventricle contracts and increases pressure
  • AV and semilunar valves closed
  • No blood entering or exiting the ventricle
  • Ends when ventricular pressure is high enough to open semilunar valves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Phases of the Cardiac Cycle: Ventricular Ejection

A

SYSTOLE

  • Pressure in ventricles > arteries
  • Semilunar valves open
  • Pressure peaks and slowly decreases as the blood leaves the ventricle
  • Ends when semilunar valve closes (Artery pressure > ventricle pressure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Phases of the Cardiac Cycle: Isovolumetric Ventricular Relaxation

A

DIASTOLE

  • Ventricle relaxes and decreases pressure
  • AV and semilunar valves closed
  • No blood entering or exiting ventricle
  • Ends when the pressure is low enough to permit AV valve to open again
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ventricular Pressure

A

Atrial Pressure: During filling phase, the final squeeze is the bump shown, marking the start of contraction

Ventricular Pressure

  • During the filling phase, there is the little bump with the atrial contraction
  • During contraction phase there is a huge increase in pressure due to the doors being closed
  • During relaxation, pressure falls to almost nothing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aortic Pressure

A
  • Ventricle contracts and dumps all the blood into the aorta
  • Aorta has to deliver all the blood to the body
  • During FILLING phase, no blood is entering the aorta, but releasing the blood for the previous phase to the body, causing decrease in aortic pressure until it reaches the minimum called DIASTOLIC PRESSURE
  • During EJECTION phase, semilunar valve opens causing pressure to increase to a maximum called the SYSTOLIC PRESSURE, which is used to pump blood into the body
  • Pressure then falls because blood leaves faster than it comes in and so it is leaky (at the end of ejection phase)
  • DICHROTIC NOTCH notes the end of the relaxation phase
  • MEAN ARTERIAL PRESSURE represents the pressure (driving force) needed to deliver blood to the systemic blood (this is what is measured at the doctor’s office)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ventricular Volume

A
  • End Diastolic Volume (EDV): Volume of blood in ventricle at the end of diastole (max ventricular volume)
  • End Systolic Volume (ESV): Volume of blood in ventricle at the end of systole (min ventricular volume)
  • Stroke Volume: Volume of blood ejected from ventricle each cycle; About 65 mL of blood remaining in the ventricle at rest
  • SV = EDV - ESV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Heart Sounds

A
  • Due to turbulent flow when valve closes
  • Correspond to beginning of contraction and relaxation when the valves close
  • First Heart Sound: Soft lubb, AV valve closes
  • Second Heart Sound: Louder dubb, SL valves close
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cardiac Output

A
  • Volume of blood pumped by each ventricle per minute
  • Autonomic input to the heart
  • CO = SV x HR
  • Average CO = 5 liters/min at rest
  • Average blood volume = 5.5 liters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Regulation of Cardiac Output

A
  • Regulate HR and SV
  • Extrinsic and intrinsic regulation
    • Extrinsic - neural and hormonal
    • Intrinsic - autoregulation
  • Parasympathetic innervation decreases HR via the vagus nerve projections actinge on the SA and AV nodes
  • Sympathetic innervation increases HR via cardiac nerve projections acting on the SA and AV nodes, and the ventricular myocardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

SA Node Firing Rate

A
  • Determines heart rate
  • SA node intrinsic firing rate = 100/min
  • SA node under control of ANS and hormones
    • Rest: Parasympathetic dominates, HR = 75
      • Acetylcholine binds to mAChRs, which causes the T-type calcium channels to close and potassium channels to open; hyperpolarization of cell occurs
    • Excitement: Sympathetic dominates, HR increases
      • Norepinephrine/Epinephrine bind to beta 1 receptors of the heart (GPCRs), which depolarize cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

AV Nodal Innervation

A
  • Sympathetic - Increases conduction velocity through node
  • Parasympathetic - Decreases conduction velocity through node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Factors Affecting Cardiac Output: Stroke Volume

A
  • Primary factors affecting stroke volume
    • Ventricular Contractility
    • End-Diastolic Volume
    • Afterload
  • Ventricles never completely empty of blood
  • Extrinsic Controls
    • Sympathetic drive to ventricular muscle fibres
      • Cardiac nerves
      • NE binds to beta 1 adrenergic receptros and increases cardiac contractility
    • Parasympathetic innervation is not significant
    • Hormonal control
      • Thyroid hormones - insulin and glucagon - increase force of contraction
  • Intrinsic Controls - Frank-Starling’s Law
    • ​What goes into the heart, must come out of the heart
    • Increase in EDV causes stroke volume to increase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Frank-Starling’s Law

A
  1. Increaes in EDV
  2. Increase in SV

Curve shifts up with increased sympathetic activity and down with decreased sympathetic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Factors Affecting End-Diastolic Volume

A
  • End-Diastolic Pressure = preload
    • Filtering time
    • Arterial pressure
    • Central venous pressure
  • Afterload - pressure in aorta during ejection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Physical Laws Governing Blood Flow and Blood Pressure

A
  • Pressure gradients in the CV system
  • Resistance in the CV system
  • Relating pressure gradients and resistance in the systemic circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pressure Gradient Across Systemic Circuit

A
  • Pressure Gradient = Pressure in aorta - pressure in vena cava just before it empties into right atrium
  • Pressure in aorta = mean arterial pressure (MAP) = 90 mmHg
  • Pressure in vena cava = central venous pressure (CVP) = 0 mmHg
  • Pressure Gradient = MAP - CAV = 90 mmHg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Pressure Gradient Across Pulmonary Circuit

A
  • Pressure Gradient = pressure in pulmonary arteries (15 mmHg) - pressure in pulmonary veins (0 mmHg)
  • Pressure Gradient = 15 mmHg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Resistance in the Cardiovascular System

A
  • Flow through both the systemic and pulmonary circuits are equal (Flow = pressure gradient/resistance)
  • Pressure Gradient: Systemic > Pulmonary
  • Resistance: Systemic > Pulmonary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Factors Affecting Resistance to Flow

A
  • Radius is inversely proportional to resistance
  • Radius of vessel in arterioles (and small arteries) is the most important regulator of blood flow because they can regulate their radius
    • Vasodilation: Decreases resistance –> Increases flow
    • Vasoconstriction: Increases resistnace –> Decreases flow
  • The length the vessel - the longer, the higher the resistance (the lower the flow)
  • Viscocity is dependent on amount of RBCs and proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Arteries

A
  • Pressure reservoir
  • Thick elastic arterial walls - stiff and flexible
  • Low compliance - a lot of pressure with little volume
  • Expand as blood enters arteries during systole
  • Recoil during diastole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Compliance

A
  • Measure of how the pressure of a vessel will change with a change in volume (change in volume/change in pressure)
  • **Low **Compliance: Small increase in blood volume causes a large increase in pressure
  • High Compliane: Large increase in blood volume required to produce large increase in pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Arterioles

A
  • Resistance vessels
  • Part of microcirculation
  • Connect arteries to capillaries or metarterioles
  • Contain rings of smooth muscle to regulate radius, and therefore resistance
  • Vascular resistance is regulated thorugh changes in the radius of arterioles, which regulates blood flow
  • Intrinsic control of blood flow distribution to organs
  • Extrinsic control of arteriole radius and mean arterial pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Active Hyperemia

A
  • Steady State
    • O2 delivered as fast as consumed
    • CO2 removed as fast as produed
  • Increased Metabolic Rate
    • O2 consumed exceeds delivery rate
    • CO2 produced faster than being removed
    • ​Leads to vasodilation, which increases blood flow to deliver more O2 and remove more CO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Reactive Hyperemia

A
  • Increasd blood flow in response to a previous reduction in blood flow
  • Blockage of blood flow to tissue
    • Metabolites increase and oxygen decreases
    • Vasodilation
  • Release blockage
    • Increased blood flow due to low resistance
    • Metabolites removed, oxygen delivered
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Regulation by Locally-Secreted Chemicals

A
  • Vasodilators
    • Bradykinin released from inflamed tissue stimulates NO release
    • Histamine released during inflamation and allergic reactions stimulates NO release
    • Prostacyclin​
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Independent Regulation of Blood Flow During Exercise

A
  • Cardiac output increases during exercise
  • Distribution of blood does not increase proportionally
    • Dilation of vessels to skeletal muscle and heart increases blood flow to muscles
    • Constriction of vessels to GI tract and kidneys decreases blood flow to these organs
  • Disproportionate flow diverts blood to muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Arterial Blood Pressure

A
  • Pressure in the aorta
  • Varies with cardiac cycle
  • Systolic BP = maximum pressure
    • Due to ejection of blood into aorta
  • Diastolic BP = minimum pressure
    • Due to elastic recoil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Veins

A
  • Volume reservoir
  • Large diameter, but thinner walls
  • Valves allow unidirectional blood flow (only present in **peripheral **veins, not central veins)
  • High Compliance - Expand with little change in pressure
    • 60% of total blood volume in systemic veins at rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Central Venous Pressure

A
  • Pressure in the large veins of the thoracic cavity that lead into the heart
  • Pressure gradient between central veins and atria drives blood back to the heart
  • Venous pressure - arterial pressure = 5-10 mmHg
  • A decrease in venous pressure decreases driving force for venous return
  • Decrease in venous return –> decrease in EDV –> decrease in SV –> decrease in CO –> decreass in blood flow to organs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Factors that Influence Central Venous Pressure and Venous Return

A
  • Skeletal Muscle Pump
  • Respiratory Pump
  • Blood Volume
  • Venomotor Tone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Factors Affecting Central Venous Pressure and Return: Respiratory Pump

A
  • Inhale
    • Decreases pressure in the thoracic cavity and increases pressure in the abdominal cavity
    • The pressure on veins in abdominal cavity creates gradient that favours blood movement in the thoracic cavity
  • Exhale
    • Increases pressure in the thoracic cavity and decreases pressure in the abdominal cavity
    • Increass in thoracic pressure drives the forward movement of blood fmor the central veins to the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Factors Affecting Central Venous Pressure and Return: Blood Volume

A
  • Increase in blood volume –> increase venous pressure (–> increase in SDV –> increase in SV –> increase in CO)
  • Decrease blood volume –> decrease in venous pressure
  • Long term regulation of BP is through regulation of blood volume
  • Directly effects mean arterial pressure so we have a reflex mechanism to help with this (negative feedback)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Factors Affecting Central Venous Pressure and Return: Venomotor Tone

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Lymphatic System

A
  • System of vessels, nodes and organs
  • Vessels involved in returning excess filtrate to circulation
  • Vessels form open system starting at capillaries
  • Also part of immune system
  • About 3 liters a day leak out of capillaries and enters the lymphatic system
  • Relies on body movement to move it around
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Mean Arterial Pressure

A
  • Determined by…
    • Heart rate
    • Stroke volume
    • Total peripheral resistance (TPR) - the combined resistance of all the organs and blood vessels that it passes through in the systemic system
  • Calculations
    • MAP = CO x TPR = HR x SV x TPR
    • CO = HR x SV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Effects on Mean Arterial Pressure: Cardiac Output

A
  • An increase in cardiac output leads to an increase in teh volume of blood contained in the aorta and an increase in MAP when total peripheral resistance reamins the same
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Effects on Total Peripheral Resistance on Mean Arterial Pressure

A
  • A constant cardiac output leads to an increase in the volume of blood contained in the aorta and an increase in MAP when TPR increases, reduces blood flow out of aorta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Neural Control of Mean Arterial Pressure

A
  • Negative feedback loops
  • Detector - Baroreceptors
  • Integration Center - CV centers in the brainstem
  • Controllers - ANS
  • Effectors - Heart and blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Arterial Baroreceptors

A
  • Locations: Aortic arch and carotid sinuses
  • Arterial baroreceptors = sinoaortic receptors
  • Respond to stretching due to pressure changes in arteries
  • Increased arterial pressure leads to increased action potential frequency of baroreceptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Cardiovascuar Control Center

A
  • Medulla oblongata - Receives information from the baroreceptors and other sensory receptors to help calculate appropriate response of ANS
  • Intergration center for BP regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Baroreceptor Reflex

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Hemorrhage

A
  • Results in a decrease in blood volume
  • Blood volume decrease –> decrease in MAP
  • Triggers baroreceptive relfex
  • GI Tract - increased resistance and decreased blood flow
  • Brain - vasculature not subject of extrinsic control so there is not change in resistance; blood diverted from GI tract to brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Functions of Blood: Transport

A
  • Gases
    • O2: Lungs –> Tissues
    • CO2: Tissues –> Lungs
  • Nutrients
    • GI Tract –> Cells
    • Storage sites –> Cells
  • Cellular Wastes
    • Cells –> Kidney
  • Excess Water
    • Cells –> Kidney
  • Hormones
    • Endocrine glands –> Target tissues
  • Heat
    • Active tissue –> Less active tissue; or to skin and lungs for elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hematocrit

A
  • The ratio of packed erythrocytes to the total blood volume in a centrifuged sample of blood
  • Expressed as a percent
  • Males: 40-54; Females: 37-47
  • An important diagnostic tool
    • Decrease in hematocrit –> Decrease in O2 carrying capacity
    • Increase in hematocrit –> Increase in viscosity –> Increase in TPR –> Increase in BP –> Increase in work load of heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Components of Plasma

A
  • Water 90%
    • Medium of transport
    • Helps maintain body temperature
  • Electrolytes
    • Na+, Cl-, H+, Ca2+, HCO3-
  • Proteins (6-8%) - Mostly synthesized in the liver and helps to maintain oncotic osmotic pressure
  • Other
    • ​Nutrients - glucose, amino acids, lipids, vitamins
    • Wastes - urea, bilirubin, creatinine
    • Gases - dissolved (oxygen and carbon dioxide)
    • Hormones

​

  • Serum - Plasma with no plasma proteins because they are being used up in the formation of the clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Components of Plasma: Proteins

A
  • Albumins
    • Major contributor to plasma oncotic osmotic pressure
    • Carriers
  • Globulins
    • Alpha and beta
      • Carriers
      • Clotting factors
      • Enzymes
      • Precursor proteins (angiotensinogen)
    • Gamma
      • Immunoglobulins
      • Part of immune system
  • Fibrinogen
    • Blood clotting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Leukocytes

A
  • Colourless but appear coloured in stained prepartions
  • Nucleated and are of several types
  • All the types of WBC constitute 7000/mm3 in comparison with 5 million RBC/mm3
  • Can exit the blood vessel to the site of infection because of amoeboid movement
  • Polymorphonuclear Granulocytes - Nucleus is multilobed and has granules
    • Neutrophils
    • Eosinophils
    • Basophils
  • Mononuclear Agranulocytes - One nucleus with no granules
    • Monocytes
    • Lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Neutrophil

A
  • Polynucleated granulocyte
  • 50-80% of leukocytes in blood
  • Phagocyte
  • Circulate in blood 7-10 hours
  • Migrate to tissues for a few days
  • Numbers increase during infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Eosinophil

A
  • Polynucleated granulocyte
  • 1-4% of leukocytes
  • Phagocytes, but not main mechanism of action
  • Defend against parasitic invaders
  • Granules contain toxic molecules that attack parasites
  • Contribute to tissue damage in allergic reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Basophil

A
  • Polynucleated granulocyte
  • <1% of leukocytes
  • Non-phagocytic
  • May defend against large parasites by releasing toxic substances
  • Contain heparin (anticoagulant) and histamine (vasodilator)
  • Often associated with connective tissue and do not really circulate in the blood
54
Q

Monocyte

A
  • Mononuclear agranulocyte
  • 5% of leukocytes
  • Phagocytes
  • New monocytes circulate in blood few hours
  • Secretes cytokines and engulf microorganisms by phagocytosis
  • Migrate to tissues and become macrophages
    • Wandering macrophages
    • Fixed macrophages
55
Q

Lymphocyte

A
  • Mononuclear agranylocyte
  • 30% of leukocytes
  • 99% of interstitial fluid cells
  • Three types
    1. ​B Lymphocytes - antibody production
    2. T Lymphocytes - cell mediated response
    3. Null cells - viral infection
56
Q

Platelets

A
  • Cytoplasmic fragments derived from megakaryocytes (aka thrombocytes)
  • Colourless
  • Cell fragments
    • No nucleus
    • Has organelles and granules
  • 100,000 - 500,000/mL blood
  • Important in hemostasis (platelet plug)
  • Granules containing secretory products
57
Q

Requirements for Erythrocyte Production

A
  • Iron
    • Component of hemoglobin (heme portion)
    • Normal hemoglobin content of blood
      • Male: 13-16 grams/dL
      • Female: 12-16 grams/dL
  • Folic Acid
  • Vitamin B12
58
Q

Anemia

A
  • Anemia: Blood hemoglobin levels are too low, leading to decrease in oxygen carrying capacity
  • Types
    1. Nutritional - Deficiency in raw material
      • ​Dietary deficiency of a factor needed for erythropoeisis
    2. Pernicious - Deficiency in absorption of prerequisites​
      • ​Inability to absorb enough vitamin B12
      • Deficiency of **intrinsic factor **produced in parietal cells
    3. Aplastic - Deficiency in production of RBC
      • Caused by failure of bone marrow to produce RBC - radiation, chemotherapy, toxic chemicals
    4. Renal - Deficiency due to decreased erythropoietin, which is responsible for telling the stem cell to differentiate into RBC
      • Consequence of renal failure
    5. Hemorrhagic - Deficiency because of blood loss
      • ​​Extensive loss of blood
    6. Hemolytic - Deficiency becasue of breakdown of RBC
      • ​​Premature rupture of excessive RBC
59
Q

Polycythemia

A
  • Primary Polycythemia/Polycythemia vera
    • Stem cell dysfunction that produces too many RBCs and WBCs
    • As high as 70% hematocrit
    • Can increase viscosity and therefore BP
  • Secondary Polycythemia
    • Induced, adaptive mechanism in response to prolonged reduction of oxygen delivery to tissues
    • Ex. High altitude living
60
Q

Erythrocyte Lifecycle

A
  • Born in the bone marrow and breakdown in the spleen
    1. ​Synthesized in the bone marrow differentiating by erythropoeisis
    2. Transport oxygen and carbon dioxide
    3. Eventually go to spleen to be broken down
    4. Spleen macrophages break down the old ones
  • Some of the byproducts of breaking down RBCs get into the blood
    • Liver metabilizes bilirubin –> bilirubin is released into the blood stream and goes to the liver for further metabolism –> metabolites are released through the bile and excreted through feces and urine
  • Most of the iron is recycled and some is transported (transferrin) in the blood stream and then stored in the liver (ferritin)
61
Q

Hemostasis

A
  1. Vascular Spasm
  2. Platelet Plug Formation
  3. Blood Coagulation

Only occurs in damaged cells –> in healthy endothelium cells, there is prostacyclin and NO to make sure that this does not occur

62
Q

Hemostasis: Vascular Spasm

A
  • Occurs as a result of vasoconstriction
  • Vasoconstriction leads to decrease in blood flow
  • Reduces blood loss but does not stop bleeding
63
Q

Hemostasis: Formation of Platelet Plug

A
  • Forms around site of vessel damage, thereby decreasing blood loss
  • Platelets are the chief platers in the formation of the plug
  • In platelet plug formation, the key protein is von Willebrand factor (vWf), which accumulates at the side of vessel damage
  • Requires presence of platelets and speficic proteins, which are floating around in the plasma
  1. Exposed collagen fibres due to damage of blood vessel
  2. Blood flow comes in contact with subendothelium tissue and vWf binds to factors to trigger binding of platelets and anchors platelets in the area of damaged blood vessel
  3. Contact between platelets and vWf changes the consistency by making them sticky and stimulating secretion of chemicals
  4. ADP stimulates morphological things in the platelets so they form aggretory mass which secrete more ADP and stimulate more aggregation (positive feedback)
  5. Also releases thromboxin A2 (TXA2), which further supports aggregation by stimulating ADP secretion, in addition to vasoconstriction
  6. Activated platelets secrete powerful vasoconstrictions - serotonin and epinephrine
64
Q

Arachidonic Acid and Platelet Aggregation

A
  • Adhered Platelets
    • Arachidonic Acid (phosopholipid in platelets) –> Thromboxane A2 –> Platelet aggregation and secretions stimulated
  • Health Endothelial Cells
    • Arachidonic Acid –> Prostacyclin (Prostaglandin I2) –> Platelet aggregation inhibited
65
Q

Hemostasis: Blood Coagulation

A
  • Liquid blood –> solid gel
  • Stops blood flow in damaged area
  • Involves as cascade with many plasma proteins - clotting factors (mostly found in liver)
    • Almost all of these are in the inactive form until one is activated, and then the cascade begins
    • Exists to help reduce formation of clots in fine blood vessels
  • SEE LECTURE 22, SLIDES 12-16
66
Q

Roles of Thrombin

A
  1. Converts fibrinogen –> loose fibrin
  2. Activates Factor XIII, which stabilizes fibrin
  3. Positive feedback for its own production
  4. Positive feedback activates intrinsic pathway
67
Q

Factors Limiting Clot Formation

A
  • Anticoagulants
    • Proteins in plasma and surface of endothelial cells
  • Tissue factor pathway inhibitor
    • Secreted by healthy endothelial cells
    • Inhibits extrinsic pathway
  • Thrombomodulin
    • Secreted by healthy endothelial cells
    • Binds to thrombin, forming complex that activates protein C
    • Inhibits **both pathways ** - thrombin is used to both clot and prevent clotting in the blood
68
Q

Some Important Points About Coagulation

A
  • Clot dissolved by fibrinolytic enzyme - plasmin
  • Inactive molecule —FXII—> Kallikrein
  • Plasminogen —Kallikrein—> Plasmin
  • Steptokinase and tissue plasminogen activator (TPA) are used clinically to promote dissolution of clots
  • During clot retraction, fluid (serum) is squeezed out from the clot
69
Q

Clotting Disorders

A
  • Thrombus: An abnormal intravascular clot attached to a vessel wall
  • Embolus: A free floating clot - can eventually enter a blood vessel and cause thromboembolism
  • Abnomal Clotting –> Too many clots
  • Clotting Defect –> Too much bleeding
70
Q

Thromboembolism

A
  • Roughened vessel surfaces associated with atherosclerosis can lead to thrombus formation
  • Imbalances in the clotting-anticlotting systems can likewise trigger clot formation
  • Slow moving blood is more apt to clot
  • Widespread clotting is occasionally triggered by the release of tissue thromboplastin into blood from large amounts of traumatized tissue
71
Q

Abnormal Clotting

A
  • Prevention - administer anticoagulants
  • Heparin inhibits the activity of thrombin
  • Citrate combines with Ca2+ and inhibit the activtiy of many clotting factors
  • Warfarin (coumadin) prevents clotting by suppressing production of vitamin K dependent clotting factors
  • Aspirin
    • Low doses - anticoagulants inhibit formation of TXA2
    • High doses - inhibits formation of prostacyclin increasing the likeliness of clot formation
72
Q

Clotting Defect

A
  • Delay of formation in fibrin
    • ​Hemophilia A - defective factor VIII
    • Hemophilia B - defective factor IX
  • Interferes with platelet adhesion to collagen
    • ​von Wildebrand disease - defective factor VIII
    • Vitamin K deficiency
    • Thrombocytopneia - platelet deficiency
73
Q

Immune System

A
  • Protects the body from disease-causing invaders
  • Removes dead or damaged tissue and cels
  • Recognizes and removes abnormal cells when normal cell growth and development goes wrong
74
Q

Bacteria vs. Virus

A
  • Bacteria
    • Cells, usually surrounded by cell wall
    • Can survive outside a host
    • Can reproduce without a host
    • Can be killed or inhibited by antibiotics
  • Virus
    • Acellular, nucleic acid core with protein envelope
    • Parasitic - must have a host cell to survive
    • Must use the genetic material and organelles of the host to reproduce
    • Cannot be killed by antibiotics, must be destroyed by host’s immune system
75
Q

Anatomy of the Immune System

A
  • Leukocytes
    • Granulocytes
      • Neutrophils
      • Eosinophils
      • Basophils
    • Agranulocytes
      • Monocytes
        • Fixed and free macrophages
      • Lymphocytes
        • B cells, T cells, Null cells
  • Other Cells
    • Mast Cells - associated with connective tissue; secrete histamine and other useful substances for immune response
    • Dendritic Cells - activate certain types of T cells
  • Lymphoid Tissues
    • Central
      • Bone Marrow - where they are made
      • Thymus - where they mature
    • Peripheral
      • Spleen - where they go to die
      • Lymph Nodes
      • Tonsils
      • Appendix
      • Peyer’s Patches
      • Collections of T cells, B cells, and macrophages
76
Q

Organizations of the Body’s Defenses

A
  • Nonspecific Defenses - Innate
    • Resist a variety of agents
    • Act against foreign agents
    • Meet the pathogen as soon as they are presented
    • Provide generalized defense by acting against anything that is non self
  • Specific Defenses - Adaptive
    • Stimulated by speficic antigens or haptens
77
Q

Nonspecific Defenses

A
  • Physical Barriers
    • Skin
    • Sebum and other secretions
    • Mucous membranes
    • High acidity
  • Inflammation
    • Most powerful defense
  • Interferons
    • Peptides that are produced by virus, infected cells
  • Natural Killer cells
  • Complement system
78
Q

Inflammation

A
  • Series of events causing accumulation of proteins, fluids, and phagocytes in area injured or area invaded
  • Bacteria enter tissue/tissue damage –>
    1. ​Macrophages engulf debris and foreign matter
    2. Mediators released
      • ​Leading to chemotaxins, increased blood flow and increased permeability
    3. Increase in leukocytes and mediators
    4. (a) Bacteria contained –> tissue repair –> regenerative AND nongenerative tissue

​(b) Bacteria remain –> additional mediators released feeding back to (2)

79
Q

Steps of Phagocytosis

A
  1. ​Attachment
    • ​Membrane dips inward to form a pouch and trap bacteria
    • Macrophage targets damaged cells that have been specifically targeted by proteins
  2. Internalization
    • ​Takes about 0.01 seconds
    • Internalizes in a vesicle (phagosome), which combines with the lysosome to form a secondary lysosome
  3. Degredation
    • ​Lysosome enzymes degrade phagosome products into glucose, amine acids and free fatty acids
  4. Exocytosis
    • ​Some degredation products and undigested microbial products (such as cell wall) are eliminated
80
Q

Phagocytosis of Pathogens

A
  1. Phagocytosis by Nearby Macrophages
    • ​Proteins in microbes are bound by macrophages, which trigger secretion and pahgocytosis
    • Macrophages also secrete cytokines (**interleukins **and TNF), which communicate within bone marrow to secrete more interleukin
  2. Dilation and Increased Permeability in Capillaries
    • Mast cells secrete histamine (vasodilator) to increase blood and plasma fluid permeability –> increased blood flow and proteins into the interstitial fluid
  3. Containment of Foregin Matter
    • Mast cells and basophils also release **heparin **(anticoagulant), so blood cells can get to area
    • Clotting proteins eventually form scab
  4. Leukocyte Proliferation and Migration
  5. Clearing of Foreign Particles
    • ​Continued activity of recruired leukocytes
81
Q

Leukocyte Proliferation and Migration

A

Monocytes migrate to area of damage and leukocyte proliferation occurs in 3 stages

  1. ​Heparin and histamine release
  2. Clotting factors florming clots in tissue preventing spread of foreign matter and eventually aiding in scab formation
  3. About an hour after microbial entering cells, neutrophil migration occurs, triggered by cytokines

Leukocyte Migration

  1. **Margination **- movement towards cell wall
  2. Attachment - attach to blood vessel wall
  3. **Diapedesis **- move out of blood vessel
82
Q

Symptoms of Local Inflammation

A
  • Redness - due to histamine
  • Warmth - due to increased bloofd flow to the region
  • Swelling (edema) - due to increased blood flow from some of the liquid leaking out of the area
  • Pus - accumulation of dead leukocytes
  • Pain - nociceptors are stimulated by the inflammation
  • Fever - via hypothalamus
83
Q

Inteferons

A
  • Briefly provide nonspecific resistance by transiently interfering with replication of same or unrelated virus in other host cells
  • In response to virus, cells produce interferon, which bind to receptor on uninvaded cells
  • Now activated, the cells produce inactive antiviral proteins, which break down viral messenger mRNA and prevents virus from multiplying in other cells
84
Q

Types of Interferons

A
  • Alpha - help treat chronic hepatitis A/B, some genital warts, etc.
  • Beta - help treat relapsing multiple sclerosis
  • Gamma - produced by particluar lymphocytes and related types of cells (killer cells)
85
Q

T Cells

A
  • Inhibit viral replication
  • Enhance macrophage activity
  • Boost antibody production
  • Help activated natural killer cells and cytotoxic T cells
86
Q

Natural Killer Cells

A
  • Recognize abnormal or infected cells
  • Can attack virus-infected cells without identifying virus
  • Specific immune response
  • Cause cells to lyse by producing perphorins, which kill the host cells due to osmotic distribution
87
Q

Complement System

A
  • Activated when foreign particles are detected
  • About 30 proteins participate in cascade resulting in major attack complex (MAC) on surface of bacteria
  • MAC pierces bacterial membrane causing lysis
  • Part of response to antibodies (specific immunity) in addition to non-specific response
88
Q

Activation of Complement System

A
  • Alternate Pathway
    • Binding to carbs on bacterial wall cells
    • Part of nonspecific defense mechanisms
  • Classical Pathway
    • Binding to antibodies attached to bacteria
    • Part of specific defense mechanisms
89
Q

Specific Defenses

A
  • Immune responses
  • Humoral Immunity
    • B cell mediated
    • Involves secretion of antibodies by plasma cells
  • Cell-Mediated Immunity
    • T cell mediated
    • Lyses of cells by cytotoxic cells
    • Part of reaction of transplant of tissues and cancer cells
  • Features
    1. ​Specificity
    2. Diversity allows immune system to recognize millions of antigens
    3. Memory - memory cells are produced to confer long term protection if the individual should be exposed to the same antigen subsequently
    4. Self-tolerance
90
Q

Hematopoietic Stem Cells

A
  • Differentiate into
    • Myeloid Stem Cells
      • RBCs, granulocytes, platelets, monocytes
    • Lymphoid Stem Cells
      • ​B Cells –> Antibody-Mediated Immune Response
      • Thymus –> T Cells –> Cell-Mediated Immune Response
        • Thymopoeitin I and II promote T cell formation from lymphocytes
        • Thymosin promotes maturation of T Cells
          *
91
Q

Specific Immune Responses: Specificity

A
  • Antigens - large, molecular substances that trigger immune response
  • Confer specificity
  • Complex proteins and polysaccharides
  • Part of foreign or self antigens
    • Foreign - Components of bacteria, pollen, animal hair, certain drugs and gfood, and transplanted tissue
    • Self - Beneficial or harmful species produced by the body to take care of specific immune responses
  • Autoimmune diseases occur when specific immune responses happen in the body in a toxic manner
    • Ex. Rheumatoid Arthritis - Antibodies attack another type of antibody, leading to inflammation of joints
  • Epitopes - Localized region on surface of antigen that are capable of producing immune response by B or T cells
  • Antigen receptors recognize only certain antigens
    • B Cells - Membrane antibodies as surface receptors
    • T Cells - T Cell receptors
92
Q

Haptens

A
  • Small molecular substances that are capable of combining with large molecules such as blood proteins to stimulate specific immune responses
  • Ex. Penicillin - binds to larger proteins that can cause allergic response
93
Q

Specific Immune Responses: Self-Tolerance

A
  • B and T cells do not attack normal cells of body
  • As cells develop in bone marrow and thymus, any that have antigen receptors against normal body cells are destroyed by apoptosis
  • Autoimmune diseases caused by failure of self-tolearnce
94
Q

B Lymphocyte Responses

A
  • Binding of antigen activates proliferation by the lymphocytes, which differentiate into plasma cells and memory cells
  • Plasma cells have a life span of 4-7 days and secrete antibodies to specific antigen, which circulate for several weeks, binding to antigens to mark them for phagocytosis
95
Q

Primary Immune Response

A
  • Initial latent period of about a week and then antibody production occurs
  • Takes 10-17 days to occur after exposure
  • Symptoms of illness occurs during these days
  • Antigen-selected B and T cells proliferate and differentiate into effector cells
    • Plasma cells
    • Cytotoxic T cells
96
Q

Secondary Immune Response

A
  • When the body is re-exposed to the same antigen, the response is much faster and longer than the primary response
  • This is the premise for immunization shots
  • Takes 2-7 days to occur
97
Q

Classes of Immunoglobulins

A
  • IgM: B cell receptors, early response; most common produced in the primary response
  • IgG: 75% of immunoglobulins; most common in the blood and major in secondary response; important in fetal and newborn immunity
  • IgE: Parasitic worms and allergic reactions
  • IgA: Secretions - saliva, tears, intestinal and bronchial mucus
  • IgD: Appear on the surface of B cells
98
Q

Antibody Actions

A
  1. Neutralization
    • ​Antibody blocks activity of antigen
    • All classes can do this
  2. Agglutination
    • ​Clumping of antigens
    • All classes can do this
  3. Opsonization
    • ​Coats the pathogen and making them better targets for phagocytosis
    • IgG
  4. Activation of complement protein
    • Formation of membrane attack complex (MAC) leading to lyses of pathogenic cells
  5. **Enhanced NK cell activity **
    • ​​NK Cells have receptors of antibody tails
    • IgG
99
Q

T Lymphocytes

A
  • Killer or Cytotoxic T Cells
  • Helper T Cells secrete cytokines that enhance B cell activity, as well as enhancing activity of macrophages and NK cells
  • Suppressor T Cells secrete cytokines that suppress B cell activity
100
Q

Major Histocompatibility Complex

A
  • T cells have antigen receptors that interact with foreign antigens, but they only do this when the antigens are associated with major histocompatibility complex (APC)
  • MHC marks cells as belonging to self and are unique to every person
  • Class I is found on the surface of almost all cells in the body
    • Recognized by cytotoxic T cells by the CD8 receptor
  • Class II is found on a few certain types of cells, including activaed B cells and macrophages
    • Recognized by helper T cells by the CD4 receptor
101
Q

Helper T Cell Activation

A
  • Helper T cells coordinate immune response
  • Events of activation
    • Bind to Class II MHC-foreign antigen complex on surface of macrophages and B cells
    • Macrophages and B cells secrete interleukin I, which induces proliferation and differentiation of helper T cells
102
Q

Helper T Cell Differentiation

A
  • Secretory cells (effector cells) secrete cytokines that stimulate and regulate immune response
  • Memory cells
  • Cytokines act on…
    • Helper T Cell
    • B Cells
    • Cytotoxic T Cells
    • Macrophages
    • Mast Cells
    • NK Cells
    • Hematopoietic stem cells
103
Q

Helper T Cells

A
  • Important lymphokines secreted by helper T Cells
    • Interleukin-2
    • Interleukin-3
    • Interleukin-4
    • Interleukin-5
    • Interleukin-6
    • Granulocyte-monocyte colony stimulating factor
    • Interferon (gamma)
104
Q

Direct Destruction of Invading Cell by Sensitized Lymphocyte

A
  • Perforins punch large holes in the membrane causing fluid from the interstitial to enter the cell and cause osmotic gradient
  • Cytotoxic cells can pull away and go off and kill more cells
105
Q

Actions of Activated Cytotoxic T Cells in Tumor Cells

A
  • Tumor cells –> Tumor antigens
  • Class I MHC bring antigens to surface and present to cytotoxic T cells, initiating killer response
  • Cytotoxic T cells destroy tumor cells
  • Some cancers and viruses inhibit production of Class I MHC molecules, thus protecting them from immune system
106
Q

Suppressor T Cell

A
  • Regulate the activities of the other cells and prevent excessive immune reactions
  • Play a role in immune tolerance
107
Q

Events in Immune Response to Virus

A
  1. ​Specific contact with macrophage presenting MHC Class II
  2. Interleukin 1 is secreted by macrophages
  3. IL-2 playes a role in B cell activation and cytotoxic T cells (either by specific contact with the pathogen or by IL-2)
  4. Fragmentins enter the cell through perforins and trigger more cell death things
108
Q

Immune Dysfunctions

A
  • Allergy
    • Hypersensitive response to allergens (nonpathogenic antigens that activate certain aspects of immune system)
    • Involve IgG class of antibodies
  • Autoimmune Diseases
    1. ​Myasenia gravis
    2. Rheumatoid arthritis
    3. Lupus - immune system generates antibodies against a widesoread amount of self
    4. Insulin-Dependent Diabetes Mellitus
    5. Multiple Sclerosis - T cells have propensity to attack myelin and infiltrate CNS to cause demyelination of nerves
  • Immunodeficiency Diseases
    • ​Severe Combined Immunodeficiency Disease (SCID) - ex. Adenosine deaminase
    • Hodgkin’s Disease - damage to lymphatic system
  • Role of Stress in the Immune Response
109
Q

Anaphylactic Shock

A
  • Life threatening allergic reaction
  • Results from widespread dilation of blood vessels
  • Leads to a significant drop in blood pressure resulting in death
110
Q

Tissue Grafts and Organ Transplantation

A
  • Human Leukocyte Antigen (HLA) molecules (MHC) stimulate rejection by inducing immune response
  • Tissue typing - match HLA between donor and recipient
  • Suppress immune response of recipient
    • Cyclosporin A
    • FK506
111
Q

Blood Types

A
  • A and B antigens are complex oligosaccharides that differ in their terminal sugar
  • Blood type denotes antigens found on surface of RBC
  • Immune system is tolerant to its own blood type antigens to they only produce antibodies to the other types
  • Antigens that are similar to A/B are common to foods and such, so newborns rapidly produce antibodies for the antigen not present on their RBCs
  • When plasma of Type A is mixed with Type B, they agglutinate
112
Q

Blood Genotypes

A
  • Blood Group –> Possible Genotypes (% of population)
  • A –> IAIA or IAi (41%)
  • B –> IBIBor IBi (9%)
  • AB –> IAIB (3%)
  • O –> ii (47%)
113
Q

Transfusion Reactions

A
  • Donor cells must be matched with recipient’s plasma to check for agglutination in a process called cross-matching
  • Universal Donor - O becuase it has no antigens
  • Universal Recipient - AB because it has no antibodies
114
Q

Rh Factor

A
  • Groups of antigens ground on most RBCs
  • Consist of several subgroups
  • **D **is the most imporatnt
    • People who have D are Rh-positive
    • People who do not have D are Rh-negative (recessive)
  • Erythroblastosis Fetalis
    • ​At birth, there is a mixing of blood betwen fetus (Rh+) and mother (Rh-)
    • Upon exposure, the mother will produce anti-Rh antibodies, which has no effect on first pregnancy
    • During the second pregnancy, the baby is born with this disorder because there is agglutination of fetal Rh+ RBCs due to antibodies from mother’s blood
    • RhoGAM is used to treat this - mixture of IgG anti-D antibodies, which bind and destroy fetal Rh+ cells that have passed from the fetus to the mother
115
Q

Breath Size

A
  • Restig Total Volume - Amount of air we breathe in and out per breath = 500 mL
  • Resting Frequency - Number of breaths per minute = 20 breaths/minute
  • Tidal Volume - Amount of air we breathe per minute = frequency x resting total volume = 10,000 mL/minute (10 L/minute)
  • Maximal Total Volume is about the size of a basketball = 5000-6000 mL
  • Vital Capacity - Maximum amount of the tidal volume possible, when we take a big breathe
116
Q

Lung Resistance

A
  • Proportional to radius: R = 1/r4
  • Expiratory Reserve Volume (ERV) - Lung reserve for air that can be expired beyond resting conditions
    • Allows us to maintain oxygen in the body so there is a continuous supply in the blood stream
    • About 1000 mL
  • Residual Volume is left in the lung and helps with some of the reserve
  • Inspiratory Reserve Volume (IRV) - Lung reserve for air that can be inspired beyond the valve for resting conditions
    • About 3000 mL
  • Vital Capacity makes up the IRV, tidal volume, and ERV
    • Can be used to measure how quickly we can blow air out of the lungs –> the more quick the air flow out, the steeper slope of the graph (timed vital capacity)
117
Q

Dead Space

A
  • Volume in our nose and throat that does not take part in gas exchange
  • Functions to filter, warm and moisten the air before it gets to the lungs
  • About 150 mL
118
Q

Alveolar Volume

A
  • Volume that does take part in gas exchange
  • Where we pick up O2 and deliver CO2 to
  • About 350 mL
119
Q

Pressure of Oxygen

A
  • Atmospheric Pressure - About 747 mmHg
    • Breakdown
      • 80% N2
      • 20.43% O2
      • 0.03% CO2
  • Inspiration Pressure: PI,O2= 20.93% x atmospheric pressure (747 mmHg) - water vapour (47 mmHg) =147 mmHg
  • Alveolar Pressure: PA,O2 = 100 mmHg
  • Mitochondrial Pressure: PM,O2 = 1 mmHg
  • Venous Pressure: PV,O2 = 40 mmHg
  • Oxygen requires a difference of 60 mmHg for transfer of oxygen into system (Alveolar - Venous)
120
Q

Pressure of Carbon Dioxide

A
  • Inspiration Pressure: PI,CO2 = 0 mmHg
  • Alveolar Pressure: PA,CO2 = 40 mmHg
  • Venous Pressure: PV,CO2 = 46 mmHg
  • CO2 is created in the mitochondria and put into the blood stream
  • Only requires pressure gradient of 6 mmHg to move from blood to lungs because it diffuses rapidly
121
Q

Alveolar Air

A
  • Last portion of breath
  • PA,CO2= Pa,CO2 (arterial) = 40 mmHg
  • We can use alveolar pressure to estimate arterial pressure
122
Q

Surfactant

A
  • Allows the lungs to expand, so that air can enter the lungs
  • Chemical released by alveoli to increase distensibility of the lung
123
Q

Oxygen Dissociation Curve

A
  • Normally we release 5 mL of oxygen from hemoglobin
  • When the concentration of H+ increases, we release 10 mL of oxygen from hemoglobin
    • Graph also shifts right with increases in temperature
124
Q

Carbon Dioxide Dissociation Curve

A
  • Normally release 20 mL of CO2
  • Hyperventilation does not effect amount of ocygen because it is fully saturated at 20 mL/100 mL of blood, but it does not effect the amount of CO2
125
Q

Oxygen and Carbon Dioxide Carriage

A
  • Deoxygenated hemoglobin picks up the hydrogen ions formed from the bicarbonate formation to form reduced hemoglobin
  • This is how we take care of 70% of H+ ions
  • Oxygen: O2 enters the body and is transported into the RBC, where is binds with hemoglobin
  • Carbon Dioxide
    1. ​​CO2 is formed in the mitochondria and transported into the RBC
    2. CO2 + H2O —carbonic anhydrase—> H2CO3 –> H+ + HCO3- (bicarbonate)
    3. Bicarbonate is what travels in the venous system
126
Q

Hyperventilation

A
  • Lightheadedness is due to lack of oxygen getting to the brain
  • Alveolar air represents our blood
  • Alveolar CO2 goes down from 5-6% to about 1.8%
    • Causes drop in hydrogen ion concentration, leading to oxygen not being kicked off hemoglobin as much –> net reduction in oxygen delivery
  • Alveolar O2 increases to room air temperature
    • Little effect on amount of oxygen being transported in the blood
  • Consequence is oxygen lack
127
Q

Control of Bleeding

A
  • Both voluntary and involuntary
  • Neural
    • Medulla has both inspiratory and expiratory centres
    • Inspiratory centre sends impulse down the frenic nerve and intercostal nerves and ribs and diaphragm, causing diaphragm to contract and rib cage to flare out, which helps increass volume of chest cavity
    • Cortex on top of medulla controls these centres for voluntary control, but the medulla can also operate on its own (involuntary control)
  • Chemical
    • ​Increase Pa,CO2 –> Increase Ventilation (VE)
      • ​Blood flows through central receptor region os the medula where there are CO2 sensitive receptors (central chemoreceptors), which pick up CO2 and become excited
      • Once CO2 is inside the medullary region, it combines with water to produce carbonic acid that produces hydorgen ions and bicarbonate ion, which increases ventilation​
    • Decrease in Pa,O2 –> Depressed VE
    • Increase in Temperature/Adrenaline –> Stimulated VE
      • Occurs via peripheral chemoreceptors, which look at blood before it gets to the brain in terms of BP (CO2 levels)
      • If CO2 is too high, body might want to increase breathing to lower CO2
      • Provide only about 10% of drive to breathe at rest
128
Q

Spirometer Experiment 1: KOH Crystals

A
  • KOH crystals absorb CO2
  • Tidal volume and frequency remain about constant at first, but start to increase after 2-3 minutes
  • Oxygen levels are down to 4.5%, so we are hypoxic
  • In terms of stimulating peripheral and central chemoreceptors, the effect is not very considerable
129
Q

Spirometer Experiment 2: Pure Oxygen

A
  • CO2 begins to accumulate because what is being made in the body is being breathed back into the body due to the bag
  • At first, tidal volume is constant
  • Breaths then get about 3x larger and much closer together than in the beginning
  • There is now considerable drive to breath
  • Oxygen levels are about 38% and CO2 levels are about 8.7%
130
Q

Spirometer Experiment 3: Closed Circuit

A
  • Begin with normal tidal volume and then begin to increase in size and frequency
  • CO2 is about 7.2% and O2 is about 8.7%
  • High CO2 is known as hypercapnia
  • Hypercapnia + hypoxia = very powerful stimulus to breath
  • Together, these stimuli to breath are synergistic in nature, so we get more ventilation than the effect due to either alone
131
Q

Control of Breathing in Exercise

A
  • Neural component is evident at the beginning of exercise
    • Ventilaton goes from 8 L/min to 20 L/min and then climbs up fairly quickly within about 3-5 seconds of beginning exercise
  • Chemical component
    • Slow increase in ventilation, that is accompanied by little increase in CO2 and increase in hormones (adrenaline and noradrenaline), as well as temperature
    • Slow rise due to humoral factors (chemical)
  • Stopping exercise is also neural in nature because once you stop, the ventilation almost immediately goes back down to resting levels
132
Q

Mitochondria and Exercise

A
  • We want to increase our mitochondria
  • VO2 is the amount of oxygen we need for mitochondria; during exercise it is VO2max
  • The higher this is, the better the quality of life
  • Breath Sound Check can be used during exercise - when we can hear ourselves breathing, we are in the aerobic stage, which is optimal for mitochondrial increase. When we care no longer able to talk while hearing our breathing, we are in the anaerobic stage.
  • Ventilatory Threshold - Minimum intensity needed to increase mitochondria and VO2max

PSL205 Basic Human Physiology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions