Physiology Sem 2 Exam week 6-8 Flashcards

(214 cards)

1
Q

What is Erythropoietin (EPO)

A

A hormone produced by kidneys, that stimulates production of RBCs in response to hypoxia (low oxygen).

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2
Q

What is Thrombopoietin (TPO)

A

A hormone produced by the liver, that stimulates platelet formation from precursors.

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3
Q

Makeup of blood - red cells, plamsa

A

RBC - 45%
Plasma - 55%
Buffy coat (wbc and platelets) - minute

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4
Q

What does plasma contain?

A

water, along with proteins, electrolytes, nutrients, gases, hormones and wastes

91.5% water
7% proteins

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5
Q

What is Haemopoesis

A

Pluripotent stem cellsdifferentiate in the red bone marrow into two further types of stem cells:

  • Myeloid -> the rest
  • Lymphoid -> T lymphoblast, B lymphoblast, NK lymphoblast
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6
Q

What are CFUs?

A

Colony-forming units created from myeloid stem cells - these cells dont divide but mature into precursor (BLAST) cells

CFU-E -erythrocyte
CFU-Meg - megakaryocyte
CFU-GM - granulocyte-macrophage

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7
Q

Sites of haemopoesis

A

Before birth - yolk sac is the site for blood cell formation followed by the liver, spleen, thymus and lymph nodes

After birth - red bone marrow (rate of production declines with age)

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8
Q

What are pluripotent stem cells?

A

not yet committed
Develop into myeloid and lymphoid stem cells
Found in red marrow in adults

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9
Q

What are myeloid stem cells?

A

Develop in red marrow - become RBC, platelets or wbc’s

Can develop into progenitor cells or into precursor cells

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10
Q

What are lymphoid stem cells?

A

Formed by pluripotent stem cells in red marrow but finish development in lymphatic tissue

Can become T cells, B cells or natural killer cells (all granulocytes)

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11
Q

What are progenitor cells?

A

Mostly created from myeloid cells
Cannot reproduce themselves, but form specific blood cells
CFU’s are sub type

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12
Q

What are precursor cells?

A

Blasts
From lymphoid and some myeloid stem cells

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13
Q

What are the formed elements of circulating blood?

A

Erythrocytes(RBCs),thrombocytes(platelets) and leukocytes (WBCs)

Some of these escape into the tissue, becomingtissue cells.

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14
Q

What are tissue cells?

A

most retain similar functions to their precursors

Whenbasophilsmigrate to connective tissue, they become mast cells.
Migratingmonocytesbecomemacrophages

B lymphocytesbecomeplasma cells.

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15
Q

RBC shape

A

biconcave disc
lack organelles including nucleus

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16
Q

Structure of haemoglobin

A

four protein (globin) chains that each have an iron-containing pigment calledhaemin the centre.

Carries 4 oxygens

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17
Q

What is Erythropoiesis?

A

The production of RBCs in the red bone marrow

stimulated by erythropoietin (90% of this made in kidney, remainder in liver)

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18
Q

How does NO work?

A

binds to haemoglobin
Made by endothelial cells in blood vessels to cause vasodilation

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19
Q

Where is carbonic anhydrase?

A

In RBCs - catalyses conversion of CO2and water into carbonic acid.

carbonic acid dissociates intobicarbonate ions(HCO3-) which is an important buffer

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20
Q

Lifespan of RBC

A

Recycled every 120 days by macrophages in spleen, liver or red bone marrow

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21
Q

Life cycle of rbc

A
  1. Worn-out RBCs phagocytosed by macrophages in the spleen, liver or red bone marrow
  2. Released Haemoglobinbroken down into haem andglobin
  3. Globinchains split intoAAsand used to synthesise new protein.
  4. Ironseparated from haem as Fe3+ and attached totransferrin
  5. In muscle fibres, liver cells and spleen, the Fe3+detaches from the Fe3+-transferrin complex and attaches toferritin for storage
  6. Iron is released from a storage site (e.g. muscle) or absorption site (e.g. gastrointestinal tract) into the blood and reattaches to transferrin.
  7. The Fe3+-transferrin complex is carried to the red bone marrow via blood and iron is taken up into RBC precursor cells via endocytosis. Here, haemoglobin is synthesised usingiron, amino acidsandvitamin B12.
  8. Erythropoiesis results in the production of reticulocytes from RBC precursor cells. Once entering blood,reticulocytesmature into RBC over 1-2 days
  9. Thenon-iron componentremaining from haem is converted to biliverdinin macrophage, thenbilirubin
  10. Bilirubin transported in blood to liver and released into bile to SI
  11. Bacteria in LI convert bilirubin to urobilinogen, some reabsorbed into blood + converted to urobilin and eliminated inurine
  12. Most urobilinogen is converted to stercobilin and eliminated in faeces
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22
Q

Erythropoiten negative feedback

A

Stimulus - low blood oxygen carrying (low RBC, haemoglobin, blood volume)

Receptor - kidney receptors detect low O2, increase EPO secretion into blood

Control centre - proerythroblasts (precursors) mature into reticulocytes in red bone marrow

Effectors - addition of RBC increases oxygen carrying capacity

Response - increased O2 delivery to tissues relieves stimulus

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23
Q

Granular WBCs

A

neutrophils, eosinophils and basophils.

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24
Q

Agranular WBC

A

monocytesand lymphocytes (B, T and natural killer cells)

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25
Two important families of cytokines needed in the production of WBCs
Colony stimulating factors Interleukin
26
What is EBC emigration?
Some WBCs (particularly neutrophils and monocytes) leave the blood to enter infected or damaged tissue by the process of emigration (also called diapedesis).
27
What are selectins and integrins?
A damaged endothelium displays adhesion ‘sticky’ molecules called selectins that stick to the carbohydrates on the surface of neutrophils. Integrins - adhesion molecules displayed by neutrophils causing them to slow down and roll along endothelial surface, then pass through endothelial cells to enter tissues
28
2 processes in innate immune response
Phagocytosis - phagocytes migrate to tissue spaces by diapedesis Inflammation - vasodilation and permeability increases, WBC secrete substances to intensify inflammatory response, basophils leave capillaries and enter tissue to release heparin, histamine and serotonin in allergic reactions
29
Mature B cell function
transform into antibody-secreting plasma cells.
30
Mature T cell function
attack invading viruses, cancer cells, fungi and some bacteria and they are responsible for allergies, transfusion reactions and transplant rejection
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What is leukocytosis
WBC count higher than 10,000/µl of blood
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What is leukopaenia
an abnormally low level of WBC below 5000/µl of blood.
33
Platelet info
disc 2-4um diameter 7-10d lifespan no nucleus has mitochondria produce finger like projections when activated Production stimulated by thrombopoietin in liver contains serotonin, Ca2+, ADP and fibrinogen involved in clotting, clot retraction and clot removal
34
Platelet appearance and granule types
Darkly stained and granular α-granules: 50-80 per platelet that contain haemostatic factors proteins such as von Willebrand factor and fibrinogen Dense granules: 3-6 in each platelet, containing ADP, serotonin, histamine and calcium Lysosomal granule: contain hydrolytic enzymes important for degrading proteins
35
3 general mechanisms reduce blood loss and prevent haemorrhage
1. Vascular Spasm 2. Platelet plug formation 3. Blood clotting (coagulation)
36
vascular spasm process
Immediate response initiated by direct injury to smooth muscle cells, the release of serotonin by activated platelets or stimulation of pain receptors Smooth muscle in vessel walls contract, vasoconstriction, decrease blood loss for minutes-hours
37
Platelet plug formation
Initiated by damage to the endothelium exposing underlying connective tissue and collagen on inner wall Attracts platelets that become sticky and adhere to site, activate and release ADP, serotonin (vasoconstrictor), thromboxane A2 forming a seal 3 Steps: 1. Platelet adhesion 2. Platelet release reaction - explained above 3. Platelet aggregation - release of ADP makes platelets sticky and adhere to make platelet plug
38
Blood clotting process
Thickens blood to protein gel consisting of serum and fibrin in which formed elements are trapped Takes 3-6 minutes to occur 3 pathways: 1. Extrinsic 2. Intrinsic 3. Common pathway
39
Extrinsic clotting pathway
Triggered by external trauma to a blood vessel Within seconds this initiates the formation of an active enzyme called prothrombinase Tissue factor (TF) escapes into the blood from the surfaces of damaged cells outside blood vessels. In the presence of Ca2+, activated factor X combines with factor V to form prothrombinase
40
Intrinsic clotthing pathway process
Triggered by internal damage to the blood vessel wall takes minutes to complete prothrombinase production Exposed collagen fibres in vessel or damaged platelets cause formation of activated factor X in presence of calcium resulting in prothrombinase production
41
Common pathway process
Prothrombinase production by other pathways begins this process 1. prothrombinase with Ca2+ catalyses conversion of inactive prothrombin into the active enzyme thrombin 2. thrombin with Ca2+ converts soluble plasma protein fibrinogen into insoluble fibrin Production of fibrin causes - acceleration of prothrombinase production and activates platelets in intrinsic pathway to reinforce aggregation
42
Examples of clotting factors
Calcium molecules derived from platelets or damaged tissues Inactive enzymes made by hepatocytes Vitamin K
43
Vitamin K role
synthesis of 4 clotting factors by hepatocytes: Factor II (prothrombin), VII, IX and X Produced in LI by bacteria
44
What is clot retraction?
after clot forms, retraction and pulling action of platelets on fibrin causes edges of damaged vessel to pull together allowing repair of endothelial cells
45
What is fibrinolysis?
breaking up of clot at site of completed repair Relies on activation of plasminogen originally incorporated into clot during formation. Activated into plasmin by tissues that is proteolytic and digests fibrin and inactivates clotting factors
46
3 methods of clotting control
1. Inhibition of platelets -> endothelial cells + WBC produce prostacyclin that opposes thromboxane A2 on platelet adhesion and release 2. Anticoagulants -> antithrombin blocks prothrombin, heparin blocks effects of thrombin, activated protein C enhances plasminogen activators 3. Thrombolytic agents - streptokinase or tissue plasminogen activator directly or indirectly activate plasminogen
47
What is an agglutinogen
genetically determined antigens made of glycoproteins and glycolipids on rbc surfaces
48
What is an agglutinin?
blood plasma antibodies that react with antigens RBC lack eg anti-A or anti-B antibodies
49
Universal recipient type
AB do not have anti-a or anti-b antibodies in their plasma
50
Transfusion reaction causes:
agglutination clumping reaction that causes donated cells to burst, liberate haemoglobin and clog kidneys
51
What is rhesus blood group?
People with Rh agglutinogens on the surface of red blood cells are called Rh+ (“Rh positive”) and those without are called Rh- (“Rh negative”). normal plasma does not contain anti-Rh antibodies, but develop only in Rh- people if exposed to the antigen On the next antigen exposure, anti-Rh antibodies can cause agglutination
52
Rhesus pregnancy risk
A pregnant Rh- woman carrying a Rh+ baby risks foetal blood leaking across the placenta into her bloodstream. The mother’s immune system creates anti-Rh antibodies. During a subsequent pregnancy with a Rh+ baby the maternal antibodies cross the placenta and haemolytic disease of the newborn may develop causing haemolysis of the foetal red blood cells.
53
Which side of the heart pumps what?
The right side of the heart pumps deoxygenated blood into the **pulmonary** **circulation** - The left side pumps oxygenated blood into the **systemic circulation**.
54
Path of blood
1. Deoxygenated blood enters right atrium from the venous circulation. 2. RA -> through right AV (tricuspid) valve -> RV 3. RV -> right semilunar (pulmonary) valve -> pulmonary trunk. 4. Deoxygenated blood carried to lungs via the pulmonary arteries. 5. In the lungs, CO2 removed, and O2 added (external respiration) 6. Oxygenated blood from the lungs -> pulmonary veins -> left atrium 7. LA -> left AV (bicuspid) valve -> LV 8. LV pumps oxygenated blood through the aortic valve into the aorta 9. The aorta branches into systemic arteries, eventually reaching tissue capillaries 10. The superior and inferior vena cava, and coronary sinus vessels all bring deoxygenated blood from the body to the right atrium.
55
Structural adaptions of cardiac muscle
Cardiac muscle fibres are connected end-to-end by thickenings of the sarcolemma called intercalated discs containing desmosomes that anchor fibres together and gap junctions permitting fast transmission of chemicals
56
Energy production of cardiac muscle
Aerobic respiration ATP generated mainly by fatty acid and glucose oxidation
57
Sarcomere of cardiac muscle
The bands and zones of a sarcomere in cardiac muscle fibres are arranged in the same way as in skeletal muscle. more and bigger Mitochondria Smaller sarcoplasmic reticulum and less intracellualr Ca storage
58
Cardiac muscle fibre cells structure
Cardiac muscle fibres connected end to end by thickenings of sarcolemma called intercalated discs
59
Cardiac sliding filament mechanisms
Just like skeletal muscle, during contraction Ca2+ binds to troponin that causes actin (in the thin filament) and myosin (in the thick filament) to slide against one another, drawing Z discs closesr and decreasing sarcomere length
60
What are autorhythmic fibres?
Form cardiac conduction system - a network of specialised fibres that provide the path for electrical excitation through the heart ensuring the chambers contract in a coordinated manner in the order of excitation no stable resting membrane potential - spontaneous depolarisation is known as pacemaker potential
61
Order of cardiac excitation:
1. SA node in right atrial wall causing atria to contract at same time 2. AV node - APs slow down 3. AV bundle of his - ap conduct from atria to ventricles 4. Right and left bundle branches - extend through right and left bundle branches towards apex of heart 5. Purkinje fibres - from apex up through interventricular septum causing ventricular contraction
62
Resting potential of contractile muscle fibres
-90mV
63
Contractile process of contractile fibres
1. Rapid depolarisation (summit) - sodium in - reaches threshold, voltage-gated Na+ channels open and a rapid influx of Na+ down the electrochemical gradient. Membrane potential increases from -90mV to +20mV. 2. Depolarisation (continue) - calcium in -> depolarisation maintained (for about 0.25 s) in the plateau phase due to opening of voltage-gated Ca2+ channels. Ca2+ moves out of the sarcoplasmic reticulum and into cytosol. During this, some voltage-gated K+ channels open and K+ leaves the cells. The balance of Ca2+ in and K+ out sustains the plateau. The membrane potential is around 0mV. 3. Repolarisation (plummet - potassium out) -> additional voltage-gated K+ channels open and increased K+ outflow results in cell repolarisation. This restores the resting membrane potential. 4. refractory -> cell is refrained from further stimulation. Outlasts the contraction period which allows for the coordinated pattern of contraction and relaxation of the myocardium and prevents tetanic contractions
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What does the P wave represent?
Atrial depolarisation - SA node sending AP across atria toward AV node causing atrial contraction Occurs in atrial systole
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What does QRS complex represent?
Ventricular depolarisation Through AV bundle, bundle of his and purkinje fibres At the same time, atrial repolarisation is occuring and atria relax (atrial diastole)
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What happens shortly after the QRS complex and ventricular depolarisation?
Ventricular systole Contraction progresses up from apex of heart As pressure in ventricle increases, AV valves shut and blood exits semilunar valves (pulmonary and aortic) into arteries out of heart
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What is the T wave?
Ventricular repolarisation Ventricular diastole
68
What happens right before the P wave?
Ventricular diastole - both atria and ventricles are relaxed for 0.2 seconds
69
What is the end-diastolic volume?
130ml Volume of blood in a relaxed ventricle Occurs following atrial systole - where blood pushed through open AV valves into the ventricles
70
What is isovolumetric contraction in the ventricles? What is the end systolic volume?
In ventricular systole, for a brief initial period when pressure rises in each ventricle, cardiac muscle fibres are contracting and exerting force however not shortening As pressure rises, the semilunar valves open and blood is pushed out of the heart. Each ventricle ejects about 70 ml of blood into its respective blood vessel- this is the stroke volume. The remaining volume after ejection is 60ml. This is called the end-systolic volume (ESV).
71
What is the relaxation period?
For a brief period all 4 valves are closed - isovolumetric relaxation. Relaxation of ventricles causes pressure to fall and when it is below atrial pressure the AV valves open and ventricle filling commences. They fill to about ¾ full and a new P wave commences.
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Which side of the heart is higher pressure?
the left
73
Heart sounds
S1 - closure of the AV valves soon after ventricular systole begins. S2 - closure of the semilunar valves (pulmonary and aortic valves) at the beginning of ventricular diastole. S3 - inaudible sound due to blood movement during ventricular filling. S4 - inaudible sound due to blood turbulence during atrial systole
74
Cardiac output equation
SV x HR Resting adult male = 5.25L/min SV=70ml/beat HR = 75
75
3 factors regulating SV
Preload -> stretch on the ventricular muscle before it contracts - greater preload increases force of contraction and proportional to volume of blood in relaxed ventricle Contractility of heart -> greater forcefulness increases stroke volume. Positive inotropes promote influx of Ca2+ (epinephrine, glucagon, thyroid hormones) and negative ionotropes decrease force, acetylcholine or acidosis block sympathetic activation Afterload -> pressure needing to be overcome in a ventricle before blood ejection occurs through the semilunar valves. Afterload decreases, the stroke volume increases.
76
Factors affecting heart rate
age, gender, fitness and body temperature. It is regulated by the autonomic nervous system (ANS) and chemicals.
77
Nervous system regulation of heart rate
Under control of a set of neurons located in the medulla oblongata in the brain- the cardiovascular centre - that receives input from higher brain centres and sensory receptors: - Proprioceptors, chemoreceptors and baroreceptors Sympathetic nerve impulses travel through cardiac accelerator nerves to increase the rate of depolarisation by the SA node (increases heart rate) and increase the contractility of cardiac muscle (increases stroke volume). Parasympathetic nerve impulses travel through the vagus nerve to decrease heart rate by ACh release and reducing spontaneous depolarisation of the SA node. Minimal contractility effects.
78
Chemicals affecting heart rate
Epinephrine and norepinephrine from the adrenal medulla, thyroid hormones and calcium ions increase heart rate and contractility. Elevated blood levels of potassium and sodium ions decrease heart rate and contractility.
79
How do blood solutes and pH affect heart rate?
low oxygen levels (hypoxia), high acidity (acidosis) and high alkalinity (alkalosis) which all have a depressive effect on cardiac function.
80
How does exercise affect cardiac output?
Elevated CO and increases metabolic rate Increases venous return, more blood in left ventricle, harder muscles work. Stroke volume increases to a certain point them levels off and further increases in CO are due to heart rate increasing
81
Capillaries structure and function
Capillaries form a branching network of passages called a capillary bed that connect the arterial outflow (blood leaving the heart) and venous return (blood going back to the heart). Exchange materials with blood and interstital fluid Structure - lack tunica media and thin walled
82
3 types of capillaries
Continuous - plasma membranes of endothelial cells form a continuous tube. Common in central nervous system, lungs, muscle and skin Fenestrated - plasma membranes of endothelial cells have many pores. Common in kidneys, small intestine, endocrine glands. Sinusoid - plasma membranes of endothelial cells have much wider fenestration. Common in liver, spleen, red bone marrow and adrenal glands.
83
Capillary exchange mechanisms
the continuous movement of substances between the blood in capillaries and interstitial fluid. 1. Diffusion -> water soluble substances use fenestrations or intercelllular clefts and lipid soluble materials like O2 and Co2, steroid hormones use lipid bilayer 2. Transcytosis -> plasma proteins and blood cells become concentrated in caveolae and go endocytosis to epithelial cell lining capillary, vesciles move across cell with help of cytoskeleton, vesicles contents are released on other side into interstitial fluid by exocytosis 3. Bulk flow -> movement of large amounts of suspended material e.g. ions in fluid, in the same direction from high pressure to low pressure
84
What is blood hydrostatic pressure?
Is generated by the pumping of the heart and is the main pressure pushing fluid out of a capillary, promoting filtration.
85
What is blood colloid osmotic pressure?
caused from remaining large proteins in capillaries that try to draw fluid back into the capillary. It is the main pressure opposing filtration and promoting reabsorption.
86
What is interstitial fluid osmotic pressure?
‘Pulls’ fluid out of capillaries into interstitial space where small amounts of leaked protein escaped, also promoting filtration.
87
What is interstitial fluid hydrostatic pressure?
Builds as more fluid accumulates in the interstitial spaces which pushes some (minimal) fluid back into the capillary, also promoting reabsorption.
88
What is net filtration pressure?
Calculated by subtracting the pressures that promote reabsorption from the pressures that promote filtration. We find that more filtration occurs at the arterial end of a capillary and more reabsorption occurs at the venous end
89
What is oedema caused by?
An abnormal increase in interstitial fluid if filtration of fluid exceeds reabsorption. Excess filtration can be caused by: increased blood pressure and increased permeability of capillaries allowing plasma proteins to escape Inadequate reabsorption may be: decreased conc. of plasma proteins or inadequate synthesis or loss of plasma proteins from liver disease, burns, malnutrition or kidney disease
90
4 factors affecting blood flow
Blood pressure - hydrostatic pressure exerted by blood Vascular resistance - the opposition to blood flow due to friction between blood and the walls of blood vessels. It is impacted by three factors: 1. A smaller vessel lumen size increases vascular resistance 2. Increased blood viscosity increases vascular resistance 3. Increased total length of blood vessels increases vascular resistance Venous return - skeletal muscle and respiratory pump Velocity of blood flow - slowest in capillaries for exchange
91
Neural regulation of blood pressure
CV centre in medulla oblongata via autonomic nervous system Sensory input -> proprioceptors, baroreceptors in aorta and neck arteries walls monitoring stretch, chemoreceptors in carotid and aortic bodies monitoring chemicals H+, CO2 and O2
92
Baroreceptor reflex
1. Stimulus - suddenly standing drops BP 2. Receptors - BP falls and feedback from baroreceptors in carotid sinus and aortic arch decreases to CV centre 3. Control centre - The cardiovascular centre reduces parasympathetic and increases sympathetic stimulation to the heart, adrenal medulla increases epinephrine 4. Effectors - increase in HR, systemic vascular resistance and force of contraction increasing CO 5. Response - Increase BP
93
What is vasomotor tone?
The sympathetic division continually sends impulses to smooth muscle in blood vessel walls via vasomotor nerves. The result is a moderate state of tonic contraction or vasoconstriction, called vasomotor tone
94
Hormonal regulation of BP
Epinephrine and NE increase sympathetic response and HR Systemic vascular resistance - angiotensin II from RAAS, ADH, norepinephrine and epinephrine cause vasoconstriction. ANP, Nitric oxide and epinephrine in arterioles in cardiac and skeletal muscle cause vasodilation Blood volume -> Aldosterone and ADH increase blood volume and pressure, ANP decreases them
95
How does aldosterone increase BP?
released by adrenal cortex increases the reabsorption of sodium and water in the kidney, which increases blood volume and pressure. 
96
How does ADH increase blood volume?
released by the posterior pituitary in response to dehydration or reduced blood volume. Causes vasoconstriction and increased water reabsorption in the kidney which increases blood volume.
97
Autoregulation of blood flow - mechanisms
Ability of a tissue to automatically adjust its _own_ blood flow to match its metabolic demand for supply of O2 and nutrients and removal of wastes. 1. Temperature changes - warmth promotes vasodilation 2. Myogenic response - reflex response of smooth muscle in arteriole walls. Increased BP -> smooth muscle stretch -> vessel responds by constricting and vice versa 3. Vasodilators and contrictors -> histamine, K+, H+ and lactic acid dilates whilst serotonin from platelets, thromboxane A2 cause constriction 4. Change in O2 -> systemic vessels dilate with low O2, pulmonary vessels constrict with low O2 allowing blood flow to better ventilated areas of lungs
98
Process of lymph formation and its components
Excess filtered fluid unable to be returned to the blood flows into lymphatic capillaries to become lymph contains components of blood plasma such as excess fluid, plasma proteins, fats and fat-soluble vitamins (e.g. A, D, E and K).
99
Features of lymphatic capillaries
wide diameter, overlapping endothelial cells and anchoring filaments higher colloid osmotic pressure creating a ‘pull’, closed end and greater permeability than blood capillaries The increased fluid pressure causes anchoring filaments to pull on endothelial cells to create larger openings between the cells, and pushes their overlapping ends open
100
How is lymph circulated?
Lymph in capillaries -> larger lymphatic vessels -> through lymph nodes for filtration -> enters one of the 5 lymphatic trunks that drain lymph from a region in the body -> Valves in lymphatic vessels and the skeletal muscle and respiratory pumps move lymph towards the heart -> From the trunks, lymph empties into one of the lymphatic ducts: 1. The thoracic duct (left lymphatic duct) receives lymph from left side of the head, neck, chest, the left upper extremity, and the entire body below the ribs. It drains lymph into venous blood at the junction of the left internal jugular vein and the left subclavian vein. 2. The right lymphatic duct receives from upper right side of the body + drains lymph into venous blood at the junction of the right internal jugular vein and right subclavian vein.
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Primary lymphatic tissues
Red bone marrow - Found in the epiphysis of long bones or interior of flat bones Thymus - bilobed organ located between the aorta and sternum B and T lymphocytes form here
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Where do B cells complete maturation?
Red bone marrow Require immunocompetence - ability to mount specific immune response
103
Path of T cells maturing
Immature pre-T cells leave the bone marrow and migrate to the thymus and gain immunocompetence.
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Secondary lymphatic tissues
lymph nodes, spleen and lymphatic nodules (follicles) like the tonsils, appendix and Peyer’s patches in the intestine
105
Where do B and T cells go from primary lymphatic sites?
Leave primary lymphatic sites via blood and colonise parts of secondary lymphatic tissues to respond to threats
106
Lymph flow through nodes
Lymph flows through nodes in one direction (afferent vessels > sinuses > efferent vessels), slowing down the flow and trapping foreign substances such as bacteria and tumour cells.
107
What does filtered lymph contain?
antibodies secreted by plasma cells and activated T cells.
108
What is the functional parenchyma of a lymph node?
cortex and medulla
109
What does the outer cortex of lymph node contain?
Aggregates of B cells in lymphatic nodules Presence of an antigen causes the dendritic cells to ‘present’ the antigen to the B cells; the B cells differentiate into antibody-secreting plasma cells and memory B cells. This is the third line of defence. The plasma cells migrate to the medulla and make their way to the efferent vessel
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What does the inner cortex of lymph node contain?
T cells which upon antigen presentation by dendritic cells stimulates their proliferation. This is also the third line of defence. T cells migrate from the lymph node to sites of antigen in the body.
111
What does white pulp of the spleen contain?
macrophages and lymphocytes (B and T cells) arranged close to the central arteries.
112
What does red pulp of spleen contain?
blood-filled venous sinuses and splenic cords containing RBCs, macrophages, lymphocytes, plasma cells and granulocytes
113
4 functions in red pulp of spleen
Macrophages remove worn-out RBCs and platelets (found in the blood). Storing platelets (1/3 of the body’s supply) Providing a blood reservoir (particularly important during haemorrhage to maintain blood volume) In the foetus the spleen also is the site of haematopoesis
114
What are lymphatic nodules?
Lymphatic nodules are egg-shaped masses of lymphatic tissue that are not surrounded by a connective tissue capsule. Nodules are scattered throughout the connective tissue of mucous membranes e.g. Peyer’s patches in small intestine
115
What is non-specific resistance?
first and second lines of defence First line -> skin, MMs, secretions of skin and MMs, physical and chemical barriers provided by the skin, coughing, vomiting Second line -> antimicrobial substances, phagocytes, natural killer cells, inflammation, and fever. Takes place when pathogens breach first line. Mechanism are also non-specific
116
What are lacteals?
lymphatic capillaries in the SI lymph draining the small intestine appears milky white in appearance and is referred to as chyle
117
What is an epitope?
a small part of antigen that triggers the immune response
118
What happens in antigen processing and presentation?
In processing the antigen is broken down into fragments in a cell and then associated with one type of MHC molecule (either class I or II). In antigen presentation, the antigen-MHC complex is then inserted into the cell plasma membrane
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How are exogenous antigens processed?
These foreign antigens are present in fluids outside of body cells e.g. bacteria and parasitic worms. They are phagocytosed by an antigen-presenting cell (APC) first and then processed with MHC-II molecules. The antigen-MHC-II complex is presented on the cell’s surface. APCs migrate to lymphatic tissue to present the antigen to T cells
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How are endogenous antigens processed?
Present within the body cells. Antigens are digested in the cytoplasm and their fragments combine with MHC-I molecules. The antigen-MHC-I complex is presented on the body cell (not an APC) membrane
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What is cell mediated immunity"
third line of defence refers to the elimination of intruders using helper T cells and cytotoxic T cells Effective against foreign antigens that are bound to our own cells (e.g. viral proteins), some intracellular pathogens (e.g. viruses), transplanted cells and cancer cells
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3 things required for cell mediated immunity
1. Activation - Activation through (1) antigen recognition and (2) costimulation. An activated T cell can then undergo clonal selection. 2. Proliferation - During clonal selection activated helper or cytotoxic T cells undergo cell division to form a clone of identical cells that recognise the same antigen 3. Differentiation - These new clones are either the effector cell which carry out the immediate immune response or long-lived memory cell
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How do cytotoxic T cells kill?
by releasing granzymes, protein-digesting enzymes that trigger apoptosis of the infected body cells. The released microbes are then phagocytosed. Also directly kill cells by releasing perforin and granulysin which add channels or holes into the target cell membrane
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How do active helper T cells cause proliferation?
secrete cytokines including interleukin-2 which is a trigger for T cell proliferation. Interleukin-2 also serves as a co-stimulator for cytotoxic T cells and B cells in their activation.
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What is antibody mediated immunity?
destruction of antigens by antibodies. Antibodies are produced and secreted by plasma cells. This form of immunity works mainly against antigens dissolved in body fluids (humors) and extracellular pathogens. B cells populate lymph nodes, spleen and mucosa-associated lymphatic tissue.
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what 3 things does antibody mediated immunity require?
1. Activation: The B cell receptor binds to an antigen which is either unprocessed (naïve - antigen alone) or processed (antigen taken up by B cell and associated with the MHC-II complex). Processed antigens are recognised by helper T cells which releases costimulators e.g. interleukin-2 that activate B cells more intensively. 2. Proliferation: Activated B cells next undergo clonal selection to increase in numbers, forming memory B cells and plasma cells. 3. Differentiation: Effector cells called plasma cells and memory B cells form.
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IgM location and function
blood and lymph Secreted after initial exposure to an antigen; bind to ABO antigens and activate complement system
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IgA location and function
Sweat, tears, saliva, mucous, breast milk, and gastrointestinal secretions Protect mucous membranes against bacteria and viruses
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IgD location and function
On B cell surfaces Act as antigen receptors; involved in the activation of B cells
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IgG location and function
Blood, lymph and intestines Enhances phagocytosis, neutralises toxins and activates the complement system. Only class of antibody to cross placenta
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IgE location and function
On mast cells and basophils Protection against parasitic worms; Involved in allergic and hypersensitivity reactions
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5 actions of antibodies
1. Neutralising antigens - bind to sites on bacteria or viruses to prevent attachment to body cells 2. Immobilising bacteria - attack cilia or flagella 3. Agglutinating and precipitating antigens - antibody-antigen complexes cross link to form lattices that clump to be phagocytosed 4. Complement activation - classical pathway 5. Enhancing phagocytosis - complement, precipitation, opsonisation
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Describe immunological memory
After the first encounter with an antigen the first class of antibody to be produced is IgM, followed by IgG days later. This is followed by a gradual decline in antibody titre. On second encounter with the same antigen, rapid proliferation of memory cells results in a far greater antibody titre (mainly of IgG) than during a primary response
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Which cells need to have self tolerance and self recognition?
T cells - need both. Self-recognition develops via positive selection in the thymus- meaning if pre-T cells possess the correct T cell receptor they will survive. Self-tolerance develops via negative selection- meaning the pre-T cells that react to own body peptides are eliminated by apoptosis.
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Which cells need self tolerance only?
B cells - because B cells mainly respond to extracellular threats as they do not use the ‘cell-cell’ response as used by T cells.
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4 types of antimicrobial substances in the body - second line
1. Interferons - trigger synthesis of antiviral proteins 2. Complement - consists of a group of normally inactive proteins in the blood plasma, that can be activated through various mechanisms during infection. Causes cytolysis, phagocytosis and inflammation 3. Iron binding proteins - inhibit growth of certain bacteria by reducing the amount of freely available iron. transferrin, lactoferrin, haemoglobin, ferritin 4. Antimicrobial proteins - chemotaxic and attract mast cells. Dermicidin from sweat glands, defensins from neutrophils, thrombocidin from platelets
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Steps of phagocytosis
1. Chemotaxis 2. Adherence - of phagocyte to microbe 3. Ingestion - of microbe via pseudopods on phagocyte to form phagosome 4. Digestion - via lysosomes 5. Killing - chemical digestion by enzymes
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5 characteristics of inflammation
Redness, heat, swelling, pain, and loss of function.
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3 stages of inflammation
1. Vascular phase -> vasodilation and increased capillary permeability allowing defence factors to enter tissues 2. Cellular phase -> phagocytes migrate into tissue spaces through diapedesis (neutrophils first to arrive then monocytes) that remove damaged tissue and invading microbes 3. Tissue repair ->Fibroblasts lay down collagen fibres and ECM, blood vessels restored and epithlial cells multiply to fill wound with new tissue. First intention healing produces minimal scarring and second intention produces more
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What is first intention healing?
Edges of skin dermis are close together and wound free of pathogens - close wound edges allow clot to form fast Tissue repair is rapid Minimal scarring
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What is second intention healing?
Occurs if wound edges further apart or wound infected Phagocytes have to clear infection before repair commences - tissue repair is longer Scabs form - healing begins from deeper layers, scab keeps fluid in so immune cells move freely. Fibroblasts lay down collagen fibres forming scar tissue
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What is fever and how is it regulated?
a systemic innate immune response of abnormally high temperature triggered by pyrogens Regulated by hypothalamus Intensifies effect of interferons, inhibits bacterial growth and speeds up tissue repair
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what 2 things does adaptive immunity require?
specificity to antigen Memory of previously encountered antigens
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2 characteristics of an antigen
Immunogenicity - ability to provoke immune response Reactivity - ability to react to cells or antibodies it provoked
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What is a hapten?
Smaller than an epitope and has reactivity but lacks immmunogenicity. Stimulates an immune repsonse when bound to a carrier molecule.
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2 steps in T cell activation
Antigen recognition - binding of foreign antigen to t cell receptor. CD4 and CD8 proteins on surface of t cell act as coreceptors to enhance binding of antigen Costimulation - secondary signal in the form of cytokine (interleukin-2) or molecules on PM of another cell
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How do helper t cells become activated?
Use their TCR to bind to an exogenous antigen fragment To aid this interaction, the CD4 receptor on the helper T cell, binds to MHC-II molecules on the surface of APCs that are associated with the antigen fragment. The APC provides costimulation and activates the helper T cell.
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How are cytotoxic t cells activated?
also use a TCR to bind to an endogenous antigen fragment The CD8 receptor on the T cell binds to antigens associated with MHC-I molecules on infected body cells, tumour cells and transplanted tissue cells.
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Basic antibody structure
four polypeptide chains (two heavy and two light chains) linked by disulfide bonds at the hinge region The variable regions of the heavy and light chains combine to form the antigen-binding site The constant regions for the stem of an antibody that serves common functions in all antibodies
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Process of inhalation
The thoracic cage expands because of two muscle actions: the diaphragm contracts and the external intercostal muscles lift the ribs. The lungs attached to the thorax also expand. Contraction of the inhalation muscles causes alveolar pressure to fall below atmospheric (758 mmHg) creating a pressure gradient that brings air into the lungs.   Active process
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Exhalation process
At rest is a passive process with no muscular contraction involved. When the diaphragm and external intercostal muscles relaxes, the elastic recoil of the chest wall and lungs pulls the thoracic cage down/in, decreasing the space (volume) Decreased space = increased pressure in lungs (alveolar pressure) = air flows out
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Process of laboured breathing
the sternocleidomastoid muscles, scalene muscles and pectoralis minor muscles contract (active process) to elevate the sternum and first 5 ribs. Occurs during exercise, stress or some respiratory conditions
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3 factors affecting pulmonary ventilation
Alveolar surface tension - inwardly directed force exerted by the alveolar fluid that coats the inside of alveoli. This force accounts for 2/3rd of elastic recoil during exhalation. Surfactant from type II alveolar cells decreases this. To inhale, muscle force expanding lungs has to overcome this. Lung compliance -> effort to stretch lungs and chest wall. High compliance = lungs expand easily. Low compliance caused by scar tissue or fibrosis Airway resistance -> Resistance increases during exhalation as bronchioles grow smaller. Constriction of bronchioles in asthma causes more resistance
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Internal vs external respiration
External respiration refers to the exchange of respiratory gases across the respiratory membrane between alveoli and red blood cells in pulmonary capillaries. Internal respiration refers to the exchange of gases between the tissue cells and red blood cells in systemic capillaries.
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minute ventilation =
resp. rate x tidal volume
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What is alveolar ventilation
The volume of air that reaches the respiratory zone each minute Respiratory rate x (tidal volume - dead space)
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The rate of gaseous exchange is determined by:
Gas partial pressure, surface area for gas exchange, diffusion distance and the molecular weight and solubility of gases
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Tidal volume
The volume (depth) of each breath, about 500ml is tidal volume.
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Inspiratory and expiratory reserves
Refers to the amount of additional air that can be forcibly inhaled or exhaled respectively.
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Vital capacity
The total volume of air that can be displaced from the lungs by maximal exhalation after a maximal inhalation is the vital capacity.
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Residual volume
A portion of non-measurable air that remains in the lungs after maximal exhalation is the residual volume.
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Total lung capacity
(6,000 ml) is the maximum amount of air your lungs hold (vital capacity + residual volume).
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Percentages of CO2 and their location in the blood
About 70% of carbon dioxide forms bicarbonate ions in plasma, the remaining 23% is bound to haemoglobin as carbaminohaemoglobin and some 7% dissolved in plasma.
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Percentage and location of O2 in the blood
(98.5%) is bound the haemoglobin in red blood cells. - Only the remaining 1.5% dissolved in plasma can escape capillaries and enter tissue cells.
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Factors affecting oxygen saturation
Partial pressure of oxygen - greater the PO2, more oxygen combines with haemoglobin until all saturated. PO2 high in pulmonary capilaries, lower in tissue capillaries so it unloads oxygen into tissues Acidity - increases, then affinity of haemoglobin for O2 decreases and dissociates. Haemoglobin can buffer H+ and bind to it when acidity is high, decreasing its affinity for O2 (Bohr effect) CO2 partial pressure - greater PCO2 = haemoglobin releases O2 and blood pH lowers also releasing O2 Temperature -> warmer, haemoglobin releases O2 more
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Foetal haemoglobin affinity for O2
Higher affinity for O2 as it binds 2,3-biphosphoglycerate (BPG) less strongly and carries more oxygen to offset low oxygen saturation in maternal blood
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What is BPG?
2,3-biphosphoglycerate - produce produced in RBC during glycolysis Greater BPG = more O2 released from haemoglobin
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Mechanism of CO poisoning
CO competes with O2 for the same binding sites on haemoglobin and has 200 times more affinity to Hb than O2.
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What is the haldane effect?
When oxyhaemoglobin is lower, more CO2 is transported in blood.
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3 ways CO2 is transported in the blood
1. Bicarbonate - 70% 2. Haemoglobin - 23% bound to globin portion 3. Plasma - 7%
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CO2 internal respiration
CO2 diffuses out of tissue cell and enters the RBC in a capillary - some binds to Hb causing oxygen displacement Some binds to water = makes carbonic acid = dissociated to bicarbonate and H+ Some bicarbonate moves out of rbc down conc. gradient, some H+ binds Hb in bufferring effect and O2 is released out of rbc
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CO2 external respiration
As deoxygenated blood passes through pulmonary capillaries CO2 dissociates from Hb and along with dissolved CO2 in plasma, the gas diffuses into the alveolar air and out of the body.
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Where is the respiratory centre? What are the two areas?
A cluster of neurons dispersed bilaterally in the brain stem Medullary respiration centre -> in medulla oblongata controls basic rhythm of respiration and contains dorsal and ventral respiratory groups - inspiratory and expiratory area respectively Pontine respiratory group -> in pons, modifies basic rhythm. Neurons active in inhalation and exhalation and transmit impulses to DRG in medulla to modify rhythm
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Regulation of quiet breathing
Dorsal respiratory group neurons generate impulse to diaphragm and external intercostals for inhalation for 2 seconds cuasing contraction Exhalation - DRG inactivates and diaphragm and external intercostals relax for 3 seconds for passive recoil of lungs
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Regulation of forceful breathing
Inhalation - neurons in VRG generate impulse to diaphragm, external intercostals and accessory muscles (sternocleidomastoid, scalenes, and pectoral minor). This results in their contraction. Exhalation - Another set of neurons in the VRG generates impulses to the accessory muscles of exhalation (internal intercostals and abdominal muscles) to contract
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Voluntary control of breathing
Cortical regulation allows conscious control Voluntary breath-holding is limited by increased H+ and CO2. If the breath is held to cause fainting, breathing resumes when consciousness is lost.
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What is the inflation reflex
Detects lung expansion with stretch receptors (baroreceptors) and limits inflation depending on ventilatory need and prevents damage. This is an important protective mechanism that comes into play during severe exercise.
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Explain the chemoreceptor reflex
Stimulus - disrupts homeostasis by altered chemical composition of blood (Co2, O2 or H+) Controlled condition - increase in PCO2 over 40mmHg is hypercapnia. A drop below 40mmHg is hypocapnia. Receptors -> 1. central chemorecepors in medulla oblongata respond to CO2 and H+ in CSF. If PO2 falls below 50 mmHg, the central chemoreceptor become depressed and the DRG fails to be stimulated -> fewer nerve impulses being sent to the breathing muscles -> possible fatal result. 2. The peripheral receptors in aortic arch and carotid artery respond to PO2, PCO2 and H+ in blood. If levels of arterial blood PO2 drop below 100 mmHg, (but still above 50 mmHg), only the peripheral chemoreceptors are activated. This negative feedback cycle results in hyperventilation (as when PCO2 is high). Control centre -> DRG recieve stimulatory signals and fire more impulses Effectors -> increased nerve stimulation of breathing muscles causing hyperventilation Response -> Increased volume of the thoracic capacity increases PO2 in inhalation and decreases PCO2 (and H+) in exhalation. This returns arterial blood levels of CO2 to normal relieving excess stimulation of the chemoreceptors.
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Stimuli that increase breathing rate and depth
PCO2 over 40 PO2 falling from 100 to 50 Increased activity of proprioceptors Increase body temp Decrease BP Stretching of anal sphincter Prolonged pain
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Stimuli that decrease breathing rate and depth
Severe pain PCO2 below 40 Decreased activity of proprioceptors Decreased body temp Increased BP
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Describe mechanical digestion in the stomach
Peristaltic movements pass over the stomach every 15 to 25 seconds to macerate food, mix it with secretions of the gastric glands and reduce it to chyme. Intense waves near the pylorus, vigorous waves in body of stomach and gentle waves in fundus. Peristaltic waves move gastric contents forward by propulsion. However, as particles are initially too big to pass through the pyloric sphincter, they are forced back up in retropulsion. The cycle continues until the food particles are small enough to pass through the pyloric sphinter.
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Describe chemical digestion of carbs in the stomach
Starts in mouth - salivary amylase continues to break down polysaccharides like starch into trisaccharides, disaccharides and short chain glucose polymers. After an hour, the amylase enzyme is inactivated by the acidity of the gastric juice.
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Describe chemical digestion of fats in the stomach
Starts in the stomach Lingual lipase (originally secreted by the tongue) is activated. Gastric lipase, secreted by the stomach chief cell, breaks down triglycerides into fatty acids and diglycerides. This enzyme has limited activity in adults.
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Describe chemical digestion of proteins in the stomach
Starts in the stomach. Pepsinogen is activated into pepsin which breakdowns proteins into peptides.
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Absorption capacity in the stomach
Absorption is limited due to the impermeability of stomach epithelial cells. Mucous cells absorb water, ions, short-chain fatty acids and certain drugs (e.g. alcohol and aspirin).
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Bile function in the liver
Producing bile salts used in bile for emulsification and absorption of lipids. Excretion of bilirubin into bile for metabolism in small intestine by bacteria and elimination in faeces from large intestine.
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Toxins - liver function
The liver has many enzymes to process toxins (e.g. alcohol) and has two detoxification processes.
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Vitamins - liver function
Activating vitamin D precursor produced by the skin
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Hormones - liver function
Processing drugs and hormone (oestrogen_
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RBC - liver function
Excreting bilirubin
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Storage - liver function
Storing glycogen, some vitamins and minerals for later use
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Metabolic processes - liver
Metabolism of lipids (storage of triglycerides), plasma protein synthesis, breakdown of glycogen
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Gall bladder functions
Stores bile between meals from liver Releases bile during meals
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Bile secretion regulation
Parasympathetic impulses and vagus nerves. Cholecystokinin (CCK): causes gallbladder to contract and release stored bile into the duodenum. Secretin: causes liver to increase its output of bile.
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Pancreas function
Pancreatic juice clear, colourless containing water, salts, sodium bicarbonate and digestive enzymes Acini cells produce the digestive enzymes that contribute to chemical digestion of starch (via pancreatic amylase), proteins (via pancreatic proteases), fats (via pancreatic lipase) and nucleic acids (via ribonuclease and deoxyribonuclease).
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Mechanical digestion in the SI
Two types of movements: segmentation and migrating motility complex (MMC). Segmentation -> localised mixing contractions that occur in portions of the intestine distended by a large volume of chyme. They occur 12 times per minute to bring food particles in contact with the mucosa for absorption. There’s no propulsion. MCC -> the type of peristalsis that occurs in the small intestine when distension of the small intestinal wall lessens (after segmentation). Each wave migrates progressively along the small intestine, reaching the end in about 90-120 minutes.
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Chemical digestion in the SI
Intestinal juice contains water, mucous, brush-border enzymes, and lysozyme. Absorptive cells lining the mucosa secrete several brush border enzymes to complete the chemical digestion of carbohydrates, proteins, fats, and nucleic acids.
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Digestion of carbohydrates
In the mouth, salivary amylase In the small intestine - pancreatic amylase break down starch and dissacharides into oligosaccharides and disaccharides - lactose, maltose and sucrose Brush border enzymes in SI (lactase, maltase, sucrase) break disaccharides into galactose, glucose and fructose
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Digestion of proteins
Pepsin in stomach in presence of HCl breaks protein into large polypeptides Pancreatic enzymes in SI (trypsin, chymotrpysin and carboxypeptidase) break large polypeptides into small polypeptides Brush border enzymes in SI (aminopeptidase, carboxypeptidase and dipeptidase) break small polypeptides into amino acids
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Lipid digestion
Unemulsified fats are emulsified by detergent action of bile salts from the liver in the small intestine Pancreatic lipase in the small intestine breaks emulsified fats into monoglycerides and fatty acids, and glycerol and fatty acids
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Absorption of monosaccharides in the SI
All carbohydrates are absorbed as monosaccharides. The indigestible cellulose and fibres are eventuially excreted in faeces from the large intestine. GLucose and galactose -> secondary active transport with Na+ Fructose -> facilitated diffusion
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Absorption of amino acids and dipeptides in SI
Majority of proteins are absorbed as amino acids (with some dipeptides and tripeptides), that occurs in the duodenum and jejunum. Amino acids - active or secondary active transport with Na+ across brush border Dipeptides and tripeptides - secondary active transport with H+
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Absorption of lipids in SI
Triglycerides are digested into monoglycerides and fatty acids, which are either short-chain (under 10-12 carbon atoms) or long-chain fatty acids. Short fatty acids -> water-soluble and dissolve in the intestinal chyme, absorbed into a capillary Larger fatty acids and monoglycerides -> absorbed into lacteals. From here, the chylomicrons enter lymphatic system -> pass into the cardiovascular system -> reaching the liver or adipose tissue
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Mechanical digestion in the LI
Haustral churning after the relaxed haustra fill and stretch. Eventually, they contract and squeeze, shifting contents to the next haustra. Mass peristalsis is a strong wave that drives contents into the rectum ~4 times daily. The defecation reflex is a spinal reflex that causes the walls of the sigmoid colon and rectum to contract and the anal sphincters to relax. With the next mass movement, the reflex is stimulated again.
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Chemical digestion in the LI
Resident bacteria ferment the remaining carbohydrates, releasing hydrogen, carbon dioxide and methane gases. Undigested proteins are converted to amino acids and broken down into aromatic compounds and fatty acids. Excess bilirubin turns into simpler pigments (such as stercobilin), giving faeces the brown colour
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Absorption in the LI
Small amounts of water, ions, and vitamins (B and K) are absorbed.
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3 phases of digestion
Cephalic phase - activated by smell, sight, thought, or initial taste of food. The neural centres in the cerebral cortex, hypothalamus, and brain stem send a message to the facial and glossopharyngeal nerves to stimulate the salivary glands to secrete saliva. Saliva then triggers the vagus nerve, which stimulates the gastric glands to secrete gastric juice. The gastric phase commences once food reaches the stomach. It is regulated by the nervous and endocrine systems (gastrin released from g cells in response to distention and high pH, inhibited with pH below 2). Gastrin stimulates gasgtric juice secretion, contracts lower oesophageal sphincter and increase gastric motility The intestinal phase begins when food enters the small intestine. It is responsible for promoting digestion of food in the small intestine and slowing the exit of chyme from the stomach. Governed by neural (enterogastric reflex) and hormonal control (secretin and CKK)
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G cell function
gastrin secretion - stimulate parietal cells to secrete H and Cl- ions into stomach lumen to form HCl Stimulates chief cells to secrete pepsinogen, contracts lower oesophageal sphincter, increases stomach motility, relaxes pyloric sphincter
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What protein is required for absorption of B12?
intrinsic factor secreted by parietal cells
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Pathway of long chain fatty acid absorption
Long-chain fatty acids and monoglycerides recombine inside absorptive cells in gut to form triglycerides. Triglycerides join with cholesterol and phospholipids to form chylomicrons that exit absorptive cells by exocytosis and enter the lacteal of villus - then to thoracic duct Short-chain fatty acids exit absorptive cells by diffusion.
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Describe the enterogastric refelx
Neural control of the intestinal phase of digestion Arises from the distention of the duodenum by the presence of chyme. Nerve impulses are sent to the medulla oblongata causing the inhibition of parasympathetic nerves and stimulation of sympathetic nerves to the stomach. This stops gastric motility and increases contraction of the pyloric sphincter to decrease gastric emptying
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What stimulates secretin? What does secretin do?
acidic chyme Stimulates pancreatic juice rich in bicarbonate that buffers acidic chyme in duodenum and slows production of stomach acid
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What stimulates CKK and what does it do?
Amino and fatty acids Increases bile and pancreatic juice in duodenum, decreases stomach emptying and produces satiety
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