Karteikarten
Integrative
Karten in diesem Stapel (162)
- 1Why is pH important in medicine?Enzyme activity is dependant on protein structure. There is competition of Ca2+ and H+ for binding sites on albumin
- 2What are Trosseau and Chvoskek's signs?Trosseau: Latent tetany in hypocalcaemia. Wrist and metacarphalangeal joints flex and the fingers adduct.
Chvostek: Abnormal reaction to stimulation of the facial nerve, results from hypocalcaemia which destabilises the membrane potential - 3What is the bicarbonate buffer system?CO2 + H20 = H2CO3 = HCO3- + H+
- 4What is the reabsorption of bicarbonate ions in the kidney stimulated by and what is the mechanism?Stimulated by angiotensin 2, which activates H+/Na+ exchanger in the proximal tubule that moves H+ into the lumen, causing HCO3- to be moved into the blood.
- 5How is bicarbonate lost in buffering regenerated by the kidney?Protons are secreted into the nephron via the H+/K+ ATPase that are trapped and excreted by ammonium. HCO3- is then reabsorbed into the blood
- 6What is metabolic acidosis?Blood pH <7.35 and HCO3- less than 22mmol/l
- 7What is the difference between high anion gap metabolic acidosis and normal anion gap acidosis?High anion gap- Affected by changes in unmeasured ions. There is an increase in ketoacids, which bicarbonate buffers
Normal anion gap- Loss of HCO3- through renal or GI excretion. Compensated for by an increase in Cl-. - 8Metabolic alkalosis?pH is elevated above 7.45 as a result of decreased H+ leading to an increased HCO3- concentration or as a direct result of increased HCO3-
- 9Difference between chloride responsive metabolic alkalosis and post hypercapina alkalosis?Chloride responsive is due to loss of HCl through vomiting. Hypercapina is a result of respiratory acidosis being compensated for with bicarbonate, which causes an alkalosis on return to normal CO2 levels.
- 10Difference between acute and chronic respiratory alkalosis?Acute- Occurs when an abrupt failure of ventilation occurs. May result due to defects in the neuromuscular chain or an obstruction to air flow.
Chronic- Secondary to disorders including COPD - 11Respiratory alkalosisIncreased alveolar respiration expels CO2. Alters the dynamic equilibrium, H+ and HCO3- are shifted to make more CO2, decreased amount of H+ ions in the circulation.
- 12How do free radicals cause ageing?Lipid per oxidation- oxidative degradation of lipids. Products include malondialdehyde, which interferes with DNA by forming mutagenic DNA adducts
Decrease enzyme acitivity - 13Genetic causes of ageing?DNA redundancy failure- As errors occur with aging, redundant sequences are used and eventually errors are expressed
Failure in chromosome replication- Telomeres shorten with each cell division, and eventually are so small cells can no longer divide. - 14Changes to eyesight associated with agingPresbyopia- Loss of elasticity in the crystalline lens, changes in the lens's curvature and loss of power of the capillary muscles. Power of accommodation decreases from 14 diopters in the young to around 0 by the age of 70.
Cataracts- Deterioration of lens function. - 15Hearing?Presbycusis- Progressive loss of hair cells within the cochlea. First associated with higher frequencies.
- 16Structural changes in the cardiovascular system associated with ageing?Decrease in myocycte number.
Increase in ratio of collagen, stiffening the myocardium.
Increase in collagen and decreased elastic tissue in the arteries. Also increased calcium deposits. Reduces compliance. - 17Functional changes in the cardiovascular system associated with ageing?Functional- Decrease in the maximum attainable heart rate (220-age) due to the decrease in B adrenoreceptors
Decrease in SV by 0.7% per annum due to increased afterload
Blood pressure rises due to increased peripheral resistance - 18How does ageing effect the baroreceptor reflex?Sensitivity is decreased in older individuals, due to decrease in arterial compliance and increased rigidity, which impair baroreceptor afferents in carotid and aortic arch.
- 19Symptoms of sarcopeniaDegenerative loss of skeletal muscle mass by 0.5-1% per year after 50. Characterised by muscle atrophy and replacement of muscle with fat and increase in fibrosis
- 20Sarcopenia on a metabolic and cellular levelCellular: Degeneration of the neuromuscular junction, decrease in muscle cell number, twitch force and SR volume. Disorganisation of sarcomeres and a decrease in the excitability of the plasma membrane.
Metabolic- Decreased mitochondrial protein synthesis and impairment of glycolytic and oxidative enzymes. Also a decrease of 10% in metabolic rate. - 21Causes of sarcopeniaFailure in satellite cell activation
Lower testosterone decreases protein synthesis.
Inactivity
Reduction in food intake
Accumulation of non-contractile material due to oxidized proteins - 22Characteristics of osteoporosisDecrease in bone mass and density. Density of 2.5 standard deviations below mean peak bone mass.
In males, after 50 loss of 0.4% per annum
In females, from 35 loss of 0.8% per annum. - 23Underlying mechanism of osteoperosis.Imbalance between bone resorption and bone formation.
1. Excessive resorption
2. Inadequate formation of new bone during remodelling
3. Inadequate peak bone mass
Hormonal factors strongly determine the rate of bone resorption. Low oestrogen increases resorption. - 24What is an intrauterine growth retardation?Affects 3-7% of all pregnancies. Defined as birth weight that is more than two standard deviations below the mean for gestation age. Defect in the mother being able to supply nutrients to the placenta. Head and limbs are normal, decreased circumference of the abdomen.
- 25Transport of CO2 across the placentaPCO2 of fetal blood is 2-3mmHg higher than maternal blood, giving a small pressure gradient, which is adequate due to solubility of CO2.
- 26How is oxygen transported across the placenta?Dissolved oxygen in the maternal sinuses pass into the blood by simple diffusion, driven by a pressure gradient of 20mmHg.
Fetal haemoglobin has higher affinity to carry oxygen - 27Difference between fetal and maternal haemoglobin?Fetal haemoglobin has two Y subunits, compared to two B subunits. At low PO2 levels of fetal blood, fetal haemoglobin can carry 20-50% more oxygen than maternal haemoglobin.
Fetal haemoglobin is 20-50% more concentrated - 28What happens to fetal haemoglobin at birth?Y subunits are switched to B subunits by glucocorticoids.
- 29How is glucose transported across the placenta?Transported across the placenta by facilitated diffusion via hexose transporters that are not dependant on insulin.
A large amount of glucose is oxidised within the placenta to lactate. - 30What is gestational diabetes and what impact does it have on the fetus?In early pregnancy, progesterone increases maternal appetite and builds fat stores.
In late pregnancy, maternal tissues become insulin insensitive, meaning more glucose is available to the mother.
Gestational diabetes causes woman to exhibit high glucose levels in pregnancy due to poor functioning insulin receptors.
Increases fetal insulin levels, leading to excessive growth, and leads the neonate with an increased risk of hypoglycaemia - 31How does the fetus use glycogen and fatty acids?Glucose storage provides for most of the fetus metabolic needs. Glycogen is stored in the liver and cardiac muscle, regulated by the fetal adrenal cortex.
Fatty acids are used for storage (white fat) and heat generation (brown fat) - 32What is the mechanism of non shivering thermeogenesis?T3 opens proton channels in the mitochondria, which short circuits the electron transport chain, which generates heat.
- 33How are amino acids transported across the placenta?Transported to the fetus by active transport by Na+ dependant channels. Substitutional metabolism of some amino acids as the cross the placenta, much of serine is converted to glycine prior to delivery to the fetus.
- 34Outline the fetal circulationBlood from the placenta is carried to the fetus by the umbilical vein. 1/3 of this enters the ductus venosus and is carried to the inferior vena cava. The rest enters the liver via the portal vein.
The blood then moves to the right artium of the heart. Blood from the left ventricle is pumped through the aorta into the body. - 35What are the shunts of the foetal circulation? Why are they needed?Ductus Venosus- shunts a portion of the left umbilical vein directly to the inferior vena cava
Ductus arteriosis- connects the pulmonary artery to the proximal descending aorta, bypassing the pulmonary circulation
Foramen ovale is a shunt between the atria.
Shunts ensure optimal distribution of blood. - 36What are the changes in the ductus venosus during pregnancy? What clues does this give us about the importance of the foetal liver?The amount of blood shunted decreases from 30% at 20 weeks to 18 at 32 weeks, suggesting a higher priority of the foetal liver than previously thought.
- 37What are the changes in the foetal circulation at birth?Supply of blood from the placenta is disrupted , decreasing blood supply to the right atrium.
Through the first couple of breaths, the pressure in the circulatory system is massively attenuated.
Leads to a reduction of blood flow through the ductus arteriosis and the foramen ovale and an increase in blood flow through the lungs. - 38What happens to the ductus arteriosis and venosus at birth?Closure due to constriction of smooth muscle as a result of decreased prostaglandins
- 39Outline the stages of foetal lung developmentThe foetus spends 1-4h every day breathing. Only occurs during REM sleep. Diaphrgmatic and move amniotic fluid in and out of the lungs, causing them to distend and stimulates growth.
- 40What are the role of glucocorticoids in foetal lung development?Increases the number of type II alveolar epithelial cells that produce surfactant
Increase the number of lamelli bodies, which are the site of surfactant production.
Mature the enzymes that produce surfactant. - 41What is respiratory distress syndrome?Affects 10-15% of newborn babies.
Charechterised by cyanosis, tachypnea and nasal flaring.
Caused by the deficiency if pulmonary surfactant and in some cases ENac deficiency - 42How does the content of the foetal lung change?For the majority of the foetal life, lungs are filled with fluid, driven by chloride movements through CFTR
Glucocorticoids promote the expression of ENac, which drives salt and water absorption in the lung, via the pulmonary circulation. - 43What are the changes in compliance at birth?Tremendous negative intraplural pressure required to open the lungs at the onset of breathing.
The volume of air in the lungs is 0 until the negative pressure has been reached. To deflate the lungs, considerable positive pressure is required because of viscous resistance.
The second breath is much easier with far less negative and positive pressures required.
Breathing does not become completely normal until about 40 minutes after birth. - 44How well is the nervous system developed at birth?Sensory organs are highly developed
Most of the reflexes involving the spinal cord and brainstem are present by the third to fourth month of pregnancy.
Cerebral cortex is less well developed even at birth. Myelinisation of some major tracts are complete only after about 1 year. - 45How alert is the foetus during pregnancy?Shows periods of slow wave and REM sleep between periods of wakefulness
- 46What is amniotic fluid? And how is it produced and excreted?Liquid that surrounds the foetus. Contains electrolytes, carbohydrates, proteins and phospholipids.
Produced via renal and pulmonary excretions.
It is turned over at least once a day, and is removed from the GI tract, amnion and lungs. - 47How do drugs affect the nervous system of the foetus?The BBB is less developed in the foetus.
Use of morphine and nicotine by the mother creates dependence.
Pain killers can depress suckling - 48What is the main organ of secretion during pregnancy? How does the renal system developThe placenta is the main organ of excretion.
Glucocorticoids increase the expression of Na+/K+-ATPase.
Foetal kidneys begin to excrete urine during the second trimester of pregnancy, and foetal urine accounts for 70-80% of the amniotic fluid.
The renal systems for regulating foetal extracellular fluid and electrolyte fluid balances are non-existent until late foetal life. - 49What is meconin and how does it help to develop the GI tract?Formed in the GI tract and are excreted from the anus into the amniotic fluid. Composed of residue from swallowed amniotic fluid and other residues of excretory products.
Allows 'practice' and provides a small contribution to the foetal nutrition. - 50How does the GI system develop in the foetus?By mid-pregnancy, the foetus begins to ingest and absorb large quantities of amniotic fluid, and during the last 2-3 months GI function approaches that of the normal neonate
Glucocorticoids cause the maturation of the GI system by stimulating Na+/K+-ATPase - 51How does the endocrine system function in pregnancy?From early pregnancy the foetus is self sufficient in its hormonal requirements.
Maternal hormones do no directly influence the foetus except in disease. - 52Describe the difference between the 'shell' and the 'core' in temperature regualtionThe 'shell' is the skin, muscle, fat and testes. At 37*C in hot environments but drops in the cold. Ranges from 20-40*C
The 'core' is the brain and internal organs. The rectal temperature is kept at a constant rate of 37.2-37.6*C. Core temperatures ranges from 35-38*C. - 53Describe variations in the skin temperature throughout the dayA diural variation is seen depending on the period of rest and activity. Lowest at 11pm to 3am and peaking at 10am to 6pm.
- 54What are the temperature variations in the menstrual cycle?During the follicular phase, the average basal body temperature ranges from 36.5 to 36.7. Within 24 hours of ovulation, women experience an elevation of 0.15 to 0.45 due to increased metabolic rate by sharply elevated levels of progesterone.
- 55Give an overview of ATP productionProduced by redox reactions using complex and simple sugars and lipids.
Complex sugars first need to be broken down into more simple molecules. Carbohydrates are hydrolysed into simple sugars such as glucose and fructose. Fats are metabolised to fatty acids and glycerol.
30 molecules of ATP are generated for each glucose molecule. - 56Outline glycolysisMetabolic pathway that converts glucose into pyruvate.
Free energy released in this process is used to form 2 ATP and 2 NADH.
Determined sequence of ten enzyme-catalysed reactions.
Anaerobic and fast. Releases 8% of glucose energy.
Occurs in the cystol. - 57What is the citric acid cycle?Series of chemical reactions that oxidises acetate derived from carbohydrates, fats and proteins to form CO2 and ATP.
Takes place in the mitochondria.
Pyruvate is decarboxylated by pyruvate dehydrogenase to acetyl-CoA
Produces 2 ATP and 1H+. - 58What is oxidative phosphorylation?Passage of electrons from NADH and FADH2 through the electron transport chain which powers the pumping of protons out of the mitochondrial matrix into the intermembrane space.
Generates potential energy in the form of a pH gradient and an electrical potential across the membrane.
ATP synthase allows protons to flow back across the membrane, and uses the energy to generate ATP from ADP
Able to generate 34 ATP
Slower than glycolysis and dependent on oxygen. - 59How many ATP molecules can be generated from a single molecule of glucose? What is the efficiency of the breakdown of glucose in the body?30 molecules of ATP is generated for every glucose molecule.
The maximum efficiency is 2/3. Other 1/3 is given off as heat.
Less ATP is generated when the body is not at optimum temperature of lack of oxygen.
Best efficiency when things are happening slowly. - 60What are the feedback systems in ATP production?End product inhibition- Due to A*B=C
Citric acid cycle reduces glycolysis as it inhibits phosphofructokinase, which catalyses the production of a precursor of pyruvate.
ADP stimulates glycolysis. - 61What is oxygen debt?The first phase if the reconstituting of the stores of ATP and creatinine phosphate (3.5L)
Lactic acid is converted back to glycogen (8L) - 62What is the length tension relationship?
- 63What are the differences between slow twitch and fast twitch muscle?Slow twitch- Type 1, small, good blood supply. Fatigue resistant, oxidative metabolism, high levels of myoglobin and mitochondria, exhibit hypertrophy.
Fast twitch- Type II, larger, extensive SR, fatigue sensitive, glycolytic metabolism. - 64What are the changes in the respiratory system in response to a single session of exercise?Unconscious increase in minute volume (VE).
Conscious control over balance of increased depth and rate.
Forced expiration alters the insp:exp ratio from 1:2 to 2:1
VE in exercise never reaches max voluntary VE.
Increased depth (Vt) and increased rate (f) of breathing - 65What are the mechanisms through which the respiratory system changes in response to a single session of exercise?Sensitivity of peripheral chemoreceptors to oscillation in PaO2 and PaCO2 is responsible to increased ventilation.
Central chemoreceptors may readjust to increase ventilation to maintain CO2 concentrations
During prolonged exercise, or at higher rates of work, increases in CO2 production, H+ and body and blood temperatures further increases pulmonary ventilation. - 66Describe changes in pulmonary ventilation in response to exerciseIncrease is seen within 1 resp cycle. There is a sudden and massive increase in then a slight reduction followed by a gradual increase over minutes.
Once exercise stops, there is a steep reduction followed by a gradual decrease from minutes to hours.
- 67How does the lung capillary transit time change with exercise?With increased exercise there is decreased lung capillary transit time.
- 68Changes to the ventilation perfusion relationship in response to exerciseAt rest, the BP at the top of the lung is less than the gas pressures so the capillaries are compressed.
At rest, the V:Q is 1:1. In exercise, the Va increase is bigger than the CO increase, so the ratio is altered and there is an increase in PaO2.
- 69Changes in the blood content during exerciseDuring severe exercise, with an increase in CO2 and H+ ions, there is a shit in the haemoglobin dissociation curve to the right, so lowered amount of haemoglobin bound to oxygen at a certain pp.
- 70What are the changes of the distribution of blood in response to exercise.Rest Hard Work Maximal work
Cardiac output 5800 17500 25000
Skeletal m 1200 12500 22000
Splanchnic 1400 600 300
Kidneys 1100 700 250
Brain 750 750 750 - 71How does the redistribution of blood in response to exercise happen?Sympathetic vasoldilation of capillaries caused by a build up of metabolites and heat generated by exercise. Decreases diffusion distance with no change in transit time
Balance of increased supply to exercising skeletal muscle vs sympathetic effects on TPR and BP. - 72What are the changes to the cardiovascualr system in response to exercise?Symapthetic increase in heart rate and force.
Increased venous return due to the skeletal muscle pump.
Increased stroke volume - 73What is the frank starling mechanism?The SV of the heart increases in response to an increase in the volume of blood filling the heart. Increased volume of blood stretches the ventricular wall, causing cardiac tissue to contract more forcefully.
- 74What is the skeletal muscle pump?Contraction of muscle compresses then decrompresses around the vein, squeezing blood through the vessels.
- 75What is the respiratory pump?interthoracic pressures decrease during inspiration, lowering the pressure on the right atrium, raising venous return
- 76What is the afterload of the heart?Tension developed in the wall of the left ventricle during ejection. Increased BP increases afterload which tends to decrease the SV
- 77What are the hormonal changes in response to exercise?AD/ND causes an increase in heart rate (B1) Dialtes BVS (a1, B2), dilates bronchioles (B2) and stimulates gluconeogenesis (B2)
Acth cortisol increases gluconeogenesis. - 78Outline fatigueIntrinsic- acute failure of EC coupling by K+ in T tubules, H+ in cells, hypoxia
Extrinsic- Metabolic H+ and CNS influence
Recovery- O2 debt and inflammation - 79What is the effect of oxygen at high pressures?At high PaO2, over 100mmHg, the amount of oxygen dissolved in water increases markedly.
Once PaO2 rises above critical level, the haemoglobin-oxygen buffer mechanism is no longer capable of keeping the tissue in the range between 20-60 mmHg.
Causes free radicals to swamp the enzymes designed to remove them.
Causes the destruction of the membrane and disrupts metabolic enzymes. Causes a cerebral vasoconstriciton. - 80What is decompression sickness?Large amounts of nitrogen is dissolved in a divers body.
When the diver comes to the surface, nitrogen bubbles develop intra or extracellularly.
If the diver is bought up to the surface slowly enough, nitrogen is eliminated through expiration. - 81Why is helium used instead of nitrogen in deep sea divingHelium is used at massive depths as it has 1/5 of the narcotic effect of nitrogen and 1/2 as much volume dissolves as nitrogen.
- 82What are the respiratory, CVS and skeletal adjustments in response to the diving reflex?Respiratory system- Normal inspiratory reflexes inhibited. Chest shape evolved to permit compression without damage. No drive for ventilation.
CVS- Decrease in HR and CO, plus a general vasoconstriction. Use of sinuses and spleen as stores of blood.
There is an ability to switch readily between aerobic and anaerobic respiration. - 83What are the short term adaptations to altitude?The decrease in HbO2 causes an increase in HR and CO. Decreased PCO2 causes an increase in pH (respiratory alkalosis)
Increased ventilation drives off CO2, shifting equilibrium to the right, decreasing H+
HCO2- is maintained by the kidneys at a low level, H+ rises to maintain equilibrium with CO2.
Hypocapina shifts haemoglobin curve to the left. - 84What are the progressive adaptations in response to altitude?Increased HCO3- excretion by the kidney. Normalises pH but decreases buffering ability.
Increased sensitivity to hypoxia
Increased haemopiosis from erythroprotein in kidney, increases haematocrit which increases blood viscosity.
Increase in CO but decrease in TPR
Vasoconstriction in the lung gives better perfusion of the lung apex - 85What are the pulmonary adaptations to exercise?There is no change in lung function/volumes, but there is an increase in maximal minute ventilation at maximal exercise
- 86What are the cardiovascular responses to exercise?Resting CO is not different after training at rest, but there is an increase in maximal CO and SV at maximal exercise.
Endurance athletes have a lower heart rate at rest, but there is no difference in peak HR.
Increased left ventricular volume, giving larger LV end diastolic pressure- frank starling mechanism- increased SV
Increased diastolic filling time, giving bradycardia at rest. - 87What is VO2 max?Maximum rate of oxygen rate of oxygen consumption measured during exercise.
Vo2 max= Qx(CaO2-CvO2) - 88What are the metabolic changes in response to exerciseMore mitochondrial content after endurance training.
Increased levels of oxidative enzymes such as succinate dehydrogenase, which converts succinate to funarate, and citric synthase which converts OAA + Acetly-CoA to citrate in the citric acid cycle.
Fat metabolism and lactate threshold is enhanced. - 89What are the pharmacological aids to increase exercise performance?Sympathomimetic amines such as amphetamines, increase CO, breathing rate and blood glucose.
Beta blockers block the effects of noradrenaline and adrenaline, reduce muscle tension.
Caffeine stimulates CNS and increases lipolyisis. - 90What are the hormonal agents used to increase exercise performanceAnabolic steroids increase fat free mass and muscle strength.
- 91What is blood doping>increases red blood cell volume and increases VO2 max
Erythroproetin increases haemoglobin by 10% and VO2 max by 8%. Side effects include thrombosis, MI, hypertension, stroke and PE. - 92What is the exterior non-specific defence?Mechanical- Tight junctions/desmosomes. Skin, thick with high turnover of cells.
Secretary- Tears, saliva, sweat, mucus. Low pH in the GI tract. Comensual organs.
Haemostasis- Primary: platelet plug, Secondary: blood coagulation - 93What are mast cells and what is their role?Mast cells- Reside in connective tissue and the mucous membrane. Associated with wound healing, and when activated release granules containing histamine and herapin, along with chemokines and cytokines.
- 94Outline phagocytosisEngulf pathoges, wrapping the membrane around the particle. The pathogen is contained inside an endosome, which is destroyed by lysosome.
Signalled for by cytokines. - 95What are macrophages?Fight long lasting infections as they are able to move across the wall of capillary vessels.
Kills pathogen through a respiratory burst.
Most efficient pathogen. - 96How are macrophages differentiated throughout the body?Lung- alveolar
Liver- Kupffer's
Kidney- Mesangial
Brain- Microglial - 97What is a respiratory burst?Rapid release of reactive oxygen species.
NADPH oxidase reduces O2 to free radicals and hydrogen peroxide.
Myeloperoxidase is used to further combine H2O2 with Cl- to produce hypochlorite, which plays a role in destroying bacteria. - 98What are neutrophils?Granulocytes.
70% of all white blood cells.
Fights early stage of infection
Respiratory burst
Made in bone marrow - 99Dendritic cellsPhagocytic cells present in tissues that are in contact with the external environment.
- 100What are natural killer cells?Type of lymphocyte in the non-specific immune system.
Do no directly attack invading microbes.
Kill 'non-self' cells, recognised by absence of MHCI.
MHC antigens are recognised by killer cell on the immunoglobulin receptors.
Inserts perforin protein into the cell membrane, disrupting intracellular balance. - 101What is the complement cascade?Recruit phagocytic cells to the site of infection and promote inflammation (C3a and C5b), plus chemotaxis
Acts as opsonins and coats pathogens with markers for destruction by phagocytes. (C3b)
Formation of membrane attack complex which disrupts cell membrane and causes cell lysis (C5b, C6-9) - 102What is the classical pathway of the complement cascade?Initiated by IgG (2 units) or IgM (one unit).
Activates Clr complex, which cleaves C4 and C2 into C2a+b and C4a+b
C2a and C4b bind to form C3 convertase, which cleaves C3 - 103What is the alternative complement cascade pathway?Does not rely on pathogen
Continuously activated at a low level as a result of spontaneous C3 hydrolysis due to the breakdown of the internal thiester bond. - 104What is the membrane attack pathway?C5b initiates the membrane attack pathway
Binds to C6 and C7. The C5b-6-7 complex binds to C8, which acts as a catalyst in the polymerisation of C9.
This region is homologous to cholesterol-dependent cytocysis from Gram-positive bacteria.
Forms a pore in the membrane of bacteria. - 105What are interferons?Signalling molecules made and released by host cells in response to the presence of pathogens such as viruses and bacteria.
They are cytokines which interfere with viral replication and increase host defences by activating immune cells by up-regulating antigen presentation by virtue of increasing the expression of MHC antigens.
IFNs activate signal transdural activator of transcription (STAT), which activates the Jans kinase STAT pathway.
Japanese encephalitis and dengue type 2 have evolved resistance to interferons. - 106What are acute phase proteins?Released from the liver in response to injury and inflammation.
Form C3 and serves as coagulation factors and opsonins. - 107Outline the 5 stages of inflammation1. Stationary macrophages attach
2. Local blood supply is increased
3. Increased capillary permeability
4. Invasion of neutrophils
5. Arrival of mobile macrophages - 108What is the point of inflammation?Response ensures that phagocytes and other substances are brought to the injured area.
- 109What is an antigen?Molecules are structures that can tigger a specific immune reaction
Production occurs in bone marrow. - 110How are antigen receptors coded?Coded for by a small number of genes
Genetic recombination allows millions of different receptors to be coded for. - 111What is the primary lymphoid tissue?Involved in the production and early clonal selection of lymphocyte tissue.
Made up of the thymus and bone marrow.
From the bone marrow, B cells immediately join the blood stream and travel to secondary lymphoid tissues in search of pathogens.
T cells travel to the thymus where they mature. - 112What is the secondary lymphoid tissue?Includes lymph nodes and spleen.
Maintains mature naive lymphocytes and initiates an adaptive immune response.
Site of lymphocyte activation by antigens, leading to clonal expansion and affinity maturation.
Mature lymphocytes recirculate between the blood and peripheral lymphoid organs until they encounter their specific antigen. - 113What is clonal expansion?An antigen, bound to specific receptors selectively activates a tiny proportion of the pool of diverse lymphocytes created by the body which results in the generation of clones as thousands of cells which are specific for and dedicated to defending against the antigen.
Produces millions of clones of a single cell. Produces both effector cells and memory cells. - 114What are B lymphocytes?Antibody (humoral) specific defence (20% of lymphocytes)
Express a unique B cell receptor (BCR), which is an immobilised antibody molecule.
All the BCR of any clone of B cells recognise and binds to only one antigen.
Last 7 days. - 115Describe the process through which B lymphocytes cause the activation of B lymphocytes.B lymphocytes binds to specific antigen via membrane antibodies
Activates lymphocytes with helper T cells.
Transforms into plasma cells which last for 2-3 days and secrete antibodies.
10% of plasma cells survive to become long-lived antigen specific memory B cells. - 116What are the different types of antibodies?IgG (72%)- One basic unit. Directly attack microbes and toxins of bacteria and increase phagocytosis.
IgA (8%)- Two basic units. Works against bacteria toxins and directly attack some microbes. Found in bile and saliza and protects mucosal surfaces.
IgM (15%)- 5 units. First on scene, activates complement system.
IgD (1%)- Acts on surface receptors on B-lymphocytes, found primarily in blood and lymph.
IgE (4%)- Antibodies bind to mast cells and facilitate inflammatory response to antigens and cause allergic reactions. - 117Describe antigen-antibody interactions1. Neutralisation- binds and blocks the activity of a microbe.
2. Agglutination- Clamping causes neutralisation and opsonisation.
3. Precipitation- Forms immobile precipitates, then phagocytosis.
4. Opponisation- enhances macrophage attachment to microbe
5. Lysis
6. Activation of classical complement cascade. - 118What is a T lymphocyte?Cellular specific defence
Involved in the destruction of virus and infected cancer cells
Have a T cell receptor on the cell surface
Develop in the thymus - 119What are helper T cells?Assist other white blood cells in immunologic processes, including maturation of B cells into plasma cells and memory B cells, and activation of cytotoxic T cells and macrophages.
Become activated when they are present with peptide antiges by MHC class II molecules.
Once activated they secrete cytokines. - 120What are killer T cells?Bridge the adaptive immune system with the non-specific
Become activated by glycolipid CDld.
Once activated, they release cytoltic/cell killing molecules.
Able to recognise and eliminate tumours and cells infected with herpes. - 121What are memory T cells?Persist long-term after an infection has resolved.
Quickly expands to large numbers of effector T cells upon re-exposure to the their cognate antigen, thus providing the immune system with 'memory' against past infection. - 122What are MHC class I proteins?Found on antigen presenting cells of the body
Their function is to display fragments of non-self proteins from within the cell to cytotoxic T cells, this will trigger an immediate response from the immune system against the particular non-self antigen displayed with the help of MHCI
Unique to each individual, and are exposed on all cells except RBCs. - 123What is the structure of MHCI proteins?Heterodimers that consist of two polypetide chains.
The a3 domain is plasma-membrane spanning and interacts with the CD8 co-receptor of T cells.
The a3-CD8 interaction hold the MHC molecule in place whilst the T cell receptor binds the cell and check the coupled peptide for antigenicity. - 124What are MHC II proteins, and what are their function?Found only on antigen presenting cells
Derived from extracellular proteins
Heterodimers with two homogeneous peptides.
As they are loaded with extracellular proteins, it is mainly concerned with presentation of extracellular pathogens.
Mainly interact with immune cells such as T helper cells. - 125What are interleukins? What are the different types?Group of cytokines that are mostly synthesised by helper CD4 T lymphocytes, as well as through monocytes, macrophages and endothelial cells.
IL-1: Stimulate helper T cells/
IL-3: Regulates blood cell production by controlling the production, differentiation and function of granulocytes and macrophages.
IL-4: Produced by CD4 T cells and stimulate B cell proliferation
IL-6: Plays an essential role in the fluid differentiaton of B cells into Ig-secreting cells/ - 126What affect does maternal obesity have on the foetus?Obesity, hyperlipidemia and hypergycemia cause inflammation of the placenta.
Leads to increased levels of rusulin and fatty acids
Causes overgrowth of the foetus, plus CNS abnormalities in serotoninergic and dopaminergic receptors. - 127What is the affect of obesity on glucose homeostasis?Impaired glucose tolerance and insulin and c-peptide levels are markedly elevated after glucose tolerance tests.
Insulin resistance, initially associated with hyperinsulinemia is the most important risk factor. Causes increased glucose tolerance.
Hypothalamic glucose-sensing is lost in obesity and recurrent hypoglycaemia. Mechanism is unclear. - 128How does leptin regulate body weight?Released from adipose tissue as a proportion of the amount of adipose.
Acts on receptors in the arcuate nucleus of the hypothalamus to regulate appetite.
Has two signalling pathways:
1. Increased leptin excites POMC neuron, increasing POMC expression, causing the release of a-MSH, increasing MC4R signalling, decreasing food intake.
2. Increased leptin inhibits AgRP neuron, reducing AgRP expression, reducing AgRP release, decreasing MC4R signalling.
Leptin receptors become insensitive to leptin at high levels of obesity. - 129Describe bariatric surgery in the treatment of obesityOnly effective obesity treatment
Roux-en-Y gastric bypass is the most common- new smaller stomach pouch and food passes through smaller small intestine
Alteration in the secretion of various hormones associated with appetite and expenditure due to increased distension signalling.
Glucose homeostasis is instantly returned to normal. - 130What are the maternal cardiovascular changes in pregnancy?Heart rate increases by 15-25%. CO increases by up to 50% by the third trimester. SV increases by 35% due to increased venous return. Left ventricle hypertrophy and dilation. Contractility remains unchanged.
1st trimester:
40-45% increase in blood volume
Cardiac hypertrophy
Haematocrit reduced in early pregnancy as red blood cell production lags behind volume expansion.
Changes are ongoing during first 2 trimesters, stabilises in 3rd and completely reversed within few days after parturition. - 131What causes the cardiovascular changes in the mother?Increase in oestrogen and progesterone, which causes vasodilatation and a fall in peripheral resistance
Relaxin is produced by the corpus luteum. Levels peak at 14 weeks of the first trimester and at delivery.
Mediates the haemodynamic changes such as increased CO, compliance and increased renal blood flow. - 132What are the neural effects of increased plasma volume?Produces decreased sympathetic tone and secretion of adrenal catecholamines.
Extradrenal receptors govern activity of sympathetic nervous system as well as production of atrial natiuretic factor and antidiuretic hormone.
Stretch of atria releases ANF which act on vagal afferents which project to paraventricular nucleus which controls sympathetic outflow to the kidney. - 133How is increased plasma volume sensed?Stretch receptors in atria, carotid sinus and aortic arch.
Stretch receptors in kidney in JGA in afferent glomerulus and macula densor cells in distal tubule. - 134What are the hormonal effects of increased plasma volume?ANP is released from atria when stretched. Acts on kidney to increase GF and decrease Na+ retention.
Vasopressin is released by pituitary in response to hyperosmolarity, augment water permeability of collecting ducts to promote water reabsorption.
Renin is converted to angiotensin II, which causes arterial constriction, promotes renal Na+ retention by increasing aldosterone secretion. - 135How does the baroreceptor reflex change in pregnancy?Baroreceptor reflex is impaired, causing an increase in BP.
Two hormonal mechanisms contribute:
1. Increased levels of neurosteroid 3a-hydroxy-dihydroprogesterone, acting in the rostral ventrolateral medulla, and reduced actions of insulin in the forebrain.
2. 3a-OH-DHP potentiates baroreflex independent GABAergic inhibition of promotor neurons in the RVLM, which decrease the range of sympathetic nerve activity that can be elicited by changes in arterial pressure. - 136What are the maternal changes in the heart?The apex of the heart is more anterior and up to the left due to the upwards displacement of the diaphragm
Increase in myocyte length. Cardiac hypertrophy.
Oestrogen stimulates NO system, increases vasodilatation and seems to be involved in cardiac remodelling. - 137What are the adverse affects of changes to the maternal cardiovascular system?Aortacaval compression:
From mid pregnancy the enlarging uterus compresses the inferior vena cava and the lower aorta when the patient lies supine.
Reduces venous return, leading to a fall in pre load and cardiac output.
Compression of the aorta leads to reduction uteroplacental and renal blood flow. - 138What are the respiratory changes during pregnancy?Elevation of the diaphragm and the subcostal angle. Anteriorposterior and transverse diameters of the chest wall increases.
Airway resistance is reduced due to progesterone mediated bronchial and tracheal smooth muscle relaxation.
Progesterone mediated hypersensitivty to CO2 increases the respiratory rate by 15% and the tidal volume by 40%. Alveolar ventilation is increased by 70% at the end of gestation.
PaO2 rises to 14kPa during the third trimester but falls to <13.5 kPa at term because the increased CO is unable to compensate for the increased O2 consumption. - 139What are the changes in the kidney function during pregnancy?Increase blood flow and CO, causes the renal plasma flow and GFR to increase progressively during pregnancy, both are 50-60% higher at term.
Increased clearance of creatinine and excretion of bicarbonate.
Mid glycosuria and proteinuria can occur because the increase in GFR may overwhelm the renal tubules ability to reabsorb glucose and protein.
Plasma osmolarity falls due to water retention secondary to increased activity of renin-angiotensin-aldosterone pathways.
Progesterone mediated uteric smooth muscle relaxation- UTI
After the 12th week, enlarging uterus compress the ureters as they cross the pelvic brim. - 140What are eosinophils?Granulocytes produced in the bone marrow.
Make up 5% of wbc.
Release catatonic granule proteins and reactive oxygen species in the response to parasites. - 141What are basophils?Represent 0.1% of WBC.
Contain large cytoplasmic glanules.
Release histamine.
Involved in parasites and allergic reactions. - 142What is the difference between temperature in the shell and core?The shell is the skin, muscle, fat and testes. 37*C in hot environments, but ranges from 20-40*C.
The core is the brain and internal organs. Ranges from 35-38*C - 143How does temperature vary throughout the day?Diural variation- lowest 11pm to 3am and peaks at 10am to 6pm.
- 144How do temperature changes vary in the menstrual cycle?During the follicular phase, the average basal temperature ranges from 36.5-36.7*C.
Within 24 hours of ovulation, women experience an elevation of 10.15-0.45*C due to increased metabolic rate by elevated levels of progesterone. - 145What are the physical process of heat loss at ambient temperatures?Radiation 60%
Conduction 3%
Convection 15%
Evaporation 22%
Respiration 1% - 146What are the changes to the way heat is lost from the body depending on exercise?
- 147Describe cutaneous vasodilation in response to heat.Regulated by the hypothalamus
Ability to adjust the vasomotor tone provides an effective means of modulating skin blood flow and therefore heat flux from the core to the skin.
Stimulated by the cholinergic nerves.
During heat stress, vasoliation causes 60% of CO to go to the skin - 148Outline heat transduction at the skinEccrine sweat glands under the skin secrete sweat which travels up the sweat duct, through the sweat pore and onto the surface of the skin. Can secrete up to 2L/hour. Cholinergic stimulation of sweat glands elicits secretion of sweat.
- 149What is cold induced vasoldilation?When the fingers are exposed to cold, vasoconstriction occurs.
After 5-10 minutes, sudden vasodilation occurs. Probably caused by a sudden decrease in the release of neurotransmitter from the sympathetic nerves to anastomoses.
A new phase of vasoconstriction follows. This is the Hunting reaction. - 150What happens to the piloerector muscles in the cold?Cause hair to stand up straight, trapping a layer of hair, reducing heat loss due to the low thermal conductivity of air.
Normal unstirred layer of air is 2-4mm, 4mph wind gives 1mm, and a woolen jumper gives 4-10mm. - 151What is the countercurrent exchange of heat?Minimises heat loss as it is recycled instead of being dissipated.
CCHE systems are made up of a complex network of peri-arterial venous plexuses that run from the heart to peripheral sites.
Each plexus consists of a singular artery containing warm blood surrounded by a bundle of veins containing cool blood from the surface.
The warm arterial blood transfers most of its heat to the cool venous blood.
Conserves heat by recirculating it back to the body core. - 152How does shivering maintain body temperature?Involuntary repetitive contractions of skeletal muscles generate heat.
Primary motor centre for shivering is located in the posterior hypothalamus near the walls of the 1/3 ventricle. Normally inhibited by signals from the heat centre in the anterior hypothalamic-preoptic area but us excited by cold signals from the skin and spinal cord.
Increased muscluar contraction results in generation of heat as a by product.
Contraction at 10-20 Hz. - 153What is non-shivering thermeogenesis?Metabolic process located primarily in brown adipose tissue and controlled by the activity of the sympathetic nervous supply of tissue via B3 receptors.
The uncouplin protein-1, present in brown fat, allows the uncoupling of protons moving down their mitochondrial gradient from the synthesis of ATP, thus allowing the energy to be dissipated as heat.
Dense vascularisation ensures optimal substrate delivery and removal of heat generated. - 154What is the distribution of brown fat in the elderly and new-borns?In newborns, located on the front and in the interscapular depot.
Newborns rely on brown fat, as shivering mechanisms are poorly developed and high SA.
In adults, brown fat is present in the neck and suprclavicular areas, and occasionally para aortic and suprarenal areas. - 155How are temperature changes detected?Warm receptors are unmyelinated C-fibres and thinly myelinated Ad fibres for cold receptors.
Sensation enters the spinal cord along the axons of Lissauer's tract, which decussate and join the spinothalamic tract.
CNS thermorecpetors are located in the Raphe nuclei of the brainstem. - 156What areas of the hypothalamus are responsible for heat loss and heat promotion?Preoptic area- heat losing sensor and posteriorly temperature sensitive areas.
Posterior nucleus- heat promoting centre. - 157What happens to thermoregulation in the elderly?General decrease in the ability to regulate body temperature.
Reduced release of noradrenaline, weakening vasoconstriction. Reduced elastin and increased collagen make peripheral vessels less elastic.
Exhibit smaller changes in metabolic rate in response to cold.
Less able to produce heat by shivering due to muscle atrophy resulting from ageing and a sedentary lifestyle.
Unable to discriminate a difference in skin temperature of 2.5-5*C, compared to 0.8*C in young. - 158What is fever? What is the difference between endogenous and exogenous pyrogens?Increase in core temperature beyond set point by more than 1*C.
Exogenous pyrogens: bacteria, viruses and some medications. Caused by inflammation
Endogenous pyrogens: cytokines produced by immune system. - 159Describe the mechanisms of feverPGE2 release comes from the arachidonic acid pathway. Increases the set point of temperature by acting on neurons in the preoptic area through prostoglandin E receptor 3.
Fever signals sent to the raphe nucleus in the medulla oblongata lead to stimulation of the sympathetic output system, which evokes non-shivering thermogenesis.
- 160What is hyperthermia?Elevated body temperature due to failed thermoregualtion that does not represent a new hypothalamic set point.
Occurs either due to defects in the thermoregualtory mechanism or despite normal hypothalamic activation of effector responses. - 161What is heat exhaustion and heat strokes.Heat exhaustion is caused by dehydration or salt deficiency due to increased sweat production. Causes hypovolemia and decreased cerebral blood flow.
Heat stroke is hyperthermia with a body temperature greater than 40.6 due to environmental heat exposure with a lack of thermoregulation. Occurs when thermoregualtion is overwhelmed by a combination of excessive metablolic production of heat, excessive environmental heat and insufficient or impaired heat loss. Leads to depression and elevated heart and respiratory rate. Disturbances in CNS function. - 162Effect of exercise in the heat?Muscle contraction leads to increased chemical energy to heat
Increased load on cardiovascular system
Reduced plasma volume.
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