Human Disease YR2

Question 1

Basic functions of the respiratory system? Overview?

Answer 1

• Gas exchange leading to energy release via aerobic respiration- Acid base balance (reg of body pH)- Protection from infection- Communication via speech

Question 2

Why do we breathe? Characteristics?

Answer 2

To produce energy: - respiration uses oxygen to produce energy, producing CO2 and wasteThe only way this works via the integration of the CVS and the respiratory system

Question 3

Gas exchange? Characteristics?

Answer 3

Exchange of gas between lungs and blood (or via blood and cells) occurs via simple diffusion down partial pressure gradientsPart 1: between atmosphere and lungsPart 2: between lung and bloodPart 3: transport of gases in bloodPart 4: between blood and cells

Question 4

Basic Respiratory anatomy? Upper and Lower tract?

Answer 4

Upper: - Pharynx- Oesophagus- Larynx- TongueLower:- Trachea- Right and Left lung- Right and Left bronchus- Diaphragm

Question 5

Lower respiratory tract - lobes and lungs?

Answer 5

• Trachea travels down into the lungs and splits into 2 primary bronchi- 5 secondary bronchi 1 to each lobe- Right lung has 2 lobes (superior, middle and inferior)- Left lung *superior and inferior) also has the cardiac notch where the heart sits

Question 6

Branching of airways? Structure?

Answer 6

• Larynx- Trachea- Primary bronchus- Secondary bronchus- Bronchiole- Alveoli

Question 7

Structure of the lung lobule?

Answer 7

• The bronchiole is surrounded by SM and the bronchial artery, vein and nerve- Bronchiole becomes the alveoli that has elastic fibres and capillary beds to allow gas exchange

Question 8

Alveolar structure?

Answer 8

Contains:- Elastic fibres- Capillaries- Endothelial cells of capillaries- TII cells (surfactant cells)- TI cells

Question 9

Resistance to air flow? Characteristics?

Answer 9

Smooth muscle in bronchial wall regulates diameter of airways:- contraction reduces diameter and increases resistance and vice versa

Question 10

Lung volumes and capacities? Names and values?

Answer 10

• Tidal volume: 500mL- Total lung capacity: 6000mL- Vital capacity: 4600mL- Residual volume: 1200mL- Expiratory reserve volume: 1100mL- Inspiratory reserve volume: 3000mL

Question 11

Lung volumes and capacities? Definition?

Answer 11

• TV - Tidal Volume. The volume of air breathed in and out of the lungs at each breath.- ERV - Expiratory Reserve Volume. The maximum volume of air which can be expelled from the lungs at the end of a normal expiration.- IRV - Inspiratory Reserve Volume. The maximum volume of air which can be drawn into the lungs at the end of a normal inspiration.- RV - Residual Volume. The volume of gas in the lungs at the end of a maximal expiration.- VC - Vital Capacity = tidal volume + inspiratory reserve volume + expiratory reserve volume.- TLC - Total Lung Capacity = vital capacity + the residual volume.- IC - Inspiratory Capacity = tidal volume + inspiratory reserve volume.- FRC - Functional Residual Capacity = expiratory reserve volume + residual volume.- FEV1:FVC = Fraction of forced vital capacity expired in 1 second.

Question 12

Gas laws? Name and explanation?

Answer 12

• Boyle’s Law states that the pressure exerted by a gas is inversely proportional to to its volume (P a 1/V)- Henry’s Law states that the amount of gas dissolved in a liquid is determined by the pressure of the gas and it’s solubility in the liquid.- Dalton’s Law states that the total pressure of a gas mixture is the sum of the pressures of the individual gases.Gases always move from areas of high Pa to areas of low Pa

Question 13

Cross-sectional structure of the lungs?

Answer 13

• Right/Left lung| - Right/Left pleural cavity

Question 14

Anatomy of the pleural sac? Structure?

Answer 14

The lungs and interior of the thorax are covered by pleural membranes between the surfaces of which is an extremely thin layer of intrapleural fluid- left/right pleural sac- parietal pleura- visceral pleura- pleural cavity filled with intrapleural fluid`

Question 15

Functions of the pleural membranes? Functions?

Answer 15

• Stick the lungs to the rib cage- Visceral pleura is “stuck” to the surface of the lungs- Visceral pleura is “stuck” to the parietal pleura via the cohesive forces of the pleural fluid- Parietal pleura is “stuck” to the rib cage and diaphragmThe lungs will therefore follow the movements of these bones and muscles

Question 16

Muscles of Breathing? Overview?

Answer 16

These muscles are responsible for creating the pressure gradient that determines air flow (remember, air flows from high pressure to low pressure)Inspiration: - Sternocleidomastoids- Scalenes- External intercostals- DiaphragmExpiration: - Internal intercostals- Abdominal muscles

Question 17

Mechanism of breathing action? Diaphragm?

Answer 17

• At rest, the diaphragm is relaxed- Diaphragm relaxes and the thoracic volume decreases- Diaphragm contracts and the thoracic volume increases

Question 18

Mechanics of breathing? Ribs?

Answer 18

Pump handle: motion increases anterior-posterior dimensions of rib cageBucket handle: motion increases lateral dimensions of rib cage

Question 19

Relevant pressures within the lungs?

Answer 19

Intra-thoracic Pa: pressure inside the thoracic cavity (inside lung)Intra-pleural Pa: pressure inside the pleural cavityTranspulmonary Pa: difference between alveolar Pa and intra-pleural Pa

Question 20

Pressure changes within the lungs during inspiration and expiration?

Answer 20

During inspiration:- the alveolar pressure decreases and increases by 1 mmHg ending at 0 Pa difference- the interapleural pressure drops by -3 mmHgDuring expiration:- the alveolar Pa increases by 1 and drops by 1 ending at a 0 Pa chnage- the intrapleural Pa increases back to -3 mmHg (from -6)

Question 21

Importance of the relationship between pleural membranes?

Answer 21

Normal:- the intrapleural Pa is subatmospheric (-3mmHg), which drives air into the lungs- elastic recoil tries to pull chest wall outward and creates and inward pullPneumothorax:- stab wound- lung collapses

Question 22

Bulk flow of air equation and explanation? lung elasticity explanation?

Answer 22

• Bulk flow of air between the atmosphere and alveoli is proportional to the difference between the atmospheric and alveolar pressures and inversely proportional to the airway resistance: F = (Patm- Palv)/R - The lungs are stretched and are attempting to recoil, whereas the chest wall is compressed and attempting to move outward. This creates a subatmospheric intrapleural pressure and hence a transpulmonary pressure that opposes the forces of elastic recoil

Question 23

Surfactant? definition and function?

Answer 23

Detergent like fluid produced by Type II Alveolar cells- Reduces surface tension on alveolar surface membrane thus reducing tendency for alveoli to collapse- surface tension occurs wherever there is an air-water interface and refers to the attraction between water molecules

Question 24

How does surfactant work? Example? Principle of surface tension?

Answer 24

Water molecules is attracted to other water molecules, forming larger dropletsAll of these droplets causes the overall force to be brought inwards that causes surface tension within the alveoliSurfactant’s role us to surround the other water molecules to stop the attractionIncreases lung compliance, reduces lung’s tendency to recoil, makes breathing easier and more effective in small alveoli

Question 25

How does surfactant prevent alveolar collapse?

Answer 25

Pa is greater in the smaller alveoli than the larger ones and so air flows into the larger alveoliSurfactant reduces surface tension which equalises the large and small alveoli, which allows greater gas exchange due to increased SA

Question 26

Pulmonary ventilation? Definition?

Answer 26

Total air movement in and out of the lungs

Question 27

Alveolar ventilation? Definition?

Answer 27

Fresh air getting to the alveoli and therefore available for gas exchange

Question 28

Anatomical dead space volume? Characteristics?

Answer 28

• 150 mL| - volume of gas occupied by the conducting airways and the gas is not available for exchange

Question 29

Inhalation and exhalation process - air volumes?

Answer 29

Exhalation: 500mL loss; - which is 150mL dead space and 350mL stale air and the remaining 150mL (stale air) is present in the conducting airwaysInhalation: 500mL gain;- 150mL stale air from the dead space enters the lungs, and only 350mL of fresh air enters the alveoli, and another 150mL of fresh air is trapped in the dead space

Question 30

Hypoventilation vs Hyperventilation? Differences?

Answer 30

Hypoventilation: Higher TV and lower frequency (but alveolar ventilation is still normal)Hyperventilation: Lower TV and higher frequency (but the alveolar ventilation is much lower)Hyperventilation is bad in a clinical sense

Question 31

Dalton’s Law? Definition?

Answer 31

The pressure of an entire gaseous mixture is equal to the sum of the pressures of the individual gases in that mixtureAtmospheric Pa - 760 mmHgComposition of air: 78% N, 21% O2 and 0.04% CO2

Question 32

Alveolar ventilation and partial pressues? PO2 and PCO2?

Answer 32

Normal ventilation: 4.2L/min- PO2: 100 mmHg- PCO2: 40 mmHgHyperventilation: >4.2L/min- PO2: 120 mmHg- PCO2: 20 mmHgHypoventilation: < 4.2L/min- PO2 30 mmHg- PCO2 100 mmHg

Question 33

Compliance? Definition?

Answer 33

Change in volume relative to change in pressure - It represents the stretchability of the lungse. g. how much does volume change for any given change in pressure

Question 34

Difference between low and high compliance?

Answer 34

HIGH COMPLIANCE = large increase in lung volume for small decrease in interpleural pressureLOW COMPLIANCE = small increase in lung volume for large decrease in interpleural pressureChanges in disease and age

Question 35

Pressure, volume and distribution of ventilation? Differences in orientation?

Answer 35

• The pressure volume curve varies between apex and base of the lung. At the base the volume change is greater for a given change in pressure.- Alveolar ventilation declines with height from base to apex.- Compliance is lower at the apex due to being more inflated at FRC. At the base the lungs are slightly compressed by the diaphragm hence more compliant on inspiration.- A small change in intrapleural pressure therefore brings about a larger change in volume at the base compared with the apex.

Question 36

Gas transport in the blood? Process?

Answer 36

• Blood transport O2 from the lungs to the tissues, used to produce energy and then the waste and CO2 is removed- Haemoglobin carries O2 (200ml/L)- Bulk of CO2 is transported in various forms

Question 37

Blood supply to the lungs? Pulmonary circulation?

Answer 37

• Consists of L and R pulmonary arteries originating from the RV- These both supply the capillary network around the alveoli and returns oxygenated blood to the LA, via the pulmonary vein (high flow - low pressure)

Question 38

The rate of diffusion across the alveoli? Factors?

Answer 38

• Directly proportional to the partial pressure gradient- Directly proportional to the solubility of the gas- Directly proportional to the available SA- Inversely proportional to the thickness of the membrane- Most rapid over short distances

Question 39

Gas exchange in the alveoli and blood? Partial Pa?

Answer 39

Alveoli: - PO2 (100)- PCO2 (40)Blood at lungs:- PO2 (40)- PCO2 (46)Blood at cells- PO2 (100)- PCO2 (40)Cells:- PO2 (<40)- PCO2 (>46)

Question 40

Alveoli to RBC transfer? Characteristics?

Answer 40

The alveoli has a very thin membrane which allows simple diffusion of o2 to the passing RBCs in the bloodstream

Question 41

Haemoglobin? Characteristic?

Answer 41

Structure: 2 alpha chains and 2 beta chains- 98% O2 bound to haemoglobinEach haemoglobin contains 4 haem groups, each of which contains one Fe which binds one o2 and so each haemoglobin can bind 4 molecules- The degree of haemoglobin binding depends on oxygen partial pressure

Question 42

Blood with haemoglobin vs blood without haemoglobin?

Answer 42

Hb effectively sequesters O2 from the plasma, thus maintaining a partial pressure gradient that continues to suck O2 out of the alveoli, until the Hb becomes saturated with O2.Partial pressure of O2 in plasma is fundamental in determining how much O2 binds to Hb.

Question 43

Oxygen-haemoglobin dissociation curve?

Answer 43

Haemoglobin is almost 100% saturated at the normal systemic arterial PO2 of 100 mm Hg. The fact that saturation is already more than 90% at a PO2 of 60 mm Hg permits a relative normal uptake of oxygen by the blood even when alveolar PO2 is moderately reduced. Haemoglobin is 75% saturated at the normal systemic venous PO2 of 40 mm Hg. Thus, at rest only 25% of the oxygen dissociates from haemoglobin and enters the tissues.

Question 44

Factors affecting the oxygen-dissociation curve? Factors?

Answer 44

• pH (reduced pH, reduced affinity and vice versa)- PCO2 (increased CO2, reduced affinity and vice versa)- Temperature (increase temp, reduced affinity and vice versa)- DPG (addition of DPG, reduces affinity)

Question 45

Carbon dioxide transport? Process?

Answer 45

CO2 transport is much simpler than the transport of O2. CO2 is much more soluble than O2 and after CO2 diffuses from the tissues into the blood down it’s partial pressure gradient, 7% remains dissolved in the plasma and is transported in simple solution.The remaining 93% moves into the red blood cells where 23% forms carbamino compounds with the now desaturated haemoglobin while the remainder is converted to bicarbonate ions, exchanged for Cl- across the RBC membrane and transported in the plasma in the form of HCO3-

Question 46

Distribution of blood flow in lungs - influenced by? perfusion? alveolar? resistance chnages?

Answer 46

The distribution of blood flow in the lung is influenced by both hydrostatic (blood) pressure and alveolar pressure. At the base of the lungs blood flow is high since perfusion pressure exceeds alveolar pressure and hence vascular resistance is low. At the apex of the lungs blood flow is low because perfusion pressure is less than alveolar pressure. This compresses the arterioles and vascular resistance is increased.

Question 47

Matching ventilation and perfusion? Characteristics?

Answer 47

In the upright position the ratio of ventilation to perfusion within the lung changes from the base of the lung (bottom) to the apex (top) owing to the effect of gravity.Over 75% of the height the healthy lung performs quite well in matching blood and air (right y-axis). The majority of the mismatch takes place in the apex. This is then auto regulated to keep the ventilation perfusion ratio close to 1.0

Question 48

Autoregulation of ventilation:perfusion?

Answer 48

Ventilation > perfusion:- alveolar PO2 rises, PCO2 falls- causes pulmonary vasodil and bronchial constrictPerfusion > ventilation:- alveolar PO2 falls, PCO2 rises- pulmonary vasoconstrict and bronchial dilation

Question 49

Ventilatory control? Innervation and brain centres?

Answer 49

• requires stimulation of the (skeletal) muscles of inspiration. This occurs via the phrenic (to diaphragm) and intercostal nerves (to external intercostal muscles)- subconcious, but can have voluntary modulation- entirely dependent on signalling from the brain (sever spinal cord above origin of phrenic nerve (C3-5) breathing ceases)

Question 50

Rhythmic breathing and voluntary override? Overview?

Answer 50

Breathing depends upon cyclical activation of the phrenic and intercostals nerves stimulating contraction of the inspiratory muscles (diaphragm/external intercostals). This neural activity is triggered by the medullary inspiratory neurones but with voluntary override

Question 51

Respiratory centres have rhythm modulated by? factors affecting rhythm?

Answer 51

• Emotion (via limbic system in the brain)- Voluntary over-ride (via higher centres in the brain)- Mechano-sensory input from the thorax (e.g. stretch reflex)- Chemical composition of the blood (PCO2, PO2 and pH) – detected by chemoreceptors.

Question 52

Respiratory centre flow chart of action? flow chart?

Answer 52

• Located in the medulla and pons of the brain- Factors affecting rhythm influence the VRG and DRG (dorsal/ventral respiratory group)- the most significant factor is chemoreceptor input- the VRG innervates the tongue, pharynx, larynx and epiratory muscles- the DRG (via the phrenic or intercostal nerves) innervate the inspiratory muscles

Question 53

Chemoreceptors? Types and overview on how they work?

Answer 53

Types:- Central and PeripheralCentral:- medulla- responds directly to the H+ (reflects PCO2)- primary ventilatory forcePeripheral:- carotid and aortic bodies- responds to plasma H+ and PO2- secondary ventilatory drive

Question 54

Central chemoreceptors in the medulla? Characteristics and what it detects?

Answer 54

• Detect changes in H+ in CSF- Causes reflex stim of ventilation following rise in H+ (driven by raised PCO2 = hypercapnea)CO2 + H20 = H2CO3 = H+ + HCO3- Ventilation is reflexly inhibited by a decrease in arterial PCO2

Question 55

Process of central chemoreceptor action? Process?

Answer 55

When arterial PCO2 increases carbon dioxide crosses the blood-brain barrier not H+Central chemoreceptors monitor the PCO2 indirectly in the cerebrospinal fluid.Bicarbonate and H+ are formed and the receptors respond to the H+Feedback via the Respiratory Centres increases ventilation in response to increased arterial PCO2 .Decreased arterial PCO2 slows ventilation rate.

Question 56

Peripheral chemoreceptors? Characteristics and what it detects?

Answer 56

• Located in the carotid and aortic bodies- Detect changes in arterial PO2 and H+- Causes reflex stim of ventilation following significant fall in arterial PO2 or a rise in H+- respond to arterial PO2 not oxygen content- increased H+ usually accompanies a rise in arterial PCO2

Question 57

Oxygen-haemoglobin dissociation curve? Description?

Answer 57

• Haemoglobin is highly saturated across many mmHg of PO2- And so a large fall in mmHg will occur before the peripheral chemoreceptors to detect a change and influence a response

Question 58

Good Chemoreceptor reflex slide

Answer 58

GHD - Resp 4

Question 59

Emotion and the respiratory centres? the link?

Answer 59

Limbic system input allows emotional responses to alter breathing e.g. rapid, shallow breathing often accompanies anxiety

Question 60

Other aspects of controlling breathing? Characteristics?

Answer 60

Descending neural pathways from cerebral cortex to respiratory motor neurons allow a large degree of voluntary control over breathingRespiration is inhibited during swallowing to avoid aspiration of food or fluids into the airways. Swallowing is followed by an expiration in order that any particles are dislodged outwards from the region of the glottis

Question 61

Pharmacological influences on ventilatory control? Drug examples and their influence?

Answer 61

• Barbiturates – e.g. thiopental (iv. anaesthesia). Inhibit phrenic nerve activity, decrease depth of breathing (alv. ventilation)- Opioids – e.g. morphine. sensitivity to pH and therefore response to PCO2 . Also peripheral chemoreceptor response to PO2- Benzodiazepines – e.g. diazepam (anxiolytic, sedative). Similar effects to opioids but much less severe. Relatively safe and widely used.- Nitrous oxide – Little effect on response to PCO2 but significantly depresses response to falling PO2. Caution with COPD patients! Widely used.

Question 62

Location of the heart?

Answer 62

Middle mediastinum

Question 63

Basic anatomy of the heart - layers?

Answer 63

4 chambers: left and right atria and ventricles| 3 layers: peri, myo and endocardium

Question 64

Basic function of the heart?

Answer 64

The right side receives deoxygenated blood from the body and the left side receives oxygenated blood from the lungs

Question 65

Pericardium? Characteristics?

Answer 65

Fibrous outer layer and serous visceral and parietal layerPericardial cavity: space between visceral and parietal later

Question 66

Orientation of the heart?

Answer 66

Left 5th intercostal space

Question 67

Right atrium? Characteristics?

Answer 67

• Opening of the superior vena cava, inferior vena cava and the coronary sinus- Interartrial spetum- Right atrioventricular orifice

Question 68

Right ventricles? Characteristics?

Answer 68

• Trabeculae carneae- Irregular muscular elevations- Right AV (tricuspid) orifice- Interventricular (IV) septum- Pulmonary valve

Question 69

Left atrium? Characteristics?

Answer 69

• Forms most of base of the heart- 4 pulmonary veins- Left AV orifice

Question 70

Left ventricle?

Answer 70

• Forms apex of the heart- Mitral valve- Aortic orifice and Aortic valve

Question 71

Heart valves?

Answer 71

• Tricuspid and bicuspid- Aortic and pulmonary valve(Semilunar valves)

Question 72

Heart valve? Anatomy?

Answer 72

• The cusp of the valve is connected to the tendinous cords which are connected to the papillary muscles- Muscles contract to close the valve

Question 73

Right coronary artery? Supply?

Answer 73

• RA- Most of the RV- Part of the LV- SAN (60%)- AVN (80%)- Part of the AV septim (post 1/3rd)

Question 74

Left coronary artery? supply?

Answer 74

• Left atrium- Most of the left ventricle- Part of the right ventricle- Most of the IV septum- SA node (40%)

Question 75

Important coronary arteries?

Answer 75

• Ascending aorta- R/L coronary artery- Atrial artery

Question 76

Venous drainage?

Answer 76

• Superior and inferior vena cava- Great cardiac vein- Small cardiac vein

Question 77

Innervation of the heart? Characteristics?

Answer 77

Sympathetic: superficial and deep plexus- stim produces dilation of coronary arteries- allows more o2 and nutrients to reach the myocardium when neededParasympathetic: vagus nerve (CN10)- stim slow HR- reduces FoC and constrict coronary arteries- saves energy

Question 78

Conduction system of the heart? Characteristics?

Answer 78

SAN: specialised cardiac muscle fibres, at the junction of SVC and the RA and is the pacemaker of the heartAVN: near the opening of the coronary sinusBundle of His and purkinje fibres

Question 79

Circulation around the body? Ascending and Arch of the Aorta? Characteristics?

Answer 79

Brachiocephalic trunk: divides into right subclavian and right common carotid arteryleft common carotid and subclavian artery

Question 80

Circulation around the body? Thoracic and abdominal aorta? Characteristics?

Answer 80

Source: descending aortaBranches: bronchial, oesophageal, posterior intercostal, abdominal aorta, superior phrenic and pericardial arteries

Question 81

Circulation around the body? Upper and lower limbs? Characteristics?

Answer 81

• Subclavian- Axillary- Brachial- Radial- Ulnar- Femoral- Popliteal- Tibial- Dorsal artery

Question 82

Pulse points?

Answer 82

• Radial artery (distal)- Brachial (cubittal fossa)- Femoral (midinguinal point)- Popliteal (popliteal fossa)- Tibial (between achilles and heel)- Dorsal (dorsum of foot)

Question 83

Circulation around the body? Head, Neck and Brain? Characteristics?

Answer 83

• Carotid (superior thyroid, lingual, facial, ascending pharyngeal, occipital and posterior auricular)- Maxillary- Basilar- Superficial temporal

Question 84

Venous circulation? Characteristics?

Answer 84

Superior vena cava: returns blood from above the diaphragm except lungs and heartInferior vena cava: returns non-oxygenated blood from lower bodyPortal venous system: collects blood of reduced o2 but rich in nutrients from the GI tract to the liver

Question 85

Portal system circulation? Composition?

Answer 85

• Portal vein- Superior mesenteric vein- Splenic vein- Inferior mesenteric vein

Question 86

Role of the lymphatic system?

Answer 86

Transports:- Interstitial fluid back to the blood- Absorbed fat from the SI to the bloodImmunological defencesSpread infection and cancer

Question 87

Lymphatic drainage?

Answer 87

Right lymphatic duct:- drains right upper quad of the bodyThoracic duct:- remainder of the body

Question 88

Structure of the CVS? Characteristics?

Answer 88

• Pumps are in series- Most vascular beds are in parallel (all tissues get oxygenated blood, allowing regional redirection)- Specialised vascular beds exist in series (portal system)

Question 89

How is blood flow produced?

Answer 89

• Pa in the vein is 0 mmHg| - Pa in the arteries is 100 mmHg

Question 90

Regulation of blood flow? Equation?

Answer 90

• Mean Art Pa - Central ven Pa = Difference in Pa- Flow = Difference in Pa/Resistance- Resistance is controlled by vessel radius

Question 91

Aorta? Composition?

Answer 91

Elastic artery: inside - out- tunica intima (elastic layer with endothelium)- tunica media- tunica externa- wide lumen and role to dampen pressure variations

Question 92

Arteries? Composition?

Answer 92

Muscular arteries: out - in- externa, media, endo and intima- wide lumen- strong non-elastic wall- low resistance

Question 93

Arterioles? Composition?

Answer 93

Resistance vessels:- Media, endo and base mem- narrow lumen, thick contractile wall- control resistance and flow

Question 94

Capillaries? Composition?

Answer 94

Exchange vessels:- narrow lumen and thin walled- endo and base mem

Question 95

Venules/Veins? Composition?

Answer 95

Capacitance vessels:- wide lumen, distensible wall- low resistance and resevoir- allows fractional distribution of blood- externa and endo (venule)- externa, media, endo and intima (veins)

Question 96

Gross structure of the heart? Valves?

Answer 96

• Right AV valve - tricuspid valve- Left AV valve - bicuspid valve- Cusps of fibrous tissue connected round AV space- connected to chordae tendinae anchored to papillary muscles (no contract)- During heart contraction the cusps inflateSemilunar valves:- aortic and pulmonary- outward facing pocket (closing valve)

Question 97

Conduction of the heart? Process?

Answer 97

• Pacemaker cells in the SAN, caused the atria to contract (signal does not pass to ventricles due to annulus fibrosis)- Signal passed to the AVN, with a delay to allow the ventricles to fill, when the signal is initiated it travels down the left and right bundle of His to the purkinje fibres that cause the ventricles to contract (apex contraction)

Question 98

Excitation-contraction coupling? Process? Muscle?

Answer 98

• Cardiac cells contain desmosomes, intercalated discs and gap junctions with all allow the passage of signal between the cardiac cells, allowing continuous depolarisation. - Depolarisation occurs causing the release of Ca that travels down the t-tubules and activating the sarcoplasmic reticulum to release further Ca that causes the contraction of the myosin-actin complex(Ca induced Ca release)

Question 99

Mechanical events of the cardiac cycle?

Answer 99

• Chambres relaxed, passive vent filling- atrial systole (atria push blood to vent)- Isovol vent contract (AV valves closed but no great enough to open SLV)- Vent eject (open SLV, and ejected)- Isovol vent relax (SLV close)

Question 100

Reg of the HR? Parasympathetic?

Answer 100

Vagus nerve:- release ACh- acts on muscarinic ACh recep on SAN- slows pacemaker cells- reduced HR (bradycardia)

Question 101

Reg of the HR? Sympathetic?

Answer 101

Sympathetic nerves:- Release NAD- act B1- recep on SAN- increases slope of pacemaker potential (threshold achieved quicker)- speed up pacemaker- increases HR +ve chonotropic (tachy)

Question 102

Preload and Afterload? Definition?

Answer 102

Preload: - volume of blood in the ventricles at the end of diastole(increased during hypervolemia, regurgitation and heart failure)Afterload:- resistance the left ventricle must overcome to circulate blood(increased during hyperten and vasoconst)(increased afterload increases cardaic load)

Question 103

Stroke volume and cardiac output? Factors affecting each?

Answer 103

CO = SV*HRHR: affected by sympth and parasympth toneSV: affected by pre/afterload and contractility

Question 104

Regulation of stroke volume? Preload? Characteristics?

Answer 104

Frank-Starling’s law of the heart:- the energy of contraction is proportional to the initial length of the cardiac muscle fibre- relation between EDV (end diastolic volume), contraction strength and stroke volume- intrinsic property of heart musclesIncreased contractility caused by sympth nerve stim causes increased stroke volume than ventricular end-diastolic volume

Question 105

Preload and EDV relationship? Explanation?

Answer 105

Preload is affected by EDV:- increased venous return, increased EDV and therefore increased stroke volume and vice versa- ensures self-reg (match SV of left and right ventricles)

Question 106

Regulation of stroke volume? Afterload? Characteristics?

Answer 106

Afterload is set by the arterial Pa against which the blood is expelledIf total peripheral resistance increases, stroke volume will reduce

Question 107

Preload and afterload affect on stroke volume?

Answer 107

Capacitance vessels affect preload and increase SVResistance vessels affect afterload which decreases SV

Question 108

Neural regulation of stroke volume? Sympth NS?

Answer 108

Sympth:- release NAD (also from adrenal medulla)- act on B1 receptor on myocyte- increases contractility (+ve inotrope), stronger but shorter- Increased SV and EDV

Question 109

Pressure and blood flow from arteries to veins? Characteristics?

Answer 109

Pressure falls throughout the vascular tree - driving force = MAP-CVPSmall drop through arteries (from ~ 95 to 90 mmHg)- low resistance conduitLarge drop through arterioles (from ~ 90 to 40 mmHg)- the resistance vesselsLeaves a small pressure difference pushing blood back through the veins (from ~ 20 to 5 mmHg) - the systemic filling pressure

Question 110

Skeletal muscle pump? Effect on Pa and flow? Veins?

Answer 110

Muscle compresses veins:- squeeze blood back- increases return, EDV and SV- CO responds to activity- valves prevent backflow

Question 111

Respiratory pump? Effect on Pa and flow?

Answer 111

Pressure gradient favours increase in venous return:- increased rate or TV increases venous return and therefore preload- CO responds rapidly

Question 112

Venomotor tone? EFfect on Pa and flow?

Answer 112

Contraction of SM in the walls of veins mobilises spare capacitance, increasing venous return and preload

Question 113

Microcirculation? Composition and Characteristics?

Answer 113

Specailised for exchange:- thin walled small diffusion barrier- large SA:VLocal control by metarterioles and precap sphinctors

Question 114

Types of capillaries? Structure and location?

Answer 114

Continious:- Base mem and tunica intima (with intracellular cleft)- skeletal muscle, adipose, lung and CNSFenestarted:- fenestartions- kidneys, intest and endocrineSinusoid:- incomplete base- intracellular gap- liver, spleen and bone marrow

Question 115

Extrinsic control of blood flow? Parasymph and symph?

Answer 115

Parasympth:- limit effect to digest, external genitalia and salivary glandsSympth: tonic discharge- releases NAD, binds a-receptor on arteries (causing constriction)- reduces blood flow and increases TPR

Question 116

Extrinsic control of blood flow? Hormonal?

Answer 116

Tissues: liver, skeletal and cardiac- adrenaline activates B2 causing arteriolar dilation, therefore increasing flow and reducing TPRPeripheral vasoconstrict diverts blood and combined vasodil promotes BF to important organse.g. liver, skeletal/cardiac muscle (all rich in b2)

Question 117

Local control? Active hyperaemia? Autoreg?

Answer 117

Active hyperaemia:- increase of CO2, H and K promotes vasodilation- increased meta increases metabolites, that increase flow by needing to wash out metabolites- match blood flow to metabolic needAutoreg:- reduced MAP reduces flow- metaboloites accumulate stim arteriole dilation(maintains blood supply despite MAP change)

Question 118

Fundamental equation of CVP?

Answer 118

MAP = CO*TPRMAP driving force behind circulation:- too low (faint)- too high (HT)

Question 119

Arterial baroreflex? Nerves to anatomy?***

Answer 119

Internal carotid arteries to brain (carotid sinus baroreceptor)aortic arch baroreceptor to brain

Question 120

Regulation of BP long term?

Answer 120

• Cardio-pulmonary baroreceptors- tends to be hormonal- act on BVs and kidenys (blood volume)

Question 121

Posture? Scenario?

Answer 121

Lying to standing:- gravity increases Pa in veins below heart- veins distended and accommodate pooling- venous return drops(reduced EDV, preload, SV, CO and MAP and so less baroreceptor firing)

Reflex response: - Reduced vagal tone increasing HR and COSympth tone:- increased contractility and SV- venoconstrict, EDV, SV and TPR

(good diagram in CVP lecture 3)

Question 122

Exercise? Scenario?

Answer 122

HR increases due to- decreased vagal tone- increased sympathetic toneContractility increases due to- increased sympathetic tone- circulating epinephrineEDV (preload) is “maintained”:- shortened systolic phase- sympathetic venoconstriction- skeletal muscle pump- respiratory pump

Question 123

Exercise? Scenario?

Answer 123

HR increases due to- decreased vagal tone- increased sympathetic toneContractility increases due to- increased sympathetic tone- circulating epinephrineEDV (preload) is “maintained”:- shortened systolic phase- sympathetic venoconstriction- skeletal muscle pump- respiratory pump

Question 124

Functions of blood?

Answer 124

Carriage of physiologically active compoundsClottingDefenceCarriage of gasThermoregulationMaintenance of ECF pH

Question 125

Composition of blood?

Answer 125

Consists of plasma, red blood cells, white blood cells and platelets.

Question 126

Plasma? Characteristics?

Answer 126

4% body weight, 95 % waterCirculates biologically active compounds, composition kept within strict limits in healthPlasma proteins subdivided into 3 categories:Albumin: most abundantGlobulin - Subdivided into 3 categories;alpha and beta globulinsFibrinogen and other clotting factorsPlasma proteins not taken up by cells, and generate and regulate oncotic pressure

Question 127

Colloid Oncotic Pressure? Description?

Answer 127

Capillary wall allows the transport of ions, glucose and water from the interstitial space to the vessel lumenThe concentration of fluid remains unchanged while volume of plasma and interstitial fluid is alteredInterstitial fluid acts as a fluid resevoir

Question 128

Erythrocytes? Characteristics?

Answer 128

Most abundant blood cell (4 - 6 x10*12 per litre), 120 day lifespan.Highly flexible BiconcaveNon-nucleatedDiameter 7-8um Contain haemoglobin: gas transport.

Question 129

Red Blood Cell Formation? Process and enhanced hormone prod?

Answer 129

Controlled and accelerated by erythropoietinSecretion - 85% kidney15% liver hepatocytesPluripotent stem cells form erythroblasts stimulated by erythropoietinErythropoietin is enhanced when o2 delivery to kidney is reduced;- hypox- haemorrage- anaemia- lung disease- cardiac dysfunction

Question 130

Haemoglobin - iron stores? development? ferritin?

Answer 130

RBC synthesise haemoglobin at the erythroblast stage of development. Essential dietary requirements: iron, folic acid, vit B12 Iron stores: 70% haemoglobin 5% muscle myoglobin 25% hepatocytes, bone marrow, spleen (stored as ferritin).Ferritin also found in soln in blood. Reflects iron status of individual. Women - 8.5mmol/L , Men 10mmol/L

Question 131

Haemoglobin breakdown? Process?

Answer 131

Haemoglobin is released from degraded RBCs which becomes globin and is broken into aasThe haem either froms new RBCs, or converted to bilirubinBilirubin is carried in the blood by albumin (unconjugated), and enters the liver and becomes conjugated with glucuronic acidSome is excreted in the urine or secreted into the bile and excreted in the faeces

Question 132

Leukocytes? Types, Characteristics and Formation?

Answer 132

Nucleated 5 x 10*10 per litreInvolved in defense against pathogensWBCs form granulocytes, monocytes and lymphocytesGranulocytes can differentiate to neutro, eosino and basoLymphocytes can differentiate to B cells and T cellsT cells differentiate to helper and killer cells

Question 133

Neutrophils? Characteristics?

Answer 133

68% of WBC population, half-life 6 hours (need to produce 100 billion per day for normal function!)Phagocytic, and can also entrap bacteria in NETS (Neutrophil Extracellular Traps) Form first line of defence.

Question 134

Eosinophils? Characteristics?

Answer 134

1.5% although number will increase rapidly during allergic responseAttack pathogens too large for neutrophils and other defense cells

Question 135

Basophils? Characteristics?

Answer 135

0.5%, Release histamine and heparin - trigger inflammation.

Question 136

Monocytes? Characteristics?

Answer 136

5%, largest WBC, life span 72 hours in circulation. Migrate to spleen, liver, lungs and lymph nodes - macrophages

Question 137

Macrophages? Characteristics?

Answer 137

Mature monocyte that has migrated from the blood to the connective tissue where it may reside for up to 3 months. Phagocytic.

Question 138

Lymphocytes? Characteristics?

Answer 138

25%Adaptive immunityB and T cells

Question 139

Platelets? Characteristics?

Answer 139

Membrane bound cell fragments (from megakaryocytes)Formation governed by Thrombopoietin10 day spanAdhere to damaged vessel walls and exposed connective tissue (via Von Willibrand Factor) to mediate blood clotting DO NOT adhere to healthy intact endothelium.

Question 140

Haematocrit? Range? Viscosity?

Answer 140

Male: 40-54%Female: 37-47%Plasma 1.8 and blood 3-4Factors temperature and flow rate

Question 141

Steps involved in haemostasis? Overview?

Answer 141

• Vasoconstrict- Platelet plug- Clot cascade- Clot retraction- Fibrinolysis

Question 142

Platelet plug? Characteristics?

Answer 142

• Starts with a damaged vessel and vasoconstrict- Adherence of platelets via their receptors to the Von Willebrand factor present on the outer-surface of the vessel, unknown to the platelet- This activates the platelet which enables it to secrete TXA2, ADP and 5-HT- These substances then chemokines then attract other platelets which bind to to the other platelets- This creates +ve feedback to create the platelet plugThe opposing BV wall secrete anticoags to reduce the formation of the plug

Question 143

Platelets? Characteristics?

Answer 143

• Released from megakaryocytes governed by IL-6 and IL-11- Canalicular system: platelets have channels that allow nutrients to enter- Surface glycoproteinsSecretions: - dense (TXA2, CA, ADR, 5-HT and ADP)- alpha (PDGF, fibrinogen, herparin antag)- lysosomal Essential for clotting - most cascade reactions take place on the platelet membrane.

Question 144

Clotting? Characteristics?

Answer 144

Convert the blood around the site of damage into a plug with a solid gel like consistencyCirculating soluble plasma proteins called fibrinogen are converted to insoluble polymer strands of fibrin which form a mesh, trapping blood cells and preventing blood loss.Conversion of fibrinogen to fibrin is the final step in a cascade of reactions which can either follow an intrinsic or extrinsic pathway.

Question 145

Intrinsic pathway? Process?

Answer 145

XII activated by collagen or other activator Act XII activates XIAct XI activates IX Act IX activates XAct X converts prothrombin to thrombin (activates XI)Thrombin converts fibrinogen to fibrin by activating XIII to cross-link fibrinEach step needs Ca as a co-factor

Question 146

Extrinsic pathway? Process?

Answer 146

Damage exposes tissue factor III which activates VII, both of these then activate IX, which then activates X (activates VII)TFPI inhibits the formation of Act X Act X converts prothrombin to thrombin (activates XI)Thrombin converts fibrinogen to fibrin by activating XIII to cross-link fibrinEach step needs Ca as a co-factor

Question 147

Factor XIII? rls?

Answer 147

Transglutaminase which links glutamine to lysine residues

Question 148

Importance of calcium? not cows milk? for clotting?

Answer 148

Main cofactor for activation of platelet factors

Question 149

Clot stabilisation Characteristics?

Answer 149

Circulating, soluble fibrinogen forms stable insoluble fibrin meshCatalysed by thrombinPolymerisation via h-bondsXIII creates cross-links allowing stabilisation, which surrounds the platelet plug

Question 150

Clot retraction? Characteristics?

Answer 150

Actin & myosin in platelets contract drawing edges of wound together (thrombin stimulates release of intracellular Ca++)

Question 151

Fibrolytic system? Characteristics?

Answer 151

• Thrombolytic system- Clot breakdown via plasmingoen/plasmin which digest fibrin- Tissue plasminogen activator (t-PA) released by endothelial cells – activates plasminogen to plasmin leading to breakdown of fibrin, fibrinogen and Factors V and VIII.- Fibrin binds increases t-PA enzymatic activity but inhibited by PAI-1

Question 152

Anti-clotting drugs? Mechanisms?

Answer 152

• Prostacyclin and NO- Heparin: binds and act antithrombin, which neutralises IX and XII- Thrombomodulin: binds thrombin (Protein C + co-factor, protein S, inactivate clotting factors V and VIII and catalyses formation of plasmin from plasminogen)- TFPI: inhibits VII

Question 153

Dental-related drugs? Problems?

Answer 153

• Aspirin and Warfarin- No clotting after extraction- Warfarin is a vit K reductase inhibitor

Question 154

Functions of saliva?

Answer 154

Protection:- lubrication, barrier and clear sugarBuffering:- protect demineralisation Pellicle:- Ca bindingMaintenance of tooth integrity:- Ca and Pi supersaturationAntimicrobial:- prots and peps with antibacterialTissue repair:- GFsDigestion:- breakdown food with enzymewTaste:- bind to taste substances

Question 155

Salivary glands - Types of saliva?

Answer 155

Serous:- watery, from parotid and submandibular Mucous:- slimy, from sublingual and minor glands

Question 156

Salivary glands - Name the major glands - cell type? Position? Duct? Innveration (para and symph)?

Answer 156

Parotid:- pure serous, in front of the external ear, from the Stensen’s duct and innervated by IXSubmandibulae:- mixed cell type mainly serous, posterior pairt of the floor of the mouth, from the Wharton’s duct and innervated by VIISublingual:- mixed but mainly mucous, anterior part of the floor of the mouth, from the Ducts of Rivinus, innervated by VII Symph: all via the superior cervical ganglion

Question 157

Salivary glands - minor salivary glands - #? Secretion type? Location? Names?

Answer 157

#:- 600-1000Secretion type:- mucousLocation:- virtually everywhere except gingival and alveolar mucosae Names:- labial, buccal, palatal and lingual

Question 158

Salivary glands - general structure - fruit comparisons and what it relates too?

Answer 158

Similar to a bunch of grapes- grapes; secretary end pieces (acini)- stems; ducts- air; CT

Question 159

Salivary glands - type of ducts - names? CT location?

Answer 159

Intercalated ductStriated ductSecretary ductCT is located surround the ducts

Question 160

Salivary glands - structural units of a salivary gland - epith? (Main part? Ducts? Special cells?) And CT? (Main part? Speta role? Location? Carries?)

Answer 160

Epith:- secretary end-pieces - ducts (intercalated, striated and secretory)- myoepith; on acini and ductsCT:- capsule- speta; divide gland into lobes and lobules - surrounded all epith units - carries; blood and nerve supply

Question 161

Salivary glands - lobes and lobules- created by? Differences?

Answer 161

Lobes:- largest unit and separated by thick spetaLobules:- smaller- separated by thin speta- contains intercalated and striated ducts (intralobular ducts)

Question 162

Salivary glands - functional arrangement of a salivary gland - anatomy? Intra to interlobular

Answer 162

Intralobular:- serous acinus, mucous acinus (myoepith cell) and serous demilune, intercalated duct leading to the striated ductInterlobular:- collecting duct

Question 163

Salivary glands - development of salivary glands - starts? Gland derivatives? CT derivatives?

Answer 163

Starts during the 6th week (parotid)Parotid and most minor gland:- from the ectodermSubmandibular: ectodermSublingual: endodermAll lingual minor glands: endodermCT:- probably ectomesenchyme

Question 164

Salivary glands - development of salivary glands - 8 weeks - Initiation? Activates? Formation? Final stage? Cellular differentiation depends on? Age changes?

Answer 164

Initiation:- start via epith-mesenchymal interactionsActivation:- this allows epith prolif, until forms a lobule shapeFormation:- lobule formationFinal stage:- epith canalisation (form the ducts via epith) and cellular differentiationContinous process until 2 years oldCellular diff:- epith-mesenchymal inter- nerves: symph and para (influence overall growth of gland)- form secretory cells (epith cells) and myoepithAge changes:- increased fat cells

Question 165

Salivary gland - resting secretion - when it occurs? Role?

Answer 165

It occurs:- throughout day and nightRole: mouth and oro-pharynx- most, lubricated and protected

Question 166

Salivary gland - volume of saliva? Flow rate equation? Rate (unstim vs stim)?

Answer 166

Volume:- 500-750 ml/day(90% major)Great variability between individualFlow rate:- volume (ml) ÷ time (mins) Unstim: 0.3ml/min (mainly submandibular)Stim: 1.75ml/ml (mainly parotid and submand)

Question 167

Salivary gland - anatomy?

Answer 167

Anatomy:| - acinus, capsule, septum, lobe, secretory units, and ducts (intercalalted, striated and collecting)

Question 168

Salivary gland - acinar cells - what are they? Role? Specialised shape? Cell types?

Answer 168

What are they:- cells comprising of acinus (secretory end piece)Role:- saliva production (serous or mucous)Specialised shape:- pyramidal shaped cells for functionCell types:- serous acinus, mucous acinus and serous demilune

Question 169

Salivary gland - serous acinus cells - nuc location? RER? Cytoplasmic apperance? Discharge secretions where?

Answer 169

Nuc loc:- basal part of cellRER:- basophilic Cytoplasmic apperance:- granularDischarge secretion:- into tubular lumen via intracellular canaluculi running between the cells

Question 170

Salivary gland - mucous acinar cells - cytoplasm (stain)? Nuc? Granules?

Answer 170

Cytoplasm:- pale, mucin lost or not easily stained, cytoplasm can appear empty in a H&E stainNuc:- flattened nucGranules:- large mucin granules

Question 171

Salivary gland - serous demilunes - what is it? Location? Discharge?

Answer 171

What is it:- crescent of serous cells Location:- mucous acinus capped by serous cellsDischarge:- via the intercellular canaliculi between the mucous cells

Question 172

Salivary gland - myoepithelial cells - located? Shape? Grouping? Process #? Function?

Answer 172

Located:- on acini and intercalated ductsShape:- star shaped Grouping:- 1,2 or 3 cells in each salivary body Process #:- 4-8 processesFunction:- contractile elements - squeeze acinus (aid secretion)- regulate duct lumen size

Question 173

Salivary gland - intercalated ducts - type of cell? Nuc?

Answer 173

Type of cell:- low cuboidal cellsNuc: - large central nuc

Question 174

Salivary gland - striated ducts - not present? Cell shape? Mod? Folding?

Answer 174

Not present:- sublingual glandsCell shape:- columnar shaped cellsModificiation:- of primary saliva Folding:- massive basal membrane folding

Question 175

Salivary gland - collecting ducts - lumen? Cell type? Merges?

Answer 175

Lumen:- large lumenCell type:- pseudostratified columnar epithMerges:- stratified near termination merges with stratified squamous oral epith

Question 176

Salivary gland - histology - parotid composition? Submandibular composition? Sublingual composition?

Answer 176

Parotid composition:- composed of serous acinu- large number of ducts- adipocytes and plasma cellsSubmandibular gland:- mixed but more serous cells, also myoepith and demilunes- intercalated and striated ducts are less than in parotidSublingual:- mixed, but mostly mucous cells- intercalated ducts are short and difficult to recognize- intralobular ducts fewer on # than parotid and submand

Question 177

Summary of major salivary glands - names? Sizes? Location? Excretory ducts? Striated ducts? Intercalated ducts? Acini? Fluid characterisitics? Innervation?

Answer 177

Parotid:- largest, encapsulated - behind the mandibular ramus, ant and inferior to ear- Stenson’s duct: open opposite max second molar on buccal mucosa- short straited ducts- long intercalated ducts- serous acibu - secreting watery, but amylase-rich- innveration XISubmandibular - intermediate, encapsulated- beneath the mandible- Wharton’s open near lingual frenum on the floor of the mouth - striated duct long- intercalated short- mainly serous - vicous, mucin rich- VIISublingual - smallest, no capsule- floor of mouth- Bartholin’s: opens at same area as the submand, with additional ducts (Rivinus) at submand folds- straited and intercalated absent- mucous- vicious and mucin rich- VII

Question 178

Summary of minor salivary gland - names? ducts? Acini? Fluid? Innveration?

Answer 178

All- rare striated and intercalated ductsPalatinal- mucous- mucin rich- VII Buccal- mucous- mucin rich- VIILabial- mucous- mucin rich- VIIVon Ebners (lingual)- serous- watery and lipid rich- IXRetromolar- mucous- mucin rich- VII/IX

Question 179

General structure of salivary glands?

Answer 179

Like a bunch if grapes:- grapes are the acini- stems are the ducts - air is the CT

Question 180

Functional arrangement of salivary glands - chronology?

Answer 180

Inner to outer:- secretary duct- striated duct- interclalated duct- acinus

Question 181

Salivary glands - serous acinar cells - organelles?

Answer 181

Organelles:- Nuc at basal cell- basophillic RER- granular apperance- cells discharge their secretions into the tubular lumen via intracellular canaliculi running between cells

Question 182

Salivary glands - mucous acinar cells - organelles?

Answer 182

Organelles:- plate cytoplasm- mucin lost ir not easily stained, so cytoplasm can appear medium in H&E Staines secretion- flattened basal nuc- large mucin granules

Question 183

Salivary glands - saliva - characterisitics? Resting state and stimulated state? Flow rate?

Answer 183

Compostion:- hypotonic fluid (99% water and 1% dry matter)- .5 -1.5 litres daily- resting state 2/3 volume prod by submand- stimated state 60% by parotid

Question 184

Salivary glands - saliva - composition? Variations?

Answer 184

Varies:- from gland to gland, rats of secretion and between speciesCompostion:- 99% water- electrolytes and inorganic constituents - formed elements and organic constituents

Question 185

Salivary glands - saliva - electrolytes?

Answer 185

Cations:- Na, K, Ca and MgAnions:- Cl, HCO3, Pi, thiocynate, SO4, F, I, and OH

Question 186

Salivary glands - salivary secretion - stage I and stage II?

Answer 186

Stage I:- electrolyte transport bu acinar cell go produce isotonic saliva Stage II:- ductal modification of electrolyte composition of primary saliva to produce hypotonic saliva ⁰

Question 187

Salivary glands - salivary gland secretion - Stage I?

Answer 187

Step I:- ACh bind muscarinic receptor on acinar cell- increased Ca influx- from increased Ca its caused Ca gated channels to remove K and take in Cl and HCO3Step 2:- Na in via paracellular to balance charge- H20 follows Na (paracell or transcell)- aquaporins allow h20- high perm to h20- causes cell shrinkage Step 3:- act of Na/K/Cl cotransporter to take in Na- Na/H exchange to take in Na- Na/K pump to take in K and remove Na (with ATP)Step 4:- stimulus removed; the free intracellular Ca, cell volume, cytoplasmic pH and transport return back to normal

Question 188

Salivary glands - salivary secretion - stage II

Answer 188

From striated ductsStep 1:- Na/K pump removes Na into plasma Step 2:- reansorption of Na and Cl via Na and Cl channels, Na/H exchanger and Cl/HCO3 transporter

All duct is impermeable so water and stays in lumen Result in saliva with increased HCO3, reduced Cl and Na

Question 189

Salivary glands - inorganic saliva composition and flow rate relation?

Answer 189

Compostion:- salivary secretion as a function of salivary flow rate compared with concentrated ions in plasma- saliva is hypotonic to plasma at all flow rates- salivary conc of HCO3, Cl and and Na increases with increasing flow rate - salivary conc of K decreases with increases flow rate

Question 190

Salivary glands - formation of organic constituents of saliva? Secretory pathways? Prot conc dependent on?

Answer 190

Mostly by acinar cells (but can be ductal too)- proteins are the major organic componentcomponent:- prot conc depend in duration of stim and flow rate (Long stim and high flow rate results in high saliva total prot conc)Secretory pathways:- constitutive exocytosis (continous) minor - regulated exocytosis (major)

Question 191

What is exocytosis?

Answer 191

• A process which a cell transports secretory products through the cytoplasm to the plasma membrane- Secreotry products are packed into teanposrt vesicles

Question 192

What is constitute exocytosis? Prot conc? Flow?

Answer 192

• prots not concentrated into secretory vesicles awaiting stimulus- continous flow of protein in small vesicles to plasma mem- responsible for a continous secretion if several proteins without stim

Question 193

What is regulated exocytosis? Controlled by? Storage? Secretion?

Answer 193

• acceleration of constitutive - controlled by symph innveration- after synthesis proteins stored in granules- stim, granules empty content into lumen

Question 194

Salivary gland - buffering action of saliva - defintion? Key components? Other buffers?

Answer 194

Buffering capacity: ability of the saliva to maintain the pH when exposed to acids HCO3:- from major glands- conc increases with flow rate - miminises drop in pH around teeth after consumption of sugar (min demineral)Buffers:- phosphate and protein

Question 195

Salivary gland - What is a Stephan curve? Fluor vs hydroxy?

Answer 195

The change in plaque pH influencing demineralisation and remineralisationFluroapatite - 4.5 demin Hydroxyapatite- 5.5 demin

Question 196

Saliva - remineralisation of teeth - composition?

Answer 196

Composition:- supersaturaed with Ca and PO4- high flow rate associated with Caz PO4, OH and pH (reduced demin, increases remin and calculus form)- helped by presence of flouride in saliva

Question 197

Saliva - organic component - constituents?

Answer 197

Constituents:- prots, carbs, lipids and small organic molecules Proteins:- amylase, lipase, mucin, statherin, IgA,

Question 198

Saliva - organic components - amylase (secreted by? Role? Function? Inactivated? Plaque?)

Answer 198

Secreted by:- parotid glandsRole:- carbohydrate digestionFunction:- breakdown starch and maltoseInactivated:- low pHPlaque:- breakdown of plaque

Question 199

Saliva - organic components - lipase? (Secreted by? Role?)

Answer 199

Secreted by:- lingual minor glands (Von Ebner)Role:- fat digestion - active at gastric pH- digestion of milk fat for newborns

Question 200

Saliva - organic components - mucin? (Molecule type? Formation of mucus? Role? Location? Function? Important role? Immune?

Answer 200

Molecule type:- complex molecule (peptide core and oligosaccardie chains)Mucus:- mucin + waterRole to lubricate Location:- on all oral soft tissues (prevents drying and provide barrier)- hydrophilic and likes water and so stops dehydration Important for pellicleAggregate bacteria

Question 201

Saliva - organic components - statherin (prevent? Pellicle?)

Answer 201

Prevent:- precipitation of Ca and PO4 (supersaturated), good for mineral- but can inhibit remineral, but cant permeate early carious lesions (not a major problem)Prevent calculusPresent in enamel

Question 202

Saliva - organic components - antimicrobial components of H20, amylase, lysozyme, peroxidase, lactoferrin, histatins and cystatins?

Answer 202

Water - cleansing Amylase - bacterial adhesionLysozyme - leaves polysacc wallPeroxidase - same as aboveLactoferrin - bind Fe inhibit bacteria growth and adherenceHistatins- inhibit growth CandidaCystatins - inhibit tissue damaging bacterial enzymes

Question 203

Saliva - organic components - IgA (secretion? Synth? Specificity?

Answer 203

Secreted by - minor glandsSynth:- plasma cells in CTSpecific:- stim by bacteria against specific antigens provides local immunity

Question 204

Salivary glands - saliva secretion - neural control (parasympth and sympth)

Answer 204

Parasymth:- from brainstem and salivary nuclei (sup pons and inf brainstem nuc)- VII nerve to the sub glands- XI nerve to the parotid via otic ganglion- to the submandibular ganglion - ACh release to muscarinic receptors in the salivary glands Sympth:- thoracic spinal cord (T1-4) - to the superior cervical ganglion - via the sympth nerve - to the salivary gland releasing NA act b-adr

Question 205

Salivary glands - saliva secretion - neural control - reflex defintion? Stimuli? Reaction?

Answer 205

Reflex:- innate, automatic, predicate, repsonse involving the CNS, to a known stimulusStimuli:- associated with feedingReaction:- complex secretomotor and vasometer innverationLack uniformity of response between gland and species Secretion dependant in reflex activity

Question 206

Salivary glands - saliva reflex - gustatory (reflex type? Stimuli? Flow? Innervation?

Answer 206

Reflex type:- unconditioned Stimuli:- via taste buds - basic tastes cause secretion Sour > Salt > Bitter > SweetFlow:- max flow achieved using 5% citric acid (7ml per min)Innervation:- VII, IX and C nerves

Question 207

Salivary glands - saliva secretion - neural control - flow chart?

Answer 207

Sensory info from mechanoreceptors and chemo receptors Cerebral cortex Salivary centre in medullaAutonomicSalivary glandsSecretion

Question 208

Salivary glands - masticatory salivary reflex (stimulus from? Innervation? Reflex pathway?)

Answer 208

Stimulus from:- mechanorecprtors afferent neurons affecting periodontal ligament, oral mucosa, TMJ and musclesImnervation:- VReflex pathway:- unilateral- stim of one side of the mouth induces ipsilateral salivation

Question 209

What is Lashley cup?

Answer 209

A measure of flow rateTo be placed near the duct opening to collect salivaOuter chamber for suction to buccal mucosa

Question 210

Salivary glands - olfactory salivary reflex (type of repsonse? Gland?)

Answer 210

A unilateral response of the parotid gland No repsonse of the parotid to the odour of lemon But taste has a reaction But with the submand gland, the odour of beef increases flow rate of salivaOlfactory parotid reflex doesn’t existOlfactory submand reflex does exist

Question 211

Salivary glands - saliva secretion - neural control (sympth nerves? Parotid gland - innervation and synapse? Submand and subling - innveration and synapse?)

Answer 211

Sympth nerves:- from the synoatheric trunk follow blood vesselsParotid gland:- receives parasynth signals from IX synoases in otic ganglionSubmand and sublingual:- parasympth signals form facial nerve synapses in the mand ganglion

Question 212

Unconditioned salivary reflex?

Answer 212

Gustatory and masticatory and olfactory| Higher centres: - facilitate, also inhibit (dry mouth with anxiety) but can enhance response

Question 213

Condition salivary reflexes?

Answer 213

Pavlov’s dogsNot easily demonstrated in man Assocaitaion of sound with food without food stimulus

Question 214

Salivary glands - saliva secretion - neural control - psychic stimuli hypothesis?

Answer 214

Mouthwatering occurs on anticipation if sight of food when hungry, but it is more of a sudden awareness of saliva in mouth rather than more

Question 215

Salivary glands - saliva secretion - neural control (signal factord)

Answer 215

Sensory recpeotes for a salivary reflex or a condition reflex But cant enhance

Question 216

Factors affecting salivary flow rate?

Answer 216

Increased presence of food in mouth - chemical and mechanical Increased of smell of foodTime of day- increased in afternoon and reduced in night Season - lowest in winter and highest in summerLight:- bright increased and dark decreased Hydration:- reduced dehydrated Body positon:- increased standing and reduced sittingDrugs:- on glands and nervesReduces with age

Question 217

Xerostomia - defintion? Causes?

Answer 217

Defintion:- unstimulated flow less than 50% of normalCauses:- disease such as systemic, intrinsic or extrinsic- medication such as analgesics antidepressants and anti-histamines - dehydration, nerve damage tobacco and alcohol and stress and anxiety

Question 218

Xerostomia affect on QoL?

Answer 218

Eating:- taste alteration- dysphagia- mastication problems- avoid foodsSocial- speech difficulties- bad breath- sip water QoL:- embarrassment and self conscious- irrtibale- discomfort with dentures

Question 219

Physical impact of Xerostomia - oral cavity? Mucosa? Tongue teeth? Lips? Saliva?

Answer 219

Oral cavity:- food debris, poorly fitting denture and bad breathMucosa:- burn sense, dry and sticky mucosa, dental mirror sticks- mucositis, ginguvigs, mouth lesions and infection- infection, ulcers and fissures, and erythematosus Tongue:- erythrma, atrophy of filiform, dry and fissuredTeeth:- dental caries (cervical and root caries) and deminLips:- cracked lips, peeling and fissuring and angular cheiltisSaliva:- reduced pooling, stringy and frothy saliva

Question 220

Sjögrens’s syndrome - what is it? Prevalence? Ages? Symptoms? Causes? Diganoses? Treatment?

Answer 220

Long term autoimmune disease affecting body moisture producing glands (mouth and dry eyes)Prevalence:- 1/100Lab test and imagingBetween 35-50More common in females Family history Symptoms:- dry eyes and dry mouth - dry throat, dry nose, cracked tongue dry skin, persistent dry cough and prolonged fatigue Causes:- unknown but combination of genetics hormonal and environmentalDiagnoses:- blood test via antibodies and rheumatoid factorSalivary flow testEye test - function of lacrimal glandsLip/salivary gland biopsy - reveal lympho closed around salivary due to gland inflammation No known treatment

Question 221

Divisions of the nervous system?

Answer 221

CNS (brain and SC)PNS - sensory and motor division (CN and SN)Motor division is split into ANS (motor invol) and SNS (motor voluntary)ANS split into para and sympathetic

Question 222

Cell types of the neural cells of the brain and their function? (v basic)

Answer 222

Neurones - propagate impulse| Glial cells - supporting cell, aid with BBB and produce myelin

Question 223

Anatomy, function and cell characteristics of a neurone - myelination and its function? Multiple sclerosis?

Answer 223

DendritesNucleusAxonCell bodyMyelin sheathSchwann cellNode of ranvierAxon terminalsTransmits impulses as APCell characteristics:- dendrites receive impulses and axons transmit them- nuc loose chromatin- high meta rate (mito)Myelination:- unmyelinated only have 1 layer of glial cell, appear grey (grey matter)- myelinated have many layers of glial cells form MS, appear white (white matter)- faster AP conduction, protection and prevent AP passing to adj cell bodiesMS:- autoimmune against Schwann and oligodendrocytes- muscle weakness, memory and problem solving issues

Question 224

Organisation of neurons in the NS - CNS and PNS? upper and lower motor neurons relation to CNS and PNS?

Answer 224

CNS:- cell bodies and unmyelinated axons form grey matter- myelinated axons form white matterPNS:- myelinated axons form nerves- cell bodies form gangliaUpper:- in CNS, leading from grey matter in brain synapsing with the grey matter of grey matterLower:- in PNS, leading from grey matter in PC to voluntary muscle outside of the CNS

Question 225

Development - neural tube - 3 layers? top layer develop? form of tube? function of neural crest cells?

Answer 225

Ectoderm, mesoderm and endodermTop layer (surface ectoderm) develops a thickening called a neural plateNeural plate thickens and folds over to form the neural tubeNeural crest cells migrate away and form other structures

Question 226

Development - vesicle formation - neural tube division? 3 primary and 5 secondary names? 2nd –> brain structures? cerebral hemisphere further development?

Answer 226

Neural tube divides into 3 primary vesicles: - forebrain, midbrain and hindbrain (4w) and then into secondary vesicles:- telencephalon and diencephalon (forebrain)- mesencephalon (midbrain)- metencephalon and myelencephalon (hindbrain) (5w)Brain structures:- telencephalon forms cerebral cortex and basal ganglia- diencephalon forms thalamus and hypothalamus- mesencephalon forms midbrain- metencephalon forms the pons and cerebellum- myelencephalon forms medullaCerebral hemisphere:- from telencephalon- C-shaped covering diencephalon and brainstem

Question 227

Ventricles of the brain - relation to vesicles? location?

Answer 227

Ventricles of the brain:- telencephalon = lateral ventricles- diencephalon = 4rd ventricle- mesencephalon = cerebral aqueduct- rhombencephalon = 4th ventricleLateral ventricles are c-shaped and lie in the cerebral hemisphereInterventricular foramen connects LV with 3rd ventricleCerebral aqueduct lies in midbrain4th ventricle diamond shaped and in hindbrain

Question 228

CT covering of the CNS - dura mater (function, location and extension?) arachnoid mater (location, function and extension?) and pia mater (location, function and extension?)

Answer 228

Dura mater: protection and outer- septa between brain hemispheres and encloses intracranial venous sinuses- extends to S2Arachnoid mater: middle, cushioning- not follow convolutions of brain- extends to S2Pia mater: innermost and impermeable to fluid- follows convolutions- form choroid plexus form CSF- extends to coccyx as fibrous strand (filum terminale)

Question 229

Extradural space - definition? bleeding? Subdural space - definition? bleeding? Subarachnoid space - definition?

Answer 229

Extradural:- def: space between dura and skull- bleeding: involving middle meningeal artery (ECA), called and extradural haematomaSubdural:- between dura and arachnoid- bleeding from haemorrhage of veins draining brain- haematoma is sickle shapedSubarachnoid:- between arachnoid and pia- filled with CSF- all BV supplying brain and CN pass through- haemorrhage can be spont due to aneurysm or trauma (vertebral and ICA branches (cirlce of WIllis)

Question 230

Protection of brain dural folds - structures?

Answer 230

falx cerebritentorium cerebellifalx cerebellidiaphragma sellae

Question 231

CSF - colour? specific gravity? pH group? cells? normal Pa? increased Pa? circulation passage (synth by? passage between via foramen?) arachnoid granulation function/

Answer 231

Clear and transparent fluid1.004-1.007 SPAlkaline and doesn’t coagulateNo cells60-150 mm PaIncreased Pa when standing coughing, sneezing, crying and compressing IJVCirculation:- synth by the choroid plexus in the lateral ventricle- from lateral ventricle to 3rd ventricle via interventricular foramen- from 3rd ventricle to 4th ventricle via cerebral aqueduct- from 4th ventricle to the subarachnoid space around brain and SC via foramen of magendie and foramen of luschkaArachnoid granulation:- allows passage of CSF into the venous system from the subarachnoid space

Question 232

Blood brain barrier - definition? content? function?

Answer 232

Definition: circumventricular organ- protective mechanism that helps maintain a stable environment for the brain and prevents harmful aas and ions present in the bloodstream and blood cells from entering the brainContent:- endothelium with tight junctions- thick basal lamina- foot processes of astrocytesFunction:- drug delivery to CNS, but need to be lipid sol or vector

Question 233

Cerebrum - size? located? 2 parts? sulci definition? gyri definition?

Answer 233

Size:- largest part of the brainLocated:- in the anterior and middle cranial fossae and the whole concavity of the vault of the skill2 parts:- cerebral hemispheres (left and right)- diencephalon (consists of thalamus and hypothalamus)Gyri:- increases Sa of the brain the cerebral hemispheres are thrown into foldsSulci:- gyri separated from each other by fissures

Question 234

Grey matter and white matter - brain and SC? 5 types of cells in the grey matter of the cerebral cortex? 6 different cortical layers?

Answer 234

Brain:- inside white (nerve fibres)- outside grey (nerve cells)SC:- inside grey (nerve cells)- outside white (nerve fibres)5 cells:- horizontal- stellate- fusiform- cells of Martinolli- pyramidal6 layers:- molecular layer- external granular layer- external pyramidal layer- internal granular layer- internal pyramidal layer- multiform layer

Question 235

White matter - composition? supported by? Commissural fibres - function? examples? Association fibres - function? short/long fibre location and function? Projection fibres - function? examples?

Answer 235

Composition:- myelinated nerve fibresSupported by:- neurogliaCommissural fibres:- connects corresponding regions of 2 hemispheres- corpus callosum (rostrum, genu, body and splenium) and fornixAssociation fibres:- connects various cortical regions within same hemisphere- short fibres located beneath cortex and connects adjacent gyri- long fibres arranged into named bundles (fasciculi)Projection fibres:- afferent and efferent nerve fibres passing to and from the brainstem to the cerebral cortex- internal capsule, corona radiata and optic radiation

Question 236

Thalamus - contains nucs? grey matter? receives tracts? function? 3 parts? split by?

Answer 236

Nuclei:- anterior, medial and lateralGrey matter:- large ovoid massTracts:- receives main sensory tracts (except olfactory pathway)Function:- integrates information it receives and relays to the cerebral cortex and subcortical regions- integrates visceral and somatic functionPart:- anterior nuclear group- medial nuclear group- lateral nuclear groupSplit by:- internal medullary lamina

Question 237

Hypothalamus - location? function? homeostatic roles? important nuclei? nuclei run into? hypothalamo-hypophyseal portal system function?

Answer 237

Location:- part of the diencephalon that extends from the optic chiasma to the post border of the mammillary bodies- lies below thalamus and separated by the hypo sulcusFunction:- main visceral control centre and homeostasisHomeostasis:- autonomic control- body temp reg- reg food intake- reg water and thirst- reg sleep cycle- control endocrineImportant nuclei:- supraoptic- paraventricularRun:- axons running down into post lobe of the pituitaryHypothalamo-hypophyseal portal system:- carry neurosecretions into the anterior lobe of pituitary gland

Question 238

Pituitary gland - anatomy? part development?

Answer 238

Anatomy:- stalk- anterior part- posterior partDevelopment:- pituitary stalk and post pituitary derived from diencephalon- anterior pituitary from ectodermal (Rathke’s pouch)

Question 239

Pineal gland - located? age changes? function? indirect function?

Answer 239

Located:- projects backwards to lie post to midbrainAge changes:- progressive calcificationFunction:- produces melatonin for circadian rhythm influenced by lightIndirect function:- controls function of other endocrine organs

Question 240

Basal ganglia - function? pathology?

Answer 240

Function:- help reg initiation and termination of movements- role in controlling motor system referred to as extrapyramidal systemPathology:- Parkinson’s and Huntington’s

Question 241

Limbic system - located? function? components?

Answer 241

Located:- surrounds corpus callosum and the diencephalonFunction:- behavior, emotion and memoryComponents:- cingulate and subcallosal gyrus- septal area and olfactory bulb- hippocampal formation (hippo gyrus, dentate gyrus and parahippo gyrus)- amygdaloid body and mammillary body- anterior nuc of thal- hypothal

Question 242

Spinal tracts - lateral pathways (function, higher centre control and examples?) ventromedial pathways (function, higher centre control and examples?)

Answer 242

Lateral pathways:- control voluntary movements of distal muscles (under direct cortical control)- corticospinal and rubrospinal tractsVentromedial pathways:- control posture and locomotion (under brainstem control)

Question 243

Lateral pathway - 2 tracts? area 4/6? the rest are? SC junction what occurs? brain relation with body? synapse of CST axon? RST starts where? loss of function with lesions in CST and RST or CST alone? CST control of spinal motor nerves?

Answer 243

Tracts:- corticospinal and rubrospinalArea 4/6:- frontal motor cortex and the rest are somatosensoryJunction:- CST crosses over at SCRelation:- right motor cortex response for left side and vice versaSynapse:- on ventral horn motor and interneurons to control musclesRST:- starts in red nic of midbrainLesions:- CST and RST; loss of fine movement of arms and hands also can’t move shoulders, elbows, wrists and fingers independently- CST alone; same as above but functions re-appear as RST takes overControl:- pyramidal neurons in motor cortex- monosynaptically excite pools of agonist spinal motoneurons - same pyramidal branch and via interneurons inhibit them

Question 244

Ventromedial pathways - function with example? pontine and medullary reticulospinal tracts (origin? function? innervates?) use of lateral and ventromedial to cause one action?

Answer 244

Function:- stabilise head and neck (VST)- eye stability as body moves (TST)Tracts:- origin from brainstem- use sense about balance, body pos and vision- reflexly maintain balance and body position- innervates trunk and antigrav muscles in limbsAction:- motor cortex can signal via both lateral and ventromedial to form a response

Question 245

Human cortex - area 4 role and function? area 6 role, function and split into with their functions? area 5 and 7 function and inputs? prefrontal and parietal cortex role and relation to area 6?

Answer 245

Area 4:- innervate specific contralateral muscles- primary motor cortexArea 6:- drive complex movements on either side of body- premotor area (PMA) and supplementary motor area (SMA)- SMA innervates distal motor units- PMA innervate proximal motor units via reticulospinalArea 5/7: post parietal cortex- form mental image of body in space formed from somatosen, proprio and visual inputsP and P:- decisions are taken about what actions to take- axons converge to area 6 and encode the actions which is converted to how it’ll be carried out- axons from area 6 go to area 4 for the action to be performed

Question 246

Basal ganglia - motor loop definition? input to area 6? anatomy? motor loop process and end product? Primary motor cortex - initiation of vol move (neurones? inputs? encode? precision encoded by?

Answer 246

Loop:- information loop cycles from cortex through thalamus basal ganglia back to SMAArea 6:- input comes from ventral lateral nuc in dorsal thalamus called the VLo (from the basal ganglia)Anatomy:- putamen- substantia nigra- subthalamus- globus pallidus- VLo - SMAProcess:- cortex to putamen (excite)- putamen to globus (inhib)- globus to VLo (inhib)- VLo to SMA (excite)- positive feedback loop (‘Go’ signal for voluntary movement)PMC:- by pyramidal neurons- inputs from thalamus - burst of activity before and after to encode force and direction- precision encoded by population of neurons- larger population input creates finer control

Question 247

Cerebellum - lesions cause? layer, area 4/6 and somatosense cortex form? connections across the brain? function? Lateral cerebellum (motor loop addition?)

Answer 247

Lesions:- ataxiaForm:- corticopontocerebellar projectionConnections:- connect cortex, pontine nuc and cerebellum- back to cortex via ventrolateral thalamusFunction:- instruct direction, timing and force of movementsLateral:- move through basal ganglia and VLo via involve of feedback loop via pons, cerebellum, thalamus back to cortex

Question 248

Cell bodies of cranial nerves - sensory? motor? autonomic?

Answer 248

Sensory- dorsal root ganglionMotor:- in CNSAutonomic- pre (in CNS) and post (in ganglion) ganglion

Question 249

CN I - function? pathway of the nerve? Fractured cribriform?

Answer 249

Function:- smellPathway:- recep in olfactory epith of nasal cavity, olfactory nerve passes through the cribriform plate of ethmoud and enter olfactory bulb in ant cranial fossa Fractured:- loss of smell tearing nerve

Question 250

CN II - function? pathway of nerve? Increased CSF Pa? Damage to the R optic nerve, optic chasm and optic tract?

Answer 250

Function:- visionPathway:- enters optic canal, nerves join forming optic chains, fibres cross to form the optic tract Increased:- causes papilloedema R optic nerve:- blindness of R eyeOptic chaisma:- loss of peripheral vision (bitemporal hemianopsia)Optic tract:- causes blindness in left temp and right nasal fields (left homonymous hemianopsia)

Question 251

CN III - function (somatic - muscles? autonomic?) pathway of nerve? drooping? pupil problems? eyeball movement?

Answer 251

Functions:- somatic via extraocular muscles (sup, medial, inf erectus and inf oblique) and eyelid (levator palpebrae superioris)- autonomic motor - parasymph to pupil causing constriction to ciliary muscles Pathway:- merges from midbrain and exits via SOFDrooping:- ptosisEyeball movement:- abducted and pointing down- no pupillary reflex- no accomodation of lens

Question 252

CN IV - function (somatic - muscles?) pathway of the nerve? diplopia?

Answer 252

Function:- somatic motor of extraocular (superior oblique moves eye down)Pathway:- emerges form the dorsal surface of mid brain and exits via SOFDiplopia: when looking down- double vision

Question 253

CN VI - functions (somatic - muscle)? pathway of nerve? diplopia?

Answer 253

Function:- somatic extraocular; lateral erectus abducts eye)Pathway:- emerges between pins and medullary exits via SOFDiplopia: medial deviation- double vision

Question 254

CN V - ophthalmic - pathway? innervated?

Answer 254

Pathway:- emerges from the pins, travels via the trigeminal ganglion and exits via SOFInnervates:- cornea, forehead, scalp, eyelids, nose and mucosa of nasal cavities and sinuses

Question 255

CN V - maxillary - pathway? Innervates?

Answer 255

Pathway:- emerges from the pins, travels via the trigeminal ganglion and exits via the foramen rotundumInnervation:- face over maxilla, maxillafybteeth, TMJ, mucosa of nose, maxillary sinuses and palate

Question 256

CN V - mandibular - pathway? Innervates (sensory and motor?) damage can cause?

Answer 256

Pathway:- emerges from the pond, travels via the trigeminal ganglion and exits via the foramen ovale Innervates:- sensory; face over mandible, mandibular teeth, TMJ, mucosa kd mouth and ant 2/3 of tongue- motor; mastication, tensor veli palatini and tensor tympaniDamage:- paralysis of masticatory muscles- loss of corneal or sneezing refelx- loss sensation to face- trigeminal neuralgia

Question 257

CM VII - functions (somatic motor? autonomic motor? special sensory? general sensory?) pathway of the nerve? Bell’s palsy?

Answer 257

Fucntions:- somatic; muscles of facial expression, scalp, stapedius- autonomic; submand and sublingual glands, lacrimal, nose and palate glands- special; taste from ant 2/3 of tongue and soft palate- general; EAMBell’s palsy:- can’t frown, clear eyelids or bare teethPathway:- emerges from between pons and medulla and exits via IAM, dividing into vestibule and cochlear nerves

Question 258

CN VIII - innervation (special and general sensory?) nerve pathway? Ringing in ear? Deafness? Loss of balance? Nystagmus?

Answer 258

Innervation:- special; vestibular sensation from semicircular ducts, cuticle, saccule fibes sense of position and movement- general; hearing from spinal organPathway:- emerges from between pons and medulla and exits via IAM, dividing into vestibule and cochlear nervesRinging: tinnitusDeafness: conductive or sensorineural Loss of balance: vertigoNystagmus: involuntary rapid eye movements

Question 259

CN IX - innervations (special? general? visceral? autonomic motor? somatic motor?) pathway of nerve? loss of gag and taste from back of tongue?

Answer 259

Innervations:- special; taste from post 3rd of tongue- general; sensations from middle ear and post oral cavity- visceral; sensation from carotid body and sinus (Pa)- autonomic; parasymph of parotid- somatic; to stylopharyngeus helps with swallowingPathway:- emerges from medulla and exits via jugular foramenLoss of:- assoc with injuries to X and IX (jugular foramen syndrome

Question 260

CN X - innervates (special? general? visceral? autonomic motor? somatic motor?) pathway nerve? Damage to pharyngeal branch or laryngeal branch?

Answer 260

Innervations:- special; taste from epiglottis and palate - general; sensation from auricle and EAM- visceral; pharynx, larynx, trachea, bronchi, heart, oesophagus, stomach and intestine - autonomic motor; para innervation of muscles in bronchi, gut and heart- somatic; pharynx, larynx, palate and oesophagusPathway:- emerges from medulla and exits via jugular foramen Pharyngeal:- difficult in swallowing Laryngeal:- difficult in speaking

Question 261

CN XI - innervates (somatic - muscles?) Loss of function? pathway of nerve?

Answer 261

Innervates:- somatic motor; striated muscle of soft palate, pharynx and larynx also SCM and trapeziusPathway:- medulla and large spinal roots exit via jugular foramen Loss of function:- weakness in head turning and shrugging shoulder

Question 262

CN XII - innervates (somatic motor - muscle?) pathway? tongue paralysis?

Answer 262

Innervates:- somatic motor to muscles of tonguePathway:- from the medulla and exits via the hypoglossal canal Tongue:- atrophy of ipsilateral half of tongue, tip deviates towards affected side

Question 263

Different types of stimuli causing different types of pain?

Answer 263

Tissue damage - nociceptive pain Inflammatory pain - inflammatory mediators Nerve injury - neuropathic painDysfunctional pain has an unknown stimuli (lower back pain)

Question 264

Pain pathway via dorsal root ganglia (stim? AP? DRG? Ascending tracts? Higher brain centres?)

Answer 264

Stimulus detected by sensory nerve endings and AP is propagatedPasses to the dorsal root ganglion and passes into the SC via synaptic transmissionProcessing and plasticity in the spinal dorsal horn Trvalss up the SC vis the spinothalamic and spinoparacbtachial tract into the limbic, thalamus and cortex

Question 265

Primary afferent fibres - Adelta? C fibres?| Diameter? Myelination? Conduction speed? Act threshold? Sensation on stim?

Answer 265

Adelta: thermal and mechanical pain- small- thin- 5-15ms- high and low- rapid sharp and localised pain- initial pain C fibres: mechanical, thermal and chemical - smallest- unmyelinated- <2ms- high- low, diffuse and dull pain - delayed pain

Question 266

Peptide production from the pain fibres? (What are they?

Answer 266

From NGF - adelta produce CGRP and sub PFrom GDNF - c fibres non-peptergic Enter different pain of the brain

Question 267

Trigeminal ganglia ascending pathway? (TRG? Passage to the brain? Nuc?)

Answer 267

Starts at the trigeminal ganglion entering the ponsDrops into the medulla where the spinal nucleus of V is presentRises through the pons and medulla to the ventroposteromedial nuc of trigeminal to the primary sensory area

Question 268

Allodynia and hyperalgesia definitions?

Answer 268

Allodynia:- increased response to normally non-painful stimuli Hyperalgesia:- exaggerated response to normally painful stimuli

Question 269

Mechanisms of pain signalling - peripheral and central sensitisation?

Answer 269

Peripheral in the skin and muscles| Central is in the dorsal horn

Question 270

Cell signalling in peripheral sensitisation - upregualting of existing receptors? Upregulati f I’d new receptors?

Answer 270

Receptors: in response to stimuli - ligands-gated chs- GPCR (PGE2 and bradykinin)- tyrosine kinase receptor New receptors:- volt-gated chsAnd so the area becomes super-excitable due to upregulatuon (Receptor and channel sensitisation with gene expression)

Question 271

Cell signalling in the central sensitisation - definition? 2 phases? New receptor expression?

Answer 271

Def:- increase in the excitabiltuy of neurons within the central nervous system so that normal inputs begin to produce abnormal responses 2 phases:- immediate but relatively transient phase- slower onset but longer-lasting phase Expression:- presynaptic release of glutamate, sub P and CGRP- greater receptor expression such as NMDA- lower threshold and opening chs therefore increasing excitabiltiy

Question 272

Referred pain from the teeth - pain source? Vice versa? Mechanism of pain?

Answer 272

Source:- pain can originate from the maxillary sinus due to their close proximity Vice:- previous treatment can also cause maxillary sinus painMexh:- nerve damage or long-term sensitisation

Question 273

Gate control theory of pain - inhibition? C fibres? Abeta fibres?

Answer 273

C fibres activated synapsing and sending pain stimuli to the brainAbeta can also be stimulated such as rubbing which activates the inhibitory internecine which inhibits the C fibres post synaptic connection and so inhibiting the pain stimuli to the brain

Question 274

Inhibition of pain stimulation - gate theory example? Rubbing?

Answer 274

Rubbing activates Abeta which activates inhibitory interventions that inhibit 2nd order dorsal horn neurons inhibiting pain signalling

Question 275

Descending inhibition pathway for pain modulation - evidence found? Mechanism of action?

Answer 275

Electrim stim of periaqueductal grey reduces pain severityMorphine produces the same reactionNaloxone administration inhibits both 1 and 2Mechanism:- morphine binds to opioid receptors- release of endorphins/enkephalins - naloxone blocks opioid receptors

Question 276

Descending pain regulatory pathway - pain stimuli? PAG? Opiate blocking?

Answer 276

Pain:- causes pain from sensory 1st order neurons - passes into dorsal horn and synapses to another neurons to the thalamusPAG- stimulated to activate an opiate interneurone which inhibits the signalling of the 1st order sensory neurons Opiate:- block NuT reelase from 1st order afferent pre-synapic - inhibit 2and order afferent post synaptic

Question 277

Higher brain centre regulation of PAG - centres example?

Answer 277

Centre: emotion/stress/arousal - cortex- hypothalamus- thalamus Can either activate or inhibit PAG

Question 278

Common analgesic targets - NSAIDs pathway (examples? Mechanism of action?) Low effectivity?

Answer 278

Examples- aspirin- paracetamol- ibuprofenMechanism:- action to inhibit COX to stop the conversion of arachidonic acid to prostaglandins Low:- due to bradykinin which increases the synthesis of prostaglandins

Question 279

Defintion of proprioception? Types of proprioceptors? Trigeminal proprioceptor types?

Answer 279

Defintion:- awareness of position of body parts in relation to each other and surroundingsType:- muscle spindles - golgi tendon organs- joint receptors Trigeminal:- muscles of mastication (spindles)- PDLMs- TMJ receptor

Question 280

Structure of muscle (fibre types, supplies by and constituents?)

Answer 280

Extrafusal:- bulk of fibre and contractile- supplies by a-motor neurons Intrafusal:- spindle, specialised within a CT capsule

Question 281

Function of muscle spindles? Example (glass filling with drink?

Answer 281

Information about muscle lengthAct to maintain muscle lengthLoad compensation  Example:- glass filling- bicep spindle stretch- increased motor neuron drive to bicep- muscle length maintained

Question 282

Masticatory muscle spindle - cell body location? Afferent synapse location?

Answer 282

Cell body:- trigeninal mesencephalic nucAfferent:- V motor nic- cerebellum and cerebral cortex

Question 283

Gamma motor neurons - functions?

Answer 283

Cause contraction of intrafusalMaintain tension in spindle and afferent activityAlpha and gamma co-activation

Question 284

Golgi tendon organs - found? Function?

Answer 284

Found:- in tendons in series with muscle fibres- role in inhibitory reflex prevention of CS stretch of muscles

Question 285

Types of joint receptors - location and function?

Answer 285

Pacinian - ligaments- acceleration Golgi - ligament- positionRuffini - capsule - movement

Question 286

Anatomy of muscle spindle - head, centre and tail (innervation, function and stimuli)?

Answer 286

End portions are contractile - head innervated by afferent II (activated by stretch, detects fibre length)- tail innervated by gamma efferent - middle is the non-contractile central portion which can be stretched and is innervates by Ia (afferent - detects length of fibre and speed of change)

Question 287

Description of a reflex arc - reflex latency (conduction time)?

Answer 287

Receptor to afferent neurons Synapses in SCTo an efferent neurons and effectorLatency:- time relayed to speed and distance - delay at synapse (0.2ms)

Question 288

Jaw reflexes - vertical and horizontal (direction and movement?)

Answer 288

Vertical:- move mandible relative to maxilla in vertical plane - jaw jerk (opening and unloading)Horizontal:- move mandible relative to maxilla in protrusive, recursive or lateral direction

Question 289

Jaw jerk reflex - Type of reflex? Stimulus? Response? Monosynaptic? (Clinical stimulus? Receptor? Synapse? Effect? Latency?) Role of jaw-jerk (phasic and tonic?)

Answer 289

Reflex:- phasic stretchStimuli:- sudden jaw openingResponse:- activation of jaw closing muscle  Monosynaptic:- jaw closing muscle spindles- jaw closing motorneuronesClinical stimulus:- chin tapReceptor:- muscle spindleSynapse:- 1 in V motor nucEffect:- contraction of masseter muscle Latency:- 8ms  Role:- phasic: load compensation during chewing and  stabilise jaw during vigour head movement - tonic: resist gravity and maintain posture

Question 290

Jaw jerk - postural position (resting position? Maintained? edentulous? Reference for?)

Answer 290

Resting with teeth apartMaintained:- minimal muscle activity or governed by muscle elasticityRemains reproducible throughout life in dentate and edentulous subjects Important reference for position and height for dentures

Question 291

Mech of mandibular posture - clinical relevance?

Answer 291

Active - stretch reflexPassive - tissue elasticity Relevance:- altered jaw relationships- vertical jaw relationship

Question 292

Inhibitory jaw reflex - stimuli? Responses? Pathways (trisynaptic or polysynaptic? - neurons type? And receptors?)

Answer 292

Stimuli:- mech or noxious stimuli in mouth- noxious around mouth or elsewhere in body Responses:- act of jaw opening (sub-primates only)- inact of jaw closing Pathway:- trisynaptic or polysnaptic- mechanoreceptive or nociceptors- interneurones - jaw closing and opening motorneurones

Question 293

Inhibitory jaw reflex pathway?

Answer 293

Nociceptors and mechanoreceptors recieve stimulusPasses to trigeminal ganglion Both interaction with supratrigeninal nucReticular formationAct inhibitory on V motor nicCausing muscle

Question 294

Function of inhibitory jaw reflexes?

Answer 294

Protective:- restrain buildup of forces between teeth during mastication- prevent overloading of periodontium, muscle and TMJFacilitate jaw opening to expel noxious material and minimise damage to lips

Question 295

Jaw unloading reflex - stimulus? Response? Pathway neurons?

Answer 295

Stimulus:- sudden jaw closure following hard bitingResponse:- inact of jaw closing muscles- activation of jaw opening muscles Pathway:- jaw closing muscle spindles - interneurons - jaw muscle motor neurons

Question 296

Jaw unloading reflex - pathway? during loading? Loading removed? Function?

Answer 296

Pathway:- jaw closing muscle activates and synapses with V mesencepahlic nuc act V motor nuc - activates jaw opening muscles During laoding:- jaw opening muscle is not stimulated Loading removed:- jaw closing muscle doesn’t stimulate the reflex Fucntion:- protection of antagonist teeth against each other

Question 297

Horizontal jaw reflexes - response to? Role for?

Answer 297

Reflex horizontal movements of jaws in response to mechanical stimuli Roles in canine guidance

Question 298

Trigeminal system - pain? innervation it provides? branches?

Answer 298

Pain:- common reason for people to seek dental treatment- prevents people from obtaining optimal dental care- big impact on lifeInnervation:- sensory innervation to the face and mucous mem- motor innervation to muscles of masticationBranches:- ophthalmic, maxillary and mandibular

Question 299

General sensory pathway - neurone pathway?

Answer 299

Primary afferent neurons to 1st synapse| 1st synapse to thalamus then to the cerebral cortex

Question 300

Studying the CNS - tracer? electrophysiological? neurological?

Answer 300

Tracer:- HRP and fluorescent dyesElectrophysiological:- exciting the nuc from peripheral stimuliNeurological:- happens if nuc destroyed by disease

Question 301

Trigeminal sensory pathway - neurons pathway?

Answer 301

Trigeminal primary afferent neurons synapses with the trigeminal sensory nuc (trigeminal ganglion present)From the nuc to the thalamus via the trigeminothalamic tract (synapses with the thalamus)Thalamus to the somatosensory cortex

Question 302

Main sensory nucleus (found? primary afferents? second order neurons? function?)

Answer 302

Found:- brainstemPrimary afferents:- V1, V2 and V3 (large myelinated afferents)Second order neurons:- cross the midline to join VTTT and terminate in VPM of thalamus- don’t corss midline and joint DTTT and terminate in VPM of thalamusFunction:- processing discriminative tactile and proprioceptive sensation

Question 303

Discriminative touch pathway from the head - first/second and third order?

Answer 303

First:- axons from face in trigeminal ganglionSecond:- pontine trigeminal nucTrigeminal lemniscusThird:- ventral post thalamic nucNeuron reaches the sensory cortex

Question 304

V spinal trigeminal nucleus - subdivisions? extension?

Answer 304

Subdivisions:- V nuc oralis- V nuc interpolaris- V nuc caudalisExtension:- both nuc and tract extend caudally to about the third cervical segment of the SC

Question 305

V nucleus caudalis - located? primary afferent? second order neurons? function?

Answer 305

Located:- most caudal part, extending from SC to obexPrimary afferent:- small, turn caudally and join spinal trigeminal tract (V1, V2 and V3)Second order neurons:- cross midline to joint TTT and terminate in VPM of thalamusFunction:- processing pain and temp from the face, mouth and nose

Question 306

Convergence, divergence and straight through?

Answer 306

For knowledge

Question 307

Pain and temperature from the head - pathway neurons (first, second and third order?)

Answer 307

First:- axon from face in the trigeminal ganglion to the secondSecond:- within the spinal trigeminal nucSpinal lemniscusThird:- in ventral post thalamic nucLeading to the sensory cortex

Question 308

V nucleus Oralis and Interpolaris - primary afferents? second order neurons? functions?

Answer 308

Primary afferent:- small, turn caudally and join STT (V1, V2 and V3)Second order neurons:- some to contralateral VPM and some to cerebellumFunctions:- tactical information- pain and temp from the teeth and intraoral structures- reflexes (corneal)

Question 309

Arrangement of afferents and their endings in spinal trigeminal system - (rostral-caudal) ophthalmic? mandibular? maxillary? (for different divisions) pain-temp sensation?

Answer 309

Ophthalmic:- spinal tract fibres most ventralMandibular:- spinal tract fibres most dorsalMaxillary:- spinal tract fibres in betweenPain-temp:- area near centre of face more rostral- area towards the back of head more caudal

Question 310

Trigeminal mesencephalic nuc - located? cell bodies found? primary afferents? synapse? second order neurons? function?

Answer 310

Located:- most rostral partCell bodies:- jaw muscle spindles afferents- some mechanoreceptive afferents from PDLPrimary afferents:- cell bodies within CNS- parent axon in V motor root (V3)Synapse:- in V motor nucSecond order neurons:- V motor neuronsFunction:- reflexes- nonconscious proprioception

Question 311

Functions of trigeminal sensory nuclei - main sensory nuc? nucleus oralis? nucleus interpolaris? nucleus caudalis?

Answer 311

Main sensory:- sensation of touch- conscious proprioceptive sensation- reflexesNuc oralis:- tactile touch- sensation of pain- reflexesNuc interpolaris:- reflexesNuc caudalis:- sensations of hot, cold and pain

Question 312

Trigeminal motor nucleus - located? inputs from? afferent? damage to nuc?

Answer 312

Located:- medial to MSN in ponsInputs:- Vms- motor cortex- hypothalamusAfferents:- exit via mtor root to mandibular division- supply muscles of masticationDamage:- ipsilateral muscle atrophy

Question 313

Mechanism of ingestion - different stages?

Answer 313

Transport:- food from lips to cheek teethMasticationTransport:- food from cheek teeth to back of tongueSwallowing

Question 314

Functions of mastication - Related to health?

Answer 314

Functions:- breakdown food- stim salivary flow- contribute to taste and smell by releasing chemicals- growth and maintenance of oro-facial tissuesHealth:- poor dentition = poor mastication- poor mastication can lead to gut disorders- poor diet = poor dentition

Question 315

The chewing cycle - time? phases? 1 full cycle? during open? during closing?

Answer 315

Time:- 0.5-1.2 secPhases:- opening- closing (fast - crushing) (slow - grinding)- intercuspal (tooth to tooth)Full cycle:- opening + closing + power strokeDuring opening:- working side head: rotates and moves slightly (Bennett Movement)- balancing side head: moves downwards, forwards and medially During closing:- working side head: moves medially (back to normal position in glenoid fossa), rotates back to normal orientation- balancing side head: moves upwards, backwards and laterally (back to normal position in glenoid fossa)

Question 316

Lateral jaw movements - working side and balancing side?

Answer 316

Working side: functional- to which mandible moves- where food is locatedBalancing side: non-functional- from which mandible moves

Question 317

Chewing cycle - food consistency? quality and quantity of tooth contact? present or absent of pain? sequence of muscle activation (opening and closing?)

Answer 317

Food consistency:- tough or brittleQuality and quantity of tooth contact:- tall cusps and deep fossae (vertical chewing stroke)- flattened or worn teeth (broader chewing stroke)Presence or absence of pain:- TMJ pain (shorter, slower and irregular pathway)Sequence:- opening; mylohyoid, digastric and lateral pterygoid- closing; lateral pterygoid, temporalis, masseter and medial pterygoid

Question 318

Masticatory performance - definition?

Answer 318

Definition:- the ability to breakdown food morsels into small particles- number of chewing strokes required to prepare a mouthful for swallowing- correlated with total occlusal contact area

Question 319

Control of mastication - voluntary? reflex and cyclical?

Answer 319

Voluntary:- result of deliberate effort of willReflex:- given sensory input evokes a stereotypes motor responseCyclical:- N/A

Question 320

Central pattern generator theory of mastication - brain centres and responses?

Answer 320

Peripheral influences act jaw and tongue reflexes that act masticatory muscle motor neurons which activate mastication Peripheral influences can also act the central neural pattern generator of the brainstem or high centres that act mastication downstream

Question 321

Antigens - definition? epitope definition?

Answer 321

Definition:- any substance capable of triggering an immune responseEpitope is the area of the antigen which the antibody attaches to (gives identity either self or non-self)

Question 322

Physical barriers - skin definition? mucus (production? produced from? composition? immune characteristics?) self-tolerance definition?Adaptive and Innate (no answer and cells?)

Answer 322

Skin:- is a barrier between internal and externalMucus:- produced by goblet cells in the resp tract and transported by cilia- consists of 95% water, 2% salts and 2% mucin and is sticky- also contains antimicrobials such as growth inhib, enzyme inhib, lysins and abs Self-tolerance:- elim lympho which react with self antigens during early development to be destroyed

Question 323

Non-specific humoral factors - growth inhibitors (function? examples? dependent?) enzyme inhibitors (function and example?) lysins (function and example?)

Answer 323

Growth inhibitors:- deprive microbes of nutrients for growth- Transferrin (bind iron) and Interferon (antiviral)- temp dependentEnzyme inhibitors:- prevent enzymes from doing their job- poison or drugsLysins:- lysis- lysozyme and complement

Question 324

Complement system - classical? alternative? lectin?| (describe each pathway) MAC?

Answer 324

Alternative pathway:- C3 clipped and forms C3a and C3b- C3b reactive (neutralised by H2)- C3b stabilised and binds to prot B- prot B clips B to form C3bBb- C3b can bind C3 convertase forming C3bBbC3b- C5 convertaseClassical:- C1 formed from C1q/r/s- C1q binds Ab and C1r/s are proteases- bind to C1q; act of C1r and act of C1s- C1s cleaves C4 to C4a/b- C4 homologous to C3- C2 binds to C4b forming C4b2b- C3 convertase- C3 bind to C3b2b making C4b2b3b - C4 convertaseLectin: sugar binding prot- triggered by Ab absence- needs plasma mannose-binding lectin- ficolins (similar to C1q) bind lectin assoc serine proteases (sim to C1r/s) and cleave C2/4- then identical to classicalMAC: membrane attack complex- C5 convertase clips C5- C5 binds with C6/7/8/9 to form MAC- C9 pore and the rest the stalk- C5 converts C5 into C5a/b, but stays on cell surface- C7/8/9 bind in succession to C5b- C5b/6/7/8 and C9 form MAC

Question 325

Membrane attack complex - safeguards for self cells? opsonisation? chemo-attactrants?

Answer 325

Safeguards:- decay acceleration factor (DAF) which accelerates breakdown the C3bBb- CD59 compete MAC before attachmentOpsonisation:- C3b clipped by a serum prot to form iC3b- macrophages can bind to iC3bChemoattractants:- C3a/C5a recruit macro and neutrophils- anaphylatoxins

Question 326

Pathology defintion - understanding and provide basis?

Answer 326

The study of disease:- understanding how they develop and progress- provide basis for treatment selection

Question 327

Understanding disease - key words?

Answer 327

AetiologyPathogenesis Prognosis

Question 328

Aetiology defintion?

Answer 328

Cause of disease:| - genetic and environmental factors

Question 329

Pathogenesis defintion?

Answer 329

How an individual disease develops and progresses| Mechanisms of disease (inflamm, neoplasms and circulatory disorders)

Question 330

Types of basic pathological mechanisms (inflamm? Neoplasia? Circulatory disorder?)

Answer 330

Inflamm:- acute- chronicNeoplasis:- benign - malignantCirculatory disorders:- thrombosis- embolism- infarction

Question 331

Inflammation - acute vs chronic?

Answer 331

Acute:- neutrophils polymorph mediated- healing and repair - abscess formationChronic:- lymphocyte- macro- plasma cells

Question 332

Neoplasia - benign vs malignant?

Answer 332

No cancer| Cancer

Question 333

Diagnostic pathology - what gives them info? Can aid to give a?

Answer 333

Macroscipic, microscopic and molecular examination of tissue samples- biopsies Clinco-pathological correlation

Question 334

Professional phagocytes - types? function?

Answer 334

Types:- monocytes- macrophages- granulocytes- dendritic cellsFunction:- phagocytosis

Question 335

Phagocytosis - process?

Answer 335

Process:- engulfs the bacterium into a small vesicles called a phagosome - phagosome fuses with a lysozyme to form a lysosome - lysosome kills the bacterium- also release debris

Question 336

Macrophages - differentiate from? Differentiate into? Found in the? Travel to? Activation causes? 3 states of readiness?

Answer 336

From:- bone marrow stem cellsDifferentiate into:- monocytes then macrophages on the tissuesFound:- in the tissuesTravel:- into the capillaries and hang around waiting for pathogens Act:- chemicals released causing redness and swellingReadiness:- resting (low MHC 2 levels)- primed (higher MHC 2 levels)- APC (engulf pathogen)

Question 337

Neutrophils - most abundant? Name derivative? Profession phagocyte? Life span? Fucntion? Not APC? Acute inflammation (follow what?)

Answer 337

Most:- WBCName:- neutral pinkProfessional:- most importantLife span:- 5 daysFunction:- phagocytosis but not APCAcute inflamm:- migrate towards site of inflamm via BVs CIA interstitial fluid, following trail of chemokines via chemotaxis

Question 338

Natural killer cells - differentiate from? types of NK cells? Found where? Function and kill what? 2nd function (FasL?) Cell recognition? Activation of NK cells (given off by?) Cooperation (macrophages secretion? LPS? IL-12? IL-2?)

Answer 338

Diff:- stem cells in BMNK types:- have diff propertiesFound:- blood and spleenFunction:- kill tumour cells, virus infected cells bacteria, parasites and fungi- form a MAC (secrete perforin)2nd function:- FasL interact with Fas in target cell connectiong and causing the cell to dieCell recog:- activation and inhibition receptors - inhibotry receptor recognises MHC I, found on all human cells- activated of the target cell doesn’t express MHC IActivation:- IFNa/b givej off by cells under viral attack- secrete IFN-yCooperation:- LPS creates hyperact of Macro- macrophages produce IL-12 and TNF to increase IFN-y secretion to increase activation - NK produce IL-2 (GF) and Macro induce receptor on NK

Question 339

Inflammaptey response - defintion? Acute vs chronic?

Answer 339

Def:- battle that macrophages, neutrophils and other immune systems wage against invaderAcute:- initial response of body to harmful stimuliChronic:- progressive shift in type of cells at inflamm site characterised by simultaneous destruction and healing of tissue from inflamm process

Question 340

Adaptive immunity - defintion? recognition of antigens (B and T lymphocytes recog specific epitopes?)

Answer 340

Def:- specific and immunological memoryRecognition:- B and T lymphocytes - B cells recog free organic antigen via BCR (surface IgM)- T cells need to be shown antigen with MHC via TCR

Question 341

T lymphocytes - Name? Function? Types? CD4 (functions?) CD8?

Answer 341

Name:- thymus derived T cellFunction:- CD4 stimulate B cell to produce antibodies- CD8 are cytotoxic CD4:- activate other immune cells- B cell ab class switch- activation and growth of TcCD8:- exposed to infected cell release perforin forming a proe and release granzyme B and induce apoptosis

Question 342

Function of MHC I and II - found on? presents what (act which response)?

Answer 342

Found on:- MHC I; all nucleated cells- MHC II; all APCsPresent:- MHC I; present virally induced peptides to CD8 T cells and trigger cytotoxic response - MHC II; present Ag to CD4 T cells and activate macro and B cells

Question 343

T cell selection - basis? positive? negative selection? Clonal expansion process? T cell memory?

Answer 343

Basis:- must learn to not recognise self antigens Positive:- thymocyte undergoes TCR gene rearrangement - positive selection of receptors for MHC (CD3/4/8)- forming CD4 and CD8 Negative:- death of cells with high affinity for self antigens Process:- immature T cell binds to an APC forming CD4 abd CD8- CD4 can activate B cells or activate more macrophages Memory:- from fully differentiated T cells

Question 344

B cells and antibodies - cell type? production of? b cells express? Tolerance?

Answer 344

Type:- from BM and mature into plasma cellsProduction:- for abs production B cells:- express sIg on the B cellTolerance:- tolerise T cell than B cell because B cells can't produce abs without T cell help

Question 345

Antibody structure - 2 parts? light chain types? heavy chain (function? regions? 5 types of heavy?) flexibility?

Answer 345

2 parts:- ag binding region (Fab)- fc regionChains:- light; lambda and kappa- heavy; define Ig, constant region (same for all Ig class) and a variable region (differ between B)- gamma, delta, alpha, u and backwards 3Flexibility:- hinge region allows flexibility

Question 346

Antibody classes - IgM? IgG? IgA? IgE? IgD? - (function of each?)

Answer 346

IgM:- fixing complement and opsonisationIgG:- opsonisationIgA:- protect mucosal surface and resistant to stomach acidIgE:- defends against parasites causes anaphylactic shock and allergiesIgD:- naive B cell antigen recep

Question 347

Functions of abs - neutralisation? opsonisation? complement activation?

Answer 347

Neutralisation:- abs neutralise the biological effects of the antigen (stop antigen binding)Opsonisation:- chemically modified to have stronger interactions with cell surface receptors on phagocytes and NK cells (C3d bind to pathogen act B cell)

Question 348

Anaphylactic shock - cell type? express recep? allergic act? release of?

Answer 348

Cell:- mast cellExpress recep:- IgEAct:- inactive until an allergen binds to IgE- binding of 2 or more IgE required to act mast cell- clustering of the IgE causes a complex sequence of reactions (release of histamine and heparin)

Question 349

Immunological memory - secondary response features? why it occurs? memory B better?

Answer 349

2nd response:- rapid- larger and often qualitatively differentWhy:- each exposure causes an expansion in the clone of lymphocytes and differentiate to memory cellsB:- memory B cells produce abs but with higher affinity than naive and rapid

Question 350

Active and passive immunity definitions? subtypes of active and passive (natural and artificial?)

Answer 350

Active:- conferred by a host response to a pathogenPassive:- conferred by adoptive transfer of abs or T lymphocytes specific for the pathogenNatural active:- during infectionArtificial active:- injection or orally (long lasting immunity)Natural passive:- mother to childArtificial passive:- abs given for a fatal diseasePassive:- memory cells only temp

Question 351

Autoimmunity - definition? treatment? theories (clonal deletion? clonal anergy? idiotype network/)

Answer 351

Def:- triggered to attach the tissues of the hostTreat:- immunosuppressionClonal deletion:- self-reactive lymphoid cells destroyed during development of immune systemClonal anergy:- self-reactive T/B cells become inactivated in normal individuals Idiotype network:- network of bas capable of neutralizing self reactive abs naturally within the body

Question 352

Vaccinations - inactivated? acellular? attenuated? subunit? DNA? (definitions?)

Answer 352

Inactivated:- pathogen particle destroyed and can't divide but can be recognised and evoke immunityAcellular:- cellular material with antigenic partsAttenuated:- reducing pathogen virulence Subunit:- part of virusDNA:- injecting genetically engineered DNA

Question 353

Functions of the lymphatic system?

Answer 353

Drainage of tissuesAbsorption and transport of FAs and FatsImmunity

Question 354

Lymphatic vessels - lymph formation? movement of lymph (intrinsic and extrinsic)? external route drainage (organs?) intrinsic route drainage (organs?)

Answer 354

Form:- when interstitial fluid from the blood enters the initial lymphatic vessels Move:- moves along vessels by intrinsic contractions of lymphatic passages or extrinsic compression of vessels by external tissue forceExternal:- head, limbs and body cavity wallsInternal:- thorax, abdomen and pelvic cavities

Question 355

Oedema - definition? clinical signs?

Answer 355

CS:- abnormal accumulation of fluid in interstitium- severe pain- swelling

Question 356

Spleen - red pulp? white pulp? function? lymphoid follicles (content? germinal centres function? release in response?)

Answer 356

Red:- CT known as cords of BillrothWhite:- contain lymphocytesFunction:- filter blood of antigens, microorganisms and defective/old RBCsFollicle:- white pulp contains plasma cells, lymphocytes and lymphatic nodules called follicles- germinal centres are sites of lymphocyte production- releases macrophages in response to foreign antigen

Question 357

High endothelial venules - definition? found where? function? lymph nodes definition (source?

Answer 357

Def:- specialised post-cap venous swelling characterised by plump endo cellsFound:- all secondary lymphoid organs (except spleen)Function:- enable lymphocytes circulating in the blood to enter directly to a lymph node (addressins)Lymph:- consists of an outer cortical and inner medullary par- source of lymphocytes

Question 358

Peyer’s Patch - found? function? role mucosally?

Answer 358

Found:- lowest portion of SI and distal jejunum and ileumFunction:- facilitate generation of response within mucosaRole:- pathogens enter intestinal tract encounter immune cells

Question 359

Tonsils - definition? infection?

Answer 359

Def:- areas of lymphoid tissue in throat involved in defence from infection of upper resp tractInfect:- asymmetrical tonsils can indicate problems

Question 360

Lymphocyte trafficking - definition? cellular adhesion molecules of T cells?

Answer 360

Def:- process of lymphocytes getting into secondary lymphoid organsCellular:- L-selectin binds GlyCAM-1 on HEV of lymph- a4b7 binds MADCAM-1 on HEV Peyer’s patches and lymph nodes

Question 361

Primary lymphoid organs - function? examples?

Answer 361

Function:- places where blood cells are produced and receive their trainingExamples:- BM and thymus

Question 362

Thymus - description? content?

Answer 362

Description:- bi-lobed organ and site of T cell maturation- divided into outer cortex and inner medulla and contrian stromal thymic epith cells

Question 363

Lymphatic system and cancerous cells - spread? cancer of lymphatics? types of lymphatic cancers? Lymphangitis (what is it?)

Answer 363

Spread:- via the lymphatic system causing metastasisCancer:- lymphomaTypes:- thymus- multiple myeloma (BM)- leukemia (BM)- tonsillar- adenoidalLymphangitis:- infection of lymph vessel walls- acute pyogenic infection- inflammation

Question 364

Acute inflammation - definition? stimuli causing inflammation (physical? irritant? infection? immune? tissue necrosis?) Cardinal signs of inflamm?

Answer 364

Def:- immediate and early response to injury undergoing a series of protective changes occurring in living tissueStimuli:- physical such as heat and cold- irritant via chemical- infection via bacteria, virus or fungi- immune such as allergy- tissue necrosis via ischemiaSigns:- heat- redness- swelling- pain- loss of function

Question 365

Acute inflammation - pathogenesis (stimuli? changes in vessels? blood cells?) chemical mediators (complement function? kininis function? other examples? collective effect?)

Answer 365

Patho:- chemically initiated- changes in vessel radius and vessel wall permeability (flow and exudation)- movement of neutrophils from vessel to extravasc spaceMediators:- complement act MAC- kinins (vasoactive increase pain)- prostaglandins, arachidonic acid and leukotrienes?- platelet act factor- cytokines- vasodil, chemotaxis, increased permeability, neutrophil adhesion + itch and pain- acute phase proteins

Question 366

Acute inflammation - vascular changes (flow? permeability? endo cells?)

Answer 366

Flow:- transient vasoconstriction - arteriolar vasodilation- neutrophils (VIP)- blood flow slows losing laminar flow causing red cell aggregation and so neutrophils found near endoPermeability:- movement of plasma (transudate)- movement of protein-rich fluid (exudate)- thicker blood and stasis - gaps between cellsEndo cells:- contraction in response to histamine, bradykinin and leukotrienes - retraction in response to TNF and IL-1 (lasts longer)

Question 367

Acute inflammation - extravasation of leukocytes (margination and rolling -sticking?) (adhesion and transmigration - adh molecules? integrins? diapedesis? platelet adhesion mol? degrad of BM?) chemotaxis and activation (migration to injury? induces?)

Answer 367

Margination and rolling:- leukocyte accumulation at periphery- interact with endo- stick via E/L/P-selectin (upregulated by TNF and IL-1)Adhesion and transmigration:- ICAM and VCAM mol (induced by TNF and IL-1)- integrins act leukocytes with high affinity binding after conformational change- diapedesis via intercellular spaces- PECAM-1 (CD-31) (platelet adh)- degrad via collagenasesChemotaxis and activation:- exo/endo attractants- bacteria- complement system (C5a)- leukotriene B4 and IL-8

Question 368

Cyclooxygenase and inflammation - process?

Answer 368

1. Phospholipids converted to arachidonic acid via PLA2 (PLA2 activated y thrombin, complement, bradykinin and abs)2. Arachidonic acid converted to either leukotrienes by lipoxygenase or prostaglandins via cyclooxygenase3. Prostaglandins are converted to prostacyclin via prostacyclin synthase via endothelium or into thromboxane A2 via thromboxane A synthase via platelets

Question 369

Painkillers - NSAIDs (mechanism of action? action?) Paracetamol (MoA? action?) Opioids (examples? MoA? action?)Nerve block (example? MoA? action? use?)

Answer 369

MoA:- inhibit COX pathway- reduce prostaglandin level and inflammationParacetamol:- inhibit COX2, poor affinity at inflamm site, reduces PGE2- metabolite inhibits anadamide uptake (cannabinoid pathway)- blocks Na chsOpioids:- natural (morphine)- semisynth (oxycodone)- synth (fentanyl)- act via endog path but don't alter inflamm directlyNerve block:- lignocaine- Na ch blocker- prevents AP

Question 370

Neutrophils - functions (phagocytosis? degranulation? consequences?)

Answer 370

Phago;- recog antigen- move towards via chemotaxis- adhere to organism (opsonins)Degranulation:- posses oxidants (H202) and enzymes (proteases)Consequences:- neutrophils die after degranulation- progresses the inflammation

Question 371

Plasma proteins - examples and function?

Answer 371

Examples:- fibrinogen a coag factor forms fibrin and clots exudate (localises inflamm)- Ig specific to antigen (humoral)

Question 372

Resolution of acute inflamm - process (agent? epith? blood cells? vasc) benefits of acute inflamm (area? plasma prots? speed?) outcomes of acute inflammation (why?)

Answer 372

Process:- agent destroyed- macrophages phagocytose and leave- epith regenerate- inflamm exudate filters away- vasc return to normalBenefits:- rapid response- transient protection of area- agent destroyed- plasma prots localise process- resolve quicklyOutcomes:- resolve- abscess (excess exudate)- organisation (excess necrosis)- advance to chronic inflamm (agent remains)

Question 373

Chronic inflammation - definition? primary chronic inflammation (causes?)

Answer 373

Def:- inflammation of prolonged duration in which active, tissue destruction and attempts at repair are proceeding simultaneouslyPrimary:- resistance of agent to phagocytosis (TB) - endog (hair)/exog (prosthesis) materials- autoimmune (RA)- diseases of unknown aetiology (ulcerative colitis)- granulomatous diseases (Crohn’s)- acute progression (osteomyelitis)- recurrent acute episodes (chronic cholecystitis)

Question 374

Chronic inflammation histology - macroscopic and microscopic appearances

Answer 374

Macroscopic appearances:- chronic ulcers- chronic abscess cavity- thickening of wall of hollow viscus- granulomatous inflammation- fibrosisMicroscopic:- cellular infiltrate (lympho, plasma, macro and eosino)- multinucleated giant cells- prod of fibrous tissue- continued destruction

Question 375

Macrophages - migration? activation? cell size and secretion? action (fibrosis and tissue injury)?

Answer 375

Mig:- monocytes migrate into extravascular tissue in early acute inflammAct:- by IFN-y (from T cell), endotoxins and chemical mediatorsCell:- increased size and lysosomal enzyme releaseAction:- fibrosis (GF and angiogenesis)- tissue injury (proteases, coag factors and NO)

Question 376

Lymphocytes - T? B?Plasma cell - from? function?Eosinophils - mediated by? secrete? Mast - secrete and produce? neutrophil - type of cell?

Answer 376

T :- cell mediated immunity- act macrophagesB:- abs prodPlasma:- diff B- absEosinophil:- mediated by IgE and parasites- release TGF, VEGF and PDGFMast:- release histamine and produce arachidonic acid oxidationNeutrophils:- phagocyte

Question 377

Inflammatory cascade by activation of (factors)?

Answer 377

KininCoagulationComplementFibrinolytic systemLeukocyte mediatorsUric acid

Question 378

Granulomatous inflammation - what is it? characterised by? examples (infectious and noninfectious)? Granulomas - what are they? content? Immune granulomas - what is it? immune response process?

Answer 378

Granulomatous inflammation:What:- distinctive pattern of chronic inflammationCharacterised by:- focal accumulation of activated macrophages which often develop epith-like pattern- TB and syphilis (infectious)- RA, Crohn’s and sarcoidosis (non-infect)Granuloma:- large vesicular nuc, folded nuc mem, plentiful eosino granular cytoplasms and indistinct cell borders- more secretoryImmune granulomas:- insol particle induce cell mediated immune response- macro enguld, process and present to T- T lymph produce IL-2 act other T and IFN-y act macro

Question 379

Giant cell - what is it? formation? Foreign body - what is it? centre?Langhans’ giant cell - found? appearance (nuc)? cytoplasm type?

Answer 379

Giant cell:What:- form whe foreign particles are too large to be ingested by 1 macroForm:- fusion of macrophages (multi nuc)Foreign body:- too big to be digested by 1 macro- foreign material at centreLanghan's giant:- found in TB- peripheral nuc rim- eosinophilic cyto

Question 380

Oral manifestation of -sarcoidosis? Crohn’s? pyogenic granulomata?

Answer 380

Sarcoidosis - are multinodular painless ulcers of mucosa, labial mucosa and palateCrohn's:- angioedema- mucogingivitis- cheilitis- glossitis- aphthous ulcers- pyostomatitisPyogenic:- caused by irritation, trauma, hormones or poor hygiene- ulcerated and bleeds readily

Question 381

Organisation (healing and repair) - what occurs?

Answer 381

Organisation:- specialised tissue repair- mature fibrovasc CT- dead tissue removed by phago- granulation tissue contracts, accumulates collagenCausing remodelling and scar formation

Question 382

Products of granulation tissue - scar? fibrosis problem?

Answer 382

Scar:- fibrous tissueFibrosis:- can cause further diseaseOngoing process of chronic inflammation

Question 383

Wound healing - sequence of events? factors which influence wound healing (impairing and favouring?Callus formation process (osteo stim? new bone? remodel?)

Answer 383

Sequence:- injury, clot, acute inflamm, fibrin- granulation tissue growth (angiogen)- phago of fibrin- myofibroblasts move in and lay down Col- contraction of scar- re-epithImpairing:- age- diabetes- poor nutrition and cleanliness- location- abnormal cholesterol metaFavouring:- clean- nutrition- normal mechanismsCallus formation:- granulation tissue stims osteoblastic and osteoclastic- osteoblasts lay woven bone- remodelling as osteoclasts remove dead bone, woven replaced by lamellar and reforming cortical and trabecular bone

Question 384

Differences between acute and chronic?

Answer 384

Acute:- rapid- cardinal signs- neutrophils- vasc damage- more exudate- little fibrosisChronic:- slower and prolonged- low cardinal signs- lymphocytes- neovasc- less exudate- high fibrosis

Question 385

Definition of inflammation?

Answer 385

A localised, protective response to injury or infection, characterised by pain, heat, swelling, redness and loss of function and which is mediated primarily by cells present in the bloodstream

Question 386

Purpose of inflammation?

Answer 386

Protection| Increase blood flow to site allowing increased defence cells to site

Question 387

Substances secreted during inflammation - cytokines (definition and examples)? prostanoids (definitions and examples)? NO? bradykinin? histamine?

Answer 387

Cytokines:- released from cells assoc with immune system that exhibit autocrine/paracrine activity (IL, chemokines, tumour necrosis factor)Prostanoids:- substances produced via action of COX (prostaglandins, prostacyclins and TXA2)NOBradykininHistamine

Question 388

Acute inflammation - primary and secondary response overview (secretion type?)

Answer 388

Primary response:- paracrine- assoc with response of local BVsSecondary response- autocrine- assoc with intracell response of cells involved in inflamm response

Question 389

Primary inflammatory response - primary role? cytokines? cell secretion? actions (vasodil? permeability? cascade? adhesion?)

Answer 389

Primary role:- specific, local vascular response to IL-1 and TNFa released from active neutrophils and macrophagesActions:- vasodilation of precapillary arterioles- increased permeability of post-cap venule (clotting, fibrinolytic, kinin and complement cascades activated)- Increased cell adhesion to endothelial wall

Question 390

Secondary inflammatory response - primary role? cytokines? signalling pathways? NF-kB inhibition?

Answer 390

Primary role:- downstream, molecular effects of TNFa and IL-1 responseSignalling pathways:- stimulated to activation of transcription factor NF-kB(COX2 and iNOS)NF-kB:- inhibited by IkB- on IL-1 and TNFa binding releases IkB- allowing NF-kB to be transcribed

Question 391

Cyclooxygenase pathway for inflammation - phospholipids? arachidonic acid? leukotrienes? prostaglandins? prostacyclin? TXA2?

Answer 391

Pathway:- phospholipid converted into arachidonic acid by PLA2 (act by bradykinin and thrombin)- arachidonic acid converted to leukotrienes by lipoxygenase- arachidonic acid converted to prostaglandins by COX- prostaglandins converted into prostacyclins by prostacyclin synthase (secreted by endothelium)- prostaglandin can also be converted into thromboxane A2 via thromboxane a synthase (from platelets)

Question 392

COX isoforms - COX1? COX2 induced by? found where? COX3? COX2 products causing inflammation?

Answer 392

COX1:- constitutiveCOX2:- inducible- induced by IL-1 and TNFaCOX3:- paracetamol targetCOX2 products:- prostanoids (PG and TXA2)- GPCR- pro-inflammatory (vasodil, hyperalgesia and reduced platelet aggregation)- directly on precapillary arteriole, post-cap venule and indirectly on C fibres

Question 393

Process of fever - stimulus? pathway?

Answer 393

Stimulus:- toxins released by cateria activate macrophages (IL-1)Pathway:- IL-1 activates COX2 converting arachidonic acid forming PGE2 causing a reset on the body thermostat

Question 394

Inhibition of COX - glucocorticoids (functions? endogenous and synthetic forms? binding? PLA2?

Answer 394

Glucocorticoids:- regulate glucose meta and potent anti-inflamm- endog: cortisol/hydrocortisone and prednisolone- synthetic: dexamethasone and betamethasoneBinding:- intracellular receptor change gene expression- inhibit NF-kB transcription- block IL-1 and TNFa codingPLA2:- activate macrophages to release more annexin which inhibits PLA2

Question 395

NSAIDs - function? side effects?

Answer 395

Function:- inhibit COX directly- inhibit prostaglandin synthesisSide:- anti-pyrogenic

Question 396

iNOS and NO - NF-kB? expressed by? function? treatment?

Answer 396

NF-kB:- increased expressionExpressed:- by cells in response to inflammatory responseFunction:- vasodilation- increased vasc permeability- increased production pro-inflamm prostanoids- inhib of platelet aggregation- cytotoxicTreatment:- iNOS inhibitors

Question 397

Bradykinin - function? isoforms? byproduct of? pathway?

Answer 397

Function:- potent pain producing agent (sensities nociceptive fibres)Isoforms:- B1 (inducible) and B2 (constitutive)Byproduct:- of clotting cascadePathway:- Factor XIIa converts prekallikrein into kallikrein- HMW-kininogen converted by kallikrein into bradykinin

Question 398

Histamine - stored in? stimulated release? different isoforms and functions?

Answer 398

Stored in;- found in granules of mast and basophilsStimulated:- by inflammatory stimuli and complement proteins- released by exocytosisIsoforms:- H1 contract SM but relax vasc SM causing vasodil and itching- H2: gastric acid secretion- H3: plasticity in CNS

Question 399

Why does inflammation occur - what’s it trying to achieve?

Answer 399

Process:- increased BF and vessel perm- increases defence cells- increased phago potential and lymphocytic activity- eliminating the pathogen

Question 400

Outcomes of inflammation - successful and unsuccessful?

Answer 400

Successful:- removal of pathogen, heal/repair and return to healthUnsuccessful:- chronic inflamm