FOM Mechs Flashcards
haemostasis
1.Vascular spasm to reduce blood flow/vasoconstriction
2.Platelet plug formation via adhesion of platelets to temporarily seal the injury.
3.Activation of the coagulation cascade (intrinsic and extrinsic pathways) leading to fibrin clot formation (fibrinogen converted to fibrin)
4.Clot retraction and tissue repair to heal the vessel.
5.Healthy tissue release messengers for Fibrinolysis to remove the clot once it is no longer needed, preventing excess bleeding or unnecessary clotting (homeostasis)
haematoposeis
-low RBC count
-hypoxia
-hypoxia detected by kidneys
-kidneys release erythropoietin
-this stimulates erythropoiesis
-increasing RBC count
-oxygen levels increase
Describe how the membrane becomes depolarised and repolarised in cardiac conduction
-resting membrane at -70 m/v
-slow influx of Na+ depolarises membrane
-T-type Ca2+ transient channels open and membrane becomes more depolarised
-then Ca2+ L-type channels open and membrane becomes more depolarised
-threshold reached, action potential fired
-K+ channels open, efflux of K+ initiates hyper polarisation
how does the autonomic NS effect heart beat frequency
asympathetic (vagal) stimulation increases the K+ efflux and causes hyperpolarisation and slows the depolarisation
-decreased vagal influence, Sympathetic stimulation increases the Ca2+ influx and causes faster depolarisation
Outline what happens in diastole
Isovolumetric relaxation (higher pressure in aorta than ventrciles)
Rapid inflow into ventricles
Diastasis (reduced inflow into the ventricles)
Atrial contraction (100% full)
(4 phases)
Outline what happens in systole
Isovolumetric contraction
Rapid ventricular ejection
Reduced ventricular ejection
(3 phases)
describe pressure changes in cardiac cycle
1.atrial pressure increases as systole is occurring, contraction causes pressure increase
2.AV valves open, blood flow into ventricles, increasing ventricular pressure
3.Ventricles contract, increasing pressure
4.Ventricle pressure>Atrial pressure so AV valves close
5.Ventricle pressure>Aortic pressure so SL valves open
6.ventricle pressure drops as blood leaves ventricle
7.Aortic pressure>Ventricular pressure, SL valves close
8.Ventricular pressure continues to drop until it goes below atrial pressure, left atrium refills (bc AV valves open) and cycle repeats
describe sympathetic innervtion of heart
-To increase HR and contractility of the myocardium: cardioacceleratory centre of medulla sends out messages via the sympathetic nerves through the paravertebral ganglion.
-These nerve fibres innervate the SA,AV node and myocardium. -This causes stimulation of adrenal medulla resulting in release of adrenaline and noradrenaline,
-these hormones bind to B1 receptors and cause depolarisation of the nodal cells (threshold is reached) and signals are sent faster, increasing HR and atrial myocardium contractility.
outline baroreceptor reflex
1.Change in blood pressure detected by baroreceptors in aortic arch and carotid sinus
2.this sensory (afferent) message is sent to cardioregulatory centres of the medulla (AP sent out faster or slower depending) via afferent cranial nerves (9,10)
3.Cardioregulatory centres send out an efferent message that triggers the sympathetic or parasympathetic NS
4. Changes in CO (SV and HR) and constriction/dilation of blood vessels
5.Increase/decrease in BP
describe parasympathetic innervation of heart
-Parasympathetic messages are sent via vagus nerve from dorsal root ganglion to the SA,AV node only (mostly impacts HR)
-Ach is released, which forces efflux of K+, causing hyperpolarisation
-therefore making it harder for HR to increase
gastric mixing
-regulated by smooth muscle in walls of stomach
-pacemaker cells generate slow wave potentials
-slow wave potentials set the basic electrical rhythm of the heart
-muscles in wall contract due to slow wave potentials
-these contractions allow for gastric mixing, which in conjunction with gastric juices, which include hydrochloric acid, pepsin, and mucus, mix with the food to form a semi-liquid substance called chyme. The acid helps break down food particles, and pepsin begins the digestion of proteins.
gastric filling
-eating triggers the stomach to relax and expands to accommodate the incoming food. This is facilitated by the vagus nerve through a process known as receptive relaxation.
- it also triggers the relaxation of folds within the mucosa (gastric Rugae) in a process called receptive relaxation
gastric emptying
-process in which food leaves stomach into small intestine
-regulated by rate at which pyloric sphincter opens
-gastric emptying is influenced by size of meal, presence of nutrients in small intestine, neural and hormonal signals form gut
- The rate of gastric emptying depends on the composition of the chyme. Liquids empty faster than solids, and carbohydrates empty faster than proteins and fats. Fats slow gastric emptying the most due to their longer digestion time and hormonal feedback mechanisms (e.g., release of cholecystokinin).
-Gastric emptying is controlled by neural signals from the enteric nervous system and hormonal signals from the small intestine. The presence of fatty, hypertonic, or acidic chyme in the duodenum triggers the release of hormones such as cholecystokinin, secretin, and gastric inhibitory peptide, which slow gastric emptying.
Outline steps of digestion in duodenum
1.fat and protein products in duodenal lumen
2.CCK released from duodenal mucosa
3.CCK is carried by blood into pancreatic acinar cells
4.secretion of pancreatic digestive enzymes into duodenal lumen
outline steps of neutralisation in duodenum
1.acid in duodenal lumen
2.secretin released from duodenal mucosa
3.secretin is carried by blood to pancreatic duct cells
4.pancreatic duct sells secrete NaHCO3- solution into duodenal lumen
mechanism of a cough
- Irritant in the respiratory tract
- Detected by mechanoreceptors
- These send afferent message to the medulla and pons via the vagus nerve
- Integrate this information and coordinate a coughing reflex
- Afferent motor messages sent to respiratory muscles, causing abdomen to contract and the internal intercostals to contract
mechanism of a fever
- Infection/pathogen
- Endogenous pyrogens released by macrophages and neutrophil
- IL1 + IL6 + TNF alpha
- Travel through bloodstream to hypothalamus
- Hypothalamus releases prostoglandens
- Increases set temperature of the body
- This thermo up regulation is achieved through shivering, vasoconstriction
- Increased body temp provides hostile environment to pathogen and increases WBC activity
- Endogenous pyrogens released by macrophages and neutrophil
Hering breur reflex
- -when lungs become overstretched stretch receptors in the bronchi and bronchioles trasnmit signals through the vagus nerve to DRG
- -switching off inspiratory signals and preventing further inspiration/prelonging expiration
- -also increases RR
- -serves as a protective reflex against over inflation of lungs
erection + orgasm
-sexual stimulation
-parasympathetic neuron’s release nitric oxide, this causes dilation of the arteries supplying the penis, thereby increasing blood flow to penis
-increasing pressure of arterial blood entering vascular spaces of erectile tissue compresses the veins of the penis, reducing flow of venous blood away from the penis
-follwoing orgasm sympathetic nerves contract the central artery of the penis and contract smooth muscle around the erectile tissues, which expels blood away from penis
Cell-mediated immunity
1.APC’s ingest pathogens and present them on cell via MHC
2.naive T cells recognise MHC via TCR’s and co-stimulatory signals (become activated)
3.T cell undergoes clonal expansion
4.T cells differentiate into Tc cells, Th cells, Treg cells
5.effector T cells migrate to site of infection via chemotaxis guided by chemokine
6.Tc cells recognise and bind to infected cells that display antigen on MHC I
7.Tc cells release cytotoxic chemical eg perforins that lead to apoptosis of infected cell
8.Th cells release cytokines to amplify immune response, attract macrophages, activate B cells
9.some T cells divide into T memory cells for long term immunity
10. Tregs suppress excessive immune response, prevent autoimmunity and maintain homeostasis