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71 Cards in this Set
- Front
- Back
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What does a bronchodilator do |
Dilate bronchi and bronchules to be able to breathe air more easilywjat |
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What are the characteristics of asthma (5) |
Imflammatory reslonse Hyperresposiveness of smooth muscle to substances that cause contraction of smooth muscel such as acetylcholine, histamine and PAF Hyporesponsiveness of smooth muscle to substances that make the smooth muscle relax such as adrenaline Neuronal imbalance Hyperplasia(smooth muscle cell division) and hypertrophy |
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In an inflammatory response innasthma whats inflammatory cell is predominantly involved |
Eosinophils- substances that cause tissue damage to the lung, can be bronchioconstrictive agents so hard to breathe |
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What are some of the structural changes in asthma |
Variety of gross morphological changes like epithelial damage, mucosal oedema, increased intraluminal secretion, basement membrane thickening, smooth muscle hypertrophy and hyperplasia and inflammation |
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What are the current 3 proposals for alteration in smooth muscle excitability |
Abnormalities in conduction properties Alteration in calcium control and contraction/ relaxation Proliferative response increases |
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Morphology of bronchital asthma |
Lungs are over distended due to over-inflation Small areas of atelectasis can be seen Occlusion of bronchi and bronchioles by thick tenacious mucus plug- most striking finding |
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Conduction properties in the smooth muscle healthy compared to asthma |
Smooth muscle is considered multi unit type i.e each cell is innervated and cell to cell communication is poor, e.g few gap junctions through which electrical signals can pass through with low resistance In asthmatics the cells become single in nature and increased occurrence of gap junctions Healthy 1nerve- 1muscle cell Asthmatic- 1 nerve-up to 20 muscle cells |
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Calcium enters the cell through what two mechanisms |
Via voltage and receptor operated calcium channels From sarcoplasmic reticulum stores |
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Explain the pathway to which calcium to come out and cause contraction (1) |
PLC connected to a GPCR allows IP3 to be formed, because IP3 is soluble in water it moves into the cytoplams and binds to a receptor and allows calcium to come out Calcium binds to CAM- only when calcium binds to CAM it binds to MLCK and activates the enzyme, THis looks for myosin light chain and puts a phosphate covalently and allows it to bind to actin Actin and myosin slide over eachother and cause contraction |
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How is this pathway different in asthmatics (2) and how to treat it |
More muscarinic receptors increase Process is activated many more times More PLC activated maybe Strength if signal increases Can block the receptor to treat respiratory disease/ block MLCK |
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What is the proliferative response that occurs in asthmatics |
Occurs in chronic asthmatics. Growth factors elicit mitogenesis and cell proliferation, this involved a complex signalling pathway involving growth factors Bronchoconstrictors can activate this pathway at several points including raf-1 and MAP kinase |
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MAP kinase is regulated through what |
Growth factors |
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explain inflammatory response late phase |
Inflammatory cells attach to epithelium and squeeze through the lining into the airway tubule, release of substances such as O2, major basic protein and PAF have a potent killing effect upon epithelial cells and extensive damage to epithelial lining is achieved |
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Whats the cells involved in the inflammatory response (1) |
Mast cells Neutrophils and basophils Macrophage Eosinophils |
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What do these cells that are involved in the immune response do (2) |
Mast cells:- respond to allergen and IgE by releasing histamine, TNF-α, LTD4 and various interleukins such as IL-1 Neutrophils+basophils- less of a role in asthma more COPD Macrophages:- release prostanoids, cytokines and leukotrienes Eosinophils:- release PAF, TNFα CSF, GMSCF AND MPB |
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(3) what does eosinophils releasing CSF AND GMCSF do |
CSF causes haemopoetic stem cells to differentiate into progenitor cells GMCSF- causes progenitor cell to differentiate into eosinophils -amplification of eosinophils |
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Explain diapedesis |
Release of IL-1 and TNFα is believed to increase the expression of ICAM/ELAM AND VCAM proteins (adhesion molecules) in endothelial cell plasma membrane These proteins lock onto adhesion molecules expressed in the eosinophil membraneX in this way the mast cell, eosinophil and macrophage can attach to the endothelium where they can squeeze in between endothelial cells |
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explain how different selectins are expressed at different times |
P-selectin appears quickly after cell sees IL-1. E-selectin- gene is already expressed and lots of mRNA for the protein but to change it into the protein is not ongoing in a healthy patient so to get the mRNA into the protein after seeing Il-1 it takes a but longer ICAM AND VCAM take 12 hours to peak- no mRNA is present but the genes are there, the genes are turned on by IL-1 and takes 12 hours to make the mRNA then the protein |
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Whats does each adhesion molecule bind to |
ELAM-1 binds sialyl lewis x expressrd more on neutrophils than eosinophils ICAM binds to VLA-4 on eosinophils ELAM on neutrophils- COPD VCAM AND ICAM- eosinophils in asthma |
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What are the major adhesion molecules |
Integrins -composed of α and β subunits, CD11/CD18 complex expressed upon leukocytes Immunoglobulin family i.e ICAM expressed on endothelial cells Selectins |
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Explain autonomic imbalance in asthma |
Parasympathetic nervous system is more stimulated Reduces adrenergic drive and reduces β adrenoreceptors and smooth muscle- β-adrenoceptors cause bronchodilaton To treat an asthmatic with a beta adrenoceptor receptor antagonist could kill patient making asthma a lot worse You want a b adrenoceptor agonist not antagonist |
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What does MAP KINASE drive |
Protein translation DNA synthesis Inflammatory mediators |
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The cholinergic nerve has what |
A presynaptic neuron going to the central nervous system Ach is released from neuron causing muscle to contract |
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What does adrenergic nerve do |
Inhibits cholinergic nerve- adrenaline is released and block cholinergic drive |
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Afferent receptors (c finres) respond to substances such as what |
Histamine, bradykinin, prostaglandins to cause a reflex bronchoconstriction |
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Defects in cholinergic innervation 4 |
Increased vagal tone Reflex bronchoconstriction Increased acetylcholine release: incrrased neurotransmission facilitated by tachkinins thromboxane and serotonin Increased post synaptic muscarinic receptor function |
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What can influence adrenergic control |
No evidence to suggest theres any defects in adrenergic neurotransmission But it is possible that inflammatory mediators such as histamine can modulate adrenergic control Post synaptic β-adrenoceptors may be dysfucntioned as could coupling mechanisms |
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How could NANC transmission be altered (1) |
Defective NANC Inhibitory nerve i.e VIPergic nerves which represent the only neuronal innervation that elicits bronchodilation Increased NANC excitatory nerves. Release of substance P and neurokinins from C-fibre sensory nerve endings in response to prostaglandins and bradykinin released as a consequence of inflammation |
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What could this then cause In NANC transmission (2) |
Reflex bronchoconstriction, hyperaemia, microvascular leakage and hypersecretion(give rise to mucus plug), local reflexes may amplify inflammation |
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Explain the early phase on inflammatory response |
Where inflammatory cells are recruited to sites in pulmonary arteries and enter into interstitial fluid and smooth muscle by squeezing through the endothelium- called diapedesis |
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MAP kinase is regulated through what |
Growth factors |
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explain inflammatory response late phase |
Inflammatory cells attach to epithelium and squeeze through the lining into the airway tubule, release of substances such as O2, major basic protein and PAF have a potent killing effect upon epithelial cells and extensive damage to epithelial lining is achieved |
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Whats the cells involved in the inflammatory response (1) |
Mast cells Neutrophils and basophils Macrophage Eosinophils |
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What do these cells that are involved in the immune response do (2) |
Mast cells:- respond to allergen and IgE by releasing histamine, TNF-α, LTD4 and various interleukins such as IL-1 Neutrophils+basophils- less of a role in asthma more COPD Macrophages:- release prostanoids, cytokines and leukotrienes Eosinophils:- release PAF, TNFα CSF, GMSCF AND MPB |
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(3) what does eosinophils releasing CSF AND GMCSF do |
CSF causes haemopoetic stem cells to differentiate into progenitor cells GMCSF- causes progenitor cell to differentiate into eosinophils -amplification of eosinophils |
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|
Explain diapedesis |
Release of IL-1 and TNFα is believed to increase the expression of ICAM/ELAM AND VCAM proteins (adhesion molecules) in endothelial cell plasma membrane These proteins lock onto adhesion molecules expressed in the eosinophil membraneX in this way the mast cell, eosinophil and macrophage can attach to the endothelium where they can squeeze in between endothelial cells |
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|
explain how different selectins are expressed at different times |
P-selectin appears quickly after cell sees IL-1 E-selectin- gene is already expressed and lots of mRNA for the protein but to change it into the protein is not ongoing in a healthy patient so to get the mRNA into the protein after seeing Il-1 it takes a but longer ICAM AND VCAM take 12 hours to peak- no mRNA is present but the genes are there, the genes are turned on by IL-1 and takes 12 hours to make the mRNA then the protein |
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Whats does each adhesion molecule bind to |
ELAM-1 binds sialyl lewis x expressrd more on neutrophils than eosinophils ICAM binds to VLA-4 on eosinophils ELAM on neutrophils- COPD VCAM AND ICAM- eosinophils in asthma |
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|
What are the major adhesion molecules |
Integrins -composed of α and β subunits, CD11/CD18 complex expressed upon leukocytes Immunoglobulin family i.e ICAM expressed on endothelial cells Selectins |
|
|
Explain autonomic imbalance in asthma |
Parasympathetic nervous system is more stimulated Reduces adrenergic drive and reduces β adrenoreceptors and smooth muscle- β-adrenoceptors cause bronchodilaton To treat an asthmatic with a beta adrenoceptor receptor antagonist could kill patient making asthma a lot worse You want a b adrenoceptor agonist not antagonist |
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What does IL-4 do |
Turns on subset of genes that make Th2 cells |
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What does MAP KINASE drive |
Protein translation DNA synthesis Inflammatory mediators |
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The cholinergic nerve has what |
A presynaptic neuron going to the central nervous system Ach is released from neuron causing muscle to contract |
|
|
What does adrenergic nerve do |
Inhibits cholinergic nerve- adrenaline is released and block cholinergic drive |
|
|
Afferent receptors (c fibres) respond to substances such as what |
Histamine, bradykinin, prostaglandins to cause a reflex bronchoconstriction |
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|
Defects in cholinergic innervation 4 |
Increased vagal tone Reflex bronchoconstriction Increased acetylcholine release: incrrased neurotransmission facilitated by tachkinins thrombocanr and serotonin Increased post synaptic muscarinic receptor function |
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|
What can influence adrenergic control |
No evidence to suggest theres any defects in adrenergic neurotransmission But it is possible that inflammatory mediators such as histamine can modulate adrenergic control Post synaptic β-adrenoceptors may be dysfucntioned as could coupling mechanisms |
|
|
How could NANC transmission be altered (1) |
Defective NANC Inhibitory nerve i.e VIPergic nerves which represent the only neuronal innervation that elicits bronchodilation Increased NANC excitatory nerves. Release of substance P and neurokinins from C-fibre sensory nerve endings in response to prostaglandins and bradykinin released as a consequence of inflammation |
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|
What could this then cause In NANC transmission (2) |
Reflex bronchoconstriction, hyperaemia, microvascular leakage and hypersecretion(give rise to mucus plug), local reflexes may amplify inflammation |
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|
Explain the early phase on inflammatory response |
Where inflammatory cells are recruited to sites in pulmonary arteries and enter into interstitial fluid and smooth muscle by squeezing through the endothelium- called diapedesis |
|
|
MAP kinase is regulated through what |
Growth factors |
|
|
explain inflammatory response late phase |
Inflammatory cells attach to epithelium and squeeze through the lining into the airway tubule, release of substances such as O2, major basic protein and PAF have a potent killing effect upon epithelial cells and extensive damage to epithelial lining is achieved |
|
|
Whats the cells involved in the inflammatory response (1) |
Mast cells Neutrophils and basophils Macrophage Eosinophils |
|
|
What do these cells that are involved in the immune response do (2) |
Mast cells:- respond to allergen and IgE by releasing histamine, TNF-α, LTD4 and various interleukins such as IL-1 Neutrophils+basophils- less of a role in asthma more COPD Macrophages:- release prostanoids, cytokines and leukotrienes Eosinophils:- release PAF, TNFα CSF, GMSCF AND MPB |
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|
(3) what does eosinophils releasing CSF AND GMCSF do |
CSF causes haemopoetic stem cells to differentiate into progenitor cells GMCSF- causes progenitor cell to differentiate into eosinophils -amplification of eosinophils |
|
|
Explain diapedesis |
Release of IL-1 and TNFα is believed to increase the expression of ICAM/ELAM AND VCAM proteins (adhesion molecules) in endothelial cell plasma membrane These proteins lock onto adhesion molecules expressed in the eosinophil membraneX in this way the mast cell, eosinophil and macrophage can attach to the endothelium where they can squeeze in between endothelial cells |
|
|
explain how different selectins are expressed at different times |
P-selectin appears quickly after cell sees IL-1 E-selectin- gene is already expressed and lots of mRNA for the protein but to change it into the protein is not ongoing in a healthy patient so to get the mRNA into the protein after seeing Il-1 it takes a but longer ICAM AND VCAM take 12 hours to peak- no mRNA is present but the genes are there, the genes are turned on by IL-1 and takes 12 hours to make the mRNA then the protein |
|
|
Whats does each adhesion molecule bind to |
ELAM-1 binds sialyl lewis x expressrd more on neutrophils than eosinophils ICAM binds to VLA-4 on eosinophils ELAM on neutrophils- COPD VCAM AND ICAM- eosinophils in asthma |
|
|
What are the major adhesion molecules |
Integrins -composed of α and β subunits, CD11/CD18 complex expressed upon leukocytes Immunoglobulin family i.e ICAM expressed on endothelial cells Selectins |
|
|
Explain autonomic imbalance in asthma |
Parasympathetic nervous system is more stimulated Reduces adrenergic drive and reduces β adrenoreceptors and smooth muscle- β-adrenoceptors cause bronchodilaton To treat an asthmatic with a beta adrenoceptor receptor antagonist could kill patient making asthma a lot worse You want a b adrenoceptor agonist not antagonist |
|
|
What does IL-4 do |
Turns on subset of genes that make Th2 cells |
|
|
What does MAP KINASE drive |
Protein translation DNA synthesis Inflammatory mediators |
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il-5 is involved in recruitment if what |
Eosinophils |
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The cholinergic nerve has what |
A presynaptic neuron going to the central nervous system Ach is released from neuron causing muscle to contract |
|
|
What does adrenergic nerve do |
Inhibits cholinergic nerve- adrenaline is released and block cholinergic drive |
|
|
Afferent receptors (c finres) respond to substances such as what |
Histamine, bradykinin, prostaglandins to cause a reflex bronchoconstriction |
|
|
Defects in cholinergic innervation 4 |
Increased vagal tone Reflex bronchoconstriction Increased acetylcholine release: incrrased neurotransmission facilitated by tachkinins thrombocanr and serotonin Increased post synaptic muscarinic receptor function |
|
|
What can influence adrenergic control |
No evidence to suggest theres any defects in adrenergic neurotransmission But it is possible that inflammatory mediators such as histamine can modulate adrenergic control Post synaptic β-adrenoceptors may be dysfucntioned as could coupling mechanisms |
|
|
How could NANC transmission be altered (1) |
Defective NANC Inhibitory nerve i.e VIPergic nerves which represent the only neuronal innervation that elicits bronchodilation Increased NANC excitatory nerves. Release of substance P and neurokinins from C-fibre sensory nerve endings in response to prostaglandins and bradykinin released as a consequence of inflammation |
|
|
What could this then cause In NANC transmission (2) |
Reflex bronchoconstriction, hyperaemia, microvascular leakage and hypersecretion(give rise to mucus plug), local reflexes may amplify inflammation |
|
|
Explain the early phase on inflammatory response |
Where inflammatory cells are recruited to sites in pulmonary arteries and enter into interstitial fluid and smooth muscle by squeezing through the endothelium- called diapedesis |
