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97 Cards in this Set
- Front
- Back
What is classed as hypertension?
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- 140/90mmHg
- 30+% of adults but age-related |
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What are the Two classes?
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- 98% Primary - Essential
- 2% Secondary - Adrenal Gland Tumours / Kidney disease / Renal artery stenosis / Genetic Disorders |
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Role of smooth muscle cells in blood vessels?
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Control vascular diameter
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Role of endothelial cells in blood vessels?
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Regulate smooth muscle cells in reponse to blood borne factors / angiogenesis / inhibit thrombosis
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What % of all human mortality is due to disruption of vascular structure & function?
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40%
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How are blood vessel smooth muscle cells regulated?
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- ANS
- Hormones / Local Released - Rhythmic contractions by pacemaker cells in GI |
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What layer of a typical muscular artery are vessels, nerves, collagen and fibroblasts found in?
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Tunica Adventitia
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What are the three layers of a typical muscular artery wall?
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Inner to Outer
- Tunica Intima - Tunica Media - Tunica Adventitia |
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Which layer of the wall are smooth muscle cells found in?
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Tunica Media
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What makes up the wall of a capillary?
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- Monolayer of endothelial
- Basal Lamina - Pericyte - No innervation |
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What makes up the layers of a vein?
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- Thin tunic media (sparse smooth muscle)
- Well Supplied with sympathetic nerves |
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What name is given to the response where pressure effects vascular tone?
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Myogenic
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Similarities between smooth & striated muscle?
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- Ca2+ triggers contraction
- Contraction by X Bridge cycling |
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Differences between smooth & striated muscle? (Answers in format: In smooth muscle . . .)
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- No troponin - regulation by myosin
- Smooth muscle shortens more - X Bridge turnover Slower - ATP consumption smaller - Contraction graded no twitch - Contraction can be stimulated by depolarisation |
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Mechanism of Myosin - Actin Interaction?
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- Myosin light chain kinase + Calmodulin
- Active Complex phosphorylates myosin which can then enter X Bridge cycle - Myosin phosphatase dephosphorylates myosin |
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What effects formation of active phosphorylating complex in smooth muscle?
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[Ca2+]
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What are the Ca2+ sources in smooth muscle?
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- Sarcoplasmic Reticulum (IP3)
- Voltage-gated Ca2+ channels (membrane depolarisation) - Na+ / Ca2+ receptor-gated channels (DAG) |
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What does EDRF stand for & What is it released by?
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- Endothelium Derived Relaxation Factor
- Released by bradykinin, ATP, Histamine, H+, CO2, Blood flow |
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What is the action of Prostacyclin & Where is it released?
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- Inhibits platelet aggregation
- Released from endothelium |
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What is the action of Endothelin & Where is it released?
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- Vasoconstrictor
- Released from endothelium |
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Mechanism of Vasodilating substances?
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- Binds to receptor & [Ca2+] increases
- Increases eNOS production - eNOS (L-arginine-->NO) - NO increases cGMP in smooth muscle decreasing [Ca2+] and causing relaxation |
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Mechanism of Vasoconstricting substances?
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- Binds to receptor
- Stimulates endothelin --> smooth muscle cell causing contraction |
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What does PDE do?
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- Increased cGMP causes K+ out of cell depolarising the membrane
- Also causes Ca2+ into Sarcoplasmic Reticulum and also out of the cell - PDE (cGMP--->GMP) |
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How does sildenafil cause relaxation?
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Blocks PDE5
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What is endothelium-derived hyperpolarisation?
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- Vasodilator binds to receptor increasing intra [Ca2+]
- K+ channels open and membrane hyperpolarises - Spreads through gap junction and decreases intra [Ca2+] causing relaxation |
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What is oxidative stress and which species contribute to the effect?
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- Overproduction of reactive oxygen species
- O2- radical Superoxide - H2O2 Hydrogen Peroxide - O2- reacts with NO o produce perioxynitrite which prevents NO mediated vasodilation |
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What other line of drugs reduce oxidative stress?
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Statins
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Agonists which increase cAMP?
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- Adrenaline on Beta Receptors
- Adenosine - Prostacyclin - Stimulate adenylate cyclase |
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What is Metabolic Hyperaemia?
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- Increased metabolism during exercise enhances production of arteriole vasodilation (K+ H+ CO2 Lactic Acid)
- Vasodilation local and Blood Flow proportional to metabolic rate |
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What is Reactive Hyperaemia?
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- Local blood flow cut off metabolites accumulate and cause vasodilation
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What makes the S1 sound?
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- Initiation of V systole
- LUB |
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What makes the S2 sound?
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- Closure of semilunar valves
- DUP |
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What makes the S3 sound?
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- Opening of AV valves
- Rapid refilling |
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What make the S4 sound?
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- Atrial Systole
- Rarely heard except when EDP Raised |
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What rhythm can develop from high EDP?
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S3S4 Gallop rhythm
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What receptors contribute to sympathetic stimulation of the heart?
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β1
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What receptors contribute to parasympathetic stimulation of the heart?
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Muscarinic
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Effect of autonomic regulation of CV system?
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- SNS increases heart rate and contractility
- PNS decreases heart rate |
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What receptors contribute to sympathetic stimulation of the vasculature?
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α1 (can raise TPR)
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What receptors contribute to parasympathetic stimulation of the vasculature?
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Muscarinic & NANC (non-adrenergic, non-cholinergic neurotransmission e.g. NO)
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What effect do β2 mediate?
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Vasodilation in skeletal muscle
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Which receptors does NA released by nerves affect?
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α1 & β1
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Which receptors does circulating adrenaline affect?
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α1 & β1 & β2
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Effects of A on heart & vasculature?
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- Increases rate / Contractility / Cardiac Output
- Constriction in Most arteries / Veins - Vasodilation in Muscle / Coronary / Liver Circulations |
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Where is Ang II mainly Produced?
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- Present on endothelial cell surface
- Major site of production = lung (enormous endothelium) |
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What is the action of ADH / Vasopressin?
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- Decreased water excretion
- Vasoconstriction |
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What are classed as Prostanoids?
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- Prostaglandins & Thromboxanes
- Vasodilators / Vasoconstrictors / Regulate Platelet Aggregation |
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Which Prostanoids are Vasodilators?
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PGE2 PGI2
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Which Prostanoids are Vasoconstrictors?
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TXA2 PGF2a
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What is the action of COX?
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- Arachidonic Acid --> PGG2 (Then differentiates to vasodilators and vasoconstrictors)
- Aspirin inhibits COX |
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What is the action of Bradykinin?
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- Vasodilatation
- Increased vascular permeability |
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What is the action of Hisamine?
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- NO Release
- Vasodilation - Increased Vascular permeability |
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What is the function of the Circle of Willis?
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- Multiple pathways for oxygenated blood
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How does CSF prevent cerebral veins from collapsing upon standing?
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- Displaces the erebral fluid downward
- Creates negative intracranial pressure (prevents cerebral veins from collapsing) |
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Structural Adaptations of Coronary circulation?
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- Formation of coronary collaterals promoted by ischaemia
- high capillary density (1 Capillary / Myocyte) |
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Structural adaptations of Cutaneous circulation?
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- Shunt blood to venous plexuses to promote heat loss
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Which fibres in the skin are heat activated?
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- Cholinergic sympathetic
- Stimulate sweating and case local production of vasodilators |
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Functional adaptations of skeletal muscle circulation?
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- Strong metabolic hyperaemia overrides sympathetic tone during exercise
- Blood flow can dop by 80% upon strong sympathetic stimulation |
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Functional adaptations of Pulmonary circulation?
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- Hypoxic pulmonary Vasoconstriction
- Matches perfusion to ventilation - Becomes problem with global alveolar hypoxia --> pulmonary hypertension |
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How does NA contribute to venous regulation?
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- Affects splanchnic & cutaneous
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How does pulce wave vary with age?
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- Youth and Normotension - Aorta Compliant (elastic)
- Age and Hypertension - Aorta Less compliant, Sall arteries Constricted and pulse waves faster - Reflected wave going from thick aorta to small capillaries also faster |
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What is the Pulse Pressure?
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Systolic - Diastolic
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What is the mean arterial pressure?
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Diastolic + (Systolic - Diastolic)/3
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What are approximate MAP in Head / Heart / Ankle?
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60 / 90 /180
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Where are the arterial baroreceptors and where are they innervated from?
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- Carotid Sinus [IX cranial nerve] glossopharyngeal
- Aortic Arch [X cranial nerve] vagus - Mechanoreceptors |
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Where in the brain do the arterial baroreceptors feed into?
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Brain Stem: Nucleus Tractus Solitarius
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For what range are the baroreceptors most sensitive?
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80-150 mmHg
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What effect does the baroreceptor signal have?
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- Increased sympathetic drive
- decreased parasympathetic drive - Increased HR & Contractility & CO |
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What effect does syncope (fainting) have on heart rate?
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- Initial Fight or flight sympathetic increases HR
- Then profound bradycardia strong parasympathetic & vasodilation from removal of sympathetic drive |
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What effect does a decreased ADH release have on diuresis?
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Increased Diuresis
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What effect does an increased ANP release have on Na+ & H2O reabsorption?
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Decreased reabsorption
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How does sympathetic nerve activity affect renin release?
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Increases renin release
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What is normal blood pressure?
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120/80
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What is EDP?
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The pressure in the ventricle at the end of diastole, measured in the left ventricle as an approximation of the end diastolic volume / preload
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What is MAP?
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The average pressure within an artery over a complete cycle of one heart beat
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What is EDV?
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- End-Diastolic Volume
- Volume of blood in right / left ventricle at end load / diastole |
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What is Primary / Essential hypertension?
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- No obvious cause
- Polygenetic predisposition - Environmental influences (high salt / stress) - RAAS / Sympathetic overactive |
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What is secondary hypertension?
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- Cause can be found
- Renal (e.g. stenosis) - Endocrine (e.g. Birth Control / Phaeochromocytoma) |
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What equation links BP CO TPR?
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BP = CO x TPR
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Which receptors does Angiotensin II Primarily act upon?
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AT1
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1st Line Anti-Hypertensive Drugs?
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Angiotensin Receptor Blockers / Ca2+ Channel Blockers / ACE Inhibitors / Thiazide-Type Diuretics
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What is the effect of β-adrenergic receptor blockers?
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- Block sympathetic stimulation of the heart - reduces CO
- Reduce renin secretion and plasma levels of angiotensin II - Reduce mortality after MI / chronic heart failure - Bronchospasm / Cardiac Depression / Fatigue |
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At what stage do α1 and AT1 receptor blockers disrupt smooth muscle contraction?
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(SMC bind --> G-Protein Activation)
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Mechanism of ACE inhibitors?
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- Block production of angiotensin II & inhibit bradykinin breakdown
- Best in Patients with high circulating renin |
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For which demographic are they first line drugs?
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- White patients < 55 y/o
- African origin & older patients tend to have lower renin |
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How does Angiotensin II compensate for arterial stenosis?
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Constricts efferent > afferent restoring glomerular capillary pressure
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Mechanism of Angiotensin Receptor Blockers (ARBs)
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- Block angiotensin II receptors
- 1st Lines drugs <55 years of age |
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Amlodipine / verapamil / Diltiazem are all?
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- Calcium channel antagonists
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What is the mechanism of Calcium Channel Antagonists?
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- Block all VG Ca2+ channels
- Decrease TPR - Tachycardia / Peripheral Oedema |
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How can Ca2+ channel act as a voltage modulated dihydropyridine receptor?
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- Large polarisation to open state
- Dihydropyridine can bind to Inactive state and repolarise myocytes |
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Mechanism of α1 adrenergic blockers?
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Block sympathetically mediated constriction of arterioles & decrease in TPR
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Mechanism of K Channel Agonsists?
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- Opens in smooth muscle cells resulting in hyperpol
- Reverse vasoconstrictor mediated depolarisation and contraction - Severe vasodilator side effects so combined with diuretics and beta blockers |
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NICE prescribing guidelines >55 / Black patients any age?
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- CCB / Diuretic
- If not effective (+ ACEI/ARB) - If not effective CCB + Diuretic + ACEI/AII antagonist - If still ineffective (+ spironolactone / B1 / A1 antagonist) |
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NICE prescribing guidelines <55?
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- ACEI / ARB
- If ineffective (+CCB / Diuretic) - If ineffective use all three - If still ineffective (+ spironolactone / B1 / A1 antagonist) |
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What is Phaeochromocytoma?
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Adrenal catecholamine (Adrenaline / Noradrenaline) secreting tumour
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What is Conn's Syndrome?
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Excess aldosterone synthesis
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What is Cushing's Syndrome?
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Excess cortisol synthesis
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