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Unit 3 Week 6 & 7


Medicine Flashcards on Unit 3 Week 6 & 7 , created by shirou masoodi on 04/06/2018.
shirou masoodi
Flashcards by shirou masoodi, updated more than 1 year ago
shirou masoodi
Created by shirou masoodi over 4 years ago

Resource summary

Question Answer
Name 4 Risk factors of CVD (2 Constitutional & 2 non-constitutional) Constitutional Genetics FH Age Non-constitutional Smoking Obesity Hypercholesterolaemia Hypertension
Outline the formation of a Transitional atheromatous plaque 1. Endothelial injury 2. Increased vascular permeability 3. LDL Accumulation & oxidation 4. Lipid-laiden foam cells 5. Platelet adhesion & PDGF 6. SM proliferation 7. ECM deposition 8. Further LDL deposition
Describe what causes TIA Mini-stroke Microemboli i.e. cardiac thrombi or artheromatous plaque embolise into cerebral circulation - MCA Cerebral hypoxia - no infarction
Compare a fatty streak to an advanced plaque Fatty streak: Lipid laiden foam cells (Oxidised LDL Flat yellow dots & lines Mature plaque: Intimal thickening - SM proliferation & ECM deposition
Name & describe the 2 methods for formation of complicated plaque 1. Denudation of endothelium - Exposure of subendothelial collagen 2. Endothelial fissuring - Fibrous cap tears off - blood enters - thrombus forms within plaque
Outline the difference between Stable & Unstable angina Stable: Only occurs on exertion (At rest blood supply meets demand - on exertion heart requires more oxygen and this demand is not met by partially occluded vessel Unstable: Occurs even at rest - Usually due to disturbance of atheromatous plaque i.e. thrombosis, embolisation
Define and name 2 causes of Prinzmetal angina Angina that occurs without provocation usually due to vasoconstrictors i.e. TxA2 - Smoking - Cold air - Cocaine
Outline the pathogenesis of MI 1. Artheromatous plaque undergoes disruption 2. Thrombus formation causes complete occlusion of epicardial vessel 3. Cessation of aerobic respiration 4. Myocardial contractility reduced 5. Damage causes leakage i.e. troponin
What is an ST elevated MI? Transmural (Involving death of all layers of heart tissue)
Which parts of the heart is supplied by Anterior interventricular artery Left Circumflex RCA Anterior interventricular artery - Anterior wall & septum Left Circumflex - Lateral wall RCA - Posterior wall & septum
Explain the following presentations in MI 1. Chest pain (Left) 2. Sweaty & Clammy 3. Shortness of breath 1. Myocardial necrosis => Bradykinin & adenosine (Inflammation) stimulates sympathetic and vagal afferents (T1-T4) 2. Reduce CO & SV => Reflexive sympathetic drive => Diaphoresis & Peripheral vasoconstriction 3. Reduced EF => Reduced tissue perfusion => tissue hypoxia => Dyspnoea
Outline which investigations should be conducted following STEMI 1. ECG 2. Trponin I & C 3. CK-MB
What is the most optimal management strategy for MI Primary angioplasty (Reduced mortality, re-infarction & ischaemia)
Why was atenolol prescribed To reduce heart rate and force of contraction
What is the mechanism of action of Simvastatin. HMG CoA reductase inhibitor - Reduces liver LDL synthesis - Increases liver LDL-R synthesis - Increases LDL clearance from circulation
Mechanism of action of Ramipril ACE inhibitor Inhibits conversion of Ang I => Ang II 1. Reduced Ang II binding to AngII-R - GQ/11 - Vasodilation 2. Reduced altosterone induced Na+ retention ANTI-HYPERTENSIVE
2 Adverse effects of warfarin 1. Haemorrhage 2. Teratogenic
Why is aspirin given to chew after MI Aspirin is an anti-platelet drug by inhibiting the production of platelet activating TxA2 Prevents clotting of blood and thrombus formation
How does a AED work? - Electrodes send info to computer analysing whether the rhythm is shockable or not - Electrical current is delivered and depolarises the myocardium allow natural pacemaker tissue to resume control
Give 2 examples of shockable rhythms 1. Ventricular tachycardia: Re-entrant pathway looping in the ventricle 2. Ventricular fibrillation: Ventricular cells are excitable and depolarising randomly
What are the 4 primary criteria when analysing ECG - Rate - Regularity - PR interval - QRS
What is the difference between systolic and diastolic HF Systolic: Inadequate myocardial contractility i.e. IHD, Hypertension Diastolic: Inability of the myocardium to fully relax and fill i.e. Hypertrophy
Explain the pulmonary presentations of LHF - Blood is not effectively pumped out of left side of body thus there is a backlog through pulmonary veins into the lungs - Pulmonary hypertension causes pulmonary oedema - Dysponoea - Cough Crackles & Rales
Outline how chronic lung disease leads to cor pulmonale (What are the clinical manifestations of this?) Chronic lung disease => hypoxaemia => Hypoxic vasoconstriction => PH => Right ventricle dilation & hypertrophy Blood backs up into the body - Hepatosplenomegaly -Raised JVP - Pitting oedema
Management of HF Basic management of HF Atenolol Ramipril Furosemide Spironolactone
What is the role of a first responder? Community volunteer trained to attend emergency calls received by ambulance services. Carry AED.
Outline the Self regulatory model of illness - Symptom perception - Cognition => Coping with illness threat - Emotion > Coping with emotion - Appraisal
Describe the cognitive and emotional response of the self regulatory model of illness Cognitive: Symptom perception (Controllability, curability & consequences) Emotional: Anxiety (Apprehension, worsened with tests & investigations) Depression - flattened response to all situation (Feeling low, loss of interest or pleasure)
Give 2 examples of positive consequences of MI - Greater appreciation of life - Healthy lifestyle changes
What is the role of cardiac rehabilitation To help recovery and reduce the risk of recurrence of cardiac illness. Includes holistic approach: Physical fitness, education, Dietician, lifestyle advice, counselling (anxiety & depression)
Define global governance Actions and means adopted by society to organise itself in the promotion and protection of health
Give 4 ways governance can achieve equity in health 1. Redistribution of resources 2. Legislation & policy development 3. Public regulation 4. Creation of public services and organisations
Compare and contrast the Beveridge model of healthcare to the out of pocket model of healthcare Beveridge: Free at the point of access where its funded by the government through tax Out of pocket: Individuals pay for their own healthcare unless they are covered by health insurance.
Outline the classification for stage 1, & 3 of hypertension Stage 1: 140/90 Stage 2: 150/ 100 Stage 3: 160/110
Name 2 constitutional and 2 non-constitutional risk factors of hypertension Constitutional: Age>55yrs Black afro Caribbean FH Non-constitutional: Smoking Obesity Physical inactivity Heavy salt consumption Stree
What is the difference between primary and secondary hypertension Primary: Idiopathic with no known obvious cause - linked to genetics and lifestyle (90-95%) Secondary: A direct cause of another disease - Causes include renal artery stenosis, endocrine origin & coarctation of aorta
Outline how left heart failure is caused by hypertension Hypertension results in increased resistance in the aorta creating and increased afterload which the left ventricle has to work against. This results in left ventricular dilation and hypertrophy so that it is able to generate enough force to overcome the increased aortic resistance.
Explain how low blood pressure is regulated by the baroreflex - Low Pa reduces arterial stretch and activation of stretch sensitive ion channels - Reduced firing from carotid and aorta sinus to NTS and CV centre in medulla - Increase sympathetic drive to B1 on heart => increase HR & SV - Increased sympathetic drive to A1 on blood vessels => Vasoconstriction
How does the kidney normalise GFR when blood pressure is increased 1. Myogenic response 2. Tubuloglomerular feedback (Explain them!)
Give 5 actions of Angiotensin 2 1. Increased thirst and Na+ appetite 2. Na+/H+ exchanger in PCT 3. Aldosterone secretion from adrenal cortex (ZG) 4. Stimulates the release of ADH from PPG 5. Direct vasoconstriction via AT1-R
Explain why patients with hypertension would present with proteinuria Increased hydrostatic pressure leads to damage to the filtration membrane resulting in loss of the negative components of the basement membrane (glycocalyx) allowing the leakage of protein into the tubular fluid
Explain the following fundoscopic findings 1. Papilloedema 2. Cotton wool spots 3. Small haemorrhages 1. Increase intracranial pressure causes fluid leakage into retina 2. Damage to nerve fibres results in the accumulation of axoplasmic material in the retina - fluffy white patches 3. Increased hydrostatic pressure => endothelial cell damage => rupture
What would you expect to happen to serum creatinine and eGFR for a patient with hypertension? Serum creatinine: Would rise because creatinine cannot be cleared as effectively due to impaired renal function (RR: 60-120umol/l) eGFR: would decrease due to mesangial cell expansion and ECM deposition causing occlusion of the glomerular capillaries
List 4 non-pharmacological interventions for hypertension 1. Weight loss BMI 20-25kg/m2 2. Exercise >30 mins 3x/week at 60% max 3. Restrict alcohol <2units/week 4. Restrict salt <!00mmol
Give 2 adverse effects of phenoxymethylbenzamine 1. Reflexive tachycardia 2. Postural hypotension 3. Incontinence
a. What class of drug is Clonidine? b. What is the mechanism of action? a. Presynaptic alpha2-R on post-synaptic sympathetic nerve endings & NTS b. suppresses NA release & suppression of central sympathetic tone thus reducing HR, SV & causes vasodilation
Amy-lee was prescribed the beta-blocker propanolol for hypertension and now finds she often has cold hands and feet. Why might this be? - Reduced CO leads to reduced blood supply to peripheral tissues - Blocked b2 mediated vasodilation of vessels supplying the skeletal muscles
Why are beta-blockers such as atenolol & bisoprolol contraindicated in diabetics? - Blockade of b2 mediated glycogoenolysis & gluconeogenesis results in hypoglycaemia. - Blockade of sympathetic response means that the usual hypoglycaemic warnings will be absent.
Abbie Randall has been suffering from a persistent cough for the past 2 weeks. Upon consultation her GP finds that she has recently started taking Ramipril. Explain Abbie's cough Ramipril is and ACE inhibitor which inhibits the breakdown of bradykinin in the lungs resulting in irritation and persistent cough
a. What is the mechanism of action of Amlodipine? b. In what circumstance would amloppine be the first line treatment for hypertension? a. Inhibits LTCC thus reducing IC Ca2+ levels in Vascular smooth muscle cells => Vasodilation b. Age>55 & Afro-carribbean (Most responsive to CCB rather than ACE inhibitor or ART)
a. what is the mechanism of action of furosemide? b. Why is the action of diuretics transient? a. Inhibits Na+/K+/Cl- co-transporter in ascending loh thus reducing Na+ & H20 reabsorption thus reducing blood volume b. Reduction in BP stimulated by diuretics triggers renin release which in turn increases BP
Identify 3 possible triggers to consultation. Identify 3 possible barriers to consultation. a. Ley referral Sudden exacerbation of symptoms Interference with social/working life b. Lack of time Family/work responsibility Normalisation of symptoms Temporalisation
Explain the pathological basis of the following presentations in pheochromcytoma: 1. Sweating 2. Nausea & vomitting 3. Hypertension 4. Palpitations - Excess catecholamines in circulation to to presence of tumour in the adrenal medulla causes increased sympathetic drive to sweat glands => diaphoresis & Heart => Palpitations - Stimulation of a1 receptors in area postrema causes nausea and vommiting
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