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CVS (Pharmacology (Beta-blockers (MOA: blocks beta-1 receptors in the…

- - - - MOA: inhibit NKCC channel (Na,2Cl-,K) at luminal surface, binds competitively to Cl
        NKCC channel usually creates a transepithelial positive gradient that drives paracellular transportation of Na,Ca, and Mg into the blood
        Inhibition decreases Na reabsorption = decreases water reabsorption = reduces CO = reduces BP
      - Used in:
        
        HTN
        
        oedema
      - ADRs:
        
        hyponatremia
        
        hypokalemia = the high Na+ will reach the DT, and stimulate increased production of aldosterone-regulated Na pumps to increase Na reabsorption for K secretion (+ H+ secretion) :star:
        
        hyperuremia = increased risk in gout
        
        metabolic alkalosis
    - - Spironaloctone = inhibits MR receptor (aldosterone receptor), which is required for transmigration of aldosterone-sensitive Na/K ATPase into basolateral surface
        
        acts from basolateral surface
        
        aldosterone increase synthesise of basolateral Na/K ATPase and luminal Na channel => increases Na+ retention => increases water retention
        
        spironaloctone inhibit this effect = reduced water retention = decreased CO = decreased BP
      - ADRs:
        
        hyperkalemia = less K+ loss
      - Used in chronic heart failure
    - - MOA: inhibit eNCC channel (Na+, CL-) on luminal surface
        Na, Cl- go in, then through Na/K ATPase at basolateral surface into interstitum
      - Used in:
        
        HTN => can be used wth ACEi
        ACEi has risk of hyperkaelemia (K+ retention) but thiazide will cause increased excretion of K+, balances out
      - ADRs:
        
        hyponatremia
        
        hypokalemia
        
        metabolic alkalosis
- - - - aortic valve: 2nd ICS, right sternal border
      - pulmonary valve: 2ICS, left sternal border
      - tricuspid valve:4/5th ICS, right sternal border
      - mitral valve: 5th CIS, mid clavicular line
    - - Artery
        Left coronary artery
        
        from left aortic sinus
        
        short segment before giving off 2 branches = LAD and left circumflex artery
        LAD = follow the anterior IV groove
        left circumflex = follow the left coronary sulcus, gives off left marginal artery at posterior
        
        Right coronary artery
        
        from right aortic sinus
        
        longer, follow right coronary sulcus to posterior
        
        gives PDA = follow posterior IV groove
        
        gives off right marginal artery
      - Venous
        great cardiac vein = follow LAD
        middle cardiac vein = follow PDA
        small cardiac vein = follow right marginal artery
        drains to coronary sinus at the posterior
        into right atrium
- - - - Left side heart failure
        Increased MABP = increased aortic pressure, which means that the LVP must increase to overcome the increased aortic pressure so that valve will open
        increased LVP caused by stronger force of contraction, will lead to LV hypertrophy and dilatation.
        Eventually the hypertrophy becomes too severe that it distorts the normal myocyte, less beta-1 receptors = less sympathetic response
        starling's law = length tension relationship, increased length too much, decreased ability to produce active tension
        laplace's law: T=Pxr, increased R, has to increase T to get the same P, meaning need increased myocardial O2 demand
        Heart starts pumping less effectively, starts to pool, will go into atria (increased LAP), and then into pulmonary circulation, causing pulmonary congestion and oedema.
        
        pulmonary oedema
        increased pulmonary capillary hydrostatic pressure, shifts starling's equilibrium so that fluid shift into interstitum
        decreased lung compliance, harder to expand => get dyspnoea
        worse at night PND due to affect all parts of lung
        crepitation at base of lung
        frothy pink sputum
        
        can lead to right side HF
        
        Right side heart failure
        backflowing of blood to right side of heart
        atrial dilatation
        peripheral oedema
        
        ankle swelling
        
        raised JVP
        
        enlarged liver
      - Treatment :red_flag:
        
        ACE inhibitor
        
        reduce oedema
    - - occur due to HTN - dilation of the atrium increases chance of re-entry pathways around AVN
      - irregular abnormal depolarization of parts of the atrium
        when the depolarization is large enough and close enough to AVN, it might trigger the AP in AVN and causes ventricular depolarlization.
        co-ordinated depolarisation of the atria does NOT occur
      - no P wave
        fibrillatory waves
        normal QRS complex morphology, but very irregular
      - Treatment
        
        prevent complications
        
        anti-platelets, anti-coagulants
        blood can eddie in the atrium, increases chances of thrombus formation, this can cause blockage and can embolize
        
        control the rate
        
        beta blockers
        
        amiodarone
        
        CCBs
        
        control the rhythm
        
        anti-arrythmic
        
        Na channel blocker = lignocaine
        
        calcium channel blocker = diltiazem
        
        drugs that prolong AP = amiodarone
        
        cardioversion
        
        shock the heart at specific time (after R wave), so abolish abnormal pathways and reset the pacemaker cells, which will hopefully take over
        
        treat the hypertension
      - Problems:
        blood eddies in the atrium - increased risk of thrombus formation
        reduced stroke volume
        increase chance of re-entry
  - - - Infective Endocarditis
        
        Subacute
        
        low virulence, opportunistic
        
        slow onset
        
        already damaged valve
        
        Strep viridans :star:
        
        turbulent blood flow through the damaged valve causes endothelium damages, exposing the underlying subendothelium, which allows thrombus formation, forms vegetation
        
        bacteria in blood can bind to vegetation and grow 'infect and colonize'
        
        inflammatory response follows, = large friable vegetation comprising of thrombotic material, bacteria and inflammatory cells
        
        Acute
        
        high virulence
        
        fast onset
        
        normal or damaged valve
        
        Staph aureus, Strep pyogenes
        
        bacteria has virulence factors (MSCRAMMS) + SERAM that allows them to stick to endothelium
        
        binding causes inflammatory response, with large friable vegetation formed
        
        damages to the endothelium causes activation of platelet
        
        features:
        
        fusion of commissure
        
        large friable vegetation
        
        thickened and distorted valve edge
        
        treatment :star:
        Staph aureus = flucloxacillin +/- gentamicin
        MRSA/Staph epidermis = vancomycin
        Strep = penicillin
        
        can be caused by prosthetic valve - platelet thrombi can form on surface of prosthetic, bacteria can bind to it
        form biofilm infection
    - - pathogenesis
        
        prior GAS oropharyngeal infection
        
        antibodies produced against the M protein in GAS reacts with structurally similar self-proteins in the heart (+ joints and brain)
        
        also, CD4 T cell specific to the Streptococcal peptide react with self-antigen in the heart producing cytokines and activating macrophages
        
        causes damage and inflammatory response
        
        healing occurs via fibrosis = thickening of valve and chordae tendinae
      - John's criteria
        2 major, or 1 major and 2 minor
        major
        
        subcutaneous nodules
        
        syndeham chorea (irregular abnormal un-coordinated movement of limbs)
        
        pancarditis
        
        erythema marginatum = red rashes
        
        arthritis poly, migratory
        
        minor
        
        increased CRP
        
        fever
        
        arthralgia
        
        prolonged P-R interval
      - Pancarditis
        Endocarditis
        
        inflammation and fibrinoid necrosis in the CT below endocardium
        
        swelling, which can bring valve cusp together
        
        forms verrucae = sterile
        
        Myocarditis
        
        most serious
        
        inflammation in myocardium with Achoff bodies and muscle necrosis
        
        Pericarditis
        
        causes pericardial effusion = sterile fibrinous exudate
  - - - endothelium injury and dysfunction causes inflammatory response with increased vascular permeability increased leukocyte and platelet adhesion, with increased expression of VCAM-1 and ICAM-1 (adhesion molecules)
        
        this allows for monocytes and LDL in blood to enter into the intima
        monocyte becomes macrophages
        LDL becomes oxidised and then engulfed by macrophages, forming foam cells
        growth factor released, attracting SMC from blood progenitor or from media, causes SMC proliferation with ECM deposition in intima
        
        70-705% causes stenosis
        forms atherosclerotic plaque
      - complications
        
        haemorrhage into plaque
        
        acute plaque change
        
        aneurysm formation => AAA can rupture into abdominal cavity, causes distal emboli and occlude branches of aorta
        
        mechanical obstruction = ischaemia
      - endothelium damaged caused by
        
        diet high in lipid
        
        high BP
        
        chemicals
        
        immune system
    - - ischaemia not severe enough to cause tissue death
      - stable MI = occurs by onset of exercise, due to increased demand
        unstable MI = random, more severe, acute palque change
    - - ECG = STEMI