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187 Cards in this Set
- Front
- Back
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t/f... the lung does not go higher than the anterior aspect of the 1st rib
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false the lung does not go higher than the posterior aspect of the 1st rib
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Why is a PA film superior to an AP CXR for viewing the heart?
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In AP, rays pass through the heart first, then the rest of the body, allowing them to diverge after the heart, which makes the heart appear larger than it is. In PA, the rays pass through the body, then the heart is very close to the film/photodetector, so it is a more accurate representation of cardiac size. This is particularly useful if assessing for cardiomegaly (heart >50% thoracic width)
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t/f... the lungs appear darker in an CXR as xrays are stopped here
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false, they pass through
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Where does the trachea start?
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C6 - pharynx divides into oesophagus and trachea
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t/f... bronchus have C shaped cartilage in their walls
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false... the bronchus has circular cartilage, the trachea has C shaped cartilage for the oesophagus to travel behind.
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What is a bronchgram?
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radioopaque dye placed into bronchi to view airways
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What changes between bonchus and bronchioles?
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<2mm diameter, lose mucus glands, lose cartilage
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Where is the minor/horizontal fissure?
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4th intercostal cartilage on right lung
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Where is the major/oblique fissure?
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Costophrenic angle to spine above middle lobe on right, and also high on the left side
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t/f... lymph nodes always drain into the ipsilateral lymphatics
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false, not always, just most of the time
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Where does the thoracic duct drain from and into?
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absorbed fat from the bowel up to drain into the venous system between the left jugular and leftsubclavian vein. not through liver, very posterior structure against the vertebrae, usually lies to the right of midline and at T6 it swaps over to the left side
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t/f... the kidneys are covered partially by the ribs
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true, the superior kidney is covered by the ribs.
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What vertebral level do the posterior intercostal arteries branch off the descending aorta?
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T4-12
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Where do the coronary arteries originate?
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aortic cusps
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Which valve has 2 cusps?
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Mitral valve
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Where do the internal mammary arteries come from?
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The subclavian arteries
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t/f the SVC passes in front of the aortic arch
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false, while the brachiocephalic trunk of the venous system does pass in front of the aortic arch, the SVC is to the right of the aorta
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What empties into the RA?
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IVC, SVC, soronary sinus
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What is the structure of the azygous system?
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collects blood from the mediastinum and chest wall drains into the SVC. The left side is called the hemizygous and the right side is called the azygous. They are in continuity with veins coming from below the thorx, called the ascending lumbar veins.
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Describe a Pulmonary angiogram?
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catheter introduced into a vein in the arm, goes all the way to the pulmoanry arteries
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Describe the appearance of the pulmonary arteries on imaging.
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the right pulmonary artery goes in front of the bronchus, and descends and has an early branch off, creating a V shape, whereas the left pulmonary artery is longer and ascends as it goes up and over the left main bronchus, creating a box shape radiographically
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t/f... the pulmonary veins are posterior to the arteries
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false, the pulmonary veins are more anterior as they are passing oxygenated blood back into the left atrium at the back of the heart
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What pierces the diaphragm?
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Aorta, azygous veins, thoracic duct
oesophagus IVC (going from posterior to anterior) |
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where does the oesophagus start?
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C6, where the pharynx becomes the trachea and oesophagus
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What nerve travels anterior against the oesophagus below the trachea bifurcation?
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vagus
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How do the recurrent laryngeal nerves travel?
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they emerge from the vagus nerves
Left - travels under and then behind the aortic arch in order to supply the laryngopharynx (left vocal cord) Right - tracels under and then behind the right subclavian to supply the laryngopharynx (right vocal cord) |
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What is the barium swallow used for?
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to picture the oesophagus/stomach
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t/f... it is normal for children to have large opacities in their central upper thoracic region not seen in adults
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true, this is the thymus, which disappears in adolescence by being replaced by fat
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t/f... the intercostal arteries, nerves, veins are on the superior aspect of the rib
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false, they are protected at the inferior/posterior surface of the rib
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What is the valsalva sinus?
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the aortic sinus/es. These occur just above the aortic valve in the ascending aorta, and give rise to the 2 coronary arteries.
Left posterior sinus - Left coronary artery Anterior sinus - Right coronary artery Right posterior sinus - non-coronary sinus |
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At rest, what is the CO?
And typically at maximum exercise? |
5L/min
25 L/min (increased HR) |
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What is stroke volume?
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volume of blood pumped out of heart, End diastolic volume substract end systolic volume (EDV - ESV)
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What does a SNS transmitter do to the pacemaker potential?
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makes the spontaneous upward depolarisation slope steeper ie brings on the next AP faster
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What does a PNS transmitter do to the pacemaker potential?
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makes the spontaneous upward depolarisation slope less steep ie delays the next AP
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Describe the If current?
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'Funny channel/current' - non specific cation current activated by hyperpolarisation of the membrane potential (others are by depolarisation), when it gets back to its threshold, turns itself off
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Describe the INCX current?
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Uses the Calcium/Sodium exchanger, brings 3 Na in, 2 Ca out, therefore bringing in more positive charge contribuitng to spontaneous depolarisation of pacemaker potential.
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Describe the ICa current?
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Calcium inward currentactivated at the AP threshold/-40mV, Calcium current that causes the rapid AP rise
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What drugs can be used to increase heart rate?
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B-agonists (heart block)
atropine (to decrease overactive PNS) |
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What drugs can be used to decrease heart rate?
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b-blockers (- inotropic, heart contractions weaker)
Ca channel blockers (- inotropic,heart contractions weaker) Ivabradine (not - inotropic, safe on overdose, as only effects the If current and won't stop SAN firing) |
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Why is there a maximum effective heart rate?
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Inadequate diastolic filling means inadequate myocardial blood flow, as diastole becomes less of a percentage of the total cycle time with increased HR. This leads to a decrease in cardiac contractility and cardiac output
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How do endurance athletes physiologicall overcome the barrier humans have of our maximum effective heart rate to improve their performance?
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training = physiological hypertrophy of the heart, increasing EDV and Stroke volume. This means they can achieve their required CO at a low heart rate e.g. 40/min. This gives them a lot higher level of modulation when they exercise to get back up to the maximum HR of 180 /min
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What is the end systolic volume decreased by?
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Increasing heart contractiliy force through:
Increased stimulation frequency increased extracellular Ca (more Ca gets in) SNS stimulation (increases HR by increasing frequency and by cAMP dehosphorylation) Cardiac glycosides (digoxin - block Na pump = increase Na, = less Ca transported out) |
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What drugs are negatively inotropic?
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Ca channel and beta-receptor blockers make the contractions of the heart weaker.
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What increases the end diastolic volume?
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Increased central venous pressure/preload
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How does increased central venous pressure cause a greater CO?
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Increased CVP = stretches cardiac muscle = greater contractility (Starling's Law) = greater SV = greater CO
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What factors do you need to increase to get the maximum cardiac output?
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increased heart rate, contractility and central venous pressure
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How does the body increase central venous pressure?
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Muscle pump - contraction of surrounding skeletal Muscle pumps blood through veins
SNS = vasoconstiriction of peripheral veins Reduced renal blood flow = RAAS = increase blood volume (1-2 days) |
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What is preload?
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the central venous pressure, filling pressure for the heart, the pressure coming into the heart
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What is afterload?
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the arterial BP, pressure into which the heart has to pump
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What is thought to help keep CO relatively constant over the physiological range of blood pressures?
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most likely as a fall in Stroke Volume leads to a rise in Central Venous Pressure, which then causes greater diastolic filling which increases Stroke Volume, opposing the SV fall.
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How does the heart maintain/attempt to maintain a constant CO in the face of increasing BP? What is the consequence for hypertensive patients?
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By increasing its work, which means consuming more energy and by consuming more O2. This leads to a higher chance of angina in HT patients, especially if they have coronary insufficiency
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What process is effective in treating hypertension and heart failure?
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afterload reduction by inducing vasodilation, such as found in using ACE inhibitors and Ca channel blockers
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What is ARF?
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Acute Rheumatic Fever = acute, often recurrent immuno-inflam disorder 1-5 weeks following an URTI due to GAS (Group A strep)
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What are the acute effects on the heart in ARF?
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Pancarditis
Fibrinous Pericarditis (haemorrhagic/'bread and butter' from fibrin exudate) Myocarditis (Aschoff nodules near BV) Endocarditis (small nodular fibirn/platelet vegetations on cusps and cordae tendinae) Arrhythmias and cardiac failure may occasionally ensue |
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t/f... GAS will be found in the heart in and ARF patient
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false, their are none of the causative bacteria present in ARF as it occurs 1-2 weeks after the URTI, it is a cross reaction response only
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What antibodies can be found in an ARF patient?
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Ab to strep enzymes = anti-streptolysin, anti-DNase B, anti-streptokinase, anti-hyaluronidase
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How many people who develop GAS as an URTI get ARF? Who gets ARF?
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3%
usually those untreated and perhaps those with a genetic susceptibility, those infected with a particularly virulent strain |
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What are the clinical features of ARF?
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1) migratory polyarthritis at the joints (adults)
2) carditis 3) subcutaneous nodules 4) skin - erythema marginatum 5) Sydenham's chorea (neuro disorder, invol. purposeless rapid mvmt) |
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What age does the first ARF usually occur?
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5-15 years
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What % of children with ARF may develop carditis?
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50-75%
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What is the Jone's criteria?
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American Heart Association criteria used to diagnose ARF. Includes:
Evidence of preceding GAS URTI plus 2 of the major ARF clinical findings or 1 major and 2 minor/non-specific signs (fever, arthralgia, acute phase proteins) |
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What are Aschoff nodules?
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Granulomatous/foreign body type immunological inflammation found close to blood vessels in the myocardium in ARF.
They contain central necrosis, collagen surrounded by lymphocytes, occasional plasma cells and plump macrophages, (either anitschkow or aschoff multinucleated giant cells). |
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What are multinucleated Aschoff giant cells?
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Coalesced larger Anitschkow cells, found in the myocardium of patients with Acute Rheumatic Fever (ARF). They are multinucleated giant cells (macrophages).
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What are Anitschkow cells?
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Enlarged macrophages within Aschoff nodules in ARF. Called caterpillar cells, as they have a large amount of CLEAR cytoplasm surrounding a rod-shaped nucleus.
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t/f... ARF vegetations are pale, small and contain no microorganisms
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true
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t/f... the tricupsid valve is commonly effected by the endocarditis in ARF
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false, it is rarely effected, the mitral and aortic valves suffer the most damage due to the increased blood pressures/turbulence in the left chambers.
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What causes rheumatic vegetations in ARF?
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Trauma - inflamation = ulceration = vegetations where cusps touch upon valve closure. High pressure in the left side of the heart makes the mechanical damage greater, and the aortic and mitral valves more commonly effected
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What is the chronic consequence to the valves from endocarditis in ARF and how is it brought about?
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Stenosis of valves. Organisation of vegetations on cusps leads to increased thickness, higher rigidity from fibrosis and calcification (hyaline), and an increase in cusp vascularity. This decreases the distance between cusp commisures. This effect is exacerbated by repeated episodes of ARF.
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What occurs to the chordae tendinae as a consequence of endocarditis from ARF?
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Chordae adhere, fuse, thicken and shorter due to organisation following vegetation formation.
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What are the cumulative effects of recurrent rheumatic endocarditis on the valves of the heart?
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aortic stenosis and regurgitation
Mitral stenosis and regurgitation tricuspid involvement (rarer) |
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What are important sequalae/pathological outcomes following recurrent rheumatic endocarditis?
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congestive heart failure (valve malfunction)
arrhythmias(La dilatation w mitral stenosis) Infective endocarditis (turbulent blood flow from anatomical changes) |
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What is congestive cardiac failure?
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abnormality of cardiac function causing failure of heart to pump blood at a rate to adequately supply metabolism
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What are your chances of dying if you have Heart Failure and are >65?
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50%
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What is systolic heart failure? eg
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unable to contract normally eg ischaemic heart disease
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What is diastolic heart failure? eg
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unable to relax/fill normally (small lumen) e.g. constrictive pericardisit, HT, hypertrophyic cardiomyopathy, myocardial fibrosis/infiltration
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What is low output heart failure? eg
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heart can't pump adequate quantities of blood to tissues (IHD, HT, dilated cardiomyopathy, valvular or pericardial disease
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What is high output heart failure? eg
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heart pumps normally but demands of the tissues are abnormally high e.g. hyperthyroidism, anaemia, pregnancy, paget's disease of the bone
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What is acute heart failure?
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a consequence of the sudden imposition of disease. See hypotension wo peripheral oedema e.g. large AMI, rupture of cardiac valve
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What is chronic heart failure?
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occurs slowly but progressively. See normal blood pressure (long time to adapt, until endstage) and often peripheral oedema e.g. dilated cardiomyopathy, multivalve disease
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What is left sided heart failure?
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left side is pumping inadequately, so wil get pulmonary congestion. long standing will result in right sided heart failure
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What is right sided heart failure?
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right ventricle is pumping inadequately, resulting in systemic congestion, causing peripheral oedema and congestion of liver spleen
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What is forward heart failure?
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Inadequate L or R ventricular contraction, leading to inadequate LV output (analogous to a mild form of shock). can cause liver cell damage, peripheral oedema, cerebral ischaemia
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What is backward heart failure?
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Can be left and/or right, leading to venous congestion in the lungs and or systemic vicera
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What can increase cardiac demand?
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physiological cause is exercise
pathological =pressure overload (HT, aortic stenosis, must work harder to overcome) =volume overload (mitral regurgitation, blood goes back into atria) |
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Describe pressure overload.
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increased systolic pressure, increases systolic wall stress, leading to parallel addition of new myofibrils which increases wall thickness = concentric hypertrophy (leads to diastolic heart failure)
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Describe volume overload.
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increase diastolic pressures (CVP), increases diastolic wall stress, leading to series addition of new sarcomeres ie increase in length which leads to chamber enlargement and wall thinning = eccentric hypertrophy
(leads to systolic heart failure) |
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What can cause strain on LV?
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myocardial disease (CM, AMI)
valve disease (stenosis or regurgitation) arrhythmias HT Hyperdynamic states (thyrotoxicosis) Congenital anomalies Constrictive pericarditis |
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What are two general mechanisms whereby valves can become less effective?
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lesion - intrinsic structural disorder (RHD, congenital disease)
functional - dilatation of annulus fibrosis disallowing valve closure (eg tricuspid in mitral stenosis) |
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What is the short term compensation mechanism of the LV to strain?
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immediate dilatation = stretching of myocytes = increased force of contraction for next beat (Frank-Starling)
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What is the middle term adaptation of the LV to strain?
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Hypertrophy of left ventricle = limited by ability to perfuse the myocytes
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What is the decompensatory response to long term, uncorrected LV strain?
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Hypertrophy followed by delayed dilatation
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t/f... the atrium has a huge ability to compensate to increased stress
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false, it is thin walled and increased stress (e.g. LV failure) will cause hypertrophy, but this will be unnoticeable due to the dilatation occurring
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What are the pathological features of pulmonary venous congestion?
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Brown induration:
congested capillaries in alveolar walls alveolar oedema/transudate RC in alveoli RC degradation by macrophages, which become harmosiderin (rusted Iron) filled pulmonary fibrosis (chronically) |
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What form of disease causes cardiac failure confined to the right side of the heart?
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chronic fibrosing lung diseases e.g. silicosis
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t/f... dilatation occurs early on in the process of right ventricular strain
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true, as it has a thin wall and the hypertrophy which occurs to adapt to the increase strain is almost immediately masked by the dilatation
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What are the effects of right heart failure?
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congestion of systemic veins = heptaosplenic congestion
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What causes central vein dilatation and the fatty change/necrosis immediately surrounding it in venous congestion from right heart failure?
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Venous pressure is increased, causing a slowing of blood flow return to the heart, which followed downstream means that the oxygenated blood coming from hepatic arterioles in the sinusoids is giving away its O2 to epitheilial cells in the periphery of each hepatic lobule first, so that there is little left for the central vein. Fatty change occurs in hypoxic cells, and then subsequent necrosis as oxygen supply is diminished.
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What are the obvious signs of systemic venous congestion?
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Elevation of JVP, pitting oedema in legs/sacrum, ascites and effusions
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What causes aortic stenosis?
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Congenital (bicuspid)
Acquired (degeneration, rheumatic fever) Subvalvar |
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What does aortic stenosis cause
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Causes a PRESSURE OVERLOAD:
LV hypertrophy Eventual dilation and failure Causes OBSTRUCTION to FLOW: Low BP, Syncope, Angina High LVEDP causes dyspnoea |
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What does an aortic stenosis sound like on auscultation?
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harsh, loud, systolic, crescendo/decersendo murmur in aortic area with a 4th sound, and paradoxical splitting of the 2nd sound
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What causes aortic regurgitation?
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Cusp Injury - infection, rheumatic fever
Prolapse - dissection and commisural injury Aortic root - Marfan’s, Ankylosing spondylitis |
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What does aortic regurgitation cause?
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Causes a VOLUME OVERLOAD
LVEDV increases to maintain stroke volume Decompensate when LVEDV increases without SV increase LVEDV increases as there is no way for better LV emptying and ejection is into high pressure system. Unlike MITRAL REGURGITATION. |
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What does an aortic regurgitation sound like on auscultation?
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soft, blowing, diastolic decresendo murmur
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What causes mitral stenosis?
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Congenital :
Abnormality of chordae or papillary muscles Cor triatriatum Acquired: Rheumatic fever Subvalvar calcification Carcinoid disease Mucopolysaccharidoses |
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What does mitral stenosis cause?
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OBSTRUCTION of FLOW to LV from LA
Pulmonary Hypertension Passive transmission of LA pressure Reactive arteriolar constriction in lung Right heart failure Tricuspid regurgitation Portal hypertension, ascites |
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What does a mitral stenosis sound like on auscultation?
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opening snap with a diasolic-presystolic reumbling murmur in the 4th Left intercostal space
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What causes mitral regurgitation?
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Abnormality of any part of the valve
Leaflets: Prolapse Endocarditis Annulus: Dilation with LV failure Chordae: Rupture or stretch with myxoid degeneration Endocarditis Papillary muscle: Infarction or ischaemia Endocarditis |
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What does a mitral regurgitation sound like on auscultation?
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soft, blowing, pansystolic murmur at the apex
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What valvular issue is associated with the worst survival rates post diagnosis?
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Aortic stenosis (30% at 10 years)
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What valvular issue is associated with the best survival rates post diagnosis?
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Mitral stenosis (60% at 10 years)
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What are surgical options in treating valvular disease?
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Mitral valvotomy
Valve reconstruction and repair Replacement with mechanical, xenograft, homograft or autograft valve |
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What are the benefits of a mechanical valve compared to a tissue valve replacement?
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Last forever, no need for reoperation
(unlike tissue) |
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What are the benefits of a tissue valve compared to a mechanical valve replacement?
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Don't need anticoagulation, lower risk of endocarditis, is fine during pregnancy
(unlike mechanical) |
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t/f... the mortality rate for either a mitral or an aortic valve replacement is equal to 10% or less
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true (Aortic = 4%, Mitral 8%, with CABG Aortic = 6% and Mitral = 10%)
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What imaging investigations are used in determining Left ventricular function?
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Cardiac catheterisation (angio/venography)
Echocardiography Gated Heart Pooling Scan (nuclear) |
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What imaging investigations are used in suspected Coronary artery disease?
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Cardiac catheterisation (angio/venography)**
CT/MRI Exercise stress test (w ECG) Nuclear perfusion |
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What imaging investigations are used in suspected Myocardial ischaemia?
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ECG
Nuclear (thallium ,sestamibi) - stress and at rest Echocardiography stress testing |
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What imaging investigations are used in suspected Cardiac valvular dysfunction?
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Echocardiography
Cardiac catheterisation (angio/venography) MRI |
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What are the advantages of plain xrays in cardiac diagnoses?
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Advantages:
Cheap Non-invasive |
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What are the disadvantages of plain xrays in cardiac diagnoses?
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Disadvantages:
Limited information on function and chamber sizes |
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What are the advantages of Angiography in cardiac diagnoses?
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Advantages:
Accurate data Multiple vascular investigations possible Enables treatment at same procedure |
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What are the disadvantages of Angiography in cardiac diagnoses?
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Disadvantages:
Invasive Anatomical not physiological data (e.g. artery may have normal diameter/shape, but is actually dilated with a huge plaque) |
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What are the advantages of a CT in cardiac diagnoses?
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Advantages:
Non-invasive Images aorta and pulmonary vessels as well as coronaries |
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What are the disadvantages of CT in cardiac diagnoses?
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Disadvantages:
Radiation dose Cardiac movement and respiration artifacts Lower resolution Problems with highly calcified vessels |
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What heart conditions are MRI scans particularly useful for imaging?
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Aortic - coarctation, dissection, TGA
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Where can the echocardiogram be taken from?
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Transthoracic
Transoesophageal (TOE) |
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What are the advantages of a echocardiography in cardiac diagnoses?
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Advantages:
Relatively cheap Non-invasive |
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What are the advantages of a echocardiography in cardiac diagnoses?
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Disadvantages:
Investigator dependent Some patients difficult to study No information regarding coronary arteries |
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What are the 3 types of nuclear studies you may wich to perform on the heart?
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Gated Heart Blood pool studies (Assessment of chamber function)
Studies of myocardial perfusion (Thallium + Sestamibi) Studies of myocardial viability |
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What is the disadvantage of a myocardial perfusion study with Thallium and sestamibi?
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It tests for regional changes in myocardial perfusion, so if the perfusion is low over the whole heart, it may appear normal.
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What are the primary, secondary and tertiary pacemakers of the heart and what are their intrinsic rates?
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SA ~ 80/min
AV ~ 50/min His-Purkinje ~ 40/min |
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What is the normal heart rate?
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80/min at rest, no more than 180/min when exercising
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t/f... the QT interval should get shorter during exercise in an ECG
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true. QT length decreases? with increased heart rate, the QTc is a way to standardise the QT interval to a common HR?
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t/f... firm pressure with a finger which leaves a dent that takes a minute or two to obliterate is a way of telling if a swelling is oedema
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true, this is called 'pitting oedema'
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What is hydrostatic pressure? Describe its effect on circulation/blood vessels.
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The pressure exerted by a fluid at equilibrium due to the force of gravity. With regards to circulation, it tends to oppose oncotic pressure by pushing fluid out of the capillaries into the surrounding tissue. It is higher on the arterial side
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What is colloid osmotic pressure? Describe its effect on circulation/blood vessels.
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Oncotic pressure. A form of osmotic pressure exerted by proteins which when high, attracts water.
With regard to circulation, it tends to oppose hydrostatic pressure by drawing in fluid from surrounding tissues into the capillaries. It is higher on the venous side. |
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What water related forces/pressures can cause oedema and how?
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Hydrostatic force - increased water and Na in the blood vessels (from RAAS etc) means greater force, which means more fluid is pushed into the tissues.
Oncotic/colloid osmotic force - lack of proteins such as in renal failure or liver disease causes reduced hydrostatic force, so that fluid is not brought back into capillaries from tissues |
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How many >65 have Atrial Fibrillation?
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2-5%
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Aetiology of Atrial Fibrillation?
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Heart disease. e.g. mitral valve disease, HT heart disease, IHD, thyrotoxicosis, cardiomyopathy
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What is the mechanism of Atrial Fibrillation?
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High atrial pressure causes stretching which causes damage and fibrosis which promotes re-entrant circuits. >6 multiple wandering wavelets will cause AF.
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What are the symptoms of Atrial Fibrillation?
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Rapid irregular palpitations, fatigue, if heart failure is developing = dyspnoea, ankle swelling and abdominal distension
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What are the signs of Atrial fibrillation?
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Hr and pulse are rapid and irregularly irregular, pulse rate may be lower than heart rate if hr is too fast for cardiac filling, cardiac failure signs may be present
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How is Atrial fibrillation diagnosed?
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using an Electrocardiogram/ECG. P waves are absent and the baseline is finely undulating at 350-600 bpm. Irregular QRS complexes present with an average of 150-200 bpm.
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What are the complications of Atrial fibrillation?
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heart failure (VT)
embolism (feeble contraction allows pockets of stasis which thrombose and can embolise) |
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How is Atrial fibrillation treated with drugs?
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control the rate:-
digoxin increase Ca to increase force verapamil blocks voltage Ca Channels Beta blockers decrease the SR Ca uptake and the voltage Ca opening Revert and prevent future AF:- sotalol (beta receptor and potassium channel blocker) amiodarone (similar to a beta receptor and potassium channel blocker) flecainide (blocks Na channel, slows AP) Anticoagulate:- Aspirin if rheumatic valve disease present give warfarin |
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How is Atrial fibrillation treated with devices?
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DC-cardioversion, where a shock to the praecordium is designed to revert the arrythmia
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How is Atrial fibrillation cured with surgery?
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Maze procedure - incisions to block re-entry circuits are made
AVN ablation with pacemaker implantation (if drugs have failed to decrease the VT) |
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t/f... the uterus low resistance vascular network contains approx 1 litre of blood at full term
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true
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t/f... progesterone induces vasodilation
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true. this occurs in pregnancy
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t/f... the only organ not to have increased blood flow in pregnancy is the brain
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true, kidney, skin, liver increase ~60%, while breast increases 200% and uterine increases 20 times
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t/f... women are prone to fainting in pregnancy
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true. low BP from progesterone induced vasodilation occurs
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When is BP the lowest in pregnancy?
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In middle trimester, due to the vasodilation from progesterone
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How much does plasma volume increase in pregnancy?
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40%
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t/f... their is increased RAAS activation in pregnancy
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true. this leads to an crease in volume, but progesterone counters the vasoconstrictive effects
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What happens to red cell mass in pregnancy?
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increases 18-20%, but as plasma increase by 40% this causes a physiological anaemia (~105-140 g/L at term)
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t/f... cardiac reserve is decreased in pregnancy
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true. an increase in CO, HR, SV and plasma volume means the heart is already working closer to its maximal capacity, and so has more difficulty increasing with effort
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t/f... pregnant women on cardiovascular medications are under no more risk of congestive heart failure than non-pregnant women
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false. pregnant women with abnormal hearts, or being treated with drugs that increase HR, drop the BP or increase blood volume are more prone to CHF
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t/f...raised jugular venous pressure is always indicative of a pathological process
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false. If patient is not positioned properly on inspection it can be raised, and it is also raised in pregnancy from 20 weeks onwards
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How many people with rheumatic heart disease have no history of a a documented episode of rheumatic fever?
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50%
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What % of people with ARF (Acute Rheumatic Fever) will develop basal ganglia involvement ie.g. chorea?
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10-15%
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What are 3 examples of cross reactivity that cause ARF?
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M-protein/cardiac myosin
membrane proteins/myocardial sarcolemma capsular hyaluronate/heart valve glyoprotein, hyaluonic acid in synovial jts |
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What is deposited into the vegetations in rheumatic heart disease?
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Immunoglobulin and complement, infiltrated by lymphocytes (mainly CD4 and cd8 T cells)
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t/f... patients with chronic RF have high titres of high affinity IgG anti-cardiac antibodies
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true
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What is the average duration of rheumatic Fever?
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3 months
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What bacteria are most likely to cause an infective endocarditis?
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>80% streptococci and staphylococci, many from normal flora
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t/f... infective endocarditis vegetations break off easily
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true, they can form emboli
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What are the initial symptoms of infective endocarditis?
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fever, anorexia, fatigue, anaemia, splenomegaly
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t/f... patients with infective endocarditis whould be placed on anticoagulation with heparin
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false, this is contraindicated (5.02 LT 8)
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What are the characteristics of the vegetations in infective endocarditis?
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bulky, irregular, friable, often composed of thrombotic debris, fibrin, inflammatory cells and organisms, found along closure lines of valve leaflets and on the chordae tendinae, causes destruction of the underlying cardiac tissues
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Describe the course of acute infective endocarditis?
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destructive, tumultuous, necrotising, ulcerative, invasive infection of a (frequently normal) heart valve with a highly virulent organism, leading to death within days to weeks. Resistant to antibiotics
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What % of people with Acute infective endocarditis die?
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50%, even with antibiotics and surgery
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Describe the course of subacute infective endocarditis?
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organisms of low virulence infect a previously abnormal heart (esp. deformed valves), causing an insidious, protracted course over weeks to months, if not treated. Patients usually recover with antibiotics.
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What host factors can predispose to infective endocarditis?
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neutropaenia, immunodeficiency, malignancy, therapeutic immunosuppression, diabetes, alcohol, IV drug use, cardiac and vascular abnormalities, poor oral hygiene
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What is the major causative organisms in infective endocarditis of a previously normal structured heart?
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streptococcus viridans (50-60% of all cases), a highly virulent organism, a major cause of Acute IE
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What bacteria is likely to be the cause of infective endocarditis in an IV drug user?
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streptococcus aureus
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What bacteria is likely to be the cause of infective endocarditis in a patient with a prosthetic valve?
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staphylococcus epidermidis
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What valves are most commonly associated with infective endocarditis?
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aorta and mitral
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What is a major cause of subacute infective endocarditis?
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streptococcus aureus (10-20% of all cases), commonly found on skin
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What % of all cases of infective endocarditis are caused by s.aureus?
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10-20%
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What group of people are more likely to have right-sided heart involvement in infective endocarditis?
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IV drug users
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What is a major complication related to infective endocarditis?
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systemic emboli due to the friable nature of the vegetations, causing infarcts, which can become septic infarcts
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What is different about the vegetations in acute and subacute infective endocarditis?
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acute = necrotising, ulcerative, more severe
subacute = granulation tissue at their bases, suggesting healing and chronicity, fibrosis, calcification over time |
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t/f... SLE causes endocarditis
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true, called LSE, characterised by small-medium vegetations on either/both sides of the valve leaflets
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What are the clinical features of acute infective endocarditis?
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Rapidly developing fever , chills, weakness, lethargy, new valvular regurgitation on auscultation
Can also cause haematuria, albuminuria, renal failure Uncommon - Petechiae, splinter haemorrhages, Janeway (nontender, palm) lesions, Osler (tender, digits) nodes |
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What are the clinical features of subacute infective endocarditis?
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Mild fever, fatigue, loss of weight, flu-like syndrome, new valvular regurgitation on auscultation
Can also cause haematuria, albuminuria, renal failure. Uncommon - Petechiae, splinter haemorrhages, Janeway (nontender, palm) lesions, Osler (tender, digits) nodes |
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t/f... adults with abnormal hearts/valves should be placed on continual prophylactic antibiotics to prevent infectiveendocarditis
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false, it is only needed in the young who have had a previous ARF, or prophylactically given a few hours prior to an invasive procedure to prevent
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