1 Flashcards
Calcified pleural plaques seen on CXR
Asbestos Exposure
Ganglion
Degenerative cysts from an adjacent joint or synovial sheath commonly seen on the dorsum of the wrist or hand and dorsum of foot
May TRANSILLUMINATE
50% will disappear spontaneously.
Aspiration with hyaluronic acid, or resection, are treatments of choice
Normal Ejection Fraction?
60-70%
Common side effect of amplodipine?
Peripheral oedema
Why is atorvastatin better then simvastatin?
Atorvastatin has been shown to reduce LDL levels by over 50% and is therefore preferable to simvastatin which has a worse LDL profile. It has come off patent in the last two years and has since gained prominence.
Treating angina
B blocker + GTN spray PRN / subligual (or if prophylaxis is required long acting nitrates such as isosorbide mononitrate 20-40 mg but with at least 8 hours a day nitrate free so tolerance does not develop. Ranolazine is a new drug which which works on ADP to improve energy use in cardiac myocytes therefore reducing oxygen requirements.
Cholangitis triad
RUQ pain + rigors + jaundice
Initial screening test for HepC?
Anti HepC Ab, followed by HepC RNA PCR and genotyping to identify specific strain and plan antiviral therapy
Who should be monitored for HCC and how?
At risk groups include (EASL):
Cirrhosis patients - Child Pugh A, B, and C
All cirrhosis Patients awaiting liver transplant
Non-cirrhotic HBV patients with active inflammation or family history of HCC
Non-cirrhotic HepC patients with F3 or above
Haemochromatosis is associated with which polymorphism?
C282Y polymorphism of HFE gene, above about 80% affected
What is the relationship between IBD and PSC?
80% of PSC patients will have IBD, of which the majority (80%) will have UC, and the minority will have CD
A VIPoma will feature a triad of:
Diarrhoea, hypokalaemia, hypercalcaemia
How do the King’s college criteria for liver transplantation differ depending on aetiology?
For Paracetamol OD - will use PT
For all other aetiologies will use Bilirubin
CCK is produced by?
Small intestine. Will increase gastric emptying and stimulates contraction of the gallbladder
Paget’s disease
Osteitis deformans. Increased bone turnover associated with increased numbers of osteoblasts and osteoclasts with resultant remodelling, enlargement, deformity and weakness. 3% over 55 years of age.
XR - localised enlargement of bone. Patchy cortical thickening with sclerosis, osteolysis and deformity. Affinity for long bones, axial skeleton and skull
Clinical features of Paget’s disease of bone
Asymptomatic in 70%, deep boring pain deformity and enlargement. Typically pelvis, lumbar spine, skull, femur, tibia.
Complications - fractures, OA, high Ca, nerve compression, osteosarcoma (10 years, usually worsening bone pain)
Treating Paget’s disease of bone
Do blood chemistry looking at Ca and ALP
Expect Ca and PO4 normal, ALP raised
Analgesia and bisphosphonates (alendronate
Pott’s Disease
Spinal TB. Usually spread from an extraspinal source. Backache, stiffness of all back movements, pyrexia, night sweats and weight loss. Progressive bone destruction leads to vertebral collapse and gibbus (sharply angled spinal curvature).
Abscess formation leads to cord compression causing paraplegia, bowel and bladder dysfunction.
Tests - Liver Screen
HBV - HBsAg HCV - Anti HCV Ab CMV/EBV - Raised IgM levels Wilson's Disease - Caeruloplasmin Levels Haemochromatosis - Ferritin AI - ANA, anti-aLKM, ASA PSC - ANCA PBC - AMA
Haemochromatosis
Autosomal recessive
Homozygous for C282Y polymorphism
Liver cirrhosis, diabetes, arthritis, testicular failure, cardiomyopathy
Treat with venesection
Disorder of Fe overload
High ferritin
High transferrin saturations
HFE gene
Truelove and Witt Criteria for UC
- Bloody Stools per day: 6 plus at least 1 systemic feature (sev)
- Pulse: 90 (sev)
- Temperature: 37.8 (sev)
- Hb: No anaemia, >11.5 (mild-mod) ; anaemia (sev)
- ESR: 30 (sev)
The septic 6 - management of sepsis
Give 3 take 3
Take –> Lactate; Cultures; Urine
Give –> Fluids; Oxygen; Antibiotics
Blood transfusion threshold
NICE recommend a Hb of
Platelet transfusions
Clinically significant bleeding and platelet count below 30 * 10^9; usually single dose transfusions.
Thinking gallstones?
Confirm - USS. FBC. CRP. LFT. AMYLASE
Treat - IV fluids, IV Abx, analgesia (diclofenac oral or if very severe iv or per rectum)
Monitor - BP, HR, UP
Refer - Surgery, laparoscopic cholecystectomy
Positive troponin indicates (3)
Acute Coronary Syndrome, PE, renal failure
How to do troponin?
If highly sensitive assay time period is 3 hours, with standard 12 hours
PE score?
Well’s Score (>6 high probability), 3 points for clinical impression
PE on ECG
S1Q3T3 (but only sinus tachycardia most common, and absence of lung findings on examination)
Angina - key to history
Relationship to effort!
DDx Angina
IDH, AS, severe pulmonary HTN
Aortic Dissection vs MI
AD instantaneous severe pain radiating to back, MI comes on in minutes and is accompanied by sweating, N&V
Canadian CV Society grading of angina
Grade 1 - strenous physical activity
Grade 2 - ordinary physical activity (stairs, hill)
Grade 3 - marked limitation on ordinary physical activity (1 flight of stairs)
Grade 4 - any activity / rest
Causes of secondary HTN
Renal (RAS, parenchymal); Endocrine (excess steroid, phaeochromocytoma); coarctation; NSAIDs; COCP
Investigating High Blood Pressure
U&E and Urine Dip - creatinine, haematuria, proteinuria
Hypokalaemia without diuretics suggests mineralocorticoid excess.
24h blood pressure monitor or repeat measurements
Examine for coarctation
Urine catecholamines
Asess for end organ damage - LVH (ecg, echo), U&E, fundoscopy
Treating HTN
ACD - ACEi; Ca channel blockers; Diuretics
White A ± C ± D
Black or >50 –> C ± A ± D
B blockers in HTN
Reduce HR and BP by antagonising adrenergic signalling. Long term benefit if LV dysfunction (bisoprolol, carvedilol)
SE B blockers
lethargy, impotence, cold peripheries, exacerbation of DM
CI to B blockers
Asthma, caution in PVD
Why do nifedipine and amlodipine need B blocker co prescribed?
Can cause reflex tachycardia. CI in hearft failure, in angina only those with heart slowing properties, if no negative chronotropic effects B blocker must be co-aministered.
SE Ca channel blockers?
Ankle swelling, flushing. Can worsen HF
Malignant HTN
Severe uncontrolled HTN –> eg 220/120 + headache, confusion, acute end organ damage like cerebral bleed, ARF, dissection
Malignant HTN is triad of HTN, high grade retinal changes and progressive renal failure. Untreated 1 year 50% mortality
Hypercholeserolaemia boundry
total cholesterol 5.2 mmol/L
Lipids in atherosclerosis
Total cholesterol >5.2 mmol/L x2 risk of CAD, at 7.4 mmol/L x 4 risk
Reducing tChol by 20% reduces coronary risk 10%
LDL:HDL ratio >4 indictates high risk
Non ACS causes of troponin raise
CRF/ARF Severe CCF Hypertensive crisis Tachyarrythmias PE Pulmonary HTN Aortic dissection Aortic valve disease Inflitration - amyloid, sarcoid, iron (haemochromatosis) Drug - 5-FU, herceptin, adramycin Rhabdomyolysis
Investigating suspected ACS
Serial ECGs @ 1, 2, 3, 4, 6, 12, 24 hours or if pain chages
CXR to look at heart size
Biomarkers - Trop at 12 (or 3h if sensitive assay), CK, AST
Hb - look for anaemia
WCC + Inflammatory markers
Cholesterol
Renal function
Immediate treatment of ACS
Morphine (pain, anxiety)
Aspirin (chewed) 300mg + Clopidogrel 300mg dual antiplatelet therapy (alternatives include prasugrel).
B blocker - IV to reduce resting HR to 50, mild HF is not a CI
SC LMWH
High dose statin (eg atorvastatin 80mg)
Long term treatment of ACS
Angiography within 72h
Dual antiplatelet therapy for 1 year
Agressive risk management using lifestyle modifications, antihypertensives, statins,
If severe LV impairment post MI think ICD or CRT
Immediate management of STEMI
M (morphine) O (oxygen) N (nitrates) A (300mg aspirin chewed) \+ PCI (gold standard, thrombolysis with tPA is acceptable if PCI not possible, but transport must be done within 24h)
+ B blocker, ACEi, diuretic for pulmonary oedema if required
Coronary calcium score
CT scanner is used to detect and measure amount of Ca in coronary arteries. Does not inform about narrowings but the likelihood of them being present. Good to rule out (high NPP), high scores will often warrant angiography
Cardiac nuclear imaging
Myocardial perfusion scintigraphy (SPECT). Technicium 99 IV taken up in tissue proportionally to blood flow. Detected by gamma camera to create 3d model
Cardiac MRI
good for showing heart structure incl previous MI, useful esp if concerns about eposure to CT radiation. Concerns if claustrophobia or renal failure.
Managing angina
Medical therapy looking at risk factors - manage lifestyle, aggressively HTN, statins, aspirin
Managing HTN - ideal BP
Prescribing nitrates for angina
Highly effective, but require a 12-14h/day nitrate free period to avoid tolerance developing. GTN, nicorandil, isosorbide mononitrate
CABG and types of grafts
Usually bypass, however off pump method exists which avoids stopping the heart.
Vein grafts - leg saphenous veins. Annual failure rate 8%. Patients advised graft expected to last no more than 10 years. If failure, can be managed medically, PCI or rarely (higher risk) repeat CABG)
Arterial grafts - most commonly LIMA (left anterior mammary artery prev. internal thoracic artery), usually mobilised to LAD.
Types of aortic dissection
A & B
A –> point of intimal tearing in ascending aorta. The dissection tracks distally and proximally to involve the descending aorta, aortic valve apparatus and pericardium
Consequences include stroke (occlusion of carotid artery), MI (occlusion of coronary artery), tamponade (rupture into pericardium), AR (stretching of valve), rupture.
B –> tear in descending aorta, typically after left subclavian artery. Rare to propagate proximally. Consequences include RF (renal artery occlusion), gut ischaemia (occlusion of coeliac plexus or mesenteric artery) and lower limb ischaemia (involvement of iliac arteries.
Occlusion of the spinal arteries can lead to paraparesis
Marfan’s Syndrome Clinically
1/5000 AD 70% fibrillin1 gene chr 15
Eyes –> Lens dislocation 50% (slit lamp examination), myopia, retinal detachment
Narrow high arched palate
Pectus excavatum
Tall and lanky, arm span:height >1.05, arachnodactyly, joint hypermobility
Aortic disease! Progressive root dilatation leading to AR and aortic dissection. B blockers and prophylactic surgery
Mitral disease! Prolapse and regurg
Backache can be caused by dural ectasia
Pericardial tamponade
Hypotension (pulsus paradoxus) and raised JVP
Managing aortic dissection
Immediately lower BP hourly mortality rate 2%. Cardiothoracic tertiary unit
Type B –> agressive BP control, surgery if life threatening complications. False lumen can clot and stabilize
Pathophysiology of Heart Failure
Cardiac damage –> Decreased CO (digoxin) –> Neuroendocrine activation (B blockers & ACEi) –> Increased peripheral resistance (vasodilators - nitrates and hydralazine) —> Decreased CO and so on
While this is taking place, fluid retention develops (diuretics)
Neuroendocrine activation - RAS & catecholamines, which provoke Na&H2O retention thus increasing cardiac afterload which decreases CO
Cytokine activation - hallmark of advanced HF incl IL-6 and TNFa. This underlines anaemia of chronic disease and progressive cachexia.
Ventricular dilatation - caused by imparied systolic function and fluid retention making heart mechanically inefficient.
New York Heart Association Classification of Heart Failure
I - No breathlessness, annual mort
Presentation of acute HF
Largely synonymous with LHF, sudden failure to maintain CO with insufficient time for compensatory mechanisms to develop. Acute pulmonary oedema. Admission and inpatient management
Presentation of chronic HF
Largely synonymous with RHF, where change is gradual and compensatory mechanisms are present (but most likely co-exists with LHF). Patients although unwell can be managed in an outpatient basis.
Systolic Heart failure
Main problem is heart not squeezing properly. Reduced EF and increased intracardiac dimentions.
Diastolic Heart Failure
Impaired relaxation of the LV. LV relaxation in an active process requiring energy, and when imparied not enough blood reaches the LV. EF is often preserved, but not enough blood gets there. Common in elderly, HTN, high BMI.
Echo can be normal. Clinically and biomarkers will tell story.
Symptoms of Heart Failure
Left:
SoB, worse lying down, bending over, PND (SoB wakes you up at night, classically open window to catch breath)
Tachypnoea, tachycardia, 3HS (gallop rhythm), inspiratory creps.
Right: Fluid retention (legs, sacrum). Raised JVP and pitting oedema.
CCF:
Cardiomegaly, cardiac cachexia, 2* mitral/tricuspid regurg
Aetiology of HF
Arrythmia - esp AF
Drug - non-compliance, fluid retaining drugs, NSAIDs
Anaemia
Infection
Thyroid
Ischaemia
Any lung condition causing pulmonary HTN (eg COPD, PE, fibrosis)
Investigating suspected HF
ECG - look for evidence of previous MI, LVH, TW changes including asymmetrical widespread TWI (cardiomyopathy)
24h ECG - arrythmias
CXR - ABCDE
Biochemistry - BNP, electrolytes and renal function, FBC (anaemia), TFTs
Echo - if normal does not rule out HF, EF, valvular disease
Treating Heart Failure
General - low salt and fluid diet, daily weight
Diuretics - symptomatic treatment (watch out for low K). Give K sparing diuretics such as spironolactone or amiloride
ACEi - interupt maladaptive neuroendocrine responce, vasodilating and lowering BP. Check U&Es
B blockers - previously thought CI, now if started on stable patients and titrated slowly. Reverse catecholamines and downregulate agrenergic receptors.
Bisoprolol, carvedilol, metoprolol
Reduce pump failure and arrythmic sudden events
Digoxin - needs monitoring. Positive inotropic effect in sinus rhythm, symptomatic improvement and reduction in hospital admissions, but no mortality benefit.
CRT - in advanced HF, dyscoordinate ventricular contraction occurs - different parts contract at different time. Cardiac resynchronisation therapy + ICD improve outcomes
Complicaitons of Heart Failure
VTE and PE, AF, progressive pump failure, ventricular arrythmias, sudden cardiac death
Young person with AS (40s and 50s)
Think congenital - bicuspid AV
Symptoms of AS
ASD
Angina (2 year prognosis)
Syncope (1 year prognosis)
Dyspnoea (1/2 year prognosis)
Causes of aortic regurg
MARRIS
Marfans Ankylosing spondylitis Rheumatic fever Rheumatoid arthritis Infective endocarditis Syphilis/SLE
Managing AS
U&E - renal function important if surgery
Chol + Glucose - can be marker of CVD
FBC - anaemia
Monitor in absence of symptoms. Early valve replacement when symptoms do occur
Fun signs in AR
CDDQT
Corrigan's - visible carotid pulsations De Musset's - head bobbing Durozier's - back and forth murmur heard over femoral Quincke's - Nail bed pulsations Traube's - Pistol Shot Femorals
Investigations for AR
CXR - heart size, aneurysm
ECG - LVH
Echo - LV function, severity, problem with root or valve?
Treating AR
Medical - ACEi, diuretics may maintain LV function for years. Increasing LV dimentions and symptoms warrant replacement
Surgical - Midline sternotomy, replacement under vision., TAVI (transcutaneous AV implanation)
Signs of mitral stenosis
F>M
Malar flush
Signs of chronic HF (JVP, oedema)
AF
RV heave if 2* pulmonary HTN develops
Tapping apex beat (palpable S1) undisplaced if no MR
Low pitched, rumbling mid-diastolic murmur best heard with bell in L lateral position with opening snap
Causes of mitral stenosis
Rheumatic fever (99%)
SLE
Atrial Myxoma
Rheumatic Mitral stenosis
Rigid, thickened leaflets, fused commisures, shortened chordae
Treating Mitral Stenosis
Medical - diuretics, digoxin, warfarin
If uncontrolled (rare) mitral valvotomy (percutaneous balloon or open thoracotomy) or mitral valve replacement (usually mechanical as warfarin is already indicated on account of AF)
Barlow’s Syndrome
Mitral valve prolapse during ventricular systole. Click heard in early mid systole, MR
MVP with MR predisposes to bacterial endocarditis
Mitral Regurgitation Causes
Primary - intrinsic valve disease (rheumatic fever, chordal rupture, myxomatous degeneration, IE, papillary rypture 2* to ischamia and necrosis)
Secondary (functional) - caused by dilatation of the valve ring, esp in LV failure.
Managing MR
TTE to establish presence, mechanism, severity, monitor LV function
CXR - ABCDE
ECF - AF, LVH
Diuretics and ACEi.
Repair or replacement if required
Causes of dliated cardiomyopathy
Toxins - alcohol
Endocrine - hypothyroid, thyrotoxicosis, phaeochromocytoma
Infection - coxsackie, trypanosoma (Chagas’ disease)
Inflitritive - sarcoid, haemochromatosis, iron overload
Genetic - familial DCM, muscular dystrophies
Managing dilated cardiomyopathy
LV ± RV enlargement and global hypokinesia (as opposed to regional which makes IDH more likely)
Signs of HF
Most commonly excess alcohol
Medical - as heart failure
Cardiac transplantation is also an option
HOCM
Genetic disease causing abnormal myocardial structure (abnormal genes for myosin, actin, troponins cause myocyte disarray and interstitial fibrosis).
Gross hypertrophy results in small LV, diastolic HF, secondary MR
Septal hypertrophy results in LV outflow tract obstruction
B block / Ca channel block - treat exertional symptoms
Amiodarone / ICD - those in high risk of sudden death
Genetic counselling and screening
Restrictive cardiomyopathy
Rigid, stiff and thick myocardium, usually 2* to infiltration or fibrosis. Amyloid (eg MM, paraproteinaemia, chronic inflammatory conditions, sarcoid, scleroderma)
Usually refractory to treatment
Pericarditis on ECG
Saddle shaped ST elevation, but PR segment depression is more specific.
