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Final Prep > 1 > Flashcards

1 Flashcards

1
Q

Calcified pleural plaques seen on CXR

A

Asbestos Exposure

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2
Q

Ganglion

A

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

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3
Q

Normal Ejection Fraction?

A

60-70%

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4
Q

Common side effect of amplodipine?

A

Peripheral oedema

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5
Q

Why is atorvastatin better then simvastatin?

A

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.

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6
Q

Treating angina

A

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.

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7
Q

Cholangitis triad

A

RUQ pain + rigors + jaundice

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8
Q

Initial screening test for HepC?

A

Anti HepC Ab, followed by HepC RNA PCR and genotyping to identify specific strain and plan antiviral therapy

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9
Q

Who should be monitored for HCC and how?

A

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

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10
Q

Haemochromatosis is associated with which polymorphism?

A

C282Y polymorphism of HFE gene, above about 80% affected

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11
Q

What is the relationship between IBD and PSC?

A

80% of PSC patients will have IBD, of which the majority (80%) will have UC, and the minority will have CD

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12
Q

A VIPoma will feature a triad of:

A

Diarrhoea, hypokalaemia, hypercalcaemia

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13
Q

How do the King’s college criteria for liver transplantation differ depending on aetiology?

A

For Paracetamol OD - will use PT

For all other aetiologies will use Bilirubin

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14
Q

CCK is produced by?

A

Small intestine. Will increase gastric emptying and stimulates contraction of the gallbladder

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15
Q

Paget’s disease

A

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

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16
Q

Clinical features of Paget’s disease of bone

A

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)

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17
Q

Treating Paget’s disease of bone

A

Do blood chemistry looking at Ca and ALP
Expect Ca and PO4 normal, ALP raised

Analgesia and bisphosphonates (alendronate

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18
Q

Pott’s Disease

A

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.

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19
Q

Tests - Liver Screen

A 
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
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20
Q

Haemochromatosis

A

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

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21
Q

Truelove and Witt Criteria for UC

A
  1. Bloody Stools per day: 6 plus at least 1 systemic feature (sev)
  2. Pulse: 90 (sev)
  3. Temperature: 37.8 (sev)
  4. Hb: No anaemia, >11.5 (mild-mod) ; anaemia (sev)
  5. ESR: 30 (sev)
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22
Q

The septic 6 - management of sepsis

A

Give 3 take 3

Take –> Lactate; Cultures; Urine
Give –> Fluids; Oxygen; Antibiotics

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23
Q

Blood transfusion threshold

A

NICE recommend a Hb of

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24
Q

Platelet transfusions

A

Clinically significant bleeding and platelet count below 30 * 10^9; usually single dose transfusions.

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25
Q

Thinking gallstones?

A

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

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26
Q

Positive troponin indicates (3)

A

Acute Coronary Syndrome, PE, renal failure

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27
Q

How to do troponin?

A

If highly sensitive assay time period is 3 hours, with standard 12 hours

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28
Q

PE score?

A

Well’s Score (>6 high probability), 3 points for clinical impression

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29
Q

PE on ECG

A

S1Q3T3 (but only sinus tachycardia most common, and absence of lung findings on examination)

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30
Q

Angina - key to history

A

Relationship to effort!

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31
Q

DDx Angina

A

IDH, AS, severe pulmonary HTN

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32
Q

Aortic Dissection vs MI

A

AD instantaneous severe pain radiating to back, MI comes on in minutes and is accompanied by sweating, N&V

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33
Q

Canadian CV Society grading of angina

A

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

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34
Q

Causes of secondary HTN

A

Renal (RAS, parenchymal); Endocrine (excess steroid, phaeochromocytoma); coarctation; NSAIDs; COCP

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35
Q

Investigating High Blood Pressure

A

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

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36
Q

Treating HTN

A

ACD - ACEi; Ca channel blockers; Diuretics
White A ± C ± D
Black or >50 –> C ± A ± D

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37
Q

B blockers in HTN

A

Reduce HR and BP by antagonising adrenergic signalling. Long term benefit if LV dysfunction (bisoprolol, carvedilol)

38
Q

SE B blockers

A

lethargy, impotence, cold peripheries, exacerbation of DM

39
Q

CI to B blockers

A

Asthma, caution in PVD

40
Q

Why do nifedipine and amlodipine need B blocker co prescribed?

A

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.

41
Q

SE Ca channel blockers?

A

Ankle swelling, flushing. Can worsen HF

42
Q

Malignant HTN

A

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

43
Q

Hypercholeserolaemia boundry

A

total cholesterol 5.2 mmol/L

44
Q

Lipids in atherosclerosis

A

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

45
Q

Non ACS causes of troponin raise

A 
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
46
Q

Investigating suspected ACS

A

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

47
Q

Immediate treatment of ACS

A

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)

48
Q

Long term treatment of ACS

A

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

49
Q

Immediate management of STEMI

A 
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

50
Q

Coronary calcium score

A

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

51
Q

Cardiac nuclear imaging

A

Myocardial perfusion scintigraphy (SPECT). Technicium 99 IV taken up in tissue proportionally to blood flow. Detected by gamma camera to create 3d model

52
Q

Cardiac MRI

A

good for showing heart structure incl previous MI, useful esp if concerns about eposure to CT radiation. Concerns if claustrophobia or renal failure.

53
Q

Managing angina

A

Medical therapy looking at risk factors - manage lifestyle, aggressively HTN, statins, aspirin

54
Q

Managing HTN - ideal BP

A
55
Q

Prescribing nitrates for angina

A

Highly effective, but require a 12-14h/day nitrate free period to avoid tolerance developing. GTN, nicorandil, isosorbide mononitrate

56
Q

CABG and types of grafts

A

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.

57
Q

Types of aortic dissection

A

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

58
Q

Marfan’s Syndrome Clinically

A

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

59
Q

Pericardial tamponade

A

Hypotension (pulsus paradoxus) and raised JVP

60
Q

Managing aortic dissection

A

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

61
Q

Pathophysiology of Heart Failure

A

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.

62
Q

New York Heart Association Classification of Heart Failure

A

I - No breathlessness, annual mort

63
Q

Presentation of acute HF

A

Largely synonymous with LHF, sudden failure to maintain CO with insufficient time for compensatory mechanisms to develop. Acute pulmonary oedema. Admission and inpatient management

64
Q

Presentation of chronic HF

A

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.

65
Q

Systolic Heart failure

A

Main problem is heart not squeezing properly. Reduced EF and increased intracardiac dimentions.

66
Q

Diastolic Heart Failure

A

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.

67
Q

Symptoms of Heart Failure

A

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

68
Q

Aetiology of HF

A

Arrythmia - esp AF
Drug - non-compliance, fluid retaining drugs, NSAIDs
Anaemia
Infection
Thyroid
Ischaemia
Any lung condition causing pulmonary HTN (eg COPD, PE, fibrosis)

69
Q

Investigating suspected HF

A

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

70
Q

Treating Heart Failure

A

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

71
Q

Complicaitons of Heart Failure

A

VTE and PE, AF, progressive pump failure, ventricular arrythmias, sudden cardiac death

72
Q

Young person with AS (40s and 50s)

A

Think congenital - bicuspid AV

73
Q

Symptoms of AS

A

ASD

Angina (2 year prognosis)
Syncope (1 year prognosis)
Dyspnoea (1/2 year prognosis)

74
Q

Causes of aortic regurg

A

MARRIS

Marfans
Ankylosing spondylitis
Rheumatic fever
Rheumatoid arthritis
Infective endocarditis
Syphilis/SLE
75
Q

Managing AS

A

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

76
Q

Fun signs in AR

A

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
77
Q

Investigations for AR

A

CXR - heart size, aneurysm
ECG - LVH
Echo - LV function, severity, problem with root or valve?

78
Q

Treating AR

A

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)

79
Q

Signs of mitral stenosis

A

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

80
Q

Causes of mitral stenosis

A

Rheumatic fever (99%)
SLE
Atrial Myxoma

81
Q

Rheumatic Mitral stenosis

A

Rigid, thickened leaflets, fused commisures, shortened chordae

82
Q

Treating Mitral Stenosis

A

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)

83
Q

Barlow’s Syndrome

A

Mitral valve prolapse during ventricular systole. Click heard in early mid systole, MR

MVP with MR predisposes to bacterial endocarditis

84
Q

Mitral Regurgitation Causes

A

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.

85
Q

Managing MR

A

TTE to establish presence, mechanism, severity, monitor LV function
CXR - ABCDE
ECF - AF, LVH

Diuretics and ACEi.
Repair or replacement if required

86
Q

Causes of dliated cardiomyopathy

A

Toxins - alcohol
Endocrine - hypothyroid, thyrotoxicosis, phaeochromocytoma
Infection - coxsackie, trypanosoma (Chagas’ disease)
Inflitritive - sarcoid, haemochromatosis, iron overload
Genetic - familial DCM, muscular dystrophies

87
Q

Managing dilated cardiomyopathy

A

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

88
Q

HOCM

A

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

89
Q

Restrictive cardiomyopathy

A

Rigid, stiff and thick myocardium, usually 2* to infiltration or fibrosis. Amyloid (eg MM, paraproteinaemia, chronic inflammatory conditions, sarcoid, scleroderma)
Usually refractory to treatment

90
Q

Pericarditis on ECG

A

Saddle shaped ST elevation, but PR segment depression is more specific.

Final Prep (19 decks)

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