5. Coronary Heart Disease Flashcards

1
Q

Non modifiable risk factors for Atherosclerosis

A

Age, Male and FHx - CV event when less than 55

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2
Q

What is significant hypertension and what may there be evidence of at this stage

A

180/110, End organ damage dug as LVH, renal impairment or retinopathy

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3
Q

What is the def. of renal impairment for pts with hyperT

A

CKD with elev. Of Cr, or may have protienuria and haematuria upon dipstick

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4
Q

When should pts be treated for hyperT

A

> 140.900 in clinic, >135.85 at home or 180/110

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5
Q

Mx for Hyper T, including resistant hypertension

A

ACEi or ARB if <55
CCB (amlodipine) if >55 or afro caribbean,
2nd line thiazide diuretic ( after first two both given)
3rd line A or BB blocker or spironolactone if K if K is low

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6
Q

Risk scoring tool for risk of development of CVD in 10 years

A

QRISK3
Framingham- not for use in elderly or diabetics

Assign- developed in Scotland, includes SES

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7
Q

When do we consider referral to lipid clinic

A

Total cholesterol >7.5 in assoc with family history of premature CAD

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8
Q

Should medication or lifetyle changes be given for hyperlipidaemia first

A

Lifestyle and diet

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9
Q

1st line Mx for hyperlipidaemia and cholesterol reduction aim

A

Statin, 40% of non hdl cholesterol

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10
Q

Sx of T2DM

A

polydipsia, uria, weight loss, recurrent infections

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11
Q

How many hba1c reading needed for T2DM diagnosis and what is the treshold

A

2 times abnormal if no Sx, 1x if Sx present
48

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12
Q

Fasting BG level for T2Dm`

A

More than 7

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13
Q

What is the threshold for pre-diabetes

A

OGTT 7.8-11.1, FG 6.1-6.9

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14
Q

Risk factors for T2DM apart from the main two

A

Main two are FHX and obesit
HIV, anti-psychotics, SLE and RA, psoriasis, long term CTS

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15
Q

Atypical pain in NSTEMI

A

Upper abdomen pain

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16
Q

Sx of NSTEMI

A

Chest pain, back, jaw pain, sweating, N+V, dyspnoea, palpitations, stomach pain

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17
Q

Signs of NSTEMU

A

Levine;s, tachy or brady, pulm oedema if HF developed, hyper or hypo T, diaphoresis

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18
Q

Diagnostic criteria for NSTEMi

A

Cardiac biomarkers > 99th percentile +/- :
Sx relating to ischaemia, new ECG changes like ST ot T wave changes, or LBBB on 12 lead, Q waves on ECG, new RWMA on echo or loss of viable myocardium

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19
Q

Mx for NSTEMI in hosp

A

Analgesia, anti-platelets including loading dose aspirin and then maint. dose, ticagrelor, clopi or prasugre for 12 mol , and anticoag like LMWH eg. fonda

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20
Q

When should PCI be used for NSTEMI

A

Within 72 hrs of presentation

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21
Q

What other drugs can be used 24 hrs of hospitl and early following AMI

A

Acei/BB and anti-angiinal for Sx benefit

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22
Q

What is dressler’s sx

A

A comp of NSTEMI - Inflm process where pt gets pericarditis and inspir chest pain post MI

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23
Q

Complications of NSTEMI

A

Death, arrhythmia, rupture, tamponade. HF, Valve disease, Aneurysm of ventrical ( sever LV dysfx and HF), Dressler’s, embolism, reccurence

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24
Q

Mx fo NSTEMI long term

A

DAPT, sec prev- chol, BP, BM
Lifestyle
Cardiac rehab

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25
How does plaque formation lead to MI
Plaque rupture or erosion leads to inflmaatory cascape or thrombus formtn, leading to coronary thrombosis
26
Where is the pain in stemi
retrosternal
27
Signs of STEMI
unwell, pallor, sweating, breathless, in pain, tachyc, bradyc (in inferior STEMI due to reduce AV node supply), clammy, could to touch, hyper/hypoT, new murmur, HF signs
28
Autonomic features in STEMI
pallor, diaphoresis, n+v, lightheadness, feeling of anxiety
29
What heart defects can STEMi cause
Mitral valve defect or VSD
30
Ix for STEMI
12 lead ECG
31
how many leads must have ST elevation to have STEMI
2 contigous leads with ST elevation of >=2.5mm in V2-V3 in men less than 40yo, > 2 in men >=40yo, >1.5 in women >1mm in all other leads
32
evolution of ST changes in STEMI
ST elevation, then depressed R wave and development of Q wave in hours, T wave inversion and Q wave depening days 1-2, ST normalization and T wabe inversion days later, and ST and T normal weeks later, but Q wave persists ( if no timely revasc)
33
what are these leads and what supplies them Lat Inf Anterior/septal Lat
I and aVL, V5 and V5: LAD II,II and AVF: RCA V1-V4: Lcx
34
35
What is observed in inferior MI
ST elevation in II, III, aVF wirh reciprocal changes (ST depression in I and aVL0
36
Tx for STEMI
Oxygen if hypoxic, morphine for pain and anxiety, nitrates for ischaemic pain, antiplately (aspirin + clopi/prasugrel/ticagrelor)
37
Post stemi care
Monitoring for vent aneurysm, echo for cardiac fx, BB + Acei+ aspirin + p2Y12 inhibitor, statin for sec prevention, hypert management, diabetets management and smoking cessation
38
What GI causes can result in chest pain
oesophageal reflux, peptic ulcer, pancreatitis, gallstones
39
If chest pain is worse lying down, what is it likely to be
GI cause
40
Signs in angina
Murmur, anaemia, xanthelesma etc.
41
Ix for angina
Blood tests: FBC to exclude anaemia UnE for normal renal fx Lipids as risk factor Glucose, Hb A1c for Diabetes 12 lead ECG- but often normal for angina Can do CTCA for further inverstigation
42
What makes angina worse
Exertion, cold weather, walking into wind
43
When to refer to cardiologists
Ongoing, limiting anginal Sx despite tx with appropraite drugs High risk indv- recent onset of Sx (<3 mo), diabetes, strong FHx, likely familial hypercholestroleamis, HGV/bus driver, prev MI
44
Further Ix for angina
CTCA first line Exercise tolerance test or adenosine/dobutmaine with imaging (Echo/CMRI/myocardial perf scan)
45
Management of angina
Intensive lifestyle intervention as always Drug therapy- sub-lingual GTN during episode, Aspirin, atrovastatin, BB and CCB as fits line, Acei or ARB for hyperT Nicorandil as second line
46
3 different levels of BP in clinic and ABPM and how to treat
140/90 or 135/85 APBM- check BP every 5 years 179/119 clinic, offer ABPM or HBPM of not tolerated, and inv for target organ damage, assess CV risk. If ABPM 149/94, Drug treatment can be considered . If 10 year CVD risk more than 10%, discuss starting drug treatment . If less than 10, only consider treating if under 60 180/120 or more in clinic , refer same day specialist review if retinal haemorrhage or papiloedema, life threatening sx or suspected pheochromocytoma. If not, assess tarbet organ damage asap and start drugs immediately if present. If not, repeat clinic BP within 7 days or monitor using ABPM and review within 7 days. If 150/95 then consider specialist eval of sec causes if <40yo. Treat and lifestyle for pts of all ages
47
Consequences of papillary muscle rupture and which kind of infarction is it more common in
Infero-posterior infarction May have Acute MR- early to mid systolic murmur
48
How quickly after MI can ventricular septal defect occur and what are the feature
First week . May have acute HR assoc with pan systolic murmur
49
Sx of left ventricular free wall rupture
Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds
50
How fast can pericarditis occur post MI and sx
The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.
51
Antiplatelet therapy for STEMI
Immmediately 300mg aspirin Pasugrel if PCI, or UFH + bailout inhibitor -- Ticagrelor following fibrinolysis if no PCI, antithrombin with fibrinulysis Swap for clopi if pt is on anticoag/ high bleed risk
52
Antiplatelet therapy for NSTEMI
Aspirin immediately, or fonda if no PCI planned. If PCI (high 6 mo mortality), give pasugrel or tica, and UFH
53
Causes of secondary hypertension
Hyperaldosteronism (Conn Sx) Cushing's Renovasc disease CKD Phaechromocytoma OSA Coarctation of Aorta- more common in males
54
What is the most common cause of Conn's sx
Bilat idiopathic adrenal hyperplasia Adrenal adenoma Uni hyperpalsia, Famililial hyperaldo Adrenal carcinoma
55
Fx of Conn's apart from hyperT
HYPOKALAEMIA- muscel weakness
56
Mx of Conn's
adrenal adenoma: surgery (laparoscopic adrenalectomy) bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
57
Causes of Cushing's syndrome
iatrogenic: corticosteroid therapy ACTH-dependent causes Cushing's disease (a pituitary adenoma → ACTH secretion) ectopic ACTH secretion secondary to a malignancy ACTH-independent causes adrenal adenoma
58
Finding of Cushing's
A hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance. Ectopic ACTH secretion (e.g. secondary to small cell lung cancer) is characteristically associated with very low potassium levels.
59
Cushing's test
Overnight (low-dose) dexamethasone suppression test first-line to test for Cushing's syndrome- morning cortisol spike will NOT be supressed 24 hr urinary free cortisol bedtime salivary cortisol
60
How to differentiate ACTH and non-ACTH dependent cushing
9am and midnight plasma ACTH (and cortisol) levels. If ACTH is suppressed then a non-ACTH dependent cause is likely such as an adrenal adenoma High dose dexa test- will supress cortisol and ACTH in Cushing's disease Will not supress cortisol and ACTH in ectopic ACTH Sx Will supress ACTH but not cortisol in Cushing's due to other causes like adrenal adenoma
61
What drug is used as antihypertensive in patients with CKD especially when GFR falls to below 45
Furosemidee
62
Fx of Renal Artery Stenosii
hypertension chronic kidney disease 'flash pulmonary oedema'
63
Features of Phaeochromocytoma and what Ix and Mx
Catecholamine secreting tumour Features are typically episodic hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety Ix include 24 hr urinary collection of metanephrines Mx includes a and then B blocker
64
What is Stage 2 hypertension and who in this group should be offered treatment
>=150/95, offer drug treatment regardless of age
65
When should hypeerT pts have specialist referral to exclude sec causes
Any hyperT pt below 40 YO
66