Condition 1 Flashcards

1
Q

Definition for Acute coronary syndrome

A

ACS refers to any group of symptoms attributed to obstruction of the coronary arteries and also includes ST elevation MI, non-ST elevation MI, unstable angina

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2
Q

What does the history, ECG and troponin level of unstable angina show?

A

inc frequency of angina, unpredictable or at rest, chest pain < 20min

ECG - normal, ST depression or T wave changes

Troponin - normal

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3
Q

What does the history, ECG and troponin level of NSTEMI show?

A

chest pain > 20 minutes

ECG - ST depression or T wave inversion

Troponin - inc

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4
Q

What does the history, ECG and troponin level of STEMI show?

A

chest pain > 20 mins

NSTEMI + ST inc (>2mm in 2 consective chest leads or > 1mm in 2 limbs leads)

troponin - inc

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5
Q

how common is acute coronary syndrome

A

5/1000 for STEMI

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6
Q

What are the causes of acute coronary syndrome

A

atherosclerosis –> narrowing of coronary artery –> cardiac-oxygen needs are still met –> on exertion caric-oxgen needs no longer met –> MI –> chest pain –> stable angina

rupture of atherosclerotic plaque –> platelets stimulated –> thrombolysis –> more frequent and severe pain –> unstable angina

thrombus forms –> occlude artery –> myocardial infraction

if thrombus move and block downstream = NSTEMI/unstable angina

100% block = infract = STEMI

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7
Q

RF for ACS

A

same for atherosclerosis as well as outflow obstruction eg aortic stenosis or hypertension obstructive myopathy

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8
Q

symptoms for ACS

A

chest pain - central > 20 mins, often unresponsive to GTN radiates to neck and down left arm

nausea, sweating, dyspnoea, palpitations

elderly may present atypical symptoms of dyspnoea, fatigue, syncope, epigastric pain, pul oedema, acute confusion state, stroke, diabetic hyperglycaemic attacks, oliguria

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9
Q

signs on exam for ACS

A

distress, pallor, sweaty, tachycardia/bradycardia, BP changes, 4th heart sound

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10
Q

differential for ACS

A

stable angina (pain on exertion relieved by rest)

acute pericarditis (burning/sharp pain, radiate to neck/shoulders worse on coughing/breathing/lying down)

GORD (meals related)

aortic dissection (pain migrates down aorta, no ecg changes, syncope if associated with pericardial tamponade

myocarditis (stabbing chest pain, systemic symptoms)

PE - acute breathlessness, dizziness/syncope, pleuritic chest pain

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11
Q

further investigation for ACS

A

ECG - 20% normal, STEMI - STE, Q wave, new LBBB, tall T waves, NSTEMI - inverted T waves

biochemical markers

  • creatinine-kinase MB (not used now)
  • cardiac troponin most sensitive and specific, level inc within 3-12 hrs onset of chest pain)
  • myoglobin not v. specific , level inc within 1-4 hrs

CXR - cardiomegaly, PE, widened mediastinum (aortic rupture)

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12
Q

management for ACS

A

risk stratification -Thombolysis in Myocardial Infraction s (TIMI) score or Global Registry of acute coronary event (GRACE)

initial risk - determined by complications of the acute throbosis

long-term risk - defined by clinical risk factors eg age, prior-MI or bypass surgery, diabetes, HF etc

high risk pts - for progression to MI or death require urgent coronary angiography

low risk pts - manage with aspirin, clopidogreal, beta-blockers and nitrates

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13
Q

what are the immediate treatment for ACS

A

ROMANCE

reassure 
oxygen - maintain sats >94% 2-4L/min
Morphine 
Aspirin 
Nitrates - GTN spray or buccal etc 
C - clopidogrel 
Enoxaprin/Fondaparinux 
ECG
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14
Q

What are treatment for NSTEMI

A

beta blocker (atenolol)
fondaparinux
nitrates
high risk pts - GP IIb/IIIa antagonist, consider clopidogrel in additon to aspirin for 12 months
low risk pts - discharge if repeat troponin is -ve

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15
Q

definition of angina pectoris

A

a clinical syndrome of chest pain that accompanies periods of myocardial ischaemia

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16
Q

how common is angina pectoris

A

> 1.4 million ppl in the UK ie very common

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17
Q

causes for angina

A

atherosclerosis –> narrowing of coronary artery –> cardia-oxygen needs are still met –> on exertion cardiac - oxygen needs are no longer met –> MI –> chest pain –> stable angina

Rupture of atherosclerotic plaque platelets stimulated thrombolysis more frequent and severe pain Unstable Angina

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18
Q

symptoms of angina pectoris

A

chest pain - heavy/tight/gripping - central/retrosternal

pain radiating to jaw and left arm

can be precipitated by cold

SOB

Sweatiness

3 main features

1 - constricting discomfort in the front of the chest, arms, neck, jaw

2 - provoked by physical exertion (after meals and in cold etc)

3 - relieved with rest or GTN spray.

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19
Q

signs on exam for angina pectoris

A

usually no signs though 4th heart sound maybe heard

should look for signs of anaemia, thyrotoxicosis, hyperlipidemia

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20
Q

treatment for STEMI

A

PCI or angioplasty
if unstable for PCI then fibrinolysis required (streptokinase)
beta blocker - atenolol 5mg
ACE-Inhibitor within 24 hrs of acute MI esp if LV dysfunction or HR

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21
Q

differential diagnosis for angina pectoris

A
  • unstable angina (pain at rest and on exertion)
  • prinzmetal’s angina - pain on rest and no RF for atherosclerosis
  • MI - sudden, severe, crushing chest pain, do not stop after 15 mins
  • Cardiac Syndrome X - pain unpredictable, occurs at rest and for loner period of time
  • decubitus angina - pain occurs when lying down, severe coronary artery disease
  • acute pericarditis - burning/sharp pain, radiates to neck/shoulders, worse on coughing/breathing/lying down
  • GORD
  • aortic dissection
  • gallstones/acute cholecystitis
  • anxiety
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22
Q

investigation for angina pectoris

A

largely clinical

resting ECG - usually normal between attack, during attack, ST depression, and T wave inversion maybe present, Q wave indicate old MI

exercise ECG - confirm diagnosis, gives indication for severity of CAD

cardiac scintigraphy - myocardial perfusion scans at rest and exercise

echocardiography - good for diagnosing CAD and exclude other causes

CV MRI
Coronary angiography

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23
Q

management for angina pectoris

A

lifestyle change
treat underlying problems eg anaemia, diabetes and HTN

medical
- aspirin - dec risk of coronary events in pts with CAD, lipid-lowering therapy if needed

  • nitrates (GTN spray/tablet) - symptomatic relieve
  • beta-blockers
  • Ca2+ channel blockers
  • ACEi
    Statin

surgery

  • PCI
  • PCI with coated stents
  • coronary artery bypass grafting - CABG
24
Q

definiton for atrial fibrillation

A

cardiac arrhythmia characterised irregular irregular ventricular rate

25
Q

what are the different type of AF

A

acute/first detected - onset within last 48 hours

paroxysmal - spontaneous termination within 7 days and often within 48 hours

persistent - not self-terminating AF last longer than a year where cardiovaersion is unsuccessful, not pursued or has relapsed

26
Q

how common is AF

A

prevalence is 1% of all the population
affects 18% >65s
prevalence inc with age

27
Q

who is affected the most by AF

A

1/3 pt after bypass surgery and 1/2 undergoing vascular surgery

28
Q

pathogenesis of AF

A

dilation of the atria –> dec in atrial muscle mass and fibrosis of the atrial muscles

this leads to area of atrial muscle tissue randomly generate disorganised electrical impulses which override the organised impulses from the SA node

this leads to irregular irregular ventricular rate with ventricular contraction maintained

29
Q

causes of muscle disturbance in AF

A

idiopathic
valvular heart disease - inc intra-cardial pressure
HTN - inc intra-cardial pressure
congestive heart failure - inc intra-cardial pressure
left ventricular hypertrophy - inc intra-cardial pressure
atherosclerosis - inc intra-cardial pressure
obesity - inc intra-cardial pressure
hyperthyroidism -
MI - inc intra-cardial pressure
PE -inc intra-cardial pressure
caffeine
alcohol
sarcoidosis - inflammatory cause
post-op hypokalaemia or hypomagnaesia - electrolyte imbalance can cause overstimulation and excitation of myocytes

30
Q

RF for AF

A
age 
obesity 
HTN 
diabetes 
metabolic syndrome 
caffeine 
alcohol 
smoking
31
Q

symptoms on history for AF

A
aysmptomatic - in up to 20% of pts 
chest pain 
palpitations 
dyspnoea
faintness - acute syncope is rare
32
Q

signs on exam for AF

A

irregularly irregular pulse rhythm
first heart sound of variable intensity/loudness
no clear P waves on ECG
narrow QRS rhythm
untreated ventricular rate of about 120-180

33
Q

differenital for AF

A

atrial flutter - regular, usually tachycardia
SVT
ventricular tachycardia

34
Q

further investigation for AF

A

ECG - irregularly irregular rhythm
no ~P waves
irregular baseline
narrow QRS complex

bloods - TFT, U+Es, cardiac enzymes

Echo - for left atrial enlargement, mitral valve disease, structural abnor

35
Q

management for AF

A

acute AF

  • give oxygen
  • emergency cardioversion - mechanical or pharmacological using IV amiodarone
  • start full anticoagulation with LMWH, continue with warfarin if embolus risk high
  • control ventricular rate - 1st line verapamil/bisprolol, 2nd line digoxin/amiodarone

paroxysam AF
- flecanide PRN

chronic AF
- ventricular rate control - beta-blocker or rate limiting Ca channel blocker, add digoxin if the above combo not work, then consider amiodarone

  • rhythm control - mechanical or pharmacological cardioversion (IV flecainide or amiodarone for pharmco)
  • anticoagulation - warfarin
36
Q

complication for AF

A

stroke - 5x inc risk

heart failure

37
Q

definition of HTN

A

BP >140/90 mmHg

38
Q

how common is HTN

A

very common - 20-30% of adult population, 40-50% in black africans

39
Q

cause/RF for HTN

A

essential/primary/idiopathic causes - 95%

  • genetics - HTN tends to run in families (shared environment?)
  • fetal birth weight - low birth weigh = inc risk of HTN
  • lifestyle/environment - obesity, smoking, alcohol, stress, sodium (salty) diet, metabolic syndrome

secondary causes - 5%
- congenital - adrenal hyperplasia, aortic coarctation

acquired

  • renal disease (diabetic nephropathy, chronic glomerulonephritis, renal artery stenosis, CKD),
  • endocrine disease - Conn’s diseae, renal hyperplasia
  • drugs - interfere with response of some anti-hypertensives eg the pill, NSAIDs, cyclosporin, steroids
  • pregnancy
  • white coat syndrome
40
Q

symptoms of HTN

A

usually asymptomatic
headache/visual disturbance
sweating, palpitation
severe HTN - headache, epistaxis, nocturia, SOB due to LVH or HF

41
Q

what are the different grades of HTN

A
grade 1 (mild) - 140-159, 90-99
grade 2(mod) - 160-179, 100-109
grade 3 (sev) - >180, >110
42
Q

differentials for HTN

A

malignant HTN - short onset, diastolic pressure over approx 140
gestational HTN/Pregnancy induced HTN

43
Q

investigation for HTN

A
repeated BP 
ECG 
urine dipstick for protein/blood 
fasting blood for lipids and glucose 
serum urea and electrolytes 
creatinine 
CXR 

fundoscopy
Grade 1: tortuous retinal arteries with thick shiny walls (silver or copper wiring)
Grade 2: A-V nipping – narrowing where arteries cross veins
Grade 3: flame haemorrhages and soft exudates (cotton wool spots) due to small infarcts
Grade 4: papilloedema - blurring of margins of optic disc
Grade 3 and 4 = diagnostic of malignant hypertension

44
Q

treatment for HTN

A

target BP 140-85

A - ACEi/ARB
C - Ca2+ antagonist
D - diuretic (thiazide)

<55yrs - A then A+c or A+D then A+C+D the add further diuretic, alpha-blockers or beta-blockers

> 55yes - C or D then A+C or A+D then A+C+D the add further diuretic, alpha-blockers or beta-blockers

45
Q

defintion for DVT

A

venous thrombus in the deep vein of the legs or pelvis. Venous throboembolism (VTE) refers to both DVT and PE

46
Q

how common is DVT

A

1/1000 people/year affected

47
Q

who is affected the most by DVT

A

affect 25-50% of surgical pts

48
Q

causes of DVT

A

virchow’s triad

stasis of blood flow
endothelial injury
hypercoagulability

this leads to clots forming

49
Q

RF for DVT

A
inc age 
BM >30
varicose veins 
continouse travel for >3hrs in preceeding 4 weeks 
immobility/bedrest >4days 
pregnancy 
previous DVT or PE 
thrombophilia 
antithrombin deficiency 
protein C or S deficiency 
factor v leiden 
prothrombin gene variant 
antiphospholipid antibody/ lupus anticoagulant 
oestrogen therapy incl the pill and HRT

disease or surgical procedures

trauma/surgery to lower limbs, plevis, hip 
malignancy 
cardiac/resp failure 
recent MI or stroke 
acute medical illness/infection 
IBD 
nephrotic syndrome 
myeloproliferative disorders 
sickle cell anaemia 
central venous catheter 
paraproteinaemia 
paroxysmal nocturnal haemoglobinuria 
prostatectomy (50% of pts)
50
Q

symptoms of DVT

A

asymptomatic - 65% of leg DVT asymptomatic and rarely embolise to the lung

calf pain 
calf swelling 
redness 
warmth
ankle swelling 
mild fever
cyanotic discolouration of limb 
ulceration
51
Q

signs of DVT on exam

A
calf warmth 
calf tenderness 
calf swelling 
erythema 
mild fever 
pitting oedema 
distention of superficial veins
Homan's sign - +ve when there is pain or resistance in the calf or popliteal region with abrupt dorsiflexion of the pt's foot at the ankle while the knee is fully extended
52
Q

differential for DVT

A

cellulitis - close resemblance, can also occur secondary to DVT, DVT can be secondary to cellulitis

venous eczema
ruptured Backer’s cyst

53
Q

investigation for DVT

A

likely 2 level wells score

proximal leg vein USS carried out within 4 hours of being requested and if -ve then D-dimer test

or

a d-dimer test and an interim 24 hour dose of parenteral anticoagulant

gold standard - contrast venography

54
Q

treatment for DVT

A

LMWH/foundaparinux - for proximal DVT start asap and continue for 5 days or until INR –>2 for at least 24 hours

warfarin - start simultaneously with LMWH, contine for 3 months

catheter-directed thrombolyic therapy - for symptomatic ilio-femoral DVT, symptoms <14 days, good functional status, life expectancy>1 yrs

compression stockings

inferior vena caval filters - if anticoagulation contraindicative or reccurent DVT depsote anticoagulation

55
Q

what are the different types of angina

A
Stable 
Unstable 
Decubitis 
Variant 
Microvascular
56
Q

when does angina class as stable

A

when an angina is not new and there is not change in frequency and severity