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Belle Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Angina

A

narrowing of the coronary arteries (e.g. atherosclerosis) reduces blood flow to the myocardium and causes CONSTRICTING CHEST PAIN radiating to the arm, jaw or neck

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2
Q

Stable (chronic) angina

A

EXERTIONAL: symptoms are precipitated by exercise, emotion and temperature and relieved by rest or glyceryl trinitrate (GTN)

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3
Q

Unstable (acute) angina

A

cardiac chest pain at rest/with crescendo pattern

not relieved by rest or GTN spray

part of the acute coronary syndromes

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4
Q

Ischaemic heart disease / Coronary artery disease / Coronary heart disease

A

Primarily caused by ATHEROSCLEROSIS

- 70-80% ca sclerosed = exertional symptoms (ANGINA - main presenting feature)

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5
Q

Non-modifiable IHD RFs

A

FHx
Age
Ethnicity (S. Asian)

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6
Q

Modifiable IHD RFs

A

Smoking
Alcohol
HTN
Obesity

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7
Q

Angina Ix

A

GOLD STANDARD: CT CORONARY ANGIOGRAPHY

Baseline Ix:

  • ECG (usually normal)
  • FBC (exclude anaemia)
  • TFT (hypo/hyper)
  • HbA1c (exclude DM)
  • Lipids: LDL level
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8
Q

Secondary prevention of stable angina

A 
4 As:
Aspirin
Atorvastatin
ACE inhibitor 
Already on a Beta-blocker for symptomatic relief
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9
Q

Long term symptomatic relief of stable angina

A

Beta-blocker e.g. bisoprolol

Calcium channel blocker e.g. amlodipine

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10
Q

Immediate symptomatic relief of stable angina

A

GTN spray (vasodilation)

  • Take when symptoms start
  • Again 5 minutes after
  • If pain still there 5 minutes after repeat dose, AMBULANCE
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11
Q

Surgical intervention indications in stable angina

A

Proximal or extensive disease on CTCA: PCI with coronary angioplasty

Severe stenosis: CABG

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12
Q

IHD: Acute coronary syndromes

A

Sudden, reduced blood flow to the heart

Majority: thrombus from an atherosclerotic plaque blocking a CA

Unstable angina
STEMI
NSTEMI

Symptoms should CONTINUE AT REST FOR >20 MINUTES

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13
Q

MI symptoms

A

Central, constricting chest pain associated with:

  • Nausea + vomiting
  • Sweating + clamminess
  • Feelings of impending doom
  • SoB
  • Palpitations
  • Pain radiating to the jaw or arms
  • 1/3 occur in bed at night
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14
Q

Silent MI

A

DIABETICS may not experience typical chest pain

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15
Q

Diagnosis of ACS

A

Troponins taken at baseline and 6-12 hours after onset

ECG: ST elevation or new LBBB = STEMI

No ST elevation > Troponin: raised + other ECG changes (ST depression/T wave inversion) = NSTEMI

Normal troponin + no pathological ECG changes = UNSTABLE ANGINA

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16
Q

NSTEMI

Coronary vessel > Myocardium > ECG

A

Partial occlusion > Subendocardial infarct > ST depression

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17
Q

STEMI

Coronary vessel > Myocardium > ECG

A

Complete occlusion > Transmural infarct > ST elevation

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18
Q

Immediate Mx of ACS at hospital

A

MONAA

Morphine
Oxygen (if hypoxic)
Nitrate
Aspirin 300mg
Anti-platelet (P2Y12)
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19
Q

STEMI definitive Mx

A

PCI within 2 HOURS OF ONSET
+ DAPT
consider GPIIb/IIIa

Fibrinolysis with IV tenecteplase (if PCI is not possible within 2 hours)
e.g. alteplase
+ DAPT

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20
Q

Troponin

A

regulates actin:myosin contraction

highly sensitive marker for CARDIAC MUSCLE INJURY
but NOT SPECIFIC for ACS

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21
Q

Aspirin MOA

A

IRREVERISBLE inactivation of COX-1

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22
Q

NSTEMI Mx

A 
BATMAN
Beta blockers
Aspirin 300mg
Ticagrelor
Morphine
ANTICOAGULANT e.g. Fondaparinux
Nitrates (e.g. GTN)

Med/high risk:
Angiography + PCI

GRACE score = 6 month mortality + risk of further cardio events

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23
Q

Secondary prevention ACS

A

ACEi
Aspirin + DAPT
Atorvastatin
Beta-blocker

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24
Q

Post-MI complications

A 
Death
Rupture of heart septum/papillary muscles
Oedema (HF)
Arrythmias
Aneurysm
Dressler's syndrome
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25
Q

Dressler’s syndrome

A

pericarditis 2-6 weeks after MI

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26
Q

Hypertension aetiology

A

95% = idiopathic (essential)

5%: ROPE
Renal disease
Obesity
Pregnancy (pre-eclampsia)
Endocrine (Conn's)
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27
Q

HTN diagnostic criteria

A

Stage 1:
BP > 140/90 in clinic (white coat syndrome)
BP >135/85 with ABPM/home reading

Stage 2:
>160/90
>150/95

Stage 3:
>180/120 in clinic (with organ damage; medical emergency)

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28
Q

HTN modifiable RFs

A 
Alcohol
Sedentary lifestyle
DM
Sleep apnoea
Smoking
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29
Q

HTN non-modifiable RFs

A

Age (>65)
FHx
Ethnicity (afro-caribbean)

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30
Q

Further investigations HTN

A

Renal failure

  • urine ACR: proteinuria
  • dipstick: haematuria
  • bloods: GFR, Hb

CVD complications
- ECG

HTN retinopathy
- fundus examination

Other:
HbA1c
Lipids

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31
Q

HTN treatment pathway: Type 2 DM, OR, Age <55 AND not of black African or African-Caribbean family origin

A

Step 1: [ACEi or ARB]

Step 2: [ACEi or ARB] PLUS [CCB] OR [thiazide diuretic]

Step 3: [ACEi or ARB] PLUS [CCB] PLUS [thiazide diuretic]

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32
Q

HTN treatment pathway: Age >55 OR black African or African-Caribbean family origin (any age)

A

Step 1: [CCB]

Step 2: [CCB] PLUS [ACEi or ARB]

Step 3: [CCB] PLUS [ACEi or ARB] PLUS [thiazide diuretic]

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33
Q

HTN treatment pathway step 4

A

Discuss adherence
Check for postural HTN

Low dose spironolactone (if K+ <4.5)
OR
Alpha-blocker or beta-blocker (if K+ >4.5)

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34
Q

Aneurysm

A

weakening of vessel wall followed by dilation due to increased wall stress

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35
Q

The most common vessel aneurysm

A

Abdominal Aortic Aneurysm (AAA)

- commonly infrarenal arteries

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36
Q

AAA RFs

A 
SMOKING
FHx
Connective tissue disorders
Age
Atherosclerosis
Male
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37
Q

Major complication of aneurysms

A

RUPTURE
Thromboembolisms
Fistula formation

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38
Q

1st line Ix aortic aneurysm

A

US

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39
Q

Mx aortic aneurysm

A

Ruptured = urgent repair

Symptomatic = repair regardless of diameter

Asymptomatic (detected incidentally) = surveillance until diameter >5.5 (men) or >5 (women)

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40
Q

Ruptured AAA Px + Tx

A

Acute onset of SEVERE, TEARING ABDOMINAL PAIN with RADIATION TO BACK, FLANK + GROIN

Painful pulsatile mass
Hypovolaemic shock
Syncope
Nausea, vomiting

Tx: URGENT SURGERY + maintain haemodynamic stability
- EVAR (endovascular aneurysmal repair)

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41
Q

Aortic dissection

A

tear in the INTIMAL layer of the aorta = collection of blood between intima and medial layer
- as the dissection propagates, flow through false lumen can occlude branches of aorta e.g. coronary, brachiocephalic, iliac

most often occurs in middle aged men

65% of cases = ASCENDING aorta

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42
Q

Aortic dissection RFs

A 
HTN (MOST COMMON)
Trauma
Vasculitis
Cocaine use
Connective tissue disorders (young adults)
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43
Q

Aortic dissection Px

A

sudden and SEVERE TEARING PAIN in CHEST radiating to the back

Hypotension
Asymmetrical blood pressure
Syncope

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44
Q

Aortic dissection Dx

A

ECG
CXR
CT (definitive)

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45
Q

Aortic dissection Tx

A

Maintain haemodynamic stability: fluid resus, inotropes, noradrenaline

Opioid analgesia for pain control

Surgical intervention: endovascular stent-graft repair

Anti-HTs

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46
Q

Peripheral vascular disease (PVD, PAD) pathophysiology

A

Atherosclerosis (most commonly) > claudication of vessels

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47
Q

PVD RFs

A 
Smoking
Diabetes
HTN
Sedentary lifestyle
Hyperlipidaemia
History of CAD
Age <40
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48
Q

PVD Px

A

Pain in lower limbs on exercise, relived by rest (intermittent claudication)

Severe: unremitting pain in foot (especially at night - hang foot out of bed)

Leg may be pale, cold, loss of hair, skin changes

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49
Q

PVD Ix

A

Ankle brachial pressure index (ABPI) = doppler ultrasonography

  • ratio arm:ankle
  • <0.9 (normal = 1)

Buergers test (angle to which the leg has to be raised to become pale whilst lying down)

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50
Q

PVD Tx

A 
Control RFs:
Smoking cessation
Regular exercise
Weight reduction
BP control, DM control
STATIN

DAPT

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51
Q

Critical limb ischaemia Px

A

End stage PVD

6 Ps:
Pain
Paraesthesia 
Pulselessness 
Pallor
Paralysis 
Perishingly cold

PVD Tx PLUS:
Revascularisation
Amputation

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52
Q

Mitral stenosis

A

Aetiology:

  • Rheumatic HD
  • IE

Px: malar flush, pulmonary congestion (SoB, haemoptysis), AF

MURMUR: mid-DIASTOLIC, low-pitched, rumbling

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53
Q

Aortic regurgitation

A

Aetiology:

  • Idiopathic
  • EDS/Marfans

Px: corrigan’s pulse (collapsing pulse)

MURMUR: early-diastolic, soft, rumbling; Austin Flint at apex

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54
Q

Mitral regurgitation

A

Aetiology:

  • Idiopathic
  • IHD
  • IE
  • Rheumatic HD
  • EDS/Marfans

MURMUR: pan-systolic, high-pitched, whistling

Complication: Congestive HF

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55
Q

Aortic stenosis

A

MOST COMMON

Aetiology:

  • Idiopathic
  • Rheumatic HD

Px: exertional syncope, slow rising pulse, narrow pulse pressure
MURMUR: ejection-systolic, high-pitched, crescendo-decrescendo; radiating to carotids

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56
Q

Cardiogenic shock

A

Aetiology: pump failure, MI
Patho: decreased CO + MAP
Px: tachycardia + pnoea, decreased UO + BP, cold peripheries, chest pain
Tx: ABCDE, resus

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57
Q

Hypovolaemic shock

A

Aetiology: low fluid volume, haemorrhage, GI bleed, dehydration (D&V), severe burns, pancreatitis
Patho: decreased CO + MAP
Px: tachypnoea, weak rapid pulse, cyanosis
Tx: ABCDE, resus, fluids, GTN

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58
Q

Septic shock

A

Aetiology: toxins in blood
Patho: decreased MAP + derangement in physiology
Px: tachycardia, D+V, decreased UO + O2 + BP
BOUNDING PULSE
Tx: Broad spectrum IV Abx, FLUIDS, O2

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59
Q

Anaphylactic shock

A

Aetiology: severe allergic reaction
Patho: histamine release, vasodilation, hypoxia
Px: rash
Tx: resus, adrenaline

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60
Q

Structural heart defects Ix

A

echo, ECG

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61
Q

Eisenmenger’s syndrome

A

shunting of septal defect is from RIGHT to LEFT = deoxygenated blood in systemic circ

62
Q

Tetralogy of fallot

A 
4 defects:
large ventricular septal defect
overriding aorta
RV outflow obstruction (pulmonary stenosis) 
RV hypertrophy
63
Q

Heart failure definition

A

CO is inadequate for the body’s requirements

64
Q

Heart failure definition

A

CO is inadequate for the body’s demands

Pathophysiological changes take place to compensate for CO

65
Q

Types of heart failure

A

Systolic: contraction failure
Diastolic: relaxation failure

Systolic or diastolic:
LVF
RVF

Acute: new onset or decompensation of chronic
Chronic: gradual progression and arterial pressure well maintained until late

66
Q

LVF aetiology

A 
IHD (MOST COMMON CAUSE) 
Myocardial infection
Cardiomyopathy
Congenital heart defects
Valvular disease
Arrhythmias
67
Q

RVF aetiology

A 
Right ventricular infarct
PHT
PE
COPD
Progression of LVF
Cor pulmonale
68
Q

Systolic HF aetiology

A

IHD
Myocardial infection
Cardiomyopathy

69
Q

Diastolic HF aetiology

A

Aortic stenosis

Chronic hypertension

70
Q

HF pathophysiology

A
  1. HF = increased preload
  2. compensatory hypertrophy > increases myocardial oxygen demand
  3. ischaemia = fibrosis = reduced contractibility
  4. more force needed to maintain CO = cells become tired = pathological
71
Q

HF signs

A 
Tachycardia
Elevated JVP
Cardiomegaly
3rd or 4th heart sounds
Ascites
Tender hepatomegaly
Bi-basal crackles
Pleural effusion
72
Q

HF Ix

A

ECG
- indicate cause of HF e.g. MI, ventricular hypertrophy

BNP (brain natriuretic peptide)

  • marker of HF
  • directly correlated to ventricular myocardial wall stress and severity of HF

CXR: ABCDE

  • Alveolar oedema (bat wing shadowing)
  • Kerley B lines
  • Cardiomegaly
  • Dilated UPPER LOBE vessels of lungs
  • Effusions (pleural)
73
Q

HF Mx

A

Lifestyle changes

Diuretics: reduce preload and pressure on the ventricles

  • Loop diuretics e.g. furosemide
  • Thiazide diuretics e.g. bendroflumethiazide
  • Aldosterone antagonist e.g spironolactone (potassium sparing)

ACEi: LVSD

  • Ramipril
  • SE of cough: ARB

B-blocker: decrease mortality
- e.g. bisoprolol

Digoxin: LVSD symptoms

74
Q

Tachycardia

A

> 100 bpm
Abnormal P waves
Normal QRS

AVNRT: absent P waves
VT: absent P + T waves, wide QRS

75
Q

Bradycardia

A

<60bpm

76
Q

Atrial fibrillation rhythm/rate

A

chaotic IRREGULAR rhythm with an IRREGULAR ventricular rate

patho: continuous rapid activation of the atria with no organised mechanical action at 300-600bpm

77
Q

HTN medication

A 
ABCD ARB
ACEi e.g. ramipril
Beta blocker e.g. bisoprolol
Calcium channel blocker e.g. amlodipine
Diuretic
Angiotensin II Receptor Blocker e.g. candesartan
78
Q

Atrial fibrillation

A

chaotic IRREGULAR rhythm with an IRREGULAR ventricular rate

patho: continuous rapid activation of the atria with NO ORGANISED mechanical action at 300-600bpm

79
Q

AF aetiology + risk factors

A 
Idiopathic
HTN
HF
CAD
Valvular HD
60+
Diabetes
High BP
CAD
Past MI
80
Q

AF Tx

A

Cardioversion

  • Give a LMWH e.g. dalteparin (to decrease risk of stroke)
  • Shock with defibrillator
81
Q

Atrial flutter

A

ORGANISED atrial rhythm at a rate of 250-350bpm

82
Q

Atrial flutter ECG

A

Saw-tooth pattern (F waves)

= definitive diagnosis

83
Q

Atrial flutter main risk factor

A

Atrial fibrillation

84
Q

Atrial flutter Tx

A

Cardioversion
Catheter ablation
IV amiodarone (restores sinus rhythm)

85
Q

Bundle Branch Block

A

a block in the conduction of one of the bundle branches (bundle of his splits off into left and right) so the ventricles don’t receive impulses at the same time

86
Q

RBBB

A

V1 MaRRoW V5+V6

Wide QRS

87
Q

LBBB

A

V1+V2 WiLLiaM V4-V6
Wide QRS + notched top
T wave inversion in lateral leads

88
Q

Bundle Branch Block

A

a block in the conduction of one of the bundle branches so one ventricle receives impulse first then spreads to the next

Often asymptomatic

Tx:

  • Pacemaker
  • CRT (cardiac resynchronisation therapy)
  • Reduce blood pressure
89
Q

RBBB

A

V1 MaRRoW V6
Wide QRS

Aetiology:
PE
IHD
AV septal defect

90
Q

LBBB

A

V1 WiLLiaM V6
Wide QRS + notched top
T wave inversion in lateral leads

Aetiology:
IHD
Aortic valve disease

91
Q

1st degree HB

A

PR interval >200ms

Asymptomatic

92
Q

2nd degree HB Mobitz I

A

Progressive lengthening of PR interval then one non-conducted P wave, repeats with shorter PR interval
= Wenckebach

Light headedness, dizziness, syncope

93
Q

2nd degree HB Mobitz II

A

Occasional non-conducted P-waves (3:1, 2:1), wide QRS

SoB, postural hypotension, chest pain

94
Q

3rd degree HB

A

Complete HB: no relationship between P waves and QRS waves, abnormally shaped QRS

Dizziness, blackouts

Tx: permanent pacemaker, IV atropine

95
Q

Heart block aetiology

A

Atheletes
IHD (esp MI)
Acute myocarditis
Drugs

96
Q

HB Tx

A

Cardioversion
Catheter ablation
IV amiodarone

97
Q

Prolonged QT causes

A

Congenital (syndrome)
Hypokalaemia
Hypocalcaemia
Drugs e.g. amiodarone, TCA

98
Q

Wolf-Parkinson-White syndrome

A

accessory pathway for conduction - the impulse can travel to the AVN and also to the ventricle quicker than the normal pathway

ECG
= short PR interval
= wide QRS complex that begins slurred (delta wave)

Tx: catheter ablation of pathway

99
Q

WPW causes

A

Congenital
Hypokalaemia
Hypocalcaemia
Drugs e.g. amiodarone, TCA

100
Q

Pericarditis

A

Inflammation of the pericardium -/+ effusion

Pericardium: fibrous layer, serous layer

  • Fibrinous (DRY)
  • Effusive (purulent SEROUS exudate; HAEMORRHAGIC exudate)
101
Q

Acute pericarditis aetiology

A

Idiopathic

Post-cardiac injury (Dressler’s)

Infectious (enteroviruses e.g. Coxsackie B, adenoviruses, TB)

Autoimmune (RA, SLE)

Traumatic + iatrogenic

102
Q

Pericarditis pathophysiology

A

Inflammation
- pericardial vascularisation: FLUID moves into pericardial tissues THICKENING the layers
- polymorphnuclear LEUKOCYTE INFILTRATION
= NARROWING of pericardial space + scarring

103
Q

Complications of pericarditis if left untreated

A

Build up of exudate can lead to PERICARDIAL EFFUSION
= puts pressure on the cardiac myocytes
= cardiac dysfunction (tamponade physiology) = decrease in CO

Immune cell adhesions = fibrosis > CONSTRICTIVE PERICARDITIS = decreased SV (compensatory increased HR)

104
Q

Signs of rheumatic fever

A 
Tachycardia 
Murmur (dependent on valve)
Pericardial rub 
Erythema marginatum (red rings) 
Prolonged PR interval
105
Q

Pancarditis

A

Inflammation of ALL LAYERS of the heart

  • endocarditis
  • myocarditis
  • pericarditis
106
Q

Jones Criteria for RF

A

Recent streptococcal infection (2-3 weeks) + 2 major or 1 major + 2 minor

E.g strep throat 2 weeks ago + carditis + polyarthritis

Major:
Polyarthritis
Carditis
Subcutaneous nodules
Erythema marginatum
Sydenham chorea

Minor:
Fever
Raised inflammatory markers
Prolonged PR

107
Q

ESR

A

Fibrinogen causes RBC to fall to the bottom of the test tube faster

108
Q

Aortic regurgitation murmur

A

Diastolic decrescendo

109
Q

Aortic stenosis murmur

A

Systolic crescendo/decrescendo

110
Q

Mitral regurgitation

A

Pan-systolic (intensity high throughout systole)

111
Q

Mitral stenosis murmur

A

Diastolic decrescendo / pre-systolic crescendo

112
Q

Pericarditis symptoms

A

Fever
Severe, sharp, pleuritic chest pain: WORSE when LAYING FLAT and heavy inspiration, RELIEVED by SITTING FORWARD
Dyspnoea

113
Q

Pericarditis signs

A

Pericardial rub on auscultation
Tachycardia
Peripheral oedema
Effusion: muffled heart sounds

114
Q

Pericarditis Ix

A

ECG: DIAGNOSTIC
SADDLE SHAPED ST ELEVATION
PR DEPRESSION

CXR: effusion may cause cardiomegaly (water bottle)

Auscultation

115
Q

Pericarditis Tx

A

Reduce physical activity
NSAIDs (ibuprofen, aspirin)
Colchicine (inhibits neutrophil migration - decreases recurrence risk)
Pericardiocentesis (in cases of severe effusion)

116
Q

Cardiomyopathy types

A

Hypertrophic
Dilated
Restricted

117
Q

Dilated cardiomyopathy aetiology

A 
Idiopathic
Ischaemia 
Alcohol abuse
Thyroid disorder
Genetic e.g HFE
118
Q

Dilated cardiomyopathy pathophysiology

A

Dilation of left ventricle with THIN muscle = poor contraction = lower SV
Diffuse interstitial fibrosis
Biventricular congestive systolic HF

119
Q

Dilated cardiomyopathy Px

A

SoB, fatigue, dyspnoea

HF, arrhythmia, thromboembolism, increased JVP

120
Q

Dilated cardiomyopathy Ix

A

CXR (enlargement)
ECG
Echo

121
Q

Hypertrophic cardiomyopathy aetiology

A

GENETIC - autosomal dominant

50% sporadic

122
Q

Signs of hypertrophic cardiomyopathy

A

Left ventricular outflow obstruction (muscle gets in the way, increasing blood velocity)
Ejection systolic crescendo decrescendo murmur
Jerky carotid pulse

123
Q

Symptoms hypertrophic cardiomyopathy

A 
SUDDEN DEATH (may occur with no prior symptoms) 
Chest pain/angina
Dyspnoea
Dizziness
Palpitations
Syncope
124
Q

Hypertrophic cardiomyopathy Ix

A

ECG: T wave inversion, Deep Q waves

Genetic analysis

125
Q

Pathophysiology hypertrophic cardiomyopathy

A

Gene mutation for sarcomere protein
Impaired diastolic filling (less chamber room and muscles less complaint)
Reduced SV
Reduced CO
= diastolic HF
Ischaemia (muscle demand) > fast arrhythmias

126
Q

Hypertrophic cardiomyopathy Tx

A

Amiodarone (anti-arrhythmic)
CCCB e.g. verapamil
Beta blocker e.g. atenolol

CONTRAINDICATED: Digoxin (increases contraction force which can increase obstruction)

127
Q

Causes of restrictive cardiomyopathy

A

Amyloidosis (TTR deposits in myocardium)
Sarcoidosis (granuloma in myocardium)
End-myocardial fibrosis
Haemochromatosis

128
Q

Restrictive cardiomyopathy Px

A

Dyspnoea, fatigue, embolic symptoms

Signs:
Increased JVP, diastolic collapse, elevated on inspiration
Hepatic enlargement 
Ascites
Oedema
3rd + 4th heart sounds
129
Q

Diagnostic Ix restrictive cardiomyopathy

A

Cardiac catheterisation

130
Q

Pathophysiology restrictive cardiomyopathy

A

Impaired ventricle filling (RIGID myocardium RESTRICTS ventricular filling - without hypertrophy)
= diastolic HF

131
Q

Most common cardiomyopathy

A

Dilated

132
Q

Most common cause of sudden death in young people

A

Hypertrophic cardiomyopathy

133
Q

Fever + new murmur

A

Infective endocarditis until proven otherwise

134
Q

Causes of non infective endocarditis

A

Pancreatic adenocarcinoma

SLE

135
Q

Infective endocarditis aetiology

A 
Viridans strep (poor dental hygiene) - MOST COMMON CAUSE IN ADULTS
Staph aureus (IV drug use, surgery) 
Staph epidermidus (prosthetic valve, catheter)
136
Q

Infective endocarditis pathophysiology

A

Turbulent blood flow > cardiac endothelial damage > blood clot formation (non-bacterial thrombotic endocarditis)
Microbial infection in BLOODSTREAM > tricuspid valve from venous system
Adherence/biofilm at blood clot = Vegetation
Virulent organisms destroy the valve = valve regurgitation + HF
Detachment of vegetations = septic emboli

137
Q

Endocarditis risk factors

A 
IV drug use (MOST CASES) 
Prosthetic valves 
Valvular disease 
Congenital defect
Rheumatic heart disease
138
Q

IV drug use affects which side of the heart in endocarditis

A

Right

139
Q

Symptoms of endocarditis

A 
FEVER
Rigours
Night sweats
Malaise
Weight loss
140
Q

Signs of endocarditis

A 
NEW MURMUR (turbulent blood flow past damaged valve)
Sepsis of unknown origin 
Embolic events of unknown origin 
Hands: splinter haemorrhages, Janeway lesions; Osler’s nodes (antigen-antibody complexes) 
Eyes: Roth spots
Skin: petechiae, embolic skin lesions 
Anaemia
Splenomegaly 
Clubbing
141
Q

Endocarditis diagnostic criteria

A

Duke Criteria

  • 3 positive cultures
  • Echocardiography (trans-oesophageal echo): visualise vegetations or valve changes
142
Q

Endocarditis treatment

A

Antibiotics

  • Staph: vancomycin (if MRSA: add rifampicin)
  • benzylpenicillin and gentamicin

Treat any complications e.g. HF

Surgery (severe cases): valve replacement

Prevention: good oral health, no IV drug use, education

143
Q

What is disseminated intravascular coagulation?

A

Disorder of primary and secondary hemostasis

  • Microvascular thrombosis
  • Consumption coagulopathy (bleeding due to depletion of platelets and clotting factors)

Often occurs after INFECTION (sepsis)

Petechial rash:

144
Q

Abdominal aorta bifurcation into right and left common iliac

A

L4

145
Q

Irregular RR interval

A

Atrial fibrillation

146
Q

Clear lung sounds + pan systolic murmur louder on expiration

A

Right sided heart failure secondary to tricuspid regurgitation

147
Q

Murmur from ATRIOVENTRICULAR regurgitation

A

(Mitral and tricuspid)

Pan systolic

148
Q

Becks triad

A
149
Q

Heart valve most commonly affected in infective endocarditis

A

Tricuspid (50%) = first heart valve to be encountered after blood has returned from SYSTEMIC circulation

150
Q

Postural hypotension definition and Tx

A

Systolic drop >20 mmHg or if systolic BP drops to less than 90

Tx: Fludrocortisone

151
Q

Unstable angina 1st line Tx

A

GTN spray and either a B-blocker (atenolol) or CCB (verapamil)

152
Q

Schobers test

A 
Standing
Locate L5
10cm above + 5cm below 
Bend over as far as possible 
Distance of <20cm = reduced lumbar movement > ankylosing spondylitis indication

Belle Phase 2a (14 decks)

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