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Cardiology > Cardio > Flashcards

Cardio Flashcards

1
Q

List the possible causes of HTN

A
  1. Essential HTN
  2. Malignant or accelerate phase HTN (visual disturbance, headaches, retinal haemorrhages)
  3. Secondary HTN
    - Diabetic nephropathy
    - Polycystic kidney disease
    - Renovascular disease
    - Conn’s syndrome
    - Phaeochromcytoma
    - Acromegaly
  4. Drugs
    - Steroids
    - OCP
    - NSAIDS
  5. Pregnancy
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2
Q

Treatment of HTN

A

Refer to flow for targets

  1. Lifestyle advice
    - weight reduction
    - low salt diet
    - reduce alcohol
    - increase exercise
    - stop smoking
  2. Pharmacological management
    Step 1 if under 55 and not afro Caribbean
    -ACEi or ARB
    - if yes CCB

Step two
- + thiazide diuretic/ CCB/ ACEi or ARB

Step three
- All three of the above combined

Step four
SEEK expert advice is not controlled on four drugs at optimal doses.
- low-dose spironolactone4 if blood potassium level is ≤4.5 mmol/l
- alpha-blocker or beta-blocker if blood potassium level is >4.5 mmol/l

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3
Q

Pharmacology of ACEi

A

Prevent the conversion of angiotensin I to angiotensin II.

  • Angiotensin II = vasoconstrictor
  • Reduces vascular resistance
  • Dilate the efferent glomerular arteriole
DOSE
start @ 1.25mg in heart failure 
start @ 2.5mg normal people 
U&E's two weeks after starting 
Take at bed
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4
Q

Side effects of ACEi

A

Hypotension
Dry cough
Hyperkalameia due to lower aldosterone levels = potassium retention

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5
Q

Pharmacology of ARBs

A

Block the action of angiotensin II on the AT1 receptor

Dose 
Losartan is common choice 
12.5mg in heart failure
50mg in other indications 
First dose before bed
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6
Q

Pharmacology of CCB

A

Decrease Ca2t entry into the vascular and cardiac cells
Relaxation and vasodilation of the arterial smooth muscle
Reduce myocardial oxygen demand by reducing cardiac cells contractility

DOSE
Hypertension: 5-10mg daily (amlodipine)
Angina: 90mg (diltiazem- non dihydropyridine)
SVT: Verapamil 40-120mg

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7
Q

Side effects of CCB

A

Ankle swelling
Flushing
Headache
Palpations

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8
Q

Pharmacology of thiazides

A

Inhibit the Na+/Cl- co transporter in the DCT of the nephron
Prevents reabsorption of sodium
Fall in extracellular volume

DOSE
Bendro and Indapmide = 2.5mg daily

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9
Q

Side effects of thiazides and thiazide like

A

Hyponatraemia
Hypokalaemia
Impotence in men

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10
Q

Pharmacology of Spirolactone

A

Aldosterone antagonist
Competitively bind to the aldosterone receptor
Increases sodium and water exception through preventing activation of the ENAc channels

Dose
100mg daily

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11
Q

Side effects of spirolactone

A

Hyperkalamia

Gynaecomastia

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12
Q

Define acute coronary syndrome

A

Unstable angina + evolving MI

Path: plaque rupture, thrombosis and inflammation

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13
Q

Risk factors of ACS

A

Modifiable

  • HTN
  • DM
  • Smoking
  • High cholesterol
  • Obesity

Non-Modifiable

  • Age
  • Male
  • FH (< 55yrs )
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14
Q

IX in suspected ACS

A 
Bloods 
- Troponin T/I ( Present from 6hrs, repeated every 6hrs)
- FBC
- U+Es
- Glucose
- Lipids and clotting 
ECG 
CXR 
- Cardiomegaly
- Pulmonary oedema 
- Aortic rupture
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15
Q

Complication of MI

A 
Death 
Pump Failure 
Pericarditis 
Rupture 
- Cardiac tamponade ( Becks triad of low BP, high JVP and muffled heart sounds) 
- Papillary muscle rupture ( Pulmonary oedema) 
- Arrhythmias 
- Ventricular aneurysm 
Embolism 
- Dresslers syndrome
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16
Q

Define Dresslers Syndrome

A

Auto antibodies avs the myocyte sarcolemma
Present 2-6 wks with recurrent pericarditis
Fever
Anaemia
High ESR

Rx: NSAIDS or steroids

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17
Q

Classification of angina

A

Stable: induced by effort
Unstable: occurs at rest, evolving MI
Decubitus: occurs lying down
Syndrome X: angina + ST elevation on exercise test no evidence of atheroscelorsis, small vessel disease

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18
Q

Ix for chest pain

A 
Bloods
ECG ( usually normal, may show 
- ST depression
- Flat inverted t waves
- Past MI 
Stress ECHO 
Perfusion scan 
Angiography ( Gold standard)
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19
Q

Treatment for angina

A
  1. Lifestyle
    - Stop smoking
    - Wt loss and exercise
    - Healthy diet
  2. Medical ( 2nd prevention)
    - Aspirin 75mg
    - ACEi
    - Statins ( simavastatin 40mg)
    - Control HTN

Anti anginals for episodes

  • GTN spray + either
    a) B blocker (atenolol 50-100mg)
    b) CCb verapamil 80mg
  • ISMN 20-40mg BD
  1. Interventional
    - PCI
    if high risk of re stenosis give clopidogrel or use drug electing stent
  2. Surgical CABG
    - If L main stem disease or triple vessel disease
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20
Q

Pathophysiology of Heart failure

A
  1. Reduced cardiac output
    - Compensation
    - Frank starling
    - RAS and ANP/BNP release
  2. Progressive decline in CO
    - impaired contractility and functional valve regurgitation
    - hypertrophy and myocardial ischaemia
    - RAS activation with NA+ and fluid retention, increase venous pressure, oedema
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21
Q

Types of heart failure

A

Heart failure with reduced ejection fraction (HFrEF): defined as heart failure with an ejection fraction less than 40%.

Heart failure with preserved ejection fraction (HFpEF). Usually relaxation rather than contraction of the left ventricle is affected, and ejection fraction is normal or at least above 40%.

Causes:

  1. IHD
  2. Cardiomyopathy
  3. HTN
  4. Mitral and aortic valve disease

Clinical features:

  • Fatigue
  • Dyspnoea
  • Nocturnal cough with pink frothy sputum
  • Weight loss
  • Displaced apex beat
  • Gallop rhythm ( 3rd heart sounds)
  • Bibasal creps

Causes:

  1. LVF
  2. Cor pulmonale
  3. Tricuspid and pulmonary valve disease

Clinical features:

  • Anorexia
  • Nausea
  • Increase JVP
  • Hepatomegaly
  • Pitting oedema
  • Ascites
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22
Q

Classification of Congestive cardiac failure

A

New York Classification of Heart Failure
I: Heart disease present but no undue dyspnoea from ordinary activities
II: Comfortable at rest; dyspnoea on ordinary activities
III: Less than ordinary activities cause dyspnoea that is limiting
IV: Dyspnoea present at rest; all activities cause discomfort

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23
Q

Discuss the relation between CCF and BNP

A 
BNP: B-type natriuretic peptide 
Secreted from the ventricles in response to
- Increase in pressure 
- Tachycardia 
- Glucocorticoids 
- Thyroid hormones

Action

  • Increase GFR and decrease renal NA reabsorption
  • Reduced preload by reducing the smooth muscles

Marker of heart failure
BNP > 100 bad sign
Correlates with LV dysfunction

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24
Q

Signs of heat failure on CXR

A
  1. Alveolar shadowing
  2. Curly B wings
  3. Cardiomegaly
  4. Diversion to the upper lobes
  5. Effusions
25
Q

Medical management of chronic heart failure

A

1st line

  • ACEi + BB+ loop diuretic
  • with the BB start low go slow

2nd line

  • Add in spiro
  • Beaware of the increasing K=
  • Vasodilators such as ISDN

3rd line
- Digoxin

Considerations

  1. BP may be low
  2. Renal function
  3. Plasma K
  4. Daily weight
26
Q

Invasive therapies used in heart failure

A
  1. Cardiac resynchronisation
  2. Intra aortic ballon counterpulsation
  3. LVAD
27
Q

Risk factors for developing infective endocarditis

A 
Prosthetic valves 
VSD, PDS, CoA 
Rheumatic fever 
Dental caries 
Post op wounds 
IVDU ( tricuspid valve) 
Immunocompromised
28
Q

Causes of infective endocarditis

A
  1. Strep viridans
  2. Strep bovis
  3. Staph aureus
  4. Strep epideremis
  5. Pseudomonas
  • ve Cultures
    1. Haemophilus
    2. Actinobacillus
29
Q

Features of infective endocarditis

A
  1. Sepsis
  2. Cardiac ( new changing murmur)
  3. Embolic phenomena
  4. Immune complex deposition

NOTE

  • Roth spots: boat shaped retinal haemorrhages with pale centre
  • Janeway lesions: painless palmer macules
  • Oslers nodes: painful purple papules on the finger pulps
30
Q

Outline the criteria used in the diagnosis of infective endocarditis

A

DUKES CRITERIA
Major
- +ve blood culture , 2 separate cultures
- Endocardium involved, +ve echo or new valvular regurgitation

Minor

  • Predispostion
  • Fever > 38
  • Emboli
  • Immune phenomenon
  • +ve blood culture not meeting major criteria
31
Q

Investigations in cases of infective endocarditis

A

Ix

  1. Bloods
    - N.chromic or N.cytic anaemia
    - Increase ESR/CRP
    - +ve IgG RF
    - Cultures +3
  2. Urine
    - Mirco haem
  3. ECG
    - AV block
  4. Echo
    - vegetations > 2mm
32
Q

Treatment in cases of infective endocardiits

A
  1. Abx specific to cultures

- Empiric Flucloc + Gent IV

33
Q

Outline the cause and pathophysiology of rheumatic fever

A

Grp A beta haemolytic strep pyogenes

  • Abs cross react following infection with S progenies
  • Type II hypersensitivity reaction with molecular mimicry
  • ABs v M protein in cell wall, cross react with myosin , muscle glycogen and SM cells
  • Development of ASCHOFF and ANITSCHKOW myocytes
34
Q

Discuss the criteria used in the diagnosis of rheumatic fever

A

Jones Criteria

  1. Evidence of Grp A strep infection
    - +ve throat ulture
    - Rapid strep Ag test
    - Increase in ASOT (antistreptolysin O tititre)
    - Recent scarlet fever
  2. Major Criteria
    - Pancarditis
    - Arthritis
    - Erythema marginatum
    - Sydenham’s chorea
  3. Minor Criteria
    - Fever
    - Increased ESR
    - Arthralgia
    - Prolonged PR interval
    - Prev rheumatic fever
35
Q

Clinical features of rheumatic fever

A
  1. Pancarditis
    - Pericarditis
    - Myocarditis
    - Endocarditis
  2. Arthritis ( large joints, esp knees)
  3. Subcutaneous nodules on elbows
  4. Erythema marginatum
    - red raised edge with central clearing

Sydenham’s chorea

  • Grimacing
  • Clumsy
  • Hypotonia
36
Q

Treatment of Rheumatic fever

A
  1. Bed rest until CRP normalised
  2. Benepn 0.6-1.2mg IM 10/7
  3. Anaglesia
  4. Chorea haldol

can develop recurrent RF or valve regurgitation

37
Q

List the causes of acute pericarditis

A

Viral: EBV, HIV
Bacterial: pneumonia, rheumatic fever, TB
Immune: Dresslers
Drugs: Penicillin, isoniazid, hydralazine

38
Q

Patient presents to A&E with a previous history of CAP. He complains of a retrosternal chest pain, is spiking a temperature of 39.5C . The pain is made worse when he lies down and radiates to the left shoulder. He can’t think of anything that may have brought it on.

Bloods and ECG reveals the following

  • Elevated ESR
  • SAddle shaped ST elevation with PR depression

What is the dx and how will you treatment him?

A

Acute pericarditis

Key ECG findings

  • Saddle shaped ST elevation
  • PR depression

Rx

  1. Rx cause
  2. Analgesia: ibuprofen 400mg/8h/PO
  3. Consider steriods or immunosuppression if severe
39
Q

As med reg on call you receive a call from the F1. He has an unwell patients with RHF with a raised JVP. He has a positive Kussmaul’s sign and a S3.
He is fluid overload.
Investigations (CXR) reveal a small heart with evidence of pericardial calcification
How to you manage this patients

A
  • Constrictive pericarditis
  • Discuss with surgeons for surgical excision

Kussmaul’s sign
- Increased JVP with inspiration

40
Q

A patient on your ward is complaining of breathlessness… On examination you notice that he has a newly raised JVP and is bronchial breathing at the left base.

You request a CXR and ECG with reveals the following

  • CXR: enlarged globular heart
  • ECG: low voltage QRS complex

What is the diagnosis and are there any further tests you would do?

A

Pericardial Effusion

Pericardiocentesis: culture, ZN stain or cytology

Warts sign: large effusion compressing the lobe.

41
Q

Pathophysiology of cardiac tamponade

A
  1. Accumulation of pericardial fluid
  2. Increase in intra-pericardial pressure
  3. Poor ventricular filling
  4. Decrease in CO
42
Q

Explain the following signs

  1. Becks triad
  2. Pulsus paradoxus
  3. Kussmaul’s sign
A

Becks: decrease in BP, increase in JVP and quiet heart sounds

Pulsus paradoxus: pulse fades on inspiration

Kussmaul’s sign: JVP increases on inspiration

43
Q

Treatment of tamponade

A
  1. Urgent pericardiocentesis
    - watch ECG while aspirating
  2. Treat causes
  3. Send fluid for cytology and culture
44
Q

List the types of cardiomyopathy

A
  1. Hypertrophic obstructive cardiomyopathy
  2. Dilated cardiomyopathy
  3. Restrive cardiomyopathy
45
Q

Explain the pathophysiology leading to hypertrophic obstructive cardiomyopathy

A
  • Obstruction due to asymmetric septal hypertrophy
  • Autosommal dominant
  • B-myosin chain mutation is the commonest causes
    Must ask about sudden death
46
Q

A young man of 24 years presents to A&E not feeling right. He describes feeling breathless with angina like symptoms and a pounding heart.

O/E you find he is in AF, has a harsh ESM with a fourth heart sounds as well as an double apex beat

What is your working diagnosis and what investigations are you going to request
What is your major concern

A

Hypertrophic obstructive cardiomyopathy

ECG:

  • LVH
  • LAD strain
  • Ventricular ectopics (VT/VF)

Echo:
ASH

Sudden death

47
Q

Outline the treatment of hypertrophic obstructive cardiomyopathy

A

Medical

  • -ve iontropes (beta blockers or verapamil
  • Amiodarone for arrhythmias
  • Anticoagulant them if in AF

Non medical

  • Spetal myomectomy (surgical or chemical)
  • Consider ICD
48
Q

Causes of restrictive cardiomyopathy

A

misSHAPEN

  • Sarcoid
  • Systemic sclerosis
  • Haemochromatosis
  • Amyloidosis
  • Primary (fibrosis of the endocardium)
  • Eosinophilia
  • Neoplasia (carcinoid)
49
Q

Causes of dilated cardiomyopathy

A

DILATE

  • Dystrophy (muscular)
  • Infection
  • Late pregnancy
  • Autoimmune (SLE)
  • Toxins ( EtOH)
  • Endocrine ( thyrotoxicosis)
50
Q

A lady in her 40’s presents with signs of LV heart failure. On examination you notice that she is in AF, has an increase JVP, displaced apex beat and a third heart sound.
She is struggling to maintain her BP. She has a PMHx of coeliac and hashimotos

CXR reveals cardiomegaly and pulmonary oedema. You request an ECG which shows T wave inversion and poor progression

What is you diagnosis?
What would be seen on ECHO

A

Dilated cardiomyopathy

Echo

  • globally dilated heart
  • hypokinetic heart
51
Q

Management of patients with dilated cardiomyopathy

A 
Bed rest 
Medical 
- Diuretics 
- ACEi
- Anticoagulation

Surgical

  • Biventricular pacing
  • Heart tx
52
Q

Name two inherited connective tissue disorders that affect the heart

A
  1. Marfan’s

2. Ehlers-Danlos syndrome

53
Q

Describe the pathophysiology of Marfan’s syndrome

A

Autosommal dominant disorder
Mutation in FBN1 gene on Chr 15
Encodes for fibrillin 1 glycoprotein which is a component of elastin

54
Q

Clinical features of marfan’s

A

Cardiac

  • Aortic aneurysm and dissection
  • MV prolapse +- regurgitation

Ocular
- Lens dislocation

MSK

  • High arched palate
  • Arm > height
  • Pectus excavatum
  • Scoliosis
  • Pres planus
  • Joint hyper mobility
55
Q

Outline the complications encountered by people with Marfans

A

Ruptured aortic aneurysm
Spontaneous pneumothorax
Diaphragmatic hernia
Hernias

56
Q

Investigations to diagnosis marfans

A 
Slit lamp examination: ectopia lentis 
CXR: widened mediastinum, pneumothorax 
ECG: Arrhythmias 
Echo: Aortic root dilatation 
Genetic testing: FBN-1 mutation
57
Q

Describe the pathophysiology of ehlers-danlos syndrome

A

Rare heterogenous group of collagen disorders

6 subtypes of varying severity with 1 and 2 being the most common

58
Q

Clinical features of ehlers dances syndrome

A 
Hyper elastic skin 
Hypermobile joints 
Cardiac ( MVP,AR,MR and aneurysms) 
Fragile blood vessels 
Poor healing

Cardiology (3 decks)

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