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Cardio Flashcards

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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

Study These Flashcards
A
  1. Alveolar shadowing
  2. Curly B wings
  3. Cardiomegaly
  4. Diversion to the upper lobes
  5. Effusions
25
Medical management of chronic heart failure
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
Invasive therapies used in heart failure
1. Cardiac resynchronisation 2. Intra aortic ballon counterpulsation 3. LVAD
27
Risk factors for developing infective endocarditis
``` Prosthetic valves VSD, PDS, CoA Rheumatic fever Dental caries Post op wounds IVDU ( tricuspid valve) Immunocompromised ```
28
Causes of infective endocarditis
1. Strep viridans 2. Strep bovis 3. Staph aureus 4. Strep epideremis 5. Pseudomonas - ve Cultures 1. Haemophilus 2. Actinobacillus
29
Features of infective endocarditis
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
Outline the criteria used in the diagnosis of infective endocarditis
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
Investigations in cases of infective endocarditis
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
Treatment in cases of infective endocardiits
1. Abx specific to cultures | - Empiric Flucloc + Gent IV
33
Outline the cause and pathophysiology of rheumatic fever
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
Discuss the criteria used in the diagnosis of rheumatic fever
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
Clinical features of rheumatic fever
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
Treatment of Rheumatic fever
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
List the causes of acute pericarditis
Viral: EBV, HIV Bacterial: pneumonia, rheumatic fever, TB Immune: Dresslers Drugs: Penicillin, isoniazid, hydralazine
38
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?
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
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
- Constrictive pericarditis - Discuss with surgeons for surgical excision Kussmaul's sign - Increased JVP with inspiration
40
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?
Pericardial Effusion Pericardiocentesis: culture, ZN stain or cytology Warts sign: large effusion compressing the lobe.
41
Pathophysiology of cardiac tamponade
1. Accumulation of pericardial fluid 2. Increase in intra-pericardial pressure 3. Poor ventricular filling 4. Decrease in CO
42
Explain the following signs 1. Becks triad 2. Pulsus paradoxus 3. Kussmaul's sign
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
Treatment of tamponade
1. Urgent pericardiocentesis - watch ECG while aspirating 2. Treat causes 3. Send fluid for cytology and culture
44
List the types of cardiomyopathy
1. Hypertrophic obstructive cardiomyopathy 2. Dilated cardiomyopathy 3. Restrive cardiomyopathy
45
Explain the pathophysiology leading to hypertrophic obstructive cardiomyopathy
- Obstruction due to asymmetric septal hypertrophy - Autosommal dominant - B-myosin chain mutation is the commonest causes Must ask about sudden death
46
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
Hypertrophic obstructive cardiomyopathy ECG: - LVH - LAD strain - Ventricular ectopics (VT/VF) Echo: ASH Sudden death
47
Outline the treatment of hypertrophic obstructive cardiomyopathy
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
Causes of restrictive cardiomyopathy
misSHAPEN - Sarcoid - Systemic sclerosis - Haemochromatosis - Amyloidosis - Primary (fibrosis of the endocardium) - Eosinophilia - Neoplasia (carcinoid)
49
Causes of dilated cardiomyopathy
DILATE - Dystrophy (muscular) - Infection - Late pregnancy - Autoimmune (SLE) - Toxins ( EtOH) - Endocrine ( thyrotoxicosis)
50
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
Dilated cardiomyopathy Echo - globally dilated heart - hypokinetic heart
51
Management of patients with dilated cardiomyopathy
``` Bed rest Medical - Diuretics - ACEi - Anticoagulation ``` Surgical - Biventricular pacing - Heart tx
52
Name two inherited connective tissue disorders that affect the heart
1. Marfan's | 2. Ehlers-Danlos syndrome
53
Describe the pathophysiology of Marfan's syndrome
Autosommal dominant disorder Mutation in FBN1 gene on Chr 15 Encodes for fibrillin 1 glycoprotein which is a component of elastin
54
Clinical features of marfan's
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
Outline the complications encountered by people with Marfans
Ruptured aortic aneurysm Spontaneous pneumothorax Diaphragmatic hernia Hernias
56
Investigations to diagnosis marfans
``` Slit lamp examination: ectopia lentis CXR: widened mediastinum, pneumothorax ECG: Arrhythmias Echo: Aortic root dilatation Genetic testing: FBN-1 mutation ```
57
Describe the pathophysiology of ehlers-danlos syndrome
Rare heterogenous group of collagen disorders | 6 subtypes of varying severity with 1 and 2 being the most common
58
Clinical features of ehlers dances syndrome
``` Hyper elastic skin Hypermobile joints Cardiac ( MVP,AR,MR and aneurysms) Fragile blood vessels Poor healing ```

Cardiology (3 decks)

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