Part 14 Flashcards

(39 cards)

1
Q

A 23-year-old woman presents to the Emergency Department with a friend from work. Around 30 minutes ago she developed a ‘fluttering’ in her chest. She reports feeling ‘a bit faint’ but denies any chest pain or shortness of breath. An ECG shows a regular tachycardia of 166 bpm with a QRS duration of 110 ms. Blood pressure is 102/68 mmHg and oxygen saturations are 99% on room air.

What is the most appropriate initial management?

Intravenous magnesium sulphate
Direct current cardioversion
Intravenous adenosine 3mg
Intravenous adenosine 6mg
Vagal manoeuvres

A

The first-line management of supraventricular tachycardia is vagal manoeuvres. Only if these fail should adenosine be given. There are no indications for direct current cardioversion as per the ALS guidelines.

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2
Q

A 52-year-old man is seen in the hypertension clinic. He was diagnosed around three months ago and started on ramipril. This has been titrated up to 10mg od but his blood pressure remains around 156/92 mmHg.

What is the most appropriate next step in management?

Add amlodipine AND indapamide
Add amlodipine OR bisoprolol
Switch ramipril to losartan
Add amlodipine OR indapamide
Add losartan

A

Add amlodipine OR indapamide

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3
Q

You are clerking a 67-year-old man who has been admitted with chest pain. His past medical history includes hypertension, angina and he continues to smoke 20 cigarettes / day. Blood tests done in the Emergency Department show the following:

Na+ 133 mmol/l
K+ 3.3 mmol/l
Urea 4.5 mmol/l
Creatinine 90 µmol/l

Which one of the following factors is most likely to explain the abnormalities seen in the electrolytes?

Enalapril therapy
Felodipine therapy
Bendroflumethiazide therapy
His smoking history
Spironolactone therapy

A

Bendroflumethiazide therapy

Bendroflumethiazide causes both hyponatraemia and hypokalaemia. Spironolactone is associated with hyperkalaemia. His smoking would only be relevant if he had lung cancer cause syndrome of inappropriate ADH secretion - there is no indication of this from the question.

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4
Q

How do thiazide and thiazide like diuretics work?

A

Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Clˆ’ symporter

Potassium is lost as a result of more sodium reaching the collecting ducts –> increased sodium reabsorption in exchange for potassium and hydrogen ions

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5
Q

Adverse effect of thiazide and thiazide like diuretics

A

Common adverse effects
- dehydration
- postural hypotension
- hypokalaemia
- hyponatraemia
- hypercalcaemia
the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones
- gout
- impaired glucose tolerance
- impotence
Rare adverse effects:
- thrombocytopaenia
- agranulocytosis
- photosensitivity rash
- pancreatitis

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6
Q

Thiazide diuretic examples

A

Whatever their name, they always have thiazide at the end
Chlorothiazide, hydrochlorothiazide, bendroflumethiazide

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7
Q

Thiazide diuretics vs loop diuretics in heart failure

A

Thiazide diuretics have a role in the treatment of mild heart failure although loop diuretics are better for reducing overload.

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8
Q

Examples of thiazide like diuretics

A

chlorthalidone, indapamide, and metolazone, quniethazone

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9
Q

A 76-year-old lady is brought in by ambulance to the emergency department. She presents with a right-sided limb weakness, a facial droop and slurred speech. A CT head was arranged which ruled out a haemorrhage, but did report a left-sided infarct. Her admission ECG shows that she has new atrial fibrillation (AF). She is treated with aspirin 300mg for the acute stroke and doing well on the ward.

Two weeks later she is reviewed. What medication should the patient be started on to reduce the risk of further stroke?

Warfarin or a direct thrombin or factor Xa inhibitor
Aspirin
Clopidogrel
Dipyridamole
Enoxaparin

A

Warfarin or a direct thrombin or factor Xa inhibitor

Aspirin/dipyridamole should only be given if needed for the treatment of other comorbidities. None are mentioned in the above scenario.

Aspirin/dipyridamole should only be given if needed for the treatment of other comorbidities. None are mentioned in the above scenario.

Enoxaparin would not be prescribed long term but can be used for bridging whilst a patient is started on warfarin, until their INR is within range

Warfarin or a new oral anticoagulant (NOAC) should be started for a patient with AF who has had a new TIA or stroke. This is because their risk of having a further cerebrovascular event is increased (2 points on the CHA‚‚DS‚‚-VASc score).

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10
Q

What is the anticoagulation regimen of choice in a patient with AF has a cerebrovascular accident?

A

If a patient with AF has a stroke or TIA, the anticoagulant of choice should be warfarin or a direct thrombin or factor Xa inhibitor

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11
Q

Management of AF patient who just had a stroke or TIA

A
  • Following a stroke or TIA it is obviously important to exclude a haemorrhage before starting any anticoagulation or antiplatelet therapy
  • For longer-term stroke prevention, NICE recommend warfarin or a direct thrombin or factor Xa inhibitor
  • The timing of when to start depends on whether it is a TIA or stroke:
    * following a TIA, anticoagulation for AF should start immediately once imaging has excluded haemorrhage
    * in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period and stopped once anticoagulation started. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed
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12
Q

A 35-year-old male presents his general practice with pain in his foot and lower limb which is worse at night. He describes that the pain improves when he hangs his leg over the edge of the bed. On further questioning, he also notes that he has been getting ‘pins and needles’ in his fingers and they feel very cold. He has no past medical history but smokes 25 cigarettes per day.

Based on the history, what is the most likely underlying diagnosis?

Buerger’s disease
Granulomatosis with polyangiitis
Peripheral vascular disease
Sickle cell anaemia
Vitamin B12 deficiency

A

Young male smoker with symptoms similar to limb ischaemia - think Buerger’s disease

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13
Q

Feature of Buerger’s disease

A

Common symptoms include paraesthesia/cold sensation in the fingers or limbs, rest pain and ulceration/gangrene may occur

Features
extremity ischaemia
intermittent claudication
ischaemic ulcers
superficial thrombophlebitis
Raynaud’s phenomenon

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14
Q

What is Buerger’s disease also known as?

A

thromboangiitis obliterans

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15
Q

A 42-year-old patient attends the emergency department complaining of feeling generally unwell. He states that he is aching all over and has been waking up at night in a cold sweat.

On examination, you note evidence of various injection marks on the antecubital fossa. His observations show a temperature of 38.1ºC, a heart rate of 122bpm, a blood pressure of 110/90mmHg, respiratory rate of 18/min and oxygen saturation of 98%.

You request urgent blood cultures and an echocardiogram.

What site is most likely affected given the diagnosis?

Aortic valve
Mitral valve
No vegetations visible
Pulmonary valve
Tricuspid valve

A

Tricuspid valve

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16
Q

Which valve is most commonly affected in infective endocarditis in IV drug users?

A

Infective endocarditis in intravenous drug users most commonly affects the tricuspid valve

17
Q

Symptoms of IE

A

Can present either as an acute clinical deterioration or a subacute, more chronic development of the following non-specific symptoms;
- Fever (90%) - associated with chills, anorexia and weight loss.
- Other non-specific features include malaise, arthralgia, myalgia, night sweats, and abdominal pain.

18
Q

Clinical signs of IE

A

most of these are not diagnostic (as they can also be present in healthy individuals) but their presence can help support clinical suspicion:
- Heart murmurs (85%)
- Cutaneous manifestations
*Petechiae on extremities or mucous membranes (30%)
* Splinter haemorrhages (reddish-brown linear lesion on the nail bed)
- Uncommon findings that are very specific for IE include;
*Janeway lesions
*Osler node
*Roth spots
- Clinical manifestations of complications (eg. Congestive heart failure) or systemic embolisation (eg. Embolic stroke) may be present at initial presentation.

19
Q

In which subset of patients will a heart murmur be heard in IE

A

Usually only present in those with left sided IE.

20
Q

What are Janeway lesions? Are thye more associated with subacute or acute cases?

A

Non-tender macules on palms and soles, more associated with acute onset

21
Q

What are Osler node?

A

tender nodules on fingers and toes

22
Q

What are Roth spots?

A

hemorrhagic retinal lesions with a pale centre seen on fundoscopy

23
Q

What is most common presentation of isolated right sided IE?

A

Pulmonary septic emboli is the most common presentation (75%) of isolated right-sided IE. This can present clinically with a cough, dyspnoea, haemoptysis or pleuritic chest pain.

24
Q

How common is isolated right sided IE

A

10% of all cases of IE

25
Investigations for IE
Blood cultures (diagnostic) At least 3 samples from different sites over 30-60 mins is recommended. Adequate blood culture samples must be taken before starting any antibiotics, regardless of the clinical decision to start empirical antibiotics or to delay treatment. Echocardiogram (diagnostic). Additional; - ECG - helps to identify any further extension of the infection that may affect cardiac functioning for example; Heart block Conduction delay Ischaemic changes (which would indicate the presence of dispersed emboli affecting the coronary circulation) - Chest x-ray - looks for pulmonary septic emboli, congestive heart failure, any abscess' or is helpful to exclude other differentials. - CT scan (thoracic, abdominal and pelvic) is especially useful to identify the location of any metastatic infections that may require drainage.
26
Type of Echo for IE
- Transthoracic (TTE) is usually the first line investigation. - Transoesophageal (TOE) has a higher sensitivity than TTE for detecting IE, particularly L sided IE and any structural cardiac complications (intracardiac abscess, leaflet perforation, or pseudoaneurysm) and if available it is preferred as the first-line.
27
Risk factor for IE
The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. The following types of patients are affected: - previously normal valves (50%, typically acute presentation) * the mitral valve is most commonly affected - rheumatic valve disease (30%) - prosthetic valves - congenital heart defects - Intravascular catheter, intracardiac devices, arteriovenous fistula - intravenous drug users (IVDUs) - others: recent piercings
28
Organism causing infective endocarditis
- Staphylococcus aureus (Most common) - Streptococcus viridans (previously most common, most common still in developing countries) - coagulase-negative Staphylococci such as Staphylococcus epidermidis - Streptococcus bovis (associated with colorectal cancer)
29
Culture negative causes of IE
prior antibiotic therapy Coxiella burnetii Bartonella Brucella HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
30
Source of coagulase-negative Staphylococci such as Staphylococcus epidermidis in IE
- commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination. - after 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)
31
Pathophysiology of IE
The causative organism enters the bloodstream through either an infected catheter that is introduced to the body or a break to the skin or a mucous membrane. Bacteraemia progresses to IE in the presence of endocardial injury or damage (this can include damage due to turbulent blood flow secondary to dysfunctional valve or congenital abnormality that disrupts efficient blood flow through the heart). Endocardial injury â→ adherence of platelet and fibrin plug â→ circulating micro-organisms leads to secondary infection of plug â→ activation of coagulation cascade â→ adherence of more fibrin and platelets â→ growth of plug/vegetation.
32
Management of IE
- Effective antibiotic therapy: If there is a strong suspicion of IE and the patient is acutely unwell, initiating empirical antibiotics is recommended, but only after adequate blood culture samples have been taken. The choice of antibiotic depends on the following factors (which may help predict the different causative organisms); *Native valve *Prosthetic valve *People who inject drugs. - When the patient is clinically stable, starting antibiotic therapy is usually delayed to choose the most effective one based on blood culture results. - Find the source of infection, and remove it if possible, to optimise successful eradication of infection (Indwelling catheters or devices, check teeth, colonoscopy of organism associated with it) - Early valve surgery - Echo following abx therapy - Follow up echo if symptoms restart after getting better,
33
Why is echo following antibiotic therapy in IE required?
Following antibiotic therapy, even with successful treatment, complete resolution of any valvular vegetation is uncommon, an echo is recommended to establish the new baseline (including valve appearance, vegetation size and heart function).
34
Complications of IE
Delay in diagnosis or treatment can lead to a variety of complications, that can be broadly divided into cardiac complications and complications associated with metastatic infection.
35
Cardiac complications of IE
- Valvular insufficiency is the most common complication of IE, which if left untreated can lead to congestive heart failure - Other cardiac complications include pericarditis (which can present with retrosternal chest pain) or a perivalvular abscess (which can disrupt cardiac conduction leading to abnormal ECG's)
36
Forms of metastatic infection in IE
Forms of metastatic infection include Embolisation (which can lead to infarction and subsequent damage to various peripheral tissues) Metastatic abscess formation Mycotic aneurysms
37
Systemic emboli in IE
These can all lead to infarction, abscesses, infection of said organs Systemic emboli affecting the brain (embolic stroke most common neurologic complication), kidneys, spleen, and other soft tissues commonly occurs in left sided IE whereas pulmonary emboli most commonly occur in right sided IE.
38
Prognosis of IE
Six-month mortality rate is variable and can be up to 27% (quoted in uptodate). Factors associated with a worse prognosis include; - Heart failure - Larger vegetation size - Microbiology (a worse outcome is associated with -staphylococcal than with streptococcal infections) - Perivalvular abscess - Poor surgical candidate (early valve surgery confers a lower mortality risk)
39
Indication of valve surgery in IE
Early surgical intervention, ie. prior to finishing antibiotic therapy, is indicated if the following complications arise: - IE-associated valvular regurgitation/dysfunction - Heart failure - Intracardiac abscess - Persistent infection or difficult to treat organism