Corrections - Cardiology Flashcards
1st line treatment of PE?
DOACs
1st line treatment of massive PE with circulatory failure (e.g. hypotension)?
Thrombolysis
Describe the pain in aortic dissection
‘Tearing’, radiates into back
What may be seen in a CXR in aortic dissection?
Widened mediastinum
Features of pericarditis?
- chest pain: may be pleuritic. Is often relieved by sitting forwards
- other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
What ECG changes are seen in pericarditis?
The changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
1) ‘saddle-shaped’ ST elevation
2) PR depression: most specific ECG marker for pericarditis
What is the most specific ECG marker for pericarditis?
PR depression
Major cardiac complicaton of Kawasaki disease?
What investigation can be used to screen for this?
Coronary artery aneurysm –> echocardiogram
What is B-type natriuretic peptide (BNP)?
a hormone produced mainly by the left ventricular myocardium in response to strain
Give some causes of an increased BNP
- LV hypertrophy
- Ischaemia
- Tachycardia
- RV overload
- Hypoxaemia (including PE)
- GFR <60 ml/min
- Sepsis
- COPD
- Diabetes
- Age >70
- Liver cirrhosis
Give some causes of an decreased BNP
- Obesity
- Diuretics
- ACEi
- Beta blockers
- Angiotensin 2 receptor blockers
- Aldosterone antagonists
What is indicated in patients with clinical signs of heart failure and raised BNP greater than 400 pg/ml?
Urgent (within 2 weeks) specialist review and echocardiogram
What should be given in addition to aspirin to all NSTEMI patients unless high bleeding risk?
Fondaparinux
Classic CXR signs in pulmonary oedema?
- Kerley lines
- Bilateral peri-hilar shadowing (‘bat wing appearance’)
What are 2 respiratory causes of erythema nodosum?
1) TB
2) sarcoidosis
What is TURP syndrome?
A rare and life threatening complication of transurethral resection of the prostate surgery.
Caused by venous destruction and absorption of the irrigation fluid.
Symptoms of TURP syndrome?
typically presents with CNS, respiratory and systemic symptoms
Risk factors for developing TURP syndrome?
surgical time > 1 hr
height of bag > 70cm
resected > 60g
large blood loss
perforation
large amount of fluid used
poorly controlled CHF
Give some causes of RBBB
1) normal variant - more common with increasing age
2) right ventricular hypertrophy
3) chronically increased right ventricular pressure - e.g. cor pulmonale
4) pulmonary embolism
5) myocardial infarction
6) atrial septal defect (ostium secundum)
7) cardiomyopathy or myocarditis
ECG features in LBBB vs RBBB
in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
What investigation is used to capture episodic arrhythmias?
Holter monitoring (24 hours)
Cardiac features of thyrotoxicosis?
1) palpitations, tachycardia
2) AF
3) high output HF
Give some symptoms of acute mitral regurgitation
Acute mitral regurgitation can lead to flash pulmonary oedema:
- acute onset shortness of breath
- bibasal crackles
- hypotension
- systolic murmur
Damage to what muscle can cause acute mitral regurg after MI?
Papillary muscles (leads to loss of competency of the mitral valve)
Main monitoring parameters in:
a) statins
b) ACEi
c) amiodarone
a) LFTs
b) U&Es
c) TFTs, LFTs
Main monitoring parameters in:
a) methotrexate
b) azathioprine
a) FBC, LFTs, U&Es
b)FBCs, LFTs
Main monitoring parameters in:
a) lithium
b) sodium valproate
a) lithium level, TFTs, U&Es
b) LFTs
Main monitoring parameters in glitazones/
LFTs
NSTEMI (managed with PCI) antiplatelet choice:
a) if taking an oral anticoagulant
b) if the patient is not taking an oral anticoagulant
a) clopidogrel
b) prasugrel or ticagrelor
What 2 things should be measured when starting an ACEi?
1) serum creatinine
2) potassium levels
What rise in creatinine and potassium is acceptable after starting an ACEi?
1) increase in serum creatinine up to 30% from baseline
2) increase in K+ up to 5.5 mmol/L
If a patient is having persistent myocardial ischaemia following thrombolysis (fibrinolysis), what should you do?
Transfer patient for PCI
In a suspected PE, if the CTPA is negative what is the next investigation?
Consider proximal leg US if DVT is suspected
Bradycardia can be a complication of an MI.
Which type of MI (i.e. which aspect of the heart) is most likely to cause bradycardia? Why?
Inferior MI (affect RCA) - can cause ischaemia of AV node causing AV block
If a patient presents with sudden HF: bibasal crackles, raised JVP, pulsus paradoxus, muffled heart sounds etc, what complication of MI is most likely?
LV free wall rupture
What investigations should be done in all new cases of hyperkalaemia?
ECG
At what K+ level should treatment be immediately offered?
> /= 6.5 mmol/L
What electrolyte abnormalities can cause a long QT interval?
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
An ECG shows progressive prolongation of the PR interval until a dropped beat occurs.
What heart block is this?
Second degree heart block (Mobitz I)
Describe the murmur in mitral stenosis
mid-late diastolic murmur, ‘rumbling’ in character
Most likely infective organism in infective endocarditis in patients with no medical history?
S. aureus
Mechanism of thiazide diuretics?
inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule
New LBBB is always pathological. Causes of LBBB?
1) Myocardial infarction (especially if new LBBB)
2) HTN
3) Aortic stenosis
4) Cardiomyopathy
Causes of RBBB?
normal variant - more common with increasing age
right ventricular hypertrophy
chronically increased right ventricular pressure - e.g. cor pulmonale
pulmonary embolism
myocardial infarction
atrial septal defect (ostium secundum)
cardiomyopathy or myocarditis
How can amiodarone affect QT interval?
Can lengthen it
Kidneys in HIV-associated nephropathy vs CKD?
HIV-associated: bilateral large or normal sized kidneys on US
CKD: bilateral small kidneys
Give 4 causes of enlarged kidneys on US
1) autosomal dominant polycystic kidney disease
2) Chronic HIV-associated nephropathy
3) amyloidosis
4) diabetic nephropathy
What is a normal cardiac variant in atheletes?
1) 1st degree heart block
2) 2nd degree heart block mobitz type 1 (Wenckebach phenomenon)
3) sinus bradycardia
All patients with suspect ACS should be given aspirin 300mg, but further drug management depends on the type of ACS and proposed intervention.
What else should be given if the patient is to receive PCI?
Dual antiplatelet therapy:
1) Aspirin and prasugrel (if the patient does not take an oral anticoagulant)
2) Spirin and clopidogren (if they do take an oral anticoagulant)
All patients with suspect ACS should be given aspirin 300mg, but further drug management depends on the type of ACS and proposed intervention.
What else is offered to patients with unstable angina or an NSTEMI who do not have a high bleeding risk?
Fondaparinux
In an obese patient with a generalised headache, blurred vision, papilloedema and nausea/vomiting, what is msot likely?
idiopathic intracranial hypertension
What triad is seen in Boerhaave syndrome?
1) vomiting
2) thoracic pain
3) SC emphysema
What are the anterior ECG leads?
V1-V4
What are the inferior ECG leads?
II, III, aVF
What is a dangerous complication of fluid resuscitation in patients with diabetic ketoacidosis?
Cerebral oedema
Symptoms of cerebral oedema?
1) deteriorating mental status/ level of consciousness
2) incontinence
3) abnormal neurogenic respiratory pattern (e.g. grunting, abnormal tachypnoea, apnoea)
4) vomiting
Pain in pericarditis vs myocarditis?
Pericarditis - burning, pleuritic, relieved by sitting forward
Myocarditis - stabbing, not relieved by sitting forward
Contraindication of nitrates?
Hypotension (<90 mmHg)
Adverse effects of PPIs?
1) hyponatraemia, hypomagnasaemia
2) osteoporosis –> increased risk of fractures
3) microscopic colitis
4) increased risk of C. difficile infections
A LV aneurysm can develop post-MI. What signs may be seen?
1) Persistent ST elevation
2) LV failure e.g. SOB, bibasal crackles, raised JVP, peripheral oedema
This is due to the ischaemic damage sustained weakening the myocardium resulting in aneurysm formation.
Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy.
There are two types of coronary reperfusion therapy. What are they?
1) PCI (percutaneous coronary intervention)
2) fibrinolysis
When can PCI be offered in a STEMI?
Should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given
When should fibrinolysis be offered in a STEMI?
should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given
If patients having a STEMI are indicated to have PCI, what must they have before?
Dual antiplatelet therapy (i.e. aspirin + 1 more)
In dual antiplatelet therapy before PCI, what should the 2nd antipplatelet be in patients not taking an oral anticoagulant?
Prasugrel
In dual antiplatelet therapy before PCI, what should the 2nd antiplatelet be in patients who are taking an oral anticoagulant?
clopidogrel
Patients with a STEMI undergoing fibrinolysis must be given what prior?
Antithrombin drug e.g. fondaparinux
Patients with a STEMI undergoing fibrinolysis, how can the success be monitored?
What are the next steps?
An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved.
If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.
1st line management of NSTEMI/unstable angina?
Aspirin 300mg + fondaparinux (if no bleeding risk) if no immediate PCI planned
After initial management with aspirin and fondaparinux in NSTEMI/unstable angina, what is next done?
Use GRACE score to establish 6 month mortality
If a patient having an NSTEMI/unstable angina has a Grace score of </= 3% (i.e. low), what is next step?
Conservative management –> give ticagrelor
If a patient having an NSTEMI/unstable angina has a Grace score of > 3% (i.e. high), what is next step?
Consider PCI:
a) immediately if clinically unstable
b) within 72 hours if stable
Give some differentials for chest pain
1) MI
2) Pneumothorax
3) Pericarditis
4) Myocarditis
5) PE
6) Dissecting aortic aneurysm
7) GORD
8) Pleural effusion
9) MSK pain
10) Pneumonia
11) Shingles
12) Boerhaaves syndrome
13) Perforated peptic ulcer
Describe pain in dissecting aortic aneurysm
‘Tearing’ chest pain radiating through to the back
Potential exam finding in dissecting aortic aneurysm?
Unequal upper limb blood pressure
Why should metformin be stopped in patients having an MI?
Due to risk of lactic acidosis
When are antihypertensives offered?
a) age <80 y/o
AND
b) ambulatory BP of >/= 135/85 mmHg
AND
c) one or more of; target organ damage, established CVS disease, renal disease, diabetes and/or QRISK 10% or more
AV block can occur following an MI affecting which part of hear?
Inferior
Features of hypernatraemic dehydration?
- jittery movements
- increased muscle tone
- hyperreflexia
- confulsions
- drowsiness or coma
In patient with HTN who is already taking ACEi and has a history of gout, what is next step?
Add CCB e.g. nifedipine (history of gout favours CCB over thiazide like diuretic)
Signs and symptoms of malignant HTN?
1) bilteral retinal haemorhages
2) papilloedema (must be present before a diagnosis of malignant HTN can be made)
3) increased cranial pressure (headache, N&V)
4) nosebleeds
5) haematuria due to kidney failure
If a patient has a BP of >/= 180/120 mmHg and no worrying signs, what is next step?
Urgent investigation for end-organ damage
If a patient having a STEMI suddently develops worsening SOB and a new pan-systolic murmur, what is most likely cause of SOB?
Flash pulmonary oedema 2ary to acute mitral valve regurg.
Features:
1) widespread systolic murmur
2) hypotension
3) pulmonary oedema
This is most likely due to rupture of the papillary muscle during MI.
Side effects of adenosine?
- Flushing
- Chest discomfort
- SOB
- Headache
- Sense of impending doom
In a patient with a PE, what is the strongest indication for thrombolysis?
Massive PE + hypotension –> thrombolyse
How does a posterior MI typically present on an ECG?
Tall R waves V1-2
What Abx should be avoided in pregnancy?
1) tetracyclines e.g. doxycycline
2) aminoglycosides e.g. gentamicin
3) trimethoprim
4) quinolones e.g. ciprofloxacin
What drugs should be avoided in pregnancy?
1) ACEi
2) ARBs
3) Statins
4) Warfarin
5) Sulfonylureas
6) Retinoids (including topical)
7) Cytotoxic agents
8) Lithium (weigh up)
The majority of antiepileptics including valproate, carbamazepine and phenytoin are known to be potentially harmful.
In what trimester are ACEi contraindicated?
2nd and 3rd
Persistent ST elevation following recent MI with no chest pain and SOB indicates what?
left ventricular aneurysm
Indapamide vs bendroflumethiazide?
Indapamide is a thiazide-like diuretic and bendroflumethiazide is a thiazide.
Only thiazide-like diuretics are recommended in HTN.
For a STEMI, in the absence of contraindications, what should patients be given?
1) Aspirin
2) P2Y12-receptor antagonist e.g. clopidogrel, ticareglor, prasugrel
3) Unfractionated heparin (alternative is warfarin) –> usually given for patients who’re are going to have a PCI.
Threshold for transfusion of RBCs in patients with ACS?
Hb level of <80 g/L
What is most common cause of acute pericarditis?
Viral infection (patient may have had flu-like symptoms)
ECG findings in acute pericarditis?
1) Widespread ‘saddle shaped’ ST elevation
2) PR depression
Is risk of falls sufficient reasoning to withold anticoagulation in AF?
No
In AF, there is a subgroup of patients for whom a rhythm control strategy should be tried first (before rate control).
What are these exceptions?
1) Coexistent HF
2) First onset AF
3) Where there is an obvious reversible cause.
When can new onset AF be considered for electrical cardioversion?
If within 48 hours of presentation
In cases of ischaemic stroke and atrial fibrillation, what is pharmacological management?
2 weeks of aspirin 300mg OD before consideration of lifelong anticoagulation.
Common contraindication of beta blockers in AF?
Asthma
What is the most likely cause of an irregular broad complex tachycardia in a stable patient?
Atrial fibrillation with bundle branch block
If a patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion.
What is an alternative?
An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus
If a patient has a new BP >= 180/120 mmHg AND retinal haemorrhage or papilloedema, what is next step?
Admit for specialist assessment
What score is used to assess the bleeding risk of anticoagulation?
ORBIT score
1st line investigation in marked tachycardia?
ECG
Overdose of tricyclic antidepressants is a common presentation to emergency departments.
What 2 are particularly dangerous in overdose?
Amitryptiline & dosulepin (dothiepin)
Early features of TCA overdose?
relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.
Features of severe TCA overdose?
- arrhythmias
- seizures
- metabolic acidosis
- coma
ECG changes seen in TCA overdose?
- sinus tachycardia
- widening of QRS
- prolongation of QT interval
What is widening of QRS interval associated with?
1) QRS > 100ms is associated with an increased risk of seizures
2) QRS > 160ms is associated with ventricular arrhythmias
1st line management of TCA overdose?
IV bicarbonate (indications include widening of the QRS interval >100 msec or a ventricular arrhythmia)
What should be avoided in TCA overdose?
1) class Ic antiarrhythmics (e.g. Flecainide)
2) class III drugs (e.g. amiodarone) should also be avoided as they prolong the QT interval
Why is amiodarone contraindicated in TCA overdose?
As it prolongs QT interval
What is the most common heart lesion associated with Duchenne muscular dystrophy?
Dilated cardiomyopathy
Driving rules surrounding hypoglycaemia?
Patient with diabetes who have had two hypoglycaemic episodes requiring help needs to surrender their driving licence
Wht is spontaneous intracranial hypotension?
a very rare cause of headaches that results from a CSF leak
Key features of headache in spontaneous intracranial hypotension?
Strong postural relationship with the headache generally much worse when upright. Patients may, therefore, be bed-bound
Major risk factor for spontaneous intracranial hypotension?
Connective tissue disorders such as Marfan’s syndrome.
What is a sudden collapse occurring soon after a rupture of membranes suggestive of?
amniotic fluid embolism.
What is the Cushing reflex?
a physiological nervous system response to increased intracranial pressure (ICP) that results in hypertension and bradycardia
Describe HR and BP in increased ICP?
1) HTN with wide pulse pressure
2) Bradycardia
What is Cushing’s triad in raised ICP?
1) HTN with wide pulse pressure
2) Bradycardia
3) Irregular breathing
1st line for treating atrioventricular nodal re-entry tachycardia (AVNRT)?
Adenosine
Adverse effects of adenosine?
- Feeling of doom
- Chest pain
- Bronchospasm
- Transient flushing
What is hypertrophic obstructive cardiomyopathy (HOCM)?
An autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins.
What is the most common cause of sudden cardiac death in the young?
hypertrophic obstructive cardiomyopathy (HOCM)
Pathophysiology of HOCM?
1) mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
2) results in predominantly diastolic dysfunction: left ventricle hypertrophy –> decreased compliance –> decreased cardiac output
Most common cause of sudden death in HOCM?
Ventricular arrhythmias
Features of HOCM?
- often asymptomatic
- exertional dyspnoea
- angina
- syncope (typically following exercise)
- sudden death
- jerky pulse, large ‘a’ waves, double apex beat
- systolic murmurs (ejection systolic murmur, pansystolic)
If a patient’s AF has been going on for >48 hours, what is most appropriate action?
1) control rate with bisoprolol (unless contraindicated)
2) anticoagulate for at least 3 weeks
3) after this period, electrical cardioversion would be safe
What is the indication for immediate electrical cardioversion in AF?
Acute presentation of atrial fibrillation plus signs of haemodynamic instability (e.g. hypotension, heart failure)
What ECG sign is considered pathognomic for cardiac tamponade?
Electrical alternans
What triad of symptoms is seen in cardiac tamponade?
1) hypotension
2) raised JVP
3) muffled heart sounds
What post-MI complication is typically associated with persistent ST elevation and left ventricular failure?
Left ventricular aneurysm
What is Takotsubo cardiomyopathy?
A type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium.
It may be triggered by stress.
Features of Takotsubo cardiomyopathy?
- chest pain
- features of heart failure
- ECG: ST-elevation
- normal coronary angiogram
Management of Takotsubo cardiomyopathy?
Supportive
What is idiopathic intracranial hypertension?
a condition classically seen in young, overweight females.
Risk factors for idiopathic intracranial hypertension?
- obesity
- female sex
- pregnancy
- drugs: COCP, steroids, tetracyclines, retinoids (isotretinoin, tretinoin) / vitamin A), lithium
Features of idiopathic intracranial hypertension?
- headache
- blurred vision
- papilloedema (usually present)
- enlarged blind spot
- sixth nerve palsy may be present (bilateral)
Do patients who’ve had a catheter ablation for atrial fibrillation still require long-term anticoagulation?
Yes - as per their CHA2DS2-VASc score
Which CCB is used in rate control AF (e.g. if beta blocker is contraindicated)?
Verapamil
N.B. Amlodipine is not a rate-limiting calcium channel blocker, and therefore unsuitable for AF
Why must patients with AF either be a) anticoagulated for 3 weeks, or b) have had symptoms for < 48 hours before cardioversion?
To reduce risk of stroke
How often should BP be checked in patients with clinic BP <140/90 mmHg?
Every 5 years (more often if closer to 140/90)
Management of patient with clinic BP of 140/90 to 179/119 mmHg?
1) Offer ABPM (or HBPM if ABPM declined or not tolerated).
2) Investigate for target organ damage: U&Es, urine dip (haematuria), urinary ACR, fundoscopy, ECG
3) Assess QRISK
What to discuss when initiating ACEi in HTN:
1) Side effects: cough (can come on years down line)
2) Safety net: angioedema
3) 1st dose: can cause postural hypotension so take sitting down
4) U&Es required 2 weeks after starting
5) Monitor BP 4 weeks after starting
6) Explain may need to be titrated up to achieve desired target
Management of patient with clinic BP of 180/120 or more?
1) Assess for target organ damage ASAP.
2) Consider starting drug treatment immediately without ABPM if target organ damage.
3) Repeat clinic BP in 7 days if no target organ damage.
what indicates the need for a same day review in patients with a clinic BP of 180/120 mmHg or more?
1) retinal haemorrhage or papilloedema (accelerated HTN) or;
2) life-threatening symptoms or;
3) suspected pheochromocytoma
Management options for patients with stage 1 HTN (135/85 to 149/94 mmHg)?
1) Offer lifestyle advice
2) Age >80 y/o with clinic BP >150/90 mmHg –> consider drug treatment
3) Age <80 y/o with target organ damage, CVD, renal disease, diabetes or QRISK >/= 10%
4) Age <60 y/o with QRISK <10%
5) Age <40 y/o need specialist evaluation of 2ary causes
When to consider drug treatment in patients <80 y/o with BP 135/85 to 149/94?
a) diabetes
b) CVS disease
c) renal disease
4) QRISK >/= 10%
5) target organ damage
Management of patients with stage 2 HTN (>/= 150/95 mmHg)?
Lifestyle AND drug treatment
What is base target for postural hypotension based on?
Standing BP
Does furosemide improve outcomes in HF?
No - symptomatic management
Management of HF with preserved EF?
1) Treat symptoms (e.g. loop diuretic)
2) If unsuccessful, refer to specialist
Acute management of HF exacerbation?
1) IV loop diuretic: furosemide/bumetanide
Possible additional treatments:
2) Oxygen
3) Vasodilators e.g. nitrates
When are vasodilators indicated in acute HF management?
Should NOT be given routinely.
May be indicated if concomitant myocardial ischaemia, severe HTN or regurgitant aortic or mitral valve disease.
What is the major side effect/contraindication of nitrates in acute HF management?
Hypotension
What is considered as 3rd line therapy for HF management in Afro-Caribbean patients (i.e. not responding to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy)?
Hydralazine and nitrate
What is a systemic complication of acute pancreatitis?
Acute respiratory distress syndrome (high mortality rate - around 20%)
Which drug is indicated as 3rd line therapy in management of HF if there is coexistent atrial fibrillation?
Digoxin
Medical management of angina?
1) All patients should be on. aspirin, statins & GTN spray (as long as no contraindications)
2) 1st line: Beta blocker or CCB
3) Increased (2) to max dose tolerated
4) Add beta blocker/CCB (whichever haven’t used)
5) If a patient is on monotherapy and cannot tolerate the addition of a CCB:
- a long-acting nitrate
- ivabradine
- nicorandil
- ranolazine
Which CCB should be used in the management of angina?
1) if monotherapy: a rate-limiting one such as verapamil or diltiazem should be used
2) if used in combination with a beta-blocker then use a longer-acting dihydropyridine CCB (e.g. amlodipine, modified-release nifedipine)
What is rapid drainage of a pneumothorax a risk factor for?
Developing re-expansion pulmonary oedema
Risk factors:
- Large pneumothorax
- History of diabetes
In patients with HF who have not responded to an ACE-inhibitor, beta-blocker and aldosterone antagonist therapy, what are next options to consider?
- ivabradine
- sacubitril-valsartan
- digoxin
- hydralazine in combination with nitrate
- cardiac resynchronisation therapy
Criteria for ivabradine in 4th line HF?
sinus rhythm > 75/min and a left ventricular fraction < 35%
How can 1ary and 2ary aldosteronism be differentiated?
Look at renin levels:
If renin low: 1ary cause more likely
If renin high: 2ary cause more likely
Most common cause of renal artery stenosis?
Atherosclerosis
Features of renal artery stenosis (secondary to atherosclerosis)?
- HTN
- CKD
- ‘Flash pulmonary oedema’
How can renal artery stenosis result in 2ary hyperaldosteronism?
ACEi can worsen stenosis, resulting in a drop in eGFR, activating RAAS.
2nd line therapy in HF?
1) aldosterone antagonist
2) SGLT-2 inhibitors e.g. dapagliflozin
What is Charcot joint?
A Charcot joint is also commonly referred to as a neuropathic joint. It describes a joint which has become badly disrupted and damaged secondary to a loss of sensation.
Causes of Charcot joint?
- Diabetic neuropathy
- Alcoholic neuropathy
- Syphilis
- Cerebral palsy
Features of Charcot joint?
- Non-tender, swollen, erythematous and hot foot
- Xray findings: osteolysis and joint dislocation
In patients with acute HF and respiratory failure, management option?
CPAP
Management option of acute HF in patients with hypotension (e.g. <85 mmHg)/cardiogenic shock?
This can be a difficult scenario to manage -
some of the treatments typically used for acute heart failure (e.g. loop diuretics and nitrates) may exacerbate the hypotension.
1) Inotropic agents e.g. dobutamine (considered for patients with severe left ventricular dysfunction who have potentially reversible cardiogenic shock)
2) Vasopressor agents e.g. norepinephrine (normally only used if insufficient response to inotropes and evidence of end-organ hypoperfusion)
3) Mechanical circulatory assistance
How does liver feel in RHF?
Firm, smooth, tender and pulsatile liver edge
Causes of hypoglycaemia?
Mneumonic: EXPLAIN
E - Exogenous drugs (typically sulfonylureas or insulin)
P - Pituitary insufficiency
L - Liver failure
A - Addison’s disease
I - Islet cell tumours (insulinomas)
N - Non-pancreatic neoplasms
What condition can thiazide diuretics (e.g. bendroflumethiazide) exacerbate?
Gout: by increasing serum uric acid levels (thiazides reduce renal uric acid excretion)
