Geratology Flashcards
What do you need to check before starting a patient on ramipril?
Ramipril (ACE inhibitor) is used for hypertension, and in combination with furosemide in heart failure (with a beta-blocker initiated afterwards if required; if the heart failure is ischaemic, patient also gets aspirin and statins)
ACE-inhibitors are nephrotoxic, so need to check U+Es - contraindicated if eGFR is <60.
Contraindicated in hypertension secondary to RENAL ARTERY STENOSIS (which is usually due to atherosclerosis, or by fibromuscular dysplasia - seen frequently in younger women). The reason ramipril is bad in this case is because autoregulation of GFR is almost exclusively dependent on changes in post-glomerular arteriolar tone (as the afferent pressure is reduced by the narrowed vessel); because ACE inhibitors reduce production of angiotensin II, whose role is normally to mediate constriction of the post-glomerular arteriole and therefore increase pressure within the glomerulus (restoring filtration), in renal artery stenosis ACE-i cause glomerular perfusion to fall, resulting in renal ischaemic nephropathy and renal failure.
Side effects of ACE inhibitors?
Dry irritating cough (due to elevated pulmonary bradykinin) Angioedema Hyperkalemia Orthostatic hypotension Renal failure
CAPTOPRIL: cough, angioedema, potassium excess, taste changes, orthostatic hypotension, pregnancy CI, renal failure/rash
Amiodarone is used for what?
Anti-arrhythmic: used for AF and atrial flutter, praoxysmal supraventricular tachycardia, ventricular tachycardia, v-fib (after defibrillation, and if refractory to 3 shocks then IV adrenaline + IV amiodarone)
Toxicities of amiodarone?
- Amiodarone contains iodine and can cause both hypothyroidism and hyperthyroidism
- Hepatotoxicity
- Pulmonary toxicity (pneumonitis) - interstitial lung disease
- Peripheral neuropathy
- Bradycardia/hypotension
Excretion is hepatic/biliary with almost no elimination via the renal route hence can be used in patients with CKD. However, when simvastatin is used with amiodarone this can cause rhabdomyolysis, which can lead to acute kidney failure.
What drugs when prescribed alongside statins can cause rhabdomyolysis?
Macrolides
Amiodarone
What are the features of digoxin toxicity?
Digoxin blocks Na/K ATPase, –> increase in intracellular calcium within cardiac myocytes –> increased inotropy.
Digoxin toxicity causes hyperkalemia, because blocking Na/K ATPase prevents its usual action of transporting K+ into cells. However, if the patient is hypokalemic this actually worsens digoxin toxicity b/c digoxin binds to the same site as K+ on the ATPase pump; therefore if there is low K+, digoxin exerts more inhibition on the pump.
- Arrhythmias (ventricular extrasystoles, atrial tachycardia with complete heart block)
- Confusion (altered mental status) especially in elderly patients
- GI signs (nausea/vomiting/abdo pain)
- Yellow vision (xanthopsia), blurred vision, photophobia
- Weakness/dizziness
How would you manage digoxin toxicity?
Investigations: serum digoxin concentration, serum K+, creatinine, urea, serial ECGs
- Stop digoxin
- Only correct hyperkalemia (e.g. within insulin/glucose) if life-threatening, due to risk of producing hypokalemia
- If patient has hypokalemia or hypomagnesaemia, give K+ or Mg2+ with careful monitoring
- Activated charcoal PO
- Rehydrate
- DSFab therapy
Do NOT give calcium gluconate to treat hyperkalemia (the usual treatment for hyperkalemia causing ECG changes is IV calcium) in patients with suspected dig tox as it may induce life-threatening arrhythmia.
What causes digoxin toxicity in old people?
- 70% of digoxin is excreted via the kidneys; if dehydrated or infection, this reduces GFR (or other drugs may be affecting the kidneys) - or in patients with CKD
- Macrolides interact with digoxin and can cause toxicity
- Other drugs that can cause dig toxicity: antimalarials, anti-arrhythmics, CCBs (especially daltezam), diuretics (due to K+ depletion)
Warfarin mechanism of action?
Inhibits conversion of inactive form of Vitamin K to active form which is needed to produce clotting factors II, VI, IX and X.
Overall this leads to a decrease in prothrombin and thrombin levels.
What is a common drug-related cause of confusion in elderly patients?
SiADH (excessive ADH secretion from the posterior pituitary in spite of plasma hypotonicity and a normal plasma volume, resulting in dilutional hyponatremia). Drug culprits: opiates, ciprofloxacin, cyclophosphamide, vincristine, SSRIs/TCAs, carbamazapine, amiodarone, benzodiazepines.
Other causes of SiADH aside from drugs are ectopic secretion by a tumour (mc small cell lung cancer), CNS disease (meningitis, abscess, head injury, SAH, stroke), lung disease (TB, pneumonia), alcohol withdrawal.
Diagnostic criteria: euvolaemic hyponatremia, low serum sodium, high urine sodium, low plasma osmolality with inappropriately high urine osmolality; absence of hypokalemia; normal renal, adrenal and thyroid function.
- Do paired serum and urine osmolality
- Short synacthen test (negative) - measures adrenal response to ACTH i.e. cortisol - used to exclude adrenal insufficiency (Addison’s or secondary adrenal insufficiency where the pituitary doesn’t produce enough ACTH)
Clinical features of SiADH?
Nausea Myalgia/muscle weakness Hyporeflexia, ataxia, tremor Headache Cheyne-Stokes respiration
Treatment of SiADH
Fluid restriction to 500-1000ml/24h
Demeclocycline (inhibits action of ADH on kidney - useful if water restriction is ineffective)
How do you reverse warfarin in an emergency? e.g. if major bleeding, or if emergency surgery is needed,
IV vitamin K
Stop warfarin
Give dried prothrombin complex (factors II, VII, IX and X) or if unavailable give fresh frozen plasma
What is the target INR for patients on warfarin?
2.5 for atrial fibrillation and indicated by CHADS2 score (risk of stroke in AF), treatment of DVT or PE, dilated cardiomyopathy, bioprosthetic mitral heart valve (treat for 3 months)
3
How is an acute stroke managed in terms of anticoagulation/antiplatelet therapy?
Aspirin 300mg ASAP once a haemorrhagic stroke is excluded; continue for 2 weeks
Statin after 48h if cholesterol >3.5
Then after 2 weeks commence clopidogrel - this is an antiplatelet (second line is aspirin + dipyridamole)
Remember: aspirin 2 weeks, statin, clopidogrel
How is a TIA managed?
Aspirin 300mg
TIA clinic - consider same-day MRI +/- carotid US
Anticoagulation: dipyridamole + aspirin (not clopidogrel)
What sort of drugs are rivoraxiban and apixiban?
DOAC (direct oral anticoagulants) also known as NOACs (novel OACs)
These require good kidney function (warfarin is an alternative in patients with low GFR)
Management post-MI?
MONA-BASH
Morphine + anti-emetic Oxygen (if SaO2 <95%, breathless, or in acute LVF) (Nitrates - GTN use is now not recommended in acute setting unless patient hypertensive or in acute LVF) Aspirin PO Beta-blocker ACE-inhibitor Statin Heparin
–> Cath lab to restore coronary perfusion, i.e. primary PCI (percutaneous coronary intervention)
Alternative is thrombolysis (if PCI can’t be performed within 2h of first medical contact, and symptom onset was within the last 12h; thrombolysis is contraindicated if >24h from onset of symptoms)
Treatment of heart failure?
ACE-inhibitor/ARB
Then once stable on this, start a beta-blocker (bisprolol).
+ diuretic to treat fluid retention symptoms (oedema/SOB)
+ aspirin and statins if ISCHAEMIC heart failure
Extras (if still symptomatic)
+/- spironolactone (K+ sparing diuretic, aldosterone antagonist) - helps to counter hypokalaemia caused by furosemide (CI: hyperkalemia, renal impairment)
+/- vasodilator (combo of hydralazine and isosorbide dinitrate) - used if intolerant of ACE/ARB, or if patient is Afro-Caribbean as an addition to standard therapy
+/- digoxin if in stage 4 NYHA i.e. dyspnea at rest
ICD indicated if LVEF <35%
Lifestyle modifications: fluid restriction <2L/day, salt restriction
What sort of drug are captopril, enalapril, ramipril, benazepril?
ACE inhibitors
What kind of drugs are candasartan and losartan?
ARB
Symptoms of asthma?
- Wheezing, chest tightness, SOB, chronic cough
- Often strong FHx of asthma/atopic disease
- Exacerbation by irritants or seasonal exposures
Symptoms of COPD?
- Smokers
- Productive morning cough that becomes constant as disease progresses; sputum quality may change with exacerbations or superimposed infection
- Frequent chest infections (bronchitis or pneumonia)
- SOB on exertion (progresses to at rest)
Differentials for chronic cough?
- Asthma
- Pneumonia
- COPD
- Upper airway cough syndrome (postnasal drip from allergic rhinitis, bacterial sinusitis, post-infectious rhinitis)
- Gastric reflux
- ACE inhibitors
Less common causes:
- TB
- Bronchiectasis
- Chronic bronchitis
- Irritants e.g. cigarette smoke
- *Bronchogenic carcinoma
- Interstitial pulmonary fibrosis (dry cough, dyspnoea of sub-acute onset)
- Sarcoidosis
- Recurrent aspiration e.g. in neurological disorders like Parkinson’s, MS
Symptoms/flags for bronchogenic carcinoma?
- Hx of smoking
- Symptoms: hronic COUGH and esp. change in character of chronic cough; haemoptysis (70%); voice hoarseness; chest pain; recurrent/slowly resolving pneumonia, weight loss/anorexia, pleural effusion
- Signs: enlarged axillary nodes, SVC syndrome (localised oedema of face/upper extremities, facial plethora, distended neck veins), Horner’s syndrome if apical tumour (Pancoast) compressing sympathetic chain, anaemia, clubbing
Symptoms/flags for TB
Chronic cough productive of sputum, occasionally haemoptysis, fever/weight loss/night sweats, having visited or lived in an endemic country, close contact with active TB, immunocompromise (e.g. HIV+, IVDU)
Symptoms of acute bronchitis?
- Cough (non-productive or mildly productive) - sputum may be clear or purulent; can take 2-3 weeks to subside
- Preceded by URI symptoms by ~5d
- Subjective SOB due to chest pain/tightness
- May have mild fever (high fever is unusual however, suggests influenza or pneumonia)
Treatment of acute bronchitis
Symptom relief (paracetamol) Inhaled beta-agonist (salbutamol) for short time if wheezing
NO ANTIBIOTICS
CXR only if worrying symptoms that suggest pneumonia or serious illness, such as mental status change, high fever, tachypnea, hypoxaemia, crackles, signs of consolidation of pleural effusion
What is pneumonia?
What are the most common organisms that cause CAP?
Infection of the lung parenchyma with consolidation
Organisms: Streptococcus pneumonia (60%), H. influenzae, Klebsiella pneumonia
In a hospital setting, S. aureus (ITU), Pseudomonas (especially if immunocompromised/COPD)
Symptoms of pneumonia
Non-specific: fever, rigors, malaise, anorexia
Specific: cough, SOB, purulent sputum, haemoptysis, pleuritic chest pain
Investigations in ?pneumonia (CAP)
CXR (shows consolidation; if negative, consider bronchitis)
SaO2 (tells you if there is hypoxia)
Bloods: FBC, U+E, LFTs, CRP, atypical serology
Viral throat swabs if appropriate (?influenza)
Blood cultures if pyrexial
Calculate **CURB-65**: - Confusion (AMTS ≤8) - Urea >7 mmol/L - RR ≥30/min - BP <90/60 mmHg - Age ≥65 A score of ≥3 indicates severe pneumonia = requires admission, co-amoxiclav + clarithromycin 2-3 = amoxicillin + clarithromycin (and potentially short admission) 0-1 = amoxicillin
Clarithromycin treats atypical organisms e.g. mycoplasma pneumonia, C. ptsittaci, Legionella pneumophilia
Complications of pneumonia?
- Pleural effusion or empyema
- Respiratory failure
- Septicaemia
- Pericarditis/myocarditis
- AKI
Management of HAP?
HAP develops ≥48h after hospital admission
Antimicrobial prescribing:
- Non-severe symptoms: co-amoxiclav PO or doxycycline if penicillin allergy
- Severe symptoms or signs (e.g. sepsis): IV piperacillin with tazobactam (pip/taz; this covers pseudomonas)
- Add vancomycin to IV abx if MRSA suspected or confirmed
Why would VTE happen in the arm?
Due to a central venous line (axillary vein thrombosis)
What is Virchow’s triad?
- Venous stasis
- Endothelial injury (central lines or other trauma, smoking)
- Hypercoagulable state (malignancy, OCP, HRT, factor V Leiden)
D/d for unilateral swollen leg?
- DVT (clot in the deep veins of the leg, pelvis or arm)
- Cellulitis (bacterial infection of the deep layers of the skin)
- Ruptured Baker’s cyst (synovial cyst due to arthritis of the knee; causes sudden swelling of the leg if it ruptures)
What happens physiologically in a PE?
- Pulmonary hypertension, which produces right heart strain
- Clot obstructs blood flow to an area of the lung –> V/Q mismatch in this area –> hypoxemia and cyanosis
- Reduced oxygen levels, so body responds by increasing CO via increased HR (tachycardia)
- CO2 is perfusion-limited, so with tachycardia (increased perfusion) and tachypnea (increased ventilation), CO2 levels drop –> this can lead to a respiratory alkalosis (though not necessarily)
PE investigations and management?
Calculate PE Well’s Score
ECG (may show right heart strain)
ABG (may show respiratory alkalosis)
If Well’s score is <2, likely NOT a PE; –> do D-dimer test (D-dimer levels will be very elevated in VTE or DIC)
If Well’s score is 4+, first-line in the JR is a V/Q scan (compares inhaled isotopes vs. injected) - time-consuming, can be difficult to interpret if lung disease
Alternative and GOLD STANDARD is a CTPA (CT pulmonary angiogram, i.e. a ‘spiral angiogram’) - need to do U+Es before as has contrast, patient needs normal kidneys (creatinine), invasive.
Treatment of PE?
Anticoagulation with HEPARIN, bridging to 5d warfarin. Alternative is a NOAC which doesn’t need bridging, but really in an acute setting you use heparin.
tPA is used in a massive PE i.e. PE and hypotension.
What does a spirometer measure?
Functional lung volumes: FEV1 (forced expiratory volume in 1s) and FVC (forced vital capacity = total amount of air exhaled during the FEV test) are measured from a full forced expiration into a spirometer. FEV1/FVC ratio is an estimate of airflow obstruction (normal ratio is 75-80%)
What does a peak flow meter measure?
Peak expiratory flow - measured by maximal forced expiration; it correlates well with FEV1.
Does asthma affect inspiration or expiration?
What questions would you ask to assess chronic symptoms?
Rapid onset of difficulty in EXPIRATION, with wheezing
1. night-time symptoms (waking), 2. day-time cough, 3. limiting daily activities?
Ask if compliant with inhaler.
Tx asthma?
SABA prn (salbutamol or terbutaline i.e. Bricanil) + ICS e.g. beclomethasone (Clenil; need to use spacer device)
Add-ons:
- Montelukast
- LABA e.g. salmeterol, formoterol - must switch ICS to combined LABA/ICS inhaler (i.e. not prescribed separately) e.g. symbicort is formoterol + budenosine.
If still uncontrolled:
- Increase ICS dose
- Trial a LAMA e.g. tiotropium
- Seek specialist advice
Tx COPD?
Bronchodilators:
SABA + either LAMA (tiatroprium) or LABA (salmeterol)
- LAMA + LABA if no asthmatic features
- LABA + ICS if asthmatic features
- Can have triple therapy (LAMA + LABA + ICS if having severe/frequent exacerbations)
Oral therapy:
- PO corticosteroids if severe COPD - Theophylline (requires monitoring, interacts with macrolides) - Azithromycin (prophylactic)
O2 therapy - consider if PaO2 < 7.3 kPa (sats of ~88%) and non-smoker, or if nocturnal hypoxaemia/pulmonary HTN/secondary polycythaemia
Other things:
- Pulmonary rehab - Vaccines (flu, streptococcal) - Smoking cessation
Tx of exacerbation: antibiotics and steroids (send sputum sample for culture so can adjust abx). Rescue pack includes abx (amoxicillin or doxycycline) and prednisolone PO.
*note: very dangerous to put someone with asthma on a LABA before putting them on inhaled corticosteroids (ICS), whereas in COPD it is LABA -> ICS
Symptoms of COPD exacerbation?
And Tx?
Wheezing, cough, + sputum
Tx:
- Abx: doxycycline or azithromycin
- Bronchodilators: salbutamol +/- ipatroprium (can be inhaler or nebulised)
- Steroids: either PO (pred) or IV (methylpred)
- If in hospital, oxygen to 88-92% sats
- If inadequate response to nebulised bronchodilators, consider IV aminophylline or salbutamol
How would you investigate TB?
Latent TB: Mantoux test or IGRA
Active TB:
1) sputum microscopy (smear) (Zeihl-Neelsen stain)
2) culture (nucleic acid amplification, allows <2h diagnosis of TB)
Treatment of TB?
Rifampicin, isoniazid, pyrazinamide, ethambutol for 2mo
Rifampicin + isoniazid for a further 4mo
Investigations for ?lung ca
- CXR
- Cytology (sputum, pleural fluid)
- FNA/percutaneous biopsy if lesion is peripheral
- CT (tumour staging, and to guide bronchoscopy)
- Bronchoscopy + biopsy
Symptoms of AF?
SOB, palpitations, syncope/dizziness, chest pain/discomfort, stroke or TIA
Investigations for ?AF
- ECG
- Bloods: U+Es (kidney function for drug choice), thyroid (hyperthyroidism can present with AF)
- Echocardiogram (to exclude valve disease, pericardial disease, and cardiomyopathies; also to check for a thrombus in the left atrium)
Why is AF treated?
a) stroke prevention
b) alleviation of symptoms
b) prevention of tachycardia-induced cardiomyopathy
What are the clinical features of circulatory shock?
Increased cap refill time, cold peripheries
Low urine output
Low BP + tachycardia
Tx of AF
Rate control: beta-blocker, or rate-limiting CCB (e.g. diltiazem, verapamil), or digoxin, or amiodarone
OR
Anti-arrhythmic:
- Dronedarone (K+ channel blocker), flecainide (Na+ channel blocker), propafenone, solatol
AND
- Amiodarone (K+ channel blocker), dofetilide, or catheter ablation
+ ANTICOAGULATION if at high risk of stroke (CHADS(2) score) - takes into account: Congestive heart failure, Hypertension, Age >75y, Diabetes, Stroke/TIA/systemic embolism, (peripheral) Vascular disease, Age ≥65y, Sex (female)
- Warfarin or NOAC if >2 points
- If anticoagulation is not indicated by CHADSVASc (0-1), give daily aspirin
What toxicities does amiodarone have?
High iodine content of amiodarone –> pulmonary fibrosis, thyroid disease, liver dysfunction peripheral neuropathy
What anti-arrhythmics should you not use for AF with concurrent coronary artery disease?
Flecainide and propafenone (class Ic agents) - they slow the atrial cycle length, allowing faster AV conduction that can –> ventricular tachycardia
Three signs of Charcot’s triad (ascending cholangitis)
Jaundice, fever (usually with rigours), RUQ abdominal pain
How is the risk of major bleeding determined when considering anticoagulation for AF?
HAS-BLED score: Hypertension, Abnormal renal or liver function, Stroke, Bleeding predisposition or prior major bleed, Labile INR, Elderly (>65), Drugs or alcohol. A score of ≥3 indicates high risk.
How do you treat alcohol withdrawal?
- Benzodiazepine: diazepam PO/IV, lorazepam (can be IM), or chlordiazepoxide PO
- IV/IM/PO thiamine (reduces risk of Wernicke’s encephalopathy and Korsakoff syndrome)
- Magnesium sulfate IV (to correct hypomagnesaemia)
- If severe withdrawal and delerium tremens, can add phenobarbital (anti-epileptic)
Diagnostic test for COPD?
Spirometry: FEV1 and FVC decreased, with FEV1/FVC ratio <0.7
What are Well’s criteria for PE risk?
Signs/symptoms of DVT
PE is top differential diagnosis
Tachycardia (>100bpm)
Immobilisation for ≥3d OR surgery in last month
Previous DVT or PE
Haemoptysis
Malignancy w/ treatment in last 6mo or palliative
Symptoms of hyperthyroidism?
Weight loss
Tachycardia, palpitations, elevated BP
Fine resting tremor
Upper eyelid retraction
Treatment of hypertension?
Cut-off is 140/90 as a clinic reading, confirmed by at least an 135/85 average for home readings
Medication:
STEP 1
- First-line is CCB if older than 55 and/or Black (any age)
- First line is ACE-i/ARB if comorbid T2DM, younger than 55, and not Black
- First line for HTN is a beta blocker if comorbid AF (and second-line is CCB) or heart failure (and second-line is ACE-i)
STEP 2
- Titrate up
- Add the medication type you haven’t used (CCB or ACEi/ARB), or a thiazide-like diuretic (indapamide, bendroflumethiazide)
STEP 4: add spironolactone (CI: hyperkalemia)
Causes of atrial fibrillation?
Mc causes of AF are:
- Chronic hypertension
- Ischaemic heart disease
- Valvular heart disease (mitral stenosis or regurgitation - due to LA dilation)
HTN, IHD, mitral stenosis/regurg!!!!
Definition of shock, and what are the different types of shock?
SHOCK = inadequate O2 perfusion of tissues
- Hypovolaemic (blood loss, dehydration e.g. cholera, profuse sweating e.g. heat stroke)
- Cardiogenic (heart failure, arrhythmia, cardiomyopathy, tension pneumothorax, cardiac tamponade, PE)
Distributive (sepsis, neurogenic, anaphylactic) - Redistributive (third spacing) - sepsis, anaphylaxis, pancreatitis (pancreatic enzymes digest surrounding vessels –> extravasion)
- Neurogenic (SC compression –> loss of sympathetic function, leading to hypotension)
Causes of congestive heart failure exacerbation? i.e volume overload from CHF (rapid worsening of symptoms/signs of heart failure)
- Non-adherence to medication (e.g. diuretics)
- Non-compliance with fluid/sodium restriction
- Acute worsening of cardiac output, i.e. decompensation of pre-existing CHF: could be due to acute arrhythmia, acute coronary syndrome, or a worsening of cardiomyopathy or valve disease
Which medications for systolic HF reduce mortality?
Beta-blockers, ACE inhibitors/ARBs, and Spironolactone
Hydralazine and nitrates also reduce mortality, especially in Afro-Caribbean patients
Drugs that DON’T reduce mortality: digoxin and diuretics - just symptom relief
Which beta-blockers are licensed to treat systolic HF?
Bisoprolol, carvedilol, or nebivolol
These are used in combination with an ACE-inhibitor (ramipril, captopril, enalapril) - start separately.
For heart failure with comorbid hypertension or angina DON’T use rate-limiting CCBs like verapamil and diltiazem; DON’T use short-acting dihydropyiridines e.g. nifedipine
As these reduce cardiac contractility (and to have systolic HF you have to have a reduced EF already) - use amlodipine instead!!!!
Symptoms of left heart failure?
Pulmonary oedema (–> basal crepitations)
SOB on exertion, PND
Fatigue
Signs: laterally displaced apex beat (LV dilation), apex beat heave (LV hypertrophy), S3
Symptoms of right heart failure?
Peripheral oedema
Ascites, splenomegaly
Distension of IJV
Causes of systolic HF?
Reduced contractility: - Ischaemic heart disease - MI - Arrhythmias Increased preload: - Dilated cardiomyopathy - Mitral or aortic regurgitation -> progressive LV dilation Increased afterload: - Hypertension (-> increased afterload) - Aortic stenosis (-> increased afterload)
Also high-output conditions (chronic anaemia, hyperthyroidism, cirrhosis, multiple myeloma)
Causes of diastolic HF? (impaired relaxation of the ventricle -> reduced ventricular filling -> reduced CO)
- Chronic*:
- Hypertension –> hypertrophic cardiomyopathy
- Aortic stenosis –> hypertrophic cardiomyopathy
- Infiltrative disease e.g. amyloidosis, sarcoidosis -> restrictive cardiomyopathy
- Acute*
- Constrictive pericarditis
- Cardiac tamponade
Symptoms of aortic regurgitation?
- Palpitations
- Exertional dyspnoea, orthopnea (pul. oedema)
- Fatigue, syncope (reduced CO)
- Angina due to reduced coronary flow (reduced diastolic perfusion pressure)
Signs:
- Collapsing pulse (‘water hammer’), wide pulse pressure
- Auscultation: early diastolic murmur
- S3 (sign of volume overload as ultra-compliant left ventricle)
- Laterally displaced apex beat (volume overload)
Symptoms of aortic STENOSIS?
SAD: syncope, angina, dyspnea
Signs:
- Slow-rising pulse (carotid)
- Narrow pulse pressure (as systolic BP is reduced, due to decreased stroke volume)
- Ejection systolic murmur (mid-systolic systolic murmur; harsh crescendo-decrescendo)
- LV hypertrophy causes apex beat heave
When do systolic murmurs occur?
Systolic are between S1 and S2; diastolic are between S2 and S1.
Why does left heart failure cause right heart failure?
Left ventricular pressure increases and transmits back to the lungs, causing pulmonary hypertension. This strains the right heart and eventually -> right HF.
The other main cause of right heart failure is lung disease.
A patient comes in with chest pain: what are the 4 life-threatening causes that should be excluded?
- ACS
- PE
- Aortic dissection
- Oesophageal rupture
5 life threatening complications of aortic dissection?
- Coronary dissection (usually dissection of the right coronary artery -> inferior STEMI)
- Carotid dissection causing stroke
- Aortic rupture
- Cardiac tamponade from rupture into pericardium
- Acute aortic valve regurgitation causing cardiogenic shock
How do you diagnose cardiac tamponade?
How do you treat it?
Beck’s triad: hypotension, muffled heart sounds, elevated neck veins
Pulsus paradoxus: abnormal if >12 mmHg
Water bottle heart (CXR)
Tx: IV fluids to increase preload and prevent RV collapse; pericardiocentesis is therapeutic.
Most common cause of mitral stenosis?
Rheumatic heart valve disease
Causes of mitral regurgitation?
Either organic (actual valve apparatus problem: endocarditis, mitral annular calcification, rheumatic heart disease), or functional due to dilation of the annulus (ischaemic cardiomyopathy, dilated cardiomyopathy, hypertrophic, left atrial dilation)
Most common causes of aortic stenosis in >70 and <70?
> 70: senile calcific aortic stenosis
<70: bicuspid aortic valve
Causes of post-operative fever?
Wind (atelectasis), water (UTI), wound (wound infection), walking (DVT), where (abscess), wonder drugs
Acute sinusitis tx?
Topical intranasal decongestants short-term (Ephedrine hydrochloride, oxymetazoline) Nasal corticosteroids (14d) if symptoms >10d
+/- phenoxymethylpenicillin PO (or co-amox PO if complications)
If frontal sinusitis, must admit for IV Abx as risk of osteomyelitis, meningitis, frontal lobe abscess formation
If ethmoidal sinusitis (children/young adults) admit for IV ABx as risk of orbital cellulitis
Rhinitis tx?
- Antihistamines or topical nasal corticosteroids (alternative: sodium cromoglicate - mast cell stabiliser)
- Topical nasal decongestants can be used short-term to relieve congestion
Nasal polyps tx?
Antihistamines + short-course topical corticosteroids, then maintenance for 3mo with steroid nasal spray e.g. fluticasone
Acute otitis externa tx?
Mild: water avoidance, hydrocortisone cream
Moderate (painful, discharging, smelly, narrowed EAC):
= microsuction and abx/steroid drops (e.g. otomise - dexamethosone/neomycin, or gentamicin drops*) for 7-14d
(also ibuprofen/paracetamol for analgesia)
If no response to abx/steroid drops and erythema is spreading, –> flucloxacillin PO
*ototoxic so can’t use if perforated TM
Tx of necrotising otitis externa (osteomyelitis of temporal bone)?
Do a CT temporal bone
Tx is IV ceftazidimine
OR IV tazocin + ciprofloxacin PO
Complications of necrotising otitis externa?
Conducive hearing loss
Lower CN neuropathies (7-12)
Abscess formatoin
Peri-auricular or pinna cellulitis
Tx of acute otitis media?
Analgesia
+/- amoxicillin if symptoms >4d, patient systemically unwell, <2yo, bilateral, otitis media with perforation
Safety net advice for complications
Document VII exam and neurological exam (CN), bedside hearing tests, and ear examination incl. mastoid area
If recurrent AOM (>3 in 6mo), abx prophylaxis (trimethoprim) + grommet surgery
Complications of AOM: facial nerve palsy, mastoiditis, meningitis, sigmoid sinus thrombosis, brain abcess
Tx of CSOM (chronic suppurative otitis media)
Squamous CSOM is cholesteatoma, mucosal CSOM is chronic discharge due to chronic infx following TM perf.
Tx: abx/steroid drops, + referral to ENT for microsuction to clean retraction pocket or make the perforation stop discharging
If no resolution, surgery (tympanoplasty or myringoplasty)
Bacterial tonsillitis tx?
Penicillin V PO (phenoxymethylpenicillin), 7-10d
Analgesia
Encourage oral fluids
Indications for abx in acute sore throat?
Tonsillitis Features of marked systemic upset Unilateral tonsillitis (quinsy) Hx of rheumatic fever Immunodeficiency
Complications of tonsillitis?
Local: quinsy, otitis media, sinusitis, meningitis, brain abscess
Systemic: glomerulonephritis, rheumatic fever, scarlet fever, PANDAS, acute guttate psoriasis
Indications for tonsillectomy?
> 7ep in 1y, or >5ep/y for 2y
Peritonsillar abscess (2 in adults)
Tonsillitis causing febrile seizures
Hypertrophy of tonsils causing airway obstruction or speech interference
Which bacteria most commonly cause tonsillitis?
Group A streptococci (S. pyogenes)
S. aureus
C. pneumoniae
Epiglottitis symptoms/signs?
Drooling, dysphagia, develops rapidly
High fever (>38.5)
STRIDOR
No cough unlike in croup
Epiglottitis management?
Blood cultures
Bloods: CRP
ABG
Admit and urgently call ENT reg to assess airway; transfer to resus if in A+E as may require prophylactic intubation or cricothyroidotomy
–> broad-spec abx and IV steroids, adrenaline nebs, NBM, humidified oxygen, fluids
Causes of B12 deficiency?
Pernicious anaemia (mc cause) Atrophic gastritis Gastrectomy Malabsorption due to Coeliac, IBD Vegan diet or poor diet Drug causes: PPI
Contraindications to thrombolysis?
Absolute CIs
Previous intracranial haemorrhage
Ischaemic stroke in past 3mo
Known cerebrovascular abnormality e.g. aneurysm, AVM
Known malignant intracranial tumour
Significant closed head trauma/facial trauma in past 3mo
Relative CIs
Side effects of diuretics?
- Hypokalemia (monitor U+E, add spironolactone if K <3.2, if patient is predisposed to arrhythmias, or if on concurrent digoxin therapy)
- Hyponatremia (Na+ depletion –> volume contraction)
- Gout
Causes of hyponatremia?
Check osmolality - if high, = hyperglycaemia or mannitol; if normal, = pseudohyponatremia; if low osmolality…
- Hypervolaemia: CHF (secondary hyperaldosteronism: RAAS –> Na+ reabsorption –> volume overload), liver failure (low albumin lowers plasma oncotic pressure; portal HTN results in fluid migration into peritoneal cavity; splanchnic vasodilation due to vasodilating factors that the liver fails to decrease reduces effective arterial blood vol –> secondary hyperaldosteronism hence Na+ retention), nephrotic syndrome (proteinuria lowers plasma oncotic pressure, reducing EABV)
- Euvolemia (oedema absent): water intoxication (increased H2O intake, but ecstasy stimulates ADH secretion resulting in reduced urine output); SiADH (inappropriate ADH secretion)
- Hypovolaemia: renal (diuretics, adrenal insufficiency*), GI (pancreatitis, GI loss of Na+), cutaneous (burns)
- lack of aldosterone results in Na+ leak and K+ retention, resulting in hyperkalemia and hyponatraemia. (aldosterone causes Na+ reabsorption via ENaC and Na/K ATPase, and results in secretion of K+ or H+). For this reason Conn syndrome causes hyPERnatremia, hyPOkalemia, and metabolic alkalosis.
Criteria for SIADH?
Hyponatremia with low serum osmlality
Inappropriately high URINE osmolality (as not excreting water)
Euvolaemic O/E
Normal renal + adrenal + thyroid function
No diuretic use
Urinary Na+ loss of >20 mmol/L (i.e. despite the hyponatremia, Na+ is not being reabsorbed)
Causes of SiADH?
Lung disease e.g. pneumonia, lung cancer, COPD
CNS disease e.g. SOL, meningitis/encephalitis, degenerative
Drug-induced (nicotine, carbamazapine, omeprazole, tricyclics, opiates)
Tumours (pancreas, uterus, leukaemias)
Features of peripheral vascular disease?
Risk factors: smoking, diabetes, hyperlipidaemia, hypertension, Hx of coronary artery disease or cerebrovascular disease
Intermittent claudication - cramping pain, discomfort or tiredness in the legs that occurs during walking or standing and is relieved by rest. claudication is most common felt in the calves but can also affect the thighs, hips, buttocks, or arms.
Erectile dysfunction
Signs of critical limb ischaemia: leg pain at rest, gangrene, non-healing ulcer/wound, muscle atrophy, shiny/scaly skin, leg hair loss
6 signs of acute limb ischaemia?
Pallor, pain, paralysis, paraesthesia, pulselessness, perishingly cold
Why would someone with diarrhoea/vomiting be tachycardic?
Dehydration
Signs of venous insufficiency?
Signs: Varicose veins, venous eczema (itchy, red, blistered, crusty plaques), atrophie blanche (white irregular scars surrounded by white spots), haemosiderin deposition, lipodermatosclerosis, venous ulcers (typically medial ankle region - shallow, large, irregular border, mildly painful - vs. arterial ulcers which are smaller, deeper, punched out, well-defined borders + acute pain)
Symptoms: leg aching or fatigue worst in evening, leg cramps
Oedema is a sign of complicated varicose veins
Lower limb arterial disease exam (main points)?
- Inspect for scars (vein harvest sites for bypass surgery), discolouration (i.e. necrosis/gangrene), loss of hair, pallor (poor vascular perfusion), muscle wasting, ulceration (look between toes and lift feet up)
- Palpate: 1) temperature, 2) capillary refill time, 3) pulses (femoral, popliteal, posterior tibial - just behind the medial malleolus, dorsalis pedis), 4) sensation
- Buerger’s test (assesses arterial supply to limb)
Risk factors for chronic venous insufficiency?
Previous DVT, family Hx, smoking in men, female sex (progesterone)
Indications for valve replacement in endocarditis?
- CHF from valvular regurgitation
- Failure of abxs to suppress the infection, or infx with difficult to treat organisms (fungal, Pseudomonas, Brucella, drug-resistant organisms)
- Valvular annular abscess
- Peripheral embolism of vegetation
- Size of vegetation >1.0 cm
Secondary causes of hypertension?
ABCDEF
Apnoea (obstructive sleep apnoea), Acromegaly
Birth control, Bad kidneys (renal artery stenosis or renal disease)
Coarctation of the aorta, Cushing’s, Conn’s, Catecholamines (pheochromocytoma)
Drugs (alcohol, nasal decongestants, oestrogens)
Endocrine disorders (hyperthyroidism), Erhythropoeitin
Fibromuscular dyplasia
*The most common causes of difficult-to-control HTN is uncontrolled sleep apnoea, followed by renal artery stenosis
Common causes of CKD?
Diabetes, glomerulonephritis (commonly IgA nephropathy), hypertension or renovascular disease, pyelonephritis and reflux nephropathy, or idiopathic.
Nephrotic syndrome triad?
Hypoalbuminaemia
Peripheral oedema
Proteinuria
(Hyperlipidemia)
Causes of glomerulonephritis –> nephrotic syndrome
Infection: HIV (as can cause amyloidosis), Hepatitis B-associated nephropathy (can be due to polyarteritis nodosa, or a separate membranous glomerulonephritis)
Tumours: malignancy
Autoimmune: SLE (MGN - immune complex deposition in the glomerular basement membrane)
Metabolic: Diabetes mellitus
Inflammation: amyloidosis (deposition of amyloid in the glomeruli - conditions associated are RA, ankylosing spondylitis, IBD, TB, Hodgkin’s lymphoma, renal cell carcinoma, HIV)
Drugs: penicillamine (Wilson’s, kidney stones), NSAIDs
Recap: NEPHROTIC syndrome causes: diabetes, hepatitis B, amyloidosis secondary to e.g. rheumatoid arthritis, IBD, TB, Hodgkin’s lymphoma, HIV; immune complex deposition in SLE, drugs e.g. penicillamine, NSAIDs
Causes of glomerulonephrosis -> nephritis
- IgA nephropathy
- Membranoproliferative glomerulonephritis (presents w/ combined nephrotic + nephritic syn) - due to deposition of IgG complexes). Can be primary or secondary to SLE, hepatitis B/C
- Post-streptococcal glomerulonephritis:
- Crescenteric glomerulonephritis (rapidly progressive to kidney failure in weeks) - can be caused by any type of GN e.g. post-infective GN, SLE, IgA nephropathy can do this, but some types only ever present as RPGN: Wegener’s granulomatosis, microscopic polyangitis, Goodpasture’s syndrome
Recap: NEPHRITIS causes: IgA nephropathy, membranoproliferative GN (primary or 2* to SLE, hepatitis B/C), post-streptococcal GN, crescenteric GN (Wegener’s, microscopic polyangitis, Goodpastures)
Quad of nephritic syndrome?
Haematuria and red cell casts
Proteinuria (small amount)
Mild hypertension
Oliguria (>300ml/day)
Causes of a prolonged QT interval on ECG?
- electrolyte abnormalities (hypokalaemia, hypocalcaemia, hypomagnesia)
- medications (quinolones, macrolides, haloperidol, class 1A and III antiarrhythmics, tricyclics)
- genetic long QT syndromes
- myocardial ischaemia
Prolonged QT can lead to torsade de points (polymorphic v-tach) - treat torsade de points with IV magnesium
How is T2DM diagnosed?
Two of:
- Fasting plasma glucose ≥7 mmol/L
- HbA1c of ≥48 mmol/mol (6.5%)
- Random plasma glucose of ≥11.1 mmol/L
May have symptoms of hyperglycaemia (polyuria, polydipsia, weakness/fatigue), however T2DM is most often diagnosed on routine screening. Screening is done if risk factors e.g. age, obesity, Black/Hispanic/Native American ancestry, FHx of T2DM, physical inactivity, hypertension, dysplipidemia, known CVD
Ask about symptoms of volume depletion (dry mucous membranes, poor skin turgor, tachycardia/hypotension).
Symptoms of more severe diabetes: blurred vision, paraesthesia, weight loss, nocturia, skin infections, UTIs, acanthosis nigricans.
T2DM investigations
- HbA1c, fasting plasma glucose, 2-hour post-load glucose after 75g oral glucose
- Fasting lipids
- Creatinine (eGFR) - check for CKD
Urine dip for ketones
Other:
- Blood pressure
- Cardiac and peripheral vascular exam (+ECG)
- Examine for peripheral neuropathy
- ABPI (peripheral vascular disease)
- Retinal examination (patients should be referred to ophthalmology upon dx of t2dm)
T2DM management
- Management of all cardiovascular risk factors to reduce risk of stroke/MI: T2DM is frequently comorbid w/ hypertension or dyslipidemia (80%). Other risk factors are smoking.
- Lifestyle modification: dietary changes and exercise
- Pharmacotherapy ** to reduce risk of microvascular (nephropathy, retinopathy, neuropathy) and macrovascular (MI, stroke, PVD) complications. **. First-line is metformin; if not at target HbA1c, add one of:
- SGLT inhibitor
- GLP-1 agonist
Third-line therapy (i.e. adding to the others) - DPP-4 inhibitor
- Sulfonylurea, e.g. gliclazide
- Insulin
Causes of lower back pain?
Common: lumbar muscular pain, herniated nucleus pulposus, spinal stenosis, compression fracture, degenerative disc disease (‘discogenic low back pain’), sacroiliitis
Less common: vertebral osteomyelitis, malignancy, ankylosing spondylitis (inflammatory arthritis of the spine)
Causes of ischaemic stroke?
- Arterial thrombosis (in situ, cardiac emboli, atherothromboembolism from carotid plaque)
- Cerebral small-vessel disease (age-related, hypertension-related, or from cerebral amyloid angiopathy)
Symptoms of MCA stroke?
MCA supplies lateral surface of cerebral hemisphere, incl. lateral frontal, parietal and temporal lobes, insula, claustrum; the deep penetrating branches (lateral lenticulostraites arteries) supply the lateral parts of the internal capsule and may be involved or spared in infarcts separately from the main cortical territory of the MCA.
Symptoms:
- CONTRALATERAL HEMIPARESIS affecting the lower part of the face (forehead is spared, as UMN lesion and there is bilateral UMN innervation of the forehead), arm and hand (leg is largely spared)
- +/- contralateral sensory loss
- CONTRALATERAL HOMONYMOUS HEMIANOPIA (visual field loss on the same side in both eyes - in right MCA for example, the left visual field is lost).
- Left MCA stroke*:
- APHASIA (expressive or receptive): superior division of left MCA supplies Broca’s area (latero-inferior frontal lobe) - tends to occur w/ motor symptoms. Inferior division of left MCA supplies the lateral TEMPORAL lobe (Wernicke’s) - may be motor-sparing. Broca = superior MCA, Wernicke = inferior MCA
- Right MCA stroke*:
- SPATIAL NEGLECT (ignoring stimuli on the left side)
Features of lateral medullary syndrome (Wallenberg’s, aka posterior cerebellar artery syndrome)
Most common brainstem stroke = occlusion of vertebral artery, PICA (branch of vertebral artery), or medullary arteries (direct branches of vertebral arteries)
- Vestibulocerebellar symptoms (ataxia, diplopia, vertigo/nausea, nystagmus)
- Ipsilateral Horner’s syndrome
- Contralateral loss of pain/temp sensation
- Ipsilateral bulbar weakness (9-11 –> hoarseness, dysphagia)
Tx after ischaemic stroke?
Acute:
<4.5h of time of onset? –> CT head to check ischaemic stroke, then thrombolysis with ALTEPLASE (tPA) if no CI
After thrombolysis:
- FU CT after 24h
- Then give aspirin 300mg if no bleeds on post-thrombolysis CT. Continue daily for 2wk
- Begin statin if cholesterol <3.5
- Then begin long-term antithrombotic Tx: clopidogrel is first-line; aspirin + dipyridamole is second-line
TIA management?
Aspirin 300mg
Specialist assessment in TIA clinic - consider same-day MRI (not CT) to determine territory of ischaemia, +/- carotid US
Causes of SAH?
- Trauma
- Berry aneurysm (smoking, HTN, alcoholism, family Hx, polycystic kidneys, connective tissue disorders)
- AVM
- Arterial dissection
- Anticoagulation
Red flags in back pain?
Cauda equina symptoms: severe back pain and radicular-type pain (sciatica-type) radiating down the legs that is asymmetrical; LMN weakness in all leg movements except hip flexion(b/c lumbosacral plexus L1-3 and femoral nerve L2-4) and leg extension (b/c femoral nerve L2-4), absent ankle jerks, Babinski reflex absent/reduced (not upgoing though as it is a LMN pathology); saddle anaesthesia; sphincter tone reduced resulting in urinary retention/overflow incontinence/urgency.
Extra symptoms if tumour: night pain
Causes of CES? / causes of cervical myelopathy?
- Lumbar disc herniation
- Spinal stenosis
- Tumour (extradural i.e. vertebral metastases; intradural i.e. meningiomas; intramedullary i.e. astrocytoma, ependymoma, haemangioblastoma)
- Infection: epidural abscess (spinal surgery/anaesthesia, spinal trauma, IVDU, septic embolus from endocarditis, extension of infx locally e.g. vertebral osteomyelitis)
- Trauma (most commonly a complication of LP)
- Epidural haematoma (AVM, spontaneous if on warfarin, trauma)
Extra things that cause cervical myelopathy:
- DISC DISEASE / SPONDYLOSIS: degeneration of the annulus fibrosus of discs +/- osteophytes –> narrowing of spinal canal and intervertebral foramina
- Cystic lesions, e.g. syringomyelia
Causes of pancreatitis?
GET SMASHED
Gallstones, ethanol, trauma, steroids, mumps (hepatitis, HIV, coxsackie B), autoimmune (polyarteritis nodosa), scorpions, hypertriglyceraemia/hypercalcemia, ERCP, drugs (steroids, sodium valproate, mesalazine, ART)
Investigations in ?pancreatitis
Bloods: - Serum amylase >1000 - Serum lipase (x3 upper limit of normal) - FBC, U+E (hypocalcaemia, hyponatremia), LFTs - Lipids (triglycerides) - Glucose - Lactate ABG (metabolic acidosis in severe cases) US of biliary system and pancreas
Management of pancreatitis?
Fluid resuscitation
Insert catheter for strict hourly fluid balance
NG tube on free drainage and 4hrly aspiration
Morphine
If gallstones are cause, lap chlolecystectomy once fit
