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
