PACES ALL concise Flashcards
Asthma - def? Presentation? Ix? Severity? Short-term/long-term Mx incl. conservative? Mneumonic for conservative long-term Mx?
Def: chronic inflammatory airway disease characterized by reversible airway obstruction + airway hyperresponsiveness
Presentation
- Dry cough, polyphonic wheeze ( worse@night/morning)
- Triggers: cold air, pollen, pollution, exercise
- Atopic features - eczema, nasal polyps
Ix:
- Peak flow variability (in peak flow diary)
- Spirometry (shows reversibility after bronchodilator)
- FeNO (fractional exhaled nitric oxide - a marker of airway inflamme, in uncertain Dx)
- On exacerbation:
- ABG, peak flows (min x4/day), CXR
- Other:
- Allergy testing - total IgE, specific IgE (RAST), serum eosinophil count
Asthma severity:
-
Life-threatening: PEF <33% of baseline/SpO2 <92%/PaO2 <8/Normal or raised PaCO2 - should be low with resp alkalosis due to excess breathing only becomes acidotic when get tired
- CHEST: Cyanosis, Hypotension, Exhaustion, Silent chest, Tachycardia
- Acute severe: PEF <50% of baseline/RR >25/HR >110/can’t complete sentence without taking a breath
- Moderate: PEF <75% of baseline
Short-term Mx:
- A-E approach, seek senior support (call for help if life-threatening)
- O2 - 15L NRM (if hypoxaemic)
- Burst therapy:
- SABA (spacer up to 10 puffs every 20 mins –> nebs)
- Ipratropium Bromide (add to nebs if poor response/severe, every 4-6hrs)
- Corticosteroids (min 5-day course, give within 1 hour, give IV if can’t take orally)
- Other Tx options:
- IV Magnesium sulfate (STAT dose if poor response above/severe) - consult senior before use
- IV salbutamol (if on ventilation) - consult senior before use
- IV Aminophylline - consult senior before use, requires ITU setting
- If less distressed/more tired/shallow breaths/confused –> call critical care outreach team (CCOT) for ITU support
Long-term Mx (>16yrs):
-
Conservative: TAME
- Technique
- Avoid triggers
- Monitor peak flow
- Educate - formulate Personalised Asthma Action Plan (PAAP), Annual flu vaccine
-
Medical:
- SABA (reliever)
- SABA + ICS (preventer)
- SABA + ICS + LTRA (leukotrine receptor antagonist e.g. montelukast)
- SABA + ICS + LABA (+ LTRA stopped unless good response)
- SABA + MART (ICS + LABA COMBO) (+ LTRA)
- NOTE: maintenance & reliever therapy (MART) - used as preventer & maintenance inhaler
- Specialist input (e.g. for oral steroids)
COPD - definition? Signs & Sx? New Dx & exacerbation Ix/Mx? Prognosis factors?
Def: chronic bronchitis (damaged to cilia in bronchi - blue bloater) + emphysema (damage to alveoli - pink puffer)
Presentation:
- Cough (productive), SoB (starts on exercise)
- RF exposure - smoking/pollution
- Signs:
- Barrel chest
- Hyper-resonant (air trapping)
- Reduced breath sounds
- Widespread expiratory wheeze
- Coarse crackles if exacerbation (mucus in airways)
- Other - asterixis (CO2 retention flap), raised JVP (cor pulmonale)
- NOTE: COPD does not cause clubbing –> cancer/bronchiectasis
New Dx Mx:
- Ix:
- Bedside - mMRC dyspnoea scale, O2 sats, ECG (cor pulmonale)
-
Spirometry - FEV1/FVC <0.7 (forced exp volume in 1s)
- Mild - FEV1 ≥ 80%
- Moderate - FEV1 ≥ 50%
- Severe - FEV1 ≥ 30%
- Very severe - FEV1 <30%
- Bloods - FBC, ABG, eosinophil count, alpha1-antitrypsin level
- Imaging - CXR, CT chest
- Other: serial peak flows if asthma DDx, sputum culture (in freq exacerbation), pul funct tests
- Mx:
- Conservative - stop smoking, influenza + pneumococcal vaccine, inhaler device training
- Persuade to stop smoking
- Pul rehab
- Prick them - influenza + pneumococcal vaccine
- Psych issues
- Medical - depends on severity - GOLD group –> solo/combo of:
- SABA e.g. salbutamol
- SAMA e.g. Ipratropium bromide
- LABA e.g. salmeterol
- LAMA e.g. tiotropium
- ± ICS e.g. beclomethasone
- Other: mucolytic e.g. acetylcysteine, O2 therapy, theophylline
- Medical pathway:
- 1 - SABA/SAMA
- 2a - Steroid-responsive (eosinophilia/atopy): LABA + ICS
- 2b - Not steroid-responsive: LABA + LAMA
- 3 - LABA + LAMA + ICS
- 4 - specialist input e.g. theophylline
- Surgical - lung reduction surgery (large bullae)
- Other: long-term O2 therapy
- Only if non-smoker (smoker –> burns)
- Only if <7.3 PaO2/<8 if also pul HTN
- Only if PaCO2 does not rise excessively on O2
- Conservative - stop smoking, influenza + pneumococcal vaccine, inhaler device training
Acute Exacerbation Mx:
- Ix: ABG, ECG, CXR
- Mx:
- 15L O2 NRM
- Nebs - salbutamol + IpB
- Steroids (PO pred/IV hydrocortisone)
- Abx if infective –> prophylactic abx if persistent infections - azithromycin
Prognosis factors:
- Body mass - worse if obese
- Obstruction - worse if reduced FEV1
- Dyspnoea
- Exercise capacity - how far can you walk in 6 minutes?
Complication –> vasoconstriction to redirect blood flow to well-oxygenated areas of the lungs –> if widespread –> pul HTN –> cor pulmonale
Pneumonia - def? Presentation? Types? Ix? Scoring? Mx?
Def: inflammation of lung caused by inf w/ visible radiographic changes
Presentation:
- Decreased chest expansion, dull on percussion, increased sound vocal resonance
- Coarse crackles
- Bronchial breathing – bronchial airflow instead of alveolar airflow (due to transmission of sounds through consolidation) – check by listening to sound at the throat
Ix: ABG, CXR, sputum culture (mod/high severity)
Scoring for CAP: CURB-65 (confusion, urea ≥7mmol/L, RR ≥30, BP <90/60, ≥65yrs)
- +1 = outpatient; +2 = outpatient/inpatient, +3 = inpatient ± ITU
- NOTE: urea is no longer used
Types & Mx –> local abx guidelines
-
CAP:
- Typical (S. pneumo, H. influenzae) –> Amox/Co-Amox
-
Atypical (Legionella, Mycoplasma, Chlamydia) –> Clari
- Dry cough (instead of productive), myalgia, confusion, diarrhoea
- NOTE: if not sure often given Co-Amox + Clari
- HAP - pneumonia arising >48hrs after admission to hospital (S. pneumo, S. aureus, P. aeruginosa) –> Taxocin (pseudomonal cover)
- Aspiration - RFs: swallowing dyfunct, reduced consciousness, reduced mental status –> elderly/frail
Goes into septic shock –> give IV fluid + senior help + check abx sensitivity (ring lab) –> ITU (intropic support - NA to increase PVR)
- Other aspects of septic-6
- NOTE: dobutamine is for cardiogenic shock to increase CO - this is not relevant here
PE - def? Sx? RFs? Scoring & Ix? Mx?
Def: occlusion of pulmonary vasculature characterized by sharp pleuritic chest pain
Sx: SYNCOPE, sudden SoB, pleuritic chest pain, haemoptysis
RFs: SICC - Surgery, Immobility, Cancer, COCP
Initial Tx:
- DOAC (e.g. Apixaban) or unfractionated heparin (if bleeding risk, can be reversed easily)
- Massive PE –> IV unfractionated heparin for hours before and after thrombolysis e.g. IV alteplase
Scoring & Ix: Well’s score
- ≤4 = D-Dimer –sign raised–> CTPA
- >4 = CTPA
- ECG useful - sinus tachycardia, right heart strain, S1Q3T3
- NOTE: Troponin = useful markers for PE severity (indicates right heart strain)
Ongoing anticoagulation - DOAC/Warfarin
- Provoked - 3 months (SICC)
- Unprovoked - >6 months + cancer & thrombophilia testing
- Ix for cancer –> any Sx?
- If yes - CT TAP
- If no - FBC, U&E, LFTs, clotting, physical exam –> if concern –> CT TAP
- Consider thrombophilia screen if no cancer for anti-phospholipid syndrome (anticardiolipin, lupus anticoagulant, anti-beta-2-glycoprotein)
- Ix for cancer –> any Sx?
Bronchiectasis - definition? causes? presentation? Ix? Mx?
Def: obstructive lung disease characterised by permanent dilation of bronchi from the destruction of elastic & muscular components of the bronchial wall
- Results from diseases causing chronic inflammation:
- Primary ciliary dyskinesia - cilia don’t move –> mucus trapped in airways –> recurrent pneumonia –> chr inflammation
- Cystic fibrosis - mucus thick & sticky –> recurrent pneumonia –> chr inflammation
- Airway obstruction - tumour inside/outside airway or inhaled foreign body –> mucus can’t clear –> recurrent pneumonia –> chr inflammation
- NOTE: worse with certain infections e.g. aspergillosis –> hypersensitivity response
- Chr inflammation - has immune cells that release cytokines –> damage ciliated epithelial cells + destroys elastin –> airways dilated + clogged with mucus –> fibroblasts deposit collagen –> stiff lungs + mucus plug –> obstructive lung disease
Presentation:
-
RFs: CF, PCD, congenital disorders of airway, host immunodef (incl. HIV), recurrent lung inf
- Less common - inhaled foreign body, connective tissue disease, IBD, alpha1-antitrypsin def
- Productive cough (large amounts of sputum) ± haemoptysis - worse lying flat/one side
- Dyspnoea (with increased severity)
- Fever (on exacerbation)
- Crackles, inspiratory squeaks & rhonchi, clubbing (from long-term hypoxia)
Ix: CXR (ring shadows, tramlines), high-res CT (signet ring sign), FBC + sputum culture & sensitivity (inf e.g. pseudomonas), pul function tests
- Genetic testing (for possible RF causes): serum alpha1-antitrypsin, serum Ig lvls (ID), specific IgE for Aspergillus, sweat Cl test (CF), rheumatoid factor (CTD), HIV test, nasal nitric oxide (PCD)
Mx:
-
Conservative:
- Persuade to stop smoking
- Pul rehab
- Prick them - influenza + pneumococcal vaccine
- Psych issues
-
Medical:
- Mucoactive agent (nebulised hypertonic saline)
- Inhaled bronchodilator (SABA/SAMA/LABA/LAMA) - ONLY If co-existing asthma/COPD
- Surgical: depending on primary cause e.g. IFB, tumour –> lobectomy/lung transplant
- Exacerbation: short-term abx (azithromycin)
Interstitial lung disease - causes? presentation? Ix? Mx? Prognosis?
Interstitial lung disease
- Refers to the tissue the gasses pass through e.g. surface of alveoli –> reducing gas exchange
Causes:
- Upper zone fibrosis: PATEN (more occupational causes)
- Pneumoconiosis (not asbestosis) - caused by inorganic dust (e.g. soot)
- Aspergillosis/ABPA
- TB
- Extrinsic allergic alveolitis - caused by organic dust e.g. animal shedding
- Negative seroarthropathies
- Lower zone fibrosis: STAIR
- Sarcoidosis
- Toxins: B-MANS (Bleomycin, Methotrexate, Amiodarone, Nitrofurantoin, Sulfasalazine)
- Asbestosis
- Idiopathic pulmonary fibrosis
- Rheum: SLE, RhA etc
- Signs of conditions associated w/ pulmonary fibrosis:
- MCP swelling - RA
- Malar rash - SLE
- Kyphosis - Ank Spond (apical fibrosis)
- Lupus pernio - sarcoidosis
- Thick skin/’bird beak’ nose - systemic sclerosis
- Aphthous ulcers, abdo scars - Crohn’s
- Grey skin - amiodarone
Main Sx: progressive SOBOE, dry cough, fatigue, weight loss
Signs: find end-insp creps, clubbing
- Other: reduced chest expansion, normal/reduced percussion, normal vocal fremitus
Investigations: spirometry, high-res CT & lung biopsy
- Bedside: spirometry (low FEV1, low FVC, FEV1/FVC>0.8 = restrictive lung disease), ECG (right heart strain), drug review
- Bloods
- FBC, U&E, LFTs, CRP, ESR, ABG (T1RF)
- AI screen - Serology (CTD): ANA, RhF, anti-CCP
- Serum ACE for sarcoidosis
- TB testing
- Imaging
- CXR: reticulonodular shadowing (honeycombing) + rule out lung cancer
- High-res CT: more detailed view of alveolar structure –> ‘honeycombing’ + lung biopsy
- Echo (right heart strain/cor pulmonale)
- Invasive
- Bronchoscopy + lung biopsy (gold-standard)
Management:
- Conservative (4Ps):
- Persuade to stop smoking, reduce exposure (meds, EAA)
- Pul rehab
- Prick them - influenza + pneumococcal vaccine
- Psych issues
- Medical: anti-fibrotic e.g. pirfenidone +/- prednisolone ± O2 (if hypoxaemic)
- Surgical: lung transplant if severe deterioration/impairment/oxygen dependent
Prognosis: 3-4yrs post-Dx (no Mx increases survival)
Pleural effusion - signs? causes? Ix? Mx?
Signs (if fluid > 300ml):
- Key:
- Stony dull in lung base
- If large: tracheal deviation away
- Reduced chest expansion
- Reduced breath sounds
- Reduced vocal fremitus
Causes:
-
Transudative (<30g/L protein)
- HEART FAILURE
- Hypoalbuminaemia: liver disease, nephrotic syndrome, malabsorption
- Hypothyroidism
- Meig’s syndrome (benign ovarian tumor + ascites + pleural effusion)
-
Exudative (>30g/L protein)
- Infection: PNEUMONIA, TB, subphrenic abscess
- Connective tissue disease; RA (also low glucose), SLE
- Neoplasia: lung cancer, mesothelioma, metastases
- Pancreatitis: high amylase in pleural fluid
- Pulmonary embolism
Ix:
- Bedside: obs, urinalysis for protein
- Bloods:
- ABG, BC
- FBC, U&E, LFTs, CRP
- Clotting (before needle aspiration), albumin (nephrotic syndrome)
- Mantoux/ELISPOT (TB)
- Imaging:
- CXR: meniscus sign, dense shadowing, pleural effusion if ≥300mL fluid
- CT chest - identify the cause
Management: US-guided pleural aspiration = thoracocentesis (21G needle, 50ml syringe) - above rib to avoid NV bundle
- LDH & protein in pleural fluid & serum + RBCs, WBCs, cytology, culture, pH & glucose of pleural fluid
- MC&S
-
Biochemistry: PPALS
- Protein (also serum)
- pH
- Amylase
- LDH (also serum)
- Sugar (glucose)
- Cytology
- Immunology - if indicated (RF, ANA, complement)
- Findings:
- Protein > 30g/L: exudate
- Protein < 30g/L: transudate
- Protein 25-35g/L: use Light’s criteria. An exudate is likely if at least 1 of:
- Pleural protein/serum protein > 0.5
- Pleural LDH/serum LDH > 0.6
- Pleural LDH > 2/3 upper limits of normal serum LDH
- Tx cause e.g. abx for infection, furosemide for HF
- Management of recurrent pleural effusion
- Recurrent aspiration (thoracocentesis)
- Pleurodesis
- Indwelling pleural catheter
Pleural fluid features:
- Heavy blood staining - mesothelioma, TB, PE, trauma
- Purulent/turbid/cloudy - empyema secondary to bacterial pneumonia –> insert chest tube to allow drainage
- Milky - chylothorax via lymphatic obstruction secondary to malignancy
Pneumothorax - Def? RFs? Causes? Ix? Mx? How do you identify a Tension Pneumothorax?
Pneumothorax = accumulation of air in pleural space (subdivided into primary and secondary)
RFs: pre-existing lung disease, Marfan’s, RA, smoking
Causes: cystic pathology, parenchymal necrosis, iatrogenic, trauma
Ix: CXR
Mx:
- Primary (no pre-existing lung disease)
- <2cm (betw lung margin & chest wall), no SoB – observe 4-6hrs ± supplemental O2
-
SoB/≥2cm – needle aspiration (16-18G) –> observe 4-6hrs
- Do NOT repeat needle aspiration x2
-
Chest drain if above fails + ADMIT ± supplemental O2
- NOTE: correct clotting before inserting if possible
- Surgery
- Secondary (pre-existing lung disease) - ADMIT all secondary pneumothorax (for at least 24hrs observation)
- <1cm - high-flow O2 + ADMIT (24hrs observation)
- 1-2cm - needle aspiration (16-18G) –> high-flow O2 + ADMIT (24hrs observation)
- SoB/≥2cm/previous failed - chest drain + ADMIT ± supplemental O2
- Surgery
Tension pneumothorax = pushes away the trachea to the opposite side
- Non-traumatic:
- IMMEDIATE peri-arrest call (2222)
- Needle decompression = emergency Tx, 2nd ICS MCL (grey cannula) + high-flow O2
- Follow-up = ADMIT + chest drain
- Traumatic:
- Open thoracostomy
- Follow-up = ADMIT + chest drain
- Traumatic non-tension pneumothorax:
- High-flow O2 + ADMIT (24hrs observation)
- If open pneumothorax/penetrating chest wound –> occlusive dressing + observe
- Refer to thoracic surgeons - chest drain/thoracotomy
Location:
- Needle aspiration = 2nd ICS, MCL
- Chest drain = triangle of safety (axilla, pectoralis major, latissimus dorsi, 5th ICS) - 4th/5th ICS, MAL
Surgery:
- Open thoracotomy (or video-assisted thoracoscopic surgery = VATS)
- Follow-up surgery –> pleurodesis (mechanical abrasion/chemical irritation)
Lung cancer - epi? presentation? types? Ix? Mx?
Epi: Second most common cancer in UK
Presentation: chronic cough, haemoptysis, FLAWS
- Monophonic wheeze, pleural effusion signs (dull on percussion, reduced BS), cachexia, SVCO (face swelling & engorged veins in venal-caval distribution), hypertrophic pulmonary osteoarthropathy (HPOA)
- RFs: smoking, asbestos exposure, FHx
Types:
- Non-small cell lung cancer (MOST)
-
Adenocarcinoma (MOST COMMON LC)
- Non-smoking women (40% cases)
-
Squamous cell carcinoma (SCC)
- Affects large airways of lungs (central)
- Classically assoc w/ paraneoplastic hypercalcaemia, as tumour may release PTHrP
- 2nd most common in non-smokers
- Most common cause of Pancoast tumour
- Keratinization (keratin pearls)
- Large cell carcinomas (Dx of exclusion)
- Alveolar cell carcinoma = ++sputum
- Bronchial adenoma = mostly carcinoid
- Carcinoid syndrome - flushing, diarrhoea, episodes of dyspnoea
- Urinary 5-Hydroxyindoleacetic Acid (5-IAA) levels may be used to screen for carcinoid syndrome
-
Adenocarcinoma (MOST COMMON LC)
- Small cell lung cancer (15%)
- Almost exclusively smokers
- Can be assoc w/ neuroendocrine syndrome (SIADH, Cushing’s)
- Early mets BUT chemo sensitive
Ix:
- Bloods - FBC, haematinics, Ca
- Imaging - CXR, CT chest (2WW referral), CT PET scan (staging, mets)
- Interventional if suspicious CXR:
- Endobronchial US-guided biopsy (EBUS) & biopsy
- Video-assisted Tracheostomy & Biopsy (VATS - BIOPSY) of accessible nodes
Mx:
- Conservative: lung cancer MDT
- Smoking cessation
- Psych support (McMillan Nurses, specialist lung cancer nurse involvement)
- Palliative care (if terminal, Sx control & planning)
- Medical:
- Systemic chemo - esp. for small cell lung cancer (chemosensitive)
- Adjuvant/radical radiotherapy
- Surgical - if NSCLC
- VATS-lobectomy
- Open lobectomy/Pneumonectomy
4Ps of respiratory conservative Mx?
Persuade to stop smoking
Pul rehab
Prick them - influenza + pneumococcal vaccine
Psych issues
Fine vs coarse creps?
Vesicular vs bronchial breathing?
FINE (inspiratory) – pulmonary oedema (HF), interstitial lung disease (pul fibrosis)
- Best heard at base of lungs
COARSE (insp & exp) – bronchiectasis, COPD (chronic bronchitis), pneumonia
- No specific area of lungs louder
Vesicular - inspiratory > expiratory
Bronchial - inspiratory = expiratory
IHD - RFs? Types? Definition? Dx? Mx? Complications?
RFs: HTN, DM, Smoking, FHx IHD, Hypercholesterolaemia
Stable angina - chest pain on exertion relieved by rest
- Path - mismatch in O2 supply and demand to the myocardium
- Ix: CT-angiogram
- Mx:
- B-blockers - reduces HR req for activity –> reduced likelihood of mismatch in O2 supply & demand
- GTN spray - reduce myocardial preload + reduces strain
- RF modification –> reduced risk of progression
Acute coronary syndrome - Sx caused by sudden reduced BF to the myocardium
- Dx:
- ST-elevation = STEMI
- Troponin raised = NSTEMI (+ dynamic T-wave inversion, ST depression)
- Unstable angina pectoris (pain at rest) = ischemia NOT infarct
- Generic ACS Mx - MONA BASH
- ALL immediate:
- 5-10mg Morphine IV + Nitrates (GTN spray)
- Dual antiplatelet therapy (DAPT) - 300mg Aspirin STAT + 300mg Clopidogrel STAT (or 180mg PO Ticagrelor)
- ALL long-term:
- Continue DAPT
- 1 year: 75mg OD Aspirin + 75mg OD Clopidogrel (or 90mg BD Ticagrelor)
- >1yr - 75mg OD Aspirin
- B-blocker (1.25-10mg Bisoprolol OD)
- ACEi (1.25-10mg Ramipril OD)
- Statin (80mg Atorvastatin OD)
- Continue DAPT
- ALL immediate:
- STEMI Mx: establish coronary reperfusion ASAP
- Sx <12hrs: PCI BUT if no PCI within 2hrs Dx –> thrombolysis (e.g. tPA - tissue plasminogen activator)
- Sx >12hrs: invasive coronary angiography ± PCI if needed
- PCI:
- If having PCI give Prasugrel (instead of Clopi/Ticagrelor)
- PCI accessed via radial (or femoral) artery, guidewire passed via X-ray guidance into the affected coronary artery AND IV unfractionated heparin during the procedure –> stent inserted impregnated with an anti-proliferative agent (e.g. Tacrolimus - to prevent adverse tissue reaction) –> takes longer for endothelialization of stent so DAPT needed for 1yr
- If PCI with stents inserted –> DAPT 12 months
- NSTEMI Mx:
- 2.5mg SC Fondaparinux (direct factor 10a inhibitor)
- Risk stratify - GRACE criteria (& others)
- High risk = invasive coronary angiography (within 48-72hrs)
Complications: FAP (failure, arrhythmias, pericarditis)
- Heart failure, arrhythmias (incl. VF)
- Pericarditis
- Early - positional chest pain day after MI –> give NSAIDs
- Late - Dressler’s syndrome - immune response @6wks (fever, pleuritic chest pain, pericarditis/pericardial effusion)
Heart failure def? Causes? Pathophysiology? Categories & Causes? Classification? Ix? Mx?
Def: pumping of blood by heart insufficient to meet the demands of the body
Causes:
- RVF:
- Acute: MI, inf endocarditis, PE
- Chr: Cor pulmonale, LVF
- LVF:
- Acute: MI, inf endocarditis
- Chronic: ischaemic/hypertensive CMO, valvular HD
Pathophysiology:
- RHF - right side of the heart pumps deoxygenated blood from the body to the lungs to be reperfused - if the RH is not pumping effectively you get the fluid collection in the peripheries = PERIPHERAL OEDEMA
- LHF - left side of the heart pumps oxygenated blood from the lungs to the body - if the LH is not pumping effectively you pooling of blood in the lungs = PULMONARY OEDEMA
- Reduced CO –> shock, tachycardia, AKI
- CO = SV*HR
- Ejection fraction = SV/End-diastolic Volume
Categories:
- HF w/ preserved ejection fraction (left ventricular >50%) = inadequate filling of ventricles during diastole (from ventricular stiffness)
- Causes of ventricular stiffness:
- Volume overload (valve regurg)
- Pressure overload (HTN)
- Decreased distensibility (constrictive pericarditis)
- Causes of ventricular stiffness:
- HF w/ reduced ejection fraction (left ventricular <40%) = inadequate emptying of ventricles during systoles (from outflow obstruction/impaired contractility)
- Causes of outflow obstruction/impaired contractility:
- MI, Cardiomyopathy, Arrythmia
- Causes of outflow obstruction/impaired contractility:
NYHA classification:
- 1 - no limitation on activity
- 2 - comfortable at rest but dyspnoea on ordinary activity
- 3 - marked limitation on ordinary activity
- 4 - dyspnoea at rest
Ix:
- Bedside: ECG - detects if anything precipitating HF (arrhythmia/ischaemic event)
- Bloods: ABG (if resp compromise from pul oedema), troponin (ACS), BNP (HF screening)
- Imaging: CXR (visualise pul oedema, cardiomegaly), ECHO (valvular abn/regional wall mov abn)
Mx: MON BA (out of MONA BASH)
- Immediate:
- Sit the patient up (reduce venous return to heart –> less strain)
- O2 15L/min NRM
- Medical:
- IV furosemide (loop diuretic) - remove excess fluid + venous dilation (reduce preload)
- Nitrates (GTN/Isosobide Mononitrate) AND Morphine - reduce preload on the heart
- Long-term:
- Reduced ejection fraction - prognostic benefit:
- B-blocker (bisoprolol) - reduce strain on heart, do not give acutely if severe HF as will kill them
-
ACEi - reduce strain on heart
- After the above if LVEF <35% & Sx –> mineralocorticoid antagonist e.g. spironolactone
- 3rd line - by specialist: Sacubitril/Valsartan (entresto), Ivabradine & CRT
- SGLT2 inhibitors (dapagliflozin)
- RF modification - poor glycaemic control/high cholesterol
- Sx (diuretics)
- Reduced ejection fraction - prognostic benefit:
Complications:
- Reduced CO (SV*HR) –> shock, tachycardia, AKI
- Congestion –> pulmonary oedema + peripheral oedema
SVT - Def? Types? Presentation - case example? Mx?
Def: regular narrow-complex tachycardia with no p-waves + supraventricular origin
Junctional types:
- AVNRT - local re-entry circuit within AV node
- AVRT - re-entry circuit between atria and ventricles –> after SVT termination = delta wave = WPW syndrome:
- Assoc w/ HOCM
- Avoid digoxin, verapamil, amiodarone (reduce conduction down SAN –> worsen retrograde conduction –> risk of VT)
- Can use B-blocker/flecainide instead
Case example: 23yrs, 1-hr palpitations + SoB, 2 similar episodes prev following alcohol, this time severe chest pain
Mx:
- Unstable tachycardia (<90 BP/chest pain/acute heart failure) –> synchronised DC Cardioversion
-
Vagal manoeuvres (increase parasympathetic stim via vagus nerve to slow conduction via AV node)
- Valsalva manoeuvre (blow out through nose while pinching + shut mouth) - breath through 50ml syringe
-
Adenosine 6mg –> 12 mg –> 12mg
- NOTE: if adenosine CI (e.g. asthma) –> VERAPAMIL (rate-limiting CCB)
- Other:
- IV B-blocker/amiodarone/digoxin
- Synchronised DC Cardioversion
Key heart murmurs? Accentuation manoeuvres?
Causes? Left vs right heart valve abn epidemiology?
Mx? Valve types? Complications of prosthetic heart valves?
Key murmurs:
-
AS = ejection systolic + radiates to carotids, slow rising pulse, narrow pulse pressure, heaving apex beat
- Sound: Wooooshhh
- Severe AS - absent/soft 2nd heart sound, reversed splitting of 2nd HS, heaving apex beat
- A longer murmur is worse (small space for blood to pass through = takes longer)
-
AR = early diastolic + sitting forward (LLSE), collapsing pulse, wide pulse pressure, displaced apex
- Sound: de woooshhhh
- Severe AR –> Austin-flint murmur = ‘Rumbling mid-diastolic murmur’
- Best heard at apex, caused by blood flowing back through aortic valve and over mitral valve
- Shorter murmur is worse (quicker to flow back through large hole)
-
MR = pan-_systolic_ + radiates to left axilla, AF, displaced thrusting apex, LVF/pul HTN
- Sound: Woooooshhh (holosystolic)
-
MS = mid-diastolic + LLP, malar flush, AF, loud/palpable S1 “tapping” apex, pul HTN (loud P2 - pul thrill)
- Sound: Wooosh de (loud S1) de (early diastolic snap)
- NOTE: same pattern for pulmonary & tricuspid (pul stenosis & tricuspid regurgitation = systolic)
- TR - pulsatile liver
- PS - radiates to back, assoc w/ Noonan’s (AD, webbed neck, wide-spaced eyes etc.)
Accentuation manoeuvres:
- R-sided murmurs (tricuspid + pulmonary) –> louder on INspiration = blood goes IN to right-side of heart
- L-sided murmurs (aortic + mitral) –> louder on EXpiration = blood EXits left-side of heart
- AS radiates to the carotids + louder on leaning forward + listen on right sternal edge
- MS louder on turning to the left, MR radiates to axilla
Causes:
-
AS (stenosis/sclerosis):
- Older - senile calcification
- Younger - bicuspid valve
-
AR:
- Acute (aortic root dilation, infective endocarditis)
- Chronic (CTD, RHD, bicuspid aortic valve)
-
MR:
- Acute: - IHD (papillary-muscle dysfunction post-MI), infective endocarditis, RHD
- Chronic - myxomatous degeneration (can be assoc with Marfan’s/Ehlers-Danlos)
- MS: rheumatic heart disease (RHD)
Left vs Right valve abn:
- Left = more common as higher pressure system, more likely in damaged valves, commonly Strep Viridans
- Right = more common in IV drug users –> tricuspid valve is first valve reached, commonly S. aureus
Ix:
- ECHO (Dx & severity) - Transthoracic incl doppler (regurg jet) ± TOE
- If the above is inconclusive:
- 2nd - Cardiac MRI - analysis of cardiac function
- 3rd - Cardiac catheterization (invasive) - pressure gradient
- If the above is inconclusive:
- ECG (LVH), CXR (pul HTN)
Management:
- AS:
- C: Asymptomatic –> monitor (6 monthly ECHO)
- S: Symptomatic –> aortic valve replacement:
- Fit (req midline sternotomy & cardiopul bypass) = Surgical aortic valve replacement (SAVR)
- Not fit = Transcatheter aortic valve implantation (TAVI)
- M:
- HF Sx (diuretics, ACEi)
- RF optimisation (statins, HTN, DM)
- AR:
- If no left ventricular dysfunction –> medical Mx
- ACEi, vasodilators e.g. nifedipine/hydralazine (if HTN)
- If left ventricular dysfunction & low surgical risk/another indication for cardiac surgery –> aortic valve surgery (replacement > repair)
- If no left ventricular dysfunction –> medical Mx
- MR - primary (valve abn/damage):
- Mitral valve surgery (repair > replacement)
- Medical - ACEi, B-blocker & diuretics
- Tx AF if present (incl. anticoagulate)
- MS:
- C: If non severe + asymptomatic –> monitor
- S: Otherwise = Balloon valvuloplasty/mitral valve replacement
- if C/Is (persistent left atrial thrombus/rigid calcified valve) –> need open surgery
- NOTE: valvuloplasty = lateral thoracotomy scar
- M: Tx AF if present (incl. anticoagulate)
Valve types:
- Tissue valve - porcine xenograft
- For older patients & females of childbearing-age - lasts 10-15yrs, less if active
- No need for Warfarin
- Mechnical valve - quiet clicking noise
- Younger people (<60yrs) - no need for repeat surgery, last 30yrs+
- Lifelong Warfarin
Complications of prosthetic heart valves: FIBAT
- Failure
- Infection
- Bleeding - MAHA
- Anaemia
- Thromboembolic phenomena
Atrial fibrillation (AF)
- Def? Causes? Ix? Mx?
Def: rapid, chaotic, and ineffective atrial electrical conduction
- ECG def: irregularly irregular narrow complex tachycardia with no p waves
Causes: idiopathic, cardio (IHD, valvular disease, cardiomyopathy), resp (PE, pneumonia), hyperthyroidism, alcohol
Ix: ECG (absence of p-waves, irregularly irreg rhythm)
Mx:
- Haemodynamically unstable (≤90 BP, chest pain, acute HF) –> DC Cardioversion
OR
- Rate control –> B-blocker (bisoprolol) OR rate-limiting CCB (verapamil - asthma)
OR
- Rhythm control - ONLY if clear reversible cause
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
- NOTE: IV heparin started prior to cardioversion
- Sx onset >48hrs –> anticoagulate for 3wks –> elective cardioversion (also anticoag for 4wks after)
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
AND
- Stroke risk - CHADS-Vasc Vs Orbit/HAS-BLED score –> DOAC (Apixaban)
- If metallic heart valve –> warfarin INR 3-3.5
- Otherwise DOAC
- NOTE: if incidental non-symptomatic AF - normal rate, no other RFs, CHA2DS2-VASc 0 –> anticoagulation not recommended
-
CHF, HTN, Age ≥75rs (2), DM, Stroke (2), Vascular disease, Age 65-74, Sex - female
- Score 1 - consider; ≥2 - DOAC/Warfarin needed
- Lifetime risk = annual risk x estimated years of life left (up to 80 yrs e.g. if 60 then x annual risk by 20)
Infective endocarditis - RFs? Ix? Dx criteria? Mx?
Acute vs subacute bacterial endocarditis - what hearts affected? who are commonly affected? What bacteria most likely?
Def: infection of heart valves (typically mitral/aortic or tricuspid in IVDU)
RFs: bacteraemia (long-term lines, IVDU, dental work), abn valves (prosthetic, RHD), prev endocarditis, VSD, piercings
Presentation: low-grade fevers, night sweats
- Exam:
- Splenomegaly
- Splinter haemorrhages, osler’s nodes, Janeway lesions, petechiae, Roth spots (eyes)
- Chronic = clubbing (rare, mostly acute now)
Ix:
- Urine dip - haematuria
- Serial BCs (x3 but start empirical abx), ESR
- Transoesophageal Echo (TOE - vegetations)
Dx: DUKE’S CRITERIA (2 major OR 1 major + 3 minor OR 5 minor):
- Major: +ve BC (typical organism), new regurg murmur/veg on echo
- Minor: RF, fever (>38), embolic (vascular) phenomena, immune phenomena, +ve BC (another organism)
- Mx: IV abx for 6wks – fluclox/vanc/gent
Acute in structurally normal heart – In IV drug user the first valve met is tricuspid valve, commonly S. aureus (also most common cause in prosthetic valve endocarditis)
Subacute in structurally abn heart – mitral & aortic valves more commonly affected as high pressure system, more likely damaged valves, commonly Strep Viridans (overall most common cause of endocarditis)
3rd & 4th heart sounds - sounds & cause?
3rd = rapid ventricular filling = volume overload e.g. HF (reduced EF/systolic)
- KEN…TU.CKY (deee. de.de)
4th = atrial contraction against stiff ventricles = pressure overload e.g. longstanding AS & other causes of left ventricular hypertrophy (HTN heart disease, HOCM, HF with preserved EF/diastolic)
- TE.NE..SSEE (de.de.deee)
2 days of chest pain following 4 days of generalised muscle aches
- Worse on inspiration & lying flat
- Low-grade fever
- Exam: pericardial rub
Causes? Dx? Ix? Mx?
Pericarditis
Causes:
- Viral (most common)
- MI (can be Dressler’s syndrome)
- TB (constrictive)
- Uraemia (CKD where urea high –> pericarditis) = indication for haemodialysis (HUMP)
- Hydralazine (AI pericarditis)
- NOTE: also causes drug-induced lupus
- SLE, RF, radiation
Presentation:
- Pleuritic chest pain, worse lying flat
- Exam: pericardial rub - “creaking/scratching”
- Tip - put on all-fours, put stethoscope on sternal edge, hold inspiration
Ix:
- ECG: ST elevation widespread
- Only slightly raised/normal troponin
Mx: colchicine (3 months) + NSAIDs (ibuprofen, max 2wks)
Ventricular tachycardia - Dx? Presentation? Ix - appearance on ECG? Mx?
VT or SVT w/ aberrancy
- SVT >200bpm, also often irregular
- VT more likely if LAD
- Acutely treat any broad complex tachy as VT until proven otherwise
Presentation: palpitations, light-headed, chest pain, syncope, seizure
- Tachycardia, LVF
- ACS most common cause
- NEVER IGNORE palpitations & light-headedness
Ix: ECG - regular broad complex tachycardia
- U&E (Mg, Ca, K), TFTs, Troponins
Mx:
- Unstable tachycardia (BP <90, chest pain, acute cardiac failure) = DC cardioversion
- Stable:
- IV amiodarone, b-blocker –> prepare for DC cardioversion
Bradycardia arrhythmia with a palpable pulse (peri-arrest) - Mx?
Innitial: A-E
- If unstable - 500mcg IV atropine (/5mins up to 3mg)
- Also considered unstable if:
- Recent asystole >3s/Mobitz T2 AV block/3rd degree heart block
- Caution in acute MI, C/I if heart transplant
- Also considered unstable if:
- If persistent –> transcutaneous pacing + analgesia/sedation (very painful)
- If can’t be achieved properly –> IV isoprenaline/adrenaline (specialist help)
- Arrange transvenous pacing (temporary if recent asystole >3s/Mobitz T2 AV block/3rd degree heart block)
Heart block causes? types? Ix? Mx? Complications?
Causes:
- MI/IHD (MOST COMMON)
- Inf (RHD, IE)
- Drugs (digoxin)
- Metabolic (hyperkalaemia)
- Infiltration of conducting system (e.g. sarcoidosis)
- Degeneration of conducting system
Types:
- First Degree AV block - fixed prolonged PR interval (> 0.2 s) - ASYMPTOMATIC
- Second degree AV block:
- Mobitz TI (Wenckebach) - progressively prolonged PR interval –> P-wave NOT followed by a QRS complex = ‘going, going, gone’
- Normally asymptomatic
- Mobitz Type II - intermittently P wave NOT followed by a QRS
- May be regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1)
- Can cause:
- Stokes-Adams Attacks (syncope caused by ventricular asystole)
- Dizziness, palps, chest pain, HF
- Mobitz TI (Wenckebach) - progressively prolonged PR interval –> P-wave NOT followed by a QRS complex = ‘going, going, gone’
- Complete AV heart block - no relationship between P waves and QRS complexes
- Presentation as in Mobitz T2
Ix: ECG
- Bloods: TFTs, Digoxin, cardiac enzymes (troponin, CK, BNP)
- CXR (cardiac enlargement, pulmonary oedema)
- Echo (wall motion abn, aortic valve disease, vegitations)
Mx:
- Acute block - if clinical deterioration:
- IV atropine
- Consider temporary transcutaneous pacing
- Chronic block:
- 1st degree monitored
- Permanent pacemaker in:
- Symptomatic Mobitz T1
- Advanced Mobitz T2
- Complete heart block
Complications: asystole, cardiac arrest, HF, surgical complications of pacemaker insertion
Types of pacemaker? When to use each type? Complications?
Types:
- Implantable Cardioverter Defibrillator (ICD, has a thicker end)
- Single-chamber pacemaker (right ventricle)
- Used in permanent AF (no organised atrial contraction so atrial lead not required to sense contraction)
- Rarely can have atrial lead only - if SA disease in young with good AV conduction
- Dual-chamber pacemaker (right atrium & ventricle)
- Can have ICD dual-chamber pacemaker
- Used in paroxysmal AF/all other scenarios (there is sometimes organised atrial contraction - this is sensed by the atrial lead)
- Cardiac Resynchronisation Therapy/Biventricular pacemaker (right ventricle, left ventricle ± right atrial lead)
- Can have ICD biventricular pacemaker
When to use each type:
- Atrial lead only → Sino-atrial disease in young people with good AV node conduction
- RV lead only → Pacing whilst in permanent atrial fibrillation
- Dual-lead → All other scenarios (paroxysmal AF, bradycardia)
- CRT → LV dysfunction + broad QRS –> end-stage HF
- Indications for ICD:
- Primary prevention = @risk of serious ventricular arrhythmia
- Familial cardiac conditions (hypertrophic cardiomyopathy, long QT)
- Previous surgical repair of congenital HD
- Previous MI + LVEF <35% + HF Sx
- Secondary prevention = had previous serious ventricular arrhythmia wo/ treatable cause
- Cardiac arrest from VT/VT
- Spontaneous sustained VT AND:
- Syncope/haemodynamic compromise OR
- LVEF <35% + sign HF Sx (NYHA 3+)
- NOTE: VT/VF from STEMI has treatable cause (open occluded vessel)
- Primary prevention = @risk of serious ventricular arrhythmia
Complications:
- Surgical complications - infection, bleeding, damage to underlying structures
- Displacement (of lead)
- Pacemaker syndrome (if ventricular lead with no atrial) –> AV node conducts in retrograde direction = mitral/tricuspid regurge + HF Sx
How do you know this is the JVP and not the carotid pulse?
- Not palpable
- Double pulsation
- Obliterated when pressure applied at base of neck
- Rises with hepatojugular reflux
- Height changes with respiration
Causes of hepatic decompensation in CLD? Key features of decompensation?
Dx & Mx of decompensated chronic liver disease?
Cause of hepatic decompensation in CLD:
- Hypokalaemia
- Constipation (given lactulose in hospital)
- Alcohol
- GI bleed (lots of protein (Hb) enters the bowel –>liver can’t cope)
- HCC
Decompensated CLD –> Ascites, jaundice & encephalopathy
- Severely scarred liver (cirrhosis) in CLD –> back pressure on portal vein –> PORTAL HTN = splenomegaly, ascites, varices - caput medusae, oesophageal & rectal
Ix:
-
Serum Ascites Albumin Gradient (SAAG) - serum albumin conc vs ascites conc - 11.1g/L
- <11.1g/L = exudative cause - peritonitis (infection), peritoneal malignancy OR n_ephrotic syndrome_ (pee out albumin so low serum albumin)
- Otherwise = transudative cause - cirrhosis, renal failure, HF
- >250 neutrophils = spontaneous bacterial peritonitis (SBP) –> Tazocin/3rd gen cephalosporin
- If protein conc <15g/L give prophylactic oral ciprofloxacin
Mx:
- Paracentesis (ascitic drain) –> post-paracentesis circulatory dysfunction (drops BP) SO if >5L drained give human albumin solution (HAS) 8g/L drained
- Spironolactone (2nd line - Furosemide) - to prevent fluid accumulation
- (Salt restrict)
- Hepatic encephalopathy (liver not dealing with toxins) - give Lactulose + Rifaximin to prevent
- Coagulopathy - OGD (check for varices) + vit K (needed for clotting)
Chronic liver disease
- Functions of liver? Outcome of failure?
- Causes? Presentation? Ix?
- Important complication?
- Scoring?
Functions of the liver –> failure:
- Albumin (plasma oncotic pressure) –> oedema
- Bilirubin metabolism –> jaundice
- Clotting factors –> coagulopathy
- Detoxification –> encephalopathy
Causes:
- Common - alcoholic liver disease, viral hepatitis, NASH (non-alcoholic steatohepatitis)
- Less common - AI hepatitis, PSC/PBC, HF, alpha1-antitrypsin def, haemochromatosis, Wilson’s disease
Presentation:
- Spider naevi (≥5, SVC distribution, flush inside to out), palmar erythema, gynecomastia, Dupuytren’s contracture (alcoholic liver disease), clubbing
- Specific signs:
- Needle marks/tattoos - hep C
- Parotid swelling - alcohol-related liver disease
- Bronzed complexion/insulin injection signs - haemochromatosis
- Obesity/DM - non-alcoholic fatty liver disease
- Xanthelasma - cholestatic disorder
Ix:
- Alcohol history
- Hep B/C serology
- Ferritin, transferrin, A1AT, ceruloplasmin (Wilson’s)
- Ig, auto-abs (ANA in AI hep, AMA in PBC)
Important complication = VARICES
- Normal venous return: GI tract –hepatic portal vein –> liver –> hepatic vein –> systemic circulation
- Physiological hepatosystemic anastomoses (connection of portal vein to systemic circulation) sites - oesophagus, spleen, umbilicus, rectum
- MEMORY AID: BUTT, GUT, CAPUT
- Pathological process:
- In the case of cirrhosis - nodules impede flow of blood through the liver to the hepatic vein –> reducing blood flow to the systemic circulation
- Backflow of blood to the hepatic portal vein = increased –> backflow to hepatosystemic anastomoses:
- Oesophagus –> Oesophageal varices
- Spleen –> Splenomegaly
- Umbilicus –> Caput Medusae
- Only from portal HTN if running from below umbilicus up
- Rectum –> Rectal varices
Score for prognosis & need for liver transplant = Child-pugh score (A = 5-6; B = 7-9; C = 10-15 –> C is most severe)
Chronic diarrhoea - ddx? Sx? Distribution? Histology? Ix? Mx?
IBD
-
Crohn’s disease
- Sx: RIF pain (terminal ileum), failure to thrive (incl. between attacks)
- Distribution: mouth to anus (esp. terminal ileum), skip lesions
- Histology: transmural, non-caseating granuloma (also in sarcoidosis)
-
Ix:
- OGD/colonoscopy/capsule endoscopy
- Gastografin follow-through
-
Mx:
- Induction:
- Steroids (induce remission)
- 5-ASA (mesalazine)
- Maintenance:
- Steroid-sparing agents (methotrexate, azathioprine, mercaptopurine)
- Biologics e.g. Anti-TNF (infliximab)
- Induction:
- Complications: strictures, obstruction, fistulae
-
Ulcerative colitis
- Sx: gen. abdo pain, PR blood & mucus
- Distribution: ONLY rectum & colon, continuous
- Histology: mucosa & submucosa, mucosal ulcers, crypt abscesses
-
Ix:
- Flexible sigmoidoscopy/colonoscopy
-
Mx:
- Induction:
- 5-ASA
- Steroids
- Maintenance:
- 5-ASA (mesalazine)
- Steroid-sparing agents (azathioprine)
- Biologics (infliximab)
- Surgery (proctocolectomy, IJ pouch)
- Induction:
- Complications: toxic megacolon, colonic carcinoma, PSC
- Extra-intestinal signs of IBD - A PIE SAC
- Aphthous ulcers (crohn’s)
- Pyoderma gangrenosum
- Iritis, uveitis, episcleritis (Crohn’s)
- Erythema nodosum
- Sclerosing cholangitis (PSC in UC)
- Arthritis
- Clubbing fingers (CD > UC)
- Truelove & Witts’ severity index = severity criteria for IBD
Coeliac disease
-
Def: inflammatory response to gluten (immune reaction to gliadin)
- DQ2/8 (on HLA typing)
-
Sx: abdo Sx (steatorrhoea, diarrhoea, bloating), failure to thrive
- Exam: blistering rash on both knees. aphthous mouth ulcers
- Assoc: T1DM
- Distribution: duodenum
- Histology: subtotal villous atrophy with crypt hyperplasia
-
Ix: (maintain normal diet - eat gluten for 6wks before testing)
- Haematinics - macrocytic anaemia, low Fe, B12/folate
- Serological testing:
- Screening: Anti-TTG & total IgA (check for selective IgA def in case this caused false ‘-ve’ anti-tTg abs)
- If weakly +ve –> anti-endomysial abs (more sensitive & specific)
- OGD & duodenal biopsy
- Histology: sub-total villous atrophy with crypt hyperplasia
- Mx: gluten avoidance
Irritable bowel syndrome - Dx of exclusion
-
Sx: bloating, related to stress, diarrhoea/constipation, relieved by defecation
- “Pellet-like stools”
- Ix: faecal calprotectin (an inflammatory marker of GI tract = less likely to be IBS, more likely IBD)
- Mx: dietary changes, stress Mx, anti-spasmodics, probiotics, laxatives/loperamide, anti-depressants
Mesenteric ischemia:
- What is the blood supply to the GI tract?
- What area of GI tract is vulnerable to ischaemia?
- Breakdown of mesenteric ischemia? Sx? Ix? Mx?
What is the difference between Mesenteric ischemia & ischemic colitis? Sx? Ix?
Blood supply
- Coeliac axis - oesophagus, stomach, start of small intestine
- Superior mesenteric artery (SMA) - most of the small intestines up to 2/3 transverse colon
- Inferior mesenteric artery (IMA) - from 2/3 along transverse colon down to rectym
- NOTE: area 2/3 along transverse colon @splenic flexure = WATERSHED ZONE (limited supply from superior & inferior mesenteric arteries) –> vulnerable to ischaemia!!
__Mesenteric ischemia
-
Acute - occlusion of SMA by thrombus/embolus
- Sx: severe abdo pain, normal abdo exam, shock
-
Ix:
- AXR (gasless abdo)
- VBG (lactic acidosis)
-
CT abdo with contrast (if suspect mesenteric ischaemia)/CT angiogram (if LA)
- If not primary surgery –> followed by mesenteric angiography (Dx non-occlusive mesenteric ischaemia)
- Mx: resus + CCOT + NBM
- Empirical abx
- Bypass ± bowel resection
- Heparin post-op
-
Chronic - narrowing of SMA by atherosclerosis (stable angina of bowel)
- Sx: colicky post-prandial abdo pain (more work for bowel to do –> pain, just like in stable angina & exercise)
- Ix: as above
- Mx: medical optimisation + bypass (angioplasty + stent if not suitable for surgery)
Ischemic colitis
- Occlusion of inferior mesenteric artery (IMA) by thrombus/embolus
- Sx: abdo pain, PR bleeding
- Ix: sigmoidoscopy/colonoscopy
- Mx: seek GI & surgical input (can develop chr ulcerating IC)
- Mild - conservative (IV abx, fluids, bowel rest, DM control)
- Prophylactic LMWH
- Segmental resection + stoma
- Mild - conservative (IV abx, fluids, bowel rest, DM control)
How do you tell between spleen & kidney on examination?
Spleen (vs kidney):
- Moves down with inspiration
- You can’t get above it
- Has a notch
- Dull to percussion & not ballotable
Upper GI bleed - scoring for need for intervention? Mx?
Blatchford score
Variceal bleed
- Massive haemorrhage –> balloon tamponade
- A-E assessment –> IV fluids, blood transfusion
- F1 Essentials:
- 2x large bore cannula
- VBG
- G&S/X-match
- Bleep the bleed reg
- F1 Essentials:
- Drugs with prognostic benefit:
- IV Terlipressin (ADH analogue –> vasoconstriction)/Somatostatin (used for same reason)
- Prophylactic abx - Ceftriaxone/Norfloxacin (abx)
- Intervention (discuss with on-call bleed registrar) –> endoscopic band ligation
Peptic ulcer disease - RFs? Types? What artery is most likely to bleed in duodenal ulcer?
Presentation? Ix? Mx? Scoring to evaluate risk of re-bleed/death?
RFs:
- H. pylori exposure
- Aspirin/NSAID use
Types:
- Gastric - pain worsened by meal (pain 30m-1hr after meal), loose weight, vomiting, assoc w/ NSAIDs
- Duodenal - MORE COMMON, pain relieved by meal (pain 2-3hrs after meal), assoc w/ H. pylori, worse by stress/at night –> radiates to back, put weight on, malaena
- Gastroduodenal artery - runs posterior to 1st/2nd parts of duodenum –> likely cause of bleeding in PUD
Presentation:
- Chr/recurrent upper abdo pain - related to eating & nocturnal
- Can be severe/radiate to back in Duodenal ulcers if ulcers penetrates pancreas
- Pointing sign on exam - show where pain is with 1-finger
- NOTE: ‘Coffee grounds’ vomiting = upper GI bleed (mostly due to PUD > gastric erosions)
Ix:
-
OGD endoscopy = gold-standard
- Immediately if dyspepsia + upper GI bleed
- Within 2wks if ≥55yrs + weight loss + dyspepsia/reflux/upper abdo pain –> exclude malignancy
- Repeat within 6-8wks to ensure ulcer healing/rule out malignancy
- H. pylori stool antigen/breath test (2wk wash out period after PPI or 4wks after abx, retest 6-8wks after starting Tx)
- Bloods - FBC
Mx: consider STOPPING NSAIDs
- Active bleed:
- Urgent evaluation (A-E + Blatchford score) + blood transfusion
- OGD endoscopy (Dx & Tx) –> high-dose IV PPI afterwards (continue oral PPI for 6wks)
- Rockall score (for risk of rebleed/death) –> if re-bleed –> repeat endoscopy & Tx endoscopically/emergency surgery
- If H. pylori +ve:
-
H. pylori eradication - triple therapy for 7 days (PPI + 2 abx = Amox + clari/metro) –> retest 6-8wks after starting Tx (leave washout 2wks after PPI, 4wks after abx)
- If pen allergic –> PPI + Clari + Metro
- If long-term NSAID/aspirin use:
- Consider stopping NSAIDs/aspirin
- Ulcer healing Tx - full-dose PPI/H2 antagonist for 8wks –> H. pylori eradication afterwards
-
H. pylori eradication - triple therapy for 7 days (PPI + 2 abx = Amox + clari/metro) –> retest 6-8wks after starting Tx (leave washout 2wks after PPI, 4wks after abx)
- If H. pylori -ve: treat underlying cause + PPI (4-8wks, 2nd line = H2 antagonist)
- If recurrent/refractory ulcers –> long-term PPI/H2 antagonist
- Joint pain in both knees, XR shows chondrocalcinosis
- Wakes at night frequently to urinate, PMHx T2DM, low albumen on blood
Dx? Classification? Presentation? Ix? Mx?
Dx: haemochromatosis
- Risk of HCC (hepatocellular carcinoma)
Classification:
- Hereditary - AR, gene on chr6 (carried by 1:10 Europeans)
- Secondary e.g. from frequent blood transfusions (SCD)
Presentation - from Fe-deposition in various tissues:
- Arthritis (esp hands), bronze DM (tan), cirrhosis
- Hypogonadism (accumulates in testis)
- Dilated cardiomyopathy (accumulates in heart)
- XR - chondrocalcinosis is assoc w/ pseudogout & haemochromatosis
Ix:
- Blood iron profile:
- TF saturation high (>55% men, >50% women)
- Ferritin normal/slightly high (>500)
- Low TIBC (as all transferrin saturated)
Mx:
- Venesection (until transferrin saturation normal)
- Desferrioxamine (iron chelator to prevent recurring)
- Monitoring ; TF saturation <50% & serum ferritin <50ug/l
Case:
- 57yrs, burning pain after eating & lying flat, improved with cold drinks, high BMI, smokes, drinks alcohol, occasional bitter taste in back of the mouth
- Difficulty swallowing in recent months
Dx? Presentation? Ix? Mx? Complication?
Dx: GORD
- Decreased lower oesophageal sphincter (LOS) pressure:
- Drugs - nitrates, CCBs (smooth muscle relaxation)
- Alcohol, smoking
- Hiatus hernia
Presentation: RFs (above), heartburn (worse lying down/at night), reflux incl bitter taste in mouth (after meals)
Ix:
- 8wk PPI trial
- If dyspepsia consider OGD for: anaemia, weight loss, dysphagia, >55yrs
- Oesophageal pH study (<4 for >4% of time = GORD)
Mx:
- Conservative: weight loss, smoking cessation, head of bed elevation/avoid eating late at night, reduce alcohol
- Medical:
- Standard-dose PPI (20mg omeprazole) - continued long-term (if Sx continue after stopping/erosive oesophagitis/Barrett’s oesophagus)
- H2 antagonist (e.g. cimetidine)
- Surgery (only if PPIs work but don’t want long-term medical Tx) e.g. laparoscopic fundoplication
Complication: Barrett’s oesophagus –> oesophageal adenocarcinoma
Anal fissure - def? RFs? Presentation? Ix? Mx?
Def: tears of the squamous lining of the distal anal canal
- <6 weeks = acute, ≥6wks = chronic
- 90% @posterior midline
RFs: constipation, IBD, STIs (HIV, syphilis, herpes)
Presentation: painful, bright red, rectal bleeding
Ix: PR exam
Mx:
- Acute <1wk:
- Soften stool - high-fibre diet + high fluid intake, fybogel (2nd - lactulose)
- Lubricants (for passing stool), topical anaesthetic, analgesia
- Chronic: maintain above + topical GTN
- After 8wks (if above not effective) –> GI referral for sphincterotomy (or botulinum toxin)
Haemorrhoids - presentation, grading, Ix, Mx?
Presentation: rectal bleeding & perianal pain
Grading:
- 1 - prominent BVs (no prolapse)
- 2 - prolapse on bearing down + spontaneous reduction
- 3 - manual reduction
- 4 - can’t be manually reduced
Ix:
- Bedside: Anoscopic exam, stool (occult haem)
- Bloods: FBC
- Imaging: Colonoscopy/flex sigmoidoscopy
Mx:
- Conservative - fibre, fluids
- Medical = G1 - topical CS
- Surgical:
- G2/3: band ligation
- G4: surgical haemorrhoidectomy
Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?
Presentation: polyuria, polydipsia, dehydration
- Ketosis - malaise, vomiting
- FHx, other endo disorders
- If known DM:
- Previous DM control (hyp/hyper)
- Micro/macrovascular complications
- Diabetic eye disease (Dx & Tx)
RFs: overweight, FHx (DM), PMHx (GDM), PCOS, HTN, dyslipidemia, CVD
Criteria for Dx (repeat test needed for Dx):
- Fasting plasma glucose of ≥7.0 (normal ≤6)
- OGTT (BM 2hours after 75g glucose-load)/ Sx + random plasma glucose of ≥11.1mmol/l (normal <7.8)
- HbA1c ≥48mmol/mol (≥6.5%) - not for young/T1DM, acutely ill, haem disease, preg, iatrogenic
T1DM Mx: exogenous insulin to avoid DKA & long-term complications
- Diet - lower fat, higher carbs = counting carbs (adjust insulin around diet rather than limiting eating)
- Diabetic specialist nurse - EDUCATE:
- Self-adjust dose - DAFNE course for T1DM (D for DM)
- Fingerprick glucose
- Calorie intake & carb counting
- Phone support
- Don’t stop insulin during acute illness, maintain calorie intake
- Insulin regimens:
- 1st line - Basal-bolus regimen
- Basal (background) - BD insulin detemir (or Levemir/Lantus/Tresiba) as basal insulin
- Bolus (before meals) - analogue rapid-acting insulin e.g. insulin Lispro (Humalog)/Aspart (Novorapid)/Neutral (Actrapid)
- Other:
- BD biphasic (premixed insulin, hypos common) e.g. Novomix, Humulin M3, Humalog Mix
- OD before bed long-acting (for T2DM)
- NOTE: intermediate-acting insulin e.g. Humulin I, Insulatard
- 1st line - Basal-bolus regimen
T2DM Mx:
- 1st line - Lifestyle changes - DESMOND course for T2DM (D for DM), dietician input, self-BM monitoring (individual HbA1c target <6.5)
- HbA1c targets:
- No hypoglycaemics - 48mmol/mol
- Hypoglycaemics - 53mmol/mol
- Escalate Tx - 58mmol/mol
- HbA1c targets:
- Medication:
- 2nd - Metformin (SEs: diarrhoea, LA - avoid if eGFR <30)
- 3rd - ADD Sulphonylurea e.g. Gliclazide (SEs: hypoglycaemia, weight gain)
- 4th - ADD other DM med:
-
Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
- C/I in HF, bladder cancer
-
SGLT-2 inhibitor e.g. Empagliflozin (SEs: Hypoglycaemia, weight loss, UTI)
- Not recommended in impaired renal funct
- DPP-4 inhibitor e.g. Linagliptin (APPROVED FOR USE IN CKD, weight neutral)
-
GLP-1 analogues e.g. Exenatide/Liraglutide (SE: weight loss - useful if BMI >35; vomiting)
- Not recommended in impaired renal funct
-
Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
- 5th - If on triple therapy & not providing control –> commence insulin
- CVD risk Mx - anti-HTN, anti-lipid, QRISK-3 score
- Diabetic nephropathy Mx:
- Monitor albumin-creatinine ratio (ACR)
- Consider ACEi/ARB early
- Diabetic neuropathy Mx:
- Annual Sx review (erectile dysfunction, autonomic neuropathy - orthostatic hypotension, gastroparesis, bladder emptying difficulties)
- Annual foot screen + specialist foot Mx, monitor for diabetic foot/ulcers ± amputation
- Diabetic retinopathy: retinal screen annually (age ≥12yrs)
- Background: need to tighten control
- Venodilation, microaneurysms (dots), hard exudates (lipid deposits)
- Tx: tighten glycaemic control, refer if near macula
- Pre-proliferative (mild) - soft exudates (cotton wool spots e.g. infarcts)
- Proliferative - neovascularization (+ floaters, reduced acuity)
- Tx: pan-retinal photocoagulation
- Diabetic maculopathy - hard exudates, oedema (+ blurred vision, reduced acuity)
- Tx: intravitreal triamcinolone acetonide decreases macula oedema
- NOTE: Pre-diabetic –> refer to diabetes prevention programme (DPP)
- Background: need to tighten control
Diabetes complications:
- Microvascular:
- Eye - diabetic retinopathy (± cataracts, glaucoma)
- Kidney - diabetic nephropathy
- Neuropathy - damage to PNS –> diabetic neuropathy (peripheral neuropathy - glove & stockings distribution) –> diabetic ulcers/gangrene
- Macrovascular:
- Brain - stroke/TIA/cog impairment
- Heart - coronary heart disease
- Extremities - PVD, diabetic ulcers/gangrene
Hyperosmolar Hyperglycaemic State
- What does insulin do? Pathophysiology of HHS?
- HHS criteria? HHS Mx? HHS Mx Targets?
Insulin:
- High level of insulin –> reduces serum BM (pushes into surrounding tissues & hepatic glucose store)
- Low level of insulin –> switches off ketone production
Pathophysiology:
- HHS = complication of T2DM
- In HHS have enough insulin to switch of ketone production but not enough to reduce BM lvls
- High glucose - osmotically active –> polyuria –> dehydration
HHS criteria:
- Hypovolaemia
- Glucose >30mmol/L
- NO ketonaemia
- Serum osmolality >320mOsmol/kg
Mx: REHYDRATE = IV 0.9% NaCl (3-6L by 12hrs, deficit 110-220mL/kg)
- Targets:
- Reduce Na by less than 10mmol/L/day (otherwise risk osmotic demyelination syndrome)
- Reduce BM by over 5mmol/L/hr
- NOTE: if targets not met by 0.9% saline –> 0.45% instead
- If fluid alone are not enough –> 0.05 units/kg/hr fixed-rate insulin infusion
Diabetes insipidus - Sx? Types? Ix? Tx?
Sx: hypernatremia (lethargy, thirst, irritable, confusion, coma, fits), polyuria, urine plasma osmolality <2 (very dilute)
Types:
- Central (lack of ADH prod in hypothalamus) – pituitary surgery, irradiation, trauma, infarction
- Nephrogenic (resistance to ADH effects) – hypercalcaemia, hypokalaemia, meds (lithium)
Ix: rule out DDx (BM, review drugs, K/Ca lvls)
- U&E, Ca, BM, serum & urine osmolarities
- Dx: 2-step fluid deprivation test = give desmopressin (DDAVP):
- Normal/primary polydipsia –> urine concentrates on fluid deprivation (>600)
- Cranial DI - giving desmopressin allows ADH prod –> urine conc
- Nephrogenic DI: urine never concentrates
- NOTE: DI excluded if urine to plasma (U: P) osmolarity ratio >2:1
- Cranial MRI - if suspect cranial DI
NOTE: Fluid deprivation test process:
- Baseline urine osmolality
- Fluid deprivation for 8hrs, take urine osmolality
- Give desmopressin, wait 8hrs, take urine osmolality
Tx:
- Nephrogenic DI –> fluids (+ monitor UO) + thiazide diuretics (hydrochlorothiazide - weird/does not make sense)
- Central DI –> fluids + desmopressin
Thyroid disease - types? presentations? causes? Mx? What is a thyroid storm?
Hypothyroidism:
- Causes:
-
Primary:
-
Hashimoto’s thyroiditis - most common hypothyroidism
- Goitre, AI disease (vitiligo, pernicious anaemia, T1DM, Addison’s)
- Elderly females
- May be initial ‘Hashitoxicosis’
- +++ Autoantibody titres
- Antithyroid peroxidase (TPO) & antithyroglobulin (TG)
-
Atrophic AI thyroiditis
- No goitre, anti-TPO/TSH
- Iodine def, meds (carbimazole, lithium), thyroid surgery
-
Hashimoto’s thyroiditis - most common hypothyroidism
-
Secondary: pituitary gland fails to produce TSH
- Tumour, vascular (Sheehan syndrome), radiation, inf
-
Primary:
- Ix:
- Bedside: ECG (pericardial effusion, ischaemia)
- Bloods: FBC, U&E, TFTs, Lipids, Prolactin, Anti-TPO/TG
- Imaging: CXR (effusions, HF)
- Mx: thyroid replacement therapy (levothyroxine)
- Monitor with serum TSH, careful with dose in elderly (prone to IHD)
- Myxoedema coma - A-E & active warming, T3 slow IV, hydrocortisone IV
- Associated complications:
- Cardiac - HF
- Serous effusions (pleural, peritoneal, pericardial, joint)
- Neuro - carpal tunnel, proximal myopathy, cerebellar dysfunction, myxedema coma
- Systemic - dyslipidemia, anaemia
Hyperthyroidism:
- Presentation:
- Weight loss, increased appetite
- Heat intolerance, tremor, sweating, palpitations
- Mood (anxious, irritable)
- Bowel habit (diarrhoea), menses (oligomenorrhoea)
- Goitre
- Eye Sx (watering, gritty, red)
- Other AI disease (vitiligo)
- Signs:
- Lid lag (eyes)
- Palmar erythema
- Brisk reflexes
- Sinus tachy/AF
- Ix: TSH low, T3/4 high, TPO (may be raised), anti-TSHr ab (in Graves), technetium 99m uptake scan (diffuse/reduced)
- Causes:
- High-uptake:
-
Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
- Eye signs: proptosis –> exophthalmos, diplopia, visual loss
- Peripheral signs: pretibial myxoedema, thyroid acropatchy, onycholysis, bruit over thyroid
- Toxic multinodular goitre aka Plummer’s disease: hot nodules, painless
- Toxic adenoma: 5%, single ‘hot nodule’ on isotope scan (1 area of uptake)
-
Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
- Low-uptake:
-
Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
- Tx: NSAIDs
- Postpartum thyroiditis (like De Quervain’s but postpartum)
-
Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
- High-uptake:
- Mx:
- Conservative: lifestyle changes, corneal lubricants
-
Medical:
- Sx relief – B-blockers
- Antithyroid meds - Carbimazole (or propylthiouracil)
- SEs: rashes, agranulocytosis - monitor
-
Radioiodine:
- acts slowly, effective, best Tx for toxic multinodular goitre
- Risk of permanent hypothyroidism (10%)
- CI in preg/lactating women
- Surgical: subtotal thyroidectomy (in large goitre/relapse)
- Monitoring with TFTs annually
-
Thyroid storm: acute state of shock, pyrexia, confusion, vomiting
- HDU/ITU support
- Propylthiouracil 600mg –> 200mg QDS
- Stable iodine (Lugol’s iodine) ≥1hr later
- Propranolol, dexamethasone & IV fluids
Adrenal anatomy? Adrenal disease breakdown? Causes? Presentations? Ix? Mx?
Adrenal anatomy (outside –> in):
- Zona glomerulosa –> mineralocorticoids e.g. aldosterone
- Zona fasciculata –> glucocorticoids e.g. cortisol
- Zona reticularis –> androgens e.g. testosterone
- Adrenal medulla (centre) –> catecholamines e.g. NA/adrenaline
Cushing’s #HighCortisol
- Causes:
- ACTH-dependent:
- Pituitary tumour (85%) = “Cushing’s disease”
- Ectopic ACTH-prod tumour (5%) - SCLC/carcinoid tumour
- ACTH-independent:
- Adrenal tumour (10%)
- Iatrogenic steroid use
- ACTH-dependent:
- Presentation:
- Thin skin, easy bruising, proximal myopathy, obesity (moon face, buffalo hump), other (hirsutism, acne)
- Exam: vertical abdo striae
- HTN, DM, osteoporosis (back/bone pain)
- Ix:
- Exclude pseudo-Cushing’s - depression, alcohol excess, chr inf (no muscle weakness)
- Confirm Dx: low-dose dex suppression test - fail to suppress cortisol in all
- Overnight dexamethasone suppression test (1g @11pm) OR
- 48hr low-dose 0.5mg/6h PO dexamethasone supression test OR
- 24-hr urinary free cortisol (test x3 as low sensitivity)
-
Plasma ACTH measured:
- High - CRH test identifies if pituitary or ectopic
- Could also do bilateral inferior petrosal sinus sampling –> if no mass –> CT contrast CAP for ectopic
- Low - adrenal tumour –> CT/MRI adrenal glands –> if nothing –> adrenal vein sampling
- High - CRH test identifies if pituitary or ectopic
- Mx: treat underlying disease e.g. withhold steroids or surgical removal of the lesion
- Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
- 2nd - pituitary radiotherapy (also used if still high cortisol post-surgery) –> progressive anterior pituitary failure
- Metyrapone & ketoconazole - sometimes before/after surgery
- 3rd - laparoscopic bilateral adrenalectomy in refractory (but require lifelong glucocorticoid/mineralocorticoid replacement + risk of Nelson’s syndrome (increased skin pigment from high ACTH
- Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
Hypoadrenalism
- Causes:
- AI: Addison’s disease (>70%)
- Malig: mets (lung, breast. kidney)
- Inf: TB (>10%), HIV (CMV adrenalitis), Fungal
- Infiltration: granulomatous disease, hemochromatosis, amyloidosis
- Iatrogenic: ketoconazole, rifampicin, phenytoin, bilateral adrenalectomy
- Congenital: congenital adrenal hyperplasia (late-onset)
- Presentation:
- Anorexia/weight loss, fatigue/weakness, postural dizziness, reduced libido, sweating
- N&V, diarrhoea, salt craving
- Signs: hyperpigmentation in skin creases/lip/mouth, vitiligo, sparse axillary/pubic hair
- Ix:
- Bedside - postural hypotension, IGRA (TB inf)
- Bloods - FBC, U&E (↑ K+, ↓ Na+), low glucose, serum Ca, AI/auto-ab screen, plasma renin & aldosterone, short snACTHen 250mcg IM test (not Addison’s if 30min cortisol rises >550nmol/L
- Imaging: CXR (past TB), adrenal CT (for TB/mets)
- Mx:
- Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
- Ppt factors: inf, trauma, surgery, missed steroid doses
- Ix: Cortisol, ACTH, U&E
- Mx: IV hydrocortisone + IV fluids ± fludrocortisone (if primary adrenal lesion)
- Monitor BM ± IV dextrose
- Bloods, urine, sputum culture ± abx
- Chronic: hydrocortisone + fludrocortisone (Na homeostasis), education (compliance, increase steroid dose if ppt factors, follow-up
- Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
Hyperaldosteronism (incl. Conn’s)
- Primary (HTN, ↑ Na+ ↓ K+):
- Conn’s - aldosterone-secreting adrenal adenoma
- Bilateral adrenal hyperplasia
- Secondary - decreased renal perfusion (high renin –> Na reabsorption –> HTN) - RAS, HF, liver failure
- Ix: aldosterone-renin ratio (ARR), CT/MRI adrenals, adrenal vein sampling
- Conn’s is very high (high aldosterone, low renin) VS BAH has both high (high aldosterone, high renin)
- Mx: spironolactone, unilateral adrenalectomy (for Conn’s)
PHaeochromocytoma #HighCatecholamines
- Cause: adrenal medulla tumour –>↑ catecholamines (adrenaline/NA)
- Presentation: episodic headache, sweating, tachycardia, hypertension, arrhythmias, death if untreated
- 10% exta-adrenal, 10% bilateral, 10% malignant
- Ix: ECG (LVF, increased ST seg, VT), 24hr urinary metanephrines, abdo CT/MRI
- Mx: specialist endo centre - alpha blockade = PHenoxybenzamine then beta-blockade –> then surgery when BP controlled (after 4-6wks)
DDx for tiredness & lethargy? Ix?
DDx:
- Anaemia - PUD, altered bowel habit? occult blood loss?
- Thyroid disease - thyroiditis?
- DM - polyuria, polydipsia, weight loss
- Adrenal insufficiency
- Primary hyperparathyroidism - constipation, urinary stones, abdo pain, depression
- Hypopituitarism
- Anxiety & depression - sleep disturbances, poor appetite, recent stress
Ix:
- FBC, U&E, LFTs, CRP, bone profile, HbA1c, TFTs, haematinics, BM, serology (anti-TSH/TPO), 9am cortisol lvls
- CXR
Diabetic Ketoacidosis (DKA)
- Normal glucose transport & during starvation?
- The problem in insulin deficiency (diabetes)? How does this relate to Sx of DKA?
- Ix? Dx criteria? Mx? Monitoring Tx & hourly targets?
Normal glucose transport: diet –> blood –insulin–> hepatic glucose store –GH, Cortisol, Adrenaline, Glucagon–> blood
- During starvating - GH, Cortisol, Adrenaline, Glucagon make sure there is enough glucose in the blood BUT liver also produces ketones
- Ketones can cross BBB providing an alternative source of fuel for the brain when low glucose
- Pancreatic beta cells –> insulin prod –> reduces glucose (high glucose has–> feedback on pancreatic beta cells –> produce more insulin)
- High insulin (associated with high glucose) –> -ve feedback on ketone prod
In insulin deficiency - high glucose but unable to produce insulin + no -ve feedback on ketone prod –> high glucose, high ketones
- High glucose - osmotically active (moves along concentration gradient into urine –> pulling more water with it) –> POLYURIA –> DEHYDRATION
- High ketones - acidic (metabolic acidosis) –> enzyme dysfunction –> COMA & DEATH
DKA Ix:
- Bedside - urine dip, ECG, continuous cardiac monitoring
- Bloods - VBG, FBC, U&E, BC, BM
- Imaging - possibly CXR
DKA Dx:
- BM: ≥11mmol/L
- Ketones: ≥3mmol/L (serum) OR ≥2+ (urine)
- Acidaemia: pH <7.3 OR Bicarb <15mmol (ketoacidosis)
DKA Mx: A-E assessment
-
IV FLUIDS (rehydrate)
- Bolus –> 1L over 1hr –> 2hr –> 3hr –> 4hr
- Add 40mmol KCL to fluids after bolus
-
0.1 U/kg/hr fixed-rate INSULIN infusion (reduce ketones)
- If BM <14 –> start 125ml/hr 10% dextrose
- Insulin infusion continues until ketones normalise (not BM)
- NOTE: follow local trust guidelines for DKA Tx as varies slightly between trusts
Monitor - BM, ketones, VBG (K conc)
- Hourly targets:
- Fall in BM ≥3
- Fall in ketones ≥0.5
- Rise in HCO3 ≥3
- Continue until: blood ketones <0.6, pH >7.3, HCO3 >18
Acromegaly cause? presentation? Ix? Mx? Complications?
Cause: macroadenoma in anterior pituitary
Presentation: coarse facial features
- Skin (acanthosis nigricans - thick & dark in creases), sweating, carpal tunnel syndrome (bilateral)
- Arthropathy, sleep apnoea, reduced sexual functioning, visual field defects (bitemporal hemianopia)
- Assoc: DM, HTN, MEN type 1 (15%)
Ix:
- Bedside: CN VI palsy, urine dip (glucose), ECG (cardiomyopathy)
- Bloods: elevated IGF-1, GH lvl during OGTT (not suppressed in acromegaly)
- Imaging: MRI brain (macroadenoma), sleep studies, colonoscopy (screening), visual field testing (driving)
Mx:
- Transsphenoidal hypophysectomy (curative)
- Medical: somatostatin analogue (octreotide)
- External pituitary radiotherapy (long-term 5-10yrs)
Complications:
- General: HTN, DM, carpal tunnel syndrome, sleep apnoea, colorectal cancer, LVH/cardiomyopathy/IHD
- Anterior pituitary hypofunction: hypogonadism
- Local compressive: bitemporal hemianopia
Hyperprolactinaemia - causes? presentation? Ix? Mx
Causes:
- Prolactinoma (macroprolactinoma >6000)
- Adenoma (non-funct pituitary adenoma 1000-5000, from compression & DA lvls)
- DA antagonist (metoclopramide, anti-psychotics, methyldopa)
- Hypothyroidism (increased TRH stimulates prolactin prod)
- Physiological (pregnancy, breastfeeding)
Presentation: irreg periods, decreased libido, galactorrhoea
- Bilateral hemianopia
Ix:
- Bedside - pregnancy test, visual fields assessment
- Bloods - serum prolactin, TFTs, U&E
- Imaging - pituitary MRI
Mx:
- Asymptomatic pre-menopausal/post-menopausal with microadenoma - observation
- Symptomatic pre-menopausal/macroadenoma post-menopausal/male:
- Dopamine agonist (Cabergoline/Bromocriptine), 2nd line - COCP (not if want pregnancy)
- Trans-sphenoidal surgery (if visual Sx/pressure effects refractory to medical Tx)
- Follow-up: monitor prolactin, check visual fields