FY1 On Call

Question 1

Reading an ABG?

Answer 1

Respiratory failure:

• Low O2 = T1RF (PaO2 <8kPa)
• Low O2 + High CO2 = T2RF (PaO2 <8kPa, PaCO2 >6kPa)

Determining acid: base balance:

• Low pH + high CO2 = Respiratory acidosis (low CO2 = metabolic)
• High pH + low CO2 = Respiratory alkalosis (high CO2 = metabolic)
• NOTE: if bicarb is high in RA = chronic RA (compensation by bicarb is slow) –> this determines if should be on scale 1/2 O2 (scale 2 = 88-92%)

Causes of acid: base balance:

• RA causes: COPD, ILD, hypoventilation, asthma (normally resp alkalosis but can be acidotic if severe)
• MA causes: lactic acid, ketoacids (CO2 blown off to compensate –> Kussmaul breathing)

Question 2

COPD - definition? Signs & Sx? New Dx & exacerbation Ix/Mx? Prognosis factors?

Answer 2

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

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
• Reassess:
  
  • If improvement (increased SaO2, reduced RR/HR):
    
    • Continue abx/steroids
    • Wean of nebs and O2
  • No improvement (after 30 mins):
    
    • NIV (BiPaP)

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

Question 3

Aspects of A-E assessment

Answer 3

Identify a problem and deal with it as going along…

• Airway - patent? look, listen and feel –> head tilt + chin lift, jaw thrust, airway adjunct
• Breathing - RR, O2 Sats (>94% - scale 1, 88-92% - scale 2 if COPD), resp exam, ABG –> Oxygen (15L/min O2 non-rebreather mask)
• Circulation - HR, BP, CRT, cardio exam –> IV fluids
• Disability - BM, pupils (PEARL - pupils equal and reactive to light), GCS/AVPU, abdo/neuro exam
• Exposure - assess everything but not all at the same time –> calf tenderness, bleeding, bruising, rashes etc.

NOTE: if put in intervention say to examiner I would reassess previous steps e.g. A&B if gave IV fluids are there any changes

Question 4

Oxygen therapy principles

Answer 4

Oxygen from wall = 100%

Peak inspiratory flow - the maximum rate of drawing in O2 normally is 20L/min (not normally measured unless ITU)

O2 therapy goal is increasing conc grad between alveoli and blood - done by increasing FiO2 (fraction of inspired O2)

Devices types: 1) variable (can’t guarantee FiO2, depends on PIF) - nasal cannula, hudson mask, non-rebreather mask 2) fixed - venturi mask (useful if COPD as need to know exactly how much O2 giving)

NOTE: If PIF increases (breathing harder) –> FiO2 decreases so more device O2 is required

High-flow nasal oxygen therapy - humidifies + warms O2 = well-tolerated –> very high flow rate can be achieved - finely controlled FiO2

Question 5

AKI - def? Severity stages? Breakdown by pathology? Key things to do? Ix? Mx?

Answer 5

Def: abrupt loss of kidney function resulting in dysregulation of fluid balance + electrolytes & retention of nitrogenous waste products

Severity defined based on creatinine/urine output:

• Stage 1: 1.5-1.9x baseline/UO <0.5mL/kg/hr for 6-12hrs
• Stage 2: 2-2.9x baseline/UO <0.5mL/kg/hr for >12hrs
• Stage 3: >3x baseline/UO <0.3mL/kg/hr for >24hrs OR anuria >12hrs

Breakdown by pathology:

• Pre-renal - HYPOPERFUSION
  
  • Hypovolemia (e.g. dehydration/upper GI bleed -> less circulating volume)
  • Sepsis/Anaphylaxis (widespread vasodilation -> reduced perfusion pressure)
  • HF (heart pumping less effectively -> less blood reaches kidneys)
  • RAS (mechanical obstruction of blood flow to kidneys)
• Renal - KIDNEY-SPECIFIC –> renal referral
  
  • Acute tubular necrosis (following pre-renal AKI, high CK)
  • Glomerulus = Glomerulonephritis
  • Interstitium = acute interstitial nephritis (low-grade fever, elevated urinary eosinophils, commonly from NSAIDs)
  • Blood vessels = vasculitis
  • Toxin accumulation = nephrotoxic drugs (ACEi, thiazide diuretic), rhabdomyolysis (myoglobin)
• Post-renal - OBSTRUCTION –> urology referral
  
  • Ureteric calculus
  • BPH
  • Cancer (prostrate, bladder)

Key things to do:

• Check trend (compared to baseline creatinine)
• Check drug chart (any nephrotoxic?) –> remove/replace
  
  • CANDA: Contrast (keep very hydrated), Aminoglycosides (Gent), NSAIDs, Diuretics, ACEi
  • NOTE: DO NOT GIVE Metformin if kidney issue/low GFR - increases risk of lactic acidosis but unlikely to cause AKI
• 3) Check fluids (pre-renal - dehydration) –> give fluids

Ix:

• Bedside - urinalysis (haematuria, inf, BM, PCR)
  
  • Red cell casts - glomerulonephritis
  • White cell casts = pyelonephritis
• Bloods - U&E, AI screen (ANCA), CK
• Imaging - renal USS (stones, vascular thrombosis)

Mx:

• Identify & Mx the cause
• Hypovolaemic - IV fluid bolus
• Hypervolaemic - if pul oedema –> loop diuretic (furosemide) + Na restriciton

Question 6

Heart failure def? Pathophysiology? Categories & Causes? Ix? Mx?

Answer 6

Def: pumping of blood by heart insufficient to meet the demands of the body

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)
• 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

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 = fluffy opacification, 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
  • If no improvement –> furosemide ± CPAP
• 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)

Question 7

Types of Non-Invasive Ventilation

Answer 7

CPAP = fixed IPAP and EPAP

• Holds open/splints airways –> for T1RF –> increase O2

BiPAP = IPAP higher than EPAP

• Gradient allows exhalation more easily –> for T2RF –> excrete CO2
• (- If had high CO2 on ABG –> increase IPAP –> more excreted CO2)

Question 8

IHD - Types? Definition? Dx? Mx?

Answer 8

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)
• 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)

Question 9

Drugs to avoid in renal failure (eGFR <30)?

Answer 9

Key: NSAIDs, ACEi (& ARBs)

Other:

• Abx: tetracyclines, nitrofurantoin, aminoglycosides
• Allopurinol (accumulates in renal dysfunction)
• Lithium
• Metformin
• IV contrast

Drugs harmful in AKI = CANDA: Contrast (keep very hydrated), Aminoglycosides (Gent), NSAIDs, Diuretics, ACEi

Question 10

Anaemia Ix? Mx?

Answer 10

Ix: FBC, haematinics, B12/folate, OGD

Blood transfusion threshold: Hb <70 or <80 AND ACS

Other options: Fe infusion, ferrous fumarate

NOTE: anaemia can exacerbate chest pain/ACS

Question 11

Atrial fibrillation (AF)

• Def? Causes? Ix? Mx?

Answer 11

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)

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)

Question 12

Types of anticoagulant

Answer 12

Heparins

• LMWH (SC) - VTE prophylaxis BUT bad for renal function
• UFH (SC/IV) - GOOD for renal function as a rapid reversal BUT heparin-induced thrombocytopenia (hypercoag state) risk needs APTT ratio monitoring

DOACs - oral + no monitoring BUT bad for renal function e.g. Apixaban (BD), Rivaroxaban (OD)

Vit K antagonist = Warfarin if weight extremes, reduced renal function or AF w/ MS/mechanical heart valve BUT INR monitoring + drug interactions

Question 13

Alcohol withdrawal management?

Answer 13

1. Chlordiazepoxide (decreasing regimen + PRN) - prevent alcohol withdrawal Sx (anxiety, shakes etc.) + CIWA scoring (dose increased inf CIWA score increases)
2. Pabrinex (thiamine, B1) - prevent Wernicke’s encephalopathy (ophthalmoplegia, ataxia, confusion)
3. Bloods - coagulation (injury, bleeds), LFTs

Question 14

What are the markets of liver synthetic dysfunction?

Answer 14

Bilirubin

Albumin - slow to change so gives good idea of chronic disease

Coagulation screen (APTT, PT, INR)

Question 15

Causes of hepatic decompensation in CLD? Key features of decompensation?

Dx & Mx of decompensated chronic liver disease?

Answer 15

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)

Question 16

Chronic liver disease

• Functions of liver? Outcome of failure?
• Causes? Presentation? Ix?
• Important complication?
• Scoring?

Answer 16

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)

Question 18

Upper GI bleed - scoring for need for intervention? Mx?

Answer 18

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
• 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

Question 19

How does lactic acidosis appear on VBG? Lactate physiology/pathology?

Answer 19

Acute metabolic acidosis - low pH, low cHCO3/low BE, high lactate

Physiology:

• Glucose –> Pyruvate –O2–> mitochondria –> ATP
• Glucose –> Pyruvate –NO O2–> Lactate (+ small ATP) –> excreted by kidney or liver/muscle –gluconeogenesis –> glucose

Pathology:

• Hypoxia
  
  • Reduced oxygen delivery - from reduced circulating volume (bleed), vascular compromise (clot)
  • Reduced oxygen carriage - reduced gas exchange, anemia
• Mitochondrial toxicity - mitochondria can’t aerobically produce ATP
  
  • Drugs - metformin, propofol, cyanide
  • Inherited - MELAS
• Reduced metabolism (of lactate) - liver/renal impairment, muscle compromise
• Increased glycolysis (more pyruvate) - both paths increase
  
  • Increased glucose uptake from adrenergic stimulation e.g. salbutamol use
  • Increased energy demand of cells - exercise

Question 20

Delirium definition? Common causes?

Delirium screen breakdown? Mx?

Answer 20

Def: Acute confusional state caused by a physical condition

Causes: U PINCHES ME

• Urinary retention
• Pain
• Infections
• Nutrition
• Constipation –> stool chart + PR exam
• Hydration
• Endo & electrolytes
• Stroke
• Medications & alcohol
• Environmental

Delirium screen:

• FBC, U&E, LFT, glucose, BC, Ca, TFTs, B12/folate
• Urine dip + MC&S
• CXR, possibly CT-head

Management: Tx cause

• Conservative: lighting, clocks, 1:1 nursing, adequate hydration, laxatives, involve family/carers
• SOS (risk to themselves/others):
  
  • Lorazepam (PO/IM/IV)
  • Haloperidol (PO/IM) - be careful if Parkinson’s –> worsens Sx

Question 21

How to think about inf for abx? What are the best broad-spectrum abx? Abx for pseudomonas cover?

Answer 21

• where is the infection? e.g. resp, skin, cardio etc.
• what are the common organisms that cause these infections? mainly G+ve or -ve?

G+ve: staph, strep, C. diff –> pneumonia, skin inf, colitis, sepsis

• B-lactams:
  
  • Penicillins (peptidoglycan cell wall) - amox, co-amox, fluclox, tazocin
  • Cephalosporins (cover -ve’s as well) - ceftriaxone, cefuroxime, cefalexin
  • Carbapenems (holy grail) - meropenem
  • NOTE: ESBL (extended spectrum b-lactamase) - bacteria that are not sensitive to Pen + Cephalosporins
  • NOTE: Carbapenemase - resistant to carbapenems as well
• Macrolides - for pen allergic = Clari, erythromycin
• Glycopeptides - vancomycin, teicoplanin (good if pen allergic)
• Oxazolidinones - linezolid (rarely used)

G-ve: E.coli, P. aeruginosa, K. pneumo, salmonella –> UTI, pneumonia, GI inf

• Aminoglycosides (nephrotoxic –> monitoring) - gent, amikacin
• Fluoroquinolones - cipro/levo/moxifloxacin
• NOTE: broad spectrum so some +ve cover

Other antibiotic types:

• Tetracyclines - doxy
  
  • Broad-spectrum intracellular pathogens (chlamydia, mycoplasma) –> STIs, pneumonia
• Nitroimidazoles - metro
  
  • Anaerobes (c. diff, bacterial vaginosis) –> aspiration pneumo, abscesses
  • NOTE: nitrofurantoin (related compound) - concentrates in bladder –> UTI

Best broad-spectrum abx:

• Co-amox: most G-ve AND +ve AND anaerobes
  
  • Does not cover pseudomonas + Neisseria spp.
• Tazocin: as above AND pseudomonas
  
  • Does not cover Neisseria gonorrhoea
• Meropenem: EVERYTHING (bar carbapenemase bacteria)

Abx for pseudomonas cover: gentamicin, amikacin, ciprofloxacin, ceftazidime

Question 22

Opioids:

1. Strength of different opioids
2. Forms of oral morphine
3. Guide to giving morphine
4. When to give oxycodone
5. Breakthrough analgesia
6. Conversion between opioid doses

Answer 22

Strength:

• Weak - codeine, dihydrocodeine
• Moderate - tramadol (surgeons love)
• Strong - morphine, oxycodone, buprenorphine, fentanyl

Oral morphine has 2 forms:

• Oral morphine has 2 forms:
  
  • Immediate-release (e.g. oromorph) - max 4-hourly
  • Modified-release (e.g. MST Continus/Zomorph/Morphgesic SR) - 12-hourly (BD) OR 24-hourly (OD)

Guide to morphine:

1. If can’t tolerate oral e.g. vomiting alot –> oral dose/2 = IV dose
2. Immediate-release PRN (max 4-hourly) –> see how much using
3. If using a huge amount –> convert to modified-release (12/24-hourly):
   
   • Add up total daily PRN dose = X
   • 24-hourly = X (OD); 12-hourly = X/2 (BD)

​When to give oxycodone: partial renal impairment (eGFR <30mL/min)

• Immediate-release: oxycodone oral solution, oxynorm
• Modified-release: oxycontin
• NOTE: same logic as above
• NOTE: fentanyl if very low eGFR

Breakthrough analgesia:

• Oral morphine/oxycodone
• 1/10-1/6 of total daily dose of modified-release morphine

Example: 60mg Oromorph –> 30mg MST BD + 6-10mg breakthrough dose

Conversion - 10mg oral morphine:

• Oxycodone - 5mg oral (x/2), 2.5mg IV (x/4)
• Tramadol/Codeine - 100mg oral/IV (x*10) - NOTE: codeine has no IV option

Question 23

Hyperosmolar Hyperglycaemic State

• What does insulin do? Pathophysiology of HHS?
• HHS criteria? HHS Mx? HHS Mx Targets?

Answer 23

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 sign. ketonaemia (<3mmol/L)
• 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

Question 24

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?

Answer 24

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

Question 25

Haemodialysis - access? How does it work? How often? Indications? Complications?

Answer 25

Access - 2 points (one for blood to come out of and one to go back into):

• AV fistula (surgical anastomoses between artery & vein) OR Tesio (tunnelled central line)

How does dialysis machine work:

• Box with dialysate fluid in it
• Blood in separate tube going through box
• Semi-permeable membrane between dialysis fluid & blood - diffusion between the two - K⁺, Na⁺, Ca²⁺, Mg²⁺, Cl^-, Glucose, Bicarbonate
  
  • End-stage renal failure will not be able to excrete potassium –> hyperkalemia - blood high in K+, dialysate low in K+ –> diffusion across concentration gradient
  • End-stage renal failure will not be able to retain bicarbonate in kidneys = at risk of metabolic acidosis - blood low in bicarbonate, dialysate high in bicarbonate –> diffusion across concentration gradient
  • End-stage renal failure = low UO –> fluid retention –> -ve pressure created in dialysate compartment –> H₂O drawn into dialysate from blood = ULTRAFILTRATION

How often - 4 times per week

Dialysis indications: HUMP

• Hyperkalaemia (refractory)
• Uraemic complications
• Metabolic acidosis (context of poor renal funct)
• Pul oedema (refractory & hypoxic)

Complications: infection, CVD, fluid balance irregularities

Question 26

Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?

Answer 26

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

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
• 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
  • 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)

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