FY1 On Call Flashcards

Question 1

Q

Reading an ABG?

Answer

A

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

Q

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

Answer

A

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

Q

Aspects of A-E assessment

Answer

A

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

Q

Oxygen therapy principles

Answer

A

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

Q

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

Answer

A

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

Q

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

Answer

A

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

Q

Types of Non-Invasive Ventilation

Answer

A

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

Q

IHD - Types? Definition? Dx? Mx?

Answer

A

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

Q

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

Answer

A

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

Q

Anaemia Ix? Mx?

Answer

A

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

Q

Atrial fibrillation (AF)

Def? Causes? Ix? Mx?

Answer

A

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

Q

Types of anticoagulant

Answer

A

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

Q

Alcohol withdrawal management?

Answer

A

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

Question 14

Q

What are the markets of liver synthetic dysfunction?

Answer

A

Bilirubin

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

Coagulation screen (APTT, PT, INR)

Question 15

Q

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

Dx & Mx of decompensated chronic liver disease?

Answer

A

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

Q

Chronic liver disease

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

Answer

A

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 17

Q

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

Answer

A

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 18

Q

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

Answer

A

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 19

Q

Delirium definition? Common causes?

Delirium screen breakdown? Mx?

Answer

A

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 20

Q

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

Answer

A

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 21

Q

Opioids:

Strength of different opioids
Forms of oral morphine
Guide to giving morphine
When to give oxycodone
Breakthrough analgesia
Conversion between opioid doses

Answer

A

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:

If can’t tolerate oral e.g. vomiting alot –> oral dose/2 = IV dose
Immediate-release PRN (max 4-hourly) –> see how much using
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 22

Q

Hyperosmolar Hyperglycaemic State

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

Answer

A

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 23

Q

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

A

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 24

Q

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

Answer

A

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 25

Q

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

Answer

A

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

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