Chapter 3: Data Interpretation Flashcards
Causes of anaemia (categorised by MCV)
Red blood cells:
- Microcytic (low MCV) = iron deficiency anaemia, thalassaemia, sideroblastic anaemia.
- Normocytic (normal MCV) = anaemia of chronic disease, acute blood loss, haemolytic anaemia, renal failure (chronic).
-
Macrocytic (high MCV) = B12/folate deficiency (megaloblastic anaemia), excess alcohol, liver disease (including non-alcoholic causes), hypothyroidism, “M” haematological causes (myeloproliferative, myelodysplastic, multiple myeloma).
- B12 deficiency includes pernicious anaemia.
Causes of neutrophilia
Neutrophilia (high) :
- bacterial infection
- tissue damage (inflammation/infarct/malignancy)
- *steroids*.
Causes of Neutropenia
Neutropenia (low neutrophils)
- viral infection
- chemotherapy/radiotherapy (may become neutropenic in response to infection, neutropenic sepsis)
- If neutropenic sepsis, must give urgent IV broad-spectrum antibiotics (hospital-specific).
- clozapine (antipsychotic)
- carbimazole (antithyroid).
Causes of lymphocytosis
Lymphocytosis (high lymphocyts)
- viral infection
- lymphoma
- CLL.
Causes of Thrombocytopenia
Thrombocytopenia (low platelets)
- reduced production
- viral infection
- drugs especially penicillamine in RA
- myelodysplasia, myelofibrosis, myeloma
- increased destruction
- heparin
- hypersplenism
- DIC
- ITP
- HUS/TTP
Causes of thombocytosis
Thrombocytosis (high platelets)
- reactive
- bleeding
- tissue damage e.g. infection/inflammation/malignancy
- post-splenectomy
- primary
- myeloproliferative disorders
Causes of hyponatraemia
Na+ 135-145 mmol/L
Hyponatraemia: assess fluid status first.
- Hypovolaemic
- fluid loss (D&V)
- Addison’s
- any diuretic.
- Euvolaemic
- SIADH
- small cell lung tumours, _i_nfection, abscess, drugs (carbamazepine + antipsychotics), head injury.
- psychogenic polydipsia
- hypothyroidism.
- SIADH
- Hypervolaemic
- heart failure
- renal failure
- liver failure (hypoalbuminaemia)
- nutritional failure (hypoalbuminaemia)
- thyroid failure (hypothyroidism – can be euvolaemic too).
Causes of SIADH
SIADH
- small cell lung tumours
- infection
- abscess
- drugs (carbamazepine + antipsychotics)
- head injury.
Causes of Hypernatraemia
Hypernatraemia: Causes all begin with “D”…
- Dehydration.
- Drips i.e. too much IV saline.
- Drugs e.g. effervescent tablet preparations or IV preparations with high Na+ content.
- Diabetes insipidus – opposite of SIADH.
Causes of Hypokalaemia (3.5-5mmol/L)
Hypokalaemia: DIRE
- drugs (loop + thiazide diuretics)
- inadequate intake or intestinal loss (D&V)
- renal tubular acidosis
- endocrine (Cushing’s + Conn’s syndrome).
Causes of Hyperkalaemia (3.5-5mmol/L)
Hyperkalaemia: DREAD
- drugs (K+-sparing diuretics + ACE-i)
- renal failure
- endocrine (Addison’s disease)
- artefact (clotted sample)
- DKA (when insulin given to treat DKA, K+ drops so needs monitoring + replacement).
Link between urea and Hb
Ur rise = AKI or upper GI haemorrhage
Hb broken down by gastric acid into Ur, then absorbed into blood
In an upper GI H’gge you may fine a low Hb, Ur rise.
nb isolated urea rise (without Creatinine rise may be seen in pre-renal causes of renal failure e.g. DEHYDRATION)
Causes of pre-renal AKI
Pre-renal = U rise > C rise (U x 10 > C).
- Dehydration (or if severe, shock) e.g. sepsis, blood loss.
- Renal artery stenosis (often triggered by drugs e.g. ACEi or NSAIDs; renal hypoperfusion)
Causes of renal AKI
Intrinsic = U rise < C rise, no bladder or hydronephrosis.
INTRINSIC
- ischaemic (prerenal AKI → ATN)
- nephrotoxic antibiotics
- gentamicin, vancomycin + tetracyclines
- tablets
- ACE-i, NSAIDs
- radiological contrast
- injury; rhabdomyolsis
- negatively birefringent crystals (gout)
- syndromes; glomerulonephridites
- inflammation; vasculitis
- cholesterol emboli.
Causes of post renal AKI
Post-renal = U rise < C rise, bladder or hydronephrosis.
- In lumen = stone or sloughed papilla.
- In wall = tumour (renal cell, transitional cell), fibrosis.
- External pressure = benign prostatic hyperplasia, prostate cancer, lymphadenopathy, aneurysm.
LFT:
- Markers of hepatocellular injury or cholestasis
- Synthetic function
- bilirubin, ALT, AST, ALP.
- Albumin, vit K dependent clotting factors (2,7,9,10) measure PT/INR
Causes of raised bilirubin (3 categories)
- Bilirubin rise only = pre-hepatic e.g.
- haemolysis
- Gilbert’s syndrome
- Crigler-Najjar syndrome
- Bilirubin + AST/ALT rise = hepatic e.g.
- fatty liver
- hepatitis
- cirrhosis
- Hepatitis + cirrhosis = alcohol, viruses (hepatitis A-E, CMV + EBV), drugs (paracetamol overdose).
- malignancy; 1⁰ or 2⁰
- metabolic; Wilson’s, haemochromatosis
- HF
- Bilirubin + ALP rise = post-hepatic i.e. obstruction…
- In lumen = gallstones, drugs (flucloxacillin, co-amoxiclav, nitrofurantoin, steroids + sulphonylureas).
- In wall = cholangiocarcinoma, PBC, PSC.
- External pressure = pancreatic or gastric cancer, lymph nodes.
Causes of raised ALP
ALKPHOS
- any fracture
- liver damage (post-hepatic)
- k for kancer
- Paget’s + pregnancy
- hyperparathyroidism
- osteomalacia
- surgery.
Thyroid Fynction tests: and Changing levothyroxine!
Check TSH (0.5-5mIU/L), and change by smallest increment offered (unless grossly hypo/hyperthyroid).
- <0.5 = decrease dose
- 0.5-5 = nil action
- >5 = increase dose.
Abnormal TFTs: Hypothyroidism
Primary hypothyroidism = ↓T4 from thyroid so ↑TSH from pituitary = Hashimoto’s, drug-induced.
Secondary hypothyroidism = ↓TSH, so ↓T4 = pituitary tumour or damage.
Abnormal TFTs: Hyperthyroidism
Primary hyperthyroidism = ↑T4, so ↓TSH = Grave’s, toxic nodular goitre, drug-induced.
Secondary hyperthyroidism = ↑TSH, so ↑T4 = pituitary tumour.
Quick review of CXR:
PIPRA + ABCDEFGH
PSA=?pneumonia/pulmonary oedema
PIPRA:
- Projection: PA (N, PA if no markings) or AP (can’t comment on heart) – should see from above clavicles to below diaphragm.
- Inspiration: 7th anterior (down-sloping) rib transects diaphragm.
- Penetration: vertebral bodies behind heart.
- Rotation: distance between spinous processes + clavicles equal.
- Artefact: if present.
ABCDEFGH:
- Airways: trachea central – if not, consider collapse (towards) or pneumothorax (away).
- Bone: rib fractures or lytic lesions.
- Cardiac: cardiothoracic ratio <50% on PA film.
- Diaphragm: air under diaphragm – bowel perforation or recent surgery; under L side is gastric bubble (N).
- Edges: costophrenic + cardiophrenic angles sharp or blunt (effusion).
- Fields: white area = effusion (unilateral + solid), pneumonia (unilateral + fluffy), oedema (bilateral + fluffy), fibrosis (bilateral + honeycomb).
- Oedema, ABCDE = alveolar oedema, kerley B lines, cardiomegaly, diversion of blood to upper lobes, effusions.
- Sail sign (triangle shape) behind heart = L lower lobe collapse.
- Gynaecomastia + other soft-tissues.
- Hila.
Quick review of ABG
- Check inspired oxygen concentration (FiO2):
- Calculate N PaO2 for patient on oxygen: subtract 10 from FiO2, and if PaO2 exceeds this number, then patient not hypoxic.
- E.g. On 60% oxygen with FiO2 of 30kPa actually hypoxic. Accurately done via arterial-alevolar gradient.
- Calculate N PaO2 for patient on oxygen: subtract 10 from FiO2, and if PaO2 exceeds this number, then patient not hypoxic.
- Check for respiratory failure: if PaO2 low or inappropriately N.
- Type 1 = low or N PaCO2 (fast breathing) → heart/lung damage causing SOB.
- Type 2 = high PaCO2 (slow breathing) → ‘blue-bloaters’ of COPD, NM failure or restrictive chest wall abnormalities.
- Check acid-base status:
- Low pH = acidosis; high pH = alkalosis.
- PaCO2 abnormal = respiratory. HCO3 abnormal = metabolic. Both = compensation (fully if pH normal, otherwise partial). Both abnormal in opposite directions = mixed.
Causes of the 4 acid base abnormalities
Respiratory alkalosis = rapid breathing – disease or anxiety.
Respiratory acidosis = same causes as T2RF. (COPD, blue bloaters, + neuromuscular failure + restrictive chest wall abn)
Metabolic alkalosis = vomiting, diuretics + Conn’s syndrome.
Metabolic acidosis = multiple causes e.g. lactic acidosis, DKA, renal failure, ethanol/methanol/ethylene glycol intoxication → narrow cause by using anion gap.
Quick review of ECG interpretation
Rate: divide 300 by # of large squares between each QRS complex; N = 60-100bpm.
Rhythm: p-waves present before QRS = sinus; PR interval not constant or >1 square = heart block → 1st degree = constant but >1 square, 2nd degree type 1 = increasing PR then misses a QRS, 2nd type 2 = 2/3 p waves for every QRS, 3rd/complete = no relationship; no p waves + irregular QRS complexes = AF.
Axis: look at direction of I and II. If I +ve and II +ve = N; If I +ve and II –ve = LAD; If I –ve and II +ve = RAD.
QRS: width <3 small squares = N, narrow-complex; >3 = BBB – WiLLiaM = LBBB, rSR (M shape) in V6, MarRRoW = RBBB, rSR in V1.
V-waves: Add largest deflection in V1 to V6; >3.5 large squares = LVH (Sokolov-Lyon); small complexes throughout = pericardial effusion.
ST segment: elevated = infarction (flat + some leads) or pericarditis (convex + all leads); depressed = ischaemia (flat + some leads) or digoxin (down-sloping, all leads).
T-waves: height > 2/3rd QRS height throughout ECG = hyperkalaemia; inversion = N in aVR + I, other leads = old infarction/LVH
What criteria would suggest the need for monitoring
name 6 common drugs that require monitoring
Drug with narrow therapeutic index; small difference in blood concentration for therapeutic + toxic effects require monitoring
- digoxin
- theophylline
- lithium
- phenytoin
- ABx: gentamicin
- ABx: vancomycin
What does drug monitoring entale (2 part)
Monitoring
- assess clinical state
- response to drug
- evidence of toxicity
- measure serum drug levels
→ adjust dose/frequency accordingly
For what reasons is the dose/freq of a drug altered (4)
Inadequate response + low serum drug level = increase dose – in general by smallest possible increment, especially if 0-order kinetics (e.g. phenytoin).
Adequate response + N/low serum drug level = no change – clinical response more important, as already therapeutic dose!
Adequate response + high serum drug level = decrease dose – if toxicity, then can omit for few days (except gentamicin).
- gent: pre-emptive decrease in frequency by 12hrs (e.g. 36 rather than 24hrs)
Toxicity + any serum drug level = (1) stop dose (+ alternative); (2) supportive measures (usually IV fluids); (3) give antidote
Common signs of drug toxicity
- Digoxin
- Lithium
- Phenytoin
- Gentamicin
- Vancomycin
- Digoxin
- confusion
- nausea
- visual halos
- arrythmia
- Lithium
- early: tremor
- intermediate: tiredness
- Later: arrhythmias
- seizures
- coma
- renal failure
- diabetes insipidus
- Phenytoin
- gum hypertrophy
- ataxia
- nystagmus
- peripheral neuropathy
- teratogenicity
- Gentamicin
- ototoxicity
- nephrotoxicity
- Vancomycin
- ototoxicity
- nephrotoxicity
Gentamicin normal dosing (&2 exceptions)
Gentamicin monitoring: IV aminoglycoside antibiotic used in severe infections.
Doses calculated via weight + renal function.
- Most treated with high-dose regimen of 5-7mg/kg once-daily;
- Renal failure patient recieve divided daily dosing (1mg/kg) 12-hourly
- Endocarditis patients recieve divided daily dosing (1mg/Kg) 8-hourly
Must monitor as high risk of nephrotoxicity + ototoxicity.
Gentamicin: Normal once daily regime monitoring
Risk of ototoxicity and nephrotoxicity
- Measure gentamicin levels at particular times e.g. 6-14h after last gentamicin infusion started.
- Use nomogram (specific to dose). If point on graph falls within 24h area, continue at same dose. If above 24h area, then change dosing:
- If in 36h area, change to 36-hourly dosing.
- If in 48h area, change to 48-hourly dosing.
- If above 48h area, repeat gentamicin level and only re-dose when concentration <1mg/L.
- Change frequency over dose as need sufficient dose to hit peak to hit minimum inhibitory concentration of organism.
Gentamicine: divided daily dosing regimes + monitoring
Divided daily dosing: Nomogram exists, but daily peak and trough levels usually used instead.
- Peak (1hr post dose) if outside of normal range (3-5mg/L (endocarditis) 5-10mg/L (all else)) adjust the dose
- Trough (just before next dose) if outside of normal range (<1mg/L (endocarditis) <2mg/L (all else)) adjust the interval
Management of paracetamol overdose (2)
- Specific = N-acetyl cysteine (NAC) if appropriate.
- Paracetamol metabolised by liver; relies on glutathione which is quickly depleted so toxic NAPQI accumulates. NAC replenishes it.
- Supportive = particularly IV fluids.
Warfarin Mechanism of action
Inhibits synthesis of vitamin K-dependent clotting factors (2, 7, 9 + 10) – prolongs PT from which INR derived.
What is INR?
INR = ratio of patient PT to N population.
Normal INR = 1. INR
Only used to monitor warfarin – use PT for liver disease/ DIC
Target INRs
Target INR for most = 2.5
if recurrent thromboembolism while on warfarin or metal replacement heart valves INR = 3.5.
If major bleed i.e. causing hypotension or bleeding in confined space (brain or eye):
- Stop warfarin
- give 5-10mg IV vitamin K
- give prothrombin complex (e.g. Beriplex).
How to manage over coagulation
If not bleeding, then look at INR to judge next step:
- INR <6 = reduce warfarin dose.
- INR 6-8 = omit warfarin for 2 days then reduce dose.
- INR >8 = omit warfarin + give 1-5mg oral vitamin K.
- If minor bleeding, with INR >5, give IV instead of oral vitamin K.
