Prescribing Safety Assessment: Data Interpretation Flashcards
Causes of thrombocytopenia?
Reduced production (infection, drugs e.g. penicilliamine, myelodysplasia/myelofibrosis/myeloma), increased destruction (ITP, heparin, hypersplenism, DIC, TTP/HUS)
Causes of thrombocytosis?
Reactive (bleeding, tissue damage [infection/inflammation/malignancy], post-splenectomy) or primary (myeloproliferative disorder)
Three causes of euvolaemic hyponatraemia?
SIADH, hypothyroidism, psychogenic polydipsia
Causes of SIADH?
SIADH mnemonic: Small cell lung tumour, infection, abscess, drugs (especially carbamazepine and antipscyhotics), head injury.
Three causes of hypovolaemic hyponatraemia?
- Fluid loss (especially diarrhoea/vomiting)
- Addison’s
- Diuretics (any type)
Five causes of hypervolaemic hyponatraemia?
- Liver failure (hypoalbuminaemia and lose oncotic pressure)
- Renal failure
- Heart failure
- Nutritional failure (albumin again)
- Thyroid failure i.e. hypothyroid (can also be euvolaemic)
Causes of hypokalaemia? (DIRE)
Drugs (loop and thiazide diruetics)
Inadequate intake or intestinal loss (D&V)
Renal tubular acidosis
Endocrine (Cushing’s/Conn’s)
Causes of hyperkalaemia? (DREAD)
Drugs (K+ sparing diuretics and ACEI) Renal failure Endocrine (Addison's) Artefact (haemolysed sample) DKA
Two causes of raised urea and clinical significance?
Kidney injury or UGI bleed (breakdown of globin chains in Hb into urea). If have normal creatinine, and not dehydrated (i.e. not pre-renal failure) then check Hb; if anaemic then may have UGI bleed
Causes and features of pre-renal AKI?
Causes include dehydration/sock of any cause e.g. sepsis, blood loss. Other cause is renal artery stenosis.
May see urea rise > creatinine rise.
Causes and features of intrinsic AKI? “INTRINSIC”
Ischaemia (pre-renal AKI becomes renal through ATN)
Nephrotoxic antibiotics (aminoglycosides)
Tablets (ACEi/NSAIDs)may be pre-renal
Radiological contrast
Injury (rhabdomyolysis)
Negatively birefringent crystals (gout)
Syndromes (glomerulonephritides)
Inflammation (vasculitis)
Cholesterol emboli.
See creatinine rise > urea, but not palpable bladder/hydronephrosis
Causes and features of post-renal AKI?
In lumen: (stone, sloughed papilla)
In wall: (tumour [RCC, transitional cell], fibrosis
External pressure: BPH, prostate cancer, lymphadenopathy, aneurysm, ?constipation.
Creatinine rise > urea, and may have palpable bladder/hydronephrosis
Causes of raised ALP? “ALKPHOS”
Any fracture Liver damage (post-hepatic) K (kancer) Paget's disease of bone and Pregnancy Hyperparathyroidism Osteomalacia Surgery
Tips for changing thyroxine dose?
Use TSH as a guide and, unless grossly hypo/hyperthyroid, change by smallest increment offered
Causes/features of pre-hepatic jaundice?
Isolated raised bilirubin.
Haemolysis, Gilbert’s
Causes/features of intrahepatic jaundice/LFT derangement?
Bilirubin and ALT/AST elevated.
Fatty liver, hepatitis/cirrhosis (alcohol, viruses [Hep A-E, CMV, EBV], drugs [paracetamol OD, statin,s rifampicin], autoimmune [PBC, PSC, AIH]), malignancy (primary or secondary), metabolic (Wilson’s/haemochromatosis), heart failure (causing hepatic congestion)
Causes/features of post-hepatic (obstructive) LFTs?
Bilirubin, GGT and ALP elevated.
In lumen: gall stone, drugs causing cholestasis [flucloxacillin, co-amox, nitrofurantoin, steroids, sulphonylureas]
In wall: tumour (cholangiocarcinoma), PBC, PSC)
Extrinsic pressure: pancreatic or gastric cancer, lymph node
Primary hypothyroidism?
Low T4 from thyroid, TSH rises to compensate. Hashimoto’s, drug-induced
Secondary hypothyroidism?
Low TSH from pituitary, get low T4. Pituitary tumour or damage.
Primary hyperthyroidism?
High T4 from thyroid, low TSH. Graves’, TMG, drug-induced
Secondary hyperthyroidism?
Raised TSH from pituitary, so T4 rises. Pituitary tumours.
Calculating normal PO2 for patient on oxygen?
Take FiO2 and subtract 10; if PaO2 exceeds this then not hypoxic.
Causes of T2 RF?
COPD, chest wall deformities (e.g. kyphosis), obesity, neuromuscular weakness (NMD, GBS), central depression of resp. centre e.g. opiate OD. Ventilation affected.
Four features of digoxin toxicity?
Confusion, nausea, visual disturbance (blurred/yellow vision), arrhythmias
Features of lithium toxicity?
Early is tremor, intermediate is tiredness, late is arrhythmia, seizure, coma, renal failure and diabetes insipidus
Features of phenytoin toxicity?
Gingival hyperplasia, ataxia, nystagmus, peripheral neuropathy, teratogenicity
When to give NAC in paracetamol OD?
If above treatment line after four hours, if staggered overdose, or if time of ingestion unknown
Major bleed on warfarin?
Stop warfarin, 5-10mg IV vit K, give prothrombin complex
Managing high INRs without bleed?
<6 = reduce dose, 6-8 = omit for two days then reduce dose, >8 = omit and give 1-5mg oral vit K
How do NSAIDs cause AKI?
Inhibit prostaglandins that dilate afferent arterioles (especially if have renal artery stenosis), mimicks pre-renal failure
How do ACEI cause hyperkalaemia/AKI?
Hyperkalaemia directly through reduced aldosterone production, and indirectly by causing renal injury by preventing efferent arterioles constricting (relies on angiotensin II). These remain dilated, causing hypotension (most marked in renal artery stenosis when renal blood flow reduced anyway)
Thing to remember with nebulised salbutamol?
With-hold salbutamol inhaler!
Enzyme inducers? “PC BRAS”
Phenytoin, carbamazepine, barbiturates, rifampicin, alcohol (chronic excess), sulphonylureas
Enzyme inhibitors? “AODEVICES”
Allopurinol Omeprazole Disulfiram Erythromycin Valproate Isoniazid Ciprofloxacin Ethanol (acute intoxication) Sulphonamides
