Prescribing Safety Assessment: Data Interpretation

Question 1

Causes of thrombocytopenia?

Answer 1

Reduced production (infection, drugs e.g. penicilliamine, myelodysplasia/myelofibrosis/myeloma), increased destruction (ITP, heparin, hypersplenism, DIC, TTP/HUS)

Question 2

Causes of thrombocytosis?

Answer 2

Reactive (bleeding, tissue damage [infection/inflammation/malignancy], post-splenectomy) or primary (myeloproliferative disorder)

Question 3

Three causes of euvolaemic hyponatraemia?

Answer 3

SIADH, hypothyroidism, psychogenic polydipsia

Question 4

Causes of SIADH?

Answer 4

SIADH mnemonic: Small cell lung tumour, infection, abscess, drugs (especially carbamazepine and antipscyhotics), head injury.

Question 5

Three causes of hypovolaemic hyponatraemia?

Answer 5

1. Fluid loss (especially diarrhoea/vomiting)
2. Addison’s
3. Diuretics (any type)

Question 6

Five causes of hypervolaemic hyponatraemia?

Answer 6

1. Liver failure (hypoalbuminaemia and lose oncotic pressure)
2. Renal failure
3. Heart failure
4. Nutritional failure (albumin again)
5. Thyroid failure i.e. hypothyroid (can also be euvolaemic)

Question 7

Causes of hypokalaemia? (DIRE)

Answer 7

Drugs (loop and thiazide diruetics)
Inadequate intake or intestinal loss (D&V)
Renal tubular acidosis
Endocrine (Cushing’s/Conn’s)

Question 8

Causes of hyperkalaemia? (DREAD)

Answer 8

Drugs (K+ sparing diuretics and ACEI)
Renal failure
Endocrine (Addison's)
Artefact (haemolysed sample)
DKA

Question 9

Two causes of raised urea and clinical significance?

Answer 9

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

Question 10

Causes and features of pre-renal AKI?

Answer 10

Causes include dehydration/sock of any cause e.g. sepsis, blood loss. Other cause is renal artery stenosis.
May see urea rise > creatinine rise.

Question 11

Causes and features of intrinsic AKI? “INTRINSIC”

Answer 11

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

Question 12

Causes and features of post-renal AKI?

Answer 12

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

Question 13

Causes of raised ALP? “ALKPHOS”

Answer 13

Any fracture
Liver damage (post-hepatic)
K (kancer)
Paget's disease of bone and Pregnancy
Hyperparathyroidism
Osteomalacia
Surgery

Question 14

Tips for changing thyroxine dose?

Answer 14

Use TSH as a guide and, unless grossly hypo/hyperthyroid, change by smallest increment offered

Question 15

Causes/features of pre-hepatic jaundice?

Answer 15

Isolated raised bilirubin.

Haemolysis, Gilbert’s

Question 16

Causes/features of intrahepatic jaundice/LFT derangement?

Answer 16

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)

Question 17

Causes/features of post-hepatic (obstructive) LFTs?

Answer 17

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

Question 18

Primary hypothyroidism?

Answer 18

Low T4 from thyroid, TSH rises to compensate. Hashimoto’s, drug-induced

Question 19

Secondary hypothyroidism?

Answer 19

Low TSH from pituitary, get low T4. Pituitary tumour or damage.

Question 20

Primary hyperthyroidism?

Answer 20

High T4 from thyroid, low TSH. Graves’, TMG, drug-induced

Question 21

Secondary hyperthyroidism?

Answer 21

Raised TSH from pituitary, so T4 rises. Pituitary tumours.

Question 22

Calculating normal PO2 for patient on oxygen?

Answer 22

Take FiO2 and subtract 10; if PaO2 exceeds this then not hypoxic.

Question 23

Causes of T2 RF?

Answer 23

COPD, chest wall deformities (e.g. kyphosis), obesity, neuromuscular weakness (NMD, GBS), central depression of resp. centre e.g. opiate OD. Ventilation affected.

Question 24

Four features of digoxin toxicity?

Answer 24

Confusion, nausea, visual disturbance (blurred/yellow vision), arrhythmias

Question 25

Features of lithium toxicity?

Answer 25

Early is tremor, intermediate is tiredness, late is arrhythmia, seizure, coma, renal failure and diabetes insipidus

Question 26

Features of phenytoin toxicity?

Answer 26

Gingival hyperplasia, ataxia, nystagmus, peripheral neuropathy, teratogenicity

Question 27

When to give NAC in paracetamol OD?

Answer 27

If above treatment line after four hours, if staggered overdose, or if time of ingestion unknown

Question 28

Major bleed on warfarin?

Answer 28

Stop warfarin, 5-10mg IV vit K, give prothrombin complex

Question 29

Managing high INRs without bleed?

Answer 29

<6 = reduce dose, 6-8 = omit for two days then reduce dose, >8 = omit and give 1-5mg oral vit K

Question 30

How do NSAIDs cause AKI?

Answer 30

Inhibit prostaglandins that dilate afferent arterioles (especially if have renal artery stenosis), mimicks pre-renal failure

Question 31

How do ACEI cause hyperkalaemia/AKI?

Answer 31

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)

Question 32

Thing to remember with nebulised salbutamol?

Answer 32

With-hold salbutamol inhaler!

Question 33

Enzyme inducers? “PC BRAS”

Answer 33

Phenytoin, carbamazepine, barbiturates, rifampicin, alcohol (chronic excess), sulphonylureas

Question 34

Enzyme inhibitors? “AODEVICES”

Answer 34

Allopurinol
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
Ethanol (acute intoxication)
Sulphonamides