Data interpretation

Data interpretation

Chapter objectives

. Learn memorable and reliable methods of interpreting the most common test results.

. Learn how to interpret (and act on) drug-specific data.

. Use 10 scenarios with worked answers to reinforce these principles.

Structure of this Section within the PSA

The ‘Data interpretation’ section will have 6 questions with 2 marks available per question, so a possible total of 12 points. The questions will be of the multiple choice style and you will be asked to select the most appropriate answer from a list of five options (A–E). See Question 3.1 for a demonstration scenario.

Introduction

The ‘Data interpretation’ section requires knowledge of drug-specific data (such as paracetamol nomograms and drug monitoring) and general data interpretation (such as biochemistry and imaging).

An overview of common investigation abnormalities will be presented, with the drug related causes (to be particularly wary of in the exam) in bold italic, while the more common causes (in real life!) are emboldened.

General Data Interpretation

Blood Tests: Haematology

The most important results of a full blood count (FBC) are the haemoglobin, the white cell count (WCC) and the platelets. The most commonly encountered abnormalities are shown in Tables 3.1–3.3.

Table 3.1

Causes of anaemia

^*B₁₂ deficiency includes pernicious anaemia.

Table 3.2

High and low white blood cells

^*Patients undergoing chemotherapy or radiotherapy may become neutropenic (or even pancytopenic) in response to infection (‘neutropenic sepsis’). This carries a much higher mortality rate so they must be given urgent IV broad-spectrum antibiotics (the choice is hospital specific).

Table 3.3

Causes of thrombocytosis and thrombocytopenia

Low haemoglobin (anaemia)

There are many causes of anaemia (see Table 3.1), so look at the mean cell volume (MCV) to narrow your differential.

Blood Tests: Biochemistry

Urea and electrolytes (U&E)

There are two principal abnormalities to glean from the U&E: high and low electrolytes (i.e. sodium or potassium), and the presence and type of kidney injury (i.e. through assessing the urea and creatinine).

Sodium (normal range 135–145 mmol/L)

Hyponatraemia: to help narrow the (wide) differential for hyponatraemia assess the patient’s fluid status (e.g.hypovolaemic/euvolaemic/hypervolaemic) (Table 3.4).

Table 3.4

Causes of hyponatraemia

^*Causes of SIADH can be remembered with the mnemonic SIADH: Small cell lung tumours, Infection, Abscess, Drugs (especially carbamazepine and antipsychotics), and Head injury.

Hypernatreamia: causes of this all begin with ‘d’: dehydration; drips (i.e. too much IV saline); drugs (e.g. effervescent tablet preparations or intravenous preparations with a high sodium content); diabetes insipidus (which is effectively the opposite of syndrome of inappropriate anti-diuretic hormone (SIADH).

Potassium (normal range 3.5–5.0 mmol/L)

Hypokalaemia and hyperkalaemia are particularly important because they cause fatal cardiac arrhythmias. Their causes may thus be remembered with the mnemonics DIRE and DREAD (Table 3.5).

Table 3.5

Causes of hypokalaemia and hyperkalaemia

Acute kidney injury (AKI)

See Table 3.6 for the causes of AKI (which was previously called acute renal failure).

Table 3.6

Causes of acute kidney injury

Note: the creatinine can rise with severe prerenal AKI; to differentiate this from intrinsic and obstructive AKI, multiply the urea by 10; if it exceeds the creatinine (showing a relatively greater increase in urea compared to creatinine) then this suggests a prerenal aetiology.

^*AKI in RAS is often triggered by drugs (ACEI or NSAIDs) and effectively causes hypoperfusion of the kidneys and thus a prerenal picture.

^**Especially gentamicin, vancomycin and tetracyclines.

Common trap

Raised urea indicates kidney injury or upper gastrointestinal (GI) haemorrhage. A raised urea usually indicates renal failure; however, because it is a breakdown product of amino acids (such as globin chains in haemoglobin), it can also reflect an upper GI bleed where haemoglobin has been broken down by gastric acid into urea, which is subsequently absorbed into the blood. The same phenomenon occurs if you eat a big (and bloody) steak. Thus, a raised urea with normal creatinine in a patient who is not dehydrated (i.e. does not have prerenal failure) should prompt a look at the haemoglobin; if this has dropped then the patient probably has an upper GI bleed.

Liver Function Tests (LFTs)

One can assess the liver by looking at markers of:

Hepatocyte injury or cholestasis such as:

alanine aminotransferase (ALT) and the less commonly measured aspartate aminotransferase (AST)

alkaline phosphatase (alk phos or ALP).

Synthetic function (i.e. the proteins it makes):

vitamin K-dependent clotting factors (II, VII, IX and X) measured via PT/INR.

LFTs help to narrow the causes of raised bilirubin (which may cause jaundice) (Table 3.7). A raised bilirubin on its own indicates prehepatic jaundice (see later in this chapter) that is rarely due to any liver problem itself (in the same way a raised urea on its own (i.e. prerenal AKI) rarely indicates an intrinsic renal problem); rather, because bilirubin is a breakdown product of haemoglobin, a solitary raised bilirubin usually indicates haemolysis.

Table 3.7

Causes of deranged liver function tests

^*Hepatitis and cirrhosis may be due to (1) alcohol, (2) viruses (Hepatitis A–E, CMV and EBV), (3) drugs (paracetamol overdose, statins, rifampicin), and (4) autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis).

^**Flucloxacillin, coamoxiclav, nitrofurantoin, steroids and sulphonylureas.

Clinical hint

A raised alk phos does not necessarily indicate posthepatic jaundice; common causes may be remembered using the mnemonic ALKPHOS: Any fracture, Liver damage (posthepatic), K (for kancer), Paget’s disease of bone and Pregnancy, Hyperparathyroidism, Osteomalacia, and Surgery.

Thyroid Function Tests (TFT)

TFTs assess the thyroid stimulating hormone (TSH) and T4; Table 3.8 shows the most common abnormal patterns and causes. In the PSA, students may be asked to change a levothyroxine dose according to TFT results for patients with hypothyroidism (Table 3.9). The trick to this is to use the TSH as a guide: target range ~0.5–5 mIU/L and, unless grossly hypo/hyperthyroid, change by the smallest increment offered.

Table 3.8

Abnormal thyroid function tests.

^*Through negative feedback from increased T4 levels.

(image at right from GeekyMedics.com, with permission)

Table 3.9

How to interpret and change levothyroxine dose following TFT results

TSH range (mIU/L)	Change to thyroxine
<0.5	Decrease dose
0.5–5	Nil action – same dose
>5	Increase dose

Chest X-Rays

As with all data, a routine must be followed to prevent questions catching you out. The most likely scenarios in the PSA will be pulmonary oedema or pneumonia. CXR interpretation involves assessing the quality of the film, the structures and the difficult areas.

Quality of film

It is important to check that the film is PRIM:

Projection (e.g. posterioanterior (PA) (normally) or anterioposterior (AP). If AP the heart will appear larger. If no markings then it is PA)

Rotation (e.g. if distance between spinous process and clavicles is equal then no rotation)

Inspiration (e.g. if the seventh anterior (down-sloping) rib transects the diaphragm then adequate)

Markings (if additional markings, e.g. ‘red marks’, then the radiographer has spotted an abnormality).

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Tags: Pass the PSA

Mar 24, 2017 | Posted by admin in PHARMACY | Comments Off

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