Interpreting investigation results Flashcards

1
Q

What are the different causes of anaemia?

A

Low haemoglobin:

  1. Microcytic (low MCV): <80
    1. Iron deficiency anaemia
    2. Thalassaemia
    3. Sideroblastic anaemia
  2. Normocytic (normal MCV): 80-100 fL
    1. Anaemia of chronic disease
    2. Acute blood loss
    3. Haemolytic anaemia
    4. Renal failure (chronic)
  3. Macrocytic (high MCV): >100
    1. B12 deficiency (includes pernicious anaemia)/ Folate deficiency
      1. megaloblastic anaemia
    2. Excess alcohol
    3. Liver dizease (including non-alcoholic causes)
    4. Hypothyroidism
    5. Haematological diseases
      1. Myeloproliferative
      2. myelodysplastic
      3. Multiple myeloma
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2
Q

What are the causes of:

  • Neutrophilia
  • Neutropenia
  • Lymphocytosis
A
  1. Neutrophilia (high neutrophils):
    1. bacterial infection
    2. Tissue damage (inflammation/infarct/malignancy)
    3. Steroids
  2. Neutropenia (Low neutrophils):
    1. Viral infection
    2. Chemotherapy or radiotherapy
      1. Patients undergoing chemotherapyor radiotherapy may become neutropenic (or even pancytopenic) in resonse to infection (‘neutropenic sepsis’). This carries a much higher mortality rate so they must be given urgent IV broad-spectrum antibiotics.
    3. Clozapine (antipsychotic)
    4. Carbimazole (antithyroid)
  3. Lymphocytosis (high lymphocytes)
    1. Viral infection
    2. Lymphoma
    3. Chronic lymphocytic leukaemia
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3
Q

What are the causes of thrombocytopenia and thrombocytosis?

A
  • Thrombocytopenia (low platelets)
    • Reduced production:
      • Infection (usually viral)
      • Drugs (esp penicillamine (e.g. in rheumatoid arthritis treatment))
      • Myelodysplasia, myelofibrosis, myeloma
    • Increased destruction:
      • heparin
      • Hypersplenism
      • Disseminated intravascular coagulation
      • Idiopathic thrombocytopenic purpura
      • Haemolytic uraemic syndrome/Thrombotic thrombocytopenic purpura
  • Thrombocytosis (high platelets)
    • Reactive:
      • Bleeding
      • Tissue damage (infection/inflammation/malignancy)
      • Post-splenectomy
    • Primary
      • Myeloproliferative disroders
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4
Q

What are the causes of HYPERnatraemia?

A

All Ds

  • Dehydration
  • Drips (too much IV saline)
  • Drugs (e.g. effervescent table preperations or intravenour preparations with a high sodium content)
  • Diabetes insipidus (opposite of SIADH - Syndrome of inappropriate anti-diuretic hormone)
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5
Q

What are the causes of hyponatraemia?

A

To help lower the wide differential, assess the patient’s fluid status:

  • Hypovolaemic:
    • Fluid loss (especially diarrhoea/vomiting)
    • Addison’s disease
    • Diuretics (any type)
  • Euvolaemic
    • SIADH
    • Psycogenic polydipsia
    • Hypothyroidism
  • Hypervolaemic
    • Heart failure
    • Renal failure
    • Liver failure (causing hypoalbuminaemia)
    • Nutritional failure (causing hypoalbuminaemia)
    • Thyroid failure (hypothyroidism; can be euvolaemic too)
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6
Q

What are the causes of hypokalaemia?

A

DIRE

  • D: Drugs (loop and thiazide diuretics)
  • I: Inadequate intake or Intestinal loss (DnV)
  • R: Renal tubular acidosis
  • E: Endocrine (Cushing’s and Conn’s syndromes)
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7
Q

What are the causes of hyperkalaemia?

A

DREAD

  • D: Drugs (potassium-sparing diuretics and ACE-inhibitors)
  • R: Renal failure
  • E: Endocrine (Addison’s disease)
  • A: Artefact (very common, due to clotted sample)
  • D: DKA (note that when insulin is given to treat DKA the potassium drops requiring regular (hourly) monitoring +/- replacement
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8
Q

What are the causes of acute kidney injury?

A
  • Pre-renal: Urea rise >> Creatinine rise
    • Dehydration (or if severe, shock) of any cause, e.g. sepsis, blood loss.
    • Renal artery stenosis
      • this is often triggerend by drugs (ACEi or NSAIDs) and effectively causes hypoperfusion of the kidneys and thus a prerenal picture
  • Intrinsic: Urea rise << Creatinine rise (Bladder or hydronephrosis not palapable)
    • INTRINSIC
      • I: Ischaemia (due to pre-renal AKI, causing acute tubular necrosis)
      • N: Nephrotoxic antibiotics e.g. Gentamicin, vancomycin and tetracyclines
      • T: Tablets (ACEi, NSAIDs)
      • R: Radiological contrast
      • I: Injury (Rhabdomyolysis)
      • N: Negatively birefringent crystals (gout)
      • S: Syndromes (Glomerulonephridites)
      • I: Inflammation (Vasculitis)
      • C: Cholesterol emboli
  • Post renal: Urea << Creatinine, Bladder or hydronephrosis may be palpable depending level of obstruction:
    • In lumen:
      • Stone
      • Sloughed papilla
    • In wall:
      • Tumour (renal cell, transitional cell)
      • Fibrosis
    • External pressure:
      • Benign prostatic hyperplasis
      • Prostate cancer
      • Lymphadenopathy
      • Aneurysm
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9
Q

What can raised urea also be a sign off?

A

Kidney injury OR Upper GI haemorrhage.

A raised urea usually indicates renal failure; however, because it is a breakdown product og aminoacids, it can also reflect upper GI bleed where haemoglobin has been broken down by gastric acid into urea and is susequently absorbed into the blood

Thus a raised urea with normal creatinine in a patinet who is not dehydrated (i.e. does not have prerenal failure) should prompt a look at haemoglobin. If this is dropped then the patient probably has an upper GI bleed

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10
Q

What are markers of synthetic function of the liver?

A
  • Albumin
  • Vitamin K-dependent clotting factors (II, VII, IX and X) measured via PT/INR
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11
Q

What are the causes of deranged liver function tests?

  • Raised bilirubin
  • Raised bilirubin and raised AST/ALT
  • Raised Bilirubin and raised ALP
A
  1. Prehepatic - raised bilirubin -
    1. Haemolysis
    2. Gilbert’s and Crigler-Najjar syndromes
  2. Intrahepatic - Raised bilirubin and AST/ALT
    1. Fatty liver
    2. Hepatitis/Cirrhosis caused by:
      1. Alcohol
      2. Viruses (Hepatitis A-E, CMV and EBV)
      3. Drugs (paracetamol overdose, statins, rifampicin)
      4. Autoimmune (primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis)
    3. Malignancy (primary or secondary)
    4. Metabolic: Wilson’s disease/haemochromatosis
    5. Heart failure (causing hepatic congestion)
  3. Post hepatic (obstructive) - Raised bilirubin and ALP
    1. In lumen:
      1. stone (gallstone)
      2. Drugs causing cholestasis
        1. Flucloxacillin
        2. Coamoxiclav
        3. Nitrofurantoin
        4. Steroid
        5. Sulphonylureas
    2. In wall:
      1. Tumour (cholangiocarcinoma)
      2. Primary biliary cirrhosis
      3. Sclerosing cholangitis
    3. Extrinsic pressure:
      1. Pancreatic or gastric cancer
      2. Lymph node
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12
Q

Describe the TFTs of primary and secondary hypothyroidsim and its causes

A
  1. Primary hypothyroidism (low T4, high TSH)
    1. Low T4 from thyroid causing compensatory rise in TSH
    2. Caused by
      1. Hashimoto’s thyroiditis
      2. Drug induced hypothyroidism
  2. Secondary hypothyroidism (low TSH and low T4)
    1. Low TSH from pituitary causing low T4
    2. Caused by
      1. Pituitary tumour or damage
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13
Q

Describe the TFTs of primary and secondary hyperthyroidsim and its causes

A
  1. Primary hyperthyroidism: Raised T4 and low TSH
    1. Raised T4 from thyroid causing low TSH
    2. Caused by;
      1. Grave’s disease
      2. Toxic nodular goiter
      3. Drug-induced hyperthyroidism
  2. Secondary hyperthyroidism: Raised TSH and T4
    1. Raised TSH from pituitary causing raised T4
    2. Caused by:
      1. Pituitary tumour
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14
Q

How do we interpret and change levothyroxine dose following TFT results?

A
  • TSH <0.5: decrease dose
  • TSH 0.5-5: Nil action - same dose
  • TSh >5: Increase dose
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