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Chemical Pathology > Part 1 Viva > Flashcards

Part 1 Viva Flashcards

1
Q

Causes of respiratory alkalosis

A

Hypoxia - altitude, anaemia, R-L shunts
Drugs – salicylate, catecholamines etc.
Pulmonary – pneumothorax, haemothorax, pulmonary oedema, pulmonary embolism, aspiration, COPD
Endocrine – pregnancy, hyperthyroidism
CNS – pain, hyperventilation, anxiety, fever, trauma, tumour, meningitis etc.

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2
Q

Causes of a low urea

A

Hepatobiliary disease due to dec synthesis – acute liver failure, alcohol abuse
Overhydration
Starvation
SIADH

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3
Q

Causes of a high urea

A

High protein diet
Increased protein catabolism
Dehydration
Renal dysfunction
Shock
Haemorrhage
GI bleed

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4
Q

Causes of hypokalaemia

A

Inadequate intake - alcoholic, anorexia etc.
Transcellular shift - insulin, ventolin, periodic paralysis etc.
Renal loss - diuretics, vomiting, RTA, Bartter’s syndrome etc.
Extra-renal loss - diarrhoea, laxitives, cancer etc.
Misc – Mg depletion etc.

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5
Q

Further investigation of hypokalaemia

A

Urine [K], [Cl], plasma [HCO3-], aldo:renin

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6
Q

Bartter syndrome lab findings

A

Hypokalemic alkalosis
Hypercalciuria/nephrocalcinosis
Increased levels of plasma renin and aldosterone

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7
Q

Biochemical investigation of hyperammonaemia

A

Mild - exclude artefactual increase and repeat
Exclude heaptic causes (LFTs)
U&E, glucose, Ca, lactate, urine ketones, INR, ABG
Plasma amino acids, urine amino acids, organic acids, orotate, plasma acylcarnitines

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8
Q

Gitelman syndrome lab findings

A

Hypokalaemic metabolic alkalosis in combination with significant hypomagnesaemia and low urinary calcium excretion

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9
Q

Biochemical investigation of a patient with renal calculi

A

Single calcium calculus - serum calcium, ionised calcium, and PTH
Recurrent - MC&S, pH, 24 h urinary calcium, phosphate, urate, oxalate, citrate, cystine, creatinine
Stone analysis for components (Fourier Transform InfraRed Spectroscopy)

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10
Q

Causes of low magnesiumm

A
  1. Low albumin – biologically active serum Mg is normal
  2. Electrolyte loss
    - GI (malabsorption, diarrhoea, short bowel)
    - renal tubular disease, e.g. chronic pyelonephritis, glomerulonephritis, recovery from acute tubular necrosis, post-transplantation
  3. Poor intake - inadequate parenteral nutrition, malabsorption, starvation
  4. Drugs - thiazides, loop diuretics, aminoglycosides, amphotericin B, cytotoxics, cyclosporine, pentamidine, laxative abuse, proton pump inhibitors, e.g. omeprazole (rare)
  5. Alcoholism - common (1/3), multiple causes: diet, diarrhoea, renal tubular losses
  6. Endocrine - hyperthyroidism, hyperparathyroidism, poorly controlled diabetes (osmotic diuresis), hyperaldosteronism, SIADH
  7. Redistribution - alkalosis, correction of acidosis, severe stress, ‘hungry bone’ syndrome after parathyroid surgery
  8. Chelation - acute pancreatitis, post-transfusion, foscarnet therapy
  9. Genetic causes - Bartter, Gitelman syndromes
  10. Late pregnancy - combination of low albumin and respiratory alkalosis
  11. High fat diet - up to 10% of patients (mechanism unclear)
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11
Q

Causes of hypoglycaemia in an infant/newborn

A
  1. Idiopathic ketotic hypoglycaemia
  2. Hormonal abnormalities
    Insulin excess (non-ketotic)
    Counter-regulatory hormone deficiency (ketotic)
    eg deficiency of growth hormone or cortisol
  3. Hepatic enzyme deficiencies (ketotic), eg
    o Involving glycogen breakdown or synthesis - Glucose-6-phosphatase deficiency, Debrancher deficiency, etc
    o Involving gluconeogenesis - Fructose-1,6-diphosphatase deficiency, etc
  4. Other enzyme deficiencies, eg
    o Fatty acid oxidation defects (non-ketotic – but not all cases)
    o Congenital disorders of glycosylation (phosphomannose isomerase deficiency)
  5. Reaction to drugs or toxins
  6. Secondary to other systemic disease
    Liver failure
    Gastroenteritis
    CNS disorders
    Reye’s syndrome, etc
  7. Iatrogenic – following fundoplication, with gastric tube feeding
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12
Q

Investigation of neonatal hypoglycaemia

A

o Glucose
o Insulin
o Cortisol
o Growth hormone
o Plasma β-hydroxybutyrate and free fatty acids
o Lactate
o Acylcarnitines (elevated in fatty acid oxidation defects)
o Urine metabolic profile (looking for abnormal patterns of organic acid excretion which may be seen in fatty acid oxidation defects, etc)
o Urine drug screen
o Ammonia (rare possibility of the hyperammonaemia, hypoglycaemia syndrome – activating mutation in glutamate dehydrogenase)
o Other tests – electrolytes and acid-base studies

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13
Q

What substances within the RBC cause interference by haemolysis?

A

Hb
AST
K
Mg
LDH
Phosphate
Adenylate kinase
Proteases

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14
Q

Rule of thumb: resp compensation for met acidosis?

A

Winter’s formula: pCO2 = 1.5HCO3 + 8 (+/-2)

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15
Q

Rule of thumb: resp compensation for met alkalosis?

A

For every 10 mmol/L increase in HCO3, pCO2 should increase by 7 mmHg (by 24 hours)

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16
Q

Expected changes in acute diarrhoea

A
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17
Q

Expected changes in chronic diarrhoea

A
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18
Q

Rule of thumb: compensation for acute respiratory acidosis

A

Every 10mmHg rise in pCO2, 1mmol/L rise in HCO3

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19
Q

Rule of thumb: compensation for chronic resp acidosis

A

Every 10mmHg rise in pCO2, 3.5 mmol/L rise in HCO3

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20
Q

Rule of thumb: compensation for acute respiratory alkalosis

A

Every 10mmHg fall in pCO2, 2 mmol/L fall in HCO3

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21
Q

Rule of thumb: compensation for chronic respiratory alkalosis

A

Every 10mmHg fall in pCO2, 5 mmol/L fall in HCO3

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22
Q

Diagnostic test for protein losing enteropathy

A

Faecal alpha-1-AT - spot or 24hr clearance
(why - A1AT shows minimal degradation and secretion by GIT, and has similar MW to albumin)

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23
Q

Calculation of 24hr clearance A1AT?

A

(stool vol x stool [A1AT])/serum [A1AT]

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24
Q

Causes of protein-losing enteropathy

A

Non GI vs GI
NonGI causes (Lymphatic obstruction vs Cardiac):
Lymphangiectasia
Portal hypertension
Fontan procedure (for univentricular heart)
Congenital heart disease
Congestive heart failure esp RHF
Pericarditis

GI causes (Erosive vs Non-erosive)
Erosive:
IBD primarily Crohn’s
NSAID abuse
Gut malignancy
GVHD
Sarcoidosis
Non-erosive:
Amyloidosis
Collagenous colitis
Sprue
Eosinophilc gastroenteritis
Lupus and ANCA vasculitis, Sjogrens

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25
Q

Causes of increased faecal A1AT

A
  1. Protein losing enteropathy
  2. GI bleeding
  3. Diarrhoea (obligate loss)
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26
Q

Gold standard test for protein losing enteropathy

A

Technetium-99m labelled human serum albumin scintigraphy

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27
Q

Causes of low faecal A1AT

A

Acid degradation (eg Zollinger-Ellison - use PPI)

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28
Q

Causes of distal RTA

A

Autoimmune diseases are the commonest cause in adults: Systemic lupus erythematosus (SLE), Sjogren syndrome, rheumatoid arthritis, systemic sclerosis, thyroiditis, hepatitis, primary biliary cirrhosis [2].

Drugs: Lithium, amphotericin B, NSAIDs, lead, antivirals, glue sniffing (toluene inhalation in recreational drug abuse)

Inherited, AD or AR: Genetic primary causes of distal RTA include mutations of genes that encode the chloride-bicarbonate exchanger (AE1) or subunits of the H-ATPase pump respectively

Genetic associations: Marfan syndrome, Ehler Danlos syndrome, sickle cell disease, congenital obstruction of the urinary tract

Nephrocalcinosis: Chronic hypercalcemia/familial hypercalciuria, medullary sponge kidney

Tubulointerstitial diseases: chronic pyelonephritis, chronic interstitial nephritis, obstructive uropathy, renal transplant rejection

Hypergammaglobulinemic states: Monoclonal gammopathy, multiple myeloma, amyloidosis, cryoglobulinemia, chronic liver disease

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29
Q

Causes of a proximal RTA

A

Hypergammaglobulinemic states: Most common cause in adults-monoclonal gammopathy (light chain), multiple myeloma, amyloidosis

Miscellaneous: Interstitial nephritis, Fanconi syndrome, vitamin D deficiency, secondary hyperparathyroidism, chronic hepatitis, idiopathic

Drugs: Lead or other heavy metals, carbonic anhydrase inhibitors (e.g., acetazolamide, topiramate) [4], out of date tetracyclines, aminoglycosides, valproate, mercury, tenofovir, and ifosfamide (nephrotoxic)

Autoimmune: Sjogren syndrome, systemic lupus erythematosus (SLE)

Inherited: AD or AR putative mutations in Na-H antiporter in apical membrane and Na-HCO3 cotransporter in the basolateral membrane of proximal tubular cells respectively

30
Q

If ferritin is increased due to inflammation, what other test for iron deficiency can be done?

A

Soluble transferrin receptor 1

31
Q

What is pyroglutamic acid (5-oxoproline)?

A

A glutathione precursor. Produced from gamma-glutamyl cysteine by gamma-glutamyl cyclotransferase. Gamma-glutamyl cyclotransferase activity is induced by glutathione depletion - in states of ongoing glutathione depletion, especially if glutathione synthase is inhibited (catalyses gamma-glutamyl cysteine conversion to glutathione), pyroglutamic acid can accumulate.

32
Q

Risk factors for pyroglutamic acidosis

A

Elderly
Paracetamol use (glutathione depletion by its metabolite NAPQI)
Sepsis (depletion of glutathione)
Flucloxacillin (inhibits 5-oxoprolinase)
Hepatic and renal impairment
Malnutrition
Pregnancy
Vigabatrin (antiepileptic drug)
Congenital enzyme deficiencies (glutathione synthase deficiency)

33
Q

Causes of increased homocysteine

A

Renal impairment
Hypothyroidism
Folate, vitamin B12, and B6 deficiency
Drugs (alcohol)

34
Q

Expected pattern of B12/folate results in nitrous oxide poisoning?

A

Normal concentrations total and active B12, increased functional B12 assays (MMA, homocysteine). Functional moieties of B12 - methyl- and adenosylcobalamin replaced by nitrosylcobalamin, impairing it’s ability to convert MMA and homocysteine.

35
Q

Causes of a discordant low total B12 and normal/increased active B12

A

Pregnancy (dilutional/reduced haptocorrin)
COCP (same mechanism as pregnancy)
HIV
Myeloma
Severe folate deficiency

36
Q

What is your lab’s insulin method?

A

2 site chemiluminescent immunoassay

37
Q

Interferences with insulin immunoassay?

A

Insulin autoantibodies
Heterophile antibodies

38
Q

Interferences with free thyroid hormone assays?

A

Anti-thyroid hormone antibodies
Heterophile antibodies
Biotin

39
Q

Definition of neonatal hypoglycaemia

A

glucose < 2.6mmol/L

40
Q

Definition of persistent neonatal hypoglycaemia

A

hypoglycaemia that continues for longer than or starts after 48 hours

41
Q

Further investigations for neonatal hypoglycaemia

A

Insulin, GH, cortisol
C-peptide
Ketones, Lactate
Ammonia
Amino acids
Free fatty acids
Urine - ketones, glucose, reducing sugars, urine amino acids, organic acids and acylglycines (urine metabolic screen), drug screen (if suspect exogenous insulin/OHAs)

42
Q

Causes of neonatal hypoglycaemia

A
  1. Hyperinsulinism
    - Transient: prem, IUGR, birth asphyxia, maternal PET/DM, intrapartum glucose infusion
    - Persistent: Beckwith-Wiedemann syndrome, defects in regulation of insulin secretion
  2. Inadequate glycogenolysis/GNG
    - Transient: LBW, SGA, sepsis, hypothermia
    - Hormone deficiencies: cortsiol, GH, hypopituitarism
    - Severe liver disease
    - Inborn errors of metabolism: glycogen storage disease, gluconeogenic defects, fatty oxidation defects, ketogenesis defects, organic acidaemias, galactosaemia, tyrosinaemia type 1
43
Q

Causes of hypogonadotropic hypogonadism in men

A

Exogenous androgens
Androgen deprivation therapy
Hypothalamic-pituitary disorders (incl haemochromatosis)
Opioids
Glucocorticoids
Chronic illness
T2DM
Obesity
Sleep apnoea

44
Q

Causes of increased uric acid

A

Gout
Preeclampsia
Tumour lysis syndrome

45
Q

Causes of random error (QC troubleshooting)

A

Damaged/blocked/poorly aligned sample/reagent pipettor
Aged photometer lamp
Expired reagent

46
Q

Actions to take if QAP is out

A

Check units, transcription errors, reconstitution errors (making up QAP sample)
Review internal QC
Check reagent lot changes and calibration results
Check if other labs are having the same problem

47
Q

Common patterns in QC troubleshooting

A

Controls in wrong cups (low is high and high is low)
Shift in mean (NLN)
Sawtooth (reagent/QC degradation)

48
Q

CSF evaluation for meningitis

A

CSF glucose, lactate, LDH, CRP, adenosine deaminase

49
Q

CSF evaluation for demyelinating disease

A

CSF index, oligoclonal banding

50
Q

What is CSF oligoclonal banding?

A

Index of intrathecal IgG synthesis
Bands present in CSF but NOT serum

51
Q

Causes of oligoclonal banding on CSF

A

Multiple sclerosis
Subacute sclerosing panencephalitis
Neurosyphilis
Neuro-AIDS
Neuro-SLE
Neuro-Behcets
Neurosarcoid
GBS
Cysticercosis
Neuro-Lyme disease

52
Q

Procalcitonin interpretation

A
53
Q

Causes of an increased CK

A

Analytical - macro CK
Non-exertional (STEEMi)
- Statins and other drugs
- Traumatic/ compressive
- Electrolyte disturbance (hypokalaemia, hypophosphataemia)
- Endocrine (hypothyroidism, acromegaly, thyrotoxic periodic paralysis etc)
- Myopathies (inflammatory- dermatomyositis, polymyositis etc)
Exertional
- Normal muscle: seizures, extreme exercise, environmental heat illness, sickle cell trait, hyperkinetic states
- Abnormal muscle: metabolic and mitochondrial myopathies, malignant hyperthermia/neuroleptic malignant syndrome, dystrophinopathies (muscular dystrophies)

54
Q

Causes of a hepatitic pattern of abnormal LFTs

A

Viral (HBV, HCV, EBV, CMV)
Alcohol
NAFLD
Medications (NSAIDs, paracetamol, AEDs)
Haemochromatosis
Alpha-1-antitrypsin deficiency
Autoimmune hepatitis
PBC
PSC
Ischaemic

55
Q

Causes of a falsely low HbA1c

A

Pathological:
Increased red cell turnover eg haemolytic anaemia, recent red cell transfusion, recent iron infusion
Chronic liver disease
Pharmacological:
Dapsone
Hydroxyurea
Antivirals (ribavirin, HAART)
Preanalytical/analytical:
Hb variant interference (HPLC/CZE)
Hypertriglyceridaemia (immunoassay)
Short EDTA sample (excessive calcium chelation) (Vitros)

56
Q

Causes of a falsely increased HbA1c

A

Pathological:
Iron deficiency with or without anaemia
CKD
B12 deficiency
Alcohol
Pharmacological:
Aspirin
Opiates
Preanalytic/analytical:
Hb variant (HPLC/CZE)
Heterophile antibody

57
Q

Causes of hypophosphataemia

A

Intracellular shift: refeeding, IV glucose/insulin, DKA, respiratory alkalosis (complex mech involving glycolysis and increased phosphorylation), burns, hungry bones
Lowered renal phosphate threshold: hyperparathyroidism, iron infusion, renal tubular defects (familial hypophosphataemia, Fanconi syndrome), oncogenic osteomalacia, alcoholism, burns
Decreased intestinal phosphate absorption: vomiting, diarrhoea, phosphate-binding antacids, malabsorption syndrome, vitamin D deficiency, alcoholism
Genetic: X-linked hypophosphataemic rickets, Dent disease
Drugs: Acetazolamide, bisphosphonates, diuretics, oestrogens, HIV therapy, salicylates, TKIs

58
Q

Causes of cholestatic LFTs

A
  1. Intrahepatic - neoplastic (primary or metastatic), infiltrative (amyloidosis, leukaemias, lymphomas), PBC, granulomatous, post-transplant cholangiopathy, AIDS, TPN
  2. Extrahepatic - gallstones, head of pancreas tumours, cholangiocarcinomas, biliary stricture (congenital biliary atresia), PSC
  3. Cholestatic hepatitis - drugs eg oestrogens and anabolic steroids, viruses
59
Q

Metabolic myopathies associated with rhabdomyolysis

A

Disorders of lipid metabolism and glycogen storage disorders including McArdle’s disease.

60
Q

DDx methaemoglobinaemia

A
  1. Drugs (most common cause) - dapsone, sulfamethoxazole, nitrates
  2. Hereditary - types I, II, IV, HbM, unstable Hb, G6PD deficiency
61
Q

Causes of a low anion gap

A
  1. High chloride, iodide, bromide
  2. Decreased albumin
  3. Increased cations (calcium, magnesium, lithium, proteins)
62
Q

Causes of increased transferrin

A

Iron deficiency
Pregnancy
Oestrogen therapy
Hepatitis

63
Q

Causes of increased serum iron

A

Recent iron infusion
High biological variability
Iron ingestion/poisoning

64
Q

Interpretation of serum iron post-poisoning

A

1-6 hrs post-ingestion
<55: unlikely to lead to clinical toxicity
55-310: mild gut toxicity
>310: liver toxicity

65
Q

Causes of raised plasma lactate

A

Preanalytical/analytical: haemolysis, red cell/plt leak, macro-LD
Heart: MI, myocarditis (LD1 and 2)
Liver: hepatocellular damage (LD5)
Skeletal muscle: trauma, muscular dystrophy, dermatomyositis, myoglobinuria (LD 5)
Misc: Infections, CTD, haemolysis, leukemia, pernicious anemia, myeloproliferative disorders, malignancy, renal infarction, pulmonary embolus, hypothyroidism, acute pancreatitis

66
Q

The only cause of increased plasma albumin

A

Haemoconcentration

67
Q

Causes of hypogammaglobulinaemia

A

Decreased synthesis
Protein loss

Decreased synth: transient (neonates), primary (immunodeficiencies), secondary
Secondary causes of hypogammaglobulinaemia:
Haem- myeloma, CLL, lymphosarcoma
Toxins- uraemia, corticosteroids, cytotoxic, diabetes mellitus, celiac disease
AIDS

Protein loss - skin, gut, kidneys

68
Q

List the 12 competitive immunoassays we run on Atellica

A

Anti-TPO
Cortisol
DHEAS
Digoxin
Oestradiol
Folate
FT4
FT3
Homocysteine
Progesterone
Testosterone
Total B12

69
Q

Causes of false positive GH suppression test

A

Poorly controlled diabetes mellitus
Malnutrition/malabsorption/anorexia nervosa
Renal disease
Liver disease
Uraemia
Heroin addiction

70
Q

Causes of low transferrin

A
71
Q

Causes of low transferrin

A

Acute inflammation
Chronic liver disease
Haemochromatosis

72
Q

Causes of increased angiotensinogen

A

Hyperthyroidism
Pregnancy/oestrogens
Glucocorticoids

Chemical Pathology (27 decks)

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