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Medicine > Bloodwork > Flashcards

Bloodwork Flashcards

1
Q

6 causes of eosinophilia

A

Common:
1. Parasitism
2. Hypersensitivity (food, skin, FEGC, eosinophilic gastroenteritis/colitis, asthma, allergic rhinitis/sinusitis)

Uncommon
3. Eosinophilic infiltration: eosinophilic bronchopneumopathy, Hypereosinophilic syndrome (rottweilers)
4.Endocrine: Hypoadrenocorticism/ hyperthyroidism
5. Chronic eosinophilic leukaemia
6. Paraneoplastic: MCT, lymphoma, carcinoma, thymoma

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2
Q

5 causes of hypercobalaminaemia

A
  1. Neoplasia
  2. SI dysbiosis
  3. Liver disease
  4. Over supplementation
  5. Pancreatitis
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3
Q

12 causes of hypercholesterolaemia

A
  1. Iatrogenic (steroids)
  2. Hyperadrenocorticism
  3. Diabetes Mellitus
  4. Nephrotic syndrome
  5. Hypothyroidism (incr LDL and HDL)
  6. Cholestatic disease (reduced clearance)
  7. Pancreatitis
  8. Familial hypercholesterolaemi - briards, rottweilers, shetland sheepdogs and dobermans
  9. Hyperlipidaemia - minature schnazers
  10. Primary hyperchylomicronemia - cats
  11. Post prandial
  12. Artifact - haemolysis
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4
Q

What is the substance can be an indirect measure of cobalamin? Is it incr or decr in hypocobalaminaemia?

A

Cobalamin deficiency can lead to accumulation of methylmalonic acid (MMA). MMA inhibits activity of carbamoyl phosphate synthetase I, an enzyme in the urea cycle that metabolizes ammonia. As a result, plasma ammonia concentrations can increase and lead to neurologic abnormalities

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5
Q

7 causes of increased urea

A
  1. Renal disease
  2. Pre- renal azotaemia
  3. Post renal azotaemia
  4. GI bleed
  5. Post prandial esp. high protein
  6. Incr protein catabolism - starvation, fever, burns, +/- steroids
  7. Artifact - icteric samples
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6
Q

7 causes of increased ALT

A
  1. Primary hepatic disease (infectious, inflammatory, toxicity, neoplasia, inherited storage dz, hypoxia)
  2. Reactive hepatopathy e.g. GI
  3. Trauma
  4. Anaphylaxis
  5. Hyperthyroidism - cats
  6. Hyperadrenocoriticism
  7. Diabetes
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7
Q

8 Causes of hyperphosphataemia

A
  1. Post prandial
  2. Artifact - haemolysis
  3. Iatrogenic - enema, diet, fluids
  4. Renal/ post renal azotaemia
  5. Endocrine: Hypoparathyroidism, HyperT4, acromegaly
  6. Growing animals
  7. Incr intake: Vit D toxicity, diet
  8. Transcellular shfit - acute tumour lysis, ST trauma, myopathy
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8
Q

Hypoalbuminaemia

A
  • decreased production: severe liver dz, compensatory (incr glob), maldigestion, malabsorption (SI dz), inflammation (neg acute phase protein), malnutrition, neonates,
  • increased loss: PLN, PLE, Addison’s, dermatological dz, effusions
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9
Q

Hypocalcaemia

A

CKD
Acute pancreatitis
Decreased albumin
Hypoparathyroidism
EG toxicity
Preeclampsia
Artifact (EDTA)

(Uncommon- malabsorption, EPI, cushings, hypovitaminosis D, nutritional secondary hyperparathyroidism, myopathies, hypercalcitonism, tetracycline/ anticoagulant drugs)

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10
Q

Hypomagnesaemia

A

Hypoproteinaemia
GI dz - malabsorption
Renal disease / diuretics
Extra cellular to intracellular shift - dka tc
Primary hypoparathryoidism
Acute pancreatitis
Hyperaldosteronism
Myocardial infarction

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11
Q

Hypocholesterolaemia

A

Decreased production - liver disease/ failure
Decreased absorption - SI dz, low fat diet
Maldigestion
Malnutrition
Incr loss - lymphangiectasia
Addison’s

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12
Q

Hyperlipidaemia

A

Endocrine- hypothyroidism, cushings, diabetes
Pancreatitis
Recent meal
Iatrogenic- steroids
Primary hyperlipaemia- schnauzers, Shetland sheepdog, collies

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13
Q

Increased urea

A
  • prerenal
  • renal
    -postrenal
  • Addison’s
  • GI bleed
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14
Q

Causes of hypercalcaemia

A

Hyperparathyroidism
Osteoclastic lesion (high cal phos product)
Granulomatous disease (makes vit d metabolites)
Spurious
Idiopathic (more in cats)
Neoplastic
Youth
Addisons (doesn’t tend to be marked)
Renal
D - vitamin d toxicity (high ca and phos)

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15
Q

Neoplastic causes of hypercalcaemia

A

Lymphoma
Lymproliferative disease
Osteosarcoma
Mammary carcinoma
PTH adenoma
Multiple myeloma
ASL

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16
Q

Causes of neutropenia

A

Consumption: inflammatory, infection

Decreased production:
- myelophthysis (neoplasia, fibrosis, fatty infiltration)
- reduced function (toxic - phenobarb, oestrogens, fenbendazole, thiamezole, infectious, iatrogenic - chemo, IM destruction)

17
Q

Differentials for PU PD

A
  1. Primary Polydipsia

Behavioural (psychogenic)

Fever

Encephalopathy

Pain

Neurologic disorder

  1. Primary Polyuria

2a Osmotic Diuresis

Diabetes mellitus

Primary renal glucosuria

Fanconi’s syndrome

Post-obstructive diuresis

2b ADH Deficiency–Central Diabetes Insipidus (CDI)

Congenital disorder

Traumatic origin

Neoplastic

2c Renal insensitivity to ADH–Nephrogenic diabetes insipidus (NDI)

Primary Nephrogenic Diabetes Insipidus (Rare)

Secondary Nephrogenic DI

Chronic renal failure

Renal medullary washout

Pyelonephritis

Pyometra

Liver disease

Hyperadrenocorticism

Hypoadrenocorticism

Hypercalcaemia

Hypokalaemia

Hyperviscosity

Drugs–phenobarbitone, furosemide, glucocorticoids

High salt diet

18
Q

What gene in Basenjis causes Franconi syndrome and what % are affected?

A

Fan1 and 10%

19
Q

Which antibodies increases first in cats with toxoplasma?

A

IgM - increased at 1-4 weeks in 80% of cats
>1:64 indicates recent infection or false positive (some healthy cats, FIV infected cats, steroid Tx)

20
Q

What is the sensitivity of acth stim for AT HAC?

a) 75%
b) 90%
C) 85%
D) 65%

A

D) 65%, Most sensitive for PDH

21
Q

Is the sensitivity or specificity of UCCR for the detection of cushings better?

A

Sensitivity - 90%, negative rules out

Ensure no stress 24 h before
Collect morning samples (best to pool 3 days)

22
Q

Hyperkalaemia

A

Pseudo: haemolysis, edta contamination, Thrombocytosis (platelets release during clotting), marked leucocytosis, potassium contamination

Decreased renal excretion:
Urethral obstruction
AKI
End stage CKD
Uroabdomen
HypoA —> hypoaldosteronism
Acidosis - decreases K+ excretion and promotes resorption in the distal nephron
Hyperreninemic hypoaldosterone: high levels of cortisol can cause inhibition of aldosterone by negative feedback.

Drugs: Trilostane, motor and, angiotensin 2 receptor blockers, aldosterone antagonists, ace inhibitors, cyclosporine, nsaids, digoxin, b blockers

Transcellular shift;
Tissue damage eg rhabomyolysis
Acute tumour lysis syndrome
Uroperitoneum
Insulin deficiency
Hyperchloraemic metabolic acidosis

23
Q

Hyperkalaemia

A

Pseudo: haemolysis, edta contamination, Thrombocytosis (platelets release during clotting), marked leucocytosis, potassium contamination

Decreased renal excretion:
Urethral obstruction
AKI
End stage CKD
Uroabdomen
HypoA —> hypoaldosteronism
Acidosis - decreases K+ excretion and promotes resorption in the distal nephron
Hyperreninemic hypoaldosterone: high levels of cortisol can cause inhibition of aldosterone by negative feedback.

Drugs: Trilostane, motor and, angiotensin 2 receptor blockers, aldosterone antagonists, ace inhibitors, cyclosporine, nsaids, digoxin, b blockers

Transcellular shift;
Tissue damage eg rhabomyolysis
Acute tumour lysis syndrome
Uroperitoneum
Insulin deficiency
Hyperchloraemic metabolic acidosis

24
Q

Hyponatraemia

A

Artefact: lipaemia or hyperproteinaemka
Iatrogenic: diuretics, hypotonic fluids

Hyperosmolar states eg diabetes; or mannitol (increased flu by 100mg/dl increases sodium by 1.6meq/L)

Volume overload (hypervolaemic)

Excessive water intake (normovolaemic) - psychogenic polydipsia, inappropriate adh release

Hypertonic fluid loss (hypovolaemia) eg diarrhoea, sequestration of sodium rich fluid, ileus

*Hypotonic fluid loss (hypovolaemia) : renal, GI, third space, Addison’s, osmotic diuresis. Sodium dilation: movement of water into the vasculature and increased drinking.

Decreased intake

Intracellular translocation (muscle injury)

Medicine (10 decks)

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