Bloodwork Flashcards
6 causes of eosinophilia
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
5 causes of hypercobalaminaemia
- Neoplasia
- SI dysbiosis
- Liver disease
- Over supplementation
- Pancreatitis
12 causes of hypercholesterolaemia
- Iatrogenic (steroids)
- Hyperadrenocorticism
- Diabetes Mellitus
- Nephrotic syndrome
- Hypothyroidism (incr LDL and HDL)
- Cholestatic disease (reduced clearance)
- Pancreatitis
- Familial hypercholesterolaemi - briards, rottweilers, shetland sheepdogs and dobermans
- Hyperlipidaemia - minature schnazers
- Primary hyperchylomicronemia - cats
- Post prandial
- Artifact - haemolysis
What is the substance can be an indirect measure of cobalamin? Is it incr or decr in hypocobalaminaemia?
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
7 causes of increased urea
- Renal disease
- Pre- renal azotaemia
- Post renal azotaemia
- GI bleed
- Post prandial esp. high protein
- Incr protein catabolism - starvation, fever, burns, +/- steroids
- Artifact - icteric samples
7 causes of increased ALT
- Primary hepatic disease (infectious, inflammatory, toxicity, neoplasia, inherited storage dz, hypoxia)
- Reactive hepatopathy e.g. GI
- Trauma
- Anaphylaxis
- Hyperthyroidism - cats
- Hyperadrenocoriticism
- Diabetes
- Causes of hyperphosphataemia
- Post prandial
- Artifact - haemolysis
- Iatrogenic - enema, diet, fluids
- Renal/ post renal azotaemia
- Endocrine: Hypoparathyroidism, HyperT4, acromegaly
- Growing animals
- Incr intake: Vit D toxicity, diet
- Transcellular shfit - acute tumour lysis, ST trauma, myopathy
- Metabolic acidosis
- Osteopathic bone lesions
Hypoalbuminaemia
- 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
Hypocalcaemia
CKD
Acute pancreatitis
Decreased albumin
Hypoparathyroidism
EG toxicity
Preeclampsia
Artifact (EDTA)
Aki - renal tubular loss and chelation with phos
Trauma
Ple
Sirs
(Uncommon- malabsorption, EPI, cushings, hypovitaminosis D (due to renal dz, malabsorption or EPI) nutritional secondary hyperparathyroidism, hypomag, myopathies, hypercalcitonism, tetracycline/ anticoagulant drugs, phos enemas, tumour lysis)
Hypomagnesaemia
Hypoproteinaemia
GI dz - malabsorption
Renal disease / diuretics
Extra cellular to intracellular shift - dka tc
Primary hypoparathryoidism
Acute pancreatitis
Hyperaldosteronism
Myocardial infarction
Hypocholesterolaemia
Decreased production - liver disease/ failure
Decreased absorption - SI dz, low fat diet
Maldigestion
Malnutrition
Incr loss - lymphangiectasia
Addison’s
Hyperlipidaemia
Endocrine- hypothyroidism, cushings, diabetes
Pancreatitis
Recent meal
Iatrogenic- steroids
Primary hyperlipaemia- schnauzers, Shetland sheepdog, collies
Increased urea
- prerenal
- renal
-postrenal - Addison’s
- GI bleed
Causes of hypercalcaemia
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)
Neoplastic causes of hypercalcaemia
Lymphoma
Lymproliferative disease
Osteosarcoma
Mammary carcinoma
PTH adenoma
Multiple myeloma
ASL
Causes of neutropenia
Consumption: inflammatory, infection
Decreased production:
- myelophthysis (neoplasia, fibrosis, fatty infiltration)
- reduced function (toxic - phenobarb, oestrogens, fenbendazole, thiamezole, infectious, iatrogenic - chemo, IM destruction)
Differentials for PU PD
- Primary Polydipsia
Behavioural (psychogenic)
Fever
Encephalopathy
Pain
Neurologic disorder
- 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
What gene in Basenjis causes Franconi syndrome and what % are affected?
Fan1 and 10%
Which antibodies increases first in cats with toxoplasma?
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)
What is the sensitivity of acth stim for AT HAC?
a) 75%
b) 90%
C) 85%
D) 65%
D) 65%, Most sensitive for PDH
Is the sensitivity or specificity of UCCR for the detection of cushings better?
Sensitivity - 90%, negative rules out
Ensure no stress 24 h before
Collect morning samples (best to pool 3 days)
Hyperkalaemia
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
Hyperkalaemia
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
Hyponatraemia
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)
Hypophataemia
Decreased intestinal absorption:
- decr diet intake
- malabsorption
- v+ and d+
- phosphate binding antacids
- vit D def
Incr urinary excretion:
- primary hyperparathyroidism
- DM and ketoacidosis
- HAC
- hyperaldosteronism
- renal tubular disease
- diuretics or bicarbonate
- hypothermia recovery
- fluids
- early changes of hypercalcaemia of malignancy
Trancellular shift;”:
- insulin
- glucose
- hyperalimentation
- reap alkalosis
