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Oral Exam Practice > Diagnostics > Flashcards

Diagnostics Flashcards

1
Q

Causes of haemolysis

A

Immune mediated destruction (primary vs associative due to haemotropic mycoplasma or protozoal disease)

Toxin induced injury (increased risk in cats due to reduced amount of intrinsic antioxidant)

Fragmentation (abnormal endothelial disease, DIC, neoplasia, vasculitis, myelofibrosis)

Membrane defects (PVK and PFK deficiencies - alter membrane integrity due to lack of ATP)

Hypophosphataemia (seen in cats with hepatic lipidosis)

Oxidant injury (onion tox,

Defective Hgb synthesis (Fe deficiency)

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2
Q

Haemotropic infections that can cause haemolytic anaemia

A

Mycoplasma felis
(M. haemominutium, M turicensis)
M haemocanis (rarely)
Leptospirosis
Anaplasma phagocytophilium (platys rarely causes RBC issues)
Babesia vogeli (mild) or gibsoni
Cytauxzoon sp (exotic)
FeLV (rare)

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3
Q

Microcytic, normo/hypochromic anaemia DDx

A

Iron deficiency - may or may not be regenerative)
PSS
nrIMHA
Chronic GI blood loss, chronic urinary blood loss

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4
Q

Expected indices for iron deficiency

A

Serum Fe = decreased
TIBC (transferrin level) = normal
% saturation = decreased

Can also assess BM stores in dogs (not cats) –> reduced haemosiderin in macrophages in iron deficient states.

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5
Q

Low Fe
Low TIBC
normal % saturation

+/- Normocytic/microcytic non-regenerative anaemia

A

This pattern is typical of inflammation of >24-48 hours duration. Both iron (inflammatory cytokines, hepcidin) and TIBC (negative acute phase protein) decrease, resulting in a normal % saturation.

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6
Q

Causes of hyperglycemia

A

Insulin resistance
Increased Diabetogenic hormones
Stress
Phaeochromocytoma
HAC
Hypersomatotropism
Dioestrus/Ovarian remnant
HyperTH

Decreased Insulin
Pancreatic immune mediated damage
Glucose toxicity
Type I diabetes

Spurious - delayed measurement, haemolysis, EDTA/Lith hep tubes.

Sepsis
Stress
Parenteral IVF or nutrition
Drugs: thiazide diuretics, B-agonists

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7
Q

Causes of hypoglycemia

A

Decreased Production
Neonates - low stores of glycogen
Hepatobiliary disease (PSS, liver failure (acute or end stage chronic), neoplasia)
Toxins: ethylene glycol, ethanol
Sepsis ( reduced hepatic production - impaired oxidative metabolism, hypoxic injury, increased anaerobic glycolysis)
Glycogen storage disease - enzyme deficiency in glycogenolysis (hypogly, hepatomegaly with vacuolation, elevated liver enzymes)

Increased Utilisation
Sepsis (insulin like substances, IL1, cytokine enhances transport of glucose into cells)
Insulinoma, or iatrogenic insulin
Paraneoplastic - HCC, leiyomyosarcoma, hepatic mets
(impaired hepatic gluconeogenesis/glycogenolysis, excess glucose utilisation, IGF 2, inhibition of counter-reg hormones)
Toxins: xylitol, ethanol, ethylene glycol
Parasitic infection: Babesia (consume glucose and deplete hepatic stores)
Primary renal glycosuria (dried chicken jerky)
Polycythemia (artefactual due to increased RBC in sample)

Deficiency in insulin antagonists (diabetogenic hormones)
Hypoadrenocorticism
Glucagon deficiency - severe pancreatitis
Hypopituitarism (low ACTH and GH rare)

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8
Q

Causes of elevated Albumin

A

Dehydration
Hormonal: Hypersomatotropism; Insulinoma

Hepatocellular carcinoma

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9
Q

Causes of decreased albumin

A

Reduced synthesis: liver disease, starvation, malnutrition
Hormonal hypoTH, DM, hypoA, Glucagonoma;

Inflammation - IL1 and IL6

Increased Loss:
PLE, PLN
Cutaneous lesions, centesis of effusions

3rd space loss from effusion

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10
Q

Causes of elevated TG/Cholesterol

A

Causes of Secondary Hyperlipidaemia - cause mild to moderate increases in TG and/or cholesterol
High fat diet
Endocrine:hypoTH, HAC, DM (cats, mainly TG)
Pancreatitis
Obesity (cats as well)
Protein losing nephropathy
Cholestasis
Hepatic insufficiency
Drugs: phenobarbitone, glucocorticoids, Oestrogen

Primary Hyperlipidemia:
Min Schnau; Beagle, Doberman, Shetland Sheepdog

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11
Q

Causes of low cholesterol

A

PLE
IBD
Intestinal Lymphoma
Hepatic failure
Histiocytic sarcoma

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12
Q

Causes of hyperkalaemia

A

Reduced renal excretion = hypoA, renal failure, LUT obstruction, bladder rupture, Whipworm, salmonellosis
Hypovolaemia reducing GFR and tubular flow (GI disease, body cavity effusions)
Repeated pleural effusion drainage

Translocation from ICF to ECF
Metabolic Acidosis
Insulin deficiency (have intracellular deficit)
Tissue injury - reperfusion, acute tumour lysis
Total parenteral nutrition

Artefact: haemolysis, EDTA, thrombocytosis, delayed serum removal;

Drugs: ACEi, B-blockers, ARBs → all reduce aldosterone effects

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13
Q

Causes of hypokalaemia

A

Increased renal excretion - affected by aldosterone, tubular flow and lumen electronegativity.
CKD or Distal renal tubular acidosis
Hyperaldosteronism (or HAC)
Post-obstructive diuresis, diuretic drugs, DKA diuresis
→ osmotic diuresis with anion like ketones drags K+ out
HyperTH polyuria
Diet induced hypokalaemic nephropathy in cats
Drugs: thiazide or loop diuretics,
Increased GI loss: Gastric vomiting; SI diarrhoea

Translocation from ECF → ICF: Alkalosis
Hyperinsulinism or after glucose containing fluid

Decreased intake: Iatrogenic fluids; Anorexia; Dietary deficiency

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14
Q

ECG findings of hyperkalaemia - why

A

Initial increase in excitability due to less negative RMP

But with this change there are less voltage gated Na channels present to open –> slower depolarisation when impulse commenced in SA node, and slower impulse conduction.

Shortened QT
T tenting (rapid repol
as K moves in quickly)
Widening of the QRS due to conduction delay
Flattening and eventual loss of P waves

Sine waves develop in severe disease

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15
Q

How does Ca alleviate hyperkalaemic arrhythmogenic effects

A

antagonises the effects of K+ on the RMP, stabilising the RMP

Does not alter the amount of K+ present so additional treatment is needed

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16
Q

How does hypokalaemia affect cardiac rhythm/ECG and why

A

Enhances the ‘funny currents’ in the SA nodal cells –> faster phase 4 depolarisation

See effects most in the purkinjie fibres –> increasing risk of ectopic foci developing

The hypokalaemia slows repolarisation through inhibition of the K+ efflux channels as well resulting in risk of re-entrant arrhythmia

Flattened T wave and development of U wave (due to delayed repolarisation)
Prolonged QU interval

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17
Q

How does hypokalaemia affect motor neuron conduction

A

Causes hyperpolarisation –> more negative RMP
–> need greater stimulus to generate AP
–> weakness

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18
Q

Causes of Hypernatraemia

A

Free water deficit –> hyperosmolality of the ECF. Approach is through assessment of volume status

  1. Hypovolaemia (isotonic water loss generally have the greatest vol depletion)
    - Renal: appropriate (osmotic or drug induced diuresis); inappropriate (CKD, nonoliguric AKI, post-obstructive diuresis)
    - Extra-renal: GI (V, D, obstruction); 3rd space (pancreatitis, pleural eff); Cutaneous
  2. Normovolaemia = pure water deficit
    - insensible loss (fever, tachypnoea)
    Hypodypsia (neurological dz, thirst centre defect, ADH defect)
    - CDI/NDI - ADH dysfunction
    Lack of water access
  3. Hypervolemia (solute gain):
    - Salt poison
    - Hypertonic fluids
    - Hyperaldosteronism
    - HAC
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19
Q

Causes of hyponatraemia

A

Generally caused by excess water –> result of non-osmotic ADH release

Most are LOW OSMOLALITY
1. Hypervolemic: renal failure, nephrotic syndrome, CHF, liver failure
(all cause perception of reduced ECV thus nonosmotic ADH release and water retention despite low osmolality) Renal failure may also be unable to excrete sufficient water.
Also water intoxication

  1. Normovolaemia: SIADH (paraneoplastic, drugs); hypothyroidism (myxoedema), Hypotonic fluids, Psychogenic polydipsia, reset osmostat
    (Low Na, high Urine osmolality and high Ur Na)
  2. Hypovolaemia:
    Addison’s, Nephropathy (salt losing); GI loss, 3rd space loss; excessive diuretic use

NORMAL OSMOLaLITY - pseudo/spurious due to increased protein or lipid (measured osmolality will be normal)

HIGH OSMOLALITY - hyperglycemia, mannitol or severe azotaemia

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20
Q

Causes of hyperchloraemia

A

Corrected for Na = [Cl] x 146 / [Na]
Hyperchloraemia is associated with tendency toward acidosis
Iatrogenic = fluids, KBr, spironolactone

Concurrent HCO3 deficit = renal Cl retention and HCO3 excretion → chronic alkalosis or renal tubular acidosis
or GI loss of HCO3
DKA - ketones excreted in place of Cl
HypoA - Na loss > Cl loss

Hypoalbuminemia
Diarrhoea - loss of Na > Cl

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21
Q

Causes of hypochloraemia

A

Corrected for Na = [Cl] x 146 / [Na]
In hypochloraemic states Cl is conserved by renal tubules until deficit resolves (usually just need to correct underlying cause) provided renal function is normal

Iatrogenic = HCO3 therapy, loop diuretics, steroids, HAC

Chronic respiratory acidosis (hypoventilation)

GI loss or sequestration - vomiting

Lipaemia (spurious)

22
Q

Causes of hypercalcaemia

A

Nonpathologic: growth, non-fasting, spurious (lipemia)
Transient: hemoconcentration, hyperproteinemia, HypoA

Parathyroid Dependent: primary hyperPTH

PTH independent: PTHrp in malignancy, bone marrow osteolysis (haematopoietic malignancy); idiopathic hyperCa, CKD, HyperVit D; granulomatous disease, AKI; Nonmalignant osteolysis (HOD, infectious); Excess supplements; Grape tox;

23
Q

Effects of hyperCa on neuron conduction and ECG

A

reduces membrane Na permeability –> reduced impulse firing

In heart this results in prolonged PT and short QT

24
Q

Causes of hypocalcaemia

A

Common: low albumin, CKD, eclampsia, AKI, acute pancreatitis, insufficient dietary intake

Drugs: Enrofloxacin, bisphosphonates,

Uncommon: hypoPTH, sudden correction of hyperCa; ethylene glycol Tox, Phosphate enemas; Overzealous PO4 supplementation, DKA, PLE, SIRS/Sepsis, hypoMg; hypovit D; HAC

Nutritional secondary hyperPTH: high Phos diet → increased PTH with low iCa
Vit D resistance (Rickets type 2) - end organ resistance to Vit D (calcitriol)
Rickets type I - deficiency in conversion enzymes for Vit D

25
Q

Effects of hypoCa on neuron conduction and ECG

A

→ increased neuromuscular excitability → cramps, seizures, tetany, behavioural change, facial rubbing
→ death from circulatory collapse, risk with respiratory alkalosis

Reduced smooth muscle excitability.

ECG: prolonged duration of AP in cardiac myocytes
→ wide deep T waves, prolonged Q-T, Bradycardia

26
Q

Causes of hyperphosphataemia

A

→ sampling timing within 12h of meal can falsely increase
Maldistribution: tumour lysis, tissue trauma
Haemolysis, extracellular shift with acidosis

Increased intake: Phosphate enemas, Vit D excess; intravenous

Decreased Excretion: AKI, CKD, uroabdomen, hypoPTH, hyperTH

Young growing animals
Spurious: lipemia, hyperproteinemia

27
Q

Causes of hypophosphataemia

A

Translocation: intracellular shift with acidosis treatment, insulin or glucose administration.
TPN or hypothermia also cause intracellular shift

Increased renal loss (reduced reabsorption)
hyperPTH; renal tubular disorder, proximal diuretics; eclampsia

Reduced intake - binders, diet deficiency, high Ca:P load, Vit D deficiency

28
Q

Causes of hypomagnesaemia and significance

A

Reduced intake or GI Loss - 2 routes of GI absorption, one is saturable. Uptake increases in deficiency
Renal Excretion - usually most is reabsorbed along with NaCl (solvent drag). Reduced by PGE2.
→ reduced in acidosis

Diabetic ketoacidosis - loss in urine and intracellular shift with acidosis resolving → lethargy, muscle weakness, seizures, fasciculations, ataxia, Further K wasting

→ deficiency can cause cardiac arrhythmia
→ can also cause hypoK due to reduced function of ATPase transporters to reabsorb.
→ in young animals deficiency may impair bone growth
→ may occur concurrent with hypoCa due to similar loss mechanisms

29
Q

Causes of D-dimer increase in dogs

A

any disorder resulting in crosslinked fibrin formation and breakdown can potentially increase D-dimer concentrations

D-dimer appears to be a very sensitive indicator of fibrinolysis in dogs with DIC (85-100% sensitive - but low specificity

neoplasia, inflammatory disease and hemorrhagic effusions

30
Q

Utility of D-dimer in cats

A

Unclear due to mixed results:

D-dimer concentrations are higher in septic versus non-septic cats, but only 18% of septic cats had classic laboratory criteria of DIC

D-dimer concentrations were NOT consistently increased in cats with detectable thrombi or acute aortic thromboembolism

D-dimer concentrations were increased in 75% and 44% of cats with and without DIC, respectively. Concentrations were also increased in 33% of healthy cats

31
Q

Indications for Thrombin-antithrombin measurement

A

High concentrations of thrombin-antithrombin complexes are a sensitive and specific indicator of thrombin activation. The assay appears to detect thrombin-antithrombin complexes in some species and has been used to identify hypercoagulability in specific research projects in dogs, cats

Both thrombin-antithrombin and plasmin-antiplasmin complexes are high in human patients with DIC and these tests could be useful in animals

32
Q

Features of hypercoagulable TEG/ROTEM trace

A

Combination of short R (CT), short K (CFT), high α, or high MA (MCF), high overall coagulation index

33
Q

Interpretation of the following TEG findings:
Combination of long R (CT),
long K (CFT),
low α,
low MA (MCF)

A

Hypocoagulable

DDx high Hct, low fibrinogen, thrombocytopenia

34
Q

Causes of elevated Lactate

A

Type A - Hypoxic
Increased O2 demand (exercise, seizures)
Decreased O2 availability (reduced perfusion due to shock, hypovolemia, heart disease or reduced arterial O2 content hypoxaemia or anemia)

Type B - Nonhypoxic
Drugs/Toxins (salicylates, ethylene glycol)
Diabetes Mellitus
Liver Failure (less removal)
Hereditary defects (mitochondrial myopathies or gluconeogenesis defects)
Hypoglycemia
Renal Failure
Sepsis

35
Q

Metabolic alkalosis causes

A

Chloride responsive - vomiting, diuretic therapy, post-hypercapnea

Chloride nonresponsive - HAC or hyperaldosteronism

Alkali administration (HCO3, cation exchange resin)

Refeeding syndrome

Severe K or Mg deficiency

36
Q

Causes of metabolic acidosis

A

High Anion gap - ketones, lactate, ethylene glycol, uraemia

Reduced H+ excretion - hypoadrenocorticism

Increased HCO3 loss
- Diarrhoea
- RTA

37
Q

Causes of Respiratory acidosis

A

Hypoventilation (LMN Dz, NMJ Dz)
Airway obstruction (mass, FB, granuloma, collapse)
Cardiopulmonary arrest; Heatstroke
Intrinsic Pulmonary disease - ARDS, severe pulmonary oedema, smoke inhalation
Pleural space disease (trauma, hernia, effusion, pneumothorax)
Obesity - Pickwickian syndrome

38
Q

Causes of respiratory alkalosis

A

Hypoxaemia (O2 chemoR stimulate hyperventilation)- RtoL shunt, diffusion impairment, pulmonary dz with V/Q mismatch, anaemia, reduced FiO2, CHF, severe hypotension

Stimulation of pulmonary stretch receptors or nociceptors to increase RR - pneumonia, PTE, interstitial lung disease, ARDS

Centrally mediated hyperventilation - liver disease, HAC, G- sepsis; central neurological disease, heatstroke, CVA

39
Q

Indications for flow cytometry

A

Immunophenotyping
Differentiating small cell/indolent lymphomas from reactive population

Differentiation of thymoma from thymic lymphoma

Differentiation of acute myeloid leukaemia types as well as acute lymphoblastic leukaemia from lymphoma

Detection of cell bound Ab is an emerging field - for diagnosis of IMHA/ITP

40
Q

Common lymphoid surface antigens used in flow/IHC

A

T cell: CD3, CD4, TCR alpha beta

B cell: CD 79a, CD 20, PAX5, BLA36

CD35 stem cells

ALL - CD35+, CD45+

Thymic - CD4 and CD8+

41
Q

Markers for AML diagnosis and exclusion of lymphoblastic leukaemia

A

No lymphoid markers are positive in myeloid leukaemias

CD11b/c, CD14, CD80
Common myeloid markers

42
Q

Bone marrow cytology findings:
15% myeloblasts
- Dysplasia of all cell lines
- mild increase in erythroblasts but overall M:E increased
- bicytopenia

A

Consistent with MDS - excess blasts.

FeLV associated and testing with DNA-provirus should be considered

The higher the blast percent the poorer the prognosis, as is multiple cytopenias and marked morphologic atypia.

43
Q

BM from non-regenerative anaemia and thrombocytopenia:
Dysplastic myeloid and erythroid lineages
Blasts 3%
Disorderly erythroid maturation and maturation arrest
Poor cellularity

A

MDS RC multilineage - no increase in blasts but affects >2 cell lines

Histopathology shoul dbe performed to look for evidence of myelofibrosis - can occur secondary to many conditions (MDS, MPD, AML, PIMA, hyperparathyroidism)though may not affect prognosis

44
Q

BM findings and causes of secondary dysmyelopoiesis

A

Often only <10% dysplastic cells in marrow (differentiates from MDS)

No increase in blast cells (differentiates from AML/myeloproliferative disease)

DDx: infectious, radiation, toxin (heavy metal); drugs (chemo, oestrogen, phenobarbitone); B12 or folate deficiency; any condition causing marrow hyperplasia (ie consumption of cells peripherally or increased demand)

45
Q

Normal M:E in bone marrow and percentage of cells that should be mature vs immature

A

0.5:1 up to 3:1
regenerative anaemia will decrease as will myeloid hypoplasia
Myeloid hyperplasia will increase

Usually Blasts are <5% of marrow with 80-90% of marrow consisting of latter stages of cell maturity (if there is orderly exponential growth of precursors).

46
Q

Tests/results that indicate immune mediated haemolysis and their sens/spec

A

SPHEROCYTES - >5/10hpf has sens of 63% Spec 95% (prior to transfusion)

DAT - Sens 70-90%; Spec 95-100%
Affected by temp, less specific in cats

Saline Ag test - sens 88%; Spec 40-100% - accuracy 95% at 49:1 dilution

Flow cytom - sens 67%; Spec 87-92%. Detects Ab bound to RBC like DAT

Osmotic fragility - poor specificity due to plethora of causes ffor increase

Carboxy Hgb - metabolism of haema containing protein causes increase.
Single study reported 96.3% sens, 96.3% spec
Not yet fully evaluated or available.

47
Q

BM FIndings in non-regen anaemia:
erythroid hypoplasia with increased M:E
Maturation arrest at rubricyte
Evidence of rubriphagocytosis
Increased erythroid blasts

A

Consistent with Precursor targetted IMHA

Can use flow cytom to look for Ab bound to precursors but not present in all cases.

FIV/FeLV testing

For pure red cell aplasia see early erythroid target like this, for PIMA the maturation arrest may be later (ie up to metarubricytes present)

Aplastic anaemia the earliest precursors are targeted - common myeloid progenitor - all cell lines affected.

48
Q

Causes for neutropenia

A

Inherited defects
Increased margination - strong inflammatory stimulus, often see degenerative neuts
Immune mediated destruction
Stem cell injury
This may be reversible: viral infection (FPV/CPV) Drugs, Toxins, B12 deficiency
Or irreversible (FeLV, myelofibrosis, myeloproliferative disease, myelodysplastic disease, grey collie cyclical haematopoiesis)

49
Q

Appropriate compensation amounts for Metab and Resp acidosis

A

Metabolic:
1mmHg pCO2 decrease for every 1mEq HCO3 decrease

Resp:
Acute: 1.5mEq increase in HCO3 for every 10mmHg pCO2 increase
Chronic: 3.5mEq increase

50
Q

Appropriate compensation amounts for Metab and Resp alkalosis

A

Metabolic:
0.7mmHg increase in pCo2 for every 1mEq increase in HCO3

Respiratory:
Acute: 2.5mEq decrease in HCO3 for every 10mmHg decrease in pCO2
5.5mEq decrease in HCO3 for every 10mmHg decrease in pCo2

Oral Exam Practice (7 decks)

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