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Final exam > Rotations > Flashcards

Rotations Flashcards

1
Q

Hypotention what to do in that situation

A

a. Check patient depth -> deep then decrease inhalant and reassess
b. Check HR -> low then administer anticholinergic (glycopyrrolate – 5-20mcg/kg, 40-60mins)
c. Normal HR –> crystalloid bolus (up to 30ml/kg – so up to 3 bolus of 10ml/kg)
d. Fluid not working but HR still good
o Vascular tone + ionotropic support – ephedrine (0.1mg/kg, lasts 10-15mins) – can give x2
o Dopamine CRI – 7-10mcg/kg/min -> (beta agonist – positive inotrope, alpha agonist – vasoconstriction – middle to large doses)
o Dobutamine (ionotropic support), Vasopressin (increase vascular tone – vasoconstricts gut so can get sloughing – diarrhoea) - BIG GUNS

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2
Q

Reasons for hypotention

A
  • hypothermia, too deep anaesthesia, vasodilating drugs (iso, ace), bradycardia, reduced contractility of the heart
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3
Q

reasons for hypertension

A
  • too light anaesthetic, pain, kidney disease, hyperthyroid, vasoconstrictive drugs (alpha-2), fluid overload
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4
Q

what drug is atropine, effects, how long lasts and side effects

A

anti-cholinergic - increase HR and BP
lasts 10-15mins
side effects - SLUD - salivation, lacrimation, urination, defecation, and ventricular tachycardia

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5
Q

what are some reasons for pale MM

A
  • decreased oxygen carrying capacity of the blood, bleeding/shock, reduced oxygen availability, pain, alpha-2 agonist
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6
Q

bradycardia during anesthesia what level, how to respond

A

(HR < 50-70 dog, <100 cat)
-Only issue if low BP or an escape rhythm (no P waves)
– give anticholinergic (ensure not hypothermic)

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7
Q

Hypercapnia at what level and how to respond

A

CO2 >60mmHg

a. Hypoventilation – provide IPPV or mechanical ventilation and reassess depth
b. Rebreathing CO2 – non-rebreathing low fresh gas flow, rebreathing – exhausted soda lime

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8
Q

which LN can you normally feel

A

popliteal, sub-mandibular, pre-scapular

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9
Q

Thrombocytopaenia what levels normal, risk of bleeding and spontaneous bleed, clinical signs and immune-mediated what need to do first

A

normal 200-500, risk of bleeding <50, spontaneous bleeding <30
- Will bruise easily, petechiae -> ear, gums, ventral obstruction, vulva, gastrointestinal (melena), eyes and brain (more serious but rare)
Immune mediated thrombocytopaenia - primary or secondary (drug - penicillin, cephalosporins, inflammatory, infectious, neoplasia (lymphoma)
- Need to evaluate as to whether secondary even though primary more common

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10
Q

maropitant what type of drug and effects

A
  • neurokinin-1 (NK-1) receptor antagonist that acts in the CNS by inhibiting the binding of substance P, which is the key neurotransmitter involved in vomiting.
  • can suppress both peripheral and centrally mediated emesis.
  • has been shown to reduce the minimum alveolar concentration (MAC) requirements of sevoflurane and to reduce visceral pain in dogs, as NK-1 receptors are stimulated by substance P
  • has been shown to possess anti-inflammatory activity
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11
Q

Mirtazapine whaa is it and effects

A
  • Tetracyclic Antidepressant; 5-HT3 Antagonist
  • appetite stimulant and anti-emetic with chronic kidney disease
  • possible anti-depressant activity with sedative effects
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12
Q

Omeprazole what type of drug and effects

A

Proton pump inhibitor

- treatment and prevention of ulcers

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13
Q

What is RER, equation and how to determine DER

A
  • RER (kcal/day) = 30 x BW (kg) + 70
  • RER (kcal/day) = 70 x BW (kg)0.75 (dogs > 45 kg) - based on ideal body weight
  • DER = RER x “lifestyle factor”
    1. Determine ideal weight (BCS)
    2. Calculate RER
    3. Determine lifestyle factor to calculate DER
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14
Q

What levels of fat and protein needed for 1) diabetic cat 2) cat with advanced renal disease 3) schauzer with hypertriglyceridaemia

A

Diabetic cat -> normal fat and high protein
Cat with advanced renal disease -> high fat low protein
Schnauzer with hypertriglyceridemia -> low fat and normal protein

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15
Q

Toxicity of gentamicin

A

Nephrotoxicity and ototoxicity (cranial nerve 8 - if tympanic membrane is ruptured DON’T USE)
Single large doses have been shown to reduce nephrotoxicity

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16
Q

Toxicity of enroflocaxin

A

Cartilage breakdown in juveniles, blindness in cats (dose related) - DON’T USE IN CAT AND JUVEINILES
- Single large dose better for preventing resistance

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17
Q

Toxicity of tetracyclines

A

Degradation products cause nephrotoxicity (ototoxicity) and hepatotoxicity and photosensitivity (if use in cattle give shade)

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18
Q

what antibiotics don’t use in horses and rabbits and why

A 
Erythromycin
Clindamycin 
Lincomycin 
Metronidazole 
GIT ISSUES
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19
Q

abnormalities where is the lesion - forced expiration and inspiratory dyspnoea

A

1) Forced expiration (most of the time increase in inspiratory effort)
- Small airway disease (Asthma)
- Fixed upper airway obstruction (will also see inspiratory)
2) Inspiratory dyspnoea (short expiration)
- Upper airway obstruction (Stertor or stridor) - more common
- Severe, chronic pleural effusion (no noise)

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20
Q

abnormalities where is the lesion - paradoxical abdominal movement

A

2) Paradoxical abdominal movement - more severe dyspnoea
- Upper airway obstruction
- Stiff lungs - less compliant
- Diaphragm dysfunction
- Severe chronic pleural effusion in cats (usually fluid)

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21
Q

abnormalities where is the lesion - inspiratory dyspnoea with an expiratory pish and short shallow respiratory

A

4) Inspiratory dyspnoea with an expiratory push
- Fixed upper airway obstruction (cannot be pushed away)
5) Short shallow respiratory
- Some pleural space lesions
- Others as well

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22
Q

what are signs of severe dyspnea and critical

A 
Signs of severe dyspnoea 
- Extended neck 
- Abducted elbows
- Open mouth breathing
- Anxious facial expression (how distressed is the animal? - chronic may be less stressed) 
Critical 
- Lateral recumbency
- Pupillary dilation - RESPIRATORY ARREST 
- Cyanosis if caused by hypoxia - OXYGEN
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23
Q

Thoracocentesis how perform

A

(8th intercostal space)
□ Cranial to rib, ventral (4o’clock) for fluid, dorsal (2o’clock) for air
□ Sterile gloves, hyperdermic needle, 3 way-tap, EDTA tube
□ Go in bevel up at 90 degrees and keep moving slowly forward until no more negative pressure, once no negative pressure then can redirect the needle (NOT BEFORE this as can tear the pleura)

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24
Q

pulmonary parenchymal disease clinical signs and causes

A

crackles, short shallow breathes as it gets worse than deep breaths, paradoxical
○ Causes
§ Neoplasia, pneumonia, PTE, oedema
□ Cardiogenic oedema
® What results - get increase in hydrostatic pressure resulting in water overload - once reduce water with diuretics (such as frusemide) then normal mechanisms take over (pneumocytes)
□ Non-cardiogenic oedema
® Upper Respiratory Obstruction
◊ Large inspiration against closed glottis, large -ve pressure build up
® Neurogenic (electrocution)
◊ Large increase in sympathetic tone results in large amount of blood flow into the lungs
® What results -
◊ Capillary rupture -> not just water within the oedema also cell debris and protein

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25
Q

Cardiac tamponade what occurs and how generally presents

A

(compression/collapse) -> increase pressure will affect the right side of the heart first (thinner wall as moving blood into lower pressure system) -> increase pressure into the vena cava (abdominal effusion) -> decrease filling during diastole -> decrease SV -> short and narrow pulses
Common presentation - Muffled heart sounds, short and narrow pulses, large breed dog, ultrasound to confirm

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26
Q

arterial blood gas what PaO2 levels that are bad, how to determine issue, what look with glucose and lactate

A
  • PaO2 = oxygenation
    ○ <75 needs oxygen
    ○ <55 life-threatening
  • Determining acid-base
    1. Look at the pH -> acidosis or alkalosis?
    2. Look at what is causing that change
    § PaCO2 - if HIGH then RESPIRATORY ACIDOSIS - correlates or compensatory mechanism
    § SBE (standard base excess - amount of base to add to get normal pH (7.4) - if NEGATIVE then not much base so METABOLIC ACIDOSIS
    3. Is there a compensatory mechanism - should always be one at about 1:1
  • Glucose - very high suggests diabetes OR close to death (massive corticosteroid release which results in insulin resistance)
  • Lactate - high - reduced perfusion
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27
Q

What are the 4 main causes of metabolic acidosis

A
  • Phosphorus and sulphates (azotaemia) - not being urinated out
  • Lactic acidosis
  • Ketone acidosis
  • Toxic - 1080, ethylene glycol
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28
Q

what are the 3 main measures of perfusion

A

1) Lactate - high
2) Venous CO2 (if low could be hypoperfusion or hyperventilation (check RR))
3) Blood pressure - direct measure - hypovolaemia

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29
Q

what is the difference between hypovolaemic and cardiogenic shock and why important

A

NEED TO KNOW - one gets fluids and one gets beta blockers
- U/S heart
○ in cardiogenic cannot contract with large blood volumes within the ventricle
○ In hypovolaemic shock the contractility is fine just don’t have the volume

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30
Q

Beta 1 and 2 receptors what do they do

A
  • Beta 1 - lusitropy (increase relaxation of myocardium to allow for filling), contractility, chronotropy (increase heart rate)
    ○ DCM - agonist - debutamine
  • Beta 2 - vasodilation, bronchodilation - lower airway disease
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31
Q

radiographs what vertebrae for underinflated vs well-inflated

A

-Underinflated lungs – cura intersect vertebrae T9
-Well-inflated lungs – cura intersect vertebrae at T12/13
o Lung pathology easiest to see if surrounded by well-aerated lung

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32
Q

Cardiomegaly what are the rules for dog radiographs - lateral (3) and VD (!)

A

Lateral
1. Size of the heart - Two thirds height of thorax from base to apex (yellow line)
2. Cranial to caudal margin of heart -> 2.5-3.5 intercoastal spaces wide
3. Trachea should deviate from thoracic spine at about 40degrees (blue)
VD -
1. heart should be 2/3rds the width of the thorax

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33
Q

Cardiomegaly what are the rules with radiographs forr cats, lateral

A

Lateral
1. 5th - 7th rib rule
• Work out distance between cranial boarder of 5th rib and caudal boarder of 7th and the heart shouldn’t be greater than that distance from cranial to caudal

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34
Q

General changes with cardiomegaly seen radio-graphically

A

– elevation of trachea, increased craniocaudal diameter of the heart (Width), increased sternal contact, valentine shaped heart (cat) – left atrium sits more cranial than in dogs

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35
Q

General changes with right-sided enlargement and left side enlargement of heart radiographically

A
  • Right sided enlargement – cranial bulging of right heart border
  • Left sided enlargement – expansion of left atrium caudal lobar area (left atrial wedge), straightening of the caudal boundary (left ventricle enlargement), bulge at 2-3 o’clock on VD (left auricle enlargement)
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36
Q

what are the most common congenital and acquired cardiac diseases for dogs and cats

A

Dogs
• Congenital - PDA (patent ductus arteriosus), pulmonic or subaortic stenosis, mitral or tricuspid valve dysplasia, persistent right aortic arch
• Acquired – DCM (dilated cardiomyopathy), ARVC (arrhythmogenic right ventricular cardiomyopathy (boxer),
Cats
• Congenital – tricuspid or mitral valve dysplasia, atrial septal defect (ASD), ventricular septal defect
• Acquired – hypertrophic cardiomyopathy, restrictive cardiomyopathy

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37
Q

Pulmonary vasculature on radiographs where located in respect to each other and what are the VD (2) and Lateral (1) rules

A

Lateral – look for pairs - Dorsal to ventral – artery, bronchus, vein
VD – veins are central to arteries
Look at vessels when cross the 9th rib
VD
1. Can be 1.2 times width of the 9th rib when cross the rib
2. The artery and vein should be the same width
Lateral
• Proximal portion of the 4th rib of the 4th intercostal space-> harder to do

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38
Q

Causes of enlarged pulmonary veins, enlarged arteries, both enlarged and small vessels

A
  • Enlarged veins - Mitral insufficiency, volume overload, patent ductus arteriosus, primary myocardial disease, left atrial obstruction (neoplasia, thrombosis)
  • Enlarged arteries (not as common) – parasitic arteritis (heartworm disease), thromboembolic disease, chronic lung disease with pulmonary hypertension
  • BOTH enlarged – iatrogenic fluid overload, left to right shunting, fluid retention, peripheral arterio-venous fistula
  • Small vessels – hypovolaemia, right to left shunting, severe pulmonary stenosis
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39
Q

Causes of alveolar vs bronchial pulmonary patterns

A

Alveolar - • Aspiration pneumonia, cardiogenic and non-cardiogenic oedema
Bronchial - • Feline asthma, bronchopneumonia, age related change, chronic inflammation, idiopathic fibrosis, lungworm, neoplasia (lymphoma, bronchogenic carcinoma) – confirm via BAL

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40
Q

Differentials for lesions in cranioventral lungs, caudodorsal, diffuse, focal and multifocal lesions

A

 Cranioventral – aspiration pneumonia (Alveolar pattern), all pneumonia, haemorrhage, neoplasia and bronchitis
 Caudodorsal – cardiogenic pulmonary oedema (dog most common), non-cardiogenic pulmonary oedema (upper airway obstruction, head trauma), haemorrhage, pneumonia, neoplasia, bronchitis and fibrosis
 Diffuse – cardiogenic pulmonary oedema, haemorrhage, pneumonia, neoplasia, bronchitis, fibrosis
 Focal – solitary masses – CHANG
• C – cyst, H – haemotoma, A – abscess, N – neoplasia, G – granuloma
 Multifocal – pulmonary metastases (need to be greater than 0.5-1cm in diameter), granulomatous disease, haemorrhage

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41
Q

What are the 4 things not to confuse with pulmonary nodules of radiograph and how to differentiate

A

 End on vessels – very small and more opaque, decrease size and number towards the periphery
 Calcified plaques ‘pulmonary osteomas’ – diffuse, irregularly margined (don’t taper towards periphery), mineralised (2-4mm)
 Nipples – need to use markers
 Subcutaneous masses

42
Q

What are the 4 most common sites for oesophageal foreign bodies

A
  1. Circo-oesophagus
  2. Thoracic inlet
  3. Base of heart
  4. Diaphragm
43
Q

Pylorus and fundus radiographically which side sit and what occurs in right and left lateral

A 
Pylorus on the right 
Fundus of the left 
Right 
•Gas in fundus 
•Fluid in pylorus  
Left 
•Fluid into fundus
•Gas in pylorus
44
Q

Small intestines what are the size rules for dogs (3) and cats (2)

A

Dogs
1) Ratio of greatest SI diameter to body of L5 no > 1.6 - most useful
2) No more than twice the width of a rib - overestimates - not really used
3) No loop greater than twice the width of others
Cats
1) No greater than 12 mm in diameter
2) No greater than twice the height of L4

45
Q

when does mineralisation of foeuts occur for dogs vs cats

A
  • Dog – 20-22 days

* Cats – 25-29 days

46
Q

what are the 3 main calculi that are radioopaque

A

1) calcium oxalate/phosphate
2) struvite (ammonium phosphate)
3) silica

47
Q

What are the 5 main causes of decreased serosal detail

A

 Young animals, thin animals, abdominal effusion, peritonitis, peritoneal neoplasia (carcinomatosis)

48
Q

location of lesions for primary bone tumours, metastatic bone tumours, bone infection, bone lesions

A

 Primary bone tumours – favour metaphysis of long bones, usually monostotic, ‘away from elbow, towards knee’ – ALSO distal femur
- Osteosarcoma -> chest radiographs for metastasis
 Metastatic bone tumours – diaphysis and polyostotic
 Bone infection – haematogenous favours metaphysis and usually polyostotic
 Bone lesions – usually subchondral bone (just below cartilage in joint)

49
Q

What are the 6 salter-harris classifications

A
  • Type 1 - straight through physis
  • Type 2 - metaphysis and physis
  • Type 3 - epiphysis and physis - into joint (Articular)
  • Type 4 - physis, epiphysis and metaphysis (articular)
  • Type 5 - compressive physis injury
  • Type 6 - peripheral injury leading to bridge formation on one side
50
Q

what is hypertrophic osteopathy

A

 Produces a generalised symmetrical palisading periosteal proliferation on diaphysis of long bones – generally distal worse, most often tarsal and carpal bones, metatarsal and metacarpal bones
 Associated with either infectious or neoplastic intrathoracic lesions

51
Q

What are the 3 main radiographic changes for cranial cruciate ligament disease

A

-Effusion on the mediolateral view:
oCompression of infrapatellar fat pad and bulging of joint capsule cranially
-Periarticular osteophytes – patella, femoral trochlear ridge, fabellae, tibial plateau
-Subluxation of tibia cranially

52
Q

Hypertrophic osteodystrophy what breeds, what radiographic changes

A

 Rapidly growing large-breed dogs, younger ages – long bones (generally distally)
 Radiographic changes
- Presence transverse radiolucent bands with metaphysis -> widened metaphysis and opacity increases -> move towards diaphysis -> periosteal new bone formation (periosteal proliferation)

53
Q

OCD in small animals what are the common locations and general radiographic findings

A

Common locations
-Caudal humeral head – also caudal part of glenoid cavity
-Medial humeral condyle – elbow dysplasia
-Lateral femoral condyle – distal part
-Medial (70%) or lateral trochlear ridge of the talus
- Lumbosacral joint: Craniodorsal corner of the sacral-body (90%) and endplate of L7 (10%)
 OC radiographic – flattening of subchondral bone (hard to see as articular cartilage), sclerosis
 OCD radiographic – osteophytes, joint mice, bony proliferation, increased lucency

54
Q

panosteitis what breeds common in and radiographic changes

A

 Generally younger animals, large breeds – 5-12 months, shifting lameness, self-limiting – on long-bones
 Thumb-print shaped foci of increased medullary opacity, blurring of trabecular pattern

55
Q

OCD lesions in horses where most common locations for flap vs fragmentation and general radiographic findings

A

Most common locations – generally in standardbreds
- Flap and fragment formations
o Trochlear ridges of femur and talus, sagittal ridge of MC/MT3, caudal humerus, medial malleolus of the tibia
- Fragmentation
o Distal intermediate ridge of the tibia and proximal plantar P1 fragments
General radiographic findings
- Discrete osteochondral fragments
- Alterations in contour of the articular surface – flattening or depression
- Irregular shape lucent zones in subchondral bone
- Sclerosis surrounding the lucent zones
- Secondary remodelling of the joints

56
Q

Subchondral cyst-like lesions in horses common locations

A

Commonly weight bearing areas

  • Medial condyle of femur – COMMON
  • Medial proximal radius
  • Glenoid
  • Proximal interphalangeal joint
57
Q

Pulmonary congestion what looks like grossly, how common and main causes post-mortem

A

Red to dark red mottled lungs
Very common rarely significant
Causes
- Barbiturates - damaging the blood vessels
- Rigor mortis and gaseous distention of GIT tract pushing blood into lungs post-mortem
- True pathology - palpate lungs often results in change of texture

58
Q

Morphological diagnosis for post-mortem reports what are the 6 descriptives neede

A

1) degree (mild, moderate)
2) duration (acute, chronic)
3) distribution (focal, local)
4) exudate - if present (serous, catarrhal)
5) modifier (necrotising)
6) tissue (nephritis, cystitis etc)

59
Q

Estimated total white cell count (WCC) how perform and what should have

A

○ Estimated total white cell count (WCC)
§ Count number of leukocytes in 1- high power fields (40x)
□ Should have 2-6/40X field
® Increased - leukocytosis
® Decreased - leukopenia
§ Calculate average number of leukocytes per high power field (divide by 10)
§ Multiply by 2 to get an estimated WCC in units 10^9/L compare to reference intervals

60
Q

Estimated platelet count how to perform, what should have

A

§ count number of platelets in 10 high power fields (100x oil)
□ Should have 10-25/100x field
§ Calculate average number of platelets per high power field (ie divide by 10)
§ multiply the average number of platelets by 15 to get platelet counts in units 109/L
□ use this to compare to appropriate reference ranges for platelets

61
Q

Platelet levels that are adequate for haemostasis, risk of haemorrhage, show spontaneous mucosal bleeding

A

§ Platelet numbers >100 x 109/L are considered adequate for haemostasis (i.e. > 7 platelets per 100x field in monolayer)
§ Patients with platelets < 50 x 109/L are at risk of haemorrhage,
§ patients with < 30 x 109/L show spontaneous mucosal bleeding (i.e. ≤ 2 platelets per 100x field)

62
Q

Impedance histograms what does platelet clump look like

A

merged RBC and platelet curve

63
Q

Flow cytometry when neutrophils and lymphocytes clouds merge and get ‘shark fin’ what occuring

A

neurtophilia with left shift

64
Q

Classification of cavity effusions in dogs and cats what makes transudate vs exudate

A

transudate
1. low protein - protein <25g/L, NCC: <3 x 10^9/L
2. high protein - protein >25g/L, NCC: <3 x 10^9/L
Exudate - protein >25g/L, NCC >3 x 10^9/L

65
Q

Classification of cavity effusions in cattle what makes transudate vs exudate

A

Transudate
1. low protein <30g/l, NCC: <5 x 10^9
2. high protein >30g/L, NCC: <5 x 10^9/L
Exudate - >30g/L, NCC: >5 x 10^9

66
Q

Classification of cavity effusions in horses what makes transudate vs exudate

A 
Transudate 
1. low protein <25g/L, NCC: <5 x 10^9/L
2. high protein >25g/L, NCC: <5 x 10^9/L
Exudate 
>25g/L, NCC:>5 x 10^9
67
Q

What are the 2 main features of degenerate neutrophils

A
  • less segmentation

- swollen and paler staining nuclei

68
Q

What are some criteria of malignancy for cytology

A 
Pleomorphism
–Anisocytosis
–Variable nuclear: cytoplasmic (N:C) ratio
–Abnormal mitotic figures
–Anisokaryosis
–Multinucleation
–Nuclear molding
–Clumped chromatin
–Prominent/Variable/Multiple/Large nucleol
69
Q

Round cells of cytology what are the 6 main differentials

A
  1. Histiocytoma
  2. Mast Cell Tumour
  3. Lymphoma
  4. Plasma cell tumour
  5. Transmissible Venereal Tumour
  6. Melanoma (some times)
70
Q

What can lead to hypokalaemia

A

– excess loss through renal (renal insufficiency, frusemide diuretics), GIT disease or reduced intake through prolonged anorexia

71
Q

Azotaemia (increase urea without increase in creatinine) Causes

A

– pre-renal (GI bleeding will result in NO increase in creatinine, dehydration also possible BUT inadequately concentrated urine), renal (inadequately concentrated urine) - hyperadrenocorticism, post-renal (NOT SEEING - stranguria/dysuria, hyperkalaemia, inadequate urine concentration)
oCreatinine – could be normal due to generalised muscle wastage (masking kidney disease)

72
Q

Causes of hyperglycaemia especially in cats

A

stress most likely in this case (mild and common in cats),
omore moderate increases: diabetes mellitus (check if persistently high – Fructosamine (binds to albumin which last 2 weeks), hyperA (less common in cats))

73
Q

Mild hypercholesterolaemia causes and why

A

protein-losing nephropathy (lose lipoprotein lipase A – which increase low-density (higher cholesterol) as reduce breakdown), post-prandial (triglycerides (chylomicrons) expect larger increase), cholestasis, endocrine disease (diabetes mellitus, hyperA (less likely in cats)), primary (rare – miniature schnauzer)

74
Q

Causes of elevation in ALT and mechanism

A

Hyperthyroidism (most likely with increase total T4), liver damage (hypoxic, inflammation/infection, neoplasia, toxic), muscle damage (BUT no increase in CK), diabetes mellitus (due to hepatic lipidosis – swelling -> release ALT as lives in cytoplasm (AST in mitochondria so doesn’t escape), HyperA (hepatic vacuolation with glycogen - -less likely in cats)

75
Q

Causes of elevation in ALP

A

hepatic lipidosis (in cats highly suggestive BUT eating), HyperT (most likely with increase total T4), liver damage (measure of function -> albumin (most trusted) -> cholesterol -> urea -> glucose -> coagulation factors), diabetes mellitus, cholestasis (BUT no increase in GGT or bilirubin)

76
Q

Thrombocytosis causes

A

corticosteroids - exogenous or endogenous STRESS LEUKOGRAM (hyperA), neoplasia (would expect large increase), reactive (chronic bleeding, iron deficiency, inflammation – will see micro-platelets), secondary (splenectomy (platelets stored in spleen), splenic contraction, drugs – tribalstin)

77
Q

Causes of hypercalcaemia

A 
H - hypoA
A - hyperparathyroid
R - renal disease
D - vit D toxicity 
I - idiopathic 
O - osteolysis 
N - neoplastic
78
Q

Causes of Leukopaenia characterised by neutropenia with a moderate left shift in horse

A

severe acute inflammation/infection - SIRS (most likely), decreased production (disease involving bone marrow – myeloproliferative disease, drugs, toxins BUT PLATELETS NORMAL)

79
Q
  • Mild Hypochloraemia and hyponatraemia causes in horses
A

GIT loss (colitis) (most likely), renal loss or third space loss (uroabdomen (BUT should have hyperkalaemia)), sweating – high exercise

80
Q

Bilateral epistaxis causes

A

– coagulopathy (inherited (recently DESEXED – WOULD HAVE SEEN THEN – less likely) vs secondary (hepatic insufficiency, fat malabsorption as Vit K is fat soluble (pancreatic insufficiency, cholestasis (cannot get bile acids into intestines to digest the fats)), hypertension, fungal disease (aspergillosis), neoplasia, trauma, foreign body (generally unilateral)

81
Q

Mild thrombocytopaenia causes

A

– increased consumption or destruction (disseminated intravascular coagulation, severe and Peracute haemorrhage, immune mediated thrombocytopaenia (BUT no inflammatory leukogram)), decreased production (drug induced – antibiotics (TMS), chemotherapy and antifungals OR primary bone marrow disease (BUT normal RBC, WBC), sequestration (splenic mass, splenomegaly)

82
Q

Increase in nucleated RBCs without regenerative anaemia causes

A

– inappropriate metrarubricytosis - splenic disease, bone marrow injury, lead poisoning, hypercortisolaemia, inflammation, dyserythropoeisis, myeloproliferative disease and heat stroke.

83
Q

What changes are seen on blood smear with regenerative anaemia

A

• Polychromasia
• Macrocytosis (often the only indication in horses), anisocytosis, hypochromasia
• Increased Howell-Jolly bodies - nuclear remnants - macrophage leaves behind some nucleus
o generally, occurs more with acceleration of production of RBCs
• Increased nRBC’s
• Basophilic stippling - blue dots, RNA left behind as cell matures

84
Q

What are 7 causes of intravascular haemolysis

A
  1. Immune mediated disease – IMHA, neonatal isoerythrolysis, transfusion reaction
    • Complement cascade can be activated - Membrane attack complex (MAC) forms pore in RBC and result in haemolysis
  2. Oxidative injury e.g. red maple in horses, paracetamol in cats, onions in dogs – heinz bodies and eccentrocytes
  3. Infections e.g. Clostridium sp, Babesia sp. - Red cell parasitised by the microbe
  4. Severe hypophosphatemia (<0.3 mmol/L) - disrupt ATPase function and therefore more prone
  5. Zinc toxicosis
  6. Copper toxicosis (sheep)
  7. Genetic disease e.g. PFK deficiency in dogs - inherited defects within RBCs
85
Q

What are 6 causes of extravascular haemolysis

A
  1. Immune-mediated disease (1◦ or 2 ◦ e.g. drugs) - IMHA
  2. Infections e.g. erythrocyte parasites (Mycoplasma, Babesia, Theileria, Anaplasma), Equine Infectious Anaemia virus, FeLV
  3. Oxidative damage (intra and extravascular) – HB, eccentrocytes - produce heinz bodies
  4. Neoplasia e.g. haemangiosarcoma, haemophagocytic diseases
  5. Fragmentation e.g. DIC, haemangiosarcoma, heartworm
  6. Genetic disease e.g. PK deficiency in dogs
86
Q

IMHA what occurs, causes and how to diagnose on blood smear

A

Intra (ghost cells) or extravascular (haemolysis) haemolysis
1. Primary Immune mediated (idiopathic autoimmune) - dogs
2. Secondary Immune mediated - cats
• Drugs, Vaccination, Infections
o Equine infectious anemia virus (EIA)
o FeLV - feline leukaemia viral infection
o Mycoplasma haemofelis
• Neoplasia e.g. lymphoma, SLE
3. Alloimmune (Ab against foreign erythrocyte antigen of same spp.)
• Neonatal Isoerythrolysis - colostrum produced antibodies
• Blood transfusions
Diagnosis
• Spherocytosis
• Auto–agglutination and in saline positive agglutination
o To determine if real agglutination or just sticky -
o If sticky proteins - non-specific- saline will stop the sticking
• Coombs test - looks for agglutination using antibodies
• Exclusion of other primary diseases e.g. neoplasia, infection, or drug therapy

87
Q

Iron deficiency what type of anaemia and causes

A

MICROCYTIC HYPOCHROMIC non-regenerative anaemia
- Erythrocyte fragments also common
Causes
• Chronic external blood loss eg heavy internal or external parasitism, chronic GIT bleeding - lost in the faeces, chronic haematuria - cannot recycle
• Defective iron transport/metabolism eg hepatic insufficiency - not large deficiency
• Very rarely due to iron deficient diet - due to recycling of the iron within the body
o Neonatal animals more likely but still doesn’t really occur

88
Q

Lead posioning clinical signs and blood smear diagnosis

A

• Principle clinical signs are GIT and nervous system signs
• Inappropriate metarubricytosis (nucleated red blood cells) and
basophilic stippling (ie not accompanying a regenerative response)
with no polychormatophils
• Anaemia usually only seen with chronic toxicity
• Diagnosis: blood lead

89
Q

What causes neutrophilia

A
  1. Inflammation – increase circulating and marginating pools, increase selectins
  2. Cortisol mediated – released from bone marrow (mature neutrophilia)
  3. Excitement – move from marginating into circulating
90
Q

What are the 4 causes of neutropaenia

A
  1. Overwhelming inflammatory demand
    - Generally, a septic process with a lot of puss formed - pyometra
    - Less disease needed for cows as they have a lower storage pool
  2. Transient margination (endotoxaemia)
    - More towards edges of the vessels so not detecting them in the sample
  3. Bone marrow disease
    - Make less neutrophils
  4. Immune-mediated destruction of neutrophils
91
Q

What are the 2 types of left-shift and causes

A

1) Regenerative left shift
o ◦ Mature (segmented) neutrophils > immature (band) neutrophils
2) Degenerative left shift
o ◦ Immature neutrophils > mature nature neutrophils
Causes
1. Inflammation – high tissue damand and reflects release from maturation pool
2. Myeloproliferative disease - chronic myeloid leukaemia (serious bone marrow disease) and neoplasia (paraneoplastic syndrome)

92
Q

Lymphocytosis what are the 4 main causes

A
  1. Chronic antigenic stimulation - Vaccination
  2. Adrenaline/Excitement (young animals)
  3. Lymphoid neoplasia
  4. Hypoadrenocorticism - lack of cortisol
93
Q

Lymphopaenia what are the 3 main causes and causes within

A
  1. Glucocorticoids/Stress - most common
    - Reduced release from LN and spleen -> Lympholysis
    - hyperA
  2. Acute inflammation
    - Generally increased stress so get lympholysis or due to movement of lymphocytes into tissues - less circulating
  3. Loss of lymphatic fluid
    - Chylothorax
    - Enteric neoplasia
    - Protein losing enteropathy
94
Q

4 main causes of eosinophilia

A
  1. Worms
    - Parasitic infection
  2. Endo- and ectoparasites
  3. Wheezes & whelts
    - Allergies/Hypersensitivity
  4. Weird diseases
    - Paraneoplastic (lymphoma, mast cell tumour)
    - Hypereosinophilic syndrome - unregulated eosinophil production, pre-disposed to certain breeds
    o Suppress with corticosteroids to control
    - Eosinophilic leukaemia
95
Q

6 main causes of basophilia

A
  1. Stress and inflammation in birds
  2. Often accompanies eosinophilia
  3. Worms - Parasitic infection
  4. Endo- and ectoparasites
  5. Wheezes & whelts
    - Allergies/Hypersensitivity
  6. Weird diseases
    - Paraneoplastic (lymphoma, mast cell tumour)
    - Hypereosinophilic syndrome
    - Basophilic leukaemia
    - Myeloproliferative diseases eg polycythaemia vera
96
Q

acute inflammatory leukogram vs overwhelming inflammatory

A 
ACUTE 
-Neutrophilia* 
-+/- Toxic change - most important 
-+/- Left shift
-+/- Monocytosis
OVERWHELMING
-Neutropenia and or degenerative left shift (not putting out mainly mature now also immature) 
-+/- Lymphopenia - don't leave lymph node as quickly 
-+/- Monocytosis
97
Q

Chronic inflammatory leukogram vs physiologic

A

CHRONIC
-Neutrophilia - mature
-+/- Slight regenerative left shift
-+/- Lymphocytosis
-Monocytosis (high)
PHYSIOLOGIC
Adrenalin/excitement mediated (young animals – cat>horse>cow>dog)
-Neutrophilia – shift from marginating to circulating
-Lymphocytosis – marginating into circulating
-+/- Monocytosis (rare)
NO left shift or toxic change

98
Q

Glucocorticoid/stress leukogram what needs

A
  • Lymphopenia - NEEDS TO HAVE * - decrease release from nodes
  • Neutrophilia – increase release from storage pool
  • Eosinopenia – decreased release from marrow
  • Monocytosis (dogs) – shift from marginating to circulating
  • Basophilia (birds)
    NO toxic shift or toxic change – may see neutrophil hypersegmentation
    *most consistent finding in all species
99
Q

Hypoadrenocorticism what called, leukogram and key biochem changes

A

(Addisons syndrome)
-Lack of stress leukogram despite chronic or severe illness - consider this in dogs
o Could also be excitement - more likely in cats
-+/- Lymphocytosis-
-+/- Eosinophilia
What key electrolyte changes can we see on biochemistry?
-Hyperkalaemia
-Hyponatraemia and hypochloridaemia
-Low Na: K ratio (<27:1)

100
Q

Myeloid leukoaemia what find and types

A
  • Moderate to marked Leukocytosis
    o No inflammatory focus found
    Types
    • Acute Myeloid Leukaemia (AML) – myeloblasts +/- differentiated cells (immature)
    • Chronic Myeloid Leukaemia (CML)– differentiated cells, mimics inflammatory leukogram
    o Neutrophilic
    o Basophilic
    o Eosinophilic
    o Monocytic
    o Polycythaemia vera - erythrocytes - high RBC count
    o Essential thrombocythaemia - excess platelet production
101
Q

Persistent pancytopaenia causes

A
  1. Infectious - eg Parvovirus (dogs & cats), FeLV, EIAV, Bacterial sepsis
  2. Toxins – eg Estrogen (dogs), Bracken fern (ruminants), Chemotherapy, Phenylbutazone
  3. Immune-mediated disease- eg IMHA targeted at precursors
  4. Endocrine disease - Typically effects RBCs - eg Hypothyroidism, Hypoadrenocorticism
  5. Neoplasia - replace bone marrow - pancytopenia
102
Q

Leukaemia vs lymphoma

A
  1. Leukaemia
    • neoplastic haematopoietic cells originate in bone marrow but often seen in circulation
    o Could be red blood cell, platelet, neutrophil
    o acute vs chronic
    o lymphoid vs myeloid (all cell lines except lymphoid)
  2. Lymphoma
    • neoplastic lymphocytes originate in solid tissue
    o lymphoid tissue outside the bone marrow eg lymph node, spleen, liver, intestine, skin
    o IF IN BLOOD – Stage V lymphoma
    How to differentiate
    o Look for original site of lymphoma – lymph nodes will be huge – will be a happy dog
    o Leukaemia – very sick, dead within a couple of weeks

Final exam (37 decks)

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