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ACVIM literature 2015-2019 > Revision notes > Flashcards

Revision notes Flashcards

1
Q

What disease processes have a strong/high recommendation for the use of antithrombotics?

A
  • IMHA
  • Feline cardiomyopathy
  • PLN
  • > 1 disease/risk factor for thrombosis
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2
Q

What disease processes should antithrombotics be considered to be used in but not always recommended?

A

moderate risk or only really risk if in combo with others:

  • pancreatitis (d)
  • glucocorticoids (d)
  • Cancer
  • Heart disease (d)
  • sepsis (d)
  • HyperA
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3
Q

What type of thrombosis is usually seen with IMHA?

A
  • PTE
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4
Q

What type of thrombosis is usually seen with feline cardiomyopathy?

A
  • Arterial (minimal evidence for venous)
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5
Q

What type of thrombosis is usually seen with PLN?

A
  • PTE >ATE> venous
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6
Q

What type of thrombosis is usually seen with pancreatitis (d)?

A
  • splenic vein thrombosis
  • ATE
  • portal vein thrombosis
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7
Q

What neoplasias are most commonly associated with thrombosis?

A
  • round cell
  • carcinoma
  • adrenal tumour
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8
Q

Are antiplatelet or anticoagulants recommended for venous thrombosis prevention? Give example of this

A
  • Anticoagulant

PTE due to HE => heparin superior to aspirin.

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9
Q

Are antiplatelet or anticoagulants recommended for ATE prevention? Give example

A
  • antiplatelet

Cats with FATE - clopidogrel

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10
Q

When is aspirin recommended?

A
  • prevention of ATE in dogs and cats
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11
Q

When is clopidogrel recommended?

A
  • prevention of ATE in dogs and cats
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12
Q

When should antithrombotic drugs be discontinued?

A
  • if high risk of thrombosis, should not be discontinued for invasive procedures but if multiple agents used, then reduce to single antiplatelet drug
  • for low to moderate risk of thrombosis, discontinue 5-7 days prior
  • if the underlying cause and the thrombus has resolved.

restart as soon as possible post op provided not ongoing bleeding.

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13
Q

What antithrombotics should be weaned before discontinuation?

A
  • UFH

- Direct Xa inhibitors.

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14
Q

What are other causes of feline pancreatitis apart from idiopathic?

A

> 95% = idiopathic.

  1. Infectious
    - parasites (Toxoplasma gondii, Eurytrema procyonis, Amphimerus pseudofelineus)
    - viruses (coronavirus, parvovirus, herpesvirus, calicivirus)
  2. Trauma inc surgery or hypotension
  3. Neoplasia
  4. Toxins:
    - topical fenthion
    - KBr
    - Phenobarb
    - hypercalcaemia
    - snake bite.
  5. Autoimmune
  6. With concurrent disease:
    - diabetes mellitus,
    - chronic enteropathies,
    - hepatic lipidosis,
    - cholangitis,
    - nephritis
    - IMHA
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15
Q

What are u/s findings of acute pancreatitis in cats?

A 
- equivocal 
or 
- pancreatic enlargement, 
- hyperechoic surrounding mesentery,
- focal abdominal effusion
- distension/corrugation of duodenum
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16
Q

What does a normal feline pancreas look like on MRI? and with pancreatitis?

A

Normal: T1 hyperintense and T2 isointense to hypointense

Pancreatitis:

  • T1 hypointensity
  • T2 hyperintensity of the parenchyma,
  • enlargement of the pancreas,
  • pancreatic duct dilatation
  • contrast enhancement.
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17
Q

What is the PPV and NPV of Spec fPL in sick cats?

A

Specific and sensitive - better with more severe cases.
PPV 90%
NPV - 76%

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18
Q

How should a “normal” and “abnormal” snap fPL be interpreted?

A
  • normal - unlikely to have pancreatitis

- abnormal - may have pancreaitis.

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19
Q

What is the difference in inflammatory cell types with acute suppurative vs chronic feline pancreatitis?

A

Acute - neutrophilic +/- necrosis, oedema

Chronic - lymphocytic or mononuclear + fibrosis or cysts

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20
Q

What are the treatment recommendations for feline acute pancreatitis?

A
  • treat any inciting cause
  • IVFT
  • Antiemetics (maropitant/ondans)
  • gastric prokinetics (metoclop may be contraindicated due to dopamine antagonism, but no clinical studies support this. otheriwse cisapirde ro erythomycin)
  • analgesia - buprenorphine/methadone/fent, maropitant, tramadol or gaba
  • appetite stim - mirtazapine or capromorellin + feeding tube if req
  • Gastrointestinal diet.

Abs and corticosteroids not recommended for the pancreatitis but may be indicated if concurrent disease would benefit from them

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21
Q

What are the treatment recommendations for feline chronic pancreatitis?

A
  • analgesia
  • nutrition support (no specific diet recommended)
  • antiemetic
  • appetite stim
  • cobalamin
  • pred at antiinflam or immunosuppressant levels provided not hyperglycaemia. if so consider cyclosporine.

Abs not recommended

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22
Q

What are the 5 main phenotypes of feline cardiomyopathy

A
  1. HCM
    - Diffuse or regional increased LV wall thickness with a nondilated LV chamber.
  2. RCM:
    - Endomyocardial form: prominent endocardial scar that usually bridges the interventricular septum and LV free wall, => fixed, mid-LV obstruction and often apical LV thinning or aneurysm;
    + LA or biatrial enlargement is generally present.
    - Myocardial form Normal LV dimensions (including wall thickness) with LA or biatrial enlargement
  3. Dilated cardiomyopathy (DCM)
    - LV systolic dysfunction with
    increase in ventricular dimensions,
    normal or reduced LV wall thickness,
    atrial dilatation.
  4. ARVC:
    - Severe RA and RV dilatation
    +/- RV systolic dysfunction and RV wall thinning.
    +/- left side affected
    - Arrhythmias and RSCHF
  5. Nonspecific phenotype/unclassified
    - A cardiomyopathic phenotype that is not adequately described by the other categories
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23
Q

What proportion of cats have HCM?

what are the main clinical presentations?

A
  • 15-30%

Presenation:

  • asymptomatic
  • CHF
  • FATE
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24
Q

What are the following genetic abnormalities associated with and in which breeds:

  • MyBPC3-A31P
  • MyBPC3-R820W
A

MyBPC3-A31P: myosin binding protein C in HCM in Maine Coon cats. = 35-42

MyBPC3-R820W: myosin binding protein C in HCM in ragdolls/

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25
Q

What are markers of increased risk of CHF or ATE in cats with HCM?

A
  • a gallop sound or arrhythmia
  • moderate to severe LA enlargement,
  • decreased LA fractional shortening (LA FS%),
  • extreme LV hypertrophy,
  • decreased LV systolic function,
  • spontaneous echo-contrast or intracardiac thrombus,
  • regional wall thinning with hypokinesis,
  • restrictive diastolic filling pattern
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26
Q

Is a palpable thrill (grade 5-6/6 murmur) in cats more likely associated with cardiomyopathy or congenital malformation?

A

Congenital malformation

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27
Q

What does an increased NT-proBNP in a cat with resp distress suggest?
What samples can it be checked on?

A
  • more likely cardiac than respiratory origin

- plasma or pleural effusion

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28
Q

What is NTproBNP used for in cats?

A

If echo is not available

Differentiate severe subclinical disease from mild or normal cats

differentiate cardiac or non-cardiac origin of resp distress/pleural effusion

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29
Q

What is normal end diastolic LV wall thickeness in most cats?

A

<5 mm

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30
Q

What treatment is recommended for stage B2 cardiomyopathy cats?

A
  • clopidogrel
    +/- aspirin
    +/- Xa inhibitor (rivaroxaban)
    (high risk - use additional meds, up to all 3)

If ventricular ectropy is present then atenolol or sotolol
if Afib - diltiazem, atenolol or sotolol

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31
Q

When should pimobendan be used in cats with cardiomyopathy?

A
  • CHF without dynamic LVOFTO, especially if signs o low cardiac output inc, hypotension, hypothermia, bradycardia (INI - dobutamine)
  • maybe chronic CHF without dynamic LVOFTO
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32
Q

Is thromboylic teatment recommended for cats with ATE?

A

no

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33
Q

In acute ATE, what drugs are recommended for cats?

When discharged home, what drugs are recommended?

A
  • analgesia (mu opioid)
  • anticoag - LMWH, uFH or Factor Xa inhibitor.
  • CHF management - frusemide, O2

at home:

  • clopidogrel + Factor Xa inhibitor
  • ongoing CHF management as appropriate
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34
Q

What are the different classes of pulmonary hypertension?

A

Group 1: pulmonary arterial hypertension including:

  • idiopathic
  • heritable
  • drugs (tramadol, cyclosporine, amiodarone, cyclophosphamide)
  • congenital hunts
  • pulmonary vasculitis
  • pulmonary vascular amyloid depoits

Group 2: secondary to left heart disease
- MMVD, DCM, outflow tract obstructions etc

Group 3: Secondary to respiratory disease, hypoxia or both:

  • chronic obstructive airway disease
  • pulmary parenchymal disease inc fibrosis, eosinofili pneumonia, infectious pnumoni, difffuse neoplasia
  • high altitude
  • westies - nonspecific interstitial pneumonitis (pred + mycophenolate)

Group 4: Pulmonary emboli, thrombi or thromboemboli.

Group 5 - parasitic (HW or angiostrongylus)

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35
Q

What are the pathophological causes of pulmonary hypertension and give examples?

A
  1. Increased pulmonary blood flow
    - L to R shunt eg PDA
  2. Increased pulmonary vascular resistance
    - pulmonary epithelial disease
    - vasc remodelling
    - perivasc inflam
    - vasc lumen obstruction
    - increased blood viscosity
    - arterial wall thickness
    - lung parenchyma destruction
  3. Increased pulmonary venous pressure
    - left heart disease
    - compression of large pulmonary vein
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36
Q

What areas are looked at on echo to assist in diagnosis of pulmonary hypertension?

A
  1. Ventricles
    - flatten IVS esp during systole
    - underfilling LV
    - RV hypertrophy
    - RV systolic dysfunction
  2. Pulmonary Artery
    - enlargement (PA/Ao >1.0)
    - early peak diastolic pul regurg > 2.5m/s
    - Right pul art distensibility <30%
    - R outflow doppler acceleration tie (<52-58m/s) pr acceleration time to jection ratio (<0.30)
    - systolic notiching of doppler RV outflow profile
  3. Right atrium or CVC enlargement
    * LA enlargement is a crude surrogate for chronically increased pul art wedge pressure
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37
Q

What measurements are used on echo to assess pulmonary hypertension?

A
  1. Peak tricuspid regurg velocity
    <3 - low
    3-3.4 - intermediate
    >3.4 - high probably of pul hypertension.
    Increased risk level if other echo signs of pul hypertension noted.
  2. Calc pressure gradient between RV and RA (= 4 x velocity {m/s}2) in diastole
    > 15mmHg supports diastolic pul art hypertension.
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38
Q

What are pre-capillary causes of pulmonary hypertension and what echo changes/measurements are expected?

A
  • Group 1 (pul art hypertension)
  • Group 3 (resp disease/hypoxia)
  • Group 4 (TE)
  • Group 5 (parasitic)

no La enlargement
mean PAP >25mHg
PAWP <15mmHg
Increased pulmonary vasc resistance.

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39
Q

What are the post-capillary causes of pulmonary hypertension and what echo changes/measurements are expected

A
  • Group 2 (Left heart disease)
  • Group 6 (multi-factorial)
  • La enlargement
  • PAP > 25mmHg

Isolated post:
Diastolic pressure gradient <7mmHg
Pul vasc resistance not increased

Mixed pre and post:
Diastolic pressure gradient >7mmHg
Pul vasc resistance increased

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40
Q

What is the recommended measurement of intermediate to high likelihood of pulmonary hypertension?

A

Tricuspid regug > 46mmHg
Tricuspid regurg velocity >3.4m/s
~moderate pul hypertension.

Take into account shoudl be present with clinical signs of pul hypertension as well.

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41
Q

When should echo be used to assess for pulmonary hypertension?

A
  1. if clinical signs + after physical exam and TXR rule out other causes
  2. If TXR shows
    - tortuous, blunted, or dilated pulmonary arteries;
    - asymmetric radiolucent lung fields
    - patchy, diffuse alveolar infiltrates
    - bulge in the region of the pulmonary trunk or right-sided cardiac enlargement
  3. Clinical signs + ascites or dilated CVC or hepatic veins.
  4. Suspected parasitic or high risk of PTE
  5. If CT shows:
    - A pulmonary trunk-to-descending aorta ratio ≥1.4170
    - Evidence of RA and RV enlargement
    - decreased pulmonary vein-to-PA ratio, increased pulmonary trunk-to-ascending aorta ratio, increased RV-to-LV ratio
    - pulmonary arterial filling defects
    - mosaic attenuation pattern showing small vessels in a region of decreased attenuation (ie, hypoperfusion) on an inspiratory scan that fails to show accentuation of the mosaic attenuation pattern on an expiratory scan (ie, ruling out air trapping)
    - Perivascular diffuse nodular to ill-defined patchy ground-glass opacity with a global distribution, compatible with pulmonary capillary hemangiomatosis (PCH) or pulmonary veno-occlusive disease (PVOD
  6. If histopath shows whide spread pulmonary vascular disease
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42
Q

What general recommendations are recommended for dogs with high probability of pulmonary hypertesion?

A
  • Exercise restriction
  • Prevention of infectious resp disease inc HW, antiostrongyulus and KC
  • Avoidance of pregnancy
  • Avoidance of high altitude and air travel
  • Avoidance of nonessential wellness procedures (eg, dental cleanings) and elective surgery requiring general anesthesia
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43
Q

With pulmonary hypertension, when is a PDE5i not recommended?

A

Group 1
- occlusive cellular or fibrotic vascular occlusive lesion (pulmonary vasculaitis or amyloid deposition) as could => pul oedema. Start in hospital if needed

Group 2
- uncontrolled LSCHF => pul oedema

All others, maybe useful? need to treat underlying disease first/concurrently.

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44
Q

What are the signs of pulmonary hypertension?

A

Strongly suggestive:

  • syncope esp with activity, with no other cause
  • Resp distress at rest
  • Activity or exercise terminating in resp distress
  • RSCHF

Possible pulmonary hypertension:

  • tachyponea at rest
  • increased resp effort at rest
  • prolonged post-exercise or post activity tachyponea
  • cyanotic or pale mucous membranes.
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45
Q

What are the signs of immune mediated RBC destruction?

A
  • Spherocytes (dog)
  • positive saline agglutination test
  • positive saline agglutination test that persists with washing
  • positive Coombes/Direct antiglobulin test or flow cytometry
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46
Q

What are signs of haemolysis?

A

Without funtion liver disease, post hepatic cholelestasis or sepsis:

  • hyperbilirubinaemia
  • significant bilirubinuria
  • icterus
  • Haemoglobinaemia
  • haemoglobinuria
  • RBC ghost cells.
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47
Q

What are non-immune mediated causes of spherocytes?

A
  • oxidative damage
  • acetaminophen
  • envenomation
  • hypersplenism (hepatosplenic lymphoma)
  • pyruvate kinase deficiency
  • RBC fragmentation (endocarditis, HSA, haemolytic uremic syndrome etc)
  • dyserythropoiesis.
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48
Q

What is the threshold of spherocytes seen in blood to be considered IMHA?
sens and spec of this?

A

> or = to 5 spherocytes/x100 oil immersion filed
63% sens
95% spec

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49
Q

What is the spec of saline agglutination test for detecting IMHA?

A

4:1 saline to blood = 100%

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50
Q

What is the sens and spec of Coombs/DAT for IMHA in dogs and cats?

A

Dog
Sens: 61-82%
spec: 94-100%

Cat
Sens: 82%
Spec: 95-100%

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51
Q

What anticoagulants are recommended (in order of preference) for IMHA management?
why?
When not to use?

A
  1. Unfractionated heparin (+/- antiplatelet)
  2. LMH or Factor Xa inhibitor
  3. Clopidogrel +/- aspirin
  4. Aspirin

Predominantly venous thrombosis => thrombi formation is more dependant on Coag/fibrin than PLTs.

Not if PLT <30

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52
Q

What drugs are recommended for immunosuppression in IMHA?

A
  1. Pred 2-3mg/kg or 50-60mg/m2/day for dogs >25kg

Second line:

  • Azathioprine
  • cyclosporine
  • mycophenolate.
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53
Q

When should a second line immunosuppressant be started in dogs with IMHA?

A

second line if:

  • severe, life threatening
  • PCV not stable with decrease >5% in 24h in the first 7 days of treatment
  • expected to have adverse reaction to pred
  • increased BUN or Tbili (negative prognostic factors in other studies)
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54
Q

When do you start weaning the immunosuppressants used for IMHA?

A

When the PCV/Hct has remained stable and >30% for 2 weeks after starting treatment,
+
an improvement in the majority of measures of disease activity (spherocytosis, agglutination, TBil level, reticulocyte count),
=> decreased prednisolone by 25%.

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55
Q

What infectious agents are associated with acute hepatitis?

A
  • toxoplasma
  • neospora
  • sarcocystis
  • Histoplasma
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56
Q

What infectious agents are associated with chronic hepatitis and what is the predominant inflammatory type?

A
  • Lepto - pyogranulomatous
  • Mycobacteria - granulomatous
  • Anaplasma - granulomatous
  • E. canis - mixed
  • babesia - non–suppurative.
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57
Q

What are the following mutations associated with? and in what breeds?

  • COMMD1 deletion mutation affecting ATP7B protein
  • ATP7A and ATP7B
A

Copper toxicity

  • COMMD1 deletion mutation affecting ATP7B protein - bedlington terrier
  • ATP7A and ATP7B - labrador.
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58
Q

What metabolic genetic conditions may be associated with chronic hepatitis and in what breeds?

A
  • alph-1 antitrypsin - cocker spaniels

- erythropoietic protoporphyria in German shepherds.

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59
Q

What is the earliest biochemical indicator of chronic hepatitis?

A

ALT followed by ALP then GGT

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60
Q

What staining can be used to provide a subjective assessment of copper accumulation?
Where does copper usually accumulate if pathologic?

A

Rhodanine/rubeanic acid staining

Pathologic = centrilobular
Periportal often non-specific:

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61
Q

What additional staining/techniques can be used to assess for infectious hepatitis on liver biopsies?

A
  • Acid fast: Mycobacteria
  • Periodic acid Schiff stain or silver stain: Fungi
  • FISH for bacteria
  • Immunohistochemistry for virus and protozoa
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62
Q

What treatment is recommended for copper hepatitis?

A
  1. dietary copper restriction
    + use distilled bottled water
  2. D penicillamine for 6-9m to normal ALT or on repeat biopsy + treat for further 1 month.
  3. Zinc after chelation
  4. SAMe or Vit E to reduce oxidative injury
  5. +/- immunomodulatory therapy
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63
Q

What immunomodulatory therapy is recommended for chronic hepatitis?

A
  • Pred +/- cyclosporine

maybe azathiopine or mycophenolate.

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64
Q

What are the criteria for stage B2 MMVD?

A
  • murmur intensity ≥3/6;
  • LA : Ao ratio in early diastole ≥1.6
  • Left ventricular internal diameter in diastole, normalized for body weight (LVIDDN) ≥1.7
  • breed-adjusted, vertebral heart score (VHS) >10.5. (or VHS >11.5 if breed adjustment to possible)

likely VLAS > or = 3

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65
Q

What medications are recommended fro dogs with stage B2 mMVD?

A

only pimobendan +/- cough suppressant

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66
Q

What is NT-proBNP useful for in dogs with clinical signs of heart failure?

A

if normal or near normal, then unlikely to be CHF and clinical signs are more likely to be pulmonary related.

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67
Q

What disease are associated with systemic hypertension?

A
  • CKD
  • AKI
  • DM
  • HyperA
  • Hyperaldosteronism
  • Phaeo
  • HypoT4
  • HyperT4
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68
Q

What toxicities are commonly associated with systemic hypertension?

A
  • Cocaine
  • Methamphetamine
  • 5-hydroxytryptophan (serotonin precursor)
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69
Q

What drugs may cause systemic hyper tension?

A
  • Glucocorticoids
  • DOCP
  • EPO
  • Phenylpropanolamine
  • Phenylephrine
  • Pseudoephedrine
  • Ephedrine
  • Toceranib
  • Cyclosporine (humans)
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70
Q

What brain damage can be seen with hypertension?

A
  • Encephalopathy (white matter oedema: occipital and parietal lobes)
  • Vascular accidents
  • Cranial cervical myelopathy (ischaemic) in old cats: tetraplegia.

CSx: altered mentation, seizures, vestibular signs, focal CN deficits.

Higher risk with rapid hypertension or hypertension greater than 180mm Hg.

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71
Q

What are the recommended first line drugs for hypertension in dogs and cats?

A

Dog - ACEi +/- amlodipine of SBP >200mmHg

Cats - amlodipine

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72
Q

What medications are recommended for the management of hypertension in patients with phaeo?

A

phenoxybenzamine (alpha adrenergic block)

+/- beta blocker (atenolol) once alpha adrenergic stim is well controlled.

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73
Q

What treatment is recommended in patients with SBP >180mmmHg and signs of intracranial target organ damage?

A

Emergency treatment.
If sustained hypertension, need to incrementally decrease BP otherwise hypoperfusion => need to be titratable drug

  1. Fenoldopam (dopamine-1 agonist): renal arterial vasodilation ** (none of the others do this), natriuriesis and increased GFR.
  2. Labetalol: alpha and beta antagonist
  3. Hydralazine: smooth muscle relaxant (direct vasodilator)
  4. Nitroprusside: NO vasodilator
  5. Phentolamine: alpha blocker, reported in phaeo surgery

If no TOD => Hydralazine or amlodipine to reduce BP faster.

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74
Q

What antibodies to borrelia burgdorferi are only present in naturally infected dogs, not vaccinated?

A

antibodies against:

  • C6
  • VLsE (variable major protine-like sequence, expressed)
  • OspF
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75
Q

Antibodies to what are stimulated by vaccination against B.burgdorferi?

A
  • OpsC
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76
Q

What antibodies to borrelia burgdorferi are present in both naturally infected and vaccinated dogs? What does this mean from a testing perspective?

A
  • OpsC

If not vaccinated and positive for Abs again OpsC then likely recent exposure.

If vaccinated and postivie for Abs against OpsC then could be exposure or vaccination => look at other abs that are not stim by vaccination (C6, VLsE or OspF)

**Presence of positive Abs doesn’t = cause of clinical signs or prediction of developing clinical signs.

77
Q

What testing is recommended to confirm borrelia b exposure in clinically unwell animals?

Which of these are quantitative and for what?

A

Serology with C6 based testing:

  • SNAP4Dx
  • SNAP4DxPlus
  • Lyme Quant C6
  • Vetscan canine lyme rapid assay
  • Accuplex4 test
  • Multiplex test.

Quantitative:

  • Lyme Quant C6 - for C6
  • Multiplex - OspA, OspC and OspF
78
Q

After treatment for lyme borreliosis what monitoring is recommended?
Why?

A

Measurement of quantitative titres to C6 +/- OspF before and 6 months post treatment

  • establish a new baseline post treatment
  • confirm reduction in antigenic load.
79
Q

What testing is not recommended for Lyme disease in clinically unwell animals?
why?

A
  • Whole cell ELISA
  • IFA
  • Western blot
  • cross reaction with other spirochete
  • IgM vs IgG because dogs do not usually present with acute illness.
80
Q

Should non clinical dogs with positive Bb serology be treated with antibiotics?

A
  • generally no.
81
Q

Should unwell or proteinuric dogs be vaccinated against lyme disease?

A
  • no
82
Q

What is the recommended treatment for lyme arthritis and lyme nephritis?

A

polyarthritis - doxycycline 10mg/kg/day for 1 month

Nephritis - doxycycline for 1-3 months
+/- mycophenolate +/- short course pred if patients are not responding to antibiotics alone + standard PLN management.

83
Q

When is it recommended to start anti-epilepsy medications?

A
  • Identifiable structural lesion present or previous history of brain disease or injury
  • Seizure ≥ 5 min duration
  • ≥ 3 generalized seizure in 24h
  • ≥ 2 seizures in 6 month period
  • Prolonged, severe or unusual postictal period.
84
Q

What initial drugs as monotherapy are recommended for dogs with seizures?

A
  • Phenobarbital
  • Imepitoin

+/- Bromide (less effective)

85
Q

When should a second anti-epilepsy medication be added?

What additional factors should be considered for this next medication?

A
  • increasing seizure frequency, severity (duration, cluster, post ictal) and overal QOL.

factors to consider:

  • Selection of an AED with a different MOA
  • Minimizing drug-drug interactions
  • Avoiding additive toxicity
  • Determination of risk-benefit of polypharmacy versus quality of life
86
Q

What adjunctive therapies could be considered for seizure managment?

A
  • Vagal nerve stimulation
  • accupuncture
  • dietary - use of medium chain triglyceride diet.
  • maybe CBD oil?
87
Q

What condition is most likely?

  1. ↑TSH, ↓ TT4, ↓ FT4, ↑ AntiTg Ab
  2. ↓ TSH, ↓ TT4
  3. ↓ TSH, ↓ TT4 + ↓ TRH
  4. ↓ TSH, ↓ TT4 + ↑ TRH
  5. ↑ TSH, normal TT4, ↑ AntiTgAb
  6. ↑ TSH, ↓ TT4, ↓ FT4, ↓AntiTgAb.
A
  1. ↑TSH, ↓ TT4, ↓ FT4, ↑ AntiTg Ab
    - overt lymphocytic/immune med hypothyroidism
  2. ↓ TSH, ↓ TT4
    - sick euthyroid
    - Secondary hypothyroid
    - Tertiary hypothyroid
  3. ↓ TSH, ↓ TT4 + ↓ TRH
    - Tertiary hypothyroid
  4. ↓ TSH, ↓ TT4 + ↑ TRH
    - secondary hypothryoid
  5. ↑ TSH, normal TT4, ↑ AntiTgAb
    - subclinical lymphocytic/immune med hypothyroidism
  6. ↑ TSH, ↓ TT4, ↓ FT4, ↓AntiTgAb.
    - likely non-inflammatory, atrophic, hypothryoidism
    (ddx sick euthyroid can occasionaly have increased TSH but not routinely)
88
Q

What genetic mutation is associated with pituitary hypoplasia?
What are the clinical signs?
What hormone production is reduced?

A
  • LHX3
  • proportionate dwarf with secondary hypothyroidism.
  • Malformation of atlantoaxial joint.

↓ Growth Hormone
↓TSH
↓ Prolactin
↓ Gonatotropin

  • ACTH ok.
89
Q

What is LHX3 mutation asssociated with?

What is the treatment?

A

Combined pituitary hormone deficiency
(↓ Growth Hormone, ↓TSH, ↓ Prolactin, ↓ Gonatotropin, normal ACTH)

  • Levoxythryine
  • Porcine growth hormone or progestin (medroxyprogesterone acetate)
90
Q

What infectious disease can cause primary hypothyroidism?

A
  • leishmania
91
Q

What are the two different types of congenital hypothyroidism and what is the clinical difference?

A
  1. Hypothalamic-pituitary acid deficit (Central congenital hypothyroidism)
    => TSH deficiency +/- ↓GH and Prolactin
    - Giant schnauzer
    - no goitre
  2. T4 receptor deficiency or or TPO mutation.
    Occurs with:
    iodine deficiency (dam or pups), dyshormonogenesis or thyroid dysgenesis.
    => goitre
    => dysproportionate dwarfism (cretinism)
92
Q

What coagulation factors could be affected by hypothyroidism?

A
  • Factors VIII and IX
  • vWF
  • Platelet adhesion.
93
Q

What changes with thyroid scintigraphy are expected with:

  • Normal dogs
  • Primary hypothryoidism
  • Secondary hypothryoidism
  • Congenital iodination defects
  • non-thyroidal illness
  • Thyroiditis
A
  • Normal dogs: 1:1 thyroid to salivary gland uptake
  • Primary hypothryoidism: <0.33 uptake and small gland
  • Secondary hypothryoidism: low/undetectable uptake
  • Congenital iodination defects: normal to increased uptake with low TT4
  • non-thyroidal illness - normal
  • Thyroiditis - can be false +ve with normal to increased uptake in hypothyroid dogs.
94
Q

What potential neurological changes are seen with hypothryoidism?

A
  • CP defecit
  • reduced spinal reflexes
  • Cranial nerve dysfunction
  • facial
  • vestibulochoclear (Vestibular)
  • trigeminal
  • laryngeal paralysis?
95
Q

What radiation is produced from I131 therapy? and what does it induce?

A
  • gamma rays and Beta particles.

B-particles=> ionising effect => follicular cell death.

96
Q

How does carbimazole/methimazole control hyperthyroidism?

A
  • concentrated within thyroid gland and inhibits:
  • oxidation of iodine
  • organification
  • couple of T3 and T4 via inhibition of thyrogloblin peroxidase
    => inhibites synthesis of thyroid hormones
  • no peripheral effects.
97
Q

What is a “cold nodule” on thyroid scintigraphy?

A
  • no uptake suggestive of either poorly differentiated or other type of thyroid tumour.
98
Q

What scintigraphy findings are suggestive of thyroid carcinoma?

A
  • ectopic tissue/mets
  • mediasteinal mass
  • distorted thryoid gland
  • multiple foci of uptake
  • hterogenous or irregular margins
  • extension into the thoracic inlet
  • linear multifocal uptake => suggest extension along fascial planes.
99
Q

On scintigraphy, what aspects assist in determining if a thyroid mass is resectable or functional?

A

resectable:

  • solitary
  • homogenous
  • well defined borders

Function:

  • homogenous and diffuse uptake.
  • usually grader the 1:1 update with salivary gland
100
Q

What medications can interfere with scintigraphy?

A
  • methimazole
  • ioheol/iodine contrast
  • ketamine and midazolam
101
Q

What is the recommended managment options for canine thyroid tumours?

  • no mets
  • non-resectable or incomplete resection
A

no mets + resectable = surgery.

non-resectable:
- debulking + chemo/I131/radiation
- radiation MST 2y
- I131
- Chemo:
metronomic chlorambucil (2y)
Doxo - 9m
palladia 6m
Cisplatin 3m
102
Q

What is the renal tubular threshold for glucose in dogs and cats?

A

Dogs - 10-12mmol/L

Cat - 11-16mmol/L

103
Q

What are the blood glucose targets in diabetes management for?

  • all values
  • average
  • nadir
  • duration of effect
A
  • all values: <17mmol/L
  • average <14mmol/L
  • nadir 4.5-7.3 mmol/L and occurring < 8h or >12h after injection.
  • Duration of effect -10-14h.
104
Q

Why are diabetic patients polyphagic?

A

Inability of glucose to enter satiety center in the brain => ongoing stimulation.

105
Q

What dose stomatostatin do in relation to blood glucose control? What are 3 drugs that mimic this effect?

A

Stomatostatin - growth hormone inhibiting hormone
- inhibits secretion of insulin and glucagon.
- inhibits growth hormone release
=> decreases/stabilizes blood glucose

Stomatostatin analogues:

  • Pasireotide
  • Lanreotide
  • Octreotide
106
Q

A reduced sensitivity to glucose by which transporter is associated with insulin resistance in cats?

A
  • GLUT-4
107
Q

When is a diabetic cat considered to be in remission?

A

no insulin + 4 weeks of normoglycaemia

  • Blood glucose between 4.5-7mmol/L
  • fructosamine <350umol/L
108
Q

What is hyperosmolar hyperglycaemia?

When does this mean for treatment?

A 
blood glucose >34mmol/L
Osmolality >350mosm/kg
- no ketosis
\+/- acidosis (lactic vs BHB so could be DKA)
Dehydration
  • Has often been going on much longer than DKA
  • Need to rehydrate first before giving insulin
  • slowly reduce blood glucose as rapid changes in BG can lead to risk of cerebral oedema from ECF osmolality changes.
  • aim for 2.8mmol/L/h reduction in blood glucose.
109
Q

What are the aims of DKA treatment?

A
  • restore hydration/water and elyte losses (K+, phos, Na+ and Mg+)
  • Give adequate insulin to suppress liposysis, ketogenesis and hepatic gluconeogenesis
  • correct acidosis (IVFT +/- biocarb)
  • Identify factors that precipitated DKA
  • Provide carbohydrate source when needed to allow ongoing insulin without hypoglycaemia
  • slowly return to normal over 24-48h
110
Q

When should you change to SC insulin from CRI in DKA patients?

A

Blood glucose <14mmol/L

  • no ketones
  • off IVFT
  • eating well.
111
Q

What changes are expected with eletrolytes with DKA and during DKA treatment?

A

K+, Mg++, Phos and Na+
- lost during DKA but serum levels variable and may be normal, ↓ or ↑

With insulin => moved intracellular or increased losses through urine
=> ↓ K+, ↓Mg++, ↓Phos, ↓Na+
all should be supplemented with insulin

↓ Mg+ =>
↓ K+ (loss via kidneys)
↓ Ca++ (due to inhib of PTH by ↓ Mg+)
↓ Na+

112
Q

What is the primary ketone produced with DKA ? How is this measured?

A

BHB

  • need to check blood levels as not detected with urine ketones.
  • can use plasma on dipstick to rule OUT DKA.
113
Q

What hormones are increased with reduced insulin?

A

↑ homone sensitive lipase => ↑lipolysis => ↑ FFA

↑Glucagon > ↑ ketosis, insulin resistance, hepatic glucose production (gluoneogenesis glycogenolysis) and ketogenesis

↑ Cortisol and growth hormone => ↑ lipolysis + block insulins action in peripheral tissues

↑ adrenaline => ↑ insulin resistance

114
Q

What are the areas of the adrenal cortex and what hormones do they predominantly produce?

A

Zona glomerulosa - aldosterone
- lacks 17aHydroxylase to make others.

Zona Fasiculata - cortisol

Zona reticularis - sex hormones

  • all areas make corticosterone and all need cholesterol/LDL
115
Q

What region of the pituitary are most masses associated with PDH located?

A

80% pars distalis

20% pars intermedia

116
Q

What other tumours can produce ectopic ACTH?

What would this show on HDDST and imaging?

A
  • hepatic carcinoma
  • metastatic neuroendocrine tumour
  • lung carcinoma
  • phaeo

No suppression with HDDST
Normal pituitary size
Bilateral adrenomegaly.

117
Q

What is the sens and spec of UCCR for HyperA diagnosis in dogs?
What are the limitations of this?

A

Sens: 995
Spec:77%

Limitation: screening only. if increased then need to do confirmation test

118
Q

What is the sens and spec of ACTH for HyperA diagnosis in dogs?
What are the limitations of this?

A

Sens: 57-90%
PDH - 80%
AT - 60%
Spec: 60-90%

Limitation:

  • lower sens than LDDST esp for adrenal tumour
  • doesn’t differentiate AT vs PDH
  • Iatrogenic and hypoA both low
  • Affected by glucocorticoids, progreatgens, ketoconazole.
  • can be low with adrenal tumours.
119
Q

What is the sens and spec of LDDST for HyperA diagnosis in dogs?
What are the limitations of this?

A

Sens: 85-1005
Spec: 44-75%

Limitation:

  • false positives with non-adrenal illness and stress
  • can only confirm PDH not AT
  • Drugst that affect cytochrome P450 may also impact strest results eg phenobarb may not show suppression due to increased P450
120
Q

What findings is consistent with hyperA for:

  1. UCCR
  2. ACTH stim
  3. LDDST
A
  1. UCCR - elevated
  2. ACTH stim - post ACTH cortisol increased
  3. LDDST - 8h post dex cortisol > lab cut off
121
Q

Which tests can be used to help differentiate PDH from AT?

A
  1. LDDST
  2. HDDST
  3. eACTH
  4. CRH Stim or ADH response test
  5. Imaging
122
Q

What LDDST results can be see with PDH?

A
  • no suppression
  • 8h no suppression + is <50% of basal cortisol
  • 8h no suppression + 4h suppression or 4h is <50% of basal cortisol.

Inverse pattern:
4h no suppression but 8h suppression.
=> suspicious - do second test.

123
Q

What LDDST results are seen with AT?

does this confirm AT?

A
  • no suppression at 4 or 8h

Doesn’t confirm AT.

124
Q

What HDDST results are seen with PDH?

A
  • no suppression
  • suppress below the lab cut off at 4 or 8h
  • suppress to <50% of basal cortisol at 4 or 8h
125
Q

What HDDST results are seen with AT?

does this confirm AT?

A
  • no suppression.

doesn’t confirm AT

126
Q

What are the limitations of eACTH to differentiate AT from PDH?

A
  • labile
  • grey zone
  • episodic ACTH secretion
  • strees, ectopic ACTh and food stimulated hyperA can cause discordant results.
127
Q

What findings would be expected with eACTH for:

  • Adrenal tumour
  • PDH
A

AT - no eACTH due to negative feedback

PDH - increased eACTH to due excessive production by pituitary.

128
Q

What findings would be expected with ADh stimulation test for:

  • Adrenal tumour
  • PDH
A

AT - no increase in cortisol with ADH/desmopressin

PDH- >10% increase in cortisol from baseline with desmopressin.

129
Q

How can food dependant hyperA be diagnosed?

A
  • doubling of UCCr in response to food
  • low plasma eACTH without an adrenal tumour but bilateral adrenal enlargement
  • prevention of meal induce increase in cortisol with the use of octreotide.
130
Q

What findings are suggestive of an adrenal carcinoma?

A

> 2cm

  • perpheral fibrosis
  • capsular invasion
  • haemorrhage and necrosis/red and friable
  • mets.
131
Q

What testing is recommended to diagnose feline hyperA?

Sensitivity?

A
  • LDDST

sens: “100%” at 8h

132
Q

What endocrine disease can ear tip curling in cats be associated with?

A

Ear tip curlin g- feline hyperA.

133
Q

What are more common clin path abnormalities in cats with hyperA?

A 
↓ K+
↓ Mg+
↓ RBC
↓ Albumin + ↓total Ca
diabetic neuropathy
↑ globulins.
134
Q

What treatment is recommended for cats with hyperA?

A
  • Surgery - hypophysectomy or uni/bilateral adrenalectomy
  • trilostane
  • radiation (pituitary)
  • Metyrapone: inhibits 11beta-hydroxylase enzyme that converts 11-deoxycortisol to cortisol, proved effective at least transiently in controlling clinical signs. suitable for pre-op stabilization.
135
Q

How is feline hypoA different from canine?

A
  • can occur with lymphoma commonly
  • ACTH stim test with cortisol at 0, 30 and 60 min and give 1/2 vial IM
  • much slower reponse time. Takes 3-5 days.
136
Q

What disease does hypoA in dogs commonly mimic on lab results?

A 
1. liver failure
↓ Blood glucose
↓ Alb
↓ Cholesterol
↓ GI haemorrhage
↑ ALT and ALP
* BATT normal
  1. Renal failure
    - azotaemia + ↓ USG
    - anaemia
    - ↑ Ca++, ↑ Phos, ↑ K+
  2. Insulinoma
    ↑ ALP and ALP
    ↓ Glucose => hypoglycaemic seizures.
4. PLE
↓ Alb
↓ Cholesterol
GI haemorrhage
Non-regen anaemia.
137
Q

What CBC changes can be seen with hypoA?

A
  • anaemia - potentially non-regen or iron deficiency
    ↑ lymphocytes
    ↑ Eosinophils

normal, mildly ↑ or ↓ Neut with no stress leukogram.

138
Q

what are the medical management options for phaeo?

A
  1. phenoxybenxamine - a-adrenoreceptor blocker.
  2. Amlodipine - CCB. reduces hypertension and vasoconstriction
  3. B blocker - propranolo/atenolol - if tachycardia or tachyarrhythmia, but must have phenoxybenzamine effective first or => severe hypertension.
  4. Metyrosine - inhib the enz that catylases the rate limiting step in catecholamine synthesis => less produced.
139
Q

What testing can be used to confirm phaeo?

A

Urine metneprhine or normetnephrine testing. both higher in urine or plasma. compare with creatinien for ration. >4 x upper limit of normal

suspicious if low inhibin with AT in desexed dog.

140
Q

What conditions is ↑PTH seen in?

What do Ca+ and Phos do in these conditions?

A

Primary hyperPTH
↑PTH, ↑ iCa++, normal to ↓ phos

Secondary renal hyperPTH
↑PTH, normal to ↓ iCa++, normal to ↑Phos

141
Q

What conditions is ↑ Vit D3 (Calcitriol) seen in?

What do Ca+, Phos and PTH do in these conditions?

A

Primary HyperPTH:
↑ Vit D3, ↑iCa++, normal to ↓ phos, normal to ↑ PTH

↑ Vit D3/Calcitriol toxicity:
↑ Vit D3, ↑ iCa++, normal to ↑ phos, ↓ PTH.

142
Q

What do cats with idiopathic hypercalcaemia usually have for their:

  • phosphate
  • PTH
  • PTHrP
  • iMg
  • 25 hydroxyvit D
  • Calcitriol
A
  • all within ref range

only increased iCa++ with no evidence of malignancy and all other levels wnl.

143
Q

What medications should be given to patients with primary hyperparathryoidism perioperatively?

A
  • Vitamin D3 (Calcitriol) +/- oral Ca++ started 12-24h before surgery or after surgery

Acute hypocalcaemia => IV calcium gluconate.

144
Q

How do patients with central DI respond to:

  • water deprivation testing
  • ADH stimulation?

What is the treatment for central DI

A
  • unable to concentrate urine
  • respond to ADH stimulation
    complete central DI= >50% increase in urine osmolality
    Partial central DI = >15% increased in urine osmolality

treat with desmopressin + always have water available

145
Q

How do patients with nephrogenic DI respond to:

  • water deprivation testing
  • ADH stimulation?

What is the treatment for nephrogenic DI

A
  • unable to concentrate urine
  • no or minimal response to ADH => no increase in urine osmolality.

treatment:

  • low sodium diet
  • thiazide diuretic
  • always have water available.
146
Q

What is the difference between somatostatin and somatotropin?

A

Somatostatin = growth hormone inhibiting hormone (statins = stops)

Stomatotropin = growth hormone
(trophin = stimulate/grows)
147
Q

What cell type is this surface protein/s associated with?

Cytokeratin Ab AE1/AE3

A

Synovial cell sarcoma

148
Q

What cell type is this surface protein/s associated with?

ALP

A

Osteosarcoma

149
Q

What cell type is this surface protein/s associated with?

- Smooth muscle actin

A

Malignant fibrous histiocytoma

150
Q

What cell type is this surface protein/s associated with?

CD34+

A

ALL

151
Q

What cell type is this surface protein/s associated with?
CD3
CD4
CD8

A

T cell lymphoma

152
Q

What cell type is this surface protein/s associated with?
CD21
CD79a

A

B cell lymphoma

153
Q

What cell type is this surface protein/s associated with?

CD 11

A

MCT

154
Q

What cell type is this surface protein/s associated with?

CD117

A

Kit mutation - MCT

155
Q

What cell type is this surface protein/s associated with?

MUM

A

plasma cell tumour

156
Q

What cell type is this surface protein/s associated with?

RF4

A

Plasma cell tumour

157
Q

What cell type is this surface protein/s associated with?

Melan A

A

Melanoma

158
Q

What cell type is this surface protein/s associated with?

PNL 2

A

Melanoma

159
Q

What cell type is this surface protein/s associated with?

S100

A

Melanoma

160
Q

What cell type is this surface protein/s associated with?
CS1a
CD11c
CD18

A

Histocytic disease including

  • histiocytic sarcoma
  • haemophagocytic histocytic sarcoma (CD11d instead of CD 11c though)
  • feline progessive histocytosis ( + CD5)
  • Histocytoma (+ E cadherin)
  • Langerhans histocytosis (+ Ecadherin)
  • Reactive cutaneous or systemic histiocytosis (+ CD4 and CD90)
161
Q

What cell type is this surface protein/s associated with?

CD11d

A
  • haemophagocytic histiocytis sarcoma
162
Q

What cell type is this surface protein/s associated with?

CD5

A

feline progressive histiocytosis

T cells

163
Q

What cell type is this surface protein/s associated with?

Ecadherin

A

histiocytoma or langerhand histiocytosis

164
Q

What cell type is this surface protein/s associated with?

CD4

A

Tcells
thymocytes
monocytes

= MCH class II

165
Q

What cell type is this surface protein/s associated with?

CD 8

A

MCH class I => cytotoxic T cells

166
Q

What cell type is this surface protein/s associated with?

CD 9

A 
PLT
immature B cells
eosionophil
basophil
activated T cells
167
Q

What cell type is this surface protein/s associated with?

CD10

A

precursor T and B cells

168
Q

What cell type is this surface protein/s associated with?

CD 14

A

Macrophages

Granulocytes

169
Q

What cell type is this surface protein/s associated with?

CD15

A

NK cells

170
Q

What cell type is this surface protein/s associated with?

CD18

A

All leukocytes

171
Q

What cell type is this surface protein/s associated with?

CD19

A

B cells and dendritic cells but not plasma cells

172
Q

What cell type is this surface protein/s associated with?

CD21

A

B cells
some T cells
dendritic cells

173
Q

What cell type is this surface protein/s associated with?

CD117

A

c-Kit assoc with tyrosine kinase

174
Q

What cell type is this surface protein/s associated with?

CD54

A

= ICAM

vasc endothelial cells

175
Q

What cell type is this surface protein/s associated with?

CD56

A

NK cells and nerve cells

176
Q

What cell type is this surface protein/s associated with?’

CD66e

A

malignant intestinal cells

177
Q

What immunohistochem markers are found in :

histocytic sarcoma

A

CD1a
CD11c (CD11d = haemophagocytic HA)
CD18

178
Q

What immunohistochem markers are found in :

osteosarc

A

ALP

179
Q

What immunohistochem markers are found in :

synovial cell sarcoma

A

cytokeratin Ab AE1/AE3

180
Q

What immunohistochem markers are found in :

malignant fibrous histiocytoma

A

smooth muscle actin

181
Q

What immunohistochem markers are found in :

ALL

A

CD34

182
Q

What immunohistochem markers are found in :

Tcell lymphoma

A

CD3
CD4
CD8

183
Q

What immunohistochem markers are found in :

B cell lymphoma

A

CD21

CD79a

184
Q

What immunohistochem markers are found in :

MCT

A

CD11

CD117 (c-kit mutation)

185
Q

What immunohistochem markers are found in :

c-kit mutation

A

CD117

186
Q

What immunohistochem markers are found in :

Plasma cell tumour

A

MUM

RF4

187
Q

What immunohistochem markers are found in :

Melanoma

A

Melan A

PNL2S100

188
Q

What immunohistochem markers are found in :

histiocytoma

A

CD1a
CD11c
CD18

Ecadherin

ACVIM literature 2015-2019 (12 decks)

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