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Year 4 small animal > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Equipment for cardiac ultrasound

A

Cut out table
Chair/stool
Correct probe for patient
Ultrasound machine
Person to restrain

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2
Q

Environment needed for ultrasound

A

Quiet
Dark
Air conditioning (ideally)
Padded table
ECG pads

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3
Q

Preparation for cardiac ultrasound

A

Clipping
Spirit
Gel

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4
Q

Machine frequencies for cardiac ultrasound

A

Cats/small dogs 7.5MHz
Medium dogs 5MHz
Large dogs 2.5-3.5MHz

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5
Q

What does reducing gain do

A

Darken image

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6
Q

What are the right side views

A

Right parasternal long axis
Right parasternal short axis

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7
Q

What is the right parasternal long axis (4 chamber) view used to asses

A

Ventricle movement
Chamber diment
Valve morphology and motion
Left ventricle wall thickness and diameter/volume

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8
Q

How do you reach right parasternal long axis (5 chamber) view from (4 chamber)

A

Rotate probe anticlockwise 20° ift wrist to angle cranially

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9
Q

How do you get to right parasternal short axis view from parasternal long axis (4 chamber) view

A

Turn probe 90° thumb to bum
Tilt probe and slide up chest wall as necessary

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10
Q

What should the La:Ao be

A

<= 1.5 in dogs
<= 1.4 in cats

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11
Q

What shape is the aortic valve

A

Mercedes Benz sign

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12
Q

What does the ‘fish mouth’ view show

A

Left atrioventricular valve

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13
Q

What do you assess on cardiac ultrasound

A

Subjectively
- ventricular movement
- chamber dimensions
- valve morphology and motion
Quantitative
- left atrium diameter
- aorta diameter
- pulmonary artery diameter
- m-mode - EPSS, LV

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14
Q

What setting is best for measuring chamber size

A

M mode in dogs
In cats 2DE due to asymmetric hypertrophy

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15
Q

Key points on measuring in M mode

A

5% of dogs outside normal ranges
Some breeds have normals if not go off size
Ensure cursor between papillary muscles transacting LV in half for measuring

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16
Q

Clinical signs of left CHF pulmonary

A

oedema
Dyspnoea
Exercise intolerance
Cough
Not lying on chest
Fainting

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17
Q

Clinical signs of right CHF pulmonary

A

Ascites and pleural effusion
Exercise intolerance
Abdominal distension
Increased RR
Dyspnoea

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18
Q

When should you take a DV radiograph

A

Before either lateral

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19
Q

Where do you collimate for a cardiac radiograph

A

Thoracic inlet to caudal edge of scapula

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20
Q

Points for interpretation of radiographs

A

Assess technical quality
Don’t just look at heart and lungs
Assess respiratory system
Assess cardiac silhouette

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21
Q

What is the difference between deep and shallow chested dogs cardiac silhouettes

A

Deep chested much more upright and less contact with sternum
Shallow chested much more sternal contact

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22
Q

What is the vertebral heart score

A

Size of heart width + length compared to number of vertebral bodies
Normal total is between 8.5 and 10.5 vertebral bodies

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23
Q

How does pericardial effusion appear on radiography

A

Grossly enlarged cardiac silhouette
Distinct outline
Globular appearance

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24
Q

What classes as generalized heart enlargement

A

Heart takes up more that 2/3rds of the thorax

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25
Q

How does microcardia normally present

A

Hypovolemia

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26
Q

What are veins compared to arteries

A

Veins are central
Veins are ventral

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27
Q

How does HCM look of radiography

A

Heart shaped heart as two large atrial

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28
Q

How big is the normal feline heart

A

Width of 2 intercostal spaces
Normal DV heart width is 0.66 width of thorax at 5th rib

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29
Q

How does an old cats heart look on radiography

A

More horizontal
Prominent aortic arch

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30
Q

What is CHD

A

Congenital heart disease
Malformations of heart/vessels still present at birth

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31
Q

What are the different types of murmurs

A

Pathological - congenital/acquired
Physiological - anaemia
Innocent

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32
Q

Diagnostics for CHD

A

History/clinical exam give clues
ECG/radiography give clues
Echocardiography to diagnose

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33
Q

What should you do in practice with juvenile murmurs

A

Grade 3+ likely congenital abnormality
< Grade 2 reassess at 3/6 months

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34
Q

Atrial septal defect

A

Quiet to moderate systolic murmur
PMI at base
Right eccentric hypertrophy when severe
Can be incidental

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35
Q

Ventricular septal defect

A

Variable grade
PMI base of left and apex of right
Systolic murmur
Left ventricular eccentric hypertrophy
Small lesion is loud murmur

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36
Q

Aortic stenosis

A

Variable intensity, loud if severe
PMI left base to right
Systolic murmur
Left ventricular concentric hypertrophy
If severe poor pulses

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37
Q

Pulmonic stenosis

A

Variable loud if severe
Base left more than right
Systolic murmur
Right ventricular hypertrophy

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38
Q

Mitral valve dysplasia

A

Variable systolic murmur
PMI right apex
Right side volume load leading to eccentric hypertrophy

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39
Q

Patent ductus arteriosus

A

Usually loud continuous murmur
PMI at base and apex
Left side volume load with eccentric hypertrophy

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40
Q

Tetralogy of Fallot

A

Variable systolic murmur
PMI at base
Right ventricular hypertrophy
Shows cyanosis

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41
Q

What is aortic stenosis

A

Narrowing of the aorta
Common in boxers, newfoundland and golden retriever
Common type is sub-aortic stenosis
Signs - lethargy, exertional weakness, syncope, sudden death

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42
Q

What is patent ductus arteriosus

A

Blood shunting from aorta to pulmonary artery causing continuous murmur in axilla
Functional closure should occur in hours and permanent in days-weeks
Hyperkinetic pulses
Left sided congestive heart failure within 12 months
Surgical treatment

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43
Q

What are the 5 types of pulmonic stenosis

A

Infundibular
Sub-valvular
Valvular
Supra-valvular (rare)
Anomalous coronary artery

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44
Q

Signs of pulmonic stenosis

A

Many asymptomatic
Right sided heart failure, syncope, exercise intolerance, sudden death
2oclock bulge on x-ray
Prominent right apical beat
Radiation cranially/ventrally
Prominent jugular pulses
High frequency systolic ejection murmur

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45
Q

What is a VSD

A

Many different locations in dogs normally high in membraneous septum
Leads to volume overload of pulmonary trunk and circulation and LV and LA
CS - exercise intolerance and LCHF

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46
Q

Primary causes of heart disease

A

Chronic degenerative valve disease (mitral)
Heart muscle disease (cardiomyopathy)
Valve/endocardial infection
Pericardial disease
Rate/rhythm abnormalities

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47
Q

What equals cardiac output

A

HR + SV

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48
Q

Pathophysiology of heart failure

A

Cause leads to cardiac output falling leading to fall in blood pressure

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49
Q

What mechanisms restore BP

A

Sympathetic NS activation
RAAS
Cardiac enlargement

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50
Q

Chronic degenerative valvular disease

A

Regurgitation means fall in forward flow and therefore fall in cardiac output

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51
Q

Dilated cardiomyopathy cause of heart failure

A

Systolic failure leads to fall in stroke volume and therefore reduce cardiac output

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52
Q

What is HCM/RCM

A

Ventricle cannot fill so cardiac output falls

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53
Q

How does the sympathetic nervous system increase cardiac output

A

Brain tells heart to pump quicker/constrict vessels to increase pressure

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54
Q

Compensatory mechanisms for heart failure

A

Increased heart rate
Vasoconstriction
Increased contractility
Retention of salt and water
Cardiac enlargement

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55
Q

Treatment of heart failure

A

Many animals present with oedema
Manipulate mechanisms with to reduce fluid build up with diuretics, antagonist RAAS and vasodilate with pimobendan
Don’t overdo treatment

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56
Q

Types of left sided heart failure

A

Mitral valve
DCM
HCM
RCM

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57
Q

Right sided heart failure

A

Primary - tricuspid valve and pericardial effusion

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58
Q

Typical presentation of heart failure

A

Cough/dyspnoea
exercise intolerance
Collapse
Heart disease
Non-specific malaise/weight loss

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59
Q

What does digoxin do

A

Improves contractility
Causes arrythmias, slows heart rate, increases vagal tone, decreases sympathetic tone, alters baroreceptor sensitivity
Narrow therapeutic range not used first line

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60
Q

What does pimobendan do

A

Increases cardiac contractility, gold standard
Calcium sensitizing positive inotrope
PDEIII inhibitor - vasodilator
Antithrombotic

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61
Q

HCM/RCM treatment

A

Heart fills poorly so
Treatment - positive lusitropes (help heart relax)
Calcium channel blockers - diltiazem/verapamil
Beta blockers - propranolol, atenolol

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62
Q

Licensed product for HCM

A

Diltiazem

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63
Q

what is cyanosis

A

blueish discolouration of the skin and mucous membranes
occurs if 2g/dl or more of deoxyhaemoglobin is present

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64
Q

central vs perhipheral cyanosis

A

central - desaturation of arterial blood or presence of Hb derivative
peripheral - desaturation of blood due to regional reduction in flow

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65
Q

what is the normal o2 saturation of arterial blood

A

95-97%

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66
Q

at what o2 saturation does an animal become cyanotic

A

below 80%

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67
Q

what priority does cyanosis have

A

emergency as severely hypoxic
overrides all emergencies except arterial bleed
normally present mouth breathing and cyanotic as ‘hungry’ for air

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68
Q

what is the pericardial sac made up of

A

inner visceral layer and outer parietal layer

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69
Q

function of the pericardium

A

prevents distension within the chest cavity
reduces friction
equalises gravitational forces
prevents overdilation
regulation between stroke volumes

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70
Q

what ligaments hold the heart in position

A

to sterum via sterno-pericardial ligament and diaphragm via phrenico-pericardial ligament

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71
Q

what can go wrong with the pericardium

A

fill with fluid - blood, exudate, transudate
neoplasia
congenital disorders - pericardial peritoneal diaphragmatic hernias, pericardial cysts
constrictive

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72
Q

what does pathology within the pericardial space cause

A

cardiac tamponade leading to low cardiac output/shock short term and right sided congestive heart failure long term

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73
Q

why is the right side of the heart more effected in pericardial disease

A

there is a greater area of contact between the pericardium and the right ventricle than the left and the thinner walls put it at higher risk

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74
Q

CS of pericardial disease

A

acute - sudden onset exercise intolerance, collapse, shock, rapid death possible
chronic - history of ascites, progressive exercise intolerance, lethargy, GI signs, collapse
CS
jugular distension, +hepatojugular reflex, ascites, tachycardia, muffled heart sounds, weak femoral pulses, paleMM, tachypnoea/dyspnoea, GIT signs

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75
Q

diagnosis of pericardial disease

A

clinical signs
echocardiography - can see effusion, mass, herniation and cysts
ECG - tachycardia with small complexes and electrical alternans (base moves up and down)
radiography - globoid silhouette with sharp outline

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76
Q

treatment for pericardial disease

A

emergency care
oxygen
iv fluids
pericardiocentesis
pericardial strip

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77
Q

pericardiocentesis procedure

A

left lateral recumbency - sterile prep with local
ultrasound guided
place catheter between 4th and 6th intercostal space at level of costochondral junction
risk related to level of effusion

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78
Q

what does it mean if your pericardiocentesis sample clots

A

it is fresh blood and could be related to damage you have caused
if it doesnt clot it has been sat around and clotting factors have been exhausted

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79
Q

complications of pericardiocentesis

A

cardiac puncture
arrhythmias
dissemination of infection/neoplasia
atrial fibrillation
myocardial stunning
neoplasia will reoccur

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80
Q

acquired disorders causing pericardial disease in dogs

A

pericardial effusion
cardiac neoplasia - haemangiosarcoma, heart base tumours, mesotheliomas, lymphosarcoma
idiopathic
left atrial rupture
coagulopathies

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81
Q

acquired disorders causing pericardial disease in cats

A

congestive heart failure
FIP

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82
Q

haemangiosarcoma of the heart

A

geriatric dogs, often GSD
normally around right atrium/right auricular appendage
metastasis common - CT before surgical resection

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83
Q

tumours of the heart base

A

chemodectomas/ectopic thyroid carcinomas
common in geriatric/brachycephalic
around aortic arch
rarely metastasise but cant treat

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84
Q

mesotheliomas

A

from serous membranes into pericardium, pleura, peritoneum and tunica vaginalis
present in rchf
treat with pericardectomy

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85
Q

idiopathic pericardial disease

A

idiopathic haemorrhage
large breed - st bernards etc
cardiac tamponade and rchf
treated by pericardiocentesis to remove fluid, pericardectomy if reoccuring 3+ times

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86
Q

left atrial rupture

A

secondary to cvd with jet lesions from severe mitral regurge
acute tamponade/forward failure (not enough blood pumped leading to BP drop and shock
do not pericardiocentese
occasionally able to repair
ckcs common

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87
Q

PPDH

A

peritoneal pericardial diaphragmatic hernia
congential
weimaraners/persians predisposed, umbilical hernias/abnormal sterum associated
often incidental finding
gi signs and cardiac tamponade can be seen
surgical correction possible

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88
Q

constrictive pericardial disease

A

complication of long term pericardial effusion
cs - rchf, exercsie intolerance and collapse
diagnosis - diminished ecg complexes in all leads, easier with history
treatment - pericardectomy

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89
Q

treatment aims of congestive heart failure

A

aims - control salt and water retention, reduce cardiac workload - decrease afterload and physical activity/stress
improve pump function

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90
Q

standard chf therapy

A

triple/quad therapy
diuretics - control salt and water
pimobendan
ace inhibitors
aldosterone antagonists
+/- anti-dysrhythmic mediation

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91
Q

Stages if heart disease

A

a - high risk but no disorders
b1 - asymptomatic, no remodelling but structural disease. wieght control and monitoring
b2 - asymptomatic with cardiac remodelling - la enlargement. consider pimobendan. regular checks
c - clinical signs - double/triple/quad therapy

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92
Q

diuretics for heart disease

A

control oedema formation
loop - furosemide - first line, very potent , 3x daily but individually tailored, vasodilator if given IV. take care in cats as can lead to restrictive/hypertrophic diseases. Torasemide - sid but more expensive.
Potassium sparing - spirolactone - aldosterone antagonist to spare potassium

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93
Q

vasodilators for chf

A

ace inhibitors
venous dilators - decrease preload, reduce fluid build up (glyceryl trinitrate)
atrial dilators - reduce afterload by increasing output and reducing valve leakage (hyralazinel)

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94
Q

drugs to decrease salt and water retention

A

imadipril
enalapril
benazepril
ramipril
care for azotaemia and hypotension, monitor renal parameters

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95
Q

what is cardalis

A

combination of ace inhibitor - benazepril - and aldosterone antagonist - spirolactone
given once a day, small tablet and good for cats

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96
Q

when is pinobendan used

A

stage b2 and c chf

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97
Q

what is stage d chf

A

obvious clinical signs
progressively worsening
obvious clinical signs at rest
death

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98
Q

emergency CHF therapy

A

presentation - coughing, dyspnoeic, cyanotic, coughing up fluid, raised chest
furosemide - 2mg/kg initially then 1mg/kg hourly
oxygen supplementation
pimobendan IV
rest - avoid stress
sedation if necessary
anti-dysrhythmics as necessary
once stable - pimobendan and start spirolactone

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99
Q

extra management for chf

A

low salt diet
exercise regime - consistency and dont push them
aspirate fluid if enough to cause any dyspnoea

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100
Q

feline thromboembolic disease

A

treat/prevent
has classic presentation
echocardiography for any without history of heart disease
reoccurrence common 1/3rd will reclot
very painful, often screaming

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101
Q

clopidogrel function

A

inhibits platelet aggregation
fairly safe - some mild neutropaenia reported
bitter tasting
give in hcm to break down clots before they form

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102
Q

monitoring of chf

A

respiratory rate
coexisting diseases - can contribute to failure/therapies used

103
Q

complications of treatment for chf

A

renal insufficiency
electrolyte imbalances
potassium loss with furosemide
potassium retention with acei

104
Q

biomarkers for chf

A

can measure natriuretic peptides - bnp/anp - are expensive
markers of myocardial disease - troponins - not well validated

105
Q

what do you assess for in chf

A

efficacy of therapeutic regime
frequency of assessment determined by - failure severity, patient stability, economic guidelines
assess for side effects/toxicity - weight, blood profiles

106
Q

causes of intractable cough

A

unstable lchf
enlarged la
bronchomalacia
co-existing chronic airway disease

107
Q

ruptured chordae tendinae

A

present as acute emergency
severe dyspnoea, cyanotic
stressed

108
Q

pulmonary hypertension causes

A

alveolar hypoxia with vasoconstriction/remodelling
pulmonary vascular obstructive disease
pulmonary overcirculation
high pulmonary venous pressure
idiopathic

109
Q

pericardial effusion due to left atrial tear

A

acute bleed into pericardium
can present with acute tamponade and poor output
avoid pericardiocentesis as can move the clot

110
Q

what is tussive syncope

A

syncope associated with coughing/wretching/gagging
disposed mechanisms
- increased intrathoracic pressure = reduced venous return
- decreased cerebral blood flow due to increased cerebral pressure
- tachyarrhythmias
usually small breed dogs with chronic bronchitis/small airway disease, CDVD, collapsing trachea, brachycephalic

111
Q

complications of feline cardiomyoapthy

A

pleural effusion
refractory heart failure
thromboembolic disease

112
Q

thromboembolic disease in cats

A

complication of hcm, rcm, fucm
sudden onset and looks like neurological/trauma
clot in atrium due to static blood, endothelial damage and hypercoaguable blood
present - cold, cyanotic, paralysed hind limbs with absent pulses, hypothermic with painful firm muscles, can be sudden death
treat with analgesia - aspirin, clopidogrel, nursing care
1/3 survive

113
Q

CDVD

A

chronic degenerative valvular disease
laxity of valve lesions leading to prolapse
can get strike lesions on atrium

114
Q

pathology of valve disease

A

degeneration of mv/+tv (60% mv only )
most pronounced at free margins leading to proliferation of the fibroblasts in the spongiosa layer. inflammation/degeneration of the fibrous layer

115
Q

classes of valvular degeneration

A

1- small discrete nodules on edge of valve
2 - thickened irregular free edges
3 - grossly thickened/nodular with lesions extending to base of CT
4 - further severity of class 3

116
Q

reason for regurgitation

A

pressure in the aorta doesnt drop below 80mmHg where as in the atrium it’s ~10mmHg meaning when the valve doesnt function blood flows back into the atrium

117
Q

signalment for valvular disease

A

middle-old
small breeds CKCS/poodles/maltese
typical history of CHF

118
Q

murmur of mitral insufficiency

A

PMI - left apex radiating dorsally
murmur grade related to severity
significant if - grade 3+, heart rate >120, loss of sinus arrythmia, precordial thrill, dysrhythmia +/- pulse deficits
history - exercise intolerance, cough, breathlessness, dyspnoea, weightloss
murmur on CE

119
Q

radiographic abnormalities for MR

A

left cardiomegaly
straightening of distal trachea
increased cardiac silhouette
straightening of caudal heart border and loss of waist
left atrial tending - bulge in 2-3 o’clock

120
Q

radiographic abnormalities of TR

A

dorsal tracheal deviation
increased sternal/diaphragmatic contact
reverse D shape in DV
can see generalised cardiomegaly
RCHF signs - ascites, pleural effusion

121
Q

endocarditis

A

bacterial infection of endocardium - typically 1 or more valves
normally presents medically with and variable murmur
can have pyrexia, shifting lameness, lethargy, anorexia and weightloss

122
Q

causes of heart murmurs

A

innocent - no cause
physiological - change in blood viscosity
pathological - acquired heart disease

123
Q

what is systemic hypertension

A

persistently elevated systemic blood pressure

124
Q

what are the cut off values for hypertension

A

systolic >160
diastolic >80
normal increase of 1-3mmHg per year over 8.
sighthounds naturally 10-20mmHg higher

125
Q

how do you calculate blood pressure

A

BP = (stroke volume x heart rate) x peripheral vascular resistance

126
Q

Initiating causes of hypertension

A

chronic fluid accumulation due to increased cardiac output
persistently increased heart rate
chronic vasoconstriction

127
Q

perpetuating causes of hypertension

A

small arteries change - extravasation of plasma into the vessel walls
vascular smooth muscle hypertrophy - increased artery tone increasing blood pressure
kidney disease - abnormal salt level increase BP

128
Q

aetiology of hypertension

A

artefacts - stress induced
primary - idiopathic - rare
secondary - with underlying disease
- renal - dogs with CRF often have hypertension
- HAC - increases renal salt/water retention
- Hyperthyroidism - increased myocardial sensitivity to cathecolamines
- Diabetes mellitus - hyperglycaemia, overproduction of renin = vasoconstriction
- drugs
- diet

129
Q

clinical signs of hypertension

A

> 180mmHg or 30mmHg in 48h
Hypertensive retinopathy
Hypertensive encepalopathy
Proteinuria
Left ventricular hypertrophy

130
Q

measurements of BP

A

Direct - arterial catheter
Indirect - compressive cuff
Doppler - wear loud headphones , need training
Oscillometric - automatic but time consuming

131
Q

what size should the cuff be BP

A

40% the cuff site circumference

132
Q

treatment for hypertension

A

treat underlying disease
restrict salt in diet
Diuretics - emergency
beta blockers - reduce heart rate/contactility
ACEI - block RAAS
Ca channel blockers - vasodilate
Angiotensin II receptor blocker

133
Q

treatment goals for hypertension

A

reduce BP - <150/95
decrease proteinuria
alleviate CS

134
Q

Pulmonary hypertension

A

pulmonary circulation usually low pressure, low resistance, high capacitance
defined as systolic pulmonary artery pressure >35mmHg and diastolic >10mmHg
caused by alveolar hypoxia

135
Q

Clinical signs of pulmonary hypertension

A

suspect when persistent respiratory difficulty, fatigue and exercise intolerance without cause
common signs;
exercise intolerance, cough, respiratory difficulty, syncope
right sided murmur

136
Q

Diagnosis of pulmonary hypertension

A

Thoracic radiographs - cardiomegaly, enlarged pulmonary arteries, Right apical murmur, right sided heart failure sign
Echocardiography - RV hypertrophy (>1/2 LV thickness), RA enlargement, pulmonary artery dilation, flattened IVS

137
Q

Treatment of Pulmonary hypertension

A

Treat underlying disease
Sildenafil -effective in some but limited capacity for dilation
Pimobendan - inodilator, antithrombotic
Oxygen
Enothelin antagonists

138
Q

What causes pulmonary overcirculation

A

left to right congenital
leads to pulmonary arterial remodelling
raises perfusion pressure and damages pulmonary vessels

139
Q

pathophysiology of chronic pulmonary venous hypertension

A

can cause structural changes in pulmonary capillaries and increase arteriole resistance
pulmonary vascular resistance leads to pulmonary oedema

140
Q

VSD

A

left to right shunt between the cranial ventricles
should close after birth

141
Q

Patent ductus arteriosus

A

communication between the pulmonary artery and the aorta leading to hypertrophy of the right ventricle

142
Q

Pulmonic stenosis

A

common in dogs
thickened/distorted pulmonary valve due to distorted fusion of valvular cushions

143
Q

Dysplasia of right atrioventricular valve

A

common in cats
focal/diffuse thickening of valve leaflets
parts of valve leaflets may be fused with ventricular wall

144
Q

HCM

A

hypertrophic cardiomyopathy
enlarged heart with symmetrical concentric hypertrophy, more prominent in LV

145
Q

Heart neoplasia

A

dog - cardiac haemangiosarcoma , often in RA, are only common neoplasm

146
Q

Causes of enlarged abdomen

A

Fat
Fluid
Feotus
Flatus/flatulence
Faeces
Ftumour
Forganomegaly

147
Q

What should you always do is presented with a dog with ascites

A

ultrasound it’s heart

148
Q

Indications for thoracic surgery

A

Pulmonary - primary lung tumour, idiopathic pneumothorax, pulmonary FB, lung lobe torsion
Cardiac - vascular ring anomaly - PRAA, PDA, pericardiectomy, mitral valve repair
Miscellaneous - thymectomy, thoracic duct ligation, oesophagostomy, tracheal avulsion, exploratory

149
Q

Thoracoscopy points

A

gives the animal unilateral pneumothorax - on lateral
triangulate ports for vision

150
Q

How is best to ligate the bronchus in a lung lobectomy

A

triple layered staples for watertight seal

151
Q

Lung lobe popping

A

can produce tension pneumothorax - pressure building with breathing
air blebs can also do the same

152
Q

Pulmonary FB treatment

A

attempt endoscopic removal
lobectomy if too deep
have been known to migrate through abdomen and burst through flank

153
Q

Lung lobe torsion

A

can be secondary to pleural effusion
more common in deep chested

154
Q

Presentation of persistent right aortic arch (PRAA)

A

outpouching of the oesophagus
dont cope moving onto solid food so often PTS with breeder

155
Q

How can a PDA be treated

A

placement of an amplatz stent - expensive
can ligate - dont cut, just double ligate as will bleed a lot

156
Q

Pericardiocentesis

A

large bore cannula with 3 way stopcock
4/5/6th ICS on right below costochondral junction

157
Q

How do you remove a thymoma

A

median sternotomy

158
Q

Indications for pacemaker implantation

A

symptomatic bradycardia
advanced 2/3rd degree AV block
sick sinus syndrome
persistent atrial standstill (no P wave)
vasovagal syncope

159
Q

DCM

A

dilated cardiomyopathy
common in dog
impaired myocardial contractility with dilation of LV +/- RV
Tachyarrythmias are common
end stage of many diseases, diagnosis of exclusion

160
Q

Pathophysiology of HCM

A

eccentric hypertrophy of LV
systolic failure - forward - not enough blood to body as ventricle flabby and does not push with enough force
diastolic failure - backward - congestion, blood stuck in the heart
left atrial dilation with increase pressure

161
Q

signalment for HCM

A

breed - doberman, newfoundland, st bernard, lab, great dane, cocker, boxer, gsd
age - middle aged but reported as young as 6m
size - >12kg
males more severe but genders equally represented

162
Q

clinical DCM exam

A

tachycardia +/- arrythmias
variable pulses/deficits
LCHF+/- RCHF
soft MR/TR murmurs
with forward failure - pale MM, sluggish CRT and cool extremities

163
Q

ECG if dysrhythmic with DCM

A

Normal
wide +/- tall complexes

164
Q

Arrhythmogenic right ventricular cardiomyopathy

A

boxers.
myofibre atrophy, fibrosis, fatty infiltration - fibrotic heart
stage 1 - asymptomatic with ventricular arrythmias
stage 2 - symptomatic - normal heart size and lV function but dogs syncopal/weak
stage 3 - CHF, poor myocardial function, CHF and ventricular arrhythmias
CS - ventricular arrythmias, syncope, sudden death
Diagnosis - 25 holter
Treatment - treat LCHF, anti-arrhythmic, sotalol commonly used

165
Q

Myocardial diseases in the cat

A

HCM - hypertropic
RCM - restrictive
DCM - dilated
ARVC - arrhythmogenic right ventricular
FUCM - feline unclassified

166
Q

how do cats present

A

dyspnoeic - panting - cats dont pant!!
heart failure
EMERGENCE

167
Q

what is anaemia

A

a decreased haematocrit, pcv or haemoglobin

168
Q

what is pcv

A

percentage of packed red cells within blood volume

169
Q

signs of anaemia

A

inadequate perfusion - pale MM, lethargy, exercise intolerance
compensatory mechanism - tachypnoea, tachycardia
other sign - poor pulse, haemic/flow heart murmur
signs related to underlying pathology - splenomegaly, lymphadenopathy, pain, pica, icterus, malaena

170
Q

grade of anaemia

A

none - canine 41-58, feline 31-48
mild - canine 30-40, feline 25-30
moderate - canine 20-30, feline 15-25
severe canine <20, feline <15

171
Q

RBC indices for anaemia

A

MCV - mean corpuscular volume, changes with large/small RBCs
MCHC - mean corpuscular haemoglobin concentration - amount of haemoglobin in RBCs, also affected by cell volume

172
Q

Regeneration factors

A

reticulocytes = regeneration - MCV increases
Anisocytosis = variable RBC size
nucleated RBCs, basophilic stippling, howell-jolly bodies, heinz bodies

173
Q

regenerative vs non-regenerative anaemia

A

regenerative - haemorrhage/haemolysis body actively trying to put out more rbcs
non regenerative - decreased bone marrow production, can be pre-regenerative or through chronic haemorrhage leading to non-regenerative

174
Q

what is the most common cause of haemolysis

A

IMHA
reaction to normal self antigen
primary immune dysfunction with loss of tolerance
can be reaction to infectious antigen bound to cell surface

175
Q

causes of non-regenerative anaemia

A

intra-marrow - infection, chronic damage, neoplasia, lack of raw materials
extra-marrow - ckd, excessive oestrogen, some types of FeLV

176
Q

clinical signs of anaemia

A

pallor
icterus
tachypnoea
pyrexia if infectious
weak, thready, bounding or absent pulses, cold extremities
haematemesis, melaena
trauma
collapse, coma, death

177
Q

treatment of anaemia

A

stabilisation
- oxygen
- temperature management
- fluid therapy
- analgesia
treat concurrent conditions
confirm and characterise anaemia
Tfast, radiography, abdominal ultrasound
haematology/biochemistry
blood products

178
Q

treatment of haemolysis

A

immunosuppressive therapy
glucocorticoids
adjunct agents - azathioprine, mycophenolate mofetil, ciclosporin, leflunomide

179
Q

Babesia

A

intracellular protozoa transmitted by ticks
CS - pallor, jaundice, pyrexia, haemoglobinuria, cardiovascular compromise, weakness, inappetance
treatment - imidocarb (unlicensed), azythromycin and doxycycline
NO corticosteroid

180
Q

oxidative damage

A

caused by heavy metals and rape/kale/cabbages and some drugs
oxidation of haemoglobin to heinz bodies

181
Q

Ehrlicha

A

tick transmission
CS - grumbling thrombocytopaenia, hyperglobulinaemia, depression, fever, weight loss, poor appetite, enlarged lymph nodes, epistaxis, petechiae, ecchymoses
Treatment - doxycycline

182
Q

CME - chronic monocytic ehrlichia

A

profound thrombocytopaenia
non-regenerative anaemia
emaciation
swelling of hindlegs/scrotum
uveitis/neuro signs from thrombocytopaenia
glomerulonephritis from hyperglobulinaemia
Doxycycline to treat

183
Q

in what breed is macrocytosis normal

A

poodles

184
Q

in what breed is microcytosis normal

A

Akitas

185
Q

what are codocytes

A

bullseye appearance erythrocytes with haemoglobinised area surrounded by pallor with haemoglobin band around the outside
seen in iron deficiency, liver disease, cholestasis and after splenectomy

186
Q

what are schistocytes

A

irregular fragmented erythrocytes
markers of DIC
fragment with trauma
seen in IMHA, thrombosis, haemangiosarcoma, glomerulonephritis, CHF, valvular heart disease, doxorubicin toxicosis and myelofibrosis

187
Q

what does rouleaux formation indicate

A

inflammation related to plasma being ‘sticky’ with increased globulin

188
Q

how does the saline agglutination test work

A

mix 1 drop blood with 1 drop saline
agglutination will persist, rouleaux will disperse

189
Q

regenerative anaemia signs

A

basophilic stippling - small dark blue aggregates in RBCs, associated with intensely regenerative anaemia but also with lead poisoning
nucleated erythrocytes - early release of RBCs
howell-jolly bodies - darkish blue remnants in RBCs

190
Q

mycoplasma haemofelis (haemobartonella felis)

A

pleomorphic, can appear as chains, discs or rods, superficial or embedded into RBC membranes
Diagnosed on PCR
CS - regenerative anaemia, pyrexia and malaise

191
Q

misleading blood results

A

MCV - swelling or shrinkage, misidentification with pairs/triplets in analyser
High MCHC - rbcs dont tend to cram in extra haemoglobin
RBCs can be miscounted/mistaken for platelets

192
Q

anaemia classification

A

Normocytic normochromic - anaemia of illness/pre regenerative, rarely non-regenerative
macrocytic hypochromic - highly regenerative
microcytic hypochromic - iron deficiency - chronic blood loss, without anaemia - portosystemic shunt

193
Q

what is relative polycythaemia

A

apparent increase in RBC due to decrease in circulatory fluid - often increases in TP/albumin
no increased RBC production
fear/excitement/pain can cause splenic contraction which can cause this
will resolve with time/rehydration

194
Q

absolute polycythaemia

A

increase in RBC mass due to increased production
Primary polycythaemia - rare myeloproliferative disorders, abnormal response of RBC precursors, normal EPO
secondary polycythaemia - chronic renal tissue hypoxia, renal tumours or cysts likely, increased EPO

195
Q

what care do you need to take with digoxin

A

can gave animals absolutely any rhythm abnormality

196
Q

primary causes of dysrhythmias

A

structural heart disease
metabolic
electrolyte disorders
trauma
drugs/toxins
sepsis and neoplasia

197
Q

when do you treat dysrhythmias

A

if treatment will improve survival or to alleviate clinical signs
disturbances if rate is too low or too high as cardiac output falls due to lack of contraction or lack of time for heart filling

198
Q

Bradydysrhythmias

A

variations of sinus arrythmia - not clinically significant
Clinically significant
- high grade 2nd degree AV block - lots of P waves not conducted
- 3rd degree block
- sinus arrest - secondary to hyperkalaemia
- sick sinus syndrome - SAN not firing
- atrial standstill - long sinus pauses
CS - weakness, lethargy, syncope
Treatment - treat primary issue eg. electrolyte disturbances, place pacemaker

199
Q

anti-dysrhythmic drug classes

A

class 1 - block sodium channels eg lidocaine
class 2 - beta blockers eg propranolol/atenolol
class 3 - potassium channel blockers eg sotalol/amiodarone
class 4 - calcium channel blockers eg diltiazem/verapamil

200
Q

management of supraventricular tachydysrhythmia

A

diltiazem/sotalol PO or
verapamil IV

201
Q

management of ventricular tachydysrhythmia

A

sotalol PO
lidocaine IV

202
Q

when to perform blood transfusion

A

decision based on; tachycardia, poor pulses, weakness, tachypnoea, collapse
PCV <20% dogs, <10-15% cats

203
Q

types of immunodeficency disorders

A

congenital - primary
acquired - FPT, chronic infection, inflammatory/neoplastic disease, drugs, malnutrition, toxins, stress

204
Q

immune system neoplasia types

A

lymphoid cell neoplasia
common - lymphoma, lymphoid leukaemia, cutaneous histiocytoma
rarer - multiple myeloma, plasmacytoma, histiocytic sarcoma

205
Q

Major immune diseases

A

haemolymphatic - IMHA, IMTP, immune mediated neutropenia
endocrine - hypothyroidism, hypoadrenocortism
cutaneous - canine dermatomyositis, discoid lupus erythematosus (DLE), pemphigus-pemphigoid complex
Musculoskeletal/neuromuscular - polyarthritis, myasthenia gravis, polymyositis/polyneuritis
CNS - MUO, granulomatous meningioencephalitis
GI - IBD/chronic enteropathy
Pancreatitis
Renal - glomerulonephropathies
Multi-systemic involvement - systemic lupus erythematosus (SLE), polyarthritis and meningitis, pancreatitis and dry eye.

206
Q

types of shock

A

cardiogenic
hypovolaemic
distributive
cryptic
obstructive

207
Q

signs of hypovolaemic shock

A

pale
slow crt
high HR
low rectal temp
weak pulses
increased RR

208
Q

signs of distributive shock

A

red MM
short/fast CRT
high HR
pyrexia
bounding pulses
increased RR

209
Q

signs of obstructive shock

A

pale
increased CRT
increased HR/RR
low temp
poor pulses
metabolic acidosis

210
Q

signs of cardiogenic shock

A

primary cardiac disease
pale
slow CRT
heart rate - high/low/arrythmic
low temp
pulses- weak/deficits
RR high

211
Q

feline blood groups

A

A (weak anti-type B)
B (strong anti-type A) - fatal
AB (no antibodies)
must blood match prior to transfusion

212
Q

feline neonatal isoerythrolysis

A

type a or ab kittens to type b queen
leads to fading puppies

213
Q

canine blood types

A

DEA - 1,3,4,5,6,7,8
can be +/-
match blood + to + and - to -
first transfusion ok. after dea 1+ to dea1- can cause acutre haemolysis/death

214
Q

what does stored whole blood lack

A

Platelets, WBCs and clotting factors

215
Q

plasma - FFP - use

A

used for coagulopathies

216
Q

what is cyroprecipitate

A

plasma fraction from FFP
concentrated clotting factors
fibrinogen, factor VIII, von willebrands
pre-treatment for vWD deficiency

217
Q

what is cyrosupernatant

A

remaining plasma fraction after cyro-precipitate formed
contains plasma proteins and vitK dependent clotting factors. used as frozen plasma

218
Q

deciding what to transfuse

A

replace what is lacking, benefits must outweigh drawbacks

219
Q

canine blood collection

A

donor - fit/healthy, 1-8yo, >25kg, good temperament, never travelled, vaccinated.
jugular vein in lateral recumbency - 450ml

220
Q

feline blood collection

A

donor - healthy 1-8yo, >4kg, preferably indoor
lateral/dorsal, jugular vein, 11-13ml/kg

221
Q

volume of blood for transfusion

A

(target pcv - recipient pcv)/donor pcv x kg x N
N = 90 in dogs, N= 60 in cats

222
Q

clinical signs of transfusion reaction

A

increase in temperature, change in respiratory/heart rate, change in MM colour, visible oedema, GI signs,

223
Q

signs of acute haemolytic transfusion reaction

A

uncommon
fever, tachycardia, dyspnoea, muscle tremors, V+, weakness, collapse, haemoglobinaemia, haemoglobinuria, shock, death
stop transfusion immediately, IVFT, corticosteorids

224
Q

delayed haemolytic reaction

A

extravascular haemolysis 3-21d post transfusion
incompatible first transfusion care occur
reduced lifespan of donated erythrocytes
hyperbilirubinaemia +/- uria

225
Q

febrile non-haemolytic transfusion reaction

A

acute hypersensitivity
most common with whole blood
mild/transient fever
leukoreduction to minimise

226
Q

acute hypersensitivity blood reaction

A

anaphylactic IgE antibodies activating mast cells, mild reactions can lead to hypotensive shock
stop transfusion

227
Q

therapeutics for transfusion reactions

A

clinical exam - CRS, temperature, haemoglobinuria
supportive treatment - IVFT, corticosteroids, oxygen, antihistamines, adrenaline, diurectics

228
Q

what is the difference between primary and secondary immunodeficiency

A

primary - genetic, rare, can affect neutrophils, lymphocytes, immunoglobulins. commonly repeated infections in young animals pure bred/multiple in a litter common
secondary - more common - immunosenesence, medical immunosuppression, specific infections (fiv/parvo), chronic disease

229
Q

IMHA

A

young-middle age antibody mediated haemolysis often resulting in anaemia
primary - no known causative trigger, inherited predisposition (cocker, springer and poodles)
secondary - underlying condition trigger eg infection, neoplasia, drugs/toxins/vaccination
cats triggered by fip.felv. chronic bacterial infection, mycoplasma

230
Q

IMHA diagnosis

A

confirm anaemia - low pcv <20%
check for regeneration
left shift neutrophilia common
check platelet levels (can have imtp too)
look for spherocytes
autoagglutination test - 4 drop saline + 1 drop blood - rouleaux = inflammation, agglutination = clumping

231
Q

treatment of IMHA

A

underlying trigger/disease
immunosuppression - glucocorticoids
** must ensure no infections beforehand
risk of death through thromboembolic disease

232
Q

IMTP

A

middle age female cocker, old english, gsd, poodles
primary - autoimmune production of antibodies against normal platelet antigens
secondary - antibodies targeting non self antigens adsorbed onto platelet surface
present with anaemia/bleeding - petechiae, eccymoses, haematomas, epistaxis, gingival bleeding, malaena

233
Q

diagnosis of imtp

A

low platelet count
in primary biochem/coagulation profiles often normal
can have concurrent anaemia

234
Q

treatment for imtp

A

acute - transfusion, not often needed. vincristine immunosuppressant activity
long term - prednisolone initially whilst azathioprine kicks in
risk of death - haemorrhage
monitor platelet levels monthly, immunosuppressive for min 4-6 months
10-15% mortality

235
Q

signs of primary haemostasis dysfunction

A

petechiae/ecchymoses
bleeding from MM
multiple bleeding sites
haematomas (rare)

236
Q

signs of secondary haemostasis dysfunction

A

peteachiae/eccymoses rare
deep/cavity bleeds more common, can bleed from MM
sometimes single bleeding sites
haematomas common

237
Q

requirements to make a clot

A

platelets, endothelial cells, von-willebrands factor protein sticks platelets together
platelet agonists such as thrombin and collagen
physiologic factors - nitric oxide/prostacyclin

238
Q

diascopy

A

does the lesion blanch under a glass slide
yes - vascular vasodilation
no - in skin haemorrhage - petechiae

239
Q

thrombocytopathia

A

inherited/drug induced defects, platelet dysplasia
diagnosis - normal PLT prolonged BMBT
normal vWF. dx of exclusion
tx - withdraw drugs eg nsaids, blod transfusion if anaemia

240
Q

what should you do before neutering a doberman

A

buccal mucosal bleeding time

241
Q

enzymatic coagulation factors

A

XI, X, IX, VII, II
factor VII depletes first - v high PT, aPTT a little high

242
Q

vitamin K deficiency

A

essential in functioning of coagulation factors II, VII, IX and X
occurs with rodenticide/slug pellets and some severe hepatic/cholestatic disease as fat soluble
wont see coag issues for a week

243
Q

wbct

A

whole blood clotting time - tube should clot within 20 mins

244
Q

one stage prothrombin time

A

OSPT
aka prothrombin time measures extrinsic and common pathways
prolonged with sufficient deficiency of any factor (<30% normal)

245
Q

activated partial thromboplastin time

A

APTT
measure of intrinsic and common pathways
single factor <30% normal prolongs

246
Q

congenital disorders of secondary haemostasis

A

haemophilia
factor VIII deficiency (haemeophilia A), factor IX deficiency (haemophilia B)
sex linked, males, spontaneous bleeding
APTT increases

247
Q

acquired disorders of secondary haemostasis

A

vitamin K antagonism - depletion of II, VII, iX and X
hepatic disease - clotting and inhibitory factors produced in liver - factors go down, coags go up

248
Q

what is the triad of contributers to thrombosis

A

endothelial injury
abnormal blood flow
hypercoagubility

249
Q

DIC

A

excessive activation of haemostatic pathways - high thrombin and microvascular thrombi
coagulation factors/platelets used up - haemorrhage
triggers - endothelial damage (electrocution/heat stroke (sepsis). platelet activation - viral disease. release of tissue procoagulants - trauma, pancreatitis, bacterial infection etc - anything can cause it
dx - thrombocytopaenia (or dropping count), hypofibrinogenaemia (coagulation factors used up), schistocytes (rbc fragments)
tx - underlying cause or death is coming

250
Q

neutrophil toxic change

A

rapid neutropoiesis
foamy cytoplasm - dispersed organellas
diffuse cytoplasmic basophilic - persistent cytoplasmic rna
dohle bodies - focal blue-grey cytoplasmic structures
asynchronus nuclear maturation

251
Q

monocytosis

A

inflammation - can imply chronic or necrosis
steroid/stress

252
Q

eosinophilia causes

A

hypersensitivity
parasitism
hypoadrenocorticism
paraneoplastic
idiopathic eosinophilic syndromes
rare - eosinophilia leukaemia

253
Q

eosinopaenia causes

A

glucocorticoids, stress, inflammation

Year 4 small animal (18 decks)

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