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Advanced Clinical Veterinary Nursing > Medical Nursing > Flashcards

Medical Nursing Flashcards

1
Q

what is the process of a lameness workup?

A

signalment and presenting complaint
history
gait exam
physical exam
differential diagnosis
diagnostic plan
aids to diagnosis
arthrocentesis

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2
Q

why is signalment and presenting complaint important in lameness work up?

A

indicates possible conditions
signalment can make conditions more likely

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3
Q

what history should be taken for lameness cases?

A

current medications
duration of lameness
onset
progression
continuous or intermittent
effect of exercise and rest
effect of ground surface - if feet affected
which limb
activity levels
concurrent issues

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4
Q

what is assessed in stance for lameness cases?

A

asymmetry
weight bearing
angular limb deformity
weight shifting - to thorax if hindlimbs

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5
Q

what are the types of angular limb deformities?

A

varus - distal medial
valgus - distal lateral

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6
Q

how do you perform gait evaluation?

A

walk and trot
stairs
circles
stride length
head nodding - down on sound
scuffing nails
ataxia
paraparesis
paraplegia
bunny hopping
lateral sway

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7
Q

how is lameness graded?

A

out of 10

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8
Q

what is lameness grade 0?

A

sound

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9
Q

what is lameness grade 1?

A

occasionally shifting weight

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10
Q

what is lameness grade 2?

A

mild lameness at slow trot

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10
Q

what is lameness grade 3?

A

mild lameness while walking

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10
Q

what is lameness grade 4?

A

obvious lameness when walking
places foot when standing

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11
Q

what is lameness grade 5-8?

A

degrees of severity of worsening lameness

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12
Q

what is lameness grade 9?

A

places toes when standing
carries limb when trotting

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13
Q

what is lameness grade 10?

A

unable to weight bear

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14
Q

what is the benefit of lameness grading?

A

consistency between care and assessment

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15
Q

why is physical exam important in lameness pateints?

A

may have more severe injuries

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16
Q

what are you feeling for when palpating lameness cases (done on standing)?

A

asymmetry
swelling
muscle atrophy
joint enlargement
abnormal conformation
compare limbs, may have bilateral disease

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17
Q

what can be seen in patients with joint disease?

A

swelling
joint effusion
pain
instability
decreased range of motion
crepitus on manipulation

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18
Q

how should you examine joints?

A

lateral recumbency
examine unaffected limbs first for comparison

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19
Q

what can be seen in patients with limb disease?

A

swelling
muscle atrophy
pain

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20
Q

why is neuro exam useful in some lameness cases?

A

neuro issues may be causing lameness

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21
Q

how is neuro exam in lameness cases performed?

A

palpate spine
screening neuro exam of proprioception and reflexes
full neuro exam if concerned

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22
Q

how is cranial drawer test performed?

A

under sedation/GA
lateral recumbency
hold tibia and femur and try to move tibia cranially to see if CrCL ruptured

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23
Q

how is tibial thrust test performed?

A

hold femur with finger on tibial tuberosity
flex hock to see if tibial tuberosity moves forwards if CrCL ruptured
can be done awake

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24
Q

how do you test for patella luxation?

A

stifle extended with quads relaxed
shift patella medially and laterally

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25
Q

how is ortolani test performed for hip laxity?

A

dorsal recumbency
subluxate hips by pressing down
abduct femurs to reduce hips
adduct femurs to subluxate hips

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26
Q

what aids to diagnostics can be used for lameness work up?

A

US
x-ray
CT
MRI
arthocentesis
EMG if neuro or muscular issue

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27
Q

what is an arthrocentesis?

A

fluid obtained from the joint to diagnose disease

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28
Q

when is joint tap indicated?

A

persistent or cyclical fever
lameness in joint localised

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29
Q

how do you determine which joint to tap?

A

systemic lameness - multiple joints
one joint affected - one joint, possibly next one along

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30
Q

how do you prep for arthrocentesis?

A

GA patient
lateral recumbency
strict asepsis - gloves, drape
clip and prep area
prepare equipment
guide with bony landmarks

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31
Q

list equipment for arthrocentesis

A

20-25G needles - solution quite viscous
5/8th-2.5 inch needles - joint dependent
2.5-5ml syringe - create negative pressure

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32
Q

what are characteristics from arthrocentesis fluids when abnormal?

A

larger volume
less viscous as diluted with plasma and serum
abnormal colour

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33
Q

why is it important to release negative pressure before drawing out needle for arthrocentesis?

A

contaminate with blood from tissue

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34
Q

what should you do with fluid samples from arthrocentesis?

A

EDTA for cytology and smear
smear most important
plain if enough for protein
plain for culture if possible infection
give info on volume, viscosity, contamination

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35
Q

what should synovial fluid look like?

A

clear
viscous
small volume

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36
Q

define tap

A

to obtain

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37
Q

define arthrocentesis

A

surgical puncture and aspiration of joint

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38
Q

what equipment is needed for scapulohumeral joint tap?

A

radiograph - assess needle length
5ml syringe
1.5-2.5 inch, 20-21G spinal needle

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39
Q

how is scapulohumeral joint tap performed?

A

palpate acromion
needle inserted distal and directly perpendicular, slightly dorsal and medial
gentle traction to open shoulder joint

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40
Q

what equipment is needed for elbow/cubital joint tap?

A

5ml syringe
1-1.5 inch, 23G needle

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41
Q

how is elbow/cubital joint tap performed?

A

elbow flexed to 45 degrees
needle inserted at level between anconeal crest and epicondyle, perpendicular to epicondylar crest alongside anconeal process

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42
Q

what equipment is needed for carpal joint tap?

A

2-5ml syringe
5/8th, 23-25G needle

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43
Q

how is carpal joint tap performed?

A

flex carpus to 90 degrees to open joint space and avoid NV bundle
insert needle perpendicular to skin
aspirate all joints

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44
Q

what equipment is needed for MCP/MTP/IP joint tap?

A

1-2ml syringe
5/8th 25G spinal needle

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45
Q

how is MCP/MTP/IP joint tap perfromed?

A

hard if no aspiration
short bevel needle so whole needle tip is in the joint and avoid contamination

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46
Q

what equipment is needed for coxofemoral joint tap?

A

5-10ml syringe
1.5-2.5inch 20G spinal needle

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47
Q

how is coxofemoral joint tap performed?

A

VD radiograph to measure needle length
needle inserted craniodorsal to greater trochanter, angled medially and caudoventrally
hip abducted and internally rotated to open up joint

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48
Q

what equipment is needed for stifle joint or femoropatella joint tap?

A

5ml syringe
1-1.5inch 21-23G needle

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49
Q

how is stifle joint tap performed?

A

stifle partially flexed
needle inserted lateral to patella ligament midway between patella and tibial tuberosity
angled caudomedially until hits bone
goes through fat pad

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50
Q

how is femoropatella joint tap performed?

A

stifle extended
needle inserted at angle between patella and femur towards proximal

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51
Q

what are benefits and risks of femoropatella joint tap?

A

benefits - avoids passing through fat pad which can impede aspiration
risks - iatrogenic damage to articular cartilage possible

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52
Q

what equipment is used for tarsal joint tap?

A

2.5-5ml syringe
5/8th-1 inch 23-25G needle

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53
Q

how is tarsal joint tap performed?

A

joint partially flexed
manipulate joint to feel articulation
angle needle perpendicular to skin into the joint
take fluid from craniolateral or caudolateral aspect of the joint
push effusion for easier access

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54
Q

what is CKD?

A

gradual, progressive, irreversible nephron loss
functional or structural disease over 3 months

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55
Q

how common is CKD?

A

most common kidney disease
3x more in cats than dogs

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56
Q

how does therapeutic management of CKD help patients?

A

slow progression of disease
maintain quality of life

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57
Q

what is the goal when managing CKD?

A

reduce workload of nephrons and prevent further damage

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58
Q

why is most CKD subclinical?

A

kidneys have considerable reserve function

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59
Q

what is seen in 50% nephron loss (one kidney or 50% reduced function overall)?

A

subclinical disease

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60
Q

what is seen in 67% nephron loss?

A

lose concentration ability
USG <1.030 dogs
USG < 1.035 cats

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61
Q

what is seen in 75% nephron loss?

A

azotemia

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62
Q

what is seen in 75-100% nephron loss?

A

decreasing quality of life to incompatible with life

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63
Q

what is the pathogenesis of CKD?

A

chronic interstitial nephritis (inflammation of renal interstitium)

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64
Q

what should be ruled out in CKD cases?

A

treatable or reversible causes:
pyelonephritis - inflammation of kidney and renal pelvis
ureterolithiasis
infection
FIP
FIV

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65
Q

describe the disease process of CKD

A

reduced GRF
initial compensatory hypertrophy of remaining nephrons
over time their increased workload leads to progressive nephron loss
progressive reduced GFR

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66
Q

list effects of CKD

A

loss of water and electrolyte regulation
PUPD
dehydration
hypokalaemia
loss of acid base regulation
acidaemia - vomiting, inappetence
azotaemia
hyperphosphatemia - vomiting, inappetence, secondary hyperparathyroidism
anaemia from lack of synthesis of erythropoietin
hypertension
end organ damage

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67
Q

describe common presentation of CKD patients

A

older cats
young if congenital disorder - polycystic or malformed kidneys
long term illness
incidental finding

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68
Q

what can you ask to screen for CKD in geriatric cats?

A

weight or condition change
PUPD
appetite
demeanour
activity
V or D
hypertension - blindness, neuro signs
ability to give meds

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69
Q

what assessments do you make in cats with CKD?

A

hydration
weakness
uraemic ulcers
uraemic halitosis
hypertensive retinopathy
small and irregular kidneys
rubber jaw (from renal secondary hyperparathyroidism)

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70
Q

how is CKD diagnosed?

A

USG
urine protein : creatinine
serum creatinine and urea
GFR - most sensitive test
SDMA/symmetric dimethylarginine
US
radiography
UOP

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71
Q

what indicates early CKD?

A

low urine conc
BW change

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72
Q

what confirms reduced renal function?

A

azotaemia with inappropriately concentrated urine
SDMA bloods

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73
Q

how is structural kidney disease diagnosed?

A

US - size and structure
x-rays - ureteroliths

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74
Q

how is hypertension associated with CKD?

A

CKD complication
makes CKD worse

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75
Q

what is the effect of hypertension in CKD?

A

blindness
neuro signs
organ damage

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76
Q

what is the goal for systolic BP in CKD patients?

A

140mmHg

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77
Q

how can you reduce stress when taking BP for cats?

A

minimal restraint
gaba
feliway
calm and patient
cat friendly
headphones on doppler

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78
Q

how does renal secondary hyperparathyroidism occur in CKD?

A

CKD increases serum phosphate as kidneys fail to excrete phosphate
more PTH secreted to low phosphate but also increased calcium
fails as kidneys cant excrete excess phosphate
progressive increase in phosphate and PTH
PTH causes bone resorption and rubber jaw

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79
Q

when is renal secondary hyperparathyroidism most commonly seen?

A

renal dysplasia

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80
Q

what causes hypokalaemia in 20-30% CKD cats?

A

inappetence
GI losses
urinary losses

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81
Q

what are the effects of hypokalaemia in CKD?

A

muscle weakness
inappetence

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82
Q

how is hypokalaemia in CKD cats managed?

A

supplementation

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83
Q
A
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84
Q

how does proteinuria in CKD occur?

A

protein leaks from the blood to urine when glomerulus damaged
more common in dogs

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85
Q

how is proteinuria measured in CKD?

A

urea to creatinine ratio

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86
Q

what causes anaemia in 30-65% CKD cases?

A

lack of erythropoietin production
reduced RBC lifespan
GI losses

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87
Q

what is the effect of anaemia in CKD?

A

weakness
lethargy
inappetence

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88
Q
A
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89
Q

what is monitored in CKD cats?

A

3-6 months when stable
appetite
drinking
GI signs
weight
BCS
BP
retinal exam
PCV
urea
creatinine
phosphate
calcium
electrolytes
urinalysis

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89
Q

how is iris staging for CKD used?

A

after diagnosis to treat and monitor CKD appropriately
once reversible problems addressed - creatinine, proteinuria, BP

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89
Q

what is stage 1 CKD?

A

non-azotemic renal abnormalities
mild SDMA increase

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90
Q

what is stage 2 CKD?

A

mild increase of creatinine
mild azotaemia
SDMA increase

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91
Q

what is stage 3 CKD?

A

moderate azotaemia
clinical signs
increased SDMA

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92
Q

what is stage 4 CKD?

A

increased clinical signs
azotaemia
increased SDMA

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93
Q

how can you manage CKD cats?

A

maintaining hydration
renal diet
supportive therapy

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94
Q

why is managing hydration so important in CKD cats?

A

dehydration advances CKD

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95
Q

what is a renal diet composed of?

A

low protein - toxins produced as by product of protein
low phosphate
good antioxidants and fatty acids - blood flow and reduce inflammation
high potassium
high bicarb - prevent acidosis

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96
Q

what supportive therapy can be done for CKD?

A

calcium channel blockers to open blood vessels and manage hypertension - amlodipine (cats) or ACE inhibitors (dogs)
renal diet and phosphate binders for hyperphosphatemia
renal diet and potassium supplements for hypokalaemia
renal diet, ACE inhibitors, omega 3 PUFAs, antiplatelets for proteinuria

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97
Q

what is a senior cat?

A

11-14yo

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98
Q

what is a geriatric cat?

A

15yo +

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99
Q

list common conditions affecting older cats?

A

hyperthyroidism
hypertension
CKD
feline cognitive dysfunction
dental disease
DJD
DM
intestinal lymphoma
IBD

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100
Q

list signs of hyperthyroid in older cat

A

PUPD
increased appetite
weight loss

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101
Q

list signs of hypertension in older cats

A

vision issues
neurological changes
systolic BP over 160mmHg

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101
Q

list signs of CKD in older cats

A

lethargic
unkept
weight loss
azotemia
generalised illness
hypertension

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101
Q

how prevalent is feline cognitive dysfunction?

A

55% cats over 11yo
80% cats over 16yo

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101
Q

list signs of dental disease in older cats

A

gingivitis
periodontal disease
tooth resorption

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102
Q

list signs of DM in older cats

A

increased urination
increased appetite
weight loss

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103
Q

what is seen in intestinal lymphoma in older cats?

A

digestive issues

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104
Q

what may be included in pre-assessment forms for screening geriatric cats?

A

behaviour changes
interactions with other pets
household changes
current medications

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104
Q

what is a sign of IBD in older cats?

A

ravenous as cant absorb food

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105
Q

how is disease detected in older cats in nurse clinics?

A

pre-assessment
history
parameters
diagnostics if concerned
clinical exam

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106
Q

what history should be taken in geriatric cat clinics?

A

parasite control
vaccination status
diet
confirm signalment

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107
Q

describe structure of geriatric cat clinics

A

done by same person ideally
patient dependent
history
weight
BP
clinical exam
diagnostic tests as needed - urinalysis, bloods
recommendations - vet referral, minor changes
summarise
arrange follow up

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108
Q

how should hydration be managed in geriatric cats?

A

always available
encourage to drink
measure intake every 6 months for any change

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108
Q

what are features of feline senior diets?

A

reduced energy and fat - less active
reduced calcium and phosphorus - manage possible kidney issues
increased fibre - increase digestion, support weight loss
wet - better support of hydration

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109
Q

how are condition scores used for geriatric cats?

A

ensure consistent weight
calculate % weight changes
BCS and MCS
<5% not significant
5-10% significant
>10% big concern

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110
Q

why is maintaining hydration in older cats so important?

A

maintain acid base balance
maintain osmoregulation

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111
Q

list effects of hypertension

A

retinal oedema
retinal haemorrhage
retinal detachment
left ventricular hypertrophy
progressive renal failure
bleeding into the CNS
ataxia
disorientation
seizures
coma
death

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111
Q

why is it important to monitor BP in older cats?

A

secondary hypertension common as a result of CKD, hyperthyroidism, other endocrine disorders

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112
Q

what can cause hypotension (<120mmHg) in geriatric cats?

A

heart failure
shock
hypovolaemia

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113
Q

what is normal SBP in cats?

A

120-160mmHg

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114
Q

what can cause SBP to be slightly elevated in cats at 160-180mmHg?

A

stress

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115
Q

what can cause hypertension (>180mmHg) in geriatric cats?

A

CKD
hyperthyroidism
endocrine disease

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116
Q

what should be assessed in clinical exam in geriatric cats?

A

slowly and cat friendly
head to toe
assess gait
auscultate
observe resp
check thyroid
examine muscles

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117
Q

what are common conditions that geriatric cats may have?

A

ear infections
neurological conditions
trauma
infections
tumours

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118
Q

what bloods are common in geriatric cats and why?

A

biochem
haem
BG
thyroid
assess organs and systems

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119
Q

what urinalysis is commonly done in cats?

A

SG
dipstick
UPC ratio

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120
Q

what are considerations for restraining geriatric cats?

A

temperament
disease
injury
preference
age
DJD
push not pull limbs
towel wrap
minimal

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121
Q

define dyspnoea

A

difficult or laboured breathing

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122
Q

define tahcypnoea

A

increased rate of respiration

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123
Q

define orthopnoea

A

upright position with extended neck to create space in chest to aid breathing

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124
Q

what is normal awake and sleeping RR?

A

awake <35, panting normal in dogs
sleeping <25

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125
Q

list causes of tachypnoea and dyspnoea

A

stress
pain
excitement
exercise
hypoxaemia
hypercapnia
respiratory disease
cardiac disease

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126
Q

what is localisation for upper airway disease?

A

nasal passages
pharynx
larynx
trachea

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127
Q

list signs of upper airway disease

A

inspiratory dyspnoea (difficulty breathing in)
stertor or stridor
abnormal sounds heard without touching patient

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128
Q

list causes of upper airway disease

A

laryngeal paralysis
BOAS
FB
neoplasia
polyps
inflammation
tracheal collapse

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129
Q

how is upper airway disease initially managed?

A

GA and intubation if obstructed
care for rapid decompensation

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130
Q

what is localisation for lower airway disease?

A

bronchi
bronchioles

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131
Q

list signs of lower airway disease

A

quick short inspiration
prolonged expiration
harsh lung sounds on auscultation
wheezes due to broncho constriction
crackles from secretions blocking airways

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132
Q

what can cause lower airway disease?

A

asthma
bronchitis
smoke inhalation
bronchopneumonia
COPD

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133
Q

list signs of lung parenchyma disease

A

expiratory and inspiratory components

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134
Q

list causes of dyspnoea caused by lung parenchymal disease

A

pulmonary oedema - cardiac or non-cardiac
pneumonia
infection
fibrosis
haemorrhage
contusion
neoplasia
thromboembolism
parasites

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135
Q

how do lung parenchymal disease appear on x-rays?

A

fluid is white
can see masses or pathologies

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136
Q

list signs of pleural space disease

A

restrictive breathing pattern
increased RR
reduced depth of inspiration - lungs cant expand

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137
Q

list causes of pleural space disease

A

penumonia
pleural effusion
masses
diaphragmatic hernia
pneumothorax
heamothorax

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138
Q

list causes of pleural effusion

A

haemorrhage
infection
neoplasia
heart failure
chylothorax

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139
Q

what changes in lung auscultations with pleural effusions present?

A

muffled heart sounds
muffled lung sounds dorsally

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140
Q

how is pleural effusions and pneumothorax diagnosed?

A

physical exam
thoracic radiographs
US

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141
Q

why are US favoured for pleural effusion and pneumothorax diagnosis?

A

quick to diagnose
can do conscious
dont have to position patient

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142
Q

how do you stabilise patients with pleural effusion or pneumothorax?

A

thoracocentesis

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143
Q

how do you do a thoracocentesis?

A

sedate
prep area
collect samples for cytology, culture, biochem
drain space

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144
Q

what is the clinical approach when presented with respiratory emergencies?

A

oxygen
clinical exam
upper or lower disease
RR and effort
MM
HR and heart abnormlaities
pulses
minimise stress

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145
Q

what is the goals of oxygen in respiratory emergencies?

A

increase oxygen content in arterial blood
increase oxygen delivery to tissues

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146
Q

what determines oxygen delivery to tissues?

A

haemoglobin concentration
blood oxygenation
CO

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147
Q

list methods of oxygen supplementation

A

flow by - inefficient but fine if nothing else
mask
nasal prongs
nasal catheter - further in so more secure and better delivery
collar - fine for temporary
oxygen cage
intubation
ventilation

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148
Q

what are considerations for using oxygen cages?

A

care for temperature, humidity and carbon dioxide
cages can control this but are expensive

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149
Q

what are considerations when giving respiratory patients oxygen?

A

is it needed
oxygen toxicity
correct rate

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150
Q

list goals of oxygen supplementation in respiratory patients

A

resolve life threatening hypoxaemia
relieve resp distress

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151
Q

when can oxygen toxicity occur?

A

100% o2 for 12-24 hours

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152
Q

how do you prevent oxygen toxicity in resp patients?

A

give less than 60% if long term
aim for lowest oxygen level can tolerate

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153
Q

what should be monitored in resp patients?

A

physical exam
arterial BG
pulse ox
RR and effort
MM
hydration
HR
pulses
stress/anxiety

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154
Q

why is it important to measure arterial BG in resp patients?

A

partial pressure of oxygen
gold standard for arterial oxygenation

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155
Q

how do you take arterial blood samples for BG?

A

dorsal metatarsal or femoral artery
keep in airtight and specific syringe
apply pressure after sample

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156
Q

what affects PaO2?

A

oxygen
barometric pressure

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157
Q

what is normal PaO2 on room air and 100% oxygen?

A

100mmHg - room air
500mmHg - 100% oxygen

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158
Q

what values are seen in hypoxaemia?

A

PaO2 <80mmHg
<95% saturation

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159
Q

what is the goal for PaO2 and saturation for resp patients?

A

PaO2 80-120mmHg
95-100% saturation

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160
Q

what does a pulse ox do?

A

measure partial oxygen saturation
calculates haemoglobin oxygen saturation
continuous and non-invasive monitoring

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161
Q

when does pulse ox work best?

A

moist, non-pigmented skin with adequate perfusion

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162
Q

what heart failure is normally seen in dogs?

A

left or right sided congestive heart failure

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163
Q

what heart failure is normally seen in cats?

A

biventricular failure

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164
Q

what are the commonly seen left sided heart failure in dogs?

A

myxomatous mitral valve disease in small dogs
dilated cardiomyopathy in large breeds (systolic dysfunction)

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165
Q

what is a common cause of right sided heart failure in dogs?

A

pericardial effusion

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166
Q

what heart failure is common in young dogs?

A

congenital heart failure

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167
Q

what heart failure is commonly seen in cats?

A

hypertrophic cardiomyopathy (diastolic dysfunction)

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168
Q

describe left sided congestive heart failure

A

backwards failure
pressure in the heart increased so pressure in pulmonary veins entering the heart have increased pressure
fluid cant enter pulmonary capillaries in due to pressure in vessels
fluid collects in pulmonary tissues

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169
Q

what are the effects on the body of left sided congestive heart failure?

A

pulmonary oedema
tachypnoea
dyspnoea
coughing due to enlarged heart pressing on receptors in trachea and bronchi

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170
Q

describe presentation of left sided heart failure

A

heart murmur - not always present or an indicator of this disease
tachypnoea
dyspnoea
tachycardia
pale MM
slow CRT
arrhythmia
weak pulses
pulse defecits

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171
Q

describe clinical approach to left sided heart failure cases

A

history
physical exam
stabilise before diagnostic tests - fragile and may decompensate

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172
Q

how do you stabilise patients with left sided heart failure?

A

minimise stress
sedate with low dose butorphanol
oxygen
furusamide IV if pulmonary oedema
pimobendan PO or IV to improve myocardial contractility

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173
Q

how does furusamide help with pulmonary oedema?

A

reduces circulating volume so reduces pressure in heart and reduces fluid not in circulation

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174
Q

how is left sided heart failure diagnosed?

A

echo
throacic radiography
ECG
BP
bloods

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175
Q

how does echo help diagnose heart failure?

A

diagnosis and severity of disease

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176
Q

how does x-rays and CT help diagnosis of heart disease?

A

identify pulmonary oedema
see heart size
find neoplasia

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177
Q

why are ECGs used in diagnosis of heart disease?

A

identify arrhythmia

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178
Q

why are BP measurements used in diagnosis of heart disease?

A

identify hypotension caused by low CO

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179
Q

why are bloods done in heart disease diagnosis?

A

electrolyte and renal parameters
diuretics can lower K, cause dehydration and azotaemia

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180
Q

what is seen on x-rays in the progression of cardiogenic pulmonary oedema?

A

begins in dorsal region, spreads caudal then ventral

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181
Q

list monitoring for left sided congestive heart failure pateints

A

RR and effort
less than 40 breaths per min
SBP above 80mmHg
HR
pulse quality
EGC if arrhythmia
x-ray if pulmonary oedema not improving

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182
Q

when is the patient seen as improving in left sided CHF?

A

RR and HR decreased

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183
Q

how is left sided CHF managed once stabilised?

A

lifelong therapy
feeding to prevent cardiac cachexia
bloods week after meds started or changed
3 monthly bloods, echo and other tests as needed (patient dependent)

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184
Q

describe right sided congestive heart failure

A

backwards failure
increased pressure in the vena cava causing effusions to form around organs as fluid cant re enter the circulation

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185
Q

what is the effect on the body in right sided congestive heart failure?

A

distended peripheral veins and jugular
ascites
pleural effusion
tachypnoea
dyspnoea

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186
Q

what are causes of right sided CHF?

A

pulmonic stenosis
tricuspid dysplasia
pericardial effusion
neoplasia

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187
Q

how is right sided CHF diagnosed?

A

history
physical exam
echo
thoracic x-ray
US
ECG
CT

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188
Q

describe a pericardial effusion

A

increased fluid in pericardium leading to tamponade as right atrium collapses due to external pressure
right side of heart filling impaired

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189
Q

what can cause left side of heart filling to be impaired in pericardial effusion?

A

septum can move with filling of the heart and breathing which can impair the left side

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190
Q

what is the impact of pericardial effusion?

A

decreased CO

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191
Q

what are common causes of pericardial effusion?

A

neoplasia
idiopathic

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192
Q

how is pericardial effusion stabilised?

A

pericardiocentesis
IVFT - counteract lower pressure in heart to improve filling and CO

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193
Q

what do you see post-pericardiocentesis?

A

HR pulses and demeanour improved

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194
Q

how do you manage patients following pericardiocentesis?

A

12-24 hour hospitalisation to monitor for arrhythmia
effusion can recur at any point

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195
Q

describe reduced cardiac output

A

forwards failure
left or right sided failure causing weak peripheral pulses and tachycardia leading to low SV

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196
Q

when is reduced CO commonly seen in heart disease?

A

DCM - reduced systolic function
end stage heart disease

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197
Q

what is the most common cause of feline cardiac emergencies?

A

HCM
can be caused by stress or anaesthesia

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198
Q

how do cats with cardiac disease present?

A

murmur
gallops
tachypnoea
dyspnoea
open-mouth breathing
tachycardia
bradycardia (more severe than tachy)
weak pulses
hypothermia
older overweight males more prone

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199
Q

when does arterial thromboembolism tend to have poor prognosis in cats?

A

when presenting with HF

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200
Q

what are signs of arterial thromboembolism in cats with HF?

A

sudden onset hindlimb paralysis/paresis
pain
pallor/cyanosis of pads and nail beds
pulselessness
poikilothermy/cold leg
poor hindlimb perfusion

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201
Q

how should you manage feline cardiac emergencies?

A

history
physical exam
stabilisation - fragile and easily decompensate
tests once stable

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202
Q

how should you stabilise cats with cardiac emergency?

A

avoid stress
oxygen
furusomide for pulmonary oedema
drain pleural effusion
gentle warming
analgesia for ATE

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203
Q

how do you diagnose feline cardiac emergencies?

A

history
exam
stabilise
echo - POC until stable
thoracic x-ray
ECG
BP
bloods

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204
Q

how do you manage feline cardiac patients in hospital following diagnosis?

A

adjust therapy to lowest effective dose
feed
manage thromboembolism - warm soft bedding and physio
home as soon as possible
manage stress

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205
Q

what is long term management for feline cardiac patients?

A

food intake to prevent cardiac cachexia
repeat bloods and echo
owner monitor RR and effort, signs of embolism

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206
Q

what is prognosis for feline cardiac patients?

A

guarded
may suddenly die

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207
Q

what is normal HR of dog?

A

60-120

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208
Q

what is normal cat HR?

A

160-220

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209
Q

what is a bradyarrhythmia?

A

HR lower than normal range

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210
Q

what is a tachyarrhythmia?

A

HR above normal parameter

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211
Q

how do patients with arrhythmias present?

A

syncope (collapse)
weakness
exercise intolerance
CHF
abnormal HR
weak pulses
pulse deficits

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212
Q

how are arrhythmias diagnosed?

A

ECG

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213
Q

define hyperpnoea

A

deeper breaths without dyspnoea

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214
Q

how do you triage a patient?

A

assess most life threatening concern
CV, resp and neurological

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215
Q

what are important considerations for dyspnoeic cat?

A

fragile
keep low stress
provide oxygen where possible

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216
Q

what should be examined in dyspnoeic cat?

A

RR and effort and pattern
clinical exam
auscultate
percussion
cranial rib spring
assess oxygenation

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217
Q

what can cause inspiratory dyspnoea?

A

dynamic extrathoracic upper airway obstruction

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218
Q

what can cause expiratory dyspnoea?

A

intrathoracic upper airway obstruction
lower airway disease

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219
Q

what does rapid shallow breathing indicate in dyspnoiec cats?

A

pleural space disease
parenchymal disease

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220
Q

what is meant by adventitious lung sounds?

A

abnormal respiratory noises

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221
Q

what can you hear on auscultation in respiratory disease?

A

breath sounds
wheezes
crackles
stertor
stridor

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222
Q

what can you palpate for in respiratory disease?

A

thoracic compressibility
percussion

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223
Q

what can cause URT obstruction?

A

FB
polyps
laryngeal tumours

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224
Q

how do you manage URT obstruction?

A

intubate

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225
Q

what can cause LRT disease?

A

asthma
bronchitis
bacterial infection
lung worm
FB
neoplasia

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226
Q

what can occur secondary to LRT disease?

A

pneumothorax

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227
Q

how do you manage general LRT disease?

A

bronchodilators

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228
Q

what causes feline asthma?

A

type 1 hypersensitivity to allergen
airway hyperresponsiveness
reverse bronchoconstriction
secondary inflammation

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229
Q

describe chronic bronchitis

A

airway inflammation
excess mucus production
airway narrowing

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230
Q

how is lower airway disease managed?

A

oxygen
minimise stress
bronchodilators

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231
Q

what are examples of bronchodilators given in cats?

A

terbutaline 0.015mg/kg IM/SC q4
salbutamol 1-2 puffs to effect

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232
Q

how is parenchymal disease managed in cats?

A

cage rest
oxygen
sedation as needed
furusomide

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233
Q

what can be the fluid in pleural effusion?

A

transudate
modified transudate
exudate

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234
Q

what are possible types of exudate in plural effusion?

A

pyothorax (septic)
neoplasia or FIP (non-septic)
chyle (CHF, trauma or idiopathic)
blood (trauma, coagulopathy, neoplasia)

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235
Q

what equipment is needed for thoracentesis?

A

clippers
sterile prep kit
sterile gloves
butterfly catheter
3 way tap
EDTA and plain tube
20ml syringe
procedures book helpful

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236
Q

describe thoracocentesis procedure

A

7-8th intercostal space, costochondral junction
EDTA for cytology
plaint tube for biochem and culture and sensitivity
IV antibiotics as needed
supportive care

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237
Q

what are examples of glucocorticoids in dyspnoic cats?

A

dexamethasone
fluticasone inhaler

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238
Q

when should you give furusomide to dyspnoeic cats?

A

if suspect HF

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239
Q

what is the action of the heart?

A

pump blood around the body and lungs

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240
Q

what is myocardium?

A

cardiac muscle that contracts rhythmically and autonomically without nervous input, controlled by electrical impulses

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241
Q

what is heartrate controlled by?

A

sympathetic and parasympathetic nervous systems

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242
Q

how does SNS control HR?

A

releases catecholamines adrenaline and noradrenaline to increase HR

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243
Q

how does PNS control HR?

A

PNS releases hormone acetylcholine to decrease HR

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244
Q

what are cardiac cells?

A

electrical cells and myocardial cells

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245
Q

what are functions of electrical cells of the heart?

A

conduction system of the heart in orderly fashion
spontaneously generate electrical impulses and respond to impulses
transmit electrical impulse along to next cell

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246
Q

what is the role of myocardial cells in the heart?

A

make up walls of the atrium and ventricles
responsible for contraction and ability to stretch

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247
Q

what needs to happen for the heart to function properly?

A

co-ordinated contraction
2 atria then 2 ventricles pushing blood to circulation and lungs

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248
Q

describe the conduction system of the heart

A

at rest cardiac cells are polarised
depolarise when stimulated by electrical impulse causing contraction
repolarise back to resting state to allow filling between contractions

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249
Q

what is the sinoartial node?

A

area of modified cardiac muscle cells in right atrium wall that initiates heart beat and controls HR influenced by PNS and SNS

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250
Q

how does the SA node initiate heart beats?

A

fires electrical impulses causing depolarisation to spread through atrial muscle cells causing atrial systole and blood to move to the ventricles

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251
Q

what is the atrioventricular node?

A

specialised group of muscle cells at the top of intraventricular septum that coordinates ventricular contraction with atrial contraction by its slow transmission of the impulse through it

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252
Q

why is it important the atrial and ventricular contraction is coordinated?

A

allows full filling of the ventricles before contraction

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253
Q

what is bundle of his?

A

bundle of nerve fibres running down the interventricular septum and divides into left and right bundle branches

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254
Q

what is the role of the bundle of his?

A

connects to the AV node to pass the impulse to the ventricles

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255
Q

what are purkinjie fibres?

A

network of specialised neurones organised into fine fibre branches connected from bundle of his going into the ventricles myocardium

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256
Q

describe ventricular contraction

A

begins at bottom of the ventricle and moves upwards causing ventricular systole and pushing blood out of the heart

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257
Q

what does an ECG do?

A

measures and records changing electrical activity of the heart using positive and negative electrodes
records changes in potential difference

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258
Q

describe how an ECG works

A

when parts of atria nearest SA node depolarise electrical potential difference is created with parts still in resting state
when negative and positive electrodes are placed either side of the heart ECG detects this depolarisation wave travelling across the heart and records as a wave deflection

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259
Q

when are ECGs used?

A

diagnose arrhythmia
triage
anaesthetic monitoring
general monitoring
critical patients
monitor idenitfied pulse defecits and arrhythmias
CPR to identify shockable rhythms
in patients with metabolic and electrolyte abnormlaities
pericardiocentesis and central line placement
hands off monitoring

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260
Q

where are the ECG leads placed?

A

red - right fore
yellow - left fore
green - left hind
black - right hind

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261
Q

what are the different types of electrodes for ecg?

A

crocodile clips directly to skin
pads on patients paws or thorax

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262
Q

what are general considerations for using ECGs?

A

remove interference sources such as mobiles
good skin contact
patient ideally in right lateral

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263
Q

list types of ECG machines and most important uses for each

A

multiparameter - continuous monitoring
paper trace - diagnosis
holter - long periods and can wear at home
telemetry - remote monitoring

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264
Q

list troubleshooting for ecg

A

check machine
check leads
minimise patient movement
ideally in right lateral
purring/panting interferes
check contact
clip fur

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265
Q

what is the p wave?

A

atrial electrical activity
positive deflection
small electrical change as small muscle mass of atria

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266
Q

what is the PR interval?

A

time between atrial and ventricular depolarisation
occurs during atrial depolarisation, wave depolarises AV node

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267
Q

what is the Q wave?

A

ventricular septum depolarises first following depolarisation wave passing bundle of his and purkinjie fibres causing small downwards wave on trace
negative deflection

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268
Q

what is the R wave?

A

majority of ventricular myocardium is depolarised causing depolarisation wave travelling towards positive electrode
large muscle mass so large deflection
positive deflection

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269
Q

what is the s wave?

A

after depolarisation of most of ventricles, final depolarisation occurs at base of the heart
small negative deflection

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270
Q

what is QRS complex?

A

waveform representing depolarisation of ventricles followed by ventricular contraction

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271
Q

what is the baseline on an ecg?

A

when atria and ventricles are depolarised there is no longer electrical potential difference before repolarisation

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272
Q

what is the t wave?

A

repolarisation of ventricles following complete depolarisation ready for next impulse
small positive deflection

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273
Q

why can the T wave be positive, negative or biphasic?

A

can be random repolarisation of myocardium

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274
Q

how should you interpret ECGs?

A

HR
complexes - present and normal
any arrhythmias

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275
Q

list types of arrhythmia

A

regularly regular
irregularly irregular
regularly irregular
bradyarrhythmia
tachyarrhythmia
intermittent
continuous
sinus
ventricular
supraventricular

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276
Q

what makes an arrythmia heart beat abnormal?

A

its rate, impulse conduction or ectopia (out of place)

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277
Q

can all cells in the heart generate electrical activity?

A

yes

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278
Q

what are types of sinus rhythms?

A

normal sinus rhythm
sinus arrhythmia

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279
Q

what is sinus rhythm?

A

normal PQRST complex
regular heart sounds
pulse on every heart beat
normal HR
regularly regular rhythm

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280
Q

what is sinus arrhythmia?

A

regular variation on HR coinciding with respiration due to PNS activity/vagal tone on SA node
normal P for every QRST
pulse for every heart beat
electrical impulse originates from SA node
regularly irregular rhythm

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281
Q

list bradyarrhythmias

A

sinus bradycardia
sick sinus syndrome
AV blocks
escape beats
hyperkalaemia

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282
Q

what is a sinus bradyarrhythmia?

A

SA node impulse and depolarisation slower than normal
normal sinus rhythm and PQRST complex
slow HR
no pulse deficits
regularly regular rhythm

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283
Q

what can cause sinus bradyarrhythmia?

A

can be normal in giant or athletic dogs
issue with SA node
secondary to disease - causing increased vagal tone, hypoadrenocorticism, hyperkalaemia, BOAS, high ICP leading to cushings reflex, hypocalcaemia
hypothermia
hypoglycaemia
hypothyroidism

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284
Q

how do you treat sinus bradycardia?

A

treat underlying cause
give anticholinergic - atropine or glycopyrrolate
positive inotrope - dopamine or dobutamine

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285
Q

what is sick sinus syndrome?

A

SA node fails to discharge electrical impulse leading to severe bradycardia or periods of asystole

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286
Q

what causes sick sinus syndrome?

A

degenerative
common in WHWT, cocker, cairn, mini schnauzer

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287
Q

how is sick sinus syndrome treated?

A

pacemaker
poor response to atropine

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288
Q

what are downsides and risks to pacemakers?

A

last 5-10 years
expensive
infection
lead dislodgement
failure to place correctly
venous thrombosis

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289
Q

list nursing considerations following pacemaker

A

no waking for 48 hours
harness only walks
no neck restraint or jug samples

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290
Q

what is an AV block?

A

impulses from SA node delayed or blocked going through AV node, signal may fail to reach the ventricles
issue with conduction system in the heart

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291
Q

what can cause AV block?

A

disease process
drugs that effect AV node

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292
Q

what is the difference between AV block and bundle branch block?

A

AV affects AV node
bundle branch block affects left or right bundle branch

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293
Q

list signs of AV block

A

decreased CO
lethargy
syncope
collapse

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294
Q

how is AV blocks treated?

A

manage underlying condition
vagolytic drugs - atropine, glycopyrrolate
pacemaker for 2nd and 3rd

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295
Q

what is a first degree AV block?

A

delayed conduction through AV node
normal PQRST
prolonged PR interval

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296
Q

what is a second degree AV block?

A

longer conduction delay
some P waves wont have QRS, dropped beat

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297
Q

what is mobitz type I second degree AV block?

A

PR interval gets longer and longer until beat is dropped and then back to normal

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298
Q

what is mobitz type II second degree AV block?

A

PQRS complex normal
occasional P wave without QRS

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299
Q

what is a third degree AV block?

A

complete lack of conduction through AV node
multiple P waves without QRS complexes
some tall QRST complexes which are ventricular escape beats acting as rescue beats
usually slow HR

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300
Q

what are rescue beats?

A

electrical impulses occurring from random cells to keep animal alive
leads to bizarre and wide complexes with absent P wave

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301
Q

how does hyperkalaemia affect bradycardia?

A

as potassium increases, severity of bradycardias and arrhythmias increase

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302
Q

what is seen in hyperkalaemia arrhythmias?

A

reduced/absent p waves
spiked t waves
short QT interval
prolonged QRS complex
progression to atrial standstil, sine wave pattern, v fib and asytsole

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303
Q

what diseases can cause hyperkalaemia?

A

urethral obstruction
AKI
hypoadrenocorticism

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304
Q

how is hyperkalaemia treated?

A

calcium gluconate bolus to reduce risk of v fib and protect cardiac myocytes from high k
insulin infusion to move k into cells
dextrose as cells uptake glucose with k to prevent hypoglycaemia

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305
Q

list tachyarrhythmias

A

sinus tachycardia
supraventricular tachycardia
atrial fibrillation
ectopic beats
accelerated idioventricular rhythm
ventricular tachycardia
r on t phenomenon

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306
Q

what is sinus tachycardia?

A

SA node generates impulse at faster rate than normal
normal PQRST complexes
regularly regular rhythm
faster HR than normal
pulse for every beat

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307
Q

when can sinus tachycardia be normal?

A

pain
stress
exercise
hypovolaemia
anaemia

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308
Q

what is supraventricular arrhythmia?

A

atrial origin
occurs at point other than SA node then conducts via AV node to the ventricles
QRS normal but often narrower and taller
p wave abnormal
premature heart beat
irregularly irregular rhythm

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309
Q

what are other names for supreventricular arrhythmia?

A

atrial premature complex
premature atrial contraction
atrial premature beat

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310
Q

what is supraventricular tachycardia?

A

3 or more supraventricular arrhythmias
rapid HR
narrow and upright QRS, may or may not be with P wave
regularly irregular rhythm

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311
Q

what is seen in slow SVT?

A

normally no clinical signs

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312
Q

whatclinical signs is seen in fast SVT?

A

weakness
collapse
poor pulse quality
poor peripheral perfusion
pale MM
prolonged CRT
inadequate diastolic filling

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313
Q

what can cause SVT?

A

cardiac disease
systemic disease causing toxicity, hypovolaemia, electrolyte imbalance, ischemia

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314
Q

how is SVT managed?

A

lower HR
treat underlying disease
beta blockers
calcium channel blockers - IV then oral for maintenance

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315
Q

what is ventricular arrhythmia?

A

ventricular origin
normal conduction pathway not followed
QRS complexes wide and bizarre

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316
Q

what is an ectopic beat?

A

beat generated not from SA node but other cells in the heart
premature and interrupts normal rhythm before SA node would initiate other rhythm
abnormal PQRST complex

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317
Q

what are types of ectopic beats?

A

atrial premature complex
junctional premature complex
ventricular premature complex
supraventricular tachycardia
escape beats

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318
Q

what is atrial fibrilation?

A

supraventricular tachyarrhythmia
rapid and irregular arrhythmia of atria
pulse deficits common
irregular pulse
ventricles contract before filling
rapid irregular HR
fibrillating baseline
taller and narrow QRS
no visible p wave
irregularly irregular rhythm

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319
Q

how is atrial fibrillation treated?

A

decrease HR
increase CO
calcium channel blockers
beta blockers
digoxin
amiodarone

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320
Q

what is junctional premature complex?

A

ectopic beat arising from area in AV junction
ventricles activated normally
premature narrow QRS before P wave

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321
Q

what is a ventricular arrhtyhmia?

A

SA node no longer controls ventricular contractions
abnormal electrical impulse at ectopic site below AV node takes control of pacemaker role
complexes wide and bizarre

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322
Q

what can cause ventricular arrythmia?

A

underlying cardiac disease
complication of GDV, splenectomy, pancreatitis, anaemia

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323
Q

what is ventricular premature complex?

A

ectopic beat occurring before normal SA node depolarisation, begins in abnormal location in ventricles
no p wave
wide and bizarre QRS
weak pulses
pulse deficits

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324
Q

what is accelerated idioventricular rhythm?

A

3 or more VPC together
elevated HR
unlikely to effect CO, hypotension or haemodynamic compromise

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325
Q

how do you manage accelerated idioventricular rhythm?

A

monitor closely for progression to v tach

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326
Q

what is ventricular tachycardia?

A

3 or more VPCs
rapid HR
bizarre and wide QRS complexes
absent P waves
large t waves

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327
Q

what are signs of v tach?

A

weak pulses and deficits
rapid irregular HR
low CO
hypotension
collapse
haemodynamic compromise
altered mentation
hypoperfusion

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328
Q

what can cause v tach?

A

primary cardiac disease
abdo pathology
inflammation
severe anaemia
abnormal autonomic activity
electrolyte disturbances
drug toxicity
neoplasia

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329
Q

list effects of v tach

A

decreased systemic tissue perfusion/cardiogenic shock
myocardial failure
malignant arrhythmia/v fib
sudden death

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330
Q

what is treatment aims for v tach?

A

convert to sinus rhythm
slow HR
improve CO and peripheral perfusion

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331
Q

how do you treat v tach?

A

manage underlying cause
lidocaine
beta blockers
amiodarone
procainamide
magnesium

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332
Q

how do you manage pulseless v tach?

A

emergency
start CPR
shock

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333
Q

what is r on t phenomenon?

A

VPC premature so superimposed on T wave of preceding complex
on sinus or ectopic beat
ventricles not fully repolarised before depolarising

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334
Q

what can be the consequences of r on t phenomenon?

A

v tach or v fib

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335
Q

list cardiac arrest rhythms

A

ventricular fibrillation
pulseless ventricular tachycardia
pulseless electrical activity
asystole

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336
Q

how does defibrillation work?

A

sends high energy electric shock to heart to reset electrical state of the heart and convert to sinus rhythm

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337
Q

which CA rhythms are shockable?

A

v fib
pulseless ventricular tachycardia

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338
Q

why is it important not to shock non-shockable rhythms?

A

can be detrimental for survival

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339
Q

what is v fib?

A

pre-terminal condition leading to patient death unless managed
no effective ventricular contractions
rapid ECG with irregular wavy baseline
no CO or pulses
can be coarse or fine

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340
Q

how do you manage v fib?

A

CPR and shock

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341
Q

what is pulseless electrical activity?

A

electrical impulses in the heart
no corresponding myocardial contractions
varied HR
normal complexes become wide and bizarre
no heart beat or pulses
can occur minutes after patient death

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342
Q

how do you manage pulseless electrical activity?

A

CPR
adrenaline
atropine
defib if converts to shockable rhythm

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343
Q

what is asystole?

A

flat line
most common arrest rhythm
no pulses or CO
associated with end stage disease caused by high vagal tone

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344
Q

how do you manage asystole?

A

CPR
shock if converts to shockable rhythm

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345
Q

what are the stages of a normal cell lifecycle?

A

interpahse - cell matures and DNA replicates
mitosis - prophase, metaphase, anaphase and telophase
prophase - preparation to split, chromosomes form
metaphase - chromosomes line up
anaphase - chromosomes split
telophase - chromosomes stretch out
cytokinesis - cell splits in 2

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346
Q

when do cells enter apoptosis?

A

after replicating a set number of times, depending on function and replication frequency controlled by the nucleus

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347
Q

what signals do cells responds to?

A

growth and environmental signals

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348
Q

what makes cancer a rare event?

A

processes in place to prevent it occuring

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349
Q

what is cancer?

A

phenotypic end result of whole series of changes that take long time to develop

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350
Q

how is cancer prevented?

A

cell cycle inhibited for repair or apoptosis
tumour suppressor genes

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351
Q

describe how cancer arises

A

accumulation of genetic mutations which eliminate cell constraints
very slow process and may not occur in lifetime of animal

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352
Q

what is one factor that is increasing the amount of cancer we see?

A

longer lifespan of animals as more mutations can accumulate

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353
Q

list environmental causes of cancer (not proven in animals but can assume as in humans)

A

chemical carcinogens
physical agents
hormonal causes
cancer causing/oncogenic viruses
(inherited cancer, not recognised in animals)

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354
Q

list types of chemical carcinogen

A

tobacco smoke
pesticides
herbicides
insecticides
cyclophosphamide (chemo drug linked with bladder cancer)

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355
Q

list physical agents that can cause cancer

A

sunlight
trauma
chronic inflammation
magnetic fields
radiation
surgery
implanted devices
asbestos

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356
Q

how can hormones effect cancer?

A

neutering can prevent some
neutering can increase risk of others such as lymphoma

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357
Q

how do oncogenic viruses lead to cancer?

A

indirect or direct action on causing cancer

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358
Q

list examples of oncogenic viruses

A

papilloma virus
FeLV

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359
Q

list mutations resulting in cancer

A

sustain proliferative signalling
evade growth suppressors
resist cell death - cant recognise DNA damage
enable replicative immortality - telomeres dont reduce on division (apoptosis when no longer present)
induce angiogenesis - new blood vessels
active invasion and metastasis

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360
Q

how many mutations are needed for cancer to occur?

A

5-6 critical mutations

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361
Q

what is a tumour?

A

benign or malignant neoplasm

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362
Q

define neoplasia

A

formation of abnormal growth that is not responsive to physiological control mechanisms
benign or malignant

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363
Q

define cancer

A

malignant neoplasms

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364
Q

define benign tumour

A

space occupying
can cause tissue distortion

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365
Q

define malignant tumour

A

locally destructive, may metastasise and cause death

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366
Q

how does chemotherapy work?

A

targets dividing cells
different drug classes work at different stages of DNA replication and cell division, or interfere with cell signalling

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367
Q

when can chemotherapy be used?

A

primary induction therapy - sole therapy
primary neoadjuvant chemo - before treatment
adjuvant chemo - mop up after surgery
consolidation chemo - haemopoietic chemo after remission
maintenance chemo - low intensity over long term
rescue or salvage chemo - failed response to previous chemo
palliative chemo - maintain quality of life, not cure

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368
Q

what are the benefits of multimodal chemo plans?

A

maximal cell kill in range of tolerable host toxicity
broader range of interaction between drugs and tumour cells
slows development of tumour drug resistance

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369
Q

what are considerations for using multimodal chemo plans?

A

only drugs with single use efficacy against tumour type
ideally use drugs without overlapping toxicity so dont have to wait for toxicity to settle before next drug
use drugs at optimum dose and schedule to lower resistance by tumour
use consistent intervals

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370
Q

list effects of chemo on cells

A

affects dna replication so go inot apoptosis

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371
Q

list types of chemo agents

A

alkylating agents
antitumour antibiotics
antimetabolites
antimicrotubule agents
corticosteroids
platinum
l-asparginase
target agents

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372
Q

what are examples of alkylating agents and how do they work?

A

cyclophosphamide, chlorambucil, lomustine
binds alkyl groups to cellular macromolecules cross linking DNA

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373
Q

what are examples of anti-tumour antibiotics and how do they work?

A

doxyrubicin, mitoxantrone
multimodal action of cellular toxicity

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374
Q

how do antimetabolites work?

A

inhibit use of cellular metabolites in cellular growth and division

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375
Q

what are examples of antimicrotubule agents and how do they work?

A

vincristine, vinblastine
interfere with cellular function and replication

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376
Q

what are examples of corticosteroids used in chemo and how do they work?

A

prednisolone
induction of apoptosis in haematologic cancers

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377
Q

what are examples of platinum used for chemo and how do they work?

A

cisplatin, carboplatin
bind DNA

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378
Q

how does L-asparginase work as a chemo drus?

A

induces apoptosis in tumour cells

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379
Q

what are examples of target agents for chemo and how do they work?

A

palladia, masivet
tyrosine kinase inhibitors, block receptors on cell surface

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380
Q

what is lymphoma?

A

diverse group of neoplasm of common origin from lymphocytes, lymph nodes, spleen, bone marrow
can affect all areas of the body

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381
Q

how does lymphoma present in cats and dogs?

A

cats - intestinal presentation
dogs - 80% have multicentric form, one of most common tumour in dogs

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382
Q

how is lymphoma treated?

A

consistent chemotherapy cycles
restrart chemo if leave remission
can live 2+ years with treatment

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383
Q

what is the CHOP protocol?

A

cyclophosphamide
hydroxydaunorubicin/doxorubicin
oncovin/vincristine
prednisolone

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384
Q

when is prednisolone given in the CHOP protocol?

A

if systemically unwell

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385
Q

how does the CHOP protocol work?

A

given over several months
discontinuous so stopped when finished and restart as needed

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386
Q

what causes chemo toxicities?

A

drugs targeting normally dividing cells

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387
Q

what is commonly affected by chemotherapy in the body?

A

bone marrow
GI

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388
Q

list side effects of vincristine

A

myelosuppression
peripheral neurotoxicity
GI
ileus

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389
Q

list side effects of cyclophosphamide

A

neutropenia
GI toxicity
haemorrhagic toxicity

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390
Q

list side effects of chlorambucil

A

myelosuppression

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391
Q

list side effects of epirubicin

A

anaphylaxis
myelosuppression
GI toxicity
cardiotoxicity - rare

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392
Q

what is a possible side effect of doxorubicin?

A

changes leading to CHF

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393
Q

list nursing considerations for chemo patients

A

feeding
toileting
barrier nurse
care pre-diagnosis, during treatment if ill and end of life care

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394
Q

list considerations for administering chemo

A

bolus or infusion, or orally for some
IV needs to be clean stick
check drug and dose
use PPE
correct protocols
correct disposal

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395
Q

what chemo drugs are group 1 vesicants?

A

vinchristine
epirubicin

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396
Q

how do you manage chemo admin gone wrong?

A

leave ICV in and aspirate
inject saline around area
heat compression

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397
Q

how do you manage excretions following chemo?

A

drug is excreted for 4-5 days
handle with gloves
double bag
urinate in low traffic areas and wash away

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398
Q

how can you support owners with chemo pets?

A

understand condition and treatment for discussion
understand owners needs
provide supportive care, curative treatment, palliative care, hospice or euthanasia as appropriate to help patient
keep owners involved
provide support as needed

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399
Q

what are the two types of dietary sensitivities?

A

non-immunologically mediated
immunologically mediated

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400
Q

what are the types of non-immunologically mediated dietary sensitivities?

A

repeatable food intolerances
non-repeatable dietary indiscretion - over eating, eating things shouldnt, gluttony
intoxication
contamination/poisoning

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401
Q

what are immunologically mediated food sensitivities?

A

repeatable
food allergy or hypersensitivity

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402
Q

define a food allergy

A

immunologically mediated adverse food reaction/AFR to dietary component

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403
Q

what is the most common dietary component causing food allergies?

A

proteins

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404
Q

what defence mechanisms does the body have against AFR?

A

constant exposure to foreign antigens
peristalsis
mucus layer
gut not designed to let large molecules through
protients hydrolysed before entering blood
oral tolerance is series of signalling and processing leading to tolerance of foreign antigens
body learns whats harful

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405
Q

when does AFR occur?

A

failure of bodys defence mechanisms against them

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406
Q

how do most AFR manifest?

A

delayed hypersensitivity/type 4
anaphylaxis in some cases

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407
Q

list the systems affected by AFR

A

dermatological
GI

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408
Q

list common food allergens in dogs

A

beef
dairy
wheat

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409
Q

list common food allergens in cats

A

beef
dairy
fish

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410
Q

what is canine epileptoid cramping syndrome?

A

severe muscle and intestinal cramps of short duration in border terriers as a result of gluten allergens

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411
Q

how is canine epileptoid cramping syndrome treated?

A

eliminating gluten

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412
Q

list cutaneous clinical signs of food allergies

A

pruritis
erythema

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413
Q

list GI signs of food allergy

A

vomiting
diarrhoea, usually LI
non-specific so need to differentiate cause

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414
Q

what is the systemic reaction to food allergies?

A

anaphylaxis

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415
Q

how do patients with food allergies present?

A

younger pets typically
derm signs
LI diarrhoea, GI signs
other causes of issues excluded

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416
Q

how are food allergies diagnosed and managed?

A

exclusion/limitation
challenge and rescue
provocation and rescue
maintenance

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417
Q

what is the exclusion/limitation phase of food trials?

A

feed novel protein or hydrolysed diet exclusively

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418
Q

what is the challenge and rescue phase of food trials?

A

feed original diet to confirm was the problem
return to elimination diet if problems return
key phase of diagnosis

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419
Q

what is the provocation and rescue phase of food trials?

A

adding individual foods to identify triggers and whats fine

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420
Q

what is maintenance phase of food trials?

A

continuing to feed whats okay and excluding triggers

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421
Q

when are blood tests not useful for food allergies?

A

when have GI manifestation

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422
Q

how long does it take to see improvement in food allergies when starting management?

A

GI signs - 6 weeks
derm signs - 10 weeks

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423
Q

what is chronic inflammatory enteropathies/CIE?

A

group of disease with chronic GI inflammation
any of vomiting, diarrhoea, dysorexia (abnormal appetite), weight loss of over 3 weeks duration

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424
Q

what needs to be done before diagnosis of CIE?

A

exclusion of other diseases such as exocrine pancreatic insufficiency, abdo organ inflammation, metabolic disease

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425
Q

how is CIE diagnosed?

A

everything else is normal and ruled out
biopsies indicate both inflammation and villi atrophy

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426
Q

what are advantages and disadvantages of intestinal biopsies via laparotomy?

A

adv - full thickness biopsies, full exploration of other organs
disadv - surgical, risk of dehiscence, peritonitis and sepsis

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427
Q

what are advantages and disadvantages of intestinal biopsies via endoscopy?

A

adv - minimally invasive
disadv - small mucosal biopsies, jejunum hard to access

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428
Q

list possible causes of CIE

A

food responsive disease/FRD
antibiotic responsive disease/ARD - common in breeds such as german sheperd
idiopathic disease

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429
Q

describe antibiotic responsive disease

A

gut flora prone to random changes causing diarrhoea and inflammation which leads to further changes in gut flora

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430
Q

how is antibiotic responsive disease managed?

A

metronidazole

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431
Q

describe idiopathic CIE

A

previously known as IBD
immunological disorder
loss of tolerance to mucosal flora
cycle of GI inflammation and shift in mucosal flora, each making each worse

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432
Q

list consequences of CIE

A

dehydration
protien malabsorption/protein losing enteropathy leading to hypoalbuminaemia leading to effusions and oedema and thromboembolic events as blood more viscous (lowers oncotic pressure)
hypocobalaminaemia/low b12
GI haemorrhage
anaemia
GI perforation leading to spetic peritonitis

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433
Q

describe supportive therapy for CIE

A

haemodynamic stability
fluid balance and electrolytes to manage hypovolaemia and hydration
manage diet
tube feed in severely effected patients
anti emetics
appetite stimulants

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434
Q

what therapy can be done for idiopathic CIE?

A

immunosuppression if immune mediated problem to allow gut to recover - preds at minimum effective dose
consider fenbendazole, metronidazole, vitamin b12, anti-platelet drugs as needed

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435
Q

describe what a diet trial is

A

exclusive feeding with food and water for upto 10 weeks
hypoallergenic not sensitivity diet
novel proteins

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436
Q

why may diseases other than food allergies respond to diet trials?

A

food is high quality and digestible

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437
Q

define a novel protien

A

proteins patient wont have come across before

438
Q

what are food options for diet trials?

A

novel proteins - home cooked or commercial, Hills d/d for example
hydrolysed proteins - hills z/d, purina HA for example

439
Q

list nursing considerations for food allergy patients

A

manage hydration, inappetence and nausea
nutrition status and caloric needs
manage potassium and B12
consider abdo discomfort
manage hypoproteinaemia
manage diarrhoea and fecal scold

440
Q

how do you manage nutrition in hospitalised patient with dietary sensitivities?

A

record food intake
monitor BCS and weight considering fluid balance
nutritional support if less than 80% RER intake, >10% BW loss after fluid balance, over 3 days hyporexia, severe underlying disease
keep GI system working even if small amounts of micronutrition
encourage eating

441
Q

what are examples of diseases that increase nutritional requirements?

A

trauma
sepsis
severe burns

442
Q

how can you manipulate diet to aid food allergy patients?

A

smaller frequent meals
adust posture of feeding
low fat - gastric emptying and for reflux
supplement fibre for large bowel function and colonic disease support

443
Q

how do you manage abdo discomfort in food allergy patients?

A

omeprazole or sucralfate - GI dilation or ulceration
postural feeding to manage reflux
avoid opioids due to ileus
buscopan - stomach cramps

444
Q

how do you manage patients with diarrhoea?

A

keep clean and dry
topical barriers - cavilon or vaseline
avoid over grooming with collar and enrichment
tail bandage
inco sheets
soft blanket on top

445
Q

list monitoring considerations for dietary patients

A

weight
appetite
demeanour
vomiting or diarrhoea
hydration
HR
RR
comfort
bloods

446
Q

what is CPCR?

A

cardiopulmonary cerebral resusitation

447
Q

list goals of CPCR

A

perfusion of heart lungs and brain - require lots of oxygen and glucose to function
ROSC

448
Q

what is ROSC?

A

self perfusion by heart pumping
cant necassarily breath or do anything else by them selves

449
Q

what is respiratory arrest?

450
Q

what is cardiopulmonary arrest?

A

no CO
apnoea

451
Q

list patients at risk of arresting

A

trauma
systemically unwell
paeds
geriatric
recently arrested
iatrogenic causes

452
Q

describe risks and benefits of a patient iatrogenically arresting

A

likely have less monitoring by will be more likely to recover due to more cardiac reserves

453
Q

what are risks and benefits of unwell patients arresting?

A

likely have close monitoring so faster response
already compromised so less likely to recover

454
Q

what is the process of starting CPCR?

A

as soon as think patient has crashed, resp arrest quickly causes cardiac
anyone can help

455
Q

how do you prepare for CPCR?

A

regular CPCR training
crash kit ready
crash alarm or call for help

456
Q

what is BLS?

A

CPCR cycles
oxygen therapy
can do without a vet

457
Q

what is ALS?

A

drugs
fluids
cardioversion
under schedule 3

458
Q

describe the CRCP algorithm briefly

A

BLS - 1 cycle is 2 minutes
ALS
evaluate patient
if ROSC go to post-cpa algorithm
if VF, pulseless VT, asytole, PEA, continue management and BLS

459
Q

describe how cardiac compressions should be performed

A

100-120 per min
50%-2/3 depth of thorax, full recoil between
compress from dorsal side of patient
ideally right lateral but either fine

460
Q

describe the cardiac pump

A

compression of thorax directly over heart, can use thumbs in cats to not cause damage
in small dogs and cats

461
Q

describe thoracic pump

A

compression on widest part of thorax
dorsal caudal thorax or over xiphisternum
medium to large breed dogs

462
Q

describe internal cardiac compressions

A

needs thoracotomy or laparotomy
good if external compressions not effective or large dogs
everyone needs to be happy to do it

463
Q

how do you provide ventilation to crash patients?

A

10-12 breaths a min
100% oxygen if possible, room air fine
CO2 to guide breaths
ambu bag
start if suspect resp arrest
CO2 to guide breaths

464
Q

how are crash trolleys managed?

A

reflect cases seen
inform people of changes
one persons primary responsibility
stocked and checked after use and regularly

465
Q

what can be found in the airway access drawer in crash trolley?

A

ETTs
laryngoscope
tube tie
cuff inflator
guide wire
plain gause swabs
intubeze
u cath with 3 ETT connector

466
Q

what can be found in IV access drawer of crash trolley?

A

various catheters
IV/IO connectors
tape
scissors
cut down kit - rarely used, swab, forceps, scalpel, kidney dish
scaplel - stab incision placement
wide bore caths for GDV

467
Q

what can be found in ventilation drawer of crash trolley?

A

paediatric and adult ambu bags
capnography connectors
inline capnograph - no prime cycle

468
Q

what can be found in drugs drawer of crash trolley?

A

low and high dose adrenaline
atropine
saline
pre-prepared syringes
ECG pads
naloxone
atipamezole
flumazenil
amiodarone
glucose
propofol

469
Q

what is adrenaline used for in CPCR?

A

given in asystole
positive inotrope so increases strength of heart beat
chronotrope so increases HR
vasopressor causing vasoconstriction
results in increased SVR and MAP

470
Q

how do you give adrenaline to crash patients?

A

low dose first - 0.1mg/ml
high dose - 1mg/ml
IV or IO or intratracheal

471
Q

how do you give meds intratracheally?

A

double dose with room air down trachea
efficacy questionable

472
Q

what is atropine used for in crash patients?

A

pre arrest when bradying down, profound bradycardia or PEA
positive chronotrope so increases HR

473
Q

how do you give atropine in crash patients?

A

IV, IO or intratracheal
only one dose

474
Q

what is the role of reversal drugs in crash patients?

A

reverse all possible drugs that may affect resus

475
Q

what is amiodarone used for in crash patients?

A

prolonged v tach or v fib
anti-dysrhythmic
sodium channel blocking
IV or IO

476
Q

why is amiodarone potentially causing anaphylaxis not a concern in crash situation?

A

is likely to be unable to generate immune response if crashed

477
Q

what is glucose used for and how in crash situation?

A

treat hypoglycaemia
IV IO or transmucosally
dilute but in emergency can give neat, may cause phlebitis

478
Q

why is propofol useful in crash patients?

A

give in respiratory distress so can intubate

479
Q

how do you manage drug doses for crash?

A

pre calculated doses
drug chart and use closest weight

480
Q

what is found in thoracotomy draw if in crash trolley?

A

gown
gloves
drapes
chloraprep
thoracotomy kit
scalpel
swabs
finochietto retractors
internal defib paddles
saline

481
Q

list other equipment useful in crash trolley

A

capnograph
suction
crash record chart
ECG
defib and gel
IO access

482
Q

what is the benefit of capnography in crash?

A

shows ventilation
informs of perfusion, gas exchange and metabolism

483
Q

what capnography values are significant in crash situation?

A

ideally maintain minimum of 12
sudden increase indicates patient alive

484
Q

what are the benefits of having suction for CPCR?

A

remove airway secretions
improve larynx visualisation
reduce aspiration risk

485
Q

what should be recorded through a crash?

A

record of events and timings

486
Q

what does ECG show in crash?

A

electrical impulse and conduction
complexes and HR

487
Q

what does a defib do?

A

resets the heart

488
Q

how do you use a defib in a crash?

A

used of v fib and pulseless v tach
increase 50% voltage per shock
likely to return to same rhythm or asystole
user is responsible for everyones safety
good idea to have fire blanket around

489
Q

when is IO access useful?

A

IV access hard
fast access to central circulation
easy to place with easy IO gun

490
Q

list IO placements

A

flat medial surface of proximal tibia - ideal
greater tubercle of humerus - small cats
trochanteric fossa of femur
tibial tuberosity
wing of ielum

491
Q

how do you manage patients post arrest?

A

likely to re arrest
treat condition and cause

492
Q

describe the process of a debrief following crash

A

done after all crashes
go through events
good and bad
improvements needed
no blame

493
Q

what are considerations for equipment in ECC nursing?

A

know equipment and how to use
make sure equipment is working
make sure everyone knows how to use
assess along side patient

494
Q

list procedures that are done in ECC settings

A

normal nursing
triage
stabilisation
sedations
GA
invasive lines
advanced procedures
ventilation
blood transfusions
coma scoring

495
Q

why are discussions so important in ECC settings?

A

client and patients advocate
calm and rationale discussions
plan what to do and what should be done

496
Q

what are considerations for end of life care?

A

can be challenging
must have discussions
all options presented
opinions shouldnt influence decisions

497
Q

how can you train in ECC setting?

A

from ourselves and others
training
CPD
active reasoning

498
Q

what are some types of ECC patients?

A

systemically unwell
immunocompromised
trauma
paeds
geriatrics
post-op/post-GA

499
Q

why is self care so important?

A

some days hard
easy to get overloaded
figure out how to care for self

500
Q

how do you initially manage spinal fractures?

A

stabilise
keep calm

501
Q

how do you initially manage 3rd degree block patients?

A

keep calm, if stressed may die as HR cant increase

502
Q

how do you manage IMHA patients?

A

cross match and transfuse

503
Q

how do you manage thrombocytopenia patients?

A

soft food
gentle handling
medical management
can give platelets

504
Q

how is blood available to give to patients?

A

stored blood
direct blood collection

505
Q

how do you manage hyperthermia patients?

A

active cooling
clip fur
manage seizures

506
Q

how do you manage airway obstruction patients?

A

emergency intubation/trach

507
Q

how does CPAP work?

A

pressure/resistance on exhalation to open airways

508
Q

what is the 5th vital sign following TPR and pain?

A

adequate nutrition

509
Q

list benefits of good patient nutrition

A

reduced mortality and morbidity
reduced hospitalisation
reduced complications

510
Q

when should nutrition be provided to patients?

A

as soon as possible

511
Q

list consequences of not eating

A

got function and patient appetite reduced

512
Q

list indicators and risk factors of malnutrition

A

poor MCS - sarcopenia or cachexia
poor BCS - >5% short term or >10% long term
reduced appetite
poor coat condition
underlying disease
increased protein losses due to disease

513
Q

define sarcopenia

A

muscle loss in old age in absence of disease

514
Q

define cachexia

A

muscle loss in presence of disease

515
Q

describe what happens in simple starvation

A

normal metabolic adaptations
utilisation of glycogen stores
conservation of protein and muscle
increased fat usage

516
Q

describe what happens in stress starvation

A

clinical disease
hypermetabolism
breakdown of protein/muscle wasting
in catabolic state
reduced time to state of malnutrition, cachexia
poorer prognosis

517
Q

what should be assessed before nutrition in patients?

A

hydration
electrolytes
acid base balance
pain

518
Q

what are aims for short term nutrition?

A

provide for ongoing nutritional needs - energy and nutrients
prevent or correct nutritional deficiencies/imbalances
minimise metabolic derangements
prevent further catabolism of lean body mass

519
Q

what are long term nutritional aims?

A

restoration of optimal body condition
provision of nutrients to the animal in own environment

520
Q

list main types of feeding tubes

A

naso-oesophageal or naso-gastric for short term
oesophagostomy, gastrostomy or jejunostomy for longer term, need GA

521
Q

what type of feeding is used where possible?

522
Q

what affects choice of feeding tube?

A

patient tolerance
risk of GA
duration needed
clinician experience
risk of complications
type of diet
owner cost
ability to use at home is needed

523
Q

what is re-feeding syndrome?

A

complex metabolic derangements that occur when enteral or parenteral nutrition is fed to severely malnourished patients or following period of prolonged starvation
potentially fatal complication

524
Q

what changes are seen in refeeding syndrome?

A

change from catabolic to anabolic state
sudden insulin release causing severe hypophosphatemia, hypokalaemia, hyponatraemia, hyperglycaemia, hypocalcaemia

525
Q

list clinical signs of refeeding syndrome

A

peripheral oedema
haemolytic anaemia
cardiac failure
neurological dysfunction
respiratory failure

526
Q

what needs to be ensured before feeding patients?

A

haemodynamically stable
fluids and electrolytes balanced

527
Q

describe approach to feeding anorexic patient

A

assess malnutrition
gradual introduction
microenteral nutrition with oral rehydration - no calories but has electrolytes
small frequent meals
tube feed until eating >85% daily RER

528
Q

how do you reach full RER in patients with no anorexia?

A

day 1 - 1/2 RER
day 2 - full RER

529
Q

how do you reach full RER in patients with less than 3 days anorexia?

A

day 1 - 1/3 RER
day 2 - 2/3 RER
day 3 - full RER

530
Q

how do you reach full RER in patients with more than 3 days anorexia?

A

day 1 - 1/4 RER
day 2 - 1/2 RER
day 3 - 2/3 RER
day 4 - 3/4 RER
day 5 - full RER

531
Q

what is parenteral nutrition?

A

providing patient with nutrition via IV route when cant do enteral

532
Q

what are considerations for parenteral nutrition?

A

highly skilled practice
referral level
many complications possible

533
Q

what is the general composition of parenteral nutrition?

A

lipids
amino acids
dextrose/glucose

534
Q

describe how to give parenteral nutrition

A

through peripheral lines only
monitor for infection or phlebitis
mix solution to prevent separation
monitor for complications
cover bag if b12 added as light sensitive
deliver through CRI pump
replace line and bag after 24-48 hours
keep lines in for walking
give microenteral nutrition to prevent intestinal atrophy
wean off as increases insulin, will cause hypoglycaemia

535
Q

list possible complications for parenteral nutrition

A

metabolic complication
occlusion
dislodgement
patient interference
sepsis
hyperglycaemia if more than 50% or 4mg/kg/min dextrose

536
Q

what are parenteral nutrition requirements for dogs and cats?

A

dogs - 4-5g protein per 100kcal
cats - 6g protein per 100kcal
then 50:50 lipid : dextrose for remaining cals

537
Q

when do you lower protein in parenteral nutrition?

A

hepatic or renal failure

538
Q

what conditions do you increase protein in parenteral nutrition?

A

protein losing conditions
sepsis
burns
head trauma

539
Q

how do you calculate RER?

A

(BW x 30) + 70

540
Q

how can you prevent complications associated with parenteral nutrition?

A

experienced people managing patient
clear protocols in place
aseptic techniques
prevent patient interference
regular monitoring and recording

541
Q

list considerations for nutrition in acute pancreatitis case

A

fluids
anti-emetics
analgesia - no NSAIDs until eating
feed depending on how long not eating
microenteral nutrition
low fat, highly digestible food
NO tube short term
daily weighing
feed to avoid increasing pancreas inflammation

542
Q

list considerations for nutrition in mandible fracture case

A

fluids as likely dehydrated
o tube
opioids
no nsaids until eating
possible refeeding syndrome
daily weighing
blood monitoring

543
Q

list nutritional considerations for AKI

A

bloods
fluids and supplements
anti-emetics
analgesia
renal diet
microentral nutrition
supplement - increased loss of water soluble vitamins
reduced protein in food
highly digestible and quality food
tube feed

544
Q

list reasons for alternative diets

A

money
beliefs
source of education
personal experience
surrounding influences
health reasons
allergies
believed better quality or healthier

545
Q

what is raw feeding?

A

BARF/biologically appropriate raw food/bone and raw food

546
Q

what are the forms of raw feeding available?

A

pre-prepared
homemade

547
Q

what is difference in dogs compared to wolves in terms of digestion?

A

dogs have increased ability to digest starch
dogs live longer
have balance of energy and other nutrients based on lifestyle

548
Q

list risks of raw feeding

A

imprecise nutritional measurement
low vitamin and mineral content
microbiological infection
salmonella, listeria, toxoplasma, crypto, mycobacterium bovis
can cause hyperthyroid if eating throat tissue

549
Q

list considerations when feeding raw

A

irradiated diet better as kills pathogens
cooking kills pathogens without changing nutrients
good hygiene important
dietary calcium and other deficiencies common
keep on top of worming
minced meat more prone to pathogens due to processing
home freezing doesnt kill pathogens
risk of bone
risk if vulnerable people in house
risk of disease to humans

550
Q

what is the WSAVA stance on raw feeding?

A

no documented evidence for raw feeding but documented risks

551
Q

what is the BSAVA stance on raw feeding?

A

can be safely fed if good hygiene and correct nutrient levels met

552
Q

what is the raw feeding veterinary society stance on raw feeding?

A

has researched health benefits
risks studied outdated
lack of evidence to support risk of ingested bones
argue against nutritional inadequacy

553
Q

how should you discuss raw feeding with owners?

A

dispel misconceptions
understand views
discuss risks
assess patient health
assess home environment
keep on top of worming
support as much as possible

554
Q

how should raw food be sourced?

A

irradiated ingredients
avoid ground meat
cook to kill bacteria
good hygiene

555
Q

why cant cats be veggie or vegan?

A

obligate carnivores
need higher protien requirement
need taurine from meat

556
Q

why is synthetic taurine not reccomended in cats?

A

unknown if biologically available

557
Q

what are negatives of commercial veggie and vegan animal diets?

A

nutritionally inadequate
low palatability
low digestibility
low biological value

558
Q

what should guide home cooking of meals for pets?

A

nutritional diplomat

559
Q

list common signs of eye pain

A

blepharospasm/increased blink rate
reduced palpebral fissure/how open eye is
ocular discharge/epiphora
hyperaemia/redness

560
Q

list local signs of eye pain

A

photophobia/light avoidance
miosis/small pupil
third eyelid protrusion
head shy
self trauma

561
Q

list systemic signs of eye pain

A

reduced appetite
quiet
depressed
headache

562
Q

how should you triage eye pain?

A

assess on the day
assess systemic signs
assess ocular signs
onset
duration
clients may not be able to accurately identify eye conditions

563
Q

why is normal pain scoring not ideal for eye pain?

A

depend on facial expressions so is effected by blepharospasm

564
Q

what is the ophthalmic pain score?

A

score specifically for eyes, needs analgesia for scores over 3
assesses demeanour, blepharospasm and rubbing of the eye

565
Q

what are options for managing ophthalmic pain?

A

topical or systemic medical options
surgery
analgesia
treat cause
advocate for patient

566
Q

list causes of ocular pain

A

scratchy dry eyelids
ulcers
cramping spasm uveitis
intractable glaucoma
orbital swelling
other

567
Q

how is dry eyelids treated?

A

lubrication with hyaluronic acid eye drops - clinitas

568
Q

how are eye ulcers treated?

A

bandage contact lens
analgesia
topical lube
infection management

569
Q

how is cramping spasm uveitis treated?

A

atropine/cyclopentolate drops

570
Q

how is orbital swelling treated?

A

NSAIDs and opioids

571
Q

how is cherry eye treated?

572
Q

how is ocular FB treated?

573
Q

how is entropion treated?

A

surgery to correct

574
Q

what are important considerations for handling ocular patients?

A

blind or reduced sight
painful
fragile eye - may rupture
go slowly
talk to patient
avoid bumps
guide through things

575
Q

how do you handle patients for ocular exams?

A

assess temperament
keep steady and calm
end of table so comfortable for examiner
rewards and reassurance

576
Q

what can cause vision loss?

A

cateract
glaucoma
SARDS
toxins
PRA
brain disease
trauma

577
Q

what are cataracts?

A

inherited or caused by diabetes
opacity of lens

578
Q

what is glaucoma and what can cause it?

A

high pressure in the eye
primary genetic defect or secondary to intraocular neoplasia, uveitis or lens luxation

579
Q

how is glaucoma treated?

A

medical management
surgical shunt implant
laser
usually enucleation

580
Q

what is SARDS?

A

sudden acquired retinal degeneration syndrome
flat line on electroretinogram
no treatment

581
Q

what are toxins that can effect the eyes?

A

ivermectin
enrofloxacin

582
Q

what is PRA?

A

progressive retinal atrophy
night vision loss then day vision loss
rods not responding on ERG
common in cocker spaniels

583
Q

how is PRA diagnosed?

A

simple maze test

584
Q

what is the order of important senses in cats and dogs?

A

smell
hearing
vision

585
Q

how can you help owners with blind animals?

A

how they feel
how patient feels and is coping well most likely
sources of support
materials such as bump bars, training to help patient
lead walks more ideal

586
Q

how long do simple ulcers ulcers take to heal?

587
Q

why are eye ulcers at risk of infection?

A

bacteria can enter as corneal epithelium not present to protect against infection

588
Q

what is keratomalacia melting (risk in eye ulcer)?

A

tear enzymes liquify cornea leading to perforation, endophthalmitis, glaucoma, phthisis, blindness, necrotic end stage eye

589
Q

define phthisis

A

shrunken globe due to reduced aqueous humour formation

590
Q

describe the layers of the eye

A

cornea
limbus
sclera

591
Q

what is the anatomy of the cornea?

A

0.5mm thick
transparent stratified squamous epithelium
corneal epithelium
corneal stroma
descemets membrane
endothelium
covered by tear film

592
Q

what is the anatomy of the limbus?

A

transitional zone between cornea and sclera
stem cells present

593
Q

what is the anatomy of the sclera?

A

white of the eye
fibrous tunic
gives glove rigidity

594
Q

what are the different layers of eye ulcers from least to worst depending on depth of stroma effected?

A

superficial
deep
descemetocele - bottom layer of cornea
perforation - ruptured

595
Q

what is meant by fragile eye?

A

over 50% stromal loss
very fragile when down to descemets layer
increase of IOP can cause rupture

596
Q

list causes of increased IOP?

A

barking
jugular bloods
coughing
vomiting
pulling on neck
firm restraint

597
Q

why are brachycephalic commonly effected by fragile eye?

A

reduced corneal sensitivity
cant blink properly
shallow globes

598
Q

how should you handle patients with fragile eye?

A

avoid pressure on neck or lids
high venous pressure results in high IOP
avoid stress
regular meds
keep eyes clean

599
Q

what is SCCED?

A

spontaneous chronic corneal epithelial defect

600
Q

how is SCCED treated?

A

algar brush
grid - not on cats or pugs
superficial keratectomy

601
Q

what is a superficial keratectomy?

A

removal of top layer of cornea

602
Q

how are stromal ulcers treated?

A

medical management
surgical graft

603
Q

how are melting ulcers treated?

A

medical management
corneal cross linking - if too mushy to operate
corneal graft

604
Q

how is descemetoceles treated?

A

tectonic or structural support
CCT/corneoconjunctival transposition - moving healthy cornea over ulcer

605
Q

what can eye ulcer perforation lead to?

A

endophthalmitis - inflammation of inner eye

606
Q

how are perforated eye ulcers treated?

A

suturing
patch
graft
enucleation

607
Q

list considerations for inpatients with ocular disease

A

low stress
smooth induction and recovery
cats separate
horses dark stables with atropine

608
Q

list post op care for ocular surgery

A

harness walks
no jug samples
buster collar
manage pain
eye meds
keep wounds clean and dry
keep patient calm

609
Q

list examples of trauma to the eye

A

sharp trauma - cat claw
blunt trauma - rta etc
proptosis - eyelid behind globe, eye out of orbit
penetrating FB

610
Q

how do you manage ocular emergencies?

A

assess ABCs
analgesia
lubrication to support ocular surface and prevent ulcers
prevent more trauma
stabilise FB
buster collar

611
Q

why are puppies susceptible to cat claw injuries to the eye?

A

menace response develops at 8-12 weeks

612
Q

what can be consequences of cat claw injuries to the eye?

A

lacerates cornea, can heal over
lens puncture
capsular tear
cataract formation
lens induced uveitis

613
Q

what is seen in glaucoma patients?

A

non-traumatic emergency, often late presenting
blue cornea
red sclera and conjunctiva
blindness
pain
chronic cases have enlarged globe
IOP over 30mmHg

614
Q

why does the high IOP in glaucoma cause rapid blindness?

A

damages photoreceptors

615
Q

what is normal IOP?

616
Q

define exophthalmos

A

protrusion of the globe

617
Q

list causes of exophthalmos

A

FB causing abscess
mass
elevator slip trauma from dental work
stick injuries

618
Q

list signs of exophthalmos

A

protruding eye
pain on opening mouth
excessive conjunctiva visible
excessive 3rd eyelid

619
Q

what is the role of lubricants for eyes?

A

protect soothe and support healing of eyes
reduce evaporation
prevent ulceration
replace missing tears

620
Q

what is an example of eye lube?

621
Q

what are antibiotics used for in eye management?

A

treatment or prophylaxis of infection

622
Q

list an example of ocular antibiotic

A

chloramphenicol

623
Q

what anti-inflammatories are used for eyes?

A

NSAIDs, steroids
acular

624
Q

what are immune modulators used for for treating eye disease?

A

immune mediated disease

625
Q

list an example of immune modulator for eye disease

626
Q

what are anti-glaucoma drugs used for and an example?

A

lower eye pressure
azarga

627
Q

what do mydriatics do and an example?

A

dilate pupil
mydriacyl

628
Q

when are LAs used for eyes and an example?

A

diagnosis and pre-op
proxymetacaine

629
Q

how do serum drops work in the eye?

A

reduces corneal breakdown as contains factors present in tears
provides replacement nutritional tear film promoting ocular surface renewal
immunological defence

630
Q

how is serum eye drops made?

A

FFP or serum
defrosted and 3ml drawn up sterilely
stored in freezer

631
Q

when are serum eye drops commonly used?

A

melting ulcers
prevent keratomalacia

632
Q

describe considerations for applying eyedrops

A

correct med
clean discharge
one drop enough
avoid touching surface of eye

633
Q

how long should be left between eye drops?

A

10 minutes between drops
60 minutes between gel and ointments

634
Q

list order of eye drop admin

A

watery aqueous drops
suspension
gel
ointment

635
Q

what is meant by OS?

636
Q

what is OD?

637
Q

what is OU?

638
Q

how do you prepare ocular patients for surgery?

A

assess physical mobility
systemic health
concurrent disease
likely diabetic if non-traumatic cause - manage insulin and feeding

639
Q

what are anaesthetic considerations for ocular surgery patients?

A

smooth induction
prevent movement of patient with vacuum bags
vet to position specifically
back end monitoring where possible
armoured ETT
NMB and vent

640
Q

describe clipping for lid surgery

A

wear gloves
copious lube in eye for hairs
small sharp clippers
scissors for eyelashes
avoid skin irritation
flush hairs and lube away with saline

641
Q

how do you prep eye for surgery?

A

povidone iodine - not scrub as contains soap or tincture as contains alcohol
1:50 for globe
1:10 for eyelid
made up with sterile saline
2 minute contact time then flush with sterile saline to prevent toxicity

642
Q

what is included on trolley for occular surgery?

A

drapes - fenestrated, sticky, drape tape
gloves
gown
chair equipment
saline flush
operating microscope
sterile handles
ventilator
phacoemulsification machine for cataracts
kits
suture material

643
Q

what kits are used in eye surgery?

A

lid kit
corneal kit
phaeco kit
intraocular kit
general eye kit in first op

644
Q

list considerations for enucleation

A

local retrobulbar block
occulo-cardiac reflex
avoid trauma to chiasm
haemorrhage
histology recommended with specialist pathologist

645
Q

describe the 2 types of enucleation

A

trans-conjunctival - 2 phases, eye and lids removed separately
trans-palpebral - eyelids sutured together then removed with eye, common in tumours

646
Q

what is the oculo-cardiac reflex?

A

reflex bradycardia on eye pressure due to vagal stimulation

647
Q

what is the chiasm of the eye?

A

fibres and nerves from eyes meet together

648
Q

what is the effect of traction on the chiasm?

A

blindness in other eye
especially prone in cats with shorter optic nerves

649
Q

how do you manage haemorrhage from removing eye?

A

haemostasis
collagen pads and powders
adrenaline
pressure

650
Q

list common eye surgeries

A

entropion
mass removal
rhytidectomy - face lift for droopy dogs
distichasis/ectopic cilla correction (management of extra hairs on eyelids) with cryosurgery or electrolysis
medial canthoplasty on pugs - correct droopy eyelids
cherry eye
lid to lid transpositions
parotid duct transposition for dry eye

651
Q

list considerations for corneal surgery

A

horizonal eye positioning
central eye with NMB or stay sutures
removal of damaged cornea or CCT

652
Q

how do you assess pre cataract surgery?

A

screen for inherited causes - BVA, KC or ISDS eye schemes
gonioscopy to check glaucoma risk post op
ERG to check retinal function, no point if blind anyway
US for tumour check and detached retina
post op meds practicality
cost
test for comorbidities
impact on owner

653
Q

what is gonioscopy?

A

assesses drainage angle in eye
assess signs of inherited glaucoma
done conscious with LA drops

654
Q

how is ocular US performed?

A

conscious
local proxymetacaine to desensitise cornea
lots of gel/lube

655
Q

what can be seen in ocular US?

A

eye structures - lens, cataracts, retinal detachment, retrobulbar mass, FB
normal lens is black

656
Q

what is the purpose of ERG?

A

records retinal electrical response to light stimulus
assessment of retinal function

657
Q

what are other methods of assessing eyes?

A

CT and MRI

658
Q

what is the risk of cataracts following diabetes diagnosis?

A

50% develop them in 6 months
75-80% develop them in year

659
Q

what are the risks of diabetic cataracts?

A

lens rupture
lens induced uveitis

660
Q

what are the positives of cataract surgery?

A

restore vision

661
Q

what is aftercare for cataract surgery?

A

meds for first week upto 12 times a day
quiet for 2 weeks
topical NSAIDs and steroids for uveitis
glaucoma meds for IOP management
antibiotics until wound healed
lube for comfort

662
Q

what are GA risks for ocular surgery?

A

usually older patients
commonly have co-morbidities
brachycephalics prone so come with risks
cardiac issues

663
Q

what analgesics are used for ocular surgery patients?

A

topical proxymetacaine
LA in skin line or retrobulbar
systemic NSAIDs, opioids, CRI

664
Q

why are NMBs useful for ophthalmic surgery?

A

provide central eye

665
Q

what is brachycephalic ocular syndrome?

A

one or multiple of:
medial entropion
shallow orbit
relative exophthalmos/bludging eye
macropalpebral fissue/excessive limbal and scleral exposure
lagophthalmos/cant close eyes
medial caruncular trichiasis/hair arising from the inner corner of eyelid
nasal fold trichiasis/facial hair contacting eyes
pigmentary keratitis/black brown pigment in cornea causing blindness
epiphoria from kinking of nasolacrimal duct and obscuring punctum
exacerbated by other conditions such as dry eye or distichiasis/eyelashes in inner eyelids

666
Q

list considerations for brachy airways in GA

A

pre-oxygenate
keep cool
reduce stress
get home soon
care for URT obstruction in recovery
extubate late

667
Q

what are considerations for brachycephalic reflux?

A

short starve so acid doesnt build up
risk of hiatal hernia
omeprazole to reduce reflux or ulceration
paracetamol if liver okay
walk to stimulate peristalsis
maintain hydration
low fat meal

668
Q

list considerations for diabetic patients undergoing ophthalmic surgery

A

monitor glucose
starve from morning and withhold insulin
hyper easier to manage than hypo
higher hypertension risk
dry eye
delayed healing and infection
higher fluid requirements

669
Q

what are considerations for communicating with clients for ocular surgery?

A

likely expensive
train for eye drops
habituate brachy puppies for drops
discuss breed specific considerations

670
Q

why are primary care clinics important for eye disease?

A

monitor for subclinical disease
educate owners
support medication compliance
training eye meds
schirmer test for high risk breeds
early tests for diagnostics

671
Q

what makes up the tear film?

A

lipid layer
aqueous layer
mucus layer

672
Q

what is the purpose of the lipid layer?

A

prevents evaporation
aids distribution

673
Q

what is the purpose of the aqueous layer?

A

supplies corneal nutrition
antebrachial properties
removal and remodelling with proteases and antiproteases

674
Q

what is the purpose of mucus layer of the eye?

A

lubrication
refractive properties
anchors aqueous layer to cornea

675
Q

what is keratoconjunctivitis sica?

A

dry eye
immune mediated adenitis/inflammation
deficiency of aqueous teat
slow onset

676
Q

what breeds are predisposed to KCS?

A

WHWT
yorkie
min schnauzer
english bulldog
pugs
pekinese
boston terrier
lhasa apso
american cocker
springer
CKCS
blood hounds

677
Q

how is KCS diagnoses?

A

schirmer tear test
clinical signs

678
Q

what is normal schirmer tear test?

A

15-25mm/min

679
Q

what schirmer tear test is seen in different levels of KCS?

A

early - 10-14mm/min
moderate - 6-10mm/min
severe 0-5mm/min

680
Q

list clinical signs of KCS

A

strings of mucus
poor corneal clarity
poor corneal shine
low STT reading

681
Q

what does a pulse ox do?

A

measure SpO2 and Hb saturation

682
Q

what does capnography measure?

683
Q

what are the types of NIBP?

A

osscillometric
doppler

684
Q

how is IBP measured?

A

arterial catheter

685
Q

why is central venous pressure not commonly used?

A

needs central venous line
other ways to measure haemodynamic status

686
Q

list common equipment in ICU

A

pulse ox
capnograph
NIBP
IBP
multiparameter
glucometer
lactate monitor
lab machines
syringe driver and infusion pump

687
Q

what should lactate be below?

688
Q

when is lactate machine useful?

A

if no blood gas machine

689
Q

what are useful lab machines in ICU?

A

biochem
haem
centrifuge

690
Q

what is pH?

A

measure of hydrogen ions

691
Q

what is PaO2/PvO2?

A

partial pressure of oxygen in arterial/venous plasma

692
Q

what is PaCO2/PvCO2?

A

partial pressure of CO2 in arterial/venous plasma

693
Q

which partial pressure of CO2 is more accurate?

694
Q

what is a base excess?

A

hydrogen ions needed to return pH back to normal
can be excess or deficit

695
Q

what is the role of bicarb?

696
Q

what is the anion gap?

A

unmeasured ions in the blood
ketones, uric acid, ethylene glycol etc

697
Q

what is normal pH?

698
Q

what is normal PaO2?

A

80-100mmHg

699
Q

what is normal PaCO2?

700
Q

what is normal bicarb?

701
Q

what is normal base excess?

702
Q

what is normal anion gap in dogs and cats?

A

dogs - 12-24mEq/L
cats - 13-27mEq/L

703
Q

define metabolic acidosis

A

pH less than 7.35
acidaemia

704
Q

what are compensatory mechanisms for metabolic acidosis?

A

bicarb buffer - results in low bicarb
hyperventilation - results in low PaCO2

705
Q

what can cause metabolic acidosis?

A

increased lactate

706
Q

define metabolic alkalosis

A

pH more than 7.45
alkalaemia

707
Q

what are compensatory mechanisms for metabolic alkalosis?

A

bicarb buffer - results in high bicarb
hypoventilation - results in high PaCO2

708
Q

define respiratory acidosis

A

PaCO2 over 45mmHg

709
Q

what is compensation for respiratory acidosis?

A

hyperventilation to remove CO2 and increase pH

710
Q

define respiratory alkalosis

A

PaCO under 25mmHg

711
Q

how is respiratory alkalosis compensated?

A

hypoventilation to retain CO2 and decrease pH

712
Q

what can cause secondary metabolic acidosis?

A

primary respiratory acidosis

713
Q

what can cause secondary metabolic alkalosis?

A

primary respiratory alkalosis

714
Q

what can cause compensatory respiratory alkalosis?

A

metabolic acidosis

715
Q

what can cause compensatory respiratory acidosis?

A

metabolic alkalosis

716
Q

list causes of metabolic acidosis?

A

diarrhoea
DKA
renal failure
addisons
lactic acidosis/sepsis

717
Q

list causes of metabolic alkalosis

A

vomiting - loss of H ions
hypoalbuminaemia - weak acids
neoplasia
dehydration

718
Q

what is the rule of 20?

A

list of critical parameters to check in critical patients, frequency depends on severity of case

719
Q

list the rule of 20 parameters

A

fluid balance
oncotic pull/albumin
glucose
electrolytes and acid base
oxygenation and ventilation
consciousness and mentation
BP
HR, contractability and rhythm
temperature
coagulation
RBC and Hb
renal function
immune status
GI motility
drug doses and metabolism
nutrition
pain control
patient mobilisation
wound care
TLC

720
Q

what are the effects of sepsis/SIRS and high inflammation on rule of 20 parameters?

A

impairs BP
impairs HR, rhythm and contractility

721
Q

what are considerations for fluids in rule of 20?

A

boluses in increments of 10ml/kg
consider blood loss and haemorrhage
losses higher in high flow oxygen therapy

722
Q

what are considerations for oncotic pull in rule of 20?

A

manage feeding to prevent hypoalbuminaemia

723
Q

what can cause glucose requirements to be increased in ECC setting?

A

head trauma

724
Q

what are considerations for ventilation in rule of 20?

A

decresed when respiratory centres effected
monitor SpO2, PaO2, PaCO2
CPAP better than ventilation as prevents ARDS

725
Q

what is ARDS?

A

acute respiratory distress syndrome
lots of surfactant produced causing lots of inflammation

726
Q

what considerations should be made for patient positioning in ECC setting?

A

tilt head up to reduce risk of regurg and lower ICP as needed

727
Q

what should be considered for BP in rule of 20?

A

cushings reflex if head trauma

728
Q

what should be considered for HR and ECG in rule of 20?

A

monitor for changes and abnormalities

729
Q

what should be considered for RBC and Hb in rule of 20?

A

any haemorrhage

730
Q

what should be considered in temperature in rule of 20?

A

risk of high temperature if pyrexia, hyperthermia
risk of hypothermia
manage as needed

731
Q

what are considerations for coagulation in rule of 20?

A

trauma may need TXA for clotting to stop bleeding
TXA can induce emesis so dilute and give slow IV

732
Q

what should be considered for renal function in rule of 20?

A

monitor UOP and ins of fluids

733
Q

when would antibiotics be appropriate to give in critical patients?

A

concern or risk of aspiration pneumonia

734
Q

what should be considered for drugs and analgesia in rule of 20?

A

case by case considerations

735
Q

what are nutrition considerations in rule of 20?

A

tube feeding or parenteral nutrition as needed

736
Q

what are considerations for mobilisation in rule of 20?

A

regular walks
turn 4 hourly if immobile
oral and eye care
physio

737
Q

what are considerations for wound management in rule of 20?

A

prevent urine scalding
manage any wounds appropriately

738
Q

what is consideration for TLC in rule of 20?

A

important for all patients

739
Q

what are considerations for nursing long term ventilator patients?

A

eye care
mouth care
airways
humidification of air flow
physio and positioning
line, drain and tube management
manage excretions
drugs
treat underlying disease
communication with team
record everything
acid base, blood gases and electrolyte management

740
Q

how should care be managed in ECC patients?

A

tailor to each patient
equipment depends on whats available
use rule of 20

741
Q

what is GCPS?

A

validated for use in hospitals to determine if need more analgesia

742
Q

what is modified glasgow coma scale?

A

measurement of mentation, should be 18/18
if drops more than 2 is a concern

743
Q

why is anaemia common in cats?

A

mask illness and disease so diagnosed later and more severe by diagnosis
have shorter RBC than dogs so clinical signs appear in shorter time
lower total RBC mass
feline haemoglobin has lower affinity for oxygen so give up oxygen to tissues easily
can be more tolerant of anaemia

744
Q

list clinical signs of anaemia in cats

A

pallor of MM, may be yellow
lethargy
weakness
hyperdynamic pulses
tachycardia
haemic murmurs (reduced viscosity of bloods so moves around heart chambers)
tachypnoea
enlarged lymph nodes and spleen
pica
signs associated with underlying case

745
Q

how is feline anaemia investigated?

A

haematological investigation
PVC to confirm presence of anaemia and type of anaemia

746
Q

what is seen on PCV for anaemia from acute blood loss?

A

normal PVC as same loss of plasma and RBCs
overall reduced oxygen carrying ability

747
Q

what is seen in PCV for chronic anaemia?

A

low RBCs to plasma
low PCV

748
Q

what is seen in volume overloaded anaemia PCV?

A

low PCV due to normal RBCs but increased plasma volume

749
Q

how do you distinguish between chronic anaemia and volume overloaded anaemia?

A

haematology

750
Q

what are normal PCVs in dogs and cats?

A

dog - 35-55%
cats - 25-45%

751
Q

what is seen in regenerative anaemia?

A

reticulocytes higher than 50x10^9/L
anisocytosis
polychromasia
increased MCV (mean cell volume)
MCHC decreased (mean cell haemoglobin concentration)
bone marrow actively trying to produce blood cells

752
Q

what is seen in non-regenerative anaemia?

A

reticulocyte lower than 50x10^9/L
normocytic
normochromic
normal MCV
normal MCHC
bone marrow not releasing more RBCs to correct anaemia

753
Q

define anisocytosis

A

variation in different RBC size

754
Q

what causes anisocytosis?

A

bone marrow releasing younger cells to increase RBC numbers

755
Q

what causes reduced MCHC in non-regenerative anaemia?

A

younger cells have less Hb carrying ability

756
Q

define polychromasia

A

variation in RBC colour due to haemoglobin

757
Q

define hypochromic

A

pale as less Hb per RBC

758
Q

why are nucleated RBCs seen?

A

earlier release from bone marrow

759
Q

define normocytic

A

normal sized RBC

760
Q

define microcytic

761
Q

define macrocytic

762
Q

what is a reticulocyte?

A

immature RBC

763
Q

what is a normoblast?

A

very early RBC

764
Q

what is an erythrocyte?

A

mature RBC

765
Q

describe RBC maturation in the cat

A

normoblasts mature into aggregate reticulocytes
mature into punctate reticulocytes
mature into erythrocytes

766
Q

what reticulocytes are seen in a normal cat and why?

A

punctate frequently
aggregate rarely
takes longer for RBCs to mature in the cat so some get released early

767
Q

what does the presence of aggregate reticulocytes in cats indicate?

A

active bone marrow regeneration
regenerative anaemia

768
Q

what is the purpose of reticulocyte count?

A

establish if anaemia is regenerative
detect presence of reticulocytes in the blood
estimate growth of patients RBCs
how quickly RBCs are being produced and released from bone marrow

769
Q

how is absolute reticulocyte count (x10^9/L) calculated?

A

observed % reticulocytes x RBC count (from haem) x 10

770
Q

what equipment is needed for complete reticulocyte?

A

new methylene blue stain or brilliant cresyl blue
EDTA with 1ml whole blood
1 eppendorf test tube
37 degree water bath
3 capillary tubes
3 glass microscope slides
pencil for labelling

771
Q

describe how to prepare a slide for reticulocyte count

A

add 3-4 drops of new methylene blue/brilliant cresyl blue to 3-4 drops of mixed EDTA anticoagulated blood to eppendorf tube
mix contents and incubate for 10 minutes in 37 degree water bath
mix blood and solution
make blood smear
label slides
air dry
examine under microscope

772
Q

describe the process of a reticulocyte count

A

look for reticulocytes in monolayer
count 500 cells and number of these that are reticulocytes
calculate % of reticulocytes
use in reticulocyte calculation

773
Q

what are safety measures for using new methylene blue?

A

PPE
safety glasses
gloves
dont eat drink or smoke during use

774
Q

what values are seen in negligible regeneration?

A

<50x10^12/L reticulocytes

775
Q

how any reticulocytes is seen in mild regeneration?

A

50-100 x 10^12/L

776
Q

how many reticulocytes is seen in moderate regeneration?

A

100-200 x 10^12/L

777
Q

how many reticulocytes are seen in substantial regeneration?

A

> 200x10^12/L

778
Q

when are the only times regenerative anaemias are seen?

A

blood loss
haemolysis

779
Q

what can affect categorising of anaemias?

A

duration of anaemia
concurrent disease

780
Q

how does duration of anaemia affect categorisation of the anaemia?

A

regenerative anaemias take 3-5 days for reticulocytes to be released from bone marrow and appear in circulation
will appear initially as non-regenerative but is pre-regenerative

781
Q

what is the effect of chronic blood loss on regenerative anaemia?

A

eventually leads to iron deficiency which impairs RBC formation
overtime becomes poorly or non regenerative

782
Q

what is the main reason for cats getting iron deficiency?

A

chronic flea infestation in kittens

783
Q

what concurrent diseases impair regeneration from bone marrow in anaemia?

A

FeLV
chronic disease
infectious disease - cat flu
inflammatory disease

784
Q

how does bone marrow respond in regenerative anaemia?

A

responds best it can to correct anaemia

785
Q

list causes of regenerative anaemia from haemorrhage in cats

A

trauma
coagulopathies
congenital or inherited clotting defects
anti-coagulant rodenticide poisoning
chronic flea infestation
infected tumours or GI tract

786
Q

what is the name of regenerative anaemia that is non-regenerative due to iron deficiency?

A

non-regenerative microcytic-hypochromic iron deficiency anaemia

787
Q

list haemolytic causes of regenerative anaemia in cats

A

FeLV
FIA/feline infectious anaemia
immune mediated - drugs, neoplasia, infection
heinz body anaemia - paracetamol or onion toxicity, lymphoma
severe hypophosphataemia - refeeding syndrome
incompatible blood transfusions
neonatal isoerythrolysis
inherited defects

788
Q

list factors that indicate haemolytic anaemia in cats

A

jaundice
haemoglobin
lymphadenopathy
splenomegaly

789
Q

what causes feline infectious anaemia?

A

mycoplasma haemofelis, spread by fleas

790
Q

how is feline infectious anaemia diagnosed?

A

demonstrating organisms on RBCs on air dried blood smears, unreliable
PCR on blood with 0.5ml EDTA blood

791
Q

list signs of feline infectious anaemia

A

pallor
lethargy
anorexia
weight loss
pyrexia
dehydration
jaundice if severe acute disease

792
Q

how is feline infectious anaemia treated?

A

doxycycline antibiotic

793
Q

what is important when giving doxycycline?

A

can cause oesophageal strictures
needs to give before food and water so moves into stomach

794
Q

what is heinz body anaemia?

A

irreversibly denatured oxidised haemoglobin
premature destruction by haemolysis

795
Q

what causes heinz body anaemia?

A

paracetamol or onion toxicity
lymphoma
DKA

796
Q

what causes neonatal isoerythrolysis to occur?

A

type b queen give birth to type a kitten
queen has agglutinating anti-a antibodies in blood which are passed onto kittens in colostrum and RBCs are haemolysed

797
Q

why type of anaemia is more common in cats?

A

non-regenerative anaemia

798
Q

what happens in non-regenerative anaemia?

A

bone marrow doesnt respond to anaemia so doesnt produce adequate new RBCs

799
Q

list causes of non-regenerative anaemia in cats

A

disorders of bone marrow
suppression of normal bone marrow due to systemic disease

800
Q

how is non-regenerative anaemia diagnosed?

A

bone marrow sampling in severe anaemia - femur or humerus

801
Q

list systemic disease causing non-regenerative anaemia

A

neoplasia
FeLV
FIV
FIP
bacterial infection
CKD
chronic inflammation

802
Q

how does chronic inflammation lead to non-regenerative anaemia?

A

leads to marrow suppressive effects of circulating toxins and suppression of iron reserves

803
Q

how does chronic kidney disease induce non-regenerative anaemia?

A

reduced RBC lifespan
blood loss
impaired iron utilisation
erythropoeitin deficiency - produced by kidneys in response to hypoxia, stimulates RBC production

804
Q

how should anaemia treatment be approached?

A

tailor depending on cause
supportive measures also good

805
Q

when can blood transfusions be useful in anaemia treatment?

A

may be lifesaving in cats in critical condition
adjunct treatment in FIA and non-regenerative anaemias
while waiting response to therapy or results

806
Q

when should blood transfusions be used in anaemia cases?

A

based of clinical signs as even with very low PVC may be coping very well

807
Q

when can erythropoietin be useful in treating feline anaemia?

A

can be successful in CKD
newer recombinant human erythropoietin can be successful

808
Q

what is bone marrow stimulation for anaemia patients?

A

anabolic steroids for first line treatment to stimulate erythroid precursors in bone marrow vie EPO activation
little evidence

809
Q

what treatment may be considered for immune mediated anaemias that have bone marrow failure?

810
Q

list general nursing considerations for anaemia patients

A

monitoring vitals
drugs
assisting diagnostics
keeping patient comfortable
managing stress
IVFT
nutritional management

811
Q

what are nursing care for haemorrhagic anaemia patients?

A

control haemorrhage
IVFT
oxygen
blood transfusion
care for specific cause

812
Q

what is nursing care for haemolytic anaemia patient?

A

IVFT
nutritional supplements - iron, folic acid, B vitamins
feeding tubes
padded bedding and turning as often recumbent
barrier nurse - on immunosupressants

813
Q

list nursing considerations for non-regenerative anaemia patients

A

treat primary systemic disease
transfusion if needed
feeding high iron, folic acid and b vitamins
feeding tube

814
Q

why is barrier nursing often important for anaemia patients?

A

may causes are from infection or patients are on immunosuppressants

815
Q

define bleeding disorder

A

abnormal condition which allows blood to escape from injured vessels in unregulated transfer or interferes with haemostasis so vessels cant repair

816
Q

how do bleeding disorders occur?

A

primary
secondary to underlying disease process

817
Q

which species more commonly has bleeding disorders?

818
Q

describe the process of primary haemostasis

A

reflex constriction of blood vessels to restrict bleeding and helps the platelet plug not be moved away
formation of platelet plug due to activation of platelets, adheres to vessel collagen at site of the damaged vessel

819
Q

why are platelet activation factors important?

A

they would be constantly forming clots if they didnt need activation

820
Q

what is von willebrands factor?

A

important in platelet adhesion
genetically coded factor
aids activation factors and makes platelets sticky to aid clumping

821
Q

what is von willebrands disease?

A

commonest inherited disorder of haemostasis, especially in dobermans
platelet adhesion and clumping impaired
caused by dominant gene with incomplete penetrance

822
Q

describe secondary haemostasis

A

stabilisation of platelet plug by fibrin mesh formation by coagulation factors
results from activation of clotting cascade
only occurs in larger vessels where the platelet plug isnt stable enough on its own compared to in small vessels where its stable enough

823
Q

describe coagulation factors

A

most are protease enzymes that are sequentially activated to produce cascade phenomenon
divided into intrinsic and extrinsic pathways with final common pathway resulting in formation of fibrin from fibrinogen
numbered by roman numerals

824
Q

how are coagulation factors synthesised?

A

in liver
requires vit k

825
Q

what can cause vitamin k deficiency leading to reduced synthesis of coagulation factors?

A

liver disease
rodenticide toxicity
problems with fat digestion or fat malabsorption - is fat soluble vitamin

826
Q

what are primary haemostatic defects?

A

quantitative and qualitative disorders of platelets
reduced number or function of platelets
vessel wall defects

827
Q

what are secondary haemostatic defects?

A

quantitative and qualitative disorders of coagulation factors
reduced amount of clotting factors
reduced function of clotting factors

828
Q

what is the clinical approach to bleeding case?

A

history
clinical signs
lab investigation

829
Q

what history can be taken for bleeding cases?

A

when owner noticed bleeding
signalment - age may show if inherited or acquired, doberman, malers affected by haemophillia as sex linked
any issues in relatives
previous bleeding, trauma, surgery, issues
toxins
drugs

830
Q

list clinical signs of primary haemostasis diseases

A

multiple minor bleeds
prolonged bleeding
petichiea
echmotic haemorrhages - large bruises
multiple sits of bleeding
surface bleeding of skin and MM

831
Q

list clinical signs of secondary haemostatic diseases

A

single large bleeds
rebleeding
haematoma
localised bleeding
delayed or re bleeding from cuts
deep cavity bleeds - joints, abdomen, thorax

832
Q

describe blood sampling for bleeding disorders

A

take sample before treatment
atraumatic collection to avoid activation of haemostasis and local platelet consumption
fill citirc acid tubes correctly
handle samples correctly

833
Q

what tests are ran for primary haemostasis?

A

platelet count - inhouse
BMBT for platelet function and vessel abnormalities

834
Q

what tests are ran for secondary haemostasis?

A

activated clotting time/ACT for intrinsic and extrinsic pathways
activated partial thromboplastin time/APTT for intrinsic and extrinsic pathways
prothrombin time for extrinsic and common pathways

835
Q

how are platelet counts done in lab?

A

collect blood into EDTA and send to lab

836
Q

describe in house platelet count

A

estimate stained blood smear from fresh EDTA
under low power to scan for platelet clumps
under oil immersion for platelet count, count 10 fields and average

837
Q

what does each platelet per high power field represent?

A

20x10^9/L platelets in circulation

838
Q

what is normal platelet count (high power field and in circulation)?

A

high power field - 11-25
platelets - 200-500x10^9/L

839
Q

what level of platelets can spontaneous bleeding occur?

A

<50x10^9/L

840
Q

what is the purpose of BMBT?

A

test platelet function and vessel wall defects

841
Q

what will be seen in BMBT if there are clotting defects?

A

poor platelet function - prolonged bleeding
normal BMBT with rebleeding - coagulation defect

842
Q

describe how to do a BMBT

A

dog awake, cat sedated
in lateral with lip folded up with bandage
standard incision to buccal mucosa with spring loaded bleeding time device
timer started
blood blotted away with filter paper without disturbing clot formation

843
Q

what is normal BMBT in dogs and cats?

A

dogs - <3.5 min
cats - <3 min

844
Q

list causes of prolonged BMBT

A

von willebrands disease
thrombocytopenia
vascular wall abnormalities
DIC/disseminated intravascular coagulation

845
Q

how do you perfrom a ACT test?

A

2ml blood collected into ACT test tube (activates intrinsic pathway)
tube gently inverted and left undisturbed for 40 seconds
invert every 10 seconds until time to complete clot formation

846
Q

what is normal ACT time?

A

<165 seconds

846
Q

how is APTT and PT carried out?

A

in lab
blood collected into sodium citrate tube, ratio 1:9 (sodium citrate : blood)

847
Q

what is normal APTT?

A

15-25 seconds

848
Q

what is normal PT?

A

7-10 seconds

849
Q

how would you triage a patient with bleeding disorder?

A

owners history
previous issues
toxins
signalment
clinical exam

849
Q

what are considerations for patients with bleeding disorders caused by liver disease?

A

thermoregulation
prolonged meds
no hepatic excreted drugs
possble encephalopathy
low clotting factors

849
Q

list general considerations for bleeding disorder patients

A

handle with care
padded kennel
keep calm
manage hypothermia especially if liver disease
analgesia
avid aspirin and heparin as affects clotting
give meds PO or through IVC
one stick IVC
buster collar to prevent interference
pressure bandage after IVC removal
blood type
harness to avoid jug pressure

849
Q

what should you monitor in bleeding disorder patients?

A

demeanour
TPR
MM
HR - tachycardia
ECG
auscultation for heart murmurs
BP - may be reduced if low circulating volume
petichiea
ecchymosis
haematoma
contusion
haematemesis
haematochezia

849
Q

how do you manage nutrition in bleeding disorder patients?

A

vitamin K supplement
liver disease diet
highly digestible and pallatable
high iron, B vits and vit K

849
Q

how is bleeding disorders treated?

A

restoration of circulating oxygen carrying capacity
manage cause
blood transfusion
antithrombotic therapy
desmopressin for VWD
admin of vit K

850
Q

why are POC analysers for clotting times beneficial?

A

can determine APTT and PT without delay on small volumes of whole blood
i-stat can do ACT and PT
thromboelastography machines can determine viscosity of blood which changes with blood clotting

850
Q

what is specific factor assays?

A

specialist labs can determine deficiencies of specific factors

850
Q

list underlying causes of bleeding disorders

A

liver disease
pancreatitis
bile duct obstruction
rodenticide poisoning
VWD

850
Q

list possible diagnostics for bleeding disorder patients

A

SpO2 and blood gas
liver parameters - ALT, AST
BMBT
PT
APTT
PCV
platelet count
haem
bone marrow sample
biochem - underlying cause
PCR for VWD

851
Q

what causes majority of the body heat?

A

muscular activity - exercise and seizures

851
Q

what controls thermoregulation?

A

anterior hypothalamus
monitored by peripheral and central thermoreceptors to detect if too hot or cold

851
Q

what happens in the body when thermoreceptors detect body is too hot?

A

heat dissipation

851
Q

what happens in the body when thermoreceptors detect body is too cold?

A

heat conservation and production

851
Q

define hyperthermia

A

increased body temperature
above 39.2 degrees

851
Q

list causes of hyperthermia

A

pyrexia
increased heat production due to increased muscular activity
heat stroke

852
Q

what is classic heat stroke?

A

reduced heat loss

852
Q

what is exertional heat stroke?

A

over exercise in high temperatures

852
Q

list causes of heat stroke

A

failure of heat dissipation
URT obstruction
increased environmental temperature/humidity
poor environmental ventilation
circulatory compromise
obesity
breed predisposition

852
Q

what are the risks of body temperature over 41.6 degrees?

A

permenant organ damage - especially kidneys and brain
cell death - due to large increase in oxygen demand
DIC

852
Q

list clinical signs of heat stroke

A

stress
hyperthermia
tachycardia
hypovolaemia - GI losses and vasodilation
hyperdynamic pulses
peripheral vasodilation
collapse
hyperaemia MM
rapid CRT
endotoxin translocation - increased intestinal mucosal permeability, impaired GI perfusion
sepsis
tachypnoea
secondary resp complications - aspiration pneumonia, pulmonary oedema, pulmonary haemorrhage
DIC - coagulopathies
AKI
CNS compromise - direct effects or hypoglycaemia
hyperbillirubinaemia
hypoglycaemia
epithelial desquamation
thrombosis
myopathy
electrolyte derangements

853
Q

what happens when advanced heat stroke patient appears normothermic?

A

peripheral perfusion is impaired so appears normothermic but core temperature is still very high

853
Q

how is most of the heat lost through the body?

A

body surface so peripheral dilation and circulation increases
leads to reduced CO and decreased perfusion of vital organs

853
Q

describe emergency management of heat stroke patients

A

actively cool if over 41 degrees by losing heat from the skin
stop cooling at 39.4 to prevent hypothermia
oxygen if needed
maintain patient airway, intubate if needed
IVFT - water lost when panting, isotonic crystalloids to support circulation, replace defecits and continually assess
bloods - PVC, TS, glucose, electrolytes, abnormal coagulation factors
monitor ICP

853
Q

what shouldnt you do for cooling patients?

A

use too cold water as peripherally vasoconstricts impairing heat loss

854
Q

why shouldnt you cool patients with pyrexia?

A

pyrexia is beneficial to patients with infection as decreases replication of pathogens and increases function of WBC
protective function

855
Q

in what cases should you treat pyrexia with drugs such as paracetamol and NSAIDs?

A

immune compromised or cancer patients

856
Q

list causes of pyrexia

A

infectious or immune mediated inflammatory disease
neoplastic disease
opioids
hepatic encephalopathy
blood transfusion

857
Q

what is meant by endoscopy?

A

to view within

858
Q

how is endoscopy images transmitted?

A

light source to body cavity
resulting image to eyepiece or monitor

859
Q

list types of endoscopy and their uses

A

flexible - GI, bronchoscopy
rigid - rhinoscopy, female cystocopy

860
Q

what are the roles of endoscopy?

A

diagnosis
therapeutic

861
Q

list diagnostic roles of endoscopy

A

observation
sampling - fluid in BAL, brush cytology for cells from linings, FNAs, biopsy

862
Q

list therapeutic reasons for endoscopy

A

FB removal
stricture dilation
feeding/gastrotomy tube placement

863
Q

list benefits of endoscopy

A

minimally invasive
low morbidity/mortality
no convalescence needed so can start steroids immediately

864
Q

list limitations of endoscopy

A

cant visualise the whole GI tract - cant see middle 6 ft
can visualise all but cant toake biopsies in capsule endoscope
only assesses appearance/morphology not function
mucosal evaluation only
cant evaluate extravascular GI disease like in surgery

865
Q

list contraindications for GI endoscopy

A

known GI disease such as perforation or mass lesion
if not adequate for full investigation
not suitable for anaesthesia - inadequate CP function, hepatic or renal function
coagulopathy
inadequate prep of pateints GI tract

866
Q

how can gastric over distension make endoscopy challenging for the operator?

A

lesser curvature has much higher angle and increased antro-pyloric motility so harder for pyloric intubation

867
Q

how do you avoid gastric overdistension during endoscopy?

A

look at stomach last as needs to fill with air to view

868
Q

how can gastric overdistension affect the GA during endoscopy?

A

caudal vena cava compression leading to reduced VR, CO and BP
diaphragmatic splinting so becomes less compliant in respiration so reduced TV

869
Q

list possible complications in endoscopy and how to manage

A

acute bradycardia +/-AV block due to vagal reflex - atropine/glycopyrrolate
aspiration - suction oesophagus and pharynx at end
transient bacteraemia in colonoscopy - antibiotics if patient at risk
GI perf if servere pathology or ulcers or abdo swelling
haemorrhage - laceration during FB removal or stricture dilation, or mucosal

870
Q

what makes up the endoscopy system?

A

light source
air/water insufflator
suction pump
endoscope and insertion tube
forceps

871
Q

describe the light source of an endoscope

A

cold light
historically tungsten halogen - cheap, red tint, not bright
can use metal halide or LED
now use xenon arc - 1000 hours, brighter and white light

872
Q

describe the air/water insufflation and suction on the endoscope

A

housed in light source
air pump for insufflation
seperate suction for deflation
water reserviour for washing lens

873
Q

list components of the flexible endoscope

A

light guide connector
light guide tube
control body
video remote switches
insertion tube
internal instrument channels
bending section

874
Q

what transmits non-coherent illumination?

A

glass fibre optics

875
Q

how are endoscopy images transmitted?

A

fibre optics
video endoscopy

876
Q

describe fibre optic transmission in an endoscope

A

individiual glass fibres coated in lower optical density glass cladding
light transmitted by total internal reflection
in coherent bundles

877
Q

how does video endoscopy work?

A

image transmitted via wire from CCD video chip behind lens

878
Q

list advantages of fibre optic transmission endoscopes

A

portable
wide range of sizes
moderate cost

879
Q

list disadvantages of fibre optic endoscopy

A

faceted/honey comb image
fragile
individual fibres can stop working
size of endoscope dictates image quality
eye piece vs video

880
Q

list advantages of video endoscopy

A

mechanically identical to fibre optic
non-coherent illumination
CCD detects image and is shown on screen
excellent image
image control buttons

881
Q

list disadvantages of video endoscopy

A

expensive
not portable
smallest diameter of scope not possible

882
Q

what are the different features possible on the insertion tube?

A

varying diameters - 5.5-9.5mm for gastro, 10-13mm for colono
varies length
front or side veiwing angle
steering in uni or multiplanar
accessory channels

883
Q

what is the importance of tip retroflexion on endoscopes?

A

visualise cardia and FB retrieval

884
Q

what affects biopsy quality?

A

smaller the channel the worse the quality
cup size
pressure
bigger biopsy the better

885
Q

list accessories available for endoscopy

A

biopsy forceps
cytology brush
sheathed needles
lavage tubes

886
Q

what are the types of biopsy forceps?

A

ellipsoid/oval
round
fenstrated
with spike
swing jaw
reusable or disposable

887
Q

which biopsy forceps are better?

A

oval better than round
fenestrated better than whole
no spike
alligator over smooth
rotatable better
non-swing jaw better

888
Q

how do you confirm endoscopy is indicated?

A

exclude extra GI causes of disease
exclude surgical disease
consider contraindications

889
Q

describe preparation for gastroscopy

A

12 hour fast to empty stomach and duodenum

890
Q

why is important the GI tract is empty before scoping?

A

visualisation
manoeuvrability
food clogs scope
decrease risk of reflux and aspiration

891
Q

what are extra considerations for fasting patients before GI scope?

A

wait 24hrs if barium used as damages scope
consider patients with delayed gastric emptying

892
Q

describe how you prepare for colonoscopy

A

fast for 24-36 hours so whole GI tract empty
oral lavage
multiple high enemas

893
Q

how is an oral lavage performed?

A

polyethylene glycol electrolyte solution/klean prep
day before scope
dogs - 25-30ml/kg x3, 2-4hrs apart
cats - 20ml/kg, x2
normally given in stomach tube (dogs) or NO tube (cats) as unlikely to drink

894
Q

list risks of oral lavage?

A

tracheal intubation and admin
aspiration
trauma from tube placement

895
Q

how is a high enema done?

A

warm water
higginson pump or enema bucket
1L/30kg in dogs, 20ml/kg in cats until clear running
1-2 hours before colonoscopy, may repeat under GA
never phosphate as can be absorbed into blood
no cleansers or laxatives

896
Q

list GA considerations for endoscopy

A

opioids may affect sphincter tone
atropine affects GI tone and motility
smooth induction to avoid aerophagia and stomach distension
familiar routine
cuff ETT
avoid nitrous as accumulates in gas filled organs
care fir gastric dilation, reflux and aspriation

897
Q

how are patients positioned for GI endoscopy?

A

left lateral for entering pylorus easier
right lateral if placing g tube to secure on left side, or for FB removal if needed
mouth gag to prevent biting scope
ETT secured

898
Q

why is it important to be careful placing mouth gags in cats?

A

may compromise blood supply to the brain and cause blindness

899
Q

how do you clean endoscopes?

A

ensure channels are clear immediately post op
flush with air and water
ethylene oxide sterilisation or disinfectant protocol
never autoclave as melts

900
Q

what colour is a serum gel/plain tube?

A

brown
pink or red vacutainer

901
Q

how does a serum gel/plain tube work?

A

contains gel which begins coagulation
or
contains CAT/clotting activation thrombin
produces serum

902
Q

what is serum gel/plain tubes used for?

A

bichemistry
hormonal assays - t4
serology - antibodies
external samples as more stable than heparin

903
Q

what colour are heparin blood tubes?

A

orange
green vacutainer

904
Q

how do heparin tubes work?

A

contains heparin anticoagulant so can test immediately

905
Q

what is heparin tube used for?

A

in house biochemistry

906
Q

what colour are EDTA tubes?

A

pink
purple vacutainer

907
Q

what are EDTA tubes used for?

A

haematology

908
Q

what colour are citrate tubes?

909
Q

what are citrate tubes used for?

A

coagulation profiles

910
Q

what colour are oxalate tubes?

A

yellow
grey vacutainer

911
Q

what are oxalate tubes used for?

A

glucose testing
rare as can do patient side

912
Q

which blood tubes contain anticoagulant?

A

heparin
EDTA
citrate
oxolate

913
Q

what is plasma and which blood tubes result in this?

A

whole blood
anticoagulant tubes

914
Q

what is serum and which blood tubes result in this?

A

clotted blood without platelets or clotting factors
serum tubes

915
Q

list the order of filling blood tubes

A

serum gel
heparin
EDTA

916
Q

why do you fill EDTA tubes last?

A

chelates/binds to calcium as blood cant clot without calcium
2 potassium per EDTA
if biochem contaminated shows low calcium and high potassium

917
Q

what is meant by reference range in lab results?

A

range in 95% animals

918
Q

what is meant by mild out of range?

A

within the range away from the reference interval

919
Q

what is meant by moderate out of range?

A

more than one range away from reference interval

920
Q

what is meant by marked out of range?

A

2 or more range away from reference interval

921
Q

list suffixes for TP, albumin, bilirubin, cholesterol and ALT, ALP and GGT?

A

TP - proteinemia
albumin - albuminemia
bilirubin - bilirubinaemia
cholesterol - cholesterolaemia
ALT, ALP and GGT - just high or low

922
Q

what are the primary and secondary causes of high ALT?

A

primary - hepatopathy/liver disease
secondary - cholestasis, artefact, muscle damage

923
Q

what determines if high ALT is determined by muscle damage?

A

high creatinine kinase - only found in muscle

924
Q

list markers of hepatocellular disease

A

ALT
AST
GLDH
SDH

925
Q

list markers of cholestasis

926
Q

what is meant by functional liver markers?

A

substances produced in the liver - cholesterol, urea, glucose, albumin, globulins, coag factors
substances conjugated and excreted by the liver - bile acids, bilirubin

927
Q

what can cause primary hepatocellular disease?

A

trauma
toxins
drugs
inflammation
infection
neoplasia
intrahepatic cholestasis
bile toxicity

928
Q

what can cause secondary hepatocellular disease?

A

anything
non-specific disease

929
Q

what is seen in decreased hepatic function on lab results?

A

increased bile acids and bilirubin
decreased albumin, cholesterol, urea, glucose, clotting factors

930
Q

what is seen in xylitol toxicity?

A

acute hepatic failure
hypoglycaemia

931
Q

how is xylitol toxicity treated?

A

plasma infusion to increase protein
vitamin k therapy for coags
liver supportive treatment
fluids to increase BP and dilute toxins
antibiotics as liver function impaired

932
Q

what are possible outcomes for xylitol toxicity?

A

recovery
death
complications such as DIC

933
Q

what is seen on a stress leukogram?

A

neutrophilia (increased)
monocytosis (increased)
lymphopenia (decreased)
eosinopenia (decreased)

934
Q

what is acanthocytes?

A

RBC membrane changing
usually artefact but can be due to toxin

935
Q

what shows mild, moderate and marked on heamatology?

A

mild - +
moderate - ++
marked - +++

936
Q

define anisocytosis

A

different sized RBCs

937
Q

what can cause hyperglycaemia on blood results even if no disease present?

938
Q

what is the impact of hyperkalaemia on the body?

A

bradycardia, even at small levels

939
Q

what tests can be done for azotemia?

A

urinalysis
USG
dipstick
sediment exam
US

940
Q

what is hypersthenuria?

A

very concentrated urine to conserve water

941
Q

what is hyposthenuria?

A

very dilute urine as kidneys putting out excess water

942
Q

what is isothenuria?

A

kidney disease
urine same concentration as plasma, kidneys not filtering

943
Q

what is the impact of antifreeze/ethylene glycol ingestion and how is it managed?

A

AKI
IVFT, supportive care, ethanol

944
Q

when may you see an absence of stress leukogram?

A

chronic disease
immunosuppression
bone marrow disease

945
Q

what is important to remember when looking at lab results?

A

consider patient and clinical signs alongside

946
Q

what is cytology?

A

study of cells
screening tests looking at cells in fluids (BAL, CSF, synovial fluid, body cavities) or tissue samples (lumps, LNs)
not diagnostic

947
Q

what are the benefits of cytology?

A

quick
cheap
easy
relatively non-invasive

948
Q

what clinical information should you provide for cytology?

A

history
lesion evolution
previous treatment
characteristics of lesion

949
Q

what information should be provided for characteristics of a lesion for cytology?

A

localisation
firm or soft
dimensions
painful or not
ulcerated or not
cutaneous or SC
adherent or non-adherent
aspirate

950
Q

how should you prep for FNA?

A

surgical prep

951
Q

when should you do a suction FNA?

A

hard cutaneous or SC masses
bone lesions
when non-suction doesnt work

952
Q

describe the process of a suction FNA

A

suction while moving around lesion
release suction before withdrawing to not pull in other cells

953
Q

when are non-suction FNAs performed?

A

soft cutaneous or SC masses
LNs
vascular lesions/organs

954
Q

how is a non-suction FNA performed?

A

insert needle into tissue
pull out
fill syringe with air
attach and push out contents

955
Q

list techniques for making cytology smear

A

line
squash
twist if few cells
star - not ideal as no monolayer
splatter if no choice

956
Q

list methods of collection that arent FNA

A

impression smear
scraping
biopsy
imprint
ear swab

957
Q

describe Malassezia found on cytology

A

yeast
peanut shaped
low numbers on normal skin, infection if multiple organisms per high power field

958
Q

how are cytology samples stained?

A

diff quick
methanol fixation
eosin eosinophillic (base) staining
methylene blue basophilic (acid) staining

958
Q

describe sample preparation for cytology smear samples

A

after collection air dry or hairdry quickly
stain
label with animal and site

959
Q

what are considerations for stains for cytology?

A

replace regularly
methylene blue deteriorates quickly
have clean and dirty sets

960
Q

how much magnification is in the eye piece of a microscope?

961
Q

what is low magnification (10x) used for?

A

looking at cellularity, preservation, staining, haemodilution, cell distribution, background

962
Q

what is the aim in cytology samples?

A

have good cellularity

963
Q

what is meant by cell preservation?

A

how well its fixed

964
Q

what is high magnification (40x) used for in cytology?

A

looking at cellular and non-cellular elements
inflammatory vs neoplasia
malignant and benign

965
Q

what is high magnification (100x) used for in cytology?

A

look for presence of cytoplasmic granules, nuclear details, presence of pathogens

966
Q

how is leishmania spread?

A

sand flies

967
Q

when are neutrophils present and what do they look like?

A

inflammation
crisp, clear nuclear outlines with purple chromatin, clear pale pink cytoplasm, segmented nucleus

968
Q

when are degenerate neutrophils seen and what do they look like?

A

toxic change such as infection
loss of segmentation, lighter fluffy nuclear chromatin, swollen appearance

969
Q

what should you do if you suspect infection but cant see bacteria on cytology?

970
Q

what is the importance of quality control?

A

ensure results are reliable and decisions correctly made based on these

971
Q

what makes results reliable in lab?

A

set up of system
maintainance of analysers and system
interpretation of results
checks ensuring values are acceptable
accurate record keeping

972
Q

list advantages of in house labs

A

fast turn around time
potential for improved monitoring
smaller volume of sample needed
available OOH
available in remote areas
may be cheaper

973
Q

what factor affects lab results?

A

total variability

974
Q

what factors affect results before sampling?

A

biological
interindividual and intraindividual factors

975
Q

what are interindividual factors that may affect lab results?

A

inherent differences between groups of animals due to different signalment (age, breed, sex, species)

976
Q

what are intraindividual factors that may affect lab results?

A

transient difference in same animal, due to environmental and external factors such as diet, stress, excitement, reproductive status, drugs, method of sampling
should be minimised

977
Q

what are the types of analytical factors affecting lab results?

A

pre-analytical
analytical
post-analytical

978
Q

list pre-analytical factors that may affect lab results

A

poor sampling techniques
haemolysed, lipaemic or icteric plasma
wrong anticoagulant to blood ratio
sterile or nonsterile container
transportation
storage

979
Q

describe sample handling for lab

A

fridge if delayed in running tests to slow metabolism
50ml postal sample limit, sealed container, leak proof bag, absorbant for full sample, rigid container

980
Q

list analytical factors that may affect lab results

A

different methods causing different results so cant compare
patient side vs lab
equipment used and function
technician training
lab environment
analytical procedure and technique

981
Q

when should quality control be done?

A

voluntary process based on recommendations
should be done regularly

982
Q

what is quality control?

A

control material of known concentration measured to check accuracy of analytical process
performed during analysis to ensure validity of results
not the same as calibration

983
Q

how do you manage if quality control fails?

A

check for obvious problems - reagent expiry or depletion, faults, clots in machine
use another control sample
repeat control
new reagent and recalibrate
run routine maintenance
consult manufacturer

984
Q

what post analytical factors can affect lab results?

A

transfer of results to patient record
archiving results
storing sample for follow up test

985
Q

what is the most common feline endocrine condition?

A

feline hyperthyroidism

986
Q

what usually causes feline hyperthyroidism?

A

benign tumour (uni or bilateral) secreting excess thyroid hormone

987
Q

what concurrent diseases are often associated with feline hyperthyroidism?

A

HCM
CKD
hypertension
are either alongside due to age or secondary to HT

988
Q

list clinical signs of feline hyperthyroidism

A

polyphagia
weight loss
tachycardia
palpable enlarged thyroid glands

989
Q

how is feline hyperthyroid diagnosed?

990
Q

how can feline hyperthyroidism be treated?

A

medical management
diet
surgery
radioactive iodine

991
Q

how can feline hyperthyroid be managed medically?

A

anti-thyroid drugs - methimazole or carbimazole
lifelong, increasing dose with growth of adenoma

992
Q

how do you monitor cats on medical management for hyperthyroid?

A

euthyorid within 2-3 weeks
check t4 3 weeks after starting treatment or changing dose
monitor haem for side effects and biochem for concurrent disease
ongoing 3-12 month monitoring also with BP and urine

993
Q

why should pregnant women be careful handling antithyroid drugs?

A

can cause fetal abnormalities

994
Q

list side effects and prevalence of antithyroid drugs

A

vomiting, anorexia, lethargy - 10-20% cats, minor
GI signs, bone marrow suppression, facial pruritis, hepatopathy - rare, stop treatment

995
Q

what diet can be used to manage feline hyperthyroid?

A

iodine restricted - hills thyroid care y/d
lifelong and sole food

996
Q

why is iodine restricted diets able to cause euthyroid in 3 weeks?

A

iodine is needed for thyroid hormone synthesis

997
Q

what are negatives to managing feline hyperthyroid with diet?

A

can be less effective than other options
cant use if severely hyperthyroid, other dietary requirements or if euthyroid cats in house

998
Q

what are curative treatments for feline hyperthryoid?

A

thyroidectomy
radioactive iodine

999
Q

why should you do medical management for feline hyperthyroid before curative treatment?

A

HT can mask kidney disease so should assess renal function after treatment before irreversible treatment
can help stabilise before surgery/GA due to metabolism effect in hyperthyroidism

1000
Q

list nursing considerations for hyperthyroid cats

A

careful handling
often fractious due to high metabolism
concurrent disease

1001
Q

what are the benefits of senior cat clinics and hyperthyroid?

A

can screen for the disease

1002
Q

what is the cause of canine hypothyroidism?

A

thyroid tissue destroyed

1003
Q

what is signalment for canine hypothyroid?

A

middle aged
doberman, boxer, malamute more prone

1004
Q

list clinical signs of canine hypothyroidism

A

weight gain
lethargy
bradycardia
endocrine alopecia
myxodema
coma

1005
Q

how is canine hypothyroid diagnosed?

A

measure t4 and TSH in blood

1006
Q

how is canine hypothyroid treated?

A

oral synthetic t4 - sodium levothyroxine

1007
Q

list nursing considerations for canine hypothyroid patients on medication

A

look for derm signs
rarely cause of weight gain
monitor treatment to find optimum dose
consistent dosing important as bioavailability affected by food

1008
Q

when should monitoring should be done long term in hypothyroid dogs?

A

t4
6-8 weeks after starting treatment
2-4 weeks after adjusting dose
long term 6-12months
measure peak (3 hours post pill) and trough (just before dose) values

1009
Q

what is the purpose of calcium in the body?

A

muscle contraction
nerve conduction
other function

1010
Q

how is calcium found in the body and is it inactive or active?

A

bones with phosphate
ionised in blood - active
complexed in blood - inactive
protein bound in blood - inactive

1011
Q

what is total calcium?

A

all calcium in the blood

1012
Q

what does PTH do?

A

increases calcium in the blood by increasing calcium resorption in the kidneys and bone
increases calcitriol formation

1013
Q

where is calcitriol/vitamin d produced?

1014
Q

what does calcitriol/vitamin d do in the body?

A

increases calcium in the blood by increasing calcium resorption in the kidney and increasing calcium absorption in the gut

1015
Q

where is calcitonin produced?

A

thyroid gland

1016
Q

what does calcitonin do in the body?

A

reduces calcium in the blood by reducing calcium release from bone

1017
Q

how is hypocalcaemia managed by the body?

A

PTH released
increased calcium resorption in kidneys, increased calcium mobilisation from bone, activation of calcitriol leading to increased calcium resporption in kidneys and increased calcium absorption in gut
increased calcium

1018
Q

how is hypercalcaemia managedby the body?

A

calcitonin released
increased calcium storage in bone, increased calcium excretion in kidneys
decreased calcium

1019
Q

list parathyroid diseases

A

primary hyperparathyroidism
secondary hyperparathyroidism
hypoparathyroidism

1020
Q

what causes hyperparathyroidism?

A

one or more parathyroids overactive usually due to benign tumour

1021
Q

what dog breed is predisposed to hyperparathyroidism?

1022
Q

list clinical signs of hyperparathyroidism

A

neurological
weakness
lethargy
exercise intolerance
trembling
GI
reduced appetite
nausea
vomiting
constipation
urinary
PUPD
urolithiasis
UTI
CV
hypotension
arrhythmias

1023
Q

how do primary hyperparathyroidism patients normally present?

A

systemically well due to mild disease
1/3 cases hypercalcaemia is incidental finding

1024
Q

how is primary hyperparathyroidism diagnosed?

A

elevated iCa
PTH

1025
Q

how is iCa measured?

A

blood gas
external lab
istat machine

1026
Q

how is primary hyperparathyroid treated?

A

surgical removal of tumour
ethanol injection
US glandular heat ablation

1027
Q

what are considerations when sending samples to the lab for iCa and PTH?

A

iCa - air can effect level
PTH - must be frozen for transport

1028
Q

what are considerations following parathyroid treatment?

A

can damage recurrent laryngeal nerve
monitor iCa as can become hypocalcaemic

1029
Q

what can cause secondary hyperparathyroidism?

A

renal failure - resorbing too much calcium
fed too little calcium or vitamin d deficient so calcium mobilised from bone

1030
Q

what is secondary hyperparathyroidism?

A

chronically low calcium leading to elevated PTH and calcium mobilised from bone

1031
Q

what is hypoparathyroidism?

A

low PTH despite low calcium

1032
Q

list causes of hypoparathyroidism

A

surgical excision of parathyroid
trauma
idiopathic
immune mediated
usually all glands affected in significant disease

1033
Q

list clinical signs of hypoparathyroidism

A

seizures
muscle twitching
weakness
ataxia
anorexia
vomiting
facial rubbing

1034
Q

how is hypoparathyroidism diagnosed?

A

measure iCa
phosphorus
PTH

1035
Q

how are severe cases of hypoparathyroidism treated?

A

IV calcium bolus or CRI calcium

1036
Q

how do you manage mild clinical signs of hypoparathyroidism?

A

oral calcium supplement
calcitriol/vitamin d supplements

1037
Q

what are important considerations when giving IV calcium?

A

close monitoring of ECG and HR
usually 10% calcium gluconate
slow admin to prevent arrhythmia and CA
can cause bradycardia
skin necrosis if not in vein

1038
Q

how do you manage IV calcium extravasion?

A

infiltrate tissue with saline and manage wound

1039
Q

what is hyperadrenocorticism?

A

excess cortisol production from adrenal gland

1040
Q

what is the typical signalment for hyperadrenocorticism?

A

dogs not cats

1041
Q

what are the three types of causes of hyperadrenocorticism?

A

pituitary dependent - 85%, pituitary tumour
adrenal dependent - 15%, adrenal tumour
iatrogenic - admin of glucocorticoids

1042
Q

list clinical signs of hyperadrenocorticism

A

PUPD
lethargy
endocrine alopecia
pot belly
thin skin
poor wound healing
panting
polyphagia
calcinosis cutis - calcium deposits in skin

1043
Q

how is hyperadrenocorticism diagnosed?

A

ACTH
LDDS - low dose dexmethasone depression test

1044
Q

how is hyperadrenocorticism treated?

A

trilostane to block synthesis of cortisol

1045
Q

what are considerations for patients on trilostane?

A

montior clinical signs
ACTH or pre-pill cortisol to monitor
side effects uncommon - GI iatrogenic hypoadrenocorticism, sudden death

1046
Q

list nurse clinic considerations for hyperadrenocorticism

A

look for signs in older patients
monitor treatment - biochem adn ACTH/pre pill cortisol 10 days after treatment or dose change then 4 weeks, 12 weeks and 3 monthly
give dose in morning
monitor for iatrogenic addisons and addisonian crisis

1047
Q

how is ACTH testing done?

A

pre-pill cortisol measured when dose due
ACTH stim 4-6 hours after dose

1048
Q

what is hypoadrenocroticism?

A

lack of glucocorticoids and mineralocorticoids

1049
Q

list signalment for hypoadrenocorticism

A

young to middle aged
females
dogs

1050
Q

list clinical signs of hypoadrenocorticism

A

vague, waxing and waning illness
vomiting
diarrhoea
weight loss

1051
Q

list signs of an addisonian crisis

A

collapse
hypotension
weakness
bradycardia
severe dehydration
hypovolaemia

1052
Q

how is hypoadrenocorticism diagnosed?

A

electrolyte abnormalities
ACTH showing no cortisol

1053
Q

how is an addisonian crisis treated?

A

fluid resus
correct electrolytes
glucose and insulin if severe hypokalaemia
ACTH stim if suspect addisons

1054
Q

what is long term treatment for hypoadrenocorticism?

A

glucocorticoid replacement - low dose preds, increase at times of stress
mineralocorticoid replacement - zycortal, 4 weekly injection
frequent bloods with starting treatment

1055
Q

what causes disease of the exocrine pancreas?

A

pancreatic enzymes prematurely activated so start digesting pancreas

1056
Q

list causes of pancreatitis

A

idiopathic
dietary indiscretion
trauma
surgery - hypoperfusion in GA

1057
Q

what are more common types of panceratitis seen?

A

mild, acute, subclinical disease

1058
Q

list clinical signs of pancreatitis

A

anorexia
vomiting
abdo pain
dehydration
lethargy
generalised inflammation
DIC
renal failure
multiorgan failure
death
vague in cats

1059
Q

what can be done to diagnose pancreatitis?

A

bloods - not reliable
abdo US

1060
Q

how is pancreatitis treated?

A

supportive care - IVFT, monitoring clinical signs, analgesia
nutrition - anti emetics, keep feeding, feeding tube as needed
long term palatable, low fat, highly digestible food

1061
Q

why is altering diet for pancreatitis in cats less important?

A

likely have concurrent disease that dietary management is more needed for

1062
Q

what is DM?

A

failure of pancreas to produce insulin

1063
Q

list signalment for DM

A

middle aged to older animals
dogs and cats
burmese predisposed
obesity

1064
Q

how is DM treated in dogs compared to cats?

A

dogs need insulin, cats may be managed without insulin

1065
Q

list clinical signs of DM

A

PUPD
polyphagia
weight loss
cateracts - dogs
peripheral neuropathy - cats, plantigrade stance
DKA - vomiting, dehydration, collapse
persistent hyperglycaemia - glucosuria

1066
Q

how can DM be treaed in cats?

A

insulin injections - pro-zinc, caninsulin
diet - low carb, high protein, regulates glucose, control calories for BCS. wet food for better glycaemic control. consistent feeding
oral liquid senvelgo - blocks 90% glucose resporption in kidneys for excretion, can absorb some to prevent hypoglycaemia

1067
Q

why is it important to monitor cats in DM remission?

A

may become diabetic again later in life

1068
Q

how is DM treated in dogs?

A

insulin - pro-zinc, caninsulin
diet and exercise to help management - high carb high fibre, consistent feeding, calorie controlled, good exercise schedule

1069
Q

describe how to correctly administer insulin

A

SC injection SID or BID - patient and insulin dependent
SID - feed in morning with insulin and 6 hours later
BID - feed at same time as insulin

1070
Q

why should insulin be given with or after food?

A

in case they dont eat and become hypoglycaemic

1071
Q

how does glucose curve assess BG?

A

measure BG every 1-2 hours
may be affected by stress

1072
Q

what are the benefits of measuring BG with freestyle libre?

A

continuous BG monitoring
more accurate as in normal routine

1073
Q

why should the first insulin be given in hospital?

A

in case become hypoglycaemic

1074
Q

how long does it take to stabilise BG after first insulin dose?

1075
Q

list clinical signs of hypoglycaemia

A

weakness
ataxia
depression
altered behaviour
muscle twitching
seizures

1076
Q

how is hypoglycaemia treated?

A

conscious - give food, rub honey on gums, contact vet
unconscious - rub honey on gums, contact vet
seizing - contact vet
treat if in doubt as high BG better than low

1077
Q

what are considerations for using insulin?

A

correct syringe for insulin type
correct storage and handling
mix before use

1078
Q

why is it important to take BG samples from the same site?

A

venous and capillary blood has different BG levels

1079
Q

what would be discussed in initial post diagnosis clinic for DM?

A

make aware of disease
teach to inject
discuss routine

1080
Q

what would be discussed in follow up clinic 7 days post DM diagnosis?

A

more info for owner, check managing okay

1081
Q

what is discussed in DM stabilisation clinics until insulin dose found?

A

check managing
discuss changes
support through

1082
Q

what should be discussed in DM maintenance clinics every 3-6 months?

A

any changes
discuss long term issues

Advanced Clinical Veterinary Nursing (4 decks)

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