diseases 🦠 Flashcards

1
Q

aetiology and pathophysiology for atopic dermatitis

A

Affected animals have a genetic predisposition to become sensitised to allergens and have abnormal skin barrier function

Allergens are proteins that, when inhaled or absorbed through the skin, respiratory tract, or GI tract, evoke allergen-specific IgE production

Ige molecules affix themselves to tissue mast cells or basophils.
When these primed cells come in contact with the specific allergen again, mast cell degranulation results in the release of proteolytic enzymes, histamine, bradykinins, and other vasoactive amines, leading to inflammation (erythema, oedema, and pruritus)

Golden Retriever
Labrador Retriever
Dalmatian
Boxer

Between 6 months and 3 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CS for atopic dermatitis

A

Pruritis – VERY ITCHY +++

Inflammation
Lesions
Alopecia
Lichenification
Erythema
Papules

DOGS -
Can be seasonal or non seasonal or non seasonal with flare ups

The feet, face, ears, flexural surfaces of the front legs, axillae, and abdomenmost commonly affected areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

diagnosis for atopic dermatitis

A

History and clinical signs
Exclusion of other causes – treat any parasites / infections / rule out other skin dx
Examination
Microscopy – tape, skin scrape
Bacterial culture
Fungal culture
Biopsy
Exclusion diet
Intradermal skin testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the aetiology of chronic renal failure

A

Idiopathic deterioration in geriatric cat – most common
Previous acute renal damage eg. Injury, toxin
Neoplasia
Polycystic kidney disease
Chronic infection/pyelonephritis/glomerulonephritis
Concurrent conditions eg. Diabetes mellitus, hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the pathophysiology of chronic renal failure

A

The kidney is unable to filter nitrogenous waste from the blood leading to uraemia
Deterioration in renal function causes pH and electrolyte imbalance (potassium and phosphate)
Reduced production of erythropoietin leads to reduced erythrocyte formation in the bone marrow
Note; reserve capacity of kidneys means signs of renal failure only appear when 2/3-3/4 of functioning tissue is lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the clinical signs of chronic renal failure

A

polyuria
polydipsia
vomiting
inappetance
dehydration
weight loss
depression
oral ulcers and halitosis
seizures
anaemia of chronic renal disease
end stage may be anuric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the diagnosis of chronic renal failure

A

Several options exist;
History and clinical signs
Physical examination
Urine testing, SG
Blood testing
Blood pressure
Radiography
Ultrasound
Determine cause and extent of azotaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

aetiology for diabetes mellitus

A

type 1- beta cells have been destroyed and can no longer synthesise insulin adequately.

presumed immune mediated and some breed predisposed such as Keeshond and cairn terrier or besties and JRTs

causes a damage to the pancreas such as during an episode of pancreatitis may lead to inability to synthesise insulin.

known as insulin dependent

type 2- reduced ability to respond to insulin due to obesity, oestrus, Cushing disease, steroids, acromegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pathophysiology for diabetes mellitus

A

absolute or relative insulin deficiency.

reduced tissue utilisation of glucose

leads to hyperglycaemia in bloodstream

low glucose levels in cells

occurs secondary to acromegaly in cats

renal threshold for glucose exceeded- glycosuria

eventually fats are broken down as cells cant access glucose which leads to ketosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

CS for diabetes mellitus

A

polyphasic
polyruria
polydipsia
glycosuria

weight loss
ketosis - vomiting, depression, dehydration
on set blindness- cataracts 70% will go blind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

diagnosis of diabetes mellitus

A

history and CS
blood tests - will have high glucose
urine tests- high glucose in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

epilepsy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the aetiology for feline leukaemia virus

A

causal agent is retrovirus from the oncornavirus cancer-causing group. the incubation period is months-years.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the pathophysiology of feline leukaemia virus

A

the virus replicates in the lymphoid tissue and enters lymphocytes and monocytes. it transports all around the body and eventually enters the bone marrow. in some cats, persistent infection leads to immune suppression or anaemia. the outcome is variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the CS fo feline leukaemia virus

A

immunosupression
recurrent infections
anaemia
tumour development
lethargy
diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the diagnosis for feline leukaemia virus

A

elisa serum test
px side test
re-test after 12wks
PCR
viral isolation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the aetiology for hyperthyroidism

A

Functional thyroid tumour

Usually benign adenomatous hyperplasia (rarely cancerous) of the thyroid gland

May affect one or both lobes (also ectopic tissue)
Inciting cause theorised but unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the pathophysiology for hyperthyroidism

A

Affected gland overproduces thyroxine

This leads to a hypermetabolic state

As thyroxine affects a number of body tissues there are a wide range of clinical signs seen

Complications such as hypertension and hypertrophic cardiomyopathy may occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the CS for hyperthyroidism

A

Polyphagia
Weight loss
Hyperactive/aggressive or restless
Tachycardia
Vomiting and diarrhoea
Poor coat/unkempt
Polydipsia
potential aortic thromboelism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the diagnosis for hyperthyroidism

A

Blood test – serum T4 levels, high levels confirm diagnosis, run in house with rapid results –

T4 is tested to show thyroid function and show increased levels.

Blood biochem – this is used to check for raised kidney enzymes or any other conditions

Scintigraphy – imaging using radioisotopes injected into the patient and imaged using a gamma camera. Used to locate thyroid tissue/plan surgery. Referral centre and ££

Evaluation of cardiac function and measurement of BP advisable – Why?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

aetiology of hyperadrenocortism

A

Caused by either
Pituitary tumour – increased production of ACTH (most common)
Adrenal tumour – direct increase of cortisol
Both lead to increased serum cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

diagnosis of hyperadrenocorticism

A

History and clinical signs
ACTH stimulation test –blood at 0 and 1hrs, inj with ACTH after first blood sample – Why would we use this test?
Low dose dexamethasone suppression test – blood at 0,4 and 8hrs, inj of dexamethasone iv after first b/s – this test distinguishes the types of cushings, it can tell us if the pituitary gland is at fault or adrenal gland
urine cortisol:creatinine ratio (UCCR)
Endogenous ACTH
Often diagnosis requires combination of tests – see recommended resources
Imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

pathophysiology for hyperadrenocorticism

A

Overactive tissue in pituitary or adrenal gland leads to increased production of cortisol (2 different aetiologies)
High levels of cortisol lead to hyperglycaemia and inhibit ADH – leading to PUPD
High cortisol also causes protein catabolism leading to muscle wasting and poor wound healing
Cortisol affects hair growth and distribution of fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the CS of hyperadrenocorticism

A

Polyuria
Polydipsia
Weight loss
Alopecia (flanks)
Pot bellied- weakness of abdominal muscles due to excess cortisol and this causes fat redisposition
large liver due to the same above
Hepatomegaly
Muscle weakness
Panting
Thinning of the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

aetiology for keratoconjunctivitis sicca

A

reduced or absence of ability to form tears
Immune mediated
Breed predisposition eg. Cocker spaniel, Shih Tzu, YT, Lhasa Apso, Bulldog breeds (particularly English bulldog)

Protruberant eye breeds
Secondary to some endocrine conditions/drug toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

pathophysiology for keratoconjunctivitis sicca

A

overproduction of mucus to keep cornea moist
immune mediated or caused by drug toxicity, trauma or surgery

variation in the degree of severity

Reduced activity in the lacrimal glands leads to inadequate formation of the aqueous tear film
As adequate tear film is essential for corneal health absence of, or reduced tear film leads to corneal drying and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

CS for keratoconjunctivitis sicca

A

vascularization
ulceration
opacity of the cornea
recurrent conjunctivitis
mucoid or mucopurulent discharge on and around eye

Mucoid/mucopurulent conjunctivitis
Any dog with sticky discharge in the medial canthus should have a test for KCS
Neovascularisation of cornea
Clouding of cornea
dull/dry appearance

This condition is painful and left untreated can lead to blindness!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

diagnosis for keratoconjunctivitis sicca

A

schirmer test to show tear production

History and clinical signs should lead to suspicion of this disease
Fluorescein to rule in/out ulceration of the cornea
After Schirmer tear test – fluorescein will alter results of schirmer

Schirmer tear test – definitive test, tear production should be more than 15mm per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

mast cell tumour

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the aetiology for mitral valve disease/ endocarditis

A

Degeneration of the AV valves – Cause is unknown.

Hereditary component.

Common in Cavalier King Charles Spaniels.

Rare in Cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the pathophysiology for mitral valve disease/ endocarditis

A

Valvular tissue degenerates, becoming thickened and develops lesions.

Valves cannot close properly

Allows regurgitation of blood from the ventricles back to the atria.

Eventually leads to cardiac enlargement and output failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the CS for mitral valve disease/ endocarditis

A

Murmur
Exercise intolerance
Coughing – Normally morning or at night.
Ascites
Dyspnoea
Later – Weight loss/anorexia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the diagnosis for mitral valve disease/ endocarditis

A

Blood tests: A complete blood count (CBC) and serum biochemistry can show abnormalities. Blood cultures can help identify the bacteria causing the infection.
Chest X-rays: Can show an enlarged heart or signs of heart failure.
Electrocardiogram (ECG): Records the heart’s electrical activity and can show an irregular heartbeat.
Echocardiogram: An ultrasound of the heart that can help identify the affected valve and the extent of damage.
Infectious disease testing: Can help identify the specific pathogen causing the infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

aetiology for osteoarthritis

A

affects 1 in 5 dogs/cats.
most common cause of lamenes.

develops from an underlying deformity or trauma

hip dysplasia, elbow displasia, or Osteochondritis dissecans will lead to OA due to abnormal wear on joint surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

pathophysiology of oesto arthritis

A

characterised by degeneration of articular cartilage often associated with the formation of new bone at joint surface
may have a gradual onset, but may also occur acutely.

(Osteoarthritis can be a primary disease of joint cartilage, but is more often secondary to abnormal stresses on joints)

slowly progressive but can have a rapid onset

chronic and progressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

CS of osteo arthiritis

A

stiffness/ lameness (worse after rest) - less common in cats
reluctant to jump or climb
reduced range of movement of affected joint
+/- swelling
alteration to gait
muscle atrophy In affected limbs
may affect appetite and personality/ behaviour dependent on severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

diagnosis of oesto arthritis

A

history and examination findings (swelling and crepitus evident on exam)

radiography of joints and contralateral joint

arthroscopy to visualise cartilage and lesions and synovial fluid

CT/MRI

synovial fluid analysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

aetiology for otitis externa

A

Infection
Parasites
Trauma
Allergy
Neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

pathophysiology for otitis externa

A

Irritation/self trauma leads to tissue hyperplasia, inflammation and excess production of wax
Any obstruction of the ear canal may lead to accumulation of cerumen, discharge and predispose to infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Cs for otitis externa

A

Head shaking, ear scratching, self trauma
Pain
Inflammation
Thick, waxy or purulent discharge
Foul, yeasty smell
Thickening of ear lining

41
Q

diagnosis for otitis externa

A

History and clinical signs
Observation and aural examination
Otoscope exam
Swabs taken for culture and sensitivity

42
Q

osteosarcoma

A
43
Q

what is the aetiology for parvovirus

A

virus belongs to the parvovirus group CPV-2. it commonly affects weaned puppies who have lost their mda between 8-12wks or adults who arent not vaccinated

44
Q

what is the pathophysiology for parvovirus

A

the virus has an affinity for rapid dividing cells in the gut wall and lymphoid tissue. the virus will multiply in the SI crypt lining cells which leads to the destruction of the lining and the inability to absorb nutrients. in severe cases the bacteria will invade from the gut to the bloodstream due to a compromise of the SI. The virus will suppress the immune system and cause leucopaenia

45
Q

what is the CS for parvovirus

A

depression,
anorexia,
severe vomiting,
haemorrhagic diarrhoea,
pyrexia,
severe weight loss,
dehydration,
shock

46
Q

what is the diagnosis for parvovirus

A

clinical signs and history
faecal ELISA test
faecal PCR
SNAP test
serum antibody

47
Q

aetiology for pyometra

A

Bacterial infection of uterus, often involving EColi
Common in unspayed older bitches who have had several seasons but can be seen in younger animals
(may have history of hormone therapy for mismating/heat suppression)

Pyometra is less common in the cat as they are induced ovulators, it can be observed in rabbits and guinea pigs too.

48
Q

pathophysiology for pyometra

A

Cystic changes in the uterus and bacterial infection occuring during the oestrus phase
Open cervix allows entry of bacteria into uterus
Large accumulation of pus due to immune response of phagocytes – open or closed
Bacterial toxins enter bloodstream – septicaemia/toxaemia (which can be fatal)

49
Q

CS for pyometra

A

vomiting
polyuria
polydipsia
weakness
lethargy
mucopurulent vaginal discharge
abdominal pain
shock

50
Q

diagnosis for pyometra

A

History (6/8 weeks post season) and clinical signs – discharge and evidence of enlarged abdomen
Radiography of abdomen – may indicate presence of enlarged uterus
Ultrasound – confirm presence of distended uterus, visualise fluid/pus and uterine lining
Bloods – haematology – leucocyte counts may indicate infection

51
Q

what is the aetiology for urolithiasis/ feline lower urinary tract disease

A

idiopathic cystitis is most common, urolithiasis (stones), crystals (urethral plug), infection - rare, multi-cat household, stress, underactive, overweight, neutered cat

52
Q

what is the pathophysiology for urolithiasis/ feline lower urinary tract disease

A

irratation/ inflammation of the bladder wall/ urethra (FIC). may get recurrent bouts of cystitis

OR

uroliths or urethral plugs may cause urinary obstruction- complete obstruction is an emergency. trauma/ iatrogenic damage may result in blader wall dysfunction or rupture of the urinary tract. inability to void urine leads to azotaemia and signs associated with acute renal failure

53
Q

what is the CS for urolithiasis/ feline lower urinary tract disease

A

cyctitis, pollakuria, dysuria, haematuria, pain, blockage causes oligura and anuria. incontinence, varying frequency/ volume, abnormal micturition (weak, interrupted), licking external genitalia, depression, vomiting, anorexia, dehydration

54
Q

what is the diagnosis for urolithiasis/ feline lower urinary tract disease

A

history and clinical signs
physical xamination
observation of micturition
neurological examination where indicated
urinalysis- visual appearance, dipstick, microscopy, culture, specific gravity
radiography
ultrasound
possibly haematology/ biochemistry

55
Q

wobblers (cervical spondylomyelopathy)

A
56
Q

what is the causal agent for feline upper respiratory disease

A
  • feline herpesvirus type 1
  • feline calcivirus
  • bordatella bronchiseptica
  • chlamydophia felis
57
Q

what is the pathophysiology for feline herpesvirus type 1 in feline upper respiratory disease

A

it replicates in the tissue of the upper r. tract and ocular systems which leads to epithelial necrosis. it causes irritation to the pharynx, larynx, and trachea. there is a secondary bacterial infection as a result of damage.

58
Q

what are the clinical signs for feline herpesvirus type 1 in feline upper respiratory disease

A

Anorexia
Pyrexia
Depression
Sneezing
Conjunctivitis
Hypersalivation
Ocular/nasal discharge
Keratitis/corneal ulceration
Dyspnoea (cough if develop pneumonia)

In worst cases - death

59
Q

what is the pathophysiology for feline calcivirus in feline upper respiratory disease

A

Similar love for respiratory epithelium as FHV however causes much milder degree of URT symptoms.
Characteristic lesions occur in the oral cavity leading to oral ulceration and erosive lesions

Occasionally if severe strain will cause pneumonia.

60
Q

what are clinical signs for feline calcivirus in feline upper respiratory disease

A

Mild ocular/nasal discharge
Sneezing
Inappetance
Depression
Pyrexia
Ulceration of palates, tongue and cheeks

61
Q

what is the diagnosis for FHV-1 and FCV

A

History
Clinical signs
Viral transport swab of oropharyngeal region for FHV-1 and FCV

62
Q

what is the pathophysiology for feline chlamydophila in feline upper respiratory disease

A

Bacterial infection
Replicates in the mucosa of ocular and oral cavity and the upper and lower respiratory tract
Frequent cause of conjunctivitis
May occur alongside co-infection with FHV-1 and/or FCV

63
Q

what is the diagnosis for feline chlamydophila in feline upper respiratory disease

A

History
Clinical signs
Conjunctival swab to isolate the organism
Zoonotic – but risk low
Can cause conjunctivitis in humans
Usually in immunosuppressed people
.

64
Q

what is the pathophysiology for feline bordatella bronchiseptica in feline upper respiratory disease

A

replicate in the r. tract. it sheds thorough saliva and nasals secretions. the bacteria survives up to 1-2wks in the environment. cats may still be infected after signs are gone

65
Q

what is the clinical signs for feline bordatella bronchiseptica in feline upper respiratory disease

A

sneexing
coughing
nasal and ocular discharge

66
Q

what is the diagnosis for feline bordatella bronchiseptica in feline upper respiratory disease

A

take a swab from pharynx by PCR

67
Q

what is the aetiology for immune mediated haemolytic anaemia

A

toxaemia from lead, copper, onion, paracetamol, some drugs, incompatible blood transfusions, mycoplasma, hemofelis, babesia canine, vaccinations. cocker spaniels are breed disposed

68
Q

what is the pathophysiology for immune mediated haemolytic anaemia

A

it destroys RBC by using the animals own immune system, or parasites/toxins will reduce the number of RBC volume. bone marrow then produces regenerative anaemia, releasing immature cells. spherocytes will be seen in the circulation. RBC breakdown products will be metabolised to bilirubin causing jaundice

69
Q

what is the CS for immune mediated haemolytic anaemia

A

collapse
pale m
fever
weakness

70
Q

what is the diagnosis for immune mediated haemolytic anaemia

A

clinical signs
blood tests
diagnostic imaging

71
Q

what is the aetiology for dilated cardiomyopathy

A

idiopathic
may be related to genetic biochemical defects
rare in dogs under 15kg and some cats are affected
long silent phase where the animal may be suffering from the disease but show no CS

72
Q

what is the pathophysiology for dilated cardiomyopathy

A

progressive thinning of the myocardium which imapirs the efficiency of the heart contraction. atria becomes enlarged and the heart wall stretches becoming ballooned. the AV valves stretch leading to regurgitation of blood. there may be abnormalities in the HR and rhythm. eventually falling c02 leads to signs of congestive heart failure.

73
Q

what is the CS for dilated cardiomyopathy

A

depression
anorexia
exercise intolerance
cough/ dyspnoea
syncope
murmur
sudden death

74
Q

what is the diagnosis for dilated cardiomyopathy

A

history and CS
thoracic auscultation
chest radiographs show enlarged heart
ECG
bp measurements
echo cardiography
haematology and biochemistry
pro BNP blood test

75
Q

what is the aetiology for tracheal collapse

A

Commonly observed in toy breeds especially Yorkshire Terriers , obese small breeds
Exact causes unclear but thought to be a combination of genetic, nutritional and/or allergic triggers

76
Q

what is the pathophysiology for tracheal collapse

A

Incomplete formation or weakening of c-shaped tracheal cartilages lead to inability to maintain patency of trachea
During inspiration the cervical portion of the trachea collapses leading to airway obstruction
during expiration the thoracic portion of the trachea collapses

77
Q

what is the CS for tracheal collapse

A

Cough at exercise
‘goose honk’
Progressive signs of resp distress that may be paroxysmal
(may be other disease eg. Heart disease, other respiratory disease, cushings)

78
Q

what is the diagnosis for tracheal collapse

A

Endoscopy (bronchoscopy) of trachea (graded according to severity)
Fluoroscopy – video x-ray for real time diagnosis
Chest radiography – less reliable as sole means
Signs are suggestive in affected breeds

79
Q

what is the aetiology for gastric dilation +/- volvulus GDV

A

Not completely understood
Large breed dogs, deep chested dogs commonly effected.
Great Danes, Weimaraner’s, St Bernard and English Setters .
Some increased incidence if relatives have had GDV.
Fed once daily or history of recent large meal.
Exercise immediately before or after feeding. (Possible associated with dry food)

80
Q

what is the pathophysiology for gastric dilation +/- volvulus GDV

A

Stomach dilates and rotates into a twisted position where upon gas cannot escape.
Distension of the stomach fills the abdominal cavity putting pressure on the caudal vena cava and disrupting venous return to the heart.
Pressure on diaphragm may compromise breathing leading to poor ventilation and damage to body tissues.

Necrosis of gastric wall/splenic tissue can occur due to disruption of blood supply to these areas.

URGENT EMERGENCY CONDITION – can lead to hypovolaemic/endotoxaemic shock and respiratory compromise.

81
Q

what are the CS for GDV

A

Restlessness
Retching
Anterior abdominal swelling*
Dyspnoea
Collapse
Shock
Death

*note that in very large breeds swelling of the stomach may not be obvious as the stomach lies under the ribs

82
Q

what is the diagnosis for GDV

A

History and clinical signs in predisposed breed
(Tympany of abdomen)
Radiography needed to confirm existence of bloat and may be suggestive or torsion.
(Nature and extent confirmed at surgery)

Is a true emergency!!

83
Q

what is the aetiology for exocrine pancreatic insufficiency EPI

A

Atrophy of exocrine pancreatic cells caused by spontaneous atrophy or secondary to pancreatitis/trauma

May be inherited.

German shepherd and rough collie predisposed.

84
Q

what is the pathophysiology for exocrine pancreatic insufficiency EPI

A

Inadequate production of digestive enzymes due to atrophy of pancreatic exocrine cells.
Animal unable to digest foodstuffs fully leading to high volume faeces containing undigested material.
Malabsorption leads to weight loss and increased appetite.

85
Q

what is the CS for exocrine pancreatic insufficiency EPI

A

History and clinical signs.

Faecal examination.

Blood test; Serum Trypsin-like immunoreactivity – looking for low levels to confirm disease.

86
Q

what is the diagnosis for exocrine pancreatic insufficiency EPI

A

blood tests
faecel tests
vitamin B12 tests- if low animal has EPI

87
Q

what is the aetiology for laryngeal paralysis

A

more common in dogs, mid to old age
Larger breeds such as Labrador, Golden Retriever more commonly affected .
Most cases are idiopathic
Some may be due to nerve damage due to trauma or neoplasia or iatrogenic damage!
Some present as part of a wider nervous system dysfunction – polyneuropathy
In some dogs hypothyroidism is associated with this condition
less commonly congenital cases have been recorded,

88
Q

what is the pathophysiology for laryngeal paralysis

A

damage to the recurrent laryngeal nerve (s) that supply the muscles of the larynx that move the vocal cords
This leads to functional failure of the vocal folds to open fully during inspiration (arytenoid cartilages do not abduct fully)
Inspiration becomes difficult as the vocal folds remain in a closed position leading to dyspnoea

89
Q

what is the CS for laryngeal paralysis

A

A slow onset disease that may present acutely particularly in hot weather/ after exertion
Initially a cough that progresses to..
Increased inspiratory noise – stridor (roar/whistle)
Exercise intolerance
May be change in voice
Problems swallowing food/water
May present as acute collapse and respiratory distress!

90
Q

what is the diagnosis for laryngeal paralysis

A

May be suspected based on presenting signs and findings on neuro exam ie older dog of large breed
Examination of the larynx should be performed under sedation using a laryngoscope or endoscope to visualise the vocal folds during inspiration
Full neurological exam to establish if polyneuropathy is present
Bloods should be run to rule out other metabolic conditions such as hypothyroidism

91
Q

what Is the aetiology for pancreatitis

A

Often idiopathic though may be linked to:
High fat diet
Some drugs e.g. corticosteroids
May occur secondary to trauma or certain toxins

Acute pancreatitis – dogs
Chronic pancreatitis – cats (cholangiohepatitis/ Irritable Bowel Disease) (may lead to Exocrine Pancreatic Insufficiency or Diabetes Mellitus)

92
Q

what Is the pathophysiology for pancreatitis

A

Pancreatic enzymes are activated prematurely within the pancreas or are unable to exit into the duodenum.
The presence of these enzymes within pancreatic tissue results in auto-digestion of the pancreatic tissue.
This process causes inflammation and necrosis of the pancreas.

93
Q

what Is the CS for pancreatitis

A

Acute
Anterior abdominal pain – ‘praying position’
Vomiting
Depression
Anorexia
Shock
pyrexia
Dehydration

Chronic
More vague and variable

94
Q

what Is the diagnosis for pancreatitis

A

History and clinical signs
Physical examination
Spec cPL dogs, spec fPL cats – blood tests to measure serum pancreatic lipase which indicates pancreatic damage.
Trypsin-like immunoreactivity (TLI), amylase, lipase blood tests – less specific particularly in cats
Radiography – may be vague changes
Ultrasound – look at pancreatic tissue
Biopsy – if suspect neoplasia underlying
Haematology

95
Q

what is aetiology for hypertrophic cardiomyopathy

A

Most commonly acquired heart disease in cats.

Can be idiopathic/genetic especially in Maine Coon.

Often secondary to hyperthyroidism.

96
Q

what is pathophysiology for hypertrophic cardiomyopathy

A

Progressive thickening of the ventricular muscle.
Enlarged heart, with thickened walls (opposite of dilated cardiomyopathy)
Chambers become narrowed reducing chamber volume.
Reduced cardiac output, backpressure and atrial enlargement results.
Signs of heart failure may only be seen in advanced stages of disease.

97
Q

what is CS for hypertrophic cardiomyopathy

A

May have a murmur or gallop rhythm.
Lethargy
Depression
Anorexia
Leading to heart failure
Dyspnoea
Tachypnoea
Occurs mainly in cats as a result of hyperthyroidism.

98
Q

what is diagnosis for hypertrophic cardiomyopathy

A

aded 1-6
Grade 1 – quieter than the normal heart beat (barely audible)
Grade 2 – same volume as the normal heart beat
Grade 3 – louder than normal heart beat but not accompanied by a thrill
Grade 4 – louder and accompanied by a palpable thrill
Grade 5 – loud enough to hear with stethoscope partially off the chest wall, plus palpable thrill
Grade 6 – audible without a stethoscope