diseases 🦠 Flashcards
aetiology and pathophysiology for atopic dermatitis
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
CS for atopic dermatitis
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
diagnosis for atopic dermatitis
History and clinical signs
FAVOROTS CRITERIA!!!!!
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
what is the aetiology of chronic renal failure
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
what is the pathophysiology of chronic renal failure
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
what are the clinical signs of chronic renal failure
polyuria - kidneys cant concentrate urine
polydipsia- due to vomiting
vomiting- due to azotaemia and urea which makes them feel sick
inappetance
dehydration- from vomiting
weight loss
depression
oral ulcers and halitosis
seizures
anaemia of chronic renal disease
end stage may be anuric
what is the diagnosis of chronic renal failure
Several options exist;
History and clinical signs
Physical examination
Urine testing, SG, urine protein levels
Blood testing- SDMA shows early indicator in deterioration, testing checks levels of urea and creatinine
Blood pressure
Radiography- can show kidneys are enlarged
Ultrasound- identifies the stage and monitoring for CRF
blood chem- assess urea or creatinine and phosphate levels
Determine cause and extent of azotaemia
aetiology for diabetes mellitus
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
pathophysiology for diabetes mellitus
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
CS for diabetes mellitus
polyphagic as body isnt absorbing the glucose so feel hungry.
polyruria and polydipsia from vomiting as glucose attracts water
glycosuria cant go into tissues and it stuck in blood.
weight loss
ketosis - vomiting, depression, dehydration
on set blindness- cataracts 70% will go blind
diagnosis of diabetes mellitus
history and CS
blood tests - will have high glucose
urine tests- high glucose in urine
aetiology for epilepsy
Neurological condition arising from disruption of forebrain function
Idiopathic epilepsy is the most common- cause unknown but genetic link suspected in a number of breeds including Border Collies, Hungarian Visla and Labradors
pathophysiology for epilepsy
Disordered electrical activity of the brain cells – imbalance in excitatory and inhibitory signals
Partial or generalised
Generalised – dogs
Partial – cats
Three phases
Pre-ictal
Ictal
Post-ictal
Prolonged seizing – status epilepticus (more than 5 mins)
CS for epilepsy
pre-ictal
confusion
stumbling
anxious
diorientated
Ictal – signs (generalised seizure)
Episode of fitting
Collapse and unconsciousness
Action varies animal to animal
Clonic paddling spasms or tonic spasms
Spasms of jaw muscles
Vocalisation
Incontinence
post-ictal
hunger
heavy panting
compulsive walking
tiredness
diagnosis for epilepsy
History and clinical signs important as important to rule conditions out
RECORD THE SEIZURE - this shows the CS to the vet
Physical examination, neurological exam
Blood testing – infection, toxicity, glucose, uraemia
MRI and/or CT- advanced imaging
CSF tap- looking for neoplasia, meningitis
what is the aetiology for feline leukaemia virus
causal agent is retrovirus from the oncornavirus cancer-causing group. the incubation period is months-years.
what is the pathophysiology of feline leukaemia virus
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
what is the CS fo feline leukaemia virus
immunosupression
recurrent infections
anaemia
tumour development
lethargy
diarrhoea
what is the diagnosis for feline leukaemia virus
elisa serum test
px side test
re-test after 12wks
PCR
viral isolation
what is the aetiology for hyperthyroidism
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
what is the pathophysiology for hyperthyroidism
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
what is the CS for hyperthyroidism
Polyphagia
Weight loss
Hyperactive/aggressive or restless
Tachycardia
Vomiting and diarrhoea
Poor coat/unkempt
Polydipsia
potential aortic thromboelism
what is the diagnosis for hyperthyroidism
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 – to see if has hypertrophic cardiomyopathy
aetiology of hyperadrenocortism
Caused by either
Pituitary tumour – increased production of ACTH (most common)
Adrenal tumour – direct increase of cortisol
Both lead to increased serum cortisol
diagnosis of hyperadrenocorticism
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
pathophysiology for hyperadrenocorticism
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
what are the CS of hyperadrenocorticism
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
aetiology for keratoconjunctivitis sicca
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
pathophysiology for keratoconjunctivitis sicca
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
CS for keratoconjunctivitis sicca
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!
diagnosis for keratoconjunctivitis sicca
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
aetiology for mast cell tumour
Neoplasia affecting the histiocytes (mast cells)
Certain breeds predisposed eg. Beagles, Boxer, Golden Ret.
Are differing grades of tumour from benign to highly malignant
Around 20% of skin tumours in dogs
MCT is the most common skin tumour in dogs, usually a single lesion, very variable in appearance
pathophysiology for mast cell tumour
Mast cells undergo malignant transformation, behaviour varies between grades
Degranulation of mast cells in the tumour can lead to systemic signs
Often skin tumours
Occasionally found in GIT, spleen, bone marrow
Graded I-III according to how well differentiated cells are – grade III has poorest prognosis.
clinical signs for mast cell tumour
The great pretender – appearance is very varied!
Usually found on the skin surface
Benign or low grade may be small slow growing masses in the skin
Higher grade masses/histamine release assoc. with swelling, inflammation, ulceration
Some can occur in the subcutaneous layer
Systemic signs of degranulation may include GI ulceration, vomiting, melaena, anaemia, perforated ulcer – these are rare, may occur in animals with large number of MCT
diagnosis for mast cell tumour
FNA – fine needle aspirate of mass and examine cells yielded under microscope, this is a reliable method to diagnose this condition, simple to perform and relatively inexpensive,
Incisional – part or parts of mass removed for sampling, can be done under sedation depending on technique but the mass is not removed, this is used to help grading and planning of surgery
Excisional – remove mass and send off, margins of 2-3cm advised
Higher grade tumours, faster mitotic rate,
Imaging – detection of mets by either radiography or CT/MRI
what is the aetiology for mitral valve disease/ endocarditis
Degeneration of the AV valves – Cause is unknown.
Hereditary component.
Common in Cavalier King Charles Spaniels.
Rare in Cats
what is the pathophysiology for mitral valve disease/ endocarditis
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.
what are the CS for mitral valve disease/ endocarditis
Murmur
Exercise intolerance
Coughing – Normally morning or at night.
Ascites
Dyspnoea
Later – Weight loss/anorexia.
what is the diagnosis for mitral valve disease/ endocarditis
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.
pro BNP to see if heart is under pressure
heart rate/ pulse/ measure resting rr, are they normal?
aetiology for osteoarthritis
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
pathophysiology of oesto arthritis
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
CS of osteo arthiritis
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
diagnosis of oesto arthritis
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
aetiology for otitis externa
Infection
Parasites
Trauma
Allergy
Neoplasia
pathophysiology for otitis externa
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
Cs for otitis externa
Head shaking, ear scratching, self trauma
Pain
Inflammation
Thick, waxy or purulent discharge
Foul, yeasty smell
Thickening of ear lining
diagnosis for otitis externa
History and clinical signs
Observation and aural examination
Otoscope exam
Swabs taken for culture and sensitivity
aetiology for osteosarcoma
Primary malignant neoplasm of bone tissue
Large breeds most commonly affected
Middle aged-older dogs
pathophysiology for oesteosarcoma
Osteocytes undergo malignant transformation leading to formation of swelling or bony growth and destruction of bone architecture
damage to bone tissue may lead to weakening of bone and pathological fracture
Commonly metastatic spread occurs to the lungs
Usually found in metaphysis of long bones
CS for osteosarcoma
Lameness – due to pain/deformity of limb, swelling of bone/lump in bone – due to infiltration of neoplastic tissue, fracture – pathological fracture due to weakening of bone, coughing – may be seen due to secondary spread, weight loss
diagnosis for osteosarcoma
Radiography – visualize affected limb and allow evaluation of lung fields, may require sed/GA, does not provide definitive diagnosis but may be used where funds/patient
preclude biopsy as an option
Bone biopsy where sample of tissue taken from affected area - invasive, provides definitive diagnosis however very invasive and painful
CT/MRI – as per radiography, associated with greater cost but full body scan possible more sensitive detection of mets
what is the aetiology for parvovirus
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
what is the pathophysiology for parvovirus
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
what is the CS for parvovirus
depression,
anorexia,
severe vomiting,
haemorrhagic diarrhoea,
pyrexia,
severe weight loss,
dehydration,
shock
what is the diagnosis for parvovirus
clinical signs and history
faecal ELISA test
faecal PCR
SNAP test
serum antibody
aetiology for pyometra
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.
pathophysiology for pyometra
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)
CS for pyometra
vomiting
polyuria
polydipsia
weakness
lethargy
mucopurulent vaginal discharge
abdominal pain
shock
diagnosis for pyometra
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
what is the aetiology for urolithiasis/ feline lower urinary tract disease
idiopathic cystitis is most common, urolithiasis (stones), crystals (urethral plug), infection - rare, multi-cat household, stress, underactive, overweight, neutered cat
what is the pathophysiology for urolithiasis/ feline lower urinary tract disease
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
what is the CS for urolithiasis/ feline lower urinary tract disease
cyctitis,
pollakuria,
dysuria,
haematuria- due to irritation to bladder wall, stones as well
pain,
blockage causes oligura and anuria. incontinence, varying frequency/ volume, abnormal micturition (weak, interrupted),
licking external genitalia- due to pain depression- due to pain
vomiting- due to azotemia
anorexia,
dehydration
what is the diagnosis for urolithiasis/ feline lower urinary tract disease
history and clinical signs
physical xamination
observation of micturition
neurological examination where indicated
urinalysis- visual appearance, dipstick, microscopy, culture, specific gravity
radiography
ultrasound- dont need to sedate
possibly haematology/ biochemistry
aetiology for wobblers (cervical spondylomyelopathy)
malformation of C vertebrae leading to spinal compression
Is complex, parimarily genetic component (particularly Dobermann, Great Dane)
Nutritional factors may play a role (protein, calcium and phosphorous)
pathophysiology for wobblers (cervical spondylomyelopathy)
Narrowing of the cervical vertebral canal due to developmental abnormalities of vertebrae (young dogs) , degenerative changes can occur in older dogs leading to narrowing of the canal
Narrowed canal impinges upon the spinal cord causing compression and the resulting neurological deficit
CS for wobblers (cervical spondylomyelopathy)
All 4 Pelvic limbs weak
More pronounced in hind limbs
May scuff nails
Inco-ordinated gait»_space; ataxia
Look wobby
Neck pain
May lead to paralysis
2 engine gait
diagnosis for wobblers (cervical spondylomyelopathy)
History and clinical signs may lead to suspicion particularly in affected breeds
Physical examination - full neurological exam to narrow down where the spinal cord is affected.
Radiography, myelography
CSF analysis may be required
MRI is diagnostic as It can show you the narrowing of the spinal cord.
myelogram- shows the spinal cord
knuckle test
what is the aetiology for immune mediated haemolytic anaemia
idiopathic
toxaemia from lead, copper, onion, paracetamol, some drugs, incompatible blood transfusions, mycoplasma, hemofelis, babesia canine, vaccinations. cocker spaniels are breed disposed
what is the pathophysiology for immune mediated haemolytic anaemia
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
what is the CS for immune mediated haemolytic anaemia
collapse
pale m
fever
weakness
what is the diagnosis for immune mediated haemolytic anaemia
clinical signs
blood tests
diagnostic imaging
what is the aetiology for dilated cardiomyopathy
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
what is the pathophysiology for dilated cardiomyopathy
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.
what is the CS for dilated cardiomyopathy
depression
anorexia
exercise intolerance due to AV valves stretching
cough- fluid from the lungs
dyspnoea- due to enlargement of heart which causes pressure in thorax
syncope (fainting) - due to abnormal rhythm in the heart being slow
murmur- due to regurg of blood
sudden death
what is the diagnosis for dilated cardiomyopathy
history and CS
thoracic auscultation- listen for murmur
chest radiographs show enlarged heart
ECG- detect for arrhythmia
bp measurements as will be very low
echo cardiography
haematology and biochemistry
pro BNP blood test
what is the aetiology for tracheal collapse
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
what is the pathophysiology for tracheal collapse
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
what is the CS for tracheal collapse
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)
what is the diagnosis for tracheal collapse
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
what is the aetiology for gastric dilation +/- volvulus GDV
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)
what is the pathophysiology for gastric dilation +/- volvulus GDV
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.
what are the CS for GDV
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
what is the diagnosis for GDV
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!!
what is the aetiology for exocrine pancreatic insufficiency EPI
Atrophy of exocrine pancreatic cells caused by spontaneous atrophy or secondary to pancreatitis/trauma
May be inherited.
German shepherd and rough collie predisposed.
what is the pathophysiology for exocrine pancreatic insufficiency EPI
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.
what is the CS for exocrine pancreatic insufficiency EPI
loose stools
weight loss
polyphagia
digestive tract issues
vomiting
anorexia
what is the diagnosis for exocrine pancreatic insufficiency EPI
History and clinical signs.
Faecal examination.
Blood test; Serum Trypsin-like immunoreactivity – looking for low levels to confirm disease.
blood tests
faecel tests
vitamin B12 tests- if low animal has EPI
what is the aetiology for laryngeal paralysis
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,
what is the pathophysiology for laryngeal paralysis
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
what is the CS for laryngeal paralysis
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!
what is the diagnosis for laryngeal paralysis
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
what Is the aetiology for pancreatitis
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)
what Is the pathophysiology for pancreatitis
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.
what Is the CS for pancreatitis
Acute
Anterior abdominal pain – ‘praying position’
Vomiting
Depression
Anorexia
Shock
pyrexia
Dehydration
Chronic
More vague and variable
what Is the diagnosis for pancreatitis
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
what is aetiology for hypertrophic cardiomyopathy
Most commonly acquired heart disease in cats.
Can be idiopathic/genetic especially in Maine Coon.
Often secondary to hyperthyroidism.
what is pathophysiology for hypertrophic cardiomyopathy
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.
what is CS for hypertrophic cardiomyopathy
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.
what is diagnosis for hypertrophic cardiomyopathy
cardiac ultrasound- echo to visualise the heart and show movement of blood and show thickening of the walls.
ascultate the heart to grade murmur-
aded 1-6 for murmur
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
