Internal medicine of small animals Flashcards
Skin diseases - Pyoderma, pyotraumatic dermatitis, pododermatitis
Pyoderma - superficial/deep
S.intermedius (dog)
S.pseudointermedius (cat)
-Once primary (commenal) bacteria colonise –> 2ndary e.coli/pseudomonas
SURFACE PYODERMA
pyotraumatic dermatitis
-self-trauma (pruritis, pain, allergy)
Intertrigo (skin fold pyo)
- S.intermedius or Malassezia pachydermatis
- Folds = moist, warm, irritated
- exudative + malodorous
SUPERFICIAL
impetigo (puppy pyoderma)
-<1yr, Multifactor (nutrition, environment, parasites)
-pustules on ventrum
Pododermatitis (ALG)
-Stress/anxiety
Allergies
-parasites, contact, food, inhalant
Malassezia
-pruritus malodorous (can be sweet)
Localised demodicosis
Plasma cell pododermatitis
-AI (FIV?) T: cyclosporin
Cs: lesion, malodour, discharge
Dx: Scrapes, swabs, biopsy or vesicle fluid
-culture, KOH stain
T: peroxide shampoo, chlorhexidine, iodine, ATB, fluconazole
SKin disease - folliculitis + furunculosis
Superficial folliculitis
-Infection of hair follicle
-Primary: S.intermedius following trauma,
-Secondary: systemic illness (lowered IS), malassezia or pseudomonas folliculitis
Cs:Moth eaten ventrum
irritant folliculitis
chemical folliculitis
occlusive folliculitis (canine acne) -overuse of emollients
Keratosis pilaris
-Follicles clogged with keratin
Deep folliculitis (hair follicle) + furunculosis (follicle + hair)
- S.int, pseudo, proteus, e.coli
- Superficial –> deep –> destroys hair –> disseminates bacteria
- If left –> cutaneous LN’s –> Lymphadenopathy + generalisation
Sycosis vulgaris
-“Barbers itch” –> post clipping irritation and infection
Eosinophilic furunculosis of face
-Occurs in dogs usually idiopathic
-Callus pyoderma
Cs: much more common on pressure points, ulceration, pus weeping, fistulation
Dx: deep scrapes , cytology, culture
T: topical (Iodine, peroxide, chlorhex) + systemic (ATB)
Recurrence? (think…)
- Long term steroid use?
- Consider Atb’s
- FAD? (other ecto’s)
- Atopy?
Skin diseases - Alopecia
Alopecia
-Focal, multifocal, diffuse, symmetrical
Mechanisms
-Self-trauma, folliculitis, endocrine, anatomical (follicle)
Primary
- Genetic
- -Alopecia X (sex hormone imbalances)
- -Pituitary dwarfism (hyposomatotropism)
- -Canine pattern baldness
- -Bald thigh syndrome
- -Hairless breeds (Sphynx cat, chinese crested dog, xolo)
- Neoplastic
- Epitheliotrophic leukaemia
- Inflammatory
- -Post clipping alopecia
- -injection reaction
Auto-immune
- -Alopecia areata
- -pemphigus
-Demodecosis
Secondary Endocrine -Hyperadrenocorticism (Cushings) -Hypothyroidism -Hyperoestrogenism
Stress
–feline psychogenic alopecia
Nutritional
- Vit B1, 2, 3, 5, 7
- Vit A + C
Onset
- Gradual : endocrine/nutritional
- Rapid: inflammatory, parasitic
- Seasonal: FAD, ectoparasites, allergies (atopy)
Distribution
- Dorsal –> lumbosacral = FAD
- Diffuse = bacterial
- Symmetrical = endocrine
Pruritic skin diseases
Signs
-trauma, saliva staining, alopecia
Age
- young : FAD, ectoparasites, genetic
- Old: Endocrine, allergy
- Seasonal?
Conditions
Parasitic - Demodex, sarcoptes, fleas, flies, mites, lice
Fungal - dermatophytosis (m. canis), malessezia
Bacterial pyoderma - primary and secondary
Viral - Mad itch (Pseudorabies)
AI - pemphigus
Endocrine - cushings, Hyper and hypo T4
Chemical - contact dermatitis, photosensitivity
Dx
- Parasites/infectious –> Allergies –> AI
- Scrapes/culture –> elimination diet ID skin test –>
Milliary dermatitis + eosinophilic complexes
Miliary dermatitis
Generalised or localised
Often develops in cats as a reaction to allergy
Due to FAD, Food allergy, Environmental allergy (Atopy)
Cs: sand like skin, grooming, 2nd trauma
Eosinophilic complexes
common inflammatory lesion of cats
usually atopy, food allergy or ectoparasites (FAD)
Ag-Ab –> recruits eosinophils
Eosinophilic (Feline indolent) ulcer -upper lip Feline eosinophilic plaque -Ventral abdomen Feline eosinophilic granuloma -foot pads (occasionally mouth) Eosinophilic furunculosis of face -Occurs in dogs usually idiopathic
Dx: cytology/histopath (eosinophils)
T: Steroids can be used if underlying isn’t infectious
Cyclosporin, anti-histamines
Atopy, FAD, food sensitivity
Atopy
- Genetic response to environment Ag’s
- 3 mnth –> 6 yr onset
- Facial alopecia
- Cyclosporin, preds, anti-serum immunotherapy
Food sensitivity
- presents <1 year
- Elimination diet
FAD Cnemidocoptes canis, felis Purlex irritans 3-5 years onset Cause Fe2+ def anaemia + transmit D.caninum FAD --> Hypersensitivity I + IV
Flea control
- Adovate (Imidocloprid + moxidectin)
- Frontline PLUS (fipronil + Methroprene)
- Frontline (Fipronil)
Cs:
Dogs - facial, digital alopecia and otitis ext
Cats - miliary dermatitis, eosinophilic ulcers
Dx
- Parasites/infectious –> Allergies –> AI
- Scrapes/culture –> elimination diet ID skin test –>
DDx: Atopy = seasonal, Food allergy = Non-seasonal
Ear diseases (otitis ext, med, int) + skin adnexa
Skin Adnexes
Sebaceous adenitis
inflammation of sebaceous gland –> destruction of gland
Cs: silver dandruff
T: Anti-seborrheic shampoo + cover with baby oil
Seborrhea
Over production of keratinocytes
primary - hyperkeratosis (distemper)
secondary (FAD, Ectos, atopy, self trauma)
Cs: scaling of pressure points and nose
Dx: Histopath (para/hyperkeratosis)
T: Keratinolytic (removes excess keratinocytes)
Keratinoplastic (normalises keratinisation)
Vit A, Vit D3, cyclosporin, preds
Ear diseases
Long/floppy ears
Primary - FB, neoplasia, AI, parasites
secondary
Otitis externa (often results in haematoma)
5-8 years
-Otodectes cynotis (mostly cats) - dark + dry
-Allergies (FAD, food, Atopy)
-FB
-Infectious (s.int, pseudo) - moist, yellow, smelly
-Fungal - waxy + brown
-endocrinopathies (Hypothyroidism, hyperoestrogenism)
-AI (Pemphigus)
T: Do not use in rupture ear drum (ototoxicity) Chlorhexidine, ATB's Auriflush Ceruminolytic agent cleaning and drying Steroids
Otitis media (tympanic mem, ossicles, tympanic nerve)
-Horners syndrome (ptosis, miosis, enopthalmus, 3rd eyelid prolapse)
T:
Bulla osteotomy, ear ablation
Otitis interna (cochlear, vestibular + semi-circ canals) Ventroflexion, torticolis, rolling, circling, nystagmus - vestibular syndrome
Dx:
Otoscopy + swab
contrast canalography
myringotomy (sample of ear fluid)
Tumours of skin and subcutis
Basal cell tumour - more common in cats
-Maybe pigmented, head + trunk
Mast cell tumour - most common skin tumour of dogs
Grades
-1: Cell differentiated well
-2: Cell semi-differentiated
-3: Cells not differentiated, high Mx chance
Darier’s sign: skin becomes red and irritated on palpation due to hyperreactive mast cells
Adenomas/adenocarcinomas
Cerumin glands (ear) - ear ablation
Sebaceous glands (skin) - rare in cats (self limiting)
Apocrine gland (Anal sac) - near anal sac
Peri-anal gland - Castration (androgen stimulated)
Melanoma
Solitary brown/black mass (ulcerated = malignant)
Occular in cats
Histiocytoma - button tumour
benign tumour of histiocyte (skin macrophage)
Papiloma/lipoma
-benign lumps
Squamous cell carcinoma
Related to sun damage –> non-healing ulcer
Cutaneous lymphosarcoma
-older animals (8-10years) linked to FeLV
TVT
Only dogs
Keratoacanthoma
Benign tumour of cells between hair follicles
young dogs only
Epidermal cysts
- inclusion: acne
- Dermoid: developmental abnormality (filled with hair, skin, pus, keratin)
Dx: Biopsy, tumour factors, clinical appearnace
T: Excision (capsular, marginal, wide), chemo (vincristine), radiotherapy
Immune-mediated diseases (pemphigus, lupus, AIHA)
Lupus
Systemic lupus erythematosus
Ab development to DNA, RBC, WBC, Platelets
Inflammation damages skin, joints, kidneys, anaemia
Skin lesions have boarder (lupus band)
Discoid lupus erythematous
similar to SLE –> mainly on face only
pemphigus complex
Ag-Ab to epithelial cells –> desmosome lysis –> acantholysis –> sloughing + clefts
P. Vegetans - benign
P. foliaceus - most common (head, ears, pads)
P. erythematous - as PF + photosensitivity + nose depigmentation
P. vulgaris - bullous lesions of palate or rectum
Dx:
IFA - samples from lesion boarders
Histopathology (acantholytic cells, inflammatory cells)
AIHA
Type II. Primary or secondary (inf, drugs, maternal)
Dx: Coombes test (binds Ag’s attached to RBC’s)
T:
immunosuppressives (cyclosporin, clenbuterol, azathioprine)
Steroids (act to suppress immune system)
Hypothyroid, hyperthyroid, hyperparathyroidism
Hypothyroidism
Dogs > Cats
Types: juvenile or acquired (primary/secondary)
Cs: bilateral alopecia, lethargy, obesity, cold, bradycardia
Dx: serum or free T4
Hyperthyroidism
Cats > Dogs
95% adenomas
Cs: Polyphagia, PU/PD, weight loss, excessive licking alopecia, goitre (USG)
Dx: T3 suppression - response to TSH -Apply T3 for 2 days (3x/day) -normal: T4 and TSH suppressed -Hyperthyroid: T4 high and TSH low (unchanged)
TSH stim test
Measure T4 pre and post appliation of TSH
-Normal: T4 increases
-hyperthyroid: T4 unchanged
T: oral antithyroid (thiamazole), surgical removal
Hyperparathyroidism
PTH –> stims Ca abs in GIT and release from bones
-Primary: adenoma
-secondary: hypocalcemia, hyperphosphatemia
Cs: hypercalcemia –> muscle weakness
T: calcitonin, surgical
Diabete mellitus, acromegaly, insulinoma
DM
B-cells of islets of langerhan
Type I - insulin dependant (Dogs) - inherited
Type II - non-insulin dependant (Cats) - obesity, acromegally, cushings, pregnancy (tissue has reduced response to insulin)
Transient diabetes
-stress –> hyperglycaemia –> prolonged insulin secretion (lowers tissue response)
Islet amyloid polypeptide (IAPP)
- lowers glucose sensitivity in pancreas (less insulin)
- lowers tissue insulin sensitivity (glucose stays in blood)
- Increases hepatic GNG
- Hyperglycaemia
Cs: PU/PD, Polyphagia, weight loss
–Glucose cannot enter cells –> fat/protein metabolism
UTI’s - glucose in urine
Retinopathy - increase BP
Ketoacidosis - lipid metabolism
Dx: Bloods (hyperglycaemia), Liver enzymes, Hepatic lipidosis (increase fat metabolism), Urinalysis (Glucose 8-10mmol/L, SG >1.015, ketones)
Insulin supplementation
-human or porcine insulin
Fructosamine
-long term blood sugar, allows us to determine owner compliance
OVH
-80% DM in complete females related to hyperP4
Somogyi effect - high insulin dose –> hypoglycaemia –> overswing to compensate –> hyperglycaemia –> next insulin dose is ineffective
Acromegaly Pituitary neoplasia --> GH increase Increased progesterone --> GH increase Anabolic effects down regulates insulin receptors = DM enlarged Jaw and feet + organomeglly
Insulinoma Insulin secreting tumour Hypoglycaemia --> neurological symptoms Surgical removal --> risk pancreatitis Diazoxide --> insulin antagonist
Polyuria/Polydipsia DDx
PU
Physiological urine output: 20-45ml/kg/day
Hypothalamus regulates hydration with ADH
PD
Physiological water intake: 20-70ml/kg/day
Factors:
Diet - high in salt, low protein (albumin)
Medication - diuretics
Persistent urethral obstruction
Potential aetiologies
- Addison’s
- Cushing’s
- DM/DI
- Hyperthyroidism
- Hepatic disease
- Pyometra
- Renal failure
Dx
Urinalysis
-Glucosuria - DM or renal damage
-Pus/bacteria - glomerulonephritis
Bloods
- increased PCV + Pancytopenia = HyperT4
- Stress leucogram = pyelonephritis, pyometra
- Non-regenerative anaemia = renal/liver failure
- No stress leucogram in sick animal = addisons
Biochemistry
- Hyperglycaemia - DM
- Azotemia - Renal, pyelonephritis
- Hyperkalemia + hyponatremia - Addison’s
- Hepatic enzymes - Liver failure
Specific tests
- ACTH stim test - Addisons/cushings
- T4, fT4, T3 suppression test - HyperT4
- ADH test - DI
- water deprivation test - DI
- creatinine clearance test - renal function
- Urine culture - pyelonephritis
- Radiographs + USG - pyometra, bladder
Hyperadrenocorticism (Cushing’s) Hypoadrenocorticism (Addison’s), Diabetes inspididus
Hyperadrenocorticism (Cushing’s)
Primary (non-pituitary) - Adrenal neoplasia (20%)
Secondary (pituitary) - Pituitary neoplasia (80%)
Iatrogenic - prolonged steroid use
Cs: PU/PD, Pot belly, Polyphagia (4 P’s), bilateral alopecia
Dx:
Bloods - stress leucoram
Biochem - Low T4 (cortisol suppresses), low BUN (due to PU)
Liver enzymes (ALP,ALT, cholesterol, hyperglycaemia)
Urinalysis
Glucose (DM is usually concurrent in cats)
Proteinuria
Specific testing
Cortisol-creatinine ratio (<13IU/L - not cushings)
ACTH stim test
-give ACTH and measure cortisol in blood, if increases = cushings
Low dose dex supp test
- 0.01mg/kg of dex
- measure in 4 + 8 hours
- if no suppression = cushings
High dose dex supp test
- 0.1mg/kg of dex
- 8 hours later
- Pituitary cushings - suppression
- Adrenal cushings - no change
USG/MRI
Treatment Medical -mitotane (cytotoxic to addrenal) -Trilostane (enzyme competitor) Surgical -Hypophesectomy
Hypoadrenocorticism (Addisons)
Primary - adrenal cortex destruction
–Disrupts mineralocorticoids (aldosterone) –> hyperK and hypoNa
Secondary - pituitary destruction
-Lower ACTH so less cortisol but no disruption to MC’s (no K or Na disruption)
Cs:
PU/PD (loss of Na = water loss)
Bradycardia (increased K)
Acidosis (increased K)
Dx: Biochem: lowered aldosterone --> loss of water, Na + Cl and increase in K BUN increase (lower GFR - hypovolemia)
ACTH stim test
- Primary: cortisol increased, aldosterone decreased
- Secondary: only cortisol is decreased
Treatment
- Fluids (hypovol) + electrolytes
- Bicarb –> acidosis
- Dex (fast acting), hydrocortisone (slow)
- MC’s if primary
Diabetes insipidus
Central = ADH deficiency
Nephrogenic = no renal responce to ADH
Congenital / acquired (neoplasia)
Cs: PU/PD –> neuro signs if severe
Dx:
Water deprivation test –> if losses >5% (BW) or SG: >1.030 = DI
ADH + WDT
Concentration of urine = central
Non-conccentration = nephrogenic
Treatment:
Central - Desmopressin (synthetic ADH)
Nephrogenic - Thiazide (diuretic)
Upper respiratory tract disease
Nose + nasal cavity
Foreign bodies
Tooth root abscess or oronasal fistula
Fungal rhinitis (cryptpococcus, aspergilus) Dx - Wrights stain --crypococcus = capsule, aspergillus = hyphae
Feline upper respiratory tract infection
-Herpes, calici, chlamydia
Neoplasia –> turbinate atrophy
Allergy
-eosinophils on blood
Naso-pharyngeal
especially eustacian tube
Nasal mites
capillaria
Cs: Uni/bilateral discharge, shaking head, sneezing
Dx: endoscope, X-Ray
OROPHARYNX
Laryngeal paralysis
-hyperthermia (panting), syncope (exercise)
Dantrolene (relaxes larynx)
Laryngitis
-KC, FB, Neoplasia
TRACHEA
Collapse
-small dogs especially, chondroitin deficiency
-cervical : inspiration
-thoracic: expiration
-Grades 1-4
-T: chondroitin supplement, horizontal mattress suture (1+2), prosthetics (2+3)
Tracheal hypoplasia
- brachycephalics
- Dx: X-Ray (trachea should be 3x width proximal ribs)
Primary ciliary dyskinesia
- congenital defect
- Dx: photoscopy, semen (tails are cilia)
Kennel cough
- Primary viral - CAV-2, para-influ, distemper, herpes
- Secondary bacterial - Bordetella, mycoplasma, pseudomonas
Brachycephalic syndrome
Anatomical abnormalities due to genetic selection
- stenotic nares + short nose
- elongated soft palate
- tracheal collapse/laryngeal collapse
- turbinate abnormalities
- hypoplastic trachea
Cs: dyspnea, snoring, swallowing issues, syncope, laying dorsal, hyperthermia
Dx: Breed, sinus arrthymia, X-Ray (soft palate enlongation and hypoplastic trachea), Laryngoscopy
During an episode: cool, intbuate, bronchodilators, steroids
T: Widen nares, shorten soft palate, widen larynx, tracheostomy
Keep weight down
LRT - Bronchi and lungs
BRONCHI
Kennel cough
Bronchiectasis
-irreversible dilation of airways (proteases neutrophils)
LUNGS
Bronchopneumonia
Factors - ciliary clearance, immune system, parasites, infection, aspiration, neoplasia
-B: mycoplasma, bordatella, pseudomonas
-V: CAV-2, Herpes, calici, Para-influ, distemper
-F: cryptococcus, aspergillus, histoplasma
-P: Angiostrongylus + aerostrongylus, pneumococcus
Non-cardiogenic pulmonary oedema
Increased thoracic pressure
Diuretics
Pulmonary eosinophilic infiltration
due to parasites or allergies
Pulmonary fibrosis
- Multi factors: genetics, irritants, infection
- Thickened alveoli –> destruction –> hypoxia
Pulmonary neoplasia
- 80% secondary Mx
- 20% Primary
Dx: BAL, X-Ray (alveolar/bronchial pattern), doppler USG
T: NSAID’s, bronchodilators, anti-tussives, mucolytics
Diseases of Pleura + Mediastinum
Pleura Pleural effusion fluid in the plural space -increased production / decrease clearance (absorption) Results from -Heart failure -renal failure -hypertension -hypoalbuminaemia -torsion or lungs -diaphragmatic hernia -pancreatitis -Thrombo-elbolism
Chylothorax - Lymph
Pyothorax - spetic inflammation
Haemothorax - coagulopathy, Vit K, Trauma
Dx: X-Ray - elevated heart from sternum, thoracocentesis, USG
T: O2, diuretics, bronchodilators, vasodilators, fluids, anti-arythmics, thoracocentesis (7-9 ICS)
Mediastinum
Mass
-Tumour (lymphoma, thyroma)
-abscess, cysts, haematoma, granuloma
Pneumothorax Open or Closed (fault in pleura make air leak from lungs) Types: -spontaneous -traumatic -iatrogenic -infectious -tension
As more air enters thorax (pressure goes up) and leaves less space for the lungs to inflate –> hypoxia
Flail chest/paradoxical breathing
Penumomediastinum
-Tracheostomy, bite wound, intubation, sudden thoracic pressure change
LRT - chronic bronchitis + feline asthma
Chronic bronchitis - obstructive
-Inf = neutrophils –> hypertrophy of goblet cells –> excess mucous production
Isolated cough for >2 weeks + BAR
Feline asthma - restrictive
-Inf to environmental Ag’s –> fibrosis of bronchi –> emphysema (destruction of bronchi walls)
Cats only cough with asthma
Dx: Bloods = Neutrophilia (CB), Eosinophilia (FA) X-Ray = Bronchial pattern Bronchoendoscopy (thickened/emphysema) BAL - cytology and culture
T:
O2, steroids/ATB (depending on if infectious), bronchodilators, anti-tussives, mucolytics, NSAID’s
Congenital heart diseases
Dogs must be >12 months of age to recieve congenital status
PDA - patent ductus arteriosus
Shunts the arcus aortae + pulmonary artery
Pressure increases in PA and decreases in aorta
Pulmonary oedema and left sided hypertrophy
T: guide wire with fluroscope from femoral artery to heart and occlude PDA (amplatz canine ductal occluder)
Open heart surgery
Atrial septal defect - PFO (patent foramen ovale)
Usually closes at birth
Ventricular septal defect
L –> R more common due to pressure
Pulmonic stenosis
R hypertrophy (more work)
congenital, infectious
Aortic stenosis
- Sub, aortic, supra
- Concentric hyperplasia
- myocardial ischemia
- arrythmia (V-Fib)
R- Ascites, thrills and distended jugular
L- Pulmonary oedema
T: shunt, balloon catheter, defib for (vfib)
Valvular defects
Mitral
Tricuspid
regurgitation –> lower stroke vol –> hyperplasia
ToF (tetrology of fallot)
- Right Vent hyperplasia
- Ventricular septal defect
- pulmonic stenosis
- dextroposition of blood
- -02 <80% saturated = syncope
Diseases of myocardium (cardiomyopathy)
Diseases of myocardium (without inflammation)
Primary / Secondary
Types of CM
Hypertrophic - more wall less chamber (male cats)
Diastolic failure (less filling)
Tachycardia
Dilated (>60% cases) Often large barrel chested dogs dilated chambers = loss of contractility systolic failure (less ejection)
Restrictive
Less relaxation + normal to decreased contractility
Fibrotic effusion in pericard –> fibrous myocard (rigid not thickened)
-Amyloidosis, calcinosis
Cs: Resp, Ascites, thromboembolism (Hind Limb paralysis)
Dx: Doppler, USG, ECG
Arrhythmogenic right ventricular cardiomyopathy
- inherited in boxers
- syncope
Myocarditis
- B: Borrelia, bacillus anthacis
- V: Parvovirus
- P: Dirofilaria, angiostrongylus
T:
Diuretics (furesomide)
beta blockers (anti arythmics - propranolol)
Diltiazem (Ca2+ blocker) relaxes myocard
Lowered Na diet
Vasodilators (Fortekor - benzapril ACE inhibitor)
Diseases of the valves and pericardium
VALVES
Mitral valve insufficiency
Regurgitation causes hypertrophy + dilation
Primary - ruptured cordae tendinae
Secondary - mitral dysplasia
Secondary - following dilated or hypertrophic CM
Cs: Pulmonary oedema
Dx: ECG - wide P (atrial enlargement). Tall QRS (ventricular enlargement)
Tricupid valve insufficiency Hypertrophy + dilation Ascites, hepatosplenomegaly Cs: Jugular distention, swollen abdomen Dx: ECG - Tall P waves
T:
ACE inhibitors (vasodilator)
Diuretics
Ionotropes (anti-arrythmics - Beta blockers or Ca2+ channel inhibitors)
Aortic valve insufficiency
Blood regurgitates into the LV causing hypertrophy
ECG - Tall R waves
Valvular + sub-valvular aortic stenosis
LV hypertrophy
Lower perfusion of coronary arteries = myocardial infarct
T: Stent
Pulmonic stenosis
RV hypertrophy
PERICARDIUM
Pericardioperitoneal diaphragmatic hernia
-Rare defect in diaphragm + pericardium allowing abdominal contents to enter pericardial space
Pericarditis infection --> exudate --> fibrous adhesions B - Mycobacteria V - FIP, Parvo F - Coccidiomycosis Dx: Pericardiocentesis
Pericardial effusion
Fluid increase –> tamponade
Hemangiosarcoma (dogs), lymphoma (cats)
Heart failure and compensatory mechanisms
Failure is syndrome resulting from the heart not meeting the demands of the body for O2
Causes:
- Congenital
- Valve degeneration (mitral valve in dogs is common cause)
- Cardiomyopathy (hypertrophic CM in cats is common cause)
- Heartworm
Types of HF
-Congestive/Backward
More common, Increased venous pressure slowing flow of blood
Characterised by oedema
-Outflow/Forward
Weakness in the heart, low stroke volume and insufficient output of blood
Stages 1 - Asymptomatic (compensation activated) 2 - Exercise intolerance (No cs at rest) 3 - Seen while walking (No cs at rest) 4 - CHF (coughing at rest)
Cs: Depends on side
Dx:
ECG - sinus tachycardia, atrial fibrillation, AV Blocks
Vertebral Heart Size (VHS)
- 8.5-11 dogs
- 6.7-8.1 cats
USG - Döppler
Compensatory mechanisms RAAS -Decreased ventricular output -lowered artery pressure -Baroreceptors --> RAAS --Vasoconstriction (Angiotensin) --Aldosterone (increased vessel volume) --ANP (concentrates urine --> increases vessel volume further)
Tachycardia
Increased adrenergic tone (vasoconstriction)
Myocardial hypertrophy (as it works harder)
T:
Cardiotonics (slower harder beat) - Digoxin
Negative ionotropes (Ca2+ channel blockers Diltiazem or beta blockers propranolol)
Diuretics
Vasodilators - ACE Inhibitors
Arrhythmias - causes, Dx, Therapy
HR:
Dog: 70-160bpm
Cat: 120-240bpm
Abnormality in rate, regularity, origin of impulse or conductivity through the heart
SA –> atrium –> AV node –> Bundle of His –> L + R bundle branches –> purkinje fibres
5 properties of cardiac muscle C - conductivity C - contractility A - automatically R - refractoriness E - excitability
cardiac cycle
Atrial systole –> ventricular systole –> diastole
PQRST
Arrhythmias
Sinus arrhythmia - >10% increase between P-P
-Bradycardia
-Tachycardia
APC (atrial premature complex)
Atrial tachycardia - >3APC
Atrial fibrillation - P waves replaced with rapid “f” waves
Ventricular premature complex
Ventricular tachycardia >3VPC
Bigeminal (every other)
Trigeminal (every third)
Ventricular fibrillation - terminal rhythm
AV Blocks
1st AV - elongated P-R interval (1:1)
2nd AV
- Morbitz I - P-R extended until P is blocked
- Morbitz II - Regular P-R with P intermediately blocked
3rd AV - SAN depolarised atria wth ectopic ventricle depolarisation (no P + QRS relation)
Left and right bundle branch blocks
Delay in either L or R BB results in the opposite side depolarising giving a delayed QRS
Escape beats
Supra-ventricular escape beats
Junctional escape beats
Ventricular escape beats
-Purkinje fibres escape –> negative QRS wave (<40 bpm)
Regenerative anaemia
Reduction in RBC or Hb (or both)
- Blood loss
- Haemolysis
- Reduced production (non-regen)
Blood loss
- coagulopathy
- bleeding tumour (haemangiosarcoma)
- parasites (ticks, fleas)
Haemolysis
- Immune mediated (AIHA, SLE)
- infection (leishmania, babesia, lepto)
- Lymphoma, leukaemia
- Drugs: Atb’s or toxins (metals, drugs, warfarin)
- Metabolic (DM, hyperthyroidism)
- Internal (splenic rupture, gastric ulceration)
Cs: dyspnea,icterus, splenomegaly (hemolysis _ hematopoiesis)
Non-regenerative anaemia
Lowered production in RBC’s
- BM suppression
- Lack of precursors (vitamins, Fe, Mins, protein)
Compensation can take time (things may look non-regen at first)
Chronic disease
- inflammation
- renal failure - reduced EPO
- infection - FeLV, FIP, Leishmania
- Hepatic disease
- Hypothyroidism + Addison’s
Chronic blood loss –> this exhausts precursors like Fe, proteins, folate
Auto-immune (maternal)
BM suppression - hyperestrogenism, neoplasia
Compensatory mechanisms
- Tachycardia
- Redistribution away from GIT
- More EPO from kidneys
- Less Hb affinity for O2 = faster tissue perfusion
Dx Bloods -decreased PCV + MCHC -Macrocytic (imature RBC's) -Polychromasia (nucleated RBC) -Serum --Yellow - EV Haemolysis --Red - IV Haemloysis
BBT
Treatment
- Fix underlying cause
- Severe anaemia transfusion
- -DEA 1-8 (dog types)
- -A,B, AB (cat types)
Mix blood to see types = agglutination (no match)
Adverse reactions usually occur with cats if recipient is B and donor is A
Coagulopathies
HYPOCOAGULATION
Thrombocytopathies
-Lowered production (Vit K, BM, neoplasia)
-Increased sequestration (Splenomegaly)
-Destruction (AI, toxins, drugs, oestrogen)
-Over utilisation (DIC, haemorrhage)
Thrombobastaenia
-Normal number with altered function
Coagulopathies
-Congenital: Von Willebrands + chediak-higashi syndrome + Heamophillia A + B
-Acquired: Liver disease, warfarin, decreased Vit K, DIC, Heam diathesis
Vasopathies (defects or damage to vessels)
HYPERCOAGULATION
DIC
Protein loss –> anti-thrombin III
Hypercholesterolaemia –> thrombus
Systemic disease –> sepsis, burns, heamolysis
Thrombocytosis –> Bleeding or adrenaline (physiological)
Cs: haematuria, petechiae, epistaxis, melana, splenomegaly
Dx: CBC (thrombocytopenia) Platelet counts clotting factors prothrombin times BBT Activated clotting time
T: Transfusion (PRP, Blood, warfarin)
Lymphoproliferative diseases
Leukosis
Proliferation of leukocyte producing tissue
Causes malignant neoplasia of R/WBC’s
Leukaemia
Acute - BM infiltration = displacement of cells and lowered immune system
Chronic - mature neoplastic lymphocytes in blood
Dx:
Bloods: leukopenia, anaemia, thrombocytopenia, monoclonal IgM spikes
Marrow cytology: lymphocyte proliferation
Bence jones protein (in urine)
T: prednisolone, vincristne, chlorambucil
Feline leukaemia virus (FeLV) Saliva + urine, replicates in tonsils Good immunity - Latent Bad immunity - progressive infection Forms -thymic -multi-centric -alimentary Immunosuppression Dx: ELISA, IFAT, LN FNA
Lymphoma/lymphosarcoma Proliferation of LN + BM Classification -Multi-centric -Mediastinal -Alimentary -Extra-nodal
Staging I - Single LN II - Multiple LN in one region III - Lymphadenopathy IV - Liver and splenic involvement V - Blood or BM involvement
Dx: FNA of LN, X-Ray, USG
T: preds, vincristine, doxorubicin
Polycythemia Increased RBC production Primary/Secondary Causes bleeding disorders T: lower PCV, chemotherapy
Lymphadenopathies + splenomegaly
Lymphadenopathies
-Reactive hyperplasia - Ag stimulation causes LN enlargement but LN’s themselves are no affected
Lymphadenitis - Neutrophils + macrophages invade LN’s
Causes: B: rickettsia, brucella, pasturella, fuscobact F: Sporotrichosis Non-Inf: allergies, immune mediated Dx:bloods, LN FNA
Splenomegaly
Primary - torsion
Secondary - disease
Types Congestive - hypertension Hyperplasia - chronic anaemia Inflammation - SLE Infection - -P: babesia, ehrlichiosis, toxoplasma -B: salmonella, mycobacteria -V: canine hepatitis, FIP -Neo: heamangiosarcoma
Localisation
- Diffuse (increased splenic work)
- Asymmetrical (tumour)
Hypersplenism - increased removal of RBC’s
Hyposplenism - decreased removal and presence of more reticulocytes
Heamangiosarcoma
Common splenic tumour
Rupture –> internal bleeding
Diseases of upper GIT
Oral cavity Stomatitis Primary -Peridontal disease -trauma -chemical -nocardia ulcerative stomatitis Secondary -AI (pemphigus, SLE) -Metabolic (cushings) -Immunosupressive -eosinophilic complexes -FOR lesions
Oral Neoplasia
- Benign: epulis, papilloma
- Malignant: Melanoma
Oropharyngeal dysphagia
Oral or pharyngeal
Structural - teeth, gums, tongue or palate, stricture
Functional - nerve damage, myasthena gravis
Cs: Halitosis, bruxism and hypersalivation
Dx: Oral x-ray
Salivary glands Sub-mandibular zygomatic parotid sub-lingual
Mucoceles -Sublingual = Ranula FB or stomatitis = obstruction Sialolith is calculi in the duct T: marsupialised the gland
Diseases of the oesophagus
Megaoesophagus
- Segmental or diffuse
- Inherited or acquired
- Regurgitation
- prokinetics (only in cats as dogs is striated not smooth)
Oesophageal FB
-Thoracic inlet, apex cordis, hiatus oesophagi
Oesophageal perforation
-contrast x-ray
Oesophagitis
-Iatrogenic, acid reflux
T: cimetidine (H2 inhib), omeprazole, prokinetic, anti-emetic (cerinia)
Stricture
Diverticulum
-Traction/pulsion
Hiatal hernia
GIT in thorax
Vascular ring anomalies
Entrapment by aorta
resect and ligate
Neoplasia
Spirocercosis (Spirocerca lupi)
Red worms found in oesophagus
Diseases of stomach + DDx of V+
Acute gastritis >1 week V+ contaminated food dietary changes FB viral - parvo, distemper Parasites
V+ characteristics Gastric - milky acidic Duodenal - yellow alkaline FB/ulceration - Red Bile - reflux, pancreatitis
Chronic gastritis
recurrence of acute
Reflux or Ulceration
T: novel proteins or hypoallergenic food
Gastric ulcers
-V with blood
GDV
twisting, stops outflow and can obstruct
VCCau
presence of air or gorging a large meal –> GDV
X-Ray: compartmentalisation
Gastropexy
Gastric outflow obstruction
-Pylorus (usually stenosis)
Gastric motility disorders
-delayed emptying due to weak contractions
Neoplasia
DDx in vomiting
- Vomit vs Regurgitation
- Timing
- -fast (gastritis, overfeeding)
- -Hours post (outflow obstruction, gastric motility disorder)
T: Anti-emetic (metoclopramide) PPI (omeprazole) H2 blocker (cerenia) Mucoprotectants (sucralfate) Probiotics (Promax) withhold food (48hrs) + try bland food (elimination) ATB + anti-parasitic
Diseases of Small Intestine
Acute D+ <3wks
Chronic D+ >3wks
D+
Secretory - increased fluid from mucosa
osmotic - poor digestion –> large particles = osmolarity
malabsorptive - lack of absorption
Acute
B - salmonella, shigella, campylobacter, e.coli toxin
V - Parvo, distemper, adeno
P - isospora, giardia, toxo, crypto, eimeria, tenia, ancylostoma
Chronic D+ (acute that lasts >3 wks)
IBD
Protein loss enteropathy
Food allergy, D+, lymphatic rupture
Villous atrophy
Predisposition in setters + german shepherds
Bacterial overgrowth + GI stasis
-Absence of digestive enzymes (gall bladder stasis)
Dx: contrast X-Ray can show slow movement
T: promote gall bladder emptying
pancreatic enzymes
surgical ileocaecal valve correction
ProMax
Ileus (Intestinal obstruction)
Mechanical - intra/extra luminal
Functional - Spastic/paralytic
Diseases of the colon, rectum + perianal region
COLON
IBD
-Hypersensitivity (Ag to mucosa)
T: Diet, hypoallergenic, chlorambucil
Acute colitis
-Giardia, campylobacter, parvo, histoplasma
Irritable bowel syndrome
-Stress + irritability
often in large working dogs
high fibre and sedatives
Ulcerative colitis
Typhlitis
-inflammation of cecum
Primary/secondary (typhlocolitis)
Megacolon
- congenital
- acquired (colon inertia - neuro, metabolic, endocrine)
Obstruction
Neoplasia
Intussusception
Hypomotility + constipation
Extra-intestinal (dehydration, endocrine, neuromuscular function alteration
Intra-intestinal (obstruction, inhibition of defecation reflex)
Perforation
RECTUM
Prostatitis
-prostate hyperplasia (leydig cell neoplasia)
Proctatitis
-inflammation of anus
Anal/rectal prolapse
-complete/incomplete
T:Hypertonic solution
Anal sac disease
- clogging or inflammation
- obese dogs, poor muscle tone
Malabsorption and maldigestion
Malabsorptive syndrome
Disruption of degradation or absorption of food
Malabsorption (SI disease) fewer enterocytes or impaired function -Inflammatory damage -Bacterial interference with micelle formation -SIBO local immunodeficiency Biliary obstruction - bile acids
Maldigestion (exocrine pancreatic insufficnecy)
- Acinar atrophy, pancreatitis
- bile duct stasis
Digestion
pancreas secretes most digestive enzymes + Bile duct secretes bile acid for fat digestion
Cs: weight loss even if polyphagic, abdominal distention (hypoprotein)
T: diet, pancreatic enzyme supps, PPI (omeprazlole), H2 blocker (cimetidine)
Diseases of the pancreas
Pancreas
- endocrine
- exocrine –>pancreatic juices
Pancreatitis
- chronic inf
- trypsinogen –> trypsin (in SI is normal, in pancreas results in auto lysis)
- Billiary tract stasis, toxaemia
- Poor diet (fatty/sugary)
Cs: steatorrhea + heamatorrhea
Exocrine pancreatic insufficiency Synthesis or secretion of enzymes -Acini atrophy -chronic pancreatitis -Masses - obstruction of duct Dx: serum trypsin
Pancreatic neoplasia
- Adenoma/adenosarcoma
- Insulinoma –> hypoglycaemia
- duct obstruction
Acute hepatopathy
Function
- Protein metabolism
- detoxification
- produces bile
- coagulation factors
Acute hepatitis
- Primary = CAV-1, toxoplasma, leptospira
- Secondary = GIT infections, toxins, fungi, drugs
Inflammation –> fibrous islets (cirrhosis)
Cs: >60% destruction results in Cs
Bloods: ALP, ALT, GGT, Glu Dehy
Increase: NH4, Cholesterol,, billirubin
Decreased: CF’s, albumin, glucose
Liver function tests
- Serum bile acids
- Ammonia tolerance test
chronic hepatic disease
Chronic hepatitis
- Proliferation and dysfunction
- Lepto, CAV
- AI, chemicals, drugs
- Cholangitis prequel
Chronic active hepatitis
-still inflammed
Hepatosis dietica (yellow liver) -Vit E + sel deficiency
Dx: shrunken nodular liver
Biopsy: parenchymal cirhosis or depositis of Fe, Cu, Vit A
Amyloidosis
- AL + SAA
- steroids or nsaids
Steatosis hepatis (fatty liver)
2ndry to anorexia in obese animals –> fatty deposits
Can be caused by DM, lack of insulin –> glucose into cells –> lipid metabolism for energy
-Pre - increased FA’s
hepatic - impaired function
post - inability to conjugate with apoproteins –> lipoproteins
Hepatic glycogenesis
- steroid induced hepatopathy
- steroids = hyperglycaemia
Cirrhosis
parenchyma –> fibrous tissue
shunting and blockage
Feline cholangitis/cholangiohepatitis syndrome (CAHS)
-2nd to GIT or pancreas
T:
Metaclopromide (anti sickness)
Hepatoprotectants (milk thistle)
Vit K supplement
Diseases of the gall bladder and bile ducts
Obstruction
Inflammation of pancreas, SI, gall bladder or duct itself
(complete) Extrahepatic cholestasis –> rupture –> bile leaks –> peritonitis
Jaundice + steatorrhea
Cholelithiasis (gall stones)
Cholesterol, salts, protein
related to chronic cholecystitis
full obstruction = Cs
Inflammation
Cholangitis - large bile duct
Cholangiolitis - small intrahepatic ducts
Cholecystitis - gall bladder itself
Reflux of bacteria from SI or haematogenous
Feline progressive lymphocytic cholangiohepatitis –> fibrosis and proliferation
Bile duct hyperplasia
Insults –> proliferation
formation of new irregular channels
Neoplasia
Cholangiomas
cholangiocarcinoma
Icterus - DDx and diagnostic approach
Icterus - presence of billirubin in tissues turning them yellow
commonly collects in:
-sclera, Kidney tubules
Forms
Pre-hepatic
heamolysis (increased serum Br)
Hepatic Hepatocyte damage (increased serum Br)
Post-hepatic
IntraHepatic - bile caniculi inside liver
Extrahepatic - main bile duct
(increased serum cBr)
Van den Berg test - differentiate Br and cBr
- Prehepatic: normal liver enzymes + increased Br
- Hepatic: Increased liver enzymes + increased Br
- Posthepatic: Liver enzymes + increased cBr
Dx
- Enzymes
- Van de Berg test
- USG
T: underlying cause
Hepatencephalopathy and portosystemic shunts
PSS, cirrhosis, liver failure –> NH4+ –> CNS
- disrupts neurotransmitters
- cerebral oedema (mannitol)
- oxidative stress
Portal hypertension Pre - portal vein obstruction Hepatic - sinusoid disruption Post - disruption between liver and heart/VCCau (hepatic vein) -Can cause PSS, ascites or peritonitis
PSS
Congenital - extrahepatic or intrahepatic
Acquired - 2nd to liver disease cirrhosis + portal hypertension
Reduced blood to liver –> impaired detoxification ability
NH4+
increased flow through oesophageal vein (oes varicies) (prone to rupture)
Ligation of shunts
Perilobular hepatic artery supplies hepatocytes as such central lobe area is most sensitive to hypoxia and the perilobular area is most sensitive to toxins
Acute renal failure
Kidney failure - >75% nephrons damaged
Pre-renal - hypovolemia
Renal - Direct damage to nephrons or interstitium
- -Glomerulonephritis - GFR
- -interstitial - lepto
- -nephrotoxic - drugs, metals
- -ischemic - emboli
Post-renal - Urinary tract obstruction or cystorrhexis
Consequences -lowered excretion --> Hyperk+ --> Acidosis + bradycardia HyperP --> increase PTH --> hyperCa2+ Creatinine + BUN
Dx: uremic breath, bradycardia
Bloods - BUN, Cr, P, K, H+, Ca2+
Urinalysis - SG 1.015-1.045, pH 6-6.5
T: fluids, charcoal, bicarb, diuretics
Chronic kidney failure
Occurs over months/years
- retained toxins
- loss of endocrine function
Acquired
-AI (SLE), nephrotoxins, infections (lepto), obstruction (calculi)
Congenital
-cystic kidneys
Impaired renal function
Decreased GFR
Buffering ability (acidosis)
Toxicosis
P –> PTH –> Ca2+
Decreased excretion Na + H2O –> oedema + ascites
Urea –> oral ulcers + melana
impaired insulin degeneration
Decreased calcitriol –> cannot bind Ca2+ in SI –> lower Ca –> PTH activated –> secondary hyperparathyroidism
Decreased EPO –> anaemia
Grading
1 - Non-azotemic
2 - Azotemia
3 + 4 - Azotemia, PU/PD, V+
Mild - PU/PD
Moderate - oral ulcers, uermic breath, V+
Severe - Seizures, blindess, fatigue
Uremic syndrome - anaemia, D+, V+, CNS, osteodystrophy, acidosis
Dx:
Non-regen anaemia
PTH, K, Na, H2O, EPO, Ca
Cre + BUN
T:
Acidosis (Bicarb)
K - KCl fluids
ACE inhibitors (vasodilator)
Diseases of the urinary bladder and urethra
Obstruction
Any obstruction –> post-renal azotemia
Intraluminal - uroliths, emboli
Intramural - neoplasia, fibrosis
Other - ectopic ureters, neurological
Hydronephrosis/urolithiasis
Obstruction of bladder or urethra –> build up of fluid in the kidney –> dilation and loss of function –> uremic syndrome
Uremia
High levels of uremia in the blood –> uremic syndrome
Uremic syndrome
- P - PTH –> Ca2+
- K (bradycardia) –> H+
- Na + H20 –> dehydration
- Ca2+ –> osteoporosis
- calcitriol –> reduced Ca abs
- EPO –> anaemia
- Uremia –> ulcerative mouth and enteritis
- Pulmonary + pericardial oedema
Urethral prolapse
Trauma, urethritis
pea-sized mass
Feline idiopathic cystitis
Sterile cystitis
stress related issue
Feline lower urinary tract disease
multifactoral - FIC, neoplasia, UTI, obstruction, uroliths
Urolithiasis
Crystals formed of various materials
High levels of salt
Retention of salts (inability to concentrate urine)
pH change that favours crystalisation (alkaline)
A scaffold exists to help form crystals
Citrate acts as a crystal formation inhibitor
Stones usually occur in urethra
damage –> inflammation + rupture
Obstruction –> hydronephrosis –> renal failure and uremic syndrome
Cs depend on location
- Ureteral: discomfort + heamaturia
- Bladder: Stranguria, abdo pain
- Urethral: straining with no urination
T: dietary (acidification of urine + citrate)
Retrograde hydropulsion
cystotomy, urethrotomy
Spec grav - <1.045
Types of stones
Calcium oxolate (cats mostly)
-Higher efficacy of citrate to inhibit
-hypercalcaemia, Vit D, protein, P (PTH)
Cystine
-Protein + low pH
Struvite (dogs mostly)
-MO’s –> urease –> alkaline urine
Urate
- uric acid
- occurs in dalmations with PSS
- Allopurinol –> metabolises urate in the bladder
Disorders of urine elimination
urinary retention Incomplete retention without obstruction Hypocontractility -bladder distention -neurogenic -electrolyte imbalance (Na)
Functional obstruction
-Sacral lesions, urethrospasm
Dx: cystoretrography
T:
metaclopromide (increases muscle tone in bladder detruser muscles)
Diazepam + acepromazine (functional obstruction - anxietolytic)
Dysautonomia (Key-Gaskell syndrome)
Dysfunction of autonomic NS
Dx: STT (<5mm), Megaesophagus, histopathology of ganglia
Parasympathomimetics
Urinary incontinence
Failure of voluntary control of micuration
-constant / intermittent
Neurological
Bladder storage dysfunction - overfilling
urethral disorders - hypoplasia
anatomical - patent urachus, ectopic ureters
Cs: urine scalding Dx: double contrast uroscopy T: Acidifying agents E2 --> spayed females A2 - agonists Urethrostomy
Epileptiform statuses
Seizures
alteration of neuronal excitability –> prolonged depolarisation
- Insufficient inhibition of excitement (GABA)
- excessive excitement (glutamate)
Localisation
- Extracranial: Metabolic, toxic
- Intracranial: tumour, haemorrhage
Types
-Focal: Motor, autonomic, behavioural
General
- Tonic (stiffness + opsitonus)
- clonic (paddling + chewing)
- Tonic-clonic
- Atonic (brief absence of muscle tone)
- Absence (transient loss of conciousness)
Stages of seizures:
Prodromal - salivation, weakness
Aura - induction of seizure, odd ECG activity
Ictal - seizure itself
Postictal - memory loss, disorientation, ataxia
Dx:
Neuro exam - menace, pupillary, cornal, placing/postural, walking, tracking
Imaging - CT, MRI
Status epilepticus;
Continuous seizure for >5mins
2 Phases;
Compensatory
-Tries to compensate for increased O2 and glucose demands in the brain by increasing blood flow –> lactic acidosis and hypoglycaemia
Decompensatory
-Compensation fails –> cerebral oedema –> decreased blood flow
> 60 mins –> organ failure
Idiopathic epilepsy
> 2 seizures in 1 month
Types
Provoked - systemic disorder causing a brain insult (heavy metals)
Idiopathic (primary) - Recurrent seizures with no lesions
-Usually genetic, with an onset of appox. 6 months
Symptomatic (secondary) - with ID’able cause;
-Intracranial: degenerative (storage disease), hydrocephalus, ischemia
-Extracranial: hepatic encephalopathy, nutritional (B1), infectious (rabies)
Juvenile epilepsy - <1 year onset
Exam Time of day? Type? duration? Neuro exam -proprioception, posture, gait, behaviour
T:
Diazepam (0.5 - 2mg/kg)
Phenobarbital (2 - 4mg/kg)
Bromide - DOGS ONLY!
Diseases of the brain - congenital & inflammatory
Brain
Cerebrum - higher functions
cerebellum - muscles, posture, movement
brain stem - automatic function
Congenital Hydrocephalus Toy or brachycephalic breeds Lack of drainage or overproduction Diuretics + mannitol
Caudal occipital malformation syndrome (COMS)
Presses on the skull –> abnormal fluid dynamics
Intracranial arachnoid cysts
Pseudocyst formed of fluid in the arachnoid space
Neuronal migration disorders
Improper migration of neurones during development leading to underdeveloped areas of the brain
Cs: scizencephaly (odd clefts)
Dandy-walker syndrome (cerebellar hypoplasia)
Toy breeds
Cs: tremors, ataxia, odd posture, behavioural changes, seizures
Diseases of the brain - degenerative & neoplastic
Degenerative
Metabolite overloading
Lysosomal storage disease
Accumulation of lysosomal byproducts
Genetic/acquired
Dementia (congenital dysfunction syndrome)
Age changes in the brain
increased amyloid deposition causing nerve degeneration
T: Anipryl
Spongy degeneration
Inherited
Aquired - hepatic enceph, rabies, TSE, intoxication
Neuronal vacuolisation
Familial disease –> intracytoplasmic vacuolation
Multi-sytemic neuronal degeneration
Hereditary in terriers
progressive from 3-6 months
Neoplastic
Arise from neuroectoderm
Glia, ganglia, myelin sheaths
Primary tumours Glioma - common CNS in dogs -astrocytomas -oligodendromas -ependymomas -medulloblastomas
Meningiomas
gangliomas
schwannomas (neurofibroma)
Secondary
Pituitary adenoma
Lymphoma
Neurological examination and other Dx procedures
Neurological exam
Localise lesions
1 - Mentation Behaviour + consciousness Normal - BAR Excitation Depression -Obtunded (somnolece) -stupor -coma
2 - posture + gait Posture -kyph, lord, scoli -Torticollis, opsitonus - Goose step, schiff-sherington (FL - tonic, HL -paralysis)
Gait
- Paralysis
- Ataxia
- Spasm
- Tremors
- Forced movements
3 - CN exam CN 2 --> 8 -pupillary: 2+3 -menace: 2+3+6+7 -dazzle: avoidance is normal -palpebral: 5+6+7
4 - postural reaction Abnormality in proprioception -Overknuckling -Placing (visual, tactile) -Hopping (initiate) -Wheelbarrowing -Hemi-walking
5 - Spinal reflexes Lateral recumbency -Bicep - Cervical -Tricep - C/T -Panniculus - Thoracic -Patellar - Lumbar -Gastrocnemius - Lumbar -Withdrawal - L/S -Peri-anal - Sacral
Reflexes are either
- Hyperreflexive - UMN
- Hyporeflexive - LMN
Important to differentiate neurological and muscular
6 Palpation
swelling or atrophy of muscle
assessment of pain
7 Nociception
Superficial - cutaneous pain
Deep - periosteal nociception –> interdigital pressure
Imaging methods
USG
MRI
CT
Vestibular disease & Horners syndrome
Vestibular syndrome
Maintains balance - includes brain stem and middle/inner ear
Vestibular syndrome
Central vestibular disease - encephalitis
Vestibular nerve - Inflammation
Peripheral vestibular disease - Otitis, ototoxicity, polyps
Cs: CVD (brain lesion) -Head tilt -Circling -Nystagmus (H, R, V) -Rolling
PVD (Vestibulocochlear nerve CN8);
- CVD Cs’s (Nystagmus is only H + R) -Horner’s syndrome
- Facial paralysis (facial n. CN7)
Dx: Otoscopy, neuroexam, Brainstem auditory evocation test
Horner’s syndrome
Loss of innervation to the eye
Central lesion - BS, SC, Hypothalamus
Pre-ganglionic - nerves going to ear (FL or neck trauma)
Post-ganglionic - Nerves going fro middle ear to eye (otitis, vestibular syndrome)
Damage to sympathetic neurons –> dominance of parasympathetic system
- 3rd eyelid prolapse
- Miosis
- Ptosis
- Enophthalmos
Dx: Cyclopentolate eye drop –> mydriasis –> if successful = postganglionic lesion)
Muscular and neuromuscular diseases
MYOSITIS Infectious myositis Suppurative myositis (C. septicum) Bites --> haematogenous Abscesses and pus
Parasitic myositis
- Toxoplasma (cats)
- Neospora (dogs)
Immune mediated myositis
Polymyositis
-Large breeds at risk
-muscle atrophy, exopthalamus, strabismus
Masticatory muscle myositis
Acute - swelling and lymphadenitis
Chronic - bilateral atrophy
Dermatomyositis
Hereditary disease of skin and muscle atrophy and megaoesophagus
MYOPATHIES Non-inflammatory degeneration Metabolic myopathies -Hyperadrenocorticism -Hypothyroidism
HypoCa2+ polymyopathy
- Feline hypoCa2+ often 2ndary to hypoK
- hypoK = increased Na sensitivity of nerves = hyporeflexivity –> weakness
Inherited myopathies
X-Linked muscular dystrophy
-Lack of dystropin
eventually fatal to male puppies
Labrador retriver myopathy
Inherited myopathy especially in temporal muscles
Myotonia
Defective muscle membrane (Cl- channel dysfunction)
Constant contraction delayed relaxation
NEUROMUSCULAR DISORDERS Myasthena gravis Dysfunction of NM junctions acquired or inherited Ab --> ACh receptors Weakness + megaoesophagus IFAT - Ab's Tensilon test - ACh responce test (tension inhibits ACh hydrolysis)
Dysautonomia
Degeneration of autonomic NS
V+, D+, decreased anal tone, absent pupillary light reflex, fewer tears, mydriasis, 3rd eyelid prolapse
Common intoxifications
Rodenticides Warfarin -Prevents prothrombin formation Warfarin - chronic Superwarfarin - 1 dose Dx: MBBT
Ethylene glycol (anti freeze) 1 Tbsp severe acidosis + renal failure
FOOD
Chocolate
-Theobromide
-T: Warm milk
Alcohol (ethanol)
- Hypothermia, glycaemia, volemia
- Respiratory collapse
Grapes + raisins
-Acute kidney failure
Garlic + onions
-haemolysis
Tea + coffee
caffeine in hepatotoxic
Chewing gum
-Xylitol –> hypoglycaemic crisis due to insulin spikes with no glucose administration
DRUGS
ACE inhibitors
-Hypovolemic shock
-T: Cola
Anti-depressants
- Hyperthermia + tachycardia
- Neurological issues
Weed (THC)
-Inhibits neurotransmitters
Paracetamol
-Cats + G.Pigs –> liver failure
PLANTS Tulips Lily's Rhododendrons Foxglove Daffodil Azalea Iris
MO’s + Mycotoxins
- Botulism
- Aflatoxin
- Ergot
- Tricenethens
- ochratoxin
- zearalenone
T:
Neutralise - lemon juice (if alkalic), soda (if acidic)
Remove
- Inhibit absorption (charcoal)
- emetics (apomorphine/xylazine)
- Lavage, Oil
- Laxative, enema
Increase excretion
-Diuretics
Supportive
- fluids (10ml/kg/hr)
- Benzo’s (seizures)
- liver protectants
- Acidosis (bicarbonate)
ABC
- Airways (clear/tracheostomy)
- Breathing (CPR)
- Circulation (Prevent shock)
Principles of detoxification
General
Contact - wash with soda (acidic), lemon juice (alkaline)
Occular - eye flush 20-30 mins
Ingestions
-Empty stomach (<2 hr ingestion) –> gastric lavage + emetics
-reduce absorption (charcoal, oil, laxatives, milk)
Supportive Seizures - benzos acidosis - bicarb volemia - fluids cardia - adrenaline or K
ABC therapy
Airways - open mouth, extend neck, pull tongue forward
Breathing
- No breath? –> cpr (12-24 BPM)
- Check for air/fluid –> thoracentesis
Circulation - HR, MM, CRT, Pulse intensity
- chest beneath elbow (80-120bpm)
- Resp rate: 15-25/min
Signs of shock
Tachycardia
Pale
Low BP –> weak pulses
EMERGENCY DRUGS
Adrenaline - 0.01mg/kg initial then 0.1mg/kg after 5 mins
-Myocardial contraction
-Vasoconstriction
Atropine (0.05mg/kg)
-Parasympatholytic effect –> increases HR
Fluids
- For correction of hypovolemia
- crystaloids/colloids
Sodium bicarbonate
-Correction of acidosis
