Internal medicine of small animals Flashcards

1
Q

Skin diseases - Pyoderma, pyotraumatic dermatitis, pododermatitis

A

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

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2
Q

SKin disease - folliculitis + furunculosis

A

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?
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3
Q

Skin diseases - Alopecia

A

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
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4
Q

Pruritic skin diseases

A

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 –>
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5
Q

Milliary dermatitis + eosinophilic complexes

A

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

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6
Q

Atopy, FAD, food sensitivity

A

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

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7
Q

Ear diseases (otitis ext, med, int) + skin adnexa

A

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)

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8
Q

Tumours of skin and subcutis

A

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

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9
Q

Immune-mediated diseases (pemphigus, lupus, AIHA)

A

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)

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10
Q

Hypothyroid, hyperthyroid, hyperparathyroidism

A

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

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11
Q

Diabete mellitus, acromegaly, insulinoma

A

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
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12
Q

Polyuria/Polydipsia DDx

A

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
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13
Q

Hyperadrenocorticism (Cushing’s) Hypoadrenocorticism (Addison’s), Diabetes inspididus

A

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)

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14
Q

Upper respiratory tract disease

A

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
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15
Q

Brachycephalic syndrome

A

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

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16
Q

LRT - Bronchi and lungs

A

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

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17
Q

Diseases of Pleura + Mediastinum

A
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

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18
Q

LRT - chronic bronchitis + feline asthma

A

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

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19
Q

Congenital heart diseases

A

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
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20
Q

Diseases of myocardium (cardiomyopathy)

A

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)

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21
Q

Diseases of the valves and pericardium

A

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)

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22
Q

Heart failure and compensatory mechanisms

A

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

23
Q

Arrhythmias - causes, Dx, Therapy

A

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)

24
Q

Regenerative anaemia

A

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)

25
Q

Non-regenerative anaemia

A

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

26
Q

Coagulopathies

A

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)

27
Q

Lymphoproliferative diseases

A

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
28
Q

Lymphadenopathies + splenomegaly

A

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

29
Q

Diseases of upper GIT

A
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
30
Q

Diseases of the oesophagus

A

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

31
Q

Diseases of stomach + DDx of V+

A
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
32
Q

Diseases of Small Intestine

A

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

33
Q

Diseases of the colon, rectum + perianal region

A

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
34
Q

Malabsorption and maldigestion

A

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)

35
Q

Diseases of the pancreas

A

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
36
Q

Acute hepatopathy

A

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
37
Q

chronic hepatic disease

A

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

38
Q

Diseases of the gall bladder and bile ducts

A

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

39
Q

Icterus - DDx and diagnostic approach

A

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

40
Q

Hepatencephalopathy and portosystemic shunts

A

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

41
Q

Acute renal failure

A

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

42
Q

Chronic kidney failure

A

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)

43
Q

Diseases of the urinary bladder and urethra

A

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

44
Q

Urolithiasis

A

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
45
Q

Disorders of urine elimination

A
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
46
Q

Epileptiform statuses

A

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

47
Q

Idiopathic epilepsy

A

> 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!

48
Q

Diseases of the brain - congenital & inflammatory

A

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

49
Q

Diseases of the brain - degenerative & neoplastic

A

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

50
Q

Neurological examination and other Dx procedures

A

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

51
Q

Vestibular disease & Horners syndrome

A

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)

52
Q

Muscular and neuromuscular diseases

A
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

53
Q

Common intoxifications

A
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)
54
Q

Principles of detoxification

A

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