1. Atopic dermatitis.

is a genetically predisposed inflammatory and pruritic allergic skin disease. Most allergic
dogs begin to show signs between 1 and 3 years of age. Golden Retrievers, Labrador
Retrievers, terriers.

Etiology and Pathogenesis involves: a genetic predisposition, impairment of the normal

skin barrier function, immunologic abnormalities.

Animals are genetically predisposed to become sensitized to allergens in the environment

including plant pollens, house dust mites, or mold spores. Allergens are proteins that evoke
allergen-specific IgE production. These allergen-specific IgE molecules affix themselves to
tissue mast cells or basophils. When these cells come in contact with the specific allergen
again, mast cell degranulation results in the release of proteolytic enzymes, histamine,
bradykinins, and other vasoactive amines, leading to inflammation (erythema, edema, and
pruritus).

Clinical Findings Pruritus (feet, face, ears, flexural surfaces of the front legs, axillae, and
abdomen are most frequent). Primary lesions consist of erythematous macules and small
papules. Lesions that develop secondary to self-trauma include alopecia, erythema,
scaling, salivary staining, hemorrhagic crusts, excoriations, lichenification,
hyperpigmentation, superficial staphylococcal pyoderma, Malassezia and bacterial
overgrowth, and allergic otitis externa. In a small number of animals chronic or recurrent
otitis may the only complaint.

Diagnosis : history and clinical signs. Clinical features: onset of clinical signs before 3 yr of
age, dogs that live mostly indoors, glucocorticoid-responsive pruritus, pruritus without skin
lesions, affected front feet, affected ear pinnae, nonaffected ear margins, and nonaffected
dorsolumbosacral areas. Allergy testing (intradermal or serologic) is a diagnostic aid.
Animals with classic clinical signs but negative allergy tests are given the diagnosis of
ALD(Acral lick dermatitis).

Treatment : cannot be cured, requires lifelong management and regular checks.

Avoidance of allergens

Relief from pruritus: via antipruritic drugs alone or in combination with allergen-specific
immunotherapy (ASIT). Bathing. Recognition and control of flare factors: include fleas,
food and environmental allergens, secondary microbial overgrowth, and poor coat hygiene.
Antipruritic drugs for acute pruritic crisis (acute flares): topical triamcinolone or
hydrocortisone aceponate spray for local pruritus. Prednisone, prednisolone, or
methylprednisone at 0.5 mg/kg. Antipruritic drugs for chronic AD: omega-3 or omega-6
fatty acids. Cyclosporine (Atopica® ).

Immunotherapy: Immunotherapy or ASIT is the best treatment option for AD, because it is
the only therapy that potentially leads to remission of signs without addition of other
medications. ASIT attempts to increase an animal's tolerance to environmental allergens.

2PETS. Flea allergy dermatitis.

most common dermatologic disease of domestic dogs. Cats also develop FAD, which is
one of the major causes of feline miliary dermatitis. most prevalent in the summer.

Pathogenesis

When feeding, fleas inject saliva that contains a variety of histamine-like compounds,
enzymes, polypeptides, and amino acids that induce Type I, Type IV, and basophil
hypersensitivity. Dogs develop either immediate (15 min) or delayed (24–48 hr) reactions,
or both, and detectable levels of both circulating IgE and IgG antiflea antibodies. Dogs
exposed continuously to flea bites have low levels of these circulating antibodies and either
do not develop skin reactions or develop them later and to a considerably less extent.

Clinical signs

allergic animals will typically have a dermatitis characterized by pruritus. signs are
:papulocrustous lesions distributed on the lower back, tailhead, and posterior and inner
thighs. Affected dogs are restless, spending much time scratching, licking, rubbing and
chewing. Hair may be stained brown from the licking and is often broken off. In extremely
hypersensitive dogs, extensive areas of alopecia, erythema, and self-trauma. Traumatic
moist dermatitis (hot spots) can also occur. The rump and tailhead areas are typically the
first, most evident, areas affected. As FAD progresses and becomes chronic, the areas
become alopecic, lichenified, and hyperpigmented, and the dog develops secondary
bacterial and yeast infections.

In cats primary dermatitis is a papule, which often becomes crusted. This miliary dermatitis
is typically found on the back, neck, and face. The miliary lesions are not actual flea bites
but a manifestation of a systemic allergic reaction that leads to generalized pruritus and an
eczematous rash. alopecia, facial dermatitis, exfoliative dermatitis, and “racing stripe” or
dorsal dermatitis.

Diagnosis: History, clinical signs, presence of fleas or flea excrements. FAD does not
ordinarily occur before 1 year of age. diagnosis is made by visual observation of fleas on
the infested pet. Intradermal skin testing may be used.

Differential diagnoses: Include atopic dermatitis, food allergy dermatitis, sarcoptic or

demodectic mange, other ectoparasites, and bacterial folliculitis. In cats, other conditions
that can result in miliary dermatitis include external parasites (cheyletiellosis, trombiculosis,
notoedric mange, and pediculosis), dermatophytosis, drug hypersensitivity, food allergy,
atopic dermatitis, bacterial folliculitis, and idiopathic miliary dermatitis.

Treatment and Control

elimination of existing pet flea infestations: imidacloprid, indoxacarb, metaflumizone

eliminate the existing infestation in the pet's environment. This can be accomplished in
several ways: 1) topical application of residual insecticides that kill newly acquired fleas
(within 24 hr) before they can initiate reproduction, 2) administration of topical, injectable, or
oral IGRs(insect growth regulators) to stop flea reproduction, 3) repeated application of
insecticides and/or IGRs to the premises, or 4) combinations of the above.

Systemic glucocorticoids- prednisone or prednisolone 0.5–1 mg/kg/day

3. Canine and feline pyoderma

Pyoderma: triggered by an overgrowth of normal resident or transient flora. The primary

pathogen of dogs is Staphylococcus pseudintermedius, staphylococci, streptococci,
Micrococcus sp, and Acinetobacter. Normal resident bacteria in feline skin include
Acinetobacter sp, Micrococcus sp, coagulase-negative staphylococci, and α-hemolytic
streptococci.

Bacterial pyodermas are either simple or complex infections. Simple infections are those
occuring in young animals that are triggered by one-time or simple events, eg, flea
infestation. Complex infections are recurrent and are associated with underlying diseases,
such as allergies, internal diseases, seborrheic conditions, parasitic diseases, or anatomic
predispositions. Either simple or complex infections can be superficial or deep. Bacterial
pyodermas limited to the epidermis and hair follicles are referred to as superficial, whereas
those that involve the dermis, deep dermis, or cause furunculosis are referred to as deep.

A)SUPERFICIAL PYODERMA

1. Acute moist dermatitis (pyotraumatic dermatitis): characterized by localized, moist,

erythematous areas. Lesions appear to arise secondary to self-induced trauma. Distinguish
between pyotraumatic dermatitis and pyotraumatic folliculitis. In pyotraumatic dermatitis, the
role of bacteria is unclear and pyotraumatic folliculitis is caused initially by a bacterial skin
infection. Etiology Hot spots are self-induced. Anything that can initiate an itch-scratch
cycle may predispose a pet to this condition. Risk factors : Young dogs, Breed/genetics -
Longhaired and thick-coated breeds, summer and other medical disorders - allergies, atopic
dermatitis etc.

Clinical signs : The lesion is erythematous, swollen, alopecic, exudative, and plaque-like.
The area is often very painful. Pruritus is usually intense and the severe self-trauma can
cause large lesions (10 cm or more). Typical lesions are located on the lateral aspect of the
face below the ear. Ear examination often reveals otitis externa, which may be acute or
chronic. Diagnosis Hot spots are rarely confused with other disorders. Treatment: clipped
and cleansed with a mild antiseptic, such as chlorhexadine. Sedation or general
anesthesia. Astringent agents such as aluminium acatate or zinc oxide. Antipruritic sprays
containing 1% hydrocortisone, 1.5% lidocaine. Oral corticosteroids (prednisone 0.5 mg/kg) .
Elizabethan collars. In the case of pyotraumatic folliculitis Cephalexin (22 mg/kg). For
pyotraumatic dermatitis, use of topical antimicrobial agents (chlorhexidine)

2.Skin fold dermatitis (Intertriginous dermatitis; intertrigo)

In breeds with pronounced facial, tail, and vulvar folds. This condition occurs when skin
folds are deep, causing abnormal rubbing and retaining moisture in an area that’s both
warm and not well aerated. These conditions are ideal for the overgrowth of normal skin
inhabitants like yeast and bacteria. Skin characteristics that include wrinkles and deep skin
folds are more common in certain breeds (Pugs). Clinical signs: typically hairless
(alopecic), reddened, and malodorous areas of folded skin. In the case of deep facial folds
brown staining of facial fur. Tail fold dermatitis can lead to deep, severe infections. Urinary
tract infection can occur as a consequence of vulvar skin fold pyoderma. Diagnosis is
based on physical examination. DD: Atopic dermatitis, Demodicosis and Malassezia
pachydermatis infection. Treatment : cleaning of the affected areas and frequent use of
topical or systemic (oral or injectable) antimicrobial medications to manage the resulting
pyodermas. Surgical intervention.

3.Impetigo (Puppy pyoderma): Impetigo is a superficial bacterial infection of sparsely

haired areas in puppies, and of the dorsal head and neck in kittens. The lesions are
nonpainful, nonpruritic, small pustules that do not involve the hair follicles. Occurs in than 1
year of age. Predisposing causes include endoparasitism, ectoparasitism, poor nutrition,
viral infections, trauma, and dirty environments. Topical therapies: Astringents: 2-5%
aluminum acetate Antimicrobial agents: mupirocin ointment, medicated shampoo.

4.Folliculitis Follicullitis or osteofolliculitis: Involve the superficial portion of the hair

follicules. Common lesions of folliculitis are erythematous papules and pustules, typically
associated with hair follicles. Crusts of variable thickness are common lesions but are
sometimes absent. Variable alopecia, erythema and hypo- or hyperpigmentation are often
present

B.DEEP PYODERMA

1)Acne vulgaris: areas of blackheads, whiteheads, pimples, greasey skin and possibly
scarring. The affectted structures of the skin include the hair follicule and the adjacent
sebaceous gland. Canine acne is a benign self-limiting disease of the chin and lips of young
dogs. The condition starts at puberty and typically resolves after one year of age. Feline
acne characterized by comedone formation and secondary bacterial inflammation of the
chin and skin adjacent to the lips. Feline acne is not associated with young age. Poor
grooming habits and defect of keratinization have been suggested as causes. Swelling of
the chin. Individual lesions may fistulate, leading to abscessation and scarring. Feline acne
is usually asymptomatic.

2)Furunculosis Furunculosis occurs when rupture of deeply infected follicules occurs

within the dermis and infection spreads to involve deep stuctures of the dermis. is rarely
seen in cats. The disease manifests as focal, multifocal, or generalized skin lesions
characterized by papules, pustules, tissue discoloration, alopecia, hemorrhagic bullae, as
well as serosanguineous to purulent draining fistulous tracts. Lesions are often pruritic or
painful. They most often involve the trunk, pressure points, interdigital and perianal area but
can appear anywhere on the body. Lymphadenomegaly .

DIAGNOSIS OF PYODERMA: a)Cytology. In skin fold pyoderma, images of « bacterial

colonization » are essentially observed, i.e. healthy neutrophils, Cocci and Bacilli in an
extracellular position and degenerated neutrophils in a state of phagocytosis.
b)Histopathology, c)Bacteriology:

ANTIBACTERIAL TREATMENT FOR PYODERMA

combining systemic and topical antibacterial treatment. Cephalosporins are the first choice
for staphylococcal pyoderma (except for cases of MRSP). Fluoroquinolones should be
reserved for gram-negative pathogens or rare cases where they exceed beta-lactams in
efficacy. Poor choices include penicillin, ampicillin, amoxicillin they are sensitive to
penicillinases.Topical therapy- antibacterial shampoos include benzoyl peroxide,
chlorhexidine, chlorhexidine-ketoconazole, and acids: glycolic, lactic acids. Dogs with
superficial pyoderma 2–3 times/wk during the first 2 wk of therapy and then 1–2 times until
the infection has resolved. Dogs with deep pyoderma daily hydrotherapy. Medicated
shampoos should be prediluted 1:2 to 1:4 before application to facilitate lathering, dispersal,
and rinsing.. Clinical improvement in superficial pyodermas may not be evident for at least
14–21 days.Other Topical Therapies for specific situations: Antiseptic sprays, lotions.
Antiseptic wipes/pads/ointment/gel for skin fold pyoderma or localized dermatitis. Mupirocin
ointment for staphylococcal lip fold pyoderma or focal deep pyoderma. Chlorhexidine with
tris-EDTA or silver sulfadiazine for Pseudomonas.

P4. Otitis Externa

Otitis externa is inflammation of the external ear canal distal to the tympanic membrane; the
ear pinna may or may not be involved. It may be acute or chronic and unilateral or bilateral.

Etiology and Classification System

Causes of otitis externa are defined as primary or secondary, with factors that contribute to
or promote disease. It is also standard of care to determine whether the cause is curable or
lifelong management is required.

Primary causes of otitis externa are those that create disease in a normal ear. They can
cause otitis without any other cause or factor and can be subtle; they often go unrecognized
by owners and veterinarians until secondary causes develop. Primary factors alter the ear
environment, which allows secondary infections to develop.

The major primary causes of otitis externa are allergy, autoimmune (eg, pemphigus),
endocrine, epithelialization disorders, foreign bodies, glandular disorders, immune-
mediated (eg, drug reactions), fungal (eg, aspergillosis), parasites, viral (eg, canine
distemper), and miscellaneous (auricular chondritis, eosinophilic diseases, juvenile cellulitis,
proliferating necrotitizing otitis of cats).

Secondary causes are those that cause disease in an abnormal ear. These causes are
relatively easy to eliminate and include bacteria, fungi, medication reactions, overcleaning,
and yeast overgrowth.

Factors are elements related to the disease or pet that contribute to or promote the otitis
externa by altering the structure, function, or physiology of the ear canal. Factors are
subdivided into predisposing factors, which are present before the development of the ear
disease, and perpetuating factors, which occur as a result of the inflammation.

Predisposing factors include conformation of the ear, excessive moisture, obstruction of

the ear canal (eg, polyp, feline apocrine cystadenomatosis), primary otitis media, systemic
diseases (eg, catabolic states), and treatment effects (eg, alterations of normal microflora,
trauma from cleaning).

Perpetuating factors include changes in the ear epithelium, ear canal (eg, edema,
stenosis, proliferation), tympanic membrane, glandular, pericartilaginous fibrosis and middle
ear (eg, filled with debris, otitis media). This system is currently referred to as the PSPP
classification system.
Curable otitis means that the component of the problem is readily resolved with treatment
(for weeks) or via surgery. Longterm management indicates that the component of the ear
problem may be resolvable, but it can take months of treatment. Lifelong treatment
indicates that the owner will need to play an active role in management for the life of the
pet.

Clinical Findings and Diagnosis

There is no recognized sex distribution for otitis externa. Young animals may be more
commonly affected. There are clear breed predispositions for otitis, which directly reflect the
breed predispositions for skin disease (eg, allergies in retrievers and terriers). The most
common historical findings are headshaking and aural pruritus.

The first step in physical examination is determination of the severity of pain. If the ear is
painful or the degree of discomfort is high, the animal should be sedated before performing
any further diagnostic testing. The second step is gentle palpation and manipulation of the
ear canal and pinna to determine the presence of swelling, pruritus, fibrosis, or calcification.
The presence or absence of these findings will help determine whether advanced
diagnostics are needed, specifically imaging of the ear canal. Next, the outside of the ear
should be examined, noting erythema, edema, crusts, scale, ulcers, lichenification,
hyperpigmentation, or exudate. The pinnae and periauricular regions should be examined
for evidence of self-trauma, erythema, and primary and secondary skin lesions. Pinnal
deformities, hyperplastic tissue in the canal, and headshaking suggest chronic otic
discomfort.

If the otitis is unilateral, the unaffected ear should be examined first to prevent iatrogenic
contamination of the unaffected ear with organisms (eg, Pseudomonas aeruginosa or
Proteus mirabilis) that may be present in the diseased ear.

Otoscopic examination is often not possible because the ear is painful, swollen, or filled
with exudate; sedation is usually required. Swelling of the ear canal often makes it
impossible to see the tympanic membrane. A handheld otoscope must have enough light
and magnification to clearly visualize the external canal to the level of the tympanic
membrane. A video otoscope provides magnifcation of the ear canal and tympanic
membrane.

During an otoscopic examination, the ear canal should be inspected for changes in
diameter, pathologic changes in the skin, quantity and type of exudate, parasites, foreign
bodies, neoplasms, and changes in the tympanic membrane. The tympanic membrane
should be examined for evidence of disease or rupture. However, in many cases of otitis,
the character of the ear canal and tympanic membrane cannot be visualized at all until the
exudate is gently flushed from the canal. Samples for cytologic evaluation and culture
should be obtained before the ear is flushed. Examination is attempted again after the ear
is dried. In chronic cases, the canal may be too stenotic, either from hyperplasia or edema,
to be examined. Systemic glucocorticoids given daily for 1 wk may reduce swelling enough
to allow examination.

If sedation is not needed, samples for ear diagnostic tests should be collected: skin
cytology from the external and inner pinnae, cytology of any exudates present, hair
trichograms and skin scrapings for Demodex, and ear swab cytology with mineral oil in
young and adult animals (especially cats, because feline demodicosis can present as
pruritic otitis). Dermatophytosis affects the hair of the pinnae and hairs in the concave
surface of the ear canal.

Cytologic evaluation of exudate or cerumen taken from the horizontal ear canal may
provide immediate diagnostic information. The external ear canals of most dogs and cats
harbor small numbers of commensal gram-positive cocci. These organisms may become
pathogenic if the microenvironment is changed and encourages their overgrowth.

Coccal organisms are usually staphylococci or streptococci. Rod-shaped organisms are

usually Pseudomonas aeruginosa, Escherichia coli, or Proteus mirabilis. The yeast
Malassezia pachydermatis is found in low numbers in the ear canals of many healthy dogs
and cats. A dark exudate in the canal usually signals the presence of either Malassezia spp
or a parasite but may also be seen with a bacterial or mixed infection.

Microbial cultures are taken before otoscopy is completed and before any cleaning is done.
Samples for culture should be taken with a sterile culturette from the horizontal canal (the
region where most infections arise) or from the middle ear in cases of tympanic rupture.
Treatment

All primary and secondary causes and predisposing factors need to be identified, managed,
and treated. Management of pain or pruritus must be included in the initial treatment
protocol. Tramadol for the first 5–7 days at 5 mg/kg, PO, may be beneficial. In addition,
otitis externa is one of the few dermatologic conditions in which glucocorticoids are
beneficial in the face of concurrent antimicrobial use or sepsis. Glucocorticoids decrease
swelling of the ear canal and may be key to successful treatment. Duration depends on the
severity. Ear hygiene is important; in particular, the hair from the pre- and periauricular area
should be clipped, as well as hair from the surface of the inner pinnae and ends of the ears.
This facilitates cleaning and treatment of the ears.

The first ear cleaning should be done in the veterinary clinic, and owners should be
instructed not to clean the ears until recheck in 5–7 days. Owners are often unable to clean
the ears and/or are too aggressive, causing further damage. It is important to remember
that topical medications are inactivated by exudates, and excessive cerumen may prevent
medications from reaching the epithelium. The ears should be gently cleaned with an ear
cleaner that will remove the debris in the canal. Thick, dry, or waxy material requires a
ceruminolytic solution such as carbamide peroxide or dioctyl sodium sulfosuccinate (DSS).
The ears should be thoroughly rinsed with warm water to remove residual ear cleaner. If the
tympanic membrane is ruptured, detergents and DSS are contraindicated; milder cleansers
(eg, saline, saline plus povidone iodine, Tris EDTA) should be used to flush the ear.

Effective treatment may require both topical and systemic antimicrobial therapy, along with
pain medications and glucocorticoids.The duration of treatment may vary from 7–10 days to
>30 days, depending on the diagnosis. In treatment of acute bacterial otitis externa,
antibacterial agents in combination with corticosteroids reduce exudation, pain, swelling,
and glandular secretions.

Most commercial topical products contain a combination of antibiotic/antifungal and

glucocorticoids. The volume of the ear canal in most dogs is 1 mL, and adequate treatment
requires instillation of at least this volume twice daily. Irritating medications (eg, home
remedies and vinegar dilutions) should be avoided.

Systemic therapy should be incorporated into the treatment regimen in most cases of
chronic otitis and in any case in which otitis media is suspected. The most common cause
of recurrent otitis externa is undiagnosed oititis media. Failure to use systemic antimicrobial
therapy is an important cause of chronic ear disease in dogs. Systemic antibiotics should
be used when neutrophils or rod-type bacteria are found on cytology, in cases of
therapeutic failure with topical antimicrobial agents, in chronic recurring ear infections, and
in all cases of otitis media. Yeast infections in dogs can be treated with oral ketoconazole 5
mg/kg/day, PO, for 15–30 days. Ketoconazole should not be used in cats.

Duration of treatment will vary depending on the individual case but should continue until
the infection is resolved based on reexamination and repeat cytology and culture. Chronic
cases may take months to resolve, and in some instances, a therapeutic regimen must be
continued indefinitely.

The best treatment of chronic otitis is prevention. In addition to identifying the cause of
acute otitis, topical and/or systemic medications should be chosen based on cytology or
culture; they should have a narrow spectrum and be specific for the current condition.
Polymyxin B and fluoroquinolone antibiotics have shown the best success in controlling
Pseudomonas infections in cases in which resistance has been identified through culture.

Maintenance Care

Owners should be shown how to properly clean the ears. The frequency of cleaning usually
decreases over time from daily to once or twice weekly as a preventive maintenance
procedure. The ear canals should be kept dry and well ventilated. Using topical astringents
in dogs that swim frequently and preventing water from entering the ear canals during
bathing should minimize maceration of the ear canal. Preventive otic astringents may
decrease the frequency of bacterial or fungal infections in moist ear canals. Clipping hair
from the inside of the pinna and around the external auditory meatus, and plucking it from
hirsute ear canals, improves ventilation and decreases humidity in the ears. However, hair
should not routinely be removed from the ear canal if it is not causing a problem, because
doing so can induce an acute inflammatory reaction.

5. Epilepsy

Recurrent seizures from an unknown cause are considered epilepsy. Primary epilepsy
(also known as congenital epilepsy or functional epilepsy) results in an abnormally lowered
seizure threshold. The exact cause of the condition in dogs is not known. Characteristics of
seizures: the first seizure generally occurs between 6 months and 5 years of age, seizures
are generally isolated at first, but become more frequent and longer in duration over time
and the seizures are generalized from the onset. Secondary epilepsy (acquired or
structural epilepsy) results from an acquired lesion in the brain. This lesion may be from
previous trauma or infection that has resolved, but left a glial scar that develops an
abnormal electrical generator. Because these are acquired, they can begin at any age and
may appear focal in onset. They often become more frequent and more intense over time.

Clinical signs

Clinical manifestation of epilepsy is characterized with recurrent seizures. The type of

seizure depends on the type and localization of the disease process in the brain. Types:

1. Generalized
a. major motor seizures (grand mal) also called classic/ tonic clonic. Has 3 phases:
the aura or prodrome, the seizure itself (aka ictus), and post-ictal (post-seizure)
behavior.
b. absence seizures (petit mal).
2. Focal (partial) sezures

The most common time for a dog to have a seizure is when they are relaxed and quiet. The
pet that has a prodrome will act upset and anxious. It may represent a focal beginning of
the seizure and thus indicate a focal seizure, but its common in generalized seizures too.

The classic seizure itself is called a tonic-clonic seizure. It begins with a stiffening of the
muscles (the tonic part). Usually the pet will fall to their side with the legs stretched out and
the head back. Once the seizure has begun, the pet is no longer conscious even though his
eyes may remain open. Sometimes they will vocalize or the face may twitch. The
vocalizations are involuntary and do not indicate pain. Often he will drool excessively or
may urinate, defecate, or empty his anal glands causing a foul smell. This tonic phase is
usually very brief (less than 30 seconds) and gives way to rhythmic movements (the clonic
part). Typically this consists of chomping of the jaws and jerking or running movements of
the limbs. Often he will not breathe well during the seizure and the tongue may turn blue.
The average seizure lasts less than 2 minutes. If the seizure goes on much longer the pet
may go into a continuous seizure. Post-ictus: Following the seizure, the pet may lay
motionless for a period of time. Often the pet appears blind and disoriented and may pace
or run about the house, bumping into objects. Sometimes they are excessively hungry.

Absence (petit mal) seizures: The other type of generalized seizures is the absence or
petit mal seizure. Petit mal seizures differ from other seizures as there is little movement
during a petit mal seizure; the person simply loses contact with the world during the seizure.
They stare blankly and may blink but do little else. They represent a storm of inhibition
rather than a storm of excitation within the brain.

In focal or partial seizures, the electrical storm begins in an isolated area of the brain. The
fact that the seizure starts in a local area suggests that localized damage has occurred
which means diseases which will cause local damage, such as a brain tumor or infection
should be considered. Simple focal seizures (also sometimes called minor motor or focal
motor seizures) originate in the area of the brain that controls movement. There is
movement of the area of the body controlled by that part of the brain. Most commonly, the
face is affected resulting in twitching or blinking. The pet is usually alert and aware. The
seizure may stop there or it may generalize. If it generalizes, the pet loses consciousness
and has a classic grand-mal seizure. Complex focal seizures originate in the areas of the
brain that control emotions and behavior (the temporal lobes) and are sometimes called
psychomotor seizures. They behave bizarrely.

Cluster seizures and status epilepticus: Most seizures are brief and isolated, but
sometimes they can be more serious. The large-breed dogs tend to have clusters of
seizures. In these cases, the dog will have one seizure and recover from it. Then a few
hours later, they have another. They never completely recover before another seizure
strikes. Sometimes this culminates in a continuous seizure that doesn't stop, a condition
called status epilepticus.
Diagnosis: is made by exclusion. Diagnostics are performed in a specific order to first rule
out reactive seizures (extracranial causes such as hypoglycaemia, hypocalcemia,
hypomagnesaemia, hepatic encephalopathy, portosystemic shunts, toxins etc.) followed by
procedures to rule out symptomatic epilepsy (intracranial causes such as neoplasia).

Treament: ideal treatment strategy is to remove the cause of the epilepsy so that the
animal will never seizure again. Antiepileptic drugs do not cure epilepsy; they simply control
the seizures. The goal of therapy is to decrease the number and severity of the seizures
(eliminate the clusters of seizures which can create life-threatening situations).

Maintenance therapy

Most of the commonly used anticonvulsant drugs (phenobarbital, potassium bromide, and
diazepam) increase GABA-activated chloride channels, act to modulate sodium or calcium
channels, or reduce glutamate-mediated excitation. Phenobarbital (PB) is the initial drug of
choice for treating seizures in dogs and cats(2.5 mg/kg). A lower dosage may be used if
seizures are infrequent and occur as single episodes. Higher dosages are recommended if
seizures are frequent or tend to occur in clusters or SE. Potassium bromide (KBr) can be
used alone or in conjunction with PB. Can be used in dogs experiencing hepatotoxicity
related to PB. Dose is 22 to 40 mg/kg. Clonazepam is effective for short-term control of
refractory seizures.

Status epilepticus therapy: If the animal presents in status epilepticus without a previous
history of seizures, then metabolic conditions such as hypoglycemia or hypocalcemia
should be considered. Hypoglycemia with 50% glucose 2 mg/kg. hypocalcemia with 10%
calcium gluconate at a dose of 4 mg/kg. Diazepam has excellent anticonvulsant properties,
rapidly crosses the blood-brain barrier and exerts its effect, and has minimal cardiovascular
or respiratory depressant effects; dose 0.5 mg/kg should be administered intravenously. If
seizures continue Pentobarbital should be administered at a dose of 3 to 15 mg/kg
intravenously slowly to effect.

6. Feline asthma

Affects the lower respiratory tract and is characterized by bronchial hyper-reaction to

different stimuli. The reduction in air flow is typically the result of a combination of
inflammation, excessive mucous accumulation, and the contraction of airway smooth
muscle which results in coughing, wheezing and respiratory distress. Is caused by an
exaggerated immune reaction towards an inhaled allergen such as smoke, dust and dust
mites, molds, polens etc.

Pathogenesis: is a predisposition to chronic airway inflammation with reversible

bronchoconstriction episodes. Pathogenic events associated with feline asthma: immune
response alteration, adrenergic-cholinergic system imbalance, and increased mucous
production. In allergic Type I hypersensitivity reaction exposure to airborne allergens
stimulates the production of IgE. If re-exposure to the allergen occurs, the IgE triggers a
reaction that acutely releases preformed mediators, mainly histamine and serotonin.
Histamine contribute to mucous secretion, increase capillary permeability and promote
granulocyte chemotaxis. Serotonin provokes a sudden contraction of smooth muscles in the
bronchi. The adrenergic system acts on the airways via β-adrenergic receptors whose
stimulation increases the production of cAMP causing bronchodilation and a reduction in
mucous production. Cholinergic stimulation is opposed to β-adrenergic action causing
respiratory smooth muscle to contract (bronchoconstriction), increasing mucous production
and provoking vasodilation. Imbalance of adrenergic-cholinergic systems of the respiratory
tract is responsible for the typical severe hyper-reaction in feline asthma. Goblet cells and
submucosal gland cells are responsible for producing mucin (main ingredient of mucous) in
the airways.

Clinical signs: different according to the degree of affliction. The most frequent signs are
coughing, wheezing, and respiratory harshness. In mild cases, short and occasional
coughing bouts. These signs tend to be chronic or to progress slowly. In severe cases daily
persistent cough with frequent acute dyspneic crises. During the dyspneic crises, cats are
lying on the floor in sternal recumbence, their head and neck extended, the mouth opened
and with wheezing respiration. If bronchoconstriction lasts long enough, the cat can
become cyanotic and the thorax can adopt a barrel shape due to air trapped inside.

Diagnosis: Wheezing can be detected when the disease is advanced or during acute
aggravation episodes. Blocked airways may have air trapped distally which reduces
thoracic compressibility. Blood tests: serum test for Toxoplasma gondii. Thoracic X-Ray:
swelling of the bronchial walls, described as “donuts” and “railway lines”, increased
radiolucency of the lungs and flattening and caudal displacement of the diaphragm.
Therapeutic trial may be used by the administration of bronchodilators. Most asthmatic cats
respond to treatment in 5-7 days with a high-dose corticosteroid therapy. Bronchoscopy.

Treatment: use of a corticosteroid drug to reduce bronchial inflammation in combination

with bronchodilator to open up the airways. they are effective both therapeutically and
preventively. Ideally an inhaler is used (Aerocat®). In mild cases corticosteroid drugs such
as fluticasone proprionate (Flovent©) and bronchodilators such as albuterol (Ventolin©). In
acute crisis administer oxygen and use as bronchodilators β-adrenergic antagonists
(terbutaline and albuterol).

7. Tracheal collapse

is progressive, dorsoventral flattening of the tracheal lumen. It is most common in middle-

aged, small-breed dogs. Initially, laxity of the trachealis muscle results in coughing and
noisy breathing as the dorsal tracheal membrane billows in and out of the tracheal lumen
with each breath. As the condition progresses, the cartilaginous rings become more ovoid
resulting in dorsoventral flattening of the trachea and increasingly severe episodes of
coughing and exercise intolerance. The tracheal lumen diameter may become so narrow
that the lumen is nearly obliterated, leading to respiratory distress and collapse.

Etiology: a combination of environmental and genetic factors. Cartilaginous rings from

affected dogs are hypocellular with decreased glycoprotein and glycosaminoglycan and
subsequent reduced water retention. Obesity, pollutants, environmental allergens, and
kennel cough may be associated with disease progression.

Clinical signs: Signs of tracheal collapse include a dry cough similar to a goose honk;
noisy breathing; and, in severe cases, dyspnea, cyanosis, and hyperthermia. Coughing
episodes may increase with excitement, tracheal pressure (eg, from a leash or collar),
exercise, eating, or drinking. A cough may be elicited by palpating the trachea at the
thoracic inlet.

Diagnosis : is based on imaging. Collapse of the trachea is best viewed in the cervical
region during inspiration and in the intrathoracic region during exhalation. Fluoroscopy
allows direct viewing of tracheal motion during all phases of respiration, is noninvasive, and
is very sensitive. Tracheoscopy enables direct viewing of the trachea and mainstem
bronchi, quantification of severity and extent of collapse, identification of concurrent
inflammation, and collection of tracheal or bronchial samples for culture and cytology.
Classification of collapsing trachea:

Grade I – tracheal membrane is slightly pendulous, cartilage maintains normal shape,

lumen reduced approximately 25%; Grade II – tracheal membrane widened and pendulous,
cartilage is partially flattened, lumen reduced approximately 50%; Grade III – tracheal
membrane is almost in contact with dorsal trachea, cartilage is nearly flat, lumen is reduced
approximately 75%; Grade IV – tracheal membrane is lying on dorsal cartilage, cartilage is
flattened and may invert, lumen is essentially obliterated.

Treatment: Dogs presenting with acute respiratory distress are administered flow-by
oxygen and mild sedation (butorphanol/acepromazine). Long-term treatment for mildly to
moderately affected dogs includes oral antitussives and tapering doses of corticosteroids.
Concurrent respiratory infections are treated with antibiotics (more commonly
Pseudomonas and Enterobacter spp). If antibiotics are chosen doxycycline, cephalexin, or
amoxicillin–clavulanate are generally effective. In more severe cases surgery is
recommended. If the collapse is in the cervical region or the thoracic inlet, plastic rings are
placed surgically around the inside of the trachea. If the collapse is deeper in the chest,
often a stent is placed in the trachea.

8. Laryngeal paralysis

Laryngeal paralysis refers to a failure of the arytenoid cartilages to abduct during

inspiration, creating an upper airway obstruction. The abductor muscles are innervated by
the left and right recurrent laryngeal nerves. If clinical signs develop, both arytenoid
cartilages are usually affected.

Etiology: most often idiopathic. Trauma or neoplasia involving the ventral neck can
damage the recurrent laryngeal nerves directly or through inflammation and scarring.
Masses or trauma involving the anterior thoracic cavity can also cause damage to the
recurrent laryngeal nerves. Dogs with polyneuropathy-polymyopathy can be presented with
laryngeal paralysis as the predominant clinical sign. Congenital laryngeal paralysis Siberian
Huskies and Bull Terriers. A laryngeal paralysis polyneuropathy complex young
Dalmatians, Rottweilers, and Great Pyrenees.

Clinical Features

Laryngeal paralysis can occur at any age and in any breed, although the idiopathic form is
most commonly seen in older large-breed dogs. Clinical signs of respiratory distress and
stridor are a direct result of narrowing of the airway at the arytenoid cartilages and vocal
folds. TMost patients are presented for acute respiratory distress. Decompensation is
frequently a result of exercise, excitement, or high environmental temperatures, resulting in
a cycle of increased respiratory efforts, increased negative airway pressures, pharyngeal
edema and inflammation, which lead to further increased respiratory efforts. Cyanosis,
syncope, and death can occur. Some dogs exhibit gagging or coughing with eating or have
overt aspiration pneumonia.

Diagnosis: definitive diagnosis made only through laryngoscopy. In laryngeal paralysis the
arytenoid cartilages and vocal folds remain closed during inspiration and open slightly
during expiration. The larynx does not exhibit the normal coordinated movement: opening
on inspiration and closing on expiration. Additional laryngoscopic findings may include
pharyngeal edema and inflammation. The larynx and pharynx are also examined for
neoplasia, foreign bodies, or other diseases that might interfere with normal laryngeal
function.

Treatment: Following stabilization surgery is usually the treatment of choice. Most cases
are idiopathic, and signs are generally progressive. Arytenoid lateralization (tieback)
procedures, partial laryngectomy, and castellated laryngoplasty. The goal of surgery is to
provide an adequate opening for the flow of air but not one so large that the animal is
predisposed to aspiration and the development of pneumonia. Several operations to
gradually enlarge the glottis may be necessary to minimize the chance of subsequent
aspiration. The recommended initial procedure for most dogs and cats is unilateral
arytenoid lateralization. If surgery is not an option, medical management consisting of
antiinflammatory doses of shortacting glucocorticoids (e.g., prednisone, 0.5 mg/kg given
orally q l2 h initially) and cage rest may reduce secondary inflammation and edema of the
pharynx and larynx and enhance airflow. Prognosis for surgically treated is good.
 9. Dilated cardiomyopathy

Cardiomyopathies diseases of the myocardium associated with cardiac dysfunction. Dilated

cardiomyopathy (DCM) is a syndrome characterized by impaired myocardial function, left
(or both) ventricular dilation and frequently, tachyarrhythmias.

Etiology: Nutritinal factors, myocardial Lcarnitine deficiency –Boxers, low taurine levels -
American Cocker Spaniels. Familial factors - Doberman pinscher, Great Dane and Boxer.
Clinical signs
The two phases
 Pre-clinical DCM - “occult”. This is the long asymptomatic phase prior to
development of clinical signs.
 Overt DCM - Clinical signs.
With overt DCM and congestive heart failure (CHF) include breathlessness or dyspnoea,
cough, depression, exercise intolerance, inappetence, syncope, weight loss, abdominal
distention, and polydipsia. Clinical examination commonly reveals dyspnoea, tachypnoea,
rales, crackles and increased breath sounds, tachycardia, arrhythymia, systolic murmur,
diastolic gallops or an audible third heart sound (S3), weak femoral arterial pulses, pulse
deficit, ascites and distension of the jugular veins, pale mucous membranes, weight loss
and muscle wasting and, sometimes, elevation of the body temperature.

Diagnosis: Increases in blood urea (azotaemia due to low cardiac output). Serum
concentrations of biochemical markers of myocardial damage, such as Troponin I, may be
slightly increased.
Arrhythmias (Atrial fibrillation), abnormal amplitude or duration of P wave or the QRS
complex indicating chamber enlargement or conduction abnormalities.
Radiographic findings in dogs with DCM: cardiomegaly, venous congestion, various
degrees of interstitial or alveolar pulmonary oedema, and sometimes pleural effusion and
ascites.
Echocardiographic diagnosis- identification of myocardial systolic
dysfunction.
Treatment
 Asymptomatic Dogs with Ventricular Dilation / Dysfunction (Occult);

Two types of therapy

1) Administration of ACE inhibitors (enalapril, 0.25-0.5
mg/kg q12hr) has been shown to slow the progression to heart failure
2) Administration of beta-blockers - still being evaluated. Carvedilol

 Dogs with heart failure:

Furosemide (1-3 mg/kg) and ACE inhibitors (enalapril, 0.25-0.5 mg/kg). Spironolactone (1-2
mg/kg) should be considered for aldosterone blocking affects. Digoxin may be added when
the heart failure becomes refractory or atrial fibrillation is observed. Pimobenden can also
be added on a case by case basis at a dose of 0.3 mg/kg.
Prognosis:
Once clinical signs have developed, death usually occurs due to heart failure or sudden
death within 6 months However, many dogs may live for years on antiarrhythmics.

10. Hypertrophic cardiomyopathy

FELINE HYPETROPHIC CARDIOMYOPATY Most common heart disease in cats and is

characterized by an abnormal thickening (hypertrophy) of one or several areas of the
ventricular walls, usually of the left ventricle. Is usually diagnosed in middle-aged cats, but
may occur in juvenile also. If the hypertrophy is mild and focal, the cat may remain
asymptomtic for all his life. However, if the hypertrophy is severe, the ventricle will have a
hard time distending, which leads to increased intra-cardiac pressure and congestive heart
failure (CHF) with fluid accumulation in or around the lungs.

Complications:
Cardiac arrhythmias- sudden death
Clot formation in the left atrium. May travel in the aorta and obstruct a major artery - FATE
(Feline Arterial ThromboEmbolism).
Myocardial infarction may supervene, leading to destruction of areas of the cardiac muscle,
a situation called remodeling.
Clinical signs: Many cats with HCM are asymptomatic. Auscultation: heart murmur(s),
arrhythmias and/or extra heart sounds are heard. Fluid build-up in (pulmonary edema) or
around (pleural effusion) the lungs, increased breathing rate

Diagnosis: Cardiac ultrasound chest radiographs, electrocardiogram (ECG), blood

pressure measurement and blood tests. Screening

Treatment

Beta-adrenergic antagonists and calcium channel blockers (-Diltiazem1.75-2.5 mg/kg) can

be used to relieve myocardial ischemia and reduce systolic gradients. Diuretics are used to
relieve circulatory congestion in cats with pulmonary edema. Furosemide- Relief of
pulmonary edema.
Supplemental oxygen also should be administered.

Immediate thoracocentesis of acutely dyspneic cats should be done in addition to

administering furosemide, nitroglycerin ointment, and oxygen. Warfarin is an alternative to
aspirin. Anticoagulation, prevention of thromboembolic complications

Prognosis
Depends on the severity of the disease:
Cats with very stiff ventricles and profound disturbances of the blood circulation, very large
atria, arrhythmias (such as atrial fibrillation), and low blood pressure have a poor prognosis.

Rapidly progressive juvenile forms of HCM also carry a poor prognosis.

11. Mitral valve disease

Is the most common cause of heart failure in dogs. The disease is characterized with
progressive degeneration and valve thickening that starts at the valve edges and causes
valve insufficiency.

Etiology The cause of MVD is unknown. Is often observed in chondrodysplastic dog

breeds.

Pathology: In general MVD is characterized by nodular distortion of the valve leaflets as

well as by thickening and, sometimes, lengthening of the chordae tendineae. In severe
cases, the leaflets are contracted, and the free edge of the leaflet prolapses toward the
ventricular endocardium, resulting in mitral valve insufficiency.

Clinical signs: Systolic murmur that is usually heard best over the left cardiac apex. The
disease can have a long asymptomatic course. The symptoms usually begin with the
development of left heart failure. Tachypnea/dyspnea, cough or syncope. Pulmonary
edema or main stem bronchus compression due to enlarged left atrium. Right heart failure
in MVD is a sign of progressive mitral valve disease and pulmonary hypertension that can
be accompanied by tricuspid valve degeneration.

Diagnosis
Thoracic radiography enlargement of the cardiac silhouette with prominent left atrium. Left
atrial enlargement precedes the development of CHF. The pulmonary vein and
corresponding artery should be the same size. If the vein is wider than the artery, this
suggests pulmonary venous congestion, which is consistent with heart failure.

Pulmonary edema: abnormal lung patterns. Echocardiography : individual chamber

enlargement, the magnitude of regurgitant flow, the severity of mitral degeneration, valve
prolapse, chordal rupture and pulmonary hypertension. Cardiac biomarkers:N-terminal
fragment of the prohormo brain-type natriuretic peptide : secreted in the heart and released
into the circulation in response to left ventricular and left atrial wall stretch and has been
shown to help with the diagnosis of heart failure caused by mitral valve disease.
Therapy

Angiotensin converting enzyme inhibitors (ACE-I). Patients having an acute episode of

heart failure: furosemide 1–4 mg/kg IV, IM or SC as bolus.

Medical treatment for dogs that have clinical signs of CHF: furosemide (1–2 mg /kg), ACE-I
(dose depends of the drug used), pimobendan (0.25–0.3 mg/kg q12 h).

Diuretic: spironolactone, potassium-sparing, digoxin (0.22 mg/m²) for rate control. Beta
adrenergic blockers in cases of atrial fibrillation to control the ventricular rate, or ventricular
arrhythmias.

Instead of furosemide: amlodipine (up to 0.1 mg/kg), hydrochlorthiazide (2–4 mg/kg) and
torsemide (0.2mg/kg).

12. Diabetes mellitus

Diabetes mellitus (DM) is an endocrine disorder that occurs in both dogs and cats. It is
caused by the relative or absolute deficiency of the hormone insulin, which is produced by
the
beta cells of the pancreas. Insulin stimulates the transport of glucose and other nutrients
across
cell membranes for cellular use and is involved in a number of anabolic processes within
the
body. A lack of insulin activity leads to elevated blood glucose levels (hyperglycemia) and
an
inability of tissues to receive the glucose that they need (glucoprivation).

Classification:

Type I diabetes (insulin-dependent). Is identified by an absolute lack of endogenous

insulin and a resultant dependence upon exogenous insulin for survival. It is caused by the
immunemediated destruction of the pancreatic beta cells by T cells and antibodies. Type II
diabetes (previously referred to as non–insulin-dependent diabetes mellitus) is
characterized by impaired insulin secretion; insulin resistance; and the deposition of
amyloid in the islets of the pancreas. Do not usually require exogenous insulin therapy.
Glucose toxicity leads to impaired insulin secretion and to the destruction and loss of beta
cells.

Clinical signs: Polyuria, polydipsia and weight loss. Muscle wasting, reduced exercise
tolerance, hepatomegaly, cataracts (dogs), recurrent bacterial infections and smell of
ketones on breath. Weight loss occurs partly as a result of glucosuria, but also because of
metabolic changes resulting from cells being 'starved' of glucose

Diagnosis: Clinical signs. Urinalysis – glucosuria. Haematology and serum biochemistry:

hypercholesterolaemia, hyperglycaemia. Elevation of liver enzymes, such as AP and
ALAT.

Treatment:: Oral hypoglycaemic drugs - type 2 diabetes, in cats.

Sulfonylureas-glipizide most often used. Stimulate insulin secretion and some B-cell
function is required for the drug to be effective. The starting dose is 2.5 mg/ cat, increased
to 5 mg/cat after 2 weeks
Insulin: -Neutral (soluble) insulin is the only preparation suitable for the intensive
management of diabetic ketoacidosis, since it has the quickest onset (within 1 hour) and
shortest duration (up to 4-6 hours) of activity, with the intravenous route having the most
immediate and shortest effect.
-Lente preparations have a biphasic activity, with 30% of the insulin, with a more
immediate effect. The remaining 70% of the insulin is in an peaks in activity at around 6- 8
hours and lasts up to 12- 24 hours. -Glargine is a synthetic insulin analogue. -The longest
lasting insulins in medical use tend to be those in which the insulin is formulated with
protamine and zinc (PZI).

Frequency :once-daily or twice-daily treatment. PZI insulin, because of its longer duration
of action, is usually given once-daily, whereas lente preparations are commonly injected
every 12 hours.
As a guide, a starting dose of insulin for dogs is usually 0.5 IU/kg. Cats are more sensitive
to insulin thus 0.25 IU/kg is recommended. It is preferable to start with a low dose and work.
Monitoring and dose adjustments: After 4-7 days of treatment, a 12-24-hour blood
glucose curve to assess progress is recommended. Changes to management will also
depend on other clinical parameters, such as appetite, thirst and general demeanour of the
patient.

Long-term complications in diabetes mellitus:ocular, dermatological ( Ulcerative skin

lesions and cutaneous xanthomas) and Hypoglycaemia.

PETS 13) HYPOTHYREOIDISM

Hypothyroidism is a disorder that results from inadequate production triiodothyronine (T3)

and its prohormone, thyroxine (T4). It is rarely seen in cats.

Primary hypothyroidism is a result of progressive destruction of the thyroid gland. Occurs

either from an immune-mediated process called lymphocytic thyroiditis in which thyroid
tissue is destroyed and replaced by fibrous connective tissue or by idiopathic atrophy in
which the thyroid tissue atrophies and is replaced by adipose tissue. Secondary
hypothyroidism is rare but may be caused by pituitary malformation or neoplasia. Most
common: Golden retrievers, Doberman pinschers. Spayed females and neutered males
are at increased risk.

Clinical signs: Thyroid hormones influence the function of almost all organ systems within
the body. At a cellular level influence multiple metabolic processes, from the regulation of
mitochondrial oxygen demand to the control of protein synthesis. Signs relate to a decline in
metabolic rate, together with a variety of dermatological changes.
Hypothyroidism is associated with a decline in metabolic rate. Related clinical signs,
including weight gain, lethargy, exercise intolerance and weakness. Weight gain and
obesity occurs despite a normal or slightly reduced appetite. Cold intolerance or heat
seeking.

Thyroid hormones play an important role in the maintenance of dermal health.

Dermatological abnormalities can be extensive. Hyperkeratosis causing scaling and
scurfing of the skin, and poor quality hair coat, is common. A dry dull coat and otitis externa
also. Thyroid hormones are necessary for the initiation of the anagen phase of hair growth
ahich causes alopecia: bilaterally symmetrical nonpruritic 'endocrine' alopecia, with hair loss
along the flanks and on the trunk, usually sparing the head and extremities. There is also
myxoedematous non-pitting thickening of the skin.

Diagnosis: Common drugs including glucocorticoids, phenobarbital, sulfa antibiotics,

furosemide have been reported to alter thyroid concentrations. Concurrent illness causing a
reduction in thyroid hormone levels nonthyroidal illness or euthyroid sick syndrome,
can be brought on by conditions such as renal disease, hepatic disease, heart failure,
severe infections, and diabetic ketoacidosis.
Abnormal findings in the CBC are a mild, normocytic, normochromic, nonregenerative
anemia, as well as leukocytosis. Abnormalities in the serum chemistry profile are
hypercholesterolemia and/or hypertriglyceridemia. Urinalysis is often normal in dogs with
primary hypothyroidism.

Endocrine testing: Total T4 values will fall below normal reference range. Iit is
recommended that a free T4 by equilibrium dialysis (fT4 [ED]) and a TSH level be
evaluated. A decreased fT4 (ED) and an increased TSH in a dog with typical signs is
suggestive of a true hypothyroid condition.
Treatment : synthetic levothyroxine sodium product (doses 0.02 mg/kg). T4 level
should be reevaluated 4–8 weeks after starting replacement therapy or after any changes in
dose or supplement brand. Peak plasma concentrations after oral dosing reportedly occur
4–12 h after administration, and the serum half-life is approximately 12–16 h. Ideally, blood
samples should be drawn immediately before the next dose is due and then 4–6 h post pill
(peak level).

Once a consistent therapeutic dose has been achieved, routine monitoring may only require
testing of peak T4 levels every 6–12 months. Clinical improvement should be observed
within 4–6 weeks of initiation of therapy. Dermatologic and reproductive abnormalities may
take several months to completely resolve.

Prognosis and survival times

With proper diagnosis, therapy, and monitoring, the prognosis for canine hypothyroidism is
excellent and life expectancy is normal.

14) HYPERADRENOCORTICISM: CUSHING’S DISEASE

HAC, also known as Cushing’s disease or Cushing’s syndrome, is the result of
hypersecretion of cortisol by a functional adrenal tumor (FAT) or secondary to increases in
ACTH from a pituitary tumor. Iatrogenic HAC can occur secondary to glucocorticoid
medications.

In normal dogs, the pituitary gland secretes ACTH, which stimulates the adrenal glands to
release cortisol. The presence of cortisol exerts a negative feedback on the pituitary gland.
In dogs with pituitary-dependent hyperadrenocorticism (PDH), this feedback loop is
disrupted by the tumor and ACTH is released despite high plasma cortisol concentrations.
In dogs with FAT, excessive amounts of glucocorticoids are released, exerting a negative
feedback on the pituitary gland, resulting in low concentrations of ACTH and atrophy of the
contralateral (normal) adrenal gland. Spontaneous HAC occurs more frequently in middle-
aged to older dogs. Dachshunds, various terrier breeds, poodles, and boxers appear to be
overrepresented.

Clinical signs: polyuria, polydipsia, and polyphagia. Other common signs include weight
gain, weakness, “pot-bellied” appearance, excessive panting, and truncal, bilaterally
symmetrical hair loss. Less common clinical signs include calcinosis cutis and facial
paralysis.

Diagnostic testing: Excessive glucocorticoids typically results in a “stress leukogram”

characterized by lymphopenia, eosinopenia, neutrophilia, and monocytosis. These changes
are nonspecific. An increase in alkaline phosphatase (ALP) activity. The urinalysis reveals
a specific gravity of less then 1.020, glucosuria, and proteinuria. Due to the
immunosuppressive effects of high cortisol concentrations, dogs have a urinary tract
infection.

Endocrine testing

ACTH stimulation test: Evaluate the adrenal gland’s response to exogenous

administration of ACTH and is most useful in differentiating spontaneous HAC from
iatrogenic HAC. Synthetic ACTH protocol: Blood samples are collected prior to and 1 h
after intravenous administration of synthetic ACTH (Cortrosyn). The dose is 5 mcg/kg.
Dogs with spontaneous HAC have an exaggerated response, whereas those with
hypoadrenocorticism or iatrogenic HAC have diminished response or normal-to-diminished
response, respectively.
Low-dose dexamethasone suppression test : The LDDST evaluates the negative
feedback loop of the hypothalamic–pituitary– adrenal axis (HPAA). Dexamethasone is
administered at 0.01 mg/kg IV and serum cortisol concentrations are collected prior to and
4 and 8 h after administration. In normal dogs, the administration of dexamethasone
suppresses the secretion of ACTH from the pituitary glands, decreasing the cortisol
concentration to less than 1.4 μg/dL at 8 h. The administration of dexamethasone has a
minimal effect on dogs with PDH or FATs and the blood cortisol concentrations remain
elevated (equal to or greater than 1.4 μg/dL [38.6
nmol/L]) at 8 h.
Differentiating PDH and FAT : Discriminating tests include the LDDST, High dose
dexamethasone suppression tests (HDDSTs) and endogenous ACTH concentration.
Treatment: selective adrenocorticolysis with mitotane (Lysodren®) or by selectively
inhibiting the synthesis of adrenal cortex hormones with trilostane (Vetoryl®). Mitotane: at
high doses (30–50 mg/kg/ day) during the induction phase (usually 4–5 days) until the dog
has a decrease in appetite or water intake. Trilostane: monitored with an ACTH stimulation
at 10 days and 1, 3, and every 3 months.The ACTH stimulation must be performed 4- to 6-h
after trilostane administration. Other less commonly utilized therapies for PDH:
ketoconazole, selegiline
hydrochloride, hypophysectomy, and RT. A unilateral adrenalectomy is the treatment of
choice for FATs. Anesthetic and analgesic consideration: induction with propofol and
inhalant anesthesia for maintenance. Nutritional considerations: mild fat restriction is
recommended.

Prognosis: only age at the time of diagnosis was negatively associated with overall
survival.

PETS 15) GASTROESOPHAGEAL REFLUX ESOPHAGITIS

Gastroesophageal reflux is a disorder of the gastroesophageal sphincter permitting reflux of

gastrointestinal fluids or ingesta into the esophagus. Varying degrees of esophagitis result
from prolonged contact of gastric acid, pepsin, trypsin, bile salts, and duodenal bicarbonate
with the esophageal mucosa.

Pathophysiology: The frequency of reflux and composition of the refluxed material

determines the severity of the esophagitis. Gastric acid alone produces a mild esophagitis,
whereas combinations of acid and pepsin or trypsin, bicarbonate, and bile salts produce a
severe esophagitis. Chronic vomiting, disorders of gastric emptying, hiatal hernia, upper
airway obstruction, and anesthesia-induced reductions in gastroesophageal sphincter
pressure are implicated in the pathogenesis.
Dogma: refluxed gastric fluid does not directly damage the esophageal mucosa, but rather
stimulates esophageal epithelial cells to secrete chemokines that attract and activate
immune cells, causing damage to the esophageal squamous epithelial cells.

Clinical Signs
In severe cases: regurgitation, fever, salivation, odynophagia, extension of the head and
neck during swallowing, and total avoidance of food.
In milder cases: may have only an occasional episode of regurgitation, particularly in the
early morning hours. The latter cases are physiologic and result from transient relaxations
of the gastroesophageal sphincter during sleep.

Diagnosis: Endoscopy is the current best method. Definitive diagnosis of

gastroesophageal
reflux requires continuous measurements of gastroesophageal sphincter pressure and 24-
hour
intraluminal pH, procedures for which most dogs and cats are not compliant. DD: Hiatal
hernia, esophagitis, and esophageal stricture.

Treatment: animals should be fed fat-restricted diets.

Diffusion barriers: Sucralfate (0.5 to 1.0 g PO), protects against mucosal damage and
promotes healing of existing esophagitis.
Refractory cases should be concurrently medicated with acid secretory inhibitors and/or
prokinetic agents. The H2 histamine receptor antagonists, cimetidine (5 to 10 mg/kg)
ranitidine (1 to 2 mg/kg), and famotidine (0.1 to 0.5 mg/kg), inhibit gastric acid secretion and
reduce the amount of acid reflux.
Omeprazole (0.7 mg/kg); esomeprazole, lansoprazole, and pantoprazole (all 1.0 mg/kg IV,);
and all H+,K+- ATPase inhibitors could be used to inhibit gastric acid secretion as an
alternative to H2 histamine receptor antagonism.
Metoclopramide (0.2 to 0.4 mg/kg,) and erythromycin (0.5-1.0 mg/kg,) may be useful in
treating gastroesophageal reflux because they increase gastroesophageal sphincter
pressure.

Prognosis
The prognosis for most animals with gastroesophageal reflux is good with medical
management.
Anatomic correction of upper airway obstruction in brachycephalic breeds should
ameliorate gastroesophageal reflux in affected patients.

16.PANCREATITIS

Pancreatitis is the most common exocrine pancreatic disease in both dogs and cats. It can
be acute or chronic, depending on whether the disease has led to permanent changes of
the pancreatic parenchyma, mainly atrophy and/or fibrosis. Both acute and chronic
pancreatitis can be subclinical, mild and associated with vague clinical signs, or severe and
associated with pancreatic necrosis and systemic complications. The determination of
whether pancreatitis is acute or chronic can only be made definitively based upon a biopsy
and histopathological examination.

Aetiology

In most cases of pancreatitis in dogs the aetiology remains undetermined. There are a
number of potential risk factors that have been identified however. Obesity has been
suggested as a risk factor for the disease, and the disease has been reported as less
severe when experimentally induced in lean dogs. Hyperlipidaemia, often grossly
recognised in patients with acute pancreatitis, may be the consequence of abdominal fat
necrosis, or may potentially induce the disease. In the case of Minature Schnauzers, there
is a possible link between the familial hyperlipidaemia and the apparent increased
incidence of pancreatitis. Glucocorticoids were long implicated,other than perhaps the very
high dose regimes sometimes used for patients with spinal cord injury.

Other drugs that have been suggested as risk factors include chemotherapeutic drugs
(Lasparaginase, vinca alkalaoids), cytotoxic drugs (azathioprine), diuretics (frusemide,
thiazides), anticonvulsants (potassium bromide), antimicrobials (sulphonamides,
tetracyclines), and NSAID such as salicylates. Some toxins have been associated with the
disease, including cholinesterase inhibitors or cholinergics. The theory is that they stimulate
hypersecretion.

Other toxins include zinc and scorpion venom. Hypercalcaemia has also been recognised
as a cause of pancreatitis in dogs. This may be spontaneous (malignancy,
hyperparathyroidism, renal failure, hypoadrenocorticism, granulomatous disease,
destructive bone disease), or may be iatrogenic (vitamin D toxicity). Reflux of duodenal
juice into the pancreatic duct can cause pancreatitis, but rarely occurs in a normal patient
because of the anatomy of the duodenal papilla, which has a muscular sphincter and is also
covered by a special piece of mucosa.

Clinical causes of pancreatic duct obstruction can include surgical manipulation of the
area, neoplasia, oedema of the duct or duodenal wall, a strategically located duodenal
foreign body, trauma, parasites, spasm of the sphincter, or biliary calculi. Other potential
causes of pancreatitis include ischaemia (associated with shock, or hypotension), infectious
agents or potentially immune mediated disease.

Pathophysiology

The basic mechanism of the disease is auto-digestion of the pancreas. There are several
mechanisms in place in the pancreas to prevent this process. The first is that the digestive
enzymes (both proteolytic and phospholipolytic) are produced and then stored in an inactive
form in zymogen granules. The process of activation is achieved by the enzymatic cleavage
of a small activation peptide from the amino terminal of the polypeptide chain.

The activation typically occurs in the small intestine after secretion of the zymogens. The
duodenal enterocytes secrete an enzyme called enteropeptidase that is very effective at
cleaving the activation peptide from trypsinogen. The activated enzyme, trypsin, then
cleaves the activation peptide from the other zymogens. It is important to remember though
that enteropeptidase and trypsin are not the only enzymes that have the capability to
activate the zymogens. There are lysosomal proteases that have this capability. A second
mechanism is the strict separation of the digestive enzymes during synthesis, storage and
secretion from other cellular enzymes, including the lysosomal enzymes. The digestive
enzymes are stored in zymogen granules, separate from lysosomes.

Calcium also plays a role in enzyme activation, and it can have both an inhibitory and
activating role. At low concentrations (as in acinar cells), calcium binding protects
trypsinogen activating peptide from exposure. Whereas at higher calcium concentrations
(as found in the pancreatic duct and intestine), calcium increases the sensitivity of
trypsinogen to activation by trypsin. Higher pH levels in the pancreas and ducts also
minimise enzyme activation.

If adequate activation of the trypsin takes place within the pancreatic cells and ducts, the
other zymogens (including proelastase and prophospholipase) will be activated,
furtherincreasing pancreatic damage. As further enzyme is activated within the pancreas, a
mild oedematous pancreatitis may progress to more severe haemorrhagic or necrotic
disease, and then more systemic signs of disease will manifest.

If activated digestive enzymes gain access to the vascular space, there are plasma
protease inhibitors that are very important in minimising their adverse effects, which may be
fatal. If they are not bound the free proteases will induce disseminated intravascular
coagulation by activating the coagulation, fibrinolytic, kinin and complement systems.

Clinical signs

Whilst any dog can be affected, middle aged and older and overweight dogs are more
commonly affected. In more severe cases common clinical signs may include anorexia,
vomiting, weakness, abdominal pain, diarrhoea, and obtundation. In some severe cases
there may be more systemic clinical signs including fever, tachypnoea or dyspnoea, or
signs of shock. Abdominal pain has not been reported as frequently in canine patients as in
human patients. Other physical examination findings may include the presence of a
palpable cranial abdominal mass, or evidence of a peritoneal effusion. Cardiac arrhythmias
may also be apparent. Some severely affected patients may be hypothermic.

Diagnosis
Routine haematology and biochemical profile changes tend to be relatively nonspecific in
the diagnosis of the disease. A neutrophilia and left shift is a relatively common finding in
affected patients. Thrombocytopaenia may be noted .The PCV may be elevated secondary
to haemo-concentration, or may be reduced. A biochemical profile may reveal azotaemia,
which could be secondary to dehydration, or could indicate renal damage and the onset of
acute renal failure. Elevated liver enzymes may be the result of bile duct obstruct ion,
ischaemia, or the drainage of toxic material from the pancreatic veins into the portal vein.

Hyperbilirubinaemia may occur for similar reasons to the hepatic enzymes. Hyperglycaemia
can be the result of elevated levels of cortisol, catecholamines and glucagon, or damage to
the endocrine pancreatic tissue. Hypoalbuminaemia may be the result of loss because of
vasculitis or effusion. Hypocalcaemia may be secondary to the hypoalbuminaema, or the
formation of calcium salts with fatty acids associated with fat necrosis.
Hypercholesterolaemia and hypertriglyceridaemia are commonly recognised. Electrolyte
and acid base abnormalities are frequently recognised, secondary to vomiting and
hypovolaemia. Urinalysis is important in affected animals to aid in the interpretation of the
biochemical profile.

The presence of azotaemia and an inappropriately low specific gravity raises questions
about renal function. Whilst the pancreas synthesises lipase, so do other tissues and the
catalytic assay utilised does not differentiate the source of lipase. Lipase elevations may
occur with renal failure, glomerulonephritis, hepatic disease, intestinal disease, the
administration of glucocorticoids (especially dexamethasone), or heat stress. The
information for serum amylase is very similar, with many non pancreatic sources.

The serum trypsinogen-like immunoreactivity test (TLI) detects trypsinogen and some
trypsin in the circulation, and is a species specific test. The test has proven to be very
specific for the diagnosis of EPI in dogs and cats. The gastrointestinal laboratory at Texas A
and M University purified classical pancreatic lipase (cPL) from dog pancreas, and
developed antisera against this in rabbits. Further testing demonstrated that the only cell
type staining positively for cPL was the pancreatic acinar cell, and a reference range was
developed using 74 clinically healthy dogs. A radiommunoassay and ELISA were
developed and validated, with the ELISA commercially available. The cPLI levels were
demonstrated to be reduced in dogs with EPI.
The cPLI was evaluated in dogs with chronic renal failure, and it was found that the levels
were within reference ranges, and promising results were obtained in patients with gastritis.
The levels are not affected by the administration of prednisolone. Abdominal radiography
has the advantage of being freely available to almost all practitioners. In patients with
pancreatitis there may be a number of possible abnormal findings.

These may include an increased density, or a loss of detail in the abdomen, or a

granularity or ground glass appearance, especially in the right cranial quadrant. The
stomach may be displaced to the left, increasing the angle between the pylorus and
duodenum, and the descending duodenum may be displaced to the right. Gas
accumulation may be noted in the descending duodenum, with a suggestion of a thickened
duodenal wall, or there may be gas accumulation in the transverse colon with caudal
displacement. There may be gas accumulation in the stomach, and if barium is
administered there may be delayed transit through the stomach and duodenum, with an
irregularity of the duodenal wall.

However none of the afore mentioned findings are definitive. Abdominal ultrasonography is
a frequently used technique for diagnosis of acute pancreatitis, but is not without limitations.
Pancreatic enlargement alone is not diagnostic, because there can be other causes of
pancreatic oedema, including portal hypertension. Local effusion alone is also not
diagnostic. Altered pancreatic echogenicity is important. The pancreatic dimensions are
variable. The surrounding tissue may be hyperechoic, typically the inflamed mesentery with
fat necrosis. The liver and biliary system should also be evaluated, especially if the patient
has elevated hepatic enzymes or icterus. Chronic pancreatitis may be associated with
increased echogenicity in the pancreas associated with fibrosis. Advanced imaging options
are available.

However both are expensive and require general anaesthesia. Pancreatic biopsy and
histopathological examination is typically considered the gold standard test for diagnosis. It
is important to note that even this technique has its limitations. The presence of
inflammation or necrosis is certainly diagnostic, but their absence does not rule out the
diagnosis. Biopsies can be obtained at laparotomy, or laparoscopically. Biopsy is the only
way to definitively classify pancreatitis as acute or chronic.

Treatment
Fluid Therapy: Intravenous fluids are the mainstay of therapy for pancreatitis. Initially fluids
should correct dehydration over the first 12–24 hours, while also meeting maintenance
needs. The fluid rate should be adjusted frequently to account for ongoing losses and to
correct fluid, electrolyte and acid-base imbalances. If needed, colloidal support can be
given in the form of fresh frozen plasma, hetastarch or dextrans (10–20 mL/kg/day).

Plasma will provide a -macroglobulins to scavenge activated proteases within the serum; it
also provides clotting factors and is indicated if there is evidence of disseminated
intravascular coagulation (DIC). Pain Management: Analgesic therapy should be
considered for abdominal pain in every animal with suspected or confirmed pancreatitis.
Intravenous or subcutaneous opioids are typically utilized while the patient is hospitalized.
Alternatively, intraperitoneal infusions of lidocaine or bupivacaine mixed with sterile saline
can be administered. Options for outpatient pain control include fentanyl patch, tramadol or
butorphanol.

Nutritional Support: Experts recommend enteral nutritional support in all patients with
pancreatitis. EN stabilizes the gut barrier, improves enterocyte health and immune function,
improves GI motility and prevents catabolism.

Enteral nutrition can be provided by a variety of feeding tubes, including nasogastric (NG)
or nasoesophogeal (NE) tubes, esophogostomy tubes, gastrostomy tubes or jejunostomy
tubes. Jejunostomy tubes bypass the pancreas and can be used in patients when vomiting
cannot be controlled. Endoscopically placed jejunostomy tubes have been described in
dogs and provide an opportunity for EN without prolonged anesthesia and surgery.

Other Treatments:

Other potential therapies for pancreatitis include antiemetics, antacids, antibiotics and
dopamine. Antiemetics will help control vomiting and allow for earlier EN. Choices include
ondansetron (Zofran®), dolasetron (Anzemet®), metoclopramide and chlorpromazine.
Antacids can either be an H2-receptor antagonist (ranitidine or famotidine IV) or a proton-
pump inhibitor (pantoprazole). Pancreatitis is usually a sterile process in dogs and
antibiotics are not indicated. Rarely, antibiotics may be used if a pancreatic abscess is
present or there is evidence of bacterial translocation from the gastrointestinal tract.

In research settings, dopamine at low doses (5 μg/kg/min) maintains mesenteric blood flow
and limits increased microvascular permeability. Monitoring During hospitalization,
pancreatitis patients must be monitored closely as their status can change rapidly.
Electrolytes, acid-base status, azotemia, icterus and coagulation status should be
reevaluated regularly (e.g., every 24–48 hours in patients with severe disease).

Abdominal ultrasound can be repeated intermittently to evaluate for the development of, or
changes in, pancreatic pseudocysts and/or abscesses. Drugs associated with pancreatitis
(e.g., potassium bromide, L-asparaginase, azathioprine, furosemide, tetracycline, aspirin,
sulfa drugs) should also be avoided in these patients.

19.FELINE IDIOPATHIC CYSTITIS

Feline lower urinary tract disease describes conditions that can affect the urinary bladder
and/or urethra of cats. Although many different diseases can affect the lower urinary tract, a
number of cats develop a disease without any obvious underlying cause ' feline idiopathic
cystitis',

Etiology: abnormalities common in cats with FIC:

- Defective bladder lining –a mucus layer composed of glycosaminoglycans (GAGs). -

Neurogenic inflammation – nerves in the bladder wall may be stimulated, which causes
release of chemicals known as neurotransmitters that can exacerbate local inflammation
and pain. - Stress - Abnormal stress responses –In healthy individuals, normally induces
release of both 'catecholamines' (adrenaline and noradrenaline), and also cortisol.
However, in cats with FIC, while catecholamine concentrations tend to be high (reflecting
an underlying stress response) they actually have sub- normal cortisol responses, and are
thus not responding in a normal way.

Clinical signs: Dysuria – difficulty or painful urination • Pollakiuria – increased frequency

of urination • Haematuria – blood in the urine • Periuria – urinating outside the litter-box •
Overgrooming – especially around the perineum. Urethral blockage as a result of severe
inflammation and spasm of the muscles surrounding the urethra, or if a urethral plug
develops. FIC can lead to severe bladder inflammation and the thickened bladder wall.

Diagnosis: no diagnostic test so a diagnosis can only be made by excluding other

recognised causes of FLUTD. This means that cats should be investigated thoroughly
through: Analysis and bacterial culture of urine samples, X-rays of the bladder (including
contrast studies), Bladder ultrasound.

Treatment

Dietary modification for cats with FIC

Encouraging more frequent urination and producing urine that is more dilute. Changing to a
wet diet. These diets include added polyunsaturated fatty acids which potentially may help
reduce inflammation (change in diet gradual, Start by mixing a very small amount of the
new food with the old, Increase the amount of the new food slowly, warming the food to
body temperature). To drink more: flavoured waters or water fountains to encourage
drinking, adding further water to the food.Environmental modification – drinking and
urinating: help reduce stress, encourage cats to drink, it is important to provide water in
different places and avoid noisy places or anywhere close to a litter box. Environmental
modification – reducing stress: identify and modify or avoid any specific stress triggers
in the environment - this could be another pet in the house, abrupt changes in diet,
overcrowding, owner stress, or changes to the people in the house.

Drugs used for management of FIC: FIC is not primarily a drug-responsive disease.
GAG replacers, if the GAG layer that lines the bladder is deficient in cats with FIC, then
repairing this should be of benefit. Tricyclic antidepressants – drugs such as amitryptiline.
Use of analgesics: FIC is a painful condition, so in acute episodes and especially if the cat
is showing signs of discomfort, the use of an analgesic drug may be valuable.