Small Animal Medicine

Fekadu Regassa
 Why SAM?
• Guarding property
• Companionship
• Herding animals (sheep/goats)
• Policing/crime investigation
• Guiding blind people
• Show biz
• Child creativity
• Racing
• Hunting
• Rodent control
 RABIES

Introduction
• The oldest infections disease Known to infect humans and animals. 23
century BC
• Caused by a fragile, enveloped RNA virus of the family rabdoviridae
• Clinical rabies infection is uniformly fatal
• The virus is easily destroyed by conventional disinfectants, uv light and
heat
 Rabies
Etiology
• Specific lyssa virus RNA, Rabies Virus
• Transmission is through innoculation of infectious
saliva through a bite wound
• Other routes: airborne
• The incidence of rabies in dog t cats correlates with the
incidence of wildlife rabies.
 RABIES

PATHOGENESIS
•
• Clinical rabies conventionally classified into
1. Mad ,hyperexcitable or psychotic rabies
2. Paralytic or dumb form
• However, the clinical signs are highly variable
• Thus they do not fit into one classification or another
• Incubation period following exposure is dogs in 3-8 wks. Can go up to six
months
 Rabies

CLINICAL SIGNS
• Initially dogs manifest signs of nervousness, anxiety and solitude.
• If bite wound is present most animal show irritation and purities at the site
viral entry.
• Dogs manifest clinical lanes for 1-10 days following the onset of clinical
signs
• Dogs with furious rabies
 Progressive restlessness and hyper excitability in response to auditory and
visual stimuli
 Terminally Progressive disorientation and grand mal seizures
 Rabies

 DOGS WITH DUMB FORM

 Progressive Lower motor neuron paralysis or cranial nerve deficits are the
1st signs
 Change of tone at the bark which is dne to laryngeal Paralysis
 Excessive salivation
 Dysphagia
 Drop-Jaw
 These signs of choking prompts owners and others to attempt to remove a
foreign body from oral cavity leading to exposure
 Following paralysis death occurs within 2-4 days from respiratory
embarrassment.
 Rabies
 DIFFERENTIAL DIAGNOSIS

 CDV

 Disease with encephalitis and Change in behaviors

 Sepsis

 Tetanus

 Botulism and intracranial neoplana

 Rabies

DIAGNOSIS
• Presumption on Clinical signs
• Direct FAT from nervous tissue (most common) but depends on
prompt handling of specimens (do not freeze)
• PCR, Histology of negri bodies.
TREATMENT
• No attempt should be provide care for animals suspected of Rabies
• It is regarded as uniformly fatal diseases in dogs cats and humans
 Rabies
PREVENTION

• Killed virus and recombinant rabies vaccines

are available for use in dogs

• The 1ts dose maybe given as early as 3 months

of age

• All dogs should receive booster dose every year

 Rabies

PUBLIC HEALTH
• Humans exposed to infections saliva of any rabid animals are at
risk.
• To recommend post-esposure immuno-Prophylaxis (Admin of
H.RIG and HDC Vaccine) ability identity and capture the
animal involved, Knowledge of any contact with saliva, wether
the attack was provoke or unprovoked, Knowledge of rabies
prerace in the region, etc. should be there.
 Rabies

• 10-14 days quarantine of the animal

• Aggressive washing of the bite wound soon

• After bite with soap and disinfectant

 CANINE DISTEMPER

INTRODUCTION
• CD is a viral disease of dogs with a wide range of clinical
presentation. It is also known as Hard pad disease.
ETIOLOGY
• The CDV is a single stranded RNA Virus belongs to the
genus of Morbilivirus.
• Immunological cross reaction with RP,PPR ,measls virus
 CANINE DISTEMPER
• The virus is unstable at room temperature and susceptible
to UV light, drying and temp of 50-60c
• It survives freezing for several weeks.
• Transmission to other animals is through infectious micro
droplets. Less aften aerosol
• Unvaccinated dogs population suffers heavy threat,
especial those between 3 and 6 months of age as maternal
immunity wanes.
 CANINE DISTEMPER

PATHOGENESIS

• The initial infection begins as CDV invades the

epithelium of the upper respiratory tract.

• Spreads quickly to local Lymph ties, tonsils and

bronchial Lymph nodes.

• Then within the 1th week of infection it spreads to

epithelial and CNS tissue
 CANINE DISTEMPER

• Following this spread the humoral immune response

correlates with clearance of the virus Dogs that
recover from acute CDV infection derive long lasting
immunity
• However dogs that fail to mount a significant
immune response softer a rapid spread of the virus to
the skin, the exocrine and endocrine glands, gastro
intestinal, respiratory and uro-genital tracts.
 Canine Distemper
CLINICAL SIGNS

• Sings range from mild to severe depending on viral

strain, environmental factors and patients response to
infection

• If signs limited to URT coughing and nasal discharge

• Puppies are most susceptible to severe systemic signs :

Pneumonia, diarrhea, dehydration, vomiting
 Canine Distemper
• Neurologic signs begin 1-3 wks following from
recovery from acute clines.

• Neurologic signs are progressive resulting in rapid

deterioration

• Additional signs in clued uveitis and optic neuratis that

leads to sudden blindness

• Hard-foot pads
 CANINE DISTEMPER

DIAGNOSIS
• Dogs with sever illness have the most characteristic
feature of CDV infection
• However, in some dogs signs are limited to
respiratory and ocular disease
• Buffy Coat smears to detect inclusion bodies in
neutrophils
• ELISA
 CANINE DISTEMPER
TREATMENT

• Supportive

PREVENTION

• Highly effective modified Live CD vaccine

 Canine Distemper
DIFFERENTIAL DIAGNOSIS
 . Rabies
 . CRD
 . Renal failure
 . Idiopathic epilepsy
 . CNS trauma
 CANINE RARVOVIRUS
Introduction
• CP is a recently discovered infectious disease of dogs causing a
rapid onset, severe viral enteritis and myocarditis in young pups
Etiology
• CPV is a small DVA Virus that reproduces best in rapidly dividing
cells. Such as myocardium of puppies and intestinal epithelium
• The virus is resistant to environmental factors and detergents and
most disinfectants.
• Different strains available
 CANINE RARVOVIRUS
PATHGENESIS
• CPV enteritis is a highly contagions disease of dogs
• Transmission is oral and nasal exposure with
contaminated feces.
• Next to initial viremia, CPV localizes in the epithelium
of small intestine, tonge, oral and oese phageal macosae
as well as in Lymphoid tissue including bone marrow.
 CANINE RARVOVIRUS
• Virus also isolated from lungs, spleen, kidneys and
myocardium
• Thus clinical signs related to actual tissues affected
• The virus replicates in the lymphoid tissues of the
oropharynx, thymus and mesentric lymph nodes
• Then it spreads to intestinal crypt of the small intestines
Necrosis
 CANIN PARVOVIRUS

CLINCAL SIGNS
• Signs are variable –range from unapparent infection
to acute fatal disease
• The most severely affected dogs are younger than 4
month of age.
• Vomiting ,diarrhea (mostly blood tinged)
• Anorexia, dehydration (hemoconcentration)
• Puppies continuously cry (Myocarditis)
 CANIN PARVOVIRUS
DIAGNOSIS
• Clinical signs
• Hematology (hemoconcentration etc.) leukopenia
and lymphenia
• ELISA to detect CPV antigens
• Histology of duodenum and Jejunum → Necrosis
.
 CANIN PARVOVIRUS
DIFFERENTIAL DX

• Intussusceptions ,intestinal obstruction (foreign body )

• Poisoning

• Intestinal parasitism,

• Addison’s disease (hypoadrenocorticism) →

mineralocorticoid → Aldosterone
 CANINE PARVOVIRUS

TREATMENT

• IV replacement fluid and electrolytes is a primary

goal of treatment

• Antimicrobial agents  gram negative sepsis

• Control vomiting –antiemetics → metoclopramide

• Antispasmodic-diphenoxyle

• Prognosis: good following the 1st seven dyes of

enteritis
 CANINE PARVOVIRUS

PREVENTION
• Recovery from natural infection cenfers a
minimum of 20 months or possibly for lifetime
protection
• Both killed and live modified vaccines
• No Public Health concern
 CANIN EHRLICHOSIS
INTRODUCTION
• Ehrlichiosis is a tick-borne systemic disease caused by a
variety of rickettsial species in the genus Ehrlichia
ETIOLOGY
• Ehrlichia canis is the cause of canine monotypic Ehrlichiosis
which is the most common form of the disease in dogs
• The brown ear-tick of dog, Rhipicephalus sanguineus, is the
arthropod vector of E.canis
• The tick cannot serve as a reservoir of infection but it can
transmit the infection for up to 155 days post-infection
 CANIN EHRLICHOSIS

PATOGENESIS
• Canine monocytic Ehrlichiosis is characterized by a
reduction in cellular blood elements
• E. canis can cause acute, sub acute and chronic form of the
disease
• In the acute form the organism multiplies within the
circulating mononuclear cells and mononuclear phagocytic
tissue of the liver , spleen and lymph nodes
 CANIN EHRLICHOSIS

• Infected cells are transported are transported in

the blood to other tissue: meninges, lungs and
kidneys where they attach to the vascular
endothelium
• This leads to vasculitis and infection of sub-
endothelial tissue [basement membranes]
 CANINE EHRLICHIOSIS

• As a result of platelet consumption sequestration and

distraction there is thrombocytopenia
• Anemia develops progressively due to suppression of
erythropoeisis and accelerated destruction of RBC
• In subclinical form there is variable persistence of
thrombocytopenia, leukopenia and anemia
• Chronic form occur in dogs unable to mount immure
response
 CANINE EHRLICHIOSIS

CLINICAL SIGNS
1. Acute Phase
 1-3 wks incubation period and lasts for 2-4 wks
 Fever, nasal discharge, in appetence, wt loss and
lymphadenomegaly
 Clinical sign typically resolve spontaneously
2. Subclinical phase
 At 2-4 months post-infection clinical signs are absent.
 Can persist for several years
 CANINE EHRLICHIOSIS

• 3 CHRONIC PHASE
Occurs in some dogs
Vague signs evident in some
Severe hematologic impairment associated with bone-
marrow suppression in others profound pancytopenia
Also in some neurologic signs : seizure, ataxia,
hyperesthesia
Polyartheritis due to immune complex can occur
 CANINE EHRLICHIOSIS

DIAGNOSIS

• Clinical sign

• Hematologic abnormalities. NR anemia and

thrombocytopenia

• Serology: indirect FAT

• Histology : Peri-vascular plasma call infiltration

 CANINE EHRLI HIOSIS

TREATMENT

• Antirickettsials such as Doxycycline

• Success depends on severity of the disease and time of

initiating the treatment. The earlier the better response.
PREVENTION

• Currently no vaccine

• Manage tick infection

• No Public health concern

 CANINE BABESIOSIS

INTRODUCTION

An infection caused by a tick- borne hematozoan, Babesia canis

ETIOLOGY

→B.canis

→Transmitted by Ixodid tick Rhipicephalus sanguineus and haemophysalis

leachi leachi

→Babesia multiply with in RBC

→Transplacental transmission in ticks possible → generations transmit the

diesase unlike Ehrlichia
 LIFE CYCLE
D Sporozoites
O enter dog (merogony)
G RBC Merozoites
in RBC

RBC lyses and

Tick feed
merozoites released
On dog

Sporozoites released Merozoites

Ingested
By tick
(sporogony)
Salivary
gland T
(gamogony) I
Zygotes C
Fuse to Transform
Migrate K
form Into gametes
zygotes

eggs
ovary
 CANINE BABESIOSIS

PATHOGENISIS
• RBC parasitized RBC are destroyed by
replication of the organism

 Haemolysis → leads to anemia

 1.P 10 day -3 Weeks

 CANIN BABESIOSIS

CIINICAL SIGNS

Acute onset anemia  Fever and lethargy

Red urine (coffee colored).

Lymphadenopathy

Spleenomegaly

Vomiting and Diarrhea

Ulcerative stomatitis and

CNS signs
 CANIN BABESIOSIS

DIAGNOSIS

• Clinical signs suggestive

• Confirmation by identification of pear-shape organism

within infected RBC

• Indirect FAT
 CANIN BABESIOSIS

TREATMENT

• Diminazene aceturate

• Imidocarp diproprionate

PREVEULION

• No vaccine

• Topical acaricide
 RESPIRATORY DISEASES
• RD Occur frequent of in dogs and cats
• Coughing is the most accompanying respiratory sign
• But not always regarded as respiratory sign only
Expected is chronic heart disease (Cardiac cough )
•URT normally supports bacteriaf (microbial) flora
• P. Multicide
•. Brondiseptica
• Colllifortms, etc
 RD
• This peaceful co-existence lasts only until respiratory mucosae are
broached by primary pathogens
Canine adenovirus Type I
Canine distemper virus
Canine parinfluenza virus
• Secondary Bacterial involvement greatly complicates the
management of respiratory disease
• Spread to susceptible contacts possible in coteries kennels ,pet-shop
and pet boarding
 RESPIRATORY DISCASES

Young Pets are more susceptible to RD due to

Short and wide air ways –inhalation of noxious

agent

Undeveloped pores of khon –poor callateral

ventilation

Immature connective tissue-easy spread

Immature immunity-poor pathogen in inactivation

 RD

• Adults Susceptible when there is

1. Immunological problems

2.Neoplasm in air passage

3.Congenital defects --Cleft palali

- tracheal collapse

-BC.breeds.
 Respiratory Disorders

There are types respiratory movements

1.Costo-abdominal breathing –usual type (10-30

per min)

2.Costal /pectoral breathing-when diaphragm

plays no part →hepa s, inflamma on)

3.Abdominal Breathing → Pleurisy, IC myositis,

fracture of ribs
 RD
 All diseases of respiratory passage alter RATE and RHYTHM
1. Cheyne- Stokes Breathing.
- Period of apnea followed by shallow respiration which
becomes progressively deeper, shallow and then apnea
- Occur is accident, neurogenic shock and uremic comas
2. Kussmauls Breathing → Bradypnea” heavy respiration“
-Deep respiration for fairly long interval
• Occur in acidosis
 Respiratory Disorder

3 . Tacky pnea
- Shortness of breath –shallow and rapid
breathing
• Occurs in ecalempsia , pyrexia, sepsis

DX .Visual inspection
. Auscultation
 Respiratory Diseases
RHINITIS IN DOGS
• Inflammation of nasal mucous membrane
• Produces serous, mucoid or muco-purulent discharge

ETIOLOGY
.. Viruses- Canine Distemper, Parainfluenza and Canine
adenovirus
.. Bacteria –Bordetella brochiseptica and P. multaicoda
.. Foreign body –grass and food particles
.. Allergens- inhaled hallogens
.. Extension from pneumonia.
 RD
SIGNS
. Rubbing of the nose
. Sneezing
. Nasal discharge
. Epistaxis
. Fever
. Facial deformity
Treatment
. Eliminate primary cause
. B.S. antibiotics
 Respiratory Diseases
RHINITIS in Cats

Virus- F.calci virus and F. Rhinotrachitis virus

The disease process is the same as in dogs.

 RD
Sinusitis

o Inflammation of sinuses

o Rarae in cats

o Usually extends from diseases of adjacent tissue

ex . . Rhinitis

.. Tooth –root disease

.. Turbinate bone fractures

• Affects Frontal and maxillary sinuses

 RD

SIGNS

• Facial deformity

• Heat and pain

• Faced swelling –abstraction of nasal

opening of the safes

 Respiratory Diseases

Teeatment

.B.S Antimicrobials (1-2 wks)

.Surgical drainage –trephining

.Tooth extraction
 RD
Pneumonia

• Inflammation of the gaseous exchange portion of the lung

(alveoli and interstitium)

ETIOLOGY

 . Viral; -parafluenzat,adenovirus type 2

 .Bacteria –Bordetella bronchiseptica

 .Systemic mycosis-Histoplasmosis, Blastomyocosis

 .Aspiration –food, gastric contents,medocations

 Respiratory Diseases

SIGNS

• Tachypnea

• Dyspnea

• Cough

• Fever

• Leukocytosis

• Depression

• Sneezing and cyanosis

 RD
• Dogs with bronchopneumonia.
Soft, high pitch respiratory räles.
• Dogs with exudative pneumonia
Louder, courser, low-pitched räles.
Purulent missal discharge
 Respiratory Diseases
Treatment

dependent on the etiology

 B.S. antibiotics

 Bronchodilators –aminophyline 10 mg 1 Kg 3X /day

 Antimycotic/anitfungal drugs –

 Cough depressant → codaine for severe non –productive cough

 Rest
PLEURAL EFFUSION

• Accumulation of abnormal volume of fluid in the pleural space –normally small

amount of lubricating fluid is there.

• Respiratory problem that affect the equilibrium between fluid absorption and
excretion → Pleural effusion

SIGNS

• Depend on quantity, type and etiology of the fluid

• Increased quantity → lung expression (Pressure on paranchyma ) → Collapse

(atalectasis )→ inflammatory adhesion

• Constant sign is Labored breathing

 Respiratory Diseases
• Non- Productive cough possible

• Muffled heart and lung sound

 RD
DX

 Lab exam of the fluid –edematous, exudate, blood etc.

 Thoracocynthesis -7th -8th IC space just below the cost-chondralt junction

 Culture and cytology of the fuid

. Blood –RBC

LAB . Exudates- neutrophils

. suppurative- bacteria

. Neoplastic- cancerous cells

 Respiratory Diseases
Treatment

. Hemorrhagic effusion -Aspiration (blood in

pleural space does not clot)

 . inflammatory effusion –B.S antibiotics (culture)

. Suppurative effusion – B.S antibiotics-systemic

. Neoplstic effusion - Euthanisia

 RD
Polmonary oedema
• Acumalation of excessive fluid in the lung (alveoli)
• Fluids come from capillaries and enter the interstitial space and
then into alveoli
ETIOLOGY
 Left side heart failure
 ↓ Pulmonary capillary osmosis –Hypoproteinemia
 Obstruction in pulmonary Lymphatic's
 Respiratory Diseases
SIGNS
• Mortly cough-cardiac
• Dyspnea
• Cyanosts
• Discomfort when lying down and
restlessness
 RD
Treatment
• Aimed at removing Odem and increase oxygenation
. Furosamide 4 mg 1 kg
 Diuresis

. Ethacyaric acid 1 mg l kg
 Bronchodilators- Morphine 1 mg 1 kg
 After all RX :remove the primary cause
.
 Cardiovasuclar Disorders
• Heart disease can occur in small animals of any age.
• In young heart failure is mostly associated with
congenital heart defects.
• In middle age animals
• Progressive congenital heart defects
• Inflammatory disorders
• Idiopathic cardiopathy
• Pericardial disease
• Heart failure secondary to other organs function

• In old age
• Chronic valvular defects (mitral and tricuspid)
 Cardiovasuclar Disorders

• All questions of heart disease(problems) are

answered by obtaining:
• a thorough history
• Conducting a physical examination
• Performing electrocardiography
• Thoracic radiography and ultrasonography
 CVD
Suggested sequence for investigation of heart
diseases
1. History
• Distinguish b/n heart disease and heart failure

• Heart failure → t he heart is unable to maintain an

adequate circulation for the need of the body at normal
venous pressure → Decreased ssue perfusion
 CVD
Clinical signs of inadequate blood supply to
tissue  Forward failure
• Weakness

• Exercise intolerance

• Syncope

• Peripheral vasoconstriction

• Prolonged capillary refill time

 CVD
Clinical signs associated with raised filling
pressure results in congestive heart failure
Backward failure
 Coughing
 Dyepnea (pulmoriary edema, pleural effusion)
• Pulmonary edema is the principal sigh of left-
side heart failure.
Increased left atrial pressare Pulmonary venous congestion
edema of Interstitial tissue and alveoli.
 CVD
Causes of left-side heart failure

Valvular diseases

1. Mtral valve

• Endocardiosis ( chronic valvular disease)

• Endocarditis

2. Aortic value

• Congenital stenosis

• Endocarditis
 CVD
Myocardial disease
• Ditaled cardiorugopalhy

• Hypertrophic cardiomyopathey

Left to right shunts

• Patent ductus arteriosis

• Ventricular septal defects

 CVD

Systemic hypertension

• Aortic Stenosis

Arhythymias

• Atria fibrillation
 CVD
 Ascitis and pleural effusion are cardinal signs
of right-side heart failure in dogs and cats.
 RSHF increases right atrial pressure
distension of jugular and hepatic veins
congestion of the liver and hepatomegally.

 CVD
Causes of right –side heart far line
• Valvular diseases
Tricuspid valve disease
• Endocas diosis (chronic valvular disease)
• Endocarditis
Pulmonary value disease
• Endocarditic
• Congenital stenos is
 CVD
Myocardial diseases

• Dilated cardiomyopathry

• Hypertrophic cardiomyopathy

Pulmonary hypertension

• Heartworm disease

Arrhythmias
 CVD
• Cardiac cahexia is a severe wasting associated with chronic
congestive heart failure
• The body weight loss can be rapidly progressive
Signs
• Lethargy
• Lethargy
• Generalized weakness
• In appetence
• Poor hair cost
 CVD
SIGNALMENT

• Bread

• AGE help in raising the index of suspicion

• SEX

• Clinical signs of heart diseases in immature animal strongly suggest

congenital condition

• Acquired disease is common in adult animals but do not preclude

congenital ones.
 CARDOVASCOLAR DISORDERS

• PHYSICAL EXAMINATION
• General condition
• Poor BCS, muscle wasting
• Dyspnea , abdominal l distension

• Mucous Membrane
• Pallor, cyanosis and prolonged capillary refill time

• Peripheral pulse
• Bath femoral pulses : disparity ? tachycardia?

• Jugular Veins
• Distension? heart disease
• Hepato-jugular reflex (Pressure on liver or cranial abdomen  jugular dilation)
 CVD
Palpation of the epicardium
• Cheek the apex beat over the 5th 1.C space
at the left side at the level of Costochondral
junction
• Presence of pericardial thrill  murmur
• Displacement rupture of the diaphragm
 CVD

Cardiac Auscultation
• Auscultation of a thorax is important part of
CVD investigation
• A abnormal heart sounds → cardiac
murmurs
• Cardiac murmurs are caused by alterations
in blood flow through the heart or its major
outflow tracts, which produce turbulence.
 CVD
Ejection Aortic stenosis
pulmonic stenosis
Atrial sepal defect
1. Systolic c murmur Functional murmur (Anemia )

Mitral regurgitation
regurgitation Tricuspid regurgitation
ventricular sepal defect
 CVD
Aortic regurgitation
2. Diastolic murmur  Decrescendo pulmonary Regurgitation
(abnormal filling of heart) Mitral stenosis
Tricuspid stenosis
heartworm disease

3. Continuous murmur  patent ductus arteriosis and other left to right

shank .

Note: The intensity of the murmur do not usually correlates with severity
cardiac pathology.
 CVD

• Radiography (stenosis, endocarditis, etc)

• Electrocardiography (Rhythms, QRS, etc)
• Echocardiography ( diagnostic US )
 Real-time - Chamber sixe
-Wall thickness
-Monition timing
 Myocardial Diseases

Dilated cardiomyopathy (DCM)

Primary myocardial disease is characterized
by cardiac chamber enlargement → impaired
ventricular function, arrhythmia, diminished
contractility and signs of heart failure (mostly
left but both )
 MCD

Cause:

• Unknown

• Nutritional deficiency (carnitineand taurine)

• Hypothyroidism
 MCD
Pathogenesis:
→Loss of contractility is due to defective intracellular
calcium transport
→Myofibril degeneration and fibrous infiltration
ultimately leads to atrial and ventricular dilation,
papillary muscle dysfunction and valvular regurgitation
→Decreased cardiac put  organ blood flow and
systemic venous congestion
 MCD
SIGNS :
• Weakness, lethargy and collapse
• Anorexia and wt loss.
• Abdominal distension, venous distension
• Tachycardia, dyspnea and cough
• Syncope and sudden death
• Poor hair coat, pale mucus membrane
 MCD

Diagnosis:
 CLINICAL SIGNS
 AUSCULTATION
• mitral Tricuspid regergitation
• Ventricular tachy-arrhythmia
• Muffled heart sound
 MCD

Treatment:
• Exercise restriction
• Low sodium diet (avoid water retention)
• Nutritional Supplement (carnitine and tanrine)
• Diuretics (Furosamiade,thiazides)
• Vaso-dilatory drugs
Hydralazine (with diuretic due to water retention)
• Anti arrhythmias
Digoxin, procanamide
• Lidocaine
 FELINE HYPERTROPHIC
CARDIOMYOPATHY

HCM is Characterized by thickening of the left ventricular wall

and inter-ventricular septum
 Left ventricular outflow obstruction
 Impaired ventricular filling due to impaired
relaxation of myocaridium
 Necrosis of myocytes and fibrous infiltration
of myocardium
 usually octets young to mid –age cats
predominantly male ones  inherited defect with
outosomal dominance
 FHCM
SIGNS:
• Acute dyspnea
• tachycardia
• Sudden death
• Pain
• paresis (paralysis of hind-limb and sometime forelimb)
 FHMC

* Asoulation

- Pulmonary crackles

- gallop sound

- soft systolic murmur (regurgitation)

 FHMC
Differential Dx:

• Hyperthyroidism

• Aortic stenosis

• Pleural effusion

Rx: Same as for congestive heart failure

 HAEMOLYPHATIC DISEASES

ANEMIA

• A Condition Characterized by:

A) Redaction in hemoglobin
B) Redaction in circulating
erythrocytes
 HLD
Anemia reflects:
• Increased destruction of RBC
• Decreased production of RBC
• Decreased production of Hemoglobin
The degree of anemia is determined by:
• Level of hemoglobin (MCHC)
• Level of PCV
• RBC wont
 HLD

Characteristics of anemia as determined by

calculated RBC indices:
• Packed cell volume (PCV)
• Mean corpuscular hemoglobin (MCH, MCHC)
• Mean corpuscular Volume (MCV)
 HLD

Reticulocyte count (young RBC) help to rule

out-which of the Two errors has occurred:
1. increased destruction of RBC or
2. Decreased production of RBC
 HLD

• Ex. Marked, sustained reticalocytosis without

increased hemoglobin and PCV increased
cell destruction
• Absence of reticulocytosis → decreased cell
production
 HLD
• Clinical Signs of anemia regardless of the cause
and species
• Pallor of the mucous membranes
• Lethargy, loss of appetite, weakness
• Increased heart and respiratory rate
• Systolic (anemic) murmur due to ↓ blood
viscosity
• Hypotension and which → Acute hemorrhagic
anemia
 HLD
Development of anemia depend on:
• Degree of anemia
• Rapidity of development (Compensatory
Problem )
• Change in the blood volume
• Cardiopulmonary function
• Age of the patient
• Activity of the patient (exercise increased
manifestation of signs)
• Causative disorder
 HLD
Anemia Can be:
1. Regenerative ( Characterized by increased
reticulocytosis
-Blood loss ( hemorrhagic)
-Blood destruction
2. Non –Regenerative (absence of reticulocytosis )
- Nutritional anemia (Fe and Cu)
- hypoplastic / Aplastic anemia
 HLD
BLOOD LOSS ANEMIA
1. Per acute blood loss
-Occurs to due to accidents / donation
-Common is dogs and cats
*The first response is splenic contraction and ECF
shift to plasma and blood volume restoration
(within 12-124 hrs )
*The second response is bone marrow release of
young bold cells –reticulocytes (72 hrs later)
 HLD
Diagnosis:
• Normochromic, normocytic, regenerative
anemia
• Decreased plasma protective
• Platelets decreased in number (due to
consumption) and are larger in size (because
young )
 HLD
Treatment:
• Stop hemorrhage
• Restore blood volume (compatible
transfusion)
 HLD
2. CHRONIC BLOOD LOSS ANEMIA
• Results from continued blood loss exteriorly for a
long time
• This leads it iron-deficiency (decreased in take or
absorption or exhausted reserve )
Dx : Microcytic, hypoctromic, NR anemia
• Ex, hookworm in puppies intestinal neoplasm in
older
• RX: Remove the cause
 HLD
ANAEMIA DUE TO BLOOD DESTRUCTION
1. Hemolytic Anemia
• Due to lysis of RBC or decreased life-span (72-120
days)
• Detected by :
. hemoglbinaemia / icterus
. hemoglobin degradation products
(bilurubin)
. increased young RBC production
 HLD
Clinical signs:
• Anorexia
• Fever
• Anemia
• Haemoglobiurea /icterus
• Marked reticulocytosis
 HLD

RBC destruction can be:

• Intravascular  Hemoglobinuria
• extravascular  lcterus
 HLD
COMMON HAEMOLYTIC DISEASES
1.1. Autoimmune hemolytic anemia
. Common in dogs and cats
. Characterized by :
- Hemolytic crises with PCV less than 10%
-Marked reticulocytosis
-Spherocytosis
-Positive coombs test
 HLD
lcterus is marked in chronic cases due to
ischemic hepatic damage .
The disease is associated with:
• systemic lupus erythromatosis (CLE)
• Rheumatoid arthritis
• Thrombocytopenia
 HLD
• The diseases is an acquired
immunohaematologic state in which the
unknown element has activated the animals
immune system to produce specific antibodies
against its own red cells .
• Binding of these AB’s to RBC elicits
destruction of RBC in R.E.S by way of type III
hypersensi vity / reac on → EXTRAVASCULAR
HEMOLYSIS
 HLD

General approach to treatment: (Though

permanent cure is impossible)
• Inhibition of AB production
→immunosuppressive drugs – predinsolone
2mg/kg (5-10 days ) and 1mg/kg (maintainance)
Recurrence possible, remission unpredictable.
• Removal of the site for cell destruction and AB
production
- Spleenectomy
 HLD
2. INFECTIOUS HEMOLYTIC DISEASES
Feline / canine haemobarotonellosis )
Hemolytic Canine babe sis → both intravascular
• Parasitaemia
• Anemia
• Haemoglobinuiria
• Reticulocytosis
 HLD
• Canine trypanosoniass / lashmaniasis/
histoplasmosis
• No haematria, no reticulocytosis,
spleenomegally, lcterus
→causes cell destruc on through RES.
 HLD
C. Hemolytic Toxic chemicals:
Lead → Heinz body,
Phosphorus deficiency
→ denatured Hg due to oxidant effect.
 HLD
Anaemia due to decreased cell production
• It’s a non-regenerative anemia (Absence of
reticulocytes in the peripheral circulation )
A. Nutritional Anemia
• Rare in dogs and cats (Fe and cu)
• Characterized by microcytic hypochromic
anemia
 HLD
B. Hypoplasion / Aplestic anemia
• Common in dogs and cats.
• Caused by bone marrow suppression.
• Characterized by normocytic, normochrmic
anaemia.
• In case of aplasia  Pancytopenia
• Cases presented as having :
- bleeding  thrombocytopenia
- infec on → panleukopenia
- Anemia → ↓erythropoiesis
 HLD
CANINE LUPUS ERYTHROMATOSIS
• A complex, multi-systemic disorder characterized
by simultaneous or sequential development of
four distinct clinical syndromes
1. Auto-immune hemolytic Anemia
2. Idiopathic thrombocytopenic purpurae
3. Glomerulo-nephritis
4. Rheumatoid polyarthertis (symmetrical)
 HLD
• Thrombocytopenic (low level platelets)
purpurae is characterized by the sudden onset
of :
– Petechae /eccymosis (skin and mucus
membranes)
– Haematuria
– Epistaxis
– Melena
 HLD
Glomerulonephritis
• The renal lesions are evident by persistent
proteinuria
• Uremia is cause of death
• Membranous glomerulonephritis autoimmune
mediated
• Urine with right specific gravity
 HLD
• Serologic abnormities contribute to CLE
• Antibodies against nucleic acids (DNA/RNA )
(Antinuclear AB’S) are hallmark
• AB’S against RBC,platelets, lymphocytes,
throglobulin, nucleoprotein are present in
some individual .
• Rx : Symptomatic
• Prognosis – bad
 HLD
Canine lymphosarcoma
• A cancerous proliferation of lymphocytes
→sided lymphoid tumor
• Commonly seen in dogs over 5 years of age
• 4 forms and clinical signs depend on the
location
 HLD
1. Multicentric form → deseminated form
involves superficial lymph
nodes(symmetrical), liver, kidney and
myocardium.
• They show painless enlargement of lymph
nodes
• Later may obstruct lymphatic flow which
leads to the edema of face and extremities
 HLD

2. Alimentary form
• Diarrhea and vomiting GIT and mesenteric
lymph nodes affected
• Protein-losing enteropathy Emaciation
 HLD
3. Cutaneous form
• Involve mainly skin (sometimes superficial
lymph nodes )
• Common form  multiple firm, raised
red/pale plaques
• Plaques usually non –pruritic.
 HLD
4. Anterior Mediastinal form or thymic form
• Rare
• Respiratory signs –dyspnea
• Respiratory osteodystrophy.
•
 HLD
Dx :
1. Radiography
2. Biopsy (number of immature lymphocytes
with frequent mitotic figures (Reliable)
 HLD
FELINE LEUKEMIA VIRUS ASSOCIALAT DISEASES.
• Contagious disease
• Caused by specific Retrovirus –FeLV (oncrnavirus)
• FeLV causes
– Lymphatic leukemia –blood and bone
– Lymph sarcoma – solid lymphoid tummy
– Myeloproliferative disease
– Aplastic anemia
• FeLV subjects the animal to infectious diseases
 HLD
Signs:
• Cats may show vague signs like anorexia, wt loss,
anemia and sometimes fever
• Dyspnea  mediastinal lymphosarcoma
• Elargement mesenteric lymph nodes intestinal
lymphosarcoma.
• Large and irregular kidneys  Renal
lynphosarcoma
• Posterior paralysis –Epidural lymphosarcoma.
 HLD
Dx :
• PCV often low ( 8-15% )
• NR normocytic, normchromic anemia
• WBC usually normal
• FAT- presence of FeLV
Rx: Feline lymph sarcoma is incurable
Px: Aplastic anemia worsen the prognosis
Diseases of Urinary and
Reproductive System
Fekadu Regassa
 DUS
• In the investigation of urinary tract disease it
is necessary to combine clinical examination
and lab tests
• Generally upon palpation of kidney area there
is painful reaction as can be seen by
– Contraction of loin muscle
– Snapping at the clinician
• But palpation is possible in lean animal
otherwise not easy
 DUS
• Palpation of the bladder is relatively easier,
the degree of thickness and distension and
even contents like stone and tumors can be
assessed
• Lab tests: urinalysis, CBC, serum chemistry
panel;
• Ultrasound and radiographs are important
tolls for investigation of urinary system
disorders.
 DUS
• Urine can be collected as follows
– During micturation
– Catheter method
– Cystocenthesis
The later is better because less risk of vaginal and
preputial contamination
Characteristics of normal urine in dogs
and cats
Item Dog Cat
Color amber yellow yellow
Appearance clear and watery clear
Odor Broth like garlicky
Specific gravity 1.020-1.050 1.035-1.036
Reaction acidic = 6.7 Acidic < 6.7
Albumin trace trace
Sugar negative negative
Ketones 1-4 mg/lt 0-2 mg/lt
Urobilin 2.9-30 mg/lt 0-2 mg/lt
Urea 20% 20%
Indican 2.9-3.0 mg/lt same
Creatinine 0.7-1.87 mg/lt same
 Urinalysis
• to assess the overall health of your dog's
urinary tract,
– including the kidneys and bladder,
– and to check for other health indicators such as
glucose regulation and liver function.
A complete urinalysis usually involves 3 steps:
• Checking and recording the color, turbidity
(cloudiness), and specific gravity of the
sample.
• Performing a chemical analysis using a multi-
test dipstick.
• Centrifuging a small portion of the sample and
examining the sediment (heavier particles)
under a microscope.
Color/turbidity/specific gravity:
• Normal urine is amber-yellow in color and
clear to slightly cloudy.
• Concentrated urine is a darker yellow.
• Dilute urine may be colorless.
• White blood cells may make the urine cloudy.
• Blood in the urine can give a red-brown tinge.
• Specific gravity is determined by placing a
drop of urine into "refractometer."
• Specific gravity indicates how well the kidneys
are able to concentrate the urine.
Chemical analysis:
• Many chemical tests can be performed on a small
quantity of urine by using a dipstick.
• A dipstick is a piece of plastic to which pads of
certain chemical reagents have been attached.
• Each pad will test for a particular substance in
the urine.
• When the urine comes in contact with the
reagents, a chemical reaction occurs which
changes the color of the pad based upon how
much of the substance is in the urine
• The color of the pad is compared to a color chart
and an approximate amount of the substance can
be determined.
Substances are just a few of the chemicals
tested during a routine urinalysis:
-Urine pH This number is a reading of how
acidic or alkaline the urine is.
-Protein Healthy animals will usually not have
any protein in their urine, although in some
cases small, trace amounts may be normal.
• Glucose If the glucose (sugar) in the blood is
significantly higher than normal, some of the
excess will be found in the urine. Normal dog and
cat urine should be negative for glucose on a
dipstick.
• Ketones are substances formed in the body
during the breakdown of lipids (fat). When excess
amounts of ketones are formed, their level rises
in the blood and the urine. Excess ketones in the
urine is termed "ketonuria. Occurs in cases of
starvation, in some diabetic patients, and in
certain other diseases. Normal pet urine should
be negative for ketones.
• Bilirubin is a pigment made by the liver from
dead or dying red blood cells. Small amounts
of bilirubin may sometimes be found in the
urine of healthy dogs. In cats it calls for other
investigation
• Urobilinogen This is a compound formed
from bilirubin by intestinal bacteria. Normal
cats and dogs have small amounts of
urobilinogen in their urine.
• Blood Healthy pets may have a few red blood
cells in their urine, but greater than normal
amounts indicate a problem.
• Nitrites may be produced by the bacteria
present in some infections.
• After a urine sample is centrifuged, the top
liquid portion is poured off, and the heavier
particles in the bottom of the centrifuge tube
are placed on a glass slide.
• Examining the sediment reveals:
– White blood cells Urine sediment should be
examined for the presence of white blood cells.
– Bacteria Urine sediment should be examined for
the presence of bacteria.
– Crystals Microscopic crystals, made up of
minerals, can sometimes be found in the urine.
Common crystals in the urine are struvite
(ammonium magnesium phosphate), calcium
oxalate, and ammonium urate.
– Casts Urine casts are small cylinder-shaped
formations of cells and debris from inside the
tubules of the kidneys. The presence of casts and
their composition can give us more information
about kidney function.
 Chronic Renal Failure (CRF)
• A condition resulting from prolonged and
progressive loss of functional nephrons,
• The condition occurs when the kidneys lose
their ability to function optimally
• Prevalence is equally high in dogs and cats
with age
• Causes: renal diseases like pyelonephritis,
amylodosis, glomerulonephritis, congenital
kidney diseases, etc
 CRF

– Oral ulceration
– Diarrhea
– Severe dehydration Terminal signs
or end stage kidney disease
– Seizures
– Stupor and death
 CRF
Diagnosis:
– No change in urine and serum specific gravity →
isothenuris (low specific gravity of urine, 1.008)
– Occasional WBS and hyaline casts in the sediment
– Elevated BUN and plasma creatinine + inorganic
posphorus
– Severe NR anemia
– Polyuria (rule out reflex polyuria)
– Uremia, hyperkalemia + acidosis (↓ NH3)
 CRF

• To determine the cause perform

– IV pyelogram (contrast →barium chloride, x-ray)
– Urine culture
– Renal biopsy
– ultrsonography
 CRF
• Prognosis depends on:
– The cause
– The extent of associated metabolic defects
– No of surviving nephrons
– Concurrent infections
• Animals can live with it for for long time due
to compensatory hypertrophy and hyperplasia
• Thia is why the disease is unnoticable before
animals are clinically ill
Renal osteodystrophy and NR anemia

CRF ↑ plasma ↓Plasma

PO4 Ca++

↓Yound -NR anemia

↓Erythropoeitin (normcytic and
RBC
normochromic)

Ca++ mobilization
for bones hyperparathyroidism

-Renal rickets
-Osteodysthrophia fibrosa
-Rubber jaw
 CRF
• Treatment:
– First terminate the vomiting dehydration cycle by
mass fluid therapy
• Use lactated ringer’s solution (if hyparkalemia is not
present)
• Correct acidosis → NaHCO3
• Supress vomi ng → an eme c drugs
• Restrict protein diet and use urine acidifiers ((NH4)2Cl3)
• BS antibiotic in bacteruria
• Rest
 Acute Renal Failure (ARF)

• Also called Acute Tubular Necrosis

• Occurs as a result of major insult to the renal
paranchyma
• The condition is reversible if diagnosed and
treated at the earliest possible time
 ARF
• Etiology
– 1. vascular collapse and hypotention → renal
ischemia
• Ex, hemorrhage , overwhelming infections (acute
interstitial nephritis), hypersensitivity, shock, severe
water and electrolyte depletion
– 2. Nephrotoxic substances
• Ex, Mercurials, phosphorus, CCl4, arsenals, antibiotics
(kanamycin, gentamycin, amphotracin B, etc), other
drugs, etc
 ARF
Clinical signs:
– Vomiting
– Anorexia
– Dehydration
– oral ulceration
– Hypothermia
– oligouria/anuria
– hematuria (in case of infection)
 ARF
• Diagnosis:
– Clinical signs
– Lab results are the same with CRF except NR
anemia
– Hyperkalemia is usually present
– Renal biopsy and urine culture to determine the
cause
– Three glass test to determine site of hemorrhage
 ARF

Treatment:
– Immediate attention for restoration of bloob
volume, extracellular fluid (ECF) and elecrolyte
– Monitor urine outflow for many days
– Keep diuresis
– Avoid acidosis
 Glomerulonephritis
• It is an inflammatory lesion of glomerulus and
associated vasculature → especially
glomerular capillary basement membrane
• Some forms are usually immune-mediated →
for example as a sequel to pyometra
• Proteiuria is characteristic of it
• Pale mucus membranes due to anaemia
 glomerulonephritis
• Edema, ascites and emacia on →nephrotic
syndromes
• Hypoalbuminemia and Lipemia
Diagnosis:
• Massive proteinuria
• Renal biopsy for etiology
Rx:
• Relive nephrotic syndromes
• Increase plasma protein
 Pyelonephritis
• An inflammatory disease of the renal pelvis
and paranchyma
• Can be acute or chronic
• Bacteria usually involved are Streptococci,
E.coli and Proteus
• Although can occur as a separate disease
entity infection can be ascending like from
cystitis, calculi, congenital defects,
 Pyelonephritis
• Expect pyelonephritis in case of calculi and
lower urinary tract (LUT) infection
• Clinical signs:
– Depresion
– Fever
– Vomiting (uremic gastritis)
– Polyuria/polydypsia
– Obstruction
 Pyelonephritis
Diagnosis:
– Examination urine sediment reveals WBC, bacteria
hematuria and hyaline casts
– Urine culture (bacteria)
– CBC (LS neutrophilia)
– Ultrasonography/radiography/IV pyelogram
Treatment:
– Long term antibiotics
– Acidify urine
– High protein diet
– High fluid intake encouraged
 Renal amyloidosis

• It is an idiopathic disease characterized by intercellular

deposition of amyloid in the gromerular basement
membrane
• It occurs in all species but common in dogs
• The cause of kidney amyloidosis remains poorly
understood.
• It is a hereditary condition in certain breeds of dog.
• It also may occur in other breeds or mixed breeds as a
reaction to chronic infections and inflammatory
conditions.
 RA
• Most dogs with kidney amyloidosis are old at
the time of diagnosis (9 is average age).
• Amyloid deposits in the kidney lead to
excessive protein loss in the urine and
eventual chronic kidney failure.
• Amyloid may also be deposited in other
organs like the liver, spleen and pancreas,
causing them to malfunction as well.
 RA
Clinical signs:
• Excessive thirst
• Excessive urination
• Poor appetite
• Weight loss
• Intermittent vomiting
• Labored breathing due to thromboembolism
(blood clots in the lungs)
• Ascites (fluid accumulation in the abdomen)
• Edema (swelling of the limbs and/or face)
 RA
Diagnosis:
• Complete blood count and chemistry panel
• Urinalysis
• Urine protein/creatinine ratio
• X-rays
• Biopsy of the kidney
 RA
• Identify and treat any underlying infectious or
inflammatory condition that may have led to
the amyloidosis
• Manage any concurrent kidney failure
• Dimethylsulfoxide (DMSO)
• Colchicine (oral AID)
 Hydronephrosis
• HN is characterized by a dilation of the renal
pelvis caused by partial or complete obstruction
of to urine outflow
• Bilateral/complete obstruction is fatal and
changes are less extensive due to short life of
pateints
• In unilateral/partial obstruction the patient can
survive with pressure atrophy to ranal
paranchyma and cystic enlargement
• Hydroureter is the concurrent condition
depending on the site of obstruction
 HN
Etiology:
• Infection of renal pelvis
• Ureter
• Bladder
• Tumors
• Calculi
• External pressure (gravid uterus, prostate
enlargement)
Clinical signs:
• Longstanding due to componsation
• Vomiting,
• pain (palpation)
• Anorexia
• Terminal uremia (in bilateral case)
 HN
Diagnosis:
• Clinical signs
• Radiography/ultrsonography
• IV pyelogram
Treatment:
• Primary objective is to restablish urine outflow
by removing obstruction (catheter, surgery,
drugs, etc)
 Congenital kidney diseases
1. Renal hypoplasia
• Diminished renal cortex → common in dogs
2. unilateral renal agenesis
• One kidney and its associated uriter are
absent → common in cats
 Uremia
• Represents the final/end/terminal stage of
kidney disease
Clinically increasingly marked by:
• lassitude (tiredness) that may progress to
complete apathy (indifference)
• Loss of skin elasticity
• Emaciation
• Marked polydypsia
 Uremia
• Auto-intoxication due to failure of kidneys to
excrete waste
• Urinous odor of the breath
• Ulcers on the mouth, tongue and grey-green
deposits
• Persistent vomiting, finally blood appears on
vomitus → gastri s
• Slow deep respiration (Stokes-kyne breath)
• Later muscular spasm and convulsion
 Uremia
• The affected dog may become unuric or
oligouric → severe nephri s
• ↑ BUN with corresponding hypochloremia, in
this progressive hypochloremia the prognosis
is unfavorable due to loss of anionic state of
the blood → acidosis.
• Finally death in uremic coma
 Uremia
Treatment:
• Same as for renal diseases
• Rinse oral lesions
• Correct acidosis
• Avoid urinary incontinence or make sure urine
flows freely, ie, no obstruction (calculi or
paralysis of bladder)
 Lower urinary tract disorders
Cystitis
• It is an inflammation of urinary bladder
• It occurs due to three main causes
1. Ascending urinary tract infection (in most
cases ascension of E. coli, Staphylococcus,
proteus, pseudomonas, etc, from urethra)
2. Hematogenic infections (TB, tumor, etc)
3. Trauma (iatrogenic, accident)
 LUT disorders
Predisposers to cystitis:
• Urine stasis
• Neurologic disorders of micturation
Clinical findings:
• Pollakiuria (frequent urina on → TDO is normal)
• Hematuria
• Dysuria
• Straining
• Unproductive urinating stance
• Ammoniac odor of urine
• Urine is viscous and stringy
 LUT disorders
Diagnosis:
• History
• Distended bladder → urethral obstruc on
• Thickened, small and firm bladder
• Rule out prostate disease
• Radiography/ultrasonography
• Urinalysis (↑WBC, RBC, bacteria, transi onal
ept, alkaline pH)
 LUT disorders
Treatment:
• Acidify the urine
• High protein diet
• BS antibiotic
 LUT disorders
• Bladder tumors:
• A bladder tumor must be considered a
possible cause for ant LUT disorders,
especially when the patient is an older pet 7
years and above
• Also the cases is rare it usually bears a grave
prognosis
• All breeds of dogs and cats are susceptible
 LUT disorders
Clinical signs:
• Urinary incontinence
• Stranguria
• Hematuria
• Dysuris
• Polyuria/polydypsia
• Urinery obstruction
 LUT disorders
Types of bladder tumors:

• Transitional cell tumors

• Liemyyoma
• Prostate adenocarcinom
• Liemycarcinoma
• Cystic papiloma
• Hemoangiocarcinoma
• Seminoma
• unknown
 LUT disorders
Causes of canine bladder tumor:

• Industrial chemicals, Ex, β-naphthylamine,

benzidine
• Metabolites of trptophan
• Chronic irritation
• Virus
• Foreign bodies
• Bracken fern
• Drugs, Ex, cyclophosphamide
 LUT disorders
• Bladder cancer seems to occur more
frequently in dogs than in cats
• One theory states that this is because of
difference between dos and cat in metabolism
of tryptophan or their susceptibility to
tryptophan metabolites
 Polyuria and polydypsia cycle
Always water consumption and urine production
are controlled by complex interaction of:
– Plasma osmolarity
– The thirst center
– The kidneys
– Hypothalamus and
– Pituitary gland
 Polyuria/polydypsia
• Presence of polyuria (PU) and polydypsia (PD)
suggests that something has gone wrong in
the area of hypothalamus-pituitary renal axis
• Different failures can result in PU/PD. But
central or pituitary PU/PD is the least common
• Cause for central PU/PD:
– congenital damage to hypothalamus or pituitary
gland
– Trauma to the head (acquired)
 Polyuria/polydypsia
• The most common cause of PU/PD in dogs
and actsare:
– Inadequate production of intracellular CAMP in
the renal tubular cells
– The loss of renal medulary hypertonic
environment
 Polyuria/polydypsia

Failure of production of Failure of ADH to react

CAMP in cells of DCT tubular receptors that
and CD activate adenylate cyclase
system

Acquired
or
Secondary diabetes insipidus
 Polyuria/Polydypsia

ATP
ce
ce
3’5’cAMP Activate kinase
Iio messanger system
receptor
ADH
Io messanger

Cell membrane
Cellular response
Adenylate cyclase system (effect depends on
the target cell)
 Polyuria/Polydypsia
• ADH promotes facilitated absorption of water by
rearranging the intracellular microtubules and
microfilament of DCT and collecting duct cells to form
micro-pores or it opens the pores in the luminal
membrane of the tubular cells
• The anti-diuretic activity of ADH is entirely dependent
on the presence of the osmotic gradient of the renal
parenchyma or renal medullar hypertonic interstitium
composed of primarily urea and Na+ and maintained by
a highly specialized renal vascular system-vasa recta
 Polyuria/Polydypsia
↓effec veness Loss of passive
Loss of hypertonic of osmotic absorption of
interstitium gradient water from renal
ultrafiltrate

Thirst IIo Polydypsia

Aortic osmoreceptors center

More urine
Hemo-concentration Polyuria produced
and ↑osmolarity
 Polyuria/Polydypsia
• This loss of renal hypertonic interstitium can
be absolute or relative
1. Absolute loss:
– Results from body’s inability to supply osmotic
particles necessary to maintain medullary osmotic
gradient (Ex, failure of liver in urea and albumin
production
– Results from excessive loss of osmotic particles,
most commonly from increased blood flow in vasa
recta (Ex, pyelonephritis, hyperthyroidism ↑aldo.)
 Polyuria/Polydypsia
2. Relative loss
– Occurs as a result of increase in the number of
osmotic particles in the tubular ultrafiltrate (Ex,
diabetes melititus
– This reduces the osmotic gradient between the
renal medullary interstitium and renal tubular
filtrate
 Polyuria/Polydypsia
• Ployuria can be primary:
– It occurs regardless of the underlying cause when
there is hypothamalic-pituitary-renal axis
dysfunction
Hyperosmolarity/ Aortic osmo-
Primary receptors
polyuria hypovolemia

Compensatory or
secondary polydypsia
 Polyuria/Polydypsia
Plydypsia can also be primary
• However, the etiology is unknown but the
following are considered possible psychogenic or
physiologic causes:
• Changes in the environmental temperature
• New introduction to the member of family
• Boredom
• misperceived of previous water deprivation
• Hyperactivity with less exercise
 Polyuria/Polydypsia

Psychogenic or Overhydration and ↑ blood flow

primary hypoosmolarity through vasa recta
polydypsia

↓Medullary interstitial
hypertonic environment

Compensatory or
Secondary polyuria
 Polyuria/Polydypsia
Diagnosis of Polyuria/Polydypsia
• Normal water consumption
– Dogs 60-70 ml/kg bwt/day
– Cats same as dogs or little less
• Normal urine output
– Dogs 21-41 ml /kg bwt/day
– Cats 22-30 ml/kg bwt/day
 Polyuria/Polydypsia
• During diagnosis identify the physiologic
responses to change in environmental
temperature, increased consumption of water
with food and pathological occurrences
 Urinary Incontinence
• To maintain urinary continence:
– The ureters must empty urine into the urinary bladder in the
correct location
M
i
– The bladder must of urine to accommodate the increasing
c
volume
t– The urethra must exert a tone greater than the resting pressure
u within the bladder
r– The neurologic pathway must be intact
• a For normal urination to occur
U t
r i – The bladder must be able to contract
i o – The bladder contraction must be coordinated with urethral
n n sphincter
a – The neurologic pathway must be intact
 UI
• UI is an involuntary passage of urine
• Cause; disorder may involve:
– Storage of urine
– Voiding of urine
– Or both

• UI may be caused by to two factors:

– Non-neurologic cause
– Neurologic cause
 UI
Non-neurologic causes:
a) Congenital conditions, seen in young pets
• Ectopic ureters
• Patent urachus
• Urethral diverticulum
b) Submissiveness -young pets
c) Chronic cystitis
• Fibrosis leads ↓detrusor muscle tone and transitional
epithelium capacity
d) Iatrogenic
• Post-surgical adhesions → ↓ bladder capacity
 UI
e) Severe urethral inflammation
• ↑ urethral incon nence
f) Urethral calculi with partial obstruction
g) Urethral luminal /extra-luminal masses →
tumors
h) Hormone-responsive incontinence
• Common in neutered pets
i) Polyuria
 UI
Neurologic causes:
• Mainly spinal injuries
– Spinal traums
– Spinal tumors
– Herniated vertebral discs
 UI
• Location of the injury to the spine is imprtnt
• 1. Lower motor neuron (above L5-L7)
– Detrusor reflex nor
 UI
Upper motor neuron (above L5-L7)
•Detrusor reflex normal
•Lack voluntary control of urethral
sphincter which leads to overflow of urine
when bladder pressure exceeds sphincter
resistance
•Perineal reflex normal
Lower motor neuron (sacral segments)
Dterusor areflexia
No voluntary control of urethral sphincter
Preineal reflex absent leading to tail
paralysis, fecal incontinence
Bladder is balloon-like when empty by
catheter or expression
 Treating urinary incontinence
• Give specific treatment of the underlying
cause
• Surgical Rx:
– Correct anatomic defects
– Remove urinary calculi
• Training
– correct behaviour (submissiveness)
 Treating urinary incontinence
• Rational drug therapy:
– Small bladder capacity → anticholinergic drugs
(smooth muscle relaxant)
– Detrusor atony → cholinergic drugs (muscle toner),
but check urethral patency otherwise rapture or urine
reflux into pelvis
– Decreased urethral tone → drugs that s mulate
sympathetic alpha receptors
– Increased urethral tone → sympathe c alpha blocking
agents or smooth muscle relaxant
– Hormone-responsive incon nence → Testosterone
and estrogen
 Disease of the Female Genital System
• Pyometra → an accumula on of pus in the
uterus
• Ultimately, pyomtra results from excessive and
prolonged stimulation of the uterus by
progesterone produced by persistent and or
cystic corpora luthea
 Pyometra

Cystic
Continuous
Persistent CL endometrial
P4
or cystic CL hyperplasia
Stimulation

Acute inflammation
and
Secondary infection

Pyometra
 Pyometra
• Patency of the cervix in pyometra is variabl
but the closure worsens clinical signs or
results in severe manifestations
• Although the disease is not initiated by
microorganisms their presence is often
followed bacteremia/septicemia/toxamia
• Organism most commonly involved are E.coli
and Streptococci
 Pyometra
Clinical signs:
• Occurs in dogs >6 years of age
• Signs begin 1-12 weeks later
• First sign is anorexia followed by depression
• Loss of condition/body weight
• Polyuria/polydypsia (due to failure of kidney
to concentrate urine)
• Vomitting frquently (due to gastritis)
 Pyometra
• Initially elevated body temperature, as a
condition progress the temperature falls and
finally becomes subnormal
• Progressive weakness develops and later the
bitch becomes recumbent
• Abdominal palpation reveals enlarged and
painful uterus (do not excessively palpate)
• There may be vaginal discharge and may be
intermittent (fetid odor)
 Pyometra
Lab finding:
• ↑ WBC count 20,000-100,000 with left-shift
degeneration
• Highest count with closed cervix
• Subnormal count in toxamia due leukopenia
• Normocytic, normocromic anemia common
• ↑ BUN due to poor renal perfusion
 Pyometra
Diagnosis:
• History
• Clinical signs
• Lab data
 Pyometra
Treament:
• Ovarohysterectomy-the best
• Supportive treatment –lactated ringers sol
• Antibiotics BS-bacteremia/septicemia and
postoperative infection
• PGF2alpha –variable result
 Acute Metiritis
• Acute metritis is an acute inflammation of the
uterus
• It is usually a disease of post-partum period
• It is often seen as a result of dystocia, retained
fetal membranes, obstetrical manipulations
and abortion
• Always followed by delayed uterine involution
due to enlarged frail and flaccid uterus
 Acute Metiritis
Clinical signs:
• Usually begins 1-3 days following parturition
and can be associated with any of the
following
• Fever
• Anorexia
• Vaginal discharge –fetid
• Loss of interest in puppies
 Acute Metiritis
Diagnosis:
• History –reference to the time of delivery
• Physical exam reveals thickened uterus/
retained fetal membranes
• Lab data -leukocytosis
 Acute Metiritis
Treatment:
• Oxytocin – 1 unit/kg in 2 hrs interval
• Intra-cervical infusion of antibiotics for 3-4 days –
oxyttc, Do not enter the uterus
• Systematic Rx- Oxyttc
• Estrogen (0.5mg/kg)- to increase the effect of
oxytocin on mymetrial activities
• Lactated ringers IV
• If no response resort to ovarohyterectomy.
 Pseudo pregnancy
• Pseudopregnancy is syndrome of physiological
and behavioral changes in non-pregnant
metestrus female
• It follows ovulation which results in the
formation of CL whether or not fertile mating
has occurredin bitches
• Therfore, it is associated with P$ activity of
the persistent CL
 Pseudo pregnancy

• Can be encountered in both young and old

and can recur after each estrus
• May lead to pyometra in older dogs
• The condition in cats occurs only following
infertile mating
• This is because cats are induced ovulators
 Pseudo pregnancy
• Not caused by progesterone because it can be
caused by removal of CL during luteal phase
• The main reason for appears to be
heavy/sharp decline in P4 after 45 days estrus
causes elevation of prolactin, a polypeptide
protein, responsible for lactation
 Pseudo pregnancy
• Bitch PO
1-3 d

E
7-9d

Anoestrus
Until BS Pregnancy
58-63d M
2-3d

Pseudo
pregnancy
50-80d
 Pseudo pregnancy
• cat PO If no coitus at BS/FA
1-3 d
E
The end of BS +no coitus 5-10d
During BS

During BS copulation
Anoestrus
Until BS Pregnancy
58-63d M
2-3d

Pseudo
pregnancy
50-80d
 Pseudo pregnancy
Clinical signs:
• Enlargement of mammary gland 6-12 weeks
after estrus
• Restlessness
• Nervousness
• Nesting/bedding
• Mothering inanimate object
• Milk ejection
 Pseudo pregnancy

Diagnosis:
• Established from history
• Clinical data - ↓ P4; ↑ prolactin
 Pseudo pregnancy
Treatment:
• Progesterones, androgens, oestrogens and
combinations given in depot or daily oral dose
• But long treatment period and reducing dose
regimen may be required
• Persistent cases can be treated with dopamine
agonists (suppress prolactin) – bormocriptine
(but control vomiting with metoclopromide)
 Pseudo pregnancy
• Also carbergolamine can be used as an agonist
and there is no vomiting
• To stop recrudescence resort to OVHX
 Pseudo pregnancy
• Pseudo pregnancy in cats is a term used for
non-pregnant lutheal phase since it only
follows sterile mating
• The only sign are absence of estrus in BS
• Cats are seasonal polyestrus
• Mammary development, lactation and
behavioral changes are not features of pseudo
pregnancy in cats
 Prevention/termination of pregnancy
• 1. Keep males away
• OVHX
• In case of mismationg occurs in breeding
females use:
– Estradiol cypionate –good for cat and dog
• Prevents embryo implantation
• Give within 2 days of mismating
• Not 100% effective though
– Dieethylstilbesterol -only for dog
 Genital emergencies in Female
1. Dystocia
• It is difficult birth
• Especiallt, when the 2nd stage of labor is
markedly prolonged resulting in difficult or
impossible delivery
• Dystocia is regarded to either maternal or fetal
in origin
 Genital emergencies in Female
• However, it should be considered in relation to defect in 3
components of birth process:
– In the expulsive force
– In the birth canal
– In the fetus per se
• Maternal causes:
– Primary uterine inertia
• Obesity
• Lack of exercise
• Infection
• Toxocity
• Chemical defect – ca++, oxytocin
• Permature birth
Genital emergencies in Female
– Secondary uterine inertia
• Muscle fatigue
– Obstruction
– Stenosis
– ↑li er size
 Genital emergencies in Female
Fetal causes
• Oversize
– Absolute oversize. Usually due to mismating and
small litter size
– Relative oversize mainly due to small pelvis
– Defomity (monsters like hydrocephalus)
– Death (reorientation and fetal hormones to
initiate parturition
 Genital emergencies in Female
Clinical stages of labor
Stage I
• Restlessness, body temperature falls, anorexia
and vomiting
• 2-12 hrs fetus pushes into the cervix, allanto-
chorion raptures (rapture of the water bag)
 Genital emergencies in Female
Stage II
• Acute labor and expulsion of the fetus1-2 hrs
later(after rapture of the water bag)
• Dog may rest 30-90 minutes between delivery
of each pup.
• This stage may take 30 hrs
 Genital emergencies in Female
Stage III
• Consists of expulsion of the placenta
• Placenta can be passed
– With the fetus
– Just prior to succeeding delivery
– 10-15 min after the last fetu
– s in bunch
 Genital emergencies in Female
Diagnosis of dystocia
• History and clinical signs and examination
• Dystocia is anticipated:
– Within 4-6 hrs after the 2nd stage labor has occurred
(normally the bitch aught to have delivered with 1-2
hrs after the onset of the 2nd stage of labor)
– 4 hrs since the last fetus is delivered and there has
been no labor
– When toxamia is present
– When there is bad smelling vaginal discharge
 Genital emergencies in Female
• Treatment
• Use drugs that stimulate uterine contractions
(if cervix is open)
• Manually manipulate the fetus
• Cesarean section if females are for breeding
• Ovaro-hyterectomy- if female is not for
breeding
 Genital emergencies in Female
2. Uterine prolapse
• It is protrusion of the uterus through the cervix
• Occurs during or after parturition
• One or both horns may be involved
• There is straining due to retained fetal
membranes or dead fetus
• Metritis usually precedes the event
• Prolapse may be partial or complete
• Complete prolapse can result in rapture of the
broad ligament, abdominal bleeding and shock
 Genital emergencies in Female
Treatment :
• Replace the prolapsed uterus with manual
tradition
• Prevent infections by antibiotics
• Inject oxytocin after replacement
• If irreplaceable due to risk of shock perform
ovaro-hysterectomy
 Genital emergencies in Female
3. Puerperal Tetany/ Ecalempsia
• Usually occurs in bitches and queens within 3
weeks following parturition
• It also occurs in immediate pre-partum period
• The reduction in the rate of magnitude of
ionized ca++ influences the onset and severity
of tetany
– Total calcium = ionized (ultra- filterable) + protein
bound
 Genital emergencies in Female
• The mechanism by which absolute or relative
hypocalcemia develops is not well defined
• Anyway it appears to involve any stage of
calcium metabolism
– Intake
– Absorption
– Excretion
 Genital emergencies in Female
Clinical signs:
• Nervousness or anxiety →pacing whining and
panting
• Ataxia with stiff-legged gait and then spastic
lateral recumbency
• Signs last minutes to hours
• Febrile due to rigorous muscle spasm
• Death due to respiratory distress or hyperthermic
cerebral edema
 Genital emergencies in Female
Diagnosis:
• Heavily depends on a compatible history of
parturient or post-parturient bitch/queen
• Typical signs
• Differential Dx →strychnine poisoning
• Do not wait for lab confirmation but take pre-
treatment blood sample
 Genital emergencies in Female
• Treatment:
• Slow IV administration of 5-10 ml of a 10%
calcium solu on → Calciumgluconate
• If therapeutic dose of calcium fails treat for
respiratory alkalosis and hypoglycemia →
bicarbonates and glucose solution
• If no response to glucose solution analysis of
the pretreatment blood sample aids definitive
diagnosis
 Genital emergencies in Male
1. Paraphymosis
• A condition where the enlarged and
edematous penis cannot be retracted into the
preputial cavity per se
• It usually follows coitus or masturbation
• The glans penis is engorged the preputial
orifice acts as constricting ring and hence
venous congestion and erection is sustained
 Genital emergencies in Male
Treatment:
• Reduce edema by use of cold hypertonic
glucose solution
• Reinsert the penis into the sheath
• If difficult sugically incise the orifice ventrally
and replace the penis after proper cleaning
• Apply local antibiotics
*to avoid reoccurrence castrate the dog
 Genital emergencies in Male
2. Trauma to penis and prepuce
• Fracture of the os-penis
– Palpation
– Surgical tx
• Rapture of penile urethra
– Surgical Tx
• Preputial edema/swelling due to hematoma/abcess
– If minor, cleaning and topical tx with antibiotics
– Let it heal as open wound
– If complicated → surgical procedure
 Genital emergencies in Male
3. Orchitis
• Inflammation of the testes
• Acute bacterial orchitis may be febrile, testicles
are swollen and painful to palpation
• Treatment:
– 14-21 days of antibiotic to ensure eradication
– Anti-inflammatory gruds to reduce edema
– If no response to Rx (if febrile and soft testicles)
castration recommended
*Serum evaluation for brucella is indicated
 Genital emergencies in Male
• 4. Proststic enlargement
• The condition is usually found in older dogs
• The clinical practice reveals difficulty in
micturation and defecation
• Diagnosis can be made from clinical signs assisted
with palpa on of the gland →swelling
• Swelling can be caused by
– Tumor → hard and irregular
– Hypertrophy → semi-solid consistency
– Abscess → fluctua on
 Genital emergencies in Male
• RX:
• Large dose of estrogens 3-4 times per week
• Ligation of vas deferens
• Castration
• Prstatectomy, but difficult