VIN Feline Info Flashcards
1
Q
Topic: FeLV
1. What type of viral disease is this?
2. How is this disease transmitted?
3. Describe the clinical signs.
4. How is this disease diagnosed?
5. How is this disease treated?
6. How is this disease prevented? What are the key risk factors.
7. What is the prognosis of this disease?
A
- A retroviral disease
- Transmitted via saliva, specifically via close, intimate contact and mutual grooming. Transmission by biting can occur but is infrequent!! Transmission may also occur through reuse of instruments and blood.
- Cats may shed the virus for months to years.
- Virus is shed in saliva, tears, urine, and feces. - Can be asymptomatic. If exhibiting c/s:
- Lymphadenopathy
- Oral lesions – gingivitis, periodontitis, stomatitis, oral ulcers
- Neutropenia, fever, development of opportunistic infections (particularly skin or respiratory infections).
- Severe emaciation
- Lymphoid depletion
- Common to see concurrent or opportunistic diseases
- Fungal – Cryptococcus, Aspergillus, dermatophytes
- Parasitic – Toxoplasma, Demodex, Hemobartonella, Giardia, Coccidia, Cryptosporidia
- Atypical bacterial – Mycobacteria, Nocardia, Actinomyces - ELISA – Detects a core antigen. Neither maternal antibody nor recent vaccination will affect the test.
● If a healthy cat tests positive: AAFP guidelines recommend confirming a positive FeLV ELISA with immediate IFA testing to differentiate between an actual vs. a transient infection. Another option is to re-test in 1-3 months because up to 98% of cats infected with FELV will have a transient, self-limiting infection, develop antibodies and then become antigen-negative. - Treat any concurrent infection, oral prophylaxis, etc.
- Key risk factors:
a. Age: Young cats are much more naturally susceptible
b. Indoor/Outdoor: Cats in close contact with other cats are most susceptible
c. Vaccine given as 2 injections 2-3 weeks apart in kittens 8-9 weeks or older, booster annually. - Up to 98% of cats may only develop a transient infection, but cats with progressive infection die
within 3 years 80% of the time.
2
Q
Should you vaccinate a cat that is FeLV positive?
A
There is NO reason to vaccinate a cat that is FELV-positive because:
a. Cats remain FELV positive despite vaccination
b. Cats remain infectious despite vaccination
c. Cats have the same risk of developing clinical signs despite vaccination.
d. The vaccine will not result in a positive test
3
Q
Topic: FIV
1. What type of viral disease is this?
2. How is this disease transmitted?
3. Describe the clinical signs.
4. How is this disease diagnosed?
5. How is this disease treated?
6. How is this disease prevented? What are the key risk factors.
A
- A retroviral disease
- Transmitted by bite wounds in most cases. An “unfriendly” cat disease. Cats can live with FIV for years particularly if identified and managed.
- Can be asymptomatic. If exhibiting c/s:
- Lymphadenopathy
- Oral lesions – gingivitis, periodontitis, stomatitis, oral ulcers
- Neutropenia, fever, development of opportunistic infections (particularly skin or respiratory infections).
- Severe emaciation
- Lymphoid depletion
- Common to see concurrent or opportunistic diseases
- Fungal – Cryptococcus, Aspergillus, dermatophytes
- Parasitic – Toxoplasma, Demodex, Hemobartonella, Giardia, Coccidia, Cryptosporidia
- Atypical bacterial – Mycobacteria, Nocardia, Actinomyces - ELISA is not a confirmatory test and should be verified by Western Blot.
● Both tests are antibody-based
● It is generally useless to test kittens under 6 months of age as they may not have seroconverted (i.e. False negative) or they may have interference with the test from maternal antibodies (i.e. False positive). - Treat any concurrent infection, oral prophylaxis, etc.
- Key risk factors:
a. Indoor/Outdoor – Outdoor cats are much more likely to be bit.
● Given as 3 injections 2-3 weeks apart in kittens 8-9 weeks or older, booster annually.
● Vaccine is considered 80% effective
● Vaccine will result in a positive test on all commercially available antibody tests.
4
Q
Topic: Feline Panleukopenia
1. What is the etiologic agent?
2. List the clinical signs
3. How is this disease diagnosed?
4. How is this disease treated?
5. How is this disease prevented?
6. Who has the highest risk of mortality?
7. How is this disease prevented?
A
- feline panleukopenia virus (FPV) is closely related to canine
panleukopenia parvovirus (CPV) but does not affect canids - Mostly subclinical, especially in adult cats
- Fever (or hypothermia) Depression, lethargy, hiding, Anorexia Vomiting (may be induced by abdominal palpation), Rapid dehydration Thick bowel loops, Sudden death (“fading kitten syndrome”), +/- Diarrhea
- Cerebellar signs secondary to hypoplasia from in utero or perinatal infection (cerebellar hypoplasia or “CH” cats) Hypermetria, Ataxia with no weakness, Intention tremors and head bobbing - CBC: Leukopenia (50-3,000 WBC/μL), especially neutropenia. Cage-side immunochromatographic test kit for fecal for CPV; often see false-negatives or false-positives
(recent vaccination).
- Cerebellar hypoplasia diagnosis is based on history, signalment, and exam findings - Supportive care & Isolation
- Aggressive IV uid therapy with isotonic crystalloid solution spiked with B vitamins; +/- add 5% dextrose
- Broad-spectrum antibiotics for secondary infections
- Fresh-frozen plasma if available
- Anti-emetics (e.g., maropitant, ondansetron, metoclopramide)
- Kittens with cerebellar hypoplasia may need early assistance with feeding - Kittens under 5 mo have the highest mortality
- Inactivated or modi ed-live vaccine starting at 6-9 wk of age then every 3-4 wk until kitten is at least 16 wk of age, then annually (do not give modi ed-live vaccine to pregnant queens)
5
Q
Topic: FIP
1. This is a disease of cats within what age group?
2. Etiologic agent?
3. How is this disease transmitted?
4. List the clinical signs
5. How is this disease diagnosed?
6. How is this disease treated?
7. How is this disease prevented?
A
- 6 mo to 2 yrs most commonly
- FIP develops from mutation of feline enteric coronavirus (FECV). Nearly all cats are exposed to
FECV but only a fraction will develop FIP. - Via fecal-oral transmission.
- There are two forms of the disease: wet and dry
- Effusive/wet: Characterized by widespread vasculitis. Leaking of protein and fibrin rich fluid into pleural and peritoneal cavities.
- Dry form: Granulomatous reaction in tissues. May involve nervous system, kidneys, eyes, lymph nodes or other sites. More difficult to diagnose. - Effusive Form - Fluid analysis (Rivalta test) is key to diagnosis
a. Is Typically dark yellow, sticky and viscous
b. Non septic, high protein (globulins), A:G ratio <0.4
● Dry Form - Challenging diagnosis but some common findings include
a. Mature neutrophilia, lymphopenia, non-regenerative anemia and a hyperglobulinemia.
b. Serology for feline coronavirus is available but can be difficult to interpret.
c. Gold standard of diagnosis remains histopathological examination of biopsied tissues. ***
i. Characteristic changes include perivascular pyogranulomatous inflammation. Often involving ileum, colon, mesenteric lymph nodes and liver. - No effective treatment/cure
a. Cyclophosphamide (Cytoxan) and corticosteroids are palliative and may reduce signs.
b. Occasional reports of treatment with interferon gamma or pentoxyfylline. - Vaccine:
a. Licensed for use in kittens over the age of 16 weeks. However, kittens may become infected after maternal antibodies wane at 4-6 weeks.
b. The current vaccine can result in false positive FECV titers
● Best prevention measures are good cattery procedures
a. Hygiene is essential. The virus is relatively unstable outside of the host and susceptible to most detergents but may persist up to 2 weeks.
b. Good nutrition, general health status, sanitation and avoiding overcrowding.
c. This disease may be a problem even in a well maintained cattery
6
Q
Topic: Rabies
- List the major clinical signs seen in feline patients with rabies.
- How is this disease diagnosed?
- How do you manage exposed UNVACCINATED pets?
- How do you manage exposed VACCINATED pets?
- How do you manage exposed UNVACCINATED humans?
- How do you manage exposed VACCINATED humans?
- What happens if a healthy animal, regardless of rabies vaccine status, bites a human?
- What happens if a stray animal bites a human?
A
- Behavior change (aggressiveness, excitability or irritability, hiding (wild
animals may become less fearful of humans) and/or vocalization are key signs that should lead you to think about rabies. - The Direct Fluorescent Antibody Test detects viral antigens and should be tested on two locations from
the brain (brainstem and cerebellum) and is the test of choice for rabies diagnosis. - If an unvaccinated pet is exposed to a rabies suspect, they are either euthanized immediately or given a rabies booster and then quarantined for 4 months (dogs and cats) 6 months (ferrets).
- If a vaccinated pet is exposed to a rabies suspect they are boostered and then quarantined for 45 days with owners. If the patient is overdue for a vaccine but has gotten one in the past, the same protocol applies.
- Give post exposure prophylaxis with rabies IG AND rabies vaccine on day of exposure on days 3,7,14.
- Gives a vaccine on day 0 and day 3.
- Quarantine animal for 10 days, DO NOT VACCINATE. Report to local health department. Euthanize and submit if any symptoms develop.
- Euthanize and submit for rabies testing immediately.
7
Q
Topic: Feline Hyperthyroidism
- What is the etiology of feline hyperthyroidism?
- What are the key clinical signs of a patient with hyperthyroidism
- How do you diagnose this disease?
- What is the preferred screening test?
- What other tests should you run? - How is this treated? List the side effects.
- What is a common comorbidity in cats with hyperthyroidism?
A
- Hyperthyroidism most commonly occurs in cats due to adenomatous hyperplasia of
the thyroid glands but can also be due to a functional thyroid carcinoma. - Key historical signs include weight loss, polyphagia, vomiting, hyperactivity.
- Elevated ALT, ALP, AST, Erythrocytosis, Hypertension
- Serum total T4 level is the preferred screening test for hyperthyroidism (>4.0 ug/dl)
- Free T4, TRH Response Testing
- T3 suppression Test - A. Oral Methimazole – treatment of choice for initial therapy; Methimazole inhibits thyroperoxidase, a crucial enzyme in synthesizing thyroid hormones. This mechanism decreases the synthesis of thyroid hormones, specifically thyroxine (T4) and triiodothyronine (T3), restoring normal thyroid function.
- Can be stopped or reduced if renal values increase
- Possible side effects: Facial excoriations, Thrombocytopenia, anemia, agranulocytosis, Hepatopathy
B. Surgery – Thyroidectomy
- Usually bilateral disease requiring bilateral thyroidectomy
- Possible side effects and surgical complications: Iatrogenic hypoparathyroidism (hypocalcemia), Hypothyroidism, Horner’s syndrome, Laryngeal paralysis (voice change)
C. Radioactive Iodine
- I-131
- Single dose, requires hospitalization, usually for several days to weeks, depending on state
radiation laws.
- Possible side effects
- Iatrogenic hypothyroidism requiring T4 supplement (<5%)
- Undertreatment requiring retreatment (5%) - It is important to monitor renal function because renal insufficiency is a common comorbid condition and the presence or severity can be masked by hyperthyroidism.
8
Q
Topic: Feline Respiratory Diseases - Rhinotracheitis
1. Etiology
2. List the clinical signs.
3. Diagnostics
4. Treatment
5. Prevention?
6. What happens once these cats recover?
A
- Feline Herpesvirus-1 (FHV-1)
- Rhinitis, clear nasal discharge, Conjunctivitis
- Presumptive by clinical signs. Account for 90% of URIs in cats.
- Determining which virus is affecting the individual cat requires mouth or eye swabs for culture or PCR - Symptomatic and supportive care.
- Early use of antivirals medications (tri uoridine, idoxuridine, cidofovir and famciclovir) are safe and effective when given orally - Vaccination does not prevent herpesvirus, but minimizes clinical signs.; Isolate ill cats to prevent transmission
- Once recovered, most cats become carriers and may continue to shed virus intermittently
9
Q
Topic: Feline Respiratory Diseases - Calicivirus
1. Etiology
2. List the clinical signs.
3. Diagnostics
4. Treatment
5. Prevention?
6. What happens once these cats recover?
A
- Calicivirus
- Tongue ulceration, Gingivitis, Ptyalism
- Presumptive by clinical signs. Account for 90% of URIs in cats.
- Determining which virus is affecting the individual cat requires mouth or eye swabs for culture or PCR - Symptomatic and supportive care.
- Early use of antivirals medications (tri uoridine, idoxuridine, cidofovir and famciclovir) are safe an
effective when given orally - Vaccination does not prevent herpesvirus, but minimizes clinical signs.; Isolate ill cats to prevent transmission
- Once recovered, most cats become carriers and may continue to shed virus intermittently
10
Q
Topic: Feline Respiratory Diseases - Chlamydiosis
1. Etiology
2. List the clinical signs.
3. Diagnostics
4. Treatment
5. Prevention?
6. What happens once these cats recover?
A
- Chlamydophila felis
- Young cats/kittens; conjunctivitis, first unilateral then bilateral; +/- Concurrent upper respiratory tract infection (nasal discharge, sneezing)
- Primarily an ocular disease diagnosed by the presence of inclusion bodies in conjunctival scrapings
- Doxycycline, topical tetracycline QID for one week post resolution of clinical signs. ; Treat all cats in household;
- Isolate ill cats to prevent transmission; Clean environment to reduce fomite transmission
- Once recovered, most cats become carriers and may continue to shed virus intermittently; Prognosis good
11
Q
Topic: Feline Skin Diseases - Dermatophytosis
- Etiology
- List the clinical signs.
- Diagnostics
- Treatment
- Prevention?
A
- 98% of cases in cats are caused by Microsporum canis, but infections with M. gypseum and Trichophyton spp. are increasing in shelters.
- Kittens are most commonly affected on head and extremities
- Patchy alopecia, often circular or ring-like - - Scaling and crusting
- +/- Pruritus
- +/- Pseudomycetomas (pyogranulomatous draining nodules) in generalized dermatophytosis - Fungal culture on dermatophyte test medium (DTM). Check daily; usually takes 3-7 d to grow but wait 3 wk before declaring negative. Repeat after 2 months of treatment, then monthly until negative
- Wood’s lamp causes bright green uorescence in about 50% of cases and helps to identify hairs to be used for culture or microscopy
- Skin biopsy: Special stains are often used - Combination miconazole/chlorhexidine rinses (miconazole or chlorhexidine alone is not effective)
- Lime sulfur dips
- Severe cases may require or griseofulvin (do not use griseofulvin in pregnant or FIV-positive cats). Itraconazole is preferred in cats
- Griseofulvin
- Perform CBC in 2 wk then monthly
- Do not use in pregnant queens
- Do not use in cats positive for FIV or FeLV
Pseudomycetomas may require surgical debulking - Prevention: Disinfect environment monthly with diluted bleach or enilconazole solution
ZOONOTIC and highly contagious Clean clippers WELL after use! 1:10 bleach solution
12
Q
What are the most common skin tumors of cats?
What are the most common skin tumors of dogs?
A
- Basal cell tumor
- Squamous cell carcinoma
- Mast cell tumor
- Fibrosarcoma
- Lipoma
- Sebaceous gland hyperplasia
- Mast cell tumor
- Histiocytoma
- Papilloma
13
Q
Topic: Cutaneous Squamous Cell Carcinoma
- What is the cause and pathogenesis? Describe this tumor’s activity level.
- Describe what is seen clinically with FELINE patients affected.
- Describe what is seen clinically with CANINE patients affected.
A
- Malignant neoplasm of keratinocytes. Locally invasive and slow to metastasize. Associated with chronic sun exposure
- Generally, occurs on the head (nasal planum, eyelids, oral cavity). Rarely found on the digit; take thoracic x-rays because digital SCC in cats may be secondary. to primary pulmonary carcinoma.
- Most common neoplasm of the digit. Also, commonly found on the trunk, limbs, scrotum, lips and anus.
14
Q
Topic: Oral SCC
1. What is important to remember about this disease?
2. What part of the body does this commonly affect?
3. List the clinical signs.
4. How is this diagnosed?
5. How is it treated?
6. Prognosis?
A
- This is the most common malignant tumor in the cat. and the second most common oral cancer in dogs.
- Gingiva
- Underlying bone
- Tongue
- Sublingual region
- Alevolar mucosa
- Palatine tonsil unilaterally
- Reluctance to eat, halitosis, hypersalivation, ulceration and bleeding from the mass, regional lymphadenopathy, +/- dysphagia.
- CT, biopsy + staging
- Surgical removal if possible; pain control.
- Local recurrence post-op is common. Prognosis is poor.
15
Q
Topic: Papilloma
- What is the cause and pathogenesis?
- Transmission?
- Incubation period?
- Age range commonly affected? - Describe what is seen clinically with patients affected.
- Is it capable of regressing?
- Commonly seen where on the body?
- How do they look on presentation?
A
- Benign tumors caused by infection of epithelial cells by species specific papillomaviruses
- Transmission: direct and indirect contact
- Incubation period: 1-2 months
- Young dogs most commonly affected - Most regress in three months, but may persist up to one year
- Commonly affects nose, conjunctiva and haired skin
- Can present as smooth white papules, plaques, or verrucous cauliflower lesions
16
Q
Topic: Lipoma
- What is the cause and pathogenesis?
- Describe what is seen clinically with patients affected.
A
- Origin: adipocytes
- Common in dogs, uncommon in cats
- Benign - Soft, dome-like masses that also may be pedunculated
- Commonly found on thorax, abdomen
and proximal limbs
17
Q
Topic: Sebaceous Gland Tumors
- What is the cause and pathogenesis?
- Describe what is seen clinically with patients affected.
A
- Sebaceous epitheliomas, sebaceous adenomas and sebaceous hyperplasia are benign tumors of sebocytes: these are all benign except sebaceous adenocarcinomas, but sebaceous adenocarcinomas rarely metastasize
- Common in dogs, uncommon in cats - Nodular, solitary, or wart-like
18
Q
Topic: Mast Cell Tumors
- What is the cause and pathogenesis?
- Describe what is seen clinically with CANINE patients affected.
- Describe what is seen clinically with FELINE patients affected.
A
- Malignant tumor of dermal mast cells
- P53 mutation and c-KIT mutation
2.Dog
a. Variable: firm to soft, papular to nodular to pedunculated, dermal or subcutaneous, or
urticarial swelling; tumors usually occur on trunk, perineum and limbs
b. Gastric ulcers and coagulopathies may be observed due to mast cell granule release (histamine, heparin, etc.)
● Cat
a. Variable: firm or soft, white to pink plaques to nodules; most commonly found on the head or neck
19
Q
Topic: Cutaneous Histiocytoma
- What is the cause and pathogenesis?
- Describe what is seen clinically with patients affected.
- Are these tumors capable of regressing?
A
- Benign: more like reactive hyperplasia
● Origin: langerhans cells
● Common in dogs, rare in cats - Single well circumscribed mass in young dogs
● Head, pinnae, limbs
● Tumors regress spontaneously in three months
20
Q
Topic: Fibrosarcoma
- What is the cause and pathogenesis?
- Describe what is seen clinically with patients affected.
- How should this be treated?
A
- Common in cats, uncommon in dogs
● Origin: dermal or subcutaneous fibroblasts
● Young cats: feline sarcoma virus
● Vaccines: rabies, FeLV is most associated - Dermal or subcutaneous, irregular or nodular in shape
● Commonly found on trunk, distal limbs, ear pinnae or vaccination site - Radical excision is key !
21
Q
Topic: Basal Cell Tumor
- What is the cause and pathogenesis?
- Describe what is seen clinically with patients affected.
A
- Origin: basal epithelial cells
● Most are benign, but certain types (basosquamous,
solid basal cell tumors) are aggressive
● Common in cats, uncommon in dogs - Commonly found on head, neck and thorax; in cats can affect planum and eyelids as well
● Solitary and well circumscribed
22
Q
Topic: Cutaneous Lymphoma
- What is the cause and pathogenesis?
- Describe what is seen clinically with patients affected.
- Where are cutaneous lymphoma lesions most commonly found?
- How is this disease diagnosed?
- How is this disease treated?
- What is the prognosis?
A
- Malignant Neoplasm
● Origin: T lymphocytes - Variable Presentation
a. Depigmentation and ulceration of mucous membrane
b. Plaques
c. Nodules
d. Patches
e. Erythroderma
f. Footpads may be hyperkeratotic and ulcerated
g. Clinical signs, including itching, alopecia (hair loss), scaly skin, skin redness, loss of skin color, ulcers, nodules, pustules, and plaques. - The most common locations to find cutaneous lymphoma lesions include the junction between mucus membranes and the skin. Examples include the lip margins, eyelids, around the nose, anus/rectum, vulva, and the prepuce of the penis.
- Skin biopsy
- Lesions can be surgically excised, however, local recurrence is common. Palliative chemo or radiation can slow progression.
- Grave prognosis - once diagnosed and receive tx cats only live 6-12 months.
23
Q
Topic: GI Lymphoma
- What is important to remember about this disease?
- What is the origin of this disease in cats?
- List the clinical signs seen?
- How is this disease diagnosed?
- How is this disease treated?
- What is the prognosis?
A
- This is the most common GI neoplasm of cats, followed by adenocarcinoma and mast cell tumors.
- Low grade GI = mucosal and T cell in origin, affect SI. High grade GI = T or B cell in origin, affect SI.
- weight loss, vomiting, and diarrhea, appetite varies.
- BW: Hypercalcemia of malignancy
- FNA, biopsy
- Radiographs: lymphadenopathy, splenomegaly, hepatomegaly
- AUS, CT
- Main tx is systemic chemotherapy with or without surgical resection of the primary tumor.
- Low grade lymphoma: Prednisone + chlorambucil
- High grade lymphoma: injectable chemotherapy; if pursue sx, adjuvant chemo is recommended - High grade = poor; even with aggressive chemo, only survive for about 2-3 months
24
Q
Topic: Fibrovascular Papilloma
- What is the cause and pathogenesis?
- Describe what is seen clinically with patients affected.
A
- May be due to trauma
● Large dogs may be predisposed - Most commonly found on bony prominences, sternum and trunk
● Firm pedunculated growths
25
Q
Topic: Injection Site Sarcomas
1. They occur in approximately _____ out of
_______ vaccine injections.
2. Describe the biological behavior of this disease?
3. What is the proposed etiology of this condition?
4. List the diagnostics
5. How is it treated?
6. Prognosis
A
- 1, 10,000
- Extremely locally invasive with tendrils or “fingerlike projections”. Metastatic rate of 20-25%
- Believed to be caused by inflammation associated with injections, particularly with the
adjuvant in vaccines.
- Rabies and FeLV vaccines historically have been most commonly implicated
b. Other injections such as the upper respiratory and panleukopenia vaccine (FVRCP+/-C), lufenuron, penicillin, microchips, etc have also been implicated. - A. FNA - often definitive
B. Biopsy:
- More accurate than FNA
● Compared to naturally occurring sarcomas, ISS histology has more necrosis, inflammation with lymphocytes and macrophages, and more mitotic figures.
- Occasionally may see macrophages containing vaccine adjuvant
● 1, 2, 3 rule: biopsy is indicated if a vaccination site lump fits any of these criteria:
a. Continues to grow after 1 month post vaccination
b. Larger than 2 cm
c. Still present after 3 months
C. Thoracic Radiographs to assess for pulmonary metastasis
D. CT or MRI
- To assess invasiveness for surgical planning.
● External tumor is considered “tip of the iceberg” and is often several times larger than
what is visible externally. - A. Surgery
B. Radiation Therapy
C. Chemotherapy
D. Prevention
26
Q
Describe surgery for ISS
A
Radical excision with 3-5 cm lateral margins and 2 fascial planes deep is recommended.
● Amputation if on a limb
● Often requires body wall resection with reconstruction or hemipelvectomy for
proximal pelvic limb tumors.
● Dorsal spinous process removal and partial scapulectomies often required for interscapular tumors.
● Time to tumor recurrence
a. About 2 months with conservative surgeries
b. About 9 months with radical surgeries performed by referral surgeons
c. About 16 months if surgical margins are “clean” or complete on histopathology.
27
Q
Describe radiation therpay tx for ISS
A
Adjuvant treatment to surgery to prolong recurrence if margins are narrow or
incomplete on histopathology.
● Can be performed before or after surgery.
28
Q
Describe chemotherapy treatment for ISS
A
Adriamycin (doxorubicin) chemotherapy has up to a 50% response rate in cats with
macroscopic ISS in small studies.
a. Response is usually not durable so it is unclear if it prolongs survival times in cats
with gross disease.
b. May be more helpful in treating cats believed to have microscopic metastatic disease or cats
with incomplete surgical excision when radiation therapy is not an option
29
Q
Describe how to prevent ISS
A
Only vaccinate for diseases that the cat may be exposed to, or if required by law
● Vaccinate as distally as possible on limbs so they can potentially be cured of their local disease with
amputation alone if ISS develops.
● Standardize and record sites of injections
a. Any vaccine containing rabies antigen in the right pelvic limb
b. Any vaccine containing FeLV antigen in the left pelvic limb
c. Feline rhinotracheitis and panleukopenia vaccines (FVRCP) in the right shoulder
d. Give all vaccines as distally in the limb as possible
30
Q
Topic: Hypertrophic Cardiomyopathy
- Are there any breeds that are predisposed to this disease? What age range is typically affected.
- What are the major clinical signs seen?
- What may you hear on physical exam?
A
- Maine Coons and Ragdolls are predisposed. They can present as early as 4 months old.
- Often present as asymptomatic but can also present with signs of thromoboembolic disease:
- Cold, cyanotic distal extremities
- Paraplegia (loss of voluntary movement of the hindlimbs)
- Non-palpable pulses
Patients may also present with signs of CHF including:
- Dypsnea, tachypnea
- open-mouth breathing
- You may hear a systolic murmur or gallop sound
31
Q
Topic: HCM cont.
1. Describe the pathophysiology of HCM.
2. What diagnostics do you run on patients suffering from HCM?
A
- HCM is a disease is diastolic dysfunction because in cases of HCM the left ventricle is hypertrophied which prevent the left ventricle from filling/holding as much blood as it normally does/should. As a result of LV hypertrophy, we will see LA dilation as well as systolic anterior motion of the mitral valve. We see systolic anterior motion of the mitral valve because during systole, when the heart contracts, the mitral valve swings in an anterior motion, aka towards the left ventricle, “leaking” blood from the LA into the LV when that should NOT be happening because the heart should simply be contracting and shooting blood from the LV into the aorta. LA dilation also prediposes the patient to atrial thrombus formation due to blood stasis. These clots can become dislodged in the aortic bifurcation (iliac arteries) –> thromboembolic disease.
2.
A. Thoracic radiographs:
- Heart can be normal in size or enlarged (cardiomegaly)
- Dilated left atrium –> classic valentine shaped heart seen on DORSOVENTRAL (DV) view.
- Pulmonary edema, congestion
- Pleural effusion
B. Echocardiography (M-mode)
- Left Atrial dilation
- Left Ventricular hypertrophy
- Papillary muscle hypertrophy
- Systolic anterior motion of the mitral valve if obstructive cardiomyopathy
C. Plasma brain natriuretic peptide (BNP)
- Levels will be high in severe cases OR compensated cats.
32
Q
Topic: HCM cont.
1. How are HCM cats treated? Why do we choose the drugs that we do?
2. What resources are available for Maine Coon and Ragdoll owners?
3. What is the prognosis?
A
- If the patient is in CHF:
- Oxygen supplementation
- Furosemide (loop diuretic)
- Nitroglycerin (vasodilatory drug)
- AVOID FLUID THERAPY AND BETA BLOCKERS UNLESS TACHYARRHTHMIA
For Chronic Treatment:
- Furosemide (loop diuretic)
- Atenolol (Beta-blocker - bind to beta receptors to prevent release of epinephrine –> reduces blood pressure and heart rate)
- Clopidogrel or baby aspirin (blood thinner; reduced risk of thromboembolic disease)
- +/- potassium supplementation if hypokalemic
The primary problem with HCM is thickening of the wall of the left ventricle, impairing diastolic filling. There is usually no problem with contractility and systolic function. Slowing the heart rate provides for longer diastolic filling, allowing the left ventricle to fill more effectively. Decreasing the heart rate also decreases the severity of systolic anterior motion of the mitral valve.
- Genetic testing - cardiac myosin binding protein C gene (autosomal dominant)
- Prognosis for cats in CHF is poor :(
33
Q
Topic: Diabetes Mellitus in Cats
1. What age range is typically affected?
2. What are the major clinical signs seen in cats with DM?
3. How do you diagnose cats with DM?
A
- Middle aged to older cats; no sex predilection
- PU/PD, polyphagic, weight loss, recurrent infections
+/- plantigrade stance due to diabetic neuropathy
+/- anorexia, vomiting, weakness if in DKA - A. Fasting blood glucose
- NOTE: Stress can lead to hyperglycemia in cats
B. Urinalysis - glucosuria +/- ketonuria if in DKA
- in “healthy diabetic” the BG will be > 300
- in a DKA patient the BG will be > 500
- NOTE: Stress can lead to glucosuria in cats
C. Fructosamine - to see BG levels over the previous 2 weeks. Will be elevated in cases of persistent hyperglycemia
D. Other bloodwork abnormalities include:
- In cases of DKA - severe metabolic acidosis
- Elevated liver enzymes and cholesterol
34
Q
Topic: Diabetes Mellitus in Cats
1. How is DM treated in cats?
A
- A. Insulin therapy
- If in DKA, start off with REGULAR insulin as it has the shortest duration of action. Once stabilized, can transition to a longer acting insulin (Lente, PZI, Glargine)
- Insulin therapy should be monitored by a blood glucose curve when possible to insure the patient is receiving the correct dose.
B. Diet:
- Cats need a high protein, low carb diet
C. +/- Oral hypoglcyemics; efficacy of Glizipide is controversial.
D. +/- IVF
- For DKA patients; use 0.9% saline +/- K and Phos supplementation if needed
E.+/- Bicarbonate therapy
- For DKA patients, can be given if in severe MA or if not improving with IVF
F. Identify any concurrent infections
35
Q
What is the optimal feline glucose range?
A
80-300 mg/dl
Note: For dogs it is 80-200 mg/dl
36
Q
What is the optimal feline glucose nadir?
A
80-150 mg/dl
Note: It is the same for dogs!
http://aaha.org/resources/2018-aaha-diabetes-management-guideline-for-dogs-and-cats/interpreting-glucose-curves/
37
Q
Topic: Hemotropic Mycoplasmosis
- What is the etiology? Describe its pathogenesis.
- What are the clinical signs?
- How is it diagnosed?
- How is it treated?
- Zoonotic potential?
A
- Caused by the microscopic bacterial parasite Mycoplasma Haemofelis, previously known as Hemobartonella felis. RBC will either breakdown or the cat’s immune system may recognize it as “foreign” and then destroy them –> anemia.
- Acute, potentially severe or fatal hemolytic regenerative anemia in healthy cats. Typical clinical signs include lethargy, anorexia, and fever.
- Microscopy or PCR
- A. Acute Infections: Tetracyclines (doxycycline, oxytetracycline)
B. Pradofloxacin and marbofloxacin have also been effective. - Zoonotic potential is possible.
38
Q
Topic: Feline Infectious Anemia
- What is the etiology?
- What are the clinical signs?
- How is it diagnosed?
- How is it treated?
- Zoonotic potential?
A
- Mycoplasma haemofelis
- Weakness, pallor of the mucous membranes, tachypnea, tachycardia, and occasionally collapse.
- A. Regenerative anemia (polychomasia and/or reticulocytosis)
B. increased numbers of nucleated RBCs,
C. Anisocytosis (different size red blood cells)
D. Howell-Jolly bodies (single small dot in RBC) - Supportive care, tetracycline antibiotics, blood transfusions, oxygen therapy
39
Q
Topic: Anemia of Chronic Disease
- What is this the most common cause of?
- What is the duration of disease development?
- What is seen on bloodwork?
A
- This is the most common cause of anemia in cats.
- One week in cats, 2 weeks in dogs
- Normocytic, normochromic, non-regenerative anemia
40
Q
Topic: IMHA
1. Felids typically develop IMHA because of?
2. What are the clinical signs?
3. What is seen on bloodwork?
4. What are some complications of IMHA?
5. How is it treated?
6. What are some DDx?
A
- Develop it secondary to another disease process
- Onset of acute:
- Anorexia, lethargy
- Tachypnea, weakness, collapse
- Pale MM
- Icterus in 50% of patients
- Heart murmur, splenomegaly
- Tachycardia, tachypnea - A. Regenerative anemia
B. Polychromasia is almost always present
C. Spherocytes (abnormally shaped RBC) IN DOGS ONLY
D. Saline test - dilute blood with saline –> autoagglutination
E. Leukocytosis
F. Thrombocytopenia
G. Positive Coomb’s test
H. Elevated ALT and bilirubin - Elevated liver enzymes due to severe anemia and hypoxia - A. Concurrent immune mediated thrombocytopenia (Evan’s Syndrome)
B. DIC
C. Thromboembolism common and often fatal (Spleen, pulmonary, liver)
5.
A. Immune suppression: prednisone = first line; cyclosporine, chlorambucil (cazts) = second line; can combine two to reduce time on pred or get faster response
B. Adjuvant IVIg: Block Fc receptors on MQ from binding to RBC and destroying them so it does not treat the patients long term, but in giving transfusion, those RBC are spared for that time. May see anemia lessen and give us time to give blood transfusion and have prednisone do the work.
C. Clopidogrel or baby aspirin (acetylsalicylic acid)
- A. Infectious = Rickettsia, Babesia, Mycoplasma, Cytaxuzoon
B. Neoplasia = Lymphoma, malignant histiocytosis
C. Toxins/Drugs = Zinc pennies made after 1982, onions, garlic, Cephalosporins, Sulfa AB
41
Q
Topic: Ethylene Glycol Toxicity
- Ethylene glycol is found in?
- How does it taste to animals?
- Describe the pathophysiology of ethylene glycol toxicity.
A
- Most commercial antifreeze
- Sweet
- Ethylene Glycol is metabolized into alcohol dehydrogenase –> glycoaldehyde –> glycolic acid –> glyoxalate and oxalic acid
42
Q
Topic: Ethylene Glycol Toxicity cont.
- Describe the c/s seen in each stage of EG toxicity.
- How is this treated?
- What is the prognosis?
A
- Stage 1: 30 min - 12 hrs post ingestion –> Neuro phase/ drunken behavior, anorexia, vomiting, PU/PD, Ca oxalate crystalluria
- Stage 2: 12-24 hrs post ingestion –> Cardio phase where you see tachypnea and tachycardia, often unnoticed
- Stage 3: 12 -72 hrs post ingestion –> Renal failure, MA, elevated osmolar gap, HypoCa, HyperGlucosemia
- In order for tx to be effective, you must start tx before toxic metabolites are generated.
- Fomepizole (4-MP) = inhibits alcohol dehydrogenase; most effective within 8 hrs of ingestion; very expensive ; can be used in cats but MUCH higher dose is necessary
- 20% ethanol = competitively inhibits alcohol dehydrogenase, less effective than Fomepizole but useful within 4-8 hrs of ingestion; Can worsen C/S
- GI protectants, IVF, Diuretics (mannitol, furosemide) in oliguric patients - Prognosis is good if therapy started within 4-8 hrs. Guarded if patient is azotemic. Grave if oliguria/anuria present w/o dialysis treatments.
43
Q
Topic: Tyelonol
- Tylenol is also called?
- Describe the pathophysiology of Tylenol toxicosis. How does it affect cats? Dogs?
- What clinical signs are seen?
- How is this disease diagnosed?
- How is it treated?
A
- Acetaminophen
- Oxidizing toxic metabolites lead to methemoglobinemia with Heinz bodies. Cats uniquely sensitive because do NOT have glucuronyl transferase Dogs may get keratoconjunctivitis sicca.
- A. Muddy mm
B. Hyperpnea
C. Tachycardia
D. Weakness/depression
E. Death!!! - A. Methemoglobinemia, Heinz Bodies
B. Abnormal liver values - A. Induce emesis
B. N-acetylcysteine slowly IV
C. Ascorbic acid
D. IV fluids
E. Blood transfusion
44
Q
Topic: SSRIs
- Describe the pathophysiology of SSRI toxicosis.
- What clinical signs are seen?
- How is this disease diagnosed?
- How is it treated?
A
- Block presynaptic serotonin receptors. “Serotonin syndrome” can occur with any drug than increases free serotonin levels.
- A. Mydriasis
B. Vomiting, diarrhea
C. Lethargy, fever
D. Ataxia, seizures, hyperactivity, vocalization
E. Increased or decreased heart rate - History and clinical signs
- A. Decontamination
B. Cyproheptadine
C. Phenothiazines - Acepromazine
D. Diazepam –> binding of the inhibitory neurotransmitter GABA at various GABA receptors throughout the CNS –> drowsiness
E. Beta-blockers
F. Do NOT use atropine
45
Q
Topic: Permethrin
- Describe the pathogenesis of Permethrin toxicity.
- Describe the clinical signs seen.
- How is this disease diagnosed?
- How is this disease treated?
A
- Permethrin is a neurotoxicant. The mechanism of action of permethrin is similar to those produced by organochlorines, such as DDT, and involves interference with the axonal sodium gate
- Hyperesthesia, generalized tremors, muscle fasiculations,
hyperthermia, and seizures are the most common signs seen.
Clinical signs can develop within hours or may be delayed up to 72 hours. Clinical signs generally last 2-3 days. - The diagnosis of permethrin toxicosis is primarily based upon exposure history and the development of associated signs.
- A. Seizure control and stabilization = Methocarbomal
B. Bathe patient
C. IVF
46
Q
Topic: Lily Toxicosis
- Describe the pathogenesis of lily toxicity. What species is this toxic for?
- Describe the c/s seen in each stage of EG toxicity.
- How is it diagnosed? What do you see on diagnostics?
- How is this treated?
- What is the prognosis?
A
- The flower part of the lily is the most toxic. Even ingesting the pollen can cause toxicity. Only true lilies, aka Lilium and Hemerocallis spp. are toxic; other plants with “lily” in the name may not be toxic. These species are only toxic to cats, no other species.
- 1-3 h: salivation, anorexia, vomiting, can be mild and resolve w/out Tx
12-30 h: polyuria, dehydration, worsening GI upset
3-7 d: worsening signs and death from renal failure - A. Evidence of plant exposure
B. > 18 hrs post ingestion: Azotemia, Hyperphosphatemia, Hyperkalemia
C. Creatinine is often disproportionately higher than the BUN
D. UA: Isosthenuria, epithelial casts, +/- glucosuria - A. Remove any pollen from fur
B. Emesis, AC 1x
C. Aggressive IVF diuresis for at least 48 hrs; longer if P is azotemic
D.GI protectants/antiemetics
E. Monitor urine output and check renal values q24 hrs x 3 days
F. If oliguric - Furosemide or mannitol
G. If anuric - dialysis
47
Q
Topic: THC Toxicity
- Describe the pathogenesis of THC Toxicity.
- Describe the clinical signs.
A
- THC is very lipid-soluble, which means that it is easily stored in the fatty tissue in the liver, brain, and kidneys before being eliminated from the body. THC is metabolized in the liver and the majority (65-90%) is excreted in the feces, while a small percentage (10-35%) is eliminated through the kidneys. The drug has to be metabolized and excreted for the effects to wear off.
- A. Ataxia
B. Hyperactive or sleepy, disoriented, and/or very vocal
C. Mydriasis
D. Urinary incontinence
E. Hypersalivation
F. Bradycardia, hypotension
G. Increase or decrease in BP - A. If early enough, can induce emesis OR pump stomach (THC inhibits vomiting so inducing emesis may not be effective)
B. Most just provide supportive care (IVF, anxiolytic, gastric protectants).
C. Keep confined in a safe safe.
48
Q
Topic: Feline Trichomoniasis
- What is the etiology of this condition?
- What age range is most commonly affected? List the risk factors.
- What are the clinical signs.
- How is this condition diagnosed?
- How is this condition treated?
- What is the prognosis?
- How is this condition prevented?
- Is this disease zoonotic?
A
- Tritrichomonas Foetus - flagellated parasite
- Very common in densely housed kittens under 2 yrs of age.
- Chronic, unresponsive diarrhea that may progress from large bowl to mixed bowel diarrhea.
- Diarrhea is yellow-green with frank blood, malodorous, hematochezia.
- Tenesmus, flatulence, incontinent.
- Anus may be inflamed and slightly protruding.
- Usually normal appetite and no weight loss - A. Gold standard = PCR (100% specificity, 80% sensitivity)
- Ronidazole
- Patients are most responsive to this medication
- Side effects/Warnings: Narrow margin of safety, increasing drug resistance, DO NOT use in pregnant cats, expensive.
- Other anti-protozoal medications such as metronidazole are not effective - Remission may occur in 5-24 mo, relapses are very common, patient may suffer from life-long infection.
- Decrease housing density is more effective than hygiene and disinfection.
- Zoonotic risk if low but infection may occur in immunocompromised people.
49
Q
Topic: Hepatic Lipidosis
- Describe a classic case of hepatic lipidosis in cats.
- How is this condition diagnosed?
- How is this condition treated?
- What is the prognosis?
A
- Obese cat with several-day history of anorexia , weight loss, jaundice, +/- ptyalism when hepatic encephalopathy (HE) present
- A. Serum biochemistry: ALP higher than ALT, total bilirubin increased, normal GGT (helps differentiate from other hepatobiliary diseases)
B. Coagulopathies
C. Abdominal ultrasound Liver fine-needle aspirate (FNA) or biopsy - A. Nutritional support is key
B. Esophagostomy tube
C. High-quality, high-protein diet (unless HE present)
D. If HE: Lactulose retention enemas - Prognosis: Fair to excellent
–> Treat hyporexic and anorexic cats promptly and aggressively
50
Q
Topic: Dermatophytosis
- What is the etiology?
- What is the typical signalment?
- What are the clinical signs?
- What diagnostics would you run?
- How is this condition treated?
- How is this condition prevented?
- Describe the zoonotic risk and contagiousness of this disease.
A
- Microsporum canis
- Kittens are most commonly affected
- C/S on head and extremities:
- Patchy alopecia, often circular or ring-like
- Scaling and crusting
- +/- Pruritus
- +/- Pseudomycetomas (pyogranulomatous draining nodules) in generalized dermatophytosis - A. DTM: Fungal culture; Takes 3-7 days to grow but wait 3 weeks before declaring negative; Repeat after 3 months of treatment and then monthly until negative.
B. Wood’s lamp: fluoresces with 50% of cases so not super helpful
C. Skin biopsy - A. Miconazole + Chlorohexidine rinses
B. Lime sulfur dips
C. itraconazole or Terbinafine
D. Miconazole or clotrimazole topical may be effective for localized cases
NOTE:
Ketoconazole should not be used in cats because it causes anorexia.
Fluconazole should not be used because this is the least effective drug for dermatophytes.
Griseofulvin is no longer recommended because itraconazole and terbinafine are superior drugs with lower risk of adverse effects. Griseofulvin can not be used in pregnant or FIV + cats.
Lufenuron is ineffective.
- Disinfect environment monthly with diluted bleach or enilconazole solution
- Zoonotic and HIGHLY contagious
FOR DOGS:
Small dogs can be cost-effectively treated with itraconazole
Larger dogs can be treated with ketoconazole or terbinafine which may be more cost-effective.
Dogs should be treated until mycological cure (eg, a negative result of fungal culture or PCR assay), which can take ≥ 4–6 weeks (1).
51
Q
Topic: Pemphigus foliaceus
- This is the most common ____________ disease of cats.
- What are the clinical signs?
- How is this disease definitively diagnosed?
- How does this differ from pemphisu vulgaris?
- How is this condition treated?
A
Pemphigus foliaceus is the most common autoimmune skin disease in cats.
Crusts (scabs) and ulcers around the eyes, ears, footpads, groin, and bridge of the nose. In cats, lesions also develop at the toenail beds creating crusty sore feet
Definitive diagnosis = biopsy of the affected skin
The absence of lesions in the mouth, and the widespread thick, crusty nature of the skin lesions, tend to differentiate pemphigus foliaceus from the much rarer pemphigus vulgaris.
Immunosuppression is required to treat the disease. High doses of glucocorticoids may be used initially; however, low-dose, alternate-day treatment is used once the disease is under control.
52
Q
Topic: Ear Mites
- Who is typically affected?
- What are the c/s?
- How is it diagnosed?
- How is it treated?
- How is this prevented?
A
- Usually kittens
- Head shaking, pruritus Erythematous ears Dark brown debris in ear canals Papules on rump, tail, neck Ear-pedal re ex present (scratching with pelvic limb when ear is rubbed)
- Otoscopy: see live mites and in fammation Cytology of ear swab in mineral oil: see mites, eggs, +/- secondary bacteria
- A. Remove debris from ears
B. Miticidal otic preparation (milbemycin, ivermectin, etc.) -AND- Systemic miticidal (selamectin, ivermectin, etc.) to treat ectopic mites
C. Very contagious, treat all dogs and cats in home - A. Clean environment
B. Separate affected and non-affected cats
Cats may be infected by dogs in the household
Prognosis is good but may recur or become chronic
53
Q
Topic: Toxoplasmosis
- What is the etiology of this disease?
- How is this disease transmitted?
- What are the clinical signs? When do they appear?
- How is this disease diagnosed?
- How is it treated?
- Describe the zoonotic risk of this disease.
A
- Toxoplasma gondii
- If outdoor cat at risk due to ingestion of birds or rodents; if indoor cats at risk via insects.
- C/S can appear months to yrs after initial infection.
A. Chorioretinitis, neuro signs, GI signs, icterus, muscle pain, coughing. - IgM or IgG paired titers (4-fold increase 2-4 wks apart)
A. Postitive IgG titer = previous exposure (yrs, even)
B. IgM titer greater than 1:64 = active infection - Clindamycin for 2-4 wks or 2 wks beyond resolution of clinical signs
A. NOTE: Corticosteroids are contraindicated - ZOONOTIC - Can cause birth defects in a developing fetus if a mother is infected for the first time in her life while pregnant
- Pregnant woman can not clean litter boxes
- Whoever does clean the box: do it at least once daily (oocysts sporulate and become infective in 24 hr) and
wear gloves
54
Q
Topic: Chronic Renal Insufficiency
- List and describe the clinical abnormalities seen in patients with CRI.
A
- A. Dehydration: Patients with CRI exhibit PU/PD –> renal hypoperfusion, pre-renal azotemia.
- Owners need to add more water to diet to help increase water consumption.
- In hospital - saline, LRS can be used.
B. Metabolic Acidosis: This occurs due to the kidney’s inability to acidify urine.
- Tx with potassium citrate or sodium bicarbonate (for patients with significant acidosis).
C. Hypokalemia: The kidneys help synthesize K, so incases of CRI there is a decrease in K.
- Tx with oral K+ supplementation
D. Uremia: Inability to excrete metabolic byproducts leads to buildup of urea and other uremic toxins in the bloodstream. This contributes to CNS depression, anorexia, nausea, vomiting, halitosis, gastritis, and other clinical signs.
E. Anorexia: May occur due to uremic ulcers and gastritis, dehydration, metabolic acidosis, and hypokalemia.
- Tx with H2-blocking drugs - famotidine, ranitidine
F. Ca/Phos Imbalance: Limiting dietary phosphorus intake and/or administering phosphate binding agents (aluminum hydroxide, aluminum carbonate)
G. Anemia: Inadequate renal erythropoietin production is a major factor.
- Tx: Recombinant human erythropoietin administration may be indicated with significant anemia that is compromising quality of life or necessitating transfusion
H. Hypertension: Common with CRI and may promote proteinuria.
- Managed with ACE inhibitors and other anti-hypertensives
55
Q
Topic: Chronic Renal Insufficiency - Cont.
- How is this condition treated (other than what you explained above).
A
- Diet:
A. Minimize uremia (low protein) and corresponding clinical signs
b. Minimize fluid, electrolyte, and mineral deficits (high moisture content)
c. Minimize acidosis
d. Promote general nutrition (palatable and with sufficient caloric density)
e. Slow progression of renal disease (reduced phosphorus)
- Dietary therapy has been shown to prolong life by 2-3 times in dogs and cats
with renal insufficiency.
56
Q
Topic: Abscess
1. What is the typical etiology?
2. How is it treated?
A
- Anaerobes - Fusobacterium spp., Bacteroides spp., and Clostridium spp. as well as facultative anaerobes such as Pasteurella spp. and Actinomyces spp.
- Because anaerobes are the most common isolates, it is believed that most cat bite abscesses can be effectively treated by establishing good drainage. Nevertheless, many if not most veterinarians, elect to additionally treat these with antibiotics. Be sure to choose an antibiotic that will be effective against anaerobes such as clindamycin or amoxicillin with clavulanate.
57
Q
Topic: Feline Urethral Obstruction
- Does this disease process have a sex predilection? Species predilection?
- What is the etiology of this disease?
- What is THE most important life-threatening electrolyte imbalance in these patients? Name the other imbalances typically seen.
- Explain why hyperkalemia occurs in these patients.
- How is hyperkalemia treated?
A
- Yes - this is more commonly seen in male cats, and to a lesser extent male dogs, than females.
- Urethral obstruction can occur either due to a physical obstruction (mucosal plug, urolith, stricture, or neoplasia) or a mechanical obstruction (urethral spasm).
- Hyperkalemia is THE most important electrolyte imbalance. Patients can also present with hypocalcemia, hyperphosphatemia, metabolic acidosis, and azotemia as well as cardiovascular compromise.
- Hyperkalemia is seen in patients with urethral obstruction due to decreased renal potassium excretion, subsequently leading to metabolic acidosis.
- A major consequence of hyperkalemia is a shift in resting cell membrane potential on cardiac myocytes –> BRADYCARDIA, on ECG see tall tented T waves, widened QRS intervals, and small/diminished p waves. - In these patients, hyperkalemia is treated by:
A. Administering IVF low in K+ = 0.9% Sodium chloride
B. To reestablish resting membrane potential and target abmormal cardiac activity = Calcium gluconate (NOTE: THIS DOES NOT LOWER K+)
C. IV Dextrose + Regular Insulin = moves K+ back into cells
D. Sodium Bicarb = moves K+ back into cells and reduces MA status.
58
Q
Topic: Feline Urethral Obstruction cont.
- Explain what causes metabolic acidosis and how it is treated.
- Explain what causes the azotemia and hyperphosphatemia and how it is treated.
- Explain what causes the hypocalcemia and how it is treated.
A
- Occurs d/t inability of the kidneys to excrete hydrogen ions –> respiratory compensation (increased RR).
A. Tx by decompressing the bladder
B. IVF therapy
C. Sodium bicarb - Azotemia and hyperphosphatemia occurs d/t inability of the kidneys to excrete waste products and urea.
A. Tx by decompressing the bladder/relieving obstruction
B. IVF diuresis - Occurs d/e hyperphosphatemia –> compromises cardiac contractility and can even result in seizures.
A. Tx with IV calcium gluconate.
59
Q
Topic: Feline Urethral Obstruction Cont.
- Describe your initial plan of action and tx for this patient.
A
- Once you have made your tentative diagnosis based on signalment, c/s, and physical exam:
A. BW: PCV/TP, BG, Electrolytes, BUN, BP.
B. IVF: 0/9% Sodium Chloride, Dextrose + insulin, Calcium gluconate, +/- Sodium bicarb
C. Relieve bladder obstruction
D. Monitor urine output and fluid rates.
E. Once stable, address underlying cause of urethral obstruction
F. Cont. appropriate analgesics
G. Leave urinary catheter in place until azotemia, electrolyte abnormalities, and post-obstructive diuresis is resolved. Observe for 12-24 hrs post-catheter removal to ensure spontaneous urination.
60
Q
Topic: Feline asthma
1. Signalment and c/s
2. Diagnostics
3. Treatment
4. Things NOT to give
A
- Siamese and Himalayans are at increased risk.
- Coughing, wheezing, Tachypnea
- +/- Dyspnea and respiratory distress (status asthmaticus) - A. Xrays: Bronchointerstitial pattern and pulmonary inflammation
B. Pulmonary hyperinflation
C. CBC: Eosinophilia
D. Bronchoalveolar lavage +/- culture for mycoplasma - A. If in dyspnea or resp distress:
- O2, minimal handling
- Bronchodilators via nebulizer (albuterol) or parenteral (terbutaline)
- Parenteral glucocorticoids (prednisolone)
B. Chronic therapy:
- Bronchodilators (theophylline, aminophylline, terbutaline)
- Glucocorticoids (prednisolone)
C.
+/- doxycycline oral suspension if concurrent airway infection
+/- cyclosporine if do not respond to prednisolone
- reduce environmental irritants
- DO NOT give bronchodilators as a monotherapy
DO NOT give beta-blockers -> worsen bronchoconstriction
61
Q
Topic: Hypokalemic myopathy
- C/S
- Diagnostics
- Tx
- Prognosis
- DDx
A
- Cervical ventro exion in an older cat, generalized weakness, stiff, stilted gait
- A. Low blood potassium level (less than 3.5 mEq/L)
B. Renal profi le
C. thyroid panel
D. CK - Oral potassium gluconate, dopamine infusion if life-threatening, DO NOT
add potassium to fl uids - Good
- Chronic renal disease, snake bite envenomation, organophosphate toxicity, polymyositis, myasthenia gravis
62
Q
Topic: Otitis media/interna
1. Etiology
2. C/S
3. Dx
4. Tx
A
- Nasopharyngeal polyps are a common cause of otitis media/externa in young adult cats
- A. Head tilt and circling (toward lesion)
B. Horizontal nystagmus (fast phase away from affected side)
C. Ataxia
D. +/- Ipsilateral facial neuropathy
E. +/- Ipsilateral Horner syndrome - A. Oropharyngeal examination – look for nasopharyngeal polyp
B. Otoscopy – opaque and bulging membrane if fluid in tympanic bulla
C. Myringotomy (puncture tympanic membrane and culture); NOTE: VENTRAL CHAMBER IN CATS CAN NOT BE DRAINED
D. CT or MRI - A. Antibiotics for several weeks
B. Bulla osteotomy
63
Q
Topic: Idiopathic vestibular diseaase
1. Etiology
2. C/S
3. Dx
4. Tx
A
- Immature 5-lined skink, commonly called “blue-tail lizard” has been implicated in southern u.s; no proven cause and effect
- A. Circling and head tilt (toward affected side)
B. Ataxia
B. Horizontal or rotary nystagmus (fast phase away from affected side) C. NO: loss of conscious proprioception, facial paralysis, Horner syndrome - Otoscopy, MRI, CT, CSF analysis –> ALL NEGATIVE
- Nursing care, sedatives, con ne to prevent jumping
- Excellent prognosis
64
Q
Topic: Polycystic kidney disease
A
65
Q
Topic: Hereditary deafness
A
