Small Mammals 6 – Diseases of Ferrets Flashcards

1
Q

Adrenal Gland Disease definition, etiology

A
  • Common, middle-aged (3.5 years)
  • Early spaying/neutering (no negative feedback)?
  • Kept indoors, genetic?
    <><>
  • Adrenal gland disease is a common disease in middle-aged to older ferrets.
    It is most commonly characterized by hair loss in both sexes, and vulvar enlargement in females. It is suspected that early spaying/neutering of ferrets is the underlying cause of adrenal gland disease. Another study suggested that it tends to occur about 3.5 years on average after neutering, regardless of age
  • Most ferrets will have a history of progressive alopecia that begins in the late winter or early spring and may continue to the point of baldness. The hair may or may not cyclically regrow. Spayed female ferrets with adrenal gland disease have a history of vulvar enlargement. Male ferrets may have a history of dysuria or urinary blockage. Both sexes can have a history of change in behavior, with increased aggression and pruritus
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2
Q

Adrenal Gland Disease

A
  • Adrenocortical hyperplasia, adenoma, or adenocarcinoma → hyperandrogenism (increased production of androgens by the zona reticularis) → sex hormones, estradiol, 17-hydroxyprogesterone, or plasma androgens increased (cortisol normal)
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3
Q

Clinical signs of adrenocortical disease in ferrets important difference

A
  • IMPORTANT: Clinical signs of adrenocortical disease in ferrets differ from those of classic Cushing’s disease in dogs. Plasma cortisol concentrations are also rarely increased in ferrets. However, the sex hormones, estradiol, 17-hydroxyprogesterone, or one or more of the plasma androgens may be increased due to adrenocortical hyperplasia, adenoma, or adenocarcinoma
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4
Q

Adrenal Gland Disease clinical signs

A
  • Progressive alopecia
  • Pruritis with erythema
  • Enlarged vulva and dark perivulvar skin
  • Prostatomegaly/ periurethral cysts → urinary blockage
    <><><><>
  • Progressive alopecia - usually begins on the rump, the tail, or the flanks and
    progresses to the lateral trunk, dorsum, and ventrum
  • Pruritus with erythema (dorsum between shoulder blades)
  • Females - enlarged vulva with dark perivulvar skin
  • Partial or complete urinary blockage in male ferrets (EMERGENCY!)
  • Due to the development of periurethral cysts in the region of the prostate/prostatomegaly
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5
Q

Adrenal Gland Disease stabilization

A

Blockedmaleferrets
* Leuprolide acetate IM
* Urethral catheterization / cystocentesis
* Monitor and treat for hyperkalemia
* Maintain and hydrate for 3 days
<><><><>
* Mainly indicated in male ferrets that are partially or completely obstructed
* In these cases, emergency treatment is indicated
* PE findings: distended and painful urinary bladder
* If urinary obstruction is associated with prostatomegaly, give leuprolide
acetate IM 200-300 ug. Most obstructions resolve without further
intervention within 24-48h. If not, needs urethral catheterization
* Urethral catheter placement is challenging in the male ferret due to their
small size and the J-shaped os penis
* Treatment:
* Premedication with midazolam + opioid (remember, ferrets are sensitive to opioids)
* Provide supplemental heat
* General anesthesia easiest
* Easy to intubate - like a cat
* Slippery Sam catheters work well (3.0 French) or red rubbers (3.5
French) for bigger ferrets
* Carefully monitor ECG for evidence of hyperkalemia: loss of P wave,
widened QRS complexes, peaked T waves
* If arrhythmia is present, treat with medical management
* Calcium gluconate 50-100 mg/kg slow bolus IV
* Insulin 0.2 U/kg IV
* 50% dextrose 1-2 g/Unit IV insulin * Monitor ins and outs once the catheter is placed
* Goal: 1-2 mL/kg/hr (approximately 140 mL/day)
* Maintain catheter for 1-3 days
* Correct metabolic and acid-base disturbances
* Give fluids to correct perfusion abnormalities
* Rehydrate patient
* Maintenance fluid: 50 mL/kg/day
* Monitor for signs of overhydration (dyspnea)
* If attempts at catheterization fail, cystocentesis can be performed (with risk
of urinary bladder rupture and uroabdomen)
* Exploratory laparotomy and cystotomy may be indicated if unable to relieve
obstruction

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6
Q

Adrenal Gland Disease Dx

A
  • Presumptive diagnosis: history, clinical signs, results of imaging techniques
    and steroid hormonal assays
  • Definitive diagnosis: histologic examination of adrenal tissue obtained
    during surgical biopsy or adrenalectomy
  • CBC: usually unremarkable; rarely nonregenerative anemia, pancytopenia
    with prolonged disease
  • PCV <15% = grave prognosis
  • Biochemistry: usually unremarkable; occasionally elevation in ALT
  • Radiographs: not helpful in diagnosing this disease (unless the adrenal is so
    large it is causing organ displacement or is calcified) but important to rule
    out other causes of disease; lung metastasis rare with adrenal tumours
  • Abdominal ultrasound: useful to determine size, side of enlargement, and
    architecture of the adrenal glands (normal sizes are reported)
  • Hormone panel: estradiol, androstenedione, 17-hydroxyprogesterone
  • One or more of these compounds may be high in ferrets with adrenal gland disease
  • Note - tests that are not useful in ferrets:
  • ACTH stimulation test
  • Dexamethasone suppression test
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7
Q

Adrenal Gland Disease definitive Dx

A

Histopathology of biopsy
or adrenalectomy

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8
Q

Adrenal Gland Disease differential Dx

A
  • Ovarian remnant or intact female ferret - enlarged vulva, alopecia
  • Seasonal alopecia of the tail
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9
Q

Adrenal Gland Disease surgical treatment

A

Surgical Removal
* Indicated only when one adrenal gland is very large, suspected to be neoplastic, or for cases nonresponding to medical treatments. NOT THE FIRST CHOICE, DOES NOT TREAT THE CAUSE AND NOT CURATIVE (as it will not address the lack of negative feedback to the pituitary)
* Important to perform a full abdominal explore at the time of surgery
* Perform a unilateral adrenalectomy if only one adrenal gland is diseased
* If both glands are diseased, a subtotal adrenalectomy, with total removal of one gland and partial removal of the other is indicated
* May require replacement corticosteroids and mineralocorticoids following surgery
* Post-operative monitoring:
* Electrolyte concentrations - may require supplementation
(but uncommon)
* Desoxycorticosterone pivalate 2 mg/kg IM q21d
* Fludrocorisone acetate 0.05-0.1 mg/kg PO q12h or
divided q12h
* Ferrets will still need to be treated with a deslorelin implant once a year

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10
Q

Adrenal Gland Disease medical management

A
  • Address the hormonal cause of the disease
  • Should also be recommended for normal healthy ferrets, as it is an
    annual implant and will prevent the development of the disease or
    neoplasia later on
  • When to recommend medical management:
  • Routine treatment of adrenal gland disease with no evidence of tumors
  • Ferret is a poor surgical candidate
  • Ferret is geriatric
  • Ferret has bilateral adrenal tumors that cannot be totally
    resected
  • Ferret has recurrent disease in the remaining adrenal after
    unilateral adrenalectomy
  • Treatment options:
  • Melatonin
  • Does not stop the progression of adrenal gland
    disease and/or inhibit the continued growth of the
    affected adrenal glands
  • Does improve hair growth and reduce prostatic size
    and vulvar size
  • Leuprolide acetate
  • 150-450 mcg IM q1month * Deslorelin
  • Duration q6-12 (or more) months
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11
Q

Insulinoma etiology, definition

A
  • Common, middle-aged
  • Pancreaticisletcell tumors → insulin → hypoglycemia
    <><><>
  • Pancreatic islet cell tumors are a common neoplasm affecting middle-aged
    to older ferrets. The clinical signs associated with the disease are related to hypoglycemia due to the excess secretion of insulin from these tumors. The neoplastic beta cells of the pancreas synthesize and release insulin autonomously despite hypoglycemia
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12
Q

Insulinoma clinical signs

A
  • Lethargy,weightloss
  • Ataxia,hindlimb weakness
  • Ptyalism, pawing at the mouth
  • Bizarrebehavior (“staring off into space”), disorientation, collapse, seizures, coma
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13
Q

PE for insulinoma

A
  • Often unremarkable aside from lethargy, generalized weakness, posterior
    weakness, weight loss
  • Oral ulcerations
  • Glazed eye appearance
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14
Q

Insulinoma stabilization

A
  • Home – Sugar solution PO, then protein meal and bring to clinic
  • Clinic
  • IV dextrose – 50% then
    2.5-5%
  • +/- anticonvulsant, corticosteroid, glucagon
    <><><><>
    Stabilization = Medical Therapy for an Acute Hypoglycemic Crisis
  • If the ferret had a hypoglycemic episode at home
  • Clinical signs: collapse, seizure, coma
  • Instruct owner to put sugar solution (Karo, corn syrup, honey) on his
    or her fingers and rub it onto the ferret’s buccal mucosa
  • DO NOT get bitten!
  • DO NOT overtreat as the more glucose you give, the more
    stimulation to release further insulin there is from the tumor
    (rebound effect)
  • If a positive response to glucose, feed a small high protein meal
    once alert and able to swallow and take the to the veterinary
    hospital immediately
  • If the ferret presents to the clinic comatose or seizing
  • Place an IV or IO catheter and administer a slow IV bolus of 50% dextrose (0.25-2 mL) to effect
  • Goal: administer enough dextrose to alleviate clinical signs without causing overstimulation of the tumor (rebound effect)
  • Maintain continuous IV infusion of 2.5-5% dextrose
  • May require anticonvulsant therapy to manage seizures (diazepam,
    midazolam, propofol)
  • Can administer an injection of dexamethasone, followed by an oral
    administration of prednisolone
  • Glucagon 5-15 ng/kg/min CRI in refractory cases can be given and works well. Only give when followed by surgery (as ferrets needing glucagon will not improve without surgery)
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15
Q

Insulinoma Dx

A
  • BG<3mmol/L
  • Insulincanbenormal (suspicious) or high (definite insulinoma)
  • NOTE – handheld glucometers give low readings
    <><><><>
  • CBC/biochemistry profile
  • BG < 3 mmol/L
  • Baseline insulin and glucose concentrations
  • If blood glucose is low and insulin is high = insulinoma
  • If blood glucose is low and insulin is normal = suspicious for
    insulinoma
  • Need to collect a sample when BG is low
  • Repeat if results are unexpected - insulin is released in a pulsatile
    manner
  • Insulin:glucose ratios
  • Not recommended - give many false positives not specific
  • Radiographs - important as part of work-up, but not likely to aid in the
    diagnosis of insulinoma
  • Ultrasound - low sensitivity in detecting islet cell tumors. Also, tumors tend
    to be multifocal
  • NOTE - handheld portable blood glucose monitoring devices measure blood
    glucose values lower than actual glucose values determined by benchtop devices (which gives them high sensitivity in diagnosing hypoglycemia, but they are poorly specific). Good for screening, but glucose needs to be confirmed at the laboratory or the blood gas machine
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16
Q

Insulinoma treatment medical mgmt

A

Medical
management
* Diet – free choice, high fat, high protein, low carbohydrates +
* Prednisolone PO +
* Diazoxide PO –
GI side effects
<><><>
Treatment = Medical Management of Chronic Hypoglycemia * Food/diet
* High fat and protein diet, low carbohydrate
* Free choice feeding
* Discontinue all treats that are high in simple sugars
* Glucocorticoids
* Prednisolone: 0.5-2 mg/kg PO BID
* Monitoring: after initiation of steroid therapy, check blood glucose
in 5-7 days
* Adverse effects: PU/PD/PP, weight gain, impaired hair regrowth
* Diazoxide
* Start in conjunction with prednisolone
* Only drug that treats the cause of the disease
* 5-10 mg/kg PO BID, start low as GI side-effects are common
* Adverse effects are common, start low: anorexia, vomiting,
diarrhea, tachycardia, bone marrow suppression, aplastic anemia, thrombocytopenia, pancreatitis, diabetes mellitus, cataract formation, sodium and fluid retention

17
Q

Insulinoma surgical Tx

A
  • Not curative, slow progression
    <><><><>
    When is surgical treatment indicated
  • Surgical therapy is not usually curative but may stop or slow the
    progression - important to warn owners of this!
  • Surgery does not necessarily remove the need for lifelong daily medication
  • Surgical options: nodulectomy, partial pancreatectomy, or both
  • Metastasis at the time of surgery is uncommon
  • Post-operative pancreatitis very rare in ferrets
  • May require post-operative dextrose if hypoglycemia occurs
  • Only recommended for non-responsive cases or a large identifiable mass is
    present
18
Q

Lymphoma etiology, definition

A
  • common
  • Solid-tissue tumors composed of neoplastic lymphocytes in visceral organs or lymph nodes
  • Young (< 2 years) – lymphoblastic, rapid, disseminated
  • Adult (> 2 years) – mature small lymphocyte, slower, lymphadenopathy
  • But either form, any age
    <><><><>
  • Lymphoma is the most common malignancy in the domestic ferret, and the
    third most common neoplasm overall (after islet cell tumors and adrenocortical neoplasia). Lymphoma denotes solid-tissue tumors composed of neoplastic lymphocytes in visceral organs or lymph nodes throughout the body
  • There is no universally accepted classification scheme of lymphoma in ferrets
  • Can occur at any age (reported as young as 2 months)
  • No color or sex predisposition
  • Young ferrets (< 2 years of age) - more common to see a lymphoblastic
    form with disseminated disease involving the spleen, liver, thymus,
    mediastinum, and rapid progression
  • Adult ferrets (> 2 years of age) - more common to see mature, well-
    differentiated small lymphocytes accompanied by peripheral
    lymphadenopathy and slower progression
  • BUT either form can occur in either age group
19
Q

Lymphoma clinical signs

A
  • Varied OR asymptomatic
    <><><><>
  • Lethargy
  • Inappetence
  • Weakness
  • Diarrhea
  • Dyspnea
  • Respiratory signs
  • OR asymptomatic
20
Q

Lymphoma Dx

A

Cytology/histology
* Include
* Grading (histology)
* Staging (classification)
* +/- phenotyping (IHC for cell origin)
<><><><>
* All diagnostic workups should include both grading (histologic description) and staging (classification of disease) information. Ideally, phenotyping (immunohistochemistry to define cell origin) would also be included
* CBC/chemistry: nonregenerative anemia is the most consistent laboratory abnormality
* NOT lymphocytosis – the most common cause of this is chronic, smoldering infection
* Chemistry changes usually consistent with disease location, hypoglycemia and ionized hypercalcemia may be present but uncommon overall
* Radiographs: look for the presence of mediastinal masses, thoracic lymphadenopathy, pleural effusion, hepatomegaly, splenomegaly, renomegaly
* Absence of abnormalities does not rule out lymphoma
* Ultrasound: evaluate abdominal and mesenteric lymph nodes, evaluate
abdominal organs
* Absence of abnormalities does not rule out lymphoma
* Cytology, histology:
* Cytology - monotonous population of lymphocytes and the absence
of peripheral blood elements
* Typically obtained from peripheral or mesenteric lymph nodes,
masses, or bone marrow aspiration

21
Q

Lymphoma blood signs

A
  • Non-regenerative anemia, not lymphocytosis
  • But–EMHinspleen and reactive lymph nodes very common
22
Q

lymphoma tx

A
  • Chemotherapy/ radiation
    <><><><>
  • Many therapeutic options are available for the treatment of lymphoma in
    rabbits
  • Chemotherapy
  • There are many different chemotherapy protocols published, with varying success. The selection of which to use often depends on the state of the ferret at the time of presentation as well as the owner’s wishes with how aggressive they would like to be
  • See Quesenberry and Carpenter and OVC Oncology service for protocol options
  • Need CBC every week
  • Vascular access port vs. repeated “clean stick” weekly
    catheterization * Radiation
  • Lymphoma is highly responsive to radiation therapy
  • Beneficial for a single enlarged abdominal or thoracic organ,
    or lymph node