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Amyloidosis 51

• Patients can have significant insensible water stress of hospitalization. If a very low dose of Client Education
loss and may require aggressive fluid admin- acepromazine (0.01-0.02 mg/kg IV) resolves • Keep all medications out of the reach of
VetBooks.ir hydration status, especially because amphet- Prevention • Make sure children know ADHD/ADD Diseases and Disorders
istration. Fluid ins and outs can help estimate
pets.
the clinical signs, they are not likely due to
toxicosis.
amines are renally excreted. Excretion of
medications can harm their pets.
amphetamines is decreased with alkaline
urine. Keep all medications out of pet’s reach, includ- SUGGESTED READING
• Signs can last up to 72 hours. Discharge ing keeping children’s backpacks in a closet or Stern LA, et al: Management of attention deficit
pets only after > 8 hours free from any hung on a high hook. disorder/attention deficit hyperactivity disorder
stimulatory signs. drug intoxication in dogs and cats. Vet Clin of N
• Cats may become more withdrawn and Technician Tips Am: Small Anim Pract 42:279-288, 2012.
stare, rather than becoming hyperactive. • Keep affected animals in a dark and quiet AUTHOR: Laura Stern, DVM, DABVT
Given the typical amount of stress that cats environment. Minimizing stimulation often EDITOR: Tina Wismer, DVM, MS, DABVT, DABT
experience when hospitalized, response to decreases the amount of sedatives needed.
acepromazine may be very helpful in dif- • Body temperature should be monitored
ferentiating a cat that is showing clinical closely because hyperthermia can lead to
signs of toxicosis from one that is showing seizures and coagulopathy.

Amyloidosis Client Education
Sheet

BASIC INFORMATION hepatozoonosis); most amyloidosis in non- chronic infection, chronic inflammatory
predisposed breeds is reactive. disease, myeloma).
Definition • Dogs:
Amyloidosis is the pathologic deposition of ○ Reactive amyloid deposition causes glo- PHYSICAL EXAM FINDINGS
polymerized proteins in a beta-pleated sheet merular disease with PLN and variable • Often unremarkable; mild enlargement of
conformation; it disrupts function of involved progression to renal failure. involved organs is possible.
organs, most often the kidneys. ○ Amyloidosis in Chinese Shar-peis: variable • For reactive amyloidosis, abnormalities
proteinuria; renal failure possible without depend on underlying inflammatory process.
Epidemiology PLN • Chinese Shar-peis may have fever, joint
SPECIES, AGE, SEX ■ History may include intermittent effusion, and arthralgia (especially distal
Uncommon in dogs; rare in cats. Middle-aged fever and inflammatory, nonerosive joints).
to older dogs (median age at diagnosis, 9 years) polyarthritis. • If nephrotic syndrome is present (p. 691)
and cats; Chinese Shar-peis present at a younger ■ Hepatic amyloidosis with or without ○ Ascites, edema, or effusion
age (median age at diagnosis, 4.5 years) renal amyloidosis may also occur. ○ Variable kidney size
• Cats: amyloid deposition can occur without ○ Evidence of thromboembolism
GENETICS, BREED PREDISPOSITION clinical signs. ○ Evidence of hypertension (e.g., cho-
• Dogs: Chinese Shar-peis (renal and hepatic ○ Abyssinians: glomerular and/or medullary roidopathy, central nervous system [CNS]
amyloidosis), English foxhounds; any breed amyloid deposition with variable severity signs)
may be affected by reactive/secondary of proteinuria; renal failure may develop • Rarely, cats with systemic amyloidosis develop
form without PLN. hepatic rupture and acute hemoabdomen.
• Cats: Abyssinians (renal amyloidosis), ○ Siamese/oriental cats: systemic amyloid • Pulmonary, cardiac, dermal, or CNS amyloid
Siamese/oriental cats (systemic amyloidosis) deposition; clinical signs depend on organs deposition and resultant organ dysfunction
affected. occur rarely.
RISK FACTORS
Chronic inflammatory/infectious/neoplastic HISTORY, CHIEF COMPLAINT Etiology and Pathophysiology
diseases predispose to reactive amyloidosis. • Clinical signs frequently absent until late in • Proteins with beta-pleated sheet conforma-
disease tion accumulate within extracellular spaces,
ASSOCIATED DISORDERS • Chinese Shar-peis may be intermittently leading to organ dysfunction.
• Protein-losing nephropathy (PLN) ± febrile and/or lame from a young age. ○ Glomeruli are the most common site of
nephrotic syndrome • Siamese or oriental cats may present with accumulation in dogs other than Shar-peis,
• Chronic kidney disease (CKD) and renal life-threatening intraabdominal hemorrhage leading to proteinuria.
failure due to liver lobe fracture secondary to ○ Deposition within the renal medulla, liver,
• Other organ dysfunction depends on sites massive hepatic deposition of amyloid. and other organs may occur with or
of amyloid deposition. • Clinical signs of uremia (p. 169) are common. without glomerular involvement.
• In Chinese Shar-peis: swollen hock syndrome, • Clinical signs of nephrotic syndrome (e.g., • Reactive amyloidosis is most common.
familial Shar-pei fever edema/ascites [pp. 79 and 284]) and/or ○ Deposited protein is amyloid protein A,
concurrent hypercoagulability (e.g., pulmo- a fragment of serum amyloid A (SAA).
Clinical Presentation nary thromboembolism [p. 842]) may be ○ SAA increases with systemic inflammation.
DISEASE FORMS/SUBTYPES noted. ○ Evidence suggests a dysregulated
• Reactive amyloidosis occurs secondary • For reactive amyloidosis, clinical signs may inflammatory response leads to amyloid
to chronic inflammatory diseases (e.g., be attributable to an underlying process (e.g., deposition.

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