Pituitary Endocrine Disorders Flashcards

1
Q

OBJ: Know and understand the clinical signs and pathophysiology of Acromegaly

A
  • Unregulated diabetes (PU/PD/PP)
  • Broad face, prominent jowls
  • Large body size
  • thick skin on head, neck, limbs
  • heart failure signs
  • arthritis/arthropathy
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2
Q

OBJ: Know and understand the clinical signs and pathophysiology of Diabetes Insipidus (DI)

A
  • excessive thirst
  • water-seeking
  • increase urine production
  • encephalopathy
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3
Q

OBJ: Know and understand the key clinical and laboratory features of Acromegaly

A
  • Hyperphosphatemia without azotemia
  • Hyperglobulinemia
  • elevated ALP and ALT
  • Proteinuria/Hyposthenuria
  • periarticular periosteal proliferation
  • Hyperostosis of the skull
  • Cardio-, hepato-, and renomegaly
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4
Q

OBJ: Know and understand the key clinical and laboratory features of Diabetes Insipidus

A
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5
Q

OBJ: Know and understand the diagnostic tests used to confirm Acromegaly

A
  • Hormone assessment
    • GH - not useful do to fluctuations and availability
    • Insulin-like Growth Factor 1
      • liver response to GH
      • reflects GH 24hr prior - Elevated in Acro
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6
Q

OBJ: Know and understand the diagnostic tests used to confirm Diabetes Insipidus

A
  • Monitor water intake for 24hr
    • obtain serial plasma and urine osmolality
  • Determine response to Osmotic stimulus and ADH
    • Water deprivation test
    • DDAVP response test (ADH analogue)
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7
Q

OBJ: Know and understand the treatment options for Acromegaly

A
  • Radiation - TOC cats
  • Hypophysectomy
  • Medical management
    • pasireotide
    • supportive care
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8
Q

OBJ: Know and understand the treatment options for Diabetes Insipidus (DI)

A
  • provide water
  • intranasal DDAVP
  • Monitor for over/under treatment
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9
Q

What is Acromegaly?

A
  • “Hypersomatotrophism”
  • Chronic excess GH secretion
    • GH (growth hormone) aka somatotrophin
    • Causes overgrowth of soft tissues, bones, and viscera (anabolic) and insulin resistance (catabolic
  • RARE
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10
Q

What is the etiology of Acromegaly in cats?

A
  • ACRO caused by GH producing pituitary tumor
  • Macroadenoma of the pituitary somatotrophs
  • Functional, benign tumor; locally expansive; rare distal metastasis
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11
Q

What is the etiology of Acromegaly in Dogs?

A
  • Excess progestin compounds
  • Exogenous or endogenous PROG stimulates GH secretion
  • Medroxyprogesterone (MPA; Depo-Provera) most commonly implicated
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12
Q

What is the common signalment/history of patients with Acromegaly

A
  • Geriatric males over-represented (mean age 10yo)
  • Unregulated diabetes (PU/PD/PP) - historical or at initial presentation
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13
Q

What are the common physical exam findings of a patient with Acromegaly?

A
  • Pronounced physical changes
    • Broad face, prominent jowls
    • Protruding jaw (prognathia), enlarged interdental spaces
    • Large body size, distended abdomen
    • Thick skin on head, neck, limbs (dogs)
    • Weight gain (*despite diabetes mellitus)
    • Heart failure signs (tachycardia, dyspnea)
    • Arthritis/arthropathy
    • Neurological signs (abnormal mentation, depression
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14
Q

Which hormones can be assessed for an Acromegaly diagnosis? which is the most useful?

A
  • GH
  • IGF-1 - MOST useful
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15
Q

Why isn’t GH as useful for diagnostics

A
  • Should be most useful, but
    • GH level fluctuates over the day and disease stage
    • GH assays not regularly available
    • GH level rarely determined in dogs and cats
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16
Q

Why is IGF-1 most useful

A
  • IGF-1 is produced in the liver in response to GH
  • IGF-1 level reflects GH secretion for 24 hr prior and is ELEVATED in Acromegaly
  • Some poorly-regulated diabetic cats have elevated IGF-1 levels that overlap with Acromegaly cats
    • very high level strongly suggests Acromegaly
  • Feline and Canine IGF-1 assays are offered by several commercial labs
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17
Q

What Laboratory Findings are common for patients with Acromegaly?

A
  • CBC - erythrocytosis
  • CHEM:
    • changes caused by diabetes - hyperglycemia, hypercholestrolemia
    • Elevations in ALP and ALT
    • Hyperglobulinemia
    • Hyperphosphatemia without Azotemia
    • Renal failure present in some cats: azotemia and hyperphosphotemia
  • Urinalysis:
    • Proteinuria
    • Hyposthenuria
    • Ketonuria is uncommon
18
Q

What findings are common during imaging of patients with acromegaly?

A
  • Enlarged soft tissues of head and neck
  • Periarticular periosteal proliferation
  • Elongated mandible
  • Hyperostosis of the skull
  • Cardio-, hepato- and renomegaly
19
Q

What are the treatment options for Acromegaly?

A
  • Radiation - TOC in cats
    • mixed results; improvement over months
  • Hypophysectomy
    • some success w/ surgical removal of tumor; limited experience/availability
  • Medical Management
    • Pasireotide (somatostatin analogue) - shows promise in European studies $$$
    • Others - bromocriptine, octreotide
      • Not useful in cats
    • Supportive therapy - address diabetes, heart failure, renal insufficiency
20
Q

What is the prognosis for patients with Acromegally?

A
  • Guarded to poor
  • survival is 18 - 36 monthsd
21
Q

How is Diabetes Mellitus regulated in cats with Acromegally?

A
  • Same treatment principles as other diabetic cats
  • Ketosis is uncommon
  • Large doses of insulin may be needed
  • May never get complete control
  • Affected cats are at risk for DM complications
22
Q

What is Diabetes Insipidus (DI)?

A
  • RARE disorder
  • Caused by ADH deficiency
    • ADH - Anti-diuretic hormone (aka “AVP”)
    • Produced from posterior pituitary
    • Main hormone involved in water balance
    • ADH deficiency = POLYURIA (increased urine volume)
23
Q

What are the different types of Canine Diabetes Insipidus (CDI)?

A
  • Complete - NO ADH secretion
  • Partial - Insufficient amounts of ADH
24
Q

What are the causes of Canine Diabetes Insipidus?

A
  • Congenital - genetic/developmental
  • Acquired - various causes
    • intracranial tumor
    • Metastatic tumor
    • Infiltrative disease
    • Infection
    • Head trauma
    • pituitary surgery
25
Q

What are the clinical signs of CDI?

A
  • Excessive thirst
  • water-seeking behavior
  • Increased urine production
  • Encephalopathy - ill animals
  • Signs of primary disease (acquired CDI)
26
Q

What Laboratory findings are common in CDI?

A
  • Hydrated animals:
    • Typically normal
    • Dilute USG (<1.008)
  • Dehydrated animals:
    • Hypernatremia (severe)
    • Neurologic impairment
    • Azotemia (pre-renal)
    • Dilute USG (<1.008)
27
Q

What are the common differential diagnoses for CDI?

A
  • Primary Polydipsia (PP)
    • young, hyperactive, excitable dogs
    • Environmental/physical stressors
    • Resolution occurs in novel situations
  • Nephrogenic Diabetes Insipidus (NDI)
    • Acquired water imbalance - secondary to other disorders (e.g. hypercalcemia, renal failure)
    • “ADH” resistance
    • Normal ADH productions
    • Kidney is insensitive to ADH
28
Q

How is CDI diagnosed?

A
  • Quantitate 24-hr water intake
  • Obtain serial plasma and urine osmolality
  • Determine response to osmotic stimulus and ADH
    • water deprivation test
    • DDAVP response test (ADH analogue)
29
Q

What is the treatment for CDI?

A
  • Ensure adequate access to water at all times
  • Intranasal DDAVP formulation
    • 1 drop q12 hors into conjunctival sac
    • Monitor to ensure patient is not over/under treated
30
Q

What is the prognosis for CDI?

A
  • Good for congenital CDI
    • as long as the owner is aware and willing to treat
  • Guarded/Poor for acquired CDI
    • depends on primary pathology
31
Q

What is the common signalment in dogs with acromegaly?

A
  • Intact females (mean 7-8yo)
  • young dogs receiving MPA
32
Q

What history is common to dogs with Acromegaly

A
  • Respiratory stridor, panting, fatigue
  • Hx of MPA administration or estrus cycling
  • Occasionally diabetes is present
  • Less common: vaginitis, pyometra, skin and joint changes
33
Q

How is acromegaly diagnosed in dogs?

A
  • Based on history of progesterone exposure
34
Q

What is the treatment for canine Acromegaly?

A
  • Medical management (TOC)
    • Discontinue exogenous progestin or perform ovariohysterectomy
    • All organ and tissue changes are expected to resolve over time
    • Diabetes in dogs with ACRO can resolve
      • Diabetes never resolves in some dogs and insulin is needed for life
    • Prognosis - good with appropriate therapy
35
Q

What is Pituitary Dwarfism?

A
  • “Hypopituitarism”
  • Extremely Rare
    • German shepherd dogs are most commonly affected
36
Q

What is the etiology and pathology of Pituitary Dwarfism?

A
  • Genetic defect - genes unknown
  • Autosomal recessive in GSD - unknown in other breeds
  • Histology:
    • pituitary hypoplasia (anterior lobe)
    • Pituitary cysts - may be cause for consequence of hypoplasia
37
Q

What clinical signs are common in Pituitary dwarfism dogs?

A
  • Growth retardation - noticed at a young age, concern about poor growth
  • Hair/coat abnormalities - retained puppy coat; alopecia may occur over time
  • Determatopathy - hyperpigmentation and dry skin/scaling
  • Reproductive abnormalities - cryptorchidism and anestrus
  • Normal activity with lethargy developing later in life
38
Q

How is Hypopituitarism diagnosed?

A
  • Requires measurement of abnormal GH secretion
  • Basal GH level test - typically low but inconsistent (NOT recommended)
  • GH stimulation test:
    • assess GH secretion after injection of GH secretogogue
    • Normal dogs = 2-4x increase
    • Not widely available
  • Ancillary Testing - needed for full patient evaluation
    • Assess thyroid, adrenal, and reproductive function
    • Pituitary imaging - Brain CT/MRI
      • small pituitary/cystic structures
39
Q

How is Hypopituitarism treated?

A
  • Optimal = GH replacement
    • Canine/Feline GH is not commercially available for hormone replacement
    • Porcine GH has bee used for dogs
    • Hypoglycemia and diabetes are potential side effects
  • Progestins may provide alternative therapy - not studied
40
Q

What responses are expected from treatment of hypopituitarism?

A
  • Growth may occur - depending on the status of the growth plates
  • Improvement in skin and coat
41
Q

What is the prognosis of Hypopituitarism?

A
  • Poor w/out treatment
  • Guarded w/ treatment