Misc Endocrinopathies Flashcards

1
Q

Hypersomatotropism

A
  • Overproduction of growth hormone
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2
Q

Acromegaly

A
  • Syndrome that results from excessive GH production
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3
Q

What causes hypersomatotropism and acromegaly?

A
  • Functional adenoma in the pars distalis of the anterior pituitary
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4
Q

What organ responds to the excessive growth hormone in acromegaly?

A
  • Liver, which produces somatomedins AKA insulin like growth factors (IGF)
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5
Q

What is the most important insulin like growth factor?

A
  • Somatomedin C (IGF-1)

- This leads to clinical signs of acromegaly

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6
Q

What condition is seen concurrently with acromegaly?

A
  • DM almost always
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7
Q

When should you consider hypersomatotropism in a patient?

A
  • Diabetic cat that is not well controlled by 2-4 months, does not go into remission with appropriate insulin and diet change, or requires an insulin dose of 1.5-2 U/kg or higher
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8
Q

Who gets acromegaly?

A
  • Typically older cats (8-14 years)

- Males

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9
Q

What is the first sign of acromegaly?

A
  • uncontrolled diabetes mellitus

- Weight gain with uncontrolled diabetes mellitus, where it should usually cause weight loss

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10
Q

Clinical signs of acromegaly

A
  • Classic enlargement of extremities, jaw, tongue, forehead
  • Clubbing of paws
  • Organ enlargement
  • Stridor due to growth of soft tissue in mouth and pharyngeal region
  • Degenerative joint disease
  • Cardiomegaly, systolic murmurs, interventricular septal thickening, thickening of left ventricle (congestive heart failure)
  • Potential hypertension
  • Potential CNS signs (large pituitary masses or diabetic neuropathy)
  • Thickening of skin and excessive skin folds around the head and neck
  • Renomegaly, proteinuria (glomerulosclerosis), diabetic nephropathy - chronic renal failure
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11
Q

Diagnosis of acromegaly

A
  • usually accomplished using a combination of history, clinical signs, and multiple diagnostic tests
  • No definitive test exists
  • Potential testing could be IGF-1 concentration, GH levels (not in US), or advanced imaging like CT or MRI of the brain
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12
Q

Treatment of acromegaly

A
  • Surgery
  • Radiation
  • Medical therapy
  • Palliative
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13
Q

Surgery to correct acromegaly

A
  • Transsphenoidal hypophysectomy

- Remission of DM common within 4 weeks

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14
Q

Radiation for acromegaly

A
  • response variable

- Can take longer than a year

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15
Q

Medical therapy for acromegaly

A
  • Somatostatin analogs, but still being researched
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16
Q

Palliative care for acromegaly

A
  • Give lots of insulin and diet change (LOTS of insulin)

- Poor long term prognosis (CHF, CRF, CNS signs)

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17
Q

What usually causes acromegaly in dogs?

A
  • Adenoma

- Excessive progesterone

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18
Q

Excessive progesterone in female dogs and acromegaly

A
  • Exogenous administration
  • Endogenous production seen in cycling older intact female dogs
  • Triggers production of GH from mammary tissue
  • Correct by spaying
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19
Q

Feline Cushing’s cause

A
  • Noniatrogenic or spontaneous hyperadrenocorticism is rare in cats
  • Iatrogenic HAC is also rare
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20
Q

Prevalence of PDH vs ADH in feline Cushing’s

A
  • PDH more prevalent (75-80%)

- ADH (20-25%)

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21
Q

Feline Cushing’s PDH

A
  • usually due to adenoma of pars intermedia or pars distalis of pituitary gland
  • rarely pituitary carcinomas have been seen
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22
Q

Feline Cushing’s ADH

A
  • usually caused by a benign functional adenoma of one adrenal (65%)
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23
Q

Clinical signs of Cushing’s in cats

A
  • Most present with signs of diabetes potentially poorly controlled
  • Excess of either endogenous or exogenous glucocorticoid leads to marked insulin resistance
  • PU/PD LESS common
  • More often weight loss
  • Abdominal distension or “pot belly appearance”
  • Panting, muscle atrophy, unkempt hair coat, bilateral symmetric alopecia
  • Predisposition for infections (urinary, skin, respiratory, abscesses, toxoplasmosis, etc.)
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24
Q

Do you see weight gain or weight loss more commonly in feline Cushing’s?

A
  • Weight loss
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25
What should you consider when handling cats with Cushing's?
- Fragile skin syndrome - Tearing of the skin under normal conditions - HANDLE GENTLY! - Do not develop calcinosis cutis
26
What signs could be due to pituitary macroadenoma in feline Cushing's?
- CNS signs | - Blindness, abnormal behavior
27
Virilization in feline Cushing's
- Spines on castrated males | - Virilization with sex hormones secreting adrenal carcinomas
28
CBC changes in feline Cushing's
- Stress leukogram inconsistent
29
Chemistry changes in Cushing's
- No steroid inducible ALP in cats
30
Urinalysis changes in feline Cushing's
- Dilute urine rare with HAC in cats - Lack of an effect of cortisol on feline ADH secretion or sensitivity - USG can be affected by glucosuria (if DM) - Can see proteinuria
31
Screening test of choice for feline Cushing's?
- LDDST | - higher dose of dex used vs dogs (10x)
32
Other screening tests for feline Cushing's
- ACTH stim (2/3 of cats with HAC will have cortisol concentrations within normal limits) - UCCR - poor specificity but good sensitivity
33
Differentiation between ADH and PDH in feline Cushing's
- HDDS (50% of PDH cats show no suppression) - Endogenous ACTH - Imaging - AUS, CT, MRI***
34
Palliative treatment in feline Cushing's
- Not really an option - They are miserable if untreated - Fragile skin and 2° infections
35
Medical treatment for feline Cushing's
- Trilostane (preferred) - Mitotane (less effective) - Metyrapone (enzyme inhibitor that may be effective in some cats)
36
Radiation in feline Cushing's
- unreliable response
37
Surgical treatment of feline Cushing's
- Hypophysectomy | - Bilateral adrenalectomy
38
Hypophysectomy
- Limited availability | - Expensive
39
Bilateral adrenalectomy for tx of feline Cushing's
- Increased risk - Poor wound healing - Lifelong supplementation
40
Etiology of hyperaldosteronism
- Adrenocortical carcinoma - Adenoma (unilateral or bilateral) - Bilateral nodular hyperplasia
41
Who gets primary hyperaldosteronism (species)?
- Most commonly seen in cats - Dogs can rarely be affected - May be the most common adrenocortical disorder in cats - Often misdiagnosed as CKD due to effects on the kidney
42
Who gets primary hyperaldosteronism (age)?
- Middle-aged to older cats | - Median 13 years old (5-20 years)
43
What are the primary clinical signs due to in primary hyperaldosteronism?
- Hypertension (end organ damage) | - Hypokalemia (not usually hypernatremia)
44
Other clinical signs of primary hyperaldosteronism
- Pendulous abdomen/mass - PU/PD - Muscle atrophy - Arrhythmia - Non-specific: panting, restlessness, anorexia, weight loss
45
Hypokalemia (<2.5mmol/L) in primary hyperaldosteronism clinical signs
- Polymopathy - Muscle weakness that is episodic or acute - Plantigrade stance (cat isn't jumping) - Cervical ventroflexion - Inability to jump - Lateral recumbency, collapse
46
Clinical signs attributable to hypertension
- Mydriasis - Hyphema - Loss of vision (retinal detachment, intraocular hemorrhage)
47
Physical exam findings with primary hyperaldosteronism
- Hypertension - Ocular changes: intraocular hemorrhage, increased tortuosity, retinal edema, detachment - hypokalemic polymyopathy - Palpable mass in abdomen - Arrhythmia
48
Laboratory abnormalities with primary hyperaldosteronism
- Hypokalemia and *metabolic alkalosis* are most important changes seen**** - Others are azotemia, increased phosphorus, increased CK, hyperglycemia, and hypernatremia
49
Diagnosis of primary hyperaldosteronism
- Ultrasound, CT, MRI - Look at adrenals for evidence of a mass - Evaluate for metastasis - Evaluate for local invasion
50
Surgical treatment for primary hyperaldosteronism
- Adrenalectomy for unilateral adenoma or carcinoma - High rate of complications leading to death - Survivors live >1 year
51
Medical treatment for primary hyperaldosteronism
- Potassium supplementation (K gluconate) - Aldosterone blocker (Spironolactone) - Antihypertensives (Amlodipine)
52
Differentials for hypoglycemia
- Malnutrition - Parasites - Artifact - Hepatic insufficiency - Cellular consumption (WBC, e.g. with hepatozoon which causes a very high WBC) - Xylitol toxicity - Endocrine: Insulinoma, IGF (many tumors), insulin overdose, hormone deficiency (cortisol, growth hormone)
53
Insulinoma overview
- Pancreatic beta-cell tumors - Excess production of insulin by a functional tumor - Most common canine islet cell neoplasia
54
Are insulinomas usually benign or malignant?
- most are carcinomas
55
Species that get insulinomas
- Dogs: uncommon - Cats: RARE - Ferrets: common!!
56
Age predisposition of insulinoma
- 9 years average
57
Breed predisposition of insulinoma
- medium ot large breed dogs
58
Sex predisposition of insulinoma
- No sex predilection
59
Clinical signs associated with insulinoma
- Associated with hypoglycemia, but otherwise healthy
60
Physical exam findings associated with insulinoma
- Usually no significant abnormalities | - Overweight; anabolic effects of insulin
61
CBC findings on insulinoma
- Normal
62
Chemistry panel findings on insulinoma
- Marked hypoglycemia - +/- mild hypokalemia - +/- elevated ALP or ALT (if metastasized to the liver)
63
Urinalysis findings on insulinoma
- Unremarkable usually
64
Diagnosis of insulinoma
- CBC/Chem/UA - Paired insulin/BG levels - Abdominal radiographs/ultrasound/CT
65
Paired insulin/BG levels - when to obtain the sample?
- Blood sample must be obtained when the animal is hypoglycemic
66
Hallmark of insulinoma with paired insulin/BG levels
- Increased blood insulin concentration despite a low blood glucose concentration
67
Abdominal radiographs for insulinoma
- Usually normal, as they are very small tumors
68
Abdominal ultrasound for insulinoma
- Pancreatic mass in 50% | - Metastatic lesions in 20% (liver, lymph nodes)
69
CT findings for insulinoma
- Pre-op for larger tumors
70
Surgery insulinoma treatment
- Treatment of choice... - Has often metastasized - High recurrence rate - Difficult to find tumors
71
Chemotherapy insulinoma treatment
- Streptozotocin - Destroys beta cells in pancreas and metastatic sites - Remission in some dogs - Nephrotoxic
72
Prognosis if insulinoma treated with chemotherapy vs surgery
- Prognosis similar to surgery | - surgery usually preferred because of the nephrotoxicity of the chemotherapeutic agents
73
Medical management of insulinoma
- Avoid sharp rises in BG - Frequent, small meals every 4-6 hours - High in protein, fat, and complex carbs - Avoid simple sugars
74
Anti-insulin drugs for insulinoma
- Glucocorticoids - Diazoxide - Somatostatin (octeotide) - Glucagon
75
Glucocorticoids for insulinoma
- Increase gluconeogenesis, decrease BG uptake, stimulate glucagon secretion
76
Diazoxide for insulinoma
- Inhibits insulin release | - Very expensvie
77
Somatostatin for insulinoma
- Extremely expensive | - Antagonizes insulin
78
Glucagon for insulinoma
- Increases gluconeogenesis
79
Prognosis of insulinoma
- 12-14 months survival time (including dogs that went to surgery)
80
Prognosis of insulinoma with young dogs
- worse
81
Insulinoma post-op hyperglycemia/normoglycemia vs hypoglycemia
- Better prognosis if hyper or normoglycemia