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SA Medicine Endocrine > Misc Endocrinopathies > Flashcards

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
Q

What should you consider when handling cats with Cushing’s?

A
  • Fragile skin syndrome
  • Tearing of the skin under normal conditions - HANDLE GENTLY!
  • Do not develop calcinosis cutis
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26
Q

What signs could be due to pituitary macroadenoma in feline Cushing’s?

A
  • CNS signs

- Blindness, abnormal behavior

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27
Q

Virilization in feline Cushing’s

A
  • Spines on castrated males

- Virilization with sex hormones secreting adrenal carcinomas

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28
Q

CBC changes in feline Cushing’s

A
  • Stress leukogram inconsistent
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29
Q

Chemistry changes in Cushing’s

A
  • No steroid inducible ALP in cats
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30
Q

Urinalysis changes in feline Cushing’s

A
  • 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
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31
Q

Screening test of choice for feline Cushing’s?

A
  • LDDST

- higher dose of dex used vs dogs (10x)

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32
Q

Other screening tests for feline Cushing’s

A
  • ACTH stim (2/3 of cats with HAC will have cortisol concentrations within normal limits)
  • UCCR - poor specificity but good sensitivity
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33
Q

Differentiation between ADH and PDH in feline Cushing’s

A
  • HDDS (50% of PDH cats show no suppression)
  • Endogenous ACTH
  • Imaging - AUS, CT, MRI***
34
Q

Palliative treatment in feline Cushing’s

A
  • Not really an option
  • They are miserable if untreated
  • Fragile skin and 2° infections
35
Q

Medical treatment for feline Cushing’s

A
  • Trilostane (preferred)
  • Mitotane (less effective)
  • Metyrapone (enzyme inhibitor that may be effective in some cats)
36
Q

Radiation in feline Cushing’s

A
  • unreliable response
37
Q

Surgical treatment of feline Cushing’s

A
  • Hypophysectomy

- Bilateral adrenalectomy

38
Q

Hypophysectomy

A
  • Limited availability

- Expensive

39
Q

Bilateral adrenalectomy for tx of feline Cushing’s

A
  • Increased risk
  • Poor wound healing
  • Lifelong supplementation
40
Q

Etiology of hyperaldosteronism

A
  • Adrenocortical carcinoma
  • Adenoma (unilateral or bilateral)
  • Bilateral nodular hyperplasia
41
Q

Who gets primary hyperaldosteronism (species)?

A
  • 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
Q

Who gets primary hyperaldosteronism (age)?

A
  • Middle-aged to older cats

- Median 13 years old (5-20 years)

43
Q

What are the primary clinical signs due to in primary hyperaldosteronism?

A
  • Hypertension (end organ damage)

- Hypokalemia (not usually hypernatremia)

44
Q

Other clinical signs of primary hyperaldosteronism

A
  • Pendulous abdomen/mass
  • PU/PD
  • Muscle atrophy
  • Arrhythmia
  • Non-specific: panting, restlessness, anorexia, weight loss
45
Q

Hypokalemia (<2.5mmol/L) in primary hyperaldosteronism clinical signs

A
  • Polymopathy
  • Muscle weakness that is episodic or acute
  • Plantigrade stance (cat isn’t jumping)
  • Cervical ventroflexion
  • Inability to jump
  • Lateral recumbency, collapse
46
Q

Clinical signs attributable to hypertension

A
  • Mydriasis
  • Hyphema
  • Loss of vision (retinal detachment, intraocular hemorrhage)
47
Q

Physical exam findings with primary hyperaldosteronism

A
  • Hypertension
  • Ocular changes: intraocular hemorrhage, increased tortuosity, retinal edema, detachment
  • hypokalemic polymyopathy
  • Palpable mass in abdomen
  • Arrhythmia
48
Q

Laboratory abnormalities with primary hyperaldosteronism

A
  • Hypokalemia and metabolic alkalosis are most important changes seen**
  • Others are azotemia, increased phosphorus, increased CK, hyperglycemia, and hypernatremia
49
Q

Diagnosis of primary hyperaldosteronism

A
  • Ultrasound, CT, MRI
  • Look at adrenals for evidence of a mass
  • Evaluate for metastasis
  • Evaluate for local invasion
50
Q

Surgical treatment for primary hyperaldosteronism

A
  • Adrenalectomy for unilateral adenoma or carcinoma
  • High rate of complications leading to death
  • Survivors live >1 year
51
Q

Medical treatment for primary hyperaldosteronism

A
  • Potassium supplementation (K gluconate)
  • Aldosterone blocker (Spironolactone)
  • Antihypertensives (Amlodipine)
52
Q

Differentials for hypoglycemia

A
  • 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
Q

Insulinoma overview

A
  • Pancreatic beta-cell tumors
  • Excess production of insulin by a functional tumor
  • Most common canine islet cell neoplasia
54
Q

Are insulinomas usually benign or malignant?

A
  • most are carcinomas
55
Q

Species that get insulinomas

A
  • Dogs: uncommon
  • Cats: RARE
  • Ferrets: common!!
56
Q

Age predisposition of insulinoma

A
  • 9 years average
57
Q

Breed predisposition of insulinoma

A
  • medium ot large breed dogs
58
Q

Sex predisposition of insulinoma

A
  • No sex predilection
59
Q

Clinical signs associated with insulinoma

A
  • Associated with hypoglycemia, but otherwise healthy
60
Q

Physical exam findings associated with insulinoma

A
  • Usually no significant abnormalities

- Overweight; anabolic effects of insulin

61
Q

CBC findings on insulinoma

A
  • Normal
62
Q

Chemistry panel findings on insulinoma

A
  • Marked hypoglycemia
  • +/- mild hypokalemia
  • +/- elevated ALP or ALT (if metastasized to the liver)
63
Q

Urinalysis findings on insulinoma

A
  • Unremarkable usually
64
Q

Diagnosis of insulinoma

A
  • CBC/Chem/UA
  • Paired insulin/BG levels
  • Abdominal radiographs/ultrasound/CT
65
Q

Paired insulin/BG levels - when to obtain the sample?

A
  • Blood sample must be obtained when the animal is hypoglycemic
66
Q

Hallmark of insulinoma with paired insulin/BG levels

A
  • Increased blood insulin concentration despite a low blood glucose concentration
67
Q

Abdominal radiographs for insulinoma

A
  • Usually normal, as they are very small tumors
68
Q

Abdominal ultrasound for insulinoma

A
  • Pancreatic mass in 50%

- Metastatic lesions in 20% (liver, lymph nodes)

69
Q

CT findings for insulinoma

A
  • Pre-op for larger tumors
70
Q

Surgery insulinoma treatment

A
  • Treatment of choice…
  • Has often metastasized
  • High recurrence rate
  • Difficult to find tumors
71
Q

Chemotherapy insulinoma treatment

A
  • Streptozotocin
  • Destroys beta cells in pancreas and metastatic sites
  • Remission in some dogs
  • Nephrotoxic
72
Q

Prognosis if insulinoma treated with chemotherapy vs surgery

A
  • Prognosis similar to surgery

- surgery usually preferred because of the nephrotoxicity of the chemotherapeutic agents

73
Q

Medical management of insulinoma

A
  • Avoid sharp rises in BG
  • Frequent, small meals every 4-6 hours
  • High in protein, fat, and complex carbs
  • Avoid simple sugars
74
Q

Anti-insulin drugs for insulinoma

A
  • Glucocorticoids
  • Diazoxide
  • Somatostatin (octeotide)
  • Glucagon
75
Q

Glucocorticoids for insulinoma

A
  • Increase gluconeogenesis, decrease BG uptake, stimulate glucagon secretion
76
Q

Diazoxide for insulinoma

A
  • Inhibits insulin release

- Very expensvie

77
Q

Somatostatin for insulinoma

A
  • Extremely expensive

- Antagonizes insulin

78
Q

Glucagon for insulinoma

A
  • Increases gluconeogenesis
79
Q

Prognosis of insulinoma

A
  • 12-14 months survival time (including dogs that went to surgery)
80
Q

Prognosis of insulinoma with young dogs

A
  • worse
81
Q

Insulinoma post-op hyperglycemia/normoglycemia vs hypoglycemia

A
  • Better prognosis if hyper or normoglycemia

SA Medicine Endocrine (8 decks)

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