Endocrine Flashcards

1
Q

What can cause dramatic pathological consequences in cats during the early growth phase of life?

A

Growth hormone (GH) deficiency

GH deficiency can lead to issues such as congenital hyposomatotropism and its effects.

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2
Q

What is congenital hyposomatotropism in cats also known as?

A

Pituitary dwarfism

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3
Q

What is a common cause of congenital hyposomatotropism in dogs?

A

Failure of Rathke’s pouch to differentiate into a normal anterior pituitary

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4
Q

What clinical presentation is typical for congenital hyposomatotropism in kittens?

A

Stunted growth becomes evident by 1–2 months of age

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5
Q

What are some additional findings in cats with isolated congenital hyposomatotropism?

A
  • Prolonged retention of deciduous teeth
  • Dry, dull hair coat
  • Bilateral corneal edema
  • Generalized weakness and lethargy
  • Clinical signs associated with hypoglycemia
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6
Q

What tests are used to diagnose GH deficiency in cats?

A

GH assays and IGF-1 testing

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7
Q

What is the significance of IGF-1 testing in diagnosing GH deficiency?

A

IGF-1 secretion is non-pulsatile and reflects GH secretion over the preceding 24 hours

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8
Q

What challenges exist in treating GH deficiency in cats?

A

Lack of feline-specific GH products and potential for adverse effects and antibody formation

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9
Q

What is the prevalence of hypersomatotropism in diabetic cats?

A

Estimates range from 18% to 32%

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10
Q

What is the most common cause of hypersomatotropism in cats?

A

A tumor of the pars distalis of the anterior pituitary

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11
Q

What environmental risk factors have been implicated in promoting endocrine tumorigenesis in cats?

A
  • Organochlorine pesticides
  • Industrial compounds (e.g., PCBs)
  • Brominated flame retardants
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12
Q

What genetic contribution has been suggested in cats with hypersomatotropism?

A

A non-synonymous SNP in exon 1 (AIP C9T>G)

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13
Q

What clinical signs may indicate hypersomatotropism in cats?

A
  • Progressive upper respiratory noise
  • Myocardial thickening
  • Unexplained weight gain
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14
Q

What is the recommended screening for newly diagnosed diabetic cats?

A

Measure serum IGF-1

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15
Q

What is the mean age of diabetic cats suspected to have hypersomatotropism in a large UK study?

A

11.3 years

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16
Q

What is the significance of the finding that only 24% of attending clinicians suspected hypersomatotropism prior to diagnosis?

A

Indicates phenotypic recognition is challenging

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17
Q

What treatment has not been effective in stimulating GH secretion in cats?

A

Progesterone therapy

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18
Q

What can be a consequence of untreated congenital hyposomatotropism in cats?

A

Poor prognosis and reduced lifespan

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19
Q

What are the higher levels observed in cats with IGF-1?

A

Higher body weights, higher fructosamine concentrations, higher insulin requirements

A wide range of body weights and insulin doses was observed, making it impossible to rule out hypersomatotropism based on phenotype alone.

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20
Q

What should veterinarians consider in poorly controlled diabetic cats?

A

Hypersomatotropism

Especially if showing weight gain, severe polyphagia, insulin resistance, or respiratory stridor.

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21
Q

What are the key pathologic changes associated with hypersomatotropism?

A
  • Hypertrophy of myocardium
  • GH stimulation of the hunger center
  • Increased soft tissue mass
  • Soft tissue growth in airways
  • Soft tissue and cartilage proliferation
  • Bone growth of face and limbs
  • Pituitary tumor expansion

These changes can lead to various clinical signs in affected cats.

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22
Q

What are common clinical signs in non-diabetic cats with hypersomatotropism?

A
  • Upper respiratory stridor
  • Weight gain or obesity
  • Broadening of the head
  • Cardiac signs such as murmurs or congestive heart failure
  • Neurologic signs due to pituitary mass

The term hypersomatotropism is preferred over acromegaly as not all affected cats exhibit classic phenotypic changes.

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23
Q

What is a known limitation of IGF-1 testing?

A

Dependence on sufficient portal insulin to stimulate hepatic IGF-1 production

Up to 9% of untreated diabetic cats may yield false-negative results.

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24
Q

What is the preferred surgical treatment for hypersomatotropism?

A

Hypophysectomy

It offers the highest rates of diabetic remission and improved quality of life.

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25
What are the contraindications for hypophysectomy?
* Risk-averse owners * Large pituitary tumors * Comorbidities that may interfere with anesthesia or recovery ## Footnote Anesthetic risks include hypothermia, hypotension, bradycardia, and airway obstruction.
26
What is the median survival time after hypophysectomy in diabetic cats?
853 days ## Footnote In one study, 95% of surviving cats had improved diabetic control.
27
What challenges are associated with radiotherapy for hypersomatotropism?
* Uncertainty of clinical improvement * Uncertainty of timing, magnitude, and duration of insulin reduction * Lack of consistent normalization of IGF-1 concentrations ## Footnote Myocardial hypertrophy often persists despite treatment.
28
What is the role of somatostatin analogs in the treatment of hypersomatotropism?
They lower serum IGF-1 and reduce mean blood glucose levels ## Footnote However, their effectiveness may be limited due to variable receptor expression.
29
What are some clinical signs of congenital GH deficiency in cats?
* Proportionate dwarfism * Disproportionate dwarfism * Retained deciduous teeth * Dull hair coat * Corneal edema * Weakness and lethargy * Hypoglycemia ## Footnote These signs typically manifest by 1–2 months of age.
30
What diagnostic tests are used to confirm hyposomatotropism?
* IGF-1 Testing * GH Assay * Other biomarkers like P3P and Ghrelin ## Footnote ELISA and radioimmunoassay are validated for IGF-1 testing.
31
What is the treatment approach for managing hypersomatotropism-induced diabetes mellitus?
* High insulin doses * Use long-acting formulations like glargine or ProZinc * Monitor with continuous glucose monitoring ## Footnote The initial approach mirrors that for uncomplicated diabetes.
32
What clinical score is useful for monitoring diabetic cats?
ALIVE Diabetic Clinical Score ## Footnote This score helps assess the overall health status of diabetic cats.
33
What medication can be considered in diabetic cats with GH-induced poylphagia?
Fluoxetine ## Footnote Fluoxetine may help manage excessive hunger in diabetic cats.
34
What condition should be considered in cats with HCM, stridor, weight gain, or insulin resistance?
Hypersomatotropism ## Footnote Recognizing this condition can be critical for appropriate treatment.
35
What is the composition of growth hormone (GH)?
Single-chain polypeptide composed of 190 amino acids.
36
Which species have identical GH sequences?
Canine and porcine.
37
What is the primary source of GH secretion?
Pituitary gland.
38
What is a secondary source of GH in dogs?
Mammary gland.
39
What hormones regulate GH secretion?
* GHRH (stimulatory) * Somatostatin (inhibitory)
40
What is the origin of ghrelin?
Secreted by the stomach.
41
How does ghrelin affect GH secretion?
Increases GH secretion, food intake, gastric/intestinal motility.
42
What is the function of IGFs in relation to GH?
Mediated anabolic effects such as protein synthesis and body size regulation.
43
What does IGF-1 inhibit?
Pituitary GH secretion.
44
What are common sources of acromegaly in dogs?
* Luteal phase of estrous cycle * Exogenous progestins * Mammary GH-secreting tumors
45
List clinical manifestations of acromegaly.
* Soft tissue swelling * Snoring, dyspnea * Stiffness, neck rigidity * Polyuria, polydipsia, polyphagia * Thick skin folds * Abdominal enlargement
46
What breed is predisposed to acromegaly?
German Shepherd Dogs.
47
What does a GHRH stimulation test assess?
Failure to increase GH after GHRH supports acromegaly diagnosis.
48
What is the primary treatment for progestin-induced acromegaly?
Discontinue PG treatment and consider ovariectomy.
49
What is pituitary dwarfism also known as?
Juvenile hyposomatotropism.
50
What is the inheritance pattern of pituitary dwarfism in dogs?
Autosomal recessive.
51
Which breed is most commonly affected by pituitary dwarfism?
German Shepherd Dogs.
52
What is the genetic basis of pituitary dwarfism?
LHX3 mutation.
53
What are common clinical manifestations of pituitary dwarfism?
* Proportional growth retardation * Retention of lanugo hairs * Truncal alopecia * Hyperpigmented skin
54
What is a key laboratory finding in pituitary dwarfism?
Low plasma IGF-1.
55
What treatment options are available for pituitary dwarfism?
* Porcine GH * Progestins * Levothyroxine
56
What is acquired growth hormone deficiency (AGHD)?
Can occur after hypophysectomy or due to traumatic brain injury.
57
What breeds are predisposed to alopecia possibly associated with GH deficiency?
* Pomeranian * Miniature Poodle * Chow Chow * Keeshond
58
What is a common clinical presentation of alopecia in affected dogs from GH deficiency?
Localized to trunk, caudal thighs, perineum, neck.
59
What is the controversy surrounding the pathophysiology of alopecia?
Normal GH response in 1/3 of affected dogs.
60
What are the treatment responses for alopecia associated with AGHD?
Varies; some respond to GH therapy, others to castration.
61
What have studies shown regarding GH stimulation tests in Pomeranians with alopecia?
No significant GH increase in either group ## Footnote This includes both affected Pomeranians and unaffected controls.
62
What are the treatment responses for heterologous growth hormone therapy?
Poor to moderate success ## Footnote This reflects the variability in treatment effectiveness across different cases.
63
What is the response to medroxyprogesterone acetate treatment in GH deficiency?
Inconsistent improvement ## Footnote This indicates that while some dogs may benefit, results are not reliable across the board.
64
What may trigger AGHD in dogs?
Hypophysectomy or trauma ## Footnote This highlights potential causes of acquired growth hormone deficiency.
65
How is adult-onset alopecia in certain breeds related to GH deficiency?
Speculatively linked to GH deficiency ## Footnote This suggests a possible connection, though further research is needed to confirm it.
66
What findings suggest that true AGHD is unlikely in most cases?
* Normal IGF-1 * Inconsistent GH stimulation results * Unreliable treatment responses ## Footnote These factors collectively indicate that the condition might not be solely due to GH deficiency.
67
What complexities might underlie the condition of AGHD?
Multifactorial, genetically influenced, and/or hormonally complex ## Footnote This suggests that AGHD may involve multiple interacting factors rather than a single deficiency.
68
What is arginine vasopressin (AVP) also known as?
Antidiuretic hormone (ADH) ## Footnote AVP is critical for water balance regulation.
69
Where is AVP synthesized?
Magnocellular neurons of the paraventricular and supraoptic nuclei in the hypothalamus
70
What are the components of the prohormone preprovasopressin?
* AVP * Neurophysin-2 * Copeptin
71
How is AVP transported to the posterior pituitary?
Along the hypothalamic-neurohypophyseal tract
72
What stimulates AVP release?
* Osmoreceptors detecting a 1–2% increase in plasma osmolality * Decrease in blood volume or pressure by 10–15% * Stress, nausea, pain, hypoglycemia * Exercise, dry food ingestion * Certain drugs
73
What is the half-life of AVP in dogs?
~5.9 minutes
74
What action does AVP have on renal collecting ducts?
Increases water reabsorption by binding to basolateral V2 receptors
75
What happens when AVP binds to V2 receptors?
Triggers insertion of aquaporin-2 (AQP2) channels into the apical membrane
76
What is the effect of AVP on urine specific gravity (USG)?
USG increases as urine volume decreases proportionally to water reabsorbed
77
What are the actions of V1A receptors?
* Cause vascular smooth muscle contraction * Stimulate platelet activation * Promote hepatic glycogenolysis and gluconeogenesis
78
How does AVP influence thirst regulation?
Thirst and AVP secretion are triggered by osmoreceptor activation
79
What inhibits AVP secretion?
Natriuretic peptides
81
What causes Central Diabetes Insipidus (CDI)?
Complete or partial AVP deficiency
81
What are common causes of CDI in dogs?
* Pituitary neoplasia
82
What is a triphasic response in humans after pituitary stalk injury?
* Phase 1: Axonal shock → central DI * Phase 2: Excessive AVP release → transient antidiuresis * Phase 3: Permanent or transient DI after AVP store depletion
83
What percentage of dogs develop CDI after hypophysectomy for hyperadrenocorticism?
* 53% develop CDI lasting >2 weeks * 22% develop permanent CDI
84
What are secondary causes of Nephrogenic Diabetes Insipidus (NDI)?
* Hyperadrenocorticism * Pyometra * Liver disease
85
What is the primary cause of familial Nephrogenic DI in humans?
Mutations in AVPR2 (V2 receptor) or AQP2 (aquaporin-2)
86
What are common clinical signs of diabetes insipidus?
* Severe polydipsia * Polyuria * Water intake up to 5–20× normal
87
What is the normal water intake for dogs?
<90–100 mL/kg/day
88
What neurologic signs may occur in dogs with CDI?
* Seizures * Obtundation * Behavior change * Tremors
89
What is the purpose of the Modified Water Deprivation Test (MWDT)?
To distinguish between Central Diabetes Insipidus, Nephrogenic Diabetes Insipidus, and Primary Polydipsia
90
What indicates a positive response to DDAVP in dogs with central DI?
Marked reduction in water intake and increase in USG
91
What is the interpretation if USG remains low during Stage 2 of MWDT?
Central DI
92
What is the risk of performing MWDT in dogs with severe PU?
Hypernatremia and dehydration signs
93
What alternative is recommended for diagnosing diabetes insipidus in cats?
DDAVP trial therapy
94
Why is AVP measurement not clinically useful?
* Pulsatile, variable secretion * Technical sample handling requirements * Limited availability of validated assays
95
What is the effect of hypertonic saline infusion in humans with central DI?
Low AVP response
96
What is measured in the Hypertonic Saline Infusion Test?
AVP response to 20% NaCl infusion
97
What AVP response is observed in Central Diabetes Insipidus (CDI)?
Low AVP response
98
What is the AVP response in Nephrogenic Diabetes Insipidus (NDI)?
Normal/high AVP, no USG increase
99
What is the AVP response in primary polydipsia?
Normal AVP, appropriate USG response
100
What does urine Aquaporin-2 (AQP2) expression correlate with?
AVP activity in healthy dogs
101
Is urine AQP2 expression validated clinically?
No, it is a research tool only
102
What is Copeptin?
A stable AVP surrogate used in humans
103
What imaging techniques are used to identify structural lesions in the hypothalamus or pituitary?
MRI and CT
104
What does the absence of T1 hyperintensity in the neurohypophysis indicate in humans?
Consistent with central DI
105
What is the treatment strategy for Central Diabetes Insipidus (CDI) when treatment is necessary?
Desmopressin (DDAVP) Therapy
106
What is the mechanism of action of Desmopressin (DDAVP)?
Synthetic analog of AVP; selective V2 receptor agonist
107
What is the effect of Desmopressin on V1A receptors?
Minimal effect; no associated hypertension
108
What is the response rate of dogs and cats with partial or complete CDI to DDAVP?
Nearly all respond
109
What are common reasons for treatment failure with DDAVP?
Improper administration, use of oral tablets with low bioavailability
110
What dietary modification is recommended for Nephrogenic Diabetes Insipidus (NDI)?
Low-sodium, low-protein diet
111
What is the mechanism of action for thiazide diuretics in treating NDI?
Reduces sodium reabsorption in distal tubules, leading to mild volume depletion
112
What is the prognosis for idiopathic or traumatic CDI?
Often long-term manageable with DDAVP
113
What is the prognosis for structural disease causing CDI?
Poorer prognosis due to progressive neurologic decline
114
What is the response rate of dogs to thiazide diuretics for NDI?
~50% show reduced urine output
115
What is the main challenge in managing primary NDI?
Variable response to treatment; long-term management can be difficult
116
What are the physiologic functions of calcium?
* Intracellular signaling * Nerve conduction * Neuromuscular transmission * Muscle contraction * Blood coagulation * Hormone secretion * Hepatic glycogen metabolism ## Footnote Disruptions in calcium homeostasis can adversely affect multiple organ systems.
117
What regulates parathyroid hormone (PTH) secretion?
The Calcium-Sensing Receptor (CaSR) ## Footnote CaSR detects extracellular calcium concentrations and adjusts PTH secretion accordingly.
118
What percentage of total serum calcium is ionized calcium (iCa)?
~50% ## Footnote Ionized calcium is biologically active.
119
What are the calcium fractions in serum?
* 50% = Ionized (iCa) * 40% = Protein-bound (mostly to albumin) * <10% = Complexed with anions (e.g., bicarbonate, citrate) ## Footnote Understanding calcium fractions is important for accurate diagnosis.
120
What key hormones regulate calcium levels?
* Parathyroid Hormone (PTH) * Parathyroid Hormone-Related Protein (PTHrP) * Vitamin D (Calcitriol/1,25-dihydroxycholecalciferol) * Calcitonin ## Footnote CaSR suppresses PTH during hypercalcemia and stimulates it during hypocalcemia.
121
What is the structure of parathyroid hormone (PTH)?
An 84-amino acid polypeptide ## Footnote PTH is synthesized and secreted by chief cells in the parathyroid glands.
122
What does PTH do to serum phosphate levels?
Decreases serum phosphate levels ## Footnote PTH increases serum calcium levels while decreasing phosphate.
123
What is the relationship between serum calcium and PTH secretion?
Inverse sigmoidal relationship ## Footnote PTH secretion is modulated by serum calcium levels.
124
What is PTHrP and its significance in adults?
A protein that mimics PTH, increasing calcium and decreasing phosphate, elevated in humoral hypercalcemia of malignancy (HHM) ## Footnote PTHrP is crucial for fetal calcium regulation but is virtually undetectable postnatally in healthy animals.
125
What stimulates the active form of Vitamin D (calcitriol)?
PTH via 1-alpha hydroxylase ## Footnote Calcitriol promotes intestinal calcium absorption and inhibits PTH synthesis.
126
What is the role of calcitonin?
Helps reduce postprandial hypercalcemia by inhibiting bone resorption and enhancing renal calcium excretion ## Footnote Calcitonin functions to oppose PTH but has a minor physiologic role.
127
What is the most common cause of primary hyperparathyroidism?
Solitary adenoma ## Footnote Other causes include carcinoma and adenomatous hyperplasia.
128
What is the pathophysiology of primary hyperparathyroidism?
Affected gland(s) secrete PTH independently of serum calcium, causing persistent elevation of PTH and hypercalcemia ## Footnote In secondary hyperparathyroidism, all four glands typically become hyperplastic.
129
What is the significance of genetic testing for hyperparathyroidism?
Evaluates CASR, MEN1, and HRPT2 mutations ## Footnote Genetic syndromes may involve sporadic or familial cases of hyperparathyroidism.
130
What is the genetic mutation associated with familial isolated hyperparathyroidism (FIHP)?
MEN1 mutations ## Footnote Sporadic cases may involve somatic MEN1 mutations in ~35% of patients.
131
What is the differential diagnosis for familial isolated hyperparathyroidism?
Familial hypocalciuric hypercalcemia (FHH) ## Footnote FHH is characterized by very low urinary calcium clearance.
132
What is the calcium:creatinine ratio in FHH cases?
< 0.01 in 80% of cases
133
What genetic mutations are typically evaluated in genetic testing for FHH?
* CASR * MEN1 * HRPT2
134
What mutations are most commonly associated with familial hypocalciuric hypercalcemia?
* CASR mutations (majority) * AP2S1 mutations * GNA11 mutations
135
Which dog breed has a known familial predisposition to primary hyperparathyroidism (PHPT)?
Keeshonds
136
What is the odds ratio for PHPT in Keeshonds?
50.7
137
What are the most common renal and urinary signs of PHPT in dogs?
* Polyuria and polydipsia (PU/PD) * Urinary incontinence * Stranguria * Hematuria * Urinary tract infections * Urolithiasis
138
What are common gastrointestinal signs associated with PHPT in dogs?
* Inappetence * Vomiting * Constipation
139
What is a classic mnemonic for remembering signs of PHPT in humans?
Stones, Bones, Abdominal Groans, Thrones, and Psychiatric Moans
140
What is the mean total calcium level observed in dogs with PHPT?
14.5 mg/dL
141
What is the mean serum phosphate level in dogs with PHPT?
2.8 mg/dL
142
What imaging tool is most useful for identifying parathyroid masses in dogs?
Cervical Ultrasound
143
Which bisphosphonate is preferred for treating hypercalcemia in dogs?
Pamidronate: 1.3–2 mg/kg in 150 mL saline over 2 hrs
144
What is the main side effect of bisphosphonates?
GI upset and hypocalcemia if overdosed
145
What is the risk of chronic kidney disease (CKD) associated with hypercalcemia in dogs?
Hypercalcemia can contribute to CKD, though some dogs may not develop it.
146
What are the mechanisms leading to urolithiasis in PHPT dogs?
* Excess filtered calcium exceeds renal reabsorption → hypercalciuria * Increased phosphate excretion contributes to urinary supersaturation * Elevated intestinal calcium absorption increases oxalate absorption
147
What is the significance of the calcium × phosphate product in predicting CKD?
Theoretically indicates risk, but poor predictive value in practice
148
What is the oral bioavailability of bisphosphonates ?
<1% ## Footnote Poor oral bioavailability indicates that less than 1% of the drug is available in the bloodstream after oral administration.
149
What is the typical dose of Pamidronate for treatment?
1.3–2 mg/kg in 150 mL saline over 2 hrs ## Footnote This dosing regimen ensures adequate delivery of the drug.
150
How long do the effects of Pamidronate last?
Up to 3 weeks ## Footnote The duration of effect is significant for treatment planning.
151
How much more potent is Zoledronate compared to Pamidronate?
100–850× more potent ## Footnote This indicates a significantly stronger effect, warranting careful dosing.
152
What are some limitations of Salmon Calcitonin?
* Expensive * Can cause vomiting and anorexia * Resistance may develop ## Footnote Understanding these limitations is essential for effective treatment planning.
153
What is the suggested dose of Mithramycin for dogs?
25 µg/kg IV in 5% dextrose over 2–4 hours ## Footnote This dosing is infrequent due to its rarity of use.
154
What does Cinacalcet interact with?
Calcium-sensing receptor (CaSR) ## Footnote This interaction helps control calcium, phosphate, and PTH levels.
155
What is the treatment of choice for Primary Hyperparathyroidism in dogs?
Surgical Parathyroidectomy ## Footnote This is indicated especially when parathyroid nodules exceed 10 mm.
156
What should be monitored during intraoperative PTH monitoring?
PTH levels pre-, intra-, and post-op (although not realistic given send out test) ## Footnote This technique aims to confirm successful excision.
157
What are the outcomes of Percutaneous Ultrasound-Guided Ethanol Ablation?
* Early reports: 72% success * Later series (30 dogs): >90% success ## Footnote This method requires general anesthesia and careful operator technique.
158
What is a key histopathologic feature of carcinomas?
Capsular invasion ## Footnote Identifying these features is crucial for accurate diagnosis.
159
What is a common practice regarding vitamin D supplementation pre-operatively?
Begin calcium + vitamin D supplementation 12–24 hours pre-op if calcium is significantly elevated ## Footnote This may help prevent post-operative hypocalcemia.
160
What is the preferred agent for IV calcium supplementation?
Calcium gluconate ## Footnote It is the least caustic and preferred for intravenous use.
161
What is the prognosis for dogs with Primary Hyperparathyroidism?
Excellent in all breeds for short-to-mid-term prognosis ## Footnote Long-term prognosis is generally good, except in Keeshonds.
162
What is the recurrence rate of Primary Hyperparathyroidism in Keeshonds?
50% recurrence ## Footnote This highlights the genetic predisposition of the breed.
163
What is Idiopathic Hypercalcemia in cats?
Most common cause of feline hypercalcemia, recognized since the 1990s ## Footnote Diagnosis is often one of exclusion.
164
What dietary management is recommended for feline hypercalcemia?
* High-fiber diets * Renal diets * Calcium oxalate stone-prevention diets ## Footnote These dietary adjustments can help manage calcium levels.
165
What is the treatment of choice for Primary Hyperparathyroidism in cats?
Surgical excision ## Footnote Prognosis post-op is generally good.
166
What causes hypocalcemia in hypoparathyroidism?
Decreased bone resorption and intestinal absorption
167
What causes hyperphosphatemia in hypoparathyroidism?
Reduced renal phosphate excretion
168
What is the role of calcium in membrane stability?
Deficiency causes neuronal hyperexcitability
169
What are common clinical signs of hypoparathyroidism in dogs?
Seizures, muscle tremors, stiff gait, jaw clamping, restlessness, anxiety, aggression
170
What age range is typical for diagnosis of hypoparathyroidism in dogs?
6 weeks to 13 years
171
What breeds are overrepresented in dogs with hypoparathyroidism?
* Miniature Schnauzers * Poodles * German Shepherds * Terriers * St. Bernards (in Australia/New Zealand)
172
What are the common clinical signs of hypoparathyroidism in cats?
Lethargy, poor appetite, similar neuromuscular signs to dogs
173
What is a key diagnostic feature of hypoparathyroidism?
Hypocalcemia and hyperphosphatemia
174
What is the critical ECG finding in hypocalcemia?
Prolonged ST segment and QT interval
175
What is the preferred form of vitamin D supplementation for long-term management?
Calcitriol (active vitamin D3)
176
What is the dosing schedule for calcitriol?
Initial: 20–40 ng/kg/day for 2–4 days; Maintenance: 10–20 ng/kg/day
177
What is the primary goal of treatment for hypoparathyroidism?
Maintain serum total calcium in the range of 8.0–9.5 mg/dL
178
What is the prognosis for dogs and cats with hypoparathyroidism with proper management?
Excellent
179
What is a potential complication of subcutaneous calcium therapy?
Calcinosis cutis
180
What is a common laboratory finding in hypoparathyroidism regarding magnesium?
Not always decreased despite its role in PTH secretion
181
What is the initial recheck schedule after starting treatment for hypoparathyroidism?
Every 2 to 3 days
182
What is the main differential diagnosis for hypocalcemia related to parathyroid issues?
Idiopathic destruction
183
What is the estimated prevalence of hypothyroidism in dogs?
General estimates range from 0.2% to 0.8%.
184
What breed of dogs has a significantly higher prevalence of hypothyroidism?
Swedish Giant Schnauzers and Hovawarts: up to 15%.
185
What is the anatomy of the thyroid gland in dogs?
The thyroid gland consists of two lobes, located on either side of the trachea, composed of microscopic follicles lined by thyroid epithelial cells.
186
What is thyroglobulin?
A large glycoprotein that contains the precursors for thyroid hormones.
187
What is the role of thyroid peroxidase (TPO) in hormone synthesis?
TPO catalyzes several steps in hormone synthesis.
188
What is the serum half-life of T4 and T3 in dogs?
* T4: 10–16 hours * T3: 5–6 hours
189
Which thyroid hormone is more potent, T3 or T4?
T3 is approximately 3 to 5 times more potent than T4.
190
What regulates thyroid hormone synthesis and function?
The hypothalamus releases thyrotropin-releasing hormone (TRH), stimulating the anterior pituitary to release thyroid-stimulating hormone (TSH).
191
What are the three types of hypothyroidism categorized by lesion location?
* Primary hypothyroidism: disease of the thyroid gland * Secondary hypothyroidism: disease of the pituitary gland * Tertiary hypothyroidism: disease of the hypothalamus
192
What causes congenital hypothyroidism?
* Thyroid hypoplasia/aplasia * Thyroid dysgenesis * Dyshormonogenesis (defective hormone synthesis)
193
What are the causes of acquired hypothyroidism?
* Pituitary neoplasia * Surgical hypophysectomy * Intracranial trauma or hemorrhage * Adenohypophysitis
194
What are the histologic patterns associated with primary acquired hypothyroidism?
* Lymphocytic thyroiditis * Thyroid atrophy
195
What is lymphocytic thyroiditis?
A destructive autoimmune process characterized by multifocal or diffuse infiltration of the thyroid by lymphocytes, macrophages, and plasma cells.
196
What is the average age of dogs diagnosed with hypothyroidism?
Approximately 7 years.
197
What are the most common clinical signs of hypothyroidism in dogs?
* Lethargy * Weight gain * Exercise intolerance * Mental dullness * Cold intolerance * Generalized weakness
198
What dermatologic abnormalities are commonly seen in hypothyroid dogs?
* Hair thinning * Dry, coarse hair coat * Alopecia * Dry, scaly skin * Seborrhea
199
What are some neurological abnormalities associated with hypothyroidism?
* Neuropathies * Central vestibular disease * Myxedema coma
200
What is the relationship between thyroid hormones and hair growth?
Thyroid hormones are critical for hair growth maintenance and immune response.
201
What is the impact of hypothyroidism on the cardiovascular system?
Hypothyroidism can lead to bradycardia and possible association with atherosclerosis.
202
What is the significance of TGAA status in hypothyroidism?
Approximately 50% of hypothyroid dogs have circulating TGAAs, correlating with lymphocytic thyroiditis.
203
What condition is associated with adult-onset demodicosis?
Hypothyroidism ## Footnote Demodicosis refers to a skin condition caused by the Demodex mite, often seen in dogs.
204
List some neurologic abnormalities associated with hypothyroidism.
* Neuropathies * Central vestibular disease * Myxedema coma * Subclinical myopathies
205
What are the clinical features of myxedema?
* Puffy appearance to skin * Skin is pale, cool to touch, non-pitting * Thickened lips * Thickened forehead skin * Drooping eyelids
206
What histologic changes are associated with myxedema?
* Predominance of hair follicles in telogen phase * Kenogen follicles * Hyperpigmentation * Atrophic or dystrophic follicles * Thickened dermis * Vacuolated arrector pili muscles
207
True or False: Hypothyroidism can impair cardiac function.
True ## Footnote The clinical importance of this impairment is controversial.
208
What are some electrocardiographic abnormalities noted in hypothyroid dogs?
* Reduced heart rate * Low voltage R and P waves * Sinus bradycardia * First- or second-degree AV block
209
What is the relationship between hypothyroidism and atherosclerosis in dogs?
Atherosclerosis is rare in dogs, but when present, hypothyroidism is often implicated.
210
What neurologic dysfunctions can result from hypothyroidism?
* Neuropathies * Central vestibular dysfunction * Rarely, seizures
211
What is myxedema coma?
A rare, life-threatening condition characterized by profound mental dullness, severe weakness, hypothermia, hypoventilation, bradycardia, and hypotension.
212
What behavioral issues are controversially associated with hypothyroidism?
Aggressive behavior ## Footnote There is little evidence to support this belief.
213
What are some muscular features associated with hypothyroidism?
* Gait abnormalities * Weakness * Exercise intolerance
214
What ophthalmic features can arise from hypothyroidism?
* Corneal lipid deposits * Reduced tear production
215
What reproductive abnormalities have been attributed to hypothyroidism?
* Decreased fertility * Parturition problems
216
Fill in the blank: Hypothyroidism is associated with __________ in dogs.
gallbladder mucocele
217
What renal features are associated with hypothyroidism?
Decreased glomerular filtration rate (GFR) ## Footnote The significance of this finding is unknown.
218
What are the clinical features of congenital hypothyroidism?
* Disproportionately wide skull * Macroglossia * Delayed dental eruption * Square trunk and short limbs
219
What is Autoimmune Polyendocrine Syndrome Type 1 (APS-1)?
A rare autosomal recessive disorder characterized by chronic mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency.
220
What is the prevalence of diabetes mellitus in hypothyroid dogs?
1.2–10%
221
What clinical pathology findings are common in hypothyroid dogs?
* Mild, normocytic, normochromic anemia * Increased red cell distribution width (RDW) * Increased white blood cell count is extremely unusual
222
How does red cell distribution width (RDW) in hypothyroid dogs compare to healthy dogs?
Higher, but with significant overlap.
223
What changes are associated with platelets and von Willebrand Factor in hypothyroidism?
* Increases in platelet count * Small platelet size * Decrease in vWF concentrations with thyroid treatment.
224
Is there a link between hypothyroidism and prolonged mucosal bleeding times?
No.
225
In hypothyroid dogs, what percentage experience hypercholesterolemia?
Approximately 75%.
226
What happens to lipid metabolism in hypothyroid dogs?
Lipid degradation is severely impaired, leading to lipid accumulation.
227
What types of lipoproteins are typically increased in hypothyroid dogs?
* Low-density lipoproteins (LDL) * Very low-density lipoproteins (VLDL) * High-density lipoproteins (HDL)
228
What percentage of hypothyroid dogs show increased serum kinase activity?
18–35%.
229
What is the presumed cause of increased fructosamine concentrations in hypothyroid dogs?
Reduced protein turnover.
230
What liver enzyme activities may mildly increase in hypothyroid dogs?
* Alkaline phosphatase (ALP) * Gamma-glutamyltransferase (GGT)
231
What is the effect of hypothyroidism on serum creatinine and symmetric dimethylarginine (SDMA) concentrations?
Mildly increased in approximately 30–50% of hypothyroid dogs.
232
What is the association of total homocysteine concentrations in hypothyroid dogs?
Approximately 75% higher.
233
What are the limitations of non-isotopic methods for thyroid hormone measurement?
They may be affected by hemolysis, lipemia, and hyperbilirubinemia.
234
Which assay method is considered the gold standard for measuring free T4?
Equilibrium dialysis (ED) followed by highly sensitive RIA.
235
What factors can significantly alter thyroid hormone concentrations?
Non-thyroidal illness (NTI) can lead to non-thyroidal illness syndrome (NTIS).
236
What do canine-specific thyroglobulin autoantibody (TGAA) assays detect?
Presence of T3 and T4 autoantibodies.
237
What is the effect of age on total T4 and free T4 concentrations in dogs?
Both decline with age.
238
What breed is known to have low total T4 values commonly?
Greyhounds.
239
Does exercise have a significant long-term effect on thyroid hormone concentrations?
Short-term exercise has limited effect.
240
What is the expected outcome for total T3 in hypothyroid dogs?
Total T3 values are within or above the reference range in up to 90% of hypothyroid dogs.
241
What is the diagnostic sensitivity of total T4 in hypothyroid dogs?
Excellent; it is the most frequently recommended screening test.
242
What is a common finding in many breeds regarding total T3 values?
Low total T3 values are common in many breeds, in non-thyroidal illness, and with various drugs.
243
What can falsely increase total T4 values?
T4 autoantibodies
244
In what percentage of dogs suspected of hypothyroidism are T4 autoantibodies present?
<2%
245
What is the concern with using total T4 as a diagnostic test?
Poor diagnostic specificity
246
What type of assays are less influenced by extra-thyroidal factors when measuring free T4?
Assays that employ a separation step (e.g., equilibrium dialysis)
247
What is considered the most accurate single test for diagnosing hypothyroidism in dogs?
Free T4
248
Why is the diagnostic sensitivity of TSH moderate?
A significant portion of hypothyroid dogs have normal TSH.
249
What is the sensitivity range of total T4 as a diagnostic test?
89–100%
250
What is the specificity range of TSH as a diagnostic test?
82–100%
251
What do positive TGAA results indicate?
Lymphocytic thyroiditis
252
What do TGAA results provide regarding thyroid function?
No direct information
253
What is the dose of human recombinant TSH (rhTSH) for the stimulation test?
50–70 µg per dog, or 100 µg for dogs >20 kg
254
What is the interpretation of total T4 <1.7 µg/dL post-stimulation with TSH?
High diagnostic sensitivity (~100%)
255
What does a good T4 response to TRH indicate?
Excludes hypothyroidism
256
What is a characteristic ultrasound finding in hypothyroid dogs?
Decreased echogenicity
257
What is the typical TCTU uptake value in hypothyroid dogs?
0.03–0.26%
258
What are the risks associated with T3 supplementation?
* Increased risk of thyrotoxicosis * Requires multiple daily administrations * May result in T4 deficiency in critical organs.
259
Why are combination T4/T3 products not recommended for dogs?
Inappropriate T4:T3 ratio leading to excessive T3.
260
How much IV T4 is required to normalize T4 concentrations?
About four times the normal daily secretion.
261
What affects the bioavailability of oral T4?
* Intraluminal contents * Dietary components * GI bacterial binding.
262
What is the effect of food on T4 bioavailability?
Bioavailability is almost halved when T4 is given with food.
263
What is the common dosing schedule for T4?
Q24h is widely accepted.
264
What percentage of dogs respond successfully to 20 µg/kg Q24h dosing?
65%.
265
What is the expected weight loss within the first few months of therapy?
Approximately 10%.
266
How long does it take for neurologic signs to begin improving?
Within 1 month.
267
What is the serum half-life of T4?
9–15 hours.
268
What indicates inadequate control during T4 therapy?
Values <2.7 µg/dL.
269
What can TSH measurement help identify?
* Poor compliance * Inadequate supplementation.
270
What are some clinical signs of T4 overdose in dogs?
* Polyuria and polydipsia * Polyphagia * Panting * Weight loss * Hyperactivity * Tachycardia * Hyperthermia.
271
What is the emergency treatment for myxedema coma?
IV T4 administration at 5 µg/kg every 12 hours.
272
What is the expected time to clinical stabilization in myxedema coma?
~30 hours.
273
What is a rare but reported issue with certain T4 preparations?
Idiosyncratic skin reactions to inactive ingredients.
274
What is the effect of daily anti-inflammatory doses of prednisolone on T4 concentrations?
Can decrease total T4 concentrations.
275
What is naturally occurring hypothyroidism in cats?
A rare clinical entity with a small number of reported cases involving congenital or adult-onset hypothyroidism.
276
What is the most common cause of low serum total T4 concentration in cats?
Non-thyroidal illness syndrome.
277
What are the reported causes of adult-onset hypothyroidism in cats?
* Lymphocytic thyroiditis * Diffuse follicular hyperplasia * Idiopathic causes
278
What is diffuse follicular hyperplasia in cats?
A condition documented in two cats and suspected in an additional five based on scintigraphic findings.
279
What is a potential manifestation of mild congenital hypothyroidism in adulthood?
Dyshormonogenesis.
280
What causes congenital hypothyroidism in cats?
* Thyroid dyshormonogenesis * Thyroid hypoplasia or aplasia * TSH resistance * Thyroiditis * Iodine deficiency
281
What is the most common form of congenital hypothyroidism in cats?
Dyshormonogenesis.
282
What is thyroiditis in cats?
A condition where a colony of cats developed thyroiditis at 40–60 days of age, with early hormone supplementation reducing severity.
283
What is the most common cause of hypothyroidism in cats?
Iatrogenic hypothyroidism following treatment for hyperthyroidism.
284
What treatments can lead to iatrogenic hypothyroidism?
* Radioactive iodine (I-131) therapy * Bilateral thyroidectomy * Administration of antithyroid drugs (e.g., methimazole) * Stereotactic radiation therapy
285
What is the prevalence range of iatrogenic hypothyroidism post-I-131 treatment?
3–79%.
286
What is required for the diagnosis of hypothyroidism in cats?
* Clinical signs * Low total T4 * Elevated serum TSH concentrations
287
What are common clinical signs of adult-onset hypothyroidism in cats?
* Lethargy * Inappetence * Mental dullness * Dermatologic abnormalities * Obesity * Polyuria and polydipsia
288
What are the clinical features of congenital hypothyroidism in kittens?
* Disproportionate dwarfism * Large head * Short, wide neck * Short, thick limbs * Facial dysmorphism * Palpable bilateral goiter
289
What laboratory findings may indicate hypothyroidism in cats?
* Normocytic, normochromic anemia * Hypercholesterolemia * Elevated creatine kinase (CK) * Azotemia
290
What does an increased serum TSH concentration indicate in cats?
It is highly specific for diagnosing hypothyroidism when associated with low total T4.
291
What is the role of T3 measurement in diagnosing feline hypothyroidism?
Measurement of serum T3 is not recommended due to its variability.
292
True or False: A normal total T4 level excludes spontaneous hypothyroidism.
True.
293
What is the typical presentation of cats with overt iatrogenic hypothyroidism?
* Decreased activity * Weight gain
294
What is a significant concern in cats with subclinical hypothyroidism?
Increased risk of azotemia.
295
What is the prevalence of hypothyroidism in cats treated with methimazole?
~20% developed decreased free and/or total T4 and increased TSH.
296
What is the standard TSH dose used for cats in TSH stimulation tests?
25 µg IV ## Footnote This is lower than the dose used in dogs.
297
What is the expected increase in total T4 for euthyroid cats after TSH administration?
2–3 fold increase after 6–8 hours ## Footnote This indicates the normal response of the thyroid gland to TSH stimulation.
298
What percentage increase in total T4 is seen in healthy cats after TSH administration?
111–300% ## Footnote This shows a significant response in healthy cats.
299
What is the total T4 increase in cats with non-thyroidal illness syndrome (NTIS) after TSH administration?
146–414% ## Footnote This indicates a heightened response in these cats despite their illness.
300
What is the total T4 increase in cats with iatrogenic hypothyroidism after TSH administration?
<11% ## Footnote This minimal response suggests a diagnosis of hypothyroidism.
301
What isotope is used for thyroid scintigraphy in cats?
Technetium-99m (99mTc) ## Footnote This isotope helps visualize thyroid function and morphology.
302
In normal cats, what is the uptake ratio of thyroid lobes to salivary glands?
1:1 ratio ## Footnote This indicates normal thyroid function.
303
What are the findings in congenital goitrous hypothyroidism during scintigraphy?
Thyroid lobes are bilaterally enlarged with homogeneous uptake ## Footnote This is indicative of congenital hypothyroidism.
304
What is the finding in atrophic hypothyroidism during scintigraphy?
No thyroid tissue can be identified ## Footnote This suggests severe thyroid atrophy.
305
What is the initial recommended dose of Levothyroxine for treating hypothyroidism in cats?
10–20 µg/kg PO every 12–24 hours ## Footnote This dosage is critical for effective treatment.
306
How long should one wait before critically assessing the treatment response to Levothyroxine?
4–6 weeks ## Footnote This allows sufficient time for the medication to take effect.
307
What are the goals of treatment for hypothyroidism in cats?
* Resolve clinical signs * Maintain serum total T4 and TSH within reference ranges * Avoid overt hyperthyroidism ## Footnote These goals guide effective management of the condition.
308
What was the median levothyroxine dose for cats with congenital hypothyroidism?
16 µg/kg PO Q12H ## Footnote This reflects the dosing needed for effective management.
309
What was the median levothyroxine dose for adult-onset hypothyroidism?
32.7 µg/kg/day ## Footnote This indicates the differences in treatment needs based on age and condition.
310
What is the prognosis for adult cats with primary hypothyroidism with appropriate treatment?
Excellent prognosis; normal life expectancy ## Footnote This emphasizes the effectiveness of treatment.
311
What factors influence the prognosis for kittens with congenital hypothyroidism?
Severity of skeletal changes and neurologic status at treatment initiation ## Footnote These factors can affect long-term outcomes.
312
What is the median survival for untreated hypothyroid azotemic cats?
456 days ## Footnote This statistic highlights the serious implications of untreated hypothyroidism.
313
What is the median survival for euthyroid azotemic cats?
905 days ## Footnote This shows a better prognosis for euthyroid cats.
314
What percentage of iatrogenic hypothyroid cats had increased TSH levels?
85% ## Footnote This indicates a common finding in these cases.
315
What percentage of euthyroid cats had increased TSH levels?
14% ## Footnote This highlights the distinction between hypothyroid and euthyroid states.
316
What percentage of affected cats have bilateral pathologic changes with hyperthyroidism?
About 70%
317
What are the common clinical signs of hyperthyroidism in cats?
* Weight loss * Polyphagia * Vomiting * Hyperactivity * Polyuria and polydipsia (PU/PD) * Panting * Poor grooming habits * Behavioral changes
318
At what age do most hyperthyroid cats typically present?
9 years of age or older, with a mean age around 13 years
319
What is the prevalence of palpable thyroid nodules in hyperthyroid cats?
98%
320
What are some common physical examination findings in hyperthyroid cats?
* Muscle wasting: 77% * Weight loss: Key early detection sign * Dehydrated appearance: Due to decreased skin elasticity * Thin body condition: 35% * Dental disease: 45% * Tachycardia: 31% * Heart murmur: 29%
321
What is the significance of thyroid hormone in hyperthyroid cats?
It has direct positive inotropic and chronotropic effects and indirect effects through peripheral vasodilation
322
What percentage of hyperthyroid cats develop secondary systemic hypertension?
Approximately 10–30%
323
What laboratory findings are common in hyperthyroid cats?
* Increased alanine aminotransferase (ALT) activities: >80% * Increased alkaline phosphatase (ALP) activities: >50%
324
What is the most common first-line screening test for hyperthyroidism?
Randomly obtained serum total T4 concentration
325
What is the sensitivity of free T4 testing in hyperthyroid cats?
Abnormal in ~98% of hyperthyroid cats
326
What are the four main treatment options for hyperthyroidism in cats?
* Anti-thyroid medications (oral or transdermal) * Iodine-restricted diet * Thyroidectomy * Radioactive iodine therapy (¹³¹I)
327
Prevalence of thyroid carcinomas in hyperthyroid cats?
Diagnosed in about 1–2% of cases
328
What should be monitored during follow-up exams for hyperthyroid cats?
Tumor growth through routine cervical palpation
329
What additional factors may contribute to hyperthyroidism in cats?
* Dietary influences such as iodine or selenium deficiency * Chronic exposure to thyroid-disrupting compounds
330
What is the prevalence of polyphagia in hyperthyroid cats?
55%
331
What is the significance of TSH measurement in diagnosing hyperthyroidism?
Almost all hyperthyroid cats have undetectable TSH concentrations
332
What is the term for the presentation of hyperthyroid cats with hyporexia, anorexia, and lethargy?
Apathetic hyperthyroidism (likely clinical signs are from concurrent illnesses)
333
What is the role of thyroid scintigraphy in diagnosing hyperthyroidism?
Offers excellent sensitivity and specificity for diagnosis
334
What are SHIM RAD tumors?
Aggressive thyroid tumors that may require specialized treatment strategies
335
What percentage of hyperthyroid cats exhibit vomiting as a clinical sign?
47%
336
What is the typical body condition of hyperthyroid cats?
Thin body condition observed in 35%
337
What is the relationship between hyperthyroidism and liver enzyme levels?
Mild-to-moderate liver enzyme elevations are typically secondary to hyperthyroidism
338
What does a marked increase in thyroid nodule size indicate?
Warrants repeat scintigraphy to assess for carcinoma
339
What do anti-thyroid drugs and diet do in the context of thyroid tumors?
They block hormone synthesis, allowing the thyroid tumor to continue growing. ## Footnote Anti-thyroid drugs do not treat the tumor itself.
340
What warrants repeat scintigraphy in thyroid nodule cases?
A marked increase in thyroid nodule size.
341
What are the long-term consequences of untreated hyperthyroidism in cats?
Increased severity of clinical signs, formation of large thyroid masses, multifocal thyroid disease, development of intrathoracic thyroid masses, increased risk of thyroid carcinoma.
342
What are the goals of treatment for hyperthyroidism?
* Normalize thyroid hormone concentrations without causing iatrogenic hypothyroidism * Improve clinical signs and quality of life * Monitor and address concurrent disease.
343
What are the most common anti-thyroid medications?
* Methimazole * Carbimazole.
344
What is the mechanism of action for anti-thyroid drugs?
They block thyroid hormone synthesis by inhibiting thyroid peroxidase.
345
What is a critical reminder regarding compounded transdermal preparations?
Quality and stability are highly variable, choose a pharmacy with a history of producing high-quality formulations.
346
What are the potential limitations of anti-thyroid drugs?
Daily medication required, mild and severe adverse effects possible, risk of iatrogenic hypothyroidism.
347
What should be done if a cat experiences mild reactions to anti-thyroid drugs?
Continue therapy for a few days, reduce dose temporarily, or discontinue until signs resolve.
348
What are life-threatening reactions to anti-thyroid drugs?
* Toxic hepatopathy * Neutropenia * Agranulocytosis * Thrombocytopenia.
349
What is the first-line drug for managing moderate to severe hypertension in hyperthyroid cats?
Amlodipine.
350
What are common side effects of methimazole?
Gastrointestinal upset and erythema of pinna (transdermal)
351
What should be done if a cat has an adverse reaction to one antithyroid drug?
Switching to the other is not helpful. Discontinuation of the medication and consider another treatment option
352
What is a critical consideration when using transdermal formulations?
They have lower bioavailability and a delayed onset compared to oral forms.
353
What is the recommended action for a cat showing signs of iatrogenic hypothyroidism?
Decrease antithyroid drug dosage by 25–50%.
354
What is the reported prevalence of hypertension in hyperthyroid cats?
5% to >20%.
355
How does hypertension in some cats respond to hyperthyroidism treatment?
Hypertension resolves with hyperthyroidism treatment. Some cats will become hyperthyroid after hyperthyroid treatment
356
True or False: ACE inhibitors are the most effective for moderate-severe hypertension in hyperthyroid cats.
False.
357
List the advantages of low-iodine diets for feline hyperthyroidism.
* Initially less expensive * Easy for owners to administer * No anesthesia, surgery, or hospitalization required.
358
What are the drawbacks of low-iodine diets for cats?
* Low palatability in approximately 25% of cats * Requires strict dietary adherence * Suboptimal control of hyperthyroidism is common.
359
What percentage of cats had serum total T4 decrease into the reference interval after 30–60 days on a low-iodine diet?
55%.
360
What should be done if euthyroidism is not clearly achieved within 3–6 months of a low-iodine diet?
Alternative treatment should be recommended.
361
What is the treatment of choice for hyperthyroidism in younger cats without significant concurrent disease?
Radioactive iodine (¹³¹I) therapy.
362
How long do cats typically need to be hospitalized after radioactive iodine therapy?
3–14 days.
363
What is a common pre-treatment for cats undergoing radioactive iodine therapy?
Pre-treatment with antithyroid drugs (during waiting period). Removal about 1 week before treatment though
364
What must be balanced when dosing radioactive iodine for treatment?
Effective cure and avoidance of iatrogenic hypothyroidism.
365
What rare adverse reaction may occur from radioactive iodine therapy?
Radiation thyroiditis.
366
What is the major surgical risk associated with thyroidectomy?
Hypocalcemia due to iatrogenic hypoparathyroidism.
367
What does hyperthyroidism lead to in terms of renal function?
Increased cardiac output, intrarenal vasodilation, decreased muscle mass, increased GFR.
368
What was the median survival for cats treated with radioactive iodine therapy in Milner et al. (2006)?
4 years.
369
What is the relationship between pre-existing renal azotemia and survival in cats?
Pre-existing renal azotemia was associated with shorter survival.
370
What percentage of all neoplasms in dogs does thyroid cancer represent?
1–4% ## Footnote Thyroid cancer is the most common neuroendocrine tumor in dogs.
371
What is the typical malignancy rate of canine thyroid tumors?
10–30% benign adenomas ## Footnote The majority of thyroid tumors in dogs are malignant.
372
What type of thyroid tumors arise from follicular cells?
Carcinomas (about 70% of cases) ## Footnote These tumors stain positively for thyroglobulin.
373
What do parafollicular (C) cells produce?
Calcitonin ## Footnote These cells account for about 30% of canine thyroid tumors.
374
What leads to clinical hyperthyroidism in dogs?
Usually carcinoma. Functional adenomas are rarely reported ## Footnote Iatrogenic causes are more common.
375
What can cause iatrogenic hyperthyroidism in dogs?
Excessive L-thyroxine supplementation or consumption of raw foods containing thyroid tissue ## Footnote Thyrotoxicosis can occur from raw or dried beef-based diets.
376
What is the role of Thyroid Stimulating Hormone (TSH) in tumor development?
Excess TSH stimulates thyroid cell mitogenesis and hormone synthesis ## Footnote It may also lead to neoplastic transformation.
377
What genetic abnormalities are implicated in human thyroid carcinoma?
Point mutations in RAS genes and abnormalities in the PI3K-AKT pathway ## Footnote These pathways involve cell surface receptors like tyrosine kinases.
378
What is the mean age at which dogs are diagnosed with thyroid tumors?
9–11 years ## Footnote Some studies suggest 10–15 years.
379
What are the clinical signs of nonfunctional thyroid carcinoma?
Dysphagia, dysphonia, coughing, upper airway dyspnea, edema ## Footnote Clinical signs often result from space-occupying effects.
380
What imaging technique is rapid, non-invasive, and reliable for identifying thyroid tumors?
Ultrasound ## Footnote It can evaluate vascularity and invasion into surrounding structures.
381
What is the gold standard for diagnosing thyroid carcinoma?
Histologic examination ## Footnote Excisional biopsy may be both diagnostic and curative.
382
What are the criteria for staging thyroid tumors?
Primary tumor size, regional lymph node involvement, presence of distant metastasis ## Footnote Staging helps determine treatment options and prognosis.
383
What is the median survival time after unilateral or bilateral thyroidectomy?
Approximately 3 years ## Footnote Surgical excision is recommended for solitary, well-encapsulated tumors.
384
What is a common complication of thyroid carcinoma surgery?
Extensive hemorrhage ## Footnote Thyroid carcinomas are highly vascular.
385
What medication is used to manage thyrotoxicosis?
Methimazole ## Footnote Dosage is typically 2.5–5 mg PO q12–24h.
386
What is the purpose of using ACE inhibitors like Enalapril in thyroid carcinoma treatment?
To manage thyrotoxic hypertension ## Footnote Monitoring blood pressure is essential.
387
What should be preserved or autotransplanted during bilateral thyroidectomy?
Parathyroid glands ## Footnote This helps in preventing hypocalcemia.
388
What is the primary differential diagnosis for a cervical mass in dogs?
Enlarged lymph nodes ## Footnote Other differentials include salivary gland enlargement and abscess.
389
What type of thyroid carcinoma has been reported in a mixed-breed dog with Alaskan Malamute ancestry?
Medullary thyroid carcinoma ## Footnote Specific breed predispositions include Labrador Retrievers and Golden Retrievers.
390
What is the dosage of Telmisartan for managing thyrotoxic hypertension?
0.1–0.5 mg/kg PO q24h ## Footnote Telmisartan is an angiotensin receptor blocker.
391
What is the recommended dosage of Alendronate for treating paraneoplastic hypercalcemia?
0.5–1 mg/kg PO q24h ## Footnote Alendronate can cause esophageal irritation and needs serum calcium monitoring.
392
What is the mechanism of Calcitriol?
Vitamin D analog ## Footnote Used to treat postsurgical hypocalcemia.
393
What are the indications for Radiation Therapy?
* Non-movable, invasive tumors unsuitable for surgery * Local control or tumor shrinkage to enable later surgery
394
What was the median survival time for dogs after radiation therapy according to a study of 8 dogs?
24.5 months ## Footnote 4 of 8 dogs died from metastatic disease.
395
What are some acute side effects of Radiation Therapy?
* Esophagitis * Tracheitis * Laryngitis * Skin erythema or alopecia
396
What is the median survival for dogs receiving I-131 therapy?
12 to 34 months ## Footnote Best outcomes were seen when used adjunctively after surgery.
397
What complication can occur if doses of I-131 exceed 0.2 GBq/kg?
Bone marrow suppression ## Footnote This is a serious and irreversible complication.
398
Which chemotherapy agent demonstrated the greatest benefit for canine thyroid carcinoma?
Cisplatin ## Footnote Median survival time was approximately 11 months.
399
What are the clinical signs of thyrotoxicosis in dogs?
* Polyuria and polydipsia (PU/PD) * Hyperactivity * Weight loss despite polyphagia * Systemic hypertension * Tachycardia
400
What is the purpose of Methimazole in the treatment of canine hyperthyroidism?
Antithyroid drug to control thyrotoxicosis ## Footnote Typical dose is 2.5–5 mg PO q12–24h.
401
What is the recommended dose of Atenolol for preventing intraoperative thyroid storm?
0.25–1 mg/kg PO q12h ## Footnote Administered the night before and morning of anesthesia.
402
What medications can be used to manage systemic hypertension in dogs with non-resectable tumors?
* ACE inhibitors (e.g., enalapril, benazepril) * Amlodipine (calcium channel blocker)
403
Fill in the blank: The median survival for dogs with metastatic disease receiving weekly fractionated radiation for thyroid carcinoma was approximately _______.
8 months
404
What is insulinoma?
A neoplasm of the pancreatic beta cells that synthesizes and secretes excessive quantities of insulin, often causing clinical signs of hypoglycemia. ## Footnote It is uncommon in dogs and rare in cats.
405
How many canine cases of insulinoma have been documented approximately?
360
406
How many well-documented feline cases of insulinoma exist?
10
407
What percentage of pancreatic islet cells are beta cells?
Approximately 70%
408
What percentage of insulinomas are solitary tumors?
Approximately 80%
409
What is the typical location of insulinomas in the pancreas?
Most often located in either the right or left limb of the pancreas.
410
What is the rate of metastatic lesions detected in dogs with insulinoma?
Ranges from 45% to 64%
411
What is the clinical staging for stage 1 of insulinoma?
T1N0M0 — primary tumor without regional lymph node or distant metastasis
412
What is the clinical staging for stage 2 of insulinoma?
T1N1M0 — primary tumor with regional lymph node metastasis
413
What is the clinical staging for stage 3 of insulinoma?
T1N1M1 or T1N0M1 — presence of distant metastasis
414
What hormones are involved in the body's counter-regulatory response to hypoglycemia?
* Glucagon * Catecholamines (epinephrine and norepinephrine) * Growth hormone * Glucocorticoids
415
What is the mean age of dogs diagnosed with insulinoma?
9 years
416
What are common clinical signs of insulinoma related to neuroglycopenia?
* Mental dullness * Disorientation * Weakness * Ataxia * Visual disturbances or apparent blindness * Collapse * Seizures
417
What percentage of dogs with insulinoma experience seizures?
48%
418
What is the significance of measuring serum insulin concentrations in suspected insulinoma cases?
Concurrent normal or elevated serum insulin concentrations despite hypoglycemia.
419
What imaging study has shown promise for identifying insulinomas in dogs?
High-quality, dual-phase, thin-section multi-detector CT
420
What is the prevalence of collapse as a clinical sign in dogs with insulinoma?
40%
421
What is the role of fructosamine in the diagnosis of insulinoma?
Low fructosamine can support a diagnosis of insulinoma.
422
What is the typical clinical sign prevalence for hindlimb weakness in dogs with insulinoma?
14%
423
What can trigger worsening signs in dogs with insulinoma?
* Fasting * Exercise * Excitement
424
What is the clinical feature of obesity in dogs with insulinoma?
Some dogs may be overweight due to insulin's anabolic effects.
425
What are common diagnostic criteria for clinical suspicion of insulinoma?
* Presence of compatible clinical signs * Persistent fasting hypoglycemia * Concurrent normal or elevated serum insulin concentrations
426
Hypoglycemia typically develops within how many hours after a meal in most insulinoma cases?
12 hours
427
What should be collected when hypoglycemia is detected in a dog?
Serum to assess insulin concentration
428
True or False: A dog may not develop hypoglycemia even after prolonged fasting with insulinomas.
True
429
What diagnostic test has low sensitivity in detecting insulinoma-associated hypoglycemia?
Glycosylated hemoglobin (HbA1c)
430
What percentage of insulinoma dogs had increased insulin concentrations with a single test?
76%. A second test increases it to 91%
431
What imaging technique is most effective for identifying pancreatic masses in humans with insulinoma?
High-quality dual-phase, thin-section multi-detector CT
432
What percentage of insulinomas were identified by CT in a study of 14 dogs?
71%
433
What is the treatment of choice for insulinoma?
Surgical resection of the primary tumor and any metastases
434
What is a common postoperative complication in dogs after insulinoma surgery?
Diabetes mellitus
435
What is the role of streptozocin in the treatment of insulinoma?
Cytotoxic treatment aimed at destroying insulin-secreting beta cells
436
What should be monitored when administering diazoxide?
Response to treatment for hypoglycemia
437
What is the median survival time for dogs undergoing partial pancreatectomy for insulinoma?
12 to 14 months
438
What are two negative prognostic factors for canine insulinoma?
* Young dogs * Persistent postoperative hypoglycemia
439
What breeds were noted in the well-described cases of feline insulinoma?
* Siamese * Domestic Shorthairs * Domestic Longhairs * Maine Coon
440
What is the mechanism of action for prednisone in managing hypoglycemia?
Increases blood glucose via gluconeogenesis and decreases tissue glucose uptake
441
What are the common side effects of octreotide in dogs?
* Mild injection site pain * Nausea * Vomiting * Abdominal pain * Constipation * Steatorrhea
442
What is the function of glucagon in the treatment of hypoglycemia?
Stimulates glycogenolysis and gluconeogenesis, raising blood glucose
443
What are common clinical signs of hypoglycemia in cats?
* Anorexia * Weight loss * Episodic weakness or falling * Mental dullness * Lethargy * Hypothermia * Bradycardia * Limb and facial twitching * Seizures ## Footnote Clinical signs vary with the severity of hypoglycemia and co-morbidities
444
What findings were reported in the first three cases regarding insulinoma identification in cats?
* One mass identified on abdominal ultrasound * Two masses discovered during exploratory laparotomy ## Footnote These findings indicate the importance of imaging in diagnosis
445
What were the insulinoma locations in the later-described cases of cats?
* 6 tumors in the left pancreatic lobe * 3 tumors in the right lobe * 1 tumor at the angle of the pancreas ## Footnote Tumor size ranged from 0.4 to 3 cm
446
What is the mainstay of treatment for pancreatic tumors in cats?
Prompt surgical extirpation ## Footnote This is critical for managing the condition effectively
447
What should cats be monitored for postoperatively?
Transient diabetes mellitus due to suppression of insulin secretion from residual atrophied pancreatic beta cells ## Footnote Postoperative monitoring is essential for early detection of complications
448
What medical management options are available if surgery is declined?
* Small, frequent meals * Oral prednisone therapy at 0.5 mg/kg PO every 12 hours ## Footnote Glucocorticoids enhance hepatic gluconeogenesis and glycogenolysis while reducing peripheral glucose uptake
449
What factors influence the prognosis of pancreatic tumors in cats?
* Disease stage at diagnosis * Malignant behavior of the mass * Completeness of surgical resection * Timing of diagnosis ## Footnote The prognosis may also be related to overexpression of glucokinase 1 in neoplastic beta cells
450
What were the reported survival times in early case reports?
Survival times ranged from 1 day to 18 months ## Footnote More recent cases report survival up to 32 months post-surgery
451
What are the defining features of Hyperosmolar-Hyperglycemic State (HHS)?
* Severe hyperglycemia * Hyperosmolality * Dehydration without significant ketosis
452
What are the shared mechanisms that lead to both DKA and HHS?
* Decreased net effective action of circulating insulin * Increased circulating counter-regulatory stress hormones
453
What are the consequences of ketone excess in DKA?
* Acidemia * Osmotic diuresis * Loss of electrolytes * Volume depletion
454
What is the relationship between insulin deficiency and counter-regulatory hormones in DKA?
Insulin deficiency, along with excess counter-regulatory hormones, worsens insulin resistance, hyperglycemia, and ketonemia
455
What causes the rapid onset of clinical signs in DKA?
Rapid metabolic changes due to insulin deficiency and ketone body formation
456
In HHS, what factors contribute to the severe hyperglycemia observed?
* Increased gluconeogenesis * Altered glycogen metabolism * Decreased peripheral glucose uptake
457
What is a key difference in the insulin levels between DKA and HHS?
DKA can have absolute or relative insulin deficiency, while HHS typically has relative insulin deficiency (enough to prevent lipolysis)
458
What are the common triggers for DKA?
* Infection * Pancreatitis
459
What concurrent diseases are commonly associated with DKA in dogs?
* Acute pancreatitis * Bacterial pneumonia
460
What is the typical blood glucose level associated with HHS?
Typically >600 mg/dL
461
What is the importance of recognizing ketone bodies in urine for DKA diagnosis?
It forms the basis of DKA diagnosis, as urine reagent strips detect ketones
462
What are the classic goals of DKA treatment?
* Replace fluid and electrolyte deficits * Administer insulin * Correct acidosis * Identify and treat concurrent diseases
463
What is the risk of administering hypotonic fluids in DKA?
They are unsuitable for correcting sodium and water deficits and can cause cerebral edema
464
What is the potential effect of extracellular osmolality in pets?
Cerebral edema ## Footnote Increased extracellular osmolality can lead to significant neurological complications.
465
What are the risks of overhydration in pets with DKA?
* Overhydration * Pulmonary edema * Third-space losses ## Footnote Close monitoring is essential to avoid these complications.
466
What are the risks of insufficient fluids in pets with DKA?
* Prolonged hypoperfusion * Tissue hypoxia * Prerenal azotemia ## Footnote Insufficient fluid therapy can lead to severe complications.
467
How is fluid deficit calculated?
Fluid deficit (mL) = Percent dehydration (as decimal) × Body weight (kg) × 1000 ## Footnote Example: 10% dehydration = 0.10.
468
What is the administration protocol for fluid boluses in shock?
Administer fluid boluses of 5–10 mL/kg over 20 minutes ## Footnote Reassess heart rate and blood pressure after each bolus.
469
What is the key consideration regarding potassium in pets with DKA?
All pets with DKA should be assumed to be potassium depleted ## Footnote Acidosis can mask total body potassium deficits.
470
How frequently should blood glucose (BG) be monitored during DKA treatment?
Every hour during the first 24 hours ## Footnote Close monitoring is essential to manage BG levels effectively.
471
What is the important note regarding insulin dosage when adding dextrose?
Do not decrease the insulin dose when adding dextrose ## Footnote This is crucial to prevent hypoglycemia and large osmotic shifts.
472
What is the typical resolution time for metabolic acidosis with fluid resuscitation and insulin therapy?
12–24 hours ## Footnote Insulin promotes ketone utilization, helping to correct acidosis.
473
Under what condition should sodium bicarbonate therapy be considered?
When plasma bicarbonate concentration <11 mEq/L after several hours of therapy ## Footnote Bicarbonate therapy carries risks and should be used cautiously.
474
What is the formula to calculate bicarbonate deficit?
Bicarbonate deficit (mEq) = Body weight (kg) × 0.4 × (12 − Patient’s bicarbonate) ## Footnote Only enough bicarbonate to bring levels up to 12 mEq/L should be given.
475
What are the major effects of insulin in DKA treatment?
* Inhibits lipolysis * Suppresses hepatic gluconeogenesis * Promotes glucose utilization * Enhances ketone body metabolism ## Footnote These effects are crucial for managing DKA.
476
When should long-acting insulin be transitioned to?
When ketosis and acidemia have resolved, hydration status is adequate, and serum electrolytes are normal ## Footnote The pet should also be eating voluntarily.
477
What are the ideal characteristics of insulin for DKA?
* Rapid onset of action * Quickly metabolized ## Footnote These characteristics allow for swift adjustments and improved safety.
478
What are the drawbacks of intramuscular (IM) and subcutaneous (SC) insulin injections?
* Variable absorption * Delay in onset * Prolonged duration of action * Increased risk of hypoglycemic events ## Footnote IV administration is preferred for rapid control.
479
What is the effect of plastic binding on insulin during administration?
Insulin binds to plastic tubing and syringes ## Footnote Precondition the line to minimize loss.
480
What are the indications for potassium supplementation in DKA?
Always supplement unless the patient has anuric kidney failure ## Footnote Delay if urine production has not started or if hyperkalemia persists.
481
What are the clinical signs of magnesium depletion?
* Lethargy * Muscle weakness * Seizures * Arrhythmias ## Footnote Monitoring is important to prevent complications.
482
What are the contraindications for phosphate supplementation?
* Hyperphosphatemia * Hypercalcemia * Anuria * Tissue necrosis ## Footnote Careful assessment is required before supplementation.
483
What are the contraindications for magnesium administration?
Administration of digitalis or cardioglycosides ## Footnote These medications can interact negatively with magnesium.
484
What is the impact of appropriate management on mortality rates in DKA?
Mortality rates have dropped from 25–35% to <10% ## Footnote This improvement is due to vigilant monitoring and therapy.
485
What are the main causes of death in DKA?
* Severe underlying medical conditions (pancreatitis, hormonal disorders, sepsis, AKI, CHF) * Financial limitations leading to euthanasia * Not typically metabolic complications of DKA itself ## Footnote Understanding these causes can help in prevention strategies.
486
In which conditions can diabetes mellitus remission occur in cats?
Possible after DKA resolution, particularly in cats with: * Concurrent pancreatitis * Glucocorticoid treatment at the time of DKA diagnosis ## Footnote These factors are linked to the potential for remission.
487
What are the clinical features of Hyperosmolar Hyperglycemic State (HHS)?
HHS animals are critically ill and may present with acute renal failure, leading to death or euthanasia ## Footnote This highlights the severity of HHS.
488
What is the initial fluid choice for treating HHS?
Isotonic 0.9% saline ## Footnote This fluid helps restore hydration status safely.
489
What electrolyte management is necessary in HHS treatment?
Serum potassium and phosphate must be monitored closely ## Footnote Correcting these electrolytes is vital for patient safety.
490
When should insulin therapy be initiated in HHS?
Delay insulin until plasma volume is restored ## Footnote This approach minimizes risks associated with rapid insulin administration.
491
What is the maximum allowable BG decrease per hour in HHS treatment?
BG should not decrease more than 50 mg/dL per hour ## Footnote This limit helps prevent complications such as cerebral edema.
492
What is the prognosis for HHS compared to DKA?
Generally guarded to poor, worse than for DKA ## Footnote This highlights the seriousness of HHS.
493
What are the key management targets for DKA?
* Fluid replacement rate: 60–80% deficit over first 12h, rest over 24h * Initial insulin administration: Start 2–4h after fluids if K⁺ normal * BG reduction target: 50–75 mg/dL/hour * Dextrose supplementation: Start when BG <250 mg/dL * Prognosis: Good with close monitoring (<10% mortality) ## Footnote These targets are essential for effective DKA management.
494
What are the key management targets for HHS?
* Fluid replacement rate: Gradual over 24–48h * Initial insulin administration: Delay until plasma volume restored * BG reduction target: <50 mg/dL/hour * Dextrose supplementation: Start when BG <250 mg/dL * Prognosis: Guarded to poor ## Footnote These targets differ from DKA due to the nature of HHS.
495
What is the estimated prevalence of diabetes mellitus in dogs?
About 0.3% in first-opinion practices and about 1% in referral/institutional practices.
496
What are the two predominant forms of diabetes mellitus in humans?
* Type 1 Diabetes Mellitus (T1DM) * Type 2 Diabetes Mellitus (T2DM)
497
What is the most common form of diabetes mellitus in dogs?
It resembles human Type 1 diabetes.
498
What are common histologic findings in pancreatic tissue from diabetic dogs?
* Reduced size and number of pancreatic islets * Reduced number of beta cells * Beta cell vacuolization, enlargement, and degeneration.
499
What factors have been implicated in beta cell dysfunction or destruction?
* Genetic Predisposition * Immune-Mediated Mechanisms * Juvenile Onset * Pancreatic Abnormalities
500
What are the two classifications of canine diabetes mellitus?
* Insulin-Deficient Diabetes Mellitus (IDDM) * Insulin-Resistant Diabetes Mellitus (IRDM)
501
What causes insulin resistance in dogs?
* Endocrine influences * Obesity * Drugs * Inflammatory mediators * Disorders of receptor function
502
How common is pancreatitis in diabetic dogs?
Histologically identifiable pancreatitis is reported in 30–40% of diabetic dogs.
503
What is a 'honeymoon period' in newly diagnosed diabetic dogs?
It is characterized by excellent glycemic control with small insulin doses.
504
What metabolic effects result from diabetes mellitus?
* Decreased tissue utilization of glucose, amino acids, and fatty acids * Accelerated hepatic glycogenolysis and gluconeogenesis * Hyperglycemia * Glucosuria
505
What age group of dogs is most commonly diagnosed with diabetes mellitus?
Middle-aged and older dogs (5–12 years) with a peak prevalence between 7–10 years.
506
Which dog breeds are at the highest risk for developing diabetes mellitus?
* Australian Terrier * Standard Schnauzer * Miniature Schnauzer * Bichon Frise * Spitz
507
What is the typical duration of the diestrus phase in female dogs?
60–90 days.
508
When should insulin therapy begin for diabetic dogs?
As soon as diabetes is diagnosed.
509
What are the therapeutic goals for managing diabetic dogs?
* Reduce or eliminate clinical signs * Prevent short-term complications (hypoglycemia, DKA) * Maintain good quality of life
510
What does tight glycemic control increase the risk of in diabetic dogs?
Hypoglycemia.
511
What are the common biochemical profile findings in uncomplicated diabetes mellitus?
* Hyperglycemia * Hypercholesterolemia * Hypertriglyceridemia (lipemia) * Mild increases in ALT (<500 U/L) and ALP (<500 U/L)
512
What should owners monitor in their diabetic dogs?
* Water intake * Urine output * Appetite * Body weight changes
513
What are the initial steps for managing a diabetic dog's treatment?
* Address contributing factors * Start insulin therapy * Manage diet
514
What types of insulin are typically used for diabetic dogs?
* Intermediate-acting (e.g., Vetsulin, NPH) * Long-acting (e.g., PZI, glargine) * Ultra-long-acting (not yet approved)
515
How does exercise affect blood glucose levels in diabetic dogs?
Lowers blood glucose by increasing insulin absorption and improving blood flow.
516
What is a common complication of high-fiber diets in diabetic dogs?
* Increased frequency of defecation * Constipation * Obstipation
517
What is the initial insulin dose for dogs starting on glargine U-300?
0.5 U/kg once daily.
518
What should owners do if their dog experiences hypoglycemia during physical activity?
Carry a glucose source.
519
What is the importance of continuous glucose monitoring for owners?
It provides owners with more control over their dog's management.
520
What is the recommended adjustment in insulin dose when switching from once-daily to twice-daily dosing?
Decrease the per-injection dose by ~30%.
521
What happens to insulin when it is frozen or heated?
Freezing or heating inactivates insulin.
522
Is storing insulin at room temperature acceptable?
Yes, but it is safest to store insulin in the refrigerator.
523
What is the recommended frequency for insulin replacement?
Monthly replacement is not necessary if insulin is properly stored and handled.
524
What is the suggested method for mixing insulin?
Gently rolling is suggested for consistency with most products.
525
Which insulin should never be diluted?
Insulin glargine. (pH based)
526
How should insulin pens be stored?
Without needles attached to prevent air entry and dilution.
527
What must owners do before using an insulin pen?
Prime the pen by loading and expelling 1–2 units upright.
528
What is the only veterinary insulin marketed with a pen device?
Vetsulin VetPen.
529
What did a study find about the accuracy of the small VetPen?
It was more accurate at low doses compared to syringes.
530
What is the recommended time to hold the pen needle subcutaneously in dogs?
5 seconds.
531
When should intact females ideally be spayed after starting insulin?
1–3 days after starting insulin.
532
What is the effect of spaying intact bitches on insulin resistance?
It reduces progesterone-driven insulin resistance.
533
What are common concurrent conditions at diagnosis that can interfere with insulin?
* Inflammatory diseases (e.g., pancreatitis) * Infectious diseases * Neoplastic conditions * Metabolic diseases (e.g., Cushing’s disease)
534
What is the reflection period for serum fructosamine?
1–2 weeks.
535
What does Hemoglobin A1c reflect?
Mean blood glucose over the preceding 2–3 months.
536
What can falsely increase Hemoglobin A1c levels?
* Extreme hypertriglyceridemia * Hyperbilirubinemia * Prolonged erythrocyte lifespan.
537
What is the recommendation regarding reference intervals for fructosamine and HbA1c?
Each laboratory should generate its own reference intervals.
538
What is an ideal target for fructosamine and HbA1c levels in diabetic dogs?
Slightly above the reference range.
539
What is the ideal blood glucose range for diabetic dogs?
80–250 mg/dL.
540
What is the recommended approach when adjusting insulin doses?
Dose changes should be limited to 10–25%.
541
What does the Freestyle Libre sensor do?
Measures interstitial glucose continuously and records data every minute.
542
What is the correlation coefficient between FGMS and blood glucose readings?
Correlation coefficient (ρ) = 0.94 ## Footnote Indicates a strong correlation between the glucose sensor readings and actual blood glucose levels.
543
What are common causes for the recurrence of clinical signs in diabetic dogs?
* Incorrect insulin type * Incorrect dose or frequency * Technical issues * Concurrent diseases ## Footnote Understanding these causes is crucial for effective management of diabetes in dogs.
544
What is the recommended insulin dosage for well-controlled diabetic dogs?
≤1 U/kg/injection subcutaneously every 12 hours ## Footnote This dosage helps maintain stable blood glucose levels.
545
Define glycemic variability.
Wide glucose excursions between hyperglycemia and hypoglycemia within a day or across days ## Footnote High variability can complicate diabetes management.
546
What are common indices for evaluating glycemic variability?
* Standard deviation (SD) of BG values * Coefficient of variation (CV) ## Footnote These metrics help assess the stability of blood glucose levels.
547
What should be done if no clear cause of glycemic variability is found?
Change insulin type; for example, switch from Vetsulin to insulin detemir or glargine ## Footnote Different insulin types may offer better control.
548
List some recognized causes of insulin ineffectiveness in dogs.
* Inactive insulin * Improper administration technique * Inadequate dose * Impaired insulin absorption ## Footnote Identifying these causes is essential for effective diabetes management.
549
What is the pathogenesis of cataract formation in diabetic dogs?
Accumulation of sorbitol and galactitol in the lens leading to osmotic swelling and fiber rupture ## Footnote This process can result in significant vision impairment.
550
What is the prognosis for diabetic dogs with committed owners?
Generally have a life expectancy similar to non-diabetic dogs of the same age, sex, and breed ## Footnote Effective management and owner engagement are key to improving outcomes.
551
What is diabetic nephropathy and its clinical relevance in dogs?
Occasionally reported but its clinical relevance remains unclear; observed microscopic changes include membranous glomerulopathy ## Footnote Chronic kidney disease is often independent of diabetic nephropathy.
552
What is diabetes mellitus (DM)?
A syndrome characterized by hyperglycemia due to defects in insulin secretion, insulin sensitivity, or both.
553
What does prediabetes refer to?
A state of abnormally increased blood glucose concentrations that do not yet meet the criteria for DM.
554
What is the primary type of diabetes mellitus in cats analogous to in humans?
Type 2 diabetes mellitus (T2DM).
555
What percentage of diabetic cats may have diabetes secondary to hypersomatotropism?
Up to 25%.
556
What are the ALIVE criteria for diagnosing diabetes mellitus in cats?
Blood glucose >270 mg/dL with classical signs of hyperglycemia and one of the following: * Increased glycosylated proteins * Glucosuria on multiple occasions OR Blood glucose between 125–270 mg/dL plus two of the following: * Classical signs of hyperglycemia * Increased glycosylated proteins * Glucosuria on multiple occasions.
557
What is the reported prevalence of DM in cats?
Ranges from 0.5% to 2%.
558
What common breeds are most affected by diabetes in cats?
Domestic shorthair and longhair cats.
559
What age group is most commonly diagnosed with diabetes in cats?
Most cats are diagnosed after 8 years of age, with a peak incidence between 10–13 years.
560
What is the relationship between obesity and diabetes in cats?
Obesity causes insulin resistance and significantly increases the risk of diabetes.
561
What is the main characteristic of type 2 diabetes mellitus in cats?
Impaired insulin secretion and peripheral insulin resistance.
562
What is remission in the context of diabetes in cats?
A state of euglycemia without the need for insulin therapy for at least four weeks after prior insulin administration.
563
What factors can help achieve remission in diabetic cats?
Reducing insulin resistance and decreasing carbohydrate load.
564
What are glucotoxicity and lipotoxicity?
Glucotoxicity refers to chronic hyperglycemia damaging beta cells, while lipotoxicity refers to hyperlipidemia damaging beta cells.
565
What is the role of incretins in insulin secretion?
Incretins stimulate insulin secretion in a glucose-dependent manner and inhibit glucagon secretion.
566
What is the significance of GLP-1 receptor agonists (GLP-1RAs) in cats?
They may improve metabolic outcomes but did not significantly increase remission rates in studies.
567
What factors are associated with higher remission rates in diabetic cats?
* Mild or early diabetes * Absence of hyperlipidemia * Shorter duration of clinical signs * Older age * History of glucocorticoid therapy.
568
What insulin formulations have been reported to achieve diabetic remission in cats?
* Protamine zinc insulin (PZI) * Lente insulin * Glargine (U100) * Detemir.
569
What is the impact of dietary strategies on achieving remission in diabetic cats?
Various dietary strategies have been used, but evidence for superiority of any particular diet is insufficient.
570
What is the importance of early diagnosis in diabetic cats?
It may allow medications and dietary interventions to be more successful in inducing remission.
571
What was the outcome of the only prospective randomized clinical trial comparing insulin types in cats?
No significant difference in remission rates between glargine (U100) and PZI, combined with a low-carbohydrate diet.
572
What are the two types of diets compared in the study regarding remission rates?
* Low-carbohydrate (3.5 g/100 kcal), low-fiber (0.1 g/100 kcal) diet * Moderate-carbohydrate (7.6 g/100 kcal), high-fiber (3.1 g/100 kcal) diet
573
What remission rates were observed in cats fed the low-carbohydrate, low-fiber diet?
68% remission
574
What remission rates were observed in cats fed the moderate-carbohydrate, high-fiber diet?
41% remission
575
What monitoring strategy showed the highest remission rate in newly diagnosed diabetic cats?
Tight glycemic control with a target BG of 60–160 mg/dL.
576
What were the remission rates in the tightly controlled group versus the traditional group?
* Tightly controlled group: 78% remission * Traditional group: 14% remission
577
What is the significance of tight glycemic control early in treatment?
It significantly improves remission rates.
578
What factors may lead to recurrence of an insulin-dependent state in cats?
* Disease progression * Increased carbohydrate intake * Worsening insulin resistance
579
What interventions are likely to help maintain remission based on pathophysiology?
* Minimizing insulin resistance * Minimizing dietary carbohydrate load * Optimizing beta cell function
580
What are some challenges of insulin therapy in cats?
* Complex nature of glycemic control * Pharmacologic limitations of insulin formulations * Caregiver burden and compliance
581
What are the primary treatment goals for diabetic cats?
* Avoiding hypoglycemia * Preventing diabetic ketoacidosis (DKA) * Preventing excessive weight loss * Reducing polyuria and polydipsia (PU/PD)
582
What is recommended for cats with mild hyperglycemia and no clinical signs?
Starting with a low insulin dose.
583
What are the general principles of insulin selection for cats?
* No perfect insulin formulation * Variability in pharmacologic properties * Consideration of owner preferences and compliance
584
What are the durations of bolus insulin secretion in different species?
* Humans: 2–4 hours * Dogs: 6–9 hours * Cats: 6–12 hours
585
What is the typical insulin increase magnitude in cats compared to humans and dogs?
1.5–3-fold increase in cats, compared to 5-fold in humans and 5-7-fold in dogs.
586
What feeding regimen may better reflect natural insulin needs in diabetic cats?
Multiple small meals.
587
What are the advantages of long-acting recombinant insulin analogs?
* No need for resuspension * More consistent absorption * Lower risk of hypoglycemia
588
What is the mechanism of action for insulin glargine?
Soluble at pH 4 and precipitates at neutral pH.
589
What are the variants of insulin glargine?
* Glargine U100 (e.g., Lantus) * Glargine U300 (e.g., Toujeo)
590
What are the characteristics of insulin detemir?
* Highly predictable action * Minimal variability * Often requires q12h dosing in cats
591
What must be done with commercially available insulin suspensions before use?
They must be evenly resuspended through gentle rolling and inversion.
592
What is the typical duration of action for Insulin Detemir in cats?
Typically too short for once-daily use; q12h dosing usually required.
593
Why should Insulin Detemir not be diluted?
It has a lower biological potency due to albumin binding in plasma.
594
What is the designed purpose of Insulin Degludec?
Ultra-long-acting basal insulin coverage in humans.
595
What is the typical duration of Insulin Degludec in cats?
About 12 hours.
596
What are the key intermediate-acting insulin formulations?
* NPH * NPH-Regular mixes * Lente * PZI * Glargine U100 * Detemir
597
What is the goal for blood glucose nadirs when using intermediate-acting insulins?
Aim for blood glucose nadirs between 80–100 mg/dL.
598
What is the aim for blood glucose peaks when using intermediate-acting insulins?
Aim for blood glucose peaks between 250–350 mg/dL.
599
What is the relationship between dosing frequency and glycemic variability in cats?
Differences between required and delivered doses can cause substantial intraday glycemic variability.
600
What is the duration of action comparison between porcine lente and PZI?
Porcine lente and NPH have shorter durations compared to PZI, glargine U100, detemir, and degludec.
601
What is a key observation regarding remission induction in cats with diabetes?
Once-daily high doses of PZI, glargine U100, or detemir may achieve acceptable clinical control.
602
What are the characteristics of long-acting basal insulin formulations?
Lasting 8–24 hours with evenly distributed time-action profiles and no distinct peak.
603
What factors influence owner compliance in diabetic cat management?
* Owner concerns about quality of life * Burden of responsibility * Injection discomfort
604
What is the recommended dosing frequency for Humulin N / Novolin N in cats?
q8–12h.
605
What is the dosing frequency for Vetsulin in cats?
q8–12h.
606
What is the dosing frequency for Prozinc in cats?
q12h or longer.
607
What should be monitored when using SGLT-2 antagonists?
Monitor for ketosis.
608
What is the mechanism of action for Exenatide Extended-Release?
Potentiates insulin secretion during hyperglycemia and promotes weight loss. GLP-1 agonist
609
What is a common side effect of Glipizide in diabetic cats?
Mild hyperglycemia.
610
What is the primary concern with insulin overdose in cats?
Excessive weight gain may signal insulin overdose.
611
What is a potential consequence of chronic hyperglycemia in diabetic cats?
Impair counter-regulatory responses.
612
What is the primary function of SGLT-2 antagonists?
Increase renal glucose excretion.
613
What is the overdose risk in heavier cats?
Greater risk of overdose ## Footnote Heavier cats have a higher risk of overdose due to their body mass and insulin requirements.
614
What challenges may owners face that affect long-term adherence to diabetic treatment?
* Financial strain * Caregiver fatigue * Concurrent diseases in the cat ## Footnote These challenges can lead to unsustainable treatment plans.
615
What does weight loss in diabetic cats suggest?
Overall insulin deficiency ## Footnote Weight loss indicates that the cat may not be receiving enough insulin.
616
What is the recommended approach if no improvement in PU/PD is seen after increasing insulin dose?
Avoid further insulin increases ## Footnote This is to reduce the risk of hypoglycemia.
617
What are non-insulin hypoglycemic agents useful for?
Early disease management or as adjuncts to insulin ## Footnote These agents can help improve glycemic control.
618
What are GLP-1 receptor agonists known for?
Favorable safety profiles ## Footnote They are particularly promising in the treatment of diabetes.
619
What is a key reason for changing insulin formulations?
If no improvement is observed after increasing insulin dose ## Footnote This may necessitate a restart of the titration process.
620
What should be done if clinical signs of hypoglycemia persist?
* Further decrease the insulin dose * Consider that the signs may not be due to hypoglycemia ## Footnote This approach helps avoid unnecessary insulin increases.
621
What is the goal when monitoring for remission in diabetic cats?
* Clinical signs * Fructosamine levels * Persistent negative glucosuria ## Footnote These factors help determine if insulin can be gradually decreased.
622
What is a limitation of using glycosylated proteins for monitoring?
Do not capture short-term hypoglycemic episodes ## Footnote High concentrations of glycosylated proteins do not rule out hypoglycemia.
623
What is the significance of Continuous Glucose Monitoring (CGM) in diabetic cats?
Measures interstitial glucose and helps expedite insulin titration ## Footnote CGMs provide valuable trend data.
624
What are common complications of feline diabetes mellitus?
* Diabetic neuropathy * Urinary tract infections (UTIs) * Chronic kidney disease (CKD) ## Footnote These complications can arise due to chronic hyperglycemia.
625
What is the relationship between obesity and insulin resistance?
Obesity predictably causes insulin resistance ## Footnote Weight gain should be expected with insulin initiation.
626
What are the dangers of hypoglycemia in diabetic cats?
* Life-threatening * Leads to long-term consequences ## Footnote Repeated mild hypoglycemia can impair counter-regulatory responses.
627
How does repeated hypoglycemia affect warning signs?
Lowers the threshold for activation of warning signs ## Footnote This results in fewer early signs before severe hypoglycemia occurs.
628
What can repeated hypo- and hyperglycemia cause?
Progressive dysfunction of the central and autonomic nervous systems ## Footnote This dysfunction leads to a lower threshold for activation of warning signs.
629
What can occur due to lowered thresholds for activation of warning signs?
Fewer warning signs, sudden seizures, coma, and even death due to neuroglycopenia.
630
What were the findings regarding cats with BG < 20 mg/dL?
About one-third exhibited only mental dullness, lethargy, weakness, and ataxia.
631
What are reported clinical signs of hypoglycemia in cats?
* Vocalization * Twitching * Seizures * Bradycardia * Hypothermia * Vomiting * Panting * Decreased appetite * Inappropriate urination * Diarrhea * Drooling
632
What do CGMs measure compared to blood glucose?
Interstitial glucose.
633
What bias is observed in CGMs and human glucometers in hypoglycemic ranges?
Reported glucose concentrations are lower than actual blood glucose.
634
What can happen in cats with interstitial glucose < 40 mg/dL?
They often show no clinical signs for several hours.
635
What is the Somogyi Hypothesis?
Proposes that hypoglycemia induces a counter-regulatory hormone surge, causing rebound hyperglycemia and insulin resistance.
636
What does scientific evidence say about the Somogyi Hypothesis?
It does not support the hypothesis; no consistent correlation between hypoglycemic episodes and subsequent hyperglycemia was found.
637
What is high glycemic variability associated with in humans?
* Worsened hyperglycemia * Diabetes-related complications
638
What does increased glycemic variability correlate with in diabetic cats?
Poorer glycemic control.
639
What was observed in a clinical study involving cats treated with exenatide extended-release?
Reduced glycemic variability was associated with higher remission rates.
640
What must be avoided even if no clinical signs are observed?
Hypoglycemia.
641
What does repeated mild hypoglycemia impair?
The body’s ability to sense and respond to future hypoglycemia.
642
What negative impact does high glycemic variability have?
It negatively impacts glycemic control and possibly long-term outcomes.
643
What strategies are essential for safe, effective management of feline diabetes?
Strategies that reduce both hypoglycemia and hyperglycemia.
644
What are the two main causes of hypercortisolism?
* Iatrogenic causes: long-term administration of exogenous glucocorticoids * Naturally occurring causes: excessive endogenous cortisol production
645
What are the two classifications of naturally occurring hypercortisolism based on ACTH dependency?
* ACTH-dependent hypercortisolism: Pituitary-dependent hypercortisolism (PDH) and ectopic ACTH syndrome * ACTH-independent hypercortisolism: Functional adrenocortical tumors and primary ACTH-independent adrenocortical hyperplasia
646
What is the most common form of naturally occurring hypercortisolism in dogs?
Pituitary-dependent hypercortisolism (PDH) ## Footnote Diagnosed in approximately 80–85% of cases.
647
What is the primary hormone produced by the zona fasciculata of the adrenal cortex?
Glucocorticoids (cortisol)
648
What regulates the secretion of mineralocorticoids in the zona glomerulosa?
Primarily by plasma potassium and angiotensin II levels; ACTH has acute effects
649
What is the role of corticotropin-releasing hormone (CRH) in the hypothalamic-pituitary-adrenal axis?
Stimulates the secretion of pro-opiomelanocortin (POMC) in the anterior pituitary
650
True or False: Dogs have a consistent circadian rhythm for ACTH and cortisol secretion.
False ## Footnote Unlike humans, dogs lack a consistent circadian rhythm for ACTH or cortisol secretion.
651
What is the effect of increased cortisol on the hypothalamus and anterior pituitary?
Negative feedback suppressing CRH and ACTH secretion
652
What features are indicative of malignancy in adrenal tumors?
* Large tumor size * Peripheral fibrosis * Capsular invasion * Trabecular growth pattern * Hemorrhage * Necrosis * Increased Ki-67 proliferative index
653
What is the Utrecht Score used for?
To predict postoperative outcomes in adrenal tumor cases
654
What is a key feature of food-induced hypercortisolism?
Cortisol secretion occurs only after food intake
655
What percentage of dogs with hypercortisolism have concurrent pituitary- and adrenal-dependent hypercortisolism?
5% of all dogs with hypercortisolism; up to 10% of dexamethasone-resistant cases
656
What is subdiagnostic hypercortisolism?
Dogs exhibiting clinical signs consistent with hypercortisolism but normal endocrine test results
657
What breeds are suggested to have an increased risk of developing hyperadrenocorticism?
* Miniature Poodles * Dachshunds * Terriers * Boxers * Standard Schnauzers
658
What is the mean age at diagnosis for hyperadrenocorticism in dogs?
Approximately 11 years
659
What is the estimated prevalence of pituitary-dependent hypercortisolism (PDH) in dogs?
0.2% ## Footnote Based on several studies.
660
What is the typical age distribution for dogs diagnosed with hypercortisolism?
Middle-aged to older dogs, with diagnosis ranging from 6 months to 20 years, and a mean age of approximately 11 years.
661
Which dog breeds are suggested to have an increased risk for hypercortisolism?
* Miniature Poodles * Dachshunds * Terriers * Boxers * Standard Schnauzers ## Footnote Breed associations should be interpreted cautiously due to variations in breed popularity across geographic regions.
662
Does hypercortisolism affect both male and female dogs?
Yes, it affects both sexes, with a slight female predisposition suggested.
663
What association does neutering have with hypercortisolism in dogs?
Neutering appears associated with an increased risk of hypercortisolism.
664
What mechanisms contribute to polyuria and polydipsia in dogs with hypercortisolism?
* Cortisol-induced inhibition of vasopressin action at renal tubules * Increased neurohypophyseal vasopressin release threshold * Central diabetes insipidus from large pituitary tumors.
665
What is the classic skin change associated with hypercortisolism?
Bilaterally symmetrical alopecia (endocrine alopecia).
666
What is calcinosis cutis?
Characterized by irregular plaques of dystrophic calcium deposits within or beneath the skin, considered a pathognomonic finding.
667
What is the most consistent abnormality found in serum biochemistry profiles of dogs with hypercortisolism?
Increased alkaline phosphatase (ALP).
668
What is the significance of the Low-Dose Dexamethasone Suppression Test (LDDST) in diagnosing hypercortisolism?
It helps determine whether cortisol levels remain elevated in dogs with hypercortisolism despite dexamethasone administration.
669
What is the sensitivity and specificity of the LDDST for diagnosing hypercortisolism?
* Sensitivity: 85–100% * Specificity: 44–73%.
670
What is the role of the Urine Cortisol-to-Creatinine Ratio (UCCR) in diagnosing hypercortisolism?
It represents an integrated cortisol measure over several hours and is used in combination with suppression testing.
671
What are the common electrolyte changes found in dogs with hypercortisolism?
* Hyperphosphatemia * Mild hypernatremia * Hypokalemia ## Footnote Hyperkalemia severity may correlate with the severity of hypercortisolism.
672
What are the common coagulation parameters found in dogs with hypercortisolism?
* Shortened prothrombin time (PT) * Increased fibrinogen concentrations * Elevated thrombin-antithrombin complexes.
673
What is the purpose of endocrine testing in suspected hyperadrenocorticism?
To confirm increased cortisol production and decreased sensitivity of the hypothalamic-pituitary-adrenal axis.
674
What is the sensitivity range for UCCR performance?
75–100%
675
What is the specificity range for UCCR performance?
20–25%
676
What does the ACTH Stimulation Test assess?
Adrenocortical responsiveness to exogenous ACTH.
677
What is the gold standard for diagnosing hypoadrenocorticism?
ACTH Stimulation Test.
678
What is a limitation of the ACTH Stimulation Test?
Does not assess negative feedback sensitivity.
679
What is the sensitivity for PDH in the ACTH Stimulation Test?
80–83%
680
What is the sensitivity for ADH in the ACTH Stimulation Test?
57–63%
681
What is the main weakness of the LDDST?
Lower specificity, requires multiple samples.
682
What suggests PDH in HDDST interpretation?
Suppression of cortisol by >50% from baseline.
683
What does a P/B ratio >0.3 mm/mm² suggest?
Pituitary enlargement.
684
What are the two tumor types identified in pituitary imaging?
* Microadenomas * Macroadenomas
685
What is the sensitivity for detecting adrenal enlargement using abdominal ultrasonography?
96%.
686
What are features suggestive of adrenal malignancy?
* Heterogeneous echotexture * Vascular invasion * Adrenal diameter >2 cm
687
What is the main benefit of adrenalectomy?
Potential cure if complete excision is achieved.
688
What is the perioperative complication rate for dogs with small adrenal tumors?
6–8%.
689
What is a common postoperative complication after adrenalectomy?
Transient or permanent central diabetes insipidus.
690
What is a significant limitation of medical therapy for hypercortisolism?
Does not eliminate the source of hormone excess.
691
What is the median survival time after hypophysectomy?
781 days.
692
What is vascular invasion in dogs with adrenal tumors?
Up to 24% of dogs with invasive adrenal tumors exhibit vascular invasion.
693
List the main perioperative complications associated with adrenal surgery.
* Hemorrhage (minor to severe) * Hypertension or hypotension * Bradycardia * Tachycardia * Death
694
True or False: Tumor capsule rupture during surgery always leads to tumor regrowth.
False
695
What are the postoperative complications following adrenal surgery?
* Pancreatitis * Thromboembolism
696
What is the range of recurrence rates for adrenal tumors in dogs?
12–30%.
697
Identify three causes of recurrence in adrenal tumors.
* Adrenal tumor regrowth * Functional metastasis * Development of new pituitary-dependent hypercortisolism (PDH)
698
What is the median survival time post-adrenalectomy for dogs?
778 to 953 days.
699
How does tumor diameter influence survival rates?
Tumors <3 cm are associated with significantly better survival than tumors ≥3 cm.
700
What is the impact of tumor thrombus extending beyond the hepatic hilus?
Increases perioperative mortality.
701
Survival rates for dogs with thrombus terminating before the diaphragm range from?
73–81%.
702
What is the reported median survival after hypofractionated stereotactic volume-modulated radiotherapy?
1,030 days.
703
What is the mechanism of action of Trilostane?
Competitively inhibits the enzyme 3β-hydroxysteroid dehydrogenase.
704
What are the primary adverse effects of Trilostane?
* Transient hypocortisolism * Hypoadrenocorticism * Risk of permanent adrenal necrosis
705
What is the approximate chance of experiencing clinical hypocortisolism within the first 2 years of Trilostane treatment?
~15%
706
What is the purpose of the ACTH stimulation test in monitoring Trilostane therapy?
Reflects adrenal reserve capacity.
707
What can low pre-pill cortisol levels indicate during Trilostane therapy?
Consider dose reduction to preserve adrenal reserve.
708
What is the median survival time for dogs treated with Mitotane?
102–476 days.
709
List common adverse effects of Mitotane.
* Anorexia * Lethargy * Weakness * Diarrhea
710
What pharmacologic target is being researched to inhibit cortisol production?
MC2R Antagonists
711
Prevalence of diabetes mellitus in dogs with hypercortisolism is described as?
One of the most common comorbidities.
712
What is the pathophysiology of diabetes mellitus in hypercortisolism?
* Induces insulin resistance * Increases hepatic gluconeogenesis * Decreases insulin secretion * Blunts the incretin effect * Causes direct beta-cell cytotoxicity
713
What is the prevalence of gallbladder mucocele in dogs with hypercortisolism?
1.6–23% ## Footnote Indicates the frequency of gallbladder mucocele among dogs diagnosed with hypercortisolism.
714
What percentage of dogs with gallbladder mucocele have hypercortisolism?
3.4–23% ## Footnote Shows the overlap between gallbladder mucocele and hypercortisolism in dogs.
715
What is the impact of hypercortisolism on in-hospital mortality for dogs undergoing cholecystectomy for mucocele?
2-fold increase ## Footnote Indicates a significant increase in surgical risk for these dogs.
716
What are the consequences of steroid excess in dogs with gallbladder mucocele?
* Higher concentrations of unconjugated bile acids * Increased bile hydrophobicity * Injury to biliary epithelium * Mucinous hyperplasia ## Footnote These factors contribute to the development and complications of mucocele.
717
What additional findings are seen in dogs with both hypercortisolism and mucocele?
Increased basal and post-ACTH dehydroepiandrosterone (DHEA) concentrations ## Footnote Suggests issues with DHEA secretion or transport.
718
What may dogs with hypercortisolism and mucocele require regarding trilostane dosage?
Higher doses ## Footnote This is likely due to decreased bile secretion affecting the absorption of lipid-soluble drugs.
719
What is the prevalence of urolithiasis in dogs with hypercortisolism?
~3% ## Footnote Indicates a specific occurrence of urolithiasis in this population.
720
What type of stones are primarily associated with urolithiasis in dogs with hypercortisolism?
Calcium oxalate stones ## Footnote Indicates the specific composition of uroliths in this condition.
721
What is the incidence of pulmonary thromboembolism in dogs with hypercortisolism?
Extremely rare ## Footnote This indicates a low occurrence rate in this population.
722
What causes pulmonary thromboembolism in dogs with hypercortisolism?
Hypercoagulability ## Footnote This is associated with several underlying mechanisms related to hypercortisolism.
723
What are some contributing factors to hypercoagulability in dogs with hypercortisolism?
* Increased fibrinogen concentration * Decreased fibrinolysis * Thrombocytosis * Changes on thromboelastography ## Footnote These factors contribute to a hypercoagulable state.
724
What is the prevalence of systemic hypertension in dogs with hypercortisolism?
37–86% ## Footnote This shows a significant correlation between hypercortisolism and hypertension.
725
What is the prognosis for feline hyperadrenocorticism compared to canine hyperadrenocorticism?
Worse prognosis in cats ## Footnote Feline HAC carries more serious consequences than canine HAC.
726
What are common comorbidities associated with feline hyperadrenocorticism?
* Diabetes mellitus * Skin hyperfragility syndrome * Other complicating comorbidities
727
What is the most common cause of feline hyperadrenocorticism?
Pituitary-dependent hyperadrenocorticism (PDH) ## Footnote Accounts for approximately 85% of feline cases.
728
What is adrenal-dependent hyperadrenocorticism (ADH)?
Represents about 15% of feline cases, typically caused by an autonomously functioning adrenal cortical adenoma or carcinoma.
729
What are the clinical signs of feline hyperadrenocorticism?
* Alopecia * Unkempt hair coat * Thin, hyperfragile skin * Pendulous abdomen * Muscle wasting * Hepatomegaly * Weight changes
730
What percentage of cats with feline hyperadrenocorticism present with concurrent diabetes mellitus?
79%
731
What common metabolic alterations are associated with feline hyperadrenocorticism?
* Diabetes mellitus * Polyuria/polydipsia (PU/PD) * Polyphagia more likely related to DM than HC
732
What is the approximate frequency of hyperglycemia in cats with feline hyperadrenocorticism?
>91%
733
What can cause increased infection risk in cats with hyperadrenocorticism?
* Immunosuppression from cortisol excess * Skin fragility * Diabetes mellitus * Concurrent CKD
734
What laboratory abnormalities are frequently observed in feline hyperadrenocorticism?
* Glucosuria * Hypercholesterolemia * Proteinuria * Anemia * Neutrophilia * Lymphopenia
735
What is the ACTH stimulation test used for in diagnosing feline hyperadrenocorticism?
To assess cortisol response; >21.7 µg/dL post-ACTH is suggestive of HAC.
736
How can imaging assist in diagnosing feline hyperadrenocorticism?
Helps identify adrenal or pituitary enlargement, invasion, or metastasis.
737
What is the median age of cats affected by feline hyperadrenocorticism?
9.5 to 13 years.
738
What is the frequency of polyuria/polydipsia (PU/PD) in feline hyperadrenocorticism?
79% (same a prevalence of DM)
739
What complications can successful treatment of feline hyperadrenocorticism reduce?
* Severe infections * Skin hyperfragility * Other serious complications
740
What is the purpose of preoperative imaging in surgical approaches for ADH?
To assess major vessel invasion and metastatic disease
741
What is the common postoperative condition following unilateral adrenalectomy?
Hypoadrenocorticism requiring prednisolone replacement
742
What is the only definitive cure for PDH?
Transsphenoidal Hypophysectomy
743
What percentage of dogs experience recurrence after initial hypophysectomy?
25%
744
What is the mechanism of action of Trilostane?
Competitive inhibitor of 3β-hydroxysteroid dehydrogenase
745
What was the survival rate of cats treated with Trilostane for more than 3 months?
17 out of 20 cats survived longer than 3 months
746
True or False: Mitotane is effective for treating feline hyperadrenocorticism.
False
747
What does Metyrapone inhibit?
11β-hydroxylase
748
What is a potential use of Metyrapone in feline hyperadrenocorticism?
Pre-surgical stabilization
749
What treatment may benefit cats with neurologic signs from large pituitary tumors?
Pituitary irradiation
750
What are positive prognostic factors for feline hyperadrenocorticism?
* Adrenal adenomas * PDH undergoing appropriate definitive treatment
751
What treatment considerations should be taken for severe skin hyperfragility?
* Staged wound closure * Use of tissue glue for recent lesions
752
Fill in the blank: The initial report of Transsphenoidal Hypophysectomy showed that ___ cats died within weeks post-surgery.
2
753
What is an adrenal incidentaloma?
Focal enlargement of the adrenal gland in a pet with no clinical suspicion of adrenal gland disease ## Footnote It is commonly found during routine abdominal ultrasound.
754
What is the incidence of incidental adrenal masses in dogs according to ultrasound?
Approximately 4% of dogs ## Footnote The incidence is higher with CT scans, at about 9%.
755
What are the common non-tumorous differentials for adrenal masses?
* Nodular hyperplasia * Cysts * Abscesses * Hematomas * Granulomas
756
What percentage of incidental adrenal masses are malignant?
14%–30% ## Footnote This statistic highlights the importance of evaluating incidental adrenal masses.
757
What imaging characteristic suggests a malignant adrenal tumor?
Poor glandular demarcation and irregular contrast enhancement ## Footnote Additionally, vascular invasion is a strong indicator of malignancy.
758
What is the recommended treatment for adrenal tumors with evidence of malignancy?
Adrenalectomy ## Footnote This is advised if the mass is enlarging or if clinical signs of hormone excess develop.
759
What is the median survival time for dogs with non-cortisol-secreting adrenal tumors not undergoing surgery?
29.8 ± 8.9 months ## Footnote Larger tumor size is associated with shorter survival.
760
What is aldosterone, and where is it produced?
A principal mineralocorticoid produced in the zona glomerulosa of the adrenal cortex ## Footnote It regulates serum sodium and potassium concentrations.
761
What characterizes primary hyperaldosteronism?
Autonomous aldosterone secretion with suppressed renin concentrations ## Footnote This is due to negative feedback mechanisms.
762
What role does aldosterone play in the kidneys?
Promotes sodium reabsorption and excretion of potassium and hydrogen ions ## Footnote This action helps conserve water and increases blood volume and pressure.
763
What is the typical age of cats diagnosed with primary hyperaldosteronism?
Most cats are >10 years old, with a median of ~13 years ## Footnote Cases have been reported in cats as young as 5 years.
764
What is the significance of the aldosterone-to-renin ratio (ARR) in diagnosing hyperaldosteronism?
A high-normal or elevated PAC with a low PRA suggests autonomous aldosterone production ## Footnote This can be useful in the initial screening for hyperaldosteronism.
765
What are the characteristics of adrenal tumors in cats compared to humans?
In cats, adrenocortical carcinomas are more common than adenomas or bilateral hyperplasia ## Footnote In humans, bilateral zona glomerulosa hyperplasia is more prevalent.
766
What is the limitation of feline PRA assays?
Not widely available, require large blood volumes, rapid processing, and frozen plasma. ## Footnote There is no established feline PRA reference range.
767
What does a high-normal or elevated PAC with low PRA suggest?
Autonomous aldosterone production, even in the absence of RAS stimulation.
768
What is the significance of a normal ARR in cats?
Does not exclude primary hyperaldosteronism (PHA) in cats.
769
What does UACR reflect?
Aldosterone secretion over time.
770
What are the benefits of using UACR?
* No special handling or cooling required * Owners can collect urine at home
771
What are the limitations of UACR testing?
* Difficult to measure aldosterone in cat urine * Wide reference range * Basal concentrations often fail to identify PHA
772
What is the mechanism of the Fludrocortisone Suppression Test?
Oral fludrocortisone suppresses aldosterone secretion in healthy cats.
773
What was the outcome of the Fludrocortisone suppression in healthy cats?
Reduced UACR by a median of 78%.
774
What are the requirements for diagnosing PHA?
* Elevated PAC * Imaging confirmation of an adrenal mass
775
What should be suspected in any cat with hypokalemia and hypertension?
Aldosteronoma.
776
What is the treatment of choice for confirmed non-metastatic aldosteronomas?
Unilateral adrenalectomy.
777
What are common postoperative complications?
* Hemorrhage * Acute kidney injury * Thromboembolism * Sepsis
778
What is the median survival time after open adrenalectomy for cats?
1,297 days (range: 2–1,582 days).
779
What is the first-line agent for controlling systemic hypertension in cats with PHA?
Amlodipine.
780
What are the reported survival times for medical management of PHA?
7 months to 984 days in 4 cats.
781
What is the main cause of primary hyperaldosteronism in dogs?
Solitary adrenal adenoma or carcinoma.
782
What are common presenting signs of PHA in dogs?
* Lethargy * Anorexia * Weakness * Polyuria and polydipsia
783
What is the confirmatory diagnosis for PHA in dogs?
* Increased baseline aldosterone concentration * Suppressed plasma renin activity
784
What hormonal support may be required postoperatively for dogs?
Fludrocortisone acetate or desoxycorticosterone pivalate (DOCP).
785
What is the prognosis for adenomas in dogs if completely excised?
Excellent prognosis.
786
What are the clinical signs associated with adrenal cortical tumors secreting sex hormones?
* Fragile skin * Aggression * Vulvar enlargement in spayed females * Mammary enlargement in males
787
What is the prognosis for cats with sex hormone-secreting tumors?
Varies based on pre-op health, metastatic status, and surgical success.
788
What should be monitored postoperatively in dogs with adrenal tumors?
Frequent serum electrolyte monitoring.
789
What is the common clinical presentation of sex hormone-secreting adrenal tumors in dogs?
Polyphagia, polyuria, and polydipsia.
790
How many well-documented cases of sex hormone-secreting adrenal tumors are reported?
2 ## Footnote Only two cases have detailed treatment data available.
791
What medication was used in the medical case of adrenal tumors?
Mitotane ## Footnote The dosage was 47 mg/kg PO daily for approximately 20 days.
792
What are the typical clinical signs of sex hormone-secreting adrenal tumors?
* PU/PD * Polyphagia * Panting * Weight gain * Abdominal distention ## Footnote These signs help in the clinical suspicion of the disease.
793
Which hormone is commonly implicated in sex hormone-secreting adrenal tumors?
Progesterone ## Footnote Hyperprogesteronemia is a key feature.
794
What association is noted with cortisol testing in these cases of sex hormone producing adrenal tumor?
Markedly suppressed cortisol despite signs of Cushing’s ## Footnote This finding is critical in evaluating potential adrenal tumors.
795
What is the variability observed in estradiol levels?
Wide; random basal elevations common ## Footnote This variability can complicate diagnosis.
796
What hormone testing approach is recommended in sex hormone producing adrenal tumors?
Baseline + post-ACTH stimulation hormone panel ## Footnote This approach aids in confirming the diagnosis.
797
What is the success rate of medical management with Mitotane in sex hormone producing adrenal tumor?
Poor response reported after 20 days ## Footnote Medical management has limited and poorly documented success.
798
Fill in the blank: Clinical suspicion of sex hormone-secreting adrenal tumors should be based on __________.
Cushingoid signs, suppressed cortisol, exclusion of iatrogenic steroid use ## Footnote These factors are crucial in forming a clinical suspicion.
799
What are the reasons for the lack of response to Mitotane?
* Short duration of therapy * Dosage possibly suboptimal * General resistance of adrenal tumors to Mitotane treatment ## Footnote These factors contribute to the poor outcomes observed.
800
Which layer of the adrenal cortex synthesizes aldosterone?
Zona glomerulosa
801
What is the primary cause of hypoadrenocorticism in humans?
Autoimmune disease
802
What is the role of 21-hydroxylase in adrenal function?
It is a steroidogenic enzyme targeted by autoantibodies in autoimmune hypoadrenocorticism.
803
What percentage of dogs with hypoadrenocorticism have P450 enzyme antibodies?
24%
804
Which dog breeds show a strong genetic predisposition to hypoadrenocorticism?
* Leonbergers * Pomeranians * Great Danes * Standard Poodles * Bearded Collies
805
What is a major genetic factor linked to hypoadrenocorticism in Portuguese Water Dogs?
CTLA-4 gene
806
What distinguishes primary from secondary hypoadrenocorticism?
Primary is due to adrenal cortex failure; secondary is due to pituitary or hypothalamic dysfunction.
807
What are the two types of primary hypoadrenocorticism?
* Typical primary HA (deficiencies in glucocorticoids and mineralocorticoids) * Atypical primary HA (deficiency of glucocorticoids only)
808
What are common clinical signs of hypoadrenocorticism?
* Anorexia * Weight loss * Vomiting * Diarrhea * Lethargy * Weakness * Polyuria/Polydipsia
809
What is the median age at diagnosis for dogs with hypoadrenocorticism?
3–4 years
810
What is the typical systolic blood pressure in dogs with hypoadrenocorticism?
90 mmHg
811
What are the hematological findings in dogs with hypoadrenocorticism?
* Lower neutrophil counts * Higher lymphocyte and eosinophil counts
812
What diagnostic test is used to confirm hypoadrenocorticism?
ACTH stimulation test
813
What can cause iatrogenic secondary hypoadrenocorticism?
* Hypophysectomy * Abrupt withdrawal of glucocorticoids
814
What is a common cause of azotemia in dogs with hypoadrenocorticism?
Dehydration
815
What clinical sign may result from hyperkalemia in hypoadrenocorticism?
Bradycardia
816
What is the significance of a lymphocyte count ≥2.0 × 10³/µL in ill dogs?
85% specific for diagnosing hypoadrenocorticism.
817
What are the mechanisms for dilute urine in dogs with hypoadrenocorticism?
* Hyponatremia reduces renal medullary concentration gradient * Osmotic effect of sodium losses impairs urine concentrating ability
818
What sodium-to-potassium ratio is highly suggestive of HA?
≤24
819
What two assessments are combined to determine the need for an ACTH stimulation test?
* Sodium-to-potassium ratio (reflecting aldosterone function) * Lymphocyte count (reflecting glucocorticoid function)
820
In dogs with HA and hyponatremia, what is the typical urine sodium concentration?
≥30 mEq/L (or mmol/L)
821
What imaging technique is recommended if acute pancreatitis is suspected in dogs with HA?
Abdominal ultrasound
822
What findings on an ECG may indicate hyperkalemia in dogs with suspected HA?
* Shortened to absent P waves * Prolonged PR intervals * Widened QRS complexes * Short R waves * Tall, peaked T waves * Ectopic beats
823
What is the preferred administration route for ACTH in severely dehydrated dogs?
IV administration
824
What alternative strategies have been explored for diagnosing HA due to cost and availability issues?
* Basal cortisol measurement * Cortisol-to-endogenous ACTH ratio * IM administration of long-acting synthetic ACTH * Plasma aldosterone-to-renin activity ratio
825
What findings are expected in secondary hypoadrenocorticism?
* Normal sodium and potassium concentrations * Low endogenous ACTH concentrations
826
What does the term 'pseudo-Addison's disease' refer to?
Dogs with illnesses mimicking HA, particularly regarding electrolyte derangements
827
What is the primary focus of treatment during an acute adrenal crisis?
Aggressive IV fluid resuscitation
828
What fluid is preferred for treating hyponatremia in dogs with HA?
0.9% Sodium chloride (NaCl)
829
What is the recommended maximum increase in serum sodium during the first 24 hours of treatment for hyponatremia?
8–12 mEq/L
830
What should be administered if persistent hyperkalemia remains after 6–8 hours of fluid therapy?
IV glucose
831
What is the starting dose for glucocorticoid replacement therapy in dogs with HA?
0.5 mg/kg PO q12h for 2–3 days after crisis stabilization
832
What is the ideal sodium-potassium ratio to maintain during long-term management of HA?
About 30
833
What should be done if a dog's sodium-potassium ratio is >32 at day 15 of DOCP therapy?
Decrease DOCP dose by ~10%
834
What is the primary cause of spontaneous HA in cats?
Abrupt steroid withdrawal
835
What is a rare condition associated with HA in cats characterized by hyponatremia and hyperkalemia?
Pseudo-hypoadrenocorticism
836
What are the reported causes of hypoadrenocorticism in cats?
* Abrupt steroid withdrawal * Neoplastic invasion of the adrenal glands ## Footnote Pseudo-hypoadrenocorticism is also characterized by hyponatremia and hyperkalemia.
837
What clinical pathology findings support the suspicion of feline hypoadrenocorticism?
* Hyponatremia * Hyperkalemia * Hypoglycemia ## Footnote These findings help differentiate HA from other disorders.
838
How does the ACTH stimulation protocol differ in cats compared to dogs?
It must be tailored appropriately for cats ## Footnote The protocol specifics can vary significantly between species.
839
What are the treatment principles for hypoadrenocorticism in cats?
* Acute stabilization * Glucocorticoid supplementation * Mineralocorticoid supplementation ## Footnote These principles are similar to those used in dogs.
840
What is the prognosis for cats with hypoadrenocorticism compared to dogs?
Worse prognosis for cats ## Footnote Delayed diagnosis and rarity of the condition likely contribute to less favorable outcomes.
841
What is the largest endocrine organ in the body?
The gastrointestinal (GI) tract ## Footnote It produces over 30 hormones that regulate digestion, metabolism, motility, and appetite.
842
What are the three manners in which gastrointestinal hormones function?
Endocrine, paracrine, and neurocrine ## Footnote These modes of action affect various physiological processes.
843
What drives hormonal diversity in the gastrointestinal tract?
Tissue-specific gene expression, alternative mRNA splicing, and post-translational modifications ## Footnote These factors contribute to the unique functions of hormones.
844
What clinical syndromes can arise from gastrointestinal hormones?
Hormone excess and hormone deficiency ## Footnote An example of hormone excess is functional neuroendocrine tumors.
845
What is the source of Gastrin?
G cells of stomach antrum and duodenum ## Footnote Gastrin is a key hormone involved in gastric acid secretion.
846
What stimulates the secretion of Gastrin?
Protein intake, gastric distension; inhibited by low gastric pH ## Footnote These stimuli help regulate gastric functions.
847
What are the actions of Gastrin?
Stimulates gastric acid and pepsinogen secretion; promotes gastric mucosal growth and motility; contributes to pancreatic enzyme secretion ## Footnote Essential for digestion and gastrointestinal health.
848
What syndrome is associated with excess Gastrin?
Zollinger-Ellison syndrome ## Footnote This condition results from gastrin-secreting tumors.
849
What is the source of Cholecystokinin (CCK)?
I cells in duodenum and jejunum ## Footnote CCK plays a role in fat and protein digestion.
850
What stimulates Cholecystokinin (CCK) secretion?
Luminal fats, amino acids, and H+ ## Footnote These nutrients signal the need for digestive enzymes.
851
What are the actions of Cholecystokinin (CCK)?
Stimulates gallbladder contraction, pancreatic enzyme secretion, relaxes sphincter of Oddi; inhibits gastric emptying ## Footnote CCK coordinates digestion processes.
852
What is the source of Secretin?
S cells of duodenum ## Footnote Secretin plays a vital role in neutralizing gastric acid.
853
What stimulates Secretin secretion?
Acidic chyme (H+) ## Footnote This response helps regulate pH levels in the intestine.
854
What are the actions of Secretin?
Stimulates bicarbonate secretion; inhibits gastric acid production and motility ## Footnote Important for maintaining intestinal environment.
855
What hormones are included in the group of Glucagon and Incretins?
Glucagon, GLP-1, GLP-2, GIP ## Footnote These hormones are crucial for glucose metabolism.
856
What is the role of Glucagon?
Promotes gluconeogenesis and glycogenolysis ## Footnote It opposes the action of insulin.
857
What is the primary action of GLP-1?
Potentiates glucose-dependent insulin secretion; inhibits gastric emptying and increases satiety ## Footnote GLP-1 plays a significant role in glucose homeostasis.
858
What is the source of Somatostatin?
D cells in GI tract, pancreatic islets (δ-cells), hypothalamus ## Footnote Somatostatin has broad inhibitory effects on various hormones.
859
What are the actions of Somatostatin?
Inhibits gastric acid, pancreatic secretion, bile release, insulin/glucagon release, and GI motility ## Footnote It regulates multiple digestive processes.
860
What is the function of Motilin?
Regulates migrating motility complexes (MMCs) in fasting; coordinates GI secretions in fed state ## Footnote Essential for digestive rhythm.
861
What is the source of Ghrelin?
Stomach ## Footnote Ghrelin is known as the hunger hormone.
862
What are the actions of Ghrelin?
Stimulates appetite and GH release ## Footnote It links energy balance with the pituitary axis.
863
What is the source of Serotonin (5-HT)?
Enterochromaffin cells and enteric neurons ## Footnote Serotonin is important for regulating GI motility.
864
What are the actions of Serotonin (5-HT)?
Stimulates GI motility and secretion ## Footnote Plays a critical role in digestive function.
865
What is the most common pancreatic neuroendocrine tumor in dogs?
Insulinoma ## Footnote It causes episodic hypoglycemia due to unregulated insulin secretion.
866
What are the clinical signs of Insulinoma?
Episodic hypoglycemia ## Footnote This occurs due to inappropriate insulin levels.
867
What is the source of Gastrinoma?
Pancreas (often right limb) ## Footnote This tumor is rare in dogs and cats.
868
What is the diagnosis for Gastrinoma?
Elevated serum gastrin; gastric pH <2.5 + gastrin >1000 ng/L ## Footnote The secretin stimulation test can also aid in diagnosis.
869
What is the source of Glucagonoma?
Pancreatic α-cells ## Footnote This tumor can lead to diabetes mellitus.
870
What are the clinical signs of Glucagonoma?
Diabetes mellitus, weight loss, necrolytic migratory erythema (NME) ## Footnote These symptoms result from glucagon excess.
871
What is the diagnosis for Glucagonoma?
Hyperglucagonemia; low serum amino acids ## Footnote Imaging can help confirm the presence of a pancreatic mass.
872
What is the origin of Carcinoid Tumors?
Enterochromaffin cells ## Footnote These tumors secrete serotonin and kinins in humans.
873
What clinical syndrome is associated with Carcinoid Tumors?
Diarrhea, abdominal cramping, flushing ## Footnote These symptoms are more common in humans.
874
What is the treatment for Carcinoid Tumors?
Surgical excision when feasible ## Footnote These tumors have a high metastatic rate.
875
What is the source of Pancreatic Polypeptidoma?
PP-producing cells ## Footnote This tumor is rare and often non-functional.
876
What are the clinical signs if Pancreatic Polypeptidoma is functional?
Vomiting, ulcers, diarrhea, hypertrophic gastritis ## Footnote These symptoms result from excessive polypeptide production.
877
What is the diagnosis for Pancreatic Polypeptidoma?
Difficult—PP is often co-expressed with other hormones ## Footnote Histopathology is required for confirmation.
878
What is a key emerging hormone with therapeutic implications in diabetes mellitus?
GLP-1 ## Footnote It has a significant role in glucose regulation.
879
True or False: Somatostatin has broad inhibitory effects and its clinical role is more theoretical than practical in veterinary medicine.
True ## Footnote It inhibits various digestive processes.
880
What is a pheochromocytoma (PCC)?
A neuroendocrine tumor arising from chromaffin cells of the adrenal gland medulla.
881
What are paragangliomas (PGLs)?
Tumors originating from non-adrenal chromaffin cells located in sympathetic and parasympathetic paraganglia.
882
What are chromaffin cells?
Modified postganglionic sympathetic neurons, devoid of axons and dendrites, derived from neural crest cells during early prenatal development.
883
What percentage of all canine tumors do PCCs account for?
Approximately 0.01% to 0.1%.
884
What is the average size of pheochromocytomas at diagnosis?
Typically have an average diameter of 5 cm, but may grow up to 15 cm.
885
What percentage of pheochromocytomas are unilateral?
More than 90%.
886
What is the rate of local invasion in pheochromocytomas?
Local invasion occurs in 66% of cases.
887
What percentage of pheochromocytomas metastasize?
Reported in 20% of cases.
888
What are common metastatic sites for pheochromocytomas?
* Regional lymph nodes * Liver * Spleen * Kidneys * Pancreas * Lungs * Heart * Bone * Central nervous system
889
What are the primary sources of circulating catecholamines?
Chromaffin cells.
890
What is the biosynthesis pathway for catecholamines starting from tyrosine?
Tyrosine → DOPA → Dopamine → Norepinephrine → Epinephrine.
891
Which enzyme is responsible for converting norepinephrine to epinephrine?
Phenylethanolamine N-methyltransferase (PNMT), stimulated by cortisol.
892
What metabolites are produced from catecholamine metabolism?
* Metanephrine (from epinephrine) * Normetanephrine (from norepinephrine) * Vanillylmandelic acid (VMA)
893
How does catecholamine secretion occur in pheochromocytomas?
Autonomously by diffusion, independent of nerve impulses.
894
What percentage of pheochromocytomas in humans are associated with genetic syndromes?
Approximately 7%.
895
What are the common mutations associated with pheochromocytomas?
* RET * NF1 * TMEM127 * VHL * SDH (especially SDHB and SDHD)
896
What percentage of cases report arterial hypertension in pheochromocytomas?
Reported in 50% of cases.
897
What are the complications associated with hypertension in pheochromocytomas?
* Epistaxis * Retinal bleeding or detachment * Acute blindness * Seizures
898
What are common coexisting endocrine neoplasms with pheochromocytomas?
* Glucocorticoid-producing adrenocortical tumors * ACTH-producing pituitary tumors
899
What laboratory abnormalities are common in dogs with pheochromocytomas?
* Mild to moderate anemia * Leukocytosis * Increased liver enzyme activity * Azotemia * Decreased urine-specific gravity * Proteinuria
900
What is the preferred testing method for diagnosing pheochromocytomas?
High-performance liquid chromatography (HPLC) assays measuring catecholamines or metanephrines.
901
What is the cutoff value for urine normetanephrine to provide excellent specificity?
≥4× the upper limit of normal (ULN).
902
What imaging modality is preferred for pheochromocytomas?
Contrast-enhanced CT.
903
What cytologic features are indicative of canine pheochromocytomas?
* Cells arranged in epithelial-like aggregates * Presence of bare nuclei * Inconsistent nuclear features * Cytoplasm with fine chromatin granules
904
Is percutaneous fine-needle aspiration (FNA) safe for diagnosing pheochromocytomas in dogs?
Complication rate for FNA is approximately 10%.
905
What are potential serious complications associated with FNA in humans?
* Hemorrhage * Hypertensive crisis * Tumor seeding * Death
906
Name two cardiovascular assessments recommended due to catecholamine effects.
* Cardiac ultrasound * Electrocardiogram (ECG)
907
What are some perioperative complications associated with adrenalectomy?
* Hypertension * Tachycardia * Arrhythmias * Hemorrhage
908
What is phenoxybenzamine?
A non-competitive, non-selective, long-acting alpha-adrenergic blocker
909
What is the recommended starting dose of phenoxybenzamine?
0.25 mg/kg PO q12h
910
What is a critical aspect of postoperative monitoring?
Continuous monitoring (ECG, blood pressure) for 48 hours postoperatively
911
What is the mainstay drug for chronic management of pheochromocytoma?
Phenoxybenzamine
912
True or False: Chemotherapy has proven benefits for pheochromocytomas in dogs.
False
913
What histopathologic features are indicative of pheochromocytoma?
* Large, round to polygonal cells * Nested, trabecular, or solid arrangements * Round to oval nuclei with possible pleomorphism
914
What is the PASS scoring system used for?
Evaluating tumor invasiveness, growth patterns, cytologic features, and mitotic activity
915
What factors can worsen the prognosis of canine pheochromocytoma?
* Advanced age * Poor general condition * Serious concurrent diseases
916
What is the average size of paragangliomas at diagnosis?
6–16 cm in diameter
917
What are some clinical signs of paraganglioma?
* Dysphagia * Dyspnea * Circulatory disturbances
918
What is the reported incidence of paragangliomas in dogs?
Approximately 0.2% of all canine tumors
919
What are the two subtypes of paragangliomas?
* Sympathetic PGL * Parasympathetic PGL
920
What type of tumor is more common in dogs: sympathetic PGL or parasympathetic PGL?
Parasympathetic PGL
921
What is the significance of chromogranin A in diagnosing pheochromocytoma?
It helps differentiate pheochromocytomas from adrenocortical tumors
922
What is the role of calcium channel blockers in managing pheochromocytoma?
May help reduce phenoxybenzamine dose
923
What clinical signs are observed in feline pheochromocytoma?
Nonspecific and vague, similar to those in dogs