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ACVIM General Boards - 2022 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Steroid hormones are derived from what?

A

Cholesterol

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2
Q

What are amine hormones?

A

Hormones derived from tyrosine

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3
Q

What are three examples of amine hormones?

A

Thyroid hormone
Epinephrine
Norepinephrine

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4
Q

What hormones diffuse across the membrane and binds to the receptor in the cell?

(2)

A

Steroid hormones
Thyroid hormone

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5
Q

The anterior lobe of the pituitary gland is linked to what? Via what structure?

A

To the hypothalamus via the hypothalamic-hypophysial portal system

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6
Q

The posterior lobe of the pituitary is derived from what?

A

Neural tissue - Cell bodies located in the hypothalamic nuclei

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7
Q

What are the hormones of the anterior lobe of the pituitary?

A
  1. Growth hormone
  2. Repro hormones (LH, FSH, prolactin)
  3. Thyroid-stimulating hormone (TSH)
  4. Adrenocorticotropic hormone (ACTH)
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8
Q

What are the products of proopiomelanocortin (POMC)?

A
  1. ACTH
  2. Melanocyte-stimulating hormone (MSH)
  3. B-lipoprotein
  4. B-endorphin
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9
Q

What is a property of growth hormone release?

A
  • Released in pulsatile fashion
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10
Q

Growth hormone release is stimulated by:

A
  • Sleep
  • Stress
  • Puberty
  • Starvation
  • Exercise
  • Hypoglycemia
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11
Q

Growth hormone release is decreased by:

A
  • Somatostatin
  • Somatomedins (insulin-like growth factor)
  • Obesity
  • Hyperglycemia
  • Pregnancy
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12
Q

How are somatomedins produced?

A

They are produced when growth hormone acts on target tissues. Then they inhibit further production of growth hormone.

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13
Q

How does growth hormone act on the tissues?

A
  1. Via somatomedin (insulin-like growth factor or IGF) - produced in liver
  2. Direct effect of GH
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14
Q

What are direct effects of growth hormone?

A
  1. Decreased glucose uptake into cells (diabetogenic)
  2. Increased lipolysis
  3. Increased protein synthesis (muscle/lean body mass)
  4. Increased production of IGF (somatomedin)
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15
Q

What are the actions of growth hormone via IGF (somatomedin)

A
  1. Increased protein synthesis (chondrocytes)
  2. Increased linear growth (growth spurt)
  3. Increased organ size
  4. Increased lean body mass
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16
Q

What does a growth hormone excess cause before and after puberty?

A

Before puberty - Gigantism

After puberty - Increased periostial bone, inc organ size, glucose intolerance

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17
Q

What is octreotide? What does it do?

A

A somatostatin analogue - Inhibits growth hormone secretion

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18
Q

What is the major hormone responsible for lactogenesis?

A

Prolactin

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19
Q

What hormone inhibits prolactin?

A

Dopamine produced by hypothalamus

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20
Q

What are the actions of prolactin?

A
  1. Milk synthesis
  2. Breast development
  3. Inhibit ovulation
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21
Q

What are the hormones of the posterior lobe of the pituitary?

A
  1. Antidiuretic hormone (ADH)
  2. Oxytocin
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22
Q

How are ADH and oxytocin produced?

A

Synthesized in the hypothalamic nuclei - then carried via axons to be secreted at posterior pituitary.

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23
Q

Where is ADH specifically synthesized?

A

Supraoptic nuclei of hypothalamus

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24
Q

Where is oxytocin originated?

A

Paraventricular nuclei of the hypothalamus

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25
Q

What is the effect of oxytocin?

A

Milk let-down

Uterine contraction

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26
Q

Which thyroid hormone is MORE biologically active?

T3 or T4?

A

T3

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27
Q

How does most of the T3 and T4 travel in blood?

A

Bound to thyroxine binding globulin (TBG)

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28
Q

How does hepatic failure affect thyroid levels?

A

Thyroxine binding globulin levels decrease - decreased total thyroid hormone - but normal levels of free hormone (clinically euthyroid)

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29
Q

Describe the hypothalamic-pituitary control of Thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH)

A

TRH - secreted by hypothalamus > stimulates release of TSH by the anterior pituitary.

TSH then increases production of thyroid hormones

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30
Q

How does thyroid hormone negative feedback work?

A

T3 downregulates TRH receptors = decreased TSH release

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31
Q

What are thyroid-stimulating immunoglobulins?

A

IgG antibodies to TSH receptors - stimulate thyroid gland to secrete T3 and T4

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32
Q

How much more potent is T3 than T4

A

T3 is 4 times more potent than T4

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33
Q

What are the layers of the adrenal cortex? (from the outside in)

A
  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona reticulosa
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34
Q

Where is aldosterone produced?

A

Zona glomerulosa

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35
Q

What does the zona fasciculata and zona reticularis produce?

A

Steroids and androgens

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36
Q

What are the layers of the adrenal cortex and what do they produce?

A
  1. Zona glomerulosa (outermost layer) - Aldosterone
  2. Zona Fasciculata (middle) - Steroids and androgen
  3. Zona reticulata (innermost) - Steroids and androgen
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37
Q

Regarding adrenocortical hormone synthesis,

19-carbon steroids are:

A

Androgens; precursors to the estrogens

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38
Q

Regarding adrenocortical hormone synthesis,

18-carbon steroids are:

A

Estrogens

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39
Q

Regarding adrenocortical hormone synthesis,

21-carbon steroids are:

A

Everything else - Progesterone, deoxycortisone, aldosterone, cortisol

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40
Q

True or false: Glucocorticoid secretion oscillates with the circadian rhythm.

A

True

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41
Q

What are the effects of ACTH in the adrenal cortex? Via what enzyme?

A

Increased synthesis of all steroid hormones by stimulating cholesterol desmolase

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42
Q

What are the effects of chronic ACTH?

A

Increased up-regulation of ACTH receptors > hypertrophy of adrenal cortex

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43
Q

Describe the hypothalamic control for corticotropin-releasing hormone (CRH)?

A

When neurons of the paraventricular nuclei (hypothalamus) are stimulated, CRH is released to the anterior pituitary => stimulates POMC and secretion of ACTH

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44
Q

How does cortisol provide negative feedback to the hypothalamus?

A

Cortisol inhibits CRH secretion from hypothalamus = decreased ACTH production

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45
Q

Where does angiogensin II work to stimulate aldosterone release?

A

Zona glomerulosa of the adrenal cortex

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46
Q

How do glucocorticoids exert their anti-inflammatory effects?

A
  1. Induce synthesis of lipocortin - Inhibitor of phospholipase A2
  2. Inhibit production of IL-2
  3. Inhibit release of histamine/serotonin
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47
Q

How do steroids suppress immune response?

A

Inhibit production of IL-2 and T lymphocytes (cellular immunity)

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48
Q

How does cortisol cause hypertension?

A
  1. Up-regulates a1 receptors on arterioles.
  2. Mineralocorticoid effects - increased volume
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49
Q

How is ketoconazole used for treatment of Cushing’s?

A

Inhibits steroid hormone synthesis

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50
Q

What is Conn’s syndrome?

A

Hyperaldosteronism by an aldosterone-secreting tumor

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51
Q

What are the clinical findings in Conn’s syndrome?

A
  1. Hypertension
  2. Hypokalemia
  3. Decreased renin
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52
Q

21B-hydroxilase is involved in production of which 2 hormones?

A
  1. Cortisol
  2. Aldosterone
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53
Q

What findings are associated with 21B-hydroxylase deficiency?

A
  1. Decreased cortisol and aldosterone levels
  2. Increased progesterone and androgens
  3. Increased ACTH (no negative feedback)
  4. Hyperplasia of zona fasciculata and reticularis (increased ACTH)
54
Q

What is the endocrine portion of the pancreas?

A

Islets of Langerhans

55
Q

What is the major stimulus for glucagon secretion?

A

Decreased blood glucose

56
Q

What are the general effects of glucagon?

A
  1. Increased blood glucose concentration
  2. Increases blood fatty acid and ketoacid concentration
  3. Increases urea production (needed for amino acid production)
57
Q

What do the beta cells of the pancreas do?

A

Secrete insulin

58
Q

What do the alpha cells of the pancreas do?

A

Secrete glucagon

59
Q

What do the Delta cells of the pancreas do?

A

Secrete somatostatin and gastrin

60
Q

What is the C-peptide?

A

Product of the cleavage of proinsulin

Packaged and secreted along with insulin - used to monitor beta cell function in DM patients

61
Q

How does glucose stimulate insulin secretion?

A
  1. Glucose binds to Glut 2 on beta cells.
  2. K+ channels close > depolarization of beta cells.
  3. Depolarization opens Ca+ channels
  4. Increased intracellular Ca+ leads to insulin release
62
Q

How do the insulin receptors work on the target cells?

A
  1. Beta subunit have intrinsic tyrosine kinase activity. And becomes intracellular once it is activated by insulin.

Therefore insulin down-regulates its own receptors in target cells

63
Q

The number of insulin receptors are (increased/decreased) in starvation, and (increased/decreased) in obesity.

A
  1. Increased
  2. Decreased
64
Q

What are the effects of somatostatin? (secreted by delta cells of pancreas)

A

Inhibits insulin, glucagon and gastrin secretion

65
Q

What percentage of the total blood calcium is bound to protein?

A

40% is bound to plasma protein

66
Q

What percent of total blood calcium is not bound to protein?

A

60%

67
Q

What is ultrafiltrable calcium?

A

Non-protein bound calcium:

  1. Ca2+ complexed to anions (e.g. phos)
  2. Free ionized calcium (biologically active)
68
Q

What cells produce and secrete PTH?

A

Chief cells of the parathyroid gland

69
Q

What are the effects of PTH on bone?

A

Increased bone resorption (Calcium and phosphorus released to blood) via hydroxyproline excretion

70
Q

Patients with increases in PTH-rp will have (high/low) PTH levels?

A

Low due to feedback inhibition from high serum Ca+

71
Q

Vitamin D deficiency in children causes:

A

Rickets

72
Q

In adults, vitamin D deficiency causes?

A

Osteomalacia

73
Q

What is the active form of vitamin D?

A

1,25-dihydrocycholecalciferol (calcitriol) - formed by the enzyme 1a-hydroxylase

74
Q

What is the overall effect of calcitriol on calcium and phosphate?

A

Increase both

75
Q

What cells secrete calcitonin?

A

Parafollicular cells of the thyroid

76
Q

How does calcitonin work?

A

Inhibits bone resorption

77
Q

Most of the cholesterol (80%) used for synthesis of steroid is provided by what?

A

Low-density lipoprotein (LDL)

78
Q

How is cortisol carried in blood? (2 proteins)

A

Cortisol-binding globulin >>>> albumin

Very small portion is free (*active form*)

79
Q

What percentage of patients with Cushing’s have PDH?

A

80-85%

80
Q

What are the more common kinds of PDH tumors?

A

Pars distalis tumor in 75% of cases

Pars intermedia tumor in 25% of cases

81
Q

When screening a clinical dog for Cushing’s with a LDDST, which cortisol is diagnostic (baseline, 4h, 8h)

A

Cortisol at 8h

82
Q

What percentage of dogs with PDH will suppress at the 4h cortisol?

A

30%

83
Q

What is the cut-off value of cortisol for suppression?

A

<1.4 ug/dL or 40nmol/L

84
Q

In an LDDST, what does an escape from suppression at the 8 hour cortisol tell you?

A

Diagnosis of PDH

85
Q

What is the sensitivity of LDDST for diagnosis of Cushing’s?

A

Sensitivity 85%-100%

Specificity 44-73%

86
Q

What test is best to identify iatrogenic Cushing’s?

A

ACTH stim

87
Q

What is the sensitivity and specificity of ACTH stim for diagnosis of Cushing’s?

A

Sensitivity 60-85%

Specificity 85-90%

88
Q

ACTH stim vs. LDDST - Which one is sensitive, which one is specific?

A

LDDST - Sensitive

ACTH stim - Specific

89
Q

How do dogs with Cushing’s respond to ACTH stim? What about iatrogenic cushing’s?

A

Dogs with Cushing’s - Exaggerated cortisol elevat

Dogs with Iatrogenic cushing’s - No increase in cortisol

90
Q

What test is used to monitor for treatment response in Cushing’s?

A

ACTH stim (lower dose used)

91
Q

Which thyroid hormone has the shortest latency period and is the quickest to reach maximum cellular activity?

A

T3

92
Q

What insulin-dependent glucose transporter (GLUT) is found in fat and muscle?

A

GLUT 4

93
Q

What percentage of the pancreas is exocrine and what percentage is endocrine?

A

Exocrine - 80%

Endocrine 20%

94
Q

What is the general cause of diabetes mellitus in dogs vs. cats?

A

Dogs - Immune destruction of beta cells, vacuolar degeneration or pancreatitis.

Cats - Islet cell amyoidosis

95
Q

What are the two types of DM?

A

Type 1 DM - Beta cell destruction w/ absolute insulin deficiency. Dogs mostly

Type 2 DM - Defect in insulin secretion/insulin resistance. Cats mostly

96
Q

Do cats with diabetes mellitus get cataracts?

A

No

97
Q

What is the ideal diet for cats with diabetes mellitus?

A

High protein with limited carbohydrate intake

98
Q

ADH is produced by which nuclei?

A

Supraoptic nuclei

99
Q

Oxytoxin is produced by which nuclei?

A

Paraventricular nuclei

100
Q

What is the difference in the etiology of acromegaly in dogs and cats?

A

Cats - Secondary to pituitary tumor

Dogs - Usually exogenous or endogenous (ovaries) progestins that stimulate GH secretion from mammary tissue. Tx - spay

101
Q

What is contained within the follicles of the thyroid gland?

A

Contain colloid, most of which is thyroglobulin

102
Q

What is the essential building block of thyroglobulin?

A

Tyrosine

103
Q

What does thyroglobulin contain?

A

T4, T3, mono- and diiodotyrosine

104
Q

What is the effect of thyroid hormone on the myocardium?

A

Stimulates production of myosin isoform that speeds the interaction between myosin and actin = increased rate of contraction

105
Q

What is a mechanism for thyroid autoregulation?

A

Wolff-Chaikoff mechanism - increasing iodide slows the rate of thyroid hormone synthesis.

106
Q

How does hyperthyroidism cause vomiting?

A

Thyroid hormone stimulates CRTZ

107
Q

What is primary hypoadrenocorticism? Is the plasma ACTH low or high?

A
  • Adrenal deficiency
  • More than 95% of cases
  • Plasma ACTH is high
108
Q

What is secondary hypoadrenocorticism?

A
  • Decreased ACTH production
  • Commonly caused by excess steroid administration
109
Q

What causes primary hypoadrenocorticism?

A
  • Immune-mediated destruction
  • Mitotane or trilostane treatment
  • Bilateral adrenalectomy
110
Q

Why does primary addison’s cause skin hyperpigmentation in people?

A

Increased ACTH production leads to increased production of a-melanocyte stimulating hormone (a-MSH)

111
Q

Feline hypersomatotropism is secondary to neoplastic transformation of which cell type?

A

Acidophil (Somatotrophs)

112
Q

MOA: Diazoxide

A

(Medication for hyperinsulinism) Direct vasodilator to peripheral arteriole smooth muscle. Directly inhibits pancreatic insulin secretion, stimulates hepatic gluconeogenesis and glycogenolysis, and stimulates beta-adrenergic system to cause ephinephrine release and inhibit tissue use of glucose.

113
Q

MOA: Pamidronate, Zoledronate

A

Biphoshonates - Inhibit bone resorption by binding to hydroxyapatite crystals. Impede osteoclast activity

114
Q

MOA: Methimazole

A

Inhibits thyroid peroxidase and interferes with iodine incorporation into tyrosyl residues of thyroglobulin, thereby inhibiting thyroid hormone synthesis.

115
Q

MOA: Desoxycorticosterone Pivalate (DOCP)

A

Long-acting mineralocorticoid. Acts at the renal distal tubule where it increases absorption of sodium. Also enhances potassium and hydrogen excretion.

116
Q

MOA: Octreotide

A

Long-acting somatostatin analog. Inhibits synthesis and secretion of insulin, glucagon, secretin, growth hormone, gastrin, and motilin.

117
Q

MOA: Desmopressin

A

Similar vasopressin, but has more antidiuretic activity and less vasopressor properties.

Also increases plasma factor VIII and plasminogen factor (tx for vWD)

118
Q

What are symptoms of acromegaly in dogs?

A

Soft tissue swelling of face and neck

Hypertrophy of tongue, pharynx

Organomegaly

Hyperglycemia

119
Q

Thyroid works on what kind of receptors?

A

Nuclear receptors

120
Q

How does thyroid hormone affect the heart muscle?

A

Stimulates production of myosin, increasing rate of contraction

121
Q

What is the primary source of cholesterol for the synthesis of adrenocortical hormones?

A

LDL

122
Q

What is the rate limiting step in production of adrenocortical hormones?

A

Cholesterol > Pregnenolone

Catalyzed by cholesterol desmolase

123
Q

Increased aldosterone leads to what acid/base status?

A

Metabolic alkalosis

124
Q

Insulin stimulates translocation of what receptor to the membrane?

A

GLUT-4

125
Q

What causes nutritional secondary hyperparathyroidism?

A

Diets low in calcium or vitamin D

Diets excessive in phosphorus

126
Q

What are the results of nutritional secondary hyperparathyroidism?

A

Increased bone resorption - osteopenia

Lamenes, limb deformity, fracture, ect

127
Q

What acid base status worses hepatic encephalopathy?

A

Alkalosis - causes more ammonia to be absorbed into CNS

128
Q

What electrolyte disturbance worsens hepatic encephalopathy?

A

Hypokalemia

129
Q

ALP elevations in cats are sensitive/specific? why?

A

Specific (cholestasis)

Cats do not have steroid isoenzime

130
Q

How is ALP cleaved in order for it to go into the bloodstream?

A

Cleaved by:

Bile acids

phospholipase D

Proteases

131
Q

What insulin is long acting due to the formation of crystals SQ?

A

Glargine

132
Q

What insulin is long acting by causing slowly reversible binding to albumin?

A

ACVIM General Boards - 2022 (16 decks)

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