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Boards Review > Endocrine Recap > Flashcards

Endocrine Recap Flashcards

1
Q

Label the diagrams with the name of the hormone signaling action:

A

A = Endocrine
B= Paracrine
C= Autocrine

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2
Q

Draw an example of each of the following hormone feedback mechanisms:

Positive Long Loop
Positive Short Loop
Negative Ultrashort loop

A
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3
Q

Discuss Magnocellular neurons.

A

Larger.
Synthesize large amounts of oxytocin, AVP, and neuropeptides.
Axons link hypothalamus to posterior pituitary where hormones are released.

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4
Q

Discuss parvicellular neurons.

A

Smaller.
Projections link hypothalamus to median eminence, brain stem, and spinal cord.
Median eminence is linked to anterior pituitary via long portal veins.
Synthesize small amounts of releasing or inhibiting neurohormones which control anterior pituitary function.
CRH, TRH, LHRH, GHRH, somatostatin (growth hormone inhibiting hormone), dopamine

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5
Q

List the hormones secreted by the anterior pituitary

A
  • ACTH
  • TSH
  • LH
  • FSH
  • GH
  • Prolactin
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6
Q

Discuss actions of ACTH

A

Stimulates adrenal cortex to produce cortisol

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7
Q

Discuss actions of TSH

A

stimulates T3/T4 production by thyroid gland

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8
Q

Discuss actions of LH

A

Triggers ovulation in females and testosterone production in males

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9
Q

Discuss actions of FSH

A

Stimulates repro germ cells in both sexes.
Induces sertoli cells to secrete androgen-binding proteins in males and increases sperm

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10
Q

Discuss actions of GH

A
  • Insulin antagonism, increased hepatic glucose production 🡪 hyperglycemia
  • Bone and muscle growth
  • Increased release and oxidation of FFA’s during fasting
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11
Q

Discuss actions of Prolactin

A

increased milk production

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12
Q

What are the functions of follicular (epithelial) cells?

A

thyroid hormone synthesis, arranged around a large central cavity filled with colloid (thyroglobulin)

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13
Q

What are the functions of parafollicular or C cells

A

Produce calcitonin

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14
Q

Draw the feedback loops involved with control of thyroid hormone.

A
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15
Q

What is the difference between T3 and T4?

A
  • T4 is fairly inactive due to lower affinity for the thyroid receptor and inability to enter the cell nucleus.
  • There is more T4 than T3 in circulation.
  • T4 is converted to T3 in peripheral tissues.
  • T4 is easier and more reliable to measure when trying to assess thyroid function (T3 is less stable).
  • Only a small portion of both circulate freely (most are bound to plasma proteins)
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16
Q

What are the basic types of hypothyroidism. (& which with the most common)

A
  1. Primary (most common (95%))
  2. Secondary
  3. Tertiary
  4. Congenital defects
  5. Dietary iodine deficiency
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17
Q

Discuss and give examples of primary hypothyroidism.

A
  • Problem is within the thyroid gland itself, most common form (95%)
  • Lymphocytic thyroiditis (immune mediated): not clinical until terminal stages of destruction. Progressive condition.
  • Idiopathic atrophy: loss of thyroid tissue without inflammation, replaced by adipose tissue
  • Follicular cell hyperplasia: rare
  • Neoplastic destruction: rare
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18
Q

Discuss secondary hypothyroidism

A

problem is with TSH (due to pituitary destruction or inhibition by hormones or drugs- ie steroids). Rare to uncommon.

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19
Q

Discuss tertiary hypothyroidism

A

problem is with TRH, not reported in dogs

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20
Q

How is T4 used to diagnose hypothyroidism in dogs?

A

Low total T4 is suggestive, but some overlap b/w hypothyroid and healthy dogs, also does not distinguish euthyroid sick, and is affected by circulating thyroid autoantibodies (will read T4 falsely high).

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21
Q

Discuss and give examples of congenital defects leading to hypothyroidism.

A
  • hypoplasia or aplasia of the thyroid gland
  • iodine metabolism defects
  • abnormalities in thyroid transport hormones
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22
Q

How is TSH used to diagnose hypothyroidism in dogs?

A

high specificity when used in conjunction with T4 or fT4. High TSH with low T4 or fT4 supports hypothyroidism and normal TSH/T4/fT4 rules out hypothyroidism.

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23
Q

How is fT4 used to diagnose hypothyroidism in dogs?

A

Not affected by circulating thyroid autoantibodies, affected less by concurrent illness (euthyroid sick).

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24
Q

What factors are documented to lower total T4 measurement?

A

Old age
Being a greyhound
Concurrent illness
Poor diabetic regulation
Cushing’s disease
Steroid administration
Phenobarbital
Sulfa drugs
NSAID administration

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25
Q

What are the causes of hyperthyroidism in cats? Which is most common?

A
  • Pretty much all are “primary”
  • Benign thyroid tumors (>95%): adenoma (multinodular or solitary)
  • Malignant thyroid tumors: thyroid carcinoma (follicular or papillary)
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26
Q

What is the most common cause of hyperthyroidism in dogs?

A

Malignant thyroid carcinoma

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27
Q

How is T4 used to diagnose hyperthyroidism in cats?

A
  • Fairly reliable, initial screening test of choice.
  • Can occasionally be normal (10%)- usually due to mild hyperT4, fluctuating concentrations, or concurrent illness (euthyroid sick).
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28
Q

How is free T4 used to diagnose hyperthyroidism in cats?

A
  • Consider when total T4 is normal or borderline and hyperthyroidism is highly suspected.
  • More sensitive than total T4, but less specific (false positives). If positive on fT4 and normal on TT4, the cat generally has mild disease.
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29
Q

How is TSH used to diagnose hyperthyroidism in cats?

A

not used

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30
Q

What are the most common negative effects of methimazole therapy in cats?

A

Worsening of GFR/uncovering CKD
Severe ear/facial pruritis
GI effects
Bone marrow effects- Thrombocytopenia/neutropenia

31
Q

What is the ultimate effect of parathyroid hormone release?

A

Increase blood calcium levels with decreased phosphorus levels

32
Q

How does parathyroid hormone release lead to increase in blood calcium levels with decreased phosphorus levels?

A
  • Kidney: Increased tubular reabsorption of calcium
    —- Direct action on the distal convoluted tubule
    —- Indirect action on the ascending thick limb of the loop of Henle by increasing the net positive charge in the nephron lumen 🡪 diffusion of Ca out of the lumen.
  • Increased bone reabsorption of calcium
    —- Immediate: increased rate of flow of calcium from deep bone to surface (osteocyte-osteoblast pump). Smaller magnitude, fine-tuning.
    —- Long-term: Increased osteoclast activity. Larger magnitude changes.
  • Increased formation of calcitriol (Vit D) by the kidney 🡪 primarily increased GI absorption
33
Q

PTH release is increased by what factors?

A

Hypocalcemia
Hyperphosphatemia
Catecholamines

34
Q

PTH release is suppressed by what factors?

A

Hypercalcemia
Vitamin D
Severe hypomagnesemia

35
Q

What is the short-term treatment for primary hypoparathyroidism in dogs?

A

IV calcium administration, +/- CRI

36
Q

What is the long-term treatment for primary hypoparathyroidism in dogs?

A

oral calcium and vitamin D (calcitriol) supplementation with close monitoring

37
Q

What are the 3 types of endocrine cells in the pancreas?

A

Beta cells
Alpha cells
Delta cells

38
Q

What do beta cells secrete?

A

Insulin

39
Q

What do alpha cells secrete?

A

glucagon

40
Q

What do delta cells secrete?

A

Somatostatin

41
Q

What is the primary stimulus for insulin release? Name a few others too…

A

GLUCOSE
Others include amino acids, hormones (insulin, GLP-1, somatostatin, Epi), and neurotransmitters (NorEpi, ACh)

42
Q

What are the short-term effects of insulin?

A
  • glucose transport into fat and muscle cells, mediated by GLUT-4
43
Q

What are the intermediate effects of insulin?

A
  • Modulation of protein phosphorylation of enzymes involved in metabolic processes in muscle, fat, and liver
  • Fat: insulin inhibits lipolysis and ketogenesis; stimulates lipogenesis (favors lipid storage)
  • Liver: insulin stimulates glucose utilization (glucose uptake, glycolysis), stimulates glycogen synthesis; inhibits glucose production (decreased gluconeogenesis)
  • Muscle: insulin stimulates glucose uptake and favors protein synthesis; also favors lipid storage
44
Q

What are the long-term effects of insulin?

A

Enhances synthesis of lipogenic enzymes and represses gluconeogenic enzymes

45
Q

What are the overall effects of insulin?

A

Anabolic

46
Q

What is different about the BRAIN as far as glucose metabolism?

A

Most brain cells are permeable to glucose (they DO NOT need insulin to facilitate uptake)

47
Q

What are the physiologic effects of glucagon?

A
  • Overall glucagon counteracts effects of insulin
  • Main physiologic effect of glucagon is to increase plasma glucose concentrations
  • Liver: stimulates hepatic glucose production (gluconeogenesis, glycogen breakdown and decreases glycolysis)
  • Adipocyte: glucagon stimulates activation f hormone-sensitive lipase 🡪 glycerol and free fatty acids are release into circulation (enhances lipolysis)
48
Q

What does stomatostatin do?

A

Generalized inhibitory effect on all GI and pancreatic exocrine and endocrine functions (inhibits both insulin and glucagon). Release is stimulated by high-fat, high-carb, and protein-rich meals and inhibited by insulin

49
Q

Describe type I Diabetes

A

Insulin-dependent (type I): absolute deficiency of insulin secretion due to destruction of β-cells.
Only kind in dogs.
Cats can be either type.

50
Q

Describe type II Diabetes

A

Non-insulin-dependent (type II)

β-cell dysfunction is crucial in development of type II DM

Progressive DM likely not related to progressive insulin resistance but to progressive declines in βcell function

Causes disruption of the normal basal oscillatory pattern of insulin release, reduced or absent first-phase insulin secretion in response to IV glucose, and insufficient conversion of proinsulin to insulin

Insulin resistance (main sites of insulin resistance are liver, muscle, and adipose tissue) → obesity is a big risk factor

51
Q

What is the renal glucose threshold? Does glucosuria always indicate the patient is diabetic?

A

BG > 180-220 in dogs, > 270-300 in cats
If stress hyperglycemia is prolonged, glucosuria can be present, especially in cats

52
Q

What ketone is measured on the urine dipstick vs the blood ketone meter? Which ketone is more prevalent in DKA?

A

Dipstick- acetoacetate

Blood ketone meter- beta hydroxybutyrate ** more prevalent

53
Q

Discuss pathogenesis and treatment of DKA

A
  • Starvation (d/t anorexia or insulin deficiency) → ketone production for energy (liver)
  • FFA’s mobilized → liver → TCA cycle (Β-oxidation of fatty acids) → acetyl-CoA → acetoacetate → β-hydroxybutyrate or acetone
    —- In nondiabetics, acetyl-CoA + pyruvate can enter the citric acid cycle to form ATP—without glucose entry into cells, pyruvate production is decreased and acetyl-CoA accumulates
  • Insulin inhibits lipolysis/FFA oxidation
  • Insulin deficiency can be relative (insulin resistance) or absolute
  • Increased counter regulatory hormones from illness: Glucagon (#1), cortisol, norepi, epi
  • Ketones help to create osmotic diuresis (more pull than glucose)
  • Dehydration from diuresis + other losses → hypovolemia → decreased GFR → worsening accumulation of ketones/glucose in blood
  • Severe hyperosmolarity is rare in DKA due to dilutional hyponatremia
54
Q

Discuss pathogenesis and treatment of HONK/HHS

A
  • In HONK, small population of functional B-cells still secreting insulin +/- glucagon resistance, preventing ketosis
  • Low GFR → severe hyperglycemia (>600) and hypernatremia
  • Serum osmolality > 350mOsm/kg
  • Fluid therapy more important than insulin- restore GFR!
55
Q

List and discuss the main differences between these types of insulin? Which are preferred in dogs vs cats?

A
  • Regular insulin: U-100, very short acting, used mostly for sick diabetics/DKA in hospital
  • NPH: U-100, intermediate acting (< 12 hrs)
  • Vetsulin: U-40, intermediate acting (< 12 hrs)
  • Lantus: U-100, long-acting, “peakless” because of overlap, 12-22 hrs
  • PZI (Prozinc): U-40, long-acting, 2 “nadirs” and lasts about 21 hrs mean
56
Q

Draw the somogyi effect.

A
57
Q

Define “insulin resistance”.

A

Requiring > 1 unit/kg in dogs, 1.5 unit/kg in cats

58
Q

What are possible causes of insulin resistance?

A
  • Obesity- over-distended fat cells are less sensitive to insulin (they are already too full!)
  • Systemic illness- UTI, other infections, pancreatitis, neoplasia, CKD, heart disease, liver disease
  • Intact female (diestrus)
  • Endocrine: Cushing’s, hypothyroid, hyperthyroid, acromegaly, pheochromocytoma
  • Exogenous steroid therapy
  • Development of anti-insulin antibodies
  • MOST COMMON: animal is NOT actually insulin resistant and is on too high a dose due to poor monitoring
59
Q

What factors are associated with obtaining “diabetic remission” in cats?

A
  • Low carb diet (<6% of energy from carbohydrate)
  • Long-acting insulin (glargine vs PZI vs lente)
  • Early initiation of tight glycemic control
    — Glucotoxicity: chronic hyperglycemia is a potential suppressor of insulin secretion—so if hyperglycemia is corrected, remission is possible
  • Recent steroid administration (and stopping it)
  • Lower mean BG concentrations after treatment with insulin and lower cholesterol concentrations
  • Older cats (maybe slower disease progression?)
  • Mean BG <288 mg/dL after 17 days of glargine treatment was significantly associated with remission
60
Q

How important is diet in obtaining diabetes regulation in cats vs dogs?

A

Very important in cats (low-CARB, not low-FAT). Minimally important in dogs (although diabetic dogs very prone to pancreatitis, so low-fat probably good).

61
Q

What is the benefit of using fructosamine for diabetes monitoring?

A

Gives an average over 1-3 weeks, so removes the effect of stress hyperglycemia. Great for DIAGNOSIS.

62
Q

What is the downside of using fructosamine for diabetes monitoring?

A

patients with Somogyi on insulin have an AVG BG that is too high- so can be misleading.
Also, low alb, hyperT4, hyperlipidemia can artificially lower fructosamine.

63
Q

List possible causes of hypoglycemia:

A
  • Artifacts: serum not separated, hemoconcentration + glucometer
  • Insulin overdose
  • Insulinoma
  • Xylitol
  • Neonate or toy breed dog with inadequate gluconeogenesis
  • Liver failure
  • Addison’s disease
  • Sepsis
  • Exercise-induced (hunting dogs)
64
Q

Draw the adrenal gland layers. What does each layer do?

A

salt, sugar, sex, adrenaline

65
Q

List the different screening tests for Cushing’s disease:

A

Urine cortisol: creatinine ratio
ACTH stim
LDDS (also differentiating test)

66
Q

List the different discriminatory tests for Cushing’s disease.

A

LDDS (sometimes)
High DDS
Baseline ACTH levels
Ultrasound, CT, MRI -> look for brain vs adrenal tumor

67
Q

Discuss urine cortisol: creatinine ratio in diagnosing Cushing’s disease.

A
  • Screening test
  • Morning urine sample collected by client reflect urine cortisol levels over a few hours
  • Normal test rules out Cushings
  • Positive results need further testing to confirm Cushings
68
Q

Discuss ACTH stim in diagnosing Cushing’s disease.

A
  • Screening test
  • Measures adrenal response to ACTH
  • Differentiate naturally vs iatrogenic Cushings
  • High response 🡪 HAC (can not tell if PDH or ADH)
  • No response 🡪 Iatrogenic
  • Can be affected by stress (false positive)
69
Q

Discuss LDDS in diagnosing Cushing’s disease.

A
  • Screening test and sometimes discriminatory test
  • Works by negative feed back mechanism on pituitary gland, suppressing ACTH secretion, and in theory cortisol levels will also decrease
  • PDH (secondary): 30% cortisol suppression in 4 hours, and rise in 8 hours, or if less than 50% suppression of cortisol at either the 4 or 8 hours sample
  • Failure to suppress- usually adrenal dependent (primary) but could still be PDH
70
Q

Discuss HDDS in diagnosing Cushing’s disease.

A
  • Discriminatory test
  • In some instances a high dose of dexamethasone is needed to see a suppression of ACTH secretion
  • PDH- will show suppression
  • Adrenal tumors will not suppress
71
Q

Discuss Baseline ACTH levels in diagnosing Cushing’s disease.

A
  • Discriminatory test
  • Only to be used once the diagnosis of Cushings is found
  • If ACTH levels are high 🡪 PDH
  • ACTH levels Low 🡪 primary adrenal
72
Q

What drugs will interfere with ACTH stimulation test results (measuring as cortisol on the assay)?

A

Prednisone
Hydrocortisone

(NOT dexamethasone, dexSP, fludrocortisone, or DOCP)

73
Q

Explain the current recommendations for diagnosis of CIRCI and use of steroids in septic patients.

A
  • Diagnosed by a delta cortisol <9 with ACTH stimulation
  • However, not recommended to use this info to determine who gets steroids
  • Give hydrocortisone 200mg/d to patients in septic shock who are NOT RESPONSIVE to fluids AND pressors (treat for 7 days before tapering)
  • Consider methylprednisolone in patients with severe ARDS (P/F <200)- treat for 14 days before tapering
  • Dex SP not recommended due to prolonged adrenal suppression

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