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VET377 SPAM > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

If you have a highly Sensitive test what does this mean?

A

Highly Sensitive means that anyone that tests negative then that means you can exclude them from further testing as they do not have the disease. Remember SNNOUT

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2
Q

If you have a Highly Specific Test what does this mean?

A

High Specific means that if they test Positive they have the disease. Remember SPPIN

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3
Q

What is the calculation to work out Sensitivity?

A

Sn = Tp/Tp+Fn

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4
Q

What is the calculation to work out Specificity?

A

Sp = Tn/Tn+Fp

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5
Q

What Does a Positive Predictive Value mean?

A

How like a patient who test positive actually has the disease

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6
Q

What does a Negative Predictive Value mean?

A

How likely a patient who tested negative actually is negative to the disease

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7
Q

When talking about Hyper and Hypothyroidism Which one is common for Cats and which is common for dogs?

A
  • Dogs - Hypothyroidism
  • Cats - Hyperthyroidism
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8
Q
  • Where is All circulating T4 produced?
  • Talk about T3 production?
  • Talk about what signals T4 to be produced
A
  • Produced by the thyroid Glands
  • Only 10-40% of T3 is produced by the thyroid glands 60-80% of T3 is generated from T4 in cells throughout the body.
  • Hypothalamus -> TRH ->Pituitary gland -> TSH -> Thyroid Glands -> T4 -> fT4 ->fT3 negative feedback loop to hyperthalamus.
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9
Q

What is the difference between T4 and Free T4

A

T4 is bound to protiens like Thyroid Hormone-Binding globulin (TBG) and to transthyretin, Albumin and apolipoprotiens.

T4 and T3 not bound to plasma protiens are called Free T4, Free T3.

Free hormone concentration is maintained constant by the feeedback regulatory system

Free hormones are the biologically active form.

fT3 is the most metabolically active form (about 3-5 times as potent as fT4)

fT4 enters most cells of the body and is converted to T3

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10
Q

What is Thyroid Hormone Action on :-

  • Development
  • Growth
  • Metabolism
A
  • Development of foetal and neonatal brain
  • Necessary for normal growth., Growth-Promoting effect of thyroid hormaones is intimately intertwined with that of GH
  • Effect on Basal Metabolic rate
    • Increase basla metabolic rate
      • Increased heart Rate, Cardiac Contractility, promote vasodialation
      • ALtered Mental State
      • Reproductive Activity
  • Effects on Lipid Metabolism
    • Stimulate fat mobilization
    • Enhance oxidation fo fatty acids
  • Effects on Carbohydrate metabolism
    • Enhancement of insulin-dependent entry of glucose into cells
    • increased gluconeogenesis and glycogenolysis to generate free glucose
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11
Q
  • In dogs explain Primary, Secondary, and Tertiary Hypothyroidism, How it occurs and why.
  • Which is the most common?
A
  • Primary Hypothyroidism
    • Caused by a thyroid gland disease
      • Aquired: Iorine deficiency (carnivorous diet)
      • Lymphocytic Thyroiditis
      • Idiopathic Atrophy
  • Secondary Hypothyroidism
    • Caused by pituitary disease
      • Pituitary neoplasia
      • Surgical Hypophysectomy
  • Tertiary Hypothyroidism
    • Caused by hypothalamus disease
      • Tumour inflitrating the hypothalamus
  • Primary is the most Common in Dogs
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12
Q

What Clinicopathological Changes would you see in an animal with Hypothroydism?

A
  1. Mild normchromic, normocytic, Non regenerative Anemia
    1. Decreased T3 and T4 result in decreased matabolic rate and thus a decreased need for O2 in peripheral tissues. The decreased need for O2 leads to decreased EPO production
  2. Hyperlipemia
    1. About 75% of dogs with hypothroidism have a fasting hypercholesterolemia, Hypertriglyceridema may or may not present. Due to decreaed exression of hepatic LDL receptors. Decreased activities of hepatic lipase and lipoprotein lipase.
  3. Increased Fructosamine
    1. Due to decreased protein turnover
  4. Increased CK
    1. Due to hypothyroidism-induce myopathy
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13
Q

WHat is Euthyroid Sick Syndrome?

A

A condition in which a systemic disease outside of the thyroid hormonal system creates hypothyroxemia (decreased fT4)

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14
Q

What are the 3 Assays availabel to measure T4 and T3?

A
  • RIA (RadioImmunoAssay) Common due to higher sensitivity)
  • ELISA (Enzyme-Linked Immune Sorbent Assay)
  • CLIA (ChemiLuminescent ImmunoAssay)

All of these are not reliable for canine serum fT4 because the tend to underestimate the canine fT4

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15
Q

To Diagnose Hypothyroidism in dogs what test/s should we use?

A

Combined Total T4 and cTSH

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16
Q

Where is Insulin and amylin produced?

What is the role of these hormones?

A

Beta Cells in the Islets of Langerhans -

Reduce Glycaemia

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17
Q

Where is Glucagon produced and what does it do?

A

alpha cells and it induces hyperglycaemia

18
Q

What does the hormone Somatostatin do?

A

Inhibits Growth Hormone Release. Produced in the S-Cells in the Islets of Langerhans

19
Q

What does Insulin activity do and How?

A

Insulin activity lowers Blood Glucose by:

  • Inhibition of hepatic gluconeogenesis
  • Promotion of hepatic glycogen synthesis
  • Increased Cellular uptake of glucose by muscles and adipose tissue
20
Q

What does Glucagone Activity do and how?

A

Glucagone Activity increased Blood Glucose by:

  • Promoting gluconeogenesis in liver and muscles
  • Promoting glycogeneolysis in liver and muscles
21
Q

Where and how can excess glucose be stored in the body?

A
  • Liver as Glycogen
  • Muscles as Glycogen
  • Adipose as Glucose itself
22
Q
  • Classify the 2 types of Diabetes Mellitus and how it comes about.
  • What Animal has type 1 more commonly over Type 2?
A
  • Diabetes Mellitus - group of metabolic disease characterized by hyperglycaemia resulting from defects in insulin secretion, insulin action or both.

Type 1

  • Beta Cell destrucgtion leading to lisulin deficiency (Common with dogs)

Type 2

  • Impaired insulin secretion/insulin resistance
23
Q

What Clinical Pathological Changes would you expect with an animal with Diabetes Mellitus?

A
  1. Hyperglycaemia - Due to absence of insulin (type1) or impaired insulin actin (insulin resistance type 2)
  2. Glycosuria - Renal tubular transport maximum for glucose in dogs 9.99-11.1mmol/L in dogs
  3. Hyperlipemia - increased lipomobilization
  4. Ketonemia
  5. Increase Fructosamine - Irreversible, non enzymatic linking of glucose to albumin
  6. Increase ALP and ALT - due to hepatic lipidosis
  7. Hyponatremia and Hypochloremia - Osmotic diureses due to glycosuria
  8. Proteinuria
24
Q

What is the pathogenesis of Diabetes mellitus type 1

A
  • Multifactorial aetiology
  • Characterized by permanend Hypoinsulinemia
  • Autoimmune destruction of Beta Cells
    • infiltration of lymphocytes into the islets
    • antibodies against B-Cell and several islet components (insulin, GAD65, IA2)
  • Genetic Susceptibility (Breed predispositin)
    • Diabetes in dogs has been associated with major histocompatibility complex class II genes (Dog leukocyte antigen (DLA) -> subgroup of type 1 termed latent autoimmune diabetes LADA
25
Q

What 2 hormones does the Adrenal Glands produce?

A
  • Cortisol - Systemic Effects
  • Aldosterone - Na & Cl retention, K & H excretion
26
Q

What effect does glucocorticoids have on :-

  • Carbohydrate Metabolism
  • Protein Metabolism
  • Anti-Inflammatory Action
  • Effects on Lipid Metabolism
  • Effects on Electrolytes and Kidney
A
  • Carbohydrate Metabolism
    • Increase gluconeogenesis
    • increase liver glycogen storage
    • decrease peripheral glucose uptake and increased metabolism
    • = hyperglycemia with secondary hyperinsulinemia
  • Protein Metabolism
    • Decreased synthesis
    • increased consumption (liver ++) for gluconeogenesis
    • =muscle atrophy
  • Anti-Inflammatory Action
    • decreased capillary permability = decreased diapedesis decreased edema
    • increased lysosomal membrane stability = decreased proteolytic enzymes release
    • decreased WBC phagocytosis ability =decreased pro-inflammatory cytokine release (think anti neutrophil
    • Immune-Suppression (++T lymphocytes)
  • Effects on Lipid Metabolism
    • Increase lipolysis = increase fatty acids and glycerol release.
    • In case of hyperinsulinemia due to hyperglycemia : increase lipogenesis and centripetal fatty deposition > intra-abdominal (pot bellied appearance) < subcutaneous (thin inelastic skin)
  • Effects on Electrolytes and Kidney
    • Increased GFR + inhibition of ADH release = Poliuria
    • Na retention increase K excretion = uncommon
27
Q

What is the other name for Hypercortisolism?

A

Cushings Disease

28
Q

What is Pituitary - Dependent Hypercortisolism (PDH)?

A
  • Over production of ACTH (by the pituitary Gland) which overstimulates the adrenal gland causing bilateral adrenal hyperplasia. This can be caused Microadenomas (85%) or Adenocarcinomas (15%)
  • This produces extra cortisol, but the negative feedback loop doesnt work due to the tumour/s in the pituatary gland and more ACTH is produced.
  • Bilaterl adrenal hyperplasia
29
Q

What is Adrenal Dependant Hypercortisolism?

A

Due to a tumor in the adrenal gland, excess cortisol is produced by the adrenal with the tumor. The other adrenal usulally atrophy in responce to the negative feedback / reduction in ACTH

30
Q

What is Iatrogenic Hypercortisolim??

A

Common when Corticosteroid administation. Due to negatiuve feedback loop production of ACTH is reduced due to excesive Cortisol circulation. This requires gradual reduction of Corticosteroid Administration otherwise HypoCortisolim occurs.

31
Q

Clinicopathological Changes for Hypercortisolism

A
  1. Stress Leucogram
    • Lymphopenia = Immune Suppressiong
    • Neutrophilia with right shift = decreased diapedesis
    • Monocytosis = Marginal Pool mobilization
    • Eosinopenia = bone marrow sequestation
  2. Policitemia
    • Rare, due to hypoxia secondary to chronic respiratory insufficience caused by respiratory muscles atrophy
  3. Increased ALP
    • in 90% of cases, 5 to 40x upper reference limit
    • Due to isoenzyme C-ALP inductin
  4. Increase ALT e GGT
    • in 50-80% of cases
    • Secondary to vacuolar hepatopathy due to increased glycogen storage and consequently hepatocytes hypoxia
    • Moderately increased
  5. Increased Bile Acids (Resting and Post-Prandial)
  6. Increased Glucose
    • Cortisol is an insulin antagonist (it causes insulin resistance)
    • Decreased number or effficacy of membrane glucose transporter (GLUT4)
    • About 10% of hyperadrenocorticism evolve in Diabetes Mellatis
  7. Hyperlypemia
    • Increase Cholesterol
    • Increase Triglycerides +/-
  8. Decreased Urea
    • Secondary to PU
  9. Decreased Creatinine
    • Decreased muscle catabolism
    • Due to Low USG
  10. ISO- and Hypost**uria
    • USG <1.015 <1.008
    • Glucocorticoid hormones inhibited ADH secretion
    • Cortisol may inhibit the responsiveness of renal tubules to ADH
  11. Proteinuria
    • Often sever UPC >6 Incidence upto 75%
32
Q
  • How is a Low Dose Dexamethason Supressin Test (LDDST) completed?
A
  • Animal hospitalized over night, Start 8 or 9am.
  • Measure Serum or Heparin Plasma before administration of dexamethasone Administration for Cortisol levels.
  • IV administration of 0.01 Dexamethason/kg body weight
  • Serum or Plasma collection after 4 and 8hours

Normal after 8 hours would return to levels before test.

Iatrogenic Hyperadreanocortism and Hypoadrenocortisim will not see any effects.

PD-HAC decrease for 4 hours then increase

AD-HAC slight decrease till 4hrs then level out.

33
Q

What is the screening test of choice for Hyperadrenocortisim?

A

Low Dose Dexamethasone Suppression Test

34
Q

What is the Gold Standard test for diagnosing Iatrogenic HyperAdrenocortism?

A

ACTH Simulation Test

  • Test blood for Cortisol
  • then I/M admini of 0.25mg of synthetic ACTH in dogs (Cats 0.125mg)
  • Serum or plasma collection after 60 mins in dogs (30 and 60mins in cats)
  • iHAC levels do not change.
  • Cortisol valuse over 600nmol/L are suggestive of HAC
  • Normal dogs cortisol increase upto 450nmol/l
35
Q

What does the Urinary Cortisol to Creatinine Ratio do for you?

A

Rules out Cushings. but does not confirm Cushings

36
Q

High Dose Dexamethasone Suppression Test does what?

A

Distinguish PDH from AT in dogs confirmed spontaneous hyperadrenocorticism

Screening test for cats suspected of HAC

37
Q

What is Addisons Disease?

A

Primary Hypoadrenocorticism

  • Immune - mediated destruction of the adrenal cortex
38
Q
  • Where is the lesion in :-
  1. Primary Hypoadrenocorticism?
  2. Secondary Hypoadrenocorticism?
A
  1. Primary Hypoadrenocorticism = Adrenal glands themselves (Called Addisons Disease)
  2. Secondary HypoArenocorticism = Pituitary lesion with decreased ACTH production. (Rare)
39
Q

What are the actions of PTH?

What does Calcitonin do?

A
  • PTH stimulates Ca2+ pumps in the osteocyte membrane system - increase Clacium
  • PTH changesthe shape of osteoblasts allowing osteoclasts to reabsorb bone = increase Calcium
  • Calcitonin prevents bone reabsorption by promoting the retraction of the brush border of osterclasts.
40
Q

What does Total Serum Calcium include?

A
  • Free Calcium (50%)
  • Complexed Calcium (5%)
  • Protein-Bound Calcium (45%)
41
Q

Where would the lesion be in PrimaryParathyroidism?

A

Small adenom of the Parathyroid Gland.

42
Q

Why do cows get “Milk Fever”

A
  • High Calcium Diet before Calving -> Dependency of GIT absorption of Calcium
  • PTH is Down regulated and the rate of bone reabsorption is low and the parathyroid glands are inactive
  • Anorexia and GIT stasis that may occur near calving interrupt uptake of calcium
  • THere is increased outflow of calcium into milk
  • Net Result is Hypocalcaemia.

VET377 SPAM (6 decks)

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