EXAM 2: THYROID AND PARATHYROID

Question 1

EFFECTS: THYROID HORMONE

Answer 1

INCREASED METABOLISM OF FATS AND CARBOHYDRATES, PROTEIN SYNTHESIS
CV: INCREASE HR, CONTRACTILITY, AND CO
NERVOUS SYSTEM: ENHANCE SYMPATHETIC NERVOUS SYSTEM AND MENTAL ACTIVITY
DEVELOPMENT: ORGANOGENESIS

Question 2

WHAT ARE DESTRUCTIVE MECHANISMS OF THYROID DYSFUNCTION

Answer 2

ATROPHY - LACK OF TROPHIC STIMULATION (PITUITARY NEOPLASIA/DESTRUCTION)
INFLAMMATORY - AUTOIMMUNE THYROIDITIS
NEOPLASIA - NONFUNCTIONAL THYROID TUMORS (USUALLY ADENOMA), NONTHYROID NEOPLASIA (E.G. LYMPHOMA)

Question 3

WHAR ARE PROLIFERATIVE LESIONS OF THYROID DYSFUNCTION?

Answer 3

FUNCTIONAL NEOPLASIA - USUALLY ADENOMA
ADENOMATOUS HYPERPLASIA

Question 4

WHAT IS THE MOST COMMON TYPE OF CANINE HYPOTHYROIDISM?

Answer 4

PRIMARY
DESTRUCTIVE/LOSS OF FOLLICLES (IDIOPATHIC FOLLICULAR ATROPHY, LYMPHOCYTIC THYROIDITIS, NON-FX TUMOR)

Question 5

LESIONS: HYPOTHYROID

Answer 5

OBESITY W NORMAL/DECREASED APPETITE
CHANGES IN MENTATION, ACTIVITY LEVELS
SKIN CHANGES (ALOPECIA, PIGMENTATION, MYXEDEMA)
HYPERCHOLESTEROLEMIA
ATHEROSCLEROSIS

Question 6

CONSEQUENCES OF HYPERCHOLESTEROLEMIA

Answer 6

ATHEROSCLEROSIS (CORONARY A, HEART, CEREBRAL A)
HEPTAOMEGALY, LIPIDOSIS
GLOMERULUAR, CORNEAL LIPIDOSIS

Question 7

PATHOGENESIS: ATHEROSCLEROSIS

Answer 7

Question 8

HYPOTHYROID: SKIN LESIONS

Answer 8

SYMMETRICAL ALOPECIA
HYPERPIGMENTATION
EPIDERMAL/DERMAL ATROPHY
MYXEDEMA

Question 9

PATHOGENESIS: PROGRESSIVE ALOPECIA

Answer 9

Question 10

PATHOGENESIS: THRYOID ATROPHY

Answer 10

SECONDARY
T3/T4 SYNTHESIS INTACT BUT STIMULATION IS LOST
DESTRUCTIVE PITUITARY LESIONS

Question 11

PATHOGENESIS: GOITER

Answer 11

SECONDARY
INADEQUATE T3/T4 SYNTHESIS
(IODINE DEFICIENT DIETS, GOITROGENIC COMPOUNDS)
HYPOTHYROID BUT PROLIFERATIVE LESION

Question 12

PATHOGENESIS: GOITER

Answer 12

Question 13

CAUSES OF INADEQUATE THYROXINE SYNTHESIS

Answer 13

Question 14

CLINICAL SIGNS: HYPERTHYROID

Answer 14

INCREASED BASAL METABOLISM
WT LOSS W INCREASED APPETITE
RENAL: PU/PD, INCREASED GFR
CV: TACHYCARDIA, HYPERTENSION, CARDIAC HYPERTROPHY, DETACHED RETINA
GI: V/D/BULKY STOOL

Question 15

HYPERTHYROID: CLIN PATH

Answer 15

HIGH T3/T4
INCREASE ALT, ALP, AST
70% HAVE SIGNS OF HYPERPARATHYROIDISM
+/- AZOTEMIA

Question 16

WHAT ARE EXAMPLES OF FUNCTIONAL PROLIFERATIVE HYPERTHYROID LESIONS?

Answer 16

UNILATERAL OR BILATERAL
NODULAR HYPERPLASIA (MULTINODULAR ADENOMATOUS HYPERPLASIA)
ADENOMA
ADENOCARCINOMA (RARE)

Question 17

PATHOGENESIS: SADDLE THROMBUS

Answer 17

Question 18

WHAT TYPES OF NEOPLASIA DO DOGS/CATS/BULLS/HORSES GET?

Answer 18

Question 19

CHARACTERISTICS: FOLLICULAR CELL CARCINOMA

Answer 19

Thyroid neoplasia

Question 20

WHAT CELLS/HORMONES ARE ASSOCIATED WITH THE PARATHYROID?

Answer 20

CHEIF CELLS
PARATHYROID HORMONE SECRETED IN RESPONSE TO HYPOCALCEMIA (LOW IONIZED CA)

Question 21

PTH EFFECTS: BONE

Answer 21

Question 22

PTH EFFECTS: KIDNEY

Answer 22

Question 23

PTH EFFECTS: INTESTINE

Answer 23

Question 24

PATHOLOGY: PRIMARY HYPERPARATHYROID

Answer 24

PROLIFERATIVE:
HYPERPLASIA (MULTIFOCAL/NODULAR)
FUNCTIONAL NEOPLASMS: PARATHYROID ADENOMA > CARCINOMA (UNILATERAL)

Question 25

PATHOLOGY: SECONDARY HYPERPARATHYROID

Answer 25

HYPERPLASIA (DIFFUSE, BILATERAL): RENAL OR NUTRITIONAL SECONDARY HYPERPARATHYROID

Question 26

PATHOLOGY: PSEUDOHYPERPARATHYROIDISM

Answer 26

HYPERSECRETION OF HORMONE ANALOGUE (PTHRP): LYMPHOMA, AGASACA, MULTIPLE MYELOMA
BILATERAL ATROPHY

Question 27

HOW DOES NUTRITION CAUSE SECONDARY HYPERPARATHYROIDISM?

Answer 27

TOO LITTLE CALCIUM OR VITAMIN D
TOO MUCH PHOSPHORUS

Question 28

HOW DOES RENAL DISEASE CAUSE SECONDARY HYPERPARATHYROIDISM?

Answer 28

PATHOGENESIS: IMPAIRED NEPHRON FUNCTION –> PHOSPHORUS RETENTION, LOSS OF CA –> HYPERPARATHYROIDISM

Question 29

PATHOGENESIS: FIBROUS OSTEODYSTROPHY

Answer 29

INCREASED OSTEOCLASTIC BONE RESORPTION
REPLACEMENT WITH FIBROUS CONNECTIVE TISSUE
ATTEMPTS AT OSTEOBLASTIC PRODUCTION OF IMMATURE WOVEN BONE (POORLY MINERALIZED)
Due to excessive PTH excretion