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Module 12 > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

what are the mechanisms of endocrine disease

A
  1. hypofunction (primary and secondary)
  2. hyperfunction (think tumours, primary and secondary)
  3. endocrine dysfunction due to neoplasia
  4. failure of target cell response
  5. abnormal hormone degradation
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2
Q

what are the 3 types of intercellular signalling

A
  1. autocrine (target sites on same cell)
  2. paracrine (secretory cell –> adjacent target cell)
  3. endocrine (hormone secretion into blood by endocrine gland)
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3
Q

what are the clinical results of endocrine disease (4)

A
  1. skin: alopecia, hirsutism
  2. nervous system: seizures
  3. urinary system: polyuria
  4. skeletal: fractures
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4
Q

what hormones are released by the anterior (adenohypophysis)

A

growth hormone (GH)

adrenocorticotrophic hormone (ACTH)

thyroid-stimulating hormone (TSH)

follicle-stimulating hormone (FSH)

luteinizing hormone (LH)

melanocyte-stimulating hormone (MSH)

prolactin (PRL)

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5
Q

what hormones are released by the posterior pituitary (neurohypophysis)

A

anti-diuretic hormone (ADH)

oxytocin

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6
Q

what are the main reasons for hypofunction (2)

A
  1. failure to develop (aplasia, hypoplasia)
  2. damage to secondary disease (inflammation, neoplasia, trauma)
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7
Q

what are the causes of hyperfunction

A

tumour

benign hyperplasia

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8
Q

what are the causes primary anterior pituitary hypofunction

A
  1. aplasia/hypoplasia: congenital, toxic, viral –> destruction secondary to space occupying
  2. lesion: cystic Rathke’s pouch, abscess, neoplasm
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9
Q

what are the secondary causes of anterior pituitary hypofunction

A

hypothalamic malfunction

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10
Q

what are the various causes of anterior pituitary hypofunction (TSH, GH, ACTH, FSH/LSH)

A
  1. decreased TSH –> decreased T3/T4 –> hair coat alterations –> altered metabolism and growth
  2. decreased GH –> altered metabolism and growth
  3. decreased ACTH –> decreased cortisol –> altered metabolism and growth, delayed parturition
  4. decreased FSH/LSH –> infertility or sub-fertility
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11
Q

what are the causes of pituitary dwarfism

A
  1. decreased growth rate
  2. abnormal hair coat
  3. hypoplasia of gonads and genitalia
  4. delayed permanent dentition, epiphyseal closure
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12
Q

what can anterior pituitary dwarfism cause in certain breeds

A

congenital cysts of Rathke’s pouch (no/very little adenohypophysis)

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13
Q

what does posterior pituitary hypofunction cause

A

diabetes insipidus

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14
Q

what is primary diabetes insipidus caused by

A
  1. destruction of neurohypophysis –> no anti-diuretic hormone (ADH), trauma, neoplasia, congenital defects, immune mediated
  2. central diabetes insipidus
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15
Q

what is secondary diabetes insipidus caused by

A
  1. nephrogenic diabetes insipidus (renal tubules can’t respond to ADH)
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16
Q

what is the role of ADH

A

increased permeability of collecting tubules and ducts –> resorption of water –> concentration of urine

17
Q

what is the most common cause of pituitary hyperfunction

A

functional neoplasms

  • adenoma
  • adenocarcinoma
18
Q

what are other causes of pituitary hyperfunction

A
  1. pituitary hyperplasia
  2. pituitary dependent hyperadrenocorticism (PDH)
19
Q

what does anterior pituitary hyperfunction lead to

A
20
Q

when is pituitary hyperplasia common

A

in aged dogs

hyperplastic nodules/microadenomas

hyperadrenocorticism (cushing’s syndrome)

21
Q

what are the clinical symptoms of pituitary hyperplasia

A
  1. non-pruritic alopecia
  2. comedones with dystrophic calcification
  3. flaccid abdominal wall due to muscle wasting
  4. canine cushings calcinosis cutis
  5. cushing’s: vascular hepatopathy –> increased glucose and glycogen metabolism –> increased deposits of lipid and glycogen
22
Q

when is equine pituitary hyperplasia common

A

in aged horses (>15yo)

23
Q

what are the causes of equine pituitary hyperplasia

A

adenomatous hyperplasia, microadenomas, adenomas of pars intermedia

24
Q

what is equine pituitary pars intermedia dysfunction (PPID)

A

pathogenesis different to cushing’s disease in dogs

normal equine pars intermedia under dopaminergic control from hypothalamus, seasonal decrease in autumn allows hair coat growth and deposition of fat

dopamine is decreased all year without inhibition, melanotrophs of pars intermedia synthesize excessive hormones, hyperplasia, micro and macroadenomas develop

25
Q

what are the signs related to deranged hypothalamic function in horses

A
  1. polyphagia, polyuria, polydipsia
  2. hyperglycemia
  3. laminitis
  4. generalized hyperhidrosis (sweating)
  5. somnolence
  6. striking hypertrichosis (hirsutism)
26
Q

what is the pathogenesis of PPID

A
  1. pressure atrophy & degeneration of hypothalamus
  2. inability to control appetite (polyphagia)
  3. excessive food intake –> hypersinulinemia
  4. down-regulation of insulin receptors on target cells
  5. insulin-resistant hyperglycemia –> glycosuria
27
Q

what is equine metabolic syndrome

A

younger horses/ponies

28
Q

what does equine metabolic syndrome cause

A
  1. increased adiposity (regional –> neck crest, lumbar fat pads)
  2. insulin resistance
  3. laminitis
  4. altered E metabolism, adipocyte function, promote thrombosis, induce inflammation and oxidant stress, alter vascular endothelial cell function
29
Q

how do you differentiate PPID from EMS

A
  1. age of onset (EMS –> younger)
  2. further clinical signs suggestive of PPID (delayed/failed coat shedding, hirsutism, excessive sweating, PUPD, skeletal muscle atrophy)
  3. positive diagnositc test for PPID (increased plasma ACTH without pain, stress)
30
Q

what is adrenal cortical hypofunction

A

Addison’s disease

31
Q

what does addison’s disease cause

A

adrenal cortical atrophy (idiopathic, any damage –> infectious, vascular, drug induced) or secondary to pituitary hypofunction

32
Q

what is the pathogenesis of adrenal cortex hypofunction

A
33
Q

what is adrenocrotical hemorrhage

A

waterhouse friderichsen syndrome

horses

massive, diffuse often bilateral hemorrhage in overwhelming sepsis

34
Q

how is PPID diagnosed

A

increased plasma ACTH without pain, stress

Module 12 (8 decks)

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