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RUSVM Pathology II 2016 > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

Primary

A

Decreased cellular activity (hypo) or increased cellular activity (hyper) of the endocrine gland

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2
Q

Secondary

A

A lesion of another organ leads to decreased (hypo) or increased (hyper) cellular activity of the endocrine gland

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3
Q

What are the clinical signs for Hyperadrenocorticism?

A 
Bilaterally symmetrical Alopecia 
Polyphagia 
PU/PD
Pot belly 
Stinks
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4
Q

What hormone is over produced in hyperadrenocorticism?

A

Cortisol

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5
Q

What is the morphological diagnosis of hyperadrenocorticism?

A

Adrenal cortical Adenoma/Adenocarcinoma

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6
Q

What are the characteristics of the liver with hyperadrenocorticism?

A

Soft to the touch
Swollen margins
Tan color
Greasy tinge

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7
Q

What is the morphological diagnosis for the histopathology of the liver with hyperadrenocorticism?

A

Vacuolar hepatocellular degeneration

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8
Q

What is the common name for hyperadrenocorticism?

A

Canine Cushings

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9
Q

What are the two types of Hyperadrenocorticism?

A

Primary

Secondary

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10
Q

What is primary hyperadrenocorticism?

A

Adenoma or carcinoma of the zona fasciculata

Not all adrenocortical tumors are “productive” and associated with Hyperadrenocorticism

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11
Q

What is secondary hyperadrenocorticism?

A

Adrenal cortical hyperplasia (due to ACTH secreting pituitary adenoma)
Most arise from the pars distalis
Majority are “productive”

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12
Q

Where is lesion for secondary Hyeradrenocorticism located?

A

Pars distalis

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13
Q

Where is the lesion for primary hyperadrenocorticism located?

A

Zona fasciculata

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14
Q

What lesion of the skin is associated with hyperadrenocorticism?

A

Calcinosis cutis

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15
Q

If the other adrenal gland is enlarged then what does the other adrenal glad look like in hyperadrenocorticism?

A

Atrophied

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16
Q

Why does the other adrenal gland appear atrophied when the partner is enlarged?

A

the cortex is receiving the message that there is enough cortisol in the body due to the decrease in ACTH production in response to the message received from the adenocarcinoma

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17
Q

What will the animal’s response to stress be like if the adrenocarcinoma is removed?

A

Very little tolerance

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18
Q

What other lesions would lead to hyperadrenocorticism?

A

Adrenocortical hyperplasia

Pituitary Adenoma

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19
Q

What is the common name for Pituitary Pars Intermedia Dysfunction?

A

Equine Cushings

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20
Q

What are the clinical signs of Equine Cushings?

A 
Hirsuitism 
PU/PD
Polyphagia 
Hyperhidrosis 
Insulin Resistance 
Abnormal fat deposition
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21
Q

Hirsuitism

A

failure to shed

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22
Q

Why is Equine Cushings different from Canine Cushings

A

Non-productive adenoma - not secreting ACTH

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23
Q

What decrease in which hormones would we expect to see in an animal with a cyst instead of a pituitary gland and what disorders?

A

ACTH - Hypoadrenocorticism
Thyroid - Hypothyroid
LH and FSH - Not reproductively active
GnRH - Dwarfism

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24
Q

Iatrogenic Cushing’s Disease

A

Caused by excessive exogenous steroid administration

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25
Q

What is the morphological diagnosis for Iatrogenic Cushing’s Disease?

A

Adrenocortical Atrophy

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26
Q

What is the pathogenesis of Iatrogenic Cushings Disease?

A

increased ACTH administration over a long period of time and negative feedback caused a decrease in ACTH production and Cortisol production from the adrenal glands

27
Q

If you withdrawal too fast from exogenous ACTH administration what disease will occur?

A

Atrophic Adrenocorticism (Addison’s Disease)

28
Q

What is primary hypoadrenocorticism?

A

immune mediated lymphocytic adrenalitis

29
Q

What hormones are deficient in primary hypoadrenocorticism?

A

Cortisol and Aldosterone

30
Q

What hormone is deficient in secondary hypoadrenocorticism?

A

Cortisol

31
Q

What are the two causes of secondary hypoadrenocorticism?

A

Idiopathic loss of anterior pituitary stimulus

Iatrogenic (long term steroid withdrawal)

32
Q

Ferret Adrenal neoplasm results in what?

A

Hyperestrogenism

33
Q

What is the gross morphological diagnosis for “Goiter”?

A

Bilateral Thyroid Hyperplasia

34
Q

What is the pathogenesis for Thyroid Hyperplasia?

A

Overproduction of TSH causing Thyroid to proliferate to compensate –> no negative feedback from T4 –> more TSH

35
Q

What are the four reasons for a decrease in T4?

A

Iodine deficient diet
Goitrogenic substances interfering with T4 production
Congenital dyshormonogenic goiter
Excess dietary iodine

36
Q

What plants contain Goitrogenic substances?

A

Brassica plants - Cabbage family

37
Q

Congenital dyshormonogenic goiter

A

defects in the enzymes that make thyroglobulin

38
Q

What other clinical sign can result from Hypothyroid?

A

Hypotrichosis

39
Q

What are the clinical signs for hypothyroidism?

A

Gain in body weight without change in appetite
Bilatterally symmetrical alopecia, scaly skin
In severe cases: Atherosclerosis and Myxedema

40
Q

What are two typical lesions causing canine hypothyroidism?

A

Lymphocytic Thyroiditis

Thyroid atrophy

41
Q

What disorder results from Nodular “adenomatous” thyroid hyperplasia?

A

Hyperthyroidism

42
Q

Are thyroid neoplasms in dogs benign or malignant?

A

Malignant and nonproductive

43
Q

Are thyroid neoplasms in cats benign or malignant?

A

Benign and productive

44
Q

Clinical Signs: Fibrous Osteodystrophy
Renal Failure
Kidney cortex is white and gritty on cut surface
Bilateral nodules on parathyroid gland

A

Parathyroid hyperplasia

45
Q

What are the two causes of Secondary hyperparathyroidism?

A

Nutritional Imbalance

Renal Disease

46
Q

What are the Nutritional cause of Hyperparathyroidism?

A 
High Phosphorus/Low calcium 
Hypovitaminosis D (Dietary or uv exposure)
47
Q

What are the Renal Disease causes of Hyperparathyroidism?

A

High Phosphorus

Decreased Vitamin D

48
Q

What is the cause of pseudoparathyroidism?

A

Neoplasm (Anal sac or Lymphoma) secreting Parathyroid hormone

49
Q

What causes Primary hyperparathyroidism?

A

Parathyroid Adenoma

50
Q

Pathogenesis of Primary Hyperparathyroidism?

A

Hypercalcemia of malignancy (paraneoplastic syndrome)

51
Q

What is another name for Pancreatic Islet cell carcinoma/adenoma?

A

Insulinoma

52
Q

What is an associated lesion with an Insulinoma?

A

Acute Cerebral cortical necrosis

53
Q

Are most Insulinomas benign or malignant?

A

Malignant

54
Q

What is a clinical sign of an insulinoma?

A

Weakness or periodic collapse

55
Q

What is the clinical syndrome of hypoinsulinism?

A

Diabetes Mellitus

56
Q

What are the two causes of hypoinsulinism?

A

Decrease in insulin

Insulin Resistance

57
Q

What are the clinical signs of hypoinsulinism?

A

Polyphagia
PU/PD
Weight loss

58
Q

What lesions cause Diabetes Mellitus?

A

Beta Cell degeneration
Beta Cell amyloidosis
Isletitis
Chronic pancreatitis

59
Q

What is the pathogenesis of Diabetes Mellitus due to Insulin Resistance?

A

Insulin resistance –> hyperglycemia –> long term intracellular accumulation of glycogen within beta cells –> vacuolar degeneration of beta cells –> insulin deficiency and diabetes mellitus

60
Q

What is the pathogenesis of Diabetes Mellitus due to Pancreatic islet cell amyloidosis?

A

Insulin antagonism –> hyperglycemia –> long term overstimulation of Beta cells –> Beta cells produce IAPP (islet amyloid polypeptide) along with insulin –> IAPP polymerizes to form amyloid –> crowding of islet cells –> islet cell atrophy –> insulin deficiency and more severe diabetes mellitus

61
Q

What are the associated lesions with Diabetes Mellitus?

A

Cataracts
Microangiopathy
Hepatic lipidosis

62
Q

What organs are affected by Microangiopathy?

A

Kidneys
Retina
Appendages

63
Q

What is the pathogenesis of diabetic nephropathy?

A

Chronic hyperglycemia –> formation of glycosylated proteins –> deposition into capillary basement membranes –> thickened basement membranes

64
Q

What is the pathogenesis of cataracts?

A

Excessive glucose is taken up by epithelium of the lens (no insulin required) –> metabolized to sorbitol by aldose reductase –> sorbitol osmotically draws water into the lens –> cataract formation

RUSVM Pathology II 2016 (11 decks)

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