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Endocrine > Midterm--Hyper, Hypo, Pathology > Flashcards

Midterm--Hyper, Hypo, Pathology Flashcards

1
Q

The 5 S’s of endocrine organ function (what are the 5 functions)

A 
sense
synthesize
store
secrete
signal
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2
Q

The only reliable indicator of malignancy?

A

Vascular invasion

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3
Q

4 potential causes for DIFFUSE atrophy of a gland?

A

excess circulating hormone
decreased stimulatory substance
autoimmune or toxic destruction
defective receptors

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4
Q

Which portion of the pituitary is responsible for most of the hormone secretion?

A

Pars distalis

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5
Q

Secondary lesions of stunted growth and retention of juvenial hair coat in a GSD might be related to?

A

Cystic Rathke’s pouch

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6
Q

A functional adenoma in the pars distalis would secrete which hormone?

Dogs

A

ACTH

this is PDH

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7
Q

Epidermal atrophy, flank alopecia, and calcinosis cutis would occur secondary to elevations in which hormone?

A

Cortisol

**Cortisol is high due to excessive ACTH secretion–>bilateral, diffuse, adrenal hypertrophy (HAC)

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8
Q

Adenomas of the pars INTERMEDIA are more common in which spp.? If functional, what do they secrete?

A 
Horses
secrete propiomelanocortin (POMC)

*can compress hypothalamus

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9
Q

How do adenomas of the pars distalis differ in cats?

A

they secrete GROWTH HORMONE

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10
Q

Excessive growth hormone in cats is related to?

3 features, 1 pathology

A

Features:
coarse facial features, increased bone growth, enlarged viscera

pathology:
insulin-resistant DM

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11
Q

Name the 3 layers of the adrenal glands and the main product of each

A

Glomerulosa–mineralocorticoids

Fasiculata–glucocorticoids

Reticularis–sex hormones

Salty, steroid, Sex

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12
Q

How can you know if a cortical adenoma is functional?

A

if the contralateral gland is atrophied

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13
Q

Functional pheochromocytomas secrete?

what two pathologic findings would be associated with it?

A

Catecholamines

1) cardiac hypertrophy
2) arteriosclerosis (related to hypertension)

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14
Q

Most common lesion in dogs diagnosed with Addison’s?

A

Idiopathic adrenal cortical atrophy

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15
Q

Due to ________ _______ tissue, follicular cell carcinomas can occur anywhere along the ventral neck (as well as in the heart)

A

ectopic thyroid tissue

*Associated with “cannonball” pulmonary mets

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16
Q

Which thyroid tumor is commonly associated with bulls fed high-calcium diets?

A

C-cell tumors

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17
Q

Finding infiltrates of lymphocytes and plasma cells in the thryoid could be indicative of?

A

Lymphocytic thyroiditis

**leads to hypothyroidism

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18
Q

Dermatologic changes and presence of atherosclerosis are pathologies associated with?

A

Hypothyroidism (no matter etiology)

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19
Q

If you find diffuse hyperplasia of the parathyroid gland, what abnormality would you expect on bloodwork?

A

low Ca levels

**ALL glands affected!!

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20
Q

Which pathologic finding is associated with hyperparathyroidism (regardless of etiology)?

A

Fibrous osteodystrophy

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21
Q

What are the 3 types of islet cell tumors that occur in the pancreas

A

insulinoma
gastrinoma
glucagonoma

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22
Q

Which pancreatic pathology is associated with uncontrolled vomiting and gastric ulceration?

A

Gastrinoma

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23
Q

Islet amyloidosis is commonly seen in which spp. with what type of disease?

A

Cats with type 2 diabetes

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24
Q

Which breed is predisposed to Chemodectomas (aortic body tumors)

A

Brachycephalics

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25
Q

What abnormality might you seen in a horse with periorbital paraganglioma?

A

Exopthalmos

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26
Q

How does the HPA axis differ in horses?

A

hypothalamus releases dopamine which acts on the pituitary’s INTERMEDIATE lobe to INHIBIT ACTH secretion

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27
Q

If you’re playing the odds with HAC (based on the 85, 15 rules):

1) where the tumor’s most likely location
2) likelihood it’s malignant
3) tumor’s likely size

A

1) anterior pituitary
2) unlikely (99% benign)
3) MICROadenoma

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28
Q

Typical signalment for a dog with HAC?

How does it differ with PDH vs. AT?

A

older (>7yr)

PDH= small dogs, both male and female

AT= large dogs; females slightly more likely

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29
Q

The 5 P’s (clinical signs) associated with HAC

A

PU, PD, polyphagia, potbelly appearance, panting

30
Q

Which clinical sign of cushing’s is more severe in cats?

A

thin skin–can develop spontaneous tears

31
Q

Though not commonly found, which dermatological manifestation of cushing’s would be pathognomonic?

A

Calcinosis cutis

32
Q

Dogs with HAC are typically polyphagic, if the dog is anorexic, they most likely have which form?

A

pituitary MACROadenoma

also see neuro signs and blindness

33
Q

More common labwork abnormality assoc. with dogs that have HAC?

A

elevated ALP

**corticosteroid induced ALP isoenzyme

34
Q

What are the two broad categories of tests we using for diagnosing cushing’s and which specific tests fall under each category?

A

1) Screening tests
- -UUCR, LDDST, ACTH stim

2) Differentiation tests
- -HDDST, Endogenous ACTH, U/S

35
Q

Concerning UCCR

1) what does it stand for
2) what is its primary use
3) what is its sensitivity and specificity

A

1) Urine cortisol : creatinine ratio
2) used to RULE OUT cushing’s (dog with a normal ratio is very unlikely to have HAC)
3) 75-95% sensitive; only 20% specific

36
Q

What sample do you primarily use when interpreting LDDST? What are you looking for?

A

8hr sample

If > 30nmol/L at 8hr, consistent with HAC

37
Q

Name 3 criteria that if present with LDDST would be consistent with PDH

A

1) suppression (< 30) at 4hr
2) 4hr < 50% baseline
3) 8hr < 50% baseline

*if none of these are present, still 50/50 chance btwn AT and PDH

38
Q

Two advantages of ACTH stim

A

1) good test if the dog has a non-adrenal illness

2) only test to prove iatrogenic cushing’s

39
Q

With ACTH stim, what type of response do we expect with:

1) AT or PDH
2) iatrogenic disease

A

1) expect a greater than normal response of cortisol secretion
2) expect cortisol to be low in the beginning and low on second sample

40
Q

Concerning ACTH:

1) can you differentiate btwn PDH and AT
2) sensitivity and specificity

A

1) NO!!! Both show greater than normal release of cortisol

2) 85% for both

41
Q

With HDDST, what responses would be consistent with PDH?

If none are met, what are chances it’s PDH?

A

1) complete suppression at 8hr
2) complete suppression at 4hr
3) <50% of baseline at 4hr
4) <50% baseline at 8hr

*If none present, 50/50 chance btwn AT & PDH

42
Q

Though endogenous ACTH is great for differentiating, what is it’s major drawback?

A

requires intense special handling of sample

43
Q

Treatment of choice for AT?

A

Surgery

44
Q

What are our two drug options for tx of cushing’s?

A

Mitotane

Trilostane

45
Q

MOA of:

1) Mitotane
2) Trilostane

A

1) destroys zona fasiculata and reticularis

2) competitively inhibits 3-beta-hydroxysteroid dehydrogenase (inhibits steroid synthesis)

46
Q

How does dosing differ btwn Triolostane and Mitotane

A

Mitotane has both a loading and induction phase; loading is BID; maintenance is 2-3x per week

Triolostane is ALWAYS given BID

47
Q

Both Mitotane and Trilostane are monitored with which test? How do they differ in timing?

A

ACTH stim

Trilostane—MUST be tested 4-6hr after pill is given

Mitotane can test any time

48
Q

When treating PDH, where do we want cortisol levels to be?

A

30-150 pre AND post ACTH

**we want below normal to manage clinical signs

49
Q

4 side effects of HAC treatment

A

1) cortisol deficiency (can see GI signs)
2) aldosterone deficiency (hypoNa/hyperK)
3) direct GI toxicity
4) Direct neurotoxicity (MITOTANE ONLY!!!)

50
Q

L-deprenyl is specifically used to treat which type of HAC?

A

PDH with tumor in intermediate lobe

**prevents dopamine breakdown by inhibiting MAOB–>antagonizes ACTH secretion from IL

51
Q

Hyperaldosteronism

1) most common in which spp.
2) predominantly benign or malignant
3) typical age of onset

A

1) CATS
2) malignant (75%)
3) avg. 11 (older cats)

52
Q

What are the two main functions of aldosterone

A

1) regulation of Na & K (Saves Na, gets rid of K)

2) raises blood pressure

53
Q

2 general types of clinical signs expected with aldosterone excess

A

1) polymyopathies (due to low K)

2) ocular signs (due to high BP)

54
Q

Aldosterone excess can cause azotemia, so how would the labwork be different from renal failure?

A

phosphorous is normal

55
Q

Two ways to raise K levels with hyperaldosteronism

A

K supplementation

Spironolactone (aldosterone antagonsit)

56
Q

Hypoadrenocorticism is ALWAYS defined by _______ and SOMETIMES includes ________

A

cortisol deficiency (ALWAYS)

Aldosterone deficiency (Sometimes—typical)

57
Q

What are the forms of Addison’s disease?

A

Primary–adrenals are issue
Secondary–pituitary is issue

Typical–aldosterone affected (HypoNa/hyperK)
Atypical–aldosterone normal

58
Q

Typical signalment for Addison’s?

A

Younger to middle-aged (6m-9yr)

females slightly more likely

59
Q

Name the 4 breeds that have a PROVEN genetic predisposition for Addion’s

A

Bearded collie
standard poodle
nova scotia DTR
Portuguese water dog

60
Q

100% of Addisonian patients present with at least what type of signs?

A

GI signs (anorexia, V/D)

61
Q

If you see which two clinical signs, you should always include addison’s on your list?

A

Sudden shock (for no apparent reason)

Severe GI hemorrhage

62
Q

What physical exam finding would be a red flag & make you think addison’s?

A

Bradycardia (in the face of stress and dehydration)

63
Q

If you see any of these 5 things, Addison’s should be on your differential list

A 
Severe GI hemorrhage
Megaesophagus
Hypoalbuminemia
Hypoglycemia
"Renal failure"

EVEN if Na/K are NORMAL

64
Q

Which test is required for diagnosis of hypoadrenocorticism?

A

ACTH stim

**dogs will have low pre and post samples

65
Q

How is baseline cortisol used in diagnosing Addison’s?

A

Used to RULE OUT the disease

If baseline is >55 it’s not addison’s

66
Q

How is endogenous ACTH test used? For which form of disease do we use it?

A

ONLY for Atypical disease

  • if ACTH is high–primary dz
  • if ACTH low–pituitary dz
67
Q

Why do we care about the results of endogenous ACTH?

A

because if it’s primary atypical disease, it can progress to typical

68
Q

Two treatment options to replace deficient mineralocorticoids?

A 
Fludrocortisone (Florinef)
Desoxycorticosterone pivalate (DOCP)
69
Q

How do Florinef and DOCP differ in their GC content?

A

Florinef–has SOME GC activity; about 50% of patients will require additional prednisone

DOCP–has NO GC activity; ALL patients on this will also need prednisone

70
Q

4 steps in addressing a hypoadrenal crisis

A

1) correct hypotension & hypovolemia (fluids)
2) provide glucocorticoids
3) correct electrolyte abnormalities
4) correct acidosis (not always necessary)

71
Q

When providing glucocorticoids during a hypoadrenal crisis, which ones do you want to avoid and why?

A

Prednisone/prednisolone

will interfere with ACTH stim if you try to run it within 12hr

72
Q

What are your 3 options for correcting electrolyte abnormalities with hypoadrenal crisis? Give brief MOA

A

1) Fluids
2) insulin & glucose (insulin drives K into cells; glucose prevents concurrent hypoglycemia)
3) Ca gluconate (protects heart from high K concentrations…doesn’t alter [K])

Endocrine (5 decks)

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