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VET433: Renal, Endocrine, Urinary > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

(71 cards)

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1
Q

what area of the adrenal cortex produces the mineralocorticoids

A

zona glomerulosa

(outermost)

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2
Q

what area of the adrenal cortex produces the glucocorticoids

A

zona fasciculata

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3
Q

what area of the adrenal cortex produces catecholamines

A

zona reticularis

(innermost)

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4
Q

pituitary adrenal axis

A
  1. hypothalamus –> CRH
  2. anterior pituitary –> ACTH
  3. adrenal cortex –> cortisol
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5
Q

functions of cortisol

A

regulate metabolism, blood sugar, lipids, mucosa health, immune function

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6
Q

functions of the RAAS system

A

renin angiotensin aldosterone system

responds to LOW blood pressure

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7
Q

steps of RAAS activation

A
  1. low BP detected by JGA in kidneys –> kidneys release renin
  2. renin converts angiotensinogen (produced in the liver) into angiotensin I (ANG I)
  3. ACE gets released from the lungs and circulates –> converts circulating ANG I into ANG II
  4. ANG II stimulates release of aldosterone from the adrenal gland
  5. aldosterone acts on the kidneys to stimulate Na and water reabsorption to increase BP
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8
Q

function of aldosterone

A

maintain blood volume by retaining Na and excreting K to increase water reabsorption

stimulated by low BP and high K

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9
Q

primary addison’s disease

A

adrenal glands don’t produce hormones due to:

  • immune mediated destruction
  • drug induced destruction
  • bilateral adrenalectomy
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10
Q

typical primary addison’s

A

destruction of both the zona glomerulosa and fasciculata

low cortisol & low aldosterone

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11
Q

atypical primary addison’s

A

destruction of the zona fasciculata ONLY

low cortisol & normal aldosterone

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12
Q

what is the expected ACTH level of a dog with primary addison’s

A

HIGH - trying to stimulate the adrenals

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13
Q

secondary addison’s

A

anterior pituitary does not produce ACTH due to:

  • exogenous steroid administration
  • hypopituitarisum (surgical removal)
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14
Q

cortisol and aldosterone levels in secondary addison’s

A

low cortisol & normal aldosterone

presents similarly as atypical primary addison’s

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15
Q

what is the expected ACTH level in a dog with secondary addison’s

A

LOW - either the pituitary is unable to produce ACTH OR it is receiving negative feedback from exogenous steroid administration

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16
Q

what type of addison’s disease is susceptible to developing addisonian crisis

A

primary typical addison’s only due to aldosterone deficiency leading to hypovolemic shock and severe electrolyte imbalance

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17
Q

what is the Na:K ratio of a patient with confirmed addison’s

A

Na:K < 27:1
hyponatremia
hyperkalemia

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18
Q

how does prerenal azotemia and hyperphosphatemia develop in addisonians

A

unable to maintain hydration –> prerenal azotemia

decreased GFR –> decreased P clearance in the kidneys –> hyperphosphatemia

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19
Q

normal resting cortisol

A

> 2.0 ug/dL

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20
Q

resting cortisol in a patient that should get an ACTH stim test

A

< 2.0 ug/dL

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21
Q

what cortisol level following ACTH stimulation if confirmatory for addison’s disease

A

< 2.0 ug/dL

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22
Q

what type of addisonians require DOCP injections monthly

A

primary typical HA

DOCP = synthetic mineralocorticoid
only needs to be replaced in aldosterone deficient patients

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23
Q

where is insulin produced

A

beta cells in islets of langerhans in the pancreas

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24
Q

functions of insulin

A

lower blood glucose by:
- promote glucose uptake by muscle and adipose cells via GLUT4
- promote glycogenesis in liver and muscles to store glucose
- inhibit gluconeogenesis in the liver
- facilitate amino acid uptake in muscles
- promote synthesis of triglycerides and inhibits lipolysis in adipose
- binds IGF-1 to promote growth

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25
what are factors that decrease BG
insulin and exercise inhibit glucagon --> low glucagon state --> inhibits gluconeogenesis + glycogenolysis
26
what are the diabetogenic hormones
hormones that oppose the effects of insulin - cortisol - glucagon - epinephrine - growth hormone all contribute to developing insulin resistance by stimulating gluconeogenesis + glycogenolysis
27
pathogenesis of weight loss and polyphagia in diabetes
1. glucose accumulates in plasma despite low glucose in cells due to insulin deficiency/resistance 2. cells starve and require alternate energy pathways 3. breakdown of muscle and fat to feed the cells 4. weight loss + polyphagia
28
pathogenesis of glucosuria and PU/PD in diabetes
once blood glucose exceeds the renal threshold --> glucosuria --> glucose in the urine triggers PU --> triggers PD to try to keep up with urination
29
what are the general management strategies of diabetes in cats
diet + weight loss management in order to reduce insulin requirement SGLT-2 inhibitors
30
how does exogenous corticosteroid administration in cats predispose to diabetes
cats on prednisolone --> increase cortisol --> counteracts insulin --> insulin resistance ALWAYS monitor blood glucose levels in cats on prednisolone
31
hypersomatotropism
excess growth hormone resulting in acromegaly in cats increased GH causes insulin resistance and development of diabetes mellitus
32
what is used to diagnose hypersomatotropism in cats
IGF-1 (acts as a proxy for growth hormone) ALL diabetic cats should be tested for hypersomatotropism
33
what is the most common cause of a stable diabetic dog developing DKA
inflammation (ex. development of pancreatitis)
34
what is the renal threshold for glucose in dogs
180 mg/dL can be hyperglycemic WITHOUT glucosuria
35
what is the renal threshold for glucose in cats
270 mg/dL can be hyperglycemic WITHOUT glucosuria
36
what other biochemical changes can be seen on a chem panel in a patient with DM
- elevated liver enzymes - hyperlipidemia (cholesterol + triglycerides) - prerenal azotemia - electrolyte imbalance
37
what are the most consistent formulations of exogenous insulin
pens + solutions
38
mL per unit in U40 syringe
0.025 mL
39
mL per unit in U100 syringe
0.01 mL
40
best insulin options for dogs
BID administration: - vetsulin - novolin SID administration: - tresiba (degludec) - toujeo (glargine)
41
best insulin options for cats
BID: - prozinc SID: - lantus - toujeo
42
what are the MOAs of oral antihyperglycemics
1. promote insulin secretion 2. increase insulin sensitivity 3. decrease glucose absorption from GIT 4. promote glucosuria
43
SGLT2
sodium glucose transporter located in the renal proximal tubule to reabsorb glucose from the urine
44
SGLT2 inhibitors
blocks SGLT2 to decrease glucose reabsorption and. promote excretion
45
is there a risk of a cat becoming hypoglycemic on SGLT2 inhibitors
no - does not block SGLT-1 receptors so there will still be some glucose absorption
46
effect of SGLT2 inhibitors on BG and glucosuria
increases glucosuria by lowering the renal threshold causes a RAPID drop in BG and transient increase in polyuria
47
when should SGLT2 inhibitors be used
insulin resistant diabetes ONLY must have endogenous insulin to prevent ketosis
48
what should always be monitored at home in a patient on SGLT2 inhibitors
serum or urine ketones if a cat becomes insulin deficient while on the medication - will cause ketosis if ketones are elevated - discontinue SGLT2 inhibitor and use insulin instead
49
forms of SGLT2 inhibitors available in vet med
bexacat + senvelgo used in place of insulin for UNCOMPLICATED, insulin resistant cats with risk factors NOT for use in cats that are on exogenous insulin
50
most important indicators of diabetes management to monitor
clinical signs (want to resolve) weight trends (stabilize)
51
what do continuous glucose monitors sample
interstitial glucose slightly delayed behind changes in blood glucose
52
goal BG for adequate DM management
BG 100-200 mg/dL nadir: low 100s highest: remains below 300
53
why are cats less likely to develop DKA
cats should have some insulin production that prevents the development of ketones dogs are insulin deficient - more likely to start producing ketones due to cell reliance on alternate metabolic pathways
54
what is the goal of nutritional diabetes management
improve glycemic control does NOT eliminate the need for insulin therapy
55
goal of nutritional DM management in dogs
provide the same AMOUNT of the same DIET at the same TIME every day always coordinate with insulin administration avoid treats if possible
56
is there a need to change diet in dogs with DM
no - as long as the patient eats the diet well, do not need to change exceptions: 1. fat intolerance (pancreatitis) 2. nutritionally responsive comorbidities can add fiber if regulation is poor
57
is obesity related insulin resistance reversible in cats
yes with weight loss - not necessarily diet dependent as long as they lose weight
58
goal of nutritional management of cats with diabetes
weight loss and stabilization overweight cats - low carb + canned diets lean cats - moderate carb + high fiber + dry diets consistent timing is less important than in dogs
59
hyperlipidemia nutritional management
fat restriction - want a diet that is HALF the amount of fat on an ME basis than current diet goal is fasted serum TG < 500 mg/dL
60
is the majority of calcium intra or extracellular
extracellular w/ 0.1% being in the ECF
61
what does total Ca measure
all calcium in the ECF ionized > protein bound > complex bound
62
what is the most reliable measure of calcium levels
ionized Ca
63
what hormones regulate Ca
1. PTH 2. vitamin D 3. calcitonin 4. FGF-23
64
what is the primary source of Ca and P in the body
dietary intake
65
does calcitonin have an important role in Ca metabolism in CKD catsq
no
66
how can FGF-23 be used in CKD cats
early biomarker of CKD - level of elevation can guide the need for phosphate restriction or binders
67
most common causes of hypercalcemia in cats
renal disease idiopathic neoplasia
68
how does granulomatous disease cause hypercalcemia
macrophages secrete 1-alpha hydroxylase --> activates vitamin D into calcitriol in the kidneys --> increased active vitamin D --> increases Ca
69
hypercalcemia of malignancy
cancer cells secrete parathyroid hormone related protein (PTHrP) --> activates PTH receptors --> increases Ca, decreases P
70
what types of cancer are most commonly associated with hypercalcemia of malignancy
lymphoma AGASACA multiple myeloma SCC (cats)
71
idiopathic hypercalcemia
mild to moderate elevations in ionized and total Ca in young to middle aged cats usually incidentally found but can cause vomiting, weight loss, constipation tx w/ high fiber diet, corticosteroids if clinical

VET433: Renal, Endocrine, Urinary (20 decks)

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