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From Flashcardlet > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Ketone bodies are synthesized from

A

acetyl-CoA (product of mitochondrial beta-oxidation of FAs)

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2
Q

Synthesis of acetyl-CoA is facilitated by…

A

decreased insulin concentrations

increased glucagon concentration

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3
Q

What are the anabolic effects of insulin?

A

conversion of glucose to glycogen
AA to protein
storage of FAs in adipose tissues

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4
Q

What are the catabolic effects of glucagon?

A

glycogenolysis, proteolysis, lipolysis

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5
Q

Where does the Kreb’s cycle occur?

A

inner matrix of mitchondria

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6
Q

Where does pyruvate come from?

A

glycolysis

pyruvate –> acetylCoA –> Kreb’s cycle

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7
Q

What is sent from the Kreb’s cycle to the electron transport chain?

A

NADH and FADH2

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8
Q

What happens in diabetics with respect to citric acid cycle?

A

glucose does not enter cells in adequate amounts, production of pyruvate by glycolysis decreased, citric acid cycle diminished, decreased utilization of acetylCoA

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9
Q

What are the 3 ketone bodies?

A

beta-hydroxybutyrate, acetoacetate, acetone

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10
Q

Where are ketone bodies made?

A

liver

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11
Q

What are the most common concurrent dzs with DKA in dogs?

A

acute panc, UTI, Cushings

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12
Q

What are most common concurrent dzs with DKA in cats?

A

HL, CKD, acute panc, bacterial/viral infections, cancer

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13
Q

Degree of Heinz body formation is correlated with what in cats (DKA)?

A

plasma BHB

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14
Q

What is pseudohyponatremia?

A

Decrease of 1 mEq/L in sodium per 62 mg/dL increase in glucose concentration

or

Decrease of 1.6 mEq/L for every 100 mg/dL increase in glucose

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15
Q

Ketone stick has what activator?

A

nitroprusside

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16
Q

Which ketone is not measured on urine dipstick?

A

BHB (which is usually the highest ketone in circulation)

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17
Q

DDx for ketosis.

A

DKA, acute panc, starvation, low carb diet, persistent hypoglycemia, persistent fever, pregnancy

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18
Q

American Diabetes Association recommends bicarb supplementation if…

A

pH < 7.0 after 1 hr of fluids

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19
Q

Risks of bicarb tx in DKAs.

A

exacerbation of hypokalemia, increased hepatic production of ketones, paradoxical cerebrospinal fluid acidosis, cerebral edema, worsening intracellular acidosis d/t increased pr0d’n of CO2

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20
Q

Dogs with what dz in conjunction with DKA are less likely to be discharged?

A

Cushings

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21
Q

Define HHS

A

Severe hyperglycemia (>600), minimal or absent urine ketones, serum osmolality more than 350 mOsm/kg

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22
Q

Insulin couterregulatory hormones.

A

Epinephrine, cortisol, glucagon, growth hormone

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23
Q

Formula for serum osmolality

A

2(Na +K) + (glu/18) + (BUN/2.8)

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24
Q

Formula for effective osmolality

A

2(Na) + (glu/18)

BUN removed b/c equilibrates readily across cell membranes

Glucose becomes an effective osmole b/c no insulin!!

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25
Q

In HHS, metabolic acidosis is due to ketones. T/F

A

F - these patients are non-ketotic!! Acidosis d/t uremia and lactic acidosis

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26
Q

What is the formula for corrected sodium with hyperglycemia?

A

Na (measured) + 1.6[(measured glu - normal glu)/100]

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27
Q

What is max rate to decrease sodium with chronic hypernatremia?

A

0.5 to 1 mEq/L/hr

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28
Q

What is the goal to decrease glucose by when treating HHS or DKA?

A

Decrase glucose by no more than 75 mg/dl/hr

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29
Q

3 sources of glucose in the body

A
  1. intestinal absorption of carbs
  2. breakdown of glycogen (glycogenolysis)
  3. production from precursors (lactate, pyruvate, AA, glycerol)
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30
Q

Insulin secreted from what cells?

A

beta cells in panc

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31
Q

Insulin secreted in response to…

A

rising concentration glucose, AA, or GI hormones (gastrin, secretin, cholecystokinin, gastric inhibitory peptide)

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32
Q

Effects of insulin

A
  1. inhibits gluconeogenesis and glycogenolysis
  2. promotes glycogen storage
  3. stimulates glucose uptake utilization by insulin-sensitive cells
  4. decreases glucagon secretion
  5. promotes triglyceride formation in adipose tissue
  6. promotes synthesis of protein and glycogen in muscle
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33
Q

Where is glucagon secreted from?

A

alpha cells of panc

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34
Q

Whipple’s triad for hypoglycemia.

A

clinical signs consistent, low measured level, resolution of signs with correction

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35
Q

T/F. Hand-held glucometers tend to overestimate glucose.

A

F - underestimate

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36
Q

What will arrest glycosis of RBC?

A

sodium fluoride

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37
Q

If insulin levels are equivocal, how do you calculate the amended inulin:glucose (AIGR) and how do you interpret?

A

AIGR = (100xinsulin) / (glucose-30)

If over 30, suggests insulinoma

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38
Q

Causes of hypoglycemia d/t artifact

A

pseudohypoglycemia

hand-held glucometer

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39
Q

Causes of hypoglycemia d/t excess insulin or insulin analogues.

A

overdose
insulinoma
paraneoplastic (hepatoma/carcinoma, leiomyoma/sarcoma, pulm, salivary, mammary carcinoma, lymphoma, plasmacytoid tumors, melanoma, HSA)
toxins (sulfonylureas)

40
Q

Causes of hypoglycemia d/t excess glucose utilization

A 
infection (sepsis, babesia)
hunting dog hypoglycemia
paraneoplastic
polycythemia
leukocytosis
pregnancy
41
Q

Causes of hypoglycemia d/t decreased glucose prod’n

A

Neonatal
Liver (PSS, hepatitis, HL, cirrhosis, cancer, glycogen storage)
Addisons
Coutnerregulatory hormone deficiency
Glygenic or gluconeogenic enzyme deficiency
Beta-blockers

42
Q

Diazoxide MOA

A

directly inhibits pancreatic insulin secretion

43
Q

streptozocin MOA

A

selectively destroys pancreatic beta cells

44
Q

octreotide MOA

A

suppress synthesis and secretion of insulin

45
Q

alloxan MOA

A

beta cell cytotoxin

46
Q

List 2 oral glucose lowering sulfonylurea drugs

A

chlorpropamide

glipizide

47
Q

How do sulfonylureas work?

A

stimulate insulin secretion from pancreas, enhance tissue sensitivity to insulin, decrease basal hepatic glucose production

48
Q

How much loss of fxnal liver tissue for hypoglycemia to occur?

A

70%

49
Q

MOA hypoglycemia in Addisons

A

loss of cortisol induced couterregulatory mechanisms

50
Q

T/F. Hypoglycemia is a poor prognostic indicator in babesiosis

A

T

51
Q

Common causes of primary DI

A

central DI, trauma and intracranial dz

52
Q

Common causes of secondary nephrogenic DI

A

hypercalcemia, gram negative sepsis, severe hypokalemia, pyelonephritis, pyometra, PSS, liver insufficiency, Addisons, hyperthyroidism

53
Q

What is primary NDI

A

congenital dz

54
Q

What is desmopressin?

A

DDAVP - 10 x antiduretic action of arginine vasopressin but 1500 x less vasoconsrictor action. half life 158 min

55
Q

What is SIADH?

A

Excess production of ADH (aka Schwartz-Bartter syndrome)

56
Q

What is the most prominent lab finding in SIADH?

A

Hyponatremia secondary to renal retention of free water and ongoing urinary sodium losses b/t secretion of renin and aldosterone is inhibited by normovolemia

57
Q

Broad categories for causes of SIADH.

A

CNS dz, lung dz, cancer, drugs, pain, nausea, psychological stress

58
Q

CNS dz associated with SIADH.

A

head trauma, hydrocephalus, CVA, brain tumor, meningitis, encephalitis

59
Q

Lung dz associated with SIADH

A

bacterial pneumonia, aspergillosis, lung tomors, PPV, HWD

60
Q

Cancers associated with SIADH

A

pancreatic carcinoma, prostatic carcinoma, thymoma, OSA

61
Q

Drugs associated with SIADH

A

antidepressants, neuroleptics, antineoplastics, NSAIDS, opioids

62
Q

Clinical signs of SIADH

A

nausea, anorexia, vomiting, irritable behavior, confusion, head pressing seizures, cardiac arrhythmias, coma

63
Q

An increased ___ excludes a diagnosis of SIADH

A

BUN

64
Q

demeclolcycline MOA

A

inhibits action of ADH in renal tubules, used to tx SIADH

65
Q

lithium MOA

A

inhibits action of ADH in renal tubules, used to tx SIADH, toxic

66
Q

Potential precipitating eents for feline thyroid storm

A

radioactive iodine therapy, thyroidal or parathyroidal surgery, abrupt w/d of antithyroid meds, stress, nonthyroidal illness, iodinated contrast dyes, iodine compounds, vigorous thyroid palpation

67
Q

methimazole MOA

A

inhibits iodine incorporation into tyrosyl residues of thyroglobulin and thus prevents synthesis of active thyroid hormone

68
Q

iopanoic acid MOA

A

prevents secretion of formed thyroid hormone, blocks peripheral conversion of thyroxine (T4) to triodothyronine (T3), blocking T3 from binding to its receptor, and inhibits thyroid synthesis

69
Q

Why may propanolol be advantageous in treating thyrotoxic cats?

A

nonselective beta blocker and inhibits peripheral conversion of T4 to T3

70
Q

Atenolol MOA

A

selective beta1 adreneragic blockade

71
Q

What breed is at risk of myxedema coma?

A

Rottweiler

72
Q

What do thyroid hormones do in the heart?

A

increase number of beta adrenergic receptors and their affinity to catecholamines, increasing the inotropic and chronotropic effects of catecholamines

73
Q

What is a common concurrent dz with myxedema coma?

A

aspiration pneumonia

74
Q

Most common bloodwork abnormalities with myxedema coma?

A

mild nonregenerative anemia, hypercholesterolemia, lipemia, increased ALP

75
Q

Pheochromocytoma is a tumor of what cell?

A

chromaffin cells of adrenal medula

76
Q

What does tyrosine hydroxylase do?

A

converts tyrosine to dopa, leading to synthesis of more NE

77
Q

alpha-methyl-para-tyrosine MOA

A

competitively inhibits tyrosine hydroxylase interfering with catecholamine biosynthesis

78
Q

Describe the HPA axis.

A

Hypothalamus rleases CRH, which stimulates anterior pituitary to release ACTH, which then stimulates ZF ans ZR of adrenal gland to produce and release cortisol. CRH has neg feedback on hypothalamus and pituiary release of ACTH

79
Q

Delta cortisol less than ___ in septic dogs was associated with nonsurvival.

A
  1. 8 mcg/dl

2. 3 in cats

80
Q

Potency of hydrocortisone.

A

4 times less than prednisone

81
Q

Breeds most commonly affected with hypoadrenocorticism.

A

Portuguese water dog, Great Dane, WHWT, Standard Poodle, Wheaton Terrier, Rottweiler

82
Q

What is secondary hypoadrenocorticsm?

A

Decreased CRH and ACTH. Most commonly iatrogenic from stopping long term steroids.

83
Q

DDX for Na:K less than 27

A 
Hypoadrenocorticism
Renal failure or obstruction
Severe GI dz
Parasitic infestation
Pregnancy
Body cavity effusions
84
Q

What increases insulin secretion?

A

Increased BG, increased FFAs, increased AAs, GI hormones (gastrin, cholecystokinin, secretin, GIP), glucagon, growth hormone, cortisol, parasympathetic stimulation, acetylcholine, beta-adrenergic stimulation, insulin resistance, obesity, sulfonylurea drugs

85
Q

What decreases insulin secretion?

A

decreased BG, fasting, somatostatin, alpha-adrenergic activity, leptin

86
Q

How does glucagon cause glycogenolysis?

A

Glucagon activates adenylyl cyclase causing formation of cAMP which activates protein kinase regulator protein which activates protein kinase, which activates phosphoylase b kinase, which converts phosphorylase b into phosphorylase a which promotes degredation of glycogen to glucose-1-phosphate, which is then dephosphorylated and the glucose is released from liver cells

87
Q

What were the findings from DeClue, JAVMA, 2011 on cortisol and aldosterone response to various doses of cosyntropin in cats?

A

Lowest doses of cosyntropin that stimulated maximal cortisol and aldosterone response were 5 and 2.5 mcg/kg (equivalent to 125 mcg/cat); lower doses resulted in shorter interval b/t IV admin and peak cortisol/aldosterone concentrations.

88
Q

Common statistical errors that invalidate studies.

A
  1. Application of statistical methods that require normally distributed data to nonnormal data
  2. Analysis of nonindependent data as if they were independent
  3. Treatment of incomplete follow up as equivalent to complete follow up
  4. Misinterpretation of results from small samples
89
Q

Insulin resistance in healthy Miniature Schnauzers. JAVMA, 2011, findings:

A

Hypertriglyceridemia is associated with insulin resistance

90
Q

Hypertriglyceridemia in mini schnauz due to

A

abnormal accumulation VLDLs or a combination of VLDLs and chylomicrons, with or w/o hypercholesterolemia

91
Q

HOMA score

A

basal serum insulin (mU/L) x basal glucose (mmol/L) / 22.5

92
Q

MOA trilostane

A

4alpha, 5-epoxysteroid competitive inhibitor of the 3B-hydroxysteroid dehydrogenase-isomerase enzyme system

blocks cortisol and aldosterone

93
Q

What dogs had poorer prognosis after adrenalectomy? Massari, JAVMA, 2011

A

tumor > 5 cm, documented metastasis, vein thrombosis

mets more common with adenocarcinoma
vein thrombosis more when tumor > 5 cm

94
Q

ACCORD study, NEJM, 2011. Diabetes and heart dz.

A

Intensive to achieve glycolated Hgb <6 was worse over a 5 year period. The intensive group stopped early at 3.7 y b/c higher risk.

95
Q

Retrospective, hyperosmolar hyperglycemia dogs, Trotman, JVECC, 2013, findings.

A

5% diabetics overall
62% survived

Poor outcome assc’d with abn mental status, low venous pH.

Hyperosmolar ketonuric dogs more likely to have acute panc (50% vs. 24%), higher temp, higher WBC, shorter duration of clinical signs than hyperosmolar nonketonuric.

Hyperosmolar nonketotic higher BUN and creat, higher calculated osmolality.

Hyperosmolar defined as >325 mOsm/kg

96
Q

Normal osmolality

A

292-308 mOsm/kg

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