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Endocrine Flashcards

1
Q

What are the HLA haplotypes associated with DM I?

A

HLA-DR3 and DR4

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2
Q

What are the antibodies that can be present in DM I? (4)

A

Anti-islet cell
Anti- glutamic acid decarboxylase
Anti-insulin
Anti Zn transpor

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3
Q

What is the test to screen for renal dysfunction in DM pts?

A

albumin-to-creatinine ratio

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4
Q

How often is HbA1c obtained for DM I patients?

A

Q 3 months

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5
Q

what happens to total K stores with DKA or HONK?

A

Decreased

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6
Q

What type of fluids should be used for initial fluid resuscitation with DKA? At what point is D5 added?

A

NS (really, not LR)

D5 added at 250 mg /dl

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7
Q

What is the MOA of metformin?

A

Inhibits hepatic gluconeogenesis and increases peripheral sensitivity to insulin

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8
Q

What is the major contraindication to metformin use?

A

Renal insufficiency

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9
Q

What is the MOA of sulfonylureas?

A

Increases endogenous insulin secretion

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10
Q

What type of drug is glipizide?

A

Sulfonylurea

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11
Q

What type of drug is glyburide?

A

Sulfonylurea

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12
Q

What type of drug is glimepiride?

A

Sulfonylurea

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13
Q

What is the MOA thiazolidinediones?

A

Increases insulin sensitivity by PPRA activation

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14
Q

What is the major contraindication of thiazolidinones?

A

CHF

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15
Q

What is the MOA of DPP-4 inhibitors?

A

Inhibit degradation of GLP-1

The mechanism of DPP-4 inhibitors is to increase incretin levels (GLP-1 and GIP), which inhibit glucagon release,

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16
Q

What is the major advantage to DPP-4 inhibitors?

A

Weight neutral

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17
Q

what is the common suffix to all DPP-4 inhibitors?

A

-Gliptins

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18
Q

What is the MOA of GLP-1 agonists?

A

binds to glucagon-like peptide 1 receptors, slowing gastric emptying and increases insulin secretion by pancreatic Beta cells

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19
Q

What is the common suffix to GLP-1 agonists?

A

tides

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20
Q

What is the advantage of GLP-1 agonists?

A

Lower risk of hypoglycemic episodes

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21
Q

What is the common suffix to SGLT2 inhibitors?

A

Flozin

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22
Q

True or false: DM automatically puts one at the highest risk category for acute coronary events

A

True

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23
Q

What is the goal BP of patients with DM? What is the agent of choice? Why?

A

Less than 140/90

ACEI and ARBS due to renal preservation effects

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24
Q

What are the annual physical exam that should be performed for DM? (5)

A 
BP
Lipids
Microalbuminuria
Retinopathy
Foot neuropathy
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25
Q

All DM pts older than 19 should receive what vaccine that other groups do not need?

A

Pneumovax

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26
Q

True or false: anti-islet cell and anti-GAD antibodies are found in DM II

A

False

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27
Q

What are the fast acting insulins?

A

Lispro
Aspart
Glulisine

(no LAG)

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28
Q

What is the intermediate acting insulin?

A

NPH

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29
Q

What are the two long acting insulins?

A

Detemir

Glargine

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30
Q

Which has more profound mental status changes: DKA or HHS?

A

HHS

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31
Q

What are the respirations like with DKA?

A

Kussmaul breathing

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32
Q

What are the glucose levels in HHK?

A

Over 600 mg/dl

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33
Q

True or false: there is a normal anion gap in HHK

A

True

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34
Q

When is bicarb used for treating DKA?

A

only if pH is less than 6.9

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35
Q

What are the screening recommendations for DM?

A

Test A1c q 3 years starting at age 45

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36
Q

When does retinopathy occur in DM?

A

when present for 3-5 years

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37
Q

What is the treatment for diabetic retinopathy?

A

Laser photocoagulation prevents further neovascularization, but does not reverse damage

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38
Q

What are the symptoms of diabetic nephropathy?

A

Glomerular hyperfiltration, followed by microalbuminuria

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39
Q

When in the course of DM does nephropathy occur?

A

over 10 years

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40
Q

What are the classic histological findings of diabetic nephropathy?

A

Kimmelstiel-Wilson nodules

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41
Q

What is the preventative treatment for diabetic nephropathy?

A

ACIEs

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42
Q

What, besides gabapentin and lyrica, can be used to treat diabetic neuropathy?

A

TCAs

NSAIDs

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43
Q

What is the treatment for gastroparesis 2/2 DM?

A

metoclopramide

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44
Q

What level of fasting glucose is prediabetes (impaired fasting glucose)?

A

between 100-126

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45
Q

What are the criteria for metabolic syndrome?

A

Central obesity
Impaired glucose
HTN
Dyslipidemia

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46
Q

What level of triglycerides may indicate metabolic syndrome?

A

Over 150 mg/dL

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47
Q

What level of HDL in men and women respectively, may indicate metabolic syndrome?

A

Less than 40 in men

Less than 50 in women

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48
Q

TSH is the best measure of thyroid function unless what?

A

There is a h/o brain injury

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49
Q

What is the preferred screening test for thyroid hormone levels (NOT thyroid disease)?

A

Free T4

TSH is best screen for thyroid disease

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50
Q

What is the most common cause of hyperthyroidism in the US?

A

grave’s disease

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51
Q

Exophthalmos, pretibial myxedema, and thyroid bruits are specific to what primary thyroid disease?

A

Grave’s disease

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52
Q

What causes increased thyroid binding globulin?

A

Pregnancy
Estrogen
Infection

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53
Q

What is the pathophysiology behind fetal thyrotoxicosis?

A

IgG TSH stimulating antibodies can cross the placenta

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54
Q

What are labs like with subclinical hypothyroidism?

A

Increased TSH, but normal T3 and T4

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55
Q

What are the labs like with euthyroid sick syndrome?

A

Normal TSH
Normal to decreased T4
Decreased T3

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56
Q

What lab finding is relatively specific for euthyroid sick syndrome?

A

Increase in reverse T3

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57
Q

What is the cause of euthyroid sick syndrome?

A

Thought to be due to caloric deprivation and increased cytokines. May have transient ↑ in TSH during recovery period.

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58
Q

What drug can be given to hyperthyroid pts to decrease symptoms?

A

Beta blockers

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59
Q

What are the two drugs that can inhibit thyroid hormone production?

A

Methimazole

PTU

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60
Q

What is the treatment for severe ophthalmopathy 2/2 hyperthyroidism?

A

Steroids

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61
Q

What is the treatment for thyroid storm? (4)

A

Antithyroid drugs
Iodine
IV esmolol
Steroids

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62
Q

What are the s/sx of thyroid storm?

A

Fever
Delirium
A-fib

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63
Q

What is the major side effect of PTU?

A

Agranulocytosis

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64
Q

What is the major side effect of methimazole?

A

Agranulocytosis

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65
Q

Which is safe to use in pregnancy: PTU or methimazole?

A

PTU

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66
Q

Which prevents the peripheral conversion of T4 to T4: PTU or methimazole?

67
Q

What happens to ophthalmopathy with radioactive iodine thyroid ablation?

A

Initially worsens

68
Q

What is the most common cause of hypothyroidism in the US?

A

Hashimoto’s thyroiditis

69
Q

What are the antibodies seen in Hashimoto’s thyroiditis?

A

Anti-thyroglobulin

Anti Thyroid peroxidase

70
Q

What is the most common cause of congenital hypothyroidism?

A

Thyroid dysgenesis

71
Q

How does congenital hypothyroidism present?

A

Failure to thrive
Umbilical hernias
Prolonged jaundice

72
Q

What happens to LDL with hypothyroidism?

73
Q

Why are thyroid disorders associated with menstrual irregularities?

A

TSH and LH/FSH share the same alpha subunit

74
Q

When should subclinical hypothyroidism be treated?

A

If TSH more than 10mU/L

75
Q

Patients with Hashimoto’s disease are at an increased risk of developing which hematological malignancy?

76
Q

What are the s/sx of myxedema coma?

A

Decreased LOC
Hypothermia
Hypotension
Hypoventilation

77
Q

What is the treatment for myxedema coma?

A

IV levothyroxine and IV cortisone if renal insufficiency has not been excluded

78
Q

What are the s/sx of subacute thyroiditis?

A

Tender thyroid
malaise
URI s/sx

79
Q

What is the treatment for subacute thyroiditis?

A

If severe, NSAIDS or corticosteroids

80
Q

True or false: most thyroid nodules are benign

81
Q

Which are more likely to be malignant: hot or cold thyroid nodules?

A

Cold–hyperfunctioning nodules are not malignant

82
Q

What are the top four most common thyroid neoplasms?

A

Papillary
Follicular
Medullary
Anaplastic

83
Q

What lab value should be checked if medullary thyroid CA is suspected?

A

Calcitonin

84
Q

What are the histological characteristics of papillary thyroid cancer?

A 
Pupil nuclei ("orphan annie eyes")
Psammoma bodies
85
Q

How does papillary thyroid cancer spread?

A

lymphatics

86
Q

How does follicular thyroid cancer spread?

A

hematologically

87
Q

what is the prognosis for papillary and follicular thyroid cancer?

A

Very good–more than 90% life 10+ years

88
Q

What is the prognosis for medullary thyroid cancer?

A

80% survive 10 years

89
Q

What is the prognosis for anaplastic thyroid cancer?

A

10% survive more than 3 years

90
Q

What should be done if a FNA of a thyroid mass reveals benign neoplasm?

A

Follow with physical exam/US to assess for continued growth

91
Q

What should be done if a FNA of a thyroid mass reveals malignant neoplasm?

A

Surgical resection with hemi or total thyroidectomy

92
Q

What should be done if a FNA of a thyroid mass reveals indeterminate neoplasm?

A

Watchful waiting vs hemithyroidectomy (10–30% chance of malignancy). If resected, await final pathology to guide further treatment.

93
Q

What is the first step in working up a thyroid nodule?

A

Determine if functioning by taking TSH

  • If low, then not malignant
  • If normal or high, workup malignancy
94
Q

What is osteomalacia?

A

a mineralization defect often due to severe vitamin D deficiency that presents with bone pain, decreased calcium/phosphorus, and 2° hyperparathyroidism.

95
Q

Which ethnicities are at an increased risk of osteoporosis?

A

Caucasians

Asians

96
Q

What are the three major risk factors for osteoporosis?

A

Smoking
Age
Corticosteroid use

97
Q

When are DEXA scans recommended for men and women?

A

Women 65+

Men 70+

98
Q

How many standard deviations are diagnostic for osteopenia?

A

between 1 and 2.5

99
Q

What will labs reveal in osteoporosis?

100
Q

Global demineralization is only apparent on x-ray after what percentage of bone loss?

101
Q

True or false: bisphosphonates are recommended for treating osteopenia?

A

False–only for osteoporosis

102
Q

What is the MOA and use of denosumab?

A

Monoclonal ab to RANK-L, to decreased osteoclast function

103
Q

What is the MOA and use of teriparatide?

A

analogue of parathyroid hormone, PTH

104
Q

What is the basic pathophysiology behind Paget’s disease?

A

Increased rate of bone turnover

105
Q

What is the classic description of Paget’s disease on histology?

A

Mosaic lamellar bone pattern

106
Q

What is the usualy presentation of Paget’s disease?

A

Asymptomatic, but s/sx include bone/joint pain

107
Q

Does Paget’s disease affect all bones, or just one?

108
Q

↑ serum alkaline phosphatase with normal gamma-glutamyl transpeptidase (GGT) points to what etiology?

109
Q

Bone pain + hearing loss = ?

A

Paget’s disease

110
Q

What are the lab values like with Paget’s disease?

A

Abnormalities include ↑ serum alkaline phosphatase with normal calcium and phosphate levels.

111
Q

What is the treatment for asymptomatic Paget’s disease?

A

Follow–nothing

112
Q

What is the treatment for symptomatic Paget’s disease?

A

Bisphosphonates, Vit D, and Ca

113
Q

What are the radiographic findings of Paget’s disease?

A

Lytic and sclerotic bone lesions

114
Q

What are the two major complications of Paget’s disease?

A

high output cardiac failure

Osteosarcoma

115
Q

What is the most common cause of hyperparathyroidism?

A

Single hyperfunctioning adenoma

116
Q

What is the cause of secondary hyperPTH?

A

Renal insufficiency (due to ↓ production of 1-25 dihydroxyvitamin D)

117
Q

What is the cause of tertiary hyperparathyroidism?

A

Seen in dialysis patients with long-standing 2° hyperparathyroidism that leads to hyperplasia of the parathyroid glands. When one or more of the glands become autonomous, 3° hyperparathyroidism results.

118
Q

What is the pathophysiology behind pseudohypoparathyroidism?

A

PTH resistance

Elevated PTH levels but ineffective at target organs. Hypocalcemia and hyperphosphatemia.

119
Q

What are the labs like with primary hyperparathyroidism?

A

Elevated Ca

low phosphate

120
Q

What are the s/sx of hypercalcemia?

A 
Stones
Bones
Moans
Groans
Psychiatric overtones
121
Q

What is the treatment for hypercalcemia 2/2 hyperparathyroidism?

A

IVFs
Loop diuretics
Bisphosphonates if malignancy

122
Q

What is the treatment for primary hyperparathyroidism?

A

Parathyroidectomy

123
Q 
What happens to
-PTH
-Ca
-PO4
with primary hyperparathyroidism?
A
  • PTH increased
  • Ca increased
  • PO4 decreased
124
Q 
What happens to
-PTH
-Ca
-PO4
with secondary hyperparathyroidism?
A
  • PTH Increased
  • Ca nl/decreased
  • PO4 increased
125
Q 
What happens to
-PTH
-Ca
-PO4
with tertiary hyperparathyroidism?
A
  • PTH Increased
  • Ca increased
  • PO4 increased
126
Q 
What happens to
-PTH
-Ca
-PO4
with ectopic PTHrP?
A
  • PTH decreased
  • Ca increased
  • PO4 nl to decreased
127
Q

What is the treatment for hypercalcemia in patients with renal insufficiency?

A

Oral phosphate binders

128
Q

What are the labs that should be ordered if suspected hypopituitarism?

A

8 am cortisol
Free T4
Testosterone/estradiol
IGF-1

129
Q

What is the hormone that is secreted from the hypothalamus to the pituitary, and causes prolactin release?

130
Q

What is the treatment for Cushing’s syndrome?

A

Surgical resection of the source

131
Q

What is Cushing’s disease?

A

overproduction of ACTH from pituitary adenoma

132
Q

What is the most common cause of acromegaly?

A

benign pituitary GH-secreting adenoma

133
Q

What happens with the low and high dose dexamethasone test with cushing’s disease?

A

In Cushing disease, cortisol secretion remains elevated with the low-dose (1 mg) dexamethasone test but is suppressed with the high-dose (8 mg) dexamethasone test.

134
Q

What are some s/sx of acromegaly?

A 
Skull enlargement (frontal bossing)
Wide-spaced teeth
Coarse facial features
Macroglossia
Skin tags
135
Q

What is a normal test for the dexamethasone suppression test, and what does it indicated?

A

Lower ACTH means no cushing’s

136
Q

What is the use of the high dose dexamethasone suppression test?

A

If ACTH suppressed, then pituitary adenoma

If not, then ectopic production

137
Q

What is the most common cause of death of acromegaly?

A

Heart failure 2/2 cardiomyopathy

138
Q

What is the treatment for acromegaly?

A

Resection of the pituitary tumor

Octreotide or lanreotide

139
Q

What is the MOA and use of pegvisomant?

A

Gh receptor antagonist, used in the treatment of acromegaly

140
Q

What is the screening lab test for acromegaly?

A

IGF-1 levels (NOT GH levels)

141
Q

What must always be r/o first in cases of hyperprolactinemia?

142
Q

What is the mechanism through which prolactinomas cause a decrease in libido, and amenorrhea?

A

Elevated prolactin inhibits GnRH secretion and consequently lowers LH and FSH secretion,

143
Q

What is the serum prolactin level in a prolactinoma?

A

Over 200 ng/mL

144
Q

What is the pharmacotherapy for a prolactinoma?

A

Dopamine agonists (cabergoline)

145
Q

When is surgery indicated as the treatment for a prolactinoma?

A

Refractory to medical management or with compressive effects

146
Q

What are two classic drugs that can cause nephrogenic DI?

A

Li

Demeclocycline

147
Q

Dehydroepiandrosterone is only produced by what organ?

A

Adrenal gland

148
Q

What causes the hyperpigmentation associated with Addison’s disease?

A

Increased ACTH increases POMC intermediate

149
Q

What is the test of choice for diagnosing addison’s disease? What is the backup?

A
  • ACTH levels

- Synthetic ACTH stimulation (cosyntropin test)

150
Q

What amount of steroids, and for what durations, may cause secondary/tertiary adrenal insufficiency?

A

More than 20g for more than 3 weeks

151
Q

What is the treatment difference for primary vs secondary adrenal insufficiency?

A

Primary = Glucocorticoid and mineralocorticoid replacement

Secondary = Glucocorticoid replacement alone

152
Q

What are the 4 S’s of adrenal crisis management?

A

Salt (0.9% NS)
Steroids (IV hydrocortisone)
Support
Search for cause

153
Q

What type of cells comprise a pheochromocytoma?

A

Chromaffin cells

154
Q

What are the s/sx of conn syndrome and/or hyperaldosteronism?

A

HTN
HA
Polyuria
Weakness

155
Q

What electrolyte is deficient with hyperaldosteronism? What acid/base disorder?

A

Hypokalemic alkalosis

156
Q

What is the test to diagnose hyperaldosteronism?

A

Increased aldosterone-to-plasma renin activity ratio

157
Q

What is the pharmacotherapy of choice for hyperaldosteronism?

A

Eplerenone (aldosterone receptor antagonist)

158
Q

Review 21 hydroxylase flow.

159
Q

What is the treatment for 21 hydroxylase deficiency?

A

Immediate IVFs

Salt repletion

160
Q

What are the components of MEN1?

A

Pituitary
Parathyroid hyperplasia
Pancreatic islet cell tumors

161
Q

What is the underlying genetic mutation in MEN2?

A

RET protooncogene

162
Q

What are the components of MEN2A?

A

Parathyroid hyperplasia
Medullary thyroid
Pheochromocytoma

163
Q

What are the components of MEN2B?

A

Mucosal neuromas
Medullary thyroid
Pheochromocytoma

Marfanoid

A1 (32 decks)

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