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PANCE Prep Pearls > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

Elevated TSH + Normal FT4

A

Subclinical hypothyroidism

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2
Q

Elevated TSH + High FT4

A

TSH-mediated hyperthyroidism (secondary or tertiary)

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3
Q

Low TSH + Low FT4

A

Secondary or tertiary hypothyroidism (rare). If present, it is usually pituitary

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4
Q

Low TSH + Normal FT4

A

Subclinical hyperthyroidism

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5
Q

Low TSH + High FT4

A

Primary hyperthyroidism or thyrotoxicosis (check RAIU to identify cause)

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6
Q

RAIU: DIFFUSE uptake

A

Grave’s disease or pituitary adenoma

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7
Q

RAIU: Decreased uptake

A

Thyroiditis

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8
Q

RAIU: hot nodule

A

Toxic adenoma

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9
Q

RAIU: Multiple nodules

A

toxic multinodular goiter

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10
Q

RAIU: cold nodules

A

Suspect malignancy

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11
Q

What is thyroiditis?

A

Transient hyperthyroidism due to thyroid inflammation/destruction causing leak of “preformed” thyroid hormones (NOT due to new hormone synthesis)

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12
Q

What is cretinism?

A

Congenital hypothyroidism due to maternal hypothyroidism or infant hypopituitarism

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13
Q

What is Riedel’s thyroiditis?

A

Normal thyroid stroma replaced by fibrotic tissue

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14
Q

Reidel’s thyroiditis: Clinical manifestations

A

Painless fixed nodular that may grow rapidly (resembles malignancy). *RARE*

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15
Q

Riedel’s thyroiditis: Management

A

Steroids, tamoxifen and levothyroxine

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16
Q

What is euthyroid sick syndrome?

A

Abnormal thyroid levels with normal thyroid gland function seen with illness (ex: surgery, malignancies, sepsis, cardiac disease)

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17
Q

Grave’s Disease: Management (4)

A
  1. Radioactive iodine: MC therapy used 2. Methimazole/propylthiouracil (PTU safe in pregnancy) 3. Beta blockers (propanolol) for symptomatic relief* 4. Thyroidectomy
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18
Q

Toxic multinodular goiter (plummer disease) and toxic adenoma treatment (4)

A
  1. Radioactive iodine: MC therapy 2. Surgery (subtotal thyroidectomy) if compressive symptoms are present 3. Antithyroid meds: Methimazole/PTU 4. Beta blockers for sx of thyrotoxicosis
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19
Q

Compressive symptoms of toxic multinodular goiter and toxic adenoma

A

Dyspnea, dysphagia, stridor, hoarseness

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20
Q

TSH secreting pituitary adenoma: Clinical manifestations (3)

A
  1. Diffuse enlarged thyroid 2. Bitemporal hemianopsia 3. Mental disturbances
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21
Q

TSH secreting pituitary adenoma: thyroid function tests

A

Increased FT4/T3 + Increased TSH (inappropriate TSH elevation in the setting of elevated FT4/T3 in the same direction)

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22
Q

TSH secreting pituitary adenoma: Management

A

Transsphenoidal surgery to remove pituitary tumor

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23
Q

Elevated TSH + Low FT4

A

Primary hypothyroidism

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24
Q

What is the MC cause of hypothyroidism in the US?

A

Hashimoto’s (chronic lymphocytic)

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25
Q

Hashimoto’s: Cause

A

Autoimmune (anti-thyroid ab)

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26
Q

Hashimoto’s: Diagnosis (4)

A
    • Thyroid Ab present: thyroglobulin Ab, antimicrosomial and thyroid peroxidase Ab
  2. TFTs (us HypOthyroid)
  3. Decreased radioactive iodine uptake (usually not needed)
  4. Biopsy: Lymphocytes, germinal follicles, Hurthle
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27
Q

Silent (lymphocytic): cause

A

Autoimmune (anti-thyroid Ab)

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28
Q

Silent (lymphocytic): Clinical manifestations

A
  1. Painless enlarged thyroid
  2. Thyrotoxicosis → hypothyroid (depend on where they present)
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29
Q

Silent (lymphocytic): Diagnosis (3)

A
    • thyroid Ab present (same as Hashimoto’s)
  2. TFT: (hyper/hypo) depend on where they present
  3. Decreased radioactive iodine uptake
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30
Q

Silent (lymphocytic): Duration/Management (3)

A
  1. Return to euthyroid state within 12-18 months w/o treatment. ASA
  2. No anti-thyroid meds**
  3. 20% possible permanent hypothyroidism
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31
Q

Post-partum thyroiditis: Cause

A

Autoimmune (anti-thryoid Ab)

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32
Q

Post-partum thyroiditis: clinical manifestations (2)

A
  1. Painless enlarged thyroid
  2. Thyrotoxicosis → hypothyroid (depend on where they present)
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33
Q

Post-partum thyroiditis: Diagnosis (3)

A
    • Thyroid Ab present
  2. TFTs: (Hyper/hypo) depend on where they present
  3. Decreased radioactive iodine uptake
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34
Q

Post-partum thyroiditis: Duration (3)

A
  1. Monitor TFTs every 4-8 weeks
  2. If hyperthyroid symptoms are present: use propanolol or atenolol until levels are normal
  3. If hypothyroid symptoms are present, use levothyroxine
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35
Q

DeQuervain’s (Granulomatous) thyroiditis cause

A

MC post viral* or viral inflammatory reaction

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36
Q

DeQuervain’s (granulomatous) thyroiditis: Clinical manifestations (2)

A
  1. PAINFUL neck/thyroid
  2. Clinical hyperthyroidism
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37
Q

DeQuervain’s (granulomatous) thyroiditis: Diagnosis (4)

A
  1. Elevated ESR (hallmark)**
  2. No thyroid Ab
  3. TFTs (us hypERthyroid)
  4. Decreased radioactive iodine uptake
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38
Q

DeQuervain’s (granulomatous) thyroiditis: Duration (3)

A
  1. Return to euthyroid state within 12-18 months without treatment. ASA (for pain, inflammation, increases T4)
  2. No anti-thyroid meds
  3. 5% possible permanent hypothyroidism
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39
Q

Which medications are most responsible for causing medication induced thyroiditis?

A

Amiodarone, lithium, and alpha interferon

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40
Q

Acute thyroiditis: Diagnosis (2)

A
  1. Increased WBC count (left shift)
  2. Euthyroid
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41
Q

Acute thyroiditis: Duration

A

Antibiotics, drainage if abscess is present

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42
Q

Thyroid storm: Management (6)

A
  1. Anti-thyroid meds: Methimazole, PTU
  2. Beta-blockers for symptoms
  3. Supportive: IV fluids
  4. Glucocorticoids
  5. Oral/IV sodium iodide
  6. Antipyretics (avoid ASA as this increases T4)
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43
Q

What is the MC malignant thyroid tumor?

A

Papillary carcinoma

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44
Q

What is the MC type of thyroid nodule?

A

Colloid (50-60%)

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45
Q

On a radioactive iodine uptake scan, what type of nodule is highly suspicious for malignancy?

A

Cold nodule

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46
Q

Papillary carcinoma: Prognosis

A

Excellent (high cure rate)

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47
Q

Follicular carcinoma: METS (2)

A
  1. Local cervical lymph node invasion less common
  2. Distant METS comon (vascular invasion of lung, neck brain, bone, liver, skin)
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48
Q

Follicular carcinoma: Prognosis

A

Excellent

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49
Q

Medullary carcinoma: Risk factors (2)

A
  1. Not associated with radiation exposure
  2. MC associated with MEN 2*
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50
Q

Medullary carcinoma: Characteristics (3)

A
  1. More aggressive. Much lower cure rate.
  2. Arises from parafollicular cells → secrete calcitonin
  3. May cause diarrhea and flushing
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51
Q

Medullary carcinoma: METS (2)

A
  1. Local cervical LN occurs early in the disease
  2. Distant METS occur late (brain, bone, liver, adrenal medulla)
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52
Q

Medullary carcinoma: Prognosis

A

Poorer prognosis

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53
Q

Medullary carcinoma: Management (2)

A
  1. Total thyroidectomy
  2. Calcitonin levels used to monitor if residual disease present after treatment or detect recurrence
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54
Q

Anaplastic carcinoma: Age

A

MC in males >65 yo

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55
Q

Anaplastic carcinoma: Characteristics (2)

A
  1. Most aggressive*
  2. Rapid growth!! Often with compressive symptoms
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56
Q

Anaplastic carcinoma: METS (2)

A
  1. Local and distant METS
  2. May invade trachea (20% of patients need tracheostomy)
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57
Q

Anaplastic carcinoma: Prognosis

A

Poor prognosis*

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58
Q

Anaplastic carcinoma: Management (3)

A
  1. Most are not amenable to surgical resection
  2. External beam radiation
  3. Chemotherapy
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59
Q

What is the MC cause of primary hyperparathyroidism?

A

Parathyroid adenoma

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60
Q

MEN 1

A
  1. Hyperparathyroidism
  2. Pituitary Tumors
  3. Pancreatic Tumors
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61
Q

MEN 2a

A
  1. Hyperparathyroidism
  2. Pheochromocytoma
  3. Medullary thyroid carcinoma
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62
Q

Why does the PTH increase with secondary hyperparathyroidism?

A

It is a response to hypocalcemia or vitamin D deficiency

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63
Q

MC cause of secondary hyperparathyroidism

A

Chronic kidney failure

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64
Q

Clinical manifestations of hyperparathyroidism

A

Stones, bones, abdominal groans, psychic moans

Decreased DTR

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65
Q

Primary hyperparathyroidism: Diagnosis (4)

A
  1. Triad: Hypercalcemia + increased intact PTH + decreased phosphate
  2. Increased 24 hour urine calcium excretion
  3. Increased vitamin D
  4. Osteopenia on bone scan
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66
Q

Hypoparathryroidism: Clinical manifesetations

A

Signs of hypocalcemia: carpopedal spasm, Trousseau & Chvostek sign, perioral paresthesias, increased DTR

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67
Q

Hypoparathyroidism triad

A
  1. Hypocalcemia
  2. Decreased intact PTH
  3. Increased phosphate
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68
Q

Hypocalcemia: ECG findings

A

Prolonged QT interval

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69
Q

Hypocalcemia: GI findings

A

Diarrhea, abdominal cramps

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70
Q

Hypocalcemia: Management (severe or symptomatic)

A

Calcium gluconate IV* or calcium carbonate IV

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71
Q

Hypocalcemia: Management (mild) (2)

A
  1. PO calcium + Vitamin D (erogcalciferol, calcitriol)
  2. K and Mg repletion may be needed in some cases
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72
Q

Hypercalcemia: ECG findings

A

Shortened QT interval

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73
Q

Hypercalcemia: Management (4)

A
  1. IV saline → Fuorsemide* (Lasix) 1st line. Avoid HCTZ (causes increased calcium)
  2. No treatment needed for mild hypercalcemia
  3. Calcitonin, bisphosphonates added in severe cases
  4. Steroids (in vitamin D access, malignancies, granulomas)
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74
Q

Osteoporosis: Dexa scan results

A

Bone density T score ≤ -2.5

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75
Q

Osteopenia: Dexa scan results

A

T score ≤ 1.0 to -2.5

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76
Q

1st line treatment for osteoporosis

A

Bisphosphonates

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77
Q

Bisphosphonates: Side effects

A

Pill esophagitis, jaw necrosis, pathologic femur fracture (esp. with IV)

78
Q

Bisphosphonates: PO medications

A

Alendronate, risedronate, ibandronate

79
Q

Bisphosphonates: IV medications

A

Pamidronate and Zoledrenic acid (most potent)

80
Q

What medication is used for osteporosis in postmenopausal women?

A

Raloxifene (SERM)

81
Q

Last-line therapy for osteoporosis

A

Calcitonin

82
Q

Osteogenesis imperfecta: clinical manifestations

A

Severe osteoporosis, spontaneous fractures in childhood, blue sclerae, and presenile deafness

83
Q

What is renal osteodystrophy?

A

Group of bone disorders (osteitis fibrosis cystica and osteomalacia present in pts with chronic kidney disease)

84
Q

Renal osteodystrophy: clinical manifestations

A

Bone and proximal muscle pain (in the context of uremia)

85
Q

Renal osteodystrophy: Labs

A
  1. Decreased calcium and increased phosphate and PTH (secondary hyperparathyroidism)
  2. Increased alkaline phosphatase
86
Q

Renal osteodystrophy: X-rays (Osteitis fibrosis cystica)

A
  1. Periosteal erosions
  2. Bony cysts with thin trabeculum and cortex
  3. “Salt and pepper” appearance of the skull on X-ray
87
Q

Renal osteodystrophy: Biopsy

A

Cystic brown “tumors” (not an actual tumor)

88
Q

Renal osteodystrophy: Management (3)

A
  1. Phosphate binders: calcium carbonate, calcium acetate, sevelamer (used if both calcium and phosphate levels are elevated)
  2. Vitamin D (ergocalciferol)
  3. Cinacalcet
89
Q

Osteomalacia and rickets: Labs

A
  1. Decreased vitamin D, decreased calcium and decreased phosphate, increased alkaline phosphate
90
Q

Osteomalacia and rickets: X-rays

A

Looser lines (zones)*: transverse “pseudo fracture” lines on X-ray

91
Q

Osteomalacia and rickets: Management

A

Vitamin D supplementation (ergocalciferol) + calcium supplementation

92
Q

Three layers of the adrenal gland

A
  1. Outer layer: Zona glomerulosa
  2. Middle layer: Zona fasciculata
  3. Inner layer: Zona reticularis
93
Q

Zona glomerulosa

A

Aldosterone (controls Na balance)

94
Q

Zona fasciculata

95
Q

Zona reticularis

A

Produces androgen/estrogen

96
Q

Etiologies for Addison’s disease (primary adrenocortical insufficiency) (5)

A
  1. Autoimmune: MC cause in industrialized countries
  2. Infection: (MC worldwide)
  3. Vascular
  4. Metastatic disease
  5. Medications
97
Q

Infectious causes for Addison’s disease (4)

A
  1. TB
  2. Fungal infections (ex: Histoplasmosis)
  3. CMV
  4. HIV
98
Q

Vascular causes for Addison’s disease

A

Thrombosis or hemorrhage in the adrenal gland (Waterhouse-Friderichsen); trauma

99
Q

Medications that may cause Addison’s disease

A

Ketoconazole, rifampin, phenytoin, barbituates

100
Q

Secondary adrenocortical insufficiency etiologies (2)

A
  1. Exogenous steroid use MC cause
  2. Hypopituitarism
101
Q

What makes secondary or tertiary causes of adrenal insufficiency different from primary cause?

A

Aldosterone is intact; there is a lack of cortisol

102
Q

Since the aldosterone is decreased in primary (in contrary to secondary) what extra clinical manifestations are found with this disease? (5)

A
  1. Hyperpigmentation
  2. Marked orthostatic hypotension
  3. Severe hyponatremia
  4. Hyperkalemia
  5. Non anion gap metabolic acidosis*
103
Q

Screening test used for adrenal insufficiency

A

High dose ACTH (Cosyntropin) stimulation test

104
Q

What test is used to differentiate between the different causes of adrenal insufficiency?

A

CRH stimulation test

105
Q

CRH Stimulation Test: Primary/Addison (adrenal) results

A

Produces high levels of ACTH but low cortisol

106
Q

CRH stimulation test: secondary (pituitary) results

A

Low ACTH + low cortisol*

107
Q

1st line treatment for primary adrenal insufficiency

A

Hydrocortisone + Fludrocortisone

108
Q

Adrenal (Addisonian) Crisis: Clinical manifestations (3)

A
  1. Shock* primary manifestation
  2. Hypotension, hypovolemia
  3. Nonspecific symptoms (abd. pain, n/v, fever, weakness, lethargy, coma)
109
Q

Adrenal (Addisonian) Crisis: lab studies (2)

A
  1. BMP=hyponatremia, hyperkalemia, hypoglycemia
  2. Cortisol levels, ACTH, CBC
110
Q

Adrenal (Addisonian) Crisis: Management (4)

A
  1. IV fluids (NS or D5NS if hypoglycemic)
  2. Glucocorticoids (dexamethasone if undiagnosed and hydrocortisone if diagnosed)
  3. Reversal of electrolyte abn.
  4. Fludrocortisone
111
Q

What is cushing’s syndrome?

A

Signs and symptoms related to cortisol excess

112
Q

What is Cushing’s disease?

A

Cushing’s syndrome caused specifically by pituitary increased ACTH secretion

113
Q

Screening tests for diagnosing Cushing’s syndrome (3)

A
  1. Low-dose dexamethasone suppression test (no suppression with Cushing’s syndrome)
  2. Increased 24 hour urinary free cortisol levels
  3. Increased salivary cortisol levels
114
Q

Differentiating tests for causes of Cushing’s syndrome (2)

A
  1. High dose dexamethasone suppression test (suppression is indicative of Cushing’s disease)
  2. ACTH levels (decreased ACTH is indicative of adrenal tumors)
115
Q

Cushing’s syndrome: Management (3)

A
  1. Cushing’s disease (pituitary) → transsphenoidal surgery
  2. Ectopic or adrenal tumors: tumor removal. Ketoconazole in inoperable patients
  3. Iatrogenic steroid therapy (Gradual steroid withdrawal)
116
Q

Primary hyperaldosteronism (4)

A
  1. Primary increased aldosteronism is RENIN INDEPENDENT (autonomous)
  2. Idiopathic or idiopathic bilateral adrenal hyperplasia
  3. Conn syndrome: adrenal aldosteronoma*
  4. Unilateral adrenal hyperplasia (rare)
117
Q

Secondary hyperaldosteronism

A
  1. Increased aldosterone due to increased renin**
  2. MC due to renal artery stenosis* or decreased renal perfusion (CHF, hypovolemia, nephrotic syndrome)
118
Q

Hyperaldosteronism: Clinical manifestations (2)

A
  1. Hypokalemia symptoms (proximal muscle weakness, polyuria, fatigue, constipation, decreased DTR, hypomagnesemia)
  2. Hypertension: esp. in patients with primary hyperaldosteronism (usu. not edematous). Diastolic pressures tend to be more elevated than systolic pressures
119
Q

Hyperaldosteronism: Labs

A

Hypokalemia with metabolic alkalosis

120
Q

Hyperaldosteronism: Aldosterone to Renin ratio screening

A
  1. Done in patients with HTN
  2. ARR >20 and plasma aldosterone >20 and low plasma rening levels → Primary aldosteronism
  3. High plasma renin levels → secondary aldosteronism
121
Q

Hyperaldosteronism: Conn’s syndrome management

A

Excision of adrenal aldosteronomas + spironolactone

122
Q

Hyperaldosteronism: Hyperplasia management

A

Spironolactone, ACEI, CCB. Correct electrolyte abn.

123
Q

Hyperaldosteronism: Secondary (renovascular HTN) management

A

Angioplasty definitive. ACEI

124
Q

Pheochromocytoma: Management (2)

A
  1. Complete adrenalectomy
  2. Preoperative nonselective alpha-blockade: Phenoxybenzamine or phentolamine x 7-14 days followed by beta blockers or CCB to control HTN
125
Q

Types of anterior tumors (5)

A
  1. Prolactinomas: MC type**
  2. Somatotropinoma (GH secreting tumor)
  3. Adrenocorticotropinomas (secretes ACTH)
  4. TSH secreting adenomas (secretes TSH)
  5. FSH/LH secreting adenoma (rare)
126
Q

Diagnosis of acromegaly (2)

A
  1. Insulin-like growth factor (screening test)
  2. Confirmatory test: oral glucose suppression test (will show increased GH levels in acromegaly)
127
Q

Adrenocorticotropinomas: Clinical manifestations

A
  1. Cushing’s disease and hyperpigmentation
128
Q

Anterior pituitary tumors: Diagnosis (2)

A
  1. MRI study of choice to look for sellar lesions/tumors*
  2. Endocrine studies: Prolactin, GH, ACTH, TSH, FSH, LH
129
Q

Anterior pituitary tumors: Management of active or compressive tumors (3)

A

Transsphenoidal surgery (TSS)

130
Q

Acromegaly: Management (3)

A
  1. TSS + Bromocriptine (dopamine agonist)
  2. Pegvisomant (GH antagonist)
  3. Octreotide: Somatostatin analogue
131
Q

Prolactinoma management

A

Cabergoline* or bromocriptine

132
Q

SIADH: CNS etiologies (6)

A
  1. MC stroke (SAH)
  2. Head trauma
  3. Meningitis
  4. CNS tumors
  5. Post-op
  6. Hydrocephalus
133
Q

SIADH: Pulmonary etiologies (2)

A
  1. Small cell lung CA
  2. Infection (ex: Legionella pneumonia)
134
Q

SIADH: Medication etiologies (8)

A
  1. Narcotics
  2. NSAIDs
  3. Anticonvulsants
  4. Carbamazepine
  5. High dose IV cyclophosphamide
  6. Antidepressants (TCA/SSRIs)
  7. HCTZ
  8. Ectasy (MDMA)
135
Q

SIADH: Endocrine etiologies (2)

A
  1. Hypothyroidism
  2. Conn’s syndrome
136
Q

SIADH: Diagnosis (3)

A
  1. Isovolemic hypotonic hyponatremia*: No signs of edema
  2. Urine: Increased urine osm* >300 (concentrated urine despite decreased serum osm.)
  3. Diagnosis must be made in the absence of renal, adrenal, pituitary, thyroid disease, or diuretic use
137
Q

SIADH: Management (2)

A
  1. H20 restriction: Mainstay of tx*. Demeclocycline in severe cases (inhibits ADH)
  2. IV hypertonic saline with furosemide: If severe hyponatremia or intracranial bleed
138
Q

What is diabetes insipidus?

A

ADH (vasopressin) deficiency (central DI) or insensitivity to ADH (nephrogenic) → inability of kidney to concentrate urine → production of large amounts of dilute urine

139
Q

Central DI: Etiology

A

No ADH production**: MC type

(Others include idiopathic, autoimmune destruction of posterior pituitary, head trauma, tumor, infection, sarcoid granuloma)

140
Q

Nephrogenic DI: Etiology (3)

A
  1. Partial or complete insensitivity to ADH
  2. Drugs: Lithium*, amphotericin B, demeclocycline
  3. Hypercalcemia or hypokalemia, acute tubular necrosis, hyperparathyroidism
141
Q

Diabetes insipidus: Clinical manifestations (2)

A
  1. Polyuria + polydipsia. Nocturia
  2. Hypernatremia if severe or decreased PO H20 intake
142
Q

Diabetes insipidus: Diagnosis (2)

A
  1. Fluid deprivation test: establishes the dx of DI. DI patients will have continued production of dilute urine
  2. Desmopressin (ADH) stimulation test
143
Q

Diabetes insipidus: Central DI management

A
  1. Desmopressin/DDAVP (synthetic ADH)*
  2. Carbamazepine
144
Q

Diabetes insipidus: nephrogenic DI

A
  1. Na/protein restriction
  2. HCTZ, indomethacin
145
Q

Diabetes insipidus: symptomatic management

A

Hypotonic fluid (pure water orally is preferred, D5W, 1/2 NS)

146
Q

With DM, what does a kidney biopsy show?

A

Kimmelstiel-Wilson*

147
Q

Diabetes Mellitus: Diagnosis (4)

A
  1. Fasting plasma glucose ≥126 mg/dL GOLD STANDARD**
  2. Hemoglobin A1C ≥6.5
  3. 2 hour plasma glucose ≥200 mg/DL: oral glucose tolerance test (GTT)
  4. Plasma glucose ≥220mg/dL
148
Q

Rapid-Acting Insulin (2)

A
  1. Lispro (Humalog)
  2. Aspart (Novalog)
149
Q

Rapid-Acting Insulin: Onset, peak, duration

A

Onset: 5-15 min

Peak: 1 hour

Duration: 3 hours

150
Q

Rapid-Acting Insulin: Insulin coverage

A

Given at the same time of meal. Often used with intermediate or long acting insulin

151
Q

Short-acting insulin

A

Regular (Humulin-R)

152
Q

Short-acting insulin: Onset, peak, and duration

A

Onset: 30 min-1 hour

Peak: 2-3 hours

Duration: 4-6 hours

153
Q

Short-acting insulin: Insulin coverage

A

Given 30-60 min prior to meal. Often used with intermediate or long acting insulin

154
Q

Intermediate-acting insulin (2)

A
  1. NPH (Humulin N or Novolin N)
  2. Lente (Humulin L or Novolin L)
155
Q

Intermediate-acting insulin: onset, peak, and duration

A

Onset: 2-4 hours

Peak: 4-12 hours

Duration: 16-20 hours

156
Q

Intermediate-acting insulin: Insulin coverage

A

Covers insulin for about half day (or overnight)

Often combined with rapid or short-acting insulin

157
Q

Long-acting insulin (3)

A
  1. Ultralente (U)
  2. Insulin glargine (Lantus)
  3. Detemir (Levemir)
158
Q

Long-acting insulin: Onset, peak, and duration

A

Onset: 6-8 hours

Peak: 12-16 hours

Duration: 20-30 hours

159
Q

Long-acting insulin: insulin coverage

A

Covers insulin for 1 full day (basal insulin)

Lantus causes fewer hypoglycemic episodes than NPH

Lantus should not be mixed with other types of insulin

160
Q

What is the Dawn phenomenon?

A

Normal glucose until 2-8 am when it rises

161
Q

Dawn phenomenon results from what?

A

Decreased insulin sensitivity and nightly surge of counter regulatory hormones (during nighttime fasting)

162
Q

Dawn phenomenon: Management

A

Bedtime injection of NPH, avoid CHO snack late at night, insulin pump usage early in the morning

163
Q

What is Somogyi effect?

A

Nocturnal hypoglycemia followed by rebound hyperglycemia (due to surge in GH)

164
Q

Somogyi effect: management

A

Prevent hypoglycemia*: decreasing nighttime NPH dose or give bedtime snack

165
Q

Insulin waning: management

A

Move insulin dose to bedtime or increse dose

166
Q

Biguanides (2)

A
  1. Metformin (Glucophage)
  2. Phenformin
167
Q

Biguanides: Mechanism of action (3)

A
  1. Mainly decreases hepatic glucose production* and increases peripheral glucose utilization
  2. No effect on pancreatic beta cells → no hypoglycemia, no weight gain
  3. Usually 1st line PO medication
168
Q

Biguanides: Side effects/caution (3)

A
  1. Lactic acidosis* (Not given in patients with hepatic or renal impairment Cr>1.5)
  2. GI complaints are common. Macrocytic anemia
  3. It should be d/c 24 hours before given iodinated contrast and resumed 48 hours after with monitoring of creatinine
169
Q

Sulfonylureas: 1st generation

A

Tolbutamide, chlorpropramide

170
Q

Sulfonylureas: 2nd generation

A

Glipizide, glyburide, glimepiride

171
Q

Sulfonylureas: Mechanism of action (1)

A
  1. Stimulates pancreatic beta cell insulin release*
172
Q

Sulfonylureas: Side effects/caution (5)

A
  1. Hypoglycemia MC side effect**
  2. GI upset, dermatitis
  3. Disulfuram reaction*
  4. Weight gain
  5. CP450 inducer
173
Q

Meglitinides (2)

A
  1. Repaglinide
  2. Nateglinide
174
Q

Meglitinides: Mechanism of action

A

Stimulates pancreatic beta cell insulin release (insulin secretagogue)

175
Q

Meglitinides: Side effects/caution (2)

A
  1. Hypoglycemia (less than sulfonylureas)
  2. Weight gain
176
Q

Alpha-glucosidase inhibitors (2)

A
  1. Arbacose
  2. Miglitol
177
Q

Alpha-glucosidase inhibitors: Mechanism of action (2)

A
  1. Delays intestinal glucose absorption
  2. Does not affect insulin secretion
178
Q

Alpha-glucosidase inhibitors: side effects/caution (2)

A
  1. Hepatitis, flatulence, diarrhea, abdominal pain
  2. Cautious use in patients with gastroparesis, IBD
179
Q

Thiazolidinediones (2)

A
  1. Pioglitazone
  2. Rosiglitazone
180
Q

Thiazolidinediones: Mechanism of action

A
  1. Increases insulin sensitivity @ peripheral receptor site adipose and muscle*
  2. No effect on pancreatic beta cells
181
Q

Thiazolidinediones: side effects/caution (2)

A
  1. Fluid retention and edema* (CHF)
  2. Cardiovascular toxicity with Rosiglitazone* (MI)
182
Q

Glucagon-Like Peptide 1 (GLP-1) Agonists (2)

A
  1. Exenatide
  2. Liraglutide
183
Q

Glucagon-Like Peptide 1 (GLP-1) Agonists: Mechanism of action

A
  1. Lowers blood sugar by mimicking incretin → Increases insulin secretion, decreases glucagon secretion, delays gastric emptying*
184
Q

Glucagon-Like Peptide 1 (GLP-1) Agonists: side effects/caution (2)

A
  1. Hypoglycemia, pancreatitis
  2. CI if h/o gastroparesis
185
Q

DPP-4 inhibitor (2)

A
  1. Sitagliptin
  2. Linagliptin
186
Q

DPP-4 inhibitor: mechanism of action

A

Dipeptidylpeptase inhibition → inhibition of degredation of GLP-1 → Increases GLP-1

187
Q

DPP-4 inhibitor: side effects/caution

A

Pancreatitis, renal failure, GI sx

188
Q

SGLT-2 Inhibitor (2)

A
  1. Canagliflozin
  2. Dapagliflozin
189
Q

SGLT-2 Inhibitor: mechanism of action

A

SGLT-2 inhibiton lowers renal glucose threshold → increases urinary glucose excretion

190
Q

SGLT-2 Inhibitor: side effects/caution

A

Thirst, nausea, abdominal pain, UTIs

PANCE Prep Pearls (7 decks)

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