Endocrine Disorders Flashcards
(191 cards)
1
Q
Elevated TSH + Normal FT4
A
Subclinical hypothyroidism
2
Q
Elevated TSH + High FT4
A
TSH-mediated hyperthyroidism (secondary or tertiary)
3
Q
Low TSH + Low FT4
A
Secondary or tertiary hypothyroidism (rare). If present, it is usually pituitary
4
Q
Low TSH + Normal FT4
A
Subclinical hyperthyroidism
5
Q
Low TSH + High FT4
A
Primary hyperthyroidism or thyrotoxicosis (check RAIU to identify cause)
6
Q
RAIU: DIFFUSE uptake
A
Grave’s disease or pituitary adenoma
7
Q
RAIU: Decreased uptake
A
Thyroiditis
8
Q
RAIU: hot nodule
A
Toxic adenoma
9
Q
RAIU: Multiple nodules
A
toxic multinodular goiter
10
Q
RAIU: cold nodules
A
Suspect malignancy
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)
12
Q
What is cretinism?
A
Congenital hypothyroidism due to maternal hypothyroidism or infant hypopituitarism
13
Q
What is Riedel’s thyroiditis?
A
Normal thyroid stroma replaced by fibrotic tissue
14
Q
Reidel’s thyroiditis: Clinical manifestations
A
Painless fixed nodular that may grow rapidly (resembles malignancy). *RARE*
15
Q
Riedel’s thyroiditis: Management
A
Steroids, tamoxifen and levothyroxine
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)
17
Q
Grave’s Disease: Management (4)
A
- Radioactive iodine: MC therapy used 2. Methimazole/propylthiouracil (PTU safe in pregnancy) 3. Beta blockers (propanolol) for symptomatic relief* 4. Thyroidectomy
18
Q
Toxic multinodular goiter (plummer disease) and toxic adenoma treatment (4)
A
- 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
19
Q
Compressive symptoms of toxic multinodular goiter and toxic adenoma
A
Dyspnea, dysphagia, stridor, hoarseness
20
Q
TSH secreting pituitary adenoma: Clinical manifestations (3)
A
- Diffuse enlarged thyroid 2. Bitemporal hemianopsia 3. Mental disturbances
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)
22
Q
TSH secreting pituitary adenoma: Management
A
Transsphenoidal surgery to remove pituitary tumor
23
Q
Elevated TSH + Low FT4
A
Primary hypothyroidism
24
Q
What is the MC cause of hypothyroidism in the US?
A
Hashimoto’s (chronic lymphocytic)
25
Hashimoto's: Cause
Autoimmune (anti-thyroid ab)
26
Hashimoto's: Diagnosis (4)
1. + 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
27
Silent (lymphocytic): cause
Autoimmune (anti-thyroid Ab)
28
Silent (lymphocytic): Clinical manifestations
1. Painless enlarged thyroid
2. Thyrotoxicosis → hypothyroid (depend on where they present)
29
Silent (lymphocytic): Diagnosis (3)
1. + thyroid Ab present (same as Hashimoto's)
2. TFT: (hyper/hypo) depend on where they present
3. Decreased radioactive iodine uptake
30
Silent (lymphocytic): Duration/Management (3)
1. Return to euthyroid state within 12-18 months w/o treatment. **_ASA_**
2. No anti-thyroid meds\*\*
3. 20% possible permanent hypothyroidism
31
Post-partum thyroiditis: Cause
Autoimmune (anti-thryoid Ab)
32
Post-partum thyroiditis: clinical manifestations (2)
1. Painless enlarged thyroid
2. Thyrotoxicosis → hypothyroid (depend on where they present)
33
Post-partum thyroiditis: Diagnosis (3)
1. + Thyroid Ab present
2. TFTs: (Hyper/hypo) depend on where they present
3. Decreased radioactive iodine uptake
34
Post-partum thyroiditis: Duration (3)
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
35
DeQuervain's (Granulomatous) thyroiditis cause
MC post viral\* or viral inflammatory reaction
36
DeQuervain's (granulomatous) thyroiditis: Clinical manifestations (2)
1. PAINFUL neck/thyroid
2. Clinical hyperthyroidism
37
DeQuervain's (granulomatous) thyroiditis: Diagnosis (4)
1. Elevated ESR (hallmark)\*\*
2. No thyroid Ab
3. TFTs (us hypERthyroid)
4. Decreased radioactive iodine uptake
38
DeQuervain's (granulomatous) thyroiditis: Duration (3)
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
39
Which medications are most responsible for causing medication induced thyroiditis?
Amiodarone, lithium, and alpha interferon
40
Acute thyroiditis: Diagnosis (2)
1. Increased WBC count (left shift)
2. Euthyroid
41
Acute thyroiditis: Duration
Antibiotics, drainage if abscess is present
42
Thyroid storm: Management (6)
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)
43
What is the MC malignant thyroid tumor?
Papillary carcinoma
44
What is the MC type of thyroid nodule?
Colloid (50-60%)
45
On a radioactive iodine uptake scan, what type of nodule is highly suspicious for malignancy?
Cold nodule
46
Papillary carcinoma: Prognosis
Excellent (high cure rate)
47
Follicular carcinoma: METS (2)
1. Local cervical lymph node invasion less common
2. Distant METS comon (vascular invasion of lung, neck brain, bone, liver, skin)
48
Follicular carcinoma: Prognosis
Excellent
49
Medullary carcinoma: Risk factors (2)
1. Not associated with radiation exposure
2. MC associated with MEN 2\*
50
Medullary carcinoma: Characteristics (3)
1. More aggressive. Much lower cure rate.
2. Arises from parafollicular cells → secrete _calcitonin_
3. May cause diarrhea and flushing
51
Medullary carcinoma: METS (2)
1. Local cervical LN occurs early in the disease
2. Distant METS occur late (brain, bone, liver, adrenal medulla)
52
Medullary carcinoma: Prognosis
Poorer prognosis
53
Medullary carcinoma: Management (2)
1. Total thyroidectomy
2. Calcitonin levels used to monitor if residual disease present after treatment or detect recurrence
54
Anaplastic carcinoma: Age
MC in males \>65 yo
55
Anaplastic carcinoma: Characteristics (2)
1. Most aggressive\*
2. Rapid growth!! Often with compressive symptoms
56
Anaplastic carcinoma: METS (2)
1. Local and distant METS
2. May invade trachea (20% of patients need tracheostomy)
57
Anaplastic carcinoma: Prognosis
Poor prognosis\*
58
Anaplastic carcinoma: Management (3)
1. Most are not amenable to surgical resection
2. External beam radiation
3. Chemotherapy
59
What is the MC cause of primary hyperparathyroidism?
Parathyroid adenoma
60
MEN 1
1. Hyperparathyroidism
2. Pituitary Tumors
3. Pancreatic Tumors
61
MEN 2a
1. Hyperparathyroidism
2. Pheochromocytoma
3. Medullary thyroid carcinoma
62
Why does the PTH increase with secondary hyperparathyroidism?
It is a response to hypocalcemia or vitamin D deficiency
63
MC cause of secondary hyperparathyroidism
Chronic kidney failure
64
Clinical manifestations of hyperparathyroidism
Stones, bones, abdominal groans, psychic moans
Decreased DTR
65
Primary hyperparathyroidism: Diagnosis (4)
1. **_Triad_**: Hypercalcemia + increased intact PTH + decreased phosphate
2. Increased 24 hour urine calcium excretion
3. Increased vitamin D
4. Osteopenia on bone scan
66
Hypoparathryroidism: Clinical manifesetations
Signs of hypocalcemia: carpopedal spasm, Trousseau & Chvostek sign, perioral paresthesias, increased DTR
67
Hypoparathyroidism triad
1. Hypocalcemia
2. Decreased intact PTH
3. Increased phosphate
68
Hypocalcemia: ECG findings
Prolonged QT interval
69
Hypocalcemia: GI findings
Diarrhea, abdominal cramps
70
Hypocalcemia: Management (severe or symptomatic)
**_Calcium gluconate IV_**\* or calcium carbonate IV
71
Hypocalcemia: Management (mild) (2)
1. PO calcium + Vitamin D (erogcalciferol, calcitriol)
2. K and Mg repletion may be needed in some cases
72
Hypercalcemia: ECG findings
Shortened QT interval
73
Hypercalcemia: Management (4)
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)
74
Osteoporosis: Dexa scan results
Bone density T score ≤ -2.5
75
Osteopenia: Dexa scan results
T score ≤ 1.0 to -2.5
76
1st line treatment for osteoporosis
Bisphosphonates
77
Bisphosphonates: Side effects
Pill esophagitis, jaw necrosis, pathologic femur fracture (esp. with IV)
78
Bisphosphonates: PO medications
Alendronate, risedronate, ibandronate
79
Bisphosphonates: IV medications
Pamidronate and Zoledrenic acid (most potent)
80
What medication is used for osteporosis in postmenopausal women?
Raloxifene (SERM)
81
Last-line therapy for osteoporosis
Calcitonin
82
Osteogenesis imperfecta: clinical manifestations
Severe osteoporosis, spontaneous fractures in childhood, blue sclerae, and presenile deafness
83
What is renal osteodystrophy?
Group of bone disorders (***osteitis fibrosis cystica and osteomalacia present in pts with chronic kidney disease***)
84
Renal osteodystrophy: clinical manifestations
Bone and proximal muscle pain (in the context of uremia)
85
Renal osteodystrophy: Labs
1. Decreased calcium and increased phosphate and PTH (secondary hyperparathyroidism)
2. Increased alkaline phosphatase
86
Renal osteodystrophy: X-rays (Osteitis fibrosis cystica)
1. Periosteal erosions
2. Bony cysts with thin trabeculum and cortex
3. ***"Salt and pepper***" appearance of the skull on X-ray
87
Renal osteodystrophy: Biopsy
***Cystic brown "tumors"*** (not an actual tumor)
88
Renal osteodystrophy: Management (3)
1. Phosphate binders: calcium carbonate, calcium acetate, sevelamer (used if both calcium and phosphate levels are elevated)
2. Vitamin D (ergocalciferol)
3. Cinacalcet
89
Osteomalacia and rickets: Labs
1. Decreased vitamin D, decreased calcium and decreased phosphate, increased alkaline phosphate
90
Osteomalacia and rickets: X-rays
Looser lines (zones)\*: transverse "pseudo fracture" lines on X-ray
91
Osteomalacia and rickets: Management
Vitamin D supplementation (ergocalciferol) + calcium supplementation
92
Three layers of the adrenal gland
1. Outer layer: Zona glomerulosa
2. Middle layer: Zona fasciculata
3. Inner layer: Zona reticularis
93
Zona glomerulosa
Aldosterone (controls Na balance)
94
Zona fasciculata
Cortisol
95
Zona reticularis
Produces androgen/estrogen
96
Etiologies for Addison's disease (primary adrenocortical insufficiency) (5)
1. Autoimmune: ***MC cause in industrialized countries***
2. **_Infection:_ (MC worldwide)**
3. Vascular
4. Metastatic disease
5. Medications
97
Infectious causes for Addison's disease (4)
1. ***TB***
2. Fungal infections (ex: Histoplasmosis)
3. CMV
4. HIV
98
Vascular causes for Addison's disease
Thrombosis or hemorrhage in the adrenal gland (Waterhouse-Friderichsen); trauma
99
Medications that may cause Addison's disease
Ketoconazole, rifampin, phenytoin, barbituates
100
Secondary adrenocortical insufficiency etiologies (2)
1. Exogenous steroid use MC cause
2. Hypopituitarism
101
What makes secondary or tertiary causes of adrenal insufficiency different from primary cause?
Aldosterone is intact; there is a lack of cortisol
102
Since the aldosterone is decreased in primary (in contrary to secondary) what extra clinical manifestations are found with this disease? (5)
1. Hyperpigmentation
2. Marked orthostatic hypotension
3. Severe hyponatremia
4. Hyperkalemia
5. Non anion gap metabolic acidosis\*
103
Screening test used for adrenal insufficiency
High dose ACTH (Cosyntropin) stimulation test
104
What test is used to differentiate between the different causes of adrenal insufficiency?
CRH stimulation test
105
CRH Stimulation Test: Primary/Addison (adrenal) results
Produces high levels of ACTH but low cortisol
106
CRH stimulation test: secondary (pituitary) results
Low ACTH + low cortisol\*
107
1st line treatment for primary adrenal insufficiency
Hydrocortisone + Fludrocortisone
108
Adrenal (Addisonian) Crisis: Clinical manifestations (3)
1. Shock\* primary manifestation
2. Hypotension, hypovolemia
3. Nonspecific symptoms (abd. pain, n/v, fever, weakness, lethargy, coma)
109
Adrenal (Addisonian) Crisis: lab studies (2)
1. BMP=hyponatremia, hyperkalemia, hypoglycemia
2. Cortisol levels, ACTH, CBC
110
Adrenal (Addisonian) Crisis: Management (4)
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
What is cushing's syndrome?
Signs and symptoms related to cortisol excess
112
What is Cushing's disease?
Cushing's syndrome caused specifically by pituitary increased ACTH secretion
113
Screening tests for diagnosing Cushing's syndrome (3)
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
Differentiating tests for causes of Cushing's syndrome (2)
1. High dose dexamethasone suppression test (suppression is indicative of Cushing's disease)
2. ACTH levels (decreased ACTH is indicative of adrenal tumors)
115
Cushing's syndrome: Management (3)
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
Primary hyperaldosteronism (4)
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
Secondary hyperaldosteronism
1. Increased aldosterone due to increased renin\*\*
2. MC due to renal artery stenosis\* or decreased renal perfusion (CHF, hypovolemia, nephrotic syndrome)
118
Hyperaldosteronism: Clinical manifestations (2)
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
Hyperaldosteronism: Labs
Hypokalemia with metabolic alkalosis
120
Hyperaldosteronism: Aldosterone to Renin ratio screening
1. Done in patients with HTN
2. ARR \>20 and plasma aldosterone \>20 and low plasma rening levels → Primary aldosteronism
2. High plasma renin levels → secondary aldosteronism
121
Hyperaldosteronism: Conn's syndrome management
Excision of adrenal aldosteronomas + spironolactone
122
Hyperaldosteronism: Hyperplasia management
Spironolactone, ACEI, CCB. Correct electrolyte abn.
123
Hyperaldosteronism: Secondary (renovascular HTN) management
Angioplasty definitive. ACEI
124
Pheochromocytoma: Management (2)
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
Types of anterior tumors (5)
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
Diagnosis of acromegaly (2)
1. Insulin-like growth factor (screening test)
2. Confirmatory test: oral glucose suppression test (will show increased GH levels in acromegaly)
127
Adrenocorticotropinomas: Clinical manifestations
1. Cushing's disease and hyperpigmentation
128
Anterior pituitary tumors: Diagnosis (2)
1. MRI study of choice to look for sellar lesions/tumors\*
2. Endocrine studies: Prolactin, GH, ACTH, TSH, FSH, LH
129
Anterior pituitary tumors: Management of active or compressive tumors (3)
Transsphenoidal surgery (TSS)
130
Acromegaly: Management (3)
1. TSS + Bromocriptine (dopamine agonist)
2. Pegvisomant (GH antagonist)
3. Octreotide: Somatostatin analogue
131
Prolactinoma management
Cabergoline\* or bromocriptine
132
SIADH: CNS etiologies (6)
1. MC stroke (SAH)
2. Head trauma
3. Meningitis
4. CNS tumors
5. Post-op
6. Hydrocephalus
133
SIADH: Pulmonary etiologies (2)
1. Small cell lung CA
2. Infection (ex: Legionella pneumonia)
134
SIADH: Medication etiologies (8)
1. Narcotics
2. NSAIDs
3. Anticonvulsants
4. Carbamazepine
5. High dose IV cyclophosphamide
6. Antidepressants (TCA/SSRIs)
7. HCTZ
8. Ectasy (MDMA)
135
SIADH: Endocrine etiologies (2)
1. Hypothyroidism
2. Conn's syndrome
136
SIADH: Diagnosis (3)
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
SIADH: Management (2)
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
What is diabetes insipidus?
ADH (vasopressin) deficiency (central DI) or insensitivity to ADH (nephrogenic) → inability of kidney to concentrate urine → production of large amounts of dilute urine
139
Central DI: Etiology
No ADH production\*\*: MC type
(Others include idiopathic, autoimmune destruction of posterior pituitary, head trauma, tumor, infection, sarcoid granuloma)
140
Nephrogenic DI: Etiology (3)
1. Partial or complete insensitivity to ADH
2. Drugs: ***Lithium***\*, amphotericin B, demeclocycline
3. Hypercalcemia or hypokalemia, acute tubular necrosis, hyperparathyroidism
141
Diabetes insipidus: Clinical manifestations (2)
1. Polyuria + polydipsia. Nocturia
2. Hypernatremia if severe or decreased PO H20 intake
142
Diabetes insipidus: Diagnosis (2)
1. Fluid deprivation test: establishes the dx of DI. DI patients will have continued production of dilute urine
2. Desmopressin (ADH) stimulation test
143
Diabetes insipidus: Central DI management
1. Desmopressin/DDAVP (synthetic ADH)\*
2. Carbamazepine
144
Diabetes insipidus: nephrogenic DI
1. Na/protein restriction
2. HCTZ, indomethacin
145
Diabetes insipidus: symptomatic management
Hypotonic fluid (pure water orally is preferred, D5W, 1/2 NS)
146
With DM, what does a kidney biopsy show?
**_Kimmelstiel-Wilson_**\*
147
Diabetes Mellitus: Diagnosis (4)
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
Rapid-Acting Insulin (2)
1. Lispro (Humalog)
2. Aspart (Novalog)
149
Rapid-Acting Insulin: Onset, peak, duration
Onset: 5-15 min
Peak: 1 hour
Duration: 3 hours
150
Rapid-Acting Insulin: Insulin coverage
Given at the same time of meal. Often used with intermediate or long acting insulin
151
Short-acting insulin
Regular (Humulin-R)
152
Short-acting insulin: Onset, peak, and duration
Onset: 30 min-1 hour
Peak: 2-3 hours
Duration: 4-6 hours
153
Short-acting insulin: Insulin coverage
Given _30-60 min prior to meal_. Often used with intermediate or long acting insulin
154
Intermediate-acting insulin (2)
1. NPH (Humulin N or Novolin N)
2. Lente (Humulin L or Novolin L)
155
Intermediate-acting insulin: onset, peak, and duration
Onset: 2-4 hours
Peak: 4-12 hours
Duration: 16-20 hours
156
Intermediate-acting insulin: Insulin coverage
Covers insulin for about half day (or overnight)
Often combined with rapid or short-acting insulin
157
Long-acting insulin (3)
1. Ultralente (U)
2. Insulin glargine (Lantus)
3. Detemir (Levemir)
158
Long-acting insulin: Onset, peak, and duration
Onset: 6-8 hours
Peak: 12-16 hours
Duration: 20-30 hours
159
Long-acting insulin: insulin coverage
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
What is the Dawn phenomenon?
Normal glucose until 2-8 am when it rises
161
Dawn phenomenon results from what?
Decreased insulin sensitivity and nightly surge of counter regulatory hormones (during nighttime fasting)
162
Dawn phenomenon: Management
Bedtime injection of NPH, avoid CHO snack late at night, insulin pump usage early in the morning
163
What is Somogyi effect?
Nocturnal hypoglycemia followed by rebound hyperglycemia (due to surge in GH)
164
Somogyi effect: management
Prevent hypoglycemia\*: decreasing nighttime NPH dose or give bedtime snack
165
Insulin waning: management
Move insulin dose to bedtime or increse dose
166
Biguanides (2)
1. Metformin (Glucophage)
2. Phenformin
167
Biguanides: Mechanism of action (3)
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
Biguanides: Side effects/caution (3)
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
Sulfonylureas: 1st generation
Tolbutamide, chlorpropramide
170
Sulfonylureas: 2nd generation
Glipizide, glyburide, glimepiride
171
Sulfonylureas: Mechanism of action (1)
1. Stimulates pancreatic beta cell insulin release\*
172
Sulfonylureas: Side effects/caution (5)
1. Hypoglycemia MC side effect\*\*
2. GI upset, dermatitis
3. Disulfuram reaction\*
4. Weight gain
5. CP450 inducer
173
Meglitinides (2)
1. Repaglinide
2. Nateglinide
174
Meglitinides: Mechanism of action
Stimulates pancreatic beta cell insulin release (insulin secretagogue)
175
Meglitinides: Side effects/caution (2)
1. Hypoglycemia (less than sulfonylureas)
2. Weight gain
176
Alpha-glucosidase inhibitors (2)
1. Arbacose
2. Miglitol
177
Alpha-glucosidase inhibitors: Mechanism of action (2)
1. Delays intestinal glucose absorption
2. Does not affect insulin secretion
178
Alpha-glucosidase inhibitors: side effects/caution (2)
1. Hepatitis, flatulence, diarrhea, abdominal pain
2. Cautious use in patients with gastroparesis, IBD
179
Thiazolidinediones (2)
1. Pioglitazone
2. Rosiglitazone
180
Thiazolidinediones: Mechanism of action
1. Increases insulin sensitivity @ peripheral receptor site adipose and muscle\*
2. No effect on pancreatic beta cells
181
Thiazolidinediones: side effects/caution (2)
1. Fluid retention and edema\* (CHF)
2. Cardiovascular toxicity with Rosiglitazone\* (MI)
182
Glucagon-Like Peptide 1 (GLP-1) Agonists (2)
1. Exenatide
2. Liraglutide
183
Glucagon-Like Peptide 1 (GLP-1) Agonists: Mechanism of action
1. Lowers blood sugar by mimicking incretin → Increases insulin secretion, decreases glucagon secretion, delays gastric emptying\*
184
Glucagon-Like Peptide 1 (GLP-1) Agonists: side effects/caution (2)
1. Hypoglycemia, pancreatitis
2. CI if h/o gastroparesis
185
DPP-4 inhibitor (2)
1. Sitagliptin
2. Linagliptin
186
DPP-4 inhibitor: mechanism of action
Dipeptidylpeptase inhibition → inhibition of degredation of GLP-1 → Increases GLP-1
187
DPP-4 inhibitor: side effects/caution
Pancreatitis, renal failure, GI sx
188
SGLT-2 Inhibitor (2)
1. Canagliflozin
2. Dapagliflozin
189
SGLT-2 Inhibitor: mechanism of action
SGLT-2 inhibiton lowers renal glucose threshold → increases urinary glucose excretion
190
SGLT-2 Inhibitor: side effects/caution
Thirst, nausea, abdominal pain, UTIs
191
