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Endocrine Flashcards

1
Q

what hormones do the anterior pituitary secrete? (also called adenohypophysis)

A 
FSH
LSH
ACTH
TSH
Prolactin
GH
Melantropin
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2
Q

What hormone does the posterior (neurohypophysis)?

A

Vasopressin
Antidiuretic hormone
ADH
oxytocin

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3
Q

What are the parts of the pancreas?

A

Islets of Langerhans (alpha, beta)
Alpha= gulcagon
B= insulin
Gamma= somatostatin

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4
Q

What are the steps of insulin?

A

pre-pro insulin to proinsulin to insulin

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5
Q

Briefly describe the mechanism of insulin?

A

Binds to insulin receptors on the cell
Induces glucose uptake
Gene transcription

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6
Q

Does insulin cross the placenta?

A

No, but glucose does

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7
Q

Which are insulin dependent transporters?

A

GLUT 4 (adipose tissue) striated muscle

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8
Q

Which one are insulin -dependent transporters?

A

GLUT 1: RBC (brain, cornea)
GLUT 2: liver, kidney, small intestine
GLUT 3: brain, placenta
GLUT 5: fructose

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9
Q

What does glucagon do? What cells secrete it?

A

1) Made by alpha cells of the pancrease
2) Catabolic effects (glycogenesis, gluconeogenesis)
3) Lipolysis and ketone production
4) Secreted in response to hypoglycemia
5) Inhibited by insulin, hyperglycemia, and somatostatin

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10
Q

What are the hypothalamic-pituitary hormones?

A

1) CRH
2) Dopamine
3) GHRH
4) GnRH
5) Prolactin
6) Somatostatin
7) TRH

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11
Q

What does CRH do?

A

Increases ACTH, MSH, B endorphin

Decreased in chronic exogenous steroid use.

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12
Q

What does dopamine do?

A

Decrease prolactin
Increase TSH
Dopamine antagonists can cause galactorrhea due to hyperprolactinemia

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13
Q

What does GnRH?

A

Increased FSH, LH

Suprreses hyperprolactinemia

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14
Q

What does prolactin do?

A

Decrease GnRH

If have a prolactinemia —>amenorrhea, osteoporosis, hypogonadism, galactorrhea

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15
Q

What does somatostatin do?

A

Decrease GH, TSH

Used to treat acromegalu

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16
Q

What does TRH do?

A

Increased TSH, prolactin

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17
Q

Function of prolactin?

A

Stimulates milk production in the breast
Inhibits ovulation in females and spermatogenesis in males
Too much prolactin leads to decreased libido

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18
Q

How does prolactin inhibit it’s own production?

A

prolactin is secreted by anterior pituary
(inhibited by dopamine)
Prolactin will inhibit its own secretion by STIMULATING dopamine

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19
Q

How are prolactinemia treated?

A

Bromocriptine (dopamine agnosit) inhibits the secretion of prolactin

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20
Q

What are side effects of dopamine antagonists? what are common dopamine antagnoists?

A

1)antipyschotics

They will stimulate the production of prolactin

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21
Q

What does the growth hormone Somatotropin do?

A

Secreted by the anterior pituitary
Stimulates linear growth and muscle mass
Secretion is increased during exercise or deep sleep
Released when pulse of GHRH
Excess GH leads to gigantism or acromegaly

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22
Q

What are the hormones responsible for appetite regulation?

A

1) Grehlin
2) Leptin
3) Endocannabinoids

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23
Q

What does Ghrelin do?

What increases production?

A

1) Stimulate hunger and GH release

2) Sleep deprivation and Prader-Willi can increase production

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24
Q

What does leptin do?

A

Satiety hormone
Produced by adipose tissue
Can be produced by sleep deprivation or starvation

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25
Q

What do endocannabinoids do?

A

Receptors in the hypothalamus

Increase the appetite (munchies)

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26
Q

Where is anti-diuretic hormone made?

What is the function?

A

1) Posterior pituitary

2) Regulates osmolarity and blood pressure

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27
Q

What happens to ADH level in diabetes insipidus?

A

ADH is decreased in central diabetes insipidus

However it can be increased in nephorgenic DI

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28
Q

How is the antidiuretic hormone regulated?

A

Osmoreceptors in hypothalamus (hypovolemia)

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29
Q

What is the source, regulation, and effects of cortisol?

A 
1) Adrenal zona fasciculata
Function:
1) Increase blood pressure
2) Increase insulin resistence
3) Increase glucogenesis
4) decrease fibroblast activity
5) Inhibit WBC adhemsion
6) Reduce esinophils 
7) decrease bone formation

Regulation:
CRH (hypothalamus) stimulates ACTH release from the pituitary

Chronic stress will prolong secretion

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30
Q

What are the three forms of ionized calciumÉ

A

Ionized (45%)
Bound to albumin (40%)
Bound to anions (15%)

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31
Q

What happens to calcium when you change the ph?

A

Increase in pH will increase the affinity of calcium

Can lead to hypocalcemia (pain, parethsis, carpopedal spasm)

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32
Q

What is source, function, and regulation of vitamin D (cholecalciferol)?

A

1) Exposure of the skin to the sun
2) eating from fish and plants
3) Both are converted to 25-OH in liver and to 1,25 in the kidney

Function:increased absoption of dietery Calcium and phosphate

Regulation: Increased PTH will lead to decreased calcium and phosphate

The 1,25 (OH) will inhibit it’s own production

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33
Q

What medical conditions are caused by deficiency of vitamin D?

A

1) Ricketts in kids
2) Osteomalacia in adults
3) Malabsorption (Decrease sunlight)

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34
Q

What is the source, function, and regulation of the parathyroid hormone?

A

1) Produced by chief cells
2) Increase bone absortpiont of Ca 2+
3) Increase absorption of Ca in the kidneys
4) Decrease resoprtion of phosphate

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35
Q

What is the source, function, regulation of calcitonin?

A

1) Parafollicular cells of the thyroid
2) Decrease bone resorption of the Ca
3) Increase serum Ca

Calcitonin opposes action of PTH

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36
Q

What are the source, function of the thyroid hormone?

A

Source: follicles of the thyroid

Function:
Bone growth
Increased B receptors of the heart
Increased basal metabolic rate 
Increase glycogenolysis
Increase glucogenesis
Increase lipolysis

Regulation:
Through the TRH (hypothalamus) stimulates the follicular cells

Can also be stimulated by TSI (thyroid stimulating immunoglobulin) in Graves disease

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37
Q

What is the difference between the T3 and T4? What does the thyroid binding globulin do?

A

T4 is the major thyroid product, and converted to T3 in the periphereal tissue

The thyroxine binding globulin binds to T3/T4 in the blood, so only free hormone is active

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38
Q

What is the Wolff-Chaikoff effect?

A

Excess iodine inhibits the thyroid peroxidase (decrease iodine organification) and decrease the T3 and T4 production

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39
Q

What is the cycle of thyroid release?

A

Hypothalamus releases the TRH—–acts on the anterior pituitary—-releases the TSH—–causes the thyroid follicular cells to release the thyroid hormone

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40
Q

What are the signalling pathways of endocrine hormones?

A

1) cAMP
2) cGMP
3) IP3
4) Intracellular receptors:progesterone, estrogen, testosterone, cortisol, aldosterone
5) Receptor tyrosine kinas: Insulin, IGF-1. FGF, PDFG, EGF
5) Non receptor tyrosine kinase: IL-2, IL-6, IFN

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41
Q

What is the effect of sex hormone binding globulin on men/women?

A

In men, increase in SHBG lowers the free testosterone causing gynecomastia

In women decrease in SHBG increases the free testosterone causing hirutism

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42
Q

What is the etiology of cushing?

A

Increased in cortisol
Cause: exogenous use (results in decreased ACTH, bilateral adrenal atrophy)

Primary adrenal adenoma

ACTH secreting adenoma

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43
Q

what are the findings associated with Cushing?

A 
HTN
Weight gain
Moon farcies
Abdominal Striae
Truncal Obesity 
Buffalo hump 
Amenorrhea
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44
Q

what is the screening test of Cushings?

A

1) Increase free cortisol on 24 hour urinalysis
2) Increase midnight salivery cortisol
3) No suppression with overnight low-dose dexamthesone test

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45
Q

How to determine if it is ACTH-independent Cushings?

A

Measure ACTH
If ACTH suppressed, then have an ACTH-independent Cushing syndrome
(do MRI do confirm an adrenal tumor)

If the ACTH is elevated, then have ACTH dependent Cushing syndrome

The next step is to do a high dose, dexamethsone suppresion test OR CRH stimulation test

CRH
(Increase ACTH, and cortisol = Cushing disease)
No increase in ACTH means ectopic (ectopics don’t respond to stimulation, they are independent).

If adequate suppression (Cushing disease)
No suppression then have ectopic ACTH secretion

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46
Q

What is adrenal insufficiency?

A

Inability to generate glucocorticoids or mineral corticoids

Symptoms: weakness, fatigue, orthostatic hypotension, weight loss, GI disturbances, sugar or salt cravings

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47
Q

How is adrenal insufficiency diagnosed?

A

Measure serum electrolytes (morning and random cortisol)

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48
Q

What is primary adrenal insufficiency?

A

Low cortisol, high ACTH
Metrapone stimulation test: (blocks least step of cortisol synthesis), normal response is decreased in cortisol and compensatory increase in ACTH. In primary, the ACTH increases, but 11-deoxycortisol remains low.

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49
Q

what are the results of secondary adrenal insufficiency?

A

low cortisol, low ACTH (hypothalamic disease)

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50
Q

What is primary adrenal insufficiency?

A

Aldosterone and cortisol
Causes:
Hypotension (hyponatremic) hyperkalemia, metabolic acidosis
Acute: sudden onset (due to hemorrage) may present with acute adrenal crisis

Chronic: Addison’s disease: adrenal atrophy or destruction by disease

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51
Q

What is the waterhouse-friderichsen syndrome?

A

Primary adrenal insufficiency due to adrenal hemorrage associated with Neisseria

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52
Q

How to seperate primary, from secondary adrenal insufficiency?

A

Decrease pituitary ACTH production (no skin/mucosal hyperpigmentation) no hyperkalemia

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53
Q

What is tertiary adrenal insufficiency?

A

Seen in patients with exogenous use of steroids
Precipitated by abrupt withdrawl
Aldosterone synthesis unaffected

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54
Q

What is hyperaldosterone?

A

Increased secretion of aldosterone from the adrenal gland

Clinical features include hypertension and metabolic acidosis

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55
Q

What is primary hyperaldosterone?

A 
Adrenal Adenoma (Conn Syndrome)
Idopathic adrenal hyperplasia 
Inceased aldosterone
Decreased renin
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56
Q

What is secondary hyperaldosterone?

A

Renovascular hypertension

Juxtaglomuler cell tumor

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57
Q

What are neuroendocrine tumors?

A

Neoplasms originating from the Kulchitsky and enterochromaffin-like cells

In the thyroid, medullary carcinoma

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58
Q

what are neuroblastoma tumors?

A

Most common tumor in children

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59
Q

what is pheochromocytoma, symptoms, findings, and treatment?

A

1) 25% of pheochromocytoma associated with germline (Nf-1, VHL, RET, Men)

Symptoms: secrete epi, nore, dopaimine, episodic hypertension

Findings: Increased catecholamines and metanephrines in urine and plasma.

Diagnosis: catecholamine and metanephrines in urine and plasma

Treatment: irreversible alpha antagonists
B blockers
Tumor resection

60
Q

What are the symptoms of hypothyroidism?

A 
Cold intolerance
Weight gain
Hypoactivity 
Constipation
Decreases reflexes 
Myxedema (facial/periorbital)
Dry, cool skin, coarse, brittle hair 
Bradycardia, dsypnea on exertion
61
Q

What are lab findings of hypothyroidism?

A

1) Increased TSH
Decrease free T3 and T4
Hypercholesterolemia due to LDL receptor expression

62
Q

What are signs for hyperthyroidism?

A 
Heat intolerance
Weight loss (increase appetite)
Hyperactivity, anxiety, insommonia
Diarrhea
Increased reflexes
Moist skin
Pretibial myxedema (Graves disease)
Chest pain, arrythmia, increased number and sensitivity of B adrenergic receptors
63
Q

What are the lab findins of hyperthyroid?

A

Decreased TSH

Increased free T3 or T4

64
Q

What are the causes of smooth/diffuse goiter?

A

Graves disease
Hashimoto throiditis
Iodine deficiency
TSH secreting pituitary adenoma

65
Q

What are the causes of Nodular goiter?

A

1) Toxic multinodular goiter
2) Thyroid adenoma
3) Thyroid cancer
4) Thyroid cyst

66
Q

What are the causes of Hashimoto thyroiditis?

A

1) Most common cause of hypothyroidsim in iodine-sufficient regions
2) Can have autoimmune disorder with antithyroid peroxidase (antimicrosmal and antithyroglobulin)
3) Associated with increased HLA-DR5
4) Increased risk of Non-Hodgkins lymphoma

* in the beginning may have hyperthyroid due to thyrotoxicosis during follicular rupture*

67
Q

What are the findings in Hashimoto hypothyroidism?

A

Moderately enlarged, non tender thyroid

68
Q

What are symtoms of congenital hypothyroidism?

A

Severe fetal hypothyroidism due to maternal hypothyroidism

Thyroid agenesis

Symptoms:Pot-bellied
Pale
Puffy face (protrubding ombilicus)
Poor brain development

69
Q

What are signs of subacute granulomatous thyroiditis9de Quervan)?

A

Usually self limiting disease
May be hyperthyroid before hypothyroid
Will have granulomatous inflammtion
High ESR

70
Q

What is Riedel thyroiditis?

A

Thyroid replaced by fibrous, inflammatory infiltrate
Extend up to the trachea and look like anaplastic carcinoma
Usuaully manifestation of IgG related systemic disease

71
Q

What are other causes of hypothyroidism?

A

Iodine deficiency
Goitrogens (amiodarone/lithium)
downrefulation in response to idodie

72
Q

What are signs of Graves disease?

A

1) Thyroid stimulating immunoglobulin (IgG type 2)

2) Can occur during stress (pregnancy)

73
Q

What are caused of hyperthyroidism?

A

1) Graves disease (due to IgG immunoglobulin)
2) Toxic multinodular goiter (hyperfunctioning cells
3) Jod-Basedow (thyotoxicosis if a patient develops iodine deficiency, and partially autonomous thyroid tissue

74
Q

Thyroid adenoma?

A

Benign growth
Usually cold nodule
Commonly follicular
Absence of capsular and vascular invasion

75
Q

How is thyroid cancer treated? What are the complications?

A

1) Treated with surgery
2) Complications: hoarseness, recurrent laryneal damage, hypocalcemia, transection of recurrent and superior laryngeal nerves

76
Q

What are the associations with papillary carcinoma?

A

1) Excellent prognosis
2) Empty nuclei
3) Psammoma bodies
Increased RET nd BRAF mutations

77
Q

What are follicular carcinoma?

A

1) Good prognosis
2) Invades thyroid capsule and vasculature
3) Associated with the RAS mutation

78
Q

What is medullary carcinoma?

A

Parafollicular C cells
Produce calcitonin
Sheets of cells in amyloid stroma
Associated with MEN 2A and 2B

79
Q

what are undifferenitated, anaplastic carcinoma?

A

Older patients, invades local structures, and very poor prognosis

80
Q

What problems with the thyroid if have lymphoma?

A

Hashimoto thyroiditis

81
Q

What are the PTH charcacteristics of hyperparathyroidism (primary and secondary) and hypoparathyroidism?

A

Primary hyperparathyroidism: hyperplasia, adenoma, carcinoma (high PTH and high CA2+ in range over 12

Secondary hyperparathyroidism: vitamin D deficiency
High PTH ( and the Ca ub tge range below 10)

Primary hypoparathroidism: (low PTH) and low ca (due to surgical ressection)

PTH independent hypercalcemia : excess hypercalciemia

82
Q

what are the signs of hypoparathyroidism?

A

Tetany
Hypocalcemia
Hyperphophatemia

83
Q

What are the physical signs of hypoparathyroidism?

A

Chvostek sign (tapping of facial nerve leads to contraction)

Trousseau sign: occlusion of the brachial artery, leads to carpel spasm

84
Q

What is pesudohypoparathyroidism type A?

A

Kidney unresponsive to PTH
Hypocalcemia despite increased PTH levels
Characterized by shortened 4th and 5 th digits
Short stature (inheritied)

85
Q

What is pseudohypoparathyroidism?

A

Have the same physical exam as Albright Heredity but with end organ PTH resistance
Occurs due to defective Gs protein from the father

86
Q

What is familial hypocalciuruic hypercalcemia?

A

Defective Ca sensing receptor (in parathyroids, and kidneys)
Higher then normal Ca levels needed to suppress the PTH
Excessies renal Ca uptaje by the kidney
Mild hypercalcemia and hypocalciuria with increased levels of PTH

87
Q

What are the causes of primary hyperparathyroidism? What are the symptoms?

A

1) Due to parathyroid adenoma or hyperplasia
2) Signs include: hypercalcemia, renal stones, hypophosphatemia
3) will have abdominal flank pain, kidney stones, depression
4) will have osteitis fibrosa: bone spaces filled with brown fibrous tissue

88
Q

What are the signs of secondary hyperparathyroidism?

A

Hyperplasia due to decrease Ca absorption, and increased Posphate (chronic renal disease)

Tertiary hyperparathyroidism: results from chronic renal disease with increased PTH and ALP

89
Q

What are signs of tertiary hyperparathyroidism?

A

1) Refractory hyperparathryoidism due to chronic renal disease

Increased PTH
and increased Ca+

90
Q

What are pituitary adenomas? Where do they arise from?

What is treatment?

A

1) Benign tumor
2) Commonly prolactinoma
Functional: produces hormone (non-functional does not)
3) Also called prolactinoma (treat with dopamine agonist, or with ressection)

91
Q

What are characteristics of Nelson syndrome?

A

You have bilateral adrenectomy (for refractory Cushing disease) and then have enlargement of existing ACTH secreting pituitary tumor.

92
Q

What are the findings, diagnosis, and treatment of acromegaly?

A

1) Excess , frontal GH in adults
2) Usually pituitary adenomo
Findings: large tongue, deep furrows, course features , frontal bossing, and glucose intolerance.
Treatement: Adenoma ressction, if not treat with octerotide.

93
Q

What are symptoms of Laron syndrome?

A

Defective growth hormone receptors
Decrease in linear growth
Increase in GH
Decrease in IGF-1

The characteristics: saddle nose, prominent forehead, delayed malnutrition, skeletal mutation, small genitilia

94
Q

What are characteristics of Diabetes Insipidus? Etiology, findings, treatment?

A

Can be central or nephorgenic

1) Thirsy, polyuria, inability to concentrate urine
2) Findings: decrease ADH, decreased urine specificity
3) Water deprivation test (> 50% increase in urine osmolality)
Treatement: Desmopressin acetate (hydration)

95
Q

What are the syndromes of nephrogenic DI?

A

1) Caused by hereditary (ADH receptor mutation)
2) Will have hypercalcemia, hypokalemia lithium
What happens to ADH levels: increased
TreatmenL HCTZ, indomethacin, amiloride, hydration (avoidance of offending agent)

96
Q

What is the syndrome of inappropriate anti-diuretic hormone?

A

1) Excessive free water retention
2) Euvolemia hyponatremia with continued urinary Na2+ excretion

3) Urine osmolarity > serum osmolarity

97
Q

What are the causes of inappropriate anti-diuretic hormone secretion?

A

1) Ectopic ADH
2) CNS disorder/head trauma
3) Pulmonary disease
4) Drugs

98
Q

What are causes of hypopituitarism?

A

1) Non secreting pituitary adenoma, carniopharyngioma
Sheehan syndrome: ischemic infarct of pituitary following post partum bleeding, pregnancy

(usually due to failure to lactate, absent mensturation, cold intolerance)

2) Empty sella syndrome (atrophy or compression of pituitary) lies within the sella turcica

3) Pituitary apoplexy: sudden hemorrage of the pituitary gland (usually an existing adenoma)
Usually due to brain injury
Radiation
Treatment: hormone replacement therapy (corticosteroids, thyroxine, sex steroids, human growth hormone).

99
Q

What are the signs of Diabetes Mellitus?

A 
Polydipsia
Polyuria
Polyphagia
Weight loss
DKA
Hyperosmolar coma
100
Q

What are the complications of DM?

A

Small vessel disease (diffuse thickening)
Large vessel disease (CAD, atherosclerosis)
Osmotic damage: neuropathy, cataracts

101
Q

What are the tests for diagnosis of diabetes?

A

1) HbA1c > 65% (reflects average blood glucose over prior 3 months)
2) Fasting plasma glucose: fasting for more > 8 hours
3) 2 hour (oral glucose tolerance) 2 hours after consumption of glucose in wateer

102
Q

What can happen with chronic hyperglycemia?

A 
Increase plasma osmolarity
Increase thrist
Increase osmotic diuresis
Loss of Na and K
Hypovolemia
Circulation failure and decrease tissue perfusion
Coma and death
103
Q

What are the differences between type 1 and type 2 diabtetes?

A

Autoimmune destruction of B cells (glutamic acid)

Type 2: increase resistence to insulin, progressive pancreatic B cell failure

104
Q 
What is the age of type 1 vs type 2?
Genetic disposition ?
Association with HLA system? 
Glucose intolerance?
Insulin sensitivity?
Occurence of ketoacidosis?
B cell numbers in the islets?
Presence of classic syntoms of polyuria, polydipsia, polyphagia, weight loss? 
What is the histology?
A

1) age 40 years
2) More in type 2
3) HLA association (no for type 2)

4) Glucose intolerance is severe in type 1
5) Insulin sensitivity is high in type 1
6) Common in type 1
7) decreased in type 1, variable with amyloid deposits
8) Common classic symptoms in type 1
9)

105
Q

What are the causes of ketoacidosis?

A

Usually due to non compliance of insulin.
Increased insulin requirements from increased stress
Increased fat breakdown
Usually occurs in diabetes type 1

106
Q

What are signs of diabetes ketoacidosis?

A

Delirium
Kussmal respiration
Abdominal pain (nausea/vomiting/dehydration)

107
Q

What do the labs show during diabetes ketoacidosis?

A

Hyperglycemia
Increase H+ and HCO3-
Anion gap metabolic acidosis
Increased blood, ketone levels

108
Q

What are the complications of DKA?

A

Life threatening mucormycosis
Cerebral edema
Cardiac arrythmias
Heart failure

109
Q

What is the treatment of DKA?

A

1) IV fluids
IV insulin
K to replete intracellular stores
Glucose to prevent hypoglycemia

110
Q

What is a glucagonoma?

A

Tumor of the pancreatic cells (overproduction of glucagon)

Presents with dermatitis, diabetes, and DVT, declining weight, depression

111
Q

What are signs of insulinoma?

A

Tumor of pancreatic B cells
Overproduction of insulin
Cause hypoglycemia

Treatment: surgical ressection

112
Q

What is Whipple triad?

A

1) low blood glucose

2) Symptoms of hypoglycemia (lethargy, syncope, diplopia)

113
Q

What are the causes of somatostatinoma?

A 
Tumor of pancreatic gamma cells
Overproduction of somatostatin
Decrease secretin
Can present as diabetes/glucose intolerance
Steatorrhea, gallstones

Treatment is ressection

114
Q

What is carcinoid syndrome?

A

Rare syndrome caused by carcinoid tumor

Treatment is surgical ressection or somatostatin analogue

115
Q

What is the rule of 1/3 in carcinoid ?

A

1/3 metastasize
1/3 secondary to malignancy
1/3 are multiple.

116
Q

what is Zollinger-Ellison syndrome?

A

Gastrin secreting tumor of the pancrease/duodenum
Presents with abdominal pain
diarrhea

How to test: gastrin levels remain elevated after adminsitratio of secretin (normally inhibits gastrin release)

117
Q

What are the different types of MEN?

A

MEN 1
MEN 2A
MEN 2B

118
Q

What are the MEN 1 tumors?

A 
Pituitary tumor (prolactin or GH)
Pancreatic endocrine tumors: Zollinger Ellison, insulinomas, VIPomas, Gluconomas
Parathyroud adenomas
119
Q

What are the MEN 2A?

A

Parathyroid hyperplasia
Medullary thyroid carcinoma
Pheochromocytomas

120
Q

What are the 2B tumors?

A

Medullary thyroid carcinoma
Pheochromocytoma
RET

121
Q

What are the treatment strategies for type 1 and type 2 diabetes?

A

Type1: low carb, insulin replacement

Type 2: dietary modification, excess weight loss, oral agents, non insulin injectables.

122
Q

What are the types of rapid acting insulin preperations?

Action/clinical use/risks?

A

1) Lispro, Aspart, Glulisine
2) Increases glucose storage in the liver
Muscle: increase glycogen, protein synthesis

Clinical uses: DM 1, DM 2

Risks: hypoglycemia, lipodystrophy, hypersensitivity

123
Q

When is insulin short acting (regular used)?

A

Used in type 1, and type 2 DM

Hyperkalemia (glucose) stress hyperglycemia

124
Q

When to offer NPH? (intermediate acting)

A

Type 1 DM

Type 2 GDM

125
Q

When are long acting insulin used? The names?

A

1) Detemir and glargine

Used for type 1 and type 2 DM

126
Q

what is the mechanism and example of Biguanides?

A

1) Decreases glucogenesis and increased glycolysis, increased peripheral glucose uptake

2) First line of therapy
3) Can be used in patients without islets function
4) An example is metformin
5) Adverse effects include GI upset, adverse effect, lactic acidosis (contra-indicated in renal insufficiency)

127
Q

What are the Sulfonylureses?

A

1) Chloropropamide, tolbutamide, glyburide
2) Stimulate endogenous insulin in type 2 DM
3) Increase risk renal failure, weight gain.

128
Q

What are the Glitazone, thiazolidinediones?

A

1) Increase insulin sensitivity in periphereal tissue
2) Used as monotherapy in type 2 DM
3) Safe to use in renal impairment
4) Weight gain, edema, hepatoxicity

129
Q

What are the oral hypoglycemic drugs (meglitinides)?

A

Postprandial insulin
Used in monotherapy for type 2 diabetes or combined with metformin

Risks: Hypoglycemia

130
Q

What are GLP-1 analogs?

A

1) Increase glucose dependent insulin release
2) Decrease glucagon release
3) Decrease gastric emptying
4) Increase satiety
5) Examples: exenatide, liraglutide

131
Q

What are DPP-4 inhibitors?

A

1) linaglipin, saxagliptin, sitagliptin
2) Increase glucose dependent insulin
3) Decrease glucagon release
4) Risks: Mild urinary or respiratory infections, weight neutral

132
Q

what are the Amylin Analogs?

A

1) Pramlintide
2) Decrease gastric emptying decrease glucagon
3) Clinical use for DM1 or DM2, cause hypoglycemia (in settings of mistimed prandial insulin) nausea

133
Q

What are the sodiu-glucose co-transporter 2 (SGLT02 inhibitors)

Canagliflozin
Dapagliflozin
Empagliflozin

A

1) Block reabsorption of glucose PCT
2) Type 2 diabetes
3) Glucosuria, UTI, vagnal yeast infection, hyperkalemia, dehydration

134
Q

What are the alpha-glucosidase inhibitors?

Acarbose, miglitol

A

Inhbit intestinal brush border alpha glucosidases
Delayed carbohydrate hydrolysis and glucose absorption
Decrease postprandial hypoglycemia

Clinical use: Type 2 DM

Risks: GI disturbances

135
Q

What are examples of Thionamides?

A

1) PTU, methimazole
Mechanism: block peroxidases
Clinical uses: Hyperthyroidsim, PTU blocks periphereal conversion and is used in pregnancy

Adverse effects: Skin rash, agranulocytosis, aplastic anemia, hepatotoxicty

136
Q

What are examples of levothyroxine?

A

1) Thyroid hormone replacement
2) Hypothyroidsim, myxedmea, off label as weight loss supplement
3) Adverse effects: tachycardia, heat intolerance, tremors, arrythmias.

137
Q

How does ADH antagonists (conivaptan, tolvaptan work)?

A

1) Used for SIADH, blocks action of ADH V2 receptor

138
Q

How does desmopressin work?

A

Central (but not nephrongenic DI)

139
Q

How does GH work?

A

GH deficiency, Turner’s syndrome

140
Q

How does oxytocin work?

A

Stimulates labor, uterine contractions, milk let-down

141
Q

How does somatostain work?

A

For acromegaly, carcinoid, and gastrinoma

142
Q

How does demeclocycline work?

A

1) ADH antagonists
2) Clinical use: SIADH
3) Adverse effects: Nephogrenic DI, photosensitivity, abnormalities of skin and bone

143
Q

How do glucocorticoids work?

A

1) Examples include Beclomethasone, dexamethasone, hydrocortisone
2) Clinical uses: adrenal insufficiancy, inflammation, asthma
3) Adverse effects: Cushings (hypertension, weight gain, moon farcies, truncal obesity)
3) Adverse effect: when drug stopped adversely after chronic use

144
Q

What is fludrocortisone?

A

1) Synthetic analog of aldosterone
2) mineralocorticoid replacement second to adrenal insufficiency
3) Similar to glucocorticoids, edema, exacerbation of heart failure

145
Q

What is Cinacalcet?

A

Sensitizes Ca 2+ sensing receptor in parathryoid gland to circulating Ca 2+ PTH
Clinical use: 1 or 2 hyperparathyroidism
Adverse: hypocalcemia

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