Test 1 (Week 2&3) Flashcards

1
Q

What are some potential manifestations of a decrease in extracellular free calcium levels?

A

–Paresthesias (numbness with “pins” and needles” sensations) –Tetanic contractions of skeletal muscle (often in hands, feet, or larynx)

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2
Q

How does 21-hydroxylase deficiency present ?

A

presents in infancy as salt wasting or childhood as precocious puberty; girls can present with virilization

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3
Q

The primary stimulus for insulin release is ____.

A

glucose

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4
Q

What is Cinacalcet and what do you use it for?

A

it’s a calcium mimetic used to decrease PTH secretion in secondary hyperparathyroidism (the result of chronic renal failure)

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5
Q

defined as adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection: Typically the pathogen is the meningococcus Neisseria meningitides. Hypotension, then shock, then DIC

A

Waterhouse-Friderichsen syndrome

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6
Q

How does diazoxide, an antihypertensive, inhibit insulin secretion?

A

it increases the activity of the ATP sensitive K+ channel on the Beta cell

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7
Q

What are the 3 things to remember about MEN type 1?

A

-Parathyroid (Hyperplasia and adenomas) -Pancreas( Gastronoma or Insulinoma) -Pituitary (Prolactinoma)

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8
Q

In Pseudohypoparathyroidism, Serum Ca2+ is low, but the PTH concentration is normal or elevated. How is this happening?

A

In most patients with pseudohypoparathyroidism, there is a congenital reduction in the activity of Gs, and PTH fails to produce a normal increase in cyclic AMP.

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9
Q

What’s the criteria for the diagnosis of diabetes mellitus based on hemoglobin A1C?

A

>6.5%

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10
Q

Whats the rate limiting step in adrenal steroidal biosynthesis?

A

transport of cholesterol to mitochondria by StAR

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11
Q

What’s the mechanism of action of Spironolactone ?

A

–Competes with aldosterone for receptors —-Prevents action of aldosterone —-K sparing diuretic

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12
Q

What’s the name of the synthetic aldosterone?

A

Fludrocortisone

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13
Q

What’s the diagnostic test for adrenal insufficiency?

A

inject Cosyntropin (first 24 Amino acids of ACTH) and measure plasma cortisol response

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14
Q

How does Calcitonin decrease serum calcium?

A

1) inhibits mobilization of calcium from bone 2) increases renal excretion of calcium

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15
Q

Cortisol can bind to the same mineralocorticoid receptor as aldosterone. How do cells with these receptors ensure that only aldosterone binds?

A

these cells have 11 beta-hydroxysteroid dehydrogenase, type 2, which converts cortisol to the inactive derivative, cortisone

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16
Q

What’s the rate limiting step in catecholamine biosynthesis?

A

conversion of tyrosine to dihydroxyphenylalanine (DOPA) by tyrosine hydroxylase

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17
Q

What do you give to treat Addison’s? What if this fails to correct fluid and electrolyte imbalances?

A

hydrocortisone b/c it has both glucocorticoid and mineralocorticoid activity; if this fails to correct fluid and electrolyte disturbances, use fludrocortisone (primarily mineralcorticoid activity)

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18
Q

What are some risk factors of Type 1 diabetes mellitus ?

A

family history (genetics), geography, viral exposure (particularly coxsackievirus)

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19
Q

What causes hypercalcemia associated with malignancy?

A

tumors that hyper secrete parathyroid hormone related protein (PTHrP)

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20
Q

What’s the mechanism of action of sulfonylureas?

A

close potassium channel in beta cell membrane –> cell depolarizes–> insulin released via increased Ca++ influx

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21
Q

How do sulfonylureas work?

A

directly inhibit the ATP sensitive K+ channels which depolarizes the membrane and activates voltage sensitive Ca++ channels which will trigger the release of insulin from the Beta cells (simply put, they lower blood glucose by stimulating insulin secretion)

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22
Q

What is the major metabolic effect of glucocorticoids (cortisol)?

A

stimulation of liver gluconeogenesis

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23
Q

What are the only two adrenal hormones essential for human life?

A

cortisol and aldosterone

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24
Q

List the second generation sulfonylureas

A

glimepiride, glipizide, and glyburide

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25
Q

What will you find in MEN-2B?

A

-thyroid medullary carcinoma -adrenal pheochromocytoma + neuromas and marfanoid body habitus

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26
Q

What are the 3 polys of diabetes?

A

polyuria, polydipsia, and polyphagia

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27
Q

List the Glitazones/thiazolidinediones.

A

pioglitazone and rosiglitazone

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28
Q

At what time of day is it best to give glucocorticoids systemically?

A

in the morning, when endogenous production is highest

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29
Q

What’s the mechanism of action of ketoconazole?

A

blocks 11 beta hydroxyls and 17,20 lyase;

primary use is anti fungal agent

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30
Q

Glucose inters Beta cells of the pancreas via what transporters?

A

GLUT 2

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31
Q

What’s the name of the amylin analog?

A

Pramlintide

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32
Q

What will you find in MEN-2A?

A

-parathyroid hyperplasia -thyroid medullary carcinoma -adrenal pheochromocytoma

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33
Q

What does aldosterone cause to be excreted?

A

potassium and hydrogen

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34
Q

What is the name of the SGLT-2 inhibitor and what is its action?

A

Canagliflozin; blocks reabsorption of glucose in proximal convoluted tubule

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35
Q

What’s the name of the syndrome where you have a solitary aldosterone secreting adenoma?

A

Conn syndrome

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36
Q

List the long acting insulin preparations.

A

Detemir and Glargine

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37
Q

What are the potential toxicities of alpha-glucosidase inhibitors?

A

GI disturbances

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38
Q

beta2-adrenergic stimulation ____ insulin secretion.

A

stimulates (increases cAMP)

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39
Q

How does 17alpha-hydroxylase deficiency present ?

A

in males: pseudohermaphroditism (ambiguous genitalia, undescended testes) in females: lack of secondary sexual development you lack production of androgens

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40
Q

Which corticosteroid is used specifically for seasonal allergies and asthma via nasal spray and inhalers?

A

beclomethasone

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41
Q

Does exercise increase or decrease glucagon secretion?

A

increases; all the glucose present gets sucked up into the muscles

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42
Q

What is Paget’s disease characterized by?

A

excessive resorption and abnormal remodeling of bone

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43
Q

What are the potential toxicities of the amylin analogs?

A

hypoglycemia, nausea, diarrhea

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44
Q

What is multiple endocrine neoplasia 2B comprised of?

A

medullary thyroid cancer, pheochromocytomas, and multiple mucosal neuromatas

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45
Q

What effect does aldosterone play on K+ and H+?

A

aldosterone increases the secretion of these ions

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46
Q

Many of the metabolic effects of insulin, particularly those that occur rapidly, are mediated by ______ and _____ reactions.

A

protein phosphorylation and dephosphorylation reactions

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47
Q

The adrenal medulla is innervated by _____.

A

cholinergic preganglionic fibers.

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48
Q

What causes secondary hyperaldosteronism?

A

activation of renin-angiotensin system; this can be caused by decreased renal perfusion, CHF, pregnancy

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49
Q

List the DPP-4 inhibitors

A

linagliptin, saxagliptin, sitagliptin

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50
Q

What are the adverse effects of Cinacalcet?

A

hypocalcemia, adynamic bone, use with caution with CYP3A4

51
Q

In skin and connective tissue, high levels of glucocorticoids will promote tissue breakdown and inhibit ______

A

collagen synthesis= thinning of skin, thinning of capillaries (easy bruising), purple striae on stomach

52
Q

List the first generation sulfonylureas.

A

chlorpropamide and tolbutamide

53
Q

What’s the most serious adverse effect of metformin?

A

lactic acidosis (thus contraindicated in renal insufficiency)

54
Q

What’s the mechanism of action of Raloxifine?

A

a selective estrogen receptor modulator; enhances calcium retention and retards bone loss; It is the only SERM approved to prevent or delay bone loss in post menopaulsal women.

55
Q

List the bisphosphonates we are supposed to know.

A

alendronate, risedronate, ibandronate, zolendronate

56
Q

What’s the most frequent oral calcium supplement given for hypocalcemia?

A

calcium carbonate

57
Q

What plasma calcium levels would qualify as severe hypercalcemia?

A

>14mg/dL

58
Q

List the rapid acting insulin preparations

A
  • aspart
  • glulisine
  • lispro
59
Q

What are the target tissues of glucagon?

A

liver and adipose tissue

60
Q

How do you make an early (and potentially life saving) diagnosis of 21-hydroxylase deficiency?

A

neonatal dried blood spot test will show increased 17alpha hydroxyprogesterone

61
Q

Amino acids stimulate insulin secretion, but they also stimulate _____ release.

A

glucagon

62
Q

beta cells of the pancreas secrete what?

A

insulin

63
Q

What are the GLP-1 analogs?

A

Exenatide and Liraglutide

64
Q

What’s the primary toxicity for bisphosphonates taken orally?

A

gastric and esophageal irritation, esophagitis

65
Q

How does 11beta hydroxyls deficiency present?

A

girls can present with virilization

66
Q

What’s the mechanism of action of alpha-glucosidase inhibitors?

A

inhibit intestinal brush border alpha glucosidases; this delays carb hyrdolysis and glucose abosorption which will decrease postprandial hyperglycemia

67
Q

What causes primary hyperaldosteronism?

A

aldosterone producing adrenal adenomas

68
Q

What is Teriparatide and how does it work?

A

It’s a PTH analog that, like PTH, when administered at low doses intermittently will produce a net increase in bone formation

69
Q

What are the potential toxicities of DPP-4 inhibitors?

A

mild urinary or respiratory infections

70
Q

Glucocorticoids decrease the number of thymus derived lymphocytes, their transport to the site of antigenic stimulation, and their function. How?

A

glucocorticoids block the release of interleukin-1 from macrophages and interleukin-2 from helper T-cells

71
Q

Does the amount of protein bound calcium increase or decrease in acidosis?

A

Acidosis decreases binding and increases ionized calcium

72
Q

How do bisphosphonates work?

A

Bisphosphonates inhibit the digestion of bone by encouraging osteoclasts to undergo apoptosis, or cell death, thereby slowing bone loss.

73
Q

What are we going to be looking for in the labs of someone we suspect of having a pheochromocytoma?

A

urinary excretion of free catecholamines and metabolites (VMA or metanephrine) as well as free plasma metanephrines

74
Q

What connects the A and B chains of insulin?

A

disulfide bridges

75
Q

The A chain of insulin contains ____ amino acids. The B chain of insulin contains ___ amino acids.

A

A=21 B=30

76
Q

How do salicylates increase insulin secretion?

A

they inhibit cyclooxygenase which is necessary for the production of prostaglandins (prostaglandins inhibit insulin release)

77
Q

What’s a side effect of Teriparatide?

A

may increase risk of osteosarcoma and bone tumors

78
Q

What are the side effects of Glitazones/thiazolidinediones?

A

weight gain, edema, hepatotoxicity, HF, increased risk of fractures

79
Q

What’s the suffix for all bisphosphonate drugs?

A

-dronates

80
Q

What are some of the more important risk factors for Type II diabetes?

A

sedentary lifestyle, obesity, family history, age

81
Q

What screening test is used to check patients for diabetic nephropathy?

A

urine microalbumin levels

82
Q

What are the bisphosphonates used specifically for Paget’s disease?

A

etidronate, pamidronate, zolandronate

83
Q

What’s the mechanism of action of metyrapone?

A

blocks 11 beta hydroxylase to prevent synthesis of cortisol

84
Q

alpha cells of the pancreas secrete what?

A

glucagon

85
Q

Glucagon increases/decreases fructose 2,6-bisphosphate concentration. What’s the consequence?

A

decreases; stimulates gluconeogenesis

86
Q

What is Virilization?

A

the development of male physical characteristics (such as muscle bulk, body hair, and deep voice) in a female or precociously in a boy, typically as a result of excess androgen production.

87
Q

What’s the emergency treatment for hypercalcemia?

A

3 pronged approach: –Volume expansion (saline infusion) –Salmon Calcitonin (inc. renal excretion) –Bisphosphonates—zolendronic acid or palmidronate

88
Q

What’s the rate limiting step for making all of the endogenous steroids?

A

the conversion of cholesterol to pregnenolone

89
Q

Which corticosteroid has the longest half life?

A

dexamethasone (36-54)

90
Q

What’s the most potent glucocorticoid?

A

Dexamethasone (9-fluoro-16-methylprednisolone)

91
Q

what’s the first line blood pressure drug for diabetics?

A

ACE inhibitors (prils)

92
Q

What are the toxicities of the GLP-1 analogs?

A

nausea, vomiting, pancreatitis

93
Q

What’s the name of the enzyme that catalyzes the conversion of NE to Epi? What induces its production?

A

phenylethanolamine N- methyl transferase; it’s production is induced by cortisol from fasciculata layer

94
Q

List the alpha-glucosidase inhibitors

A

acarbose and miglitol

95
Q

What causes Addison’s disease?

A

Addison’s Disease occurs when the adrenal glands do not produce enough adrenocorticosteroid hormones —AKA “chronic adrenal insufficiency”

96
Q

In those cells in which insulin increases facilitated diffusion of glucose, this is due to increased recruitment of _____ transporter units.

A

GLUT 4

97
Q

What’s the IV drug of choice for a hypocalcemia patient?

A

Calcium gluconate

98
Q

delta cells of the pancreas secrete what?

A

somatostatin

99
Q

What are the three mechanism by which Cushing syndrome occurs endogenously?

A
  1. Hypothalamic-pituitary disease with hypersecretion of ACTH
  2. Hypersecretion of cortisol by adrenal adenoma, carcinoma or nodular hyperplasia
  3. Secretion of ectopic ACTH by non-endocrine neoplasms
100
Q

rare autoimmune mediated destruction of the adrenal cortex

A

Addison’s disease

101
Q

What are the 3 release stimulators of aldosterone?

A

1.Renin-angiotensin system 2.Extracellular potassium and sodium 3.ACTH

102
Q

When removing a pheochromocytoma, what must be given perioperatively to prevent a hypertensive crisis?

A

phenoxybenzamine (irreversible alpha blocker)

103
Q

What is the cause of most cases of Cushing syndrome?

A

administration of exogenous glucocorticoids

104
Q

Infants born to diabetic mothers often have what?

A

high birth weights and large organs (macrosomia)

105
Q

How do you treat moderate to severe Paget’s disease?

A

salmon calcitonin, human calcitonin, bisphosphonates

106
Q

What are the potential toxicities of SGLT-2 inhibitors?

A

glucosuria, UTIs, vaginal yeast infections

107
Q

How does theophylline, a phosphodiesterase inhibitor, stimulate the release of insulin?

A

inhibition of phosphodiesterase in beta cells increases cAMP (thereby reading intracellular Ca++)

108
Q

How do you test for Cushings?

A

24 hour urinary free cortisol; >250micrograms/d = cushings

109
Q

What’s normal plasma glucose levels?

A

90 mg/dl

110
Q

What are the primary target tissues of insulin ?

A

muscle, liver, and adipose tissue

111
Q

What’s the mechanism of action of Glitazones/thiazolidinediones?

A

increase insulin sensitivity in peripheral tissue by binding to and activating PPAR-gamma nuclear transcription factor

112
Q

What is 90% of cortisol bound to?

A

corticosteroid binding globulin (CBG)

113
Q

Which cells secrete renin?

A

juxtaglomerular cells

114
Q

How are patients with pheochromocytoma typically going to present?

A

Classic presentation–abrupt onset of BP elevation with tachycardia, palpitations, headache, sweating, tremor and apprehension

115
Q

What drug class is Metformin in?

A

biguanides

116
Q

What’s an intermediate acting insulin preparation?

A

NPH

117
Q

A number of congenital enzyme deficiencies in the pathways of adrenocortical hormone synthesis occur. Which is by far the most prevalent?

A

21-hydroxylase deficiency

118
Q

alpha2- adrenergic stimulation ____ insulin secretion.

A

inhibits (decreases cAMP)

119
Q

What blood glucose level is considered diabetic?

A

fasting: 126 mg/dl and above

120
Q

Glucocorticoids (like cortisol) inhibit the synthesis of prostaglandins, thromboxanes, and leukotrienes, substances thought to play important roles in inflammation. What do they block specifically to accomplish this?

A

block phospholipase A2 (Which was making arachidonic acid from phophatidyl choline)

121
Q

What does renin do?

A

converts angiotensinogen to angiotensin 1

122
Q

How do you treat mild cases of Paget’s disease?

A

analgesics and anti-inflammatory drugs

123
Q

Does the amount of protein bound calcium increase or decrease in alkalosis?

A

Alkalosis increases binding and decreases ionized calcium.