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Board Review > Endocrine > Flashcards

Endocrine Flashcards

1
Q

iinsulins effect on fat synthesis, kidneys, protein synthesis

A

increases fat synthesis, increases sodium retention in the kidneys, increases routine uptake and synthesis within muscles

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2
Q

does insulin cross the placenta

A

no but glucose does

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3
Q

which one of the GLUT molecules are insulin-dependent, what organs are they on?

A

GLUT-4, muscle and adipose tissue

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4
Q

what tissues possess GLUT 1

A

red blood cells, corneas, blood brain barrier

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5
Q

what tissues possess GLUT 2, what is the special property?

A

GLUT 2 iis bidirectional, son pancreatic beta cells, liver, kidney, and the G.I. tract

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6
Q

GLUT-3, on which organ

A

Brain, mostly neurons

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7
Q

GLUT-5? Cells, molecule of transport

A

on spermocytes and GI tract.

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8
Q

mnemonic for insulin independent organs

A 
BRICK L (insulin-independent glucose uptake):
Brain, RBCs, Intestine, Cornea, Kidney, Liver
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9
Q

how do beta agonist effect insulin release

A

beta agonist increase insulin release

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10
Q

how does growth hormone affect insulin release

A

growth hormone increases insulin resistance, leading to increased insulin

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11
Q

what cellular pathways responsible for the trophic factors associated with insulin

A

RAS/MAPK

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12
Q

how this insulin increase the number of glucose channels on the surface of insulin-dependent organs

A

Insulin -> PI3K -> increase glycogen, lipid, and protein synthesis, increase vesicles containing GLUT 4 on the surface of cells.

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13
Q

how do glucose levels lead to insert release from beta cells,

A

glucose comes in > Glycolysis > Increase ATP> ATP sensitive potassium channels close> Pancreatic beta cell depolarization> Intracellular calcium increase the opening of calcium channel> release vesicles containing insulin.

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14
Q

with the effects of glucagon on adipose tissue

A

increased lipolysis and ketone production within the liver

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15
Q

what GHRH analog is used to treat HIV related lipodystrophy

A

tesamorelin

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16
Q

what is prolactin’s effect on gonadotropin release

A

inhibitory

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17
Q

how does prolactin inhibit its own secretion

A

it increases dopamine secretion from the hypothalamus thus increasing tonic dopamine release and continued prolactin inhibition

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18
Q

what medications can be used to treat prolactinomas

A

dopamine agonists such as bromocriptine

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19
Q

how do OCP and pregnancy affect prolactin secretion

A

the increase in estrogens which then go on to increase prolactin secretion.

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20
Q

what two activities increase the amount of growth hormone secretion

A

exercise and sleep

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21
Q

how does growth hormone respond to increasing glucose levels?

A

increasing glucose levels inhibits the secretion of growth hormone

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22
Q

what is the negative feedback pathway for growth hormone secretion

A

growth hormone increases the amount of IGF 1 or Somatomedin C in circulation, Somatomedin activate somatostatin secretion, thus in turn inhibiting growth hormone secretion.

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23
Q

Effects of Ghrelin on appetite? organ that produces it? what two conditions increase the amounts of Gherlin

A

increased hunger, made in the stomach, increased with increased sleep loss and Prader Willi.

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24
Q

the effects of leptin on appetite, produced by what organ, what effects do sleep deprivation have on leptin levels?

A

leptin is a signal of satiety that comes from the adipose tissue, mutations in leptin or the leptin receptor lead to congenital obesity. Sleep deprivation decrease leptin levels.

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25
Q

affects of endocannabinoids

A

activate reward centers, increase craving for high-fat foods

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26
Q

ADH, which receptors regulate osmolarity, which receptors regulate blood pressure?

A

V1 regulates blood pressure, V2 regulates osmolarity

One heart two kidneys.

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27
Q

were the aquporins inserted into within the kidney

A

into the plasma membrane of principle cells residing within the collecting ducts of the kidney/

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28
Q

in terms of osmolarity and volume, what does the hypothalamus it’s regulatory input

A

osmolarity is paramount, followed by volume, but then hypothalamus will often increase volume at the expense of osmolarity

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29
Q

17 A hydroxylase deficiency: what steroid is in excess, what steroids are missing

A

aldosterone is in excess, cortisol is missing along with testosterone and DHEA

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30
Q

17 A hydroxylase deficiency: what are the clinical features for boys, girls? both?

A

boys: pseudo-hermaphrodite, ambiguous genitalia.

Girls: lack of secondary sex characteristics due to lack of peripheral conversion of testosterone to estrogen by aromatase.

elevated blood pressure, hypokalemia.

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31
Q

11 beta hydroxylase deficiency: what steroid is in excess, what is low?

A

11-deoxycorticosterone is in excess, low aldosterone and low cortisol. sex hormones are increased due to shunting.

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32
Q

11 beta hydroxylase deficiency: what are the clinical features in boys? both genders? laboratory studies

A

boys undergo early virilization,

blood pressure is up (11-deoxycorticosterone behaves like aldosterone), hyperkalemia. Renin will be down.

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33
Q

21 hydroxylase deficiency: what hormones are in excess? which are missing?

A

DHEA and Androstedione are in excess, aldosterone and cortisol are low.

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34
Q

21 hydroxylase deficiency: clinical features in boys versus girls?
Both genders? Labs?

A

boys demonstrate precocious puberty. girls demonstrate virilization

Blood pressure is low, salt wasting is high, sex hormones are quite high, and patients are hyperkalemic

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35
Q

in 11, 21, and 17 hydroxylase deficiencies what is the size of the adrenal glands and why is it the size

A

the adrenal glands are quite large, due to the fact they all present with a cortisol deficiency,. And lack of negative feedback leads to increased release of ACTH. Acting as a trophic factor

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36
Q

how does cortisol affect fibroblast function and bone osteoblast function

A

cortisol inhibits fibroblast function leading to poor wound healing, and inhibits osteoblasts function, leading to bone demineralization.

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37
Q

what are the three forms that calcium exist within the body?

A

45% of it is ionized, 40% of it is bound to albumin, 15% of it is bound to anions.

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38
Q

how does vitamin D effect levels of calcium within the bones

A

vitamin D actually increases bone resorption of calcium and phosphate, increasing plasma levels of calcium and phosphate.

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39
Q

how does activated vitamin D affect its own production

A

1,25-(OH)2 feedback inhibits its own

production

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40
Q

how to calcium levels, parathyroid hormone levels, and phosphate levels affect vitamin D production

A

low calcium levels, increase parathyroid hormone, and low potassium

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41
Q

when enzyme is responsible for the production of activated vitamin D, where is it located

A

1A hydroxylase, located within the kidneys

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42
Q

how does parathyroid hormone affect osteoclast activity?

A

parathyroid hormone increases osteoblast secretion of rank L, which binds to rank on the surface of osteoclast, leading to osteoclast maturity and increased activity. Increased bone resorption occurs.

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43
Q

PTHrP - what is it and how does it relate to paraneoplastic syndrome.

A

PTHrP can be released from many different types of malignancies, and lead to excessive bone resorption

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44
Q

how does magnesium affect parathyroid hormone release

A

low levels of magnesium lead to increased parathyroid hormone release

Very low levels of magnesium lead to decreased parathyroid hormone release.

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45
Q

common causes of magnesium deficiency

A

alcoholism, diarrhea, aminoglycosides, diuretics

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46
Q

cells responsible for secreting calcitonin

A

Parafollicular or C cells of the thyroid

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47
Q

hormones that rely on cAMP as a signaling pathway

A

FSH, LH, ACTH, TSH, CRH, hCG, ADH
(V2-receptor), MSH, PTH, calcitonin, GHRH,
glucagon

FLAT ChAMP Gam Gam

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48
Q

hormones that rely on cGMP as a signaling pathway

A

ANP, BNP, NO (EDRF)

Think vasodilators

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49
Q

hormones that rely on IP3 as a signaling pathway

A

GnRH, Oxytocin, ADH (V1-receptor), TRH,
Histamine (H1-receptor), Angiotensin II,
Gastrin.

GOAT HAG

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50
Q

hormones that rely on intracellular receptors in signaling pathways

A 
Vitamin D, Estrogen, Testosterone, T3/T4,
Cortisol, Aldosterone, Progesterone
VETTT CAP (think steroids)
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51
Q

hormones that rely on intrinsic tyrosine kinases for signaling pathways.

A

Insulin, IGF-1, FGF, PDGF, EGF MAP kinase pathway

Think growth factors

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52
Q

hormones that rely on receptor associated tyrosine kinases for signaling pathways.

A

Prolactin, Immunomodulators (e.g., cytokines
IL-2, IL-6, IFN), GH, G-CSF, Erythropoietin,
Thrombopoietin.

JAK/STAT pathway
Think acidophils and cytokines
PIGGLET

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53
Q

The effect of increased increased sex hormone binding globulin in men

A

increased SHBG leads to decreased levels of testosterone, causing things like gynecomastia

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54
Q

effect of decreased sex hormone binding globulin and women.

A

decreased sex hormone binding globulin and women increases levels of free testosterone, cause hirstuism .

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55
Q

how does thyroid hormone affect bone growth

A

it increases bone growth and work synergistically with growth hormone.

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56
Q

how does thyroid hormone increase basal metabolic rate

A

increased activity of the sodium potassium atpase

leading to increased oxygen demand

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57
Q

how the thyroid hormone affect glucose and lipid metabolism

A

increase glycogenolysis, gluconeogenesis, and lipolysis

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58
Q

Wolff-Chaikoff effect?

A

When excess iodine saturates thyroid peroxidase and leads to decreased activity of the enzyme t4/t43 production

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59
Q

what situations increase the amount of thyroid binding globulin? what situations decrease it?

A

pregnancy and use of OCPs lead to increased TBG, liver failure and use of steroids decreases TBG.

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60
Q

what enzyme is responsible for the conversion of T4 to T3

A

5-deiodinidase

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61
Q

what is pseudohyperaldosteronism?

A

cortisol has an affinity for the aldosterone receptor within cells, but is degraded by enzymes,. in scenarios of cortisol excess, cortisol can exceed the Vmax of this enzyme and exert aldosterone effects including increasing sodium absorption from the collecting ducts, and increase excretion of potassium. thus causing elevated blood pressure and hypokalemia, independent of cortisol’s affect on vasculature

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62
Q

what effect does Cushing’s syndrome have on the menstrual cycle.

A

cortisol inhibits the normal ovulatory cycle.

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63
Q

what are the primary screening test for detection of Cushing’s syndrome

A

24-hour cortisol collection, midnight salivary cortisol, failure of suppression with eight hour low dose (8mg) dexamethasone therapy.

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64
Q

how will a ACTH secreting tumor respond to high-dose dexamethasone? CRH?

how will ectopic ACTH response to high-dose dexamethasone? CRH?

A

with dexamethasone, ACTH will decrease with administration and increase with CRH

ectopic ACTH will not respond to either dexamethasone or CRH

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65
Q

what are some specific findings associated with adrenal insufficiency

what is the clinical use of metyrapone.

A

sugar and salt craving, orthostatic hypotension,

metyrapone blocks last step of cortisol
synthesis (11-deoxycortisol to cortisol). Normal
response is decreased cortisol and compensatory
increased ACTH. In adrenal insufficiency, ACTH
remains low after test.

66
Q

what is the etiology of hyperpigmentation surrounding adrenal insufficiency

A

increase ACTH production also includes an increase in MSH production as a byproduct leading to melanin production.

67
Q

what is the cause of secondary adrenal insufficiency

A

decrease ACTH production, no pigmentation of the skin.

68
Q

what is the most common tumor of the adrenal medulla in children? what age group? what sells to the tumor cells originate from

A

the most common tumor is neuroblastoma, it tends to present in children under the age of four and the tumor cells originate from the neural crest cells

69
Q

how does neuroblastoma acute renal medulla present? what is the blood pressure of the people who present with these?

A

usually abdominal mass that can cross the midline, that can present with, opsoclonus-myoclonus syndrome (“dancing eyes-dancing feet”). less likely to be associated with hypertension

70
Q

what testing can be used to detect a neuroblastoma the adrenals.

A

Homovanillic acid
(HVA; a breakdown product of dopamine) and vanillylmandelic acid (VMA; a breakdown product
of norepinephrine)  in urine. Bombesin and neuron-specific enolase ⊕

71
Q

what genes are associated with neuroblastoma of the adrenals

A

c-myc mutations

72
Q

what is the key finding on histology for neuroblastoma of the journals

A

Homer Wright rosettes.

73
Q

what cells are pheochromocytoma derived from

A

chromaffin cells of the adrenal medulla.

74
Q

what is the role of tens with pheochromocytoma

A 
Rule of 10’s:
10% malignant
10% bilateral
10% extra-adrenal (paraganglionic
10% calcify
10% kids
75
Q

what are the primary secretary products of the pheochromocytoma

A

Most tumors secrete epinephrine,
norepinephrine, and dopamine, which can
cause episodic hypertension

76
Q

treatment for pheochromocytoma

A

phenoxybenzamine, and after alpha block is obtained, give beta blockers prior to surgery.

77
Q

how does thyroid hormone affect tthe expression of LDL receptors

A

increase thyroid hormone leads to increased expression of LDL receptors, and hypocholesterolemia.

78
Q

would HLA is Hashimoto’s thyroiditis associated with

A

HLA DR5

79
Q

why might a person with Hashimoto’s thyroiditis be hyperthyroid?

A

the autoimmune destruction of the thyroid in the beginning of the disease could lead to the release of preformed thyroid and thyrotoxicosis

80
Q

what cancerous Hashimoto’s thyroiditis associated with

A

non-Hodgkin’s lymphoma

81
Q

what is the histological finding with Hashimoto’s thyroiditis

A

Hürthle cells, lymphoid aggregate with germinal centers.

82
Q

what is the clinical finding of Hashimoto’s thyroiditis

A

enlarged nontender, thyroid

83
Q

what is the clinical presentation of cretinism.? Primary cause?

A

Pot-bellied, Pale, Puffy-faced child with Protruding umbilicus, Protuberant tongue, and
Poor brain development: the 6 P’s

84
Q

how does subacute thyroiditis typically present? what is seen on histology?

A

Post flulike illness, the patient is hyperthyroid and then becomes hypothyroid, ESR, jaw pain, early inflammation, very tender thyroid.

on histology, granuloma formation’s are likely seen, with perhaps a multi-nucleated cells.

85
Q

Riedel thyroiditis?

primary cause?

A

Thyroid replaced by fibrous tissue (hypothyroid). Fibrosis may extend to local structures (e.g.,
airway), mimicking anaplastic carcinoma.

manifestation of IgG4-related systemic disease (e.g., autoimmune pancreatitis,
retroperitoneal fibrosis, noninfectious aortitis)

86
Q

Riedel thyroiditis clinical finding

A

fixed, hard (rock-like), painless goiter

87
Q

primary cause of goiter in thyroid in the world

A

iodine deficiency

88
Q

how does Graves’ disease affect extra ocular muscles

when does Graves’ disease typically present?

A

increase swelling within the extra ocular muscles as well as the ocular connective tissue.

typically during stressful events such as childbirth

89
Q

toxic multi-nodular goiter presentation? ultrasound?

are these nodules malignant

A

hypothyroidism with a large corridor, many hot nodules on ultrasound?

these nodules are rarely malignant, although the due process a cellular change that makes them overly sensitive to TSH

90
Q

Typical presentation of thyroid storm

what findings from bone turnover might be seen in labs

treatment for thyroid storm includes

A

Agitation, delirium, fever, diarrhea, coma, and
tachyarrhythmia (cause of death).

increase alkaline phosphate

propranolol, PTU, and prednisone

91
Q

Jod-Basedow phenomenon?

A

Thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.

92
Q

what nerves are at risk of being compromised during thyroidectomy? what arteries are associated with them?

A

recurrent and superior laryngeal nerves (during ligation of

inferior thyroid artery and superior laryngeal artery, respectively).

93
Q

what are the histological features of papillary carcinoma. chance of lymphatic invasion.

major risk factors for developing papillary carcinoma genetic and extrinsic.

A

Empty-appearing nuclei with central clearing (“Orphan
Annie” eyes) A , psammoma bodies, nuclear grooves. Lymphatic invasion common

Increased risk with
RET and BRAF mutations, childhood irradiation.

94
Q

features and invasion pattern of follicular carcinoma of the thyroid

A

Good prognosis, invades thyroid capsule (unlike follicular adenoma), uniform follicles.

95
Q

invasion pattern, prognosis, and population, of anaplastic thyroid tumor

A

Older patients, invades local structures, very poor prognosis.

96
Q

cell line for medullary tumors, primary protein product,

Histological features, and genetic mutations associated with

A

From parafollicular “C cells”; produces calcitonin, sheets of cells in an amyloid stroma
hematogenous spread common. Associated with MEN 2A and 2B (RET mutations).

97
Q

definition of trousseau sign?

A

Trousseau sign—occlusion of brachial artery
with BP cuff (cuff the Triceps) leading to carpal
spasm. evidence of hypocalcemia

98
Q

Pseudohypoparathyroidism (Albright

hereditary osteodystrophy)? primary pathology? physical features? inheritance pattern?

A

unresponsiveness
of kidney to PTH. Hypocalcemia, shortened
4th/5th digits, short stature. Autosomal
dominant.

99
Q

likely cause of low calcium and low PTH

Hi calcium and low PTH (

Hi PTH and low calcium

Hi PTH and high calcium

A

Hypoparathyroidism (surgical removal ,autoimmune destruction

PTH-independent hypercalcemia (excess Ca2+ ingestion, cancer)

secondary hyperparathyroidism ( renal failure, low vitamin D)

parathyroid neoplasia or paraneoplastic syndrome

100
Q

Familial hypocalciuric hypercalcemia? pathology? lab findings?

A

Defective Ca2+-sensing receptor on parathyroid cells.
PTH cannot be suppressed by an increase in Ca2+ level mild hypercalcemia with normal to
increased PTH levels.

101
Q

presentation of primary hyperparathyroidism,blood levels? renal? muscles? G.I.? neurological?

A

hypophosphatemia, hypercalcemia, hypercallcuria. muscle weakness along with constipation, abdominal/flank pain
(kidney stones, acute pancreatitis), depression

“Stones, bones, groans, and psychiatric
overtones

102
Q

Osteitis fibrosa cystica

A

cystica—cystic bone spaces
filled with brown fibrous tissue A (“brown
tumor” consisting of deposited hemosiderin
from hemorrhages; causes bone pain

103
Q

Renal osteodystrophy?

A

bone lesions due to 2° or 3° hyperparathyroidism due in turn to renal
disease

104
Q

Tertiary hyperparathyroidism

A

automatous action of the parathyroid, secondary to hyperplasia achieved by renal failure. parathyroid hormone is increased and calcium is increased

105
Q

what is the treatment protocol for acromegaly, pharmacologic?

A

surgical resection of the pituitary adenoma, if not cured octreotide (somatostatin analog) or pegvisomant (growth hormone receptor
antagonist).

106
Q

what is the difference between the ADH level in central diabetes insipidus versus nephrogenic diabetes insipidus

A

in central diabetes insipidus, ADH levels will likely be decreased in nephrogenic diabetes insipidus, ADH levels will likely be normal.

107
Q

Treatment for diabetes insipidus of nephrogenic origin?

A

hydration, diuretics including hydrochlorothiazide and amlioride.

108
Q

what is the primary reason for hyponatremia in SIADH?

A

increase volume ADH activity leads to suppression of the renin-angiotensin system, decreasing aldosterone and decreasing sodium absorption leading to a euvolemic hyponatremia.

109
Q

what can be the effects of hyponatremia?

A

cerebral edema, and seizures, delirium

110
Q

Causes of SIADH

A

Ectopic ADH (e.g., small cell lung cancer)
CNS disorders/head trauma
Pulmonary disease
Drugs (e.g., cyclophosphamide)

111
Q

What population is most susceptible to empty sella syndrome

A

obese women.

112
Q

What are causes of pituitary apoplexy.

A

Competitions associated with pituitary adenoma
brain injury from trauma
radiation

113
Q

Diabetes mellitus can be caused by what other hormones other than insulin

A

excessive growth hormone, excessive glucagon, or epinephrine, cortisol

114
Q

what are the effects of non-enzymatic glycosylation on small vessels, in the eye, kidneys,

A

diffuse thickening of basement membrane) Ž retinopathy (hemorrhage,
exudates, microaneurysms, vessel proliferation), glaucoma, neuropathy, nephropathy
(nodular glomerulosclerosis, aka Kimmelstiel-Wilson nodules Ž progressive proteinuria and
arteriolosclerosis leads to hypertension; both lead to chronic renal failure).

115
Q

what are the effects of non-enzymatic glycosylation on large vessels especially in the heart brain, and limbs?

A

Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, gangrene Ž limb loss,
cerebrovascular disease. MI most common cause of death.

116
Q

wwhat are the effects of sorbitol accumulation within cells without adequate sorbitol dehydrogenase

A

Neuropathy (motor, sensory, and autonomic degeneration)

Cataracts.

117
Q

what are the three test utilized to diagnose diabetes?

over what time period does hemoglobin A1c give information about glucose status

A

Fasting serum glucose, oral glucose tolerance test, HbA1c.

hemoglobin A-1 C gives information about glucose status over the last three months

118
Q

what is the genetic predisposition to type I diabetes, type II diabetes

A

weaker for type I diabetes with a 50% concordance with identical twins, very strong and type II diabetes with a 90% concordance with identical twins.

119
Q

what is one of the major precipitating factors associated with development of ketoacidosis?

A

increase insulin demand due to stress, such as an illness.

120
Q

what are the clinical features of ketoacidosis? G.I., neurological, respiratory?

A 
Kussmaul respirations (rapid/deep breathing), nausea/vomiting, abdominal pain, psychosis/
delirium, dehydration. Fruity breath odor (due to exhaled acetone).
121
Q

what are the cardiac cerebral complications of ketoacidosis

A

life-threatening arrhythmia, cerebral edema, heart failure

122
Q

what are the primary features of Glucagonoma

A

overproduction of glucagon. Presents with dermatitis (necrolytic
migratory erythema), diabetes (hyperglycemia), DVT, and depression.

123
Q

what is Whipple Triad?

A

low blood glucose, symptoms of hypoglycemia (e.g., lethargy, syncope, diplopia), and resolution of
symptoms after normalization of glucose levels

124
Q

what cell line is responsible for the production of carcinoid tumors?

primary secretary product?

A

neuroendocrine cells, often within the G.I. tract.

secrete high levels of serotonin (5-HT). Not seen if
tumor is limited to GI tract (5-HT undergoes
first-pass metabolism in liver)

125
Q

What are the findings associated with carcinoid tumor? Dermatological, G.I., cardiovascular?

A

recurrent diarrhea, cutaneous flushing,
asthmatic wheezing, right-sided valvular
disease.

126
Q

What are the findings in Labs that indicate carcinoid tumor?

A

increased 5-hydroxyindoleacetic acid (5-HIAA)
in urine, niacin deficiency (pellagra). this is because tryptophan is needed for the formation of niacin, as well as serotonin,

127
Q

what is the rule of thirds for carcinoid

how is carcinoid treated?

A 
1/3 metastasize
1/3 present with 2nd malignancy
1/3 are multiple
Most common malignancy in the small
intestine.

Treatment: surgical resection, somatostatin
analog (e.g., octreotide).

128
Q

what is the cellular origin of Zollinger-Ellison syndrome and what are the secreted

what are the consequences of Zollinger-Ellison syndrome

A

neuroendocrine cells from the pancreas or small bowel that are excreting gastrin.

ulcers within the duodenum and jejunum

129
Q

what test is utilized to test Zollinger-Ellison syndrome

A

Positive secretin stimulation test: gastrin levels remain

elevated after administration of secretin, which normally inhibits gastrin release

130
Q

what is the inheritance pattern for MEN syndrome

A

autosomal dominant

131
Q

what are the clinical features of MEN 1

what is the mutation involved MEN 1

A 
Parathyroid tumors
Pituitary tumors (prolactin or GH)
Pancreatic endocrine tumors—Zollinger-
Ellison syndrome, insulinomas, VIPomas,
glucagonomas (rare)

the mutation is in of MEN1 gene
(menin, a tumor suppressor)

132
Q

one of the clinical features seen in MEN 2A

what mutation is seen?

A

Parathyroid hyperplasia
Pheochromocytoma
Medullary thyroid carcinoma (secretes
calcitonin)
Associated with marfanoid habitus; mutation in
RET gene (codes for receptor tyrosine kinase)

133
Q

One of the clinical features of MEN 2B

what mutation is seen?

A

Pheochromocytoma
Medullary thyroid carcinoma (secretes
calcitonin)
Oral/intestinal ganglioneuromatosis (mucosal
neuromas)
Associated with marfanoid habitus; mutation in
RET gene.

134
Q

what are the recommendations for type I diabetics for therapy lifestyle and medication

A

low-carbohydrate diet, insulin replacement?

135
Q

What are the names of the fast acting insulins

A

Aspart, Glulisine, Lispro

136
Q

Metformin: mechanism

indication: weight changes?

A

Exact mechanism unknown. increases insulin sensitivity.

Oral. First-line therapy in type 2 DM, causes modest weight loss

137
Q

metformin: side effects

A

GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal insufficiency)

138
Q

Sulfonylureas: first-generation drugs ? second generation drugs?

Mechanism:

A

First generation: Chlorpropamide, Tolbutamide

Second generation: Glimepiride, Glipizide, Glyburide

Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM.

139
Q

Side effects associated with Sulfonylureas:

A

Risk of hypoglycemia in renal failure.
First generation: disulfiramlike effects.
Second generation: hypoglycemia.

140
Q

Glitazones/
thiazolidinediones drug names

Mechanism?

A

Pioglitazone, Rosiglitazone

increased insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.

141
Q

side effects associated with TZD?

A

Weight gain, edema. Hepatotoxicity, HF, risk of fractures.

142
Q

GLP-1 analogs:

mechanism:

A

Exenatide, Liraglutide

increase insulin, decrease glucagon release.

143
Q

GLP-1 analogs: side effects

A

nausea, vomiting, pancreatitis

144
Q

DPP-4 inhibitors:

mechanism:

A

Linagliptin, Saxagliptin, Sitagliptin

increase insulin, decrease glucagon release.

145
Q

DPP-4 inhibitors: side effects

A

mild risk of upper respiratory and urinary infections

146
Q

Amylin analogs

mechanism

indication:

A

Pramlintide

decreased gastric emptying, decreased glucagon secretion

Indicated for both type I and type II diabetes

147
Q

Amylin analogs:side effects

A

Hypoglycemia, nausea, diarrhea.

148
Q

SGLT-2 inhibitors: ?

mechanism?

A

Canagliflozin

Block reabsorption of glucose in
PCT.

149
Q

SGLT-2 inhibitors: side effects

A

glucosuria, urinary tract infections, increased risk of vaginal candidiasis

150
Q

α-glucosidase inhibitors:

mechanism.

A

acarbose, miglitol

Inhibit intestinal brush-border
α-glucosidases. Delayed carbohydrate hydrolysis
and glucose absorption
decreased postprandial hyperglycemia.

151
Q

α-glucosidase inhibitors: side effects

A

G.I. disturbances

152
Q

Propylthiouracil, methimazole: which one of these as indicated in pregnancy. Which one of is tteratogenic

A

Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy. Methimazole is teratogenic

153
Q

Propylthiouracil, methimazole: side effects : hematological, G.I.

A

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil). Methimazole is
a possible teratogen (can cause aplasia cutis).

154
Q

Levothyroxine (T4), triiodothyronine (T3)

A

Tachycardia, heat intolerance, tremors, arrhythmias

155
Q

ADH antagonists :? area of action

A

conivaptan, tolvaptan? V2 receptors

156
Q

growth hormone: pharmacological indications

A

GH deficiency, Turner syndrome.

157
Q

Somatostatin

(octreotide): indications , the pituitary, cancer, cardiovascular,

A

Somatostatin

(octreotide): indications , the pituitary, cancer, cardiovascular,

158
Q

Demeclocycline: mechanism

indication

side effects

A

ADH antagonist (member of tetracycline family).

SIADH.

Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.

159
Q

fludrocortisone: what is special about this glucocorticoid

A

mineralocorticoid and glucocorticoid activity

160
Q

what is the primary mechanism of action of glucocorticoids

A

inhibition of phospholipase A2, and inhibition of

transcription factors such as NF-κB

161
Q

Cinacalcet: mechanism

indication

A

Sensitizes Ca2+-sensing receptor (CaSR) in parathyroid gland to circulating Ca2+ decreased levels of PTH.

Hypercalcemia due to 1° or 2° hyperparathyroidism.

162
Q

Cinacalcet: side effects

A

side effect is hypocalcemia.

Board Review (7 decks)

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