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STEP1 2015 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

cAMP hormones

A

FSH, LH, ACTH, TSH (all ant. pit) FLAT

and also hcG
MSH
GHRH
CRH

PTH
Calcitonin

Glucagon
V2 vasopressin receptor

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2
Q 
Gq 
Inositol triphosphate (IP3) pathway
A

hypothalamic hormones
GnRH
TRH- thyrotropin releasing hormone

post pit:
Oxytocin
Vasopressin at the V1 receptor

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3
Q

Tyrosine kinase receptor

A 
growth factors
growth hormone (GH)
prolactin
insulin
insulin-like growth factor (IGF1)
platelet- derived growth factor (PDGF)
fibroblast growth factor (FGF)
cytokines
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4
Q

cGMP

A 
nitric oxide (NO)
antrial natriuretic peptide (ANP)

these both act to vasodilate

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5
Q

steroid receptors

A 
estrogens, progesterones, testosterone
glucocorticoids
aldosterone
thyroid hormone
vitamin D
  1. intracellular
  2. gene transcription

these receptors are found intracellularly. When bound, the receptor undergoes coformational change whereby DNA- binding domain is exposed. This leads to binding of a gene enhancer region

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6
Q

stimulates bone and muscle growth

A

growth hormone via insulin like growth factor (IGF1), which stimulates TKR

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7
Q

stimulates milk production

A

prolactin

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8
Q

stimulates milk secretion during lactation

A

oxytocin

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9
Q

responsible for female secondary sex characteristics

A

estradiol

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10
Q

stimulates metabolic activity

A

T4, T3

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11
Q

increases blood glucose level and decreases protein synthesis

A

glucacorticoids

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12
Q

responsible for male secondary sex characteristics

A

testosterone

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13
Q

prepares endometrium for implantation/ maintenance of pregnancy

A

progesterone

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14
Q

stimulates adrenal cortex to synthesize and secrete cortisol

A

ACTH- adrenocorticotropic hormone

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15
Q

stimulates follicle maturation in females and spermatogenesis in males

A

follicle stimulating hormone

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16
Q

increases plasma calcium, increases bone resorption

A

parathyroid hormone

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17
Q

decreases plasma calcium, increases bone formation

A

calcitonin

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18
Q

stimulates ovulation in females and testosterone synthesis in males

A

luteinizing hormone

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19
Q

stimulates the thyroid to produce TH and uptake iodine

A

thyroid stimulating hormone

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20
Q

where does growth hormone come from?

A

anterior pituitary

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21
Q

where does thyroid hormone come from?

A

thyroid

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22
Q

glucocorticoids

A

adrenal cortex (zona fasciculata)

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23
Q

progesterone

A

ovaries, and placenta if there is one

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24
Q

prolactin

A

anterior pituitary

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25
Q

oxytocin

A

hypothalamus (paraventricular nucleus)

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26
Q

atrial natriuretic hormone

A

atria of the heart

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27
Q

glucagon

A

alpha cells of the pancreas

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28
Q

testosterone

A

testes (men) ovaries (women), and in a small amount, in the zona reticularis of the adrenal cortex

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29
Q

vasopressin (ADH)

A

posterior pituitary for storage, ,made in the hypothalamus (supraoptic nucleus)

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30
Q

calcitonin

A

parafollicular cells of the thyroid

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31
Q

thyroid stimulating hormone (TSH)

A

anterior pituitary

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32
Q

epinephrine and norepinephrine

A

chromaffin cells of the adrenal medulla

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33
Q

insulin

A

beta cells of the pancreas

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34
Q

estradiol

A

ovaries

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35
Q

estriol

A

placenta

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36
Q

estrone

A

fat cells

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37
Q

estrogen in males

A

testes

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38
Q

PTH

A

parathyroid glands

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39
Q

somatostatin

A

delta cells of pancreas

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40
Q

luteinizing hormone (LH)

A

anterior pituitary

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41
Q

mineralocorticoids (aldosterone)

A

zona glomerulosa

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42
Q

adrenocorticotropic hormone (ACTH)

A

anterior pituitary

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43
Q

androgen binding protein

A

binds testosterone

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44
Q

embryological origins of anterior pituitary

A

Rathke’s pouch (ectodermal diverticulum)

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45
Q

embryological origins of posterior pituitary

A

invagination of hypothalamus (neuroectoderm)

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46
Q

2 proteins produced in the hypothalamus and stored in the posterior pituitary

A

oxytocin, ADH

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47
Q

ADH

A

antidiuresis by increasing water reuptake in the DCT of the kidney

more ADH for concentrate urine in small amounts
ADH promotes vascular constriction

this is why and how vasopressin can be used to stimulate an increase in BP

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48
Q

how do nicotine and opiates affect ADH levels?

A

increase (less urine)

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49
Q

how do decreased serum osmolarity, ethanol and atrial natriuretic factor affect ADH?

A

They decrease ADH, promoting diuresis

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50
Q

oxytocin

A

pregnancy breastfeeding hormone

causes uterine contractions, important for delivering baby as well as for stopping bleeding afterwards.

oxytocin release is stimulated by uterine dilation during labor

stimulates milk ejection from the breast, upon suckling
this is inhibited by alcohol and stress

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51
Q

anterior pituitary hormones

A

stimulated by upstream hormones, and have downstream targets at various glands. middle men

pulsatile release of GnRH–>
pulsatile release of FSH –> gonads

constant GnRH inhibits LH and FSH release

GnRH--> LH --> gonads
ACTH
TSH
Prolactin
Intermediate- MSH
GH
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52
Q

inhibin

A

inhibits FSH

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53
Q

progesterone and testosterone affects on LH

A

inhibition

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54
Q

four hormones that share a common alpha subunit

A

LH, FSH, TSH, hCG

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55
Q

ACTH

A

stimulated by CRH from the hypothalamus, and stress

ACTH induces cortisol production at the adrenal gland, which has a negative feedback effect on ACTH

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56
Q

MSH

A

anterior pituitary, stimulates melanocytes of skin

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57
Q

ACTH, MSH, and proopiomelanocortin (PMC)

A

ACTH is synthesized as part of a large precursor called POMC.
POMC contains sequences for other hormonal peptides including lipotropin, MSH, beta-endorphin

When ACTH is in excess, it stimulates MSH receptors, leading to hyperpigmentation in for example, Addison disease

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58
Q

TSH

A

stimulated by thyroid releasing hormone from the hypothalamus

it in turn, stimulates thyroid hormone production and secretion from the downstream thyroid gland

T3 and T4 will directly inhibit TSH secretion

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59
Q

Growth hormone (somatotropin)

A

helps grow, decreases glucose uptake, increases protein synthesis, increases organ size and lean body mass

increased by growth hormone releasing hormone (GHRH)

and inhibited by growth hormone inhibiting hormone (GHIH), aka somatostatin

downstream hormone (rather than gland) is IGF1, or insulin growth factor 1, which stimulates growth in peripheral tissues

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60
Q

things that stimulate growth hormone release

A

GHRH, exercise, sleepp, puberty, hypoglycemia, estrogen, stress, endogenous opioids

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61
Q

things that inhibit growth hormone release

A 
somatostatin
somatomedins
obesity
pregnancy
hyperglycemia
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62
Q

prolactin functions

A 
stimulates breast development
inhibits ovulation (inhibits GnRH, which inhibits release of FSH, LH, and thereby decreases the likeliihood of pregnancy while breast feeding)
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63
Q

what hormone stimulates prolactin release?

A

thyrotropin releasing hormone

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64
Q

what inhibits prolactin release

A

DA, which comes from the hypothalamus and is a constant tonic inhibitor of prolactin

65
Q

hyperprolactinemia- causes

A

pregnancy/ nipple stimulation
stress (physical or psychological)
prolactinoma (associated with bitemporal hemianopia)
dopamine antagonists- antipsychotics (haloperidol, risperidone), domperidone, metoclopramide

66
Q

hyperprolactinemia- symptoms in premenopausal females

A

hypogonadism
infertility, oligo/amenorrhea, rarely, galactorrhea

postmenopausal females may not have symptoms since they are already hypogonadal

67
Q

symptoms of hyperprolactinemia in males

A

hypogonadism (low testosterone), decreased libido, impotence, infertility (low sparm counts), gynecomastia, rarely glactorrhea

68
Q

pituitary adenoma

A

amenorrhea, galactorrhea, low libido, infertility, bitemporal hemianopia

Treat with bromocriptine or cabergoline, which are dopamine agonists

surgical resection if symptoms are severe

69
Q

Acromegaly

A

large tongue with deep furrows and indentations, increased spacing of teeth, deep voice, large hands and feet, coarse facial features (nose, ears), impaired glucose tolerance (opposite from insulin in some ways)

70
Q

Gigantism

A

excess bone growth of linear bones, tall/big children

excess growth hormone

71
Q

how to diagnose acromegaly/ gigantism

A

diagnose by checking IGF1, which is a stable downstream protein. Growth hormone itself is pulsatile, so depending on when you check it you will get different levels (highest at night)

confirm with oral glucose tolerance test (check GH after glucose intake) because insulin usually suppresses growth hormone, but this is not the case in acromegaly

72
Q

hot to treat acromegaly/gigantism

A

surgical resection/ octreotide

73
Q

somatostatin

A

produced in several places in the body:
D cells in the GI mucosa
pancreatic islet cells
nervous system

actions:
1. reduced splanchnic flow, reduces GI motility and gallbladder contractions, inhibits secretion of most GI hormones

  1. decreases exocrine secretion in the pancreas, which affects digestion
  2. decreases hormone secretion in the CNS, PNS, and endocrine organs
74
Q

clinical uses for somatostatin analogs (octreotide, somatostatin LAR, lanreotide-P)

A

pituitary excesses: acromegaly, thyrotropininoma, ACTH- secreting tumors

GI endocrine excess: SE, carcinoid, VIPoma, glucagonoma, insulinoma

certain diarrheal diseases

need to reduce splanchnic circulation: portal hypertension (bleeding varices), bleeding peptic ulcers

75
Q

Sheehan syndrome

A

postpartum hemorrhage leading to underperfusion of the pituitary

pituitary necrosis and hypopituitarism

presentation:

  • agalactorrhea due to deficient prolactin
  • amenorrhea after delivery
  • secondary hypothyroidism leading to fatigue, cold intolerance, and weight gain
  • hyponatremia (rare)
76
Q

empty sella syndrome

A

asymptomatic, symptoms of pituitary hormone deficiency of one or more hormone

77
Q

Primary hyperaldosteronism

A

HTN
Hypokalemia
Metabolic alkalosis due to potassium out, H in
low renin

78
Q

Secondary hyperaldosteronism

A

high aldosterone secondary to high renin
possibly due to
renal artery stenosis
congestive heart failure (low LV EF leading to poor renal perfusion)
low protein states such as cirrhosis and nephrotic syndrome that lead to low intravascular volume

79
Q

Symptoms of pheochromocytoma

A 
pressure (increased BP)
pain (HA)
perspiration
palpitations (tachycardia)
pallor

pheo may secrete EPO –> polycythemia

80
Q

tumors that secrete erythropoitin

A

pheochromocytoma
RCC
HCC
hemangioblastoma

81
Q

treat pheo

A

phenoxybenzamine, non-selective irreversible alpha blocker.

Alpha blockade must be achieved before giving beta blockers to avoid a hypertensive crisis.

Just giving a beta blocker alone will make the HTN worse since epinephrine stimulates alpha receptors even when beta blockers have been blocked

alpha receptors are vasoconstrictors

follow with surgical resection

82
Q

symptoms of Addison disease

A 
hypotension
hyponatremia
hyperkalemia
weakness
malaise
anorexia
weight loss
skin hyperpigmentation
83
Q

what causes Addison disease?

A

autoimmune destruction of adrenal glands leading to decreased production of aldosterone and cortisol

84
Q

MEN1

A 
parathyroid tumors
pituitary tumors (prolactin or GH)
pancreatic endocrine tumors- ZE, insulinomas, VIPomas, glucagonomas (Rare)

associated with menin tumor suppressor mutation (MEN1 gene)

85
Q

MEN2A

A

parathyroid hyperplasia
pheochromocytoma
medullary thyroid cancer

associated with RET gene mutation (TKR), marfanoid habitus

86
Q

MEN2B

A

pheochromocytoma
medullary thyroid carcinoma (secretes calcitonin)
oral/intestinal ganglioneuromatosis (mucosal neuromas)

associated with marfanoid habitus, mutation in RET gene

87
Q

catecholamine metabolites in a pheo patient’s plasma and urine

A

Plasma: metanephrine, normetanephrine

urine: VMA (vanillylmandelic acid)

88
Q

what pancreatic cell type makes glucagon

A

alpha

89
Q

what pancreatic cell type makes insulin

A

beta

90
Q

what pancreatic cell type makes somatostatin

A

delta

91
Q

GLUT 2 receptors are found on which cell types?

A

beta cells of pancrease
liver
small intestine
renal cells (kidney)

92
Q

GLUT 4 is insulin responsive. What cell types is it found on?

A

adipose tissue

skeletal muscle

93
Q

GLUT 1 receptors are found on which cell types

A

brain

RBCs

94
Q

what kind of receptor is the insulin receptor?

A

tyrosine kinase

95
Q

DM initial presentation

A

hyperglycemia, polyuria, polydipsia, polyphagia, weightloss

96
Q

1DM HLA associations

A

HLA DR3 DQ2

HLA DR4 DQ8

97
Q

cell types that don’t have sorbitol dehydrogenase

A

schwann cells
lens
retina
kidney

98
Q

Biguanides (metformin)

A 
advantages:
effective
low risk for hypoglycemia
no weight gain 
low cost
few side effects

can be used in prediabetes to prevent progression as well as in PCOS to prevent diabetes onset

99
Q

lactic acidosis is a rare but worrisome risk with this medication

A

metformin

100
Q

MC SE is hypoglycemia

A

insulin

and sulfonylureas, since these enhance beta cell function in the pancrease

101
Q

recommended first- line treatment for most patients

A

metformin (2DM), insulin (1DM)

102
Q

not sage in patients with symptoms of CHF or fluid balance problems

A

TZDs

103
Q

should not be used in patients with abnormal kidney function

A

SGLT2 inhibitors, metformin (increased risk of lactic acidosis)
sulfonylureas (increased risk of hypoglycemia in renal failure)

104
Q

Not associated with weight gain, may help with weight loss

A

metformin, DPP4, inhibitors, GLP1 analogs, SGLT inhibitors

105
Q

metabolized by the liver, could be used in patients with renal dysfunction

A

TZDs

106
Q

MOA: closes + channel on beta cells
leading to depolarization leading to calcium influx
and ultimately, insulin release

A

sulfonylureas, meglitinides

107
Q

MOA: inhibits alpha- glucosidase ta intestinal brush border

A

alpha- glucosidase inhibitors (acarbose, miglitol)

108
Q

MOA agonist at PPARgamma receptors leading to improved target cell response to insulin

A

glitazones/TZDs

109
Q

MOA: decreases hepatic gluconeogenesis

A

metformin, and also to a lesser extent TZDs

110
Q

MOA: decreases glucose reabsorption at renal tubules

A

SGLT-2 inhibitors

111
Q

possible non-insulin treatment for patients with organ failure (renal, liver, heart)

A

DPP4 inhibitors

112
Q

Hypocalcemia causes

A 
hypoparathyroidism (parathyroidectomy 2/2 thyroidectomy)
autoimmune destruction of parathyroids
pseudohypoparathyroidism (kidneys unresponsive to PTH due to mutated PTH receptor- Albright hereditary dystrophy)
DiGeorge syndrome (branchial apparatus)

Albright:
short stature, obesity, shortened 4th and 5th digits
Osteitis fibrosis cystica

Vitamin D deficiency
nutritional deficiency, paucity of sunlight
chronic renal failure

Acute pancreatitis
calcium precipitates out of the abdomen and forms soaps

113
Q

Chvostek sign

A

tap the cheek (facial nerve) and get contraction of facial muscles

114
Q

Trousseau sign

A

tighten BP cuff on arm

carpopedal spasm

115
Q

What does vitamin D do?

A

increases dietary absorption of calcium
increases dietary absorption of PO43-
increases bone turnover

116
Q

how does PTH affect calcium?

A

PTH increases calcium by increasing bone resorption and increasing renal reabsorption at the DCT

117
Q

how does PTH affect phosphate?

A

PTH pulls phosphate from bone and excretes it in the urine

118
Q

What cells make PTH?

A

chief cells of parathyroid

119
Q

What cells make calcitonin?

A

parafollocular C cells of thyroid

120
Q

Obesity causes

A

cultural habits
food choices
medications: atypical antipsychotics, mirtazapine, insulin, TZDs, sulfonylureas, some progestins

genetics

121
Q

Metabolic syndrome diagnostic criteria

A 
Any 3 of the following:
ABD OBESITY:
-waist circumference
   > 40 in men or
   >35 in women
not all metabolic syndrome patients are overweight

ELEVATED TG:
>150mg/dL

LOW HDL:
130/85 mmHg

ELEVATED GLUCOSE:
*FSG > 100mg/dL
(or 2 hour post oral glucose > 140 mg/dL)

122
Q

medical complications of obesity

A

2DM, HTN, atherosclerotic disease (CAD, MI, PAD, OSA, gout, gallstones, PCOS, fatty liver, which can become NASH, stroke)

osteoarthritis
candidal infections in skin folds
cancer (esophageal, colon, liver, gallbladder, pancreatic)

breast, ovarian, uterine cancer

prostate cancer
non-hodgkin lymphoma
multiple myeloma

123
Q

Non alcoholic steatohepatitis

A

fat in the liver cells causing inflammation/irritation

LFT increases in inflammation
is a progression from non-alcoholic fatty liver. Suspect NASH if LFTs are chronically elevated

MCC: obesity, 2DM, hyperlipidemia, insulin resistance leading to lipid accumulation in the liver

NAFL to NASH to cirrhosis

diagnosis; image the liver (US, CT, MRI)
Magnetic resonance spectroscopy is gold standard
liver biopsy

124
Q

at what BMI is a pt considered obese?

A

> 30

125
Q

mcc hypercalcemia in outpatients

p.321

A

primary hyperthyroidism (solitary parathyroid adenoma 90-95%)
parathyroid hyperplasia (5%)mcc hypercalcemia in inpatients
p.321
malignancy

squamous cell cancer (especially lung, head, and neck, via PTH- related peptide PTHrp)
RCC PTHrp
Breast mets to bone PTHrp

multiple myeloma (via local osteolytic factors)

126
Q

most common location for ectopic thyroid tissue

A

tongue

127
Q

how would pregnancy affect thyroid hormone levels?

A

increased thyroid binding globulin (TBG), which increases with estrogen. the body senses this and increases T4 and T3

free T4 and T3 remain constant

TSH may be low due to its similarity to beta HCG

128
Q

hypothyroidism, symptoms

A 
cold intolerance
weight gain
constipation
deepening of the voice
menorrhagia
slowed mental/ phyisical function
dry skin
coarse brittle hair
reflexes showing slow return phase
129
Q

Levothyroxine

A

synthetic analog of T4, which gets converted to T3 in the peripheral tissues

tachycardia
heat intolerance
tremors
arrhythmias
if dosed too high
130
Q

Congenital hypothyroidism- causes

A
  • thyroid- related enzyme deficiency
  • dysfunctional hormone production, transport, or function
  • TSH resistance
  • Transfer of anti-thyroid medication or anti-thyroid antibodies from the mother
  • iodine- deficient diet in the mother during pregnancy
131
Q

congenital hypothyroidism- presentation

A

impaired physical growth
intellectual disability
enlarged tongue
enlarged/distended abdomen

every baby is screened in order to intervene early if needed

132
Q

Hashimoto thyroiditis

A

autoimmune disorder, HLADR5, HLAB5
more common in women

histology: Hurthle cells, lymphoid aggregate with germinal centers
thyroglobulin and thyroid peroxidase antibodies
painless goiter
hypothyroidism
dense infiltrate of lymphocytes into the thyroid gland that cause eventual destruction of all hormone production, in some

Early: 
euthyroid
positive antibody
normal TS, TSH
Asymptomatic
possibly with a goiter

Inflammation- hyperthyroidism, transient, as T3, and T4 spill into the blood, lasting a few months

Destruction of thyroid: patient becomes hypothyroid, develops a scarred and shrunken gland in the hypothyroid state, resembling a lymph node

133
Q

thyroiditis with granulomatous inflammation

A

Subacute thyroiditis

134
Q

thyroiditis with lymphocytic inflammation

A

Hashimoto thyroiditis

135
Q

Riedel’s thyroiditis

A

fixed, hard, rock-like painless goiter

histologically: fibrosis, macrophages, eosinophils

136
Q

thyroiditis with macrophages and eosinophils

A

Riedel’s thyroiditis, where thyroid is replaced by fibrous tissue, and this fibrosis can extend into adjacent structures, mimicking anaplastic carcinoma (consider cancer if the patient is older)

137
Q

most common type of thyroid cancer

A

papillary carcinoma

138
Q

second most common type of thyroid cancer

A

follicular carcinoma

139
Q

activation of receptor tyrosine kinases

A

papillary and medullary carcinoma

140
Q

hashimoto thyroiditis is a risk factor

A

for B- cell lymphomacancer arising from parafollicular C cells

141
Q

medullary carcinoma

A

commonly associated with either a RAS mutation or a PAX8-PPARgamma1 rearrangement

142
Q

follicular carcinoma

A

commonly assocaited with rearrangements in RET oncogene or NTRK1

143
Q

papillary carcinoma

A

most common mutation is the BRAF genepapillary carcinoma

144
Q

causes of CAH

A

iodine deficient diet in mother
thyroid dysgenesis
thyroid developmental defect
failure of thyroid descent during development
transfer of antithyroid antibodies or medication from mother to fetus

145
Q

Thyrotoxicosis

A 
tachycardia
palpitations
anxiety
weightloss
heat intolerance
hyperactivity
warm skin
diarrhea
hyperreflexia
hyperactivity
pretibial myxedema (Grave's disease)
periorbital edema
warm, moist, skin, fine hair
increased free or total T3, T4
hypercholesterolemia 2/2 increased LDL receptor expression
decreased or absent menstrual flow

phenomenon

146
Q

Graves’ disease

A

autoimmune disorder
TSI binds to TSH receptor and stimulates the thyroid gland to secrete T3 and T4

HLA-DR3, HLA-B8, 4:1 female predominance

increased uptake on radioactive iodine study

exophthalmos due to connective tissue deposition in the orbit and extraocular muscles

pretibial myxedema- thickening of the skin on the front of the shins

147
Q

Jod- Basedow phenomenon

aka iodine- induced hyperthyroidism

A

thyrotoxicosis with a patient with iodine deficiency goiter is made iodine replete

148
Q

Propylthyiouracil

A

block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine. This leads to inhibition of thyroid hormone synthesis.

blocks 5’deiodinase, and leads to the decrease of peripheral conversion of T4 to T3

Toxicity: skin rash, agranulocytosis, aplastic anemia, HEPATOTOXICITY
causes fetal goiter and hypothyroidism, preferred over methimazole in the 1st trimester

149
Q

Methimazole

A

Block thyroid peroxidase, inhibiting the oxidation of iodide and the organification (coupling) of iodine. This leads to inhibition of thyroid hormone synthesis.

causes aplasia cutis (scalp defect) preferred over PTU in 2nd and 3rd trimesters of pregnancy

150
Q

toxic adenoma/ multinodular goiter

A

Mutation in TSH receptor leading to focal patches of hyper-functioning follicular cells

radioactive iodine uptake and scan, “hot nodules”
reassuring because these are not malignant.

151
Q

subacute thyroiditis

A

focal destruction of thyroid with granulomatous inflammation
3:1 female predominance
associated with HLA-B35
viral infections

thyrotoxicosis early in the course, which later switches to hypothyroidism

self- limited

152
Q

Thyroid storm

A 
increased body temperature
altered mental status
tachycardia
arrhythmias
vomiting
diarrhea
dehydration
coma 
death
stress- induced catecholamine surge seen as a serious complication of thyrotoxicosis due to disease and other hyperthyroid disorders

Treat with propanolol, PTU, corticosteroids such as Prednisolone
20% mortality
ow

153
Q

Struma ovarii

A

thyroid tissue teratoma that presents as hyperthyroid

154
Q

hyperthyroid and extremely tender thyroid gland

A

subacute (de Quervain) thyroiditis

155
Q

hyperthyroid and pretibial myxedema

A

graves’ disease

156
Q

hyperthyroid and pride in recent weightloss, medical professional

A

thyroid hormone abuse

157
Q

hyperthyroid and palpation of single thyroid nodule

A

toxic thyroid adenoma

158
Q

hyperthyroid and palpation of multiple thyroid nodules

A

toxic multinodular goiter

159
Q

hyperthyroid and recent study using IV contrast (iodine)

A

Jod- Basedow phenomenon

STEP1 2015 (30 decks)

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