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Kumar and clark endocrine > day3 > Flashcards

day3 Flashcards

1
Q

acute tenderness in goitre in a diffuse swelling, sometimes with severe pain is suggest of

A

acute viral thyroiditis (de quervains)

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2
Q

in multi nodular goitre what is the thyroid levels usually

A

euthyroid

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3
Q

what is the most common cause of tracheal and or oesophageal compression and can lead to laryngeal nerve palsy

A

multi nodular goitre

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4
Q

you get fibrotic nodular goitre in

A

riedels thyroiditis

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5
Q

what should be a concern in a solitary nodule

A

malignancy

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6
Q

are majority of solitary nodules cystic or benign

A

yes

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7
Q

most thyroid cancers are

A

painless and slow growing

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8
Q

fibrotic goitre producing a woody gland

A

riedels thyroidits

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9
Q

a goitre associated with euthyroidism rarely requires intervention and the patient can be reassured that spontaneous resolution is likely during

A

puberty and pregnancy

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10
Q

carcinomas derived from thyroid epithelium may be

A

papillary, folliciular or anaplastic

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11
Q

medullary carcinomas arise from calcitonin producing c cells

A
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12
Q

most common thyroid carcinoma

A

papillary

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13
Q

papillary carcinoma is common in what kind of people

A

young

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14
Q

what can be used as a tumour marker in thyroid carcinomas after thyroid ablation

A

thyroglobulin

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15
Q

what do you use for residual thyroid tissue post op

A

RAI ablation

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16
Q

what can you give to minimise risk of recurrence of papillary and follicular carcinomas

A

levothyroxine

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17
Q

when is the measurement of thyroglobulin(tumour marker) most sensitive

A

when TSH is high so requires withdrawal of levothyroxine

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18
Q

what can be used to stimulate thyroglobulin without stopping levothyroxine

A

recombinant TSH

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19
Q

what suggests recurrence of papillary/follcular carcinomas

A

detectable thyroglobulin

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20
Q

medullary carcinoma is often associated with

A

Men2

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21
Q

approx 1 in 4 patients diagnosed with medullary thyroid cancer have a mutation on the

A

RET proto oncogene

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22
Q

people with MEN2 mutations are advised to have what as early of 5 years of age to prevent the development of medullary thyroid carcinoma

A

prophylactic thyroidectomy

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23
Q

is local invasion or metastasis frequent in medullary thyroid carcinoma

A

yes

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24
Q

what is usually indicated in medullary thyroid carcinoma

A

total thyroidectomy and wide lymph node clearance

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25
Q

what controls progression through puberty and the capacity for reproduction

A

hypothalamo- pituitary gonadal axis

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26
Q

what is primary amenorrhoea

A

failure to begin spontaneous menstruation by age 16

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27
Q

what is secondary amenorrhoea

A

absence of menstruatuon for 3 months in a woman who has previously had cycles

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28
Q

GnRH is released from where

A

hypothalamus

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29
Q

GnRH stimulates

A

LH and FSH release from the pituitary

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30
Q

in males, LH stimulates

A

testosterone

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31
Q

FSH stimulates what cells in males to produce mature sperm

A

Sertoli cells

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32
Q

in females, LH and FSH stimulates

A

androgen and oestrogen production

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32
Q

in females, LH and FSH stimulates

A

androgen and oestrogen production

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33
Q

what indicates primary gonadal disease

A

high gonadotrophins with low testosterone or oestradiol

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34
Q

normal or low LH/FSH with low testosterone/oestridiol

A

hypothalamic pituitary disease

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35
Q

what test to exclude hypogonadism in males

A

basal testosterone

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36
Q

what test in female to exclude hypogonadism

A

basal oestradiol

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37
Q

male with an extra X chromosome

A

klinefelters syndrome

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38
Q

early indications of klinefelters syndrome

A

cryptochidism (absence of a test) , behavioural problems, tall stature and learning difficulties

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39
Q

pea sized but firm tsts

A

klinefelters syndrome

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40
Q

isolated GnRH deficiency

A

kallmans syndrome

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41
Q

what is gynaecomastia

A

development of breast tissue in the male

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42
Q

causes of gynaecomastia

A

hyperthyroidism, hyperprolactinaemia, renal and liver disease, hypogonadism drugs

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43
Q

common drugs to cause gynaecomastia

A

digoxin and spironolactone

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44
Q

cause of gynaecomastia in young person

A

oestrogen excess

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45
Q

cause of gynaecomastia in older male

A

aromatase activity increases

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46
Q

low testosterone increases risk of

A

osteoporosis

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47
Q

most common presentation of female gonadal disease

A

amenorrohea (absence of periods)

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48
Q

what is oligomenorrhoea

A

irregular infrequent periods

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49
Q

what is the most common cause of oligomenorrhoea and amenorrhoea

A

polycystic ovary syndrome

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50
Q

premature menopause before the age of 40 is called

A

premature ovarian insufficiency

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51
Q

what is a cause of premature ovarian insufficiency, frequently with delayed puberty and primary amonohorrea

A

turners syndrome

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52
Q

phenotype is a female with female external genitalia

A

turners

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53
Q

features of turners

A

short stature, webbing of the neck, wide carrying angle of the elbows, high arched palate and low seat ears

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54
Q

what confirms diagnosis of premature ovarian insuffiecny

A

elevation of LH and FSH to menopausal levels

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55
Q

if oestrogen deficiency is not reversed in premature ovarian insuffiency what should be given

A

hormone replacement therapy

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56
Q

increased hair in sex hormone dependent areas is most likely

A

polycystic ovary syndrome

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56
Q

excess hair in sex dependent hormone areas is due to

A

increased ovarian adrenal androgen production

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57
Q

most common cause of hirsutism

A

polycystic ovary syndrome

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58
Q

what is characterised by multiple small cysts within the ovary and and by excess androgen production from the ovaries

A

polycystic ovary syndrome

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59
Q

what is PCOS associated with

A

hyperinsulinaemia and insulin resistance, hypertension, hyperlipidaemia and increased cardiovascular risk

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60
Q

most patients with PCOS present with what

A

amonehoorhoea/oligomenorrhoea and or hirsutism and acne shortly after starting period

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61
Q

should diet and exercise be indicated in polycystic ovarian syndrome

A

yes

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62
Q

what worsens androgen excess and insulin resistance

A

obesity

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63
Q

what is in oral contraceptives

A

oestrogen

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64
Q

increasing SBHG levels does what

A

reduce free androgens

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65
Q

treatment if only symptom if menstrual disturbance

A

cyclical oestrogen/ progestogen

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66
Q

treatment for fertility in PCOS

A

clomifene or ietrozole

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67
Q

what is a strong determinant of timing of puberty

A

timing of parental puberty

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68
Q

GHRH is under inhibitory control by

A

somatostatin

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69
Q

gh binds to a receptor in the

A

liver

70
Q

-increasing collagen and protein synthesis
- promoting retention of calcium, phosphorus and nitrogen(necessary substrates for anabolism)
-opposing action of insulin
are

A

metabolic actions from growth hormones

71
Q

gh release is mainly

A

nocturnal

72
Q

what stimulates gh

A

stress and exercise

73
Q

what suppresses gh

A

hyperglycaemia

74
Q

inhibition of GnRH

A

initiating puberty

75
Q

what peptide plays a crucial role in the regulation of GnRH production and timing of puberty

A

KISS1R

76
Q

what are low in the prepubertal child

A

Lh and FSH

77
Q

what is more helpful than current height in measuring growth

A

height velocity

78
Q

what is associated with short stature in females

A

turners

79
Q

hypo or hyper thyroids can cause short stature

A

hypothyroidism

80
Q

chromosomal abnoramlitites that can cause tall stature

A

klinefelters syndrome and marfans syndrome

81
Q

in obesity are SHBG levels reduced or increased and same with androgens

A

shbg reduced and androgens increased

82
Q

specific features of acromegaly

A

prognathism(extension or bulging out of lower jaw), interdental separation, large tongue, spade like hands and feet

83
Q

gh excess causes what in children and what in adults

A

gigantism in children and acromegaly in adults

84
Q

gigantism and acromegaly are due to gh secreting pituitary tumour called

A

somatotroph adenoma

85
Q

acromegaly usually occurs

A

sporadically

86
Q

what is common in acromegaly

A

sleep apnoea

87
Q

what is very common in acromegaly

A

headaches

88
Q

how useful is gh levels in acromegaly

A

may exclude acromegaly if they are undetectable but a detectable value is not diagnostic alone

89
Q

what test for acromegaly is diagnostic if there ice no suppression of gh

A

glucose tolerance test

90
Q

example of a visual defect in acromegaly

A

bitemporal hemianopia

91
Q

what do people die from in acromegaly

A

heart failure, coronary artery disease or hypertension

92
Q

first line therapy in acromegaly

A

trans-sphenoidal surgery

93
Q

3 receptor targets in acromegaly

A

pituitary somatostatin receptors
dopamine receptors
Gh receptors

94
Q

side effects of somatostatin analogues eg octreotide and ianreotide

A

gallstones

95
Q

what drugs are most effective in GH producing or prolactin producing tumours

A

dopamine agonists

96
Q

growth hormone antagonist

A

pegvisomant

97
Q

what is mainly controlled by tonic inhibition by hypothalamic dopamine

A

prolactin

98
Q

what stimulates JAK2

A

prolactin

99
Q

what does prolactin do

A

stimulate milk secretion (but not breast tissue development) and inhibits gonadal activity

100
Q

what produces hypogonadism even when the pituitary gonadal axis is intact

A

prolactin

101
Q

what can these drugs cause:
oestrogen (contraceptive pill)
dopamine antagonists
antidepressants
antiemetics eg metoclopramide
verapamil

A
102
Q

common signs in hyperprolactinaemia

A

galactorrhea (nipple milk discharge)
oligomenorrhoea
decreased libido (sex drive)

103
Q

common signs in hyperprolactinaemia

A

galactorrhea (nipple milk discharge)
oligomenorrhoea
decreased libido (sex drive)

104
Q

how is hyperprolactinaemia confirmed

A

repeat measurements

105
Q

what can be a cause of hyperprolactinaemia

A

primary hypothyroidism

106
Q

hyperprolactinaemia is controlled with a dopamine agonist eg

A

cabergoline

107
Q

in prolactianemia what is done If dopamine agonists aren’t working

A

transphenoidal surgery- only for micro adenoma

108
Q

where is ash synthesised

A

hypothalamus

109
Q

predominant site of adh/vasopressin

A

kidneys

110
Q

what does vasopressin do

A

allows collecting ducts to to become permeable to water

111
Q

vasopressin results

A

retention of water

112
Q

problems involving vasopressin

A

diabetes insipidus and SIADH

113
Q

what is a common cause of hyponatraemia in hospital patients

A

syndrome of inappropriate antidiuretic hormone (SIADH)

114
Q

most common cause of diabetes insidipidus

A

hypothalamic pituitary surgery

115
Q

excess secretion of dilute urine so compensatory increase in thrust so can lead to dehydration

A

diabetes insipidus

116
Q

what can mask diabetes insidious

A

cortisol defiency

117
Q

absent or poorly developed posterior pituitary

A

DIDMOAD syndrome

118
Q

treatment of choice in cranial DI

A

synthetic vasopressin called desmopressin

119
Q

polyuria can be helped with

A

thiazide diuretics

120
Q

water deprivation test for

A

DI and primary polydipsia

121
Q

psychiatric disturbance characterised by the excessive intake of water

A

primary polydipsia

122
Q

retention of water and hyponatraemia

A

SIADH

123
Q

retention of water and hypernatraemia in plasma

A

DI

124
Q

is there oedema in SIADH

A

no

125
Q

symptoms of SIADH

A

vague with confusion, nausea and can lead to coma

126
Q

what is absent in SIADH

A

hypokalaemia or hypotension

127
Q

management fo SIADH

A

fluid intake restriction

128
Q

what drug inhibits the action of vasopressin o the kidney and can eb used for SIADH

A

demeclocycline

129
Q

serum calcium levels are mainly controlled by which 2 things

A

parathyroid hormone and vitamin D

129
Q

serum calcium levels are mainly controlled by which 2 things

A

parathyroid hormone and vitamin D

130
Q

mild hypercalcaemia is mainly due to

A

primary hyperthyroidism

131
Q

what cells secrete parathyroid hormone

A

chief cells

132
Q

parathyroid levels rise as

A

serum ionised calcium falls

133
Q

PTH acts to

A

increase plasma calcium

134
Q

what does these:
increase osteoclastic resorption of bone
increase intestinal absorption of calcium
increase excretion of phosphate

A

PTH

135
Q

most common cause of excess pTH secretion

A

primary hyperparathyroidism but adenoma is still common

136
Q

most primary hyperparathyroidism is caused by what

A

single parathyroid adenomas

137
Q

secondary hyperparathyroidism is compensatory of

A

hypocalcaemia

138
Q

when is there hypocalacemia often

A

chronic kidney disease or vitamin D deficient

139
Q

genereal symptoms of hypercalcaermia

A

tiredness, malaise, dehydration and depression

140
Q

brown tumours occurs in advanced disease of

A

hyeprcalcemia

141
Q

corneal calcification is a marker of

A

longstanding hypercalcaemia

142
Q

severe hypercalcemia is usually associated with

A

malignant disease, hyperparathyroidism, chronic kidney disease, or vitamin D therapy

143
Q

what is the hallmark of primary hyperparathyroidism

A

hypercalcaemia and hypophosphataemia with detectable PTH LEVELS DURING HYPERCALCAEMIA

144
Q

if undetectable PTH level in context of hypercalcemia need to exclude

A

malignancy

145
Q

medical management for primary hyperparathyroidism

A

high fluid intake and replaectn of vitamin d if needed

146
Q

how does acute hypercalaemia present

A

dehydration, nausea, vomiting,nocturia(causes you to wake up in night to pee), polyuria, drowsiness and altered consciousness

147
Q

treatments for acute severe hypercalcemia

A

rehydrate
IV Biphosphanates (treatment of choic)

148
Q

what is the major danger after operation

A

hypocalcemia

149
Q

causes of hypocalcaemia

A

chronic kidney disease and phosphate therapy (increased phosphate levels)
acute pancreatitis
calcitonin , biphosphanatates
ostemalacis/rickets
surgery around neck
severe vitamin D deficiency

150
Q

most common cause fo hypocalcemia is

A

chronic kidney disease

151
Q

hypocalcemia presents as

A

neuromuscular irritability, paraesthesia, anxiety, tetany

152
Q

2 signs of hypocalcemia

A

chvosteks sign and trousseaus sign

153
Q

what sign is this: gentle tapping over the facial nerves causes twitching of the ipsilateral facial muscles

A

chvosteks sign

154
Q

what sign is this: inflation of the sphygmomanometer cuff above systolic pressure for 3 min induces titanic spasm of the fingers and wrist

A

trousseaus sign

155
Q

what may cause prolonged qt interval on ecg

A

hypocalcemia

156
Q

diagnostic of hypocalcemia

A

Low serum calcium

157
Q

most appropriate treatment fro hypcalcemia if vitamin d deficient

A

cholecalciferol

158
Q

presenting features fo insulinoma

A

Diplopia (seeing double)
sweating, palpitations
confusion

159
Q

classic presentation of insulinoma

A

fasting hypoglycaemia

160
Q

whiles triad for insulinoma:

A

symptoms are associated with fasting or exercise
hypoglycaemia is confirmed during these episodes
glucose relieves the symptoms

161
Q

medical treatment for insulinomas

A

diazoxide

162
Q

what is a problem in acute hepatic failure

A

hypocalcemia

163
Q

drugs that can cause hypoglycaemia

A

sulphonylureas
propanolol

164
Q

alcohol inhibits what

A

gluconeogenesis

165
Q

can alcohol cause hypoglycaemia

A

yes

166
Q

what is the name given to the simultaneous occurrence of tumours involving a number of endocrine glands

A

multiple endocrine neoplasias (MEN)

167
Q

men 2 caused by mutations of

A

RET on chromosome 10

168
Q

all glands are typically involved in

A

MEN1

169
Q

essence of management in MEN is

A

annual screening

170
Q

first manifestation of MEN1

A

hyperparathyroidism

171
Q

useful tumour marker in medullary carcinoma of the thyroid

A

calcitonin

172
Q

carcinoid syndrome is due to what tumour

A

neuroendocrine

Kumar and clark endocrine (3 decks)

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