ENDOCRINE Flashcards

1
Q

infarction of macroadenoma can lead to

A

panhypopituitarism

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2
Q

often cystic

A

craniopharyngioma

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3
Q

most common cause of hypopituirasm

A

non function pituitary macro adenomas

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4
Q

panhypopituiriasm refers to

A

deficiency of all anterior pituitary hormones

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5
Q

panhypopituiriasm refers to

A

deficiency of all anterior pituitary hormones

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6
Q

what does hypoadrenalism cause

A

mild hypotension, hyponatraemia and CV collapse

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7
Q

what is the classical picture fo longstanding panhypopituiriasm

A

pallor with hairlessness

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8
Q

what identifies pituitary adenomas

A

MRI

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9
Q

difference in definitions between cranial and nephrogenic DI

A

cranial- insufficient levels of circulating ADH
nephrogenic - renal resistance to ADH

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10
Q

urine/serum osmolality should be

A

> 2

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11
Q

if cranial DI is diagnosed what should be done

A

CT or mRI to rule out brain tumours especially craniopharyngioma

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12
Q

what can be used before surgery for acromegaly

A

somatostatin analogues eg sandostain

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13
Q

what can increase risk of colon polyps or colon cancer and may be presenting feature

A

acromegaly

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14
Q

drugs that reduce dopamine

A

metoclopramide, phenothiazines

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15
Q

what is the main treatment for prolactinoma

A

cabergoline - v good so rarely need surgery

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16
Q

symptoms of rubella syndrome in baby

A

microcephalic;y, patent ductus arterioles and cataract

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17
Q

what tests for tubal patency

A

hysterosalpingiogram

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18
Q

what vitamin should take before pregnancy and for first 12 weeks

A

folic acid

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19
Q

what is a hydrosalpinges

A

Fallopian tube filled with water

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20
Q

what detects oestrogen defieicny

A

negative progesterone challenge test

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21
Q

kallamans is what class of pituitary failure

A

1 - hypothalamic pituitary failure

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22
Q

turners syndrome comes into what class?

A

3 ovarian failure

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23
Q

what is oligomenorrhoea

A

cycles greater than 42 days

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24
Q

diffeerence between primary and secondary amenorrhoea

A

primary - never mensutrated
secondary - menstruated then stop

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25
Q

what to do if infertility but got regular periods

A

midluteal serum progesterone

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26
Q

what to do if got irregular cycles

A

hormone evaluation

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27
Q

what challenge test should introduce a period

A

progesterone

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28
Q

what could consider if not responding to clomifene citrate for pros in getting pregnant

A

methotrexate

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29
Q

what acts as a co- gonadotrophin to LH

A

glucose

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30
Q

what lowers SHBG that can contribute to hyperandrogegism

A

insulin

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31
Q

inflammatory disorder eg chlamydia, gonorrhoea can cause what

A

hydrosalpinx

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32
Q

what is a hydrosalpinx

A

Fallopian tube is blocked and fills with serous or clear fluid near the ovary

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33
Q

pelvic inflammatory disorder presents as

A

abdo/pelvic pain
febrile
vaginal discharge

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34
Q

uterus on US may be fixed and retroverted and may show chocolate cysts

A

endometriosis

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35
Q

klinefelters biochem

A

primary hypogonadism - low testosterone and high LH/FSH

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36
Q

kallman and prader will have what biochem

A

low testosterone and low fish/LH

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37
Q

if primary hypogonadism in males what tests next

A

karyotyping or iron studies

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38
Q

in secondary hypogonadism what do you need to exclude

A

medications and prolactin and pituitary hormones

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39
Q

when does testosterone peak

A

morning

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40
Q

most common genetic cause of hypogonadism in men

A

klinefelters

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41
Q

klinefelters presents

A

infertile and small firm testes

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42
Q

increased incidence off what in klinefelters

A

cryptorchidism (abscence of testes from scrotum)

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43
Q

klinefelters increase risk of what

A

breast cancer and non Hodgkin lymphoma

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44
Q

red green colour blindness and clip palate are associated with

A

kallamsn

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45
Q

there is an isolated GnRh deficiency in

A

Kallman

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46
Q

are men autosomal dominant or recessive

A

dominant

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47
Q

men 1 3 symptoms

A

pituitary adenoma, hyperparathyroidism and pancreatic tumour eg insulinoma

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48
Q

Ret in men 2 is a

A

proto oncogene

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49
Q

mutations in RET activate what

A

receptor tyrosine kinase

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50
Q

men 2a or b more common

A

2a - 90-95%

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51
Q

men 2a features

A

medullary thyroid cancer, phaeochromocytoma and parathyroid tumours

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52
Q

men 2b features

A

MTC, phaechromocytoma and marfanoid features - mucosal neuromas

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53
Q

what is typically the first presentation of MEN 2

A

MTC

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54
Q

von hippel Lindau is tumors where

A

central nervous system

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55
Q

bone lesions in NF 1

A

sphenoid dysplasia or thinning of long bone cortex

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56
Q

cushings, acromegaly and thyroid carcinoma

A

carney complex

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57
Q

mccune Albright syndrome has mutations of what

A

GNAS

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57
Q

mccune Albright syndrome has mutations of what

A

GNAS

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58
Q

what is a trophoblast tumour secretion hCG

A

choriocarcinoma

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59
Q

what are thyrotoxicosis not associated with hyperthyroidism

A

thyroiditis

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60
Q

what drug can cause drug induces thyroiditis

A

amiodarone

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61
Q

what does a thyroid bruit reflect

A

hypervascualrity of thyroid - graves

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62
Q

pretibial myxoedema is seen in graves and what else

A

hashimotos thyroididts

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63
Q

what scan is done if suspect graves by antibodies are negative so look for toxic nodular disease

A

scintiscan

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64
Q

first line for graves

A

carbimazoel

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65
Q

what is first line treatment for relapsed graves dn nodular thyroid disease

A

radioiodien

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66
Q

what is used when radio iodine is contraindicated eg in pregnancy

A

thyroidectomy

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67
Q

what has a painful diffuse firm goitre

A

de quervains

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68
Q

what often occurs after viral infection in young woman

A

de quervains thyroiditis

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69
Q

in dequervains there is a hyperthyroid phase followed by

A

hypothyroidism phase

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70
Q

drug induced thyroiditis can be caused by

A

amiodarone and lithium

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71
Q

what does amiodarone inhibit

A

DI01

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72
Q

hormone results from amiodarone

A

increase t4, decrease t3 and normal TSH

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73
Q

hasmimotos like de quervains can have

A

hyoperthyroid then hypothyroid phase

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74
Q

de quervains tends to occur in what aged females vs hashimotos

A

dequervains - 20-50
hashimotos- 45-60

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75
Q

hurthle cell - follicular cells with eosinophils cytoplasm can be seen in

A

hashimotos thyroiditis s

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76
Q

periorbital oedema is only seen in

A

hypothyroidism

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77
Q

in hypothyrodisims wha cardiac feature

A

dilated cardiomyopathy

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78
Q

obstructive sleep apnoea can occur in what thyroidism

A

hypo

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79
Q

congenital hypothyrodisim is called

A

cretinism

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80
Q

after treatment for hypothyroidism what should be checked every 12 months

A

TSH

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81
Q

TSH is unreliable in

A

secondary hypothyroidism

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82
Q

long standing complication of autoimmune hypothyroidism

A

B cell non Hodgkins Lymphoma in the affected gland

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83
Q

TSh elevated and normal t3/4

A

subclinical hypothyroidism

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84
Q

when should you always treat sublcinctal hypothyroidism

A

pregnancy

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85
Q

subclinical hyperthyroidism is often seen in

A

multi nodular goitre

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86
Q

when is treatment generally advised in subclinical hypo/hyperthyroidism

A

hypo: TSH >10
hyper: TSH <0.1 or osteoporosis or AF

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87
Q

can benign thyroid nodules painful/ tenderness

A

yes

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88
Q

most common malignant thyroid nodule

A

papillary thyroid carcinoma

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89
Q

difference between benign and malignant thyroid nodule?

A

benign is mobile and malignant is immobile

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90
Q

if a lump moves on swallowing what does this mean

A

it is in the thyroid invested in pretracehal fascia

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91
Q

toxic nodule may have signs of what

A

hypothyroidism

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92
Q

what can tell the differcen between hot and cold nodules

A

scintigraphy

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93
Q

are hot nodules always malignant

A

no -only rarely malignant

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94
Q

what mainly diagnosis thyroid nodules

A

US- FNA

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95
Q

what tumour in thyroid has a thin fibrous capsule

A

follicular adenoma

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96
Q

why is the management for follicular adenoma lobectomy with biopsy instead of FNA

A

FNA cannot distinguish between follicular adenoma and follicular carcinoma

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97
Q

papillary carcinoma is associated with what

A

hasminotos and ionising radiation

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98
Q

follicular carcinoma rates are more in

A

iodine deficient areas

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99
Q

what carcinoma can be multifocal, often cystic and may be calcified (psammoma bodies)

A

papillary

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100
Q

follicular carcinomas spread via

A

haemtogenosu

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101
Q

what usually confirms papillary or follicular carcinoma

A

us - FNA

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102
Q

what is done 3-6 months post op of thyroidectomy

A

whole body iodine scan

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103
Q

what are patients treated with to minimise risk of recurrence of papillary or follicular carcinoma

A

levothyroxine to suppress TSH

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104
Q

tumour marker for papillary and follicular carcinoma

A

thyroglobulin as made by thyroid follilculae epithelial cell

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105
Q

what does not respond to RAI

A

anapaestic carcinoma

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106
Q

what are composed of spindle or polygonal cells in nests

A

MTC

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107
Q

what is associated with amyloid deposition

A

mTC

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108
Q

diarrhoea in MTC suggests production of what

A

VIP

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109
Q

thyroid lymphoma often has a background of what

A

auto-immune hypothyroidism

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110
Q

what presents as a rapid onset mass in thyroid

A

lymphoma

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111
Q

a rise in what stimulates goitre

A

TSH

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112
Q

what nodules have an increase risk of malignant transformation

A

toxic

113
Q

difference in t3/4 for multi nodular goitre if toxic

A

t3/4 normal in inactive
t3/4 increased in toxic

114
Q

isotope scan can tell if

A

toxic or non toxic

115
Q

how to trat toxic multomdular goitre

A

antithyroid drugs

116
Q

when does hCG associated thyrotoxicosis resolve

A

20 weeks

117
Q

hcg thyrotoxicos does not have

A

TRab antibody

118
Q

what antibodies can cause neonatal transient hyperthyroidism

A

TRab

119
Q

what is first line for hyperthyroidism with pregnancy

A

wait and see as often settles

120
Q

post partum thyroididts occurs within how long of giving birth

A

6 months

121
Q

25-50% of post partum thyroiditis will have what beyond 1 year

A

hypothyroidism

122
Q

what is the aim for diabetes hbA1c

A

<53

123
Q

diabetes in late 30s

A

LADA

124
Q

viral infection that can contribute to type 1

A

cocksackie

125
Q

gada and IA2 linked to

A

type 1 diabetes

126
Q

what is not used in the diagnosis of type 1 but used to monitor disease after

A

HbA1c

127
Q

insulin analogues reduce what

A

hypoglycaemia risk

128
Q

what transports insulin to skeletal muscle

A

GLUT4

129
Q

what is involves in insulin resistance in adipose tissue

A

TNF alpha

130
Q

gold standard fo measuring insulin sensitivity

A

hyperinsulinaemiac euglycaemia clamp

131
Q

in diabetes there is increased activity of what

A

tyrosine kinase activity

132
Q

drug fro atherosclerotic cvd in diabetes

A

Metformin + GLP-1

133
Q

most common mutation in MODY

A

transcription factor

134
Q

what has progressive hyperglycaemia

A

transcription factor

135
Q

if suspect MODY do what

A

oral glucose tolerance test

136
Q

what MODY glucose will come down with oral challenge

A

gluokinase

137
Q

mody is not dependent on

A

Insulin

138
Q

neonatal diabetes has mutation in what mechanism

A

ATP sensing K channel

139
Q

a component of the ATP sensing K channel

A

kir6.2

140
Q

neonatal diabetes if under

A

6 months

141
Q

treatment for neonatal diabetes

A

sulphonylureas

142
Q

what is the function of insulin resistance when pregnant

A

divert nutrients to foetus

143
Q

gestational diabetes can be asscociated with

A

polyhydramnios

144
Q

what drugs should avoid in gestational diabetes

A

acei - use labetalol, nifedipine and methyldopa instead

145
Q

gestation diabetes and all high risk pregnancies should start what at 12 weeks

A

aspirin

146
Q

can stay on what during pregnancy

A

metformin

147
Q

what2 things can cause osmotic damage

A

sorbitol and fructose

148
Q

macular oedema if referable if hard exudate is within

A

1 disc diameter of the fovea

149
Q

complication sof diabetic retinopath y

A

cataracts and glaucoma

150
Q

glucose is converted to what in diabetic getting a cataract

A

sortibol

151
Q

what should you do twice as false postitive readings are common

A

measure acr/pcr for diabetic nephropathy

152
Q

what will not chow up on protein dipstick

A

microalbuminuria

153
Q

acei / arb do what to renal arterioles

A

dilate afferent and efferent to reduces GFR

154
Q

what should a diabetic with microalbuminuria be started on irrespective of HBA1c

A

SGLT2i

155
Q

nsaids affect on arteriole

A

nsaids- constrict afferent
ace- vasoodilate efferent

156
Q

nsaids affect on arteriole

A

nsaids- constrict afferent
ace- vasoodilate efferent

157
Q

argyll rovertson pupil is highly specific to neurosyphilis but may also be a sign in

A

diabetic nephropahty

158
Q

what is argylll Robertson pupil

A

small bilateral pupils that do not constrict when exposed to bright light but do constrict when focused on a nearby object c

159
Q

treatment for diabtevi neuropathy

A

amitryptiline

160
Q

glycopyrolate

A

excess sweating in diabetic

161
Q

postural hypotension can be due to autonomic neuropathy

A
162
Q

what are ketone bodies important for

A

heart muscle and renal cortex

163
Q

euglycaemic DKA is a rare complication of what

A

SGLT2i

164
Q

insulin effect on potassium

A

can cause hypokalaemia

165
Q

amylase is often raised in

A

DKA

166
Q

management for DKA

A

NaCL

167
Q

what increases risk of thromboembolism in DKA

A

dehydration

168
Q

what should all patients in ska receive to prevent thromboembolism

A

LMWH

169
Q

2 complications of DKA?

A

cerebral oedema and hypokalaemia

170
Q

what should be given after NaCl once blood glucose conc falls below 14

A

glucose

171
Q

what should be given after NaCl once blood glucose conc falls below 14 in DKA

A

glucose

172
Q

what are common precipitating factors of HHS

A

glucose rich fluids, thiazides and steriods and illness

173
Q

in HHS there is still

A

small amount of insulin being secreted by the pancreas

174
Q

in HHS there is profound hyperglycaemia and what

A

hyperosmolaltity

175
Q

how to calculate osmolailtity

A

2x Na + glucose +urea

176
Q

in HHS what is the ph and bicarbonate

A

ph >7.3 and bicarbonate >15 (no acidosis)

177
Q

treatment fo HHS

A

SALINE WITHOUT INSULIN

178
Q

what is glucose levels in alcoholic ketoacidosis

A

normal or low due to combined effect of alcohol and starvation

179
Q

alcoholic has same biochemistry to DKA except

A

glucose is normal or may be low

180
Q

What is IV pabrinex for

A

alcoholic ketoacidosis to prevent wenicke encephalopathy

181
Q

PTH AND CALCIUM IS HIGH IN

A

PRIAMRY AND TERIOTARY HYPERPARATHYRROIDSM

182
Q

what is low or normal in secondary hyperparathyroidism

A

calcium

183
Q

causes of primary and tertiary hyperaprathryoidsm

A

primary - tumour
tertiary - hyperplasia

184
Q

what activates osteoclasts

A

PTH

185
Q

in hyperparathyroidism is Pth secretion stopped

A

no

186
Q

osteoporosis, brown tumours and osteitis

A

fibrosa cystica

187
Q

osteoporosis has prominent effects to which part of the bone

A

cortical

188
Q

hypercalcaemia can be caused by which drugs

A

vit D, thiazides

189
Q

hallmark of primary hyperparathyroidism

A

hypercalcaemia and hypophosphataemi with detectable or elevated intact PTH levels

190
Q

undetectable what() with hypercalcaemia requires further investigation for malignancy

A

PTH

191
Q

what is raised in hypercalcaemia of malignancy

A

serum alkaline phosphatase

192
Q

how does familial hypocalciuric hypercalcaemia present

A

mild hypercalcaemia, reduced urine calcium excretion and PTH may be elevated

193
Q

management of acute hypercalaemia

A

salien
consider loops once rehydrated

194
Q

what diuretic to avoid in hypercalemia

A

thiazides

195
Q

what is a drug for primary hyperparathyroidism if surgery not indicated

A

cinacalcet

196
Q

calcium release from cells is dependent on

A

magnesium

197
Q

paraesthesia suggest

A

hypocalcaemia

198
Q

chovesteks sign

A

tapping facial nerve

199
Q

QT prolongation is

A

hypocalcaemia

200
Q

hypocalcaemia with low PTH has to be

A

Hypoparathyroidism

201
Q

low calcium, high PTH and low cacidiol, low or normal phosphate

A

VIT D defiecjy

202
Q

low calcium, high PTH, high phosphatee

A

hyperpohospahtemia or pseudohypoparathyroidism

203
Q

low calcium with high PTH and high phosphate AND CREATINIEN

A

CKD

204
Q

LOW CALCIUM , HIGH PTH AND LOW MAGNESIUM

A

MALABSORPTION OR ALCOHOLISM

205
Q

management of hypocalcaemia

A

calcium glutinate

206
Q

oral vit d drug

A

alphacalcidiol

207
Q

injection of vit d

A

cholecalciferol

208
Q

drugs that can cause low magnesium

A

thiazides and PPIs

209
Q

what has dysfunction of GNAS

A

Pseudohyoparathyroidism

210
Q

condition associated with resistance to the parathyroid hormone

A

pseudohypoparathyroidism

211
Q

shortened 4 th finger

A

pseudohypoparathyroidism

212
Q

pseudo -pseudohypoparathyroidism

A

no abnormaliiteis in calcium metabolism

213
Q

acth independent or dependent that causes nodular adrenal enlargement

A

independent

214
Q

what cancer can cause ectopic ACTH production

A

Small cell

215
Q

what can secrete excess CRH

A

medullary thyroid carcinoma

216
Q

pigmentation in cushings syndrome only occurs with

A

ACTH dependent causes

217
Q

frontal balding in women

A

cushings

218
Q

how should cortisol level respond to administration of deaxmethasoen

A

should decrease

219
Q

what suggests ACT dependent cushings

A

if serum ACTH are high

220
Q

what is last lien for cushings

A

bilateral adrenalectomy

221
Q

what is a drug management that can be given if surgery fails in cushings

A

metyrapoen

222
Q

what investigation if ACTH independent

A

CT or MRI

223
Q

what 2 tests can tell the difference between pituitary and ectopic ACTH

A

high dose dexamethasone suppression or exogenous CRH

224
Q

adrenal adenoma emerges from where

A

adrenal cortex

225
Q

what in younger patients can be associated with Li- fraumeni syndrome

A

adrenocortical carcinoma

226
Q

what are regulators of aldosterone

A

angiotensin II and potassium

227
Q

conns syndrome is an adrenal

A

adenoma

228
Q

what is the commonest secondary cause of hypertension

A

primary hyperaldosternoism

229
Q

what presents with significant hypertension, hypokalaemia and alkalosis

A

primary hyperaldosteronism

230
Q

what is next test you do for primary hyperaldosteronism if plasma aldosterone: rennin ratio is increased

A

salien suppression test

231
Q

if plasma aldosterone doe snot suppress by how much with 2 litres of water can primary hyperaldosteronism then Bec confirmed

A

50%

232
Q

what is the treatment fro bilateral adrenal hyperplasia

A

mineralocorticoid receptro antagonists eg spironolactone or eplerenone

233
Q

when do renin/ aldosterone ration and get high aldosterone and high renin this indicates

A

secondary hyperalodsteronism

234
Q

most cases of secondary hyperaldosternism are due to

A

renal artery stenosis

235
Q

cause of secondary hyperaldosteronism in young females

A

fibromuscular dysplasia

236
Q

what looks for renal artery stenosis

A

CT angiogram or MR angiography

237
Q

treatment for secondary hyperaldosteronism

A

aldosterone antagonist eg spironolactone

238
Q

what treats renal artery stenosis

A

perucataneous renal artery angioplasty

239
Q

what involves destruction fo the entire adrenal Cortex

A

Addisons

240
Q

what is the most common cause of Addisons?

A

autoimmune adrenalitis

241
Q

anticoagulant treatment can cause adrenal haemorrhage which can cause

A

Addisons

242
Q

as there is decreased mineralocorticoids this will result in

A

K retention and Na loss

243
Q

Addisons decreases glucocorticoids causing

A

hypoglycaemia

244
Q

acth contains a sequence for what within it

A

Melanocyte stimualting hormone

245
Q

skin pigmentation is not seen in

A

hypopituitarism

246
Q

black spots in buccal mucosa, dark palmar creases and dark finger spaces

A

Addisons

247
Q

what is positive in 70% of Addisons

A

antibodies

248
Q

I know not the primary investigation but what is renin: aldosterone levels like in Addisons

A

renin high and aldosterone decreased

249
Q

manageement for Addisons

A

hydrocortisone and fludrocortisone

250
Q

pre op in Addisons need to increase

A

steriod replacement

251
Q

exogenous steriod use does what

A

inhibit CRH and ACTH production so gland becomes atrophied and so unable to produce cortisol even if ACTH given endogenously

252
Q

difference in secondary and tertiary adrenal insufficiency as opposed to primary

A

secondary and tertiary - skin pale as no increase in ACTH and aldosterone production is intact so no hypotension

253
Q

what is investigation for secondary/ tertiary adrenal insuffiecny

A

insulin tolerance test or CRH stimulation test

254
Q

management for secondary/ tertiary adrenal insuffiency

A

hydrocortisone - fludrocortisone is unecessary

255
Q

Addison crisis caused by stress in adrenal insuffiency or sudden discontinuation of steroids

A
256
Q

treatment for Addisons criss

A

NACL

257
Q

what tumour from the sympathetic nervous system originates from neural crest cells

A

neuroblastoma

258
Q

composed of primitive appearing cells but can show maturation towards gangliod cells

A

neuroblastoma

259
Q

application of what in neuroblastoma predict a poor outcome

A

N-myc and telomerase

260
Q

derived from chromaffin cells

A

phaeochromocytoma

261
Q

paragangliomas are typically found in the

A

head and neck

262
Q

10%of phaechromocytomas are not associated with

A

HYPERTENSION

263
Q

pheochromocytoma associatd with

A

NF 1, men 2, VHL< succinate dehydrogenase enzymes and tuberose sclerosis

264
Q

what has a tendency for skeletal metastasis

A

phaechromocytoma

265
Q

classic triad of phaeochromocytoma

A

hypertension, headache and sweating

266
Q

paraoxysmal sweating

A

phaeochromocytoma

267
Q

postural hypotension is seen in how many pheochromocytoma cases

A

50%

268
Q

7% of phaechromocytoma had normal 24hr urianry catecholamines so

A

secretion is episodic so take samples when patient symptomatic

269
Q

ideally take plasma metalephrites or catecholamines

A

at time of symptoms

270
Q

hyperglycaemia, low K, mild hypercalcaemai and lactic acidosis

A

phaeochromocytoma

271
Q

pre op for phaechormocytoma what do you give first

A

alpha blocker - phenoxybenzamine

272
Q

defintive management for phaechromocytoma

A

laparoscopic surgery

273
Q

what is congenital adrenal hyperplasia

A

deficiency in one of the enzymes necessary for cortisol synthesis

274
Q

90% of CAH are due to autosomal recessive

A

21 alpha hydroxyls defiecny

275
Q

21 alpha hydroxyls mutation prevents the production of what

A

aldosterone and cortisol

276
Q

why does CAH have increases testosterone and dihydrotestosterone

A

as can’t produce aldosterone or cortisol then precursors are diverted into the androgen pathway

277
Q

how does classic cat presents

A

birth - genital ambiguity in females
adrenal failure- hypotension, hypoglycaemia

278
Q

non classic CAH is partial

A

21 alpha hydroxyls defeicny

279
Q

how does non classic CAH present

A

in adolescents with precocious puberty, hirsutism, acne , infertility

280
Q

investigation for CAH

A

17- OH progesterone

281
Q

management of CAH

A

glucocorticoid replacement