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FRACP Shuyu > RPA endo > Flashcards

RPA endo Flashcards

1
Q

Diagnosis of diabetes in haemoglobinopathies

A

OGTT

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2
Q

what virus is proven to cause T1DM

A

congenital rubella unproven: coxackie, rotavirus, mumps, reovirus, herpes, cows’ milk

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3
Q

genetics of T1DM - what chromosome is involved

A

chromosome 6

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4
Q

what MHC is involved in beta cell destruction

A

MHC II - on antigen presenting cells

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5
Q

what HLA is protective of T1DM

A

DR2 is protective

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6
Q

what HLA is a risk factor of T1DM

A

DR3 and DR4 are expressed in 95% of white patients with Type 1 diabetes

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7
Q

does the mother or father confer higher risk for T1DM

A

father is 6.1% risk mother is 2.1% risk

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8
Q

what antibodies are implicated in T1DM

A

anti GAD anti IA2 zinc transporter 8 first 2 more clinically important

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9
Q

which autoantibody is most important for the development of T1DM

A

anti GAD

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10
Q

screening for T1DM - what tests to do

A

HLA DR3/DR4 nmeasure anti GAD and anti IA2 ab insulin secreting potential

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11
Q

pathogenesis of T2DM

A

insulin resistance but also relative insulin deficiency due to defect glucorecognition

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12
Q

does the mother or father confer higher risk for T2DM

A

mothers intrauterine environment is important for the development of type 2 DM

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13
Q

what type of genes are affected in T2DM

A

majority relate to beta cell function loss only a small inter related to insulin resistance

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14
Q

most important gene for T2DM

A

TCF7L2 - mechanism unknown

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15
Q

MODY genetics

A

autosomal dominant single gene defects MODY1-5 enzyme defect - HNF-4alpha, glucokinase (mild hyperglycaemia), HNF-1alpha (very sensitive to sulphonylureas), IPF-1

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16
Q

clinical features MODY

A

onset <25 for at least another family member correction of fasting hyperglycaemia for at least 2 years without insulin no ketotic events impaired insulin secretion

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17
Q

HNF-1alpha characteristics

A

MODY enzyme defect very sensitive to sulphonylureas

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18
Q

glucokinase clinical significance

A

MODY enzyme defect mild hyperglycaemia usually does not require treatment

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19
Q

impaired glucose tolerance prevention for diabetes

A

lifestyle - diet, exercise +/- weight loss effects seen without weight loss rosiglitazone reduced new DM by >60% small increase in heart failure however practically lifestyle

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20
Q

sulfonylurea MOA, adverse effects

A

stimulates release insulin from the beta cells may have weight gain hypoglycaemia is possible gliceride preferred as metabolites not active and lower risk of hypo CVS impact is neutral on latest study

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21
Q

what allergies should avoid for sulfonylureas

A

sulfur allergies

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22
Q

biguanides MOA and aderse effects

A

increases insulin action decrease hepatic gluconeogenesis does not cause hypos by itself but can potential hypos in combination with other things lactic acidosis - rare GI side effects start low and go slow

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23
Q

metformin eGFR cut off

A

<30

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24
Q

metformin contradindications

A

liver damage (pregnancy) nephropathy eGFR <30

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25
Q

acarbose MOA and adverse effects

A

decrease HbA1c by 0.5% at most (very weak agent) AE: flatuence and diarrhoea in 80%! malabsorption

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26
Q

TZD - thiazolidinediones

A

Activates PPAR_gamma nucleus receptor central to insulin action Tosiglitazone + pioglitazone AE: weight gain, fluid retention/CCF, ?cardiac disease (rose), fractures, ?bladder cancer (pio)

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27
Q

incretic mimetics

A

GIT hormones - GLP-1, GIP GLP-1 analog - exenatides, dulagutide (both weekly injections)

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28
Q

what does incretin and GLP1 do

A

increase insulin release and inhibit glucagon to lower blood glucose

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29
Q

what does DPP-4 do

A

inactivates GLP-1 (so DPP-4 inhibitors increase endogenous GLP-1)

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30
Q

GLP-1 analog advantages

A

potent weight loss ++ low risk of hypos dual/tripe therapy CV outcome studies

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31
Q

GLP1 A

A

expensive injection nausea ++

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32
Q

DPP-4 inhibitors

A

gliptins

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33
Q

DPP-4 advantages

A

tablet otherwise similar to GLP1

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34
Q

DPP-4 AE

A

depends on endogenous production of GLP-1 which is already decreased in T2DM not as potent as GLP-1 no weight loss (As weaker) neutral CV outcome studies

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35
Q

what has positive CVS outcome studies

A

SGLT-2 and GLP-1

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36
Q

SGLT-2 transported

A

transports 90% of glucose out of the tubular lumen

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37
Q

pros SGLT-2

A

relatively potent 0.5-1% HbA1c reduction weight loss lowers BP

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38
Q

cons SGLT-2

A

genital fungal infections euglycaemia DKA

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39
Q

SGLT2 eGFR cut off

A

<45

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40
Q

when does SGLT2 need to be stopped before surgery..procedure or fasting

A

2-3 days prior

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41
Q

lispro insulin, aspart, glulisine vs actrapid

A

absorbed faster than act rapid

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42
Q

what is the next step if someone has good BSL at bedtime but wakes up with high pre breakfast BSL

A

measure BSL at 3am to see whether it’s dawn phenomenon or somogyi effect to see whether it’s too little insulin (dawn) or too much (somogyi) causing rebound hyperglycaemia after 3am hypo

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43
Q

HbA1C aim T1DM

A

6.5-7

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44
Q

tighter control and weight in T2DM

A

tighter control = more weight gain

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45
Q

good glucose control and micro and macrovascular in T2DM

A

less micro vascular and maybe macrovascular EDIC showed reduced in major cardiovascular events in group that had initial good HbA1C control (2 groups of good and poor HbA1C but long term both groups had good glucose control but initial good control group early on) so macrovascular outcomes may only be apparent after many years

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46
Q

intense glucose control in T2DM

A

ACCORD study short term outcomes aimed for 6% and lower excessive mortality now we aim for 7% in cardiac disease

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47
Q

good glucose control and macrovascular outcomes

A

improves macrovascular but over long term and need initial good control

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48
Q

HBA1C aims T2DM no CV + metformin

A

<6%

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49
Q

glitazone in CVS

A

rosiglitazone worsen lipids pioglitazone possibly decreases cardiac outcomes however both should not be used oedema

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50
Q

gliptin (DPP4) on CVS

A

sitaglipin does not increase HF saxagliptin does increase hospitalisation for HF

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51
Q

empagliflozin/dapagliflozin none endo effects

A

3 point MACE heart failure reduced renal composite outcomes note empa has trend towards increased stroke

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52
Q

significance of dulagltide for CVS

A

other studies had populations w established CVS disease the rewind study of dulaglutide included 69% without baseline CV disease so it is showing the dulaglutide as PRIMARY prevention

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53
Q

BP lowering DM agents

A

SGLT2s and GLP1

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54
Q

insulinoma testing

A

prolonged fast when the person gets a hypo, simultaneous c peptide,, insulin insulinoma does not produce hypoglycaemia w OGTT

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55
Q

impaired glucose tolerance hypoglycaemia

A

high-isa C-peptide rapid reactive/postprandial hypoglycaemia

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56
Q

c peptide in sulfnoyureas hypoglycaemia

A

high c-peptide

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57
Q

diabetes and VGEF

A

vgef is the bad guy in pathogenesis in retinopathy

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58
Q

treatment of retinopathy

A

anti-VGEF intravitreal

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59
Q

type 2 DM vs type 1 DM - proteinuria and prevention of renal progression

A

Type 2 DM - ARB Type 1 DM - ACE I

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60
Q

bp targets in DM

A

accord study - no difference SBP 120-140 so aim now 140/80 if microalbuminuria; 140/90 no microalbuminuria

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61
Q

fenofibrate in DM

A

retinopathy add on to statin slow progression of retinopathy does not prevent retinopathy

62
Q

production sites of T4 and T3

A

T4 soley from the thyroid gland

T3 mainy from the peripheral tissue

63
Q

what happens to TFTs in first trimester of pregnancy, hyperemesis gravidarum, hydatidiform mole

A

TSH is suppressed

can present like a thyrotoxicosis picture

64
Q

Glucocorticoids TSH

A

Low TSH

normal T4, low T3

65
Q

TRAb

A

very high sensitivity and specificity but can occasionally be negative in Graves and occasionally positive in Hashimoto’s

66
Q

effect of biotin on TFTs

A

low TSH

High T3 and T4

TSHRAb positive

(False positive Graves disease picture; normalising after biotin is ceased)

67
Q
A

Graves disease

68
Q
A

Multinodular goitre

69
Q

most common cause of Hyperthyroidism

A

Graves disease

70
Q

clinical dx of graves

A

symmetrically enlarged thyroid

Graves orbitopathy

mod to severe hyperthyroidism

71
Q

when is scintigraphy contraindicated

A

pregnancy and lactation

72
Q

what is more elevated (T3 vs T4) in Graves disease

A

T3 more elevated than T4

73
Q

what BB can blocker T4 to T4 conversion

A

propanolol

74
Q

what treatment if contraindication in bad graves eye disease

A

radioactive iodine because it causes an initial rise in TRAb

75
Q

how long to treat with anti-thyroid medications in Graves disease

A

until TRAb becomes undetectable

76
Q

what treatment for Graves disease has the highest rate of remission

A

anti-thyroid drugs

77
Q

prevalence of eye disease in Graves’ disease

A

30-50%

5% will develop severe eye disease

78
Q

what is the most common sign of eye disease in Graves?

what is the most specific sign

A

most common = eyelid retrction of both eyes

most specific - exophthalmos

79
Q

what is the most common eye muscle affected in Graves disease

A

inferior rectus

80
Q

management of Graves eye orbitopathy

A

Mild - selenium

Mod-severe - Pulse glucocorticoird

Surgery and orbital decompression

Teprotumumab (IGF-1 receptor inhibitory monoclonal antibody; SE - hyperglyaemia)

81
Q

when to treat subclinical hyperthyroidism

A

Suppressed TSH <0.1

>65 treat

82
Q

amiodarone induced tyroiditis pathophysioogy

A

37.3% iodine by weight

can induce both hypothyroidism and hyperthyroidism

Type I - Jod-Basedow phenomenon; treated with antithyroid medications

Type II - destructive thyroiditis 5-10% patients, need glucocorticoids

83
Q

treatment of amiodarone induced hyperthyroidism

A

both carbimazole and prednisolone

84
Q

who to treat for subclinical hypothyroidism

A

<70 years of age

AND TSH >10

between TSH 7-10, treat if there are other high risk factors

85
Q

what’s the size cut off for FNA of thyroid nodule

A

>1cm

86
Q

USS features of malignancy for thyroid nodule

A

microcalcification

nodule hypoechogenicity compared with surrounding thyroid/muscle

Irregular margins - infiltrative, microlobuated, spiculated

Taller than wide on a transverse view

cyst more likely to be benign

87
Q

hyperthyroidism and warfarin

A

hyperthyroidism increases efficacy of warfarin through increasing catabolism of vitamin K dependent clotting factors

88
Q

DIagnosis of diabetes insipidus

A

water deprivation test (DI patients will continue losing water)

Central DI has response to DDAVP

Peripheral DI does not have response to DDAVP

hypertonic saline insulin test is more sensitive and specific but might not be suitable for use in hypontraemia

Arginine-stimulation and measuring copeptin is aso sensitive/specific

89
Q

gold standard for hypothalamic-pituitary adrenal axis

A

insulin tolerance test

90
Q

what can insulin tolerance test be used to test

A

growth hormone and cortisol production

91
Q

pituitary tumour classification

A

<1cm microadenoma

>1cm macroadenoma (has capaticy to compress on the pituitary)

92
Q

acromegaly diagnosis

A
93
Q

treatment of acromegaly

A
  1. Surgery
  2. Radiotherapy
  3. Somatostatin receptor ligand
    1. octreotide acting on SSTR2
    2. Pasireotide acts on 4 somatostatin receptors
      1. Hyperglycaemia and diabetes
  4. Growth hormone receptor antagonist
    1. Pegvisomant - most efficacious (>90%)
  5. Dopamine Agonist
94
Q

screening test for Cushing’s syndrome

A

dexamethasone 1mg suppression test

95
Q

cushing’s confirmatory testing

A

late night salivary cortisol (high sensitivity and specificity)

96
Q

pituitary adenoma treatment

A
  1. Medical therapy first line
    1. Cabergoline
  2. Visual field
  3. Pregnancy
    1. Microadeoma - cease treatment during pregnancy
    2. Macroadenoma - cont treatment, switch to bromocriptine
    3. Visual fields testing once a trimester
97
Q

which immunotherapy is most likely to cause hypophysitis

A

anti-CTLA4

98
Q

diagnosis of congenital adrenal hyperplasia

A

basal 17-OHP

confirmation testing with 250mcg of synacthen test and seeing if 17-OHP increases

treatment is not indicated in classical non symptomatic

99
Q

what’s the most common cause of primary hyperaldosteronism

A

bilateral adrenal hyperplasia

100
Q

pathogenesis of obesity

A

leptin deficiency (long term appetite suppressant)

cholecystokinin (short term satiety factor that regulates meal size)

ghrelin: appetite trigger

Genetic factors:

  • MC4R deficiency(causes reduction of appetite; most common monogeneic cause of paediatric obesity)
  • FTO - found with GWAS; linked to IRX3 which is another gene which is shown to have an effect of browning white fat; small effect size
101
Q

marker of brown fat

A

UCP1

browns fat burns energy rather than storing it

102
Q

orlistat

A

blocks gastrointestinal lipase

causes fatty diarrhoea

-2.75kg over 52 weeks treatment

only works if there is fat consumption

103
Q

phentermine + topiramate

A

does lead to ~10% weight loss

but note topiramate can cause depression in an already high risk group

104
Q

mean weight loss following bariatric surgery

A

25% over 12months

105
Q

physiological changes after gastric bypass

A

increase in GLP-1 and PYY (appetite regulator) (possibly explains sustained weight loss)

106
Q

what outcome has not been demonstrate in bariatric surgery RCTs

A

mortality diet

(likely because there has not been a long enough follow up)

107
Q

osteocyte - what does it secrete

A

see slides

108
Q

what is the role of RANK ligand in bone remodelling

A

rank L are secreted by osteoblasts

they bind to the RANK receptor on the osteoclast

activated RANk causes the osteoclast to be activated and resorb bone

OPG is a decoy receptor that prevents RANK ligant to activate the osteoclast.

109
Q

what happens to RANKL in aging

A

RANK L goes up

OPG goes down

110
Q

remodlling of bone in aging

A

cortex thins

holes in the cortex (cortical porosity)

less trabecular bone and loss of connectivity

can lead to skeletal fragility and fracture risk

111
Q

MOA of bisphosphonates and RANK- inhibiter

A
  1. gets uptaken by osteoclasts and kills them
  2. stops osteoclast activation
112
Q

what is the z score good at identifying

A

not as clinically helpful as T scores

but they may be helpful to identify those with underlying accelerated causes of bone loss

113
Q

who to treat for osteoporosis

A
  1. fragility fracture in post menopausal woman or man >50 years
  2. vertebral fractures (loss of weight 20% of front or middle vs back end)
  3. No existing fracture but on the basis of risk (but note larger NNT to prevent future fractures). E.g. 70 year olds with low bone density. 20% risk of fracture over 10 years
    1. Low BMD
    2. Age
    3. Previous fracture - HIGHEST RISK
  4. iatrogenic
    1. Prednisolone: >7.5mg for 3 months and T score < -1.5
    2. SERM: treat T<-2 or #
    3. Angrogenic dep: treat if T <2.5 or #
114
Q

steroids and bone

A

dose dependent but any dose will cause bone loss.

short duration results in reversible bone loss.

occurs very quickly (6-12% in the first year)

inhaled and topical no significant effects

115
Q

HRT in osteoporosis

A

only if they arehaving sx of menopause and know the risks (increased breast CA and CVS)

116
Q

raloxifene and osteoporosis

A

useful in people with a persona concern of breast cancer

117
Q

what should be avoided in AF and osteoporosis problem

A

zolendronic acid

118
Q

what fractures are the most resistance to osteoporosis therapy

A

non vertebral non hip

(e.g. humerus, colles)

119
Q

denosumab and discontinuation

A

rebound fractures due to intense trabeculae remodelling

120
Q

alendronate discontinuation

A

slow decline in bone density

re-evaluate risk after a few years

121
Q

SE of antiresorptive therapy

A
  1. osteonecrosis of the jaw (bisphosphonates, denosumab)
  2. atypical femoral fractures (presents with pain in thigh that occurs months before fracture occurs)
    1. Declines with drug holidays
    2. Subtrochanteria (no communication, transverse at the lateral cortex, medialslike, diffuse cortiacl thickening, local lateral cortical thickening)
    3. Increased by duration of therapy
      4.
122
Q

management of atypical fractures

A

Discontinue anti-resorptive therapy

Consider nail fixation

Consider teriparatide

Monitor the contralateral hip (imagine w XR +/- bone scan or MRI)

123
Q

anabolic therapy

A
  1. PTH
    1. Once daily injection
    2. stimulate osteoblast and clast - which forms the anabolic window of ~18 months which is where osteoblast activity > osteoclast
  2. New targets - Romosozunab
    1. Sclerostin inihibiting mAb
    2. LRP5 - a receptor that is important for osteoblast function. LRP5 is inihibited by Sclerostin and DKK
    3. TGA but not PBS yet
    4. Potent anabolic therapy
124
Q

Paget’s pathogenesis

A

osteoclasc activity is increased

  • > increased bone turn over
  • > weakening of the bone
  • > deformity
  • > fracture

on imaging - alternating areas of lucency

can affect 1 bone or multiple bones

Investigations: ALP, XR, Bone scan

125
Q

paget’s treatment

A

indications fo treatment: high risk of fracture, critical area

zolendronic IV 5mg once every few years

126
Q

hypergonadotropic primary ovarian failure sex hormones

A

high FSH, low E2

next step - karyotype

127
Q

hypogonadotropic amenorrhoea causes

A

most commonly functional: weight loss, anorexia, exercise, debilitating disease, psychologic stress

or structural causes

128
Q

amenorrhoea and elevated gonadotropin Ddx

A

turner syndrome

premature ovarian failure

129
Q

what cardiac diseases to screen for in Turner’s

A

co-arctation and aortic dissection

130
Q

definition of premature ovarian failure

A

<40 years amenorrhea

hypergonadotrophic amenorrhea

131
Q

ancillary studies in PCOS

A

endometrial carcinoma

flucose intolerance

lipids

OSA

132
Q

PCOS fertility tx

A
  1. Weight loss
  2. Letrozole
  3. Metformin (but not as effective as letrozole)

Clomiphene should be combined with metformin

133
Q

tall, gynaecomastic male

high LH, FSH

features of hypogonadism

A

Consider kleinfeltter’s

XXR

134
Q

MOA of iodine and carbimazole/PTU

A

iodine: decreases thyroidal iodide uptake, dcreases iodide oxidation and organification and blocks release of thyroid hormones

PTU./carbimazole: prevent synthesis of new thyroid hormone. PTU can also inhibit the conversion of T4 to T4 at high levels

135
Q

waht happens to the thyroid after Iodine I-131

A

hypothyroidism depending on how much of the thyroid take up radioactive iodine

e.g. in Graves, the patients almost always be hypothyroidism but for a single nodule, the patient woudl be euthyroid

136
Q

Wolff-Chaikoff effect

A

During the use of a high dose short duration of iodine (usually used as bridge to surgery or to control thyroid storm)

an autoregulatory phenomenon that inhibits organification in the thyroid gland, the formation of thyroid hormones inside the thyroid follicle, and the release of thyroid hormones into the bloodstream

137
Q

Jod-Basedow effect

A

iodine exposure in uderlying thyroid disease may lead to hypersecretion of thyroid hormones

usually seen in pre-existent thyroid disease or subclinical thyroid disease

138
Q

adrenal crisis w/ hypoNa hyperK+ b/g metastatic melanoma on pembrolizumab - cause?

A

adrenal metastasis

(adrenalitis is extremely rare)

139
Q

C-RET

A

mutation of MEN2A

140
Q

MEN 1

A

parathyroid

pacnreatic

pituitary

genetic MEN1

141
Q

VHL - Von Hippel-Lindau syndrome

A

hemangioblastomas

renal cell carcinoma

phaeo

gene (VHL)

inheritance AD

142
Q

cushing’s syndrome w normal ACTH

A

most likely cushing’s disease

143
Q

cushing’s syndrome confirmed, next step

A

ACTH

144
Q

pituitary apoplexy first management step

A

hydrocort

145
Q

what might precipitate addisonian crisis on adrenal replacements

A

CYP3A4 inducers:henobarbital, phenytoin and rifampicin

146
Q

menopause management

A

depends if they have the uterus

if no uterus, can give unopposed estrogen

if uterus, then need progesterone

initially estrogen then cyclical progesterone but after 1-2 years can do oral oestrogen and continuous progesterone

also depends if there are risk factors for thromboembolic diseases or if she has hypertriglyceridaemia - use transdermal if possible

also consider non hormonal treatments - 2nd or 3rd line

147
Q

reason for low morning testosterone in obese male

A

decreased sex hormone inding globulin

148
Q

High Ca2+ and high PTH next step

A

factional excretion of Ca2+

Familial hypocalciuric hypercalcemia vs primary hyperparathyroidism

149
Q

dumping syndrome

A

rapid gastric emptying -> early vs late dumping

after bypass surgery

150
Q

rapid correction of glucose levels adverse effect

A

retinopathy or neuropathy

151
Q

amyotrophy diabetes

A

it’s a plexopathy

occurs in poorly controlled diabetes

152
Q

T4 elevated and TSH normal

most likely cause

A

exogenous thyroxine intake

but can also be caused by pituitary thyrotorphy and thyroid homrone resistance and increased heterophile antibodies

FRACP Shuyu (65 decks)

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