Endocrinology Flashcards

1
Q

Which MODY uses sulfonylurea for treatment?

A

MODY3

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2
Q

Diagnostic criteria for diabetes

A

Hba1c > 6.5%
Fasting glucose > 7
Random glucose > 1.1
OGTT - meeting above criteria

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3
Q

GDM diagnosis

A

OGTT 24-28 weeks
Fasting > 5
1 hour > 10
2 hour > 8.5

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4
Q

MoA of metformin

A

Suppresses hepatic gluconeogenesis

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5
Q

SLGT2 benefit in diabetic nephropathy - mechanism

A

Reduce intraglomerular pressure due to increased afferent arteriole resistance

Reduced hyperfiltration

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6
Q

Which SGLT2 has higher risk of amputations?

A

Canglifozin

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7
Q

Benefit of degludec vs lantus/levemir

A

Reduces overnight hypoglycaemia

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8
Q

Types of Type 1 Diabetes

A

Type 1A - immune.
- Usually polygenetic
- Monogenic - AIRE (Polyendocrinopathy), FOXP3 (IPEX)

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9
Q

Polyendocrinopathy
X linked
Enteropathy

A

IPEX

FOXP3 gene

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10
Q

HLA associated with diabetes

A

HLA DR3 and HLA DR4 (have both = 50%)

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11
Q

Pathophys of T1DM

A

T cell mediate process

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12
Q

T1DM Ab’s

A

GAD
Insulin
IA-2
ZnT8

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13
Q

Anti-CD3 reducing time of onset T1DM

A

Tepiluzimab

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14
Q

Name of principal where long term complications of diabetes occur if there is poor control early

A

Metabolic memory

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15
Q

Glargin vs detemir

A

Gargine - hexamers under skin, delay absoprtion

Detemir - binds albumin, prolongs half life

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16
Q

Meal ratio calculation

A

500/TDD

1 unit of insulin for how many g for of CHO

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17
Q

Insulin sensitivity factor

A

100/TDD

1 unit of insulin drops BGL by how manny mmol/L

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18
Q

Evidence for CGM (continuous gucose monitor)

A

REduction in Hba1c
Reduces hypos
Improves time in range (closed loop therapy)

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19
Q

Whipple’s triad

A

Symptoms of low BGL
Low BGL
Symptoms imrpove after correcting BGL

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20
Q

Lymphocytic hypophysitis
- Features
- Differentiate from Sheehan syndrome

A

Hypopituitarism and headaache postpartum, no PPH

Sheehan - PPH, ischaemic infarction of pituitary causing hypopituitarism

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21
Q

Apoplexy

A

Haemorrahge into pituitary adenoma

Acute headache, diplopia, hypopituitarism

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22
Q

GH physiology
- Period when it is highest
- Stimulator and Inhibitor
- MoA

A

Puberty

GHRH stimulates, somostatin inhibits

Binds to receptors on liver, causing dimerisation + phosphorylation and IGF-1 release.
Effects - CHO and fat breakdown, protein buildup

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23
Q

Diagnosis of Acromegaly

A

Elevated IGF1? - diagnoses

Equivocal
- OGTT - GH not adequately suppressed

Proceed to pituitary MRI

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24
Q

Treatment of acromegaly

A

Somostatin analogues
- Octreotide
- Pasireotide - causes new onset diabetes in 60%

Pegvisomant
- Recombinant GH molecule, prevents receptor dimerisation. Enhances insulin sensitivity

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25
Q

Test for GH deficiency

A

Serum IGF1

Equivocal, do provocation tests:
- Macromelin test (grehlin, stimulates GH release)
- GHRH test

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26
Q

Treatment prolactinoma

A

Cabergoline - ergot Da receptor agonist

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27
Q

A/E of cabergoline

A

Valvular heart disease

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28
Q

False positive elevated PRL, without any symptoms (galactorrhoea, amenorrhoea)

A

Macroprolactin - PRL bound to Ig’s

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29
Q

Ostoporosis agents
- Prevent breakdown

A

Bisphopsphonate - prevent osteoclast binding and induce apoptosis

Denosumab - RANK-L

SERM’s - inhibit osteoclasts through upregulating OPG

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30
Q

Bone anabolic agents

A

Teriparitide - increase osteoblast activity

Romosozumab -inhibits sclerostin, which inhibits osteoblast formation. Increases osteoblast activity

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31
Q

Physiology of FGF23
- When released
- Effects
- Klotho

A

Hyperphosphataemia

Decreases phosphate reabsorption
Decreases calcitriol synthesis (reducing intestinal absorption)
Suppresses PTH (suppress vit D)

Klotho is a co-receptor that enhanced FGF23. Depleted in CKD, so reduced efefct of FGF23 in CKD (on kidneys, parathyroid) –> lead to CKD MBD

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32
Q

Calcium sensing receptor
- Function
- Defects

A

Senses iCa, increases PTH release in response to low levels

Inactivation - causes familial hypocalcuric hypercalcaemia (excess PTH release as iCa not sensed)

Cincalcet - CasR sensitiser, sensitising to Ca and suppressing PTH release (in CKD-MBD)

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33
Q

Bone resorption markers

A

Urine NTX
Serum CTX

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34
Q

Bone formation markers

A

BSAP
PINP

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35
Q

Ca replacement when on PPI

A

Ca citrate

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36
Q

Denosumab
- Risk of not taking within 4 weeks

A

Spontaneous vertebral fractures
- Need to take bisphosphonate cover

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37
Q

Denosumab - cf with bisphosphonates

A

Increased eczema and infection risk

Less renal dose adjustment

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38
Q

Atypical femur fracture
- Presentation
- Management

A

Indolent groin pain whilst on bisphosphonate

Stop bisphopshonate/denosumab immediately and refer to orthopaedic centre

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39
Q

Bisphosphonates duration

A

5 years for oral, 3 years for IV

Continue in high risk (Age > 70, low T score, high risk fragility fracture)

Drug holiday for 2-3 years, recheck T score

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40
Q

Phentermine
- MoA
- Use
- A/E

A

Adrenergic agent suppresses appetite

Obesity

Adrenergic A?E

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41
Q

Orlistat
- MoA
- A/E

A

Lipase inhibitor, reduces fat absorption

Steatorrhoea, flatulence, oxalate stones

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42
Q

Criteria for bariatric surgery

A

BMI > 40
BMI >35 and failed medical therapy

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43
Q

Pathogenesis of thyroid eye and skin disease

A

TSH receptors and IGF-1 receptors on orbital fibroblasts and skin

Excess TSH stimulates receptors in eye muscles and skin
–> excess GAG secretion, fluid accumulation.
–> Extraocular muscle swelling, proptosis, pretibial myxoedema

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44
Q

Specific and non-specific features of Grave’s disease

A

Specific - periorbital oedema, proptosis, conjunctival inflammation

Non-specific - lid lag, stare

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45
Q

Treatment of Grave’s eye disease
- Everyone
- Mod/severe

A

Treat hyperthyroid, stop smoking, conservative with drops

Severe
- steroids
- Teprotumumab - IGF-R inhibitor

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46
Q

Thyroid storm
- Features

A

Hyperthyroid

Fever
Tachycardia
CNS - psychosis, seizure, coma
Heart failure
Hepatic dysfuncton

47
Q

MoA of PTU in thyroid storm

A

Blocks T3/T4 synthesis

Blocks peripheral T4 –> T3

48
Q

MoA of Lugol’s iodine in thyroid storm

Remember it is iodine solution

A

Blocks T3/T4 release

49
Q

MoA of Dex in thyroid storm

A

Blocks T4 –> T3 peripherally

50
Q

When to treat hyperthyroidism in pregnancy

A

Graves - TSHRAb positive, as this can cross placenta
- PTU 1st trimester
- Carbimazole other times

Do not treat gestational

51
Q

Episodes muscle weakness
Low K

Cause?
Differentiate from?

A

Hypokalaemia periodic paralysis

Exclude thyroid disease
Exclude Anderson syndrome (ECG for long QT)

52
Q

Test for primary hyperaldosteronism

A

Plasma aldosterone high, plasma renin low. If K low, confirms

Confirmatory tests
- Oral Na load
- Saline suppression
- Fludrocort suppression

53
Q

Phaeo management
- Imaging
- Genetic testing
- Medical

A

MRI/CT ABdo - look for unilateral or b/l

Genetic - vHL, MEN2, can have bilateral

Medical - ALWAYS alpha blocker first

54
Q

AIRE

A

Autoimmune polyendocrine syndrome 1
- adrenal insufficiency

55
Q

Diabetic
Collapse of midfoot/arch
Acute hot, red swollen foot

?cause
?other considerations

A

Charcot’s (diabetic) neuroarthropathy

Charcot’s think midfoot/arch.

Exlude osteomyelitis, gout

56
Q

Management of charcot’s

A

Contact casting/podiatry to offload foot

57
Q

Function of kisspeptin

A

Stimulates GnRH release (remember pulsatile fashion)

58
Q

Requirements for functional GnRH secretion

A

GnRH neurons must migrate appropriately (through olfactor bulb) - error = Kallmans’ syndrome

Must secrete in pulsatile manner - continuous (GnRH agonists) = suppression

59
Q

Pathophys of PCOS

A

Functional ovarian hyperandrogenism -increased sensitivity to LH

Functional adrenal hyperandrogenism

Selective insulin resistance - insulin acts on theca cells to increase androgen synthesis

60
Q

Diagnosis of PCOS

A

Amenorrhoea/oligomenorrhoa

> 20 follicles U/S

High testosterone
- Clinical - hirsuitism
-Elevated testosterone

61
Q

Test for CAH

A

21 a hydroxylase deficiency

Check 17 OH levels - high indicates 21a hydroxylase deficiency

62
Q

Fertility management for PCOS

A

Metformin/weight loss - by 10% can improve fertility

Ovulation induction
- Letrozole, aromatase inhibitor increased ovarian oestrogen

Clomiphene - oestrogen receptor antagonist, increases FSH production

63
Q

Diagnosis of relative energy deficiency (functional hypothalamic amenorrhoae

A

Amenorrhoea

Low FSH, LH and oestradiol

63
Q

Diagnosis of relative energy deficiency (functional hypothalamic amenorrhoae

A

Amenorrhoea

Low FSH, LH and oestradiol

Trigger - eating disorder, excercise, stress

64
Q

Mullerian ducts/structures

A

Uterus
Fallopian tubes
Superior part of vagina
Female external genitalia

65
Q

Male sex development from embroy

A

XY - Y has SRY gene which causes gonad to become testes

Testis produce 3:
- AMH - regress Mullerian ducts
- 5a DHT - male sex characteristics
- testosterone - wollfian ducts

66
Q

Female characteristic development

A

XX - default ovaries produced

Mullerian ducts form –> female sex characteristics

Lack of SRY, or lack of AMH from testis (gonadal dysgenesis) cause female characteristics

67
Q

Female sex characteristics
Normal pubarche, adrenarche
Streak gonads

A

46XY gonadal dysgenesis

68
Q

Amenorrhoea
Female characteristics, absence of hair, adrenarche
46XY

A

Androgen insensitivity syndrome

69
Q

Evaluation of possible primary ovarian insufficiency

A

TSH and PRL - ensure normal

Check FSH, LH, E2 and AMH
- E2 low, FSH and LH high –> likely POI

AMH low also supports diminshed ovarian reserve

70
Q

2 most common causes POI

A

Idiopathic
Autoimmune -APS1 (AIRE)

71
Q

When to use transdermal ostrogen rather than oral

A

Hypertriglyceridaemia
Imapired Liver
Migraine with aura

72
Q

Woman with uterus - formulation for HRT?

A

Combined oestrogen and progesterone

73
Q

Absolute contraindications to HRT

A

ABCD
Acute liver disease
Bleeding - undiagnosed vaginal bleeding
Cancer (rbeast/uterine), Cardiovascular disease
DVT( or thrombophilia)

74
Q

Low test
Low FSH/LH
Anosmia

A

Kallman’s syndrome

Failure of migration of GnRH neurons through olfactory bulb with olfacotry neurons

75
Q

When to treat euvolemic HypoNa with Hypertonic saline

A

Na < 120

Cerebral symptoms - decreased GCS, seizure, headache

76
Q

Inhibitors of growth hormone

A

IGF1
Leptin
Somostain (GHIH)
Hyperglycaemia

LISH

77
Q

High TSH
High T4

A

Heterophile antibody - can interfere with assay

78
Q

Hyperthyroid
No uptake on nuclear scan
TPO positive

DDx?

A

Silent thyroditis - spectrum with Hashimoto’s (progresses to Hashimoto’s with alter hypothyroid)

Postpartum - within 12 months of birth/miscarriage

79
Q

Dequarvain’s thyroiditis Rx

A

NSAIDs first line
Pred 2nd line

BB for symptoms

80
Q

Hypercalcaemia
AKI
Metabolic alkalosis

A

Milk Alkali syndrome

81
Q

Activating mutation of TSH receptor causes?

A

Thyroid adenoma or toxic multinodular goitre

82
Q

Treatment of hypercalcaemia

A

IV fluids ALWAYS 1st line

2nd line - IV bisphosphonate

83
Q

Aldosterone levels in primary vs secondary adrenal insufficiency

A

2nd - usually preserved aldosterone

84
Q

Which fracture site is at greatest risk with steroid osteoporosis?

A

Vertebral

85
Q

High oestrogen, low LH, normal testosterone.

YOung male, gynaecomastia.

Next ix?

A

Suggests aromatisation of testosterone. Can be done by HCG from teste tumour

Testicular U/S

86
Q

Factor greatest effect on peak bone mass?

A

Genetics

87
Q

Osteoporosis men with hypogonadism

A

Treat with testosterone

88
Q

Testosterone changes in obesity

A

Low SBG - inhibition of liver. Causes decrease total testosterone

Increase peripheral conversion by aromatase from testosterone to oestrogen

89
Q

ACTH dependant Cushing’s, no lesion on MRI

Next step?

A

Petrosal sinus sampling - confirm if from pituitary.

Sometimes MRI won’t pick up pituitary adenoma

90
Q

Mechanism of steroid induced osteoporosis

A

Decreased production of OPG

91
Q

Low BSL

Insulin high
C peptide normal

A

Insulinoma

92
Q

MoA of GLP-1 agonists

A

Stimulate glucose dependant secretion of insulin by beta cells

Delay gastric emptying

93
Q

Most specific sign of Cushing’s

Most specific sign in already obese person that points to Cushings

A

Abdominal striae

Proximal myopathy

94
Q

Drug taken with bisphopshonates that reduces absorption

A

CaCO3

95
Q

REsponse to hypogylcaemia in order

A

1) Glucagon

2) Adrenaline

3) Cortisol and GH

96
Q

2nd cause hyperipidaemia most assocaited with increased LDL

A

Hypothyroid

97
Q

Therapy for proliferative diabetes
- First line
- 2nd line

A

1st line - panretinal photocoagulation - best to prevent vision loss

VEGF in short term (until photocoagulation)

2nd line - vitrectomy

98
Q

Therapy for macular oedema

A

Anti-VEGF agents

99
Q

Changes in T2DM

A

1) Impaired glucose tolerance - impaired post prandial

2) Beta cells increase insulin secretion. Can’t keep up
- Increased hepatic GNG causing fasting hyperglycaemia

100
Q

Mechanism of insulin translocating GLUT4 transporter to cell surgace

A

Activating tyrosine kinase receptor on cell surface

101
Q

Steroid induced osteoporosis
- Acute mechanism
- Long term mechanism

A

Acute - decreased OPG, increase RANK-L , increase bone resorption

Long term - decrease bone formation

102
Q

Cushing’s
- Agents that target adrenal

A

KM

Ketoconazole - inhibit androgen synthesis

Metarypone - Stops GC synthesis (inhibit 11b hydroxylase)

103
Q

Cushing’s disease (pituitary)
- Agents that target ACTH
- Agents that target GC receptor

A

PM

ACTH - pasireotide, inhibit ACTH formation

GC receptor - mifepristone

104
Q

Monitor treatment in 2nd hypothyroidism

A

Free T4

105
Q

Causes of increased CBG? (and hence elevated total cortisol)

A

Oestrogen - pregnancy, COCP

Insulin resistance

106
Q

Why take alendronate BEFORE meals

A

Taken with dairy/food, can form mineral complexes

107
Q

Gynacomastia and testicular cancer - cause?

A

bHCG production and direct effect on testicular tissue

108
Q

Bisphosponate associated with impaired bone mineralisation

A

Etidronate

109
Q

Thyroid and PRL
- What causes elevated PRL

A

Hypothyroid

110
Q

TSH receptor AB
- when can treatment for Grave’s be stopped?

A

When TSH r AB low

111
Q

Test to confirm primary adrenal insufficiency

A

Short synacthen (ACTH) test

112
Q

Test to confirm secondary adrenal insufficiency

A

ACTH and cortisol

AND

Synacthen test

113
Q

Sick Euthyroid
- Circumstances
- Labs findings

A

In critically ill patients, functional central hypothyroid to prevent catabolic state

Low T4, low T3, low normal TSH