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MED4 CPY > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the name of the diagnostic criteria for DM?

Draw the table of details

A

American Diabetic Association

  1. Fasting plasma glucose
    • > = 7: DM
    • 5.6~7: IFG
  2. 2h post-OGTT glucose / Random plasma glucose
    • > = 11.1: DM
    • 7.8~11: IGT

(5678, 711)

  1. HbA1c
    • > =6.5%: DM
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2
Q

Time of fasting for fasting plasma

A

> =10h

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3
Q

Procedure for 2h post-OGTT plasma glucose

A

overnight fasting >=8h
1. Record plasma glucose at t0
2. Drink 75g anhydrous glucose in 300ml water in 10 mins
3. Sit quietly and check at 120min (additional check at 60min in case of pregnancy)

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4
Q

FP and FN of HbA1c results (4+3)

A

FP: splenectomy, pregnancy, IDA, prolonged aspirin intake

FN: splenomegaly, haemolytic anaemia, anti-oxidant

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5
Q

Alternative for HbA1c

A

Fructosamine (reflect 1~3 weeks)

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6
Q

Gestational diabetes diganosis by OGTT

A

[t0]
5.1~6.9: GDM
>=7: DM

[60min]
>=10: GDM

[120min]
8.5~11: GDM
>=11.1: DM

(511085)

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7
Q

Complications of gestational diabetes (2)

A

macrosomia –> difficult labour
faetal hyperinsulinaemia –> neonatal hypoglycaemia

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8
Q

Monitoring of glycation level for DM patients (3)

A

Point-of-care glucometry
Lipid profiles
Albuminuria & GFR

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9
Q

ADA therapeutic goals for DM patients
(HbA1c, pre-prandial BG, post-prandial BG, SBP, DBP, TG, LDL-C, HDL-C)

A

<7%
5~7.2
<10
<130
<80
<1.7
<1.8
>1.1 for male, >1.3 for female

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10
Q

Vascular complications of DM (6)

A

retinopathy, neuropathy, nephropathy
cerebrovascular disease, CAD, PVD

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11
Q

2 ketones and their formation in DKA

A

acetoacetate, beta-hydroxybutyrate

↓ insulin/glucagon ratio –> ↑ lipolysis & FA oxidation –> ketoacids

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12
Q

Precipitating factors of DKA / HHS (2)

A

stress
discontinued injection of insulin

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13
Q

HHS full form

A

Hyperosmolar hyperglycaemic state

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14
Q

Na and K status in DKA / HHS

A

early hypoNa, late hyperNa
N or hyperK but total K deficit

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15
Q

Explain for the hyperK in DKA

A

ICF to ECF shift caused by insulin deficiency & hyperosmolality

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16
Q

Whipple’s triad

A
  1. plasma glucose <=2.5 by laboratory method
  2. hypoglycaemic symptoms
  3. symptoms relief after elevation of plasma glucose
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17
Q

Aetiology of hypoglycaemia (fasting, reactive)

A

Fasting:
- excessive utilization: insulin administration, oral hypoglycaemic, insulinoma, extra-pancreatic tumours
- diminished glucose production: adrenal insufficiency, GH deficiency, liver disease, renal disease, autoimmune cause

Reactive:
- post-gastrectomy syndrome

Others: alcohol

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18
Q

Further testing for fasting hypoglycaemia (4)

A

Serum insulin
C-peptide
IGF-2, IGFBP3

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19
Q

Triple function test for pituitary deficiency

A
  1. insulin tolerance test
  2. GnRH stimulation test
  3. TRH stimulation test
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20
Q

Hyperprolactinaemia DDx

A

Physiological: pregnancy, stress
Primary: Prolactinoma
Secondary: NFPAH, dopamine depleting / receptor blocking agents, hypothalamic disease
Tertiary: Primary hypothyroidism
Others: chronic renal failure, liver cirrhosis

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21
Q

Free androgen index

A

= T/SHBG *100

> =5: hyperandrogenaemia

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22
Q

Klinefelter syndrome

A

47, XXY (primary hypogonadism in men)

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23
Q

Turner syndrome

A

45, X (primary hypogonadism in women)

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24
Q

Kallmann syndrome, Prader-Willi syndrome

A

hypogonadotrophic hypogonadism

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25
Q

Aim for progesterone withdrawal test

A

investigation of amenorrhoea

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26
Q

Iodine deficiency and excess aetiology (2+3)

A

Deficiency: pregnancy, malnutrition

Excess: contrast, amiodarone, eye drops & ointments

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27
Q

Jod-Basedow effect

A

failure to downregulate NIS in iodine excess –> hyperthyroidism

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28
Q

Wolff Chaikoff effect

A

iodine exposure –> inhibit iodide organification

Failure of escape –> hypothyroidism

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29
Q

Anti-thyroid antibodies involved in Dx of Hashimoto thyroiditis (2)

A

Anti-Tg Ab
Anti-TPO Ab

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30
Q

Anti-thyroid antibody involved in diagnosis of Graves disease

A

Thyoid stimulating IgG (TSI)

31
Q

3 MC causes of hyperthyroidism

A
  1. Graves’ disease
  2. Toxic multinodular goitre / Plummer’s disease
  3. Toxic adenoma
32
Q

Anti-thyroid drugs (2): mechanisms, preference

A

Carbimazole, Propylthiouracil

Mechanisms: inhibit TPO, iodination, coupling (PTU inhibits peripheral conversion of T4 to T3)

Preferences: PTU in pregnancy and thyroid storm

33
Q

Which iodine is used for thyroid scan? Which is used for radioactive iodine treatment?

A

I-123
I-131

34
Q

Management of hypothyroidism and monitoring (2)

A

L-thyroxine

Monitoring: TSH, cortisol

35
Q

3 zones of adrenal cortex

A

zona glomerulosa, zona fasciculata, zona reticularis

36
Q

Screening test for Cushing syndrome (3)

A
  1. Overnight dexamethasone suppression test
  2. 24h urine free cortisol
  3. Late night salivary cortisol
37
Q

RR for insulin

A

<3

38
Q

RR for C-peptide

A

<0.6

39
Q

Discriminatory tests for Cushing syndrome (3)

A
  1. Plasma ACTH
  2. High dose dexamethasone suppression test
  3. CRH stimulation test
40
Q

Interpretation of high dose dexamethasone suppression test

A

50% suppression ==> pituitary problem
⨉ suppression ==> ectopic ACTH

41
Q

MC cause for renal artery stenosis in young patients

A

fibromuscular dysplasia

42
Q

Gene for apparent mineralocorticoid excess (AME) (pathogenesis)

A

HSD11β2

↓ 11β-hydrosteroid dehydrogenase type 2 –> ↑ cortisol binds to mineralocorticoid receptors –> pseudohyperaldosteronism

43
Q

Confirmatory test for hyperaldosteronism

A

Salt loading test / saline suppression test / captopril test

44
Q

Salt loading test: measurement (2, RR)

A

urine aldosterone (<38)
urine Na (>200)

45
Q

Discriminatory tests for hyperaldosteronism
(Interpretations)

A
  1. Spot aldosterone-renin ratio
    • ↑ : primary
    • N/ ↓: secondary
  2. Postural test
    • physiological rise: bilateral adrenal hyperplasia
    • paradoxical fall: Conn’s syndrome
46
Q

Test for adrenal insufficiency (Interpretation)

A

Short synacthen test
a. cortisol rise <200 above baseline: primary cause
b. cortisol rise >200 above baseline with level <500: secondary cause
c. cortisol rise >200 above baseline with level >550: normal

47
Q

MC congenital adrenal hyperplasia

A

21-hydroxylase deficiency

48
Q

RR for overnight dexamethasone suppression test

A

<50

49
Q

Screening tests for suspecting phaeochromocytoma (3) and the second line test for borderline results

A
  1. 24h urine catecholamines, metanephrine, VMA
  2. Plasma catecholamines
  3. Plasma metanephrines
  4. Overnight clonidine suppression test
50
Q

Overnight clonidine suppression test interpretation

A

NA/Cr >60 or adrenaline /Cr >20 : phaeochromocytoma

51
Q

Investigation for midgut carcinoid tumour

A

urine 5-HIAA

52
Q

Side effects of anti-thyroid drugs

A

Allergy, agranulocytosis, hepatotoxicity

53
Q

What is the HVA/VMA ratio that indicates a poor prognosis for neuroblastoma?

A

<1

54
Q

Secretion of carinoid tumour in different regions

A

Foregut: 5-HT, His
Midgut: serotonin
Hindgut: /

55
Q

Metabolic pathways of tyrosine & tryptophan

A

tyrosine => DOPA => dopamine => NA => A
- D => HVA
- NA => notmetanephrine => VMA
- A => metanephrine => VMA

tryptophan => 5-HT => serotonin => 5-HIAA

56
Q

Which CAH leads to androgen deficiency?

A

17α hydroxylase deficiency

57
Q

How does DM lead to abnormal lipid profile?

A

High VLDL —> high TG —> high LDL-C —> low HDL-C

  • hyperinsulinemia & hyperglycaemia → + hepatic VLDL synthesis → ↑ hepatic release of TG & LDL
  • insulin resistance → ↓ inhibition of lipolysis in adipocytes
  • insulin resistance → ↓ lipoprotein lipase activity of muscles and adipocytes
58
Q

Why urine ketostix could be negative in severe DKA?

A

↑ NADH/NAD ratio → acetoacetate converts to β-hydroxybutyrate → FN in urine ketostix

59
Q

Examples of extra-pancreatic tumour that leads to tumour-associated hypoglycaemia (2)

A

retroperitoneal fibrosarcoma, hepatoma

60
Q

How does liver disease lead to hypoglycaemia?

A

↓ glycogen reserve

61
Q

How does renal disease lead to hypoglycaemia?

A

multifactorial
uraemia –> inhibit liver gluconeogenesis & lead to poor appetitie
↓ insulin clearance

62
Q

2nd causes of hyperaldosteronism (3)

A

renal artery stenosis
juxtaglomerular apparatus tumour
renin-secreting tumour

63
Q

How does DM lead to atherosclerosis?

A

apoB glycation –> ↓ affinity of LDL to LDL-R –> ↓ LDL catabolism –> ↑ LDL in circulation –> atherosclerosis

64
Q

normal GH response in glucagon stimulation test

A

up to 20 ng/mL

65
Q

FP for 24h urine catecholamine, metanephrine, VMA (4)

A

medications (e.g. β blockers, α blockers…), food (e.g. caffeine, tobacco), physical stress, OSA

66
Q

Why is glucagon stimulation test not used anymore for phaeochromocytoma?

A

hypertensive crisis risk

67
Q

Risk for overnight clonidine suppression test

A

hypotensive crisis

68
Q

Compare pros and cons between urinary and plasma metanephrines (3+4)

A

Urine:
a. Pros:
- well-established, widely available
- urinary conc. make analysis relatively easy
- easy to implement
b. Cons:
- 24h collection inconvenient for patients
- reliability problem
- difficult to control dietary & daily life influence
- inappropriate for patients with renal failure

Plasma (the opposite)

69
Q

Why genetic testing should be considered in all patients who present with PPGL? (3)

A
  • > = 1/3 of all patients with PPGLs have disease-causing germline mutations
  • mutations of SDHB lead to metastatic disease commonly
  • earlier diagnosis & treatment of PPGLs & other manifestations in relatives
70
Q

Suppression test for high prolactin level

A

Bromocriptine suppression test

71
Q

DDx for high testosterone level (in female) (3)

A

polycystic ovarian syndrome
Cushing syndrome (active adrenal)
ovarian tumour

72
Q

How does hypothyroidism lead to high lipid profile?

A

low LDL-R & lipoprotein lipase activity –> LDL cannot be recycled back to liver –> ↓ LDL metabolism —> remain in circulation –> ↑ cholesterol

73
Q

Confirmation laboratory test for GH secreting tumour

A

IGF-1

74
Q

Management of DKA / HHS (5)

A

Insulin
Rehydration
KCl
Close monitoring
Treat underlying cause

MED4 CPY (14 decks)

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