Endocrinology Flashcards

1
Q

MOA of Denosumab

A

MAB that inhibits RANK ligand.
RANK ligand promotes osteoCLAST differentiation and activation.
Therefore Denosumab prevents osteoclast maturation.

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2
Q

Steroids which do NOT have mineralocorticoid activity

A

Dexamethasone

Betamethasone

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3
Q

Mechanism of Hepcidin

A

Inhibits iron transport by internalisation and breakdown of ferroporin on basolateral surface of enterocytes.

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4
Q

radioiodine ablation is associated with which complication

A

worsening of graves ophthalmopathy

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5
Q

Symptoms of carcinoid tumours

A

Diarrhoea, flushing, telangictasia, wheeze, valvular lesions

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6
Q

Location of carcinoid tumours

A

Mid gut, bronchial

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7
Q

Test for carcinoid tumour

A

24hr Urine 5-HIAA

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8
Q

Effect of PTH on Ca, Phosphate, Vit D and FGF23 levels

A

Increases Ca
Decreases Ph
Increases Vit D
FGF23 decreases PTH

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9
Q

MEN1

A

3P’s - above the umbilicus

  • Pancreatic tumor
  • Pituitary tumor
  • Parathyroid hyperplasia
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10
Q

MEN 2A

A

2P’s 1M - below the head

  • Parathyroid hyperplasia
  • Pheochromocytoma
  • Medullary thyroid cancer
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11
Q

MEN 2B

A

1P 2M’s

  • Phaeochromocytoma
  • Medullary thyroid cancer
  • Mucosal neuromas
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12
Q

Management of incidental adrenal mass >4cm

A

adrenalectomy + hormone evaluation

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13
Q

Management of incidental adrenal mass <4cm

A

hormone evaluation

  • hormonally active lesion -> adrenalectomy
  • hormonally inactive -> follow up imaging
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14
Q

effect of hypophosphatemia in Hb curve

A

Shift to the Left due to reduced 2,3 BPG

As 2,3 BPG works by adding a phosphate molecule to haem to stop O2 binding

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15
Q

Why do obese men have lower testosterone?

A

reduced sex-hormone binding globulin.

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16
Q

MOA of exenatide

A

Stimulates glucose dependant secretion of insulin by pancreatic beta cells (incretin)

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17
Q

Manifestation of GH deficiency

A

short stature and reduced growth velocity

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18
Q

Decreased growth hormone occurs in what state

A

hyperglycaemia

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19
Q

What is sheehan syndrome

A

Damage to the pituitary, usually from hypoperfusion, in pregnancy/childbirth.

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20
Q

Test for GH deficiency

A
  1. IGF-1

2. GHRH

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21
Q

Most common cause of familial hypercholesterolemia

A

Low-density lipoprotein (LDL) receptor defect.

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22
Q

How does Sarcoidosis cause hypercalcaemia.

A

Increased 1,25(OH)2-vitamin D synthesis.

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23
Q

How does malignancy cause hypercalcaemia

A

Secretion of parathyroid hormone-related peptide (PTHrP).

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24
Q

Carbimazole MOA

A

Thyroid peroxidase activity.

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25
Q

Haemachomatosis arthritis joints

A

Metacarpophalangeal.

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26
Q

Investigation of adrenal incidentalomas

A
  1. If malignant features (>20 houndsfields, irregular shape, delayed contrast washout, >4cm, calcification) then - biopsy or interval imaging.
  2. No malignant features - check plasma metanephrines, Renin:Aldo ratio, dexamethasone suppression test for functioning lesion.
  3. Follow up - imaging in 6-12 months + yearly dexamethasone suppression tests and plasma metanephrines for 4 years.
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27
Q

In diabetes, sudden change in diabetic control causes which complication?

A

Retinopathy

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28
Q

Bone pain + muscle weakness + waddling gait = ?

A

Osteomalacia

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29
Q

Specific changes in Osteomalacia (that differentiate it from Osteoporosis)

A
  1. blurred vertebral body trabeculae on imaging.
  2. softening leads to a concavity of the vertebral bodies called codfish vertebrae. The vertebral disks appear large and biconvex.
  3. Looser zones = Looser pseudofractures - fissures, or narrow radiolucent lines, 2 to 5 mm in width with sclerotic borders, often are bilateral, symmetric, and lie perpendicular to the cortical margins of bones. commonly found at the femoral neck, on the medial part of the femoral shaft, and in the pubic and ischial rami.
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30
Q

Causes of Osteomalacia

A

Vit D deficiency
Vit D resistance
Phosphate wasting conditions.

31
Q

Management of HTN in Pheochromocytoma

A
  • Use alpha blockers first.
  • If beta blockers are used then the adrenaline can cause unopposed vasoconstrictive α-adrenergic stimulation that aggravates hypertension.
32
Q

MOA of steroids in bone resorption

A

Act on osteoblasts and inhibit growth and differentiation of osteoblasts.
Inhibit osteoprotegerin production thereby preventing osteoclast inhibition. Increase NFKB and CSF1.
Inhibit ILGF.

33
Q

MOA of Bisphosphonates

A

Bisphosphonates attach to hydroxyapatite binding sites on bony surfaces. When osteoclasts resorb bone, the bisphosphonate released during resorption impairs the ability of the osteoclasts to form the ruffled border, to adhere to the bony surface, and to produce the protons necessary for bone resorption.
Decrease osteoclast differentiation and increase apoptosis.

34
Q

Next investigation of a thyroid nodule and hyperthyroidism.

A

Radionucleotide thyroid scan.

Not for FNA unless non-functioning.

35
Q

Marker in medullary thyroid cancer

A

Calcitonin

36
Q

What is a VIPoma

A

Neuroendocrine tumor. watery diarrhea that persists with fasting. Stools are tea-colored and odorless with stool volumes exceeding 700 mL/day.

37
Q

Whipples triad

A

Symptoms of neuroglycopenia
Low BSL
resolution of symptoms with treating hypoglycaemia.

NOT necessarily insulin related.

38
Q

Thyroid changes in pregnancy

A

Decreased TSH
Increased TBG
Stimulation of the TSH-receptors by bHCG
Increase in TOTAL T3, T4 (not free T3, T4)

39
Q

Pathology changes seen in Addisons disease

A
Hyperkalaemia 
Hypercalcaemia 
Hyperchloremia
Hyponatremia 
Metabolic acidosis 
Increased urea and creatinine 
Anaemia 
Lymphocytosis 
Eosinophilia
40
Q

MODY subtypes, gene and management.

A

memory tool –> HHH, GIN between the H’s. All 4 One and 1 for all.

MODY 1 - HNF4a - reduced insulin response, treat with sulfonylureas.

MODY 2 - Glucokinase gene - defective glucokinase, treat with diet modification only.

MODY 3 - HNF1a - most common, decreased insulin secretion, glycosuria, treat with sulfonylureas.
MODY 4 - IPF1
MODY 5 - HNF1b - insulin
MODY 6 - NDF1 - insulin

41
Q

Aim for rate of glucose decrease per hour in DKA protocol

A

3mmol/hr

42
Q

Test to avoid in possible pheochromocytoma

A

Dexamethasone suppression test - can cause catecholamine crisis

43
Q

When to treat subclinical hypothyroidism

A
  1. If TSH >10
  2. If TSH >7 and pt <65yrs
  3. If they also have autoantibodies
  4. If they have symptoms
44
Q

What is the primary MOA of metformin

A

reduces liver gluconeogenesis

45
Q

Cardiac drug which increases the risk of developing diabetes

A

Statins

46
Q

Risk of Denosumab cessation

A

Treatment cessation is associated with risk of bone remodeling overshoot associated with increased risk of multiple vertebral fractures

47
Q

Pasireotide MOA, uses and SE

A

MOA: (somatostatin analogue) - peptide inhibitor of multiple endocrine, neuroendocrine, and exocrine mechanisms. In patients with Cushing disease, pasireotide binds to somatostatin receptor (sst1-5), with highest affinity for the sst5 subtype, resulting in inhibition of ACTH secretion which leads to decreased cortisol secretion. In patients with acromegaly, pasireotide binds to sst2 and sst5, resulting in decreased GH and IGF-1.

Uses: for treatment of refractory acromegaly and Cushing’s disease

SE: Hyperglycaemia.

48
Q

Reason for replacing GH in Growth hormone deficiency

A

recommended for body composition, exercise capacity, bone and CV health

49
Q

Management of hyperprolactinemia

A

Cabergoline - Dopamine agonist

50
Q

SE Cabergoline

A

Increased compulsive disorders - eg. gambling, sexual.

51
Q

Treatment of Acromegaly

A
  1. Surgical resection of pituitary tumour.
  2. Octreotide
  3. Pegvisomant is a GH receptor antagonist
  4. Carbergoline
52
Q

First line investigation for diabetes insipidus

A

hypertonic saline–stimulated plasma copeptin

NOT water deprivation test.

53
Q

Treatments for adrenal Cushings and Cushings disease

A

Adrenal Cushings - Ketoconazole, Etomidate, Metyrapone

Cushings disease - Pasireotide

54
Q

Pathophys of Pagets

A

Marked increase in activity of both osteoclasts and osteoblasts. Bone remodelling is increased and
disorganised, resulting in bone which is structurally impaired and prone to deformity and fracture.

55
Q

Hormone levels in PCOS

A
  • High LH
  • Low FSH
  • High testosterone
  • High DHEAS
  • > 20% have elevated 17OHP (but usually means CAH)
  • low serum SHBG concentrations
  • High AMH
56
Q

Findings in hypocalciuric hypercalcaemia

A
  • low urine calcium
  • high PTH
  • High serum calcium

–> due to defect in calcium sensing receptor

57
Q

Through what network does the hypothalamus and pituitary communicate

A

Hypophyseal portal system. Goes from arcuate nucleus to anterior pituitary

58
Q

Management of insulinoma

A
  1. Surgical resection

2. Somatostatin analogue for hypoglycaemia

59
Q

At what age is HBA1c lowest in T1DM

A

20-30 - young adult

60
Q

Risk of stopping denosumab

A

atypical vertebral fractures

61
Q

Order of investigations for Cushings

A
  • ACTH

If ACTH independent - adrenal CT
If ACTH dependant - Desmopressin stimulation/ dexamethasone suppression test/ pituitary MRI
Intermediate result - desmopressin test

62
Q

Fracture risk assessment score

A

FRAX

63
Q

Contraindications to bisphosphonate therapy

A
  • esophageal disorders
  • inability to follow the dosing requirements
  • chronic kidney disease [eGFR] rate <30 mL/min
64
Q

When to start anti-resorptive therapy

A
  1. History of hip or vertebral fracture.
  2. T-score ≤-2.5 (DXA) at the femoral neck or spine, after appropriate evaluation to exclude secondary causes.
  3. T-score between -1 and -2.5 at the femoral neck or spine, and a 10-year probability of hip fracture ≥3 percent or a 10-year probability of any major osteoporosis-related fracture ≥20 percent based upon the United States-adapted WHO algorithm.
65
Q

Management of atypical femoral fractures in osteoporosis on bisphosphonates

A

only likely due to be from bisphosphonates if treatment duration >5 years. As prolonged therapy can lead to oversuppression of bone turnover (“frozen bone”)
A patient with an atypical femur fracture in one leg is at risk for a fracture in the other leg - therefore should xray other leg too. When bisphosphonates are stopped, the risk of atypical fracture declines.

66
Q

Highest risk ethnicity for atypical femoral fractures on bisphosphonates

A

Asians

67
Q

High risk HLA in T1DM

A

HLA DR3 and HLA DR4

68
Q

Protective HLA in T1DM

A

HLA DR2

69
Q

T1DM autoantibodies

A

GAD65
IAA
IA-2
ZnT8

70
Q

Therapies for infertility in PCOS

A

Letrozole
Clomiphene
Gonadotrophin therapy
IVF

71
Q

Types of Amiodarone induced thyrotoxicosis

A
  1. Type 1 - occurs in 3-4 months post amiodarone - it is the Jod Basedow effect due to underlying multinodular goitre or graves.
  2. Type 2 - occurs in 2-3 years after amiodarone and is due to a destructive thyroiditis - should be treated with steroids.
72
Q

When is RAI contra-indicated

A

when there is thyroid eye disease.

73
Q

Cinacalcet MOA

A

Increases sensitivity of CaSR - calcium sensing receptor

74
Q

Treatment for adrenal carcinoma

A

Mitotane