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Bpt > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Mifepristone

A

Synthetic steroid
Can be ised for tx of hyperglycemia in patients with cushings syndrome
Glucocorticoid receptor antagonist

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2
Q

Monitoring for nonfunctioning Pituitary adenomas

A

Macro:
-6 monthly MRI

Micro:
yearly MRI

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3
Q

Tx of pituitary adenomas producing prolactin

A

Dopamine Agonist

  • Carbegoline
  • Bromocriptine
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4
Q

Cut offs for prolactin level to suggest functioning vs non functioning macroadenoma

A

> 4000 = functoning macroadenoma

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5
Q

ADH

A

Increases permeability of cells in distal tubule and medullary collecting ducts

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6
Q

What is water deprivation test used for

A

Assessing for diabetes insipidus

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7
Q

Interpreting water deprivation:
-Nil significant increase in urine osmolality as tiem goes

Post desmopressin
-Significant increase in urine osmolality

A

Central DI

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8
Q

Interpreting water deprivation:
–Nil significant increase in urine osmolality as tiem goes

Post desmopression:
-No elevation in urine osmolality

A

Nephrogenic DI

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9
Q

Interpreting water deprivation:
-Incraseing urine osmolality >600 mosmol/kg

Post desmopression:
-No response

A

Primary polydipsia

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10
Q

Urine Osm suggestive of DI

A

<300 mosmol/L

Associated with High-normal Serum osm

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11
Q

MX of Central DI

A

Mild polyuria <3L/Day no Tx needed if thirst centre intact

OTherwise desmopressin 100 microg BD-TDS

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12
Q

Mx of SIADH

A

Fluid restriction
Salt tablets and frusemide in some cases
Severe: Hypertonic saline

Vasopressin receptor angatonists (Vaptans)

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13
Q

CAuses of decreased GH

A

DaytimeHyperglycemiaAgingObesity

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14
Q

Control of GH

A
  • Ghrelin (gastric derived peptide) à stimulates GH release
    * Somatostatin à inhibits GH secretion

IGF-1 (insulin-like factors) à negative feedback loop; inhibits release

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15
Q

Diagnosis of GH Deficiency

A

Most specific: IGF-1 measured in insulin tolerance test (low)

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16
Q

Ix for Acromegaly

A

Oral glucose tolerance test:
1. IGF -1 level High

NORMAL = GH <1ng/mL after 75g of oral glucose

Acromegaly = GH >2ng/mL

• Pituitary MRI
If NEGATIVE = Chest/abdo CT to identifies ectopic source

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17
Q

Tx of Acromegaly

A
  1. Stomatostatin analgoue (octreotide, pasireotide)
  2. Dopamine agonist (carbegoline, bromocriptine)
  3. GH receptor antagonist (pegvisomant)
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18
Q

APS 1

autoimmune polyglandular syndrome

A

hypoparathyroidism/chronic mucutaneous candidiasis (Th17) in mid 20s followed by adrenal insufficiency

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19
Q

APS 2

A

presents age 40; primary adrenal insufficiency (main feature), autoimmune thyroid disease and T1DM

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20
Q

Ix for Addison’s

A

Morning Cortisol <90 nmol/L

Short synacthen test
-Only useful in ruling out primary hypoadrenalism
○ Normal = rise >250 nmol/L with 30 minute value of >550 nmol/L
-Primary insufficiency = sub-normal increase

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21
Q

Gold standard Ix for hypoadrenalism

A

Insulin tolerance test

-CAuses hypoglycemia which is stressful and shuld produce ACTH

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22
Q

Adrenoleukodystrophy

A

XLR

Features:
-Addison's
○ Dementia
○ Blindness
-Quadriparesis
○ Spasticity
-Polyneuropathy

Diagnosed on plasma very long chain fatty acids (VLCFA) and gene testing

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23
Q

Adrenal incidentaloma Mx

A

• Functioning – surgical removal
• Non-functioning:
• <4cm and non suspicious features on scanning à repeat scan in 6 to 12 months
• >4cm and suspicious features on scanning à remove surgically
-<2cm – no follow-up required as rule; unless concerning features on screening

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24
Q

Specific features of Cushings

A

• Facial plethora
• Proximal myopathy
Purple striae

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25
Q

Pseudocushings

A

Suppressed with low dose dexamethasone testing

Mild hypercortisolism

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26
Q

Tx of Cushings disease

A
  1. Transphenoidal resection of pit adeno
  2. RTx
  3. MEdical
    - Ketoconazole SE androgen inhibition
    - Pasireotide: Somatostatin receptor antagonist sE Hyperglycemia
    - Mifepristone
    - MEtyrapone
  4. Bilateral adrenalectomy
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27
Q

CAH pathophys

A

Autosomal recessive disorder of 21-hydroxylase deficiency

CYP21 gene on chromosome 6

21-hydroxylase deficiency (93%) results in decreased aldosterone and cortisol synthesis, high ACTH levels and subsequent adrenal stimulation with diversion of the steroid precursors into androgenic pathways

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28
Q

CLASSIC 21-HYDROXYLASE DEFICIENCY (CONGENITAL ADRENAL HYPERPLASIA)

A

salt-wasting and adrenal sufficiency or with virilisation as neonates

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29
Q

• NON-CLASSIC 21-HYDROXYLASE DEFICIENCY

A

present in young adulthood with signs of androgen excess

Late childhood – premature pubarche, acne, accelerated bone age

Adolescent and adult females – acne, hirsutism, menstrual irregularity

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30
Q

Ix for CAH

A

○ High serum 17-hydroxyprogesterone

○ Exaggerated response to ACTH stimulation test (synacthen) with ↑ 17-hydroxyprogesterone levels

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31
Q

Tx CAH

A

○ Women – cyproterone acetate/OCP – for hirsutism, acne, oligomenorrhoea; dexamethasone for ovulation induction
○ Men – not necessary unless testicular masses or oligospermia, possibly dexamethasone

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32
Q

Ix for Conn’s

A

ARR >30 and Plasma aldosterone concentration >20ng/dl = 90% sensitivity/specific for hyperaldosteronism

Other tests:

  • SAline infusion test: positive if no suppression of plasma aldosterone
  • Salt suppresion test
  • Fludrocortisone suppresion test
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33
Q

Mx of Conn’s

A

Adrenalectomy

Medical

  • Spiro
  • Amiloride
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34
Q

Carney Triad

A

gastric stromal tumour, pulmonary chondaromas, phaeo

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35
Q

Ix for Phaeo

A

Best test:
-24 hour urine catecholamines and metanephrines

Best screening:
Plasma fractionated metanephrines

Confirmation tests:

  • Clonidine suppression test: if no suppression, then phaeo
  • Chromogranin A elevated
  • Neuropeptide Y elevated
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36
Q

Mx of Phaeo

A

Resect lesion

Medical: Alpha blockers
Phenoxybenzamine
prazosin

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37
Q

Hormones that increase appetite

A

Ghelin

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38
Q

Hormones that decrease appetite

A

CCK
GLP1
PYY
Leptin

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39
Q

MEN1

A

Hyperparathyroid
Pituitary macroadenoma
Pancreas - insulinoma, gastrinoma

MEN1/MENIN

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40
Q

MEN2A

A

TAP
Thyrioid - medullary cancer
Adrenal - Phaeo
Primary prarthyroid hyperplasia

RET

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41
Q

MEN2B

A

TAN
Thyroid - medullary cancer
Adrenal - pheao
Neuromas, marfanoid habitus, Hirschsprungs

RET

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42
Q

Carcinoid Syndrome

A
  • Serotonin secretion
  • Associated with metastatic midgut carcinoid tumor
  • FEatures: flushing/diarrhea/TR/pellegra like skin lesions

Ix:

  • 5-HIAA in urine
  • Urine/plasma 5-HT

Mx:

  • Ondansetron
  • Octreotie
43
Q

Zollinger Ellison Syndrome

A

• Non-beta islet cell gastrin-secreting tumour of the pancreas
○ Usually located in pancreas, duodenum or abdominal lymph nodes

Ix
○ Secretin infusion – increase in gastrin >200 pg within 15 minutes of secretin injection = >90% of sensitivity and specificity
○ Fasting gastrin levels
○ Gastric acid secretion – normal = 10mEq/hour; ZES > 15 mEq/hour

Mx – PPI/H1 receptor antagonists; octreotide

44
Q

VIPoma

A

80% solitary pancreatic masses; usually >3cm at diagnosis

Features
-Large volume watery diarrhea, hypokalemia, hypochlorhydria, dehydration

Persistance of diarrhea on fastin means secretory

45
Q

Kallman’s Syndrome

A

• Hypogonadtrophic hypogonadism and anosmia
Failure of migration of GnRH neurons

Features:
• Male – delayed puberty +/- micropenis
Female – delayed puberty and lacks of secondary sex characteristics

Assocaitions:
-Cleft palate, hearing loss, color blindness

46
Q

DKA Criteria

A

Hyperglycemia >14
Ketosis
pH <7.3 (Bicarb <20 mmol)

47
Q

HHS Criteria

A

Hyperglycemia >30
Minimal ketoisis
Serm OSm >320

48
Q

When to start giving IV Dextrose in DKA to prevent cerebral dextrose

A

DKA serum BG <11.1 swap to IV Dextrose and halve insulin infusion rate (HHS serum BG<15)

49
Q

Hospital target for BSLs

A

5-10

in and out of ICU

50
Q

Which DDP4i does not need renal dose adjustment

A

linagliptin

51
Q

Hba1c target in pregnancy

A

<6

52
Q

T1DM in which family member increases the risk of most of someone getting T1DM

A

Sibling!

Then Father

53
Q

HLA DR associated with T1DM

A

DR3 and DR4

54
Q

T1DM Retinopathy screening

A 
At diagnosis
•
Then every 1 to 2 years
•
Children -commence at puberty
55
Q

PRimary pigmented nodular adrenal disease mutation

A

PRKAR1A mutation

56
Q

Diagnostic criteria for PCOS

A

2 of 3:

  • Oligo/anovulation
  • Clinical and/or biochemical hypernadrogenism
  • Polycystic ovaries
57
Q

Diagnostic criteria for hypergonadotrophic hypogonadism

A

2 x FSH > 40 U/L at least 1 month apart or ↓ [oestradiol] & elevated FSH, in the context of amenorrhoea and menopausal symptoms

58
Q

Female athlete triad

A

Amenorrhoea, low bone density and eating disorder among female athletes

59
Q

Corr Sodium when hyperglycemic

A

Divide BSL by 3 and add to Na

60
Q

MAx correction of NA per day in chronic hyponatremia

A

8 mmol/day

61
Q

Severe and symptomatic hyponatremia management

A

100-150 ml 3% saline over 15 mins
-Rises Na by 2-3 mmol

Aim to increase by 4-6 mmol over 2-3 hours

62
Q

Sick euthyroid

A

Diagnosis –
•
If TSH>10 –true hypothyroidism
•
If T3 raised and TSH undetectable -hyperthyroidism
•
If low T4 and T3 and TSH < 10 -exclude pituitary disease (Prolactin/LH/FSH/Cortisol)

63
Q

Tx of MNG/Toxic adenoma

A 
•
Same option as for Graves’ disease
•
I131 particularly suited to TA
•
MNG -I131 or surgery if large goitre, obstructive symptoms or suspicion of malignancy
•
Thionamidetherapy less favoured as remission is unlikely
64
Q

Type 1 Amiodarone Thyrotoxicosis

A

Increased thyroid hormonse synthesis due to iodine load

Vascularity normal or reduced

Tx: CMZ

65
Q

Type 2 Amiodarone thyrotoxicosis

A

Thyrocye cytotoxicity

IL-6 and TG elevated

Reduced vascularity

PRednisolone

66
Q

Subclinical hyperthyroidism

A

Subnormal TSH with normal T4 and T3

Tx:
-if TSH <0.01, MNG, existing OP/heart disease, older patients

67
Q

Consequences of TSH <0.01 in subclinical hyperthyroidism

A

Progression to overt disease
OP
AF
HEart failure

68
Q

Thyroid storm Mx

A

IV propanolol
PTU Q4H (lowers T3 faster than CMZ)
Lugol’s solution - only in prep for emergency thyroidectomy - use >4 days exacerbates thyrotoxicosis
Hydrocort - Blocks T4 to T3 conversion
Cholestyramine - to increase T4 clearance
PLEX

69
Q

Hypothyroid Mx

A 
•
L thyroxine -dose adjusted to achieve TSH around 1mIU/L
•
No dose adjustment for 2 weeks
•
Start low (25 or 50ug) if IHD
•
T3 not needed
•
Increase by 50% in pregnancy
•
In pituitary disease beware unmasking HPA axis dysfunction
70
Q

Subclinical Hypothyroid

A

Higher with higher iodine intakes and in Down syndrome and type 1 diabetes

Symptoms, lipids and cardiac function may improve if TSH > 10
•
TSH < 10 no evidence of benefit (symptoms do not improve in placebo controlled studies)
•
Treat if pregnant (TSH >4.0) or contemplating pregnancy

71
Q

Myxoedema Coma Mx

A

Hydrocort in case of any adrenal insufficiency
T4 loading
Avoid water overload

72
Q

Subacute Thyroiditis

A

Likely due to viral infection

Painful swollen thyroid
Thyrotoxicosis
Sx for 2-8 weeks
No isotope uptake
USS - enlarged hypoechoic gland with reduced vascularity

Thyrotoxicosis then hypothyroidism then recovery

Mx:

  • NSAIDS
  • Can trial PNL 40 mg then taper
  • Can have thyroxin for hypothyroid phase

90% resolves completely

73
Q

Lymphocytic and post partum thyroiditis

A

Painless enlarged thyroid
Low echogenisity on USS and zero isotope uptake

Thyrotoxicosis is limited, followed by hypothyroidism that persists in 20-30%

High risk of eventual hypothyroidism

74
Q

Thyroid lesions fo rFNA

A

•
TSH –if suppressed (<0.01 mIU/l) lesion may be “hot” and isotope (Tc99m) uptake scan should be performed. If hot –no FNAC
•
Lesion > 2cm and not a cyst or spongioformlesion then FNA
•
Lesions 1-2 cm selected on the basis of high risk US features TI-RADS 3-5
•
Lesions < 1 cm repeat evaluation in 6-12 months
•
Lesions that increase by 30% volume or 10% in diamshould be biopsied

75
Q

Papillary Thyroid carcinoma

A

Most common thyroid cancer

Overlapping nucleii, grooves, “orphan annie”
and Psammomabodies

USually indolent, but can be metastatic to bone and lung

Usually BRAF mutation

76
Q

Follicular thyroid carcinoma

A

Loss of follicular structure and increased atypia in undifferentiated tumours

Distinguished from FA by capsular and vascular invasion post surgery

Poor prognosis due to usually presenting late

77
Q

Teprotumumab

A

For thyroid eye disease

78
Q

Bad features of thyroid nodules

A

-Solid
-Very hypoechoic
-Taller than wider
-Lobulated/irreguler
Extrathyroidal extension
-Microcalcifications
-Punctate echogenic foci

79
Q

P1NP

A

Synthesised by osteoblasts

Procollagen type 1 has short N-and C-terminal extensions that we can measure when cleaved during conversion from procollagen to collagen

80
Q

Vit D Deficiency classification

A 
•
Adequate ≥ 50 nmol/L
•
Mild deficiency 30–49
•
Moderate deficiency 12.5–29
•
Severe deficiency < 12.5
81
Q

Alendronate

A

Increased spine BMD by 9% and hip BMD by 6% over 3 years

Incidence of new fractures reduced by ~50% compared with placebo

82
Q

Risendronate

A

Increased spine BMD by 4–5% and hip BMD by 2–4% versus placebo over 3 years

risedronatereduced vertebral fractures by 40–50%

83
Q

Zolendronic Acid

A

Most potent bisphosphonate

Vertebral fractures reduced by 70%
•
Hip fractures reduced by 41%
•
Non vertebral fractures reduced by 25%
84
Q

Duration of bisphosphonates

A

•
In women at high risk (low hip T-score, hxfracture), continuation of treatment for up to10 years oral and 6 years IV should be considered with periodic evaluation
•
For women not at high risk after 3-5 years, a drug holiday of 2-3 years can be considered

85
Q

Risk factors for ONJ

A 
High-dose IV bisphosphonates,
•
Longer duration of treatment with bisphosphonates
•
Glucocorticoid use
•
Alcohol abuse and tobacco use
•
Cancer
•
Advanced age
•
Poor dental hygiene and those who undergo a dental procedure such as dental extraction
86
Q

Teriparatide

PBS Criteria

A

PBS Criteria:
A bone mineral density (BMD) T-score of –3.0 or less AND
•
2 or more fractures due to minimal trauma AND
•
At least one new symptomatic fracture after at least 12 months of continuous treatment with antiresorptive therapy at adequate doses

87
Q

Teriparatide SE and CI

A

Main SE dizziness, leg cramps, pain at injection site

Benefit in terms of BMD seems to wane after discontinuation unless followed by an antiresorptive

CI-Paget’s disease, skeletal irradiation, unexplained increases in ALP, pre-existing malignancy, renal stones, gout

88
Q

Denosumab

A

Human monoclonal antibody to the receptor activator of nuclear factor kappaBligand (RANKL), an osteoclast differentiating factor

nhibits osteoclast formation, function and survival
•
Decreases bone resorption

9% gain BMD LS and 4% hip

Reduction in VF-68%
•
Reduction in non vertebral fracture-40%
•
Reduction in hip fracture-20%

When discontinuing denosumabtherapy, bisphosphonates should be considered to prevent or reduce the rebound increase in bone turnover

89
Q

Denosumab + Teriparatide

A

Two years of concomitant teriparatide and denosumabtherapy increases BMD more than therapy with either medication alone and more than has been reported with any current therapy.

90
Q

Insulinoma

A

Gold standard testing:
• 72hour fast with measurements of insulin, glucose and C-peptide

C peptide: <200 pmol = no insulinoma; >200 pmol = diagnostic of insulinoma

FEatures
• Hypoglycaemia = typically early in morning or just before meal
○ Diplopia, weakness
Rapid weight gain

91
Q

Paget’s Disease

A 
Ix
		• High ALP
		• High C and N-telopeptides
			○ High in both serum and urine 
High osteocalcin

Indication for Tx
• Severe bone pain – not responding to analgesia
• Neurological Cx
• High output cardiac failure
• Hypercalcaemia
Preparation for elective orthopaedic surgery

Tx

  • NSAIDS
  • Bisphosphonates
92
Q

Romosozumab

A

Sclerostin is an osteoblast inhibitor
mAB to sclerostin
Better than teriparatide/alendronate for vertebral fractures and reduction in clinical fractures

Rebound in BMD on cessation

93
Q

Medullary thyroid cancer

A

Vandetanib improves progression free survival

Calcitonin levels correlate with tumor burden

Test for RET mutation

neuroendocrine tumour of para-follicular/C-cells of thyroids – secretes calcitonin

94
Q

HNF1A mutation

A

MODY 3

-sensitive to sulphonurea

95
Q

GCK mutation

A

MODY 2

-Ccan stop glucose lowering therapy once reached baseline

96
Q

Anti-thyroid perioxidase (TPO)

A

90% of Hashimoto’s thyroiditis, 75% of Grave’s disease, 10% of multi-nodular goitre

97
Q

Anti-thyrogloublin (TG)

A

70% of Hashimoto’s thyroiditis; 60% of idiopathic hypothyroiditis, 30% of Grave’s disease

98
Q

TSH receptor antibodies

A

70 to 100% of Grave’s disease

99
Q

Thyroxine malabsorption

A
  • Malabsorption:
    • Coeliac disease
    • Small bowel surgery
    • Oestrogen therapy
    • Drugs that interfere with T4 absorption = ferrous sulfate, cholestyramine
• Increased clearance:
	• Lovastatin
	• Amiodarone
	• Carbmazepine
Phenytoin
100
Q

Post PArtum Thyroiditis

A
  • Occurs within 1 years after childbirth
  • Anti-TPO antibody = high in 60 – 85% of patients
  • Risk factors:
    • Anti-TPO positive prior to pregnancy
    • T1DM
    • Previous episode of post-partum thyroiditis
  • Treatment:
    • Propranolol can be safely used even if breast-feeding
101
Q

Thyroid in Pregnancy

A
  • Increased in thyroxine-binding globulin (TBG)
    • Increase is due to decreased hepatic clearance and increases synthesis (triggered by oestrogen)

Beta HCG mimics TSH and increases production of T3/T4

102
Q

Gestational Hyerthyroidism

A

• Non-autoimmune; no goitre
• Almost all patients resolved by 20 weeks
• LOW, maternal tachycardia may occur
• Only 12% will have elevated FT3
If persistent beyond 20 weeks à then treat; consider Grave’s disease

103
Q

Anaplastic Thyroid cancer

A

; undifferentiated tumour of thyroid follicular epithelium

Generally in age 65

Extensive local invasion and compression Sx are prominent

104
Q

Thyroid lymphoma

A
  • Often arises in background of Hashimoto’s thyroiditis; diffuse large B cell lymphoma is the most common
  • Highly sensitive to the external radiation

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