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BPT > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the inhibitory hypothalamic hormones, and what do they inhibit?

A

Somatostatin: Growth Hormone and TSH release
Dopamine: Prolactin release

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2
Q

Aldosterone

A

Mineralocorticoid, synthesised in zona glomerulosa
Released stimulated by Angiotensin II in response to hypotension and hyponatraemia
Target: DCT + collecting ducts → upregulated NaK pumps + ENaC channels, Hydrogen ion secretion

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3
Q

Cortisol

A

Glucocorticoid, synthesiased in zona fasciculata
Release stimulated by: ACTH in response to stress and hypoglycaemia

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4
Q

Androgens

A

SHEA produced in Zona reticularis, precursor to other steroids, particularly testosterone (converted in Leydig cells), and Oestradiol

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5
Q

Catecholamines

A

Adrenaline and Noradrenaline
Synthesised in adrenal medulla, not steroid hormones and not cholesterol based

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6
Q

Structures at risk in cavernous sinus syndrome

A

CN III, IV, V1, V2, VI
Carotid Artery

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7
Q

Most effective method of weight loss in obesity

A

Bariatric surgery

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8
Q

Criteria for metabolic syndrome

A

3 of the 5:
- Increased waist circumference
- Wait: hip ratio used
- Males >0.9
- Females >0.85
- Hypertension
- Triglycerides >1.7
- HDL <1.0
- Impaired glucose tolerance/insulin resistance

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9
Q

Key features of MEN1

A
  • Primary hyperparathyroidism due to parathyroid adenoma -> severe hypercalcaemia
  • Pancreatic tumours
  • Pituitary adenomas, mostly prolactinoma

(3 Ps: Parathyroid, Pancreas, Pituitary)

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10
Q

Key features of MEN 2A

A
  • Medullary Thyroid Carcinoma
  • Pheochromocytoma
  • Primary hyperparathyroidism
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11
Q

Key Features of MEN 2B

A
  • Medullary thyroid carcinoma
  • Multiple neurinomas
  • ## Marfinoid Habitus
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12
Q

Gold standard management for BPH

A

TURP

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13
Q

Metabolites of Testosterone

A

5-alpha-reductase: Produces dihydrotestosterone, key for external genitalia formation, prostate development, hair follicles

Aromatase: produces oestradiol, acts on bone and brain and key for epihyseal fusion, bone mass, verbal memory

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14
Q

Most common congenital cause of primary hypogonadism?

A

Klinefelter Syndrome
Karyotype 47, XXY or Mosaic 46 XY
Small firm testes, infertility, learning difficulties

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15
Q

How are LH and FSH results interpreted in hypogonadism (i.e. low Testosterone)?

A

LH + FSH raised: Primary Hypogonadism
LH + FSH low: Secondary Hypogonadism, functional hypothalamic disorder

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16
Q

Congenital Causes of Secondary Hypogonadism

A

Kallmann’s Syndrome: associated with anosmia
Prader Willi

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17
Q

Contraindication to Testosterone Replacement Therapy

A

Hormone responsive tumours: prostate cancer, breast cancer

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18
Q

Key side effects of Testosterone Replacement

A

Erythrocytosis
Prostatic enlargement
Detection of subclinical prostate cancer
Acne
Gynaecomastia
Male pattern baldness
Worsening of heart failure
Transient worsening of OSA
Infertility due to reduced spermatogenesis

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19
Q

What are the Rotterdam Criteria for PCOS?

A

Need two of the three, with other endocrinological conditions excluded
- Oligo-ovulation and/or anovulation
- Hyperandrogenism (Acne, alopecia, hirsutism)
- Enlarged and/or polycystic ovary on ultrasound (volume ≥10ml and/or multiple cystic follicles in one or both ovaries)

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20
Q

PCOS Management

A
  • Weight loss most effective - restores ovulation, increases insulin sensitivity, increased SHBG (reducing testosterone)
  • COCP → increased SHBG, reduces free androgens
  • Androgen blockade (i.e. Spiro)
  • Letrozole and Clomiphene can be used for induction of ovulation
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21
Q

Gold standard test to distinguish central and nephrogenic Diabetes Insipidus?

A

Fluid deprivation test
- No change in urine output = DI
- Desmopressin given:
- Urine output drops: central DI
- Urine output unchanged: nephrogenic

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22
Q

What is Copeptin?

A

Prohormone for vasopressin.

Give patient hypertonic saline, which should drive rise in ADH to retain water and thus copeptin rises. In central DI, ADH not released, Copeptin level will be low.

Can do arginine stimulated copeptin level if serum sodium is normal, and then if very low indicates central DI

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23
Q

Key drug cause of Diabetes Insipidus?

A

Lithium

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24
Q

Management of Diabetes Insipidus

A

Central: Desmopressin, treat cause
Nephrogenic: Desmopressin doesn’t work. Need to remove cause

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25
Q

Differentiate Psychogenic Polydipsia and Diabetes Insipidus

A

Psychogenic Polydipsia:
- Low sodium, normal glucose
- Low plasma osmolality
- Dilute urine with low osmol <100
- Low urine sodium <10

Diabetes Insipidus
- High plasma osmolality
- Low urine osmolality <300
- Normal or high urine sodium

(So essentially in psychogenic polydipsia the kidney is trying to retain fluid, retaining sodium)

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26
Q

What is the gold standard diagnostic testing for Acromegaly?

A

OGTT is gold standard, but best test now is IGF-1 → elevated = diagnostic

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27
Q

Primary treatment for Acromegaly?

A

Surgical resection is first line, 80% success rate. IGF-1 levels for surveillance post op.

Somatostatin analogues such as Octreotide if levels high post op or can’t have surgery. Reduced GH release → reduce systemic symptoms and also reduce size of adenoma improving mass effect.

RTx also for recurrence post op

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28
Q

What is a key rare complication of Pegvisomant used for Acromegaly? Why does this occur?

A

Can cause tumour enlargement. This is because it doesn’t target the tumour directly, but instead prevents the excess GH from binding to its target. Also means GH levels/ IGF-1 levels remain high.

Second line agent after Octreotide. GH receptor antagonist.

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29
Q

HLA and Type 1 Diabetes

A

High Risk: DR3, DR4
Protective: DR2

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30
Q

Auto antibodies in Type 1 Diabetes Mellitus

A

Glutamic Acid Decarboxylase
Insulinoma Associated Ab
Proinsulin
Zinc Transport

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31
Q

Latent Autoimmune Diabetes of Adulthood

A

Subtype of T1DM
Initially responds to oral agents as Beta cells not yet depleted

Criteria:
- Age of onset ≥30
- Positive titre for a least one T1DM autoantibody
- Not treated with insulin within the first 6 months

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32
Q

Which other autoimmune disease is most closely associated with Type 1 Diabetes?

A

Autoimmune thyroid disease (27%)
Coeliac Disease (12%)

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33
Q

Key benefit of using closed loop system for T1DM?

A

Key benefit is lowering risk of severe hypoglycaemia. Also small HbA1c benefit

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34
Q

Benefits and Adverse Effects of intensive insulin therapy?

A

Reduces microvascular complications, particularly retinopathy and nephropathy.

Increases risk of severe hypoglycaemia and weight gain.

Benefits greater, and adverse effects lessened by insulin analogues compared to human insulin.

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35
Q

Estimation of Insulin requirements

A

0.5U/kg/day
Half given as basal
Half split through day as bolus doses, guided by patient

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36
Q

Insulin carbohydrate ratio and insulin sensitivity factor

A

ICR: grams or carbs/unit of insulin (around 500/total daily insulin)

ISF: effect 1U rapid acting insulin will have over a couple of hours (around 100/total daily insulin requirement)

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37
Q

SGLT2i in Type 1 Diabetes Mellitus

A

Not approved in Australia, but:
- reduce HbA1c
- Body weight reduction
- Lower daily insulin requirement
- Lower SBP
- Increased risk of ketosis

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38
Q

Metformin and Type 1 Diabetes

A

Small reduction in weight and lipids
No effect on HbA1c

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39
Q

Benefits of continuous glucose monitoring

A

Reduced time in hypoglycaemia without compromising HbA1c
Improve time in target range
Improve HbA1c

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40
Q

Benefits of Continuous SC insulin Infusion

A

Reduced hypoglycaemic events without increasing HbA1c
Improves Hb1c
Reduced hospitalisation for hypoglycaemia and ketoacidosis
Reduced work absenteeism
Improved QOL

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41
Q

Neurogenic/Autonomic Hypoglycaemia symptoms

A

Adrenergic: Palpitations, tremor, anxiety/arousal, pallor
Cholinergic: Sweating, hunger, paraesthesia

Occur at BGL <4

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42
Q

Neuroglycopaenic Hypoglycaemia symptoms

A

Cognitive impairment
Behaviour change
Psychomotor abnormalities
Seizures
Coma

Occur with BGL <3

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43
Q

Risk Factors for hypoglycaemia unawareness

A

Increasing age and long diabetes duration
Aggressive glycaemic control
Frequent hypoglycaemia
Autonomic neuropathy
Medications, e.g. beta blockers

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44
Q

Diagnosis of HHS

A

Serum BGL >30
Serum Osmolality >320
Dehydration
pH >7.3
Low ketones (<3)
Altered level of consciousness

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45
Q

Diabetic Neuropathy

A

Microangiopathy of vasonervorum causes nerve ischaemia

Length dependent sensory > motor neuropathy
Paraesthesia most common symtpom
Don’t forget autonomic neuropathy

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46
Q

Earliest manifestation of diabetic microvascular disease?

A

Retinopathy

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47
Q

Non Proliferative Diabetic Retinopathy

A

Subclinical, normal vision.
Microaneurysms, dilated venules, flame haemorrhages, cotton wool exudates, macular oedema

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48
Q

Proliferative Diabetic Retinopathy

A

Small vessel damage → reduced blood flow → VEGF release → neovascularisation → new vessels fragile and prone to rupture

Extensive neovascularisation
Retinal ischaemia
Fibrosis
Vitreal haemorrhage
Retinal detachment

Management: laser photocoagulation, intravitreal anti-VEGF (Bevacizumab)

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49
Q

Risk Factors for recurrence of diabetic ulcers

A

Loss of vibration (No. 1)
Preulcerative lesions
Peripheral arterial disease
Previous ulcer
Osteomyelitis
High GDS

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50
Q

Glucose transporters

A

GLUT2 brings glucose into beta cells which drives Insulin release
GLUT4 brings glucose into peripheral cells

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51
Q

Mature Onset Diabetes of the Young

A

Autosomal Dominant hereditary form of DM.
MODY3: most common and most severe, due to mutations of hepatocyte nuclear transcription factor. Treat with Sulphonylurea

MODY2: second most common, due to mutation of glucokinase. Mild hyperglycaemia, minimal treatment needed.

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52
Q

What is the first change seen in type 2 diabetes/impaired glucose tolerance?

A

Loss of first phase insulin secretion → post prandial hyperglycaemia

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53
Q

Treatment targets in Type 2 Diabetes

A

General <7.0%
New onset aim <6.0%
Reduction improves microvascular outcomes
Intensive control <6.5% increases mortality

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54
Q

SGLT2 Inhibitors

A

Block glucose reabsorption in proximal convoluted tubule. Low risk of hypoglycaemia, but have risk of euglycaemic ketoacidosis and UTIs. Contraindicated in renal impairment (Empa <30, Dapa <25)

Benefits.
Reduced HbA1c
Weight loss
Reduced blood pressure
Reduced MACE
Reduced HF hospitalisation, Empa reduced HF mortality and all cause mortality
Renoprotective

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55
Q

Metformin

A

Inhibit hepatic gluconeogenesis, no risk of hypo, modest weight decrease.

First line unless contraindicated. Severe renal impairment is key contraindication.

Risk of lactic acidosis, GI side effects. Hold when unwell

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56
Q

Sulfonylurea

A

Bind to ATP sensitive K channels on Beta cells → calcium influx → insulin secretion. High risk of hypoglycaemia which rises with age and renal/hepatic impairment.

Lead to weight gain. Contraindicated in hypoglycaemia and pregnancy as well as CrCl <15.

Not used much now. Gliclazide key example.

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57
Q

DPP4 Inhibitors

A

Inhibit DPP4 → reduced GLP-1 breakdown → Increased glucose dependent insulin secretion, slowed gastric emptying, inhibition of glucagon release, reduced appetite.

No risk of hypo with monotherapy. Contraindicated in renal impairment, and can worsen CCF (esp Saxagliptin). Linagliptin can be used in any CrCl.

End in “gliptin”

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58
Q

GLP-1 Agonists

A

Increase GLP-1 activity which increases glucose dependent insulin secretion, slowed gastric emptying, reduced glucagon release, reduced appetite, reduced hepatic steatosis.

Minimal hypoglycaemia risk, marked decrease in weight.

Mortality benefit for Liraglitide. Others reduce MACE and stroke risk. Semaglutide slows CKD progression.

Contraindicated in renal impairment, CrCl <30 (<15 for Dulaglutide)

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59
Q

Insulinoma

A

Insulin secreting neuroendocrine tumour of the beta cells, most common neuroendocrine tumour and most common cause of endogenous hyperinsulinism. Mostly benign.

5% part of MEN1. Present with sympathetic symptoms then neuroglycopaenic symptoms. High C peptide and proinsulin.

Tumour resection for localised disease. Octreotide can work while awaiting surgery.

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60
Q

Features of Thyroid Nodules concerning for malignancy

A

Hypoechoic
Height greater than width
Irregular margins
Calcification
Increased vascularity
Size >10mm

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61
Q

Workup for thyroid nodule

A

TFTs to ensure euthyroid
Ultrasound then done
Tc-99 scan can be done to further assess risk. Hot nodules typically benign, cold nodules concerning for malignancy
Biopsy lesions >10mm with high risk features and all >20mm

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62
Q

Thyroid Follicular Adenoma

A

Most common type of thyroid adenoma. 10-15% malignant but can’t tell on FNA so need to excise. If surgical excisional biopsy shows cancer then completion thyroidectomy + adjuvant therapy indicated

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63
Q

Monitoring thyroid cancers for response to therapy and recurrence

A

Medullary: Calcitonin
Follicular and Papillary: Thyroglobulin

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64
Q

Thyroid Cancer Subtypes

A

Papillary (80%): young females, good prognosis
Follicular (10%)
Medullary (5%): part of MEN2
Anaplastic (1%): Worst prognosis

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65
Q

Management of Papillary thyroid cancer

A

<1cm: Hemi or total thyroidectomy followed by surveillance
>1cm: Total thyroidectomy, radioactive iodine treatment with TSH stimulation, annual screening (USS, Thyroglobulin)

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66
Q

Mechanisms of Amiodarone thyroid toxicity

A

Type 1: increased thyroid synthesis due to excessive iodine (from the Amiodarone), responds to antithyroid drugs, occurs early in course of treatment

Type 2: Due to direct thyrocyte toxicity leading to inflammation. Typically self limiting, not responsive to antithyroid drugs. Responsive to steroids. More common

Colour doppler reduced in type 2, as it Sestamibi scan/

When in doubt use both steroids and ATDs

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67
Q

Benefit of Propranolol in Thyrotoxicosis

A

Slows heart rate like other beta blockers, but also reduces peripheral conversion of T4 to T3.

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68
Q

Indications for Radioactive Iodine in Hyperthyroidism

A

Second line after antithyroid medications.

Indicated in failed medical therapy or patients with contraindications to medical therapy

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69
Q

Hashimoto Thyroiditis Pathology/Pathophysiology

A

Antibodies to thyroid peroxidase drive CD8 T lymphocyte and Th1 lymphocyte response leading to thyroid gland destruction.

Lymphocytic infiltrates, plasma cells, new germinal follicles, colloid atrophy present in histology. Collagen deposition is a marker of longstanding disease.

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70
Q

What other Autoimmune conditions are associated with Hashimoto Thyroiditis?

A

Coeliac Disease
Type 1 Diabetes Mellitus
Vitiligo

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71
Q

Most common cause of hypothyroidism worldwide?

A

Iodine deficiency

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72
Q

Testing for Iodine Deficiency

A

Negative autoantibodies
High TSH, low T3/T4
24 hour urinary iodine post oral iodine loading will be low (as iodine is retained rather than excreted)

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73
Q

Complications of Iodine supplementation

A

Excessive replacement: hyperthyroidism (Jod-Basedow effect)

Wolff-Chiakoff effect: worsening of hypothyroidism initially due to transient downregulation of iodine uptake in follicular cells due to sudden rise in iodine concentration.

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74
Q

Threshold to treat subclinical hypothyroidism

A

TSH >10

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75
Q

What peripheral tissues can convert T4 to T3?

A

Liver
Kidneys
Skeletal muscle

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76
Q

Drug Causes of Graves’s Disease

A

Alemtuzumab (Humanised anti CD52)
Anti-retroviral therapy

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77
Q

Drugs that can influence TFT results

A

Amiodarone (High TSH, high T4, low T3)
Carbamazepine (low T4 and T3)
Enoxaparin (High T4 and T3)
Heparin (High T4 and T3)
Phenytoin (Low T3)
Biotin (High T4, low TSH)

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78
Q

Lithium and thyroid function

A

Causes hypothyroidism with goitre.

Due to reduced pinocytosis which impairs thyroglobulin release. Accumulates in cells and results in goitre formation.

Not linked to therapeutic range/dose. More common in women, prolonged use, TPO antibodies.

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79
Q

Common causes of impaired Thyroxine absorption

A

PPI
Antacid
Calcium carbonate
Alcohol
Soy
Milk

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80
Q

Features of a Pituitary Microadenoma

A

<1cm in diameter
Monoclonal
Majority are non functioning
<5% enlarge
Hypodense after gadolinium, due to reduced blood supply

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81
Q

Features and assessment of Pituitary Macroadenoma

A

> 1cm in diameter
To assess for function: Prolactin, TSH, fT4, Urinary Free Cortisol, IGF-1
Assess visual fields for mass effect

82
Q

What does visual field defect indicate in assessment of pituitary adenoma?

A

Macroadenoma

83
Q

What is the most likely aetiology of a pituitary mass that causes diabetes insipidus?

A

Metastasis - mets mainly spread to the posterior pituitary, so DI is classic of metastatic spread to the pituitary

84
Q

Order of hormonal loss in hypopituitarism

A

GH, LH, FSH, TSH, ACTH

85
Q

Craniopharyngioma

A

Embryonic remnants of Rathke’s pouch
BRAF V600E mutation
Mostly in kids, but make up 1% of adult intracranial tumours
Often calcified, with cystic component

86
Q

Key mutations in Congenital Hypopituitarism

A

HesX-1
Pit-1 (GH, TSH, Prolactin)
Prop-1(Low GH, TSH, prolactin, FSH)

87
Q

Pituitary Apoplexy

A

Generally due to haemorrhage. Don’t bleed into normal pituitary
Can mimic SAH
Need to give steroid as acute ACTH deficiency can be life threatening
Key indication for surgery is visual impairment

88
Q

Radiotherapy and Pituitary function

A

Usually quite delayed, minimal in first 3 years
GH deficiency common, almost all at 5 years post
Then LH/FSH, ACTH, TSH

89
Q

Lymphocytic Hypophysitis

A

Key cause of primary hypophysitis
More common in women, and particularly during pregnancy or post partum.
ACTH deficiency most commonly

90
Q

Most common cause of immunotherapy related hypophysitis, and details

A

CTLA-4 (Ipilimumab)
(Some pituitary cells express CTLA-4)
ACTH most affected (ACTH only in PD1, total anterior pituitary in CTLA-4)
Visual field defects rare
DI is rare

91
Q

What is the key receptor present on Pituitary Adenomas that allows treatment?

A

Somatostatin receptor
SST2: Octreotide (GH)
SST5: Likely to respond to Pasireotide (ACTH, GH)
D2: Dopamine agonist

92
Q

Management of non functioning Pituitary Adenomas (PitNETs)

A

Asymptomatic don’t need anything acute if non functioning and vision normal
Transphenoidal pituitary surgery indicated if there are visual problems or enlarging
30% will regrow post surgery (more likely if silent corticotroph)
Post op RTx if regrowing post surgery
Medical therapy doesn’t work well for mass effect (doesn’t shrink tumour)

93
Q

Why does compression of the pituitary stalk lead to hyperprolactinaemia?

A

Compression of stalk → reduced dopamine flow to pituitary → reduced inhibition of prolactin secretion → hyperprolactinaemia

94
Q

What do the findings of a repeat MRI for a pituitary incidentaloma indicate?

A

If no growth on repeat MRI at 1 year, and remains non functioning, no further monitoring required

If any chiasmal compression or hypopituitarism

95
Q

What is the key complication of pasireotide?

A

Reduces insulin and incretin levels → hyperglycaemia in 33%

GLP agonists particularly effective in managing this

96
Q

What marker suggest poor response to Octreotide

A

High Ki-67 index

97
Q

Assessment of adult GH deficiency

A

IGF-1 is useful but not diagnostic, can be normal despite deficiency.

The more other hormones are deficient, the more likely GH is to be deficient (3 deficient = 96% chance GH deficient)

Stimulation testing: Glucagon response <3 (<1 if obese) diagnostic

98
Q

Impact of oral GH supplementation

A

Reduced cholesterol, improved cardiac function, improved quality of life, reduced body fat, improved insulin sensitivity.

No impact on cancer risk

Can increase conversion of cortisol to inactive form → may need glucocorticoid replacement

Oral oestrogens (e.g. women taking the pill) are relatively resistant to oral GH

99
Q

Key spurious and physiologic causes of hyperprolactinaemia (Things to rule out)

A

Macroprolactinaemia (prolactin bound together by Ig, increases half life in circulation)
Pregnancy
Drugs: Metoclopramide, Domperidone, Fluoxetine, Verapamil, Oestrogens

If no clinical sequelae, not pregnant and not on any causative drugs, check macroprolactin levels.

100
Q

Who do women present earlier with hyperprolactinaemia?

A

Women present earlier as menstrual cycle far more sensitive than testicular axis to changes in prolactin levels, and thus develop symptoms earlier.

Thus if men do present they typically present with a macroadenoma

101
Q

What intermediary hormone/signalling molecule is inhibited in hyperprolactinaemia?

A

Kisspeptin - inhibited by prolactin and thus reduces the usual pulsatile GnRH secretion → bloackade of oestrogen induced LH surge.

Reduced gonadal steroid production results.

102
Q

Which pituitary tumour is most common in MEN1, and what proportion of these tumours are part of MEN1 when they do occur?

A

Prolactinoma
10% of prolactinomas are part of MEN1

103
Q

Management of Prolactinaemia

A

Dopamine agonism key
Bind to D2 receptor → increased dopamine → reduced prolactin synthesis and release

Normalise prolactin levels and shrink tumour

Cabergoline: more specific to D2 receptor than bromocriptine
Can cause valvular heart fisease, so need TTE if higher doses
Impulse control disorder is significant issue, need to screen

Tumour shrinkage occurs within days so often can avoid surgery evenin in patients with visual field defects

20% can remain in remission after discontinuation of Cabergoline

104
Q

What electrolyte imbalances can mimic nephrogenic DI?

A

Hypercalcaemia and hypokalaemia can down regulate AQP2 channels → clinical picture similar to nephrogenic DI

105
Q

What additional activity does PTU have over Carbimazole?

A

Also reduces peripheral conversion of T4 to T3

106
Q

Which patients are most likely to go into remission with medical therapy for Graves Disease?

A

> 40 years old
Mild disease (fT4 <40)
Low TRAB levels (<3x ULM)
No goitre

107
Q

Key risk factors for PTU that mean Carbimazole is preferred

A

Hepatotoxicity can be fulminant with PTU
PTU can also induce an ANCA positive, Lupus like vasculitis

Only times PTU us preferred: 1st trimester pregnancy, Thyroid storm

Carbimazole can cause pancreatitis

108
Q

What is the key contraindication to Radioiodine therapy for Graves Disease?

A

Active Graves orbitopathy - radioactive iodine still stimulates TSH receptors, leading to worsening of gravers ophthalmopathy

109
Q

What is an additional therapy that can improve mild Graves Orbitopathy?

A

Selenium 100mcg BD

Other treatment for severe disease:
- IV Methylprednisolone
- Cyclosporin, RTX, Toci

110
Q

How does non toxic goitre progress?

A

Initially due to combination of genetic and environmental factors, typically relating to low iodine intake. Initially causes diffuse hyperplasia, but over time somatic mutations lead to focal epithelial proliferation and formation of nodules. These nodules may become hyper functioning (toxic) nodules which are autonomous → hyperthyroidism

111
Q

Management of Toxic Nodule Goitre and Toxic Adenoma (and post treatment outcomes)

A

Radioactive Iodine is treatment of choice, works very well

Rates of post op hypothyroidism are low because the remainder of the thyroid doesn’t take up the iodine due t low TSH

112
Q

Conditions that don’t show any uptake on Thyroid Scintigraphy

A

Thyroiditis, exogenous thyroid hormone excess, Iodine exposure

113
Q

Thyroiditis

A

Inflammation leads to release of thyroid hormone stores. No overproduction of thyroid hormones

114
Q

Wolff Chaikoff Effect

A

Expected response post iodine load - transient reduction in thyroid hormone production due to downregulation of sodium iodine transporter

Euthyroid state returns within 24-48hr

115
Q

Jod-Basedow Phenomenon

A

Pathological response to exogenously administered iodine.

Occurs in patients with impaired thyroid autoregulation

Results in thyrotoxicosis as thyroid can take up iodine autonomously

116
Q

Drug induced thyroid disorders

A

Alemtuzumab: reconstitution syndrome → Graves
ICI: Graves
TKI: Hypothyroidism

117
Q

When to treat subclinical hypothyroidism

A

Pregnancy
<70 years of age and TSH >10
All other situations unclear

Should send TPO antibodies - 60-80% actually have undiagnosed Hashimoto’s

118
Q

Subclinical Hyperthyroidism

A

Mild: TSH 0.1-0.4; Severe <0.1
Increases risk of cardiac mortality and AF as well as fracture risk
Treat if: TSH <0.1, also consider when mild if >65 or known cardiac disease

119
Q

What occurs in sick euthyroid?

A

Impaired peripheral conversion of thyroxine, and reduced TSH, so everything usually low initially

No treatment required, no evidence of benefit for thyroid replacement. Just repeat once well

120
Q

Why are higher doses of thyroxine needed during pregnancy?

A

Some increased demand, but also higher thyroid binding globulin, meaning more needed to saturate this and have normal functional free thyroid hormone

121
Q

Leading cause of mortality in Myxoedema coma?

A

Respiratory failure

122
Q

Leading cause of adrenal insufficiency?

A

Autoimmune Adrenalitis >90%
Key HLA: DR3-DQ2, DR4-DQ8
Driven by CD8+ T cells, reacting against 21-hydroxylase

60% is autoimmune polyendocrine syndrome
AIRE gene mutation
Accompanied by hypoparathyroidism, candidiasis (type 1)
Autoimmune thyroid disease and T1DM (type 2)

123
Q

Adrenal insufficiency + Neurological features

A

Adrenoleukodystrophy

124
Q

Why is TSH high in adrenal insufficiency?

A

Loss of cortisol’s inhibitory effect

125
Q

Testing for Adrenal Insufficiency

A

Normal Synacthen, high ACTH, low Aldosterone, high renin, low DHEAS, 21-hydroxylase antibodies,

Ab negative: check VLCFA in males, image adrenal for mets, TB, lymphoma, APLS Ab

126
Q

Critical Illness Corticosteroid Insufficiency

A

Prolonged high cortisol, plus opioids and possibly steroid use lead to significant suppression of ACTH.

Over time response blunted, can’t then stimulate cortisol release

Clinical diagnosis, no good testds

127
Q

Key investigation for Congenital Adrenal Hyperplasia

A

17-hydroxyprogesterone

Mutation of CYP21A2 gene, leading to 21-hydroxylase deficiency

Loss of cortisol and if severe aldosterone

Can be salt wasting, and need mineralocorticoid replacement to manage this

128
Q

Primary Hyperaldosteronism

A

Most common cause of secondary hypertension
Increasess risk of: stroke, MI, CCF, AF, renal impairment

Mx: Adrenalectomy for unilateral hyperaldosteronissm. MRA for bilateral forms

Majority is bilateral hyperplasia

Only 25% have hypokalaemia. If present need to correct before doing aldosterone:renin ratio, as hypokalaemia suppresses aldosterone production

129
Q

Aldosterone:renin ratio and impact of different medications

A

Raised ratio = hyperaldosteronism
Stop diuretics and spiro 6 weeks before testing
Others 2-4 weeks prior

Beta blockers: decrease renin (can cause false positive)
ACEi: drop Aldosterone, increase Renin (false negative)
Diuretics: increase renin (false negative)
DHP CCB: decrease aldo, increase renin (false negative)

So all cause false negatives except beta blockers

Agents to use: non DHP CCB, Prazosin, Hydralazine, moxonidine

130
Q

Confirmatory testing for hyperaldosteronism

A

ARR has poor specificity, so confirmatory testing important
Can skip if: hypokalaemia, undetectable plasma renin, plasam aldo >550

IV Saline test → Aldosterone >171
Captopril test: Aldosterone drops, renin rises, ARR reduced

Then do CT: if unilateral adenoma and patient <35, presume functioning. Can identify carcinomas, and find hyperplasia which just needs medical mnagement.

Adrenal venous sampling otherwise - gold standard for subtyping

131
Q

Familial Hyperaldosteronism

A

Rare, but type 1 can be treated with dex, so important to be aware of
Check if PA in very young patient
CYP11B1, CYP11B2

132
Q

Target for medical management of bilateral adrenal hyperplasia

A

Not used for secretory adenoma (Surgery better, though no mortality benefit).

Aim for normal BP, normal K, normal plasma renin

133
Q

Predominant type of adenoma when found incidentally

A

Non functioning (75%)
Of remaining functional, cortisol producing most common

134
Q

Adrenal mass and metastasis

A

Only time biopsy is indicated (once phaeo excluded)
An adrenal mass found in a patient with history of malignancy will be a met in 20% of cases

135
Q

Management of suspicious adrenal lesion

A

Adrenalectomy usually
Can do biopsy if high likelihood of met

136
Q

Confounders when testing metanephrines

A

TCAs, SNRI, MAOI, Levodopa, Methyldopa, CCB, Beta blockers, labetalol, Caffeine, Paracetamol, Mesalazine, Sulfasalazine

If not >3x ULN with these medicatiosn avoided, do Clonidine suppression test

137
Q

Normetanephrine vs metanephrine

A

Normetanephrine higher when lesion is extra-adrenal. i.e. Paraganglioma

138
Q

Management of phaeochromocytoma

A

Surgery, but need to control hormones first to avoid haemodynamic instability.

Give alpha blockade before beta blockade, but do give both
To prevent unopposed alpha activity which can cause circulatory collapse

Metastatic disease: chemotherapy or radiotherapy options

139
Q

Mutations in Phaeochromocytoma

A

SDHB, SDHD, VHL, RET, NF1

Plus associated with MEN-2

140
Q

Benefit of 1mg overnight dex suppression test

A

High NPV, useful in shift workers, best test for cortisol secreting adrenal adenomas.

141
Q

When to do 24hr urinary free cortisol

A

Pregnancy, on OCP, on Carbamazepine, Malabsorption

142
Q

Highly specific test for Cushing’s Disease

A

Desmopressin test: ACTH secreting adenomas express vasopressin V1b receptors, prodsucing an increase in plasma ACTH concentration after desmopressin injection

143
Q

Next steps once Cushing’s Syndrome confirmed

A

ACTH:
High → image pituitary → inferior petrosal sinus sampling
Low → image adrenals

Can do CRH levels, Desmopressin test, etc. if MRI pituitary shows large mass, to confirm this is the cause

144
Q

Location of ectopic ACTH producing NETs

A

Neck and Chest mostly

145
Q

Management and Recurrence of Cushing’s Syndrome causes

A

Cushing’s Disease: pituitary surgery → repeat surgery or medical therapy or radiotherapy
Ectopic Cushing’s: surgery if possible
Adrenal adenoma: Adrenalectomy, unusual to recur unless carcinoma → poor prognosis

146
Q

Pathophysiology of PCOS and blood test results

A

ABnormality of GnRH pulsatile release → Increased LH release → raised LH/FSH ratio
Insulin resistance due to obesity
Ovulatory dysfunction → hyperandrogenism, follicular arrest
Low oestrogen, high testosterone is result

Bloods: Raised testosterone, low SHBG, raised DHEAS, raised LH/FSH ratio, elevated AMH (this isn’t in diagnostic criteria)

OGTT is best test in PCOS for diabetes

147
Q

What to exclude when trying to diagnose PCOS

A

CAH: 17OH progesterone (<6 = excluded)
Hyperprolactinaemia
Cushing’s Syndrome, 24h UST, DST
Acromegaly: IGF-1
Hypothyroidism
Androgen secreting tumours: imaging

148
Q

Most effective means to induce ovulation in PCOS

A

Letrozole (i.e. Aromatase Inhibitor)

149
Q

Functional Hypothalamic Amenorrhoea

A

Absence of menses due to stress, weight loss, xercise
No identifiable anatomic/organic cause
Under or normal weight
GnRH pulsatility suppressed → high cortisol, low/N TSH, low T3, low IGF-1, low leptin, low FSH, low LH, low oestrogen
Low bone density
FGFR1 most common gene associated with risk

Need to exclude pregnancy
Check prolactin and pituitary function
Provera challenge to exclude PCOS (get withdrawal bleed if PCOS), no bleed with FHA

Weight gain is key management
Calcium and Vit D for Osteoporosis

150
Q

Primary Ovarian Insufficiency

A

Essentially menopause early, <40 years of age
Diagnosis: raised FSH in menopausal range (usually >40) on ≥2 occasions
Most cases idiopathic/unknown, but can be induced by chemo, radiotherapy, Fragile X, autoimmune (autoimmune polyendocrine syndrome 1 and 2)

Tests: raised FSH, low oestradiol, FMR-1 for Fragile X,

Management: HRT, donor oocytes for fertility
Spontaneous pregnancy can occur

151
Q

46XY Complete Gonadal Dysgenesis

A

Essentially should be male based on karyotype, but SRY gene on Y chromosome not working → female phenotype, but ovaries don’t develop properly as need both X chromosomes for this → have female external genitalia but only gonadal streak

Leads to primary amenorrhoea

Gonadal streaks need to be removed
High FSH and LH
Low Oestradiol
Normal testosterone

Management: HRT → development of secondary female sex characteristics, remove streak gonads, assisted reproduction

152
Q

Complete Androgen Insensitivity Syndrome

A

Female external genitalia, but no internal structures as mullerian inhibitory factor present to block this. Testis present → tesotsterone aromatased → normal breast development
46XY karyotype, normal or high testosterone, LH normal or high

153
Q

Turner Syndrome

A

1:2500 live female births
Loss of whole or part of X chromosome → 45X most common karyotype
Short stature
90% have ovarian failure

Oocytes lost rapidly, all lost by puberty → infertile

Bicuspid aortic valve (16%), Coarctation of aorta (11%)
30% hypothyroidism
Hypertension
SNHL
Renal tract abnormalities
Diabetes

Give GH, HRT

154
Q

Use of HRT in Menopause

A

Is risk of breast cancer with long term use, as well as cardiovascular disease
If used in patients <60 without history of CVD, Breast rCa, VTE → risks minimised
Generally can use safely if within 10 years of menopause

Need E and P to prevent endometrial cancer

SSRIs can be useful

155
Q

Kallman Syndrome

A

Hypogonadotrophic hypogonadism + anosmia
Men
ANOS1 or KAL1 X lnked recessive
GnRH and Olfactory neurons don’t work properly

Presents at puberty

Check for renal agenesis, SNHL

lfactory bulkb/tract absent on MRI
HRT with testosterone → induced puvberty
Induction spermatogenesis
Can recover spontaneously

156
Q

Klinefelter Syndrome

A

47XXY, or 46XY/47XXY mosaic
Tall, feminized physique, mild IQ impairment, poor beard growth, bresst development

Raised FSH and LH, low testosterone

Associated with T2DM, Osteoporosis, Thyroid disease, ILD, Breast cancer

Mx: Testosterone, increased risk of chromosomal abnormalities in offspring

157
Q

What needs to be excluded prior to commencing testosterone replacement for male hypogonadism?

Other risks

A

Prostate Cancer

Doesn’t increase risk of cardiovascular disease, but can cause polycythaemia

158
Q

Phases of Menstrual Cycle

A

Median length 28 days
Follicular phase: 1st day of menses to ovulation. Oestradiol levels secreted by developing follicles → stimulates LH surge → ovulation
Ovulation
Luteal phase: corpus luteum formed post ovulation, secretes progesterone which stimulates endometrial growth

159
Q

Key hormone for diagnosis of CAH (and hormone deficient)

A

Test 17-OH progesterone
But 21 hydroxylase is what’s lost → prevents conversion of 17-OH progesterone into cortisol and progesterone into aldosterone in most severely affected patients

Steroid replacement for management

160
Q

In what form is the majority of calcium in the body?

A

Ionised

161
Q

Calcium reabsorption

A

Passive paracellular reabsorption in PT and TAL (90%)
- Calcium sensing receptor regulates calcium absorption in TAL
- This reabsorption is tied to Mg reabsorption
Active reabsorption in DCT (10%) - mediated by PTH

162
Q

Familial Hypocalciuric Hypercalcaemia

A

Inactivating mutation of Calcium Sensing Receptor → doesn’t stop calcium reabsorption (in kidneys), doesn’t turn of PTH production (in parathyroids)

Leads to mild-moderate PTH dependent hypercalcaemia

AD inheritance. CaSR gene, G alpha 11 gene

Key for diagnosis: Inappropriately low urinary calcium excretion
Hypermagnesaemia common
Doesn’t cause kidney stones or osteoporosis another key differentiator

163
Q

PTH action on kidney

A

Stimulates transcellular calcium reabsorption in DCT
Phosphate excretion in PT
Stimulates 1-alpha-hydroxylase → 1,25 Vit D synthesis

164
Q

FGF23

A

Key regulator of phosphate levels
Levels rise when phosphate rises, blocking PT reabsorption, and downregulates bone resorption
Decreases PTH synthesis

Release stimulates by: PTH, phosphate levels, 1,25 Vit D

165
Q

What cells produce PTH?

A

Parathyroid chief cells

166
Q

Benefits of Parathyroidectomy

A

Reduced fracture risk
Reduced kidney stones
Slows progression of CKD

Indications: Renal involvement key, CRCl <60, nephrolithiasis, nephrocalcinosis

167
Q

Routine imaging for parathyroids

A

Ultrasound and Technetium 99 sestamibi to identify location of nodes and any enlargement

168
Q

Non operative options for management of hyperparathyroidism

A

Bisphosphonates if only issue is reduced BMD. Improves BMD as much as PTx

Cinacalcet for those unfit for surgery with severe/symptomatic hypercalcaemia. Doesn’t improve BMD. Stimulates CaSR.

169
Q

Romosozumab mechanism and other detail

A

Inhibits sclerostin → increased bone formation, reduced resorption

Contraindicated with history of MI/Stroke

Used only when people have very poor BMD despite being on another antiresoprtive agent and still having fractures

170
Q

Osteoblasts

A

Form bone, can be inhibited by high PTH levels
ALso make hydroxyappatite, important for bone mineralisation

171
Q

Osteocytes

A

Osteoblasts initially, that get trapped in cortical bone and then become osteocytes

At baseline secrete sclerostin, inhibiting bone formation (i.e. block Osteoblast activity). With mechanical stress to bone, sclerostin production stops → bone remodelling to respond to stress

Produce RANKL which stimulates osteoclastogenesis and increases bone resorporption

172
Q

Osteoclast

A

Bone resorption
Formation and activation stimulated by osteoblasts/osteoclasts via RANKL

RANKL activity stimulated by PTH and Vitamin D

RANK on osteoclasts precurors stimulated.

Osteoprotegerin is a soluble decoy receptor for RANKL, so increased level blocks osteoclast activation (Denosumab mimics this)

173
Q

Oral calcium and peak bone mass

A

Small benefit

174
Q

Who to treat for osteoporosis

A

T score < -2.5
Fracture of hip or vertebra regardless of T score
Osteopaenia at femoral neck or total hip with 10 year FRAX risk ≥3% or MOF risk ≥20%
Osteopaenia with other fragility fractures (wrist, pelvis, proximal humerus)

175
Q

Role of Trabecular Bone Score

A

Assess actual microstructure of the bone, can adjust FRAX probability of fracture

176
Q

Role of Z score in Osteoporosis

A

For assessment of secondary causes of osteoporosis, by comparing to expected for age: If within 2 SD of expected, unlikely to have secondary osteoporosis

177
Q

Role of bone turnover markers and bisphosphonate use

A

Crosslaps (CTX) should be low when on bisphosphonates
Should be used to monitor effect
Can use CTX, ALP, P1NP to monitor for wearing off of effect during bone holiday

178
Q

Which patients should receive calcium and Vitamin D supplements

A

Those on bisphosphonates, and those in RACF. Plus Vit D for those who are deficient in community, and calcium for those without adequatedietary calcium. But if levels normal, not required.

179
Q

Bisphosphonate mechanism

A

Inhibit osteoclast activity by inducing osteoclast apoptosis

180
Q

When to repeat DEXA post antiresorptive commencement

A

Need to wait at least 2-3 years, otherwise won’t necessarily have seen benefit

181
Q

Compare fractures related to bisphosphonate (atypical femoral fractures) and fractures related to osteomalacia

A

Bsiphosphonate fractures begin at lateral cortex
Osteomalacia medial cortex

182
Q

Denosumab side effects

A

Osteonecrosis of jaw, atypical femoral fracture
Cellulitis and Eczema are classic issues
Rapid loss of BMD if stopped without replacement

183
Q

Key serious risk of Teriparatide

A

Osteosarcoma

184
Q

Physiologic function of Sclerostin

A

Binds to Wnt to block Osteoblast formation -> reduced bone formation

185
Q

Mechanism of Romosozumab

A

Inhibits sclerostin activity -> stimulates bone formation, inhibits bone resorption
Possible increase in cardiovascular risk
Used in patients with severe osteoporosis, still having fractures despite antiresorptive therapy
Reduces risk of vertebral and hip fractures

186
Q

Mechanism of steroid induced osteoporosis

A

Glucocorticoids inihibit osteoblastogenesis and also damage osteocytes -> reduced bone formation, and reduced remodelling in response to mechanical stress = poor quality bone

So someone on steroids will have lower bone quality and strength than someone not on steroid with same BMD

187
Q

Who to treat for steroid related osteoporosis?

A

Previous fracture OR age >70 OR Prednisolone dose >7.5mg/day
If not previous fracture, age <70 or Pred dose <7.5mg/day, then treat if T score < -2.5, FRAX MOF >20% or Hip Fracture >3%

Bisphosphonates first line, but Denosumab and Teriparatide also work

188
Q

Role of testosterone replacement in hypogonadism for osteoporosis

A

Testosterone treatment doesn’t lower incidence of fracture compared to placebo

189
Q

When to use calcium citrate over calcium carbonate?

A

When patient is on a PPI. Carbonate required stomach acid to assist with absorption and should be taken with food.

190
Q

Vitamin D and calcium absorption

A

Vitamin D promotes active transcellular absorption via TRPV channels in proximal small intestine

191
Q

Paget’s Disease of the Bone

A

Consider with isolated ALP rise
Only treat if symptomatic or in high risk location

192
Q

Waist circumference cut offs

A

Men: 102cm
Women 88cm

193
Q

Basal Metabolic Rate and obesity

A

Rising as weight increases, not decreasing. Makes up 50-70% of total daily energy expenditure

194
Q

Leptin

A

Secreted by white adipose tissue
Low leptin drives appetite
Overweight individuals are resistant to Leptin, so body thinks it has low levels

195
Q

Ghrelin

A

Orexogenic - released during fasting to stimulate appetite
Released by Oxyntic glands in fundus and body of stomach
Increases with fasting
Increases gastric emptying

196
Q

GLP-1

A

Anorexigenic - released post prandially and induce satiety
Secreted by enteroendocrine L cells
Release stimulated by presence of food in small intestine
Stimulates insulin release, decreases gastric emptying and increases beta cell mass

197
Q

CCK

A

Anorexigenic - released post prandially and induce satiety
Secreted by Intestinal I cells when fat and protein in duodenum
Also stimulates gall bladder contraction, slows gastric emptying and promotes pancreatic enzyme secretion

198
Q

Pancreatic Polypeptide

A

Anorexigenic - released post prandially and induce satiety
Secreted by pancreatic F cells in presence of food, particularly high protein content
Regulates pancreatic exocrine secretion, modules gastric acid release and GI motility

199
Q

Neurohormonal mechanisms and bariatric surgery

A

Key mechanism for effect - essentially get food into small intestine earlier = earlier release of satiety hormones

200
Q
A

BPT (16 decks)

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