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Endocrine Flashcards

1
Q

hyperthyroidism definition

A

over-production of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), by the thyroid gland

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2
Q

thyrotoxicosis definition

A

refers to effects of an abnormal and excessive quantity of thyroid hormones in the body

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3
Q

primary hyperthyroidism

A

due to thyroid pathology
thyroid is behaving abnormally and producing excessive thyroid hormone

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4
Q

secondary hyperthyroidism

A
  • pathology in the hypothalamus or pituitary
  • pituitary gland produces too much thyroid-stimulating hormone, stimulating the thyroid gland to produce excessive thyroid hormones.
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5
Q

subclinical hyperthyroidism

A
  • thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low)
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6
Q

what is grave’s disease?

A
  • an autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism
  • These TSH receptor antibodies stimulate TSH receptors on the thyroid
  • most common cause of hyperthyroidism
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7
Q

what is Toxic multinodular goitre?

A
  • a condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones
  • It is most common in patients over 50 years.
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8
Q

which hormones are released by anterior pituitary

A

FLAT PEG

  • FSH
  • LH
  • Adrenocorticotropic hormone (ACTH)
  • Thyroid-stimulating hormone (TSH)
  • Prolactin
  • Growth hormone (GH)
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9
Q

briefly outline the thyroid axis?

A
  1. hypothalamus releases thyrotropin-releasing hormone (TRH)
  2. TRH stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH)
  3. TSH stimulates the thyroid gland to release triiodothyronine (T3) and thyroxine (T4)

NB hypothalamus and anterior pituitary respond to T3 and T4 by suppressing the release of TRH and TSH = negative feedback

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10
Q

which hormones are release by posterior pituitary?

A

Oxytocin
Antidiuretic hormone (ADH)

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11
Q

briefly summarise the growth hormone axis

A
  1. hypothalamus produces growth hormone-releasing hormone (GHRH)
  2. GHRH stimulates the anterior pituitary to release growth hormone (GH)
  3. Growth hormone stimulates the release of insulin-like growth factor 1 (IGF-1) from the liver
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12
Q

what hormone inhibits growth hormone release from anterior pituitary?

A

somatostatin

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13
Q

what does insulin-like growth factor do?

A
  • stimulates fat breakdown
  • releases glucose from liver
  • cell division
  • protein synthesis
  • increased bone density
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14
Q

causes of hyperthyroidism?

A

G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule - usually benign adenoma
T – Toxic multinodular goitre

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15
Q

causes of thyroiditis (gland inflammation that causes hyperthyroid then hypothyroid) ?

A
  • DeQuervain’s - transient inflammation of thyroid after viral infection
  • Hashimoto’s
  • Post-partum
  • Drug-induced - amiodarone, iodine, lithium
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16
Q

Hyperthyroidism Px

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination

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17
Q

Graves specific Px ?

A

Diffuse goitre (without nodules)
Graves’ eye disease, including exophthalmos (eye bulging)
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)

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18
Q

Hyperthyroidism Ix

A
  • TFTs - high T3/4, TSH low (high in 2ndary)
  • Thyroid ABs - TSHR-Ab, TPO-Ab, TgAb
  • CRP / ESR - thyroiditis
  • baseline FBC, U/E
  • US thyroid - if lump
  • thyroid isotope scan
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19
Q

Hyperthyroidism Mx

A

1st line = carbimazole (start high, titrate down, block and replace by adding lego)
2nd line = propylthiouracil

  • radioactive iodine
  • subtotal / total thyroidectomy

beta blockers can be used for symptom control

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20
Q

possible side effects of carbimazole?

A

risk of:
- neutropenia
- agranulocytosis
- congenital malformations

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21
Q

What is a thyrotoxic crisis (aka thyroid storm) and how do you manage it?

A
  • rapid T4 increase / release
  • eg stress, infection, surgery, stopping anti-thyroid drugs

Px
- high temp, tachy, restless, delirium, coma, death

Mx
- IV fluids, corticosteroids, BBs, carbimazole / propylthiouracil
- potassium iodide

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22
Q

what is hypothyroidism? define primary and secondary?

A

Low TH - T3/4

Primary - thyroid gland disease - T3/4 low, TSH high

Secondary - disease of hypothalamus / pituitary - T3/4 low, TSH low

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23
Q

Causes of primary hypothyroidism

A

Primary:
1. Hashimoto’s - autoimmune inflammation
2. iodine deficiency
3. hyperthyroidism Tx
4. lithium

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24
Q

Causes of secondary hypothyroidism

A

Secondary:
1. Tumours (e.g., pituitary adenomas)
2. Surgery to the pituitary
3. Radiotherapy
4. Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
5. Trauma

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25
Q

what antibodies are associated with Hashimoto’s?

A
  • anti-thyroid peroxidase (anti-TPO) antibodies
  • anti-thyroglobulin (anti-Tg) antibodies
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26
Q

what is Sheehan’s syndrome?

A

major post-partum haemorrhage causes avascular necrosis of the pituitary gland leading to hypopituitarism

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27
Q

Hypothyroidism Px

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

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28
Q

Hypothyroidism Ix

A
  • TFTs
  • thyroid ABs - anti-TPO, anti-Tg
  • FBC - anaemia
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29
Q

Hypothyroidism Mx

A
  • levothyroxine
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30
Q

Myoxedema coma

A
  • severe hypothyroidism

Px
- confusion, coma, hypothermia, hypoglycaemia, hyponatraemia

Mx
- T3/4 replacement (T3 causes arrhythmias)
- IV glucose
- hydrocortisone if needed
- fluids / supportive care

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31
Q

describe the renin-angiotensin aldosterone system

A

1) low bp sensed by juxtaglomerular cells in afferent arterioles of kidneys stimulating renin secretion

2) renin converts angiotensinogen (from liver) to angiotensin 1

3) angiotensin 1 converted to angiotensin 2 by ACE (released by lungs)

4) angiotensin 2 stimlates aldosterone secretion from adrenals

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32
Q

what are the actions of aldosterone?

A
  • increase Na reabsorption
  • increased K secretion from distal tubules
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33
Q

adrenal axis: mechanism of glucocorticoid release?

A

stress and time of day (AM) stimulate hypothalamus to secrete corticotropin-releasing hormone (CRH)

CRH stimulates anterior pituitary to secrete adrenocorticotrophic hormone (ACTH)

ACTH stimulates adrenals to secrete glucocorticoids (cortisol, cortisone, corticosterone)

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34
Q

6 actions of cortisol?

A

1 - stimulates metabolic rate
2 - increases alertness
3- increases sodium and water reabsorption
4 - increases blood sugar levels
5 - inhibits immune system
6 - inhibits protein synthesis / bone formation

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35
Q

What is cushing’s syndrome ?

A

refers to signs and symptoms of prolonged high levels of glucocorticoids in the body.

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36
Q

Cushing’s disease?

A

refers to a pituitary adenoma secreting excessive adrenocorticotropic hormone (ACTH), which stimulates excessive cortisol release from the adrenal glands

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37
Q

Causes of cushing’s syndrome ?

A

C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
P – Paraneoplastic syndrome
E – Exogenous steroids (patients taking long-term corticosteroids)

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38
Q

Cushing’s features?

A
  • Round face (known as a “moon face”)
  • Central obesity
  • Abdominal striae (stretch marks)
  • Enlarged fat pad on the upper back (known as a “buffalo hump”)
  • Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
  • Male pattern facial hair in women (hirsutism)
  • Easy bruising and poor skin healing
  • Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)

may also see: HTN, T2DM, osteoporosis, dyslipidaemia, mental health problems

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39
Q

Cushing’s Ix

A
  1. low dose dexamethasone suppression test to confirm cushing’s
  2. high dose dexamethasone suppression test to determine cause of Cushing’s
  3. FBCs and U&Es
  4. MRI/ CT TAP
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40
Q

what are the low/high dose dexamethasone suppresion tests?

A

low dose
- give 1mg dex at night and measure ACTH and cortisol in the AM. dex will normally suppress cortisol so failure to suppress suggests Cushing’s

high dose
- give 8mg dex at night and measure ACTH and cortisol in the AM. high dos is enough to suppress cortisol caused by pituitary adenoma (cushing’s disease) but not if due to adrenal adenoma / ectopic ACTH

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41
Q

Cushing’s Mx

A
  • stop steroids
  • Cushing’s - transsphenoidal resection of adenoma
  • Adrenal adenoma - adrenalectomy
  • adrenal carcinoma - surgery / radio / mitotane
  • ectopic ACTH - surgery / metyrapone / ketoconazole
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42
Q

Nelson’s syndrome

A

development of an ACTH-producing pituitary tumour after the surgical removal of both adrenal glands due to a lack of cortisol and negative feedback. It causes skin pigmentation (high ACTH), bitemporal hemianopia and a lack of other pituitary hormones

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43
Q

Hyperaldosteronism: primary versus secondary

A

excess aldosterone

Primary
- adrenals producing too much aldosterone, renin low due to high BP

Secondary
- high renin levels leading to high aldosterone

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44
Q

Causes of hyperaldosteronism: primary and secondary

A

Primary
- Adrenal adenoma - Conn’s syndrome
- bl adrenocortical hyperplasia (more common)

Secondary
- reduced renal perfusion e:g
- renal artery stenosis
- HF
- liver cirrhosis / ascites

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45
Q

Hyperaldosteronism Px

A
  • asym
  • HTN, headaches, flushing
  • metabolic alkalosis - H secretion
  • hypokalaemia - weakness, cramps, paraesthesia, polyuria, polydipsia, constipation, arrhythmias
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46
Q

Hyperaldosteronism Ix

A

1) aldosterone-to-renin ratio (ARR)
2) Raised blood pressure (hypertension)
3) Low potassium (hypokalaemia)
4) Blood gas analysis (alkalosis)
5) CT / MRI
6) renal artery imaging - eg doppler, angiography
7) adrenal vein sampling - which adrenal gland is producing more aldosterone

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47
Q

aldosterone-to-renin ratio (ARR) results in primary versus secondary hyperaldosteronism

A

High aldosterone and low renin indicate primary hyperaldosteronism
High aldosterone and high renin indicate secondary hyperaldosteronism

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48
Q

Hyperaldosteronism Mx

A
  • oral spironolactone or eplerenone

Surgical removal of the adrenal adenoma
Percutaneous renal artery angioplasty via the femoral artery to treat renal artery stenosis

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49
Q

adrenal insufficiency defintion

A

underproduction of adrenal cortex hormones - mineralocorticoids (aldosterone) and glucocorticoids (cortisol)

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50
Q

primary adrenal insufficiency: pathology site and causes?

A

damage to adrenal glands means not enough hormones are produced

causes: Addison’s, infection, surgery, malignancy

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51
Q

secondary adrenal insufficiency: pathology site and causes?

A

damage to pituitary (so not enough ACTH)

causes: pituitary adenoma, Sheehan’s syndrome, pituitary injury (infection/surgery/malignancy)

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52
Q

tertiary adrenal insufficiency: pathology site and causes

A

inadequate CRH release from hypothalamus

causes:
cessation of long term steroid use (>3m)

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53
Q

what is Sheehan’s?

A

major post-partum haemorrhage causes avascular necrosis of the pituitary gland

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54
Q

Adrenal insufficiency presentation?

A
  • tanned, toned, tired, tearful
  • fatigue, muscle weakness, cramps, dizziness, fainting, thirst, wt loss, abdo pain, N+V, depression, reduced libido, vitiligo, bronze hyperpigmentation, postural hypotension
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55
Q

what do you see bronze pigmentation in adrenal insufficiency?

A

ACTH stimulates melanocytes to produce melanin

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56
Q

Adrenal insufficiency Ix

A

1) bloods
2) short synacthan test
3) ACTH test
4) adrenal autoantibodies
5) CT/MRI of adrenals or MRI pituitary

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57
Q

autoantibodies that may be present in autoimmune adrenal insufficiency?

A

Adrenal cortex antibodies
21-hydroxylase antibodies

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58
Q

biochemical findings you might see in someone with adrenal insufficiency?

A

Hyponatraemia (low sodium)
Hyperkalaemia (high potassium)
Hypoglycaemia (low glucose)
Raised creatinine and urea due to dehydration
Hypercalcaemia (high calcium)

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59
Q

what is the short synacthan test?

A
  • give dose of synthetic ACTH
  • check blood cortisol before and 30 mins after dose
  • cortisol level should double

failure to double suggests Addison’s or significant adrenal atrophy due to secondary insufficiency

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60
Q

Adrenal insufficiency Mx

A
  • hydrocortisone (double when ill) = glucocorticoid replacing cortisol
  • fludrocortisone = mineralocorticoid replacing aldosterone
  • steroid card, ID tag, IM hydrocortisone
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61
Q

Adrenal crisis

A
  • acute severe adrenal insufficiency - eg infection, trauma

Px
- low GCS, hypotension, low BMs, low Na, high K

Mx
- IM/IV hydrocortisone (100mg stat), IV fluids, IV dextrose

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62
Q

Acromegaly

A
  • excess GH in adults due to pituitary adenoma (most common) or ectopic production of hormones involved in growth hormone axis (GH/ GHRH) (usually cancer e.g. lung/pancreas)
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63
Q

what visual field defect might be seen with a pituitary tumour?

A

bitemporal hemianopia

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64
Q

Acromegaly Px

A

Excess growth hormone causes tissue growth:
- Prominent forehead and brow (frontal bossing)
- Coarse, sweaty skin
- Large nose
- Large tongue (macroglossia)
- Large hands and feet
- Large protruding jaw (prognathism)

Additional features include:
- headaches
- Hypertrophic heart
- Hypertension
- Type 2 diabetes
- Carpal tunnel syndrome
- Arthritis
- Colorectal cancer

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65
Q

Acromegaly Ix

A
  • IGF-1 = raised
  • growth hormone suppression test = 75g glucose drink with growth hormone tested at baseline and 2 hours following the drink.Glucose should suppress GH level. Failure to suppress GH suggest acromegaly.
  • MRI pituitary
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66
Q

Acromegaly Mx

A
  1. surgical = transsphenoidal resection of adenoma
  2. medical = IM octreotide (somatostatin analogue)
    - oral cabergoline, bromocriptine (dopamine agonist)
    - SC pegvisomant (GH receptor antagonist)
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67
Q

growth hormone deficiency: Px, Ix and Mx

A

Px = small physical features, low energy levels, short stature

Ix = low IGF-1

Mx = daily injections of recombinant human growth hormone

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68
Q

T1DM

A

Autoimmune destruction of beta cells in pancreas leading to lack of insulin production and a high blood glucose

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69
Q

T1DM Px

A
  • DKA
  • polyuria
  • polydipsia
  • wt loss
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70
Q

ideal blood glucose ?

A

4.4 – 6.1 mmol/L.

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71
Q

where is insulin produced?

A

beta cells in the Islets of Langerhans in the pancreas

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72
Q

how does insulin work?

A

insulin causes:
- cells to take up glucose from blood
- prompt muscle/liver cells to absorb glucose and store it a glycogen (glycogenesis)

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73
Q

where is glucagon produced?

A

alpha cells in the Islets of Langerhans in the pancreas

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74
Q

how does glucagon work?

A
  • released in response to low blood glucose / stress
  • prompts liver to breakdown glycogen to release as glucose = glycogenolysis
  • prompts liver to convert fat/protein into glucose = gluconeogenesis
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75
Q

T1DM Ix

A
  • usually clinical
  • urine dip for glucose and ketones
  • fasting glucose and random glucose
  • ? c-peptides - not routine
  • ? autoantibodies to distinguish T1 and T2
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76
Q

fasting and random blood glucose thresholds in T1DM

A

if symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l

random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test

asymptomatic? as above but on 2 separate occasions

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77
Q

T1DM Mx

A
  1. Subcutaneous insulin
  2. Monitoring dietary carbohydrate intake
  3. Monitoring blood sugar levels upon waking, at each meal and before bed
  4. Monitoring for and managing complications, both short and long term

S/C insulin
- ideal is basal-bolus regime

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78
Q

T1DM: what is a basal bolus regimen

A
  • Background, long-acting insulin injected once a day
  • Short-acting insulin injected 30 minutes before consuming carbohydrates (e.g., at meals)
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79
Q

T1DM: what is an insulin pump?

A

pumps that continuously infuse insulin at different rates to control blood sugar levels. They are an alternative to basal-bolus regimes

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80
Q

T1DM sick day rules

A
  • Don’t stop insulin
  • Check BMs more frequently
  • Consider checking ketones
  • Maintain normal meal pattern if possible - carb drinks if necessary
  • Drink plenty fluids
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81
Q

T1DM complications: macrovascular + acute complications

A
  • atherosclerosis
  • stroke
  • IHD
  • PVD

Acute
- DKA, HHS, hypos

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82
Q

T1DM complications: microvascular

A
  • diabetic retinopathy
  • nephropathy
  • neuropathy
  • infections (UTI, pneumonia, skin)
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83
Q

insulin adverse effects?

A
  • hypos
  • lipodystrophy
  • weight gain
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84
Q

T2DM - pathophysiology

A

increased insulin resistance and decreased production, leading to persistent hyperglycaemia

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85
Q

T2DM risk factors

A
  • non-modifiable - older age, Black / South Asian, FHx
  • modifiable - obesity, sedentary lifestyle, high sugar die
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86
Q

T2DM Px

A
  • asym
  • fatigue
  • polyuria, polydipsia
  • wt loss
  • opportunistic infections - eg oral thrush
  • slow wound healing
  • acanthosis nigricans
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87
Q

what HbA1C suggests pre-diabetes?

A

HbA1c of 42 – 47 mmol/mol indicates pre-diabetes

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88
Q

T2DM diagnosis

A

HbA1C >48 mmol (6.5%)

[asymptomatic? need two positive tests. symptomatic? 1 positive test]

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89
Q

glucose cut of values for diabetes mellitus Dx [fasting, random, OGTT]

A

Serum blood glucose
- fasting >7, IGT 6.1-6.9
- random >11.1, IGT 7.8-11

OGTT
- >11.1 2hrs after 75g glucose - diagnostic

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90
Q

T2DM: HbA1C treatment targets

A

48 mmol/mol for new type 2 diabetics

53 mmol/mol for patients requiring more than one antidiabetic medication

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91
Q

T2DM Mx - lifestyle

A

lifestyle:
- Low-glycaemic-index, high-fibre diet
- exercise
- weight loss
- manage complications e.g. HTN

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92
Q

T2DM Mx - medical - 4 stages

A

1st line = metformin [ + SGLT-2 if cardiovascular disease or HF ]

2nd line = add sulfonylurea / pioglitazone / DPP4 inhibitor / SGLT-2 inhibitor

3rd line = triple therapy [metformin + 2 of the 2nd line drugs] or insulin therapy

4th line (triple therapy failure and patient BMI >35) = GLP-1

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93
Q

T2DM sick day rules

A
  • Some OHAs may be stopped, restart once feeling better
  • Metformin - stop if risk of dehydration
  • Sulfonylureas - increase hypo risk
  • SGLT-2 - check ketones
  • GLP-1 - stop if dehydrated
  • Monitor BMs more
94
Q

DVLA diabetes rules

A

Group 1
- insulin - can drive if has hypo awareness, <1 bad hypo in last 12mo, no visual impairment
- tablets - no need to notify DVLA
- diet controlled - no need to notify

Group 2 must meet
- no severe hypos <12mo
- control of condition, monitoring etc
- understand hypo risks
- no cx of DM

95
Q

Diabetic neuropathy?

A
  • Glove + stocking sensory loss
  • If painful - neuropathic pain meds, pain clinic

Also GI autonomic neuropathy
- Gastroparesis - erratic blood control, bloating, vomiting, Mx with metoclopramide, domperidone, erythromycin
- Chronic diarrhoea
- GORD

96
Q

Diabetic foot

A
  • from neuropathy / PAD
  • loss of sensation, absent foot pulses, reduced ABPI
  • calluses, ulcers, Charcot’s arthropathy, cellulitis, osteomyelitis,
  • screen annually - palpate pulses, 10g monofilament
97
Q

Biguanides - metformin
Mechanism and S/E

A
  • increases insulin sensitivity and decreases glucose production by the liver

S/Es
- GI Sx: including pain, nausea and diarrhoea (depending on the dose)
- Lactic acidosis (e.g., secondary to acute kidney injury)

NB does not cause weight gain or hypoglycaemia

98
Q

SGLT-2 inhibitors - cana/empa/dapa-gliflozin

Mechanism and S/E

A
  • block action of sodium-glucose co-transporter 2 protein in kidneys, inhibiting glucose resorption and increasing urinary glucose loss

S/Es
- increased frequency of UTI and genital thrush
- DKA
- Fournier’s gangrene
- inreased urine output

99
Q

Thiazolidinediones / glitazones - pioglitazone, rosiglitazone

Mechanism and S/E

A
  • increase insulin sensitivity, decrease liver glucose production

S/Es
- Weight gain
- Heart failure
- Increased risk of bone fractures
- small increase in bladder Ca risk

100
Q

Sulfonylureas - gliclazide, tolbutamide

Mechanism and s/e

A
  • stimulate insulin secretion from pancreas

S/Es
- Weight gain
- Hypoglycaemia

101
Q

DPP4 inhibitors - sita/lina/saxa-gliptin

Mechanism and S/E

A
  • enhance incretin effect (increased insulin response to oral glucose) - increase insulin, lower glucagon

S/Es
- nausea, headaches
- pancreatitis

102
Q

GLP-1 agonists - exanatide, liraglutide

Mechanism and S/E

A
  • injectable S/C - increase incretin effect

S/Es
-Reduced appetite
- Weight loss
- GI sx including discomfort, nausea and diarrhoea

103
Q

What is DKA?

A
  • diabetic emergency usually due to inadequate insulin
  • 3 key features: ketoacidosis, dehydration, potassium imbalance
104
Q

DKA: why does ketoacidosis happen?

A
  • liver starts producing ketones to use as fuel
  • this builds up and kidneys start producing bicarb to counteract ketone acids
  • over time ketone acids use up bicarb and blood becomes acidotic
105
Q

DKA: when can insulin infusion continue til?

A
  • Ketosis and acidosis should have resolved
  • They should be eating and drinking
  • They should have started their regular subcutaneous insulin
106
Q

DKA Px

A
  • pear drop breath
  • Kussmaul’s respiration
  • reduced LOC
  • vomiting
  • abdo pain
  • dehydration - dry mucous membranes, slow CRT, tachycardia, hypotension
107
Q

DKA Ix

A
  • CBG - hyperglycaemia
  • ketone - blood ketones > 3
  • VBG - acidosis
  • investigate precipitant e.g. infection (CXR)
108
Q

criteria for DKA dx

A

all 3 of:
1. Hyperglycaemia (e.g., blood glucose above 11 mmol/L)
2. Ketosis (e.g., blood ketones above 3 mmol/L)
3. Acidosis (e.g., pH below 7.3)

109
Q

DKA Mx

A

F – Fluids – IV fluid resuscitation with normal saline (e.g., 1 litre in the first hour, followed by 1 litre every 2 hours)
I – Insulin – fixed rate insulin infusion (e.g., Actrapid at 0.1 units/kg/hour)
G – Glucose – closely monitor blood glucose and add a glucose infusion when it is less than 14 mmol/L
P – Potassium – add potassium to IV fluids and monitor closely (e.g., every hour initially)
I – Infection – treat underlying triggers such as infection
C – Chart fluid balance
K – Ketones – monitor blood ketones, pH and bicarbonate

110
Q

DKA Cx

A
  • Hypoglycaemia
  • Hypokalaemia
  • Cerebral oedema, particularly in children
  • Pulmonary oedema secondary to fluid overload or acute respiratory distress syndrome
111
Q

HHS

A
  • rare but potentially fatal complication of type 2 diabetes.
  • characterised by hyperosmolality (water loss leads to very concentrated blood), high sugar levels (hyperglycaemia) and the absence of ketones, distinguishing it from ketoacidosis
112
Q

HHS Px

A
  • polyuria
  • polydipsia
  • weight loss
  • dehydration
  • tachycardia
  • hypotension
  • confusion
113
Q

HhS Ix

A
  • CBG - usually hyperglycaemia
  • serum osmolarity - >320 mOsm/kg
  • ketones - no ketones
  • VBG - no sig. acidosis
  • U+Es - hypo/hypernatraemia, hypo/hyperkalaemia, dehydration
  • investigate precipitant e.g. septic screen, MI etc
114
Q

HHS Mx

A
  • 0.9% NaCl - 0.5-1l/hr
  • correct electrolytes
  • insulin - give if BM stops falling with fluids
  • LMWH for VTE prophylaxis
115
Q

Hypoglycaemia

A

BM <4

116
Q

Causes of hypoglycaemia

A

EXogenous drugs - insulin, OHAs, alcohol, quinine, quinolones
Pituitary insufficiency - no GH/cortisol
Liver failure - no glycogen stores
Adrenal failure - no cortisol
Insulinomas / immune hypoglycaemia
Non-pancreatic neoplasms

117
Q

Hypoglycaemia Px

A

Adrenergic
- sweating, palpitations, tremor, anxiety/irritable, hunger, feel cold

Neuroglycopenic
- confusion, dizziness, tingling, blurred vision, slurred speech, headache, N+V, seizure, coma

  • fatigue, weakness
118
Q

Hypoglycaemia Ix

A
  • CBG
  • ix for cause
119
Q

Hypoglycaemia Mx

A
  • conscious, orientated - oral glucose
  • conscious, confused, IV access - 100mls 20% / 200mls 10% glucose
  • conscious, confused, no IV access - 1mg IM glucagon
  • unconscious / fitting - as above
  • give long-acting carb on recovery
  • review meds etc
120
Q

Hyperglycaemia

A
  • high BMs

Causes
- decompensated / undiagnosed DM
- stress - acute illness
- Cushing’s, pheochromocytoma, acromegaly, hyperthyroidism
- meds - eg steroids, BBs

121
Q

Hyperglycaemia Px

A
  • weakness, headache, blurred vision, polyuria, polydipsia, palpitations, N+V, abdo pain, drowsiness, seizure, coma
122
Q

Hyperglycaemia Ix

A
  • CBG, VBG, bloods, HbA1c
123
Q

Hyperglycaemia Mx

A
  • Novarapid if need to bring down BM
  • diabetic team review
  • meds review
  • tx cause
124
Q

describe the parathyroid axis?

A

PTH released from chief cells in 4 parathyroid glands in response to low calcium

125
Q

3 key actions of PTH?

A

1) increases activity and number of osteoclasts in bone causing bone resorption

2) stimulates calcium reabsorption in the kidneys

3) stimulates the kidneys to convert vitamin D3 into calcitriol, the active form of vitamin D - vitamin D promotes calcium absorption from food in intestine

net effect = serum calcium increases and serum phosphate decreases

126
Q

Hyperparathyroidism

A

high PTH

127
Q

symptoms of hypercalcaemia ?

A

Kidney stones
Painful bones
Abdominal groans (constipation, nausea and vomiting)
Psychiatric moans (fatigue, depression and psychosis)

128
Q

Primary hyperparathyroidism

A
  • excess PTH production from parathyroid tumour -> hypercalcaemia
  • mostly solitary adenoma, also hyperplasia, multiple adenoma, carcinoma
129
Q

Primary hyperparathyroidism: blood results (PTH, Ca, phosphate

A

high PTH
high Ca
low Phosphate

130
Q

hyperparathyroidism Ix

A
  1. bloods - PTH, calcium, phosphate, ALP
  2. urine calcium
131
Q

Primary hyperparathyroidism Mx

A
  • total parathyroidectomy - risk of low Ca / recurrent laryngeal nerve injury
  • calcimimetic (cinacalcet)
  • bisphosphonate - alendronate
132
Q

Secondary hyperparathyroidism

A
  • insufficient vitamin D or CKD reduces calcium absorption from the intestines, kidneys and bones.
  • results in low blood calcium
  • parathyroid glands react to the low serum calcium by excreting more parathyroid hormone
133
Q

Secondary hyperparathyroidism: blood results (PTH, Ca, phosphate

A
  • PTH high
  • Ca normal (or low)
  • phosphate high
134
Q

Secondary hyperparathyroidism Mx

A
  • Tx cause - vit D replacement, renal transplant
  • maybe cinacalcet
135
Q

Tertiary hyperparathyroidism? blood results (PTH, Ca, phosphate

A
  • occurs after long period of secondary hyperparathyroidism resulting in hyperplasia of PTH glands -> autonomously produce high PTH
  • high PTH leads to inappropriately high Ca absorption

bloods
- PTH very high
- Ca very high
- phosphate high

136
Q

Hypoparathyroidism

A

Low PTH, leading to low Ca

137
Q

Primary hypoparathyroidism

A

Low PTH due to PT gland failure

Causes - acquired / congenital
- DiGeorge syndrome
- Autoimmune cause
- Lack of PT gland at birth
- Genetic mutations

138
Q

Secondary hypoparathyroidism

A
  • low PTH after damage

Causes - physiological
- Parathyroidectomy / thyroidectomy (most common)
- Radiation
- Hypomagnesaemia - Mg required for PTH secretion

139
Q

Pseudohypoparathyroidism

A
  • PTH present but body unable to respond to it due to genetic mutations in PTH receptors
140
Q

Pseudopseudohypoparathyroidism

A
  • Same phenotypic defects as pseudo- without abnormalities of Ca metabolism
141
Q

Hypoparathyroidism Px

A

hypocalcaemia signs :
trousseau’s sign - carpopedal spasm caused by BP cuff
chvostek’s sign - facial contraction caused by tapping facial nerve

hypocalcaemia symptoms:
- muscle cramps / pain
- fatigue
- twitching
- paraesthesia
- confusion

142
Q

Hypoparathyroidism Ix

A
  • bloods - PTH, calcium, phosphate, ALP
  • test for underlying causes (genetics, auto-antibodies, infection)
  • test for complications (ECG - see long QT with hypocalcaemia)
143
Q

Hypoparathyroidism blood results: hypo, pseudo and pseudo pseudo

A

Hypo - normal appearance, low PTH, low Ca, high phosph

Pseudo - skeletal defects, high PTH, low Ca, high phosph

Pseudopseudo - skeletal defects, normal PTH, normal Ca, normal phosph

144
Q

Hypoparathyroidism Mx

A
  • IV calcium if severely low
  • Ca supplements
  • calcitriol - active vit D
145
Q

where is ADH secreted from and what does it do?

A

Antidiuretic hormone (ADH) is produced in the hypothalamus and secreted by the posterior pituitary gland aka vasopressin

ADH stimulates water reabsorption from the collecting ducts in the kidneys

146
Q

2 key sources of excess ADH?

A
  • Increased secretion by the posterior pituitary
  • Ectopic ADH, most commonly by small cell lung cancer
147
Q

what happens if a person has too much ADH?

A
  • Excessive ADH results in increased water reabsorption in the collecting ducts, diluting the blood
  • excess water reduces the sodium concentration (hyponatraemia)
  • extra water is not usually significant enough to cause fluid overload
  • SIADH results in euvolaemic hyponatraemia
148
Q

what happens to the urine if a person has excess ADH?

A
  • urine becomes more concentrated as kidneys excrete less water
  • SO patients with SIADH have high urine osmolality and high urine sodium
149
Q

top 3 causes of SIADH?

A
  • post-operative
  • SSRIs
  • small cell lung cancer
150
Q

SIADH Px

A
  • symptoms related to hyponatraemia:
  • Headache
  • Fatigue
  • Muscle aches and cramps
  • Confusion

severe? seizures, low gcs

151
Q

Primary polydipsia (a DDx of SIADH)

A
  • excessive water consumption, no cause
  • euvolaemic hyponatraemia, but low urine Na/osmolality also
152
Q

SIADH Ix

A
  • euvolaemic
  • FBC, U/E - low Na, low serum osmolality
  • urine studies - high Na, high osmolality >100
  • Ix for cause - CXR, CT TAP, short synacthen test, TFTs, serum cortisol
153
Q

SIADH Mx

A
  1. Admission if symptomatic or severe (e.g., sodium under 125 mmol/L)
  2. Treating the underlying cause (e.g., stopping causative medications or treating the infection)
  3. Fluid restriction
  4. Vasopressin receptor antagonists (e.g., tolvaptan)
154
Q

why is it essential to raise sodium slowly?

A

risk of osmotic demyelination syndrome

155
Q

Diabetes insipidus (DI) definition (+ detail on types!)

A
  • lack or production or loss of sensitivity to ADH

Cranial DI ‘ low ADH’ = reduced ADH secretion from post pituitary

Nephrogenic DI ‘insensitivity to ADH’ = impaired response of kidney to ADH

156
Q

causes of cranial DI

A
  • Brain tumours
  • Brain injury
  • Brain surgery
  • Brain infections (e.g., meningitis or encephalitis)
  • Genetic mutations in the ADH gene (autosomal dominant inheritance)
  • Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
157
Q

causes of nephrogenic DI?

A
  • Medications, particularly lithium (used in bipolar affective disorder)
  • Genetic mutations in the ADH receptor gene (X-linked recessive inheritance)
  • Hypercalcaemia
  • Hypokalaemia
  • Kidney diseases (e.g., polycystic kidney disease)
158
Q

DI Px

A
  • polyuria
  • polydipsia, chronic thirst
  • nocturia
  • dehydration
  • postural hypotension
159
Q

DI Ix

A
  • urine collection - >3L/24hrs
  • high/normal serum osmolality
  • low urine osmolality

water deprivation test

160
Q

what is the water deprivation test?

A

used in DI

  • no water for 8 hours
  • given desmopressin and measure urine osmolality before and after

cranial DI? urine osmolality high
nephrogenic DI? urine osmolality low

161
Q

DI Mx

A

Cranial DI
- oral desmopressin

Nephrogenic DI
- tx cause
- low salt / protein diet
- thiazide diuretics
- NSAIDs - ibuprofen

162
Q

Pheochromocytoma: definiton and risk factors

A
  • tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline)
  • secrete adrenaline in bursts -> intermittent sx

RFx: MEN II, NFT1, von-Hippel-Lindau

163
Q

Pheochromocytoma Px

A
  • periodic sx
  • anxiety, sweating, headache, tremor, palpitations, HTN, tachycardia
164
Q

Pheochromocytoma Ix

A
  • plasma free metanephrines
  • 24hr urine catecholamines
  • CT / MRI
  • genetic testing
165
Q

Pheochromocytoma Mx

A
  • alpha blockers - phenoxybenzamine, doxazosin
  • BBs
  • partial adrenalectomy
166
Q

Thyroid cancer (&RFx)

A
  • cancer of thyroid gland
  • papillary, follicular, anaplastic, lymphoma, medullary cell

RFs
- radiation exposure
- hx of goitre, nodule, thyroiditis, FHx, female, Asian

167
Q

Thyroid cancer Px

A
  • thyroid nodule
  • hard / irregular thyroid
  • cervical lymphadenopathy
  • mets to lungs, brain, hepatic, bone
  • hoarse voice
168
Q

Thyroid cancer Ix

A
  • fine needle aspiration biopsy / cytology
  • Bloods - TFTs
  • US thyroid
  • thyroglobulin
169
Q

Thyroid cancer Mx

A
  • papillary / follicular - total thyroidectomy / radioactive iodine
  • anaplastic / lymphomas - external radiotherapy
  • medullary - thyroidectomy, lymph node removal
  • levothyroxine - keep TSH reduced
  • chemotherapy
170
Q

what hormone is released from hypothalamus that acts on anterior pituitary to inhibit prolactin release?

A

dopamine

continuously secreted in absence of pregnancy

171
Q

important hormonal S/E of dopamine inhibiting medications?

A

prolactin will be secreted

172
Q

what does prolactin do?

A
  1. stimulates milk production
  2. inhibits GnRH secretion so inhibits FSh and LH release (they regulate menstruation) –> so during lactation, a period of amenorrhoea will occur

NB oxytocin inhibits dopamine so promotes prolactin production

173
Q

what is a prolactinoma?

A

pituitary adenoma secreting prolactin

174
Q

signs of prolactinoma in males?

A

gynacomastia
erectile dysfunction
loss of libido
galactorrhea

NB generic pituitary adenoma too - headaches / bitemporal hemianopia

175
Q

signs of prolactinoma in females?

A

amenorrhoea
galactorrhea
infertility

NB generic pituitary adenoma too - headaches / bitemporal hemianopia

176
Q

prolactinoma ix?

A

bloods - GH, prolactin, ACTH, FSH, LH, TFTs
MRI head

177
Q

Prolactinoma Mx

A

Medical = dopamine agonist - cabergoline, bromocriptine
Surgical = transsphenoidal pituitary resection

178
Q

Hyperkalaemia

A
  • high serum K

Classification
- Mild - 5.5-5.9
- Moderate - 6.0-6.4
- Severe - >6.5

179
Q

Causes of hyperkalaemia

A

Renal
- AKI, CKD, Addison’s,
- drugs - spironolactone, ACEi, ARBs, NSAIDs, ciclosporin, heparin

Increased circulation of K
- exogenous - foods, blood transfusion
- endogenous - rhabdo, crush, burns, tumour lysis syndrome

IC->EC
- DKA, metabolic acidosis
- digoxin toxicity, BBs, sux, theophylline

Pseudo
- haemolysed sample

180
Q

Hyperkalaemia Px

A
  • asym
  • Palpitations
  • Chest pain
  • Dizzy
  • Muscle weakness
  • Stiffness
  • Fatigue
181
Q

Hyperkalaemia Ix

A
  • VBG, U/E, FBC, LFTs, BMs
  • serum cortisol / aldosterone if adrenal insufficiency suspected

ECG
- tall tented T waves
- flattened P waves
- PR prolongation
- broad QRS
- sine wave pattern
- then VF

182
Q

Hyperkalaemia Mx

A
  • ABCDE
  • remove cause
  • calcium gluconate / chloride (if >6.5 / ECG changes)
  • insulin + dextrose - 10-20 units in 500mls of 10% glucose
  • salbutamol
  • furosemide, calcium resonium (GI binder), sodium bicarb, dialysis
183
Q

hypokalaemia

A

serum K<3.5

184
Q

Hypokalaemia causes

A
  • not enough K in fluids
  • GI losses - D+V, malabsorption, laxatives, high output stoma, poor oral intake / inadequate feed
  • Renal losses - genetic syndromes, Conn’s, Cushing’s, renal tubular acidosis, furosemide, thiazides
  • Intracellular shift - alkalosis, insulin, adrenaline, salbutamol
185
Q

Hypokalaemia Px

A
  • asym
  • Muscle weakness
  • Hypotonia
  • Hyporeflexia
  • Tetany
  • Constipation
  • Palpitations
  • Light-headed
186
Q

Hypokalaemia Ix

A
  • U/E

ECG
- small / inverted T waves
- Long PR
- prominent U waves
- ST depression
- long QT, Torsades de Pointes

187
Q

Hypokalaemia Mx

A
  • tx cause

Mild >3.1
- oral sando-K

Severe <3.1
- IV KCl - no quicker than 10mmol/hr
- lower - ITU discussion

188
Q

Hypercalacaemia

A
  • normal serum Ca 2.1-2.6

Classification
- mild 2.65-3 - asym
- moderate - 3.01-3.40 - asym/sx
- severe >3.40 - arrhythmias, coma

189
Q

Causes of hypercalcaemia

A

High/normal PTH
- hyperparathyroidism

Low PTH
- malignancy - SCLC, bone mets, myeloma, ectopic
- sarcoidosis, TB
- Drugs - Ca/vit D, antacids, thiazides, lithium, theophylline
- rhabdo
- adrenal insufficiency, thyrotoxicosis, phaeo

190
Q

Hypercalcaemia Px

A

Bones
- bone pain, fractures, osteopenia, osteomalacia, osteoporosis

Stones
- renal / biliary stones

Groans
- abdo pain, pancreatitis, malaise, nausea, constipation, polydipsia, dehydration, confusion

Moans
- depression, anxiety, cognitive dysfunction, insomnia, coma

  • sx of malignancy etc
191
Q

Hypercalcaemia Ix

A
  • hydration
  • Bloods - bone profile, vit D, ALP, U/E
  • ECG - short QT, brady, 1st HB
  • CXR, isotope bone scan, CT / MRI
  • serum ACE (sarcoidosis)
192
Q

Hypercalcaemia Mx

A
  • 0.9% NaCl 4-6l/24hrs
  • IV bisphosphonates - zolendronate
  • dialysis
  • cinacalcet, denosumab, calcitonin, prednisolone
193
Q

Hypocalcaemia

A

Ca <2.1

194
Q

Causes of hypocalcaemia

A
  • total thyroidectomy / parathyroidectomy / hypoparathyroid
  • vit D deficiency
  • CKD
  • low Mg (PPIs)
  • pancreatitis
  • rhabdo, tumour lysis syndrome
  • Loop diuretics, steroids, gent, phosphates, theophylline
  • massive transfusion
195
Q

Hypocalcaemia Px

A

SPASMODIC
- Spasms - Trousseau’s
- Perioral paraesthesia
- Anxious, irritable, irrational
- Seizures
- Muscle tone increase in smooth muscle - wheeze
- Orientation impaired and confused
- Dermatitis
- Impetigo herpetiformis - reduced Ca and pustules in pregnancy
- Chvostek’s sign, cataracts, cardiomyopathy (long QT)

196
Q

Hypocalcaemia Ix

A
  • Bloods - bone profile, U/E, Mg, vit D, PTH, amylase, CK
  • ECG - prolonged QT
197
Q

Hypocalcaemia Mx

A

Mild >1.9
- oral sandocal / adcal
- vit D - colecalciferol
- IV Mg if low
- may need calcitriol in para/thyroidectomy

Severe <1.9 / sx
- cardiac monitor
- calcium gluconate bolus / infusion
- tx cause

198
Q

Hypophosphataemia

A

low serum phosph <0.8 (normal 0.8-1.5)

199
Q

Hypophosphataemia causes

A
  • redistribution into cells - resp alkalosis, insulin, adrenaline
  • increased urinary excretion - acidosis, DKA, hyperparathyroid
  • decreased intestinal absorption - antacids, vit D deficiency, D+V, malabsorption
  • refeeding syndrome
  • chronic alcohol
  • acute liver failure
200
Q

Hypophosphataemia Px

A
  • Asymptomatic
  • Myopathy, rhabdomyolysis, weakness
  • Resp failure
  • Arrhythmias, cardiomyopathy
  • Irritable, confused, hallucinations, lethargy, seizure, coma
  • Rickets / osteomalacia if chronic
201
Q

Hypophosphataemia Ix

A
  • bloods - bone profile, Ca, phosph, U/E
202
Q

Hypophosphataemia Mx

A
  • oral phosphate sandoz
  • IV phosphates polyfusor / sodium glycerophosphate
203
Q

Hypomagnesaemia

A
  • low serum Mg (normal 0.7-1.05)
204
Q

Hypomagnesaemia causes

A
  • refeeding syndrome
  • D+V, high output stoma
  • alcoholism
  • hypercalcaemia
  • SIADH, DKA, aldosteronism
  • renal losses
  • post-parathyroidectomy
  • drugs - diuretics, gent, PPIs
205
Q

Hypomagnesaemia Px

A
  • asym
  • irritable, lethargy
  • N+V
  • confusion, depression, psychosis
  • tremors, cramps, tetany, weakness, seizures
206
Q

Hypomagnesaemia Ix

A
  • ECG - PR prolongation, ST depression, altered T waves, ventricular arrhythmias, eg VF
  • Bloods - U/E, Ca, Mg
  • urinary Mg
207
Q

Hypomagnesaemia Mx

A

0.4-0.7
- oral Mg salts

<0.4 / tetany, arrhythmias, seizures
- IV Mg

208
Q

Hypernatraemia

A
  • serum Na >145
209
Q

Causes of hypernatraemia

A

Hypovolaemic hypernatraemia - salt + water lost, but more water
- D+V, sweating, burns, loop diuretics, osmotic diuresis

Normovolaemic hypernatraemia - loss of purely water
- impaired thirst / water intake -> dehydration - dementia, decreased access to water
- diabetes insipidus

Hypervolaemic hypernatraemia - rare, iatrogenic
- hypertonic saline
- hypertonic dialysis
- hyperaldosteronism

210
Q

Hypernatraemia Px

A
  • Thirst, lethargy, weakness, nausea, loss of appetite
  • Severe - myoclonic jerks, intracranial haemorrhage, coma, death
211
Q

Hypernatraemia Ix

A
  • assess fluid status
  • bloods - U/E, glucose, Mg, Ca
  • urine / serum osmolalities
212
Q

Hypernatraemia Mx

A
  • tx cause
  • oral fluids
  • 0.9% NaCl (unless hypervolaemic)
  • correct <0.5mmol/L/hr (cerebral oedema risk)
213
Q

Hyponatraemia

A
  • low serum Na <135

Severity
- Mild – 130-134
- Moderate – 120-129
- Severe – <120

214
Q

Hyponatraemia causes

A

Hypovolaemic hyponatraemia - loss of Na and water
- diuretics, Addisonian crisis, D+V, MDMA, pancreatitis
- exercise induced hyponatraemia (EAH)

Euvolaemic hyponatraemia - volume expansion, no oedema
- SIADH
- hypothyroidism
- beer potomania
- adrenal insufficiency

Hypervolaemic hyponatraemia - Na and water increase, more water
- HF, liver failure, nephrotic syndrome, excessive water consumption

215
Q

False hyponatraemia?

A
  • lab results show low Na, but no hypotonicity
  • eg glucose - draws water into blood - appears like Na low
216
Q

Hyponatraemia Px

A
  • asym

early
- Headache
- Lethargy
- N+V
- Dizziness
- Confusion
- Muscle cramps

late
- seizures
- coma
- cardio-respiratory arrest

217
Q

Hyponatraemia Ix

A
  • fluid status
  • U/E
  • serum / urine osmolality
  • urinary sodium
  • if fluid overloaded - BNP, LFTs, urine dip, protein:creatinine ratio
  • TFTs, 9am cortisol
218
Q

Hyponatraemia Mx

A

Severe sx, Na <120
- HDU / ITU
- hypertonic saline - 3% NaCl

Hypovolaemic
- 0.9% NaCl

Euvolaemic
- fluid restrict 500-1000ml/d
- tolvaptan / demeclocycline

Hypervolaemic
- fluid restrict 500-1000ml/d
- furosemide / tolvaptan

219
Q

Osmotic demyelination syndrome

A
  • from rapid over-correction of hyponatraemia
  • astrocyte/oligodendrocyte apoptosis -> demyelination

Px
- irreversible sx
- dysarthria, dysphagia, paralysis, seizures, confusion
- coma - locked-in-syndrome

Mx
- avoid - Na levels raised by 8mmol/L/24hrs

220
Q

Bartter’s syndrome

A
  • autosomal recessive disease of severe hypokalaemia
  • defective NKCC2 transporter - like lots of furosemide
    Px
  • childhood - failure to thrive
  • polyuria, polydipsia
  • hypokalaemia
  • normotension
  • weakness
221
Q

Insulinoma

A
  • NE tumour derived from pancreatic Islets of Langerhans cells
    Px
  • hypoglycaemia - early morning, just after meal
  • rapid weight gain
    Ix
  • high insulin, raised proinsulin:insulin ratio
  • high c-peptide
  • supervised prolonged fasting
  • CT pancreas
    Mx
  • surgery
  • diazoxide / somatostatin
222
Q

Liddle’s syndrome

A
  • autosomal dominant - disordered Na channels in distal tubules -> increased Na reabsorption
  • HTN, hypokalaemic alkalosis
    Mx
    amiloride / triamterene
223
Q

Maturity-Onset Diabetes of the Young (MODY)

A
  • monogenic diabetes, autosomal dominant inheritance
  • impaired insulin secretion
    Px
  • mild, non-ketotic hyperglycaemia
    Ix
  • genetic testing
    Mx
  • Sulfonylurea / insulin / nothing depending on type
224
Q

what is Multiple endocrine neoplasia

A
  • autosomal dominant disorders causing different endocrine glands to grow benign, malignant or non cancerous growths
225
Q

what are the 3 types of MEN?

A

MEN-1
- parathyroid, pituitary, pancreas, adrenal, thyroid
- commonly px with hypercalcaemia

MEN-2a
- medullary thyroid cancer, parathyroid, phaeo

MEN-2b
- medullary thyroid cancer, phaeo, marfanoid body habitus, neuromas

226
Q

Gynaecomastia

A
  • abnormal breast tissue in males - increase in oestrogen:androgen ratio

Causes
- Physiological: normal in puberty
- Syndromes with androgen deficiency: Kallman’s, Klinefelter’s
- Testicular failure: e.g. mumps
- Liver disease
- Testicular cancer e.g. seminoma secreting hCG
- Ectopic tumour secretion
- Hyperthyroidism
- Haemodialysis
- Drugs - spironolactone, cimetidine, digoxin, cannabis, finasteride, GnRH agonists, oestrogens, anabolic steroids

227
Q

Thyroid eye disease Px

A
  • affects 25-50% pts with graves
  • May be eu/hypo/hyperthyroid
  • Exophthalmos
  • Conjunctival oedema
  • Optic disc swelling
  • Ophthalmoplegia
  • Eyelid retraction
  • Inability to close eyelids -> sore, dry eyes
228
Q

Thyroid eye disease Mx

A
  • stop smoking
  • topical lubricants
  • steroids
  • radiotherapy
  • surgery

Urgent ophthal review if
- Unexplained deterioration in vision
- Change in colour vision
- Hx of eye popping out – globe subluxation
- Corneal opacity
- Cornea visible when eyelids closed
- Disc swelling

229
Q

BMI ranges for overweight and obesity

A

Overweight 25 - 30
Obese class 1 30 - 35
Obese class 2 35 - 40
Obese class 3 > 40

230
Q

obesity management options

A

conservative: diet, exercise
medical
- orlistat
- liraglutide
surgical

231
Q

Orlistat

A

a pancreatic lipase inhibitor used in the management of obesity

only prescribed for adults as part of a plan who have:
- BMI of 28 kg/m^2 or more with associated risk factors, or
- BMI of 30 kg/m^2 or more
- continued weight loss e.g. 5% at 3 months
- orlistat is normally used for < 1 year

232
Q

current NICE criteria for Liraglutide use?

A
  • person has a BMI of at least 35 kg/m²
  • prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)

finals (21 decks)

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