Endocrine Flashcards

1
Q

A CT head shows bleeding on the pituitary gland, what is this and what is the most common cause?

A
  • Pituitary apoplexy is heamorrage of pituitary gland

- Often caused by tumour (macro adenoma)

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2
Q

What investigations should you do for pituitary apoplexy, IN THE ORDER OF MOST IMPORTANT?
What would you expect to see?

A

1) CT head-bright white in middle by pituitary gland
2) pituitary hormones
- cortisol>CHECK ASAP-if low give hydrocortisone
- thyroid
- sex hormones
- growth hormones
3) visual field problems (bilateral hemianopia a.k.a tunnel vision) caused by compression of the optic chiasma

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3
Q

If hypercalcemia is parathyroid dependant what would you expect to see?

A
  • raised PTH

- high Calcium, low Phosphorus

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4
Q

treatment for thyroid storm?

A

Thyroid storm

1) Propylthiouracil
2) Hydrocortisol (prevent peripheral conversion of T3 and T4)
3) Symptom control
- Beta blocker
- IV fluids

**monitor heart for arrhythmias

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5
Q

Explain the negative feedback loop of the hypothalamus, anterior pituitary gland and the adrenal glands

A

Negative feedback loop
1. Hypothalamus produces cortico-trophic releasing hormone CRH

  1. This causes Anterior pituitary gland to release ACTH (adreno-cortico-trophic hormone)
  2. ACTH causes the adrenal cortex to release
    a) mineralocorticoids(aldosterone)
    b) glucocorticoids (cortisol)
    c) androgens
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6
Q

What are the effects of the 3 hormones secreted by the adrenal gland?

A

Adrenal gland hormone

  1. Mineralocorticoids (aldosterone)
    - Na+ and water retention>↑BP
  2. Glucocorticoids (cortisol)
    - immunosuppressant and anti inflammatory
    - skin thinning
    - metabolism (weight gain and insulin resistance
    - bone effects (↑osteoclasts>osteopenia and osteoporosis)
  3. Androgens
    - more effect for females
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7
Q

Presentation of adrenal insufficiency?

A

ADRENAL INSUFFICIENCY PRESENTATION

  • fatigue, depression, ↓self-esteem, psychosis
  • tan/pigmentation (skin/buccal mucosa/palmar creases)
  • anorexia and weight loss (can be mistaken for anorexia)
  • signs of dehydration
  • dizzyness/syncope
  • nausea, vomiting (↓Na+)
  • abdo pain, constipation or diarrhoea
  • arthralgia/myalgia
  • decreased libido
  • low grade fever
  • loss of hair
  • can present ACUTELY with circulatory collapse
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8
Q

Investigations and findings of adrenal insufficiency? (bedside, bloods, imaging,special)

A

Bedside

  • low BP and signs of dehydration
  • ECG (tachy to compensate for low BP)

Bloods

  • Us+Es (HYPONATREMIA, HYPERKALEMIA)
  • 9am serum cortisol QUICKEST TEST (reduced)
  • Glucose (hypoglyceamic-due to ↓cortisol)
  • ABG (metabolic acidosis due to↓aldosterone> ↓HCO3- )

Imaging
-Could do if concerned primary malignancy, mets or infection (TB-CXR)

Special test

  • SynACTHen test (diagnostic ∆ ) <420nmol/L cortisol suggests primary adrenal deff -however takes longer so would prob just treat before results
  • Adrenal antibodies (21 hydroxylase Ab + ve 80% in Addisons). If negative consider TB
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9
Q

Long term management for Adrenal insufficiency?

A

ADRENAL INSUFFICIENCY MANAGMENT

  1. Mineralocorticoid replacement: fludrocortisone (only in primary because RASS has less effect)
  2. Glucocorticoid replacement: daily hydrocortisone (divided doses throughout day-mimic normal fluctuations)
  3. Androgen replacement: DHEA (Dehydroepiandrosterone is produced by adrenals whereas testes produce androgens)
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10
Q

What are the clinical effects of
↓Mineralocorticoids
↓ Glucocorticoids
↓Androgens

A

↓Mineralocorticoids (aldosterone)

  • Hyperkaleamia ↑K+
  • Hyponatreamia (↓Na+and ↓water retention)>↓BP> compensatory ↑HR
  • Metabolic Acidosis (aldosterone reabsorbs bicarb(↓HCO3-)

↓Glucocorticoids

  • weight loss
  • fatigue
  • ↓gluconeogenesis ↓blood glucose

↓Androgens (more effect on women)

  • ↓libido
  • ↓Pubic hair

-skin pigmentation our to compensatory hyper-pituitary activity → ↑melanocyte stimulating hormone

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11
Q

Causes of adrenal insufficiency

A

Causes of adrenal insufficiency

  • ADDISONS DISEASE (autoantibodies against adrenal cortex +/- hydroxylase autoimmunity)
  • infection
  • malignancy or mets
  • infiltration diseases (heamochromatosis or amyloidosis)
  • adrenal heamorrage (warfarin) or infarction
  • iatrogenic (Surgery)
  • congenital adrenal hyperplasia
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12
Q

What are the cut-offs for cortisol test?

What does high ACTH mean? What does low/norm ACTH mean?

A

9am ↓Cortisol and ACTH
-allows differentiation of 1 vs 2

Cortisol < 100 (Addison’s likely admit to hospital )
100-500 (do Synacthen test);
> 500 (unlikely Addison’s)

↑ACTH = primary (pituitary trying to compensate);
↓ or norm ACTH = secondary (↓pituit. sec is the issue)

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13
Q

What things might interfere with cortisol test?

What would you do to overcome this?

A
  • shift workers
  • patients on long term steroids
  • patients on oestrogen therapy
  • do ACTH test instead
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14
Q

How does the ACTH stimulation test work?

A

-Synacthen® ACTH stimulation test is diagnostic ∆

  1. First, measure plasma cortisol
  2. Then, give IM Synacthen (tetracosactide), wait 30 min
  3. Then, measure plasma cortisol
    - If 30 min cortisol < 500 nmol/L = Addison’s
    - If 30 min cortisol > 550 nmol/L = not Addison’s

Refer to endocrinologist

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15
Q

What advice can you give to someone taking steroids for adrenal insufficiency?

A

STEROIDS ADVICE-ADRENAL INSUFFICIENCY

  • Warn not to abruptly stop steroids (risk of crisis)
  • DOUBLE hydrocortisone dose alone in febrile illness
  • provide IM hydrocortisone if vomiting prevents oral intake
  • give blue steroid card
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16
Q

Symptoms of addisonian crisis?

A

Addisonian crisis

  • dehydration>hypotension>HYPOVOLEAMIC SHOCK>altered consciousness>death
  • seizures
  • stroke or cardiac arrest
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17
Q

What is the ACUTE management for Adrenal insufficiency?

A

ACUTE adrenal insufficiency

1) Sugar (dextrose)
2) Steroids (IM or IV)
2) Saline
3) Search for cause

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18
Q

What is Waterhouse-Friderichsen syndrome

A
  • complication of sepsis (particularly meningococcal sepsis)
  • hemorrhagic necrosis of the adrenal glands
  • cause adrenal crisis
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19
Q

Explain how parathyroid hormone works?

A
  • low levels of calcium detected in blood
  • causes PTH gland to release PTH
  • PTH causes:
    a) ↑osteoclast activity and ↑calcium resorption from bone
    b) Activates vitamine D so ↑Ca2+ absorption from gut
    c) ↑Ca2+ reabsorption from kidneys

PTH also stimulates vitamin D production from kidneys

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20
Q

What is the most common cause of primary hyperparathyroidism

A

PRIMARY HYPERPARATHYROIDISM CAUSES

  • Most common cause is Parathyroid adenoma (80%)
  • Hyperplasia (20%)
  • Parathyroid carcinoma (<0.5%)
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21
Q

What are risk factors for primary parathyroidism?

A

PRIMARY HYPERPARATHYROIDISM

  • post menopausal women
  • MEN1/2a
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22
Q

Symptoms of hyperparathyroidism? (nervous system, cardiac, GI, urinary, MSK)

A
PRIMARY HYPERPARATHYROIDISM (symptoms of high calcium- MOANS/BONES/ GROANS/ THRONES
Nervous system 
-cognitive impairment 
-depression/fatigue 
-confusion>drowsy>siezures>coma 

Cardiac
-Arrhythmias (do ECG)

GI system

  • abdo pain
  • N and V
  • loss of appetite
  • constipation

Urinary system

  • kidney stones (most common)
  • increased urination
  • increased thirst

MSK

  • bone pain
  • muscle weakness

70-80% are asymptomatic and diagnosis is often incidental

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23
Q

What investigations would you do for hyperparathyroidism and what would they show? (bedside, bloods, imaging, special)

A
PRIMARY HYPERPARATHYROIDISM 
Bedside 
-Blood pressure (↑HTN)-PTH>aldosterone 
-ECG – may present with short QT interval  
-24hr Urinary Ca2+ (↑Ca2+) 

Bloods (calcium should be corrected for albumin)

  • U+Es (↑PTH / ↑Ca2+ / ↓PO4, check Mg (PPI causes low Mg and low Ca2+)
  • LFTS - ↑ALP (bone resorption – osteopenia)

Imaging
-DEXA scan – determine level of osteoporosis/dystrophy (see complications)

Special- biopsy
-if ?carcinoma

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24
Q

What are the 2 options for hyperparathyroidism treatment?

A

PRIMARY HYPERPARATHYROIDISM

  1. Conservative if:
    - kidneys working well with no stones
    - only slightly elevated Ca2+
    - bone density okay
    - if surgery unsuccessful or unsuitable
  2. Surgery
    - high serum/urinary calcium
    - osteoporosis
    - ↓renal function/renal calculi
    - age <50 years
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25
Q

What is the conservative management of primary hyperparathyroidism? (4)

A

Conservative treatment:

  • ↑fluid intake and avoid thiazide diuretics
  • Calcimimetics (Cinacalcet) -when surgery unsuitable/unsuccessful) ↑sensitivity of parathyroid cells to ca2+ levels → ↓PTH secretion
  • Bisphosphonates if ↑fracture risk
  • Replenish Vitamin.D (Cholecalciferol – non-active)
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26
Q

what is the surgical treatment for hyperparathyroidism?

What are the complications of surgical treatment?

A

SURGERY
-Parathyroidectomy

Complications

  • hypothyroidism
  • recurrent laryngeal nerve damage (hoarse voice)
  • symptomatic ↓Ca2+ (check Ca2+ daily for ≥ 14 d post-op)
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27
Q

What type of lung cancer is associated with ↑PTH?

A

-Squamous cell carcinoma is associated with ↑PTH (also seen in breast and renal cancer)

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28
Q

What are two complications of primary Hyperparathyroidism (2)

A

Osteitis fibrosa cystica

  • bones replaced by fibrous tissue
  • salt and pepper skull
  • brown tumours of long bones
  • dissapearance of distal clavicle

Nephrocalcinosis-loads of calcium in kidneys

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29
Q

Define:

  1. primary Hyperparathyroidism
  2. secondary Hyperparathyroidism
  3. tertiary Hyperparathyroidism
A

Primary Hyperparathyroidism
-excess PTH independant of Ca2+ levels

Secondary Hyperparathyroidism
-excess PTH in response to chronic hypocalcaemia

Tertiary Hyperparathyroidism

  • prolongued secondary hyperparathyroidism
  • when secondary is treated, the PTH baseline is still increased → HYPERcalcaemia
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30
Q

What would the PTH/ calcium/vit D/phosphate/ALP be in primary/secondary/tertiary hyperparathyroisim?

osteomalacia?

A

Primary
↑PTH / ↑Ca2+ / ↑vitamine D / ↓phosphate/ ↑ALP

Secondary:
↑PTH /Ca2+↓ or normal /↓Vitamin D/ ↑phophate

Tertiary
↑↑PTH / ↑ Ca2+/ ↓Vitamin D/↓phosphate if CKD normal phosphate (if kidneys transplant)/ ↑ALP

Osteomalacia
↓Vit D ↓Ca ↓Ph ↑PTH ↑ALP

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31
Q

What is secondary hyperparathyroidism?

What is the most common causes?

A

SECONDARY HYPERPARATHYROIDISM

  • excess PTH in response to chronic hypocalcaemia
  • causes hyperplasia of PT gland to compensate for low calcium

Common causes:

  • CKD (common)
  • ↓Calcitrol (active vit.D)> ↓GI tract Ca2+ absorption> ↓free calcium ions
  • Vitamine D defficiency (↓Calcitrol)
  • lack of sunlight, poor vitamin D intake

-Bowel absorption problems/liver problems

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32
Q

What are the symptoms of secondary hyperparathyroidism?

A

SECONDARY HYPERPARATHYROIDISM
(symptoms of low calcium)

  • Starts with confusion/tiredness
  • Tetany – twitching, cramping, spasms
  • Perioral paraesthesia
  • Siezures
  • Trousseau (BP cuff and cramp)
  • Chvostek’s sign (tap parotid, causing facial twitch)
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33
Q

What is the treatment of secondary hyperparathyroidism?

A

SECONDARY HYPERPARATHYROIDISM

  • Correct cause – treat CKD or Vitamin D def (Ergocalciferol-high dose. Colecalciferol for maintenance)
  • Cinacalcet if PTH ≥ 85
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34
Q

What is tertiary hyperparathyroidism?

What is the treatment of tertiary hyperparathyroidism?

A

Tertiary hyperparathyroidism
-prolongued secondary >HYPERcalceamia

Treatment: surgery to remove hyperplasia glands and return PTH to baseline

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35
Q

What is the 2nd most common cause of hypercalceamia?

A

Cancer is 2nd most common cause of hyperparathyroidism (after primary HP)

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36
Q

What would the calcium/phosphate/PTH/phosphate/ALP be in hypercalcemia due to malignancy?

A
  • ↑Ca2+ and ↓phosphate (↑Urine phosphate)
  • normal or ↓ (compensation) PTH
  • ↑Serum ALP
  • low albumin
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37
Q

What would you see on ECG with HYPER calceamia?

A
ECG IN HYPERCALCEMIA 
Most common: Short Q/T interval
-wide T-waves
-BBB
-prolonged PR interval
-arrhythmia
-J waves
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38
Q

Treatment of hypercalcemia of malignancy

A

HYPERCALCEMIA MALIGNANCY
Fluids → bisphosphonates

STEP 1: Fluids

  • IV Fluids (rehydration)
  • normal Saline 0.9% 3-4L/day (rate 250ml/hr) with adequate K+ (20 or 40mmols)
  • administer with Furosemide if ↑risk of fluid overload (also promotes ↑Ca2+ excretion ☺)

STEP 2 IV BISPHOSPHONATES
- Zolindronic acid or Pamidronate (inhibit osteoclast bone resorption) if Ca2+ > 3

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39
Q

What are some causes of SECONDARY hyperlipidemia?

A

Secondary hyperlipidaemia

  • Cushing’s synd
  • Hypothyroidism
  • Nephrotic syndrome
  • Cholestasis (↓bile)
  • Anorexia nervosa
  • Alcohol
  • Obesity
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40
Q

What are some signs of hyperlipidemia?

A

HYPERLIPIDEAMIA

  • Premature corneal arcus – white grey opaque ring in corneal margin
  • Tendon xanthomata – hard, non-tender nodular enlargement of tendons (knuckles and Achilles
  • Xanthelasma – yellow plaques around eye
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41
Q

What bloods would you get in hyperlipideamia?

A

Hyperlipideamia (get full lipid profile)

  • total cholesterol (refer to speilaist if >9)
  • HDL-C
  • non HDL-C
  • Triglycerides
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42
Q

Phaeochromocytoma
Features?
Test?
Treatment?

A

Phaeochromocytoma (features are typically episodic)

  • hypertension (around 90% of cases, may be sustained)
  • headaches
  • palpitations
  • sweating
  • anxiety

Tests
-24 hr urinary collection of METANEPHRINES

Treatment:
-Surgery is the definitive management.
-The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)

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43
Q

What is the negetive feedback loop of thyroid hormones?

A

Hypothalamus produces thyotropin releasing hormone (TRH)

  • Anterior pituitary gland produces TSH
  • Thyroid gland produces T3 and T4 (thyroxine-converted to T3 in cells
44
Q

What are the normal effects of T3 (more active hormone)

A
T3 normal functions  
↑Basal metabolic rate
↑glucose  ↓cholesterol
↑Cardiac output and contractility 
↑vasodilation 
↑gut motility 
↑Bone resorption → thins bones   
↑sympathetic nervous system
-fetal and childhood growth
45
Q

What are the autoimmune causes of primary HYPOthyroidism ?

Which one presents with a goitre?

A

Autoimmune primary HYPOthyroidism

  1. Hashimottos (most common cause of hypo in UK)
    - hypertrophy + hyperplasia therefore causes goitre
  2. Atrophic hypothyroidism (common in elderly)
46
Q

What is the most common cause of HYPOthyroidism worldwide?

A

Iodine deficiency most common cause of HYPOthyroidism world-wide

47
Q

what drugs cause HYPOthyroidism

A

HYPOthyroidism causing drugs

  • antithyroid drugs
  • amiodarone (can cause Hyper and hypo)
  • iodine
  • lithium
48
Q

HYPOthyroidism symptoms

A

HYPOthyroidism symptoms

  • Tiredness + lethargy
  • Depression
  • Cold
  • Weight gain but decreased appetite
  • Constipation
  • Menorrhagia
  • Poor cognition
  • Hoarse voice
  • Myalgia + Cramps
  • ↓Libido
  • ↓Memory + ↓Cognition → dementia like symptoms
49
Q

What are the signs on examination of hypothyroidism (remember the mnemonic)?

A

BRADYCARDIC

Bradycardia ↓HR
Reflexes relax slowly 
Ataxia (cerebella)   
Dry thin hair and skin (loss of lateral eyebrow)
Yawning 
Cold 
Ascites, pericardial or pleural effusion  
Round puffy face 
Defeated demeanour 
Ileus 
Cystic fibrosis
50
Q

Treatment of hypothyroidism?

Who should you start at lower doses? and why?

A
  • Thyroxine replacement (levothyroxine) T4 is then converted to T3 in periferies (prescribed by GP)
  • (if elderly/IHD start lower dose and titrate up because it can precipitate angina/MI and worsen osteoporsosis)
51
Q

Thyroid function tests

  1. primary hypothyroidism
  2. secondary hypothyroidism look like?
  3. subclinical hypothyroidism (and your plan)
A

Thyroid function tests
1. Primary HYPOthyroidism
TSH = high (compensate)
T4/T3 = low

  1. Secondary HYPOthyroidism (pituitary tumour/hypothamous trauma)
    TSH = normal or low if there is a lack from pituitary
    T4/T3 = low
  2. Subclinical hypothyroidism
    TSH high
    T3/T4 normal
    RE-TEST in 2-4 months to see if TSH still high (would also want to look at TPO to see if you’ve caught HYPOthyroidism early)
52
Q

What antibodies are found in hashimottos?

What antibodies are found in Graves?

A

Anti-TPO Ab=hashimottos (hypo)

TSH-receptor stimulating Ab (TRAB) GRAVES (hyper)

53
Q

What is the most common cause of hyperthyroidism?

Explain what it is?

A

Grave’s disease

  • Autoimmune disease caused IgG antibodies binding to TSH receptors
  • Causing thyroid enlargement and increase in T3 and T4
  • Also bind to antigens in extra ocular muscles (inflammation/proptosis/exopthalmous)
54
Q

What is the name of ultimate hypothyroid state before death?

Management?

A

Myxodema coma (ITU and IV T3 or levothryoxine AND IV corticosteroids coexisting adrenal insufficiency has been excluded)

55
Q

Causes of HYPERthyroidism?

A
  • Graves disease
  • Toxic multinodular goitre=multiple nodules that secrete thyroid hormones
  • Toxic adenoma = solitary nodule producing T3 and T4
  • Ectopic thyroid tissue - metastatic follicular thyroid cancer
56
Q

What causes a painful goitre?

Treatment?

A
  • Painful Goitre – subacute De-Quevain (following on from viral infection.
  • Self limiting-treat with NSAIDS
57
Q

How do you treat Graves disease

What is curative treatment?

A

Graves disease
-Carbimazole for 12-18 months!!! (relapse high)
(either on its own or part of a BLOCK AND REPLACE therapy with levothyroxine-less relapse)
-Aim is to try and make euthymic then just reassess
-Surgery diffinitive (more rarely done now)

58
Q

What are some dangerous side effects of carbimazole?

A

Agranulocytosis-low neutrophils which can lead to sepsis

59
Q

What are TFTs like in hyperthyroidism? (primary, secondary, subclinical)

A

PRIMARY HYPERTHYROIDISM
TSH = low (suppressed)
T4 + T3 = high

SECONDARY HYPERTHYROIDISM (TSH secreting pituitary adenoma)
TSH= high
T3/T4 high 

SUBCLINICAL HYPERTHYROIDISM
TSH = low (suppressed)
T4 + T3 =normal
(recheck in 2 months)

60
Q

What are graves specific signs? (4)

A

Graves specific signs

  • Eye disease (exophthalmos, opthalmoplegia (paralysis of muscles within or surrounding eye → diplopia)
  • Pretibial myxoedma – oedematous, discoloured swelling above lateral malleoli (also seen in hypothyroid)
  • Thyroid Acropatchy – extreme manifestation with clubbing, painful finger + toe swelling
  • Also Bruits (due to ↑vascularity in thyroid)
61
Q

What is a hyperthyroid crisis called ?

What could precipitate it?

A
  • Thyroid storm

- Precipitated by surgery/radioactive iodine (also infection, MI, trauma)

62
Q

How does a thyroid storm present?

A
Severe hyperthyroidism:
Fever 
AF 
Diarrhoea + vomiting
Agitation>confusion>coma
63
Q

Treatment of a thyroid storm?

A
  1. THYROID BLOCKING
    - propylthiouracil
  2. CORTICOSTEROIDS (stops the peripheral conversion of T3/T4). E.g. hydrocortisone
  3. SYMPTOM CONTROL
    - IV propanolol or CCB
    - IV fluids
    - Paracetamol (anti-pyrexial)
64
Q

1st line treatment for Toxic nodular goitre?

A

Toxic nodular goitre
1st line: radioactive iodine
(taken up preferably by autonomous nodule)
(toxic afterwards-stay clear of kids/pregnant ppl)

-surgery/drugs if radioactive iodine unsuitable (pregnancy/lactation) or if compressive symptoms

65
Q

Thyroid function tests
1. ↑TSH and ↑T3/T4

  1. ↓TSH ↓T3/T4
A
  1. ↑TSH and ↑T3/T4
    - Pituitary tumour (rare)
    - Poor compliance with thyroxine, focus on TSH for monitoring (T3/T4 can be normal)
  2. ↓TSH ↓T3/T4
    - Sick euthyroid (sick hospital inpatient)
    - Pituitary insufficiency
66
Q

How does thyroiditis present?
What causes it?
Whats the treatment?

A

ACUTE THYROIDITIS

  • Acute heat intolerance, tremor, neck discomfort
  • Viral: de Quervians
  • Drugs (amiodarone)
  • Postpartum

Treatment: self limiting

67
Q

Complications in hyperthyroidism?

A

Complications in hyperthyroidism

  • AF
  • High output HF
  • Thyroid storm (precipitated by surgery, trauma or infection)
  • Osteopenia/osteoporosis
  • Upper airway obstruction (goitre)
  • Visual effects/corneal ulcers
68
Q

Cushings syndrome vs cushings disease?

A

Cushing’s syndrome
-the clinical state produced by chronic glucocorticoid excess (most common cause-exogenous steroids)

  • Cushing’s disease
  • excessive ACTH from the pituitary (due to a benign pituitary adenoma)
69
Q

Aside from Cushing’s disease, what is another ACTH-dependent cause of Cushing’s syndrome?

A

Ectopic ACTH tumours e.g. small cell lung cancer

The classical symptoms of Cushing’s are absent in this one

70
Q

What does a Cushing’s person look like?

A
Cushings
Catabolic (inc androgens)
-Skin thinning
-Myopathy 
-Purple abdominal striae 
-Muscle/tendon wasting - recurrent Achilles tendon rupture 
-Osteoporosis 
-Acne 
-Hirsutism 
-Gonadal dysfunction - erectile dysfunction, irregular periods (↓GRH)

Glucocorticoid

  • Diabetes/hyperglycaemia (↑Glucose)
  • Infection prone + Poor healing wounds (↓inflam mediators)
  • Truncal obesity/intrascapular fat pad
  • Moon face

Mineralcorticoid

  • HTN (↑BP)
  • Hypo↓kalmia (opposite of addisons)

*Depression /Psychosis

71
Q

What do you need to confirm a diagnosis of Cushing’s?

A

Confirm diagnosis with raised plasma cortisol

72
Q

What is the first-line test (after establishing a raised plasma cortisol) for Cushing’s?

A

1st line Overnight dexamethasone suppression test

  • give 1mg dexamethasone at midnight
  • do serum cortisol at 8am
  • normally, cortisol suppresses to <50nmol/L

Cushing’s = NO SUPPRESSION – cortisol remains high
False + ve in obesity, alcohol, phenytoin, rifampicin

73
Q

What is an alternative to the overnight dexamethasone suppression test?

A

24 hour urinary free cortisol

  • 3 collections
  • also measures creatinine excretion
  • diagnosed in 2+ collections measure cortisol excretion as >3 times the lab upper limit of normal
74
Q

What is 2nd line test (if 1st line tests were abnormal) for Cushing’s?

A

48 hour dexamethasone suppression test
- give dexamethasone 0.5mg 4 times per day for 2 days
- measure cortisol at 0 and 48 hours
Cushing’s = NO SUPPRESSION

75
Q

Apart from oral steroids, what are some other ACTH-independent causes of Cushing’s?

A
  • Adrenal adenoma (do an adrenalectomy)

- Adrenal nodular hyperplasia

76
Q

What test can you do to localise the cause of Cushing’s? (whether or not ACTH dependent)

A

Plasma ACTH

  • LOW in cushings syndrome (adrenal tumour)
  • HIGH in Cushings disease (ACTH-dependent cause)
77
Q

How do you distinguish between a pituitary cause or ectopic ACTH producing cause of Cushing’s?

A

High dose dexamethasone suppression test

  • pituitary adenoma >cortisol suppressed
  • ectopic >no change
78
Q

How does a growth hormone-producing tumour (pituitary adenoma) in children or adults?

A
Children = gigantism (most commonly prolactinoma)
Adults = acromegaly
79
Q

What visual defects do you get from a pituitary adenoma and why?

A

Bilateral temporal hemianopia due to compression of the optic chiasm

80
Q

What other condition can be caused by pituitary adenoma?

A
  • Diabetes insipidus (which is not related to diabetes mellitus).
  • Characterised by polydypsia and polyuria (nocturia)
  • It is due to reduced ADH secretion from the posterior pituitary
  • Diagnostic test used is the water deprivation test.
81
Q

When treating hypothyroidism secondary to hypopituitarism, what must you give before levothyroxine and why?

A

Steroids because thyroxine could precipitate and Addisonian crisis (=adrenal crisis)

82
Q

What visual field problem would you see in pituitary adenoma?

A

PITUITRY ADENOMA-VISION

-bilateral temporal hemianopia a.k.a tunnel vision

83
Q

What antibody is seen in Addisons adrenal insufficiancy?

A

ADDISONS: 21 hydroxylase Ab + ve

84
Q

What is Conns syndrome?

What are the signs?

What is the 1st line investigation

A

Conns is a cause of primary hyperaldosteronism

HYPERTENSION and HYPOkalaemia (can be normal)

1st line investigation
- renin-aldosterone ratio will be high-renin high to compensate for low aldosterone (ideally, this should be taken whilst the patient is not taking any antihypertensives)

Treatment:

  • surgery if adenoma,
  • aldosterone antagonist e.g. spironolactone if hyperplasia
85
Q

What is diabetes insipidous? (2 types)

Symptoms?

A

Diabetes insipidus

  • issues with ADH action:
    a) Cranial (HYPO ADH secretion)
    b) Nephrogenic (Insensitivity of ADH) e.g. lithium
86
Q

Symptoms of diabetes insidious?

A

Diabetes insipidus symptoms

  • thirst
  • polyuria (>3 litres per day)
  • nocturia
87
Q

What is the serum and urine osmolarity in diabetes insipidus?

Treatment?

A

Diabetes insipidus
↑Serum osmolarity (concentrated-hypernatremia)
↓Urine osmolarity (not very concentrated)

Tx: desmopressin (causes hyponatreamia)

88
Q

What is the diagnostic test for diabetes insipidus?

A

Diagnostic test used is the water deprivation test. (deprived water, given ADH, reassessed)

(although if taking lithium-do Ca2+ first to rule out hypercalceamia)

89
Q

What is the diagnostic test for acromegally?

A

Acromegally

-increased insulin like growth factors

90
Q

After a water deprivation test what would you see for both nephrogenic and neurogenic diabetes insipidious?

A

After 8 hour water deprivation test
-both neurogenic and nephrogenic URINE OSMOLARITY would be LOW (normal responce would be to increase ADH to retain water but they cant)

91
Q

After desmopressin test what would you see for both nephrogenic and neurogenic diabetes insidious?

A

After desmopressin test

  • Neurogenic URINE OSMOLARITY would INCREASE (cos now they have ADH)
  • Nephrogenic URINE OSMOLARITY would still be LOW (cos they dont know how to use ADH) e.g. lithium
92
Q

What does HIGH osmolarity mean?

A

High osmolarity=high concentration

93
Q

What are periods like in hyper/hypo thyroidism?

A

Hypo=irregular/heavy :(

Hyper=AMMENORREA no periods :)

94
Q

How do we monitor responce to thyroxine?

A

Look at TSH (aim for 0.2-2)

  • aim for a LOWER TSH than the general population
  • If still high> bad compliance or not high enough
95
Q

What tumours commonly metastasise to bone?

A
  • Myeloma/melanoma
  • Breast
  • Lung (squamous most commonly) /lymphoma
  • Thyroid
  • Kidney
  • Prostate
96
Q

What is calcitonin?

A

Produced by the thyroid gland to LOWER CALCIUM by preventing osteoclasts

97
Q

What is cholecalciferol?

A

Used for Vit D defficiency maintenance

98
Q

What is Cinacalet?

When is it used?

A

REDUCES PTH!!!

  • MOST COMMONLY used in primary hyperparathyroidism when parathyroidectomy is inappropriate!!!!!!
  • Also used in secondary hyperparathyroidism (as well as treating cause)
99
Q

What are some causes of hyPOparathyroidism?

A

Rarer than hyper

  • Following thyroid surgery/radiotherapy
  • Digeorge syndrome (parathyroid/cardiac/cleft palate)
  • Infiltrative (Wilsons/haemachromatosis)
100
Q

Treatment of addisonian crisis?

A

Addisonian crisis

1) STEROIDS
- 100mg hydrocortisone IV

2) SUGAR
- 200mg hydrocortisone IV in 5% glucose

3) SALINE
- 500ml 0.9% NaCl
- then rehydrate 3-4L over 24 hours

4) SEARCH FOR CAUSE
(suddenly stopped steroids/illness/surgery/trauma)

101
Q

1st line treatment for micro- and macroprolatinomas?

A

Cabergoline (a dopamine agonist) is the first-line treatment for a micro- and macroprolatinomas.

102
Q

What drug can be used to treat high cortisol in bushings disease

A

Metyrapone

103
Q

If you cant find source of cusgings disease, what can you do?

A

Bilateral adrenalectomy

can also give adrnenolytic drug mitotane

104
Q

What is a complication of Bilateral adrenalectomy

A

Nelsons syndrome (pituitary adenoma expands due to removal of adrenals-do MRI and monitor ATCH follow up after adrenalectomy)

  • Dark
  • Head
  • bitemporal hemionopia
105
Q

What is the treatment for prolactinomas (pituitary adenomas)

A

Carboligine (or bromocriptine)

Dopamine agonists