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Year 4 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the most common type of thyroid cancer?

A

Papillary - 70-80%
20-40y
early lymphatic spread

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2
Q

What type of thyroid cancer need a diagnostic thyroidectomy?

A 
Follicular carcinoma (20%) spread by haematgenous route** so worse prognosis. 
(Follicular adenoma -80%)
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3
Q

What type of thyroid cancer get genetic testing?

A

Medullary. 20% Associated with MEN 2A and 2B

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4
Q

What are the types of thyroid cancer and their key features?

A

Papillary - most common - 70-80%

Follicular - spread via blood and need diagnostic hemithyroidectomy. Chronic TSH stimulation (usually due to iodine deficiency)

Medullary - C-cells (calcitonin and CEA) associated with MEN 2A and MEN 2B. usually in upper 2/3 of thyroid

Anaplastic - Undifferentiated follicular cells. poor prognosis <6months. Rapidly infiltrates local structures and mets. dysphagia, hoarse voice, compromised airway

Lymphoma - from non-hodgkins B cell. elderly women. Usually on a back ground of Hashimotos

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5
Q

How is a thyroglossal cyst formed?

A

Remnant of the foramen cecum

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6
Q

Give some differentials of a neck lump.

A

Thyroid nodule, lipoma, skin cancer, parotid tumour (or other salivary gland tumour), reactive lymphadenopathy, thyroglossal cyst.

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7
Q

What are the features of MEN 1 (on Ch 11, encoded Menin)

A

3 P’s
Parathyroid tumour
Pancreatic islet cell tumour
Anterior pituitary tumour

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8
Q

What are the features of MEN 2 (ch 10, mutation to RET photo-oncogene)

A

MEN 2A - Medullary thyroid carcinoma, Pheochromocytoma, Primary hyperparathyroidism

MEN 2B - Medullary thyroid carcinoma, pheochromocytoma, Mucosal neuroma

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9
Q

What signs may indicate a retrosternal goitre?

A

Facial flushing and venous distention

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10
Q

What is secondary hyperparathyroidism?

A

Usually due to CKD or vit D deficiency. PTH increased in response to hypocalcaemia

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11
Q

What conditions can hyperparathyroidism cause

A

Pancreatitis
Gout
Renal stones

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12
Q

Give a complication of hypothyroidism.

A

Thyroid lymphoma, generally non-hodgkins

AF, osteoporosis, myxoedema coma (multi organ failure), angina, resistant hypothyroidism

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13
Q

What is first line treatment in hyperthyroidism?

A

40mg PO propanolol - symptom control then

Carbimazole SE - rash, agranulocytosis

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14
Q

What is Conn’s syndrome?

A

Syndrome of HTN, severe hypokalaemia and aldosterone hypersecretion with suppression of plasma renin activity. A adrenal adenoma

HTN with LOW renin **
(secondary hyperaldosterone has high renin and Aldos)

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15
Q

What tests would you do in Primary hyperaldosteronism?

A

Serum K (<3mmol/L) and urinary K (>40mmol/L)

Serum aldosterone and renin levels

Ratio of plasma aldosterone conc:Plasma renin activity (>2PAC:PRA, can get false +ve in renovascular hypotension, diuretics, ACEi, malignant HTN, Cablockers)

Aldosterone suppression test (inability for aldosterone to be suppressed by high Na diet)

CT/MRI adrenals
Adrenal venous sampling

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16
Q

What AI might suggest Addison’s disease?

A

Autoantibodies to 21-hydroxylase

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17
Q

What is the max amount of Na you can give?

A

10mmol/L in 24 hours

risk of cerebral oedema

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18
Q

What causes increased levels of growth hormone?

A

Acromegaly, stress, pregnancy, sleep, puberty

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19
Q

What treatment options are available in acromegaly?

A
  1. Trans-sphenoidal surgery - if fails ->
  2. Somatostatin analogue (octreotide) + domaine agonist (cabergoline) ± radiotherapy
  3. GH receptor antagonist (pegvisomant)
  4. Radiotherapy
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20
Q

How might someone with sever hyponatraemia present? (Sr Na <120)

A

Reduced mental state, confusion, irritability, restlessness, seizures, coma

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21
Q

How can you calculate serum osmolality?

A

2X (Na) +urea + glucose

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22
Q

What are some causes of SIADH?

A

Small cell lung cancer
infection - Legionella pneumonia, lung abscess
Meningitis
Head injury or port-op from a major surgery
Stroke, haemorrhage
SSRIs, carbamazepine, thiazide diuretics, NSIADs (mood stabilisers and anti-epileptic)

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23
Q

How could you treat symptomatic hypocalcaemia?

A
  1. 10ml of 10% calcium gluconate diluted in N saline or dextrose, (SLOW!) over 10min with cardiac monitoring (giving it fast - arrhythmias)
  2. Followed by a slow infusion of 100ml 10% Ca gluconate in 1L N saline. ~50ml/hr. Titre dose to maintain Sr Ca at low-normal range. Monitor 2X daily

If Mg low - add 20ml (~40mmol/L) 50% MgSO4 to 230ml N saline and infuse at 50ml/10min then 25ml/hr

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24
Q

What are the treatment options for hyperprolactinaemia?

A

Bromocriptine or cabergoline - dopamine agonist

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25
Q

What are some causes of hyperkalaemia?

> 6

A 
The body CARED too much for K
Cellular movement of IC K to EC in burns and tissue damage
Adrenal insufficiency / Addison's 
Renal failure
Excessive K intake
Drugs - ACEi, NSAIDs, spironolactone

Tumour lysis syndrome, metabolic acidosis, massive blood transfusion, rhabdomyolysis

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26
Q

What are some symptoms of hyperkalaemia?

A

MURDER
Muscle weakness
Urine output little to none
Respiratory failure (due to muscle weakness)
Decreased cardiac contractility
Early muscle twitches/ cramps
Rhythm changes - tall peaked T wave, prolonged PR

Cardiac arrhythmia - VF - Fatal
>7 - bradycardia
>9 - Cardiac arrest

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27
Q

What are the ECG changes seen in hyperkalaemia?

A

Tall peaked T wave
Broad QRS
Flattened or absent P waves
Prolonged PR

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28
Q

How would you manage hyperkalaemia? (K > 6.5?)

A

Insuline (10U actrapid), dextrose (50ml of 50%) and IV calcium gluconate

Nebulised salbutamol
If renal failure acidotic - sodium bicarbonate
Dialysis is recurrent and severe and renal failure

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29
Q

How might you manage mild hyperkalaemia?

A

Oral calcium resonium - draws K out of gut and into stool

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30
Q

What are some causes of hypokalaemia?

< 2.5

A

The body is trying to DITCH the K
Drugs - diuretics, laxatives, hydrocortisone
Inadequate consumption of K
Too much water intake
Cushings or Conn’s (kidneys excrete K)
Heavy fluid loss - vomiting/ diarrhoea**, wound drainage, NG tube suction, intestinal fistula

alkalosis, renal tubular failure, pyloric stenosis

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31
Q

What are some signs and symptoms of hypokalaemia?

A 
7 L's
Lethargic
Low, shallow respiration .. failure
Lethal cardiac dysrhythmias
Lots of urine (freq &amp; large volume)
Leg cramps
Limp muscles
Low BP (severe)
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32
Q

What are some causes of hypoglycaemia in non-diabetics?

1st line fir hypoglycaemia testing - short synacthen test
then 72 hour fast

A 
EXPLAIN
EXogenous drugs - lithium, beta blockers
Pituitary insufficiency/ Addison's 
Liver failure 
AI hypoglycaemia
Islet cell tumour - insulinoma
Non-pancreatic neoplasm 
Miscellaneous - sepsis, anorexia, starvation
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33
Q

What must you have to get DKA?

A

Known T1DM or glucose > 11 (1st presentation?)
Acidotic pH <7.3 or bicarb <15 or H > 45
Ketone ++ in urine +/- blood >3mmol/L

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34
Q

What are the first line drugs in T2DM and what comes after?

A

1st - Metformin or sulphonylurea
2nd - Metformin/SU + SU or SGLT2 inhibitor or DPP-4 inhibitor or Glitazone
3rd - or add GLP-1 agonist

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35
Q

What level is the thyroid at ?

A

C5-T1 inferior to the thyroid cartilage

Deep to the sternothyroid and sternohyoid

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36
Q

What is Hypopituitarism?

A

Dysfunction of the hypothalamus, pituitary stalk or pituitary gland that causes a reduction in the anterior pituitary hormone release.
Can be due to trauma, inflammation, ischaemia or infection

GH affected first, ACTH last

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37
Q

Give some examples of causes of hypopituitarism.

A

Hypothalamis - Kallmann’s syndrome, tumour, ischaemia, infections - TB, meningitis, inflammation
Pituitary stalk - Carotid artery aneurysm, meningioma, trauma, surgery
Pituitary gland - Infiltration (HH, amyloidosis, mets), ishcaemia (Sheehan’s syndrome, pituitary apoplexy), tumour, irradiation, inflammation

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38
Q

What are some signs of hypothyroidism?

A 
BRADYCARDIC
Bradycardia
Reflexes relax slowly
Ataxia
Dry skin 
Yawning - tiredness and fatigued
Cold hands
Ascites 
Round puffy face 
Defeated demeans 
Immobile
CCF
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39
Q

What does GH do and what Sx would show a deficiency of it?

A

Stimulates IGF-1 in the liver and controls metabolism, growth, sleep, food intake and memory. It increases muscles mass and reduces body fat.

Sx -
Central obesity, short height, low blood sugar, reduced muscle mass and exercise tolerance, reduced strength, atherosclerosis, dry, wrinkled skin

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40
Q

What affect would gonadotrophin deficiency have on males?

A

FSH-Spermatogenesis via ABP from sertoli
LH- stimulates testosterone by leydig

Reduced secondary sex characteristic, reduced libido, reduced muscle bulk, erectile dysfunction, small testes

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41
Q

What affect would gonadotrophin deficiency have on females?

A

FSH - development of the ovarian follicle
LH - maturation of follicle, formation of corpus lute, ovulation

Reduced libido, reduced fertility, breast atrophy, osteoporosis, oligo/amenorrhoea

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42
Q

What might cause unexplained abdominal pain and vomiting?

A

Addiosns - primary adrenal insufficiency

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43
Q

What affect would corticotrophin deficiency have?

A

Cortisol - released during stress, regulates metabolism, anti-inflammatory, glucose met

fatigue, myalgia, low mood, loss of appetite, increased thirst, N&V, dizziness

NO hyperpigmentation

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44
Q

Give an example of a cause of iatrogenic hypothyroidism.

A

Post-thyroidectomy, post radioactive iodine, amiodarone

Lithium: Block the TSH from binding to its receptor
Before starting they should get a neck exam and TFTs checked. 6 monthly TFTs

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45
Q

What is sick euthyroid syndrome?

A

Abnormal TFTs in the presence of systemic disease e.g. critical illness, starvation. Switches the body into a catabolic state. T4/T3 low TSH - low or normal

Gland is functioning normally but there is less deiodinase and dysregualtion of thyrotrophic feedback control (reduced TSH, TRH) - due to catabolic state (immune cells produce cytokines (IL-6/TNF-alpha) which act directly on hypothalamus and pituitary)

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46
Q

What antibodies are seen in hashimotos thryoiditis?

A

Anti-thyroglobulin*, anti-thyroid peroxidase, anti-TSH receptor

Destruction of follicular cells - release of T3/T4 = transient hyperthryoid phase, but long term low T3/4

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47
Q

In Hashimotos thyroiditis, how might a goitre form?

A

Chronic inflammation leads to
Build up of connective tissue
Infiltration of immune cells
Less functional thryoid tissue

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48
Q

What do thyroid hormones do?

A

Increase the bodys basal metabolic rate and heat production.
Increases SNS - Increases CO, RR, mental awareness
Inc long bone growth, brain development, hair follicle growth
Inc sebaceous and sweat gland secretion, increases glucose metabolism

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49
Q

What are the types of AI thyroiditis in hypothyroidism?

A

Hashimotos - In areas with water/salt fortified with iodine. Goitre formation
Primary myxoedema/atrophic - similar to above but NO goitre
Reidels thyroiditis - IgG4 mediated. Dense fibrous tissue replaces thyroid- Fibrosis extends beyond thyroids fibrous capsule - goitre (Associated with RETROPERITONEAL FIBROSIS)

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50
Q

What is subclinical hypothyroidism?

A

A state of thyroid function where thyroid hormones are normal level but TSH is raised.
TH may be in range but a FALL from a previous level

More common to progress to overt hypo if:
Higher TSH, especially >10mU/L–> give Levothyroxine
Anti-thyroid peroxidase

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51
Q

Sheehans syndrom is a cause of secondary hypothyroidism, what is it?

A

Post partam pituitary necrosis caused by ishcaemic necrosis due to blood loss/ hypovolaemia during child birth

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52
Q

What is the most common cause of hypothyroidism in the UK and worldwide?

A

UK - Hashimotots

World wide - iodine deficiency - hypertrophy of the gland causing a goitre

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53
Q

List some causes of secondary hypothyroidism?

A

Pituitary tumour - bitemporal hemianopia
Sheehans syndrome
Sick euthyroid syndrome
Head trauma

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54
Q

What investigations would you do to investigate thyroid dysfunction?

A

US
FNA
Thyroid uptake scan
MRI head

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55
Q

What is a goitre?

A

A symmetrical swelling at the front of the neck that moves on swallowing

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56
Q

What causes the clinical features in graves disease?

Triad - thyrotoxicosis, goitre, eye signs

A

Fibroblasts are stimulated by TSH receptor antibodies which causes deposition of glycosaminoglycans which causes fluid retention

Exopthalmos - inflammation, hypertrophy and swelling of retro orbital structures push eye forward. - this causes limited eye movement - Ophthamoplegia
Depositions in the skin causes non-pitting oedema and skin thickening - pretibial myxoedema

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57
Q

Why is there lid lag and retraction in Graves?

A

Overactivity of SNS? and so over activity of the lelevator palpebral superiors

Corneal ulceration - more prone to dry eyes

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58
Q

What is the most common cause of hyperthyroidism in iodine deficient areas?

A

Toxic multi nodular goitre (plummers disease)

Toxic - nodules autonomously secrete excess TH

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59
Q

How does a toxic multinodular goitre form?

Radioactive iodine 1st line for toxic nodular HypERthyroidsim

A

Multinodular goitre - Low levels of T4/T3 feeds back to pituitary - TSH
Increased TSH causes follicular hyperplasia and thyroid hypertrophy - uneven growth die to responsiveness
Inc no. of follicular cells can result in pt being euthryoid
If iodine decency worsen it can undergo hypertrophy and hyperplasia again in reposne to TSH

Toxic - Mutation in a dividing follicular cell
TSH receptor constantly activated - excess TH secretion

60
Q

What is De Quervians thyroiditis or subacute thryoiditis?

A

Precipitated by a viral infection - mumps, influenza, cocksackie virus (target the thyroid)
Painful inflamed thyroid, there is destruction of follicular cells - relates of TH - transient mild hyperTH
should return to normal function in 6months
Rarely do not completely recover - hypothyroidism

61
Q

What is a cause of secondary hyperthyroidism?

A

Pituitary adenoma

62
Q

What results are seen in subclinical HypER thryodisim?

A

Low TSH, normal T4/T3

63
Q

What are the 2 ways of giving of antithyroid treatment in hyperthyroidism?

A

Dose titration: Give antithyroid drugs to make you euthryoid

Block and replace: Antithyroid drugs and a thyroxine replacement

64
Q

What are some complications of hyperthyroidism?

A

Heart problems - heart failure, AF
osteoporosis
Thyroid storm - HR, Bp and body temp can sore to dangerously high levels - medical emergency

65
Q

What are some causes of hyperparathyroidism?

A

Primary - Pituitary single adenoma, hyperplasia, multiple adenomas, carcinomas. Low PO4
Secondary - Vit D deficiency or renal failure /Uraemia due to long term dialysis. Response to hypoCa. High PO4
Tertiary - Prolonged secondary HPT causes PT hyperplasia. seen in CKD. high Ca, PO4

66
Q

What are some scans that can be performed of the parathyroid gland.

A

SPECT CT scan
Sestamibi scan of the neck- localise a PT adenoma
US

67
Q

What is Cinacalcet?

A

Its a calcimmetic
Reduces PTH secretion
Increases Ca receptors sensitivity to activation by EC Ca
Inhibition of PTH and so Ca reduced
Treat 2ndary HPT with ESRD on dialysis
Primary HPT when parathryoidectomy inappropriate

68
Q

List some immediate and late complications of thyroid surgery.

A

Immediate - haemorrhage, RLN palsy, resp obstruction (due to laryngeal oedema due to tension haematoma?), infection, thyroid crisis/storm
Late - thyroid insufficiency, recurrent thryrotoxicosis, hypertrophic scar ot keloid scar

69
Q

A late complication of thyroid surgery is PTH insufficiency/ permanent hypoCa, how might this present?

A

Sudden changes in ionised sr Ca can cause perioral and distal extremity paraesthesia (lips and finger tingling)
Triad: Carpopedal spasm, stridor, convulsions
Give calcitriol or Ca, and Vit D

70
Q

What are causes of hypothyroidism?

A 
Hashimotos thyroiditis
Reidels thyroiditis 
Atrophic thyroiditis 
De quervians thyroiditis 
Iodine deficiency 
Iatrogenic hypo - Lithium 
Subclinical hypo
Pituitary adenoma
71
Q

What are some dynamic tests for checking hormone axis defiencies and what do they test?

A

Short synacthen test - adrenal axis
Insulin intolerance test - Adrenal and GH axis
(if contraindicated glucagon stimulation test)
GHRH-arguinine test (arguine is a AA which inhibits somatostatin allowing GH release) - GH axis

72
Q

What does somatostatin do?

A

Inhibits TSH and GH

73
Q

The commonest hormonal disturbance of the pituitary is hyperprolactinoma (PRL>390), what might high levels of PRL lead to?

A

High PRL inhibits GnRH
Leading to hypogonadism, infertility, osteoporosis
Sx relate to FSH and LH def - Galactorrhoea, reduced libido, erectile dysfunction, oligo/amenorrhoea

74
Q

What are some causes of hyperprolactineamia?

1st line - Dopamine agonist - Bromocriptine or cabergoline

A

PROLACTINS
Prolactinoma/Physiolgical -pregnancy/breastfeeding/stress
Renal failure
Ocp and meds - (most common) haloperidol, melthydopa
Liver failure
Adenoma (PRL secreting)
Chest wall disease (herpes zoster, surgery)
Thyroid disease (hypothyroidism)
Infiltrative disease - HH, sarcoidosis
Nipple stimulation/ nursing
Stalk damage

75
Q

How would you test for hyperprolactinaemia?

A 
Review medications
Basal PRL
Pregnancy test **
LFTs, TFTs, U&Es
MRI pituitary
76
Q

How could you tell if the hyperprplactinaemia was causes by an adenoma and what size?

A

> 5000 PRL usually due to prolactinoma
Microprolactinoma <10mm - ~1000-3000PRL Dopamine agonist then if intolerant trans-sphenoidal surgery
Macro- >10mm on MRI, ~3000-6000PRL. Usually have Sx such as Optic atrophy. ophthalmoplegia, reduced visual fields and visual acuity, diplopia due to compressing optic chiasm. Treat same as micro

77
Q

How can you treat DI?

A

Cranial - IM desmopressin

Nephrogenic - Thiazide diuretics like bendroflumethiazide

78
Q

How would you diagnose SIADH?

Tx
1. Fluid restriction 
2. Treat underlying cause 
3. Tolvaptan - ADH receptor blocker 
Or Demeclocycline - inhibits ADH
A

Initial diagnosis:
Exclude: Adrenal insufficiency (short synacthen test), CKD/AKI, Hx excessive water intake, diuretic use, D&V, burns, excessive sweating, fistula

Establish cause: CXR, MRI brain, CT TAP, review drugs. recent surgery?

Urine Osmo and urine Na HIGH
Plasma Osmo and plasma Na LOW

79
Q

What is free (ionic) plasma calcium dependent on?

A 
Arterial pH (in acidosis there is reduced protein binding and so increased free ca)
Plasma albumin

Corrected Ca = Measured Ca + [40-sr albumin] x0.02

80
Q

What are some Sx seen in hypERcalcaemia?

A

Asymptomatic, Polyuria, polydipsia, dehydration, abdo pain, constipation, N&V, depression, anorexia, HTN, weakness, nephrogenic DI*, bone pain
Severe - cardiac dysrhythmia (bradycardia or arrhythmias), confusion, kidney stones, risk of cardiac arrest

81
Q

Why might there be muscle weakness and absent or slow reflexes in hyperCa?

A

Too much Ca increases the threshold for depolarisation in neurones so they are less excitable - slower contraction

82
Q

Causes of Hyper Ca?

A

PASER MOD
Primary (or 3) hyperpapthryoidism - single PT adenoma (INC PO4 EXCRETION SO LOW PO4)
Addisons
Sarcoidosis or amyloidosis
Endocrine tumours - gastrinoma
Renal failure
Malignancy - PTHrP or osteolytic bone mets
Overdose of vit D
Drugs - lithium, thiazide diuretics, theophylline toxicity

83
Q

How would you treat HyperCa?

A

IV normal saline ~3-6L/24hr - depends on fluid status - monitor fluid balance
Once rehydrated, continued IV N saline infusion and give 20-40mg/2-4hr Furosemide to prevent PO
Monitor K & Mg- may need added (esp after rehydration)

If fails:
BIsphosphonates - Pamidronate 30-60mg/4-6hr IV
Calcitonin
Steroids in sarcoidosis, myeline or vit D toxicity

84
Q

Give some Sx of Hypernatraemia (Na>145mmol/L).

A

Confusion, AMS, dehydration, polydipsia, muscle spasm/twitches, weakness, fatigues, seizures, irritable

85
Q

What are some causes of hypernatraemia?

A 
COID BRD
Cushings or conns syndrome
Osmotic diuresis in HHS
Iatrogenic 
Diabetes insipidus 
Burns 
Respiratory losses
Diarrhoea and vomiting
86
Q

What are the Sx and causes of hypomagnesaemia?

< 0.6mmol/L

A

Sx - Paraesthesia, ataxia, teteny, seizures, headache, fatigue, arrhythmia, digitalis toxicity exacerbated

Causes - Alcohol Abuse, TPN, Severe diarrhoea, diuretics, ketoacidosis, loss or low other electrolytes (Ca, K, PO4),

87
Q

What are the Sx and causes of hypermagnesaemia?

> 1mmol/L
5 - severe

A

Sx: Drowsy, N&V, hypotension, reduced pulse, coma, Neuromuscular depression, CNS& resp depression, heart block, hyporeflexia

Causes: renal failure, iatrogenic (excessive antacids)

88
Q

When might blood results show hyperkalaemia but not be true?

A

Haemolysis (Break down of RBC, falsely elevated K)
Contamination
Thrombocythemia - K leaks out of platelets during clotting
Delayed analysis

89
Q

What ECG changes are seen in hypokalaemia?

A

Small, T waves, prominent U waves, ST depression

90
Q

How would you manage a patient if the had K < 2.5 ± dangerous Sx such as shallow resp, cardiac arrhythmia or where lethargic?

A

IV K
DO NOT GIVE MORE THAN 20mmol PER HOUR
OR CONC MORE THAN 40mmol/L
NEVER give as a fast bolus

91
Q

Hyponatraemia (Na <135) is usually asymptomatic unless severe Na < 120, what are some clinical signs?

A

Gait instability, seizures, confusion, AMS, irritability, postural hypotension, drowsy, ataxia, coma

92
Q

List some causes of hypoNa.

A

Hypovolaemic, hypoNa - When you are losing fluid and electrolytes in the blood - Renal losses - diuretics, addisons, hypoTH. (renal cause has HIGH urinary Na)
Non-renal - D&V, burns, peritonitis, pancreatitis (low urinary Na)

Normovolaemic and hypoNa - normal or inc ECV or losing Na somewhere? - SIADH, trauma, malignancy (small cell, leukaemia, lymphoma), stroke, Infections- pneumonia, TB, CF, vasculitis

Hypervolaemic hypoNa - Fluid overload - Nephrotic syndrome, CCF, cirrhosis with ascites, severe renal failure

93
Q

Osmotic demyelination can occur if hypONa is corrected too fast, what are some Sx?

A

Can be delayed onset by 2-5 days
often irreversible
Dysarthria, dysphasia, paraparesis or quadriparesis, lethargy, coma or seizures

94
Q

How do you test for the type of hyponatraemia?

A
  1. Serum osmolarity - Pseudo-hyponatraemia (isotonic hypoNa), True hypoNa (hypotonic hypoNa), hypertonic hypoNa (HHS, radiocontrast, hyperglycaemia, mannitol)
  2. Fluid staus - Hypovolaemia, euvolaemia (SIADH, severe myxoedema), Hypervolaemia (CCF, nephrotic syndrome, cirrhosis with ascites)
  3. Urinary Na- Renal losses in hypovolaemic hypoNa (Diuretics, addisons)- HIGH URINARY NA
    Non-renal hypovol hypoNa (D&V, burns, pancreatitis) LOW URINARY Na
95
Q

How would you treat the different causes of hypoNa?

A

Symptomatic (coma, seizures) may need airway management- Hypertonic 3% saline, preferabley down a central line in HDU

If dehydrated - normal 0.9% saline and recheck U&Es, may need to Monitor fluid

If not dehydrated with SIADH - restrict fluid
CCF - Furosemide?

96
Q

What is peudohyponatraemia?

A 
Severely elevated cholesterol - hyperlipidaemia - 
Isotonic hyponatraemia  (isotonic sr Na 285-295mosm/kg)
97
Q

What are some causes of hypocalcaemia?

A

Vit D deficnecy, CKD, Sepsis, buruns, Mg deficiency, loss from circulation such as in acute pancteatits, chemotherapy (cisplatin), hypoparathyroidism, post-PT, thyroid or neck surgery

98
Q

How might hypocalcaemia present?

A

abnormal neurological sensation and neuromuscular excitation
SPASMODIC
Spasms - carpopedal spasm In Trousseau’s sign
Perioral and distal limb paraesthesia
Anxious, irritable
Seizures
Muscle tone increased (smooth m) - dysphagia, wheeze
Orientation impaired and confusion
Dermatitis
Impetigo herpetifformis
Chvosteks sign/ cardiomegaly

QT prolonged

99
Q

What signs can be used in testing for hypocalcaemia?

A

Chvostek’s sign - tapping facial nerve at anterior of ear causing contraction of facial muscles

Trousseau’s sign - inflating BP cuff for 3-5min, 10-20mmHg above SPB causing mild ischaemia - hyper excitability - carpal spasm

100
Q

Acromegaly is due to increased GH secretion usually due to a pituitary tumour, what are some Sx?

A

Acroparaesthesia, frontal bossing, large hands and feet. macroglossia, arthralgia/arthritis, headache, reduced libido, amenorrhoea, OSA, proximal myopathy, coursing face, snoring, acanthosis nigracans, goitre

101
Q

What are some complications of acromegaly?

A

Impaired glucose tolerance - DM - ketoacidosis
(normally GH is inhibited by high glucose)
Inc BP - LVH, cardiomyopathy, arrhythmias, CCF, stroke
Inc risk of Colon cancer

102
Q

How could you test for acromegaly?

A
  1. IGF-1 level
  2. Oral glucose TOLERANCE test (OGTT)- GH level remains high
  3. Random sr GH
    MRI, visual fields, ECG, Echo
103
Q

What is a pheochromocytoma?

A

Catecholamine secreting tumour of the adrenal medulla (Dopamine, NA, adrenaline)

Triggered by mechanical pressure on tumour - defecation, exercise, labour, GA, alcohol, sex. or MEN2

Palpitations, headache, sweating, HTN (persistent or parsoxysmal), dizzy, irritable, shaky, weakness

104
Q

How would you test for a pheochromocytoma?

A 
24 hour urinary catecholamine collection - NA and VMA levels (Vanillylmandelic acid)
Clonidine suppression test (failure of urinary catecholamine levels to fall after dose)
Thoracoabdominal CT or MRI - 1st line 
MIBG scan (nuclear medicine)
105
Q

How can you tell if primary hyperaldosterone is due to a single adenoma (Conn’s) or bilateral hyperplasia?

A

Posture test:

Aldos plasma con rises in bilateral hyperplasia after 4 hours of standing but falls in unilateral adenoma

106
Q

What treatment can you give in cushings syndrome?

A

Due to Excess levels of plasma cortisol.

Medical - Metyrapone or Ketoconazole - reduced cortisol synthesis
Unilateral (adenoma) or bilateral adrenaletomy (failed pituitary surgery for ACTH secreting adenoma or bilat adrenal hyperplasia)
WITH CORTISOL REPLACEMENT - PO prednisolone (50-100mg IV hydrocortsone initially after surgery)
and Fludrocortsine 0.1mg in bilateral

*inform about addisonian crisis

107
Q

Explain the investigations for checking if there is excess cortisol in cushings syndrome.

A

Late night salivary cortisol - elevated levels at 9am and 12am shows loss of normal circadian rhythm of cortisol
24-hour urinary cortisol - constantly elevated
Dexamethasone suppression test - 1mg in evening then measure in the am - Failure of cortisol to be inhibited - Cushings syndrome

ACTH levels - Low in adrenal disease (-ve feedback), high in pituitary adenoma (cushings disease) or ectopic source (small cell lung cancer)

108
Q

What tests can indicate addisons?

IV 200mg/24hr hydrocortisone

A

Suspicious biochem - hypONa, HypERK, hypOglycaemia
Morning cortisol <83nmol/L = insufficiency
Short Synacthen test - Measure cortisol before (should be >250 baseline) and 30min after IV ACTH = <450 after = insufficiency
ACTH really high
Renin High aldosterone low
autoantibodies - 21- hydroxylase

109
Q

List some causes of primary hypoadrenalism?

A

AI - 21-hydroxylase autoantibodies
Infections - TB, pseudomonas, meningiococcal
Bilateral adrenal destruction by mets - lung, breast, stomach, lymphoma
Adrenal haemorrhagic infarction - warfarin or heparin
Drugs - ketoconazole or metyrapone (cushings), mitotane (adrenocortico carcinoma)
Congenital adrenal hyperplasia (deficiency of 21-hydroxlayse)

110
Q

What are babies with diabetic mums at risk of?

A

Neonatal hypoglycaemia
Polycythaemia, jaundice, congenital heart disease, cardiomyopathy

Pregnancy - macrosomia and large for date foetus

111
Q

What are causes of insulin resistant and insulin deficient diabetes?

A

Deficient - T1DM, MODY (secondary diabetes - CF, Haemochromatosis, pancreatitis)
Resistant - T2DM, gestational (secondary - cushings, acromegaly)

112
Q

Give an example of a causes of hypogonadism due to hypogonadotrophic hypogonadism?

A

Kallmann’s syndrome - isolated deficiency in LH and FSH (gonadotrophin)
Failure of GnRH cells to migrate to hypothalamus from factory placodes.
Aplasia or hypoplasia of olfactory lobes - anosmia or hyposmia
Deafness, cleft palate, micropenis ± cryptorchidism

113
Q

Give an example of a causes of hypogonadism due to primary gonadal failure.

A

Klinefelters syndrome: XXY presents at puberty
Raised LH & FSH but seminiferous tubules regress and leydig cells don’t function properly
Behavioural issues, learning difficulties, azospermia, gynaecosmatsia, testicular atrophy, lack of male 2nd sex characteristic, delayed puberty

114
Q

What symptoms may present in hypoglycaemia (<3mmol/L)?

A

Autonomic - palpitations, sweating, pallor, tremor, irritability, nausea
Neuroglycopenic - lack of concentration, drowsy, incoordination, weakness, dizzy, seizures, headache

115
Q

An insulinoma is a benign islet cell tumour that can be seen in MEN 1, how might it present?

A

Fasting hypoglycaemia + whipples triad:

  1. Symptoms consistent with hypoglycaemia
  2. Plasma glucose conc low < 50mg/dL
  3. Relief of symptoms when plasma glucose level raised
116
Q

What are some causes of acute breast pain?

A

Normal pre-menstrual cyclical pain, breast trauma, fibrocystic change, infection, MSK pain

117
Q

What are some causes of nipple discharge?

A

Breast cancer, pregnancy or previously breast feeding, galactorrhea, duct ectasia, intraductal papilloma

118
Q

Give some egs of developmental benign breast disease.

A

Ectopic breast tissue - breast tissue outwith the breast. Milk line anywhere from axilla to groin. can be just nipple ± glandular tissue

Breast hypoplasia - associated with turners, Polands, ulnar-mammary syndrome

Congenital nipple inversion - IF NEW inversion - Cancer?

119
Q

Give soma examples of inflammatory breast cancer.

A

Acute mastitis - Associated with breast feeding. Fissuring of the skin allows access of organisms. Stagnant milk allows growth. - Abscess, cellulitis

Granulomatous conditions - TB or sarcoidosis (systemic)

Periductal mastitis/ mammary duct ectasia - SMOKING. Central/Subareolar mammary ducts, become inflamed, blocked and dilated, chronic inflam &scarring, a keratin plug. Abscess & fistulas- red, swollen, hot, tender. Nipple discharge - bloody or yellow-green. non-cyclic mystalgia
Tx - Metronidazole or co-amox, drainage?

Fat necrosis - damage to fat tissue - degeneration and scarring of fat. Firm, irregular, fixed Lump ?bruise - external trauma, surgery - chronic inflammation - fibrosis - necrosis

120
Q

Describe feature of the benign breast neoplasm Fibroadenoma.

A

Breast mouse - Smooth, well circumcised, painless, firm, mobile lump. Benign tumour of the stroma. Younger its - 20s, often asymptomatic

121
Q

Describe features of the hyper plastic benign breast disease fibrocystic breast disease (fibroadenosis)

(radial scar is also a hyperplastic bbd - flower head or star shaped)

A

Women menstruating. Hormone driven* - fluctuating cyclical change. Usually arises prior to period (~10d) and goes once finished.
Bilateral breast lumpiness, bilateral breast pain/tenderness, fluctuations in breast size.
NSAIDs, weight loss, supportive clothes, avoid OCP

122
Q

What is a phyllodes tumour?

A

A large, fast growing, periductal stroma cell neoplasm. 50% benign 25% borderline 25% malignant (squamous metaplasia) 40-50y. Well defined large mass
WLE or mastectomy

123
Q

Describe feature of the benign breast neoplasm Intraductal papilloma.

A

Presents after menopause. Within breast duct
Serous or bloody discharge. Breast ductography
Benign but can indicate and increase risk of breast cancer
Excised and vigilant breast screening

124
Q

The stage before invasive malignancy is dysplastic lesions. What are features of these?

A

Within basement membrane, do NOT extend into the breast stroma, no communication with blood vessels or lymphatics, no possible mets - DCIS, LCIS

125
Q

Give some signs of breast cancer.

A

Breast lump - painless, fixed, immobile, tethered, asymmetrical, ill-defined, hard
Armpit lump
Nipple changes - inverted, deviated, bloody discharge
Skin changes - peu d’orange, dimpling, puckering, ulceration
Systemic - bone pain, weight loss, malignant pleural effusion, pericardial effusion, fever, night sweats, anaemia

126
Q

List some risk factors for breast cancer.

A

Early menarche, late menopause, nulliparity, late first pregnancy, number of children. Breast feeding
HRT, OCP, radiation exposure
Alcohol, smoking, age, obesity
BRAC1 (chr 17) or 2 (13), family history

127
Q

What does HER2 normally do in a healthy breast and what does it do in HER2+ve cancer.

A

Normally the HER2 gene helps control breast cells grow, divide and repair themselves.
In HER2 +ve its over expressed and so there is uncontrollable growth and division

128
Q

What Medication options are available for breast cancer its?

A

Pre-menopasual ER+ - Tamoxifem (SERM- selective oestrogen receptor modulator) Binds and blocks Oestrogen receptor. SE - risk of osteoporosis, indigestion
Post-menopausal ER+ - Aromatase inhibitor (Letrozole, anastrozole) blocks conversison in e.g. fat by aromatase to oestrogen. Reduce amount of oestrogen made by the body. SE - risk of osteoporosis, menopausal Sx, fatigue
Herceptin (trastuzumab) Her2+ - monoclonal ab, given WITH chemo! MONITOR HEART FUNCTION

Can give ovarian suppression - Goserline/zoladex (LHRH agonist)

129
Q

Radiotherapy is a localised breast cancer treatment, what are some SE?

A

Skin reactions (10-14d after), hair loss in armpit, changes to the breast size, shape and colour (darker), lymphadenopathy, oedema, pain in breast or chest, sore throat, tiredness and fatigue

130
Q

What risk comes with axillary node clearance?

A

Chronic lymphoedema -achy, heaviness, difficulty moving

DO NOT TAKE BLOOD FROM THIS ARM.

131
Q

When are you offered Breast screening?

A

50-70 every 3 years

132
Q

What bias might be seen in screening?

A

Lead time - Screen detects cases that survive longer even without the benefit of earl treatment
Length time - it detects slower growing or slower progressive cases that have a better prognosis
Selection - compliers are better educated and more health conscious so have inherently better prognosis

133
Q

List some screening criteria?

A
  1. Condition is an important health problem
  2. cost effective
  3. continuous provess
  4. facilities for diagnosis and treatment
  5. Suitable test or examination
  6. acceptable treatment for pt with the disease
  7. a recognisable early symptomatic stage
  8. natural Hx of the condition is adequately understood
  9. acceptable test to the population
  10. an agreed policy on who to treat
134
Q

Define T1DM.

A

A metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances in carbohydrate, protein and fat metabolism resulting from defects in insulin secretion, action or both. Absolute insulin deficiency.
Type 4 hypersensitivity reaction specific for Beta cells.
5% of all diabetes.
HLA DR3/4 on chr 6
Only presents when 70-90% of beta cells are destroyed.

135
Q

How do you test for T1DM?

A
  1. Establish if diabetes:
    Fasting blood glucose >/=7 OGTT 2-hour post >/=11.1
    1 + symptoms OR 2 if asymptomatic
    HbA1c >/=48
  2. Type of diabetes
    a. Ketone/bicarb - ketones >1.5mmol/L = hyperglycaemic
    b. autoAb - 80% GAD65 (glutamic acid decarboxylase65), I-A2 (insulinoma-associated antigen2), islet cell Ab
    c. C-peptide level - endogenous insulin - high in T2, low or absent in T1 -no insulin made. Measure in blood or urine
    d. Age, BMI, PMHx
  3. Investigate for complications?
    DKA? Bicarb <15, venous pH <7.3
    Check ECG, urinary microalbuminuria, nerve coduction etc
136
Q

How would you manage a patient with hypoglycaemia?

A

Mild - Get them to eat a rapidly absorbed/ fast acting carbohydrate - 15-20g - 4-7 glucotabs, 150-200mls pure fruit juice - try every 10-15min up to 3X. if fails –>
If in coma or confused - IM glucagon or IV 10% glucose

Once >4mmol/L give a long acting carb - 2 biscuits, 1 slice of bread

137
Q

What may indicate that a patient has severe DKA?

DKA triggered by sepsis/infection, stress, skipping insulin/ non-compliance, sickness, first presentation

A

GCS <12, pH <7.1, HCO3 <5, H >80, cerebral oedema, hypokalaemia on admission K <3.5, anions gap >16, pulse > 100 or < 60, SBP < 90, ketones > 6

138
Q

How would you manage a DKA?

A
  1. Fluid rehydration - 0.9% NaCl via infusion pump
    (if hypotensive - STAT 500ml)
  2. Fixed infusion of insulin, 50 units in 50ml N saline - Actrapid of humulin S. If on long acting insulin continue this.
  3. Reassess pt - RR, temp, BP, pulse, O2 sats, GCS, cap and lab glucose, K, pH, PO4, Mg, U&Es, FBC, blood cultures, ECG, CXR, MSU
  4. May need K replacement - KCl in 500ml 0.9% NaCl, if glucose falls < 14 - IV 10% dextrose

May need HDU/ICU input, central line, arterial line, catheter, severe acidosis, oliguric, hypotensive

NBM for 6 hours as gastroparesis common
NG tube if GCS reduced to prevent aspiration
LMWH - enoxaparin

139
Q

What is T2DM?

A

A chronic progressive metabolic disorder characterised by hyperglycaemia and insulin resistance with a relative insulin deficiency.
90% of diabetes. C-peptide HIGH
1. risk factors 2. Insulin resistance 3. hyperinsulinaemia 4. exhausted beta cells 5. hyperglycaemia

140
Q

How might you treat T2DM?

A

Weight loss and lifestyle changes

  1. Metformin or if intolerant Sulphonylurea (glimepride, glipizide)
  2. ADD SU or SGLT2 or DDP-4 inhibitor, or Glitazone
  3. ADD either another form above or GLP-1 or insulin (injectables)
  4. 4 agents from list above
141
Q

What is the criteria for HHS?

A

Hyperglycaemia >30mmol/L
High serum osmolality >320mmol/Kg [2x (Na ±K) + glucose + urea]
Absence of significant ketoacidosis < 3
Severely dehydrated - hypovolaemic - drowsy
Bicarb >15, venous H <50
(May not have known diabetes)

142
Q

How might you treat HHS?

A

A-E - may need to manage airway, Oxygen?
1. IV fluid - may need up to 8-10L in 48hr.
1L IV 0.9% NaCl over 1 hour (then less regularly)
if Na >160 - 0.45% NaCl for first 3L
2. Insulin, start IV insulin infusion 2-4U/Hr
when blood glucose reaches 15mmol/L commence 5% dextrose and stop insulin

  1. May need K replacement (put in N saline bag)
    Monitoring (sats, fluid balance (catheter?), bloods etc) and reassessment
    Treat underlying cause
    LMWH
143
Q

What might trigger HHS?

A

First presentation, poor control
Infection (UTI, pneumonia, sepsis, cellulitis), MI, TIA, stroke, pancreatitis, AKI, PE, HyperTH, cushings, GI bleed
Metformin, diuretics, BB, Ca channels, prednisolone, alcohol, TPN, cocaine

144
Q

Adrenal crisis includes?

A

Shock, collapse, pyrexia

When you suddenly stop steroids - post-op
e.g. Post-op asthma patient (long term steroid user)

Give IV fluids and Hydrocortisone

145
Q

Causes of Addisons

A 
Meningiococcal septicaemia syndrome
Anti-phospholipid syndrome 
HIV
Mets
TB

Year 4 (14 decks)

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