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3B > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the primary causes of hypothyroidism?

A

Atrophic hypothyroidism
Hashimotos thyroiditis
Iodine deficiency

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2
Q

What are secondary causes of hypothyroidism?

A

Drugs - lithium + amiodarone

Thyroidectomy

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3
Q

What abs may be seen in hypothyroidism?

A

Anit thyroid peroxidase abs TPO

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4
Q

What are some of the signs of hypothyroidism?

A

BRADYCARDIC
Reflexes down, ataxia, Dry skin, Yawning (tired), Cold peripheries, Ascites, Round puffy face, Depressed, Immobile +/- ileus, CCF

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5
Q

What are the 3 main causes of hyperthyroidism?

A

1) Graves disease
2) Toxic multi nodular goitre
3) Solitary toxic adenoma

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6
Q

What abs are associated with hyperthyroidism?

A

TSH receptor abs

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7
Q

What investigations can you do in hyperthyroidism?

A

T3, T3, TSH
TSH receptor abs
Thyroid USS
Radioisotope uptake scan

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8
Q

What are the medical options for treating hyperthyroidism?

A
  • Symptomatic: BB - propranolol (stop the conversion of T4–>T3)
  • Anti-thyroid: Carbimazole
  • Propylthiouracil (for pregnancy or thyroid storm)
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9
Q

What are the SE of carbimazole?

A

Agranulocytosis + neutropenic sepsis as it causes myelosupression

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10
Q

Give a very brief pathophys behind graves disease

A

TSH receptor abs mimic TSH –> gland hyperplasia and high T3/T4

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11
Q

Give 4 signs specific to graves disease?

A

1) Ophthalmoplegia
2) Exopthalmos
3) Pretibial myxoedema
4) Thyroid acropathy

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12
Q

Give some causes of high serum prolactin levels

A

Benign pituitary adenoma
Hypothyroidism Cushings syndrome
Drugs: AP, Dopamine antagonists (domperidne and metoclopramide) and anti-depressants

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13
Q

At what levels do prolactin have to be to be a true prolactinoma?

A

> 5000

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14
Q

You suspect your patient has acromegaly, what investigation work up do you do?

A
  • Bloods: BM, phosphate, calcium and triglycerides
  • OGTT - glucose should decrease, if no response –> acromegaly
  • Serum IGF -1 if normal that excludes acromegaly
  • Serum GH (but it has episodic production)
  • MRI pituitary and hypothalamus
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15
Q

Explain how the OGTT works to dx acromegaly

A

With acromegaly they have high GH levels
Hyperglycaemia should have a negative FB on GH and cause a decrease in GH levels

The patients are fasted and then given a glucose solution to drink. Their BM and GH levels are monitored every 30ms and the GH levels do not decrease with increased BMs in acromegaly

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16
Q

What are the medical and surgical treatment options for acromegaly?

A

M

  • somatostatin analogues (inhibits GH) = ocretotide
  • GH antagonists = pegvisokmant

S = Tran sphenoidal surgery

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17
Q

What is Cushing’s disease caused by?

A

Bilateral adrenal hyperplasia from an ACTH secreting pituitary adenoma

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18
Q

What tests can you do to dx someone with cushings syndrome?

A

1) dexamethasone suppression test (no suppression seen)

2) 24 hour urinary free cortisol

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19
Q

You have dx someone with Cushings syndrome - what do you look at next to determine the cause of the problem?

A

Drug chart - are the on exogenous steroids?

ACTH high - from the pituitary

  • -> pituitary tumour = cushing’s disease
  • -> ectopic = NSCLCa

ACTH low - from the adrenals

  • ->pituitary adenoma
  • -> pituitary carcinoma
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20
Q

What abs are seen in AI Addison’s?

A

21 hydroxylase Abs

21
Q

How would a person with Addison’s present?

A

Thin - anorexia, N+V wt loss
Tanned - ACTH cross reacts with melanin
Tired - fatigue
Tumbling - weakness + faintness due to low BP

22
Q

How do you dx someone with Addisons?

A

Short ACTH stimulation test = synactin test
Addisons if there is no increase in cortisol following the synactin (which is a chemical copy of ACTH)
Addisons can be excluded if cortisol levels increase >500

23
Q

A 55 year old thin, tanned man presents with N + V, fever, muscle cramps and confusion
His ABG shows low sodium and glucose, high K+ and Cr.
What is happening and how do you treat it?

A 
Addison's crisis 
Rx: 
IM/IV hydrocortisone 100mg if adult 
IV fluids (must rehydrate) 
Further hydrocortisone and glucose
24
Q

What is Conns disease?

A

(Opposite of Addison’s)
= Primary hyperaldosteronism
Excessive production of aldosterone independent of RAAS system
Due to adrenal adenoma (80%) // bilateral adrenal hyperplasia

25
Q

How would someone with Conns disease present?

A

Oedema, HTN,
Hypokalaemia - weakness, cramps, paraesthesia
Metabolic alkalosis (H low due to more K in urine)
Polyuria - inability to concentrate urine

26
Q

What normal serum test would exclude Conns disease?

A

Renin

DD = renal artery stenosis // diuretics

27
Q

How can you treat Conn’s?

M + S

A

M - aldosterone antagonist = spironolactone

S - laproscopic adrenalectomy

28
Q

What can cause high potassium?

A

Renal causes - AKI/CKD, Addisons, renal tubular acidosis
Drugs - ACE-I, NSAIDs, heparin
Shift from IC–> EC = BB and DKA
Increased circulation - burns, tissue damage

29
Q

What is phaeochromocytoma?

A

A rare catecholamine secreting tumour derived from the chromaffin cells in the adrenal medulla

30
Q

How would someone with phaeochromocytoma present?

A

1) Headache
2) Sweating
3) Palpitations
4) Tremor
+ N, anxiety, C and wt loss
HTN

31
Q

What investigations do you do for phaeochromocytoma?

A

Bloods - high: glucose, ca and Hb. Plasma metanephrines
Urine - 24hour free urine collection for Cr, total catecholamines and metanephrines
Imaging - Abdo CT

32
Q

Give 2 differentials for phaeochromocytoma?

A

Multiple Endocrine Neoplasms (bilateral tumours)

Neurofibromatosis

33
Q

How do you treat phaeochromocytoma?

A

Surgical resection of tumour in adrenal medulla
+ pre surgery alpha blockade
+ post surgery beta blockade

34
Q

What are carcinoid tumours?

A

They are neuroendocrine tumours occurring in cells of the neuroendocrine system - occurs usually in the midgut

35
Q

How do people with hypernatremia present?

A 
FRIED 
Fever 
Restless 
Increased fluid retention + high BP 
oEdema 
Dry mouth and decreased UO
36
Q

What are 4 ECG changes seen in hyperkalaemia?

A

P - no P waves
PR - Prolonged
QRS - Broad
T - Tall, tented

37
Q

How do you treat hyperkalaemia?

A

1) Calcium gluconate 10% 10ml
2) Insulin (10u act rapid) with 50% 50ml dextrose
// 10mg salbutamol nebs
3) Calcium resonium 15-45mg

38
Q

What are the ECG changes seen in hypokalaemia?

A 
PRSTTU 
PR - long
ST - depression 
T - inversion 
U - prominent 
(looks like a wavy baseline)
39
Q

How do you treat hypokalaemia?

Mild + severe

A

Mild = SandoK
Severe = < 10mmol/hr K+ slowly
Need cardiac monitoring and regular bloods

40
Q

Does DI cause hyper or hyponatraemia?

A

Hypernatraemia

41
Q

You suspect someone has DI.

What investigation work up do you do?

A

Bloods: serum osmolality + U&Es
Urine: dip, 24hour urine collection, osmolality <300
Imaging: MRI pituitary + hypothalamus
ST: Water deprivation test with desmopressin response

42
Q

What are some of the causes of hyponatraemia?

A

Low volume - D + V, diuretics
N volume - addison’s, SIADH, low thyroid
High volume - heart/liver/renal failure

43
Q

What are some of the causes of SIADH?

A

Malignancy - SCLC, GI, GU
Drugs - SSRIs, Opiates
CNS disorders - infection, stroke, head injury, GBS, SLE

44
Q

You have a patient who is euvolaemia hypotonic hyponatraemia and they have concentrated urine.
They are acutely unwell. How to you treat acute SIADH?

A

IV hypertonic saline (3%)
Furosemide
+ treat the cause

45
Q

In patients who have hypercalcaemia, cinacalet can be used to reduce calcium. How does it do this?

A

Cinacalet is a calcimimetic. It acts on calcium receptors on chief cells in the parathyroid gland making them more sensitive to calcium levels. They are the main negative feedback regulator cells so reduce the amount of PTH produced and thus calcium

46
Q

What investigation results would make you suspect DKA?

A

Hyperglycaemia >11
Ketones >3
Metabolic acidosis on ABG <7.3

47
Q

What are the main causes of hyponatraemia?

A 
Medical illnesses: HF, pneumonia, ca, MI 
\+ SALTED 
SIADH 
Age >70 
Lower limb surgery 
Energy + nutrition 
Drugs - SSRIs, diuretics, PPI
48
Q

How should you group the causes of hyponatraemia?

A

Hypovolaemic - V, D, diuretics
Euvolaemic - SIADH, addison’s, hypothyroidism
Hypervolaemic - Heart, liver & renal failure

49
Q

What is the complication that the patient are at risk of if you hydrate them too quickly when they have hyponatraemia?

A

Pontine myelunolysis

3B (21 decks)

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