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Year 6 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Phaeochromocytoma - Definition and key facts

A

Catecholamine secreting tumour (typically in the adrenal medulla).

Most commonly occur in the 3rd-5th decade of life

  • 10% malignant
  • 10% bilateral

Can be familial (associated with MEN2a, MEN2b, NF1, VHL).

Paragangliomas are catecholamine producing tumours that originate from chromaffin cells (derived from the neural crest) in the autonomic ganglia)

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2
Q

Phaeochromocytoma - signs, symptoms and Ix findings

A

Symptoms: episodic BP crises with paroxysmal (throbbing) headaches, diaphoresis, heart palpitations, anxiety, abdominal pain, nausea and pallor.

Signs: HTN,

Investigation Findings:

  • plasma catecholamines
  • raised urinary metanephrines (e.g. vanillylmandelic acid -> have higher diagnostic sensitivity than plasma catecholamines)
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3
Q

Phaeochromocytoma - Management

A
  1. alpha block (phenoxyenzamine - competitive irreversible antagonist of adrenaline)
  2. beta block (propranolo)
  3. surgical removal of the tumour/adrenal gland

You alpha block first to prevent hypertensive crisis

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4
Q

Blood supply of the adrenals

A

superior, middle and inferior adrenal artery

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5
Q

Why are phaeochromocytomas dangerous and what life-threatening presentations can they cause?

A

can cause a dangerous surge of adrenaline

this can lead to:
- arrhythmias
- MI
- cerebral haemorrhage
- sudden death

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6
Q

What % of gynaecomastia is drug related?

A

25%

-> therefore always review the medication the patient is taking

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7
Q

What is neonatal gynaecomastia?

A
  • due to placental transfer of maternal estrogens
  • sex independent, and spontaneously resolves within a few weeks or months
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8
Q

Management of gynaecomasta

A
  • stop causative drugs
  • medication to fix hormone imbalance
  • surgery
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9
Q

Which tests are useful in distinguishing between type 1 and type 2 diabetes?

A

C-peptide (low in type 1)
anti-GAD (glutamic acid decarboxylase) antibodies

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10
Q

What is type 3c diabetes?

What prescriptions do these patients need?

A

Can happen when the pancreas is damaged and stops producing enough insulin

can be as a result of: pancreatitis, pancreatic cancer, CF, haemochromatosis

patients present with lower GI sx (e.g. steatorrhoea, diarrhoea) and T1 diabetes sx (weight loss, can have hypoglycaemia) -> they have endocrine and exocrine dysfunction

they also don’t make glucagon so it needs to be prescribed.

  • insulin, glucagon, creon
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11
Q

What is the general rule of thumb in prescribing insulin in T1 diabetes?

A

0.5 units / kg body weight
-> half should be long lasting, half should be the post meal doses

e.g. if someone weights 60 kg their total daily requirement is 30 U;
baseline long acting insulin: 15 U
5U with every meal (3 meals)

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12
Q

What acid base abnormality can be seen in Cushing’s syndrome?

A

hypokalaemia metabolic alkalosis

(increased potassium excretion; increased bicarbonate resorption in the tubules)

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13
Q

Sick day rules for adrenal hormone replacement

A

double the GC dose
keep normal MC dose

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14
Q

How can sarcoidosis cause diabetes insipidus?

A

sarcoidosis can result in the formation of granulomas in the pituitary gland which can lead to neurogenic diabetes insipidus

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15
Q

What are the metabolic risks of acromegaly?

A

increased risk of
- diabetes
- HTN
- vascular disease (incl. cerebral aneurysms)
-> raised morbidity

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16
Q

What causes acromegaly

A

benign pituitary adenoma causing excessive secretion of GH and IGF-1 (in adults; in children this would lead to gigantism, but in adults you don’t get linear growth because the epiphyses have fused)`

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17
Q

Investigations in ?acromegaly

A

IGF-1 levels
OGTT with GH measurement
cranial MRI (pituitary)

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18
Q

Main cause of death in acromegaly

A

cardiovascular disease

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19
Q

Pathophysiology of acromegaly

A

increased GH -> increased IGF-1 -> overstimulation of cell growth and proliferation

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20
Q

How can you measure GH to test for acromegaly?

A

Not random GH measurement! Pulsatile secretion, therefore a high measurement would not be helpful/diagnostic.
If ‘0’, it could exclude acromegaly

-> measure by doing OGTT; normally, this would suppress GH to zero. If there is no suppression or even an increase in GH, this suggests a somatotroph adenoma.
-> measure baseline GH and 2h GH

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21
Q

Management options for acromegaly

A

All patients should be discussed in the MDT

medical:
- dopamine agonists (some patients respond)
- somatostatin analogies (octreotide, lanreotide)
- GH antagonists (pegvisomant)

Surgery
- transsphenoidal adenomectomy

Radiotherapy

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22
Q

What is the best single test for acromegaly?

A

Serum IGF-1 concentration

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23
Q

How do you test for acromegaly?

A
  1. serum IGF-1 -> if elevated to OGTT; if normal, acromeglay is ruled out
  2. OGTT with baseline and 2h GH -> if GH is suppressed, acromegaly is ruled out. If GH not suppressed: acromegaly confirmed, conduct pituitary MRI to determine the source of excess GH
  3. pituitary MRI
    adenoma -> confirmation of GH secreting adenoma

normal -> screen for an extra-pituitary cause

24
Q

waterhouse friedrichsen syndrome

A

acute primary insufficiency of the adrenal gland most commonly caused by adrenal haemorrhage (commonly associated iwht meningococcal meningitis; rarer causes include DIC, endotoxic shock and septicaemia due to other pathogens).

can be fatal

treat the underlying cause, parenteral fluid therapy and management of disorders of sodium balance

25
Q

What is LADA?

A

latent onset diabetes of adulthood

autoimmune diabetes
autoimmune cell failure is slow (much slower than T1DM) - takes longer to become insulin dependent

anti-GAD antibodies are present

26
Q

What ranges are diagnostic diabetes?

A

HbA1c: >48 mmol/mol (but not for 1st diagnosis)

Randon glucose: >11mmol/L

Fasting glucose: >7mmol/L

In patients that are asymptomatic, don’t diagnose based on one reading. repeat it.

27
Q

Management of diabetes

A
  • refer to diabetes/endo for individualised care plan
  • provide advice and support e.g. Diabetes UK
  • provide advice on lifestyle measures
  • offer immunisations (influenza and pneumococcus)
  • HbA1c monitoring 3-6 monthly
  • eye/kidney/foot monitoring
  • monitoring medical management
28
Q

Drugs for T1DM

A

Insulin
education on self monitoring of glucose and optimal targets

(devices such as FreeStyle Libre, insulin pump)

29
Q

What diabetic medication is good in pts with heart disease?

A

SGLT2 inhibitors

30
Q

T2Dm meds

A

1st line: metformin

CVS/HF SGLT2i

add info to this

30
Q

Management of DKA

A

ADMIT
IVF
IV insulin + potassium replacement

ix: urinalysis (ketones), blood gas shows acidosis (ketones high)

31
Q

do DKA patients always need admission?

A

yes

32
Q

management of HHS

A

delete

33
Q

How is DKA and HHS different?

A

no ketones in HHS

34
Q

learn ranges for Addison’s

A
  • Fluids! (IV sodium chloride)
  • VTE prophylaxis (hyperviscosity)
  • insulin should only be given in blood sugars stop falling while giving IV fluids.
35
Q

steroid induced vs addisons

A

paradoxically appear cushingoid
lack hyperpigmentation, high K+ and salt cravings
preserved MR activity secretion in GC induced addisons

36
Q

Which O/E findings can help distinguish between primary and secondary adrenal insufficiency?

A

hyperpigmentation is primary (POMC -> ACTH + alpha MSH)

37
Q

Management of Addison’s including doses, sick day rules

A
  • Hydrocortisone (20-30mg/day in 2-3 divided doses with the majority taken in the first half of the day)
  • Fludrocortisone

In intercurrent illness take double the dose of hydrocortisone

Also need a steroid card (alert/info)

38
Q

weight gain DDx

A

Cushing’s syndrome / disease
PCOS
hypothyroidism
malignancy

39
Q

Causes of Cushing’s

A

ACTH dependent:
- Cushing’s disease -
- ectopic ACTH (SCLC) - 10%

ACTH independent

Pseudo

insert

40
Q

Ix for ?Cushing’s

A

give 1mg dex at night
if at 8 am you see cortisol spike -> Cushing’s

insert more info

41
Q

IPSS

A
42
Q

What is Nelson’s syndrome?

A
  • also known as ‘post adrenalectomy syndrome’
  • rare
  • seen in pts post bilateral adrenalectoym
  • pts who have an undeteced pituitary adenoma -> adrenals removed -> no -ve feedback from cortisol on the hypothalamus -> ↑ CRH production → uncontrolled enlargement of preexisting but undetected ACTH-secreting pituitary adenoma → ↑ secretion of ACTH and MSH → sx
  • Symptoms: headache, bitemporal hemianopia (mass effect), cutaneous hyperpigmentation
43
Q

Mx of hyperthyroidism

A
44
Q

How do you differentiate Graves’ vs other causes of thyrotoxicosis?

A

Eye signs:
exophthalmos
proptosis
ophthalmoplegia

might also get derm signs

45
Q

complications of hyperthyroidism

A

AF (common)
Congestive HF
bone loss
dermopathy

46
Q

Schmidt’s syndrome

A

Addison’s + AI hypothyroidism + T1DM

47
Q

What is the Zuckercandl organ?

A

Chromaffin body derived from the neural crest locaated at the bifurcaation of the aorta or the origin of the IMA

also known as para-aortic body

have the potential for deadly paragangliomas (surgical cause of HTN)

48
Q

Management of hyperthyroidism in pregnancy according to TM

A

1st: Propylthiouracil (because there is a lower risk of congenital abnormalities, incl. facial malformations and VSD)

2nd and 3rd TM: carbimazole (due to lower risk of hepatotoxicity)

49
Q

How do sulfonylureas work?

A

stimulate the release of insulin from the pancreas which can lower blood sugar levels (therefore they are associated with a risk of hypos - especially if the medication is not taken with food or if the patient is fasting)

50
Q

What medication can you use in the management of primary hyperparathyroidism in patients that are not suitable for surgery?

A

cinacalcet

(it is a calcimimetic - a drug that ‘mimics’ the action of calcium on tissue by allosteric activation of the calcium-sensing receptor)

51
Q

Precipitating factors for HHS

A

intercurrent illnesss
dementia
sedative drugs

52
Q

What is exposure keratopathy and in which endocrine condition can it occur in?

A

= damage to the cornea du to dryness

can occur in thyroid eye disease (Grave’s disease) due to the inability to close eyes

53
Q

Summarise the features of the MEN disorders?

A

MEN I
- Pituitary adenoma
- Parathyroid hyperplasia
- pancreas tumours

MEN IIa
- parathyroid hyperplasia
- phaeochromocytoma
- medullary thyroid carcinoma

MEN IIb
- phaeochromocytoma
- medullary thyroid carcinoma
- mucosal neuroma
- marfanoid body habitus

54
Q

Zollinger-Ellison syndrome

A

= condition characterised by excessive levels of gastrin secondary to a gastrin-secreting tumour.

The majority of these tumours are found in the first part of the duodenum, with the second most common location being the pancreas.

  • Around 30% of gastrinomas occur as part of MEN type I syndrome.

Features
- multiple gastroduodenal ulcers
- diarrhoea
- malabsorption

Year 6 (37 decks)

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