Endo Flashcards

1
Q

What is the most common cause of increased cortisol?

A

Iatrogenic (meds). 70% of non-iatrogenic cortisol is pituitary.

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2
Q

If the increased cortisol is due to pituitary then what else will you see?

A

Increased ACTH

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3
Q

What is Conn’s syndrome?

A

Adrenal Adenoma - that leads to increased Aldosterone production

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4
Q

What is secondary hyperaldosteronism?

A

Overactive RAAS system - due to increased renin secreting tumour or renal artery stenosis

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5
Q

What is Cushing’s disease

A

Primary hyper-cortisol production.Generally due to basophils with microadenoma and no leading to bitemporal hemianopia

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6
Q

What is Cushing syndrome?

A

Range of symptoms due to ectopic ACTH production or adrenal adenoma/adrenal hyperplasia

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7
Q

Cushingoid features:

Bam Cushingoid

A

BAM CUSHINGOID

Buffalo Hump
Amenorrhea
Moon facies

Central/truncal obesity  - proximal myopathy
Ulcers
Skin changes - Easy bruising, Hirsutism, Acne, Plethora, Striae, pigmentation
Hypertension, Hypercholestrolaemia
Infection
Necrosis of femoral head
Glaucoma
Osteoporosis
Immunosuppression
Diabetes - Hyeprglycaemia
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8
Q

What would you see on bloods for Hyperaldosterone?

A

Hypertension, Hypokalaemia

The low K+ levels may cause muscle weakness, N/V, and alkalosis due to H+ secretion

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9
Q

How does the dexamethasone test work?

What is a positive finding?

A

Dexamethasone provides negative feedback to the pituitary gland to suppress the secretion of ACTH by the pituitary.

A normal result is a decrease in cortisol levels on admisitration of a low dose dexa(2mg)

results indicative of Cushing’s disease involve o change in cortisol on low dose dexa but inhibition of cortisol on high dose dexa (8mg)

If cortisol levels are unchanged after both low and high dose then it may be indicative of primary adenoma (undetectable or levels of ACTH) or Ectopic ACTH syndrome (Elevated ACTH)

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10
Q

How do you investigate for Hyper-aldo?

A

Serum aldosterone:renin ratio

Aldo:renin ratio is increased in Primary hyperaldo, normal in secondary hyperaldo (as renin is high there)

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11
Q

Ix for Hyper-cortisol / Hyper-aldo?

A

Dexa suppression, ACTH levels, Abdo +chest CT, pituitary MRI, Serum aldosterone:Renin ration

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12
Q

Differentials for increased aldosterone levels?

A

Primary aldosteone - Idiopathic adrenocortical hyperplasia (most common), Conn’s syndrome (Adrenal adenoma), Familial hyperaldosteronism, Congenital adrenal hyperplasia

Liddle syndrome, Renal artery stenosis, RAAS dysfunction

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13
Q

What is Liddle Syndrome?

A

pseudohyperaldosteronism - Involves abnormal kidney function with excess reabsorption of sodium and loss of potassium from the renal tubule.

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14
Q

How to differentiate from Conn’s Syndrome and Idiopathic adrenal hyperplasia?

A

CT?

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15
Q

How do you manage pituitary adenoma?

A

Pituitary adrenal mass resection with post-op glucocorticoid replacement, at least in the short term (temporary suppression of ACTH post op)

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16
Q

What is Nelson’s Syndrome?

A

In extreme circumstances of hyper-cortisol you do a bilateral adrenalectomy - which can lead to Nelsons Syndrome:
Sudden removal of cortisol and negative feedback on AP allows pre-existing pituitary tumours to grow rapidly and produce increased amount so ACTH and MSH. Since no cortisol can be produced there is hyperpigmentation from MSH and muscle weakness

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17
Q

Mx of hyper-aldo?

A

If Primary adrenal adenoma - laprascopic surgical resection
If bilateral adrenal hyperplasia then risky to operate - hence use aldosterone anattagonist (spironlactone)

In both regularly assess Serum K for 4-6 weeks after

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18
Q

Does increased cortisol lead to increased or decreased osteoblastic function.

A

Decreased osteoblastic function and hence osteoporosis

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19
Q

3 common AIDS defining illnesses?

A

PCP, Kaposi’s Sarcoma, Oesophageal Candida

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20
Q

Diagnosis of HIV?

A

ELIZA test confirmed by Western Blot

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21
Q

Signs of Haemachromatosis?

A

Bronzed, joint pain,

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22
Q

Managing Haemachromatosis?

A

Screen (gene analysis), Transferrin saturation, Consider liver biopsy (if symptomatic)

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23
Q

Does transferrin saturation and serum transferrin go up/down in Fe deficiency?

A

Serum transferrin would go up (since we try to move more iron) and Saturation would be down (Because not enough iron)

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24
Q

A patient with Dm. Start with Metformin and if more drugs need to be added you add..

A

Sulfonylurea, Gliptin, Poiglitazone, SGLT2 inhibitor

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25
Q

If FBG or RBG less than 5.5 then…

A

diabetes unlikely

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26
Q

Cut off to diagnose DM - for FBG, RBG or HbA1C

A

FBG > 7
RBG > 11 (OGTT 2hr > 11)
HbA1c >6.5%

  • Each on 2 separate occasions
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27
Q

OGTT normal results for Fasting and 2hr?

A

FBG

28
Q

What are the four phases of De Quervian’s thyroiditis (Subacute thyroiditis)

A
Phase 1 (3-6 weeks): Hyperthyroidism, painful goitre, raised ESR
Phase 2 (1-3 weeks): Euthyroid
Phase 3 (weeks-months): Hypothyroidism
Phase 4: Thyroid structure and function goes back to normal
29
Q

How does Subacute Thyroiditis present?

A

Its presents after a viral infection with a tender goitre, hyperthyroidism and raised ESR

30
Q

Common problems with poiglitazone?

A

Weight gain, Liver impairment

Fluid retention, Some studies show Bladder on 2 separate occasions)

31
Q

How to Mx Addison’s disease?

A

Glucocorticoid and Mineralcorticoid=

Hydrocortisone + Fludrocortisone

32
Q

What are the causes of Addisonian Crisis (3):

A
  • Sepsis or surgery causing an acute exacerbation of chronic insufficiency (addison’s, hypopituitarism)
  • Adrenal Haemorrhage e.g. Waterhouse-Friderichsen syndrome
  • Steroid withdrawl
33
Q

How to manage Addisonian crisis?

A

High dose hydrocortisone with Normal Saline fluids.

(No fludrocortisone required because high dose hydrocortisone accommodates for it

34
Q

What are the 3 causes of malignany associated hypercalcaemia?

A

Lytic Bone disease metastasis
Myeloma
PTH like tumour

35
Q

Test to diagnose Addison’s disease?

A

Short ACTH test: Short synacthen test

36
Q

4 features of hypercalcaemia?

A

Bones, stone, abdominal groans and psychic moans

37
Q

3 features seen on Graves disease but not other Thyroiditis?

A
  1. Eye signs - exopthalmos, opthalmoplegia
  2. Pretibial Myxedema
  3. Thyroid Acropachy
38
Q

Prediabetes is defined y HbA1c between ______

A

6.0 and 6.5%

39
Q

How to manage Hyperthyroidism medically?

A

Carbimazole

40
Q

How to manage Hypothyroidism?

A

Levothyroxine

41
Q

How to diagnose Acromegaly?

A

OGTT with serial GH measurements

In normal patients GH is suppressed to

42
Q

Hypokalaemia with hypertension points towards a diagnosis of __________

A

primary hyperaldosteronism.

Barteter’s Syndrome is associated with normotension.

43
Q

Which diabetic medication acts to increase insulin sensitivity:

A

Pioglitazone

44
Q

__________ is caused by systemic illness. With this, the patient may have an apparently low total and free T4 and T3, with a normal or low TSH. Note that the levels are only mildly below normal.

A

Sick Euthyroid

45
Q

What is the most common thyroid cancer?

A

Papillary carcinoma

46
Q

Psammoma bodies and so called “orphan Annie nuclei”

A

Papillary carcinoma

47
Q

This type of thyroid cancer tends to spread haematogenously. This translates into a higher mortality rate.

A

Follicular thyroid carcinoma

48
Q

Papillary or follicular - which are more accurately diagnosed on fine needle aspiration?

A

Papillary carcinoma -

49
Q

Typically metastasise via the lymphatics and thus laterally located apparently ectopic thyroid tissue is usually a metastasis from a well differentiated __________

A

Papillary carcinoma

50
Q

__________ thyroid carcinoma tend to occur in elderly female. The disease usually at advanced presentation and often only palliative decompression and radiotherapy can be offered.

A

Anaplastic

51
Q

________ thyroid tumours are of the Parafollicular cells (C-Cells) and are of neural crest origin

A

Medullary

52
Q

In _______ carcinoma, the serum calcitonin may be elevated and hence used when monitoring for recurrence

A

Medullary carcinoma

53
Q

Spread of this thyroid cancer can be haematogenous or lymphatic and these tumours are not derived primarily from thyroid cells and are not responsive to radioiodine

A

Medullary

54
Q

TSH: high, T4: Normal

A

Poor compliance with Thyroxine

55
Q

Sick Euthyroid presents with TSH and T4 as?

A

TSH low, T4 low

56
Q

Nuclear scintigraphy reveals patchy uptake with thyroid

A

Toxic Multinodular goitre

57
Q

_______ work by stimulating the pancreatic beta cells to secrete insulin

A

Sulfonylureas

58
Q

_____ have an increased risk of pancreatitis and side effects include n/v

A

GLP-1 agonists (-tides)

59
Q

A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

A

Maturity onset diabetes of the young - MODY

60
Q

Hypothyroid with a painful goitre and raised ESR

A

De Quervain’s - Subacute hypothyroiditis

61
Q

Is Post partum thyroiditis Hyper- or Hypo?

A

Initially brief hyperthyroid phase followed by longer hypothyroid phase

62
Q

Two most common causes of hyperthyroidism?

A

Grave’s disease and Toxic multinodular goitre

63
Q

Two disease which cause an initial brief phase of hyperthyroidism and then prolonged hypo

A

Subacute thyroditis (De Quervain’s) and Post-partum thyroiditis

64
Q

gliclazide and glimepiride are _____

A

Sulphonylurea

65
Q

anti-TPO antibodies are seen in

A

Hashimoto’s thyroiditis

66
Q

works by increasing insulin sensitivity and decreasing hepatic gluconeogenesis
Notes

A

Metformin

67
Q

Side effects of Sulphonylureas?

A

Hypoglycaemia, weight gain and hyponaetraemia