DUMS Endo Flashcards

1
Q

What is homeostasis

A

Physiological regulation of the body to keep processes in a stable equilibrium

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2
Q

What is autocrine signalling

A

A response produced by a cell which acts on itself

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3
Q

The retropharyngeal space lies between which two fascial layers

A

the pretracheal and prevertebral fascia layers

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4
Q

Which fascial layer encloses all the other neck fascial compartments

A

Investing (deep) fascia

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5
Q

Which fascial layer is the most superficial out of all the deep fascial layers

A

Investing fascia

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6
Q

Which of the pituitary secretions is mainly controlled by inhibition and by why chemical

A

Prolactin is mainly controlled by the inhibitory effect of dopamine

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7
Q

Asides from being inhibited by dopamine, how else is prolactin secretion controlled

A

Secretion caused by TRH

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8
Q

what is the difference between a pituitary macroadenoma and a microadenoma

A
MACROadenoma = >1cm 
MICROadenoma = ≤ 1cm
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9
Q

Which structure can a non-functioning macroadenoma compress and where does this structure lie

A

Optic chiasm

which is superior to the pituitary gland

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10
Q

Which cranial nerves are at risk of being compressed by a pituitary tumour

A

3, 4, 6

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11
Q

How can a non-functioning pituitary adenoma cause the likes of HYPO -adrenalism, -gonadism, -thyroidism

A

Can grow and wipe out cells that usually produce hormone – ACTH cells wiped out = hypoadrenalism etc

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12
Q

How can a non-functioning pituitary adenoma cause diabetes insipidus

A

Grow and compress the posterior pituitary thus decreasing/ stopping the production of ADH

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13
Q

Which visual field defect can a pituitary growth cause

A

Bitemporal Hemianopia

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14
Q

What is the most common type of pituitary tumour

A

Prolactinoma

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15
Q

What gender-specific symptoms will a prolactinoma present with

A

Males -> impotence

Females -> cycle irregular

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16
Q

Which investigation should be carried out if you suspect a pituitary tumour…

A

MRI pituitary fossa

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17
Q

What is the treatment for a prolactinoma and how does it work

A
Dopamine agonist (Cabergoline) 
Inhibits prolactin release
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18
Q

How is acromegaly diagnosed

A

IGF1
Glucose Tolerance Test (75g Oral)
-> diagnostic if GH unchanged or > 1ug/L (normal <0.4)

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19
Q

What GI symptoms can Acromegaly present with

A

Colon Polyps

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20
Q

Which MSK hand condition can Acromegaly put you at higher risk of

A

Carpal tunnel syndrome

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21
Q

What is the 1st line treatment for Acromegaly and what should be done after this

A

Pituitary surgery/ Radiotherapy to pituitary fossa

Repeat GTT

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22
Q

Is surgery is unsatisfactory for Acromegaly, what drugs can be used and how do they work

A
Dopamine agonist (dopamine inhibits GnRH) 
Somatostatin analogue (somatostatin inhibits GH)
Pegvisomant (GH receptor antagonist)
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23
Q

What do parafollicular C cells secrete

A

Calcitonin

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24
Q

What is calcitonin involved in

A

Minor role in calcium regulation

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25
Q

What is the major regulatory step in the HPT axis

A

TSH release from the anterior pituitary regulated by TRH

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26
Q

Which two carrier molecules are responsible for transporting thyroxine around the body

A

Thyroxine-binding-globulin

Transthyretin

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27
Q

What is a dietary cause of hypothyroidism

A

Lack of iodine in diet

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28
Q

Antibodies for Hashimoto’s thyroiditis

A

Thyroid peroxidase antibodies (Anti-TPO)

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29
Q

What is the management of hypothyroidism

A

Levothyroxine 50-100 MICROgrams

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30
Q

How often should you check TSH levels for someone being treated for hypothyroidism

A

TSH every 2 months after any dose change
4 weeks after first starting
Once stable 12-18 months

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31
Q

What kind of menstrual irregularities can hyperthyroidism cause

A

Less frequent periods

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32
Q

What is De Quervain’s thyroid pathology and what is it caused by

A

Sub acute thyroiditis – viral trigger

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33
Q

A smooth symmetrical goitre and symptoms of hyperthyroidism should make you think of what

A

Grave’s disease

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34
Q

An asymmetrical goitre and symptoms of hyperthyroidism should make you think of what

A

Multi-Nodular goitre

Toxic Nodule - thyroid adenoma

35
Q

What drugs can be given to treat thyrotoxicosis and the symptoms of thyrotoxicosis

A

Beta Blockers –> for symptomatic relief

Carbimazole/ PTU –> to lower thyroxine

36
Q

Which nerve is at risk from thyroid surgery and how would an injury to this structure present

A

Recurrent laryngeal nerve

Hoarse voice

37
Q

What are the three treatments you could consider in acute hypercalcaemia

A

Fluids- rehydrate with 0.9% saline 4-6L in 24hours
Loop diuretics once rehydrated- avoid thiazides
Bisphosphonates

38
Q

Which biochemical marker will be high in Paget’s

A

ALP

39
Q

What will PTH levels be like in a bone malignancy

A

Very low

physiological response to high Ca

40
Q

What is the difference between rickets and osteomalacia

A

Rickets is in kids

Osteomalacia is in adults

41
Q

What is the normal range of blood sugar

A

4-6mmol/L

42
Q

What is the normal range of HbA1c for a diabetic

A

48-58mmol/l

43
Q

What are 3 different ways to diagnose T2DM

A

Random blood sugar test > 11mmol/l
Fasting blood sugar > 7 on 2 occasions
OGTT > 11mmol/l after 2 hours

44
Q

What is a rare but serious side effect of Metformin

A

Lactic Acidosis

45
Q

After what age are TZD’s not recommended and why

A

Over 65’s due to increase in fracture risk

46
Q

How are GLP-1 agonist administered

A

Sub-cutaneous injection

47
Q

Which malignancy can GLP-1 agonists cause

A

Pancreatic cancer

48
Q

What is the most common GLP-1 agonist

A

Exenatide (synthetic Exendin-4)

49
Q

Which GLP-1 agonist is DPP-IV resistant

A

Liraglutide

50
Q

What is the most commonly used DPP-IV inhibitor

A

Sitagliptin

51
Q

What level of ketonaemia is diagnostic of DKA

A

> 3mmol/L

52
Q

What blood glucose level is diagnostic of DKA (with relevant symptoms/ history)

A

> 11mmol/l

53
Q

What bicarbonate and pH levels diagnose DKA

A

Bicarbonate < 15mmol/L

pH < 7.3

54
Q

What kind of breathing is specific to DKA

A

Kussmaul’s breathing

55
Q

What is Kussmaul’s breathing trying to achieve in DKA

A

Attempt to blow off CO2 to lower pH of the blood

Attempt to compensate for the metabolic acidosis

56
Q

Which condition is blood glucose typically higher in, DKA or HHS

A

HHS

57
Q

When checking blood sugar, where should the lancet be used

A

Lancet against the side of the distal portion of a finger.

Don’t use the lancet on the finger pad.

58
Q

What is the major regulator of aldosterone production

A

RAAS

59
Q

When is RAAS activated

A

A decrease in blood pressure

60
Q

How does angiotensin 2 increase blood pressure

A

direct (vasoconstriction) and indirect (aldosterone)

61
Q

What are 4 possible causes of primary adrenal insufficiency

A

Addison’s
Congential Adrenal Hyperplasia
Adrenal Tb
Malignancy

62
Q

What are 3 possible causes of secondary adrenal insufficiency

A

Lack of ACTH stimulation
Iatrogenic (excess exogenous steroid)
Pituitary/hypothalamic disorders

63
Q

How is Addison’s diagnosed

A

SHORT synACTHen test

Measure cortisol 30 mins after ACTH administration. Should be > 550 mmol/l

64
Q

What is the management of Addison’s

A

Hydrocortisone (Corisol mimic)

Fludrocortisone (Aldosterone mimic)

65
Q

In someone with Addison’s, where will they have areas of hyperpigmentation

A

Classically mucosal membranes, extensor surfaces and palmar creases

66
Q

Why do you not give fludrocortisone in secondary adrenal insufficiency

A

Because the adrenal gland is functioning fine and the RAAS system will be regulating the release of Aldosterone just fine so no replacement needed

67
Q

What is a common way in which an Addisonian crisis can occur

A

Steroid therapy stopped suddenly

Adrenal glands have ‘gone to sleep’

68
Q

Why is myopathy a feature of Cushing’s syndrome

A

Glucocorticoids alter protein metabolism

Reduced protein synthesis

69
Q

What are the 2 categories of causes of Cushing’s

A

ACTH dependent

ACTH independent

70
Q

Name 3 ACTH dependent causes of Cushing’s

A

Pituitary adenoma -> most common
Ectopic ACTH production
Ectopic CRH

71
Q

Name 3 ACTH independent causes of Cushing’s

A

Adrenal adenoma
Adrenal carcinoma
Nodular hyperplasia

72
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease

A
Syndrome = Excess Cortisol due to any cause
Disease = Excess Cortisol due to pituitary pathology
73
Q

How is Cushing’s diagnosed

A

Overnight dexamethasone suppression test - screening

Short dexamethasone suppression test

74
Q

What is the commonest cause of 2ndary hypertension

A

Conn’s syndrome

75
Q

What does renin do

A

Converts angiotensinogen into Ang I

76
Q

What happens to angiotensin I in the RAAS

A

Angiotensin I converted to Ang II by ACE

77
Q

Where is ACE found

A

Pulmonary vascular endothelium

78
Q

What is the commonest cause of Conn’s syndrome

A

Bilateral adrenal hyperplasia

79
Q

How is Conn’s diagnosed

A

Aldosterone: Renin ratio
Saline suppression test
(Failure to suppress aldosterone by 50% with 2L of saline is diagnostic)

80
Q

What is done after Conn’s is diagnosed, via a saline suppression test, to work out the treatment plan

A

Adrenal CT to demonstrate adenoma

81
Q

What is the treatment of Conn’s syndrome

A

Spironolactone/ eplerenone if bilateral hyperplasia

Laparoscopic Adrenalectomy if unilateral adenoma

82
Q

What is the treatment of PCOS

A
Antioestrogens (Clomifene citrate or Tamoxifen)
Aromatase inhibitors (Letrozole)
83
Q

What is the normal range of HbA1c for a non-diabetic

A

below 41mmol/L