iv. Endocrinology Flashcards

1
Q

L76: Where are the adrenal glands located?

A

Right above the kidneys

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2
Q

L76: What type of hormones do they adrenal glands secrete and can you provide examples of these?

A
  • Endocrine hormones;
  • Adrenaline;
  • Steroids (aldosterone + cortisol).
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3
Q

L76: What part of the adrenal glands produce steroids?

A

Outer cortex

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4
Q

L76: What part of the adrenal glands produce adrenaline?

A

Inner medulla

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5
Q

L76: What disease can destruction of adrenal tissue lead to?

A

Addison’s Disease - gland can’t make steroids (primary)

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6
Q

L76: What disease can excess adrenal action (glucocorticoids) lead to?

A

Cushing’s Disease

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7
Q

L76: What hormone is cortisol production, by the adrenal glands, stimulated by?

A

ACTH (adrenocorticotrophic hormone) from pituitary gland

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8
Q

L76: What hormone is ACTH production, by the pituitary gland, stimulated by?

A

CRH (corticotrophin releasing hormone) from hypothalamus

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9
Q

L76: By what type of feedback system is cortisol production regulated by?

A

Negative feedback (HPA axis)

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10
Q

L76: What is cortisol (and other steroids) produced from?

A

Cholesterol

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11
Q

L76: What is the main function of aldosterone?

A

Salt and water regulation to control blood pressure

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12
Q

L76: How does aldosterone regulate salt and water absorption?

A
  • Renin-angiotensin system;
  • Enhances Na+ reabsorption and K+ loss;
  • Indirect effect on blood pressure.
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13
Q

L76: What drugs inhibit aldosterone?

A
  • ACE inhibitors (angiotensin converting enzyme);
  • AT2 blockers (block angiotensin receptors).

[both dilate blood vessels to reduce bp]

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14
Q

L76: List some side effects of ACE inhibitors.

A
  • Cough;
  • Angio-oedema;
  • Oral lichenoids.
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15
Q

L76: Why do ACE inhibitors often cause patients to develop a cough?

A

Prevent the breakdown of compounds such as bradykinin which in turn accumulate in respiratory tract

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16
Q

L76: Why can ACE inhibitors cause angio-oedema?

A
  • Elevated levels of bradykinin;
  • Tissues act as if they’re inflamed;
  • Sudden onset of fluid retention in tissues.
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17
Q

L76: If a patient presents with oral lichenoids as a result of their ACE inhibitors, what should you do?

A
  • This is a tissue reaction to the medication (ulceration);
  • Ask GP to change pt to AT2 blocker;
  • bp still maintained without effect on tissues.
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18
Q

L76: What part of cells does cortisol act upon?

A
  • Works inside nucleus of cells;

- Changes protein transcription.

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19
Q

L76: Naturally, when is most cortisol produced in the body?

A

During the night, circadian release

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20
Q

L76: What effect does cortisol have on insulin?

A

Inhibits insulin, stimulates gluconeogenesis and fat/ protein breakdown

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21
Q

L76: What effect does cortisol have on the immune system?

A

Lowers immune reactivity

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22
Q

L76: What effect does cortisol have on bone?

A

Inhibits bone synthesis

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23
Q

L76: Name a therapeutic steroid.

A
  • Hydrocortisone;
  • Prednisolone;
  • Triamcinolone;
  • Dexamethasone;
  • Bethamethasone.
24
Q

L76: What suffix do steroids usually end in?

A
  • one
25
Q

L76: What is the cortisol equivalent of hydrocortisone?

A

1

26
Q

L76: What is the cortisol equivalent of prednisolone?

A

4

27
Q

L76: What is the natural amount of steroids produced by the body per day?

A

14-15mg

28
Q

L76: What happens to natural production of steroids if someone is receiving therapeutic steroids?

A
  • Natural levels ‘swamped’;
  • Negative feedback;
  • Adrenal glands stop producing.
29
Q

L76: What is the major issue with receiving long term therapeutic steroids?

A
  • Adrenal gland atrophy;

- Shrink away and fail to ‘switch back on’ once therapy has stopped.

30
Q

L76: How do the effects or therapeutic steroids generally compare to natural steroid production?

A
  • Enhance glucocorticoid effect;

- Enhance mineralocorticoid effect.

31
Q

L76: List some side effects of therapeutic steroids.

A
  • Hypertension;
  • Type 2 diabetes (prolonged raised insulin to combat inhibition by steroids);
  • Osteoporosis;
  • Increased infection risk;
  • Peptic ulceration;
  • Thinning of the skin;
  • Easy bruising;
  • Cataracts and glaucoma;
  • Hyperlipidaemia (atherosclerosis);
  • Increased cancer risk;
  • Psychiatric disturbance.
32
Q

L76: What can cause hyperfunction of the adrenal glands?

A
  • Adrenal tumour (primary);

- Pituitary tumour (secondary).

33
Q

L76: What is Conn’s Syndrome?

A

Hypertension caused by excess aldosterone in the adrenal glands (adrenal tumour or hyperplasia)

34
Q

L76: What is the main function of aldosterone?

A
  • Mineralocorticoid;

- Na+ conservation in the kidneys.

35
Q

L76: Other than Addison’s disease, what can cause hypofunction of the adrenal glands?

A

Pituitary failure - can’t ask gland to make steroids (secondary)

36
Q

L76: What are the signs (will see) of Cushing’s Syndrome?

A
  • Centripetal obesity;
  • Moon face + buffalo hump;
  • Hypertension;
  • Thin skin + purpura (blood spots);
  • Muscle weakness;
  • Osteoporotic changes + fractures.

[effects lipid/ fat metabolism and muscles/ bones]

37
Q

L76: What are the signs (will experience) of Cushing’s Syndrome?

A
  • Diabetes mellitus features;
  • Poor infection resistance;
  • Back pain/ bone fractures (due to osteoporotic changes);
  • Psychiatric disorder (inc. depression);
  • Hirsuitism (excess body hair);
  • Skin + mucosal pigmentation (due to ACTH);
  • Ammenorrhoea, impotence + infertility.
38
Q

L76: Why does excess ACTH cause pigmentation of the skin/ mucosa?

A
  • Interaction between ACTH and MSH (melanocyte stimulating hormone);
  • Changes in protein sequences;
  • Become more tanned/ pigmented;
  • Often presents on oral mucosa.
39
Q

L76: What can cause adrenal gland failure and subsequent hypofunction?

A
  • Autoimmune gland destruction;
  • Infection;
  • Infarction.
40
Q

L76: What can cause pituitary gland failure and subsequent hypofunction?

A
  • Compression from other adenoma;

- Sheehan’s Syndrome (sudden drop in bp to gland during childbirth).

41
Q

L76: What are the major causes of Addison’s Disease?

A
  • Infection (TB);

- Autoimmune adrenalitis.

42
Q

L76: Addison’s Disease usually has a slow onset, what are the signs of it?

A
  • Postural hypotension (salt and water depletion);
  • Weight loss and lethargy;
  • Hyperpigmentation (not w secondary hypofunction);
  • Vitiligo.
43
Q

L76: What are the symptoms of Addison’s Disease?

A
  • Weakness;
  • Anorexia;
  • Loss of body hair (females).
44
Q

L76: What would a diagnostic test for Cushing’s Syndrome show?

A

High cortisol all of the time, independent of circadian rhythm

45
Q

L76: What would a diagnostic test for Addison’s Disease show?

A
  • High ACTH levels;

- Negative response (no plasma cortisol rise) to ACTH injection.

46
Q

L76: When diagnosing the cause of adrenal hyperfunction, how do you distinguish if the issue is primary or secondary to the adrenal glands?

A
  • Primary: i.e. adenoma in adrenal gland: Low ACTH but high cortisol (correct pituitary response);
  • Secondary: i.e. adenoma in pituitary or ectopic ACTH production: High ACTH and high cortisol (pituitary is not responding to high plasma cortisol).
47
Q

L76: When diagnosing the cause of adrenal hypofunction, how do you distinguish if the issue is primary or secondary to the adrenal glands?

A
  • Primary i.e. destruction of the adrenal glands: High ACTH, low cortisol and negative to synthetic ACTH (pituitary gland is working to increase cortisol but adrenal glands do not respond);
  • Secondary i.e. destruction of pituitary gland: Low ACTH, low cortisol but positive to synthetic ACTH (pituitary not producing ACTH to stimulate cortisol production).
48
Q

L76: What is an Addisonian crisis?

A
  • Not enough cortisol or aldosterone;
  • Takes time to develop;
  • Hypovolaemic shock (low bp/ faint/ vomit/ collapse);
  • Hyponatraemia (loss of salts).
49
Q

L76: How do you treat an Addisonian crisis?

A
  • Give pt saline (to treat the Addison’s);
  • Then steroid replacement;
  • Hydrocortisone (cortisol);
  • Fludrocortisone (aldosterone).

[done in A&E after ambulance referral]

50
Q

L76: When must a patient with Addison’s Disease increase their dose of steroids?

A
  • When the body would usually increase cortisol production;
  • Increased physical stress (difficult extractions);
  • Significant infection;
  • Perioperative treatment (under GA);
  • Vomiting (pills will not be kept down).
51
Q

L76: Why is steroid therapy more complicated than thyroxine therapy?

A

Thyroxine levels are the same day to day, cortisol levels change

52
Q

L76: When should steroid prophylaxis (usually) be given for the following treatments: routine restorative, simple extractions, minor oral surgery, severe dental infection?

A

Minor oral surgery and severe dental infection

53
Q

L76: At what dose of therapeutic steroids do you not require steroid prophylaxis?

A

Above 15mg prednisolone

54
Q

L76: For patients on 1-15mg/ day doses of prednisolone, what prophylaxis cover should be given?

A

Double oral dose, perioperatively (surgery ± 2 days)

55
Q

L76: Why must a patient’s steroid history over the past 6 months be taken?

A
  • Effects (on glands) will be there for months;

- Might require prophylaxis dose (IM if no tablets).