Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 MedEd > Endo2 > Flashcards

Endo2 Flashcards

Adrenal

1
Q

What are the 4 regions of the adrenal glands?

A 
Adrenal medulla
Adrenal cortex:
-zona reticularis
-zona fasciculata
-zona glomerulosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is produced by the adrenal medulla?

A

Catecholamines (adrenaline, noradrenaline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is produced by the zona reticularis?

A

Androgens (DHEA, androstenedione)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is produced by the zona fasciculata?

A

Glucocorticoids (cortisol, corticosterone, cortisone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is produced by the zona glomerulosa?

A

Mineralocorticoids (aldosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What effect do catecholamines have on the body?

A

Increased cardiac activity, blood pressure, glycogen breakdown, blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What effect do glucocorticoids have on the body?

A

Release AA from skeletal tissue, lipids from adipocytes, promote liver formation of glucose and glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What effect do mineralocorticoids have on the body?

A

Increased renal reabsorption of Na+ and H2O, renal K+ excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the adrenal medulla stimulated by?

A

Sympathetic preganglionic fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the zona reticularis stimulated by?

A

ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the zona fasciculata stimulated by?

A

ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the zona glomerulosa stimulated by?

A

Angiotensin II, high K+, low Na+, inhibited by ANP/BNP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the hypothalamic-pituitary-adrenal axis?

A 
Hypothalamus
Corticotrophin releasing hormona (CRH)
Anterior pituitary
Adrenocorticotrophic hormone (ACTH)
Adrenal cortex
Cortisol (supplies -ve feedback to the hypothalamus and anterior pituitary)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is adrenal insufficiency?

A

an adrenal cortex disorder where there is a decreased production of adrenocortical hormones (cortisol, aldosterone, DHEA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the causes of primary adrenal insufficiency?

A

Addison’s disease (80%, autoimmune, common in females)

Tuberculosis (commonest cause in endemic countries)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the causes of secondary adrenal insufficiency?

A

Pituitary adenoma

Sheehan’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of tertiary adrenal insufficiency?

A

Brain tumour

Sudden withdrawal of long term corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the main thing you would be looking for in a Pt with glucocorticoid deficiency?

A

Hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the main thing you would be looking for in a Pt with mineralocorticoid deficiency?

A

Hyponatraemia

Hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms of adrenal insufficiency?

A 
Fatigue
Anorexia
Weight loss
Nausea and vomiting
Arthralgia and myalgia
Abdominal pain
Depression
Salt cravings
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the signs of adrenal insufficiency?

A

Hyperpigmentation in buccal mucosa and sun exposed areas (due to raised ACTH stimulating melanocytes)
Hypotension
Loss of body hair (in females)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the first line investigation you should do in a Pt with adrenal insufficiency?

A

9am cortisol (will be low)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the diagnostic investigation you should do in a Pt with adrenal insufficiency?

A

synACTHen test

250mcg tetracosactide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

At what cortisol levels can you rule out adrenal insufficiency?

A

Baseline cortisol >170nmol/L

30 min cortiosl >600nmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What other investigations can be done in a Pt with adrenal insufficiency?

A

Long synACTHen test (1mg tetracosactide, check at 1, 2, 3, 4, 5, 8, 24 hrs)
Adrenal antibodies
Adrenal CT/MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the management for adrenal insufficiency?

A

Lifelong glucocorticoids and mineralocorticoids
eg. hydrocortisone + fludrocortisone
Raise dosage if stressed eg. trauma, surgery, infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the complications of adrenal insufficiency?

A

Addisonian crisis
Secondary Cushing’s syndrome
Osteoporosis (long term XS glucocorticoids)
Hypertension (long term XS glucocorticoids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is an Addisonian crisis?

A

Acute adrenal insufficiency with major haemodynamic collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the causes of an Addisonian crisis?

A

Sepsis/surgery with a background of chronic insufficiency
Steroid withdrawal
Adrenal haemorrhage (Waterhouse-Friderichsen syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the presentation of an Addisonian crisis?

A 
Hypotensive shock
Tachycardia
Abdo pain
Confusion
Lethargy
Coma
Hyperkalaemia
Hypercalcaemia
Hypoglycaemia
Hyponatraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the management of a Pt with an Addisonian crisis?

A

Hydrocortisone sodium succinate 50-100mg IV every 6-8 hrs
1L saline followed by 2-4L over 24 hrs
Glucose to correct hypoglycaemia, risk of worsening hyponatraemia

32
Q

What is Cushing’s syndrome?

A

Chronic inappropriate elevation of free circulating cortisol

33
Q

What are the causes of Cushing’s syndrome?

A 
Exogenous Cushing's syndrome:
-chronic excess steroid use
ACTH-dependant:
-excess ATCH from pituitary adenoma (Cushing's disease)
-excess ATCH from ectopic tumour
ACTH-independant:
-excess cortisol from adrenal adenoma
34
Q

What are the symptoms of Cushing’s syndrome?

A 
Weight gain
Fatigue
Depression/psychosis
Insomnia
Amenorrhoea/oligomenorrhoea
Poor libido
Hirsutism/acne/balding
Thin skin
Easy bruising
Back pain
Muscle weakness
Polyuria/polydipsia
35
Q

What are the signs of Cushing’s syndrome?

A 
Moon face
Facial plethora
Interscapular fat pad
Hirsutism/acne/balding
Thin skin
Bruising
Hypertension
Ankle oedema
Pigmentation
Proximal myopathy
Osteoporosis
Pathological fractures
Skin infections
36
Q

What are the key symptoms of Cushing’s syndrome?

A 
Weight gain
Fatigue
Muscle weakness
Easy bruising
Menstrual irregularities
37
Q

What are the key signs of Cushing’s syndrome?

A 
Bruising
Proximal myopathy
Purple/red striae
Facial plethora (facial rounding)
Diabetes (early-onset)
Hypertension (early-onset)
Osteoporosis (early-onset)
Pathological fractures (ribs & vertebrae)
38
Q

What are the investigations for Cushing’s syndrome?

A

24hr urinary free cortisol (>50mcg)
Late night salivary/plasma cortisol
48hr low dose dexamethasone suppression test

39
Q

How is the 48 hour low dose dexamethasone suppression test performed?

A

Measure 9am plasma cortisol
Administer 0.5mg dexamethasone orally at 6hr intervals for 48hrs
Measure 9am plasma cortisol again

40
Q

What are the investigations for Cushing’s syndrome?

A 
High dose dexamethasone suppression test
-slight suppression if pituitary tumour
Inferior petrosal sinus sampling
-measure ACTH from pituitary
Adrenal CT/MRI
-adrenal adenoma/hyperplasia/tumour
Pituitary MRI
CT CAP
-ectopic sources
41
Q

What is the management for Cushing’s syndrome?

A

ACTH pituitary tumour:
-trans-sphenoidal pituitary adenectomy
Ectopic ACTH tumour:
-Surgical resection/ablation

Pre-surgery: somatostatin analogue, steroidogenesis inhibitor, glucocorticoid receptor antagonist
Post-surgery: pituitary hormone replacement therapy

42
Q

What are the complications of Cushing’s syndrome?

A 
Adrenal insufficiency post-treatment
Cardiovascular disease (main cause of mortality)
Hypertension
Diabetes mellitus
Osteoporosis
43
Q

What is hyperaldosteronism?

A

Autonomous overproduction of aldosterone from the adrenal glands

44
Q

What are the causes of hyperaldosteronism?

A

Primary:

  • adrenal adenoma (Conn’s syndrome) 70%
  • adrenal cortex hyperplasia 30%

Secondary:

  • glucocorticoid-supressible hyperaldosteronism
  • aldosterone producing adrenal carcinoma
45
Q

What are the risk factors for hyperaldosteronism?

A

FHx of aldosteronism/early HTN/stroke

46
Q

What are the clinical features for hyperaldosteronism?

A 
Asymptomatic unless hypokalaemic
Hypokalaemia:
-lethargy
-polyuria/polydipsia
--nephrogenic diabetes insipidus secondary to hypokalaemia
-muscle weakness
-paraesthesia
-tetany

Key signs: HTN

47
Q

What are the investigations for hyperaldosteronism?

A

Plasma potassium
-low
Aldosterone/renin ratio (best initial)
-increased
Fludrocortisone suppression test (best diagnostic)
-4 days of fludrocortisone, plasma cortisol should be suppressed
Saline infusion test
Adrenal CT/MRI
Adrenal venous sampling (to determine unilateral/bilateral Dx)

48
Q

What is the management for hyperaldosteronism?

A

If bilateral hyperplasia: aldosterone antagonists (spironolactone, amiloride, epleronone)
If aldosterone producing adenoma: adrenalectomy, post-op aldosterone antagonist if ongoing hyperaldosteronism

49
Q

What is a phaeochromocytoma?

A

Catecholamine producing tumour

50
Q

What are the causes of a phaeo?

A

Adrenal medullary chromaffin cells (90%)
Extra-medullary tumour (10%)
35% have familial link (MEN2, VHL, NF1 etc)

51
Q

What is the rule of 10’s for a phaeo?

A

10% are extra-medullary
10% are bilateral
10% are malignant

52
Q

What are the symptoms of a phaeo?

A 
Paroxysmal episodes of:
Headache (90%)
Palpitations (60%)
Diaphoresis (65%)
Chest pain
Dyspnoea
Epigastric pain and nausea
Diarrhoea
Tremor
Anxiety
53
Q

What are the signs of a phaeo?

A 
Hypertension (95%)
Tachycardia
Hypertensive retinopathy
Pallor
Impaired glucose tolerance
Orthostatic hypotension
54
Q

What are the investigations for a phaeo?

A

24hr urinary catecholamines, metanephrines, normetanephrines, and creatinine
Plasma metanephrines and normetanephrines (will be continuously elevated unlike catecholamines)

Genetic testing
CT/MRI AP
I-123 metaiodobenzylguanidine (MIBG) scintigraphy

55
Q

What is the management for a phaeo hypertensive crisis?

A

5-20mg phentolamine IV single dose

56
Q

What is the management for a phaeo?

A 
IV fluids if dehydrated
Alpha blockers (eg. phenoxybenzamine)
Beta blockers (eg. atenolol, propanolol)
-once alpha blockade is sufficient
-prevents reflex tachycardia (due to a2 blockade)
Surgical excision of tumour
57
Q

What is the normal range of potassium and what hormones can affect potassium levels?

A

3.5-5.0 mmol/L

Angiotensin II, aldosterone

58
Q

What are the causes of hyperkalaemia?

A 
Renal impairment- decreased GFR
Decreased renin production
ACEi
Ang II receptor blockers
Addison's
Aldosterone antagonists
Rhabdomyolysis
Blood acidosis
59
Q

At what level do Pts with hyperkalaemia become symptomatic?

A

> 6.0mmol/L

60
Q

What are the symptoms of a Pt with hyperkalaemia?

A

Muscle weakness
ECG changes
-tall tented T waves
-loss of P waves

61
Q

What is the management for hyperkalaemia?

A

10ml 10% calcium gluconate
100ml 20% dextrose and 10 units of insulin (drives K+ into cells)
Nebulised salbutamol

62
Q

What are the causes of hypokalaemia?

A 
Gastrointestinal loss (D+V)
Renal loss
-diuretics: loop/thiazide diuretics
-genetic defects
-hyperaldosteronism
-excess cortisol (binds to mineralocorticoid receptors)
-osmotic diuresis
Redistribution of K+ into cells (insulin, beta agonist, blood alkalosis)
63
Q

what are the signs of hypokalaemia?

A

Muscle weakness
ECG changes
-ST depression, reduced T wave amplitude, increased U wave amplitude
Polyuria/polydipsia (nephrogenic DI due to hypokalaemia)
Rhabdomyolysis, renal abnormalities, cardiac arrhythmias

64
Q

What is the management for hypokalaemia?

A 
Reduce K+ loss
-stop diuretics/laxatives etc
Replenish K+ stores
-oral replacement, IV if ECG changes/severe symptoms
Monitor for complications eg. ECG
65
Q

What is polycystic ovarian syndrome?

A

Syndrome characterised by:

  • oligomenorrhoea/amenorrhoea
  • hyperandrogenism
  • polycystic ovaries
66
Q

What is the cause of PCOS?

A

Unknown cause

Associated with obesity, insulin resistance, T2DM, dyslipidaemia

67
Q

What are the symptoms of PCOS?

A 
Irregular menstruation (75%)
Oligomenorrhea/amenorrhoea
Infertility
Hirsutism (60%)
Acne (20%)
Hair loss (scalp) (5%)
Oily skin
Excess sweating
68
Q

What are the signs of PCOS?

A

Hirsutism
Overweight
Hypertension
Acanthosis nigricans

69
Q

What is the criteria used to diagnose PCOS?

A

Rotterdam criteria (2/3 needed for diagnosis)

  1. menstrual irregularity
  2. clinical/biochemical evidence of hyperandrogenism
  3. polycystic ovaries on US
70
Q

What are the investigations for PCOS?

A 
Tests to exclude other causes (prolactin, TFT etc)
LH/FSH ratio >3
Serum total/free testosterone (elevated)
Serum DHEAS elevated
Oral glucose tolerance test- diabetes
Fasting lipid profile- dyslipidaemia
Pelvic ultrasound
71
Q

A 40 year old female presents to the GP with chronic fatigue, myalgia and depressive type symptoms. On examination you notice hyperpigmentation of the buccal membrane. Routine blood tests reveal a hyponatraemia and hyperkalaemia.
Which of the following investigations should be done?

A. Low dose dexamethasone suppression test
B. High dose dexamethasone suppression test
C. Short SynACTHen test
D. TRH stimulation test
E. Glucose tolerance test

A

C. Short SynACTHen test

72
Q

A patient with Addison’s disease is found unconscious on the bus. She is brought to the A+E where is she found to be hypotensive and slightly feverish. Routine blood tests are sent off which are normal except for the U+E’s.
Na+ = 130 mmol/L
K+ = 5.4 mmol/L
Urea = 9 mmol/L
Creatinine = 80 mcmol/L
What is the most appropriate immediate therapy?

A. IV hydrocortisone and fludrocortisone
B. IV hydrocortisone
C. IV fludrocortisone
D. Start sepsis 6
E. Give IV fluid bolus
A

A. IV hydrocortisone and fludrocortisone

?not severe enough to be classified as an Addisonian crisis, where the management would be B. IV hydrocortisone

73
Q

A 58 year old man attends the GP concerns about the stretch marks on his stomach. On examination, there are purple striae on his abdomen and you notice he is overweight with adipose tissue predominantly centrally and subscapular. You send for a dexamethasone supression test with come back with the following:
Initial 9am cortisol = 600 nM. 48 hours later: cortisol = <50 nM.
What of the following is the most likely cause?

A. Cushing’s syndrome
B. Alcohol excess
C. Cushing’s disease
D. Hypothyroidism
E. Addison's disease
A

B. Alcohol excess

74
Q

A 38 year old female has a routine blood test for health insurance. She is referred to her GP after a mild hypokalaemia was detected. She reports some fatigue and lethargy but no other symptoms. Her examination is normal except for a blood pressure of 150/90.
What is the most appropriate 1st investigation?

A. Fludrocortisone suppression test
B. Thyroid function tests
C. Aldosterone/Renin Ratio
D. Renal duplex ultrasound
E. Low dose dexamethasone suppression test
A

C. Aldosterone/Renin Ratio

75
Q

A 35 year old man has headache, palpitations, and sweating. Examination reveals hypertension, which is paroxysmal in nature. Additionally, there are café au lait spots. A diagnosis of phaeochromocytoma is suspected. Which investigation would provide confirmation?

A. thyroid stimulating immunoglobulin antibody levels
B. TFTs
C. 24-hour urinary catecholamine and metanephrine Levels
D. aldosterone/renin ratio

A

C. 24-hour urinary catecholamine and metanephrine Levels

Phaeochromocytoma secondary to NF1

76
Q

A nurse bleeps you (the on-call SHO) at 7pm as a patients blood tests have come back showing a severe hyperkalaemia of 7.4 mmol/l. You burst into the ward and find the patient. He responds cheerily to you and asks how you are doing.
What is the best appropriate next step?

A. Ask the nurse to do an ECG on him
B. Do a venous blood gas
C. Repeat the blood test
D. Give 10ml 10% calcium gluconate
E. Warm up the defibrillator
A

C. Repeat the blood test

77
Q

A 22 year old female presents to the GP with excessive hair growth along persistent acne. She mentions that’s she’s been having painful irregular periods for many years and would also like treatment for that.
What is the most likely diagnosis?

A. Physiologically normal 
B. PCOS
C. Hypothyroidism
D. Delayed puberty
E. Hyperthyroidism
A

B. PCOS

Year 3 MedEd (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions