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Year 2 - Endocrinology > Hyperadrenal Disorders > Flashcards

Hyperadrenal Disorders Flashcards

1
Q

Clinical features of Cushing’s?

A 
x Excess cortisol
x Centripetal obesity
x Moon face & buffalo hump
x Proximal myopathy (muscle weakness)
x Hypertension
x Hypokalaemia
x Red striae
x Thin skin & bruising
x Osteoporosis
x Diabetes
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2
Q

Link between fat, protein & Cushing’s?

A
  • SYNTHESISE too much FAT

- Break DOWN too much PROTEIN

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3
Q

Potential causes of Cushing’s?

A

x Taking too many steroids (glutocorticoids)
x Pituitary dependent Cushing’s Disease
x Ectopic ACTH from lung cancer
x Adrenal adenoma (secretes cortisol)

Last 3 are endogenous causes

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4
Q

Difference between Cushing’s Syndrome & Disease?

A

If Cushing’s DISEASE - has a pituitary source!

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5
Q

What are the investigations to determine the cause of Cushing’s Syndrome?

A
  1. 24h urine collection for urinary free cortisol
  2. Blood diurnal cortisol levels
  3. Low-dose dexamethasone suppression test
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6
Q

How does the blood diurnal cortisol levels test work?

A

Varying levels depends upon time of say (highest at 9am, lowest at midnight)

Cushing’s - cortisol HIGH at ALL times

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7
Q

LDDST?

A

Low-dose dexamethasone suppression test

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8
Q

How does LDDST work?

A

Dexamethasone = artificial steroid

Normal - will suppress cortisol to 0 as excess cortisol
Cushing’s - will FAIL to suppress cortisol (ANY cause/type of Cushing’s)

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9
Q

Can you determine type of Cushing’s after the 3 investigative tests?

A

Nope - need more tests to see TYPE of Cushing’s (pituitary OR ectopic OR adrenal)

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10
Q

How can pharmacology be used in the treatment of Cushing’s>

A

Manipulate the steroids

  • Enzyme inhibitors
  • Receptor blocking drugs
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11
Q

Specific drugs used in the treatment of Cushing’s?

A

Metyrapone

Ketoconazole

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12
Q

Metyrapone MOA?

A

Inhibits 11beta-hydroxylase:

  • blocks production of cortisol
  • ACTH secretion increases (feedback systems)
  • plasma deoxycortisol increases
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13
Q

Why does plasma deoxycortisol increase through the use of Metyrapone?

A

Steroid synthesis in zona fasciculata (and reticularis) arrested at 11-deoxycortisol stage (has NO feedback effect) so levels increase

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14
Q

Clinical uses of Metyrapone?

A

Control of Cushing’s Syndrome prior to surgery:

  • dose adjusted to cortisol
  • improves patient’s symptoms & promotes post-op recovery

Control of Cushing’s symptoms AFTER radiotherapy (usually slow to take effect)

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15
Q

What are some unwanted actions associated with Metyrapone?

A

x Hypertension - deoxycorticosterone accumulates in z. glomerulose which has aldosterone-like activity leading to salt retention & hypertension

x Hirsutism - increased androgen production

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16
Q

History of Ketoconazole?

A

Main use as an antifungal work - not anymore

At HIGHER [ ], off-label use in Cushing’s Syndrome

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17
Q

Ketoconazole MOA?

A

Inhibits steroidogenesis (gluco/mineralcorticoids & sex steroids)

As blocks main enzyme converting cholesterol to pregnenolone (first-step)

18
Q

Uses of Ketoconazole?

A

(similar to Metyrapone)

x Treatment and control of symptoms prior to surgery
x Orally active

19
Q

Ketoconazole unwanted effects?

A

Liver damage

20
Q

Other than drugs, how else can you treat Cushing’s?

A

Surgery

21
Q

Different types of surgery available for Cushing’s?

A

Depends on cause

x Pituitary surgery (transsphenoidal hypophysectomy)
x Bilateral adrenalectomy
x Unilateral adrenalectomy for adrenal mass

22
Q

Conn’s Syndrome?

A

A benign adrenal cortical tumour (zona glomerulosa)

23
Q

What does Conn’s Syndrome lead to?

A

Excess aldosterone so hypertension & hypokalaemia

This is due to water retention, aldosterone enhances Na+ reabsorption and K+ excretion in the kidneys

24
Q

Type of diagnosis that can be reached for those with Conn’s Syndrome?

A

1o hyperaldosteronism

RAAS should be suppressed to exclude 2o hyperaldosteronism

25
Q

Treatment available for Conn’s?

A

x Aldosterone receptor antagonists i.e. Spironolactone & Epleronone

x Surgery

26
Q

Mineralcoticoid Receptor Antagonists used for Conn’s?

A

Spironolactone

Epleronone

27
Q

When is Spironolactone used?

A

For 1o hyperaldosteronism (Conn’s)

28
Q

Spironolactone MOA?

A

Converted to several active metabolites:

x CANRENONE being one - a competitive antagonist of the MR

29
Q

In Spironolactone MOA, how do the metabolites work?

A

Block Na+ resorption & K+ excretion in the kidney tubules (potassium sparing diuretic)

30
Q

Pharmacokinetics of Spironolactone?

A

x Orally active
x Highly protein bound
x Metabolised in the liver

31
Q

Spironolactone unwanted actions?

A

x Menstrual irregularities [women] (via. + progesterone receptors)

x Gynaecomastia [men] (via. - androgen receptor)

32
Q

Similarities & differences of epleronone to spironolactone?

A
  • also a MR antagonist
  • similar affinity to MR

BUT

-LESS binding to androgen & progesterone receptors so better tolerates

33
Q

Phaeochromocytomas?

A

Tumours of the adrenal MEDULLA which secrete catecholamines (A or NA)

34
Q

What are the clinical features of phaeochromocytomas?

A 
x sudden episode of hypertension (in young people as well)
x sweating
x headache
x sudden dizziness
x sudden anxiety
35
Q

Defining clinical feature of phaeochromocytomas?

A

Episodic SEVERE hypertension (after abdominal palpation - squeezes more A out)

More common in certain inherited conditions

36
Q

Difference between phaeochromocytomas and Conn’s?

A

Conn’s hypertension is episodic in the older population not in the young

37
Q

Why is the episodic severe hypertension so dangerous in phaeochromocytomas?

A

Can cause MI or stroke

High adrenaline can cause VI & death if not treated SO is a medical emergency

38
Q

How can phaeochromocytomas be managed?

A

Eventually need surgery
BUT
anaesthetic needs careful preparation as can precipitate a hypertensive crisis (causes releases of A)

Remember: this is curable so important!

39
Q

Before surgery, what is the first step for phaeochromocytomas treatment?

A

Alpha-blockade!

  • patients may need IV FLUID during this as will see a severe DROP in BP
  • beta-blockage is added to prevent tachycardia

This ensures that even if there is A released, can have NO EFFECT as the receptors are blocked

40
Q

Some key facts of phaeochromocytomas?

A

x 10% are extra-adrenal (down the SN chain)
x 10% are maligant
x 10% are bilateral

VERY RARE

Year 2 - Endocrinology (19 decks)

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