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CAM304: Endocrinology > B1: RMcC Adrenal Gland > Flashcards

B1: RMcC Adrenal Gland Flashcards

1
Q

Embryological origin od adrenal gland, when does it form?

A

Neuroectodermal cells - medulla
Mesenchyma - cortex

Adrenal Glands present in fetuses ~2months development

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2
Q

Basic anatomy of adult adrenal gland

A

3-4cm wide, ~1cm thick, 4-6g
Located on superior poles of kidneys
Blood supply from suprarenal / adrenal branches from abdominal aorta

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3
Q

Zones of Medulla/Cortex

A

Cortex = 80%

  • Outer Capsule
  • Zona Glomerulosa (15%)
  • Zona Fasciculata (75%)
  • Zona Reticularis

Medulla = 20%

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4
Q

Hormones secreted, by area:

A

All hormones synthesized and secreted by cortex are derived from choelsterol*

Zona Glomerulosa = Aldosterone
Zona Fasciculata = Cortisol
Cona Reticularis = Androgens & Estrogens

Medulla = Epinepherine and Nor-epinephrine

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5
Q

Normal feedback loop - cortisol

A

Hypothalamus -> secretion of CRH
Anterior Pituitary -> Secretion of ACTH
-> Adrenal Cortex (zona fasciculats) -> Cortisol

Cortisol then feeds back to inhibit secretion of both CRH and ACTH

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6
Q

How is cortisol circulated, and when does it carry out its action?

A

Secreted unbond
Travels in plasma, bound to plasme proteins

Active form = unbound

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7
Q

Actions of Cortisol:

A
  • Decreased immune responses
  • Bone reabsorption and decreased bone formation
  • Decreased connective tissue
  • Increased muscle function and decreased muscle mass
  • Wakefulness
  • Modulation of emotional tone
  • Increased glomerular filtration and free water excretion
  • Supports CO and peripheral tone
  • Facilitates fetal maturation
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8
Q

Describe how the SNS acts on the body - including the adrenal gland (general terms)

A

Various structures feed input into Hypothalamus, which feeds into the brainstem (ANS centres) and SC

Sympathetic nerves -> Sympathetic Ganglia -> Postganglionics -> NA/A onto specific innervated tissues

Alternatively: Postganglionic axons release ACh onto Adrenal Medulla -> release of Epinephrine / Norepinephrine into blood circulation -> systemic effect

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9
Q

Epidemiology of Adrenal Insufficiency

A

Prevalence: 40-110/1,000,000
F:M ratio = 2.6:1
Usually diagnosed in 3rd-5th decades

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10
Q

Primary Adrenal Insuffciency - Causes

A

Autoimmune Adrenalitis -> 70% of cases

Other causes:

  • haemorrhagic adrenal damage (coagulopathies, heparin)
  • Infective causes (HIV, TB, Histoplasmosis)
  • Polyglandular autoimmune 2
  • Adenoleukodystrophy
  • APECED
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11
Q

Secondary Adrenal INsufficiency - what is it, and causes

A

Adrenal ‘insufficiency’ that is secondary to problems ‘upstream’ -> results in low corticoid release

  • Glucocorticoid Use -> HPA Axis Suppression
    (Dexamethasone most prominantly does this, followed by Fludrocortisone, Prednisolone, Methylprednisolone, then cortisol itself)
  • Anterior Pituitary Problems:
    e. g. Pituitary Adenomas, Haemorrhage affecting pituitary, Metastatic Malignancy
  • Developmental Abnormalities
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12
Q

Clinical Features of Adrenal Insufficiency:

A 
Skin:
- Increased pigmentation of face, palms, areas subject to friction, skin folds, scars, freckling, dair darkening, mucous membranes, nipples
- Decreased skin pigmentation
Weakness
Weight loss, emaciation
Anorexia, Diarrhoea, Vomiting
Salt Cravings
Hypotension
Hypoglycemic Episodes
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13
Q

Diagnosing Adrenal Insufficiency:

A

Can be done with ‘Endocrine Stimulation Test’
*want to isolate primary adrenal insufficiency as cause -> not due to secondary causes

Give synthetic ACTH 250mcg IV
Normal Response (measured free cortisol)
@ 0 mins - cortisol - 220mmol/L
@ 30 mins -------------550
@ 60 mins -------------550

If cortisol fails to rise in response to synthetic ACTH, then it is adrenal insufficiency

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14
Q

How can we test for secondary or tertiary abnormalities associated with decreased cortisol levels?

A

Metyrapone Testing

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15
Q

Describe Metyrapone Testing:

A

Tests for 2ndary or 3iary abnormalities assoc. w/ low cortisol

Metyrapone prevents cortisol synthesis by inhibiting the 11B-deoxycortisol conversion to cortisol

Premise: giving metyrapone will prevent cortisol production, which should therefore result in both increased 11B-deoxycortisol AND ACTH

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16
Q

Steroid-induced HPA axis suppression: in order of most HPA-suppressing to least so

A 
Dexomethasone - most
Fludrocortisone (most salt retention)
Prednisolone
Methylprednisolone
Cortisol - least
17
Q

Problems with metyrapone testing?

A

Can induce adrenal crisis

Requires: fluid rescusitation (saline + sucrose)

And 100mg IV bolus hydrocortisone + Q6hr 100mg IV

18
Q

Aldosterone - where is it produced and what does it do in the body?

A

Produced by Zona Glomerulosa of Adrenal Cortex
Acts on Distal Tubules of the Nephron, resulting in:
- Increased Na+ reabsorption
- (and thus increased water reabsorption)
- Increased K+ loss in urine

19
Q

What is Hyperaldosteronism - signs

A

Over-production of Aldosterone
(Believed to account for a significant proportion of mod-severe HTN)

Signs:

  • HTN (often resistent)
  • Hypokalaemia
  • High serum aldosterone
  • loe serum renin (*remember ald feeds back to suppress renin in the RAS)
20
Q

Primary Causes of Hyperaldosteronism

A
  • Bilateral Idiopathic Adrenal Hypertrophy
  • Adrenal Adenoma (Adenomatous Primary Aldosteronism)

(Rarer causes: congenital adrenal hyperplasia; adrenal carcinoma)

21
Q

Secondary causes of Hyperaldosteronism

A

Usually due to overactivity of the RAS, which can be due to:

  • Juxtaglomerular cell tumour (produces renin -> stimulates RAS)
  • Renal artery stenosis (reduced flow to juxtaglomerular cells -> stimulates RAS)
22
Q

Overview of RAS

A

Decreased flow to juxtaglomerular cells -> Releases Renin

Renin converts Angiotensinogen to Angiotensin I

ACE converts Angiotensin I to Angiotensin II

Angiotensin II (and angiotensin III) causes release of Aldosterone

Aldosterone acts on distal nephron (increased Na+ and H2O reabsorption and increased K+ loss)

Aldosterone feeds back to suppress Renin activity

23
Q

Coming to a diagnosis for primary hyperaldosteronism: i.e. differentiating between adenoma and bilateral hyperplasia

A

Patient Presents with: Resistant HTN and Unprovoked Hypokalaemia

Test Aldosterone-Renin-Ratio (ARR) -> if normal, excluse primary hyperaldosteronism as cause

Is ratio is high -> want to re-test after making some adjustments

Adjustments:

  • Normalize serum K+ levels
  • Adequate Na+ intake
  • Cease BP medication if possible
  • Repeat ARR
  • Conduct 24hr urine aldosterone

If repeated ARR normal -> excluse PA as cause
If ratio still high, conduct ADRENAL CT SCAN

On scan:

  • If micronodules Medical Treatment -> Diagnosis = Bilateral Adrenal Hyperplasia
  • If still suspicous of adenoma, can do Adrenal Venous Sampling, to check for lateralization. Lateralization indicates Adenomatous Primary Aldosteronism. No lateralization = Bilateral Adrenal Hyperplasia
  • If mass(es) >1cm are present:
  • > and patient is >40 years old, conduct AVS to check for lateralization.
  • > If patient <40 years old…

Treatment is Unilateral Adenalectomy
As diagnosis is Adenomatous Primary Aldosteronism

24
Q

What is Cushing’s Syndrome:

A

A collection of clinical features (signs and symptoms) associated with chronically elevated cortisol

25
Q

Major Clinical Features of Cushing’s Syndrome

A
  • Central Obesity
  • HTN
  • Glucose Intolerance
  • Easy Bruising
  • Amenorrhoea or Impotency
  • Decreased Libido, Depression
  • Purple Striae
  • Moon Face and Facia Plethora
  • Osteoporosis
  • Hirsutism (excessive hairiness on woman)

(Less common: acne, personality changes, edema, headache and poor wound healing)

26
Q

Exogenous Cause of Cushing’s?

A

Glucocorticoid administration

E.g. due to asthma, rheumatoid arthritis, immunosuppression in post-transplant patients

27
Q

Endogenous Causes of Cushing’s:

A

Most common (70% of endogenous cushing’s) caused by Pituitary Ademona -> secretes lots of ACTH -> stimulates cortisol secretion from adrenal cortex

Less commonly, adrenal cushing’s due to adrenal adenoma, or adrenal hypertrophy

28
Q

What is Congenital Adrenal Hyperplasia

A

One of several genetic conditions involving mutations in the genes responsible for forming enzymes involved production of hormones derived from cholesterol - i.e. Adrenal Cortex Hormones

(aldosterone, androgens, cortisol)

29
Q

How might COngenital Adrenal Hyperplasia first present?

A

Sexually ambiguous genitalia - “virulization” - due to lack of androgens

30
Q

Congenital Adrenal Hyperplasia involves deficiencies of which cytochrome P450 enzymes?

A

21-OH and 11-OH Deficiencies

CAM304: Endocrinology (3 decks)

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