Brainscape's Knowledge GenomeTM

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


See full index

Semester 2 MEH > L19: The adrenal glands > Flashcards

L19: The adrenal glands Flashcards

1
Q

What are the adrenal glands? Where are they located?

A

Endocrine glands–> secrete directly into the blood
Pair of glands situated at the superior part of the kidney
Touch the inferior border of the diaphragm in the retroperitoneal space (outside the peritoneum)
6-8g combined weight

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

Describe the structure of the adrenal gland? What does each part secrete?

A

Capsule
Cortex
–> Zona Glomerulosa –> Mineralocorticoids (aldosterone)
–> Zona Fasiculata–> Glucocortocoids (cortisol)
–> Zona Reticulata–> Glucocorticoids + (small amount) Androgens (sex hormones- testosterone and oestrogen)
Medulla–> chromaffin cells
–> Adrenaline
–> Noradrealine

GFR- Salt, Sugar Sex

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

Embryologically where is the cortex and medulla derived from?

A

Cortex–> mesoderm

Medulla–> neural crest

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

What type of hormones are the hormones in the adrenal glands? What are the collectively known as?

A 
All steroid hormones 
Synthesised from cholesterol 
Lipid soluble 
Modulate gene transcription by binding to nuclear receptors 
Called corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is congenital adrenal hyperplasia?

A

Deficiency in 21 hydroxylase enzyme
Meaning synthesis of mineralocorticoids and glucocorticoids is inhibited
Synthesis directed towards androgens leading to development of indistinguishable sex organs

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

How do corticosteroids exert their action?

A
  1. Diffuse across the plasma membrane
  2. Bind to glucocorticoid receptors (or receptor for whatever hormone) in the cytosol
  3. Binding result in dissociation of chaperone proteins (e.g. heat shock protein 90)
  4. Receptor-ligand complex translocates to the nucleus
  5. Dimerisation with other receptors can occur
  6. Receptors bind to hormone response elements (glucocoricoid response elements (GREs)) or other TF
  7. Alter gene experion
    - -> Upregulate (most common)
    - -> Downregulate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is aldosterone?

A

Mineralocorticoid hormone
Produced in the Zona Glomerulosa
Major role in regulation of plasma Na+ (ENaC) and K+ (ROMK) and therefore arterial blood pressure

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

Where does aldosterone function? How does it get there?

A

Main action on the distal tubules and collecting ducts of nephrons
Transported bound to carrier protein serum albumin (lesser extent transcorin)

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

What does aldosterone do? How?

A

Controls the reabsorption and secretion of Na+, K+ and water
Increases the expression of the Na+/K+ pump on the basolateral surface of kidney cells
Pumps 3Na+ out of the cell and 2K+ into cell
Creates a concentration gradient into the interstitial fluid which water follows
Retention of Na+ and Water
Excretion of K+ into urine
Upregulates expression of epithelial sodium channels (ENaCs) in collecting ducts and colon–> promotes Na+ absorption
Key role in renin-angiotensin-aldosterone system

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

How does the renin-angiotensin-aldosterone system work?

A

RAAS
Increase blood pressure and regulate Na+ concentration
1. ↓ renal perfusion detected by Juxtaglomerular cells of the kidney and drop in BP detected by baroreceptors in carotid sinus stimulate release of renin from the kidneys
2. Renin acts on angiotensinogen released from the liver
3. Angiotensinogen cleaved to produces Angiotensin I
4. Angiotensin I cleaved by ACE released from the lungs to produce angiotenin II
5. Angiotensin II
–> Potent vasoconstrictor–> ↑ arterial BP
–> Adrenal cortex–> aldosterone–> ↑ resorption of Na+ and water, ↑ excretion of K+–> ↑ BP and volume
–> Posterior pituitary–> ↑ ADH secretion–> translocation of aquaporins –> ↑ water reabsorption

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

What is hyperaldosteronism? What are the different types?

A

Too much aldosterone produced
Primary–> defects in adrenal cortex
Secondary–> overactivity of RAAS

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

What could cause primary hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia –> increase in cell number
Aldosterone secreting adenoma (Conn’s syndrome)
Low renin levels (high aldosterone:renin ratio)

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

What could cause secondary hyperaldosteronism?

A

Renin producing tumour–> rare–> JXA tumour
Renal artery stenosis
High renin levels (low aldosterone: renin ratio)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the signs of hyperaldosteronism?

A 
High blood pressure
LV hypertrophy (heart has to work hard due to ↑BP)
Stroke
Hypernatraemia 
Hypokalaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the treatment options for hyperaldosteronism?

A

Depend on whether its primary or secondary
Aldosterone-producing adenomas removed by surgery
Spironolactone (mineralocorticoid receptor antagonsit)

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

What is cortisol?

A

Glucocorticoid
Released from Zona fasciculata in response to ATCH
Major role in metabolism and stress response

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

What are the main actions of cortisol?

A 
↑ protein breakdown
↑ lypolysis
↑ gluconeogenesis
Resitance to stress
Anti inflammatory effects
Depression of immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What regulates cortisol secretion?

A

Adrenocorticotropic hormone (ACTH) secreted from the anterior pituitary
Secreted with a circadian rhythm with pulsatile secretion superimposed
Peak 7.00am
Trough 7.00pm
Time should be noted when taking cortisol blood sample

Negative feedback loop
Cortisol feedsback onto the hypothalamus and AP to inhibit secretion of CRH and ACTH respectively

19
Q

What regulated ACTH secretion?

A

Cortisol releasing hormone (CRH) from hypothalamus

Released in response to physical (temperature, pain), chemical (hypoglycaemia) and emotional stressors

20
Q

What is ACTH?

A

39aa single chain polypeptide hormone
Initally–> 250aa called POMC (proopiomelanocortin)
Post-transaltional processing produces range of biologically acitve peptide–> ACTH, α-MSH (meloncytes stimulating hormone) and endorphins
α-MSH is within ACTH –> ACTH has some properties

21
Q

How does ACTH cause cortisol release?

A 
ACTH is hydrophilic
Bind to high affinity receptors in Zona fasciculata and reticularis (GPCR)--> Melanocortin receptor (type 2)--> cAMP as second messenger 
Activation of cholesterol esterase
Cholesterol esters--> cholesterol (free)
Cholesterol--> cortisol
22
Q

How is cortisol transported in the blood?

A

Lipophilic hormone

Carrier protein–> transcortin (aka corticosteroid binding globulin (CBG))

23
Q

How does cortisol act on target cells?

A

Cross the membrane of target cells
Forms hormone/receptor complex–>cortisol-receptor complex
Enters the nucleus
Interacts with specific region of DNA–> glucocorticoid response element
Changes rate of transcription of specific genes

24
Q

What is the net effect of glucocorticoid actions on metabolism?

A
  • Increased glucose production (in the liver, gluconeogenesis from AA and glycerol)
  • Increased lipolysis (breakdown of fat- releases glycerol, and re-distribution of fat abs, supraclavicular, dorso-cervical (buffalo hump) and face (moon face)
  • Increased proteolysis (muscle breakdown release AA, cortisol inhibits insulin-induced GLUT4 translocation in muscle–> prevents glucose uptake–> glucose sparing effect)

Increased glucose production
–> gluconeogenesis from glycerol and AA
–> glucose leads to increased insulin–> increases glycogen store (paradoxal effect)
–> Cortisol–> inhibits insulin-induced GLUT4 translocation in muscle–> prevents glucose uptake–> glucose sparing effect
Break down of protein
–> muscle
Redistribution of fat–> abdomen, supraclavicular fat pads, dorso-cervical fat pad (buffalo hump) and face (moon face)

25
Q

What is Cushing syndrome? What is it caused by?

A

Chronic excessive exposure to cortisol
Endogenous causes
–> Adrenal tumour–> Adrenal Cushings
–> Cushing disease–> Benign anterior pituitary adenoma secreting ACTH
–> Non pituitary-adrenal tumours producing ACTH (or CRH)
Exogenous
–> Prescribe glucocoritcoid (and steroids)

26
Q

What are the signs and symptoms of Cushing’s syndrome?

A 
Plethoric moon shaped face
Buffalo hump
Abdominal obesity 
Purple Striae--> protein in skin broken down--> becomes transparent
Acute weight gain
Hyperglycaemia
Hypertension
27
Q

What are steroid drugs used to treat? What are the side effects?

A

Anti-Inflammatory and immunomodulatory effects
Treat–> inflammatory disease (asthma, IBD, Rheumatoid, autoimmune conditions), suppress immune reaction to organ transplant
Side effects–> cortisol levels are increased–> side effects same as Cushing’s syndrome and can have mineralocorticoid effects

28
Q

What is important to remember if a patient on steroid drugs has side effects?

A

Cannot be stopped immediately
Need weening off them
Gradually reduce dose

29
Q

What is Addisons disease? What is it causes by?

A

Chronic adrenal insufficiency
Destructive atrophy from autoimmune response
Exact reason for autoimmune response unknown
Rarer causes–> fungal infection, adrenal cancer, adrenal haemorrhage

30
Q

What are the signs and symptoms of Addison’s disease?

A 
Postural hypotension 
Lethargy 
Weight loss
Anorexia
Increased skin pigmentation 
Hypoglycaemia
31
Q

Why do you get hyperpigmentation in Addison’s?

A

Decreased cortisol
Anterior pituitary
More POMC–> ACTH and α-MSH produced
α-MSH–> melanin stimulating hormone–> increased pigmentation
ACTH can also bind to melain receptor–> hyperpigmentation

32
Q

What is Addisonian Crisis? What causes it?

A

Life threatening emergency
Adrenal insufficiency
Precipitated by:
Severe stress, salt depravation, infection, trauma, cold exposure, over exertion, abrupt steroid drug withdrawal

33
Q

What are the signs and symptoms of Addisonian crisis?

A

Nausea, Vomiting
Pyrexia (↑body temp)
Hypotension
Vascular collapse

34
Q

How is Addisonian Crisis treated?

A

Fluid replacement

Cortisol

35
Q

What are androgens?

A

Weak hormone secreted from Zona Reticularis
Dehydroepiandrosterone (DHEA) and androstenedione
Partially controlled by CRH and ACTH secretion

36
Q

What is DHEA converted into? What does it promote?

A

Males–> Testosterone in testes (only before puberty–>after insignificant as testes secretes more)
Females–> Oestrogens (promotes libido, after menopause only source)
Axillary and pubic hair growth

37
Q

What is unusual about the adrenal medulla?

A

Modified sympathetic ganglion

Neuroendocrine system–> neuronal input for hormonal output

38
Q

What are the secretory cells in the adrenal medulla called?

A

Chromaffin cells

Technically postganglionic cells

39
Q

What do the chromaffin cells secrete?

A

Catecholamines–> Adrenaline (80%) and Noradrenaline (20%)

40
Q

How are the catecholamines synthesised? Why do some cells secrete NA?

A

Enzyme catalysed steps
Tyrosine–> Levodopa–> Dopamine–> Noradrenaline–> Adrenaline
NA–> adrenaline requires N-methyl transferase enzyme some cells lack the enzyme

41
Q

What are the adrenergic receptors? What types of receptors are they? How do they work?

A

α1 and 2 receptors
β1 and 2 receptors
GPCR
α1–> Gαq protein (activates phospholipase C–> PIP2 –> DAG and IP3–> PKC and Ca2+ release via IP3 receptors–> target proteins)
α2–> Gαi protein (inhibits Adenyl cyclase)
β1 and β2–> Gαs protein (activated AC–> cAMP–> PKA–> target protein)

42
Q

What are the actions of adrenaline?

A

‘Fight or flight’–> response to stressful situations, sympathetic release

  1. Heart–> β1 receptors increase HR and contractility
  2. Lungs–> β2 bronchiodilation
  3. BV–> α1 vasoconstriction (skin, gut) β2 vasodilation (skeletal muscle)
  4. Kidney–> renin secretion (β1, β2)
  5. Muscles–>increase glycolysis and glycogenolysis (α1, β2)
  6. Liver–> increase glycogenolysis and gluconeogenesis (α1, β2)
  7. Pancreas–> increase glucagon secretion (α2), decrease insulin secretion (α2, β2)
  8. Adipose–> increase lipolysis (β2)
43
Q

What causes over-secretion of adrenaline?

A

Chromaffin cell tumour–> Phaeochromocytoma
(dark, colour, cell–> tumour stains dark with chromium salts)
Rare–> catecholeamine secreting tumour (mainly NA)
May precipitate life threatening hypertension

44
Q

What are the consequences of over-secretion of adrenaline?

A 
Severe hypertension 
Headaches
Palpitations 
Diaphoresis (excessive sweating)
Anxiety 
Weight loss 
Elevated blood glucose

Semester 2 MEH (23 decks)

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