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BMS2031 > ENCDOCRINOLOGY > Flashcards

ENCDOCRINOLOGY Flashcards

1
Q

Location of the hypothalamus:

A

Location of the third ventricle

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2
Q

What do magnocellular neurons secrete in the posterior pituitary?

A
  • Secrete ADH and oxytocin (from either supraoptic nucleus OR paraventricular nucleus
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3
Q

What is the blood supply of the ANTERIOR PITUITARY

A

Internal carotid artery which goes into the hypophyseal arteries–> form median eminence –> divides into veins (portal veins) –> come down and supply anterior pit.

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4
Q

What is the blood supply of the posterior pituitary?

A
  • MIddle hypopyseal artery

- Inferior hypophyseal arteries

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5
Q

Where does the pituitary gland sit?

A
  • In pituitary fossa
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6
Q

What is the pituitary gland surrounded by?

A
  • Carnevous sinus (contains carotid arteries), cranial nerves, Sphenoid sinus
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7
Q

What will a tumor in the pituitary gland affect?

A
  • The surrounding structures, puts pressure on the optic chiasm–> double vision
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8
Q

What does a tumor in the pituitary gland putting pressure on the canernous sinuses cause?

A

Bad headaches

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9
Q

What can a pituitary tumor that presses LATERALLY on the cranial nerve (oculomotor) cause?

A
  • Transmission can be affected (lesions)

- Eye muscles don’t work properly

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10
Q

Where does the posterior pituitary develop from?

A
  • Develops from BRAIN (buds off and moves down)
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11
Q

Where does the anterior pituitary develop from?

A
  • Develops from roof of mouth and moves UP during development
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12
Q

What are the 5 cell types from the anterior pituitary and what do they secrete?

A 
SOMATOTROPHS--> Growth Hormone (GH) 
LACTOTROPHS--> Prolactin (PRL)
THYROTROPHS--> TSH (thyroid stimulating hormone)
GONADOTROPHS-->FSH AND LH
CORTICOTROPHS--> ACTH
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13
Q

Where are the parvocellular neurones and where do their nerve terminals go?

A
  • Within paraventricular nucleus area of hypothalamus

- Nerve terminals go TO median eminence

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14
Q

Is the posterior pituitary a gland?

A
  • NO! It is an extension of the hypothalamus (embryo-buds off from brain)
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15
Q

When are ADH or oxytocin released in terms of APs?

A
  • If the nerves ARE electrically stimulated (AP)
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16
Q

Where are oxytocin and ADH made?

A
  • Paraventricular nucleus and supraoptic nucleus clusters
  • WIthin cell bodies of neurones
  • Then transported DOWN axon and stored in axon terminal
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17
Q

What is oxytocin (what type of structure) and what is it inoolved in?

A
  • 9aa peptide
  • Involved in lactation
  • Involved in suckling (positive feedback via mechanoreceptors) –> oxytocine released
  • Labour (positive feedback) -stretch recepotrs–> signals to brain and hypothalamus
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18
Q

What does prolactin cause?

A
  • Milk production
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19
Q

What does oxytocin casue in terms of feeding?

A
  • Milk let down
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20
Q

Which two things is ADH most sensitive to?

A
  1. Change in plasma osmolarity (1% changes it is sensitive to)
  2. Change in BP (10-15% changes it is sensitive to) –> baroreceptors in aortic arch and carotid bodies + low pressure vol. receptors in atria and pulm venous system in chest.
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21
Q

Which receptors does ADH act on in kidney and blood vessels and what do these receptors do when ADH is bound?

A

Kidney= V2 receptors
Blood vessels= V1
- These receptors when activated cause more aquaporins to migrate to renal tubule membranes

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22
Q

Is the secretion of anterior pituitary hormones a balance between positive and negative hypothalmic influences?

A
  • YES!
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23
Q

Is there a hypothalmic stimulator and inhibitor for each anterior pituitary hormone?

A
  • YES!
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24
Q

What is hyperplasia?

A
  • Increase in the number of cells
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25
Q

What is hypertrophy?

A

-Increase in the size of cells

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26
Q

What is GH secreted by and what does it stimulate?

A
  • Secreted by anterior pituitary and stimulates insulin like growth factors to be secreted from LIVER
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27
Q

What do problems in the thyroid hormones, sex steroids and glucocorticoids lead to?

A
  • Decrease in growth rate and neuro development
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28
Q

What do excess glucocorticoids lead to?

A
  • Premature fusion of the epiphyses of bone bodies (long bones)
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29
Q

What 4 functions does GH have?

A
  1. Stimulates LIVER to release insulin like growth factor (IGF-1)
    2INCREASES Ca2+ retention
  2. INCREASES muscle mass (hypertrophy of sarcomeres)
  3. INCREASE in protein synthesis
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30
Q

What is a feature of GH and when does its secretion peak?

A
  • Pulsatile and circadian secretion

PEAKS during SLEEP

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31
Q

What 6 things is GH secretion stimulated by?

A
  1. SLEEP
  2. EXERCSIE
  3. STRESS/TRAUMA
  4. FASTING/PROTEIN DEFFICIENCY
  5. HYPOGLYCEMIA
  6. GHRELIN
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32
Q

Which 5 things is GH secretion inhibited by?

A
  1. SOMATOSTATIN
  2. POST PRANDIAL HYPERGLYC
  3. INCREASED FATTY ACIDS
  4. INCREASED IGF-1 (Neg feedback)
  5. AGING
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33
Q

Which two chemical molecules are needed for bone growth?

A
  • Ca2+ and PO43-
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34
Q

What does a Ca2+ and PO43- defficiency result in (bones)?

A
  • Rickets

- Bowing of bones

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35
Q

What does GH stimulate in terms of bone growth?

A
  • Stimulates LONG BONE GROWTH at epyphyseal cartilages

- Stimulates DEPOSITION of new cartilages and INCREASES osteoblast activity

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36
Q

What is the intake of calcium PER DAY and how much of this is abosrbed in the intestine and where does it go after absorption?

A
  • 1g
  • 35% reabsorption in intestine
  • Goes to ECF–> Kidneys–> Excreted in urine (10%)
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37
Q

Which 4 things regulate the amount of Ca2+ that is ingested?

A
  1. VIt D
  2. PTH (parathyroid hormone)
  3. Cortisol
  4. T3/T4
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38
Q

What is the ECF calcium dependent on?

A
  • How much is absorbed and excreted by the kidney and gut
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39
Q

How much Ca2+ is stored by the bones?

A
  • 1kg (1,000,000mg)
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40
Q

Which 4 factors increase bone resoprtion (Ca2+ OUT of bone)?

A
  1. Vit D3
  2. PTH
  3. Cortisol
  4. T3/T4
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41
Q

Which 3 factors increase bone mineralisation?

A

`1. E2 (Estrogen)

  1. Testosterone
  2. GH (growth hormone)
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42
Q

Which 3 factors is balancing Ca2+ levels dependent on?

A
  • Storage of calcium in bone (increasing or decreasing plasma calcium)
  • Absorption from gut
  • Actions of kidneys
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43
Q

Which two hormones regulate Ca2+?

A
  1. PTH (parathyroid hormone)

2. 1,25dihydroxy vitamin D (Calcitrol)

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44
Q

Where is PTH made and secreted?

A
  • Made and stored in vesicles in parathyroid (contains Ca2+ binding receptor on cell membrane)
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45
Q

What stimulates PTH?

A

LOW Ca2+ level

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46
Q

What inhibits PTH?

A

HIGH Mg2+ level

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47
Q

What do catecholamines stimulate?

A
  • PTH secretion
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48
Q

As Ca2+ levels decrease……….what increases?

A
  • PTH levels increase
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49
Q

What is the half life of PTH, what type of hormone is it, and what stimulates its secretion?

A
  • Large polypeptide chain (protein hormone)
  • 2-4 min half life
  • LOW Ca2+ levels stimulate secretion
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50
Q

What substance is bone made up of?

A
  • Hydroxyapatite

[Ca10(PO4)6(OH)2]

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51
Q

Is bone CONSTANTLY being remodelled?

A
  • YES!
52
Q

If bone is being layed down what happens to Ca2_ and PO42-?

A
  • Taken FROM plasma TO bone
53
Q

If bone is being resorbed what happens to Ca2+ and PO42-?

A
  • RELEASED from BONE TO PLASMA
54
Q

Which structure does PTH act on?

A
  • Kidney
55
Q

What do osteoclasts do?

A
  • Break DOWN bone
56
Q

What does PTH stimulate osteoblasts to make and what does this thing do?

A
  • RANK ligand (RANKL)

- RANK Ligand binds to RANK receptor on OSTEOCLASTS –> stimulates osteoclast activity

57
Q

What do sex steroids stimulate the production of and what does this thing do?

A
  • OPG protein

- Sits on RANKL and stops RANKL from binding to osteoclasts so inhibits GONE RESORPTION *

58
Q

What are the 3 targets for PTH?

A
  1. Bone –> causes resoprtion (increased Ca2+ levels in plasma) and decreased PO43-
  2. KIDNEY—> Increases Ca2+ and decreases PO43- reabsorption (excretion occurs)
  3. Gut (indirectly to increase Ca2+ absorption)
    - Increases 1,25OH VIt D3 (converts inactive form of Vit D to Active Vit D)–> ACTS ON GUT TO INCREASE CA2+ ABSORPTION
59
Q

What type of hormone is VItamin D?

A

Steorid hormone

60
Q

What is the rate limiting step in vitamin D formation (liver)?

A
  • Adding the second OH group to C1 convertes inactive Vit D (25alphahydroxy vit D3) —-> 1,25dihydroxy-VitD3
  • VIA 1ALPHAHYDROXYLASE
61
Q

What is the enzyme 1alphahydroxylase stimulated by?

A

PTH in kidney and LOW PO43-

62
Q

What does Vitamin D supress?

A
  • PTH secretion
63
Q

What does Vitamin D act on the gut to do?

A
  • INCREASE Ca2+ reabsorption and INCREASE PO43- reabsorption
64
Q

What does VItamin D stimulate the differentiation of ?

A
  • Osteoblasts and RANKL production
65
Q

Laying down bone will happen automatically IF there is enough….

A

Calcium and phosphate

66
Q

What does Calcitronin (hormone) do?

A
  • Decreases plasma Ca2+ concnetration and plasma PO43-
  • Does’t have a massive effect on the plasma Ca2+ levels
  • Acts on bone to inhibit osteoclasts resorption (OPPOSITE ACTION TO PTH)
67
Q

What is Calcitronin used clinically for?

A
  • To treat Pagets disease (disrupts replacement of old bone tissue with new bone tissue)
  • to treat hyperglycemia (hyperparathyroidsim–> increases bone resorption, increases Ca2+ resorption in gut, decreases Ca2+ excretion (renal) –> hyperpolarises cells
  • To treat osteoperosis
68
Q

What is hypocalcemia and what is it caused by?

A

Cells depolarise much more easily (tetany, seizures)

- Caused by FAILURE of PTH, Vitamin D defficiency or resistance

69
Q

Do you die if you have no adreal gland?

A

yes!

70
Q

What is the adrenal gland under control by?

A
  • ACTH (adrenocroticotropin releasing hormone)
71
Q

Where in the adrenal medulla are the steroid hormones released from?

A
  • The cortex
72
Q

Which tissue is the adrenal medulla derived from?

A

-Neural Tissue –> catecholamines–> Adrenaline

73
Q

What are the steps of the sympathoadrenal system (neural arm)?

A

STRESS (detected by higher brain centres)
BRAIN stimulated –> brainstem –> sympathetic nerves ACTIVATED (spinal cord pathways) –move down s.c.–> pre ganglionic fibres nerve endings SECRETE ADH onto CHROMAFIN cells in Adrenal MEDULLA –> Chromaffin cells release adrenaline (80% ) + NA (20%)

  • Adrenaline–> SYSTEMIC CIRCULATION–> heart increase HR and contractility
  • NA released at synapses of sympathetic nerves –> stimulate SA node and cardiomyocytes to INCREASE FORCE OF CONTRACTION
74
Q

Which two aspects are organs getting a sympathetic response from?

A
  1. Release of NA

2. Adrenaline circulating

75
Q

What is the sympathoadrenal system (endocrine arm)?

A

CRH (corticotropin releasing hormone) and ADH released from HYPOTHALAMUS –> Stimulates release of ACTH from pituitary –> acts on cortex (to release cortisol-steroid hormone)

76
Q

What are the symptoms of addnsons disease?

A
  • Fatigue
  • Hypotension
  • Skin pigmentation (degeneration of adrenal gland)
77
Q

What occurs in Cushings syndrome?

A
  • Too much cortisol is released
78
Q

What hormone does the zona glomeulose (cortex of adrenal gland) cells reelase?

A
  • Aldosterone (mineralcorticoid)
79
Q

Which hormone does the zona fasciculate (cortex of adrenal gland) release?

A
  • CORTISOL (glucocorticoid)
80
Q

What does the zona reticularis cells (cortex of adrenal gland) release?

A
  • Sex steroids (androgens–> pubertal growth)

also technically cortisol is released from here aswell

81
Q

What are ALL steroids made from?

A
  • Pregnenolone (cholesterol is substrate)
82
Q

In the different layers of the adrenal cortex, what determines which hormone will be made by particular cells?

A
  • Different enzymes produced by the different layers
83
Q

Which two main things is alsdosterone important in?

A
  1. Conservation of Na+

2. Maintaining normal blood volume (water follows sodium)

84
Q

When there is low Na+ or high K+ what does this cause (aldosterone)?

A
  • Casues more aldosterone to be released from ADRENAL CORTEX
  • acts on kidney tubules –> Na+ reabsorption INCREASES and K+ secretion increases
85
Q

Does Na+ or K+ have a DIRECT effect on the adrenal glands?

A
  • K+ has DIRECT EFFECT and Na+ has indirect effect
86
Q

Which steroids does the adrenal cortex secrete?

A
  • Sex steroids–> androgens (DHEA and androstenedione)
87
Q

What is the precursor for pregnenolone/progesterone and thus DHEA and androstenedione?

A
  • Cholesterol

- Need 17,20 lyase

88
Q

What is the androgen level like compared to the gonads?

A
  • It is LOW
89
Q

What is Conn syndrome?

A
  • Adrenal hyperfunction for aldosterone (excessive secretion of aldosterone)
90
Q

What are the effects of Conn syndrome?

A
  • retention of Na+ and H20
  • Retention of Na+ and H20
  • Systemic hypertension and urinary loss of K+- cardiac arrhythmia (normal K+ is low in plasma)
91
Q

What does hypersecretion of estrogens lead to?

A
  • Feminisation (breast development)
92
Q

What does hypersecretion of androgens lead to?

A
  • virilisation (Increase in facial hair and acne)
93
Q

What is the major glucocorticoid in humans?

A
  • Cortisol
94
Q

What does the glucocoregulatory counter regulatory hormone do?

A
  • Opposes action of insulin

- Just like glucagon adrenaline and GH

95
Q

Do all cells have cortisol receptors?

A
  • YES (pretty much)
96
Q

Where (in tissue) is the main regulatory role of cortisol?-

A
  • Skeletal muscle, liver and adipose tissue
97
Q

Does cortisol act alone?

A
  • NO! Acts in conjunction with glucagon, adrenaline, and GH
98
Q

What is the main hormone secreted when responding to stress?

A
  • Cortisol
99
Q

Is cortisol secreted in non stress situations?

A
  • YES! There is a basal level that is produced to maintain NORMAL blood pressure (A and NA)
100
Q

What effect does cortisol have on the immune response?

A
  • Inhibits immune system and inflammatory response
101
Q

Which class of drug is prescribed to reduce inflammation?

A
  • corticosterioid (glucocorticoids–> cortisol)
102
Q

What is the secretion pattern of cortisol like?

A
  • Pulsatile and circadium rhythm
103
Q

When does cortisol level secretion peak?

A
  • During sleep

- Cortisol pulses follow ACTH

104
Q

Which 3 main factors stimulate the parvicelllar neurones in the PVN to secrete CRH and ADH?

A
  • Circadium rhythm
  • Stress
  • Negative feedback
105
Q

Where are CRH and ADH released into?

A
  • Hypophyseal portal blood (local)
106
Q

Are androgens also secreted with cortisol?

A
  • YES! (negatively feedback to anterior pituitary)
107
Q

CRH stimlates the secretion of ____ from the _____

A

CRH stimulates the secretion of cortisol from the adrenal gland

108
Q

What does a decrease in CRH release and ADH have on the pituitary?

A
  • Makes it less responsive to CRH and ADH

- Thus DECREASE in ACTH

109
Q

What does a chronic high ACTH level lead to?

A
  • (Hyppoplasia) –> Not enough ACTH

- Hypertrophy of adrenal cortex

110
Q

What effect does cortisol have on metabolism in muscle?

A
  • Increases plasma glucose
  • Decreases protein synthesis
  • Increases protein degradation (aa release)
  • Decreases glucose uptake (so muscles are more dependent on on glycogen supply for energy)
111
Q

What effect does cortisol have on metabolism in adipose tissue?

A
  • Stimulates lipolysis–> glycerol + FAs
  • Glycerol–> Glucose
  • FAs –> Ketone bodies
112
Q

What are some physiologyical effects of the stress response when A and NA released from adrenal medulla?

A
  • Increased HR and BP
  • Glycogen–> glucose
  • Dilation of bronchioles
  • Decreased blood to GIT
  • Increased metabolic rate
113
Q

What is the really general pathway for the stress response in terms of A and NA ?

A
  • Stress–> nerve impulses–> Pre ganglionic symathetic fibres–> adrenal medulla
114
Q

What is the pathway for the stress response in terms of Aldosterone and Cortisol?

A
  • Stress (in hypothalamus)
  • CRH released into local circulation (hypophyseal portal)
  • CRH acts on Corticotroph cells of anterior pituitary to release ACTH —goes into systemic circulation—–> adrenal cortex
  • Releases mineralcorticoids (aldosterone–> prolonged high ACTH) and glucocorticoids (cortisole)
115
Q

What happens in the long term stress response?

A
  1. Retention of the Na+ and H20 by kidneys

2. Increase in blood volume and blood pressure

116
Q

What is cushings syndrome?

A
  • Too much cortisol
117
Q

What is a primary cause of cushings syndrome?

A
  • Tumor –> leading to hypertrophy
118
Q

What is a secondary cause of cushings syndrome?

A
  • versecretion by hypothalamus or pituitary - HIGH cortisol and HIGH ACTH levels
119
Q

What are the effects of increased cortisol?

A
  • Weight gain
  • Fat deposits on face (moon face)
  • Insulin resistance
  • Protein wasting
  • Calcium effects
  • Increased MSH (skin pigmentation–> melanocyte skin hormone)
120
Q

Why do people with cushings syndrome put on weight?

A
  • High level of glucose in blood
121
Q

What is addinsons disease?

A
  • Decreased levels of cortisol
122
Q

What is the primary cause of addinsons?

A
  • Autoimmune destruction of adrenal cortex (low cortisol and increased ACTH –> but ACTH is independent)
123
Q

What is a secondary cause of addinsons?

A
  • Under secretion by the hypothalamus or pituitary
  • DECREASED cortisol
  • DECREASED ACTH or CRH (ACTH dependent)
124
Q

What are the effects of decreased cortisol?

A
  • Weakness
  • Fatigue
  • Anorexia
  • Weight loss
125
Q

What is the treatment for addinsons?

A
  • Glucocorticoids (Cortisol)
126
Q

What does glucocorticoid treatment for primary casue of addinsons turn off?

A
  • Patients own ACTH (production of own cortisol)

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