Endocrine refined Flashcards

1
Q

Endocrine glands

  • Function
  • Vascularity
A
  • Function: secrete hormones directly into the bloodstream upon stimulation
  • Vascularity: highly vascularised
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2
Q

The three arrangements of endocrine tissue

A

1- Endocrine organ
2- Distinct clusters of cells within an organ
3- Individual cells scattered throughout an organ

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3
Q

Major hormone products of the hypothalamus

  • RH and IF
  • Examples
A
  • Releasing hormones and inhibiting factors

- E.g. CRF, GnRH, GHRH, TRH, dopamine

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4
Q

Major products of the posterior pituitary (2)

A
  • Anti-diuretic hormone (ADH)

- Oxytocin

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5
Q

Major hormone products of the anterior pituitary (6)

  • ACTH
  • GH
  • P
  • FSH
  • LH
  • TSH
A
  • Adrenocorticotrophic hormone (ACTH)
  • Growth hormone
  • Prolactin
  • Follicle stimulating hormone (FSH)
  • Luteinising hormone (LH)
  • Thyroid stimulating hormone
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6
Q

Major hormone products of the thyroid gland (3)

A
  • Thyroxine (T4)
  • Tri-iodothyronine (T3)
  • Calcitonin
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7
Q

Major hormone product of the parathyroid gland

A
  • Parathyroid hormone
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8
Q

Major hormone products of the adrenal gland (2)

A
  • Adrenaline

- Cortisol

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9
Q

Major hormone products of the pancreas (2)

A
  • Glucagon

- Insulin

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10
Q

Major hormone products of the gonads (3)

A
  • Progesterone
  • Oestrogen
  • Testosterone
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11
Q

Modes of hormone action

  • Autocrine and Paracrine
  • Endocrine and Neuroendocrine
A
  • Autocrine and Paracrine: Local diffusion

- Endocrine and neuroendocrine: Circulation

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12
Q

Chemical nature of hormones is related to …. (5)

  • How they are….
  • Nature of the H….
  • Ability to b…..
  • degradation
A
  • How they are synthesised
  • Nature of the hormone receptor they bind to
  • Ability to bind to other proteins (e.g. transport proteins)
  • How they partition in tissues
  • How they are degraded
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13
Q

Steroid hormone examples:

  • Prog…
  • Gluco…
  • Mineral…
  • And….
  • Oest…..
A
  • Progestagens
  • Glucocorticoids
  • Mineralocorticoids
  • Androgens
  • Oestrogens
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14
Q

Non-steroid hormones

  • Poly…
  • Glyco…
  • Eico….
  • Pep….
  • Ami….
A
  • Polypeptides
  • Glycoproteins
  • Eicosanoids
  • Peptides
  • Amines
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15
Q

Hypothalamus-pituitary axis:

A
  • Interface between central nervous system and endocrine system
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16
Q

Hypothalamus-pituitary axis controls homeostatic regulation of (7)

  • S and I F
  • R
  • G and D
  • W/E B
  • E B/A C
  • T
  • S/W
A
  • Stress and immune function
  • Reproduction
  • Growth and development
  • Water/electrolyte balance
  • Energy balance/appetite control
  • Thermoregulation
  • Sleep/wakefulness
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17
Q

Hypothalamus, anatomical boundaries:

  • Anterior: OC
  • Posterior: MB
  • Superior: T
  • Inferior: ME
A
  • Anterior: Optic chiasm
  • Posterior: Mammillary bodies
  • Superior: Thalamus
  • Inferior: Median eminence
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18
Q

Hypothalamus structure: (2)

A
  • Divided into anatomical nuclei

- Contains hypothalamic neurosecretory cells

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19
Q

Action of the hypothalamus: (2)

  • HNC R P F AT A to C
  • I NI F BS, LS a HA, W R A
A
  • Hypothalamic neurosecretory cells release peptides from axon terminals adjacent to capillaries
  • Integrates neural inputs from brainstem, limbic system and hypothalamic areas, which regulate activity
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20
Q

Pituitary (hypophysis): two gland in one

A
  • Posterior lobe: under DIRECT control

- Anterior lobe: under INDIRECT control

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21
Q

Tissue of the posterior lobe:

A
  • Neural tissue: axons and nerve terminal endings of neurosecretory cells
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22
Q

Tissue of the anterior lobe:

A
  • Glandular tissue: cells controlled by releasing hormones, delivered via hypophyseal portal system
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23
Q

Vascular supply of the pituitary gland:

  • Anterior
  • Posterior
  • Drainage: CSS/IPS
A
  • Anterior lobe: primary portal plexus transports releasing hormones to the secondary plexus
  • Posterior lobe: a single plexus
  • Drainage: cavernous sinus superior / inferior petrosal sinus
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24
Q

Anterior pituitary lobe: hormones secreted (6)

A

Hormones with trophic action

  • Follicle stimulating hormone (FSH)
  • Luteinising hormone (LH)
  • Adrenocorticotrophic hormone (ACTH)
  • Thyroid stimulating hormone (TSH)
  • Growth hormone (GH)
  • Prolactin
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25
Hormones with trophic action:
- They go on to regulate a third hormone
26
"Tripartite" neuroendocrine system:
- The idea that 3 separate hormones are involved in a system 1. Releasing hormone 2. Tropic hormone 3. Hormone (hits target cells)
27
Tripartite neuroendocrine system is prominent in control of major glands e.g. (3)
- Thyroid gland - Adrenal gland - gonads (ovary/testis)
28
What controls biorhythms?:
- The hypothalamic suprachiasmatic nucleus (SCN), the body's master clock
29
Role of the hypothalamic SCN: (2) | - Partial control on …. Of …. Release from rhythm generators in the SCN
- Partial control on pulsatile patterns of hormone release from rhythm generators in the SCN - E.g. paraventricular nucleus receives circadian input from SCN, regulating hypothalamus-pituitary-adrenal (HPA) axis activity and cortisol release
30
Polyuria: Polydipsia:
- Excessive production and passing of urine | - Excessive thirst
31
What causes polyuria:
- In uncontrolled diabetes mellitus, osmotic diuresis (glucosuria) causes increased passive water loss
32
Principles of metabolic regulation:
- The flow of metabolites through pathways must be regulated to maintain homeostasis - Homeostasis occurs when metabolite concentrations are at a steady state
33
Reasons why the levels of required metabolites may vary: (3) Hint:exercise
- To increase the rate of glycolysis during exercise - To reduce the rate of glycolysis after exercise - To increase the rate of gluconeogenesis after exercise
34
What is the Km of a reaction:
- Rates are more sensitive to concentration near or below their Km
35
Km variation in glucose transporters:
- Different tissues have different glucose transport proteins present. - The Km for each GLUT type varies due to its tissues function
36
GLUT1: - Tissue/organ: - Km
- Red blood cells | - 3 mM
37
GLUT 2: - Tissue/organ - Km
- Liver, pancreas | - 17 mM
38
GLUT3: - Tissue/organ - Km
- Brain | - 1.4 mM
39
GLUT4: - Tissue/organ - Km
- Muscle, adipose tissue | - 5 mM
40
Contact-dependant signalling:
- A cell-surface-bound signal molecule binds to a receptor protein on an adjacent cell, no molecules are released
41
Paracrine signalling:
- Paracrine signals are released by cells into the EF, acting as a local mediator
42
Cell surface receptors: - Most signalling molecules.... - instead, they bind to .....
- Most signalling molecules are large and hydrophilic, they can't cross the plasma membrane. - Instead, they bind to cell-surface receptors which generate intracellular second messenger signalling molecules
43
Intracellular receptors: - Some small hydrophobic.... pass through the target cells plasma membrane binding to …. - That regulate, for example.....
- Some small hydrophobic extracellular signalling molecules pass through the target cells plasma membrane, binding to intracellular receptors. - That regulate, for example, gene transcription
44
Apoptosis:
- A form of cell suicide that occurs when a cell does not receive the necessary signals to survive
45
Timescales of a cell's response - Fast - Slow
- Fast: processes that rely on altered protein function; movement, secretion and metabolism - Slow: processes that rely on altered protein synthesis; differentiation, growth and division
46
Ion-channel-coupled receptors: - Signal molecules..... - Causing a change in...... - Thus, a chemical change.....
- Signal molecules (acetylcholine) cause the receptors to open in response to binding, - causing a change in the electrical potential across the membrane - Thus, a chemical signal is transducer into an electrical signal
47
G-Protein coupled receptors are transmembrane proteins: - Extracellular - Intracellular
- Extracellular portion of a GPCr binds to signalling molecules - The cytoplasmic portion binds to a G-protein
48
The two most common enzyme targets of G-proteins are: - Adenyl cyclase action: - Phospholipase C action:
- Adenyl cyclase catalyses the formation of the second messenger cyclic AMP (cAMP) - Phospholipase C produces the second messengers inositol triphosphate (IP3) and diacylglycerol (DAG). IP3 promotes the accumulation of cytosolic Ca2+, another 2nd messenger
49
The effect of adrenaline on skeletal muscle: - Adrenaline indicates a ..... - Adrenaline activates a ..... - The increase in cAMP activates..... - Phosphorylase kinase activates......
- Adrenaline indicates a requirement for glucose in muscle - Adrenaline activates a GPCR, activating a G-protein which activates cAMP - The increase in cAMP activates protein kinase A (PKA), which phosphorylates, activating phosphorylase kinase - Phosphorylase kinase activates glycogen phosphorylase, the enzyme that breaks down glycogen
50
GPCRs and cholera:
- Cholera toxin affects cells of the intestinal epithelium - Modifies a G protein, preventing it from deactivating, so it continually activates adenylyl cyclase - Causes continuous outflow of Cl- and H2O - Causing diarrhoea, dehydration and death
51
Growth hormone: - Location - Effect - Action
- Anterior pituitary - Causes growth in most tissues and promotes differentiation in some cell types - Binds to GH receptor in target tissues
52
Effect of somatostatin on GH secretion:
- Somatostatin inhibits GH secretion
53
Effect of GRH dopamine on GH secretion:
- GRH dopamine increases GH release
54
GH secretion frequency:
- Periodic secretion, affected by sleep
55
Feedback control of GH: - SS - GH
- GH stimulates somatostatin (SS), SS inhibits GH release | - GH also inhibits GHRH release and GH release
56
GH action: acute - Protein - Lipid - Carbs - Key effect
- Protein: Increased amino acid uptake and usage, increased protein synthesis. Decreased protein catabolism - Lipids: decrease in lipogenesis increase in lipolysis - Carbohydrates: decrease in glucose uptake and oxidation Increase in blood glucose -KEY EFFECT: PROTECTS PROETIN
57
Regulation of bone growth: IGF-1 - PM - R of P C - M of D S
- Pro-mitogenic - Recruitment of precursor cells - Maintenance of differentiated state
58
Regulation of bone growth: Glucocorticoids - P - Chronic effect
- Permissive: presence required for normal processes | - In chronic high doses leads to bone loss and catabolism
59
Regulation of bon growth: Androgens | - T S
- Testosterone surge during puberty accelerates closure of growth plates
60
Effects of an abnormal increased GH secretion:
1. Gigantism (before epiphyseal growth plate has sealed) | 2. Acromegaly (after growth plate closure)
61
Adrenal cortex zones: (3) - g - f - r
- Zona glomerulosa - Zona fasiculata - Zona reticularis
62
Hormone produced in the zone glomerulosa:
- Aldosterone
63
Hormone produced by zona fasiculata:
- Cortisol (and androgens)
64
Hormone produced by zona reticularis:
- Androgens (and cortisol)
65
Hormones produced by the adrenal medulla
- Adrenaline | - Noradrenaline
66
Synthesis of adrenocortical steroids
- All based on cholesterol, synthesised as required | - Expression of key enzymes regulated
67
Cortisol (glucocorticoid): - secretion: - regulation:
- Secreted by zona fasiculata - Release controlled by CRH/ACTH CRH: Cortisol releasing hormone ACTH: adrenocorticotrophic hormone
68
Circadian rhythm for Cortisol: - Synchronisation - Effect of stress
- CRH secretion synchronised with sleep cycle. | - Stress-induced CRH secretion increases glucocorticoid secretion approx. 20 fold
69
Cortisol actions: - Metabolic effects - Cardiovascular effects - Other
- ME: Stimulates gluconeogenesis and glycogenolysis (provides fuel) - CE: Maintains blood volume (protects CVS) - OE: Anti-inflammatory, immunosuppressive
70
Cortisol action on CVS:
- Increases contractility - Increases peripheral resistance Amplifying the effects of noradrenaline and adrenaline
71
``` Cortisol effect on inflammatory/immune response: -INHIBITS . S of C . H R . P of I C . S of A ```
``` - Inhibits: . Secretion of cytokines . Histamine release . Proliferation of immune cells . synthesis of antibodies ```
72
Regulation of cortisol release: tripartite 1. 2. 3.
1. Hypothalamus: releases CRH 2. Anterior pituitary: releases ACTH 3. Adrenal cortex: cortisol CRH: corticotropin releasing hormone ACTH: adrenocorticotropic hormone
73
Feedback control of cortisol - Positive - Negative
- Positive: stressors (physical/emotional) | - Negative: Pituitary, hypothalamus
74
Aldosterone: - Secretion - Half-life
- Zona glomerulosa | - 30 mins
75
What stimulates the release of cortisol?:
- Angiotensin 2 | - Low Na stimulates renin release in kidney, renin cleaves angiotensin into Ang1
76
What does aldosterone stimulate?: - Answer - Effect
- aldosterone stimulates Na-K ATPase in renal collecting ducts - Na reabsorbed in filtrate, K secreted into filtrate, Water retention
77
Corticosteroid receptors: | - two cytosolic receptors
- Glucocorticoid receptor (GR) . Cortisol - higher affinity at GR . Most cells have GR - Mineralocorticoid receptor (MR) . Aldosterone - higher affinity at MR . MR mainly in kidney and gut
78
Termination of action (adrenocorticoid): - Half-life: - Liver - Kidney
- Half-life: . Cortisol: 60 mins . Aldosterone: 15 mins - Liver: cortisol and aldosterone inactivated - Kidney: inactivated forms excreted in urine
79
Dysregulation of glucocorticoid release (2)
- Addison's: too little cortisol | - Cushing disease: too much cortisol
80
Paths to dysregulation: 1. Primary 2. Secondary 3. Tertiary
1. Primary: failure of adrenal cortex to secrete cortisol 2. secondary: failure of pituitary to secrete ACTH 3. tertiary: failure of hypothalamus to secrete CRH
81
Addison syndrome: too little cortisol | -Symptoms(6)
Symptoms: - Hypotension - Hypoglycemia - Hyponatremia - Hypovolumia - Hyperpigmentation - Hyperkalemia
82
Addison's disease : - Main cause - Other cause
- Main cause: autoimmune destruction of adrenal cortical cells (primary adrenocortical insufficiency) - Other causes: . Chronic glucocorticoid treatment . Infection
83
Cushing's SYNDROME: - ACTH??? - Causes????
- ACTH low - Adrenal neoplasm or hyperplasia - Chronic glucocorticoid treament
84
Cushing's disease:
- ACTH high | - Excessive and unregulated pituitary ACTH secretion
85
Glucocorticoid treatment: - wanted effects - unwanted effects
- Wanted effects: - reduces inflammation and suppresses immune system - Unwanted effects: - Atrophy of the zona fasicula (cortex)
86
Cushing's treatment:
- Remove or destroy source of ACTH or cortisol
87
Cushing's treatment:
- Remove or destroy source of ACTH or cortisol
88
General thyroid and parathyroid anatomy: - TG - PTG
- Thyroid gland has lateral lobes connected by isthmus | - Parathyroid glands are located behind the lateral lobes of the thyroid
89
T4 and T3 synthesis: -Location 1. Active uptake of..... I 2. Production of ..... Thy 3. Iodination of ...... tyr 4. Reabsorption of..... thy 5. Digestion by .....
- Occurs in the thyroid follicles 5 steps 1. Active uptake of iodide I- 2. Production of thyroglobulin 3. Iodination of tyrosine on thyroglobulin (in colloid) 4. Reabsorption of thyroglobulin 5. Digestion by lysosomal enzymes causes secretion of T4 and T3
90
Dietary iodide facts: - Daily requirement: - AVG. daily intake - Efficiently absorbed - Absorbed into.... - Removed from EP by .... - Kidneys... - Thyroid contains.....
- Daily requirement: >75 micro grams - Avg. daily intake: 500 micro g - Efficiently absorbed: only 15 micro g lost from gut in bile - Absorbed into extracellular pool: 150 micro g. - Removed from EP by thyroid or kidneys - Kidneys excrete 485 micro gram/day - Thyroid contains huge iodide store in colloid (8000 micro g)
91
Actions of thyroid hormones: - TBG - Method of action - Target genes - Target cells
- >99% is reversibly bound to proteins - thyroid binding globulin (TBG) - T4 and T3 operate through nuclear receptors regulating gene transcription (latency of several days) - Genes regulating cell differentiation and metabolism - Affects most tissues
92
Hypothyroidism: in early development - Definition - Symptoms (4)
- Cretinism: complete absence of thyroid hormone during development - symptoms: Neurological deficits (retardation) - Small stature and immature appearance - Puffy hands and face - Delayed puberty
93
Hypothyroidism in adulthood: symptoms (9) - L BMR and C S - B - S S - L - W G - C - M A - D T S - S M F
- Low BMR and cold sensitivity - Bradycardia (abnormally low resting HR) - Slow speech - Lethargy - Weight gain - Constipation - Menstrual abnormalities - Dry thickened skin - Slow mental function
94
Hyperthyroidism symptoms:
- Nervousness - High BMR, raised temp - Tachycardia (abnormally high resting HR) - Increased appetite/ weight loss - Tiredness
95
``` Physiological role of calcium: (6) - B S - B C _ N E - M I T - E R - C ```
- Bone strength - Blood coagulation - Neuromusclular excitability - Membrane ion transport - Enzyme regulation - Contraction
96
3 hormones of Ca regulation:
- PTH - Calcitonin - Vitamin D
97
Normal plasma calcium range:
- 2.2 to 2.6 mmol/L
98
Low Plasma Ca2+ response:
- Parathyroid glands (chief cells) secrete PTH, increasing plasma Ca2+
99
High plasma Ca2+ response:
- Thyroid parafollicular C cells secrete calcitonin, lowering plasma Ca2+
100
Hypocalcaemia: - Cause - Symptoms - Increased N E - T, M C, T - C and D (severe)
- Caused by hypoparathyroidism, caused by accidental damage to parathyroid glands during thyroid surgery - Symptoms: - Increased neuromusclular excitability - Twitching, muscle cramps, tetany - Carpodeal spasm - Coma and death (severe)
101
Hypercalcaemia: - Cause - Symptoms
- Associated with primary hyperparathyroidism and malignancy - Symptoms of stones bones and groans
102
Insulin: - Role: - Secreted:
- Role: signals the fed state, lowers blood glucose levels | - Secreted by beta-cells in the pancreas
103
Insulin synthesis: 1. Starts as preproinsulin, signal sequence.... 2. A and B peptides linked by .... 3. Mature insulin leaves .....
1. Starts as preproinsulin, signal sequence directs it into the endoplasmic reticulum 2. A and B peptides linked by disulfide bonds, proinsulin cleaved twice by a protease, removing C peptide 3. Mature insulin leaves Golgi network and enters a secretory vesicle
104
Insulin action: - Insulin binds to ......... .......... ......... on the surface of muscle and adipose cells - ...... is activated, auto phosphorylating .......... - Phosphorylated receptor binds to ..... allowing ..... to be converted to ....... - ........ activated ....... which activates Akt - Activated Akt increases cell glucose uptake
- Insulin binds to enzyme-coupled receptors on the surface of muscle and adipose cells - RTK is activated, auto phosphorylating tyrosines - Phosphorylated receptor bind to IRS-1 allowing PIP2 to be converted to PIP3 - PIP3 activates PDK1, which activates Akt - Akt ac
105
Effect of activated Akt on GLUT4 transporters:
- Activated Akt causes GLUT4 transporter vesicles to fuse to the cell surface membrane, increasing glucose uptake 15x
106
Glucose regulates insulin secretion from beta-cells: - Glucose enters..... - Glycolysis causes an..... - ATP binds to ..... - Membrane depolarisation causes..... - Causing more .... - Triggering insulin release via .....
- Glucose enters the beta-cell via GLUT2 - Glycolysis causes an increase in ATP - ATP binds to ATP-gated K+ channels, closing them - Membrane depolarisation causes opening of Ca2+ channels - Causes more Ca2+ to be released by the ER - Triggering insulin release via exocytosis
107
Sulfonylurea drugs in treating diabetes:
- Binds to SUR1 subunit, closing K+ channel, causing insulin release
108
Insulin main aim:
- Stimulate the uptake of glucose into cells, lowers plasma blood sugar levels
109
Glucagon main aim:
- Glycogen breakdown, raises plasma blood sugar levels
110
Diabetes symptoms: - Mutual (2) - Type 1 specific: ketoacidocis
- Elevated blood sugar - Excessive urination and thirst In type 1: - Accelerated fat break down, increase in ketone bodies, some of which are ketoacids, raising [H+], causing ketoacidosis
111
Long-term effects of raised blood sugar:
- Hemoglobin becomes glycated, compromising O2 deliveries (especially to extremities)
112
Luteinizing hormone (LH) role:
- Stimulation of testosterone secretion
113
Follicle-stimulating hormone role: (2)
- Spermatogenesis | - Oestrogen synthesis
114
DHEA (Dehydroepiandrosterone) role:
- Weaker androgens, no effect in males
115
Testosterone role:
- Secondary male sexual characteristics | - Spermatogenesis
116
Oestrogen role: (2)
- Secondary sexual characteristic development | - Growth of ovarian follicles/proliferation of endometrium
117
Progesterone role:
- Prepares the uterus for ovulation, thickens wall lining etc.