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
Q

Hormones with trophic action:

A
  • They go on to regulate a third hormone
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26
Q

“Tripartite” neuroendocrine system:

A
  • The idea that 3 separate hormones are involved in a system
    1. Releasing hormone
    2. Tropic hormone
    3. Hormone (hits target cells)
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27
Q

Tripartite neuroendocrine system is prominent in control of major glands e.g. (3)

A
  • Thyroid gland
  • Adrenal gland
  • gonads (ovary/testis)
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28
Q

What controls biorhythms?:

A
  • The hypothalamic suprachiasmatic nucleus (SCN), the body’s master clock
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29
Q

Role of the hypothalamic SCN: (2)

- Partial control on …. Of …. Release from rhythm generators in the SCN

A
  • 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
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30
Q

Polyuria:
Polydipsia:

A
  • Excessive production and passing of urine

- Excessive thirst

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31
Q

What causes polyuria:

A
  • In uncontrolled diabetes mellitus, osmotic diuresis (glucosuria) causes increased passive water loss
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32
Q

Principles of metabolic regulation:

A
  • The flow of metabolites through pathways must be regulated to maintain homeostasis
  • Homeostasis occurs when metabolite concentrations are at a steady state
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33
Q

Reasons why the levels of required metabolites may vary: (3)
Hint:exercise

A
  • To increase the rate of glycolysis during exercise
  • To reduce the rate of glycolysis after exercise
  • To increase the rate of gluconeogenesis after exercise
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34
Q

What is the Km of a reaction:

A
  • Rates are more sensitive to concentration near or below their Km
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35
Q

Km variation in glucose transporters:

A
  • Different tissues have different glucose transport proteins present.
  • The Km for each GLUT type varies due to its tissues function
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36
Q

GLUT1:

  • Tissue/organ:
  • Km
A
  • Red blood cells

- 3 mM

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37
Q

GLUT 2:

  • Tissue/organ
  • Km
A
  • Liver, pancreas

- 17 mM

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38
Q

GLUT3:

  • Tissue/organ
  • Km
A
  • Brain

- 1.4 mM

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39
Q

GLUT4:

  • Tissue/organ
  • Km
A
  • Muscle, adipose tissue

- 5 mM

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40
Q

Contact-dependant signalling:

A
  • A cell-surface-bound signal molecule binds to a receptor protein on an adjacent cell, no molecules are released
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41
Q

Paracrine signalling:

A
  • Paracrine signals are released by cells into the EF, acting as a local mediator
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42
Q

Cell surface receptors:

  • Most signalling molecules….
  • instead, they bind to …..
A
  • 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
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43
Q

Intracellular receptors:

  • Some small hydrophobic…. pass through the target cells plasma membrane binding to ….
  • That regulate, for example…..
A
  • Some small hydrophobic extracellular signalling molecules pass through the target cells plasma membrane, binding to intracellular receptors.
  • That regulate, for example, gene transcription
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44
Q

Apoptosis:

A
  • A form of cell suicide that occurs when a cell does not receive the necessary signals to survive
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45
Q

Timescales of a cell’s response

  • Fast
  • Slow
A
  • Fast: processes that rely on altered protein function; movement, secretion and metabolism
  • Slow: processes that rely on altered protein synthesis; differentiation, growth and division
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46
Q

Ion-channel-coupled receptors:

  • Signal molecules…..
  • Causing a change in……
  • Thus, a chemical change…..
A
  • 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
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47
Q

G-Protein coupled receptors are transmembrane proteins:

  • Extracellular
  • Intracellular
A
  • Extracellular portion of a GPCr binds to signalling molecules
  • The cytoplasmic portion binds to a G-protein
48
Q

The two most common enzyme targets of G-proteins are:

  • Adenyl cyclase action:
  • Phospholipase C action:
A
  • 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
Q

The effect of adrenaline on skeletal muscle:

  • Adrenaline indicates a …..
  • Adrenaline activates a …..
  • The increase in cAMP activates…..
  • Phosphorylase kinase activates……
A
  • 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
Q

GPCRs and cholera:

A
  • 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
Q

Growth hormone:

  • Location
  • Effect
  • Action
A
  • Anterior pituitary
  • Causes growth in most tissues and promotes differentiation in some cell types
  • Binds to GH receptor in target tissues
52
Q

Effect of somatostatin on GH secretion:

A
  • Somatostatin inhibits GH secretion
53
Q

Effect of GRH dopamine on GH secretion:

A
  • GRH dopamine increases GH release
54
Q

GH secretion frequency:

A
  • Periodic secretion, affected by sleep
55
Q

Feedback control of GH:

  • SS
  • GH
A
  • GH stimulates somatostatin (SS), SS inhibits GH release

- GH also inhibits GHRH release and GH release

56
Q

GH action: acute

  • Protein
  • Lipid
  • Carbs
  • Key effect
A
  • 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
Q

Regulation of bone growth: IGF-1

  • PM
  • R of P C
  • M of D S
A
  • Pro-mitogenic
  • Recruitment of precursor cells
  • Maintenance of differentiated state
58
Q

Regulation of bone growth: Glucocorticoids

  • P
  • Chronic effect
A
  • Permissive: presence required for normal processes

- In chronic high doses leads to bone loss and catabolism

59
Q

Regulation of bon growth: Androgens

- T S

A
  • Testosterone surge during puberty accelerates closure of growth plates
60
Q

Effects of an abnormal increased GH secretion:

A
  1. Gigantism (before epiphyseal growth plate has sealed)

2. Acromegaly (after growth plate closure)

61
Q

Adrenal cortex zones: (3)

  • g
  • f
  • r
A
  • Zona glomerulosa
  • Zona fasiculata
  • Zona reticularis
62
Q

Hormone produced in the zone glomerulosa:

A
  • Aldosterone
63
Q

Hormone produced by zona fasiculata:

A
  • Cortisol (and androgens)
64
Q

Hormone produced by zona reticularis:

A
  • Androgens (and cortisol)
65
Q

Hormones produced by the adrenal medulla

A
  • Adrenaline

- Noradrenaline

66
Q

Synthesis of adrenocortical steroids

A
  • All based on cholesterol, synthesised as required

- Expression of key enzymes regulated

67
Q

Cortisol (glucocorticoid):

  • secretion:
  • regulation:
A
  • Secreted by zona fasiculata
  • Release controlled by CRH/ACTH
    CRH: Cortisol releasing hormone
    ACTH: adrenocorticotrophic hormone
68
Q

Circadian rhythm for Cortisol:

  • Synchronisation
  • Effect of stress
A
  • CRH secretion synchronised with sleep cycle.

- Stress-induced CRH secretion increases glucocorticoid secretion approx. 20 fold

69
Q

Cortisol actions:

  • Metabolic effects
  • Cardiovascular effects
  • Other
A
  • ME: Stimulates gluconeogenesis and glycogenolysis (provides fuel)
  • CE: Maintains blood volume (protects CVS)
  • OE: Anti-inflammatory, immunosuppressive
70
Q

Cortisol action on CVS:

A
  • Increases contractility
  • Increases peripheral resistance
    Amplifying the effects of noradrenaline and adrenaline
71
Q
Cortisol effect on inflammatory/immune response:
-INHIBITS
. S of C
. H R
. P of I C
. S of A
A
- Inhibits:
. Secretion of cytokines
. Histamine release 
. Proliferation of immune cells
. synthesis of antibodies
72
Q

Regulation of cortisol release: tripartite
1.
2.
3.

A
  1. Hypothalamus: releases CRH
  2. Anterior pituitary: releases ACTH
  3. Adrenal cortex: cortisol
    CRH: corticotropin releasing hormone
    ACTH: adrenocorticotropic hormone
73
Q

Feedback control of cortisol

  • Positive
  • Negative
A
  • Positive: stressors (physical/emotional)

- Negative: Pituitary, hypothalamus

74
Q

Aldosterone:

  • Secretion
  • Half-life
A
  • Zona glomerulosa

- 30 mins

75
Q

What stimulates the release of cortisol?:

A
  • Angiotensin 2

- Low Na stimulates renin release in kidney, renin cleaves angiotensin into Ang1

76
Q

What does aldosterone stimulate?:

  • Answer
  • Effect
A
  • aldosterone stimulates Na-K ATPase in renal collecting ducts
  • Na reabsorbed in filtrate, K secreted into filtrate, Water retention
77
Q

Corticosteroid receptors:

- two cytosolic receptors

A
  • 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
Q

Termination of action (adrenocorticoid):

  • Half-life:
  • Liver
  • Kidney
A
  • Half-life:
    . Cortisol: 60 mins
    . Aldosterone: 15 mins
  • Liver: cortisol and aldosterone inactivated
  • Kidney: inactivated forms excreted in urine
79
Q

Dysregulation of glucocorticoid release (2)

A
  • Addison’s: too little cortisol

- Cushing disease: too much cortisol

80
Q

Paths to dysregulation:

  1. Primary
  2. Secondary
  3. Tertiary
A
  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
Q

Addison syndrome: too little cortisol

-Symptoms(6)

A

Symptoms:

  • Hypotension
  • Hypoglycemia
  • Hyponatremia
  • Hypovolumia
  • Hyperpigmentation
  • Hyperkalemia
82
Q

Addison’s disease :

  • Main cause
  • Other cause
A
  • Main cause: autoimmune destruction of adrenal cortical cells (primary adrenocortical insufficiency)
  • Other causes:
    . Chronic glucocorticoid treatment
    . Infection
83
Q

Cushing’s SYNDROME:

  • ACTH???
  • Causes????
A
  • ACTH low
  • Adrenal neoplasm or hyperplasia
  • Chronic glucocorticoid treament
84
Q

Cushing’s disease:

A
  • ACTH high

- Excessive and unregulated pituitary ACTH secretion

85
Q

Glucocorticoid treatment:

  • wanted effects
  • unwanted effects
A
  • Wanted effects:
  • reduces inflammation and suppresses immune system
  • Unwanted effects:
  • Atrophy of the zona fasicula (cortex)
86
Q

Cushing’s treatment:

A
  • Remove or destroy source of ACTH or cortisol
87
Q

Cushing’s treatment:

A
  • Remove or destroy source of ACTH or cortisol
88
Q

General thyroid and parathyroid anatomy:

  • TG
  • PTG
A
  • Thyroid gland has lateral lobes connected by isthmus

- Parathyroid glands are located behind the lateral lobes of the thyroid

89
Q

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 …..
A
  • 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
Q

Dietary iodide facts:

  • Daily requirement:
  • AVG. daily intake
  • Efficiently absorbed
  • Absorbed into….
  • Removed from EP by ….
  • Kidneys…
  • Thyroid contains…..
A
  • 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
Q

Actions of thyroid hormones:

  • TBG
  • Method of action
  • Target genes
  • Target cells
A
  • > 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
Q

Hypothyroidism: in early development

  • Definition
  • Symptoms (4)
A
  • Cretinism: complete absence of thyroid hormone during development
  • symptoms: Neurological deficits (retardation)
  • Small stature and immature appearance
  • Puffy hands and face
  • Delayed puberty
93
Q

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
A
  • 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
Q

Hyperthyroidism symptoms:

A
  • Nervousness
  • High BMR, raised temp
  • Tachycardia (abnormally high resting HR)
  • Increased appetite/ weight loss
  • Tiredness
95
Q
Physiological role of calcium: (6)
- B S 
- B C 
_ N E
- M I T
- E R 
- C
A
  • Bone strength
  • Blood coagulation
  • Neuromusclular excitability
  • Membrane ion transport
  • Enzyme regulation
  • Contraction
96
Q

3 hormones of Ca regulation:

A
  • PTH
  • Calcitonin
  • Vitamin D
97
Q

Normal plasma calcium range:

A
  • 2.2 to 2.6 mmol/L
98
Q

Low Plasma Ca2+ response:

A
  • Parathyroid glands (chief cells) secrete PTH, increasing plasma Ca2+
99
Q

High plasma Ca2+ response:

A
  • Thyroid parafollicular C cells secrete calcitonin, lowering plasma Ca2+
100
Q

Hypocalcaemia:

  • Cause
  • Symptoms
  • Increased N E
  • T, M C, T
  • C and D (severe)
A
  • 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
Q

Hypercalcaemia:

  • Cause
  • Symptoms
A
  • Associated with primary hyperparathyroidism and malignancy
  • Symptoms of stones bones and groans
102
Q

Insulin:

  • Role:
  • Secreted:
A
  • Role: signals the fed state, lowers blood glucose levels

- Secreted by beta-cells in the pancreas

103
Q

Insulin synthesis:

  1. Starts as preproinsulin, signal sequence….
  2. A and B peptides linked by ….
  3. Mature insulin leaves …..
A
  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
Q

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

A
  • 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
Q

Effect of activated Akt on GLUT4 transporters:

A
  • Activated Akt causes GLUT4 transporter vesicles to fuse to the cell surface membrane, increasing glucose uptake 15x
106
Q

Glucose regulates insulin secretion from beta-cells:

  • Glucose enters…..
  • Glycolysis causes an…..
  • ATP binds to …..
  • Membrane depolarisation causes…..
  • Causing more ….
  • Triggering insulin release via …..
A
  • 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
Q

Sulfonylurea drugs in treating diabetes:

A
  • Binds to SUR1 subunit, closing K+ channel, causing insulin release
108
Q

Insulin main aim:

A
  • Stimulate the uptake of glucose into cells, lowers plasma blood sugar levels
109
Q

Glucagon main aim:

A
  • Glycogen breakdown, raises plasma blood sugar levels
110
Q

Diabetes symptoms:

  • Mutual (2)
  • Type 1 specific: ketoacidocis
A
  • 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
Q

Long-term effects of raised blood sugar:

A
  • Hemoglobin becomes glycated, compromising O2 deliveries (especially to extremities)
112
Q

Luteinizing hormone (LH) role:

A
  • Stimulation of testosterone secretion
113
Q

Follicle-stimulating hormone role: (2)

A
  • Spermatogenesis

- Oestrogen synthesis

114
Q

DHEA (Dehydroepiandrosterone) role:

A
  • Weaker androgens, no effect in males
115
Q

Testosterone role:

A
  • Secondary male sexual characteristics

- Spermatogenesis

116
Q

Oestrogen role: (2)

A
  • Secondary sexual characteristic development

- Growth of ovarian follicles/proliferation of endometrium

117
Q

Progesterone role:

A
  • Prepares the uterus for ovulation, thickens wall lining etc.