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Physiology Year 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Major Endocrine glands

A

Hypothalamus and Pituitary Gland, Thyroid, adrenal cortex and gonads, Pancreas and parathyroid glands

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2
Q

Hypothalamus secretion

A

Releasing and inhibiting hormones

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3
Q

Pituitary gland secretion

A

Anterior lobe- trophic hormones

Posterior lobe- Oxytocin and vasopressin (ADH)

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4
Q

Thyroid gland secretion

A

Thyroxine, tri-iodothyronine

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5
Q

Adrenal gland secretion

A

Cortex- Cortisol, aldosterone

Medulla- Adrenaline/noradrenaline

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6
Q

Gonads secretion

A

Oestrogens, androgens, progestogens

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7
Q

Pancreas secretion

A

insulin, glucagon

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8
Q

Parathyroid gland secretion

A

Parathyroid hormone

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9
Q

Other secretions

A

Kidney(Vit.D, EPO), CVS(ANP, endothelins), pineal(melatonin), thymus(thymic hormone), bone(phosphate), adipose tissue(leptin)

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10
Q

Main signalling mechanisms

A

Endocrine, paracrine, autocrine, intracrine

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11
Q

Endocrine signalling

A

Hormones released by an endocrine cell into the general circulation and acting on distant target sites

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12
Q

Paracrine signalling

A

Hormones released by an endocrine cell which act locally on adjacent cells

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13
Q

Autocrine signalling

A

Hormones released by a cell which act back on the same cell

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14
Q

Intracrine signalling

A

Conversion of an inactive hormone to an active hormone that acts within that cell

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15
Q

General Functions of hormones

A

Reproduction, Growth and development
Maintenance of internal environment
Energy production, utilisation and storage

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16
Q

Reproduction, growth and development

A

sex steroids, thyroid hormones, prolactin, growth hormone

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17
Q

maintenance of internal environment

A

aldosterone, parathyroid hormone, vitamin D

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18
Q

Energy production, utilisation and storage

A

insulin, glucagon, thyroid hormones, cortisol, growth hormones

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19
Q

Chemical classification of hormones

A

Protein/peptide hormones, Steroid hormones(cholesterol), Amino acid derivatives(tyrosine/tryptophan), Fatty acid derivatives

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20
Q

Protein/peptide hormones eg

A

Hypothalamic hormones, pituitary hormones, insulin, PTH, Calcitonin

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21
Q

Steroid hormone eg

A

Cortisol, aldosterone, oestrogens, androgens, progestogens, Vitamin D

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22
Q

Amino acid derivatives

A

Adrenaline, noradrenaline(tyrosine), thyroid hormones(tyrosine), melatonin(tryptophan)

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23
Q

Fatty acid derivatives

A

Prostaglandins, thromboxanes, prostacyclin

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24
Q

Half lives and transport

A

proteins and peptides: Minutes and mainly unbound
Tyrosine derivatives and Thyroid hormones: Seconds (CA’s), Hours (thyroid) and thyroid hormones bound to plasma proteins
Cholesterol: Hours-Days and bound to plasma proteins

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25
Q

Magnocellular hormones

A

In the hypothalamus, synthesise and release posterior pituitary hormones

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26
Q

Other neurosecretory cells

A

In the hypothalamus, release their hormones into the portal capillaries in which they are transported directly to endocrine cells of the anterior pituitary gland

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27
Q

Glands controlled by the hypothalamic pituitary axis

A

Hypothalamus – (releasing/inhibiting neurohormones)–> anterior pituitary gland–Trophic hormones–>TSH(Thyroid), ACTH(Adrenal cortex), LH/FSH(Gonads)

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28
Q

How are the main ways disorders are caused?

A

Excess or deficiency of hormones, impaired synthesis, transport and mechanism of hormones, resistance to hormone action

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29
Q

Control of cortisol secretion

A

Hypothalamus-> CRH->Anterior pituitary->ACTH->Adrenal cortex->cortisol

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30
Q

Cortisol functions

A

Glycogenesis, Protein mobilisation, fat mobilisation, anti-inflammatory effects

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31
Q

Lack of/excess Cortisol =

A

Lack off= Addison’s disease

Excess= Cushing’s Disease

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32
Q

Homeostasis

A

The maintenance of an internal steady state in the face of changing external and internal conditions.

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33
Q

Components of a feedback system

A

Regulated/controllable variable(set point, error signal), detector/sensor (afferent path), comparator/control centre(determines set point of variable; intrinsic: local= cell or tissue, extrinsic: endocrine), effector(returns variable to set point(efferent path)), response

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34
Q

Eg of regulated factors/controlled variables

A

Physical entities, blood pressure, core temperature, Circulating concentrations of chemical substances, Ions: Na+, Ca2+, Nutrients: blood glucose concentration, hormones

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35
Q

Regulation of body temp:

A

Shivering, vasoconstriction, increased metabolism, vasodilation, sweating

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36
Q

Benefits of an increased body temperature

A

Inhibits bacterial growth, speeds up metabolic reactions, increases delivery of white blood cells to infection sites

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37
Q

How does body temp increase and why?

A

Pyrogens (bacterial or viral infections) change the site point to a higher level resulting in fever.
Blood flow shifted to core conserve heat- increased muscle activity (shivering), chills stop when high temp reached

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38
Q

Time course of a typical fibril attack

A

The actual body temperature lags behind the rapid shift in set point and though regulation is maintained during the fever it is less precise.

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39
Q

Role of vasopressin

A

Vasoconstriction = increased arterial pressure

Renal fluid reabsorption-> increased blood volume -> vasoconstriction

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40
Q

Following a haemorrhage

A

Blood volume and hence blood pressure are reduced. To help restore blood pressure several homeostatic controls systems activated:
The baroreceptor reflex to increase cardiac output and total peripheral resistance
Stimulation of vasopressin (ADH) secretion to increase blood volume

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41
Q

Integrated feedback

A

Loops in the control of sodium balance, blood pressure and fluid volume

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42
Q

Negative feedback

A

Increase in a controlled variable results in decrease in a controlled variable

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43
Q

Positive feedback

A

Increase in a controlled variable results in a increase in controlled variable.

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44
Q

+ feedback control: Haemostasis

A

Less common physiologically ( due to less control)

The response of the effector output reinforces the stimulus e.g. blood clotting, ovulation, childbirth

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45
Q

+ feedback: Control of uterine contractions in labour by oxytocin

A

1) In labour, oxytocin stimulates contraction of uterine muscles
2) Cervix dilates and activate stretch receptors
3) Action potentials signal to hypothalamus
4) Stimulates further release of oxytocin

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46
Q

Peptides and Proteins

A

Water soluble, made large precursor molecules-prohormones

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47
Q

Steroids and iodinated tyrosines

A

Lipid soluble, made from low molecular weight precursors

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48
Q

Synthesis of Protein/peptide (transcription)

A

1- Transcription of DNA to RNA
2- Post transcriptional processing: RNA-> mature RNA- excision of introns, modifications of 3’ and 5’ ends
3- Translation of mature RNA into protein using tRNA to transfer amino acids
4- Post-transcriptional processing cleavage of large pre-prohormone, folding of proteins, additions of sugars (glycosylation)

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49
Q

Synthesis of Large precursor proteins -> active hormone

A

Pre-prohormone (signal sequence + prohormone) = signal, hormone, peptide sequence(s)( these sequences get cleaved)
Prohormone (hormone + peptide sequence(s)) = hormone + peptide sequence(s)

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50
Q

Synthesis of insulin

A

1- Transcription of RNA
2- Excision of introns to mRNA
3- Removal of signal sequence and formation of disulphide bonds in RER
4- Pre-proinsulin-> proinsulin
5- Transfer to golgi apparatus, excision of C peptide and packaging into secretory granules

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51
Q

Thyroid

A

Thyroid stimulating hormone ( TSH) stimulates Thyroid to release T3 and T4

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52
Q

Adrenal Cortex

A

ACTH stimulates adrenal cortex to release cortisol/aldosterone

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53
Q

Gonads

A

LH/FSH stimulates gonads to release oestrogen/testosterone

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54
Q

Control of Steroid synthesis from Cholesterol

A

1- cholesterol bound to sterol carrier protein transported to mitochondria
2- StAR protein transports cholesterol to inner mito. membrane (rate limiting)
3- Cholesterol to pregnenolone by side chain cleavage enzyme, P450scc (rate limiting)
4- Between mito. and SER steroids synthesised by hydroxylase enzymes

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55
Q

Synthesis of Thyroid hormone

A

1- Active uptake of iodine into follicular cell
2- Transport across the apical membrane
3- Oxi of iodine to iodinated intermediate , by thyroid peroxidase (TPO), which is activated by H2O2
4- Iodination of tyrosine residues of thyroglobulin
5-Coupling of iodinated tyrosine residues
6-Storage of T3 and T4 in colloid
7- Uptake of thyroglobulin droplets into follicle cell
8- Release and secretion of T3 and T4 stimulated by TSH

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56
Q

Signalling pathways for receptors with tyrosine kinase activity

A

Raf/MEK ERK Pathway
PI3-Kinase/Akt Pathway
JAK STAT Pathway

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57
Q

Steroid Hormone Receptors

A

A family of transcription factors

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58
Q

Domains

A

Different functional regions of the receptor

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59
Q

C domain

A

The DNA binding region is made up of 2 zinc fingers which can slot into the helix of the DNA

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60
Q

Pro and pep disorder

A 
Obesity class III>- 40 BMI 
type 1: autoimmune destruction of the pancreatic islets: absolute insulin deficiency 
type 2: insulin resistance, partial loss of insulin production( insulinopaenia) - often  associated with obesity
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61
Q

Protein and peptide disorder

A 
Obesity class III>- 40 BMI 
Diabetes 
type 1: autoimmune destruction of the pancreatic islets: absolute insulin deficiency 
type 2: insulin resistance, partial loss of insulin production (insulinopaenia) - often  associated with obesity
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62
Q

Steroid hormone disorder

A

Aromatase deficiency
Men: unable to synthesise oestrogens from androgens -> no epiphyseal closure -> long stature
Women: Virilisation of XX fetuses, Clitoromegaly, Ambiguous genitalia
Girls develop male-type characteristics
Boys show early sexual development due to excess androgens

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63
Q

Steroid receptor disorder

A

Inactivating mutations of steroid receptors e.g. androgen receptor (nuclear receptor)
Androgen insensitivity syndromes (AIS)

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64
Q

Resistance to hormone action

A

When you cannot respond to steroid hormones

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65
Q

Thyroid hormone disorder

A

Goitre- Enlargement of thyroid gland
causes: Lack of iodine in the diet leads to deficiency in T3 and T4 (hypothyroidism), Graves disease (hyperthyroidism), Thyroid adenoma

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66
Q

Thyroid hormone disorder Graves’ Disease

A

Autoantibodies to the TSH Receptor act on the thyroid gland, stimulate excess thyroid hormones and can cause disease

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67
Q

Proptosis

A

Bulging of eye

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68
Q

Thyroid hormone Cancer

A

Activating mutation of the TSH receptor- a G protein coupled receptor

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69
Q

Signalling

A

Any physiological function can be analysed in molecular terms as a succession of interactions occurring either in a solution or in a membrane system. The key mechanism in the ordering of the cascade is the conformational recognition of the two partners at each step. Each interaction results in the change of conformation of a recognized protein that in turn becomes a recognizer for the following molecule.

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70
Q

Neuroendocrine cells

A

Neurosecretory cells that release signal molecules (hormones) from their synaptic terminals into the blood.

controlled via synaptic transmission (neuroendocrine integration)

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71
Q

Embryology of the Pituitary gland

A

Evagination of floor of 3rd ventricle (neural ectoderm), Evagination of oral ectoderm (Rathke’s pouch), Ratheke’s pouch pinched off

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72
Q

Hypothalamus

A

Composed of various nuclei (cell clusters)

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73
Q

Parvocellular nuclei

A

Neurosecretory cells release hormones to capillaries of median eminence (supplied by superior hypophysial artery); conveyed by portal veins to anterior pituitary

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74
Q

Magnocellular Nuclei

A

Project to posterior pituitary and release to capillaries supplied by inferior hypophysial artery

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75
Q

Posterior pituitary hormones

A

Oxytocin and vasopressin
PP is an extension of the hypothalamus with hormones stored in hypothalamic neuron terminals. Released under neural control into hypophysial capillaries, inferior hypophysial vein

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76
Q

Growth hormone functions

A

Growth and development (anabolic)

Couples growth to nutritional status

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77
Q

Secretion of Growth hormone

A

GH (Somatotropin) synthesised and secreted by somatotropes of the anterior pituitary

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78
Q

Ghrelin

A

‘hunger hormone’ secreted by endocrine cells of the stomach

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79
Q

GH-releasing hormone

A

Hypothalamic neurosecretory cells

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80
Q

Somatostatin

A

Hypothalamic neurosecretory cells

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81
Q

GH Negative feedback control by:

A

GH in circulation, IGF-1 (released by liver in response to GH)

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82
Q

Insulin Tolerance Test

A

Monitor blood every 30 min for 2 hr after insulin injection. Insulin will lower blood sugar, GH (and cortisol) will rise in response, if pituitary function is normal.

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83
Q

Partial list of factors controlling GH secretion

A 
Stimulatory 
GHRH
Ghrelin
Hypoglycemia
Decreased fatty acids
Fasting 
Exercise, sleep
Stress 
Inhibitory 
Somatostatin (GHIH)
GH
Hyperglycemia
Increased fatty acids
IGF-1
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84
Q

GH action

A

Stimulates production of IGF-1 by liver
Increases lipolysis: raises free fatty acids (FFA)
Increases gluconeogenesis: raises blood sugar
Increases amino acid uptake into muscle, protein synthesis and lean body mass
Stimulates chondrocytes: linear growth
Stimulates somatic growth: increased organ/tissue size

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85
Q

XS GH : Acromegaly

A

Most common due to pituitary adenoma: increase in GH secreting somatrophs
Less commonly secondary: tumour elsewhere secretes GHRH
Diagnosed with glucose tolerance test. Monitor blood GH every two hours following 75 g glucose in oral solution. GH levels should be supressed, but doesn’t occur in acromegaly.
Excess GH leads to insulin resistance
Many patients will have impaired glucose tolerance and hyperinsulinemia. Also hypertriglyceridemia due to inhibition of lipoprotein lipase.

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86
Q

Endocrine signalling

A

Hormone secreting gland cell -> blood -> target cell (just taken up by capillaries and vessels)

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87
Q

‘Neurocrine’ signalling

A

Nerve cell -> Nerve impulse -> neurotransmitter -> neuron or effector cell (synaptic transmission)

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88
Q

Neuroendocrine signalling

A

Nerve cell -> neurotransmitter-> neurohormone -> blood -> target cell (mixture of both)

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89
Q

Local Endocrine signalling

A

Local cell -> paracrine agent -> target cell
or
local cell -> autocrine agent ->back to the local cell

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90
Q

Neuroendocrine reflex

A

Initiated by stimulation of sensory neurons that cause a release of a neurohormone from the neurosecretory cells. It is the simple neural reflex that controls the neuroendocrine reflex. The natural progression of events in this system is sensory nerves respond to a stimulus, be it thermal, tactile, or visual. These sensory nerves then synapse with interneurons in the spinal cord. Where efferent neurons, or neurons conducting impulses outwards from the brain or spinal cord, travel to the hypothalamus where the hypothalamic neurons release neurohormones. These neurohormones then enter the blood and activate the target tissues, such as the anterior lobe of the pituitary, mammary glands, or the epididymis.

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91
Q

pH of liquid

A

-log10 its hydrogen ion concentration

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92
Q

normal pH range of bodily fluids

A

7.35-7.45, corresponds to a hydrogen ion concentration of ≈0.00000004 moles per litre, or 40 nM

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93
Q

Carbon dioxide dissolves in the aqueous environment of the body to produce carbonic acid:

A

CO2 + H2O ↔ H2CO3

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94
Q

Carbonic acid is a volatile acid that readily dissociates into hydrogen ions and carbonate ions:

A

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

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95
Q

3 complementary tactics of maintaining pH

A

ECF&ICF Buffers, Respiratory excretion, retention of CO2, Renal excretion, retention, synthesis of HCO3-

96
Q

3 main buffering systems in the blood

A

Biggest: Bicarbonate
H+ + HCO3- ↔ H2CO3 ↔ CO2 + H2O

Second: Phosphate
H+ + HPO42- ↔ H2PO4-

Third: Protein (inc haemoglobin)
H+ + Pr- ↔ HPr

All these systems work together

97
Q

Bicarbonate Buffer System

A

Henderson-Hasslebalch Equation : Can calculate pH using pK and log10 of the bicarbonate ion conc/ CO2 ion conc

Is the most important buffer
Plasma(CO2) proportional to partial pressure of CO2 (pCO2) in plasma

math constant to covert pCO2 (mmHg) to [CO2] mmol/L is 0.03 = pH 6.1 + log[24mmol/L] / 0.03 x [40mmHg]

measured clinically = 20.1
measure pH w/ arterial blood gases (ABG)

98
Q

+/ -‘s of Bicarbonate Buffering

A

-
@ 6.1 the pK of CO2-HCO3 buffer not close to desired plasma pH of 7.4 = purely from a chemical POV, it is x

\+
Abundant source of CO2 from metabolism 
Alveolar ventilation controls PCO2
Kidneys Control [HCO3]ECF 
the last two have (independent regulation) = physiologically it is really ✓
99
Q

Renal control of acid-base levels

A 
Kidneys control acid-base levels by excretion of acidic or basic urine
Primary renal mechanisms involved: 
'Re-absorption' and secretion of HCO3-
Formation of 'new' HCO3-
Secretion of [H+] into tubular fluid
Buffer secretions within tubule that react with secreted [H+] are: 
HCO3-:H2CO3
HPO42-:H2PO4-
NH3: NH4+
100
Q

PCT

A

85-90% of filtered HCO3- ‘reabsorbed’

Great capacity to secrete [H+]

101
Q

Intercalated cells of late DCT & Collecting duct

A

In distal part of nephron [HCO3-] is low and H+ react with other buffers
H+ATPase pump most important

102
Q

(other buffers)-Phosphate

A

Further H+ secreted into lumen buffered by HPO42-
Very effective buffer because pK=6.8 (close to pH of filtrate)

Cl-HCO3- exchanger predominant within intercalated cells

103
Q

(other buffers)- Ammonia

A

Tubular epithelium produces NH3 from glutamine with the enzyme glutaminase

Excretion of ammonia salts increases tenfold during metabolic acidosis- from 30-50mmol/day to 300-500mmol/day

Urinary excretion of ammonium salts

1 glutamine molecule gives rise to 2HCO3-

104
Q

Role of Respiratory System

A

Chemosensitive area in medulla oblogata regulates respiration

Monitors [H+] of plasma indirectly, via CSF

Charged ions can not cross BBB, but CO2 can

105
Q

Metabolic acidosis

A

Characterised by low pH as a result of increase ECF [H+] or decrease ECF [HCO3-]

caused by:
severe sepsis or shock = lactic acid
uncontrolled diabetes = overprotection of 3-OH-butyric acid & other ketoacids

Diarrhoea = loss of HCO3 from GI Tract

106
Q

Metabolic Alkalosis

A

Characterised by high pH cause by increase ECF [HCO3-] or decrease ECF [H+]

caused by: 
excessive diuretic (thiazide0 use= chronic loss of Cl-, Na+ & K+ = increase H+ secretion
Vomiting = loss of H+ from GI tract 
Ingestion of alkaline antacids 
Hypokalaemia
107
Q

Kidney to Ureter pathway

A

Urine from all collecting ducts of all nephrons -> empty into renal pelvis -> urine enters ureter

108
Q

Urine in ureter

A

Urine enters- distends it and smooth muscles around contract.

Peristaltic waves in ureter occur @ freq 1-6 contractions/minute

Ureters squeeze urine to pressure of 10-20mmHg

109
Q

Ureter to bladder

A

Ureter open obliquely into bladder. Prevents reflux of urine back into ureters by passive flap-valve effect
Ureteric peristalsis is myogenic in origin and not under CVS control
Coordination required between peristalsis and changing urine volume.

110
Q

Bladder

A

Can hold up to 400ml without much increase in pressure => spherical structure

111
Q

Sphincters of bladder

A

Internal Sphincter: Extension of detrusor muscle => Not under voluntary control

External Sphincter: Two striated muscles(compressor urethrae & bulbocavernosus) surrounding urethra => these muscles are responsible for continence

112
Q

Female bladder & Urethra

A

Short Urethra-only carries urine
External sphincter less developed
More prone to incontinence particularly after childbirth

113
Q

Male Bladder & Urethra

A

Carries urine and semen

Urine elimination aided by contraction of bulbcavernosus muscles in penis

114
Q

Bladder summary

A 
Bladder: 
Lining- transitional epithelium 
Bladder muscle- detrusor
Impermeable to salt& water
Permeable to lipophilic molecules

Outlet of bladder intro urethra:
Internal sphincter- smooth muscle, involuntary
External sphincter- striated muscle, voluntary

115
Q

Kidney stones (renal calculi)

A

Most common disorder of urinary tract
Develop from crystals that separate from urine within urinary tract
Normal urine contains inhibitors (citrate) to prevent this
Calcium is present in nearly all stones (80%), usually as calcium oxalate or less often as calcium phosphate
Others made up of uric acid (<10%), struvite(<10%), cysteine(<5%)

more common in men because of testosterone

116
Q

Kidney stones causes

A 
XS dietary intake of stone-forming substances 
Poor urine output/obstruction
Altered urinary pH
low conc of inhibitors 
infection
117
Q

Ureterolithiasis

A

Kidney stones can form anywhere in the urinary tract

symptoms:
Dysuria (painful urination)
Haematuria
Loin pain/back pain
Reduced urine flow
Urinary tract obstruction: pressure reaches 50mmHg-causes considerable pain ‘renal colic’
If stone approaches tip of urethra- intense pain can inhibit micturition- ‘strangury’

118
Q

The bladder circuits

A

Neural circuits in brain & SC co-ordinate activity of the bladder & sphincters
Circuits act as on-off switches to alternate between storage & elimination.

119
Q

The nerves in the bladders

A

Sympathetic (hypogastric nerve)
Parasympathetic (pelvic nerve)
Somatic (pudendal nerve)

120
Q

The types of innervation

A

Sensory(afferent): gives sensation (awareness) of fullness and also pain from disease

Motor(efferent): causes contraction and relaxation of detrusor muscle and external sphincter to control micturition

121
Q

Motor innervation

A

Parasympa. neurons:
Contract detrusor via Ach(muscarinic) & ATP(purigenic R)
Relax internal sphincter via NO(cGMP) & Ach(nicotinic R)
THEY ALL ENCOURAGE MICTURITION

Sympa. neurons:
Relax detrusor: Indirectly via NA(α-R), directly via NA(β-R)
Contract internal sphincter via NA(α-R)

Somatic neurons:
Contract external sphincter via Ach (nicotinic R)

SYMPA. + SOMATIC INHIBIT MICTURITION

122
Q

Types of afferent (sensory) nerve fibre

A

‘A Fibres’: sense tension in detrusor
i. filling of bladder
ii. detrusor contraction
=> bladder fullness, discomfort

‘C Fibres’: respond to damage & inflammatory mediators
=> PAIN (urgent desire to micturate)

123
Q

Afferent sensory innervation

A

Main afferent pathway is via pelvic nerve (parasympathetic):
Small myelinated Aδ–fibres = micturition reflex
Stretch receptors = signal wall tension
Volume receptors = signal bladder filling
Unmyelinated C fibres = endings in/near epithelium
Nociceptors = pain (e.g. during infection of bladder lining – cystitis; excessive distension)

Hypogastric (sympathetic) & Pudendal (somatic) pathways
Nociceptors
Flow receptors (external sphincter)

124
Q

Bladder filling

A

Initially – bladder empty
Sphincters closed
(tonic activity sympathetic & somatic nerves)
Bladder pressure low

Arrival of urine
Detrusor relaxes progressively 
(sympathetic activity inhibiting parasympathetic transmission)
Little increase in pressure
Sphincters still closed
= ''RECEPTIVE RELAXATION'
125
Q

Bladder emptying (micturition)

A
  1. Micturition is an autonomic reflex
    e. g. in babies (<18months), adults with spinal cord transected above sacral region
  2. Reflex is modified by voluntary control
    Inhibited or initiated by higher centres in the brain
    Maturation of bladder complete by >6 years

3.Basic circuits act as on/off switches to alternate between 2 modes of operation: storage and elimination

4.Disease/injury/ageing to nervous system in adults disrupts voluntary control of micturition
bladder hyperactivity & urge incontinence
stress incontinence

126
Q

Micturition reflex

A
  1. filling bladder: receptors in bladder wall ‘fire off’ as tension increases
    2.Aδ-fibre afferent signals to the SC, which will return via parasympathetic efferent
    stimulation
  2. = contraction of detrusor muscle and also relaxation f the internal sphincter
  3. = urine begins to leave the bladder = Urine flow activates flow receptors in urethra = pudendal afferents excited
    5.Tonic contraction of external sphincter removed by inhibition of somatic input

Sacral reflex is important to reinforce micturition till bladder is empty

127
Q

Modification of micturition reflex by higher centres

A

The activation pattern during micturition superimposed on averaged MRI scans.

A widespread involvement of cortical and subcortical areas including specific pontine micturition centre (PMC).

128
Q

Voluntary Modification of reflex

A

Higher centres can modify micturition reflex for a while:

Contract external sphincter & levator muscle consciously

Increase sympathetic firing to bladder and internal sphincter (voluntary??)

Interferes with positive feedback to bladder emptying by inhibition of parasympathetic transmission

Tightens internal sphincter

Urine stream can be halted by “strangury” (urethral pain) due to urethritis (inflammation of urethra from STI or renal calculi)

Pinching glans penis can inhibit micturition

At night, if bladder fills to capacity, recognised by PMC and arousal centre wakes you up

129
Q

Voluntary control of micturition

A

The bladder is contained in the floor of the abdominal cavity

By contracting abdominal muscles:

The increased intra-abdominal pressure is transmitted to the bladder and urethra.

Reflex contraction of peri-urethral striated muscles also helps compress the urethra ⇒ micturition reflex aided

130
Q

Importance of bladder emptying

A

Urine
Normally sterile
Occasional bacterial entry
Complete emptying restores sterility
Bacteria in retained urine seeds fresh urine
Retained urine = clinical infection (UTI)
Repeated infections can destroy renal function if ascend to kidney

131
Q

Urinary Tract Infections (UTI’s)

A

Can happen anywhere along the urinary tract

UTIs have different names, depending on area of infection:
Bladder – an infection in the bladder is called cystitis or a bladder infection
Kidneys – an infection of one/both kidneys is called pyelonephritis
Ureters – rarely the site of infection
Urethra – an infection of the urethra is called urethritis

132
Q

UTI Risk factors

A

More common in women because of short urethra

Common in men over 40 due to prostatic disease, causing bladder outflow obstruction

Some risk factors:
Diabetes mellitus; long-term catheterisation; pregnancy; enlarged prostate; prolonged immobility; kidney stones; bowel incontinence; advanced age

133
Q

Problems of aging bladder 1

A 
Slow urine stream: 
Prostate enlargement (BPH -benign prostatic hyperplasia): most common cause of lower urinary tract symptoms in men (25% of men > 40yrs)

Slow urine stream → incomplete emptying → infection

134
Q

Problems of aging bladder 2

A

Incontinence
Causes
Weakening of sphincters (e.g. stress incontinence): common in women after child-birth, weakened pelvic floor muscles

Failure of nervous control
Overactive bladder (OAB) – detrusor contracts spastically – results in sustained high bladder pressure – urge incontinence

Consequences
Socially embarrassing
Diminishes self-esteem
Reduces quality of life

135
Q

Treatments

A

Anti-muscarinics  relax smooth muscle & ↓ detrusor contraction
(eg non-specific muscrarinic receptor antagonist Oxybutynin – wide ranging side effects)

Bladder retraining (used for stress & urge incontinence): Timetable & Kegel exercises

Surgery:
Bladder neck suspension
botulinum toxin/collagen injections into muscles around urethra → relaxes bladder (OAB)

Sacral Nerve Stimulation (SNS):
implanted neurostimulation system
electrical impulses to sacral nerve

Stem cell therapy
cultured stem cells into bladder wall= 90% no leakage
Limited by supply of stem cells (bone marrow)

Tissue engineered bladder
Synthetic and natural scaffolds to form 3D structure using human tissue.
Currently in phase II trials.

136
Q

Stored and circulating nutrients

A 
Circulating: 
Glucose
Fatty acids
Amino acids
Ketone bodies 
Lactate

Stored:
Glycogen
Triglycerides
Body proteins

137
Q

Plasma glucose

A

constant = 5mmol/L
brain depends of glucose metabolism

<2.5mmol/L is critical (hypoglycaemia- ultimately coma and death)

(hyperglycaemia- chronic exposure to raised glucose concentrations leads to protein damage via non-enzymatic glycation)

138
Q

How much glucose?

A

60/40/20
60% of body weight is water
40% of body weight is intracellular water
20% of body weight is extracellular water

e.g. 70kg male, 14L extracellular water gives total of 14x5 = 70mmol glucose
brain:30mmol/hr
skeletal muscle(exten.): 300mmol/hr

139
Q

2 sources of plasma glucose

A

Diet, Organs that can export glucose into the circulation

140
Q

What prevents plasma glucose surging after a meal and plummeting between meals?

A

Hormones regulate the integration of carb ,fat, and protein metabolism to maintain constant plasma glucose level

141
Q

2 phases of metabolism

A

Absorptive (fed state) and fasting(between meals, also called post absorptive phase)

142
Q

Hormones and met.

A

regulate metabolic pathways promoting energy storage or release

143
Q

Insulin and met.

A

Promotes storage, decreases plasma glucose

144
Q

Counter-regulatory hormones

A

Promote nutrient release, raise plasma glucose:
glucagon
adrenaline (epinephrine)
cortisol, growth hormone (somatotrophin)

145
Q

Major effects of insulin

A

STIMULATES nutrient storage:
uptake of glucose by skeletal muscle, adipose, and other tissues
Glycogen synthesis in liver, skeletal muscle
Uptake of FA and amino acids
INHIBITS nutrient release
inhibits release of glucose from liver(hepatic glucose production)
Inhibits fat and protein breakdown (lipolysis and proteolysis

146
Q

Major effects of counter-regulatory hormones

A

glucagon: principle effects in liver- stimulates hepatic glucose production
Adrenaline (and sympathetic NS): stimulates hepatic glucose production
stimulates liposis: release of FA from adipose tissue stores
Growth hormone: stimulates hepatic glucose production, lipolysis
Cortisol: stimulates hepatic glucose production, lipolysis, stimulates proteolysis: release of amino acids from the body protein (skeletal muscle)

147
Q

Metabolic pathways serving energy storage

A 
Glycogenesis
lipogenesis
Triglyceride synthesis
Glycogenolysis
Gluconeogenesis
Lipolysis
Beta-oxidation 
Ketogenesis
148
Q

glycogenesis

A

synthesis of glycogen from glucose

149
Q

lipogenesis

A

synthesis of FA from acetyl CoA

150
Q

Triglyceride Synthesis

A

esterification of FA for storage as TG

151
Q

Glycogenolysis

A

release of glucose from glycogen stores

152
Q

Gluconeogenesis

A

De novo synthesis of glucose from non-carbohydrate substrates

153
Q

Lipolysis

A

Release of FA from TF breakdown

154
Q

Beta-oxidation

A

FA to Acetyl Co A

155
Q

Ketogenesis

A

Production of ketone bodies from Acetyl CoA

156
Q

Defences against HypOglycaemia

A

ST:
glucagon, epinephrine, sympathetic NS
Medium term: ketogenesis: fat reserves can provide a partial substitute for glucose, spring muscle tissue from the destruction that would otherwise be needed to provide amino acid substrates for gluconeogenesis
LT: Cortisol stimulates proteolysis to supply amino acid substrates for gluconeogenesis

157
Q

Defences against HypERglycaemia

A

Insulin: stimulates glucose uptake by tissues, inhibits hepatic glucose production

Lack of insulin action = hyperglycaemia, diabetes mellitus

Type 1: insulin deficiency
Type 2: insulin insufficiency combines with insulin resistance

158
Q

Plasma glucose regulation locations

A

Liver, skeletal muscle adipose tissue

159
Q

How does glucose get into cells? I

A

Sodium-Glucose cotransporters (SGLTs)

Secondary active transport

SGLT1: Glucose absorption from gut
SGLT1,SGLT2: Glucose reabsorption from kidney (PCT)

160
Q

How does glucose get into cells? II

A

Family of glucose transporters (GLUTs)

GLUT 1, GLUT 2, GLUT 3

GLUT 4(muscle and adipose tissue)-medium affinity for glucose. Insulin dependent transporters = insulin- dependent uptake of glucose into cells

161
Q

Islets of Langerhans

A

Clusters of endocrine cells surrounded by exocrine pancreas

162
Q

Islets of Langerhans: What they release

A

alpha cells- glucagon
beta cells- insulin
delta cells- somatostatin

163
Q

Synthesis of insulin pathway

A

Original transcript: pre-pro insulin

Signal sequence removed: proinsulin (in rough endoplasmic reticulum)

Transfer to Golgi apparatus

Peptidases break off the C peptide leaving an A and B chain linked by disulphide bonds

One mole of C-peptide is secreted for each mole of insulin

164
Q

Release of insulin into the circulation

A

Pancreas supplied by branches of the coeliac, super mesenteric, and splenic arteries.

The venous drainage of the pancreas is into the portal system.

Half of the secreted insulin is metabolized by the liver in it’s first pass; the remainder is diluted in the peripheral circulation

C-peptide is more accurate index of insulin secretion in peripheral circulation (not metabolized by liver)

165
Q

Factors regulating insulin secretion

A

Plasma glucose (+ incretin hormones), amino acids, glucagon , parasymp
ALL INCREASE
somatostatin, alpha adrenergic
ALL DECREASE

= BETA CELLS = INSULIN

166
Q

Factors regulating glucagon secretion

A

Plasma glucose, somatostatin, insulin
ALL DECREASE

Amino acids, Beta-adrenergic, parasymp
ALL INCREASE

=ALPHA CELLS = GLUCAGON

167
Q

insulin and glucagon secretion

A

insulin and glucagon secretion are exquisitely sensitive to blood glucose levels.
Insulin: Glucagon ratio varies over physiologically significant range of glucose concentrations

168
Q

How do beta cells sense rise in glucose?

A

No glucose receptor,

GLUT2/ Glucokinase can be thought of as the sensor

Effector is rise in ATP due to glucose oxidation

169
Q

Thyroid Function

A

Development: essential for normal development, esp. CNS & bone

Metabolic: essential for normal metabolism of many body tissues

170
Q

Anatomy of the thyroid gland

A

Rich blood supply: more blood per unit weight than kidney
Inferior thyroid artery from subclavian
Superior thyroid artery from carotid

171
Q

Histology of the Thyroid gland

A

Follicular cells, colloid(mainly thyroblobulin), C-cell(parafollicular cell),

172
Q

Follicular cells

A

Synthesise and secrete TH

173
Q

C cells

A

secrete calcitonin

174
Q

Where are thyroid hormones derived from?

A

2 iodinated tyrosine molecules

175
Q

Thyroid hormones T3+T4

A

T4: Major form released to blood, less active (prohormone)
T3: active form, converted in target cells

176
Q

Circulating Thyroid hormones

A

Over 99% bound to plasma protein, mainly thyroid-binding globulin (approx. 70%), also transthyretin (approx. 10-20%), albumin (approx. 10-20%)

177
Q

TH Synthesis

A
  1. Active uptake of I- across basolateral membrane, against concentration and electrical gradient, by Na/I symporter (NIS). Stimulated by TSH.
  2. Iodide efflux (diffusion) across apical membrane via exchanger known as pendrin (PDS).
  3. At extracellular apical membrane iodide is oxidized to iodine and covalently bound to tyrosine residues within the thyroglobulin (TG) macromolecule. Requires thyroid peroxidase (TPO) and H2O2.
  4. Tyrosine residues may be iodinated in one (mono-iodotyrosine, MIT) or two (DIT) positions. Coupling of iodotyrosine residues (catalysed by TPO) produces T4 (DIT-DIT) and a smaller amount of T3 (MIT-DIT
178
Q

TH Release

A
  1. Under the influence of TSH, colloid droplets consisting of thyroid hormones within the thyroglobulin molecules are taken back up into the follicular cells by pinocytosis.
  2. Fusion of colloid droplets with lysosomes causes hydrolysis of thyroglobulin and release of T3 and T4.
  3. About 10% of T4 undergoes mono- deiodination to T3 before it is secreted. The released iodide is reutilized. Several-fold more iodide is reused than is taken from the blood each day but in states of iodide excess there is loss from the thyroid.
  4. Approximately 100 μg TH secreted per day (90% T4 and about 10% T3). Secretion probably relies on membrane transporter
179
Q

TH Receptors

A

Belong to the nuclear receptor superfamily.
Ligand-activated transcription factors.
High affinity for T3: activation requires dimerization with another TR or Retinoid X receptor (RXR)
TR’s encoded by 2 genes: TR alpha and TR beta

180
Q

Metabolic regulation of THs

A

Controlled in target tissues
3 iodothyronine selenodeiodinases, D1-3 is essential in diet
Tissue-specific expression
Regulate the amount of T3 actually available to bind with receptor
T2, rT3: inactive metabolites of T3/T4

181
Q

TH transporters

A

TH previously thought free to diffuse across cell membrane, but transporters are required, some recently identified, e.g., MCT8, OATP1C1

MCT8: mutations in gene discovered to underlie an X-linked condition, Allan–Herndon–Dudley syndrome, which is associated with psychomotor retardation

182
Q

Functions of TH

A

Increase metabolic rate: Number and size of mitochondria, enzymes in metabolic chain, Na/K ATPase activity, positive inotropic and chronotropic effects on heart, synergizes with sympathetic nervous system

Energy metabolism:
Partially antagonizes insulin signalling, gluconeogenesis, lipolysis

Growth and development

183
Q

Hypothalamic-pituitary-thyroid axis

A

Negative feedback control of thyroid hormone synthesis and secretion, via the hypothalamo-pituitary axis

Hypothalamic neurosecretory cells release thyrotrophin-releasing hormone (TRH) into the portal capillaries

TRH stimulates thyrotrophs of anterior pituitary to secrete thyroid stimulating hormone (TSH)

184
Q

Actions of TSH

A

Increases iodine uptake
Stimulates other reactions involved in TH synthesis (e.g., TPO)
Stimulates uptake of colloid
Induces growth of thyroid gland (which can lead to goitre)

185
Q

Euthyroid

A

Normal thyroid function

186
Q

Hyperthyroidism

A

XS TH
Primary: problem is thyroid gland itself
Secondary: problem is pituitary regulation

187
Q

Hypothyroidism

A

TH deficiency

188
Q

Grave’s disease

A 
primary hyperthyroidism 
Autoimmune
High circulating TH, low TSH
Weight loss, tachycardia, fatigue
Diffuse goitre (TSH receptor stimulation)
Opthalmopathy
189
Q

Hashimoto’s

A 
primary hypothyroidism
Autoimmune
Low circulating TH, high TSH
Lethargy, intolerance to cold
Lack of growth and development
Diffuse goitre
190
Q

Steroids of Adrenal cortex

A

Glucocorticoids: principally cortisol in mammals
Mineralocorticoids: aldosterone
Androgens

191
Q

Adrenal blood flow and functional Zonation

A

Blood flows from outer cortex to inner medulla

Layer-specific enzymes; steroid synthesis in one layer can inhibit different enzymes in subsequent layers

Results in functional zonation of cortex with different hormones made in each layer

192
Q

Actions of adrenal steroids

A

Mineralocorticoids: salt and water balance

Glucocorticoids: metabolism and immune function. Stress increases release, but minimal levels essential for normal function

Androgens: so called ‘weak androgens’

193
Q

Mineralocorticoid function

A

Sodium retention (whole body sodium): active reabsorption of sodium (with associated passive reabsorption of water), active secretion of potassium

Volume regulation (part of RAAS)

194
Q

Circulating concentrations of cortisol much higher than aldosterone so why doesn’t cortisol stimulate salt and water retention?

A

Cortisol is rapidly metabolized to inactive cortisone in the kidney

Requires enzyme, 11beta-hydroxysteroid dehydrogenase type 2

195
Q

Apparent Mineralocorticoid Excess (AME)

A

Rare inactivating mutation of 11B-HSD2 leads to syndrome of apparent mineralocorticoid excess (AME). Liquorice contains a compound that blocks this enzyme

196
Q

Glucocorticoid receptor

A

Member of the nuclear receptor super-family

Characteristic 3-domain structure

197
Q

Transactivation:

A

glucocorticoid receptor (GR) enhances transcription of target gene

198
Q

Transrepression:

A

GR represses transcription of target gene

Many anti-inflammatory effects of GCs thought to be due to transrepression – major therapeutic research target

199
Q

ACTH in detail

A

ACTH is synthesized from the pro-opiomelanocortin prohormone.

ACTH receptor is member of the melanocortin group of receptors

Different forms of melanocyte-stimulating hormones bind to melanocortin receptors

Can also bind to other melanocortin receptors

XAs circulating ACTH may cause skin pigmentation

200
Q

Adrenal insufficiency

A

Addison’s disease: primary adrenal insufficiency

Secondary (hypopituitarism; secondary to failure in RAAS)

Enzyme defect in steroid synthesis pathways

201
Q

Clinical features of Addison’s

A 
Primary adrenal insufficiency
Low circulating adrenal steroids
Plasma [Na+]: normal to low
High ACTH
Plasma [K+]: normal to high
Elevated plasma renin
May be unmasked by significant stress or illness – shock, hypotension, volume depletion (adrenal crisis)
202
Q

Hypercortisolism

A

Cushing’s syndrome: excess glucocorticoid

ACTH-DEpendent:
Cushing’s disease: due to increased ACTH secretion (typically due to pituitary adenoma: secondary)

Ectopic ACTH-secreting tumour

ACTH-INdependent:
Adrenal adenoma or carcinoma (primary)

Latrogenic; effect of GC therapy

203
Q

Hypercortisolism: clinical features

A

Hypertension (salt + water retention)
Hyperglycaemia
Truncal obesity (changes in protein and fat metabolism)
Fatigue, muscle weakness
Virilization (hirsutism in females) (changes in sex hormones)
Depression, mood or psychiatric disturbances

204
Q

Diagnosis of Cushing’s

A

First step: confirm hypersecretion of cortisol
24-hour urinary cortisol
Cortisol at nadir of increased secretion (around midnight)

Next, determine the cause
Plasma ACTH
Dexamethosone suppression test

205
Q

Most common cause of Cushing’s syndrome…

A

…Is iatrogenic.

Exogenous glucocorticoids activate cortisol receptor

@ high doses will shut down HPA

Adrenal cortex atrophies with lack of ACTH stimulation

Several days may be required for adrenal to become responsive to ACTH again

206
Q

Dexamethasone suppresion test

A

Dexamethasone: exogenous steroid

Low doses will normally supress ACTH secretion via negative feedback

Low dose fails to supress ACTH secretion with pituitary disease (Cushing’s)

Higher dose will supress ACTH secretion in Cushing’s

No suppression with low or high dose: suggests ectopic source of ACTH (e.g., tumour elsewhere

207
Q

Pituitary gland location and info

A

2 lobes
Under the brain, in the Sella Turcica
The anterior lobe(adenohypophysis) is derived from and invagination of the roof of the embryonic oropharynx= Rathke’s pouch
Notochordal prjection forms the pituitary stalk, which connects the gland to the brain and also the posterior lobe of the pituitary (neurohypophysis)

208
Q

Pituitary Gland blood supply

A

dual blood supply: 1st is via the long + short pituitary arteries, 2nd is from the hypophyseal portal circulation. Begins as a capillary plexus around the Arc.

209
Q

Pituitary cells

A

Originally classified by their staining characteristics w/ acidic (orange-G) and basic (aldehyde fuscin) dyes

210
Q

Anterior pituitary hormones

A

ACTH, TSH, GH, LH/FSH, PRL

211
Q

Posterior pituitary hormones

A

ADH, Oxytocin,

212
Q

Pituitary gland layers

A

Primary = end organ
Secondary = pituitary
Tertiary = hypothalamus
This allows endocrine control.

213
Q

Clinical features of pituitary features

A

Hormone hypersecretion, space occupying lesion (Headaches, visual loss(field defect), cavernous sinus invasion) , hormone deficiency states (interference with surrounding normal pituitary)

214
Q

XS pituitary hormone diseases

A 
GH: Acromegaly
ACTH: Cushing's disease 
TSH: Secondary Thyrotoxicosis
LH/FSH: Non-functioning pituitary tumour 
PRL: Prolactinoma
215
Q

Systemic effects of XS GH/IGF-I

A 
Acral enlargement
Increased skin thickness 
Increased sweating
Skin tags and acanthosis nigricans
Change appearance
Visceral enlargement
Metabolic Changes
Impaired fasting glucose
Impaired glucose tolerance
Diabetes mellitus
Insulin resistance
Reduced total cholesterol 
Increased triglycerides
Increased nitrogen retention
Cardiomyopathy
Hypertension
Bowel Polyps
Colonic Cancer 
Multinodular goiter
Hypogonadism
Arthropathy		
OSA
216
Q

Actions of Cortisol

A 
Increases plasma glucose levels
Increases lipolysis 
Proteins are catabolised
Na+ and H2O Retention
Anti inflammatory
Increased gastric acid production
217
Q

Prolactinomas

A

Common
PRL different control to all other anterior pituitary hormones - tonic release of DA inhibits PRL release
Positive feedback

218
Q

Prolactinomas drugs

A

Many drugs interfere with DA and PRL secretion:
Antiemetics
Antipsychotics
OCP/HRT

219
Q

Features of XS PRL (hypogonadism)

A 
Infertility	
Oligoamenorrhoea
Amenorrhoea	
Galactorrhoea
Reduced libido	
 Impotence
220
Q

Prolactinomas treatment - dopamine agonists

A

Bromocriptine
Cabergoline
not surgery

221
Q

Non-functioning pituitary tumours

A

30% of all pituitary tumours
No syndrome of hormone excess produced
Cause symptoms due to space occupation( headache, visual field defects, nerve palsies, interfere with rest of pituitary function - deficiencies of hormones)

222
Q

Non-functioning pituitary tumours treatment

A

surgery (transsphenoidal approach) ± radiotherapy

no effective medical therapy

223
Q

Loss of pituitary w/ an expanding tumour

A 
LH/FSH - sex 
GH - growth
TSH - metabolism
ACTH - survival
Prolactin - stalk compression 
ALL DECREASE (based on biological importance)
224
Q

Treatment of pituitary Adenomas

A

Surgery:

  • Transsphenoidal
  • (Adrenalectomy - Nelson’s syndrome)

Radiotherapy:
-Slow

Drugs:

  • Block hormone production
  • Stop Hormone Release
225
Q

Causes of Pituitary failure

A 
Tumour(benign, malignant)
Trauma
Infection
Inflammation(sarcoidosis, histiocytosis) 
Iatrogenic
226
Q

Hypopituitarism

A

Thyroid (bradycardia, weight gain, cold intolerance, hypothermia, constipation)

sex steroids (oligomenorrhoea, reduced libido. hot flushes, reduced body hair)

reduced cortisol( tiredness, weakness, anorexia, postural hypotension, myalgia)

reduced GH( tired, central weight gain)

227
Q

Hypopituitarism treatment

A

Thyroid- thyroxine
sex steroids- testosterone, oestrogen
reduced cortisol- hydrocortisone
reduced GH- growth hormone

228
Q

Syndrome of Inappropriate ADH (SIADH)

A

Too much ADH
Brain injury/infection
Lung cancer/infection asthma IPPV
Metabolic (Hypothyroidism, Addison’s)

229
Q

SIADH Diagnosis

A

Plasma Na+
Plasma osmolality
Urine osmolality
Urine Sodium

230
Q

SIADH Treatment

A 
Fluid restriction
Demeclocyline 
ADH Antagonist (Tolvaptan)
231
Q

Diabetes Insipidus

A

Underproduction ADH
Cranial (Lack of Production)

Nephrogenic(Receptor resistance)

232
Q

Diabetes Insipidus Diagnosis

A 
Polyuria (>3l)
Polydipsia:
- Plasma Na+
- Plasma osmolality (> 295 mosmol/kg)
- Urine osmolality     (< 700 mosmol/kg)
- Urine Na+
233
Q

Water Deprivation test

A 
Discard urine 
Collect Plasma 1
Collecting urine 1 ml
Discard urine 
Collect plasma 2 
Collect U2 ml 
Discard urine 
Collect P3
Collect P4
Collect U4
give DDAVP 
Collect U5
Collect U6
Collect U7
Collect U8
234
Q

Water Deprivation test

A

before DDAVP:

after DDAVP:

235
Q

Pseudocushing’s Syndrome

A

Depression, alcoholism, anorexia nervosa, obesity

Physiology Year 1 (5 decks)

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