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Primary FRCA > Physiology 20 > Flashcards

Physiology 20 Flashcards

1
Q

How are oral and rectal body temperature related?

A

rectal is usually 0.5°C higher than oral

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2
Q

what is a normal scrotal temperature?

A

32°C

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3
Q

What is the normal circadian fluctuation in temperature?

A

0.5-0.7°C

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4
Q

What processes contribute to heat production in the body during exercise?

A

BMR (60%)
Thermogenic effect of food (digestion/absorption/storage) (8%)
Non-exercise activity thermogenesis (NEAT) (7%)
Exercise (25%)

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5
Q

What is ‘countercurrent heat exchange?’

A

Transfer of heat from arteries to adjacent veins warms blood returning to the core

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6
Q

To what extent is the skin able to control heat loss?

A

Up to eightfold increase in temperature conductance between full contriction and dilation of skin vessels

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7
Q

What are the main mechanisms of body heat loss?

A

At room temperature:

Radiation (60%)
Evaporation (22%)
Conduction/convection via air (15%)
Conduction via contact eg. chair (3%)

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8
Q

Outline the thermoregulatory mechanism

A

Posterior hypothalamus receives afferents from peripheral (via lateral spinothalamic tracts) and central cold thermoreceptors

Anterior hypothalamus (preoptic nuclei) receives afferents from peripheral heat thermoreceptors via lateral spinothalamic tracts. This centre can exert an inhibitory effect on the shivering / cold centre in the posterior hypothalamus

Efferents act to:

  • Modify vascular tone
  • Modify behaviour
  • Stimulate/inhibit shivering/sweating
  • Stimulate thermogenesis
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9
Q

Discuss peripheral thermoreceptors

A

Two types:

Skin:

  • Cold receptors - most numerous. in dermis. Discharge regularly and periodicallym increasing frequency below 25°C. via Aδ fibres.
  • Warm receptors - maximal discharge rate at 45-50°C. Type C fibres

Deep tissue:
-Mainly in spinal cord, abdo viscera and great veins. Can induce shivering when core temperature falls by 0.5°C

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10
Q

Summarise the structure and function of sweat glands

A

Two components - Gland and duct

Gland secretes ‘primary secretion’ similar to plasma and duct reabsorbs Na, Cl and H2O.

Reabsorption almost total at low levels of sweating. At high levels of sweating, significant loss of NaCl and H2O can occur.

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11
Q

How does acclimatisation to heat occur?

A

Release of aldosterone limits sodium loss

Takes 4-6 weeks

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12
Q

What is chemical thermogenesis?

A
  • Production of heat that is not related to ATP production
  • Happens as a result of uncoupling proteins (which cause mitochondrial H+ ions to bypass ATP synthase) so produce heat without ATP

Occurs with sympathetic excitation, raised thyroxine levels and in brown adipose tissue found in infants

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13
Q

What is the function of the ‘set point’ for temperature regulation?

A
  • The temperature below which the posterior hypothalamus will exhibit an effector response eg. shivering.
  • It is modified by skin temperature ie. set point is lower if skin temperature is higher
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14
Q

How may epidurals during labour affect body temperature?

A

Basal temperature increases following epidural/CSE analgesia - ‘epidural fever’

Thought to be due to disturbance in central thermoregulation

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15
Q

What is the classical description of an endocrine gland?

Why is this concept of limited use?

A

Ductless and specalised

Limited as hormones are also produced and released by other tissues eg. heart or liver tissue

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16
Q

When is the term ‘neurocrine’ most appropriate?

A

The hypothalamus and posterior pituitary release hormones directly from nerve tissue and are thus ‘neurocrine’ glands

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17
Q

Contrast the terms endocrine, paracrine and autocrine

A

Endocrine: chemical release affects distant tissue
Paracrine: chemical release affects nearby cells in the same organ/tissue
Autocrine: chemical released influences the releasing cell

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18
Q

How are hormones classified chemically?

A

Proteins/peptides:
-Diverse in origin, structure and function

Amines:

  • Derived from tyrosine
  • All have an alpha amino group on a benzene ring
  • Includes catecholamines and thyroid hormones

Steroids:

  • Derived from cholesterol
  • Includes adrenal hormones, sex hormones and vitamin D
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19
Q

What is the difference between a peptide and a protein?

A

Peptide: 3-100 amino acid chain

Protein: >100 aa chain

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20
Q

How are peptide/protein hormones produced?

A

RER -> prehormone

SER / Golgi apparatus -> completed hormone, stored in vesicles

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21
Q

How are peptide hormones released?

A

Secretory vesicles are exocytosed in response to increased IC [Ca2+]

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22
Q

Where do peptide hormones exert their effects?

A

On membrane-bound receptors of target cells due to water solubility and inability to cross membranes

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23
Q

How does the adrenal medulla produce adrenaline?

A

-It possesses the enzyme phenylethanolamine N-methyltransferase, which produces adrenaline from NA

[this enzyme is usually lost in phaeochromocytoma]

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24
Q

How are amine hormones stored and released?

A

Catecholamines:

  • Stored as secretory vesicles
  • When released are 50% albumin bound

Thyroid hormones:

  • Stored complexed with thyroglobulin
  • When complex is split, T3/4 diffuses out of the cell and binds to thyroid binding protein, leaving little free hormone with a large, stable bound reserve
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25
Q

What is the common structure of steroid hormones?

A
  • 4-ring structure: 3 hexamic; 1 pentamic

- Physiological differences relate to side chain modifications

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26
Q

How are steroid hormones produced and released?

A
  • Hormone precursors/intermediaries pass between several enzymes within the producing cell prior to completion.
  • Once complete, they diffuse out into the ECF, being highly lipid-soluble
  • There is no intracellular storage of steroid hormones
  • They are highly bound in plasma
27
Q

What are the main factors that affect hormone activity?

A
  1. Rate of production and release
  2. Rate of removal
  3. End-organ sensitivity
28
Q

What systems exist to control the rate of production and release of hormones?

A

Feedback: +ve and -ve

Neuronal control: ANS

29
Q

Where do cyclical variations in hormone activity originate?

A
  • Not in the glands themselves

- CNS activity alters trigger thresholds

30
Q

Where is the circadian rhythm generated?

A

Suprachiasmatic nucleus of hypothalamus

External stimuli eg. Light/dark adjusts intrinsic ‘clock’ of the cells.

31
Q

What is the most important mechanism influencing the circadian rhythm?

A

Melatonin production by the pineal gland
Levels increase 10 fold at night
Retinal photoreceptors have a communication with the pineal gland

32
Q

Which anterior pituitary hormones exhibit a circadian rhythm?

A

GH

ACTH

33
Q

What are some important second messengers?

A

Adenylate cyclase - phosphorylates other proteins. Inactivated by phosphodiesterase

Phospholipase C - activates protein kinases and Ca2+ channel opening -> calmodulin activation

34
Q

Summarise the structure and function of receptor tyrosine kinase (RTK)

What are examples?

A

Single, transmembrane monomer with extracellular receptor and intracellular tyrosine chain.

When activated by ligand, monomers join to form dimers which are then phosphorylated by ATP and induce a cellular response through protein activation.

Eg. Insulin and IGF receptors.

35
Q

Which hormones act on intracellular targets?

Where are the receptors usually found? How do they exert an effect?

A

Steroid and thyroid hormones

Receptors are usually cytosolic -> then the complex enters the nucleus and binds to DNA, modifying gene expression

36
Q

Outline the location and activity of thyroid hormone receptors

A

Located within the nucleus, bound to target DNA and inhibiting gene expression in the resting state.

Activated when bound to T3/4, initiating mRNA production

37
Q

Summarise the nature and duration of effect of thyroid hormones on BMR

A

T3/4s effect in promoting production of many proteins indirectly increases BMR.

T3/4 can remain receptor-bound for many days and has a large, bound intravascular reservoir, thus the thyroid hormones have the longest latency of all hormones

38
Q

What are the main hormone assay techniques?

A

Radioimmunoassay - traditional technique

Immunometric assay - faster and more specific

39
Q

Describe the development of the pituitary gland

A

Anterior develops as Rathke’s pouch in the embryonic oral cavity. Becomes separated by the sphenoid bone and sits in the sella turcica

Posterior develops as a downward projection of neural tissue from floor of 3rd ventricle. Upper part is the median eminence of the hypothalamus, lower is the infundibular process

40
Q

What hormones does the anterior pituitary produce?

A

Six:

ACTH
TSH
GH
LH
FSH
PRL (prolactin)
41
Q

What hormones are released from the posterior pituitary?

A

ADH

Oxytocin

42
Q

Outline the blood supply to the pituitary

A

Median eminence and stalk - Superior hypophyseal artery -> capillary plexus -> portal veins -> anterior pituitary plexus -> venous sinuses

Posterior pituitary - Inferior hypophyseal artery -> few portal veins to anterior but mainly drains into dural sinuses

43
Q

What are the main hypothalamic functions relating to the endocrine system?

A
  • ANS regulation
  • Temperature regulation
  • Regulation of food intake
  • Regulation of water intake
  • Regulation of pituitary secretion
44
Q

What type of receptor is the ADH receptor?

Where are they located?

A

G-protein-linked

V1R: Gαq. Mainly smooth muscle and visceral organs
V2R: Gαs. Renal DCT and collecting ducts
V3R: Gαq. ACTH-secreting cells of anterior pituitary

45
Q

What are the characteristics of ADH?

A
  • Nonapeptide hormone
  • Synthesised in supraoptic hypothalamic nuclei
  • Released by axon terminals of magnocellular neurones in post pit
  • Released by neuronal depolarisation in response to increasing plasma osmolality / [Na}
  • Suppressed by water intake and fall in plasma osmolality / [Na}
  • 1-2% sensitive to change in {Na}
  • Short half life (<5 mins)
  • Unbound
46
Q

Other than plasma osmolality / {Na}, what factors stimulate ADH release?

A
  • > 10% drop in BP
  • Fall in blood volume
  • Fall in CO
  • Standing
  • IPPV
  • Physiological stress
  • N&V
  • Drugs (TCAs, analgesics, antiepileptics, nicotine)
  • ATII
47
Q

Other than plasma osmolality / {Na}, what factors inhibit ADH release?

A
  • Increase in blood volume
  • ANP
  • Drugs (α agonists, ethanol)
48
Q

Describe the effect of ADH on the renal tubular cells

A

Binds to V2R (Gαs) -> increased cAMP -> mobilisation of Aquaporin 2 storage vesicles in cell to apical membrane

49
Q

What are the subtypes of aquaporin channels?

Where are they found?

A

Aquaporin 1: Constitutively expressed in proximal and descending renal tubules

Aquaporin 2: Expression in DCT and collecting ducts induced by ADH

Aquaporin 3 + 4: Found in capillary membrane of renal tubular cells

50
Q

What are the extrarenal effects of ADH?

A

Vasoconstrictor action in high concentrations / haemorrhage (esp. coronary/splanchnic)

Can induce ACTH release

51
Q

What are the characteristics of oxytocin?

A
  • Nonapeptide hormone
  • Derived from paraventricular hypothalamic nuclei
  • Very similar in structure to ADH (isoleucine at position 3 instead of phenylalanine) but no physiological overlap
  • Main function is to eject milk from lactating breasts
  • Physiologically and pharmacologically induces and augments labour
  • Thought to modulate sexual arousal and behaviour
52
Q

What are the characteristics of TSH?

A
  • Glycoprotein
  • MW 28000 daltons
  • Induced by thyrotrophin releasing hormone (TRH) from parvicellular neurons of hypothalamus
  • Inhibited by increase in thyroid hormones (mainly T3)
  • In normal situations TRH release remains relatively constant - control of TSH release is through modulation of response to TRH
  • TSH functions to stimulate thyroid function, hyperplasia and hypertrophy
53
Q

What factors modulate TRH/TSH release?

A

Fasting / temperature change / other hormones

Fasting: Reduced TRH release -> reduced TSH -> reduced BMR

Hypothermia: Increased TRH -> Increased TSH -> Increased BMR

Somatostatin, dopamine, cortisol and GH all inhibit TSH production/release

54
Q

What are the characteristics of ACTH?

A
  • Peptide hormone
  • MW 4500 daltons
  • Derived from cleavage of pro-opiomelanocortin -> ACTH + β lipotrophin
  • β lipotrophin -> β-endorphin + α,β & γ melanocyte stimulating hormone (MSH). All these are stored and released with ACTH
  • Major mediator of release is corticotrophin releasing hormone (CRH) from paraventricular nuclei of hypothalamus, which acts on CRH-1 receptors (GPCR) of ‘corticoptrophic’ ant pit cells
  • Diurnal release (peak early morning, trough late afternoon)
  • Pulsatile secretion (3x per hour)
  • Causes increased production and release of cortisol via MC2R and adrenal cortical hyperplasia
  • Also causes stimulation of melanocytes
  • Half life 15 mins
  • Unbound
55
Q

What factors inhibit ACTH release?

A

Cortisol, opioids/encephalin and somatostatin

56
Q

What factors increase ACTH release?

A

Fall in cortisol (eg. adrenalectomy / pharmacological block) -> Increase in CRH -> Increase in ACTH

Hypoglycaemia
Anaesthesia
Trauma/surgery
Critical illness
- All inhibit negative feedback of cortisol on ACTH release
57
Q

What are the characteristics of growth hormone (GH)?

A
  • aka somatotrophin
  • Peptide hormone, 191 aa
  • Produced by 50% of anterior pituitary cells (somatotrophs), whach are acidophil-type cells
  • 300-500mcg released daily (~5% of store) from granules
  • Release is stimulated by GHRH and inhibited by somatostatin from hypothalamus
  • GHRH release stimulated by exercise, stress, fasting, hypoglycaemia and sleep
  • T3/4 and cortisol also increase GH production and release
  • Released in 2-hour cycles, with an additional nocturnal peak
  • Receptors to GH on all cells of the body
  • Plasma T1/2 of 20 mins
  • Highly protein bound
58
Q

How does GH release change throughout life?

A

Highest at birth, falls to age 12, then increases with puberty, falling to adult levels around age 18 and continuing to fall slowly into old age

59
Q

What are the actions of GH?

A

Anabolic / Acute metabolic

Anabolic:

  • Promotes growth and protein synthesis
  • Bone mineralisation and lengthening
  • Visceral, endocrine, muscular and connective tissue hypertrophy / hyperplasia
  • Enhanced organ function
  • Increases ECF volume through ANP inhibition

Acute metabolic:

  • seen in 2-3h
  • Antagonistic to insulin
  • Lipolysis / ketogenesis
  • Reduced insulin sensitivity
  • Increased gluconeogenesis, glycogenolysis & non-esterified fatty acids
  • Increased aa transport into cells and protein synthesis
60
Q

Discuss the role of somatomedins in GH mediation

A
  • aka insulin-like growth factors (IGFs)
  • Produced by individual tissues with paracrine activities
  • Also produced by the liver (IGF-1 and IGF-2) with endocrine effects, modulating hypothalamic GH regulation and stimulating growth of bone and muscle mass
  • IGF-1 and -2 are highly protein bound in plasma
  • Levels of somatomedins remain relatively constant throughout the day
  • Exact role unknown
61
Q

What effect does IGF-1 have on insulin?

A
  • Insulin sensitiser
  • Maintains B cells
  • Both low and high levels are associated with reduced insulin secretion
62
Q

Compare the effects of carbohydrate or protein intake on GH and insulin release

A

Protein:

  • Increased GH + insulin
  • Protein anabolism
  • Balanced effect on carbohydrate anabolism

Carbohydrate:

  • Increased insulin; decreased GH
  • Relatively reduced protein anabolism
  • Dominant carbohydrate anabolism
63
Q

What is the effect of fasting on GH?

A
  • Increased GH secretion in context of reduced insulin and somatomedin secretion
  • Protein and fat mobilisation
  • Fatty acid and ketone metabolism
64
Q

What are the characteristics of prolactin?

A
  • Structurally similar to GH
  • Produced in ‘lactotrophs’
  • Tonically inhibited by dopamine
  • Oestrogen increases number of lactotrophs and prolactin levels
  • Acts mainly on breast tissue, promoting growth of milk-producing tissue and production of milk.
  • Also suppresses luteal cell proliferation and has immunomodulatory action

Primary FRCA (34 decks)

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