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BDS1 > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

How is hormone secretion regulated?

A

1) Humoral e.g high blood glucose = insulin secretion
2) Neural e.g. SNS = epinephrine
3) Hormonal e.g. pituitary gland hormones = testosterone

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2
Q

Name the endocrine glands (11)

A

1) Pituitary gland
2) Hypothalamus
(3) Pineal gland)
4) Thyroid gland
5) Parathyroid gland
(6) Thymus)
7) Pancreas (Islets of Langerhans)
8) Endocrine cells in GI Tracts
9) Adrenal (supra-renal) Glands
10) Gonads: ovaries and testes
11) Placenta gland

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3
Q

What are the classification of endocrine hormones?

A

1) Steroid

2) Non- steroid

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4
Q

Name the steroid endocrine hormones (5)

A

1) Cortisol
2) Aldosterone
3) Testosterone
4) Oestrogen
5) Progesterone

(Based on cholesterol ring structure)

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5
Q

What are the classes of non-steroid endocrine hormone?

A

1) Amino acid derivatives
2) Peptides
3) Glycoproteins

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6
Q

What are the non-steroid endocrine amino acid derivatives?

A

1) Amines
Adrenaline/ epinephrine
Noradrenaline /norepinephrine
Melatonin

2) Iodinated amino acids
tri-iodo-thyronine (Thyroxine)
tetra-iodo-thyronine

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7
Q

What are the non-steroid endocrine peptides?

A 
1) Long chain ('proteins')
 antidiuretic hormone
 oxytocin
 melanocyte stimulating hormone
 somatostatin 
 thyrotropin releasing hormone
 gonadotropin releasing hormone
 atrial natriuretic hormone
2) Short chain ('proteins')
 growth hormone
 prolactin
 parathyoid hormone
 calcitonin
 adrenocorticotropic hormone
 insulin
 glucagon
 GI tract hormones (secretin, CCK, gastrin)
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8
Q

What are pro-hormones?

A

inactive precursor to peptide hormones

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9
Q

Describe the processing of pro-hormones

A

In endoplasmic reticulum, the pre pro-hormone –> pro-hormone. Pro-hormone packaged in golgi apparatus and becomes active. Active hormone secreted

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10
Q

What are glycoproteins

A

carbohydrate groups attached to the amino acids

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11
Q

What are the non-steroid endocrine glycoproteins? (4)

A
  • Follicle stimulating hormone
  • Luteinizing hormone
  • Thyroid stimulating hormone
  • Chorionic gonadotropin
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12
Q

Name three “local tissue” hormones (paracrine)

A

Prostaglandins
Leukotrienes
Thromboxanes

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13
Q

What are the functions of local tissue hormones

A

regulation of blood flow
haemostasis
mucosal protection (stomach)
inflammation

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14
Q

How do non-steroid hormones act on target cells

A

via second messenger in target cells

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15
Q

Name two common second messengers

A

Cyclic AMP

Calcium ions

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16
Q

Do steroid hormones need the use of second messengers?

A

No, because they pass through the outer cell membrane to reach intra cellular receptors

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17
Q

Give a brief overview of hormone action

A

1) synthesis/ storage
2) released in response to a stimulus
3) transport in blood
4) action on target cell (2nd messenger)
5) metabolism (liver) /excretion (kidney)

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18
Q

Target cell mechanism of steroid hormones

A

1) Plasma protein carrier molecules in blood vessel carries the steroid hormone
2) Enters the cell via cell wall
3) Steroid hormone attaches to hormone-receptor complex
4) transcription ->mRNA
5) ribosomes -> protein
- making proteins takes time

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19
Q

Target cell mechanism for non-steroid hormones

A

1) non steroid hormone (first messenger) attaches to protein receptor in cell wall
2) enters cell
3) causing GTP to couple with G protein
4) activating adenyl cyclase -> ATP
5) cAMP (second messenger)
6) Activates protein kinase
7) Activates specific enzyme
8) Substrate becomes product

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20
Q

How are most hormone systems regulated

A

negative feedback

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21
Q

How does negative feedback work in parathyroid glands with plasma ca2+ concentration

A

Low plasma calcium concentration
Parathyroid gland secrete parathyroid hormone
actions on target cells
increase in plasma calcium concentration
feedback to parathyroid gland

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22
Q

what is excess secretion called?

A

Hypersecretion

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23
Q

What is decreased secretion called?

A

hyposecretion

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24
Q

What is upregulation?

A

More receptors, in target cell, increases sensitivity

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25
Q

What is downregulation?

A

Less receptors, in target cell, decreases sensitivity

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26
Q

What is hyper function?

A

Excess production and secretion

Up regulation of receptors

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27
Q

What is hypo function?

A

Decreased production and secretion
Down regulation of receptors
receptors non-functioning

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28
Q

the connection between the hypothalamus and the pituitary gland is called

A

Infundibulum

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29
Q

What is the function of the hypothalamus? (4)

A 
Thermoregulation
Circadian Rhythm
Motivation
Emotions
Hormone secretion
1) Primary hormones
2) Trophic hormones
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30
Q

Describe how thermoregulation works

A

Core temperature is down ->
thermoregulator in hypothalamus ->
compare to set point ->
Effectors -> heat production -> raise temperature -> (or heat loss)

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31
Q

When is your body temperature lowest

A

When you are sleeping

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32
Q

When does your set temperature raise?

A

After meals

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33
Q

How do hormones pass from the hypothalamus to the anterior pituitary?

A

Via blood vessels: Hypothalamic - pituitary portal vessels

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34
Q

What hormone does the hypothalamus secrete

A

releasing hormone (from neurosecretory cell)

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35
Q

What does the releasing hormone from the hypothalamus cause?

A

They trigger secretion of hormones from anterior pituitary

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36
Q

How to hormones produced in the hypothalamus pass to the posterior pituitary

A

Via nerve axons ->

then released in to circulation

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37
Q

Where is the Adenohypophysis?

A

Anterior pituatory

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38
Q

Where is the Neurohypophysis?

A

Posterior pituatory

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39
Q

Name hypothalamic hormones (trophic)

A 
Corticotrophin releasing hormone (CRH)
Gonadotrophin releasing hormone (GRH)
Thyrotropin  releasing hormone (TRH)
Growth hormone releasing hormone (GHRH)
Somatostatin (SS) (GH inhibiting hormone)
Prolactin releasing hormone (PLRH)
Dopamine (DA) ( also PLIH)
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40
Q

Name some anterior pituitary hormones

A 
Adrenocorticotropic hormone (ACTH)
Follicle stimulating hormone (FSH)
Luteinising hormone (LH)
Thryroid stimulating hormone (TSH)
Growth hormone (GH)
Prolactin (PL)
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41
Q

Describe the negative feedback involving corticotrophins

A 
Stressor -> 
Hypothalamus ->
Hormone 1: corticotrophin releasing hormone
Anterior pituitary gland ->
Hormone 2: Adrenocorticotropin releasing hormone (ACTH)
-> Adrenal cortex ->
Hormone 3: cortisol ->
Action
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42
Q

Describe the negative feedback involving Gondotropins

A

Stimulus ->
Hypothalamus ->
hormone 1: gondatropin release hormone
anterior pituitary gland ->
Hormone 2: Follicle stimulating hormone (FSH)
ovaries or testes
ovum maturation & oestrogen production/ sperm production

or Hormone 2: Luteinising hormone (LH)
ovaries or testes
ovulation (oestrogen/ progesterone) / testosterone production

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43
Q

Describe the negative feedback involving Thyrotrophins

A 
Stimulus ->
Hypothalamus ->
hormone 1: Thyrotrophins releasing hormone
anterior pituitary gland ->
Hormone 2: Thyroid stimulating hormone
thyroid gland
Hormone 3: thyroid hormones
action
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44
Q

Describe the negative feedback involving Somatotrophins

A

Hormone 1: Growth hormone releasing hormone or Growth hormone inhibiting hormone
Hormone 2: growth hormone
action

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45
Q

Describe the negative feedback involving Prolactin

A

Hormone 1: Prolactin RH or Prolactin IH
Hormone 2: Proaction
action: breast development and milk production

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46
Q

Name some posterior pituitary hormones

A 
Antidiuretic hormone (ADH)
Oxytocin
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47
Q

What neurons produce oxytocin and antidiuretic hormone?

A 
supraoptic nucleus (Oxy)
paraventricular nucleus  (ADH)
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48
Q

Describe the pathway involving antidiuretic hormone

A 
Stimulus ->
Hypothalamus ->
hormone 1: ADH (axonal transport)
posterior pituitary gland ->
Hormone 2: ADH in plasma
Kidney
action: water reabsorption in collecting duct
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49
Q

Describe the pathway involving antidiuretic hormone

A

Stimulus: uterus stretching or infant suckling
Hypothalamus
Hormone 1: oxytocin (axons)
posterior pituitary gland
Hormone 2: oxytocin in plasma
action: contraction of uterus (parturition) or milk ejection

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50
Q

What hormones do the thyroid gland produce?

A

T3, T4
Thyroid hormone
calcitonin (regulates calcium lvl)

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51
Q

Where are thyroid hormones produced?

A

From cells around the follicles

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52
Q

Where is Calcitonin produced?

A

from para-follicular C cells

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53
Q

What is T4 a precursor for?

A

T3, which is more potent

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54
Q

What are the actions of thyroid hormones?

A

Increase metabolic rate of all cells
Determines basal metabolic rate
Essential for normal fetal and childhood growth
Permissive effect on action of adrenaline by up regulating adrenoreceptors.

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55
Q

Name the disorders of thyroid hormones when there is under secretion

A

Hypothyroidism (congenital)

Cretinism, Myxoedema (Adult)

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56
Q

Name the disorders of thyroid hormones when there is over secretion

A

Hyperthyroidism
Grave’s disease
Exophthalmos - eye bulging

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57
Q

What is simple goitre

A

Thyroid swelling associated with iodine deficiency

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58
Q

How does simple goitre occur?

A

Hormone is produced but in low levels

low levels of thyroxine result in increased secretion of Thryoid Stimulating Hormone (TSH) -> thyroid swelling

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59
Q

What is used to cure simple goitre?

A

Iodine

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60
Q

What hormones do parathyroid glands produce?

A

Parathyroid hormone

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61
Q

What does parathyroid hormone do?

A

regulate blood calcium levels

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62
Q

Where do the pancreatic islets contain?

A

Alpha cells - secrete glucagon
Beta cells - secrete insulin
Delta cells - secrete somatostatin

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63
Q

How much of the pancreatic tissue does the islets of Langerhans occupy?

A

1 -2 %

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64
Q

What do the islets of Langerhans produce?

A

Insulin
Glucagon
Somatostatin

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65
Q

Describe how the secretion of insulin is promoted

A 
Insulin is released in response to:
increased blood glucose
increase blood amino acid
glucose- dependent insulinotropic peptide
vagus nerve activity
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66
Q

What does insulin do?

A
  • lowers blood glucose
  • facilitates glucose entry into:
    Muscle cells
    adipocytes
    (but not liver - as glucose uptake by liver is not insulin-dependent)

Promotes formation of:
Glycogen
triglycerides
facilitates protein synthesis

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67
Q

What inhibits secretion of insulin

A

increased adrenaline
sympathetic nerves
somatostatin - causes body tissue to be less sensitive to insulin so more glucose available

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68
Q

When is glucagon released?

A

When there is low blood glucose?

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69
Q

What does glucagon do?

A

Acts to raise blood glucose

by:
glycogenolysis in liver
gluconeogenesis in liver
lipolysis and ketone synthesis

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70
Q

What promotes secretion of glucagon?

A

decreased blood glucose
increased blood amino acid
Cholecystokinin
autonomic nerve activity

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71
Q

What inhibits glucagon secretion

A

Insulin

somatostatin

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72
Q

What is diabetes mellitus

A

elevated blood glucose concentration
reduced glucose uptake by cells
metabolic changes:
gluconeogenesis; lipolysis

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73
Q

What are the clinical features of diabetes mellitus

A

polyuria (increased urine production)
polydipsia ( increased fluid intake; thirst)
Glycosuria (glucose in urine)
Diabetic neuropathy
skin and oral diseases including periodontitis, xerostomia

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74
Q

What are the feature of diabetes mellitus type 1

A 
insulin dependent
decreased insulin secretion
because of destruction of beta-cells
Autoimmune?
10% of cases
"Early" onset
insulin injections and diet
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75
Q

What are the features of diabetes mellitus type 2

A 
insulin independent
insulin level "normal"
decrease target cell responsiveness to insulin
related to overweight
"Late" onset
Diet, oral hypoglycaemic agents
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76
Q

Where are the Adrenal Glands

A

On top of the kidneys (supra-renal)

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77
Q

Name the sections of the adrenal gland

A

Cortex
Medulla
Capsule

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78
Q

Name the sections in the adrenal gland cortex

A

zona glomerulosa
zona fasciculata
zona reticularis

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79
Q

What hormones are produced in the adrenal gland cortex

A

Corticosteroids:
Aldosterone
Cortisol
Androgens

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80
Q

What hormones are produced in the adrenal gland medulla

A

The Medulla is a modified sympathetic ganglion which secretes adrenaline/epinephrine

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81
Q

Where cortisol produced?

A

The cells of zona fasciculata of adrenal cortex

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82
Q

What controls cortisol?

A

Adrenocorticotropic hormone (ACTH) from the anterior pituitary

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83
Q

What are the actions of cortisol?

A

Metabolic effects
permissive effects
anti-inflammatory, immunosuppressant

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84
Q

What type of hormone is cortisol?

A

Glucocorticoid hormone

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85
Q

What type of hormone is aldosterone?

A

Mineralocorticoid

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86
Q

Where is aldosterone produced?

A

cells of zona glomerulosa

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87
Q

What controls the release of aldosterone?

A

renin-angiotensin system

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88
Q

What are the actions of aldosterone?

A

Promotes reabsorption of Na+ and H2O in kidney (DCT)

Increases excretion of H+ and K+

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89
Q

Describe the renin - angiotensin aldosterone system

A

1) Stimulus occurs in the juxta-glomerular apparatus
2) Renin acts on angiotensionogen to form angiotensin 1
3) Angiotensin converting enzyme (ACE) acts on angiotensin 1 to form angiotensin II
4) causing the adrenal cortex to increase aldosterone release
5) increased Na+ is reabsorbed in cortical collecting ducts

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90
Q

What type of hormone is androgens?

A

Gonadocorticoid hormone

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91
Q

Where is androgen produced?

A

zona fasciculata and

zona reticularis

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92
Q

What are the actions of androgens?

A

Contribute to growth and 2 sexual characteristics in boys and girls
pubertal growth spurt

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93
Q

What occurs with excess glucocorticoid

A

Cushing’s syndrome

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94
Q

What are some characteristics of Cushing’s syndrome?

A 
Moon face
Red cheeks
Fat pads
Bruisability with ecchymoses
Thin skin
Pendulous abdomen
striae (stretch marks)
poor muscle development
poor wound healing
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95
Q

What occurs with excess androgens?

A

Andro-genital syndrome

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96
Q

What are the characteristics of andro-genital syndrome

A 
Baldness/ receding hairline
Hirsutism (excess body hair)
Androgenic flush
small breasts
male escutcheon (pubic hair distribution)
Heavy arms and legs
enlarged clitoris
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97
Q

What is the adrenal medulla controlled by?

A

pre- ganglionic sympathetic nerve (because it is a modified sympathetic ganglion)

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98
Q

What does the adrenal medulla produce?

A

adrenaline - this augments the action of the sympathetic nervous system

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99
Q

What does adrenal insufficiency cause?

A

Addison’s disease

100
Q

What is Addison’s disease?

A

Decreased adrenal function and reduced levels of adrenal hormones:
glucocorticoids
mineralocorticoids
Very serious condition

101
Q

How is water gained in the body?

A

ingestion
formed during metabolism

Food 700 ml/day
Drink 1400
Metabolic 300

total: 2400

102
Q

How is water lost from the body?

A

Excretion: urine and faeces
Evaporation: sweat, in expired air

Urine 1500
Faeces 100
Evaporative sweat, breathing 800

total: 2400

103
Q

In water balance which function is the only one under homeostatic control

A

urinary excretion

104
Q

What are the structures in a nephron?

A 
Glomerulus 
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
collecting ducts
105
Q

What is the purpose of glomerulus?

A

Filtration of blood plasma (from blood cells)

106
Q

What is the glomerular filtration rate?

A

It is the rate at which the kidneys filter blood

It is 120ml/min

107
Q

What is the renal blood flow?

A

1200ml/min

108
Q

How do the filtration pressures change in the glomerulus?

A

Pressures vary along length of glomerular capillary from afferent arteriole to efferent arteriole

capillary hydrostatic (blood pressure) 45-50mmHg
Plasma protein oncotic pressure 25-35mmHg
Capsular pressure 10mmHg

Net filtration pressure 10-15mmHg

109
Q

What occurs in the proximal convoluted tubule?

A

Obligatory reabsorption of 60 - 70% of the glomerular filtrate (no control over what is reabsorbed)

reabsorbs : ions, small organic molecules
secretes: H+ (acid - base balance)
Active transport, facilitated diffusion

110
Q

What is the renal blood flow?

A

1200ml/min

111
Q

How do the filtration pressures change in the glomerulus?

A

Pressures vary along length of glomerular capillary from afferent arteriole to effectent arteriole

112
Q

What is the net reabsorption of fluid in the Loop of Henle?

A

10% of glomerulus filtration rate

113
Q

What occurs in the Loop of Henle

A

important for urine concentration (countercurrent exchange)

concentration of urine depends on active transport pumps in thick, ascending limb of the loop of henle

114
Q

In the distal convoluted tube - what hormones control its activity?

A

Aldosterone
Atrial natriuretic hormone
Anti diuretic hormone
Parathyroid hormone

115
Q

What is the net reabsorption of fluid in the Loop of Henle?

A

10% of glomerulus filtration rate

116
Q

What occurs in the distal convoluted tubule?

A

Reabsorption: Water, Na+, Cl-, Ca2+

Secretion of H+, K+

117
Q

In the distal convoluted tube - what hormones control its activity?

A

Aldosterone
Atrial natriuretic hormone
Anti diuretic hormone
Parathyroid hormone

118
Q

What happens in the collecting duct?

A

Water reabsorption -> moves along osmotic gradient (count current exchange mechanism)

  • > used ADH
  • > creates membrane channels for water reabsorption
119
Q

What hormones regulate water and electrolytes

A

ADH
Renin-angiotensin-aldosterone
Atrial Natriuretic Hormone (ANH, ANF, ANP)

120
Q

What is the main control for water?

A

ADH

121
Q

What is ADH also know as?

A

Vasopressin

122
Q

What does ADH do?

A

Acts on distal convoluted tube (distal end) +
collecting ducts
-> increase water permeability
-> inserts aquaporin channels
-> passive water movement along osmotic gradient between tubule lumen and interstitial fluid

123
Q

Describe the ADH secretion pathway

A

1) decreasing plasma volume (/blood pressure) (a bleed)
decreasing baroreceptor distension (low pressure receptors in atria and great veins)
increased ADH (from p. pituitary)
increased water permeability of collecting ducts

2) increased plasma osmolarity (dehydration)
increased osmoreceptor activation (In hypothalamus)
increased ADH (from p. pituitary)
increase water permeability of collecting ducts

124
Q

What increases ADH secretion?

A

Decreased ECF volume

Increased ECF osmolarity

125
Q

What effect does ADH have on blood vessels?

A

Constriction

126
Q

What does drinking 1 litre of fluid do to urine output?

A
  • isotonic NaCal output around 50ml/30mins

- Water output varies

127
Q

What determines control of electrolytes?

A

The kidneys - how much is excreted

homeostatic control

128
Q

Where are electrolytes found?

A

ICF + ECF

129
Q

name the electrolytes?

A

Na+
Ca2+
K-
H+

130
Q

What controls Na+

A

1) Renin-angiotensin-aldosterone system
- > reabsorbs Na+ (and water)
- > exchange for K+ and H+
- > angiotensin = potential vasoconstrictor

2) Atrial Natriuretic Hormone
- > increases excretion of Na+ (and water)
- > opposite effects to aldosterone

131
Q

Describe the ANH section pathway

A 
Increased plasma volume
increased atrial distention
increased ANH release
decreased Na+ absorption + increased GFR
increased Na+ excretion
132
Q

What regulates K+?

A

Aldosterone

Na+ is swapped for K+ and H+

133
Q

What does ECF [K+] effect

A

Membrane potential

Nerve/muscle function

134
Q

What occurs when there is hypo secretion of ADH?

A

Diabetes insipidus

-> increased urination

135
Q

What occurs when there is hyper secretion of ADH?

A

Syndrome of inappropriate ADH (SIADH)

excess ADH = water retention

136
Q

What effect does K+ have on muscle function?

A

Increased ECF [K+] -> depolarisation

  • > axons to fire AP
  • > MP ≠ resting levels
  • > axons = extended refractory period
137
Q

What is used in sensitive toothpaste?

A

K salt

138
Q

What do the manufacturer’s of sensitive toothpaste claim?

A 
K+ ions diffuse from the paste along tubules
Raise [K+] at inner end of tubule
nerves depolarised
Na+ channels inactivated
prolonged refractory period
139
Q

What is the problem with sensitive toothpaste?

A

K+ build up does not persist

140
Q

Describe the pathway for renin secretion

A

1) Decreased plasma volume (dehydration?)
leads to increases sympathetic nerve activity in J-A apparatus
decreased renal blood flow
decreased stretch of JG baroreceptors
J-G A
increased secretion of renin

2) from decreased renal bF
decreased GFR
decreased Na+ in tubular fluid
macula densa
J-G A
increased secretion of renin
141
Q

What does decreased blood volume result in?

A

Fall in blood pressure
impaired delivery of nutrients to cells

ie. shock

142
Q

What are the physiological responses to blood loses

A

Immediate: stop the bleeding (haemostasis)
Short term: restore blood pressure
Medium term: restore fluid volume
Long term: replace blood constituents

143
Q

What components occurs in the immediate physiological responses to blood lose?

A

1) Vascular response
2) Platelet response
3) Plasma response (coagulation)

144
Q

What occurs in the vascular response?

A

1) Smooth muscle (of blood vessel)
- spasm due to trauma
- > decrease in blood flow + increase blood pressure
* myogenic response (constriction of blood vessels)
* humoral factors (vasoconstriction)

2) Endothelium
- When injured secrete: platelet adhesion and aggregation (initial formation of clot?)
- Normally release: anticlotting and fibrinolysis

145
Q

What occurs in the platelet response?

A

1) Damage to blood vessel
- > turbulent blood flow
- > platelets come into contact with vessel wall (collagen)

2) Aggregate: platelets adhere; clump together
3) Release chemicals that cause further aggregation (positive feedback)
4) formation of platelet plug

146
Q

What mechanism does platelet plug formation use?

A

Positive feedback

147
Q

What chemical use involved in platelet formation?

A

ADP induced Thromboxane A2

  • > vasoconstrictor
  • > platelets; aggregate + release of chemicals
148
Q

Where are most clotting factors made?

A

The liver

149
Q

What does the synthesis of several clotting factors require?

A

vitamin K

150
Q

How are clotting factors activated?

A

Enzyme cascade

151
Q

What occurs in coagulation?

A

Plasma proteins and tissue components combine:

Fibrinogen -> fibrin to form blood clot

  • Numerous clotting factors are involved
  • > made in liver
  • > need vit K.
  • > enzyme cascade
152
Q

Describe the coagulation: common pathway

A

Prothombin -> (Factor Xa (ca2+, phosopholipid, Factor V) -> Thrombin

Thrombin -> (Factor XIII) -> Factor XIIa
Fibrinogen -> (Thrombin) -> soluable fibrin
Soluable -> (Factor XIIIa) -> insoluable fibrin

153
Q

Name the blood clotting factors

A 
1 Fibrinogen
2 Prothrombin
3 Tissue factor (Thromboplastin)
4 Calcium ions
5 Proaccelerin
6
7 Proconvertin
8 Antihaemophilic globulin
9 Christmas factor
10 Stuart - Prower factor
11 Plasma Thromboplastin antecedent 
12 Hageman factor
13 Laki -Lorkand factor

Some factors may be missing due to genetics e.g. haemophilia.

154
Q

What are the two coagulation pathways?

A

Intrinsic + extrinsic

155
Q

Describe the coagulation intrinsic and extrinsic pathways

A

Factor X -> (phospholipid, calcium ions (important)) Factor Xa ->

156
Q

Describe the coagulation intrinsic pathway

A

Intrinsic pathway:
Vascular damage,
contact activation involving factors XII, XI, IX, VIII

157
Q

Describe the coagulation extrinsic pathway

A

extrinsic pathway:
Tissue damage,
Tissue factors (‘tissue thromboplastin’) factor VII

158
Q

When is the extrinsic pathway more important?

A

in initiating clotting after an injury

159
Q

When does the intrinsic pathway occur?

A

It serves to maintain the process once it has started

Maybe have a role in thrombosis -> blood clot forms inside an intact blood vessels.

160
Q

What is Fibrinolysis?

A

When the blood clot is broken down

161
Q

What is the enzyme in fibrinolysis

A

Plasmin

162
Q

Describe the fibrinolysis pathway

A

Plasminogen -> (Plasminogen activator) -> Plasmin

Fibrin -> (Plasmin) -> Soluble fibrin fragments

163
Q

What components occurs in the short term in physiological responses to blood lose?

A

Overall restore blood pressure

Haemorrhage: changes in blood pressure

  • Loss of blood volume
  • Fall in blood pressure
  • compensatory mechanisms triggered by the arterial baroreceptors
164
Q

What are baroreceptors reflexes mediated by?

A 
Sympathetic nerves + hormones:
Adrenaline
Angiotensin II
Vasopressin (ADH)
-> mechanism for restoring BP
165
Q

Describe the baroreceptor flexes

A

deceased blood volume
decreased blood pressure
decreased baroreceptor firing
CVS centres (brainstem)
increase in sympathetic NS activity
1) increased heart rate -> increased cardiac output
2) ventilation control-> increased stroke volume -> increased cardiac output -> increased mean arterial BP
3) venous constriction -> increased stroke volume etc
4) arteriole constriction -> increased peripheral resistance -> mean arterial BP

166
Q

Describe what occurs what happens in a haemorrhage to stroke volume, heart rate , cardiac output (SV x HR), total peripheral resistance, mean arterial pressure (CO x TPR)

A 
SV: decrease
HR: increase
CO: decrease
TPR: increase
MAP: decrease
167
Q

What components occurs in the medium term in physiological responses to blood lose?

A

restore blood volume:

  • Shifting interstitial fluid back into blood vessels
  • Decrease fluid loss in kidney
  • Increasing fluid intake
168
Q

What factors are important in Starling’s Forces?

A 
Hydrostatic pressure (blood pressure)
Oncotic pressure (plasma proteins)
169
Q

Normally in Starling forces describe the pressures

A

Arterioles: 35mmHg hydrostatic pressure
Venules: 15mmHg hydrostatic pressure
Oncotic pressure remains constant at 25mmHg

more filtration on arteriole end
more reabsorption on venules end

filtration ≈ reabsorption

170
Q

Through baroreceptor reflexes reduced arterial blood pressure causes:

A

1) vasoconstriction of arterioles
Increased TPR
Decreased capillary BP
-> causes decrease of hydrostatic pressure pushing fluid out of the capillary
-> more fluid is drawn back into the capillaries by the oncotic pressure

171
Q

What occurs to the Starling forces in a capillary during a haemorrage?

A 
-> constricted arteriole 
oncotic pressure (plasma protein) does not change: 25mmHg
hydrostatic pressure: 25mmHg -> 10mmHg

reabsorption > filtration

172
Q

During the medium term of haemorrhage - describe the decrease of fluid loss in the kidney

A 
decreased Glomerular filtration
increased reabsorption of Na+ and water by stimulating release of:
renin- angiotensin-aldersterone
antidiuretic hormone
-> both are vasoconstrictors
173
Q

What area is important in thirst?

A

Hypothalamus

174
Q

What promotes thirst?

A 
increased plasma osmolarity
decreased ECF volume
Angiotensin II -> promotes thirst
Dry mouth
stretch receptors in stomach suppress drinking: feed forward regulation
175
Q

Long term response in haemorrhage

A 
restore plasma protein
(replaced from liver 3-4 days)
replace blood cells esp RBC
erythropoiesis
-> regulated by erythropoeitin (EPO)
-> EPO released from kidney
-> Stimulated RBC production in bone marrow
-> return to normal in 2-3 months
176
Q

Describe the Erythropoietin pathway

A 
decreased RBC numbers ->
decreased oxygen delivery ->
 kidney ->
erthropoietin ->
red bone marrow ->
increased RBC production
177
Q

What is shock?

A

inadequate blood flow to tissues

178
Q

What is inadequate blood flow associated with

A

decreased cardiac output

decreased blood or ECF volume

179
Q

what are the 2 main types of shock

A

reversible and irreversible

180
Q

what types of shock are there

A

1) hypovolaemic shock
reduced ECF, due to haemorrhage, sweating, diarrhoea, burns etc
2) low resistance (distribution shock)
reduced peripheral resistance, due to widespread vasodilation e.g. anaphylactic shock
3) cardiogenic shock
heart fails as pump

181
Q

What are some types of stressor:

A 
1) Physical
Injury, surgery
Infection, shock
Pain
Exposure to cold
Sustained exercise

2) Threats
Imprisonment
torture
exams

182
Q

What body systems are involved in stress?

A

Nervous
Endocrine
Immune

183
Q

What do the effects of stress depend on?

A
  • duration and severity of stressor

- effectiveness of any responses

184
Q

What are the stages in stress

A 
1) Alarm reaction
Fight, flight, fright response
Physiological effects
2) Resistance phase
adaptation to stressor
3)Exhaustion phase e.g sleep deprivation 
severe, persistant stress
responses futile; system fail
pathological effects
185
Q

What is General Adaptation Syndrome (Seyle)

A

The stages in stress

  • alarm reaction
  • resistance phase
  • exhaustion phase
186
Q

What are the components of the alarm reaction

A 
Physiological response to threat
Neural: Sympathetic NS
Hormonal: Adrenal glands:
1) Adrenaline (Adrenal medulla in thoraco-lumbar)
2) Corticosteroid (Adrenal cortex)
187
Q

In the alarm reaction, what occurs in the neural component?

A

1) Increased cardiac output
Increased heart rate
increased ventricular contractility

2) redistribution of cardiac output
Increased flow to muscles
Decreased flow to gut, kidney

3)Metabolic
Glycogen breakdown -> glucose release
Mobilisation of fat stores (release of free fatty acids)

4) Stimulation of adrenaline release

188
Q

In the alarm reaction, what occurs in the hormonal component?

A
  • Adrenaline released from adrenal medulla (functionally part of SNS.
    -> augments and prolongs actions on SNS
    increases cardiac output
    redistribution of cardiac output
    metabolic effects
  • Glucocorticoids secreted from adrenal cortex
    E.g steroid like cortisol
    Cortisol compliments actions of SNS and adrenaline
    harmful if persistent, high secretion
189
Q

What is the main stress hormone

A

Cortisol

190
Q

What are the actions of Cortisol

A 
1) metabolic
Increased energy production from glucose, amino acids and fats
increased protein breakdown
2) enhances the actions of adrenaline
"permissive effect"
3) Anti-inflammatory action
4) Immunosuppression
191
Q

Glucocorticoids have an anti-inflammatory and immunosuppressant action. What can happen in the immune system?

A
  • Inhibit release of prostaglandins + leukotrienes

- Inhibit macrophages and helper T lymphocytes

192
Q

Many people receive corticosteroid drug therapy. What can it cause

A

Increased incidence of illness at times of stress

193
Q

What is one reason someone might be taking corticosteroids?

A

As an anti-inflammatory for arthritis

194
Q

What can long term use of corticosteroids potentially do?

A

Disrupt normal control mechanism:
- suppress Corticotrophin Releasing Hormone (CRH) an Adrenocorticotrophic Hormone (ACTH) release -> and therefore the naturally stress response

  • makes patients are risk during e.g dental extractions
195
Q

What is stress analgesia?

A

When pain is diminished during physical stress

196
Q

What causes stress analgesia?

A

Release of

1) endogenous opioid peptides
2) endrophins
3) enkephalins in CNS
- > suppress nociception and pain

197
Q

How is stressed assessed?

A

changes in:
HR
BP

198
Q

What increases dental stress in patients

A

Anticipation of treatment = stressful
Oral surgery > scaling
effects greater in : anxious patients < dental phobics
pain increases amount of stress
LA, noise, masks + gowns, if child = stressful
women = high HR.
women and men = no diff in BP

199
Q

Talk about the size of stress-induced effects

A

Range of changes:
Sys BP + 5-20mmHg
Dia BP + 4-8mmHg
HR +20

example of BP during treatment without LA
210/115 mmHg

200
Q

What increases dental stress in dentists

A

When standing
Complex procedure
anxious patient

201
Q

What happens to the individual if the stressors continue to present?

A

1) Adaptation phase (resistance)
- persistant exposure to stressor = diminished response to stress
- effective is perceived threat is removed

2)Exhaustion phase
Adrenal failure
immunosuppression
peptic ulcers
CVS disease
death
202
Q

What are the functions of calcium

A 
bone and tooth structure
mineral store
AP (cardiac muscle)
Membrane excitability
2nd messenger
 - non steroid hormone action
 - gland secretion
- Muscle: excitation - contraction coupling
co factor in metabolic pathway
blood clotting
203
Q

Calcium concentrations

A

Diffusible calcium

  • ionised calcium 1.2mmol/l
  • calcium bound to citrate 0.2mmol/l

Non-diffusible calcium
- calcium bound to protein 1.2mmol/l

total 2.6mmol/l (Homeostatic conc.)

204
Q

Describe the calcium turnover pathway

A

Calcium from diet -> GI tract -> faeces

calcium in GI tract plasma and interstitial fluid exchangeable bone ‘stable bond’

Plasma and interstitial fluid kidney -> urine

205
Q

What hormones are used in calcium homeostasis

A

1) Parathyroid hormone
2) Calcitonin
3) Vitamin D

206
Q

How is parathyroid hormone involved in calcium homeostasis

A

Low plasma Ca2+ concentration -> PTH secretion
-> increase plasma Ca2+ by

1) increased reabsorption of bone (osteoclasts)
2) Increase Ca2+ reabsorption in kidney (with decreased PO4 resorption)
3) Increase uptake of Ca2+ from intestines (assisted by Vit D)

207
Q

Describe the parathyroid hormone pathway for calcium homeostasis

A

decreased plasma Ca ->
PT gland -> PTH ->
1) Kidney: formation of 1,25 OH vit D ->
Intestines: increased absorption of Ca

2)Kidney: Increased Ca resorption
Increase PO4 excretion

3) Bone: resorption + release of Ca +PO4

All lead to Increased Plasma Ca

208
Q

How is Calcitonin involved in calcium homeostasis

A

responds to high plasma Ca
-> Calcitonin secreted from thyroid glands

Lowers plasma Ca by:

  • increased formation of bone (osteoblasts)
  • decreased ca resorption in kidney
  • no major role in calcium homeostasis
209
Q

describe the calcitonin pathway in calcium homeostatsis

A 
increased plasma ca
thyroid gland (c-cells) release calcitonin 
1) Kidney: increase ca excretion
2) Bone: deposition
lowers plasma ca
210
Q

Describe the vit D pathway in calcium homeostatsis

A

Overall: increased levels of plasma Ca and Po

Dietart Vit D + 7-dehydrocholesterol synthesised in skin
->
Vit D3 (cholecalciferol)
-> (Liver + 25hydroxylase) ->
25(OH)cholecalciferol
-> kidney 1alpha hydroxylase (regulated by PTH)->
1,25 (OH2) Cholecalciferol or calcitrol
1) Intestine: Ca resorption
2) Kidney: Ca retention; PO retention
3) Bone: Ca release; PO4 released

-> all Plasma: increased Ca and PO4

211
Q

What hormones cause increased bone formation and increased bone mass

A 
Calcitonin 
Growth Hormone
IGF
Insulin
Oestrogen
Testosterone
212
Q

What hormones cause increase bone resorption and decreased bone mass

A

Parathyroid hormone
Cortisol
Thyroid Hormones

213
Q

What do osteoblasts do?

A

Synthesis and secrete collagen fibres

  • > forming matrix
  • > later mineralised by calcium salts
214
Q

What are osteocytes?

A

trapped osteoblasts in the bone matrix
lie within bony lacunae
contact other cells via long cytoplasmic processes

215
Q

What are osteoclasts?

A 
Reabsorb bone
large
multinucleated cells
derived from macrophages
lie in depressions: Howship's lacunae
216
Q

Describe bone remodelling

A

1) Resting bone surface: PTH + collagenase = osteoclast precursor
2) Reabsorption: osteoclasts
3) Reversal: mononuclear cells
4) Formation: secretion of osteoblasts
5) Reminerization: osteoids
6) Resting: inactive osteoblasts

217
Q

What is hypercalcaemia?

A

Raised [Ca2+]

218
Q

What is hypocalcaemia?

A

Reduced [Ca2+]

219
Q

What causes Hypocalcaemia Tetany?

A

Decrease Ca2+ intake
Excess loss of Ca2+
Alkalosis -> low [Ca2+] in blood

220
Q

What occurs in Alkalosis?

A

Low [Ca2+] in blood = increased nerve excitability
pins and needles; muscle spasms
Trousseau’s sign
Chvostek’s sign

221
Q

What can cause alkalosis?

A

Hyperventilation

by blowing off CO2

222
Q

How can you cure alkalosis?

A

rebreathing expired air into a bag

trapped CO2 in patient’s lungs

223
Q

Name some disorders of hormones regulating calcium

A

Over secretion + under secretion of:

1)PTH
hyperPT: Osteitis Fibrosa Cystica
hypoPT: defective mineralisation

2)Vit D
Rickets (children)
Osteomalacia (adults)

3) Calcitonin
No effect -> no essential for regulation of plasma [Ca2+]

224
Q

What is Osteitis Fibrosa Cystica?

A

Areas of demineralisation in skull and leg bones

Primary hyperparathyroidism

225
Q

What is vit D deficiency?

A 
Dietary deficiency
failure to synthesis in body:
reduced Ca up from GI track
undermineralised bone
bone lack rigidity
226
Q

Name some bone diseases

A

Osteoporosis - decreased bone mass and density

Osteopetrosis - increased bone mass and density

227
Q

What is osteoporosis?

A 
Reduced bone density
Loss of matrix with 2ndry loss of mineral
fractures common
common in elderly
in both genders
menopause
other causes:
Corticosteriods
nutrition deficiency
228
Q

What is osteropetrosis?

A 
Increased bone density
reduced blood supply
prone to fracture and chronic infection
difficult extraction
tooth roots indistinct on radiographs
mandible > maxilla
229
Q

What is hyperplasia?

A

Increase in cell numbers

230
Q

What is hypertropia

A

Increase in cell size

231
Q

Which cells can regenerate?

A

Skin
Liver
Blood

232
Q

Which cells can’t regenerate?

A

Nerve

233
Q

What affects growth?

A

Genetics

Environment:
Nutrients
Disease
Growth factors e.g hormones

234
Q

Which hormones influence growth?

A

Thyroid
Growth H
Sex H

others:
Insulin
Cortisol
Vit D
PTH
235
Q

In growth, what does the thyroid hormone do?

A

Indirect effect

Needed for:
Normal development + growth
protein synthesis in brains of fetus and infant
normal development of neurons

Faciliates:
actions of growth hormone
SNS

236
Q

Symptoms of hypothyroidism

A

Deficiency of thyroid hormone

Fetal/neonate ->
sparse hair
large tongue
permanent mental impairment

in childhood ->
impedes brain development and skeletal growth
delayed tooth eruption

Treatment: Thyroxine
recovery: depends on onset and duration.

237
Q

Growth hormone

A

mainly indirect

Metabolic and growth-promoting actions

Growth action: in postnatal period, infancy and adolescence

Metabolic action (indirect):

  • increases blood glucose levels (anti insulin)
  • decreases glucose uptake in calls
  • increases lipolysis - making fatty acids available for
  • energy production
  • facilities uptake of AA for protein synthesis (esp. liver and muscle)

IGF-1 (from liver) exerts effects:

  • cartilage, bone, soft tissue, viscera
  • IGF-1 -> cartilage proliferation in long bones, until epiphyses (growth centres) close
238
Q

Types of dwarfism

A

hypothyroid

hypopituitary

239
Q

Sex hormones

A

Testostetone, oestrogen
-> growth spurts

Mediated by:
increases secretion of GH and IGF-1:
-stimulate bone growth but accelerate closure of epiphyseal growth plates

testosterone:
anabolic effects on protein synthesis, increase muscle bulk

240
Q

In growth, what does insulin do?

A

no direct effect on growth promoting actions but:

Promotes foetal growth
promoting post-natal growth by stimulating secretion of IGF-1
Faciliating protein synthesis (by making glucose available for energy production)

241
Q

In growth, what does cortisol do?

A

higher then normal level -> inhibits growth

stimulates protein catabolism
suppresses bone growth
promotes bon resorption -> osteoporosis

childhood: stress/illness = cortisol = growth inhibition

242
Q

In growth, what does, Vit D + PTH do?

A

contribute to growth by
- ensuring Ca2+ + PO4 available for bone formation

  • Vit D = Ca2+ absorption in gut
  • PTH raises plasma Ca2+
243
Q

What occurs if there is excess growth hormone?

A

Childhood:
Gigantism

Adulthood:
Acromegaly (Hands, feet, jaw = bulky)
Class 3 - greater growth of mandible/gap between teeth

244
Q

What do you see in tumour of pituitary gland

A

Enlarged sella turcica

245
Q

Achondroplasia

A

Defective cartilage growth
- effects:
long bones
cartilage growth centres e.g spheno-occipitial synchondrosis (in cranial base)

246
Q

What happens to cells in ageing?

A 
Decline in ability of cells to divide
as they divide, accumulate:
Errors in DNA sequence
Abnormal proteins
Damage to organelles e.g. mitochondria
free radicals; shortening of telomeres
247
Q

What is apoptosis

A

programmed cell death

occurs in:
development - tooth germs, nervous system
to replace worn out cells
to destroy tumour cells

BDS1 (9 decks)

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