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Finals > REB Endocrine > Flashcards

REB Endocrine Flashcards

1
Q

what are the types of hormones?

A
  1. steroid
  2. amine
  3. peptide
  4. protein
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2
Q

what are steroid hormones derived from?

A

cholesterol

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3
Q

what are amine hormones derived from?

A

from amino acid modification of tryptophan and tyrosine

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4
Q

what are peptide hormones derived from?

A

multiple amino acids linked together

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5
Q

what type of hormones need transport proteins?

A

steroid hormones

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6
Q

steroid hormones arrive at the nucleus with the help of transport proteins. what does the activated receptor bind to?

A

HREs (hormone response elements) of DNA

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7
Q

what are HREs?

A

regions of DNA that contain a consensus sequence located upstream to the initiation site and associated with transcription factors

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8
Q

hormone signalling duration is _____ but effect duration is _____

A

short

long

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9
Q

how is cAMP signalling controlled

A

negative feedback by pKA

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10
Q

what does pKA activate?

A

phosphodiesterases

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11
Q

what do phosphodiesterases do?

A

deactivate cAMP

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12
Q

what substance is activated by G-proteins and cleaves membrane-bound phospholipids

A

phospholipase C

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13
Q

phospholipase C cleaves membrane-bound proteins into

A

IP3 and DAG

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14
Q

what causes the phosphorylation cascade?

A

protein kinases activated by DAG

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15
Q

IP3 increases release of

A

Ca2+

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16
Q

Ca 2+ acts as a second messenger by binding tp

A

calmodulin

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17
Q

what does calmodulin do

A

modulates protein kinase activity within the cells

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18
Q

what is the second messenger of a GPCR dependent reaction?

A

calcium

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19
Q

what is the second messenger of a GPCR independent reaction?

A

cGMP

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20
Q

explain a GPCR independent reaction

give an example

A

involves the conversion of GTP to GMP when ligand binds by membrane-bound receptor guanylate cyclase
eg. ANP –> increase Na excretion –> decrease ECF

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21
Q

explain the binding of insulin

A

insulin binds
tetramer dimerises and autophosphorylation occurs
the insulin response element is then phosphorylated and hence activates

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22
Q

describe a sandwich elisa

A

monoclonal antibodies plates –> antigen binds –> sandwiched by second monoclonal antibody modified with enzyme –> colour produced

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23
Q

in a sandwich elisa what is the relationship between colour produced and amount of antigen

A

colour produced directly proportional to amount of antigen

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24
Q

describe a competitive elisa

A

antibody incubated with sample –> mixture added to wells coated with the same antigen –> bound to antibodies in mixture washed away ; free antibodies will bind to antigen (2nd antibody is added for colour)

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25
Q

in a competitive elisa what is the relationship between colour produced and amount of antigen

A

colour produced inversely proportional to amount of antigen

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26
Q

where does the anterior pituitary gland arise from

A

Rathke’s pouch - epithelioid nature

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27
Q

where does the posterior pituitary gland arise from

A

neural tissue outgrowth from hypothalamus - glial type

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28
Q

what types of neurons are in the posterior pituitary. where are their cells?

A

neurosecretory neurons in the hypothalamus

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29
Q

what are the main nuclei in the posterior pit

A

supraoptic

paraventricular

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30
Q

what hormones are produced by the posterior pit

A

vasopressin/ADH

oxytocin

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31
Q

what nuclei produces vasopressin

A

supraoptic mostly

1/6 by the paraventricular

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32
Q

what nuclei produces oxytocin

A

paraventricular mostly

1/6 by the supraoptic

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33
Q

vasopressin and oxytocin are produced as

A

prohormones

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34
Q

vasopressin and oxytocin are bound to carrier proteins called

A

neurophysins

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35
Q

how long does it take to transport vasopressin and oxytocin to go to the posterior pituitary

A

several days

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36
Q

nervous impulses cause the release of both neurophysins and hormones into the

A

capillaries (they separate immediately)

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37
Q

Unlike the post pit gland, the anterior pituitary gland synthesises its own hormones. What are these hormones?

A
  1. somatotrophs (GH)
  2. corticotrophs (ACTH)
  3. Gonadotrophs (FSH and LH)
  4. Lactotrophs (prolactin)
  5. Thyrotropes (TSH)
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38
Q

all hormones are trophic except

A

prolactin

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39
Q

what hormones control the release of anterior pituitary hormones

A

hypothalamic releasing and inhibitory hormones

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40
Q

the hypothalamus releases hormones which control secretions of the anterior pituitary by the

A

hypothalamic hypophyseal portal system

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41
Q

where does the hypothalamic hypophyseal portal system begin?

A

median eminence (base of hypothalamus)

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42
Q

the hypothalamic hormones act on the ________ of the anterior pituitary

A

glandular cells

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43
Q

anterior pituitary hormones are regulated by

A
  1. hypothalamic hypophysiotropic hormones

2. negative feedback

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44
Q

what are the types of feedback loops

A
  1. ultrashort
  2. short
  3. long
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45
Q

how are ultrashort feedback loops regulated

A

hypothalamic hormones self-inhibit

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46
Q

how are short feedback loops regulated

A

pituitary hormones inhibit hypothalamic hormones and other pituitary hormones

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47
Q

how are long feedback loops regulated

A

hormones from peripheral endocrine glands

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48
Q

PIH is identical to

A

dopamine (has more than 1 effect)

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49
Q

a hormone may be regulated by more than one hormone. example….

A

GH by GHRH and GHIH

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50
Q

what is primary hypo/hyper secretion

A

hypo/hyper secretion of the anterior pit cells

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51
Q

what is secondary hypo/hyper secretion

A

hypo/hyper secretion of the hypophysiotropic hormones

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52
Q

what is tertiary hypo/hyper secretion

A

hypo/hyper secretion of endocrine gland

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53
Q

what is panhypopituitarism

A

decrease in secretion in all anterior pituitary hormones

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54
Q

effect of panhypopituitarism on children

A

rate of development is decreased and they never go through puberty

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55
Q

effect of panhypopituitarism in adults

A

become sterile but can be treated with thyroid/ adrenocortical hormones

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56
Q

what illness is characterized by:

  • decrease in secretion in all anterior pituitary hormones
  • rate of development is decreased and they never go through puberty
A

panhypopituitarism in children

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57
Q

what illness is characterized by:

  • decrease in secretion in all anterior pituitary hormones
  • person becomes sterile but can be treated with thyroid/ adrenocortical hormones
A

panhypopituitarism in adults

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58
Q

what cells produce growth hormone

A

somatotropes

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59
Q

treatment of panhypopituitarism in adults

A

thyroid/ adrenocortical hormones

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60
Q

which hormones are closely related to GH and its function

A

thyroid hormone

sex hormones

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61
Q

what i sthe most abundantly produced ant pit hormone

A

GH

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62
Q

secretion of GH _____ with age

A

decreases

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63
Q

is GH secreted after growth has seized

A

YEP

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64
Q

metabolic effects of GH are triggered by

A

direct binding to the target hormone

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65
Q

what are the metabolic effects of GH

A
  1. metabolization of FA in adipose tissue for energy. this increases FA in the blood and conserves glucose for the brain
  2. decreased rate of glucose utilization throughout the body (decreases uptake) –> GH induced insulin resistance eg Muscles uptake of glucose decreases
  3. increased rate of protein synthesis
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66
Q

growth- promoting effects are done by stimulating

A

somatomedins

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67
Q

somatomedins are structurally and functionally similar to

A

insulin called insulin-like growth factor (IGF1 or somatomedin C)

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68
Q

where is IGF 1 produced

A

liver

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69
Q

what is the purpose of IGF?

A

promotes growth upon stimulation (bone growth and protein synthesis)

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70
Q

bone growth occurs through

A

thickening of the epiphyseal plate and increase in bine length

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71
Q

regulation of GH

A
  1. negative feedback on GHRH and GHIH secretions (short loop)
  2. diurnal rhythm - GH secretion increases 1hr into sleep
  3. other factors - low blood glucose (GH conserves glucose), exercise (fat usage instead), high protein (protein synthesis) and decrease in plasma FA (mobilisation)
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72
Q

GH deficiency in children can lead to what conditions/ illnesses?

A

dwarfism
laron dwarfism
african pygmies

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73
Q

symptoms of Dwarfism

A

short stature
decrease in development of muscles
increase in subcutaneous fat

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74
Q

cause of laron dwarfism

A

blood GH normal but GH receptor is abnormal

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75
Q

cause of african pygmies

A

blood GH normal, receptor normal, lack of IGF 1

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76
Q

symptoms of african pygmies

A

no growth function but normal metabolism

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77
Q

symptoms of GH deficiency in adults

A

reduced skeletal muscle mass
increased bone density
increased risk of heart failure

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78
Q

excess GH in children can lead to what conditions/ illnesses?

A

gigantism

hyperglycemia (GH conserves glucose)

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79
Q

symptoms of GH excess in adults

A

bones and tissue thicken and proliferate
hyperglycemia
** shows mostly in face

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80
Q

explain the change in glucose level if there is a GH deficiency

A

normally after a meal, insulin should decrease glucose levels which should trigger GH secretion, allowing glucose to rise again.
if deficient, glucose levels cannot rise again

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81
Q

what test can be done to determine if a person has excess GH secretions

A

glucose loading test

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82
Q

explain the glucose loading test and its result if GH is excessively secreted

A

patient given glucose –> increase in glucose –> increased GHIH –> decrease glucose normally
if excess, decrease would not be as significant either due to not enough GHIH or too much GH acting

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83
Q

what does prolactin normally stimulate

A

proliferation and branching of ducts in the breasts

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84
Q

what does prolactin stimulate in pregnancy

A

development of lobules of alveoli for milk production

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85
Q

what does prolactin stimulate post partum

A

milk production and secretion

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86
Q

what effect does prolactin have on immunity

A

decreases immune responses to accept foetal tissue

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87
Q

prolactin increases during pregnancy until

A

mother stops breastfeeding

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88
Q

deficiency in prolactin leads to

A

inability to lactate

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89
Q

how is prolactin regulated

A

short-loop negative feedback by PRH and PIH or dopamine

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90
Q

how does excess prolactin specifically affect women

A

infertility, loss of menstruation, inappropriate lactation

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91
Q

how does excess prolactin specifically affect men

A

decreased testosterone levels, sperm production, breast development

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92
Q

how does excess prolactin generally affect both genders

A

decreased libido

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93
Q

treatment of excess prolactin

A

dopaminergic drugs (perform PIH functions)

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94
Q

what stimulates oxytocin secretion

A

positive feedback when suckling or birth canal stretch

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95
Q

what are the functions of oxytocin

A

milk ejection

contraction of uterus

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96
Q

what are the functions of vasopressin

A

enhances retention of water by kidneys

constriction of arterial smooth muscle

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97
Q

what stimulates the release of vasopressin

A
  1. osmotic: osmoreceptors increased osmolality and increased firing rate –> ADH secretion
  2. volume: decreased volume of BP causes release detected by baroreceptors or stretch receptors located in the walls of the left atrium and pulmonary veins
  3. age: older –> more ADH
  4. ethanol: suppresses ADH release (this is why you get thirsty)
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98
Q

explain ADH levels after hemorrhage

A

during low volume

ADH is secreted 50 times more to bring back blood volume

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99
Q

what is a deficiency in vasopressin caused by

A

diabetes (hyperglycemia –> increased blood osmolarity)

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100
Q

symptoms of vasopressin deficiency

A

same as the symptoms of diabetes (hyperglycemia, polyuria, polydipsia, nocturia)

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101
Q

symptoms of excess vasopressin

A

electrolyte disturbance

CNS symptoms from too low osmolarity

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102
Q

source of thyroglobulin

A

epithelial cells surrounding the colloid space or lumen

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103
Q

where is thyroglobulin stored

A

lumen

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104
Q

where is parathyroid hormone released from

A

parathyroid gland

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105
Q

what is the effect of parathyroid hormone of Ca

A

increases calcium levels

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106
Q

where is calcitonin released from

A

parafollicular (C) cells

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107
Q

what is the effect of calcitonin of Ca

A

decreases calcium levels

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108
Q

where are parafollicular (C) cells located?

A

between follicles in the thyroid gland

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109
Q

what regulates thyroglobulin synthesis

A

TSH through active transport of Iodine (iodinating tyrosine residues)

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110
Q

steps of thyroid hormone synthesis

A
  1. thyroglobulin is synthesised by epithelial cells and transported into the colloid space
  2. TSH causes cells to actively transport iodine into the cytosol. once inside, they are trapped to prevent escape and oxidised into the active form by peroxide.
  3. iodine enters the lumen through NIS (sodium, iodide symporter). thyroperoxidase iodinates tyrosine molecule on thyroglobulin forming either 2MITs or 1DIT (# of iodine attacks)
  4. MIT and DIT –> T3 and 2DIT –> T4
  5. epithelial cells ingest the colloid by endocytosis and fuses the vesicle with lysosomes where thyroglobulin is cleared releasing 90% T4 and 10% T3.
  6. since the thyroid hormones, T3 and T4, are lipid soluble, they diffuse across the membrane and into the bloodstream.
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111
Q

what hormone causes cells to actively transport iodine into the cytosol?

A

TSH

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112
Q

what oxidises iodine in the cytosol?

A

peroxide

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113
Q

iodine enters the lumen through

A

NIS

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114
Q

what iodinates tyrosine molecules on thyroglobulin

A

thyroperoxidase

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115
Q

thyroperoxidase iodinates tyrosine molecule on thyroglobulin forming

A

either 2MITs or 1DIT

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116
Q

1MIT and 1DIT forms

A

T3

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117
Q

2DIT forms

A

T4

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118
Q

of the total TH made, how much is T4 and how much is T3

A

90% T4 and 10% T3

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119
Q

T4 is a ____ of T3

A

prohormone

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120
Q

which TH is more biologically active

A

T3

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121
Q

deiodination of T4 forms

A 
T3
reverse T3 (metabolization of T4)
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122
Q

iodine is converted to ____ by bacteria in the gut

A

iodide

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123
Q

how is iodide transported in the blood

A

bound to serum proteins

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124
Q

how does the NIS work in transporting iodine

A

transfers both iodine and sodium in one direction using gradient of sodium

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125
Q

how is TH regulated

A
  1. TRH secretion - stimulated by exposure to cold; inhibited by T3 and T4 levels
  2. TSH secretion from anterior pituitary by thyrotropes - stimulated by TRH during the day and inhibited by T3 (beta subunit) during the night
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126
Q

what part of the T3 inhibits TSH

A

Beta subunit

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127
Q

what is the significance of the binding of TH to a transport protein

A

to prevent free diffusion into random cells

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128
Q

Active TH are _____ and can hence freely diffuse into cells to elicit an action.

A

unbound

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129
Q

what transport proteins are TH bound to and describe their affinity and capacity

A
  1. thyroxine-binding globulins (TBG) - high affinity, low capacity
  2. albumin - low affinity, high capacity
  3. thyroxine binding prealbumin (TBPA) - low affinity, high capacity
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130
Q

describe the genomic action of TH

A

TH are steroid hormones (hydrophobic). they diffuse into the cell and T4–>T3 in the cytoplasm. T3 binds to the thyroid receptor activating it. the receptor then complexes with TRE and Retinoid X receptor).

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131
Q

what stimulates and inhibits TRH secretion

A

stimulated by exposure to cold; inhibited by T3 and T4 levels

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132
Q

what stimulates and inhibits TSH secretion

A

stimulated by TRH during the day and inhibited by T3 (beta subunit) during the night

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133
Q

TH increases the body’s sensitivity to

A

catecholamines (adrenaline and noradrenaline)

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134
Q

temporal effects of TH levels

A

Daytime - low - anabolic - low metabolic rate - protein and glycogen synthesis
night time - high - catabolic - high metabolic rate - protein and glycogen breakdown

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135
Q

Explain the effects of TH on metabolism

A 
presence of TH --> catabolism 
increased glucose absorption 
glycogenolysis
gluconeogenesis 
increased fat mobilization --> increased FA
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136
Q

what is the metabolic function of TH

A

increases overall BMR
most important regulator of oxygen consumption and energy expenditure
it degrades fats and glycogen but doesn’t affect proteins

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137
Q

what is the calorigenic effect of TH

A

increases metabolic activity –> increases heat production

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138
Q

what is the effect of TH on the nervous system of children

A

TH is essential for myelination and CNS development

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139
Q

what is the effect of excess TH on the nervous system of adults

A

restlessness and hypersensitivity

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140
Q

what is the effect of a TH deficiency on the nervous system

A

lethargy and mental deficit

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141
Q

what the effect of TH on growth

A

stimulates GH secretion and increases synthesis of IGF-1 and promotes GH and IGF effects on growth and development

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142
Q

what the effect of TH deficiency on growth in children

A

stunts growth –> dwarfism (african pygmies)

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143
Q

what is the effect of TH on the cardioresp system

A

TH increases blood flow and increases sensitivity to catecholamines which increase HR, SV and BP

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144
Q

what is the primary cause of hypothyroidism

A

Gland tissue

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145
Q

what is the secondary cause of hypothyroidism

A

anterior pituitary/ hypothalamus

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146
Q

symptoms of hypothyroidism

A 
reduces BMR 
poor tolerance to cold 
slow mental response 
weight gain 
weak pulse 
lethargy
husky voice 
dry scalp/skin
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147
Q

what is myxedema

A

severe hypothyroidism
increased H2O retention of carbs
increases interstitial fluid

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148
Q

clinical presentation of myxedema

A

edemic appearance (puffy) with bagginess under eyes and face swelling

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149
Q

clinical presentation cretinism

A

congenital –> since birth
they experience dwarfism (no IGF-1) and mental retardation
**effects may not show before birth as the mother supplies the embryo

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150
Q

cretinism can be caused by hypothyroidism or

A

can also be due to iodine deficiency

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151
Q

treatment of cretinism

A

T4 supplements few weeks after birth or permanently

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152
Q

diagnostics of hypothyroidism (test and results)

A

done by measuring TSH and T4 levels in blood
people with hypothyroidism should have high TSH and low T4 (low negative feedback)
if issue is secondary, then low TSH and TRH

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153
Q

most common cause of hyperthyroidism

A

grave’s disease

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154
Q

what is grave’s disease

A

autoimmune disease characterised by the production of LATS that also target TSH receptors (not TH)
growth and secretion continue unchecked

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155
Q

what does grave’s disease stimulate

A

growth and secretion of thyroid gland

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156
Q

grave’s disease has a similar function to

A

TSH

** but it is not inhibited by TH

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157
Q

symptoms of grave’s disease

A

elevated BMR
increased appetite and weight loss
intolerance to heat
degradation of fat, protein and carb stores at an abnormal rate
HR and SV increase significantly –> palpitations
excessive degree of mental awareness –> anxiety

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158
Q

clinical signs of grave’s disease

A

inflammation and swelling of eye muscles –> eye bulge out and lids cannot close –> irritation

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159
Q

diagnostics of grave’s disease

A

done by measuring TSH and Thyroxine (TH) in plasma

TSH should be very low (inhibited) but TH levels very high.

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160
Q

what is a goitre

A

an enlarged thyroid thyroid gland

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161
Q

when are goitres present (in relation to TH release)

A

they are present in hypo and hyperthyroidism or none

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162
Q

when in hypothyroidism is a goitre present?

A

issue with thyroid gland or lack of iodine

where there is excessive stimulation of the gland by TSH but no TH is being secreted

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163
Q

when in hyperthyroidism is a goitre present?

A
  1. Grave’s disease (PRIMARY) - hypersecretion due to LATS which acts like TSH but has no inhibition (continuous stimulation)
  2. Secondary defect - excessive TSH secretion due to tumor leads to excessive stimulation –> goitre
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164
Q

when in hypothyroidism is a goitre not present?

A

when the issue is with hypothalamus or anterior pituitary since there is no TSH secretion –> no stimulation –> no goitre

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165
Q

when in hyperthyroidism is a goitre not present?

A

when there is excessive secretion without extra stimulation –> thyroid tumor

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166
Q

where is calcium stored

A

bone reservoir, ECF and cells

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167
Q

disorders of Ca are closely related to disorders of

A

magnesium

phosphates

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168
Q

what are the functions of calcium

A
  1. muscle contraction and nerve excitability. Ca2+ deficit causes hyperexcitability of neurons and excess Ca2+ causes increased contractility
  2. NT and hormone release into synaptic cleft
  3. Blood coagulation (essential cofactor for clotting factors)
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169
Q

regulation of calcium is done by

A

parathyroid hormone released from parathyroid glands –> increases Ca2+
calcitonin released from thyroid gland –> decreases Ca2+

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170
Q

effect of parathyroid hormone on Ca

A

increases Ca2+

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171
Q

effect of calcitonin on Ca

A

decreases Ca2+

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172
Q

calcium is absorbed in the ____ but requires ____

A

small intestine

vitamin D

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173
Q

how is plasma Ca2+ levels controlled by the kidney

A

regulation of excretion of extra calcium and reabsorption if levels are low

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174
Q

if there is impairment of intestines, parathyroid glands and kidneys, how is plasma Ca2+ maintained

A

at the expense of bone calcification

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175
Q

what are the functions of PTH

A
  1. increases Ca2+ and Mg2+ reabsorption in the kidneys
  2. increases Ca2+, Mg2+ AND HPO4- uptake from GI tract into blood
  3. increases activity of osteoclasts –> bone breakdown –> increased Ca2+ levels
  4. promotes vitamin D formation by increasing Ca2+ absorption in small intestine
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176
Q

PTHrP is structurally similar to

A

PTH

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177
Q

what are some additional functions of PTHrP (beside those similar to PTH)

A

mammary gland development
lactation
placental transfer of Ca2+

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178
Q

where is PTHrP secreted from

A

breast and lung tumors

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179
Q

unlike PTH, PTHrP does not stimulate

A

vitamin D synthesis

nor calcium absorption (bone decalcification only)

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180
Q

what are the PTH receptors

A

type 1 - high affinity for both PTH and PTHrP and is a G-protein receptor located in the bone and kidney
type 2 - binds to PTH but low affinity for PTHrP

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181
Q

which PTH receptor has a low affinity for PTHrP

A

type 2

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182
Q

which PTH receptor has a high affinity for both PTH and PTHrP

A

type 1

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183
Q

calcitonin is produced by

A

parafollicular (C) cells

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184
Q

calcitonin binds to a ____ receptor

A

Calcitonin

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185
Q

where is the calcitonin receptor located

A

on osteoclasts (inhibiting fxn)
osteoblasts ( promotes fxn)
kidneys

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186
Q

what type of receptor is the calcitonin receptor

A

GPCR

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187
Q

effect of calcitonin receptor on osteoclasts

A

inhibits fxn

188
Q

effect of calcitonin receptor on osteoblasts

A

stimulates fxn

189
Q

mRNA in C-cells contain _____ exons which code for _______

A

4 of 6 exons

pre procalcitonin

190
Q

calcitonin opposes the fxn of §

A

PTH

191
Q

mRNA in CNS contain _____ exons which code for _______

A

5 of 6 exons

calcitonin-gene related peptide (CGRP)

192
Q

what is the function of CGRP

A

potent vasodilator

193
Q

vitamin d can be obtained through the diet as __ in vegetables and __ in meat

A

D2

D3

194
Q

how can vitamin D be obtained other than through the diet

A

endogenously through UV action on the skin producing Calcitriol

195
Q

formation of vitamin D

A

7 dehydrocholesterol –> vitamin D3 – liver (hydroxylation) –> 25 hydroxyvitamin D3 – kidney (hydroxylation) —> Calcitriol (1,25 dihydroxyvitamin D3)
enzyme of last step - 25 hydroxyvitamin 1 alpha hydroxylase

196
Q

where does 1 alpha hydroxylase work

A

kidney

197
Q

____ stimulates 1 alpha hydroxylase

A

PTH

198
Q

____ inhibits 1 alpha hydroxylase

A

vitamin D (calcitriol)

199
Q

____ inhibits PTH

A

calcitriol

200
Q

vitamin D is transported in the blood bound to

A

vitamin D-binding protein

201
Q

inactive form of vitamin D is

A

25-hydroxyvitamin D

202
Q

active form of vitamin D is

A

1,25-hydroxyvitamin D (calcitriol)

203
Q

25-hydroxyvitamin D is from the

A

liver

204
Q

1,25-hydroxyvitamin D is from the

A

kidney

205
Q

vitamin D has a lower affinity for which form of vitamin D

A

25-hydroxyvitamin D (inactive)

206
Q

which form of vitamin D has a longer half life

A

25-hydroxyvitamin D (inactive)

207
Q

when vitamin D binds to its receptor, it forms a complex with

A

RXR (like TH) which then goes onto the vitamin D response element

208
Q

functions of vitamin D

A
  1. increases calcium uptake
  2. mineralises excretion of Ca2+ from kidney by increasing Ca2+ reabsorption
  3. stimulates osteoclast activity

** same as PTH

209
Q

calcium is mostly reabsorbed in the

A

PCT but some in the loop of henle

210
Q

the functions of vitamin D are similar to that of

A

PTH

211
Q

does vitamin D increase or decrease calcium uptake

A

increases calcium uptake

212
Q

____% of Ca2+ in the body is found in the blood
____% is bound to albumin or an anion (inactive)
____% is found in it’s free form (Ca2+ ionised form) (active)

A

0.1
45
55

213
Q

changes in albumin alters the ________ of calcium but NOT the ________

A

total amount

fraction of free ionized Ca+

214
Q

does changes in H+ alter fraction of free ionized Ca+?

A

YEP

215
Q

How does changes in H+ alter fraction of free ionized Ca+?

A

H+ competes with Ca2+ to bind to anions –> increase H+ –> increase acidity –> increase free ionised Ca2+

216
Q

describe the effect of alkalosis and acidosis on the fraction of free ionised Ca2+

A

Alkalosis –> less H+ –> decreased free ionized Ca2+

Acidosis –> more H+ –> increased free ionized Ca2+

217
Q

what are the different types of cells involved in bone turnover and what is the purpose of each

A
  1. osteoclasts - bone forming
  2. osteoblasts - bone-resorbing cells
  3. osteocytes - embedded osteoblasts - they regulate concentration if osteoblasts and osteoclasts
218
Q

what is hyperparathyroidism

A

excess PTH –> increased bone resorption (break down)

219
Q

what is osteomalacia and rickets

A

vitamin D deficiency
osteomalacia - demineralizing of pre-existing bones
rickets - in the children version where there is continued collagen formation but incomplete mineralization

220
Q

In rickets, there is continued ______ formation but incomplete mineralization.

A

collagen

221
Q

what is osteoporosis

A

disorder of reduced bone matrix

** not a disorder of Ca+ metabolism

222
Q

osteoporosis resembles _______ but normal plasma Ca2+

A

osteomalacia

223
Q

treatment of osteoporosis

A

treated with calcitonin to increase mineralisation

224
Q

what is paget’s disease

A

increased osteoclast activity
there is new bone formation but osteoclasts make it weaker
(easy to fracture)

225
Q

diagnosis of paget’s disease

A

increased serum alkaline phosphatase (ALP)

226
Q

symptoms of hypocalcemia

A

constipation and arrhythmia

227
Q

clinical presentation of hypercalcemia

A

trousseau’s sign (wait sign)

chvostek’s sign (twitch of lip or facial spasm)

228
Q

symptoms of hypercalcemia

A

muscle cramps

excess Ca2+ –> increase muscle contraction

229
Q

insulin is secreted by

A

B cells of Langerhan in the pancreas

230
Q

when is insulin released in the blood

A

when glucose levels in the rise after parasympathetic stimulation

231
Q

insulin facilitates the uptake of

A

glucose into the cell

232
Q

what are the cell types in the islets of langerhans and what do they produce

A
  1. alpha cells (20%) - glucagon
  2. beta cells (75%) - insulin
  3. delta cells (5%) - somatostatin
233
Q

somatostatin is inhibits

A

GH secretion

release of pancreatic and GI hormones

234
Q

somatostatin is released by

A

Hypothalamus and delta cells

235
Q

insulin inhibits

A

somatostatin and glucagon

236
Q

somatostatin inhibits

A

insulin and glucagon

237
Q

glucagon promotes

A

insulin and somatostatin

238
Q

why does glucagon promote insulin production

A

it is needed for glucose transport

239
Q

insulin synthesis

A
  1. synthesised initially as pre proinsulin with 4 domains (in beta cells)
  2. removal of N-terminus signal peptide becoming proinsulin with 3 domains. Amino B, Middle C and Carboxyl A.
  3. removal of C peptide forms mature insulin with only 2 domains linked by alpha sulfide bonds –> mature –> amino B and carboxyl A
240
Q

what domain is removed from insulin first

A

N-terminus

241
Q

what domain is removed from inulin second

A

C peptide

242
Q

mature insulin and C-peptide are packaged into secretory vesicles by

A

Golgi

243
Q

insulin release is triggered by the

A

influx of glucose

244
Q

describe the steps in insulin release

A
  1. glucose enters beta cells via facilitated diffusion through the GLUT 2 transporter
  2. Glucose metabolised by glucokinase into G-6-P trapping it in the cell
  3. ATP generated via glycolysis for K+ channels
  4. closure of ATP-sensitive K+ channels –> no K+ influx –> depolarises cell leading to opening of Ca+ channel –> Ca2+ influx
  5. increased intracellular Ca2+ triggers the release of insulin - containing vesicles/ granules.
245
Q

the 2 domains left on the mature insulin molecule is linked by

A

alpha sulfide bonds

246
Q

insulin release - glucose enters beta cells via facilitated diffusion through the

A

GLUT 2 transporter

247
Q

insulin release - Glucose metabolised by _____ into G-6-P trapping it in the cell

A

glucokinase

248
Q

insulin release - ATP generated via glycolysis for

A

K+ channels

249
Q

insulin release - closure of ATP-sensitive _____ –> depolarises cell leading to opening of _____–>

A

K+ channels

Ca+ channel

250
Q

insulin release - increased intracellular Ca2+ triggers the release of _____

A

insulin - containing vesicles/ granules

251
Q

hyperinsulinism can be induced by

A

tumors or by excessive insulin intake

252
Q

hyperinsulinism can lead to

A

hypoglycemia which can cause brain damage

253
Q

regulation of insulin release

A
  1. nutrients - glucose and amino acids leucine, isoleucine, alanine, arginine
  2. pancrine via somatostatin and glucagon (inhibition)
  3. GI hormones - GIP, glucagon-like peptide (GLP) and catecholamines (noradrenaline and adrenaline)
254
Q

glycogen is synthesised by

A

aloha cells

interstitial neuroendocrine L cells (gut) and brain

255
Q

glucagon is secreted is stimulated by

A

low glucose
high protein
catecholamine stimulation

256
Q

glucagon is first synthesized as _____ before undergoing post-translational processing

A

proglucagon

257
Q

proglucagon in pancreatic alpha cells is converted to (3)

A
  1. glucagon
  2. GRPP (glicentin related pancreatic peptides)
  3. major proglucagon fragment (MPF)
258
Q

proglucagon in pancreatic alpha cells is converted by what hormone

A

prohormone convertase 2 (PC2)

259
Q

proglucagon in neuroendocrine or enteroendocrine L cells is converted to

A
  1. glicentin
  2. GLP 1 (glucagon-like peptides) - stimulator of insulin secretion and somatostatin secretion but inhibit glucagon secretion
  3. GLP 2 - useless
260
Q

function of glicentin

A

stimulator of insulin secretion, inhibits secretions of gastric acid, and reduces gut motility
(increases beta secretions)

261
Q

effect of glicinten on pancreatic cells

A

increases secretion of B cells

262
Q

effect of GLP 1 on pancreatic cells

A

decreases secretion of alpha cells

increased secretion of B and D cells

263
Q

proglucagon in neuroendocrine or enteroendocrine L cells is converted by

A

prohormone convertase 1 and 3

264
Q

what are the immediate effects of insulin

A

increased transport of glucose, amino acids and K+ into cells

265
Q

what are the intermediate effects of insulin (4)

A

increased entry of AA
increases glycolysis and glycogen synthesis
decreased gluconeogenesis and glycogenolysis
decreased protein degredation

266
Q

what are the delayed effects of insulin

A

Increase in mRNA for lipogenic enzymes to store glucose in the form of lipids in adipose tissue

267
Q

the insulin receptor is an RTK receptor which has an ____ subunit extracellularly and a ____ subunit intracellularly

A

alpha

beta

268
Q

when insulin binds to its receptor, it causes

A

auto-phosphorylation of tyrosines in the beta subunit

269
Q

auto-phosphorylation of tyrosines in the beta subunit allows the receptor to phosphorylate

A

IRS-1

270
Q

when insulin binds, the whole receptor moves intracellularly allowing

A

lysosomes degrade insulin

271
Q

what glucose transporter is found on muscle and adipose?

do they require insulin?

A

GLUT 4

YUP

272
Q

what glucose transporter is found on brain and kidneys? do they require insulin?

A

GLUT 3

NOPE

273
Q

what glucose transporter is found on liver and pancreas?

do they require insulin?

A

GLUT 2

NOPE

274
Q

what glucose transporter requires insulin

A

GLUT 4

275
Q

hypoglycemia is due to

A

insulinomas or congenital

276
Q

type 1 diabetes is caused by

A

immune-mediated B cell destruction –> hyperglycemia

277
Q

describe the onset of type 1 diabetes

A

fast

278
Q

type 1 diabetes may cause

A

ketoacidosis

279
Q

type 2 diabetes is caused by

A

B cell dysfunctional insulin resistance and associated with obesity and sedentary lifestyle

280
Q

describe the onset of type 2 diabetes

A

slow

281
Q

type 2 diabetes may cause

A

blurred vision

slow healing

282
Q

diagnosis of type 2 diabetes

A

hyperglycemia but with normal insulin levels

283
Q

diabetic ketoacidosis is a symptom of

A

uncontrolled diabetes

284
Q

without insulin, the body cannot break down glucose.

what is the new fuel source

A

break down of fat instead

285
Q

the break down of fat produces

A

ketone bodies

286
Q

a buildup of ketone bodies in the liver after beta oxidation can lead to

A

keto acidosis

287
Q

keto acidosis is caused by

A

a buildup of ketone bodies in the liver after beta oxidation

288
Q

where does beta oxidation occur

A

liver

289
Q

explain the cause of glycosuria

A

too much glucose –> kidney cannot reabsorb 100% of glucose –> its in piss
therefore, with a high glucose concentration in urine, volume increases and there is more piss

290
Q

normal glycogen levels in the body is

A

70-120 mg/dL (3.9-7.1 mmol/L)

291
Q

glucagon regulates blood glucose levels by

A

stimulating glycogen breakdown

292
Q

process of glucagon secretion

A
  1. hypoglycemia causes intracellular glucose concentration to fall
  2. reduction in glycolysis ATP –> K+ channels close
  3. intracellular K+ concentration rises –> depolarises cell –> Ca2+ channels open –> influx of Ca2+
  4. influx of Ca2+ causes secretion of glucagon through exocytosis
293
Q

in glucagon secretion, there is a reduction in glycolysis ATP which causes the closure of the

A

K+ channels

294
Q

in glucagon secretion, the influx of ____ causes secretion of glucagon through endocytosis

A

Ca2+

295
Q

what factors stimulate glucagon release (3)

A
  1. low blood glucose
  2. protein rich meal (secreted with insulin)
  3. catecholamines (glucagon levels increase in anticipation for increased glucose use)
296
Q

what factors inhibit glucagon release (2)

A
  1. high blood glucose

2. insulin

297
Q

metabolic effects promoted by glucagon (3)

A

glycogenolysis
gluconeogenesis
ketogenesis (liver and adipose tissue)

298
Q

metabolic effects inhibited by glucagon (2)

A

glycogenesis

glycolysis

299
Q

what type of receptor is the glucagon receptor

A

GPCR

300
Q

what type of reaction is catalysed by enzymes which are active when phosphorylated

A

catabolism

301
Q

what type of reaction is catalysed by enzymes which are active when dephosphorylated

A

anabolism

302
Q

what is whipple’s triad

A
  1. hypoglycemic symptoms - motor impairment, NSB problems
  2. blood glucose levels < 50 mg/dL (normal 70-120)
  3. symptoms resolve after glucose administration
303
Q

types of hypoglycemia (4)

A
  1. insulin-induced
  2. post-prandial
  3. fasting
  4. alcohol-induced
304
Q

cause of insulin-induced hypoglycemia

A

self-injection

305
Q

what is postprandial hypoglycemia

A

exaggerated insulin release after a meal

306
Q

how is postprandial hypoglycemia treated

A

eating less

more frequently

307
Q

cause of fasting hypoglycemia

A

insulinoma, adrenal insufficiency (catecholamines stimulate glucagon), liver damage

308
Q

risk group for alcohol-induced hypoglycemia

A

alcoholics that take irregular meals

309
Q

how does alcohol consumption increase the risk of hypoglycemia

A

metabolism of alcohol –> excess NADH –

> diverts oxaloacetate away from gluconeogenesis –> increased the risk of hypoglycemia

310
Q

prediabetes is also known as

A

intermediate hyperglycemia

311
Q

plasma glucose concentration of prediabetes

A

6.1-6.4 mmol/L

312
Q

plasma glucose concentration of diabetes

A

> = 7 mmol/L

> 125 mg/dL

313
Q

plasma glucose concentration of acute hyperglycemia

at what glucose concentration is the person symptomatic

A

> = 8 mmol/L

symptomatic at >= 15 mmol/L

314
Q

symptoms of hyperglycemia (6)

A
  1. decreases glucose entry into tissues and increased hepatic output
  2. glycosuria
  3. osmotic diuresis - polyuria and polydipsia (increased thirst)
  4. polyphagia - (increased appetite since body thinks its hypoglycemic)
  5. weight loss - excess metabolism of proteins and fats
  6. increase HbA1C - especially following an episode as diagnostic trace. it is glycated hemoglobin
315
Q

how does osmotic diuresis affect electrolyte composition

A

excess loss of Na+ and K+ –> dehydration

316
Q

diabetic ketoacidosis is caused by

A

alteration of carb, protein and lipid metabolism

317
Q

DKA is a hallmark of what type of diabetes

A

type 1

318
Q

what causes the increases ketosis in DKA

A

severe insulin deficiency and/or elevated levels of counter-regulatory hormones

319
Q

what the counter-regulatory hormones of insulin secretion

A

glucagon
catecholamines
cortisol

320
Q

the excess ketone production in DKA is from the breakdown of

A

fat and protein

321
Q

excess ketone production by the breakdown of fats and proteins can lead to

A

metabolic acidosis

322
Q

what hormone is responsible for the shift of K+ into cells

A

insulin

323
Q

explain the effect of insulin deficiency on K+ levels of patients

A

they can be normal or elevated due to extracellular migration
however, cells are being depleted of K+ –> hypokalemia

324
Q

what is ketogenesis

A

it is the enhanced lipolysis of lipids in adipose tissue

325
Q

ketogenesis leads to the release of ____ into the bloodstream

A

FA

326
Q

FA are taken up from the blood by the liver where ______ of FA occurs

A

B oxidation

327
Q

the B oxidation of FA occurs in the

A

liver

328
Q

the B oxidation of FA results in the production of _____ from acetyl coA

A

ketone bodies

329
Q

the B oxidation of FA results in the production of ketone bodies from

A

acetyl coA

330
Q

how is acetone produced

A

spontaneous decarboxylation of acetoacetate

331
Q

how is acetone eliminated from the body

A

slowly through urine

332
Q

what is ketonemia

A

presence of abnormally high concentrations of ketones in blood

333
Q

what is ketonuria

A

excretion of abnormally large amounts of ketone in urine

334
Q

symptoms of DKA (3)

A
  1. dehydration
  2. fruity breath
  3. CNS shit
335
Q

DKA can eventually lead to

A

coma
shock
death

336
Q 
Diagnosis of DKA 
give the corresponding values for 
hyperglycemia
ketonemia 
acidemia 
anion gap
A

hyperglycemia >11 mM
ketonemia >3mM
acidemia pH<7.3
anion gap >12 mmol/L

337
Q

what is an anion gap

A

difference between measured cations and anions

338
Q

how is DKA treated

A

IV fluid replacement
IV insulin
potassium replacement

339
Q

in the treatment of DKA, what IV fluids are used

A

isotonic initially

hypotonic when Na concentration is fixed

340
Q

in the treatment of DKA, when should insulin therapy be started

A

after fluid replacement

only if K>3.3 mmol/L

341
Q

if DKA is resolved through treatment, the patient starts to take

A

subcutaneous insulin

342
Q

chronic hyperglycemia can be caused by

A

microvascular and macrovascular complications

343
Q

microvascular complications involve the formation of ______ caused by prolonged (chronic) hyperglycemia and protein glycation

A

advanced glycation end-products (AGE)

344
Q

microvascular complications involves the nonenzymatic binding of

A

glucose with amino groups ( m- terminal) of proteins

345
Q

what causes the accumulation of AGEs

A

binding to structural and functional proteins causes permanent changes (resembles protein denaturation) –> alters fxn of protein

346
Q

what is the receptor for AGEs

A

RAGE

347
Q

effect of binding of AGE to its receptor on endothelial cells

A

altering intracellular signalling and gene expression which leads to the release of proinflammatory molecules and free radicals –> extracellular matrix degradation

348
Q

effect of binding of AGE to its receptor on platelets

A

causing aggregation –> vascular proliferation

349
Q

effect of binding of AGE to its receptor on vascular smooth muscle cells

A

uncontrolled proliferation

350
Q

where in the body are RAGE located

A

epithelial cells
platelets
vascular smooth muscle

351
Q

binding of AGE to its receptor on _____ leads to extracellular matrix degradation

A

epithelial cells

352
Q

binding of AGE to its receptor on _____ leads to uncontrolled proliferation

A

vascular smooth muscle

353
Q

binding of AGE to its receptor on _____ leads to vascular proliferation

A

platelets

354
Q

what is the most common cause of chronic kidney failure

A

diabetic nephropathy

355
Q

cause of diabetic nephropathy

A

causes kidney failure –> leads to unhealthy glomerulus where protein spills into urine due to damage at the capillary wall

356
Q

what is the predictor of diabetic nephropathy

A

microalbuminuria (albumin in urine)

357
Q

cause of diabetic retinopathy

A

changes in vessels of the eye

358
Q

complication of diabetic retinopathy

A

exudates (lipoprotein leaks)
microaneurysms
hemorrhage

359
Q

complications of diabetic retinopathy contribute to ischemia which leads to the activation of

A

hypoxia-induced factor (HIF)

360
Q

The activation of HIF in diabetic retinopathy is due to

A

ischemia by complications of diabetic retinopathy which are:
exudates (lipoprotein leaks)
microaneurysms
hemorrhage

361
Q

The activation of HIF in diabetic retinopathy leads to the formation of ___

A

new vessels

362
Q

how will the new vessels formed by activation of HIF in diabetic retinopathy be affected by AGE

A

AGE makes them leaky again

363
Q

symptoms of diabetic retinopathy

A

sudden and complete loss of vision
discoloured spots
blurred vision

364
Q

diabetic neuropathy develops as a result of

A

AGEs leading to ischemia and nerve cell injury (stroke)

365
Q

what are the 2 types of neuropathy

A
  1. peripheral

2. autonomic

366
Q

what does peripheral neuropathy affect

A

limbs (numbness, burning, pain)

367
Q

what complication can arise from peripheral neuropathy

A

minor skin injuries may lead to serious infections because of the loss of sensation

368
Q

what is autonomic neuropathy

A

damage of nerves including myelin degeneration

it affects autonomic function

369
Q

autonomic neuropathy is the damage to nerves involved in autonomic regulation of

A

autonomic regulation of BP, cardiac function, respiratory, urinary and GI systems

370
Q

what does autonomic neuropathy affect

A

weight loss, erectile dysfunction, no sensations of heart attacks
** it affects autonomic function

371
Q

how do macrovascular complications contribute to hyperglycemia

A

damages vascular endothelium, increases platelet aggregation, decreases thrombolysis, making it difficult to restore blood as well as promoting pro-inflammatory responses

372
Q

how do macrovascular complications affect platelet aggregation

A

increases platelet aggregation,

373
Q

how do macrovascular complications affect thrombolysis

A

decreases thrombolysis

374
Q

macrovascular complications lead to

A

heart disease
stroke
peripheral vascular disease

375
Q

what are the 3 main types of microvascular complications

A
  1. diabetic nephropathy
  2. diabetic retinopathy
  3. diabetic neuropathy
376
Q

what are the regions of the adrenal gland

A
  1. zona glomerulosa
  2. zona fasciculata
  3. zona reticularis
  4. medulla
377
Q

what hormone is produced in the zona glomerulosa

A

mineralocorticoids –> aldosterone

378
Q

what hormone is produced in the zona fasciculata

A

glucocorticoids –> cortisol

379
Q

what hormone is produced in the zona reticularis

A

androgens –> DHEA

380
Q

what hormone is produced in the medulla

A

catecholamines –> adrenaline and noradrenaline

381
Q

cortisol can be made in the zona fasciculata and the

A

zona reticularis

382
Q

androgens can be made in the zona reticularis and the

A

zona fasciculata

383
Q

what hormones are produced by the ovaries

A

estrogens and progesterone

384
Q

what hormones are produced by the testes

A

large amounts of androgens

385
Q

in what part of the cell does steroid hormone synthesis occur

A

mitochondria

ER

386
Q

are steroid hormones lipid soluble?

A

yes

387
Q

can steroid hormones be stored?

A

nope

388
Q

adrenocorticoids are bound to _______ to prevent reentry into the cell

A

plasma proteins

389
Q

where is cholesterol synthesised

A

liver

390
Q

cholesterol is synthesised in the liver as an _____ molecule

A

amphiphatic

391
Q

all steroids are synthesised from

A

cholesterol

392
Q

all steroid are synthesised from cholesterol via what process

A

hydroxylation of steroid nucleus

393
Q

what is the RLS of steroid synthesis

A

conversion of cholesterol to pregnenolone catalysed by cytochrome P450
this step requires NADPH and oxygen

394
Q

what protein controls the uptake of cholesterol into the mitochondria

A

Star

395
Q

what enzymes involved in steroid synthesis are found in the ER

A

3B-OH
delta 5,4 isomerase
17-OH
21-OH

396
Q

what enzymes involved in steroid synthesis are found in the mitochondria

A

11B-OH

18-OH

397
Q

conversion of cholesterol to pregnenolone catalysed by ______ . it also requires ______ and _____

A

cytochrome P450

this step requires NADPH and oxygen

398
Q

in steroid synthesis, pregnanalone is converted to

A

progesterone

399
Q

conversion of pregnenolone to progesterone is catalysed bv

A

3B-OH

delta 5,4 isomerase

400
Q

3B-OH and delta 5,4 isomerase catalyses the conversion of

A

pregnenolone to progesterone

401
Q

cytochrome P450 catalyses the conversion of

A

cholesterol to pregnenolone

402
Q

describe aldosterone synthesis from progesterone

A

progesterone –> 11-deoxycorticosterone (21-OH)
11-deoxycorticosterone –> corticosterone (11B-OH)
corticosterone –> aldosterone (18-OH, aldosterone synthase)

403
Q

describe cortisol synthesis from progesterone

A

progesterone –> 17 hydroxyprogesterone (alpha 17-OH)
17 hydroxyprogesterone –> 11-deoxycortisol (21-OH)
11-deoxycortisol –> cortisol (11B-OH)

404
Q

which hormones are used in aldosterone synthesis

A

21-OH
11B-OH
18-OH, aldosterone synthase

405
Q

which hormones are used in cortisol synthesis

A

alpha 17-OH
21-OH
11B-OH

406
Q

how does hypersecretion of mineralocorticoids affect electrolytes

A

increases Na in ECF
K depletion
–> hypokalemia and hypertension

407
Q

mineralocorticoids are released in response to

A

decreased ECF volume

high K+ concentration

408
Q

the secretion of mineralocorticoids stimulate the transcription of the Na/K pump by

A

increasing numbers of sodium pumps on the basolateral membrane of epithelial cells
** facilitates uptake of sodium and water from the tubular lumen

409
Q

Na+ is reabsorbed in the kidney at the expense of K+ and H+. how does this affect ECF volume and electrolyte concentration

A

increase in ECF volume (dec BP)
decreased K+
INCREASED Na+

410
Q

what parts of the nephron does aldosterone act

A

DCT

collecting ducts

411
Q

aldosterone is secreted by activation of

A

RAAS

412
Q

RAAS activation promotes secretion of

A

aldosterone

413
Q

what is the main function of glucocorticoids

A

inhibit anabolism and stimulate catabolism

414
Q

how do glucocorticoids inhibit anabolism and stimulate catabolism

A

reverses insulin functions

breakdown of muscle and aa uptake into liver for gluconeogenesis and lipolysis of adipose tissue

415
Q

what is congenital adrenal hyperplasia (CAH)

A

autosomal recessive disorders of cortisol biosynthesis

416
Q

CAH is caused by deficiency in which hormones

A

3B-OH
17 alpha-OH
21 alpha-OH
11B-OH

417
Q

explain the effect of a deficiency of 3B-OH

A

no conversion of pregnenolone to progesterone and hence the pathway to all steroid hormones are affected –> salt excretion in urine and female-like genitalia

418
Q

explain the effect of a deficiency of 17 alpha-OH

A

no conversion of progesterone to 17-hydroxyprogesterone
no androgens or cortisol can be produced but there will be high amounts of aldosterone secretion –> increased fluid retention –> hypertension and hypokalemia
female-like genitalia

419
Q

explain the effect of a deficiency of 21 alpha-OH

A

no conversion of progesterone to 11-deoxycorticosterone and 11-deoxycortisol
no mineralocorticoids and no glucocorticoids but there is an increase in androgens –> masculinization of external genitalia in females and early sterilization in men

420
Q

explain the effect of a deficiency of 11B-OH

A

no conversion of 11-deoxycorticosterone to corticosterone and 11-deoxycortisol to cortisol
no mineralocorticoids and no glucocorticoids but there is an increase in androgens –> masculinization of external genitalia in females and early sterilization in men
increased production of deoxycorticosterone –> fluid retention (hypertension)

421
Q

a protein shortage leads to

A

muscle wasting
poor healing
weakened skeleton

422
Q

effects of an increase and a decrease of aldosterone

A

i - hypokalemia; hypertension

d - hyperkalemia; salty urine; decreased BP and volume

423
Q

effects of an increase and a decrease of cortisol

A

i - adrenal diabetes; fat digestion; decrease in protein

d - hypoglycemia, increased ACTH, dark skin

424
Q

effects of an increase and a decrease of androgens

A

i - male-like genitalia

d - female like genitalia

425
Q

In CAH, a deficiency in which enzymes cause female-like genitalia

A

deficiency of 3B-OH

deficiency of 17 alpha-OH

426
Q

In CAH, a deficiency in which enzymes cause masculinization

A

deficiency of 11B-OH

deficiency of 21 alpha-OH

427
Q

In CAH, a deficiency in which enzymes cause hypertension

A

deficiency of 11B-OH

deficiency of 17 alpha-OH

428
Q

what is the metabolic function of glucocorticoids

A

increases glucose concentration at the expense of proteins and lipids
- catabolism

429
Q

what is the permissive function of glucocorticoids

A

enhances glucagon and catecholamines

430
Q

what is the immune function of glucocorticoids

A

anti-inflammatory, decreases stress, and boosts immune response following tissue injury
- important of transplants

431
Q

what are the factors which control glucocorticoid secretions (3)

A
  1. CRH –> ACTH from corticotropin –> zona fasciculata –> cortisol –> CRH and ACTH (by negative feedback)
  2. diurnal rhythm which acts on the hypothalamus to vary CRH secretion
    - highest in morning, lowest at night
  3. dramatic increases in stress increases CRH release
432
Q

what is cushing’s syndrome

A

cortisol hypersecretion

433
Q

adrenal diabetes is caused by

A

excessive glucose (hyperglycemia)

434
Q

clinical features of cushing’s syndrome

A

extra glucose deposited as fat in face, abdomen and shoulder but thin otherwise

435
Q

what is the significance of DHEA in males and in females

A

males - overpowered by testosterone

female - governs androgen-dependent processes (pubic hair, growth spurts, sex drive)

436
Q

in both sexes, the zona reticularis produces

A

estrogens

androgens

437
Q

what controls secretions of the adrenal cortex

A

ACTH

438
Q

DHEA inhibits

A

GRH

439
Q

the inhibition of GRH by DHEA inhibits

A

FSH and LH

440
Q

do adrenal hormones feedback to the axis?

A

NOPE

441
Q

hypersecretion of androgens may be caused by

A

tumour or defect in part of the cortisol pathway.

442
Q

what is the effect of hypersecretion of androgens in newborn females

A

male type external genitalia

443
Q

what is the effect of hypersecretion of androgens in adult females

A

secondary male characteristics

444
Q

what is the effect of hypersecretion of androgens in prepubescent boys

A

early puberty but no sperm production

445
Q

what is the effect of hypersecretion of androgens in adult males

A

overpowered by testosterone

446
Q

If one adrenal gland is non-functional, will there be renal insufficiency? why?

A

nope

the second one can take over

447
Q

What is Addison’s disease?

A

Primary adrenocortical insufficiency where all layers of the adrenal cortex are undersecreting due to an autoimmune disease that destroys cells of the adrenal cortex
There is a decrease in aldosterone and the cortisol

448
Q

Explain the resultant aldosterone deficiency of Addison’s disease

A

K retention –> hyperkalaemia –> disturbs cardiac rhythm (smooth muscle contraction)
Na depletion –> excessive urinary loss of sodium –> salty urine
Reduced ECF volume –> reduce in pressure –> hypotension, shock

449
Q

Explain the resultant cortisol deficiency of Addison’s disease

A

Poor response to stress
decrease in gluconeogenesis
hyperglycaemia
no ACTH negative feedback therefore increased ACTH release and darkening of skin

450
Q

What is a secondary adrenocortical insufficiency?

A

Pituitary or hypothalamic abnormality only cortisol is affected.

451
Q

What is hormones or affected by a primary adrenocortical insufficiency?

A

Aldosterone and cortisol

452
Q

What is hormones or affected by a secondary adrenocortical insufficiency?

A

Cortisol only

453
Q

What are chromaffin cells and where are they located?§

A

Modified sympathetic neurons which are part of the adrenal medulla (modified part of SNS)

454
Q

What do chromaffin cells produce and how much (%)?

A

Adrenaline 80% and noradrenaline 20%

455
Q

Do the axonal fibres of chromaffin cells terminate at the effector organ?

A

nope

456
Q

the axonal fibres of chromaffin cells do not terminate at the effector organ. Release of Catecholamines is stimulated by….

A

Released directly into circulation upon stimulation by preganglionic fibres

457
Q

Secretions of chemicals by preganglionic fibre is by the __NS

A

ANS

458
Q

Adrenaline is produced exclusively by the

A

Adrenal Medulla

459
Q

Noradrenaline is produced in far greater quantities by

A

SNS postganglionic fibers

460
Q

What is the function of catecholamines?

A

Involved in the flight or fight response

461
Q

Effects of catecholamines on heart, GI system and skeletal muscle

A

Increases stroke volume, heart rate, blood pressure and shifting blood to heart and skeletal muscles (vasodilation) and includes respiration
reduces digestive activity
inhibits insulin and stimulates glucagon secretion

462
Q

Catecholamines inhibit

A

Insulin

463
Q

Catecholamines stimulate

A

Glucagon

464
Q

Secretions of the adrenal Medulla are controlled by

A

Sympathetic input into gland

465
Q

Now you have to do REB endocrine 2

A

SHIT!

Finals (17 decks)

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