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Medicine yr1 > ENDO-SOM > Flashcards

ENDO-SOM Flashcards

1
Q

what are hormones?

A
  • chemical messengers that have an effect on target organs

- only specific target cells with specific receptor will respond to hormone

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2
Q

what are the 4 classifications of hormones?

A
  • steroid hormones (lipid-derived hormones)
  • amino acid derived hormones
  • peptide hormones
  • Eicosanoids (chemical messengers derived from fatty acid
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3
Q

what is autocrine signalling?

A

when a cell sends signals to itself

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4
Q

what is endocrine signalling?

A

signalling using the circulatory system to transport ligands

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5
Q

what is paracrine signalling?

A

neighbouring cells signal to each other

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6
Q

what are examples of steroid hormones hormones?

A

mineralcorticoids
glucocorticoids
sex hormones-androgens

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7
Q

what are steroid (lipid derived) hormones derived from?

A

cholesterol—>pregnenolone…

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8
Q

where are amino acid derived hormones generally derived from?

A

tyrosine

tryptophan

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9
Q

what are examples of amino acid derived hormones?

A
  • thyroid hormones-T3/T4

- catecholamines

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10
Q

what are peptide hormones formed from?

A

amino acid chains

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11
Q

what type of hormones are the most common?

A

peptide

eg oxytocin/ TSH/ prolactin/ insulin

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12
Q

why can’t peptide hormones pass through phospholipid bilayer?

A

not lipid-soluble

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13
Q

what are chemical messengers derived from fatty acids important in?

A

inflammation , blood pressure , clotting

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14
Q

what is a receptor?

A

protein molecule usually embedded within plasma membrane surface of cells
-receives chemical signals from outside of cell

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15
Q

what are the different types of receptors?

A
  • intracellular (eg steroid hormone receptors)

- cell surface

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16
Q

what do cell surface receptors do?

A

perform signal transduction-converting extracelular signal to intracellular signal

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17
Q

what are the types of cell-surface receptors?

A
  • G protein-linked receptors
  • enzymes-linked receptor
  • ion channel-linked receptors
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18
Q

how does binding to G protein-linked receptors work?

A
  • ligand binds to receptor
  • activates G protein
  • G protein interacts with either iron channel or enzyme in mem
  • each receptor has own specific extracellular domain and G-protein binding site
  • GDP—–>GTP once bound to G protein receptor
  • GTP binds to adenyl cyclase-activates it
  • catalyses conversion of ATP to cAMP
  • cAMP activates PKAs
  • GTP is hydrolysed to GDP + pi
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19
Q

how do enzyme-linked receptors work?

A

-cell surface receptors with intracellular domains are associated with enzymes
-have large extracellular and intracellular domains
-when ligand binds to extracellular domain-signal is transferred-activates enzyme component of the receptor which leads to a response
Eg-tyrosine kinase-insulin binds to

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20
Q

how do ion channel-linked receptors work?

A
  • Ligand binds to receptor
  • conformational change in protein structure-allows ions eg Na+, Ca2+, Mg2+ and H+ to pass through
  • change activity of ion-binding enzymes and voltage-sensitive channels-to produce response
  • eg neurons with ACh and serotonin
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21
Q

what is receptor down-regulation?

A

-receptors exposed to excessive ligands results in ligand-induced desensitisation or internalisation of that receptor

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22
Q

what is receptor up-regulation?

A

-super sensitised cells after repeated exposure to drug or prolonged absence of ligand

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23
Q

are receptor agonists up-regulation or down-regulation of their respective recpetors?

A

down-regulation of their respective receptors

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24
Q

are receptor antagonists up-regulation or down-regulation of their respective receptors?

A

up-regulation

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25
Q

what is the blood vessel network called that connects the pituitary gland to the hypothalamus?

A

hypothalamohypophyseal-portal system

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26
Q

what are the 5 subtypes on anterior pituitary cells and what do they secrete?

A
  • somatotroph- GH secreting
  • corticotroph- ACTH secreting
  • thyrotroph- TSH secreting
  • gonadotroph- LH/ FSH secreting
  • lactotroph- prolactin secreting
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27
Q

where is the anterior pituitary derived from in embryology?

A

from the ectoderm of Rathke’s pouch

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28
Q

where is the posterior pituitary derived from in embryology?

A

from the downward extension of neural ectoderm forming the floor of diencephalon

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29
Q

what are the types of hypothalamic signals to the pituitary?

A
  • stimulatory

- inhibitory

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30
Q

what are the main functions of growth hormone in children?

A

-linear growth

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31
Q

what are the main functions of GH in adults?

A
  • protein synthesis
  • carbohydrate metabolism
  • lipolysis
  • calcium homeostasis
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32
Q

what is IGF-1?

A

insulin-like growth factor 1

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33
Q

what is the role of IGF-1?

A

-produced in the liver in response to GH stimulation, mediates most GF effects

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34
Q

what can be used to help diagnose GH abnormalities?

A

plasma levels of IGF-1

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35
Q

what are the 3 parts of the adrenal cortex?

A
  • zona glomerulosa (outermost)
  • zona fasciculata (middle)
  • zona reticularis (inner)
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36
Q

what hormones are secreted by the zona glomerulosa and what does it help to regulate?

A

-secretes mineralcorticoids
important in fluid homeostasis.
EG. aldosterone-regulates absorption/uptake of K+ and Na+ levels in the kidney

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37
Q

what hormones are secreted by the zona fasciculata? Give an example of a specific hormone and what it does.

A

-secretes glucocorticoids -important for carbohydrate, protein and lipid metabolism
EG.cortisol which raises blood glucose and cellular synthesis of glycogen

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38
Q

what is the secretion of cortisol controlled by?

A

Its secretion is controlled by a hormone from the pituitary - ACTH.

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39
Q

what is secreted by the zona reticularis?

A

secretes androgens

(and small amounts of glucocorticoids)

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40
Q

what are glucocorticoids?

A

class of steroid hormone-widely used for inflammatory and autoimmune diseases e.g. cortisol

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41
Q

what are mineralcorticoids?

A

Mineralocorticoids are a class of steroid hormones that regulate salt and water balances e.g. Aldosterone

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42
Q

describe the CRH-ACTH-cortisol axis.

hypo-pit-adrenal axis

A
  • hypothalamus releases CRH (corticotropin-releasing hormone)
  • stimulates anterior pituitary gland to release ATCH (adrenocorticotropic hormone)
  • stimulates adrenal cortex (z.f.) to release cortisol
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43
Q

what are the main functions of cortisol?

A
  • increase glucose production (increase gluconeogeneis/ hepatic glycogen synthesis/ inhibits peripheral glucose uptake)
  • inhibits protein synthesis
  • increases protein breakdown
  • stimulates lipolysis
  • increases appetite
  • increases sodium retention and potassium loss-inflammatory response
  • make vessels vasoconstrict-raise BP
  • suppress immune response
  • forms essential part of the body’s response to stress-fight or flight
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44
Q

describe the negative feedback loops in the CRH-ACTH-cortisol axis.

A
  • cortisol can reduce its own secretion via feedback to the anterior pituitary to reduce ACTH and the hypothalamus to limit the secretion of CRH
  • ACTH also provides negative feedback limiting its secretion via CRH
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45
Q

describe the TRH-TSH-thyroid axis.

hypo-pit-thyroid axis

A
  • hypothalamus releases TRH (thyrotropin-releasing hormone)
  • stimulates anterior pituitary to release TSH (thyroid-stimulating hormone)
  • stimulates thyroid to release T3/ T4-which produce effect on target tissues/organs
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46
Q

describe the negative feedback loops in TRH-TSH-thyroid axis.

A

Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland

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47
Q

outline the main functions of thyroid hormones (T3/4).

A
  • CARDIOVASCULAR: increase heart rate and cardiac output
  • BONE: increased bone turnover and resorption
  • GI: increased gut motility
  • LIPIDS: increased lipolysis
  • SYMPATHETIC NERVOUS SYSTEM: increased catecholamine sensitivity
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48
Q

which hormones are released from the posterior pituitary?

A
  • oxytocin

- ADH (vasopressin)

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49
Q

what are the roles of vasopressin (ADH)?

A
  • increase in reabsorption of water
  • increases blood vol
  • increases blood pressure
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50
Q

what are the roles of oxytocin?

A
  • roles in female reproduction. -released in large amounts during labor, and after stimulation of the nipples
  • a facilitator for childbirth and breastfeeding.
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51
Q

what are the limits in which normal blood glucose is regulated within?

A

4.0-7.0 mmol/L

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52
Q

what are the 2 main pancreatic endocrine hormones involved in regulating blood glucose?

A
  • glucagon

- insulin

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53
Q

what are the 4 main glucose receptors and where are they situated?

A
  • GLUT1-brain/ RBCs/ placenta
  • GLUT2-liver/kidneys/ intestine
  • GLUT3-brain
  • GLUT4-muscle/ adipose tissue
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54
Q

how is glucose uptake from gut and glomerular filtrate in kidney achieved?

A

by Na+ dependent glucose transporters not GLUT
1-Na+ gradient from lumen to the cell is needed for glucose uptake
2-transport is saturable -if glucose in lumen rises above certain level not all glucose is absorbed-causes glucosuria in diabetes (glucose in urine)

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55
Q

what are the 2 minor pancreatic endocrine hormones?

A
  • somatostatin-inhibits secretion of pancreatic hormone-including insulin and glucagon
  • pancreatic polypeptide-secreted by PP cells decreases food intake and increases energy expenditure
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56
Q

what are the pancreatic endocrine cells called?

A

Islets of Langerhans

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57
Q

which cells make up the Islets of Langerhans and what do they secrete?

A
  • alpha cells-secrete glucagon

- beta cells-secrete insulin

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58
Q

what stimulates insulin release?

A
  • high blood glucose
  • parasympathetic system
  • Gastric inhibitory polypeptide GIP and GLP-1 (2 primary incretin hormones) secreted from the intestine upon ingestion of glucose to stimulate insulin secretion
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59
Q

how many amino acids make up insulin?

A

51

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60
Q

state the steps outlining how beta cells work to release insulin.

A

1-K channels open at rest- K+ ions diffuse out of cell creating PD across cell (inside more -ive than outside)
2-when glucose conc high-enters beta cells through GLUT2 transporter
3-glycolysis occurs in b-cell-generating ATP
4-causes K+ channel to close-PD across cell becomes +ive
5-chanmge in PD causes Ca2+ V.G. channel to open
6-Ca2+ enters cell
7-causes vesicles containing insulin to fuse with p. membrane and release
8-increase in GLP1 stimulates the release of insulin

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61
Q

what are the actions of insulin?

A
  • increases glucose uptake into fat and muscle
  • stimulates glycogen synthesis
  • stimulates storage of triglyceride in adipose tissue
  • increases protein synthesis
  • decreases hepatic gluconeogenesis
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62
Q

what is the role of GLUT4 in glucose uptake?

A

-insulin binds to receptor and initiates recruitment of GLUT4 to cell surface-integrated into cell mem allow glucose to be transported into cell

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63
Q

what are the effects of feeding on the liver?

A
  • rise in nutrients
  • increased in glycogen synthesis
  • reduced gluconeogenesis-(reduced glucose/ ketones/ amino acids in blood)
  • increased protein synthesis
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64
Q

what are the effects of feeding on fat?

A
  • increased lipogenesis

- decreased lipolysis- (reduced fatty acids in blood)

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65
Q

what are the effects of feeding on muscle?

A
  • increased glycogen synthesis
  • reduced gluconeogenesis
  • increased protein synthesis
  • switch to carbohydrate oxidation
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66
Q

what is the effect of glucagon on blood glucose levels?

A

-raises blood glucose level

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67
Q

what is the main target organ of glucagon?

A

liver

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68
Q

how does glucagon raise blood glucose levels?

A
  • stimulates glycogen breakdown and inhibits glycogen synthesis
  • inhibits FA synth by diminishing production of pyruvate
  • stimulates gluconeogenesis in liver and blocks glycolysis
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69
Q

what state is the body in to stimulate glucagon?

A

fasting

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70
Q

what effect does fasting state have on liver?

A
  • reduced glycogen synth
  • reduced protein synth (low glucose/ high ketone/ low AA in blood)
  • increased gluconeogenesis
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71
Q

what effect does fasting state have on fat?

A
  • reduced lipogenesis (increased FA in blood)

- increases lipolysis

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72
Q

what effect does fasting state have on muscle?

A
  • reduced glycogen synth
  • increased gluconeogenesis
  • reduced protein synth
  • switch to lipid oxidation -fat burning
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73
Q

how many amino acids make up glucagon?

A

29

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74
Q

whats the half-life of insulin?

A

5 mins

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75
Q

whats the half-life of glucagon?

A

4-6mins

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76
Q

what stimulates glucagon release?

A

low blood glucose

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77
Q

what inhibits insulin release?

A

sympathetic activity

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78
Q

name the different types of diabetes?

A
  • TYPE 1
  • TYPE 2
  • TYPE 3c
  • LADA
  • MODY
  • SCONDARY DIABETES
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79
Q

what is type 3c diabetes secondary to?

A

pancreatic disease

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80
Q

what is LADA diabetes?

A

late inset autoimmune disease leading to diabetes

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81
Q

what is MODY diabetes?

A

maturity onset diabetes of the young-rare inherited form of type 2

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82
Q

what is secondary diabetes?

A

Secondary diabetes is diabetes that results as a consequence of another medical condition.
eg from crushing’s syndrome/ haemochromatosis

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83
Q

what is the ration of people in the UK who suffer from type 1 diabetes?

A

1:3000

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84
Q

what is hyperglycaemia?

A

blood sugar exceeds normal limits

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85
Q

what is hypoglycaemia?

A

blood sugar below normal limits

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86
Q

what caused type 1 diabetes?

A

-autoimmune disease causing islet cell destruction

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87
Q

how does type 1 diabetes affect how insulin works?

A
  • complete insulin deficiency
  • uncontrolled gluconeogenesis
  • failure of glucose uptake into muscles and fats
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88
Q

what does type 1 diabetes lead to if untreated?

A
  • development of hyperglycaemia
  • ketoacidosis- ketone build up
  • eventual coma and death
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89
Q

what can occur is there is insulin excess?

A

hypoglycaemia

  • can occur in diabetes treatment
  • serious as brain starved of glucose
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90
Q

what are the risk factors for type 2 diabetes?

A
  • older age (as generally late onset 40+)
  • obesity
  • inactivity
  • family history
  • ethnicity
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91
Q

what is type 2 diabetes caused by?

A
  • insulin resistance

- insulin deficiency

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92
Q

how does insulin resistance cause type 2 diabetes?

A
  • peripheral tissues not responsive to insulin
  • higher levels of insulin required to keep blood glucose in normal range
  • genetic component
  • exacerbated by obesity and lack of physical activity
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93
Q

how does progressive insulin deficiency cause type 2 diabetes?

A
  • pancreas does not make enough insulin
  • amyloid and fat deposits
  • defective incretin response
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94
Q

what effect does type 2 diabetes have on fat cells?

A
  • reduced insulin response
  • high cholesterol
  • high blood pressure
  • inflamed arteries
  • increased blood clotting
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95
Q

how can type 2 diabetes lead to hyperglycaemia?

A
  • pancreatic beta-cells initially compensate for insulin resistance by increasing production-maintaining normal blood glucose levels
  • in. most patients b-cell function worsens-leading to hyperglycaemia
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96
Q

where is the thyroid gland located?

A

-thyroid gland located immediately below the larynx and anterior to upper part of trachea

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97
Q

what is the name of the narrow band that connects the 2 lobes of the thyroid gland?

A

isthmus-which overlies 2nd to 4th tracheal cartilage

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98
Q

what are the functional units of the thyroid gland?

A

follicles

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99
Q

which cells are interspersed between follicles in the thyroid gland and what do they secrete?

A

C cells

-secrete calcitonin for calcium homeostasis

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100
Q

what do thyroid gland follicles consist of?

A
  • layer of epithelium

- central cavities containing colloid-constiuents=large glycoproteins/ thyroglobulin

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101
Q

what are follicular cells of the thyroid gland dependent on?

A

TSH

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102
Q

which molecules are essential for synthesis of thyroid hormones?

A
  • iodine

- tyrosine

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103
Q

what is tyrosine synthesised from?

A

thyroglobulin

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104
Q

outline the steps in thyroid hormone synthesis.

A

1-IODINE TRAPPING- iodine is actively transported and iodide into cytosol of follicular cells in response to TSH
2-SYNTHESIS OF THYROGLOBULIN (TGB)- TGB produced in RER and golgi packaged in secretory vesicles-released into follicle lumen by exo
-occurs at same time as iodine trapping
3-OXIDATION OF IODINE
-I- is oxidised to iodine-when it passed through membrane into follicle lumen
4-IODINATION OF TYROSINE
-iodine reacts with tyrosine aas of TGB
-binding of single I forms monoiodtyrosine
-binding of 2-diiodotyrosine
-region of TGB with attached I atom=colloid
5-COUPLING OF T1 and T2
2x T2= T4
T1 + T2= T3
5-PINOCYTES AND DIGESTION OF COLLOID
-parts of colloid re enter follicular cells via pinocytosis and merge w lysosomes
-TGB broken down by digestive enzymes, T3/ T4 cleaved off

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105
Q

what % of hormones released from the thyroid appear as T4 and what happens to the majority of T4 hormones?

A

90%

-mostly converted to from T4 to T3 (from monoiodoination of T4)

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106
Q

where does the conversion of T4 to T3 occur?

A

liver

kidneys

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107
Q

describe the secretion of thyroid hormones

A
  • T3 and T4 are lipid soluble (even though aa derivatives) so diffuse out of follicular cell into interstitial fluid via plasma membrane then into blood
  • T3 and T4 bind to thyroxine binding protein in the blood to be transported to target cells
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108
Q

what are some physiological roles of thyroid hormones?

A
  • increase ATP production-Na+/ K+ ATPase synthesis, ^ mitochondria/ ^ respiration enzymes
  • increase heart rate, BP, and force of heart beat-up-reg B-andrenergic receptors-increase catecholamine binding
  • BMR can increase by 60-100%
  • increase production of GH and IGFs-results in increase of formation of ossification centres in bone
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109
Q

what is the sympathomimetic effect of thyroid hormones?

A

thyroid hormone increase target cell responsiveness to catecholamines-SNS/ ADRENAL

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110
Q

what is a sympathomimetic effect?

A

any action like one produced by the sympathetic nervous system

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111
Q

describe the mechanism of thyroid hormone release

A
  • TSH binds to TSH receptor on cell surface

- activates secondary messenger-cAMP from ATP

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112
Q

which hormone do thyroid hormones stimulate?

A

-growth hormone-important i promoting growth and development of brain during fetal and postnatal life

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113
Q

what are the symptoms of hypothyroidism?

A
  • weakness
  • cold intolerant
  • mental slowness
  • dry skin
  • depression
  • muscle cramps
  • infertility
  • Mild weight gain
  • hoarseness
  • constipation
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114
Q

what are the signs of hypothyroidism?

A
  • bradycardia
  • dry skin
  • relayed relaxation
  • hypertension
  • slow speech
  • slow movements
  • non-pitting edema
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115
Q

what are some of the causes of hypothyroidsim?

A
  • autoimmune (Hashimoto’s) thyroiditis
  • atrophic
  • iodine 131 treatment
  • pituitary disease
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116
Q

what are some of the causes of hypothyroidism?

A
  • autoimmune (Hashimoto’s) thyroiditis
  • atrophic
  • iodine 131 treatment
  • pituitary disease
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117
Q

how could you assess hypothyroidism in a labortory evaluation?

A
  • -increased TSH-most sensitive test-primary hypo

- -anti-thyroid peroxidase TPO and anti-thyroglobulin Tg antibodies-suggest Hashimoto’s thyroiditis

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118
Q

what can be used as a therapy for hypothyroidism?

A

T4

-can alleviate symptoms

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119
Q

what is T4?

A

Thyroxine

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120
Q

what is T3?

A

triiodothyronine

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121
Q

what is primary hypothyroidism caused by?

A

low levels of blood thyroid hormone due to destruction of the thyroid gland.

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122
Q

what is secondary hypothyroidism?

A

-failure of the pituitary gland to secrete thyroid stimulating hormone (TSH). –This is usually caused by a tumor in the region of the pituitary.

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123
Q

what specific roles is T3 involved in?

A
  • maintain muscle control
  • brain function
  • development
  • heart functions
  • digestive functions
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124
Q

what specific roles is T4 involved in?

A
  • metabolism
  • mood
  • body temperature
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125
Q

what shape is used to describe the suprarenal glands?

A

pyramidal

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126
Q

how much do the suprarenal glands weigh?

A

5g

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127
Q

why are the adrenal glands yellow on colour?

A

high lipid content

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128
Q

which artery supplies the suprarenal glands?

A

superior suprarenal artery

129
Q

which vein drains the adrenal glands?

A

suprarenal veins

130
Q

what percentage of the adrenal cortex does the zona glomerulosa make up?

A

15%

131
Q

what percentage of the adrenal cortex does the zona fasciculata make up?

A

80%

132
Q

what percentage of the adrenal cortex does the zona reticularis make up?

A

5%

133
Q

what is the role of aldosterone?

A

regulates blood pressure-
stimulates the conservation of sodium and eliminate potassium, enhancing the absorption of water by kidneys and other glands

134
Q

how is aldosterone production regulated?

A

renin-angiotensin system

135
Q

describe the renin-angiotensin system in aldosterone production

A
  • change in blood pressure (low-renal perfusion) -detected by baroreceptors (or low Na+ detected by macula densa cells) stimulates the release of renin to be released from the kidney
  • renin acts on angiotensin to form angiotensin I
  • angiotensin-converting enzyme is released from lungs
  • ACE acts on angiotensin I to from angiotensin II
  • angiotensin II acts on adrenal glands to stimulate release of aldosterone from zona g. of adrenal cortex
136
Q

how is aldosterone synthesised?

A

in zona glomerulosa

  • Angiotensin II binds to GPCR
  • ATP—>cAMP
  • activates protein kinase C
  • PKC and calcium stimulate the conversion of cholesterol to aldosterone in the mitochondria
137
Q

what are examples of diseases of the adrenal cortex due to hormonal overproduction?

A
  • Conn’s syndrome

- Cushing’s syndrome

138
Q

what causes Conn’s syndrome?

A
  • excess of mineralcorticoid-aldosterone

- controls sodium and potassium in the blood

139
Q

what causes Cushing’s syndrome?

A

-glucocorticoid excess-excess cortisol

140
Q

what are the clinical features of Cushing’s syndrome?

A
  • irritability
  • moon faced
  • interscapular fat
  • hypertension
  • diabetes
  • osteoporosis
  • bruising
  • muscle weakening
  • striae (stretch marks)
141
Q

how would you confirm diagnosis of Cushing’s syndrome?

A

-24 hour urine free cortisol
-salivary cortisol
-midnight cortisol
Overnight dexamethasone suppression test
-serum ACTH
-CRH/ high dose dexameth suppression test
-pituitary MRI scan
-inferior petrosal sinus sampling
-CT scan adrenals

142
Q

what does high levels of aldosterone (Conn’s) cause?

A
  • hypertension
  • hypokalaemia
  • metabolic alkalosis
143
Q

how would you confirm Conn’s syndrome?

A
  • high aldosterone to renin ratio
  • use CT/MRI SCAN
  • adrenal vein sampling-allows differentiation between unilateral and bilateral aldosterone production
  • surgical Rx-adrenalectomy
  • medical rX-aldosterone antagonists-spironolactone, amiloride, triamterene
144
Q

how is cortisol synthesised?

A
  • in zona f.
  • ACTH binds to GPCR receptor
  • ATP—>cAMP
  • activates protein kinase A
  • stimulates the conversion of cholesterol to cortisol in mitochondria
145
Q

when are cortisol levels highest?

A

morning

146
Q

what are the actions of cortisol in gluconeogenesis?

A
  • hepatic glycogen synthesis

- inhibit peripheral glucose uptake

147
Q

what are the actions of cortisol in lipolysis?

A
  • Increased appetite

- Fat deposition

148
Q

what are the actions of cortisol in protein catabolism?

A

Decreased protein synthesis

149
Q

what are the actions of cortisol affecting sodium retention?

A
  • Potassium loss

- Anti-inflammatory

150
Q

what are the causes of primary adrenal insufficiency of cortisol?

A
  • autoimmune adrenalitis
  • infections
  • neoplastic infiltration and metastasis
  • infiltration
  • thrombosis
  • adrenal haemorrhage
151
Q

what are the causes of secondary adrenal insufficiency of cortisol?

A
  • pituitary diseases

- drugs-long term steroids

152
Q

what are the clinical features of Addison’s disease?

A
  • weight loss
  • skin pigmentation-^ACTH–> ^melanin
  • dizziness and postural hypotension-low aldosterone–>low blood vol (due to low reabsorption by kidneys)-also dehydration
  • hypoglycaemia-low cortisol=reduced gluconeogenesis-causes fatigue
153
Q

what is the name of primary adrenal insufficiency of cortisol?

A

Addison’s disease

and insufficient aldosterone

154
Q

what is the name of secondary adrenal insufficiency of cortisol?

A

Hypopituitarism

155
Q

what could be used to diagnose adrenal insufficiency?

A
  • hyponatraemia and hyperkalaemia
  • inappropriately low cortisol for the level of stress
  • short synacthen
  • anti-adrenal antibodies
  • Endocrine tests for thyroid/ pit
  • imaging CT-abdomen/ MRI-pituitary
156
Q

how would you initially treat adrenal insufficiency?

A

IM/ IV hydrocortisone

157
Q

how would you later treat adrenal insufficiency?

A

oral hydrocortisone and fludrocortisone

158
Q

what are examples of 2 adrenal androgens?

A
  • —>dehydroepiandrosterone (DHEA)

- —–>androstenedione

159
Q

where are adrenal androgens secreted from?

A

zona reticularis

160
Q

what is the secretion of androgens controlled by?

A

ACTH

161
Q

what are androgens?

A

hormones that contribute to growth and reproduction in both men and women

162
Q

what may excess adrenal androgens lead to in pre pubertal boys?

A

precocious development of secondary sexual characteristics

163
Q

what may excess adrenal androgens lead to in female foetus?

A

pseudo hermaphroditism

164
Q

which class of hormones are secreted from the adrenal medulla?

A

catecholamines

165
Q

which hormones are examples of catecholamines?

A
  • adrenaline

- noradrenaline

166
Q

how is adrenaline synthesised?

A

1-catecholamines formed by hydroxylation and decarboxylation of tyrosine
2-tyrosine transported into catecholamine-secreting neurons and adrenal medullary cells
3-converted in to DOPA and Dopamine in cytoplasm
4-catecholamines are released from autonomic neurons and adrenal medullary cells by exocytosis

167
Q

outline the actions of catecholamines

A
  • prepare body for sympathetic fight-or-flight response
  • breakdown of glycogen to glucose-glycogenolysis
  • breakdown of fats—->fatty acids
  • increase rate and force of cardiac muscle contraction
  • enables body to deal with physical and psychological stress
168
Q

what is pheochromocytoma?

A

adrenal medullary catecholamine secreting tumour

example of adrenal medullary hormone hypersecretion disorders

169
Q

what is the clinical representation of pheochromocytoma?

A
  • hypertension
  • palpitations
  • sweating
  • heat intolerance
  • pallor
  • flushing
  • pyrexia
  • headache
170
Q

how would pheochromocytoma be diagnosed?

A

-high 24hr catecholamine excretion
-high plasma meta and noretanephrines
-MRI/ CT
MIBG scan

171
Q

how could you manage and then treat pheochromocytoma?

A

manage: alpha and beta blockers
treatment: surgery

172
Q

how much is the total body calcium?

A

approx 1000g

173
Q

what percentage of calcium is stored in bones as hydroapatite?

A

99%

174
Q

where is 1% located of calcium located?

A
  • blood
  • extracellular fluid
  • soft tissues
175
Q

what are the functions of calcium in the body?

A
  • cell division
  • plasma membrane integrity
  • protein secretion
  • neural excitability
  • cell adhesion
  • glycogen metabolism
  • muscle contraction-includes cardiac
  • neuronal excitability
  • blood coagulation
176
Q

what is the daily calcium requirements for children?

A

350-550 mg/day

177
Q

what is the daily calcium requirement for teens?

A

800-1000 mg/day

178
Q

what is the daily calcium requirements for adults?

A

700 mg/day

179
Q

what is the normal range of Ca levels in serum?

A

2.18 to 2.62 mmol/L

180
Q

what happens if blood calcium levels drop?

A

1-release of PTH from chief cells of the parathyroid

2-causes effects on bone/ kidneys/ intestines increasing blood calcium levels

181
Q

what are the effects of PTH on bone?

A
  • inhibits osteoblasts
  • stimulates osteoclasts
  • bone is broken down-releasing calcium ions into bloodstream
182
Q

what are the effects of PTH on the kidneys?

A
  • PTH stimulates kidney tubule cells to recover waste calcium from the urine
  • PTH stimulates kidney tubule cells to release calcitriol
183
Q

what are the effects of calcitriol on the intestines?

A

-stimulates intestines to absorb calcium from digesting blood

184
Q

what happens if blood calcium levels are high?

A

-high conc of calcium stimulate parafollicular cells in the thyroid to release calcitonin

185
Q

what are the effects of calcitonin on bone (target organ)?

A
  • stimulates osteoblasts
  • inhibits osteoclasts
  • calcium is removed from blood and used to build bone
  • lowering blood calcium
186
Q

what are 80% of phosphates stored as in the bones and where is the rest stored?

A
  • stored as hydroxyapatite in bones

- in soft tissues both as inorganic and organic molecules

187
Q

what do phosphates in bones help with?

A

-skeletal integrity

188
Q

what are the roles of phosphate in the body?

A
  • bone and teeth formation
  • DNA synthesis
  • ATP synthesis
  • cell membrane constituent-phospholipids
189
Q

what is the daily requirement of phosphates?

A

550mg

190
Q

what is the range of blood phosphate levels?

A

0.8-1.5 mmol/L

191
Q

what is the systematic regulation of phosphates maintained by and where?

A

maintained by:

  • PTH feedback
  • vitamin D
  • intestines
  • kidney
  • bones
192
Q

name 2 disorders of phosphate homeostasis?

A
  • hypophosphataemia

- hyperphosphataemia

193
Q

name 2 disorders of phosphate homeostasis?

A
  • hypophosphataemia

- hyperphosphataemia

194
Q

what are the features of hypophosphataemia?

A
  • decreased intestinal absorption
  • increased renal wasting
  • redistribution of ECF into cells
195
Q

what are the clinical consequences of hypophosphataemia?

A
  • 5% of hospitalised patients/ 30% in alcoholics
  • poor growth in children
  • fatigue, weakness, loss of appetite
  • bone pain/ fragile bones
196
Q

what are the features of hyperphosphataemia?

A
  • decreased renal excretion
  • acute exogenous phosphate load
  • redistribution of intracellular phosphate to extracellular space
197
Q

what are the clinical consequences of hyperphosphataemia?

A
  • hypocalcaemia
  • soft tissue calcification
  • calcification of arteries and heart valves
198
Q

where are the parathyroid glands situated and how many are there?

A

-4 small glands on posterior part of thyroid gland

199
Q

name the 2 cell types which make up the parathyroid gland.

A
  • chief cells

- oxyphil cells

200
Q

what are chief cells of the parathyroid responsible for?

A

synthesising and secreting parathyroid hormone-PTH

201
Q

where do the parathyroid glands develop from?

A

-develop from endoderm of 3 and 4 pharyngeal pouches

202
Q

what is the role of the parathyroid glands during gestation?

A

control calcium balance in foetus

203
Q

how does PTH act on bones?

A

PTH—->stimulates osteoblasts—->stimulates RANK ligand——>allows differentiation from osteoblast to osteoclast——->cause resorption of bone—–>Ca released into blood stream

204
Q

how does PTH act on kidneys?

A
  • Increases Ca reabsorption—–>decreased phosphate reabsorption
  • increases activation of Vit D
205
Q

describe the indirect effect of PTH on small intestines.

A
  • increase in active Vit D due to its action on kidneys

- Vit D increases absorption of Ca and phosphate from intestines

206
Q

what are 3 disorders of the parathyroid?

A
  • hyperparathyroidism
  • hypoparathyroidism
  • pseudohypoparathyroidism
207
Q

what is hypoparathyroidism due to?

A

-high levels of PTH and Ca

208
Q

what are the 3 different types of hyperparathyroidism?

A
  • primary (PHPT)-abnormality of parathyroid gland itself
  • leads to loss of bone tissue
  • secondary (SHPT)-in response to low calcium
  • tertiary (THPT) -after secondary HPT is treatment-very rare
209
Q

what are the clinical features of hyperparathyroidism (and hyperCa)?

A
  • nausea/ vomiting
  • constipation
  • ECG changes-short QT interval
  • kidney stones
  • bone pain
  • osteoporosis
  • psychosis/ altered mental state
210
Q

what are the clinical features of hyperparathyroidism (and hyperCa)?

A
  • nausea/ vomiting
  • constipation
  • ECG changes-short QT interval
  • kidney stones
  • bone pain
  • osteoporosis
  • psychosis/ altered mental state
211
Q

what does hypoparathyroidism suggest about PTH and Ca levels?

A

-low Ca
-low PTH
(most likely caused by autoimmune disorders)

212
Q

what are the clinical features of HypoPTH and HypoCa?

A 
-muscle weakness and cramps 
Nerve function:
-peroral numbness and tingling 
-Chvostek’s sign 
-Trousseau’ sign 
-Tetany
213
Q

what is pseudohypoparathyroidism due to?

A
  • target organ is resistant to PTH

- PTH is present just not effective so pseudo

214
Q

what are the roles of sex steroids?

A
  • promote sexual differentiation
  • development of secondary sexual characteristics
  • regulate sexual behaviour
  • supporting normal reproductive function
  • support bone growth and maintain bone mass
215
Q

which enzyme converts testosterone and androstendone to oestrogen?

A

aromotase

216
Q

describe the actions of steroid hormones

A
  • enter cell (lipid soluble)
  • bind to receptors in nucleus
  • then bind to DNA sequences-creating a hormone response element
  • this response then induces a transcription of mRNA in order to produce effector proteins-bring about physiological effects in several organs in body
217
Q

what do steroid hormones act as?

A

transcription factors

218
Q

which cells produce testosterone?

A

-Leydig cells in testicles

219
Q

which hormone can control testosterone release?

A

LH (stimulates Leydig cells to secrete test)

220
Q

when are testosterone levels highest and lowest?

A
  • highest-waking up and midnight-when melatonin peaks

- lowest in afternoons/ evenings

221
Q

what are the functions of testosterone in males?

A
  • primary sex hormone in males

- influences sexual characteristics and increases bone building-increases bone thickness/ increases basal metabolic rate

222
Q

what are the functions of testosterone in females?

A
  • tends to be used as a precursor to make estrogens
  • small influence on sexual characteristics
  • increases bone building
223
Q

what are the 3 types of estrogens?

A
  • estrone
  • estradiol-main type
  • estriol
224
Q

where are estrogens generally produced?

A

ovaries by granulosa cells

225
Q

how is estradiol produced?

A

from conversion of circulating androgens by aromatisation

226
Q

what is estrogen secretion under the influence of?

A

LH

FSH

227
Q

where are LH and FSH secreted from?

A

anterior pituitary gland

228
Q

what type of hormones are LH and FSH?

A

gonadotropin hormones

229
Q

what are the functions of estrogens?

A
  • influences sexual characteristics
  • responsible for secretory activity within genital tract
  • regulates GnRH secretion
  • responsible for ovulation during menstrual cycle
  • regulates cardiovascular physiology and neuronal growth
  • decreases bone breakdown
230
Q

describe the hypothalamic-pituiutary-ovarian axis

A
  • hypothalamus secreted GnRH
  • stimulates anterior pituitary to secrete LH anf FSH
  • LH causes theca cells to secrete androgens (test)
  • androgens and FSH cause granulosa cells to secrete estrogens
231
Q

where is progesterone secreted from?

A

corpus luteal cells

232
Q

what are the roles of progesterone?

A
  • embeds a fertilised ovum and maintains pregnancy
  • encourages growth of the endometrial wall-allows rooting of ovum and forming of bed for its development
  • inhibits uterine contractions
  • increases viscosity of cervical mucus
  • promotes breast development
  • increases body temperature
  • inhibits GnRH release
233
Q

what cells secrete testosterone in the ovaries?

A

theca interna cells of ovary

234
Q

which cells of testis secrete estradiol?

A

sertoli cells of testis

235
Q

what are the 2 phases of the ovarian cycle and what days of the cycle do these include?

A
  • follicular-days 0-14

- luteal-14-28

236
Q

which tissues is aromatase present in?

A
  • gonads
    • vascualr endothelium
    • endometrium
    • skin
    • bone
    • brain
    • adipose tissue
    • placenta
237
Q

which hormone conversions is aromatase responsible for?

A

androstenedione—–>estrone

Testosterone———–>estradiol

238
Q

what does aromatase deficiency in peripheral tissues lead to and how does this differently affect females and males?

A
  • results in overproduction of testosterone
  • less oestrogen production
  • females: ambiguous genitalia
  • males: not enough oestrogen can affect skeletal growth and final height
239
Q

what is hypogonadism?

A

inability of testicles or ovaries to produce enough testosterone or oestrogen

240
Q

what are the 2 types of hypogonadism?

A
  • —>primary-due to defect at level of the gonad-ie testicles or ovaries
  • —->secondary-due to defect at level of pituitary or hypothalamus-causing reduced amplitude or pulsality of FSH/ LH or GnRH secretion
241
Q

what is the effect of oestrogen on LH/FSH in the follicular phase?

A

oestrogen has stimulatory effect on LH /FSH

242
Q

what is the effect of oestrogen in the luteal phase?

A

oestrogen inhibits LH and FSH in luteal phase

243
Q

what is the effect of progesterone in the luteal phase?

A

progesterone has inhibitory effect on pituitary LH and FSH secretion

244
Q

what happens to the corpus luteal cells is pregnancy occurs?

A

corpus luteum is maintained by HCG secreted by trophoblast

245
Q

what happens to the corpus luteum if there is no pregnancy?

A

corpus luteum is degenerated into corpus albicans-by luteolysis

246
Q

what is ovulation triggered by?

A
  • ovulation is triggered by rapid rise in oestradiol level

- positive feedback of oestradiol at pituitary and hypothalamus results in LH surge-causing ovulation

247
Q

what is the LH surge essential for in the menstrual cycle?

A

release of ovum and formation of corpus luteum

248
Q

in the luteal phase do oestrogen levels fall or rise again?

A

rise again

249
Q

what are the 2 types of adipose tissue?

A
  • white adipose tissue

- brown adipose tissue

250
Q

what is the structure of white adipose tissue?

A

-contains single large fat droplet, forces the nucleus to be squeezed into a thin rim at the periphery

251
Q

what are the functions of white adipose tissue?

A
  • lipid storage tissue

- has receptors for insulin, adrenaline and sex steroids-these can trigger lipolysis-breakdown of WAT to generate energy

252
Q

what is the structure of brown adipose tissue?

A

small lipid droplets and numerous-iron rich mitochondria giving the brown appearance

253
Q

what is the function of brown adipose tissue?

A
  • helps them survive cold temperatures-transfer energy from food into heat
  • may contribute to energy homeostasis in adults
254
Q

what does the ovarian cycle involve?

A

involves the growth of the ovum and follicle

255
Q

what does the uterine cycle involve?

A

involves breakdown and growth of the endometrial wall

256
Q

when are ghrelin levels high?

A

before a meal when stomach is empty

257
Q

when do ghrelin levels decrease?

A

shortly after eating when stomach is full

258
Q

what are the 3 stages of the uterine cycle and what days these include?

A
  • menses days 0-7
  • proliferative phase days 7-14
  • secretory phase days 14-28
259
Q

where does aromatisation usually occur?

A

reaction tends to occur in the peripheral fat of the body

260
Q

describe the hypothalamic -pituitary-testicular axis

A
  • hypothalamus releases GnRH
  • stimulates anterior pituitary to release LH and FSH from gonadotrophs
  • LH stimulates testes-Leydig cells to secrete testosterone
  • FSH stimulates sertoli cells-stimulating spermatogenesis and estrogen production
261
Q

what is an example of negative feedback in the hypothalamic-pituitary-testicular axis?

A

sertoli cells in testes (stimulated by FSH) release inhibition B to stop the release of FSH and LH (negative feedback loop)

262
Q

what is an example of negative feedback in the hypothalamic-pituitary-ovarian axis?

A

granulosa cells of the ovaries (stimulated by FSH)

release inhibition B to stop the release of FSH and LH-negative feedback loop

263
Q

what is the role of FSH in males?

A

stimulates spermatogenesis in sertoli cells

264
Q

what is the role pf FSH in females?

A

stimulates oogenesis in the granulosa cells

265
Q

what are eicosanoids (FA derived hormones) made from?

A

arachidonic acid

266
Q

what are examples of eicosanoids?

A

prostaglandins

267
Q

what hormone types are hydrophobic?

A

steroid hormones

amino acid derived hormones

268
Q

which family of receptors do catecholamines bind to?

A

GPCR-specifically alpha and beta adrenergic receptors

269
Q

which hormone is hydrophilic?

A

peptide-mostly use receptors embedded in membrane

270
Q

which receptors do steroid hormones use?

A

nuclear/ intracellular

271
Q

what is adipose tissue?

A

-tissue deicated to lipid storage-safely stores fatty acids as triglycerides

272
Q

why are fatty acids an important energy molecule?

A
  • they undergo beta-oxidationo to produce acetyl CoA

- must be stored if not used as toxic in blood

273
Q

what is the difference between fasting and post-prandial phase?

A
  • fasting-triglyceride undergoes lipolysis to FAs and glycerol-produce ATP
  • post-prandial-ATP and glycerol undergo lipogenesis to form triglyceride to store
274
Q

what are the 4 important adipose tissue regulators?

A
  • Adiponectin
  • Leptin
  • Ghrelin
  • Insulin
275
Q

where is adiponectin released from and where does it bind to?

A

released from: adipose tissue

binds to:

  • ADIPOR1-skeletal muscle
  • ADIPOR2-liver
276
Q

where is leptin released from and where does it bind to?

A

released from: adipose tissue

binds to: hypothalamus

277
Q

where is ghrelin released from and where does it bind to?

A

released from: stomach

binds to: hypothalamus
NPY and AgRP receptors

278
Q

insulin is released from beta cells of pancreas, where does it bind to?

A

hypothalamic arcuate nucleus

-GLUT receptors

279
Q

what is the function of adiponectin?

A
  • enhances cells sensitivity to insulin
  • makes it easier to uptake glucose
  • good marker for whether or not someone has developed insulin resistance
280
Q

what is the function of leptin?

A
  • anorexigenic hormone-released after you eat high fat food-tells you to stop eating by binding to hypothalamus-activate thyroid and HPO axis
  • increases lipolysis
281
Q

what would a mutation in leptin gene cause?

A

hyperphagia- overeating

282
Q

what is the function of ghrelin?

A

orexigenic hormone-hunger hormone

  • binds to NPY and AgRP receptors in hypothalamus to stimulate you to eat and store fat you eat in meals
  • increased lipogenesis
283
Q

what is released after eating to stimulate insulin?

A

Glucagon-like peptide 1

284
Q

what type of hormone is insulin in eating?

A

anorexigenic hormone-binds to arcuate nucleus in hypothalamus and promotes glucose storage

285
Q

what is the hypothalamic arcuate nucleus (ARC)?

A

an area of the hypothalamus that is key for regulation of appetite

286
Q

what 2 peptide types does ARC express?

A
  • orexigenic-NYP and AgRP-encourages eating (ghrelin binds)

- anorexigenic-POMC-discourages eating

287
Q

which other nuclei in the hypothalamus does ARC work with?

A
  • ventromedial nucleus-satiety centre
  • -stimulation decreases eating
  • -lesion or disease results in overeating
  • dorsomedial nucleus
  • paraventricular nucleus
288
Q

what are the roles of androgens in males and females?

A

released from zona r. of adrenal gland-used to make testosterone and oestrogens (precursor to sex cells)

289
Q

what are the effects of angiotensin II?

A
  • aldosterone production
  • stimulates ADH release-increases BP
  • arterial vasoconstriction-increases BP (binds to AT-R receptor on vascular endothelium)
  • degrades bradykinin
290
Q

how does bradykinin cause vasoconstriction?

A
  • bradykinin synthesises nitric oxide-NO
  • NO is vasodilator
  • ACE degrades bradykinin
  • so less vasodilation-more vasoconstriction
291
Q

where do all female estrogens come from after menopause?

A

the conversion of adrenal androgens

292
Q

what is Addison’s disease caused by?

A

autoimmune disease that attacks the adrenal cortex (primary adrenal insufficiency)

293
Q

How does Addison’s disease cause hyperpigmentation?

A
  • low cortisol triggers release of ACTH
  • excess ACTH binds to melanocytes
  • stimulates melanocytes to secrete melanin
294
Q

why does secondary adrenal insufficiency not cause hyperpigmentation?

A

the secretion of ACTH is not increased

295
Q

what is tertiary hypothyroidism?

A

insufficient TRH production form hypothalamus

296
Q

how is vitamin D synthesised?

A
  • UV converts 7-dehydroxycholestrol to vit D in keratinocytes in skin (lipid soluble as steroid)
  • can be absorbed in GI tract via dietary sources
297
Q

what are the effects of vitamin D?

A

in liver:

  • vit D is converted to calcidiol via 25-hydroxylase
  • calcidiol is converted to active calcitriol in the kidney-stimulated by PTH
  • vit D increases osteoclast activity and increases osteoclast uptake from GI tract
298
Q

what is the stimulator and inhibitor of calcitonin?

A
  • stimulus= high Ca+

- inhibitor= low Ca+

299
Q

what type of hormone is calcitonin?

A

peptide

300
Q

what is calcitonins, PTH receptor type?

A

GCPR

301
Q

what is T3/T4 receptor type?

A

nuclear

302
Q

what is Vit D receptor type?

A

nuclear

303
Q

what is the stimulus and inhibitor of GH?

A

stimuli

  • hypoglycaemia
  • low FAs
  • high aas
  • ghrelin

inhibitor
-somatostatin

304
Q

what is the stimulus and inhibitor of ACTH?

A

stimuli

  • stress
  • low glucose

inhibitor
-cortisol

305
Q

what is the stimulus and inhibitor of TSH?

A

stimuli
-low T3/ T4

inhibitor

  • T3
  • T4
306
Q

what is the stimulus and inhibitor of LH/FSH?

A

stimulus
-oestrogens

inhibitors

  • oestrogen
  • progesterone
307
Q

what are is the stimulus and inhibitor of prolactin?

A

stimuli

  • low dopamine prior to menses
  • baby sucking on nipple

inhibitor
-dopamine

308
Q

what is the stimulus and inhibitor of oxytocin?

A

stimuli
-uterine stretching during labour

inhibitor
-catecholamines

309
Q

what is the stimulus and inhibitor of vasopressin?

A

stimuli
-osmoreceptors in the hypothalamus detect high blood osmolarity-low water levels

inhibitor

  • alcohol
  • low blood osmolality-high water levels
310
Q

what are the locations of GLUT1?

A

brain
RBCs
placenta
fetal tissue

311
Q

what are the locations of GLUT2?

A

liver
kidney
intestine
beta cells

312
Q

what is the location of GLUT 3?

A

brain

313
Q

what are the locations of GLUT 4?

A

muscles and adipose tissue

314
Q

what are the locations of GLUT 5?

A

jejunum

315
Q

describe the mechanism of GLUT 2

A
  • glucokinase sites become occupied with glucose=converting glucose to glucose-6-phosphate
  • increase in glucose-6-phosphate and insulin action leads to build up of glycogen stores in liver
  • this glycogen can be released as glucose when blood glucose levels are low
  • inulin accelerates uptake of glucose not necessary
316
Q

describe the mechanism of GLUT4

A

1-insulin binds to tyrosine kinase receptor
2-triggers protein kinase cascade
3-glut4 transporters travel to cell surface membrane by exocytosis
4-glucose enters cell

adipose-glucose to FAs
muscle and liver-glucose to glycogen

317
Q

what are SDGLTS?

A

sodium dependent glucose transporters
-contribute to renal glucose absorption

-found in small intestine and proximal tubule of nephron

318
Q

what do pancreatic polypeptide cells do?

A

inhibit secretion of spomatostatin

319
Q

how do beta cells work?

A
  • glucose enters cell via GLUT2
  • glucose to glucose-6-phosphate via glucokinase
  • G6P stimulates glycolysis to produce ATP
  • ATP sensitive K+ channels close
  • K+ builds up in cell-change in potential differnece causes V.G. Ca2+ channels to open
  • increased calcium induces secretion of insulin

Medicine yr1 (55 decks)

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