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Physiology > Endocrine 4 > Flashcards

Endocrine 4 Flashcards

1
Q

Where are the adrenal glands located?

A

Embedded above each kidney in a capsule of fat

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2
Q

What are the divisions of the adrenals?

A

Cortex and medulla

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3
Q

What does the adrenal cortex (outer) have a similar origin to?

A

Gonads

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4
Q

What does the adrenal cortex produce? (adrenal steroids)

A 
Mineralocorticoids (outer gland)
– aldosterone
• Glucocorticoids (middle gland)
– cortisol (corticosterone)
• Androgen sex steroids (inner gland)
– DHEA (dehydroepiandrosterone)
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5
Q

What is the adrenal medulla (inner) composed of?

A

Chromaffin cells

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6
Q

Where does the adrenal medulla originate from?

A

Sympathetic nervous system

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7
Q

What does the adrenal medulla produce?

A

Catecholamines
– epinephrine (adrenaline)
– norepinephrine (noradrenaline)

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8
Q

What are the 3 layers / zones that the adrenal cortex consists of?

A
  • Zona glomerulosa – outermost layer
  • Zona fasciculata – middle and largest portion
  • Zona reticularis – innermost zone
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9
Q

What are the categories of adrenal steroids?

A
  • Mineralocorticoids
  • Glucocorticoids
  • Sex hormones
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10
Q

Mineralocorticoids, role and main one

A

– Mainly aldosterone

– Influence mineral balance, specifically Na+ and K+ balance

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11
Q

Glucocorticoids, main one and role

A

– Primarily cortisol

– Major role in glucose metabolism as well as in protein and lipid metabolism

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12
Q

What are the sex hormones of the adrenal cortex similar to?

A

To those produced by gonads

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13
Q

What is the most abundant and physiologically important sex hormone produced by adrenal cortex?

A

Dehydroepiandosterone (male “sex” hormone)

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14
Q

What is aldosterone?

A

A major mineralocorticoid

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15
Q

What does aldosterone maintain?

A

electrolyte balance

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16
Q

Aldosterone feedback

A
  1. low plasma Na++ or high K+
  2. activates renin-angiotensin system
  3. Angiotensin II increases aldosterone release from adrenal glands
  4. acts on distal renal tubules
    • increase Na++ & water retention
    • increase excretion of K+ & H+ ions
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17
Q

What is cortisol (hydrocortisone)?

A

A major glucocorticoid in humans

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18
Q

Cortisol secretion rhythm regulation

A

Diurnal rhythm

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19
Q

Cortisol function

A 
– plays role in stress
– increase blood glucose
– increase blood fatty acids
– control water and electrolyte balance
– anti-inflammatory/immunosuppressive
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20
Q

Cortisol feedback

A

negative feedback on hypothalamus (CRH) & anterior pituitary (ACTH)

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21
Q

Release of ACTH

A

Hypothalamus neurons CRF (41aa peptide) → anterior pituitary
ACTH → adrenal cortex corticosteriods

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22
Q

What does the adrenal cortex (sex h)

A

Both male and female sex hormones in both sexes

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23
Q

Dehydroepiandrosterone (DHEA)

A

The only adrenal sex hormone that has any biological importance

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24
Q

What is dehydroepiandrosterone (DHEA) overpowered by?

A

By testicular testosterone in males

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25
Q

What does DHEA govern in femailes

A

– Growth of pubic and axillary hair
– Enhancement of pubertal growth spurt
– Development and maintenance of female sex drive

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26
Q

Epinepherine and Norepinerphrine primary stimulius

A

Activation of sympathetic nervous system by stress

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27
Q

Where is Epinephrine / Adrenaline secreted?

A

Into blood

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28
Q

Where is Epinephrine / Adrenaline secreted?

A

Into blood

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28
Q

Where is Epinephrine / Adrenaline secreted?

A

Into blood

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29
Q

Funciton of Epinephrine / Adrenaline x 4

A

– “fight-or-flight” responses
– Maintenance of arterial blood pressure
– Increases blood glucose
– Increases fat metabolism (increase blood fatty acids)

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30
Q

Glucocorticoids x 4

A

hydrocortisone, prednisolone, dexamethasone, betamethasone

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31
Q

Glucocorticoids clinical

A

Replacement therapy: in adrenal failure (Addison’s disease)

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32
Q

Anti-inflammatory/immunosuppressive disorders ‘chemical’ treatment

A

Reduce T cell proliferation, release of IL-2, TNF-a, IL-1

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33
Q

Anti-inflammatory/immunosuppressive disorders x 6

A

– asthma (inhaler)
– eczema (topical cream)
– arthritis (systemic injections)
– ulcerative colitis (rectal suppositories)
– prevent graft rejection of the transplant
– cancer patients (anti-emetic; reduce oedema in brain tumours)

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34
Q

Benefit vs glucocorticoid use

A

Benefit > Risk of glucocorticoid use

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35
Q

Risk of glucocorticoid use x 4

A

– Immune system limited (delay tissue repair, gastric/peptic ulcers)
– Cushing’s symptoms
– Osteoporosis (alter function of bone cells osteoblasts/osteoclasts)
– Adrenal insufficiency due to sudden withdraw

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36
Q

What activity does fludrocortisone have?

A

Glucocorticoid and mineralocorticoid activity

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37
Q

How is fludrocortisone used as a treatment?

A

Used in mineralocorticoid replacement therapy (eg) in Addison’s disease.

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38
Q

What are the 3 major targets of mineralocorticoids?

A

Kidneys, bladder and colon

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39
Q

Addison’s disease hormone levels

A

Low glucocorticoid (cortisol) & mineralocorticoid (aldosterone)

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40
Q

Cause of primary Addison’s disease

A

Damage adrenal gland (TB or autoimmunity)

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41
Q

Cause of secondary Addison’s disease

A

Low ACTH release

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42
Q

Symptoms of Addison’s disease

A
  • hypoglycaemia
  • decreased liver glycogen
  • fatigue, anorexia, nausea, weight loss, dizziness, hypotension, psychiatric
  • death if untreated
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43
Q

Treatment for Addison’s disease

A

Steroid replacement therapy

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44
Q

Cushing’s disease hormone levels

A

Excess glucocorticoids (cortisol)

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45
Q

Cause of Cushing’s disease

A

ACTH secreting tumor in pituitary

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46
Q

Symptoms of Cushing’s disease

A
  • hyperglycemia
  • elevated blood pressure
  • obesity (abdominal fat, thin arms & legs)
  • muscle wasting, osteoporosis, cataracts
  • poor wound healing
  • buffalo hump, moon face, red cheeks
  • psychiatric symptoms (depression, euphoria, hallucinations)
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47
Q

Treatment for Cushing’s disease

A
  • remove tumor
  • antiglucocorticoids
  • surgical adrenalectomy
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48
Q

Hyperplastic of adrenal cortex image

A
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49
Q

Conn’s syndrome hormone levels

A

Excessive mineralocortocoids (aldosterone)

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50
Q

Primary Conn’s syndrome cause

A

tumour

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51
Q

Secondary Conn’s syndrome cause

A

Excessive renin-angiotensin action in kidney disease, cirrhosis of liver, congestive heart failure

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52
Q

Symptoms of Conn’s syndrome

A
  • sodium and water retention

* increase in extracellular fluid and hypertension

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53
Q

Treatment for Conn’s syndrome

A
  • antagonist of aldosterone (spirono-lactone)

* unilateral adrenalectomy

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54
Q

generalised stress response LEARN

A
  • ↑ epinephrine secretion from adrenal medulla (chromaffin cells)
  • ↑ CRH-ACTH-cortisol (HPA axis) that mobilises metabolic resources
  • ↓ insulin & ↑ glucagon secretion to raise blood glucose & fatty acids
  • ↑ renin-angiotensin-aldosterone system & vasopressin secretion to maintain blood volume and blood pressure
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55
Q

What does chronic stress cause?

A

Causes heart disease, hypertension, atherosclerosis, immune-suppression

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56
Q

What does prolonged release of CRH cause?

A

Anxiety & depression

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57
Q

What may CRF1 receptor antagonists treat?

A

Anxiety, depression, drug dependence and irritable bowel syndrome

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58
Q

Stress response from hypothalamus diagram

A
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59
Q

Cortisol feedback

A
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60
Q

Main glucocorticoids

A

Cortisol

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61
Q

Upstream hormones of cortisol

A

Adreno-corticotropic Hormone (ACTH)

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62
Q

Hypersecretion of cortisol causes

A

Cushing’s disease (high glucocorticoids)

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63
Q

Hyposecretion of cortisol causes

A

Addison’s disease

low corticoids

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64
Q

Main mineralocorticoids

A

Aldosterone

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65
Q

Upstream hormones of Aldosterone

A

Angiotensin II

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66
Q

Hypersecretion of aldosterone causes…

A

Conn’s Syndrome (high mineralocortocoids)

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67
Q

Hyposecretion of aldosterone causes…

A

Addison’s disease (low corticoids)

68
Q

Hyposecretion of aldosterone causes…

A

Addison’s disease (low corticoids)

69
Q

Fed state

A

Store amino acids, glucose and triglycerides

70
Q

Hungary state

A

Mobilise stored reserves

71
Q

Tissue to breakdown in blood diagram

A
72
Q

Glycogenesis reaction

A

Glucose → glycogen

73
Q

Glycogenolysis reaction

A

Glycogen → glucose

74
Q

Gluconeogenesis reaction

A

Amino acids → glucose

75
Q

Protein synthesis reaction

A

Amino acids → protein

76
Q

Protein degradation

A

Protein → amino acids

77
Q

Fat synthesis (Lipogenesis or Triglyceride synthesis)

A

Fatty acids and glycerol → triglycerides

78
Q

Fat breakdown (Lipolysis or Triglyceride degradation)

A

Triglycerides → fatty acids and glycerol

79
Q

Blood consequence of glycogenesis

A

↓ blood glucose

80
Q

Blood consequence of protein synthesis

A

↓ Blood amino acids

81
Q

Blood consequence of fat synthesis

A

↓ Blood fatty acids

82
Q

Blood consequence of glycogenolysis

A

↑ Blood glucose

83
Q

Blood consequence gluconeogenesis

A

↑ Blood glucose

84
Q

Blood consequence of protein degradation

A

↑ Blood amino acids

85
Q

Blood consequence of fat breakdown

A

↑ Blood fatty acids

86
Q

Anabolism defn

A

Build up or synthesis of larger organic macromolecules from small organic subunits

87
Q

Anabolism require..

A

ATP

88
Q

Anabolism results in…

A
  • Manufacture of materials needed by the cell
  • Storage of excess ingested nutrients not immediately needed for energy production or needed as cellular building blocks
89
Q

Catabolism defn

A

Breakdown or degradation of large energy rich organic molecules within cells

90
Q

The two levels of catalytic breakdown are ….

A
  • Hydrolysis of large cellular molecules into smaller subunits
  • Oxidation of smaller subunits to yield energy for ATP production
91
Q

Summary of the major pathways involving organic nutrient molecules diagram

A
92
Q

Where does most interconversion of organic molecules occur?

A

In the liver

93
Q

What happens to excess circulating glucose?

A
  • Stored in liver and muscle as glycogen
  • Once liver and muscle stores are “filled up”, additional glucose is transformed into fatty acids and glycerol and stored in adipose tissue
94
Q

What happens to excess circulating fatty acids?

A

Becomes incorporated into triglycerides

95
Q

What happens to excess circulating amino acids?

A

Converted to glucose and fatty acids

96
Q

What is the circulating form of carbohydrate?

A

Glucose

97
Q

What is the circulating form of fat?

A

Free fatty acids

98
Q

What is the circulating form of protein?

A

Amino acids

99
Q

What is the storage from of carbohydrate?

A

Glycogen

100
Q

What is the storage from of fat?

A

Truglycerides

101
Q

What is the storage from of protein?

A

Body proteins

102
Q

What is the major storage site of carbohydrate?

A

Liver, muscle

103
Q

What is the major storage site of fat?

A

Adipose tissue

104
Q

What is the major storage site of protein?

A

Muscle

105
Q

Carbohydrate percentage of total body energy content

A

1%

106
Q

Fat percentage of total body energy content

A

77%

107
Q

Protein percentage of total body energy content

A

22%

108
Q

Reservoir capacity of carbohydrate

A

Less than a day’s worth of energy

109
Q

Reservoir capacity of fat

A

About two months’ worth of energy

110
Q

Reservoir capacity of protein

A

Death results long before capacity is fully used because of structural and functional impairment

111
Q

Role of carbohydrate

A

First energy source, essential for brain

112
Q

Role of fat

A

Primary energy reservoir, energy source during a fast

113
Q

Role of protein

A

Source of glucose for the brain during a fast; last resort to meet other energy needs

114
Q

Role of liver in metabolic states

A
  • Primary role in maintaining normal blood glucose levels

- Principal site for metabolic interconversions such as gluconeogenesis

115
Q

Role of adipose tissue in metabolic states

A
  • Primary energy storage site

- Important in regulating fatty acid levels in the blood

116
Q

Role of muscle in metabolic states

A

Muscle

  • Primary site of amino acid storage
  • Major energy user
117
Q

Role of brain in metabolic states

A
  • Normal can only use glucose as an energy source
  • Does not store glycogen
    Mandatory blood glucose levels be maintained
118
Q

Factors that increase blood glucose

A
  • Glucose absorption from digestive tract
  • Hepatic glucose production; Through glycogenolysis and
    gluconeogenesis
119
Q

Factors that decrease blood glucose

A
  • Transport of glucose into cells: for utilisation for energy production and for storage as glycogen through glycogenesis and as triglycerides.
  • Urinary excretion of glucose
120
Q

Hormones regulating metabolism

A
  • Anterior Pituitary gland
  • Growth hormone, ACTH, TSH
  • Liver
  • Somatomedins (IGF’s)
  • Thyroid gland (T3 T4 )
  • Thyroxine
  • Gonads
  • Sex steroids
  • Adrenal cortex
  • Glucocorticoids (cortisol)
  • Adrenal medulla
  • adrenaline (noradrenaline)
  • Pancreatic (Islets of Langerhans)
  • Insulin & glucagon
121
Q

What do exocrine cells of islets of langerhans secrete?

A

Proteases into small intestine

122
Q

How much of pancrease does the endocrine Islet of Langerhans comprise?

A

1%

123
Q

What is the endocrine Islet of Langerhans surrounded by?

A

Capsule

124
Q

Where are endocrine Islet of Langerhans located?

A

Scattered throughout pancreas

125
Q

Endocrine Islet of Langerhans blood supply function

A

Rich blood supply for hormone drainage

126
Q

Endocrine Islet of Langerhans composition

A

Clusters composed ~3000 endocrine secretory cells

127
Q

What does pancreas removal cause

A

Symptoms of diabetes

↑[glucose]plasma 20-30mM

128
Q

Location and structure of the pancreas diagram

A
129
Q

Cell types in the islets of Langerhans diagram

A
130
Q

3 secretory cells of islets of Langerhans

A

─ β cells
─ α cells
─ δ cells

131
Q

What do the secretory cells of islets of Langerhans produce?

A

peptide hormones

132
Q

Beta cells function

A

Insulin production - promotes glucose uptake

133
Q

Alpha cells function

A

Glucagon production - opposite effect to insulin

134
Q

Delta cells function

A

Somatostatin production -

potentiates glycogen breakdown activity of glucagon

135
Q

Where is insulin stored and secreted from?

A

Cytoplasmic granules

136
Q

Insulin fed state

A

Anabolic hormone

137
Q

Insulin in fed state effects

A
  • Glucose to glycogen
  • Fatty acids to triglycerides
  • Amino acid to protein
138
Q

‘Organ’ effects of insulin

A
  • ↓ glucose, amino acid and fatty acid in blood
  • ↑ glucose, amino acid and fatty acid uptake in muscle
  • ↓ breakdown of glycogen, fat (triglycerides) and protein
139
Q

Glucagon in hungry state

A

Catabolic hormone

140
Q

Effects of glucagon

A
  • Glycogen to glucose
  • Triglycerides to fatty acids
  • Protein to amino acid
141
Q

Effects of glucagon in blood

A
  • ↑ glucose, amino acid and fatty acid in blood
  • ↓ glucose, amino acid and fatty acid uptake in muscle
  • ↑ breakdown of glycogen, fat (triglycerides) and protein
142
Q

glycogenolysis/lytic

A

glycogen breakdown

143
Q

gluconeogenesis

A

glucose synthesis

144
Q

gluconeogenesis

A

glucose synthesis

145
Q

lipolysis

A

lipid/fat breakdown

146
Q

lipogenesis

A

Lipid/fat synthesis

147
Q

What is insulin synthesised as?

A

Prohormone

148
Q

What is insulin cleaved to?

A

Mature peptide

149
Q

Half life of insulin and glucagon

A

I - t1/2 = 30 minutes

G - t1/2 = 10 minutes

150
Q

Stimulation of insulin secretion by glucose via excitation secretion couplinf

A
  1. Glucose enters Beta cells by diffusion via GLUT- 2. Glucose is phosphorylated to glucose-6-phosphate.
  2. Oxidation of glucose-6-phosphate produces ATP.
  3. ATP acts on ATP-sensitive K+ channels, closing it.
  4. Reduced exit of K+ depolarises membrane.
  5. Depolarisation opens voltage-gated Ca2+ channels.
  6. Ca2+ enters Beta cell.
  7. Ca2+ triggers exocytosis of insulin vesicles.
  8. Insulin is secreted
151
Q

Factors controlling insulin secretion

A
152
Q

What is the most common of all endocrine disorders?

A

Diabetes Mellitus

153
Q

Most prominent feature of Diabetes Mellitus?

A

Hyperglycemia

154
Q

What is hyperglycemia

A

Elevated blood sugar

155
Q

What is the only hormones capable of lowering blood sugar

A

Insulin

156
Q

2 varients of Diabetes Mellitus

A

Type 1 Diabetes and Type 2 Diabetes

157
Q

Diabetes word meaning

A

“siphon” or “running through” – reference to the large urine volume accompanying this condition

158
Q

Mellitus work meaning

A

“sweet” – acquires its sweetness from secretion of excess glucose in this condition

159
Q

x 6 points about Type 1 diabetes

A
  • Symptoms develop rapidly
  • Childhood onset
  • Affects 10-20% diabetics
  • Loss of b cell function
  • Insulin secretion none/low
  • Insulin injections for treatment
160
Q

x 6 points about Type 2 diabetes

A
  • Symptoms develop slowly
  • Adulthood onset
  • Affects 80-90% diabetics
  • Insulin insensitivity
  • Insulin secretion normal/high
  • Treatment - diet/exercise and oral drugs
161
Q

4 effects of severe diabetes

A
  1. Excessive eating
  2. Dehydration and thirst
  3. Coma
  4. Brain cells are glucose obligate cells
162
Q

Excessive eating in severe diabetes

A
  • Cells starved of carbohydrate

- Hypothalamic center leads to excessive eating

163
Q

Dehydration and thirst in severe diabetes

A
  • Low glucose uptake, blood glucose rises
  • Glucose appears in urine, increases urinary vol
  • Dehydration and thirst
164
Q

Coma in severe diabetes

A
  • Cells unable to use glucose increases
  • Lipolysis generates fatty acids and ketoacids
  • Ketoacids lower blood pH
  • Decreased brain O2 and coma
165
Q

Brain cells are glucose obligate cells in severe diabetes

A
  • Low glucose, brain stops working

- Coma and respiratory paralysis

166
Q

Glucose tolerance test chart

A
167
Q

Counteracting actions of glucagon and
Insulin on blood glucose during absorption
of a high protein meal. diagram

A
168
Q

slide

A

42 finish it lol

Physiology (28 decks)

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