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CBL Year 1 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

When does concentration of metabolites need to be altered rapidly

A

increase in rate of glycolysis during exercise
Reduce rate of glycolysis after exercise
Increase rate of gluconeogenesis after exercise

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2
Q

What is Km

A

Michealis constant

substrate concentration at which half the enzyme molecules are associated with the substrate

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3
Q

What tissue are GLUT1 transporters in and what Km do they need

A

red blood cells and some other tissues 3mM

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4
Q

What tissues are GLUT2 transporters in and what Km do they need

A

Liver, pancreas 17mM

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5
Q

What tissue is GLUT3 transporters in and what Km do they need

A

brain, 1.4mM

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6
Q

What tissues are GLUT4 transporters in and what Km do they need

A

muscle and adipose tissues, 5mM

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7
Q

Why is glucose absorption through GLUT3 always constant

A

because the brain need fuel, low Km allows their to be a constant flow unless starved

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8
Q

What happens when glucose gets into the cell

A

it is phosphorylated into glucose-6-phosphate by hexokinase or glucokinase

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9
Q

Differences and similarities between nervous system and endocrine system

A

nervous system releases neurotransmitters to local areas whereas endocrine system releases hormones into the bloodstream to target organs
Both are directly connected by the hypothalamus and pituitary

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10
Q

What is signal transduction

A

process of converting one type of signal into another

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11
Q

Four types of signals?

A

neuronal, contact-dependent signalling, paracrine, endocrine

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12
Q

Describe neuronal signalling

A

action potentials are transmitted electrically along a nerve axon, when the signal reaches the nerve terminal it causes a release of neurotransmitters onto adjacent cells

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13
Q

Describe contact-dependent signalling

A

cell-surface-bound signal molecule binds to a receptor protein on an adjacent cell. no molecules are released
(A communicating junction links the intracellular compartments of two adjacent cells, allowing transit of relatively small molecules.)

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14
Q

Paracrine

A

signals are released by cells in the extracellular fluid in their neighbourhood and act as local mediators

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15
Q

Endocrine

A

hormones are secreted into the bloodstream and are widely distributed throughout the body

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16
Q

Describe cell surface receptors

A

extracellular molecules are usually large and hydrophilic (peptides and proteins) so they cannot cross the plasma membrane
therefore they bind to cell surface receptors which generate intracellular secondary messenger signalling molecules
(most common type of receptor)

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17
Q

Describe intracellular receptors

A

some small extracellular hydrophobic molecules can pass through target cells plasma membrane and bind to the intracellular receptors in the cytosol or nucleus than then regulate things such as gene transcription

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18
Q

True/false: cells can receive and respond to many signals simultaneously

A

true

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19
Q

What is apoptosis

A

cell programmed death

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20
Q

What are processes that rely on altered protein function and how fast are they

A

movement, secretion and metabolism

fast (

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21
Q

What are processes that rely on altered protein synthesis and how fast are they

A

differentiation, growth and division

slow (minutes to hours)

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22
Q

Three types of effector proteins

A 
metabolic enzyme (alters metabolism)
cytoskeletal protein (alters cell shape or movement)
transcription regulator (alters gene expression)
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23
Q

What are the three main types of cell surface receptors

A

ion channel coupled receptors
G protein coupled receptors
enzyme coupled receptors

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24
Q

What is another name for ion channel coupled receptors

A

transmitter-gated ion channels

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25
Q

Describe an ion channel coupled receptor

A 
they are responsible for transmission of signals across synapses in the nervous system
signal molecules (such as acetylcholine) cause the receptors to open in response to binding , causing a change in the electrical potential across the cell membrane
so a chemical signal is transduced (converted into another form) into a electrical signal
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26
Q

Describe G protein coupled receptors

A

they are transmembrane proteins
the extracellular portion of the GPCR bind to signalling molecules
cytoplasmic portion binds to the G protein

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27
Q

What are the two most common enzyme targets of G protein coupled receptors

A

adenylyl cyclase and phospholipase C

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28
Q

What does adenylyl cyclase do (in related to GPCRs)

A

catalyses the formation of the secondary messenger signalling molecule cAMP

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29
Q

What does phospholipase C do (in relation to GCPRs)

A

produces the second messengers inositol triphosphate (IP3) and diacylglycerol (DAG)

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30
Q

What does inositol triphosphate do

A

promotes the accumulation of cytosolic Ca2+ (calcium ions) which is another common second messenger

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31
Q

What is the effect of adrenaline on skeletal muscle

A

Adrenaline activates a GPCR which activated a G protein that activates adenylyl cyclase which produces cAMP (a secondary messenger)
increase in cAMP activates protein kinase A (PKA) which phosphorylates and activates phosphorylase kinase
this activates glycogen phosphorylase (enzyme that breaks down glycogen)
This all occurs within seconds

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32
Q

What are the thyroid glands lateral lobes connected by

A

the isthmus

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33
Q

What does the thyroid gland form the floor of

A

the pharynx

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34
Q

Where are the parathyroid glands located

A

behind the lateral lobes of the thyroid gland
four glands (two superior and two inferior)
approximate diameter of 12mm each

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35
Q

Where does T3 and T4 synthesis occur (thyroxine)

A

in the thyroid follices

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36
Q

Describe T3 and T4 synthesis

A

Thyroglobulin (precursor for T3 and T4) is produced by thyroid follicular cells
iodine is actively absorbed from bloodstream by iodine trapping (sodium is co-transported with iodine from basolateral side of membrane into the cell and is then concentrated in the follicular cells by about 30 times)
through reaction with enzyme called thyroperoxidase, tyrosine is bound to thyroglobulin to form monoiodotyrosine (MIT) and diiodotyrosine (DIT)
linking two moieties of DIT produce T4 and one MIT and one DIT produce T3

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37
Q

Describe dietary intake of iodine

A

absorbed first into the extracellular pool
then removed from their by the thyroid or kidneys
thyroid contains huge iodine store in colloid

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38
Q

Describe cretinism (Congenital iodine deficiency syndrome)

A

neurological deficits
small stature and immature appearances
puffy face and hands
delayed puberty

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39
Q

What is hypothyroidism, describe it in adulthood

A 
under active thyroid gland
insidious onset (very gradual)
low BMR and cold sensitivity
bradycardia
slow, hoarse voice
lethargy and slow movements
constipation
menstrual abnormalities
one weight gain
dry thickened skin
slowing of mental function
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40
Q

What is hyperthyroidism, describe it

A

over active thyroid gland
nervousness, restlessness, tremors or anxiety
tachycardia and palpitations
Increased appetite but associated with weight loss
tiredness
increased number of bowel movements per day
decreases menstruation
most common type is Graves disease with characteristic eye signs (bulging eyes, redness and retracting eyelids)

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41
Q

what are the biological roles of calcium

A

blood coagulation
neuromuscular excitability, neurotransmitter release and hormone secretion
membrane ion transport (and permeability to sodium ions)and second messenger functions
enzyme regulations
contraction (including skeletal and cardiac muscle)

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42
Q

what three hormones is plasma calcium concentration precisely controlled by

A

parathyroid hormone (PTH) (counter-regulatory hormone)
calcitonin (Counter-regulatory hormone)
vitamin D

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43
Q

What do counter regulatory hormones do? what does this mean in the examples of PTH and calcitonin

A

any deviations have considerable impact with severe consequences
hypercalcaemia (high calcium levels) trigger the release of calcitonin
Hypocalcamia (low calcium levels) trigger the release of PTH

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44
Q

If calcium levels decrease in the blood plasma then what happens

A

increase in parathyroid gland (chief cells)

which then increase the levels of PTH which then increase the levels of calcium

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45
Q

If calcium levels rise too much in the blood plasma then what happens

A

increase in thyroid parafollicular C cells

which increase calcitonin release which decreases the levels of calcium

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46
Q

What hormone regulates the calcium homeostasis minute by minute and what hormone is more in case of emergency

A

minute by minute is PTH

emergency is calcitonin

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47
Q

What is hypocalcaemia caused by and what are some symptoms

A

caused by hypoparathyroidism following accidental removal or damage to parathyroid glands during thyroid surgery
symptoms include: increased neuromuscular excitability, twitching, muscle cramps, tetany, carpopedal spasm, coma and death

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48
Q

What is hypercalcaemia associated with and what are some symptoms

A

with primary hyperparathyroidism and malignancy
symptoms of stones, bones and groans
slowing of nerve impulses, sluggish reflexes and muscle weakness, mood and cognitive dysfunctions may also see polydipsia and polyuria
in extreme cases can cause neurotoxicity, coma and death

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49
Q

What is a PCHR (personal child health record) used for

A 
family and birth related information
routine screening
immunisations
growth
advice and support
early education
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50
Q

Three factors that influence growth

A

nutrition
genetics
environment

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51
Q

Difference between hypertrophy and hyperplasia

A 
hypertrophy = increase is size of cells
hyperplasia = increase in number of cells
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52
Q

What is GHRH, describe it

A

growth hormone releasing hormone
Produced in the hypothalamus and secreted from nerve endings into the portal system
is an anterior pituitary peptide hormone
can cause growth in most tissues that grow, promotes differentiation of some cell types
binds to GH receptors in target tissues
works often in combination with insulin-like-growth-factor-1 (IGF-1)

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53
Q

Describe growth hormone (GH) secretion

A 
it is periodic - think circadian rhythms 
things that promote secretion:
sleep
acute stress
hypoglycaemia
exercise
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54
Q

Metabolic actions of the growth hormone

A 
increase in amino acid uptake
increase in protein synthesis
decrease in protein catabolism
decrease in lipogenesis 
increase in lipolysis
decrease in glucose uptake and oxidation
increase in blood glucose (stimulate gluconeogeneis and glycogenolysis)
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55
Q

what does endocrine mean? exocrine?

A

endo- internal secretion, secrete hormones directly into bloodstream upon stimulation
exo- secrete into glands (Such as salivary glands, sweat glands, and glands of GI tract)

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56
Q

Describe the three distinct types of endocrine tissue

A

1) endocrine organ devoted to hormone synthesis
2) distinct clusters of cells within an organ
3) individual cells scattered diffusely throughout an organ

57
Q

Name two major endocrine organs that are NOT under pituitary control.

A

parathyroid gland and pancreas

58
Q

what type of hormones does the pituitary produce

A

releasing hormones and inhibiting factors

59
Q

What hormones does the posterior pituitary produce (endocrine)

A

arginine vasopressin (AVP), antidiuretic hormone (ADH) and oxytocin

60
Q

What hormones does the anterior pituitary produce (endocrine)

A 
adrenocorticotropic hormone (ACTH)
growth hormone
prolactin
follicle stimulating hormone (FSH)
Luteinising hormone (LH)
Thyroid stimulating hormone (TSH)
61
Q

What hormones does the thyroid gland produce (endocrine)

A

thyroxine T4, tri-iodothyronine T3, calcitonin

62
Q

What hormones does the parathyroid gland produce (endocrine)

A

parathyroid hormone (PTH)

63
Q

what hormones does the adrenal gland produce (endocrine)

A

adrenaline

cortisol

64
Q

what hormones does the pancreas produce (endocrine)

A

glucagon and insulin

65
Q

what hormones do the gonads produce (endocrine)

A

progesterone, oestrogen and testosterone

66
Q

What are the steroid hormones

A 
progestagens
glucocorticoids
mineralocorticoids
androgens
oestrogens
67
Q

What are the non-steroid hormone classes

A

polypeptide/protein (growth hormone, insulin, glucagon, PTH)
glycoproteins (FSH, LH, TSH and gonadotropins )
Eicosanoids (prostaglandins, leukotrienes)
Peptides (oxytocin, gonadotropin releasing hormones)
Amines (adrenaline, thyroxine, noradrenaline)

68
Q

What receptors do steroid hormones and non-steroid hormones use

A

steroid use intracellular receptors whereas non-steroid use cell surface receptors

69
Q

What is the hypothalamus-pituitary axis

A

interface between central nervous system and endocrine system

70
Q

What are the other names for the anterior and posterior pituitary gland

A

anterior is also called Adenohypophysis

posterior is called neurohypophysis

71
Q

Describe the posterior (neurohypophysis) lobe of the pituitary gland

A

under direct control

neural tissue comprises of axons and nerve terminal endings of the hypothalamic neurosecretory cells

72
Q

Describe the anterior (adenohypophysis) lobe of the pituitary gland

A

under indirect control
glandular tissue comprises of cells controlled by releasing hormones (or inhibitory factors) delivered by the hypophyseal portal system

73
Q

Mnemonic to remember layers of adrenal cortex from outermost to innermost

A

GFR (glomerular filtration rate)
zona glomerulosa
zona fasciculata
zona reticularis

74
Q

What class of hormones does the adrenal cortex produce

A

corticosteroids

75
Q

what class of hormones does the adrenal medulla produce

A

catecholamines

76
Q

What does the zonea glomerulosa of the adrenal cortex produce

A

aldosterone

77
Q

what does the zona fasciculata of the adrenal cortex prpduce

A

cortisol (and androgens)

78
Q

What does the zona reticularis of the adrenal cortex produce

A

androgens (and cortisol)

79
Q

What does the adrenal medulla produce (hormones)

A

adrenaline and noradrenaline

80
Q

What are adrenocortical hormones

A

they are all steroids (so all derived from cholesterol)

they are synthesised as required and not stored

81
Q

What is cortisol and what is it regulated by

A

it is a glucocorticoid

release is controlled by CRH and ACTH

82
Q

What are the three main sections of glucocorticoid actions

A 
metabolic (mobilisation of glucose in liver, stimulates catabolism of fats and proteins, increases plasma concentration of fatty acids glucose and amino acids)
Immune system (anti-inflammatory and immunosuppressive)
Cardiovascular (maintains blood volume, maintains vascular responsiveness to catecholamines)
83
Q

Give an example of how cortisol acts on metabolism (with low blood glucose)

A 
insulin decreases
glucagon increases
growth hormone increases 
cortisol increases
glucose from liver increases
release of fats from white fat and liver increases
fat oxidation (beta oxidation) for cellular respiration increases
hunger increases
84
Q

Give an example of how cortisol acts on there cardiovascular system

A

increases contractility
increases peripheral resistance
increases effects of noradrenaline and adrenaline
increases expression of androgenic receptors (specifically alpha 1)
increases number of angiotensin receptors

85
Q

Give an example of how cortisol acts on the immune system

A 
(anti-inflammatory and immunosuppressive) 
inhibits secretion of cytokines
inhibits histamine release (mast cells)
inhibits proliferation of immune cells
inhibits synthesis of antibodies
86
Q

What does the gonadotropin releasing hormone (GnRH) from the hypothalamus stimulate and where does it go

A

FSH and LH secretion from the anterior pituitary to the gonads

87
Q

What does the corticotropin releasing hormone (CRH) from the hypothalamus stimulate and where does it go

A

secretion of adrenocorticotropic releasing hormone (ACTH) from the anterior pituitary to the adrenal cortex to then produce cortisol

88
Q

what does the thyrotropin releasing hormone (TRH) from the hypothalamus stimulate and where does it go

A

secretion of thyroid stimulating hormone (TSH) from the anterior pituitary to the thyroid

89
Q

What does the prolactin releasing hormone (PRH) from the hypothalamus stimulate and where does it go

A

stimulation of prolactin from the anterior pituitary to the mammary glands

90
Q

what does dopamine from the hypothalamus stimulate and where does it go

A

inhibition of secretion of prolactin from the anterior pituitary to the mammary glands

91
Q

What does growth hormone releasing hormone (GHRH) from the hypothalamus stimulate and where does it go

A

stimulation of secretion of growth hormone (GH) from the anterior pituitary to the liver (and all body)

92
Q

What does somatostatin from the hypothalamus stimulate and where does it go

A

inhibition of secretion of the growth hormone from the anterior pituitary to the liver and rest of the body

93
Q

Where does ADH (or vasopressin) come from and where does it go

A

secreted from the posterior pituitary gland (stimulated by neurosecretory cells from the hypothalamus) to the kidney

94
Q

Where does oxytocin come from and where does it go

A

secreted from the posterior pituitary gland (stimulates by neurosecretory cells from the hypothalamus ) to the mammary glands

95
Q

Negative feedback (-) of cortisol and stressors (+)

A
  • : pituitary (short)
    hypothalamus (long)
    + : physical (exercise, injury, infection, dehydration)
    emotional (anxiety, pain, depression)
96
Q

What type of hormone is aldosterone

A

a mineralocorticoid

97
Q

Describe the hormone aldosterone

A

controls regulation of body fluid and composition (osmolarity)
produced from progesterone in the zona glomerulosa in the adrenal cortex
has a half life of 30 mins
raises blood pressure and fluid volume
increases sodium uptake by the kidneys

98
Q

Describe the release of aldosterone

A

release is stimulated by angiotensin
low sodium ion levels stimulate renin being released in the kidneys
renin then cleaves angiotensin to angiotensin I
angiotensin I is then converted into angiotensin II

99
Q

Describe corticosteroid receptors

A

steroids are fat soluble so they can cross cell membranes
they have two cytosolic receptors
A glucocorticoid receptor (GR) (most cells have one, cortisol has a higher affinity here)
A mineralocorticoid receptor (MR) (aldosterone has a higher affinity here, mainly found in gut and kidney)

100
Q

Describe a primary deficit of cortisol

A

the failure of the adrenal gland to secrete cortisol

consequences are: loss of feedback on CRH and ACTH secretion so both increase

101
Q

Describe a secondary deficit of cortisol

A

Failure of the anterior pituitary to secrete ACTH
consequences are: loss of negative feedback on CRH secretion so CRH secretion increases but the ACTH secretion is low which causes atrophy (wastage) of the adrenal cortex

102
Q

What is Addisons disease

A

adrenocortical insufficiency or hypoadrenalism

103
Q

Describe the symptoms of Addisons disease

A

hyoptension (low blood pressure)
hypoglycaemia (low blood sugar)
hyponatreamia (low sodium conc)
hypovoleamia (low blood volume)
Hyperpigmentation (only from primary deficit, high ACTH stimulates MSH receptors on melanocytes so melanin increases)
Hyperkaleamia (high potassium suggests lack of aldosterone)

104
Q

Main causes of Addisons disease

A

autoimmune destruction of adrenal cortical cells (leads to primary adrenocortical insufficiency

105
Q

What are some other causes of Addisons disease

A

chronic glucocorticoid treatment (causes secondary adrenocortical insufficiency)
Infection (TB or HIV)
drugs that inhibit cytochrome P450 enzyme
cortical resistance - rare

106
Q

Describe Cushings disease

A

excessive pituitary ACTH secretion

(too much cortisol)

107
Q

Describe Cushings syndrome

A

adrenal neoplasm or hyperplasia
from chronic glucocorticoid treatment
(too much cortisol)

108
Q

Describe the acute phase response to stress from trauma or surgery

A

interleukin 6 produced by macrophages
results in fever
increased blood count of granulocytes especially neutrophils and platelets
liver increases production of proteins such as C reactive protein (CRP) (a protein that adheres to bacteria and promotes complement activation and phagocytosis)

109
Q

What are the components of a full blood count (FBC)

A 
platelets
total white cell count
neutrophils
Eosinophils 
lymphocytes
110
Q

Describe the activation of the fight or flight response from the alpha adrenoreceptors

A 
relaxation of smooth muscle in wall of GI tract
pupil dilates (mydriasis)
constriction of arterioles in skin and splanchnic circulation
111
Q

Describe the activation of the fight or flight response from the beta adrenoreceptors

A

relaxation of smooth muscle in wall of GI tract
increased heart rate and contractility
bronchodilation
relaxation of detrusor muscle in bladder wall
dilation of arterioles in skeletal muscle

112
Q

what are the actions of insulin

A

increases formation of glycogen
decreases glycolysis and gluconeogenesis
increases protein synthesis
increases fat deposition
decreases lipolysis
increases potassium uptake into cells by stimulating Na-K-ATPase
decreases blood amino acids, fatty acids, ketoacids, and potassium

113
Q

What are the clues of systemic inflammatory response syndrome (SIRS)

A

temperature of more than 38 degree or less than 36
heart rate of 90bpm
resp rate of more than 20 breaths per minute
abnormal white blood cell count

114
Q

Describe what happens in the fasting state

A

primary aim is to maintain blood glucose
liver glycogen is broken down into glucose-6-phosphate and then to glucose which is released into the bloodstream
amino acids from protein and glycerol from fatty acids is used for gluconeogenesis
liver uses fatty acids as its fuel source

115
Q

Describe what happens in the fed state

A

insulin stimulates glucose uptake by the tissues
in the liver excess glucose is converted into acetyl-coA which is used to synthesise fatty acids for export to adipose and muscle tissue

116
Q

Four hormones involved in glucose homeostasis

A

glucagon
insulin
adrenaline
glucocorticoids (especially cortisol)

117
Q

describe insulin in glucose homeostasis

A

signals the fed state

secreted in response to high blood glucose from the beta cells of the pancreas

118
Q

Describe glucagon in glucose homeostasis

A

signals the fasting state

secreted in response to low blood glucose from the alpha cells of the pancreas

119
Q

Describe adrenaline in glucose homeostasis

A

secreted from the adrenal medulla in response to low blood glucose (and fear)
stimulates fuel mobilisation especially in muscle and adipose tissue

120
Q

Describe glucocorticoids in glucose homeostasis

A

secreted largely in response to stress and starvation

exert long-term effects on the expression of enzymes involved in fat and carbohydrate metabolism

121
Q

Describe the hormone testosterone

A

an androgen
male sex hormone synthesised in the testes
responsible for secondary sex characteristics
synthesised from progesterone

122
Q

Describe the hormone oestradiol

A

an oestrogen
principal female sex hormone produced in the ovaries
responsible for secondary female sex characteristics

123
Q

Describe the hormone progesterone

A

a progestestin
produced directly from the pregnenolone and secreted from the corpus luteum
responsible for changes associated with the luteal phase of the menstrual cycle
differentiation factor for mammary glands

124
Q

Describe the relationship between cortisol (and other steroid hormones) and regulating transcription

A

the hormones act by regulating transcription
they are transported in the blood bound to transporter proteins
inside the cell membrane they bind to members of the nuclear receptor family
nuclear-receptor signal complexes bind specific DNA sequences and regulate gene expression

125
Q

When does cortisol begin to lose its positive effect and start to cause damage

A

after prolonged exposure (weeks)

126
Q

Describe what the cells in the islets of langerhans in the pancreas produce

A

alpha cells produce glucagon
beta cells produce insulin
delta cells produce somatostatin

127
Q

Describe how secretion of insulin is biphasic

A

1st phase: fusion of granules with plasma membrane

2nd phase: synthesis and translocation of granules to the membrane

128
Q

What are some factors that affect insulin secretion

A 
adrenaline (inhibitory)
amino acids (stimulatory)
Fatty acids (stimulatory)
129
Q

Describe what happens in insulin binding

A

binds to an enzyme-coupled receptor on the surface of adipose and muscle tissues
Receptor is a member of the RTK tyrosine kinase class
(when insulin binds RTK is activated and auto-phosphorylates tyrosine)
phosphorylated receptor can now bind IRS-1 (insulin receptor substrate 1) allowing PIP2 to be converted to PIP3 which activates PDK1 which activates Akt (also known as protein kinase B) which activates a host of responses including metabolic control and gene transcription

130
Q

Describe how glucose regulates insulin secretion from beta cells

A

glucose enters beta cells through GLUT2 transporters, glycolysis leads to ATP increase
ATP binds to ATP-gated K+ channels and they close, depolarising the plasma membrane
triggers the opening of the voltage-gated Ca2+ ion channels
increased cytosolic ca2+ triggers more ca2+ release from the ER and this wave of calcium inside the cell triggers insulin secretion by exocytosis

131
Q

What is type 1 diabetes

A

(juvenile onset or insulin dependent)
due to failure to produce or to secrete insulin, usually from an autoimmune destruction to beta cells
develops early on in life
treated with insulin injections

132
Q

Describe type 2 diabetes

A 
(maturity onset or non-insulin dependent)
Due to failure to respond to insulin
usually develops in late adulthood
usually associated with diabetes 
controlled by diet and/or drugs
133
Q

How do you diagnose diabetes

A

urine glucose analysis
oral glucose tolerance test
glycated haemoglobin
measurement of plasma insulin

134
Q

what does diabetes resemble? describe it?

A

resembles a starving state
gluconeogenesis produces glucose as fuel for the brain
proteins are broken down and glucogenic amino acids yield glucose as fuel for the brain
NH3 from amino acid deamination is converted into urea and is excreted

135
Q

early symptoms of diabetes

A 
frequent urination
increased thirst
blurred vision
fatigue
headache
136
Q

Later symptoms of diabetes

A 
breath smells of pear drops (acetone)
nausea and vomiting
shortness of breath
dry mouth
abdominal pain
weakness
confusion
coma
137
Q

Describe the oral glucose tolerance test

A

solution of 75g is given to patients who have fasted overnight
blood sample is taken before giving it to them and at thirty minute intervals for two hours

138
Q

describe the normal and abnormal levels in an oral glucose tolerance test

A

Normal: fasting - <6.1(mmol/l), 2hrs - <7.8
impaired fasting glycaemia: fasting ≥6.1 & <7, 2hrs- <7.8
impaired glucose tolerance: fasting <7, 2hrs -≥7.8
Diabetes mellitus: fasting ≥7, 2hrs - ≥11.1

CBL Year 1 (7 decks)

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