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
Describe an ion channel coupled receptor
``` 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 ```
26
Describe G protein coupled receptors
they are transmembrane proteins the extracellular portion of the GPCR bind to signalling molecules cytoplasmic portion binds to the G protein
27
What are the two most common enzyme targets of G protein coupled receptors
adenylyl cyclase and phospholipase C
28
What does adenylyl cyclase do (in related to GPCRs)
catalyses the formation of the secondary messenger signalling molecule cAMP
29
What does phospholipase C do (in relation to GCPRs)
produces the second messengers inositol triphosphate (IP3) and diacylglycerol (DAG)
30
What does inositol triphosphate do
promotes the accumulation of cytosolic Ca2+ (calcium ions) which is another common second messenger
31
What is the effect of adrenaline on skeletal muscle
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
32
What are the thyroid glands lateral lobes connected by
the isthmus
33
What does the thyroid gland form the floor of
the pharynx
34
Where are the parathyroid glands located
behind the lateral lobes of the thyroid gland four glands (two superior and two inferior) approximate diameter of 12mm each
35
Where does T3 and T4 synthesis occur (thyroxine)
in the thyroid follices
36
Describe T3 and T4 synthesis
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
37
Describe dietary intake of iodine
absorbed first into the extracellular pool then removed from their by the thyroid or kidneys thyroid contains huge iodine store in colloid
38
Describe cretinism (Congenital iodine deficiency syndrome)
neurological deficits small stature and immature appearances puffy face and hands delayed puberty
39
What is hypothyroidism, describe it in adulthood
``` 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 ```
40
What is hyperthyroidism, describe it
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)
41
what are the biological roles of calcium
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)
42
what three hormones is plasma calcium concentration precisely controlled by
parathyroid hormone (PTH) (counter-regulatory hormone) calcitonin (Counter-regulatory hormone) vitamin D
43
What do counter regulatory hormones do? what does this mean in the examples of PTH and calcitonin
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
44
If calcium levels decrease in the blood plasma then what happens
increase in parathyroid gland (chief cells) | which then increase the levels of PTH which then increase the levels of calcium
45
If calcium levels rise too much in the blood plasma then what happens
increase in thyroid parafollicular C cells | which increase calcitonin release which decreases the levels of calcium
46
What hormone regulates the calcium homeostasis minute by minute and what hormone is more in case of emergency
minute by minute is PTH | emergency is calcitonin
47
What is hypocalcaemia caused by and what are some symptoms
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
48
What is hypercalcaemia associated with and what are some symptoms
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
49
What is a PCHR (personal child health record) used for
``` family and birth related information routine screening immunisations growth advice and support early education ```
50
Three factors that influence growth
nutrition genetics environment
51
Difference between hypertrophy and hyperplasia
``` hypertrophy = increase is size of cells hyperplasia = increase in number of cells ```
52
What is GHRH, describe it
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)
53
Describe growth hormone (GH) secretion
``` it is periodic - think circadian rhythms things that promote secretion: sleep acute stress hypoglycaemia exercise ```
54
Metabolic actions of the growth hormone
``` 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) ```
55
what does endocrine mean? exocrine?
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)
56
Describe the three distinct types of endocrine tissue
1) endocrine organ devoted to hormone synthesis 2) distinct clusters of cells within an organ 3) individual cells scattered diffusely throughout an organ
57
Name two major endocrine organs that are NOT under pituitary control.
parathyroid gland and pancreas
58
what type of hormones does the pituitary produce
releasing hormones and inhibiting factors
59
What hormones does the posterior pituitary produce (endocrine)
arginine vasopressin (AVP), antidiuretic hormone (ADH) and oxytocin
60
What hormones does the anterior pituitary produce (endocrine)
``` adrenocorticotropic hormone (ACTH) growth hormone prolactin follicle stimulating hormone (FSH) Luteinising hormone (LH) Thyroid stimulating hormone (TSH) ```
61
What hormones does the thyroid gland produce (endocrine)
thyroxine T4, tri-iodothyronine T3, calcitonin
62
What hormones does the parathyroid gland produce (endocrine)
parathyroid hormone (PTH)
63
what hormones does the adrenal gland produce (endocrine)
adrenaline | cortisol
64
what hormones does the pancreas produce (endocrine)
glucagon and insulin
65
what hormones do the gonads produce (endocrine)
progesterone, oestrogen and testosterone
66
What are the steroid hormones
``` progestagens glucocorticoids mineralocorticoids androgens oestrogens ```
67
What are the non-steroid hormone classes
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
What receptors do steroid hormones and non-steroid hormones use
steroid use intracellular receptors whereas non-steroid use cell surface receptors
69
What is the hypothalamus-pituitary axis
interface between central nervous system and endocrine system
70
What are the other names for the anterior and posterior pituitary gland
anterior is also called Adenohypophysis | posterior is called neurohypophysis
71
Describe the posterior (neurohypophysis) lobe of the pituitary gland
under direct control | neural tissue comprises of axons and nerve terminal endings of the hypothalamic neurosecretory cells
72
Describe the anterior (adenohypophysis) lobe of the pituitary gland
under indirect control glandular tissue comprises of cells controlled by releasing hormones (or inhibitory factors) delivered by the hypophyseal portal system
73
Mnemonic to remember layers of adrenal cortex from outermost to innermost
GFR (glomerular filtration rate) zona glomerulosa zona fasciculata zona reticularis
74
What class of hormones does the adrenal cortex produce
corticosteroids
75
what class of hormones does the adrenal medulla produce
catecholamines
76
What does the zonea glomerulosa of the adrenal cortex produce
aldosterone
77
what does the zona fasciculata of the adrenal cortex prpduce
cortisol (and androgens)
78
What does the zona reticularis of the adrenal cortex produce
androgens (and cortisol)
79
What does the adrenal medulla produce (hormones)
adrenaline and noradrenaline
80
What are adrenocortical hormones
they are all steroids (so all derived from cholesterol) | they are synthesised as required and not stored
81
What is cortisol and what is it regulated by
it is a glucocorticoid | release is controlled by CRH and ACTH
82
What are the three main sections of glucocorticoid actions
``` 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
Give an example of how cortisol acts on metabolism (with low blood glucose)
``` 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
Give an example of how cortisol acts on there cardiovascular system
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
Give an example of how cortisol acts on the immune system
``` (anti-inflammatory and immunosuppressive) inhibits secretion of cytokines inhibits histamine release (mast cells) inhibits proliferation of immune cells inhibits synthesis of antibodies ```
86
What does the gonadotropin releasing hormone (GnRH) from the hypothalamus stimulate and where does it go
FSH and LH secretion from the anterior pituitary to the gonads
87
What does the corticotropin releasing hormone (CRH) from the hypothalamus stimulate and where does it go
secretion of adrenocorticotropic releasing hormone (ACTH) from the anterior pituitary to the adrenal cortex to then produce cortisol
88
what does the thyrotropin releasing hormone (TRH) from the hypothalamus stimulate and where does it go
secretion of thyroid stimulating hormone (TSH) from the anterior pituitary to the thyroid
89
What does the prolactin releasing hormone (PRH) from the hypothalamus stimulate and where does it go
stimulation of prolactin from the anterior pituitary to the mammary glands
90
what does dopamine from the hypothalamus stimulate and where does it go
inhibition of secretion of prolactin from the anterior pituitary to the mammary glands
91
What does growth hormone releasing hormone (GHRH) from the hypothalamus stimulate and where does it go
stimulation of secretion of growth hormone (GH) from the anterior pituitary to the liver (and all body)
92
What does somatostatin from the hypothalamus stimulate and where does it go
inhibition of secretion of the growth hormone from the anterior pituitary to the liver and rest of the body
93
Where does ADH (or vasopressin) come from and where does it go
secreted from the posterior pituitary gland (stimulated by neurosecretory cells from the hypothalamus) to the kidney
94
Where does oxytocin come from and where does it go
secreted from the posterior pituitary gland (stimulates by neurosecretory cells from the hypothalamus ) to the mammary glands
95
Negative feedback (-) of cortisol and stressors (+)
- : pituitary (short) hypothalamus (long) + : physical (exercise, injury, infection, dehydration) emotional (anxiety, pain, depression)
96
What type of hormone is aldosterone
a mineralocorticoid
97
Describe the hormone aldosterone
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
Describe the release of aldosterone
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
Describe corticosteroid receptors
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
Describe a primary deficit of cortisol
the failure of the adrenal gland to secrete cortisol | consequences are: loss of feedback on CRH and ACTH secretion so both increase
101
Describe a secondary deficit of cortisol
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
What is Addisons disease
adrenocortical insufficiency or hypoadrenalism
103
Describe the symptoms of Addisons disease
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
Main causes of Addisons disease
autoimmune destruction of adrenal cortical cells (leads to primary adrenocortical insufficiency
105
What are some other causes of Addisons disease
chronic glucocorticoid treatment (causes secondary adrenocortical insufficiency) Infection (TB or HIV) drugs that inhibit cytochrome P450 enzyme cortical resistance - rare
106
Describe Cushings disease
excessive pituitary ACTH secretion | (too much cortisol)
107
Describe Cushings syndrome
adrenal neoplasm or hyperplasia from chronic glucocorticoid treatment (too much cortisol)
108
Describe the acute phase response to stress from trauma or surgery
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
What are the components of a full blood count (FBC)
``` platelets total white cell count neutrophils Eosinophils lymphocytes ```
110
Describe the activation of the fight or flight response from the alpha adrenoreceptors
``` relaxation of smooth muscle in wall of GI tract pupil dilates (mydriasis) constriction of arterioles in skin and splanchnic circulation ```
111
Describe the activation of the fight or flight response from the beta adrenoreceptors
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
what are the actions of insulin
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
What are the clues of systemic inflammatory response syndrome (SIRS)
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
Describe what happens in the fasting state
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
Describe what happens in the fed state
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
Four hormones involved in glucose homeostasis
glucagon insulin adrenaline glucocorticoids (especially cortisol)
117
describe insulin in glucose homeostasis
signals the fed state | secreted in response to high blood glucose from the beta cells of the pancreas
118
Describe glucagon in glucose homeostasis
signals the fasting state | secreted in response to low blood glucose from the alpha cells of the pancreas
119
Describe adrenaline in glucose homeostasis
secreted from the adrenal medulla in response to low blood glucose (and fear) stimulates fuel mobilisation especially in muscle and adipose tissue
120
Describe glucocorticoids in glucose homeostasis
secreted largely in response to stress and starvation | exert long-term effects on the expression of enzymes involved in fat and carbohydrate metabolism
121
Describe the hormone testosterone
an androgen male sex hormone synthesised in the testes responsible for secondary sex characteristics synthesised from progesterone
122
Describe the hormone oestradiol
an oestrogen principal female sex hormone produced in the ovaries responsible for secondary female sex characteristics
123
Describe the hormone progesterone
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
Describe the relationship between cortisol (and other steroid hormones) and regulating transcription
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
When does cortisol begin to lose its positive effect and start to cause damage
after prolonged exposure (weeks)
126
Describe what the cells in the islets of langerhans in the pancreas produce
alpha cells produce glucagon beta cells produce insulin delta cells produce somatostatin
127
Describe how secretion of insulin is biphasic
1st phase: fusion of granules with plasma membrane | 2nd phase: synthesis and translocation of granules to the membrane
128
What are some factors that affect insulin secretion
``` adrenaline (inhibitory) amino acids (stimulatory) Fatty acids (stimulatory) ```
129
Describe what happens in insulin binding
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
Describe how glucose regulates insulin secretion from beta cells
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
What is type 1 diabetes
(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
Describe type 2 diabetes
``` (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
How do you diagnose diabetes
urine glucose analysis oral glucose tolerance test glycated haemoglobin measurement of plasma insulin
134
what does diabetes resemble? describe it?
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
early symptoms of diabetes
``` frequent urination increased thirst blurred vision fatigue headache ```
136
Later symptoms of diabetes
``` breath smells of pear drops (acetone) nausea and vomiting shortness of breath dry mouth abdominal pain weakness confusion coma ```
137
Describe the oral glucose tolerance test
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
describe the normal and abnormal levels in an oral glucose tolerance test
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