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Phase 2 > Endocrine lecture notes > Flashcards

Endocrine lecture notes Flashcards

1
Q

endocrine vs exocrine

A

endocrine - glands secrete into bloodstream

exocrine - glands secrete through a duct to site of action

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2
Q 
describe water soluble hormones in terms of:
transport
cell interaction
half-life
clearance
examples
when are they syntehsised/stored?
A

transport: unbound
cell interaction: bind to surface receptor
half-life: short
clearance: fast
eg peptides, monoamines
- stored in vesicles and secreted when needed

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3
Q 
describe fat soluble hormones in terms of:
transport
cell interaction
half-life
clearance
eg
when are they synthesised?
A 
transport: protein bound
cell interaction: diffuse into cell
half-life: long
clearance: slow
eg. thyroid hormone, steroids
 - synthesised on demand
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4
Q

What are some roles of thyroid hormone?

A
  • increased food metabolism
  • increased protein synthesis
  • stimulates carb metabolism
  • enhances fat metabolism
  • increased CO and HR so increased BP
  • increased ventilation rate
  • increased growth rate
  • brain development. foetal and post natal
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5
Q

What are some roles of cortisol?

A
  • bone development
  • BP
  • anti-inflammatory, immune system
  • skin: texture of collagen
  • released as a reaction to stress
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6
Q

what are the results of too much cortisol?

A

protein breakdown, put on weight, increased blood sugar

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7
Q

How is the balance between energy expenditure and energy intake maintained normally in the body?

A

By hormones of the…

  • GI tract: eg CCK
  • brain: eg vagus nerve stimulated by gastric stretch to stop appetite
  • adipose tissue
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8
Q

What are the components of the satiety cascade?

A
  • internal physiological drive
  • feeling prompts thought of food - psychological
  • time of day
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9
Q

Where is the centre of appetite regulation? whithin this, where us the hunger centre compared with the satiety centre?

A

Appetite regulation occurs in the hypothalamus.
Hunger = lateral hypothalamus
Satiety = ventromedial hypothalamic nucleus

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10
Q

what role does the arcuate nucleus of the hypothalamus have in apetite regulation?

A

Has fenestrated blood brain barrier so can sample peripheral hormones.
Secretes leptin hormone, which switches off appetite and is immunostimulatory.
Blood levels increase after a meal and decrease after fasting.

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11
Q

What stimulates an individual to want to eat?

A
  • Ghrelin hormone, expressed in the stomach, stimulates GH release and appetite
  • olfactory, gustatory, cognitive and visual stimuli
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12
Q

Describe the Pituitary - thyroid axis

A

Hypothalamus releases TRH which stimulates pituitary to release TSH. TSH stimulates production of T4 and T3 from the thyroid, which has a negative feedback effect on both TRH and TSH secretion.

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13
Q

How would removal of the thyroid, vs an overactive thyroid, affect TSH levels?
Can levels of this hormone therefore be used in screening for thyroid problems?
What about in screening for pituitary disease?

A

Removal: increased TSH
Overactive: decreased TSH
Levels are used to screen for thyroid problems but NOT for pituitary disease

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14
Q

Why is prolactin unusual as a hormone released from the anterior pituitary?
Which drugs may be relevant in affecting prolactin levels?

A

Its axis
Prolactin is under negative control by dopamine from the hypothalamus.
Drugs such as anti-psychotics which inhibit the release of dopamine can cause increased prolactin levels

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15
Q

How is benign pituitary adenoma usually picked up?

A

Usually accidentally on MRI. It is relatively common.

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16
Q

Describe the 3 different presentations of a pituitary tumour

A
  1. Pressure on local structure, e.g optic nerve causing bitemporal hemianopia
  2. Pressure on normal pituitary (hypopituitarism)
  3. Functioning tumour (of hormone releasing cells)
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17
Q

What is the effect of hypopituitarism caused by pressure on the normal pituitary due to a tumour?

A

Slow onset
If child: poor growth
Adult: pale, no body hair, central obesity… Need steroid replacement, often wear bracelet explaining this in case of emergency

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18
Q

Describe 3 examples of functioning pituitary tumours. Which hormones are over produced?

A

Prolactinoma - prolactin
Cushing’s - ACTH
Acromegaly - GH

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19
Q

why is important to be aware of acromegaly?

A

Uncommon, but its slow progression means it can go undiagnosed for years and co-morbidities can cause significant harm.

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20
Q

Describe briefly the pathogenesis of acromegaly

A

Too much GH
GH stimulates the production of IGF-1 from the liver.
IGF- 1 targets other organs in the body leading to clinical signs.

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21
Q

What are common co-morbidities of acromegaly?

A

Arthritis (due to bone overgrowth), cerebrovascular events, headache, sleep apnea, diabetes (GH has antagonistic effects to insulin), hypertension, heart disease.
It is important to treat these co-morbidities alongside the acromegaly.

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22
Q

What are 2 ways, other than looking at clinical features, of diagnosing acromegaly?

A
  1. Normally, GH secretion is pulsatile, stimulated by GHRH from hypothalamus. In acromegaly the pulses are disrupted so GH secretion will be dysregulated. Levels will also never by completely gone, as with normal inividuals.
  2. Normally, glucose promptly supresses GH, but not with acromegaly. Therefore a glucose tolerance test is an important diagnostic tool.
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23
Q

3 modes of treatment of acromegaly?

A
  • pituitary surgery
  • medical therapy (dopamine agonist, somatostatin analogues, GH receptor antagonist)
  • radiotherapy (interrupts vascular supply, prevents DNA division)
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24
Q

What is a key principle of endocrinology in terms of the pathway for diagnosing an endocrine issue?

A

Clinical suspicion –> biochemistry –> scan
In that order.
This is because scan may show accidental findings.

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25
Q

Why is recognising prolactinoma important?

A

Common: 10 in 100000
Easily treated.
Causes infertility.

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26
Q

Define prolactinoma

A

lactotroph call tumour of the pituitary
OR
non-functioning: interruption of pituitary stalk means dopamine can’t reach the pituitary so prolactin levels increase uninhibited

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27
Q

What effect does dopamine have on a prolactinoma?

A

Tumour cells are not under inhibition by dopamine

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28
Q

Describe the clinical features of someone which may indicate that they have a prolactinoma

A

Galactorrhoea (milk in the breast)
Amenorrhoea, infertility, loss libido, visual defect, hypogonadism.
More common in women

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29
Q

What is the treatment for prolactinoma? How does this differ from other pituitary treatment?

A

Management is medical, not surgery.

Dopamine agonists used.

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30
Q

Adrenal insufficiency - what are the primary, secondary and tertiary causes?

A

Primary: autoimmune, Addison’s
Secondary: hypopituitarism
Tertiary: suppressed HPA

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31
Q

what is the HPA axis?

A

Hypothalamus stimulates ACTH prod. from the anterior pituitary, which stimulates the adrenal cortex to secrete cortisol, which has a negative feedback effect on both the hypothalamus and ant. pituitary.

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32
Q

Principles of endocrinology:
What test when looking for a deficiency?
What test when looking for an excess?

A 
Deficiency = stimulatory test
Excess = suppression test
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33
Q

Acute administration of what can save someone in adrenal crisis? how?

A

Hydrocortisone.

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34
Q

Treatment for adrenal insufficiency?

A

Hydrocortison 2/3 times daily in attempt to mimic cortisol levels throughout the day.
However, hard to replace mid night cortisol spike.

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35
Q

Examples of thyroid autoimmunity?

A 
Post partum thyroiditis (after pregnancy)
Graves disease (immune system antibodies stimulate the thyroid) - MOST COMMON CAUSE OF HYPERTHYROIDISM
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36
Q

What are factors that predispose to thyroid autoimmunity?

A
  • female (onset common post partum)
  • genetic: HLA-DR3 and other immunoregulatory genes
  • environmental: stress, high iodine intake, smoking
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37
Q

Describe autoimmune hypothyroidism

A
  • immune system (cytotoxic T cell mediated) attacks thyroid, follicles break down and there is an invasion of lymphocytes and a build up of fibrotic
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38
Q

describe Graves disease

symptoms?

A

Most common type of hyperthyroidism, 70-80% cases.
Thyroid stimulating antibodies stimulate the thyroid.
This causes thickening of the cells and overproduction of thyroid hormone.
Affects other systems
Symptoms: periorbital oedema, weight loss, enlarged thyroid, tachycardia, hyperphagia, anxiety, tremor, heat intolerance, sweating, diarrhoea, lid lag and stare, menstrual disturbance

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39
Q

What is goitre?

A

Palpable and visible thyroid enlargment.

Commonest endocrine disorder, has a variety of causes.

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40
Q

What investigations will reveal primary hyperthyroidism? What about secondary hyperthyroidism?

A

Primary: increased free T4 and T3, suppressed TSH
Secondary: increased free T4 and T3, inappropriately high TSH

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41
Q

What is primary hyperthyroidism? Secondary?

A

Primary: abnormal functioning of the thyroid gland itself. 80% occurs due to single benign adenoma.
Secondary: dysfunction is caused by factors extrinsic to the thyroid gland (i.e., not due to a disorder in the gland).

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42
Q

What is primary hypothyroidism? Secondary?

A

primary - dysfunction of the thyroid gland

secondary/tertiary - pituitary/hypothalamic dysfunction

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43
Q

Treatment for hypothyroidism?

A

synthetic thyroxine

1.6mg/kg body weirgh

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44
Q

treatment for hyperthyroidism?

A

antithyroid drugs
radioiodine
surgery

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45
Q

Which drugs/therapies that pts may be on require thyroid function monitoring?

A
  • amiodarone/lithium

- immunotherapy

46
Q

What is the role of PTH?

Which structures does it act on?

A

Maintenance of serum calcium.
Secreted in response to low serum Ca2+ and acts on:
BONE: increased bone resorption > bone formation
KIDNEY: increased Ca2+ reabsorption (decreased Phosphate reabsorption, increased hydroxylation 25-OH vit D)
GUT: increased Ca2+ absorption (not direct effect, increases 1,25(OH)2 vit D)

47
Q

Vitamin D deficiency (2ndary hyperparathyroidism)
Describe levels of:
PTH
Calcium
Phosphate
Are PTH levels appropriate to maintain Ca balance, or inappropriate, causing the imbalance?

A

PTH increased
Calcium decreased
Phosphate decreased
PTH levels appropriate

48
Q 
Hypoparathyroidism
Describe levels of:
PTH
Calcium
Phosphate
Are PTH levels appropriate to maintain Ca balance, or inappropriate, causing the imbalance?
A

PTH decreased
Calcium decreased
Phosphate increased
PTH levels inappropriate

49
Q

Pseudohypoparathyroidism (PTH resistance)
Describe levels of:
PTH
Calcium
Phosphate
Are PTH levels appropriate to maintain Ca balance, or inappropriate, causing the imbalance?

A

PTH increased
Calcium decreased
Phosphate increased
PTH levels appropriate

50
Q 
Primary hyperparathyroidism
Describe levels of:
PTH
Calcium
Phosphate
Are PTH levels appropriate to maintain Ca balance, or inappropriate, causing the imbalance?
A

PTH decreased
Calcium increased
Phosphate decreased
PTH levels inappropriate

51
Q

Common causes of hypocalcaemia?

A
  • osteomalasia due to vit D deficiency
  • hypoparathyroidism
  • pseudohypoprathyroidism
52
Q

Consequences of hypocalcaemia

A

parasthesia, muscle spasm (- premature labour, larynx could be dangerous), seizures, cataracts, ECGa bnormalities (lengthens QT interval)

53
Q

How to calculate corrected calcium? (some ionised, some bound to ambumin)

A

total serum calcium + 0.2 x (40 - serum albumin)

54
Q

Clinical features of pseudohypoparathyroidism (resistance to PTH)

A

Short stature, obesity, short 4th metacarpals, other hormone resistance

55
Q

What is chostek’s sign? (indicating hypocalcaemia)

A

tap over facial nerve where it leaves the parotid and observe spasm of facial muscles

56
Q

What is trousseau’s sign? (indicating hypocalcaemia)

A

inflate BP cuff, hand goes into characteristic spasm

57
Q

Symptoms of hypercalcaemia?

A

thirst, polyuria, nausea, constipation (due to gut stasis), confusion –> coma
Long termm: renal stones, short QT interval on ecg

58
Q

describe the QT interval on an individual with hypo vs hypercalcaemia

A 
hypo = long
hyper = short
59
Q

Causes of hypercalcaemia?

A

90% cases:
malignancy
primary hyperparathyroidism

60
Q

what is tertiary hyperparathyroidism?

what will it lead to if left untreated over a long period of time?

A

Renal failure - can’t activate vitamin D
Leads to decreased Ca2+ absorption, leads to increased PTH.
Over time, this causes nodular hyperplasia and autonomy of parathyroid glands (stop responding) –> hypercalcaemia

61
Q

How do the breasts/testes indicate start of puberty according to Tanner?

A

Boys: testes > 3mL
Dependent on normal functioning of germ cells
Girls: breast bud palpable (thelarche = breast development)
Acts as marker of oestrogen effect:
- ductal proliferation
- adipose deposition
- enlargement of areola and nipple

62
Q

what is adrenarche?

A

maturation of the adrenal gland

leads to mild advanced bone age, axillary hair, oily skin, mild acne, body odour

63
Q

describe the HPG axis

A

hypothalamus –> pulsatile secretion of GnRH
This stimulates pituitary to secrete LH and FSH
These act on gonads to produce gonadal sex hormones,

64
Q

In case of true precocious puberty in boys, what must be investigated?

A

Brain tumour

65
Q

What is hypogonadism?

What is hypogonadic hypogonadism?

A

Hypogonadism is a condition in which the male testes or the female ovaries produce little or no sex hormones. Hypogonadotropic hypogonadism (HH) is a form of hypogonadism that is due to a problem with the pituitary gland or hypothalamus.

66
Q

How is hypogonadism named primary secondary / tertiary?

A

According to where the problem is.
Hypothalamus = tertiary
Pituitary = secondary
Gonads = primary

67
Q

main ions intracellularly?
extracellularly?
L water in each

A

intra: 2/3 potassium, magnesium, phosphate
extra: 1/3, sodium

68
Q

describe the feedback loop when water has been ingested that leads to decreased total body water?

A

Ingestion water –> decreased plasma osmolality –> increased cellular hydration –> decreased thirst & decreased vasopressin –> increased water excreted as urine from kidney –> decreased total body water –> ingestion water

Negative feedback loop

69
Q

How is ADH release controlled in an emergency eg extreme blood loss?

A

By baroreceptors in brainstem and great vessels

70
Q

Where is ADH synthesised and released?

Where does it act?

A

Synthesised in hypothalamus and released from the posterior pituitary into the blood stream.
It binds to V2 receptors on collecting duct principle cells, where it initiates the insertion of aquaporin channels

71
Q

what is osmolality?

A

conc. solutes per kilogram of solvent

72
Q

What is the main determinant of serum osmolality? what other molecules affect osmolality, and do their effects vary?

A

Sodium is the main determinant, as it is the major extracellular cation. The total body water is also a main determinant.
Osmolality is affected by Na, K, Cl, HCO3-, urea, glucose.
Conc solutes depends on number, not size, of particles, so all will exert the same relative effect.

73
Q

What should serum osmolality be compared with urine osmolality?
What does an abnormality suggest?

A

Should be double urine osmolality.

If abnormal ,indicates ADH deficiency, consistent with Diabetes Insipidus.

74
Q

what are the 2 major symptoms that indicate diabetes insipidus?

A

Thirst and high urine output

75
Q

How is hyponatraemia diagnosed from a serum test?

What is the cut off for severe hyponatraemia?

A

serum sodium <135 mmol/l

severe = serum sodium <125mmol/l

76
Q

Why is it important to be aware of and investigate hyponatraemia?

A

It is common, but investigation and management is poor.

It has high mortality: 1 in 3 die

77
Q

What are signs and symptoms of hyponatraemia, in order of decreasing Na level?

A 
progresses from...
asymptomatic
headache
lethargy
anorexia, abdo pain
weakness
confusion/hallucination
firring 
coma
78
Q

In the management of hyponatraemia, what is the danger if Na levels are raised quickly?
(in chronic hyponatraemia, where the CNS adapts)

A

Osmotic demyelination can occur, which can result in coma.

Correction must be slow, <8mmol/24hr

79
Q

What tests are important when hyponatraemia presents?

A 
plasma osmolality
cortisol
TSH
urine dip for protein
plasma glucose
urine osmolality
urine sodium
80
Q

what are common causes of hyponatraemia?

A

renal failure
malignancy
SIADH
E+D

81
Q

What is Syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
what are the 3 main causes?
how is it treated?

A

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a condition in which the body makes too much antidiuretic hormone (ADH).
Causes:
1. drugs
2. respiratory causes
3. CNS disorders
tumours
Treated by fluid restriction (740ml-1L/day)

82
Q

components of the anterior lobe of the pituitary vs the posterior lobe

A 
anterior = glandular, 75% weight
posterior = nerve tissues, axons that originate in the hypothalamus
83
Q

What are some possible local mass effects of pituitary mass lesions

A

Visual field defect (bitemporal hemianopia) due to pressing on optic chiasm.
Leakage CSF from nose. (CSF rhinorrhea)
Palsy
Headache

84
Q

what are the 3 main types of pituitary mass lesions?

A
  1. Most common = non-functioning pituitary adenomas
  2. endocrine active
  3. Malignant tumours - functional and non-functional
85
Q

What are measures of agression of non-functioning pituitary adenomas, which account for 14-28%pituitary adenomas?
How are non-functioning pituitary adenomas usually discovered?

A

size, invasion cavernous sinus.

50% are incidentally discovered

86
Q

what 3 things are you looking for in an individual with pituitary dysfunction?
what investigations would you carry out, in what order?

A
  1. Tumour mass effects
  2. Hormone excess
  3. Hormone deficiency
    Investigation:
    Hormonal tests
    If these are abnormal, or there are tumour mass effects, perform an MRI.
    (biochemical before radiological)
87
Q 
Hormone axises can be used to diagnose pituitary malfunctions. What are symptoms associated with malfunction in production of the following hormones?
GH
LH/FSH
TSH
ACTH
How can these deficiencies be treated?
A

GH - short, reduced muscle
LH/FSH - hypogonadal, infertility, menstruation problems
TSH - hypothyroidism
ACTH - adrenal failure
Treatment = pituitary hormone replacement

88
Q

what are the insulin independent tissues and how/from where do they receive glucose in the fasting state?

what about insulin dependent?

A

the brain, red blood cells, kidney tubular cells, pancreatic beta cells, liver and small intestine lining - all have different glucose receptors (not GLU4)
In the fasting state they receive glucose from the liver (and kidney) by glycogenolysis and gluconeogenesis.

For adipose and skeletal muscle cells glucose enters via GLU4. Muscle uses FFAs for fuel in the fasting state.

89
Q

In the post prandial state, what is the effect of rising glucose concentration?

A

Stimulates insulin secretion (beta cells) and suppresses glucagon (alpha cells).
40% of the glucose in the blood goes to the liver, 60% to periphery (muscle), helping to replenish glycogen stores.
HIGH insulin and glucose levels suppress lipolysis and FFAs.

90
Q

What hormones are involved in carbohydrate metabolism? what effect do they have

A

Insulin = key regulator.
Glucagon = counter regulatory: increases glycogenolysis and gluconeogenesis.
Others: adrenaline, cortisol and GH all have similar effects to glucagon.

91
Q

What is diabetes mellitus? (in words)

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia.

92
Q

In diabetes mellitus, what morbidities & mortality is associated with:

  • acute hyperglycaemia
  • chronic hyperglycaemia
  • hypoglycaemia
A
  • acute hyperglycaemia: Diabetic ketoacidosis (DKA), coma
  • chronic hyperglycaemia: tissue complications - macrovascular complications (coronary artery disease, peripheral arterial disease, and stroke) and microvascular complications (diabetic nephropathy, neuropathy, and retinopathy).
  • hypoglycaemia: as an affect of treatment - loss consciousness, seizures, faint/weak etc.
93
Q

Definition of diabetes (by blood components)

A
  • Symptoms + random plasma glucose>11mmol/l
  • Fasting plasma glucose > 7mmol/l
  • No symptoms but above^ repeatedly
  • HBA1c of 48mmol/mol (65%)
94
Q

Describe the pathogenesis of type 1 diabetes.
What is it?
What problems is it often accompanied by?
- is it purely genetic?

A

An insulin deficiency disease, characterised by loss of beta cells due to autoimmune destruction. Beta cells express HLA antigens, activating a chronic cell mediated response –> ‘insulitis’.
Often accompanied by other endocrine problems such as thyroid problems. This can help in diagnosis/differentiation from type 2.
NOT purely genetic! only 50% genetic.

95
Q

what is the key factor for distinguishing type 1 diabetes from type 2?

A

Unrestrained gluconeogenesis, lipolysis and muscle breakdown leading to weight loss.
Type 1 don’t have microvascular complications.
DKA

96
Q

What effect does the lack of insulin secretion in type 1 diabetes have on carbohydrate metabolism?

A
  • increased glycogenolysis
  • unrestrained lipolysis and muscle breakdown
  • inappropriate increased hepatic glucose output and suppression of peripheral glucose uptake
  • urinary glucose losses as renal threshold exceeded
97
Q

If type 1 diabetes is not treated with insulin, what will happen?

A
  • increased glucagon –> even more glucose
  • ketoacidosis
  • weight loss and eventual death
98
Q

why do you not see DKA in individuals with type 2 diabetes, but you do in type 1?

A

Even low levels of insulin prevent muscle catabolism and ketogenesis - therefore in type 2, profound muscle breakdown and gluconeogenesis are restrained and ketone production is rarely excessive.
/Low insulin is sufficient to suppress catabolism and prevent ketogenesis.
Therefore DKA is not seen in type 2 diabetes.

99
Q

Type 2 diabetes has genetic and environmental origin. Genetic = impaired insulin secretion, environment = insulin resistance
What do these factors lead to? How does this contribute to the progressive nature of type 2 diabetes?

A

Both lead to impaired glucose tolerance, which eventually crosses a threshold and is diagnosed as type 2 diabetes.
Type 2 diabetes -> progressive hyperglycaemia and high FFAs.
This has a positive feedback effect, further impairing insulin secretion and increasing insulin resistance.

100
Q

What is the diagnostic criteria for type 2 diabetes?

A

Diabetes symptoms (e.g. polyuria, polydipsia and unexplained weight loss for Type 1) plus:

  • a random venous plasma glucose concentration ≥ 11.1 mmol/l or
  • a fasting plasma glucose concentration ≥ 7.0 mmol/l (whole blood ≥ 6.1 mmol/l)
101
Q

why does obesity cause type 2 diabetes?

A

it impairs insulin action

102
Q

What are the principles of pharmacological treatment of type 2 diabetes ?

A
  • control symptoms
  • prevent acute emergencies, ketoacidosis, hyperglycaemic hyperosmolar states
  • prevention of long term microvascular complications (eg with statins)
103
Q

what is the ideal treatment of type 2 diabetes?

A

weight loss and exercise will reverse hyperglycaemia

104
Q

Management of type 1 diabetes uses basal-bolus insulin.

What is basal vs bolus insulin? How and why do the types of insulin used for each differ?

A

A bolus dose is insulin that is specifically taken at meal times to keep blood glucose levels under control following a meal. Bolus insulin needs to act quickly and so short acting insulin or rapid acting insulin will be used.

The role of basal insulin, also known as background insulin, is to keep blood glucose levels at consistent levels during periods of fasting. Basal insulin need to act over a relatively long period of time and therefore basal insulin will either be long acting insulin or intermediate insulin.

105
Q

What are the drawbacks of basal-bolus control of type 1 diabetes?

A

Calculating bolus dose can be difficult, as it depends on carbohydrate/glucose content of meal as well as specific person.
Management asks a lot of the patient!

106
Q

How does treatment of type 2 diabetes differ from basal-bolus control of type 1?

A

Earlier initiation of insulin is necessary for type 2 - clinical inertia still exists.
Basal insulin + oral therapy for type 2 diabetes improve glycaemic control and reduce hypoglycaemia (intensification and bolus insulin sometimes necessary).
Can also be managed by controlling diet and exercising.

107
Q

why is it crucial that hypoglycaemic episodes in diabetics are avoided?

A

More than 1 episode per year = driving license revoked.

At level 3 episodes, cognitive function is impaired.

108
Q

Common symptoms of hypoglycaemia:
autonomic?
neuroglucopenic(shortage glucose to brain)?
non-specific?

A

autonomic?
trembling, palpitations, sweating, anxiety, hunger
neuroglucopenic(shortage glucose to brain)?
difficulty concentrating, confusion, weakness, drowsy/dizzy, vision changes, difficulty speaking
non-specific?
nausea, headache

109
Q

In non-diabetics, what protective mechanisms do we have against hypoglycaemia?

A

Insulin secretion switched off by beta cells as glucose falls, stabilising glucose levels.

110
Q

with diabetes, why do protective mechanisms against hypoglycaemia (insulin secretion switched off) not occur?

A

Injected bolus of insulin continues to lower glucose levels.
Glucagon defense response progressively disappears and is not released during hypoglycaemia. Adrenal mechanism threshold also begins to fall progressively.
ADditionally, cognitive response is impaired.

Phase 2 (16 decks)

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