Endocrinology Flashcards

1
Q

Where is the hypothalamus situated in relation to the pituitary? Which hormones are released?

A

Hypothalamus sits above the pituitary gland and stimulates it with various hormones

Pituitary gland has anterior and posterior section that releases separate hormones.

Anterior pituitary gland releases:
- TSH (thyroid stimulating)
- ACTH (adrenocorticotropic hormone)
- FH
- LH
- GH
- prolactin

Posterior pituitary gland releases:
- oxytocin
- ADH (antidiuretic hormone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Thyroid axis

A

Hypothalamus releases TRH (thyrotropin releasing hormone)

TRH stimulates anterior pituitary to release TSH

TSH stimulates thyroid gland to release T3 and T4

Negative feedback loop
When T3 and T4 levels are high, the hypothalamus and pituitary suppress the release of TRH and TSH to decrease levels of T3 and T4

With lower levels of T3 and T4, there is less suppression of TRH and TSH, so more is released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Adrenal axis

A

Cortisol is released by adrenal glands which sit above each kidney
- it is released in response to stress
- has diurnal variation - peaks early morning and is lowest at night

Cortisol release is controlled by the hypothalamus

Hypothalamus releases CRH (corticotropin release hormone)

CRH stimulates anterior pituitary to release ACTH (adrenocorticotrophic hormone)

ACTH stimulates adrenal gland to release cortisol

Adrenal axis is also controlled by negative feedback
- when cortisol is high, CRH and ACTH is suppressed and v.v.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What actions does cortisol carry out

A
  • inhibits immune system
  • inhibits bone formation
  • raises blood glucose
  • increases metabolism
  • increases alertness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Growth hormone acis

A

Hypothalamus releases GHRH (growth hormone releasing hormone)

GHRH stimulates anterior pituitary to release GH

GH stimulates liver to release IGF-1 (insulin like growth factor 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Functions of growth hormone

A

GH works directly and indirectly on almost all cells of the body

Main functions:
- stimulates muscle growth
- increases bone density and strength
- stimulates cell regeneration
- stimulates growth of internal organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Relationship between parathyroid hormone and calcium levels

A

PTH (parathyroid hormone) is released from the 4 parathyroid glands, situated in the 4 corners of the thyroid gland

PTH is released in response to
- low serum calcium
- low magnesium
- high serum phosphate

PTH role is to increase serum calcium concentration and it does this in 3 ways:
1. increases activity and number of osteoclasts in the bone - causing reabsorption of calcium from the bone, therefore increasing conc

  1. stimulates increased calcium reabsorption from kidneys meaning less is excreted in urine
  2. stimulates kidneys to convert vitamin D3 into calcitriol, which is an active form of vitamin D that promotes calcium reabsorption from food in the small intestine

When serum calcium is high, PTH is suppressed via negative feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does the renin-angiotensin system affect blood pressure

A

Renin is a hormone/enzyme that is secreted by the juxtaglomerular cells in the afferent arterioles of the kidney

The afferent arterioles can sense blood pressure

When BP is low they secrete more renin, and when it is high they secrete less renin.

Renin is an enzyme.
It converts angiotensinogen from the liver into angiotensin 1.

Angiotensin 1 is converted into angiotensin 2 in the lungs by ACE (angiotensin converting enzyme).

Angiotensin 2 causes vasoconstriction of blood vessels, which increases the blood pressure.

It also stimulates the release of aldosterone from the adrenal glands.

Aldosterone is a mineralocorticoid steroid hormone. It acts on the nephrons in the kidney to:
- increase Na reabsorption in distal tubule
- increase K secretion in distal tubule
- increase H secretion from collecting ducts

This leads to an increase in intravascular volume, and subsequently BP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cushing’s syndrome vs Cushing’s disease

A

Cushing’s syndrome = signs and symptoms that develop after prolonged abnormal elevation of cortisol.

Cushing’s disease = a specific condition where a pituitary adenoma secretes excessive ACTH, which stimulates adrenal gland to secrete cortisol.

Cushing’s diseases causes Cushing’s syndrome
but Cushing’s syndrome is NOT always caused by Cushing’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Features of Cushing’s syndrome

A

In terms of appearance, think of a patient who is round in the middle with thin limbs
- round moon face
- central obesity
- abdominal striae
- buffalo hump (fat pad on upper back)
- proximal limb muscle wasting

Other features of high stress include
- hypertension
- cardiac hypertrophy
- hyperglycaemia, type 2 diabetes
- depression
- insomnia
- easy bruising and poor skin healing
- osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes of Cushing’s syndrome

A
  • patients on long term, high dose steroids
  • cushing’s disease (pituitary adenoma)
  • adrenal adenoma
  • paraneoplastic Cushing’s/ ectopic ACTH - cancer elsewhere like in lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the main test for diagnosing Cushing’s syndrome?

A

Dexamethasone suppression test

Dexamethasone is a synthetic glucocorticoid steroid.

You start with the Low dose test (1mg dexamethasone)
- patient takes it at night and then ACTH and cortisol levels are measured in the morning

Normally dexamethasone would suppress cortisol via negative feedback. Hypothalamus would reduce CRH secretion, therefore less ACTH secretion from pituitary and therefore low cortisol.
NORMAL RESULT = EXCLUDE CUSHING’S

If the cortisol levels are not lowered in the morning, then you would do a high dose dexamethasone test.

In the high dose test the patient is given 8mg, and this is performed to differentiate the causes.

If the patient has Cushing’s syndrome because of Cushing’s disease (PITUITARY ADENOMA) - the pituitary will still show some negative feedback and 8mg will be enough to suppress cortisol.

If the patient has Cushing’s syndrome because of an ADRENAL ADENOMA, cortisol will not be suppressed but ACTH will be suppressed.

If the patient has Cushing’s syndrome because of an ECTOPIC ACTH - neither cortisol nor ACTH will be suppressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Other potential tests for Cushing’s syndrome

A
  • 24hr urinary free cortisol - can diagnose Cushing’s but does not indicate underlying cause
  • FBC - raised WBC
  • electrolytes - low K if aldosterone is being secreted by an adrenal adenoma
  • MRI brain for pituitary adenoma
  • chest CT for ectopic ACTH due to lung cancer
  • abdominal CT for adrenal tumours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Treatment of Cushing’s syndrome

A
  • remove underlying cause - surgical removal of tumour

if surgical removal is not possible - remove both adrenal glands and give patient replacement steroid hormones for life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is adrenal insufficiency?

A

where the adrenal glands do not produce enough steroid hormones, particularly cortisol and aldosterone

this is a life threatening condition if the hormones are not replaced

there are 3 types of insufficiency - primary, secondary and tertiary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is primary adrenal insufficiency

A

also known as Addison’s disease

a specific condition where the adrenal glands have been damaged

leading to reduced secretion of cortisol and aldosterone

main cause is autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is secondary adrenal insufficiency

A

a result of inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release

this is due to loss or damage of the pituitary gland

which can be due to surgical removed of pituitary tumour, infection, loss of blood flow or radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is tertiary adrenal insufficiency

A

a result of inadequate CRH (corticotropin releasing hormone) being released by the hypothalamus

usually a result of long term oral steroids (>3 weeks) causing suppression of the hypothalamus

this is why steroids have to be tapered off so adrenal axis can regain function, rather than withdrawn suddenly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Signs and symptoms of adrenal insufficiency

A

Symptoms
- nausea
- fatigue
- cramps and abdominal pain
- reduced libido

Signs
- bronze hyperpigmentation of the skin (because ACTH stimulates melanocytes to produce melanin)
- hypotension

Hyponatraemia - key clue, can sometimes be the only presenting deature

Hyperkalaemia is also possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the test of choice to diagnose adrenal insufficiency

A

Short synacthen test

Usually performed in the morning

Patient is given synacthen, which is synthetic ACTH

Then blood cortisol is measured at baseline, then 30 and 60 minutes after administration

The synthetic ACTH should stimulate healthy adrenal glands to produce cortisol, and the levels should at least double

A failure of cortisol to rise less than double the baseline indicates primary adrenal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Treatment of adrenal insufficiency

A

Replacement steroids that are titrated according to signs, symptoms and electrolyte levels.

Hydrocortisone is used to replace cortisol. It is a glucocorticoid hormone.

Fludrocortisone is used to replace aldosterone. It is a mineralocorticoid hormone.

Doses should not be missed because they are essential for life.

Doses are doubled during acute illnesses.

Patient should be given a steroid card and emergency ID tag to alert emergency services that they are dependent on steroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is an Addisonian Crisis (also known as Adrenal Crisis)

A

it is an acute presentation of severe Addison’s diseases, where the absence of steroid hormones becomes life threatening.

Patients present with:
- reduced consciousness
- hypotension
- hypoglycaemia
- hyponatraemia
- hyperkalaemia

It can be the first presentation of Addison’s disease
or in a patient with established Addison’s it can be triggered by infection, trauma or other acute illness
or in can happen in someone who suddenly stops taking their steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Management of Addisonian crisis

A
  • parenteral steroids
    IV hydrocortisone 100mg stat
    then 100mg every 6 hours
  • IV fluid resuscitation
  • correct hypoglycaemia
  • monitoring and balance of fluid and electrolytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Thyroid function tests and their levels in hypo- and hyperthyroidism

A

TSH can be used first as a screening test.

If TSH is abnormal then you can measure T3 and T4.

In hyperthyroidism, there is high thyroid hormones (T3 and T4), so TSH will be low.

In hypothyroidism, there are low T3 and T4, so TSH will be high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

In what exceptional case would a patient have hyperthyroidism but also have elevated TSH?

A

If they have a pituitary adenoma as they release TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the 3 main antibodies that could be present in thyroid disease?

A
  1. anti-TPO antibodies
    (anti thyroperoxidase antibodies)
    antibodies against the thyroid gland itself
    present in Grave’s and Hashimoto’s
  2. Antithyroglobulin antibodies
    antibodies against thyroglobulin, which is a protein produced and present only in the thyroid gland.
    can be present in Grave’s, Hashimoto’s, thyroid cancer, but also in healthy individuals
  3. TSH receptor antibodies
    autoantibodies that mimic TSH and bind to the TSH receptor to cause thyroid hormone release
    cause of Grave’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What imaging tests can be used to detect thyroid diseases?

A
  1. thyroid ultrasound
    - useful for detecting thyroid nodules and differentiating between whether they are cystic or solid nodules
  2. Radioisotope scan
    - used to investigate hyperthyroidism and thyroid cancer
    - radioactive iodine is given either orally or IV, which then travels to they thyroid where it is taken up
    - normally iodine is taken up by the thyroid anyway to produce thyroid hormones
    - the more active they thyroid cells are, the faster the iodine is taken up
    - a gamma camera is used to detect the gamma rays emitted from the radioactive iodine
    - more gamma rays = more iodine taken up

Diffuse, high uptake = Grave’s disease

Focal, high uptake = toxic multinodular goitre and adenoma

Abnormally low uptake = thyroid cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Primary vs secondary hyperthyroidism

A

Primary hyperthyroidism is due to thyroid pathology
- the thyroid itself is behaving abnormally and releasing excess thyroid hormones

Secondary hyperthyroidism is due to pathology in the hypothalamus or pituitary
- the thyroid produces excess thyroid hormones due to overstimulation by TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the symptoms of hyperthyroidism?

A
  • anxiety and irritability
  • sweating and heat intolerance
  • tachycardia
  • weight loss
  • fatigue
  • frequent loose stools
  • sexual dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is Grave’s disease

A

an autoimmune condition where TSH receptor antibodies cause hyperthyroidism

these are autoantibodies that mimic TSH and bind to the TSH receptor to cause thyroid hormone release

Grave’s disease is the most common cause of hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the 3 main features of Grave’s disease?

A
  1. diffuse goitre without nodules
  2. exophthalmos = bulging of the eyeball out of the socket
    occurs due to inflammation, swelling and hypertrophy of the tissue behind the eyeball that forces the eyeball forward
  3. pretibial myxoedema = discoloured, waxy, oedematous appearance of the skin over the pre-tibial area due to deposits of mucin under the skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is toxic multinodular goitre

A

this is a condition where firm nodules develop on the thyroid gland

they act independently of the normal negative feedback system

and continuously produce excessive thyroid hormone

most patients are aged over 50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is a solitary toxic thyroid nodule

A

a single abnormal thyroid nodule that acts alone to release thyroid hormones

nodules are usually benign adenomas

treated with surgical removal of the nodule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is De Quervain’s thyroiditis

A

a viral infection with fever, neck pain and tenderness
as well as dysphagia and features of hyperthyroidism

there is a hyperthyroid phase, followed by a hypothyroid phase due to negative feedback

self-limiting condition treated with NSAIDs and beta blockers for symptomatic relied

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is a thyroid storm

A

also known as thyrotoxic crisis

it is a rare, more severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Management of hyperthyroidism

A
  1. First line antithyroid drug = CARBIMAZOLE
    - usually successful in treating Grave’s
    - patients have normal thyroid after 4-8wks
    - then the dose is titrated to either maintain normal levels, or to completely block all production of TSH but with this the patient has to take levothyroxine
    - complete remission within 18mnths of treatment
  2. Second line antithyroid drug = PROPYLTHIOURACIL
    - similar MOA, but has additional risk of severe hepatic reactions
  3. RADIOACTIVE IODINE
    - patient drinks a single dose of radioactive iodine
    - this is taken up by the thyroid and the emitted radiation destroys a portion of thyroid cells
    - reduction in cells = decrease in thyroid hormone production = remission
    - remission takes 6 months
    - patient might be left hypothyroid after and will require levothyroxine replacement
    - pt cannot be pregnant + must limit contact with everyone, esp children and pregnant women
  4. BETA BLOCKERS
    - do not treat the condition, used to control symptoms
    used to block adrenaline related symptoms of hyperthyroidism
    - propranolol is preferred because its non-selective
  5. SURGERY
    - removal of whole thyroid or toxic nodules
    - effectively stops the production of thyroid hormone
    - pt will be left hypothyroid and will require levothyroxine replacement for life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the causes of hypothyroidism

A
  • Hashimoto’s thyroiditis
  • iodine deficiency
  • hyperthyroidism treatments have potential to cause hypothyroidism
  • medications such as lithium or amiodarone which inhibit thyroid hormone production
  • pituitary gland tumours which means pituitary gland fails to produce enough TSH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Presentation and features of hypothyroidism

A
  • weight gain
  • fatigue
  • dry skin
  • coarse hair and hair loss
  • fluid retention
  • amenorrhoea
  • constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Primary vs secondary hypothyroidism

A

Primary is caused by thyroid gland insufficiency.
T3 and T4 will be low, and TSH will be high because there is no negative feedback to the brain so the pituitary produces lots of TSH to get the thyroid working

Secondary is caused by pituitary pathology that results in low production of TSH. Thyroid hormones will be low due to low TSH

40
Q

What is the main management of hypothyroidism

A

Replacement of thyroid hormone with oral levothyroxine
- this is synthetic T4 which metabolises to T3 in the body
- the dose is titrated until TSH levels are normal

Levels have to be measured monthly until stable,
If TSH levels are high, dose is too low and needs to be increased and v.v.

41
Q

2 main hormones that control blood sugar

A
  1. INSULIN - produced by the beta cells in the Islets of Langerhans in the pancreas
    - insulin increases when blood sugar increases
    - it causes cells in the body to absorb glucose and use it
    - also causes muscle and liver cells to absorb glucose from the blood and store it as glycogen
    - without insulin cells cannot take up and use glucose
  2. GLUCAGON - produced by alpha cells in the Islets of Langerhans in the pancreas
    - glucagon increases when blood sugar decreases
    - causes liver to break down stored glycogen into glucose
    - and also to convert proteins and fats into glucose
42
Q

What is ketogenesis

A

when there is insufficient glucose
and glycogen stores are exhausted
the liver takes fatty acids and converts them into ketones

e.g. in prolonged fasting

ketones are water soluble fatty acids that can cross the blood brain barrier

producing ketones is normal and not harmful unless produced in excess amount, where it can cause diabetic ketoacidosis

43
Q

What is type 1 diabetes

A

a condition where the pancreas stops being able to produce adequate insulin

without insulin, cells cannot absorb glucose from the blood and use it for energy

because cells cannot absorb glucose, they think there is no glucose available

at the same time, glucose levels in the blood keep rising, causing hyperglycaemia

44
Q

Causes of diabetes

A
  • unclear
  • possible genetic component
  • can be triggered by certain viruses, e.g. Coxsackie B and enterovirus
45
Q

What is the classic triad of hyperglycaemia symptoms that people with type 1 diabetes may present with?

A
  1. polyuria - excessive urine
  2. polydipsia - excessive thirst
  3. weight loss - mainly through dehydration
46
Q

What is diabetic ketoacidosis?

A

occurs in type 1 diabetes where the person is not producing enough insulin themselves
and is also not injecting enough to compensate for it

can occur as the initial presentation of diabetes;
or in a diabetic pt who has an infection;
or a diabetic pt who is not sticking to their insulin regime

47
Q

What are the 3 key features of diabetic ketoacidosis that can cause serious harm to a patient?

A
  1. ketoacidosis
  2. dehydration
  3. potassium imbalance
48
Q

What is ketoacidosis?

A

type 1 diabetic pts have a lack of insulin

without insulin the body’s cells cannot recognise glucose even though it is present in the blood

so the liver converts fatty acids into ketones to use those for energy instead

over time, glucose and ketone levels rise

at first, the kidneys produce bicarbonate to counteract the ketone acids and maintain a normal pH

but eventually the ketones use up the bicarbonate and the blood becomes acidic = ketoacidosis

49
Q

How does diabetic ketoacidosis cause dehydration?

A

hyperglycaemia overwhelms the kidneys
resulting in glucose being filtered into the urine

glucose in the urine draws water out of it via osmotic diuresis

this causes polyuria which results in severe dehydration
which results in polydipsia

50
Q

How does diabetic ketoacidosis cause potassium imbalance?

A

insulin normally drives potassium into cells

without it, potassium does not enter and is not stored in cells

so serum potassium will be high or normal (because kidneys balance it with the potassium excreted in urine)

but total body potassium will be low because there is none in the cells

when pts start insulin treatment, they can quickly develop severe hypokalaemia (low serum K), leading to fatal arrhythmias

51
Q

What symptoms does diabetic ketoacidosis present with?

A
  • polyuria
  • polydipsia
  • nausea and vomiting
  • acetone (fruity) smell to breath
  • dehydration
  • weight loss
  • altered consciousness
52
Q

A diagnosis of diabetic ketoacidosis requires which 3 factors?

A
  1. hyperglycaemia (blood glucose >11mmol/L)
  2. ketosis (blood ketones > 3mmol/L)
  3. acidosis (pH < 7.3)
53
Q

Management of diabetic ketoacidosis

(can be remembered by FIG-PICK)

A

F - FLUIDS - IV fluid resuscitation with normal saline (1L in the first hour, followed by 1L every 2hrs)

I - INSULIN - fixed rate insulin infusion (Actrapid at 0.1units/kg/hr)

G - Glucose - monitor blood glucose and add glucose infusion if levels drop < 14mmol/L

P - Potassium - add potassium to IV fluids and monitor closely, correct as required. In general, potassium should NOT be infused at a rate of more than 10mmol/hr

I - INFECTION - treat any underlying triggers such as infections

C - CHART FLUID BALANCE

K - KETONES - monitor blood ketones, pH and bicarbonate

54
Q

Autoantibodies which may be present in type 1 diabetes include

A
  • anti-islet cell antibodies
  • anti-GAD antibodies
  • anti-insulin antibodies
55
Q

Long-term management of type 1 diabetes

A
  1. subcutaneous insulin
  2. monitoring dietary carbohydrate intake
  3. monitoring blood sugars when you wake up, before/after each meal and before bed
  4. monitoring for and managing any complications
56
Q

What is a basal-bolus regime of insulin?

A

It involves a combination of:

  1. long-acting insulin - injected once a day
  2. short-acting insulin - injected 30 mins before meals
57
Q

What is the difference between basal bolus and sliding scale

A

Basal bolus aims to prevent hyperglycaemia

Sliding scale (dose is dependent on blood sugar levels pre-meals, higher blood sugar means higher dose) - used after hyperglycaemia has occurred

58
Q

Why is it important for patients to cycle their insulin injection sites?

A

Injecting into the same spot can cause lipodystrophy

which is where the subcutaneous fat hardens

these areas do not absorb insulin properly

59
Q

What are insulin pumps

A

an alternative to basal-bolus regiments

they are small devices that continuously infuse insulin at different rates to control blood sugar

the pump pushes insulin through a small cannula inserted under the skin

the cannulas are replaced ever 2-3 days

60
Q

advantages and disadvantages of an insulin pump

A

advantages:
- better blood sugar control
- more flexibility with eating
- less injections

disadvantages:
- difficulties learning to use the pump
- it is attached at all times
- small risk of infection

61
Q

How can patients monitor their blood glucose levels? (4 ways)

A
  1. HbA1c = glycated haemoglobin (how much glucose is attached to Hb).
    Reflects the average glucose level over the past 3 months (because RBC have 3-4months lifespan)
  2. Capillary blood glucose / finger-prick test
    measured using blood glucose monitor, gives immediate result
  3. Flash glucose monitor, e.g. FreeStyle Libre 2
    a sensor on the skin measures the glucose levels of the interstitial fluid in the subcutaneous tissue
    - usually a 5 min lag with results
    - but records at short intervals
    - sensors need replacing every 2 weeks
    - pts swipe phone over sensor to collect reading
  4. Continuous glucose monitors
    similar to flash glucose monitors except readings are sent over bluetooth
62
Q

What are the 2 short term complications of type 1 diabetes

A
  1. hypoglycaemia
    - first give rapid-acting glucose (e.g. drink with high sugar like lucozade)
    - once blood glucose improves, have a slower-acting carb like biscuit or toast to stop it dropping again
    - if severe - requires IV dextrose and intramuscular glucagon
  2. hyperglycaemia & DKA
    - short episodes may not require treatment
    - DKA needs to be admitted to hospital
63
Q

Long term complications of type 1 diabetes

A
  • coronary artery disease
  • peripheral ischaemia - diabetic foot ulcers
  • stroke
  • peripheral neuropathy
  • retinopathy
  • kidney disease like glomerulosclerosis
  • UTIS
  • fungal infections like candidiasis
64
Q

What is type 2 diaebetes

A

when a combination of insulin resistance and reduced insulin production causes persistently high blood sugar levels

65
Q

why do people with type 2 diabetes have reduced insulin production?

A

repeated exposure to glucose and insulin makes the cells in the body resistant to insulin effects

so more insulin is required to stimulate cells to take up glucose

over time the pancreas becomes fatigued and damage from producing so much insulin, and so insulin production is reduced

66
Q

non-modifiable risk factors of type 2 diabetes

A
  • older age
  • ethnicity (black, south asian)
  • family history
67
Q

modifiable risk factors of diabetes

A
  • obesity
  • sedentary lifestyle
  • high carb diet
68
Q

what are the presenting features of type 2 diabetes

A
  • tiredness
  • polyuria and polydipsia
  • unintentional weight loss
  • opportunistic infections (oral thrush)
  • slow wound healing
  • glucose in urine on dipstick
69
Q

what physical feature is assosciated with insulin resistance

A

acanthosis nigricans
= thickening and darkening of the skin often at neck, axilla and groin

70
Q

what test levels indicate pre-diabetes (HbA1c, fasting and OGTT levels)

A

HbA1c = 42-47mmol/L

fasting glucose = 6.1-6.9mmol/L

OGTT at 2 hours = 7.8-11.1mmol/L

  • patient should be education about risk of diabetes and lifestyle changes they should make to reverse it
71
Q

what test levels indicate type 2 diabetes (HbA1c, fasting and OGTT levels)

A

HbA1c = 48mmol or above

fasting glucose > 7mol/L

OGTT >11mmol/L

72
Q

what is the first line option for medical management of type 2 diabetes

A

Metformin - initially 500mg once daily
titrated up as tolerated

it is a biguanide - increases insulin sensitivity and decreases glucose production by the liver

does not cause weight loss/gain

can cause gastro symptoms like diarrhoea; and lactic acidosis

73
Q

what is the second line option for medical management of type 2 diabetes

A

based on individual factors and drug tolerance, add either of the following:
- sulfonylurea
- pioglitazone
- DPP-4 inhibitor
- SGLT-2 inhibitor

74
Q

What are SGLT-2 inhibitors

A

sodium-glucose co-transporter 2 protein inihibitors
e.g. dapagliflozin; empagliflozin

SGLT-2 are proteins found in the proximal tubules of the kidneys
- they reabsorb glucose from the urine back into the blood

SGLT-2 inhibitors block this so more glucose is excreted in urine

preferred drug especially in patients with existing heart or kidney diseases because they can also help this

2 main side effects
1. increased UTIs and thrush bc lots of sugar passing through urinary tract
2. diabetics ketoacidosis

75
Q

What is pioglitazone

A

a thiazolidinedione
- increases insulin sensitivity and decreases liver production of glucose

does not cause hypoglycaemia but can cause
-weight gain
-heart failure
-increased risk of bone fractures

76
Q

what are sulfonylureas

A

most common is gliclazide
- stimulate insulin release from pancreas

can cause weight gain and hypoglycaemia

77
Q

What are incretins

A

hormones which are normally produced by the GI tract in response to large meals to reduce blood sugar by
- increasing insulin secretion
- inhibiting glucagon production
- slowing absorption by the GI tract

the main incretin in GLP-1 (glucagon like peptide 1)

incretins are inhibited by an enzyme called DPP-4 (dipeptidyl peptidase 4)

78
Q

what are DPP-4 inhibitors

A

e.g. sitagliptin, alogliptin

they block the action of DPP-4 so that incretins are not blocked and their activity is increased

therefore incretins can continue
- increasing insulin secretion
- inhibiting glucagon production
- slowing absorption by the GI tract

do not cause hypoglycaemia

79
Q

what is the third line option for medical management of type 2 diabetes

A

there are 2 options:

  1. triple therapy with metformin and two of the second-line drugs
  2. metformin with insulin therapy
80
Q

What are the 5 types of insulin that can be given

A
  1. RAPID ACTING - NovoRapid
    start after 10mins, last 4 hours
  2. SHORT ACTING - Actrapid
    start after 30mins, last 8 hours
  3. INTERMEDIATE ACTING - Humulin
    start after 1hr, last 16 hrs
  4. LONG ACTING - Lemevir, Lantus
    start after 1hr, last 24hrs or more
  5. COMBINATION = rapid acting : intermediate acting
    Humalog 25 (25:75)
    Humalog 50 (50:50)
    Novomix 30 (30:70)
81
Q

Key complications of type 2 diabetes

A
  • infections like thrush and infected ulcers
  • diabetic retinopathy
  • peripheral neuropathy
  • chronic kidney disease
  • diabetic foot
  • gastroparesis (slow emptying of stomach)
  • hyperosmolar hyperglycaemic state
82
Q

What is the first line drug to manage hypertension in type 2 diabetic patients

A

ACE inhibitors

83
Q

What drugs are used to manage chronic kidney disease in type 2 diabetic patients

A

When ACR (albumin:creatine ratio) > 3mg/mmol = ACE Inhibitors

When ACR > 30mg/mmol = ACEI and an SGLT-2 inhibitor

84
Q

What drugs are used for gastroparesis in type 2 diabetic patients

A

prokinetic drugs like metoclopramide

can have cardiac side effects so use with caution

85
Q

What drugs can be used for neuropathic pain in patients with type 2 diabetes

A
  • amitriptyline - tricyclic antidepressant
  • duloxetine - SNRI antidepressant
  • gabapentin - anticonvulsant
  • pregabalin - anticonvulsant
86
Q

What is HHS (hyperosmolar hyperglycaemic state)

A

rare by fatal complication of type 2 diabetes - medical emergency

characterised by 3 things:
1. hyperosmolality (water loss leads to very concentrated blood)

  1. hyperglycaemia
  2. absence of ketones (used to distinguish from DKA)

Presents with polyuria, polydipsia, weight loss, tachycardia, dehydration, hypotension and confusion

IV fluids and monitoring required

87
Q

What is acromegaly

A

a result of excessive growth hormone

88
Q

most common cause of unregulated growth hormone secretion

A

pituitary adenoma

89
Q

If acromegaly is caused by a pituitary tumour, what 2 other symptoms can you expect

A
  1. headaches
  2. Bitemporal hemianopia = visual field defect caused by pressure on the optic chiasm, which is just above the pituitary gland.
    The patient has loss of outer half of vision in both eyes
90
Q

Excess growth hormone can cause tissue growth. What symptoms can this cause

A
  • frontal bossing = prominent forehead and brow
  • large nose
  • large tongue (macroglossia)
  • large hands and feet
  • large protruding jaw (prognathism)
  • coarse, sweaty skin
  • arthritis from imbalanced growth of joints
91
Q

Excess growth hormone can cause organ dysfunction, this includes:

A
  • hypertrophic heart
  • hypertension
  • type 2 diabetes
  • colorectal cancer
  • bilateral carpal tunnel syndrome
92
Q

What 3 tests can be carried out to diagnose acromegaly

A
  1. Blood sample to test for IGF-1 (insulin like growth factor)
    - this indicates GH levels and is raised in acromegaly
    - testing GH directly is unreliable because it fluctuates throughout the day
  2. GH suppression test
    - pt consumes 75g glucose drink and GH is measured at baseline and after 2 hours
    - glucose should suppress GH, failure to do so indicates acromegaly
  3. MRI of pituitary to diagnose an adenoma
93
Q

What is the definitive treatment for acromegaly caused by a pituitary adenoma

A

Trans-sphenoidal surgery
- removal of pituitary tumour through the nose and sphenoid bone

94
Q

What are the medical options available for treating acromegaly when surgery isn’t suitable

A
  1. Pegvisomant = GH receptor antagonist
    given daily via subcutaneous injection
  2. Somatostatin analogues, octreotide
    block GH release
  3. Dopamine agonists, bromacriptine
    block GH release
95
Q
A