Endocrinology Flashcards
Where is the hypothalamus situated in relation to the pituitary? Which hormones are released?
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)
Thyroid axis
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
Adrenal axis
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.
What actions does cortisol carry out
- inhibits immune system
- inhibits bone formation
- raises blood glucose
- increases metabolism
- increases alertness
Growth hormone acis
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)
Functions of growth hormone
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
Relationship between parathyroid hormone and calcium levels
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
- stimulates increased calcium reabsorption from kidneys meaning less is excreted in urine
- 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 does the renin-angiotensin system affect blood pressure
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.
Cushing’s syndrome vs Cushing’s disease
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
Features of Cushing’s syndrome
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
Causes of Cushing’s syndrome
- patients on long term, high dose steroids
- cushing’s disease (pituitary adenoma)
- adrenal adenoma
- paraneoplastic Cushing’s/ ectopic ACTH - cancer elsewhere like in lungs
What is the main test for diagnosing Cushing’s syndrome?
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
Other potential tests for Cushing’s syndrome
- 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
Treatment of Cushing’s syndrome
- 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
What is adrenal insufficiency?
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
What is primary adrenal insufficiency
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
What is secondary adrenal insufficiency
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
What is tertiary adrenal insufficiency
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
Signs and symptoms of adrenal insufficiency
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
What is the test of choice to diagnose adrenal insufficiency
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
Treatment of adrenal insufficiency
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.
What is an Addisonian Crisis (also known as Adrenal Crisis)
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
Management of Addisonian crisis
- parenteral steroids
IV hydrocortisone 100mg stat
then 100mg every 6 hours - IV fluid resuscitation
- correct hypoglycaemia
- monitoring and balance of fluid and electrolytes
Thyroid function tests and their levels in hypo- and hyperthyroidism
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
In what exceptional case would a patient have hyperthyroidism but also have elevated TSH?
If they have a pituitary adenoma as they release TSH
What are the 3 main antibodies that could be present in thyroid disease?
- anti-TPO antibodies
(anti thyroperoxidase antibodies)
antibodies against the thyroid gland itself
present in Grave’s and Hashimoto’s - 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 - TSH receptor antibodies
autoantibodies that mimic TSH and bind to the TSH receptor to cause thyroid hormone release
cause of Grave’s disease
What imaging tests can be used to detect thyroid diseases?
- thyroid ultrasound
- useful for detecting thyroid nodules and differentiating between whether they are cystic or solid nodules - 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
Primary vs secondary hyperthyroidism
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
What are the symptoms of hyperthyroidism?
- anxiety and irritability
- sweating and heat intolerance
- tachycardia
- weight loss
- fatigue
- frequent loose stools
- sexual dysfunction
What is Grave’s disease
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
What are the 3 main features of Grave’s disease?
- diffuse goitre without nodules
- 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 - pretibial myxoedema = discoloured, waxy, oedematous appearance of the skin over the pre-tibial area due to deposits of mucin under the skin
What is toxic multinodular goitre
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
What is a solitary toxic thyroid nodule
a single abnormal thyroid nodule that acts alone to release thyroid hormones
nodules are usually benign adenomas
treated with surgical removal of the nodule
What is De Quervain’s thyroiditis
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
What is a thyroid storm
also known as thyrotoxic crisis
it is a rare, more severe presentation of hyperthyroidism with pyrexia, tachycardia and delirium
Management of hyperthyroidism
- 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 - Second line antithyroid drug = PROPYLTHIOURACIL
- similar MOA, but has additional risk of severe hepatic reactions - 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 - 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 - 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
What are the causes of hypothyroidism
- 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
Presentation and features of hypothyroidism
- weight gain
- fatigue
- dry skin
- coarse hair and hair loss
- fluid retention
- amenorrhoea
- constipation
Primary vs secondary hypothyroidism
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
What is the main management of hypothyroidism
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.
2 main hormones that control blood sugar
- 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 - 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
What is ketogenesis
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
What is type 1 diabetes
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
Causes of diabetes
- unclear
- possible genetic component
- can be triggered by certain viruses, e.g. Coxsackie B and enterovirus
What is the classic triad of hyperglycaemia symptoms that people with type 1 diabetes may present with?
- polyuria - excessive urine
- polydipsia - excessive thirst
- weight loss - mainly through dehydration
What is diabetic ketoacidosis?
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
What are the 3 key features of diabetic ketoacidosis that can cause serious harm to a patient?
- ketoacidosis
- dehydration
- potassium imbalance
What is ketoacidosis?
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
How does diabetic ketoacidosis cause dehydration?
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
How does diabetic ketoacidosis cause potassium imbalance?
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
What symptoms does diabetic ketoacidosis present with?
- polyuria
- polydipsia
- nausea and vomiting
- acetone (fruity) smell to breath
- dehydration
- weight loss
- altered consciousness
A diagnosis of diabetic ketoacidosis requires which 3 factors?
- hyperglycaemia (blood glucose >11mmol/L)
- ketosis (blood ketones > 3mmol/L)
- acidosis (pH < 7.3)
Management of diabetic ketoacidosis
(can be remembered by FIG-PICK)
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
Autoantibodies which may be present in type 1 diabetes include
- anti-islet cell antibodies
- anti-GAD antibodies
- anti-insulin antibodies
Long-term management of type 1 diabetes
- subcutaneous insulin
- monitoring dietary carbohydrate intake
- monitoring blood sugars when you wake up, before/after each meal and before bed
- monitoring for and managing any complications
What is a basal-bolus regime of insulin?
It involves a combination of:
- long-acting insulin - injected once a day
- short-acting insulin - injected 30 mins before meals
What is the difference between basal bolus and sliding scale
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
Why is it important for patients to cycle their insulin injection sites?
Injecting into the same spot can cause lipodystrophy
which is where the subcutaneous fat hardens
these areas do not absorb insulin properly
What are insulin pumps
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
advantages and disadvantages of an insulin pump
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
How can patients monitor their blood glucose levels? (4 ways)
- 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) - Capillary blood glucose / finger-prick test
measured using blood glucose monitor, gives immediate result - 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 - Continuous glucose monitors
similar to flash glucose monitors except readings are sent over bluetooth
What are the 2 short term complications of type 1 diabetes
- 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 - hyperglycaemia & DKA
- short episodes may not require treatment
- DKA needs to be admitted to hospital
Long term complications of type 1 diabetes
- coronary artery disease
- peripheral ischaemia - diabetic foot ulcers
- stroke
- peripheral neuropathy
- retinopathy
- kidney disease like glomerulosclerosis
- UTIS
- fungal infections like candidiasis
What is type 2 diaebetes
when a combination of insulin resistance and reduced insulin production causes persistently high blood sugar levels
why do people with type 2 diabetes have reduced insulin production?
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
non-modifiable risk factors of type 2 diabetes
- older age
- ethnicity (black, south asian)
- family history
modifiable risk factors of diabetes
- obesity
- sedentary lifestyle
- high carb diet
what are the presenting features of type 2 diabetes
- tiredness
- polyuria and polydipsia
- unintentional weight loss
- opportunistic infections (oral thrush)
- slow wound healing
- glucose in urine on dipstick
what physical feature is assosciated with insulin resistance
acanthosis nigricans
= thickening and darkening of the skin often at neck, axilla and groin
what test levels indicate pre-diabetes (HbA1c, fasting and OGTT levels)
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
what test levels indicate type 2 diabetes (HbA1c, fasting and OGTT levels)
HbA1c = 48mmol or above
fasting glucose > 7mol/L
OGTT >11mmol/L
what is the first line option for medical management of type 2 diabetes
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
what is the second line option for medical management of type 2 diabetes
based on individual factors and drug tolerance, add either of the following:
- sulfonylurea
- pioglitazone
- DPP-4 inhibitor
- SGLT-2 inhibitor
What are SGLT-2 inhibitors
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
What is pioglitazone
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
what are sulfonylureas
most common is gliclazide
- stimulate insulin release from pancreas
can cause weight gain and hypoglycaemia
What are incretins
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)
what are DPP-4 inhibitors
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
what is the third line option for medical management of type 2 diabetes
there are 2 options:
- triple therapy with metformin and two of the second-line drugs
- metformin with insulin therapy
What are the 5 types of insulin that can be given
- RAPID ACTING - NovoRapid
start after 10mins, last 4 hours - SHORT ACTING - Actrapid
start after 30mins, last 8 hours - INTERMEDIATE ACTING - Humulin
start after 1hr, last 16 hrs - LONG ACTING - Lemevir, Lantus
start after 1hr, last 24hrs or more - COMBINATION = rapid acting : intermediate acting
Humalog 25 (25:75)
Humalog 50 (50:50)
Novomix 30 (30:70)
Key complications of type 2 diabetes
- infections like thrush and infected ulcers
- diabetic retinopathy
- peripheral neuropathy
- chronic kidney disease
- diabetic foot
- gastroparesis (slow emptying of stomach)
- hyperosmolar hyperglycaemic state
What is the first line drug to manage hypertension in type 2 diabetic patients
ACE inhibitors
What drugs are used to manage chronic kidney disease in type 2 diabetic patients
When ACR (albumin:creatine ratio) > 3mg/mmol = ACE Inhibitors
When ACR > 30mg/mmol = ACEI and an SGLT-2 inhibitor
What drugs are used for gastroparesis in type 2 diabetic patients
prokinetic drugs like metoclopramide
can have cardiac side effects so use with caution
What drugs can be used for neuropathic pain in patients with type 2 diabetes
- amitriptyline - tricyclic antidepressant
- duloxetine - SNRI antidepressant
- gabapentin - anticonvulsant
- pregabalin - anticonvulsant
What is HHS (hyperosmolar hyperglycaemic state)
rare by fatal complication of type 2 diabetes - medical emergency
characterised by 3 things:
1. hyperosmolality (water loss leads to very concentrated blood)
- hyperglycaemia
- absence of ketones (used to distinguish from DKA)
Presents with polyuria, polydipsia, weight loss, tachycardia, dehydration, hypotension and confusion
IV fluids and monitoring required
What is acromegaly
a result of excessive growth hormone
most common cause of unregulated growth hormone secretion
pituitary adenoma
If acromegaly is caused by a pituitary tumour, what 2 other symptoms can you expect
- headaches
- 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
Excess growth hormone can cause tissue growth. What symptoms can this cause
- 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
Excess growth hormone can cause organ dysfunction, this includes:
- hypertrophic heart
- hypertension
- type 2 diabetes
- colorectal cancer
- bilateral carpal tunnel syndrome
What 3 tests can be carried out to diagnose acromegaly
- 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 - 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 - MRI of pituitary to diagnose an adenoma
What is the definitive treatment for acromegaly caused by a pituitary adenoma
Trans-sphenoidal surgery
- removal of pituitary tumour through the nose and sphenoid bone
What are the medical options available for treating acromegaly when surgery isn’t suitable
- Pegvisomant = GH receptor antagonist
given daily via subcutaneous injection - Somatostatin analogues, octreotide
block GH release - Dopamine agonists, bromacriptine
block GH release
