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FinalMB Part I - Medicine > Diabetes > Flashcards

Flashcards in Diabetes Deck (52)
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1
Q

Ideally the body wants to keep blood glucose at at a concentration between ?

A

4.4 and 6.1 mmol/L

2
Q

Where is insulin produced ?

A

The beta cells in the Islets of Langerhans in the pancreas

3
Q

What type of hormone is insulin ?

A

It is an anabolic hormone

4
Q

How does insulin reduce blood sugar levels ?

A
  • It causes cells in the body to absorb glucose from the blood and use it as fuel
  • It causes muscle and liver cells to absorb glucose from the blood and store it as glycogen
5
Q

Where is glucagon produced ?

A

The alpha cells in the Islets of Langerhans in the pancreas

6
Q

What type of hormone is glucagon ?

A

It is a catabolic hormone

7
Q

What is glucagon released in response to ?

A

Low blood sugar levels and stress

8
Q

How does glucagon increase blood sugar levels ?

A
  • Glycogenolysis

- Gluconeogenesis (It tells the liver to convert fats and proteins into glucose

9
Q

When does ketogenesis occur ?

A

When there is insufficient glucose supply and glycogen stores are exhausted, such as in prolonged fasting

10
Q

What happens in ketogenesis ?

A

The liver takes fatty acids and converts them into ketones. Ketones are water soluble fatty acids that can be used as fuel. The can cross the BBB and can be used by the brain. Producing ketones is normal and not harmful in healthy pts when under fasting conditions or on very low carbohydrate, high fat diets.

11
Q

How can ketone levels be measured ?

A
  • Urine dip stick

- In the blood using a ketone meter

12
Q

People with ketosis have a characteristic what smell on their breath ?

A

Acetone smell

13
Q

Ketone acids (ketones) are buffered in normal pts so the blood does not become acidotic. When underlying pathology (i.e. type 1 diabetes) causes extreme hyperglycaemic ketosis this results in what ?

A

A life threatening metabolic acidosis. This is called diabetic ketoacidosis.

14
Q

Pathophysiology of DKA ?

A

DKA occurs in type 1 diabetes where the person is not producing adequate insulin themselves and is not injecting adequate insulin to compensate for this. It occurs when the body does not have enough insulin to use and process glucose. The main problems are ketoacidosis, dehydration and potassium imbalance.

KETOACIDOSIS:
-As the cells in the body have no fuel and think they are starving they initiate the process of ketogenesis so that they have a usable fuel. Over time the pt gets higher and higher glucose and ketone levels. Initially the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH. Over time the ketone acids use up the bicarbonate and the blood starts to become acidic. This is called ketoacidosis.

DEHYDRATION:
-Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine. The glucose in the urine draws water out with it in a process called osmotic diuresis. This causes polyuria. This results in severe dehydration. The dehydration stimulates the thirst centre to tell the pt to drink lots of water causing polydipsia.

POTASSIUM IMBALANCE:
-Insulin normally drives potassium into cells. Without insulin potassium is not added to and stored in cells. Serum potassium can be high or normal as the kidneys continue to balance blood potassium with the potassium excreted in t the urine, however total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts pts can develop severe hypokalaemia very quickly and this can lead to fatal arrhythmias

15
Q

Presentation of DKA ?

A

This is a life threatening medical emergency. The pathophysiology described previously leads to:

  • Hyperglycaemia
  • Dehydration
  • Ketosis
  • Metabolic acidosis (with a low bicarbonate)
  • Potassium imbalance

The pt will therefore present with symptoms of these abnormalities:

  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Acetone smell to their breath
  • Dehydration and subsequent hypotension
  • Altered consciousness
  • They may have symptoms of an underlying trigger (i.e. sepsis)
16
Q

Note:

A

The most dangerous aspects of DKA are dehydration, potassium imbalance and acidosis. Therefore the priority is fluid resuscitation to correct the dehydration, electrolyte disturbance and acidosis. This is followed by an insulin infusion to get the cells to start taking up and using glucose and stop producing ketones.

17
Q

Diagnosis of DKA ?

A

Check the local DKA diagnostic criteria for your hospital. To diagnose DKA you require:

  • Hyperglycaemia (i.e. blood glucose > 11 mmol/L)
  • Ketosis (i.e. blood ketones > 3 mmol/L)
  • Acidosis (i.e. pH < 7.3)
18
Q

Treatment of DKA ?

A

FIG-PICK

Follow local protocols carefully

F - Fluids - IV fluid resuscitation with normal saline (e.g. 1 litre stat, then 4 litres with added potassium over the next 12 hours)
I - Insulin - Add an insulin infusion (e.g. Actrapid at 0.1 Unit/Kg/hour)
G - Glucose - Closely monitor blood glucose and add a dextrose infusion if below a certain level (e.g. < 14 mmol/L)
P - Potassium - Closely monitor serum potassium (e.g. 4 hourly) and correct as required
I - Infection - Treat underlying triggers such as infection
C - Chart fluid balance
K - Ketones - Monitor blood ketones (or bicarbonate if ketone monitoring is unavailable)

Establish the pt on their normal subcutaneous insulin regime prior to stopping the insulin and fluid infusion.

Remember as a general rule potassium should not be infused at a rate of more than 10 mmol per hour.

19
Q

Long term management of type 1 diabetes ?

A

Patient education is essential. Monitoring and treatment is relatively complex. The condition is life-long and requires the pt to fully understand and engage with their condition. It involves the following components:

  • Subcutaneous insulin regimes
  • Monitoring daily carbohydrate intake
  • Monitoring blood glucose on waking, at each meal and before bed
  • Monitoring for and managing complications, both short term and long term

Insulin is usually prescribed as a combination of a background, long acting insulin given once a day and a short acting insulin injected 30 minutes before intake of carbohydrates (i.e. at meals). Insulin regimes are initiated by a diabetes specialist.

Injecting into the same spot can cause a condition called “lipodystrophy”, where the subcutaneous fat hardens and pts do not absorb insulin properly from further injections in this spot. For this reason pts should cycle the injection sites. If a pt is not responding to insulin as expected, ask where they inject and check for lipodystrophy.

20
Q

Short term complications of type 1 diabetes ?

A
  • Hypoglycaemia

- Hyperglycaemia (and DKA)

21
Q

Most pts are aware when they are hypoglycaemic by their symptoms however some pts can be unaware until severely hypoglycaemic. Typical sypmtoms are ? & More severe hypoglycaemia will lead to what ?

A
  • Tremor, sweating, irritability, dizziness and pallor.

- Reduced consciousness, coma and death unless treated.

22
Q

How is hypoglycaemia treated in type 1 diabetics (include treatment for severe hypoglycaemia ?

A
  • A combination of rapid acting glucose such as lucozade and slower acting carbohydrates such as biscuits and toast for when the rapid acting glucose is used up.
  • Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.
23
Q

How is hyperglycaemia treated in type 1 diabetes ?

A

If the pt is hyperglycaemic but not in DKA then may require their insulin dose to be increased. Pts will get to know their own individual response to insulin and be able to administer a dose to correct the hyperglycaemia. Be conscious that it can take several hour to take effect and repeated doses could lead to hypoglycaemia. If they meet the criteria for DKA they need admission for treatment of DKA.

24
Q

Long term complications of type 1 diabetes ?

A

Chronic exposure to hyperglycaemia causes damage to the endothelial cells of blood vessels. This leads to leaky, malfunctioning vessels that are unable to regenerate. High levels of sugar in the blood also causes suppression of the immune system, and provides an optimal environment for infectious organisms to thrive.

Macrovascular complications:

  • Coronary artery disease is a major cause of death in diabetics
  • Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
  • Stroke
  • Hypertension

Microvascular complications

  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis

Infection related complications

  • Urinary tract infections
  • Pneumonia
  • Skin and soft tissue infections, particularly in the feet
  • Fungal infections, particularly oral and vaginal candidiasis
25
Q

Monitoring of type 1 diabetes ?

A
  • HbA1c
  • Capillary blood glucose
  • Flash glucose monitoring (e.g. FreeStyle Libre)
26
Q

What is a HbA1c, how often is it measured/why is it measured in diabetic pts?

A

When we check HbA1c we are counting glycated haemoglobin, which is how much glucose is attached to the haemoglobin molecule. This is considered to reflect the average glucose level over the last 3 months because RBCs have a lifespan of around 3 to 4 months. We measure it every 3 to 6 months to track progression of the pts diabetes and how effective the interventions are. It requires a blood sample to be sent to the lab, usually a red top EDTA bottle.

27
Q

How is capillary blood glucose measured ?

A

Using a little machine called a glucose meter that gives an immediate result. Pts with type 1 and type 2 diabetes rely on these machines for self monitoring their sugar levels.

28
Q

Flash glucose monitoring (e.g. Freestyle libre) ?

A

This uses a sensor on the skin that measures the glucose level of interstitial fluid. There is a lag of 5 minutes behind blood glucose. This sensor records the glucose readings at short intervals so you get a really good impression of what the glucose levels are doing over time. This user needs to use a “reader” to swipe over the sensor and it is the reader that shows the blood sugar readings. Sensors need replacing every 2 weeks for the FreeStyle Libre system. It is quite expensive and NHS funding is only available in certain areas at present. The 5 minute delay also means it is necessary to do capillary blood glucose checks if hypoglycaemia is suspected.

29
Q

Simplified pathophysiology of type 2 diabetes ?

A

Repeated exposure to glucose and insulin makes the cells in the body become resistant to the effects of insulin. It therefore requires more and more insulin to produce a response form the cells to get them to take up and use glucose. Over time, the pancreas (specifically the beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less. A continued onslaught of glucose on the body in light of insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia. Chronic hyperglycaemia leads to microvascular, macrovascular and infectious complications as previously described.

30
Q

Risk factors for type 2 diabetes ?

A

Non-modifiable

  • Older age
  • Ethnicity (Black, Chinese, South Asian)
  • Family history

Modifiable

  • Obesity
  • Sedentary lifestyle
  • High carbohydrate (particularly refined carbohydrate) diet
31
Q

Note:

A

Consider type 2 diabetes in any pts fitting the risk factors previously mentioned. It is easy to screen for diabetes with a HbA1C and early treatment goes a long way to prevent the long term complications. It is possible to reverse diabetes with the proper diet and lifestyle, therefore knowing about it early is worthwhile.

32
Q

Symptoms of diabetes that should prompt testing ?

A
  • Fatigue
  • Polydipsia and polyuria
  • Unintentional weight loss
  • Opportunistic infections
  • Slow healing
  • Glucoseuria (on dipstick)
33
Q

How does an oral glucose tolerance test work + what is it testing ?

A

It is performed in the morning prior to having breakfast. It involves taking a baseline fasting plasma glucose result, giving a 75g glucose drink and then measuring plasma glucose 2 hours later. It tests the ability of the body to cope with a carbohydrate meal

34
Q

What is pre-diabetes ?

A

It is an indication that the pt is heading towards diabetes. They do not fit the full diabetic diagnostic criteria but should be educated regarding diabetes and implement lifestyle changes to reduce their risk of becoming diabetic. They are not currently recommended to start treatment at this point..

35
Q

Pre-diabetes diagnosis ?

A

It can be diagnosed with a HbA1c or by “impaired fasting glucose” or “impaired glucose tolerance”. Impaired fasting glucose means their body struggles to get their blood glucose into normal range even after a prolonged period without eating carbohydrates. Impaired glucose tolerance means their body struggles to cope with processing a carbohydrate meal.

  • HbA1C - 42-47 mmol/mol
  • Impaired fasting glucose - fasting glucose 6.1 - 6.9 mmol/L
  • Impaired glucose tolerance - plasma glucose at 2 hours 7.8 - 11.1 mmol/L on an OGTT
36
Q

Diabetes diagnosis ?

A

Diabetes can be diagnosed if the pt fits the criteria on plasma glucose, an oral glucose tolerance test or HbA1c .

  • HbA1c > 48 mmol/mol
  • Random glucose > 11 mmol/L
  • Fasting glucose > 7 mmol/L
  • OGTT > 11mmol/L
37
Q

Management of type 2 diabetes ?

A

Dietary modification:

  • Vegetables and oily fish
  • Typical advice is low glycaemic, high fibre diet
  • A low carbohydrate diet may in fact be more effective in treating and preventing diabetes but is not yet mainstream advice

Optimise other risk factors:

  • Exercise and weight loss
  • Stop smoking
  • Optimise treatment for other illness, for example HTN, hyperlipidaemia and CVD

Monitoring for complications:

  • Diabetic retinopathy
  • Kidney disease
  • Diabetic foot
38
Q

Treatment targets for type 2 diabetes ?

A

SIGN Guidelines and NICE Guideline 2015 recommend the following HbA1c treatment targets:

  • 48 mmol/mol for new type 2 diabetics
  • 53 mmol/mol for diabetics that have moved beyond metformin alone
39
Q

Medical management of type 2 diabetes ?

A

NICE Guidelines 2015 (updated 2017):

First line: metformin titrated up as tolerated. Initially 500mg once daily.

Second line add: sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor. The decision should be based on individual factors and drug tolerance.

Third line:

  • Triple therapy with metformin and two of the second line drugs combined, or;
  • Metformin plus insulin

SIGN Guidelines 2017 suggest the use of SGLT-2 inhibitors (e.g. empagliflozin) or GLP mimetics (e.g. liraglutide) preferentially in pts with CVD.

40
Q

What is metformin, how does it work, what is it considered to be and does it have any side effects ?

A

Metformin is a “biguanide”. It increases insulin sensitivity and decreases liver production of glucose. It is considered to be “weight neutreal” and does not increase or decrease body weight.

Notable side effects:

  • Diarrhoea and abdominal pain. This is dose dependant and reducing the dose often resolves the symptoms
  • Lactic acidosis
  • Does NOT typically cause hypoglycaemia
41
Q

What is pioglitazone, how does it work and list some notable side effects ?

A

Pioglitazone is a “thiazolidinedione”. It increases insulin sensitivity and decreases liver production of glucose.

Notable side effects:

  • Weight gain
  • Fluid retention
  • Anaemia
  • Heart failure
  • Extended use may increase risk of bladder cancer
  • Does not typically cause hypoglycaemia
42
Q

What is the most common sulfonylurea, what do sulfonylureas do and name some notable side effects ?

A

The most common sulfonylurea is “gliclazide”. Sulfonylureas stimulate insulin release from the pancreas.

Notable side effects:

  • Weight gain
  • Hypoglycaemia
  • Increased risk of CVD and MI when used as monotherapy
43
Q

What are incretins, what are they secreted in response to and what do they do ?

A

Incretins are hormones produced by the GI tract. They are secreted in response to large meals and act to reduce blood sugar. They:

  • Increase insulin secretion
  • Inhibit glucagon production
  • Slow absorption by the GI tract.
44
Q

What is the main incretin ?

A

Glucagon-like peptide-1 (GLP-1)

45
Q

Incretins are inhibited by an enzyme called what ?

A

Dipeptidyl peptidase-4 (DPP-4)

46
Q

What is the most common DPP-4 inhibitor, what effect does it have and name some notable side effects ?

A

The most common DPP-4 inhibitor is “sitagliptin”. It inhibits the DPP-4 enzyme and therefore increases GLP-1 activity.

Notable side effects:

  • GI tract upset
  • Symptoms of upper respiratory tract infection
  • Pancreatitis
47
Q

GLP-1 mimetics ?

A

These medications mimic the action of GLP-1. Two common GLP-1 mimetics are “exenatide” and “liraglutide”. Exenatide is given as a subcutaneous injection either twice daily by the pt or once weekly in a modifiable-release form. Liraglutide is given daily as a subcutaneous injection. They are somtimes used in combination with metformin and a sulfonylurea in overweight pts.

Notable side effects

  • GI tract upset
  • Weight loss
  • Dizziness
  • Low risk of hypoglycaemia
48
Q

What suffix do SGLT-2 inhibitors end with and give some examples ?

A

The suffix “-gliflozin”. Examples include empagliflozin, canagliflozin and dapagliflozin.

49
Q

How do SGLT-2 inhibitors lower blood glucose ?

A

The SGLT-2 protein is responsible for reabsorbing glucose from the urine into the blood in the proximal tubules of the kidneys. SGLT-2 inhibitors block the action of this protein and cause glucose to be excreted in the urine.

50
Q

Note:

A

Empagliflozin has been shown to reduce the risk of CVD, hospitalisation with HF and all cause mortality in type 2 diabetes. Canagliflozin has been shown to reduce the risk of MI, stroke, death and hospitalisation with HF in type 2 diabetes. These reduced risks are likely related to the class rather than the individual medications but have not been proven for all SGLT-2 inhibitors.

51
Q

Notable side effect of SGLT-2 inhibitors ?

A
  • Glucoseuria (glucose in the urine)
  • Increased rate of UTIs
  • Weight loss
  • Diabetic ketoacidosis, notably with only moderately raised glucose. This is a rare complication.
52
Q

Examples of insulin ?

A

RAPID ACTING INSULINS - These start working after around 10 minutes and last around 4 hours:

  • Novorapid
  • Humalog
  • Apidra

SHORT-ACTING INSULINS - These start working in around 30 minutes and last around 8 hours:

  • Actrapid
  • Humulin S
  • Insuman Rapid

INTERMEDIATE-ACTING INSULINS - These start working in around 1 hour and last around 16 hours:

  • Insulatard
  • Humulin I
  • Insuman Basal

LONG-ACTING INSULINS - These start working in around 1 hour and lasts around 24 hours:

  • Lantus
  • Levemir
  • Degludec (lasts over 40 hours)

COMBINATION INSULINS - These contain a rapid acting and an intermediate acting insulin. In brackets is the proportion of long to short acting:

  • Humalog 25 (25:75)
  • Humalog 50 (50:50)
  • Novomix 30 (30:70)