Type 2 Diabetes Flashcards
(109 cards)
1
Q
What causes type 1 diabetes?
A
A culmination of lymphocytic infiltration and destruction of insulin-secreting beta cells of the islets of Langerhans in the pancreas. As beta-cell mass declines, insulin secretion decreases until the available insulin is insufficient to maintain normal blood glucose levels.
2
Q
What causes type 2 diabates?
A
When cells in the muscle, fat, and liver become resistant to insulin, causing them to no longer take in enough sugar. The pancreas then can’t produce enough insulin to keep blood sugar levels within a healthy range.
3
Q
What are some common symptoms of type 2 diabetes?
A
Polydipsia - thirst
Polyuria – frequent urination
Blurred vision
Unexplained weight loss
Recurrent infections
Tiredness
Acanthosis nigricans – skin condition caused by dark pigmentation of skin folds. Suggests insulin resistance.
4
Q
What is persistent hyperglycaemia defined as?
A
HbA1c 48mmol/L (6.5%) or more
Fasting plasma glucose 7mmol/L or more
Randome plasma glucose 11.1mmol/L or more in the presence of symptoms of diabetes.
5
Q
In which groups should HbA1c not be used to determine persistent hyperglycaemia?
A
<18
Pregnant women
2 months postpartum
<2 months diabetes symptoms
Medication which cause hyperglycaemia e.g., longterm corticosteroids.
Acute pancreatic damage
End-stage renal damahe
HIV
6
Q
Why should diabetes not be diagnosed based on a one-off blood test?
A
Hyperglycaemia can be due to trauma, infection, stress
7
Q
What are risk factors for type 2 diabetes?
A
Obesity and inactivity
Family history
Ethnicity - Asian, African, Afro-Caribbean
History of gestational diabetes
Diet - low fibre or high glycaemic index foods
Drug treatments - statins, corticosteroids
PCOS
Metabolic syndrome
Low birth weight
8
Q
What is the target HbA1c level if T2D managed by lifestyle changes alone?
A
48mmol/mol (6.5%)
9
Q
What is the target HbA1c level if T2D managed by lifestyle changes with a single drug not associated with hypoglycaemia?
A
48mmol/mol (6.5%)
10
Q
What is the target HbA1c level if T2D managed by drug treatment associated with hypoglycaemia?
A
53mmol/mol (7%)
11
Q
When should HbA1c levels be measured?
A
3-6 monthly intervals until stable, then every 6 months.
12
Q
What lifestyle advice should be given to someone with type 2 diabetes?
A
Join group education programme such as DESMOND.
Eat high fibre, low-glycaemic index sources of carbohydrates such as fruit, vegetables, wholegrains, and pulses.
Eat low-fat dairy products.
Oily fish.
Reduce foods containing high-saturated fats, sugar, and salt.
Minimise time spent being sedentary.
Advise regular exercise to lower blood glucose levels, improve CVD risk, and reduce excess weight.
If drinking, eat a snack containing carbohydrates before and after drinking as alcohol can exacerbate and prolong effects of antidiabetic drugs leading to hypoglycaemia.
13
Q
How should T2D be treated?
A
- Metformin
- SGLT2 inhibitor – if have or at risk of CH or CVD. Can use SGLT2 inhibitor alone if metformin contraindicated or not tolerated.
- DPP4 inhibitor OR pioglitazone OR sulfonylurea OR SGLT2 inhbior (if not using already) – dual therapy if monotherapy insufficient.
- insulin therapy OR DPP4 inhibitor OR pioglitazone OR sulfonylurea OR SGLT2 inhbior (if not using already) – triple therapy if dual therapy insufficient.
- If triple therapy ineffective, not tolerated, or contraindicated, consider switching one drug to a GLP-1 receptor antagonist if their BMI is 35kg/m2 or higher, or if it is lower an insulin therapy would have implications, or if obesity would benefit an obesity-related comorbidity.
14
Q
How does metformin work?
A
Metformin opposes glucagon and activates AMPK which inhibits hepatic gluconeogenesis (production of glucose from precursors such as glycerol, lactate, pyruvate etc)
15
Q
How should metformin be initiated?
A
Gradually increased weekly (usually by 500mg) over several weeks to minimise the risk of adverse effects and to identify the minimum dose for adequate glycaemic control. If there are intolerable GI adverse effects, consider a trial on MR metformin.
16
Q
What are some adverse effects of metformin?
A
GI – nausea, flatulence, abdominal pain, diarrhoea, appetite decreased.
Lactic acidosis – lactic acid build up in the blood stream which can cause GI discomfort, exhaustion, muscle cramps, respiratory compensation/dyspnoea, and hypothermia. Discontinue immediately. Higher risk in patients with heart failure.
Reduced vitamin B12 levels at high doses – breathlessness, fatigue, light-headedness. Monitor levels and supplement, continue metformin as long as it is tolerated.
Skin reactions such as erythema, pruritis, and urticaria.
17
Q
What monitoring does metformin require?
A
Renal function – baseline and annually (at least) or 6 monthly if risk factors.
Do not start if eGFR <30ml/min/1.73m2.
If at review eGFR <45ml/min/1.73m2, review dose.
Stop treatment if eGFR <30ml/min/1.73m2 or patient at risk of tissue hypoxia or sudden deterioration in renal function.
B12 (folate) serum levels
Test levels if deficiency suspected.
Consider periodic monitoring in patients with risk factors.
18
Q
What are some common drug interactions of metformin?
A
Alcohol – increased risk of lactic acidosis.
Beta-blockers – warning signs of hypoglycaemia (such as tremor) may be masked during concurrent treatment.
Ketotifen – platelet count may be depressed.
Topiramate – plasma concentrations of metformin increased.
Hypoglycaemic effects may be enhanced by other anti-diabetic drugs, ACE inhibitors, MAOIs, anabolic steroids.
Hypoglycaemic effects may be prevented by corticosteroids, diuretics, oestrogen/progesterone.
19
Q
When should an SGLT-2 inhibtor be prescribed in type 2 diabetes?
A
In combination with metformin first line if at risk of CHF or CVD
Alone if metformin contraindicated.
20
Q
How should SGLT-2 inhibitors be prescribed with metformin?
A
Sequentially - start metformin, then when tolerability confirmed, initate SGLT-2 inhibitor
21
Q
How do SGLT-2 inhibitors work?
A
Inhibit sodium-glucose cotransport-2 to reduce renal tubule glucose reabsorption, producing a reduction in blood glucose without stimulating insulin release.
They also have a mild diuretic effect and decrease sodium, which results in sodium homeostasis and a decrease in plasma volume which decreases BP and improves cardiac blood flow, which plays a role in treating heart failure.
22
Q
Name 3 SGLT-2 inhibitors.
A
Dapagliflozin
Canagliflozin
Empagliflozin
23
Q
What are some common side effects of SGLT-2 inhibitors?
A
Constipation
Nausea
Dyslipidaemia
Hypotension
Vulvovaginitis, UTO, urosepsis.
24
Q
What are some serious side effects of SGLT-2 inhibitors?
A
Renal impairment.
Fournier’s gangrene – a rare but life-threatening necrotizing fasciitis of the genitals and perineum which presents as severe pain or tenderness, erythema, and swelling in genital area, with fever and malaise. Stop SGLT-2 inhibitor immediately and seek medical attention.
Diabetic ketoacidosis – occurs when the body doesn’t have enough insulin to allow blood sugar into the cells to use as energy. Instead, liver breaks down fat for fuel which produces ketones at a rapid rate which can build up dangerous levels in the body. This can lead to thirst, polyuria, dyspnoea, stomach pain, nausea, and fruit smelling breath.
25
What monitoring do SGLT-2 inhibitors require?
Renal function – do not initiate treatment if eGFR < 60ml/min/1.73m2. However, dapagliflozin is licensed for use in CKD and can improve renal function but should not be used if eGFR <15ml/min/1.73m2.
Monitor for symptoms of DKA – stop immediately and seek medical attention.
26
What are some common drug interactions of SGLT-2 inhibitors?
Thiazide and loop diuretics – additive effects which can increase risk of dehydration and hypotension.
Insulin and other antidiabetic drugs – hypoglycaemia.
Enzyme-inducers such as St John’s wort, rifampicin, phenytoin, carbamazepine.
Lithium – increased renal lithium excretion and decreased blood levels
27
Name 2 SPP4 inhibitors?
Saxaglipin
Alogliptin
28
How do DPP4 inhibitors work?
Bind to dipeptidyl peptidase-4 and prevent it from destroying incretin, a hormone involved in glucose homeostasis which stimulates insulin production and inhibits glucose production when required.
29
What monitoring do DPP4 inhibitors require?
LFTs - baseline, every 3 months for 1 year, periodically thereafter. Avoid in heoatic impairment.
Renal function - baseline, annually. Use with caution in renal impairment.
30
What are some adverse effects of DPP4 inhibitors?
GI – constipation, vomiting, nausea, reflux, dyspepsia.
Dizziness and tremor
Pruritis, urticaria, angioedema, rash.
Pancreatitis (acute) – short-term inflammation of the pancreas. Seek urgent medical attention and stop treatment if patient develops jaundice or other signs of liver dysfunction such as nausea, diarrhoea, indigestion, fever, tenderness of abdomen, and dark urine.
Hepatic – hepatitis and hepatic failure – RARE.
31
What are some common drug interactions of DPP4 inhibitors?
Beta-blockers – warning signs of hypoglycaemia (e.g., tremor) may be masked.
ACE inhibitors – increased risk of angioedema with vildagliptin.
Digoxin – sitagliptin increases plasma concentrations of digoxin.
Rifampicin – decreases linagliptin effects.
Hypoglycaemic effects may be enhanced by other anti-diabetic drugs, alcohol, MAOIs, anabolic steroids.
Hypoglycaemic effects may be prevented by corticosteroids, diuretics, oestrogen/progesterone.
32
What is pioglitazone?
A synthetic ligand for PPARs which alter the transcription of genes influencing carbohydrate and lipid metabolism, which results in reduced insulin resistance and gluconeogenesis in the liver.
33
Before treatment with pioglitazone, what do patients need to undergo?
LFTs – If ALT is >2.5x the upper limit of normal do not start. Monitor LFTs regardless periodically based on clinical judgement.
Risk of heart failure – contraindicated. Monitor for signs and symptoms of heart failure throughout treatment such as weight gain or oedema. Stop treatment if decline in cardiac function seen.
Risk of bone fracture – can cause this.
Risk of bladder cancer - risk factors include age, smoking history, certain drugs, and pelvic radiation therapy. Do not start in individuals with bladder cancer. Risk of bladder cancer development. Seek urgent medical attention if symptoms develop such as unexplained weight/appetite loss, dysuria, DVT, UTI.
Assess the safety and efficacy of pioglitazone 3-6 months after treatment is initiated and regularly thereafter. Stop treatment where response is not adequate.
34
What are some adverse effects of pioglitazone?
Pee cancer (bladder cancer
Insomnia
Optic - visual impairment
Gain weight
Liver impairment
Increased risk of infection and bone fractures
## Footnote
PIOGLI
35
What are some common drug interactions with pioglitazone?
Beta-blockers – warning signs of hypoglycaemia (e.g., tremor) may be masked.
NSAIDs – peripheral oedema and cardiac failure. Stop treatment if decline in cardiac function seen.
Liver-enzyme inducing drugs may reduce plasma concentration of pioglitazone and may warrant dose change. These include: rifampicin, phenytoin, carbamazepine, St John’s wort.
Hypoglycaemic effects may be enhanced by other anti-diabetic drugs, alcohol, MAOIs, anabolic steroids.
Hypoglycaemic effects may be prevented by corticosteroids, diuretics, oestrogen/progesterone
36
Name 4 sulfonylureas.
Gliclazide
Glimepiride
Glipizide
Tolbutamide
37
How do sulfonylureas work?
Bind to sulfonylurea receptors to close ATP-sensitive K-channels in the beta-cell plasma membrane to stimulate insulin release.
38
What monitoring do sulfonylureas require?
Blood glucose at start of treatment to monitor for hypoglycaemia
Renal and hepatic function - baseline. Continuous monitoring in moderate impairment. Avoid in severe.
39
What are some adverse effects of sulfonylureas?
GI – abdominal pain, nausea, vomiting, diarrhoea, and constipation.
Hepatic impairment.
Skin – rash, pruritis, urticaria, photosensitivity.
Blood – leucopenia, thrombocytopenia, anaemia.
Hypoglycaemia.
40
What are some common drug interactions of sulfonylureas?
Beta-blockers – warning signs of hypoglycaemia (e.g., tremor) may be masked.
Colesevelam – decreased sulfonylurea absorption – separate by 4 hours.
Fluconazole, Fluvastatin – increased sulfonylurea plasma concentration.
Phenytoin – increased phenytoin plasma concentration.
Hypoglycaemic effects may be enhanced by other anti-diabetic drugs, alcohol, MAOIs, anabolic steroids, NSAIDs, ACE inhibitors, some antibiotics.
Hypoglycaemic effects may be prevented by corticosteroids, diuretics, oestrogen/progesterone, and pehnothiazines.
41
How do GLP-1 agonists work?
Bind to glucagon-like peptide-1 receptor on islet beta-cells and gamma cells to stimulate insulin and somatostain (SMS) secretion, respectively. Insulin works to promote glycogenesis and inhibit gluconeogenesis, while SMS inhibits glucagon secretion from islet cells.
42
How are GLP-1 receptor agonists administered?
Once weekly via SC injections.
43
Who shoudln't be prescribed GLP-1 receptor agonists?
Patients with:
Ketoacidosis
Pancreatitis
Renal impairment
Severe hepatic impairment
Severe GI disease
44
What is a beneficial side effect of GLP-1 receptor agonists?
They bind to the GLP1 receptors in the brain which are involved in appetite and also decrease gastric emptying, resulting in weight loss.
45
What are some adverse effects of GLP-1 agonists?
GI – decreased appetite, altered taste, nausea, vomiting, constipation, delayed gastric emptying.
Headache
Dizziness
Fatigue and drowsiness
Acute pancreatitis - short-term inflammation of the pancreas. Seek urgent medical attention and stop treatment if patient develops jaundice or other signs of liver dysfunction such as nausea, diarrhoea, indigestion, fever, tenderness of abdomen, and dark urine.
Gastroporesis
46
What are some common drug interactions of GLP-1 agonists?
Beta blockers – warning signs of hypoglycaemia (e.g., tremor) may be masked.
Paracetamol – paracetamol absorption may be lower
Warfarin – enhanced anticoagulation effect of warfarin – monitor INR.
Hypoglycaemic effects may be enhanced by other anti-diabetic drugs, alcohol, MAOIs, anabolic steroids.
Hypoglycaemic effects may be prevented by corticosteroids, diuretics, oestrogen/progesterone.
47
What is insulin?
A polypeptide hormone secreted by pancreatic beta cells which lowers blood glucose to prevent hyperglycaemia via stimulating glycogenesis (formation of glycogen from glucose to be stored in liver and muscle cells) and inhibiting gluconeogenesis (production of glucoses from glycerol, lactate and other precursors).
48
What are the different types of insulin?
Rapid-acting insulins – taken immediately before meals or as a correction dose. Start working within 5-10 minutes and lasts 2-5 hours.
Short-acting insulins – mimic physiological secretions of insulin which occurs in response to the glucose absorbed from the diet. Usually taken about 30 minutes before meals or just after eating. Starts working in 30mins-1 hour and lasts up to 8 hours.
Intermediate – mimic basal insulin which is secreted continuously throughout the day. Taken once or twice a day. Starts working with 2 hours and lasts 8-14 hours.
Long-acting - mimic basal insulin which is secreted continuously throughout the day. Taken once or twice a day. Starts working with 2 hours and lasts 18-24 hours.
49
What are some examples of rapid-acting insulins?
o Insulin aspart e.g., Novorapid
o Insulin lispro e.g., Humalog
o Insulin glulisine e.g., Apidra
50
What are some examples of short-acting insulins?
o Human soluble insulin e.g., Humulin S, Insuman Rapid, Actrapid/
51
What are some examples of intermediate-acting insulins?
Isophane insulin e.g., Insulutard and Humulin I.
52
What are some examples of long-acting insulins?
Insulin detemir – Levemir
Insulin glargine – Lantus, Abasaglar
Insulin degludec - Tresiba
53
What are 1/2/3 insulin injection per day regimens?
Insulin used once/twice/thrice daily containing a mixture of shorter and intermediate acting insulin, usually taken with meals. Insulin dose is constant for each dose and doesn’t depend on the amount of carbohydrates eaten, so patients must maintain the same amount of carbohydrates with each meal.
54
What is multiple daily injection basal-bolus insulin regimen?
Combination of a basal (long-acting) insulin once or twice a day with bolus (short/rapid-acting) insulin at each meal which relates to the amount of carbohydrates consumed.
55
What are some counselling points for insulin pens?
Use a new needle for every injection and ensure it is tightly screwed on.
Use a needle that is the right length.
Make sure insulin is at room temperature.
Shake the pen 6-10 times till it appears cloudy to ensure it is well mixed.
To test for air bubbles or blockages, perform the “2 unit test”, where you dial up 2 units then watch to see if it comes out of the end of the needle.
Inject into fatty tissue underneath the skin usually of lower stomach, buttocks, or outer thighs at a 90 degree angle. Change injection site regularly.
When injecting, hold the button until the whole dose has been released, plus an extra 10 seconds (minimum) before removing needle and putting in sharps bin.
Store pens in use away from direct sunlight and at room temperature (maximum 1 month). Store pens not used yet in the fridge.
56
What are insulin pumps/CSII?
continuous subcutaneous insulin infusion (CSII) electronic devices are small devices which can be attached to a belt or waistband and deliver quick-acting insulin continuously via a small plastic cannula under the skin. This is done at a basal rate, although additional bolus doses can be administered by pressing the bolus button when eating carbohydrates or if blood glucose is too high.
57
What are the pros and cons of insulin pumps?
Pros:
Constant levels of insulin absorption
Reduced hypoglycaemia risk
More personalised basal rate
Fewer injections
Cons:
Must be worn all the time
Requires intensive training.
58
What do closed loop systems consist of?
An insulin pump and a continuous glucose monitor which work together to act as an “artificial pancreas”.
59
What are the 2 types of closed-loop systems?
Low glucose suspend systems – glucose sensor notifies pump when blood glucose is going low and to stop insulin infusion until the glucose rises again.
Hybrid closed-loop system – glucose sensor communicates all changes in blood glucose to the pump which automatically adjusts the basal rate of insulin infusion.
60
What are the pros and cons of closed-loop systems?
Pros:
Fewer injections
Improved blood sugar control
Improved QOL
Cons:
Very expensive and only available on NHS under strict circumstances.
Requires carbohydrate counting
Patients must be aware of things which can cause significant/rapid changes in blood sugar (e.g., sugar) as the system will not respond quickly enough.
61
What are some counselling points for insulin use?
Insulin passport – paper record of insulin regimen, information of what to do in emergency if they are found ill/unconsciousness, and emergency contacts. Recommended to carry on them at all times.
Symptoms of hypos – sweating, pale, dizziness, trembling, palpitations.
How to prevent hypos – eat regularly, don’t drink on empty stomach, take insulin as prescribed, always carry snacks and meters.
62
What should be considered when travelling abroad with insulin?
* Carry lots of insulin – double the amount you think you need to be on the safe side. If travelling for a long-time, ask for a supplier to arrange insulin to be sent to a particular pharmacy or collection point, or find out the availability of it in the country.
* Plane – keep insulin in hand luggage as the hold can drop below freezing. Use a cool box or ice pack (but not directly next to pens) to keep insulin cool while travelling, and transfer to fridge once you get there.
* Quality – check appearance of insulin before using it. If it appears cloudy, thick, lumpy, brownish, or frosted appearance, it may have gone off. Check what this looks like for your insulin.
* Heat - Avoid overheating in hot countries or freezing in cold countries and avoid bright light. Glucose meters and test strips can also be affected by extreme temperatures so check manual before you go. Perform a quality control check using glucose solution to check it is accurate.
63
What should be done if a diabetic patient becomes unwell with any incurrent illnesses?
1. Screen for the possibility of DKA, HHS, or AKI.
2. Admit to hospital if at risk of above, appear dehydrated, vomiting for 2+ hours, unclear underlying condition, or their blood glucose can't be controlled.
3. If low risk, assess and manage illness as appropriate. Follow sick-day rules.
64
What are the "sick-day rules" in diabetes?
During acute illness, some medication may be stopped and restarted once they are feeling, eating, and drinking better for 24-48 hours. These drugs include:
o ACE inhibitors, ARBs, diuretics, NSAIDs, and GLP-1 receptor agonists – if risk of dehydration to reduce risk of AKI.
o Metformin – if risk of dehydration to reduce risk of lactic acidosis.
o Sulfonylureas – may increase risk of hypoglycaemia if dietary intake reduced.
o SGLT-2 inhibitors – check for ketones and stop treatment of acutely unwell and/or at risk of dehydration due to risk of DKA.
Self-monitor blood orr urinary ketones every 3-4 hours and record results. Urine ketone level >2 or blood ketone level >3mmol/L, seek immediate medical advice.
Do not stop insulin therapy. Recommend to increase frequency of blood glucose monitoring.
Maintain normal eating pattern (especially fluids and carbohydrates) where possible. If unable to eat or vomiting, replace meals with carbohydrate-containing drinks such as milk, milkshakes, sugary drinks.
Can use ORT sachets to prevent dehydration.
Can use glucose tablets or gel to prevent hyoglycaemia.
65
What are some complications of hyperglycaemia?
Diabetic ketoacidosis
Hyperosmolar hyperglycaemic state
Retinopathy
Foot problems
Diabetic kidney disease
Peripheral and autonomic neuropathy
66
What is DKA?
DKA happens when the signal from insulin in the body is so low that glucose can't go into cells to be used as a fuel source, the liver makes a large amount of glucose, and fat is broken down too rapidly for the body to process.
The fat is broken down by the liver into a fuel called ketones. Ketones are normally produced by the liver when the body breaks down fat after it has been a long time since your last meal. These ketones are normally used by the muscles and the heart. When ketones are produced too quickly and build up in the blood, they can be toxic by making the blood acidic.
67
What are some symptoms of DKA?
CATSPAWS
Confusion
Abdominal pain
Tachycardia and tachypnoea
SOB
Polydipsia and polyuria
Acetone breath (fruit smell)
Weight loss
Serum or urinary ketone
68
What is hyperosomolar hyperglycaemic state?
A condition characterised by:
Hypovolaemia
Hyperglycaemia (> 30 mmol/L)
Mild or absent ketonaemia (blood ketones < 3 mmol/L)
High osmolality (> 320 mOsm/kg)
69
What HHS caused by?
1. Relative lack of insulin is coupled with a rise in counter-regulatory hormones (e.g. cortisol, growth hormone, glucagon) leads to a profound rise in glucose.
2. Since the renal proximal tubules only have a certain capacity for reabsorption of glucose. once this is reached, the remaining glucose is passed through the renal nephrons causing diuresis.
3. This leads to massive osmotic diuresis with a loss of sodium and potassium.
4. As water is lost, there is profound dehydration and reduced circulating volume, resulting in hyperosmolarity and marked hyperglycaemia.
4. The increase in osmolality increases compensatory mechanisms such as release of anti-diuretic hormone (ADH) and stimulation of thirst.
5. Renal water loss (e.g. elderly patients with co-morbidities) then hypovolaemia develops with progression to acute kidney injury, electrolyte disturbances, hypotension and coma.
6. The hyperosmolar state of the condition leads to hyperviscosity that increases the risk of arterial and venous thrombosis (e.g. stroke, DVT).
70
What is retinopathy?
A diabetes complication which is caused by high glucose levels causing damage to the blood vessels of the light-sensitive tissue at the back of the eye (retina) which can lead to vision loss and blindness if left untreated.
71
How is retinopathy detected?
Diabetic eye screenings are performed every 1-2 years to check the eyes in general and a photograph of the back of the retina.
72
What are some red flags for diabetic retinopathy?
Seek emergency assessment if:
Sudden vision loss
Formation of abnormal blood vessels oniris
Pre-retinal haemorrhgae.
73
How is retinopathy treated?
Control blood sugar.
Prevent progression using blood pressure management, statins, and fibrates.
Panretinal photocoagulation (high-risk patients).
Anti-VEGF therapy (if panretinal photocoagulation unsuccessful or unsuitable)
Cataract surgery.
74
How do foot problems occur in diabetes?
Hyperglycaemia can impact the sensation in the feet, as well as circulation. Therefore, patients will have issues identifying cuts or sores on their feet, and reduced blood supply will reduce its healing.
75
How can you reduce the risk of diabetic foot issues?
Check feet every day for any changes. Use a mirror if this is easier.
Be careful while cutting nails – don’t cut them too short, trim with nail clippers and file down, clean them with a nail brush.
Wear shoes and socks that fit well. Shoes should be broad fitting, have a deep/rounded to area, be flat, and be fastened by a lace or buckle to stop feet sliding around.
Use an emollient every day to prevent cracks which can get infected. Avoid getting it between toes as it can build up and cause issues.
Stop smoking – worsens circulatory issues.
Look out for foot problems – swelling, pain/burning, tingling sensation, numbness, ache, hair loss, cramps in calves.
If you notice changes in colour/shape, hot/cold feet, blisters/cuts that you see but don’t feel, and a foul smell from a wound, see foot team urgently.
76
How is mild diabetic foot infection treated?
1. Flucloxacillin 500mg-1g qds for 7 days.
2. Clarithromycin 500mg bd for 7 days or Doxycylin 200mg for one day, then 100mg od for 7 days.
3. Erythromycin 500mg qds for 7 days.
77
How is moderate/severe diabetic foot infection treated?
1. Flucloxacillin 1g qds orally or 1-2g qds IV
with or without….
Gentamicin 5-7mg/kg od IV
and/or…
Metronidazole 400mg tds orally or 500mg tds IV
2. Co-amoxiclav 500/125mg tds orally or 1.2g tds IV
with or without…
Gentamicin 5-7mg/kg od IV
3. Cotrimoxazole (penicillin allergy) 960mg bd orally or 960mg bd IV
with or without…
Gentamicin 5-7mg/kg od IV
and/or…
Metronidazole 400mg tds orally or 500mg tds IV
4. Ceftriaxone 2g od IV + Metronidazole 400mg tds orally or 500mg tds IV.
For 7 days – 6 weeks (osteomyeleitis).
78
How should suspected MRSA diabetic foot be treated?
1. Vancomycin 15-20mg/kg bd-tds IV (max 2g per dose).
2. Teicoplanin 6mg/kg every 12 hours for 3 doses then 6mg/kg od IV.
Reassess if symptoms worsen rapidly or do not start improving within 1-2 days. Consider an X-ray to determine extent of issue and presence of osteomyeleitis.
79
How do penicilli antibiotics work?
Binds to and inhibits penicillin binding proteins to prevent cross-linking between linear peptidoglycan chains which make up the major component of the cell wall of Gram-positive bacteria.
80
What are some common drug interactions of flucloxacillin?
MTX - reduced clearance
Warfarin - monitor INR
Cholera and typhoid vaccine - efficacy reduced
81
What are some common side effects of flucloxacillin?
GI discomfort
Hepatic disorders
Thrombocytopenia
82
What class of antibiotic is gentamicin?
Aminoglycoside
83
How do aminoglycosides work?
Binds electrostatically to bacterial cell membranes to displace divalent cations and increase membrane permeability, allowing cell entry. Then targets 30s ribosome and causes mistranslation of proteins and disruption of the cytoplasmic membrane.
84
What is some side effects of gentamicin?
GI discomfort
Risk of deafness in patients with mitochondrial mutations and in infant if used in pregnancy. Patients should undergo R65 genetic testing.
85
What monitoring does gentamicin require?
Serum concentration for IV/IM doses.
86
What is gentamicin contraindicated in?
2nd/3rd trimester pregnancy
Mitochondrial mutations.
87
Name a drug interaction of gentamicin?
Potent diuretics - increased ototoxicity
88
What class of antibiotics is metronidazole?
Nitroimidazole
89
How do nitroimidazoles work?
Bacterial nitroreductases reduce the nitro group on the drug, resulting in the formation of highly reactive intermediates that cause loss of helical DNA structure and strand breakage to inhibit protein synthesis.
90
What are some side effects of metronidazole?
Dark urine
Jaundice
Liver disorders
Psychotic disorders
91
What conditions is metronidazole contraindicated in?
Pregnancy 1st trimester
Severe liver disease or hepatic encephalopathy (1/3rd dose)
Peripheral or CNS disease (neurological aggravation),
Cockayne syndrome (hepatotoxicity, fatalities).
92
What drugs do metronidazole interact with?
Alcohol - increased RR & PR, fludhing, nausea, headache
Warfarin - monitor INR
Ciclosporin - elevated ciclosporin levels
Lithium - raised lithium and renal damage
93
What class of antibiotic is vancomycin?
Glycopeptide
94
How do glycopeptides work?
Binds to acyl-D-ala-D-alanine on NAM/NAG-peptides of growing cell wall of actively dividing Gram-positive bacteria and prevents their incorporation into the peptidoglycan matrix, preventing formation of the cell wall. Also alters cell-membrane permeability and RNA synthesis.
95
What are some side effects of vancomycin?
Blood disorders
Cardiac arrest
Dizziness
Ear - transient loss of hearing
Flushing of face and upper body
GI discomfort
Hypotension
Impairment - renal
96
When is vancomycin contraindicated?
Inflammatory disorders - higher risk of AEs
Renal impairment
Underlying hearing loss
Breastfeeding - diarrhoea, fungal infection, and sensitisation in infant
Concurrent use of ototoxic or nephrotoxic medications.
97
What is diabetic nephropathy/diabetic kidney disease?
High glucose levels lead to high blood pressure which damages the renal blood vessels
and kidney over time. This causes symptoms such as foamy urine, swelling of feet/ankles/hands/eyes, confusion, SOB, loss of appetite, nausea, and vomiting.
98
How is diabetic kidney disease detected?
All adults with type 2 diabetes have annual screenings for diabetic kidney disease which consists of an early morning first-void urine sample to measure ACR (assess microalbuminuria) and serum creatinine (ceGFR).
99
What is required for diabetic kidney disease to be diagnosed?
Persistent reduction in kidney function: eGFR <60ml/min/1.73m2 for 3 months or more
and/or
Persistent proteinuria: urine ACR >3mg/mmol for 3 months or more.
100
What should be done after diagnosis of diabetic kidney disease?
Optimise blood glucose control, lipid levels, and BP to reduce risk of progressive kidney disease.
Classify stage - stage 3 or more and/or microalbuminuria warrants atorvastatin 20mg + ACE inhibitor.
101
What does a CVD risk factor assessment for diabetics include?
Annual review of:
Smoking status
Blood glucose control
Blood pressure (140/90mmHg) – aim for 120-139/90mmHg if ACR<70mg/mmol and 120129/90mmHg if ACR>70mg/mmol.
Albuminuria
Full lipid profile – total cholesterol, LDL, HDL, and triglycerides.
Aim for 40% reduction in non-HDL cholesterol.
Family history of CVD
Height, weight, waist circumference, and BMI.
102
How is hypertension treated in diabetes?
1. ACE inhibitor or ARB
2.+ CCB or thiazide-like diuretic
3. + CCB or thiazide-like diuretic (other one)
103
When do diabetics require statins for CVD prevention?
No established CVD but >85 or QRISK >10 = atorvastatin 20mg od
Established CVD = 80mg atorvastatin od
104
What is peripheral neuropathy?
A disorder in which peripheral nerves are damaged throughout the body (mainly legs and feet), with autonomic neuropathy causing more damage to the autonomic nerves (balance, sweating, digestion) than somatic nerves.
105
How does diabetes cause autonomic neuropathy?
High blood sugar levels cause damage the small blood vessels which supply the nerves, depriving them of nutrients and leading to damage.
106
What are the main symptoms of peripheral neuropathy?
Numbness, burning, shooting pains, or tingling of the hands or feet often at night which may be relieved by activity.
Muscle weakness, wasting, cramps, or twitching.
107
What are the main symptoms of autonomic neuropathy?
Postural hypotension (drop in systolic BP of 30mmHg from lying to standing) – ask about drug treatments which can cause this.
Diabetic gastroparesis – delayed gastric emptying, nausea, bloating, vomiting. Symptoms can be relieved by having small portions of mashed or pureed food.
Lower GI issues – abdominal pain, nocturnal and unexplained diarrhoea.
Unexplained urinary symptoms such as hesitancy, reduced frequency, inadequate bladder emptying, retention.
Sweating abnormalities.
## Footnote
SHLUG
108
What is first line treatment for painful neuropathy?
Amitriptyline, duloxetine, gabapentin, or pregabalin.
109
Explain how gluceose homeostasis works in a normal body.
After consumption, glucose is absorbed into the blood and causes high plasma levels. This stimulates beta cells to produce and secrete insulin. Insulin mediates uptake of glucose into cells as a fuel source. The spike in insulin also notifies the liver of high glucose levels causing it to absorb glucose and convert it into glycagon for storage.
When glucose levels in the blood get too low. Alpha cells in the pancreas secrete glucagon which stimulates the liver to perform glycogenesis (conversion of glycogen back to glucose) and gluconeogenesis (production of glucose from other sources) to raise plasma glucose levels again. This in turn stimulates insulin and the cycle starts again to maintain a safe level in the blood.
