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Type 2 diabetes Flashcards

Overview, aetiology & pathophysiology, molecular action

1
Q

What are the different types of diabetes?

A
  1. Type 1 (autoimmune destruction of beta cells)
  2. Type 2 (insulin resistance and beta-cell dysfunction)
  3. Gestational (develops in pregnancy)
  4. Type 3c (pancreatic-related)
  5. Type 1.5 (Latent Autoimmune Diabetes in Adults)
  6. Double (type 1 diabetes with significant insulin resistance)
  7. Neonatal (infants 6 months old)
  8. Steroid induced (cause hyperglycaemia, make liver less sensitive to insulin)
  9. Monogenic (GCK, HNF1a, HNF4a, HNF1b) - mutation in a single gene
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2
Q

What are the syndromic forms of diabetes?

A

Alström Syndrome (genetic disorder causes obesity, organ dysfunction and health issues) (type 2 diabetes is a symptom)
Wolfram Syndrome (genetic disorder affecting body’s systems (diabetes mellitus due to a lack of insulin or diabetes insipidus cannot concentrate urine)
Glucagonoma Syndrome (pancreatic tumour secretes too much glucagon (raising blood sugar)
Pheochromocytoma Syndrome (tumour in adrenal gland producing too much catecholamines like adrenaline and noradrenaline, can manifest as impaired glucose tolerance as interferes with insulin production)

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3
Q

Why is diabetes a growing problem in the UK?

A

5 million people live with diabetes (1 in 14 individuals)
In some constituencies, prevalence reaches 1 in 9
Prevalence: 9% rise in 2018 and 13% rise in 2023
Major weekly impact: 185 amputations, 700 strokes, 2,000 heart attacks and 500 early deaths

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4
Q

What are the risk factors for type 2 diabetes?
Non-modifiable
Modifiable
Emerging factors

A
  1. Family Hx, ethnicity, age, Hx of gestational diabetes, gender
  2. Obesity, diet and physical inactivity, high blood pressure, smoking & alcohol use, sleep disorders and chronic stress
  3. Gut microbiome imbalance and Polycystic Ovary Syndrome (PCOS)
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5
Q

How is type 2 diabetes diagnosed?

A

Symptoms: Polyuria, polydipsia, fatigue, weight loss, blurred vision, gento-urinary and skin infections, DKA symptoms
Blood tests: HbA1C >48 mmol/mol (measure of 3-month glucose control)
Traditional x2 to confirm diagnosis
Random plasma blood glucose
Fasting Plasma Glucose (FPG) >7 mmol/L
Oral Glucose Tolerance Test (OGTT)
Caveats: HbA1C not suitable for acutely ill patients or those with abnormal haemoglobin.

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6
Q

What are the complications of diabetes?

A

Macrovascular: Cardiovascular disease, stroke, peripheral arterial disease (PAD)
Microvascular: Retinopathy, neuropathy, nephropathy
Acute: Diabetic ketoacidosis (DKA), hyperosmolar hyperglycaemic state (HHS)

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7
Q

What treatments are available for diabetic retinopathy?

A

Fenofibrate
Laser therapy
Monoclonal antibodies (e.g. Bevacizumab)
Implantable steroid treatments
Surgery for advanced cases

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8
Q

How does PAD (peripheral arterial disease) relate to diabetes and treatment?

A

12-20% of people aged >65 have PAD
Diabetes increases PAD risk, raising cardiovascular event risk 4-5 fold
Symptoms include leg cramps, cold extremities, and discolouration
Treatments: Clopidogrel, angioplasty, bypass surgery

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9
Q

What are the types of diabetic neuropathy and treatment?

A

Sensory neuropathy: Tingling, numbness, “pins and needles”
Autonomic neuropathy: Gastroparesis, bladder dysfunction, erectile dysfunction
Motor neuropathy: Muscle weakness, leading to falls
Treatment: Medications include duloxetine, gabapentin, pregabalin, and lidocaine plasters

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10
Q

What causes diabetic nephropathy and prevention?

A

High blood glucose damages renal blood vessels
Leads to albuminuria and reduced filtration
Prevention: control glycaemia, blood pressure, and lipids or use ACE inhibitors, ARBs, or SGLT2 inhibitors

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11
Q

What lifestyle changes can help manage type 2 diabetes?

A

Diet: Avoid “diabetic foods,” swap to low-GI alternatives, monitor labels
Exercise: 150 minutes of moderate aerobic activity weekly (e.g., brisk walking, cycling)
Weight management: Engage with weight loss programmes (e.g., Slimming World)
Strength training: Particularly beneficial for glucose metabolism

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12
Q

What is diabetic gastroparesis and how is it managed?

A

Symptoms: Nausea, vomiting, bloating, early satiety, weight loss
Diagnosis: Imaging (barium swallow) and endoscopy
Management:
First: Dietary adjustments
Second: Prokinetic medications (e.g., erythromycin, domperidone)
Third: Surgical interventions (e.g., gastric stimulation)

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13
Q

What are the exercise guidelines for people with diabetes?

A

Aerobic exercise: 150 minutes per week (e.g., brisk walking, water aerobics)
Vigorous exercise: Running, cycling uphill, skipping
Strength training: Builds muscle, improves glucose control
Tips: Make it social and realistic, plan ahead

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14
Q

How can type 2 diabetes be prevented?

A

Screen at-risk populations using:
- BMI assessments
- Blood tests (FPG, HbA1C)
Focus on lifestyle interventions:
- Healthy eating habits
- Physical activity
- Weight reduction
Regular monitoring for high-risk groups

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15
Q

Type 2 prevention strategies eligibility

A

Adults aged 40-74
Adults 25-39 from high-risk ethnics
Adults with high-risk co-morbidities (CVD, HTN, Non-Alcoholic Fatty Liver Disease, PCOS, obesity, Gestational Diabetes Mellitus, stroke & mental health illness/treatments)

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16
Q

Type 2 diabetes assessment outcomes:
Possible diagnosis
What A1c means

A
  1. FPG>7, A1C>48mmol/mol, refer to GP for additional testing
  2. If A1c>48 & diabetes symptoms present = T2DM
    If A1c>48 & symptoms not present = repeat A1c in 3 months
    If FPG >7 test A1c to confirm (<48 ‘high risk’ and act accordingly) (>48 diagnose T2DM)
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17
Q

Type 2 diabetes assessment outcomes:
Low risk
Moderate risk
High risk

A
  1. Brief advice
  2. High risk score with normal blood glucose/A1c, brief intervention & re-assess A1c or FBG every 3 yrs
  3. High risk score with ‘pre-diabetes’ A1c or raised FBG, refer to local lifestyle change programme, provide further info and contacts for healthcare, re-assess A1c or FBG annually
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18
Q

What is HbA1c? How does it work?

A
  1. Glycated haemoglobin, measures % of haemoglobin in RBCs that are coated with glucose
  2. Glucose in blood binds to Hb in RBCs, level of glyctaed Hb increases when glucose consistently high
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19
Q

Limitations of HbA1c testing

A

Conditions affecting RBC turnover: anaemia, recent blood transfusions, haemoglobinopathies (sickle cell)
Acute conditions: sudden onset of diabetes symptoms (<2 months), recent severe illness
Other: CKD, medication (steroids)

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20
Q

Type 2 diabetes diagnostic measures and what they are?

A

HbA1c
Fasting plasma glucose (FPG): blood glucose after an 8 hour fast
Oral glucose tolerance test (OGTT): measures glucose 2 hours after glucose solution
Random plasma glucose: useful in symptomatic patients

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21
Q

Type 2 diabetes pathophysiology:
Normal glucose homeostasis
Pathogenesis of T2DM
Factors contributing to hyperglycaemia

A
  1. Overview of insulin action, glucose uptake & regulation by pancreas, liver & muscle
  2. Insulin resistance: mechanism at cellular level (adipose tissue, liver and muscle)
    Beta-cell dysfunction: progressive loss of pancreatic beta-cell function
    Role of incretin hormones (GLP-1 & GIP)
  3. Increased hepatic glucose production, reduced glucose uptake by peripheral tissues & increased lipolysis & free fatty acid levels
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22
Q

Who is HbA1c not suitable for?

A

Symptoms for <2 months
High diabetes risk and acutely ill
Treatment causing hyperglycaemia
Acute pancreatic damage
End-stage chronic kidney disease
HIV patients

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23
Q

Who is HbA1c a caution for?

A

Abnormal Hb
Anaemia
Altered RBC lifespan
Recent blood transfusion

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24
Q

Diabetic retinopathy:
Nonproliferative
Proliferative

A
  1. Haemorrhage, cotton wool spots, macular oedema, microaneurysm
  2. Abnormal blood vessel growth
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Bevacizumab MOA
1. VEGF-A binds VEGF receptors (VEGFR-1 and 2) on endothelial cells, triggering downstream pathways that promote proliferation, survival, vasodilation and endothelial cell migration (blood vessel formation essential) 2. Bevacizumab binds VEGF-A preventing interaction with VEGF receptors, blocking signalling pathways for blood vessel formation 3. Anti-angiogenic effect useful in preventing new leaky blood vessel formation
26
What is bevacizumab?
Monoclonal antibody that inhibits angiogenesis by targeting vascular endothelial growth factor A Off-label diabetic macular oedema and proliferative diabetic retinopathy treatment
27
What is peripheral arterial disease (PAD)?
Narrowed arteries reduce blood flow to the limbs, often due to atherosclerosis
28
Stages of arterial blockage in PAD
1. Normal Artery: Blood flows freely with no obstruction 2. Atherosclerotic Plaque Build-Up: Cholesterol and inflammatory cells accumulate, narrowing the artery 3. Plaque Blocking Blood Flow: Severe plaque formation significantly obstructs blood flow, leading to tissue damage and ischaemia
29
How does atherosclerosis cause PAD?
By causing plaque buildup in the arterial walls This plaque consists of lipids, cholesterol, inflammatory cells, and cellular debris Over time, it hardens and narrows the arteries, restricting oxygen-rich blood flow to the limbs, particularly the legs If untreated, this can lead to pain (claudication), ulcers, gangrene, and increased risk of CV events like heart attacks and strokes
30
Components of atherosclerotic plaque
1. Platelet: Blood cells involved in clot formation, which can contribute to blockages 2. Fibrous Cap: A tough outer layer that forms over the plaque, preventing rupture 3. Core: Contains lipids and cholesterol, forming the bulk of the plaque 4. Transformed Macrophages (Foam Cells): Immune cells that engulf cholesterol but contribute to plaque growth 5. Transformed Muscle Cells (Foam Cells): Smooth muscle cells that also take up lipids and contribute to the thickening of the artery wall
31
What are the main treatment options for PAD?
1. Angioplasty & Stenting – A minimally invasive procedure using a balloon and stent to open narrowed arteries 2. Bypass Graft Surgery – A surgical procedure that redirects blood flow around a blocked artery using a graft 3. Endarterectomy – A procedure to remove plaque buildup from an artery to restore blood flow.
32
Nephropathy - kidney damage and protein leakage
Filtration process: normally waste products pass into urine but in nephropathy proteins also do Normal metabolic waste is expelled into urine
33
What is Type 2 Diabetes Mellitus (T2DM)?
Chronic condition characterised by high blood glucose Due to insulin resistance and beta-cell dysfunction Leading to insufficient insulin secretion
34
What are the key factors involved in the development of Type 2 Diabetes?
1. Insulin resistance 2. Beta-cell dysfunction and death 3. Genetic predisposition 4. Environmental and lifestyle factors (e.g., obesity, poor diet, lack of exercise)
35
How is diabetes mellitus classified by the WHO?
Fasting glucose ≥ 7 mmol/L 2-hour post-prandial glucose ≥ 11.1 mmol/L
36
What are the six variables used in the novel diabetes typology?
1. Glutamic acid decarboxylase (GAD) antibodies 2. Age at diagnosis 3. Body Mass Index (BMI) 4. HbA1c levels 5. Insulin resistance 6. Beta-cell function
37
What are the primary risk factors for Type 2 Diabetes?
Obesity (most significant risk factor) Socioeconomic status (higher prevalence in deprived groups) Ethnicity (higher risk in Black, South Asian populations at lower BMI) Age (increased risk with ageing) Low birth weight (associated with future risk) Hx of gestational diabetes
38
How does genetics contribute to Type 2 Diabetes?
- 30%-70% of T2DM risk is attributed to genetics - Family studies show 15% risk if one parent has T2DM, 75% risk if both parents have it - Monozygotic twin concordance ~70% - Dizygotic twin concordance ~20%-30% - GWAS studies have identified multiple diabetes susceptibility genes
39
What are the two main components of Type 2 Diabetes pathophysiology?
1. Insulin Resistance – Insulin-sensitive tissues fail to respond to insulin 2. Beta-cell Dysfunction and Death – Beta cells become dysfunctional, reducing insulin secretion
40
What is insulin resistance, and how does it develop?
A reduced ability of insulin-sensitive tissues to respond to insulin 1. Decreased sensitivity and reduced responsiveness 2. Reduced maximum response-curve due to impaired insulin signalling
41
What are the key features of beta-cell dysfunction in Type 2 Diabetes?
1. Loss of pulsatile insulin secretion (early feature) 2. Loss of first-phase insulin secretion 3. Reduced glucose-stimulated insulin secretion 4. Decreased insulin content 5. Increased proinsulin secretion
42
What is the role of ectopic fat in insulin resistance?
Excess fat is stored in non-adipose tissues (e.g., muscle, liver) Leads to increased fatty acid metabolites, which inhibit insulin signalling Results in lipotoxicity, contributing to insulin resistance
43
What are the causes of beta-cell failure in Type 2 Diabetes?
Glucolipotoxicity: High glucose and fatty acids are toxic to beta cells Beta-cell exhaustion: Increased insulin demand leads to depletion ER stress: Overproduction of insulin exceeds cellular processing capacity Amylin deposits: Accumulation of amylin damages beta cells Inflammation: Systemic and local inflammation impairs function Genetics: Determines susceptibility to stress and ability to compensate Reduced incretin effect: Incretin hormones (GLP-1, GIP) are less effective
44
What 5 subclassification groups for T2DM were made by the 6 variables?
1. Severe autoimmune 2. Severe insulin-deficient 3. Severe insulin-resistant 4. Mild obesity-related 5. Mild age-related
45
Why is there an association between T2DM and obesity?
As age increases, weight increases Beta cells compensate for insulin-resistance by producing more insulin BUT 30% of insulin-resistant individuals B cells cannot produce enough insulin to compensate weight, increasing blood glucose
46
Beta cell compensation: Compensation Decompensation
1. Increase function & mass leading to increase in insulin secretion - NO diabetes 2. Reduced beta cell function & mass (reduced insulin secretion) - diabetes Increased beta cell mass and function in response to increased demand
47
What is the insulin signalling pathway and why is it important?
Regulates glucose metabolism, protein synthesis, and lipid storage Involves insulin binding to its receptor, triggering a cascade of intracellular signals that control key metabolic processes in the liver, muscle, and adipose tissues
48
How does insulin activate its receptor in insulin signalling?
1. Insulin binds to the extracellular insulin receptor, a transmembrane protein 2. This activates the tyrosine kinase domain of the receptor 3. Receptor undergoes autophosphorylation, adding phosphate groups (P) to specific tyrosine residues 4. Activated receptor recruits insulin receptor substrates (IRS-1, IRS-2, IRS-3, IRS-4)
49
PI3K activation and downstream signalling: What happens after IRS proteins are phosphorylated?
1. IRS proteins activate phosphoinositide 3-kinase (PI3K) 2. PI3K converts PIP2 (phosphatidylinositol-4,5-bisphosphate) into PIP3 (phosphatidylinositol-3,4,5-trisphosphate) 3. PIP3 recruits AKT/PKB (Protein Kinase B) to the membrane 4. AKT/PKB is activated via phosphorylation, leading to various metabolic effects
50
What are the effects of insulin signalling in the liver?
✔️ Glycogen Synthesis: Insulin promotes glucose storage by activating glycogen synthase. ❌ Inhibits Gluconeogenesis: Insulin suppresses the production of glucose from non-carbohydrate sources by inhibiting phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase)
51
How does insulin affect muscle metabolism?
✔️ Protein Synthesis: Insulin stimulates protein synthesis by activating mTOR (mechanistic target of rapamycin), which enhances muscle growth ✔️ Glucose Uptake: Insulin promotes glucose uptake into muscle cells by increasing GLUT4 (glucose transporter type 4) translocation to the cell membrane
52
What are insulin's effects on fat (adipose) tissue?
✔️ Lipogenesis: Insulin enhances fat storage by activating acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) ❌ Inhibits Lipolysis: Insulin suppresses fat breakdown by inhibiting hormone-sensitive lipase (HSL), preventing the release of free fatty acids
53
How does insulin promote glucose uptake in muscle and adipose tissue?
1. Activated Akt/PKB stimulates the translocation of GLUT4 transporters to the cell surface 2. GLUT4 facilitates the uptake of glucose into muscle and adipose cells 3. This reduces blood glucose levels, storing glucose as glycogen (muscle) or fat (adipose)
54
Metformin (1st line) MOA
Reduces hepatic glucose production (gluconeogenesis & glycogenolysis). Increases insulin sensitivity in muscle and fat. Delays intestinal glucose absorption. Activates AMP-activated protein kinase (AMPK).
55
Metformin: Administration Excretion Common SEs Key C/Is
- Oral, immediate-release (IR) or extended-release (ER). - Unchanged in urine (renal clearance). - GI upset, nausea, diarrhea. - Renal impairment (risk of lactic acidosis).
56
Thiazolidinediones (TZDs/Glitazones) Pioglitazone MOA
Binds to PPAR-γ receptor, increasing insulin sensitivity. Enhances glucose and fatty acid uptake.
57
Thiazolidinediones (TZDs/Glitazones) Pioglitazone Administration Adverse effects Safety concerns
- Oral. - Weight gain, fluid retention, increased risk of fractures. - Cardiovascular risk (Rosiglitazone withdrawn).
58
Sodium-glucose co-transporter 2 inhibitors (SGLT2i) Dapagliflozin, Canagliflozin, Empagliflozin MOA
Inhibits SGLT2 in kidney tubules, preventing glucose reabsorption. Increases glucose excretion via urine.
59
Sodium-glucose co-transporter 2 inhibitors (SGLT2i) Dapagliflozin, Canagliflozin, Empagliflozin Administration Additional benefits Adverse effects
- Oral. - Weight loss, cardiovascular protection. - Increased risk of UTIs, dehydration, ketoacidosis.
60
Sulphonylureas: Gliclazide, Glimepiride MOA
Stimulates insulin secretion from pancreatic β-cells. Closes ATP-sensitive potassium channels, leading to calcium influx and insulin release.
61
Sulphonylureas: Gliclazide, Glimepiride Administration Adverse effects C/Is
- Oral (once/twice daily). - Hypoglycemia, weight gain. - Renal or hepatic impairment, elderly (higher hypoglycemia risk).
62
Gliptins (DPP-4 Inhibitors) Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin MOA
Inhibits DPP-4 enzyme, prolonging GLP-1 action. Enhances insulin release and suppresses glucagon.
63
Gliptins (DPP-4 Inhibitors) Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin Administration Adverse effects C/Is
- Oral. - Nasopharyngitis, headache, pancreatitis (rare). - Severe renal impairment (dose adjustment needed)
64
GLP-1 receptor agonists Exenatide (Byetta), Liraglutide (Victoza), Semaglutide (Ozempic) MOA
Mimics GLP-1 hormone, stimulating insulin secretion. Suppresses glucagon release. Delays gastric emptying, promotes satiety.
65
GLP-1 receptor agonists Exenatide (Byetta), Liraglutide (Victoza), Semaglutide (Ozempic) Administration Additional benefits Adverse effects
- Subcutaneous injection. - Weight loss, cardiovascular protection. - Nausea, vomiting, pancreatitis risk.
66
Insulin therapy: Types MOA Administration Adverse effects
- Used when oral agents fail. - Rapid-acting, short-acting, intermediate, long-acting (e.g., Lantus, Levemir). - Directly replaces insulin, lowering blood glucose. - Subcutaneous injection. - Hypoglycemia, weight gain.
67
Biguanides (Metformin): Mechanism Advantages Disadvantages Monitoring
- Sensitizes cells to insulin, reduces hepatic glucose production, increases glucose uptake. - Weight neutral, no hypoglycaemia risk, proven cardiovascular benefits, inexpensive. - GI side effects, lactic acidosis risk, B12 deficiency. - Renal function, Vitamin B12 levels.
68
Sulphonylureas: Mechanism Advantages Disadvantages Monitoring
- Stimulates insulin secretion. - Effective, quick glucose reduction, useful in steroid-induced hyperglycaemia. - Hypoglycaemia risk, weight gain, β-cell exhaustion, cardiovascular risks. - Blood glucose, risk of falls in elderly patients.
69
Thiazolidinediones (Pioglitazone): Mechanism Advantages Disadvantages Monitoring
- Increases insulin sensitivity by activating PPAR-γ. - No hypoglycaemia risk, HbA1C reduction, useful in NASH. - Weight gain, oedema, fracture risk, bladder cancer risk. - Liver function, heart failure symptoms.
70
Alpha-Glucosidase inhibitors (Acarbose): Mechanism Advantages Disadvantages Monitoring
- Delays carbohydrate absorption by inhibiting α-glucosidase. - No hypoglycaemia risk, weight neutral. - GI side effects, minimal HbA1C effect. - Liver function tests (LFTs).
71
DPP-4 inhibitors: Mechanism Advantages Disadvantages Monitoring
- Enhances incretin effects to increase insulin secretion and decrease glucagon. - Weight neutral, no hypoglycaemia risk, once-daily dosing. - Risk of pancreatitis, potential heart failure risk (Saxagliptin). - Symptoms of pancreatitis, renal function.
72
GLP-1 receptor agonists: Mechanism Advantages Disadvantages Monitoring
- Enhances glucose-dependent insulin secretion, slows gastric emptying. - Weight loss, cardiovascular and renal benefits (Semaglutide), alternative to insulin. - Expensive, GI side effects, retinopathy risk. - GI symptoms, retinopathy signs.
73
SGLT-2 inhibitors: Mechanism Advantages Disadvantages Monitoring
- Inhibits glucose reabsorption in kidneys, increasing glucose excretion. - Weight loss, cardiovascular and renal protective effects, low hypoglycaemia risk. - UTIs, dehydration, euglycaemic DKA risk, Fournier’s gangrene. - Kidney function, infection signs, hydration status.
74
Steroid-induced hyperglycaemia
Monitor CBG; intervene if >12 mmol/L. Use Gliclazide 40mg OM, titrate up as needed. Consider evening gliclazide or basal insulin if persistent.
75
Enteral feeding and diabetes
First-line: Intermediate basal insulin (e.g., Humulin I). Short-acting insulin may be added if glucose remains high. Monitor glucose pre-feed and every 4-6 hours during feeding.
76
End of life care
Minimize interventions that cause distress. Consider stopping non-essential diabetes medications.
77
Sick day management
Continue glucose monitoring. Maintain hydration and carbohydrate intake. Avoid stopping insulin unless instructed.
78
Key monitoring parameters in T2DM: HbA1C Renal function Liver function CVD risk
- Check every 3-6 months, individualize targets. - Key for Metformin, SGLT2 inhibitors, DPP-4 inhibitors. - Pioglitazone, Acarbose. - Monitor BP, lipid profile, weight changes.
79
9 Care Processes (NICE Guidelines)
Annual monitoring of HbA1C (3-6 months) BP (annual, intervene at 140/90) Cholesterol (annual lipid profile) Renal function (serum creatinine and albumin:creatinine ratio annually) Foot health (risk stratification) BMI Smoking status Emotional health Medication review (retinal screening yearly)
80
Self-Monitoring of blood glucose (SMBG) not routine unless...
On insulin or sulphonylureas. Operating heavy machinery (e.g., HGV drivers). Pregnant.
81
DVLA blood glucose monitoring advice
Check blood glucose before driving and every 2 hours. Keep glucose levels >5 mmol/L before driving. Carry fast-acting carbohydrates in the vehicle.
82
HbA1C targets and what based on?
Patient factors (age, comorbidities, occupational risks) Non-diabetic range: <42 mmol/mol. Well-controlled diabetes: 48-58 mmol/mol. Requires intervention: >74 mmol/mol. Emergency intervention: >103 mmol/mol.
83
Blood pressure monitoring and treatment
BP Threshold for Intervention: >140/90 mmHg. Confirm hypertension with second measurement (white coat effect possible). 1st Line: ACE inhibitors (or ARBs if not tolerated). 2nd Line: Add calcium channel blocker or thiazide-like diuretic. 3rd Line: Combination of ACEi/ARB + CCB + thiazide. 4th Line: Add spironolactone (monitor electrolytes).
84
Cholesterol monitoring and treatment: Lipid profiles Targets Statin therapy
Total cholesterol (TC), Low-density lipoprotein (LDL), High-density lipoprotein (HDL), Triglycerides (TG) LDL: <2.0 mmol/L. Total cholesterol: <4.0 mmol/L. Triglycerides: <2.3 mmol/L. - Primary Prevention (No CVD): Atorvastatin 20mg OD if 10-year CVD risk >10%. - Secondary Prevention (CVD Present): Atorvastatin 80mg OD. - Consider ezetimibe, fibrates, PCSK9 inhibitors for uncontrolled cases.
85
Challenging statin intolerance
Re-challenge with different statins (e.g., rosuvastatin weekly, then increase gradually). Hydrophilic statins (rosuvastatin, pravastatin) have lower muscle side effect risk. Monitor creatine kinase (CK) levels if myalgia occurs.
86
Diabetic foot care: Symptoms and history Visual inspection Physical exam
Any pain, numbness, skin breakdown? Nail health, calluses, deformities. Vascular (pulses), Neurological (monofilament test).
87
Diabetic foot care: Risk stratification and monitoring frequency
Low Risk: Annual check. Moderate Risk: Every 3-6 months. High Risk: Every 1-2 months. Active Problem (Ulcer/Infection): Weekly or emergency care.
88
Renal disease monitoring: Diagnosing diabetic kidney disease Prevention
Annual ACR & Serum Creatinine Measurement. D: ACR >30 mg/g, Creatinine Clearance (CrCl) <60 ml/min, 95% of T1DM nephropathy patients also have retinopathy → Check eyes! P: Optimize glycaemic control, BP, cholesterol.
89
Weight management: Recommended weight loss Approach
5-10% body weight. Regular, sustained weight loss over time. Avoid ‘diabetic’ processed foods (often high in fat). Reinforce lifestyle improvements positively.
90
Smoking cessation and psychological support
Nicotine replacement therapy, varenicline, bupropion, behavioral support. Use person-first language (e.g., ‘person with diabetes’ instead of ‘diabetic’). Acknowledge emotional struggles linked to diabetes. Encourage engagement without blame (avoid “non-compliant” language).

Pharmacy 302 (32 decks)

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