Diabetes Mellitus (type 2)

Screening Diagnosis GDM Overt DM

FBS ≥5.6 mmol/L Prediabetes: 6.1- 6.9 mmol/L ≥5.1 mmol/L ≥7.0 mmol/L
Diabetes: ≥7.0 mmol/L
RPG ≥7.8 mmol/L ≥11.1 mmol/L ≥7.8 mmol/L ≥11.1 mmol/L +
symptoms
confirm with FPG/ OGTT/ confirm with FPG/ RPG/
HbA1c OGTT

OGTT results. What patient has?

FPG 6.2
2hr FPG 7.0
ANS: Impaired fasting glucose ONLY. Not IGT because 2hr FPG <7.8
HbA1c: average plasma glucose level over 3 months

Investigations → determine baseline

 Fasting plasma glucose (FPG)
  HbA1c
 Renal + Lipid profile
 Liver function test
 Urinalysis for albumin, microalbuminuria if albuminuria is absent
 ECG

Treatment

Class Drug name MOA (simplified) Dosage Side effects

Biguanides Metformin Lower hepatic Initial dose: Diarrhoea
gluconeogenesis 500 mg OD
NO insulin production Max: 1000 mg
BD

Sulphonylureas (SU) Gliclazide ↑ insulin 40 mg OM Hypoglycaemia

Max: 160 mg
BD
 Meglitinides Repaglinide SA insulin secretagogues 0.5 mg with
Taken 10 mins BEFORE main meals
meals Max: 4mg with
main meals

Alpha-glucosidase Acarbose ↓ postprandial glucose → ↓ Initial dose: 50 GI disturbances: bloating,

inhibitors (AGIs) absorption of ps mg OD abdominal discomfort, diarrhoea,
Max: 100 mg flatulence
TDS

Thiazolidinediones Pioglitazone PPAR-γ agonists à ↑insulin 15 mg OD !!: CCF, liver failure

(TZD) sensitivity Max: 45 mg
OD
Incretins: DPP4-i, Sitagliptin GLP-1, GIP: Glucose- 25 mg OD
induced insulin secretion Max: 100 mg
(-) glucagon release OD
GLP-1 analogue Exenatide 5 μg BD
Max: 10 μg BD

SGLT2-i Dapagliflozi ↓ glucose reabsorption 5 mg OD UTI, Mycotic infection

n Max: 10mg OD

Class Drug name MOA (simplified) Action

SA Actrapid Insugen Prandial: short onset of controlling postprandial glucose Onset: 30-60
R min
Peak: 2-4 hrs
RA Aspart Onset: 0-20 min
Lispro Glulisine Peak: 1-3 hr

Intermediate acting, Insulatard Basal: Covers insulin requirements between meals + night à Onset: 1-2 hr
NPH Insugen N Last 24hr Peak: 4-8 hr

Long-Acting Analogue Glargine Onset: 30-

60mins

Premixed Mixtard biphasic insulin: SA/RA + intermediate Onset: 30 mins

Dual peak

Lifestyle modification
 Medical nutrition therapy (MNT) → counselling with dietitian (Low CHO diet/ GI)
 PA + smoking cessation

Dyslipidaemia: > 40 years old→ statin regardless of baseline LDL cholesterol level
Management of complications

A. Retinopathy
Screening:
1. Visual acuity: Snellen + pinhole
2. Fundus examination
T(x) goals:
1. Delay onset and progression: improve glycaemic + BP control

B. CKD

ACEi/ ARB is preferred for CKD patients  antiproteinuric effect

OAD: Metformin, SGLT2-i, GLP1-RA

C. Diabetic symmetric polyneuropathy (DSPN)

Screening: Monofilament test

Diagnosis: Sensory examination for DM

Diabetic emergencies
Hypoglycaemia

Autonomic: Trembling, Palpitations, Sweating, Anxiety, Hunger, Nausea, Tingling

CNS: Difficulty concentrating, Confusion, Weakness/stroke like symptoms, Drowsiness, Vision changes, Difficulty speaking,
Headache, Seizures/coma

1. GIVE Simple CHO: 1 tbsp honey/ 150-200 ml of fruit juice/ 3tsp sugar + water à measure rbs after 15 mins
2. If still <3.9 mmol/L, repeat until > 3.9 mmol/L

DKA: Diagnosed by fulfilment of ALL criterias:

1. Capillary plasma glucose >11 mmol/L

2. Capillary ketones >3 mmol/L or urine ketones ≥2+
3. Venous pH <7.3 and/or bicarbonate <15 mmol/L

Principles of management

1. IMMEDIATE Correction of dehydration

2. Correction of electrolyte imbalance: maintain serum potassium between 4-5 mmol/L

3. Insulin therapy: › 50 units short-acting human insulin or rapid-acting insulin analogue made up to 50 ml with 0.9% saline
solution.

** Delay insulin infusion if the initial potassium <3.5 mmol/L until serum potassium is corrected.

4. Treatment of precipitating factor

5. Prevention of complications

Continue IV insulin infusion until resolution of DKA

Resolution is defined as:505 (Level III) › pH >7.3 › Plasma ketone <0.6 mmol/L

GDM
 Body mass index (BMI) >27 kg/m2
 Previous history of GDM
 First-degree relative with diabetes mellitus (DM)
 History of macrosomia (birth weight >4 kg)
 Bad obstetric history [unexplained IUD, congenital anomalies (NTD, cardiac defects), shoulder dystocia]
  Glycosuria ≥2+ on two occasions
 Current obstetric problems (PIH, polyhydramnios, current use of corticosteroids)

Management
Medical nutrition therapy (MNT) → high risk of developing/ diagnosed with GDM/ PMH of DM

Preconception counselling→ women with DM

 T2DM who are planning pregnancy: switch (OAD) to insulin
 Patients who are already on metformin may continue treatment
 pre-existing diabetes + PCOS may continue metformin for ovulation induction.
 Prior to conception/ detection of pregnancy→ discontinue: ACEi/ ARB, statins

Glycaemic control
Aim for HbA1c <6.5% — if possible without causing hypoglycemia
Self-monitoring of blood glucose at home

Glycaemic target
• fasting: ≤5.3 mmol/L
• 1-HPP: ≤7.8 mmol/L
• 2-HPP: ≤6.4-6.7 mmol/L

Medical nutritional therapy

 CH controlled (Low GI diet) — women with GDM intake of 175g
 If can’t be controlled after 1-2 weeks→ START OAD: metformin, glibenclamide
 If either/ both fail to meet target glycaemic control → initiate insulin
o blood glucose targets are not met after MNT + metformin
o metformin is contraindicated or unacceptable
o FPG ≥7.0 mmol/L (+- metformin)
o FPG of 6.0-6.9 mmol/L + macrosomia/ polyhydramnios +-metformin (start insulin immediately)
 Human insulin (preferred)
 Rapid-acting Insulin Analogues: Lispro/ Aspart
 Long-acting (Basal) Insulin Analogues: Detemir/ Glargine

Differentiate between GDM and pre-existing PMH: DM mothers

Complications
 Retinal Assessment: booking + week 28 (REPEAT)
 Renal Assessment: Mother (pre-existing DM) done 3 months before/ 1st antenatal visit. REFER nephrology if:
o serum creatinine > 120 µmol/L
o urinary albumin: creatinine ratio (ACR) >30 mg/mmol
o total protein excretion >0.5 g/day
Delivery method (IOL)
pre-existing diabetes
 (-) complications: between 37+0 and 38+6 weeks
 (+) complications, deliver: before 37+0 weeks
GDM
 (-) complications: no later than 40+6 weeks
 (+) complications: before 40+6 weeks

Postpartum glucose monitoring

 insulin-treated pre-existing diabetes→ step-down insulin immediately after birth + monitor their blood glucose levels
(estimate dosage)
GDM→ able to discontinue their insulin immediately after delivery
Dyslipidaemia
Dyslipidemia
 Total cholesterol <4.0 mmol/L
 LDL-C <2.0 mmol/L
 HDL-C ≥1.0 mmol/L

Framingham General CVD risk score tool → assess 10-year risk of developing CVD (heart disease, strokes, PAD and heart failure)
 > 20% - High CV Risk
 10-20 % - Intermediate (Moderate) CV Risk
 < 10% - Low CV Risk

A 40 years old man with newly diagnosed dyslipidaemia was started on statin. DM on Metformin. Ideal LDL-C?
ANS: <4.2

Management
Therapeutic lifestyle changes (TLC)
Lipid lowering drugs
Statin: (-) HMG CoA reductase → lower LDL
Target LDL achieved → maintain dose & repeat lipid profile 6-12 months
Not achieved → first step-up dosage, if remains add non-statin drugs

Statin associated muscle symptoms

myalgia (normal creatine kinase (CK)), myositis (CK > ULN) and rhabdomyolysis (CK > 10X of ULN)
Find out function of creatine kinase

Cholestyramine
Fenofibrate

Lipid Targets in Diabetes

>40 years → give statin

Heart Failure
All patients with HF due to CHD should be on statins but not recommend in non ischemic HF

Elevated TG: fasting TG > 1.7 mmol/L

Mild-to-moderate Elevations in TG (>1.7–<10.0 mmol/L)
1. Lifestyle change + control DM (if present)
2. Increase statin dosage + fibrates (combination therapy)

Severe Elevations in TG (> 10mmol/L)

Asymptomatic: repeat fasting TG + find [2] cause
Pancreatitis: Gemfibrozil, Fenofibrate

Hypertension

An otherwise healthy 65-year-old man comes to the physician for a follow-up visit for elevated blood pressure. Three weeks ago,
his blood pressure was 160/80 mmHg. Subsequent home blood pressure measurements at days 5, 10, and 15 found: 165/75 mm
Hg, 162/82 mm Hg, and 170/80 mmHg, respectively. He had a cold that was treated with over-the-counter medication 4 weeks ago.
Pulse is 72/min and blood pressure are 165/79 mm Hg.
This older patient has a wide pulse pressure with elevated SBP and normal DBP

 Isolated systolic hypertension: < arterial elasticity and compliance associated with aging  manifests with wide pulse
pressure.
 High risk of renal dysfunction and cardiovascular events (MI, stroke)
 Antihypertensive agent: thiazide diuretic or CCB— <risk of a cardiovascular event
 Isolated Office (“White-Coat”) Hypertension: BP persistent 140/90 mmHg but home systolic/ diastolic BP
measurements < 135/85 mmHg.
 Masked hypertension: normal clinic blood pressure but > home blood-pressure level (≥135/85 mmHg). Prognosis of
masked hypertension is worse than isolated office hypertension

Target BP
 <80 years old: SBP <140 mmHg and DBP <90 mmHg
 80 years and above: target of <150/90 mm

Non-Pharmacological Management
1. Weight Reduction
2. ↓Na intake, ↑K intake, Healthy eating
3. Alcohol consumption
4. Regular PA
5. Smoking cessation
6. Relaxation therapy

Pharmacological Management
 Stage 1 + low CVS risks → healthy lifestyle for 3-6 months
 1st line monotherapy in uncomplicated case: ACEIs, ARBs, CCBs and diuretics
 ß-blockers:
o intolerance or contraindication to ACEIs and ARBs
o women of child-bearing potential
o >> sympathetic drive
Framingham Risk Score
Hypertensive crisis
 Hypertensive urgency: BP >180/110 mmHg without acute end organ damage/complication

 Blood pressure measurement should be repeated after 30 minutes of bed rest

1. Rest in quiet room for at least 2 hours
2. Initiate oral anti-hypertensive agents if BP remains >180/110 mmHg
3. Hypertensive urgency discharge plan

 Hypertensive emergency: new or progressive EOD/EOS: acute heart failure, dissecting aneurysm, acute
coronary syndromes, hypertensive encephalopathy, acute renal failure, subarachnoid haemorrhage and/or
intracranial haemorrhage
 Should be admitted for immediate intervention and monitoring
 BP reduced by 10%-25% within certain minutes to hours but not lower than 160/90 mmHg

Other comorbidities (HPT +)

 DM
o target BP: <140/80 mmHg; <130/80 mmHg in younger patients and those at higher risk of cardiovascular
disease
o ACEi is drug of choice → cardiovascular benefits and reno-protective effects in patients with diabetic kidney
disease

 Non- diabetic CKD: high serum creatinine, proteinuria and/or haematuria

o target BP should be <140/90 mmHg for patients with CKD
o <130/80 mmHg for those with proteinuria ≥1g/24hours
o ACEi conferred an anti-proteinuric and reduction in ESRD

1. CHD: target BP <130 / <80 mmHg

o Cardio-selective ß-blockers: symptomatic & stable angina
o Short-acting nifedipine should not be used.
 Heart failure, AFib, PAD: Treat blood pressure to <140 / <90 mmHg.
  Resistant Hypertension: uncontrolled hypertension (>140/90 mmHg) with good medication adherence while on 3/4 anti-
hypertensive agents (+ diuretic) in adequate doses
 Refractory hypertension: patients whose BP are not controlled after ≥5 antihypertensives

This patient has hypertension and a history of increasingly frequent migraine headaches, making a specific medication more
appropriate in this case.
 ACE inhibitors avoided in female patients of reproductive age that are sexually active and use contraception
inconsistently, as they are known to be teratogenic.
 both hypertension + history of migraine requiring prophylactic therapy— beta blockers (propranolol)
 Hypertension + no other comorbidities: thiazide diuretics, ACE inhibitor, calcium channel blockers, and/or angiotensin-
receptor blockers should be tried first, before administering a beta blocker.

PIH (Refer PIH)

A 26-year-old woman, gravida 2, para 1, at 28 weeks' gestation comes to the physician for a prenatal visit. She feels well. Pregnancy
and delivery of her first child were uncomplicated. Her temperature is 37.2°C (99.0°F) and blood pressure is 165/115 mm Hg. Her
blood pressure measured 5 hours ago at home was 160/112 mm Hg. Pelvic examination shows a uterus consistent in size with a 28-
week gestation. A complete blood count and serum concentrations of electrolytes, creatinine, and hepatic transaminases are within
the reference ranges. Urinalysis is within normal limits. Which of the following is the most appropriate next step in management?

 Preeclampsia with severe features diagnosed in patients at > 20 weeks' gestation SBP ≥ 160 mm Hg / DBP ≥ 110 mm
Hg, even if other abnormalities characteristic of preeclampsia are absent on clinical or diagnostic evaluation.
 Antihypertensive therapy ASAP: hydralazine, intravenous labetalol, oral nifedipine.
 Magnesium sulfate for seizure prophylaxis
 Patients (24 weeks' - 34 weeks')  antenatal corticosteroid therapy for foetal maturation.

 ACE inhibitors: absolutely contraindicated during pregnancy  permanent renal damage in the foetus + congenital
malformations of CVS, CNS
 Methyldopa is safe, Severe hypertension: parenteral labetalol, parenteral hydralazine, nifedipine.
Prophylaxis: aspirin, Ca, Vit D

Bronchial Asthma & Chronic Obstructive Pulmonary Disease (COPD)

 Asthma usually caused by triggers/ allergen

 SOB in panic attacks: sudden onset + spontaneous resolution with peripheral numbness
 History of asthma may have no relation to SOB experienced by patient
Assesment of asthma control
Pharmacological treatment

Inhaled LABA without ICS should NOT use as reliever monotherapy in stable asthma.
Types of prescriptions
1. As-needed reliever therapy: asthma symptoms OR need for SABA (less than twice a month)
AND
 no waking up at night due to asthma in last month
 no risk factors for AEBA— no exacerbation in the last year

Control of symptoms
2. Low dose ICS: asthma symptoms or need for SABA between twice a month and twice a week
OR
 wakes up at night due to asthma >x1 a month with no risk factors
 For patients who remain symptomatic in Step 1

3. Low dose ICS/ LABA: troublesome asthma symptoms more than twice a week
OR
 wakes up at night due to asthma once a week or more
 AND with any risk factors
 For patients who remain symptomatic in Step 2

4. Medium/high dose ICS/ LABA: troublesome asthma symptoms more than twice a week
AND
 wakes up at night due to asthma once a week or more
 AND with any risk factors
 OR AEBA requiring hospital admission
 For patients who remain symptomatic in Step 3

5. Referral to respiratory physician

6. Monoclonal antibodies for poorly controlled asthma: Omalizumab (expensive)

Non pharmacological treatment

 Quit smoking
 Breathing exercise
 Weight loss
  LTRA (Montelukast) is added in case of uncontrolled asthma (with low- dose ICS)
o additional control of asthma symptoms
 ICS trial considered if patient use SABA inhaler but have not been using ICS
 If after addition of LTRA  uncontrolled, indicate for referral

AEBA  immediate referral to hospital

 sit forward (Tripod position)
 speak in words or short phrases
 use of accessory muscles
 agitation/altered consciousness
 tachypnoea
 tachycardia
 hypoxia
 silent chest

Management
 Hypoxemia in AEBA  maintain SpO2 at >94%
 β2-agonists to relieve bronchospasm
 Ipratropium bromide: moderate to severe AEBA in the ED or equivalent care setting.
 Corticosteroids  resolution of exacerbations and prevention of relapse
 Magnesium sulphate in severe asthma

Asthma in Pregnancy
 Management same as for non-pregnant patients
 Advise on patient education on good asthma control
 frequent monitoring (4 - 6 weeks)
 maintenance, reliever, LTRA continue
 stepping down  after delivery if asthma is well controlled
Peak Flow Metre & Asthma diary
COPD
 symptoms of chronic cough, sputum production or dyspnoea
 History of exposure to risk factors  >> cigarette smoking.
Status asthmaticus
1. Tachypnoea
2. Pulsus paradoxus
3. Silent chest
4. Inability to talk in sentence
5. Subcostal recession

Anaemia
Haemoglobin level:
 ♀: < 12 g/ dL (120 g per L)
o Pregnant: 1st/3rd trimester  <11 g/dL, 2nd trimester  <10.5 g/dL, Postpartum: <10 g/dL
o Severe anaemia (Hb <7.0 g/dL)
 ♂: <13 g/ dL (130 g per L)

Haemodynamic instability
Volume loss: light-headedness, syncope, hypotension
↓ oxygen-carrying capacity: weakness, fatigue, SOB, >>exacerbation of comorbidities

Mean corpuscular volume

1. Microcytic (< 80 fL),  IDA, Thalassemia
2. Normocytic (80 to 100 fL), 
Haemolytic: Hemoglobinopathies (Sickle cell), G6PD, PNHb, Hereditary spherocytosis, AHA, MAHA
Non-haemolytic: Anaemia of chronic kidney disease
3. Macrocytic (> 100 fL) 
Megaloblastic: Vit B12, Folate deficiency
Pregnancy
1. IDA
2. Haemoglobinopathy  May coexists +IDA (Hb analysis)

Do FBC + serum ferritin (POCT) during booking  early detection

R(x)
1. Prevention
 Daily oral iron: 30-60 mg of elemental iron OR EOD (reduce GI side effects)
 If not acceptable  Weekly oral iron: 120mg

2. Treatment (<11 g/dL)

 Daily oral iron: 120mg
 Once corrected  standard daily antenatal iron dose
(++ Folic acid 400mcg for daily/EOD, 2.8mg for weekly)
 IV Iron  ONLY if not tolerated, non-compliant, poor response
NO IM (never), NO IV in 1st trimester

For asymptomatic:
Hb <7 g/dL and POA <34weeks – refer FMS
Hb <7 g/dL and >34weeks – refer O&G

For symptomatic  refer O&G

Joint Pain (including Gout)

  Osteoarthritis: stiffness >> activity
Pain: worse by the end of the day, aggravated by use, relieved by rest,
Painful and limited range of motion, crepitus, effusions, instability, or deformities

Principles of management
1. Provide explanation and reassurance
2. Correct modifiable risk factors: obesity, injury, overuse
3. Control pain and maintain function with appropriate drugs

 Rheumatoid arthritis: Joint pain and swelling  symmetrical polyarthritis for >6 weeks
Early morning stiffness lasting ≥30 minutes
Clinical synovitis, joint tenderness + boggy swelling
Restricted range of motion
Polymyalgia rheumatica syndrome (refer Dizziness > Giant cell/ temporal arteritis)

Non- PMT
 Patient education
 When in pain  rest joint.
Once resolved  regular, gentle exercise (low impact aerobic exercises, strengthening, stretching and range-of-motion)
 Adaptations of house  prevent accidents
 Occupational Therapy  joint protection by hand strengthening + mobilisation exercise
 Physiotherapy to reduce pain
 Footwear

Pharmacological
1. NSAIDs: relieve joint pain and swelling
2. Corticosteroids: short term treatment for joint inflammation
3. DMARDs: treat joint inflammation and slow progression (long-term)
 Methotrexate
 Sulfasalazine
 Hydroxychloroquine
 Leflunomide
  Gout: Persistent hyperuricemia  deposition of MSU crystals + gout flare, chronic gouty arthritis, OR subcutaneous
tophus

Clinical stages of gout

1. Gout Flare
 Acute inflammation induced by MSU crystals PAINFUL
 Occurs abruptly with joint pain peaking in intensity within 24 hours and resolves spontaneously within 1 - 2 weeks
 Usually occurs at night, with the patient’s sleep interrupted due to severe joint pain

2. Intercritical gout: asymptomatic period after or between gout flares + persistence of MSU crystals
3. Chronic Gouty Arthritis: persistent joint inflammation induced by MSU crystals

 Chronic arthritis, with or without tophi,

 Chronic joint pain,
  Functional disability,
 Structural joint destruction/ deformity

Main differentials

1. Septic arthritis: common at knee joint

 Systemic features: fever, ill or septic-looking
 Leukocytosis and raised C-reactive protein

2. Acute calcium pyrophosphate crystal arthritis

 Age >60 years old
 Involvement of a degenerative joint

3. Psoriatic arthritis: psoriasis, nail dystrophy (pitting, onycholysis or crumbling)

4. Reactive arthritis: urethral discharge or ulcer, rash on soles, conjunctivitis  postinfectious autoimmune
5. Gonococcal arthritis: sexually active

Non PMT
Patient education
1. Compliance to ULT
2. Healthy lifestyle follow DASH  discourages purine-rich red meat (except omega 3), fructose-rich foods, full fat
dairy products and saturated fats
3. Reduce weight for obese/overweight

Pharmacological treatment
 Urate-lowering therapy  Allopurinol
o Recurrent gout flares (≥2 flares in 12 months)
o OR presence of ≥1 tophi
o OR presence of radiographic damage attributable to gout

Gout flare (Monotherapy)

 1. Colchicine for pain relief
2. NSAIDs
3. Corticosteroids
4. Prophylaxis: (3 to 6 months when initiating ULT)

Muscle Weakness

Intrinsic muscle weakness  unable to perform first repetition of the task

Asthenia: exhaustion (–) muscle weakness
 Degenerative disc/ Spinal cord injury/ TIA/ CVA: neurological deficits –paraesthesia, numbness, paralysis
 Botulism
GBS Poliomyelitis Multiple sclerosis Muscular dystrophy
Stocking-glove distribution Paralytic poliomyelitis: Optic neuritis (unilateral) Progressive muscle paresis
Back + limb pain Asymmetric acute flaccid UMN weakness and atrophy
Respiratory involvement paralysis ascending Cerebellar involvement: poor Duchenne: Gower + dilated
paralysis postural control/ imbalance cardiomyopathy (young)
Becker: Slower progression <
DMD

Muscle fatigue  inability to continue performing a task after multiple repetitions;

 Electrolyte imbalance: hypokalemic or hyperkalemic periodic paralysis): recurrent episodes of muscle weakness after
exercise/ diet change/ medications
 Lambert Eaton syndrome: muscle strength improves with repetitive/ ongoing use + autonomic symptoms  dry
mouth, constipation
 Myasthenia gravis: weakness of extraocular muscle + worsen with repetitive use
  Addison disease
 Fibromyalgia
 Drug: Simvastatin
 Dengue

UMN vs LMN