CBM Flashcards
Common triggers for asthma
Allergens (e.g. pets, pollen, dust mites). Cold air Emotions Smoking Viral infection Pollution Drugs (e.g. NSAIDs, beta-blockers).
Pathophysiology of asthma
Triggers activate mast cells to relate spasmogens and chemotaxins.
EARLY PHASE - bronchospasm due to spasmogens
LATE PHASE - inflammation due to chemotaxins (causes attraction of eosinophils/monocytes).
Types of asthma
cause and timing of onset?
- EXTRINSIC - type I hypersensitivity
=> early onset/younger patients (may improve with age)
=> subtype - occupational asthma - INTRINSIC - non-immune mechanisms (often no cause identified).
=> late onset/middle-aged patients
Occupational asthma
extrinsic asthma (but may be later onset due to not working until adulthood)
Occurs due to occupational triggers - chemicals, enzymes in flour, animal substances, dust
Symptoms will be better on days off work/holidays
Asthma - symptoms
Wheeze, SOB, cough (worse at night/early morning/on exercise).
Chest tightness +/- reflux symptoms
Asthma - history
FHx or PMHx of atopy Typical Sx with diurnal variation Identifiable trigger(s)
Asthma - investigations
History + auscultation
Objective measurements - spirometry/BDR test/FeNO/PEF variability
What peak flow results are indicative of asthma?
PEF with >20% variability
What spirometry results are indicative of asthma?
FEV1:FVC <70%
What BDR results are indicative of asthma?
FEV1 >12% improvement after bronchodilator
or >200ml volume increase
What FeNO results are indicative of asthma?
FeNO >40ppb
Management of chronic asthma
- SABA + Low-dose ICS
- Add LABA or LTRA
- increase dose of ICS
- referral to specialist, potentially oral steroids.
Safety netting
Lifestyle factors - smoking, weight loss, avoiding triggers
Asthma reviews
What is important to remember with LABAs in the management of asthma?
do not use without an ICS
Safety netting in chronic asthma
Return if symptoms are getting worse/interfere with daily life/waking up at night.
Will have an annual review for their asthma.
Signs of an acute attack and how to manage:
- reliever inhaler isn’t helping
- too breathless to speak/eat/sleep
- very tight chest/coughing a lot
- RR increasing/feels like can’t get enough air in
=> Puff or PRN inhaler - up to 10 times. Ring 999 if no improvement.
Components of an annual asthma review
- LEVEL OF CONTROL?
- using SABA >3x per week
- night symptoms
- interfering with activities
- chest tightness, wheeze - EXACERBATIONS?
- COMPLIANCE/TECHNIQUE
- SIDE EFFECTS OF MEDICATIONS
What is COPD?
= chronic, progressive, POORLY REVERSIBLE airway obstruction
including chronic bronchitis and emphysema
Chronic bronchitis
CHRONIC BRONCHITIS (“blue bloaters”)
- increased mucous production and inflammatory cells, scarred/thickened epithelium => increased airway resistance
- chromic productive cough
- poor alveolar ventilation => T2RF (CO2 retention, loss of hypoxic drive)
Emphysema
EMPHYSEMA (“pink puffers”)
- Increased protease activity destroys alveoli, decreased elasticity and recoil, enlarged air spaces (decreased SA).
- increased RR and HR to compensate for reduced gas exchange
- cachexia (higher energy demand for respiration).
- poor gas exchange => T1RF (normal CO2)
Risk factors for COPD
Smoking
Occupational dust
Childhood infections
Alpha1-antitrypsin deficiency
COPD - symptoms
Productive cough (clear, white sputum)
Progressive dyspnoea + wheeze
Frequent LRTIs
COPD - signs
Increased RR, flapping tremor, cyanosis, barrel-chest
Reduced chest expansion, hyper-resonance
Polyphonic expiratory wheeze, decreased breath sounds.
What might you hear on auscultation in a person with COPD?
Polyphonic expiratory wheeze
(or decreased breath sounds).
MRC Dyspnoea scale
1 - only SOB on strenuous exercise
2 - SOB if hurrying/walking up hill
3 - SOB on flat
4 - Stop for breath after 100m
5 - SOB with ADLs, at rest, etc.
COPD - diagnosis
- Hx and Examination
- Spirometry + BDR
=> BDR - no improvement
=> FEV1 <80%
=> FEV1:FVC <0.7
=> PEF - little variation
- CXR
What might a CXR show in COPD?
hyperinflation
flat diaphragms
decreased peripheral markings
What might an ABG show in COPD?
Decreased O2
Either normal or increased CO2 (depending on type of respiratory failure).
Severity of COPD by spirometry
Mild - FEV1 >80%
Moderate - FEV1 50-79%
Severe - FEV1 30-49%
Very severe - FEV1 <30%
What is the only intervention in COPD that decreases mortality?
Smoking cessation
COPD - management
- SMOKING CESSATION
- OPTIMISE WEIGHT
- PULMONARY REHAB
=> exercises to improve SOB
=> educate and promote self-management - MUCOLYTICS (e.g. carbocysteine)
=> may help chronic productive cough
=> review after 4 weeks, stop if no benefit. - VACCINATIONS
=> pneumococcal and flu
How can you help someone stop smoking pharmacologically?
Nicotine replacement - patches/gum
Varenicline - nicotine receptor partial agonist.
Bupropion - NA/DA reuptake inhibitor
E-cigarettes - lack long-term evidence but potentially safer
When is inhaled therapy for COPD offered?
only when lifestyle interventions have been tried and still SOB
inhaled therapy for COPD
SABA or SAMA (salbutamol or ipratropium)
If asthmatic features
=> LABA + ICS (e.g. Fostair)
=> Add LABA for triple therapy
If no asthmatic features (steroids won’t help)
=> LABA + LAMA
What are asthmatic features in COPD?
Previous asthma/atopy OR increased eosinophils
Substantial FEV1 variation
Substantial diurnal PEF variation
What role do SABAs/SAMAs have in COPD?
Relieve acute bronchochonstriction
What role do LABAs/LAMAs have in COPD?
Increase FEV1 and improve SOB
What are some anti-muscarinic side effects?
Constipation Urinary retention Dry mouth Blurred vision Confusion
What are signs of an acute COPD exacerbation?
Altered sputum volume/colour
Reduced exercise tolerance
Fever/malaise/lethargy
COPD exacerbation - management
Bronchodilators (neb) - SABA & SAMA
Oral corticosteroids - 30mg prednisolone o.d. 5 days
Oxygen - aim for 88-92%
Possibly antibiotics
COPD exacerbation - investigations
Sputum sample (if purulent)
Bloods - FBC, U&Es, ABG
CXR, ECG
COPD - safety netting
- Signs of exacerbation (increased SOB, increased cough/wheeze, cyanosis, confusion).
=> May give rescue pack (steroid + Abx) - Warn of risk of pneumonia and pneumothorax
COPD - follow up
At least once a year!
- Measure FEV1 and FVC
- Assess on MRC dyspnoea scale
- Review for referral to specialist services
COPD complications
Acute exacerbations Polycythaemia Respiratory failure Cor pulmonale Pneumothorax Lung carcinoma
What is Atrial Fibrillation?
= a rapid, irregular heart rhythm due to uncoordinated contraction of the atria.
What are the types of AF?
- PAROXYSMAL - recurrent, sudden, self-limiting episodes
- PERSISTENT - AF >7 days
- PERMANENT - long-term AF
Causes of AF
“Mrs SMITH”
S - sepsis M - mitral valve stenosis I - IHD T - thyrotoxicosis H - HTN
Complications of AF
- STROKE!
- Vascular dementia
- decreased left ventricular function
- decreased QoL
Symptoms of AF
SOB
Syncope / dizziness
Palpitations
Chest pain
Diagnosis of AF
- Examination - irregularly irregular pulse
- 12-lead ECG (if normal do 24-hour ECG)
- Bloods - FBC, TFT, U&Es, LFTs, glucose
- CXR / echo - investigate cause
What signs indicate AF on an ECG?
Absent P-waves
Irregular R-R interval
>150 bpm
What are the aims of management of AF?
- Rate and Rhythm control
2. Stroke prevention (anticoagulation)
AF - Rate & Rhythm control
RATE - Target HR 60-80 bpm
=> beta-blocker (OR RL CCB if contraindicated BB, OR combine either with digoxin).
RHYTHM
=> flecanide/amiodarone
=> cardioversion
=> ablation
What options should be avoided in rate management in AF?
NOT BB + RL CCB
NOT Digoxin as monotherapy
AF - haemodynamically unstable patient
Acute heart failure/chest pain/hypotension
=> CARDIOVERSION
AF - Stroke Prevention
Anticoagulation
- Assess stroke risk with CHA2DS2-VASc score
- Assess bleeding risk with HASBLED score
=> HASBLED of 3+ needs closer anti-coag monitoring/alternative
CHA2DS2-VASc score
C - congestive HF H - HTN A2 - age >74 (score = 2), age 65-74 (score =1) D - diabetes S2 - prev stroke/TIA (score = 2) Va - vascular disease Sc - sex category - female
HASBLED score
H - HTN A - Abnormal liver/renal function S - Stroke B - bleeding predisposition L - labile INR E - elderly >65 D - drugs (NSAIDs, aspirin, alcohol, etc)
What lifestyle factors can be managed in AF?
weight loss, diet, exercise
reduce alcohol and caffeine, reduce smoking
optimise co-morbidities
AF - Safety netting and follow-up
Safety Net:
- Signs of MI/stroke (LoC, severe chest pain/SOB, dizziness)
Follow-up:
- in 1 year to check Sx of AF
- annual review of stroke and bleed risk.
Risk factors for HTN
Age >65 Male FHx Obesity Sedentary lifestyle High salt diet Alcohol/caffeine DM Renal disease
Primary vs Secondary HTN
Primary (95% cases) - cause unknown
Secondary (5% cases)
- renal disease (80%)
- endocrine
- drugs
- other (pregnancy, aortic coarctation).
What are renal causes of secondary HTN?
Glomerulonephritis
CKD
Renal artery stenosis
PCKD
What drugs can cause secondary HTN?
Steroids, NSAIDs, OCP
What are endocrine causes of secondary HTN?
Conn’s (increased aldosterone)
Cushing’s (increased cortisol)
Acromegaly (increased GH)
Phaeochromocytoma (increased adrenaline)
What is essential HTN?
What are the symptoms?
Gradual increase in BP over years
Asymptomatic
What is malignant HTN?
What are the symptoms?
Rapid, sustained increase in BP
Headaches, visual disturbances, renal dysfunction
Complications/consequences of HTN
Heart - LVH (eventually failure)
Aorta - AAA, aortic dissection
Brain - IC haemorrhage and stroke
Kidney - CKD
Eyes - hypertensive retinopathy
Stage 1 HTN
Clinic BP >140/90
ABPM >135/85
Stage 2 HTN
Clinic BP >160/100
ABPM >150/95
Stage 3 HTN
Clinic SBP >180 or DBP >110
HTN - investigations
- Clinic BP - 2 readings >140/90
- ABPM
3. Investigate end-organ damage => U&Es and urine dip => HbA1c, cholesterol, lipids => Fundoscopy => ECG
- QRISK2 - to assess 10-year CVD risk
QRISK2 score
Used to assess 10-year risk of CVD
Based on age, sex, ethnicity, BMI, DM, CKD, AF, FHx, cholesterol
HTN - lifestyle management
Diet - low salt, fruit&veg, low fat
Exercise - >30 mins 4-5x a week
Weight loss (if necessary)
Smoking cessation and alcohol reduction
HTN - when is pharmacological management required?
If <80 years old and 1 or more of:
- CVD/renal disease
- QRISK >20%
- DM
- End-organ damage
All stage 2 and 3 HTNs
HTN - pharmacological management
1.
If <55 or diabetic - ACEI
If >55 or black - CCB
- Add either ACEI/CCB or thiazide-like diuretic
- A+C+D
- Beta-blocker / alpha-blocker / other diuretic
HTN - annual review
Review BP
Review risk factors - smoking, alcohol, BMI, HbA1c
Review medications and symptoms
SBP and DBP goals of treating HTN
if <80 - BP <140/90
If >80 - BP <150/90
Side effects of ACEIs?
What monitoring is required?
Cough
Hyperkalaemia
Angioedema
Decreased renal function
Monitor U&Es - stop if big increase in CR or decrease in eGFR
ACEIs - contraindications
Renovascular disease
Caution with spironolactone (hyperkalaemia)
Avoid in pregnancy
Side effects of ARBs?
What monitoring is required?
Hyperkalaemia
Decreased renal function
Monitor U&Es
Side effects of thiazide-like diuretics?
What monitoring is required?
Hypokalaemia
Postural hypotension
Impaired glucose control
Exacerbate gout
Monitor U&Es, BP
what do you need to remember about efficacy of thiazide diuretics?
Rely on good renal function - need to be really excreted in order to work
Contraindications of thiazide-like diuretics
Renal impairment
Gout
DM
Side effects of spironolactone?
What monitoring is required?
Hyperkalaemia
Gynaecomastia
Monitor U&Es
Contraindications of spironolactone
Renovascular disease
Caution with ACEI (risk of hyperkalaemia)
Side effects of calcium-channel blocker?
What monitoring is required?
Headaches, flushing, ankle oedema, hypotension
Monitor BP, HR
Contraindications of CCBs
Don’t use RL CCB in CHF
Don’t use in combination with BBs
Contraindications of Beta-blockers
Asthma (bronchospasm)
Side effects of alpha-blockers
Postural hypotension
Dyspepsia symptoms
abdo pain, bloating, N&V, heartburn, food/acid regurgitation
Dyspepsia - DDx
GORD
Peptic Ulcer disease (gastric/duodenal)
Gastric ca
Oesophageal ca
Symptoms of GORD
Dyspepsia
=> worse lying/bending down and with hot liquid/alcohol
=> relieved by antacids
Waterbrash Odynophagia Atypical chest pain Nocturnal wheeze/cough Tooth decay
Causes of GORD
- ANATOMICAL
- sphincter dysfunction, hiatus hernia (sliding/rolling) - PHYSIOLOGICAL
- smoking/alcohol
- spicy/fatty/starchy food, large meals late at night
- increased IAP
Complications of GORD
ADULTS
- Oesophagitis/ulcers
- Barret’s oesophagus => adenocarcinoma
CHILDREN
- aspiration pneumonia
- frequent otitis media
INFANTS
- feeding difficulties => reduced growth
Causes of peptic ulcer disease
H. pylori (causes PUD / gastric cancer)
NSAIDs
Zollinger-Ellison syndrome
Smoking/Caffeine
Duodenal vs Gastric ulcers
Duodenal are 4x more common
Duodenal typically younger incidence
Duodenal - pain relief on eating/milk
Gastric - pain worse on eating
Duodenal - no anorexia and vomiting
Gastric - anorexia and vomiting
Symptoms of peptic ulcer disease
Dyspepsia
Burning epigastric pain (related to food/hunger)
+/- Haematemesis
+/- Melaena
Dyspepsia - ALARMS55 Symptoms
Anaemia Lost weight Anorexia Recent onset + progressive Sx Melaena/Haematemesis Swallowing difficulties
55+ years old
(i.e. over 55 and at least one of the above symptoms)
Dyspepsia - investigations
History
FBC - anaemia?
Barium swallow - anatomical causes?
Endoscopy
=> ONLY IF ALARM SYMPTOMS (urgent 2ww referral) or Tx resistant dyspepsia
Dyspepsia - Initial management
- LIFESTYLE
- Weight loss, reduce smoking and alcohol, reduce stress, smaller meals
- Medication review - NSAIDs, steroids, bisphosphonates, etc. - SYMPTOM RELIEF
- Antacid/Alginates - MEDICAL TREATMENT
- Full dose PPI (4-8 weeks)
- H. Pylori - triple therapy
H. Pylori triple therapy
1 week of PPI and 2 Abx (amoxicillin and either clarithromycin or metronidazole).
Continue PPI for 4-6 weeks
Confirmed GORD - management
1st Line - PPI (4-8 weeks at lowest dose)
2nd Line - H2RA
Signs of Oesophageal Malignancy
- Progressive dysphagia
- Weight loss + anorexia
- Retrosternal chest pain
- Lymphadenopathy
- Cough/aspiration
Safety netting in dyspepsia
Return immediately if develop any ALARM symptoms
Upper GI 2WW referral if…
- Dysphagia
- Dyspepsia and at least 1 ALARM symptom
- Recent onset dyspepsia in >55s
- Dyspepsia and other cancer RF
How common is IBS?
When is peak onset?
Up to 20% of the population
F:M - 2:1
Peak onset = age 20-30
What is IBS?
IBS is a group of abdominal symptoms for which no organic cause is found
A - abdo pain/discomfort
B - bloating
C - change in bowel habits
How is IBS diagnosed?
> 6 months of abdominal pain/discomfort
=> relieved on defecation OR associated with altered bowel frequency/stool form
and at least 2 of:
- bloating/distension
- passage of mucous
- incomplete evacuation/straining/urgency
- symptoms worsened by eating
+/- non-intestinal Sx
Non-intestinal Sx of IBS
urinary Sx, headache, fatigue, back pain, dysmenorrhoea
RFs/causes of IBS
- Gastroenteritis
- Antibiotics
- Stress, anxiety, depression
- Eating disorders
- Trauma/surgery
IBS - investigations
Careful Hx and examination
FBC, CRP - r/o IBD
Faecal calprotectin - r/o IBD
Coeliac screen
CA-125 - in older women to r/o ovarian cancer
Lower GI 2WW if…
- Weight loss
- Melaena
- altered bowel habit >60yo
- FHx colon cancer <50yo
- Abdo or rectal mass
=> 2WW for colonoscopy
IBS - prognosis
Not associated with any serious long-term disease
Sx may fluctuate in severity
IBS - Management
- DIET/LIFESTYLE
=> low fodmaps diet
=> regular meals
=> lots of fluids, but avoid caffeine/fizzy drinks - PSYCHOLOGICAL
=> CBT, hypnotherapy, acupuncture, herbal therapies - PHARMACOLOGICAL
=> Constipation - laxatives
=> Diarrhoea - anti-diarrhoeals
=> Pain - antispasmodics, low-dose TCAs
How is chronic/resistant pain in IBS managed?
Low dose TCAs
SSRIs 2nd line
IBS - follow-up
Agreed between clinician and patient, depending on Sx and response to Tx.
SAFETY NET FOR RED FLAGS OF BOWEL CANCER
What is hyperthyroidism?
= raised circulating thyroid hormones T3 and T4
General Sx of hyperthyroidism
- Anxious, irritable, insomnia
- Fatigue/weakness
- Hot/sweaty
- Tremor/palpitations
- Menorrhagia/diarrhoea
- Weight loss (but increased appetite)
General Signs of hyperthyroidism
Increased HR / arrythmia
Increased SBP
Hyperreflexia
+/- goitre
Signs of Hyperthyroidism specific to Grave’s Disease
Goitre
Pre-tibial myxoedema
Acropachy (swollen hands and clubbing)
Grave’s ophthalmology
What are the components of Grave’s ophthalmology ?
- Exophthalmos (bulging eyes)
- Lagophthalmos (cannot close eyes)
- Periorbital oedema
What are the causes of hyperthyroidism?
Grave’s Disease (70%)
Toxic Multinodular Goitre
Solitary toxic adenoma
Drug-induced
Secondary causes - TSH-secreting pituitary adenoma, pregnancy
What drugs can induce hyperthyroidism?
Iodine, Amiodarone, Lithium
Hyperthyroidism - what is toxic multi nodular goitre?
What are the risk factors?
T3/T4 secreting nodules, irresponsive to -ve feedback
RFs - elderly, iodine deficient
Hyperthyroidism - what is a solitary toxic adenoma?
Benign T3/T4 secreting nodule, irresponsive to -ve feedback.
Grave’s Disease - pathophysiology
Autoimmune process
involves IgG autoantibody stimulation of thyroid follicular cells
Grave’s disease - risk factors
PMHx or FHx of autoimmune disorders
TFTs - primary hyperthyroidism
raised T3/T4
low TSH
TFTs - secondary hyperthyroidism
raised TSH
raised T3/T4
TFTs - subclinical hyperthyroidism
normal T3/T4
low TSH
Investigations for ?hyperthyroidism
Hx and examination
TFTs
Autoantibodies
Technetium uptake scan (if no autoantibodies)
=> patchy uptake in nodules
=> diffuse uptake in Grave’s
Assess eye disease (Grave’s)
Hyperthyroidism - management options
NEEDS SPECIALIST INPUT!
- Symptomatic relief - beta-blockers
- Anti-thyroid drugs - carbimazole/propylthiouracil
- Radioactive iodine
- thyroidectomy
When would a thyroidectomy be done in hyperthyroidism?
Compression Sx
Malignant nodule
Tx resistant disease
What anti-thyroid drug regimens are there?
- TITRATION - high dose then titrate down to euthyroid
- BLOCK & REPLACE - maintain high dose and levothyroxine replacement
=> not in pregnancy
Also: Beta-blockers for symptom relief.
What are contraindications for radioactive iodine therapy in hyperthyroidism?
Pregnancy/breastfeeding
<16 years old
Anti-thyroid drug side effects
Rash/cholestatic jaundice
Agranulocytosis - infection/bleeding risk
=> FBC before Tx and monitor closely
Hyperthyroidism - safety netting
- Signs of agranulocytosis
=> sore throat, mouth ulcer, bruising - Signs of thyroid crisis
=> severe tachycardia and increase in temp, confusion - Signs of tracheal compression
=> SOB/stridor/dysphagia - Regular TFT monitoring
What is hypothyroidism?
= low circulating thyroid hormones T3 and T4
Symptoms of hypothyroidism
Depression/psychosis/slowed intellectual activity Fatigue/weakness Cold Amenorrhoea/constipation Weight gain Decreased libido
Signs of hypothyroidism
Low HR
Anaemia
Hyporeflexia
Dry skin/ hair loss
+/- non-pitting oedema
+/- goitre
Investigations in ?hypothyroidism
Hx & Examination
TFTs
FBC
Autoantibodies (TPO and Tg)
Causes of hypothyroidism
- Hashimoto’s Thyroiditis (most common in UK)
- Primary atrophic thyroiditis
- Iodine deficiency (most common worldwide)
- Drug-induced
- Congenital
- Postpartum Thyroiditis
- Secondary causes (very rare)
=> hypopituitarism (pituitary adenoma, Sheehan’s syndrome, etc.)
What drugs can cause HYPOthyroidism?
Amiodarone, Lithium, carbimazole, excess iodine
Also - post-thyroidectomy or radioactive iodine therapy.
What is primary atrophic thyroiditis?
Autoimmune gland destruction
=> Excessive lymphocyte infiltrate atrophies the gland
=> No goitre
What is Hashimoto’s thyroiditis?
Autoimmune condition
Autoantibodies against TPO and thyroglobulin
Gradual gland destruction, lymphocyte infiltration and fibrosis => GOITRE
There is an initial hyperthyroid state before hypothyroidism (damage causes release of T3 and T4)
What is the cause of congenital hypothyroidism?
due to absence/underdevelopment of the thyroid gland
TFTs - primary hypothyroidism
low T3/T4
high TSH
TFTs - secondary hypothyroidism
low TSH
low T3/T4
TFTs - subclinical hypothyroidism
raised TSH but T3/T4 normal
Sick euthyroid syndrome
low TSH which is transient during a period of illness
DDx for ?hypothyroidism
DM Adrenal insufficiency Coeliac disease Anxiety/Depression Dementia
Hypothyroidism - management
LIFELONG Thyroid hormone replacement therapy
Levothyroxine - low dose and titrate up until desired TSH levels reached.
Starting dose depends on age
=> 18-49yo - 50-100 mcg
=> >50 or CVD - 25 mcg
How often is levothyroxine dose reviewed?
Every 3-4 weeks initially
Then every 4-6 months once stable.
When might hypothyroidism need referring to secondary care endocrinologist for management?
Patients with goitre Suspected malignancy Cardiac disease Tx resistant Patients planning a pregnancy
pathophysiology of T2DM
a combination of insulin resistance and deficiency, resulting in persistent hyperglycaemia and beta cell decline.
due to a combination of genetic and environmental factors
Risk factors for T2DM
Genetics - FHx, south asian/afro-caribbean, male
Increasing age
Metabolic syndrome
Obesity, sedentary lifestyle, poor diet
Smoking/alcohol
What is metabolic syndrome?
Central obesity
Increased BP
Increased lipids/cholesterol
Increased glucose
Symptoms of T2DM
GRADUAL ONSET
Polyuria, polydipsia
Fatigue
Recurrent infections
OFTEN COMPLICATIONS ARE 1st PRESENTATION
Complications of T2DM
MICROVASCULAR
- Retinopathy (visual blurring)
- Polyneuropathy (pain/numbness)
- Nephropathy
MACROVASCULAR
- Erectile dysfunction
- CVD (MI)
- Cerebrovascular disease (stroke)
T2DM - Management
Lifestyle modifications - trial for 3 months
MONOTHERAPY
If HbA1c >48, then add metformin/sulphonyurea depending on renal function.
DUAL THERAPY
Add sulphonyurea, DPP4 inhibitor, pioglitazone.
TRIPLE THERAPY
INSULIN THERAPY (or GLP1 mimetic)
What is important to remember when prescribing metformin?
Patient needs good renal function (contraindicated if eGFR <45)
Can cause GI upset
Lifestyle modifications in T2DM
Diet - low GI carbs, low fat, high fibre (inc. F&V)
Weight loss - calorie restriction AND exercise
Reduce smoking/alcohol
What is the goal of pharmacological management in T2DM?
Aim for HbA1c <48 (6.5%)
Monitoring diabetes control
HbA1c - over 3 months
Finger-prick - if on insulin
Urine dip - glucose, ketones, protein
How does metformin act?
Decreases gluconeogenesis
Increases glucose utilisation
What are advantages of metformin?
Decrease CV risk
No weight gain
How do pioglitazones work?
Decrease insulin resistance
Disadvantages of pioglitazones
Cause weight gain
Increased risk of CVD
Fluid retention
How do sulphonyureas work?
Increase insulin secretion via K+ channel closure
Disadvantages of sulphonyureas
Can cause hypos
Can cause weight gain
What is an advantage of GLP1 mimetics?
Also cause weight LOSS
T2DM follow-up/review
At least once a year
- Review glucose control
- Screen for complications - fundoscopy, foot check, urine dip
- Reduce CVD risk - BP <140/80, QRISK
- Ensure access to sufficient education and understand the risk of long-term complications
Risk of complications with T2DM when counselling a patient
MI x4 chance Stroke x2 chance Increased risk of infection and ulcers Risk of vision loss/blindness Risk of kidney damage /failure
Safety netting in T2DM
1. Signs of hypos => lethargy, confusion, aggression => sweaty, pale, shaking => RISK DRIVING => Mx = glucose PO 10-20g
- Reiterate risks of complications of diabetes
What is the 1st line antihypertensive for a patient with T2DM?
ACE inhibitors are the first choice anti-hypertensive in patient’s with T2DM, irrespective of family background and age.
