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CCC CO 1 > Long term CCs part I > Flashcards

Long term CCs part I Flashcards

1
Q

Define Asthma

A

Episodes of reversible airway obstruction characterised by wheeze, cough, sputum and SOB

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2
Q

What percentage of the population does asthma affect and in what proportion?

A

5-8% of the population
Children: boys >girls
Adults: Girls > boys

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3
Q

What are the 3 factors which contribute to bronchial airway narrowing?

A
  1. Bronchial muscle contraction triggered by stimuli
  2. Mucosal swelling/ inflammation caused by masts cell and basophil degranulation= release of inflammatory mediators
  3. Increased mucus production
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4
Q

Risk factors for asthma?

A 
Cold air 
Exercise 
Emotion 
Allergens e.g. dust mite/ pollen fur 
Infection/ URTI esp in children 
Smoking 
Pollution 
FamHx of atopy 
Social deprivation
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5
Q

Key features of an asthma history?

Any questionnaires that can be used?

A

Ask about other atopic disease e.g. eczema, hayfever, allergy or FamHx
Ask about house setting, pets, carpet, feather pillows or duvet
Ask about occupation: if symptoms remit at the weekend work may provide trigger
Quantify exercise tolerance and effect on ADLs
Quantify nights of disturbed sleep

Asthma control questionnaire can be used (ACQ)

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6
Q

Clinical signs of Asthma

Clinical signs of life threatening asthma?

A 
Tachypnoea 
Hyperinflated chest
Hyper-resonant percussion note
Decreased air entry 
Audible wheeze

Confusion: due to cerebral hypoperfusion
Exhaustion
Silent chest
Cyanosis= (PaO2 <8kPa but PaCO2 4.6-6.0, SPO2<92%)
Bradycardia: heart is fatigued

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7
Q

Define FEV1 and FVC and explain their ratios

A

FEV1: The volume of air that an individual can forcefully exhale in 1 second: time dependent: reflects airway caliber

FVC: Forced vital capacity: The amount of air that can be forcibly exhaled from the lungs after taking the deepest breath possible- volume dependent: reflects lung volume not caliber

FEV1/FVC Ratio: This is used to distinguish between obstructive and restrictive conditions

  • Ratio <0.7= obstructive: due to narrowing of airways
  • Ratio >0.7= restrictive: due to reduced total lung capacity
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8
Q

What’s the NICE diagnostic algorithm for children <5

A

To treat symptoms based on observation- review the child regularly

Use skin prick test to aeroallergens or specific IgE tests to identify triggers after formal diagnosis made

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9
Q

What’s the NICE diagnostic algorithm for children ages 5-17?

What are the positive thresholds?

A
  1. Perform Spirometry in children and young people with asthma symptoms
  2. If they can’t do 1. Treat based on observation/ clinical judgement and try doing the tests again every 6-12 months
  3. If still unsure after spirometry and Bronchodilator reversibility, consider FENO
  4. If still unsure after 1-3, monitor peak flow variability for 2-4 weeks

Positive thresholds

  • Obstructive spirometry: FEV1/FVC<0.7/ 70% or below the lower limit of their normal
  • FENO 35ppb or more
  • BDR: Improvement in FEV1 of 12% or more
  • Peak flow variability: Over 20%
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10
Q

What’s the NICE algorithm for adults?

What are the positive thresholds?

A

Confirm occupational asthma first- then refer to specialist if positive. Otherwise…

  1. Measure FENO first then Spirometry with symptomatic adults
  2. If unsure after FENO, spirometry and BDR- monitor peak flow variability for 2-4 weeks
  3. If still unsure after peak flow variability, refer for a histamine or methacholine direct bronchial challenge test
  4. If Meta or bronc.chall. test is unavailable- suspect asthma and review diagnosis after treatment OR refer to a center with access to histamine or methacholine challenge

Thresholds

  • Obstructive spirometry: FEV1/FVC<0.7/ 70% or below the lower limit of their normal
  • FENO 40ppb or more
  • BDR: Improvement in FEV1 of 12% or more and increase in volume of 200m or more
  • Peak flow variability: Over 20%
  • Direct bronchial challenge test with histamine or methacholine: PC20 of 9mg/ml or less
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11
Q

Explain to your patient how to perform a peak flow test

A

o Standing or sitting up – preferably standing
o Ensure pointer at zero and fingers not obstructing
o Full breath in, rapid forced expiratory puff through meter, tight seal around mouthpiece
o Best of 3 readings recorded

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12
Q

What mnemonics would you use to explain a diagnosis of asthma (or any disease tbh)

A

BUCES, Brief history, understanding, concerns, explanations, summarise

NWCPM, Normal anatomy/ physiology, what the disease is, cause, problems/ complication and management

see osce notes for more info

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13
Q

What are the 2 main self management methods in asthma?

A

Patient education: Should include discussion of issues such as trigger avoidance and occupational exposure to support people and their families living with asthma. Encourage a smoke free environment

PAAP: : Asthma.org.uk contains good examples: There’ll be specific advice about recognising loss of asthma control, assessed by symptoms or peak flows or both

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14
Q

Differentiate between primary, secondary and tertiary management

A

Primary: Stop yourself from getting it. Secondary, detect disease early and prevent it from getting worse
Tertiary- trying to improve your quality of life and reduce symptoms of a disease you already have

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15
Q

What are the methods of non-pharmacological management

A

Avoidance of aeroallergens
Reduce pet contact
Food allergen avoidance- esp eggs. This should not be offered as primary prevention advice, just be aware of it
Breastfeeding: has potential protective effect in relation to early asthma
Weight reduction is recommended in obese patients
Warn patients and families about the dangers of smoking and second-hand tobacco smoking exposure

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16
Q

What is a phased approach in asthma management

A

Aims to abolish symptoms asap and optimise peak flow by starting treatment at the level most likely to achieve this.
Aim for early control and step up or down as required
Before starting something new, practitioners should check adherence with existing therapies, check inhaler technique and eliminate trigger factors

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17
Q

Pharma management step 1 Asthma?

A

Intermittent reliver therapy: SABA: Salbutamol PRN. Fastest working short term reliever therapy PRN

18
Q

Pharma management step 2 Asthma? When is it indicated?

A

Regular preventer therapy: Inhaled corticosteroids. Start dose in relation to severity: 200-800 micrograms Beclometasone dipropionate and budesonide

Indicated:
Increased use of SABA 3 + times a week
Waking up one night a week
Adult/ child who has had asthma attack requiring oral CS in the last 2 years

If ICS not tolerated/<5yrs – consider leukotriene receptor antagonist (monteleukast, zafirlukast and pranlukast)

19
Q

Pharma management step 3 Asthma- Initial add on therapy?

A

Consider ADDING a long-acting β2 agonist (LABA) e.g. salmeterol if Sx still uncontrolled with ICS (should ONLY be used with an ICS) 🡪 usually combination inhaler (Symbicort)

If no response to LABA consider stopping LABA

20
Q

Pharma management step 4 Asthma- additional add on therapy?

A

Assess response to LABA:
Good response 🡪 continue LABA
Partial response 🡪 continue LABA + increase ICS to 800μg/day
No response 🡪 stop LABA + increase ICS to 800μg/day 🡪 if still inadequate:

Refer for specialist care

21
Q

Pharma management step 5 asthma- high dose therapies

A

Increase ICS to max dose = 2000μg/day OR
ADD 4th drug – e.g. leukotriene receptor antagonist, SR theophylline, LAMA e,g. tiotropium bromide, or oral β2 agonist tablet

Refer to specialist care

22
Q

Pharma step 6 management asthma- oral therapies

A

Use daily oral steroid tablet (e.g. prednisolone) + maintain high-dose ICS + consider other Rx to minimize steroid tablet use
Refer for specialist care

23
Q

What is the pharma management chain for children (both under and over 5 yo) with asthma?

Clue (SIMR, SIL8OR)

A

SIMR (<5): SABA, ICS, monteleukast, refer

SIL8OR (>5): SABA, ICS, LABA, 8 (increase ICS to 800 micrograms), oral steroids, refer

24
Q

Medical management in acute attack of asthma?

OSISM

A

Oxygen 15L/min – prioritise nebulizing salbutamol with face mask rather than high oxygen without nebulizing- Sit pt. up

Salbutamol 5mg (or terbutaline) nebulised with oxygen, repeated at 15-20 min intervals (in all types of attack; although if mild with normal sats – 10 puffs inhaled and observe, discharge if PEF >75% with 1mg beclametasone)

S/E of salbutamol 🡪 hypokalaemia (so be careful)
Steroid: 40-50mg PO prednisolone or 100mg IV hydrocortisone (if moderate, severe or life-threatening)
Ipratropium bromide 0.5mg with oxygen (if severe or life-threatening) – 4-6 hourly
If life-threatening features: contact critical care outreach team 🡪 Magnesium sulphate 2g IV over 20 mins/ aminophylline infusion/ salbutamol infusion (if life-threatening) + call anaesthetist for intubation/ventilation (worsening hypoxia/hypercapnia despite max therapy)

25
Q

Grading severity of asthma?

A
  • Moderate: PEFR >50-75%, normal speech and no features of acute severe or life-threatening asthma
  • Acute severe: PEFR 33-50% or RR 25/min in people aged >12
  • Life threatening: PEFR <33% or oxygen sats <92% or altered consciousness or exhaustion or cardiac arrhythmia
26
Q

Define diabetes

What are the 2 types of T1DM?

A

Metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency/ reduced effectiveness of insulin

AI T1DM: Characterised by absolute insulin deficiency and presence of antibodies to pancreatic beta cells
Idiopathic: Uncommon form characterised by absence of antibodies- more common in African/ asian ancestry

27
Q

How common is it and who is affected?

A

T1DM= 5-10% of all diabetes patients

Usually adolescent onset but can occur at any age. M:F; 1.5: 1

28
Q

What’s the pathophys of T1DM?

A

Insulin deficiency from autoimmune destruction of insulin-secreting pancreatic beta cells: this causes persistent hyperglycaemia

Pts can’t use glucose > this stimulates secretion of glucagon, adrenaline, cortisol and GH > this promotes gluconeogenesis, glucogenolysis and ketogenesis in the liver > patients present with hyperglycaemia and anion gap metabolic acidosis

29
Q

Risk factors for T1DM?

A 
Genetics: HLA D3 and HLAD4 linked
Poor diet (low vit D, early exposure to cow’s milk)
Family or personal Hx of autoimmunity
30
Q

Symptoms of T1DM

A 
Polydipsia (↑ thirst)
Polyuria (↑ urination)
Lethargy
Boils/slow-healing sores
Visual blurring
Genital thrush/pruritis vulvae
Frequent, recurrent or prolonged infections – esp. gum, skin, vaginal, UTIs
Unexplained weight loss despite extreme hunger
Ketosis
31
Q

Define DKA and the parameters

What are the symptoms?

A 
Diabetic ketoacidosis: ketonaemia 3 mmol /l and over or significant ketonuria (more than 2 + on standard urine sticks) 
blood glucose over 11 mmol /l or known diabetes mellitus.
venous bicarbonate (HCO3 ) ) below 15 mmol /l and /or venous pH less than 7.3
  • Lethargy/ confusion
  • Visual disturbance
  • Increased thirst and urinary frequency
  • Inability to tolerate fluids
  • Fruity smell of acetone on breath
  • Persistent vomiting and or diarrhoea
  • Abdominal pain
  • Weight loss
32
Q

Signs of T1DM

Signs of DKA?

A

Persistent hyperglycaemia
Ketonuria
Tachypnoea
Lethargy

Kussmaul breathing
Dehydration: dry skin, mucus membranes, reduced skin turgor. Sunken eyes and prolonged cap refill in severe cases
Shock: resulting from severe dehydration- tachycardia, poor peripheral perfusion, lethargy drowsiness and decreased consciousness

33
Q

What are the microvascular complications of diabetes?

What about macro complications?

A 
Vascular disease 
Nephropathy 
Diabetic retinopathy 
Diabetic feet
Neuropathy: Direct damage to the nerves by hyperglycaemia and decreased blood flow to nerves

DM is a risk factor for the development of atherosclerosis which increases the risk of HF, stroke and PAD

34
Q

How is T1DM specifically diagnosed?

How is T2DM specifically diagnosed?

A

Low C-peptide + presence of autoantibodies – islet cell antibodies (ICA) and anti-glutamic acid decarboxylase (GAD) antibodies

HbA1c >48mmol/mol

35
Q

What are the 2 main ways to diagnose DM?

A
  • Symptoms of hyperglycaemia (3 main of polyuria, polydipsia, unexplained weight loss, visual blurring, genital thrush, lethargy) AND raised venous glucose detected once:
  • Fasting >7mmol/L
  • Random >11.1mmol/L

OR

  • Raised venous glucose on two separate occasions with no Sx OR raised oral glucose tolerance test (OGTT) – gold standard:
  • 2h value >11.1mmol/L – OGTT: pt. fasts overnight, then in the morning the fasting blood glucose is taken. Then you give them a sugary drink and periodically test blood sugar for the next 2 hours > results are based on value after 2 hours.
36
Q

What are the 5 main steps of conservative management for T1DM?

A

Provide an individual care plan
Offer a structured education programme e.g. DAFNE
Provide info on communicating with diabetes specialist care team
Manage lifestyle issues: meal planning, carb counting, avoid drinking alcohol on empty stomach, spread weekly units over min 3 days, advise on smoking misuse
Provide up to date info on diabetes support groups e.g. diabetes UK

37
Q

What are the targets for T1DM (4 main ones)

What advice would you give re driving and diabetes? What are the thresholds?

A

HBA1C <48mmol/mol
Fasting plasma glucose 5-7mmol/L
Plasma glucose before meal 4-7mmol/L
Plasma glucose after meal 5-9mmolL- 90 mins after eating

Pt needs to be careful and have a fast acting carbohydrate in the car, avoid driving if meal is delayed, check glucose before starting the journey and 2 hours into the journey. Young people driving- target is 5mmol/L
Pt can be fined up to £1000 if they fail to tell the DVLA about a condition
For cars and motorcycle: must have an awareness of hypoglycaemia and no more than 1 episode of hypo while awake in the preceding 12 months

38
Q

DKA management?

Hypoglycaemia management?

A

1L of 0.9 normal saline over 1 hour- when K+ result available start replacement
50 units of actrapid in 49.5ml of 0.9% NaCl
Insulin: rate: 0.1 units/kg of bodyweight/ hour IV

Advise patient to consume 10-20g of fast acting carbohydrate preferably in liquid form. Recheck blood glucose after 10-15 mins. If person is unconscious- IM glucagon should be administered immediately. Call 999 for children <8/ IM glucagon not available or alcohol is the cause

39
Q

What are the 4 speeds of insulin?

What are the 3 types of insulin?

A

Rapid acting insulin: onset 15 mins, duration 2-5 hours. E.g. Humalog and Novorapid

Short acting insulin: onset 30-60 mins, duration 8 hours. E.g. Actrapid and Humalin S

Intermediate acting (isophane) insulins: onset 1-2 hours, duration 11-24 hours. E.g. Humulin I and Insulatard

Long acting insulins: duration of up to 24 hours. Steady state level achieved after 2-4 days to produce a constant level of insulin

  1. Human Insulins- produced by recombinant DNA and have the same amino acid sequence as human insulin
  2. Human insulin analogues: Same make up as human insulin but modified to have extended duration of action or faster absorption
  3. Animal insulins: Extracted and purified from animal sources- bovine or porcine- not commonly used
40
Q

What is the preferred order for insulin regimes?

General advice for insulin injection?

Factors that affect insulin absorption

A

1Multiple daily injection basal bolus insulin regime: Offer twice daily insulin detemtir as the long-acting basal insulin therapy. Offer RA insulin analogue injected before meals for mealtime insulin replacement
If 1 is not possible consider a twice-daily human mixed insulin regimen
3. Insulin pump therapy recommended if multiple daily injections results in severe hypoglycaemia or HBA1C levels have remained high

Subcut injection as it’ll be destroyed by gastric acid otherwise and not absorbed across the gut mucosa.
General advice: leave for 30 mins at room temp prior, check expiry date before administration, read manufacturer’s advice, use a new needle for each injection, choose appropriate injection site. Needle should be injected at 90 degrees to skin- pinch skin

a. Large dose
b. Accidental IM injection due to poor injection technique
c. Exercise: faster absorption due to increased blood flow at injection site
d. Injection site- rate depends on which site is used
e. Age: faster in younger children as they have less subcut fat
f. Fat mass: absorption is slower if there is a large amount of subcut fat

41
Q

T2DM Definition

Prevalence

Pathophysiology

A

Insulin resistance and relative insulin deficiency result in persistent hyperglycaemia

Higher prevalence in South Asia

Decrease in insulin secretion with or without insulin resistance. Pancreas is unable to secrete enough insulin to compensate

42
Q

T2DM risk factors?

A

Obesity
Lack of exercise
Calorie and alcohol excess: low fibre, high glycaemic index diet may increase the risk of being overweight
FamHx: People with a fam Hx are 2-6 times more likely to have diabetes
Ethnicity: People of Asian, African and Black communities are 2-4times more likely to develop
History of gestational diabetes: 7 fold increased risk of developing T2DM
Drug treatment: Statins, corticosteroids and a combined treatment with a thiazide diuretic + beta blocker can increase risk of T2DM
Polycystic ovarian syndrome: This increases the risk of impaired glucose regulation
Metabolic syndrome
Low birth weight for gestational age

CCC CO 1 (7 decks)

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