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CP2 > CBM > Flashcards

CBM Flashcards

1
Q

Common triggers for asthma

A 
Allergens (e.g. pets, pollen, dust mites). 
Cold air
Emotions
Smoking
Viral infection
Pollution
Drugs (e.g. NSAIDs, beta-blockers).
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2
Q

Pathophysiology of asthma

A

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).

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3
Q

Types of asthma

cause and timing of onset?

A
  1. EXTRINSIC - type I hypersensitivity
    => early onset/younger patients (may improve with age)
    => subtype - occupational asthma
  2. INTRINSIC - non-immune mechanisms (often no cause identified).
    => late onset/middle-aged patients
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4
Q

Occupational asthma

A

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

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5
Q

Asthma - symptoms

A

Wheeze, SOB, cough (worse at night/early morning/on exercise).

Chest tightness +/- reflux symptoms

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6
Q

Asthma - history

A 
FHx or PMHx of atopy
Typical Sx with diurnal variation
Identifiable trigger(s)
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7
Q

Asthma - investigations

A

History + auscultation

Objective measurements - spirometry/BDR test/FeNO/PEF variability

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8
Q

What peak flow results are indicative of asthma?

A

PEF with >20% variability

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9
Q

What spirometry results are indicative of asthma?

A

FEV1:FVC <70%

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10
Q

What BDR results are indicative of asthma?

A

FEV1 >12% improvement after bronchodilator

or >200ml volume increase

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11
Q

What FeNO results are indicative of asthma?

A

FeNO >40ppb

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12
Q

Management of chronic asthma

A
  1. SABA + Low-dose ICS
  2. Add LABA or LTRA
  3. increase dose of ICS
  4. referral to specialist, potentially oral steroids.

Safety netting
Lifestyle factors - smoking, weight loss, avoiding triggers
Asthma reviews

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13
Q

What is important to remember with LABAs in the management of asthma?

A

do not use without an ICS

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14
Q

Safety netting in chronic asthma

A

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.

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15
Q

Components of an annual asthma review

A
  1. LEVEL OF CONTROL?
    - using SABA >3x per week
    - night symptoms
    - interfering with activities
    - chest tightness, wheeze
  2. EXACERBATIONS?
  3. COMPLIANCE/TECHNIQUE
  4. SIDE EFFECTS OF MEDICATIONS
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16
Q

What is COPD?

A

= chronic, progressive, POORLY REVERSIBLE airway obstruction

including chronic bronchitis and emphysema

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17
Q

Chronic bronchitis

A

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)
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18
Q

Emphysema

A

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)
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19
Q

Risk factors for COPD

A

Smoking
Occupational dust
Childhood infections
Alpha1-antitrypsin deficiency

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20
Q

COPD - symptoms

A

Productive cough (clear, white sputum)
Progressive dyspnoea + wheeze
Frequent LRTIs

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21
Q

COPD - signs

A

Increased RR, flapping tremor, cyanosis, barrel-chest

Reduced chest expansion, hyper-resonance

Polyphonic expiratory wheeze, decreased breath sounds.

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22
Q

What might you hear on auscultation in a person with COPD?

A

Polyphonic expiratory wheeze

(or decreased breath sounds).

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23
Q

MRC Dyspnoea scale

A

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.

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24
Q

COPD - diagnosis

A
  1. Hx and Examination
  2. Spirometry + BDR

=> BDR - no improvement
=> FEV1 <80%
=> FEV1:FVC <0.7
=> PEF - little variation

  1. CXR
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25
Q

What might a CXR show in COPD?

A

hyperinflation
flat diaphragms
decreased peripheral markings

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26
Q

What might an ABG show in COPD?

A

Decreased O2

Either normal or increased CO2 (depending on type of respiratory failure).

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27
Q

Severity of COPD by spirometry

A

Mild - FEV1 >80%

Moderate - FEV1 50-79%

Severe - FEV1 30-49%

Very severe - FEV1 <30%

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28
Q

What is the only intervention in COPD that decreases mortality?

A

Smoking cessation

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29
Q

COPD - management

A
  1. SMOKING CESSATION
  2. OPTIMISE WEIGHT
  3. PULMONARY REHAB
    => exercises to improve SOB
    => educate and promote self-management
  4. MUCOLYTICS (e.g. carbocysteine)
    => may help chronic productive cough
    => review after 4 weeks, stop if no benefit.
  5. VACCINATIONS
    => pneumococcal and flu
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30
Q

How can you help someone stop smoking pharmacologically?

A

Nicotine replacement - patches/gum

Varenicline - nicotine receptor partial agonist.

Bupropion - NA/DA reuptake inhibitor

E-cigarettes - lack long-term evidence but potentially safer

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31
Q

When is inhaled therapy for COPD offered?

A

only when lifestyle interventions have been tried and still SOB

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32
Q

inhaled therapy for COPD

A

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

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33
Q

What are asthmatic features in COPD?

A

Previous asthma/atopy OR increased eosinophils

Substantial FEV1 variation

Substantial diurnal PEF variation

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34
Q

What role do SABAs/SAMAs have in COPD?

A

Relieve acute bronchochonstriction

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35
Q

What role do LABAs/LAMAs have in COPD?

A

Increase FEV1 and improve SOB

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36
Q

What are some anti-muscarinic side effects?

A 
Constipation
Urinary retention
Dry mouth
Blurred vision
Confusion
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37
Q

What are signs of an acute COPD exacerbation?

A

Altered sputum volume/colour
Reduced exercise tolerance
Fever/malaise/lethargy

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38
Q

COPD exacerbation - management

A

Bronchodilators (neb) - SABA & SAMA

Oral corticosteroids - 30mg prednisolone o.d. 5 days

Oxygen - aim for 88-92%

Possibly antibiotics

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39
Q

COPD exacerbation - investigations

A

Sputum sample (if purulent)

Bloods - FBC, U&Es, ABG

CXR, ECG

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40
Q

COPD - safety netting

A
  • Signs of exacerbation (increased SOB, increased cough/wheeze, cyanosis, confusion).
    => May give rescue pack (steroid + Abx)
  • Warn of risk of pneumonia and pneumothorax
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41
Q

COPD - follow up

A

At least once a year!

  • Measure FEV1 and FVC
  • Assess on MRC dyspnoea scale
  • Review for referral to specialist services
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42
Q

COPD complications

A 
Acute exacerbations
Polycythaemia
Respiratory failure
Cor pulmonale
Pneumothorax
Lung carcinoma
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43
Q

What is Atrial Fibrillation?

A

= a rapid, irregular heart rhythm due to uncoordinated contraction of the atria.

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44
Q

What are the types of AF?

A
  1. PAROXYSMAL - recurrent, sudden, self-limiting episodes
  2. PERSISTENT - AF >7 days
  3. PERMANENT - long-term AF
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45
Q

Causes of AF

A

“Mrs SMITH”

S - sepsis
M - mitral valve stenosis
I - IHD
T - thyrotoxicosis
H - HTN
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46
Q

Complications of AF

A
  • STROKE!
  • Vascular dementia
  • decreased left ventricular function
  • decreased QoL
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47
Q

Symptoms of AF

A

SOB
Syncope / dizziness
Palpitations
Chest pain

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48
Q

Diagnosis of AF

A
  1. Examination - irregularly irregular pulse
  2. 12-lead ECG (if normal do 24-hour ECG)
  3. Bloods - FBC, TFT, U&Es, LFTs, glucose
  4. CXR / echo - investigate cause
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49
Q

What signs indicate AF on an ECG?

A

Absent P-waves
Irregular R-R interval
>150 bpm

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50
Q

What are the aims of management of AF?

A
  1. Rate and Rhythm control

2. Stroke prevention (anticoagulation)

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51
Q

AF - Rate & Rhythm control

A

RATE - Target HR 60-80 bpm
=> beta-blocker (OR RL CCB if contraindicated BB, OR combine either with digoxin).

RHYTHM
=> flecanide/amiodarone
=> cardioversion
=> ablation

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52
Q

What options should be avoided in rate management in AF?

A

NOT BB + RL CCB

NOT Digoxin as monotherapy

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53
Q

AF - haemodynamically unstable patient

A

Acute heart failure/chest pain/hypotension

=> CARDIOVERSION

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54
Q

AF - Stroke Prevention

A

Anticoagulation

  1. Assess stroke risk with CHA2DS2-VASc score
  2. Assess bleeding risk with HASBLED score
    => HASBLED of 3+ needs closer anti-coag monitoring/alternative
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55
Q

CHA2DS2-VASc score

A 
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
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56
Q

HASBLED score

A 
H - HTN
A - Abnormal liver/renal function
S - Stroke 
B - bleeding predisposition
L - labile INR
E - elderly >65
D - drugs (NSAIDs, aspirin, alcohol, etc)
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57
Q

What lifestyle factors can be managed in AF?

A

weight loss, diet, exercise

reduce alcohol and caffeine, reduce smoking

optimise co-morbidities

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58
Q

AF - Safety netting and follow-up

A

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.
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59
Q

Risk factors for HTN

A 
Age >65
Male
FHx
Obesity
Sedentary lifestyle
High salt diet
Alcohol/caffeine
DM
Renal disease
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60
Q

Primary vs Secondary HTN

A

Primary (95% cases) - cause unknown

Secondary (5% cases)

  • renal disease (80%)
  • endocrine
  • drugs
  • other (pregnancy, aortic coarctation).
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61
Q

What are renal causes of secondary HTN?

A

Glomerulonephritis
CKD
Renal artery stenosis
PCKD

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62
Q

What drugs can cause secondary HTN?

A

Steroids, NSAIDs, OCP

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63
Q

What are endocrine causes of secondary HTN?

A

Conn’s (increased aldosterone)
Cushing’s (increased cortisol)
Acromegaly (increased GH)
Phaeochromocytoma (increased adrenaline)

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64
Q

What is essential HTN?

What are the symptoms?

A

Gradual increase in BP over years

Asymptomatic

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65
Q

What is malignant HTN?

What are the symptoms?

A

Rapid, sustained increase in BP

Headaches, visual disturbances, renal dysfunction

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66
Q

Complications/consequences of HTN

A

Heart - LVH (eventually failure)

Aorta - AAA, aortic dissection

Brain - IC haemorrhage and stroke

Kidney - CKD

Eyes - hypertensive retinopathy

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67
Q

Stage 1 HTN

A

Clinic BP >140/90

ABPM >135/85

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68
Q

Stage 2 HTN

A

Clinic BP >160/100

ABPM >150/95

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69
Q

Stage 3 HTN

A

Clinic SBP >180 or DBP >110

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70
Q

HTN - investigations

A
  1. Clinic BP - 2 readings >140/90
  2. ABPM
3. Investigate end-organ damage
=> U&Es and urine dip
=> HbA1c, cholesterol, lipids
=> Fundoscopy
=> ECG
  1. QRISK2 - to assess 10-year CVD risk
71
Q

QRISK2 score

A

Used to assess 10-year risk of CVD

Based on age, sex, ethnicity, BMI, DM, CKD, AF, FHx, cholesterol

72
Q

HTN - lifestyle management

A

Diet - low salt, fruit&veg, low fat

Exercise - >30 mins 4-5x a week

Weight loss (if necessary)

Smoking cessation and alcohol reduction

73
Q

HTN - when is pharmacological management required?

A

If <80 years old and 1 or more of:

  • CVD/renal disease
  • QRISK >20%
  • DM
  • End-organ damage

All stage 2 and 3 HTNs

74
Q

HTN - pharmacological management

A

1.
If <55 or diabetic - ACEI
If >55 or black - CCB

  1. Add either ACEI/CCB or thiazide-like diuretic
  2. A+C+D
  3. Beta-blocker / alpha-blocker / other diuretic
75
Q

HTN - annual review

A

Review BP

Review risk factors - smoking, alcohol, BMI, HbA1c

Review medications and symptoms

76
Q

SBP and DBP goals of treating HTN

A

if <80 - BP <140/90

If >80 - BP <150/90

77
Q

Side effects of ACEIs?

What monitoring is required?

A

Cough
Hyperkalaemia
Angioedema
Decreased renal function

Monitor U&Es - stop if big increase in CR or decrease in eGFR

78
Q

ACEIs - contraindications

A

Renovascular disease

Caution with spironolactone (hyperkalaemia)

Avoid in pregnancy

79
Q

Side effects of ARBs?

What monitoring is required?

A

Hyperkalaemia
Decreased renal function

Monitor U&Es

80
Q

Side effects of thiazide-like diuretics?

What monitoring is required?

A

Hypokalaemia
Postural hypotension
Impaired glucose control
Exacerbate gout

Monitor U&Es, BP

81
Q

what do you need to remember about efficacy of thiazide diuretics?

A

Rely on good renal function - need to be really excreted in order to work

82
Q

Contraindications of thiazide-like diuretics

A

Renal impairment
Gout
DM

83
Q

Side effects of spironolactone?

What monitoring is required?

A

Hyperkalaemia
Gynaecomastia

Monitor U&Es

84
Q

Contraindications of spironolactone

A

Renovascular disease

Caution with ACEI (risk of hyperkalaemia)

85
Q

Side effects of calcium-channel blocker?

What monitoring is required?

A

Headaches, flushing, ankle oedema, hypotension

Monitor BP, HR

86
Q

Contraindications of CCBs

A

Don’t use RL CCB in CHF

Don’t use in combination with BBs

87
Q

Contraindications of Beta-blockers

A

Asthma (bronchospasm)

88
Q

Side effects of alpha-blockers

A

Postural hypotension

89
Q

Dyspepsia symptoms

A

abdo pain, bloating, N&V, heartburn, food/acid regurgitation

90
Q

Dyspepsia - DDx

A

GORD
Peptic Ulcer disease (gastric/duodenal)
Gastric ca
Oesophageal ca

91
Q

Symptoms of GORD

A

Dyspepsia
=> worse lying/bending down and with hot liquid/alcohol
=> relieved by antacids

Waterbrash
Odynophagia
Atypical chest pain 
Nocturnal wheeze/cough
Tooth decay
92
Q

Causes of GORD

A
  1. ANATOMICAL
    - sphincter dysfunction, hiatus hernia (sliding/rolling)
  2. PHYSIOLOGICAL
    - smoking/alcohol
    - spicy/fatty/starchy food, large meals late at night
    - increased IAP
93
Q

Complications of GORD

A

ADULTS

  • Oesophagitis/ulcers
  • Barret’s oesophagus => adenocarcinoma

CHILDREN

  • aspiration pneumonia
  • frequent otitis media

INFANTS
- feeding difficulties => reduced growth

94
Q

Causes of peptic ulcer disease

A

H. pylori (causes PUD / gastric cancer)
NSAIDs
Zollinger-Ellison syndrome
Smoking/Caffeine

95
Q

Duodenal vs Gastric ulcers

A

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

96
Q

Symptoms of peptic ulcer disease

A

Dyspepsia
Burning epigastric pain (related to food/hunger)
+/- Haematemesis
+/- Melaena

97
Q

Dyspepsia - ALARMS55 Symptoms

A 
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)

98
Q

Dyspepsia - investigations

A

History

FBC - anaemia?

Barium swallow - anatomical causes?

Endoscopy
=> ONLY IF ALARM SYMPTOMS (urgent 2ww referral) or Tx resistant dyspepsia

99
Q

Dyspepsia - Initial management

A
  1. LIFESTYLE
    - Weight loss, reduce smoking and alcohol, reduce stress, smaller meals
    - Medication review - NSAIDs, steroids, bisphosphonates, etc.
  2. SYMPTOM RELIEF
    - Antacid/Alginates
  3. MEDICAL TREATMENT
    - Full dose PPI (4-8 weeks)
    - H. Pylori - triple therapy
100
Q

H. Pylori triple therapy

A

1 week of PPI and 2 Abx (amoxicillin and either clarithromycin or metronidazole).

Continue PPI for 4-6 weeks

101
Q

Confirmed GORD - management

A

1st Line - PPI (4-8 weeks at lowest dose)

2nd Line - H2RA

102
Q

Signs of Oesophageal Malignancy

A
  • Progressive dysphagia
  • Weight loss + anorexia
  • Retrosternal chest pain
  • Lymphadenopathy
  • Cough/aspiration
103
Q

Safety netting in dyspepsia

A

Return immediately if develop any ALARM symptoms

104
Q

Upper GI 2WW referral if…

A
  • Dysphagia
  • Dyspepsia and at least 1 ALARM symptom
  • Recent onset dyspepsia in >55s
  • Dyspepsia and other cancer RF
105
Q

How common is IBS?

When is peak onset?

A

Up to 20% of the population

F:M - 2:1

Peak onset = age 20-30

106
Q

What is IBS?

A

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

107
Q

How is IBS diagnosed?

A

> 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

108
Q

Non-intestinal Sx of IBS

A

urinary Sx, headache, fatigue, back pain, dysmenorrhoea

109
Q

RFs/causes of IBS

A
  • Gastroenteritis
  • Antibiotics
  • Stress, anxiety, depression
  • Eating disorders
  • Trauma/surgery
110
Q

IBS - investigations

A

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

111
Q

Lower GI 2WW if…

A
  • Weight loss
  • Melaena
  • altered bowel habit >60yo
  • FHx colon cancer <50yo
  • Abdo or rectal mass

=> 2WW for colonoscopy

112
Q

IBS - prognosis

A

Not associated with any serious long-term disease

Sx may fluctuate in severity

113
Q

IBS - Management

A
  1. DIET/LIFESTYLE
    => low fodmaps diet
    => regular meals
    => lots of fluids, but avoid caffeine/fizzy drinks
  2. PSYCHOLOGICAL
    => CBT, hypnotherapy, acupuncture, herbal therapies
  3. PHARMACOLOGICAL
    => Constipation - laxatives
    => Diarrhoea - anti-diarrhoeals
    => Pain - antispasmodics, low-dose TCAs
114
Q

How is chronic/resistant pain in IBS managed?

A

Low dose TCAs

SSRIs 2nd line

115
Q

IBS - follow-up

A

Agreed between clinician and patient, depending on Sx and response to Tx.

SAFETY NET FOR RED FLAGS OF BOWEL CANCER

116
Q

What is hyperthyroidism?

A

= raised circulating thyroid hormones T3 and T4

117
Q

General Sx of hyperthyroidism

A
  • Anxious, irritable, insomnia
  • Fatigue/weakness
  • Hot/sweaty
  • Tremor/palpitations
  • Menorrhagia/diarrhoea
  • Weight loss (but increased appetite)
118
Q

General Signs of hyperthyroidism

A

Increased HR / arrythmia
Increased SBP
Hyperreflexia
+/- goitre

119
Q

Signs of Hyperthyroidism specific to Grave’s Disease

A

Goitre
Pre-tibial myxoedema
Acropachy (swollen hands and clubbing)
Grave’s ophthalmology

120
Q

What are the components of Grave’s ophthalmology ?

A
  • Exophthalmos (bulging eyes)
  • Lagophthalmos (cannot close eyes)
  • Periorbital oedema
121
Q

What are the causes of hyperthyroidism?

A

Grave’s Disease (70%)
Toxic Multinodular Goitre
Solitary toxic adenoma
Drug-induced

Secondary causes - TSH-secreting pituitary adenoma, pregnancy

122
Q

What drugs can induce hyperthyroidism?

A

Iodine, Amiodarone, Lithium

123
Q

Hyperthyroidism - what is toxic multi nodular goitre?

What are the risk factors?

A

T3/T4 secreting nodules, irresponsive to -ve feedback

RFs - elderly, iodine deficient

124
Q

Hyperthyroidism - what is a solitary toxic adenoma?

A

Benign T3/T4 secreting nodule, irresponsive to -ve feedback.

125
Q

Grave’s Disease - pathophysiology

A

Autoimmune process

involves IgG autoantibody stimulation of thyroid follicular cells

126
Q

Grave’s disease - risk factors

A

PMHx or FHx of autoimmune disorders

127
Q

TFTs - primary hyperthyroidism

A

raised T3/T4

low TSH

128
Q

TFTs - secondary hyperthyroidism

A

raised TSH

raised T3/T4

129
Q

TFTs - subclinical hyperthyroidism

A

normal T3/T4

low TSH

130
Q

Investigations for ?hyperthyroidism

A

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)

131
Q

Hyperthyroidism - management options

A

NEEDS SPECIALIST INPUT!

  1. Symptomatic relief - beta-blockers
  2. Anti-thyroid drugs - carbimazole/propylthiouracil
  3. Radioactive iodine
  4. thyroidectomy
132
Q

When would a thyroidectomy be done in hyperthyroidism?

A

Compression Sx
Malignant nodule
Tx resistant disease

133
Q

What anti-thyroid drug regimens are there?

A
  1. TITRATION - high dose then titrate down to euthyroid
  2. BLOCK & REPLACE - maintain high dose and levothyroxine replacement
    => not in pregnancy

Also: Beta-blockers for symptom relief.

134
Q

What are contraindications for radioactive iodine therapy in hyperthyroidism?

A

Pregnancy/breastfeeding

<16 years old

135
Q

Anti-thyroid drug side effects

A

Rash/cholestatic jaundice

Agranulocytosis - infection/bleeding risk
=> FBC before Tx and monitor closely

136
Q

Hyperthyroidism - safety netting

A
  1. Signs of agranulocytosis
    => sore throat, mouth ulcer, bruising
  2. Signs of thyroid crisis
    => severe tachycardia and increase in temp, confusion
  3. Signs of tracheal compression
    => SOB/stridor/dysphagia
  4. Regular TFT monitoring
137
Q

What is hypothyroidism?

A

= low circulating thyroid hormones T3 and T4

138
Q

Symptoms of hypothyroidism

A 
Depression/psychosis/slowed intellectual activity
Fatigue/weakness
Cold
Amenorrhoea/constipation
Weight gain
Decreased libido
139
Q

Signs of hypothyroidism

A

Low HR
Anaemia
Hyporeflexia
Dry skin/ hair loss

+/- non-pitting oedema
+/- goitre

140
Q

Investigations in ?hypothyroidism

A

Hx & Examination

TFTs
FBC
Autoantibodies (TPO and Tg)

141
Q

Causes of hypothyroidism

A
  • 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.)
142
Q

What drugs can cause HYPOthyroidism?

A

Amiodarone, Lithium, carbimazole, excess iodine

Also - post-thyroidectomy or radioactive iodine therapy.

143
Q

What is primary atrophic thyroiditis?

A

Autoimmune gland destruction
=> Excessive lymphocyte infiltrate atrophies the gland
=> No goitre

144
Q

What is Hashimoto’s thyroiditis?

A

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)

145
Q

What is the cause of congenital hypothyroidism?

A

due to absence/underdevelopment of the thyroid gland

146
Q

TFTs - primary hypothyroidism

A

low T3/T4

high TSH

147
Q

TFTs - secondary hypothyroidism

A

low TSH

low T3/T4

148
Q

TFTs - subclinical hypothyroidism

A

raised TSH but T3/T4 normal

149
Q

Sick euthyroid syndrome

A

low TSH which is transient during a period of illness

150
Q

DDx for ?hypothyroidism

A 
DM
Adrenal insufficiency
Coeliac disease
Anxiety/Depression
Dementia
151
Q

Hypothyroidism - management

A

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

152
Q

How often is levothyroxine dose reviewed?

A

Every 3-4 weeks initially

Then every 4-6 months once stable.

153
Q

When might hypothyroidism need referring to secondary care endocrinologist for management?

A 
Patients with goitre
Suspected malignancy
Cardiac disease
Tx resistant
Patients planning a pregnancy
154
Q

pathophysiology of T2DM

A

a combination of insulin resistance and deficiency, resulting in persistent hyperglycaemia and beta cell decline.

due to a combination of genetic and environmental factors

155
Q

Risk factors for T2DM

A

Genetics - FHx, south asian/afro-caribbean, male

Increasing age

Metabolic syndrome

Obesity, sedentary lifestyle, poor diet

Smoking/alcohol

156
Q

What is metabolic syndrome?

A

Central obesity
Increased BP
Increased lipids/cholesterol
Increased glucose

157
Q

Symptoms of T2DM

A

GRADUAL ONSET
Polyuria, polydipsia
Fatigue
Recurrent infections

OFTEN COMPLICATIONS ARE 1st PRESENTATION

158
Q

Complications of T2DM

A

MICROVASCULAR

  • Retinopathy (visual blurring)
  • Polyneuropathy (pain/numbness)
  • Nephropathy

MACROVASCULAR

  • Erectile dysfunction
  • CVD (MI)
  • Cerebrovascular disease (stroke)
159
Q

T2DM - Management

A

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)

160
Q

What is important to remember when prescribing metformin?

A

Patient needs good renal function (contraindicated if eGFR <45)

Can cause GI upset

161
Q

Lifestyle modifications in T2DM

A

Diet - low GI carbs, low fat, high fibre (inc. F&V)

Weight loss - calorie restriction AND exercise

Reduce smoking/alcohol

162
Q

What is the goal of pharmacological management in T2DM?

A

Aim for HbA1c <48 (6.5%)

163
Q

Monitoring diabetes control

A

HbA1c - over 3 months

Finger-prick - if on insulin

Urine dip - glucose, ketones, protein

164
Q

How does metformin act?

A

Decreases gluconeogenesis

Increases glucose utilisation

165
Q

What are advantages of metformin?

A

Decrease CV risk

No weight gain

166
Q

How do pioglitazones work?

A

Decrease insulin resistance

167
Q

Disadvantages of pioglitazones

A

Cause weight gain
Increased risk of CVD
Fluid retention

168
Q

How do sulphonyureas work?

A

Increase insulin secretion via K+ channel closure

169
Q

Disadvantages of sulphonyureas

A

Can cause hypos

Can cause weight gain

170
Q

What is an advantage of GLP1 mimetics?

A

Also cause weight LOSS

171
Q

T2DM follow-up/review

A

At least once a year

  1. Review glucose control
  2. Screen for complications - fundoscopy, foot check, urine dip
  3. Reduce CVD risk - BP <140/80, QRISK
  4. Ensure access to sufficient education and understand the risk of long-term complications
172
Q

Risk of complications with T2DM when counselling a patient

A 
MI x4 chance
Stroke x2 chance
Increased risk of infection and ulcers
Risk of vision loss/blindness
Risk of kidney damage /failure
173
Q

Safety netting in T2DM

A 
1. Signs of hypos
=> lethargy, confusion, aggression
=> sweaty, pale, shaking
=> RISK DRIVING
=> Mx = glucose PO 10-20g
  1. Reiterate risks of complications of diabetes
174
Q

What is the 1st line antihypertensive for a patient with T2DM?

A

ACE inhibitors are the first choice anti-hypertensive in patient’s with T2DM, irrespective of family background and age.

CP2 (8 decks)

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