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My Phase 3a Revision > GP - CARDIO, RESP, GI & NEURO > Flashcards

GP - CARDIO, RESP, GI & NEURO Flashcards

1
Q

HTN
What are the types of HTN?

A
  • Primary/essential (95%)
  • Secondary HTN (5%)
  • Malignant HTN
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2
Q

HTN
What are the risk factors for HTN?

A

Modifiable:
- alcohol intake
- sedentary lifestyle
- diabetes mellitus
- sleep apnoea
- smoking

Non-modifiable:
- Increasing age
- family history
- ethnicity - afro-Caribbean

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3
Q

HTN
What are the causes of essential HTN?

A

Unknown cause - multifactorial involving:
- genetic susceptibility
- Excessive sympathetic nervous system activity
- Abnormalities of Na+/K+ membrane transport
- High salt intake
- Abnormalities in renin-angiotensin-aldosterone system

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4
Q

HTN
Name 4 conditions that hypertension is a major risk factor for

A
  1. Stroke
  2. MI
  3. HF
  4. Chronic renal failure
  5. Cognitive decline
  6. Premature death
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5
Q

HTN
What are some causes of secondary HTN?

A

ROPE –
- Renal disease
- Obesity
- Pregnancy induced or pre-eclmapsia
- Endo (Conn’s, Cushing’s, acromegaly, pheochromocytoma)

most common = primary hyperaldosteronism (Conn’s syndrome)

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6
Q

HTN
Name 3 endocrine disease that can cause secondary hypertension

A
  1. Conn’s syndrome - hyperaldosteronism
  2. Cushing’s syndrome - excess cortisol –> increase BP
  3. Phaemochromocytoma - adrenal gland tumour, excess catecholamines –> high BP
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7
Q

HTN
What is malignant HTN?

A

Rapid rise in BP –
- Fibrinoid necrosis
- Retinal haemorrhages
- Papilloedema
- Exudates
Severe HTN ≥180/120

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8
Q

HTN
How might malignant HTN present?
Management?

A
  • Headache ± visual loss, typically younger + black patients
  • Same day specialist referral if Sx if not Ix for end-organ damage
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9
Q

HTN
What are some complications of HTN?

A
  • IHD
  • CVA
  • Hypertensive retinopathy + nephropathy
  • Heart failure
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10
Q

HTN
How would you diagnose HTN?

A
  • Clinical BP ≥140/90mmHg
  • ABPM to confirm diagnosis of ≥135/85mmHg (excludes white coat HTN >20mmHg rise)
  • 2 measurements/hour during waking hours
  • HBPM if unsuitable
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11
Q

HTN
After a diagnosis of HTN what other investigations would you do?

A
  • QRisk 3 + check for end-organ damage:
    – Urine dipstick (proteinuria + haematuria
    – Fundoscopy for hypertensive retinopathy
    – 12 lead ECG
    – First urine albumin creatinine ratio (ACR)
  • blood tests: HbA1c, U+Es, creatinine, cholesterol
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12
Q

HTN
In terms of clinical and ABPM/HBPM, how would you diagnose…

i) stage 1 HTN?
ii) stage 2 HTN?
iii) severe HTN?

A

i) ≥140/90 or ≥135/85
ii) ≥160/100 or ≥150/95
iii) ≥180 or ≥110 (clinical)

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13
Q

HTN
What is first line management of HTN?

A

lifestyle modifications
- Smoking + alcohol cessation
- Regular exercise
- Healthy diet, reduce dietary sodium, discourage caffeine

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14
Q

HTN
In terms of medication, what is first line treatment for…

i) 45 + T2DM?
ii) <55y/o?
iii) ≥55y/o?
iv) Afro-Caribbean?

A

i) ACEi or ARB
ii) ACEi or ARB
iii) CCB
iv) CCB

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15
Q

HTN
In terms of HTN medication, what is…

i) step 2?
ii) step 3?
iii) step 4?

A

i) The alternative (ACEi/ARB or CCB)
ii) Diuretics - Bendroflumethiazide, furosemide
iii) Beta-blocker, alpha-blocker, spironolactone if low potassium

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16
Q

HTN
What is an example and mechanism of action of ACEi?

A

Ramipril,

inhibit conversion of angiotensin I>II

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17
Q

HTN
What is an example and mechanism of action of CCB?

A

Amlodipine,

act on L-type Ca2+ channels

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18
Q

HTN
What is an example and mechanism of action of thiazide-like diuretic?

A

Indapamide,

locks Na+ reabsorption at DCT by blocking Na+/Cl- symporter

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19
Q

HTN
What is an example and mechanism of action of ARB?

A

Candesartan,

blocks effects of angiotensin II at the AT1 receptor

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20
Q

HTN
What are the side effects of ACEi?

A

Dry cough + rash (bradykinin),
hypotension,
hyperkalaemia,
AKI (check renal function 1-2w after starting)
teratogenic

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21
Q

HTN
What are the side effects of CCB?

A

Oedema,
headache,
flushing
palpitations

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22
Q

HTN
Name 4 classes of diuretics

A
  1. Thiazides
  2. Loop
  3. Potassium sparing
  4. Aldosterone antagonists
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23
Q

HTN
Where in the kidney do thiazide diuretics work?

A

The distal tubule

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24
Q

HTN
Name a thiazide

A

Bendroflumethethiazide

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25
Q

HTN
Name a loop diuretic

A

Furosemide
Bumetanide

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26
Q

HTN
Name a potassium sparing diuretic

A

Spironolactone
Eplerenone

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27
Q

HTN
Why are potassium sparing diuretics especially effective?

A

They have anti-aldosterone effects too

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28
Q

HTN
Give 5 potential side effects of diuretics

A
  1. Hypovolaemia
  2. Hypotension
  3. Reduced serum Na+, K+, Mg+, Ca2+
  4. Increased uric acid –> gout
  5. Erectile dysfunciton
  6. Impaired glucose tolerance
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29
Q

HTN
Name 3 beta blockers

A
  1. Bisoprolol (beta 1 elective)
  2. Atenolol
  3. Propranolol (beta 1/2 nonselective)
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30
Q

HTN
What are the side effects of beta-blocker?

A

Headache,
hypotension,
erectile dysfunction

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31
Q

HTN
when are beta blockers contraindicated?

A

DO NOT GIVE in asthma, heart failure/heart block, hypotension and bradyarrhythmia

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32
Q

HTN
What are the side effects of ARB?

A

Hyperkalaemia
hypotension
renal dysfunction
rash

contraindicated in pregnancy

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33
Q

HTN
What are the clinical + ABPM/HBPM HTN treatment targets for…

i) <80?
ii) >80?
iii) diabetics?

A

i) <140/90 or <135/85
ii) <150/90 or <145/85
iii) <130/80

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34
Q

ANGINA
What is angina?

A

Type of ischaemic heart disease
It is a symptom of O2 supply/demand mismatch to the heart

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35
Q

ANGINA
What is the pathophysiology?

A

On exertion there is increase O2 demand
Coronary blood flow is obstructed by an atherosclerotic plaque –> myocardial ischaemia –> angina

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36
Q

ANGINA
What are the 4 types of angina?

A
  • Stable = induced by effort, relieved by rest or GTN
  • Unstable (ACS) = crescendo, increasing frequency or severity, occurs at rest (higher risk of MI)
  • Decubitus = precipitated by lying flat
  • Prinzmetal = due to coronary artery spasm
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37
Q

ANGINA
What are some causes of angina?

A
  • Atherosclerosis
  • Increased distal resistance (LVH)
  • Reduced oxygen carrying capacity (anaemia)
  • Thrombosis
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38
Q

ANGINA
What are the non-modifiable risk factors for angina?

A
  1. Increasing age
  2. Family history
  3. Gender - Male
  4. ethnicity - south Asian
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39
Q

ANGINA
What are some modifiable risk factors for angina?

A
  1. Smoking
  2. Diabetes
  3. Hypertension
  4. Hypercholesterolaemia
  5. Sedentary lifestyle/obesity
  6. Stress
  7. alcohol
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40
Q

ANGINA
What 3 things are used to assess whether it is typical angina, atypical pain or non-anginal pain?

A
  1. Have central, tight, radiation to arms, jaw and neck
  2. Precipitated by exertion
  3. Relieved by rest or GTN spray
    3/3 = Typical angina
    2/3 = Atypical pain
    1/3 = Non-anginal pain
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41
Q

ANGINA
How does angina present?

A
  1. Crushing central chest pain
  2. Pain is relieved with rest or GTM spray
  3. Pain is provoked by physical exertion
  4. Pain may radiate to arms, neck or jaw
  5. Dyspnoea
  6. Nausea
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42
Q

ANGINA
What are some investigations for angina?

A
  1. ECG - usually normal, sometimes ST depression, flat or inverted T waves
  2. Echocardiography
  3. CT angiography - high NPV and good at excluding disease (gold standard)
  4. Exercise tolerance test - induces ischaemia
  5. Invasive angiogram - tells you FFR (pressure gradient across stenosis)
  6. SPECT - radio labelled tracer taken up by metabolising tissues
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43
Q

ANGINA
What primary prevention may be offered in angina?

A
  • QRISK3 score >10% = start on statin (or pts with CKD or DM)
  • Lifestyle advice
  • low dose aspirin
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44
Q

ANGINA
What is the secondary prevention of angina?

A

4As –
- Aspirin 75mg OD (+ second antiplatelet like clopidogrel for 12m)
- Atorvastatin 80mg ON
- Atenolol (or bisoprolol) titrated to max tolerated
- ACEi (ramipril) titrated to max tolerated

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45
Q

ANGINA
What short term treatment can be given in angina?

A
  • Glyceryl trinitrate (GTN) spray for vasodilation
  • Take when Sx start, wait 5m, repeat spray, wait 5m > ambulance
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46
Q

ANGINA
What are some long-term symptomatic relievers of angina?

A
  • Beta-blocker (in secondary prevention)
  • CCB (amlodipine)
  • Long-acting nitrates (isosorbide mononitrate)
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47
Q

ANGINA
Ultimately, what 2 treatments may resolve angina?

A
  • Percutaneous coronary intervention (PCI) with coronary angioplasty
  • Coronary artery bypass graft (CABG)
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48
Q

ACS
What is ACS?
What occurs?

A
  • Unstable angina, NSTEMI + STEMI
  • Atheroma ruptures causing platelet aggregation leading to thrombus formation completely occluding artery.
  • Irreversible ischaemia > infarction + necrosis of cells (troponin release) > permanent myocardium damage
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49
Q

ACS
Describe type 1 MI

A

Spontaneous MI with ischaemia due to a primary coronary event e.g. plaque erosion/rupture, fissuring or dissection

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50
Q

ACS
Describe type 2 MI

A

MI secondary to ischaemia due to increased O2 demand or decreased supply such as in coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension

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51
Q

ACS
How does an MI present?

A
  • Central crushing chest pain, may radiate to jaw, neck, arm
  • pain occurs at rest
  • Dyspnoea + palpitations
  • Sweating, N+V
  • Pallor, anxiety
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52
Q

ACS
Give 3 signs of MI

A
  1. Hypo/hypertension
  2. 3rd/4th heart sound
  3. Signs of congestive heart failure
  4. Ejection systolic murmur
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53
Q

ACS
What investigations would you do on someone you suspect to have ACS?

A
  1. ECG
  2. Blood tests - troponin levels and rule out anaemia
  3. Coronary angiography
  4. Cardiac monitoring for arrhythmias
  5. Chest x-ray
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54
Q

ACS
On an ECG, how would a STEMI appear?

A

New LBBB or ST-elevation,
hyperacute T waves
(T-wave inversion + pathological Q waves occur later)

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55
Q

ACS
On an ECG, how would an NSTEMI appear?

A

ST depression + T-wave inversion

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56
Q

ACS
Where on the ECG would indicate a circumflex artery (lateral) occlusion?

A

I, V5, V6

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57
Q

ACS
Where on the ECG would indicate right coronary artery (inferior) occlusion?

A

II, III, aVF

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58
Q

ACS
Where on the ECG would indicate left anterior descending (LAD) artery (anterior) occlusion?

A

V1–V4

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59
Q

ACS
What other investigations may you consider in ACS?

A
  • ECHO after event to assess functional damage
  • CT coronary angiogram to assess for IHD
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60
Q

ACS
What are the complications following ACS?

A

DREAD –
- Death
- RUpture of heart septum or papillary muscles
- oEdema
- Arrhythmia or Aneurysm
- Dressler’s syndrome

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61
Q

DRESSLER’S SYNDROME
What is Dressler’s syndrome?

A
  • 2-3w post MI autoantibody formation against heart > pericarditis
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62
Q

DRESSLER’S SYNDROME
How does it present?

A
  • 2-3w post MI
  • Pleuritic CP,
  • low grade fever,
  • pericardial rub ± effusion
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63
Q

DRESSLER’S SYNDROME
what are the investigations?

A
  • ECG = global ST (saddle shaped) elevation + T-wave inversion,
  • raised CRP/ESR
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64
Q

DRESSLER’S SYNDROME
what is the management?

A

NSAIDs or steroids if severe

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65
Q

ACS
What is the pre-hospital management of ACS?

A

MONA
- Morphine
- Oxygen
- Nitrates
- Aspirin (300mg)

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66
Q

ACS
What is the pre-hospital management of ACS?
What is the management of STEMI?

A

primary PCI (≤2h)
thrombolysis (>2h) with streptokinase or alteplase

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67
Q

ACS
What is the management of NSTEMI?

A

BATMAN
– Beta-blocker
– Aspirin 300mg
– Ticagrelor 180mg
– Morphine
– Anticoagulant (LMWH)
– Nitrates (GTN)

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68
Q

ACS
What is the secondary prevention of ACS?

A

5As:
– Aspirin 75mg OD
– Another antiplatelet (clopidogrel or ticagrelor for 12m post PCI to prevent thrombus on stent)
– Atorvastatin 80mg ON
– ACEi
– Atenolol (or bisoprolol)

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69
Q

ACS
How does aspirin work?

A

Antiplatelet
Irreversibly inhibits COX –> reduced thromboxane 2 synthesis –> platelet aggregation reduced

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70
Q

ACS
What is a caution when prescribing aspirin?

A

Gastric ulceration

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71
Q

ACS
How does clopidogrel work?

A

Antiplatelet
P2Y12 inhibitor –> prevents platelet activation

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72
Q

HEART FAILURE
What is heart failure?

A
  • CO insufficient to meet metabolic demands of body + suggests the efficiency of heart as pump is impaired
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73
Q

HEART FAILURE
What compensatory mechanisms are seen in heart failure and what is seen when they decompensate?

A
  • Dilatation > impaired contractility + valve regurg
  • Hypertrophy > myocardial ischaemia
  • RAAS > Na+ + fluid retention > increased venous pressure > oedema
  • Sympathetic activation > increased afterload > decreased CO
  • Natriuretic peptide release (diuretic, hypotensive + vasodilating properties)
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74
Q

HEART FAILURE
What are the two broad categories of heart failure and what do they mean?

A
  • Systolic failure (EF < 40%) = inability of ventricles to contract normally > reduced CO (normal filling volume, less output)
  • Diastolic failure (EF > 50%) = inability of ventricles to relax + fill normally > increased filling pressures
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75
Q

HEART FAILURE
What are the 2 main types of systolic heart failure and what causes them?

A
  • Left ventricular systolic dysfunction (IHD, HTN, structural)
  • Right ventricular systolic dysfunction (secondary to LVSD, cor pulmonale = RHF due to lung disease leading to pulmonary HTN)
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76
Q

HEART FAILURE
What is diastolic failure also referred as and why?
What can cause it?

A
  • Heart failure with preserved ejection fraction = less volume fills + low volume output so ejection fraction higher
  • Cardiac tamponade, cardiomyopathies, pericardial effusion
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77
Q

HEART FAILURE
What is the New york Heart Association classification of heart failure?

A
  • I = no limitation (asymptomatic)
  • II = slight limitation (mild cardiac failure)
  • III = marked limitation (moderate)
  • IV = inability to carry out any physical activity without discomfort (severe)
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78
Q

HEART FAILURE
What are the 3 cardinal symptoms of heart failure?

A
  • Dyspnoea (+ orthopnoea due to pulmonary oedema, lots of pillows)
  • Fatigue
  • Peripheral oedema
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79
Q

HEART FAILURE
What are some classic features of left heart failure?

A
  • Nocturnal cough ± white or pink frothy sputum
  • Paroxysmal nocturnal dyspnoea
  • Cold peripheries
  • Signs = S3 + tachy (gallop), bibasal crackles from pulmonary oedema
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80
Q

HEART FAILURE
What are some classic features of right heart failure?

A
  • Peripheral oedema, ascites, nausea
  • Signs = raised JVP, hepatomegaly
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81
Q

HEART FAILURE
What are some investigations for heart failure?

A
  • ABG ?T1 resp failure (hypoxia w/out hypercapnia)
  • N-terminal pro-B-type natriuretic peptide (NT-proBNP)
  • ECG (?arrhythmias which can cause HF like AF)
  • ECHO = diagnostic
  • CXR (ABCDE)
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82
Q

HEART FAILURE
What NT-proBNP values are suspicious for heart failure?

A
  • > 2000ng/L = urgent referral
  • 400-2000ng/L = raised
  • <400ng/L = unlikely HF
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83
Q

HEART FAILURE
What can falsely raise and decrease NT-proBNP levels?

A
  • Raise = LVH, ischaemia, DM, COPD, sepsis, PE
  • Decrease = obesity, diuretics, ACEi/ARBs, beta-blockers
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84
Q

HEART FAILURE
Why is an ECHO diagnostic?

A
  • Assess function of LV + any structural function
  • Can measure ejection fraction (% of blood squeezed out with each ventricular contraction)
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85
Q

HEART FAILURE
What might you see on a CXR in heart failure?

A

ABCDE
- Alveolar oedema (Bat’s wings)
- kerley B lines (interstitial oedema)
- Cardiomegaly
- Dilated prominent upper lobe vessels
- pleural Effusion

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86
Q

HEART FAILURE
What is the acute management of heart failure and likely cause?

A
  • Pour SOD (#1 = MI)
    –Pour (stop) any IV fluids (monitor fluid balance)
    – Sit pt upright
    – Oxygen if desaturating
    – Diuretics (IV furosemide 40mg stat to reduce circulating volume
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87
Q

HEART FAILURE
What is the mechanism of action of furosemide?

A
  • Loop diuretic
  • Inhibits Na-K-Cl co-transporter in thick ascending limb of loop of Henle to reduce absorption of NaCl
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88
Q

HEART FAILURE
What is the general management of heart failure?

A
  • Yearly flu + PCV
  • HF specialist nurse input
  • Lifestyle changes
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89
Q

HEART FAILURE
What is the first line medical treatment for heart failure?

A
  • ACEi = #1 in those with LVSD to improve prognosis/survival after MI
  • Beta-blockers
  • Loop diuretics (furosemide 40mg PO) for Sx relief or aldosterone antagonist (spironolactone) if Sx not tolerated)
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90
Q

HEART FAILURE
What other methods of management may be considered in heart failure?

A
  • ?Digoxin if all else fails but monitor for toxicity
  • Avoid CCBs like verapamil + diltiazem in HF with reduced ejection fraction
  • Surgical intervention if severe aortic stenosis or mitral regurgitation
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91
Q

ATRIAL FIBRILLATION
What is the pathophysiology of AF?

A
  • Contraction of atria is uncoordinated, rapid + irregular due to disorganised electrical activity overriding SAN
  • AVN struggles to keep up so responds intermittently giving irregular ventricular rhythm
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92
Q

ATRIAL FIBRILLATION
What are some causes of AF?

A
  • idiopathic
  • Sepsis
  • Mitral valve (stenosis/regurg)
  • IHD
  • Thyrotoxicosis
  • HTN
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93
Q

ATRIAL FIBRILLATION
What is the clinical presentation of AF?

A
  • Palpitations, dyspnoea, syncope, CP
  • Irregularly irregular pulse
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94
Q

ATRIAL FIBRILLATION
What is paroxysmal AF?

A
  • Comes/goes in episodes, usually <48h (up to 7d)
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95
Q

ATRIAL FIBRILLATION
what is the management of paroxysmal AF?

A

Anticoagulate based on CHADSVASC,
may use “pill in the pocket” with flecainide if infrequent episodes
no underlying structural heart disease

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96
Q

ATRIAL FIBRILLATION
What does the ECG in atrial fibrillation look like?

A
  • Absent P waves
  • Irregularly irregular ventricular rhythm
  • Narrow QRS complex tachycardia
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97
Q

ATRIAL FIBRILLATION
What is the main complication of AF?
Management?

A
  • Embolic stroke due to stagnation of blood in atria due to ineffective mechanical action of atria
  • Calculate CHADSVASC score + ≥2 = anticoagulate
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98
Q

ATRIAL FIBRILLATION
How can you control the rate in AF?

A
  • Beta-blocker first line
  • Rate-limiting CCB
  • Digoxin only if they fail
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99
Q

ATRIAL FIBRILLATION
How would you control the rhythm acutely?
What can be used?

A
  • Immediate cardioversion if AF <48h + haemodynamically unstable
  • Elective cardioversion if AF present >48h + stable
  • Pharma = flecainide or amiodarone if structural heart disease
  • Electrical = sedation or GA using cardiac defib
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100
Q

ATRIAL FIBRILLATION
What other treatment can be used in AF?

A
  • Catheter ablation if not responded or wish to avoid antiarrhythmic meds, must be anticoagulated 4w before
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101
Q

ATRIAL FIBRILLATION
What should you use for anticoagulation in AF?
Which is better?

A
  • Warfarin (vit K antagonist) or DOACs such as apixaban, rivaroxaban (factor Xa inhibitors)
  • DOACs = no INR monitoring, no major interactions, equal effect but no reversal
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102
Q

COPD
What are the two diseases that make up COPD?
What is the main cause of COPD?

A
  • Pink puffers = emphysema
  • Blue bloaters = chronic bronchitis
  • Smoking (alpha-1-antitrypsin is a major protease inhibitor that can be inactivated by smoke)
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103
Q

COPD
What causes emphysema?

A
  • Alveoli lose elastic recoil > air trapping after exhalation
  • Unable to oxygenate so hyperventilate (puffing), no cyanosis
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104
Q

COPD
What causes chronic bronchitis?

A
  • Bronchoconstriction = less oxygen enters alveoli, less carbon dioxide leaves so V/Q mismatch + hypoxia leads to cyanosis
  • Capillaries compensate + vasoconstrict to shunt blood to better ventilated alveoli > pulmonary HTN > RHF > cor pulmonale
  • Cyanotic but not breathless
  • Resp centres insensitive to carbon dioxide so rely on hypoxic drive
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105
Q

COPD
What are the 3 typical signs of COPD?
What are some other signs?

A
  • Chronic cough, sputum (often clear white), dyspnoea
  • Pursed lip breathing, tachypnoea, hyperinflated barrel chest, cachexic
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106
Q

COPD
How is COPD classified into stages?

A
  • 1 = mild (FEV1 ≥80% predicted)
  • 2 = mod (FEV1 50–79% predicted)
  • 3 = severe (FEV1 30–49% predicted)
  • 4 = very severe (FEV1 <30% predicted)
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107
Q

COPD
What are some investigations for COPD?

A
  • ECG = ?P pulmonale
  • FBC to exclude secondary polycythaemia
  • Spirometry = obstructive pattern (FEV1/FVC <0.7 with FEV1 ≤80%) and no post-bronchodilator reversibility
  • CXR = hyperinflation, flat hemidiaphragm, bullae
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108
Q

COPD
What is the conservative management of COPD?

A
  • Smoking cessation
  • Annual flu vaccine
  • One off PCV
  • Pulmonary rehab (exercise, nutrition, breathing exercises)
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109
Q

COPD
What are steps 1 and 2 of the COPD management?

A
  • 1 = SABA or SAMA
  • 2:
    – FEV1>50% = LABA and/or LAMA
    – FEV1 <50% LABA + ICS and/or LAMA (also offered in those with asthma/atopic features)
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110
Q

COPD
What is step 3 of COPD management?
Any other management?

A
  • FEV1>50% = LABA + ICS or same as FEV1<50%
  • FEV1<50% = LAMA + LABA/ICS combination (FOstair)
  • Consider PO theophylline or mucolytics like carbocysteine
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111
Q

COPD
What is the mechanism of action of LAMA?
Give an example
What about SAMA?

A
  • Block ACh receptors which are stimulated by parasympathetic nervous system causing bronchial smooth muscle contraction so overall effect is bronchodilation (Tiotropium)
  • Same but shorter action, ipratropium
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112
Q

COPD
When would you consider long-term oxygen therapy?
When is it contraindicated?

A
  • 2 separate ABGs showing PaO2 <7.3kPa or paO2 7.3–8 with pulmonary HTN or polycythaemia or peripheral oedema
  • Smokers as fire hazard
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113
Q

COPD
What is an acute exacerbation of COPD?
What is the most common cause?

A
  • Acute worsening of Sx such as cough, dyspnoea, wheeze + sputum (?purulent)
  • Haemophilus influenzae (#1), strep. pneumoniae, Moraxella catarrhalis
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114
Q

COPD
What are some investigations for acute exacerbation of COPD?

A
  • FBC (raised WCC), CRP, ?blood cultures if septic
  • Sputum MC&S
  • CXR may show consolidation
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115
Q

COPD
What is the management of an acute exacerbation of COPD?

A
  • Oxygen therapy for SpO2 88–92% via venturi mask 24-28%
  • Nebulised salbutamol + ipratropium
  • PO prednisolone for 1-2w
  • Abx if infection
  • Consiver NIV (BiPAP) or intubation + ventilation with ICU admission
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116
Q

PNEUMONIA
What are the 3 classifications of pneumonia?

A
  • Community-acquired = develops outside hospital
  • Hospital acquired = develops >48h after hospital admission
  • Aspiration = acute aspiration of gastric contents (stroke, MG, MS, MND)
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117
Q

PNEUMONIA
What are the most common causes of CAP?

A
  • Strep. pneumoniae #1
  • Haemophilus influenzae
  • Moraxella catarrhalis
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118
Q

PNEUMONIA
What are some atypical pneumoniaes?

A
  • Mycoplasma pneumoniae (erythema multiforme, neuro Sx in younger, atypical chest/XR findings)
  • Chlamydophila pneumoniae (school aged child)
  • Legionella pneumophila (infected water supplies + air con, can cause hyponatraemia > SIADH
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119
Q

PNEUMONIA
What is a cause of fungal pneumonia?
How does it present?
Management?

A
  • Pneumocystis jiroveci pneumonia (PCP) in immunocompromised
  • Dry cough, SOB on exertion, night sweats
  • Co-trimoxazole
120
Q

PNEUMONIA
What are some risk factors for pneumonia?

A
  • Elderly + infants
  • Comorbidities = DM, COPD, bronchiectasis
  • Smokers, alcoholics
  • Immunocompromised + nursing home residents
121
Q

PNEUMONIA
What are the…

i) symptoms
ii) signs
iii) exam findings

in pnuemonia?

A

i) Dyspnoea, cough with purulent sputum (dry in atypicals), fever
ii) Pyrexia, tachypnoea, tachycardia
iii) Bronchial breath sounds, focal coarse crackles, dullness to percuss

122
Q

PNEUMONIA
What are some investigations for pneumonia?

A
  • FBC (neutrophilia, raised WCC)
  • CRP, U+Es, ABG
  • Sputum MC&S + blood cultures
  • Pneumococcal + legionella urinary antigen tests
  • CXR = consolidation
123
Q

PNEUMONIA
What score can be used to assess severity of CAP?
How does this guide your management?

A
  • Confusion
  • Urea >7mmol/L
  • RR ≥30/min
  • BP <90 or 60
  • 65 ≤ age
  • 0-1 = PO amoxicillin in community
  • 2 = PO amoxicillin + clarithromycin in hospital
  • ≥3 = severe IV co-amoxiclav + clarithromycin ?ICU
124
Q

PNEUMONIA
What is the general management for pneumonia?

A
  • Oxygen therapy
  • IV fluids
  • PCV vaccine in children
  • Flu vaccine if ≥65y, immunocompromised or medical co-morbidities
  • Smoking cessation
125
Q

PNEUMONIA
What typical antibiotics might you use in…

i) HAP?
ii) aspiration?
iii) atypicals?

A

i) Aminoglycoside like gentamycin + cephalosporin
ii) IV cephalosporin + metronidazole to cover gut anaerobes
iii) Macrolides (clarithromycin), fluoroquines (levofloxacin) + tetracyclines (doxycycline)

126
Q

LUNG CARCINOMA
What are the 2 broad categories of lung cancer?

A
  • Non-small cell lung carcinoma (NSCLC)
    –Squamous = Smokers
    – Adenocarcinoma = non-smokers, asbestos
    – Large cell (poorly differentiated)
  • Small cell lung carcinoma
127
Q

LUNG CARCINOMA
What can happen in SCLC?

A
  • Arise from Kulchitsky (endocrine) cells so can cause paraneoplastic syndromes like SIADH (think low sodium), Cushing’s, Lambert-Eaton myasthenic syndrome
128
Q

LUNG CARCINOMA
In terms of lung cancer, what are some…

i) symptoms?
ii) signs?
iii) signs of mets?

A

i) Cough + haemoptysis, CP, dyspnoea, weight loss, night sweats, recurrent pneumonia
ii) Finger clubbing, lymphadenopathy (supraclavicular)
iii) Bone tenderness, hepatomegaly, neurology (seizures, headache)

129
Q

LUNG CARCINOMA
What are some investigations for lung cancer?

A
  • CXR first line (opacity, hilar enlargement, effusion, collapse)
  • CT CAP for staging or if CXR clear
  • Bronchoscopy with EBUS + biopsy
130
Q

LUNG CARCINOMA
What are some complications from lung carcinoma?

A
  • L recurrent laryngeal nerve = hoarse voice
  • Phrenic nerve = diaphragm weakness + dyspnoea
  • SVC obstruction = facial swelling, distended veins in neck + upper chest
  • Brachial plexus = shoulder pain
  • Sympathetic ganglion = Horner’s (miosis, anhidrosis + ptosis often Pancoast)
131
Q

LUNG CARCINOMA
Complication of squamous cell carcinoma?

A
  • Hypercalcaemia from ectopic PTH-rP = primary hyperparathyroidism
132
Q

LUNG CARCINOMA
What is the management of lung cancer?

A
  • NSCLC = lobectomy if isolated, radio/chemo
  • SCLC = chemo ± radio
  • Supportive = analgesia, anti-emetics, ?tracheal stenting if bronchial obstruction
133
Q

CONSTIPATION
What is constipation?
What are some causes?

A
  • Infrequent bowel movements (<3/w) or with straining
  • Obstruction, hypothyroid, neuro (MS, cauda equina), dehydration, IBS
134
Q

CONSTIPATION
What is the management of constipation?

A
  • Hydration + increased fibre
  • Bulking agents = increased faecal mass + peristalsis (ispaghula husk)
  • Osmotic = retain fluid in bowel (lactulose)
  • Stimulant = increased intestinal motility (Senna)
  • Phosphate enemas
135
Q

GORD
What is GORD?
Risk factors?

A
  • Regurg acidic gastric contents into lower oesophagus injuring squamous epithelium
  • Obesity + pregnancy, smoking, alcohol, caffeine, hiatus hernia
136
Q

GORD
What are the clinical features or GORD?

A
  • Heartburn (oesophagitis) can be retrosternal/epigastric (worse after meals or lying down)
  • Acid regurg
  • Dysphagia/odynophagia
  • Nocturnal cough (aspiration)
137
Q

GORD
What are some investigations for GORD and when would you do them?

A
  • OGD if new onset ≥55y or weight loss, melaena, haematemesis etc.
  • 24h oesophageal pH monitoring
138
Q

GORD
What are some complications of GORD?

A
  • Benign stricture > dysphagia
  • Oesophageal adenocarcinoma
  • Barrett’s oesophagus = metaplasia squamous?columnar may lead to dysplasia to adenocarcinoma
139
Q

GORD
What is the general management of GORD?

A
  • Reduce caffeine + alcohol, weight loss, stop smoking, smaller meals
  • PRN OTC antacids like Gaviscon or Rennie
140
Q

GORD
What treatments can be given for GORD?

A
  • PPI like omeprazole
  • H2 antagonists like ranitidine
  • Laparoscopic fundoplication to narrow lower oesophageal sphincter last line
141
Q

DIVERTICULAR DISEASE
What is…

i) diverticulum?
ii) diverticulosis?
iii) diverticular disease?
iv) diverticulitis?

A

i) Pouch of colonic mucosa herniating through muscularis propria lying in the thin subserosa fat
ii) Presence of diverticula but asymptomatic
iii) Implies symptomatic diverticula
iv) Inflammation of a diverticulum

142
Q

DIVERTICULAR DISEASE
What causes a diverticulum?

A
  • High intraluminal pressures force mucosa to herniate through muscle layers of gut at weak points (adjacent to penetrating vessels)
143
Q

DIVERTICULAR DISEASE
What can cause high intraluminal pressures?
How does it present?

A
  • Low fibre, sigmoid colon as smallest diameter
  • > 60y, asymptomatic or LIF pain, altered bowel habit, fever, bleeding
144
Q

DIVERTICULAR DISEASE
What causes diverticulitis?
How does it present?

A
  • Trapped faeces
  • # 1 = descending colon, LIF pain, fever, tachycardia, ?intestinal obstruction
145
Q

DIVERTICULAR DISEASE
Investigations for diverticulitis?
Management?

A
  • Bloods, FBC (WCC raised), ESR/CRP, tender colon ± peritonism
  • Mild = bowel rest ± Abx if severe = analgesia, NBM, IV fluids + Abx, surgery if peritonitis
146
Q

DIVERTICULAR DISEASE
Investigations for diverticular disease?
Management?

A
  • Erect CXR (?perf), AXR, contrast CT, incidental finding at colonoscopy
  • Antispasmodics like Buscopan, Hartmann’s if perforation or obstruction
147
Q

COLORECTAL CANCER
What are some causes of colorectal cancer?
Risk factors?

A
  • Hereditary nonpolyposis colorectal cancer #1 = AD
  • Familial adenomatous polyposis (FAP) = AD
  • Peutz-Jeghers syndrome = AD
  • Red + processed meat, alcohol, smoking, IBD
148
Q

COLORECTAL CANCER
What are some features of…

i) FAP?
ii) HNPCC?
iii) Peutz-Jeghers?

A

i) >100 polyps as teenager, 100% lifetime risk
ii) Accelerated progression of adenoma > carcinoma as no DNA repair proteins
iii) Mucocutaneous hyperpigmentation (macules on palms + buccal mucosa), multiple GI hamartomatous polyps

149
Q

COLORECTAL CANCER
What is the clinical presentation of colorectal cancer?

A

Majority L sided:
- PR bleed/mucus, altered bowel habit, obstruction
R sided + caecum:
- Weight loss, Fe anaemia
RectumL
- Fresh blood, mass, tenesmus

150
Q

COLORECTAL CANCER
Investigations for colorectal cancer?

A
  • FBC (Fe anaemia)
  • Faecal occult blood screening 2y 60–74
  • Colonoscopy + biopsy
  • CT CAP for Duke’s staging
151
Q

COLORECTAL CANCER
In terms of colorectal cancer management…

i) prevention?
ii) adenoma?
iii) colorectal adenocarcinoma?

A

i) ?NSAIDs prevent adenomas
ii) Endoscopic resection ideally end-end anastomosis
iii) Surgical resection if no spread, chemo + palliative care if metastatic

152
Q

COLORECTAL CANCER
What is Duke’s staging in colorectal cancer?

A
  • A = bowel mucosa
  • B = extends through bowel wall
  • C = regional LNs
  • D = distant mets
153
Q

GALLSTONES
What causes gallstones?
Risk factors?

A
  • Imbalance between cholesterol + bile salts (75% mixed, 20% large yellow cholesterol, 5% bilirubinate)
  • Fat, Female, Forty, Fertile
  • Crohn’s as malabsorption of bile salts from terminal ileum
  • Haemolytic anaemias as increased bilirubin > bilirubinate stones
154
Q

GALLSTONES
Management of gallstones?

A
  • FBC, U+Es, amylase, LFTs (ALP + bilirubin raised in attacks)
  • USS shows dilated ducts (MRCP if case)
  • Conservative (analgesia + fluids) with elective lap chole
155
Q

ACUTE CHOLECYSTITIS
What is acute cholecystitis?

A
  • Inflammation of gallbladder following impaction of stone in cystic duct or neck of gallbladder obstruction bile emptying > damage to mucosal lining
156
Q

ACUTE CHOLECYSTITIS
What is the clinical presentation of acute cholecystitis?

A
  • RUQ pain radiating to tip of scapula
  • FEVER (differentiates from biliary colic), N+V
  • Murphy’s sign = tenderness worse on inspiration with 2 fingers on RUQ
  • NO jaundice (differentiates from ascending cholecystitis)
157
Q

ACUTE CHOLECYSTITIS
Investigations for acute cholecystitis?

A
  • FBC (raised WCC), LFTs,
  • USS shows gallstones + distended gallbladder with thickened wall
  • Sonographic murphy’s
158
Q

ACUTE CHOLECYSTITIS
Management of acute cholecystitis?

A
  • Conservative = NBM, IV fluids, pain relief, IV Abx
  • Lap chole
159
Q

ANGINA
What are some non-modifable risk factors for angina?

A
  • Non-modifiable = age, FHx, male
  • Modifiable = smoking, obesity, high cholesterol, HTN, DM
160
Q

PERIPHERAL VASCULAR DISEASE
what is the epidemiology?

A

Men > Women
usually affects the aorta-iliac and infra-inguinal arteries

161
Q

PERIPHERAL VASCULAR DISEASE
what is the clinical presentation of PVD?

A

Pain in lower limbs on exercise, relieved on rest- intermittent claudication
Severe unremitting pain in foot (esp at night- hangs foot out of bed)
Leg may be pale, cold, loss of hair, skin changes

162
Q

PERIPHERAL VASCULAR DISEASE
what is the pathophysiology of PVD?

A

Commonly atherosclerosis leading to claudication of vessels
Other (rarer) causes of claudication:
- aortic coarctation,
- temporal arteritis,
- Buerger’s disease.
End stage PVD= Critical Limb Ischaemia (6 P’s)

163
Q

PERIPHERAL VASCULAR DISEASE
what are the investigations for PVD?

A

1st line = ankle brachial pressure index (ABPI), duplex ultrasound

<0.3 = critical ischaemia

164
Q

PERIPHERAL VASCULAR DISEASE
what is the treatment for critical limb ischaemia?

A

revascularisation (e.g. stenting, angioplasty, bypassing)
Amputation if unsuitable

165
Q

ATRIAL FIBRILLATION
what score is used to calculate the risk of stroke in someone with atrial fibrillation?

A

CHA2D2 VASc

166
Q

ATRIAL FIBRILLATION
What is the treatment for AF?

A
  • cardioversion - LMWH (enoxaparin) and DC shock
  • rate control - 1st line = beta blocker, 2nd line = CCB
  • rhythm control - BB (bisoprolol), CCB (verapamil), digoxin, anti-arrhythmic (amiodarone)
  • anti-coagulation
167
Q

ARRHYTHMIAS
Give 2 effects of hypokalaemia on an ECG

A
  1. Flat T waves
  2. QT prolongation
  3. ST depression
  4. Prominent U waves
168
Q

ARRHYTHMIAS
Give an effect of hypocalcaemia on an ECG

A
  1. QT prolongation
  2. T wave flattening
  3. Narrowed QRS
  4. Prominent U waves
169
Q

ARRHYTHMIAS
Give an effect of hypercalcaemia on an ECG

A
  1. QT shortening
  2. Tall T wave
  3. No P waves
170
Q

ARRHYTHMIAS
What controls the sinus node discharge rate?

A

Autonomic nervous system

171
Q

ARRHYTHMIAS
Define sinus rhythm

A

A P wave precedes each QRS complex

172
Q

ARRHYTHMIAS
Define cardiac arrhythmia

A

Abnormality of cardiac rhythm

173
Q

ARRHYTHMIAS
Give 3 potential consequences of arrhythmia

A
  1. Sudden death
  2. Syncope
  3. Heart failure
  4. Chest pain
  5. Palpitations
    May also be asymptomatic
174
Q

ARRHYTHMIAS
Define bradycardia

175
Q

ARRHYTHMIAS
Define tachycardia

176
Q

ARRHYTHMIAS
Give 2 causes of bradycardia

A
  1. Conduction tissue fibrosis
  2. Ischaemia
  3. Inflammation/infiltrative disease
  4. Drugs
177
Q

ARRHYTHMIAS
Give 2 broad categories of tachycardia

A
  1. Supraventricular tachycardias
  2. Ventricular tachycardias
178
Q

ARRHYTHMIAS
Where do supra-ventricular tachycardia’s arise from?

A

Atria or atrio-ventricular junction

179
Q

ARRHYTHMIAS
Do supra-ventricular tachycardia’s have narrow or broad complex QRS complexes?

A

Narrow QRS complexes

180
Q

ARRHYTHMIAS
Name 3 types of supraventricular tachycardia

A
  1. Atrial fibrillation
  2. Atrial flutter
  3. AV node re-entry tachycardia
  4. AV re-entry tachycardia (accessory pathway)
181
Q

ARRHYTHMIAS
Where do ventricular tachycardia’s arise from?

A

The ventricles

182
Q

ARRHYTHMIAS
Do ventricular tachycardia’s have narrow or broad complex QRS complexes?

A

Broad QRS compelxes

183
Q

ARRHYTHMIAS
What is the commonest supra-ventricular tachycardia?

A

AV node re-entry tachycardia (AVNRT)

184
Q

ARRHYTHMIAS
Do you see P waves in AV node re-entry tachycardia (AVNRT)?

A

Loss of P waves

185
Q

ARRHYTHMIAS
what is the clinical presentation of AV node re-entry tachycardia (AVNRT)?

A

Rapid regular palpitations – abrupt onset, sudden termination
Chest pain and breathlessness
Neck pulsations
Polyuria

186
Q

ARRHYTHMIAS
Describe the acute treatment of AV node re-entry tachycardia (AVNRT)

A

Vagal manoeuvre,
carotid sinus massage
catheter ablation and adenosine (block AVN to terminate the SVT)

187
Q

ARRHYTHMIAS
What drugs might you give someone to suppress further episodes of AV node re-entry tachycardia (AVNRT)?

A

Beta blockers, CCB

188
Q

ARRHYTHMIAS
Describe the pathophysiology of atrioventricular reciprocating tachycardia - AVRT (accessory) arrhythmias

A

Congenital muscle strands connect atria and ventricles = accessory pathway
Result in pre-excitaiton of ventricles

189
Q

ARRHYTHMIAS
Describe 3 characteristics of an ECG from someone with accessory pathway arrhythmia

A
  1. Delta wave
  2. Short PR interval
  3. Slurred QRS complex
190
Q

ARRHYTHMIAS
Give an example of an atrioventricular reciprocating tachycardia - AVRT (accessory) arrhythmia

A

Wolff-Parkinson-White Syndrome

191
Q

ARRHYTHMIAS
Give 4 causes of sinus tachycardia

A
  1. Physiological response to exercise
  2. Fever
  3. Anaemia
  4. Heart failure
  5. Hypovolaemia
  6. pain
192
Q

ARRHYTHMIAS
Why do ventricular tachycardia’s arise?

A

Extra circuits in ventricles or abnormal muscle depolarisation
Can come from previous MI or cardiomyopathy

193
Q

ARRHYTHMIAS
What ECG changes might you see with someone with ventricular tachycardia?

A

Crescendo-decrescendo amplitude = torsades de pointes

194
Q

ARRHYTHMIAS
What is the treatment for ventricular tachycardia in an urgent situation?

A

DC cardioversion

195
Q

ARRHYTHMIAS
What is long term treatment for ventricular tachycardia in high risk patients

A

Implantable cardioverter defibrillator (ICD)

196
Q

ARRHYTHMIAS
What is the treatment for stable ventricular tachycardia?

A

IV beta blockers (bisoprolol) and IV amiodarone

197
Q

ATRIAL FLUTTER
What is atrial flutter?

A

Fast but organised waves in the atrium
Atrial rate 250-350 bpm

198
Q

ATRIAL FLUTTER
Describe the ECG pattern taken from someone with atrial flutter

A
  1. Narrow QRS
  2. Saw tooth flutter (F) waves
199
Q

ATRIAL FLUTTER
Describe the pathophysiology of atrial flutter

A

the P wave produces a sawtooth pattern with regular conduction to the ventricles
- Wave of contraction around the atria causing the repolarisation of the AV node

200
Q

ARRHYTHMIAS
What are ectopic beats?

A

Non sustained beats arising from ectopic regions of atria or ventricles
Very common, generally benign arrhythmias caused by premature discharge

201
Q

ARRHYTHMIAS
what are the causes of long QT syndrome?

A
  1. Congenital
  2. hypokalaemia,
  3. hypocalcaemia
  4. Drugs - amiodarone, tricyclic antidepressants
  5. bradycardia
  6. Acute MI
  7. diabetes
202
Q

ARRHYTHMIAS
what is the clinical presentation of long QT syndrome?

A
  1. Palpitations
  2. Syncope
    - may progress to VF
203
Q

HEART BLOCK
Where can heart blocks occur?

A
  1. Block in either AVN or bundle of His = AV block
  2. Block lower in conduction system = Bundle Branch Block
204
Q

HEART BLOCK
Describe a first degree heart block

A

Fixed prolongation of the PR interval due to delayed conduction to the ventricles
- PR interval >0.22s
- asymptomatic

205
Q

HEART BLOCK
Describe a second degree heart block

A

There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles

206
Q

HEART BLOCK
Describe a Mobitz type 1 second degree heart block

A

PR interval gradually increases until AV node fails and no QRS is seen
PR interval returns to normal and the cycle repeats

207
Q

HEART BLOCK
Describe a Mobitz type 2 second degree heart block

A

Sudden unpredictable loss of AV conduction and so loss of QRS
PR interval is constant but every nth QRS is missing
wide QRS

208
Q

HEART BLOCK
Describe a third degree heart block

A

Atrial activity fails to conduct to the ventricles
P waves and QRS complexes occur independently
ventricular contractions are maintained by spontaneous escape rhythm originating below the block

209
Q

HEART BLOCK
What are the treatments for heart blocks?

A

1st = asymptomatic, watch and wait –> atropine
Mobitz 1 = no pacemaker
Mobitz 2 = pacemaker
3rd = permanent pacemaker

210
Q

HEART BLOCK
what are the causes of heart block?

A

Athletes
Sick sinus syndrome
IHD – esp MI
Acute myocarditis
Drugs
Congenital
Aortic valve calcification
Cardiac surgery/trauma

211
Q

HEART BLOCK
What kind of heart block is associated with wide QRS complexes with an abnormal pattern?

A

Right bundle branch block (RBBB) and Left bundle branch block (LBBB)

212
Q

HEART BLOCK
Explain the pathophysiology of a BBB

A

Lack of simultaneous ventricular contractions
LBBB = R before L
RBBB = L before R

213
Q

HEART BLOCK
What changes would you see on an ECG from someone with a LBBB?

A

WiLLiaM
slurred S wave in V1 (resembles W)
R wave in V6 (resembles M)

wide QRS with notched top in V6

214
Q

HEART BLOCK
What changes would you see on an ECG from someone with a RBBB?

A

MaRRoW
R wave in V1 (resembles M)
slurred S wave in V6 (resembles W)

wide QRS
RSR pattern in V1

215
Q

ARRHYTHMIAS
Cardiac arrhythmias: what is the treatment of choice in a patient who is hemodynamically unstable due to the underlying rhythm?

A

DC cardioversion

216
Q

ATRIAL FLUTTER
what are the causes of atrial flutter?

A
  • idiopathic
  • CHD
  • hypertension
  • heart failure
  • COPD
  • pericarditis
  • obesity
217
Q

ATRIAL FLUTTER
what are the risk factors for atrial flutter?

A
  • atrial fibrillation
218
Q

ATRIAL FLUTTER
what is the management for atrial flutter?

A
  • Cardioversion
    - Give a LMWH
    - Shock with defibrillator
  • Catheter ablation = definitive treatment – creates a conduction block
  • IV Amiodarone – restore sinus rhythm
219
Q

ARRHYTHMIAS
what are the risk factors for AVNRT?

A

exertion
emotional stress
coffee
tea
alcohol

220
Q

HEART BLOCK
what are the causes of RBBB?

A

Pulmonary embolism
IHD
Atrial ventricular septal defect

221
Q

HEART BLOCK
what is the pathophysiology of RBBB?

A

Right bundle doesn’t conduct
Impulse spreads from left ventricle to right
Late activation of RV

222
Q

HEART BLOCK
what is the clinical presentation of RBBB?

A

Asymptomatic
syncope/presyncope

223
Q

HEART BLOCK
what is the treatment for RBBB?

A

Pacemaker
CRT – cardiac resynchronisation therapy
Reduce blood pressure

224
Q

HEART BLOCK
what is the clinical presentation of LBBB?

A

Asymptomatic
syncope/presyncope

225
Q

HEART BLOCK
what is the pathophysiology of LBBB?

A

Left bundle doesn’t conduct
Impulse spreads from right ventricle to left
Late activation of LV

226
Q

HEART BLOCK
what is the treatment for LBBB?

A

Pacemaker
CRT – cardiac resynchronisation therapy
Reduce blood pressure

227
Q

HEART BLOCK
what are the causes of LBBB?

A

IHD
Aortic valve disease

228
Q

HEART BLOCK
what are the investigations for heart block?

229
Q

HEART BLOCK
what is the treatment for heart block?

A

Cardioversion
- Give a LMWH
- Shock with defibrillator
Catheter ablation – creates a conduction block
IV Amiodarone – restore sinus rhythm

230
Q

HEART BLOCK
what is the presentation of first degree heart block?

A

asymptomatic

231
Q

HEART BLOCK
what is the clinical presentation of Mobitz type 1 second degree heart block?

A

light-headedness
dizziness
syncope

232
Q

HEART BLOCK
what is the clinical presentation of Mobitz type 2 second degree heart block?

A

SOB
postural hypotension
chest pain

233
Q

HEART BLOCK
what is the clinical presentation of third degree heart block?

A

dizziness
blackouts

234
Q

IBS
Give an example of a functional bowel disorder

235
Q

IBS
Describe the mil-factorial pathophysiology of IBS

A

The following factors can all contribute to IBS:

  • Psychological morbidity - trauma in early life
  • Abnormal gut motility
  • Genetics
  • Altered gut signalling (visceral hypersensitivity)
236
Q

IBS
Give 3 symptoms of IBS

A
  1. Abdominal pain
  2. Bloating
  3. Change in bowel habit
  4. Mucus
  5. Fatigue
  6. Backache
237
Q

IBS
Give an example of a differential diagnosis for IBS

A
  1. Coeliac disease
  2. Lactose intolerance
  3. Bile acid malabsorption
  4. IBD
  5. Colorectal cancer
238
Q

IBS
What investigations might you do in someone who you suspect has IBS?

A

Rule out differentials

  1. Bloods - FBC, U+E, LFT
  2. CRP
  3. Coeliac serology
  4. Colonoscopy
239
Q

IBS
Describe the non pharmacological treatment of IBS

A

Education
Resistance
Dietary modification - reduce caffeine, plenty of fluids, increase fibre intake

240
Q

IBS
Describe the pharmacological treatment of IBS

A
  1. Antispasmoidics for bloating - mebeverine
  2. Laxatives for constipation
  3. Anti-motility agent for diarrhoea - loperamide
  4. Tricyclic antidepressants
241
Q

HAEMORRHOIDS
what are haemorrhoids?

A

-disrupted and dilated anal cushions due to swollen veins around the anus

242
Q

HAEMORRHOIDS
what is the epidemiology of haemorrhoids?

A
  • prevalence increases with age (peak = 45-65yrs
  • male=female
243
Q

HAEMORRHOIDS
what are the main causes of haemorrhoids?

A
  • constipation (with prolonged straining)
  • diarrhoea
  • effects of gravity due to posture
  • congestion from pelvic tumour, pregnancy, portal hypertension
  • anal intercourse
244
Q

HAEMORRHOIDS
what is the pathophysiology of haemorrhoids?

A
  • effects of gravity, increased anal tone and effect of straining make anal cushions become bulky and loose -> protrude
  • are vulnerable to trauma and bleed easily
  • protrusions can strangulate
245
Q

HAEMORRHOIDS
where do internal haemorrhoids occur?

A

above dentate line
have 4 degrees

246
Q

HAEMORRHOIDS
where do external haemorrhoids occur?

A

below dentate line
may be visible externally
- are painful due to sensory nerve supply

247
Q

HAEMORRHOIDS
what is the clinical presentation of haemorrhoids?

A
  • bright red rectal bleeding that coats stool/seen on tissue/drips into toilet
  • mucus discharge and itchy bottom
  • severe anaemia
  • weight loss
  • change in bowel habit
248
Q

HAEMORRHOIDS
what investigations are undertaken for haemorrhoids?

A
  • abdominal exam
  • PR exam - prolapsing piles obvious, internal haemorrhoids not palpable
  • proctoscopy - see internal haemorroids
  • sigmoidoscopy
249
Q

HAEMORRHOIDS
what is the treatment for 1st degree haemorrhoids?

A
  • increase fluid and fibre
  • topical analgesia and stool softener
250
Q

HAEMORRHOIDS
what is the treatment for 2nd and 3rd degree haemorrhoids?

A
  • rubber band ligation
  • intra-red coagulation
251
Q

HAEMORRHOIDS
what is the treatment for 4th degree haemorrhoids?

A

surgery
- elective haemorrhoidectomy

252
Q

ANAL FISSURE
what is an anal fissure?

A

Painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line resulting in pain on defecation

253
Q

ANAL FISSURE
what is the epidemiology of anal fissures?

A
  • 90% are posterior
  • Anterior ones follow childbirth
  • FEMALES affected more than males
254
Q

ANAL FISSURE
what are the causes of anal fissures?

A
  • Main causes:
    * HARD FAECES
    * Spasm may constrict the inferior rectal artery resulting in ischaemia which makes healing difficult and perpetuates the problem
  • Rare causes:
       - Syphilis 
   - Herpes 
   - Trauma 
   - Crohn’s 
   - Anal cancer
255
Q

ANAL FISSURE
what is the clinical presentation of anal fissures?

A
  • Extreme pain especially on defecation
  • Bleeding
256
Q

ANAL FISSURE
what investigations are undertaken for anal fissures?

A
  • Can usually be made on history alone
  • Confirmed on perianal inspection
  • Rectal examination is often not possible due to pain and sphincter spasm
257
Q

ANAL FISSURE
what is the treatment for anal fissures?

A
  • Increase dietary fibre and fluids to make stools softer
  • LIDOCAINE OINTMENT + GTN OINTMENT or topical BOTOX INJECTION (2nd line)
  • Surgery if medication fails
258
Q

HIATUS HERNIA
what are the 2 types of hiatal hernia?

A

sliding
rolling

259
Q

HIATUS HERNIA
what is a sliding hiatal hernia?

A

the gastro-oesophageal junction and part of the stomach slides up into the chest via the hiatus so that it lies above the diaphragm

260
Q

HIATUS HERNIA
what is a rolling hiatal hernia?

A

the gastro-oesophageal junction remains in the abdomen but part of the fundus of the stomach prolapses through the hiatus alongside the oesophagus

261
Q

HIATUS HERNIA
what are the clinical features of hiatus hernia?

A

50% have GORD

262
Q

HIATUS HERNIA
what investigations are undertaken for hiatus hernia?

A

barium swallow = best diagnostic test,
upper GI endoscopy = visualizes the mucosa, but cant reliably exclude hiatus hernia

263
Q

HIATUS HERNIA
what is the treatment for hiatus hernia?

A

lose weight,
treat reflux symptoms,
surgically treat to prevent strangulation

264
Q

VARICOSE VEINS
what are they?

A

Varicose veins are dilated, tortuous, superficial veins that occur secondary to incompetent venous valves, allowing blood to flow back, away from the heart

265
Q

VARICOSE VEINS
where do they most commonly occur?

A

They most commonly occur in the legs due to reflux in the great saphenous vein and small saphenous vein.

266
Q

VARICOSE VEINS
what are the risk factors for varicose veins?

A
  • increasing age
  • female gender
  • pregnancy - the uterus causes compression of the pelvic veins
  • obesity
267
Q

VARICOSE VEINS
what is the clinical presenation?

A

For many patients, the cosmetic appearance may prompt presentation.
However other patients may complain of symptoms:
- aching, throbbing
- itching

268
Q

VARICOSE VEINS
what are the complications?

A
  • a variety of skin changes may be seen:
    - varicose eczema (also known as venous stasis)
    - haemosiderin deposition → hyperpigmentation
    - lipodermatosclerosis → hard/tight skin
    - atrophie blanche → hypopigmentation
  • bleeding
  • superficial thrombophlebitis
  • venous ulceration
  • deep vein thrombosis
269
Q

VARICOSE VEINS
what are the investigations?

A

venous duplex ultrasound: this will demonstrate retrograde venous flow

270
Q

VARICOSE VEINS
what is the conservative management of varicose veins?

A

leg elevation
weight loss
regular exercise
graduated compression stockings

271
Q

VARICOSE VEINS
what would be the reasons for referral to secondary care for varicose veins?

A

significant/troublesome lower limb symptoms e.g. pain, discomfort or swelling
previous bleeding from varicose veins
skin changes secondary to chronic venous insufficiency (e.g. pigmentation and eczema)
superficial thrombophlebitis
an active or healed venous leg ulcer

272
Q

VARICOSE VEINS
what are the treatments?

A

endothermal ablation: using either radiofrequency ablation or endovenous laser treatment
foam sclerotherapy: irritant foam → inflammatory response → closure of the vein
surgery: either ligation or stripping

273
Q

ACUTE BRONCHITIS
what is it?

A

Acute bronchitis is a type of chest infection which is usually self-limiting in nature. It is a result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum.

274
Q

ACUTE BRONCHITIS
how long it the disease course?

A

The disease course usually resolves before 3 weeks, however, 25% of patients will still have a cough beyond this time

275
Q

ACUTE BRONCHITIS
what is the clinical presentation?

A

cough: may or may not be productive
sore throat
rhinorrhoea
wheeze

The majority of patients with have a normal chest examination, however, some patients may present with:
Low-grade fever
Wheeze

276
Q

ACUTE BRONCHITIS
how do you differentiate acute bronchitis from pneumonia?

A
  • history = Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia.
  • Examination = No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze.
    Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia.
277
Q

ACUTE BRONCHITIS
what are the investigations?

A

acute bronchitis is typically a clinical diagnosis
however, if CRP testing is available this may be used to guide whether antibiotic therapy is indicated

278
Q

ACUTE BRONCHITIS
what is the management?

A

analgesia
good fluid intake
consider antibiotic therapy - doxycycline (amoxicillin in children/pregnancy)

279
Q

ACUTE BRONCHITIS
when would you consider antibiotic therapy?

A

are systemically very unwell
have pre-existing co-morbidities
have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)

280
Q

BRONCHIOLITIS
what is it?

A

Bronchiolitis is a condition characterised by acute bronchiolar inflammation

281
Q

BRONCHIOLITIS
what is the most common causative pathogen?

A

Respiratory syncytial virus (RSV) is the pathogen in 75-80% of cases

282
Q

BRONCHIOLITIS
what is the epidemiology?

A

most common cause of a serious lower respiratory tract infection in < 1yr olds (90% are 1-9 months, with a peak incidence of 3-6 months). Maternal IgG provides protection to newborns against RSV
higher incidence in winter

283
Q

BRONCHIOLITIS
what is the clinical presentation?

A

coryzal symptoms (including mild fever) precede:
dry cough
increasing breathlessness
wheezing, fine inspiratory crackles (not always present)
feeding difficulties associated with increasing dyspnoea are often the reason for hospital admission

284
Q

BRONCHIOLITIS
According to NICE guidelines, when would you immediately refer (call 999 ambulance)?

A

apnoea (observed or reported)
child looks seriously unwell to a healthcare professional
severe respiratory distress, for example grunting, marked chest recession, or a respiratory rate of over 70 breaths/minute
central cyanosis
persistent oxygen saturation of less than 92% when breathing air.

285
Q

BRONCHIOLITIS
According to NICE guidelines, when would you consider referring to hospital?

A

a respiratory rate of over 60 breaths/minute
difficulty with breastfeeding or inadequate oral fluid intake (50-75% of usual volume ‘taking account of risk factors and using clinical judgement’)
clinical dehydration.

286
Q

BRONCHIOLITIS
what are the investigations?

A

immunofluorescence of nasopharyngeal secretions may show RSV

287
Q

BRONCHIOLITIS
what is the management?

A

Management is largely supportive
- humidified oxygen is given via a head box and is typically recommended if the oxygen saturations are persistently < 92%
- nasogastric feeding may be needed if children cannot take enough fluid/feed by mouth
- suction is sometimes used for excessive upper airway secretions

288
Q

PNEUMONIA
What are the most common causes of HAP?

A
  • S. aureus
  • Klebsiella pneumoniae
  • Pseudomonas aeruginosa
289
Q

VENOUS ULCERS
what are venous ulcers?

A

A venous ulcer is a long-lasting (chronic) sore that takes more than 4 to 6 weeks to heal. They usually develop on the inside of the leg, just above the ankle.

290
Q

VENOUS ULCERS
what is the clinical presentation?

A
  • painful ulcer that takes >1 month to heal
  • ankle oedema
  • discolouration around ulcer (dark red, brown or purple)
  • hardened skin around ulcer
  • heavy feeling in legs
  • aching in legs
  • varicose eczema (red, flaky itchy skin on legs)
  • varicose veins
  • unpleasant + foul smelling discharge
291
Q

VENOUS ULCERS
what are the signs of an infected venous ulcer?

A
  • worsening pain
  • a green or unpleasant discharge coming from the ulcer
  • redness and swelling of the skin around the ulcer
  • a high temperature (fever)
292
Q

VENOUS ULCERS
what are the causes?

A
  • sustained venous hypertension
  • chronic venous insufficiency
  • venous valve incompetence (varicose veins)
  • impaired calf muscle pump
293
Q

VENOUS ULCERS
what are the risk factors?

A
  • obesity
  • previous DVT
  • varicose veins
  • immobility
  • increasing age
294
Q

VENOUS ULCERS
what are the investigations for venous ulcers?

A
  • physical examination
  • doppler study to measure ABPI (to rule out arterial disease)
295
Q

VENOUS ULCERS
what is the management of venous ulcers?

A
  • cleaning and dressing ulcers
  • compression bandages
  • emollient for eczema
  • elevate legs to reduce oedema
296
Q

VENOUS ULCERS
hoe can you reduce the risk of recurrence?

A
  • long term use of compression hosiery
  • lifestyle changes

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