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Junior blocks > Cardiorespiratory > Flashcards

Cardiorespiratory Flashcards

1
Q

Give an example of a class 1a and 1b anti arrhythmic and what it might be used for.

A

A Quinidine
B lidocaine

Both for vt and vf

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2
Q

Give an example of a class 1c anti arrhythmic and what it might be used for.

A

Flecainide

Paroxysmal AF
Rentrant rhythms e.g. WPW

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3
Q

Give an example of a class 2 anti arrhythmic and what they might be used for.

A

Beta blockers
Bisoprolol or atenolol

Post MI
Angina
AF

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4
Q

Give an example of a class 3 anti arrhythmic and what they might be used for.

A

K channel blockers e.g. Amiodarone. Or sotalol at high dose has class 3 effects

VT or VF
Chemical cardioversion
SVT

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5
Q

Give an example of a class 4 anti arrhythmic and what they might be used for.

A

Calcium channel blocker eg Verapamil, diltiazem, amlodipine

Fast AF
SVT
Hypertension

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5
Q

What are the main 5 side effects of beta blockers?

A

Vagal GI disturbance - vomiting, diarrhoea, abdo pain, anorexia.
Bradycardia
Exacerbation of Reynauds and Claudication
Bronchospasm
Dizziness/ postural hypotension

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6
Q

What are the contra indications to beta blockers?

A

Asthma
Bradycardia/ hypotension
Heart block

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7
Q

Which ca channel blocker works more on the blood vessels than the myocardium?

A

Amlodipine

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8
Q

What are the indications for GTN spray?

A

Stable angina

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9
Q

What are the contra indications for ca channel blockers?

A

Heart failure - verapamil contraindicated. Can give amlodipine
Beta blockers - verapamil contraindicated
Heart block

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10
Q

What are the indications for IV gtn?

A

Unstable angina

Acute heart failure

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11
Q

What are the side effects of gtn?

A

Tolerance
Postural hypotension
Headache
Dizziness

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12
Q

What are the 4 effects of ACE inhibitors?

A

Inhibits angiotensin 2 therefore

  1. Decreases sympathetic
  2. Direct vasodilation
  3. Decrease aldosterone - decrease in Na (and fluid) retention via ENac
  4. Decrease ADH - decrease in fluid (and Na) retention via removal of Aquaporin2 channels from the apical membrane of collecting ducts.
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14
Q

What are the effects of ACE in CKD and AKI?

A

Protective in CKD by reducing the workload

Toxic in AKI by causing renal artery constriction

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15
Q

What are the indications for ACE inhibitors?

A

Hypertension (unless old, black, diabetes)
Heart failure
Post MI
CKD - especially diabetic

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16
Q

What are the side effects of ACE inhibitors?

A 
Dry cough
Angio oedema
Hyperkalaemia
Pancreatitis 
Renal impairment
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17
Q

What are the contra indications for ACE inhibitors?

A

Renal artery stenosis
Aortic stenosis
Pregnancy

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18
Q

What is furosemide and where does it act?

A

Loop diuretic.

Na k cl transporter in the thick ascending loop of henle

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19
Q

What are the indications for furosemide?

A

Symptomatic relief of pulmonary oedema
Refractive hypertension
CKD
Nephrotic syndrome

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20
Q

What are the common side effects of furosemide?

A 
Hypokalaemia
Hyponatraemia 
Low ca and mg
Metabolic alkalosis 
Hypovolaemia
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21
Q

What monitoring is required for furosemide?

A

Regular u and e for k and Na levels

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22
Q

What is bendroflumethiazide and where does it act?

A

Thiazides diuretic

Na cl channel on the distal convoluted tubule

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23
Q

What indications for bendroflumethiazide?

A

pulmonary oedema in heart failure

Second/third line in hypertension

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24
Q

What are the side effects of bendroflumethiazide?

A

Hypokalaemia
Hyponatraemia
Low ca and mg
Hyperglycaemia metabolic alkalosis

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25
Q

What is spironolactone and where does it Act?

A

K sparing diuretic

Aldosterone antagonist

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26
Q

What are the indications for spironolactone?

A

Heart failure
Liver failure
Offset loop or thiazides

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27
Q

What are the side effects of spironolactone?

A 
Gynaecomastia
Impotence
Menstrual problems
Lethargy 
GI
Hyperkalaemia
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28
Q

What is the mechanism of action of statins?

A

HMG co a reductase inhibitors

Inhibit liver synthesis of Cholesterol. Upregulates ldl receptors so that more is absorbed out of the circulation

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29
Q

Give some side effects of statins

A 
Hepatitis
Myositis
Rhabdomyelisis 
Parasthesia 
Headache
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30
Q

What are the contra indications for statins?

A

Cirrhosis/ liver disease

Pregnancy

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31
Q

What should be monitored when on a statin?

A

LFTs - hepatotoxic

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32
Q

Why should statins be taken in the evening?

A

Most cholesterol synthesis occurs when dietary intake is low.

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33
Q

What is gemfibrozil? Why might it be given? When should it not be given?

A

Fibrate

Lowers triglycerides more than ldl.
Can’t be given with a statin because it increases the risk of rhabdomyelisis

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34
Q

What are the contraindications to adenosine?

A

Haemodynamically unstable - go straight to cardioversion of presumed VT
Asthma

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35
Q

What is the effect of adenosine in a narrow complex tachycardia?

A

Returns to normal if AVNRT / SVT

Or will reveal atrial tachy/ AF / atrial flutter

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36
Q

What is the effect of adenosine in a broad complex tachycardia?

A

Testing a Broad complex tachy to see if it is vt or SVT with aberrancy
If the rhythm goes back to normal it is SVT with aberrancy.

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37
Q

Which drugs can be cardio toxic?

A

Digoxin
Na blockers -Tricyclics, lidocaine, carbamazepine, class 1 anti arrhythmic
K blockers - citalopram, erythromycin, antihistamines, amiodarone, antipsychotics

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39
Q

How is atherosclerosis formed?

A 
Endothelial damage
LDL oxidation and accumulation in intima
Taken up by macrophages- foam cells
Cytokines released - platelet aggregation, fat and smooth muscle proliferation 
Lipid core and fibrous cap.
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40
Q

What happens to an atherosclerotic plaque to cause an acute coronary syndrome?

A

Rupture
Platelet aggregation and adhesion
Localised thrombus concludes the vessel

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41
Q

Which group of patients commonly present with silent MI? How does it present?

A

Diabetics and elderly
No chest pain.
Week long history of breathlessness.
Can progress into pulmonary oedema due to acute heart failure.

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42
Q

What causes a raised troponin? (5 things)

A 
MI
PE
Pericarditis 
Sepsis 
Tachyarrhythmias
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43
Q

How long after an MI does the troponin increase? How long before it comes down?

A

6-14 hrs after onset.

Remain high for 14 days

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44
Q

How long after an MI does the creatinine kinase rise? Hoe long does it stay high?

A

4 hours

Falls within 72 hours

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45
Q

What are the criteria for an acute MI?

A

Raised biochemical marker plus one of -

Ischaemic symptoms
Pathological q waves
St elevation/depression

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46
Q

How do the ecg changes develop in a STEMI?

A

ST depression and T wave inversion
ST elevation and pathological Q
Q waves persist

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47
Q

List the investigations you would order for a suspected MI and give a reason for each.

A
  1. Fbc - anaemia can precipitate MI in angina
  2. U and e - Possible AKI due to poor perfusion in MI. Also MI is a proarrhythmic state and hyperkalaemia is a big risk.
  3. Troponin and creatinine kinase
  4. LFTs
  5. Glucose and lipids - need to keep tight control of risk factors.
  6. CXR - widened mediastinum of aortic dissection - do not thrombolyse!!! Hypertrophy- HF. Pulmonary oedema can form after a few hours of MI as it causes acute HF
  7. ECG - to identify MI
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48
Q

Where is the MI located if ST elevation is seen in leads v1-4?

A

Anterior

LAD

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49
Q

Where is the MI located if ST elevation is seen in leads II, III and AVF?

A

Inferior

RCA or circumflex

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50
Q

Where is the MI located if ST elevation is seen in leads v4-6, aVL and I?

A

Lateral

Circumflex

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51
Q

Where is the MI located if ST elevation is seen in leads v1-6?

A

Anterolateral

Proximal LAD/ left main stem

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52
Q

What are the pathological differences between STEMI, nstemi, unstable angina, angina?

A

STEMI - complete occlusion of artery by thrombus and full thickness infarct. Troponin positive
NSTEMI - partial occlusion of artery by thrombus - partial thickness infarct or infarct in small vessel. Troponin positive (mild)
Unstable angina - partial occlusion of artery by thrombus. No infarct. Troponin negative.
Angina - no thrombus. Partial occlusion by atheroma. Relieved by rest.

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53
Q

What are the complications associated with an MI?

A

Ischaemic - recurrence, angina

Mechanical - aneurysm, heart failure, mitral regurgitation, ruptured papillary muscles, cardiogenic shock, embolism

Arrhythmia

Dresslers - pericarditis

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54
Q

Where is the MI located if ST depression is seen in leads v1-2?

A

Posterior
Right coronary
Do v7 8 and 9 to confirm

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56
Q

Describe the management of an acute MI

A 
MONA
5-10mg morphine IV with 10mg metoclopramide
Oxygen - 15L via non rebreather mask
GTN - 2 puffs sublingual 
Aspirin 300mg
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56
Q

What is the difference between the type of clots found on a mechanical heart valve and in IHD? What is the significance?

A

Mechanical heart valve - fibrin rich
IHD- platelet rich

Antifibrin - warfarin
Antiplatelet - prasugrel/ticagrelor/clopidogrel

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57
Q

What are the contra indications for thrombolysis in an acute MI?

A 
Recent stroke or GI bleed
Brain tumour
Bleeding disorder
Aortic dissection 
(Pregnancy, warfarin)
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58
Q

What are the complications of thrombolysis?

A 
Bleeding
Hypotension 
Intracranial haemorrhage
Embolism
Allergic reaction
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59
Q

Give 3 causes of AF

A

IHD
Hyperthyroidism
Valvular disease

Plus previous cardiac surgery, sleep Apnoea, caffeine

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60
Q

Which scores would you use in tandem to decide whether to anticoagulate a patient with AF?

A

CHADSVAS

HASBLED

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62
Q

How would you initially treat an anaphylactic reaction?

A 
Oxygen 
Fluid
100mg hydrocortisone IV
Adrenaline 0.5mg every 5 mins
10mg chlorpheniramine IV
Protect airway - consider intubating
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63
Q

What tests would you request in an anaphylactic reaction?

A 
General observations
BM
Abg for lactate
Chest x Ray 
CT head if loss of consciousness
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64
Q

What can cause a positive D Dimer?

A 
PE
Pregnancy
Surgery
Trauma
Infection
Hepatorenal disease
Cancer
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65
Q

Which systems are affected by cystic fibrosis?

A

Respiratory - thickened mucus, recurrent infection, bronchectasis
Pancreas - enzymes and insulin
GI - malabsorption, steattorea and low body weight due to low pancreatic enzymes
Reproductive - males due to cftr in vas deferens. Females have 70-80% fertility due to cftr in Fallopian tube.

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66
Q

What is creon?

A

Pancreatic enzyme replacement for cf patients

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67
Q

What are the radiological signs of left sided heart failure?

A 
A - a large heart 
B - batwing oedema
C - Kerley B lines
D - dilated upper lobe vessels
E - effusion
F - fluid in the fissure
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68
Q

What are the emergency complications associated with cystic fibrosis?

A

Recurrent infection
Pneumothorax
Hypersensitive drug reactions
Meconium ileus / DIOS distal intestinal obstruction syndrome

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68
Q

What is different about cf associated diabetes?

A

Transient insulin levels (go up and down)

Requires insulin treatment

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68
Q

What lifestyle advice would you give to a patient with cf?

A 
Stay away from other cf patients
Don't smoke
Avoid people with colds
Avoid jacuzzis- pseudomonas
Avoid stables and compost aspergillus fumigatus
Flu jab
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68
Q

Which drugs are given to a patient after an MI?

A 
Bisoprolol 
Aspirin
Ramipril
Atorvastatin
Prasugrel (STEMI)
Ticagrelor (nstemi)
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69
Q

What is Dressler’s syndrome?

A

Autoimmune pericarditis triggered by a recent MI.

Treat with steroids.

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70
Q

What causes acute left ventricular failure?

A 
MI
Hypertension
Aortic stenosis
Aortic regurgitation 
Mitral regurgitation
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71
Q

How does acute L ventricular failure present?

A 
Breathless
Cough
Frothy pink sputum
Orthopnoea and pnd
Arrest

Tachy
Fine bilateral crepitations
3rd heart sound - gallop rhythm

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72
Q

Which drugs actually improve morbidity in heart failure? Which are for symptomatic relief?

A

Morbidity- spironolactone, beta blocker.

Symptoms - loop diuretic, ACE inhibitors, nitrates, ionotropes - dopamine, digoxin

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73
Q

What is a normal/abnormal ejection fraction?

A

Normal is above 50%

Borderline - 41-50

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74
Q

How does heart failure present on a chest x Ray?

A 
Batwing oedema 
Pleural effusion 
Fluid in the fissure
Kerley B lines 
Upper lobe blood vessel dilation
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75
Q

Give some differentials for palpitations

A 
Arrhythmia - AF, flutter, wpw, ectopics, avnrt, SVT, long qt
Anxiety - sinus tachycardia 
Hyperthyroidism 
Caffeine
Hypertrophic cardiomyopathy
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76
Q

Give some differentials for haemoptysis.

A 
Lung cancer
Pneumonia/ TB
Bronchiectasis 
PE
Lung abcess
Vasculitis
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77
Q

Give some differentials for shortness of breath

A

Asthma/ COPD
Pneumonia/ TB
Pneumothorax/ pleural effusion
PE

Pulmonary oedema / heart failure
Arrhythmia
Valve disease

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78
Q

Give some differentials for pleuritic chest pain.

A 
PE
Pneumothorax 
Pleural effusion/ empyema
Endocarditis 
Irritation of diaphragm
Gastric reflux
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79
Q

Which antibiotic is used for a septic patient?

A

Meropenem

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81
Q

Which antibiotic is given to a curb 3-5 pneumonia?

A

Co amoxiclav and doxycycline
Or
Meropenem and doxycycline

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82
Q

What is CURB 65? What does it stand for?

A 
Measure of severity of pneumonia
C - confusion
U - urea above 7
R - Resp rate above 30
B - bp below 90/60
65 years or older

Score 1 for each

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83
Q

What is the follow up for a patient with pneumonia following discharge?

A

Chest X-ray in 6 weeks.

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84
Q

What are the causes of copd?

A

Smoking
Alpha 1 anti trypsin
Industrial exposure - soot

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85
Q

What is the pathophysiology of emphysema?

A

Alveolar wall destruction - irreversible enlargement of airspaces distal to terminal bronchioles. Bulla formation. Loss of surface area for gas exchange.

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86
Q

What is the outpatient care bundle for copd?

A

Smoking cessation
Pulmonary rehab to break the deconditioning cycle
Bronchodilators - salbutamol or ipratropium
Steroids - fluticasone
Mucolytic - carbocysteine

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87
Q

How long must oxygen therapy be used per day to have a survival benefit?

A

16 hours

88
Q

When is long term oxygen therapy offered for copd?

A

pO2 below 7.3 or below 8 with cor pulmonale

89
Q

Why is it important to check the ankles in a respiratory examination?

A

Cor pulmonale - right heart failure caused by pulmonary hypertension from lung pathology

90
Q

What is the care bundle for acute copd exacerbation?

A

Venturi mask for controlled oxygen therapy - 88-92 sats
Salbutamol and ipratropium nebs
Prednisolone 30mg stat and OD for 7 days
Consider NIV if becomes acidotic 7.25-7.35
Below 7.25 call ITU

91
Q

How are pack years calculated?

A

Packs of 20 each day x years of smoking

So 10 a day for 5 years is 1/2 x 5 = 2.5 pack years

92
Q

What is the pathophysiology of chronic bronchitis?

A

Mucous gland hyperplasia

Chronic inflammation of the bronchi

93
Q

What is the pathophysiology of bronchectasis?

A

Chronic dilatation of the bronchi
Mucous plugging
Damage to ciliary escalator - recurrent infection
Haemoptysis due to damage to the bronchial arteries

94
Q

What is the pattern of spirometry in copd?

A

Obstructive pattern
Scooped out edge
Reduced fev1 /fvc (less than 70%) and reduced fev1 (less than 80%)

95
Q

What is the role of pulmonary rehab in copd patients?

A

Break the cycle of deconditioning

96
Q

Give 5 causes of non resolving pneumonia

A 
Empyema
Immunocompromise
PE
Cancer
Wrong dose/wrong antibiotic
Organising pneumonia
96
Q

What organisms commonly cause hospital acquired pneumonia?

A

Staph aureus - MRSA

Pseudomonas aeruginosa

96
Q

What organisms are commonly found in infections in CF patients?

A

Staph aureus - MRSA
Pseudomonas aeruginosa
Haemophillus influenza

Burkholderia cepacia

96
Q

Which copd treatments affect survival?

A

Long term oxygen therapy - 16 hours a day at least
NIV if acidotic
Smoking cessation

97
Q

What organisms commonly cause community acquired pneumonia?

A

Strep pneumoniae
Haemophillus influenza
Group A strep - like strep throat - pyogenes

99
Q

Why is uncontrolled oxygen therapy dangerous in copd patients?

A

The choroid plexus has reset to accept a hypercapnia so that it is no longer the main driver for respiratory effort. Instead hypoxia is the main driver so needs to be maintained.

Also there is hypoxic vasoconstriction in copd to maximise the perfusion to well sventilated areas. So there is a compensatory v/q mismatch. Too much oxygen causes these areas to reperfuse even though they are inefficient at gas exchange so the compensation is overridden.

101
Q

What questions would you ask a patient with asthma?

A

Diurnal variation? (Worse in morning and night)
Atopy? (Hay fever, allergy, eczema)
Ever been in ICU?

102
Q

What are the definitions for mild moderate severe life threatening and near fatal asthma?

A 
Mild - over 75% peak flow
Moderate - 50-75%
Severe - 33 - 50%
Life threatening- less than 33%
Near fatal - rise in co2
103
Q

What is the significance of eosinophilia in a patient with asthma?

A

Aids diagnosis - Indicates atopical traits

Generally responsive to steroids

108
Q

Give some differentials for a pleural effusion

A 
Usually transudate - 
Heart failure - congestive
Nephrotic syndrome 
Glomerulonephritis 
SVC obstruction
Cirrhosis
109
Q

Give some differentials for pulmonary oedema.

A

Exudative - pneumonia, PE, lung cancer
Transudative - heart failure,cirrhosis, nephrotic syndrome
Other - MI, valve disease, tamponade, dissection, fluid retention

110
Q

What might cause a transudate effusion?

A

Heart failure
Cirrhosis
Nephrotic syndrome

111
Q

How would you treat a new Left bundle branch block?

A

As a STEMI

112
Q

Give some causes of ST elevation

A 
STEMI
Pericarditis- diffuse st elevation with saddle shape
Coronary artery spasm
PE
Hyperkalaemia
113
Q

Give 4 causes of coarse crepitations

A

Pneumonia
Bronchiectasis
TB
Cystic fibrosis

114
Q

Describe the classic ecg of PE

A

S1-Q3-T3
Large S in I
Q inversion in III
T inversion in III

Although generally just a sinus tachycardia

115
Q

Describe the classic ecg of hyperkalaemia

A

Tall tented T
Flat p
Broad qrs
Slurring into a sine wave

116
Q

Give 3 causes of fine crepitations

A

Pulmonary oedema
ILD/fibrosis
Chronic bronchitis

117
Q

Give 5 respiratory causes of clubbing

A 
Lung cancer 
Cystic fibrosis
Bronchiectasis 
Lung abcess
ILD
118
Q

Give 5 non respiratory causes of clubbing

A

Congenital heart defects, Infective endocarditis
Cirrhosis
Celiacs
Crohns

Hyperthyroidism

119
Q

Give 6 signs of infective endocarditis

A 
Clubbing
Splinter haemorrhage 
Osler nodes and janeway lesions
Changing heat murmur
Microscopic haematuria
Roth spots
120
Q

Give 5 ways that lung cancer can present

A 
Asymptomatic/ incidental findings
Haemoptysis 
Horners
Superior vena cava obstruction 
Mets / paraneoplastic
121
Q

Give 5 risk factors for lung cancer

A 
Smoking
Family history
Copd
ILD
Exposure to asbestos
122
Q

What is the WHO performance status scale?

A 
0 - normal
1 - able to do lîght work
2 - ambulatory and self caring
3 - some self care. confined to bed/chair for 50% waking hours 
4 - cannot self care. Confined to bed.
5 - dead
123
Q

What are the treatment options for stage 1-2 lung cancer?

A

Curative surgery

Curative CHART radiotherapy

124
Q

What are the treatment options for stage 3-4 lung cancer?

A

Chemo

Palliative radiotherapy

125
Q

What is the 5 year survival rate for lung cancer?

A

13%

126
Q

Describe the ecg of pericarditis

A

Diffuse st elevation with no regional pattern

Saddle qrs

127
Q

Describe the ecg of digoxin toxicity

A

Inverted reverse tick T

Plus or minus AF

128
Q

What might cause an exudate effusion?

A

Infection
Cancer
PE

129
Q

What is the difference between a transudate and an exudate?

A

Lights criteria -
Exudate if effusion/serum protein ratio greater than 0.5
Or effusion/serum LDH ratio greater than 0.6

130
Q

What hormone is commonly secreted by a bronchial squamous cell carcinoma? What about a small cell carcinoma?

A

Squamous - PTH

Small cell - ADH and acth - cortisol

131
Q

What are the 2 main types of lung cancer?

A

Small cell

Non small cell - inc squamous and adenocarcinoma

132
Q

How does ILD present?

A

Dry non productive cough
Exertional progressive sob
?exposure to methotrexate, nitrofurantoin, amiodarone
?exposure to asbestos

133
Q

What are the signs of ILD?

A

Late inspiratory fine crackles

Clubbing

134
Q

What causes early inspiratory and expiratory fine crackles?

A

Alveoli pop open early because there is hyperinflation

COPD - chronic bronchitis

135
Q

What causes late inspiratory fine crackles?

A

Alveoli popping open late after being held shut by fibrosis/oedema/negative pressure

ILD
Pneumonia
Pulmonary oedema
Atelectasis - collapsed lung

136
Q

What causes early inspiratory coarse crackles?

A

Excess fluid on the lung

Pulmonary oedema
Bronchiectasis
CF
Pneumonia

137
Q

What causes a polyphonic vs a monophonic wheeze?

A

Mono- single obstruction

Poly - general bronchial obstruction

138
Q

What causes an expiratory wheeze?

A

Asthma

COPD

139
Q

What causes an inspiratory wheeze?

A

Stiff stenosis - cancer, scarring

140
Q

What causes a pleural rub? What does it sound like?

A

Pleurisy
Pneumothorax
Pleural effusion

Walking in snow

141
Q

What do you normally hear in a pleural effusion?

A

Reduced/absent breath sounds

Can have a pleural rub

142
Q

What are the causes of ILD?

A

Idiopathic- ipf
Drugs - methotrexate, amiodarone, nitrofurantoin
Rheumatoid- sarcoidosis, SLE, arthritis, sjrojens.
Occupational - asbestos, soot

143
Q

What are the radiological findings in ILD?

A

CXR- Reticular nodular opacities

CT - honeycombing or ground glass

144
Q

What is the spirometry pattern in ILD?

A 
Restrictive
Reduced FVC (less than 80) but normal fev1
145
Q

What might cause central cyanosis?

A

Desaturation of central arterial blood. Colour is caused by desaturated haemoglobin.

Severe lung disease - COPD, acute severe asthma, PE, severe pneumonia, high altitude

Right to left cardiac shunt (some blood avoids the lungs) - fallots, pda

Abnormal haemoglobin (doesn’t uptake o2) - genetic or drug induced - quinones, sulfonamides.

146
Q

What might cause peripheral cyanosis?

A 
Central cyanosis 
Vasoconstriction- reynaud, beta blockers
Reduced cardiac output - heart failure, shock
Peripheral arterial disease
Peripheral venous disease
147
Q

Why might sats be normal but pa02 down?

A

Anaemia
All the existing haemoglobin is saturated, there is just not enough of it to maintain o2 levels so they are hypoxic. They may not be cyanotic.

148
Q

Which patient groups should have especially tight control of hypertension?

A

Those with existing cardiovascular risk factors

Hyper cholesterol 
Smoking 
CKD
Diabetes
Previous IHD
Rheumatoid arthritis
149
Q

Why might the sats be down but the pa02 normal?

A

Polycythaemia - Increased rbcs measured by an increase in haematocrit

Not all haemoglobin may be saturated and therefore some deoxygenated haem causes cyanosis. But there is so much in total that the pa02 is normal and they are not hypoxic.

150
Q

Is cyanosis related to sats or pa02? Which is more important?

A

Cyanosis is a sign of low sats because the colour comes from deoxygenated haemoglobin.

Pa02 is more important because it is a marker of o2 that reaches the tissue.

151
Q

What is the definition of hypertension?

A

140/90

152
Q

What mechanisms might cause secondary hypertension?

A

Raised sympathetic drive - increases renin - increases raas activation

Decreased perfusion to nephron - increases renin - increase raas activation

Decreased egfr - decreases Na cl in Dct - increases renin - increases rasa activation

Increased aldosterone - increased Na uptake at enac channels

153
Q

Give a lost of causes of secondary hypertension.

A

Horners
Phaeochromocytoma
Carcinoid syndrome

Renal artery occlusion

CKD
Polycystic kidney disease

Conn’s - aldosterone secreting tumour
Cushing’s - high concentration cortisol acts on mineralocorticoid receptor

154
Q

What complications are associated with hypertension?

A

LVH - HF

Atherosclerosis- IHD, stroke

Intracranial haemorrhage

Peripheral vascular disease
Aneurysm
Nephropathy
Retinopathy - aneurosis fugax

155
Q

What investigations would you ask for to investigate secondary hypertension?

A

U and e and Renal ultrasound - renal function
Then CT renal - renal artery stenosis

Urinary catecholamines - phaeochromocytoma
Urine cortisol and dexamethasone suppression- cushings

156
Q

What signs and symptoms would make you suspect a secondary cause of hypertension?

A

Young - under 35
Greater than 180/110, retinopathy, HF at a young age

Sweating, dizziness, tachycardia - high sympathetic
Different bp in each arm - renal artery stenosis
Cushingoid appearance

157
Q

Describe the management of primary hypertension

A

Weight loss and exercise
Reduce salt
Reduce alcohol

Address cardiac risk factors
- smoking, cholesterol

ACE - ramipril for under 55, not pregnant, not diabetic, not black.
Otherwise ca channel blocker - amlodipine.

158
Q

What is the difference between the ca channel blockers? What are they each used for?

A

All act on L type ca channels.

Amlodipine - greater affinity when channels inactive - more often in blood vessels - used in hypertension

Verapamil- greater affinity when channels open - more often in sa node - used in arrhythmia . Don’t use in hf because decrease contractility in any open channels!!

Diltiazem - more often in cardiac myocytes - used in angina

159
Q

How is losartan different from ramipril?

A

Arb - angiotensin receptor blocker .
Same effect except no effect on bradykinin

Therefore decreased side effects - no dry cough or angio oedema

160
Q

What is the appropriate follow up for a patient with hypertension?

A

Yearly checkup

End organ damage - fundoscopy, pulses
Urine dip
ECG
U and e
Cholesterol and lipid profile 
BM
Echo if LVH
161
Q

What is the significance of differentiation between small cell and non small cell lung cancer?

A

Small cell = Short history, aggressive, likely to metastasise quickly
But chemo sensitive

162
Q

What are the causes of angina symptoms?

A 
Atherosclerosis 
Arteriospasm
Aortic stenosis
Anaemia 
Hyperthyroidism
163
Q

What are the side effects of salbutamol?

A

Sympathetic agonist

Tachycardia
Palpitations
Tremor
Hypokalaemia

164
Q

What type of drug is theophylline and how does it act?

A

Xanthine

Antagonises sleepy adenosine just like caffeine

165
Q

What side effects of theophylline?

A

Same as salbutamol..

Tachycardia
Arrhythmia
Tremor
Hypokalaemia

166
Q

How does tiotropium / ipratropium bromide work? What is the difference?

A

Both anticholinergics. Non specific but inhaled acts on M3

Tiotropium - spireva inhalerfor copd control
Ipratropium - nebs for acute exacerbation

167
Q

What are the side effects of ipratropium or tiotropium?

A

Anticholinergic…

Urinary retention
Constipation
Tachycardia
Palpitations

168
Q

Give some differentials for syncope?

A

Cardiac -

Tacchyarrthmia
Bradyarrhthmia
Stoke-Adams attack - transient asystole
Outflow obstruction- aortic or pulmonary stenosis, pulmonary hypertension, hypertrophic cardiomyopathy

Non cardiac

Epilepsy 
Hypo
Postural hypotension 
Vasovagal - hyper stimulated vagus - av node block - Brady
PE
Sepsis
169
Q

Give 3 causes of aortic stenosis

A

Bicuspid aortic valve - under 65
Age related calcification- over 65
(Rheumatic fever)

170
Q

Give the main causes of aortic regurgitation

A

Rheumatic fever
Infective Endocarditis
Marfans
Syphilis

171
Q

Give the main causes of mitral stenosis

A

Rheumatic fever

Calcification from old age

172
Q

Give the main causes of mitral regurgitation

A

Cardiomyopathy (any kind)
Post MI papillary muscle rupture
Rheumatic fever
Connective tissue disorders - marfans, ehlers Danlos, osteogenesis imperfecta

173
Q

What are the main types of cardiomyopathy?

A

Ischaemic - post MI heart failure
Hypertrophic - genetic
Dilated - genetic/viral/autoimmune/thyroid

174
Q

What kind of history would make you suspect aortic stenosis?

A

Exercise induced syncope
Then later
(Angina, Dyspnoea)

175
Q

What are the signs of aortic stenosis?

A

Slow rising pulse
Narrow pulse pressure (difference between systolic and diastolic)
Left sided heave

176
Q

Describe the murmur of aortic stenosis

A

Ejection systolic
Crescendo decrescendo
Radiates to carotid
Variable volume of first heart sound

Lub whoosh. Dub

177
Q

What indicates a severe aortic stenosis?

A

Absent 2nd heart sound
Left sided heave
Narrow pulse pressure

178
Q

What is the mechanism of action of digoxin?

A

Blocks Na k atpase therefore blocking the av node

179
Q

What is digoxin used for?

A

Not much. Potent av node blocker so useful in AF when there is a big difference between the apex and radial pulse.

180
Q

What causes radioradial delay?

A

Coarctation of the aorta

Subclavian stenosis

181
Q

Why must you measure an irregular pulse at the apex with the Stethoscope?

A

Some impulses are not transmitted fully as the refractory period is so quick, so the radial pulse is an underestimate.

182
Q

What are the most common organisms associated with infective endocarditis?

A

Natural valve - Streptococcus viridans (from upper Resp tract)
Prosthetic valve - Staph aureus

183
Q

What makes up vegetation found in Endocarditis?

A

Fibrin rich
Some platelets
Adherence and colonisation of bacteria

184
Q

Why is infective endocarditis so life threatening?

A

Host defences struggle to reach the vegetation because-

No blood supply to valves
Fibrin blocks them

185
Q

What are the most common murmurs associated with endocarditis?

A

Aortic regurgitation

Mitral regurgitation

186
Q

What are dukes major criteria for endocarditis?

A

Typical Organism found in 2 cultures or any Organism in 3
Plus
Endocardial involvement- on echo or new regurgitation

187
Q

What are dukes minor criteria for endocarditis?

A

Predisposition
Fever over 38
Vascular signs
Positive culture or echo that don’t meet major criteria

188
Q

Define infective endocarditis according to dukes criteria

A

2 major criteria
1 major 3 minor
5 minor

189
Q

What causes a split second heart sound?

A

Young on inspiration - physiological

Fixed - MI, cardiomyopathy, heart failure, hypertension

190
Q

What is the empirical treatment for infective endocarditis?

A

Benzylpenecillin plus gentamicin
Or
Vancomycin plus gentamicin

191
Q

What are the main risk factors for infective endocarditis?

A 
IVDU
Valve disease
Congenital abnormality 
Prosthetic valve
Previous endocarditis
192
Q

What is a sign of LVH? What is a sign of cardiomegaly?

A

LVH - left sided heave

Cardiomegaly- displaced apex beat

193
Q

What are the signs of mitral regurgitation?

A

Malar flush
Displaced apex beat - Cardiomegaly
Palpable thrill

193
Q

Describe the murmur of mitral regurgitation

A

Pan systolic
Radiates to axilla
Rumbling

194
Q

What are the signs of mitral stenosis?

A

AF
Malar flush
Loud 1 st heart sound

195
Q

Describe the murmur of aortic regurgitation

A

High pitched early diastolic
Like a cymbal
Lub d tahhh
Exaggerated left sternal edge on expiration

196
Q

What are the signs of aortic regurgitation?

A 
Collapsing pulse
Wide pulse pressure 
Displaced apex beat - cardiomegaly 
Quincke's sign - capillary pulsation
De Musset's sign - head bobbing
197
Q

Describe the murmur of mitral stenosis

A

Rumbling low pitch mid diastolic murmur with an opening snap
Exaggerate with the bell at apex leaning left

Lub de derrrr

198
Q

Describe the severity grading of COPD

A

FEV1 % predicted

> 80% Stage 1 - Mild
50-79% Stage 2 - Moderate
30-49% Stage 3 - Severe
< 30% Stage 4 - Very severe

199
Q

What is Kartagener’s syndrome?

A

dextrocardia or complete situs inversus
bronchiectasis
recurrent sinusitis
subfertility

200
Q

Give 4 causes of bronchiectasis

A

CF
Post infective - TB, pertussis, pneumonia
Ciliary dysmotility eg Kartagener’s
Allergic bronchopulmonary aspergillosis

201
Q

What is the most common type of lung cancer in non-smokers?

A

Adenocarcinoma

202
Q

What is your first differential for an ecg with a rate of 150?

A

Atrial flutter with 2:1 block

203
Q

What are the differences between type 1 and type 2 respiratory failure?

A

Type 1 is low o2
Caused by Alveolar issues across the the membrane. Peripheral o2 chemoreceptors in the carotid and aortic arch trigger hyperventilation so co2 is blown off
Eg, PE, pneumonia, ASD, VSD

Type 2 is low o2 plus high CO2
Caused by pump failure as even though chemoreceptors are triggered, hyperventilation is not possible.
Eg tiring in near fatal asthma, neuromuscular, opioids, obesity, COPD

204
Q

How long is the window of opportunity to treat an MI with PCI?

A

2 hours

otherwise thrombolysis

205
Q

How is torsades de pointes treated?

A

IV magnesium

206
Q

Describe the ECG of hypokalaemia

A

In hypokalaemia U have no pot of T, but a long PR and a long QT

U waves
Absent T
Long PR
Long QT

207
Q

What are the main causes of torsades de pointes?

A

Long QT
Hypokalaemia
Antipsychotics

208
Q

How would you decide whether to use rate control or rhythm control for chronic AF?

A

Rate - elderly, hx of IHD

Rhythm - young, symptomatic, heart failure

209
Q

What drugs are used to rate control AF?

A 
Beta blockers (not sotalol)
Ca channel blocker (verapamil or diltiazem)
Digoxin
210
Q

What drugs are used to rhythm control AF?

A

Sotalol
Flecainide
Amiodarone

211
Q

What is the treatment for paroxysmal AF?

A

Flecainide

“Pill in pocket”

212
Q

How would you treat acute fast AF?

A

Electrical cardioversion

or amiodarone if not available

213
Q

What are the side effects of amiodarone?

A

Pulmonary fibrosis
Hypo and hyperthyroid
Heptatotoxic
CYP inhibitor

214
Q

What is amiodarone used for?

A

Chemical cardiovesion of:

Acute fast AF (when electrical unavailable)
VT
VF

215
Q

What are the causes of heart block?

A

Beta blockers
Ca channel blockers
Digoxin

IHD
Infiltrative - sarcoidosis, haemochromatosis
Infective - endocarditis, Lyme disease

216
Q

What are the contraindications to PCI for MI?

A

Onset of symptoms greater than 2 hours

Intolerance to antiplatelet

217
Q

Which drugs are contraindicated in heart block?

A

Beta blockers
Ca channel blockers
Digoxin
Amiodarone

218
Q

How is heart block treated?

A

Pacemaker

Atropine if haemodynamcally unstable

219
Q

What is the relevance of Starling’s curve to heart failure?

A

Left ventricular dysfunction leads to decreased contractility of the heart (the gradient of the starling curve)

This means that for any given end diastolic volume, there is a decreased cardiac output

Junior blocks (12 decks)

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