13 Flashcards

1
Q

How do class Ia, Ib, Ic antiarrhythmics work?

A
  • Ia – Lengthen AP duration
  • Ib – Shorten AP duration
  • Ic – No significant effect on AP
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2
Q

What are some common symptoms of pulmonary TB?

A
  • Haemoptysis.
  • Cough.
  • Sputum.
  • Chest pain.
  • Systemic symptoms of infection.
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3
Q

Antimuscarinics MOA in asthma

A

o Block the activity of the muscarinic acetylcholine receptor (blocks ACh binding to muscarinic receptors)
o This results in bronchial dilation + decreased secretions

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4
Q

Side effects of amiodarone (class III anti-arrthymatic)

A
  • Blue-grey skin discolouration
  • Photosensitivity
  • Lung fibrosis
  • Corneal deposits
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5
Q

What is coarctation of the aorta?

A

Narrowing of a short section of the aorta

It’s rare

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6
Q

MOA of streptokinase

A

Activates plasminogen to plasmin which is a fibrinolytic enzyme

Used in acute MI

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7
Q

How are diffusion and perfusion affected in obstructive lung disease?

A

Not much, it is a ventilatory problem.

  • Diffusion affected in emphysema due to parenchyma destruction.
  • Perfusion affected in end stage (cor pulmonale).
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8
Q

What do Th2 cells produce?

A

IL-4 which stimulates IgE

IL-5 which activates eosinophils

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9
Q

What does an atheroma contain?

A

o Macrophage cells
o Lipids
o Calcium
o Variable amount of fibrous connective tissue

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10
Q

What 2 types of test for TB are there?

A

1) Mantoux tuberculin skin test.

2) Interferon gamma release assay.

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11
Q

Blue bloaters (bronchitis)

A
  • Coughs up lots of sputum
  • Oedematous ankles
  • Cyanosed
  • Overweight
  • Sleep apnoea
  • Do into ventilatory failure early on
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12
Q

Tissue changes in the kidney in hypertension

A
  • Glomerular damage
  • Shrink
  • Renal artery stenosis
  • Arteriosclerosis leading to progressive ischaemia of the nephrons
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13
Q

What happens when you breathe out if you lack alveolar integrity?

A

Pleural pressure will exceed > pressure in small airway, so it would collapse prematurely on exhalation.

Hyperexpanded chest in asthma and emphysema

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14
Q

What are arterial blood gases? When is it indicated?

A

Gives you:

  • PaO2.
  • PaCO2.
  • Acid-base balance (pH, HCO3, H+ etc).
  • When oxygen sats are 90-92% or lower.
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15
Q

Overview of pharmacological treatment of patients with LV HF

A

Patients w/ LV HF should be on ACE inhibitors, beta blockers + ARBs for the rest of their life – because the cumulative effect of these drugs doubles life expectancy (triple therapy)

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16
Q

What is the point of a granuloma? What happens within it in TB? What is the main disadvantage of this?

A

To try and contain the focus of infection.

  • Caseating necrosis to prevent dissemination of TB.
  • Dampens the host immune response.
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17
Q

1st degree heart block

A

QRS normal
P wave present
Long PR interval

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18
Q

What is wheeze?

A

A musical noise produced by air moving through narrowed airways (airway obstructed)

o Obstruction of airways within chest causes wheezing w/ expiration – airways get narrower because lungs get smaller

Contrast with stridor which occurs in inspiration – e.g. whooping cough, epiglottitis, foreign body

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19
Q

How is sinus bradycardia treated?

A

Investigate and remove cause:

  • Beta blockers
  • Hypothyroidism
  • Heart block - recent MI, digoxin toxicity, B-blockers

Usually manged consevatively

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20
Q

Which cytokine is skewed in asthma?

A

Greater Th2 production

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21
Q

Haemodynamic model for progression of heart failure

A
  • Sympathetics and RAAS activated
  • Increased preload and afterload
  • Consequence is very dilated heart
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22
Q

MOA and example of a biguanide

A
  • Metformin

- Increases utilisation of glucose by increasing uptake and decreasing gluconeogenesis

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23
Q

List and explain the 3 factors regulating stroke volume

A

o Preload: the degree of stretch before contraction

o Contractility: the forcefulness of contractions

o Afterload: the pressure that must be exceeded for the ventricle to eject blood

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24
Q

Non-dihydropyridines

A

Calcium antagonists

  • Verapamil, diltiazem (class IV anti-arrithymatics)
  • Slow heart rate
  • Useful for angina
  • Not for use in heart failure
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25
Q

MOA of acarbose

A

Inhibits intestinal alpha-glucosidases and delays absorption of starch and sucrose

Antidiabetic drug for DM2

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26
Q

What does low compliance indicate?

A

Stiff lung which indicates high elastic recoil.
E.g. pulmonary fibrosis

Compliance affects how much energy is required to generate pressure gradient for ventilation.

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27
Q

Torsades de pointes

A

o Commonly seen in patients w/ pre-existing bradycardia especially if give class I anti-arrhythmic drugs

o A feared side-effect of drugs

o Exacerbated by low potassium and magnesium

o Treatment – magnesium

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28
Q

Microbiology of Mycobacterium Tuberculosis

A
  • Gr+
  • Obligate aerobe
  • Stains with Ziehl-Neelson
  • Bacilli are non-motile, non-sporing and non-capsulated
  • Rod
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29
Q

What are the results of left ventricular dysfunction?

A
  • SOB
  • Peripheral oedema
  • PND
  • Raised JVP
  • Orthopnoea
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30
Q

Name some common restrictive lung diseases.

A
  • Pulmonary fibrosis (IPF).
  • Chest wall deformity (kyphosis).
  • Obesity.
  • Neuromuscular disease.
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31
Q

Pheochromocytoma

A
  • Adrenal medullary (neuroendocrine) tumours secreting catecholamines
  • Alpha mediated vasoconstriction
  • Beta mediated cardiac stimulation
  • Raised BP and tachycardia (may cause cardiomyopathy)
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32
Q

MI treatment for STEMI

A

o Primary percutaneous coronary intervention (PCI)

o Thrombolysis >20% of patient given thrombolysis do not achieve reperfusion so start with PCI
 Significantly lower mortality w/ PCI compared to thrombolysis because of high rate of reperfusion

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33
Q

What % of all CHD deaths are attributable to smoking?

A

20

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34
Q

Left bundle branch block

A

Negative V1 - W
Positive V6 - M

WiLLiaM

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35
Q

Causes of tachycardia due to increased SNS activity

A
  • Exercise (after the 1st minute)
  • Fear
  • Heart failure
  • Adrenaline
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36
Q

Cardiogenic shock

A
  • Extreme version of heart failure
  • Large heart attack where they kill off so much heart and become shocked
  • Stop perfusing brain and kidneys properly
  • Results in death
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37
Q

Step 3 asthma treatment

A

Corticosteroid + long acting beta agonist combination (salmeterol) - Regular use

Short acting beta agonist (symptomatic)

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38
Q

2nd degree type 1 heart block

A
  • QRS irregular
  • P wave present
  • AV node slows till P wave delivered which doesn’t get conducted to ventricles
  • PR interval becomes progressively longer until QRS fails to appearbu
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39
Q

Class IV example and effect on AP

A

Verapamil, Diltiazem

  • Blocks Ca2+ channels
  • Prolong conduction and refractoriness in SA and AV node
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40
Q

Pathophysiology of right sided heart failure

A

Fall in CO –> fall in renal perfusion –> increased ADH, increased aldosterone –> Na+ and H2O retention

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41
Q

What is alveolar ventilation?

A

The amount of air sitting in the terminal airways where gas exchange is taking place.
- (Tidal volume - dead space) x respiratory rate.

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42
Q

3 unique properties of cardiac cells

A
  1. Automaticity
  2. Excitability
  3. Refractoriness
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43
Q

When are beta blockers contraindicated?

A
	Asthma
	Cardiogenic shock
	Hypotension
	AV block
	Untreated pheochromocytoma side effects (neuroendocrine tumour of medulla of adrenal glands)
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44
Q

What 3 factors contribute to the level of transmission of TB?

A

1) Number of individuals susceptible to the disease.
2) Number of people exposed to the disease.
3) Duration of time a person with TB is undiagnosed and infectious for.

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45
Q

What is cardiac neurosis?

A

Da Costa’s Syndrome

  • A set of symptoms similar to heart disease e.g. chest pain, dyspnoea, fatigue etc.
  • No physical findings
  • It’s considered as a form of anxiety disorder
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46
Q

Causes of haemoptysis

A

o Lung cancer – haemoptysis is a red flag for lung cancer; is most common cause of cancer deaths

o TB – kills 3,000,000 people every year (more than AIDS +tropical diseases (malaria) combined)

o Bronchiectasis – chronic mucoid sputum production, may have v. inflamed, fragile airways so may

o Pulmonary oedema – causes pink frothy sputum

o Pulmonary embolism – sudden blockage of a major artery in the lung, usually by a blood clot

o Pneumonia – causes rusty sputum, blood is mixed through the purulent sputum

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47
Q

What tests would you perform prior to treating TB?

A
  • HIV.
  • Hep B and C.
  • Liver function test, ALT.
  • Visual acuity when using ethambutol.
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48
Q

Which sites are involved in TB?

A

Pulmonary TB (85% of all cases)

Extra-pulmonary sites

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49
Q

Aortic dissection

A
  • Sudden, tearing, knife-like pain
  • Excruciating
  • Radiate to back
  • Abdominal pain (20-40% of cases)
  • Often seen in elderly population w/ hypertension
  • Seen in people with stressful jobs with hypertension at a young age
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50
Q

Bronchopneumonia

A
  • Inflammation of walls of bronchioles w/ multiple foci of consolidation, affecting 1 or more lobules
  • Most common form
  • Infants + elderly more susceptible
  • Any organism
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51
Q

List rapid (hrs) causes of breathlessness

A

Acute asthma
Pneumonia
Pulmonary oedema
Acute hypersensitivity pneumonitis

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52
Q

Which immune cells are involved in asthma?

A

o Antigen presenting cells
o T cells (CD4+)
o B cells – produce IgE which stick to mast cells + eosinophils
o Mast cells – activate eosinophils vis leukotriene B4
o Eosinophils – cause late reaction

High eosinophil count means allergy or parasites (worms)

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53
Q

MOA of Isoniazid

A

Disrupts synthesis of mycolic acid

TB drug (bacteriostatic)

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54
Q

Class Ib example and effect on AP

A

Lidocaine

  • Block Na+ channel
  • Shortens AP
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55
Q

QRS narrow and ragged atrial spikes rather than P waves

A

Atrial fibrillation

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56
Q

How is any tachycardia with hypotension/collapse treated?

A

 Emergency electrical cardioversion w/ sedation if necessary
 Treatment for collapsed patient with VT same for VF

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57
Q

What happens to the granuloma in latent TB?

A

The TB bacilli become dormant inside the granuloma.

- Only pathogenic again upon reactivation.

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58
Q

When are class IV antiarrhythmics used?

A

Prevent recurrence of paroxysmal supra-ventricular tachycardia

Reduce ventricular rate in patients with atrial fibrillation

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59
Q

Tissue changes in the heart in hypertension

A
  • Coronary atheroma
  • Left ventricular hypertrophy
  • Increased peripheral resistance
  • Decreased flow in cardiac vessels and endothelial dysfunction
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60
Q

Define atheroma

A

A nodular accumulation of degenerative material in the tunica intima of the artery walls

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61
Q

How do ADH antagonists work?

E.g. tolvaptan

A

Bind to vasopressin receptors + block the action of ADH – this is a newer treatment

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62
Q

What happens in the early phases of hypertension?

A

Blood volume and cardiac output increase due to sodium and water retention

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63
Q

What is the primary site of infection known as in TB?

A

The Ghon focus.

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64
Q

Asthma spirometry findings

A

FEV1 - significantly reduced
FVC - normal
FEV1/FVC = <70%

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65
Q

How to diagnose aortic coarctation?

A

Compare femoral pulse to radial pulse.

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66
Q

What happens when exercise/stress level increases and expiration becomes more forceful?

A

Becomes an active process.

- Internal intercostals and abdo muscles used.

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67
Q

Innate defences of the respiratory tract

A
  • Alveolar macrophages - phagocytose and produce cytokines
  • Macrophages - phagocytose and APC
  • Dendritic cells - APC and cytokine production
  • Intravascular macrophages
  • Cytokines important for inflammatory response
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68
Q

What type of diuretics are these?

o	Bendroflumethiazide
o	Chlortalidone
o	Cyclopenthiazide
o	Metolaone
o	Indapamide
A

Thiazide (block Na+/K+¬¬ cotransport in DCT)

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69
Q

The combined presence of S3 and S4 is a quadruple gallop.

When does it occur?

A

 Also known as a hello-goodbye gallop

 Occurs in patients with heart failure

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70
Q

What is primary hypertension?

A

o 90-95% of patients with hypertension have primary hypertension
o Unknown cause
o Probably environmental (high salt intake) or genetic
o There are 2 phases of abnormally as people develop hypertension – early + late

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71
Q

Other than the SAN, what other pacemaker sites are there?

A

Bundle of His - 40 bpm

Purkinje cells - 15 bpm

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72
Q

MOA of Cholestyramine

A

A positively charged drug which binds to negatively charged bile acids, inhibiting their absorption.

It is a bile acid sequestant.

Cholestyramine may also be used to treat itching in people with too much bile acid caused by a certain type of liver/bile duct disease (partial biliary obstruction). This medication is known as a bile acid-binding resin. It works by removing bile acid from the body.

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73
Q

Causes of bardycardia caused by increased PNS activity

A
  • Sleep
  • Vasovagal syncope (fainting)
  • Fitness – elite athlete may have HF of 30bpm
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74
Q

What is the definition of type 2 respiratory failure (hypercapnia)? What does it indicate?

A
  • Low PaO2 (less than 8kPa).

- High PaCO2 (greater that 6kPa).

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75
Q

What causes the right heart to fail?

A

Left sided failure

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76
Q

Location of ectopic pacemakers can change its effect on SAN and its rhythm. List 3 different types of pacemakers

A

o Atrial pacemaker: an ectopic pacemaker located in the atria - can cause atrial conduction to be faster
o Junctional pacemaker: ectopic pacemaker located near AVN and septum
o Ventricular pacemaker: located in ventricles

o Other pacemakers can lie within the pulmonary vein and thoracic vein walls

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77
Q

What class of antiarrhythmics are the following?

Quinidine
Ajmaline
Procainamide
Disopyramide

A

Ia

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78
Q

MoA of amiodarone (class III antiarrhythmic)

A

 Potassium channel blocker

 Extends the action potential (refractory period) and delays repolarisation

 Blocks transmission of abnormal signals and terminating arrhythmia

 Also acts like a beta blocker (class II)

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79
Q

How do baroreceptors determine BP?

A

 From moment to moment the firing of the baroreceptors (they are the most important system in BP control)

 V. sensitive to changes in BP – change firing rate within course of a single heartbeat (diastolic vs systolic pressure)

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80
Q

How is pneumonia classified microbiologically?

A

Typical and atypical

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81
Q

Examples of obstructive lung diseases

A
  • COPD
  • Asthma
  • Bronchiectasis
  • CF
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82
Q

Myocardial rupture

A
  • Fibrous scar tissue following MI
  • Usually occurs within first 2 weeks
  • Sudden deterioration
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83
Q

What happens to pleural pressure as you breathe out?

A

Pleural pressure increases which leads to collapsed airway wall

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84
Q

What is purulent sputum?

A

Yellow/green

  • Due to myeloperoxidase from granulocytes (neutrophils/eosinophils)
  • Myeloperoxidase involved in free radical generation pathway to kill bacteria
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85
Q

List causes of HF

A
o	Past heart attacks
o	CHD
o	High blood pressure
o	Heart valve disease
o	Heart muscle disease or inflammation of the heart
o	Congenital heart defects
o	Lung conditions
o	Alcohol/drug abuse
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86
Q

What is pleuritic pain?

A

o Injured/inflamed parietal pleura

o Sharp, stabbing, worse on inspiration

o Pneumonia, pulmonary embolism, pneumothorax

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87
Q

Name some of the processes that contribute to respiratory physiology.

What are the 4 categories that they can be broken down into?

A
  • Respiratory drive (CO2 or hypoxic drive).
  • Ventilation (air flow): chest wall w/muscles, airway resistance, lung compliance.
  • Diffusion (gas exchange): alveoli.
  • Perfusion: blood O2 carrying capacity and pulmonary circ.
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88
Q

Colours of sputum

A

 Mucoid (clear/creamy)
 Purulent (yellow/green)
 Bloodstained – haemoptysis

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89
Q

JVP waveform summary

A
  • A wave– produced by atrial systole
  • X – descent occurs when atrial contraction finishes
  • C wave – caused by rapid increase in RV pressure before tricuspid valve closure
  • V wave – develops as venous return fills the RA during ventricular systole
  • Y descent – follows the V wave when the tricuspid valve opens (atrial empty into ventricle)
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90
Q

Adverse effects of thiazide diuretics?

A

o Hyponatraemia, hypokalaemia, hypomagnesemia

o Hyperuricemia, hypercalcaemia

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91
Q

What can cause acidaemia (low pH) in the blood?

A
  • Resp: high CO2 (hypercapnia).

- Metabolic: low HCO3.

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92
Q

Stenosis vs sclerosis

A

Aortic stenosis is thickening and tightening of the valve that leads to the heart having to work harder and the possibility of not enough blood being delivered to the body.

Aortic sclerosis is thickening of the valve without any significant effect on the function of the valve itself.

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93
Q

Langerhans giant cells (TB)

A

 What you see when looking at TB under microscope

 Fused macrophages oriented around tuberculosis antigen w/ multiple nuclei in periphery

 It represents the most successful type of host tissue response
 When the population of activated lymphocytes reaches a certain size:
• Cutaneous delayed reactivity to tuberculin, or tissue hypersensitivity manifests
• The spread with which this occurs, varies, but generally will have development within 3-9 weeks after infection
 Some macrophages may migrate to lymph nodes + carry bacterium  spreads infection

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94
Q

Cause of type II respiratory failure

A

Alveolar hypoventilation

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95
Q

What are class V antiarrhythmics?

A

Agents that work by other or unknown mechanisms

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96
Q

3rd degree (complete) heart block

A
  • QRS regular
  • Unrelated P wave to QRS
  • Ventricular rate usually less than 40bpm
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97
Q

Examples of upper respiratory tract infections

A
  • Pharyngitis, tonsilitis, laryngitis, sinusitis

- Otitis media - due to eustachian tube

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98
Q

Describe Phase 3 cardiac myocyte action potential

A

Second period of repolarisation caused by continual outflow of K+ and closure of Ca2+ channels

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99
Q

MOA of cisplatin

A
  • Forms a reactive complex that causes intrastrand cross-linking and denaturation of DNA
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100
Q

Atopy and asthma

A
  • Dendritic cell presents to T cell which causes the production of IL-4 and IL-5
  • Th2 signals to B cells to produce IgE
  • Mast cells degranulate when antigen binds
  • Cytokines activate T and B lymphocytes and attract eosinophils
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101
Q

What can cause normal ventilation but decreased perfusion?

A
  • Right to left cardiac shunt (no oxygenation of blood).
  • Pulmonary emboli (areas left un-perfused).
  • V/Q mismatch.

Enough ventilation but not being perfused!

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102
Q

Course of heart failure

A
  • First acute event e.g. MI
  • Acute heart failure
  • Treated and recovery OR chronic heart failure
  • Chronic heart failure can only occur if acute is treated
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103
Q

MOA of digoxin

A
  • Blocks Na+/K+ ATPase pump
  • Increases intracellular Na+
  • Decreases intracellular K+
  • Increased Na+ reduces Ca2+ exchange by reducing Na+ gradient
  • Overall result is increased intracellular Ca2+ producing a POSITIVE INOTROPIC EFFECT
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104
Q

Does eosinophilic and neutrophilic reactions produce green or yellow sputum?

A

Green

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105
Q

Chemo-reflexes in HF

A

o Reflex initiated by the stimulation of chemoreceptors (e.g. carotid + aortic bodies) by changes in CO2, H+, O2 conc. in blood
o This is abnormally activated in people with HF and leads to increased ventilation

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106
Q

What do alveolar macrophages produce?

A

Cytokines

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107
Q

How do beta blockers improve myocardial function?

A
  • Protect cardio myocytes
  • Slowing the heart
  • Increases diastolic coronary blood flow and reduce myocardial oxygen demands
  • Anti-ischaemic
  • Anti-arrhythmic
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108
Q

What causes ventilatory failure?

A
  • Ventilatory demand (amount of ventilation to exchange CO2) increases.
  • Outweighs ventilatory capacity (amount of ventilation we can maintain before respiratory muscle fatigue).
  • Can’t expel CO2 properly.
  • Type 2 resp failure?
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109
Q

MOA and examples of sulphonylureas

A
  • Gliclazide and tolbutamide
  • Block ATP dependent K+ channels in membrane of pancreatic beta cells, causing depolarisation, calcium influx and insulin release
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110
Q

When are class III antiarrythmics used?

A

In Wolff-Parkinson-White syndrome

(Sotalol:) ventricular tachycardias and atrial fibrillation

(Ibutilide:) atrial flutter and atrial fibrillation

(Amiodarone): hemodynamically stable ventricular tachycardia[6]

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111
Q

How would you treat stable supraventricular tachycardia?

A

IV adenosine

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112
Q

What is anasarca?

A

Anasarca: gross fluid retention, extreme generalised oedema

 Pitting oedema - Needs 5kg weight increase + is gravitational
 Ascites
 Pleural effusions
 Develops over many days/weeks
 Not all ankle oedema is due to HF, differential diagnoses include:
• Stasis
• Chronic venous insufficiency – varicose veins, DVT
• Drugs – dihydropyridines (calcium antagonists)
• Hypoalbuminaemia – e.g. due to nephrotic syndrome

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113
Q

Panacinar emphysema

A

Dilatation of terminal acinus

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114
Q

Describe changes in the brain due to hypertension

A

o Clear associated between hypertension + stroke

o Thrombotic
 Increased carotid atheroma
 Small penetrating arteries – internal capsule

o Haemorrhagic
 Small arteries (charcot-bouchard aneurysms)
 Tiny aneurysms develop in small arteries + may rupture causing intracerebral haemorrhage

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115
Q

MOA of minoxidil

A
  • Opens K+ channels
  • Good vasodilator - hence it’s used for hypertension
  • Fall in peripheral resistance: reflex increase in CO and fluid retention
  • Use with diuretic and beta-blocker
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116
Q

Examples of lower respiratory tract infections

A
  • Bronchitis
  • Pneumonia
  • Lung abscesses
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117
Q

Would patients with obstructive lung disease have more difficulty breathing in or out?

A

Breathing out.

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118
Q

Treatment of AF

A

ABCDE treatment of AF:
• Anticoagulants - warfarin or NOACs not aspirin
• Beta blockers - ventricular rate control
• Calcium channel blockers (verapamil) - ventricular rhythm control
• Digoxin - ventricular rate control
• Electro-cardioversion - rhythm control

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119
Q

Atypical community acquired pneumonia - what is it caused by?

A

Cough and dyspnoea but usually no sputum

Caused by:

  • Mycoplasma pneumonia
  • Chlamydophilia pneumoniae
  • Legionella pneumophilia

Children and young adults

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120
Q

Class III example and effect on AP

A

Amiodarone

  • Blocks K+ channels
  • Prolongs AP
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121
Q

ACS (acute coronary syndrome) is an umbrella term for what?

A
  1. Unstable angina
  2. ST elevation myocardial infraction (STEMI)
     Blocked (full) coronary artery
  3. Non-ST elevation myocardial infarction (NSTEMI)
     Partially occluded coronary artery + raised troponi
  • Acute chest discomfort that lasts more than 10 minutes
  • Usually some myocardial necrosis, evident by rise in cardiac enzymes
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122
Q

Symptoms of simple bronchitis

A
  • Illness begins with irritating, non-productive cough + discomfort behind the sternum
  • Later the cough becomes productive with yellow or green sputum
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123
Q

What type of immune cells combat TB in the lungs?

A

Alveolar macrophages.

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124
Q

Tissue changes in the brain in hypertension

A
  • Thromboembolic stroke - carotid atheroma, effects internal capsule
  • Haemorrhagic stroke - small vessels
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125
Q

Give 6 factors that make TB more common in low/middle income settings.

A

1) Stigma (don’t seek treatment).
2) Infrastructure problems.
3) Conflict.
4) HIV (immunosuppression).
5) Migration.
6) Poverty (cramped conditions no healthcare).

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126
Q

Hypoxia can be caused by?

A

o Impaired diffusion
o Hypoventilation
o Ventilation/perfusion (V/Q mismatch)

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127
Q

Which beta blockers are used for heart failure?

A

o Carvedilol – blocks beta 1, 2 and alpha receptors
o Metoprolol
o Bisoprolol

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128
Q

What happens to the lungs in restrictive lung disease?

A
  • SA reduces.
  • Reduced compliance.
  • Thickened alveolar membrane.
  • Relatively normal airways and airflow

Impaired diffusion.

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129
Q

Silicosis

A
  • Rare
  • Caused by inhalational of silicone dust
  • Upper lobe nodules and lymph node calcification
  • Looks like sarcoidosis - this also affects upper lobes and is associated with granuloma formation
  • Predisposes to TB and lung cancer
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130
Q

Chest wall compliance is affected by which factors

A
	Curvatures of spine (kyphosis, scoliosis)
	Rib fractures
	Ossification of costal cartilage
	Obesity
	Position (supine/prone)
	Pneumothorax, hydrothorax
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131
Q

Typical pneumonia causative agents

A
  • Streptococcus pneumonae
  • Haemophilus influenzae
  • Moraxella catarrhalis
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132
Q

Symptoms of heart block

A
  • Dizziness
  • Fainting
  • Fatigue
  • SOB
  • Chest pain
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133
Q

Aortic valve stenosis

A
  • Aortic S2 often soft
  • Slow rising carotid pulse
  • Often left ventricular hypertrophy on ECG
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134
Q

At what systolic pressure would you treat hypertension?

A

140

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135
Q

What does QRS complex correspond to?

A

Ventricular depolarisation

o Reflects slow conduction from the AVN, down the bundle of His and up the purkinje fibres

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136
Q

Why must TB droplets be small?

A
  • To remain suspended in the air for a longer period of time.
  • To reach the terminal air passages (alveoli).
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137
Q

Where on the cardiac action potential do class IV drugs work?

A

Phase 2

  • Blockage of Ca2+ channels prevents Ca2+ influx
  • Prolongs conduction and refractoriness in SA and AV nodes
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138
Q

Describe chronic primary hypertension

A

Usually blood volume + CO are normal

Confirming that the major underlying factor is an increase in systemic vascular resistance at this stage
o Thickening of wall of vessels
o Reduction in lumen diameters

What came first? – structural changes in the vasculature or increased BP

Abnormalities can be seen in small vessels
o E.g. renal glomerulus (L is normal, R shows hypertension – eosinophilic material fills vasculature)

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139
Q

What is protodiastolic gallop aka ventricular gallop?

A

S3 added heart sound

 Sounds like Kentucky
• S1 = ken
• S2 = tuck
• S3 = y

 Heard at beginning of diastole after S2

 Low pitch

 Benign in youth, some trained athletes, sometime in pregnancy

 Occurs with cardiac problems – failing LV + dilated congestive HF

 Caused by oscillation of blood back + forth between the walls of the ventricles after a rush of blood from atria

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140
Q

What class of antiarrhythmics are the following examples of?

Adenosine
Digoxin
Magnesium sulphate
Atropine

A

Class V

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141
Q

Small cell carcinoma treatment

A

Limited stage (to one side of chest, above diaphragm)
• Radical chemotherapy + radiotherapy
• Median survival time 18 months, <20% achieve cure, 5 year survival 25%

Extensive
• Palliative chemotherapy + radiotherapy
• Median survival time 9 months

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142
Q

List changes which cause fluid to leave capillaries and accumulate in tissues (oedema).

A
  • Decreased colloid osmotic pressure – e.g. due to low albumin levels, less pressure pulling fluid into tissues so fluid leaks out
  • Damage to alveolar-capillary membrane – becomes less resistance and causes pulmonary oedema
  • Lymphatic blockage – e.g. in some cancers

• Increase in hydrostatic pressure (main factor):
o In the failing heart, heart requires progressively higher pre-load to work enough to keep you alive
o At a critical point, the increased filling pressure in the LV causes the hydrostatic pressure in pulmonary capillaries to go up so high that the fluid transudes out of capillaries into tissues faster than lymphatics can take it away - If this happens in the pulmonary circulation, it leads to pulmonary oedema

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143
Q

What does giant V waves (JVP waveform) indicate?

A

Tricuspid regurgitation

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144
Q

What could an incomplete rupture lead to?

A
  • Frank rupture
  • Formation of false aneurysm
  • LV diverticulum
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145
Q

What is an acid-fast bacteria?

What type of test is used for this?

A

Maintains its colour integrity when acid is applied to it.
- Ziehl-Neelsen stain.

Acid-fast organisms like Mycobacterium contain large amounts of lipid substances within their cell walls called mycolic acids.

These acids resist staining by ordinary methods such as a Gram stain. It can also be used to stain a few other bacteria, such as Nocardia.

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146
Q

Causes of type I respiratory failure

A
  • V/Q mismatch

- Asthma, pulmonary oedema, PE, pneumonia

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147
Q

Ectopic foci

A

Ectopic foci can initiate and maintain electrical impulses in emergency situations e.g. is SAN blocked

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148
Q

Phase 1 of cardiac action potential

A
  • Closure of Na+ channels
  • K+ still continues to move out down concentration gradient
  • Voltage gated K+ channels open
  • Cl- influx
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149
Q

MOA of alpha blockers (treats HTN)

A
  • Block peripheral alpha-1 receptors
  • First dose hypotension
  • Example: doxazosin
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150
Q

Pulmonary oedema

A
  • Abrupt (mins)
  • Breathlessness
  • Difficulty talking
  • Orthopnoea – lying down may kill them becuasefluid accumulates in alveolar spaces.
  • Frightening – experience ‘angor animi’ fear of certain impending death
  • Use of accessory breathing muscles
  • Pink, frothy sputum – alveolar fluid with blood
  • Sweating
  • Cold, clammy
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151
Q

What is the main virulence factor of TB and the reason it isn’t phagocytosed?

A

It’s thick waxy mycolic acid capsule.

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152
Q

What is NEP? How is it involved in diuresis?

A
  • Neutral endopeptidase
  • Converts ANP and BNP to breakdown products
  • Blocking it gives more ANP and BNP so more diuresis

E.g. Sacubitril

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153
Q

What are the 2 types of drug resistant TB and what are they resistant too?

A

1) MDR (multi drug resistant) TB: Rifampicin and isoniazid.

2) XDR (extensively drug resistant) TB: Rifampicin, isoniazid, fluroquinolone, other drugs.

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154
Q

Law of Laplace

A

Tension in wall of left ventricle = pressure within ventricle x volume within ventricle DIVIDED by wall thickness (this ratio is the other factor in setting the afterload).

  • As ventricle dilates, wall tension increases
  • As heart starts to contract, it has to exceed wall tension before it contracts
  • As afterload increases, CO decreases
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155
Q

How can you diagnose occupational asthma?

A

Ask if symptoms worse at work and better when they are away

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156
Q

What test is used to test lung (ventilation) function most accurately?

How can this be used to determine the type of lung disease a patient has?

A

Spirometry.

  • FEV1/FVC ratio of 0.7 = obstructive.
  • FEV1/FVC ratio of 1 = restrictive.

For obstructive FEV1 is reduced but FVC is normal.

For restrictive both FEV1 and FVC would be reduced so ratio remains normal.

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157
Q

What is tachypnoea?

A

Faster breathing that normal (>24 breaths per min)

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158
Q

MI treatment for NSTEMI

A

o Anti-platelets – aspiring and one of: clopidogrel, ticagrelor, prasugrel
o LMWH
o Statin – high dose to reduce cholesterol + stabilise plaque
o Anti-ischaemic (beta blocker, nitrates) – beta blocker therapy decreases heart rate + amount of stress of plaque

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159
Q

Workplace infections

A

Human sources - influenza, pneumococcus C, pneumoniae, ,tuberculosis.

Animal sources - anthrax, psittacossis (from birds).

Environmental sources - legionellosis.

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160
Q

QRS regular, P wave present, 35bpm

A

Sinus bradycardia

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161
Q

Dihydropyridines

A

Calcium antagonists (e.g. nifedipine)

  • Block Ca2+ entry into smooth muscle so smooth muscle relaxes + vasodilates

Treatment of hypertension

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162
Q

MoA of calcium channel blockers

A

 Slows the movement of calcium into the heart and blood vessel walls

 Reduces heart rate, LV contraction, blood pressure and reduced myocardial O2 demand

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163
Q

Simple pneumoconiois

A
  • Associated with dust inhalation

- Nodules on x-ray

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164
Q

Examples of angiotensin II receptor blockers (ARBs) and their suffix

A
  • Losartan
  • Valsartan
  • Candesartan

-sarta

Used to lower blood pressure

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165
Q

What are the 2 types of presentation of TB by timing?

A

1) Primary TB.

2) Latent/reactivated TB

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166
Q

Large volume of sputum expected in?

A

Bronchiectasis and bronchioloalveolar carcinoma

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167
Q

What 3 features characterise asthma?

A
  1. Reversible airflow obstruction
  2. Airway inflammation
  3. Increased airway responsiveness
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168
Q

MOA of nicotinic acid

A

Vitamin B3
- Increases HDL + reduces release of VLDL from the liver

lipid disorders and atherosclerotic cardiovascular disease

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169
Q

What are U waves on ECGs?

A

The source of the U wave is unknown. 3 common theories regarding its origin are:

  1. Delayed repolarisation of Purkinje fibres
  2. Prolonged repolarisation of mid-myocardial “M-cells”
  3. After-potentials resulting from mechanical forces in the ventricular wall

Prominent U waves seen in bradycardia.

Abnormally prominent U waves are seen in severe hypokalaemia.

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170
Q

What are the 2 types of presentation of TB by site?

A

1) Pulmonary TB.

2) Extra-pulmonary TB.

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171
Q

Pathogenesis of hospital-acquired pneuomonia (HAP)

A
  • Inhalation/aspiration
  • Direct spread - ET tube
  • Ventilator associated pneumonia - pneumonia 48hrs after being ventilated
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172
Q

List causes of chest pain

A
o	Pleural pain
o	Cariac pain
o	Upper retrosternal pain (tracheitis)
o	Musculoskeletal pain
o	Retrosternal pain – mediastinal tumour
o	Bone pain – rib metastases
o	Spinal root pain
o	Herpes zoster (shingles)
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173
Q

What can cause normal perfusion but reduced ventilation?

A
  • Pneumothorax.
  • Obstructive lung disease.

Not enough ventilation!

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174
Q

Neurohormonal model for progression of heart failure

A
  • ADH - drink more and retain more fluid
  • Natriuretic peptide - ANP, BNP - excrete more Na+, and hence water
  • Aldosterone (Na+ and water retention, K+ and Mg2+ loss)
  • Endothelin - vasoconstrictor
  • Neuropeptide Y - adrenaline
  • VIP - parasympathetic
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175
Q

What is miliary TB? What is it an example of?

A

Invasion of a blood vessel by TB resulting in spread of TB around the bloodstream.

  • Lungs and bone marrow most often affected.
  • Appears as dots on a CXR.
  • Miliary tuberculosis is present in about 2% of all reported cases of tuberculosis and accounts for up to 20% of all extra-pulmonary tuberculosis cases (liver, spleen, kidneys)
  • Left untreated, miliary tuberculosis is almost always fatal
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176
Q

Modifiable risk factors for atheroma

A
  • Smoking
  • Hypertension
  • Obesity
  • Diabetes mellitus
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177
Q

What is “gas trapping” in obstructive lung disease?

A

When part of the lung cannot empty.

  • Keep filling and filling, hyper-expansion.
  • Ventilation-perfusion mismatching occurs.
  • Results in hyperventilation.
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178
Q

Large cell carcinoma

A
  • Poorly differentiated

- Poor prognosis

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179
Q

How is TB identified in a lab?

A
  • Identification of TB bacillus.
  • Send 3 sputum samples to lab for TB microscopy.
  • Ziehl-Neelsen stain to test for acid fast bacteria.
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180
Q

What is Extra-pulmonary TB (EP.TB)?

What type of patient is it found in?

A
  • TB that is outside the lung via haematogenous or lymphatic spread.
  • More common in children and old people, immunosuppressed
  • TB of spine can cause back pain
  • TB of kidneys can cause blood in the urine
  • Miliary TB
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181
Q

Atheroma risk factors

A

o Modifiable: smoking, DM, obesity, hyperlipidaemia, hypertension, lack of physical activity

o Non-modifiable: family history, gender, age, ethnicity

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182
Q

Consequences of pulmonary hypertension

A

Cor pulmonale

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183
Q

Second degree heart block type 1

A

 Irregular QRS complexes:

 3:2 heart block – 3 P waves for every 2 QRS

 AV node is becoming refractory

 There is an intermittent delay in conduction of normal sinus impulses from the atria to ventricles

 PR interval becomes progressively longer until QRS complex fails to appear

 This sequence is then typically repeated

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184
Q

Treatment of stable ventricular tachycardia

A

 Check and correct hypokalaemia and hypomagnesaemia

 Intravenous amiodarone (preferably via a central line)

 Electrical cardioversion if goes on for 10-15 minutes

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185
Q

Class Ia example and effect on AP

A

Disopyramide

  • Block Na+ channels
  • Prolongs AP
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186
Q

Where is the infarction in an inferior MI?

A

Right coronary artery

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187
Q

Which TB drug may cause vision problems?

A

Ethambutol.

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188
Q

What is farmers lung?

A
  • Allergic reaction to organisms in mouldy hay
  • Inhalation of hat dust or mould such as aspergillus
  • In CT scan you can see centriolobular nodules
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189
Q

What are type 2 cardiac cells?

A

Myocytes

They only fire when simulated (depolarised)

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190
Q

How does digoxin alter the frank-starling curve?

A

Up and to the left

- It is a positive inotrope

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191
Q

Physiological defences of the respiratory tract

A
  • Cough
  • Epiglottic reflex
  • Nasopharynx clears organism for swallowing
  • Epithelial cells produce airway surface liquid
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192
Q

Ventricular fibrillation

A

o Chaotic depolarisation of the ventricles, resulting in an arrested cardiac pump function and immediate death

o VF can only be treated by immediate defibrillation

o Rate is O – no QRS complexes

o Rates are so rapid that the ventricles twitch in a disorganised and chaotic manner

o ECG shows no identifiable waves, no pattern of impulses – hence no CO

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193
Q

Why do patients with heart failure under diuresis become hypokalemic?

A
  • Aldosterone from RAAS causes K+ excretion

- Effect of diuretics results in more Na+ in DCT resulting in more K+ being lost

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194
Q

What happens if you decrease colloid osmotic pressure?

A

Movement of fluid out of the capillaries

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195
Q

Atypical pneumonia causative agents

A
  • Legionella pneumophila
  • Mycoplasma pneumoniae
  • Chlamydiophila pneumoniae
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196
Q

Special points about digoxin

A
  • Big loading dose
  • Narrow therapeutic window
  • Excreted unchanged by the kidneys - don’t use if kidney diseased
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197
Q

Emphysema

A
  • Abnormal enlargement of airspace, distal to terminal bronchioles
  • Destruction of alveoli walls
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198
Q

Which drugs should be avoided in HF?

A

o Calcium antagonists – e.g. amiodipine

o Positive inotropes – e.g. digoxin, levosimendan

o Antiarrhythmics – stop antiarrhythmic in people with HF except amiodarone which is ok

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199
Q

Give examples of normal perfusion but reduced ventilation

A

 Pneumothorax
 Pneumonia
 Obstructive lung diseases (e.g. asthma)

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200
Q

What are the 2 mineralocorticoid (aldosterone) antagonists?

A
  • Spironolactone

- Eplerenone - new + expensive

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201
Q

What type of immunity is important to keep TB in check?

A

Cell mediated

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202
Q

What is renal artery stenosis?

What is its effect on blood pressure?

A
  • Fibromuscular hyperplasia
  • In young women with hypertension which is difficult to control
  • Kidneys don’t get enough blood so they think BP is low
  • Decreased pressure in the afferent arteriole
  • Increase in renin release = increase in angII and aldosterone
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203
Q

Where do loop diuretics work?

A

Block Na+/K+/2Cl- cotransporter in the thick ascending loop of Henle

• Work from lumen of the tubule – need some glomerular function to filter the drug into the tubule

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204
Q

Signs and symptoms of L sided heart failure

A

 Increased rate + work of breathing

 Dyspnea, orthopnoea, paroxysmal nocturnal dyspnoea

 Fatigue

 Rales or crackles heat in lung bases (if heard throughout the lung this indicates pulmonary oedema)

 Cyanosis

 Laterally displaced apex beat (occurs if the heart is enlarged)

 Gallop rhythm

 Heart murmurs may indicate the presence of valvular heart disease as either a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure

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205
Q

At which phase of cardiac myocyte action potential do class III agents work?

A

Phase 3 – Second period of repolarisation caused by continual outflow of K+ and closure of Ca2+ channels

• Class III agents block these K+ channels and prolongs the duration of the AP

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206
Q

Ventricular tachycardia

A

o Is a sequence of 3(+) ventricular beats

o Frequency is usually 110-250bpm

o Often origin around old scar tissue in the heart – e.g. post-MI

o CO is strongly reduced during VT, resulting in hypotension and loss of consciousness

o Can deteriorate into ventricular fibrillation

o Due to rapid discharge of ectopic beats from multiple sites in vernicles

o Patient has palpations and need defibrillation

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207
Q

What is ventilation/perfusion mismatch?

A
  • Part of the lung is not ventilated but IS being perfused.
  • Part of the lung is being ventilated but IS NOT being perfused.
  • Hypoxia.
  • Results in shunt of deoxygenated blood from R -> L heart.
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208
Q

Treatment of asthma

A

o Inhaled corticosteroids and bronchodilators are fine for most people

o Some people make too much IgE (highly atopic) – some drugs can mop up excess IgE

o Monoclonal antibodies

o IL-5 blocker e.g. Mepoluzimab – work for people who have a high eosinophil count in airway + lungs

o If the patient is receiving treatment and not getting better may be due to:
 Poor compliance – not taking medication
 Poor technique – not using proper inhaler technique
 Misdiagnosis

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209
Q

What are the causes of loss of consciousness?

A

Cardiac
o Sudden onset, no aura, no jerks/incontinence, injury common, very pale, immediate recovery

Neurological
o Prodrome/aura, convulsive movements, incontinence, self-harm (tongue), post-ictal confusion

Vasodepressor syncope
o After prolonged standing response to stress, gradual developing faintness, greying out of vision

Carotid sinus hypersensitivity
o Rubbing neck causes syncope

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210
Q

What are some of the side effects of Rifampicin?

A
  • Orange secretions (pee, tears).
  • Nausea.
  • Abdo pain.
  • Hepatitis.
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211
Q

Pre-load

A

Pressure in the ventricles before it starts to contract

- Also called filling pressure

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212
Q

Pink puffers (emphysema)

A

• Thin because of work of breathing
• Pursed lips breathing + leaning forwards
o To give ‘auto ‘PEEP’ expiratory resistance to prevent airway collapse
o Prominent use of accessory breathing muscles
• Go into ventilatory failure later
• May be very breathless but have normal blood gases up to end of disease

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213
Q

Mutations in non-small cell carcinoma

A

EGFR, KRAD, CD44, P16

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214
Q

LRT infections

A

o Pathogens that cause lower RTI - Viral, bacterial, mycobacterial, fungal, protozoal infections

o Includes: bronchitis, pneumonia, lung abscesses

o LRTI as the leading cause of death among all infectious diseases

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215
Q

Describe early primary hypertension

A
  • Increased blood volume + cardiac output
  • Increased sodium retention could account for increase in blood volume
  • May mean that hypertensive patients cannot handle sodium appropriately, or cannot easily excrete sodium
  • Unknown how initial increase in blood volume + CO initiates subsequent changes in systemic volume
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216
Q

What is the anterolateral papillary muscles blood supply?

A

LAD and Left circumflex

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217
Q

Name 2 classes of potassium sparing diuretics

A

Mineralocorticoid receptor antagonists (used to be called aldosterone antagonists because they block effects of aldosterone)

Epithelial sodium channel blockers (ENaC) - block K/Na pump

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218
Q

Frank-starling law

A

o The more the heart fills with blood, the greater the force of contraction
 Increasing pre-load leads to increases ventricular work

o In people with HF, the curve falls downwards and to the right until patient needs an extremely high preload just to have heart function at rest

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219
Q

MoA of digoxin

A

 Inhibits Na+K+ATPase membrane pump, resulting in increased intracellular Na+ and decreased intracellular K+

 Sodium calcium exchanger tries to extrude the sodium by pumping in more calcium – positive inotropic effect

 Strengthens ventricular contractions so that the heart is able to pump more blood with each beat

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220
Q

Chronic bronchitis involves?

A

o Mucus glands hypertrophy
o Smooth muscle hypertrophy
o Goblet cell hyperplasia
o Inflammatory cell infiltrate – lymphocytes + neutrophils (not eosinophils)
o Excess mucus – because goblet cells + mucus glands increase in number

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221
Q

Atrial flutter with 2:1 AV conduction

A
  • 2 P waves for every 1 QRS
  • Sawtooth appearance of P wave!!
  • Narrow complex tachycardia
  • Atrial rate 280bpm, ventricular 140bpm
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222
Q

What are some of the problems with the Mantoux test? (TST).

A
  • False positives: Low specificity. Previous BCG or incorrect reading.
  • False negatives: Low sensitivity. Immunosuppression could impact.
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223
Q

What are some systemic symptoms of infection?

A
  • Fever.
  • Chills.
  • Weight loss.
  • Fatigue.
  • Appetite loss.
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224
Q

Chronic airway changes in asthma

A

Subepithelial fibrosis

Smooth muscle hypertrophy

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225
Q

Causes of pneumoconiosis

A

o Coal dust
o Silica
o Asbestos

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226
Q

What is essential hypertension?

A
  • Primary hypertension
  • 90-95% of cases
  • No known causes
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227
Q

Chronic heart failure symptoms

A

o Exertional breathlessness, relieved by rest – may also be related ischaemia
o Orthopnoea
o Swollen abdomen – ascites caused by severe LV dysfunction, R heart failure
o Nocturnal cough
o Episodes of PND
o Ankle oedema

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228
Q

MOA of furosemide

A

Loop diuretics

  • Block Na+/K+/2Cl- co-transpotrter in the thick ascending loop of Henle
  • Can cause hyponatraemia, hypokalaemia and hyperuricaemia
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229
Q

Why is pyridoxine indicated in TB?

A
  • To prevent peripheral neuropathy
  • Side effect of isoniazid
  • It is vitamin B6
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230
Q

Where is a murmur with aortic regurgitation best heard?

A

Left 4th IC space (pulmonary valve)

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231
Q

Pulmonary embolism

A
  • Over infarcted area
  • Pleuritic pain
  • Associated with SOB
  • Tachycardia/AF
  • Tachypnoea
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232
Q

Which conditions can trigger acute heart failure?

A
o	Infection
o	Kidney disease/poor kidney function
o	Anaemia
o	Abnormal heart rhythm
o	Overactive thyroid gland
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233
Q

Asthma medications

A

o Short acting beta agonists (SABA)
o Long-acting beta agonists (LABA) - Formoterol + salmeterol
o Inhaled corticosteroids
o Leukotriene receptor antagonists - Block leukotriene receptors, prevent bronchoconstriction
o Combination inhalers - Mixture of LABA + corticosteroid

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234
Q

QRS regular, P wave absent, Long PR interval

A

1st degree heart block

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235
Q

What does the PR segment represent?

A

PR segment – conduction from the AVN, down the bundle of his and up the purkinje fibres

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236
Q

What type of resp failure is seen in acute asthma (normal)?

A

Type 1.

  • Hyperventilation with hypoxia.
  • They have ventilatory capacity to match the demand.
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237
Q

What happens in complete heart block?

A

Blockage of normal electrical connection across annulus fibrosus

  • SA node can’t dominate
  • Bundle of His takes over - 40 bpm
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238
Q

How does renal artery stenosis cause secondary hypertension?

A

Narrowing of arteries that carry blood to kidneys leads to decreased pressure in afferent arteriole

Kidney thinks BP is low so it releases renin

Renin increases BP by increasing angiotensin II and aldosterone

Angiotensin II promotes cardiac and vascular hypertrophy

Increased blood volume, cardiac output, vascular resistance all leads to hypertension

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239
Q

How should diuretics be used?

A
  • Administered IV to bypass oedematous gut
  • Infusion better than bolus
  • Change loop diuretic - bumetanide + torsemide are more predictable and have fewer side effects
  • Progressive nephron blockade – can work down the nephron tubule + block different things, add thiazide
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240
Q

What are class II antiarrhythmics?

A

Agents that are anti-sympathetic nervous systemic (most a beta blockers)

241
Q

Interleukins

A

o IL4 – stimulates production of IgE
o IL5 – Activates locally recruited eosinophils
o IL13 – stimulates mucus secretion from bronchial submucosal glands + also promote IgE production by B cells

242
Q

Mycobacterium species

A

M. tuberculosis – main cause of TB
o Rod shaped bacterium
o Mycolic acid present in cell wall making it acid-fast
o Aerobic + non-motile
o Multiplies slowly and can remain dormant for decades

M. afriticanum – important opportunistic infection in HIV; commonly found in West Africa

M. bovis – Widespread; causes bovine TB in cattle, cats, dogs, badgers, deer, possums…
o Nonvirulent vaccine strain of M bovis used in the BCG vaccine

M. canatii – emerging disease in East Africa

M. microti – mostly infects voles, human infections are rate (more common in immunocompromised patients

243
Q

Clinically what is pneumonia classified as?

A

 Community acquired: Patients seen by GP or new admission

 Hospital acquired: in hospital for ?48hrs (or recently discharged)

244
Q

Extra-pulmonary TB

A

Metastatic spread to any organs: abdomen, bone, brain, retina, muscles, lymph nodes

~30% of TB cases are exclusively extra pulmonary
o TB of spine may cause back pain + kyphosis
o TB of kidney may cause blood in the urine
o Extra-pulmonary TB should be considered in the differential diagnosis of ill persons who have systemic symptoms + who are at high risk for TB

245
Q

Why is the SAN the pacemaker?

A

Fastest intrinsic firing - 105 bpm

246
Q

FVC

A

Forced vital capacity - total amount of air you can blow out of your lungs

247
Q

MOA of pioglitazone

A

Reduce peripheral insulin resistance, leading to reduction in plasma glucose

Drug for DM II

248
Q

Non-modifiable risk factors for atheroma

A

Age - older
Gender - male
Ethnicity - Asian
Family history

249
Q

What is the Mantoux tuberculin skin test? (TST).

A
  • Intadermal injection of tuberculin.

- If T cells have been previously sensitised, inflammatory response at the site within 48-72 hours.

250
Q

Where is the AVN?

A

Base of the interatrial septum - only connection across the annulus fibrosus

251
Q

Second line drugs (list is extensive)

A
  • Amikacin
  • Kanamycin
  • Capreomycin
  • Streptomycin
  • Cycloserine
252
Q

Assessment and treatment of Da costa’s syndrome

A

o Physiological and psychological assessment

o Understanding – Discuss diagnosis and meaning (‘it’s all in your head’)

o Pathway – Regular visits to same physician/team

o Pharmacological treatment

o Psychological support and/or training

o Education

o Lifestyle factors

253
Q

Phase 3 of cardiac action potential

A
  • Ca2+ channels close
  • K+ still leaking out but voltage gated K+ channels close
  • Repolarisation
  • -90mV
254
Q

Bundle branch block

A
  • Block either in right or left bundles that branch from the Bundle of His
  • Wide double peak QRS
  • Inverted T wave
255
Q

What are Janeway lesions?

A
  • Non-painful, black spots on thenar + hypothenar eminences of hands + feet
  • Septic emboli within dermis of skin
256
Q

Left sided heart failure

A

L side is responsible for receiving oxygen rich blood from the lungs + pumping it forward to the systemic circulation

Failure of the L side of the heart causes blood to back up into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood

There are 2 types of left-sided heart failure:
 Systolic failure – L chamber lacks the force to push enough blood into the circulation
 Diastolic failure – L chamber fails to relax normally because the muscle has become stuffer + filling is impaired

257
Q

When are calcium channel blockers (class IV) contraindicated?

A
	Pregnancy
	Cardiogenic shock
	Severe bradycardia
	Moderate to severe heart failure
	Patients on modified release formulations should be maintained on the same brand
258
Q

Define opportunistic infection

A

An infection caused by a microorganism that normally does not cause disease but becomes pathogenic when the body’s immune system is compromised

259
Q

MOA of alteplase

A

Activates plasminogen to plasmin which digests fibrin and fibrinogen

Used in acute MI

260
Q

What is grade II cancer?

A

Cancer cells that don’t look like normal cells and are growing faster than normal cells

261
Q

What is grade I cancer?

A

Cancer cells that resemble normal cells and aren’t growing rapidly

262
Q

What is Fick’s Law of Diffusion? How does it apply to the lungs?

A

The rate of transfer of a gas through a tissue is proportional to the tissue area, and inversely proportional to thickness.

  • Large and thin = lots of transfer.
  • Large SA in the lungs (50-100sq. metres) and extremely thin alveoli.
263
Q

Commensals of the respiratory tract

A
  • Streptococcus pneumoniae
  • Haemophilus influenza e
  • Streptococcus viridian’s group
264
Q

Ventricular flutter

A

o Mostly caused by re-entry with a frequency of 300bpm
o The ventricles depolarise in a circular pattern, which prevents good function
o Most often this results in a minimal CO and subsequence ischaemia
o Often deteriorates into VF

265
Q

What is omapatrilat?

A

A combined ACEi and NEP inhibitor which increases diuresis

Omapatrilat is an experimental antihypertensive agent that was never marketed. It inhibits both neprilysin (NEP) and angiotensin-converting enzyme.

NEP inhibition results in elevated natriuretic peptide levels, promoting natriuresis, diuresis, vasodilation.

266
Q

How can hypokalaemia be prevented in patients with HF under diuresis?

A

Give K+ sparing diuretic e.g. spironolactone or amiloride

267
Q

Class Ic example and effect on action potential

A

Flecainide

  • Block Na+ channel
  • No effect on duration of AP
268
Q

What is presystolic gallop (aka atrial gallop)?

A

S4 added heart sound

 Sounds like Tennessee gallop
• S4 = tenn
• S1 = es
• S2 = see
 Heard just after atrial contraction + end of diastole before S1
 Best heart at the cardiac apex
 Produced by the sound of blood being forced into a stiff or hypertrophic ventricle
• Caused by aortic stenosis, hypertension, hypertrophic cardiomyopathy

269
Q

Describe changes in the heart due to hypertension

A

o Coronary atheroma – increases risk of MI
o Atheroma in L side circulation doesn’t affect pulmonary artery – pulmonary atheroma only seen in pulmonary hypertension, this shows that hypertension is vital in pathogenesis of atheroma
o Concentric LV hypertrophy (fairly early on in hypertension) - myocyte no. remains constant but individual cells hypertrophy

There also may be fibroblast proliferation and LV fibrosis which would lead to impaired LV relaxation

270
Q

What is centrilobular emphysema?

A
  • Primarily the upper lobes, occurs with loss of the respiratory bronchioles in the proximal portion of the acinus, with sparing of distal alveoli
  • Centrilobular emphysema is one of the first changes in smokers
271
Q

TB transmission

A

Person-to-person
 Through the air by person w/ active TB (droplet infection)

Ingestion of M. bovis
 Found in unpasteurised milk

Inoculation

Transplacental route (rare)

272
Q

What is dead space?

A

The volume of air which is inhaled that does not take part in the gas exchange, either because it;

  • Remains in the conducting airways (mouth/nose etc.).
  • Reaches alveoli that are not perfused or poorly perfused
273
Q

Causes of tachycardia from decreased PNS activity

A
  • 1st seconds of exercise
  • Falling arterial pressure (blood loss etc. until syncope)
  • Heart failure
  • Atropine (muscarinic receptor blockade
274
Q

List sudden (mins) causes of breathlessness

A
Pulmonary oedema
Pneumothorax
Pulmonary embolism
Anaphylaxis
Foreign body inhalation
275
Q

Development of atherosclerosis

A
  1. Development of fatty streak which forms an intermediate atherosclerotic region
  2. Fibrous cap can develop over it - the lipid core can become necrotic
  3. Thinning and rupture of fibrous plaque
  4. Necrotic core ruptures which exposes lipid below to circulating blood resulting in thrombus formation
276
Q

If in diagnostic doubt whether SVT or VT inject what?

A

 Incremental boluses (6-18mg) of adenosine

 Adenosine should slow rate markedly if it is SVT

277
Q

Phase 2 of cardiac action potential

A
  • Plateau
  • Slow inward movement of Ca2+
  • K+ still flowing out

Class IV agents block these Ca2+ channels and prolng conduction and refractiveness in SAN + AVN

278
Q

What is the QT interval and what does it represent?

A
  • Beginning of Q to end of T
  • Reflects repolarization of the ventricles
  • Time between onset of ventricular depolarization and end of repolarization
  • Less than 12 small squares
279
Q

What is the difference between obstruction and restriction?

A
  • Obstruction: narrowing of the airways, increased resistance to air flow (like breathing through a straw).
  • Restriction: increased work to expand the chest or reduced lung compliance/increased stiffness.
280
Q

There are 2 main subtypes of lung carcinomas. Name them

A

o Non-small cell carcinoma (87%)

o Small cell carcinoma (13%)

281
Q

How is bradycardia due to bundle branch block treated?

A

Pacemaker – mostly monitors heart;

If HR too slow, it sends electrical impulses to prevent bradycardia

282
Q

What is brady-tachy syndrome?

A

Intermittent episodes of slow and fast rates from SA node

283
Q

Aortic stenosis

A
  • Obstruction to normal flow through the valve
  • Usually a result of calcification or genetically bicuspid aorta
  • Stenosed valve increases after load of left ventricle = increasing the force required to eject blood into aorta
  • Causes left ventricular hypertrophy
  • Reduction in CO can cause breathlessness
  • Inadequate perfusion to brain can cause syncope
  • Reduced myocardial perfusion can cause angina
284
Q

How is sinus tachycardia treated?

A
Investigate and remove cause:
•	Hyperthyroidism
•	Anxiety
•	Heart failure
•	Hypovolaemia
•	Septicaemia
285
Q

Risk factors for pneumonia

A
  • Alteration in host consciousness
  • Smoking
  • Alcohol
  • Sepsis
  • Immunosuppression
  • Iatrogenic manipulation
  • Drugs
  • Congenital
286
Q

What are Osler’s nodes?

A

Tender red nodules on finger pulps/thenar eminence (infective endocarditis)

  • Painful lesions on finger pulps
  • Deposition of immune complexes in fingers
287
Q

Viral, fungal, mycobacterial + parasitic causes of pneumonia

A
  • Viral - Influenza A, B + respiratory syncytial virus (RSV)
  • Fungal - Aspergillus
  • Mycobacterium - mycobacterium tuberculosis
  • Parasitic - pneumocystitis jirvecci
288
Q

Acute airway changes in asthma

SMOPS

A
  • Smooth muscle contraction
  • Mucus hypersecretion
  • Oedema
  • Plasma leakage
  • Sensory nerve
289
Q

Anatomical defences of the respiratory tract

A
  • Nasal hair
  • Nasal turbintes
  • Cilia
  • Sneezing
  • Saliva
290
Q

Triggers of asthma

A
  • Smoke
  • Faeces of dust mites
  • Mould spores
  • Foods
  • Industrial chemicals
  • Pollen
291
Q

Non-infective causes of consolidation

A
  • Fluid - inflammatory/heart failure
  • Cells - cancer
  • Protein - alveolar proteinois
  • Blood - pulmonary haemorrhage
292
Q

Pathophysiology of left bundle branch block

A

LBBB: aortic stenosis, dilated cardiomyopathy, MI, CAD

293
Q

What does high CO2 indicate? What sign is characteristic of this?

A

Ventilatory failure.

- Flapping tremor

294
Q

How is TB spread?

A

By inhalation of droplet nuclei.

- Infectious particles are aerosolised by coughing, sneezing or talking.

295
Q

If d-dimer test (inflammation and clot measure) negative after 6 hours. What is unlikely?

A

Aortic dissection + pulmonary embolism unlikely

296
Q

Occupational causes of COPD

A
o	Coal mining
o	Agriculture
o	Construction
o	Dock workers
o	Brick making
297
Q

Non-small cell carcinoma treatment

A

Early stage (I and II)
• Hasn’t spread to peripheral lymph nodes
• Surgical resection – 5-year survival 23-60%
• Radical radiotherapy may be offered if unfit for or refuses surgery (almost as effective)

Advanced stage (III and IV)
• Palliative chemotherapy and/or radiotherapy
• 5-year survival <1%

298
Q

What type of resp failure is seen in late severe asthma?

A

Type 2.

  • Respiratory muscles get tired and can’t expel all the CO2.
  • Worrying sign.
299
Q

What species is the definitive host of TB?

A

Humans

300
Q

What is secondary hypertension?

A

o Raised blood pressure with an identifiable underlying cause
o 5-10% of causes
o Often renal or endocrine causes

301
Q

How does damage to papillary muscle present?

A

 Acute onset of hypertension + pulmonary oedema with a mid-, late- or holosystolic murmur
 The intensity of the murmur does not necessarily correlate with severity

302
Q

Atrial fibrillation

A

o Commonest sustained arrhythmia (1% of adults)
o Prevalence increases with age
o Increases risk of stroke by x4
o Can cause tachycardiomyopathy if untreated
o ~1/2 patients with AF also have HF
o ~1/3 of patients with HF have AF

303
Q

What is the QRS interval and what does it represent?

A
  • Beginning of Q wave to end of S wave
  • Reflect slow conduction through ventricular myocardium
  • Onset and end of depolarization
  • Less than 3 small squares
304
Q

Aortic regurgitation

A
  • Valve fails in its function to prevent back flow
  • Can result from infective endocarditis, dilatation of aortic root e.g. Marfan’s
  • Back flow into left ventricle causes left ventricular hypertrophy
  • In order to maintain CO, hypertrophy occurs
305
Q

How would you treat stable ventricular tachycardia?

A
  • IV amiodarone

- Electrical cardioversion

306
Q

Non-pharmacological treatment of pulmonary oedema?

A

Ventilatory support
 CPAP – continuous positive airways pressure
 IPPV – intermittent positive pressure ventilation

Inotropic support
 Try to avoid as may cause worse prognosis – only used when shock/incipient shock
 Usually dobutamine

307
Q

Typical pathogens that cause pneumonia

A

Streptococcus pneumoniae (pneumococcus):
o Typically colonises the respiratory tract, sinuses, and nasal cavity, wo/ causing harm
o However, in susceptible individuals with weaker immune systems, the bacterium may become pathogenic and spread to other locations to cause disease
o It Is the main cause of community acquired pneumonia + meningitis in children and the elderly

Haemophilus influenzae:
o Most strains of H. influenzae are opportunistic pathogens

Moraxella catarrhalis:
o Causes bronchitis + pneumonia at any age with underlying chronic lung disease
o Occasionally a cause of bacteraemia + meningitis, especially in immunocompromised persons

308
Q

What is grade III cancer?

A

Cancer cells that look abnormal and may grow or spread more aggressively

309
Q

Rupture of interventricular septum

  • Where does it develop?
  • What does it cause?
A
  • Rupture develops at margin of necrotic and non-necrotic myocardium
  • Left to right shunting
  • Loud, harsh murmur
310
Q

What is asbestosis?

A
  • Chronic inflammatory and fibrotic medical condition caused by inhalation of asbestos
  • Restrictive - lungs small and thick
  • Worse at bottom of lungs than at top
311
Q

Retinal complications of hypertension

A
  • Hypertensive retinopathy

- Papilloedema

312
Q

List the main drugs used in the treatment of chronic HF

A

ACE inhibitors

Angiotensin receptor blockers (ARBs)

Beta-blockers

Mineralocorticoid receptor antagonist (MRAs)

313
Q

Peripheral model for failing heart

A
  • People with heart failure develop abnormal skeletal muscle
  • Shift from type I slow twitch aerobic to type II fast twitch anaerobic
314
Q

What are the 2 types of cells in the heart?

A

Type 1 - SAN, AVN, conducting tissue - these are automatic/spontaneous

Type 2 - atria, ventricles - depolarise upon stimulation

315
Q

What are the 4 steps of TB infection?

A

1) TB bacilli reach the alveoli.
2) The bacilli multiply and and phagocytosed by alveolar macrophages.
3) Alveolar macrophages attempt to destroy the TB but made difficult by thick waxy mycolic acid capsule.
4) Bacilli replicate inside the macrophage and kill it OR be presented to the immune system.

316
Q

Causes of acute pulmonary oedema?

A
  • Acute ischaemia
  • Arrhythmia – AF, flutter, VT
  • Mechanical disaster – e.g. rupture of papillary muscle to mitral valve
  • Non-compliance with medication
  • PE
  • Environment – stress, drugs
317
Q

What can affect the outcome of a diffusion test?

A

Thickness of the alveolar membrane.

318
Q

Describes the forces acting on fluid balance across a capillary in a tissue?

A

 Hydrostatic pressure: pressure in capillary that is forcing fluid out
 Colloid osmotic pressure: osmotic pressure provided by albumin + other proteins (pull the fluid back in again)

Other influences:
 Lymphatic drainage – drains any excess fluid outside of tissues
 Alveolar-capillary membrane – provides some resistance against the movement of fluid

319
Q

Alpha blockers

A

o Block peripheral alpha 1 receptors which normally mediate sympathetic vasoconstriction

o Side effect – first dose hypotension (vasodilation)

o Doxazosin is the only one commercially available for hypertension treatment

320
Q

What can cause hypoxia?

A
  • Impaired diffusion.
  • Hypoventilation.
  • V/Q mismatch.
321
Q

Can tetanus occur in cardiac muscle?

A

No

322
Q

What is the definition of type 1 respiratory failure (hypoxaemic)?

A
  • Low Pa02 (less than 8kPa).
  • Low or normal PaCO2 (less that 6kPa.

Hypoxia without hypercapnia.

323
Q

Describe Phase 0 cardiac myocyte action potential

A
Phase 0 – Rapid depolarisation associated w/ fast inflow of Na+ via Na+ channels
•	All class I agents block these Na+ channels + reduce the rate of depolarisation
324
Q

What is the risk with AF?

A

Increases risk of stroke by 4x

325
Q

Incomplete/subacute rupture of LV free wall

A

Can occur when organised thrombus + the pericardium seals the perforation

This may progress to either:
 Frank rupture
 Formation of pseudo-aneurysm (false aneurysm) – walled off by pericardial tissue + communicating w/ the LV through the perfusion
• True aneurysm – lined w/ muscle itself
 Formation of a left ventricular diverticulum

326
Q

Apart from lab work, what other techniques are used to identify TB?

A

CXR.

327
Q

What are the most common sites of EP.TB?

A
  • Pleura (pleural TB).
  • Brain (Tuberculoma).
  • Spine (Pott’s disease).
  • Lymph node (Adenitis).
  • CSF (TB meningitis).
  • Retina (retinal TB).
328
Q

What are the risk factors for DR TB (drug resistant TB)?

A
  • People with a history of TB drug use.
  • Poor compliance.
  • Malabsorption of drugs.
  • Foreign born people from areas of DR TB.
  • People receiving inadequate treatment regimes.
329
Q

What is malar flush?

A

A plum-red discolouration of the high cheeks classically associated with mitral stenosis due to the resulting CO2 retention and its vasodilatory effects.

• Can be associated with SLE or polycythemia rubra vera

330
Q

MOA of amiodarone

A
  • Class III and some class I, II, IV activity
  • Prolongs AP
  • Used in SVT and VT
  • 6 days onset
  • Long elimination
331
Q

What can cause alkalaemia (high pH) in the blood?

A
  • Resp: low CO2.

- Metabolic: high HCO3.

332
Q

What would a wide QRS interval suggest?

A

Intra/interventricular conduction delay

333
Q

What is carbocysteine?

A

A mucolytic - agent which dissolves thick mucus, used to help relieve breathing difficulties

334
Q

What are the 3 outcomes of a macrophage being infected by TB?

A

1) Clearance of the infection: TB is presented to the immune system and destroyed.
2) Latent infection: Bacteria in the macrophage become dormant until patient is immunosuppressed.
3) Primary TB: Macrophage is killed. Progression to TB disease.

335
Q

What class of antiarrhythmics are the following?

Encainide
Flecainide
Propafenone
Moricizine

A

Ic

336
Q

What is bronchoalveolar carcinoma

A

o Glandular cells produce lots of mucus (bronchorrhoea)

337
Q

What cells form a granuloma?

A
  • Macrophages.
  • Giant cells (langhans).
  • T lymphocytes.
  • B lymphocytes.
  • Fibroblasts.
338
Q

Radiologically what is pneumonia classifed into?

A

Lobarpneumonia vs bronchopneumonia

339
Q

What is bronchiectasis?

A

o Airways abnormally dilated
o Secretions pool + aren’t properly cleared by the mucociliary escalator
o Gets infected + colonise w/ bacterial
o Patient constantly coughs up purulent sputum

340
Q

How is stable supraventricular tachycardia (SVT) managed?

A

 Many revert spontaneously

 Vagotonic manoeuvres – stimulates increased vagal tone e.g. get patient to blow out against pressure, put child head under cold water, press on carotid sinus

 Rapid IV adenosine bolus

 Avoid digoxin and verapamil unless you are expert

341
Q

What is Poiseuille’s law?

A

Flow = radius4

 Baroreceptors alter sympathetic outflow to all the smooth muscle cells in the vasculature of the body (arterioles)
 Flow down a tube – proportional to 4th power of radius so only have to change radius a tiny bit to affect BP

342
Q

Acute bronchitis

A
  • Acute infection of trachea and bronchi
  • Usually viral
  • Influenza
  • Adenovirus
  • Rhinovirus
  • No change on CXR
343
Q

Medical uses of class Ia antiarrhythmics?

A

Ventricular arrhythmias

Prevention of paroxysmal recurrent atrial fibrillation (triggered by vagal overactivity)

Procainamide in Wolff-Parkinson-White syndrome

Increases QT interval

344
Q

Some patients (especially w/ mitral stenosis) can develop compensatory mechanisms such as?

A
  • Thickened alveolar capillary membrane

* Increased lymphatic drainage

345
Q

What is theophylline?

A

Example of methylxanthine which acts as bronchodilator (used in COPD and asthma)

346
Q

How is perfusion measured?

A

Imaging type tests.

  • CT pulmonary angiogram to check for PE and malformations of vasculature.
  • Echocardiogram to check for shunts.
347
Q

Sinus arrest

A

Failure of sinus node discharge resulting in absence of atrial depolarization
- Periods of ventricular asystole

348
Q

Atrial flutter

A

Atria contract at 300 bpm

349
Q

What groups other than immigrants is TB present in in the UK?

A
  • Homeless
  • IV drug users
  • Alcoholics
  • Prison inmates
  • Urban poor
350
Q

When are steroids indicated in TB?

A
  • TB meningitis.

- Pericardial TB.

351
Q

Risk factors for HAP

A
  • Over 70
  • Severe underlying disease
  • Surgical procedures
352
Q

What do Th1 cells produce?

A

IFN-gamma

IgG

353
Q

At which phase of cardiac myocyte action potential do class I agents work?

A

Phase 0 - Rapid depolarisation associated w/ fast inflow of Na+ via Na+ channels

• All class I agents block these Na+ channels + reduce the rate of depolarisation

354
Q

What are class IV antiarrhythmics?

A

Agents that affect calcium channels and the AVN

355
Q

Speed of propagation is determined by the gradient of phase what?

A

Phase 0

356
Q

What is pulse oximetry?

A
  • A machine placed on the finger.
  • Shines a red light and measures light absorption, gives estimation of O2 sats.
  • Oxygenated blood is red, deoxygentaed dark red/purple colour.
357
Q

How do long acting muscarinic antagonists (LAMA) work in asthma treatment?

E.g. Tiotropium – causes a 20% improvement in FEV1

A

o Response is the same a year later – shows deterioration of patient

o Delays lung function deterioration by around 4 years, reduced mortality, but doesn’t make it stable

o In people under 50 w/ milder disease there is a disease modification so improved outcomes

358
Q

Type B personality

A
  • Work steadily
  • Enjoy achievement
  • Don’t mind defeat
359
Q

Syncope is a symptom, the defining clinical characteristics of which are?

A
  • Transient
  • Self-limited loss of consciousness
  • Leads to falling
  • Onset is relatively rapid
  • Recovery is spontaneous, complete, and usually prompt
360
Q

How many people in the world have TB?

A

1/3rd of the worlds population infected with TB

361
Q

Differential diagnosis for ankle oedema

A
  • Nephrotic syndrome
  • Chronic venous insufficiency e.g. previous DVT or varicose veins
  • Drugs - dihydropyridines
  • Hypoalbuminaema
  • Fat
362
Q

How do we confirm a diagnosis of angina?

A

Stress testing

363
Q

What does high compliance indicate?

A

Pliable lung (low elastic recoil)

E.g. emphysema/COPD

364
Q

Where on the cardiac action potential do class II drugs work?

A

Phase 4

  • Block SAN conduction
  • Beta-blockers
365
Q

MOA of pyrazinamide

A

Is converted to pyrazinoic acid which disrupts membrane and inhibits membrane transport in mycobacterium tuberculosis

366
Q

What type of lung disease is there with an FEV1/FVC ratio of less than 70%

A

Obstructive

367
Q

MOA of paclitaxel

A

Binds to tubulin, keeping the microtubules polymerised, preventing spindle formation in dividing cells and stopping them in mitosis

It is an anti-microtubule agent, used for non-small cell lung cancer in patients unsuitable for curative treatment

368
Q

Where on the cardiac action potential do class III drugs work?

A

Phase 3

- Block K+ channels which prolongs AP

369
Q

Atrial flutter treatment

A

 Anticoagulants – due to stroke risk

 External electrical cardioversion

 Electrophysiological ablation

370
Q

An anti-leukotriene is a drug which functions as either?

A

o Leukotriene-related enzyme inhibitor
o Leukotriene receptor antagonist

They oppose leukotrienes (product released by mast cells that cause bronchoconstriction, inflammation, microvascular permeability, mucus secretion in asthma, and COPD)

371
Q

How are ventilation and perfusion matched in the body?

What can be a complication of chronic hypoxia because of this?

A
  • Ventilated areas receive more perfusion.
  • Hypoxia in the lungs causes vasoconstriction, so that well ventilated areas are perfused instead.

Cor pulmonale.

372
Q

Medical uses of class II antiarrhythmics (beta-blockers mostly)?

A

Decrease MI mortality

Prevent recurrence of tachyarrhythmias

373
Q

Lobar pneumonia

A
  • Involve a whole/large continuous area of lobe
  • Bacterial – Streptococcus pneumoniae, Klebsiella spp.
  • Most lobar pneumonia’s are pneumococcal – but most pneumococcal pneumonia are not lobar
374
Q

What are ventilatory capacity and ventilatory demand? How are they balanced in health?

A
  • Ventilatory capacity: maximum amount of ventilation we can maintain before respiratory muscle fatigue.
  • Ventilatory demand: amount on ventilation required to maintain a normal CO2 level.

In health, capacity far outweighs demand.

375
Q

What does the ST segment correspond to?

A

ST segment – time when the ventricles are depolarised during the plateau phase of action potential

376
Q

Myocardial wall rupture

A

o When there is thin damaged myocardium next to healthy, actively contracting myocardium, this is a hinge point where the damage myocardium can rupture

o Sudden deterioration

o Leads to arterial bleeding into the pericardium + rapid death – not survivable

377
Q

What is the ergo-reflex?

A

o Reflex generation by exercising muscles – with exercise, muscle being exercised sends signals to the brain to breath more

o The ergo-reflex increases as exercise capacity falls + increases as ventilatory response to exercise increases

  • Normally ventilation increases with exercise, decreases after
  • In heart failure, ergoreflex is activated meaning heavy breathing long after exercise
378
Q

First line drugs for TB

A

RIPE (first line drugs)
• Rifampin: inhibits RNA synthesis - Often turns urine bright orange if taken properly
• Isoniazid: inhibits cell wall synthesis
• Ethambutol: inhibits cell wall synthesis
• Pyrazinamide: exact target unclear, disrupts plasma membrane + energy metabolism

Rifampicin + isoniazid are given for 6 months w/ pyrazinamide + ethambutol for those first 2 months

379
Q

What is breathlesness?

A
  • Defined as an unpleasant sensation of feeling increased demand for breathing
  • It is a symptom not a sign – do not say ‘the patient appears breathless’
  • Poor correlation with: respiratory rate (tachypnea), hypoxaemia, hypercapnia
380
Q

What are propanolol and timolol examples of?

A

Non-selective (B1 and B2) beta blockers

381
Q

Side effects of spironolactone

A
  • Gynaecomastia

- Hyperkalaemia

382
Q

Which asbestos fibres are the most damaging?

A

Straight fibres - blue/brown

383
Q

MOA of ethambutol

A

Obstructs the formation of the cell wall in dividing TB bacilli

384
Q

What is afterload?

A

Peripheral resistance

The load against which the heart has to eject blood

 Altered by the state of the blood vessels

 Approximately equal to blood pressure
• Higher the BP, harder the heart works

 Leads to ventricular hypertrophy

385
Q

Acute community acquired pneumonia

A
  • Older patients and elderly

- Peak mid-winter/spring

386
Q

Where is the infarction in a lateral acute MI?

A

Left circumflex artery

387
Q

What class of antiarrhythmics are the following examples of?

Verapamil
Diltiazem

A

Class IV

388
Q

Cases of uneven radial pulses

A

Aortic dissection
Coagulation of aorta
Atheroscleoris

389
Q

What is torsades de pointes exacerbated by?

A

Low potassium and magnesium

390
Q

Cardiac markers

A
  • Troponin I
  • Troponin T
  • Myoglobin
  • CK-MB
391
Q

What is minute ventilation? How is it calculated?

A

The amount of breath taken in and out in a minute.

  • Tidal volume x respiratory rate.
392
Q

Causes of COPD

A

 Tobacco – main cause, need ~15 pack years to develop emphysema
 Recreational drug use
 Passive smoking
 Chronic asthma
 Biofuels
 Occupational – coal mining, cotton, wielding
 Familial – alpha-1 antitrypsin deficiency

393
Q

What is Ebstein’s anomaly?

A

A congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle of the heart

About 50% of individuals with Ebstein’s anomaly have evidence of Wolff-Parkinson-White syndrome, secondary to the atrialized right ventricular tissue

394
Q

What type of respiratory failure would you see in restrictive lung disease patients?

How does this differ from interstitial lung disease (i.e. IPF)?

A

Type 2: chest wall deformities etc. cause ventilatory failure earlier than IDL.

ILD is type 1, CO2 rise is a sign of morbidity.

395
Q

Causes of bradycardia

A
  • Sick sinus syndrome - damage to SAN (tachy-brady syndrome)
  • AV block
  • Drugs
  • Non-cardiac - hypothyroidism etc.
396
Q

Aortic valvue sclerosis

A
  • Normal or loud S2
  • Carotid pulse often brisk or normal
  • Usually no LV hypertrophy unless severely hypertensive
  • Due to wear + tear to valve overtime
397
Q

What is malignant hypertension?

A

A recent significant elevation over the baseline BP that is associated with target organ damage
- Before effective treatment, the life expectancy was less than 2 years
- It is v. rare because hypertension is treated very early
o E.g. papilloedema indicated raised ICP – so called malgnant hypertension

398
Q

What is elevated JVP due to?

A
o	Heart failure
o	Constrictive pericarditis
o	Cardiac tamponade
o	Renal disease
o	SVC obstruction
399
Q

Where is a rupture most common in papillary muscles?

A

Posteromedial as there is only 1 blood supply from posterior descending artery

400
Q

Types of non-small cell carcinoma?

A

Adenocarcinoma (>40-50%)

Squamous cell carcinoma (20%)

Large cell carcinoma (2%)

401
Q

Describe changes in the aorta due to hypertension

A

o Atheroma
o Aneurysm – may rupture/dissect
o Aortic dissection – quite common, cystic medial necrosis, aortic wall tears (intima is torn off rest of the aorta by the pressure)

402
Q

What is FVC?

A

The maximum amount of air that can be expelled in forced expiration.

403
Q

NSTEMI ECG features

A
  • Frequently normal
  • May be minor T wave changes/inversion
  • May be significant ST depression
404
Q

When are type Ib antiarrhythmics used?

A

Treatment and prevention of, during and immediately after myocardial infarction, though this practice is now discouraged given the increased risk of asystole

Ventricular tachycardia

405
Q

How can aortic coarctation cause secondary hypertension?

A

Above the narrowing (coarctation) = hypertension

Below the coarctation = normotension of hypotension

If kidneys are hypo-perfused , RAAS activated which increases BP

406
Q

Platinum based drugs like cisplatin and carboplatin is used to treat what percentage of cancer patients?

A

50%

407
Q

Torsades de pointes

A
  • Commonly seen in patients with pre-existing bradycardia, especially if given type I anti-arrhythmias
  • Patient conscious but ECG looks like VF
  • Long QT
408
Q

What are ARBs?

A

Angiotensin receptor blockers

Block the angiotensin I receptors, inhibiting angII

409
Q

What would the spirometry of a patient with restrictive lung disease show?

A
  • Reduced FEV1.
  • Reduced FVC.
  • No change or raised FEV1/FVC.
410
Q

Tissue changes in the aorta in hypertension

A
  • Atheroma
  • Aneurysm
  • Dissection
411
Q

Which are the anterior ECG leads?

A

V1-V6

412
Q

Is TB a fast-growing or a slow-growing mycobacteria?

A

Slow-growing

413
Q

MOA of thiazides

A
  • Block Na+/Cl- co-transport in DCT

- Loss of Na+, K+ and Mg2+

414
Q

What happens in the chronic phases of hypertension?

A
  • Blood volume and CO normal

- Increase in systemic vascular resistance

415
Q

What happens to the granuloma in primary TB?

A

It is liquefied and the macrophage is killed, TB bacilli released.

  • TB may be spread by connection to the bronchi.
  • May be other spread by blood or lymphatic system.
416
Q

Why is psychology important in cardiovascular disease?

A
  • Link between psychological distress and CVD well established
  • Comparable to physical risk factors e.g. hypertension
  • Leads to physical risk factors
  • Strong gradient between levels of depressive symptoms and likelihood of adverse cardiac event
417
Q

What are the 2 factors involved in homoeostasis of ventilation?

A
  • Ventilatory capacity.

- Ventilatory demand.

418
Q

Describe kidney changes due to hypertension

A

o Small vessel (hypertensive) disease causes glomerular damage

o Gradual parenchymal loss accelerates decline in function

o Large vessel atheromatous disease

419
Q

MOA of dobutamine

A
  • B1-agonist catecholamine

- Can cause arrythmia through toxicity

420
Q

Which cells in the heat conduct fastest?

A

His and purkinje cells conduct the fastest (2-5m/s

421
Q

How is anasarca treated?

A

By inducing diuresis

o Bed rest – legs up + catheter below level of bladder
 Need to give heparin or LMWH to prevent DVT
o Fluid restriction
o Diuretics

422
Q

What is the ARP?

A

Absolute refractory period

  • Between S and T waves
423
Q

Nature of simple bronchitis

A
  • Cells of bronchial tissue irritated
  • Mucous membrane becomes hyperaemic and oedematous
  • Diminishes bronchial mucocilliary function
  • Air passages become clogged with debris and irritation increases
  • Copious secretion of mucous develops causing characteristic cough
  • Infection with Strep pneumoniae or H. Influenzae
424
Q

Consequnces of atheroma

A
  • Ventricular fibrillation + sudden death
  • ½ of all patients have MI, die before getting to hospital
  • Cardiovascular disease is second only to cancer as cause of death for men + women
425
Q

MOA of GTN

A

Nitroglycerin is converted to NO which stimulates cGMP synthesis. Ca2+ ions released resulting in SM relaxation and vasodilation.

426
Q

What is preload?

A

Filling pressure

The pressure (blood) in the ventricles just before they start to contract

 Heart detects this as stretch on myocytes (leads to ventricular dilation)

 Roughly equates to end diastolic pressure/volume

427
Q

Which disease causes more fibrosis and mucous, COPD or asthma?

A

COPD

428
Q

How do the kidneys respond to heart failure?

A
  • Less perfusion to kidneys
  • Activates RAAS
  • Retains Na+ and H2O
  • Increases blood volume
  • Increases preload
429
Q

What can untreated AF cause?

A

Tachy-cardiomyopathy

430
Q

What happens to the baroreflex in heart failure?

A

It’s turned off

431
Q

Which questions should be considered when assessing the heart rhythm?

A

o How is the patient? Need to act quickly if there is no output/severe hypotension

o What is the ventricular rate?

o Is the ventricular rate regular or irregular?

o Are the QRS complexes narrow or wide (>120ms)?

o Are P waves visible?

o What is the relationship between P waves and QRS complexes?

o What is the PR interval?

432
Q

What class of antiarrhythmics are the following?

Lidocaine
Phenytoin
Mexiletine
Tocainide

A

Ib

433
Q

Name some common obstructive lung diseases.

A
  • Asthma.
  • COPD.
  • Bronchiectasis (mixed).
434
Q

Phenotypes of COPD patients

A

Blue bloaters - predominantly bronchitis

Pink puffers - predominantly emphysema

435
Q

Potential causes of secondary hypertension?

A

 Renal artery stenosis

 Chronic renal disease

 Primary hyperaldosteronism

 Pheochromocytoma

 Coarctation of the aorta

 Cushing’s disease – excess production of glucocorticoids, all cause some salt + water retention

 Pregnancy – towards the end of pregnancy, BP increases in some women (may lead to pre-eclampsia)

 Thyroid disease

 Sleep apnoea

 Alcohol

 Syndrome of apparent mineralocorticoid excess – autosomal recessive; causes hyperextension, hypokalaemia

 Liddle syndrome – rare hereditary abnormality of intra-renal metabolism

436
Q

What is hypersensitivity pneumonitis?

Due to: bird features/droppings, mouldy hay, metalworking fluids.

A

o Hypersensitivity pneumonitis is a type 3 hypersensitive reaction (immune complex deposition)

o It’s an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic dust

o Symptoms include: cough + breathlessness

o Lung function test: there is a restrictive effect because it mainly affects lung interstitium

437
Q

Uses of Ic class antiarrhythmics?

A

Prevents paroxysmal atrial fibrillation

Treats recurrent tachyarrhythmias of abnormal conduction system

Contraindicated immediately after myocardial infarction

438
Q

What is papilloedema?

A

Optic disc swelling

439
Q

Whereabouts in the lung does TB usually accumulate?

A

The upper lobe.

440
Q

How do B2 agonists work in asthma treatment?

A

Bronchoconstriction is contraction of bronchial smooth muscle

o They relax muscles of the airways – widens airways + results in easier breathing
o Act on beta-adrenoceptors found on bronchial smooth muscles
o Activated adenylate cyclase which leads to activation of cAMP, this activates protein kinase A (PKA) which phosphorylates target proteins
o Ultimately induces smooth muscle relaxation

441
Q

Atenolol

Acebutolol

A

Selective (B1 only) beta blockers

442
Q

How does hypoxia in the lungs differ to the rest of the body?

A
  • Hypoxia in systemic tissues causes vasodilation.

- Hypoxia in pulmonary tissues causes vasoconstriction.

443
Q

Pathogenesis of consolidation

A

Inflammatory changes in region of lung affected

444
Q

Chlamydophilia pneumoniae

A
  • Mild and self limiting in adults

- Acute exacerbations of COPD

445
Q

Use of lidocaine and MoA?

A

Used in VT when amiodarone is contraindicated or ineffective

Mechanism of action:
 Sodium channel blocker
 Raises the depolarisation threshold
 Making the heart less likely to initiate or conduct early action potentials that may cause an arrhythmia

446
Q

What would eliciting a bronchodilator response distinguish between?

A

COPD and asthma

- Asthma responds, COPD doesn’t

447
Q

Siderosis

A

o Is the deposition of iron in tissue, it usually refers to an environmental disease of the lung

o CXR – shadowing of iron

o Not associated w/ any symptoms or functional abnormality

o Iron stays in lung but has no effect – no associated fibrosis or narrowed airways

448
Q

Diagnosis of lung carcinoma

A

o Cytology – bronchial brush + wash, BAL
o Biopsy – bronchoscopy
o Surgery – lobectomy, pneumonectomy

449
Q

Atrial flutter with variable block

A
  • 300bpm atria contract
  • Ventricles contract at slower rate - 150bpm
  • Due to refractory period in AV node
  • Multiple P waves
  • Regular QRS
450
Q

What percentage occlusion is there for angina?

A

75%

451
Q

What factors may influence transmission of TB droplets?

A
  • Infectivity of droplets (small).
  • Duration and level of exposure.
  • Susceptibility of exposed person.
452
Q

What is alpha-1 antitrypsin deficiency?

A
  • Lobular
  • Neutrophils attracted to airways which produce proteolytic enzymes
  • Enzyme needs to be switched off
  • People with this do not have anything to switch it off
  • Neutrophil elastase therefore destroys alveoli wall
453
Q

Which drug leads to reduced rna synthesis in the bacterial cell?

A

Rifampicin - inhibits bacterial DNA-dependent RNA polymerase

454
Q

Neutrophils vs eosinophils in COPD and asthma?

A

Asthma - eosinophils present

COPD - neutrophils present

455
Q

What peripheral changes occur as the LV fails?

A

o BP falls, this is sensed and there is sympathetic outflow which causes vasoconstriction which increases afterload + BP rises
o The heart does not perfuse the kidneys properly, this triggers AAS which leads to salt + water retention, increasing blood volume + hence preload – BP rises

456
Q
Where on cardiac action potential do class I drugs work?
Phase 0
A
  • Block Na+ channels
457
Q

Subacute (wks) causes of breathlessness

A

Heart failure
Anaemia
Pleural effusion
Lung cancer

458
Q

Why do you get a cough with ace inhibitors?

A

ACE breaks down kinins so if you block ACE you have more kinins which increases vasodilation but also induces cough

459
Q

What is the posteromedial papillary muscles blood supply?

A

Posterior descending artery

460
Q

How does the SNS respond to heart failure?

A
  • Sympathetics activated
  • Vasoconstriction
  • Increases afterload
461
Q

Which is more likely to be a diffusion problem, CO2 or O2? What does this mean?

A

O2.

  • CO2 not affected as it diffuses extremely quickly.
  • Hypercapnia is more likely to be a ventilation problem i.e. emphysema.
462
Q

How does chronic renal disease lead to secondary hypertension?

A

Kidney damaged (e.g. due to diabetic nephropathy, glomerulonephritis)

Loss of pressure diuresis due to decreased sodium excretion hence water retention. This leads to increased blood volume and cardiac output

Due to kidney damage, kidney wants to increase its own perfusion by increases BP to restore GFR so it increases renin release –> Ang II and aldosterone –> increased blood volume and CO

463
Q

With increased blood volume the heart stretches, this releases what?

A

Natriuretic peptides into circulation which go to the kidney and cause increased urination, getting rid of salt and water

464
Q

List 4 major determinants of BP

A

Baroreceptors
Poiseuille’s law
Renin angiotensin aldosterone system
Renal function

465
Q

Paroxysmal nocturnal dyspnoea symptoms

A
o	Wake from sleep (2-4 hours)
o	Cough, wheeze
o	Have to sit up while sleeping – asking how many pillows hey sleep with at night
o	Frightening
o	Last 15-30 minutes
466
Q

On a standard ECG, how many small squares does the normal PR interval, QRS complex and QT interval contain?

A

PR = <6 small squares

QRS = <3 small squares

QT = <12 small squares

467
Q

How does the PNS affect the SA node?

A
  • Increased PNS causes a decrease in HR
  • Sleep
  • Vasovagal syncope
  • Fitness
468
Q

What is a full thickness (transmural) infarct?

A

 Involves entire thickness of LV wall (isolated infarct of RV + RA are extremely rare)
 E.g. block anterior intraventricular descending artery from L coronary artery – supplies left side of heart

469
Q

Adverse effects of loop diuretics like furosemide, bumetanide, torsemide?

A

o Hyponatraemia – low blood sodium levels

o Hypokalaemia = low blood potassium level

o Hyperuricemia – excess uric acid in blood, acute gout is v. common

470
Q

Toxic pneumonitis

A
  • Acute, usually by inhalation

- Irritant gases of high NH3 or NO2, organic chemicals such as paraquat, metallic Hg, Cd and complex mixtures

471
Q

Examples of stress tests

A
  • Exercise ECG
  • Stress ECHO
  • Myocardial perfusion scan
472
Q

Name some countries in which TB is particularly prevalent.

A
  • Russia.
  • India.
  • China.
  • Kenya.
  • South Africa.
  • Indonesia.
473
Q

How does primary hyperaldosteronism cause secondary hypertension?

A

Excess production of aldosterone by adrenal glands (usually due to adrenal tumours or more commonly, hyperplasia) –> leads to low renin levels by negative feedback

High aldo, low K+, and low renin means problem at adrenal glands with aldosterone overproduction

474
Q

Which medication would you give to someone following a STEMI?

A
  • Anti-ischaemics - nitrates/beta-blockers
  • Statin
  • Anti-platelet - clopidogrel, aspirin
  • LMWH
475
Q

What happens to hydrostatic pressure in a failing heart? What are the consequences of this?

A

It increases

  • Heart requires a higher filling pressure in order to fill heart enough
  • There becomes a point where heart filling pressure in the left ventricle causes the hydrostatic pressure in the pulmonary circulation to go so high that fluid move out into pulmonary bed faster than lymphatics can drain it away = pulmonary oedema
476
Q

In what way do respiratory gases not diffuse identically?

A

CO2 diffuses across the membrane 20x faster than oxygen

477
Q

How can dead space become a problem?

A

In hyperventilation, not much of the air actually reaches the alveoli.

  • Small volumes of air shifted.
  • Emphysema etc.
478
Q

Nodal action potential

A

o Automaticity – spontaneous depolarisation until threshold potential reaches when cell fires (phase 0)
o Phase 0 – depolarisation, inwards Ca2+ ¬influx instead of Na+, slower rise, less overshoot
o Phase 3 – repolarisation, no rapid inactivation of Na+ channels, slow increase in K+ outflow, slow inactivation of Ca2= inflow
o Phase 4 – spontaneous depolarisation, increase slow Na2+ current

479
Q

What are the 2 types of COPD patients?

A
  1. Blue bloaters - overweight, cyanotic, oedema & sleep apnoea - chronic bronchitis
    - respiratory failure earlier
  2. Pink puffers - pursed lip breathing, leaning forward, prominent accessory muscles - respiratory failure late
480
Q

HF causes almost every hormone system in he body to become abnormal. Name these systems

A
o	Activation of RAAS – biggest one
o	Adrenergic activation
o	Increased endothelin (vasoconstrictor)
o	Increase ADH – increases thirst + fluid retention
o	Increased natriuretic peptides
481
Q

Pathology of chronic bronchitis

MEGIS

A
Mucous gland atrophy 
Excess mucous 
Goblet hyperplasia 
Inflammatory cell 
Smooth muscle hypertrophy
482
Q

Eosinophils in sputum is a marker of what?

A

Asthma

483
Q

What is the bacteria that mainly causes TB?

A

Mycobacterium tuberculosis.

484
Q

Step 1 asthma treatment

A

Inhaled short acting B2 agonist - salbutamol

485
Q

Which agent is the most important class-Ib antiarrhythmic?

A

Lidocaine

486
Q

Causes of tachycardia

A
  • Supraventricular - AF, atrial flutter

- Ventricular - VT, VF, torsades de pointes

487
Q

How does resistance affect flow rate?

A

Narrowing of the airway, increased resistance, flow reduced.

488
Q

Step 2 asthma treatment

A

B2 agonist and steroid

489
Q

Phase 4 of cardiac action potential

A
  • High K+ intracelluar
  • Intracellular negative ions unable to penetrate resting membrane and can’t accompany K+ out, therefore always slight negative charge at rest
  • Diastole
490
Q

Occupational causes of asthma

A

 Bakers
 Welders
 Paint sprayers
 Laboratory workers

491
Q

Which are the inferior leads of an ECG?

A

II, III, AVF

492
Q

2 types of acquired immunity

A

Humoral - antibody production

Cell-mediated - associated with CD8

493
Q

How does the SNS affect the SA node?

A
  • Increased sympathetic = increased heart rate
  • Exercise (after first minute)
  • Heart failure
  • Salbutamol
  • Adrenaline
494
Q

How is COPD and asthma treatment different?

A

 Eosinophilic bronchitis responds to steroids

 Neutrophilic bronchitis does not

 Yet every patient is give corticosteroids on admission w/ obstructive airway problem

495
Q

What class of antiarrhythmics are the following examples of?

Carvedilol
Propranolol
Esmolol
Timolol
Metoprolol
Atenolol
Bisoprolol
Nebivolol
A

Class II

They are mostly beta-blockers

496
Q

Causes of cough hypersensitivity

A
o	Airway/lung infection 
o	Left heart failure
o	Lung cancer
o	Foreign body inhalation
o	Interstitial lung disease/pulmonary fibrosis/pneumoconiosis
o	Tracheal compression by lymph nodes, aortic aneurysm, tumour
o	ACE inhibitors
o	Asthma
o	Gastro-oesophageal reflux
o	Chronic bronchitis + emphysema (COPD)
497
Q

What is S1 and S2 heart sounds due to?

A

S1 - 1st heart sound – closure of atrioventricular valves (tricuspid + mitral)

S2 - 2nd heart sound – closure of semilunar valves (aortic and pulmonary)

498
Q

Normally, which of inspiration and expiration is passive, and which is active?

A
  • Inspiration: active.

- Expiration: passive (elastic recoil).

499
Q

What are some of the issues of DR TB?

A
  • Difficult to treat.
  • Toxic treatments.
  • Expensive drugs.
  • Isolation and quarantine of patients.
  • Higher mortality rate.
500
Q

Chronic heart failure can be classified using NYHA classification. From Class I to IV describe how they are defined.

A

o Class I – no symptoms
o Class II – symptoms on severe exertion, but more than a normal person
o Class III – symptoms on modest exertion
o Class IV – symptoms at rest - mortality after 1 year of class IV = 50%

501
Q

What is the body’s response to heart failure?

A

Same response to acute blood loss

Sympathetic outflow:
 Raised BP, HR
 Preserved flow to vital organs at expense of limbs

Salt + water conservation:
 Thirst, ADH
 Shut down kidneys

502
Q

What is pulmonary oedema?

A

Fluid in air spaces of lungs

 Impaired LV requires higher filling pressure to maintain output, eventually the pressure exceeds the lymphatic drainage + fluid accumulates in the alveoli

 Early stage CXR – heart enlarged, interstitial lines, beginnings of alveolar oedema, lungs look white wit ‘bat-wing’ appearance if fluid stretching out from the hila of the lungs

503
Q

Small cell lung cancer

A
  • Develops from bronchial endocrine or APUD cells
  • Associated with paraneoplastic syndrome
  • Mutations in p53, RB, MYC
504
Q

Adenocarcinoma

A
  • Most common type in people who have smoked less than 100 cigarettes in their lifetime
  • Tumours arise from glands e.g. clara cells, type II pneumocytes + goblets cells
  • Slowest rate of growth
  • Most common in women
505
Q

Findings of investigation of bronchitis?

A

o Bloods – often normal
o Spirometry – obstructive picture
o Chest x-ray – normal

506
Q

Conduction velocities of ventricular and atrial muscles and AVN?

A

Ventricular + atrial muscles (1m/s)

AVN conducts the slowest (0.05m/s)
 Allows atria sufficient time to contract before ventricles are activated

507
Q

2nd degree type 2 heart block

A
  • QRS regular

- 2x P waves for every 1 QRS

508
Q

Paraseptal emphysema

A

Involves air spaces at periphery of lobule

509
Q

Atrial flutter

A

Usually not stable over a long period of time
 Revert to sinus rhythm
 Likely to recur
 Often degenerates to AF

Difficult to modify atrial rate or control ventricular rate:
 Changing block creates abrupt change in HR
 2:1  4:1 block means ventricular rate drops from 150mp to 75bpm

510
Q

Summary of asthma Tx

A
  • Treat the 2 components of asthma – bronchoconstriction + inflammation
  • We use 2 hormone receptors = corticosteroid + adrenaline
  • Inhalers at the correct dose can minimise systemic effects
  • Getting the right combination of therapy is key
  • Step 1 – salbutamol (if pt. using more than once per day) –> step 2 corticosteroid (if ineffective) –> step 3 long acting beta agonist
    o Long acting beta agonist + corticosteroid combination regular use + short acting beta agonist when required
511
Q

What is post-primary/secondary TB?

A
  • Reactivation or reinfected TB
  • Occurs in immune deficiency such as disease, drugs and old age
  • Reactivation as granuloma breaks up
512
Q

Management of bronchitis

A
o	Symptomatic
o	Bronchodilators
o	Steroids – inhaled vs oral
o	Possibly antibiotics
o	Limited evidence of benefit from treatments
513
Q

What is an ectopic pacemaker?

A

Ecopic pacemaker: an excitable group of cells that cause a premature heart beat outside the normally functioning SAN
- An ectopic pacemaker can reside within a part of the electrical conduction system of heart or within muscle cells of atria or ventricles

514
Q

Complicated coal-workers pneumoconiosis

A
  • Rare
  • AKA progressive massive fibrosis (PMF)
  • Coal they worked with contaminated with silicase
  • Marked disability
515
Q

What happens when a muscle is stimulated to contract by an action potential?

A
  • Calcium channels open in the sarcoplasmic reticulum
  • Release calcium into sarcoplasm
  • Calcium then binds to troponin, causing it to change shape and reveal the myosin binding site on actin
  • Cross-bridge forms
  • Contraction can occur
516
Q

Mechanism of asthma

A

o Dendritic cells present allergen antigen to t-cell
o Th2 cells produce IL4, IL5, IL13
o Production of these interleukins signals B cells to produce IgE
o IgE binds to mast cells in the airways
o In the presence of the antigen, IgE causes mast cells to degranulate
o Degranulation of mast cells releases inflammatory mediators like histamine, leukotrienes (promote bronchospasm)
o These cytokines activate T and B lymphocytes further + attract eosinophils

517
Q

What is pan-lobular emphysema?

A
  • Involves all lung fields, occurs w/ loss of all portions of the acinus from respiratory bronchiole to alveoli
  • This pattern is typical for alpha-1 antitrypsin deficiency
518
Q

Clinical course of pulmonary oedema

A

o Patients get better or die
o Time course of hours – not a chronic problem
o Following recovery, the patient is started on oral diuretics + ACE inhibitors – treatment for chronic heart failure

519
Q

Second line drugs for TB

A
  • Capreomycin
  • Cycloserine - inhibits early stages of peptidoglycan synthesis
  • Streptomycin - inhibits bacterial protein synthesis
  • Flouroquinolones
520
Q

MOA of ezetimibe

A
  • Blocks sterol carrier protein in brush border of enterocytes therefore reducing amount of biliary and dietary cholesterol delivered to liver via chylomicrons
521
Q

What class of antiarrhythmics are the following examples of?

Amiodarone
Sotalol
Ibutilide
Dofetilide
Dronedarone
E-4031
Vernakalant
A

Class III

522
Q

Which cells conduct the fastest?

A

His-Purkinje cells - 205m/s

523
Q

What is the Interferon gamma release assay? (IGRA). What is the advantage of IGRA over TST?

A
  • Blood test to measure cell mediated immune response by quantifying IFN-g released by T cells in response to TB antigens.
  • More specific and sensitive than Mantoux.
524
Q

Atypical pathogens that cause pneumonia

A
Legionella pneumophilia:
o	Legionella resides in stagnant water
o	Causes 2 syndromes: Legionnaire’s disease (pneumonia) + Pontiac fever (less severe)
o	Severe disease associated w/ extra-pulmonary findings:
	Fever
	Diarrhoea
	Headaches
	Liver enzyme rise
	Mental state changes
	Hyponatraemia
o	CXR: patchy infiltrates
o	Treat with macrolide or quinolone

Mycoplasma pneumoniae:
o More common in older children + young adults
o Course usually mild but can be severe when multiple systems involved
o CXR: much more extensive than clinical chest findings (discrepancy)

Chlamydophila pneumoniae:
o Usually milk in adults/self-limiting
o Associated w/ exacerbations of COPD

525
Q

Why are large TB droplets not infectious?

A
  • Fall out of the air due to the size.

- Are removed from the body by coughing and mucociliary action.

526
Q

Conn’s syndrome

A
  • Primary hyperaldosteronism
  • Tumour in adrenal gland producing aldosterone
  • Increased aldosterone leads to increased sodium and water retention
  • Hypertension with low K+ = Conn’s
  • Renin:aldosterone ratio is wrong
527
Q

How to differentiate between renin overproduction and aldosterone overproduction causing secondary hypertension?

A
  • High aldosterone, low K+, low renin means – problem at adrenal glands with aldosterone overproduction
  • High aldosterone, high renin – means problem at kidneys with renin overproduction
528
Q

MOA of spironolactone

A

Aldosterone antagonist (aka mineralocorticoid nuclear receptor antagonist)

Competitive binding to receptors on the aldosterone dependent Na+/K+ exchanger in the DCT

529
Q

What are the 4 models of progression for heart failure?

A
  1. Haemodynamics
  2. Neurohormonal
  3. Peripheral
  4. Metabolic
530
Q

What is pericarditis?

Symptoms, causes and changes on ECG of pericarditis

A
Pericardial inflammation
•	Sharp, stabbing
•	Worse with inspiration
•	Worse lying flat
•	Eased by sitting up + NSAIDs
•	Hours to days

Causes:
o Infection – bacterial, viral
o Pericardial infusion – with infection, malignancy, lymphoma

Changes on ECG:
o Concave scooped ST elevation – different to ST elevation in MI
o PR depression – best seen on lead 4

531
Q

Differential diagnosis of breathlessness in women or diabetics

A

Angina

532
Q

What rate would a denervated heart beat at?

A

105 bpm (SANs intrinsic rate)

533
Q

How much time does blood spend in the pulmonary capillaries on exercise and rest? What is the significance of this?

A
  • 3/4 of a second at rest.
  • 1/4 of a second on exercise.
  • CO2 diffuses very quickly so unaffected, is then ventilated out.
  • On exercise, not enough O2 is always taken up in the short amount of time.
  • In respiratory illness within thickened membrane it is even worse.

Not enough time for gas exchange to take place!

534
Q

Most prosthetic valve produce a normal flow murmur. Difference between aortic valve and mitral valve prosthesis?

A

 Aortic valve prosthesis – systolic ejection murmur

 Mitral valve prosthesis – diastolic flow murmur

535
Q

Causes of multi-drug resistant TB

A
	Poor treatment compliance
	Single drug therapy
	Poor calculation or regimes
	Malabsorption of drugs
	Prescribing/dispensing errors
536
Q

Estimating risk/benefit of treating hypertension?

A

o There is a linear relationship between increasing BP + increasing risk to health

o There is risk associated with treatment of hypertension

o Should only treat people when risk from hypertension exceeds risk from treatment – there are a lot of people who are treated prematurely + they are at high risk from side effects of treatment

537
Q

Describe the electrical pathway of the heart

A

o Electrical impulses begin at SAN

o Signals spread from SAN across atria causing atrial muscular contraction)

o Signals stimulate AVN and AVN delays the signal

o Impulses pass down bundle of His and splits into the left and right

o Impulses pass up the purkinje fibres which are spread throughout the ventricles

o Impulses cause the ventricles to contract from base up

o Repolarisation takes a while in cardiac muscle to prevent the muscle from going into tetanus

538
Q

What is the baroreflex?

A
  • Baroreceptors in carotid sinus and aortic arch
  • Detect BP change
  • Carotid sinus signals via glossopharyngeal nerve to nucleus tractus solitarus in the medulla
  • Aortic arch signals via vagus nerve to nucleus tractus solitarus in the medulla
539
Q

Causes of hypersensitivity pneumonitis

A

Bird fancier’s lung
• Due to feathers + bird droppings

Farmer’s lung
• Due to mouldy hay (moulds + bacteria)

Metalworking fluids HP
• Due to mist from metalworking fluids (no-TB mycobacterium)

540
Q

Centrilobular emphysema

A

Dilatation of respiratory bronchioles

541
Q

Steroids are very effective at getting rid of eosinophils, they cause apoptosis.

How to they work?

A

Steroid molecule attaches to inactive steroid receptor  activating it

Receptors form a dimer

Dimer acts on DNA by:
 Up regulating beta-receptor gene – more beta receptors
 Down regulating cytokine genes – less inflammation

542
Q

What is a granuloma? When would one form in TB.

A

A collection of immune cells that from a wall around a foreign substance that they are unable to destroy.

  • In latent TB.
  • Consists of macrophages, giant cells, T lymphocytes, B lymphocytes, fibroblasts.
543
Q

Where is the infarction in an anterior acute MI?

A

Left anterior descending artery

aka

The anterior interventricular branch of left coronary artery is a branch of the left coronary artery.

544
Q

Pathophysiology of acute heart failure

A
  • Gets you admitted to hospital

- Fluid in the wrong place e.g. peripheral or pulmonary oedema

545
Q

What is the difference between compensated and decompensated type 2 resp failure in COPD?

A
  • Decompensated = acutely unwell, CO2 rapidly goes up.

- Compensated = chronic over time, bicarbonate from the kidneys.

546
Q

Spectrum of coronary disease

A
  • Asymptomatic
  • Stable angina
  • Acute coronary syndrome
  • Heart failure
  • Sudden death
547
Q

What does aldosterone do?

A
  • Potentiates the effect of sympathetic activation
  • Pro-arrhythmic
  • Causes salt + water retention
  • Triggers fibrosis within failing heart
  • Na+ and water retention
  • Increases K+ and Mg2+ loss
548
Q

What is mesothelioma?

A

A type of cancer that develops from thin layer of tissues + covers internal organs

Most commonly affected are is lining of lungs + chest well

It is almost invariably caused by occupational exposure to asbestos:
• Long latency (approximately 40 years) 

• Only small exposures needed 

• Highly dependent on fibre type

549
Q

What are type 1 cells in heart?

A

Pacemaker cells

o Automatic: spontaneously depolarises wo/ stimulation
o SAN, AVN, conductive tissue (His bundle, bundle branches, purkinje fibres)

550
Q

What would the spirometry of a patient with obstructive lung disease show?

A
  • FEV1 is reduced in obstruction.
  • FVC is normal.

Reduced FEV1/FVC ratio, less that 0.7 ratio.

551
Q

Systemic effect of lung carcinoma

A

o Metastatic spread

o Paraneoplastic syndromes secondary to ectopic production of hormones by the lung cancer cells

o Lambert-Eaton myasthenia syndrome – Auto-antibodies against neuronal calcium channels
o Peripheral neuropathy
o Dermatological abnormalities – e.g. acanthosis nigrans
o Haematological abnormalities – e.g. leukaemia reactions
o Hypertrophic pulmonary osteoarthropathy w/ finger clubbing

552
Q

URT infections

A

o Airway above glottis – Nose, sinuses, pharynx, larynx

o Pathogens that cause UPRI - Viral, bacterial, fungal

o Includes: tonsillitis, pharyngitis, laryngitis, sinusitis, common cold, otitis media

o Symptoms: nasal congestion, runny nose, sore throat, cough, sneezing, headache, facial pain and fever

553
Q

What is Wolff-Parkinson-White syndrome?

A

A disorder due to a problem with the electrical system of the heart

The underlying mechanism involves an accessory electrical conduction pathway between the atria and the ventricles

554
Q

What are amiloride and triamterene examples of?

A

Epithelial sodium channel blockers which are potassium sparing diuretics

Treatment of hypertension and congestive heart failure.

555
Q

MoA of class II antiarrhythmics?

A

 Beta adrenergic receptor antagonists – Non-selective/cardio-selective

 Inhibits sympathetic stimulation – Blocks the effects of adrenaline

 Reduces heart rate, contractility LV and blood pressure - Improve myocardial O2 supply/demand ratio

 Reduce excitability of cardiac tissue and prevalence arrhythmias

556
Q

MOA of gemfibrozil

A
  • Fibrate
  • Increase transcription of genes for lipoprotein lipase and ApoA1 + ApoA5
  • Increased risk of gallstones
557
Q

What should the ratio of FEV1/FVC be?

A

Greater than 75%

558
Q

Histological changes in accelerated hypertension?

A

o Fibrinoid necrosis of small arteries + arterioles

o Damage to RBCs – as they negotiate vessels obstructed by fibrin with resulting microangiopathic haemolytic anaemia

559
Q

Why is troponin (I or T) the only cardiac markers we tend to use?

A

o Very early peak within day then gradually level reduces
o Need to take 2 measurements to observe elevation of the enzyme
o Goes back to baseline level after around 1-2 weeks
o Troponin is sensitive to damage to myocardium but it’s not specific for MI

560
Q

Describe Phase 4 cardiac myocyte action potential

A

Na2+ and Ca2+ channels close, open K+ channels keeps membrane potential at -90mV

561
Q

Which are the lateral ECG leads?

A

I, V5, V6, AVL

562
Q

List all cardiac markers

A
o	Troponin I
o	Troponin T
o	CK
o	CK-M8
o	LDH
o	Myoglobin
563
Q

Name the 2 major types of emphysema?

A

 Panlobular

 Centrilobular

564
Q

First degree heart block

A

 Rate is 75bpm – not bradycardiac in terms of ventricular rate
 Regular QRS complexes
 P wave before each QRS
 PR interval is prolonged – delay in conduction of impulses from atria to ventricles

565
Q

Pharmacological treatment of pulmonary oedema

A

Diamorphine - anxiety relief, possible role as vasodilator

Oxygen - patient will be. hypoxic

Diuretic - almost always IV furosemide

Vasodilator:
 Often given nitrate IV – GTN, isosorbide mononitrate, etc.
 Titrated against BP
 Drops blood pressure (may be a problem in very ill people)
 Acutely reduce left ventricle end diastolic pressure by vasodilation

566
Q

How can pneumonia be classified?

A

Radiological
lobar or bronchopneumonia

Clinical
CA or HA

Microbial
typical or non-typical

567
Q

How does resistance to acute pulmonary oedema occur?

A

Mitral stenosis!!

  • Thickened alveolar capillary membrane
  • Increased lymphatic drainage
568
Q

Symptoms of stable angina

A
  • Central tight chest pain
  • Radiates to jaw, teeth, back and arm
  • Brought on by exercise, big meals, cold etc.
  • Relieved by rest and nitrates
569
Q

What is cor pulmonale?

A
  • Right sided heart failure as a result of chronic lung disease
  • Ventilation-perfusion mismatch due to chronic hypoxia of the alveoli
  • Constriction of capillaries, results in pulmonary hypertension
  • RV has to work harder against resistance, becomes dilated - can become RHF
  • If so raised JVP and peripheral oedema (ankles) due to stasis
570
Q

Left ventricular aneurysm

A
  • Ballooning out of heart
  • Associated with signs and symptoms of heart failure
  • Decreased cardiac output
  • LV thrombus formation
  • Ventricular arrhythmias and sudden death
571
Q

How can psychological risk factors lead to physical risk factors?

A

Psychological risk factor –> health behaviours –> disease outcomes

Stress –> smoking –> COPD/Angina

572
Q

When are class V antiarrhythmics used?

A

Used in supraventricular arrhythmias, especially in heart failure with atrial fibrillation.

Contraindicated in ventricular arrhythmias.

Magnesium sulfate used in torsades de pointes.

573
Q

Common presentations of lung carcinoma

A

o Cough (75%)
o Weight loss (40%)
o Chest pain (40%)
o Dyspnoea (20%)

574
Q

Pathophysiology of R bundle branch block

A

RBBB: atrial septal defect, PE, MI

575
Q

Give some examples of 1st line TB medication.

A
  • Rifampicin: Inhibits RNA synthesis.
  • Pyrazinamide: Disrupts plasma membrane.
  • Isoniazid: Inhibits cell wall synthesis.
  • Ethambutol: Inhibits cell wall synthesis.
576
Q

Large A waves on JVP can indicate what?

A

o Pulmonary hypertension
o Tricuspid stenosis
o Cannon waves in CH8 or VT
o If not A wave present – AF

577
Q

What does aldosterone do?

A

Encourages excretion of K+ in exchange for reabsorption of Na+ in the late DCT.

578
Q

How is bradycardia due to heart block treated?

A

Investigate and remove cause
• Recent (inferior) MI
• Digoxin toxicity, beta-blockers, rate limiting calcium channel blockers
• Intravenous atropine

2nd/3rd degree heart block usually requires pacing

579
Q

Mitral papillary muscles

A

The mitral valve has 2 cusps, help by papillary muscles

 The posteromedial papillary muscle is typically supplied via the posterior descending artery
• 80% of people PDA Is supplied by RCA
• 20% of people PDA is supplied by LCx

 The anterolateral papillary muscle has a dual supply from the LAD + LCx
• Collateral supply means if there is an anterior infarct, you can still get blood supply from the LCx

 Rupture of the posteromedial papillary muscle occurs 6-12x more frequently than anterolateral papillary muscle

580
Q
  • Methylxanthines act as bronchodilators by relaxing bronchial smooth muscle + helps the constricted airways to dilate
  • They are used in the treatment of asthma + COPD

What is their MOA?

A

Exact mechanism is no well understood but it’s thought to…

o Inhibits phosphodiesterase (which usually degrades cAMP)
o Increases concentration of cAMP
o Activates PKA
o Inhibits TNF-alpha + leukotriene synthesis
o Reduces inflammation + innate immunity

581
Q

Pathophysiology of chronic stress

A
  • Increased output from sympathetic nervous system and increased HPA output
  • Results in insulin resistance, central obesity, bone density drops, inflammation, hypertension and ANS dysfunction
582
Q

What group is TB most prevalent in in the UK?

A

Non-UK born citizens

583
Q

What does a ventricular rate of 40 bpm suggest?

A

Complete heart block where the bundle of His has taken over as dominant pacemaker

584
Q

What can cause a ventilation/perfusion mismatch?

A
  • Infection i.e. pneumonia, infection and inflammation cause vasodilation so perfused despite no ventilation.
  • Pulmonary embolism, part of the lung is normally ventilated but not perfused.
585
Q

List classes of drugs used for hypertension treatment

A

A - Ace inhibitors
B - Beta blockers
C - Calcium antagonists
D - Diuretics

586
Q

What is the annulus fibrosis?

A

Fibrous ring separating atria and ventricle

587
Q

Examples of thiazide drugs

A
  • Bendroflumethiazide
  • Chlortalidone
  • Metolazone
588
Q

Slow (mnths/yrs) causes of breathlessness

A

COPD

Interstitial lung disease (e.g. idiopathic pulmonary fibrosis)

Pneumoconiosis (occupational lung disease)

Pulmonary arterial hypertension

589
Q

Give examples of normal ventilation but decreased perfusion

A

 Pulmonary embolism
 Right to left cardiac shunt
 (but not normally obstructive or restrictive diseases)

590
Q

Right sided heart failure

A

o R side is responsible for receiving deoxygenated blood from systemic circulation + pumping it to lungs to be oxygenated
o This may be due to muscle injury, MI localised to RV, damage to valves in R side of heart or elevated pressure in the lungs
o However, HF commonly affects both sides of the heart and this is called biventricular HF
o The R heart fails usually because the L heart fails

591
Q

Systemic disease associated with COPD

A

Muscle wasting, increased osteoporosis, peripheral neuropathy and depression

592
Q

What conditions cause a wheeze?

A

o Acute bronchitis
o Asthma
o COPD
o Large airway obstruction – tracheal/laryngeal tumour

593
Q

Paraneoplastic syndromes secondary to ectopic production of hormones by the lung cancer cells.

In particular SCC and SqCC

A

 ADH – Hyponatraemia (commonly in small cell carcinoma).

 Parahormone – Hypercalcaemia (commonly in squamous cell carcinoma)

594
Q

Mnemonic – No (Na blocker) Boy (beta blocker) Keeps (K blocker) Clean (calcium blocker)

A

Type I anti-arrthymatics are Na channel blockers (phase 0)

Type II - beta blockers mainly

Type III - K channel blockers (phase IV)

Type IV - Ca channel blockers (phase III)

595
Q

Causes of pulmonary oedema?

What would be observed in a CXR?

A

o Causes: MI, left ventricular dysfunction, renal artery stenosis

o CXR – cardiomegaly, bats-wing appearance (fluid + congestion, fluid in interstitial spaces

596
Q

What is the mechanism of action of atrial natriuretic peptide?

A. Suppress sympathetic tone

B. Agonist of aldosterone

C. Hydrolyses angiotensinogen to angiotensin I

D. Antagonist of angiotensin II

E. Agonist of angiotensin I

A

D. Antagonist of angiotensin II

597
Q

How does B-type or brain natriuretic peptic work?

BNP named as such because it was originally extracted from pig brain

A

B-type natriuretic peptides suppress sympathetic tone and the RAAS

598
Q

Causes of aortic regurgitation?

A

Rheumatic fever,

Infective endocarditis,

Marfan’s syndrome,

Syphilis

599
Q

Most common cause of infective endocarditis?

A

Streptococci viridans. It is found in the mouth and so is associated with poor dental hygiene or after dental procedure.

Staphylococcus epidermidis is a cause of infective endocarditis, but is associated with patients with prosthetic valves.

Staphylococcus aureus is a cause of infective endocarditis, commonlpy associated with injecting drug users.