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Year 2 > Block 13 > Flashcards

Block 13 Flashcards

1
Q

What are the sudden causes of breathlessness?

A

Pulmonary oedema (additional nocturnal dyspnoea)
Pneumothorax (additional pluritic chest pain)
PE (additional syncope)
Anaphylaxis (additional swelling, itch, urticaria)
Foreign body inhalation (onset whilst eating)

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2
Q

What are the rapid (hour onset) causes of breathlessness?

A

Acute asthma
Pneumonia
Pulmonary oedema
Acute hypersensitivity pneumonitis

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3
Q

What are the subacute (week onset) causes of breathlessness?

A

Heart failure
Anaemia
Pleural effiusion
Lung cancer

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4
Q

What are the slowly progressive causes of breathlessness?

A

COPD
Interstitial lung disease
Pneumoconiosis
Pulmonary arterial hypertension

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5
Q

What are some causes of cough?

A 
Infection
Left heart failure
Lung cancer
Foreign body inhalation
ACE inhibitors
Asthma
COPD
GO reflux disease
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6
Q

What are some factors to note about sputum?

A

Colour:
Mucoid? Purulent? Bloodstained?

Volume:
Large volume in bronchiectasis and bonchioalveolar carcinoma

Odour:
Putrid in anaerobic infection

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7
Q

What are the causes of haemoptysis?

A 
Lung cancer
TB
Bronchiectasis
Pulmonary oedema
Pulmonary embolism
Pneumonia
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8
Q

What are the causes of wheeze?

What is the difference between wheeze and stridor?

A

Wheeze = expiratory sound produced by air moving through narrowed airways.

Acute bronchitis
Asthma
COPD
Large airway obstruction

Stridor = an inspiratory sound in: whooping cough, epiglottitis, foreign body obstruction, laryngeal obstruction

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9
Q

What are the causes of chest pain?

A

Pleuritis
Pneumonia (sharp, stabbing, worse on inspiration)
PE (sharp, stabbing, worse on inspiration)
Pneumothorax (sharp, stabbing, worse on inspiration)
Tracheitis
Mediastinal tumour (retrosternal pain)
Rib mets (bony pain)
Spinal root pain
Herpes zoster (dermatomal)

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10
Q

What are the causes of wheeze - heard on auscultation?

A 
Asthma = polyphonic and high pitched
Monophonic = large airway obstruction
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11
Q

What are the causes of crackles - heard on auscultation?

A

Clearing with coughing = consolidation - lots of causes. Main being pneumonia.

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12
Q

What is the incidence of lung cancer?

A

The 2nd most common cancer in the UK ~45000

The leading cause of cancer death ~35000

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13
Q

What is the survival rate for lung cancer?

A

Poor.
1yr survival = 50%
5yr survival = 10%

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14
Q

What are the risk factors for developing lung cancer?

A

FHx
Environmental factors (asbestos, chemical dust, radiation)
Smoking

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15
Q

What are the main forms of lung cancer?

A

Small cell
Adenocarcenoma
Squamous cell carcinoma
Large cell carcinoma

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16
Q

Describe the features of small cell carcinoma.

A

The most malignant form of lung cancer
Metastasises early and widely
Histologically - lots of small, highly nucleated cells. Very fragile = crush artefacts
Closely associated with smoking
Necrosis is usually present and extensive throughout the lung
Common mutations (p53, KRAS, 3p)
Commonly associated with a PARANEOPLASTIC syndrome.

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17
Q

Describe the features of a lung adenocarcinoma.

A

Most common form of lung cancer
Not associated with smoking. (Usually found in young, non-smoking females)
Slow growing but can metastasise early
Usually sound in the periphery of the lung

Atypical adenomatous hyperplasia –> adenocarcinoma in situ.

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18
Q

Describe the features of squamous cell carcinoma.

A

As with small cell carcinoma, strongly associated with smoking rates.
Usually found in large, main, bronchi.

Squamous metaplasia –> dysplasia –> CIN –> neoplasm

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19
Q

Describe the features of large cell carcinoma.

A

Uncommon form of lung cancer (5-10%)
Linked with smoking - not as much as SCC and SCC
Undifferentiated, epithelial tumours.

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20
Q

What is a pancoast tumour?

A

An apical lung tumour which impinges on nerves in the mediastinum - particularly: recurrent laryngeal, vagus, sympathetic trunk.

Causes: Horners syndrome (enopthalmos, ptosis, miosis, anhidrosis)

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21
Q

What are the early –> late symptoms found in lung cancer?

A

Early:
Productive cough w/ blood, chronic cough, weight loss

Mid:
Chest pain, SVC syndrome, effusion, pneumonitis, atelectasis

Late:
Bone pain, heptaomegaly, neurological change, Addisons.

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22
Q

What percentage of heavy smokers develop lung cancer?

A

~11%

Suggesting that there is a strong genetic involvement

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23
Q

Give some examples of the common 2˚ pathology that can arise from lung cancer?
(10)

A

Partial lung obstruction = focal emphysema
Total lung obstruction = atelectasis
Venous blockage = pulmonary oedema
Invasion of pleura = pleuritis / pleural effusion
Vascular compression = superior SVC syndrome
Pericardial spread = pericarditis / tamponade
Recurrent laryngeal nerve = hoarsness
Sympathetic trunk = horners syndrome
Oesophageal invasion = dysphagia
Chest wall invasion = rib pain / destruction

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24
Q

What are the common clinical presentations of lung cancer?

A

Chronic cough
Weight loss
Chest pain
Dyspnea (SOB)

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25
Q

What are the main treatments for lung cancer?

A

Lobectomy
Pneumonectomy
Chemotherapy and radiotherapy (little effect on small CC)
EGFR inhibitors (adenocarcinoma)

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26
Q

What is the incidence of TB?

A

Extremely common cause of morbidity and mortality worldwide (>1.7billion infected)
2nd most common cause of deaths worldwide

UK incidence ~10/100,000

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27
Q

What are the main risk factors for TB?

A 
Overcrowding
Poverty
Poor hygiene
Concurrent chronic illness
HIV infection
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28
Q

What organism causes TB?

A

Most commonly mycobacterium TB (can be mycobacterium bovis)

Acid fast bacillus (Zhiel Neilson stain)

Spread by droplet infection

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29
Q

What is the pathophysiology of 1˚ TB?

A

Droplets into the lungs - usually effects lung apices as M.tb is an aerobic organism.
Taken up by alveolar macrophages + phagocytosis
TB released substance which prevents lysosome fusion
Replication and proliferation within macrophages
Causes a 1˚ infection which generally goes unnoticed (subclinical or flu-like infection)
After 3w antigens are taken to lymph and cell-mediated immune response begins.
T-cells release INF-gamma which causes macrophages to coagulate and form fibrous capsule around the infected area GHON FOCUS

GHON COMPLEX is formed with lymph nodes become involved.

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30
Q

What is the pathophysiology of 2˚ TB infection?

A

Reactivation of a latent ghon focus due primarily to immunosuppression (drugs, disease, age).
Causes a severe - localised inflammatory reaction.

Cavitation when the necrosed centre of the lesion erodes into a bronchiole and has a method of escape.
Haemoptysis, pleural effusion, emphysema, pleuritis

GHON COMPLEX is formed with lymph nodes become involved.

Miliary TB = seeding of other organs with lesions of TB (particularly the liver) causing widespread infection.

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31
Q

What component of the cell wall causes TB to be acid fast?

A

Myocolic acid

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32
Q

What are the two forms of drug resistant TB?

A

Multidrug resistant = ioniazid and rifampicin resistant

Extensively drug resistant = as MDR +1 of: ethambutol, streptomycin, pyrazinamide

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33
Q

What are the main components that are seen in spirometry?

A

Vital capacity = max inhalation to max expiration. Should be >80%. Is decreased in restrictive airway disease

FEV1 = max air expelled in 1 sec. Decreased in both restrictive and obstructive

FEV1:FVC = proportion of vital capacity expelled in 1 sec. Decreased in obstructive disease.

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34
Q

What FEV1:FVC ratio is indicative of obstructive lung disease?

A

<70%

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35
Q

What spirometry pattern is seen in obstructive lung disease?

A

Normal FVC

FEV1 reduced >70%

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36
Q

What spirometry pattern is seen in restrictive lung disease?

A

FVC reduced
FEV1 reduced
As both reduced by same quantity ratio is normal

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37
Q

What spirometry pattern is absolutely indicative of asthma?

A

A 15% improvement of FVC1 after administration of Beta agonists.

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38
Q

What is the test for infection with TB?

A

Mantoux = subcutaneous PPD

No differentiation between infection and disease?

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39
Q

What is the difference between TB infection and disease?

A

Infection = latent infection after 1˚ TB disease

Disease = current, active infection and inflammation.

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40
Q

What is respiratory failure?

A

Failure of the lungs and respiratory system to provide the oxygen requirements and CO2 secretion required by the body.

Can be type 1, type 2 or somewhere between the two extremes.

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41
Q

What is type 1 respiratory failure?

A

‘pink puffer’
Hypoxia without hypercapnia.

Hunched over, struggling to breathe, pursed lip breathing, barrel chest, accessory muscles of inspiration, hyperventilation

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42
Q

What is type 2 respiratory failure?

A

‘blue bloater’
Hypoxia and hypercapnia

Cyanosis, hypoventialtion, diminished drive

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43
Q

What are the two forms of emphysema?

A

Panacinar = total alveolar enlargement. Mainly caused by congenital disease (alpha-1 amitrypsin deficiency)

Centriacinar = enlargement at the levels of respiratory bronchioles. Caused by damage from smoking.

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44
Q

Define emphysema.

A

Lung parenchyma destruction without fibrosis and insufficient wound repair.

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45
Q

Describe the pathophysiology of emphysema.

A

A combination of genetic and environmental factors - mainly smoking.
Causes inflammation of the lung parenchyma (anti-inflamamtories a-1 amitrypsin deficiency)
Activation of proteases, elastases, cytokines, oxidants.

Causes: necrosis, apoptosis, ECM destruction

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46
Q

What are the major symptoms of COPD?

A 
Progressive dyspnea (SOB)
Chronic cough
Wheezing
Weight loss (misconstrued as neoplasia)
FEV1:FVC <70%
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47
Q

Describe the pathophysiology of chronic bronchitis.

A

A cough lasting longer than 3 consecutive months in two consecutive years.

Mucus hyper secretion caused by hyperplasia of goblet cells within the large bronchial walls - caused by excessive chemical stimulation.

Hypersecretion of mucus –> outflow obstruction –> mucus plugs, inflammation, fibrosis –> 2˚ microbial infection

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48
Q

What are the main features of asthma?

A 
Reversible airflow obstruction
SOB - particularly brought on by exercise 
Diurnal variation
Wheeze (possibly stridor)
Inflammatory airway obstruction
Eosinophil infiltrate
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49
Q

What is the main difference between COPD and asthma

A

COPD is irreversible whereas asthma is reversible (time and medication)

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50
Q

What are the common airway irritants in asthma?

A

Dust + dust mites, mould, pet dander, chemicals, pollen, shellfish, nuts

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51
Q

What is the main piece of legislation that has decreased occupational asthma in the last 50 years.

A

Clean air act (1950)

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52
Q

What is the difference between occupational asthma and workplace asthma?

A

Occupational asthma = caused by work

Workplace = current asthma exacerbated by the workplace.

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53
Q

What are the main diseases of the airway?

A 
Occupational asthma
Occupational COPD
Pneumoconiosis
Toxic pneumonitis
Occupational infections (TB)
Malignancies (lung and pleura)
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54
Q

What are the most common allergens to cause occupational asthma?

A

Flour (bakers asthma)
Solder
Isocyanates

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55
Q

How can occupational asthma be distinguished from ‘normal’ asthma?

A
  • Are the symptoms worse at work
  • Do the symptoms get better when away from work - at weekend and on holiday.
  • Peak flow diary to measure this
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56
Q

What is simple pneumoconiosis?

A

A restrictive airway disease caused by the inhalation of dust - specifically coal dust found in mines.

57
Q

What is silicosis?

A

A rare, restrictive lung disease (found in sand blasters) that causes fibrosis and predisposes to many conditions - infective and malignancy.

58
Q

What is asbestosis?

A

A restrictive lung disease
Fibrosis of the lungs caused by inhalation of fibres from asbestos - used in building and roofing.
3 main types of asbestos (blue, white, brown) - blue and brown asbestos cause mesothelioma.

59
Q

What is toxic pneumonitis?

A

A rare - acute condition
Usually caused by acute chemical inhalation (NH3, NO2, etc.)
Usually required supportive treatment and oxygen but is usually self limiting and leaves no long term consequences.

60
Q

What is hypersensitivity pneumonitis?

A

Commonest among pigeon keepers and farmers (pigeon fanciers pneumonitis and farmers lung).
Presents like a chronic pneumonia
Treated by oral steroids

61
Q

What are the broad defence mechanisms within the respiratory tract?

A

Physical: nasal hair, turbinates, mucus

Mechanical: mucociliary escalator, air flow, sneezing, coughing

Microbial: alveolar macrophages, secreted antimicrobial substances, IgA secretion, resident microbial flora in upper tract.

62
Q

Which of the following organisms are NOT colonising organisms?

S. pneumonia
H. influenzae
Group A strep
Staph aureus
Legionella spp.
M. pneumonia
C. pneumonia
Gram -ve (E.coli, Klebsiella spp.)
A

Group A strep
Legionella
M. pneumonia
C. pneumonia

63
Q 
Give an example of organisms that cause respiratory infections:
Viral
Fungal
Parasitic
Mycobacteria
A

Viral = rotavirus, influenzae A/B

Fungal = aspergillus

Parasitic = Pneumocystis jirovecii

Mycobacteria = M.tuberculosis

64
Q

What are the common symptoms of upper respiratory infection?

A 
Runny nose
Nasal congestion
Sore throat
Cough
Sneezing
Headache
Pain
Fever
65
Q

What is bronchitis?

A

An inflammatory condition of the larger airways and bronchi. Associated with generalised respiratory infection. It is a diagnosis of exclusion - when no other cause can be found for the cough.

66
Q

What are the different ways of classifying pneumonia?

A

Hospital acquired (s. aureus, s. pneumonia, legionella, enterobacterioacea)

Community acquired (s. pneumonia, h. influenza, rotavirus, influenza, pseudomonas, m. catarrhalis)

Lobar (affecting an entire lobe)

Bronchopneumonia (spots of inflammation with multiple areas of consolidation)

Typical (s. pneumonia, h. influenzae, m. cararrhalis)

Atypical (legionella, mycoplasma, chlamydia, )

67
Q

What are the main differences in broncho and lobar pneumonia?

A

Bronchopneumonia = most common form. Most seen in extremities of age and can be caused by any organism.

Lobar pneumonia = bacterial (s. pneumonia, klebsiella). Most lobar pneumonia is pneumococcal but most pneumococcal is bronchopneumonia.

68
Q

What is ‘atypical’ pneumonia?

A

Cough and dyspnea but with no sputum production.
Due to inflammation of the alveolar walls without consolidation of the spaces.

Mycoplasma pneumonia, chlamydia pneumonia, legionella pneumonia

69
Q

What are the main symptoms of pneumonia?

A 
Fever
Cough +- sputum
Dyspnea
Chest pain
Fatigue and joint pain
Tachypnea and tachycardia
Headaches 
Loss of appetite
70
Q

What are the chronic and acute changes of asthma?

A

Acute: smooth muscle inflammation, eosinophil infiltrate, mucus hypersecretion, oedema

Chronic: sup-endothelial fibrosis and smooth muscle hypertrophy. MUCUS PLUGGING

71
Q

What is the most important inflammatory cell found in asthma. What is the equivalent cell found in COPD?

A

Asthma = eosinophil (mediates most of the damage)

COPD = neutrophils (release enzymes that cause ECM damage / necrosis)

72
Q

What is bronchial hyper reactivity?

A

A 2˚ care test - lung function laboratories.
To measure the ‘twitchiness of the airway’
Measuring the levels of histamine required to induce a substantial reduction in FEV1

73
Q

What are some of the occupational causes of COPD?

A 
Coal dust
Cotton dust
Grain
Heavy metals
Oil fumes
74
Q

What is for pulmonale and describe the basic pathology for its cause?

A

Right sided heart failure caused by increased vascular resistance in the lungs. (COPD)
Increased resistance is caused by capillary loss and capillary construction due to V/Q matching.

Increased resistance –> increased after load –> increased force of contraction –> right distention and hypertrophy –> failure

75
Q

Describe the pathophysiology of bronchiectasis.

A

Caused by recurrent lung infections during childhood.
Bronchial dilation - recurrent infection - mucus hypersecretion
Cystic fibrosis is the most common cause
Secretions and fibrosis causes obstruction of airflow in the small airways.

76
Q

What are some common radiological findings in COPD

A

Bullae formation.

Large airspaces that have become walled off = increasing the residual volume and decreasing the vital capacity.

77
Q

Draw a diagram of the wave form resultant from a spirometery reading.
Label all of the areas on the graph with its proper name.

A

Normal breathing waves with large inspiration and expiration.

Tidal volume
Inspiratory reserve volume 
Expiratory reserve volume
Residual volume
Vital capacity
Total lung capacity.
78
Q

What are the most common symptoms of lung disease?

A 
Dyspnea (SOB)
Cough (+- sputum)
Wheeze
Haemoptysis 
Chest pain

TIME COURSE AND RELATIONSHIP ARE IMPORTANT

79
Q

What would the expected findings be on a clinical examination of a patient with consolidation?

A 
SOB
Tachypnea
Decreased or normal expansion
Increased tactile resonance
Dull percussion
Bronchial breath sounds
Crackles 
Increased vocal resonance
80
Q

What would the expected findings be on a clinical examination of a patient with pleural effusion?

A 
Decreased chest expansion
Stony dull percussion note
Diminished breath sounds
No added sounds
Decreased vocal resonance
81
Q

What would the expected findings be on a clinical examination of a patient with airway obstruction?

A

Possibly only expiratory wheeze

- resonant percussion?

82
Q

What would the expected findings be on a clinical examination of a patient with pneumothorax?

A 
Deviated trachea - away (tension pneumothorax)
Reduced chest expansion
Hyperresonant percussion
Diminished or absent breath sounds
Reduced vocal resonance
83
Q

What would the expected findings be on a clinical examination of a patient with atelectasis?

A 
Deviated trachea - towards
Reduced chest expansion
Dull percussion note
Diminished breath sounds
Reduced vocal resonance
84
Q

What would the expected findings be on a clinical examination of a patient with fibrosis?

A 
Reduced chest expansion
Dull percussion note
Normal breath sounds
Normal vocal resonance 
Possibly crackles
85
Q

What is Flick’s law of diffusion?

A

About the rate of gas transfer though a membrane.

The rate of transfer is proportional to the area of the membrane, the diffusion constant and the difference in partial pressure. It is inversely proportional to the thickness of the membrane

86
Q

How can a respiratory acidosis be differentiated from a metabolic acidosis.

A

Respiratory = high CO2

Metabolic = low HCO3

87
Q

What are the two types of type 2 respiratory failure?

A

Compensated = no respiratory acidosis as compensated by kidney HCO3 retention.

Decompensated = respiratory acidosis as failure is so severe it cannot be compensated for.

88
Q

What is the most common cause of lung fibrosis?

A

Idiopathic pulmonary fibrosis

89
Q

What is the difference between chronic and acute for pulmonale?

A 
Acute = dilatation 
Chronic = hypertrophy
90
Q

What are the signs and symptoms of cor pulmonale?

A 
SOB - particularly on exertion 
Chronic cough
Peripheral oedema
Ascites
Raised JVP
Hepatomegaly
91
Q

What are the acute causes of cor pulmonale?

A

PE
Exacerbation of chronic CP
Acute Respiratory Distress Syndrome

92
Q

What are the chronic causes of for pulmonale?

A

COPD
Fibrosis (sarcoidosis, pneumoconiosis)
1˚ pulmonary hypertension

93
Q

What are the stages of asthma treatment?

A 
1 = short acting beta agonist (salbutamol)
2 = addition of inhaled steroid 
3 = addition of long acting beta agonist
4 = addition of inhaled leukotriene antagonist (montelukast)
5 = addition of oral prednisolone tablets
94
Q

What is the incidence of coronary artery disease?

A

Primary cause of death worldwide.
7 million deaths.
Prevalence of 2.3 million in the UK

95
Q

What are the main diseases under the banner of ‘coronary artery disease’

A

Myocardial infarction
Angina pectoris
Sudden cardiac death
Heart failure

96
Q

What are the causes of myocardial ischaemia?

A 
Atherosclerosis
Thrombus formation
Embolus (air, fat, blood, etc.)
Shock
Myocardial hypertrophy 
Tachycardia
97
Q

Define atherosclerosis?

A

Progressive stenosis of an artery through inflammation and the deposition of fats, collagen, cholesterol and minerals.

98
Q

What are the different consequences of typical stable angina and their pathologies?

A

atherosclerosis –> plaque disruption

  • -> healing –> chronic ischaemic heart disease
  • -> thrombus formation –> unstable angina
  • -> large thrombus and occlusion –> MI
99
Q

What is unstable angina?

A

Precipitated by plaque rupture and sudden, massive artery occlusion.
Severe chest pain on minor exercise or at rest.
Warning of an impending MI
(Used to be called pre infarction angina)

100
Q

What are the risk factors for thrombosis?

A

VIRCHOW’S TRIAD:
hypercoagulability, vascular injury, disturbance to flow

Diabetes
Hypertension
Pregnancy 
Turbulence 
Thrombophilia
101
Q

What are the risk factors for coronary heart disease and atherosclerosis?

A 
Hypertension
High cholesterol
Diabetes
Smoking
Alcohol
Obesity
High fat intake 
Low exercise
FHx
Ethnicity
102
Q

What are some of the minor causes of angina?

A 
Vasospasm
L atrial thrombus
Vegitations from infective endocarditis
Vasculitis
Sickle cell
Shock
103
Q

Describe what occurs in cardiac muscle cells during a myocardial infarction

A

20mins = anaerobic respiration
20mins –> 30mins = decreasing contractility (reversible)
>30mins = myocardium death

This only occurs when flow rate drops below 10% of normal.

104
Q

What are the 3 main arteries that CVD occurs in?

A

Left anterior descending (~50%)
Left circumflex (~20%)
Right coronary artery (~30%)

105
Q

What are the two forms of myocardial infarction?

A

Total occlusion = transmural = ST elevation (STEMI)

Partial occlusion = subendocardial = Non ST elevation (NSTEMI)

106
Q

What is reperfusion injury?

A

Injury that occurs when cells that have previously undergone infarction are resupplied with blood - as in a myocardial infarction and catheterisation.

Cells that have necrosed release certain toxins - free radicles, Ca2+, Inflammatory mediators, cytokines

When these toxins reach another area of healthy cells they can cause damage.
Haemorrhage, fibrillation, arrhythmia, microvascular occlusion

107
Q

What are the clinical features of coronary artery disease?

A 
Rapid, weak pulse
Profuse sweting
Dyspnea
Severe chest pain
Fatigue
Nausea and vomiting 
Confusion
108
Q

What are some of the blood markers of myocardial infarction?

A

Increased plasma myoglobin
Cardiac troponin T and I
Increased creatine kinase
Increased lactate - (acidosis??)

109
Q

What are the complications of myocardial infarction?

A 
Arrhythmia
Contractile dysfunction = heart failure
Pulmonary oedema
Cardiogenic shock
Myocardial rupture = 3-5 days post (failure, tamponade)
Pericarditis
Thrombus formation
110
Q

What are the two main forms of heart failure?

A

Chronic heart failure = progressive contractility failure of the left ventricle as a response to ischaemic change, mainly following a myocardial infarction.
Progressive failure to pump blood around the body to supply required oxygen.

Sudden cardiac death = ventricular failure with no prior symptoms of cardiac disease. Mainly caused by myocardial atherosclerosis.

111
Q

What are ectopic pacemakers?

A

A group of cells (outside the SA node) that causes a premature heartbeat

112
Q

Why does the SA node usually regulate the heartbeat when all of the heart is neurogenic?

A

It is the area of cells with the fastest natural beat.

113
Q

What are the main causes of obesity?

A

Modifiable:
fat intake, cholesterol intake, exercise levels, smoking, stress, poor diet

Non-modifiable:
Genetics (FHx), Age, gender, ethnicity, co-morbidities

114
Q

What are some of the consequences of obesity?

A 
Cardiovascular disease (MI, stroke)
Osteoarthritis
Non-alcoholic fatty liver disease
Type 2 diabetes
Hypertension
Sleep apnea
115
Q

What are some of the theories that give insight into how to decrease dangerous lifestyle factors (like obesity).

A

Theory of planned behaviour
(intention to change is the best predictor of change)

Health belief model
(Change is based on perceived threat and perceived susceptibility and perceived benefit of treatment)

Stages of change
(Pre-contemplation –> contemplation –> preparation –> action –> maintenance (–> lapse and relapse))

The E’s of behavioural change

  • Enable
  • Encourage
  • Engage
  • Exemplify
116
Q

Through which mechanisms can the heart compensate for heart failure?

A

Frank-starling mechanism:
increased preload –> increased stretch –> increased force of contraction. Maintenance = compensated heart failure
However, increased O2 requirements and if can’t maintain perfusion = decompensated.

Sympathetic activation

RAAS activation

Structural changes of myocytes themselves.

117
Q

What are the common causes of left sided heart failure?

A

Systemic hypertension
Mitral or aortic valvular disease
1˚ diseases of the myocardium (amyloidosis)

118
Q

What are the macroscopic changes observed in left sided heart failure?

A

Ventricular dilatation and hypertrophy
Possible mitral insufficiency = rate of AF
Back-pressure to the lungs (pulmonary hypertension)
Interstitial transudate = fluid filled alveoli
(pink, frothy sputum)
Extravision of RBC’s are phagocytosed by macrophages = haemociderin build up = HEART FAILURE CELLS

119
Q

What are the common early symptoms of left sided heart failure?

A 
Dyspnea
Cough
Orthopnea
Paroxysmal nocturnal dyspnea 
Tachycardia
Basal lung crackles
120
Q

What are some consequences of left ventricular failure?

A 
Mitral regurgitation and AF
Thrombus formation due to stasis
Stroke
Pulmonary oedema
Prerenal azotemia
Hypoxic encephalopathy
121
Q

What are the two main causes of right sided heart failure?

A

Cor pulmonale

Left sided heart failure that causes pulmonary hypertension and increases right sided after load.

122
Q

What are some consequences of right sided heart failure?

A 
Portal hypertension
Hepatomegaly and splenomegaly
Cardiac cirrhosis 
Peripheral oedema
Anasarca
123
Q

What are the causes of anasarca?

A

Liver cirrhosis = portal hypertension

Severe renal failure = no excretion

Nephrotic syndrome = reduced capillary oncotic pressure

Right sided heart failure =

Severe malnutrition and protein deficiency (kwashikor)

124
Q

What is the difference between kwashiorkor and marasmus?

A

Kwashiokor = protein malnutrition

Marasmus = calorie malnutrition

125
Q

What are the main causes of bradycardia?

A

Sinus bradycardia (fit, young individuals) = reduced sympathetic or increased parasympathetic

Heart block (usually result of damage to the AV node)

126
Q

What are the expected ventricular rate of the:
SA node
AV node
Ventricles

A

SA = 60-100bpm
AV ~50bpm
Ventricles ~25bpm

127
Q

What are the types of heart block?

A

1st degree = increased PR interval

2nd degree type 1 (Wenkenbach) = increased PR interval and dropping of QRS complex

2nd degree type 2 = Random dropping of QRS complex

3rd degree = No impulse from atria to ventricles so totally independent in their rhythm.

128
Q

What would an ECG of a bundle branch block show?

A

Widened QRS complex as impulse from remaining bundle branch has to traverse more of the heart.
Rate = normal

Characteristic ‘M’ shape in V1 and V2 / V5 and V6

129
Q

What are the causes of tachycaria?

A

Increased pacemaker activity = sympathetic activity = SINUS TACHYCARDIA = exercise etc…

Sick sinus syndrome (can also cause bradycardia)

Re-entry tachycardia

  • atrial fibrillation / ventricular tachycardia
  • wolff-parkinson-white syndrome (bundle of kent)
Delayed repolarisation (long QT syndrome)
R on T phenomenon
130
Q

Describe the pathophysiology of atrial fibrillation.

A

A form of re-entry tachycardia
Caused by a scar tissue focus that prevents passage of action potential through it.
If one side of the ‘normal tissue’ can repolarise faster than the other side, a circuit can develop that is continuously causing depolarisation.

= random, fast beating.

131
Q

How long is a normal PR interval?

A

3-5 small squares (<200ms)

5 small squares in one large square

132
Q

How long is a normal QRS complex ?

A

<100ms)

133
Q

How can a supraventricular tachycardia be differentiated from a ventricular tachycardia via ECG?
THE GOLDEN RULE

A

Supraventricular = normal (thin) QRS = 1/2 large square

134
Q

What is premature atrial or ventricular contraction?

A

A random, ectopic beat (not from the SA) node that causes systole.
It is very common and not connected to any pathology.

135
Q

How could a supraventricular tachycardia be distinguished from a ventricular tachycardia?

A

Both >100bpm
Supraventricular = thin QRS complex
Ventricular = wide QRS complex

Ventricular tachycardia = broad complex tachycardia
Life threatening
Requires defibrillation!

136
Q

How is a ventricular fibrillation be distinguished from a ventricular tachycardia?

A

Both are broad complex
Tachycardia = regular complexes
Fibrillation = no regularity = CHAOS

Both require defibrillation!

137
Q

What is the most common heart arrhythmia?

What does it look like on ECG?

A

Atrial fibrillation
Irregularly irregular QRS complexes
No P waves
CHAOS between the QRS complexes - the systolic rhythm proper = normal QRS but irregularly irregular

138
Q

What is cardiac flutter?

What does it look like on ECG?

A

An extreme form of tachycardia
Can occur in either the atria or the ventricles
A sequence switching between flutter and fibrillation

Atrial flutter = saw tooth between QRS

139
Q

What are the common pathologies that can be seen on ECG?

A

STEMI

Arrhythmias:
(bradycardia), (supra ventricular tachycardia), (ventricular tachycardia), (flutter - atrial or ventricular), (ventricular fibrillation), (atrial fibrillation)

Heart block:
1st degree
2nd degree - Mobitz type 1 - Wenkenbach
2nd degree - Mobitz type 2 
3rd degree 
Bundle branch block

Year 2 (7 decks)

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