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Year 2 - Theme A > Block 13 > Flashcards

Block 13 Flashcards

1
Q

Define: dyspnoea

A

Breathlessness

An unpleasant sensation of a feeling of an increased demand for breathing

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2
Q

What are some causes for breathlessness?

A 
Pulmonary oedema
Pneumothorax
Pulmonary embolism
Acute:
- Anaphylaxis
- Acute asthma
- Pneumonia

Subacute:

  • heart failure
  • pleural effusion
  • lung cancer
  • anaemia

Slowly progressive:

  • chronic bronchitis and emphysema
  • interstitial lung disease
  • pneumoconiosis
  • pulmonary arterial hypertension
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3
Q

What are some causes of cough?

A 
Airway/lung infection
Left heart failure
Lung cancer
Foreign body inhalation
ACE inhibitors
Asthma
Pulmonary fibrosis
COPD
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4
Q

Risk factors for TB

A 
Elderly
Immunocompromised
Diabetes
Hodgkin lymphoma
Chronic lung disease
Chronic kidney failure
Malnutrition
Alcoholism
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5
Q

What are the pathological manifestations of TB?

A

Caseating granulomas

Cavitation

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6
Q

Describe secondary TB

A

Arises in previously sensitised host
Appears when host immune system compromised
Cavitation occurs readily
Erosion of cavities = coughing up bacteria = INFECTIOUS
Reactivation of latent infection or exogenous reinfection

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7
Q

What are some of the carcinogens that can cause lung cancer?

A 
Radon
Arsenic
Asbestos
Outdoor air pollution
Cigarette smoke
Hydrocarbons
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8
Q

What are some of the carcinogenic substances in cigarette smoke?

A

43 known

Carcinogenic metals - arsenic, nickel, cadmium, chromium

Potential promoters - acetaldehyde, phenol

Irritants - nitrogen dioxide, formaldehyde

Cilia toxins - hydrogen cyanide

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9
Q

What are the targets of genetic damage in cancer?

A

Growth promoting oncogenes
Growth inhibiting cancer suppressor genes
Genes that regulate programmed cell death
Genes that regulate repair of damaged DNA

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10
Q

What is the histology of normal respiratory epithelium?

A

Pseudostratified, columnar, ciliated

Squamous if damaged

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11
Q

Describe what is seen in dysplasia

A

Disordered cell growth

Loss of normal architecture and of uniformity of cells

Pleomorphic, hyperchromic nuclei

Increase in mitotic figures often at abnormal locations

Precedes but does not necessarily lead to cancer

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12
Q

Squamous cell carcinoma

A

Develops from squamous metaplasia

Excessive growth of abnormal squamous cells

Locally invasive

Able to form metastases

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13
Q

How does carcinoma of the lung present?

A

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

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14
Q

What are the local effects of lung cancer, what causes them?

A

Pneumonia, lobar collapse, abscess - obstruction of airway

Lipid pneumonia- obstruction

Pleural effusion - spread to pleura

Hoarseness - invasion of recurrent laryngeal nerve

Dysphagia - oesophageal invasion

Diaphragm paralysis - phrenic nerve invasion

Rib destruction - chest wall invasion

SVC syndrome - SVC compression

Horners syndrome - invasion of sympathetic ganglia (Pancoast)

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15
Q

What are the systemic effects of lung cancer?

A

Metastatic spreak

Ectopic production of hormones - ADH, ACTH, Parathyroid hormone, calcitonin, gonadotropins, serotonin

Peripheral neuropathy

Dermatological abnormalities

Haematological abnormalities

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16
Q

What are the 2 main subtypes in lung cancer?

A

Non small cell carcinoma 80%

Small cell carcinoma 20%

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17
Q

What are the 3 sub groups of non small cell carcinoma?

A

Squamous cell carcinoma 25-40%

Adenocarcinoma 25-40%

Large cell carcinoma 10-15%

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18
Q

Describe adenocarcinoma (lung)

A

Infiltration of lung by abnorma glandular structures

Shows glandular differentiation

  • tubular/acinar/papillary structures
  • Mucin production

Precursor lesions - atypical alveolar cell hyperplasia (alveoli lined by atypical cuboidal epithelial cells)

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19
Q

Describe small cell carcinoma (lung)

A

Shows neuroendocrine differentiation

Crowded small cells with hyperchromatic glassy nuclei and extremely scanty cytoplasm

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20
Q

What are the 2 main factors for rapid spread of TB?

A

Crowded living conditions

A population with little native resistane

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21
Q

Where is prevalence of TB highest?

A

China
India
Southern Africa

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22
Q

What is the incidence of TB in the UK?

A

13 per 100,000

Highest in London

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23
Q

What groups are most at risk of TB?

A 
Alcoholics
Intravenous drug users
Homeless
Prison inmates
Urban poor
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24
Q

How is TB spread?

A

Inhalation of droplet nuclei

Aerosolised by coughing, sneezing or talking

8 hours of close contact required - prolonged exposure

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25
Q

Describe the process of TB infection

A
  • Bacteria multiply freely in alveolar space or within macrophages
  • Proceeds for weeks
  • Development of tissue hypersensitivity
  • CD4 recognise the antigens presented by macrophages
  • Cytokine release
  • Form Langhans giant cells (fused macrophages)
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26
Q

Describe caseous necrosis in TB

A

Inherently unstable

Liquifies and discharges through the bronchial tree producing a tuberculous cavity

Infectious material sloughed from a cavity can allow bronchogenic spread

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27
Q

What questions should be asked in taking a history from a patient with TB?

A 
History of TB exposure
Country of origin
Age
Ethnic or racial group
Occupation
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28
Q

What is the presentation of TB?

A 
Productive, prolonged cough (over 3 weeks)
Chest pain
Haemoptysis
Fever
Chills
Night sweats
Appetite loss
Weight loss
Fatigue
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29
Q

What happens in primary TB infection?

A

Rapid destruction of bacteria and the infective process is arrested (only evidence is positive ManToux test)
Ghon focus occurs but is stopped

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30
Q

What happens in post primary infection?

A

Immune deficiency which allows reactivation as macrophage and granuloma break up

Causes bronchial spread as necrosis occurs

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31
Q

Where are the main sites of spread for extra-pulmonary TB?

A

Can be to any organ

Abdomen
Bone
Brain
Muscle
Retina
Lymph node
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32
Q

What percentage of TB cases are purely extrapulmonary?

A

19-30%

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33
Q

What is the stain used for acid fast bacilli?

A

Ziehl- Neelson

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34
Q

What tests can be used to check immunity to TB?

A

Man toux test (only specific for mycobacteria)

IFN-g (specific for TB)

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35
Q

What tests should be carried out if you suspect TB?

A 
Chest X-ray
Sputum specimens
Routine drug susceptibility testing
HIV testing
Hepatitis testing
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36
Q

What are the first line drugs for TB treatment?

A 
Isoniazid
Rifampicin
Pyrazinamide
Ethambutol
Rifabutin
Rifapentine

Viractiv - one tablet for all 4 drugs

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37
Q

Name some occupational lung diseases

A 
Occupational asthma
COPD
Pneumoconiosis
Toxic pneumonitis
Hypersensitivity pneumonitis
Benign pleural disease e.g. asbestos
Infective - TB
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38
Q

Outline occupational asthma

A

Underdiagnosed
Most common cause of occupational lung disease
Baker ,soldering, Paint spraying, animal housing.

Can prevent lifelong asthma if picked up early enough

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39
Q

Outline simple pneymoconiosis

A

Coal miners lung
Causes chronic bronchitis
Normal lung funtion
Cough and sputum

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40
Q

Outline silicosis

A 
Coal workers (mixed)
Sand blasters (pure)

Rare
Upper lobe nodules and lymph node calcification and enlargement

Predisposes to TB and lung cancer

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41
Q

Outline siderosis

A

Inhaled iron

Doesn’t cause disability or decrease lung function

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42
Q

Outline hypersensitivity pneumonitis

A

Form of pulmonary fibrosis (presents like pneumonia - breathing difficulties and fever)

Farmers lung (mouldy hay - fungal spores) and pigeon fanciers lung

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43
Q

Describe the pathogenesis of TB

A
  1. Macrophages are infected by mycobacterium tuberculosis
  2. Bacteria replicate within the macrophage
  3. 3 weeks post infection - TH1 response activates macrophages
  4. TH1 release IFN gamma.
  5. TH1 stimulates formation of granlomas and caseous necrosis
  6. Infection is controlled within the macrophages
  7. It can be reactivated or reexposed
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44
Q

Describe secondary TB

A

Arises in previously sensitised host

Reactivation when immune system decreased or re-exposure

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45
Q

What are the clinical features of secondary TB?

A 
Insidious in onset
Malaise
Anorexia
Weight loss
Low grade fever
Sputum
Haemoptysis
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46
Q

Describe the morphology of TB

A
  • Small area of white inflammation with consolidation - Ghon focus
  • Centre undergoes caseous necrosis
  • Ghon complex = lung lesion and node involvement
  • It undergoes progressive fibrosis then calcification (Ranke complex)
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47
Q

Outline miliary pulmonary disease

A

Occurs when organisms drain through lymphatics

Consolidation scattered throughout lungs

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48
Q

Define chronic bronchitis

A

Defined clinically as persistent cough with sputum production for at least 3 months in at least 2 consecutive years

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49
Q

What can result from persistent chronic bronchitis?

A

Progress to COPD
Lead to cor pulmonale and heart failure
Cause atypical metaplasia and dysplasia of respiratory epithelium

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50
Q

What is the pathogenesis of chronic bronchitis?

A

Long standing irritation of inhaled substances
Hypersecretion of mucus in large airways (hypertrophy of glands)
Proteases released from neutrophils
Marked increase in goblet cells
Damage to cilia and epithelium

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51
Q

Outline the morphology of chronic bronchitis

A
  • Hyperaemia, swelling and oedema of mucous membranes
  • Excessive mucinous secretions
  • Hyperplasia of mucous glands
  • Increased Reid index
  • Marked narrowing of bronchioles
  • Obliterations of lumen due to fibrosis (extreme)
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52
Q

What are the clinical features of chronic bronchitis?

A 
Persistent cough, productive of sputum
Dyspnoea on exertion
Hypercapnia
Hypoxaemia
Mild cyanosis
Impairment of respiratory function
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53
Q

What are the changes seen in chronic bronchitis?

A 
Squamous metaplasia
Glandular hyperplasia
Goblet cell hypertrophy
Smooth muscle cell hypertrophy
Mucociliary dysfunction

LYMPHOCYTES not eosinophils

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54
Q

What is the incidence of lung cancer?

A

Occurs most frequently between 40-70 years
Peak incidence at 50-60
5 year survival rate = 16%
Incidence and mortality rates have been decreasing

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55
Q

Outline pathogenesis of lung cancer

A

Stepwise accumulation of genetic abnormalities

  • 87% are smokers
  • Heavy smokers (10 pack years) are 60x increased risk
  • Gene mutations: KRAS, EGFR, p53, RB1, p16
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56
Q

What are the features of a lung adenocarcinoma?

A

Malignant epithelial tumour with glandular differentiation

Most common in women and non-smokerss

Peripheraly located and tend to be smaller

Slow growth - wide and early metastasis

KRAS mutation

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57
Q

What are the features of a small cell carcinoma?

A

Highly malignant with distinctive cell type - high mitotic count

No cell differentiation, necrosis is common and extensive

Neuroexcretory granules
Strong relationship to cigarette smoking

p53 and RB1

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58
Q

What are the features of a squamous cell carcinoma (lung)

A

Most common in men
Closely correlated with smoking
Keratinisation
p53 mutations

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59
Q

What are the uses of radiotherapy in lung cancer?

A

External radiotherapy (more common) and internal during bronchoscopy

Shrink tumour blocking an airway

SE: fatigue, anaemia, skin soreness, hair loss in area, difficulty swallowing

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60
Q

What are the uses of chemotherapy in lung cancer?

A

Small cell lung cancer
Can be used for non-small cell after surgery

SE: tiredness, nausea and vomiting, mouth ulcers, diarrhoea, constipation, hair loss, increased infection

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61
Q

What are the uses of surgery in lung cancer?

A 
Non-small cell lung cancer
Lobectomy
Sleeve resection
Pneumonectomy
Segmentectomy
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62
Q

Mycobacterium tuberculosis

A 
large non-motile baccili
obligate aerobe (upper lobes)
Intracellular parasite of macrophages
Acid fast
High lipid content
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63
Q

Why is the high lipid content of M. tuberculosis important?

A

Impermeability to stains and dyes
Resistance to many antibiotics
Resistance to killing by acidic and alkaline compounds
Resistance to osmotic lysis via complement deposition
Resistance to lethal oxidations and survival inside macrophages

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64
Q

Define multi-drug resistant TB

A

Resistant to at least 2 of the best anti-TB drugs

Isoniazid and rifampicin

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65
Q

Define extensively drug resistant TB

A

XDR TB
Rare
Resistant isoniazid and rifampicin plus resistant to any fluroquine and at least 1 of 3 injectable 2nd line drugs e.g. kanamycin, capremycin

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66
Q

Define asthma

A

Chronic inflammatory disorder of the airways that causes recurrent episodes of wheezing, breathlessness, chest tightness and cough, particularly at night and//or in early morning.

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67
Q

What are the hallmarks of asthma?

A

Increased airway responsiveness to various stimuli
Causing episodic bronchoconstriction
Inflammation of bronchial walls
Increased mucus secretion

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68
Q

What are the common triggers of asthma?

A 
Respiratory infections 
Environmental exposure to irritants (smokes, fumes)
Cold air
Stress
Exercise
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69
Q

What are the 4 different types of asthma?

A

Atopic
Non-atopic
Drug-induced
Occupational

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70
Q

What is atopic asthma?

A

Type 1 IgE mediated hypersensitivity reactions

  • Begins in childhood
  • Positive family history common
  • Triggered by allergens
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71
Q

What is non-atopic asthma?

A
  • Respiratory infections are common triggers
  • Hyperirritability of bronchial tree
  • Virus induced inflammation lowers threshold of the subepithelial vagal receptors to irritants
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72
Q

Describe the pathogenesis of asthma

A
  1. Genetic predisposition for atopy
  2. Initial sensitisation to allergen which stimulates production of TH2 cells
  3. TH2 cells secrete cytokines IL4, 5 and 13
  4. Promotes inflammation and stimulates B cells to produce IgG and the antibodies
  5. IgE, eosinophils and mucus secretion
  6. IgE coats mast cells, repeat exposure to release granule contents
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73
Q

Describe the early phase reaction in asthma?

A

Bronchoconstriction - triggered by direct stimulation of subepithelial vagal receptors

Increased mucous production
Variable degrees of vasodilation
Increased vascular permeability

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74
Q

Describe the late phase reaction in asthma?

A

Inflammation with recruitment of leukocytes and eosinophils, neutrophils and T cells

Eotaxin activates eosinophils

Prolonged bronchoconstriction - leukotrienes C4.D4.E4. ACh, histamine. prostaglandin D2.

75
Q

What are the features of airway remodelling?

A
  • Hyperplasia and hypertrophy of bronchial smooth muscle
  • Epithelial injury
  • Increased airway vascularity
  • Increased mucus gland hypertrophy
  • deposition of subepithelial collagen
76
Q

Epidemiology of asthma

A

1 in 10 children

1 in 12 adults

77
Q

What are the clinical features of asthma?

A

Chest tightness
Dyspnoea
Wheezing
Cough with or without sputum production

78
Q

Define emphysema

A

Condition of the lung characterised by irreversible enargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis

79
Q

What are the different types of emphysema?

A

Centriacinar
Panacinar
Paraseptal
Irregular

80
Q

Outline centriacinar emphysema

A

Central or proximal parts of acini (respiratory bronchioles)
Terminal alveoli are spared
Lesions are more common and more severe in upper lobes
Inflammation around bronchi and bronchioles common
Occurs predominantly in heavy smokers

81
Q

Outline panacinar emphysema

A

Acini are uniformly enlarged from the level of respiratory bronchiole to the terminal blind alveoli
Entire acinus
Occurs more commonly in lower zones and anterior margins
Associated with alpha 1 antitrypsin deficiency

82
Q

Outline paraseptal/ distal acinar emphysema

A 
Proximal part of the acinus is normal
Distal part is predominantly involved
At margins of lobules and adjacent to pleura
More severe in upper part of lungs
Forms cyst like structures
Underlies most spontaneous pneumothorax
83
Q

Outline the pathogenesis of emphysema

A
  • Activated inflammatory cells release mediators - IL8, TNF that damage lung structures and sustain neutrophilic inflammation
  • Protease antiprotease mechanism and imbalance of oxidants and antioxidants (deficiency of antiprotease alpha 1 antitrypsin)
  • Increased neutrophil elastase
  • Causes tissue damage
  • Loss of elastic tissue which causes respiratory bronchioles to collapse during expansion
84
Q

What are the cellular findings in emphysema?

A

Goblet cell metaplasia
Inflammatory infiltration of walls with neutrophils, macrophages, B cells, CD4 and 8 T cells
Thickening of bronchiolar wall due to smooth muscle hypertrophy and peribronchial fibrosis
Loss of elastic recoil

85
Q

Outline the morphology of emphysema

A 
Voluminous lungs overlapping heart
Upper 2/3 of lung more affected
Large alveoli separated by thin septa
Loss of attachment of alveoli to outer wall of small airways
Decrease in capillary bed
86
Q

What are the clinical features of emphysema?

A 
No symptoms until at least 1/3 is damaged
Dyspnoea
Cough or wheeze
Expectoration
Weight loss
Barrel chest and dyspnoic
Prolonged expiration
Sits hunched over with pursed lip breathing
87
Q

What is type 1 respiratory failure?

A

Hypoxaemic
Low O2
Normal or low CO2
Caused by ventilation-perfusion mismatch
- Underventilated alveoli
- Venous blood bypasses ventilated alveoli
Hyperventilation increases CO2 removal but does not increase oxygenation

88
Q

What is type 2 respiratory failure?

A

Hypercapnic
Increased CO2
Indicated inadequate alveolar ventilation
Can be acute or chronic

89
Q

Causes of type 1 respiratory failure

A 
COPD
Pneumonia
Pulmonary oedema
Pulmonary fibrosis
Asthma
Pneumothorax
PE
Pulmonary hypertension
90
Q

Causes of type 2 respiratory failure

A 
COPD
Severe asthma
Drug overdose
Myasthenia gravis
Obesity
91
Q

Define forced vital capacity

A

Volume of lungs from full inspiration to forced maximal expiration

Reduced in restrictive disease

92
Q

Define FEV1

A

Forced expiratory volume in one second

Volume of air expelled in the first second of forced expiration

93
Q

Define FER

A

Forced expiratory ratio

FEV1/FVC x100

94
Q

What would you expect in a FEV1/FVC to be in obstructive disease?

A

FVC normal or reduced
FEV1 reduced <80%
Ratio reduced below 70%

95
Q

What would you expect in a FEV1/FVC to be in restrictive disease?

A

FVC reduced <80%
FEV1 reduced
Ratio remains the same

96
Q

What are the 5 steps in asthma treatment?

A

Step 1 - short acting beta agonist (salbutamol)
Step 2 - Inhaled steroid (beclometasone)
Step 3 - Long acting beta agonist (salmetrol)
Step 4- Leukotriene receptor antagonist and increased steroid (montelukast)
Step 5- Oral steroid (prednisolone)

97
Q

What are the symptoms of life threatening asthma?

A 
Severe breathlessness
Unable to complete sentences
Tachypnoea
Tachycardia
Silent chest
Cyanosis
Collapse
98
Q

Define MI

A

Death of cardiac muscle due to prolonged severe ischaemia

99
Q

What is the incidence of MI?

A

Frequency rises with age
Men at more risk
10% under 40
45% in over 65s

100
Q

What is the pathogenesis of MI

A

Sudden change in atheromatous plaque which causes coronary artery occlusion

  • exposed subendothelial collagen, platelets adhere and become activated
  • Release of granule contents (aggregation)
  • Vasospasm stimulated by mediators released from platelets
  • Tissue factor activates coagulation pathway
  • Thrombus occludes lumen

Myocardial response

  • Ischaemia and myocyte death
  • Cessation of aerobic metabolism
  • Accumulation of noxious metabolites (lactic acid)
  • Loss of contractility
  • Cell death (if ischaemia longer than 20-30 minutes)
101
Q

What are the 2 forms of MI?

A

Transmural

Subendocardial

102
Q

Describe transmural infarction

A

Ischaemic necrosis involves full or nearly full thickness of ventricular wall in the distribution of coronary artery

ST elevation

103
Q

Describe subendocardial infarction

A

Ischaemic necrosis limite to inner 1/3 or 1/2 of ventricular wall which is the area most vulnerable to decreased blood flow

non ST elevation

104
Q

Which arteries are most commonly affected in MI?

A

Left anterior descending 40-50%
Right coronary artery 30-40%
Left circumflex 15-20%

105
Q

What are the dangers of reperfusing the heart after MI?

A 
Arrythmias
Haemorrhage
Irreversible cell damage
Microvascular injury
Prolonged ischaemic dysfunction
106
Q

What are the clinical features of an MI?

A

Rapid weak pulse
Profuse sweating
Dyspnoea
10-15% asymptomatic

107
Q

How would you diagnose an MI?

A

Cardiac troponins T and I
MB fraction of creatine kinase
ECG

108
Q

What are the complications of MI?

A

Contractile dysfunction (pulmonary oedema, ventricular failure, cardiogenic shock)
Arrythmia - VT, VF, tachycardia, asystole
Myocardial rupture
Pericarditis

109
Q

What is the mortality after MI?

A

30% in the first year

3-4% with each year after

110
Q

Define angina

A

Angina pectoris
Characterised by paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort caused by transient myocardial ischaemia

Doesn’t cause myocyte necrosis

Stable and unstable

111
Q

Outline stable angina

A

Most common

Caused by an imbalance in coronary perfusion due to chronic stenosing coronary atherosclerosis relative to myocardial demand

Pain caused by increased cardiac load - physical activity and emotional excitement

112
Q

Outline unstable angina

A

Pattern of increasingly frequent pain, often of prolonged duration that is precipitated by progressively lower levels of physical activity

Can occur at rest
Caused by disruption of atherosclerotic plaque with thrombosis, possibly embolisation or vasospasm

113
Q

Outline the conduction system of the heart

A 
SA node (pacemaker)
Bachmanns bundle
Anterior, middle, posterior to AV node
Bundle of His
Left and right bundle branch
Purkinje fibres
114
Q

What is the arterial supply tot he AV node?

A

Right coronary artery 85-90%

Left circumflex artery 10-15%

115
Q

What is the arterial supply to the SA node?

A

Right coronary artery 55-60%

Left circumflex artery 40-45%

116
Q

Define ventricular tachycardia

A

Broad complex tachycardia originating from a ventricular ectopic focus

3 or more ventricular extrasystoles in succession at a rate of more than 120bpm

117
Q

What are the features of ventricular tachycardia?

A

Rate >120bpm
Broad QRS complexes
Can be monomorphic - regular rhythm from single focus
Can be polymorphic - irregular with different QRS complexes

118
Q

What is sustained VT associated with?

A 
Late phase MI
Cardiomyopathy
Right ventricular dysplasia
Myocarditis
Drugs e.g. class 1 anti-dysrhythmic
119
Q

What is the presentation of VT?

A 
Chest pain
Palpitations
Dyspnoea
Dizziness
Syncope
120
Q

What are the risk factors for VT?

A

Coronary heart disease
Structural heart disease
Triggered by electrolyte deficiency
Sympathomimetic agents e.g. caffeine

121
Q

What is VF?

A

Ventricular fibrillation - cause of cardiac arrest and sudden cardiac death.

Ventricular muscle fibres contract randomly causing a complete failure of ventricular function

122
Q

What are the risk factors for VF?

A 
Anti-dysrhythmics
Ischaemia
Shock during cardioversion
Hypoxia
AF
Electrical shock
123
Q

What is the presentation of VF?

A

Chest pain
Fatigue
Palpitations

124
Q

What is an ectopic pacemaker?

A

Abnormal pacemaker sites within the heart (outside SA node) that display automaticity
Can cause additional beats or take over the SA node
Generally produce a rhythm of 30-40bpm
Spread of depolarisation is not normal as it takes longer to spread
Prolongs duration of QRS complex

125
Q

What is ischaemic heart disease?

A

Leading cause of death worldwide

Myocardial ischaemia is reduced blood flow due to obstructive athersclerotic lesions in coronary arteries

126
Q

What is the presentation of ischaemic heart disease?

A

Myocardial infarction
Angina pectoris
Chronic IHD with heart failure
Sudden cardiac death

127
Q

What is the pathogenesis of IHD?

A

Insufficient coronary perfusion relative to myocardial demand due to chronic progressive atherosclerotic narrowing of coronary arteries, superimposed acute plaque change, thrombosis and vasospasm.

128
Q

What are the risk factors for atheroma/ CVD?

A 
Increasing age
Male
Family history
Race - south Asians
Smoking
Lack of exercise
High fat diet
High alcohol intake
Psychological factors e.g. depression, stress
Hypertension
Diabetes
Hyperlipidaemia
Obesity
Systemic inflammation
129
Q

What is the management for obesity?

A 
Dieting
Exercise
Weight loss programs
Orlistat - inhibits pancreatic lipase
Bariatric surgery
130
Q

What are the physical consequences of obesity?

A 
Increased risk of:
CHD
Hypertension
Stroke
Type 2 diabetes
Cancer
Fertility problems/ high risk pregnancy
Decreased life expectancy
Joint problems
131
Q

What are the psychological consequences of obesity?

A 
Depression
Anxiety
Low quality of life
Low self-esteem
Body dissatisfaction
Poor concentration
Lower academic success 
Social exclusion
132
Q

What are the social consequences of obesity?

A

More likely to suffer from discrimination
- in employment, travel, school, healthcare, retail
Less friends
Lower educational achievement
Lower employment

133
Q

Where are the 3 main places that myocardial rupture can take place?

A

Myocardial rupture of L ventricular wall
Myocardial rupture of ventricular septum
Myocardial rupture of papillary muscle

134
Q

What are the features of a myocardial rupture of the ventricular septum?

A

Size of defects determine magnitude of Left to right shunt
Haemodynamic compromise
Harsh, loud, holsystolic murmur

135
Q

What are the 4 classes in the New York Heart Classification?

A

Class 1 - no limitation of physical exercise. No symptoms on ordinary physical activity

Class 2 - slight limitation of physical activity. Symptoms on ordinary activity

Class 3 - Marked limitation of physical activity. Symptoms on less than ordinary activity

Class 4 - inability to carry out any physical activity without discomfort

136
Q

What is cardiac neurosis?

A

Occurs in relative or friend of individual who has recently been diagnosed with cardiac condition or in the period following myocardial infarction

Dyspnoea, fatigue, rapid pulse, palpitations and chest pain with exertion

Psychological disorder associated with exhaustion and emotional strain

137
Q

Describe the cardiac action potential

A

Phase 0 - rapid depolarisation, fast inflow of Na+
Phase 1 - short initial rapid repolarisation due to closure of Na+ channels, Cl- influx and outflow of K+
Phase 2 - Plateau, delay repolarisation, slow inward movement of Ca2+ and continual outflow of K+
Phase 3 - second period of repolarisation caused by continual flow of K+ and inactivation of Ca2+ inflow

138
Q

Describe the waves on an ECG

A

P wave - spread of excitation through atria
PR interval - atria contract, excitation within AV node
QRS complex - spread of excitation through ventricles
QT interval - ventricles contract, action potential pahse 2
T wave - ventricles repolarise

139
Q

What are the average lengths of the peaks in an ECG?

A 
PR = 0.12-0.2s
QRS = 0.08-0.12s
QT = 0.3-0.46s
140
Q

How do you measure HR using an ECG?

A

300/ number of large boxes between successive R wave peaks

141
Q

What time is represented by 1 ECG grid box (small square)?

A

0.04s

142
Q

What are the different types of heart block?

A 
1st degree
2nd degree
- Mobitz type 1
- Mobitz types 2
3rd degree (complete)
143
Q

Describe 1st degree heart block

A

PR interval >0.2s

Asymptomatic, no treatment required

144
Q

Describe Mobitz type 1 heart block

A

2nd degree
Wenckebach
Progressive PR interval prolongation until P wave fails to conduct
No treatment unless symptomatic

145
Q

Describe Mobitz type 2 heart block

A

Sinus rhythm with normal PR interval but occasionally the p wave is not followed by QRS complex
Close monitoring - could progress to complete heart block

146
Q

Describe a 3rd degree heart block

A

Complete heart block
Normal p wave
No QRS complex
ICU or CCU

147
Q

What is bundle branch block?

A

Block of either the right or left bundles that branch from the bundle of His

In right BBB - right heart activation follows left
In left BBB - left heart activation follows right

Wide double peaked QRS complex and inverted T wave

148
Q

What are the symptoms of heart block?

A 
2nd and 3rd degree
Fainting
Dizziness
Fatigue
SOB
Chest pain
149
Q

Outline AF

A 
Atrial fibrillation
Atrial activity poorly defined
Ventricular response is irregularly irregular
Atrial rate = 350-650bpm
P wave is fibrillatory.
QRS <0.12s
150
Q

How can you manage arrythmias?

A 
Treat cause (if possible)
Vagotonic manoeurves
DC cardioversion
Pacemakers
Surgery
Medication
151
Q

What are the causes of bradycardia?

A

HR < 60bpm

Physiological - athletes
Cardiac - AV block or sinus node disease
Non-cardiac - vasovagal, hypothermia, hypothyroidism, hyperkalaemia
Drugs - Beta blocker, diltazem, digoxin, amiodarone

152
Q

How can you treat bradycardia?

A

atropine
glucagon
digoxin specific antibody fragments
external pacing

153
Q

What are the causes of haemopysis?

A 
Lung cancer
TB
Bronchiectasis
Pulmonary oedema
Pulmonary embolism
Pneumonia
154
Q

What are the causes of stridor?

A 
Whooping cough
Epiglottitis 
Foreign body
Laryngeal/tracheal tumour
Laryngeal oedema
155
Q

What would you expect to find on examination of consolidation?

A 
Mediastinal shift - NO
Percussion note - DULL
Added sounds - CRACKLES
Chest expansion - NORMAL OR DECREASED
Breath sounds - BRONCHIAL
Vocal resonance - INCREASED
156
Q

What would you expect to find on examination of pleural effusion?

A 
Mediastinal shift - NONE OR AWAY
Percussion note - STONY DULL
Added sounds - NONE
Chest expansion - DECREASED
Breath sounds - DIMINISHED/ABSENT
Vocal resonance - DECREASED
157
Q

What would you expect to find on examination of airway obstruction?

A 
Mediastinal shift - NONE
Percussion note - NORMAL
Added sounds - WHEEZE
Chest expansion - SYMMETRICAL
Breath sounds - NORMAL
Vocal resonance - NORMAL
158
Q

What would you expect to find on examination of pneumothorax?

A 
Mediastinal shift - AWAY
Percussion note - HYPER RESONANT
Added sounds - NONE
Chest expansion - DECREASED ON SIDE OF
Breath sounds - ABSENT/DIMINISHED
Vocal resonance - INCREASED
159
Q

What would you expect to find on examination of collapse?

A 
Mediastinal shift - TOWARDS
Percussion note - DULL
Added sounds - NONE OR CRACKLES
Chest expansion - REDUCED
Breath sounds - DIMINISHED
Vocal resonance - REDUCED
160
Q

What would you expect to find on examination of unilateral fibrosis?

A 
Mediastinal shift - TOWARDS
Percussion note - DULL
Added sounds - CRACKLES
Chest expansion - REDUCED
Breath sounds - NORMAL
Vocal resonance - NORMAL
161
Q

What is congestive heart failure?

A

Occurs when the heart is unable to pump blood at a rate sufficient to meet metabolic demands of tissues or can only do so at an elevated filling pressure

  • Ischaemic heart disease
  • Chronic work overload
  • Acute haemodynamic stresses e.g. large MI
162
Q

What is the Frank-Starling mechanism?

A

Increased filling volumes dilate the heart and increases functional cross bridge formation, enhancing contractility

163
Q

What mechanisms maintain perfusion and pressure?

A 
Frank-Starling mechanism
Myocardial adaptations - hypertrophy and ventricular remodelling
Activation of neurohumoural systems
- Release of NA by ANS
- Activation of RAAS
- Release of ANP
164
Q

Outline the formation of cardiac hypertrophy

A

Increase mechanical work due to pressure or volume overload - cause myocytes to increase in size

Pressure overload hypertrophy -
Response to increase in pressure. Concentric increase in wall thickness. Expanding cross sectional area of myocytes

Volume overload hypertrophy -
Ventricular dilatation. Wall thickness can be: increased, decreased or stay the same.

165
Q

Describe how cardiac dysfunction occurs

A

Hypertension (pressure overload)
Vascular disease (pressure +/- volume overload)
MI (volume overload)

  • Increased cardiac load
  • Increased wall stretch
  • Cell stretch
  • Hypertrophy +/- dilation
  • Cardiac dysfunction
166
Q

What are the characteristics of congestive heart failure?

A

Variable degrees of decreased cardiac output and tissue perfusion
Pooling of blood in venous system

167
Q

What are the causes of left sided heart failure?

A

Ischaemic heart disease
Hypertension
Aortic and mitral valvular disease
Myocardial diseases

168
Q

Define left sided heart failure

A

Congestion of pulmonary circulation, stasis of blood in the left sided chambers and hypoperfusion of tissues leading to organ dysfunction

169
Q

What are the consequences of left sided heart failure?

A

Left ventricle is hypertrophied and often dilated
Can cause dilation of left atrium and increase risk of AF
Pulmonary congestion and oedema
Perivascular and interstitial oedema (Kerley B lines)
Progressive oedematous widening of alveolar septa
Accumulation of fluid in alveolar spaces
RBC in fluid = phagocytosed = iron in macrophages

Decreased output causes decrease in renal perfusion
Activation of RAAS
Induces retention of salt and water
Expansion of interstitial and intravascular fluid volumes

170
Q

What are the clinical signs of left sided heart failure?

A

Cough
Dyspnoea (initially in exertion, later at rest)
Orthopnoea
Paroxysmal noctural dyspnoea

171
Q

What is systolic dysfunction?

A

Failure of the pump function
Decreased ejection fraction (less than 45%)
Destruction or dysfunction of cardiac myocytes

Ventricle inadequately emptied
Ventricular end-diastolic pressures and volume increases
Pressure transmitted to atrium then pulmonary vasculature

172
Q

What is diastolic dysfunction?

A

Failure of the ventricle to adequately relax - stiff ventricle wall
Heart can’t increase output without demand
Any increase in pressure causes pulmonary oedema

173
Q

What is right sided heart failure?

A

Most commonly caused by left sided heart failure
Increased pressure in pulmonary circulation burdens the right

Pure right sided heart failure is from lung disorders

174
Q

What are the causes of right sided heart failure?

A

Parenchymal diseases of lung
Primary pulmonary hypertension
Recurrent pulmonary thromboembolism
Hypoxia

175
Q

What is the incidence of hypertension?

A

35 years - 30%
45-54 years - 30%
Over 75 years - 70%

176
Q

What are the different stages of hypertension?

A

Stage 1 - BP in surgery 140/90+
Stage 2 - BP in surgery 160/100+
Severe hypertension - BP in surgery 180/110+

177
Q

What are the causes of hypertension?

A

Primary - essential hypertension (unknown 95%))

Secondary 5%
Renal disease
Endocrine (cushings, crohns, acromegaly, hyperparathyroidism)
Coarction
Pre-eclampsia
Drugs and toxins
178
Q

What are the long term consequences of hypertension?

A 
Atherosclerosis
Stroke
MI
Aneurysm
Kidney disease
Vascular dementia
Eye damage
179
Q

Define preload

A

Filling pressure, pressure in ventricle just before it starts to contract

180
Q

Define afterload

A

Pressure at which the heart has to eject blood

181
Q

What is Starlings Law?

A

Increase in preload leads to increased heart work and increased force of contract

Caused by increased cross linking of myofibrils in syncytium

182
Q

What are the precipitants of heart failure?

A 
acute ischaemia
arrythmia AF, VT
mechanical disaster
intercurrent illness
non-compliance
PE
Stress
Drugs
183
Q

What is chronic heart failure?

A

Cardiac dysfunction at rest
Symptoms of heart failure
Responds to treatment

Year 2 - Theme A (7 decks)

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