PBL 3 Flashcards

1
Q

What general aspects of the lungs do pulmonary functions tests test for?

A
  • How much air volume can be moved in and out of the lungs
  • How fast the air in the lungs can be moved in and out
  • How stiff are the lungs and chest wall - a question about compliance
  • The diffusion characteristics of the membrane through which the gas moves (determined by special tests)
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2
Q

Pulmonary Function Tests are used for the following reasons:

A
  • Screening for the presence of obstructive and restrictive diseases
  • Evaluating the patient prior to surgery
  • Evaluating the patient’s condition for weaning from a ventilator.
  • Documenting the progression of pulmonary disease - restrictive or obstructive
  • Documenting the effectiveness of therapeutic intervention
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3
Q

When is a patient’s condition good enough to try weaning from a ventilator?

A

If the patient on a ventilator can demonstrate a vital capacity (VC) of 10 - 15 ml/Kg of body weight, it is generally thought that there is enough ventilatory reserve to permit (try) weaning and extubation. Be careful to ensure they are not suffering from malnutrition.

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4
Q

What factors affect the “normal” pulmonary function test scores predicted for a particular patient? (4)

A
  • Age: As a person ages, elasticity of the lungs decreases, so we have decreasing lung volumes and capacities as we age.
  • Gender : Usually the lung volumes and capacities of males are larger than those of females.
  • Body Height & Size: Body size has a tremendous effect on PFT values. A small man will have a smaller PFT result than a man of the same age who is much larger. If a patient becomes too obese, the abdominal mass prevents the diaphragm from descending as far as it could and the PFT results will demonstrate a smaller measured PFT outcome then expected.
  • Race: Race affects PFT values. Black people, Hispanics and Native Americans have different PFT results compared to Caucasians. Therefore, a clinician must use a race appropriate table.
  • Other factors such as environmental factors and altitude may have an affect on PFT results but the degree of effect on PFT is not clearly understood at this time.
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5
Q

What is FVC? What units is it expressed in? Which type of disease is it particularly useful for diagnosing?

A

FVC - Forced Vital Capacity - after the patient has taken in the deepest possible breath, this is the volume of air which can be forcibly and maximally exhaled out of the lungs until no more can be expired. FVC is usually expressed in liters. This PFT value is critically important in the diagnosis of obstructive and restrictive diseases

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6
Q

What is FEV1?

A

FEV1 - Forced Expiratory Volume in One Second - this is the volume of air which can be forcibly exhaled from the lungs in the first second of a forced expiratory manuever. It is expressed as liters. This PFT value is critically important in the diagnosis of obstructive and restrictive diseases.

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7
Q

What does FEV1/FVC - FEV1 Percent (FEV1%) - show?

A

FEV1/FVC - FEV1 Percent (FEV1%) - This number is the ratio of FEV1 to FVC - it indicates what percentage of the total FVC was expelled from the lungs during the first second of forced exhalation - this number is called FEV1%, %FEV1 or FEV1/FVC ratio. This PFT value is critically important in the diagnosis of obstructive and restrictive diseases.

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8
Q

What is FEV3?

A

FEV3 - Forced Expiratory Volume in Three Seconds - this is the volume of air which can be forcibly exhaled in three seconds - measured in Liters - this volume usually is fairly close to the FVC since, in the normal individual, most of the air in the lungs can be forcibly exhaled in three seconds.

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9
Q

What does FEV3/FVC show?

A

FEV3/FVC - FEV3% - This number is the ratio of FEV3 to the FVC - it indicates what percentage of the total FVC was expelled during the first three seconds of forced exhalation. This is called %FEV3 or FEV3%.

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10
Q

What is PEFR? What units is it measured in?
What is it useful for?

A

PEFR - Peak Expiratory Flow Rate - this is maximum flow rate achieved by the patient during the forced vital capacity maneuver beginning after full inspiration and starting and ending with maximal expiration - it can either be measured in L/sec or L/min - this is a useful measure to see if the treatment is improving obstructive diseases like bronchoconstriction secondary to asthma.

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11
Q
  • What are.
  • FEF25%
  • FEF50%
  • FEF25%-75%
A
  • FEF25% - This measurement describes the amount of air that was forcibly expelled in the first 25% of the total forced vital capacity test.
  • FEF50% - This measurement describes the amount of air expelled from the lungs during the first half (50%) of the forced vital capacity test. This test is useful when looking for obstructive disease. The amount of air that will have been expired in an obstucted patient is smaller than that measured in a normal patient.
  • FEF25%-75% - This measurement describes the amount of air expelled from the lungs during the middle half of the forced vital capacity test. Many physicians like to look at this value because it is an indicator of obstructive disease.
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12
Q

What is MVV, when is it used and what caution should the clinician be aware of?

A

MVV - Maximal Voluntary Ventilation - this value is determined by having the patient breathe in and out as rapidly and fully as possible for 12 -15 seconds - the total volume of air moved during the test can be expressed as L/sec or L/min - this test parameter reflects the status of the respiratory muscles, compliance of the thorax-lung complex, and airway resistance. Surgeons like this test value because it is a quick and easy way to assess the strength of the patient’s pulmonary musculature prior to surgery. One major cautionary note is that this test is effort dependant.

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13
Q

If flow of air out of the lungs is impeded, what type of defect is the cause?
If volume of the lungs is reduced, what type of defect is the cause?

A

If flow is impeded, the defect is obstructive
If volume is reduced, the problem is restrictive

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14
Q

What are the 5 Stages?
Pulmonary Function Tests - A Systematic Way To Interpretation

A
  • Step 1. Look at the forced vital capacity (FVC) to see if it is within normal limits.
  • Step 2. Look at the forced expiratory volume in one second (FEV1) and determine if it is within normal limits.
  • Step 3. If both FVC and FEV1 are normal, then you do not have to go any further - the patient has a normal PFT test.
  • Step 4. If FVC and/or FEV1 are low, then the presence of disease is highly likely.
  • Step 5. If Step 4 indicates that there is disese then you need to go to the %predicted for FEV1/FVC. If the %predicted for FEV1/FVC is 88%-90% or higher, then the patient has a restrictive lung disease. If the %predicted for FEV1/FVC is 69% or lower, then the patient has an obstructive lung disease
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15
Q

Microbiological sputum samples are usually used to look for infections by which organisms? (4)

A
  • Moraxella catarrhalis,
  • Mycobacterium tuberculosis,
  • Streptococcus pneumoniae
  • Haemophilus influenzae.
  • Other pathogens can also be found.
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16
Q

What three kinds of Bloody Sputum (Hemoptysis) are there? What do they show? (3)

A
  • blood-streaked sputum - inflammation of throat, bronchi; lung cancer;
  • Pink sputum - sputum evenly mixed with blood, from alveoli, small bronchi;
  • massive blood - cavitary tuberculosis of lung, lung abscess, bronchiectasis, infarction, embolism
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17
Q

What does Rusty colored sputum indicate?

A

Rusty sputum - usually caused by pneumococcal bacteria (in pneumonia)

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18
Q

What 4 types of Purulent sputum are there? (containing pus)
What do they each indicate?

A
  • A yellow-greenish (mucopurulent) color suggests that treatment with antibiotics can reduce symptoms. Green color is caused by Neutrophil Myeloperoxidase.
  • A white, milky, or opaque (mucoid) appearance often means that antibiotics will be ineffective in treating symptoms.
  • Foamy white - may come from obstruction or even edema.
  • Frothy pink - pulmonary edema
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19
Q

What is lung compliance?

A

How easy it is for the lung to change shape due to the stiffness of the lungs and chest wall

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20
Q

What is a restrictive lung disorder?

A

Restrictive disorder: one in which the lungs ability to expand is impaired, eg pulmonary fibrosis or kyphoscoliosis

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21
Q

What is an obstructive disorder of the lungs?

A

Obstructive disorder: one in which there is narrowing of the airways eg asthma, bronchitis

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22
Q

What are the different reasons for performing PFTs?

A
  • Screening for the presence of obstructive and restrictive diseases
  • Evaluating the patient prior to surgery
  • Evaluating the patient’s condition for weaning from a ventilator. If the patient on a ventilator can demonstrate a vital capacity (VC) of 10 - 15 ml/Kg of body weight, it is generally thought that there is enough ventilatory reserve to permit (try) weaning and extubation.
  • Documenting the progression of pulmonary disease - restrictive or obstructive
  • Documenting the effectiveness of therapeutic intervention
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23
Q

What is a Spirograph?
What is a Spirogram?

A
  • Spirograph: device attached to the spirometer, measures the movement of gas in and out of the chest.
  • Spirogram: sometimes the spirograph is replaced by a printer. The resulting tracing is called a Spirogram
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24
Q

you use a bronchodilator to test the reversibility of airflow of an airway disease. How do you tell if the airway is reversible by pulmonary function test?

A
  • Reversible airway obstruction that is responsive to medication, 2 out of 3:
  • FVC: an increase of 10% or more
  • FEV1: an increase of 200 ml or 15% of the baseline FEV1
  • FEF25%-75% : an increase of 20% or more
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25
Q

Infection of the lower respiratory tract may be considered as a process involving 5 steps, what are they?

A
  • exposure to the pathogen,
  • inhalation or aspiration of the organism into the lungs,
  • adherence to the respiratory epithelium,
  • failure of clearance,
  • invasion of tissues and initiation of an inflammatory and immune response
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26
Q

What are the main defences of the lungs against infection? (3)

A
  • The mucociliary escalator.
  • Anti microbial peptides present in lung secretions. These include lactoferrin, transferrin, lysozyme, defensins and cathelicidins.
  • Immunoglobulin A in lung secretions
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27
Q

As the lungs fight infection, respiratory disease evolves through four classical stages, which represent the gross appearances of the lung during the various stages of the inflammatory response. What are they?

A
  • congestion,
  • red hepatisation,
  • grey hepatisation and
  • resolution
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28
Q

If infection is not cleared, how does it lead to lung damage?

A

If the infection is not cleared the phase of resolution fails to occur. A persistent, uncontrolled inflammatory response results in tissue damage, which disrupts the epithelium and the mucociliary escalator.
This encourages adherence of bacteria to the mucosa causing further inflammation and progressive lung damage.

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29
Q
  • What are the microbiological approach to respiratory infections? (3)
  • What are the clinical aspects of a respiratory infection? (2)
  • They must be viewed together to manage the patient.
A

Microbial:

  • the identification of the pathogen
  • its characteristics
  • its susceptibility to antimicrobial therapy.

Clinical:

  • the site in the respiratory tract involved,
  • the characteristics of the patient
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30
Q

In respiratory infection, which areas can the infection spread to?

A
  • Upper respiratory tract (many are self-limiting)
  • Lower respiratory tract infections may be:
  • Confined to the bronchi (bronchitis)
  • Spread to the lung parenchyma (pneumonia)
  • The pleural space (empyema)
  • Bloodstream (septicaemia)
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31
Q

The initial clinical approach is to classify pneumonia one of three things:

A
  • Community-acquired
  • Hospital-acquired (nosocomial)
  • Pneumonia in the immunocompromised patient
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32
Q

What are the pathogens which cause community-acquired pneumonia, including the percentage of illnesses caused by each. (7)

A
  • Streptococcus pneumoniae (G+) 60-70%
  • Mycoplasma pneumoniae 10%
  • Haemophilus influenza 5-10%
  • Viruses (e.g. influenza) 5-10%
  • Staphylococcus aureus 3%
  • Legionella pneumophila 2-5%
  • Others (e.g. Chlamydia pneumoniae) 5%
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33
Q

What are the clinical features of community acquired severe pneumonia associated with an increased risk of death? (7)

A
  • Respiratory rate > 30/min
  • Diastolic blood pressure < 60 mmHg
  • Age > 60 years
  • Underlying disease
  • Confusion
  • Atrial fibrillation
  • Multilobar involvement
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34
Q

What are the laboratory features of community acquired severe pneumonia associated with an increased risk of death?

A
  • Serum urea > 7 mmol/L
  • Serum albumin < 35 g/L
  • Hypoxaemia: Po2 < 8 kPa (60 mmHg)
  • White cell count < 4000 x 10^9/L
  • White cell count > 20 000 × 10^9/L
  • Bacteraemia
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35
Q

What partial pressure of oxygen in arterial blood is generally considered too low?

A

an abnormal PaO2 has not been defined because a threshold below which tissue hypoxia occurs has not been identified. However, it seems reasonable to consider a PaO2 <80 mmHg abnormal.

36
Q

What is the definition of Hospital-acquired Pneumonia?

A

Hospital-acquired pneumonia is defined as pneumonia developing two or more days after admission to hospital for some other illness. It is, therefore, a secondary infection in patients compromised by other diseases

37
Q

Chronic bronchitis is characterised by (4)

A
  • cough
  • sputum production
  • mucous gland hypertrophy (enlargement) and hypersecretion
  • disruption of the mucociliary escalator.
38
Q

What are the main characteristics of emphysema?

A
  • The terminal air spaces are dilated with destruction of their walls.
  • There is loss of elastic tissue support, resulting in airway collapse.
39
Q

What do you see in an exacerbation of COPD?

A

During exacerbations of COPD, the patient becomes more breathless with an increase in cough, sputum production and sputum purulence.

40
Q

What are the main signs that COPD is progressing in a patient?

A
  • As COPD progresses:
  • exacerbations become more frequent and alarming
  • airways obstruction and gas exchange deteriorate
  • mortality and morbidity are substantial.
41
Q

In COPD, how do infections gain a foothold, and what does this cause?

A

Disruption of the mucociliary escalator allows colonisation of the lower respiratory tract by bacteria such as H. influenzae, Strep. pneumoniae and Moraxella catarrhalis. Infection promotes inflammation and a vicious circle of infection and inflammation further compromises lung clearance mechanisms.

42
Q

In COPD, what causes exacerbations?

A

Exacerbations may be precipitated by viral infections, which further compromise lung defences and permit secondary bacterial proliferation and invasion.
More recently organisms such as Myc. pneumoniae and Chl. pneumoniae have also been linked to exacerbations.

43
Q

In general, how are antibiotics used in COPD?

A

The best use of antibiotics in exacerbations of COPD is uncertain, and it is difficult to distinguish colonisation from active infection. Patients are often given antibiotics in combination with corticosteroids, bronchodilator therapy, oxygen and supportive care so that it is difficult to define the benefit of any one intervention. Treatment tends to be given empirically: trial and error. In general, antibiotics are beneficial for patients with more severe exacerbations, but the role of antibiotics in milder exacerbations is uncertain.

44
Q

Why is long term antibiotic treatment not used in COPD? (3)

A

Long-term prophylactic antibiotic therapy may reduce the frequency of exacerbations in advanced disease, but this strategy is now rarely used, because of concerns about antibiotic resistance, alteration of the normal oropharyngeal flora and unwanted effects such as Clostridium difficile colitis.

45
Q

15-20% of strains of H. influenzae are resistant to which antibiotic?
90% of which bacteria produce beta lactamase?

A

About 15-20% of strains of H. influenzae are amoxycillin-resistant.
90% of strains of M. catarrhalis produce beta lactamase, so the optimal choice of antibiotic in COPD is unclear.

46
Q

What vaccinations do COPD patient get given?

A

Influenza vaccination and Pneumococcal vaccinations may also be useful.

47
Q

What is the most common cause of COPD? What percentage of cases are caused by this?

A

Smoking is the most common cause of COPD and is responsible for 80 per cent of cases.

48
Q

How many smokers develop emphysema compared to non smokers?

A

Almost all smokers develop emphysema, hardley any non smokers do.
It’s estimated that 94 per cent of 20-a-day smokers have some emphysema when the lungs are examined after death, while more than 90 per cent of non-smokers have little or none.

49
Q

At what age does COPD typically develop?

A

COPD typically starts between the ages of 35 and 45 when lung function starts to decline anyway.

50
Q

How much faster is lung decline in smokers compared to nonsmokers?
How does quitting smoking help lung decline?

A

In smokers, the rate of decline in lung function can be three times the usual rate. As lung function declines, breathlessness begins.
Lung damage from COPD is permanent, but giving up smoking at any stage reduces the rate of decline in lung capacity.

51
Q

What characterises COPD? (3)

A

COPD is a combination of chronic bronchitis, airways obstruction and emphysema

52
Q

In the UK how many people die from COPD each year, and how many working days are lost?

A

In the UK about 30 000 people die and about 30 million working days are lost each year as a result of COPD.

53
Q

The initial immune response to lung infection can be broken up into 6 stages. What are they?

A
  • Activation of alveolar macrophages.
  • Inflammatory mediators released: results in a systemic inflammatory response.
  • Release of cytokines, chemotaxins and interleukins (for the recruitment of other cells)
  • About two hours, neutrophil leucocytes migrate into the alveoli through the endothelium and alveolar epithelium.
  • Monocytes appear about six hours later.
  • Leakage of fluid and proteins, including complement and immunoglobulins, takes place into the alveoli.
54
Q

What is the antibody commonly found in the healthy lungs? What does it do?

A

Immunoglobulin A (IgA) is the major immunoglobulin of the healthy respiratory tract and it can combine directly with and neutralise pathogenic micro-organisms.

55
Q

Which are the main antibodies made during lung infection? What are the major actions of these antibodies?

A
  • The main immunoglobulin produced during the primary immune response is IgM,
  • The main immunoglobulin produced during the secondary immune response is IgG
  • In addition to activating complement, immunoglobulins bind to bacterial antigens and this facilitates their phagocytosis.
56
Q

Why do you need to be cautious of sputum microbiological results? (2)

A
  • Many of the major respiratory pathogens also colonise the respiratory tract, so the identification of an organism in respiratory tract secretions may not be sufficient to implicate it as the cause of illness.
  • The same microbe may also cause various illnesses, such as otitis or bronchitis, and different infecting agents may cause identical clinical syndromes, such as pneumonia.
57
Q

What is pneumonia, what is pneumonitis?

A
  • ‘pneumonia’ is inflammation of the lung parenchyma caused by infection
  • ‘pneumonitis’ is inflammation due to physical, chemical or allergic stimuli.
58
Q

In the UK, how many people are admitted to hospital with pneumonia? Of these, how many die from pneumonia?

A

In the UK each year about 1 in 1000 of the population are admitted to hospital with pneumonia, and the mortality in these patients is about 10%. About 25% of all deaths in the elderly are related to pneumonia, but this is often the terminal illness in a patient with serious concomitant disease.

59
Q

What has led to an increase in the number of patients who are particularly vulnerable to pneumonia

A
  • The ageing population: Developments in many areas of medicine have resulted in improved survival for patients with chronic complex diseases.
  • Immunosuppressive therapies: now more widely used in the fields of autoimmune diseases, oncology and organ transplantation.
60
Q

Which antibiotics are commonly used in pneumonia with an increased mortality or the need for admission to intensive therapy?

A

Dual antibiotic therapy: amoxycillin and erythromycin
or cefuroxime and erythromycin in patients with more severe pneumonia.

61
Q

How many hospital patients does pneumonia affect?

A

Hospital-acquired pneumonia affects about 0.5-1% hospital admissions with an incidence 20-fold higher in patients who are mechanically ventilated

62
Q

What is the most common cause of hospital acquired pneumonia?

A

Gram negative bacteria from the oropharynx can be inhaled and cause pneumonia. Oropharyngeal colonisation by Gram-negative bacilli increases as patients develop more severe systemic illness, so that about 35% of patients with moderately severe illness and 73% with critical illnesses develop it. These Gram-negative bacilae are acquired from endogenous sources: the upper gastrointestinal tract, subgingival dental plaque and the periodontal crevices.

63
Q

What conditions (8), drugs (6) and procedures (2) predispose to oropharyngeal colonisation by Gram negative bacteria?

A
  • Poor oral hygiene, coma, malnutrition, debility of chronic disease, hypotension, diabetes, alcohol misuse and uraemia (the illness accompanying kidney failure).
  • Sedatives, anaesthesia, corticosteroids, broad-spectrum antibiotics, cytotoxic drugs,H2 antagonist drugs used as prophylaxis against stress gastritis
  • prolonged surgery,use of nasogastric tubes.
64
Q

What is the prognosis for most upper respiratory infections?

A

Although unpleasant, most upper respiratory tract infections are mild and self-limiting, but some may give rise to serious problems, most notably:

  • acute epiglottitis in children
  • influenza A in the elderly
65
Q

Which upper respiratory tract infection can be serious in children?

A

In children respiratory syncytial virus (RSV) infection is very common and may cause serious disease, such as bronchiolitis or pneumonia, whereas subsequent infections cause less severe illness usually amounting only to a mild ‘cold’ in adults

66
Q

What type of antibiotic is Cefuroxime? What is its trade name?

A

Cefuroxime is a second-generation cephalosporin antibiotic. GlaxoSmithKline sells the antibiotic in the United Kingdom under the name Zinnat.

67
Q

What is the mode of action of Cefuroxime and other Cephalosporins?
What type of bacteria are they most active against?

A

Cephalosporin mechanism of action is similar to penicillin; they interfere with bacterial peptidoglycan synthesis. Penicillin and cephalosporins are beta-lactam antibiotics becasue they have a beta-lactam ring that can bind to penicillin-binding-proteins (beta-lactam-binding proteins). This disrupts the final cross-linking step in the production of peptidoglycan, the main component of the (inner) cell wall.

68
Q

What type of bacteria are Cefuroxime and the other cephalosporins most active against?

Which bateria is it commonly used to counter? (7)

A
  • Cefuroxime is potent against Gram -negative bacteria, but less so against Gram positive bacteria.
  • Used for: staphylococci (+), group B streptococci (+), H. influenzae (-), E. coli (-), Enterobacter (-), Salmonella (-), and Klebsiella (-)
69
Q

What causes antibiotic resistance to cephalosporins and penicillin? Which bacteria in particular are showing this resistance?

A

Resistance to these antibiotics is increasing due to the production of beta-lactamase by bacteria. Nearly all Gram negative bacteria produce beta-lactamase that is more active in hydrolysing cephalosporins than penicillin

70
Q

What are the side effects of Cefuroxime? (6) Who should you be cautious about giving cefuroxime to and why?

A
  • Cefuroxime is generally well tolerated and side effects are usually transient. Cefuroxime, if ingested with food, is less likely to cause its most common side effects of diarrhea, nausea, vomiting, headaches/migraines, dizziness and abdominal pain.
  • There is a widely quoted cross-allergy risk of 10% between cephalosporins and penicillin, so 10% of people allergic to penicillins will also be allergic to cephalosporins
71
Q

What type of antibiotic is erythromycin? What is its mode of action and which patients is it often used for?

A

Erythromycin is a macrolide antibiotic. The macrolides inhibit bacterial protein synthesis by an effect on translocation. They bind to the 50S subunit on the ribosome of the bacteria.
It has an antimicrobial spectrum similar to or slightly wider than that of penicillin, and is often used for people who have an allergy to penicillins.

72
Q

What type of bacteria is erythromycin most active against?

A
  • Erythromycin is very effective against Gram positive bacteria and spirochaetes, but not against most Gram negative organisms,
  • (the exceptns being N. gonorrhoea and to a lesser extent, H. Influenza, Mycoplasma pneumoniae, legionella sp.)
73
Q

What is the measure socioeconomic status?

A

Socioeconomic status (SES) is an economic and sociological measure of an individual’s or families position in relation to others.

74
Q

What is the Socioeconomic status (SES) measure based on? (3-4)

A

When placing a family or individual into an SES category any or all of the three following variables can be assessed:

    • income
    • education
    • occupation.
  • A 4th variable, wealth, may also be examined.
75
Q

Socioeconomic status is typically broken into which three categories.

A
  • high SES
  • middle SES
  • low SES
76
Q

Low SES has shown to be a strong predictor of which problems? (4)

A
  • Respiratory viruses, arthritis, coronary disease, and schizophrenia.
  • These may be due to environmental conditions in the workplace, or in the case of mental illnesses, may be the entire cause of that persons social predicament to begin with.
77
Q

How is low SES perpetuated through generations?

A

Low income families focus on meeting immediate needs and do not accumulate wealth that could be passed on to future generations, thus increasing inequality.

78
Q

What are some psychological effects on the children of high SES parents?

A

Children of parents with a high socioeconomic status tend to express more “disengagement” behaviors than their less fortunate peers: actions such as fidgeting with other objects and drawing pictures while being addressed.
Those born into less favored circumstances tend to make more eye contact, head nods and signs of happiness when put into a social environment. Authors hypothesize that the more fortuitous peers felt less inclined to gain rapport with their group because they saw no need for their assistance in the future.

79
Q

What is the chemical equation of the (CO2) buffering of the blood?

A

CO2 + H2O <> H2CO3 <> HCO3- + H+
Carbon Dioxide and Water
Carbonic Acid
Bicarbonate and Hydrogen ions

80
Q

What are the three buffering systems in the body?

A
  1. Protein buffer systems: help regulate pH in the intracellular fluid (ICF) and extracellular fluid (ECF). These of the systems interact with the other two systems
  2. The carbonic-acid-bicarbonate buffer system is most important in extracellular fluid
  3. The phosphate buffer system has an important role in buffering the pH of the ICF and urine.
81
Q
  • What is the normal pH of extracellular fluid (includes blood and intracellular fluid)?
  • What are the upper and lower limits beyond which pH can quickly cause death?
A
  • normal pH ECF: 7.35-7.45
  • You could not survive long with an ECF pH below 6.8 or above 7.7
82
Q
  • Which body systems are particularly susceptible to changes in pH?
  • How does severe acidosis cause death? (3)
A
  • The nervous and cardiovascular systems are particularly sensitive to pH fluctuations

Severe acidosis causes:

  • Central nervous system function to deteriorate: coma
  • Cardiac contractions become weak: irregular: heart failure
  • Peripheral vasodilation produces a dramatic drop in blood pressure which can cause circulatory collapse.
83
Q

What is the most important factor affecting pH in the body tissues?

A

PCo2

84
Q

When the blood becomes more alkaline than it should be, what is the response of the kidneys?

A

Bicarbonate is filtered at the glomerulus and is not reabsorbed: it is excreted in urine, so the blood pH becomes more acidic.

85
Q

When the blood becomes more acidic than it should be, what is the response of the kidneys?

A
  • Reabsorbing bicarbonate (secretion at the glomerulus then reabsorbed at the tubules)
  • Making new bicarbonate in the kidney tubule cells
  • Secretion of hydrogen ions
86
Q

Renal mechanisms are the slowest mecahnism to affect pH in the body. What are they particularly important for?

A

Important for the elimination of fixed acids from the body, which are produced in metabolic processes.