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Clinical Medicine > Pulmonolgy > Flashcards

Pulmonolgy Flashcards

1
Q

asthma

A

chronic pulmonary disorder characterized by episodic reversible airflow obstruction

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2
Q

what causes airflow obstruction in asthma

A

smooth muscle contraction, vascular congestion, edema, thick sputum

brought on by airway inflammation

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3
Q

evidence for airway inflammation as the primary underlying cause of asthma

A

increased inflammatory cells (eosinophils, basophils, etc) on bronchial washings and lung biopsy even when assymptomatc

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4
Q

two main types of asthma

which is more prevalent

A

allergic and idosyncratic

allergic

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5
Q

differentiate allergic asthma from idiosyncratic

A

allgeric asthma often has a personal of FHx of allergic disease and commonly present at an early age

idiosyncratic has no Hx, negative skin tests, normal serum IgE

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6
Q

two long term complications of asthma

A

airway remodeling in response to chronic inflammation leading to gradual decline in pulmonary function

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7
Q

treatment strategies for asthma

A

reduce inflammation

increase airway diameter

improve airway secretions

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8
Q

asthma treatment principles

A

preventing inflammation is key

use Beta-2 agoninsts for acute episodes

prevent recurrence with anti-inflammatories and long actings Beta-2

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9
Q

types of goals of two asthma intervention

A

acute: relieave acute bronchspasm
chronic: reduce frquency of acute episodes

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10
Q

outpatient devices for inhalation treatment of asthma

A

metered dose inhalers

dry powder inhaler

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11
Q

deliniate where particles of varying sizes can be used in aerosol therapy fo asthma

>10 microns

1-5 microns

<.5 microns

A

>10microns: mouth and oropharynx

1-5: smaller airways

<0.5: minimal deposition (in and out)

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12
Q

ingeneral how much of an aersol asthma medication is inhaled vs swallowed

A

2-10%

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13
Q

what is the goal of corticosteroid treatment for asthma

A

to reduce underlying inflammation related to chronic asthma

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14
Q

typical methods of adminstration for corticosteroids

A

inhaled aerosol (most common)

oral or parenteral (emergency situation)

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15
Q

what is needed to use the dry powder inhalers

A

a good inspiratory effort, because inspiration is what breaks up the powder

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16
Q

three inhaled glucocorticoids

A

¨Flunisolide (Aerobid)

¨Budesonide (Plumicort)

¨Fluticasone (Flovent)

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17
Q

typical dosage of inhaled glucocortocoids for asthma treatment

A

200-400 mcg/day

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18
Q

adverse drug reactions related to corticosteroid treatment of asthma

A

pituitary-adrenal suppression >1600 micrograms/day

bone loss

hyperglycemia significant >1000mcg/day

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19
Q

thrush prevention in corticosteroid treatment of asthma

treatment

A

use a spacer to catch larger particles that would deposit in the mouth

rinse mouth with water after dose

nystatin

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20
Q

T/F most patients will benefit from some level of corticosteroid therapy for asthma

A

true

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21
Q

two good glucocortcoid inhalers that have high compliance

A

¤Fluticasone (Flovent) or budesonide (Plumicort)

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22
Q

why does long term corticosteroid therapy cause adrenal suppression

A

because the pituitary-adrenal axis takes time to adjust when corticosteroid therapy is disonctinued

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23
Q

when are oral corticosteroids used in asthma treatment

dose?

goal?

taper?

A

in severe attacks

40-60 mg prednisone/day 5-10days or 1mg/kg/day

prevent hospitalization

not if the course lasts less than 14 days

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24
Q

non-steroid anti-inflammatory choices

A

leukotriene inhibitors

cromolyn

anti-IgE monoclonal antibodies

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25
Q

what is the function of leukotriene inhibitors

A

decrease action to prevent bronchoconstriction

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26
Q

two leukotriene receptor agonists

5-lipooxygenase inhibitor

A

¤Zafirucast (Accolate)

¤Montelukast (Singulair)

¤Zileuton (Zyflo)

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27
Q

what is the function of 5-lipooxygenase

A

it converts arachadonic acid to leukotrienes

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28
Q

what leukotriene is 1000x more potent than histamine

A

LLTD4

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29
Q

uses of leukotriene inhibitors in asthma treatment

A

lowered glucorticoid dose

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30
Q

adverse effects of leukotriene inhibitos

A

liver toxicity (esp zilueton) that requires peroidic liver enzyme testing

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31
Q

what is the function of cromolyn

A

stabilizes mast cells to prevent antigen induced broncospasm but has no bronchdilating properties

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32
Q

when is cromolyn the first line treatment of asthma

A

mild to moderate cases

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33
Q

Anti-IgE Monoclonal Antibody treatment for asthma

why is it saved for difficult cases

A

¨Omalizumab (Xolair)

it is costly

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34
Q

methods for reducing bronchospasm assocaited with asthma

A

relax bronchial smooth muscle by stimulating Beta2 sympathetic receptors

block parasympathetic muscarinic receptors

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35
Q

effect of beta-2 agonists

adverse drug reactions

A

bronchdilation

hyperglycema, tachycardia, poss HTN

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36
Q

examples of short acting beta 2 agonists

A

¨Albuterol (Proventil, Ventolin)

¨Metaproterenol (Alupent)

¨Terbutaline (Brethine, Bricanyl)

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37
Q

which method of treating bronchospams is associated with asthma is more effective

A

beta2 agonists

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38
Q

beta-1 agonist effects from Beta-2 crossover

A

HTN, tachycardia

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39
Q

short acting beta2 onset

duration

benefits

A

1-5 minutes

2-6 hours

bronchodilation with minimal anti-inflammatory effects

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40
Q

what is a patient controlled adverse effect of short acting Beta2 treatment of asthma

A

patient mange deteriorating asthma due to progressive inflammation with more frequent doeses

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41
Q

long acting beta2s

A

¨Salmeterol (Servent)

¨

¨Formoterol (Foradil)

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42
Q

duration and utility of long acting beta2’s

A

duration: 12 hours
utility: preventing recurrent acute attacks

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43
Q

cautionary statements of long acting beta2’s

A

not effective for acute attacks

15% of patients will not respond as predicted

increased mortality if used as the sole treatment

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44
Q

examples of long acting Beta2’s with glucocortcoids

A

¨Fluticasone + salmeterol (Advair)

¨Mometasone + formoterol (Dulera)

¨Budesonide + formoterol (Symbicort)

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45
Q

two examples of muscarinic receptor blockers used in asthma treatment

action

A

ipratropium, tiotrpoium

helps relieve bronchospasm, reduces airway secretion

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46
Q

what is the action of theophylline

A

inhibits phosphodiesterase to decrease muscarinic receptor function

some anti-inflammatory effect

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47
Q

how are theophyllines used in treatment of ashtma in kids

adults

A

kids: in place of inhaled glucocortcoids
adults: time release for nocturnal asthma

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48
Q

strategy to block secretions in asthmatic patients

A

¨Decrease bronchial secretions with anticholinergic/ anti-muscarinic agents

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49
Q

derivatives of atropine used as anticholinergic/muscarinic drugs in management of secretions in asthma

side effects

A

¨Ipratropium (Atrovent), ¨Tioptropium (Spiriva)

urinary retention, constipation, glaucoma

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50
Q

¨Ipratropium (Atrovent) and Tioptropium (Spiriva) are synergistic with what other asthma treatments

A

beta 2 inhalers (ipratropium + albuterol)

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51
Q

types of emergency asthma therapy

A

1st line: beta2 inhlaers

subQ epi is useful

corticosteroid IV or oral

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52
Q

cautionary statements of using beta2 agonists in asthma treatment

A

frequen use may reduce effectiveness due to down regulation

bronchospasm may worse in some patients with long acting beta2

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53
Q

treatments safe for asthma and pregnancy

A

¤Beta 2 agonists

¤Glucocorticoids

¤Cromolyn

¤Ipratropium, tiotropium

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54
Q

typical causes of hay fever (allergic rhinitis)

A

¤Pollens, animal dander, dust, molds, etc.

¤Hyperemia, enhanced secretions

¤IgE involved in inflammatory cascade

¤Histamine & other mediators

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55
Q

rhinitis treatment strategies

A

avoid allegerns

desensitize the immune system

prevent mast cell degranulation

block histamine

reduce nasopharyngeal hyperemia

block/reduce inflammtion

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56
Q

drugs used to prevent IgE activation in the treatment of allerigc rhinitis

A

cromolyn nose spray before allergen exposure

omalizumab as an anti-IgE monoclonal antibody

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57
Q

1st generation antihistamines

drawbacks

A

Chlortrimeton, Benadryl

effective but cause drowsiness

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58
Q

2nd generation antihisamines

are 1sts or 2nd gen better

A

Loratadine (Claritin), cetirizine (Zirtek), Fexofenadine (Allegra)

2nd gens

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59
Q

why do 1st generation anti-histamines cause drowsiness

A

they can cross the blood brain barrier

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60
Q

what is the action of alpha adrenergic agonists in treatment of allergic rhinitis

A

vasoconstriction to reduce hyperemia

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61
Q

long and short acting alpha agonists used in the treatment of allergic rhinitis

A

¨Phenylephrine (Neosynephrine) - Short acting drops/spray

¨Oxymetazoline (Afrin) - Longer action (12 hours)

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62
Q

reactive hyperemia

A

after 2 or three days of alpha adrenergic use your nose will swell up due to compensatory mechcanisms activated in response to ischemia

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63
Q

what are nasal glucoortcoids used for in treating allergic rhinitis

how often are they dosed

how long will it take to get effective

what is their most effecitve use

A

block or reduce inflammation

1-2x daily

1-2 wks

most effective for seasonal allergic rhinitis

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64
Q

three types of nasal corticosteroids

A

¨Beclomethasone (Beconase, Vancenase)

¨Fluticasone (Flonase)

¨Flunisolide (Nasalide)

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65
Q

useful combination in the treatment of allergic rhinitis

A

¨Inhaled glucocorticoids as main preventative

¨Cromolyn/nedocromil added if needed to keep steroid dose low

¨Inhaled antihistamine

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66
Q

types of inhaled antihistamines

benefit of use

A

¨Azelastine nasal spray (Astelin)

¨With fluticasone: Dymista

¨Risks of sedation seem very low

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67
Q

treatment of allergic conjunctivitis

A

systemic antihistamines work

topical is better

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68
Q

pathophysiological hallmarts of COPD

A

¤Airflow obstruction

¤Alveolar dilation and destruction

¤Airway infection (chronic and acute)

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69
Q

possible etiology of COPD

A

¤Cigarette smoking (99%)

¤Other toxins (such as coal dust, silica)

¤Genetic (Cystic fibrosis, A-1antiproteinase (anti-trypsinase) deficiency)

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70
Q

differentiate between chronic bronchitis and emphysema

A

chronic bronchitis is caused by airway obstruction that destroys alveoli

emphysema is cause by alveolary loss that least to air way obstruction

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71
Q

two main symptoms of chronic bronchitis

A

¤Chronic productive cough

¤Mucopurulent sputum

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72
Q

two main symptoms of emphysema

A

¤Shortness of breath (dyspnea) with exertion

¤Shortness of breath at rest

73
Q

how is COPD related to asthma

A

smoke damaged epithelium, leading to frequent infection, chronic inflammtion, and asthma like reactive airways

74
Q

COPD treatment strategies are preventing new damange and improve airways

how to prevent new damage

A

reducing exposure to irritants

ABx to control infetion

75
Q

COPD treatment strategies are preventing new damange and improve airways

how to improve airways

A

¤Bronchodilators

¤Glucocorticoids

¤Other anti-inflammatory drugs (leukotriene inhibitors)

¤Improve or reduce airway mucus (Respiratory therapy, Drugs such as ipratropium (Atrovent))

76
Q

T/F nearly all asthma treatments can be used with COPD and are very effective

A

false, asthma treatment for COPD is less effective depending on how extensive the damage is

77
Q

what is the value of ABx use in COPD treatment

A

they are valuble to prevent acute flare of bronchitis but have dubious value in long term treatment

78
Q

two benefits of supplmental oxygen treatment of COPD

A

improves activty tolerance and improves survivability

79
Q

where is capilary blood flow in the lungs greatest

A

in the bases due to gravity

80
Q

T/F pulmonary arteries have a very low resistance to blood flow

A

true

81
Q

glucorticoids deal with what

mineralocortoids deal with what

A

inflammation

fluid retention

82
Q

where must gas diffusion happen for O2 and CO2 exchange

A

alveolar gas

alveolar and capillary walls

plasma

membrane and cytoplasm of RBC

83
Q

oxygen in blood is found in what two places

A

either bound to Hgb or dissolved in plasma

84
Q

%O2 is determined by whay

A

arterial Po2

Hbg level

85
Q

tissue oxygenation depens on what

A

oxygen content in the arterial blood

cardiac output

86
Q

pulmonary infection types

A

Pneumonias (Community acquired, (CAP)Hospital acquired, (HAP)Fungal)

Tuberculosis

Acute Bronchitis

Influenza

Pertussis

Acute Bronchiolitis

Acute epiglottitis

Croup

87
Q

three pulmonary diseases commonly found in kids

A

Acute Bronchiolitis

Acute epiglottitis

Croup

88
Q

how is diffusion measured

A

DLCO (diffusion capacity of the lung to carbon monoxide)

89
Q

three types of pulmonary neoplasms

A

solitary nodules

mesothelioma

lung cancer

90
Q

what is the common cause of mesothelioma

A

asbestosis

91
Q

two types of lung cancer

A

small cell (oat cell)

non-small cell

92
Q

three types of non-small cell lung cancer

A

squamous cells carcinoma

adenocarcinoma

large cell carcinoma

93
Q

four types of obstructive pulmonary disease

A

bronchiectatsis (tumors, foreign bodies)

  • Asthma
  • Chronic obstructive pulmonary disease (COPD)
  • Cystic Fibrosis
94
Q

three pleural disorders

A
  • Pleuritis (“pleurisy”)
  • Pleural effusion
  • Pneumothorax
95
Q

three disorders of pulmonary circulation

A
  • Pulmonary thromboembolism
  • Pulmonary hypertension
  • Pulmonary vasculitis
96
Q

three types of restricive lung disease

A
  • Idiopathic fibrosing interstitial pneumonia
  • Pneumoconioses ()Asbestosis, Coal dust, Silicosis)
  • Sarcoidosis
97
Q

three miscellaneous pulmonary disease

A
  • Acute Respiratory Distress Syndrome (ARDS)
  • Foreign Body Aspiration
  • Hyaline Membrane Disease (pre-term infants)
98
Q

two cardinal symptoms of pulmonary disase that can be identified in a history

A

Dyspnea

Cough

99
Q

notable features associated with dyspnea that can be picked up on history

cough

A

Acute or progressive, Triggers

Duration, Productive of sputum, Acute or chronic

100
Q

PE findings correlated with pulmonary disease

A

low O2 sat

tachypnea, bradypnea

adventitious breath sounds

cyanosis or clubbing

suspected or visible foreign bodies

101
Q

pneumoconioses are pulmonary disease acquired from what

A

work place exposure to things like silica and coal dust

102
Q

adventitious breath sounds associated with pulmonary disease

A

stridor

wheeze from airway obstruction

Rhonchi (obstruction of medium bronchi)

crackles and rales

no breath sounds

103
Q

rhonchi are associated with what pulmonary disease

A

bronchitis, COPD, bronchiectasis

104
Q

cor pulmonale

A

right sided heart failure which may or may not be precipitated by left sided heart failure

105
Q

crackles and rales are signs of what

A

alevolar disease

pneumonia

pulmonary edema

106
Q

egophony can be used to differentiate between what

A

cracklse of pneumonia and interstitial pulmonary ffibrosis

107
Q

T/F stridor is often present in the lower airway

A

false, stridor is usually found in the neck and upper respiratory tract

108
Q

conditions that may result in absent or decreased breath sounds

A

emphysema (quiet or diffuse)

pneumothorax

pleural effusion

109
Q

increase tactile fremitus is indicative of what

A

lung consolidation

110
Q

decreased tactile fremitus and/or dullness on percussion is indicative of what

A

pleural effusion

111
Q

hyperresonance on percussion is indicative of what

A

pneumothorax

112
Q

signs of pulmonary disease in other systems

A
  • Pedal edema
  • JVD
  • Joint examination
  • Skin examination
  • Clubbing
113
Q

what is the goal of PFTs

A

objective assessment of a pesron with known or suspected pulmonary disorder

determine if teh lung disease is sufficient to explain the patients symptoms

is the functional pattern of the disease obstrictive or restrictive

114
Q

indications for PFTs

A
  • Pre-operative evaluation of pulmonary risk
  • Assess the severity of pulmonary disease
  • Evaluation of dyspnea or other pulmonary complaints
  • Evaluate abnormal findings on other studies
  • To measure and evaluate response to treatment
  • To quantitate the improvement or deterioration in a patient’s condition
  • To measure the effects of environmental exposures
  • To evaluate disability
115
Q

three main categories of information in PFTs

A

the size of the lungs (lung volumes)

measurement of maximum flow rates in the air way

how readily gas exchanges between alveoli and capillaries (diffusion)

116
Q

spirometry

A

a meassure of pulmonary function based on assessing air flow obstruction

117
Q

what is the criteria for diagnosis of an obstuctive condition based on spirometry

A

Decreased forced expiratory volume in 1 second (FEV1)/ forced vital capacity (FVC) defined as <70% of predicted is diagnostic of obstruction

118
Q

what should be done when spirometry is normal or with symmetric decreases in FEV 1 and FVC get

A

lung volumes, total lung volume less than 80% indicates restictive

DLCO, restruction plus decreased DLCO indicates parenchymal disease

119
Q

what spirometry values are indicative of obstructive diseas

restrictive

A

decrease in FEV1, increase in residual volume

decrease in TLC, FEV1/FVC remains normal

120
Q

lab tests of pulmonary disease

A
  • Arterial Blood Gas
  • Complete Blood Count
  • Chemistry profile
  • Sputum gram stain, culture, sensitivity
  • Pleural Fluid Analysis
  • Cytologies
121
Q

indications for arterial blood gas measurement

A
  • Assessing and managing a patient’s respiratory (ventilation) and metabolic (renal) acid-base and electrolyte homeostasis
  • Assess adequacy of oxygen
122
Q

normal ABG values

pH

PaO2

PaCO2

HCO3

A

pH 7.35 - 7.45

PaO2 70-100mmHg

PaCO2 35-45mmHg

HCO3 22-30 nm or 22-26 mEq/L

123
Q

increased pH indicates what

decreased pH indicates what

A

respiratory and metabolic alkalosis

respiratory and metabolic acidosis

124
Q

decreased PaO2 indicates what

A

oxgenation issues (pneumonia)

125
Q

HCO3 changes are indicative of what

as HCO3 increases what happens to pH

A

acid-base equilibrium

HCO3 increases lead to pH increases

126
Q

distrubances in acid base balance

A
  • Metabolic acidosis
  • Respiratory acidosis
  • Metabolic alkalosis
  • Respiratory alkalosis
127
Q

metabolic causes of acidosis

A

Metabolic

  • Renal failure
  • Ketoacidosis
  • Ingestion of acidic compounds (i.e. aspirin overdose)
128
Q

respiratory causes of acidosis

A

Respiratory failure (high PaCO2, causing acidosis)

COPD (Increased PaCO2 and HCO3-) (Ions increased to compensate for chronic hypoventilation)

129
Q

metabolic causes of alkalosis

A

Metabolic

  • Prolong vomiting
  • Ingestion of large amounts of bicarbonate
130
Q

respiratory causes of alkalosis

A

Respiratory

  • Hyperventilation (low PaCO2)
  • Hypoxemic states (cystic fibrosis, PE, acute severe pulmonary disease)
  • Breathing increased and CO2 is blown off
131
Q

how does pulmonary compensation take place in falling pH (acidosis)

A

ventilation rate increases

causes a fall in PaCo2 that increases HCO3

132
Q

pulmonary compenstion in response to rising pH levesl

A

ventilation falls to increase PaCO2, increase pH

133
Q

what is the goal of pleural fluid analysis

A

helps determine between transudative or exudative effusion based appearance, protein, glucose content

134
Q

two causes of transudative effusions

A

heart failure, cirrhosis with ascities

135
Q

two causes of exudative effusions

A

infection and cancer

136
Q

diagnostic imaging for pulmonary conditison

A
  • Chest radiography
  • Chest computerized tomography (CT)
  • Magnetic resonant imaging (MRI)
  • Ventilation and Perfusion Scan
  • PET Scan
137
Q

structures and patterns that can be assessed on CXR

A

Structures

  • Mediastinum (lymph nodes, vessels, tumor)
  • Pleura (effusions, air space)
  • Lung parenchyma (infiltrates, lesions)

Patterns

  • Interstitial (lacy, reticular, reticulonodular)
  • Airspace (lobar, segmental, air bronchograms)
138
Q

what is the key advantage of chest CT over xray

A

excellent resolution

Cross-sectional images allow distinction between densities super-imposed on plain films

Can characterize tissue density= accurate size of lesions

139
Q

chest CT allows for better delination of what

A

uParenchymal processes

uPleural disease

uHilar and mediastinal masses

uMasses or nodules

uLarge airways

uAny unclear lesion or problem on routine chest radiograph

140
Q

why is MRI less used than chest CT

A

breathing causes motion artifact, less detail between parenchymal structure

141
Q

what is chest MRI used for

A

discriminating between enlarged mediastinal vessels and lymphadenopathy

142
Q

what is a Ventilation perfusion scan used for

A

Used in the detection of PE and evaluation of lung function in patients considering lung resection

143
Q

what is thoracentesis used for

A

Diagnostic sampling of pleural fluid by blind needle aspiration or US guided

Allows for collection and evaluation of fluid- micro and cytology

144
Q

what is bronchoscopy used for

A

Direct visualization of the tracheobronchial tree

Done with flexible fiberoptic instrument

Done to retrieve foreign bodies and obtain endobronchial pathology for cytology, stains, cultures, etc.

145
Q

different types of mycobacterium that people can be exposed to and hwere they cause issues

A

tubercolsis (lungs)

Bovis (gut)

leprae (skin leprosy)

abscessus and fortinuitum (skin)

avium (bone marrow)

146
Q

T/F late stages of tuberclosis can affect all organs in the body

A

true

147
Q

what percentange of the world’s population has active or inactive TB

A

20-43%

148
Q

what US citizens are most at risk based on ethnicity

A

asian (25x)

hispanic (7.3x)

non hispanic black (6.6x)

149
Q

what is the primary method of transmission for TB

A

breathing, except for non-pulmonary TB

150
Q

what is required for transmission of TB

how effiecient is it

A

fairly close, prolonged contact

23%

151
Q

how many peole will an untreated person with active TB infect per yar

A

15-20

152
Q

what is the key pathphyisologic finding in TB

A

caseating granuloma with necrotic center caused by the body’s attempt to wall of the infection

153
Q

what determines the chance of a person exposed to TB will be come infected

A

the innate and active immune responses

154
Q

conditions that can alter immune response and make people susceptible to TB

A

Calcified / fibrotic lung lesions

Silicosis

Chronic RF

DM

IV Drug use

Immunosuppresive Rx HIV infection & Others

155
Q

risk factors for TB exposure and infections

A

—HIV positive? 7.7%

—Are you homeless? 5.6%

—Do you drink excessive alcohol? 12.1%

—Have you been in prison? 4.2%

156
Q

symptoms of latent TB

are people with latent TB infectious

A

usually none with a positive skin test

not infectious

157
Q

symptoms of active TB

A

high fever with night sweats

weight loss

cough/hemoptysis

fatigue

malaise

158
Q

how is the diagnosis of TB made

A

HP

chest xray

PPD/TB gold/T-SPOT

159
Q

how can you confirm your diagnosis of TB without skin or blood tests if you have high suspicion

A

sputum evaluation

blood evaluation

160
Q

two types of sputum evaluation for Dx of TB

drawbacks of each

A

acid fast smear (only a screen, any mycobacterium will be +)

culture (takes 2-6 weeks)

161
Q

two types of blood evaluation for Dx of TB

if these tests are positive, can you assume TB infection

A

—Nucleic Acid Amplification test detection (NAAT-TB)

—Nucleic Acid Amplification test resistance marker (NAAT-R)

yes, assume they have TB and start treatment

162
Q

should bronchoscopy be used in Dx of TB

A

for the most part, no

163
Q

are CT and MRI used to Dx TB

A

Ct may be useful for distinguishing undertermined masses

MRI not typical but can be used

164
Q

how does the PPD test work

A

it injects a protein derivative from the TB cell wall into the skin and looks for an inflammatory reaction

165
Q

a PPD test produces a lesion >=5mm

when might that indicate TB infection

A

HIV, exposure, immunosuppresion, fibrotic changes from old TB

166
Q

a PPD test produces a lesion >=10mm

when might that indicate TB infection

A

people coming from overseas

IVDA

residents or employees of prison, hospitals, homeless shelters

167
Q

a PPD test produces a lesion >=15mm

when might that indicate TB infection

A

anyone

168
Q

what might cause false negatives on a PPD test

A

patients with disseminated TB

immunocompromised patients

reading the test too soon

169
Q

what would produce a false positve

A

people who received the BCG vaccine

170
Q

BCG (Baccile Calmette-Guerin)

A

a vaccine derived from a weak strain of TB commonly used in the UK with variable efficaacy

171
Q

what is the benefit of Interferon Gamma Release Assays (IGRAs such as TB fold or Tspot)

A

24-48 hours to interpret

less susceptible to false recordings

172
Q

what patients are most at risk for widespread miliary TB

A

—Infants

—The elderly

—Immuno-compromised adults

173
Q

booster phenomenon

A

repeat PPD tests can be false negatve due to decreased reactivity of the immune system, may need a second exposure in close proximity to trigger a true result

174
Q

four different approaches for latent TB treatment

A

—INH (+B6) daily or twice weekly for 9 months

—Or INH (+B6) daily or twice weekly for 6 months

—Or INH and Rifapentine – once weekly for 3 months

—Or Rifampin – daily for 4 months

175
Q

treatment regimines for active TB

A

—Daily for 8 weeks (EMB may be d/c is drug susceptible TB)

INH / Rifampin (RIF) / Ethambutol (EMB)/ Pyrazinamide (PZA)

—Daily or two-times weekly for 18 more weeks

INH and RIF

176
Q

what determines what treatment regimine to use for active TB

A

population demographic

risk factors

how long it take to convert to latent TB

177
Q

after treatment for latent TB, when should CXR be done

A

only if the patient develops signs or symptoms suggestive of TB

178
Q

factors that can cause the conversion of latent TB to active

A

HIV infection

iatrogenic immune depression form chemo, steroids, DMARDs

starvation

179
Q
A

Clinical Medicine (11 decks)

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