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411 > Week 7: COPD > Flashcards

Week 7: COPD Flashcards

1
Q

What things decrease oxygen affinity for hemoglobin (shift curve right) ?

A

Low pH
High blood CO2
High temperature
Added BPG

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2
Q

3 distinct components of neural control of breathing

A

Factors that:

  1. Generate alternating inspiration/expiration rhythm
  2. Help regulate the magnitude of ventilation
  3. Modify respiratory activity for other purposes
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3
Q

What is respiratory Center

A

Medulla oblongata and pons

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4
Q

What does pons regulate ?

A

Rate of breathing

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5
Q

What muscles are used for expiration during active ventilation ?

A

Internal intercostal muscles

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6
Q

Dorsal respiratory group (DRG) function

A
  • inspiratory neurons that discharge during inspiration and stop discharging during expiration
  • generate RAMP signal
  • initiate inspiration with weak burst of APs that gradually increase in frequency then cease for next 3 seconds until new cycle
    —> gradual increase in lung volume during inspiration
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7
Q

Pontine respiratory Center function

A

Modify rate and pattern of respiration

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8
Q

Apneustic centre

A

Sends stimulatory discharge to inspiratory neurons promoting inspiration
Removal of its effects—> shallow, irregular respiration

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9
Q

Pneumotaxic centre function

A

Regulation of respiratory volume and rate
Controlling cessation of inspiratory RAMP signal from DRG
Switch off DRG and Apneustic centre —> expiration

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10
Q

Central chemoreceptors pathway

A

Lying just beneath ventral surface of medulla
Relay most important sensory input about changes in their close environment to respiratory center in pons and medulla
- sensitive to change in PACO2

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11
Q

How are central chemoreceptors stimulated by an increase in arterial PCO2 ?

A

CO2 crosses blood brain barrier
—> CO2 + H2O —> H2CO3–> HCO3- + H+
And H+ stimulate central chemoreceptors

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12
Q

Peripheral chemoreceptors

A

In direct contact with arterial blood
Afferent neurons project to medullary respiratory control areas
Respond mostly to changes in PAO2 or pH

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13
Q

what is the most common cause of massive hemoptysis ?

A

Something wrong with bronchial circulation

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14
Q

Important history for hemoptysis diagnosis

A 
TB or lung disease 
Environmental or TB exposures 
Smoking 
Travel 
Immune status 
Toxins and drug use
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15
Q

Important laboratory data for patients presenting with hemoptysis

A 
HCT/platelets 
Renal function and urinalysis 
Coagulation factors 
ABG 
Type and cross
Sputum
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16
Q

Advantages of rigid bronchoscopy

A

Secure airway
Large port: greater suction
Greater visualization than flexible

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17
Q

Endobronchial tamponade vs selective intubation

A

ET: inflated tracheal cuff and inflated bronchial cuff in bad lung
SI: inflated bronchial cuff in good lung

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18
Q

Topical therapy examples for hemoptysis

A

Cold saline irrigation —> vasoconstriction
Vasoconstrictive agent: epinephrine
Topical coagulants: fibrinogen, thrombin

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19
Q

4 common chronic obstructive diseases:

A

Asthma
COPD
Bronchiectasis
Bronchiolitis

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20
Q

What airways are involved with asthma ?

A

Secondary bronchus - respiratory bronchiole

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21
Q

What airways are involved with COPD ?

A

Bronchioles - respiratory bronchioles

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22
Q

4 common symptoms of chronic obstructive airway diseases

A

Cough
Sputum
Wheeze
Dyspnea

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23
Q

Sources of mucus

A

Goblet cells

Bronchial mucus glands

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24
Q

Causes of dyspnea in obstructive lung diseases

A

Increased work of breathing due to increased airway resistance
Hypoxemia
Hyperinflation

25
Q

Mechanisms of increased resistance

A 
Smooth muscle contraction 
Wall thickening 
Luminal occlusion 
Decreased lung elasticity 
Obliteration
26
Q

Primary mechanisms of increased resistance in asthma

A

Smooth muscle contraction
Wall thickening
Luminal occlusion

27
Q

Primary mechanisms of increased resistance in COPD

A

Decreased lung elasticity

Obliteration

28
Q

Inflammatory trigger in bronchiectasis

A

Bacteria

29
Q

Bronchiectasis definition

A

Irreversible dilation of the bronchial tree

  • obliteration of peripheral small airways
  • repetitive of persistent infection of proximal airways
30
Q

Bronchiectasis etiologies

A 
CF 
Ciliary dysfunction syndromes 
Foreign bodies 
Tracheomalacia 
Relapsing polychrondritis 
Infective
31
Q

What spirometry measure is decreased in asthma and COPD

A

FEV1: rate of lung emptying

32
Q

What measure detects airway obstruction ?

A

Maximal expiratory flow (MEF)

33
Q

Characteristics of squamous cell carcinoma

A

Central
Often cavitate
Keratin formation and intercellular bridges

34
Q

Characteristics of adenocarcinoma

A

Mostly peripheral
Commonest type in non-smokers
Gland formation and/or mucin production

35
Q

Characteristics of small cell carcinoma

A

Mostly central
Highly malignant and often disseminated at time of presentation
Cells with small oval hyperchromatic nuclei and scanty cytoplasm
Tumour cells exhibit neuroendocrine differentiation

36
Q

Characteristics of large cell carcinoma

A

Often peripheral

Composed of large polygonal cells with vesicular nuclei and often prominent nucleoli

37
Q

What mutation testing is done with adenocarcinoma

A

EGFR and ALK

38
Q

3 ways that lung cancer can spread

A

Locally
Lymphatically
Hematogenously

39
Q

Treatments for relieving dyspnea in COPD patients

A

Oxygen
Pulmonary rehabilitation
Smoking cessation
Short acting opioids

40
Q

MPOWER

A

Monitor epidemic in your country
Protect your population from 2nd hand smoke
Offer treatment for those who want to quit smoking
Warn, labels on tobacco products
Enforcement on advertising bans
Raise taxes

41
Q

Mechanism of action of nicotine in CNS

A

Nicotine binds preferentially to nACh receptors in CNS (primary is a4B2 nACh in VTA )

After nicotine binds a4B2 nACh receptor in VTA —> release of dopamine in nucleus accumbens (nAcc) —> reward

42
Q

Drugs for smoking cessation

A

Bupropion SR

Varenicline

43
Q

What happens to FEV1 and FVC in COPD and asthma

A

Asthma: decreased FEV1, normal FVC
COPD: decreased FEV1 and FVC

44
Q

Airway hyperresponsiveness

A

Allergen exposure —> smooth muscle contraction —> limited airflow to respiratory airways for gas exchange
Inflammation, edema, and mucus further close off conducting airways

45
Q

Mechanism of action of B2 adrenergic receptor

A

Removal of Ca2+ from the cell
Uncoupling of actin-myosin filaments
—> smooth muscle relaxation

46
Q

Treatment for asthma

A

mild: SABAs
Severe: LABAs + corticosteroid

47
Q

Side effects of B2 agonists

A

Agitation
Tremor
Tachycardia

48
Q

Common symptoms of COPD

A 
Dyspnea 
Chest tightness 
Wheezing 
Sputum production 
Shortness of breath
49
Q

Mechanism of muscarinic antagonists

A

Relax smooth muscle by blocking the muscarinic acetylcholine receptors

50
Q

Treatment for COPD

A

B2 adrenergic receptor agonists
SAMAs
LAMAs

51
Q

Corticosteroid mechanism

A

Binds GC receptor —>
Trans-repression: prevents translocation of inflammatory transcription factors from cytosol to nucleus
Trans-activation: up regulates anti-inflammatory mediators by binding to glucocorticoid response elements

52
Q

Thoracentesis

A

Insert needle through chest wall into the pleural space and drain pleural fluid

53
Q

2 layers of pleura

A

Visceral: covers lungs
Parietal: lines inside of thoracic cavity

54
Q

Histology of parietal pleura

A

Loose CT
Blood vessels and lymphatic lacunae
Thin layer of mesothelial cells

55
Q

What happens when there is differences in hydrostatic and osmotic pressures between vessels and pleural space ?

A

Fluid builds up in pleural space

56
Q

What causes increased fluid entry in pleural effusion ?

A

Increase in permeability
Increase in micro vascular pressure
Decreased pleural pressure
Decreased plasma oncotic pressure

57
Q

Work up of pleural effusions

A

Cell count and differential
Bacterial culture, AFB sweat and atypical mycobacterial culture
Mycoplasma PCR and strep pneumoniae PCR

58
Q

Transudate LUCKI ME

A 
Liver 
Urinothorax 
CHD 
Kidney 
Iatrogenic 
Myxedema 
Embolic

411 (16 decks)

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