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KHI > Robert parker > Flashcards

Robert parker Flashcards

1
Q

Define chronic bronchitis

A

Chronic inflammation of the bronchi resulting in a productive cough; lasting for at least 3 months over 2 consecutive years.

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2
Q

What is the main cause of bronchitis?

A

Smoking.

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3
Q

Name 4 infections that can cause chronic bronchitis

A

Influenza
Staph aureus
Step
Mycoplasma pneumonia

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4
Q

What GI problem can cause bronchitis

A

GERD

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5
Q

List 4 causes of bronchitis

A
  1. Smoking
  2. Air pollutants
  3. Infection (staph/strep/mycoplasma/influenza)
  4. GERD
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6
Q

List 4 complications of chronic bronchitis

A
  1. Progression to COPD
  2. Cor pulmonale
  3. Epithelial metaplasia -> dysplasia (SCC)
  4. Bronchial hyper-responsiveness
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7
Q

List 3 morphological features of chronic bronchitis

A
  1. Mucus gland hypertrophy (reid index > 0.4) with hypersecretion of mucus
  2. Goblet cell hyperplasia
  3. Bronchial inflammation (from release of inflammatory cytokines IL-8)
  4. Epithelial metaplasia (squamous) -> Dysplasia
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8
Q

outline the pathophysiology of chronic bronchitis

A

Response to injurious agent e.g. smoking

*Hypertrophy of mucus gland
*Hyperplasia of goblet cells
—-> Hypersecretion of mucus -> mucus plugging.

*Oedema of bronchus due to:
—>release of pro-inflammatory cytokines (IL-8)
—>neutrophil infiltrate to submucosa
—>epithelial cells impaired from releasing usual regulatory substances to modulate inflammation such as angiotensin-converting enzymes/ can’t convert inflammatory substances to inert forms = chronic inflammation + vasodilation.
—> defective mucocilliary function

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9
Q

What is the Reid index

A

Measures the ratio of mucus gland to thickness to that of bronchial wall - usually < 0.4 and measured at post-mortem.

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10
Q

5 clinical sings of chronic bronchitis

A
  1. Cough
  2. Wheeze (obstruction)
  3. Crackles (mucus)
  4. Dyspnea (poor ventilation)
  5. Cyanosis (shunting)
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11
Q

What type of epithelium lines the bronchus

A

pseudostratified ciliated columnar

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12
Q

What is meant by carcinoma in situ

A

Dysplasia confined to epithelium and does not cross the basement membrane.

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13
Q

Define emphysema

A

Emphysema is an enlargement of the airspaces distal to the terminal bronchiole (i.e. the acinus) due to destruction of the alveolar wall leading to air flow limitation.

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14
Q

Name the 3 types of emphysema, the primary cause of each and their most common locations within the lung

A
  1. Centriacinar
    –> Proximal acinus affected
    –> upper lobes usually
    –> smokers
  2. Panacinar
    —> Entire acinus affected
    —> Lower borders and anterior margins
    —> Alpha-1 antitrypsin deficiency
  3. Paraseptal
    —> most accentuated on outer margins/adjacent to septa or pleura
    —> often adjacent to areas of fibrosis / atelectasis
    —> often upper lobes.
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15
Q

What type of emphysema is associated with premature babies?

A

Interstitial emphysema.
—> associated with positive airway pressure in an attempt to offset affects of infant respiratory distress syndrome.
—> rupture of alveolar walls results in air leakage into the lung interstitium.

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16
Q

Outline the pathophysiology of alveolar breakdown in emphysema

A

Underlying cause is an imbalance between proteases (elastase) + antiproteases.

  1. Smoking results in increased elastase production from neutrophils + macrophages -> results in elastin breakdown.
  2. Alpha-1 antitrypsin deficiency
    –> AAT usually functions to protect elastin from elastase
    –> AATD results in unopposed action of elastase -> elastin break down.

Loss of elastin = loss of elastic recoil of alveoli = bronchiole collapse + air trapping.

17
Q

Where is Alpha-1 Antitrypsin produced and What is the underlying cause of AATD.

A

Produced in liver hepatocytes

Misfolding of AAT due to a glutamate-lysine substitution- folds into an insoluble polymer/amyloid fibril

18
Q

What is meant by elevated V/Q ratio

A

elevated V/Q ratio (mismatch) means that there is much more ventilation in the alveoli than there is perfusion. In other words, the oxygen is being wasted.

Pulmonary embolism can cause elevated V/Q as the ventilation is ok but it is the blood (Q) that is obstructed.

19
Q

What is meant by low V/Q ratio? List 3 causes

A

Low V/Q (mismatch) means that there is less ventilation to the alveoli than there is blood supply. in other words the blood is wasted/not getting oxygen.

This can occur in:

Chronic bronchitis
Pulmonary odema
Cystic fibrosis
Phsyical air obstruction from foreign object

20
Q

What is the physiological response to Low V/Q ratio?

A

Low V/Q ratio can result in shunting to try offset the severity of hypoxemia. This is facilitated through vasoconstriction of the vasculature supplying the hypoxic alveoli to redirect blood to better ventilated alveoli - however the redirected blood may not partake in sufficient gas exchange.

21
Q

Why do people with shunting physiology respond poorly to oxygen therapy?

A

Because the redirected blood will often fail to participate in gas exchange by bypassing unventilated alveoli. As well as this, the blood that is passing these ventilated alveoli will already be saturated so can’t pick up anymore O2. Therefore oxygen therapy will not improve the hypoxemia.

22
Q

Why would LMW heparin be given in COPD?

A

To prevent blood clots due to secondary polycythenia (caused by chronic hypoxemia)

23
Q

What group of drugs does heparin belong to? What is its MOA

A

Anti-coagulants

Heparin increases activation of antithrombin III by binding to it.

Increased activity of antithrombin III will result in increased inhibition of factors Xa and IIb. This dampens the common pathway of coagulation cascade, preventing fibrin activation (Ia), platelet activation and ultimately clot formation.

24
Q

3 goals of oxygen therapy in COPD

A
  1. Offset chronic hypoxemia
  2. Prevent further polycythenia
  3. Prevent cor pulmonale by inducing vasodilation of pulmonary vasculature thereby reducing degree of pulmonary hypertension.
25
Q

clinical signs of cor pulmonale

A
  1. Raised JVP (increased pressure from Rt ventricle -> Rt atrium -> SVC -> Rt brachiocephalic -> Rt jugular)
  2. Hepatomegaly
    -> Pressure from Rt atrium -> IVC -> hepatic veins.
  3. Hypotension due to systemic vasodilation in response to hypoexmia.
  4. Tachycardia
  5. Peripheral oedema -> back flow of blood
26
Q

list 4 other non-COPD causes of cor-pulmonale

A
  1. Kyphoscoliosis
  2. Myasthenia Gravis
  3. Obesity.
  4. Recurrent pulmonary microembolism.
27
Q

Distinguish between hypoxia and hypoxemia. List the 4 types of hypoxia

A

Hypoxemia refers to a low PaO2 in arterial blood.

Hypoxia refers to low/inadequate oxygen supply to organs and tissues.
(1) Hypoxemic-hypoxia
(2) Anaemic hypoxia
(3) Circulatory hypoxia
(4) Histotoxic/cytotoxic hypoxia: oxygen is available but cells can’t utilise it: seen in sepsis.

28
Q

What % o2 sat should you aim for when treating COPD patients with oxygen?

A

88-92% , delivering 24-28% oxygen via venturi mask.

29
Q

FEV1, FVC, FEV1:FVC ratio in obstructive disease?

A

All reduced, FEV1 reduced more than FVC

Reduced FEV1 and FVC means <80% of predicted

Low ratio means <0.7

30
Q

FEV1, FVC and ratio in restrictive diseases?

A

FEV1 + FVC reduced, usually by same amount , therefore ratio may be normal or else increased.

31
Q

What is the most effective means of preventing further decline in FEV1 in COPD?

A

smoking cessation.

KHI (16 decks)

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