Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the main cause of bronchitis?

A

Smoking.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name 4 infections that can cause chronic bronchitis

A

Influenza
Staph aureus
Step
Mycoplasma pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What GI problem can cause bronchitis

A

GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

List 4 causes of bronchitis

A
  1. Smoking
  2. Air pollutants
  3. Infection (staph/strep/mycoplasma/influenza)
  4. GERD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

5 clinical sings of chronic bronchitis

A
  1. Cough
  2. Wheeze (obstruction)
  3. Crackles (mucus)
  4. Dyspnea (poor ventilation)
  5. Cyanosis (shunting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of epithelium lines the bronchus

A

pseudostratified ciliated columnar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is meant by carcinoma in situ

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

32
Q

Define cor pulmonale

Name 4 conditions that can pre-dispose someone to cor pulmonale

A

Cor pulmonale refers to right ventricular hypertrophy, dilation and often failure due to pulmonary hypertension caused by a primary disorder/disease of the lung parenchyma.

  1. Myasthenia gravis
  2. Cystic fibrosis
  3. Recurrent pulmonary thromboemboli
  4. Obesity
33
Q

State two anti-cancer functions of the tumour suppressor p53 also called the “guardian of the genome”.

A

P53 can respond to DNA damage by inhibiting progression of the cell through the cell cycle. It does so by activating P21 which can then inhibit cyclin-CDK complexes from driving a cell through the cell cycle to mitosis. This allows for P53 to induce cellular repair mechanisms.

*If a cell’s DNA cannot be fixed, p53 will induce apoptosis in the cell through promotion of pro-apoptotic gene expression. These pro-apoptotic mediators such as BAX can then release cytochrome C from the cell mitochondria resulting in a downstream cascade ending in apoptosis.

KHI (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions