Brainscape's Knowledge GenomeTM

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


See full index

Semester 2 Case Studies > Case 3 > Flashcards

Case 3 Flashcards

1
Q

what is COPD a combination of

A

bronchitis and emphysema

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

what is bronchitis

A

cough and sputum production on most days for at least three moths during the last two years

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

what is emphysema

A

enlarged air spaces distal to the terminal bronchioles with destruction of the alveolar walls

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

is there any reversibility with COPD obstruction

A

no

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

from 1-10 how leading is COPD as a cause of death

A

4th leading cause of death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

percentage of smokers who will develop COPD

A

10-20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what deficiency causes emphysema

A

alpha 1 anti tyrpsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

percentage of adult population it affects

A

1-4%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how many causes in UK - diagnosed and undiagnosed

A

3 million undiagnosed, 1 million diagnosed

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

how many deaths per year in UK

A

30,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

odds of hospital admissions

A

1 in 8

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

symptoms

A

breathlessness
cough
regulat exacerbations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

some unusual signs

A
  • use of accessory muscles during respiration
  • reduced cricosternal distance
  • pursed lip breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does gas trapping lead to

A

increase in dead space and hyperinflation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is FVC

A

forced vital capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what Is the predicted FVC value

A

<80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the FEV

A

forced expiratory volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is value of FEV/FVC ratio

A

<0.7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is bullae

A

complications of emphysema. Air pockets grow, take up space in the chest cavity and encroach on the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what can the heart look like in a COPD chest X-ray

A

cylindrical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what would readings on an ECG show

A

right atrial and ventricular hypertrophy, leading to large P waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what would an ABG test show

A

decreased PaO2

increased PaCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how is COPD diagnosed

A

through spirometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

are there any clinical features of this diagnosis

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is FEV value for severe COPD

A

<40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

why is there a hyper secretion of mucus

A

due to marked hypertrophy of mucus-secreting glands and hyperplasia of goblet cells. also reduces lumen size and increasing distances for gas diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

when is the process irreversible

A

when the larger airways become infected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is main cell involved in chronic bronchitis

A

the main cell involved is the neutrophil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the two main kinds of emphysema

A

centrilobular - associated with smoking

pan lobular - inherited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the three main pathological effects of COPD

A
  • loss of elasticity of the alveoli
  • inflammation and scarring - reduces the size of the lumen as well as reducing elasticity
  • mucus hyper secretion - reducing the size of the lumen and increasing the distance gases have to diffuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what do tobacco products release from white cells

A

predominantly neutrophil polymorphs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what does tobacco inhibit

A

alpha 1 antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is pulmonary fibrosis

A
  • loss of type 1 pneumocytes
  • replaced by type 2 pneumocytes - failure of normal maturation
  • excessive deposition of collagen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

which disease is finger clubbing associated with

A

pulmonary fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how common is lung cancer

A

second most common cancer diagnosed in the UK after breast cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the histological classifications of primary lung cancer

A
  • squamous cell carcinoma
  • small cell carcinoma
  • adenocarcinoma
  • large cell undifferentiated carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is an exacerbation of COPD

A

defined as a change in the patients baseline symptoms such as;

  • worsening SOB
  • increase cough
  • increase sputum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what does goblet cell hyperplasia lead to

A

cough and sputum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what does airway narrowing lead to

A

breathlessness and wheeze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what does alveolar deconstruction lead to

A

breathlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

normal FEV/FVC ratio

A

70-85%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is pulmonary rehabilitation

A

multidisciplinary programme of care for people with chronic respiratory impairment. it is individually tolerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

who do NICE recommend making pulmonary rehabilitation available to

A

everyone with copd

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what does pulmonary rehabilitation include

A
  • physical training
  • disease education
  • nutritional education
  • physical and behavioural intervention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

after 20 mins

A

pulse returns to normal

46
Q

after 8 hours

A

nicotine is reduced by 90% and carbon monoxide levels in blood reduce by 75%. circulation improves

47
Q

after 24 hours

A

carbon monoxide and nicotine removed from the body. ability to taste and smell improves

48
Q

after 72 hours

A

breathing is easier. bronchial tubes begin to relax and energy levels increase

49
Q

2-12 weeks

A

circulation improves

50
Q

1 month

A

physical appearance improves

51
Q

3-9 months

A

coughing and wheezing is reduced

52
Q

1 year

A

excess risk of a heart attack reduces by hand

53
Q

10 years

A

risk of lung cancer falls to about half of a continuing smoker

54
Q

after 15 years

A

risk of a heart attack falls to the same as someone who has never smoked

55
Q

what is pneumonia

A

infection of the lung interstitium, alveoli and airways

56
Q

what does CAP, HAP AND VAP stand for

A

CAP - community acquired pneumonia
- HAP - hospital acquired pneumonia
VAP - ventilatory acquired pneumonia

57
Q

how many pneumonia’s require hospitalisation

A

1 in 3

58
Q

what is tachypnoea

A

hast breathing

59
Q

what is tachycardia

A

fast pulse

60
Q

what is the treatment for acute bronchitis

A

supportive only unless prolonged illness

61
Q

treatment for ‘exacerbation’

A
  • bronchodilators
  • steroid
  • oxygen
62
Q

treatment for pneumonia

A

PROMPT antibiotics. must cover streptococcus

63
Q

treatment of COVID 19

A
  • antivirals - remdesivir

- anti inflammatioies - tocilxumab

64
Q

when does a lung infection become chronic

A

lasts more than 6-8 weeks

65
Q

transfer is proportional to

A
  • pressure gradient
  • surface area available for diffusion
  • 1/length of the pathway
  • solubility
  • 1/(square route) molecular wight
66
Q

what is the resting cardiac output

A

5L/min

67
Q

what scale measures severity of dyspnoea

A

MRC dysponaie scale

68
Q

COPD management in community

A
  • bronchodilators
  • antibiotics
  • oral corticosteroids
69
Q

hospital management of COPD

A

ABC assessment
controlled oxygen therapy
blood gas measurement
CXR

70
Q

what is addiction

A

an inability to stop using a substance or engaging in a behaviour even though it is causing psychological and physical harm

71
Q

what does nicotine exert their actions by elevating

A

the synaptic levels of dopamine, noradrenaline and serotonin

72
Q

what is the serotonin pathway called

A

the dopamine reward pathway

73
Q

mode of action of nicotine

A
  • nicotine enters the brain, stimulating the release of dopamine inducing nearly immediate feelings of pleasure
  • initiates acetylcholine and binds to the nicotinic receptors and mimics the action of Ach
  • body increases levels of Ach to all unregulated stimulation
  • heightened activity in cholinergic pathways to the brain
74
Q

what is the second transmitter nicotine stimulates and describe

A
  • stimulates release of glutamate
  • it is involved in the learning and memory and enhances the connections between sets of neurone
  • these stronger connections may create a memory loop of the good feelings you get and further drive the desire to use nicotine
75
Q

how does smoking affect the lungs

A
  • toxins break the thin walls of the alveoli leaving larger, less efficient air sacs
  • they also lose their bounce making it harder to exchange oxygen
  • signals the start of emphysema
76
Q

how does smoking make you cough

-

A
  • cells that produce mucus in your lungs and airways grow in size and number so amount of mucus increases and thickens
  • lungs can’t clean out this mucus and makes you cough
77
Q

what does black mucus indicate

A

fungal infection

78
Q

what does rust coloured sputum suggests

A

pneumococcal infection

79
Q

how does amoxicillin work

A

interfere with ability of bacteria to form cell walls

- impaired the bonds that hold the bacterial walls together and allows holes to appear and kills the bacteria

80
Q

action of cefuoxime

A
  • attaches via B lactan ring to the target in the cell (penicillin binding protein)
  • changes the functional group of the protein on the cell wall and uses inhibition of the transpeptidation enzyme that cross links the peptide chains attached to backbone of the peptidoglycan
  • as cell wall grows in coordination with bacterial growth, the cell wall is weakened and crumbles. extracellular fluid enters and leads to the death
81
Q

what is the enzyme bacteria can produce to stop penicillin working

A

B-lactamase

82
Q

what is cefuroxime used to treat

A

pneumonia

83
Q

what bacteria is pneumonia caused by

A

pneumococci

84
Q

COVID mechanism

A
  • uses the human ACE2 receptor for viral entry and cell tropism for infectivity
  • infection of circulating immune cells is abortive
  • viral structural spike protein that binds to ACE2 receptor
  • the type 2 transmembrane serine protease present in the host cell, promotes viral uptake by cleaving ACE2 and activating the s protein
85
Q

what are the host cells for COVID

A

alveolar epithelial type II cells

86
Q

what is scarring called in lungs

A

pulmonary fibrosis

87
Q

how do anticholinergic bronchodilators work

A
  • bind to muscarinic receptors and block action of acetylcholine
  • reduce the bronchomotor tone which leads to bronchodilator
88
Q

what is the drawback from using a combination inhaler

A

loss of flexibility in dosing of component drugs in the inhaler

89
Q

how long does it take nicotine to reach the brain

A

10 seconds

90
Q

what is 2,3-BPG

A

molecule that binds to haemoglobin and decreases its affinity for oxygen

91
Q

what role does Hering Bruer reflecx play in breathing

A

terminates inspiration to stop inflammation of the lungs

92
Q

a pink puffer does not have what symptom

A

cyanosed skin

93
Q

what is mechanism of action of clarithromycin

A

binds to 50 s subunit of bacterial ribosome and inhibits translation of peptides

94
Q

what happens to PEFR value

A

it is low

95
Q

what happens to blood gases in severe COPD

A

hypoxemia and hypercapnia

96
Q

what is aim of oxygen therapy

A

to increase Pa02 to at least 8kPa (60mmHg)

97
Q

what percentage of oxygen is usually administered

A

24-28%

98
Q

who does centrelobular emphysema affect

A

smokers

99
Q

who does pan lobular emphysema affect

A

alpha 1 antitrypsin deficient

100
Q

what is distal acinar (paraseptal) emphysema

A
  • underlies many of the cases of spontaneous oneumotharox
101
Q

what cells are increased in the lung

A

macrophages, CD8+, CD4+ T lymphocytes and neutrophils

102
Q

what is alpha 1 antitrypsin

A

is it a proteinase inhibitor which is produced in the liver, secreted into the blood and diffuses into the ling
- it inhibits proteolytic enxymens such as neutrophil elastase which are capable of destroying alveolar wall connective itusse

103
Q

what do neutrophils and macrophages activate

A

the transcription factor NF-xB which switches on genes that encode TNF and chemkines

104
Q

what is hyperaemia

A

excess of blood in vessels

105
Q

what kind of bacteria is streptococcus pneumonia

A

gram positve

106
Q

what type of bacteria is HAP

A

gram negative

107
Q

what are the four stages of substance use

A
  • initiation
  • maintenance
  • cessation
  • relapse
108
Q

what is varenicline

A

partial agonist of the alpha 4 beta 2 subtype of the nicotinic acetylcholine receptor. stimulates receptors more weakly than nicotine. does not greatly increase downstream release of dopamine.

109
Q

eryhtromycin mechanism

A
  • macrolides inhibit bacterial protein synthesis by an inhibitory effect on translocation
110
Q

where do macrolide antibiotics bind to

A

the P site on the submit 50s of the bacterial ribosome. considered bacteriostatic

Semester 2 Case Studies (11 decks)

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