CR Revision 5 Flashcards

1
Q

What determines the alveolar to arterial PO2 difference? [1]

What is usual Alveolar-arterial O2 difference not normally greater than? [1]

A

Shunting determines the alveolar to arterial PO2 difference

The normal A-a O2 difference is not normally greater than 1.3 kPa

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2
Q

How do you calculate normal aterial PaO2? [1]

A

Normal PaO2 = 13.6 – (0.044 x age in yrs) kPa

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3
Q

What is shunting (of the lungs)? [1]

What can shunting be caused by [1]

]

A

When an area of the lung is perfused but not ventilated. Blood is transported through the lungs without taking part in gas exchange

Can be caused by Arteriovenous malformations (AVMs)

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4
Q

What causes changes in oxygen dissociation curve?

A

Shifts to L → Lower oxygen delivery, caused by:

Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature

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5
Q

Label A & B [2]

A

A: Lung failure
B: Pump failure

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6
Q

Type 2 Respiratory Failure is an imbalance between which three factors? [3]

A

Imbalance between:
- Neural respiratory drive
- Load of resp. muscles
- Capacity of the resp. muscles

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7
Q

LEARN ! Name 4 reasons that could cause hypoventilation

A

Increased resistance as a result of airway obstruction (e.g.COPD)

Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity).

Reduced strength of the respiratory muscles (diaphragm) (e.g. Guillain-Barré, motor neurone disease)

Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates)

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8
Q

Name three consequences of CO2 retention [3]

State for each their clinical signs [3[

A

End-organ hypoxia
- Altered mental status
- Bradycardia and hypotension (late)

Haemoglobin desaturation
- Cyanosis

CO2 Retention
- Flap (asterixis): ask a patient to extend arms out, close eyes, should be able to hold for 30 secs
- Bounding pulse

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9
Q

What would be the threshold limit pulse ox saturation (SpO2) that is a critical threshold?

A

~94% is a critical threshold. Below this level a small fall in PaO2 produces a sharp fall in SpO2

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10
Q

If the SpO2 is >94% the the PaO2 should be >[]kPa

A

If the SpO2 is >94% the the PaO2 should be >10kPa

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11
Q

First line of treatment for respiratory failure? [1]

A

Oxygen

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12
Q

If giving oxygen therapy, what is SpO2 target?

A

94-98%
Avoid hyperoxia in patients recieving supplemental oxygen !

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13
Q

Which type of patients would require the following?

  • Oxygen masks / nasal cannulae
  • Face mask with reservoir bag
  • Venturi mask
A

Oxygen masks, nasal cannulae
Patient with normal vital signs (post-op)

Face mask with reservoir bag
Higher O2 concentration needed (asthma attack, pneumonia, sepsis)

Venturi mask
Controlled treatment in long-term respiratory failure (COPD)

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14
Q

Describe how conduct oxygen therapy?

A

High flow Oxygen

Continuous oximetry should be started immediately

Monitor:
Vital signs
ABGs

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15
Q

What are the two main mechanisms that cause ischaemic stroke? [2]

A
  1. Thrombosis: The formation of a blood clot in an artery normally at the site of an atheroma or atherosclerosis.
  2. Embolism: An embolus blocks a downstream artery after originating from somewhere else in the body, usually having broken off from a thrombus.
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16
Q

Explain MoA of how atherosclerosis causes ischaemic stroke

A

Endothelial damage allows lipoproteins and monocytes to adhere to the vessel wall and enter the intima.

Monocytes differentiate into macrophages and engulf the lipoprotein and become known as foam cells.

Further accumulation of cholesterol and foam cells forms a fatty streak.

Foam cells release pro-inflammatory cytokines which leads to smooth muscle cell proliferation. and connective tissue to deposition in the fatty streak.

These changes form a fibrous cap over the lipid core.

A necrotic core can form due to the lack of capillaries.

Plaque rupture removes the endothelium which exposes the fibrous cap leading to thrombosis and occlusion of the artery

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17
Q

What is a watershed ischaemic stroke? [1]

A

Sudden BP drop by more than 40mmHg, then there is low cerebral blood flow = global ischaemia leading to ‘watershed infarcts’ in vulnerable areas of cortex between boundaries of different arterial territories

brain ischemia that is localized to the vulnerable border zones between the tissues supplied by the anterior, posterior and middle cerebral arteries

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18
Q

When is common to see watershed stroke?

A

Sepsis patients

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19
Q

What is the most important risk factor for Haemorrhagic stroke? [1]

A

Hypertension !

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20
Q

Whats the difference between Intracerebral haemorrhage vs Subarachnoid haemorrhage (SAH)?

Which causes a thunderclap headache?

A

Intracerebral haemorrhage is bleeding into the brain parenchyma: basal ganglia particularly effected

SAH is bleeding into the subarachnoid space. thunderclap headache

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21
Q

Which artery is most common to have a stroke in? [1]

A

Middle cerebral artery

22
Q

Which drug classes would use for primary prevention of stroke? [3]

Control of which disease would allow prevention of stroke? [1]

A

Primary prevention:

  • Cholesterol: statin
  • AF: anticoagulation
  • Good diabetic control
  • BP: antihypertensives
23
Q

What are the 3 overlying causes of cellular death in stroke? [3]

A

Mechanical compression
Cerebral Oedema
Excitotoxicity

24
Q

Excitotoxicity of stroke

A
25
Q

What is first step for diagnosis you do when suspect stroke patient? [1]

A

Get them to have a non-contrast CT scan: rule out haemorrhage stroke

26
Q

How would you treat acute ischameic stroke:

  • if within 4.5 hrs of onset [1]
  • if outside 4.5 hrs of onset [1]
A

Thromboylsis:
- using drug - Alteplase
- Must occur within 4.5 hours of onset
- haemorrhage has to be excluded

Mechanical thrombectomy
- endovascular removal of a thrombus from a large artery.

27
Q

What drug would you initially give to non-haem stroke? [1]

A

Aspirin !

28
Q

How would you manange an acute TIA?

A

300mg Aspirin
Refer urgently to TIA clinic (to be seen within 24 hours). In clinic: work out if was stroke or not.
Might do ECG to see if have AF

29
Q

draw the circle of willis xxx

A
30
Q

Label A-C

A

A: anterior cerebral artery
B: middle cererbral artery
C: internal carotid artery

31
Q

What are a common consequence of prolonged or recurrent inflammation, particularly allergic inflammation in respiratory system? [1]

A

Nasal polyps are oedematous protrusions of the respiratory mucosa and are a common consequence of prolonged or recurrent inflammation, particularly allergic inflammation.

32
Q

Describe 3 histological changes seen in asthma Ptx? [3]

A

Asthma causes:

  • SM hyperplasia (due to increase in muscle use
  • Basement membrane thickening
  • Mucus hyperplasia
Fig. 6 Endoscopic biopsy from a patient with severe asthma shows mucus hyperplasia, extensive thickening of the subepithelial layer and marked infiltration of inflammatory cells—in particular, eosinophils.
33
Q

Which part of the respiratory system is the main site of SABA action? [1]

A

Smaller airways in tracheal / bronchial tree: requires smooth muscle to be there (to relax)

34
Q

Which secretory protein is associated with pathologies such as COPD and asthma? [1]
Which cell secretes? [1]

A

Secretory protein C16: associated with pathologies such as COPD and asthma.
non-ciliated bronchiolar Clara cells This protein increasingly appears to protect the respiratory tract against oxidative stress and inflammation

35
Q

What histological changes do you see in bronchitis? [4]

A

goblet cell metaplasia

mucous plugging

inflammatory cell infiltration (lymphocytes and macrophages)

fibrosis

mucus gland hypertrophy

36
Q

What are the histopatholigcal features of TB? [4]

A

Langhan cells

immune cell infiltration

granulomas; have central necrosis and cavitation

tissue destruction

37
Q

Which of the following depicts the Langhan cell in TB Ptx?

A
B
C
D

A

Which of the following depicts the Langhan cell in TB Ptx?

A
B
C
D

38
Q

Histopathological features in pneumonia? [1]

A

aggregates of neutrophils (almost like an abscess) in the alveolar

39
Q

Where are sq cell carcinomas (SCCs) most often found (lung)? [1]

A

Hilum

40
Q

Name a risk factor for squamous cell carcinoma [1]

What are histological changes are induced by ^? [2]

A

Often centrally located close to hilum
Smoking is a risk factor:
- Leads initially to metaplasia (from respiratory to squamous epithelium) then dysplasia.
- Smoke procarcinogens can be converted to carcinogens via P450

41
Q

What may be indicative of paraneoplastic syndrome due to Squamous Cell Carcinoma? [1]

A

Hypercalcemia may be indicative of paraneoplastic syndrome due to SCC

42
Q

Cytological features of Squamous cell C? [3]

A
  • small cells
  • Pleomorphic, Polygonal cells [1]
    with high nuclear to cytoplasmic ratio [1]
    with island of keratinisation
    [1](orange, Normal bronchial cells are azure/blue)
  • Larger tumours may have extensive necrosis
43
Q

Histopathological features of Cytological features of Squamous cell C? ? [5]

A
  • Small, malignant cells often very large with eonisophilic cytoplams [1] and large vesicular nucleus [1]
  • High nuclear:cytoplasm ratio
  • Intercellular bridges
  • Keratin pearls [1]
44
Q

Histopathological features of adenocarcinoma? [3]

A

irregular, closely packed glands effacing normal lung appearance with atypical cells lining the gland lumen

glandular hyperplasia

desmoplastic (fibrotic) stroma around them.

45
Q

Histopathological features of small cell carcinoma? [3]

A

malignant neuroendocrine neoplasm found centrally in the lung

small oval rounded cells with scarce cytoplasm and irregular borders: morphology where can only see nuclei - looks like nuclei molding

extensive necrosis

mitosis ++++++++++++++

46
Q

What type of T helper cells are found in granulomas? [1]

A

TH1 subtype

47
Q

Describe that pathophysiology of granuloma formation

A
  • Antigen taken up by macrophage & presented to CD4+ helper T cells
  • CD4+ helper T cell convert to TH1 subtype
  • TH1 cells screte IL-2 and INy
  • T cell proliferation and macrophage activation
  • Macrophages and T cells secrete TNFa
  • Causes increase in inflammatory cells
  • Causes repeat of TH1 cells screte IL-2 and INy etc
48
Q

Label A-D of this granuloma

A
49
Q

Which of the following is lobal pneumonia and which is bronchopneumonia?

A

Left: Bronchopneuomia
Right: Lobal pneumonia

50
Q

What changes do COPD small airways undergo with developement on the disease? [1]

A

COPD small airways demonstrate marked remodelling, with the overall thickness of the airway wall increased compared to smokers without airflow limitation

  • epithelial changes
  • mucoid plugs
  • increased density of inflammatory cell
  • smooth muscle hyperplasia and fibrosis
Histopathological features of small airways disease in COPD. a A COPD bronchiole with a thickened airway wall due to fibrotic remodeling and excessive deposition of collagen bundles (blue colouration). Section stained with Masson’s Trichrome (10X magnification). b A COPD bronchiolevascular bundle whereby the bronchiole contains a large intra-luminal mucous plug (red arrow) (2X magnification). Section stained with hematoxylin and eosin. c A COPD bronchiole with increased numbers of goblet cells (greenarrows) in the epithelial lining (20X magnification). Section stained with hematoxylin and eosin. d The wall of a COPD bronchiole with increased numbers of inflammatory cells (black arrows) (20X magnification). Section stained with hematoxylin and eosin
51
Q

Name the type of lung cancer depicted

A

metastatic small cell carcinoma - blue cluster

note:
- orange myeloid precursors
- fat cells
- blue erythoid precursors
- megakaryocytes

52
Q

Which of the following arrows shows a thickened basement membrane in asthma patient?

A
B
C
D

A

Which of the following arrows shows a thickened basement membrane?

A
B
C
D