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First Year random > resp facts > Flashcards

resp facts Flashcards

1
Q

Define MLCK

A

MLCK stands for Myosin Light Chain Kinase. It’s an enzyme that phosphorylates (adds phosphate groups to) the regulatory light chain of myosin, a protein involved in muscle contraction. When MLCK phosphorylates the myosin light chain, it activates the myosin molecule, leading to muscle contraction.

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2
Q

Explain M1 receptors

A
  • Found primarily in the central nervous system, particularly in regions involved in cognitive function and memory.
  • Activation of M1 receptors can enhance cognitive function and memory formation.
  • Blocking M1 receptors may result in cognitive impairment and memory deficits.
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3
Q

Explain M2 receptors

A
  • Predominantly found in the heart (cardiac tissue), where they regulate heart rate and contractility.
  • Activation of M2 receptors leads to a decrease in heart rate and contractility.
  • Blocking M2 receptors may increase heart rate and contractility.
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4
Q

Explain M3 receptors

A
  • Found in various peripheral tissues, including smooth muscle cells in the respiratory tract, gastrointestinal tract, and blood vessels.
  • Activation of M3 receptors leads to smooth muscle contraction, glandular secretion, and vasodilation.
  • Blocking M3 receptors may result in relaxation of smooth muscles, decreased glandular secretion, and vasoconstriction.
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5
Q

If the goal is to dilate bronchial smooth muscles in respiratory conditions like asthma or COPD. What receptor would be best to use?

A

M3

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6
Q

If the goal is to treat bradycardia or heart block, what receptor would be best to use?

A

M2

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7
Q

If the goal is to improve cognitive function in conditions like Alzheimer’s disease. What receptor would be best to use?

A

M1

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8
Q

Why is it a good thing that drugs like sama and lama reduce mast cells

A

mast cells cause bronchoconstriction and inflammation in airways

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9
Q

Why is it a good thing that drugs like sama and lama reduce macrophages

A

play a role in inflammation and the immune response which is bad in COPD

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10
Q

Why is it a good thing that drugs like sama and lama reduce eosinophils

A

Eosinophils are a type of white blood cell involved in allergic reactions and asthma. They release inflammatory substances that contribute to airway inflammation and constriction.

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11
Q

Child with a barking cough

A

Croup

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12
Q

D sign on XRAY

A

Empysemia

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13
Q

Non smoker + lung cancer

A

adenocariconoma

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14
Q

Squamous + small cell lung cancers

A

central

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15
Q

Treat (i) mild C. Difficile
(ii) Severe C. Difficile

A

(i) - metronidazole
(ii) - Oral Vacomysin

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16
Q

Type 1 resp failure definition

A

PaO2 < 8 kPa
PaCO2 Normal

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17
Q

Type 2 resp failure definition

A

PaO2 < 8 kPa
PaCO2 > 6 kPa
PH- resp acidosis

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18
Q

How does resp 1 failure happen?

A

Ventilation-perfusion (V/Q) mismatch. The volume of air passing in and out of the lungs is comparatively smaller than the volume of blood perfusing the lungs

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19
Q

How does resp 2 failure happen?

A

Alveolar hypoventilation. This means that the lungs fail to effectively oxygenate and blow off carbon dioxide.

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20
Q

What are the causes of type 1 resp failure?

A

(1) Asthma
(2) Congestive Cardiac Failure
(3) Pulmonary embolism
(4) Pneumonia
(5) Pneumothorax

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21
Q

What are the causes of type 2 resp failure?

A

(1) COPD
(2) Restrictive lung diseases - idiopathic pulmonary fibrosis
(3) Depression of the respiratory centre
(4) Neuromuscular disease – Guillan-Barre syndrome, motor neuron disease
(5) Thoracic wall disease – rib fracture

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22
Q

Kerly B lines
Bat wing shadowing

A

Heart failure

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23
Q

Tram line shadowing

A

bronchostatsis

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24
Q

wedge shaped infract

A

pulmonary embolism

25
Q

Pleural mass with lobulated margin

A

mesothelioma

26
Q

Ground glass appearance

A

Fibrosis

27
Q

Honeycomb glass appearane

A

Fibrosis late

28
Q

Young non-smokers and potentially liver damage could be caused by what

A

Alpha 1-antitypsin deficiency

29
Q

What are the PIDs of the innate immune system?

A
  1. Severe congenital neutropenia
  2. Leukocyte adhesion deficiency
  3. Chronic granulomatous disease
30
Q

What are the PIDs of the adaptive immune system?

A
  1. Severe combined immunodeficiency
  2. X-linked SCID
  3. Bruton’s X-linked hypogammaglobulinaemia
  4. Defects in the IL-12: IFN𝛾 network
  5. Transient hypogammaglobinemia of infancy
31
Q

What is Severe Congenital Neutropenia (SCN)?

A

Characterised by low levels of neutrophils.

The most common form, Type I, is caused by an autosomal dominant mutation in the gene responsible for neutrophil elastase, leading to impaired neutrophil development

32
Q

What is Leukocyte Adhesion Deficiency (LAD)?

A

Caused by a defect in the CD18 integrin gene, resulting in neutrophils being unable to recognize markers on endothelial cells.

This leads to a failure in neutrophil adhesion and migration, compromising the immune response

33
Q

What is Chronic Granulomatous Disease (CGD)?

A

Macrophages cannot produce oxygen and nitrogen free radicals.

This impairment reduces their ability to kill intracellular microorganisms, resulting in excessive inflammation and the formation of granulomas

34
Q

What is Severe Combined Immunodeficiency (SCID)?

A

Results in a failure to produce lymphocytes, compromising both T and B cell-mediated immunity

35
Q

What is X-linked SCID?

A

X-linked SCID is caused by a mutation in the IL-2 receptor gene, leading to an inability to respond to cytokines.

This results in the failure of T and natural killer (NK) cell development and the production of immature B cells

36
Q

What is Bruton’s X-linked Hypogammaglobulinemia?

A

Mutations in the BTK gene, which is essential for B cell development.

This leads to reduced levels of immunoglobulins, compromising the body’s ability to mount an effective immune response.

37
Q

What are defects in the IL-12: IFN𝛾 network?

A

Defects in the IL-12: IFN𝛾 network impair the body’s defence against intracellular mycobacteria, compromising the immune response to these pathogens

38
Q

What is Transient Hypogammaglobulinemia of Infancy?

A

Temporary condition where infants have low levels of immunoglobulins.

This can lead to increased susceptibility to infections early in life but typically resolves on its own as the child’s immune system matures

39
Q

Clinical presentation of PIDS - primary immunodeficient disorders

A

Weight loss
Eczema
Chronic diarrhoea
Mouth ulceration
SPUR infections - serious, persistent, unusual, recurrent

40
Q

Tests for PIDS

A

FBC + IG levels

41
Q

Management of PIDS

A

IV iG

Aggressive management of infection - antibiotics, antifungals

Definitive therapy - stem cell transplant, gene therapy, recombinant G-CSF for SCN

42
Q

Explain Anaphylaxis

A

Type 1 (immediate) hypersensitivity (IgE)
Caused by (1) Hypotension (vasodilatation and plasma exudation) → circulatory collapse (shock)

(2) Angioneurotic oedema (lips, tongue → face, larynx, bronchi)

43
Q

Acute treatment for Anaphylaxis

A

M Epinephrine
(adrenaline) - MAIN
- IV antihistamine
- IV corticosteroid
- High flow O2
- Nebulised bronchodilators
- Endotracheal intubation if necessary

44
Q

Long-term management for anaphylaxis

A

Allergen avoidance

Desensitisation (immunotherapy) if the trigger is known - e.g. bee venom

Self-administered epinephrine (EpiPen)

45
Q

Explain IPEX syndrome

A

X-linked mutation on a gene called FOXP3.

This gene is important for the development of a type of immune cell called T regulatory cells (TREGs), which help regulate the immune system and prevent it from attacking the body’s tissues

46
Q

Explain HLA genes encoding for MHC cell

A

HLA genes are responsible for encoding proteins called major histocompatibility complex (MHC) molecules. These molecules play a key role in the immune system by presenting antigens (pieces of foreign substances) to immune cells, allowing the immune system to recognize and respond to them.

Certain variations (alleles) of HLA genes have been identified that can increase the risk of developing autoimmune diseases. This means that individuals with these specific HLA alleles may be more likely to develop autoimmune disorders where the immune system mistakenly attacks the body’s own tissues

47
Q

Calculate the alveolar ventilation (in litres) in one minute

A

VA = (Vt –Vd) x RR where:

VA = Alveolar ventilation (L/min)
Vt = Tidal volume (L)
Vd = Dead space (L)
RR = Respiratory rate (/min)

48
Q

What is an example of a peripheral chemorecepor

A

Carotid bodies in the bifurcation of the common carotid arteries

49
Q

The volume of air that can only be expelled from the lungs using energy. Refers to what term?

A

Expiratory reserve volume (ERV)

50
Q

What is the best investigation to diagnose type 2 respiratory failure?

A

Arterial blood gas

51
Q

What is the role of lung surfactant?

A

To reduce alveolar surface tension, reduce collapsing pressure and increase lung compliance

52
Q

Which part of the respiratory tree is predominantly involved in the pathophysiology of emphysema?

A

Alveoil sacs

53
Q

Mucus and cilia help protect the respiratory system by trapping pathogens and by wafting the mucus upward so it can subsequently be swallowed, respectively.

In which areas of the respiratory tract are mucus and ciliated epithelium absent?

A

Avelio

54
Q

Which muscles if any, are most active during normal expiration?

A

none

55
Q

Forced expiration is an active process, which requires the contraction of a group of muscles. Which muscle or muscle groups are used during forced expiration?

A

Internal intercostal

56
Q

Central chemoreceptors are involved in regulating breathing. Where are the central chemoreceptors located?

A

Ventral medulla

57
Q

Central chemoreceptors are involved in regulating breathing. Which of the following stimulates activation of central chemoreceptors?

A

H ions

58
Q

What best describes the Minimum Alveolar concentration?

A

The concentration of drug required to abolish a response to surgical incision in 50% of subjects

First Year random (35 decks)

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