VIVA QUESTIONS Flashcards

1
Q

Define APO

A

An accumulation of fluid in the tissues of the lung and alveoli, forming a barrier to gas exchange

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2
Q

What are the two main causes of APO?

A
  1. Haemodynamic distubances (LVF), and

2. Increased capillary permeability

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3
Q

What is the cause of Paroxysmal Noctural Dyspnoea?

A

Negative feedback system based upon hypoxia. Metabolism slows during sleep, HR slows, reduces myocardial force of contraction and CO. Exacerbates already hypoxic system. HR speeds up to compensate, further hypoxia, back pressure of blood in pulmonary system, cycle continues until person is woken with APO.

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4
Q

Describe the pathphysiology of cardiogenic APO

A

LVF->ventricle stiffens->LV pressure increases->pressure back on atria and pulmonary circulation->pulmonary capillary pressure increased->fluid portion of blood forced into interstitium and alveoli->insufficient lymphatic drainage to cope->barrier to gas exchange, surfactant washout(decreased surface tension)->increased work of breathing

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5
Q

List the symptoms of APO

A

SOB, pale, cyanotic, crackles/gurgles on auscl, tachycardic, hypertensive, decreased O2 sats, cardiac wheeze, ALOC

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6
Q

Describe the management of APO

A

DRABC, posture (upright), high flow oxygen, monitor, GTN (systolic of 100 as a guide) per 5 mins, consider salbutamol for wheeze???

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7
Q

Describe the action of GTN

A

Absorbed by mucosa into vascular system, metabolised by vascular smooth muscle to form nitric oxide, decreased intracellular Ca2+ lvls, smooth muscle relaxation and vasodilation, = decreased preload, afterload, reduced myocardial workload and oxygen demand

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8
Q

WHy are phosphodiesterase inhibitors contraindicated in the use of GTN?

A

They inhibit the breakdown of cAMP and cGMP resulting kin elevated levels, potentiate the effect and duration of GTN

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9
Q

List the 3 main cardiac causes of APO

A

CCF, LVF, mitral valve regurgitation

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10
Q

List the 3 main non-cardiac causes of APO

A

ARDS, toxic inhalation, direct lung injury

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11
Q

What is the difference between osmotic, oncotic, and hydrostatic pressure?

A

Osmotic refers to the pressure produced by a solution due to a differential of solute concentration, oncotic refers to the pressure exerted on a solution by proteins and hydrostatic pressure refers to the pressure exerted on a semi-permeable membrane by a solution

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12
Q

What is oedema?

A

excess fluid in the interstitial space

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13
Q

What are the 4 causes of oedema?

A
  1. Increased hydrostatic pressure
  2. decreased oncotic pressure
  3. increased vascular permeability
  4. lymphatic blockage
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14
Q

What do the pneumonics COP, CHP, IFOP and IFHP mean?

A
COP = capillary oncotic pressure (protein levels)
CHP = capillary hydrostatic pressure (blood pressure)
IFOP = interstitial oncotic pressure (proteins in interstitium)
IFHP = interstitial hydrostatic pressure (lymphatic drainage)
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15
Q

What are the two main physiological effects of APO, and what symptoms do they produce?

A
  1. increased thickness of respiratory membrane = decreased gas exchange and hypoxemia,
  2. Washout of surfactant = alveolar collapse, increased WOB, and V/Q mismatches
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16
Q

WHy would a patient suffering APO become acidotic?

A
  1. Decreased gas exchange = increased pCO2, low pH (respiratory acidosis)
  2. increased anaerobic respiration of tissues because of hypoxia leads to lactic acid production (metabolic acidosis)
17
Q

What is capillary epithelium breakdown and what can cause it?

A

Breakdown of the capillary wall, and can be caused by toxic inhalation, aspiration, and inflammatory mediators

18
Q

Why would adrenaline be contraindicated in APO?

A

It would vasoconstrict peripheral vessels and increase HR and force of contraction, which would increase myocardial workload (increased hypoxia on heart) and increased hydrostatic pressures within pulmonary vessels.

19
Q

Define Anaphylaxis

A

A severe form of life threatening allergic reaction caused by repeated exposure to an antigen (usually a protein), resulting in systemic inflammatory response initiated by IgE mediated mast cell degranulation, causing hypotension, bronchospasm, and oedema

20
Q

What is an antigen?

A

Molecule capable of initiating an immune response

21
Q

What is an allergen?

A

Its an antigen capable of initiating a type 1 hypersensitivity response in atopic people (means they have a predisposition to having allergic reactions

22
Q

What are mast cells and how do they initiate an immune response?

A

Mast cells are bags of granules located in loose connective tissue which wen stimulated release inflammatory mediators such as histamine and basophils, which are granulocytes similar to mast cells.

23
Q

Explain what effect mast cell degranulation has on H1 and H2 receptors

A

Mast cell degranulation releases histamine which stimulates H1 receptors in the bronchial smooth muscle causing bronchoconstriction and increased vascular permeability leading to oedema, and H2 receptors in the stomach which release gastric acid

24
Q

List the clinical features of anaphylaxis

A

Bronchospasm, conjunctivitis, rhinitis, itching, angioedema, peripheral vasodilation

25
Q

List the symptoms of anaphylaxis

A

SOB, tachypnoea, hypotension, airway compromise, rash, nausea and vomiting

26
Q

Discuss the role of adrenaline in anaphylaxis

A

Adenaline has a positive inotropic, chromotropic, and dromotropic effect –> peripheral vasoconstriction, increased HR and FOC, bronchodilation, decreased mucous production, decreased mast cell degranulation

27
Q

What is the prehospital treatment of anaphylaxis?

A

DRABC, high flow oxygen, posture, adrenaline 10mcg/kg up to 0.5mg IM every 5 mins if required, IV fluids for adequate BP (adults only), clinical support early for paeds, transport and notify.