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Life Support > Week 6 > Flashcards

Week 6 Flashcards

1
Q

What is hypoxia vs hypoxaemia?

A

hypoxia = inadequate level of tissue oxygenation for cell metabolism

hypoxaemia - abnormally low oxygen tension in the blood

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2
Q

What are the four types of hypoxia?

A

Hypoxic hypoxia - low oxygen tension
Hypoxaemic hypoxia - low blood content
Circulatory hypoxia - low cardiac output/delivery
Histotoxic hypoxia - poor tissue usage

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3
Q

How do you measure oxygen transport and delivery (two equations)

A

Oxygen bound to Hb + Oxygen carried in plasma = total carrying capacity

Total carrying capacity x cardiac output = oxygen delivery to tissues

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4
Q

Describe and give potential causes of hypoxic hypoxia

A

Hypoxic hypoxia - low oxygen tension, issue is getting air to the plasma
Examples: AIRWAY OBSTRUCTION, LACK OF ATMOSPHERIC OXYGEN, HYPOVENTILATION, VQ MISMATCH

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5
Q

What are the causes of hypoventilation? (3 examples)

A

Coma, COPD, obesity

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6
Q

What are the endpoints of VQ mismatch? (low ventilation, low perfusion)

A

Low ventilation results in shunt (deoxygenated blood moviving through, mixing with oxygenated)

Low perfusion results in deadspace ventilation (blood can’t move through to be oxygenated)

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7
Q

Describe and give potential causes of hypoxameic hypoxia

A

Hypoxaemic hypoxia - low blood content

Examples: LOW HAEMOGLOBIN
ABNORMAL HAEMOGLOBIN (SICKLE, THALASSAEMIA), CO POISONING
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8
Q

Describe and give potential causes of circulatory hypoxia

A

Circulatory hypoxia - low cardiac output/delivery / CIRCULATION ISSUE

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9
Q

Describe and give potential causes of histotoxic hypoxia

A

Histotoxic hypoxia - poor tissue usage / CELL LEVEL

Examples: SEPSIS, DRUGS, CYANIDE

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10
Q

Why do we need to use anticoagulants? (3)

A

Stroke prevention
Venous thromoembolic disease
Arterial thrombotic disease

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11
Q

DVT - incidence, relevance of position in the leg, fatality rate

A

Incidence 1/1000 per year
50-70% above the knee embolise
1-2% incidence of fatal PE

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12
Q

What do anticoagulants do?

A

Prevent development of clots
Does NOT thin blood
Does NOT dissolve existing clots

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13
Q

What is a risk factor?

A

Any characteristic which identifies a group at increased risk of disease now or in the future

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14
Q

How would we calculate the relative risk of VTE in people who have flown?

A

Risk of VTE in people exposed (have flown) / risk of VTE in people who are not exposed (not flown)

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15
Q

What are the factors increasing risk of VTE? (3)

A

Virchow’s triad
Reduced rate of blood flow
Increased coagulability of blood
Damage to venous endothelium

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16
Q

What are the common underlying causes of VTE? (7 examples)

A 
Immobility
Heart failure
Severe injury
Malignancy
Pregnancy
Oral contraceptives / HRT
Dehydration
Heredity causes
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17
Q

How soon does VTE generally occur following flying?

A

Approx 3 days - 2 weeks

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18
Q

What are the strengths of a case control study? (4)

A

Quick to carry out
Relatively cheap
Good for uncommon disease
Can look at several possible exposures

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19
Q

In case control study, beware of: (2)

A

Confounding - Things that can cause the disease with or without the factor you are focusing on
Bias -

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20
Q

Random vs systematic error

A

Random error is imprecision, but the more research you do, the closer you will get

Systematic error is caused by bias which leads you to believe the answer is completely different

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21
Q

Factors to consider when designing your case control study? (6)

A 
Hypothesis and confounding factors
Size / statistical power of study
Selection of cases
Selection of controls
Study conduction - how is exposure measured? How are cofounding factors managed?
Approach to analysis
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22
Q

What is the difference between selection and information bias?

A

Selection in cases and/or controls is related to exposure under study

Information on their exposure is obtained differently from cases and controls

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23
Q

Describe conducting vs respiratory portions of airway (anatomy)

A

Trachea, bronchi, conducting bronchioles

respiratory bronchioles, alveolar ducts and alveoli

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24
Q

Describe role of diaphragm and abdominal muscles during respiration

A

Diaphragm contracts, moving down, abdominal muscles contract outwards (bucket handle), sternum moves anterior (pump)

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25
Q

What are the attachments of the diaphragm? What are its apertures? What are the structures that pass through the diaphragm?

A

It is attached anteriorly to the xiphoid process and costal margin, laterally to the 11th and 12th ribs, and posteriorly to the lumbar vertebrae.

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26
Q

What are the major features / functions of the pharynx and larynx?

A

Pharynx - naso, oro, laryngo - warms air, food passes through mouth, houses tonsils
Separated by epiglottis
Larynx - beginning of airway, provides structure

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27
Q

What is the clinical significance of the crossing of the digestive and respiratory passages in the pharynx?

A

food / air can move into the wrong passages.

Issues affecting trachea / oesophagus may have implications for other system

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28
Q

Describe the arrangement and subdivisions of the lung pleura (including blood supplies, innervations and lymphatic drainage)

A

Parietal - responds to temp, touch, pressure, pain
Intercostal, phrenic nerves
Blood supply from costal veins/arteries

Visceral - only reacts to stretch, innervated by pulmonary plexus
Blood supply from bronchial arteries/veins

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29
Q

What structures make breathing friction free?

A

Pleural cavity - air-filled space and some serous fluid

30
Q

What changes happen at birth to allow neonate to breathe independently? (5)

A

Clearance of fetal lung fluid
Surfactant secretion, and breathing
Transition of fetal to neonatal circulation
Decrease in pulmonary vascular resistance and increased pulmonary blood flow
Endocrine support of the transition

31
Q

What are the chief mechanical processes of inspiration and expiration?

A

Muscles, pleural cavity, relaxation during expiration

32
Q

What is the gross structure / function of the pleural membrane?

A

Outside, inside, space

Reduces friction, pressure required for breathing prcoess

33
Q

What is reflection?

A

Learning through experience toward gaining new insights or changed perceptions of self and practice

Intention of improving and developing

34
Q

Describe the haemostatic response to injury

A

Endothelium injury - platelets come in and adhere to the location of damage - coagulation (fibrin comes in to create mesh which allows platelets to leave and WBCs to come rebuild tissue)

35
Q

What are the principles / objectives of haemostasis

A

Life preserving process design to maintain blood flow

  • respond to tissue injury
  • curtail blood loss
  • restore vascular integrity
  • promote healing
  • limit infection
36
Q

Primary (3) vs secondary (2) haemostasis - followed by what? And approx time frames

A

Primary - vasoconstriction (seconds), platelet adhesion (seconds), aggregation and contraction (minutes)

Secondary - activation of coagulation factors (seconds), formation of fibrin minutes)

Then fibrinolysis (activation within minutes, lysis of plug within hours)

37
Q

Significance of Von Willebrand factor

A

Anchor / glue
Carries and protects factor 8
Protein in circulation that sticks to collagen and platelets
Deficiency prevents clotting, commonest clotting disorder

38
Q

What is haemophilia A?

A

Deficiency of factor 8

Most severe bleeding disorder

39
Q

Describe changes in platelets during clotting

A

Shape changes as they are activated during clotting, develop feet and then flatten

40
Q

Where are most clotting factors made?

A

Liver

41
Q

What does blood do outside of the body?

A

Due to its charge, it essentially wants to become solid outside the body and gets sticky

42
Q

What does the endothelial wall do?

A

xxx

43
Q

What is the role of thrombin? What factor is it?

A

Thrombin turns fibrinogen into fibrin. Factor 2

44
Q

Describe fibrinolysis

A

clot limiting mechanism
plasminogen turned into plasmin (by tPA which is in endothelium) to destroy fibrin clot
Fibrin degradation products (such as D dimers produced)

45
Q

What is the role of streptokinase?

A

Thrombolytic - thrombolytics by activating plasminogen to form plasmin, which degrades fibrin and so breaks up thrombi

46
Q

What are PT and APTT?

A

Prothrombin tine looks at extrinsic pathway
Add tissue factor

APTT looks at intrinsic pathway
At foreign material

Both tell you if something is wrong (if they take longer) but don’t tell you exactly what the problem is

47
Q

How can you do coagulation test without the blood clotting in test tube?

A

Add citrate / calcium xxx LOOK AT THIS

48
Q

What is serum vs plasma?

A

Serum doesn’t have clotting factors

49
Q

What is a mixing study?

A

50% normal plasma, 50% test plasma, shows you if there is a antibody blocking clotting rather than a lack of particular clotting factors

50
Q

What are the models of behaviour change? (4)

A

Health belief model
Theory of planned behaviour
Cognitive dissonance theory
PRIME theory

51
Q

What makes a good theory (5)

A 
Explain a related set of observations
Generate testable predictions / hypotheses
Simplest set of concepts / elements
Comprehensible and coherent
Not contradicted by observations
52
Q

Describe the health belief model - what are its shortcomings?

A

If I believe I can escape a negative consequence, I will take precaution
Doesn’t work very well if consequences are long term
Threat (alongside cues, your own modifying factors and your susceptibility) can drive behaviour change

Smoking, drinking, drugs behaviour not well explained by this model

53
Q

What did Taylor and Brown study in 1988 find?

A

People (non-medical) underestimate the possibility of bad things (medical, accidents) happening to them and overestimate good things (intelligence, attractiveness, etc)

54
Q

Describe theory of planned behaviour

A

Based on our intention to do things
Your attitudes, norms and perceived control all contribute to intentions, which CAN lead to behaviour change (depends on your ability to actually change behaviour)

55
Q

Describe transtheoretical model

A

pre-contemplation, contemplation, preparation, action, maintenance, relapse

Stages vary significantly

56
Q

Describe cognitive dissonance theory

A

Competing thoughts - they contradict each other. Holding two at once causes negative feelings

57
Q

Examples of concepts needed to be added into new models of health behaviour to make them more accurate

A

Identity, impulses, triggers, spontaneous/chaotic change, plans, memory, conditioning, positive illusions

58
Q

Why do we need anticoagulants? (3)

A

Stroke prevention
VTE
Arterial thrombotic disease (ACS, MI, failed arterial grafts, etc.)

59
Q

What do/don’t anticoagulants do?

A

They do NOT break up the clot, they prevent further clot development and aim to give the body a break so it is has a chance to break up the clot

60
Q

What does heparin do? Two types, monitoring required, reversal agent, don’t use with

A

Interact with anti-thrombin
UFH has activity on factor 10 and thrombin, reversal = protamine, monitoring = APTT, can be used with kidney issues
LMWH has more activity on thrombin, no reversal agent, no monitoring required, don’t use in kidney issues but can use in pregnancy

61
Q

If a patient is pregnant and needs an anticoagulant, what would you use?

A

LMWH

62
Q

What are the three main heparin side effects?

A

Bleeding
Heparin induced thrombocytopenia
Osteoporosis

63
Q

How does warfarin work?

A

Interferes with use of Vitamin K in the liver - interferes production of Clotting factors 2, 10, 9, 7 & protein c, s

64
Q

Quick description of cytochrome p450 system

A

xxx

65
Q

Why do you need to start warfarin with heparin?

A

xxx

66
Q

Why do you use INR and PT?

A

PT changes between hospital based on reagent used, machine, population
INR provides standarised result for use by other hospitals

67
Q

Why does target INR vary?

A

Depends on reason you are giving warfarin

68
Q

Warfarin side effects

A

Skin necrosis
Crosses placenta - early skeletal deformity, later haemorrhage
Bleeding

69
Q

How do you reverse warfarin?

A

PCC (prothrombin complex concentrate) - most commonly used
Fresh frozen plasma only works short term
Vitamin K for long term

70
Q

What are the advantages of DOACs? (6)

A 
Oral
Rapid onset / offset of action
Short half life (easy to control, stop for surgery)
Little food/drug interactions
Limited drug-drug interaction
Predictable means little/no monitoring

Life Support (5 decks)

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