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Phase 1 JD > CVR > Flashcards

CVR Flashcards

1
Q

What is the lifespan of an RBC?

A

100 -> 120 days.

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2
Q

How big is an RBC?

A

~ 7 x 2.2 um

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3
Q

What is the function of an RBC?

A

O2/CO2 carrier.

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4
Q

Describe some problems with RBCs.

A
  • Anaemia-hypoxia.
  • Polycythaemia (PRV)-
    thrombosis.
  • Sickle cell disease.
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5
Q

Give corpuscular examples of anaemia.

A

Membrane, haemoglobin, and enzymes.

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6
Q

Give extra-corpuscular examples of anaemia.

A

Reduced production, increased destruction/loss, and redistribution.

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7
Q

What is the lifespan of a WBC?

A

Normally hours or days, some for years.

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8
Q

How big is a WBC?

A

7 -> 30 um (bigger than RBCs).

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9
Q

What is the function of a WBC?

A

Non-specific and specific immunity.

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10
Q

List some WBC abnormalities.

A
  • Neutrophil leukocytosis/
    neutropenia.
  • Eosinophilia/ eosinopenia.
  • Basophilia.
  • Monocytosis/
    monocytopenia.
  • Lymphocytosis/
    lymphopenia.
  • Myeloid malignancies.
  • Lymphoid/ plasma cell
    malignancies.
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11
Q

What is GVHD?

A

Graft-versus-host-disease.
WBCs in donated stem cells/bone marrow attack your own body cells, as it sees them as foreign.

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12
Q

What are BiTE molecules?

A

Molecules designed to form a bridge between cancer cells and cytotoxic T cells. Cytotoxic T cells are WBCs that can destroy other cells that pose a threat.

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13
Q

What is CAR-T therapy?

A

Chimeric antigen receptor T-cell therapy. Reprogramming patients T-cells to enable them to locate and destroy cancer cells more effectively.

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14
Q

What is the difference between humoral and cellular immunity?

A

B cells activate humoral, T cells activate cellular.
Humoral produces antigen specific antibodies, cellular does not depend on antibodies.

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15
Q

Describe lymphocyte maturation.

A

B cells mature in bone marrow.
T cells mature in thymus.
Mature cells enter the circulation and peripheral lymphoid organs surveying for pathogens or tumours.

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16
Q

What is haematopoiesis?

A

The formation of a wide variety of blood cellular components.

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17
Q

What is the lifespan of a platelet?

A

7 -> 10 days.

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18
Q

How big is a platelet?

A

2 -> 5 um.

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19
Q

Where are platelets found?

A

In bone-marrow blood.

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20
Q

What is the function of platelets?

A

Essential for blood clotting.

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21
Q

What makes up the structure of platelets?

A

Plasma membrane, cytoskeleton, dense tubular system, secretory granules (alpha, dense, lysosome, peroxisome).

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22
Q

What are the platelet activation stages?

A

Initiation, propagation, and stabilisation.

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23
Q

What are the two different types of bleeding?

A
  • Platelet type: thrombocytopenia /thrombocy topathy.
  • Haemophilia type : factor deficiency.
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24
Q

Describe the presentation/history of platelet type bleeding.

A
  • History of skin and mucosal bleeding (gastrointestinal and genitourinary).
  • Early post procedural bleeding (minutes).
  • Petechial rash.
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25
Q

What can cause platelet-type bleeding?

A
  • Medication reactions.
  • Liver disease.
  • Renal disease.
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26
Q

Describe the presentation/history of haemophilia-type bleeding.

A
  • History of muscle/joint bleeding.
  • Late post procedural bleeding (hours/days).
  • Large suffusions, haematomas.
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27
Q

What can cause haemophilia type bleeding?

A
  • Haemophilia A, B, C.
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28
Q

What is plasma? What % of blood volume can be attributed to it?

A
  • Liquid component of blood, holding cellular elements in suspension.
  • 55% of total blood volume.
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29
Q

What is plasma made up of?

A
  • Water (up to 95%).
  • Electrolytes.
  • O2, CO2.
  • Proteins: albumin, globulins, coagulation factors, transport proteins.
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30
Q

What is blood serum?

A

Blood plasma without clotting factors.

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31
Q

How is cryoprecipitate prepared?

A

FFP is thawed to 4 degrees celsius, the fibrinogen rich layer is skimmed off, and the precipitate is collected.

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32
Q

What does every cell in our body need?

A
  • To be bathed in fluid.
  • To be within 2mm of a source of oxygenation.
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33
Q

What are the four major types of blood group? What is the name of a rare variant?

A
  • A, B, AB, O.
  • Bombay subtype.
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34
Q

How many antigens are on the surface of an erythrocyte? How many of these are blood group antigens?

A
  • Millions of antigens.
  • Several hundred are blood group antigens.
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35
Q

Which blood group is the universal recipient?

A

AB.

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36
Q

Which blood group is the universal donor?

A

O.

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37
Q

What ages and what weights can donate blood?

A

17 -> 65 year olds.
Body weight: 50->158kg.

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38
Q

What are temporary blood transfusion exclusion criteria?

A
  • Travel.
  • Tattoos/body piercings.
  • Lifestyle.
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39
Q

What are permanent blood transfusion exclusion criteria?

A
  • Certain diseases.
  • Received blood products or organ/tissue transplant since 1980.
  • Notified at risk of vCJD.
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40
Q

Which tests are mandatory in blood donation?

A
  • Hep B.
  • Hep C.
  • Hep E.
  • HIV.
  • Syphilis.
  • HTLV.
  • Groups and antibodies.
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41
Q

Which tests are sometimes done before blood donation?

A
  • CMV.
  • West Nile Virus.
  • Malaria.
  • Typanosoma.
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42
Q

How do antibodies against other ABO antigens occur?

A

Naturally, without ever being exposed to the other blood types - potently antigenic system.

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43
Q

Where does coding for ABO antigens occur? How?

A
  • By genes on chromosome 9, one gene has 2 alleles: A and B (co-dominant), a different gene has just O alleles (recessive).
  • The genes code for enzymes that produce the sugars that differentiate the blood groups.
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44
Q

What determines an individuals blood group?

A

Antigens on RBCs.

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45
Q

What is the similarity and difference between the ABO antigens?

A
  • All have common H antigen.
  • Different groups have different sugars added to the H antigen.
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46
Q

When do we develop ABO antibodies?

A
  • First true ABO antibodies start developing at ~ 3 months old.
  • Infants less than 3 months old have only maternal antibodies.
  • Maximum concentration of ABO antibodies occurs between 5 -> 10 years old.
  • Decreases with age.
  • Mix of IgG and IgM types.
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47
Q

How many different Rh antigens are there?

A

More than 45.

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48
Q

Where does coding for Rh antigens occur? How?

A
  • Genes on chromosome 1.
  • RHD gene codes for Rh D
  • RHCE gene codes for Rh C and Rh E.
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49
Q

How do antibodies against other Rh antigens occur?

A

Only have antibodies if exposed to the opposite type.

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50
Q

How does haemolytic diseases of the fetus and newborn (HDFN) occur?

A
  • Rh+ father and Rh- mother.
  • Develop anti-Rh antibodies in mothers bloodstream.
  • Attacks second child if they are Rh+.
  • Severe fetal anaemia and hydrops fetalis.
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51
Q

How is blood cross-matched?

A

Mix recipient serum with donor RBCs to check for either an exact match (A+ for A+) or compatible blood (O+/- for A+)

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52
Q

What is the difference between direct and indirect antiglobulin tests?

A
  • Indirect = detects antibodies in patients serum.
  • Direct = detects antibodies on patients RBCs.
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53
Q

When giving blood, what can you donate?

A
  • Whole blood.
  • Apheresis removes and externally separates blood - plasma, platelets.
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54
Q

Describe the storage of RBCs.

A
  • Stored at 4 degrees celsius.
  • Shelf life = 35 days.
  • Some units irradiated to eliminate risk of GVHD.
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55
Q

Describe the storage of platelets.

A
  • Stored at 22 degrees celsius.
  • Shelf life = 7 days
  • ## Most units pooled from 4 donations, some single-donor units.
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56
Q

Describe FFP.

A
  • From whole donations of apheresis.
  • Patients born > 1996 can only receive FFP from low vCJD risk (not UK).
  • Single donor packs have variable amounts of clotting factors, pooled donations can be more standardised.
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57
Q

Describe immunoglobulin.

A
  • Made from large pools of donor plasma.
  • Normal and specific IVIg.
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58
Q

Describe granulocytes.

A
  • Used very rarely.
  • Effectiveness = controversial.
  • Must be irradiated to kill T cells.
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59
Q

Describe factor concentrates.

A
  • Single factor concentrates.
  • Prothrombin complex concentrates.
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60
Q

What is an indication for RBCs?

A

Severe anaemia.

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61
Q

What is an indication for platelets?

A

Thrombocytopaenia.

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62
Q

What are 2 indications for FFP?

A
  • Multiple clotting factor deficiencies and bleeding. (DIC)
  • Some single clotting factor deficiencies where no concentrate available.
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63
Q

When is it appropriate to use cryoprecipitate?

A
  • DIC with bleeding.
  • Massive transfusion.
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64
Q

When is normal IVIg used?

A

To treat immune conditions e.g. ITP.

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65
Q

Give an example of use of a specific IVIg.

A

Anti D immunoglobulin used in pregnancy to neutralise any RhD positive antigens.

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66
Q

When is it appropriate to use granulocytes?

A

With severely neutropaenic patients with life threatening bacterial infections.

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67
Q

Give an example of the use of a single factor concentrate?

A

Factor VIII for severe haemophilia A.

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68
Q

Give an example of the use of prothrombin complex concentrates.

A

The rapid reversal of warfarin.

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69
Q

How can you provide the safe delivery of blood?

A
  • Patient identification.
  • 2 sample rule.
  • Hand-written patient details.
  • Blood selected and serologically matched.
  • Mistakes can happen.
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70
Q

Give 3 examples of ways to avoid blood transfusion.

A
  • Cell salvage.
  • IV iron if severely iron deficient.
  • Some people can tolerate lower haemoglobin concentrations.
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71
Q

Describe an ABO incompatability reaction.

A

Rapid intravascular haemolysis -> cytokine release -> acute kidney failure and shock -> DIC -> rapidly fatal.
Can be acute or delayed.

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72
Q

How can you treat/manage an ABO incompatibility reaction?

A

Stop transfusion immediately.
Send bloods to the lab for further typing.
Report to SHOT.

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73
Q

Describe a bacterial contamination reaction.

A

Most common with platelets.
Symptoms start soon after transfusion begins, and include fevers, hypotension, shock, and rigors.
Abnormal colouration may be seen in the unit.

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74
Q

How can you treat/manage a bacterial contamination reaction?

A

Stop transfusion immediately.
Send bloods to the lab for further typing.
Treat the infection.

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75
Q

Describe a transfusion-related lung injury (TRALI).

A

Inflammation causes plasma to leak into alveoli.
Symptoms include SOB, cough with frothy sputum, hypotension and fever.

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76
Q

Describe a transfusion-associated circulatory overload (TACO) reaction.

A

Acute/worsening pulmonary oedema within 6hrs of transfusion.
Older patients = higher risk.
Symptoms include respiratory distress, evidence of positive fluid balance, and raised blood pressure.

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77
Q

What is the importance of platelets in disease?

A

Platelets contribute to thrombosis, having a central role in arterial thrombosis which can lead to heart attack, stroke, or sudden death.

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78
Q

What is thrombosis?

A

The formation of a clot (thrombus) inside a blood vessel.

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79
Q

What happens to platelets when they are activated? What does this do and allow?

A
  • They change shape, from smooth discoid -> spiculated with pseudopodia.
  • Increases surface area, therefore increasing possibility of cell-cell interactions.
  • They activate GP IIb/IIIa receptors to allow platelet aggregation via fibrinogen cross-linking.
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80
Q

Where are glycoprotein IIb/IIIa receptors found?

A

On the surface of platelets. 50,000 -> 100,000 copies on resting platelet.

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81
Q

How does platelet activation affect GPIIb/IIIa receptors?

A
  • Increases number of receptors.
  • Increases receptors’ affinity for fibrinogen.
  • Fibrinogen links receptors, binding platelets together (platelet aggregation).
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82
Q

How do platelets/ platelet receptors respond to atherosclerotic plaque rupture of a vessel?

A
  • Collagen receptors on the platelet bind to exposed subendothelial collagen.
  • GP IIb/IIIa also binds to von Willebrand factor which is attached to collagen.
  • Soluble agonists are also released and activate platelets.
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83
Q

What role does aspirin play involving platelets? How does this work?

A

Inhibits the thromboxane A2 amplification pathway.
Low-dose aspirin inhibits COX-1 -> inhibition platelet activation.
High-dose aspirin inhibits COX-1 and 2 -> inhibition of inflammatory pathways.

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84
Q

Which G proteins are linked to platelet P2Y receptors?

A

P2Y1 linked to Gq protein.
P2Y12 linked to Gi protein.

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85
Q

What binds to and activates platelet P2Y receptors?

A

Adenosine diphosphate (ADP).

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86
Q

What does the activation of P2Y1 do?

A

Causes platelet activation and therefore platelet aggregation.

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87
Q

What does the activation of P2Y12 do?

A

Amplifies platelet activation and aggregation, and the release of granules.

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88
Q

Describe the platelet activation and amplification loop.

A

ADP -> activates P2Y receptors -> platelet activation.
Dense granules from the platelet -> ADP -> activates P2Y receptors -> further platelet activation.
Activation of GPIIb/IIIa also amplifies platelet activation.

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89
Q

How is thrombin involved in platelet activation?

A

Thrombin activates protease-activated receptors (PARs) on platelets -> platelet activation and release of ADP -> amplifies activation through P2Y receptors.

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90
Q

What does platelet procoagulant activity produce and cause?

A

Drives thrombin generation, creating a thrombin-mediated amplification loop increased platelet activation, whilst also linking with coagulation.

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91
Q

How are platelet-fibrin clots formed?

A

Platelets aggregate, thrombin cleaves fibrinogen to form fibrin strands, that form a mesh with the aggregated platelets creating a clot, and trapping RBCs.

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92
Q

Describe the role of the fibrinolytic system.

A

To maintain homeostasis and avoid thrombosis.

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93
Q

What is the function of platelet alpha granules?

A

Released during platelet activation, have coagulation factors, but also inflammatory mediators. Also mediate the expression of surface P-selectin.

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94
Q

How can platelets interact with leukocytes, and what does this interaction lead to?

A

Leukocytes have a PSGL-1 counter receptor, allowing a platelet to bind and link to a leukocyte using P-selectin. This connection contributes to both the thrombotic response and the inflammatory response.

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95
Q

What are the typical setting on an ECG?

A

Speed = 25mm/sec
Voltage = 10mm/mV

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96
Q

How do you calculate rate (bpm) from an ECG?

A

Either:
300/(no. of large squares between cardiac cycles)
OR
(Cycles in 10 secs) x 6

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97
Q

What does an ECG measure/show?

A

The net change in voltage in the whole heart.

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98
Q

What does the P wave on an ECG represent?

A

Atrial depolarisation.

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99
Q

What does the QRS complex on an ECG represent?

A

Ventricular depolarisation.

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100
Q

What does the T wave on an ECG represent?

A

Ventricular repolarisation.

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101
Q

Describe atrial fibrillation.

A
  • Random atrial activity.
  • Random ventricular capture.
  • Irregularly irregular rhythm.
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102
Q

Describe atrial flutter.

A
  • Organised atrial activity ~300/min.
  • Ventricular capture at ratio to atrial rate (usually 2:1, so 150bpm).
  • Usually regular.
  • Can be irregular if ratio varies.
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103
Q

What are the normal values for the PR interval?

A

120 -> 200ms (3 -> 5 small squares).

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104
Q

What does a prolonged PR interval suggest?

A

Conduction disease (heart block).

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105
Q

What are the normal values of the QRS complex width?

A

Less than 120ms (less than 3 small squares).

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106
Q

What does a prolonged QRS interval width suggest?

A

Issue in conduction system -> bundle branch block, when one ventricle is depolarising faster than the other.

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107
Q

What are the normal values for the QT interval?

A

Men: 350 -> 440 ms.
Women: 350 -> 460ms.

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108
Q

What does a prolonged QT interval suggest? What can cause a prolonged QT interval?

A

Serious arrhythmia.
Drugs (most common) and genetic predisposition.

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109
Q

How can you identify left axis deviation on an ECG?

A

Lead I = positive.
Lead II = negative.
(L)eaving each other = (L)eft axis deviation.

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110
Q

How can you identify right axis deviation on an ECG?

A

Lead I = negative.
Lead II = positive.
(R)eaching for each other = (R)ight axis deviation.

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111
Q

Describe leads I and II on a normal axis.

A

Both positive.

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112
Q

What does ST elevation suggest?

A

Blocked coronary artery, can tell which by which leads are affected on the ECG.

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113
Q

Which limb leads are involved with the lateral wall of the LV, which artery are they therefore involved with?

A

aVl and lead I.
Circumflex artery.

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114
Q

Which limb leads are involved with the inferior wall of the LV, which artery are they therefore involved with?

A

Leads II, aVF, and III.
Right coronary artery.

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115
Q

Which chest leads are involved with the septal wall of the LV?

A

V1 and V2.

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116
Q

Which chest leads are involved with the anterior wall of the LV?

A

V3 and V4.

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117
Q

Which chest leads are involved with the lateral wall of the LV?

A

V5 and V6.

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118
Q

Which are the bipolar limb leads? How do they work?

A
  • Leads I, II, and III.
  • Measure potential difference between two electrodes (one designated +ve and the other -ve).
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119
Q

Which are the unipolar limb leads? How do they work?

A
  • aVL, aVF, aVR.
  • Measures the potential difference between a +ve electrode, and a -ve combined reference electrode.
  • AKA augmented leads.
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120
Q

What are the names of the chest leads? Are these unipolar or bipolar?

A
  • V1, 2, 3, 4, 5 and 6.
  • Unipolar.
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121
Q

How are cardiac muscle cells connected?

A

Intercalated discs that contain gap junctions, adhering junctions, and desmosomes.

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122
Q

What is the role of gap junctions in cardiac muscle?

A

Allow direct communication between cells, for example if iron changes in one cell, iron will change in the next.

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123
Q

What is the role of desmosomes in cardiac muscle?

A

Physical link between cardiac muscle cells, ensure that they work together and contract as a unit.

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124
Q

What is the resting membrane potential of the heart?

A

Around -90mV.

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125
Q

Explain negative membrane potential.

A
  • High K+ conc inside.
  • Low Na+ and Ca2+ conc inside.
  • K+ diffuse out (high -> low).
  • Anions cannot follow.
  • Excess of anions inside = -ve membrane potential.
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126
Q

What is phase 0 of cardiac action potential?

A

Depolarisation, Na+ in.

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127
Q

What is phase 1 of cardiac action potential?

A

Initial repolarisation, K+ out.

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128
Q

What is phase 2 of cardiac action potential?

A

Plateau, Ca2+ in, K+ out.

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129
Q

What is phase 3 of cardiac action potential?

A

Repolarisation, K+ out.

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130
Q

What is phase 4 of cardiac action potential?

A

Resting potential, 2K+ in for every 3Na+ out. Against their gradients, therefore requires active transport and ATPase for energy,

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131
Q

What is the Nernst Equation used for?

A

To work out membrane potential under non-standard conditions.

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132
Q

What is action potential propagation?

A

Wave of depolarisation in which action potential spreads across membrane via gap junctions, kicking off sodium channels through the whole myocardium.

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133
Q

What is the point of cardiac action potential?

A
  • Calcium!!!
  • Contraction of heart muscle requires appropriately-timed delivery of Ca2+ ions to the cytoplasm.
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134
Q

Describe calcium in cardiac muscle cells.

A
  • Excitation-contraction coupling.
  • Calcium enters, triggers release of more from the sarcoplasmic reticulum.
  • Calcium tightly regulated, kept in SR.
  • Conc in cytoplasm usually low, high in SR.
  • Ryanodine receptors activated by calcium influx of cytoplasm, allow calcium to leak out of SR.
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135
Q

Describe the troponin-tropomyosin-actin complex.

A
  • Calcium binds to troponin.
  • Conformational change in tropomyosin reveals myosin binding sites.
  • Myosin head cross-links with actin.
  • Myosin head pivots, causing cardiac muscle contraction.
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136
Q

Describe the sino-atrial node’s cardiac action potential phases.

A
  • Upsloping phase 4.
  • Less rapid phase 0.
  • No discernable phase 1 or 2.
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137
Q

What is the velocity of conduction in the specialised fibres of the hearts conduction system?

A

Atrial and ventricular muscle fibres = 0.3 -> 0.5m/s.
Purkinje fibres = 4m/s.

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138
Q

What is the pacemaker of the heart? Why? What would happen is this was lost?

A
  • Sinoatrial node as it has the fastest leak of current between impulses to trigger depolarisation.
  • Heart beat would still occur if lost as all cardiac tissue leaks some charge that eventually triggers depolarisation, but it would be unreliable and slow.
  • Next fastest will take over e.g. atrioventricular node.
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139
Q

What is sympathetic stimulation of the heart controlled by?

A
  • Adrenaline and noradrenaline, and Type 1 beta adrenoreceptors.
  • Increases adenylyl cylcase -> increases cAMP.
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140
Q

What does increased sympathetic stimulation of the heart cause?

A
  • Increased heart rate (up to 180->250bpm).
  • Increased force of contraction.
  • Increase in cardiac output (by up to 200%).
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141
Q

What does decreased sympathetic stimulation of the heart cause?

A
  • Decreased heart rate.
  • Decreased force of contraction.
  • Decreased cardiac output (by up to 30%).
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142
Q

What is parasympathetic stimulation of the heart controlled by?

A
  • Acetylcholine
  • M2 receptors inhibit release of acetylcholine.
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143
Q

What does increased parasympathetic stimulation of the heart cause?

A
  • Decreased heart rate (temporarily pause or as low as 30->40 bpm).
  • Decreased force of contraction.
  • Decreased cardiac output (by up to 50%).
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144
Q

What does decreased parasympathetic stimulation of the heart cause?

A
  • Increased heart rate.
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145
Q

What is the refractory period of myocardial contraction?

A

A period of time during which a cell is incapable of repeating an action potential.

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146
Q

What are the 3 states of sodium channels involved in the refractory period and myocardial contraction?

A
  • Open and activatable.
  • Closed and inactivatable.
  • Closed but activatable (resting).
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147
Q

What is the normal refractory period of ventricles and atria?

A

Approx 0.25s for ventricles, less for atria.

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148
Q

What is the purpose of the refractory period of myocardial contraction?

A

Prevents excessively frequent contraction, and allows time for the heart to fill.

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149
Q

What is the absolute refractory period?

A

Period in which another impulse cannot be stimulated, so another depolarisation cannot occur.

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150
Q

What is the relative refractory period?

A

Period in which a high stimulus is needed to trigger another impulse, so it is difficult to get another depolarisation to occur.

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151
Q

What are the main components of the myocardium?

A
  • Contractile tissue.
  • Connective tissue.
  • Fibrous frame.
  • Specialised conduction system.
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152
Q

What does the cardiac myocyte do?

A

Pumping action of the heart is dependent on interactions between contractile proteins in muscular walls. These proteins are activated by excitation-contraction coupling.

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153
Q

Describe the working myocardial cell.

A
  • Filled with cross-striated myofibrils.
  • Plasma membrane regulated E-C coupling and relaxation.
  • Plasma membrane produced part of T-tubule.
  • Plasma membrane separates cytosol from extra-cellular space and sarcoplasmic reticulum.
  • Mitochondria: ATP, aerobic metabolism, oxidative phosphorylation.
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154
Q

Describe myocardial metabolism.

A

Aerobic: relies on free fatty acids (efficient energy production).
Anaerobic: during hypoxia, no free fatty acids, relies on glucose metabolism.

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155
Q

What is the A-band of a myocardial working cell?

A

Region of the sarcomere occupied by thick filaments.

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156
Q

What is the I-band of a myocardial working cell?

A

Region occupied only by thin filaments that extend towards the centre of the sarcomere from the Z-lines. Also contain tropomyosin and troponins.

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157
Q

What are the Z-lines of a myocardial working cell?

A

Bisect each I-band.

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158
Q

What is a sarcomere?

A
  • The functional basic unit of contractile apparatus.
  • Defined as the region between a pair of Z-lines.
  • Contains two half I-bands, and one A-band.
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159
Q

What is the sarcoplasmic reticulum?

A

Membrane network surrounding contractile proteins, consists of the sarcotubular network and the subsarcolemmal cisternae.

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160
Q

What is the sarcolemma?

A

The plasma membrane of muscle.

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161
Q

What is the transverse tubular system (T-tubule)?

A

Lined by a membrane continuous with the sarcolemma, so the lumen carries extracellular space towards the centre of the myocardial cell.

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162
Q

What are the important contractile proteins of the heart?

A
  • Myosin.
  • Actin.
  • Tropomyosin.
  • Troponin (I, T, and C).
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163
Q

Describe myosin.

A
  • Thick filament.
  • 2 heavy chains (responsible for dual heads).
  • 4 light chains.
  • Heads are perpendicular at rest, join with actin, bend towards centre of sarcomere during contraction.
  • ATPase in head.
  • Alpha and beta myosin.
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164
Q

Describe actin.

A
  • Thin filament.
  • Globular protein (G-actin).
  • Linear polymers of globular proteins (F-actin).
  • Double-stranded macromolecular helical structure.
  • Has a myosin binding site, partially covered by tropomyosin and held in place by troponin
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165
Q

Describe tropomyosin.

A
  • Thin filament.
  • Elongated molecule, made of two helical peptide chains.
  • Wire like structure occupying each of the longitudinal grooves between two actin strands.
  • Regulates interactions between the other three contractile proteins.
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166
Q

Describe troponin.

A
  • Thin filament.
  • 3 types: I,T, and C.
  • I: inhibits actin and myosin interaction.
  • T: binds troponin complex to tropomyosin.
  • C: high affinity calcium binding sites, signalling contraction, also drives troponin I away from actin, allowing its interaction with myosin.
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167
Q

When is the myocardium normally perfused?

A

During diastole, via the coronary arteries.

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168
Q

Describe physiologic systole.

A

Isovolumetric contraction and ejection.

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169
Q

Describe cardiologic systole.

A

From M1 -> A2, between 1st and 2nd heart sounds.

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170
Q

Describe physiologic diastole.

A

Reduced ejection, isovolumetric relaxation, and filling phases.

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171
Q

Describe cardiologic diastole.

A

A2 -> M1 interval.

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172
Q

Describe preload.

A

Amount of blood present in ventricles just before ventricular contraction has started.

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173
Q

Describe afterload.

A

The pressure against which you heart has to contract to eject the blood.

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174
Q

What is Starling’s Law (1918)?

A

The greater the stretch on the myocardium before systole, the stronger the ventricular contraction.

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175
Q

Define force-length interaction.

A

Force produced by skeletal muscle declines when the sarcomere is less than optimal length.

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176
Q

Define contractility.

A

The state of the heart which enables it to increase its contraction velocity, to achieve higher pressure, when contractility is increased (independent of load).

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177
Q

Define elasticity.

A

The myocardial ability to recover its normal shape after removal of systolic stress.

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178
Q

Define compliance.

A

The relationship between the change in stress and the resultant strain. (dP/dV).

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179
Q

Define diastolic distensibility.

A

Pressure required to fill the ventricle to the same diastolic volume.

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180
Q

What are the components of the circulation?

A
  • Anatomy.
  • Blood.
  • Pressure (CO).
  • Volume.
  • Flow.
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181
Q

Which structures hold the greatest proportion of blood volume in the circulation?

A

Small veins and venules (43%).

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182
Q

Describe arteries.

A
  • Low resistance conduits.
  • Elastic.
  • Cushion systole.
  • Maintain blood flow -> organs during diastole.
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183
Q

Describe arterioles.

A
  • Principle site of vascular flow resistance.
  • TPR (total peripheral resistance), basically arteriolar resistance. Determined by local, neural and hormonal factors.
  • Major role in determining arterial pressure.
  • Major role in distributing flow to tissue/organs.
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184
Q

Describe TPR.

A
  • Total peripheral resistance, basically arteriolar resistance.
  • Vascular smooth muscle (VSM) determines radius.
  • VSM contracts: radius decreases, resistance increases, flow decreases.
  • VSM relaxes: radius increases, resistance decreases, flow increases.
  • Vasoconstriction and vasodilation.
  • VSM never completely relaxed = myogenic tone.
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185
Q

Describe capillaries.

A
  • 40,000km and large area = slow flow.
  • Allows time for nutrient/waste exchange.
  • Plasma or interstitial fluid flow determines distribution of ECF between compartments.
  • Flow determined by arteriolar resistance and the number of open pre-capillary sphincters.
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186
Q

Describe veins.

A
  • Low resistance conduits.
  • Compliant.
  • Capacitance vessels.
  • Valves aid venous return against gravity.
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187
Q

Describe lymphatics.

A

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188
Q

Equation for blood pressure:

A

Blood pressure = CO x TPR
(cardiac output x total peripheral resistance).

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189
Q

Equation for cardiac output:

A

CO = HR x SV
(heart rate x stroke volume).

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190
Q

Equation for pulse pressure:

A

PP = systolic - diastolic pressure

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191
Q

Equation for mean arterial pressure:

A

MAP = diastolic pressure = 1/3 pulse pressure

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192
Q

Describe systolic BP.

A

Ventricles contract, highest BP (100 -> 150 mmHg).

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193
Q

Describe diastolic BP.

A

Ventricles relax, lowest BP (not 0, 60 -> 90 mmHg).

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194
Q

How is BP measured?

A

Using a sphygmomanometer on the brachial artery as it is convenient to compress, and level to the heart.

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195
Q

Describe the basics of Korotkoff sounds.

A

0) BP greater than systolic, no flow = no sounds.
1) Systolic, high velocity = sounds.
2) Between S and D = thud.
3) Diastolic = sounds disappear.

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196
Q

What is autoregulation?

A

The intrinsic ability of a structure to maintain constant blood flow despite perfusion pressure changes.

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197
Q

Which organs/systems have excellent autoregulation?

A
  • Renal.
  • Cerebral.
  • Coronary.
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198
Q

Which organs/systems have moderate autoregulation?

A
  • Skeletal muscle.
  • Splanchnic.
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199
Q

Which organs/systems have poor autoregulation?

A
  • Cutaneous.
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200
Q

In which scenarios are extrinsic and intrinsic control of blood flow dominant?

A
  • Brain and heart: intrinsic.
  • Skin: extrinsic.
    Skeletal: rest = extrinsic, exercise = intrinsic.
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201
Q

In local control of blood flow, name 2 vasoconstrictors:

A
  • Endothelin-1.
  • Internal blood pressure.
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202
Q

In local control of blood flow, name 8 vasodilators:

A
  • Hypoxia.
  • Adenosine.
  • Bradykinin.
  • NO.
  • K+.
  • CO2.
  • H+.
  • Tissue breakdown products.
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203
Q

Describe the blood flow control functions of endothelium.

A
  • Essential for circulation control.
  • Rubbing off endothelium -> constriction.
  • Nitric oxide released = vasodilator.
  • Prostacyclin released = vasodilator.
  • Endothelin released = potent vasoconstrictor.
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204
Q

Name 3 circulating (hormonal) vasoconstrictors:

A
  • Epinephrine (skin).
  • Angiotensin II.
  • Vasopressin.
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205
Q

Name 2 circulating (hormonal) vasodilators:

A
  • Epinephrine (muscle).
  • Atrial natriuretic peptide (ANP).
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206
Q

Where are primary/arterial baroreceptors found?

A
  • Carotid sinus.
  • Aortic arch.
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207
Q

Where are secondary/cardiopulmonar baroreceptors found?

A
  • Vein.
  • Myocardium.
  • Pulmonary vessels.
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208
Q

Describe the baroreceptor reflex in regulating blood pressure.

A

Increased BP -> increased baroreceptor activity -> increased impulse firing -> increased PSNS and decreased SNS -> decrease in CO, and vasodilation to reduce BP.

Vice versa for BP decrease.

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209
Q

What are the main neural influences on the medulla?

A
  • Baroreceptors.
  • Chemoreceptors.
  • Hypothalamus.
  • Cerebral cortex.
  • Skin.
  • Changes in blood [O2] and [CO2].
210
Q

What effects on BP and HR occur when different parts of the hypothalamus are stimulated?

A
  • Anterior stimulated -> decreased BP and HR.
  • Posterolateral stimulated -> increased BP and HR.
211
Q

What important role does the hypothalamus have regarding skin blood flow?

A

Regulates skin blood flow in response to temperature.

212
Q

What effect does stimulation of the cerebral cortex have on blood pressure?

A

Stimulation -> vasoconstriction -> increased BP.

213
Q

What effect can emotion have on blood pressure (via the cerebral cortex)?

A

Emotion -> vasodilation and depressor responses e.g. blushing and fainting.
Can be direct or mediated via medulla.

214
Q

How do chemoreceptors affect blood pressure?

A
  • Chemosensitive regions in medulla.
  • Increased PaCO2 -> vasconstriction -> increased BP.
  • Opposite for decreased PaCO2.
  • Similar changes occur with pH level changes.
215
Q

What is responsible for short term BP regulation?

A

Baroreceptors.

216
Q

What are the physiological relevancies of control of the circulation?

A
  • Cold.
  • Standing up.
  • Running.
  • Lifting.
  • Injury.
  • Blood loss.
217
Q

Describe the intrinsic pathway of the coagulation cascade.

A
  • Mainly within blood vessel by breakdown of wall and release of collagen.
  • Collagen = primary activator of factor XII -> activates factor XI -> factor IX -> VIII -> X.
  • Positive feedback loops within.
218
Q

Describe the extrinsic pathway of the coagulation cascade.

A
  • Tissue factor released at site of injury, combines with inactivated factor VII, activating it.
  • Activated factor VII -> activates factor X.
219
Q

What is the purpose of the plasminogen pathway n the coagulation cascade?

A

To maintain balance.

220
Q

Name 4 functions of the nose:

A
  • Temperature of inspired air.
  • Humidity.
  • Filtration.
  • Defence.
221
Q

Describe the area from the anterior nares to the vestibule.

A
  • Skin lined.
  • Stiff hairs.
222
Q

Where are turbinates of the nasal cavity found? How many are there? What do they do?

A
  • On the lateral nasal wall.
  • 3 large shelves effectively.
  • Increase SA.
223
Q

What are the three turbinates called? What lies beneath each of these?

A
  • Superior, middle, and inferior turbinates.
  • Superior, middle, and inferior meatuses lie beneath respectively.
224
Q

What are the paranasal sinuses? How many are there? What are they called?

A
  • Pneumatised areas of the frontal, maxillary, ethmoid and sphenoid bones.
  • 4: named after their bones.
225
Q

How are the paranasal sinuses arranged?

A
  • In pairs.
  • Not necessarily symmetrical.
226
Q

Describe how the paranasal sinuses are related to the nasal cavity.

A
  • Evagination of mucous membrane from nasal cavity.
  • Extension of mucosa, like a ‘room’ of nasal cavity with the same lining.
227
Q

Describe the nerve supply of the frontal sinuses.

A

Ophthalmic division of the trigeminal nerve (CN V).

228
Q

Describe the nerve supply of the ethmoid sinuses.

A

Ophthalmic and maxillary divisions of trigeminal nerve (CN V).

229
Q

Describe the nerve supply of the sphenoid sinuses.

A

Ophthalmic division of trigeminal nerve (CN V).

230
Q

Describe the location of the frontal sinuses.

A
  • Within frontal bone.
  • Midline septum.
  • Over orbit and superciliary arch.
231
Q

Describe the location of the maxillary sinuses.

A
  • Within body of the maxilla.
  • Pyramidal shape:
  • Base = lateral wall of nose.
  • Apex = zygomatic process of the maxilla.
  • Roof = floor of orbit.
  • Floor = alveolar process.
232
Q

Describe the location of the ethmoid sinuses.

A
  • Between the eyes.
  • Labyrinth of air cells/pockets, not a single space.
233
Q

Describe the location of the sphenoid sinuses.

A
  • Medial to the cavernous sinus.
  • Very close to carotid artery, CN III, IV, V, and VI.
  • Inferior to optic canal, dura, and pituitary gland.
234
Q

What is the function of the larynx?

A
  • Valvular function.
  • Prevents liquids and food from entering the lungs.
235
Q

How many cartilages make up the larynx? How many are single, how many are paired?

A
  • 9 cartilages.
  • 3 single.
  • 3 pairs.
236
Q

What are the 3 single cartilages of the larynx called?

A
  • Epiglottis.
  • Thyroid.
  • Cricoid.
237
Q

What are the 3 pairs of cartilages of the larynx called?

A
  • Cuneiform.
  • Corniculate.
  • Arytenoid.
238
Q

Which cranial nerve is responsible for innervation of the larynx? What are the names of its branches responsible?

A
  • The vagus nerve (CN X).
  • Superior laryngeal nerve.
  • Recurrent laryngeal nerve.
239
Q

Describe how the superior laryngeal nerve innervates the larynx.

A
  • Divides into internal and external.
  • Internal brings sensory innervation to the larynx.
  • External innervates only the cricothyroid muscle.
240
Q

Describe how the recurrent laryngeal nerve innervates the larynx.

A
  • Innervates all muscles except cricothyroid.
  • Divides into left and right branches.
241
Q

How much gas exchange area is there per lung?

A

20 metres squared.

242
Q

Where is the trachea found?

A
  • Commences at cricoid cartilage.
  • From larynx -> carina.
  • Down the midline, slightly to the left.
243
Q

Describe the structure of the trachea.

A
  • C-shaped cartilages,
  • Trachealis muscle joins incomplete circuit.
  • Pseudostratified ciliated columnar epithelium.
  • Goblet cells.
244
Q

What provides sensory innervation to the trachea?

A

Recurrent laryngeal nerve.

245
Q

What provides the arterial supply of the trachea?

A

Inferior thyroid artery.

246
Q

How many main bronchi are there? Where do they occur?

A
  • 2: right and left.
  • Sharp division at the carina.
247
Q

Describe the right main bronchus.

A
  • More vertically disposed than L main.
  • 1-> 2.5cm long.
  • More likely to aspirate into.
  • Related to R pulmonary artery.
248
Q

Describe the left main bronchus.

A
  • Less vertically disposed than R main.
  • 5cm long.
  • Less likely to aspirate into.
  • Related to aortic arch.
249
Q

What do the lobar bronchi supply?

A

Right: upper, middle, and lower lobes.
Left: upper and lower lobes, and lingular.

250
Q

What are the names of the right segmental bronchi?

A
  • Upper lobe: apical, anterior, posterior.
  • Middle lobe: medial and lateral.
  • Lower lobe: apical, anterior, posterior, medial and lateral.
251
Q

What are the names of the left segmental bronchi?

A
  • Upper lobe: apico-posterior and inferior anterior.
  • Lingular: superior and inferior.
  • Lower lobe: apical, anterior, posterior, and lateral.
252
Q

If you are listening to the back of the chest, which lobe/s of the lungs are you predominantly listening to?

A

The lower lobes.

253
Q

If you are listening to the front of the chest, which lobe/s of the lungs are you predominantly listening to?

A

Upper and middle lobes.

254
Q

As the bronchi continue to divide, what happens to the walls?

A

They become thinner.

255
Q

What are the names of the 2 types of pleura?

A

Visceral and parietal.

256
Q

Where can the visceral and parietal pleuras be found?

A
  • Visceral: lung surface.
  • Parietal: internal wall of chest.
257
Q

Describe the pleura.

A
  • Each a single cell layer.
  • Pleural cavity with pleural fluid between them to maintain surface tension.
  • Continuous with each other at the lung root.
258
Q

What are the three type of host defence?

A
  • Intrinsic.
  • Innate.
  • Acquired/adaptive.
259
Q

Describe intrinsic host defences. Give an example.

A
  • Always present.
  • Physical and chemical.
  • E.g. apoptosis.
260
Q

Describe innate host defences. Give an example.

A
  • Induced by infection.
  • E.g. macrophages.
261
Q

Describe acquired/adaptive host defences. Give an example.

A
  • Tailored to a pathogen.
  • T cells.
262
Q

What do host defences in the respiratory tract rely on?

A
  • Epithelium.
  • Physical barriers (mucus).
  • Products of the submucosal glands.
263
Q

How does epithelium play a role in host defence?

A
  • Epithelium = intrinsic physical barrier.
  • Secreted molecules from epithelium = intrinsic chemical barrier.
  • Secreted molecules from most/all epithelial cells include:
    • Antiproteinases.
    • Anti-fungal peptides.
    • Anti-microbial peptides.
    • Antiviral proteins.
    • Opsins.
264
Q

Describe airway mucus.

A

Viscoelastic gel containing:
- Water.
- Carbohydrates.
- Proteins.
- Lipids.

265
Q

Describe the production of airway mucus.

A

Secretory product of mucous cells, both goblet cells of the epithelium, and submucosal glands.

266
Q

How does airway mucus play a part in host defence?

A

Protects epithelium from foreign material and fluid loss.

267
Q

How is mucus moved in the airways?

A
  • By air flow and mucociliary clearance (via the mucociliary escalator).
  • Cilia beat in directional waves to move mucus.
268
Q

Describe coughing as a defence mechanism.

A

An expulsive reflex that protects the lungs and respiratory passages from foreign bodies.

269
Q

What causes coughing?

A
  • Irritants.
  • Diseases/conditions.
  • Infections.
  • Can be voluntary of reflexive.
270
Q

What are the 2 pathways of coughing as a defence reflex?

A
  • Afferent limb: receptors within the sensory distribution of the trigeminal, glossopharyngeal, superior laryngeal, and vagus nerves.
  • Efferent limb: recurrent laryngeal nerve, and the spinal nerves.
271
Q

Describe sneezing as a defence mechanism.

A

The involuntary expulsion of air containing irritants from the nose.

272
Q

What causes sneezing?

A
  • Irritation of nasal mucosa.
  • Excess fluid in the airway.
273
Q

Describe epithelial repair.

A

Following an injury, airway epithelium can often effect a complete repair as it exhibits a level of functional plasticity in multiple cells.

274
Q

What happens if there is an abnormal epithelial response to injury? Give examples.

A
  • Epithelium repair does not happen as it should.
  • This can cause lung diseases.
  • Goblet cell metaplasia: airway epithelial cells differentiate -> mucin producing goblet cells.
  • Obstructive lung disease: mucus plugs/inflammation blocking the airway, which can be fatal
275
Q

Is all airway epithelium the same?

A

No, it is different in distinct regions to reflect the different functions needed.

276
Q

Describe the pulmonary circulation.

A
  • From right ventricle.
  • Supplies the lungs with oxygenated blood.
  • 100% of blood flow (4.5 -> 8L/min).
  • Red cell transit time = 5 secs
  • 280 million capillaries.
  • 300 million alveoli.
  • SA for gas exchange = 50 -> 100m squared.
277
Q

Describes the bronchial circulation.

A
  • Supplies the architecture of the lungs.
  • 2% of left ventricular output.
278
Q

Describe pulmonary arteries.

A
  • Thin vessel walls.
  • Minor muscularisation.
  • No need for redistribution in their normal state.
279
Q

Describe systemic arteries.

A
  • Thick vessel walls.
  • Significant muscularisation.
  • Need for redistribution.
280
Q

What causes the differences in pulmonary and systemic arteries?

A
  • Pulmonary circulation has much lower pressure than systemic.
  • LV sees higher pressure than RV.
281
Q

Which area of the heart is being measured in pulmonary arterial wedge pressure?

A

The left atrium.

282
Q

Give the equation for pressure based on Ohm’s Law:

A

Pressure = cardiac output x resistance.

283
Q

Define Pouiseuille’s Law:

A

Resistance =
(8 x length x viscosity)/
(pi x r^4)

284
Q

Which measurement of a vessel is important to resistance?

A

The radius.

285
Q

What are the two ways to reduce pulmonary vascular resistance?

A
  • Recruitment of closed vessels of the capillary bed.
  • Distention of vessels.
286
Q

What are 4 causes of hypoxaemia?

A
  • Hypoventilation.
  • Diffusion impairment.
  • V/Q mismatch.
  • Shunt.
287
Q

Describe the 3 types of diffusion impairment and the effects of these.

A
  • Gaseous diffusion impairment = pulmonary oedema.
  • Membrane diffusion impairment = interstitial fibrosis.
  • Blood diffusion impairment = anaemia.
  • All of which can cause hypoxaemia.
288
Q

Describe the pressures and perfusion of zone 1 of the lung.

A

PA > Pa > PV.
(Alveolar > arterial > venous).
No perfusion.

289
Q

Describe the pressures and perfusion of zone 2 of the lung.

A

Pa > PA > PV.
(Arterial > alveolar > venous).
Some perfusion, increasing as you go down the zone.

290
Q

Describe the pressures and perfusion of zone 3 of the lung.

A

Pa > PV > PA.
(Arterial > venous > alveolar).
Constant perfusion.

291
Q

What is the trend of perfusion across the lung?

A

Increases down the lung with gravity.

292
Q

What is the trend of ventilation across the lung?

A

Increased down the lung, less steep change than perfusion.

293
Q

What is the ideal V/Q across the lung?

A

1.

294
Q

Describe V/Q at the top of the lung.

A
  • High V/Q.
  • Wasted ventilation.
295
Q

Describe V/Q at the bottom of the lung.

A
  • Low V/Q.
  • Wasted perfusion.
296
Q

What is the average V/Q across the lung?

A

0.8.

297
Q

Describe how V/Q mismatch can cause hypoxaemia.

A

Reduced ventilation caused by pneumonia or COPD -> low V/Q, as perfusion remains steady. This means some blood isn’t undergoing gas exchange -> hypoxaemia.

298
Q

Describe how a shunt can cause hypoxaemia.

A

Complete blockage causing no ventilation such as a lobar collapse -> V/Q = 0. Blood isn’t undergoing gas exchange -> hypoxaemia.

299
Q

What is shunting?

A

Large amount of blood bypassing the alveolar bed.

300
Q

What are three types of shunting? Give examples.

A

Pulmonary:
- Complete lobar collapse.
- Arteriovenous malformation.

Intracardiac:
- Ventricular septal defect, Right -> left shunt. (Eisenmenger’s Syndrome).

Physiological:
- Bronchial arteries.

301
Q

Describe the symptoms of Eisenmenger’s syndrome.

A
  • Cyanosis.
  • Clubbing.
  • Erythrocytosis.
302
Q

Describe hypoxic pulmonary vasoconstriction.

A
  • Low alveolar oxygen -> pulmonary vasoconstriction.
  • Redistributes blood away from poorly ventilated areas.
  • Trying to maintain V/Q matching.
303
Q

When is hypoxic pulmonary vasoconstriction a good/bad thing?

A

Good: in one area of the lung, maintains V/Q.
Bad = throughout the lung, increases resistance, meaning heart may not be able to handle pressure increase.

304
Q

Describe partial reduced perfusion and it’s effect on V/Q.

A

Reduced perfusion due to peripheral pulmonary embolism -> high V/Q, as ventilation remains steady.

305
Q

Describe dead space ventilation.

A

Complete blockage of pulmonary arterial perfusion due to central pulmonary embolism -> alveolar dead space -> V/Q = infinity, as ventilation remains steady.

306
Q

How do pulmonary embolisms generally start?

A

As a clot in a vein in the leg.

307
Q

What are two differential diagnoses for pulmonary embolism?

A
  • Deep-vein thrombosis.
  • Skin infection.
308
Q

What are the 2 types of pulmonary embolism?

A
  • Minor PE.
  • Major PE.
309
Q

What can we use to determine how prone an individual is to clots?

A

-Virchow’s Triad:
- Circulatory stasis.
- Endothelial injury.
- Hypercoagulable state.

310
Q

Describe pulmonary hypertension.

A
  • Increased pulmonary vascular resistance.
  • Lumen becomes increasingly smaller.
  • Afterload will increase significantly.
  • Right ventricle becomes larger, left becomes much smaller.
311
Q

Describe what a pulmonary arteriovenous malformation is.

A
  • Direct connection between an artery and vein.
  • Large amount of blood shunts through the lungs, without going near capillaries or alveoli, for example.
312
Q

What are the 2 main dangers of pulmonary arteriovenous malformations?

A
  • Low oxygen (hypoxaemia).
  • Capillaries normally filter the blood for things such as small clots, as these are being shunted, clots could remain and cause issues elsewhere in the body.
313
Q

What is FeNO/eNO? Explain it’s clinical significance.

A
  • Simple measure of nitric oxide in exhaled breath.
  • Measured in ppb.
  • Not diagnostic, but generally increased in asthma.
  • Reflects eosinophilic airway inflammation: high >50ppb, normal <25ppb.
314
Q

What percentage of asthma is related to occupation?

A

15%.

315
Q

Give 6 examples of high molecular allergens involved in asthma.

A
  • Latex.
  • Grain.
  • Flour.
  • Laboratory animals.
  • Enzymes.
  • Sea food.
316
Q

Give 5 examples of low molecular allergens involved in asthma.

A
  • Sterilising agents.
  • Isocyanate paints.
  • Metal working fluids.
  • Chemicals.
  • Metals.
317
Q

What percentage of people have asthma worldwide?

A

5 -> 16%.
Wide variation between countries.

318
Q

When was there an increased prevalence of asthma?

A

Second half of 20th century, now plateaued mostly.

319
Q

Give 4 other influences on asthma than occupation.

A
  • Infectious agents.
  • Fungi.
  • Pets.
  • Air pollution.
320
Q

What percentage of COPD is related to occupation?

A

Around 15%.

321
Q

What is the main cause of COPD?

A

Tobacco smoking.

322
Q

Give 5 occupational exposures that can cause COPD.

A
  • Silica.
  • Coal.
  • Grain.
  • Cotton.
  • Cadmium.
323
Q

Give 5 asbestos associated conditions.

A
  • Pleural plaques.
  • Pleural thickening.
  • Benign pleural effusions.
  • Asbestosis.
  • Lung cancer.
324
Q

What is hypersensitivity pneumonitis?

A

Inflammation of the alveoli within the lung, caused by hypersensitivity to inhaled agents.

325
Q

Give 6 environmental influences for hypersensitivity pneumonitis.

A
  • Farmers lung.
  • Bird fanciers lung.
  • Metal working fluids.
  • Mouldy straw.
  • Mould in saxophone.
  • Hot tub lung.
326
Q

Describe asthma in relation to genes.

A
  • Runs in families.
  • Children of asthmatic parents at greater risk.
  • Not caused by a single mutation in one gene.
  • Does not follow simple Mendelian inheritance.
327
Q

Describe the possible future treatment of asthma.

A
  • Personalised medicine.
  • Individualise pharmacotherapy based on genetic polymorphisms.
  • Certain drugs only administered to those likely to respond.
328
Q

What is the most common lethal autosomal recessive genetic disorder in Caucasians?

A

Cystic fibrosis.

329
Q

Describe the prevalence of cystic fibrosis in the UK.

A

More than 10,000 affected.
1/25 are carriers.
1/2500 births have CF.

330
Q

Describe cystic fibrosis.

A
  • Chronic genetic disease.
  • Multi-organ involvement.
  • Defect in long arm of chromosome 7, which codes for CFTR protein.
331
Q

How many mutations of the CFTR gene have been identified? Which is the most common cause of CF?

A
  • More than 1600 mutations identified.
  • 90% within a panel of 70.
  • F508del is most common mutation causing CF.
332
Q

Describe how cystic fibrosis can be diagnosed.

A
  • Genetic profile and neonatal screening (day 5 IRT).
  • Clinical symptoms: frequent infections, malabsorption, and failure to thrive.
  • Raised skin salt due to abnormal salt/chloride exchange.
333
Q

At what age do most diagnoses of cystic fibrosis occur?

A

50% diagnosed by 6 months.
90% diagnosed by 8 years old.

334
Q

Describe the pancreatic pathophysiology of cystic fibrosis.

A
  • Blockage of exocrine ducts.
  • Early activation of pancreatic enzymes.
  • Eventual auto-destruction of exocrine pancreas.
335
Q

Describe the intestinal pathophysiology of cystic fibrosis.

A

Bulky stools, causing intestinal blockage.

336
Q

Describe the respiratory pathophysiology of cystic fibrosis.

A
  • Mucus retention.
  • Chronic infection.
  • Inflammation, which destroys lung tissue.
337
Q

How many different genotypic classifications are there of cystic fibrosis?

A

6, called class I -> class VI.
Different properties of CFTR mutation.

338
Q

How can cystic fibrosis symptoms be prevented?

A
  • Segregation.
  • Surveillance (review every 3 months min.).
  • Airway clearance - physio and exercise.
  • Suppressing chronic infections.
  • Bronchodilation.
  • Anti-inflammatories.
  • Vaccinations.
339
Q

What are cystic fibrosis rescue antibiotics?

A

2 week course of IV antibiotics, at home or hospital.

340
Q

What are some issues with frequent antibiotic use?

A
  • Allergies.
  • Renal impairment.
  • Resistance.
  • Access problems.
341
Q

What is cystic fibrosis bacteriophage therapy?

A

Use of lytic phages (bacteria specific viruses) to kill infectious bacteria.

342
Q

Give 2 examples of genotype directed therapies, and which class of mutation they target?

A

Ivacaftor in G551D = class III mutations.
Lumacaftor/Orkambi in F508del = class II mutation.

343
Q

What are some challenges in treating cystic fibrosis?

A
  • Adherence to treatment.
  • High treatment burden.
  • High cost.
  • Allergies/intolerances.
  • Different infectious organisms and their resistance to drugs.
344
Q

What type of condition is alpha-1 antitrypsin deficiency?

A

Autosomal recessive disorder

345
Q

What is the normal SERPINA1 gene phenotype in a healthy individual?

A

PiMM.

346
Q

How many different mutations have been found of SERPINA1 gene?

A

80.

347
Q

Which chromosome is the SERPINA1 gene forund on?

A

Chromosome 14.

348
Q

What is the most harmful phenotype of SERPINA1? Which other phenotype has major disease associations?

A

PiZZ.
Both S and Z phenotypes have major disease associations

349
Q

What is a possible consequence of alpha-1 antitrypsin deficiency?

A

PiZZ -> early onset emphysema and bronchiectasis.

350
Q

What is the usual age of onset of asthma vs COPD?

A

Asthma = <50.
COPD = >35.

351
Q

What is the usual smoking history of patients with asthma vs COPD?

A

Asthma = no clear aetiology.
COPD = >10 pack-years.

352
Q

What is the usual disease course of asthma vs COPD?

A

Asthma = stable, with exacerbations.
COPD = progressive, with exacerbations.

353
Q

What is the usual sputum production in asthma vs COPD?

A

Asthma = infrequent.
COPD = common in chronic bronchitis.

354
Q

What is the usual spirometry with asthma vs COPD?

A

Asthma = likely to normalise with treatment.
COPD = may improve, but never normal.

355
Q

What is the usual treatment response with asthma vs COPD?

A

Asthma = responds well.
COPD = less responsive.

356
Q

What is ACOS?

A

Asthma and COPD Overlap Syndroe.

357
Q

What are the two systems within the autonomic nervous system?

A

Parasympathetic system, and sympathetic system.

358
Q

Describe the autonomic nervous systems general structure.

A

2 neurons, separated by the autonomic ganglion; pre- and post-ganglionic fibres.

359
Q

Describe the parasympathetic nervous systems structure.

A
  • Ganglion within/very close to effector organ/their target.
  • Short post-ganglionic fibres.
360
Q

Describe the sympathetic nervous systems structure.

A
  • Ganglion is within a chain adjacent to the spinal cord.
  • Long post-ganglionic fibres.
361
Q

Describe parasympathetic bronchoconstriction.

A
  • Vagus nerve neurons terminate in ganglia near airway wall.
  • Short post-ganglionic fibres reach muscle and release acetylcholine.
  • ACh acts on muscarinic receptors of M3 subtye on the muscle cells.
  • Stimulates airway smooth muscle contraction.
362
Q

Would stimulation or inhibition of the parasympathetic nervous system be beneficial in asthma and COPD?

A

Inhibition, as stimulation narrows the airway.

363
Q

Which drugs can inhibit the parasympathetic systems effects on the airway? How?

A

Anti-muscarinics, which block the M3 receptors that ACh acts on to constrict the airway.

364
Q

What are SAMAs? Give an example.

A

Short-acting muscarinic antagonists.
E.g. ipratropium bromide.

365
Q

What are LAMAs? Give an example.

A

Long-acting muscarinic antagonists.
E.g. tiotropium.

366
Q

Are SAMAs or LAMAs more widely used?

A

LAMAs, but SAMAs still used in high doses in nebulisers for severe asthma and COPD.

367
Q

What do SAMAs do?

A

Inhaled treatment to relax airways in asthma and COPD.

368
Q

What do LAMAs do?

A

Increased bronchodilation and relieve breathlessness in asthma and COPD. Seem to also reduce exacerbations and have other benefits,

369
Q

Which nervous system is ‘fight or flight’?

A

Sympathetic.

370
Q

Which nervous system is ‘rest and digest’?

A

Parasympathetic.

371
Q

How does the sympathetic nervous system have an effect on the airways?

A
  • Nerve fibres release noradrenaline, which activates adrenergic receptors.
  • Two types of these receptors: alpha or beta.
  • Mainly innervate blood vessels, but airway smooth muscle cells have beta adrenergic receptors.
  • Activating beta2 receptors in airway smooth muscle cells causing muscle relaxation by activating adenylate cyclase, raising cyclic AMP.
372
Q

What are SABAs? Give an example.

A

Short-acting beta2-agonists.
E.g. salbutamol.

373
Q

What are LABAs? Give an example.

A

Long-acting beta2-agonists.
E.g. formoterol, salmeterol.

374
Q

How are SABAs and/or LABAs usually given in asthma?

A
  • Both given.
  • With steroids.
375
Q

How are SABAs and/or LABAs usually given in COPD?

A
  • Often without steroids,
  • Often with a LAMA.
376
Q

What are the 3 main effects of beta2-agonists?

A
  • Prevent bronchoconstriction.
  • Acute rescue of bronchoconstriction.
  • Reduce rates of exacerbations.
377
Q

What are the 3 fundamentals of treatment of asthma or COPD?

A

Concordance with therapy = poor.
Inhaler education = key.
Device selection = vital.

378
Q

What are the 3 main goals of treatment of asthma or COPD?

A
  • Aim to improve patients control.
  • Address important issues for patient.
  • Maximum relief of symptoms for minimum side effects.
379
Q

Describe the immediate management of an asthma attack.

A
  • Oxygen is needed to maintain O2 sats 94 -> 98%.
  • Salbutamol nebuliser 5mg.
  • Ipratropium nebuliser 0.5mg.
  • Prednisolone 30 -> 60mg (+/- hydrocortisone 200mg iv).
  • Magnesium of aminophylline iv.
380
Q

What are 6 adverse effects of beta-2 agonists?

A
  • Raising cAMP may activate NA/K pump -> cellular influx of potassium.
  • Tachycardia.
  • Tremors.
  • Cramps.
  • Headache.
  • Hyperglycaemia.
381
Q

What is the role of the immune system?

A

To kill infection and heal tissues.

382
Q

What can happen if there is unwanted or excessive activation of the immune system?

A

Healthy tissue can be damaged.

383
Q

Describe the innate immune system.

A
  • First line of defence.
  • Immediate response.
  • Phagocytes, NK cells, mast cells, basophils, eosinophils.
  • E.g. sputum and cilia.
384
Q

Describe the adaptive immune system.

A
  • Often second line.
  • Delayed response, often >4 days.
  • B and T-lymphocytes.
  • E.g. pus, swelling, and granuloma.
385
Q

What are antibodies/ immunoglobulins produced by, and what do they do?

A
  • Produced by B-lymphocytes.
  • Neutralise or eliminate pathogens.
  • May also cause disease.
386
Q

What are the 5 types of antibody/immunoglobulin?

A
  • IgM.
  • IgG.
  • IgE.
  • IgA.
  • IgD.
387
Q

How many types of hypersensitivity are there?

A

4 (named type I, II, III, IV).

388
Q

Describe type I HP. (Give mediators, timing, and examples).

A

Mediators: IgE antibodies.

Timing: immediate (within 1hr).

Examples: anaphylaxis and hayfever.

389
Q

Describe type II HP. (Give mediators, timing, and examples).

A

Mediators: cytotoxic, antibodies bound to cell antigen.

Timing: hours to days.

Examples: transfusion reactions and Goodpastures (Anti GBM disease).

390
Q

Describe type III HP. (Give mediators, timing, and examples).

A

Mediators: Deposition of immune complexes.

Timing: typically 7 -> 21 days.

Examples: hypersensitivity pneumonitis and lupus.

391
Q

Describe type IV HP. (Give mediators, timing, and examples).

A

Mediators: T-cells (lymphocytes).

Timing: days to weeks/months.

Examples: tuberculosis, sarcoidosis, and Stevens-Johnson syndrome.

392
Q

What is the predominant mediator in type I HP?

A

Histamine.

393
Q

Which 2 antibodies are usually involved in type II HP?

A

IgG and IgM.

394
Q

When are antigen-immunoglobulin complexes formed in type III HP?

A

On exposure to the allergen.

395
Q

How long can a secondary reaction in type IV HP take?

A

2 -> 3 days.

396
Q

Which type of HP requires primary sensitisation?

A

Type IV.

397
Q

What are 5 consequences of T-cell hyperactivity?

A
  • Diabetes.
  • Thyroid disease.
  • Hepatitis.
  • Nephritis
  • Life threatening pneumonitis.

(Any -itis really!).

398
Q

What is dead space in ventilation?

A

Volume of air inspired not contributing to ventilation/gas exchange.

399
Q

How much air do we inspire in a breath?

A

Around 500ml.

400
Q

How much total dead space is there, how is this calculated?

A

Anatomic = approx. 150mls.
Alveolar = approx. 25 mls.
Physiological = anatomic + alveolar.
Therefore = approx. 175mls.

401
Q

What can cause dead space?

A
  • Air not reaching alveoli (anatomic).
  • Air reaching alveoli, but alveoli is damaged or not perfusing properly (alveolar).
402
Q

How much gas does the respiratory pump need to move per minute?

A

5 litres/minute.

403
Q

How many capillaries are there per alveolus?

A

1000 capillaries per alveolus.

404
Q

Does each erythrocyte only come into contact with one alveolus, or multiple alveoli?

A

Each may come into contact with multiple alveoli.

405
Q

At rest, how far through the capillary is haemoglobin fully saturated?

A

25% through.

406
Q

What 3 things can perfusion of capillaries depend on?

A
  • Pulmonary artery pressure.
  • Pulmonary venous pressure.
  • Alveolar pressure.
407
Q

Describe hypoxic pulmonary vasoconstriction.

A
  • Blood seeks areas of oxygen.
  • Therefore, would not perfuse alveoli without oxygen.
  • Vasconstriction.
  • Opposite of normal hypoxia, in which the systemic system causes vasodilation to increase oxygen to hypoxic area.
408
Q

What are the four main acid-base disorders?

A
  • Respiratory acidosis.
  • Respiratory alkalosis.
  • Metabolic acidosis.
  • Metabolic alkalosis.
409
Q

What is normal pH and why is this maintained? What system is crucial to this maintenance?

A
  • Normal = 7.40 (7.36 -> 7.44).
  • Maintained to ensure optimal function.
  • Respiratory system crucial to maintenance.
410
Q

What do these stand for:
TLC,
VC,
RV,
FRC?

A

TLC = total lung capacity.
VC = vital capacity.
RV = residual volume.
FRC = functional residual capacity.

411
Q

What do these stand for:
FEV1,
FVC?

A

FEV1 = forced expiration volume in one second.
FVC = forced vital capacity.

412
Q

What do these stand for:
PEF,
FEF25?

A

PEF = peak expiratory flow (single measure of highest flow during expiration).
FEF25 = flow at point when 25% of total volume to be exhaled has been exhaled.

413
Q

What is the equation for TLC?

A

TLC = VC + RV.

414
Q

How do you determine if an FEV1 is normal?

A

Compare to a predicted value; if 80% +, result is normal.

415
Q

How do you determine is an FVC is normal?

A

Compare to a predicted value; if 80% +, result is normal.

416
Q

At what point is the FEV1/FVC ratio considered abnormal? What does this suggest?

A

< 0.70.
Suggests airway obstruction.

417
Q

What apparatus is used to measure FEV1 and FVC?

A

A spirometer.

418
Q

Give one problem with spirometry,

A

It is effort dependent.

419
Q

What is a problem with expiratory procedures measuring?

A

Doesn’t measure residual volume (RV).

420
Q

Give 2 methods for measuring RV.

A
  • Gas dilution.
  • Body box (total body plethysmography).
421
Q

Describe the gas dilution technique of measuring RV.

A

Measures all of the air in the lungs that communicates with the airways.
Won’t measure areas of non-communication.

422
Q

Describe the total body plethysmography technique of measuring RV.

A

Measures all air, including air trapped in non-communicative areas.
Ask patients to pant against a closed shutter to produce change in box pressure proportionate to volume of air in the chest.

423
Q

What is a TL CO test?

A

A gas transfer test, using carbon monoxide due to its high affinity for haemoglobin.

424
Q

What does a TL CO test measure (6)?

A

The interaction of:
- Alveolar surface area.
- Alveolar capillary perfusion.
- Physical properties of the alveolar capillary interface.
- Capillary volume.
- Haemoglobin concentration.
- Reaction rate of carbon monoxide and haemoglobin.

425
Q

Describe the TL CO tests administration and make-up.

A

Single 10 second breath-holding technique.
Breathed in substance is:
10% helium,
0.3% carbon monoxide,
21% oxygen,
68.7% nitrogen.

426
Q

In asthma, what changes would we expect in:
FEV1,
FVC,
PEF,
TLC,
TL CO,
eNO?

A

FEV1 = normal or reduced.
FVC = normal.
PEF = typically variable.
TLC = normal or high.
TL CO = normal or elevated.
eNO = high.

427
Q

In COPD, what changes would we expect in:
FEV1,
FVC,
PEF,
TLC,
TL CO,
eNO?

A

FEV1 = reduced significantly.
FVC = normal or reduced.
PEF = typically not variable.
TLC = normal or high.
TL CO = low.
eNO = normal.

428
Q

In asbestosis, what changes would we expect in:
FEV1,
FVC,
PEF,
TLC,
TL CO,
eNO?

A

FEV1 = reduced significantly.
FVC = reduced significantly.
PEF = typically not variable.
TLC = reduced.
TLCO = low.
eNO = normal.

429
Q

What would be the typical blood gases in asthma?
(PaO2, PaCO2, pH, and HCO3-).

A

PaO2 = normal.
PaCO2 = low.
pH = normal or elevated.
HCO3- = normal.

430
Q

What would be the typical blood gases in COPD?
(PaO2, PaCO2, pH, and HCO3-).

A

PaO2 = low.
PaCO2 = low in type I, high in type II.
pH = normal.
HCO3- = may be elevated (if chronic acidosis).

431
Q

What would be the typical blood gases in asbestosis?
(PaO2, PaCO2, pH, and HCO3-).

A

PaO2 = low.
PaCO2 = low.
pH = normal.
HCO3- = low.

432
Q

What is asbestosis?

A

Pulmonary fibrosis due to asbestos.

433
Q

What are the 3 requirements of respiration?

A
  • Ensure haemoglobin is as close to full saturation with oxygen as possible.
  • Efficient use of energy source.
  • Regulate PACO2 carefully.
434
Q

What are the two types of chemoreceptor?

A

Central chemoreceptors, and peripheral chemoreceptors.

435
Q

Where can central chemoreceptors be found?

A

In the brainstem. at the pontomedullary junction.
Not within DRG/VRG complex.

436
Q

Where can peripheral chemoreceptors be found?

A

In carotid bodies (bifurcation of common carotid, and CN IX afferents) and in aortic bodies (ascending aorta and CN X afferents).

437
Q

Describe how central chemoreceptors are stimulated/triggered.

A

Sensitive to PaCO2.

  • Blood-brain barrier = relatively impermeable to H+ and HCO3-.
  • PaCO2 preferentially diffuses into CSF.
  • Change in pH of CSF is detected (H+ is detected).
  • This triggers chemoreceptors to cause ventilation.
438
Q

Describe how peripheral chemoreceptors are stimulated/triggered.

A

Respond to reduced PaO2, also respond to PaCo2.
Carotid bodies also detect pH. Aortic bodies do not.

439
Q

Which type of chemoreceptor can be desensitised over time by hypoxaemia?

A

Central chemoreceptors.

440
Q

Which type of chemoreceptor has a greater impact on ventilation control?

A

Central chemoreceptors.

441
Q

What are the 3 types of lung receptor?

A
  • Pulmonary stretch receptors.
  • ‘J’ (juxtacapillary) receptors.
  • Irritant receptors.
442
Q

Are lung receptors slow or fast-adapting?

A

A combination.

443
Q

What do lung receptors do in relation to respiration?

A

Assist with lung volumes and responses to noxious inhaled agents.

444
Q

Which two types of airway receptors can be found in the nose, nasopharynx and larynx?

A

Chemoreceptors and mechanoreceptors.

445
Q

What do airway receptors in the nose, nasopharynx and larynx appear to sense and monitor?

A

Flow.

446
Q

What do airway receptors in the pharynx appear to be activated by?

A

Swallowing.

447
Q

Where is basic breathing rhythm generated?

A

Pons:
- Pnuemotaxis centre.
- Apneustic centre.

Medulla oblongata:
- Dorsal respiratory group (DRG).
- Ventral respiratory group (VRG).

448
Q

When is the DRG predominantly active?

A

During inspiration.

449
Q

When is the VRG predominantly active?

A

During both inspiration and expiration.

450
Q

Are the DRG and VRG unilateral or bilateral? Are they connected to one another?

A

Both are bilateral. Interconnected by a complex system of neurons.

451
Q

Describe the central pattern generator.

A
  • Neural network.
  • Located within DRG/VRG.
  • Precise functional location = unknown.
452
Q

Where can muscle proprioreceptors be found?

A

In all parts of the moving thorax there are joint, tendon and muscle spindle receptors.

453
Q

Define respiratory failure.

A

Failure of gas exchange, causing an inability to maintain normal blood gases.

Low PaO2 (<8kPa), +/- an elevated PaCo2 (>6.5kPa).

454
Q

Give the blood gases of type I respiratory failure.

A

Low PaO2 (hypoxaemia -> hypoxia).

Low/normal PaCO2 (hypocapnia/normal).

455
Q

Give 4 mechanisms of type I respiratory failure.

A
  • Ventilation/perfusion mismatch.
  • Shunting.
  • Diffusion impairment.
  • Alveolar hypoventilation.
456
Q

Give 5 specific causes of type I respiratory failure with examples.

A

Infection -> pneumonia.

Congenital -> cyanotic congenital heart disease.

Airway -> COPD/asthma.

Vasculature -> pulmonary embolism.

Parenchyma -> pulmonary fibrosis.

457
Q

What are 4 treatments for type I respiratory failure.

A
  • Airway patency.
  • Oxygen delivery.
  • Increasing FiO2.
  • Treat the primary cause (e.g. antibiotics for pneumonia).
458
Q

Is type I or type II respiratory failure more common?

A

Type I - most pulmonary and cardiac causes produce type I respiratory failure.

459
Q

Give the blood gases of type II respiratory failure.

A

Low PaO2 (hypoxaemia -> hypoxia).

High PaCO2 (hypercapnia).

460
Q

Give 3 mechanisms of type II respiratory failure.

A
  • Lack of respiratory drive.
  • Excess workload.
  • Bellows failure.
461
Q

Give 3 specific causes of type II respiratory failure with examples.

A

Airway -> COPD/asthma.

Drugs/metabolic -> opiates, poison.

Neurological -> head and cervical spine injury.

462
Q

Give 3 treatments for type II respiratory failure.

A
  • Airway patency.
  • Oxygen delivery.
  • Treat the primary cause (e.g. antibiotics for pneumonia).
463
Q

Which treatment can be more difficult with type II respiratory failure than type I? Why is this?

A

Oxygen delivery.
As central chemoreceptors have habituated to high levels of CO2, their drive to breath comes from low O2 instead.
If O2 is given, drive to breath could stop = stop breathing.

464
Q

Define hypoxia.

A

Reduced level of tissue oxygenation.

465
Q

Define hypoxaemia.

A

Decrease in level of oxygen in the blood.

466
Q

Give 7 symptoms of hypoxia.

A
  • Central cyanosis (oral cavity).
  • Irritability.
  • Reduced intellectual function.
  • Reduced consciousness.
  • Convulsion.
  • Coma.
  • Death.
467
Q

In what type of patient may hypoxia not be obvious?

A

Anaemic patients.

468
Q

Give 9 symptoms of hypercapnia.

A
  • Irritability.
  • Headache.
  • Papilloedema.
  • Warm skin.
  • Bounding pulse.
  • Confusion.
  • Somnolence (abnormal drowsiness).
  • Coma.
  • Death.
469
Q

Does hypercapnia present the same in all patients?

A

No, it is variable patient-to-patient.

470
Q

What is the purpose of systemic vessels?

A

To deliver oxygen to hypoxic tissues.

471
Q

What is the purpose of pulmonary vessels?

A

To pick up oxygen from oxygenated lung.

472
Q

Name the vasodilator/s of systemic vessels.

A

Hypoxia, acidosis, CO2.

473
Q

Name the vasoconstrictor/s of systemic vessels.

A

Oxygen.

474
Q

Name the vasodilator/s of pulmonary vessels.

A

Oxygen.

475
Q

Name the vasoconstrictor/s of pulmonary vessels.

A

Hypoxia, acidosis, CO2.

476
Q

What is Boyle’s Law?

A

P1V1 = P2V2
As a constant temperature, the absolute pressure of a fixed mass of gas is inversely proportional to its volume.

477
Q

At 150m depth, how many atmospheres would this be?

A

16 (multiple of 10 it is = 15, +1 = 16).

478
Q

What is Dalton’s law?

A

The total pressure exerted by a mixture of gases is equal to the sum of the partial pressures of the individual gases.

479
Q

Describe apnoea diving.

A
  • Diver inhales (pre-hyperventilation).
  • Diver descends whilst holding breath, gas compresses.
  • PaO2, PaN2, PaCO2 rise.
  • Eventually CO2 builds up to induce desire to breathe.
  • Diver returns to surface, PaO2, PaN2, and PaCO2 fall.
480
Q

Describe the diving reflex.

A

Occurs when cold water is splashed on the face.
Causes apnoea, bradycardia, and peripheral vasoconstriction to optimise respiration by preferentially distributing oxygen stores to the heart and brain.

481
Q

When may apnoea diving be commonly used? Why?

A

Military operations to remain covert.

482
Q

Describe SCUBA diving.

A
  • SCUBA = self contained underwater breathing apparatus.
  • Gas on demand.
  • Gas delivered on inhalation at ambient pressure.
483
Q

Describe pulmonary oxygen toxicty.

A
  • PiO2 > 0.5 ATA.
  • Cough, chest tightness and pain, SOB.
  • Also a problem with ITU patients.
  • Relief with PiO2 < 0.5 ATA.
484
Q

Describe CNS toxicity’s symptoms and how to remember these.

A

Use ‘ConVENTID’.

Con = convulsion (common final, and often first, sign).
V = vision (tunnel vision etc).
E = ears (tinnitus).
N = nausea.
T = twitching.
I = irritability.
D = dizziness.

485
Q

Describe inert gas narcosis.

A

Commonest in nitrogen narcosis.
Worsens with increasing pressure.
First noticed between 30 -> 40 msw. Increased PiN2.
Individual variation.
Influencing factors; cold, anxiety, fatigue, drugs, alcohol.

486
Q

Describe the symptoms of inert gas narcosis.

A

10 -> 30m: mild impairment of performance.
30 -> 50m: over confidence, sense of well being.
50 -> 70m: loss of memory, stupefaction.
90+m: unconsciousness, death.
Death may occur at much shallower depths.

487
Q

Describe decompression illness.

A

N2 = poorly soluble.
Ascent -> fall in pressure, fall in solubility, gas bubbles of nitrogen formed in tissues and blood.
O2 supportive treatments and urgent recompression.

488
Q

Describe arterial gas embolism.

A

Scuba dives 3m deep on air, panicked and returned quickly, shortly after - week R arm, generalised seizure.
Gas gets into the circulation via torn pulmonary arteries.
Small transpulmonary pressures can lead to AGE.
Normally occurs within 15 minutes of surfacing.
Urgent recompression necessary.

489
Q

Describe pulmonary barotrauma.

A

Air leaks from burst alveoli -> pneumothorax, pneumomediastinum, subcutaneous emphysema.

490
Q

What is the death zone? At what height does this occur?

A

Death zone = altitude above which it is difficult to sustain life without added O2.
Over 8000m.

491
Q

What heights are described as high altitude, very high altitude, and extremely high altitude?

A

High = 1500 -> 3500m.
Very high = 3500 -> 5500,.
Extremely high = 5500+m.

492
Q

What is the altitude and atmospheric pressure at sea level?

A

Altitude = 0m.
Atmospheric pressure = 100kPa.

493
Q

What is the equation for pressure of inspired gas (PiGas)?

A

PiGas = FiGas x Patm.

494
Q

What is the equation for alveolar oxygen pressure (PAO2)?

A

PAO2 = PiO2 - PaCO2/R.
(R = 0.8).

495
Q

What os the equation for arterial oxygen pressure (PaO2)?

A

PaO2 = PAO2 - (A-aDO2).

A-aDO2 = alveolar arterial O2 difference (approx 1kPa).

496
Q

Give the normal blood gas range of PaO2.

A

10.5 -> 13.5 kPa.

497
Q

Give the normal blood gas range of PaCO2.

A

4.5 -> 6.0 kPa.

498
Q

Give the normal blood gas range of pH.

A

7.36 -> 7.44.

499
Q

What shape is the oxygen dissociation curve?

A

Sigmoidal.

500
Q

Give 4 factors that mediate a shift in the oxygen dissociation curve.

A
  • Acidity.
  • 2,3 DPG.
  • Increased temp.
  • Increased PCO2.
501
Q

What happens to FiO2 and PiO2 as altitude increases?

A

FiO2 remains constant at 0.21.
PiO2 falls.

502
Q

Describe the normal response to elevation.

A

Hyperventilation:
- Increases minute ventilation.
- Lowers PaCO2.
- Initially become alkalotic.
- Become tachycardic.

503
Q

Which system compensates for alkalosis? How?

A

The renal system. by excreting bicarbonate to restore acid-base balance.

504
Q

Describe elevation in terms of blood gases.

A

Ascend = PiO2 falls.
- Decreased PAO2.
- Decreased PaO2.

Peripheral chemoreceptors fire, activates increased ventilation, reducing PaCo2.
- Increased PAO2.
- Increased PaO2.

505
Q

Give the altitude, atmospheric pressure, PiO2 and PaO2 of Mont Du Vallon.

A

Altitude = 3000m.
Atmospheric pressure = 62kPa.
PiO2 = 13kPa.
PaO2 = 8kPa approx.

506
Q

Give the normal blood gases for Mont Du Vallon.

A

PaO2 = 7.0kPa.
PaCO2 = 3.0kPa.
pH = 7.44.

507
Q

Give the altitude, atmospheric pressure, PiO2 and PaO2 of Everest.

A

Altitude = 8848m.
Atmospheric pressure = 33.5kPa.
PiO2 = 7kPa.
PaO2 = 5kPa approx.

508
Q

Give the normal blood gases for Everest.

A

PaO2 = 4.0kPa.
PaCO2 = 1.5kPa.
pH = 7.56.

509
Q

What is AMS?

A

Acute mountain sickness.

510
Q

What factors put a person at risk of acute mountain sickness (AMS)?

A
  • Recent travel to over 2500m (a few hours).
  • Normal dwelling at sea level.
  • Altitude, rate of ascent, and history of AMS.
  • Being a younger person.
511
Q

How is AMS diagnosed?

A

Lake Louise score of 3+.
Must have a headache and at least one other symptom.

512
Q

How is AMS treated?

A

Only reliable treatment is descent, NEVER go up higher with AMS.

513
Q

What is HAPE?

A

High altitude pulmonary oedema.

514
Q

What are the symptoms of HAPE?

A

Cough and SOB.

515
Q

Which factors increase the risk of HAPE?

A
  • Rapid ascent above 8000ft.
  • Sleeping above 6000ft.
  • Speed of ascent (rapid = higher risk).
  • Individual susceptibility.
  • Exercise.
  • Respiratory tract infection.
516
Q

How is HAPE treated?

A
  • Descend urgently.
  • O2.
  • Gamow bag.
  • Steroids?
  • Ca2+ blockers?
517
Q

What is HACE?

A

High altitude cerebral oedema.

518
Q

What are the symptoms of HACE?

A
  • Confusion.
  • Behaviour change e.g. agitation, lethargy.
  • AMS is not necessarily a pre-requisite.
519
Q

How is HACE treated?

A
  • Immediate descent needed.
  • Symptoms may resolve relatively quickly.
  • May need gamow bag recompression.
520
Q

Give the altitude, atmospheric pressure, effective cabin atmosphere, and cabin pressure of a Dreamliner.

A

Altitude = 10,000m.
Atmospheric pressure = 21kPa.
Effective cabin atmosphere = 1890m.
Cabin pressure =81kPa.

521
Q

In what cases may individuals need assessment before going on an aircraft? Why?

A

If they have lung disease, or low sea level O2.
To ensure they do not desaturate.

522
Q

When should individuals avoid flying?

A
  • Pneumothorax.
  • Infectious TB.
  • Major haemoptysis.
  • Very high O2 requirements at sea level (> 4 litres/minute).

Phase 1 JD (5 decks)

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