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Perioperative Care > General Physiology > Flashcards

General Physiology Flashcards

1
Q

Structure of cell membrane

A
  • Phospholipid bilayer
  • Hydrophobic lipid tails on inside
  • Hydrophilic phosphate groups on outside
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2
Q

Contents of cytoplasm

A
  • Water (70-85%)
  • Electrolytes - potassium, magnesium, sulphate and bicarbonate
  • Proteins
  • Lipids
  • Carbohydrates
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3
Q

What supports the structure of the cytoplasm

A
  • Actin filaments

- Cytoskeleton of tubulin microtubules

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4
Q

What surrounds the cell nucleus

A

Double phospholipid membrane which is penetrated by nuclear pores

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5
Q

What protein is DNA wrapped around within the nucleus

A

Histone

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6
Q

How is mRNA formed

A
  1. DNA unwinds from histone when gene is activated
  2. Two strands separate
  3. Transcription factor enzyme binds to the promoter region
  4. Allows RNA polymerase to produce complimentary copies of the gene
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7
Q

How is energy derived from glucose

A
  1. Enters cell via facilitated diffusion under control of insulin
  2. Inside the cell glucose is phosphorylated to glucose-6-phosphate
  3. Either stored as a polymer (glycogen) or immediately for energy via glycolysis
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8
Q

What maintains the resting potential of a cell

A

Na/K ATPase

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9
Q

What is the average cell resting potential

A

-70mV

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10
Q

What causes an action potential

A

When a stimulus alters the resting potential of the cell by a significant enough amount to cause depolarisation

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11
Q

Outline the physiology of the action potential

A
  1. Stimulus alters resting potential of the cell membrane
  2. Alters the permeability to sodium ions (via voltage-gated sodium channels)
  3. Sodium influx into the cell
  4. Membrane potential continues to increase
  5. Peaks at +50mV
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12
Q

How is the cell repolarised

A

Depolarisation causes voltage-gated potassium channels which causes potassium to move out of the cell to compensate for the Na influx

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13
Q

What is the refractory period

A

Time taken for resting potential of the cell to be re-established

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14
Q

What causes the action potential plateau in cardiac and smooth muscle cells

A

Slow release of calcium ions causes delay to recovery of the resting potential and allows for prolonged contraction

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15
Q

What are the nodes of Ranvier

A

Bare area that transmits action potentials in myelinated neurons

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16
Q

What is Saltatory conduction

A

Conduction of action potentials in myelinated nerves

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17
Q

Outline the function of a synapse

A
  1. Action potential arrives at synapse
  2. Stimulates opening of calcium ion channels
  3. Influx of calcium draws secretory vesicles to the presynaptic membrane
  4. Vesicles exocytose their contnets and they travel across the synaptic cleft
  5. Stimulates post-synaptic receptors and alters the post-synaptic membrane to sodium 6. This change in resting potential stimulates post-synaptic action potential
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18
Q

Outline the structure of the neuromuscular junction

A
  1. Action potential reaches terminal of the nerve and causes calcium influx
  2. Triggers the release of secretory vesicles of Acetycholine into the synaptic trough
  3. Muscle membrane of the trough has multiple Ach receptors which act as gated ion channels
  4. On binding Ach via nicotinic Ach receptors these channels allow sodium to flood into the cell
  5. This depolarises the membrane, generating an action potential
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19
Q

How is the action potential transmitted through the muscle fibre

A

Via T-tubules

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20
Q

Outline the mechanism of skeletal muscle contraction (excitation-contraction coupling)

A
  1. Action potential transmitted through muscle via T-tubules
  2. Depolarisation of T-tubule membrane causes release of calcium from SR in the muscle fibre
  3. Calcium causes actin and myosin molecule to slide over one another
  4. Causes muscle contraction
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21
Q

Describe slow-twitch muscle fibres

A
  • Type 1
  • Smaller with extensive blood supply
  • Contain myoglobin to act as oxygen store
  • Contain mitochondira for oxidative phosphorylation
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22
Q

Describe fast-twitch muscle fibres

A
  • Type 2
  • Larger
  • Extensive sarcoplasmic reticulum for rapid release of calcium ions
  • Minimal blood supply
  • No myoglobin and so appear white
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23
Q

Difference between actin and myosin contraction in smooth muscle compared to skeletal muscle

A

Smooth muscle contains calmodulin in the place of troponin

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24
Q

Methods of smooth muscle activation/relaxation

A
  • Nervous impulse (as for skeletal muscle)
  • Local tissue factors e.g. hypoxia
  • Hormones
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25
Q

Method of cardiac muscle contraction

A

Striated - contains actin and myosin filaments which contract the same as skeletal muscle

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26
Q

What makes up an actin fibre

A
  1. Actin
  2. Tropomyosin
  3. Troponin
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27
Q

How do actin and myosin filaments slide over each other on contraction

A
  1. Tropomyosin and troponin form a complex that covers/inhibits the active site
  2. When this complex binds with 4 calcium ions a change occurs which uncovers the active site
  3. Myosin molecule cross-bridges contain ATPase heads which bind to the actin active site
  4. ATP is used to walk the myosin along the actin
  5. Calcium ions are then pumped back into the sarcoplasmic reticulum
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28
Q

List the 3 main types of blood cell

A
  1. Erythrocyte (RBC)
  2. Leucocyte (WBC)
  3. Thrombocytes (platelets)
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29
Q

What is the haematocrit

A

Percentage of blood volume made up of erythrocytes

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30
Q

Normal haematocrit

A

45%

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31
Q

List the 5 types of leucocyte

A
  • Neutrophil
  • Eosinophil
  • Basophil
  • Lymphocyte
  • Monocyte
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32
Q

Lifespan of neutrophils

A

Spend 14 days in the bone marrow but have a half-life of 7 hours in the blood

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33
Q

Role of neutrophils

A
  • Major cell in acute inflammation

- Role against bacteria

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34
Q

List the 3 types of lymphocyte

A
  1. B cells
  2. T cells
  3. Natural killer cells
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35
Q

Fate and role of B cells

A

Once activated convert into plasma cells and produce antibodies (the humoral response)

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36
Q

Role of T-cells

A

Produce the cell-mediated immune response

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37
Q

Role of T-helper cells

A

Activate macrophages and B cells

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38
Q

Role of Basophils

A

Initiate immediate hypersensitivity via histamine release

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39
Q

How are thrombocytes (platelets) produced

A

Produced from megakaryocytes via cytoplasmic fragmentation

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40
Q

Causes of primary polycythaemia

A

Polycythaemia rubra vera:

  • Excess erythrocyte production despite low EPO
  • Due to proliferation of pluripotent stem cells
  • Unknown cause
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41
Q

Diagnostic Hb in polycythaemia rubra vera (male and females)

A
  • Male Hb >180

- Female Hb >160

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42
Q

Secondary polycythaemia - causes with appropriate rise in EPO in response to hypoxia

A
  • Altitude
  • Cardiac disease
  • Pulmonary disease
  • Smoking
  • Haemoglobinopathy
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43
Q

Risks of polycythaemia

A
  • Increase in blood viscosity

- Increase risk of clots

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44
Q

List the causes of lymphocytosis

A
  • Viral infection
  • Chronic infection e.g. TB, toxoplasmosis
  • CLL, lymphoma
  • Acute transient response to stress (24 hours only)
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45
Q

Causes of platelet production failure

A
  • Aplastic anaemia
  • Cytotoxic drugs
  • Alcohol
  • EBV, CMV
  • Leukaemia, myelofibrosis, myeloma
    Hereditary thrombocytopenia
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46
Q

Causes of reduced platelet survival

A
  • Idiopathic thrombocytopenic purpura
  • Heparin, penicillamine, gold
  • Meningococci
  • Subacute bacterial endocarditis
  • Thrombotic thrombocytopenic purpura
  • DIC
  • Dilutional from blood transfusion
  • HUS
  • Extracorporeal bypass
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47
Q

What occurs in DIC

A

Simultaneous activation of coagulation and fibrinolytic systems:

  • Widespread microvascular thrombosis
  • Fibrin deposition
  • Bleeding due to consumption of clotting factors
  • Fibrinolysis
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48
Q

How long should aspirin and clopidogrel ideally be stopped prior to operating

A

7 days

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49
Q

When and why does sickle cell disease manifest itself

A

6 months of age - when fetal Hb levels fall to be replaced by adult Hb

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50
Q

Diagnostic investigations of sickle cell disease

A
  1. FBC
  2. Blood film
  3. Sickle solubility test
  4. Confirmed with Hb electrophoresis
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51
Q

Sickle cell inheritance pattern

A

Autosomal recessive

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52
Q

Clinical features of sickle cell

A
  1. Haemolytic anaemia
  2. Pigment gallstone formation
  3. Vaso-occlusive crisis
  4. Ischaemic pain in fingers, chest, kidney, liver and penis
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53
Q

Sites of haemopoeisis in adults

A

Red marrow remains only in the axial skeleton, ribs, skull, proximal ends of femur and humerus

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54
Q

Sites of haemopoeisis in the fetus

A
  • Bone marrow
  • Spleen
  • Liver
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55
Q

How are RBCs removed from the circulation

A
  • Removed by macrophages in the spleen
  • Broken down into haem and globin
  • Haem releases iron that attaches to transferrin
  • Remaining haem is converted to bilirubin
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56
Q

When does the proportion of reticulocytes in the blood stream increase

A

When bone marrow production of erythrocytes increases e.g. after haemorrhage

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57
Q

Laboratory evidence of haemolysis

A
  1. Increased unconjugated bilirubin
  2. Reduced serum haptoglobin
  3. Morphological evidence of damage e.g. spherocytes
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58
Q

Cause of osteomyelitis in sickle cell anaemia

A

Salmonella

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59
Q

Treatment of hereditary spherocytosis

A

Splenectomy delayed until aged 10

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60
Q

Pathophysiology of hereditary spherocytosis

A

Defect in red cell membrane

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61
Q

Platelet survival time

A

8-10 days

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62
Q

List the four components of haemostasis

A

(1*Vascular injury with exposure of subendothelial tissue factor and collagen)

  1. Vasoconstriction
  2. Platelet activation
  3. Coagulation mechanism
  4. Fibrinolytic system
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63
Q

What mediates vasoconstriction

A
  • Local reflexes
  • Thromboxane A2 released from activated platelets
  • Serotonin released from activated platelets
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64
Q

Describe the process of platelet adherence

A
  1. Vessel injury causes loss of endothelium and exposure of collagen
  2. Platelets adhere to damaged area and there is activation of the intrinsic pathway via thromboplastim
  3. Damaged endothelial cells release VWf which is necessary for platelet adhesion
  4. Platelet granules release ADP which is needed for platelet aggregation
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65
Q

Describe the process of platelet aggregation

A
  1. Platelet phospholipids release arachidonic acid
  2. Thromboxane A2 is produced by the arachidonic acid
  3. Thromboxane A2 induces further platelet aggregation
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66
Q

What forms the platelet plug

A
  • Platelets
  • Thrombin
  • Fibrin
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67
Q

What clotting factor is activated as the result of the enzyme reactions in the intrinsic and extrinsic pathway

A

Factor X

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68
Q

What is required for the initiation of the extrinsic pathway

A

Tissue thromboplastin and factor 7

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69
Q

Outline the intrinsic coag pathway

A
  1. Subendothelial damage
  2. Formation of primary complex on collagen by kininogen, prekallikrein, factor 12
  3. Prekallikrein is converted to kallikrein and factor 12 is activated
  4. Factor 12 activates factor 11
  5. Factor 11 activates factor 9
  6. Activated factor 9 forms tenase complex with factor 8a
  7. Activates factor 10
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70
Q

Outline the extrinsic coag pathway

A
  1. Tissue damage
  2. Factor 7 binds to tissue factor
  3. Activates factor 9
  4. Activated factor 9 and factor 7 activated factor 10
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71
Q

Outline the common coag pathway

A
  1. Activated factor 10 causes conversion of prothrombin to thrombin
  2. Thrombin hydrolyses fibrinogen bonds to form fibrin
  3. Thrombin also activates factor 13 to form cross-links between fibrin molecules
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72
Q

How is fibrin removed

A

Via the fibrinolytic system during the repair process in blood vessels and healing wounds

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73
Q

Outline the fibrinolytic system

A
  1. Tissue plasminogen activator is released by endothelial cells
    (regulated by plasminogen-activator inhibitor 1 from endothelial cells)
  2. Permits conversion of plasminogen to plasmin
  3. Plasmin breaks down fibrin into fibrin degradation products
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74
Q

What minimum platelet count is required for surgical haemostasis

A

70

75
Q

At what platelet count does spontaneous bleeding occur

A

20

76
Q

What does a prolonged bleeding time imply

A
  • Thrombocytopenia
  • Platelet defects
  • Failure of vascular contraction
77
Q

What does Prothrombin time (PT) test and thus detect

A
  • Integrity of the extrinsic pathway and common pathway

- Detects deficiencies in factors 1, 2, 5, 7, and 10

78
Q

What does the activated partial thromboplastin time (APTT) test and detect

A

Intrinsic system (i.e. all factors except factor 7)

79
Q

What is haemophilia A

A

Inherited deficiency of factor 8

80
Q

Haemophilia A inheritance pattern

A

X-linked recessive affecting males and carried by females

81
Q

Haemophilia clotting test results

A
  • APTT increased
  • PT normal
  • Bleeding time normal
82
Q

What is Von Willebrand disease

A
  • Due to deficiency of VWf
  • Vascular endothelium releases reduced amounts of factor 8
  • Defective interaction of platelets with endothelium
83
Q

Von Willebrand disease clotting test results

A
  • APTT increased
  • PT normal
  • Bleeding time increased
84
Q

What clotting factors is vitamin K required for the production of

A

2, 7, 9, 10

85
Q

Vitamin K deficiency clotting test results

A
  • APTT increased
  • PT increased
  • Bleeding time normal
86
Q

What confirms the diagnosis of DIC

A
  • Thrombocytopenia
  • Decreased fibrinogen
  • Elevated fibrin degradation products
  • Prolonged PT, APTT, TT
  • Fragmented RBCs
87
Q

Describe the role of antithrombin 3

A
  • Inhibitor of thrombin

- Action potentiated by heparin

88
Q

Inheritance pattern of congenital antithrombin 3 deficiency

A

Autosomal dominant

89
Q

Where and how are Proteins C and S made

A
  • In the liver

- Dependant on vitamin K

90
Q

Function of Protein C

A
  • Degrades factor Va and 8a
  • Inactivates plasminogen-activator inhibitor 1
  • Thus promotes fibrinolysis
91
Q

Function of Protein S

A

Co-factor of Protein C and enhances its activity

92
Q

Symptoms of inherited protein C deficiency

A
  • PE
  • Superficial thrombophlebitis
  • Cerebral venous thrombosis
93
Q

Mechanism of action of heparin

A

Potentiates the action of antithrombin 3

94
Q

Monitoring of heparin

A

APTT - aim for 2-2.5x normal

95
Q

Side effects of heparin

A
  • Thrombocytopenia
  • Hypersensitivity reactions
  • Alopecia
  • Osteoporosis
96
Q

What clotting factors does heparin inhibit

A

7a, 9a, 10a, 11a, kallikrein, plasmin

97
Q

What clotting factor does LMWH inhibit

A

Factor 10a

98
Q

Heparin half-life

A

1 hour

99
Q

Mechanism of action of warfarin

A
  • Vitamin K antagonist

- Interferes with factors 2, 7, 9, 10

100
Q

Drug of choice for anticoagulation in pregnancy and why

A

Heparin - does not cross placenta

101
Q

Mechanism of action of NOACs

A

Direct inhibitors of activated factor 10

102
Q

Management of haemophilia A

A
  • Factor 8 concentrate

- Desmopressin in mild disease

103
Q

Management of haemophilia B

A
  • Prothrombin complex concentrate

- Factor 9 concentrate

104
Q

Treatment of antithrombin 3 deficiency

A
  • Antithrombin 3 concentrate

- Anticoagulation

105
Q

Treatment of protein C deficiency

A
  • Replacement

- Anticoagulate with warfarin

106
Q

Management of DIC

A
  • Fluid resus
  • FFP
  • Cryoprecipitate
  • Platelets
107
Q

Reversal of heparin

A

IV Protamine - 1mg for every 100units

108
Q

Shelf life of RBCs

A

42 days at 4 degrees

109
Q

Storage of RBCs results in loss of

A
  • Granulocyte and platelet function

- Factors 5 and 8

110
Q

Biochemical changes from RBC storage

A
  • Increased lactate
  • Increased potassium
  • Increased phosphate
  • Decrease in pH
  • Haemolysis
111
Q

Make up of platelet transfusion

A

Platelets suspended in plasma

112
Q

Contents of FFP

A

Contains all clotting factors

113
Q

Contents of cryoprecipitate

A
  • Factor 8 (primarily)
  • Fibrinogen
  • Von Willebrand factor
114
Q

Fast reversal of Warfarin

A

Human prothrombin complex (reversal within 1 hour)

115
Q

Indications for platelet transfusion

A
  • Haemorrhage in presence of thrombocytopenia
  • Thrombocytopenia prior to invasive procedures
  • Consumptive coagulopathy e.g. DIC
116
Q

Indications for FFP transfusion

A
  • Replace clotting factors in major haemorrhage
  • Liver disease, rapid reversal of warfarin
  • DIC
  • Prophylaxis in patients with clotting defects
117
Q

Indications for cryoprecipitate transfusion

A
  • Haemophilia
  • Von Willebrands disease
  • Fibrinogen deficiency e.g. DIC
118
Q

Cause of immediate haemolytic transfusion reaction

A

ABO incompatibility

119
Q

Symptoms of immediate haemolytic transfusion reaction

A
  • Pyrexia
  • Dyspnoea
  • Chest pain
  • Severe loin pain
  • Collapse/hypotension
  • Haemoglobinuria
  • Oliguria
  • Jaundice
  • DIC
120
Q

When does delayed haemolytic transfusion reaction occur

A

5-10 days post transfusion

121
Q

Most likely blood product to cause urticaria

A

FFP

122
Q

Why does urticaria occur in plasma transfusions

A

Patient’s IgE antibody complexing with a protein present in the donor plasma

123
Q

Why does TRALI occur

A

Incompatibility between donor antibodies and recipient granulocytes

124
Q

Autologous blood predonation amount

A

4 units over 4 weeks

125
Q

How much blood can safely be removed from a patient without cardiac disease

A

2L

126
Q

What occurs in transfusion reaction to white blood cells and why

A
  • Febrile reaction
  • Fever and flushing soon after the start of the transfusion
  • Due to recipient leucocyte antibodies
127
Q

List the potential complications of massive blood transfusion

A
  • Overload
  • Cardiac arrhythmia due to cold blood
  • Citrate toxicity causing hypocalcaemia
  • Hypothermia
  • Hyperkalaemia
  • Metabolic acidosis from acidity of stored blood
  • Haemorrhage due to coagulopathy
  • DIC
  • ARDS
128
Q

When does delayed haemolytic transfusion reaction occur

A

5-10 days after transfusion

129
Q

What are the signs of delayed haemolytic transfusion reaction on blood film

A
  • Spherocytosis

- Reticulocytosis

130
Q

What is the fluid composition of a 70kg man

A
  • TBW = 46L
  • Intracellular water = 25L
  • Extracellular water = 19L (3L = plasma, 15L = interstitial fluid, 1L = trancellular fluid)
131
Q

What are the two types of diuresis

A
  1. Water

2. Osmotic

132
Q

Describe water diuresis

A
  1. Excess water ingested
  2. ADH suppressed
  3. Collecting ducts become impermeable to water
  4. Water is lost without solute
133
Q

Describe osmotic diuresis

A

This results when more solute is presented to the tubules than they can reabsorb

134
Q

Give examples of osmotic diuresis

A
  • DM
  • Mannitol (a filtered by non-reabsorbed solute)
  • Inhibition of tubular function (e.g. drugs that block NaCl reabsorption)
135
Q

What are the main cations in intracellular fluid

A
  • K+

- Mg2+

136
Q

What are the main cations in extracellular fluid

A

Na+

137
Q

What 2 factors determine the osmolality of the bodies fluid compartments

A
  1. Adjustments in ADH

2. Thirst

138
Q

Where in the brain is thirst and ADH secretion controlled

A

By the osmolality of the plasma-perfusing nuclei in the hypothalamus

139
Q

What biochemical abnormality is associated with pure water deficiency

A

Hypernatraemia

140
Q

How is pure water deficiency corrected

A

5% dextrose

141
Q

Where is sodium reabsorbed in the nephron

A
  • 65% in the PCT
  • 25% in the loop of Henle
  • 10% in the DCT/collecting ducts
142
Q

What is the effect of ANP on body sodium

A

ANP increases excretion of Na+:

  • Increases GFR
  • Inhibits Na reabsorption in the collecting ducts
  • Reduces secretion of renin and aldosterone
143
Q

How should symptomatic severe (<119) hyponatraemia be treated

A

Hypertonic saline

144
Q

What is the effect of aldosterone on potassium balance

A
  • Increases renal excretion by effects on DCT

- Exchanges for H+

145
Q

What is the effect of acid-base balance on serum potassium concentration

A

Acidosis results in increased serum K+ due to reduced entry into cells and reduced urinary excretion

146
Q

What are ECG changes associated with hyperkalaemia

A
  • Peaked T-waves
  • Loss of P-waves
  • QRS widening
147
Q

What are the ECG changes associated with hypokalaemia

A
  • Low broad T-waves

- U-waves

148
Q

What catalyses the carbonic acid-bicarbonate system

A

Carbonic anhydrase

149
Q

What does the Henderson-Hasselbach equation prove

A

That pH depends on the ration of HCO3 (kidney function) to pCO2 (respiratory function)

150
Q

How can the Henderson-Hasselbach equation be simplified

A

pH = constant + (kidney function/respiratory function)

151
Q

Describe the compensation that occurs in respiratory acidosis

A
  • Increased bicarbonate by buffer

- Reduced H+ by kidneys

152
Q

How can acute and chronic CO2 retention be differentiated on ABG

A
  • Acute = bicarb may be normal as not enough time to change

- Chronic = pH may be normal as bicarb increased

153
Q

List the causes of metabolic alkalosis

A
  • Vomiting
  • NG aspirations
  • Gastric fistula
  • Thiazides and Loop diuretic
  • Cushing’s syndrome
  • Conn’s syndrome
  • Milk-alkali syndrome
154
Q

List the GI causes of metabolic acidosis

A

From excessive loss of base:

  • Diarrhoea
  • Intestinal, biliary, pancreatic fistulae
155
Q

What does a high base excess indicate

A

Metabolic alkalosis

156
Q

What does a low base excess indicate

A

Metabolic acidosis

157
Q

How is the anion gap calculated

A

(Na + K) - (HCO3 + Cl)

158
Q

What is the normal anion gap

A

10-19

159
Q

What causes an increased anion gap

A

Metabolic acidosis resulting from production of an acid

160
Q

When does the ebb phase occur in response to trauma and what is its purpose

A
  • First few hours (<24 hours)

- Protective mechanism to conserve circulatory volume and minimise demands on the body

161
Q

What modulates the ebb phase

A
  • Catecholamines
  • Cortisol
  • Aldosterone
162
Q

What physiological changes occur in the ebb phase

A
  • Reduced O2 consumption
  • Reduced enzymatic activity
  • Reduced CO
  • Reduced basal metabolic rate
  • Reduced body temperature
  • Increased production of acute phase proteins
163
Q

When does the flow phase occur in response to trauma and what is its purpose

A
  • > 24 hours after insult
  • Hypermetabolic state
  • Initially catabolic (3-10 days) allowing for mobilisation of the building blocks for repair
  • Later anabolic (10-60 days) with repair of tissue
164
Q

Why is the body predisposed to gut bacteria translocation following trauma

A
  • Gut mucosal integrity relies on amino acids (specifically Glutamine)
  • This is reduced post-trauma
165
Q

What is the primary fuel of the catabolic phase

A

Glucose - liver produces this from catabolism of fats and protein to maintain high serum levels

166
Q

How much energy is supplied by 1g of carbohydrate

A

4.1 kcal

167
Q

How much energy is supplied by 1g of protein

A

5.3 kcal

168
Q

How much energy is supplied by 1g of fat

A

9.3 kcal

169
Q

What occurs to fluid balance following surgical trauma

A
  • ADH and aldosterone is released
  • Na is retained and K excreted
  • Water conserved
170
Q

By how much does fever increase maintenance fluid requirements

A

By 20% for each 1 degree rise in temperature

171
Q

How much fluid does an average adult lose over a 24 hour period

A

2.5 - 3L

172
Q

Which colloids are suitable for short-term volume expansion

A
  • Gelatin (Gelofusin)

- Dextran

173
Q

Which colloids are suitable for medium-term volume expansion

A
  • Albumin

- Pentastarch

174
Q

Which colloids are suitable for long-term volume expansion

A
  • Hetastarch
175
Q

What cautions must you be aware of with Dextran use

A
  • Interferes with cross-matching
  • Interferes with coagulation (reduces factor 8, inhibits platelet aggregation)
  • High incidence of allergy
176
Q

Where are gelatins derived

A

Bovine collagen

177
Q

What are the general problems associated with plasma expanders

A
  • Dilution coagulopathy
  • Allergic reactions
  • Interferes with cross-matching (Dextran 70)
178
Q

In a given volume of crystalloid, how much remains in the intravascular compartment and how much moves to the ECF

A
  • Intravascular = 1/3rd

- ECF = 2/3rd

179
Q

What safety measures should be taken when using K+ containing fluids

A
  • Urine output at least 40ml/hr
  • No more than 40mmol to be added to 1L bag
  • Infusion fate no faster than 40mmol/hr (typically 10mmol/hr)
180
Q

What does the Starling Equilibrium explain

A

The relationship between hydrostatic pressure, oncotic pressure, and fluid flow across the capillary membrane

181
Q

Where are the body’s temperature-sensitive receptors located

A

Anterior hypothalamus

182
Q

Describe the reflex vasoconstriction loop

A
  • Direct contact with cold stimulus
  • Afferent neuron = cutaneous nerve
  • Centre = hypothalamus and spinal cord
  • Efferent = sympathetic fibres
183
Q

Describe the reflex vasodilatation loop

A
  • Application of radiant heat
  • Afferent neuron = cutaneous nerve
  • Centre = above C5 of spinal cord
  • Efferent pathway = sympathetic fibres (reduced activity)
184
Q

Which clotting factors are produced by hepatocytes

A

5, 7, 9, 10, 11, 12

Perioperative Care (6 decks)

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