PBL Topic 2 Case 9 Flashcards

(141 cards)

1
Q

What is an acid?

A
  • A molecule containing hydrogen atoms that can release protons
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2
Q

What is a strong acid? Give an example of a strong acid

A
  • One that rapidly dissociates and releases large amounts of protons
  • Hydrochloric acid
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3
Q

What is a weak acid? Give an example of a weak acid

A
  • One that has a lower tendency to dissociate protons

- Carbonic acid

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4
Q

What is a base?

A
  • A molecule that can accept a proton
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5
Q

What is a strong base? Give an example of a strong base

A
  • One that reacts rapidly and strongly with protons

- Hydroxide ion

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6
Q

What is a weak base? Give an example of a weak base?

A
  • One that reacts much more weakly with protons

- Bicarbonate ion

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7
Q

How does one calculate pH from [H+]?

A

pH = -log [H+]

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8
Q

What is the normal pH of blood?

A

7.4

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9
Q

Why is the pH of venous blood lower than that of arterial blood?

A
  • Carbon dioxide is released from tissues to form carbonic acid
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10
Q

Why is intracellular pH lower than plasma pH?

A
  • Metabolism of cells produced carbonic acid
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11
Q

Identify three systems that help regulate [H+]

A
  • Buffer systems
  • Respiratory centre
  • Kidneys
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12
Q

What is a buffer?

A
  • Any substance that can reversible bind H+
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13
Q

What is Ka and how is it calculated?

A
  • The concentration of the acid relative to its dissociated ions
  • Ka = [H+][A-] / [HA]
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14
Q

What is pKa and how is it calculated?

A
  • Negative log of the Ka value

- pKa = -log [Ka]

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15
Q

What is the pKa in the bicarbonate buffer system?

A
  • 6.1
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16
Q

Give the Henderson-Hasselbalch Equation

A

pH = 6.1 + log [HCO3-] / (0.03 x [PCO2])

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17
Q

In the Henderson-Hasselbalch Equation:

Why is [CO2] calculated rather than H2CO3?

A
  • H2CO3 rapidly dissociated into CO2

- Which is proportional to the amount of undissociated H2CO3

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18
Q

Using the Henderson-Hasselbalch Equation:

What is the result of an increase in [HCO3-]

A
  • pH increases

- Shift towards alkalosis

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19
Q

Using the Henderson-Hasselbalch Equation:

What is the result of an increase in pCO2

A
  • pH decreases

- Shift towards acidosis

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20
Q

Why is a change in the [HCO3-] referred to as a metabolic disturbance?

A
  • [HCO3-] is regulated by the kidneys
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21
Q

Why is a change in the pCO2 referred to as a respiratory disturbance?

A
  • PCO2 is controlled by the rate of respiration
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22
Q

An increase in [HCO3-] is termed a [A]

A decrease in pCO2 is termed a [B]

An increase in pCO2 is termed a [C]

A decrease in [HCO3-] is termed a [D}

A
  • [A] Metabolic alkalosis
  • [B} Respiratory alkalosis
  • [C] Respiratory acidosis
  • [D] Metabolic acidosis
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23
Q

What is the effect of increased ventilation on [H+]

A
  • Reduced CO2 from extracellular fluid

- Reduced [H+]

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24
Q

What is the effect of decreased [H+] on ventilation

A
  • Alveolar ventilation decreases

- Reduced [H+]

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25
Explain why respiratory acidosis occurs in emphysema
- Loss of elastic recoil - Airflow limitation - Build up of CO2
26
Outline the mechanism by which the kidneys excrete acidic or basic urine
- HCO3- is filtered into the tubules, thus removing base from the blood - H+ is filtered into the tubules, thus removing acid from the blood - Net effect is based on relative concentrations in tubular lumen
27
How does the removal of HCO3- raise the extracellular [H+] in alkalosis
- Kidneys fail to reabsorb HCO3- - Increased excretion of bicarbonate - Decrease in HCO3- shifts acid base balance towards acidosis (Henderson-Hasselbalch equation)
28
How does the reabsorption of HCO3- reduce the extracellular [H+] in acidosis
- Increase in HCO3 shifts acid base balance towards alkalosis (Henderson-Hasselbalch equation)
29
In which region of the kidneys does HCO3- reabsorption and H+ secretion not occur?
- Loop of Henle
30
Outline the features of metabolic acidosis
- pH < 7.4 | - PO2 > 40 mm Hg
31
What is the compensatory mechanism for metabolic acidosis?
- Increased ventilation - Reduced pCO2 - Reduced H+ - Increased pH
32
Outline the features of a respiratory acidosis
- pH < 7.4 | - HCO3- <24 mEq/L
33
What is the compensatory mechanism for respiratory acidosis?
- Increased H+ secretion - Increased reabsorption of bicarbonate - Increased pH
34
Outline the features of a metabolic alkalosis
- pH > 7.4 | - PO2 < 40 mm Hg
35
What is the compensatory mechanism for metabolic alkalosis?
- Decreased ventilation - Increased CO2 - Increased H+ - Reduced pH
36
Outline the features of a respiratory alkalosis
- pH > 7.4 | - HCO3- > 24 mEq/L
37
What is the compensatory mechanism for respiratory alkalosis?
- Reduced H+ secretion - Reduced reabsorption of HCO3- - Reduced pH
38
Define circulatory shock
- Generalised inadequate blood flow | - Damage to body tissues due to lack of oxygen and other nutrients
39
Outline the three stages of shock
- Non progressive / compensatory stage - Progressive stage - Irreversible stage
40
What is meant by the term hypovolaemia?
- Reduced blood volume
41
What is the most common cause of hypovolaemia?
- Haemorrhage
42
How does haemorrhage result in shock?
- Reduced filling pressure - Reduced venous return - Reduced cardiac output
43
Identify the sympathetic reflexes that occur as a result of decreased arterial pressure after haemorrhage
- Arterioles constrict, increasing total peripheral resistance - Veins and venous reservoirs constrict, increasing venous return - Increased heart rate
44
Identify the role of baroreceptors in non-progressive shock
- Elicit powerful sympathetic stimulation of the circulation
45
Identify the role of the CNS ischaemic response in non-progressive shock When is this response activated?
- Elicits even more powerful sympathetic stimulation of the circulation - When the arterial pressure falls below 50 mm Hg
46
What is the role of reverse stress-relaxation in non-progressive shock ?
- Contraction of blood vessels around the diminished blood volume
47
What is the role of angiotensin in non-progressive shock ?
- Constriction of peripheral arteries | - Decreased output of water and salt by the kidneys
48
What is the role of ADH in non-progressive shock ?
- Constricts arteries and veins | - Greatly increases water retention by the kidneys
49
What causes cardiac depression?
- Fall in arterial pressure - Reduced coronary blood flow - For adequate nutrition of the myocardium - Weakness of the heart muscle
50
What causes vasomotor failure?
- Reduced cardiac output | - Reduced blood flow to the vasomotor centre
51
How does failure of the vasomotor centre cause a decreased cardiac output?
- Vascular dilation - Venous pooling of blood - Decreased venous return
52
Identify three effects of sluggish blood flow
- Tissue metabolism continues despite low flow - Large amounts of acid continue to empty into the local vessels and increase the acidity of the blood - Resulting in agglutination and blood clots - Leading to plugging of small vessels
53
Why is there increased capillary permeability and what is the effect of this?
- Due to hypoxia | - Decreased cardiac output
54
Explain what occurs to the phosphate reserves in irreversible shock
- Creatine phosphate is degraded - ATP is degraded to ADP - ADP is degraded to AMP - AMP is degraded to adenosine - Which diffuses out of cells and is converted to uric acid - Uric acid cannot re=enter the cells
55
Explain how intestinal obstruction can result in hypovolaemic shock
- Distension of intestine block venous return - Increase in capillary pressure - Fluid leakage from capillaries into intestinal wall and lumen - Reduced plasma volume
56
Explain how severe burns can result in hypovolaemic shock
- Loss of plasma through the denuding skin
57
Why does blood viscosity increase in hypovolaemic shock? What is the effect of this?
- Increased red cell concentration | - Increased sluggishness of blood
58
Identify four causes of hypovolaemic shock caused by dehydration
- Excessive sweating - Fluid loss in diarrhoea or vomiting - Fluid loss by nephrotic kidney - Inadequate intake of fluid and electrolytes
59
Outline the pathophysiology of neurogenic shock
- Loss of vasomotor tone - Massive dilation of veins - Reduced mean systemic filling pressure - Reduced venous return - Increased venous pooling
60
Explain how anaesthesia causes neurogenic shock
- Blockage of sympathetic nervous outflow from nervous system
61
Explain how brain damage causes neurogenic shock
- Brain ischaemia is prolonged | - Inactivation of vasomotor centre
62
Identify a cause of compartment syndrome
- Bone fracture
63
Outline the pathophysiology of compartment syndrome
- Tissue hypoxia - Release of histamine like substances - Causing vasodilation - Increased endothelial permeability - Transudation of plasma into the intramuscular compartment - Swelling and oedema
64
What causes the collapse of a vessel in compartment syndrome?
- Increased critical closing pressure
65
Outline the treatment of compartment syndrome
- Incision through the deep fascia - To open up the compression - To cause decompression
66
Outline the pathophysiology of anaphylactic shock
- Antigen-antibody reaction - Release of basophils and mast cells - Release of histamine - Increased venous dilation and decreased venous return - Dilation of arterioles and reduced arterial pressure - Increased capillary permeability - Loss of fluid into the tissue spaces
67
What is the main cause of sepsis?
- 'Blood poisoning' | - Caused by bacterial infection
68
Outline the clinical features of hypovolaemic shock stemming from inadequate perfusion
- Cold, pale and clammy skin with slow capillary refill - Anuria and oliguria - Drowsiness, confusion and irritability
69
Outline the clinical features of hypovolaemic shock stemming from increased sympathetic tone
- Tachycardia - Hypotension - Sweating
70
Outline the clinical features of cardiogenic shock
- Raised jugular venous pressure - Pulmonary oedema - Gallop rhythm - Basal crackles - Pulmonary oedema
71
Outline the clinical features of anaphylactic shock
- Low blood pressure and tachycardia (vasodilation) - Bronchospasm - Oedema of the face, pharynx and larynx - Nausea, vomiting, abdominal cramps and diarrhoea
72
Outline the clinical features sepsis
- Pyrexia and rigors - Nausea and vomiting - Hypotension - Bounding pulse
73
Outline the management of shock
- Oxygen (via endotracheal tube where necessary) - Antibiotics for sepsis - Fluid Replacement by wide-bore intravenous cannula
74
What is packed cell volume?
- Proportion of blood made up of red blood cells | - Essentially the same thing as hematocrit
75
When giving fluid replacement what is the optimal packed cell volume and why is this the case?
- 30-35% - Balance oxygen carrying capacity - And tissue flow
76
A massive transfusion involves the transfer of how many units of blood?
- 80 > 100 units of red cells
77
Why can blood transfusion cause hypothermia?
- Bank blood is stored at four degrees celsius
78
Why can blood transfusion cause coagulopathy
- Bank blood contains few platelets or clotting factors
79
Why can blood transfusion cause hypocalcaemia?
- Citrate stored in blood binds to calcium ions reducing ionised calcium levels
80
Why can blood transfusion cause increased oxygen affinity
- 2,3-BPG in stored blood is reduced - Oxygen dissociation curve shifts to the left - Increased affinity and reduced unloading
81
What do crystalloid fluids involve? Identify an example of a crystalloid
- Addition of volume to blood - Addition of electrolytes - Saline
82
What do colloid fluids involve? Identify an example of a colloid
- Volume expanders resulting in an increase in blood volume, blood flow, cardiac output and oxygen transportation - Gelofusine
83
Which are preferred colloids or crystalloids?
- Colloids | - Since the volume of crystalloid needed to produce the same effect as colloid is far greater
84
Identify two potential sites of heart block
- AV Block in AV node or Bundle of His | - Bundle Branch Block in lower conductive system
85
What is a Stokes-Adams attack?
- Associated with heart block | - Causes syncope
86
What is seen on an ECG with first degree heart block?
- Prolongation of PR interval greater than 0.22
87
Identify three types of second degree AV block
- Mobitz 1 Block (Wenckeback block) - Mobitz II Block - 2:1 or 3:1 Block
88
What is seen on an ECG with Mobitz 1 block
- Progressive PR prolongation | - Until P wave fails to conduct
89
Where is Mobitz I block most likely to occur?
- AV Node
90
What is seen on an ECG with Mobitz II block?
- A dropped QRS complex | - Not preceded by PR interval prolongation
91
Where is Mobitz II block most likely to occur?
- Bundle of His
92
What is seen on an ECG with a 2:1 or 3:1 advanced block?
- Every second or third P wave conducts to the ventricles
93
Identify two types of third degree AV block
- Congenital complete heart block | - Acquired complete heart block
94
What is seen on an ECG with a congenital complete AV block?
- QRS complex is narrow | - QRS rate is rapid
95
What is seen on an ECG with an acquired complete AV block?
- QRS complex is broad | - QRS complex is slow
96
What is seen in right bundle branch block on an ECG?
- Deep S waves in leads I and V6 | - Tall R wave in lead V1
97
What are the clinical features of right bundle branch block?
- Splitting of the second heart sound
98
What is seen in left bundle branch block on an ECG?
- Deep S wave in lead V1 | - Tall R wave in leads 1 and V6
99
What are the clinical features of right bundle branch block?
- Reverse splitting of the second heart sound
100
Identify the two functioning systems that determine consciousness
- Ascending Reticular Activating System (ARAS) | - Cerebral Cortex
101
Identify the three principal causes of coma
- Diffuse brain dysfunction e.g. traumatic brain injury or drug overdose - Direct effect within brainstem e.g. haemorrhage or infarction - Pressure effect on brainstem e.g. tumour, oedema, abscess
102
What does Glasgow Coma Scale record?
- Best Eye, Verbal and Motor Responses
103
A Glasgow Come Scale score of less than which value denotes a coma?
- 8
104
What is meant by the term delirium?
- Confusion state - Reduced attention - Altered behaviour
105
What is a Swan-Ganz catheter?
- Balloon Flotation Catheter | - Used to determine pulmonary artery pressure
106
Identify two locations where the Swan-Ganz catheter may be inserted?
- Femoral Vein | - Antecubital Fossa
107
Identify three conditions that can be diagnosed using a Swan-Ganz catheter
- Cardiac tamponade - Pulmonary hypertension - Cardiomyopathy
108
Identify three conditions that are often monitored using a Swan Ganz catheter
- Heart failure - Cardiogenic Shock - Doubtful fluid status
109
Why is the pulmonary artery pressure recorded a reasonable reflection of left atrial pressure?
- Catheter becomes so wedged | - Due to fluid between the catheter lumen and left atrium
110
Identify two invasive means of ventilating a patietn
- Endotracheal tube | - Tracheostomy
111
Explain how sedation, muscle anaesthesia and muscle relaxation can cause hypotension
- Loss of sympathetic drive | - Vasodilation
112
Explain how positive pressure ventilation can cause hypotension
- Increased intrathroacic pressure - Reduced venous return - Reduced cardiac output
113
When is a tracheostomy performed?
- When endotracheal intubation is likely to be required for a prolonged period - Typically over 14 days
114
What is IPPV and how is it achieved?
- Intermittent Positive Pressure Ventilation - Intermittent inflation of lungs with positive pressure - Air is forced into lungs - Elastic recoil carries out expiration
115
When is CMV used and outline two ways in which it is achieved
- Controlled Mechanical Ventilation - With patients in whom respiratory efforts are absent - Volume controlled ventilation - Pressure controlled ventilation
116
Outline the process of volume controlled ventilation
- Tidal volume and respiratory rate are preset | - Airway pressure varies according to the ventilator setting and the lung mechanics (e.g. resistance and compliance)
117
Outline the process of pressure controlled ventilation
- Inspiratory pressure and respiratory rate are preset | - Tidal volume varies according to patient's lung mechanics
118
What is IMV ?
- Intermittent mandatory ventilation - Allows patient to breathe spontaneously between the mandatory tidal volumes delivered by ventilator - Timed to coincide with patients own respiratory efforts
119
What is weaning?
- Process of progressively reducing and eventually removing external ventilatory support
120
How is the decision made to wean a patient from artificial ventilation?
- Subjective criteria including responses to short periods of spontaneous breathing - Objective criteria based on blood gas analysis, lung mechanics and muscular strength - Patient's mood, and consciousness level, as well as any drugs
121
Identify two causes of a fall in cardiac output associated with artificial ventilation
- Positive pressure to the lungs impeded venous return | - Stretching of pulmonary capillaries causing a rise in pulmonary vascular resistance
122
What is barotrauma and how is it associated with artificial ventilation
- Damage to body tissues caused by a difference in pressure - Caused by high tidal volumes and PEEP - Which may rupture alveoli and cause air to dissect along the perivascular sheath
123
Identify three sets of signs of a tension pneumothorax associated with artificial ventilation
- Hypoxia and hypercapnia - Hypotension and tachycardia - Mediastinal shift and tracheal displacement
124
How may ventilator associated pneumonia occur?
- Leakage of infected oropharyngeal secretions | - Promoted by regurgitation of colonised gastric fluid
125
Identify three organisms associated with ventilator associated pneumonia
- Pseudomonas aeruginosa - Klebsiella pneumoniae - Staphylococcus aureus
126
Identify a specific marker that be may helpful when there is suspected ventilator associated pneumonia
- Serum procalcitonin
127
Outline the pathophysiology of disseminated intravascular coagulation
- Endothelial damage results in platelet aggregation - Tissue injury results in thrombin - Vascular occlusion and consumption of platelets
128
Outline how tranexamic acid is used in disseminated intravascular coagulation
- Inhibits plasminogen activation - Prevents fibrinolysis - Given orally or by IV injection
129
What is an opioid?
- Any substance that produces morphine like effects
130
Identify a drug that blocks opioids
- Naloxone
131
What is the function of u receptors?
- Analgesic effects of opioids
132
Outline the mechanism of action of opioids
- Opening of inward K+ channels causing hyperpolarisation | - Closure of Na+ channels resulting in reduced Ca2+ entry
133
Outline how opioids can result in physical dependence
- Inhibition of adenylyl cyclase and MAP activation
134
Identify three regions of the brain where analgesics have an effect
- Insular cortex - Amygdala - Hypothalamus
135
What is diamorphine?
- Prodrug that has a high analgesic potency -
136
Why does diamorphine give a greater 'buzz' than morphine
- Greater lipid solubility | - More easily crosses the blood brain barrier
137
How is diamorphine metabolised?
- By glucuronide in the liver | - Metabolised to 6-monoacetylmorphine
138
Why does morphine cause respiratory depression?
- Decrease in sensitivity of receptors to arterial PCO2
139
Why does morphine cause constipation?
- Increased tone | - Reduced motility in GI system
140
Why does morphine cause urticaria and itching?
- Release of histamine from mast cells
141
Why are opioids unsuitable for asthmatic patients?
- Release of histamine from mast cells | - Causing bronchoconstriction and hypotension