Physiology Flashcards
1
Q
What are the functions of the respiratory system?
A
Gas exchange
Regulation of acid/base balance
Immune surveillance and Host defence
2
Q
Asthma and COPD are an example of what kind of abnormal gas exchange?
A
Airway disorders
3
Q
Emphysema is an example of what type of abnormal gas exchange?
A
Alveolar disorder
4
Q
Asbestosis is and example of what type of respiratory disorder?
A
Fibrotic lung disease
5
Q
What does nasal breathing do?
A
Filters air
Warms air
Humidifies air
6
Q
How is Humidification in nasal breathing achieved?
A
Mucous galnds
Seromucous glands
Goblet cells
7
Q
How is heating achieved in Nasal Breathing?
A
The use of a rich capillary network.
8
Q
Three examples of disorders caused by abnormal mucosal defence?
A
Pneumonia
Lung abscesses
Bronchiectasis
9
Q
What causes respiratory acidosis and alkalosis?
A
Acidosis - inadequate clearance of CO2
Alkalosis Hyperventilation leading to too little CO2
10
Q
What is type 1 respiratory failure and Type 2?
A
Type 1 - Low PaO2 and normal or low PaCO2
Type 2 - Low PaO2 and high PaCO2
11
Q
Where does type 2 respiratory failure normally occur?
A
COPD
Neuromuscular Disease
Primary and secondary abnormalities of ventilation control.
12
Q
What is the equation for pressure?
A
N/unit area (m2)
13
Q
What is the partial pressure of a gas?
A
The individual pressure that one gas exerts.
14
Q
What does Daltons law state?
A
That the total pressure is equivalent to the sum of the partial pressures.
15
Q
At equilibrium the partial pressure of a gas in solution is what to it in it’s gaseous state?
A
Equal.
16
Q
What is henry’s law?
A
[gas] = partial pressure x solubility coefficient.
17
Q
What are the normal values for the PaO2 and % Hb saturation of arterial blood and of mixed (venous) blood?
A
Arterial: 13.3 kPa, 97-98%
Venous: 5.3 kPa, 75%
18
Q
IN what two forms is oxygen transported around the body?
A
dissolved in blood plasma
bound to Hb
19
Q
Why is Haemoglobin so important?
A
Increases oxygen carriage capacity.
The body needs around 250ml/min of Oxygen, the [O] in the blood is only 3ml, if only dissolved Oxygen was present then this quota could not be reached.
20
Q
How does oxygen get delivered to tissues?
A
Through diffusion, there is a massive diffusion gradient into mitochondria (their Po2 is only 0.1 kPa compared to arterial blood’s 13.3 kPa.
21
Q
What is the structure of Haemoglobin?
A
Consists of 4 subunits, each subunit consists of a glob in chain (peptide) and a haem group.
22
Q
1g of Hb binds how many ml’s of O2?
A
1.36
23
Q
if 1g of Hb binds 1.36ml’s of O2, what is the O2 content (ml/l) of a person with an [Hb] of 15g/100ml?
A
204ml/l
24
Q
What does anaemia result from?
A
A lack of Hb in the blood caused by:
Impaired production
Increased breakdown
Blood loss
Fluid Overflow - haemodilution.
25
What is anaemia?
A lack of Hb in the blood.
26
What are the different types go haemoglobin, what are they made up of and what is the percentage proportion of those types in the adult body?
Adult haemoglobin (HbA) (97%)
- 2 alpha chains
- 2 beta chains
HbA2 (2%)
- 2 alpha chains
- 2 delta chains
HbF (fetal haemoglobin) 1%
- 2 alpha chains
- 2 gamma chains
27
When does the switch from fetal haemoglobin to Adult Hb happen?
between 3-6 months of age.
28
What's thalassaemia?
A defect in the synthesis of the globin chain of Hb.
29
What is sickle cell disease?
A defect in the structure of the globin chain of Hb
30
What are the two types of thalasseamia?
Alpha and Beta, Alpha affects only Major HbA, Beta affects all forms.
31
What is the genetic cause of sickle cell disease?
A specific mutation in the ß-chain.
32
What are the two forms of sickle cell disease and their symptoms?
Heterozygous Hb (carrier)
- generally asymptomatic
- anoxia can manifest in stress situations such as air travel
- protection against malaria
33
What is the name of the process of O2 binding to Fe2+ in the porphyrin ring?
Oxygenation.
34
What does an Hb saturation of 50% mean?
| The molecules are all half loaded with O2 or half the molecules are fully loaded?
Half of the molecules are fully loaded, half are not at all.
35
What is cooperative binging of O2?
The fact that once O2 has binded to Hb then it is much more likely to bind again.
This is why there are a negligible amount of half filled Hb molecules.
36
At what paO2 does Hb begin to desaturate?
About 8 kPa
37
What is the use of Hb not desaturating until about 8 kPa?
Means there is a large functional reserve of O2, if PaO2 should fall.
38
Do all tissues have the same O2 functional reserve? use the examples of the heart and Kidney.
No, The heart receives uses a lot of the O2 from the blood it receives and so has little functional reserve and to increase output blood flow must increase
The kidney receives a lot of blood, due to its excretory role and so has a very large functional reserve, as it does not use much of the O2
39
What are the three major factors that alter Hb affinity?
Temperature
The Bohr effect (H+) - pH
BPG
40
Will increased or decreased temperature increase the Hb affinity?
Decreased temp will increase Hb Affinity.
41
Will increased H+ increase or decrease the Hb affinity and O2 delivery? Why?
Increased H+ will decrease Hb affinity, as H+ stabilises Hb.
Decreased H+ will also increase O2 delivery because O2 at the site of the tissue is no longer bound to Hb and so will diffuse into that tissue.
42
Tissues in anaerobic respiration produce H+ and metabolically active tissues produce more Co=O2, why is this useful in terms of oxygen?
Both will make the blood more acidic and will increase O2 delivery.
43
What is the role of BPG in oxygen delivery? how is this accomplished?
At high altitude or in chronic hypoxia BPG levels increase, thus increasing the delivery of oxygen.
This is because BPG stabilises Deoxy-Hb (attaches between the two ß-chains), so this prevents binding of O2 to it.
44
BPG does not affect HbF why is this important?
Because The bobby needs a lower oxygen saturation, to take O2 from the Mother.
45
What is Methaemoglobin (MetHb) and how is it formed?
It is formed when O2 oxidises Fe2+ to Fe3+ and so it cannot bind O2
46
How can MetHb be formed?
Spontaneously
Side effects of drugs such as nitrates sulphonamides
47
How are levels of MetHb controlled within the body?
MetHb reductase (keeps MetHb levels at 1.5% of total Hb)
48
What happens when MetHb reductase is deficient? How can this be treated?
Can allow MetHb concentration to rise to levels up to 25%, Treated with reducing agents such as Vit. C and methylene blue.
49
What can happen to Hb if a patent has high blood plasma glucose, what does this mean?
Can form Glycosylated Hb (HbA1c) when glucose attaches to ß-chains, has no direct effect on oxygen carriage.
50
Levels over what percentage of HbA1c can be problematic?
Over 7.5%, normal is 4-6%
51
What is cyanosis and what causes it?
Inadequate oxygenation of the blood, caused by the blue colour of deoxy-Hb.
52
What are the two forms of Cyanosis?
Peripheral cyanosis: Poor tissue perfusion leading to increased O2 extraction from available blood (turning it Blue)
Central Cyanosis: Poor oxygenation of blood to the lungs.
53
Is Cyanosis more likely to be seen in patients with Polycythaemia (increased [Hb]) or in patients with Anaemia (decreased [Hb])
Polycythaemia
54
What is Carboxyhaemoglobin?
Hb bound to CO.
55
What would a Carboxyhaemoglobin % of 0.7, 5 and 60 mean?
0.7% - normal
5% - smoker
60% - loss of consciousness
56
average values of PCO2 for arterial and venous blood?
Arterial: 5.3 kPa
Venous: 6.1 kPa
57
What are the three forms that CO2 can be carried in the blood? What proportion is carried by each?
Dissolved CO2 - 10%
Carbamino compounds - 10%
Bicarbonate ions - 80%
58
How are Carbamino compounds formed?
What's the most common?
Reactions of CO2 with Amine groups on proteins
Most common is caraminohaemoglobin, the Co2 binds to the globin chains not the Haem.
59
Where is bicarbonate formed? With what enzyme?
In erythrocytes using carbonic anhydrase
60
What is the Haldane effect?
The fact that Oxy-Hb is a stronger acid than Deoxy-Hb and so [H+] increases in the lungs when O2 is taken into Hb, this promotes the separation of bicarbonate into CO2 and H2O.
61
What's Myoglobin?
Similar to Hb but found in muscle, is equivalent to one globin chain and one haem group.
62
What is the use of myoglobin?
Facilitates diffusion of O2 from plasma membrane to mitochondria (creates a larger concentration gradient)
Acts as a small store (one or two heartbeats)
63
What is caisson disease?
The bends. When the patient has gone under high pressure and N2 solubility has increased, at lower pressures the N2 escapes and this causes the symptoms of the condition.
64
How do you treat Caisson disease?
Re-pressureise and then gradually depressurise.
65
How much oxygen is consumed and carbon dioxide produced per minute?
250ml of O2 consumed
200ml of CO2 produced
66
What is the determining factor for ventilation, [CO2] or [O2] why?
[CO2] this is because CO2 controls the bodies acid-base balance, and if PaCO2 is okay then normal PaO2 is too.
67
What is PAO2 and PaO2?
PAO2 is alveolar partial pressure of O2
PaO2 is arterial Partial pressure of O2
68
What are the three lines of defence in the airway?
1st - Nose and nasal passages of upper airway warm, moisten and filter for pathogens.
2nd - mucociliary escalator.
3rd - White blood cells in CT of lung tissue
69
What is the dead space of the lungs?
The conducting zone of the lungs that does not take part in gas exchange
70
What is the functional residual capacity?
The volume of air left inside the lungs after a normal quiet expiration.
Expiratory reserve volume + residual vol
71
What is the vital capacity?
The total volume of gas it is possible to inhale or exhale with a single breath.
72
What is residual volume?
The volume of gas left in the lungs at the end of a maximum expiration.
73
How do you work out the minute volume?
Tidal vol. x Rate
74
What is the alveolar ventilation and how do you work it out?
The Alveolar Ventilation (VA) is the amount of air actually passing through the gas-exchanging parts of the lung a minute.
(Tidal volume - Dead Space) x rate/min
75
What is the respiratory quotient, and what can it be used to measure?
CO2 Production/O2 consumption
Measures what someone is metabolising, if someone were metabolising pure glucose it would be 1.
76
What is PiO2?
The air arriving in the alveoli.
77
How do you calculate PAO2? what can this be used to do?
PiO2 (19.9 - usually) - PACO2/R (rate of respiration).
Compared the PAO2 to the PaO@ and if they are different there is a gas exchange issue.
78
If the PaCO2 is low the patient is Hypo/Hyperventilating?
Hyperventilating.
79
If the alveolar ventilation doubles what happens to the PACO2?
Halves.
80
Why is the Arterial PCO2 such a good indicator of Alveolar PCO2?
Because CO2 is so soluble.
81
If the PAO2 and the PaO2 do not mismatch what is the most likely explanation?
A V/Q mismatch or shunt.
82
What four mechanism helps maximise ventilation/Perfusion (Q) matching?
Gravity ensures the bases of the lungs are better perfused
Because lungs hang in the chest the lower parts of the lungs are better ventilated
Oxygen in the lungs is a vasodilator
Areas of the lung that are better perfused have more CO2 which is a bronchodilator.
83
What is the difference in a V/Q mismatch and a shunt?
A V/Q mismatch is when there is reduced ventilation to part of the lung
A shunt is when pulmonary arterial blood reaches the systemic circulation without being exposed to ventilation.
84
In a ventilation perfusion mismatch the PaO2 will be reduced, how is it possible that the PaCO2 can remain normal?
Because the body can over-ventilate the parts of the lungs that are being perfused and will therefore release enough CO2, these areas already have a Hb of 100% so this is not possible for paO2.
85
How is it possible to diagnose a Ventilation perfusion mismatch (V/Q or shunt)?
If the PaO2 is reduced, but the PaCO2 is normal.
86
Will supplementary oxygen improve the situation of a V/Q mismatch or a Shunt?
It will improve the situation in a V/Q mismatch as this results from poor ventilation, however it will not help in a shunt because the blood passing through the shunt will not be affected.
87
If the PaCO2 is normal but the PaO2 is less than predicted what is the problem (ventilation or gas exchange) and a likely diagnosis?
Ventilation is fine, there is a gas exchange problem, e.g. pulmonary oedema.
88
If the PaCO2 is elevated and the PaO2 is normal what is the problem (ventilation or gas exchange) and a likely diagnosis?
gas exchange is fine, there is a ventilation issue, hypoventilation. e.g. respiratory depressant drug (e.g.morphine)
89
If the PaCO2 is elevated and the PaO2 is less than calculated, what is the problem (ventilation or gas exchange) and a likely diagnosis?
Hypoventilation and a gas exchange problem e.g. COPD
90
If the PaCO2 is reduced, but the PaO2 is normal what is the problem (ventilation or gas exchange) and a likely diagnosis?
No gas exchange issue, only hyperventilation e.g. panic attack.
91
The PaCO2 is reduced and so is the PaO2 what is the problem (ventilation or gas exchange) and a likely diagnosis?
Hyperventilation and gas exchange. e.g. asthma.
92
What muscles are used in inspiration and which in expiration?
Inspiration - Diaphragm, external intercostals and shoulder girdle muscles
Expiration - Internal intercostals and abdominal wall muscles
93
What three conditions require the expiratory muscles to actually be used?
- To go below FRC
- To achieve High pressures
- To achieve high flow rates
94
What contributes to elastic recoil?
The elastic fibres of lung tissue
Surfactant in the alveoli
95
What contributes to the alveolar pressure?
The Pressure acting on the outside of the alveolus (pleural) and the pressure generated by the elastic recoil of the alveolus.
96
Explain the concept of flow limitation.
The fact that there is a maximal flow for each lung volume which cannot be exceeded. This occurs because the resistance to flow determines the air flow.
97
Why does airway collapse happen on forced expiration?
Happens as the pleural pressure becomes greatly positive, more so than the pressure at the critical closing point.
98
Why do pink puffers breath through pursed lips?
In order to raise airway pressure and avoid collapse.
99
What conditions might affect the capacity to inspire?
If lungs are abnormally stiff e.g. Fibrosis, pulmonary oedema.
100
What is orthopnoea?
Shortness of breath when supine, can occur in obese patients that struggle to depress the diaphragm.
101
What increases airway resistance?
Bronchoconstriction, swelling of the wall or airway by secretions.
102
In what situations is lung compliance increased and in what situations is it decreased?
Increased in emphysema as a result of elastin and also surface area which can lead to loss of surface tension.
Decreased in restrictive conditions such as asbestosis and fibrosis.
Decreased in left side heart failure as the pulmonary vessels are engorged with blood and there is pulmonary oedema.
103
What is surfactant mostly made up of?
Lipids.
104
What is the function of surfactant?
Allows alveoli to be expanded in inspiration and prevent alveolar collapse at expiration
105
What are the two types of receptors involved in controlling ventilation?
1. Mechanoreceptors e.g. in limbs, chest wall and airways.
2. Chemoreceptors e.g. Central chemoreceptors (in brain), Peripheral (aortic and carotid bodies - normal contribute little, but important in 'hypoxic drive')
106
What are the two types of lung diseases? examples?
Restrictive - decreased lung compliance (smaller lungs), e.g. tumours or fibrosis.
Obstructive - impaired airflow, especially during expiration, normally involving airway narrowing and or obstruction. e.g. Asthma, COPD.
107
What is emphysema? what causes it?
Enlargement of the airspaces distant to the terminal bronchiole. Due to breakdown of alveolar walls, normally due to excessive protease activity caused by smoking.
108
What is bronchitis?
Chronic over-production of mucus in the bronchial tree, with periods of infection.
109
What happens to the FEV1 and FVC in bronchitis and in emphysema?
Decreased FVC and FEV1 in emphysema and bronchitis
110
What is COPD?
Normally chronic lung disease has features of both emphysema and bronchitis and is categorised as COPD
111
How does H+ react with proteins?
Reacts with negative charges on proteins.
112
What is the normal arterial pH rang?
7.35-7.45
113
Difference in strong and weak acids?
Strong acids dissociate completely in solution.
114
What are buffers?
Weak acids or weak bases.
115
What are three physiological buffers in the human body?
Bicarbonate buffer (HCO3-)
Proteins (they can accept H+ due to -ve charges)
Phosphate buffer (important in urine) - H2PO4
116
How are acid product dealt with in the body?
1. buffered by physiological buffers.
| 2. Eliminated via lungs and kidneys
117
Where are Co2 and metabolic acids eliminated
CO2 in the lungs
metabolic acids in the kidneys
118
What is carbonic anhydrase?
The enzyme that catalyses the bicarbonate buffer reaction
119
In relation to carbonic anhydrase what do RBC's do in the body and then differently in the lungs?
In the body they take up CO2 and convert it to HCO3- and H+
In the lungs they take up HCO3- and H+ to convert to CO2
120
What does the kidney do to HCO3-?
Resorbs it in the proximal tubule
121
What will Increasing pH/CO2 do to the respiratory system?
will increase rate and depth and more CO2 will be expired – increasing pH
122
What do clinical acid-base machines measure, how do they measure [HCO3-]?
Measure PaCO2, PaO2 & pH (via an electrode), then the [HCO3-] is determined from the henderson-haselbach eq.
123
What are the measurements that determine respiratory acidosis and alkalosis?
PaCO2 > 6.1
| PaCO2 < 4.8
124
What would a proportionate change in PaCO2 and HCO3- suggest, and what would a disproportionate one suggest?
Proportionate: A respiratory acid-base imbalance.
Disproportionate: Metabolic imbalance
125
What is base excess (BXS)?
The change in [HCO3-] produced only by the metabolic component of the acid/base balance.
126
Is the base excess positive or negative in metabolic acidosis?
Not enough bicarbonate so negative
127
Is the base excess positive or negative in respiratory acidosis?
effectively 0.
128
What is the standard bicarbonate?
It is an estimate of what the HCO3- would be if the PaCO2 was normal
provides the same info as Base excess.
129
What are the two ways in which we control our respiration?
Voluntary control - Cerebral cortex
Involuntary - Brainstem
130
Is normal expiration passive or active?
Passive.
131
What are the two medullary centres controlling ventilation? What does each do?
Dorsal respiratory group:
- causes inspiration, expiration occurs passively.
Ventral respiratory group:
- involved in inspiration and expiration when there is increased demand to breathe, e.g. in exercise.
132
What are the two types of neurones that are part of the dorsal respiratory group
1. I alpha that are inhibited by lung inflation
| 2. I alpha excited by lung inflation
133
How does the ventral respiratory group work in an increased drive to breathe?
Uses accessory muscles for increased inspiration and abdominal muscles for forced expiration.
134
What is the role of the pons in ventilation?
Controls filling duration of the lungs and rate and depth of breathing.
135
What do the central chemoreceptors respond to?
Increased PaCO2 and decreased pH
136
What are the carotid and aortic bodies sensitive to?
Aortic have minimal role and are mostly sensitive to total O2 flow
Carotid bodies are only sensitive to PO2
137
If H+ ions cannot diffuse across the blood-brain barrier how are central chemoreceptors sensitive to H+?
Co2 indirectly influences the pH by increasing the number of H+ ions through bicarbonate.
138
What is the pentose phosphate pathway and how does it differ from glycolysis?
An alternative pathway (to glycolysis) of glucose metabolism; provides raw materials for cellular functions such as NADPH and pentose phosphates.
Does NOT produce ATP
Does NOT oxidise glucose completely
139
What is the Hexose monophosphate shunt?
The point of glycolysis (at Glc-6-phosphate) that the pentose-phosphate shunt can occur.
140
What are the two main stages of the pentose phosphate pathway?
What do the produce?
An irreversible redox stage
- NADPH and pentose phosphates
A reversible interconversion stage
- Excess pentose phosphates are converted into glycolytic intermediates.
141
What can the pentose phosphates be used for in the cell?
Production of DNA and RNA.
142
What happens in the redox stage of the Pentose Phosphate Pathway (PPP)?
What can then happen to the product?
First reaction produces 6-phosphogluconate, in a dehydrogenase reaction with the enzyme Glucose-6-Phosphate dehydrogenase.
Final reaction produces ribulose-5-phosphate, in a dehydrogenase reaction using the enzyme 6-phosphogluconate dehydrogenase.
Ribulose-5-phosphate can then be used for DNA/RNA synthesis, or put into the interconversion stage.
143
What determines whether the ribulose-5-phosphate produced from the redox stage of the PPP then gets used for DNA/RNA or goes into the interconversion stage?
The need for NADH over the need for DNA/RNA synthesis.
In dividing cells they need pentose phosphates to produce DNA/RNA
In non-dividing cells there is an increased need for NADH and so pentose phosphates can be put back into glycolysis.
144
What happens in the interconversion stage of the PPP?
Re-arrangement of carbon in three 5-Carbon ribulose-5-phosphates to produce:
Glyceraldehyde-3-Phosphate (3C)
and 2x fructose-6-phosphate (6C)
They are then fed back into glycolysis.
145
What is the difference in NADPH and NADH, and what is the advantage of having both in a cell?
The single phosphate has no effect on electron carrying ability, it serves to distinguish the two electron carriers. This is so that the cell can regulate both pathways independently and have access to both oxidising and reducing agents for two sets of reactions in a cell.
146
What is reduced glutathione (GSH), and how is NADPH relevant?
Reduced glutathione converts dangerous metabolites in the cell e.g. H2O2 to H2O
NADPH reduces GSSG to 2x GSH
147
What is Glucose-6-phosphate dehydrogenase (G6PD) deficiency? how does it confer protection to malaria?
X-linked recessive condition, mutating G6PD altering it's structure/stability.
Malaria relies on a metabolite produced by G6PD
148
What are the other biochemical effects of G6PD deficiency?
G6PD also regulates NADPH levels in the cell, so NADPH is reduced:
- NADPH converts GSSG to GSH, which means if there is little GSH H2O2 cannot be converted to to H2O, if not reduced H2O2 will degrade rbc's
149
What do patients with G6PD present with?
Neonatal Jaundice
Haemolytic anaemia:
- Oxidative stress with no GSH can result in loss of Hb function, can result after oxidative drugs are administered e.g. aspirin, anti-malarial drugs.
150
What reflex do the Nasal, Epipharangeal, Larangeal and Tracheal receptors all produce? What nerve enervates them?
Nasal - Sneeze (Trigeminal)
Epipharangeal - Aspiration (Glossopharangeal)
Larangeal - Cough (Vagus)
Tracheal - Cough (Vagus)
151
What is tidal volume?
Volume of air inspired and expired during quiet breathing.
152
What is the Inspiratory reserve volume?
The maximal volume of air that can be inhaled after a normal tidal volume inspiration.
153
Expiratory reserve volume?
Maximum amount of air that can be exhaled from the resting expiatory level.
154
Residual volume?
Volume of air remaining in the lungs at the end of maximum expiration.
155
Vital capacity?
Volume of air that can be exhaled from the lungs after maximum inspiration
156
What is FEV1 and FVC?
FEV1: Volume of air that can be exhaled in 1 second from full inflation.
FVC: Total volume of air that can be exhaled from full inflation.
157
Examples of obstructive airway disorders?
COPD, Asthma.
158
What characterises obstructive expiratory disorders?
Limitation in expiratory airflow.
Decreased FEV1 and FEV1/FVC ratio.
159
What are restrictive airways disorders caused by?
Diminished lung volume, by alteration of lung tissue or other disease.
160
What are restrictive airways disorders characterised by?
Low FVC and FEV₁
161
How are lung volumes clinically measured?
Dilutional methods such as 100% oxygen or helium.
Body plethysmography
162
How is pulmonary function clinically tested?
Blood gasses, cardiopulmonary exercise tests, metabolic measurements.
163
What are Mucins?
A substance secreted by goblet cells and mucous glands in the upper respiratory tract that provides stickiness to the mucous and traps particles.
164
What is the first line of defence against pathogens that reach the alveolar space?
Alveolar Macrophages
165
What receptors are present on alveolar macrophages?
TLR (toll-like receptors)
PRR, Pattern recognition receptors.
166
What are the primaryAPC of the respiratory system?
Dendritic cells
167
What is IgA's role in mucous defence?
inhibits:
bacterial adhesion
inflammatory effects of other immunoglobulins
Neutralises bacterial/viral toxins
168
What is Bronchiectasis?
Permanent dilation of the Bronchi, generally accompanied by suppurative inflammation (sputum production)
169
What are the two main heart sounds caused by?
The first 'lub' is the closure of the atrioventricular valves
The second is the closure of the aortic and pulmonary valves
170
When is ventricular and atrial systole occurring in relation to the heart sounds?
Ventricular - in-between the first and second heart sounds
Atrial - just before the first sound
171
What part of the ECG represents electrical event happening at atrial systole and which at ventricular systole?
Atrial - P wave
Ventricular - QRS
172
What is isovolumic contraction?
Occurs in systole when the ventricular pressure rises but the ventricular volume is constant.
173
What causes an early systolic murmur?
When the AV valves fail to close fully in atrial systole, or when aortic/pulmonary valves do not full open.
174
What can cause an early diastolic murmur?
If the aortic or pulmonary valves fail to close fully in diastole.
175
What are the 3rd and 4th heart sounds caused by?
Both are not always heard:
3rd: 'sail flapping in the wind' Due to rapid ventricular filling.
4th: Heard due to atrial systole, heard due to ischaemic heart disease or hypertension. Heard when a hypertrophied left atrium pumps into a stiffened left ventricle.
176
Quick way to work out heart rate from an ECG?
Count the squares between two QRS complexes and divide by 300
177
What are the two types of limb leads in an ECG?
Bipolar limb leads (I,II and III)
Unipolar limb leads (aVR, aVL and aVF)
178
Apart from the Limb leads, what else is included on the ECG?
The 6 Chest leads
179
What direction do all the limb leads travel?
I: RA to LA
II: RA to LL
III: LA to LL
aVR: (LA-LL) to RA
aVL: (RA-LL) to LA
aVF: (RA-LA) to LL
180
What is idiopathic ventilation?
Sustained alveolar and arterial hypocapnia. during rest and exercise.
181
Cause of idiopathic ventilation?
inappropriate cortical processing.
182
What are some respiratory adaptations to training?
Pulmonary ventilation increases at maximal effort, by increasing strength of inspiratory muscles.
Pulmonary diffusion increases at maximal work rates
Slight increase in total lung capacity
Decreased respiratory rate and pulmonary ventilation at rest.
183
Why is there less haematocrit in the capillaries?
To reduce resistance.
184
What are the major features of cardiac muscle?
Striated
Branched
Intercalated discs
185
Main mechanism of control of cardiac muscle?
Increased intracellular calcium to increase strength of contraction.
All positive inotropic drugs work this way
186
Three ways in which Intracellular calcium concentrations are raised?
Enters the cell from the outside
Released from intracellular stores
Calcium mediated calcium release
187
How are calcium level returned to resting in cardiac muscle cells? (3)
Active calcium extrusion (pump)
Active Na+/Ca2+ exchange
Active uptake into SR
188
What is the cause of a stiff ventricle due to cardiac ischaemia?
Slowed uptake of calcium, causing a raised resting potential in cardiac muscle cells.
189
Is the contractile mechanism in cardiac muscle the same or different to the mechanism in skeletal muscle?
the same.
190
Phases of the ventricular action potential?
Phase 0 - Depolarisation due to sodium influx
Phase 1 - Initial depolarisation caused by potassium efflux
Phase 2 - Plateau caused by calcium influx and potassium efflux.
Phase 3 - actual depolarisation by potassium efflux
Phase 4 - resting potential
191
how does hyperkalaemia cause cardiac arrest?
The membrane may not return to it's normal resting value due to high K+ concentration and Na+ channels may not be fully reset, therefore dialling contraction.
192
Two examples of positive inotropes and their mechanism of action?
Beta agonists (dobutamine): Speed Ca++ uptake into intracellular stores
Cardiac Glycosides (Digoxin): Inhibit Na+/K+ ATPase, increasing intracellular [Na+], thus decreasing Na/Ca exchange and increasing intracellular [Ca++]
193
Two examples of negative inotropes, and their mechanism of action?
Calcium channel blockers: Guess.
Beta Blockers: Decrease Ca++ uptake into intracellular stores
194
Factors which determine preload?
```
Gravity
Thoracic pump
The muscle pump
Co-localisation
Venomotor tone
Blood volume
```
195
How does gravity affect preload?
In the upright position the preload is increased form the SVC and decreased from the IVC.
196
What is the thoracic pump and how does it affect preload?
On inspiration preload falls due to decreased thoracic pressure.
197
What is co-localisation?
The fact veins are bound together with arteries and when the artery pulses the blood moves up the vein.
198
What is venomotor tone, and how does it affect preload?
The fact some of the great veins have smooth muscle that is stimulated by a-1 receptors, making it contract increasing preload.
199
Increased preload increases what?
Increased end diastolic volume, the same systolic volume and increased cardiac output
200
Increased after load increases what?
Increased end diastolic volume but maintained stroke volume and cardiac output
201
What is the molecular basis of increased force of contraction due to increased preload/afterload?
The actin and myosin strands are thought to be drawn closer together.
202
What is an increase in contractility e.g. from an inotropic drug ?
An increase in the fore of contraction that does not result from increased stretch.
203
Process of events that result after left ventricular ischaemia?
The right ventricle function better than the left
The right continues to pump blood to the lungs but it is ineffectively cleared by the left, and so pulmonary and left atrial bp rise.
Eventually ventricular balance will be restored as the left ventricle will move up it's starling curve, at the cost of pulmonary congestion and possible oedema.
204
What is orthopnoea?
Breathlessness when lying flat, commonly due to left side heart failure.
205
What causes pain due to hypoxia?
Na+/K+ pump malfunction.
206
Corneal arcus and xanthelasmata are commonly caused by what?
Hypercholesterolaemia
207
Process of fat digestion and absorption in the small intestine?
Chyme (partially digested food) is mixed with Bile,
Pancreatic juice and Intestinal juice.
This is then emulsified, digested and absorbed.
208
What is the function of pancreatic lipase?
It hydrolyses triglyceride contained within the fat droplet.
209
Four main types of lipoprotein?
Chylomicron very large, formed in small intestine enterocytes.
VLDL - very low density lipoprotein - triglyceride rich and formed in the liver
LDL - Cholesterol rich formed by VLDL
HDL - Cholesterol rich (less than LDL's) formed in the liver
210
Functions of apolipoproteins?
The actual protein component of lipoproteins.
To solubilise the lipid particle
Maintain structural integrity
To confer specificity on the lipoprotein particle and therefore direct it's metabolism.
211
What is lipoprotein lipase?
Enzyme found on the surface of capillaries/hepatocytes that hydrolyses the TG to release fatty acids near the tissue.
212
Where are renin, ACE and angiotensinogen produced?
Renin is produced by the kidneys
ACE is produced in the lungs
Angiotensinogen is continuously produced by the liver
213
What does renin do to angiotensinogen and what does ACE then do?
Renin converts Angiotensinogen to Angiotensin I and then ACE converts Angiotensin I to II (the active form)
214
What is the interaction between ACE and bradykinin?
Bradykinin is a vasodilator (in the lungs) ACE will break it down and so ACE inhibitors can affect this (can cause dry cough)
215
Actions of Ang II?
Vasoconstriction
Aldosterone release
Increased sympathetic stimulation
Promotes Na+ retention
216
What factors increase renin release?
Low arterial BP
Low Blood Volume
Altered sodium handling
217
Factors that decrease renin release?
High arterial BP
Increased Blood Volume
Angiotensin II (negative feedback)
218
What are the two Ang II receptors, and their features?
AT1 receptors
- Mitogenic
- Pro-fibrotic
- Vasoconstriction & increased BP
AT2 receptors
- Anti - mitogenic
- Anti - fibrotic
- Vasodilation & decreased BP
219
How do AT1 receptors cause vasoconstriction?
Direct action on vascular smooth muscle
Release of ADH
potentiation of Sympathetic NS
220
How do AT1 receptors act on the Sympathetic NS?
Act on peripheral nerve endings
- potentiate noradrenaline release
- block noradrenaline reuptake
- increase noradrenaline synthesis
noradrenaline leads to vasoconstriction.
221
How is aldosterone regulated and what does it do?
Regulated by Ang II
Aldosterone promotes water retention:
- increases Na+ retention in kidney and gut
- increases ADH secretion
- potent dipsogen (promotes thirst)
222
What are the actions of AT2 receptors?
Stimulates vasodilation
Increased activity of collagenases
Decrease growth factor expression
223
What are the interactions of Ang II in heart failure?
Ang II can increase cardiac remodelling due profibrotic/mitotic effects
224
What drugs block the RAAS system?
Beta-blockers
Renin inhibitors
ACE inhibitors
AT receptor antagonists
225
Two types of exercise?
Static or dynamic
226
Two different types of muscle?
Slow Twitch:
- Dependent of oxidative phosphorylation, good blood supply
Fast Twitch:
IIa: oxidative
IIb: glycoloytic
- Dependent on Creatine Phosphate
227
In what three ways is an oxygen debt incurred after exercise begins?
- Depletion of cellular ATP
- Depletion of creatine phosphate
- Build up of Lactic Acid
228
How is oxygen repaid after oxygen debt is acquired?
Fast: Rephosphorylation of ATP/Creatine
Slow: Lactate converted back to glucose/glycogen
Very Slow: Increased metabolic rate following exercise
229
Main physiological adaptations to exercise?
Increased HR
Increased SV
Decreased total peripheral resistance
Changes in distribution of blood flow
230
How is heart rate and Stroke volume mediated by the body?
Heart rate increased by the Sympathetic Nervous System, and decreased by the parasympathetic
Stroke volume modulated by preload and contractility.
231
What blood vessel mostly determines total peripheral resistance?
The arterioles
232
What is metabolite induced vasodilation? What are some examples?
When increased metabolism increases the amount of metabolites including; CO2, H+, lactate, K+ and Adenosine. These induce vasodilation.
233
Do arterial blood gasses change in response to exercise?
No
234
What are the parts of the body that act to increase ventilation in exercise?
Higher centres in the brain, peripheral chemoreceptors, skeletal muscles (chemo and mechanoreceptors)
235
What are the physiological changes to the lungs in exercise?
respiratory rate and ventilation increase.
236
What are the changes to the baroreceptor response in exercise?
The brain alters the 'set point' of blood pressure and so blood pressure is perceived as being too low. So heart rate is increased to compensate.
237
What is the limiting system to increase VO2 max?
Cardiovascular system
238
Responses in the muscle to training?
```
Muscle hypertrophy
Increased number of myofibrils
Increased mitochondrial enzymes
Increased ATP and Phospho-creatine
Increased glycogen
```
239
Effects of training on Respiration?
Reduced ventilation at the same work rate.
240
Main difference in the CV system's response to static exercise?
There is no significant drop in peripheral resistance.
241
What's VO₂ max used to measure?
The functional capacity of the entire cardiopulmonary system.
242
Reasons for termination of an exercise test?
Moderate to severe angina
dizziness or syncope
Subject wishes to stop
243
What does it tell you if the murmur is long?
Possibly a septal defect.
244
What is a wide pulse pressure and what does it mean?
A large gap between the systolic and diastolic blood pressures, represents a stiff aorta normally if the systolic is raised.
245
What are the two theories on the auto regulation of blood pressure in tissues?
Which applies to the afferent arterioles?
Metabolic theory: improved blood flow increases metabolism and has vasoactive effects?
Myogenic theory: Smooth muscle constricts when stretched, via an increase in intracellular [Ca].
246
What is Tubuloglomerular feedback?
When the fluid content is monitored in the DCT in the macular dense and there is feedback to the glomerulus and GFR is modified.
247
If the Na+ and Cl- is too high in the DCT what changes will happen to the afferent arteriole?
Afferent constriction.
248
What is the difference in the blood flow/O2 Consumption to the cortex and to the medulla?
The Cortex receives a lot of blood and has a relatively low O2 consumption
In the medulla each nephron is individually supplied by the vasa recta and so blood flow is low and O2 consumption is relatively high, leaving little residual capacity
249
What are the two characteristics that determine whether a molecule will pass through the glomerular filter.
Charge (Negative will be repelled), Size
250
What kind of things are not filtered into the PCT?
Cells and proteins
251
What effect will afferent arteriole constriction have on Blood flow into the glomerulus, Glomerular pressure and GFR?
Decrease for all.
252
Mediators of Afferent arteriole Vasoconstriction/dilation?
Constriction:
Sympathetic tone
Adenosine
Endothelin
Dilation:
NO
ANP
Prostaglandins
253
What effect will Efferent arterial dilation have on Blood flow out of the glomerulus, Glomerular pressure and GFR?
Decrease Blood flow out
Increase Glomerular pressure and GFR
254
What are the Mesangial cells in the glomerulus?
Cells that support the glomerular filter
Phagocytic and contractile.
255
Contraction of Mesangial cells does what?
decreases surface area and decreases GFR
256
What's the textbook GFR?
125ml/min
257
What's compensatory SNGFR?
Increases in single nephron GFR, through hypertrophy of blood vessels and tubules, can maintain GFR following nephron loss.
258
Definition for renal clearance?
Volume of plasma that is completely cleared of a marker per unit time
259
What are the properties which mean a clearance marker can be use to measure GFR
```
Freely filtered in the glomerulus
Not secreted nor reabsorbed
non-toxic
Not metabolised in the kidney
No effect on GFR
```
260
How do you work out the amount of marker excreted?
(Urine [marker] x vol) / Time
261
How do calculate the amount of marker filtered?
GFR x Urine [marker]
262
How do you calculate clearance of a marker, and GFR if it's suitable?
(U x V / P x T)
263
What are the markers usually used to measure GFR?
Inulin (gold standard)
Creatinine (routine) Urea
264
Why is inulin not commonly used?
Too time consuming as it is not endogenous
265
How is creatinine handled by the kidney?
Freely filtered
Not reabsorbed
Slightly secreted (about 10% discrepancy)
266
What factors can affect [Creatinine]?
Muscle mass
Age
Gender
267
How is Urea handled by the Kidneys?
Freely absorbed and not secreted
About 40% reabsorbed
268
What factors affect [urea]?
Protein turnover
Hydration status (due to release of ADH)
269
Why is the Urea:Creatinine Concentration useful?
Both should be equally affected by any change in GFR so if they change disproportionately there may be underlying problems (e.g. dehydration)
270
To measure renal plasma flow what properties must a marker exhibit?
An example?
Freely filtered not reabsorbed
Must be mostly secreted
e.g. PAH (90% cleared)
271
How do you calculate Renal Plasma flow?
UxV / PxT
272
Two main types of nephron? What's the difference?
Cortical Nephrons Glomeruli in outer cortex short loop of henle
Juxtamedullary nephrons Glomeruli near the boundary between Cortex/Medulla the loop of henle descends into the medulla.
273
Main functions of the nephron?
Resorption of solutes
Secretion
Regulation of urine volume
274
What is the mechanism of obligate reabsorption in the proximal convoluted tubule?
Na+ dependent active transport across the membrane.
275
Why is glucose seen in uncontrolled diabetes?
When there is so much glucose in the plasma that the glucose transported in the PCT are saturated and have reached 'renal threshold'
276
If the GFR increases what will happen to the PCT resorption of Na+/K+?
doesn't change this is because there is a set proportion absorbed independent on the amount
277
How is Na+ reabsorbed in the PCT?
Actively with glucose/amino acids and also as an H+/Na+ anti-port
278
In the proximal tubule what is the rate of bicarbonate reabsorption?
90%
279
How is water reabsorbed in the PCT?
The amount of solutes being reabsorbed creates an osmotic gradient (where sodium flows water follows)
280
How are Cl-, K+ and Urea reabsorbed in the PCT?
The reabsorption of Na+ and water causes a chemical gradient and a diffusion gradient is created.
281
What things are secreted into the PCT and how does this occur?
Organic acids and bases, occurs through active transport.
282
Very basic overview of what is permeable in the loop of henle?
Thin descending limb permeable to water and not Na+ or Cl-
Thin ascending permeable to Na+ and Cl-
Thick ascending limb actively pumps Na+ and Cl-
283
What happens to Na+/K+ and Cl- in the thick ascending limb exactly?
Na+/K+/2Cl- active transport from the tubular epithelium to the epithelial cell
Na+ is pumped into medullary interstitium, Cl- diffuses into the medullary interstitium, K+ diffuses back into the tubule
284
Detail on how the loop of henle functions.
The Na+ and Cl- efflux from the Thick ascending limb causes the interstitium to be hyperosmolar
Drawing water out of the descending limb, making the electrolytes inside more concentrated
Then when the fluid reaches the thin ascending limb it is permeable to Na+ and Cl- and they diffuse out.
then the Na+ and Cl- and K+ are actively pumped out of the thick ascending limb
285
If the collecting duct is permeable to water where will it diffuse?
What hormone causes this?
Out of the collecting duct and into the hyperosmolar medulla
ADH
286
Where is ADH made and secreted, due to what stimulus, in response to what receptors?
MAde in the soma of the hypothalamus neurones and transported to the pituitary. Secreted if the fluid increases in osmolarity.
Due to the osmoreceptors or from input from the medulla
287
How does ADH increase permeability?
Inserts aquaporins in the collecting duct, they are water channels.
288
What stimuli can cause ADH secretion?
```
Increased osmotic pressure of plasma
Decreased Extracellular fluid
Pain, emotion, stress
Exercise
Nausea/vomiting
Angiotensin II
```
289
What stimuli can decrease ADH secretion?
Decreased Osmotic pressure
Increased ECF volume
Drugs e.g. alcohol
ANP
290
What are the different sensory inputs for water and salt regulation?
Osmoreceptors in hypothalamus
Low pressure receptors in the atria
High pressure baroreceptors in aortic arch and carotid sinus
Juxtaglomerular apparatus
291
What stimuli cause thirst?
Increased plasma osmolarity
Decreased blood volume
During meals
292
What is diabetes insipidus?
The inability to concentrate urine as a lack of ADH activity, either not secreted or nephron does not respond.
293
Where is sodium reabsorption regulated?
Regulated in the distal nephron
Ascending loop of henle
Distal tubule
Early collecting duct
294
What hormones control Na+ regulation?
Aldosterone
| ANP
295
How is Na+ reabsorbed in the DCT?
Through a Na+/Cl- co-transporter from lumen to cell
and through the Na+/K+ antiport from cell to interstitium
296
Two major cell types in the collecting ducts?
Principle cells: Resorb Na+ and secrete K+
Intercalated cells: secrete H+, maintain acid/base balance
297
What happens in the early collecting duct?
Na+ resorption by principle cells, Na+ leaves through water filled channels and is not linked to any other ion.
298
What does aldosterone do, and how does aldosterone work?
Promotes Na+ retention and K+ excretion & H+
Priniciple cell:
Increases the amount of Na+ and K+ channels in the luminal membrane, also promotes Na+/K+ ATPase activity in the basolateral membrane
Intercalated cell:
Increase the Na+/H+ symporter
299
Examples of aldosterone antagonists? what type of diuretic are they?
Spironolactone, they are potassium sparing diuretics.
300
What factors affect aldosterone action?
High [PGE₂] inhibits Na+/K+ ATPase
it is produced by endothelia and ANP
301
What are the main actions of Natriuretic peptides?
Examples?
Mostly oppose the actions of the RAAS pathway.
ANP - atrial natriuretic peptide
BNP - brain natriuretic peptide
302
Problems with hypo/hyperkalaemia?
Hyper - membrane potential increased, particularly crucial in the heart, causing sudden cardiac death syndrome
Hypo - Membrane potential decreased, causing muscle weakness and arrhythmia
303
Causes of hypokalaemia?
Alkalosis
V&D
Diuretics
Eating Clay
304
Causes of hyperkalaemia
Acidosis
Strenuous exercise
Inadequate hormonal control
305
how do you calculate excretion?
[Urine] x vol / time
306
What plasma protein has the highest concentration in the plasma?
Albumin.
307
How are proteins reabsorbed in the PCT?
Epithelial cells in the PCT engulf the proteins through endocytosis
308
What are healthy reasons why proteins are found in the urine?
Protein release in the tubule
Glomerular leakage (where the amount of protein exceeds the reabsorption capacity)
309
What is tubular proteinuria?
When tubule-intestinal disease impair tubular function so that the tubule cannot reabsorb protein and it appears in the urine
310
What is Overflow proteinuria?
Excess production of small proteins which are filtered at too great a quantity to be reabsorbed in the PCT.
311
What is Glomerular proteinuria?
Reflects an increase in the permeability of the glomerulus to protein. Capillaries or the basement membrane may be damaged.
312
Common causes of Glomerular Proteinuria?
Hypertension/Diabetes
313
What is Nephrotic syndrome?
Umbrella term for an increase in the glomerular permeability to proteins
Associated with Salt and water retention and Hypoalbuminaemia causing oedema.
314
What is microalbuminuria?
Albumin excretion of >30mg but less than 150mg a day
First indicator of Diabetic nephropathy
315
What does a dipstick test test for?
Will test for proteinuria and will give positive if the urine is alkaline
316
What do you do if a dipstick test is positive?
24hour urine collections or a albumin/creatinine ratio
317
What would you define as a lower UTI?
Infection of bladder or urethra
318
What's cystisis?
Inflammation of the lining of the bladder
319
What would you define as an uncomplicated UTI?
No co-morbidity (healthy people)
320
Whats pyuria?
Raised white cell count in the urine.
321
What's an upper UTI?
Pyelonephritis (kidney infection)
322
Formula for CO and BP?
CO = SV x HR
BP = CO x TPR
323
What is starlings law of the heart?
Ventricular filling is proportional to SV by the increased contractility of the myocytes.
324
What are the cardiac responses to a fast haemorrhage?
Increased sympathetic drive manages to maintain stroke volume through increased contractility, but decreases left atrial pressure
325
Other cardiovascular responses to haemorrhage?
Vasoconstriction, Venoconstriction.
326
Where does sympathetic vasoconstriction occur in response to haemorrhage?
Skin, Kidneys, GI tract and skeletal muscle
327
Physiological advantage to venoconstriction?
Raised central venous pressure
Increased preload
Increased SV and CO
328
At what percentage blood loss in a haemorrhage would it become likely to be fatal?
Above 30%
329
During haemorrhage what happens to the net movement of fluid in capillaries? What is this called?
There is net movement into the capillary, due to decreased capillary hydrostatic pressure, Internal transfusion.
330
What ways does the body raise blood pressure to maintain perfusion?
Internal transfusion
Baroreceptor response
331
How does the body replace the volume of blood in the long term?
Salt and water retention.
RAAS, ADH, and thirst
332
What does ANP do?
Promotes Na+ and water excretion (not an appropriate response to haemorrhage)
333
What is decompensated (irreversible) shock?
Shock following >30% blood loss and a 3 hour delay in replacing fluids.
there is prolonged vasoconstriction in some organs leading to failure, e.g. kidney and liver
334
Examples of replacement fluids?
Blood
Crystalloids
Colloids
335
How does Dextrose/Colloids/saline work as a replacement fluid?
Colloids cannot move from blood vessels and will expand the fluid in blood vessels
Saline can move to the ECM and expand it
Dextrose can move into cells and will expand the ICM
336
General signs of shock?
Weakness
Lethargy
Tachycardia
Cyanosis
337
Definition of renal failure?
A decrease in GFR resulting in increased [creatinine] and [urea]
338
What are the names for acute and chronic renal failure?
AKI (acute kidney injury)
Chronic Kidney Disease
339
Is AKI defined by GFR or urine flow or both?
Only by GFR, not defined by urine flow (although it may decrease)
340
What is oliguria and anuria?
Oliguria is less than 400ml/day
Anuria is less than 50ml/day
341
Clinical signs of AKI?
Decline in GFR
Often oliguria
Rise in plasma [urea] and [creatinine]
342
What are the three classifications of AKI?
Prerenal: before the nephron
Intrarenal: in the nephron
Postrenal: after the nephron
343
What could cause Prerenal kidney injury?
Inadequate perfusion of the glomerulus
e.g. renal artery stenosis
hypotension
heart failure
344
What are some examples of drug induced prerenal injury?
NSAID drugs: block PGE2 induced dilation of afferent arteriole
ACE/AT1 receptor antagonists: Block constriction of efferent arteriole by Angiotensin II
345
Causes of Intrarenal injury?
Acute tubular necrosis
Acute glomerulonephritis
endogenous or exogenous toxins
interstitial nephritis
346
Two types of acute tubular necrosis?
Toxic
Ischaemic
347
What happens in acute tubular ischaemia?
Occlusion or obstruction leads to ischaemia, which produces paradoxical vasoconstriction mediated by endothelins and involving Ca2+ and ROS
348
A raised urea to creatinine ratio will often mean the condition is what type of AKI?
Pre-renal
349
What are buffers?
Weak acids or bases
350
What are the physiological buffers of the body?
Bicarbonate buffer
Proteins
Phosphate buffer
351
Two types of acid produced in metabolism?
CO2 (blown off in lungs)
Metabolic acids taken away by the kidneys
352
Examples of metabolic acids are produced by the body?
Sulphuric acid
Phosphoric acid
Lactic acid
Ketone Bodies
353
What Reaction does carbonic anhydrase catalyse?
CO2 + H2O = H2CO3
354
What roles do the kidneys play in the acid/base balance?
Reabsorbs filtered bicarbonate
Excretes excess acid
Generates new bicarbonate
355
How does reabsorption of filtered bicarbonate occur in the PCT?
The Na from the HCO3- & Na+ gets pumped into the epithelium and the Na+ is replaced by H+ to make H2CO3.
This is then converted into H20 and CO2 by carbonic anhydrase. The CO2 diffuses back into the epithelium and can then be used to make H2CO3 again and be pumped out.
356
How does excess acid excretion occur in the DCT?
In the distal nephron H2O and CO2 is also converted to H2CO3 where H+ is secreted into the lumen and HCO3 is secreted into the interstitium
357
How is the excreted H+ in the urine buffered?
Phosphate
ammonia
358
Does aldosterone cause secretion or reabsorption of H+?
secretion
359
Four different types of acid/base disturbances in the body?
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
360
Causes of metabolic acidosis?
Increased acid intake
Increased metabolic acid production
Increased GI loss of bicarbonate
Decreased acid excretion
361
Causes of metabolic alkalosis?
Increased alkali intake
Increased loss of H+
Increased HCO3 generation in kidneys
362
What does a proportionate change in PaCO2 and HCO3 suggest?
what does a disproportionate change suggest?
Proportionate: respiratory acid base imbalance
Disproportionate: metabolic imbalance
363
What is the base excess a measure of?
The change in [HCO3-] produced solely by the metabolic component of an acid-base disturbance.
364
If the base excess is positive what does it mean?
Metabolic alkalosis
365
If the base excess is negative what does that mean?
Metabolic acidosis
366
Increased anion gap represents what?
Metabolic acidosis
