1. Sanjay’s Malaise
Ventilation-Perfusion Relationships
1. What is pulmonary blood flow in L/min?1
2. What is approximate ventilation of the lungs in mL/min?2
3. What is the normalVa/Q (ventilation-perfusion) matching for normal gas
exchange?3
4. Why could you have a normal pulmonaryVa/Q but poor gas exchange?4
5. Which veins account for the 2% of venous blood which does not pass through the
lungs?5
6. What two deformities of the heart could initially cause L to R shunt in newborns?
6
7. How does constant high pressure in the pulmonary circulation cause right to left
shunts?7
8. List the four heart malformations that make up Fallot’s tetraolgy8
9. Does ventilation or breathing 100% oxygen help a patient with right to left shunt?9
10.Would an area of high perfusion low ventilation be described as dead space or
shunt effect?10
1 5000ml/min blood
2 7500ml/min air
3 0.8
4 Ventilation/perfusion could be matched on pulmonary level but also need to be matched on alveolar level
5 Bronchial veins and small veins draining the wall of the L.vent go into arterial circulation
6 Atrial and septal defects
7 Pulmonary vascular resistance and remodelling
8 Overriding aorta (middle of heart rather than left), ventricular septal defect, R.vent hypertrophy, pulmonary
stenosis (narrowing caused by hypertrophy of heart wall).
9 Little, because the haemoglobin is already fully saturated, it cannot open up the unventilated/unperfused
areas or dead space
10 Shunt - dead space would be a high ventilation/perfusion (because it means poor gas exchange taking
place)

2. 11.Why do highVa/Q areas not compensate for low ones?11
12.What would aVa/Q of zero indicate?12
13.What normal mismatch could occur due to gravity in normal lungs?13
14.How is the response of pulmonary vasculature different to that of other tissues in
hypoxic conditions?14
15.Why does load on the right heart increase in respiratory failure?15
16.What is the normal alveolar-arterial pressure gradient in mmHg for a healthy
adult, why is this caused?16
Respiratory Failure
1. What defines respiratory failure in terms of pO2 and pCO2?17
2. What is the difference between type 1 (hypoxaemic) respiratory failure and type 2
(hypercapnic) respiratory failure?18
3. What pathologies can cause right to left shunts?19
4. List the factors that could cause type 1 respiratory failure?20
11 More blood tends to come from the low Va/Q areas as the high Va/Q areas are mostly caused by poor
perfusion. High Va/Q areas do not have higher O2 content because the blood is already fully saturated. So
increasing PO2 does little to increase O2 content.
12 A completely collapsed lung or one where perfusion is completely blocked
13 Gravity improves both perfusion and ventilation at the bottom of the lungs but effect on perfusion is larger
than effect on ventilation. So the Va/Q is higher at the top and lower at the bottom.
14 Vasoconstriction in some areas to divert blood from poorly ventilated areas to better ventilated ones, so
improves Va/Q matching. So using vasodilators in the case of poor ventilation to certain areas of the lung
may in some cases be detrimental.
15 Because of vasoconstriction in the pulmonary vasculature
16 5-10mmHg, pressure difference is caused by gravity (top of lung more efficient)
17 When arterial pO2 falls below 8kpa and pCO2 rises to above 6
18 Hypoxaemic respiratory failure = due to failure of alveolar gas exchange, Hypercapnic = ventilatory (e.g.
airway) failure.
19 Cyanotic (congenital) heart malformation, pulmonary emboli, pulmonary edema
20 Failure of CNS, spinal cord damage, myesthenia gravis, airway obstruction, COPD, asthma, muscular
dystrophy

3. 5. Why does CO2 retention not occur in type 2 respiratory failure (ventilation
failure)?21
6. What effect would hypoventilation have on arterial pCO2 and pO222
7. What are the possible causes of hypoventilation?23
8. What is the most important chemical factor out of plasma pH, PaO2 and PaCO2
in control of ventilation?24
9. Where would these chemical changes be picked up?25
10.Why does a change in plasma pH alone not affect the central chemoreceptors?26
11.What O2 sats would you begin to notice central cyanosis?27
Respiratory Tract Bacteria and Viruses
1. What organisms can be found in the normal flora of the upper respiratory tract
and lower respiratory tract?28
2. What is the difference between endogenous and exogenous respiratory infections
and give relevant examples?29
3. What are the two main common cold viruses?30
21 Because CO2 diffuses across the alveolar membrane 20x better than O2, so if perfusion is normal it will
get across the membrane. In the case of diffusion impairment, compensatory hyperventilation can actually
result in a lower than normal pCO2.
22 Low paCo2 and high PaCO2. Hypoventilation is the only cause of hypoxaemia that will increase paCO2,
others lead to reflex hyperventilation.
23 Structural - failure of adequate chest wall movement (CNS damage), Failure of breathing control (loss of
chemoreceptor sensitivity to CO2), COPD, sleep apnoea, obstructive
24 PaCO2
25 In the central chemoreceptors in the medulla, respond to pH of the CSF which is made more acidic by a
higher presence of CO2.
26 H+ cannot diffuse across the blood-brain barrier so pH of the CSF affected mostly by plasma CO2, which
can cross the blood brain barrier
27 85% or lower, may not occur in anaemic patients, blueness comes from lots of deoxygenated haemoglobin
28 Commensal bacteria, strep pneumoniae, haemophilus influenzae, some viruses. Lower respiratory tract is
normally sterile.
29 Exogenous = airborne from another infected patient/animal. Endogenous = inhaled from URT, sometimes
gut bacteria can increase and enter lungs via stomach and esophagus (if patients are on antacids).
30 Rhinovirus 30%, Coronavirus 10%

4. 4. What is the common name for pharyngitis?31
5. What is the bacterial (30%) cause of pharyngitis and the early and late
complications of this kind of infection?32
6. What are the pathogenic effects of the C diptheriae toxin?33
7. What is quinsey in relation to bacterial pharyngitis?34
8. What is Haemophilus influenzae?35
9. What is sinusitis?36
10.List 3 examples of lower respiratory tract infections?37
11.What is the link between haemophilus influenzae and blood?38
12.Why does legionella pneumophila only grow in water?39
Treatment of Infection 1
1. What is normal blood platelet count?40
2. List the main classes of antibiotics41
31 Sore throat (pharynx-itits), 70% viral
32 Strep Pyogenes. Complications = (early) scarlet fever, local abscess, (late) glomerulonephritis, rheumatic
fever
33 toxaemia (toxins in blood), myocarditis (infection of myocardium), neutritis (inflammation of nervous
system), toxin inhibits protein synthesis at the host cell ribosome
34 Complication of tonsilitis consisting of a collection of pus beside the tonsil
35 Life threatening swelling of epiglottis that can cause respiratory obstruction within hours especially in
young children
36 viral URTI leads to defect on mucous membrane which results in blockage of sinuses. Symptoms are
headache, facial cellulitis and purulent discharge. Caused by haemophilus influenzae which can be present
in normal URT flora.
37 Any of Strep Pneumoniae, Haemophilus influenzae, mycoplasma pneumoniae, chlamydia, influenza,
adenovirus, mycobacterium tuberculosis TB, legionella pneumophila
38 It needs blood factors in order to grow
39 It grows inside amoebae which are present in water
40 150-400 x10^9/L
41 Penicillins/cephalosporins, Macrolides (e.g. erythromycin, clarithromycin), chloramphenicol,
aminoglycosides, metronidazole, tetracyclines, quinolones, glycopeptides

5. 3. What is the difference between an antibiotic and an antimicrobial agent?42
4. What is antibiotic prophylaxis?43
5. Which gram type of bacteria have an outer membrane?44
6. By what mechanism do bacteria resist penicillins and caphalosporins?45
7. What part of the bacteria is targeted by macrolides such as erythromycin?46
8. By what mechanism does MRSA resist antibiotics?47
9. How does vancomycin resistant enterococci resist vancomycin?48
10.Why is penecillin not effective against Pseudomonas and E. coli?49
11.What does the tet (A) gene do in some resistant coliforms?50
12.What 3 ways are resistance genes spread between bacteria?51
13.What are MIC and MBC?52
14.What is the MIC in mg/L for penicillin?53
42 Antibiotic is a natural substance produced by an organism, an antimicrobial agent may be synthetic or
natural
43 Pre-emptive treatment with antibiotics before an invasive procedure
44 Gram negative bacteria, so antibiotics used against them must contain beta lactams to penetrate this
45 Penecillins depend on beta lactams which target the bacterial cell wall peptidoglycan cross-links. Bacteria
then produce beta-lactaminases which attack the 4 membered ring of the antibiotic
46 prokaryotic 70S ribosome of sterptococci and staphylococci
47 Alters target site by producing a new PBP that is not inhibited by methicillin/flucloxacillin
48 Again by an altered target site mechanism, altered cell wall pentapepdite instead of D-alanine to which
vancomycin normally binds
49 Because they have an outer membrane which it cannot penetrate
50 Resists tetracycline which has penetrated the membrane by pumping it out of the bacteria
51 Conjugation (transmission of DNA between two cells), Transformation (when a bacterium takes up
resistant DNA from a dead organism), Transduction (when DNA is spread by bacteriophages), viruses that
infect bacteria.
52 Minimum inhibitory concentration and minimum bactericidal concentration, a measure of how easily an
antibiotic inhibits or kills a bacterium
53 0.25mg/L, after incubation, bugs are killed at this concentration but not below it

6. Influenza
1. What is the approximate size range for viruses?54
2. What is the capsid?55
3. Name the virus that causes influenza56
4. Describe the structure of this virus including names of its surface proteins57
5. How does the influenza virus enter new host cells?58
6. How many subtypes are there of the surface proteins, therefore varieties of
influenza A?59
7. What genes are these based on and where are they found as a reservoir?60
8. What is the difference between antigenic shift and antigenic drift?61
9. What were the 3 major pandemics of H/N flu in the 20th century?62
10.How many different types of H and N are known to exist in nature?63
11.How many cases per 100,000 population do you need to see before flu is
considered an epidemic?64
54 20-300nm
55 A virusesʼ protein coat containing its receptors, forms nucleocapsid together with nucleic acid core.
56 orthomyxovirus
57 Lipid envelope with 2 surface glycoproteins (Hemagglutinin, neuraminidase), matrix proetin on inner
surface and pores composed of M2 protein
58 By attachment with host proteins, endocytosis into cell, dispersal of viral DNA and budding from cell
59 15 variants of haemagglutinin, 9 variants of neuraminidase
60 Based on H & N genes, found as a reservoir in birds and some mammals e.g. pigs
61 Antigenic drift = minor changes, seasonal outbreaks, DNA replication as error accumulation. Antigenic shift
= sudden and major changes, accounts for pandemic, genetic segment of virus changes, forms completely
new virus so host is no longer resistant (not seen in influenza B or C) e.g. mixing of animal strain with human
strain
62 H1H1 Spanish flu 1918, H2N2 Asian flu 1957, H3N2 Hong Kong flu 1968
63 16 H, 9 N
64 200 per 100,000, this is considered higher than average and therefore epidemic

7. 12.How effective as a % is the flu vaccination?65
13.What may be used as an treatment against influenza A?66
14.What are neuraminase inhibitors?67
15.What process is blocked by Relenza and Tamiflu?68
Thermoregulation
1. What is the difference between a poikilotherm and a homeotherm?69
2. Why is an aural temperature reading relatively quick and accurate?70
3. The skin contains temperature receptors, where are the three deep body
temperature receptors located?71
4. Which part of the brain controls temperature regulating mechanisms, including
regulation of signals from all of the areas in (3)?72
5. What controls the regulation of venous plexus under the skin to moderate
radiative heat loss?73
6. What is a countercurrent exchange?74
65 70% annually, varies with different strains
66 M2 channel blockers such as amantadine, blocks entry of virus into nuclear envelope and secretion
pathway when in high concentrations
67 target the protein on the influenza and prevent it from binding to other cells to replicate. Inhibits budding
and release.
68 These are neuraminidase inhibitors, inhibit budding of new virus from invaded host cells, so cannot
replicate effectively
69 poikilotherms body temp varies with changes in environmental temp, homeotherms have to have a core
body temperature maintained within narrow constant range despite variations in environmental temperature
70 because it is close to the brain, which has 10x the blood supply of any other area of the body, aural
thermometer detects infra red radiation from the hear drum.
71 Spinal cord, abdominal viscera, great veins (SVC, IVC and pulmonary veins)
72 Hypothalamus
73 Sympathetic outflow moderated by hypothalamus.
74 Deep veins in the limbs are positioned alongside arteries so that heat lost by the arteries is conserved by
the veins. In situations where the body wants to lose heat, countercurrent deep veins are constricted and the
blood is routed to the skin.

8. 7. What are arteriovenous anastemoses?75
8. What is the composition of sweat when it is first secreted, at the bottom of the
sweat gland?76
9. How does the composition of sweat change as it moves up the duct towards the
skin?77
10.How does sweat capacity change in someone acclimatized to high temperatures
for a week?78
11.How many times over can heat production be raised by maximum shivering?79
12.Why is it of crucial importance that neonates are kept (incubated) at a fixed
temperature?80
13.What is the muscle mechanism responsible for shivering?81
14.What things can limit shivering?82
15.What is ‘brown fat’?83
16.What hormones are responsible for stimulating non-shivering thermogenesis?84
17.What is a pyrogen?85
75 arterio-venous plexuses in the skin which can constrict or dilate to regulate temperature enabling higher
blood flow to the skin than would otherwise be possible
76 Essentially the same as plasma but without albumin (and other proteins)
77 At low sweating rates, most of the salt and water are reabsorbed as sweat moves up the duct, at high
sweating rates more salt than water is reabsorbed but salt in surface sweat is still 50% of plasma levels.
78 Sweat capacity increases 2-3 fold. There is a 5 fold reduction in salt loss during sweating, mostly due to
increased aldosterone secretion resulting from lowered plasma Na+, aldosterone increases absorbtion of
Na+ from sweat glands as well as in the kidneys
79 x5
80 They have a poorly developed reflex for increasing temperature (particularly shivering)
81 Stretch reflex centres in muscle are activated, causes feedback loop responsible for shivering
82 Glycogen depletion, hypoglycaemia, hypoxia and some drugs.
83 Type of adipose tissue especially important in newborns. Replaces function of shivering by maintaining
warmth, it contains numerous mitochondria which make it brown.
84 thyroxine and epinephrine, increase transcription of UCP1 and UCP3, release free fatty acids that activate
uncoupling
85 A substance which causes an increase in body temp by resetting the hypothalmic set-point, e.g. toxin