Get Through MRCP Part 1:BOFs

Clinical sciences: Answers Clinical sciences: Answers

1) c.

C1q, C1r, C1s, C2 and C4 are parts of the classical complement pathway
which is activated by IgG, IgM and C-reactive protein. This activation

leads to the formation of C3 convertase which then forms C5 convertase,
ending in the formation of membrane attack complex (MAC). Although

IgA may activate the alternative pathway, generally this pathway does not

require an antibody for activation; there is continuous autoactivation of

C3 so that when this fragment encounters a microbe it will stick to its
surface and activate the alternative pathway.

Classical complement Mannan- AlternaƟve
pathway. AcƟvaƟon by Binding lecƟn complement pathway.
Ab-Ag complex; IgG or AcƟvaƟon by microbial
IgM. pathway surfaces and
polysaccharides.
C1, C2, C4
MASP1, C3b, Factor B,
MASP2, Factor D,
MBL Factor P

C

C5, C6, C7, C8, C9 (the membrane 289
aƩack complex; MAC)

Complement system. This system can be activated by three pathways.
The end result of each is the formation of the membrane attack complex
(MAC). The lectin pathway is activated by the binding of a lectin to a sugar.
MASP-1 and MASP-2 are proteases (similar to C1r and C1s, respectively)
which cleave C2 and C4. MASP, mannan-binding lectin-associated serine
protease; MBL, mannan-binding lectin; Ag, antigen; Ab, antibody.

© 2008 by Taylor & Francis Group, LLC

Clinical sciences: Answers2) c.
Deficiency of the early complement components (C1– 4) predisposes to
the development of autoimmune diseases (SLE and rheumatoid arthritis),
while deficiencies of the late complement components are associated
with susceptibility to disseminated Neisseria infections. Deficiency of the
alternative pathway’s regulatory proteins carries a risk for Neisseria
meningitides infections. The majority of these complement deficiencies are
inherited in an autosomal co-dominant pattern, except properdin and
factor-D deficiencies which are inherited in an X-linked pattern, and C1
inhibitor deficiency which is inherited in an autosomal dominant pattern.
Therefore, properdin deficiency fits the clinical scenario.

3) c.
Mannan-binding lectin, which is part of the complement lectin pathway,
attaches repeating mannoses to the surface of microbes. This serum
protein resembles C1q; both are oligomers which have a globular domain
at one end and a collagenous domain at the other end.

4) c.
CD55 (decay accelerating factor, DAF) and CD59 are abnormal in
paroxysmal nocturnal haemoglobinuria. CD55 is a regulatory cell surface
protein for C3 and C5 convertases; it disintegrates these convertases and
prevents cell lysis. CD59 is a glycolipid-anchored protein and a
complement system regulator that binds to C8 and C9; it blocks the
attachment of membrane attach complex and hence cell lysis. CD25 is an
interleukin-2 receptor. Basiliximab and daclizumab are antibodies against
CD25. Rituxumab is a monoclonal antibody against CD20.

5) c.
Serum levels of C3, C4 and CH50 (total haemolytic complement) are low
during SLE flare-ups and indicate activation of classical and alternative
complement pathways. Low serum levels of C3 and CH50 with normal
serum C4 indicate classical pathway activation, while low serum C4 and
CH50 with normal C3 indicate activation of the alternative pathway.
Elevation of these serum complements is a reflection of the acute phase
response. Very low (or even zero) CH50 with normal C3 and C4 indicates
inherited deficiency of other complement system proteins or in vitro
activation.

6) d.
Cystic fibrosis has a carrier rate of 23% while that of hereditary
haemochromatosis is 10%. Three per cent is the usual carrier rate of
a1-antitrypsin deficiency. Cystic fibrosis is an autosomal recessive disease
which usually results from mutation in the CFTR gene. The HFE gene is
mutated in 85% of cases of hereditary haemochromatosis.

7) b.
Myotonia dystrophica has a non-coding repeat expansion involving CTG in

290 the DMPK 30UTR gene on chromosome 19, while GAA repeat is

© 2008 by Taylor & Francis Group, LLC

abnormally expanded in the non-coding sequence of the frataxin gene on Clinical sciences: Answers
chromosome 9. Friedreich’s ataxia is an autosomal recessive disorder,
while other hereditary spinocerebellar ataxias (e.g. type 1 and 2) are 291
autosomal dominant.

8) d.
Kearns–Sayre syndrome is a mitochondrial cytopathic disease which
presents with progressive external ophthalmoplegia, heart block, raised
CSF protein and sensorineural deafness. Li–Fraumeni is an autosomal
dominant disease due to mutation in the tumour suppressor gene p53,
resulting in increased risk of developing tumours of the brain, breast,
adrenal gland, leukaemia and sarcomas. Renal cell carcinoma (which may
be bilateral), phaeochromocytoma and intracranial haemangioblastoma
are seen in patients with von Hippel–Lindau. Apart from gastrointestinal
tumours, cancers of the endometrium, ovary and breast may occur with
Peutz–Jeghers syndrome. Patients with hereditary retinoblastoma may
develop osteosarcoma.

9) c.
Microdeletion syndromes are syndromes caused by a chromosomal
deletion spanning several (contiguous) genes that is too small to be
detected under the microscope using conventional cytogenetic methods.
Depending on the size of the deletion, other techniques, such as FISH or
other methods of DNA analysis, can sometimes be employed to identify
the deletion. These are monosomy 1p36 syndrome, Williams’ syndrome,
WAGR syndrome, Angelman’s and Prader–Willi syndromes, Miller–
Dieker syndrome, Smith–Magenis syndrome, neurofibromatosis type 1
(only 5%), Alagille’s syndrome and DiGeorge syndrome. Machado–Joseph
disease is hereditary spinocerebellar ataxia type 3. Wilms’ tumour
aniridia, genitourinary abnormalities and mental retardation constitute
WAGR syndrome which is due to a microdeletion involving chromosome
11. DiGeorge syndrome is the commonest microdeletion syndrome with
hypoparathyroidism (absent parathyroids), facial dysmorphism, congenital
heart disease, cleft palate and thymic aplasia with low circulating T cells
and impaired T-cell function.

10) e.
Common variable immune deficiency syndrome is a sporadic non-
inherited disease; there is no risk of inheritance by offspring. Although the
number of circulating B cells is normal, these cells fail to differentiate into
antibody-secreting plasma cells. Relatives of individuals with this disease
might have selective IgA deficiency. Patients may develop repeated
sinopulmonary infections, malabsorption, pseudo-lymphoma, lymphoid
interstitial pneumonia, amyloidosis and non-caseating sarcoid-like
granulomata of the liver, spleen, lung and skin.

11) b.
S-100 is not an oncogene and is seen in tumours of neural crest
origin. Her-2/neu over-expression is seen in 20% of cases of breast cancer.

© 2008 by Taylor & Francis Group, LLC

Clinical sciences: Answers CA-125 is a fetal antigen that is present in blood in very small quantities;
high levels are encountered in epithelial cancers of the ovaries. a-
fetoprotein is produced by the fetal yolk sac and its serum level is very
low in normal individuals. Tissues with malignant degeneration have the
ability to synthesize and secrete this protein and a serum level
.10 000mg/ml is almost always seen in non-seminoma germ cell
tumours. Its half life is 5 days (b hCG’s half life is 1 day); therefore, it needs
time to achieve a lower level following successful treatment of these
tumours. False elevation in alpha-fetoprotein can be encountered in
hepatocellular carcinoma and other hepatic pathologies (e.g. hepatitis and
cirrhosis).

12) a.
At least 90% of Burkitt’s patients have a translocation between c-myc
(long arm of chromosome 8) and at least one of the following:
immunoglobulin heavy chain locus on chromosome 14, kappa light chain
locus on chromosome 2, or lambda light chain locus on chromosome 22.

13) d.
Her-2 receptor is one of the epidermal growth factor receptors which are
important in the cellular transduction activation pathways controlling
epithelial cell growth, differentiation and angiogenesis. There is over-
expression of these cell surface receptors in 20% of breast cancer
patients; a target for trastuzumab (Herceptinw). BRCA1 and BRCA2
mutations increase the risk of hereditary breast (and ovarian) cancers.
Mutations in the p53 tumour suppressor gene are seen in many cancers
(like lung and colon).

14) b.
Selective IgA deficiency has a prevalence of 1:700 population and 1:333
blood donors. Up to 45% of these have antibodies against IgA; a situation
that may result in severe anaphylactic reaction upon receiving blood or
blood product. Usually other immunoglobulins are normal; however,
serum IgG2 subtype may be low and low molecular weight IgM may be
raised. There has no curative therapy and regular immunoglobulin
replacement has not been successful. The only management is proper
treatment and prevention of infections.

15) b.
This is the classical scenario of INF-gR1 mutation on chromosome 22.
Asplenic patients or patients with hypogammaglobulinaemia are
predisposed to infection by encapsulated organisms. Deficiencies of the
late complement components (C5–9) carries a risk of disseminated
Neisseria infections. CMV retinitis is especially seen in advanced HIV
infection (CD4þ count ,50/ml3).

292

© 2008 by Taylor & Francis Group, LLC

16) a. Clinical sciences: Answers
The CD40 ligand (CD154) is present on the surface of B cells and
activated CD4þ T cells; the interaction between CD154 and CD40
results in antibody isotype switching from IgM to IgA and IgG. Failure of
this process will result in low serum IgA and IgG with increased number
of IgM (which are polyclonal and sometimes of low molecular weight).
The DNA-dependent kinase is mutated in ataxia telangiectasia which
shows a combined selective IgA deficiency and defective T-cell function.
Janus kinase (JAK) III mutations on chromosome 19 and adenosine
deaminase mutations are parts of the abnormal targets in severe
combined immune deficiency syndrome with abnormalities in B, T and
natural killer cells. Mutated CD18 affects leucocyte adhesion molecule
type 1. The mutated IL-2Ra in lymphoproliferative syndrome results in
poor T-cell responses, impaired apoptosis, increased bcl-2 and
autoimmunity.

17) d.
Hepatic nuclear factor 1a mutation is responsible for two-thirds of cases
of MODY in the UK. Hyperglycaemia in these cases is mainly seen in
adolescents and is usually progressive, requiring antidiabetic medication.
Mutations in the glucokinase gene cause 10% of cases of MODY, and
usually mild hyperglycaemia is present at birth and can be controlled with
diet alone. All MODY types are inherited in an autosomal dominant
pattern.

18) c.
The clinical scenario only fits Wiscott–Aldrich syndrome. Survival
beyond adolescence is rare and most patients die from overwhelming
infections, haemorrhagic complications and Epstein–Barr virus-
associated malignancies. Serum IgG may be normal or low. It is one of the
diseases that impairs both humeral and cell-mediated immunities; other
diseases are purine nucleoside phosphorylase deficiency, cartilage-hair
hypoplasia, ataxia telangiectasia and MHC class I and II deficiencies.

19) a.
Serum levels of IgA, IgM and IgG are normal as is the peripheral count of B,
T and NK cells. In spite of blood and sputum eosinophilia, chest allergic
symptoms are usually absent. Histopathological examination of lymph
nodes and spleen reveals striking eosinophilia. The eczematous skin rash
is not atopic and is usually not persistent (unlike that of Wiskott–
Aldrich). Residual pneumatoceles usually follow recurrent chest
staphylococcal infections. Low serum levels of IgG are seen in, for
example, common variable immune deficiency syndrome and X-linked
agammaglobulinaemia.

293

© 2008 by Taylor & Francis Group, LLC

Clinical sciences: Answers20) b.
These episodic brawny non-pitting oedemas usually involve the
extremities, but external genitalia and mucosal surfaces (especially the
upper aerodigestive system) can also be involved. Many attacks have no
clear-cut precipitants, but some form of trauma (usually pressure) is
usually implicated. Many patients notice increased attack frequency when
they are emotionally upset. Between attacks, serum levels of C2 and C4
are low and they further decrease during attacks; serum C3 is
characteristically normal during and between attacks. Fresh frozen
plasma infusion usually terminates these episodes and long-term danazol
therapy is useful to elevate the endogenous level of C1 inhibitor. About
85% of hereditary angioedema cases are associated with quantitatively
abnormal C1 inhibitor; the rest (15%) have abnormal function of
that enzyme.

21) d.
The T cells form about 75% of the lymphatic cell pool, and CD4þ cells
constitute around 65% of the T-cell population, and the remainder are
CD8þ cells. CD3 is part of the T-cell receptor complex and is present
virtually on all T-cells (not B-cells). TH1 CD4þ cells recognize antigen on
the surface of macrophages and are the maestro of cell-mediated
immunity by secreting interleukin-2 and interferon-g. TH2 CD4þ cells
recognize antigens on the surface of B cells, and when activated they
enhance humoral immunity by secreting interleukin-4, -5, -6 and -10.
CD4þ cells interact with antigen on antigen-presenting cells in
association with MHC class II, while CD8þ cells recognize antigen on the
surface of macrophages in association with MHC class I.

22) b.
TNF-a is secreted by macrophages and activates T and B cells. This
cytokine enhances angiogenesis, potentiates acute phase responses and
stimulates the secretion of interleukin-6 and GM-CSF. Note that TNF-b
is secreted by activated T-lymphocytes. TH1 cell responses enhance the
synthesis and secretion of TNF-a.

23) c.
Questions about NNT (number needed to treat), absolute risk reduction
and relative risk reduction are very common in the MRCP examinations.
Absolute risk reduction (ARR) is calculated as ARR ¼ treated
group2control group; this study produced an ARR of 4%. Relative
risk reduction (RRD) is measured as RRR ¼ (treated group2control
group)/treated group; this study demonstrates an RRR of 36%. NNT is
obtained by dividing 1 by the ARR; 25 patients need to be treated to
prevent one cerebral vasospasm.

294

© 2008 by Taylor & Francis Group, LLC

24) e. Clinical sciences: Answers
The positive and negative predictive values of various tests for the
screening/diagnosis of disease can be calculated from:

Positive testing Disease present Disease not present
Negative testing A B
C D

Positive predictive value reflects the percentage of individuals who test

positive and who actually have the disease, while the negative

predictive value reflects the true percentage of individuals who are

negative for the test and who do not have the disease. Positive predictive
value ¼ A/(A þ B); it is 86% in this question [95/(95 þ 15)]. Negative
predictive value ¼ D/(C þ D).

25) b.
The sensitivity and specificity of various tests for the screening/diagnosis
of diseases can be calculated from:

Positive testing Disease present No disease present
Negative testing A B
C D

Sensitivity ¼ A/(A þ C); it is 98% in this question [98(98 þ 2)].
Specificity ¼ D/(B þ D).

26) c.
At the end of a research project, the question needs to be asked ‘is there
any difference between the two samples studied?’. The null hypothesis
always states that there is no difference between the studied groups, e.g.
there is no difference between disability scores in patients taking a novel
medication and those taking conventional therapy for multiple sclerosis.
A type I error is said to be present when the null hypothesis is rejected
when it is in fact true. A type II error occurs when the alternative
hypothesis (fails to reject the null hypothesis) is rejected when it is in fact
true. Note that clinical significance does not correspond to statistical
significance.

27) e.
Parametric tests use normally distributed data; these tests are the
Student’s t-test and the Pearson’s coefficient of linear regression. As well
as the first four options, Kandall’s and Sign tests are non-parametric tests
which are based on ‘ranks’.

28) b.
Cross-sectional studies are ideal for detecting the prevalence of a disease
in a given population, while the incidence of a disease in that population
is better studied using a cohort study.

295

© 2008 by Taylor & Francis Group, LLC

Clinical sciences: Answers29) e.
Note the data given are not normally distributed and have been provided
with a contingency 2Â2 table. This makes the chi-square test the test
of choice.

30) d.
Note that the data can be assumed to be normally distributed and the use
of a parametric test, like the Student t-test, is reasonable. However, as
two groups are being compared for one variable, a ‘paired’ Student t-test
is the correct answer. Anderson–Darling and Kuiper’s tests are non-
parametric tests.

31) d.
The activity of leucocyte alkaline phosphatase reflects an increased
intracellular metabolic activity. Its main use is to differentiate between
leukaemoid reaction and the chronic phase of chronic myeloid leukaemia
(CML). The LAP score is decreased in the chronic phase of CML (while
the blastic crisis has an increased activity and score), paroxysmal
nocturnal haemoglobinuria and some cases of myelodysplastic
syndromes. Apart from paroxysmal nocturnal haemoglobinuria, the
other options are associated with increased LAP score.

32) c.
The supravital stains (methylene blue and brilliant cresyl blue) are used
to demonstrate the presence of RNA aggregates in reticulocytes;
Howell–Jolly bodies, Pappenheimer bodies and Heinz bodies also take the
stain. This stain is used clinically to demonstrate polychromasia,
denatured haemoglobin (as in G6PD deficiency) and haemoglobin-H
disease.

33) d.
The impaired respiratory burst in chronic granulomatous disease of
childhood renders the nitroblue tetrazolium reduction test negative. In
this test, the peripheral blood neutrophils are incubated with an activating
agent and nitroblue tetrazolium; the neutrophils release superoxide upon
activation and this would normally reduce the dye into insoluble dark blue
formazan (practically seen as granular precipitate within neutrophils). The
routine haematoxylin/eosin staining in these patients is unremarkable.
Non-specific esterase is positive within blasts of acute lymphoblastic
leukaemia and acute myeloblastic leukaemia M4 and M5 subtypes. Bone
marrow Prussian blue stain is used for iron stores.

34) c.
The myeloid antigens are CD33, CD34, CD117 and HLD-DR. The
lymphoid antigens are CD3, CD5, CD10, CD19, CD20 and CD22.
Monocytic antigenic markers are CD4, CD11b, CD11c, CD64 and
CD36.

296

© 2008 by Taylor & Francis Group, LLC

35) d. Clinical sciences: Answers
p53 is a tumour suppressor gene that plays a central role in the control of
apoptosis during cellular division. It is mutated in many cancers of the
breast and colon, and is the fundamental defect of Li–Fraumeni
syndrome. Other options are proto-oncogenes.

36) c.
The hepatocytes form only about 60% of the total liver cellular mass.
Kupffer cells are fixed macrophages that sit in the space of Disse. Ito
(stellate) cells are fat-storing mesenchymal cells that are very important
in the storage of vitamin A; in liver cirrhosis, Ito cells transform
themselves into collagen-forming myofibroblasts. In normal conditions,
liver portal tracts have a few scattered lymphocytes and an even smaller
number of other inflammatory cells; however, in inflammatory diseases of
the liver and chronic liver disease, these cells increase prominently in
number and arrange themselves into lymphoid follicles. About two-thirds
of the liver blood supply comes from the portal vein; the remainder is
from the hepatic artery. This dual blood supply is responsible for the red
colour of liver infarctions.

37) c.
The apex is formed by the left ventricle. The free wall of the right
ventricle is usually 4 mm thick while that of the left ventricle may reach
15 mm. The normal pericardial fluid is ,20–30 ml. The AV node lies in
the interatrial septum just above the orifice of the coronary sinus. The
Z-lines separate the myocyte sarcomeres; this is seen with the aid of
electron microscopy.

38) e.
The vertebral arteries unite to form the basilar artery which runs in a
groove on the ventral (anterior) surface of the pons. The anterior
communicating artery connects the proximal portions of both anterior
cerebral arteries. The inferiomedial temporal lobe is supplied by the
posterior cerebral artery; posterior cerebral arteries are the cephalic
continuation of the basilar artery. The internal carotid artery gives rise to
the anterior choroidal artery, ophthalmic artery and anterior cerebral
artery, and continues as the main stem of the middle cerebral artery.

39) a.
Woven bone is not normally found in the adult skeleton; it is seen in areas
of bone fractures, bone restructuring diseases (e.g. renal osteodystrophy)
and chronic osteomyelitis. The newly formed bone is not solid and is
composed mainly of haphazardly arranged collagen fibres.

297

© 2008 by Taylor & Francis Group, LLC

Clinical sciences: Answers40) c.
The size and structure of melanosomes together with the type of melanin
determine the skin colour; the number of melanocytes has no effect
on skin colour. The upper dermis is the papillary dermis while the
reticular dermis forms the lower part. Melanocytes are found in the basal
layer of the epidermis. The epidermis is clearly demarcated from the
dermis by the dermo-epidermal junction.

41) e.
The vasa recta supply the inner and outer medulla and participate in the
counter-current exchange system of fluids and minerals. Although 170 L
of fluids are filtered by the kidneys each day, the tubular reabsorption
of that filtrate lessens it to only 1 L. Both kidneys receive about 20–25%
of the cardiac output. The juxtaglomerular apparatus is composed of
macula densa (of the distal convoluted tubules), juxtaglomerular cells
(of the afferent arterioles) and Lacis non-granular cells.

42) c.
Insulin cell surface receptors have an intracellular domain with tyrosine
kinase activity. G-protein-coupled receptors are beta-adrenoceptors and
acetylcholine (muscarinic) receptors. Acetylcholine (nicotinic) and
glutamate receptors are examples of ligand-gated ion channels. Steroid
receptors are nuclear.

43) b.
Albumin has the largest capacity to bind T4 while thyroid-binding globulin
has the highest affinity to bind that hormone. Under normal conditions,
about 99.98% of T4 is bound and the remainder is the free fraction. The
half-life of T4 is about 7 days. Many medications and drugs can raise the
serum concentration of T4-binding proteins, resulting in an increase in the
serum levels of total T4 while leaving the free fraction constant and
the TSH unchanged; oestrogen, heroin, methadone and clofibrate are
the usual culprits, as well as pregnancy. In contrast, glucocorticoids,
L-asparginase, androgens and danazole decrease the serum levels of
T4-binding proteins; the net result is a reduction in the serum
concentration of total T4, but again this does not affect the free T4
fraction and TSH.

44) e.
A cardiac ectopic beat or an unsynchronized DC shock that coincides
with the vulnerable period might easily precipitate ventricular fibrillation.
This vulnerable period lies in the mid-portion of the Twave, i.e. when part
of the myocardium is depolarized, part is partially repolarized and part is
completely repolarized. This constellation produces a highly favourable
environment for establishing a re-entry and circus movement.

298

© 2008 by Taylor & Francis Group, LLC

45) b. Clinical sciences: Answers
The adrenal cortical enzyme 21b-hydroxylase catalyses the formation of
11-deoxycorticosterone and 11-deoxycortisol from progesterone and
17-hydroxyprogesterone, respectively. The latter two products will enter
the cell mitochondria to undergo hydroxylation resulting in the formation
of corticosterone and cortisol by the action of the cytochrome
enzyme 11b-hydroxylase. These hormones are present in the zona
reticularis and fasciculata from where they diffuse into the systemic
circulation.

Cholesterol

Pregnenolone a Progesterone b 11-Deoxycorticosterone c Corticosterone f Aldosterone

17-hydroxylase 17-hydroxylase

17OH-Pregnenolone a 17OH-Progesterone b 11-Deoxycortisol c Cortisol

17,20-lyase 17,20-lyase

Dehydroepiandrosteron a Androstenedione d Testosterone e Dihydrotestosterone

aromatase d aromatase
Oestron Oestradiol

(a) = 3b-hydroxysteroid dehydrogenase
(b) = 21-hydroxylase
(c) = 11b-hydroxylase
(d) = 17b-hydroxysteroid dehydrogenase
(e) = 5a-reductase
( f ) = aldosterone synthetase

Diagram illustrating the major steroid biosynthetic pathways in the
adrenal cortex. Note that many enzymes catalyse these reactions;
therefore, congenital adrenal hyperplasias have diverse manifestations
due to the accumulation of certain metabolites and deficiency in others.

46) d.
Fibres from the olfactory mucosa high up in the nasal cavity enter the
anterior cranial fossa through the cribriform plate of ethmoid bone to
terminate in the mitral cells of the olfactory bulb. The amygdala are
involved in the emotional reflexes and responses towards olfactory
stimuli while the entorhinal cortex is probably involved with olfactory
memories. The calcarine cortex is concerned with vision.

299

© 2008 by Taylor & Francis Group, LLC

Clinical sciences: Answers47) c.
Cholecystokinin-pancreozymin (CCK-PZ) is a gut hormone that is
secreted by the I-cells of the upper small bowel. However, it is also found
in the brain (mainly in the cerebral cortex) and in the peripheral nerves in
the body. It has a multitude of effects: contraction of the gallbladder,
stimulation of the pancreas to secrete its juices rich in enzymes, inhibition
of gastric secretion and emptying (and perhaps contraction of the
pylorus), stimulation of the release of enterokinase (and enhancing the
motility of the small and large bowels) and (together with gastrin)
stimulation of the secretion of glucagon (i.e. control of blood glucose).

48) a.
The first step is the combining of acetyl-CoA with oxaloacetate to form
citrate. This is followed by a series of reactions ending in the formation of
oxaloacetate which forms pyruvate thereafter. The Krebs cycle is the
major oxidation pathway for carbohydrates and fats (and some amino
acids as well). Aerobic metabolism of 1 mol of blood glucose via the Krebs
and Embden–Meyerhof pathways yields 38mol of ATP.

49) b.
The fear reaction can be reproduced consciously in animals by stimulating
the amygdala and hypothalamus. Damage to the amygdaloid nuclei will
prominently abolish the fear reaction and its autonomic manifestations.
Frontal eye field 8 is concerned with saccadic eye movements.

50) c.
Factors that shift the oxyhaemoglobin dissociation curve to the right (and
hence facilitate O2 delivery to tissues) are: rise in body temperature
(fever and hyperthermia), increased concentration of red cell 2,3-DGP
(this is low in banked blood; its synthesis is increased by anaemia) and
reduction in blood pH (acidosis; chronic renal failure would produce
systemic acidosis). Fetal haemoglobin has low affinity for 2,3-DGP;
consequently, red cells rich in fetal haemoglobin have greater affinity for
O2 and this facilitates the movement of O2 from the maternal blood to
the fetal blood.

300

© 2008 by Taylor & Francis Group, LLC

51) Clinical sciences: Answers

Hypothermia, Percentage
O2
Alkalosis, saturaƟon
of
100 Decreased Hemoglobin
PCo2, (0–100%)
Decreased

RBCs 2,3-DGP,

Carboxyhaemo-

globin, Foetal

Haemoglobin

50 Fever,
Acidosis,
Increased
PCo2,
Increased
RBCs 2,3-
DGP,
Hypoxia,
Sickle Cell
Anemia

0 100
26
PO2 (mmHg)

Oxyhaemoglobin dissociation curve illustrating factors that
‘shift’ the curve to the right or left. Note that at 26mmHg
partial pressure of O2, 50% of the haemoglobin is saturated (the
so-called P50).

301

© 2008 by Taylor & Francis Group, LLC