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340 Physiological changes occurring in pregnancy
Table 16.1 The foetus contains 50% genes from the father. These could render the foetus as for-
eign material which could be rejected by the mother’s immune system. Here are some
reasons why the maternal immune system does not attack and reject the foetus, i.e. the
foetus becomes an immunological privileged site
Subject Mechanism
Placenta Forms a barrier to the immune system between the mother and
the foetus.
Neurokinin B This comes from the placenta and contains phosphocholine
which binds with proteins to form compounds that suppress the
maternal immunity.
Trophoblasts Produced by the placenta, these cells lack certain HLA
1
molecules. These HLA molecules would trigger an immune
response from the mother. Their absence allows the foetal cells
to prevent an attack from maternal immunity cells.
Lymphocytic suppressor cells These cells block maternal immunity T-cells
2
from destroying the
foetus.
Syncytium
3
The placental cells have very little extracellular space between
them. This results in a barrier that prevents potential antigenic
cells from moving out of the placenta and reaching the maternal
immune system.
PREGNANCY
Corpus
luteus
Ovary
LABOUR
Cortisol
CRH
ADRENAL ADRENAL
Cortisol
CRH
ACTH
ACTH
AL PL
PITUITAR
Y
GLAN
D
P
r
o
l
a
c
t
i
n
BREAST
O
x
y
t
o
c
i
n
Prostaglandins
˜
relaxin
O
e
s
t
r
a
d
i
o
l
Progesterone
U
T
E
R
U
S
Figure 16.2 The main hormones in pregnancy and labour. Left: During pregnancy, the ovarian cor-
pus luteum produces oestrogen (oestradiol) and progesterone until it is replaced by the
placenta, which takes over the production of these hormones, and the corpus luteum
then disappears. The placenta also produces corticotropin-releasing hormone (CRH),
which stimulates adrenocorticotropic hormone (ACTH) from the pituitary gland (ante-
rior lobe, AL), and this then stimulates cortisol from the adrenal cortex. Prolactin, also
from the pituitary gland (anterior lobe, AL), prepares the breasts for lactation. Right:
During labour, oxytocin, from the pituitary gland (posterior lobe, PL), contracts uterine
muscles to expel the baby, along with some prostaglandins and the hormone relaxin
and also allows the cervix to dilate.
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Physiological changes occurring in pregnancy 341
Thyroid-stimulating hormone (TSH) from the pituitary is raised slightly at the end of
the rst trimester but is otherwise remains stable in pregnancy. The free thyroid hormones
(T
3
and T
4
; see Chapter 4) are normally a little lower in the second and third trimesters.
Biochemical changes
Iron, folate and iodine requirements during pregnancy are increased. Iron intake should
increase by as much as 2 to 3 times when pregnant. Iron is required for both maternal and
foetal haemoglobin.
Folate (vitamin B
9
) intake should increase by 10 to 20 times. Folate is essential to pre-
vent foetal neural tube defects (NTDs) such as spina bida (a defect of the spinal cord)
and anencephaly (a serious defect of the head and brain). Additional supplements of folic
acid in the maternal diet, starting just before becoming pregnant, and for up to 12 weeks
of pregnancy, are usually recommended.
Iodine intake during pregnancy should rise from the average 100 mg/day before preg-
nancy to 150–200 mg/day during pregnancy. Iodine in pregnancy is required for the
foetus, and a shortage in the diet may induce a maternal goitre (i.e. enlargement of the
thyroid gland).
Twice as much vitamin B
12
(see Table 7.3, page 142) than normally consumed is also
required during pregnancy to prevent maternal anaemia and for the foetal blood.
Glucose and lipid metabolism undergo signicant changes during pregnancy in order
to supply both mother and foetus with glucose for energy. These changes involve an
increase in pancreatic beta cells producing higher levels of insulin. However, insulin
resistance starts to occur in the second trimester and peaks during the third trimester.
This resistance is due to a cocktail of hormones, including progesterone and cortisol,
that disturb peripheral insulin receptor efciency. Foetal glucose uptake and additional
glucose storage as glycogen in the maternal tissues may contribute to a relative hypogly-
caemia. Lipolysis provides an additional source of energy as serum cholesterol, notably
low-density lipoproteins, LDL (see Figure 4.5, page 75) and triglycerides rise during preg-
nancy. The higher LDL level becomes important as a substrate in the production of ste-
roidal hormones in the placenta. The rise in triglycerides may provide more of the energy
needs for the mother, thus allowing the foetus to use the glucose.
Protein metabolism mainly involves providing the additional required amino acids
for foetal growth and development. Much of these extra amino acids will come from the
maternal diet by increasing protein intake. The normal turnover and breakdown of the
mother’s protein is reduced to allow fat reserves to be preferentially used for maternal
energy.
Calcium is required for foetal growth, particularly during the third trimester when
development of the skeleton is increasing. The main source of calcium is the maternal
diet, and calcium absorption from the digestive tract is signicantly increased after 12
weeks gestation. Maternal bone absorption and replacement also increases in the third
trimester, providing additional calcium for the foetus.
Renal and uid balance changes
The hormone relaxin is produced by the corpus luteum and placenta, and the level rises
to a peak in the rst trimester. Relaxin stimulates the production of other hormones called
endothelins (ETs), the most important being ET-1. These bind to two types of endothelin
receptors, ET
A
and ET
B
. The binding of ET-1 to these receptors in smooth muscle causes
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342 Physiological changes occurring in pregnancy
arterial vasoconstriction, and therefore a rise in blood pressure. In cardiac muscle it
increases the force of contraction. ET
B
receptors are also found on the endothelial lin-
ing cells of arteries. When endothelin binds to the endothelial ET
B
receptors, nitric oxide
(NO) is produced, and this reduces ET-1 production causing vasodilation and reduc-
ing the blood pressure. This is particularly important regarding the renal arteries, which
dilate, creating an increase in the renal blood ow during pregnancy (Figure 16.3).
The result of increased renal blood ow is a rise in the glomerular ltration rate
(GFR) (see Chapter 8). The kidneys enlarge slightly to accommodate the increased vas-
cular glomeruli and raised urinary volumes. Dilation of the urinary collecting system
within the kidneys can lead to a mild hydronephrosis, an accumulation of urine in the
kidney, in as many as 80% of pregnant women, with some degree of urinary stasis.
Glucose is normally excreted by the glomerulus and then fully reabsorbed (see
Chap-
ter8), but in pregnancy the reabsorption is not as effective, and therefore about 90% of
pregnant women have some glucose in their urine. This should return to normal after
delivery. High levels of glucose in the urine may be the sign of gestational diabetes.
E
N
D
O
T
H
E
L
I
A
L
C
E
L
L
S
S
M
O
O
T
H
M
U
S
C
L
E
C
E
L
L
S
A
N
D
C
A
R
D
I
A
C
M
U
S
C
L
E
C
E
L
L
S
NO
ET-1
Ca
2+
IP
3
ET
B
ET
A
SR
ET
B
Figure 16.3 Endothelin (ET-1) is released from endothelial cells lining blood vessels and binds
to two ET receptor types, ET
A
and ET
B
on vascular smooth and cardiac muscle cells.
ET-1 binding to both receptor types raises (↑) IP
3
, an intracellular messenger molecule.
Raised IP
3
causes release of calcium (Ca
2+
) from the cell’s sarcoplasmic reticulum (SR)
and this causes smooth muscle contraction (i.e. vasoconstriction) and increased car-
diac muscle contraction (i.e. increased cardiac output) both leading to raised blood
pressure. ET-1 binding to ET
B
receptors on the endothelial cells causes production of
nitric oxide (NO) which reduces (↓) ET-1 production.
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Physiological changes occurring in pregnancy 343
This may return to normal or it may require investigation and treatment (NHS 2022).
Similarly, protein and uric acid may appear in the urine when the kidney’s ability to
prevent this loss is compromised.
Antidiuretic hormone (ADH), a hormone from the hypothalamus via the posterior
pituitary gland, increases in pregnancy, causing water retention and hypervolaemia. The
maternal blood volume increases by 45%, with plasma volume increasing by 30–40%,
rising to 50–60% by the end of pregnancy. Extracellular uid also increases by 30–50%.
The volume increase in circulation is important for the maintenance of the blood ow to
the uterus and placenta.
Sodium retention in pregnancy is the result of activation of the renin-angiotensin-
aldosterone cycle (see Figure 3.6, page 47). Aldosterone conserves sodium from the sec-
ond convoluted tubules and collecting ducts of the nephron (see page 162), and the level
of aldosterone in circulation rises steadily throughout pregnancy. Sodium retention is
partly the reason for the hypervolaemia since higher levels of sodium in the blood attracts
water back into circulation (see Chapters 3 and 8). However, sufcient sodium is still lost
in the urine to prevent sodium overload, and this is the result of the increased GFR, which
is excreting more sodium, combined with the anti-aldosterone effect of progesterone.
Pre-eclampsia and eclampsia
As identied above, normal blood pressure falls by mid-pregnancy and then returns to
normal by full term (Figure 16.1). Pre-eclampsia is a condition that occurs in 5–7% of
pregnant women, mostly in late pregnancy (after 20 weeks gestation). It is characterised
mainly by high blood pressure (Tables 16.2 and 16.3) and protein in the urine. It may
progress, and it sometimes leads to the onset of seizures (called eclampsia).
The symptoms of pre-eclampsia include any combination of the following:
• high blood pressure (see Chapter 3 and Tables 16.2 and 16.3)
• protein in the urine (called proteinuria; see Chapter 8) and reduced urine output (olig-
uria; see Chapter 8)
Table 16.2 The systolic and diastolic pressure values for normal blood pressure, mild, moderate and
severe hypertension
Blood pressure Systolic (mmHg) Diastolic (mmHg)
Normal
Mild hypertension
Moderate hypertension
Severe hypertension
110–120
140–149
150–159
> 160
70–80
90–99
100–109
> 110
Table 16.3 Terms used for hypertension at different stages of pregnancy. Chronic hypertension is
probably pre-existing before pregnancy and is therefore unrelated to the pregnancy.
Gestational hypertension is due to the pregnancy
Gestation (week when rst discovered) Type of hypertension
0–20 Chronic (pre-existing)
20–40 Gestational
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344 Physiological changes occurring in pregnancy
Table 16.4 Red and amber ag warnings of deteriorating condition
O Red Flag = serious situation which needs urgent medical attention.
O Amber Flag = important to get a medical assessment as soon as possible.
Flag Details
warning
O Red Flag
Abdominal pain or asthma attack during pregnancy.
Vaginal bleeding or discharge.
Seizures during pregnancy (eclampsia).
O Amber Flag Contact with chicken pox, measles, scarlet fever, rash, inuenza or shingles
during pregnancy.
Fever during pregnancy.
Diarrhoea, vomiting with weight loss or headache during pregnancy.
Urinary infection.
Symptoms of high blood pressure (pre-eclampsia).
(After Hill-Smith and Johnson 2021, with permission)
• severe headaches
• excessive vomiting and nausea (see Chapter 9)
• dizziness (vertigo; see Chapter 9)
• rapid weight gain and swelling of the legs, feet and hands, caused by uid retention
(see Chapter 6)
• abdominal pain.
Pre-eclampsia must be recognised as early as possible and intervention is required
quickly. Complications include liver and kidney malfunction, hypercoagulability of the
blood (due to raised levels of clotting factors) leading to increased risk of circulatory
thrombosis, pulmonary oedema and the risk of seizures (eclampsia). The mother and
baby may both be at risk of harm.
The pathology of pre-eclampsia is complex and not fully understood, but it does
appear that the placental is central to the problem (Hladunewich et al. 2016). Abnormal
arterial disease within the placenta prevents adequate blood ow through the placenta,
reducing oxygen and nutrient exchange with the foetal circulation. The very early stages
of the disease may be asymptomatic, and this may be the reason diagnosis is delayed
until later in the pregnancy. Termination of the pregnancy (and therefore removal of the
placenta) at the earliest possible time preterm, provided the child is survivable outside
the uterus, may be the only way available to safeguard the mother and child against
further harm.
Eclampsia is the presence of tonic-clonic seizures (see Chapter 11, page 235) dur-
ing pregnancy as a result of raised blood pressure. It is a severe complication of pre-
eclampsia and affects about 1 in 200 pregnant women who had previously developed
pre-eclampsia.
Key points
• The maternal changes in pregnancy are normal, and they accommodate and sustain a
developing child.
• There are three stages of pregnancy, the rst (weeks 1 to 12), second (weeks 13 to 27)
and third (weeks 28 to 40) trimesters.
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Physiological changes occurring in pregnancy 345
• Blood changes during pregnancy provide the foetus with nutrition and uid.
• Blood pressure drops slightly over the rst half of pregnancy but restores to normal by
full term.
• The heart becomes enlarged during pregnancy, with a greater force of contraction and
in labour cardiac output increases by 15% (rst stage) and by 50% (second stage).
• Blood clotting factors increase in pregnancy to prevent bleeding during birth, but this
leads to an increased risk of thrombosis.
• There is 20% increase in oxygen consumption during pregnancy.
• Progesterone remains high in pregnancy to maintain the endometrium, and oestrogen
rises.
• Oxytocin reaches a peak at the onset of labour and causes uterine contractions and
dilation of the cervix.
• Folate (vitamin B
9
) intake should increase in pregnancy in order to prevent foetal neu-
ral tube defects. Iron and iodine intake should increase also.
• Glucose and lipid metabolism changes occur in pregnancy to supply energy to mother
and foetus.
• Renal changes in pregnancy include an increase in the glomerular ltration rate (GFR),
sodium and water retention due to increased aldosterone, and the loss of some glucose
in the ltrate.
• High blood pressure and protein in the urine are symptoms of pre-eclampsia.
• Eclampsia means seizures occur as a result of the high blood pressure.
Notes
1 HLA is a group of human leukocyte antigens which nucleated cells produce on their surfaces.
They are part of the cells ability to regulate the immune system.
2 T-cells are part of the body’s immunity which can destroy cells that are foreign (antigenic cells).
3 Syncytium is a collection of cells closely united and acting together as a single unit.
References
Hill-Smith I. and Johnson G. (2021) Little Book of Red Flags. National Minor Illness Centre,
Bedfordshire.
Hladunewich M., Karumanchi S.A. and Lafayette R. (2016) Pathophysiology of the clinical manifes-
tations of preeclampsia. Clinical Journal of the American Society of Nephrology, 2(3): 543–549.
http://doi.org/10.2215/CJN.03761106
National Health Service (NHS) (2022) www.nhs.uk/conditions/gestational-diabetes/ (Accessed 3rd
March 2023). Due for update 8th December 2025.
Soma-Pillay P., Nelson-Piercy C., Tolppanen H., Mebazaa A., Tolppanen H. and Mebazaa A. (2016)
Physiological changes in pregnancy. Cardiovascular Journal of Africa, March–April, 27(2): 89–94.
http://doi.org/10.5830/CVJA-2016-021
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Index
25-hydroxycholecalciferol see vitamins, D
ABCDE: mole (nevi) changes 216; physical
assessment
113–114
abducens nerve (cranial nerve VI) 272
ABO blood groups 93–94
absences (petit mal ts) see ts
accommodation (of the eye) 273
acetoacetic acid 166
acetone 7, 166, 168
acetylcholine 299, 317
acetyl-CoA (acetyl coenzyme A) 2, 7
acetylsalicylic acid (aspirin) 16, 18–19,
188, 258
acid-base balance (in urine) 173
acidosis 174
acne 213
acrophobia 325
acupuncture 264
acute renal failure 164
Addison disease 70, 83
adenosine diphosphate (ADP) 2, 5–6;
triphosphate (ATP) 2, 5–6, 166
adipose 148, 201
adjuvant therapy 263–264
adrenaline 54, 81–82
adrenocorticotropic hormone (ACTH)
81–82, 339
A/G ratio 68–69
agglutination (of blood) 94
agonist (drug) 120, 315, 329
air: hunger 108; pressure 12–13; rareed 108
akathisia 300, 322
akinesia 299, 322
alanine aminotransferase (ALT) 80
albumin 67–68, 171
albuminuria 171
aldosterone 54, 79, 157, 162–163, 170
alkaline phosphatase (ALP) 80
alkalosis 106–107, 174
allergies 330–331
alopecia 327–328
alpha-fetoprotein (AFP) 71
alpha receptor 60
altered states of consciousness 230–231, 240
alveolar: air 99, 102; ventilation rate (AVR) 103
alveoli 98–99
Alzheimer disease (AD) 95
amino: acids 7, 136–137, 148; group 7, 137
ammonia (NH
3
) 8, 76, 168
amygdala 224
amylase 80, 141
amyotrophic lateral sclerosis (ALS) 177, 302
amyotrophy 302
anabolism 79
anaemia 83, 92; haemolytic 92, 173; iron-
deciency 78, 93, 144; pernicious 73,
93, 142; sickle-cell 92
anaesthetic drugs 242–243
analgesia 257–265, 327; patient-controlled
(PCA) 264–265; spinous 260; supra-
spinous 260
analgesic ladder 262–263
anaphylactic shock (anaphylaxis) 55–56, 330
angina 24, 37, 327
angiotensin 46, 80
angiotensin converting enzyme (ACE) 47, 80
anions 131–132
anorexia (loss of appetite) 148, 317, 324
antagonist (drug) 315, 329
anterior cingulate cortex (gyrus) 221–222
anti-arrhythmic drugs 36–40
antibiotics 184–185, 187, 314
antibodies (immunoglobulins) 86–88, 330–331
anticholinergics 195
anticipatory nausea and vomiting (ANV) 191
anticoagulant drugs 87
antidiuretic hormone (ADH) 54, 81–82, 157,
162–163
anti-emetics 195
antigen 91, 93–94, 330
antihistamines 195, 324
antimuscarinic side effects 318–319
antioxidants 74
antipyretic drugs 18–19
anuria 164
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Index 347
aorta 24
aortic valve 24
apex beat 29–30
Apgar score 115
aphasia 237
apneustic: breathing 105–106; centre 105
apnoea 104, 106; sleep apnoea 109
apraxia 300
arachidonic acid 18
arachnoid: mater 238–239; villi 238
area postrema 188, 195
Argyll Robertson pupil 276
arrhythmias (cardiac) 33–35
arsenic 89
arteriosclerosis 54
ascites 128
ascorbic acid see vitamins, C
aspartate aminotransferase (AST) 81
aspirin see acetylsalicylic acid
asthma 108
astrocytes 227
asystole 34
ataxia 304, 322
ataxic breathing see Biot (ataxic) breathing
atelectasis (of the lung) 100, 109
athetosis 306
atrial: brillation 33–34; utter 34; septal
defects (ASD)
30
atrioventricular: (AV) node 26; valves 23
Atwater number 2
auditory cortex (of brain) 223
auscultation 35, 49, 111
autoimmune disease 167
autonomic nervous system (ANS) 24, 299, 318
AVPU system 232
ballism 306
baroreceptors 45
basal: ganglia 291–293, 320–321; metabolic
rate 8, 551–552; motor loop
293–294
basophils 91
B-cell lymphocyte 68, 90
beriberi 72, 142
beta-adrenergic receptors 57, 60; blockers
(antagonists) 57–59, 324–325
beta hydroxybutyric acid 166
bicarbonate 76–77, 132
bicuspid valve 23
bilirubin 77, 168, 172; in urine 172
biliverdin
172, 205
binding protein C 94–95; output 26, 47;
parameters in pregnancy 337
bioavailability 312
bioelectric impedance analysis (BIA) 152
Biot (ataxic) breathing 105–106
bladder (urinary) 155–156
blood: cells 91–93; chemistry 76–79; clotting
factors 85–86; enzymes 79–81; in
faeces 183–184; fats 74–75; gas
tensions 88–89, 107; groups 93–94;
hormones 81–85; immunity 86–88; pH
88–89; plasma 65–67; pressure (BP)
42–57, 337–338, 343–344; protein
67–71; tests 65–95; toxic substances
89–90; transfusion 94; urea nitrogen
(BUN)
77; in urine 171–172; vitamins
71–74; volume 65
blurred vision 320
body: mass index (BMI) 150–152; weight
150–151
Bohr effect 112
bone marrow stem cells 90
botulism 192–193
Bowman’s capsule 156, 158–159
Boyle’s law 101
brachial artery 49; pulse 27–28
Braden (pressure sore) scale 210–211
bradycardia 28–29
bradykinesia 322
bradykinins 248–249
brain 220–226; reexes 230; stem 230
breathing 100–102; childhood 114–115
Broca’s area (of the brain) 232
Brodmann numbers 222–223
bronchi 98
bronchial pneumonia 109
bronchioles 98, 118
bronchitis 108
bronchoconstriction 98
bronchodilation 98; bronchodilators 116–119
brown fat 14
bruise (ecchymosis) 55, 205
B-type natriuretic peptide (BNP) 68–69
buffers 173–174
bulimia 148
bundle branches 25–26; of His 25–26
burns (of the skin) 211–213
cachexia 7, 148
caffeine 323
calciferol see vitamins, D
calcitonin 81–82
calcium 76–77, 144, 147, 170, 341
calculi (renal) 175
cancer fatigue syndrome (CFS) 322
cannabinoids 195
capillary rell time 21, 48
carbohydrates 140–141
carbon dioxide (CO
2
) 97, 99, 104–105,
106–109
carbonic acid 77, 104
cardiac: arrest 34, 114; arrhythmias 33–35; axis
32; centre 26; conduction 25; cycle
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348 Index
26, 33; enzymes 70–71; failure 109;
hypertrophy 54; incompetence 35;
muscle 24; myosin-cardiogenic shock 55
carotid: artery 236; chemoreceptors 45; pulse
27–28
casts (in urine) 169
catabolism (catabolic) 79, 180–181
cataracts 273–274
cations 131–132
caudate nucleus 306, 321
Celsius (centigrade) 12
central: aortic systolic pressure (CASP) 52–53;
nervous system (CNS) 289, 317;
neurogenic hyperventilation 105–106;
venous pressure (CVP) 56, 127
cerebellar ataxia 304
cerebellum 188, 293, 295–296
cerebral: anoxia 278; arteries 236; cortex
221–223; hemispheres 221; infarcts
237; lobes 221; oedema 129–130
cerebrospinal uid (CSF) 238–239, 284
cerebrovascular accident (CVA) (stroke) 234,
236–237, 300
ceruloplasmin 77
chemoreceptors 45
chemoreceptor trigger zone (CTZ) 188–189
Cheyne-Stokes respiration 105–106
childhood: blood pressure 56–57;
breathing 114–116; defecation 183;
electrocardiogram (ECG) 35; uid
balance 327; nutrition 145–147; pain
257; pulse 30; temperature 14–17;
urinary system 161
chloride (Cl) 131–133, 144
cholesterol 74–75; ratio 75
chorea 306
choreoathetosis 306
chronic: bronchitis 108; cough 110–
111;
energy imbalance 135–136;
hypertension 53–54; pain 248; protein
deciency 136–137; renal disease 164;
respiratory disease 108
circle of Willis 236–237
cirrhosis (of the liver) 193
citric acid cycle (Krebs cycle) 2–4
Clostridium botulinum 192–193
clotting factors 85–86, 337
cluster breathing 105–106
codeine 262
coenzyme Q
(CoQ ) 324
10 10
colic, digestive 184; renal 175
colostomy 187–188
colour: nail bed 48; plate 1; skin 202–204;
stools 183–184, 187–188; urine 87,
168–169; urine test sticks plate 3
coma scales 231–233
commensals 181
compensatory mechanism: (in hypotension) 54;
(in raised intracranial pressure) 240–241
complement system 88, 331–332
compression (intracranial) 237, 239
concussion 129, 237, 239
conduction: heart 25–26; heat 10; nerve
226–229
confusion 185, 231
congenital heart defects 30
congestive cardiac failure (CCF) 54, 109, 150
coning (of the brain) 241, 278
connectivity (of the brain) 220
consciousness 219–226; observations
230–233
constipation 185–186, 316, 319–320
contracoup injury 238
contusion (of the brain 239
convection (of heat) 10
copper 76–78, 144
core temperature 9
corneal reex see reexes
coronary arteries 24
corpus: callosum 221; striatum 220, 306
corticobulbar tracts 290–
291
corticospinal tracts 287–289
corticotropin releasing hormone (CRH) 339
cortisol 54, 81–82, 339
cough 110–111; reex (see reexes)
coupled beats 39
C-peptide 69, 167
cranial nerves 272, 290; abducens (VI) 272;
facial (VII) 290; glossopharyngeal (IX)
290; oculomotor (III) 272, 279–280;
optic (II) 268–269; spinal accessory
(XI) 290; trigeminal (V) 290; trochlear
(IV) 272; vagus (X) 189–190, 290;
vestibulocochlear (VIII) 188–189,
231, 295
C-reactive protein 68, 70
creatine-kinase-MB 71
creatinine 78, 175; clearance 175
Crohn’s disease 184
cromoglicate see sodium, cromoglicate
crossed extensor reex 297–298
croup 111
cyanocobalamin see vitamin, B
12
cyanosis 111–112, 129, 203–204
cyclo-oxygenase (COX) 18, 258–259, 317
cystatin C 76, 78
cysteine proteases 78
cystic brosis 116
cytochrome P450 oxidases (CYP) 329
dead space (in respiration) 102
deamination (of proteins) 7
deceleration trauma 238
decerebration 304–305
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Index 349
decortication 304–305
decubitus ulcers see pressure sores
deep: coma 232; tendon reex 297
defecation 182
dehydration 130
delirium 230; post-operative 243
delta (δ) receptor 260
density of urine see urinalysis,
specic gravity
deoxyribonucleic acid (DNA) 136–137, 169
depolarisation 31
deposits (in urine) 169
dermatitis: atopic 214; contact 214, 331;
incontinent-associated 210; primary
irritant 214
dermis 199–201
dermorphins 261
D-factor (rhesus factor) 94
diabetes 7, 78, 164–168, 242; gestational
342; insipidus 164; latent autoimmune
disease in adults (LADA)
167; maturity
onset of the young (MODY) 167;
mellitus 164–168
diagonal diplopia see diplopia
diamorphine (heroin) 260–261
diarrhoea 183–185, 316
diastole 26, 28, 43
diastolic pressure 43
diffusion 99
digestion 180–182
digestive system 181
digoxin 39
dilated pupils 319–320
diplopia 281–282
diuresis 164, 166
diuretics 129, 177–178
diurnal (24 hour) pattern 13
diverticular disease 182
dizziness 324
dopamine 321; antagonist 321; receptors
195, 326
dorsalis pedis pulse 27–28
dorsal respiratory group (DRG) 105
drowsiness 324
drugs: absorption 328; allergies 330
–333;
distribution 328–329; elimination 329;
interactions 328–330; metabolism 329;
side effects 316–328
dry: eyes 319–320; mouth 130, 319–320
Duchenne’s muscular dystrophy (DMD) 302
dura mater 238
dynorphins 252, 261
dyskinesia 300, 322; tardive 321
dyspepsia 317
dyspnoea 108, 129
dyspraxia 300–301
dystonia 322
ecchymosis see bruise
eclampsia 343–344
ectopic beats 34
eczema 214
eicosapentaenoic acid (EPA) 139
elderly: hypotension 54–55; nutrition 147–148;
trauma
205, 239
electrocardiogram (ECG) 31–35, 264
electroencephalogram (EEG) 230, 264
electrolytes (ions) 31–33, 143, 182; balance
130–132
electron transport system 3–5
elimination: drugs 329; faeces 181–188; urine
162–164, 174
embolus (emboli) 236
emesis 188
emphysema 108, 110–111
encephalitis 242
endocardium 35
endometrium 338
endomorphines 261
endorphins 252, 261
endothelin (ET) 341–342
energy 135–136, 147; balance 135–136
enkephalins 252, 261
enterococci 174
enzymes 79–81; blood 79–81
eosinophils 90–91
epidermal growth factor (EGF) 199
epidermis 197–199
epidural: infusion 264; space 264
epilepsy see ts
epileptogenic focus 234
epistaxis 193
erythema 203
erythrocytes 90–92, 172–173; sedimentation
rate (ESR) 92
erythropoietin (EPO) 82–83
Escherichia coli (E. coli) 161, 174
essential hypertension 54
expiratory reserve volume (ERV) 102, 104
extensor muscle 297–298
extracellular (tissue) uid (ECF) 122–124
extradural: haematoma 239; space 239
extrapyramidal tract: side effects 320–321;
system 195, 289–292, 320–321
eyes: anatomy 268–273; intraocular pressure
274; movements 271–272; muscles
272; papilloedema 283–284; pupils
272, 274–278
facial nerve (cranial nerve VII) 290
faecal (faeces) 181–186; blood 183–184; fat
184; mucus 184
Fahrenheit 12–13
failure to thrive (in infants) 19
fainting 204, 242, 324–325
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