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5 Endocrinology
Fig 5.
https://t.me/med1917
27
Galactorrhoea can be prolific enough to create medium- sized galaxies (bottom right).
In the Birth of the Milky Way Hera is depicted by Rubens in her chariot, being drawn through the
night sky by ominous black peacocks. Between journeys, she enjoyed discussing dicult endocrinological topics with her husband Zeus (who was also her brother), such as whether women
or men find sexual intercourse more enjoyable. Hera inclined to the latter— and it is on this flimsy
evidence, and her gorgeous galactorrhoea, that we diagnose her hyperprolactinaemia (which is
known to decrease desire, lubrication, orgasm, and satisfaction). In the end, this issue was settled,
in favour of Zeus’s view, by Tiresias, who had unique insight into this intriguing question: every time
this soothsayer saw two snakes entwined, (s)he changed sex, so coming to know a thing or two
about sex and sexual pleasure. This is a primordial example of an ‘N- oftheir own control. Generalizability can be a problem with this methodology.
1
’ trial, where the subject is
Image is in the public domain.
231
5 Endocrinology
Acromegaly
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232
This is due to secretion of GH (growth hormone) from a pitu-
99
itary tumour (
GH-
topic
Incidence:
p
217
). GH stimulates bone and soft tissue growth through
(
%) or very rarely hyperplasia, eg via ec-
releasing hormone from a carcinoid tumour. :
UK
3/ million/ yr. ~5% are associated with
secretion of insulin- like growth factor-
Symptoms Acroparaesthesia (akron = extremities); amenor-
rhoea; libido; headache; sweating; snoring; arthralgia; backache;
fig
5.28
: ‘My rings don’t fit, nor my old shoes, and now I’ve got a
wonky bite (malocclusion) and curly hair. I put on lots of weight,
all muscle and looked good for a while; now I look so haggard’.
Signs (See
by >
BOX
4
‘Signs of acromegaly’.) Often predate diagnosis
yrs. If acromegaly occurs before bony epiphyses fuse (rare),
gigantism occurs.
Complications (May present with
• Impaired glucose tolerance (~40%), DM (~15%).
• Vascular: BP, left ventricular hypertrophy (±dilatation/
cardiomyopathy, arrhythmias. There is risk of ischaemic heart
disease and stroke (?due to
induced increase in fibrinogen and decrease in protein
• Neoplasia: colon cancer risk; colonoscopy may be needed.
Acromegaly in pregnancy (Subfertility is common.) Pregnancy
may be normal; signs and chemistry may remit. Monitor glucose.
Te st s
IGF- 1:
as secretion is pulsatile and during peaks acromegalic and normal
levels overlap.
Normally
detectable. In acromegaly
• If
preferred screening test. GH Don’t rely on random GH
GH
also in: stress, sleep, puberty, and pregnancy.
GH
secretion is inhibited by high glucose, and GH hardly
IGF-1
(p
226
), an oral glucose tolerance test (
GH
If the lowest
value during
acromegaly is confirmed. With general use of very sensitive assays, it has been said that this cut- o be decreased to
0.9
m
IU/ L
).22 Method Collect samples for GH glucose at: 0, 30,
L (
60, 90, 120, 150
hepatic and renal disease, anorexia nervosa, and
•
MRI
scan of pituitary fossa. • Look for hypopituitarism (p
• Visual fields and acuity. •
Check Hb
min. Possible false + ves: puberty, pregnancy,
A1
c.
Tre at me nt Aim to correct (or prevent) tumour compression by
excising the lesion; aim for a
3
- part strategy: 1 Trans- sphenoidal surgery is often 1st line. 2 If
A
surgery fails to correct
analogues (
SSA
S) and/ or radiotherapy,
ferred. Example: octreotide (Sandostatin
lanreotide (Somatuline
:
ab dom ina l c ramp s, flat ule nce , lo os e st ool s, gallstones; impaired
tinal
glucose tolerance.
analogue) is used if resistant or intolerant to
to normal in
so monitor closely.
3
The GH anta gonist p egvisoma nt (recombina nt GH
90
%, but GH levels may rise; rarely tumour size increases,
Radiotherapy If unsuited to surgery or as adju-
vant; may take years to work.
diovascular risk reduction, intermittent colonoscopy, photos (
Prognosis Ma y ret urn t o nor mal (any exce ss mo rta lity is mo stl y vas -
16
% get diabetes with
cular).
1
(
IGF- 1
).
CCF
or ketoacidosis.)
BP
± insulin resistance and GH-
GH
release fai ls to su ppress.
OGTT
is above 1mcg/ L (3m
OGTT
) is needed.
S
0.3
DM
.
ECG
, echo. Old photos if possible.
GH
level of <1mcg/ L and normal
GH/ IGF-1
hypersecretion, try somatostatin
SSA
S being generally pre-
LAR
LA
®). SE: pain at the injection site; gastrointes-
Fol low- up Yearly GH,
®, given monthly IM), or
SSA
. It suppresses
IGF-1
±
OGTT
fig
SSA
S vs ~
13
Fig 5.
My life with acromegaly. (
% after surgery.
28
Acromegaly. Courtesy of Omar Rio.
http:// odel rio.blogs pot.com)
).
226
≈
1
MEN- 1
CCF
16
IU/ L
mcg/
).
IGF-1
IGF-1
, car-
5.29
:1.
),
),
.
).
5 Endocrinology
(a) (b)
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Fig 5.
29
(a) and (b) Coarsening of the face and growth of hands and mandible (prognathism).
Signs of acromegaly
• Growth of hands (fig
encroach on the dorsum).
• Coarsening face; wide nose.
• Big supraorbital ridges.
• Macroglossia (big tongue).
• Widely spaced teeth.
• Puy lips, eyelids, and skin (oily and large- pored); also skin tags.
• Scalp folds (cutis verticis gyrata; due to expanding but tethered skin).
• Skin darkening (fig
• Acanthosis nigricans (fig
• Laryngeal dyspnoea (fixed cords).
• Obstructive sleep apnoea.
• Goitre (thyroid vascularity).
• Proximal weakness + arth ropathy.
• Carpal tunnel signs in 50%, p
• Signs from any pituitary mass: hypopituitarism ± local mass eect (p
hemianopia); fits.
5.29b
; may be spade- like), jaw (fig
5.29
).
12.29
, p
561
).
497
.
5.29a
), and feet (sole may
226
233
; vision;
5 Endocrinology
Diabetes insipidus (DI)
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234
Physiology This is the passage of large volumes (>3L/ day) of dilute urine due to im-
paired water resorption by the kidney, because of reduced
terior pituitary (cranial
Symptoms Polyuria; polydipsia; dehydration; symptoms of hypernatraemia (p
Polydipsia can be uncontrollable and all- consuming, with patients drinking anything
and everything to hand: in such cases, if beer is on tap, disaster will ensue!
Causes of cranial DI • Idiopathic (50%). • Congenital: defects in
12
DIDMOAD.
• Tu mou r (may present with DI + hypopituitarism): metastases,
craniopharyngioma, pituitary tumour.
stalk as proximal nerve endings grow out to find capillaries in scar tissue and begin
direct secretion again.
• Infiltration: histiocytosis, sarcoidosis.13 • Vascu lar: haemorrhage.14 • Infection:
meningoencephalitis.
Causes of nephrogenic DI •Inherited. •Metabolic: low potassium, high calcium.
•Drugs: lithium, demeclocycline. •Chronic renal disease. •Post- obstructive uropathy.
Te st s
estimate
285– 295
is
tration. Significant
2:1
, provided plasma osmolality is no greater than
2
+
U&E
, Ca
, glucose (exclude DM), serum and urine osmolalities. Serum osmolality
≈
2 × (Na+ + K+ ) + ure a + glucose (a ll in mm ol/ L). Normal plasma osmolality
mOsmol/ kg, and urine can be concentrated to more than twice this concen-
DI
plasma osmolality, urine is dilute with a
be dilutional hyponatraemia— and as hyponatraemia may itself cause mania, be cautious of saying ‘It’s water intoxication from psychogenic polydipsia’.
Diagnosis Water deprivation test See
it is often dicult to dierentiate primary polydipsia from partial
etics or lithium use;
primary polydipsia causes symptoms of polydipsia and polyuria
with dilute urine. Its cause is poorly understood;
phrenia or mania (± Li
tumour; encephalitis; brain injury;
the kidneys may lose their ability to fully concentrate urine, due to a wash- out of
the normal concentrating gradient in the renal medulla. In the absence of a water
deprivation test, if available, plasma copeptin (a surrogate marker of vasopressin
secretion) can be used to diagnose nephrogenic
Treatment Cranial DI
desmopressin, a synthetic analogue of
IV
including
, intranasal, sublingual, and oral preparations.
Nephrogenic Treat the cause. If it persists, try bendroflumethiazide 5mg PO/ 24h.
NSAID
S lower urine volume and plasma Na
prostaglandins locally inhibit the action of
Emergency management
• Seek urgent Endocrinology or Nephrology advice.
• Do urgent plasma
carefully and check
•
IVI
to keep up with urine output. If severe hypernatraemia, do not lower Na+ rapidly as this may cause cerebral oedema and brain injury. If Na
saline initially— this contains
10
less than
• Desmopressin 2mcg IM (la sts 12– 24h) may be used as a therapeutic trial if polyuric.
12
Deafness (also known as Wolfram’s syndrome).
13
Suspect neurosarcoidosis if
diabetes insipidus (
(
12
%), optic atrophy (12%), hearing loss (12%), or nystagmus (9%).
14
Sheehan’s syndrome is pituitary infarction from shock, eg postpartum haemorrhage. It is rare.
15
Most of us could drink 20L/ d and not be hyponatraemic; some get hyponatraemic drinking 5L/ d; they may
have
leading to atrial natriuretic peptide,
mmol/ L per day. Use of 0.45% saline can be dangerous.
DIDMOAD
is a rare autosomal recessive disorder: Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and
21
%), hemiparesis (17%), psychosis (17%), papilloedema (15%), ataxia (13%), seizures
Psychosis, Intermittent hyponatraemia, and Polydipsia (
ADH
DI
) or impaired response of the kidney to
se cret ion from the p os-
ADH
(ne phrog enic DI).
ADH
• Trauma: temporary if distal to pituitary
• Hypophysectomy. • Autoimmune hypophysitis (p
is excluded if urine to plasma (
U:P
BOX
+
therapy), or, rarely, hypothalamic disease (neurosarcoid;
HIV
encephalopathy). As part of this syndrome,
MRI
(head); test anterior pituitary function (p
U&E
, and serum and urine osmolalities. Monitor urine output
U&E
twice a day initially.
CSF
protein (seen in 34%), facial nerve palsy (25%),
p
ADH.
150
mmol/ L of sodium. Aim to reduce Na+ at a rate of
135
, hence natriuresis and hyponatraemia.
U:P
) osmolality ratio is more than
295
mOsmol/ kg. In DI, despite raised
ratio <2. In primary polydipsia there may
‘The 8- hour water deprivation test’.
DI
. DM; diur-
15
it may be associated with schizo-
DI
(>21.4pmol/ L).
226
It is available in multiple formulations
+
by inhibiting prostaglandin synthase:
ADH
.
+
is ≥
170
, use 0.9%
CSF
pleocytosis (23%),
PIP
syndrome), ?from intravascular volume
664
gene,
226
NB:
). Give
).
).
5 Endocrinology
The 8- hour water deprivation test
https://t.me/med1917
Tests the ability of kidneys to concentrate urine for diagnosis of
spite of dehydration), and then to localize the cause (
before establishing that urine volume is >
+
plasma Na
• Stop test if urine osmolality >~
• Free fluids until 07.30. Light breakfast at 06.30, no tea, no coee, no smoking.
and osmolality excludes significant disturbance of water balance).
3
600
mOsmol/ kg in stage 1 (DI is excluded).
table
L/ d (output less than this with normal
DI (
dilute urine in
5.6
). Do not do the test
Stage 1 Fluid deprivation (0– 8h): for diagnosis of DI. Start at 08.00.
• Empty bladder, then no drinks and only dry food.
• Weigh hou rly. If >3% weight lost during test, order urgent serum osmolality.
300
mOsmol/ kg, proceed to stage 2. If <
If >
• Collect urine every 2h; measure its volume and osmolality.
• Venous sample for osmolality every 4h.
• Stop test after 8h (16.00) if urine osmolality >
300
, continue test.
600
mOsmol/ kg (ie normal).
Stage 2 Dierentiate cranial from nephrogenic DI.
• Proceed if urine still dilute— ie urine osmolality <
• Give desmopressin 2mcg IM. Water can be drunk now.
• Measure urine osmolality hourly for the next 4h.
Table 5.
6
Interpreting the water deprivation test
Diagnosis Urine osmolality
Normal
Primary polydi psia
Cranial
DI
Nephrogenic
Urine osmolality >
concentrating ability)
Urine concentrates, but less than normal, eg >
Urine osmolality increases to >
sin (if equivocal an extended water deprivation test may be tried
(no drinking from
No increase in urine osmolality after desmopressin
DI
600
mOsmol/ kg in stage 1 U:P ratio >2 (normal
18:00
600
mOsmol/ kg.
600
mOsmol/ kg after desmopres-
the night before))
400– 600
mOsmol/ kg
235
Syndrome of inappropriate
In
SIADH, ADH
plasma volume. Diagnosis requires concentrated urine (Na
osmolality >
osmolality, having excluded adrenal insuciency and hypothyroidism. Causes are
numerous. See
continues to be secreted in spite of low plasma osmolality or large
100
mOsmol/ kg) in the presence of hyponatraemia and low plasma
p
665
.
ADH
secretion (
SIADH
)
+
>20mmol/ L and
6
https://t.me/med1917
Gastroenterology
Contents
Healthy eating
Nutritional disorders
The mouth
Procedures
Endoscopy and biopsy
Some presenting symptoms
Dysphagia
Nausea and vomiting
Dyspepsia and peptic ulcer
disease
Gastro- oesophageal reflux
disease (
Upper gastrointestinal
bleeding
Gastro- oesophageal varices
Diarrhoea
Constipation
Diseases and conditions
Ulcerative colitis (UC)
Crohn’s disease
Gastrointestinal malabsorption
Coeliac disease
Chronic pancreatitis
Gastrointestinal motility
disorders
Irritable bowel syndrome (
Neuroendocrine tumours
Zollinger– Ellison syndrome
Jaundice
Liver failure
Cirrhosis
Viral hepatitis
Alcohol misuse
Primary biliary cholangitis (
Primary sclerosing cholangitis
Autoimmune hepatitis (
Non- alcoholic fatty liver disease
(
NAFLD
Wilson’s disease/ hepatolenticular
degeneration
Liver tumours
Hereditary haemochromatosis
(
HH
α1- antitrypsin deficiency
238
240
242
244
246
246
248
GORD
)
250
252
254
256
258
260
262
262
264
268
270
272
274
)
281
282
)
284
276
281
AIH
IBS
266
)
286
PBC
252
Fig 6.
1
Suering in silence: Ludwig van Beethoven’s
gastrointestinal symptoms began in his late teens,
262
soon after the death of his mother from tuberculosis
and the lapse of his father into alcoholism. Like the
stark rhythmic motifs that increasingly characterized
his compositions, a pattern of recurrent abdominal
cramping and alternating bouts of severe diarrhoea
)
264
and constipation emerged as an underlying constant
in his life. The aiction rose to a stifling crescendo
267
with prostration, anorexia, a host of rheumatic problems, and even jaundice and ascites proving debilitating modulations. His renowned deafness began
with high- frequency loss and tinnitus at the age of
28
, becoming relentlessly progressive. Multiple theories to explain his hearing loss have been proposed.
Beethoven’s own supposition that his deafness had its
)
278
root in the abdomen may well have been correct, des-
278
pite his physicians’ uniform dismissal. Bilateral sen-
280
sorineural hearing loss in the context of immunopathy
is well described. Inflammatory bowel disease, with
its weaving counterpoint of extra- intestinal manifestations and the oft- associated primary sclerosing cholangitis provides an all- encompassing source. A source
not only of his symptoms but quite possibly the suffering as a wellspring of his genius, bubbling with
emotion and gushing with harmonious floods of the
most profound and inspiring sounds yet conceived.
Reproduc ed from Bald win A. Oxford Handbook of
Clinical Specialties (
2020
), with permission from
Oxford University Press.
We thank Simon Campbell, our Specialist Reader for this chapter.
6 Gastroenterology
Lumen
https://t.me/med1917
We learn about gastroenterological diseases as if they were separate entities, independent species collected by naturalists, each kept in its own dark matchbox—
collectors’ items collecting dust in a desiccated world on a library shelf. But this is
not how illness works. Otto had diabetes, but refused to see a doctor until it was
far advanced, and an amputation was needed. He needed looking after by his wife
Aurelia. But she had her children Warren and Sylvia to look after too. And when
Otto was no longer the bread- winner, she forced herself to work as a teacher,
an accountant, and at any other job she could get. Otto’s illness manifested in
Aurelia’s duodenum— as an ulcer. The gut often bears the brunt of other people’s
worries. Inside every piece of a gut is a lumen
gut is in the world. But the light does not always shine. So when the lumen filled
1
— the world is in the gut, and the
with Aurelia’s blood, we can expect the illness to impact the whole family. Her
daughter knows where blood comes from (‘straight from the heart . . . pink fizz’).
After Otto died, Sylvia needed long- term psychiatric care, and Aurelia moved to
be near her daughter. The bleeding duodenal ulcer got worse when Sylvia needed
electroconvulsive therapy. The therapy worked and now, briefly, Sylvia, before
her own premature death, is able to look after Aurelia, as she prepares for a
gastrectomy.
The story of each illness told separately misses something; but even taken in
its social context, this story is missing something vital: the poetry, in most of our
patients lived rather than written— tragic, comic, human, and usually obscure—
but in the case of this family not so obscure. Welling up, as unstoppable as the
bleeding from her mother’s ulcer came the poetry of Sylvia Plath.
237
1
Lumen is Latin for light (hence its medical meaning of a tubular cavity open to the world at both ends),
as well as being the
power, whether by insightfully interpreting patients’ lives and illnesses to them, or by acts of kindness— even
something so simple as bringing a cup of tea.
SI
unit of light flux falling on an object— ie the power to illuminate. All doctors have this
6 Gastroenterology
Healthy eating
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238
Nutritional science is plagued by its own media success. Even the lowest quality research enjoys an editorial queue jump to the headlines. The result is a diet both rich
and varied in contradictory advice served directly to an increasingly confused and
frustrated public. A study on the latest diet, ground- breaking 'superfood', or newly
purported harm/ benefit of something we eat is sure to whet journalistic appetite.
Guidelines on healthy eating must also be updated when diet- outcome associations
are revised. Observational research at the heart of nutritional epidemiology is particularly prone to bias from measurement error (typically we cannot remember
what we ate yesterday, never mind details on exact portion sizes), confounding,
reverse causation, and biomarkers that poorly represent intake. Eggs went from
shunned one day to encouraged the next. Red meat and a daily glass of red wine
rapidly followed the opposite trajectory. In the ensuing confusion, we risk rejecting
simple and undisputed tenets of healthy eating based on large, high- quality prospective epidemiological studies. In particular, balancing intake across food groups
and eating less (for the majority of the population) should be encouraged.
The u rgent problems at both ends of the dietary spectr um
• 2 in 3 UK adults and 1 in 3 children are overweight or obese.
• The prevalence of obesity has doubled in the last two decades.
• More than 3 million people in the UK are malnourished/ at risk of malnutrition.
• The cost to health services of obesity and malnutrition exceeds that of smoking.
Important components of a healthy diet
Balancing energy in and out
of normal weight (
men and
adults are inactive, making caloric balance more dicult.
Carbohydrate Aim for around ⅓ of energy consumed to derive from starchy
carbohydrate (pasta, rice, potatoes, bread); low- carbohydrate diets with meat replacement are associated with higher mortality.
Protein Good sources include lean meat, fish, eggs, beans, and nuts. Processed and
red meat consumption has been associated with increased mortality compared
with white meats. Aim for
3
omega-
Fibre 30g per day is recommended, and there is a dose– response relationship with
higher consumption associated with greater reduction in vascular disease, type
diabetes, colorectal cancer, and breast cancer risk.
Fat The type of fat consumed is more important than the quantity; avoid trans fats
completely (not yet banned in the
goods) and limit saturated fat (replace with mono- and polyunsaturates).
Eat enough fruit and vegetables Aiming for 5 portions of a variety per day.
Eat some dairy produce/ alternatives Lower fat & sugar options where possible.
Limit alcohol U/ wk for both men and women, spread over 3 or more days.
There is no ‘safe’ level (apparent protective eects were largely artefactual).
Caeine There is insucient evidence to either promote or discourage tea/ coee
consumption, despite possible mortality benefits in cohort studies. Beware the 'tea
and toast' diet, a common form of malnutrition in the elderly.
Supplements There is scant evidence for most nutritional supplements in those
able to follow a balanced diet. Women attempting to conceive should take
400
mcg/ day folic acid from (pre- )conception until 13wks. Vitamin D supplements
10
mcg/ day) should be considered by all in the UK during autumn and winter.
(
This diet is not appropriate for all • <5yrs old. • At risk of malabsorption or
dietary deficiency (eg
may be dierent in
liver failure (
BP
(p
110
BMI
2000
for women. Physical activity should be encouraged for all; 1 in 2
fatty acids (probable reductions in vascular risk).
p
270
); chronic pancreatitis (p
).
Energy intake should equal expenditure for those
18.5–25
; table
6.1
). UK guidelines recommend
1
2
servings of fish per week, including oily fish rich in
2
UK
and present in some spreads, fried and baked
IBD
, p
260
Dyslipidaemia (p
). • Special diet (coeliac disease, p
682
); DM (p
200
); obesity; constipation (p
262
); renal failure (less protein) (p
2500
kcal/ d for
262
). Emphasis
256
296
2
);
);
6 Gastroenterology
Screening for malnutrition
OHCS
https://t.me/med1917
Impact of malnutrition The notion that malnutrition is a problem restricted to
UK
the developing world is a myth. It aects ⅓ of
those aged >
65
yrs in the community. Malnutrition increases mortality, prolongs
hospital inpatients and 10% of
hospital stay, and increases healthcare use.
Malnutrition Universal Screening Tool The
to identify adults at risk of malnutrition. Patients should be screened at hospital
admission or at their first outpatient appointment.
loss, and the presence of acute disease are used to calculate a simple risk score.
A score of ≥
2
should prompt referral to a dietitian.
MUST
is a validated screening tool
BMI, %
unplanned weight
Losing weight— why and how?
Health consequences of obesity The risks have been appreciated since the time
of Hippocrates. Obesity is a disease associated with a significant increase in mortality, vascular disease, type
ease, sleep apnoea, osteoarthritis, depression, and social stigma.
2
diabetes, hypertension, cancer, hepatobiliary dis-
Losing weight Motivational and behaviour- modification therapy, in combination
with dietary adherence (regardless of the type of diet). Exercise is less successful
for weight loss but is a powerful predictor of loss maintenance.
Drugs or surgery for obesity? The most desirable treatment for obesity is still
primary prevention, but pharmacotherapy does work. Orlistat lowers fat absorption (hence
potential for significant weight loss in appropriately selected patients but also
significant morbidity (see
of the anatomical and physiological eects of weight loss surgery but with less
SE
of oily faecal incontinence)— see
p
618
). Endoscopic management: may replicate some
p
830
. Surgery: carries
morbidity.
Calculating body mass index
Table 6.
BMI
<18.
5
18.5– 24.9
25– 29.9
30– 39.9
≥
40
Caveats:
1
BMI
= (weight in kg)/ (height in m)
State Some implications within the categories
Underweight
Healthy range
Overweight We ight los s sh ould be cons ide red
Obesity
Extreme/ morbid obesity
BMI
is reliable and easy to measure, but does not take into account
2
Consider pathology (incl. eating disorder)
32
is uns uitable fo r day- case general surgery
>
40
is an i ndication for bariatric surg ery
≥
the distribution of body fat, overestimates body fat mass in those who are very
muscular, and is harder to interpret for children and adolescents. This classification underestimates risk in Asian populations; guidelines define overweight
BMI
23–
25 and obesity as
as
measure in those with a
omental fat and correlates better with risk than does
BMI
>25. Waist circumference is especially useful to
BMI
25–35; >94cm in men and >80cm in women reflects
BMI
.
239
6 Gastroenterology
Nutritional disorders
OHCS
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240
Vitamin deficiency syndromes are making a worrying return in Western countries,
even in obese individuals.
Always consider their co- occurrence (table
Scurvy This is due to lack of vitamin C. Is the patient poor, pregnant, or on an odd
Signs 1 Listlessness, anorexia, cachexia (p35). 2 Gingivitis, loose teeth, hali-
diet?
3
Bleeding from gums, nose, hair follicles (fig
tosis.
4
Muscle pain/ weakness. 5 Oedema. Diagnosis No test is completely satisfactory.
WBC
s: ascorbic acid. Dietary education;2 ascorbic acid ≥
6.2
), or into joints, bladder, gut.
250
mg/ 24h PO.
Beriberi There is heart failure with oedema (wet beriberi) or peripheral neuropathy
B
(dry beriberi) due to lack of vitamin
brown rice, legumes). For treatment and diagnostic tests, see Wernicke’s enceph-
p
700
alopathy (
).
(thiamine, present in yeast, whole grains,
1
Pellagra = Lack of nicotinic acid (meat, yeast, grains, seeds, nixtamalized maize).
Classical triad:
fig
6.3
in carcinoid syndrome and antiAfrica (non- treated corn).
Diarrhoea, Dementia, photosensitive Dermatitis (Casal’s necklace,
) ± neuropathy, depression, insomnia, tremor, rigidity, ataxia, fits. It may occur
TB
drugs (isoniazid). It is endemic in China and
Education, nicotinamide
100
mg/ 4h.
Xerophthalmia This vitamin A (liver, egg yolk, butter) deficiency syndrome is a
major cause of blindness in the Tropics. Conjunctivae become dry and develop oval/
triangular spots (Bitôt’s spots). Corneas become cloudy and soft. Night blindness.
Give vitamin
must be avoided. Re- educate and monitor diet.
Table 6.
Vitamin/ nutrient Site of absorption Deficiency syndrome
F
A
B
(thia mine)
1
B
(riboflavin)
2
B
(niac in)
3
B
(pyridoxine )
6
B
12
C
F
D
F
E
F
K
Fol ic ac id Jejunum
A
(
p
374
). Get special help if pregnant: vitamin A embryopathy
2
Deficiency syndromes and the sites of nutrient absorption
Small intestine
Small intestine
Proximal small intestin e
Xerophthalmia
Beriberi; Wernicke’s encephalopathy (p
Angular stomatitis; cheilitis (p
Jejunum Pell agra
Small intestine Polyn europa thy
Te rm i n a l il e u m
Macrocytic anaemia (
p
242
glossitis (
Proximal ileum Scurvy
Jejunum as free vitamin
Rickets (
p
676
Small intestine Haemolysis; neurological deficit
Small intestine
Bleeding disorders (
Macrocytic anaemia (
p
328
)
); osteomalacia (p
p
342
p
328
Mineral
Calcium
Copper
Duodenum + je junum
Stomach + jejunum
p
668
Menkes’ kinky hair syndrome
Fluoride Stomach Dental caries
Iodid e
Small intestine
Iron Duodenum + jejunum
Magnesium Small intestine
Goitre; hypothyroidism
Microcytic anaemia (
p
671
p
326
Phosphate Small intestine Osteoporosis; anorexia; weakness
Selenium
Zinc Jejunum Acrodermatitis enteropathica; poor wound
F
= fat- soluble vitamin, thus deficiency is likely if there is fat malabsorption.
Small intestine
Cardiomyopathy (
p
671
healing (
)
p
671
); myopathy
6.2
).
242
)
); neuropathy;
676
)
)
), glossitis (p
)
242
700
)
)
2
That oranges and lemons prevent ‘the scurvy’ was noted by the naval surgeon James Lind in
may rank as the first ever clinical trial, he randomly divided
same basic diet but each group received a unique dietary intervention. The
lemons both made a good recovery.
1753
12
sailors with scurvy into 6 groups, given the
2
sailors receiving oranges and
. In what
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