Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5595_Библиотеки_им_академика_М_И_Перельмана.pdf
362 Chapter 14 Diabetes mellitus and obesity
e osmotic diuresis promoted by the excretion of glucose
produces a small decrease in blood pressure by lowering
plasma volume (see Chapter 5). is is a benecial eect,
as hypertension dramatically increases the risk of
complications suered by diabetic patients (see Section 14.3).
14.6 Management of diabetes
e management of diabetes is complex, combining diet
modications with pharmacological agents. e longterm complications associated with the disease can be
reduced if the condition is well managed, and if it is
treated early. As obesity is a signicant predisposing
factor, weight loss is an important part of the
management of the condition for overweight patients.
Weight loss can lead to attenuation of insulin resistance
and of metabolic syndrome. Bariatric surgery may be
considered and is extremely eective in restoring
metabolic control (see Section 14.8).
As seen in the previous section, a large number of
antidiabetic drugs are available. A scheme for treatment is
presented in Box 14.2; treatment is individualized,
though, according to presenting features (e.g. need for
weight loss, HbA1C level).
Treatment aims to achieve good control over blood
glucose levels, with targets for most patients of between 4
and 7 mmol/l for pre-meal levels and <10 mmol/l after
e gliozins are taken orally once a day. e main
adverse eect is increased incidence of urinary tract
infections because of the presence of glucose. e
diuretic eect can lead to volume depletion, resulting in
hypotension.
meals. Glycaemic control is reected in the HBA1C level,
with an optimal target of 7% being common.
Good control of blood glucose levels is obviously
important, but management of other factors is equally
benecial. Regulation of blood pressure is crucial as the
coexistence of hypertension and diabetes exacerbates
kidney damage and neuropathy, and most importantly
increases the risk of cardiovascular disease. e target
blood pressure for diabetic patients is therefore usually
lower than that for non-diabetic patients. Angiotensinconverting enzyme (ACE) inhibitors are prescribed or, if
not tolerated, an angiotensin II receptor blocker (ARB or
sartan). A calcium channel blocker is prescribed for
patients of African origin (see Chapter 5).
e involvement of circulating lipopoteins in the
atherosclerotic process also necessitates regulation of
cholesterol through cholesterol-lowering drugs, typically
statins (see Chapter 6). Many of these aspects of
managing diabetes are explored in Workbook 11.
14.7 Obesity
Obesity is dened as an illness in which the patient’s
health is adversely aected by excess body weight. It is a
growing health problem which is reaching epidemic
proportions and represents an enormous healthcare
burden to society. Currently 1 in 4 adults and 1 in 3
children in the UK are described as obese; similar
numbers are reported in Australia and Canada. In the
USA over a third of the adult population is obese,
predicted to rise to around 50% if the current trend
continues.
Obesity occurs when, over time, more calories are
consumed than are used by the body, and the excess
energy is stored as triglycerides in adipose tissue. ere is
an increase rstly in the size of the existing fat-storing
cells or adipocytes. Once these are full to capacity, more
cells are made.
14.7.1 Causes of obesity
e cause of obesity is not as simple as it might at rst
appear. Regulation of body weight involves numerous
factors such as calorie intake, extraction of energy, energy
expenditure, and basal metabolic rate. Accordingly,
obesity is multifactorial; numerous possible causes
combine and underlie the condition, including both
genetic and environmental factors.
• Genetic predisposition—numerous genes have been
identied that predispose people to gaining weight
more easily. It is likely that obesity is contributed to by
many of these genes. Amongst those implicated is that
encoding the melanocortin receptor (see below);
mutations in the receptor have been noted in obese
patients. ese receptors may be a target for future drug
Box 14.2
Approaches to the management of type II diabetes
Step-up if control is not achieved
5
Insulin
4
3
Add
sulfonylurea
or metformin
2
1
Lifestyle modication—diet and exercise
cardiovascular risk factor modication
Figure b
1. Diet and exercise are a fundamental part of the management of type II diabetes. Pharmacological treatment cannot
replace these treatments. Consideration should also be given to cardiovascular risk factors, such as hypertension
and hyperlipidaemia.
2. Initial treatment is with either metformin or a sulfonylurea. The best choice for overweight patients is metformin.
Elderly patients may not tolerate metformin, and repaglinide may be preferred.
3. Combination of metformin with a sulfonylurea.
4. If the combination of sulfonylurea and metformin is not tolerated, or does not yield a satisfactory response, either one
may be substituted by an alternative agent (e.g. pioglitazone, GLP-1 receptor agonist, gliflozin, or gliptin).
5. Sulfonylurea and metformin can be combined with another oral antidiabetic drug (gliptin, pioglitazone) or parenteral
incretin mimetic. Triple therapy may lead to increased risk of hypoglycaemia. Early addition (within a few months) of
insulin to patients who are poorly controlled on dual or triple therapy has been shown to improve outcomes in type II
diabetes. It can be given as a single daily dose of long-acting insulin, usually in the evening.
(i.e. combination
therapy)
Metformin or sulfonylurea
Add/substitute
glitazone, GLP-1
mimetic, acarbose,
gliptin, or gliozin
Dual or
triple
therapy
364 Chapter 14 Diabetes mellitus and obesity
therapy for obesity. Genetic variation is also believed to
underlie the dierences seen in the suppression of
ghrelin (see below) by eating that have been observed
in obese people.
• Variation in the body’s eciency in extracting energy
from food—obese people may have more energyecient systems.
• Variation in energy expenditure, e.g. underactivity in
the sympathetic nervous system or decreased
metabolic rate.
• Defects in the hypothalamic appetite centre (see
below) or in the signalling pathways that provide its
input (e.g. decreased inuence of leptin; see below).
• Dierences in composition of gut bacterial
populations—obese people may have more ecient
gut ora, increasing the availability of absorbable
nutrients in the digestive tract.
• Diet, lack of exercise.
• Emotional disturbance, stress.
14.7.2 Obesity is associated with
significant morbidity and mortality
Obesity often coexists with other factors, particularly
hypertension, hyperlipidaemia, and insulin resistance.
is cluster of disorders is known as the metabolic
syndrome, and often precedes the development of type II
diabetes. Indeed, as noted above, around 80% of people
with type II diabetes are obese.
In particular, it is fat that is distributed around the waist
(visceral fat, surrounding the abdominal organs) that
increases the risk of an obese individual suering a wide
range of serous conditions, including cardiovascular
disease, respiratory disorders, liver disease, cancers,
dementia, and type II diabetes (see Section 14.2.1).
14.7.3 Adipose tissue participates in
energy balance
It is now recognized that rather than being an inert store
for excess energy, adipose tissue actively participates in
energy balance in the body and contributes to
physiological functions, such as inammation and
immunity. Indeed, adipose tissue has endocrine
functions, secreting a wide variety of proteins known as
adipokines. Amongst these are molecules with hormonelike properties, as well as a range of cytokines and
chemokines (see Section P3.3 in the Introduction to
Part 3). ey are released both from adipocytes and from
macrophages and other immune cells that inltrate the
adipose tissue in large numbers, particularly in visceral
fat. ese cytokines include tumour necrosis factor-
(TNF-) and interleukin-6 (IL-6), important mediators of
the inammatory response (see Section P3.3 and Chapter
9, Section 9.1.1). is gives rise to a chronic low level
inammatory state with detrimental consequences,
including promotion of the atherosclerotic process that
underlies cardiovascular disease (see Chapter 6, Box 6.1).
e pattern of adipokine release from visceral and
subcutaneous fat is dierent. More inammatory
mediators are released in visceral fat and the
inammatory process is therefore promoted. is
correlates with the increased risk of cardiovascular
disease in obese people with a high abdominal
distribution of fat.
Numerous adipokines have already been identied, and
doubtless many more are yet to be discovered. Some, like
adiponectin, have benecial eects, whereas others, such
as resistin, are implicated in the development of insulin
resistance and cardiovascular complications. Amongst
those that have already been identied are the following.
• Leptin, the earliest known adipokine, is secreted by
dierentiated adipocytes in direct proportion to the
amount of fat present. Leptin increases sensitivity of
skeletal muscle and liver to insulin, and encourages the
-oxidation of fatty acids. Importantly, it suppresses
appetite; leptin resistance is implicated in the
development of obesity.
• Adiponectin released from adipocytes improves insulin
sensitivity of tissues. It increases glucose uptake and
promotes -oxidation of fatty acids. It has protective
eects in the vascular endothelium, and is therefore
anti-atherogenic. Adiponectin levels are decreased in
obesity.
• Resistin released from inamed visceral fat is believed
to promote insulin resistance, and increase production
of inammatory cytokines.
• TNF- produced by macrophages that have inltrated
adipose tissue is a pro-inammatory mediator and is
implicated in the induction of insulin resistance.
• Plasminogen activator inhibitor-1 expressed and
secreted by adipocytes inhibits the activation of
plasminogen, the precursor of plasmin, which is
responsible for the dissolution of clots. It is therefore
pro-thrombotic. Levels are increased in obese subjects,
and correlate with increased cardiovascular risk.
14.7 Obesity 365
14.7.4 Control of food intake (appetite)
Food intake is regulated by various factors in the blood
that signal the body’s nutritional state, or energy status.
e overall control is coordinated in the brain, which
receives and integrates a large number of inputs and
ensures that in the long term calorie intake and total
energy output are well matched so that body weight
remains more or less constant (Figure 14.4).
Particular regions of the hypothalamus, including the
arcuate nucleus, the paraventricular nucleus, the
ventromedial hypothalamic nucleus, and the
dorsomedial hypothalamic nucleus, are central to
appetite control. Importantly, these regions are often
accessible to circulating hormones and are innervated by
nerves, including the nucleus of the solitary tract which
receives input from the vagal nerves.
A large number of hormones have important regulatory
roles. ese include the following.
1. Ghrelin, a peptide released primarily by cells in the
stomach: levels decrease when food is ingested and
increase when fasting. Ghrelin acts in the
hypothalamus to increases levels of neuropeptide Y
(NPY) and agouti-related protein (AgRP), both of
which have important orexigenic (appetite-stimulant)
properties. e eect of ghrelin is to increase appetite,
encouraging food intake.
2. e adipokine leptin (see above) has opposing actions
to ghrelin, resulting in appetite reduction. Leptin acts
by reducing levels of NPY and AgRP. It also increases
the levels of pro-opiomelanocortin, which causes
release of -melanocyte-stimulating hormone to
inhibit feeding.
3. Insulin is important in long-term control of body
weight, acting to inhibit the release of NPY in the
hypothalamic regions to suppress food appetite.
4. Cholecystokinin and GLP-1 are secreted from the gut
in response to eating. ey also suppress appetite by
acting at the hypothalamus.
e concerted actions of these (and other) factors control
food intake and contribute to energy homeostasis.
Derangements in these systems have been implicated in
the obese state. For example, resistance to the eects of
leptin, possibly through faulty receptors or changes in the
signalling pathway after receptor occupation, may lead to
loss of its appetite-suppressant action.
A number of neurotransmitters act in concert with the
hormonal controls to regulate appetite. ese include
serotonin (5-hydroxytryptamin; 5-HT), noradrenaline,
dopamine, and histamine. In addition, a range of
endogenous peptides, including opioids and
endocannabinoids, also provide input to the appetite
regulation of appetite are summarized in Table 14.5.
Stomach
Hypothalamus
ARC
Brainstem
Insulin
Vagus
Pancreas
Food intake
Leptin
CCK
GLP-1
Ghrelin
Adipose tissue
Figure 14.4 Inputs into the regulation of appetite.
The regulation of: ARC, arcuate nucleus; CCK, cholecystokinin; GLP-1, glucagon-like
protein-1.
366 Chapter 14 Diabetes mellitus and obesity
()
()
=×
Table 14.5 Hormones and neurotransmitters involved in appetite
Neurotransmitter/hormone Receptor/mode of action Effect on appetite
Ghrelin
Leptin
Insulin
Cholecystokinin (CCK)
Glucagon-like peptide-1 (GLP-1)
Serotonin 5-HT
Dopamine D
Noradrenaline
Histamine H
Endogenous opiates (e.g. endorphins)
Endocannabinoids (e.g. anandamide) CB
Neuropeptide Y
Agouti-related protein
Vagal stimulation
Neuropeptide Y
Agouti-related protein
Pro-opiomelanocortin
Neuropeptide Y
Vagal activity (CCKA receptors)
CCKB receptors in VMH and PVN
Neuropeptide Y
Gastrointestinal motility
Delays gastric emptying
Stimulates insulin release
2C
2
1
2
2
1
, ,
1
LHA, lateral hypothalamic area; PVN, paraventricular nucleus; VMH, ventromedial hypothalamic nucleus.
14.7.5 Diagnosis of obesity
BMIkg/m
Obesity is diagnosed by measuring body mass index
(BMI) of the individual. e BMI is the weight divided by
the square of the height. e formulas below are used to
()
BMIkg/m
()
calculate BMI:
A BMI of over 30 is the arbitrary boundary for a diagnosis
of obesity (see Table 14.6).
Table 14.6 NICE treatment guidelines based on BMI and waist measurements
Waist circumference
a
Classification BMI (kg/m2) Low High Very high
Overweight 25–29.9
Obesity I 30–34.9
Obesity II 35–39.9
Obesity III 40 or more
a
For men, waist circumference of less than 94 cm is low, 94–102 cm is high, and more than 102 cm is very high. For women, waist
circumference of less than 80 cm is low, 80–88 cm is high, and more than 88 cm is very high.
General advice on healthy weight and lifestyle
Diet and physical activity
Diet and physical activity; consider drugs
Diet and physical activity; consider drugs; consider surgery
Weight in pounds
2
Height in inches
Weight in kg
2
=
Height in metres
Comorbidities present
703
2
2
14.8 Management of obesity 367
BMI is useful for guiding treatment choice and
monitoring its eectiveness. is measure of body
composition does not, however, take account of
anatomical fat distribution, and as noted earlier it is
visceral fat that is most damaging. For this reason, it is
14.8 Management of obesity
Obesity is a chronic condition requiring long-term
management. Lifestyle changes to diet and exercise
regimes are central to managing the condition. Weight
loss can lead to attenuation of insulin resistance and
metabolic syndrome, reducing the risk of complications.
Often, though, dieting only leads to short-term weight
loss, and any weight that is lost is easily regained. Bariatric
surgery can be considered (e.g. gastric stapling) and is by
far the most eective option available, with a successful
outcome in over 70% of patients who show excellent
metabolic recovery.
14.8.1 Drug treatment for obesity
Despite the range and diversity of potential targets for
anti-obesity drugs, there is a paucity of pharmacological
agents available to treat the condition. A number of drugs,
some of which were eective, have had to be withdrawn
due to safety concerns. Research is ongoing in the search
for new, safer agents; modulation of the pathways
involved in satiety signals may provide clinically useful
drugs.
Lipase inhibitors
Fats are the most caloric of the foodstus we consume,
and inhibiting their breakdown in the gut is currently the
only pharmacological method for treating obesity that is
licensed in the UK.
Ingested fats are broken down in the gut by gastric and
pancreatic lipases into free fatty acids and glycerol, which
are then absorbed. Orlistat is an irreversible lipase
inhibitor, derived from lipstatin, a naturally occurring
irreversible pancreatic lipase inhibitor produced by the
bacterium Streptomyces toxytricini. Orlistat is not absorbed
into the systemic circulation, and its eects are restricted
to the intestines, where it blocks the absorption of around
30% of dietary fat. Use of the drug, combined with a low
calorie diet, can lead to modest weight loss (~5%).
Orlistat is sold without prescription in many countries. Its
adverse eects on the gastrointestinal tract can be
more informative to consider BMI in combination with
waist circumference. Table 14.6 summarizes the
recommendations from the National Institute of Health
and Care Excellence (NICE) in the UK on when and how
to initiate treatment for obese patients.
signicant: for example, loose and oily stools, atulence
associated with discharge, and faecal incontinence, as
well as bloating and cramps. e absorption of fat-soluble
vitamins may be reduced, and supplements may be
necessary. e absorption of a number of drugs,
including antivirals and the antibacterial ciclosporin, may
be reduced by orlistat. Interestingly, the drug has been
found to increase the uptake of other drugs, and this may
necessitate a reduction in dose. Such an interaction has
been reported with insulin and pravastatin, and may
therefore be relevant in the treatment of overweight
diabetic patients.
Appetite suppressants
Serotonin/noradrenaline reuptake inhibitors As noted
in Table 14.5 both serotonin (5-HT) and noradrenaline
have important roles in appetite regulation. Sibutramine
is a selective serotonin and noradrenaline reuptake
inhibitor, which has been used in the past to treat obesity.
e drug increases extracellular brain levels of both 5-HT
and noradrenaline, leading to enhanced stimulation of
5-HT2C receptors and 1- and 2-adrenoceptors (see Table
14.5) to enhance satiety. In addition, sibutramine
stimulates the sympathetic nervous system, leading to
increased glucose usage and heat production in
breakdown of brown adipose tissue.
Although an eective appetite suppressant, sibutramine
has a long list of serious adverse drug reactions and was
withdrawn from the market in 2010 following concerns of
increased risk of heart attack and stroke.
Amphetamines have been used for weight reduction
since the early 1950s. ey act by increasing dopamine
and noradrenaline release from nerve endings in the
brain, including in the hypothalamus, to reduce appetite.
In most countries amphetamines are no longer
recommended for weight loss—they produce euphoria
and increase feelings of reward, which is due to an
increase in monoaminergic transmission in mesolimbic
parts of the brain, and as such have potential for abuse
368 Chapter 14 Diabetes mellitus and obesity
(see Chapter 21). ey can also cause lethargy, rebound
depression, and binge eating.
Cannabinoid receptor antagonists e CB1 cannabinoid
receptor is a relatively new target for treating obesity. CB1
receptors are expressed in the mesolimbic system and the
hypothalamus where they enhance reward and stimulate
appetite, respectively (see also Chapter 21). e receptor
is Gi-coupled, activation leading to decreases in cyclic
AMP levels. It also blocks pre-synaptic calcium channels
Key references and suggested reading
Greeneld JR, Chisholm DJ. iazolidinediones—mechanisms
of action. Aust Prescr 2004; 27: 67–9.
Harrold JA. Hypothalamic control of energy balance. Curr Drug
Targets 2004; 5: 207–19.
Hiller-Sturmhfel S, Bartke A. e endocrine system. Alcohol
Health Res World 1998; 22: 153–64.
Holst JJ. e physiology and pharmacology of incretins in type 2
diabetes mellitus. Diabetes Obes Metab 2008; 10: 14–21.
Kilov G, Leow S, omas M. SGLT2 inhibition with
dapagliozin: a novel approach for the management of type 2
diabetes. Aust Fam Physician 2013; 42(10): 706–10.
National Evidence Based Guidelines for the Management of
Type 2 Diabetes Mellitus. Canberra, National Health and
and activates potassium channels, leading to an
inhibition of synaptic transmission.
Rimonabant is a CB1 receptor antagonist which acts
centrally to reduce appetite, and peripherally to increase
insulin sensitivity and fatty acid oxidation in muscles and
the liver. It was found to be an eective agent in
encouraging weight loss but had to be withdrawn from
the market because of serious psychiatric eects,
including depression and suicidal ideation.
Medical Research Council, 2004. https://www.nhmrc.gov.
au/guidelines-publications/di7-di8-di9-di10-di11-di12di13.
Obesity Prevention. National Institute for Health and Care
Excellence Clinical Guidelines CG43, 2006. http://www.nice.
org.uk/guidance/cg43.
Type 2 Diabetes in Adults: Management. National Institute for
Health and Care Excellence Clinical Guidelines NG28, 2015.
http://www.nice.org.uk/guidance/ng28.
Vincent RP, Ashraan H, le Roux CW. Mechanisms of disease:
the role of gastrointestinal hormones in appetite and obesity.
Nature Clin Pract Gastroenterol Hepatol 2008; 5: 268–77.
SUMMARY OF DRUGS USED FOR DIABETES AND OBESITY
14.8 Management of obesity 369
Therapeutic class Drugs Mechanism of action Common clinical
uses
Insulins Short-acting:
Actrapid
Mimic effects of endogenous
insulin by activating insulin
receptor
Type I diabetes
Type II diabetes
Rapid acting:
Insulin aspart
Insulin lispro
Insulin glulisine
Intermediate acting:
Insulin mixtard (different
strengths)
Long-acting:
Insulin glargine
Insulin detemir
Biguanides Metformin Mechanism of action not fully clear
Type II diabetes Causes weight reduction
Potentiates effects of insulin by
sensitizing insulin receptor
Decreases hepatic
gluconeogenesis, and glucose
absorption from the GI tract
Sulfonylureas Tolbutamide
Glibenclamide
Glimepiride
Gliclazide
Glipizide
Blocks ATP-dependent K+
channels on -cells to cause
depolarization
Influx of Ca
2 +
through voltage-
gated channels, stimulates release
Type II diabetes Gliclazide and glipizide have the
of insulin by exocytosis
Meglitinides Nateglinide
Repaglinide
Act in the same way as
sulfonylureas, but by binding to a
distinct site to block the ATPdependent K+ channel on -cells
to stimulate the release of insulin
Thiazolidinediones (glitazones) Pioglitazone Selective agonist at peroxisome
Type II diabetes Liver function needs monitoring
proliferator activator receptor
(PPAR)
Increases transcription of genes
involved in insulin signalling
Comments Common adverse drug
reactions
Injected 30–45 min before
meals
Used in infusion for some type I
patients
More flexible because of quick
absorption, given immediately
Hypoglycaemia
Lipodystrophy weight gain
Allergic reactions
Local reactions (e.g.
erythema, reddening and
itching)
before food
Onset of action up to 2 h, and
duration of effect up to 20 h
Onset of action within 4 h, and
duration around 24 h
Used in conjunction with
short-acting insulins
GI disturbances (abdominal
First-line agent
Contraindicated in renal
impairment
distension and pain,
nausea, diarrhoea)
Malabsorption of vitamin B
Lactic acidosis
Hypoglycaemia
lowest risk of hypoglycaemia
Weight gain
Nausea
Diarrhoea
Rapid onset and short duration
of action
Can be taken immediately
before food
Peripheral oedema
Contraindicated postmyocardial infarction, and in left
ventricular heart failure
Weight gain
Headache
Dizziness
12
370 Chapter 14 Diabetes mellitus and obesity
Therapeutic class Drugs Mechanism of action Common clinical
Comments Common adverse drug
uses
-Glucosidase inhibitors
Dipeptidylpeptidase-4 inhibitors
(gliptins)
Incretin mimetics Exenatide
Sodium–glucose co-transporter
2 (SGLT2) inhibitors
Glucagon Glucagon Opposite action to insulin
Lipase inhibitor Orlistat Blocks the action of lipase, the
Amphetamines Increases dopamine and
GI, gastrointestinal; GLP-1, glucagon-like peptide-1; HDL, high-density lipoprotein; LDL, low-density lipoprotein; PPAR, peroxisome proliferator activator receptor .
Acarbose Reversible inhibition of
Sitagliptin
Vildagliptin
Alogpitin
Linagliptin
Saxagliptin
Lixisenatide
Liraglutide
Dapagliflozin
Canagliflozin
Empagliflozin
-glucosidase
Reduces post-prandial peak in
glucose levels, by slowing
intestinal glucose absorption
Competitive inhibitors of
dipeptidylpeptidase-4, the enzyme
that inactivates endogenous
incretins, potentiating their effects
Mimic actions of GLP-1
Direct effect on -cells of pancreas
enhancing glucose-mediated
release of insulin, and inhibiting
glucagon release by -cells
Reversible inhibition of renal
co-transporter of glucose (SGLT2)
Reduces glucose reabsorption,
and promotes excretion of glucose
in the urine
Binds to Gs-coupled receptor to
increase intracellular cAMP levels
Promotes increases in blood
glucose levels
enzyme that breaks fat down for
absorption
noradrenaline release from nerve
endings in the feeding centre in
the hypothalamus, reducing
appetite
Type II diabetes
(effective in type I
diabetes, but rarely
used)
Type II diabetes Used in conjunction with other
Type II diabetes Useful in obese patients and
Type II diabetes Often given in combination with
Hypoglycaemia Can be given for emergency
Obesity Only drug in this class Loose and fatty stools
Not recommended for use in most countries Lethargy
Used in combination with other
oral antidiabetic drugs
antidiabetic drugs
those unable to take insulin
metformin or a sulfonylurea
Promotes osmotic diuresis to
give beneficial reduction in
blood pressure
treatment of hypoglycaemia by
intramuscular or subcutaneous
injection, e.g. to an unconscious
patient
reactions
Bloating
Flatulence
Diarrhoea
Headache
Nausea
Infections
Nausea
Vomiting
Diarrhoea
Dyspepsia
Abdominal pain
Urinary tract infections
Hypotension
Nausea
Vomiting
Hypokalaemia
Flatulence
Bloating and cramps
Rebound depression
Binge eating
WORKBOOK 11
Diabetes mellitus and obesity
Andreas Kaiser: a simplified case history
Andreas has been admitted directly to hospital following a third visit to his GP regarding the
ulcer on his left little toe, which will not heal. The GP had taken his blood pressure and
temperature and rung the hospital to chase up the results of his recent blood tests. Once he
heard the results, the GP had sent him straight to hospital.
After3hoursofwaiting,Andreasisnallyseenbytheconsultantwhohashisclinicalnotes.
A table of clinical clerking abbreviations is given on page xviii.
CLINICAL CLERKING FOR ANDREAS KAISER AT A&E
DEPARTMENT
Age: 38 years
PC: Worsening ulcer on left little toe and general feeling of lethargy. Increased thirst and urinary
frequency.
HPC: Admitted via GP following aggravation of toe ulcer. Emergency visit to GP revealed pyrexia (fever).
Blood test results indicated elevated random blood glucose of 25 mmol/l and elevated white cell count.
Andreas’s random blood glucose level was a lot higher than the normal range of 3.5–10 mmol/l.
Random blood glucose levels >11.1 mmol/l in combination with his symptoms point to a diagnosis of
diabetes.
Elevated white cell count indicates infection, probably from his ulcerated toe. Foot ulcers are very
commonindiabetes—aresultofneuropathy(nervedamage),vasculardisease,andhyperglycaemia.
PMH: Hypertension; hypertensive crisis a year ago.
Andreas is hypertensive and had a life-threatening hypertensive crisis last year.
DH: Losartan and indapamide
Andreas has been taking these two drugs for his blood pressure.
Losartan is an angiotensin receptor blocker (ARB) which was started after he developed a dry cough
with lisinopril (ACE inhibitor).
Indapamide is a thiazide-like diuretic.
SH: Lives with wife and twin daughters. Smokes 10 cigarettes a day. Weight = 98 kg (overweight).
Mother is diabetic (type II).