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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5230_Библиотеки_им_академика_М_И_Перельмана.pdf
T2DM(E OHCMp. 200.)
Symptoms As for TDM, but can also present with diabetic complica-
tions, eg visual problems, neuropathy, MI, CVA, claudication.
Signs Foot ulcers, infections, peripheral neuropathy, poor visual acuity
and retinopathy, evidence of cardiovascular disease.
Investigations blds Confirm diagnosis based upon plasma glucose testing
±OGTT (E p. 342), HbA
Treatment
T2DM may initially be controlled by a healthy diet with min-
(Box .7), U+E, lipid profile;ECG.
c
imal rapid- release carbohydrates (as found in sugary drinks or sweets)
and weight loss. If medication required, uptitrate pharmacological agents
(usually to triple therapy) before adding in insulin therapy (Table.).
Chronic management E p. 344. See Box.8.
Table. Medications forglycaemic control inT2DM
Class Examples Comment*
Biguanides Metformin st line;
Sulphonylureas
Thiazolidinediones
DPP- 4
inhibitors
SGLT2
inhibitors
GLP-
agonists
Insulin
α- glucosidase
inhibitors
*For more information, see NICE guidelines are available at
Gli clazide Add to metformin or st line if metformin not tolerated;
Pioglitazone Add to metformin 2nd line.
Sitagliptin Add to metformin or st line if metformin not
Dapagliflozin Add to metformin or st line if metformin not
Exenatide,
liraglutide
Isophane
(given SC)
Acarbose Rarely used in current practice;
icellular glucose uptake and dappetite;
avoid if eGFR <30
iinsulin secretion, but causes weight gain. Cautious use in
elderly and renal failure due to risk of hypoglycaemia
commonly used due to side eect profile. Avoid in
heart failure
tolerated; reduces breakdown of incretins (GLP-
and GIP) with iinsulin and dglucagon secretion
tolerated; iincreases renal glucose excretion.
Growing evidence for benefit in heart failure
If other drugs not tolerated or eective, especially if iBMI;
iinsulin and dglucagon secretion
Added eg if triple oral therapy insucient (or if
metformin not tolerated and dual therapy insucient)
absorption; causes flatulence
dinsulin resistance; less
dcarbohydrate
Mguidance.nice.org.uk/NG28
343DIABETES MELLITUS
K Box .8 Sick dayrules
Educate diabetic patients about what to do if they are feeling unwell:
• Drink plenty offluids
• If not eating, try milk, soup, fruit juice, or fizzy drinks instead
• Increase frequency of blood glucose monitoring (+ ketones if glucose
>5mmol/L) to at least 4 times/ day
• Seek medical attention if they cannot keep fluids down, are becoming drowsy or
confused, blood glucose <4mmol/ L or persistently >20mmol/ L
• If on insulin 3This should never be stopped; hyperglycaemia can arise from
intercurrent illness, regardless of calorie intake. Consider increasing insulin dose if
blood glucose >3mmol/ L even if unable to eat
• If on tablets SGLT2 inhibitors must be stopped in acute illness. Metformin
should be stopped if dehydrated or pre-existing renal impairment.
344 CHAPTER Endocrinology
Long- term management ofdiabetes mellitus
K Diabetes mellitus is associated with macrovascular (IHD, CVA, PVD)
and microvascular (nephropathy, neuropathy, retinopathy) complications. Large, long- term studies show reductions in complications with
control of risk factors; these should be assessed at least annually in a
formal review.
,2
Education and lifestyleEnsure understanding and motivation for glycaemic
control (including self- monitoring, medication compliance, and diet as
well as assessing risk of hypoglycaemic unawareness). Modify risk factors for complications (physical activity, smoking cessation, foot care).
Refer for education classes.
Glycaemic controlMeasure HbA
after. Adjust therapy accordingly (Box .7). Consider revising target if
every 3– 6mth until stable, annually there-
c
tight control unacceptable to patient based upon individual risk profile.
BPAim for BP <40/ 80 (uncomplicated T2DM) or <35/ 85 (uncompli-
cated TDM); if end- organ damage aim for BP <30/ 80 (E pp. 278–8).
Use an ACEi as st line (plus diuretic or Ca
2+
channel blocker if African-
Caribbean descent).
Lipids Measure lipid profile and consider cardiovascular risk factors.
Oer statin therapy in T2DM if 0yr CVD risk >0% (using QRISK assessment tool). In TDM oer if over >40yr, had TDM for >0yr or
end organ disease. st-line primary prevention is atorvastatin 20mg,
titrate to response.
Nephropathy Test early morning urine albumin:creatinine ratio; if ≥2 re-
peated measurements show microalbuminuria (>3mg/ mmol), tighten BP
control, initiate ACEi, and consider renal referral.
RetinopathyArrange annual retinal screening; sudden loss of vision, rubeosis
iridis, pre- retinal or vitreous haemorrhage, or retinal detachment require
emergency ophthalmology review; new vessel formation requires urgent referral; pre- proliferative retinopathy, significant maculopathy, or unexplained
change in visual acuity require routine referral.
Footcare Assess annually for ulcers, peripheral pulses, sensory function,
and foot deformity. If ulcers present, refer urgently to a specialist diabetic
footcare team. Those with previous ulcers, absent pulses, or impaired
sensation require referral to a footcare team for frequent review.
Neuropathy Assess for autonomic neuropathy in the form of unex-
plained vomiting (gastroparesis— consider trial of prokinetic agents, eg
metoclopramide), erectile dysfunction (oer phosphodiesterase- 5 inhibitor, eg sildenafil), nocturnal diarrhoea, bladder voiding problems, or
orthostatic hypotension. Neuropathic pain
4
requires oral neuropathic
agent (eg gabapentin, amitriptyline, duloxetine). Refractory or severe
pain may require opioid analgesia and specialist pain service referral.
Vaccination Oer one-o pneumococcal vaccination; ‘flu vaccine should
be given annually to all patients.
3
For NICE guidelines on management of TDM see Mguidance.nice .org.uk/ NG7
2
For NICE guidelines on management of T2DM, see Mguidance.nice .org.uk/ NG28
3
For NICE guidelines on footcare in T2DM, see Mguidance.nice.org.uk/ NG9
4
For NICE guidelines on neuropathic pain, see Mguidance.nice.org.uk/ CG73
Pituitaryaxis
Hypopituitarism
K Failure of secretion may aect one or more anterior pituitary hormones.
CausesDamage to the hypothalamic– pituitary axis after surgery, irradiation,
tumours, ischaemia, infection (eg meningitis), autoimmune, or infiltration (eg
amyloidosis, haemochromatosis).
Symptoms and signsSpecific to each hormone lost, eg growth hormone (GH)
loss:weakness, malaise, dcardiac output, hypoglycaemia; gonadotropin (LH,
FSH) loss: amenorrhoea, dlibido, erectile dysfunction; TSH loss: hypothyroidism (E pp. 348–9); ACTH loss:glucocorticoid insuciency (Ep. 346).
Investigations Tests of pituitary function include LH, FSH, TSH, paired
with target organ hormones: testosterone/ oestradiol, T
insulin- like growth factor- (IGF- , a marker of growth hormone secretion). Dynamic testing (eg short Synacthen
®
test E p. 599) is also in-
formative. Generally, testing of pituitary function should be undertaken
and interpreted with specialist advice.
Treatment Identify and treat underlying cause; appropriate hormone replace-
ment may be required, eg hydrocortisone (E p. 20) or thyroxine (Ep. 204).
3On the ward, the most important point is to ensure any patient with
panhypopituitarism gets regular steroids (increased in acute illness and given
IV if necessary) with early endocrinologist involvement (E p. 346).
Diabetes insipidus
K Inability to form concentrated urine due to loss of either ADH secre-
tion (neurogenic) or renal response (nephrogenic).
Causes Neurogenicidiopathic, brain tumour or metastases, head trauma,
cranial surgery;
obstructive uropathy, iCa
SymptomsPolyuria, thirst (may be extreme).
SignsDilute urine, clinically dehydrated (Epp. 402–5).
InvestigationsCheck U+E, Ca
Nephrogenic inherited, drugs (eg lithium), CRF, post-
2+
,dK+.
2+
, and glucose, 3exclude DM. Look for:
durine osmolality (<400mOsmol/ kg), iplasma osmolality, and iNa
In the water deprivation test (fluid balance, weight, urine, and plasma
osmolality recorded over 8h without fluids)— failure to concentrate urine
(>600mOsmol/ kg) confirms DI. Desmopressin (an ADH analogue) is
then given— the production of a concentrated urine at this point implies
neurogenic DI; failure to concentrate implies nephrogenicDI.
Treatment Identify and treat the cause. In neurogenic DI, intranasal
desmopressin may be used regularly. In nephrogenic DI, bendroflumethiazide or NSAIDs may beused.
Acromegaly
K Hypersecretion of GH from a pituitary tumour drives soft tissue and
skeletal growth resulting in characteristic facial and body features.
Symptoms and signsEnlarged hands and feet, coarse facial features, prog-
nathism, macroglossia; headache ±bitemporal hemianopia. Sweating,
hypertension, and hyperglycaemia are markers of disease activity.
InvestigationsIGF- levels reflect GH secretion; OGTT and other tests of
pituitary function under specialist guidance; pituitaryMRI.
TreatmentTranssphenoidal resection of pituitary tumour where possible;
medical therapy includes somatostatin analogues (eg octreotide).
, cortisol and
4
345PITUITARYAXIS
+
.
346 CHAPTER Endocrinology
Adrenal disease
Cushing’s syndrome(E OHCMp. 28.)
K Excess of glucocorticoids (eg cortisol); ‘Cushing’s disease’ when due
to an ACTH- producing pituitary tumour. ACTH may also be produced ectopically, eg by small- cell lung cancers. Adrenal adenomas or
carcinomas are ACTH- independent causes (and will suppress ACTH).
Apatient on steroids may become ‘Cushingoid’.
SymptomsWeight gain, depression, psychosis, tiredness, weakness, oligo-
or amenorrhoea, hirsutism, impotence, infections,DM.
SignsCentral obesity (bualo hump), moon- face, water retention, iBP,
thin skin, striae, bruising, peripheral wasting; hyperpigmentation only in
Cushing’s disease or ectopic ACTH production.
Investigations iglucose, i24h urinary cortisol, plasma ACTH and 8am cortisol,
dexamethasone suppression tests (E OHCM p. 29); imaging tests are
problematic due to high rates of ‘incidentalomas’ on adrenal CT or pituitary
MRI and are only done after biochemical confirmation of the diagnosis.
TreatmentLocalize and remove source of cortisol, eg transsphenoidal resec-
tion of pituitary adenoma, adrenalectomy for adrenal adenoma. If surgical
treatment fails or unsuitable (eg ectopic ACTH from metastatic lung cancer),
suppress steroidogenesis, eg with ketoconazole or metyrapone. If iatrogenic
cause, try to taper steroid dose (E p. 75). Consider bone protection with
bisphosphonate and vitamin D; monitor for iglucose.
ComplicationsOsteoporosis, DM, infection, poor healing, infertility.
Adrenal insuciency(E OHCMp. 220.)
K Adrenal deficiency caused by: withdrawal of long- term steroid therapy,
pituitary failure, ° adrenal (Addison’s) disease including autoimmune (commonest in UK), TB (commonest worldwide), metastases (eg lung, breast),
Waterhouse– Friderichsen syndrome (sepsis and adrenal haemorrhage).
Symptoms Tiredness, lethargy, weight loss, weakness, dizziness, depres-
sion, abdo pain, diarrhoea or constipation, vomiting, myalgia.
SignsVitiligo, postural hypotension, hyperpigmentation of creases, scars,
and mouth from iACTH.
Investigations dNa
If suspected perform short Synacthen
from pharmacy, once this arrives send a blood sample for cortisol and ACTH
levels, give the Synacthen
Addison’s is excluded if initial, or 30min cortisol is >550nmol/ L.
TreatmentHydrocortisone 20– 30mg/ day in divided doses to mimic normal
circadian rhythm. May also need fludrocortisone (50– 200micrograms PO
OD) if electrolytes deranged or postural hypotension. 2If unwell, double
dose of oral steroids for duration of illness. If vomiting, needs IV/ IM
hydrocortisone— 00mg STAT and seek medical attention. Provide steroid
emergency card for patients to carry with them.
2
Addisonian crisis Shock, dGCS, or hypoglycaemia in a patient with
Addison’s disease or stopping long- term steroid therapy. Give hydrocortisone (00mg IV STAT, then 200mg/ 24h in divided doses) and fluid
resuscitation with 0.9% NaCl; seek urgent endocrinologist advice.
+
, iK+, iurea, may have abnormal FBC (eosinophilia) and LFT.
®
IM/ IV (E p. 599); repeat cortisol levels in 30min.
®
test:order 250micrograms Synacthen®
347ADRENAL DISEASE
Hyperaldosteronism(E OHCMp. 222.)
K Excess aldosterone secretion, resulting in Na
+
and water retention; typ-
ically from an adrenal adenoma (Conn’s syndrome), or adrenal hyperplasia.
SymptomsThirst, polyuria, weakness, muscle spasms, headaches.
SignsHypertension (especially if refractory to multiple antihypertensive
agents or young age of onset).
Investigations dK
+
, normal or iNa+, metabolic alkalosis; measure plasma
renin and aldosterone together after 30min supine (postural changes affect renin secretion). Ideally the patient should be o all antihypertensives
apart from α- blockers. iAldosterone with drenin supports the diagnosis;
consider CT abdo (but beware ‘incidentalomas’:abnormal CT findings,
such as a small adrenal mass of no clinical significance).
Treatment Spironolactone; if adenoma, surgical resection may be at-
tempted after 4wk medical therapy once electrolytes and BP controlled.
Secondary hyperaldosteronism This occurs when renal perfusion is de-
creased, leading to high renin secretion. Common causes include diuretics, heart failure, liver failure, and renal artery stenosis. Features are
similar, but aldosterone:renin ratio will not be high. Manage with spironolactone orACEi.
Phaeochromocytoma(E OHCMp. 222.)
K Catecholamine (eg noradrenaline) production from tumours within the
adrenal medulla, or more rarely extra- adrenal source. Consider in those
with drug- resistant or young- onset hypertension, or typical symptoms.
Symptoms Episodic anxiety, sweating, facial flushing, chest tightness,
breathlessness, tremor, palpitations, headaches, abdo pain, vomiting, or
diarrhoea.
SignsEpisodic hypertension.
InvestigationsPlasma and urine (24h collection) metanephrines. Imaging if
biochemistry positive.
Treatment Surgical resection of tumour can safely be performed only
after adrenoreceptor blockade. α- blockers (eg phenoxybenzamine) are
given prior to β- blockers (eg propranolol) to avoid hypertensive crisis of
unopposed α- adrenoreceptor stimulation. See Box.9.
2Box .9 Cautious prescribingneeded
Many drugs can precipitate a crisis in a patient with phaeochromocytoma. Think before prescribing and if in doubt, seek advice. Put a
warning on the patient’s drug charts to alert prescribers. Common
culprits are opioids, β- blockers, dopamine receptor antagonists, and
steroids.
348 CHAPTER Endocrinology
Thyroid disease
Hyperthyroidism
K Hypermetabolic state driven by excess thyroxine.
Causes Graves’ disease (50– 60%; agonistic autoantibodies to TSH re-
ceptor), toxic multinodular goitre (5– 20%), subacute thyroiditis (5%;
self- limiting, with painful granulomatous infiltrates as de Quervain’s
thyroiditis, or painless lymphocytic infiltrates), toxic adenoma (5%),
amiodarone (either due to excess iodine or drug-induced thyroiditis),
excess exogenous replacement.
Symptoms Weight loss, agitation, anxiety, psychosis, sweating, heat in-
tolerance, diarrhoea, tremor, oligomenorrhoea.
SignsThin, iHR, irregular pulse, warm hands, tremor, goitre ±nodules, lid
lag, lid retraction, muscle weakness;
ophthalmoplegia, pretibial myxoedema, thyroid acropachy.
Investigations TSH used as screening test— if d then measure fT
thyroxine, ie active, not bound to plasma proteins); antithyroid peroxidase (TPO) antibodies positive in Graves’ and other forms of thyroiditis
(TSH receptor antibodies more specific for Graves’ but not routinely
measured);
ECGto exclude AF;USSThyroid, or nuclear scintigraphy may
help localize lesion and assess uptake.
Treatment Symptom relief with propranolol 40mg/ 6h (or rate limiting
calcium-channel blocker if asthmatic); suppress thyroid function using
carbimazole in dose titrated to TFTs, or with thyroxine in ‘block and replace’
approach. Other options include radioiodine ablation or surgical resection.
ComplicationsCCF, AF, ophthalmopathy, osteoporosis.
3
Thyrotoxic storm This is caused by infection, severe illness, recent thy-
roid surgery, or radioiodine. Tachycardia, ±AF, fever, agitation, confusion,
or coma with ifT
get senior help. Propranolol (suppresses sympathetic response, blocks
T
to T3 conversion, and alleviates symptoms), propylthiouracil (inhibits
4
T
/ T4 production and T4 to T3 conversion), and hydrocortisone (reduces
3
iodine uptake and inhibits T
Carbimazole (inhibits T
but may be preferred to propylthiouracil since it has a longer duration of
or iT3. Resuscitate as required (E pp. 478–9) and
4
/ T4 production) has a slower onset of action
3
action and is less hepatotoxic.
Specic toGraves’ disease Exophthalmos,
to T3 conversion) are the main treatments.
4
(free
4
Hypothyroidism
K Common and insidious; characterized by insucient thyroxine release
(Box.0).
Causes Hashimoto’s thyroiditis (autoimmune destruction), resolution
stage of subacute thyroiditis, drugs (eg amiodarone, lithium), iatrogenic
(post surgery or radioiodine), iodine deficiency (commonest worldwide). See also Box..
SymptomsFatigue, lethargy, weight gain, hair loss, depression, confusion,
dementia, cold intolerance, constipation, menorrhagia, infertility.
Signs Obese, bradycardia, dtemp, cold/ dry hands, macroglossia, jaundice,
pitting oedema, goitre, peripheral neuropathy, slow relaxing reflexes.
Investigations iTSH, dfT
Treatment Levothyroxine (T
up into range 50– 50micrograms/ 24h based upon monthly TFTs until
; +ve thyroid autoantibodies.
4
): 50micrograms/ 24h PO, gradually titrated
4
TSH in normal range; yearly TFT once stable. Beware of worsening
underlying ischaemic heart disease:consider propranolol 40mg/ 6h PO to
preventiHR.
ComplicationsAngina from treatment, myxoedemacoma.
K Box .0 Subclinical thyroid disease
Patients with normal fT4 and T3 but i or dTSH have subclinical (hypo/
hyper) thyroid disease. Although some will progress to frank hypo/
hyperthyroidism, there is no management consensus. Positive autoantibodies increase likelihood of progression to overt thyroid dysfunction. Threshold for treatment lower if patient symptomatic. Recheck
TFTs after 3mth; if TSH grossly i or d (eg >0 or <0.mU/ L) then
consider levothyroxine/ carbimazole or surveillance. dTSH and dfT
suggests ‘sick euthyroidism’ in systemic illness— recheck after recovery.
349THYROID DISEASE
4
I Box . Thyroid disease covered elsewhere
Parathyroid diseaseEp. 4
Chapter2
Neurology
2Coma and reduced GCS emergency 352
Coma and reduced GCS 354
Focal neurology 355
Functional neurological disorder 358
2Adult seizures emergency 359
2Paediatric seizures emergency 360
Seizures 36
Neurodegenerative disorders 364
2Stroke/ CVA/ TIA emergency 365
Stroke 366
Back pain 368
Headache 370
Dizziness 374
351
352 CHAPTER2 Neurology
2Coma and reduced GCS emergency
2 Airway
2 Breathing
2 Circulation
2 Disability
Check airway is patent; consider manoeuvres/ adjuncts
If no respiratory eort—
If no palpable pulse—
If GCS ≤8—
CALL ANAESTHETIST
CALL ARREST TEAM
CALL ARREST TEAM
3Call for senior help early if patient unwell or deteriorating.
Airway and C- spine
• Stabilize cervical spine if there is any risk of injury (egfall)
•
Look inside the mouth, remove obvious objects/ dentures
•
Listen for upper airway compromise (gurgling, stridor, snoring)
• Wide- bore
•
Jaw thrust/ chin lift; oro/ nasopharyngeal airway if tolerated.
suction under direct vision if secretions present
Breathing
• 5L/ min O2 if SOB/ sats <94%; beware if previous COPD/ CO2 retainer
• If hypoxicEp. 284
•
Monitor SpO
•
Bag and mask ventilation if poor/ absent respiratory eort
•
ABG, but don’t leave the patientalone.
satsandRR
2
Circulation
• Venous access, take bloods:
•
VBG, FBC, U+E, LFT, glucose, Ca2+, troponin, clotting, G+S, bld
cultures, paracetamol, salicylate, and alcohollevels
•
ECG and treat arrhythmias (tachy E p. 262; brady Ep. 270)
• Start
IV uids if shocked
•
Monitor HR, cardiac trace, andBP.
Disability
• Check blood glucose
• Check for sedatives:
•
opioids, benzodiazepines, antihistamines, TCAs, baclofen, alcohol
• Control
• GCS (Box 2.), pupil reexes, limb tone, plantar responses, neuroobs:
• Call
seizures (Ep. 359)
•
look for brainstem, lateralizing or meningeal signs (Table2.)
anaesthetist for airway support if GCS ≤8 or airway concerns.
Exposure
• Check temperature
• Look over whole body for evidence of injury orrashes
• Ask ward sta for a brief
•
Examine patient brief RS, CVS, abdo, and neuroexam
• Request urgent portable
history and check medicalnotes
CXR
• Stabilize and treat, see following sections
• Call for
seniorhelp
• Reassess, starting with A, B, C…