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_2720_Библиотеки_им_академика_М_И_Перельмана
.pdf
404
https://t.me/med1917
404
CHAPTER12 Gastrointestinalmedicine
Pancreatictumours
Pancreatic cancer accounts for 3% of all malignancies causing ~7800
deaths/ y in the UK. 80% of cases occur in patients >60y. > (3:2).
Riskfactors
• Smoking— causes 25– 30% of pancreatic cancers in the UK. Risk returns
to non- smoker levels 10– 20y after cessation
• Chronic pancreatitis— usually related to excess alcohol
• Type 2 (non- insulin dependent) DM— relative risk 81.8
• Obesity— i risk by 19%
• Genetic— 5% pancreatic cancers are hereditary— characterized
presentation aged <30y and +ve FH
• Occupation— cancer is i among nickel workers, and workers exposed
to insecticides, radiation, lead, iron, or chromium
Tumourcharacteristics
• The majority of pancreatic tumours develop in the exocrine part of the
gland. 95% of tumours are adenocarcinomas. Rarely tumours develop
from the endocrine part— these have better prognosis
• 75% arise in the head of the pancreas, 15% from the body, and 10%
from the tail. Tumours arising in the head of the pancreas tend to
present earlier and are easier to remove
• Spread to local LNs occurs early and metastatic spread to the
peritoneum, liver, and lungs is frequently found at presentation
Presentation Non- specic with:
• Gradual deterioration in health or fatigue
• Anorexia or weight d;
• Pain— epigastric ± radiation l back— may be relieved by sitting forward
• Diarrhoea/ steatorrhoea due to malabsorption
• Early satiety, dyspepsia, or nausea/ vomiting (gastric outlet obstruction)
• Obstructive jaundice
• Pancreatitis
Examination Check for weight d, epigastric or left upper quadrant
mass, hepatomegaly, jaundice. If jaundice is present the gallbladder may be
palpable as a small rounded mass beneath the liver.
Primary care management Refer for urgent assessment (in <2wk)
To a team specializing inupper GI cancer if:
• Upper abdominal mass consistent with pancreatic cancer
• Aged ≥40y + jaundice
For direct access CT (or USS if CT not available) if ≥60y + weight loss
AND ≥1 of:
• Diarrhoea
• Back pain
• Abdominal pain
For direct access USS if Upper abdominal mass consistent with enlarged liver
or gallbladder.
• New DM
• Spontaneous venous thrombosis
• Nausea/ vomiting
• Constipation
• New- onset diabetes
N
.
https://t.me/med1917
PANCREATICTUMOURS
Specialist management Diagnosis is conrmed using a combination
of USS, CT, MRI, and/ or ERCP. The only potentially curative treatment is
surgery but <15% of patients are suitable for surgery at presentation. The
operation of choice is a Whipple’s procedure (pancreaticoduodenectomy).
Surgery is associated with signicant morbidity; mortality 5– 15%.
Prognosis Those undergoing surgical resection have 5y survival of 7– 25%
(median survival 11– 20mo) but those that survive 5y are likely to survive
long- term. Median survival for those with irresectable locally advanced disease is 6– 11mo, and 2– 6mo if metastatic disease.
Palliative treatment Patients with locally advanced/ metastatic disease
may benet from surgical bypass of common bile duct and/ or duodenal
obstruction. An alternative is a biliary stent. Chemotherapy may give some
survival benet. Refer for palliative care support early.
Endocrine tumours In all cases specialist management is required:
Glucagonoma Islet cell tumour of the pancreas. Most are malignant and 90%
have liver or LN metastases at presentation. 5– 20% of tumours occur as
part of multiple endocrine neoplasia (MEN- I) syndrome. Presents with:
• Attacks of hyperglycaemia (DM in >50%)
• Skin changes— sore mouth, necrolytic migratory erythema (70%— rash
which starts as an erythematous rash then blisters before crusting)
• Weight d/ cachexia (60%)
• Tendency to venous
thrombosis(11%)
Insulinoma Tumour of the APUD cells of the Islets of Langerhans. >90%
are benign. 7– 8% are associated with MEN-Isyndrome. Presents with episodes of hypoglycaemia, especially when exercising or fasting. i appetite
and frequent food intake to avoid hypoglycaemia often results in substantial
weight gain.
Somatostatinoma Uncommon islet cell tumour. Most are large tumours
(>5cm) in the head/ body of the pancreas. Presents with gallstones, steatorrhoea, and DM.
0 Extrapancreatic somatostatinomas can present in association with
neurobromatosis type Iand phaeochromocytoma.
Verner Morrison syndrome An intestinal vasointestinal peptide (VIP) producing tumour results in profuse watery diarrhoea l dehydration, metabolic
acidosis, and d K+. Also associated with insulin resistance and impaired
glucose tolerance. VIPomas account for <10% islet cell tumours. 60% are
malignant.
• Anaemia
• Diarrhoea
• Depression/ psychosis
Further information
NICE (2015, updated 2017)Suspected cancer:recognition and referral.
Mwww.nice.org.uk/ guidance/ ng12
Advice and support forpatients
Cancer Research UK F 0808 800 4040 M www.cancerhelp.org.uk
Macmillan Cancer Support F 0808 808 0000 M www.macmillan.org.uk
405
ALGRAWANY
406
https://t.me/med1917
https://t.me/med1917
Chapter13
Renal medicine and
urology
Laboratory tests 408
Estimating renal function 410
Presentation of renal disease 412
Chronic kidney disease 414
Specic kidney diseases 416
Renal stones 418
Haematuria, bladder and renal cancer 420
Urinary tract infection 422
Incontinence of urine 424
Aids and appliances for incontinence 426
Urinary tract obstruction 428
Benign prostatic hypertrophy 430
Prostate cancer 434
Treatment of prostate cancer 436
Conditions of the penis 438
Testicular disease 440
407
ALGRAWANY
408
https://t.me/med1917
408
CHAPTER13 Renal medicine and urology
Laboratorytests
Serum creatinine (Cr) Commonly ordered test to detect renal dys-
function. Can be used to calculate estimated glomerular ltration rate
(eGFR) when corrected for age, sex, weight, and ethnicity (E p. 410). d in
GFR is associated with i in serum Cr.
Urea Commonly ordered test to detect renal dysfunction. While a d in
GFR is associated with an i in serum urea, serum urea may also vary independently of the GFR. Causes of abnormal serum urea:
• i serum urea (>6.7mmol/ L) Renal failure, GI bleeding, high- protein
diet, drugs (e.g. high- dose steroids, tetracycline), dehydration
• d serum urea (<2.5mmol/ L) Liver disease (d urea production), anabolic
state, high ADH levels (high GFR), starvation or low- protein diet, pregnancy
• Plasma potassium >6.5mmol/ L needs urgent treatment.
• Check it is not an artefact, e.g. due to haemolysis inside the bottle
• Admit for investigation of cause and treatment
Hyperkalaemia High serum potassium (>5mmol/ L). Causes:Table 13.1.
Treat the cause.
ECG changes associated with hyperkalaemia Tall, tented T waves; small P
wave; wide QRS complex becoming sinusoidal, VF.
Hypokalaemia Low serum potassium (<3.5mmol/ L). Presents with
muscle weakness, hypotonia, cardiac arrhythmias, cramps, and tetany.
Causes:Table 13.1. If K+ >2.5mmol/ L and no symptoms, give oral potas-
sium supplement. 0 If the patient is taking a thiazide diuretic, hypokalaemia >3.0mmol/ L rarely needs treating.
• Plasma potassium <2.5mmol/ L needs urgent treatment— admit.
ECG changes associated withhypokalaemia Small/ inverted T waves; prominent U wave; prolonged P– R interval; depressed ST segment.
Hyponatraemia Low serum sodium (<135mmol/ L). Rarely symptom-
atic in general practice. May present with signs of water excess— confusion,
ts, i BP, cardiac failure, oedema, anorexia, nausea, muscle weakness.
Causes: Table 13.1. Management: treat the cause. If unwell admit for
investigation.
Hypernatraemia Excess serum sodium (>145mmol/ L). R are in general
practice. Presentation: thirst, confusion, coma, ts, signs of dehydration—
dry skin, d skin turgor, postural hypotension, and oliguria if water decient.
Causes:Table 13.1. Management:admit for investigation.
Glycosuria E p. 312
Proteinuria Excess protein in the urine. Risk factor for renal disease and
CVD. Usually renal in origin. Urine dipsticks are not sensitive for low levels
of proteinuria/ albuminuria. If proteinuria on dipstick, exclude UTI and
repeat. If persists, check dipstick for haematuria, albumin:creatinine ratio
(ACR) or protein:creatinine ratio (PCR), serum Cr, and BP.
https://t.me/med1917
LABORATORYTESTS
Table13.1 Causes ofaltered serum electrolytes
i potassium
(>5mmol/ L)
Renal failure
Drugs, e.g. ACE
inhibitors, excess
K+ therapy, K+sparing diuretics
Addison’s disease
Metabolic acidosis
(DM)
Artefact
(haemolysed
sample)
d potassium
(<3.5mmol/ L)
Diuretics
Cushing’s
syndrome/
steroids
Vomiting and/ or
diarrhoea
Conn’s syndrome
Villous adenoma
of the rectum
Purgative or
liquorice abuse
Intestinal stula
Renal tubular
failure
Hypokalaemic
periodic
paralysis—
intermittent
weakness lasting
<72h
i sodium
(>145mmol/ L)
Fluid loss
without water
replacement
(e.g. diarrhoea,
vomiting, burns)
Diabetes
insipidus—
suspect if large
urine volume
Osmotic diuresis
Primary
aldosteronism:
suspect if i BP,
dK+, alkalosis
d sodium
(<135mmol/ L)
Drugs— especially
antidepressants (SSRIs
most common) or
diuretics (thiazides
most common)
Renal failure or
nephrotic syndrome
Gut— diarrhoea/
vomiting; stula; rectal
villous adenoma; small
bowel obstruction
Endocrine— SIADH
(E p. 341); severe
hypothyroidism;
Addison’s disease;
gluco- corticoid
deciency
Cardiac failure
Cirrhosis
Cystic fibrosis (E
p. 300)
Heat exposure
Water overload (e.g.
polydipsia)
Postural (orthostatic) proteinuria 2– 5% adolescents; rare >30y. Proteinuria
disappears on early- morning sample. No long- term eects.
Urine ACR and PCR Check using a laboratory urine sample if per-
sistent proteinuria on dipstick, or annually for all patients with DM or eGFR
<60mL/ min/ 1.73m2. If initial result is abnormal and ACR<70mg/ mmol,
conrm with early morning sample. Denitions:
• Microalbuminuria ACR >2.5mg/ mmol (♂) or >3.5mg/ mmol (♀) or
albumin concentration >20mg/ L
• Proteinuria ACR ≥30mg/ mmol or albumin concentration >200mg/ L
0 Use ACR in preference to PCR in most patients as more sensitive to
low levels of proteinuria. Use PCR in preference to ACR if high levels of
proteinuria, in children (<18y) and in pregnant women.
ACR and risk ofadverse outcomes Figure 13.1, E p. 411.
409
In people without diabetes Consider proteinuria to be clinically signicant if ACR is ≥30mg/ mmol (approximately equivalent to PCR ≥50mg/
mmol, or a urinary protein excretion ≥0.5g/ 24h).
In people withdiabetes Consider microalbuminuria to be clinically signicant if ACR >2.5mg/ mmol in ♂ or ACR >3.5mg/ mmol in ♀.
ALGRAWANY
410
https://t.me/med1917
410
CHAPTER13 Renal medicine and urology
Estimating renalfunction
Direct measure of glomerular ltration rate (GFR) using 24h plasma or
urinary clearance is most accurate but is time- consuming and dicult in
practice. Instead, other methods are often used to estimate GFR.
Renal function d with age (~1mL/ min/ y >40y). Always assume a
degree of renal impairment in all patients >75y.
Urine ACR and PCR E p. 409
Estimated glomerular ltration rate (eGFR) Method of calcu-
lation of renal function based on serum creatinine levels. Various equations
exist but, in the UK, laboratories report eGFR using the Chronic Kidney
Disease Epidemiology Collaboration (CKD- EPI) formula. This is adjusted
for body surface area and uses age, sex (× 1.018 if ♀) and ethnicity (×1.159
if of Afro- Caribbean origin) as variables.
Limitations ofeGFR calculation Do not use if rapidly changing renal function
or AKI. May be aected by some drugs (e.g. trimethoprim) and dependent
on muscle mass and diet:
• Overestimates eGFR If elderly, low- protein diet, amputee or muscle-
wasting disorder (e.g. myasthenia gravis, late- stage muscular dystrophy)
• Underestimates eGFR If high muscle mass (e.g. high- level sport or body
builder), high protein diet (e.g. taking protein supplements), muscle
breakdown (e.g. after heavy exercise, myositis, muscular dystrophy)
Interpretation ofeGFR Table 13.2 and Figure 13.1
eGFR cystatin C Method of calculating eGFR using blood cystatin
Clevels instead of creatinine. Consider at initial diagnosis if:
• Standard eGFR (using creatinine) is 45– 59mL/ min/ 1.73m2, sustained for
≥90d, and
• No proteinuria (ACR <3mg/ mmol) or other marker of kidney disease
Under these circumstances, do not diagnose CKD if eGFR cystatin
C>60mL/ min/ 1.73m2.
0 Interpret eGFR cystatin C with caution if uncontrolled thyroid disease:falsely i with hypothyroidism and d with hyperthyroidism.
Cockcroft and Gault formula Box 13.1. Preferred method for
estimating renal function if elderly (≥75y), high or low BMI (>40kg/ m2 or
<18kg/ m2), or at extremes of muscle mass. Provides an estimate of creatinine clearance (CrCl).
Box 13.1 Formula forcalculatingCrCl
CrCl=[(140 − age in years)] × (weight in kg) ÷ serum Cr in micromol/
L × 1.23 (♂) or 1.04 (♀)
0 Use ideal body weight where fat may be a major contributor to body
mass. Use actual body weight if <ideal body weight or high BMI is due to
i muscle bulk.
Ideal body weight in kg=50 (♂) or 45 (♀) + 0.91 x (height in cm − 152.4)
https://t.me/med1917
ESTIMATING RENALFUNCTION
Table13.2 Interpretation ofeGFR results
eGFR in mL/ min/ 1.73m2
>90 60– 90 45– 59 <45
Normal eGFR
0 If serum
Cr i >20%,
may indicate
signicant d in
renal function
Does not indicate
CKD unless other
markers of kidney
damage are present,
e.g. ACR ≥3mg/ mmol,
persistent microscopic
haematuria, or
structural abnormality,
e.g. polycystic kidneys
May indicate CKD if
proteinuria or other
markers of kidney
disease are present. If
no proteinuria (ACR
<3mg/ mmol) and no
other markers of kidney
disease, consider checking
eGFR cystatin C
On 2 readings
>90d apart,
indicates CKD
(E p. 414)
411
Figure13.1 Classication of CKD using eGFR and ACR categories
Reprinted from Kidney International, 85, Levin Aetal., Summary of KDIGO 2012 CKD
Guideline: behind the scenes, need for guidance, and a framework for moving forward, 49– 61.
Copyright©2013, with permission from the International Society of Nephrology.
ALGRAWANY
412
https://t.me/med1917
412
CHAPTER13 Renal medicine and urology
Presentation ofrenaldisease
Renal disease may present to the GP with:
• Haematuria (E p. 420)
• Proteinuria (E p. 408)
• d renal function (E p. 410)
• Outow tract obstruction (E
p. 428)
Acute kidney injury (AKI)
oliguria/ anuria. Investigate for AKI by checking serum Cr and comparing
with baseline if acutely unwell and any of the following factors apply:
• Age >65y
• Heart failure
• CKD (especially if eGFR is usually <60mL/ min/ 1.73m2)
• Hypovolaemia (e.g. diarrhoea, vomiting, diuretics, fever)
• Disability that may limit access to uids (e.g. cognitive impairment,
neurological condition)
• Potentially nephrotoxic drugs in the past week (e.g. NSAIDs, ACE
inhibitor/ ARB, diuretics, iodinated contrast agent)
• Oliguria (urine output <0.5mL/ kg/ h)
• History of, or condition predisposing to, urological obstruction
Diagnostic criteria forAKI
• i in serum Cr of ≥26 micromol/ L in <48h
• ≥50% i in serum Cr known/ presumed to have occurred in <7d
• d in urine output to <0.5mL/ kg/ h for >6h in adults and >8h in
children/ young people
• ≥25% d in eGFR in children/ young people in <7d
Management If AKI is suspected, admit to hospital as an emergency.
Follow- up Monitor for development or progression of CKD for at least 2–
3years after AKI, even if Cr has returned to baseline.
• Hypertension (E p.218)
• UTI/ pyelonephritis (E p. 422)
• Nephrotic syndrome
• Nephritic syndrome
N
d renal function over hours/ days ±
• Sepsis
• Past history of AKI
• Liver disease
• DM
Prevention Consider ‘sick day rules’. If a patient is unwell with fevers,
sweats/ rigors, or vomiting/ diarrhoea (unless minor), stop:
• ACE inhibitors and ARBs, e.g. losartan, candesartan, ramipril, lisinopril
• NSAIDs, e.g. ibuprofen, naproxen
• Diuretics, e.g. furosemide, bumetanide, bendroumethiazide
• Metformin (i risk lactic acidosis when dehydrated)
Chronic kidney disease (CKD) E p. 414
Nephrotic syndrome Proteinuria, hypoalbuminaemia, and oedema.
Often associated with i cholesterol. Causes:
• Minimal change
glomerulonephritis (GN)
(90% children, 30% adults)
• Membranous GN
• Focal segmental
glomerulosclerosis
• Membranoproliferative GN
• DM
• Amyloid
• Neoplasia
• Endocarditis
• PAN
• SLE
• Sickle cell disease
• Malaria
• Drugs (penicillamine,
gold)
https://t.me/med1917
PRESENTATION OFRENALDISEASE
Presentation Swelling of eyelids and face; ascites, peripheral oedema;
urine froth due to protein. Nephrotic crisis:unwell with oedema, anorexia,
vomiting, pleural eusions, and muscle wasting.
Investigation Urine:ACR (>220mg/ mmol); microscopy for red cells and casts;
Blood: U&E, creatinine, eGFR, albumin (<25g/ L), cholesterol, FBC, ESR/ CRP.
Management Refer all suspected cases of nephrotic syndrome to a renal
physician. Complications include:
• Thromboembolism • Hypercholesterolaemia
• Infection— especially pneumococcal— if persistent nephrotic syndrome,
oer vaccination
• Hypovolaemia and renal failure
• Loss of specic proteins, e.g. transferrin (causes hypochromic anaemia
which is iron resistant)
Nephritic syndrome Central feature is blood and protein in the urine
from glomerular inammation.
• Causes GN (may occur after throat, ear, or skin infection with group
Aβ- haemolytic streptococci), vasculitis
• Features Oliguria, haematuria and proteinuria, uid retention, i BP,
uraemia, and i creatinine
• Management Refer suspected cases immediately to renal medicine
• Risks Hypertensive encephalopathy, pulmonary oedema, acute
kidney injury
• Prognosis Excellent in children; in adults some proteinuria/ urine
sediment may persist. CKD is rare
Nephrocalcinosis Deposition of Ca
tion. May cause symptoms of UTI or renal stones. Cause:
• Medullary (95%) Hyperparathyroidism, distal renal tubular acidosis,
medullary sponge kidney, idiopathic calciuria, papillary necrosis, oxalosis
• Cortical Serious renal disease or chronic GN
2+
in the kidneys. X- ray: calcica-
Anaemia and renal disease 2° anaemia due to d kidney erythropoi-
etin production is universal among people with severe renal disease (G4/ 5).
Exclude other causes. Recombinant erythropoietin is given if Hb <10.5g/ dL.
Specic kidney diseases E p. 416
Patient support and information
Kidney Patient Guide M www.kidneypatientguide.org.uk
The National Kidney Federation F 0800 169 0936 M www.kidney.org.uk
413
ALGRAWANY
Соседние файлы в папке Библиотека им академика М.И. Перельмана