MRCP Part 1 Jan 06

Discussion in 'MRCP Forum' started by yc, Jan 26, 2006.

  1. yc

    yc Guest

    Hello, I thought I'll contribute some of the questions I remembered from the exam. The answers are what I have written and I am not certain about them.

    Cardiovascular
    Patient in heart failure. Which beta blocker would you give
    Ans : Carvedilol

    Young lady - collapse a few times. Father passed away from sudden death. Whats the likely cause.
    Ans : Cardiac Syncope (My guess is HOCM)

    Prolonged QT --> Torsades. How would you treat
    Ans : Magnesium

    Prolonget QT --> Which drug is causing them
    Ans : ?sotalol

    Pharmacology
    Rash in sunlight
    Ans : Amiodarone

    Drugs causing pancreatitis
    Ans : Lamotrigine. I think real answer is Carbamazepine

    Drugs causing polyuria
    Ans : Lithium

    Infectious Disease
    Young lady, visiting West Africa. Came back with fever, petechial rash. No lymph nodes
    Ans : Dengue, ?possibly Malaria

    Respiratory
    Small cell lung cancer, tumour growing on R main bronchus. How would you treat
    Ans : laser therapy (most prob wrong) other options include radiotherapy, chemotherapy, surgical

    Neurology
    Patient with guillain barre syndrome. Severely breathless, Sats 95%. Unable to measure VC What would you do
    Ans : Intubate, ?increase O2 to 100%

    Patient with absense ankle reflex
    Ans : Common Peroneal Nerve lesion

    Basic sciences
    Breakdown of peptides
    Ans : Peroxisomes, ?proteases

    Gastroenterology
    Watery diarrhoea, stool chart with weight + showing fasting
    Ans : VIPoma (didn't made sense to me)

    Long history of alcoholism, abdo pain, weight loss, clay coloured stool. Whats the diagnosis
    Ans : Chronic Pancreatitis

    Long history of alcoholism, abdo pain, weight loss, clay coloured stool. Best investigation
    Ans : CT scan

    Acute Medicine
    Someone in anaphylactic shock
    Ans : 0.5ml 1:1000 adrenaline IM.

    Statistics
    - Can't remember the questions but they were relatively straightforward
    - Question on calculating NNT
    - Question on calculating specificity (i think ans was 95+percent)
    - Question on understanding p value <0.02

    Rheumatology
    Patient with asthma develops haematuria ?churg strauss
    Ans : antimyeloperoxidase

    Patient with Raynauds, which is likely to suggest autoimmune disease
    Ans : History of chillbains

    Endocrinology
    Patient develop polyuria, erectile dysfunction and avascular necrosis
    Ans : check blood glucose, ?possibly cortisol

    Psychiatry
    Patient in uni, became withdrawn, thinks lecturers are against him. Hears auditory hallucination
    Ans : ?cannabis induced schizophrenia. Not sure if it was cannabis, could be other drugs

    Patient developing dementia, extensor plantar
    Ans : ?B12 def.

    Renal Medicine
    Patient developing diarrhoea + renal failure --> HUS
    Ans : Treat with dialysis?

    Patient with nephrotic syndrome develops clot. Why?
    Ans : dec. antithrombin 3
  2. yc

    yc Guest

    Rheumatology
    Lady developing swollen knee, red eye ?cause
    Ans : ?reactive arthritis, nongonococcal arthritis

    Gastroenterology
    Patient develop lesion on the anus
    Ans : ?wart

    Dermatology
    Patient develop smooth lesion on forehead
    Ans : sebaceous cyst

    Cardiology
    Patient with known clotting tendency, on warfarin for DVT. Develop hemiplegia. What will be seen on echo
    Ans : normal

    Renal
    Patient with grey legs, aortic thrill. Develops proteinuria
    Ans : ?hepatic vein thrombosis

    Psychiatry
    Known IV drug abuser, complaining of pain. Yawning, pupils reactive to light
    Ans : ?methadone

    Neurology
    Patient with SAH. Has aneurysm + polycystic kidney. How would you screen relative
    Ans : ?to do kidney USS on 1st degree relative. Other option includes MRI relatives

    TI lesion, which dermatomes
    Ans: dun remember

    Haematology
    Which virus predisposed to hodgkin's lymphoma
    Ans : EBV

    Respiratory
    pleural effusion - protein 40 glucose 1.5, what is the most likely cause
    Ans : ?adenocarcinoma, mesothelioma, rheumatoid arthritis, don't remember the other 2 option

    Infectious Disease
    Patient with ?gonorrhea or nongonococcal urethritis
    Ans : treat with doxycycline
  3. Guest

    Guest Guest

    - There was a question regarding the cardiac enzymes to be used for diagnosing MI after 3 days. I dont remember the answer.

    - insurance company question..... serum urate level more than normal. which test to do ???

    - PCR question....
  4. Nath

    Nath Guest

    1. Athelet girl which hormone is suppressed - LH
    2. Source of Folic Acid - Liver
    3. Gentamycin Half Life - 2 hr
    4. Erythromycin action in Gastroparesis - Gastric Emptying ( Made a mistake here- choose inh bac overgrowth )
    5. Relative risk - 10%
    6. Specificity - 950/970
    7.NNT - 100/18-8
    8.Statin action - Inh endogenous synth of cholesterol
    9.Cranial Nerve Palsy - Jugular Foramen
    10.P value 0.01 in a study - 1 in 50 chance of drinking fruit juice helpful in crohns
    11. WPW - radiofrequency abl
    12. addition of 5th anithypertensive ,adverse effect --- ?
    13. pancreatitis in pt with epilepsy and Htn - valproate( Choose nife )
    14.Cannabis use with schizophrenic symp - drug induced schizo was not an option,is it paranoid schizo?
    15. PCR - DNA Amp
    16 - breaking of polypeptide - Protease?
    17. Clonig - right ans is Nuclear Transer ( Mistake )
    18.Preg lady with PE - V/Q Scan
    19. High Calorie - Cheese?
    20. Pt with MI with BP 205/115 - ?
    21 - Rate conrol in Af - Digoxin
    22 - Pt with Patch on Back and rash - P.Rosea
    23 - Pt with erisypelas ,which org - Strep.Pyogens
    24 - Crest Synd - Anticentromere
    25 - Raynouds which is associted - history of Chilblains
    26 - Diplopia,6th nerve palsy,contralateral leg weakness ,ext plantar - Brain tsem infarc,pontine lesio,cerebellpontine,cerebellarhemorrhage --- ans ?
    27 - treatment of Torsedes - Magnesium
    28 - drug cusing torsedes - Sotalol
    29 - refractory Asthma treatment - Magnesium
    30 - retrosternal goitre - flow volume loop
    31 - Asthma,Upperlode Collapse - Churg Staruss
    32 - pt with extensive p.versicolor front and back - Ket cream,Tebinafine cream,Oral Itraconazole - Ans ? ( Choose Oral as extensive)
    33. Lt knee sweeling in a girl after returning from holiday - Gonococcal
    35 - Reiters - HLA B27
    36. child with HUS ,treatment - Plasmapheresis
    37. Tall guy with hypogonadotrophic hypogonadism - Kallmanns
    38. raised calcium,Alp,next investigation - PTH
    39. Pt with pagets,next investigation - Calcium
    40. epoitin resistance,raised PTH - Hyperparathyroidsm
    41. ligh micros of child with Sore throat and haematuria - no change by light microscopy?
    42 - pt with s.clerosis,htn,drug - ACE inhibitor
    43. pt with recurrent thromboembolism - 6 months warfarin
    44. Pt having spinothalamic symp ,dorsal colum spared,acute onset - ant spinal artery aneysm
    45. treatment for BEtremor - propanolol
    46. pt with intermittent diarrhea and constipation - IBS
    47. Pt with occ bloody diarrhea and siggy shows loss of houstr and erythematous friable mucosa - UC?
    48.PAS positive ,Diarrhea - Whipples
    49.24hr h/o blood diarrhea - ? Sheigella
    50.best inv for pancreatic ca - ERCP
    51. endocarditis after 6 weeks of valve replacement - Str.epider
    52. pt with fever,c3 low - SBE
    53. Pt with septic arthritis ,invest - joint aspiration
    54. Pt with stump infection,treatment - Fluclox + Penicillin
    55. Antibiotic for Gram Neg Diplococci - Cipro
    56. Pt with kyphoscoliosis,what Pulmonary f.test - Reduced VC
    57.Pt with pul fibrosis ,PFT shows - PEFR of <50%
    58.Monitoring of colon ca - CEA
    59. malignant melanoma on rt arm,prognsis depends on - Depth of the lesion
    60. Pt with symptoms of tamponade,best Inv - Echo
    61. Pt received carbimazole,monitoring - TSH
    62.Treatment of Hyperthyroidsm in preg - Propylthiouracil
    63.pt with small cell ca,treatment - Chemo
    64.Pt with headache,lacrimation - cluster
    65.Another question on headache with hemiparesis - cerebral venous thrombosis.
    66. Pt presenting with ARF and Rash after Coronary angio - Cholesterol embolism
    67.T1 root lesion - ? Ans ( I choose Horners)
    68. Pt with sore eyes,arthritis - Sjogrens synd
    69.Pt with Lymphoma,which virus - EBV
    70.Pt admitted with vague symptoms,multiple admissions - Somatisation
    71.Pt with Neuroleptic maligant syndrome,which will be the other symptom - ?Fever (other option is Limb tremor)
    72. Treatment /Antibiotic for Tetanus - ? Ans (
    Choose gentamycin ,is the correct ans Metro?)
    73.Young girl with apthous ulcers - Crohns
    74. Pt with arthralgia,skin lesions on the shins,diarrhea - Pyoderma gang
    75.compression of common peroneal nerve at fubula - ? Ans - weakness of everters,loss of sensation over medial lower leg etc.. no foot drop as an option
    76.Pt diarrhea stopped after admission - Laxative abuse
    77.Pt with anaphylaxis,raised BP stridor ,treatment - Options were Inhaled adrenaline,S/C adrenaline,IV And IM adrenalline - ? Ans
    78.One more question on adrenaline - cant remember exactly
    79.Olanzapine blocks Dopamine 2 receptor,which other receptor would enhance it effect - Options were Dopamine 1 ,Seratonin,Alfa 1 etc.
    80. pt with cerebral embolism,dvt,what will u see on echo - normal appearence.
    81. Outbreak of diarrhea on the ward . patients resolving after 48hr. ?close ward, isolate patient etc.
    82. 65yr old lady with Lt hemisphere cerebral infarct, has Lt complete stenosis, and 30% stenosis in Rt Cart. ? no Sugery other otpions arterectomy.+/- angioplasty.
    83. 36yr from Zimbabwe with calcification in bladder on X-ray- Schisto.
    84. Patient with sarcoidosis what wud lead u to start prednisolone-? Hypercalceamia
    85. RTA type 1 common attribute- Renal stones.
    86. Post cholecystectomy bile stone is found best Ix- ?ERCP, CT.etc
    87.Diabetic patient, notices swelling in knee a week later has calf tenderness and ankle swelling-? backers'cyst #. cellulitis
    88. myelofirbrosis likey feature- fatigue etc.
    89. 68yr old man with AS what wud reduce pressure gradient across valve.- ?VSD, AR, MR etc.
    90. Sciatica with severe pain reqiured immediate symptom relief- ?Physio, Analgesia,intra-epidural steroid, bed rest.
    91. COPD with lobar pnemunia treatment. Amoxycillin, Clarythr+Amoxy, Ceftr, etc.

    PS. Q1 paper 2. returned from Visit in West Africa , fever, anemia thromboctypaenia, rash etc options, malaria, dangue fever, Lassa, hiv seroconversion

    92. asymptomatic hyperuricemia, next investigation - ? lipids profile (increase risk IHD)
    93. pt with waldestrom's - cyroglobulinemia, retinal vein thrombosis, etc
    94. pt with cholestasis, which medication responsible - co-** ans: augmentin
    95. ischemic ATN, long term HD prognosis - 20-30%?
    96. solidary thyroid nodule, next step investigation - FNA, radioactive isotope uptake etc
    97. pt with high calcium and phosphate and suppressed PTH ? hypercalcemia of malignancy; initial management - IV lasix, IV normal saline, IV biphosphates
    98. ataxia, parkinsonism and postural drop in BP - multiple systems atrophy
    99. west africa visit with fever, anemia, thrombocytopenia and rash - dengue
    100. what clinical signis would suggest Severe aortic stenosis - radiation to carotids, etc
    101. Road traffic accident - 2 weeks later developed anxiety symptoms. Evaluated 6 months after RTA. Diagnosis? - anxiety, PTSD, etc
    102. h/o splenectomy - give pneumococcal vaccine
    103. s/p kidney transplant with worsening renal function. biopsy shows acute rejection. What mediators? - receipient's T cells
    104. bloody LP with predominantly lymphocytes (100%). Diagnosis - HSV encephalitis
    105. Crytococcus vs toxoplasmosis- CT head with contrast?
    106. Chronic alcoholic with visual hallucinations 3 days after admission - DT
    107. Hep C treatment. What labs to follow? ALT, HCV RNA titers etc
    108. presents with electrolytes imbalance suggestive of DI - medications? lithium
    109. Works in the kitchen. Hand rash with fissures on finger pads. Manangement? ellioments, gloves, etc
    110. pt with heart failure on many medications. What else to add? carvedilol
    111. pt with CRF. What would he most likely die from? AMI/IHD, etc
    112. pt with odynophagia to both solids and liquids. next step investigation? esophageal manomotry studies, etc
    113. sick euthyroidism - low T3, elevated T4 and normal TSH
    114. admitted for AMI, which test would suggest reinfarction? CK, AST, trop I, T
    115. pt with intermittent palpitations associated with dyspnea n dizziness. occurs ~1/week. investigation of choice? holter, loop recorder, event recorder, etc
    116. Poor prognosis in CAP: BUN > 16
    117. heroin addict admitted for pain control. drug of choice for pain control? diclofenac, methadone, tramadol, etc..
    118. Young pt out drinking, had a fall. admitted with neck stiffness. CT head normal. investigation of choice: CSF investigation
    119. father with VZ, wanted to fly to attend daughter's wedding. What to do? fit to fly, give IVIG and fly, give -cyclovir and fly, not fit to fly, etc
    120. features of hypersensitivity pneumonitis: eosinophilia, upper lobe fibrosis, neutrophilia, etc
    121. photosensitivity rash. which medication: amiodarone, aspirin, ACEI, etc
    122. physical findings of a pt presenting with AN: fine hair on body ie lanugo hair
    123. acromegaly seen for increased sweating. reason? sweat gland hypertrophy
    124. action of statins: decrease liver production of cholesterol
    125. best screen for hemachromatosis: ferritin level
    126. pancytopenia and diarrhea: pernicious anemia, celiac disease, etc
    127. leukamogenesis of acute promyelocytic leukemia: fusion of 2 genes?
    128. recurrent pneumonia, elevated total whites with lymphocytosis. etiology? CLL, CVHG, etc
    129. 16 y/o out drinking - developed transient afib. management? lifestyle
    130. family h/o PCKD. best screen? u/s all 1st degree relatives
    131. microalbuminuria. best management? ACEI
    132. action of aldosterone
    133. site which remains impermeable to ADH.
    134. action of DDAVP in vWD. released stored vWF
    135. pt with headache and symptoms of temporal arteritis. next step? esr, prednisolone, analgesics, CT head, etc
    136. role of metformin in PCKD. increase peripheral glucose uptake? (decrease insulin resistance)
    137. role of NAC in paracet poisoning. replenish glutathione concentration
    138. pt with polyuria, decreased libido. What tests to order? ferritin level?
    139. HTN on multiple drugs. c/o edema. which drug? nifedipine?
    140. htn, depression on multiple drugs and lithium. lithium toxic level - induced by which medication? ACEI?
    141. pathology caused by myeloma: activation of osteoclasts.
    142. asthmatic on inhaled steroids and b blockers. c/o dysphagia: esophageal candidiasis?
    143. absent knee reflexes with extensor plantars: b12 deficiency
    144. management of chronic fatigue syndrome
    145. gastric adenocarcinoma on biopsy. what histological features: columnar cells, signet ring cells, diminished goblet cells, etc
    146. cushing's syndrome. what metabolic disorder? metabolic alkalosis
    147. osteoporotic bone pain. on paracetamol. What immediate course of action? add calcitonin? other analgesics
    148. acute red eye: closed angle glaucoma
    149. suicidal attempt on long acting propanolol. bradycardia unresponsive to atropine. next course of action: glucagon
    150. suicidal attempt on TCAs. wide complex tachycardia without p waves. HR 160s. SBP 90. course of action: Dc shock, amiodarone, hco3, MgSO4 etc
    151. white nodular exudate on sigmoidoscopy: pseudomembraneous colitis?
    152. diabetic with frozen shouder: adhesive capsulitis
  5. Guest

    Guest Guest

    gr8 work by NATH. all of us must appreciate
  6. Guest

    Guest Guest

    good work by all who have contributed
  7. Nath

    Nath Guest

    Thanks Ahmadd,Its a group work and I hope some more friends would contribute to the remaining questions.
    Praying for all of us.
  8. Guest

    Guest Guest

    Inv of choice for chronic pancreatitis - ERCP

    DOC for ctrlling rate in AF- Beta/ Ca channel blockers

    Treatment of torsade pointes- Mg

    R u sure that the answer for the man who travelled back from africa is Dengue & not HIV

    Feature of lat epicondylitis- difficulty in pronation

    Treatment of gonococcal urethritis-? 1st choice ceftriaxone not there in the given choices...dont exactly remember the rest

    R u sure that the rash on back is P Rosea & not dermatitis herpetiformis....

    Thyroid profile in Pneumonia patient: Hypothyroidism seen

    Treaatment of chroni fatigue syndrome: antidepressants. Behavioural therapy is the 1st choice whic's not given...decond choice is antidepressants

    There was a Q on early morning headache....ans?

    Rx of small cell Ca: chemotherapy

    Olanzapine : action on D2 & serotonin receptor

    Dr. Anoop George Alex
  9. yc

    yc Guest

    Additional info on questions + other questions.

    Additional information added in blue

    4. Erythromycin action in Gastroparesis - Gastric Emptying, relaxation of pylorus, release of cholecyskinin

    14.A young boy with history of depression and suicidal. Has paranoid delusions, Clinical examination mental state is flat, withdrawn, admits to occasional cannabis use with schizophrenic symp - drug induced schizo, psychotic depression

    16 - Area where this occurs - breaking of polypeptide - Protease, golgi apparatus, endoplasmic reticulum, mitochondrion, peroxisomes

    20. Pt with MI, >2mm ST elevation in V2-6, with BP 205/115, already given morphine and aspirin - the next appropriate management - iv GTN, iv streptokinase, iv tPA,

    25 - A patient has a history of Raynaud's syndrome, which other clinical findings would be associated with underlying connective tissue disease - history of Chilblains, recurrent abortions

    31 - A man with a history of chronic Asthma presented with breathlessness of 4 weeks duration. CXR showed Upperlode Collapse - Churg Staruss, acute bronchopulmonary aspergillosis

    33. Lt knee sweeling in a girl after returning from holiday, also noted to have conjunctivitis, now presents with bilateral ankle swelling - Gonococcal, reactive arthritis

    40. A patient with renal failure on hemodialysis for a few years, has been on epoetin before, with baseline Hb of 11-12. Now noted anemia, Hb 8.0, MCV low, with raised Ca, PO4 and raised PTH, what is the cause of epoitin resistance - Hyperparathyroidsm, occult malignant disease, inadequate epoetin dosing

    42 - pt with systemic.clerosis, is now hypertensive with cotton wool spots on fundoscopy as well as acute renal failure, what is the next management ,drug - ACE inhibitor, oral atenolol, iv nitruprusside, iv labetalol

    43. A lady with a past history of DVT is now on heparin due to a DVT confirmed on doppler. She previously had abortions. What is the next appropriate managment - 6 months warfarin, warfarin indefinitely

    53. Pt with a long history of rheumatoid arthritis which is currently quiescent, complained pain of the right knee. Patient is otherwise apyrexial. What is the next immediate investigation that you would do? with septic arthritis - X-Ray of the right knee, joint aspiration, ESR, CRP

    65.Another question on headache with hemiparesis that resolves after the attack - cerebral venous thrombosis, migraine

    81. Outbreak of diarrhea on the ward . patients resolving after 48hr. ?close ward, isolate patient, stop visitors from coming, use bottled water for drinking

    99. A lady who has been to west africa for 6 months returned. 4 weeks after presents with fever, anemia, thrombocytopenia and rash - dengue, lassa fever, falciparum malaria, typhoid, acute HIV seroconversion

    100. what clinical signis would suggest Severe calcified aortic stenosis - radiation to carotids, loud second heart sound A2, hyperdynamic apex beat

    101. Road traffic accident - 2 weeks later developed anxiety symptoms, headache. Evaluated 6 months after RTA and was found normal. Diagnosis? - anxiety, PTSD, post concussion syndrome

    112. A young lady presents with difficulty swallowing solids and liquids. BMI within normal limits. She vomits after taking 3 mouthfuls of food, OGD done, found food residues at the lower part of esophagus. pt with odynophagia to both solids and liquids. next step investigation? esophageal manomotry studies, barium follow through

    114. admitted for AMI, which test would suggest reinfarction after 3 days? CK, AST, trop I, T

    118. Young lady out drinking the night before, had a fall(?). Had a headache that woke her up and associated with vomiting. has low grade temperature, admitted with neck stiffness. CT head normal. investigation of choice: CSF investigation, MR brain, MR angiography

    138. pt with polyuria, decreased libido, right hip pain. What tests to do in order to confirm the diagnosis? ferritin level, cortisol level, blood sugar level

    Additional recall questions:

    139. An African man has had depressive illness for the past 3 winters. Currently feeling suicidal. Also known to smoke cannabis. What is the diagnosis? Schizophernia, cyclothymic disorder, seasonal related affective disorder

    140. 70yo lady has a history of facial rash exacerbated by sunlight and alcohol. Clinically there is an arythematous papular rash with pustules. Weakly positive rheumatological markers. What is the most approriate treatment? prednisolone, flucloxacillin, dapsone

    141. 80yo lady c/o fatigue, polyarthralgias and alopecia. She has a history of Raynaud's phenomenon. Clinically joints are normal. Diagnosis? Hypothyroidism, SLE, Sjogren's

    142. Patient recently started on carbamazepine for seizures. Came in for breakthrough seizure a few months after and noted subtherapeutic level of anticonvulsants. Pill count showed patient is compliant. What is the explanation? Alcoholic binge, enzyme induction

    143. An elderly gentleman was found to be in AF. Pulse 96, BP 124/84. What is the next step in management? DC cardioversion, aspirin, warfarin

    144. 48yo lady with type I DM for 2 years, but long history of rheumatoid arthritis. Urinanalysis showed proteinuria. Likely renal pathology? amyloidosis, DM nephropathy, NSAIDS induced nephropathy

    155. Young lady with acute leukemia received chemotherapy that consisted of doxoburicin and vincristine. 3 weeks later she complained of abdominal pain with constipation. What is the cause? doxoburicin, vincristine, hypercalcemia

    156. Young woman complained transient aphasia and left sided hemiparesis. She just returned to London from Australia. What is the likely echo findings?

    157. A patient recently started on oral prednisolone. What is the treatment of choice for steroid induced osteoporosis? Ca/D, bisphosphanates

    158. Where is the G protein located ? membrane, mitochondrion, nucleus

    159. A pregnant woman with DM has episodes of loss of consciousness without any warning. What is the cause? fetal insulin secretion, tight glycemic control

    160. Patient came in for decompensated cardiac failure. JVP raised, oliguric, bilateral pedal edema. What test can identify the cause of deterioration? echocardiogram, CXR, Urea and electrolytes, trop T

    161. A patient with compensated type 2 respiratory failure. pH normal. What treatment improves prognosis? Long term O2 therapy, O2 concentrator, pulmonary rehab

    162. A young lady admitted for depression. There was history of recent bereavement. She was given some medication that ran out 7 days ago. Clinically, distressed, tachycardic, has a tremor. What is the likely diagnosis? benzo withdrawal, depression

    163. A young boy with history of acne on minocycline still has acne with scarring. What is the next appropriate management? tetracyline, topical retinoids, oral isoretinoin

    164. drug causing proteinuria - Gold

    165. prognostic factor in Pneumonia - Na 130, Urea 11 ?166.Pt with ataxia,demntia and incontinence - Normal pressure hydrocephalus

    167.Pt with syncopal attacks,father has the same - Cardiac Syncope

    168.Patient with nephrotic syndrome develops clot - ? ans

    169.Patient develop lesion on the anus

    170.Patient develop smooth lesion on forehead -Ans ?

    171.pleural effusion - protein 40 glucose 1.5, what is the most likely cause - Mesothelioma

    172.Patient with ?gonorrhea or nongonococcal urethritis,Antibiotic - ? Doxy
  10. Guest

    Guest Guest

    Yes man i think the same the person from west africa:::: ans::; aaacute HIV

    Outbreak in the ward ::: self limiting :::: use bottle water



    any comments
  11. Guest

    Guest Guest

    there are 2 versions of the 'west african' scenario i think. my scenario was some guy returned from west africa? zimbabwe? (can't remember exact place) presented with pancytopenia and rash (no mention of lymphadenopathy nor any symptoms/signs of mononucleosis) and dx is likely dengue (a similar question was on onexamination).

    those who are interested we have posted questions on mcqs.com as well,
  12. yc

    yc Guest

    HI all, just sat the MRCP part 1 in January, it wasn't as bad as I thought it would be, but I wouldn't say it was easy. ONexamination.com's questions come very very close.


    Resp

    1. Which respiratory test for enlarged obstructive goitre?

    2. Scenario with community acquired pneumonis- you need to memorise the CURB 65 critieria by heart

    Cardio

    1. Scenario with anterior MI, need to know contraindications to thrombolysis to answer this

    2. 68yr old man with AS what wud reduce pressure gradient across valve, i think heart failure is answer

    Resp
    1. Small cell lung cancer, tumour growing on R main bronchus. How would you treat

    2. young man severe guillain barre, FEV1 unrecordable, sats 95%
    what is immediate management? choices: high flow oxygen vs intubation

    How to manage anaphylactic shock, must choose the right does of adrenaline i.e. 0.5mg of 1:1000

    Statistics
    quite straight foward
    1 was on calculating specificity, 2 were on calculating number to treat
    1 was on a trial, with "an intention to treat" vs control, what exactly are they testing?

    infectious
    36yr from Zimbabwe with calcification in bladder on X-ray- Schisto.

    gastro
    gastric adenocarcinoma on biopsy. what histological features: columnar cells, signet ring cells, diminished goblet cells, etc
  13. Guest

    Guest Guest

    Hi to all of u ,,
    and wish u best of luck ,,,,,,,,,,,,,,,IT WASNT AN EASY EXAM
    regarding the man who came from africa with fever,rash........etc
    i remember that he developed the symptoms 6 weeks after arrival so its not dengue cuz dengue has an incubation period of 3-7 days but from the list which also contained typhoid,brucellosis, hiv ,,,,HIV is the most likely answer cuz it has the longest incubation period among all other options.
  14. Guest

    Guest Guest

    Yes i'm also talking abt the same question with incubation period of 6 months.

    and i agree with u ppl that this was not easy paper specially part 2 of the paper
  15. I WILL SEND SOME OF QESTION WITH ANSWER OF MRCP I 24 -1-2006

    1-LEADY PREGNANT 12 W PRESENTED WITH PALPITATION TREMER
    TFT REVELD HIGH T3 T4 LOW TSH
    ANSWER WAS OBSERVATION NO DRUGS

    CROSS REACTIVITY OF TSH RECEPTOR BY HIGH HCG LEVEL IN FIRST
    TRIMESTER

    2-PATIENT WITH BLOODY DIARRHEA WITH HUS
    TREATMENT PLASMA EXCHANGE

    3-LEADY WITH MISSCHRAGE BEFORE WITH THROMBO EMBOLISM
    TREATMENT WARFARINE INDEPENDTILY

    4-OLD AGE WITH AF
    TREATMENT WARFARINE

    5- PATIENT WITH UREATHRAL DISGHARGE G NEG DIPLO COCCUS
    TREAT MENT FIRST THIRD GENERATION CEPHALOSPORINE BUT NOT PRESENT IN OPTIONS. SO TR IS CIPLOX

    5 PATIENT TRAVEL FROM USTRALIA TO LONDON BY AIR LINE GET CVA
    PATENT FORAMINE OVALE

    6-PART OF KIDNEY IMPERMABLE TO WATER ASCENDING LOOP OF HENLE

    OLD AGE WITH RECCERENT PNEMONIA HIGH WBC CLL

    7-PROMYELOCYTIC LEK (M3) FUSION OF GENE(17-15)

    8-patient with headace sign of temporal arteritis (prednosolone)

    9-PATIENT WITH OAT CELL CA TREATMENT CHEMOTHERAPY

    10 CARDIC PATIENT RECIEVE AMIODARONE GET PHOTOSENSEVITY REACTION
  16. Guest

    Guest Guest

    Why not in a pregnant lady... propylthiouracil.....as there are symptooms present i:e palpitations.

    Secondaly why is the diagnosis of a person on aeroplane getting CVA is "Patent Foramen Ovale"
  17. hello ahmaddd

    regarding preqnant lady with tremor and palpitatio


    CROSS REACTIVITY OF TSH RECEPTOR BY HIGH HCG LEVEL IN FIRST
    TRIMESTER .
    because two hormones tsh and hcg have (common alpha unit)
    propyl thiouracil is safe and can be use but is often unnecessary.

    regarding leady travel from australia to london she was health before
    travel get dvt due to long tavel then emboli from vein to rt side of heart
    throw patent foramine ovali to lt side to cerebral circulation.this is the senario of this qestion
    thank
    dr kadhaum
  18. Guest

    Guest Guest

    My contribution to Naths list.

    thank you Nath for all your work.
    here is what I want to add.

    Additional questions I do not think are on the list:

    74yr male. drowsy and confused. Normal anion gap acidosis: acetazolamide.
    Other answers were causes of raised anion gap acidosis.

    Questions on your list which I disagree with your answers. See what you think.

    10. P value 0.01 means that there is a less than 1 in 50 cheance that the nul hypothesis is correct. "Fruit juice is helpful in Crohns" implies causation, which a p value cannot tell you.

    19. High calorie food- I think butter.

    43. Recurrent thromboembolism - lifelong warfarin. (Give 6 months warfarin in 1st embolism, lifelong in subsequent emboli.)

    77. Anaphylaxis pt from prawns. I think the answer is do nothing because he was already hypertensive and has normal sats and presented 2hrs after ingestion. Close observation would be the treatment and steroids would be the real treatment, not further adrenaline.

    90. Sciatica pain- physio.

    My answers to the questions you did not specify the answer:

    109. Works in kitchen, skin reaction: Wear gloves.

    115. Intermittent palpitations - event recorder.

    121. Photosensitivity rash - amiodarone.

    135. Temporal arteritis - give prednisolone.

    161. Type II resp failure in COPD - I think longterm nebs but I'm not so sure about this one.

    162. Young lady, depression. Recent bereavement. Stopped meds 7 dayys ago: I think benzo withdrawal.

    163. Young boy with acne - I think isoretinoin.


    170 Forehead lesion: I think sebaceous cyst. (Although no punctum, nothing else fitted this description.

    So that is my contribution. Feel free to comment.

    thank you Nath for all your work. I will continue to try to find out some answers.

    God bless.
    D.
  19. sawsan s

    sawsan s Guest

    some Answers corrections
    breaking of polypeptide: proteasome
    rate control in AF: flecainide
    Patients with painful, isolated third nerve palsy with pupillary involvement are assumed to have posterior communicating artery aneurysm until proven otherwise.
    child with sore thraot and heamaturia: hypercellularity
    24 hour h/o bllody diarrhea: I think campylobacter
    malignant melanoma: I think the site of lesion is the answer
    COPD with lobar pneumonia, Rx: amoxicillin only!
  20. shabana

    shabana Guest

    lower right chest pain 15 minutes after liver biopsy?
    hemobilia
    bilairy peritonitis
    pneumothorax
    subphrenic hematoms?

    what is the answer please?
  21. Guest

    Guest Guest

    investigation for the diagnosis of a secoend mi within 3 days is the ckmb
  22. Guest

    Guest Guest

    i think lower chest pain after liver biopsy ----------- subphrenic haematoma.


    and thanx to all for ur help and corrections.
  23. regarding opthalmologica guestions

    1-PATIENT WITH RT EYE PUPIL LARGE THAN LT EYE LOW RESPONCE TO LIGHT AND ACCOMIDATION
    HOLMES AEDI PUPIL

    2-PATIENT WITH NEW VESSLE FORMATION IN EYE TREATMENT LASER THERAPY


    PATIENT WITH PTB NEED LIVER F T BEFORE GIVEN ANTI TB

    PATIENT WITH CHRONIC EXTERNAL ALLERGIC PULMONARY ALVEOLITIS
    NOT ESONOPHILIA BECAUSE IT IS TYPE3 HYPER SENSITIVITY REACTION IMMUNE COMPLEX REACTION
    MY ANSWER WAS APICAL PULMONORAY FIBROSIS
  24. shabana

    shabana Guest

    hey guys..
    what do u think the pass mark will be?

    what was the pass mark of sept 2005?
  25. Guest

    Guest Guest

    hi guys i hope all r doinng well and fine and wish u all best of luck,,
    1- Regarding the question of melanoma for which u have to choose the most important prognostic factor :i think the right answer is the duration of the lesion cuz generally when talking about prognosis of a tumor we talk about the duration from which u can expect dissemenation ,but the site ,the depth of the lesion this will depend on the type of melanoma ,e.g when considering the superficial spreadng type we will look for the extent,if the acral type we will look for the depth and for the lentigous type we will look for all ,,so it wasnt specified in the question what type of melanome we are dealing with so the duration well be of the greatest significant applying for all 4 types.
    2-Regarding rate control in AF its digoxin(an av blocker) but fleccanide will be for the paroxism of AF
    3-High calorie food i think its butter from the list as it has more than 65% fat 1g=9 kcal while cheese has less that that
    4-COPD imropve long prognosis long O2 THERAPY
    i will be happy to see ur replys
    Best of luck
  26. shabana

    shabana Guest

    diabetic patient with new vessel formation at optic disc. visual acuity in both eyes not affected (6/9). what is the managment?

    a-tight glycemic control
    b-BP control
    c-repaeat ophthalmoscopy in 3 months
    d-aser treatment
    e-couldnt remember the last option!!

    asymptomatic patient has a brother with hemocromatosis
    what is the screening test?
    a- HFE gene
    b- serum ferritin
    c- serum iron
    d-serum transferrin saturation
    e- TIBC
  27. SHABANA

    SHABANA Guest

    WHAT WAS THE ANSWER FOR THE 62 YEAR OLD LADY WITH LETHARGY, POLYARTHRALGIA AND HAIR LOSS. ON EXAMINATION..HORMAL JOINTS?

    -SLE
    -HYPOTHYROIDISM
    -FIBROMYALGIA RHEUMATICA
    -POLYMYALGIA RHEUMATICA/ GIANT CELL ARTERITIS
    -COULDNT REMEMBER THE LAST OPTION!!!
  28. Guest

    Guest Guest

    FOr haemochromatosis

    Answer::: Transferrin Saturation

    For Diabetic Retinopathy

    Answer:::: Laser THerapy
  29. Nath

    Nath Guest

    hi
    For diabetic retinopathy,they mentioned in the question that there are new vessel formation near the optic disc,So i think the correct ans is Photocoagulation.

    Haemocromatosis - Agree T Saturation
    COPD - LTOT
    Melanoma - Not sure I choose depth of the lesion

    Praying for all of us.
  30. Nath

    Nath Guest

    What was the answer for the pt presenting with complete obstruction of lt corotid with 40% stenosis on rt side.
    anyone...

    cheers
  31. regarding asympthomatic man . his brother has hemachromatosis
    the screening test was

    HFE GENE

    (HARRISON PAGE 2299 16 EDITION)
  32. Guest

    Guest Guest

    FACTS/
    -Regarding heamochromatosis
    for screening best is ferritin level
    for diagnosos T saturation graeter than 60% plus other measures
    -Regarding the carotid obstruction(from published evidances) its highly recommended to ectomize the the artery if it stenosed more than 70% ,so in the question the answer is to remove the completed obtructed one 100% stenosis and to leave the other one with 40%.
  33. Nath

    Nath Guest

    hi,
    Regarding Hemochromatosis ,it looks as if T.St is the right answer.However,I am not sure,whoever asked that question actually knew the correct answer.....Bl--dy
    This article was taken from Internet.


    Screening methods! The most effective biochemical screening test, serum transferrin saturation (TS) identifies about 70% of men and 60% of women with hereditary haemochromatosis at a 0.3% false positive rate (TS cut offs 70% and 65% respectively)[2] ! DNA based testing for C282Y homozygosity (blood or buccal samples) identifies about 83% of individuals with clinically diagnosed hereditary haemochromatosis (reported range 64-100%); the false positive rate is likely to be very low.[3-7][10] Suchtesting is not readily available and has not been costed Subsequent tests! A repeat fasting TS test in individuals with raised elevated TS levels can reduce the false positive rate with little loss ofdetection. In addition, serum ferritin measurements can be used to determine total body iron stores ! Diagnostic tests include: - DNA based testing for HFE mutations after a positive TS screening test - Liver biopsy to assess the degree of liver damage (fibrosis or cirrhosis) and to quantify excess iron, based on hepaticparenchymal cell stainable iron (grade 1-4+) and liver iron concentration (µmol/g dry weight). The hepatic iron index (µmol/g dry weight divided by age at the time of biopsy) is helpful in differentiating hereditary haemochromatosis fromalcoholic liver disease [1] - Quantitative phlebotomy. Removal of 5g or more of iron before the packed cell volume falls is consistent with hereditary haemochromatosis Treatment! Initially remove 500ml of blood (as in blood donation) once or twice a week until the packed cell volume begins to fall and TS and serum ferritin levels return to low normal ! Then, remove 500ml every two to six months to maintain low normal TS and serum ferritin levels Unresolved screening issuesThe case for population screening is not yet made because: ! The size of the effect of screening on reducing morbidity and mortality is uncertain ! There is a need for more detailed information on the prevalence and severity of hereditary haemochromatosis clinical manifestations according to age in the general population ! A better understanding is needed of the correlations between genotype, iron status markers (TS, serum ferritin, hepatic iron), and clinical severity ! The initial screening test of choice (TS or DNA testing) is unresolved ! The best age for screening in men and women is not specified ! Designs for delivering screening related services need to be developed and evaluated 1 Witte DL, Crosby WH, Edwards CQ, Fairbanks VF, Mitros FA. Practice guideline development task force of the College of American Pathologists: HereditaryHemochromatosis. Clin Chim Acta 1996;245:139-200. 2 Bradley LA, Haddow JE, Palomaki GE. Population screening for haemachromatosis: expectations based on a study of relative of symptomatic probands. J Med Screen 1996;3:171-7. 3 Feder JN, Gnirke A, Thomas W, Tsuchihashi Z, Ruddy DA, Basava A et al. A novel MHC class I-like gene is mutated in patients with hereditary haemachromatosis. Nature Genetics 1996;13:399-408. 4 Jouanolle AM, Gandon G, Jezequel P, Blayau M, Campion ML, Yaouang J et al. Haemachromatosis and HLA-H. Nature Genetics 1996;14:251-2. 5 Beutler E, Gelbart T, West C, Lee P, Adams M, Blackstone R et al.Mutation analysis in hereditary haemachromatosis. Blood Cells Mol Dis 1996;22:187-94. 6 Borot N, Roth MP, Malfroy L, Demangel C, Vinel JP et al. Mutations in theMHC class I-like candidate gene for hemachromatosis in French patients. Immunogenetics 1997;45:320-4. 7 Carella M, D'Ambrosio L, Torato A, Grifa A, Valentino MA, Piperno A, et al. Mutation analysis of the HLA-H gene in Italian hemachromatosis patients. Am J Hum Genet 1997;60:828-32. 8 Roberts AG, Whatley SD, Morgan RR, Worwood M, Elder GH. Increased frequency of the haemachromatosis Cys282Tyr mutation in sporadic porphyria tarda. Lancet 1997;349:321-3. 9 Merryweather-Clarke AT, Pointon JJ, Shearman JD, Robson KJH. Global prevalence of putative haemochromatosis mutations. J Med Genet 1997;34:275-8. 10 Jazwinska EC, Cullen LM, Busfield F, Pyper WR, Webb SI, Powell LW et al. Haemachromatosis and HLA-H. Nature Genetics 1996;14:249-51.
  34. shabana

    shabana Guest

    a diabetic parient with 60 mg protein/24 hour urine. what is the most likely subsequent complication?

    -retinopathy
    -myocardial infarction
    -neuropathy
    -renal failure
    -couldnt rememcer the last option!!!!!!


    a diabetic patient with microalbuminuria. what is he likey to die from?
    hypertensive heart disease or dilated cardiomyopathy?
  35. Nath

    Nath Guest

    \Hi
    I think its Renal failure due to diabetic nephropathy.Any comments.
  36. Nath

    Nath Guest

    a diabetic patient with microalbuminuria. what is he likey to die from?
    hypertensive heart disease or dilated cardiomyopathy

    I think the question was .Pt on 5 yr haemodialysis,what is he most likely to die from.
    Options were CAD,Dilated Cardiomyopahty.
    I choose CAD as he is most likely to die from MI.
    However,not sure,Any comments.
  37. regarding cushing s question associated with metabolic alkalosis
    but in question put two options
    1-hypochloriemic m alkalosis
    2- hyperchloriemic m alkalosis

    my answer option 1( hypo ch metabolic alkalosis )
  38. Guest

    Guest Guest

    Patient on haemodialysis dies of - The right answer is CAD as they die of IHD then next comes the cardiac failure and the last cerebrovascular disease. REF - OHCM pg no.278 complications of dialysis.
  39. Guest

    Guest Guest

    Guest User

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    Have a go at the question of the day
    Try today's question based on topics from the December 2004 exam and compare your scores with others. Registered users have access to all questions with detailed feedback. Revising online lets you know exactly how your performance compares to others that are sitting the exam.
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    Score: 1 (100%)

    A 65-year-old man presented with a four week history of pleuritic chest pain associated with shortness of breath and dry cough. He also reported weight loss of nearly 10kg in the past six months.
    He had a past history of myocardial infarction 20 years earlier from which he had made a good recovery. He did not suffer from any exertional chest pain subsequently. He lived alone and had not seen his general practitioner for two years. He seldom saw his General Practitioner, but had attended the surgery twice recently with mild recurrent pain in his left knee that responded well to treatment with simple analgesia. He was an ex-smoker of 15 cigarettes per day, having given up smoking 20 years previously. His only medication was aspirin.
    On examination of his chest he had reduced expansion, dull percussion note and decreased breath sounds on the right. A chest X-ray confirmed a right-sided pleural effusion.
    Analysis of a pleural aspirate revealed:
    Pleural fluid protein content 42 g/L
    Pleural fluid glucose 1.3 mmol/L
    What is the diagnosis?

    Available marks are shown in brackets
    1 ) bronchial carcinoma
    [0]
    2 ) cardiac failure
    [0]
    3 ) mesothelioma
    [0]
    4 ) rheumatoid arthritis

    [100]
    5 ) tuberculosis
    [0]

    Comments:
    The pleural fluid protein is greater than 30g/l which demonstrates it is an exudate and effectively excludes cardiac failure. If pleural fluid protein is 25-35 g/l then Light’s Criteria is more accurate in determining whether the effusion is an exudate or transudate. It is an exudate if 1 or more of the following criteria are met (a) pleural fluid protein divided by serum protein > 0.5 (b) pleural fluid LDH divided by serum LDH > 0.6 (c) pleural fluid LDH > 2/3rds upper limits of normal serum LDH.
    The pleural glucose level is very low. Levels less than 3.3 mmol/l are found in empyema, rheumatoid arthritis, lupus, malignancy, oesophageal rupture and tuberculosis. The lowest levels are found in rheumatoid effusions and empyema with pleural glucose in rheumatoid effusions rarely being above 1.6 mmol/l.

    Registered users average score for this question is 37.2% (answered 4094 times)
  40. Guest

    Guest Guest

    The above two replies have been posted by the same guest in order to make all the MRCPians aware as these questions can appear in the next forthcoming mrcp exam-
    The question with PL effusion with Pr > 40 and Glu < 1.5 mmol/L which appeared in JAN 06 mrcp1 - the right answer is RHEUMATOID ARTHRITIS as you could read the above copy of a question which was a free a day question from onexamination.com last JAn 2005.
  41. Guest

    Guest Guest

    hi,
    Regarding Hemochromatosis ,it looks as if T.St is the right answer.However,I am not sure,whoever asked that question actually knew the correct answer.....Bl--dy
    This article was taken from Internet.




    Yes Dr.Nath the rt answer is Transferrin Saturation-


    The answer for the renal problem like after proteinuria, subsequently the patient goes into RENAL FAILURE
  42. Afshaan

    Afshaan Guest

    Hi

    Dear Doctors

    Could u please list me the books required to give MRCP EXAM and if some one is selling them do let me know.



    Thanks
  43. shabana

    shabana Guest

    why was the answer to the patient with COPD and lobar pnemonia amoxicillin and not amoxicillin+ clarithromycin?
  44. Nath

    Nath Guest

    not sure about the answer but I choose amox + clar,,.......anyone

    cheers
  45. shabana

    shabana Guest

    what immediately reverses the effect of warfarin?
    cryoprecipitate
    fresh frozen plasma
    oral vit k
    parenteral vit k
    ?
  46. fresh frozen plasma
  47. shabana

    shabana Guest

    what was the answer for the patient with left complete stenosis of the common carotid and 30% stenosis of the right?
    no surgical intervention or left carotid endarterectmy?
  48. sawsan s

    sawsan s Guest

    The Dutch College of General Practitioners (NHG) Practice Guideline

    This NHG Practice Guideline is a translation of the Dutch guideline. It is specifically written for Dutch general practitioners in the Dutch enviroment. The advice which is given may therefore not be in accordence with the views of general practitioners in other countries.


    --------------------------------------------------------------------------------

    NHG Practice Guideline 'COPD: treatment' (May 2001)
    R.M.M. Geijer, C.P. van Schayck, C. van Weel, A.P.E. Sachs, B.J.A.M. Bottema, I.J.M. Smeele, H.A. Thiadens, W. van Hensbergen, C.F.H. Rosmalen

    This practice guideline and its scientific basis have been updated with respect to the previous version (NHG Practice Guidelines for the General Practitioner 1, 1999). The most important points are:

    Cessation of smoking is the most significant intervention for improving the prognosis.
    Bronchodilators should be given for symptomatic treatment.
    Cooperation with the pulmonologist is indicated for diagnostic problems, patients with severe COPD, and patients with moderately severe COPD with a rapidly progressive course.
    New:

    Pulmonary function (FEV1) should be monitored once yearly. More frequent pulmonary function measurements are no longer recommended in the initial years after COPD has been diagnosed.
    The accelerated deterioration of lung function is not inhibited by a high dose of inhaled glucocorticoid.
    Cooperative agreements with the pulmonologist are described in detail in the Landelijke Transmurale Afspraak COPD [National Transmural Agreement on COPD].


    INTRODUCTION
    The NHG Practice Guideline 'COPD: treatment' provides guidance for the treatment of COPD (Chronic Obstructive Pulmonary Disease). The diagnosis of COPD and the treatment of asthma are covered in separate practice guidelines.1

    The typical starting point is a patient, usually over 40 years of age, who has complaints of almost constant dyspnoea and/or coughing, with or without mucus production, in whom

    Reversibility with bronchodilators can not be shown, and
    normal pulmonary function, measured by FEV1, cannot be achieved, even after a diagnostic trial with 30 mg prednisone or prednisolone for 14 days.
    The short-term aim of the treatment is to reduce symptoms, improve exercise tolerance, improve pulmonary function, and prevent exacerbations.

    The long-term aim of treatment is to prevent or slow progressive deterioration of pulmonary function, delay or prevent complications and disability, and improve disease-related quality of life.

    The most important component of the treatment is talking with patients about the effects of smoking and motivating them to stop, since this can improve pulmonary function in the short term and slow further deterioration of pulmonary function in the long term.2 Drug therapy for COPD is less research-based than that of asthma. Complaints are treated symptomatically with bronchodilators. There is no evidence that an inhaled glucocorticoid has a beneficial effect on pulmonary function, but there are indications that an inhaled glucocorticoid diminishes the complaints and reduces the frequency of severe exacerbations in patients with moderately severe COPD. The benefits of prophylactic treatment with acetylcysteine are still uncertain.

    Parameters for the effectiveness of the treatment are exercise tolerance, the severity of the complaints, and the degree of bronchial obstruction. The preferred method for determining the degree of bronchial obstruction is measurement of FEV1, expressed as a percentage of the reference or 'predicted' value. The measurement must be made under certain controlled conditions. If the general practitioner cannot provide these, the measurement should be made in a general practice laboratory or in the pulmonary function department of a hospital. Making regional agreements for this is advisable.

    The severity of bronchial obstruction can be classified as follows:

    mild: FEV1 reduced but >70% of the predicted value
    moderate: FEV1 >50% and <70% of the predicted value
    severe: FEV1 <50% of the predicted value or <1.5 litre
    For the sake of simplicity, the terms 'mild,' 'moderately severe', and 'severe' COPD will be used hereafter to represent the FEV1 categories. In addition to FEV1, however, the severity of COPD is determined by the severity of the dyspnoea and other complaints (coughing, mucus production), the severity and frequency of the exacerbations, the limitations of exercise tolerance, and the presence of comorbidity.3 Limitations of exercise tolerance due to dyspnoea can be classified as follows, taking into account the patient's normal level of activity:

    grade 1: no restriction of physical activity due to dyspnoea
    grade 2: limited restriction (problem-free at rest but normal physical activity causes dyspnoea)
    grade 3: moderate restriction (problem-free at rest but less than normal physical activity causes dyspnoea)
    grade 4: severe restriction (mild physical activity such as ADL causes dyspnoea, or dyspnoea at rest)
    .

    The general practitioner can test and treat most patients with mild or moderately severe COPD, provided that the practice has a spirometer and the general practitioner is capable of interpreting the results of the lung function test. COPD patients with severe lung disease (FEV1 <50% of the predicted value) or COPD patients with less severe lung disease but rapidly progressive complaints of dyspnoea or reduced exercise tolerance despite receiving optimal treatment, should be referred to the pulmonologist.



    MANAGEMENT GUIDELINES
    Information
    COPD is a chronic disorder in which pulmonary function has deteriorated rapidly. The most significant cause is smoking. In the long term, smoking causes irreversible damage to the lungs in susceptible individuals, resulting in limitations in daily functioning due to shortness of breath, sometimes at a relatively young age. Smoking cessation slows this rapid deterioration of pulmonary function.2 Viral and bacterial infections can greatly worsen the symptoms temporarily. Influenza carries a greater risk of complications in COPD patients4 and influenza vaccination is therefore indicated.

    Inhalation is the preferred method of administering medications for COPD. This should be discussed and demonstrated. An agreement should be made that the patient brings his inhaler(s) when coming for a consultation. If the complaints worsen, patients who have been carefully instructed in the use of short-acting bronchodilators can increase the dose themselves, up to the recommended maximum. Patients should contact the general practitioner if there is insufficient improvement, a continually increased need for bronchodilators, or an increase in the dyspnoea associated with fever or malaise.



    Preconditions
    The care of patients with asthma and COPD can be partly delegated to a well-trained practice assistant or to a practice nurse who can provide some or all of the following:

    information
    conservative advice, such as guidance on stopping smoking
    lung function testing (annual spirometry at COPD follow-up)
    instruction on inhalation
    scheduling and implementation of influenza vaccinations
    scheduling and participation in follow-ups


    Non-medicinal interventions
    Smoking cessation is the most important step in treating COPD.2 A structured approach is advisable, such as the one described in the NHG DKB Smoking Cessation workbook. Nicotine replacement therapy is recommended to support the process of giving up smoking.2 For those who are unmotivated or who do not succeed in stopping, the motivation to quit smoking and any potential blocks can be brought up again at a later time. Discourage smoking in the presence of the patient by others in the patient's house.

    The general practitioner should give the patient advice on improving physical fitness (cycling, walking, swimming), taking into consideration the patient's interests and possibilities. The general practitioner should discuss the importance of a healthy diet.5 If overweight, the patient should try to lose weight.

    For all patients with COPD who continue to have limitations and handicaps despite optimal medical care, a rehabilitation programme should be discussed after referral to the pulmonologist (see the section 'Consultation and referral').

    If there are signs of worsening of symptoms due to factors in the patient's workplace, discuss taking up contact with the Occupational Health and Safety Department about options for modifying the work or changing jobs. If work-related factors are jeopardizing the patient's work or career track, referral to the pulmonologist is indicated.



    Drug therapy
    Inhaled medications are used in the management of COPD. Options include metered-dose aerosols and dry powder inhalers.6

    With metered-dose aerosols, the dosage delivery and the average particle size do not depend on the inspiratory force, and deposition in the lung is primarily determined by hand-lung coordination. This coordination problem can be overcome by using a spacer or a 'breath-actuated' metered-dose aerosol. With dry powder inhalers, the dosage delivery and the average particle size depend on the inspiratory force, which largely determines the deposition in the lung. Most types—with the exception of the multidose inhalers—are somewhat awkward to prepare for use. The deposition in the lung is greater with some dry powder inhalers (due to the physical properties of the device) or some metered-dose aerosols (due to a smaller particle size). Because of this, the same preparation may have different recommended doses, depending on the type of inhaler or metered-dose aerosol.

    The above properties and the patient's skill with the device should be taken into consideration when choosing an inhalation form. In general, a dry powder inhaler or a metered-dose aerosol can be used by patients with adequate inspiratory force and adequate hand-lung coordination. For older patients (with inadequate inspiratory force and/or poor coordination) or patients with severe dyspnoea, use of a spacer is preferable.6 7 When prescribing multiple medications, aim for consistency in the method of administration.8

    The following inhalation instructions should be given (for more information see the Skill Promotion Packet of the Dutch College of General Practitioners (NHG) on Asthma/COPD: Treatment):

    Metered-dose aerosol: shake well before use, inhale slowly while depressing the nebulizer, and hold the breath for at least 5 seconds.
    Dry powder inhalation: inhale forcefully and deeply.
    Spacer: shake the metered-dose aerosol well before use, spray one puff at a time depending on the size of the spacer, and inhale immediately after spraying, to minimize deposition of medication on the spacer walls. Wash and air-dry plastic spacers regularly, to minimize deposition on the spacer walls due to static electricity.
    Over the course of time, particularly if medication changes are being considered, attention should be devoted to:

    cessation of smoking
    compliance with treatment
    the inhalation technique


    Bronchodilators

    For COPD patients, try different bronchodilators or combinations of bronchodilators to determine which is most effective (see Table 1).9 10 11

    The following short-acting bronchodilators can be used:
    an anticholinergic agent (ipratropium bromide),
    or a short-acting beta2 sympathomimetic agent (salbutamol, terbutaline or fenoterol).
    If there is inadequate clinical improvement in two weeks, change to a different type of bronchodilator.
    If the alternative medication still gives insufficient improvement after two weeks, use both bronchodilators simultaneously.
    The lowest effective dose of one of the two alternatives or a combination of the two should be prescribed as a maintenance dose.
    For mild exacerbations, temporarily increase the dose to the maximum.
    There are limited indications for prescribing a different bronchodilator or another method of administration.

    For patients whose nightly sleep is disturbed by dyspnoea despite continuous use of a short-acting beta2 sympathomimetic agent and ipratropium bromide, prescribe a long-acting beta2 sympathomimetic agent in place of a short-acting beta2 sympathomimetic agent (see Table 2).11
    For COPD patients who are unable to inhale adequately using a dry powder inhaler or a metered-dose aerosol, discuss the use of a spacer.
    The addition of theophylline can be considered for patients who still have symptoms despite optimal symptomatic treatment with inhaled bronchodilators.12 This applies primarily to patients with severe COPD. The pulmonologist should decide whether it is indicated.


    Table 1. Short-acting bronchodilators

    Medication
    Powder inhalation

    dosage (maximum)
    Metered-dose aerosol

    dosage (maximum)

    Lower doses are used for some metered-dose aerosols or dry powder inhalers: consult the Farmacotherapeutisch Kompas [Pharmacotherapeutic Compass]

    Ipratropium bromide*
    40 mcg 4 times daily 1 (4 times daily 2)
    20 mcg 4 times daily 1 (4 times daily 2)

    Salbutamol#
    100-400 mcg 4 times daily 1 (4 times daily 2)
    200 mcg 4 times daily 1 (4 times daily 2)

    Terbutaline#
    500 mcg 4 times daily 1 (4 times daily 2)
    250 mcg 4 times daily 1 (4 times daily 2)

    Fenoterol#
    200 mcg 4 times daily 1(4 times daily 2)
    200 mcg 4 times daily 1 (4 times daily 2)


    *anticholinergic # beta2 sympathomimetic agent



    Table 2. Long-acting beta2 sympathomimetic agents

    Medication
    Dosage (maximum)

    Lower doses are used for some metered-dose aerosols or dry powder inhalers: consult the Farmacotherapeutisch Kompas [Pharmacotherapeutic Compass]

    Formoterol
    6-12 mcg twice daily 1 (twice daily 2)

    Salmeterol
    50 mcg twice daily 1 (twice daily 2)




    Other medications

    Treatment with inhaled glucocorticoids or acetylcysteine is not recommended for all COPD patients.13 14 15

    For COPD patients with a history of asthma and/or atopy, or with no history of smoking, a therapeutic trial with an inhaled glucocorticoid is indicated.
    If there is subjective improvement in 3-6 months, the treatment is continued; if not, the treatment is discontinued.

    If there are frequent exacerbations (3 or more in a year or in the previous winter period), a choice can be made between a trial treatment with (see Table 3):
    a high-dose of inhaled glucocorticoid, for patients with (moderately) severe COPD
    acetylcysteine
    If the number of exacerbations declines (assessed after 12 months and measured as the number of courses of oral glucocorticoid or antibiotic, or hospitalizations due to COPD), the treatment is continued; if not, the treatment is discontinued.

    It is unclear whether inhaled glucocorticoids are also indicated for patients with moderately severe COPD and many complaints and/or limitations.
    In exceptional cases, a maintenance programme with antibiotics may be advisable in order to reduce the number of exacerbations.16 The pulmonologist should decide whether this is indicated.


    Table 3. Inhaled glucocorticoids, acetylcysteine

    Indication
    Purpose
    Medications and dosage

    Lower doses are used for some metered-dose aerosols or dry powder inhalers: consult the Farmacotherapeutisch Kompas [Pharmacotherapeutic Compass]

    Medical history:

    -with asthma and/or atopy

    -without smoking
    Treatment of inflammation
    400 mcg beclomethasone or budesonide or 250 mcg fluticasone, twice daily for 3-6 months (see NHG Practice Guideline 'Adult asthma: treatment')

    Frequent exacerbations (>3 in the previous winter and/or year)
    Reducing the frequency of exacerbations
    800-1600 mcg beclomethasone or budesonide daily or 500-1000 mcg fluticasone daily in 2-4 doses for 12 months

    600 mg oral acetylcysteine once daily for 12 months




    Follow-ups
    A 'new' COPD patient should be seen every 2 weeks after changing the treatment—sooner if there is severe dyspnoea, of course—to determine whether the patient is improving satisfactorily.

    When the situation is acceptable, the frequency of follow-ups can be cut back to once every 6-12 months.17 Parameters for the clinical course are the severity of the complaints, exercise tolerance, physical limitations, and FEV1.

    The follow-up consists of:

    evaluating the symptoms, physical limitations, exercise tolerance, and nutritional condition
    evaluating the effect of the current treatment ('24-hour history')
    discussing problems in quitting smoking and, if necessary, offering additional guidance and support
    monitoring compliance and inhalation technique
    physical examination, if necessary, including weight measurement
    annual spirometry17
    giving attention to any comorbidity, such as heart failure (see the relevant practice guideline) and lung cancer
    noting any side effects of the medication, particularly if the patient is on long-term use of high doses of an inhaled glucocorticoid or is on an oral glucocorticoid18


    Consultation or referral
    Diagnostic problems
    Referral is indicated for:

    a discrepancy between the severity of the complaints and the objective findings (e.g., spirometric results)
    COPD at a relatively young age (arbitrary cut-off <50 years)
    lingering doubts as to whether the reduced exercise tolerance is caused by COPD or by concomitant heart failure (For patients with COPD and signs of heart failure, even after additional examinations and tests under the general practitioner's supervision (chest x-ray, ECG, spirometry), there may be lingering doubts about the degree to which pulmonary or cardiac causes contribute to the decrease in exercise tolerance. Refer to a cardiologist or pulmonologist, depending on the suspected cause of the worsening of the complaints.)
    Referral for additional diagnostic studies is also indicated if any of the following disorders are suspected (not an exhaustive list):19

    lung cancer
    pulmonary disease with reduced lung volume (restrictive pulmonary diseases) such as lung fibrosis and pneumoconiosis
    pulmonary diseases in which gas exchange is hampered by disorders of the interstitial lung tissue (diffusion disorders), such as extrinsic allergic alveolitis (e.g., allergens from pigeons or parakeets)
    a pneumothorax, tuberculosis, or other pulmonary disease


    Failure or inadequacy in attaining treatment goals
    When the response to the treatment is unsatisfactory, consider the exercise tolerance in patients with COPD to be permanently reduced.

    Refer patients having a severe form of COPD, as when:

    FEV1 is <50% of the predicted value or <1.5 litres, despite optimal treatment. When referring, request additional diagnostic studies (to exclude other causes or disorders) and treatment recommendations.19
    The clinical course is rapidly progressive (increased dyspnoea, decreased exercise tolerance) despite maximal treatment with bronchodilators and an inhaled glucocorticoid (even if FEV1 is >50% of the predicted value).20
    There is unintended weight loss of 5% or more within 1 month or 10% or more within 1 year.19 24
    There have been more than two exacerbations per year for which oral glucocorticoids or hospitalization was necessary, despite treatment with a high-dose of inhaled glucocorticoid and/or acetylcysteine, if indicated. A possible cause is bronchiectasia, which could require surgical intervention.
    There may be an indication for oxygen therapy, the purpose of the referral being to quantify the hypoxaemia by measuring blood gasses.21
    The following situations are indications for referral to the pulmonologist, with the question of whether a pulmonary rehabilitation programme is indicated:

    · Despite optimal medical care, the patient continues to have limitations and handicaps.

    · The disorder is so severe that the patient has inadequate control over his symptoms, impairments, disabilities, and handicaps.

    The components of a pulmonary rehabilitation programme include optimizing the drug therapy, giving conservative advice and inhalation instruction, giving support in smoking cessation, improving general fitness, strengthening the respiratory muscles,22 23 and nutritional supplementation, if needed.24 A combined approach (improving fitness, psychosocial support, attending to compliance and inhalation technique, improving nutrition) is preferable to a single intervention. It is not clear which components of pulmonary rehabilitation are most effective.



    COPD in combination with heart failure. The most significant comorbidity in COPD is heart failure. Based on the history and physical examination, it is not always clear whether the reduction in exercise tolerance is caused by COPD, heart failure, or both.25 Nocturnal shortness of breath, coughing, and a prolonged, wheezy expiration can occur in both heart failure and COPD. See the relevant NHG practice guideline for diagnosis of heart failure. In patients with COPD and signs of heart failure, there may be uncertainty about the degree to which pulmonary or cardiac causes are contributing to lowering exercise tolerance, even after additional examinations and tests are done under the general practitioner's supervision (chest x-ray, ECG, spirometry). In these cases, the primary treatment is for the heart failure, using diuretics.



    Treatment in the terminal stage of COPD often requires intensive supervision and good teamwork with other physicians who are treating the patient.26 It is recommended that the general practitioner and/or pulmonologist, in mutual consultation and at a calm and appropriate time for the patient, discuss early on what options still are or no longer are medically advisable. At this time, the patient's wishes concerning the use of a respirator or reanimation can be discussed. For the transfer of relevant information during observation, it is recommended that a copy of the most important data from the medical record be kept at the patient's home. Since there is often comorbidity, the total medication should be kept as manageable as possible (e.g., managed by one person and with the aid of a daily medication organizer case). It may be necessary to hire intensive home care, both for care of the patient and to relieve the patient's partner or other carers.



    Management of exacerbations
    An exacerbation is defined as a period of increased dyspnoea and coughing, with or without mucus production.27 In most cases the exacerbations are mild or moderately severe, without dyspnoea at rest or respiratory failure.

    The treatment of an exacerbation and the frequency of the follow-ups for it are determined by the severity of the current clinical picture and the effectiveness of treatment prescribed for previous exacerbations.

    The general practitioner:

    inspects the patient and examines the thorax
    looks into the cause of the exacerbation, to the extent possible (e.g., infection, discontinuation of the medication on the patient's own initiative)
    decides whether there is a cause for the worsening of dyspnoea, other than COPD
    For the treatment of most exacerbations, the following will suffice:

    Start or resume a bronchodilator, temporarily doubling the dose or combining two types of bronchodilator (see section 'Symptomatic treatment')
    If the effect is inadequate, an oral glucocorticoid can be added temporarily.


    An exacerbation can also be severe, the criteria being:

    reappearance or worsening of dyspnoea at rest, difficulty in speaking a full sentence, inability to lie flat
    respiratory rate >25/min (in very severe exacerbations the respiratory rate decreases again!)
    heart rate >110/min
    use of accessory respiratory muscles
    The treatment of a severe exacerbation is as follows (see Table 4):8

    Give a beta2 sympathomimetic agent by spacer (4-10 puffs, one puff at a time), or subcutaneously, if necessary (1 ml of 0.5 mg/ml), or via an electric-powered jet nebulizer (5 mg/ml 0.5-1 ml). Wait with the patient for it to take effect. After several minutes repeat the inhalations of the beta2 sympathomimetic agent, and if there is insufficient improvement, give additional ipratropium bromide (2-4 puffs, one puff at a time). In less severe cases, a follow-up can be scheduled for a few hours later.
    If there is improvement, the general practitioner prescribes:
    a course of oral glucocorticoid (It is advisable to carry a starting dose of prednisone or prednisolone tablets or a glucocorticoid for intravenous administration in the doctor's bag.)27
    instructions for bronchodilator use during the next 24 hours (e.g., a double dose or inhalation using a spacer)
    A follow-up should be scheduled for the following day, to:
    evaluate the patient’s symptoms and limitations
    examine the lungs
    investigate the reason for the exacerbation, reviewing especially compliance, the inhalation technique, and exacerbating factors
    adjust the management, if indicated
    An antibiotic (amoxicillin, doxycycline, or another broad-spectrum antibiotic for 7 days) is only advised for:16
    clinical signs of infection (temperature >38.5°C, general malaise)
    very poor pulmonary function (FEV1 known to be <30% of the predicted value)
    insufficient improvement after 4 days
    For a severe exacerbation the patient should be referred if:

    no improvement occurs within a half hour
    care options at home are inadequate
    previous exacerbations have always required hospitalization
    exhaustion leads to a decreased respiratory rate, reduced consciousness, a 'more placid' patient. These are alarm signs for which emergency hospital admission is indicated.


    Table 4. Drug therapy for acute severe dyspnoea

    Medication
    Administration and dosage
    Comments

    beta2 sympathomimetic agent such as salbutamol
    metered-dose aerosol with spacer, 4-10 puffs of 200 mcg (1 puff at a time in spacer)
    Repeat inhalations after several minutes and if improvement is not adequate, give additional ipratropium bromide (2-4 puffs, one puff at a time).

    if necessary, by SC injection (1 ml of 0.5 mg/ml) or nebulizer (0.5 ml of 5 mg/ml)
    Refer if there is no improvement within half an hour.

    Prednisone or prednisolone
    orally, 30 mg once daily for 7-10 days
    Either stop abruptly or taper off, depending on the clinical picture


    --------------------------------------------------------------------------------

    note 1

    Other consensus texts were considered when the guidelines were written.1-3 The guidelines are in keeping with the other practice guidelines on asthma and COPD.4 5

    Siafakas NM, Vermeire P, Pride P, et al. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). A consensus statement of the European Respiratory Society. Eur Respir J 1995:8;1398-420.
    Commissie diagnostiek astma bronchiale en COPD, NVALT [Committee on diagnosis of bronchial asthma and COPD, NVALT]. Standaard diagnostiek van astma bronchiale en COPD [Practice guideline on diagnosis of bronchial asthma and COPD]. Pulmoscript 1994;3:31-46.
    Ferguson GT, Chernick RM. Management of chronic obstructive pulmonary disease. N Engl J Med 1993;328:1017-22.
    Geijer RMM, Thiadens HA, Smeele IJM, et al. NHG-Standaard COPD en Astma bij volwassenen: Diagnostiek [NHG Practice Guideline 'COPD and adult asthma: diagnosis']. Huisarts Wet 2001;44:107-17.
    Geijer RMM, Van Hensbergen W, Bottema BJAM, et al. NHG-Standaard Astma bij volwassenen: Behandeling [NHG Practice Guideline 'Adult asthma: treatment']. Huisarts Wet 2001;44:153-64.
    note 2

    In a randomized study, two interventions were compared with no intervention: smoking cessation plus ipratropium bromide, smoking cessation without ipratropium bromide, and no intervention.1 The study included 5,887 smokers aged 35-60 years, having a mild form of COPD (FEV1 mean 75% of predicted value) for 5 years. Thirty-five percent of the subjects in the intervention groups quit smoking; 5 years later, 22% were still non-smokers. In the non-intervention group, these percentages were 10% and 5%, respectively. Five years later, pulmonary function (mean FEV1) was better in both intervention groups than in the non-intervention group. The beneficial effect on pulmonary function was greatest in those who had permanently quit smoking: their FEV1 increased in the first year and then gradually decreased (mean overall reduction 72 ml in 5 years). In those who continued to smoke, FEV1 decreased by a mean of 300 ml in 5 years. Treatment with ipratropium bromide had no long-term effect on pulmonary function. No research was found on the effect of smoking cessation in patients over the age of 60.

    Nicotine replacement. A meta-analysis of the effect of nicotine replacement therapy on smoking cessation covered 53 trials (a total of over 18,000 subjects, 42 trials with chewing gum, 9 with patches, 1 with nasal spray, and 1 with inhalation).2 Nicotine replacement increased the probability of smoking cessation for 6-12 months: 19% in the nicotine groups compared with 10% in the control groups (odds ratio 1.71, 95% CI 1.56-1.87). In a study (n = 227) with a follow-up of more than 3 years, the final percentage of non-smokers was only half that at the 1-year follow-up. The relative difference between treatment and a placebo remained constant: with nicotine spray, 28% were still non-smokers 1 year later and 15% were 3 years later, compared with a placebo, 13% were still non-smokers 1 year later and 6% were 3 years later. In absolute terms, however, the percentage of non-smokers in the group using a nicotine spray decreased more sharply.3

    In a placebo-controlled study (n = 237), 5 months of nicotine patches combined with 1 year of nicotine nasal spray was more effective than nicotine patches alone: abstinence after 1 year was 27% for patches plus spray compared with 11% for patches alone, and after 6 years it was 16% compared with 9%.4 Nicotine replacement therapy is also recommended in British guidelines for smoking cessation.5

    Antidepressants. In a placebo-controlled study (n = 893), smoking abstinence after 12 months was determined in smokers treated with bupropion (an antidepressant) for 9 weeks, with or without the additional use of nicotine patches, and in those receiving a placebo (point prevalence). After 12 months, the proportion abstaining from smoking was 15.6% for a placebo, 16.4% for the nicotine patch, 30.3% for bupropion, and 35.5% for bupropion combined with the nicotine patch. The statistics for continuous abstinence (not smoking for an entire year) were lower: 5.6% for a placebo, 9.8% for the nicotine patch, 18.4% for bupropion, and 22.5% for the combination. The drop-out rate was 34.8%; since there was no intention-to-treat analysis, the absolute percentages are somewhat inflated. The study population was recruited via advertisements.6 In three other placebo-controlled studies with bupropion, there was a positive abstinence percentage after 1 year (point prevalence).7 Only one of these three studies has been fully reported.8 In one study, there was 30% abstinence after 6 months among those on fluoxetine, compared with 20% among those receiving a placebo.7 In another study there was higher abstinence after 6 months among those on nortriptyline than among those receiving a placebo.9

    Anxiolytics. In two studies buspirone proved to be no more effective than a placebo after 12 months, and in another study buspirone was just as effective as a nicotine patch.7 Other studies have shown that diazepam, meprobamate, and beta-blockers are not noticeably effective.

    Conclusions:

    The simple advice to stop smoking results in 5% stopping; a brief but methodical approach (the 'minimal intervention strategy') increases this to 10-20%.10
    All forms of nicotine replacement (chewing gum, nasal spray, inhalation, patch) double the rate of abstinence compared with a placebo (about 20% after 1 year). This is by far the most extensively investigated therapy.
    There is some evidence that bupropion and other antidepressants such as nortriptyline and fluoxetine are effective, but as yet there are no data on their use and effectiveness in the usual general practice setting. There has been only one study comparing an antidepressant with the current standard treatment (nicotine replacement).
    Combinations of different types of nicotine replacement therapy (such as patches plus spray), or combination of nicotine replacement therapy with bupropion, result in higher abstinence after 1 year. Over the long term, abstinence declines, but there is still a positive difference compared with a placebo.
    The preference of the work group is for advising smoking cessation, combined with the minimal intervention strategy; for initial support, nicotine replacement therapy is recommended.
    Anthonissen NR, Connett JE, Liay JP, et al. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. JAMA 1994;272:1497-505.
    Silagy C, Mant D, Fowler G, Lodge M. Meta-analysis on efficacy of nicotine replacement therapies in smoking cessation. Lancet 1994;343:139-42.
    Stapleton JA, Sutherland G, Russell MAH. How much does relapse after one year erode effectiveness of smoking cessation treatments? Long term follow-up of randomised trial of nicotine nasal spray. BMJ 1998;316:830-1.
    Blondal T, Gudmundsson LJ, Olafsdottir I, Gustavsson, Westin A. Nicotine nasal spray with nicotine patch for smoking cessation: a randomised trial with six year follow-up. BMJ 1999;318:285-9.
    Raw M, McNeill A, West R. Smoking cessation guidelines for health professionals. A guide to effective smoking cessation interventions for the health care system. Thorax 1998:53(Suppl5):5-9.
    Jorenby DE, Leischow SJ, Nides MA, et al. A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation. N Engl J Med 1999;340:685-91.
    Hughes JR, Stead LF, Lancaster T. Anxiolytics and antidepressants for smoking cessation. (Cochrane review). In: The Cochrane Library, issue 3, 1999. Oxford: Update Software.
    Hurt RD, Glover ED, Sachs DPL, et al. A comparison of sustained-release bupropion and placebo for smoking cessation. N Engl J Med 1997;337:1195-202.
    Hall SM, Reus VI, Munoz RF, et al. Nortriptyline and cognitive-behavioral therapy in the treatment of cigarette smoking. Arch Gen Psychiatry 1998;55:683-90.
    NHG-DKB- Stoppen met roken - cahier [NHG DKB Smoking cessation - workbook]. Utrecht; Nederlands Huisartsen Genootschap [Dutch College of General Practitioners], 1995.


    note 3

    Classification of the severity of COPD based on the FEV1 does not correlate well with quality of life. Even patients with mild bronchial obstruction sometimes have a substantial decline in quality of life.1

    Ferrer M, Alonso J, Morera J, et al. Chronic obstructive pulmonary disease stage and health-related quality of life. Ann Intern Med 1997:127:1072-9.
    note 4

    Twenty-five percent of the excess mortality from influenza occurs in patients with a chronic lung disease. The reason for this has not been found. Influenza vaccination is recommended.1

    A study in 189 COPD patients (FEV1 <1.5 l), one-half of whom were vaccinated with a pneumococcal vaccine while the other half received an injection of physiological salt solution, revealed no difference in mortality or hospitalizations after 2 years.2 In a retrospective study in elderly patients with chronic lung disease, of whom1,280 had been vaccinated with pneumococcal vaccine and 618 were not vaccinated, there were 40% fewer hospitalizations and 29% fewer deaths among those who were vaccinated. However, the groups were not entirely comparable.3

    Conclusion: Influenza vaccination is recommended but there is as yet no consensus about pneumococcal vaccination.

    Van Essen GA, Sorgdrager YCG, Salemink GW, Govaert ThME, Van den Hoogen JPH, Van der Laan JR. NHG-Standaard Influenza en influenzavaccinatie [NHG Practice Guideline 'Influenza and influenza vaccination']. In: Thomas S, Geijer RMM, Van der Laan JR, Wiersma Tj. NHG-standaarden voor de huisarts II, 1996 [NHG Practice Guidelines for the General Practitioner II, 1996].
    Leech JA, Gervais A, Ruben FL. Efficacy of pneumococcal vaccine in severe chronic obstructive pulmonary disease. Can Med Am J 1987;136:361-5.
    Nichol KL, Baken L, Wurenma J, Nelson A. The health and economic benefits associated with pneumococcal vaccination of elderly persons with chronic lung disease. Arch Intern Med 1999;159:2437-42.
    note 5

    A cross-sectional study in the Netherlands in over 13,000 individuals demonstrated that with an above-average consumption of fruit and whole-grain products plus low consumption of alcohol (1-3 U/day), pulmonary function was better (FEV1 139 ml higher) and there were fewer respiratory complaints than in persons with a lower than average consumption of fruit and whole-grain products and no consumption of alcohol. This difference was found in both smokers and non-smokers and might be explained by the protective effect of antioxidants such as vitamin C and $-carotene on the respiratory tract. This study supports the general recommendations for healthy nutrition.

    Tabak C. Epidemiological studies on the relation between diet and COPD. Wageningen: University of Wageningen, 2000.
    note 6

    For inhalation therapy there is a choice between a dry powder inhaler and a metered-dose aerosol.1 With a dry powder inhaler, deposition in the lung depends primarily on the inspiratory force; at a lower inspiratory force, the dose delivered from the device decreases and the average particle size increases, which decreases powder deposition in the lung. With a metered-dose aerosol, deposition in the lung depends primarily on hand-lung coordination; the inspiratory force does not affect the dose delivered or the average particle size. If deliberate inhalation is not possible, a metered-dose aerosol with spacer is preferred. If deliberate inhalation is possible, the inspiratory force and the patient’s coordination determine the choice between a metered-dose aerosol ('breath-actuated') with or without a spacer, or a dry powder inhaler.

    Dekhuijzen PNR. Inhalatiemedicatie bij volwassenen met obstructieve longaandoeningen: poeder of aërosol? [Inhalation medication for adults with obstructive pulmonary diseases: powder or aerosol?] Ned Tijdschr Geneeskd 1998;142:1369-74.
    note 7

    Three studies compared the effectiveness of a dry powder inhaler and a metered-dose aerosol with a nebulizer.1-3 Twenty-five COPD patients who used a nebulizer (FEV1 29% of predicted value, 0.73 l, age 66 years), were included in a randomized, double-blind, crossover study.1 The participants were younger on average, and used the nebulizer for a shorter period than the non-participating patients. A comparison was made between 2 weeks of 2.5 mg terbutaline powder inhalation (Turbuhaler) 3 times daily, and 5 mg terbutaline 3 times daily using a nebulizer (Pariboy). Sixteen patients preferred the powder inhalation and 9 the nebulizer. This difference was not significant (p = 0.09).

    In a two-day randomized, double-blind, crossover study of 28 patients with COPD (FEV1 29% of predicted value, 0.73 l, age 67 years), a single dose of 1.6 mg salbutamol inhaled in powder form (Diskhaler) was compared with a dose of 2.5 mg delivered by a nebulizer (Pariboy).2 Patients were unfamiliar with the use of the nebulizer. The increase in the FEV1 was greater in the group inhaling the powder than in the group using the nebulizer after 85 and 145 minutes. Sixty percent of the active ingredients in the nebulizer did not reach the patient, because of precipitation on the wall of the device, and an additional portion was lost through evaporation and leakage.2

    A study of 47 COPD patients (FEV1 33% of predicted value, age 58 years) compared 40 mcg ipratropium bromide by metered-dose aerosol with progressively increasing doses of ipratropium bromide by nebulizer (100, 200, 400, and 600 mcg).3 The effect of 40 mcg by metered-dose aerosol was found to be comparable to 100 mcg via a nebulizer, but provided only about 70% of the effect of the highest dose by nebulizer. The study concluded that the optimal dose of ipratropium bromide administered by nebulizer is 400 mcg.

    In a literature overview, six studies were found in which the efficacy of metered-dose aerosols was compared with that of spacer nebulizers.4 The conclusion was that the two methods of administration are equally effective for an exacerbation of COPD. A double-blind, crossover study of 20 COPD patients (FEV1 0.71 l, age 68 years) concluded that 4 puffs of salbutamol by metered-dose aerosol with spacer (360 mcg total) is just as effective as 2.5 mg salbutamol by nebulizer.5

    Conclusion: A metered-dose aerosol with spacer is usually sufficient, even in severe dyspnoea. For patients who are exhausted, for those with very severe obstruction, and for those who cannot manage a metered-dose aerosol with spacer, a nebulizer is preferred.1

    Hansen NCG, Evald T, Ibsen TB. Terbutaline inhalations by the turbuhaler as replacement for domiciliary nebulizer therapy in severe chronic obstructive pulmonary disease. Resp Medicine 1994;88:267-71.
    Hansen NCG, Andersen PB. Salbutamol powder inhaled from the diskhaler compared to salbutamol as a nebulizer solution in severe chronic airways obstruction. Resp Medicine 1995;89:175-9.
    Gross NJ, Petty TL, Friedman M, Skorodin MS, Silvers GW, Donohue JF. Dose response to ipratropium as a nebulized solution in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1989;139:1188-91.
    Kuhl DA, Olakundbi A, Agiri A, Mauro LS. Beta-agonists in the treatment of acute exacerbation of chronic obstructive pulmonary disease. Ann Pharmacotherapy 1994;28:1379-88.
    Berry RB, Shinto RA, Wong FH, Despars JA, Light RW. Nebulizer vs. spacer for bronchodilator delivery in patients hospitalized for acute exacerbations of COPD. Chest 1989;96:1241-6.
    note 8

    Van der Palen J, Klein JJ, Van Herwaarden CLA, Zielhuis GA, Seydel ER. Multiple inhalers confuse asthma patients. Eur Respir J 1999;14:1034-7.



    note 9

    A search for English-language articles on beta2 sympathomimetic agents for the treatment of acute exacerbations of COPD in Medline (1977-1993) and the Index Medicus (1984-1993) yielded a small number of articles which differed greatly in quality.1 Among other things, it was concluded that combining ipratropium bromide with beta2 sympathomimetic agents for an exacerbation of COPD has no advantages over the use of beta2 sympathomimetic agents alone. The included studies were all conducted in hospitals and are difficult to compare because of differing dosage regimens and differences in the duration of follow-up.2-4 In a crossover study of 32 patients with severe COPD (age 62 years, FEV1 <0.70 l), a beta2 sympathomimetic agent appeared to have a bronchodilatory effect equivalent to that of ipratropium bromide, after 90 minutes. The effect of ipratropium bromide peaked later, however.5

    There is ambiguity about the optimal dose and recommended interval between administrations with regard to effectiveness and side effects. A dose of 800-1,000 mcg of salbutamol (4-5 puffs of 200 mcg) or an equivalent dose of another beta2 sympathomimetic agent administered by metered-dose aerosol with spacer (or a dose more than 10 times greater administered by nebulizer) seems to be effective and safe for an exacerbation of COPD.1.6

    Conclusion: Despite the lack of evidence of the added value of ipratropium bromide for an exacerbation of COPD, adding it is recommended because its value in exacerbations of asthma has been confirmed, it is current practice, and it is safe.

    Kuhl DA, Olakundbi A, Agiri A, Mauro LS. Beta-agonists in the treatment of acute exacerbation of chronic obstructive pulmonary disease. Ann Pharmacotherapy 1994;28:1379-88.
    Rebuck AS, Chapman KR, Abboud R, et al. Nebulized anticholinergic and sympathicomimetic treatment of asthma and chronic obstructive airways disease in the emergency room. Scan J Rehabil Med 1987;82:59-64.
    O'Driscoll BR, Taylor RJ, Horsley MG, Chambers DK. Nebulised salbutamol with and without ipratropium bromide in acute airflow obstruction. Lancet 1989;ii:1418-20.
    Patrick DM, Dales RE, Stark RM, Laliberte G, Dickinson G. Severe exacerbations of COPD and asthma. Incremental benefit of adding ipratropium to usual therapy. Chest 1990;98:295-7.
    Karpel JP, Pesin J, Greenberg, Gentry E. A comparison of the effects of ipratropium bromide and metaproterenol sulfate in acute exacerbations of COPD. Chest 1990;98:835-9.
    Van Grunsven PM. Behandeling van acute, ernstige dyspnoe bij astma en COPD in de huisartspraktijk. Een literatuuronderzoek [Treatment of acute, severe dyspnoea in asthma and COPD in primary practice. A review of the literature]. Huisarts Wet 1997;40;54-62.
    note 10

    A search via Medline (obstructive lung disease and drug therapy or therapy 1984-95)—excluding studies, reviews, and theses concerning beta2 sympathomimetic agents not available in the Netherlands—provided seven controlled studies comparing the efficacy of ipratropium bromide or beta2 sympathomimetic agents with a placebo and with a combination of the two types of drugs.1-7 Most of these studies were small, short-term, and of limited quality.1-4 6 7 All of the studies concluded that ipratropium bromide or a beta2 sympathomimetic agent was more effective than a placebo. It is not clear whether one of the two medications is more effective than the other. The combination of ipratropium bromide and a beta2 sympathomimetic agent was investigated in five of the seven studies.1 2 4-6 Three studies found that the combination had no more efficacy than the medications given separately1 2 4 but two studies5 6 did find additional efficacy from the combination.5

    One of the latter was a larger and higher-quality study which investigated the effect of a salbutamol and ipratropium bromide combination compared with each medication separately, in 538 COPD patients for 85 days.5 The indicator of treatment effectiveness was the change in FEV1 with respect to the initial value on the study days. During the first 4 hours after administration the combination was more effective than either medication taken separately, and separately they did not differ in efficacy. The mean increase in the peak FEV1 values with respect to the initial value was 38% for the combination and approximately 30% for the individual medications.

    One study compared different doses and combinations and found 80 mcg ipratropium bromide combined with 400 mcg salbutamol (by metered-dose aerosol) to be more effective than a half dose of each, which in turn was more effective than 40 mcg ipratropium bromide or 400 mcg salbutamol alone.6 In a dose-response study of ipratropium bromide and fenoterol, the latter proved to be more effective but had more side effects (rapid pulse, tremor). Maximum bronchodilation occurred with a dose of 280 mcg of ipratropium bromide.7

    In 35 COPD patients (FEV1 0.91, age 68) maximum bronchodilation was provided by 430 mcg salbutamol per administration by metered-dose aerosol and by 1,160 mcg terbutaline per administration.8 The efficacy of progressive doses of terbutaline was tested in 25 patients with COPD (FEV1 0.94 l, age 68 years).10 At doses of more than 500 mcg given 4 times daily, the increase in FEV1 was not clinically relevant. In an equivalent type of study with increasing inhalation doses of salbutamol powder (0, 0.4, 1, 2, and 4 mg) in 30 patients with COPD (FEV1 0.9 l, age 63 years), the optimal dose (best balance between effect and side effects) was 1 mg salbutamol powder.10

    A new, long-acting anticholinergic agent (tiotropium bromide) that can be given once daily seems to be effective for COPD. This medication has not yet been marketed.11

    Conclusion: Studies of the differences in efficacy between ipratropium bromide and beta2 sympathomimetic agents have produced conflicting results. Even at high doses, ipratropium bromide has almost no adverse effects, in contrast to beta2 sympathomimetic agents. There is a slight preference for ipratropium bromide.12 Maximum bronchodilation per administration is reached at doses of 70-80 mcg ipratropium bromide, 400 mcg salbutamol (metered-dose aerosol), 800 mcg salbutamol (powder inhalation), and 500-1,000 mcg terbutaline. Some patients do not respond to ipratropium bromide but do respond to beta2 sympathomimetic agents, and the reverse is also true. Due to the poor pulmonary function in COPD, bronchodilators should be given continuously, and not on an as-needed basis.

    Easton PA, Jadue C, Dhingra N, Anthonissen NR. A comparison of the bronchodilating effects of beta-2 adrenergic agent (albuterol) and an anticholinergic agent (ipratropiumbromide) given by aerosol alone or in sequence. N Engl J Med 1986;315:735-9.
    Barnes D, Delaney JC. A comparison of salbutamol and ipratropium in chronic bronchitis and chronic airflow limitation. Br J Clin Practice 1988;42:372-88.
    Braun SR, Levy SF, Grossman J. Comparison of ipratropium bromide and albuterol in chronic obstructive pulmonary disease: a three-center study. Am J Med 1991;91(Suppl 4a):28S-32S.
    Imhof E, Elsasser S, Karrer W, Grossenbacher M, Emmons R, Perruchoud AP. Comparison of bronchodilator effects of fenoterol/ipratropium bromide and salbutamol in patients with chronic obstructive lung disease. Respiration 1993;60:84-8.
    Petty TL for the combivent inhalation aerosol study group. In chronic obstructive pulmonary disease, a combination of ipratropium and albuterol is more effective than either agent alone. An 85-day multicenter trial. Chest 1994;105:1411-9.
    Ikeda A, Nishimura K, Koyama H, Izumi T. Bronchodilating effects of combined therapy with clinical dosages of ipratropium bromide and salbutamol for stable COPD: comparison with ipratropium bromide alone. Chest 1995;107:401-5.
    Ikeda A, Nishimura K, Koyama H, Izumi T. Comparative dose-response study of three anticholinergic agents and fenoterol using a metered dose inhaler in patients with chronic obstructive pulmonary disease. Thorax 1995;50:62-6.
    Jaeschke R, Guyatt GH, Cook D, et al. The effect of increasing doses of ß-agonists on airflow in patients with chronic airflow limitation. Resp Med 1993;87:433-8.
    Jaeschke R, Guyatt GH, Willan A, et al. Effect of increasing doses of beta agonists on spirometric parameters, exercise capacity and quality of life in patients with chronic airflow limitation. Thorax 1994;49:479-84.
    Vathenen AS, Britton JR, Ebden Ph, Cookson JB, Wharra HJ, Tattersfield E. High-dose inhaled albuterol in severe
    Chronic airflow limitation. Am Rev Respir Dis 1988;138:850-5.Barnes PJ. New therapies for chronic obstructive pulmonary disease. Thorax 1998;53:137-47.
    Rennard SI, Serby CW, Chafouri M, Johnson PA, Friedman M, Extended therapy with ipratropium is associated with improved lung function in patients with COPD: a retrospective analysis of data from seven clinical trials. Chest 1996;110:62-70.
    note 11

    In five studies in COPD patients1-5 salmeterol was more effective than a placebo (symptomatic improvement, less use of short-acting beta2 sympathomimetic agents, minor improvement in pulmonary function). A Cochrane review of three of those studies came to the same conclusion.6 In two studies salmeterol was more effective than ipratropium bromide (pulmonary function, symptoms).3 7 In two studies the combination of salmeterol with ipratropium bromide was somewhat better than salmeterol alone (FEV1, quality of life).4 8 Formoterol has not been studied for use in COPD, to our knowledge.

    Ulrik CS. Efficacy of inhaled salmeterol in the management of smokers with chronic obstructive pulmonary disease: a single centre, randomised, double blind, placebo controlled, crossover study. Thorax 1995;50:750-4.
    Boyd G, Morice AH, Pounsford JC, Siebert M, Peslis N, Crawford C. An evaluation of salmeterol in the treatment of chronic obstructive pulmonary disease (COPD). Eur Resp J 1997;10:815-21.
    Mahler DA, Donohue JF, Barbee RA, et al. Efficacy of salmeterol xinafoate in the treatment of COPD. Chest 1999;115:957-65.
    Van Noord JM, De Munck DR, Bantje TA, Hop WC, Akveld, ML, Bommer AM. Long-term treatment of chronic obstructive pulmonary disease with salmeterol and the additive effect of ipratropium. Eur Resp J 2000;15:878-85.
    Jones PW, Bosh TK. Quality of life changes in COPD patients treated with salmeterol. Am J Respir Crit Care Med 1997;155:1283-1289.
    Appleton S, Smith B, Veale A, Bara A. Regular long-acting beta-2 adrenoreceptor agonists in stable chronic obstructive airways disease. In: The Cochrane Library, issue 1, 2000. Oxford: Update Software.
    Anderson W, Wisniewski M, Barbee R, Rickard K. A comparison of Serevent and ipratropium on pulmonary function in COPD patients reversible to ipratropium. Am J Respir Crit Care 1997;155:A277.
    Rutten van Molken M, Roos B, Van Noord JA. An empirical comparison of the St. George's Respiratory Questionnaire (SGRQ) and the Chronic Respiratory Disease Questionnaire (CQR) in a clinical setting. Thorax 1999;54:995-1004.
    note 12

    Inhaled bronchodilators are preferred for treatment of COPD. The question is whether theophylline has an additional effect when the effect of the bronchodilators is insufficient.

    In a study in 84 patients with COPD (average age 62 years, FEV1 <1l) the combination of ipratropium bromide, salbutamol, and theophylline was more effective (FEV1) than ipratropium bromide alone or the combination of theophylline and salbutamol.1 A randomized, crossover study in 60 COPD patients showed improved respiration and decreased dyspnoea, probably due to better performance of the respiratory muscles.2 Another small study showed no difference in the effect (FEV1) between adding theophylline and adding a placebo to the usual medication.3 In 24 COPD patients (FEV1 37% of predicted value) theophylline was added to maximum doses of ipratropium bromide and beta2 sympathomimetic agents. One-third of the patients reported subjective improvement. The post-bronchodilator FEV1 improved in those with subjective improvement and not in those without subjective improvement.4

    In a study in 38 stable COPD patients (FEV1 31-38% of predicted value), there was a clinically-relevant exacerbation in 72% of those in whom theophylline was discontinued, compared with15% of those in whom it was continued.5

    The therapeutic range of theophylline is small. With the use of multiple medications there is an elevated risk of intoxication, especially in the elderly. Chronic intoxication often occurs because patients themselves gradually increase the medication.6

    Conclusion: Few good studies were found on the efficacy of theophylline for COPD. For a limited group of COPD patients, there may be an additive effect; other consensus guidelines mention theophylline as an option. Because theophyllines are only considered for patients with very severe COPD, the decision on whether it is indicated should be left to the pulmonologist.7

    Karpel JP, Kotch A, Zinny M, Pesin J, Alleyne W. A comparison of inhaled ipratropium, oral theophylline plus inhaled beta-agonist, and the combination of all three in patients with COPD. Chest 1994;105:1089-94.
    Murciano D, Auclair MH, Pariente R, Aubier M. A randomized, controlled trial of theophylline in patients with severe chronic obstructive pulmonary disease. N Engl J Med 1989;320:1521-5.
    Fink G, Kaye C, Sulkes J, Gabbay U, Spitzer SA. Effect of theophylline on exercise performance in patients with severe chronic obstructive pulmonary disease. Thorax 1994;49:332-4.
    Nishimura K, Koyama H, Ikeda A, Sugiura N, Kawakatsu K, Izumi T. The additive effect of theophylline on a high-dose combination of inhaled salbutamol and ipratropium bromide in stable COPD. Chest 1995;107:718-23.
    Kirsten DK, Wegner RE, Jörres RA, Magnussen H. Effects of theophylline withdrawal in severe chronic obstructive pulmonary disease. Chest 1993;104:1101-7.
    Ramsdell J. Use of theophylline in the treatment of COPD. Chest 1995;107 (Suppl 5):206S-9S.
    Siafakas NM, Vermeire P, Pride P, et al. Optimal assessment and management of chronic obstructive pulmonary disease (COPD). A consensus statement of the European Respiratory Society. Eur Respir J 1995:8;1398-420.
    note 13

    For a meta-analysis of studies on the effectiveness of prednisone for COPD patients outside exacerbations, 15 placebo-controlled studies found via Medline (1966-1989) were selected by several previously-established criteria. The total number of patients in these 15 studies was 445 and the great majority were 60-year-old male smokers with a mean FEV1 of 1l. The standard treatment of 40 mg prednisone daily for 14 days was compared with a placebo. The combined results of these studies, expressed as the percentage of patients in whom FEV1 was improved 20% or more, was 10% (95% CI 2-18%). This improvement was found in about 30% of the patients in the prednisone group and about 20% of those in the placebo group. The results were independent of the size of the trial, the mean initial value of FEV1, the average age of the population, and the 'age' of the trial.1

    After 1989, four more placebo-controlled, short-term (<6 weeks) trials were found in which the results were similar.2-5 One study showed no difference in efficacy between prednisone and a placebo, which could be explained by the stringent exclusion of patients with asthma characteristics in this study.4 The other three showed a modest beneficial effect from prednisone compared with a placebo.2 3 5

    Two placebo-controlled trials compared the effect of prednisone with that of an inhaled glucocorticoid.2 3 Prednisone appeared to be more effective than an inhaled glucocorticoid. The efficacy of inhaled glucocorticoids for the subgroups with emphysema and expiratory airway collapse was not clear. A beneficial effect of prednisone on FEV1 in the ISOLDE study did not appear to be related to a beneficial effect (on the complaints, exacerbations, or general well-being) of treatment with an inhaled glucocorticoid.6

    Conclusion: The dose of prednisone used in the studies was 30-40 mg daily. It is worthwhile to check the effect of a course of prednisone or prednisolone (30-40 mg daily for 10-14 days) in all patients with COPD.

    Callahan CM, Dittus RS, Katz BP. Oral corticosteroid therapy for patients with stable chronic obstructive pulmonary disease. A meta-analysis. Ann Intern Med 1991;114:216-23.
    Weir DC, Burge PS. Effects of high dose inhaled beclomethasone dipropionate, 750 micrograms and 1500 micrograms twice daily, and 40 mg per day oral prednisolone on lung function, symptoms, and bronchial hyperresponsiveness in patients with non-asthmatic chronic airflow obstruction. Thorax 1993;48:309-16.
    Weir DC, Gove RI, Robertson AS, Burge PS. Response to corticosteroids in chronic airflow obstruction: relationship to emphysema and airways collapse. Eur Respir J 1991;4:1185-90.
    Syed A, Hoeppner VH, Cockcroft DW. Prediction of nonresponse to corticosteroids in stable chronic airflow limitation. Clin Invest Med 1991;14:28-34.
    Weir DC, Gove RI, Robertson AS, Burge PS. Corticosteroid trials in non-asthmatic chronic airflow obstruction: a comparison of oral prednisolone and inhaled beclomethasone dipropionate. Thorax 1990;45:112-7.
    Burge PS, Calverley PMA, Jones PW, Spencer S, Anderson JA, Maslen TK on behalf of the ISOLDE study investigators. Randomised, double blind, placebo controlled study of fluticason propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ 2000;320:1297-303.
    note 14

    In recent years, five randomized, placebo-controlled studies have been published,1-5 as well as a fresh analysis of a subpopulation of patients with moderately severe COPD in three other studies.6 For the characteristics and results of these studies see Table.

    In the EUROSCOP study, patients with mild COPD were treated with a moderate dose of budesonide for 36 months. In the first few months there was improvement in FEV1, compared with a placebo, without any effect on the decline in lung function over the long term.1 In the Copenhagen study, the effect of a usually moderate dose of budesonide was investigated in patients with mild COPD for 36 months. There was no difference in FEV1 or in the number of exacerbations.2

    In patients with moderately severe COPD who were treated for 6 months with a high dose of fluticasone, Paggiaro et al. found fewer exacerbations (both moderate and severe), a small but significant improvement in pulmonary function, and an increase in exercise tolerance.3 In patients with moderately severe COPD treated with a high dose of fluticasone, the ISOLDE study found a small initial increase in FEV1, a reduction in the number of exacerbations, and improvement in the functional condition.4

    In a two-year study in patients with severe COPD treated with a high dose of beclomethasone, Van Grunsven found an increase in FEV1, not only in the initial phase but also during the entire study. He found no difference in the number of treatments with an oral glucocorticoid or antibiotics, nor in dyspnoea or well-being.5

    A reexamination6 of the data from three studies5 7 8 in a selected subpopulation of COPD patients (n = 183, FEV1 45-55% of predicted value, 1,500 mcg beclomethasone or 1,600 mcg budesonide) who were treated with inhaled glucocorticoids for two years, revealed that FEV1 increased in the treated group, not only during the first 6 months but also thereafter. Conversely, there was no effect on the frequency of exacerbations.

    Discussion:

    There was initial improvement (in the first 6 months) in FEV1 in four of the five studies. This initial improvement was observed in the three studies in patients with more severe forms of COPD (Paggiaro, ISOLDE, Van Grunsven) and in one of the two studies in patients with mild forms of COPD (EUROSCOP).
    In three studies, FEV1 decreased after this initial period (ISOLDE, Copenhagen, EUROSCOP), as before. Paggiaro's study was for only 6 months, so it is not possible to evaluate the change in FEV1 after the initial phase in this study. There was a less dramatic decrease in FEV1 after the initial phase only in the study of Van Grunsven and in the same author's re-examination of the data from his own study plus two other small studies.
    With regard to the number of exacerbations, four of the five studies used the frequency of exacerbations as an outcome indicator. Two studies found a difference: ISOLDE (reduction in the number of exacerbations) and Paggiaro (no difference in the number of exacerbations, but a difference in the severity of the exacerbations). Two studies did not: Van Grunsven and Copenhagen. The varying definitions of the term 'exacerbation' (worsening of symptoms, the necessity for courses of antibiotics/glucocorticoid, or for consultation with the practitioner or hospitalization) make it difficult to draw a clear conclusion.
    With regard to symptom scores/functional condition, four of the five studies measured a symptom parameter. These parameters improved in two studies: ISOLDE (less decrease in scores on St. George's questionnaire) and Paggiaro (less coughing, less mucus production, increase in walking distance). They did not improve in two: Van Grunsven (dyspnoea, general well-being) and Copenhagen (coughing/mucus production). No symptom parameter was measured in the EUROSCOP.
    There appears to be a dose-response relation, as well as a relation to the severity of the COPD. High doses do seem to be effective for moderately severe COPD, as used in ISOLDE (fluticasone 1,000mcg, moderately severe COPD), Paggiaro (1,000 mcg fluticasone, moderately severe COPD), and Van Grunsven (1,500 mcg beclomethasone, severe COPD). A lower dose for mild COPD, as used in EUROSCOP (800 mcg budesonide, mild COPD) and the Copenhagen study (predominantly 800 mcg budesonide, mild COPD) does not seem to be effective.
    Conclusion:

    Benefits of treating mild forms of COPD (FEV1 >70% of predicted value) with inhaled glucocorticoids have not been proved (EUROSCOP, Copenhagen). With the exception of an initial improvement in FEV1 in the EUROSCOP (about 80 ml difference from a placebo is not very relevant), there was no difference in the deterioration in FEV1, the exacerbation frequency, or symptom scores.
    Treatment of moderately severe forms of COPD (FEV1 50-70% of predicted value) results in fewer and/or less severe exacerbations as well as improvement of the functional condition (Paggiaro, ISOLDE). Both studies showed initial improvement in FEV1 (75-150 ml). That information alone does not seem to be enough to support prescribing inhaled glucocorticoids as a maintenance programme for this group of patients. However, for patients with moderately severe COPD, with frequent exacerbations and possibly many complaints/limitations, a maintenance programme of a high dose of inhaled glucocorticoid does appear to be advisa
  49. shabana

    shabana Guest

    smoker with expectoration of cupfull of sputum daily
    how to diagnose? was the answer spirometry or high resolution CT chest?
  50. Guest

    Guest Guest

    spirometry

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