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Transcript of Magdy Abbas (1)
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Dr. Rami Abazid
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MAGDY ABBAS
BRAIN MAP
FOR
PACES
PREPARED BY:
DR. RAMI ABAZID
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TO:THE SOUL OF MY PARENTS
TO: Jailan, Diaa,
Mariam and Reham
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PREFACE
This edition of the brain map for
PACES is basically designed for the
busy dynamic young doctors who
intended to go through the exam.
I hope this will help candidates to
pass with case.
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ACKNOWLEDGEMENTS
I would like to express my sincere feelings and
thanks to the following people.
Dr. Abdulfatah Arafaa-Medical Consultant in the
Farouk Charity Hospital-Cairo
Dr. Abdulla Hamed Abo Jabal-Consultant in Tropical
Medicine, Embaba Fever Hospital-Cairo
Dr. Mohamed Samer-Senior Cardiologist in Mubarak
Hospital-Kuwait
Dr. Samy Zaki-Professor of Gastroenterology-Al
Azhar University-Cairo
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ABOUT THE AUTHOR
DR. MAGDY ABBAS
Graduate from Cairo University worked as a
Registrar in Kasr El Aini Hospital (Cairo)
Senior Registrar In Adan University (Kuwait)
Consultant in Embaba Fever Hospital (Cairo)
Participated in many Teaching programmed in
Egypt
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THE PACES EXAMINATION:
Cardiology
10 mins.
Communication
Skill
20 mins.
Brief Clinical
Consultation
10 mins.
Brief Clinical
Consultation
10 mins.
(5) (4)(3)
(1) (2)
Neurology
10 mins.
History taking
20 mins.
Chest
10 mins.
Abdomen
10 mins.
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ST TION I
MAP FOR
ABDOMEN
&
CHEST
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ABDOMEN CASES
With stigmata of without stigmata of
CLD CLD
Cirrhosis
Hepatomegally hepatosplenomegally Splenomegaly Ascites
Abdominal masses
I would like to complete my examination
1-Per rectal examination2-External genitalia3-Hernia orifices4-Lymph nodes5-Urine dipstick6-BP T (temperature)
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C L D
Signs Decompensated D-D Investigation
Signs General* CBC
Spider Clubbing Ascites * electrolyte complicationsNaevi Arms leuconychia
Fistula Hands Palmer erythma Assess
Dupuytrens Jaundice Liver & FP
Contracture Function
Hepatic Encephalopathy -S. Bil. U/SFlap -S. Alb
. -PT
-ALT Search
-AST for the
Parotid cause
Swelling
Jaundice
Wasting Face
Pallor Spider
Anthelasma Naevi
Chest reduced axillary hair hepatitis H.chr. Wilson
Gynaecomastia C. B.Alcohol PBC Virdogy
Shrunken Drugs Study
Liver
Hepatomegaly AIH Alpha 1,AT Auto Immune Iron
Splenomegaly Abdomen Study Study
Ascites
venous
Hum ---L.L. oedema Metabolic Wilson
Alpha1 AT
Caput Medusa -Testicular Atrophy
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COMPLICATION
OF
CIRRHOSIS
Portal hypertension Hepato Cellular Dysfunction
Varices Ascites hepato Encephalopathy Hepato
Renal cellular
Syndrome carcinoma
Coagulopathy
Bleeding Spontaneous
Bacterial
Peritonitis
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POOR PROGNOSTIC FACTORS
IN
LIVER CIRRHOSIS
Encephalopathy Na Albumin PT < 120 25g/L
FACTORS PRECIPITATE HEPATIC ENCEPHALOPATHY
Infection Diuretics Electrolyte Sedative Surgery
Diarrhea Imbalance
Vomiting Paracentesis
GI Bleeding
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TREATMENT OF ASCITES
IN
C L D
Salt restriction Furosemide Serial
to 78 If Na is < 125mmol/L
mmol/dayup to 400mg/day
TIPS
Transjugular
Intra hepatic
Portal systemicShunt
(Aim: one KG weight loss/day)
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PRIMARY PREVENTION OF VARICEAL BLEEDING
DIAGNOSIS OF CIRRHOSIS
O G D
No varices Grade I Varices Grade 2 or 3 varices
Repeat OGD repeat OGD one year Propranolol
3-4 years 80-160mg/day
HR60
Band ligation if
Propranolol intolerant
or Verapamil
Diltiazem
MANAGEMENT OF VARICEAL BLEEDING
IN CIRRHOSIS
TIPS
Blood transfusion Octreotide Endoscopic Endoscopic Balloon
Sclerotherapy ligation Tamponade
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HEPATOMEGALY
3 C 3 I
1-Cirrhosis 1-Infection
2-Cardiac CCF -HBU
3-Cancer -HCU
-T.B.
-Brucella
2-Infiltrative
-Amyloid
-Sarcoid
-Myeloproliferative
3-Immune
-AIH
-PBC
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SPLENOMEGALLY
Mild Moderate Massive
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MOST COMMON CAUSES OF ASCITES
Pancreatitis
Cirrhosis Malignancy Heart Failure Tuberculosis
TRANSUDATIVE OR EXUDATIVE
S-A ALBUMIN GRADIENT
11 g/L 11 g/L
Transudative Exudative
MYXAEDEMA MAGs SYNDROME
CLD CHC CRF MALIGNANCY T.B. INFECTION
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RENAL ANGLE MASS
Polycystic Renal Cell Hydronephrosis
Carcinoma Adrenal mass
Retroperitoneal
Mass
WHY RENAL MASS
Can get Minimal Resonant to
Above it Ballottable No movement with Percussion
Notch inspiration
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SURGICAL INTERVENTION IN
POLYCYSTIC KIDNEY
Massive Recurrent Transplant Recurrent Possible
Cysts Pain work up Infected Malignancy
Cysts
ASSOCIATED INHERITED CONDITION
WITH RENAL CYSTIC DISEASE
Autosomal
Tuberous Von-Hippel Autosomal recessive
Sclerosis Lindou disease dominant polycystic Polycystic
Kidney Kidney
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CHEST C SES
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INTERSTITIAL LUNG DISEASE
Dry S.O.B. Fine Endispiratory
Cough Crackles
C A U S E S
TIP
Rheumatological
- Rh. Arthritis Vasculitis
- S.L.E. - PAN
- Systemic Sclerosis -Wegners Pneumocomosis- Polymyositis -Churg-Strauss -Asbestosis Drugs
- Dermatomyositis -Good Pastures Silicosis Amiodarone
- Ankylosing Spondilitis -Beryliosis Nitrofurnatone
- MCTD Busulphan
- Sjogrens Syndrome Bleomycine
Allergic Gold
Radiation Methotraxte
OTHERS
Extrinsic Gauchers
Allergic Lymphangiomyelomatosis
Alveolitis Niemann Pick
NF
Tuberous Sclerosis
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IDIOPATHIC INTERSTITIAL PNEUMONIATIP
N D A R U C Linda
Usual lymphoid
Interstitial Interstitial
Pneumonia Pneumonia
(UIP) (LIP)
Non Specific
Interstitial Desefuamative Respiratory Cryptogenic
Pneumonia Interstitial Bronchiolitis organizing
(HSIP) Pneumonia Interstitial Pneumonia
(DIP) Lung disease (COP)
(RB-ILD)
Acute Interstitial
Pneumonia
(AIP)
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INVESTIGATIONS OF ILD
Lab. Radiology Respiratory
-FBC better for
-Inflammatory markers upper lobe
-immunoglobulin
-autoimmune profile CXR HRCT MRI
ANA Pul. Function lung
ENA Test biopsy
ANCA restrictive
Anti G-BM pattern
Reticular Coarse Ground
Shadowing reticular glass B A L
-Precipitins
-Serum ACE
-ABG Honey combing neutrophils lymphocytes
Not responded
To cortisone
Good response
To corticosteroid
Bad prognosis Good prognosis
Respond to
Corticosteroid
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MANAGEMENT OF ILD
Non Pharmacological Lung Transportation
Smoke Avoid exposure long term corticosteroids Young Patent
Cessation to toxic oxygen + rapidly
Substance Azathoprine progressive
Disease
If not tolerate
Corticosteroids if not tolerate
Azathoprine alone Azathoprine
Cyclophosphamide
Discontinuation
Of toxic medication
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UNILATERAL LUNG FIBROSISEXAMINATION
Flattening of
The affected side
Heterogenous Breath sounds trachea is
percussion of reduced shifted to
the affected + the affected
side coarse crackles side
not changed with
cough
+VR
on the affected side
Reduced movement
Of the affected side
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CAUSES OF APICAL FIBROSIS
Histoplasmosis
Old T.B. Radiation Ankylosing
Spondolitis Sarcoidosis
Extrinsic allergic
Alveolitis
CAUSES OF BASAL FIBROSIS
ILD
Aspiration Asbestosis Drugs Connective
Tissue disease
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PLEURAL EFFUSION
Chest expansion breath sounds
On the affected side bronchial breathing
Above the effusion
Stony dullness on
Percussion
PLEURAL EFFUSION
Exudates Pl. Protein between Transudates
PL. protein>35g/L (25-35) g/L Pl. protein
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PLEURAL EFFUSION
Exudates Transudates
Protein >35g/L between Protein 0.5
Pl. Fluid LDH
DRUGSSerum LDH >0.6
Amiodorone Phenytoin
Methotrexate
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PNEUMONECTOMY
Chest wall
Chest expansion Trachea
Scar Flattering of the
Affected side
Absent on Grossly deviatedThe affected side to the affected side
Breath sounds
absent on
the affected side
LOBECTOMY
Scar
Chest wall Chest expansion Trachea Breath sounds
localized reduced on the deviated to the reduced on the
Deformity affected lobe affected lobe affected lobe
On upp.lobectomy
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LUNG CONSOLIDATION
Chest wall Chest expansion Trachea Percussion
normal
Reduced not shifted dullness
Except if associatedCollapse
Breath
Sounds
C A U S E SBronchial
breathing
crepitations
Infection Vasculitis malignancy Cysts
Vocal
Infarction resonance
Granuloma
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BRONCHIECTASIS
Investigations
Lab Radiology Special
-Sputum CLS
-Sputum AFB
-Sputum gram stain CXR HRCT Bronchoscopy-Immunoglobulins for malignancy
-Rheumatology profile
-Na Sweat Test
-Genetic Screening for C.F. Tranlines shadows Signet ring sign
Ring shadows Thickened dilated
Bronchi Larger than
Vascular bundle
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BRONCHIECTASIS MANAGEMENT
Non Pharmacological Medical
-Stop smoking
-Pulmonary Rehabilitation Vaccination Surgery-Multi-disciplinary -annual Influenza for localized
Management -H. influenza -Antibiotic disease
-Pneumococcal for exacerbation
-long term antibiotic
-bronchodilators
-Inhaled corticosteroid
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OBSTRUCTIVE AIRWAY DISEASES
Chronic Asthma Chronic
Obstructiveairway disease
COAD
Reversible Cause Chronic Emphysema
Bronchitis
Diurnal
Variation Smoking
Irreversible No Cause
Diunalvariation Pollution
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INVESTIGATIONS OF OBSTRUCTIVE
LUNG DISEASE
Lab.
Others
-FBC Radiology E.C.G.
-urea Electrolytes
-LFT -CXR -Rt. ventricles
Hypertrophy
-Inflammatory markers -HRCT -P. Pulmonale
-S. & antitypsis for emphysemia
-ABG -Echo
-Sputum -RFTCLS (Spirometry)
gram
Stain
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MANAGEMENT OF OBSTRUCTIVE
AIR WAY DISEASE
Non pharmacological Vaccination Pharmacological
-Stop smoking
-Pul. Rehabilitation
Annual H. Influenza Pneumococcal
Influenza PneumoniaVaccine
Bronchial Asthma
C O A D
B2 against or LABA LABA
Anticholinegic + +
SABA inhaled inhaled
Or SAMA corticostriods +
Theophylline
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BRITISH THORACIC SOCIETY GUIDELINES
STEP STEP STEP =step 4Add beclomethasone +
100-400 ug/12h -oral Prednisolone
Occasional
Short acting
Inhaled B2 against STEP STEP
+-LABA -Beclomethasone to 1000 ug/12h
- dose of oral TheophyllineBeclomethasone oral leukotrene antagonistTo 400ug/12h
If > than once daily oral B2 againstOr nightTime symptoms oral leukotrene receptor
oral Theophylline
STEP
12
3
4
5
2
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STATION 3
MAP FOR
CARDIOLOGY
NEUROLOGY
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CARDIOLOGY EXAMINATION
Non Auscultatory Auscultatory Rt. A.S.
Carotid
Thrill
Pulse
Lf. P.S.
Both
Radial
AF JVPor not
-small pulse
Or
-Big pulse volume
-Average
Collapsing
Water V Wave w/
Hammer Carotid TR
Or not
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AUSCULTATORY
APEXAxilla 2
ndRt. Intercostal 3
rdleft intercostals space
Soft Pansystolic space while patient leans forward
Murmur -1st
H.S. after expiration early
MR ejection systolic diastolic murmur
Murmur A.S.
H.S. MurmursLower left A.R.
Sternal edge 2nd
left
TR (Insp.) intercostal
4th
H.S. Left sternal Carotid
Near the 1st
H.S. edge R A.S.
V.S.D. L P.S.
2ndH.S. opening A.S.D. 2nd H.S.
snap near it
fixed splitting
2nd
H.S.
HOCM
valsalvis
1st
H.S.
P. HTN
normal M.R. A.S.
P.S.
M.S.
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AORTIC STENOSIS
A.S.
Symptoms Non Auscultatory Auscultatory
Findings
Ejection systolic
Murmur with
Expiration radiate to
neck
Dyspnoea Syncope -small pulse
Volume Apex
heaving
-Slow Rising
Chest pain Pulse
-Narrow PulsePressure Systolic thrill in
Aortic area
SIGNS OF SEVERITYPul. HTN
Pul.
congestion
Slow-rising pulse
Small Pulse volume
Narrow Pulse Pressure Heaving Systolic Soft 2nd
4th
H.S. Long
Apex Thrill heart sound murmurs
A2
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Bicuspid Congenital Rheumatic Degenerative
Indications for Aortic
Valve replacement
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AORTIC REGURGITATION A.R.
SYMPTOMS NON AUSCULTATORY AUSCULTATORY
FINDINGS FINDINGS
SIGNS OF SEVERITY
Long duration of
The murmur Austin Flint murmur P.HTN
Wide Pulse 3rd
H.S.
Pressure
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A.R.
CAUSES INDICATION FOR SURGERY
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MITRAL STENOSIS
SYMPTOMS NON AUSCULTATORY AUSCULTATORY
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M.S.
COMPLICATION DD SIGNS OF SEVERITY
Left Atrial myxoma Clinical Echo
Austin-flint murmur
INDICATION OF SURGERY
Pul. Pul. Recurrent
Congestion HTN thromboembolic
Events despite
Anticoagulation
Haemoptysis
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MITRAL REGURGITATION
Symptoms Non Auscultatory Auscultatory
1st
H.S. S3
Pan-systolic murmur
soft and radiating
to axilla
===========================================================================
CAUSES INDICATIONS FOR SURGERY
Acute Chronic Symptomatic Asymptomatic
Despite optimum
Prolapse Medical therapy LVEF LVES D
Rupture MI NYAH III-IV 60% 45mm
Rheumatic Functional EF~35-50%
3 act. Endocarditis
Connective tissue
Disease
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SOME CONGENITAL ANOMALY
A.S.D. V.S.D. HOCM PDA
On Pulmonary at the lowerarea sternal edge
Coarctation Thrill left
of Aorta Inter-space
Thrill fixed splitting
2nd
H.S. thrill at machinery
Lower sterna murmurs
Ejection systolic Edge loudest below
Murmur left clavicleEjection systolic
Murmur valsalvi
Systolic Pansystolic
thrill murmur
no radiation
Fallotscontinuous
V.S.D. Rt. vent. Pul. Stenosis radiofemoral murmur radiating
Hypertrophy delay to back
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