MORNING REPORT

Tuesday, May 17 2016

st

Co-Ass INCHARGE:
IA

MODERATOR : dr.
Dokter Jaga + Notulen: dr.
dr.
 Summary of Database
Mr. R/Male /74 y.o

Chief complaint : Shortness of breath

Patient suffered from shortness of breath since 1

month ago which was getting worse since 2 days ago
when he walking from his bedroom to toilet. Patient
said that he was oftenly awake in the night because of
cough and shortness of breath.
Patient complained that since 1 month ago he easily
felt fatigue when walking in short distance. He
complained cough since 1 month ago.
 Patient also complained Nausea (+),
vomitting (+) with frequency 4 time,
containts whitish liquid., Floating
headache (+), epigastric pain (+) since 1
week ago, He felt it like being stabbed
continuously, and getting worse when he
had late lunch or late dinner.
Patient had history of smoking about 40
years ago
 Past Medical History
Patient had been diagnosed with long
standing hipertension
Patient also consumsed NSAID and
herbal medicine about 20 years ago
Patient had history of dyspepsia
about 10 years ago
 Physical examination in
BP =
Kenanga Ward
PR : 120 tpm, regular RR = 30 tpm, T ax 36,9oC
150/100mmHg

General appearance looked severely ill GCS 456

Head Anemic (-) Icteric (-)
Neck JVP 5+2 cmH2O

Thorax Invisible Palpable at Ictus ICS VI MCL S,

Heart RHM SL D, LHM as ictus,
S1 S2 single, mur mur (-), gallop (-)

lung Simetric, SF D = S SS v v Rh - - Wh - -
SS v v - - - -
SS v v - - - -

Abdomen Convex, Soefl, Hepar : Liver span 12 cm, tenderness in

epigastric region

Extremities Oedema (-), CRT < 2s

ECG in ER
 Interpretation
Rhytm: Sinus Rhytm
Heart Rate: 125 bpm
Frontal Axis: Normoaxis
Horizontal axis: CWR
PR Interval: 0,12
QRS complex : 0,12
QT interval : 0,28
Abnormality wave: Bifasic P wave in lead V2 with
predominantly positif deflection, QRS complex positif
deflection in lead V1, ST depression in lead II and AVF

Concl: Sinus tachicardia with HR 125 bpm, with RAE,

Incomplete RBBB and ischemia at inferior wall
 Interpretation
AP position, symmetric
Soft tissue and bone normal
Trachea in the middle
ICS D/S wide
Left and right costophrenicocostalis angle are sharp
Hemithorax : hyperaeration
Heart : site normal, Size 61%, tear drop shape
Lung : Bronchovascular pattern normal in both lungs

Concl: emphysematous lung with cardiomegaly

 Lab Value Lab Value

Leukocyte 8.000 3500;10000 Ureum 80 10-50mg/dL

/L
Haemoglob 12,3 11,0- Creatinin 1.47 0,7-1,5mg/dL
in 16,5g/dl e
MCV 86,1 80-97 SGOT 26 11-41U/L

MCH 29,0 26,5-33,5 SGPT 17 10-41U/L

Thrombocy 79 150000-
te 390000/L
RBG 106 (<200)mg/d
L
CUE AND CLUE PROBLE INITIAL PLANNIN PLANNING PLANNING
M DIAGNOSE G THERAPY MONITORI
LIST DIAGNOS NG
E
Male/74 yo 1. SOB 1.1 Heart BNP Semi fowler VS
Ax: Failure Echocar position Complai
SOB, PND (+), Stage C Fc diograph O2 2 4 lpm per n
DOE (+), nasa canule
III y Diet : Na
Orthopnea(+).
Smoking history Restriction, Water
40 years, long 1.2. Chronic Restriction (800-
standing HT lung 1000 cc if there is
disease overload, 1500 cc if
CXR : 1.2.1. COPD there is no
emphysematous overload)
lung with Diuretik
cardiomegaly (Furosemide 1
x40mg iv)
ECG : sinus ARB (Irbesartan
tachycardia with 1x75 mg)
HR 125 bpm with B-blocker
Right atrial (Bisoprolol
enlargement, 1x2,5mg)
Incomplete RBBB Spironolacton
and Iskemia 1x25mg
Inferior wall Digoxin 1x 0,25 mg
CUE AND CLUE PROBLEM INITIAL PLANNING PLANNING PLANNI
LIST DIAGNOSE DIAGNOSE THERAPY NG
MONITO
RING

Male/ 74 yo 2. 2.1 Gastric - Inj. Omeprazole VS

Ax: Dyspeps ulcer Endoscopy 1 x 40 mg IV complai
Epigastric pain,
ia 2.2. (EGD) Inj. n
nausea (+), Doudenal Ondansentron 1
vomitting (+). syndrom
ulcer x 8 mg IV
History of e
analgetik and
traditional herbal
medicine
consumption to
relieve his fatigue,
History of
Dyspepsia
syndrom 10 years

PE:
Abd : flat, soepel,
bowel sound (+)
N, tenderness in
epigastrium region
CUE AND CLUE PROBLEM INITIAL PLANNING PLANNING PLANNI
LIST DIAGNOSE DIAGNOSE THERAPY NG
MONITO
RING

male/ 50 yo 3. 3.1. Lipid profil Diet low salt Lab

Ax: Hyperte Esential Irbesartan 1 x finding
-History
nsion HT 300 mg tab p.o
uncontrolled HT 3.2.
Stage 1
Secondary
PE:
BP:160/90mmhg
HT
CUE AND CLUE PROBLEM INITIAL PLANNING PLANNING PLANNI
LIST DIAGNOSE DIAGNOSE THERAPY NG
MONITO
RING

male/ 50 yo 4. 4.1 due to - Blood Confirm dx Lab

Ax: Tromboc no. 1 smear finding
-
ytopenia
PE:
-
Lab:
Pltl : 79.000
CUE AND CLUE PROBLEM INITIAL PLANNING PLANNING PLANNI
LIST DIAGNOSE DIAGNOSE THERAPY NG
MONITO
RING

male/ 50 yo 2. 2.1 due to - Confirm dx Lab

Ax: Azotemi no. 1 finding
-
a Pre
PE: Renal
-
Lab:
Ur: 160
Cr: 2,3
 Present conditions
SOB (+) , cough (+), Nausea (-),
Vomiting (-)
GA : good GCS E4V5E6
BP : 140/80 mmHg
HR : 94 bpm
RR : 24 tpm
Monitoring ECG
THANK YOU
Terapi
 Mechanism of Anemia in AI
RBC destruction: increased erythrocyte
destruction is caused by the activation of hosts
factors such as macrophages that prematurely
remove aging erythrocytes from the
bloodstream. The explanation is consistent with
the predominance of young erythrocytes in AI.
Suppressive effects of inflammation on
erythropoietic precursors: chiefly tumor necrosis
factor (TNF)-, IL-1, and the interferons, exert a
suppressive effect on erythroid colony formation.
 Inadequate erythropoietin secretion and resistance to
erythropoietin: In support of the EPO suppression
hypothesis are experiments with EPO-producing cell lines
indicate that production of the hormone is inhibited by
inflammatory cytokines including TNF- and IL-1. The
inhibition is mediated by the effects of the transcription
factor GATA-1 on the EPO gene promoter, and the
suppression of EPO production can be reversed by a GATA
inhibitor. Moreover, both baseline and hypoxia-induced
EPO gene expression is suppressed in rats treated with 551
Chapter 37: Anemia of Chronic Disease bacterial
lipopolysaccharide or IL-1 to mimic a septic state.
However, suppression of EPO production is not the major
mechanism of AI.
Erythropoiesis restriction as a result
Of iron unavailability