2.

CASE DESCRIPTION
2.1 Patient’s Demographic
Patient initial : Mr MBI
Age : 81 yrsold
Gender : Male
Race : Malay
Height : 160 cm
Weight : 55 kg
BMI : 21.5
ADL : Bed mobility dependent
DOA : 22/09/2019
Ward/bed : 7A/37

2.2 HISTORY OF PRESENTING COMPLAINTS

He had less responsive - 2/7 , him son claimed patient is having difficulties in answering questions and
facial asymmetry -1/7, slumpty of speech , decrease oral intake ,lost meal was lunch @12 pm episodes
of choking meals since yesterday n of admission. Him son claims cough x-2/7 and patient unable to
expectorate. Otherwise she did not experience any temperature spike, vomiting, abdominal pain,
diarrhea, SOB, chest pain, trauma/fall. He also does not have any symptoms of UTI or URTI

2.3 PAST MEDICAL AND MEDICATION HISTORY

Patient previously had multiple comorbidities. He was diagnosed with hypertension and
dyslpidemia since 2009.Him son claimed the patient not complaint to medication (sometimes took high
dose medication). Antiplatelet has been withold since December 2018, family unsure of reason, no
history of bleeding tendency, malaena, drug intolerance . Simvastatin and aspirin off actually by KK (
government health clinic ). The patient was had few medications in outpatient as stated below :

Medication Dose
Tab. HTCZ 25 mg OD
Tab. Perindopril 4 mg OD

Patient had multiple admission in hospital at 2018 :

1. The patient on 13th September2018 was admitted to the hospital and diagnosed with cerebrovascular
accident with right hemiparesis, to Hypertensive emergency BP : 170/91, Dyslipidemia. In ward
given Tablet Perindopril 6 mg OD then subsequently BP normalize ( BP range 120-134/62-84 mm
 th
hg). CT Brain (15 September2018)with result Multifocal infarct with varying ages. Started on
Tablet Cardipin 100 mg OD and Tablet Simvastatin 20mg ON only.
2. The patient on 16th December2018 was admitted to the hospital and diagnosed with atypical
pneumonia, history of cerebrovascular accident with right hemiparesis, Hypertension, Dyslipidemia,
resolved acute kidney injury secondary to dehidration. He was had few medications in ward as
stated below :
Medication Dose
Tablet. Simvastatin 20 mg ON
Tablet. Cardipin 100 mg OD
Tablet. Perindopril 6mg OD
Tablet. Azithromycin 500 mg x 4/7
IV. Augmentin 1,2 g TDS x 4/ 7

2.4 SOCIAL HISTORY

Ex smoker 40 years 40 pack /month and stopped 1 years ago (September 2018)
Home :

 stay in elderly wife (73 y/o)- wife is a retired teacher.

 Patient previous a school security guard-receiving pension
 Has 4 children – 2 in seremban (sons) another 2 daughter in klang and johor
 Single storey house , squatty toilet (at terachi)
 Has standard quadripod

Carer : wife

2.5 FAMILY HISTORY

Nil

2.6 EXAMINATION DETAILS

BP : 178/79
HR : 99
Reflo : 5.2mmol/l
SP02 : 96%
2.7 Compliance Assessment : Him son claimed the patient not complaint to medication

2.8 Allergies
NKDA

2.9 DIAGNOSIS :
Cerebrovascular accident (CVA)
Recurrent CVA

2.10 CLINICAL PROGRESS

Day Progress
1 Arrived in ED at 04:50 PM with had less responsive - 2/7 , him son claimed
patient is having difficulties in answering questions and facial asymmetry -
1/7, slumpty of speech , decrease oral intake ,lost meal was lunch @12 pm
episodes of choking meals since yesterday n of admission. Him son claims
cough x-2/7 and patient unable to expectorat. Appeared weak. Otherwise
no chest pain/SOB, no fever, no vomiting, no h/o trauma/fall,
Admitted to 7A by 06.25 PM under neurology.
Provisional diagnosis: Cerebrovascular accident (CVA)
Recurrent CVA
Start Tablet aspirin 300 mg at 07.00 PM via RT ( Ryle’s tube)

2 Diagnosis: Cerebrovascular accident (CVA) Recurrent CVA

Patient appeared weaknes, difficulty in speaking, difficulty in eating Plan: to
start back Tablet cardipin 100 mg after review FBC, IVD NS 2 kolf/24 hours
3 Patient appeared
2.11 Lab Results and Impression
2.12 VITAL SIGN MONITORING
PATHOPHYSIOLOGY OF THE ILLNESS

Smoking is a trigger for the occurrence of UC and the most studied environmental factor in UC.
Quitting smoking increases the risk to develop UC in the following years, and this risk remains elevated
over 20 years. Passive smoking is not protective against UC, and it predisposes to ileal disease (pouchitis
and backwash ileitis) compared to non-passive smokers(Higuchi dkk., 2012) ; (Aldhous dkk., 2007).
Smoking is associated with lower onset risk, fewer hospitalizations, lower relapse rate and decreased
need for colectomy in UC The pathomechanism of the effect of smoking in IBD is not yet established.
However, it is generally believed that the beneficial effect of smoking in UC is mostly related to nicotine.
Nicotine increases mucine secretion in the colon, provokes the release of NO, and has several
anti-inflammatory properties (Bastida dan Beltrán, 2011). IgA concentration is markedly decreased in
the intestinal fluid of smoking UC patients compared to healthy non-smokers. Smoking also increases
the level of suppressor CD8+ T cells, decreases. the synthesis of proinflammatory molecules, such as Il-
1β, IL-2, IL-8, TNF-α, and impairs phagocytosis, which may explain its positive effects in UC(Kyte dkk.,
2018).
Ulcerative colitis (UC) is an inflammatory condition of the large intestine, but it cancause
disturbances in other organ systems. It is typified by abdominal pain, chronic loose bloody stools, and
fatigue

PEMBAHASAN
Ulcerative colitis (UC) is an inflammatory condition of the large intestine, but it cancause disturbances in
other organ systems. It is typified by abdominal pain, chronic loose bloody stools, and fatigue[91].
Nicotine increases mucine secretion in the colon, provokes the release of NO, and has several anti-
inflammatory properties [92-94]. IgA concentration is markedly decreased in the intestinal fluid of
smoking UC patients compared to healthy non-smokers [95]. Smoking also increases the level of
suppressor CD8+ T cells, decreases the synthesis of proinflammatory molecules, such as Il-1β, IL-2, IL-8,
TNF-α, and impairs phagocytosis, which may explain its positive
effects in UC [91].
[92-94].
IgA concentration is markedly decreased in the intestinal fluid of
smoking UC patients compared to healthy non-smokers [95].
Smoking also increases the level of suppressor CD8+ T cells, decreases
the synthesis of proinflammatory molecules, such as Il-1β, IL-2, IL-8,
TNF-α, and impairs phagocytosis, which may explain its positive
effects in UC [91].
dapus
Aldhous, M.C., Ph, D., Drummond, H.E., Hons, B.S., Anderson, N., Ph, D., dkk., 2007. Smoking Habit and
Load Influence Age at Diagnosis and Disease Extent in Ulcerative Colitis. American Journal of
Gastroenterology, 102: 589–597.
Bastida, G. dan Beltrán, B., 2011. Ulcerative colitis in smokers , non-smokers and ex-smokers. World
Journal of Gastroenterology, 17: 2740–2747.
Higuchi, L.M., Khalili, H., Chan, A.T., Richter, J.M., Bousvaros, A., dan Fuchs, C.S., 2012. A Prospective
Study of Cigarette Smoking and the Risk of Infl ammatory Bowel Disease in Women. Am J
Gastroenterology, 107: 1399–1406.
Kyte, S.L., Toma, W., Bagdas, D., Meade, J.A., Schurman, L.D., Lichtman, A.H., dkk., 2018. Nicotine
Prevents and Reverses Paclitaxel-Induced Mechanical Allodynia in a Mouse Model of CIPN s. The
Journal of Pharmacology and Experimental therapeutics, 364: 110–119.