LAPORAN KASUS

Oleh : Geha Sholichah

Pembimbing : dr. H. Miftah, SpPD

RUMAH SAKIT MUHAMMADIYAH JOMBANG FAKULTAS KEDOKTERAN UNIVERSITAS MUHAMMADIYAH MALANG 2014

IDENTITAS PASIEN
Nama Jenis Kelamin Usia Alamat Status Pekerjaan Tanggal MRS No. RM : Ny. Mufatikah : Perempuan : 43 tahun : KH Dewantara Gg II No. 23 Jombang : Menikah : Ibu Rumah Tangga : 24 April 2014 (18.15 WIB) : 12.19.32

KELUHAN UTAMA Nyeri Perut

RIWAYAT PENYAKIT SEKARANG Pasien datang ke IGD RSMJ dengan keluhan nyeri pada perut, nyeri pada perut bagian uluhati, kanan atas dan perut terasa sebah dan perih. Hal ini dirasakan pasien hilang timbul sejak 1 minggu SMRS. Mual + setiap hendak mau makan, namun tidak sampai muntah. Nafsu makan menurun dan badan pasien terasa lemas. Tidak ada keluhan panas badan. Pada saat BAK, warna air kencing kuning, nyeri - panas (-), keluar pasir (-). BAB dalam batas normal.

RIWAYAT PENYAKIT DAHULU

Hipertensi (+) rutin kontrol berobat ke dr. Miftah, Sp.Pd Gastritis (+) rutin kontrol berobat ke dr. Miftah, Sp.Pd ISK (+) 1 minggu yll, (nyeri berkemih +, panas +)
RIWAYAT PENYAKIT KELUARGA Ibu pasien menderita hipertensi (+) dan Gastritis (+) Bapak pasien meninggal RIWAYAT SOSIAL Pasien sehari-hari bekerja sebagai Ibu rumah tangga

PEMERIKSAAN FISIK
Vital Sign Kesadaran : Compos Mentis GCS : 456 KU : Lemah Tekanan Darah : 170/80 mmHg Nadi : 106 x/menit Respiratory rate : 22 x/menit Temperature : 37,2C

 Kepala-Leher : Anemis (-/-), Ikterik (-/-), Cyanosis (-), Dyspneu (-) Pembesaran KGB (-) Thorax
Pulmo
I: bentuk dada normal, gerakan dada simetris, retaksi dada -, massa P: gerakan dinding dada simetris, fremitus simetris P: sonor/sonor A: vesikular, wh -/-, Rh -/-

Cor
I: icyus cordis tdak tampak P: iktus cordis tdk kuat angkat P: batas jantung normal A: S1 S2 tunggal regular, bising -

Abdomen : I : Flat, asites-, massaP : Soefl, nyeri tekan (+) epigastrium, dan suprapubik H/L ttb P : Timpani A : Bising usus (+) Normal Extremitas : Akral Hangat kering merah Edema -/CRT 2 detik

PEMERIKSAAN PENUNJANG
Hb : 14,6 Leukosit : 11.600 Hitung Jenis Granulosit : 66 Limfosit : 27 Monosit : 7 LED : 16/33 Trombosit : 251.000 Hmeatokrit : 39 Eritrosit : 4,6 SGOT : 40 SGPT : 24 Ureum : 35,0 Creatinin : 0,8 Asam urat : 7,0 GDA : 128

PEMERIKSAAN PENUNJANG
Warna : Kuning Tua pH 6,5 Protein : Negatif Glukosa : Negatif Urobilin : Negatif Keton : Negatif Nitrit : Negatif Blood : Negatif Lekosit : Negatif Berat jenis : 1,010 Sedimen : Eritrosit : 3-4/lp Lekosit : 6-8/lp Epitel : penuh Kristal : Bakteri : Positif Lain-Lain : -

ASSESSMENT
UTI HT Stage II Dyspepsia Sndroma

PLANNING THERAPY
Terapi di IGD Infus Ringer Laktat 1000cc/24 jam Injeksi ranitidin 2 x 1 ampul Oral : Bisoprolol 1x1 Amlodipin 5mg 1x1

Di Ruangan : Infus Ringer Laktat 20tpm Injeksi ranitidin 3 x 1 ampul Drip NSB 5000 1x1 Drip Civell 1flash PO : Vosedon 3x1 Bisoprolol 1x tab Amlodipin 1x 5mg Lesicol 2x1 Sulcolon 3x 2 tab Librozym 3x1 tab Omeprazol 1x1 Becombion F

PLANNING THERAPY

Tanggal
24/April

Keluhan
S : Badan Lemas (+), Nyeri Perut ulu hati (+), sebah (+), mual (+), intake O : KU : Lemah TD : 170/100 N/S : 88/36,9 Dyspepsia Syndroma + HT STAGE II Planning dx : Lab DL, dan UL IVFD RL 20 tpm Inj. Ranitidine 3x1 Drip Neurosanbe 5000 1x1 PO : Vosedon 3x1 Bisoprolol 1x1 Amlodipin 1x5mg IVFD RL 20 tpm Inj. Ranitidine 3x1 Drip Civell 1flash PO : Vosedon 3x1 Bisoprolol 1x tab Amlodipin 1x 5mg Lesicol 2x1 Sulcolon 3x 2 tab Librozym 3x1 tab Omeprazol 1x1 Becombion F

25/April

S : Nyeri Perut ulu hati (+), sebah (-), mual (), nyeri pinggang, intake cukup O : KU : Cukup TD : 150/90 N/S : 88/36,2 Hasil Lab DL dan UL Leukosit : 11.600 LED : 16/33 OT : 40 Sedimen : -Eritrosit : 3-4/lp -Lekosit : 6-8/lp -Epitel : penuh -Kristal : -Bakteri : Positif

UTI + Gastritis + HT

26/April

S : Nyeri Perut (-) intake meningkat O : KU : Cukup TD : 130/90 N/S : 86/36,2

UTI +Gastritis +HT

IVFD RL 20 tpm Inj. Ranitidine 3x1 Drip Civell 1flash PO : Vosedon 3x1 Bisoprolol 1x tab Amlodipin 1x 5mg Lesicol 2x1 Sulcolon 3x 2 tab Librozym 3x1 tab Omeprazol 1x1 Becombion F

TINJAUAN PUSTAKA...

SISTIM URINARIA

Urinary Traktus Infection

Wanita Gender (females>males) Dewasa 50% Age Pregnancy and menopause Use of diaphragm Sexual intercourse Vesicoureteral reflux Congenital abnormalities Stone (kidney or any part of tract) Urinary catheters Diabetes mellitus Inadequate fluid intake

Community-acquired : Escherichia coli* Klebsiella pneumoniae Proteus mirabilis Staphylococcus saprophyticus Enterococcus faecalis Hospital-acquired Escherichia coli Pseudomonas aeroginosa Proteus sp. Enterobacter sp. Serratia sp. Enterococcus sp.

UTI Upper 1. Pyelonefritis ( PNA & PNK) 2. Ureter ( Uretritis) Urinary Traktus Infection UTI Lower 1. VU ( Sistitis) 2. Urethra ( Uretritis) 3. Prostat (Prostitis)

Urinary Traktus Infection

Hematogen

Limfatik

Ascending infeksi

Eksogen

Kolonisasi uretra & introitus vagina

Mikroorganisme

Multiplikasi bakteri dan pertahanan menurun

Naiknya bakteri ke ginjal

Urinary Traktus Infection

-ISK.bawah (Sistitis): nyeri atau rasa panas saat kencing, polakisuria, Nyeri suprapubik -ISK.atas (Pielonefritis): demam menggigil, nyeri pinggang malaise, mual, muntah, nyeri kepala

Lokal - Disuria - Polakisuria - Inkontinensia - Stranguria - Tenesmus - Nokturia - Urgensi

- Prostatismus - Nyeri Uretra - Nyeri VU - Nyeri kolik (menyebar) - Nyeri ginjal - Eneurisis nokturnal

Sistemik - Demam sampai menggigil - Septikemia & syok

Perubahan urinalisisis - Hematuria - Chylusuria - Piuria - Pnematuria

Diagnosa ISK
Anamnese Pemeriksaan fisik Laboraturium Urinalisis: lekosituri, hematuri Bakteriologis: mikros., kultur Tes kimiawi: tes reduksi Griess-nitrate Tes plat-celup (Dip-Slide) Pem.penunjang: Mencari kausa : batu, anomali sal.kemih IVP, USG, CT-Scanning

Komplikasi
- Dapat terjadi Ascending infection dari saluran
kemih ke ginjal

Pielonefritis dapat menyebabkan gagal ginjal,sepsis - Dapat menjadi kronis, dan mengarah ke kerusakan ginjal yang permanen

 Gastritis proses inflamasi pada mukosa dan submukosa lambung. Etiologi : helicobacter pylori 90%

The normal gastric mucosa

Cardia mainly mucus-secreting cells Fundus (body) acid producing parietal cells, pepsin producing chief cells Pylorus hormone (gastrin) production

Function of stomach
Mixing of food with acid/pepsin Unique acid environment requires functional gastric surface mucus barrier, bicarbonate buffering and epithelial integrity

Mucosa protective factors

Pathogenesis
In normal acid/pepsin attack is balanced by mucosal defences Increased attack by hyperacidity Weakened mucosal defence the major factor (H. pylori related)

Acute gastritis
Drugs (non-steroidal antiinflammatory drugs NSAID), alcohol cause acute erosion (loss of mucosa superficial to muscularis mucosae). Can result in severe haemorrhage Acute Helicobacter infection has a prominent neutrophil infiltrate

Chronic gastritis
A autoimmune B bacterial (helicobacter) C - chemical

Autoimmune chronic gastritis

Autoantibodies to gastric parietal cells Hypochlorhydria/achlorhydria Loss of gastric intrinsic factor leads to malabsorption of vitamin B12 with macrocytic,megaloblastic anaemia

Morphology of chronic gastritis

Chronic inflammatory cell infiltration Mucosal atrophy Intestinal (goblet cell) metaplasia Seen in Helicobacter and autoimmune gastritis (not chemical)

Helicobacter pylori
Causes cell damage and inflammatory cell infiltration In most countries the majority of adults are infected

Helicobacter gastritis
Acute inflammation mediated by complement and cytokines Polymorphisms infiltrate epithelium and may be partly responsible for its destruction An immune response is also initiated (antibodies may be detected in serum)

Helicobacter gastritis
2 patterns of infection
Diffuse involvement of body and antrum (pan gastritis associated with diminishing acid output) Infection confined to antrum (antral gastritis, associate with increased acid output)

Chemical gastritis
Commonly seen with bile reflux (toxic to cells) Prominent hyperplastic response (inflammatory cells scanty) With time intestinal metaplasia

Regulation of gastric acid secretion

Blood Pressure Classification(JNC7)

BP Classification SBP mmHg DBP mmHg

Normal
Prehypertension Stage 1 Hypertension Stage 2 Hypertension

<120
120139 140159 >160

and
or or or

<80
8089 9099 >100

Etiology
Essential (95%) Secondary about 5%-10% of cases Renal : renal artery stenosis ; parenchymal disease Endocrine : Pheochromocytoma; Hyperaldosteronism; hyperthyroidsm ; Cushing syndr; Exogenous agent Vascular: Coarctation of aorta, Aortic insufficiency Toxemia of pregnancy

Causes of secundary hypertension

Primary renal disease Oral contraceptives Pheochromocytoma (about one-half of px have paroxysmal hypertension) Primary hyperaldosteronism (triad of hypertension, unexplained hypokalemia, metabolic alkalosis) Renovascular disease Chusing syndrome Hyperthyroid, hyperparathyroid Sleep apnea syndrome Coartation of the aorta

Risk factors
Race (more common and more severe in blacks) Age > 60 years Sex (men and postmenopausal women) Family history of CVD Smoking High cholesterol diet Co-existing disorders such as DM, obesity, and hyperlipidemia Sodium intake High intake of alcohol

Standard work-up
Conformation of real hypertension Identify Etiology of H/T Access of End-organ damage Identify cardiovascular risk

Laboratory test
Routine screen ,including CBC ,biochemistry Urinalysis : albumin , microalbumin Serum potassium , Calcium ,Creatinine Thyroid function , Cortisol level Cholesterol , TG EKG Chest X-Ray Catecholamines only in presence of diastolic pressure >110 mmHg in patient younger than 30

Echocardiography

Target organ damage

Heart
Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revasculariztion

Brain
Stroke or transient ischemic attack

Chronic kidney disease Peripheral arterial disease Retinopathy

Complications
Cerebrovascular disease: tromboembolic, intracranial bleeding, TIA Cardiovascular disease: MI, HF, CAD LVH: enhanced incidence of HF, ventricular arrythmia, sudden cardiac death Periveral vascular disease Renal failure

JNC 7: Treatment Algorithm for Hypertension

Lifestyle modifications
Not at goal blood pressure (<140/90 mm Hg) (<130/80 mm Hg for those with diabetes or chronic kidney disease)

Initial drug choices

Without compelling indications

With compelling indications

Stage 1 hypertension (SBP 140159 or DBP 9099 mm Hg) Thiazide-type diuretic for most. May consider ACEI, ARB, BB, CCB, or combination.

Stage 2 hypertension (SBP 160 or DBP 100 mm Hg) Two-drug combination for most (usually thiazide-type diuretic and ACEI or ARB or BB or CCB).

Drugs for compelling indications Other antihypertensive drugs (diuretic, ACEI, ARB, BB, CCB) as needed.

Not at goal blood pressure

Optimize dosages or add additional drugs until goal blood pressure is achieved. Consider consultation with hypertension specialist.

SBP=systolic blood pressure; DBP=diastolic blood pressure; ACEI=angiotensinconverting enzyme inhibitor; ARB=angiotensin receptor blocker; BB=b-blocker; CCB=calcium channel blocker

JNC 7. May 2003. NIH publication 03-5233.

JNC 7: Classification and Management of Blood Pressure for Adults

Initial Drug Therapy
BP Classificatio n
Normal Prehypertens ion

SBP* (mm Hg)

<120 120139

DBP* (mm Hg)

and <80 or 80 89

Lifestyle Modificati on
Encourage Yes

Without Compelling Indications

No antihypertensive drug indicated. Thiazide-type diuretic for most. May consider ACEI, ARB, BB, CCB, or combination. Two-drug combination for most (usually thiazide-type diuretic and ACEI or ARB or BB or CCB).

With Compelling Indications

Drug(s) for compelling indications. Drug(s) for compelling indications.

Stage 1 hypertension

140159

or 90 99

Yes

Stage 2 hypertension

160

or 100

Yes

Other antihypertensive drugs (diuretic, ACEI, ARB, BB, CCB) as needed.

JNC 7. May 2003. NIH publication 03-5233.

Lifestyle Modifications to Manage HTN

Modification Recommendations
Approximate Systolic Blood Pressure Reduction

Weight Reduction
Adapt eating plan Dietary sodium reduction Increase physical activity

Maintain normal body weight (BMI 18.5-24.9)

Consume diets rich in fruits, vegetables, low fat dairy and low saturated fat Reduce sodium to no more than 2.4 g/day sodium or 6 g/day NaCl Engage in regular aerobic activity such as walking (30 min/day on most days) than 2 drinks/d for men and 1 drinks/day for women.

5-20 mm Hg for each 10 kg weight loss

8-14 mm Hg 2-8 mm Hg 4-9 mm Hg 2-4 mm Hg

Moderate alcohol consumption Limit alcohol to no more

Source: The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure JNCVII. JAMA. 2003;289:2560-2572.

Again: Treatment Algorithm

Lifestyle Modification

Not at goal BP

Initial Drug Choices

W/O Compelling Indications

With Compelling Indications

Stage 1

Stage 2

Drug for Indication

Thiaz, ACE, ARB, BB, CCB

2 Drug Combo

Not at Goal BP Adjust Dose or add additional agents

Obat hipertensi oral yang sering digunakan di Indonesia

Obat
Nifedipin 5-10 mg

Dosisi
Diulang 15 menit

Efek

Lama kerja

Efek samping
Gangguan koroner

5-15 menit 4-6 jam

Kaptopril 12,5- Diulang jam 25mg

15-30 menit

6-8 jam

Stenosis a.renalis

Klonidin 75150 mg

Diulang/jam

30-60 menit 15-30 menit

8-16 jam

Mulut kering. Ngantuk Bronkokonstriksi, Blok jantung.

Propanolol 10- Diulang setiap 40 mg jam

3-6 jam

Buku Ajar Ilmu Penyakit Dalan jilid II