Lapsus Gege FIX2

Oleh :Geha Sholichah

Pembimbing :dr. H. Miftah, SpPD

RUMAH SAKIT MUHAMMADIYAH JOMBANGFAKULTAS KEDOKTERAN

UNIVERSITAS MUHAMMADIYAH MALANG2014

LAPORAN KASUS

IDENTITAS PASIEN

Nama : Ny. MufatikahJenis Kelamin : PerempuanUsia : 43 tahunAlamat : KH Dewantara Gg II No. 23 JombangStatus : MenikahPekerjaan : Ibu Rumah TanggaTanggal MRS : 24 April 2014 (18.15 WIB)No. RM : 12.19.32

PEMERIKSAAN FISIK

Vital SignKesadaran : Compos MentisGCS : 456KU : LemahTekanan Darah : 170/80 mmHgNadi : 106 x/menitRespiratory rate : 22 x/menitTemperature : 37,2⁰C

• 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-, massa-P : Soefl, nyeri tekan (+) epigastrium, dan suprapubik

H/L ttbP : TimpaniA : Bising usus (+) NormalExtremitas :Akral Hangat kering merahEdema -/-CRT 2 detik

PEMERIKSAAN PENUNJANG• Hb : 14,6• Leukosit : 11.600• Hitung Jenis

Granulosit : 66Limfosit : 27Monosit : 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 ampulOral :• Bisoprolol 1x1• Amlodipin 5mg 1x1

PLANNING THERAPYDi Ruangan :• Infus Ringer Laktat 20tpm• Injeksi ranitidin 3 x 1 ampul• Drip NSB 5000 1x1• Drip Civell 1flashPO :• Vosedon 3x1• Bisoprolol 1x ½ tab• Amlodipin 1x 5mg• Lesicol 2x1• Sulcolon 3x 2 tab• Librozym 3x1 tab• Omeprazol 1x1• Becombion F

Tanggal Keluhan

24/April S : Badan Lemas (+), Nyeri Perut ulu hati (+), sebah (+), mual (+), intake ↓O : KU : LemahTD : 170/100N/S : 88/36,9

Dyspepsia Syndroma + HT STAGE II

Planning dx : Lab DL, dan ULIVFD RL 20 tpmInj. Ranitidine 3x1Drip Neurosanbe 5000 1x1PO :Vosedon 3x1Bisoprolol 1x1Amlodipin 1x5mg

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

UTI + Gastritis + HT IVFD RL 20 tpmInj. Ranitidine 3x1Drip Civell 1flashPO :Vosedon 3x1Bisoprolol 1x ½ tabAmlodipin 1x 5mgLesicol 2x1Sulcolon 3x 2 tabLibrozym 3x1 tabOmeprazol 1x1Becombion F

26/April S : Nyeri Perut (-) intake meningkatO : KU : CukupTD : 130/90N/S : 86/36,2

UTI +Gastritis +HT IVFD RL 20 tpmInj. Ranitidine 3x1Drip Civell 1flashPO :Vosedon 3x1Bisoprolol 1x ½ tabAmlodipin 1x 5mgLesicol 2x1Sulcolon 3x 2 tabLibrozym 3x1 tabOmeprazol 1x1Becombion F

TINJAUAN PUSTAKA...

SISTIM URINARIA

Urinary Traktus Infection

Community-acquired :Escherichia coli*Klebsiella pneumoniaeProteus mirabilisStaphylococcus saprophyticusEnterococcus faecalis

Hospital-acquiredEscherichia coliPseudomonas aeroginosaProteus sp.Enterobacter sp.Serratia sp.Enterococcus sp.

Gender (females>males)AgePregnancy and menopauseUse of diaphragmSexual intercourseVesicoureteral refluxCongenital abnormalitiesStone (kidney or any part of tract)Urinary cathetersDiabetes mellitusInadequate fluid intake

Wanita Dewasa 50%

Urinary Traktus Infection

UTI Upper1. Pyelonefritis ( PNA & PNK) 2. Ureter ( Uretritis)

UTI Lower1. VU ( Sistitis)2. Urethra ( Uretritis)3. Prostat (Prostitis) ♂

Urinary Traktus Infection

Hematogen Limfatik Ascending infeksi

Eksogen

Urinary Traktus Infection

Lokal- Disuria - Prostatismus- Polakisuria - Nyeri Uretra - Inkontinensia - Nyeri VU- Stranguria - Nyeri kolik (menyebar)- Tenesmus - Nyeri ginjal- Nokturia - Eneurisis nokturnal- Urgensi

Sistemik- Demam sampai menggigil- Septikemia & syok

Perubahan urinalisisis- Hematuria - Chylusuria- Piuria - Pnematuria

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

Diagnosa ISK• Anamnese• Pemeriksaan fisik• Laboraturium

Urinalisis: lekosituri, hematuriBakteriologis: mikros., kulturTes kimiawi: tes reduksi Griess-nitrateTes plat-celup (Dip-Slide)

Pem.penunjang: Mencari kausa : batu, anomali sal.kemihIVP, 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 anti-inflammatory 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)

metaplasiaSeen 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)Blood Pressure Classification(JNC7)

NormalNormal <120<120 andand <80<80PrehypertensionPrehypertension 120120––139139 oror 8080––8989Stage 1 Stage 1 HypertensionHypertension

140140––159159 oror 9090––9999

Stage 2 Stage 2 HypertensionHypertension

>>160160 oror >>100100

BP BP ClassificationClassification

SBP SBP mmHgmmHg

DBP DBP mmHgmmHg

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 EKGChest 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

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

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

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

Not at goal blood pressure

Without compelling indications

Stage 1 hypertension(SBP 140–159 or DBP 90–99 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).

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

With compelling indications

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

Initial Drug TherapyInitial Drug TherapyBP BP ClassificatiClassificationon

SBP* SBP* (mm (mm Hg)Hg)

DBP* DBP* (mm (mm Hg)Hg)

Lifestyle Lifestyle ModificatModificat

ionion

Without Without Compelling Compelling IndicationsIndications

With With Compelling Compelling IndicationsIndications

NormalNormal <120<120 and and <80<80 EncourageEncourage

No No antihypertensive antihypertensive drug indicated.drug indicated.

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

PrehypertePrehypertensionnsion

120–120–139139

or 80–or 80–8989 YesYes

Stage 1 Stage 1 hypertensiohypertensionn

140–140–159159

or 90–or 90–9999 YesYes

Thiazide-type Thiazide-type diuretic diuretic for most. May for most. May consider ACEI, consider ACEI, ARB, BB, CCB, ARB, BB, CCB, or combination.or combination.

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

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

Stage 2 Stage 2 hypertensiohypertensionn

160160 or or 100100 YesYes

Two-drug Two-drug combination combination for most (usuallyfor most (usuallythiazide-type thiazide-type diuretic diuretic and ACEI or ARB and ACEI or ARB or or BB or CCB).BB or CCB).

JNC 7: Classification and Management of Blood Pressure for Adults

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

Lifestyle Modifications to Manage HTN

ModificationModification RecommendationsRecommendations Approximate Systolic Approximate Systolic Blood Pressure Blood Pressure

ReductionReductionWeight ReductionWeight Reduction Maintain normal body Maintain normal body

weight (BMI 18.5-24.9)weight (BMI 18.5-24.9)5-20 mm Hg for each 5-20 mm Hg for each 10 kg weight loss10 kg weight loss

Adapt eating planAdapt eating plan Consume diets rich in Consume diets rich in fruits, vegetables, low fruits, vegetables, low fat dairy and low fat dairy and low saturated fatsaturated fat

8-14 mm Hg8-14 mm Hg

Dietary sodium reductionDietary sodium reduction Reduce sodium to no Reduce sodium to no more than 2.4 g/day more than 2.4 g/day sodium or sodium or 6 g/day NaCl6 g/day NaCl

2-8 mm Hg2-8 mm Hg

Increase physical activityIncrease physical activity Engage in regular Engage in regular aerobic activity such as aerobic activity such as walking walking (30 min/day on most (30 min/day on most days)days)

4-9 mm Hg4-9 mm Hg

Moderate alcohol Moderate alcohol consumptionconsumption

Limit alcohol to no more Limit alcohol to no more than 2 drinks/d for men than 2 drinks/d for men and 1 drinks/day for and 1 drinks/day for women.women.

2-4 mm Hg2-4 mm HgSource: 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

Stage 1 Stage 2

With Compelling Indications

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 Dosisi Efek Lama kerja

Efek samping

Nifedipin 5-10 mg

Diulang 15 menit

5-15 menit 4-6 jam Gangguan koroner

Kaptopril 12,5-25mg

Diulang ½ jam 15-30 menit

6-8 jam Stenosis a.renalis

Klonidin 75-150 mg

Diulang/jam 30-60 menit

8-16 jam Mulut kering. Ngantuk

Propanolol 10-40 mg

Diulang setiap ½ jam

15-30 menit

3-6 jam Bronkokonstriksi, Blok jantung.

Buku Ajar Ilmu Penyakit Dalan jilid II