CONSTIPATION AND GASTROPARESIS ( Gastrointestinal Problems )

Wednesday, October 28, 2009

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CONSTIPATION

Constipation is a symptom rather than a disease and is the most common digestive complaint in the United States. A standard set of criteria has been suggested that includes at least 2 of the following symptoms present for at least 3 months:

  • Hard stools
  • Straining at defecation
  • Sensation of incomplete evacuation at least 25% of the time
  • Two or fewer bowel movements per week

EXAMINATION

History is most relevant regarding the etiology of constipation. Understanding the type and degree of disability caused by the symptoms is important. Disability may include the following:

  • Length of time attempting rectal evacuation
  • Number of bowel movements per week
  • Presence of chronic straining and/or hard stools

The patient may be totally asymptomatic or complain of the following:

  • Abdominal bloating
  • Pain on defecation
  • Rectal bleeding
  • Spurious diarrhea
  • Low back pain

The following also suggest that the patient may have difficult rectal evacuation:

  • Feeling of incomplete evacuation
  • Digital extraction
  • Tenesmus
  • Enema retention

However, the following signs and symptoms should be concerning:

  • Rectal bleeding
  • Abdominal pain
  • Vomiting
  • Unexplained weight loss

General physical examination often is of no benefit in determining etiology or deciding on treatment. The following are exceptional findings:

  • A localized mass on abdominal examination
  • Local anorectal lesions, which can cause or contribute to constipation (eg, anal fissures, fistulae, strictures, cancer, thrombosed hemorrhoids)
  • Visible intussusception during straining

Digital rectal examination provides information about the following:

  • Anorectal masses
  • Tone of the internal anal sphincter
  • Strength of the external anal sphincter and puborectalis muscle
  • Presence of gross blood or occult bleeding by checking the stool guaiac
  • Stool amount and consistency: In pelvic outlet dysfunction, more stool is present in the rectal vault than in colonic inertia or irritable bowel syndrome, in which little or no stool remains in the rectum between defecations. Pelvic floor dysfunction manifests by failure of descent of the examining finger and contraction of the upper segment of the sphincter during straining.
TREATMENT
Emergency
  • Most patients have chronic constipation, which does not lend itself to a specific etiology at time of presentation.
  • A comprehensive history should readily identify the most common causes of fecal impaction including (1) postoperative constipation, (2) prolonged bed rest, (3) residual barium from barium enemas, or (4) medication-related constipation (eg, opioids, anticholinergics).
  • In elderly bedridden patients, it is important to exclude severe dehydration and electrolyte abnormalities.
  • Exclude any life-threatening complication of constipation (eg, volvulus) and remember that the patient might present with intestinal perforation after tap water enemas performed at home.
  • Specifically focus therapeutic interventions on facilitating rectal evacuation rather than increasing bowel movement.
Consultations
  • Consult a general surgeon if you suspect intestinal obstruction or volvulus.

GASTROPARESIS

Gastroparesis presents with symptoms of gastric retention and nongastrointestinal manifestations, with objective evidence of delayed gastric emptying in the absence of mechanical obstruction. Diabetic, idiopathic, and postsurgical gastroparesis are the most common forms, although many other conditions are associated with symptomatic delayed gastric emptying ( Table 1 ).

Table 1. Etiologies of Gastroparesis

Disorder

N

%

Idiopathic

52

35.6

(Postviral)

12

8.2

Diabetic

42

28.8

Postsurgical

19

13.0

Parkinson's disease

11

7.5

Collagen vascular disease

7

4.8

Intestinal pseudo-obstruction

6

4.1

Miscellaneous

9

6.2

Gastroparesis presents with a constellation of symptoms. In one study, nausea was reported by 93% of patients whereas early satiety and vomiting were noted by 86% and 68%, respectively. In another series, nausea, vomiting, bloating, and early satiety were reported by 92%, 84%, 75%, and 60% of patients, respectively. Many patients in both case series (89% and 46%) also reported abdominal pain ( Table 2 ).

Table 2. Characteristics of Pain in 28 Gastroparesis Patients

Characteristic

%

Localized

76

Upper abdominal location

36

Constant

28

Burning, vague, or crampy

64

Nocturnal

80

Exacerbated by meals

60

Relief by meals

15

ETIOLOGY

Gastroparesis has many causes. In a case series of 146 gastroparesis patients seen at a large US tertiary medical center, 29% had underlying diabetes, 13% developed symptoms after gastric surgery, and 36% were idiopathic. The mean age of onset for gastroparesis is 34 years. Eighty-two percent of cases occur in women.

THERAPY

Therapies for gastroparesis include nutritional modifications, medications to stimulate gastric emptying, drugs that reduce vomiting, endoscopic and surgical approaches, and psychological interventions. To facilitate treatment selection, a gastroparesis severity classification has been proposed. Grade 1 (mild) gastroparesis is characterized by intermittent, easily controlled symptoms with maintenance of weight and nutritional status, and is treated with dietary modification and avoidance of medications that slow emptying. Grade 2 (compensated) gastroparesis is characterized by moderately severe symptoms with infrequent hospitalizations that are treated with combined prokinetic and antiemetic agents. Grade 3 (gastric failure) gastroparesis patients are medication-unresponsive, cannot maintain nutrition or hydration, and require frequent emergency department or inpatient care. Individuals with grade 3 gastroparesis may need intermittent intravenous fluids and medications, enteral or parenteral nutrition, and endoscopic or surgical therapy.

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READ MORE - CONSTIPATION AND GASTROPARESIS ( Gastrointestinal Problems )

PATOLOGI HATI 1 ( Do you have a heart ? )

Tuesday, October 13, 2009

HEART LOU

GAMBARAN UMUM PENYAKIT HATI

Ada 3 aspek yang perlu diketahui :

A. Pola jejas dan cedera pada hati.

Pola jejas dan cedera pada hati yaitu perubahan morfologik yang terjadi pada hati akibat jejas dan cedera. Secara umum terdapat 5 respon / reaksi akibat cedera pada hati, yaitu :

  1. Degenerasi
  2. Nekrosis : nekrosis fokal, nekrosis zonal, nekrosis submasif, nekrosis masif, nekrosis sentrilobular, neokrasis mid-zonal, nekrosis periportal, nekrosis geografik.
  3. Inflamasi / peradangan
  4. Regenerasi
  5. Fibrosis

B. Kegagalan hati dan sirosis.

Kegagalan hati : apabila kemampuan hepar membentuk dan mensekresi empedu hilang yang ditandai oleh ikterus, maka ini merupakan refleksi terjadinya kegagalan hati yaitu berupa kerusakan semua fungsi hati. Gangguan yang menyebabkan kegagalan hati dibagi menjadi 3 kategori :

  1. Nekrosis hepatik yang masif
  2. Penyakit hati kronik
  3. Disfungsi hati tanpa nekrosis yang terbuka

Sirosis : yaitu terbentuknya nodul – nodul regeneratif yang dikelilingi fibrosis pada jaringan hati. Penyebab antara lain : Alcohol abuse, hepatitis kronik, penyakit biliar, hemokromatosis primer, penyakit Wilson, defisiensi antitrypsin alfa 1, dll.

Terdapat 3 karakteristik pada sirosis :

  1. Septa jembatan fibrosis
  2. Nodul parenkimal
  3. Perubahan atau pecahnya arsitektur seluruh jaringan hati

Patogenesis dari sirosis :

  • Kolagen tipe I dan III dalam lobulus
  • Menciptakan serabut sepa yang halus dan banyak
  • Menghambat darah di sekitar parenkim
  • Terjadi deposisi terus menerus dari kolagen pada space of Disse
  • Hilangnya fenetrasi sl endotelial sinusoid
  • Rongga sinusoid menjadi lebih mirip seperti kapiler
  • Sekresi protein dari sel – sel hati mengalami kegagalan

Picture4-2

Gambaran klinik sirosis :

  • Hipertensi porta
  • Ascites
  • Portosystemic shunt
  • Splenomegali
  • Varices esophagus
  • Malnutrisi
  • dll

C. Jaundice atau ikterus dan kholestasis.

Jaundice atau ikterus : merupakan gejala klinik dimana kulit dan sklera berwarna kuning akibat pigmen bilirubin meningkat dalam darah dan dideposit di jaringan tubuh.

Pembentukan Bilirubun :

  • Heme dioksidasi menjadi biliverdin
  • Direduksi menjadi bilirubin yang mengikat albumin ( bilirubin albumin complex )
  • Proses di hepar
  • Berkonjugasi dengan molekul glucoronic acid
  • Kebanyakan bilirubin glucoronida di dekonjugasi oleh bakteri beta glucoronidase didegenerasi menjadi urobilinogen

Terdapat 2 fungsi dari empedu hati :

  1. Emulsifikasi lemak makanan
  2. Menghilangkan sisa / kotoran atau debris produk sistemik

Patofisiologi Ikterus :

  • Peningkatan produksi bilirubin
  • Pengurangan pelepasan oleh hati
  • Kegagalan konyugasi oleh hati
  • Penurunan ekskresi bilirubin
  • Kegagalan aliran intrahepatik dan ekstrahepatik

Tiga mekanisme pertama menghasilkan hiperbilirubinemia unconjugated. Dua mekanisme terakhir menghasilkan hiperbilirubinemia conjugated.

Kholestasis : keadaan kholestasis yang disebabkan oleh disfungsi hepatoseluler atau obstruksi biliar ekstra intrahepatik juga bisa disertai ikterus.

PENYAKIT HATI INFEKSI

Infeksi virus sistemik pada hati bisa disebabkan oleh :

  1. Infeksi mononukleosis, misal : Virus Ebstein Barr
  2. Infeksi Cytomegalovirus
  3. Yellow fever, Rubella, Adenovirus, Herpes, Enterovirus, dll.
  4. Infeksi virus hepatitis : Virus hepatitis A,B,C,D dan E

A. Hepatitis Virus.

Hepatitis virus akut : setiap virus hepatotrofik bisa menyebabkan hepatitis virus akut. Apapun agennya penyakit ini terdiri dari 4 fase :

  1. Fase Inkubasi
  2. Fase preikterik
  3. Fase ikterik
  4. Fase convalesent

B. Hepatitis Virus Kronik.

Adalah penyakit hepar yang secara simptom, biokimia atau serologik tejadi perlangsungan terus menerus atau berlangsung lebih dari 6 bulan. Hepatitis kronik dibagi atas :

  1. Hepatitis kronik persisten
  2. Hepatitis kronik aktif
  3. Hepatitis kronik lobular

PENYAKIT HATI AUTOIMUN

A. Hepatitis Autoimun

adalah hepatitis kronik dengan penyebab yang tidak diketahui, yang khas pada penyakit hepatitis autoimun yaitu memberikan respons yang baik dan memuaskan terhadap terapi imunosupresif.

PENYAKIT HATI ALKOHOLIK

Alkohol abuse merupakan bentuk utama penyakit hati di negara bagian barat. Terdapat 3 bentuk penyakit hati yang berbeda, sekalipun bisa overlaping :

  1. Steatosis Hepatik
  2. Hepatitis Alkoholik
  3. Sirosis Hepatik

A. Steatosis Hepatik

Secara morfologik, sesudah pemakaian alkohol dalam jumlah yang sedang ( moderat ), maka hepatosit meimbun droplet lemak kecil ( mikroveskuler ).

B. Hepatitis Alkoholik

Secara morfologik hepatitis alkoholik menonjolkan hal – hal sebagai berikut :

  1. Nekrosis sel hati
  2. Mallory Bodies
  3. Reaksi Netrofilik
  4. Fibrosis

 

 

 

READ MORE - PATOLOGI HATI 1 ( Do you have a heart ? )

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