DR.

ANAM NAVEED KHAN RESIDENT MEDICAL UNIT 4 CHK

 Name:

Ayesha d/o Ateeq khan Age: 20 yrs Residence: Hyderabad Status: Unmarried D.O.A: 2-6-2011

She presented with 1 month history of.

Swelling

over both feet Vomiting, loose motions Abdominal pain Severe weight loss

month ago, the patient noticed swelling over both limbs, initially mild but gradually it progressed uptil thigh.
was followed by vomitings, 4-6/day, watery, non foul smelling, non bloody, associated with nausea, anorexia, increased thirst & central abdominal pain and with loose motions.

This

 Loose

motions were watery, 6-8/day, moderate in amount, non bloody, no mucus present, but tenesmus and fecal incontinence was present.
also complains of dry skin, generalized weakness, severe weight loss and bone pains.

Patient

 Nothing

significant.

Appetite: decreased Diet: normal Sleep: normal Micturation: no complains Bowel habits: As per presenting complains Addiction: nil Weight loss: significant loss noticed

 K:

13 yrs

Flow:

decreased during last cycle

4/30

Cycle:

 No

history of TB in family, parents and siblings alive and healthy.

 Belongs

to a poor family.

ABDOMEN: Pain in whole abdomen.

CHEST: No chest pain, cough, breathlessness etc.

CVS: No chest pain, dyspnea, PND, orthopnea or palpitations.

CNS: No dizziness, blackouts, limb weakness etc. MUSCULOSKELETAL: Generalizaed weakness, bone pains.

GENITO-URINARY: No complains.

 APPEARANCE:

Young girl of good height, cachectic, pale, looking ill, lying on bed, conscious and oriented x 3 and co-operative.
VITALS:

B.P: 100/80 mm Hg Pulse: 92b/min R/R: 20/min Temp: Afebrile

 Anemia

++
++

Dehydration Edema Tongue Angular

++ dry and smooth chelosis, dry skin

INSPECTION: Scaphoid shaped abdomen, centrally placed umbilicus, moving equally with respiration. Scratch marks all over abdomen.
PALPATION: No tenderness, no visceromegaly, no lymphadenopathy. Free fluid present in flanks. Shifting dullness positive. AUSCULTATION: Gut sounds normal.

 CHEST:

NVB all over chest with no added sounds.

CVS:

S1+S2 audible in all 4 areas with no added sounds.

CNS:

Grossly intact but generalized reduced muscle bulk.

20 yrs old Ayesha with no known comorbids presented with 1 month history of bilateral lower limbs swelling, vomiting & loose motions, abdominal pain & severe weight loss. On general examinaion, she was vitally stable, cachectic, moderately anemic & dehydrated. Pedal edema & signs of vitamin deficiency were present. Systemic examination was significant for free fluid in the abdomen.

CBC:

Hb = 10.1 gm% MCV = 96.2 MCH = 32.2 TLC = 8.6 N = 72% PLTs = 140,000

ESR: 10 mm in 1st hr

UCE:

Na+ = 140meq/l K+ = 3.1 meq/l cl- = 107meq/l BUN =3 Creatinine + 0.5

RBS: 86mg%

LFTs =
T.bili = 0.83 SGPT = 23 Alk. phosohatase = 74

 Vitamin

B12= <150 pg/ml (193-982)

Folic

acid=
8.93 (3-17)

Iron=

38 (37-145)

 PROTIEN

A/G RATIO: Total= 4.9 Albumin= 2.5 Globulin= 2.4 Ratio= 1.0

 CALCIUM:

6.5 (corrected Ca= 7.7)

Mg=

1.2 ( 1.6-2.6)
PHOSPHATE=

3.0 (2.7-4.5)
PT/INR:

1.44

 URINE

D/R: Sp.gravity = 1.01 Nitrites= +ve Red cells= Nil Pus cells= 1-2 Casts= Nil Bacteria= ++

 VIRAL

MARKERS: Hep B and Hep C negative by ICT.

 Normal

 ULTRASOUND

ABDOMEN: Increased echogenicity of liver, moderate ascites.

MT:

Negative with 0 mm.

 ASCITIC

D/R: Appearance= turbid, blood stained Proteins= 1gm% Albumin= 0.8gm% Amylase= 12U/l RBC= +++ WBC= 57/mm3 (lymphos: 81%) No organism seen----- AFB not seen SAAG Ratio : 1.7

 CT

SCAN ABDOMEN WITH CONTRAST: Normal

MP:

Not seen

 OGD:

Gastritis, lax esophageal sphincter Biopsies taken from antrum and D2.

 STOOL

D/R: ph= acidic mucus= Nil RBC= Nil WBC= +/HPF Parasite cyst/ ova= None

 SPUTUM

AFBx 3:
Negative

TTG=

IgA: 4.57 (<20 neg) IgG: 0.083 (<1.0 neg)

 CBC

repeated.

Hb: 8.1 MCV: 101 TLC: 18.7 Plts: 71,000

 Report

of blood c/s showed staph aureus (? Contamination). of urine c/s showed no growth.

Report

 COLONOSCOPY:

Normal GI mucosa. Biopsies taken from sigmoid and caecum.

Retic

count: 1.8%

 BIOPSY

FROM ANTRUM AND D2: Moderate chronic non specific duodenitis.

 BIOPSY

REPORT OF SIGMOID AND CAECUM: Mild to moderate non specific colitis.

ESR:

71 mm 1st hr

 HYDROGEN

BREATH TEST: Negative at 120 minutes

NOTE: In malabsorption, breath hydrogen peaks (>20 ppm) at 60-90 min after lactose ingestion.

 BARIUM

STUDIES: Due.

TSH:

Awaited

MALABSORPTION SYNDROME

TYPE???????

Defective absorption of fats, fat-soluble and other vitamins, proteins, carbohydrates, electrolytes, minerals and water. Most common clinical presentation is chronic diarrhea.
Hallmark: Steatorrhea that causes excessive fecal fat excretion and produces nutritional deficiencies and GI symptoms.

1.

INTRALUMINAL DIGESTION
TERMINAL DIGESTION In the brush border of the small intestinal mucosa TRANSEPITHELIAL TRANSPORT Through vessels and lymphatic channels.

2.

3.

Mechanism Maldigestion

Specific Disease Chronic pancreatitis, cystic fibrosis, pancreatic carcinoma

Bile Salt deficiency

Cirrhosis, cholestasis, bacterial overgrowth, impaired ileal reabsorption, bile salt binders
Massive intestinal resection, gastrocolic fistula, jejunoileal bypass Lymphoma, Whipples disease, intestinal lymphangiectasia Constrictive pericarditis, rightsided heart failure, mesenteric arterial or venous insufficiency Infection (esp.Giardia, Whipples disease, tropical sprue), Inflammatory diseases , radiation enteritis.

Inadequate Absorptive surface

Lymphatic obstruction Vascular disease

Mucosal disease

ABDOMINAL TUBERCULOSIS

Tuberculous abdomen is a condition in which there is tuberculous infection of the peritoneum or other organs in the abdomen.

 Abdominal

TB is usually secondary to pulmonary TB.

evaluation often shows no evidence of lung disease. pulmonary disease is present in <50% of the patients.

Radiologic

Active

Nonhealing ulcers of the mouth or anus.

Difficulty swallowing with esophageal disease.

Abdominal pain mimicking peptic ulcer disease with stomach or duodenal infection.
Malabsorption with infection of the small intestine. Abdominal pain, diarrhea, or hematochezia with infection of the colon.

 Is

the most common area of involvement

Basis

of which is the abundance of lymphoid tissue and slower rate of passage of luminal contents.
any area of GIT can be involved.

However

Natural course of gastrointestinal tuberculosis may be:

Ulcerative Hypertrophic Ulcero-hypertrophic

1. Small intestines: Ulcerative form

2. Ileocaecal Region: Hypertrophic form 3. Tuberculous Mesenteric Adenitis

4. Tuberculous Peritonitis

 The

cecum becomes conical, shrunken, and retracted out of the iliac fossa due to fibrosis within the mesocolon.

Ileocecal

valve becomes fixed, irregular, gaping, and incompetent.

 Acute

tuberculous peritonitis
tuberculous peritonitis

Chronic

Tuberculous

stricture of the small intestine causing subacute intestinal obstruction caecal tuberculosis presenting with a mass in the right iliac fossa

Ileo

1.

Ascitic Form
Encysted Form Purulent Form

2.

3.

4.

Dry Plastic Adhesive Form

Abdominal Pain Fever Loss of Weight Ascites Night Sweats Abdominal Mass

90% 60% 60% 60% 37% 26%

 Abdominal

TB mimics any abdominal pathology, including cancers. tests are suggestive, but PPD testing can be negative especially in patients with weight loss or AIDS.
stain and culture yield is very low.

Skin

AFB

 ULTRASONOGRAPHY
CT

Scan

ENDOSCOPY,

COLONOSCOPY: May demonstrate mucosal hyperemia, an ulcerated mass, multiple ulcers with steep edges and small sessile polyps, small ulcers or erosions or divertivcula most commonly in the ileocecal region.

Gastrointest Endosc 2004;59:362-8.

Can show mucosal ulceration, thickening or stricture formation.

In the early stages, spasm and hypermotility with edema of the ileocecal valve.
Later thickening of the ileocecal valve. A widely gaping ileocecal valve with narrowing of the terminal ileum (Fleischner sign) A narrowed terminal ileum with rapid emptying of the diseased segment through a gaping ileocecal valve into a shortened, rigid, obliterated cecum (Stierlin sign)

 LAPAROSCOPY:

Fluid for staining and culture and tissue for biopsy can be obtained.
diagnosis by either endoscopic or surgical biopsy. reveals acid fast bacilli, caseating granuloma or positive cultures. of tubercle bacilli in biopsy specimen by PCR is the most sensitive means of diagnosis.

Final

Biopsy

Detection

 Intestinal Fistula

obstruction

formation

Hemorrhage

Once diagnosed, ATT is started.

1.

Isoniazid

2. 3. 4.

Rifampicin
Pyrazinamide Ethambutol

 Diagnostic

Laparoscopy or Laparotomy
for:

Therapeutic

Relieving obstructions Removing Masses Draining Abscesses

 Very

good, if diagnosed before complications. increase morbidity and mortality.

Complications Disseminated

miliary TB has worse prognosis

 The

definitive diagnosis of intestinal tuberculosis is made by:

Identification of the organism in tissue, either by direct visualization with an acid-fast stain. By culture of the excised tissue.

By a PCR assay.

 Can

be established in:

A patient with active pulmonary TB and radiologic and clinical findings that suggest intestinal involvement. Response to anti-TB therapy.

CELIAC DISEASE

Autoimmune disorder, prevalence of 0.5 to 1 percent in the US. HLA-DQ2 or HLA-DQ8. Inappropriate immune response to the dietary protein gluten, which is found in rye, wheat, and barley. Manifestations from no symptoms to overt malabsorption with involvement of multiple organ systems. Increased risk of some malignancies.

RISK FACTOR

PREVALENCE AMONG THOSE WITH RISK FACTOR 100% 5 to 22% 1.5 to 14% 5 to 12% 2 to 10% 3 to 8% 2 to 5%

Dermatitis herpetiformis 1st degree relative with celiac disease Autoimmune thyroid disease Down syndrome Turner's syndrome Type 1 diabetic: Children Adults

Common
Diarrhea Fatigue Borborygmi Abdominal pain Weight loss Abdominal distention Flatulence

Uncommon
Osteopenia/ osteoporosis Abnormal LFTs Vomiting Iron-deficiency anemia Neurologic dysfunction Constipation Nausea

Up to 38 % Asymptomatic

 Serum

IgA endomysial Ab and IgA tissue transglutaminase Ab ( Sensitivity and specificity > 95%) for gliadin antibodies is no longer recommended because of the low sensitivity and specificity. tTG antibody is the recommended single serologic test for celiac disease screening in the primary care setting.

Testing

The

 Required

disease.

to confirm the diagnosis of celiac

Should

also be considered in patients with negative serologic test results who are at high risk. to total villous atrophy, or subtle crypt lengthening or increased epithelial lymphocytes. avoid false-negative results, obtaining at least four tissue samples is recommended.

Partial

To

Normal small intestine

Normal villi

Celiac Disease

Villous atrophy

 Gluten

free diet.

Eliminate

all wheat, rye, barley and their derivatives. take 6-12 months for intestines to heal.

May

 Flour/meal Barley Phosphated Flour Barley malt/extract Bran Rye Couscous Semolina Bromated or durum flour Triticale (cross between Enriched or Self Rising wheat/rye) Flour Wheat Gram Flour Wheat Bran Wheat germ Wheat starch

 Osteoporosis Thyroid

dysfunction

Deficiencies Increased

in folic acid, vitamin B12, fatsoluble vitamins, and iron risk of malignancy:

Non-Hodgkin's lymphoma (3-6x more likely)

Oropharyngeal, esophageal, and small intestinal adenocarcinoma.

Protozoal infection of upper small intestine.

Caused by flagellate Giardia lamblia.

Most abundant in areas with poor sanitation.

Only the cyst form is infectious, trophozoites are destroyed by gastric acidity. Hypo-gammaglobulinemia, low IgA levels in gut, achlorydria, malnutrition are the favouring factors.

50% , no discernable infection.

10% , asymptomatic cyst passers.

25-50% , acute diarrheal illness------ followed by chronic diarrhea.

Abdominal cramps, bloating, flatulence, nausea, malaise & anorexia. Stools greasy & frothy with no pus, blood or mucus.

Weight loss is common.

 Identification Antigen

of cyst or trophozoites in stool.

assays.

 Metronidazole
Tinidazole Nitazoxanide

Furazolidine
Albendazole