What is Geographic Tongue !!

This 61-year-old man was referred for treatment of painless white lesions on his tongue that had appeared 1 month earlier. He had been treated with topical and systemic antifungal drugs for presumed oral candidiasis, but the lesions remained unchanged. The patient reported that a similar episode 1 year earlier had resolved spontaneously.
Lingual examination revealed multiple erythematous patches with an annular, well-demarcated white border. A diagnosis of geographic tongue was made.

Geographic tongue (benign migratory glossitis) is a benign inflammatory condition that affects approximately 2% of the world's population. The classic manifestation is a maplike distribution of erythema caused by atrophy of the filiform papillae of the tongue, surrounded by a white hyperkeratotic rim. The lesions typically resolve spontaneously without sequelae but can develop quickly in other areas of the tongue.

Nonalcoholic Fatty Liver Disease NAFLD

Endoscopic Management of Acute Bleeding from a Peptic Ulcer

Acute upper gastrointestinal hemorrhage, which is defined as bleeding proximal to the ligament of Treitz, is a prevalent and clinically significant condition with important implications for health care costs worldwide. Negative outcomes include rebleeding and death, and many of the deaths are associated with decompensation of coexisting medical conditions precipitated by the acute bleeding event. This video focuses specifically on endoscopic management of acute bleeding from a peptic ulcer.

Extra GI causes of Voiting

VOMITING :

• Vestibular disturbance/ Vagal (reflex pain)
• Opiates
• Migrane/ Metabolic (DKA, gastroparesis, hypercalcemia)
• Infections
• Toxicity (cytotoxic, digitalis toxicity)
• Increased ICP, Ingested alcohol
• Neurogenic, psychogenic
• Gestation

Excellent videos explain Crohn's Disease

ART 1



PART 2

Rectal bezoars in children

A bezoar is a solid mass formed in the gastrointestinal tract as a result of the consumption of indigestible or poorly digestible substances. Bezoars most commonly form in the stomach, but can occur in the small intestine and, rarely, in the colon or rectum. They are usually classified according to the material of which they are derived, for example, trichobezoars (hair), lactobezoars (milk curd), phytobezoars (plant fibre) and medication bezoars. The term originates from the Arabic term badzehar, meaning "antidote," a reference to historical medicinal use of these concretions found in animal gastrointestinal tracts in the treatment of human poisonings.

See this case of a previously well 8 year-old boy was brought to the emergency department with a three-day history of constipation. He had consumed three handfuls of flavoured unshelled sunflower seeds four days previously. His mother had unsuccessfully tried several sodium biphosphate and sodium phosphate enemas at home, as well as the use of bran to aid defecation. On examination, the patient’s abdomen was soft and nontender with normal bowel sounds. A bolus of stool mixed with unshelled sunflower seeds was visible at the anus.

A radiograph of the abdomen showed stool extending from the descending colon down to the rectum, which contained a large mass . Oral phosphate soda and a mineral oil enema were ineffective. The patient was taken to the operating room for digital and instrumental extraction under general anesthesia. He was monitored in hospital for 24 hours and discharged when he was taking liquids and passing soft stool.

Although small rectal bezoars may pass spontaneously, options for the care of patients presenting to clincians with symptomatic rectal bezoars include the use of enemas and extractions with conscious sedation or general anesthesia. Formation of bezoars from sunflower seeds may be more likely in children or preteens who are unable or unwilling to spit out the shells, particularly with flavoured shells.

Radiation Proctitis

A 70-year-old man presented with a 2-month history of intermittent hematochezia. Ten years earlier, he had undergone 6 months of radiation therapy for the treatment of prostate cancer. The total dose of radiation was 64 Gy, and the prostate cancer was cured.

On physical examination, the temperature was 36.5°C, the blood pressure was 150/90 mm Hg, the pulse was 90 beats per minute, and the respiration was 14 breaths per minute. The abdomen was soft, with normal bowel sounds and without tenderness.
On rectal examination, there were blood clots and friable mucosa that bled easily but no hemorrhoids or palpable masses. The results of analyses of blood and urine were normal.

Colonoscopy revealed fine, tortuous blood vessels and telangiectasias in the rectum (figure). Histopathological evaluation revealed telangiectatic blood vessels with adjacent hyalinization of the lamina propria. Radiation proctitis was diagnosed, and the patient was given argon plasma coagulation therapy.
During 15 months of follow-up, he had mild tenesmus and infrequent, small amounts of hematochezia that did not require further intervention.

What`s Caroli Disease and Caroli syndrome??

Caroli disease is one of non-obstructive biliary diseases that cause biliary dilatation,Once you have excluded obstruction, you have to think about nonobstructive biliary diseases as:

1- Caroli disease
2- Choledochal cyst
3- Recurrent pyogenic cholangitis
4- Primary sclerosing cholangitis

Caroli disease is an autosomal recessive disease secondary to malformation of the ductal plate .
It is associated with polycystic kidney disease, medullary sponge kidney and medullary cystic disease.
So looking at the kidneys can sometimes help you make this diagnosis.

In images below Notice the intrahepatic duct dilatation and the normal caliber of the choledochal duct (extrahepatic bile duct).

Saccular intrahepatic duct dilatation with normal sized choledochal duct in Caroli disease

Saccular bile duct dilatation in Caroli disease

**The hallmark of Caroli disease is intrahepatic duct dilatation.
The dilatation can be very large and saccular as seen in the image or it can be very linear.

The duct dilatation in Caroli disease is due to a congenital malformation of the ductal plate, which is the precursor of the intrahepatic bile ducts.we can see in this diagram the normal development of the ductal plate .
Embryologically each bile duct starts as a single layer of cells that surrounds a portal vein.after that this layer duplicates.
Portions of this double layer fuse and resorb leaving unfused portions that become the bile ducts.

So in the normal condition each portal vein is surrounded by interconnecting bile ducts .However if the patient has ductal plate malformation, the bile ducts are too numerous and they are ectatic (as seen below).
Whether or not we see this on imaging depends on which portion of the bile ducts is affected.
If the large ducts are involved, we see this as Caroli disease.
However if only the very small ducts are involved, the result is congenital hepatic fibrosis.
If all ducts are involved, then there is a combination of fibrosis and Caroli disease, which is also known as the Caroli syndrome.

Crohn's disease PIC and x-ray

Synonyms: regional ileitis, terminal ileitis, regional enteritis or granulomatous enteritis.

Crohn's disease causes inflammation in the small intestine. Crohn's disease usually occurs in the lower part of the small intestine, called the ileum, but it can affect any part of the digestive tract, from the mouth to the anus. The inflammation extends deep into the lining of the affected organ. The inflammation can cause pain and can make the intestines empty frequently, resulting in diarrhea.

Crohn's Disease, X-Ray
This lower abdominal X-ray shows narrowing (stenosis) of the end of the small intestine (ileum)with loss of mucosal pattern and bowel wall thickening. Crohn's disease typically affects the small intestine. A solution containing a dye (barium), was swallowed by the patient. When it passed into the small intestines, this X-ray was taken (lower GI series).

For more information: WATCH THE VIDEO

Appearance of Cricopharyngeal achalasia in X-ray

It appeares as :Hemispherical or horizontal, shelflike protrusion on the posterior aspect of the esophagus at approximately the C5-C6 level.

Short Comment.......It is Failure of the upper esophageal sphincter to relax. Can result in dysphagia by obstructing the passage of a swallowed bolus. In severe disease, can cause aspiration and pneumonia.

Epidemiology & Natural History of Hepatitis C Virus

Dr. Miriam Alter, Director of Infectious Disease Epidemiology at the University of Texas Medical Branch in Galveston TX, discusses the appearance and spread of Hepatitis C.

Schatzki Ring by Endoscopy

It appears in endoscopy as smooth, concentric narrowing of the lumen at the esophagogastric junction.
...... 82 year-old woman with nausea refractory to therapy; endoscopy also demonstrated gastritis and duodenitis.






In this 53 year-old man with pyrosis (heartburn) and dyspepsia (indigestion),Schatzki ring is often seen in the setting of reflux esophagitis, as seen here with linear, longitudinal esophageal ulcers.

All about COLONOSCOPY PROCEDURE

It is the endoscopic examination of the colon and the distal part of the small bowel with a CCD camera or a fiber optic camera on a flexible tube passed through the anus. It may provide a visual diagnosis and grants the opportunity for biopsy or removal of suspected lesions.IT differs from sigmoidoscopy in allowing an examination of the entire colon while sigmoidoscopy allows to vizualize only the final two feet of the colon.

INDICATION:
1. Gastrointestinal hemorrhage
2. Suspicion of malignancy
3. Inflammatory bowel disease (chron's disease & ulcerative colitis)
4. Unexplained drop in hematocrit (In anemia)
5. Positive feacal occult blood test
6. Unexplained changes in bowel habit
7. If any abnormality found on colon x- ray or a CT scan



PROCEDURE:
Bowel preparation

* The colon must be free of solid matter for the test to be performed properly
* For one to three days, the patient is required to follow a low fiber or clear-liquid only diet
* Patient should be well hydrated
* The patient should be given appropriate Colonic Cleansing
* Most medications should be continued as usual, but some may interfere with the examination.
* If the patient is on Aspirin products, blood thinners (Coumadin, etc.), arthritis medications, insulin, and iron preparations that may require special instructions
## Regimens For Colonic Cleansing Before Colonoscopy:-
a.Diet - Dietary modifications alone, such as a clear liquid diet, are inadequate for colonoscopy

b.Enemas - Used in patients who present to endoscopy with a poor distal colon preparation and in patients with a defunctionalized distal colon

c.High-Volume - Gut Lavage such as mannitol

d.Rectal Pulsed Irrigation - Rectal pulsed irrigation administered immediately before the procedure combined with magnesium citrate given the evening before the procedure is a reasonable alternative to full-volume (4-liters) polyethylene glycol (PEG) in those individuals who cannot tolerate per oral administration of PEG

e.PEG (Electrolyte Lavage Solution) -
faster, more effective, and better-tolerated method
PEG is safer than osmotic laxatives/sodium phosphate (NaP) for patients with electrolyte or fluid imbalances, such as renal or liver insufficiency, congestive heart failure, or liver failure
PEG regimens (2–3 liters given the night before the colonoscopy and 1–2 liters on the morning of procedure)

f.Aqueous Sodium Phosphate - An equal alternative to PEG solutions except for pediatric and elderly patients, patients with bowel obstruction, and other structural intestinal disorders, gut dysmotility, renal failure, congestive heart failure, or liver failure

-Contraindications of NaP

* In patients younger than five years of age
* Those with serum electrolyte imbalances
* Advanced hepatic dysfunction
* Acute and chronic renal failure
* Recent myocardial infarction, unstable angina, congestive heart failure
* Ileus, malabsorption, and ascites

IN THE PROCEDURE:

* It usually takes 15 to 60 minutes
* The patient is often given sedation intravenously such as fentanyl or
midazolam
* Monitoring the Vital parameters
* Patients will be lying on their left side or back
* First step is usually a digital rectal examination, to examine the tone of the
sphincter and to determine if preparation has been adequate
* Then endoscope is passed to visualize the entire colon
* Suspicious lesions may be cauterized, treated with laser light or cut with an
electric wire for purposes of biopsy or complete removal polypectomy
* Medication can be injected, e.g. to control bleeding lesions

COMPLICATIONS:
1. Gastrointestinal perforation, which is life-threatening
2. Bleeding
3. Splenic rupture
4. On very rare occasions, intracolonic explosion

Causes of Calcified Liver Masses on CT

1- Inflammatory hepatic lesions
oMost common cause of calcified hepatic lesions
. Inflammatory conditions

• For example, granulomatous diseases (tuberculosis).
• Calcification involves entire lesion
• Appears as a dense mass

. May produce artifacts on CT scans
o Echinococcus cysts have curvilinear or ring calcification
. Central water density in cyst



2- Benign neoplasms
o Hemangiomas, especially large ones, may contain large, coarse calcifications; may be seen at CT in 20% of cases or radiography in 10%



3- Malignant liver neoplasms
o Hepatocellular adenoma
. Calcifications may be solitary or multiple
. Usually located eccentrically within complex heterogeneous mass.
o Fibrolamellar carcinoma
. Calcifications reported in 15%-25% of cases at CT
. Occurs in many patterns
o Intrahepatic cholangiocarcinoma
. Calcifications are typically accompanied by a desmoplastic reaction
. Visible at CT in about 18% of cases.
o Calcified hepatic metastases
. Most frequently associated with mucin-producing neoplasms such as colon, or less likely ovarian, carcinoma

Calcified liver and peritoneal metastases from ovarian carcinoma

A Case of Constipation as a Chief Complaint

A 61-year-old African American Obese female was admitted to the hospital with a chief complaint of bilateral knee pain for 2 weeks. She was diagnosed with severe osteoarthritis and opioid pain medications were started.

The patient's last bowel movement (BM) was one week prior to admission and she did not have any BM after that despite multiple laxatives. She also admitted to feeling depressed.

With past history of Hypertension (HTN), gout, COPD, hypothyroidism following a radioactive iodine treatment for hyperthyoridism in the remote past.

Medications: Telmisartan/hydrochlorothiazide (Micardis), furosemide (Lasix), levothyroxine (Synthroid) 100 mcg p.o. q.d, indomethacin, lorazepam.

Family history of Gout, stroke.

Physical examination:
VS:Temp.=36.9 R.R.=16 H.R=53 BL.P.=170/95.
Chest: CTA (B).
CVS: Clear S1S2.
Abdomen: Soft, NT , absent BS.
Extremities: the knee examination showed bilateral knee swelling, left greater than right. No joint fluid. Joint tenderness was present. No pitting edema or cyanosis.

Investigation:
The right knee X-rays showed severe degenerative joint disease and several loose bodies in the joint. An orthopedics consultation was called and the patient agreed to a total knee replacement at a later date.

Laboratory results:


TSH and T4 levels.


What happened next?
TSH was 41.40 mU/L, and her Synthroid dose was increased to 150 mcg po qd. A selective serotonin reuptake inhibitor (SSRI) was started for depression.

The patient constipation persisted despite multiple medications prescribed for the problem.

A list of medications given for the constipation without success.

Her constipation gradually resolved with T4 replacement and lactulose. She will need a recheck of her TSH in 6-8 weeks.


Final diagnosis : Hypothyroidism.


What did we learn from this case?

1. Constipation is a classic presenting symptom of uncontrolled hypothyroidism.
2. Uncontrolled HTN and bradycardia are also common presenting symptoms of hypothyroidism.
3. Opiods, prescribed to this patient for knee pain, made the constipation worse. Most inpatients on opioid therapy will require a stimulant laxative such as senna 2 tabs PO QHS for regular BM.

Ranson's criteria and CT scoring system in Pancreatitis

photo of ClarkRansonR

Present on Admission - GA LAW

Blood Glucose greater than 200 mg/dl
Age greater than 55 years
Serum LDH greater than 350 I.U./L
SGOT (AST) greater than 250 I.U./L
WBC greater than 16,000/ul

NB - Amylase is NOT one of Ranson's criteria!
# Serum amylase has low sensitivity and specificity
# 20% cases of pancreatitis have normal serum amylase (particularly alcoholic aetiology)


Developing During the First 48 Hours: - C HOBBS

Serum Calcium less than 8 mg/dl
Hematocrit fall greater than 10%
Arterial Oxygen saturation less than 60 mm Hg
BUN increase greater than 8 mg/dl
Base deficit greater than 4 meq/L
Estimated fluid Sequestration greater than 600 ml

*Ranson score of 0-2, minimal mortality
*Ranson score of 3-5, 10%-20% mortality
*Ranson score of >5 has more than 50% mortality and is associated with more systemic complications.

Contrast-enhanced CT scoring system
Grade........................................... Criteria
A ................................ .......... ............. Normal
B ................................. Focal or diffuse glandular enlargement

Small intra-pancreatic fluid collection

C ....................................................... Any of the above

Peripancreatic inflammatory changes

Less than 25% gland necrosis

D ............................ .................................Any of the above

Single extrapancreatic fluid collection

25-50% gland necrosis

E ....................... .......................................... Any of the above

Extensive extrapancreatic fluid collection
Pancreatic abscess
More than 50% gland necrosis

The Digestive System animation