Final From Material Flashcards
Difficulty in the digestion or absorption of nutrients from food in teh small intestine
Malabsorption syndrome
Etiology malabsorption syndrome
Infections Structural defects Postsurgery Mucosal abnormalities Systemic diseases Enzyme deficiencies
Malabsorption syndrome
Infectious
Bacteria (E. Coli, whipple disease, TB)
Virus (HIV)
Parasites (Giardia lamblia)
Malabsorption syndrome
Etiology
Structural defects
IBD (crohn’s disease) Autoimmune diseases (SLE)
Malabsorption syndrome
Etiology
Postsurgery
Gastroectomy
Weight loss surgery
Short bowel syndrome (resection of small intestine)
Malabsorption syndrome
Etiology
Mucosal abnormalities
Celiac disease
Malabsorption syndrome
Etiology
Systemic diseases
Diabetes mellitus
Addison’s disease
Malabsorption syndrome
Etiology
Enzyme deficiencies
Lactose intolerance
Pancreatic insufficiency
Signs and symptoms malabsorption syndrome
Chronic diarrhea with steatorrhea
Abdominal bloating
Signs of malnutrition
Signs of malnutrition
Edema anywhere in the body (protein deficiency)
Muscle cramping
Osteomalacia, osteoporosis (vit D and calcium deficiency)
Anemia (vit B12, folic acid, iron deficiencies) - megaloblastic
Bleeding tendencies
Weight loss (deficiency of all nutrients)
Diagnosis malabsorption syndrome
Blood tests
Signs of anemia
Hypoalbuminemia
Decreased amount of pancreatic enzymes
Malabsorption syndrome
Diagnosis
Stool tests
Identification of bacteria
Identification of protozoa
Presence and concentration of fat
Malabsorption syndrome
Diagnosis
Blood tests Stool tests Schilling test Lactose intolerance test CT or MRI
Malabsorption syndrome
Diagnosis
Schilling test
To establish vit B12 deficiency
Urine test - distal portion ilium absorption test
Diagnosis malabsorption syndrome CT or MRI
Only for ruling out structural abnormalities
Malabsorption syndrome treatment
Depends on etiological factors
Restoration of nutrients, vitamins, minerals, enzymes
Gluten and lactose free diet
Bromamine - decrease inflammation
Celiac disease aka
Celiac sprue
Non-tropcial sprue
Gluten enthesopathy
Gluten intolerance
Autoimmune disorder that occurs in all age people with genetically predisposed damage of the small intestine villi
Celiac disease
The problem associated with presence of unexpected antigen on chromosome 6
Celiac disease
AMHC type 1 and 2 human leukocyte antigen
Celiac disease is often associated with
Diabetes mellitus type 1
Autoimmune thyroiditis (aka hasimoto’s disease)
SLE
Rheumatoid arthritis
Abnormal chormosome 6 MHC type 2
Celiac disease etiology
Gluten which is found in
Wheat Rye Barley Oat Triticale
Risk factors celiac disease
Severe emotional stress
Pregnancy
After surgery
Pathophysiology celiac disease
Zonulin works like the traffic conductor
Celiac disease signs and symptoms
Abdominal pain and cramping Bloating Chronic diarrhea and steatorrhea Lactose intolerance Weight loss Fat-soluble vitamin deficiencies Osteomalacia, osteoporosis Recurrent painful mouth ulceration (aphthous stomatitis) Dermatitis herpetiformis Unexplained anemia (iron-deficiient or megaloblastic) Joint pain Numbness and tingling in feet and hands
Dermatitis herpetiformis
Itchy rash on the elbows
Knees
Buttocks
Scalp
Diagnosis celiac disease
TTGA-test - Ig
A anti-tissue transglutaminase antibodies - 90% specificity for celiac disease
Endoscopy of small intestine, especially with biopsy of descneidng duodenum
Hypoalbuminemia
Low levels of iron, vitamins (B12, 9,6), calcium, fat soluble vitamins
Gold standard for diagnosis of celiac disease
Endoscopy of small intestine, especially with biopsy of descneidng duodenum
Treatment celiac disease
No contraindication for adjustments
Lactose-free diet
Gluten free diet life-time requirement
Absolute avoidance of products with
Wheat, barley, rye, oat, triticale
Strong diet could result in healing of small intestine in celiac disease
3-6 months in children
Several years in adults
Whipple disease aka
Intestinal lipodystrophy
Infectious systemic disease, most likely caused by gram-positive bacterium tropheryma whipplei
Whipple disease
This disease affects small intestine, joints, CNS, cardiovascular ssytem
Whipple disease
The characteristic pathomorphological sign of whipple disease is
Thickening of intestinal wall
Whipple disease etiology
Gram-positive bacillus tropheryma whipplei
Whipple is most common in
Male 30-40 years old
Source of tropheryma whipplei
Soil
Animals
Whipple disease ____ transmitted from person to person
Is not
Signs and symptoms of whipple disease
Joint pain - usually initial symptom
Joints - knee elbow fingers
Joint involvement without joint deformity
GI tract manifestations several years after joint involvement - malabsorption - diarrhea/steatorrhea, weight loss, abdominal pain, peripheral edema due to hypoalbuminemia
Systemic manifestations of whipple disease
Fever, chills Uveitis Bacterial endocarditis Lymphadenopathy Darkness or grey color of the skin
More advanced stage of whipple disease
CNS involvement
Oculomasticatory myorythmia - highly characteristic of whipple disease
Eye movmenet disturbances and rapidly repetitive movements of the facial muscles
Oculomasticatory myorythmia
CNS involvement whipple disease
Vision problems Memory problems or personality changes Dementia Facial numbness Headaches Msucle weakness or twitching Difficulty walking Hearing loss or ringing in the ears
Whipple disease diagnosis
Duodenal endoscopy with biopsy, which reveals presence of bacteria
PCR
Highly sensitive test that amplifies the DNA of the tropheryma whipplei from tissue samples
PCR - polymerase chain reaction
Treatment whipple disease
Long-term antibioticotherapty (1-2 years)
If the disease is untreated, mortality is 100%
A true congenital diverticulum, is a slight bulge in the small intestine present at birth, and represents a remnant of incompletely obliterating omphalomesenteric duct (also called the viteline duct)
Meckel’s diverticulum
The omphalomesenteric duct normally undergoes obliteration at
7-8 week of gestation
The most common congenital abnormality of the small intestine
Meckel’s diverticulm
Meckel diverticulum is characterized by
Blind end
True diverticulum that contains all layers of the wall
Usually found in the ileum (distal 3rd)
Tip of the diverticulum is free in 75% of cases or is attacehd to the anterior abdominal wall
In the case of diverticulum’s attachment to the anterior abdominal wall the following anomalies could be found in meckel’s diverticulum
Fibrous cord
Umbilicoileal fistula
Umbilical sinus
Fluid-filled cysts located either intra-abdominally or just below the umbilical skin
Characteristics of meckel’s diverticulum (rule of 2’s)
Occurs in 2% of the population
Male-to-female ratio is 2:1
Peak age of presentation is 2 years old
Locates 2 feet from ileocecal junction (distal portion of ileum)
2cm in diameter
2in in length
2 types of common ectopic tissue (gastric and pancreatic)
The majority of people with a meckel’s diverticulum are
Asymptomatic (silent meckel’s diverticulum
Symptoms often occur during the first few years of life
Clinical manifestations of meckel’s diverticulum come to the clinical attention in teh form of complications
Bleeding
Obstruction
Diverticulitis
Tumors
Meckel’s diverticulum
Bleeding is more common among ___ occurs when acid secreted from ____ in the diverticulum ulcerates the adjacent ileum
Young children less than 5
Ectopic gastric mucosa
Repeated episodes of painless rectal bleeding which is usually not severe enough to cause shock
Stools are birght red like currany jelly or black and tarry
Adults may also bleed in form of melena
Meckel’s diverticulum
Meckel’s diverticulum
Intestinal obstruction can occur at ____ but is more common in ___
Any age
Older children and adults
Intestinal obstruction is manifested by
Cramping abdominal pain
Abdominal tenderness
Nausea, comiting
Severe or complete constipation
Later intestinal obstruction is manifested by
Acute peritoneal signs due to intestinal ischemia or infarction
Acute meckel’s diverticulum can occur at ___ but is more common in ____
Any age
Older children
Acute meckel’s diverticulum is characterized by
Either focal or diffuse abdominal pain and tenderness
Pain typically localized in epigastric or periumbilical regions
The pain is similar to one typical for appendicitis (but not same location!!!!!_)
Persistence of periumbilical pain or a history of bleeding from rectum may be helpful in distinguishing this entity from appendicitis
Meckel’s diverticulum
Meckel’s diverticulum
Tumors
Rare and occur mainly in adults
Benign = leiomyoma, angioma, neuroma, lipoma
Malignant = carcinoid, sarcoma, adenocarcinoma
Routine laboratory findings are ___ helpful in establishing the diagnosis of meckel diverticulum
Not
tests necessary for meckel’s diverticulum
CBC
Stool
CBC meckel’s
Hemoglobin and hematocrit (low)
Signs of iron def anemia and signs of megaloblastic anemia can be seen
Stool test meckls
For occult blood
Technetium-99m (99mTc) scan
Aka meckel scan
Investigation of choice to diagnose meckel’s diverticulum
99mTc can detect ____ since approx 50% of symptomatic meckel’s diverticula have ectopic gastric or pancreatic cells locating within them, they are displayed as a spot on the scan distant from the stomach itself
Gastric mucosa
In children, the meckel scan is
Highly accurate
Noninvasive
95% specificity and 85% sensitivity
In adults meckel sca is
9% specific and 62% sensitive
Diagnosis GI bleeding meckel’s diverticulum
Screening colonoscopy
Angiography
Diagnosis intestinal obstruction meckel’s diverticulum
Plain -xray of abdomen may reveal evidence of signs of air or air-fluid levels or perforation
US could demonstrate the omphaloenteric duct remnants or cyst
Diagnosis nonbleeding or bleeding or inflammatory complications meckel’s
CT scan - blind ended and inflamed structure in the mid-abdominal cavity which is not an appendix
Treatment meckel’s diverticulum
No symptoms = no treatment required
Symptoms = surgery to remove diverticulum
Blood loss = iron therapy or blood transfusion to replace lost blood
Group of idiopathic autoimmune inflammatory conditions of the small intestine and colon with genetic predisposition
Inflammatory bowel diseases
Two major types of IBD
Crohn’s disease
Ulcerative colitis
Crohn’s disease aka
Regional enteritis
An idioptahic chronic systemic autoimmune inflammatory disease which can involve any segment of GI tract from teh mouth to the anus, as well as other systems
Crohn’s disease
Typical age of onset for crohn’s
13-30 yo
Crohn’s disease is characterized by
Inflammation and ulceration of all layers of involved GI tract wall
A classic feature of crohn’s disease is
The sharp demarcation of diseased segments fro adjacent uninvolved part
Abrupt transition between unaffected tissue and the ulcer - characteristic sign of crohn’s known as
Skip lesions
When multiple segments are involved the intervening part is essentially
Normal
Risk factors for crohn’s disease
Smoking (high risk factor)
Increased intake of animal proteins, milk proteins
Emotional stress or surgery
Crohn’s etiology
Unknown but these could contribute:
Genetic predisposition
Abnormal host immunoreactivitiy
Infection (mycobacterium paratuberculosum
Signs and symptoms crohn’s disease
Chronic recurring periods of flare-ups and remissions
Abdominal pain due to inflammation and ulcerations, predominately in lower right side of abdomen
Diarrhea from mild to severe bowel movements (5-20 a day)
Sometiems stool contains mucus, blood, pus
Weight loss and fatigue due to malabsorption diarrhea
Fever
Dysphagia or upper abdominal pain due to ulceration of esophagus or stomach
Aphthous ulcers
Aphthous ulcers
Non-helaing sores if the mouth is involved
Crohn’s disease has an increased risk for formation of
Gallstones
Gallstone risk is due to
Decrease in bile acid reabsorption in the ileum and the bile gest excreted in the stool which causes the cholesterol/bile ratio to increase in the gallbladder an dinc risk for gallstones
Systemic manifestations crohn’s
Seronegative spondyloarthritis Eye involvement Skin involvement Thrombosis Anemias Nervous system involvment
Seronegative spondyloarthris crohn’s disease
Infalmmation of one or more joints and/or AS
Chromosome 1
HLA-B27
Eye involvment crohn’s
Uveitis (iridocyclitis)
Uveitis characterized by
Inflammation of iris, acocmpanying by eye pain, photofobia
Skin involvment crohn’s
Erythema nodosum - due to inflammation of subcutaneous tissue
Pyoderma gangrenosum - painful ulcerating nodules
Thrombosis crohn’s
Of lower extremity veins which could result in pulmonary embolism and lung infarction
Anemias crohn’s
B12-def anemia due to involvement of ileum
B9 def anemia due to involvment of jejunum
Iron def anemia due to blood loss or dec iron absoprtion in duodenum
Autoimmune immunohemolytic anemia
Nervous system involvement crohn’s
Peripheral neuropathy due to malabsorption of group B vitamins
Depression and headache
Diagnosis crohn’s
Endoscopy and colonoscopy with biopsy (in 50% of cases the granulomas of GI wall are found)
Aggregations of macrophages most specific for crohn’s disease
Granulomas
Granulomas in crohn’s do not show a ___ appearance on microscopic examination
Cheese-liek
Other diagnosis for crohn’s
Capsule endoscopy because small intestine difficult to access
CT or MRI for complicated areas
CBC for diagnostics of anemia, leukocytosis
Stool test for presence of blood or bacteria
Complications crohn’s
Bowel obstruction due to development of bowel stricture
Fistula to adjacent organs or perforation
Colorectal cancer
Malnutrition disorders - osteoporosis, osteomalacia, gallstones
Internal bleeding
Management crhon’s
Quit smoking
Avoid: alcohol, high fiber food, nuts and seeds, raw fruits and vegetables, soft drinks, coffee, chocolate, butter and mayo
High calorie liquid diet
Probiotics
Treatment crohn’s
Medical treatment is mandatory
Corticosteroids
Aminosalicylates (sulfasalazine)
Immunomodulators
Antibiotics
Surgery could be necessary
Chronic idiopathic autoimmune inflammatory ulcerative disease affecting superficial inner lining of teh colon and rectum
Ulcerative colitis
This disease always starts in the rectum and then moves up, diffusely involving all other parts of the colon
No skip lesions
Ulcerative colitis
Etiology ulcerative colitis
Unkown
Risk factors ulcerative colitis
Northern european white people
Genetic predisposition
Viral or bacterial infection of the colon
Physical and/or emotional stress
Unlike crohns disease ____do not predispose to ulcerative colitis
Smoking and food
Peaks of age ulcerative colitis
15-30 and between 50-70
Signs and sypmtoms of ulcerative coitis depend on whether the disease
Is restricted by rectum or involves other parts of the colon
The farther from the rectum ulcerative colitis
The more severe the clinical manifestations are
Signs and symptoms ulcerative colitis
Bloody diarrhea Tenesmus Left abdominal pain Fever Weight loss Fatigue, loss of energy
Ineffective painful urge to defecation altough bowels are empty
Tenesmus
In a case of the entire colon involvement ulcerative colitis (pancolitis aka fulminant colitis) the clinical manifestations develop in the following order
Severe diarrhea with blood and pus
Severe abdominal pain due to severe inflammation and pus formation
High fever with night sweat
Dehydration due to fever, diarrhea, lack of water absorption
Shock could develop
Systemic manifestations ulcerative colitis
Oligoarthritis
AS
Mouth ulceration due to depletion of B vitamins
Skin ulceration, predominately of low extremities
Iron def anemia
Sclerosing cholangitis
Disease of the bile ducts that causes inflamamtion and subsequent obstruction of bile ducts both at a intrahepatic and extrahepatic levels
Sclerosing cholangitis
Diagnosis ulcerative colits
Colonoscopy with bopsy presence of continuous ulceration
Anti-neutrophil anti-cytoplasmic autoantiboidies - p-ANCA ONLY in UC
CBC - anemia neutrophilia
Stool specimens - to exclude infection and parasites
Blood in stool
CT, MRI, x-ray with liquid barium
Inflammation may devlep anywhere in GI tract
Crohn’s (CD)
Patholgoical process may extend thorugh entire thickenss of wall of GI tract organ
CD
Characterized by patchy areas of inflammation - skip lesions
CD
Inflammation limited to large intestine
UC
Pathological process occurs in teh superficial lingin gof large intestine wall
UC
Always starts in rectum and characterized by continuous area of inflammation
UC
Diarrhea may or may not be bloody
CD
Smoking is always a high risk of the disease development
CD
Pain is commonly presented in the right side of abdomen RLQ
CD
Diarrhea Is always bloody
UC
Smoking is risky just in 30%
UC
Pain is common in left part of abdomen LLQ
UC
Fistulas and stenosis are common
CD
Tenesmus may present
CD
Colon wall may be thickend and may have granulomas
CD
Fistulas and stneosis are rare
UC
Tenesmus are more common
UC
Colon wall is thinner and shows continuous inflammation
UC
Complications of ulcerative colitis
Colon rupture
Osteoporosis
Hypovolemic shock
Colon cancer
Treatment ulcerative colitis
Diet - high calorie diet but eliminate raw fruits, vegetables, nuts and seeds, sugar, high fiber food
Hydration - drink small portions frequently
Probiotics
Pig whipwomr therapy duration 12 weeks
Corticosteroids
Antibiotics if needed
Aminosalicylates
In cases of serious complications ulcerative colitis
Surgery is necessary
Any mass of tissue that arises from the bowel wall and protrudes into the lumen
Colon/rectal polyps
Etiology colon/rectal polyps
Unkown
Risk factors colorectal polyps
Stronly associated with increasing age
Age over 50
African-americans
Strong family history
Lifestyle (smoking, low fiber meal and fatty meal)
Morphologically the colorectal polyps are divided into 2 groups
Pedunculated
Sessile
Attached to intestinal wall by a stalk
Pedunculated
Grow directly from intestinal wall broad based
Sessile
Histologically the colorectal polyps are divided into 3 groups
Benign (hyperplastic polyps)
Premalignant (tubular adenoma)
Malignant (colorectal adenocarcinoma)
Colorectal polyps divided into 4 groups
Hyperplastic polys
Serrated polyps
Adenomatous (neoplastic) polyps
Inflammatory (pseudoinflammatory) polyps
Usually do not develop into colon cancer
Hyperplastic polyps
Having a notched edge or saw-like teeth - lesss common but may develop into colon cancer over time
Serrated polyps
May devleop into colon cancer over time
Adenomatous polyps
Usually small and on the left side of hte colon
Polyps that do not carry a risk of developing into cancer
Large ones on the right are ofconcern and should be removed
Hyperplastic polyps
Rarely malignant
Usually less than .5cm in diameter
Occurs in recto sigmoid region
Small serrated polyps
Precancerous
Typically flat more tahn .5cm in diameter
Difficult to detect, they locate in the right upper colon
Large serrated polyps
About 2/3 of all polyps
Can be benign premalignant or malignant
Only a small percentage of them actually become cancerous
Nearly all malignant polyps are this
Adenomatous polyps (neoplastic polyps)
These polyps are associated with IBD
Having ulcerative colitis or crohn’s disease increases overall risk of colon cancer
Inflammatory (pseudoinflammatory) polyps
Signs and symtpoms colorectal polyps
Not usually associated with symptoms
First sign could be rectal bleeding or bloody stool
Later the manifestations may include fatigue (due to iron def anemia), diarrhea (large villous adenomas), abodminal pain, bowel obstruction with severe constipation, nausea and vomiting
The larger the poly
The higher probability of its malignancy
Diagnosis colorectal polyps
Fecal occult blood test Stool DNA test Digital rectal exam Flexible sigmoidoscopy Colonoscopy
Treatment colorectal polyps
The polyps can be removed during a colonoscopy or sigmoidoscopy
FAP
Familial adenomatous polyposis
A genetic condition, when a person develops multiple (more than 100) noncancerous (benign) adenomatous colon polyps
FAP
Etiology FAP
Passed from generation to generation in a family
APC gene (tumor supressor gene) is linked to FAP
A mutation in the APC gene gives a person an increased lifetime risk of developing
Colorectal cancer or other cancers of the GI tract
Familial adenomatous polyposis may begin to develop in the colon
As early as teenage years
More than 95% of people with FAP will have multiple colon polyps by age
35
The average age at which an individual develops colon cancer in classic familial adenomatous polyposis is
39-40 yo
Symptoms FAP early stages
None
Symptoms of FAP as condition progresses
Blood in the stool (iron def anemia)
Diarrhea (mucous drainage)
Abdominal pain
Intestinal obstruction
FAP always affects the ____ but the mutation is present in every cell int he body and other organs are affected
Colon
As a reult of other organs being affected, tumors are sometimes found in other places of the body with FAP
Stomach (usually NOT precancerous)
Duodenum (precancerous)
Bones, skin, brain, teeth (may cause jaw pain)
Three subtypes of classic FAP
Attenuated FAP (AFAP)
Gardner syndrome
Turcot syndrome
Multiple adenomatous colon polyps, and polyps and cancer of the stomach and small intestines
Attenuated FAP
Multiple adenomatous colon polyps typical of FAP, along with benign tumors in many different organs (osteomas - most commonly on the skull and mandible, dental problems, soft tissue tumores), and sometimes carcinomas
Gardner syndrome
Multiple adenomatous colon polyps, an increased risk of colorectal cancer, and an increased risk of brain cancer
Turcot syndrome
Diagnosis colorectal polyps
Genetic test to detect an APC mutation gene
Flexible sigmoidoscopy or colonoscopy every 1-2 years
Fecal occult blood tests
US, CT or MRI of abodmen
Tests to diagnose colorectal polyps should be performed starting at age
10-12
Complications of FAP
GI hemorrhage
GI obstruction
Colorectal cancer
If FAP is not recognized and treated, there is almost a 100% cahnce that a person will develop _____ by age 40
Colorectal cancer
Treatment colorectal polyps
Prophylactic surgery may be recommended before the age of 25
NSAIDs have been shown to significantly decrease the number of polyps
Malignant tumor that grows from uncontrolled cells of the large intestine
Colorectal cancer
Etiology colorectal cancer
Unkown
Predisposing factors colorectal cancer
Neoplastic adenomatous polyps
Right side colon hyperplastic polyps
Multiple polyposis (FAP)
IBD
Alcohol abuse
Fatty food
Age after 50
Family hisotry of colorectal cancer
Two types of colorectal cancer depending on its location
Right side cancer in ascending colon
Left side cancer in descending colon
Right side cancer characterized by
Ascending colon
Exophytic shape of the tumor
Development of anemia
Left side cancer characterized by
Descending colon
Tendency to be circumferential
High frequency of the bowel obstruction
Types of colorectal cancer depending on histology
Adenocarcinoma
Lymphoma
Squamous cell carcinoma
Adenocarcinoma colorectal cancer
Originates from goblet or endocrine cells
Lymphoma colorectal cancer originates from
Peyer’s patches
Squamous cell carcinoma originates from
Colorectal cancer
Epithelial cells
Signs and symptoms colorectal cancer early stages
Blood in stool (bright or very dark)
Change in bowel habits (constipation change to diarrhea)
Worsening constipation**
Stool is narrower than usual
Frequent gas or cramps
Worsening constipation is classic sign
Colorectal cancer
In terminal stages of colorectal cancer, patients demonstrate
Fatigue Night perspiration Unexplained weight loss - 10 lb a month Abdominal pain Pelvic pain, back pain Unexplained anemia
More than 80% of colorectal cancer arises from ____ making this cancer amenable to screening
Adenomatous polyps
Diagnosis of colorectal cancer through screening tends to occur
2-3 years before the first manifestations of cancer
Screening tests have the potentials to reduce colorectal cancer death by
60%
Diagnosis colorectal cancer
Fecal occult blood test DNA screening stool test (cologuard) Blood tests (CBC) Tumor markers Flexible sigmoidoscopy with biopsy Colonoscopy Virtual colonoscopy via a CT-scan CT-scan of chest, abdomen and pelvis PET and MRI
For invisible blood in the stool
Should be done every year in the age after 40
Fecal occult blood test - colorectal cancer
could indicate cancer or pre-cancer of a large intestine
Should be done every year starting at age 50
DNA screening stool test (cologuard)
Blood test colorectal cancer
CBC - ESR increased, IDA
Tumor markers colorectal cancer
Carcinoembryonic antigen CEA - colorectal**
CA-19-9 - pancreas**, colorectal, liver
CA 125 - ovarian cancer**, breat, colorectal, liver
CA 27.29 - breast***, colorectal, liver
The most accurate way to detect polyps should be done every 3-5 years in age after 50 with biopsy
Colonoscopy
In teh process of ____ and _____ the polyps can be removed immediately
Sigmoidoscopy
Colonoscopy
Appears as good as standard colonoscopy for detecting cancers and large adenomatous polys
Virtual colonoscopy via CT-scan
Disadvantages to virtual colonoscopy via CT-scan
Expensive
Associated iwth radiation exposure
Cannot remove abnormal growth and polyps like standard colonoscopy can
CT-scan determines ___ for colorectal cancer
Metastases
Colorectal cancer spreads first to ____ of the peritoneum
Lymphatic nodes
Colorectal cancer spread to lymphatic nodes of peritoneum may be manifested by
Bloating
Swollen belly
Feeling of fullness
Loss of appetite
Colorectal cancer also spreads to the
Liver
Liver spread from colorectal cancer can be manifested by
Pain in upper right side of the abdomen
Bloating
Loss of appetite
Feeling of fullness
Colorectal cancer also spreads to the lungs which can be manifested by
Cough
Blood in sputum
Hard time breathing
Colorectal cancer also spreads to bones especially to the spine, hips, and pelvis. Can be manifested by
Constant bone pain which can awaken a patient in the night
Back pain
Colorectal cancer also spreads to the brain. It may cause problems with
Memory
Concentration
Ataxia
Movements
If colorectal cancer is diagnosed early then ____ can be curative
Surgery
In addition to surgery treatment for colorectal cancer may include
Chemotherapy
Radiation therapy
Congenital abnormality of distal part of large intestine characterized by lack of ganglion cells resulting in functional obstruction and dilation of proximal part of affected colon
Hirschprung’s disease
Hirschprung’s disease aka
Congenital aganglionic megacolon
Congenital megacolon
Hirschprung’s disease often coexists with
Down’s syndrome
Hirschprungs boys vs girls
Boys more often affected 5:1
Most common segment in boys hirschprung’s disease
Short aganglionic segment of colon
Most common segemnet girls hirschprung’s disease
Long aganglionic segment
Hirschprung’s disease etiology is unclear. It is not caused by
Nything the mother did while being pregnant
Possible genetic predisposition is found for hirschprung’s disease
Several genes and specific regions of chromosomes have been shown to be associated with hirschprung’s disease
Pathogenesis of hirschprung’s disease
During normal fetal development between 7-12 weeks the cells from the neural crest migrate into the muscular layer of the large intestine to form the networks of nerves called Auerbach’s and Meissner’s plexus
Normally auerbach’s and meissner’s plexus ganglion cells account for _____ which plays a significant role in peristalsis
Relaxation of smooth muscle cells in the GI tract
Pathomorphologically in hirschprung’s disease these ganglion cells in the affected colon
Are absent
Due to absence of ganglion cells the affected segment of the colon
Cannot relax and pass stool through the colon
The absence of ganglion cells without the reciprocal relaxation results in a ___ in the affected regions leading to spasm of affected colon smooth muscles, creating an obstruction
Overstimulation of nerves
Usually hirschprungs diseaase affects the part of the colon ____ but sometimes more regions could be involved
Near the anus
Signs and symptoms hirschprungs in a newborn birth-1month
First manifestation occurs usually in first 24-48 hours after birth because a baby fails to pass meconium and first stool
If stool does not occur baby may develop vomiting with green or brown color vomiting masses within first 24 hours after birth
Swelling of the abdomen which may cause baby to breathe fast
After the stool pass, baby may have watery diarrhea
Constipation - no regular bowel movement
Signs and symptoms hirschprung’s disease 1 motnh -1 year of age
Slow than expected weight gain
Constipation - bowel movement once every 3-5 days
Swollen abdomen
Episodes of vomiting and diarrhea due to intoxication from delayed feces
Signs and symptoms hirschprung’s children 1 year and older
Severe chronic constipation (stool 1x/5-7 days) Malnutrition Easy palpable fecal masses Abdominal distention Emotional instability Delayed physical development
Complications hirschprung’s disease
Perforation or rupture of intestine
Electrolyte imbalance
Enterocolitis due to overgrowth of opportunistic bacteria (e. Coli)
Toxic megacolon
Diagnosis hirschprung’s disease
X-ray with liquid barium for children older than 3 months
If only a small anal part is involved x-ray won’t reveal signs of the disease
Colonoscopy with biopsy of rectum
CT-scan of abdomen
Gold standard for hirschprung’s disease
Colonoscopy with biopsy of rectum
Treatment hirschprung’s disease
Corrective surgery, I.e. removal of aganglionic segment of colon
Chronic functional disorder of large intestine without inflammation or morphological changes in bowel tissue (without organic basis of disease) - all cells and tissues normal
IBS - irritable bowel syndrome
IBS aka
Spastic colon
Irritable colon
Mucous colitis
(Prolonged spasm)
IBS ___ cause more serious conditions such as colorectal cancer or IBD
Does NOT
IBS is more common
In young than elderly
Females 2:1
People over age 50 are less likely to develop IBS for the first time in life, so it is more likely that similar symptoms may be caused by
Another problem
Etiology IBS
Not known
Often results from combination of physical and stress related factors
Genetic predisposition is possible
Chriopractor is super helpful for
IBS
Risk factors for IBS
Abnormality of innervations of large intestine
Abnormally decreased serotonin level
Pscyhological/psychosomatic factors (anxiety, depression, fibromyalgia, stressful lifestyle)
Change of hormonal level (females before menses)
Abnormalities in gut flora (overgrowth of opportunistic bacteria, decrease in bifidobacteria and lactobacteria - good bactera)
After long-term therapy with antibiotics (more than 2 weeks)
Food intolerance for IBS
Chocolate Sugar Alcohol Vegetables High fiber fruits like mango Chewing gums with sweeteners Coffee
IBS appears to reflect motor disturbances of the ____ in response to stimuli
Entire colon
The contraction of the bowel wall in IBS
Can be stronger and lasts longer than normal
Contraction of gallbladder and stimulation of smooth muscle
Cholecystokinin
The patient may be hypersensitive to hormones ___ and ____ which result in hypercontraction of the bowel smooth muscles in IBS
Gastrin
Cholecystokinin
The abnormal decreased produciton of serotonin by brain and IG cells is associated with
Abnormal digestive function and mood
Biochemically derived from tryptophan
Serotonin
Primarily found in GI tract - 90% - used to regulate intestinal movements
Serotonin
Serotonin is found in and stored in
Platelets
Neurotransmitter of the CNS - regulation of mood, appetite, sleep (melatonin)
Serotonin
IBS-D
Predominately characterized by diarrhea
IBS-C
Predominately characterized by constipation
IBS-A
Predominately characterized by pain or alternating stool patterns
Signs and symptoms IBS
Abdominal discomfort or pain lower than bellybutton occurs 1 hour after meal or stress Association with diarrhea or constipation (no blood or pus) Presence of mucous in the stool Fatigue Headaches Depression in 60% of patients Unpleasant taste in the mouth Backache Insomnia Heart palpitation
IBS pain disappears after
Bowel movement and passage of gas
IBS close to age
40
Diagnosis IBS
Non-specific and based on ruling out of other more serious disaeses
Blood tests - rule out celiac disease
CBC - rules out inflammation, allergy, cancer
Stool microscopy and culture - rule out infection
Stool for parasites
Fecal occult test
Thyroid functional test - rule out thyroid diseases (myxedema)
Colonoscopy - rule out IBD - only over 40
X-ray with liquid barium
Cancer ESR level
High with more than 40 ml/hr
Treatment IBS
No single type of treatment works best for everyone. Treatment is individual and basaed on IBS form
Adjustments are super helpful
IBS-D treatment
Fructose free diet (no honey, apples, pears, corn, corn syrup, dry figs, grapes, red sweet pepper, mango, maple syrup) Lactose free diet Avoid artifical sweeteners Avoid alcohol Avoid coffee and fried foods
IBS-C treatment
Soluble fibers 20 g per day
Non-soluble fibers will worsen symptoms (cellulose, lignins, cereal grains)
Regular exercises may help reduce constipation (swimming, biking, walking)
Recommend raw or steamed vegetables - steamed is best, olive oil, hydration
IBS-A treatment
Avoid foods that increase gas production
Beans, cabbage, uncooked cauliflowers, broccoli
Recommended for all forms IBS treatment
Chiropractic
Meditation
Normalize serotonin with Vit B 1,3,6,9; calcium, magnesium, sunlight exposure not less than 30 min/day, 7-8 hours of sleep
Medications for IBS
Antidiarrhea or laxative meds
Antidepressants
Probiotics (bifidobacteria and lactobacteria) - 20-60mg
Antispasmodic meds (peppermint oil)
Outpocketing of colonic mucosa and submucosa through weakness of muscle layers in the colon wall
Diverticular disease
Diverticular disease is most prevalent in
Men over age 40
Most common site for diverticula is in the
Sigmoid colon
Diverticula may develop in
Esophagus Stomach - usually precursor of peptic or neoplastic diseases of stomach Duodenum near hepatopancreatic ampulla Jejunum Ileum - meckel’s - congenital anaomaly
Etiology diverticular disease
Unkown
Risk factors diverticular disease
Increasing age - 50% of people 70 or over have this
Chronic constipation
A high fiber diet and inc frequency of bowel movement
Connective tissue disorders that may cause weakness in the colon wall (marfan’s syndrome)
Genetic predisposition
Physical inactivity
Clinical forms diverticular disease
Diverticulosis
Diverticulitis
Diverticulum is present but asymptomatic, no inflammation
Diverticulosis
Inflamed diverticula may cause potentially complications - fatal obstruction, bleeding, abscess, perforation, fistula to adjacent organs, peritonitis
Diverticulitis
Diverticula probably result from ___ on an area of weakness in GI wall where blood vessels enter
High intraluminal pressure
In ___ the fecal masses and bacteria accumulate in the diverticular sac. They affect blood supply to the thin wall of the sac making them more susceptibel to attack by colonic bacteria
Diverticulitis
Signs and symptoms of diverticulosis
80% of patients are asymptomatic
20% of patients experience irregular defecation or bloating
Signs and symptoms of acute diverticulitis
Characterized by triad - sudden left lower quadrant pain worsening with movement, chills and fever, leukocytosis Nausea, vomiting Diarrhea or constipation Tenderness in the lower abdomen Feeling of fullness
Signs and symptoms of chronic diverticulitis
Constipation Ribbon-like stool Abdominal rigidity and pain Diminished bowel sound (normal is 5-35, less than 5 is constipation) Nausea, vomiting
Diagnosis diverticulosis is occasional finding while performing
Plain x-ray of the abdomen with liquid Barium
CT-scan
MRI
Colonoscopy (gold standard)
Diagnosis acute diverticulitis contraindications
Colonoscopy and plain x-ray with liquid barium because could result in perforation of colon
Diagnosis acute diverticulitis
CT-scan
MRI
US
Complications diveticular disease
More common in patients taking NSAIDS esp long-term (over 6 months, over age 70)
Bleeding Abscess Rupture of colon Perforation of colon Fistula to adjacent organs Peritonitis Sepsis
First time bleeding from the rectum especially in patients over 40 yo requires ruling out of
Colorectal cancer
Inflammatory bowel diseases
Colon polyps
In uncomplicated diverticular disease there is no specific treatment it is recommended
Adjust
Decrease consumption of nuts, sunflower seeds, popcorn, pumpkin seeds
In complicated diverticular disease only ___ and ___ are indicated for treatment
Antibioticotherapy
Surgery
Inflammation of the appendix
Appendicitis
Untreated cases of acut appendicitis have
High mortality rate
Appendicitis is classified as
Medical emergency
Location of appendix
Base of appendix at 2cm below ileocecal valve, tip of appendix can vary from being retrocecal (74%) to being in the pelvis to being extraperitoneal
There are some rare congenital variations of appendix
Agenesis
Duplication
Triplication
Situs inversus
Etiology appendicitis
Lymphoid hyperplasia
Obstruction of appendix
Appendicitis
Etiology
Lymphoid hyperplasia due to
Viral infection (measles, mono, respiratory viral infeciton)
Crohn’s disease
Bacterial enterocolitis
Amebiasis
Lymphoid hyperplasia etiology is more typical for
Children, young people before age 20
Appendicitis
Etiology
Obstruction of appendix due to
Foreign bodies
Constipation with fecal stasis
Parasites
Neoplasms
More typical for adults age 25 and older
Clinical forms appendicitis
Acute - typical, atypical
Chronic - aka rumbling or recurrent appendicitis
Signs and symptoms acute appendicitis appear in strict sequence
Pain
Vomiting, nausea
Fever
Acute appendicitis
The first symptom is ___
Sudden mild pain in upper epigastric area or around the umbilicus lasting 4-6 hours
after first symptoms acute appendicits
The pain gets more sharp, severe, constant and goes down towards RLQ (typical) LLQ or RUQ (atypical)
Pain characteristic depending on locations of tip of appendix
Flank or back pain (retro/paracecal) - could mimic kidney stone migration
Crampy pain associated with diarrhea (paraileal)
Suprapubic pain associated with increased urinary frequency (pelvic) - mimics bladder inflammation
In children before 8 yo acute appendicitis the pain localizes around
The umbilicus
The pain is reduced when the patient being in supine or side position flex the hips and draw their knees up toward the chest right side
Fetal position
Acute appendicitis
The second manifestations are
Nausea, vomiting, reduced appetite
Acute appendicits
The third manifestation is
The fever from low to high degrees
Acute appendicitis after 12-20 hours the following symptoms usually come to the clinical attention
Chills
Constipation
High fever
Severe constant pain
If after first three manifestations the sudden relief of pain occurs within next 2-4 hours, it could indicate
Rupture of appendix
If after few hours the pain becomes significantly worse, the development of ___ might be suspected
Peritonitis
Chronic appendicitis develops rare, usually in ___ never in ___
Age 16 and over
Children
All patients with chronic appendicitis have experienced before
One or more episodes of acute appendicitis
Chornic appendicitis is characterized by
Fibrotic thickening or scaring of the appendix wall as a result of previous acute inflammation
Pain characteristics chronic form
Pain in RLQ or lower abdomen for 3 or more weeks of duration
Pain intensity from mild to moderate, it gets worse within one to more weeks
If pain gest severe and constant, it indicates the rupture of appendix
Nausea and vomiting are not always present in
Chronic appendicitis (unlike acute form)
Fever chronic appendicitis
Is NOT present
If develops, the peritonitis must be suspected
In pregnancy the appendix migrates in CCW direction towards
The right kidney, rising above the iliac crest
RLQ pain and tenderness dominate in
First trimester of pregnancy
After 20 weeks of pregnancy the pain may present in RUQ or right flank, and could mimic the
Kidney or gallbladder problems
Complications appendicitis
Gangrenous appendicits with local peritonitis
Diffuse peritonitis
Sepsis
Death
Diagnosis appendicits most specific physical findings are
Pain on percussion of abdomen
Rebound tenderness - Rowsing sign
Psoas sign
Obturator sign
The most specific physical findings of appendicitis are
Rigidity and guarding of abdominal muscles in RLQ
Positive dunphy sign (sharp pain in RLQ with coughing)
Positive sitkovsky sign (an increase of pain in the RLQ when a patient lies on left side)
Positive blumberg sign - indicates the development of peritonitis
Diagnosis appendicits
CBC - leukocytosis acute, neutrophilia acute, normal blood chronic
Urinalysis to rule out UTI is normal
US - esp in children and chronic cases
CT-scan only for chronic form
Treatment appendicitis
Surgery ASAP
