causes:

friction

trauma (oral appliances)

-resolves quickly

-painful

causes:

injury

trauma

menstrual cycles

stress

-which lead to hyperkeratosis

-resolves in 1 week

-gray circumference and does not bleed

-very painful

white raised patch

not easily removed

causes: cigarette smoking

associated with epstein barr or HIV virus

keratosis on the lateral surface of the tongue

white plaque

-readily removed

-bleeds

-self limiting

-causes: oral fungal infection

persistent bleeding

can enlarge

-can look like other lesions > confirm by biopsy

painful sensation during swallowing

common for geriatrics: take pill without water and the gelatin capsule gets lodged into the esophagus and leeches and causes pain

anatomical anomaly > protrusion of stomach above the diaphragmatic esophageal opening

associated with lower esophageal pain and can be mistaken for GERD

1. GERD

2. GU/DU (gastric and duodenal ulcers)

3. SRMD (stress related mucosal damage)

4. NSAIA induced ulceration

transient LES relaxation > reflux of acid to the esophagus which causes epigastric burning pain (heartburn)

-common after eating (postprandial) because meals stimulate acid production

symptoms:

-common: heartburn

-uncommon: hoarseness, coughing (acid irritating trachea), chest pain, pain upon swallowing, weight loss, anemia (significant bleed in stomach)

1. overeating: stimulates acid production

2. alcohol: vasodilator effect

3. smoking: prevents healing of epithelia

4. spices and carminatives = spearmint, mint

5. caffeine, other xanthines: vasodilator effect

6. fatty foods

1. anticholinergics: decrease vagal tone of LES

2. opiates

3. benzodiazepines

4. oral contraceptives

5. glucocorticoids: steroids shut down protein production > weakens wall of esophageal tract

1. weight loss: abdominal fat puts pressure on stomach that forces it up the esophagus

2.reduce alcohol and cigarette smoking

3. raise level of bed in the thoracic region to increase esophageal clearance

4. not eating within 3 hr of bedtime

-usually caused by h.pylori but 10% from systemic disease

-h.pylori infection verified by biopsy, culture and urease activity

-split into 2 diseases depending on location: duodenal, gastric ulcer

1. symptoms: pinpoint epigastric pain, burning pain, WEIGHT GAIN

2. onset: 1-3 after meals (when acid secretions enter the duodenum), pain is relieved by food

3. gastric acid: normal to high

1. symptoms: diffuse pain, NV, WEIGHT LOSS

2. onset: immediately after meals

3. gastric acid normal to low

1. h.pylori burrows deep into the lining of the GI tract

2. causes inflammation and destroys the mucus barrier > leads to acid influx which causes ulceration

3. uses urease to break down urea into ammonia

-ulcers can spontaneously heal or rupture leading to mortality

causes: systemic response to stress (an intensive care unit disorder) > increases systemic glucocorticoids

-CNS injury

-mechanical ventilation

-coagulopathy

-extensive burns

-sepsis, trauma, shock 

-can be asymptomatic

treat primary disease to prevent blood loss, mucosal damage and mortality

diffuse vs discrete lesions

located in acid producing region vs. in duodenum and antrum

perforation rare vs perforation common

bleeding from superficial capillaries vs bleeding from major arteries and veins

mix between SRMD and PU

misoprostol (prostaglandin analog): restores prostaglandins (gastroprotective) produced by COX and decreased by NSAIDS > reverses damage

1. gastric ulcer predisposition

2. genetic factors

3. dietary factors

4. infectious disease factors

neoplasm causes are multifactorial!

personality disorder

altered sense of body image with self induced starvation

behavioral disorder

binge eating with vomiting

-transit time: 40-180 min normally

-decreased transit time caused by: 

1. uncoordinated contractions

2. obstruction

3. herniation: twisting of the valves

symptoms:

1. NV

2. cramping or severe pain

3. peritonitis

4. fever and sepsis

1. osmotic

2. secretory

3. infectious

poorly absorbed solutes

decreased digestive capacity

viral, bacterial or parasitic causes

self limiting

lethal in very old, young, immunosupressed

rotavirus damage to villae

-cells that regrow are immature and dysfunctional > lose absorptive capabilities

-can spontaneously resolve but severe in neonates

immune reaction to wheat protein that causes villus atrophy, diarrhea and malabsorption

treat by restricting wheats > special diets

caused by AIDS infection and kaposi's sarcoma

type of malabsorption syndrome

inability to control bowel movements > not the same as diarrhea

causes:

1. surgery

2. hemorrhoids

3. aging

4. crohn's disease

5. trauma

6. diabetic neuropathy

7. AIDS

1. lactose intolerance

2. quantitative stool fat (fat is readily absorbed in small intestine): collect stool for a few days and measure the amount of fat in the feces > excess fat in feces > malabsorption problem or pancreas/liver problem

3. D-xylose (readily absorbed in the small intestine): give to patient with water > if there is D-xylose in feces/urine > then no malabsorption problem

nutrient absorption (fats, proteins, carbs, vitamins, minerals) is impaired

-anemias

-vit b12 deficiencies

-hypocalcemia

-osteoporosis

-etc.

2 major forms: crohn's disease and ulcerative colitis

-genetic and microbial based factors involved in an autoimmune disorder against intestinal mucosa

regional enteritis vs. diffuse bleeding

fistulas common vs. fistulas uncommon

Th1 cytokine activity (enhanced cell mediated immunity) vs TH2 cytokine activity (enhanced humoral immunity)

TNFalpha prominent in crohn's disease

smoking exacerbates vs smoking protects

-caused by mesenteric artery occlusion (embolus in ped/geriatric or atherosclerosis in geriatric)

-symptoms:

1. severe abdominal pain

2. hypotension

3. acidosis

4. fever

5. blood loss

-complications:

1. ischemia

2. necrosis

3. peritonitis

4. death

treatment: bowel resection

-painless premalignant growths into the lumen of the colon 

-most common in men/women age 40 or older

-NEED TO SCREEN BY ENDOSCOPY AT AGE 50 OR HIGHER

-always removed because if not caught they can lead to cancer

-outpouchings of colon (usually sigmoid colon)

-causes: low fiber diet

diverticula that become inflamed because of fecal impaction or lodging of seeds/nuts in the diverticula

-symptoms:

1. left sided pain: where the sigmoid colon is

2. fever

3. constipation

4. feeling of fullness with lack of appetite

treatment for mild diverticulitis (no perforations):

1. bland liquid diet with antibiotics

repeated episodes can cause:

1. abscesses

2. ulceration

3. scarring transmural adhesions

4. fistulas

form of anatomical diverticula

can be either acute or chronic

-inflammation, ulceration and perforation is a medical emergency > can lead to peritonitis

-symptoms

1. NV

2. uncommonly diarrhea

3. reflexive pain upon abdominal compression and release

-abdominal pain with increased/decreased GI motility and spasm

-associated with dietary, emotional, environmental changes

-treatment is not curative: antidepressants, anticholinergics

masses of areolar rectal tissue with inflammed arteries and veins

-extremely painful

-associated with pregnancy, aging, heavy lifting, changes in bowel habits

-can be transient

-can be removed through laser or surgery

1. fatty liver: fatty acid oxidation is impaired and triglyceride levels increase

-REVERSIBLE

2. alcoholic hepatitis: hepatocellular necrosis with hepatomegaly

-fever: build up of bacteria

-jaundice: build up of bilirubin

3. alcoholic cirrhosis: hepatic scarring, collagen formation and diffuse connective tissue replacement > inflammation causes normal cells to be replaced

-firm liver: from all the connective tissue

LIVER TRANSPLANT

-scar tissue in the liver blocks the portal vein > cannot bring blood into the liver > portal HTN > blood flows to other areas in the body (back flow)

-results in

1. splenomegaly

2. varices (esophageal and others): swelling of the veins > can eventually burst

3. ascites: passage of fluid from hepatic circulation (increasing capillary hydrostatic pressure) into the intracellular space and peritoneal cavity

4. peritonitis: stasis of blood flow allows bacteria to flow into peritoneum and circulation

LEADS TO LIVER FAILURE

causes: alcohol, acetaminophen (fulminant/acute liver failure can occur within 8 weeks of acetaminophen overdose), mushroom toxin

symptoms:

1. fatigue: liver can't process waste products and nutrients 

2. ND: inability to process nutrients, body rejects enteric nutrition

3. jaundice: inability to metabolize heme and bilirubin

4. bleeding: liver is responsible for clot factor synthesis (II, VII, IX, X)

5. edema and ascites: decreased plasma protein production (decreased colloid osmotic pressure) and activation of renin-angiotensin-aldosterone system

6. hepatic encephalopathy: mild confusion to comas, liver is responsible to metabolize ammonia and mercaptans from the intestines

gallstones formed in gallbladder (also other areas of the biliary system: pancreas and liver) by precipitation of cholesterol and bile tract components (bilirubinates, calcium, etc)

-can grow to large stones over many years

-symptoms: pain after meals is common

gallstones with greater than 50% cholesterol

-greater prevalence in women

-causes: excess biliary cholesterol in relationship to bile acid solubilization > too much cholesterol and not enough bile acids > free cholesterol can precipitate

-mainly in gallbladder

1. black pigment (calcium bilirubinate): hemolysis and cirrhosis are predisposing factors

2. brown pigment (calcium bilirubinate with salts of fatty acids): higher incidence in asia

-gallstones (from pancreas or liver or gallbladder) get pushed down to the sphincter of oddi because of a meal> can block the sphincter

-obstruction of pancreas > leads to pancreatitis

-symptoms: flank pain, nausea, increase in serum amylase and lipase (not getting into the duodenum)

-treatments: surgery or non surgery (scopes can reach the sphincter of oddi)

-female prevalence

-associated with oral contraceptive use

-usually benign but can present with a liver function problem if progressive

-male prevalence

-commonly associated with alcohol and androgen abuse

-may be associated with hep B and C

associated with

1. cholelithiasis

2. high triglyceride levels: provides substrates for the lipases released from the pancreas and will increase fatty acid levels which can cause pancreatitis

-picornavirus

-single stranded RNA genome

-viremia is transient

-generates IgG and IgM response > can be used for diagnostic procedure

-25-50% of US population has serologic evidence of exposure

-oral-fecal

-contaminated shellfish or water

-incubation period: 14-49 days

-HAV appears in stools 2 wks prior to symptoms > asymptomatic is highest levels of cross contamination

-HAV disappears 3 wks after onset of symptoms

mostly asymptomatic or mild flu like symptoms (fever, fatigue, nausea, abdominal pain)

-can have 

1. mostly asymptomatic

2. mild flu like symptoms (fever, fatigue, nausea, abdominal pain)

3. pale colored stools

4. dark urine

5. jaundice

6. elevated transaminases: transaminases found in hepatocytes to break down AA > if liver damage then you have higher transaminase in the blood

-cases resolve in 6 mo for normal people

-geriatric, children, concurrent alcoholic liver disease > can lead to liver failure or cirrhosis

-no specific treatment > rest and dietary measures

-prophylaxis: HAV immune globulin is of limited protection for exposed

-HAV immunization (VAQTA and HAVRIX) are effective but length of protection is variable

-hepadnavirus 

-partially double stranded genome

-outer coat of the viron is produced in excess >diagnostic procedure looks for hepatitis B surface antigen or HBsAg > shows active disease

-saliva, blood,seminal contact

-incubation period: 28-160 days

-transmission can be through asymptomatic individuals

-10% of infections result in a persistent carrier state

2 stages

1. preicteric stage: influenza like illness that lasts for several days

2. icteric stage: jaundice, fever, arthralgias (joint pain), increased fatigue, abnormal liver function tests > persists for several weeks prior to resolution

10% leads to chronic hepatitis, cirrhosis and liver cancer

variable > depends on initial response

-coinfection with hep D > 80% incidence of chronic hepatitis

-bed rest, dietary measures

-drug therapy gradually improving response

-hep b immune globulin and vaccine for exposed individual > protection for 5-7 yrs

-booster is controversial

RNA containing flavavirus

diagnostic procedures:

1. anti HCV antibody

2. RT PCR (real time PCR) for HCV RNA > more accurate diagnosis

-blood contamination

-sexual transmission less frequent than with hep B

-greater than 70% infected contribute to asymptomatic carrier group

generally milder than hep B > cyclical symptoms or asymptomatic

-anti HCV antibodies develop slowly 10-39 weeks after onset of symptoms > diagnostic procedure by looking at antibodies is not definitive, need to use RT PCR

although milder than HBV > 70% of infected HCV develop chronic hepatitis, liver failure and cancer

-treatments are also variable and no vaccine for HCV > 50% prognosis

-bed rest for acute (preicteric) phase is essential

-restricted alcohol and hepatotoxic drug (isonazid and acetaminophen) use

-treatment regimens (antivirals, interferons) > limited success