Block 2 Gi Flashcards
Oral cavity:
Describe the following for Cleft lip & palate:
What is it?
What causes it?
Patho:
When the facial prominences fail to fuse during early pregnancy (they usually appear together)
Causes:
Teratogenic drugs
Patho:
When the facial prominences fail to fuse during early pregnancy (they usually appear together)
Causes:
Teratogenic drugs
Describes which condition?
Cleft Lip & palate
Describe the following for aphthous ulcers:
What are they?
What causes them?
Patho:
Aka cancer sores that look gray/blue with surrounding erythema. They are painful & superficial sores in the mouth
Causes:
Stress/illness
Bechet syndrome
Patho:
Aka cancer sores that look gray/blue with surrounding erythema. They are painful & superficial sores in the mouth
Causes:
Stress/illness
Bechet syndrome
Describes which type of ulcer?
Aphthous ulcer
Describe the following for Oral herpes:
What is it?
What causes it?
What is a complication of a primary infection?
Patho:
An infection causes the mucosal vesicles to rupture resulting in shallow & painful red ulcers (cold sores)
Causes:
HSV-1 infection
Comp:
If you contract a primary HSV-1 infection in childhood the lesions will heal but the virus will lie dormant in the trigeminal ganglia & can reactivate in response to stress & sunlight (life long)
Patho:
An infection causes the mucosal vesicles to rupture resulting in shallow & painful red ulcers (cold sores)
Causes:
HSV-1 infection
Comp:
If you contract a primary HSV-1 infection in childhood the lesions will heal but the virus will lie dormant in the trigeminal ganglia & can reactivate in response to stress & sunlight (life long)
Describes which condition?
Oral herpes (HSV-1)
Describe the following for Bechet syndrome:
What is it?
What causes it?
Patho:
Immune complex vasculitis affecting smaller blood vessels causes recurrent uveitis, aphthous & genital ulcers.
Causes:
Typically post viral infection
Patho:
Immune complex vasculitis affecting smaller blood vessels causes recurrent uveitis, aphthous & genital ulcers.
Causes:
Typically post viral infection
Describes which condition?
Bechet syndrome
Describe the following for Squamous cell cancer (mouth):
What is it?
What causes it?
- risks
What are the lab findings?
- histology
What are the differentials?
Patho:
A malignant neoplasm of squamous cells lining the mouth. It presents with precursor lesions i.e leukoplakia & erythroplakia
Causes/risks:
- Smoking
- Drinking
- Genetics
Lab/histo:
Leukoplakia (A white plaque that can’t be scraped off)
Erythroplasia (A red plaque aka vascularized squamous cell dysplasia)
Both represent squamous cell dysplasia
Differentials:
- Oral Candidiasis (white plaque that’s easily scraped off usually in immunocompromised )
- Hairy leukoplakia (lateral side tongue plaque seen in immunocompromised plp with EBV infection)
Patho:
A malignant neoplasm of squamous cells lining the mouth. It presents with precursor lesions i.e leukoplakia & erythroplakia
Causes/risks:
- Smoking
- Drinking
- Genetics
Lab/histo:
Leukoplakia (A white plaque that can’t be scraped off)
Erythroplasia (A red plaque aka vascularized squamous cell dysplasia)
Both represent squamous cell dysplasia
Differentials:
- Oral Candidiasis (white plaque that’s easily scraped off usually in immunocompromised )
- Hairy leukoplakia (lateral side tongue plaque seen in immunocompromised plp with EBV infection)
Describes which condition?
Squamous cell cancer (mouth)
Describe the following for Mumps:
What is it?
What causes it?
What are the symptoms?
What are the lab findings?
What is a possible complication?
Patho:
Infection causing bilateral parotid inflammation & swelling
Causes:
Mump virus
Signs:
1) Orchitis (inflamed testes)
2) Pancreatitis
3) Aseptic meningitis
Labs:
Elevated serum amylase
Comp:
Sterility in teenagers
Patho:
Infection causing bilateral parotid inflammation & swelling
Causes:
Viral infection
Signs:
1) Orchitis (inflamed testes)
2) Pancreatitis
3) Aseptic meningitis
Labs:
Elevated serum amylase
Comp:
Sterility in teenagers
Describes which condition?
Mumps
Describe the following for a pleomorphic adenoma:
What is it?
What are the symptoms?
What are the lab findings?
- histology
What is a rare complication?
Patho:
A benign tumor in the salivary glands (#1 Parotid). It is a mobile, painless, & circumscribed mass at the angle of the jaw it has a high rate of reoccurrence
Signs:
1) Facial nerve damage
Labs/histo:
Tumor is made from Stromal (cartilage) & epithelial tissue
&
There is extension of tumor islands outside the tumor capsule (incomplete resection)
Comp:
It rarely progresses to a carcinoma
Patho:
A benign tumor in the salivary glands (#1 Parotid). It is a mobile, painless, & circumscribed mass at the angle of the jaw it has a high rate of reoccurrence
Signs:
1) Facial nerve damage
Labs/histo:
Tumor is made from Stromal (cartilage) & epithelial tissue
&
There is extension of tumor islands outside the tumor capsule (incomplete resection)
Comp:
It rarely progresses to a carcinoma
Describes which condition?
Pleomorphic adenoma
A patient presents to the clinic with facial palsy & a painless mobile mass at the jaw angle.
What is a possible diagnosis?
What is the concern with surgery?
What is a possible complication?
Diagnosis:
Pleomorphic adenoma
Surgery concern:
The tumor has many small island extensions outside of the original tumor capsule making it difficult to resect completely (high recurrence rate)
Comp:
In rare cases it can transform into a carcinoma (malignant tumor)
Which is the most common benign tumor of the salivary gland?
Pleomorphic adenoma (parotid)
Which is the 2nd most common benign tumor of the salivary gland?
Warthin tumor (parotid)
What is the most common malignant tumor of the salivary gland?
Mucoepidermoid carcinoma (parotid)
Describe the following for a Warthin tumor:
What is it & what are the lab findings (histo)?
Patho/histo:
A benign cystic tumor with lots of lymphocytes & germinal centers (lymph node-like stroma)
It’s the second most common benign tumor of the salivary (parotid) gland
Patho/histo:
A benign cystic tumor with lots of lymphocytes & germinal centers (lymph node-like stroma)
It’s the second most common benign tumor of the salivary (parotid) gland
Describes which condition?
Warthin tumor
Describe the following for a mucoepidermoid carcinoma:
What is it & what are the lab findings (histo)?
Patho/labs (histo):
A malignant tumor made of mucinous & squamous cells
It is the most common malignant tumor of the salivary gland (parotid)
Patho/labs (histo):
A malignant tumor made of mucinous & squamous cells
It is the most common malignant tumor of the salivary gland (parotid)
Describes which condition?
Mucoepidermoid carcinoma
Describe the following for a transesophageal fistula:
What is it?
- most common variant
What are the symptom?
Patho:
A congenital defect resulting in a connection between the esophagus & trachea
most common var:
A proximal esophageal atresia with & the distal esophagus connecting to the trachea
Signs:
1) Vomiting
2) Polyhydramnios
3) Abdominal distension & aspiration (air)
Patho:
A congenital defect resulting in a connection between the esophagus & trachea
most common var:
A proximal esophageal atresia with & the distal esophagus connecting to the trachea
Signs:
1) Vomiting
2) Polyhydramnios
3) Abdominal distension & aspiration (air)
Describes which condition?
Tracheoesophageal fistula
A 1-month-old is brought in because of difficulty feeding. Baby will vomit immediately after a meal & their belly appears to be distended. During pregnancy mom had confirmed polyhydramnios.
What is the diagnosis?
Transesophageal fistula
Describe the following for esophageal web:
What is it?
What are the symptoms?
What is a possible complication?
What is the associated condition?
Patho:
A thin protrusion of the esophageal mucosa (upper esophagus)
Symptoms:
1) Dysphagia when food isn’t chewed well
Comps:
High risk of esophageal squamous cell carcinoma
Ass cond:
Plummer-Vinson syndrome
Patho:
A thin protrusion of the esophageal mucosa (upper esophagus)
Symptoms:
1) Dysphagia when food isn’t chewed well
Comps:
High risk of esophageal squamous cell carcinoma
Ass cond:
Plummer-Vinson syndrome
Describes which condition?
Esophageal webs
What is the triad of Plummer-Vinson syndrome?
1) Severe iron-def anemia
2) Esophageal webs
3) Beefy red tongue with atrophic glossitis
1) Severe iron-def anemia
2) Esophageal webs
3) Beefy red tongue with atrophic glossitis
Describes the triad of which condition?
Plumber Vinson syndrome
Describe the following for Zenker diverticulum:
What is it & what causes it?
What are the symptoms?
Patho/cause:
It’s outpouching of the pharyngeal mucosa through an acquired defect (false diverticulum). It sits above the upper esophageal sphincter at the junction of the esophagus & pharynx
Signs:
1) Dysphagia
2) Obstruction
3) Halitosis (bad breath)
Patho/cause:
It’s outpouching of the pharyngeal mucosa through an acquired defect (false diverticulum). It sits above the upper esophageal sphincter at the junction of the esophagus & pharynx
Signs:
1) Dysphagia
2) Obstruction
3) Halitosis (bad breath)
Describes which condition?
Zenker diverticulum
Describe the following for Mallory-Weiss syndrome:
What is it?
What causes it?
What are the complications?
What is a complication?
Patho:
A longitudinal laceration/tears at the gastroesophageal junction
Causes:
Severe vomiting attributed to alcoholism or bulimia
Signs:
1) Painful hematemesis (bloody vomit)
Comps:
Risk of progressing to Boerhaave syndrome
Patho:
A longitudinal laceration/tears at the gastroesophageal junction
Causes:
Severe vomiting attributed to alcoholism or bulimia
Signs:
1) Painful hematemesis (bloody vomit)
Comps:
Risk of progressing to Boerhaave syndrome
Describes which condition?
Mallory-Weiss syndrome
What is Boerhaave syndrome & what condition is it associated with?
It’s rupture of the esophagus (GE junction) resulting in air going into the mediastinum & subcutaneous emphysema
It’s associated with Mallory-Weiss Syndrome
Describe the following for esophageal varices:
What is it?
What causes it?
- explain why
What are the symptoms?
What is a complication?
What is a key associated condition
Patho:
It’s dilated submucosal veins in the lower esophagus
Cause:
Portal HTN
(normally the distal esophageal vein drains into the portal vein via the L. gastric vein, but during portal HTN the L.gastric vein backs up into the esophageal veins resulting in dilation/varices)
Signs:
1) Painless hematemesis
Comps:
Main COD in cirrhosis
Patho:
It’s dilated submucosal veins in the lower esophagus
Cause:
Portal HTN
(normally the distal esophageal vein drains into the portal vein via the L. gastric vein, but during portal HTN the L.gastric vein backs up into the esophageal veins resulting in dilation/varices)
Signs:
1) Painless hematemesis
Comps:
Main COD in cirrhosis
Describes which condition?
Esophageal varices
Describe the following for Achalasia:
What is it?
What causes it?
What are the symptoms?
What is a complication?
Patho:
It is disordered esophageal motility & it can’t relax the lower esophageal sphincter (LES)
Causes:
Damage to the ganglion cells of the myenteric plexus (Auerbach plexus)
1) Trypanosoma cruzi infection in Chaga’s disease
2) Trauma
Signs:
1) Dysphagia (solids & liquids)
2) High LES pressure on esophageal manometry
3) Bird-beak app on barium swallow
Comp:
Risk of esophageal squamous cell carcinoma
Patho:
It is disordered esophageal motility & it can’t relax the lower esophageal sphincter (LES)
Causes:
Damage to the ganglion cells of the myenteric plexus (Auerbach plexus)
1) Trypanosoma cruzi infection in Chaga’s disease
2) Trauma
Signs:
1) Dysphagia (solids & liquids)
2) High LES pressure on esophageal manometry
3) Bird-beak app on barium swallow
Comp:
Risk of esophageal squamous cell carcinoma
Describes which condition?
Achalasia
Explain how infection with trypanosome cruzi in Chagas disease can lead to achalasia?
What is the cause?
What are the symptoms
- acute
- chronic
Patho/cause:
Infection from the kissing/reduviid bug (Latin America) with Trypanosome cruzi leads to Chagas disease.
Causes achalasia:
It damages the ganglion cells of the myenteric plexus (responsible for reg both muscularis propria layers (reg bowel movement) & relaxing the LES)
Signs:
Acute
- 1) Chagoma (edema at bite site usually the face)
- 2) Romana sign (unilateral eyelid edema)
Chronic
- 1) Chagas cardiomyopathy (biventricular dilation & atrophic apex)
- 2) Achalasia
- 3) Megaesophagus
- 4) Megacolon
Describe the following for GERD:
What is it?
What causes it?
-risks
What are the symptoms?
What are the complications?
Patho:
Reduced LES tone results in acid reflux
Causes/risks
#1 Smoking
Other (Drinking, Fat-filled diet, Obesity, Caffeine & Hiatal Hernia)
Symptoms:
1) Heart burn
2) Asthma (adult onset) with cough
3) Enamel erosion
Comps:
Ulceration with stricture
Barrett’s esophagus
Patho:
Reduced LES tone results in acid reflux
Causes/risks
Smoking
Drinking
Fat-filled diet
Obesity
Caffeine
Hiatal Hernia
Symptoms:
1) Heart burn
2) Asthma (adult onset) with cough
3) Enamel erosion
Comps:
Ulceration with stricture
Barrett’s esophagus
Describes which condition?
GERD
Describe the following for Barrett’s esophagus:
What is it & what causes it?
What are the complications?
Patho/causes:
Metaplasia of the lower esophageal mucosa changing from stratified squamous to non-ciliary columnar epi with goblet cells in response to acid reflux (GERD)
Comps:
Progression to dysplasia & adenocarcinoma
Patho/causes:
Metaplasia of the lower esophageal mucosa changing from stratified squamous to non-ciliary columnar epi with goblet cells in response to acid reflux (GERD)
Comps:
Progression to dysplasia & adenocarcinoma
Describes which condition?
Barrett’s esophagus
Describe the following for esophageal carcinomas:
What are the subtypes?
1) Adenocarcinoma (most common esophageal cancer in the west)
2) Squamous cell carcinoma (esophagus) (most common world wide esophageal cancer)
3) Esophageal carcinoma (presents late & has a poor prognosis :( )
Describe the following for adenocarcinoma (esophagus):
What is it?
What is an associated condition?
Patho:
A subclassification of esophageal cancer, that involves malignant proliferation of the glands.
Ass cond:
Barrett’s esophagus
Patho:
A subclassification of esophageal cancer, that involves malignant proliferation of the glands.
Ass cond:
Barrett’s esophagus
What’s the condition?
Adenocarcinoma of the esophagus
Describe the following for squamous cell carcinoma:
What is it?
What is an associated condition?
Patho:
Malignant proliferation of the squamous cells (most common esophageal cancer world-wide)
Ass cond:
Smoking
Alcohol
Very hot tea
Achalasia
Esophageal webs (Plummer-Vinson)
Esophageal injury (lye ingestion hair straightener)
Patho:
Malignant proliferation of the squamous cells (most common esophageal cancer world-wide)
Ass cond:
Smoking
Alcohol
Very hot tea
Achalasia
Esophageal webs (Plummer-Vinson)
Esophageal injury (lye ingestion hair straightener)
Describes which condition?
Squamous cell carcinoma (esophagus)
Describe the following for Esophageal carcinoma:
What is it?
What are the symptoms?
Where does it spread?
Patho:
A malignant/metastatic cancer that presents late & has a poor prognosis :(
Signs:
1) Progressive dysphagia (from solids to liquids)
2) Weight loss
3) Pain
4) Hematemesis (bloody vomit)
5) Hoarseness (rec. laryngeal nerve involvement)
Spread:
- If cancer is in the upper 1/3 of the esophagus (cervical LN spread)
- If cancer is in the middle 1/3 of the esophagus (mediastinal or tracheobronchial LN spread)
- If cancer is in the lower 1/3 of the esophagus (celiac or gastric LN spread)
Patho:
A malignant/metastatic cancer that presents late & has a poor prognosis :(
Signs:
1) Progressive dysphagia (from solids to liquids)
2) Weight loss
3) Pain
4) Hematemesis (bloody vomit)
5) Hoarseness (rec. laryngeal nerve involvement)
Spread:
- If cancer is in the upper 1/3 of the esophagus (cervical LN spread)
- If cancer is in the middle 1/3 of the esophagus (mediastinal or tracheobronchial LN spread)
- If cancer is in the lower 1/3 of the esophagus (celiac or gastric LN spread)
Describes which condition?
Esophageal carcinoma
Describe the following for gastroschisis:
What is it?
Patho:
A congenital malformation of the anterior abdominal wall failing to form resulting in exposed abdominal contents
Patho:
A congenital malformation of the anterior abdominal wall failing to form resulting in exposed abdominal contents
Describes which malformation?
Gastroschisis
Describe the following for an Omphalocele:
What is it?
What causes it?
Patho:
When bowels herniate through the umbilical cord during development & persist (get trapped), this results in them being covered by the peritoneum & amnion of the cord
Causes:
Failure of the herniated intestines to return to the abdomen during development
Patho:
When bowels herniate through the umbilical cord during development & persist (get trapped), this results in them being covered by the peritoneum & amnion of the cord
Causes:
Failure of the herniated intestines to return to the abdomen during development
Describes which condition?
Omphalocele
Describe the following for a pyloric stenosis:
What is it?
What are the symptoms?
What is the treatment?
Patho:
A congenital hypertrophy of the pyloric smooth muscle (more common in males) that obstructs the passage of food/liquids, symptoms typically present 2wks after birth
Signs:
1) Projectile non-bilious vomiting
2) Visible peristalsis
3) Olive mass in the abdomen
Rx. Myotomy
Patho:
A congenital hypertrophy of the pyloric smooth muscle (more common in males) that obstructs the passage of food/liquids, symptoms typically present 2wks after birth
Signs:
1) Projectile non-bilious vomiting
2) Visible peristalsis
3) Olive mass in the abdomen
Rx. Myotomy
Describes which condition?
Pyloric stenosis
Describe the following for acute gastritis:
What is it?
What causes it?
- risks
What are the effects on the stomach lining?
Patho:
When there is an imbalance between mucosal defenses & the acidity of the stomach resulting in acidic damage to the mucosa, usually with neutrophilic infiltrate
Causes/risks:
1) Severe burns from fire/food/drink (curling ulcer) leads to hypovolemia & less blood supply
2) NSAID (Lowers PGE)
3) Chemotherapy
4) Increased intracranial ulcer (Cushing ulcer stimulation of the vagus nerve increasing acid production)
5) Shock (stress ulcers in ICU patients)
Comp of mucosa:
1) superficial inflammation
2) erosion (loss of superficial mucosa)
3) ulcers (loss of mucosa)
Patho:
When there is an imbalance between mucosal defenses & the acidity of the stomach resulting in acidic damage to the mucosa
Causes/risks:
1) Severe burns from fire/food/drink (curling ulcer) leads to hypovolemia & less blood supply
2) NSAID (Lowers PGE)
3) Chemotherapy
4) Increased intracranial ulcer (Cushing ulcer stimulation of the vagus nerve increasing acid production)
5) Shock (stress ulcers in ICU patients)
Comp of mucosa:
1) superficial inflammation
2) erosion (loss of superficial mucosa)
3) ulcers (loss of mucosa)
Describes which condition
Acute gastritis
Describe the following for Chronic gastritis:
What is it?
- subtypes
Patho:
It is chronic inflammation of the stomach mucosa which is divided into 2 subtypes:
1) Chronic auto-immune gastritis
2) Chronic H. pylori gastritis
Describe the following for Chronic auto-immune gastritis:
What is it?
What are the lab findings?
- histology
What are the symptoms?
What are the complications?
Patho: Subtype of Chronic gastritis
Autoimmune destruction of gastric parietal cells in the fundus & body of the stomach. It is a type IV hypersensitivity reaction that is mediated by T cells (though it has Abs against parietal cells & intrinsic factor)
Labs/histo:
Atrophy of mucosal & intestinal metaplasia
&
Achlorhydria with increased gastrin levels & antral G hyperplasia
Signs:
1) Megaloblastic (pernicious) anemia because of the Abs vs intrinsic factor
Comps:
High risk of progressive to gastric adenocarcinoma (intestines)
Patho:
Autoimmune destruction of gastric parietal cells in the fundus & body of the stomach. It is a type IV hypersensitivity reaction that is mediated by T cells (though it has Abs against parietal cells & intrinsic factor)
Labs/histo:
Atrophy of mucosal & intestinal metaplasia
&
Achlorhydria with increased gastrin levels & antral G hyperplasia
Signs:
1) Megaloblastic (pernicious) anemia because of the Abs vs intrinsic factor
Comps:
High risk of progressive to gastric adenocarcinoma (intestines)
Describes which condition?
Chronic autoimmune gastritis (subtype of chronic gastritis)
Describe the following for Chronic H. pylori gastritis:
What is it?
What is a symptom?
What are the complications?
What are the treatments?
Patho:
The ureases & proteases from H. pylori along with inflammation damage the mucosal defenses usually in the antrum
Symptoms:
1) Epigastric abdominal pain (better with food)
Comps:
1) peptic ulcer disease
2) gastric adenocarcinoma (intestines)
3) MALT lymphoma
Rx: triple treatment
resolve the gastritis/ulcers
reverse metaplasia
eradicate h.pylori
(-ve urea breath test & stool antigen test)
Patho:
The ureases & proteases from bacteria along with inflammation damage the mucosal defenses usually in the antrum
Symptoms:
1) Epigastric abdominal pain (better with food)
Comps:
1) peptic ulcer disease
2) gastric adenocarcinoma (intestines)
3) MALT lymphoma
Rx: triple treatment
resolve the gastritis/ulcers
reverse metaplasia
eradicate infection
(-ve urea breath test & stool antigen test)
Describes which condition?
Chronic H. pylori gastritis
Peptic ulcers includes which 2 types of ulcerations?
Duodenal ulcers
Gastric ulcers
Describe the following for duodenal ulcers:
Where are they?
- most common vs less
What are the causes?
- main & other
What are the symptoms?
What are the lab findings?
- histology
What is a complication
Differential?
Location:
1) Most commonly appear in the anterior duodenum
2) Less common in posterior duodenum
Causes:
Main: H.pylori
other: Zollinger ellison
Symptoms:
1) Epigastric pain (better with meals)
Labs (histo):
Endoscopic biopsy shows ulcers with hypertrophy of the Brunners glands (ant duodenum)
Comps:
If ulcers in the posterior duodenum it can lead to gastroduodenal artery bleeding or acute pancreatitis
Diff:
Almost never malignant
Location:
1) Most commonly appear in the anterior duodenum
2) Less common in posterior duodenum
Causes:
Main: H.pylori
other: Zollinger ellison
Symptoms:
1) Epigastric pain (better with meals)
Labs (histo):
Endoscopic biopsy shows ulcers with hypertrophy of the Brunners glands (ant duodenum)
Comps:
If ulcers in the posterior duodenum it can lead to gastroduodenal artery bleeding or acute pancreatitis
Diff:
Almost never malignant
Describes which condition?
Duodenal ulcers due to Peptic ulcer disease
Describe the following for Gastric ulcers:
What/where is it?
What are the causes
- most common
- other
What are the symptoms?
What are the complications?
Patho/location:
Appear lesser curve of the stomach as well demarcated, punched out lesions surrounded by radiating folds of mucosa
Causes:
Most: H.pylori
Other: NSAIDs, Bile reflux, or gastric carcinoma
Signs:
1) Epigastric pain (worse with food)
Comps:
Rupture risks a big bleed from the L. gastric A
Patho/location:
Usually appears along the lesser curve of the stomach
Causes:
Most: H.pylori
Other: NSAIDs, Bile reflux, or gastric carcinoma
Signs:
1) Epigastric pain (worse with food)
Comps:
Rupture risks a big bleed from the L. gastric A
Diff:
Small well demarcated “punched out” lesions surrounded by radiating folds of mucosa
Describes which condition?
Gastric ulcers due to peptic ulcer disease
What are the 2 subtypes of gastric carcinomas?
1) Intestinal type
2) Diffuse type
Describe the following for gastric carcinoma intestinal type:
What is it/what are the lab findings?
- histo
What are the causes
- risks
Patho/labs (histo):
The more common subtype.
The ulcers are large & irregularly shaped with heaped up margins appearing on the lesser curve of the antrum
Cause/risks:
1) Intestinal metaplasia (H.pylori or autoimmune gastritis)
2) Nitrosamines (smoked foods Japan)
3) Blood type A
Patho/labs (histo):
The more common subtype.
The ulcers are large & irregularly shaped with heaped up margins appearing on the lesser curve of the antrum
Cause/risks:
1) Intestinal metaplasia (H.pylori or autoimmune gastritis)
2) Nitrosamines (smoked foods Japan)
3) Blood type A
Describes which condition?
Intestinal type gastric carcinoma
Describe the following for gastric carcinoma diffuse type:
What is it/What are the lab findings?
- Histo
What is it not associated with?
Patho/labs (histo):
Less common type
It has signet ring cells that diffusely infiltrate the gastric wall & cause desmoplasia resulting in linitis plastica (aka thickened stomach wall)
NOT ass with
h.pylori, intestinal metaplasia, or nitrosammines
Patho/labs (histo):
Less common type
It has signet ring cells that diffusely infiltrate the gastric wall & cause desmoplasia resulting in linitis plastica (aka thickened stomach wall)
NOT ass with
h.pylori, intestinal metaplasia, or nitrosammines
Describes which condition?
Gastric carcinoma diffuse type
Describe the following for gastric carcinomas:
What is the presentation
- both
What are the complications?
- Both
- Spread of intestinal type
- Spread of diffuse type
Later presentation:
1) Weight loss
2) Abdominal pain
3) Anemia
4) Early satiety
5) acanthosis nigricans or Leser-Trelat sign (RARE)
Comps:
Both: proximal spread to the left supraclavicular LN (Virchow node) or distal to liver
Intestinal (periumbilical region via sister-mary-joseph node)
Diffuse (bilateral ovaries via Krunkenberg tumor)
Describe the following for duodenal atresia:
What is it & what causes it?
What is it associated with?
What are the symptoms?
Patho/Cause:
Congenital failure of the duodenum to canalize
Ass cond:
Down syndrome
Signs:
1) Polyhydramnios
2) Distension of the stomach with a blind loop duodenum (double bubble sign)
3) Bilious vomiting
Patho/Cause:
Congenital failure of the duodenum to canalize
Ass cond:
Down syndrome
Signs:
1) Polyhydramnios
2) Distension of the stomach with a blind loop duodenum (double bubble sign)
3) Bilious vomiting
Describes which condition?
Duodenal atresia
Describe the following for Meckel diverticulum:
What it is?
What causes it?
What are its rule of 2s?
What are the symptoms?
Patho:
Outpouching of all 3 layers of the bowel wall (true diverticulum)
Causes:
When the vitelline duct doesn’t involute (untwist)
Rule of 2s:
- 2% of the pop
- 2 inches long & located within 2 ft of the ileocecal valve
- presents in the first 2yrs of life with bleeding
Signs: Usually asymptomatic
1) Volvulus (twisted bowel)
2) Intussusception or obstruction (mimic appendicitis)
Patho:
Outpouching of all 3 layers of the bowel wall (true diverticulum)
Causes:
When the vitelline duct doesn’t involute (untwist)
Rule of 2s:
- 2% of the pop
- 2 inches long & located within 2 ft of the ileocecal valve
- presents in the first 2yrs of life with bleeding
Signs: Usually asymptomatic
1) Volvulus (twisted bowel)
2) Intussusception or obstruction (mimic appendicitis)
Describes which condition?
Meckel diverticulum
Describe the following for Juvenile polyp:
What is it? & What causes it?
What’s the treatment?
Patho/cause:
A sporadic hamartomatous (benign) polyp that happens in kids under 5yrs old. It’s usually a solitary rectal polyp that eventually prolapses & bleeds
Labs:
Cystic spaces with proliferation of lamina propria & mucosal glands
Rx:
Polypectomy
Patho/cause:
A sporadic hamartomatous (benign) polyp that happens in kids under 5yrs old. It’s usually a solitary rectal polyp that eventually prolapses & bleeds
Labs:
Cystic spaces with proliferation of lamina propria & mucosal glands
Rx:
Polypectomy
Describes which condition?
Juvenile polyp
Describe the following for Juvenile polyposis:
What is it?
What is a complication?
Patho:
Formation of multiple juvenile polyps in the stomach & colon
Comps:
More polyps means a higher risk of progressing to carcinoma
Patho:
Formation of multiple juvenile polyps in the stomach & colon
Comps:
More polyps means a higher risk of progressing to carcinoma
Describes which condition?
Juvenile polyposis
Describe the following for Peutz-jeghers syndrome:
What is it & what causes it?
What are the symptoms?
What are the complications?
Patho/cause:
An auto-dominant mutation that causes benign polyp grows throughout the GI & hyperpigmentation of mucosa linings
Signs:
1) Hamartomatous (benign) polyps throughout the Gi tract
2) Mucocutaneous hyperpigmentation on the lips, mouth, & genitals
Comps:
High risk of developing colorectal, breast or gynecological cancers
Patho/cause:
An auto-dominant mutation that causes benign polyp grows throughout the GI & hyperpigmentation of mucosa linings
Signs:
1) Hamartomatous (benign) polyps throughout the Gi tract
2) Mucocutaneous hyperpigmentation on the lips, mouth, & genitals
Comps:
High risk of developing colorectal, breast or gynecological cancers
Describes which condition?
Peutz-jeghers syndrome
Describe the following for Familial adenomatous polyposis (FAP):
What is it?
What causes it?
What is the treatment?
- complication of no treatment?
What are the associated conditions?
Patho:
The formation of 100-1000s colonic adenomatous polyps spreading from the colon to the rectum
Cause:
An auto-dominant inheritance of a mutated APC on chromosome 5 which increases development of adenomatous polyps
Rx:
As prophylaxis remove the colon & rectum
comp of no Rx:
progression to carcinoma by age 40yrs
Ass conds:
Gardner syndrome
Turcot syndrome
Patho:
The formation of 100-1000s colonic adenomatous polyps spreading from the colon to the rectum
Cause:
An auto-dominant inheritance of a mutated APC on chromosome 5 which increases development of adenomatous polyps
Rx:
As prophylaxis remove the colon & rectum
comp of no Rx:
progression to carcinoma by age 40yrs
Ass conds:
Gardner syndrome
Turcot syndrome
Describes which condition?
Familial adenomatous polyposis (FAP)
Describe the following for Gardner syndrome:
What is it?
What are the lab findings?
-histo
Patho:
A mix of FAP with fibromatosis & osteoma formations
Labs(histo):
Fibromatosis (proliferation of fibroblasts in the retroperitoneum which destroys the tissue
&
Benign bone tumors (aka osteomas usually on the skull/hands)
&
desmoid tumors (soft tissue)
Patho:
A mix of FAP with fibromatosis & osteoma formations
Labs(histo):
Fibromatosis (proliferation of fibroblasts in the retroperitoneum which destroys the tissue
&
Benign bone tumors (aka osteomas usually on the skull/hands)
&
desmoid tumors (soft tissue)
Describes which condition?
Gardner syndrome
Describe the following for Turcot syndrome:
What is it?
What are the lab findings?
-histo
Patho:
A mix of FAP with CNS tumors
Labs(histo)
Medulloblastomas/astrocytoma’s
Glial tumors
Patho:
A mix of FAP with CNS tumors
Labs(histo)
Medulloblastomas
Glial tumors
Describes which condition?
Turcot syndrome
Describe the 3 that can be involved in the adeno-carcinoma progression sequence
APC & K-ras mutations both lead to polyp formation
&
P53 mutation with increased expression of COX (turns adenomatous polyps into carcinomas)
What drug interferes with the adeno-carcinoid progression sequence?
Aspirin
Describe the following for colonic polyps:
What are they?
-subtypes?
What are the lab findings?
- screening
Patho:
They’re raised protrusions of the colonic mucosa. The most common types are the hyperplastic & adenomatous types.
Lab (screening):
Colonoscopy
Fecal occult blood
Patho:
They’re raised protrusions of the colonic mucosa. The most common types are the hyperplastic & adenomatous types.
Lab (screening):
Colonoscopy
Fecal occult blood
Describes which condition?
colonic polyps
Hyperplastic polyp type (colonic polyps):
What is it?
What are the lab findings?
- Histology
Patho:
It’s the most common type of that is due to hyperplasia of the glands. The benign polyps appear in the left colon (rectosigmoid)
Labs (Histo):
Glands have a serrated appearance (sawtooth app)
Polyps have nipple app
Patho:
It’s the most common type of that is due to hyperplasia of the glands. The benign polyps appear in the left colon (rectosigmoid)
Labs (Histo):
Glands have a serrated appearance
Describes which condition?
Hyperplastic polyp type (colonic polyps)
Describe the following for adenomatous polyp type (colonic polyps):
What is it?
What are the complications?
Patho:
It is neoplastic proliferation of the glands.
It’s the 2nd most common polyp type that is benign but that is considered premalignant because of its potential to progress to carcinoma via the adeno-carcinoma sequence (APC, K-ras, or P53 (COX) mutations).
Comp:
Progression to adenocarcinoma
Patho:
It is neoplastic proliferation of the glands.
It’s the 2nd most common polyp type that is benign but that is considered premalignant because of its potential to progress to carcinoma via the adeno-carcinoma sequence (APC, K-ras, or P53 (COX) mutations).
Comp:
Progression to adenocarcinoma
Describes which condition?
adenomatous polyp type (colonic polyps)
Describe the following for carcinoid tumors:
What is it
What are the complications?
What are the lab findings?
Patho:
A low grad malignant proliferation of neuroendocrine cells which can arise anywhere (usually the small bowel) & it grows like a submucosal polyp which can secrete serotonin.
Signs:
1) Flushing
2) Diarrhea
3) Tricuspid insufficiency
4) Pulmonary stenosis
Comps:
The serotonin secreted by a carcinoid tumor can bypass liver metabolism & leak into systemic circulation via hepato-systemic shunts resulting in carcinoid syndrome or carcinoid heart disease (fibrotic effects on heart)
Labs:
Elevated Serotonin
Elevated 5HIAA
Carcinoid tumor of TIPS
Tricuspid insuf
Pulmonary stenosis
Patho:
A low grad malignant proliferation of neuroendocrine cells which can arise anywhere (usually the small bowel) & it grows like a submucosal polyp which can secrete serotonin.
Comps:
The serotonin secreted by a carcinoid tumor can bypass liver metabolism & leak into systemic circulation via hepato-systemic shunts resulting in carcinoid syndrome or carcinoid heart disease
Descsribes which condition?
A carcinoid tumor
Describe the following for a carcinoid syndrome:
What is it?
What are the symptoms?
Patho:
When patients with a carcinoid are stressed or alcohol consume excess alcohol the tumor secretes excess serotonin resulting in carcinoid syndrome
Signs:
1) Bronchospasms
2) Diarrhea
3) Flushed skin
4) TIPS
Patho:
When patients with a carcinoid are stressed or alcohol consume excess alcohol the tumor secretes excess serotonin
Signs:
1) Bronchospasms
2) Diarrhea
3) Flushed skin
Describes which condition?
Carcinoid syndrome
Describe the following for carcinoid heart syndrome:
What it it/causes it?
What are the symptoms?
Patho/cause:
Carcinoid tumor secretion eventually leads to fibrosis of the heart tissue
Signs:
1) Right sided valvular fibrosis (increased collagen)
2) Tricuspid regurgitation
3) Pulmonary regurgitation
Patho/cause:
Carcinoid tumor secretion eventually leads to fibrosis of the heart tissue
Signs:
1) Right sided valvular fibrosis (increased collagen)
2) Tricuspid regurgitation
3) Pulmonary regurgitation
Describes which condition?
Carcinoid heart disease
List the symptoms of carcinoid syndrome vs carcinoid heart disease
Carcinoid syndrome:
Bronchospasms
Cyanosis
Diarrhea & cramps
Skin flushing
Hypotension
Pellagra
Telangiectasia
Carcinoid heart disease:
Ascites
Dyspnea
Fatigue
Elevated JVP
Peripheral edema
Plural effusion
Systolic murmur (tricuspid & pulmonary regurg)
Describe the following for volvulus:
What is it?
Where is it?
- elderly vs young adults
Patho:
When the bowel is twisted among its mesentery, resulting in obstruction of the bowel & blocked blood flow causing infarcts
Location:
elderly = sigmoid colon
young adult = cecum
Patho:
When the bowel is twisted among its mesentery, resulting in obstruction of the bowel & blocked blood flow causing infarcts
Location:
elderly = sigmoid colon
young adult = cecum
Describes which condition?
Volvulus
Describe the following for duodenal atresia:
What is it/what causes it?
What are the symptoms?
What is a lab finding?
-xray shows
What is an associated condition?
Patho/cause:
A congenital defect where the duodenum doesn’t canalize during development
Signs:
1) Polyhydramnios
2) Stomach distension
3) Bilious vomiting
Labs(xray):
Shows a blind loop of the duodenum with a double bubble sign.
Ass cond:
Down syndrome
Patho/cause:
A congenital defect where the duodenum doesn’t canalize during development
Signs:
1) Polyhydramnios
2) Stomach distension
3) Bilious vomiting
Labs(xray):
Shows a blind loop of the duodenum with a double bubble sign.
Ass cond:
Down syndrome
Describes which condition?
Duodenal atresia
Describe the following for intussusception:
What is it?
What causes it?
- associated with what?
- children vs adults
What is a complication?
Patho:
When the proximal segment of the bowel “telescopes” (involutes) into the distal segment of the bowel because of the force of peristalsis (basically shortening the bowel) resulting in bowel obstruction & reduced blood flow
Causes:
It is associated with a leading edge in the bowel (aka a point to focus traction that causes peristalsis to push the bowel in on itself)
- Children
(Lymphoid hyperplasia of peyers patches which pulls the ileum into the cecum (via rotavirus or Adenovirus infection))
& - Adults
(Tumor via polyps)
Comp:
Infarct
Patho:
When the proximal segment of the bowel “telescopes” (involutes) into the distal segment of the bowel because of the force of peristalsis (basically shortening the bowel) resulting in bowel obstruction & reduced blood flow
Causes:
It is associated with a leading edge in the bowel (aka a point to focus traction that causes peristalsis to push the bowel in on itself)
- Children
(Lymphoid hyperplasia of peyers patches which pulls the ileum into the cecum (via rotavirus or Adenovirus infection))
& - Adults
(Tumor via polyps)
Comp:
Infarct
Describes which condition?
Intussusception
Describe the following for a small bowel infarct:
What is it?
What causes it?
- artery vs veins
What are the symptoms?
What are the lab findings?
Patho:
Transmural infarct aka reduced blood flow to a section of the small bowel
Causes:
1) Superior Mesenteric artery (thrombosis or embolism)
2) Mesenteric vein (thrombosis)
3) Mitral stenosis (resulting in embolism in SMA/IMA)
Signs:
1) Diffuse Abdominal pain
2) Bloody diarrhea
3) Absent bowel sounds
Labs:
1) Thumbprint sign on barium swallow
2) Neutrophilic leukocytosis
3) Elevated amylase
Patho:
Transmural infarct aka reduced blood flow to a section of the small bowel
Causes:
1) Superior Mesenteric artery (thrombosis or embolism)
2) Mesenteric vein (thrombosis)
3) Mitral stenosis (resulting in embolism in SMA/IMA)
Signs:
1) Diffuse Abdominal pain
2) Bloody diarrhea
3) Absent bowel sounds
Labs:
1) Thumbprint sign on barium swallow
2) Neutrophilic leukocytosis
3) Elevated amylase
Describes which condition?
Small bowel infarct
What do the myenteric (Auerbach) plexus & submucosal (Meissner’s) plexuses each normally regulate?
Myenteric (gut motility)
Submucosal (blood flow, secretions, & absorption)
Describe the following for Hirschsprung disease:
What is it?
What causes it?
What are the symptoms?
What is an associated condition?
Patho:
When there is defective relaxation & peristalsis of the rectum & distal sigmoid colon resulting in massive dilation
Cause:
Congenital failure of neuroendocrine derived ganglion cells to descend to the myenteric & submucosal plexuses during development
Signs:
1) Fail to pass meconium (1st poop)
2) Empty rectal vault
3) Megacolon proximal to the obstruction
Patho:
When there is defective relaxation & peristalsis of the rectum & distal sigmoid colon resulting in massive dilation
Cause:
Congenital failure of neuroendocrine derived ganglion cells to descend to the myenteric & submucosal plexuses during development
Signs:
1) Fail to pass meconium (1st poop)
2) Empty rectal vault
3) Megacolon proximal to the obstruction
Describes which condition?
Hirschsprung disease
How would you treat Hirschsprung disease & why?
Resect the affected bowel because the rest of the bowel (proximal to the disease segment) will have its ganglion & function normally
Describe the following for abetalipoproteinemia:
What is it/ what causes it?
What are the symptoms?
Patho/cause:
An auto-recessive deficiency of apolipoprotein B-49 & B-100
Signs:
1) Malabsorption (B-45 def due to poor chylomicron formation)
2) Absent plasma VLDL & LDL (B-100 def)
Patho/cause:
An auto-recessive deficiency of apolipoprotein B-49 & B-100
Signs:
1) Malabsorption (B-45 def due to poor chylomicron formation)
2) Absent plasma VLDL & LDL (B-100 def)
Describes which condition?
Apolipoproteinemia
Describe the following for Whipple disease:
What is it?
What causes it?
What are the lab findings?
What are the symptoms?
Patho:
Systemic tissue damage in the small bowels lamina propria, or other areas that occurs in response to a t. whippelii infection. Macrophages ingest organism, clog lysosomes, block transfer of chylomicrons from enterocytes to lymph.
Causes:
Happens during a trophyrema whippelii infection.
Labs/histo:
Foamy macrophages filled with glycoprotein-rich granules (PAS +ve)
Signs:
1) Fat malabsorption
2) Steatorrhea
3) Hyperpigmentation
4) Fever
5) Polyarthritis
6) Lymphadenopathy
7) Cardiac valve issues
Patho:
Systemic tissue damage in the small bowels lamina propria, or other areas that occurs in response to a t. whippelii infection. Macrophages ingest organism, clog lysosomes, block transfer of chylomicrons from enterocytes to lymph.
Causes:
Happens during a trophyrema whippelii infection.
Labs/histo:
Foamy macrophages filled with glycoprotein-rich granules (PAS +ve)
Signs:
1) Fat malabsorption
2) Steatorrhea
3) Hyperpigmentation
4) Fever
5) Polyarthritis
6) Lymphadenopathy
7) Cardiac valve issues
Describes which condition?
Whipple disease
Acid fast rods that imitate whipple disease (malabsorption & diarrhea)
Mycobacterium avium intracellulare
Describe the following for Tropical spruce:
What is it?
What causes it?
What are the symptoms?
What is the treatment?
Patho:
Infection causes small bowel villi damage in the jejunum & ileum
Causes:
Post infection with a tropical organism
Signs:
1) Malabsorption (vit B12 & folate deficiencies)
Rx:
Antibiotics
Patho:
Infection causes small bowel villi damage in the jejunum & ileum
Causes:
Post infection with a tropical organism
Signs:
1) Malabsorption (vit B12 & folate deficiencies)
Rx:
Antibiotics
Describes which condition?
Tropical spruce
Describe the following for colorectal cancer:
What is it?
- right vs left
What causes it?
What are the lab findings?
- screening
What is the treatment?
Patho:
The 3rd most common site of cancer, affects the colon/rectal mucosa. It usually peaks in 60-70yr olds.
1) left sided (napkin-ring lesions)
2) right sided (raised lesions)
Causes:
1) Usually from the adenocarcinoma-sequence (progression of polyps into cancer via APC, K-ras, or P53 mutations)
2) Microsatellite deletions resulting in DNA copy mechanism defects
Labs (screening/obs)
Colonoscopy & fecal occult blood (screening)
CEA (tumor marker for recurrence)
Rx:
Surgery (goal catch cancer before symptom onset)
Patho:
The 3rd most common site of cancer, affects the colon/rectal mucosa. It usually peaks in 60-70yr olds.
1) Left sided (napkin-ring lesions)
2) Right sided (raised lesions)
Causes:
1) Usually from the adenocarcinoma-sequence (progression of polyps into cancer via APC, K-ras, or P53 mutations)
2) Microsatellite deletions resulting in DNA copy mechanism defects
Labs (screening/obs)
Colonoscopy & fecal occult blood (screening)
CEA (tumor marker for recurrence)
Rx:
Surgery (goal catch cancer before symptom onset)
Describes which condition?
Colorectal cancer
Describe the differences between right vs left colorectal cancer types:
- Lesion type
- Symptoms
- Complications
Right:
Raised lesions
1) Iron def anemia (older pers always assume C/R cancer unless proven otherwise)
2) Vague pain
3) occult blood
Left:
Napkin-ring lesions
1) decreased stool caliber
2) LLQ pain (colicky)
3) Blood streaked stool
Explain how microsatellite instability can lead to cancer
The repeating sequence of non-coding DNA is normally kept stable during cell division. If it’s not it leads to defect in DNA copy mechanisms (ex DNA mismatch repairs)
How does microsatellite instability cause Hereditary non-polyposis colorectal cancer (HNPCC)?
Microsatellite instability results in defective DNA repair enzymes & increase the overall risk of developing colorectal, ovarian, & endometrial cancers
Describe the tumor staging of a classic case of colorectal cancer:
T
N
M
T (aka depth of invasion) tumors of the mucosal rarely spread because they don’t have direct access to lymph
N if it does spread it spreads to the regional LNs
M if it spreads to a distant site it’s almost always the liver
Describe the following for lactose intolerance:
What is it?
What causes it?
What are the symptoms?
Patho:
A deficiency of lactase enzyme which is needed to break down the lactose in milk into glucose & galactose
Causes:
Congenital (rare auto-recessive)
Acquired (usually in late childhood ME!)
Temporary intolerance post small bowel infection
Signs:
1) Abdominal distension
2) Diarrhea
After drinking milk
Patho:
A deficiency of lactase enzyme which is needed to break down the lactose in milk into glucose & galactose
Causes:
Congenital (rare auto-recessive)
Acquired (usually in late childhood ME!)
Temporary intolerance post small bowel infection
Signs:
1) Abdominal distension
2) Diarrhea
After drinking milk
Describes which condition?
Lactose intolerance
Describe the following for celiacs disease:
What is it?
What causes it?
- associated with which genotype?
What are the symptoms?
What are the lab findings?
What are the complications?
What is the treatment?
Patho:
An immune mediated attack against the villi of the small bowel when it’s exposed to gluten. Though most celiac patients have IgA deficiency the IgA’s are formed when exposed to gluten & are targeted against their own endomysium & transglutaminase deaminase as well as the gliadin from gluten resulting in flattening villi.
Causes:
associated with the HLA-DQ2 & DQ8 genotypes
Signs:
Kids
1) Abdominal distension
2) Diarrhea
2) Failure to thrive
Adults
1) Chronic diarrhea
2) Bloating
3) Dermatitis herpetiformis (IgAs in the tips of dermal papillae cause lesions)
Labs:
Duodenal biopsy shows
1) Flattened villi
2) Hyperplastic crypts
3) Elevated intraepithelial lymphocytes
IgAs vs endomysium, tTG, & gliadin (exp to gluten)
Elevated IgG (there’s usually IgA def)
Comp:
Small bowel cancer
Tcell lymphoma
Rx: Gluten free diet
Patho:
An immune mediated attack against the villi of the small bowel when it’s exposed to gluten. Though most celiac patients have IgA deficiency the IgA’s are formed when exposed to gluten & are targeted against their own endomysium & transglutaminase deaminase as well as the gliadin from gluten resulting in flattening villi.
Causes:
associated with the HLA-DQ2 & DQ8 genotypes
Signs:
Kids
1) Abdominal distension
2) Diarrhea
2) Failure to thrive
Adults
1) Chronic diarrhea
2) Bloating
3) Dermatitis herpetiformis (IgAs in the tips of dermal papillae cause lesions)
Labs:
Duodenal biopsy shows
1) Flattened villi
2) Hyperplastic crypts
3) Elevated intraepithelial lymphocytes
IgAs vs endomysium, tTG, & gliadin (exp to gluten)
Elevated IgG (there’s usually IgA def)
Comp:
Small bowel cancer
Tcell lymphoma
Rx: Gluten free diet
Describes which condition?
Celiac disease
Patho:
Chronic & relapsing inflammation of the bowel that usually occurs in young women. The subclasses are ulcerative colitis & Chron’s disease
Location:
Splenic flexure (because it’s a watershed area between the SMA & IMA putting it at risk of atherosclerosis)
Causes:
An abnormal immune response to the enteric flora
White & eastern European jews are at high risk
Signs:
1) Recurrent bouts of bloody diarrhea
2) Abdominal pain
Describes which condition?
Irritable bowel disease
Describe the following for acute appendicitis:
What is it?/What causes it?
-adults vs kids
What are the symptoms?
What are the complications?
Patho/causes:
inflammation of the pancreases due to
1) adults (obstruction from a fecalith)
2) kids (destruction from lymphoid hyperplasia due to viral inf)
Signs:
1) periumbilical pain
2) pain that localizes to RLQ (McBurneys)
3) Fever
4) Nausea
Comps:
Rupture can result in peritonitis (guard with rebound)
Peri appendiceal abscess (common)
Patho/causes:
inflammation of the pancreases due to
1) adults (obstruction from a fecalith()
2) kids (destruction from lymphoid hyperplasia)
Signs:
1) periumbilical pain
2) pain that localizes to RLQ (McBurneys)
3) Fever
4) Nausea
Comps:
Rupture can result in peritonitis (guard with rebound)
Peri appendiceal abscess (common)
Describes which condition?
Acute appendicitis
Describe the following for irritable bowel disease:
What is it?/What causes it?
What are the symptoms?
What is the treatment?
Patho/cause:
Relapsing bouts of abdominal pain that feels better after pooping. It’s likely due to disturbed intestinal motility ( usually seen in middle aged women)
Signs:
1) Abdominal pain
2) Flatulence
3) Change in bowel habits (i.e diarrhea or constipation)
Rx dietary fiber
Patho/cause:
Relapsing bouts of abdominal pain that feels better after pooping. It’s likely due to disturbed intestinal motility ( usually seen in middle aged women)
Signs:
1) Abdominal pain
2) Flatulence
3) Change in bowel habits (i.e diarrhea or constipation)
Rx dietary fiber
Describes which condition?
Irritable bowel syndrome
Describe the following for Ischemic colitis:
What is it?
What causes it?
What are the symptoms?
What is a complication?
Patho:
Ischemic damage to the colon usually at the splenic flexure (because it’s a watershed area of the SMA) as a result of low blood flow
Causes:
#1 Atherosclerosis of the SMA
Signs:
1) Postprandial pain (post food)
2) Weight loss
3) pain & bloody diarrhea (Infarct sign)
Comp:
Infarction
Patho:
Ischemic damage to the colon usually at the splenic flexure (because it’s a watershed area of the SMA) as a result of low blood flow
Causes:
#1 Atherosclerosis of the SMA
Signs:
1) Postprandial pain (post food)
2) Weight loss
3) pain & bloody diarrhea (Infarct sign)
Comp:
Infarction
Describes which condition?
Ischemic colitis
Describe the following for Hereditary hemorrhagic telangiectasia:
What is it/What causes it?
What are the symptoms?
Patho/causes:
An auto-dominant disorder resulting in thin-walled blood vessels in the mouth & Gi tract
Signs:
1) Rupture (bleeding)
Patho/causes:
An auto-dominant disorder resulting in thin-walled blood vessels in the mouth & Gi tract
Signs:
1) Rupture (bleeding)
Describes which condition?
Hereditary hemorrhagic telangiectasia
Describe the following for ulcerative colitis:
What is it?
What protects against it?
What are the symptoms?
What are the lab findings?
What are the complications?
Patho:
Ulcers in the mucosa & submucosa of the rectum & cecum
Protective:
Smoking
Signs:
1) LLQ pain
2) Bloody diarrhea
3) Arthritis
4) Uvetis
5) Erythema nodosum
6) Pyoderma gangrenosum
7) Primary sclerosing cholangitis
Labs:
Histo shows
1) crypt abscesses with neutrophils
2) psuedopolyps
3) loss of haustra (lead pipe sign)
4) P-ANCA +ve
5) HLA B27 +ve ankylosing spondylitis
Comp:
Toxic megacolon & carcinoma (if the disease progresses over 10 years)
Patho:
Ulcers in the mucosa & submucosa of the rectum & cecum
Protective:
Smoking
Signs:
1) LLQ pain
2) Bloody diarrhea
3) Arthritis
4) Uvetis
5) Erythema nodosum
6) Pyoderma gangrenosum
7) Primary sclerosing cholangitis
Labs:
Histo shows
1) crypt abscesses with neutrophils
2) psuedopolyps
3) loss of haustra (lead pipe sign)
4) P-ANCA +ve
5) HLA B27 +ve ankylosing spondylitis
Comp:
Toxic megacolon & carcinoma (if the disease progresses over 10 years)
Describes which condition?
Ulcerative colitis
Describe the following for Chron’s disease:
What is it?
What causes it?
-risk
What are the symptoms?
What are the lab findings?
What are the complications?
Patho:
Full thickness inflammation of the mucosa with knife like fissures anywhere from the mouth to the anus (ileum is the most common)
Cause/risk:
Smoking
Signs:
1) RLQ pain
2) Non-bloody diarrhea
3) arthritis
4) erythema nodosum
5) pyoderma gangrenosum
6) primary sclerosing cholangitis
Labs:
Histo shows
1) Lymphoid aggregates with granulomas (40% cases)
Cobblestone mucosa
Creeping fat
Strictures (string sign)
P-ANCA +ve
Comps:
Malabsorption & Nutritional deficiency
Calcium oxalate nephrolithiasis
Fistula
Carcinoma
Patho:
Full thickness inflammation of the mucosa with knife like fissures anywhere from the mouth to the anus (ileum is the most common)
Cause/risk:
Smoking
Signs:
1) RLQ pain
2) Non-bloody diarrhea
3) arthritis
4) erythema nodosum
5) pyoderma gangrenosum
6) primary sclerosing cholangitis
Labs:
Histo shows
1) Lymphoid aggregates with granulomas (40% cases)
Cobblestone mucosa
Creeping fat
Strictures (string sign)
P-ANCA +ve
Comps:
Malabsorption & Nutritional deficiency
Calcium oxalate nephrolithiasis
Fistula
Carcinoma
Describes which condition?
Chron’s disease
Describe the following for angiodysplasia:
What is it?
What are the symptoms?
Patho:
An acquired malformation of the mucosal & submucosal capillary beds usually in the cecum or right colon because of the higher wall tension
Signs:
1) Hematochezia (rupture aka bleeding rectum typically in older adults)
Patho:
An acquired malformation of the mucosal & submucosal capillary beds usually in the cecum or right colon because of the higher wall tension
Signs:
1) Hematochezia (rupture aka bleeding rectum typically in older adults)
angiodysplasia
Describe the following for colonic diverticulum:
What is it?
What causes it?
What are the complications
Patho:
Outpouching og the mucosa & submucosal layers through the muscularis propria (false diverticulum) usually in the vasa recta transverse muscular propria because it is the walls weakest point
Causes:
It’s associated with wall stress
Adults
1) constipation
2) straining
3) low-fiber diet
4) older age (sigmoid colon most at risk)
Comps:
Hematochezia (rectal bleeding)
Diverticulitis (LLQ pain mimics appendicitis)
Fistula (the inflamed diverticulum ruptures & reattached to the nearest structure i.e colovesicular fistula where urine has poop & air in it)
Patho:
Outpouching og the mucosa & submucosal layers through the muscularis propria (false diverticulum) usually in the vasa recta transverse muscular propria because it is the walls weakest point
Causes:
It’s associated with wall stress
Adults
1) constipation
2) straining
3) low-fiber diet
4) older age (sigmoid colon most at risk)
Comps:
Hematochezia (rectal bleeding)
Diverticulitis (LLQ pain mimics appendicitis)
Fistula (the inflamed diverticulum ruptures & reattached to the nearest structure i.e colovesicular fistula where urine has poop & air in it)
Describes which condition?
Colonic Diverticulum
Undercooked beef can lead to infection with ETEK,EHEK, or shigella all of which result in which condition?
Hemolytic uremic syndrome look for schistocytes & helmet cells of smear
antibiotics like ampicillin or clindamycin can cause diarrhea because of what?
Loss of normal gut flora leading to an overgrowth of C. difficile causing pseudomembranous colitis
Single acid fast oocytes that cause diarrhea?
- What are they
- What condition are they associated with?
- What is the diagnostic test?
Cryptosporidium parvum
Ass with AIDS
Diagnostic string test
Paired acid fast oocysts that cause diarrhea
Isospora belli
Desentry with flask shaped ulcers in the cecum are due to which pathogen? & what is a histological liver finding you can expect?
Entamoeba histolytica
Anchovy sauce appearance
What are the differentials for Chrons vs Ulcerative colitis
Chrons:
Sharp demarcations
Transmural (all layers)
Mouth to ass skip lesions (ileum**)
Non caseating granulomas
Fistulas
Cobblestone app (creeping fat)
Ulcerative colitis:
Megacolon
Rectum & left colon usually
Bloody diarrhea
Wet & glaring mucosa
Risk of adenocarcinoma
RLQ pain
Recurrent non-bloody diarrhea
Fever
Chrons
Primary biliary cirrhosis predisposes what condition?
Ulcerative colitis
Tubular vs villous adenomas
Tubular:
Sigmoid
ass as a precursor to colon cancer
Villous:
Velvety/flat
Hypoproteinemia/Hypokalemia
Over bleeding
Highest malignancy risk
Right vs left colon cancer differentials
Right:
Polypoid tumors
Blood in stool
Iron def
Left:
Annular & napkin ring app
Constipation or diarrhea with/wo blood
What is the most common cause of Gi occlusion?
Improper cleaning during surgery resulting in bowel adhesions
Liver failure leads to these symptoms:
Palmar erythema
Spider angiomas
Gynecomastia
Hypogonadism
Because of the livers inability to metabolize which horome?
Estrogen (hyperestronism)
How does Portal hypertension lead to hyperaldosteronism?
Portal HTN is due to liver failure which means the liver isn’t producing proteins like albumin.
This causes hypoalbuminemia (reduced oncotic pressure) which tricks the kidneys into thinking there’s low BP thus activating RAAS (up renin & aldosterone)
Which bilirubin form is water or fat soluble?
Conjugated = water soluble
can’t cross BBB but can enter bile
Unconjugated = fat soluble
Can cross BBB (Kernicterus)
