Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
152 Cards in this Set
- Front
- Back
|
What is cleft lip and palate? |
Full-thickness defect of lip and palate. Due to failure of the facial prominences/processes to fuse.
|
|
|
Cleft lip and palate usually occur _________ (in isolation/together).
|
together
|
|
|
What is the most common congenital abnormality of the oral cavity?
|
Cleft lip and palate
|
|
|
What is an aphthous ulcer?
|
Painful, superficial ulceration of oral mucosa. Arises in relation to stress and resolves spontaneously, can recur.
|
|
|
Aphtous ulcer is characterized by a ________ base surrounded by __________.
|
grayish base (granulation tissue); erythema
|
|
|
What is a derivative syndrome involving aphtous ulcers? Describe it.
|
Behcet syndrome.
(1) Recurrent aphthous ulcers, genital ulcers and uveitis (2) IC vasculitis involving small vessels (3) Can be seen after viral infection. Etiology is unknown. |
|
|
What is oral herpes? What is it usually due to?
|
When you have vesicles involving the oral mucosa that rupture, resulting in shallow, painful, red ulcers. Usually due to HSV-1.
|
|
|
Primary infection with oral herpes occurs in ___________ (childhood/adulthood).
|
childhood
|
|
|
In oral herpes in childhood, the lesions heal but the virus remains dormant in _______________.
|
the ganglia of the trigeminal nerve
|
|
|
What can cause reactivation of herpes virus?
|
(1) Stress
(2) Sunlight |
|
|
Reactivation of a herpesvirus leads to what?
|
Leads to vesicles that often arise on lips and these are called cold sores.
|
|
|
Tobacco and alcohol are major risk factors for this cancer in the oral mucosa, what is it?
|
Squamous cell carcinoma
|
|
|
Where do SCC usually occur in the oral cavity?
|
Floor of the mouth
|
|
|
Often before getting squamous cell carcinoma of the oral cavity you can get _________.
|
dysplasia in the form of leukoplakia and erythroplakia
|
|
|
Leukoplakia has a ___% rate of progression to oral cancer while erythroplakia has a ___% rate of progression to oral cancer.
|
30;60
|
|
What would you do if you saw this?
|
Biopsy to rule out squamous cell carcinoma.
|
|
|
A man comes in with a white plaque on his tongue. You take a tongue scraper and try to scrape it off, and it comes off. What is this most likely?
|
Oral candidiasis. Leukoplakia you would not be able to scrape off.
|
|
|
What is hairy leukoplakia?
|
A "shaggy" leukoplakia of the lateral aspect of the tongue. Due to EBV. Associated with an immunocompromised state.
|
|
|
Hairy leukoplakia represents ______________ (hyperplasia/dysplasia) of the squamous mucosa.
|
hyperplasia
|
|
|
What do erythroplakia mean to you in terms of malignancy?
|
It means you have a vascularized leukoplakia (would suggest angiogenesis)
|
|
|
What three major salivary glands are there?
|
(1) Parotid
(2) Submandibular (3) Sublingual |
|
|
How many minor salivary glands do we have?
|
Thousands
|
|
|
Mumps virus classically infects the ___________ resulting in a ______________.
|
parotid glands; bilaterally inflamed parotid glands
|
|
|
What else outside the parotid gland can the mumps virus infect?
|
(1) Testicles (orchitis)
(2) Pancreas (pancreatitis) (3) Meninges (aseptic meningitis) |
|
|
This is a feared complication of mumps.
|
Sterility (teenagers)
|
|
|
Patients less than 10 yo __________ (do/do not) get orchitis while patients greater than 10 yo (do/do not).
|
do not; do
|
|
|
What would an increased serum amylase in a patient with mumps infection suggest to you?
|
Infection of salivary glands or pancreas (or both?)
|
|
|
What type of pathogen is mumps?
|
Paramyxovirus
|
|
|
Most cases of orchitis in context of mumps is _____________ (unilateral/bilateral).
|
unilateral
|
|
|
What is sialadenitis?
|
Inflammation of salivary gland
|
|
|
What is sialadenitis usually due to?
|
Most commonly due to obstructing stone (sialolithiasis) leading to S. aureus infection
|
|
|
Sialadenitis is usually ___________ (unilateral/bilateral).
|
unilateral
|
|
|
Principle: Any time you block a tube, you are gonna get ___________.
|
infection behind that block
|
|
|
This is the most common tumor of salivary glands. What is it? Describe.
|
Pleomorphic (multiple types of tissue) adenoma.
Benign tumor composed of stromal (e.g., cartilage) and epithelial tissue (e.g., glands). |
|
|
Pleomorphic adenoma usually arises in the __________.
|
parotid
|
|
|
A tumor composed of both stroma and epithelium we call that a __________ tumor.
|
biphasic
|
|
|
How does a pleomorphic adenoma present as?
|
Mobile, painless, circumscribed mass at angle of jaw.
|
|
|
Why is a pleomorphic adenoma painless?
|
It hasn't invaded the facial nerve which run through the parotid gland. Benign tumors don't invade and infiltrate.
|
|
|
A pleomorphic adenoma has a high rate of __________. Why?
|
recurrence
Extension of small islands of tumor through tumor capsule often results in incomplete resection (irregular margin). |
|
|
True or false: Pleomorphic can transform into carcinoma.
|
True, but rarely. It presents with signs of facial nerve damage.
|
|
|
A patient has had a mass in his parotid gland for 12 years. He claims it was always painless, but lately his face has started to ache. What might be going on?
|
Transformation of pleomorphic adenoma to carcinoma involving facial nerve.
|
|
|
What is the second most common tumor of salivary glands? Describe it.
|
Warthin tumor
Benign cystic tumor with abundant lymphocytes and germinal centers. Almost always arises in the parotid. |
|
|
Warthin tumor is basically a cystic tumor with _________ tissue.
|
lymph node
|
|
|
Why does Warthin tumor almost always arise in the parotid?
|
It is not uncommon embryologically for lymph node tissue to be associated with the parotid. This gland is the last gland to separate itself from adjacent stroma embryologically.
|
|
|
A mucus carcinoma of salivary gland. What is its name? Describe it.
|
Mucoepidermoid carcinoma.
Malignant tumor comprised of mucinous and squamous cells. Usually arises in the parotid; commonly involves facial nerve. |
|
|
What is a TE fistula?
|
Tracheoesophageal fistula. A fistula is an abnormal connection between two tubes. It's a congenital defect.
|
|
|
What is the most common variant of a TE fistula?
|
|
|
|
How would a baby with TE fistula present?
|
(1) Regurgitation of food
(2) Polyhydramnios (can't swallow) (3) Abdominal distention (4) Aspiration |
|
What is this?
|
TE fistula
|
|
|
What is an esophageal web?
|
Mucosal protrusion. Most often in upper esophagus.
|
|
|
How does esophageal webs present?
|
(1) Dysphagia for poorly chewed foods
|
|
|
Patients with esophageal webs have an increased risk for what?
|
(1) Esophageal squamous cell carcinoma
|
|
|
Chronic iron deficiency can lead to what syndrome? Describe it.
|
Plummer-Vinson syndrome.
(1) Severe iron deficiency anemia (2) Esophageal web (3) Beefy-red tongue due to atrophic glossitis |
|
|
What is a Zenker diverticulum?
|
Outpouching of pharyngeal mucosa through acquired defect in the muscular wall.
|
|
|
Where does a Zenkers diverticulum usually arise?
|
Arises above upper esophageal sphincter at junction between esophagus and pharynx. Due to abnormal pressure in the pharynx when swallowing.
|
|
|
How does Zenker diverticulum present?
|
(1) Dysphagia
(2) Obstruction (3) Halitosis |
|
|
Zenker diverticulum is known as a ___________ (true/false) diverticulum.
|
False. It means you protruded only one part of the wall through the defect. Most diverticuli in GI tract are false.
|
|
|
What is Mallory-Weiss syndrome?
|
Longitudinal laceration of mucosa at GE junction.
|
|
|
What is Mallory-Weiss syndrome usually caused by?
|
(1) Severe vomiting (Bulimia)
(2) Alcohol |
|
|
How does Mallory-Weiss syndrome present clinically?
|
(1) Painful hematemesis
|
|
|
A patient with Mallory-Weiss syndrome is at risk for what?
|
Boerhaave syndrome.
|
|
|
What could be seen in Boerhaave syndrome?
|
Subcutaneous emphysema. Air bubbles are beneath the skin, especially in the region of the neck. Pushing in them makes a crackling sound.
|
|
|
What are esophageal varices?
|
Dilated submucosal veins in lower esophagus.
|
|
|
Esophageal varices can arise secondary due to ______________.
|
portal HTN
|
|
|
There are two ways by which the vv. of the esophagus drain, explain.
|
Most esophageal blood actually drains via the azygos vein into the superior vena cava. However there is some blood that drains via the left gastric vein into the portal vein.
|
|
|
How does esophageal varices present?
|
It is asymptomatic, but risk of rupture is present, which would create a painless hematemesis (contrast with Mallory-Weiss which is painful).
|
|
|
MCC of death in patients with cirrhosis?
|
Rupture of esophageal varices. Since it's seen in context of cirrhosis, a coagulopathy often complicates the situation.
|
|
|
What is achalasia?
|
Disordered esophageal motility with inability to relax LES. Due to dmg-ed ganglion cells in the myenteric plexus.
|
|
|
How does the damage to ganglion cells in achalasia occur?
|
Damage can be idiopathic or secondary to known insult (e.g., Chagas disease).
|
|
|
What are clinical features of achalasia?
|
(1) Disordered motility leads to dysphagia for both solids and liquids.
(2) Putrid breath (3) 'Bird beak' sign (4) Increased risk for esophageal squamous cell carcinoma (5) High LES pressure on esophageal manometry |
|
|
What sign can be seen in achalasia with imaging?
|
Bird beak sign.
|
|
What disease is this?
|
This is a bird-beak sign. It is achalasia.
|
|
|
What is GERD?
|
Gastroesophageal reflux disease. Reflux of acid from stomach due to low LES tone.
|
|
|
Risk factors for GERD?
|
(1) Alcohol
(2) Tobacco (3) Obesity (4) Caffeine (5) Hiatal hernia (6) Fat-rich diet |
|
|
Describe the normal histologic layers of the GI tract.
|
|
|
|
What is the MC type of hiatal hernia?
|
Sliding type. Paraesophageal is much less common.
|
|
|
A child has bowel sounds in the lung fields. What might be going on?
|
Paraesophageal herniation
|
|
|
Clinical features of hiatal hernia?
|
Based on the fact that you are shooting acid into the esophagus.
(1) Heartburn (mimics cardiac chest pain) (2) Asthma and cough (3) Damage to enamel of teeth (4) Ulceration with stricture (5) Barret esophagus |
|
|
What would you consider in your differential if you saw new-onset asthma in an adult?
|
Hiatal hernia with constant acid reflux. It may cause adult-onset asthma.
|
|
|
What happens in an ulceration?
|
You are knocking out the mucosa. This means you remove the stem cells so it heals by fibrosis (stricture e.g. in esophagus).
|
|
|
How is esophageal carcinoma divided?
|
(1) Adenocarcinoma
(2) Squamous cell carcinoma |
|
|
Adenocarcinoma is a malignant proliferation of _________.
|
glands (kjertel)
|
|
|
What is the most common type of esophageal carcinoma in the west?
|
Adenocarcinoma
|
|
|
Barret esophagus arises in the _____________ (middle/lower) 1/3 of the esophagus.
|
lower
|
|
|
What is the most common esophageal cancer worldwide?
|
Squamous cell carcinoma
|
|
|
Where does squamous cell carcinoma of the esophagus usually arise?
|
Usually arises in the upper or middle third of the esophagus.
|
|
|
Risk factors for squamous cell carcinoma of the esophagus?
|
Summed up in one word: Irritation
(1) Alcohol & tobacco (2) Very hot tea (3) Achalasia (rotting food irritates) (4) Esophageal web (5) Esophageal injury (e.g., lye ingestion) |
|
|
A 54 year old chinese man from southern china has lately lost a lot of weight unexplained by his lifestyle. He has trouble swallowing solid foods. What risk factor may have lead to his underlying condition?
|
Drinking very hot tea regularly, this is possibly squamous cell carcinoma of the esophagus
|
|
|
Esophageal carcinoma generally presents at what point in its course?
|
Late
|
|
|
How does esophageal carcinoma present?
|
(1) Progressive dysphagia (first solids, then liquids)
(2) Weight loss (3) Pain (4) Hematemesis (5) Hoarse voice (recurrent laryngeal n.) (6) Cough (trachea) (5) and (6) are due to invasion. |
|
|
Esophageal carcinoma first spreads to _________ then to _________ and _________.
|
lymph nodes; lungs; liver
|
|
|
There are differences in lymph node spread based on where the cancer arises in the esophagus. Explain.
|
Upper 1/3 – cervical spread
Middle 1/3 – mediastinal or tracheobronchial nodes Lower 1/3 – celiac and gastric nodes |
|
|
What is gastroschisis?
|
Schisis means to split. It refers to a split stomach. Congenital malformation of the abdominal wall. Exposes contents
|
|
|
What is an omphalocele?
|
Persistent herniation of bowel into umbilical cord. Due to failure of herniated intestine to return to body cavity during development.
|
|
What is this?
|
Omphalocele. contents are covered by peritoneum and amnion of umbilical cord.
|
|
|
What is pyloric stenosis?
|
Congenital hypertrophy of pyloric SMC.
|
|
|
Pyloric stenosis is most common in ___________ (females/males).
|
males
|
|
|
True or false: Pyloric stenosis presents at birth.
|
False. There is no pyloric stenosis right after birth, it presents about 2 weeks after birth.
|
|
|
How will infants with pyloric stenosis present?
|
(1) Food is not gonna pass through the pylorus. Pressure builds up until projectile vomiting happens. It is nonbilious.
(2) There is a lot of peristalsis against the pyloric block, and that peristalsis can actually be seen on the stomach of the infant. |
|
|
On physical exam of a baby with pyloric stenosis you could observe what?
|
You can feel the pyloric stenosis as an olive-like mass.
|
|
|
Treatment of pyloric stenosis?
|
Myotomy
|
|
|
What is acute gastritis.
|
Acidic damage to mucosa.
|
|
|
What types of gastritis are there? Explain how they occur.
|
(1) Acute gastritis
- A story of burning of the stomach by acid. - ↑ acid or decreased protection (2) Chronic gastritis - Subdivided into chronic autoimmune gastritis, chronic H. pylori gastritis |
|
What is this?
|
Pyloric stenosis
|
|
|
Epithelial cells lining the stomach and producing mucus are also known as ________ cells.
|
foveolar
|
|
|
What are important defences of the stomach against damage by acid?
|
(1) Mucus and bicarbonate secretion
(2) Normal blood supply Remember prostaglandins role: increased secretion and increased blood flow. |
|
|
Risk factors of acute gastritis?
|
Blood supply is insufficient:
- Severe burn causes hypovolemia (Curling ulcers in stomach) - Shock --> severe decreased in flow to vital organs --> multiple stress ulcers - NSAIDs Damage to mucosa: - Heavy alcohol consumption - Chemotherapy (knock out cells that turn over) - Increased intracranial pressure (Cushing ulcer) because of increased vagal stimulation --> Acetylcholine --> Acid production |
|
|
Acidic damage resulting in acute gastritis is gonna result in what?
|
(1) Superficial inflammation
(2) Erosion (3) Ulcer |
|
|
Erosion is loss of _________, ulceration is loss of _________.
|
epithelium; mucosa
|
|
|
Mnemonic. AB-pairing. What does it mean?
|
Autoimmune in the Body
Bacteria in the Antrum |
|
|
What happens in chronic autoimmune gastritis?
|
Autoimmune destruction of gastric parietal cells (body and fundus [AB pairing; autoimmune - body]). T-cell mediated (type IV hypersensitivity), and as a CONSEQUENCE of this you get antibodies in the blood vs proton pump or intrinsic factor. Thickness of mucosa is reduced and we get atrophy of mucosa.
|
|
|
Are antibodies in chronic autoimmune gastritis the cause of side effect of any damage caused?
|
Side effect
|
|
|
Clinical features of chronic autoimmune gastritis?
|
(1) Lack of intrinsic factor with megaloblastic (pernicious) anemia.
(2) Achlorhydria with increased gastrin and G-cell hyperplasia (3) Atrophy of mucosa |
|
|
This is the MCC of vitamin B12 deficiency.
|
Pernicious anemia
|
|
|
Patients with chronic autoimmune gastritis are at increased risk for what? And why?
|
Gastric adenocarcinoma.
Chronic inflammation is gonna induce intestinal metaplasia (we have Peyer's patches there; cells in stomach start to 'act' like cells in the intestine) |
|
|
A mass may arise as a complication of chronic gastritis and achlorhydria. What may be seen?
|
(1) Hyperplastic polyp
- Most common type (Hamartoma vviih no malignant potential) (2) Adenomatous polyp - Neoplastic polyp (Potential for malignant transformation) |
|
|
What is the most common form of chronic gastritis?
|
H. pylori chronic gastritis (90%).
|
|
|
How can H.pylori induce acute and chronic inflammation of the stomach?
|
H. pylori ureases and proteases and inflammation weakens mucosal defences. It can also lower the amount of somatostatin producing cells somehow.
|
|
|
Where do H. pylori like to hang out in the stomach?
|
Most common site is antrum (AB-pairing; Bacteria in Antrum)
|
|
|
Presentation of patients with H. pylori chronic gastritis?
|
(1) Epigastric abdominal pain
(2) Increased risk for ulceration, gastric adenocarcinoma, and MALT lymphoma. |
|
|
Why and how is there a risk for MALT lymphoma in chronic H. pylori gastritis?
|
Chronic inflammation creates germinal centers. This creates post-germinal center B-cells (marginal zone).
|
|
|
Memory help: Compare complications of chronic H. pylori gastritis with treatment of this disease.
|
Three complications and three treatments.
Ulceration, epigastric pain and lymphoma and something called TRIPLE therapy (PPI combined with metronidazole/amoxicillin plus clarithromycin). |
|
|
How could you confirm eradication of H. pylori from the stomach?
|
Negative urea breath test and lack of stool antigen confirm eradication of H. pylori.
|
|
|
What is peptic ulcer disease?
|
Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%).
|
|
|
Duodenal ulcer is almost always due to what?
|
H. pylori
|
|
|
Duodenal ulcer may rarely be due to?
|
Zollinger Ellison syndrome.
|
|
|
Investigation shows ulcers in the jejunal mucosa. What should you consider?
|
Zollinger ellison. This is characteristic for this cancer.
|
|
|
With duodenal ulcers, pain ____________ (worsens/improves) with meals.
|
improves (because it prepares itself for potential receiving of acidic stomach contents)
|
|
|
How could you absolutely confirm that you have an ulcer in the duodenum?
|
Endoscopic biopsy. It would show ulcer with hypertrophy of Brunner glands.
|
|
|
Complications of duodenal ulcer?
|
(1) Rupture
- Leads to bleeding from gastroduodenal artery or acute pancreatitis (posterior ulcers) |
|
|
Most common site for duodenal ruptures to occur?
|
anterior wall
|
|
|
What is a gastric ulcer usually due to? Other causes?
|
H. pylori. Other causes include NSAIDs and bile reflux.
|
|
|
How does gastric ulcers present?
|
With epigastric pain that worsens with meals.
|
|
|
If you were to have a gastric ulcer, where would it usually be located?
|
Along the lesser curvature of the stomach (antrum)
|
|
|
Rupture of gastric ulcer carries the risk of what?
|
Left gastric artery bleeds
|
|
|
What is a differential diagnosis when you have ulcers of the GI tract (stomach)?
|
Cancer.
Gastric ulcers could be caused by gastric carcinoma while duodenal ulcers are almost never malignant. |
|
|
How could you tell if a gastric ulcer was benign or malignant by looking at it through an endoscope?
|
Benign ulcer: Small, looks punched out, margins are flat and normal
Malignant ulcer: Looks irregular, larger, piling up of mucosa at edge of ulcer. However, biopsy is needed to confirm. |
|
|
What is a gastric carcinoma?
|
Malignant proliferation of surface epithelial cells (adenocarcinoma because they are columnar cells)
|
|
|
How is gastric carcinoma divided?
|
(1) Intestinal type
(2) Diffuse type |
|
|
How does the intestinal type of gastric carcinoma present on endoscopy?
|
Large, irregular ulcer with heaped up margins.
|
|
|
Intestinal type of gastric carcinoma usually involves what part of the stomach?
|
Lesser curvature of stomach. Also where gastric ulcers in peptic ulcer appear.
|
|
|
Risk factors for the intestinal type for gastric carcinoma?
|
(1) Intestinal metaplasia (chronic autoimmune gastritis/chronic H. pylori gastritis)
(2) Nitrosamines in smoked foods (3) Blood type A |
|
|
What could help you remember that blood type A is a risk factor for gastric carcinoma?
|
Gastric carcinoma = Gastric cA = A
|
|
|
What is the most common type of stomach cancer?
|
Intestinal type of gastric carcinoma.
|
|
|
Describe the diffuse type of gastric carcinoma.
|
Signet ring cells that diffusely infiltrate gastric wall. This results in a reaction to the cancer called desmoplasia (fibrous tissue and blood vessels). Stomach wall thickens resulting in linitis plastica.
|
|
|
Diffuse type of gastric carcinoma is NOT associated with these risk factors [...]
|
(1) H. pylori
(2) Nitrosamines (3) Intestinal metaplasia |
|
|
Gastric carcinoma usually presents ___________ (early/late).
|
late
|
|
|
Classic signs of gastric carcinoma?
|
(1) Weight loss
(2) Abdominal pain (3) Anemia (4) Early satiety (classic in diffuse type) |
|
|
These signs are rarely associated with gastric carcinoma.
|
Thought to be paraneoplastic syndromes.
Acanthosis nigricans (thickening/darkening of skin, particularly in axillary region) Leser-Trélat sign (patient gets dousins of seborrheic keratoses over their bodies) |
|
|
Gastric carcinoma will spread to where?
|
Lymph nodes.
Often spreads to left supraclavicular node called Virchow's node. |
|
|
Distant metastasis of gastric carcinoma usually involves what?
|
Most commonly the liver.
Also: (1) Periumbilical region (Sister Mary Joseph nodule); seen with intestinal type (2) Bilateral ovaries (Kruckenberg tumor); seen with diffuse type |
|
|
A underweight woman with early satiety and fatigue has a bilateral adnexal mass on palpation. What type of gastric carcinoma could it be?
|
Diffuse type
|
