Topics B43-48 Lips, Oral cavity, Pharynx, Salivary Glands, Esophagus, Stomach Flashcards
2 infections/inflammations of the lips?
- Aphthous Ulcers (Canker Sores): painful, recurrent, unclear etiology, more common in first 2 decades of life
- Herpes Simplex Virus: HSV1 is more typical, while HSV-2 (genital herpes) is becoming more common. Majority of adults have latent HSV-1. Reactivation is called “cold sore.” May also appear in nasal orifice, buccal mucosa, gingiva, and hard palate
3 infections/inflammations of the lips
- Aphthous Ulcers (Canker Sores): painful, recurrent, unclear etiology, more common in first 2 decades of life
- Herpes Simplex Virus: HSV1 (labial herpes) is more typical, while HSV-2 (genital herpes) is increasingly common too. Majority of adults have latent HSV-1. Reactivation is called “cold sore.” May also appear in nasal orifice, buccal mucosa, gingiva, and hard palate
- Stomatitis: inflammation of mouth and lips (general term)
4 infections or non-infectious inflammations of the oral cavity that are NOT related to AIDS
- Tonsillitis: generally viral (adenovirus, rhinovirus, influenza) or S. pyogenes infection
- Ulcerative Necrotizing Gingivitis: massive necrotizing hemorrhagic inflammation. Used to be caused by agranulocytosis; now more commonly from cytostatic anti-cancer drugs + mixed bacteria -> necrotizing inflammation
- Pemphigus: autoimmune disease with anti-desmosome antibodies, affects skin and mucous membranes
- Dental caries from S. mutans producing acid from sucrose metabolism
3 infections of the oral cavity that ARE related to AIDS or other conditions of immuno-suppression
- Candida albicans: responsible for oral thrush - pseudomembrane on mucosa of buccal region, tongue. Oral candidiasis can also be erythematous or hyperplastic.
- Hairy leukoplakia: keratinizing of mucosa due to EBV infection - “hair-like” appearance. NOT the same as premalignant leukoplakia.
- Kaposi sarcoma can also appear on hard palate, due to HHV-8
3 infections of the oral cavity that ARE related to AIDS or other conditions of immuno-suppression
- Candida albicans: responsible for oral thrush on mucosa of buccal region, tongue
- Hairy leukoplakia: keratinizing of mucosa due to EBV infection - “hair-like” appearance
- Kaposi sarcoma can also appear on hard palate, due to HHV-8
3 benign neoplasms of the oral cavity
- Papilloma (squamous papilloma) - common finding, caused by HPV 6 and 11.
- Fibromas: submucosal nodular fibrous tissue mass from chronic irritation
- Pyogenic granulomas: found in gingiva of children, young adults, and pregnant women. Can transform to dense fibrous masses, become an ossifying fibroma, or regress.
1 oral cavity malignant neoplasm
Squamous cell carcinoma: can be keratinizing or non-keratinizing. Strong relation to tobacco and drinking, also HPV 16 and 18.
Hungary is #1 in mortality from this in Europe
What is the word for inflammation of salivary glands? What are 4 etiologies?
Sialadenitis
Etiologies:
- Viral: mumps [rarely due to vaccine], CMV
- Bacterial: S. viridans or S. aureus
- Autoimmune: Sjogrens
- Mucocele (cyst, obstruction) that causes leakage of saliva into CT stroma
Duct obstruction or dehydration may predispose the salivary gland to infection.
4 benign tumors of the salivary gland
- Pleiomorphic Adenoma (mixed tumor) - most frequent, located in parotid gland. Can be extremely large, disfiguring. Remember that although it’s encapsulated, it can recur after surgery because some is left on the facial nerve and surgeons don’t remove it.
- Warthin Tumor: multi-cystic tumor of Parotid gland. Risk in smoking. Huge amount of lymphoid tissue; salivary gland tissue is trapped in lymph node
- Oncocytoma: “swelling of the cells” due to proliferation of mitochondria
- Monomorphic Adenomas, e.g. cystadenoma or basal cell adenoma
4 Malignant tumors of the salivary gland
+ 1 more on the list that was not elaborated on
- Mucoepidermoid carcinoma: most common; mixture of neoplastic sqaumous and mucous secreting cells.
- B-Cell non-Hodgkin Lymphoma: associated with Sjogren syndrome
- Adenoid Cystic Carcinoma: small dark-stained cells that look like lymphoid cells
- Adenocarcinoma from pleiomorphic adenoma
(5. Acinic cell carcinoma)
3 congenital malformations of the esophagus
- Agenesis: no esophagus
- Atresia: esophagus does not canalize.
- Tracheo-esophageal fistula: septum which separates esophagus and trachea is defective. Life-threatening due to aspiration.
3 types of Esophageal Diverticula (out-pouching)
- Zencker: upper esophageal (pharyngeal-esophageal) - due to weakness of cricopharyngeus muscle. Food gets trapped.
- Traction: middle esophagus. Tent-like. Result of tuberculosis with hilar lymph node involvement
- Epiphrenic: lower esophagus, due to dysfunction of LES.
What is achlasia? What are the primary and secondary forms?
not mentioned in lecture, only Robbins
Achlasia is a dysfunction of the lower esophageal sphincter with 3 components: incomplete LES relaxation, increased LES tone, and esophageal aperistalsis.
Primary achlasia: failure of esophageal inhibitory neurons, idiopathic
Secondary achlasia: can arise in Chagas disease (T. cruzi)
(achlasia-like disease may be seen in diabetic neuropathy, infiltrating malignancy, lesions of dorsal motor nuclei, etc.)
3 causes of esophagitis
- Reflux: LES is flaccid, gastric acid flows upward, GERD. Complications: strictures (narrowing), leukoplakia (keratinization), and Barrett metaplasia (intestinal epithelium in place of squamous. preneoplastic for adenocarcinoma)
- Infection: Candidiasis, herpes, CMV. Necrotizing lesions from CMV are common in people on immunosuppressants after organ transplants
- Corrosive agents: suicide attempts or regularly drinking high-concentration alcohol (note: chemical irritants/allergenic foods may also cause eosinophilic esophagitis)
2 forms of bleeding in the esophagus
- Esophageal Varices: dilated esophageal veins due to portal hypertension. Rupture -> hematogaster, hematemesis, melena, risk of hypovolemic shock
- Mallory-Weiss tears / lacerations: rupture with multiple tears at esophago-gastric junction, occurs with alcoholics due to severe vomiting. (remember Mallory bodies also seen in alcoholics)
2 types of malignant esophageal cancer
+ 3 complications?
- Squamous cell carcinoma: can arise anywhere in esophagus, strong correlation with smoking, drinking, male gender.
- Adenocarcinoma: typically in lower esophagus due to transformation of Barrett metaplasia.
Complications:
- Obstruction (causing cachexia, can’t eat)
- Fistula formation between trachea and esophagus (may aspirate tumor)
- Mediastinal infiltration (causing ichorous mediastinitis)
2 examples of esophageal dysphagia (both of which are generally not GI-specific disorders)
- CREST syndrome (E is esophageal dysmotility) in scleroderma
- Plummer-Vinson syndrome seen in chronic iron deficiency
What is hiatal hernia?
What are the 2 types?
Separation of diaphragmatic crura, protrusion of stomach into thorax through the gap. May be congenital, most are acquired. Usually asymptomatic but if there are symptoms, they’re similar to GERD.
- Almost all cases are “sliding” - gastroesophageal junction moves above the diaphragm with proximal stomach coming too.
- Some cases are “rolling” - gastroesophageal junction remains at level of diaphragm, while the stomach herniation comes up on the side of the esophagus.
2 types of Gastritis
not all the details are on this answer card, will elaborate later.. gastritis is an entire topic somehow
- Acute: Zalatnai said this is not really the subject of pathology but I’ll elaborate more on other cards anywhere because it is a topic
- Chronic: causes are “ABC” autoimmune, bacterial, chemical
Some causes and clinical signs of acute gastritis
again we were told this is not really subject of pathology, but it’s worth knowing and it’s fairly intuitive
Causes: any gastric irritants. Heavy use of NSAIDs, excessive alcohol consumption, infections
Clinical signs: acute mucosal inflammation. May be neutrophilic infiltration, hemorrhage/petechiae, ulcers. May cause hematemesis, melena, and iron deficiency.
3 causes of Chronic Gastritis
ABCs:
1. Autoimmune atrophic gastritis: pernicious anemia (megaloblastic) due to loss of parietal cells and intrinsic factor. Mucosa becomes flattened.
- Bacteria: especially H. pylori makes ulcers in pylorus or antrum. Visualize with Giemsa stain (cheap) and see lymphocytes, plasma cells, and eosinophils. H. pylori has CagA oncoprotein that disrupts epithelial differentiation; related to gastric adenocarcinoma and MALT lymphoma
- Chemical: e.g. alcoholic gastritis
2 complications of chronic gastritis
- Severe parietal cell loss -> intrinsic factor deficient, B12 deficiency
- Intestinal metaplasia (seen with flattening of mucosa, atrophic gastritis) has strong risk for transformation to gastric cancer
2 conditions that lead to peptic ulcer formation
- H. pylori infection
- Mucosal exposure to excessive gastric acid (e.g. ZES/gastrinoma, NSAIDs, CMV. Zalatnai also mentioned extremely stressful situations with abnormal cerebrovisceral reflexes)
5 complications of chronic peptic ulcers
note that this is definitely on their list of favorite crap to memorize, was emphasized in lecture
- Bleeding: deep erosion destroys vessels
- Perforation: hole produced that leads out into peritoneum
- Penetration: ulcer occurs near another abdominal organ, so for example the ulcer penetrate tothe pancreas. Can even penetrate diaphragm and affect the lung.
- Stenosis: CT proliferation -> narrowing of lumen
- Malignant transformation: mucosal layer transforms to adenocarcinoma
How are chronic peptic ulcers different than erosions / acute ulcerations?
Chronic ulcerations go deep enough to penetrate the muscle layer, which makes the mucosa unable to be regenerated. Becomes replaced with connective tissue scar; firm on palpation.
The collagen becomes stretched, causing a deep ulcer to be surrounded by ruggae in a star-shaped radiation.
Note that the edges of the ulcer are the most at risk for malignant transformation, so they must always be included in biopsy.
What are the 4 layers of connective tissue accumulation in chronic peptic ulcer, as seen in histology? Arranged from the lumen of the stomach towards the wall.
- Epithelial slough
- Fibrinoid necrosis
- Granulation tissue: proliferating capillaries and PMNs
- Connective tissue scarring: deepest part of ulcer. Collagen is proliferating, resulting in stretching of the mucosa.
3 kinds of benign gastric neoplasma?
- Hyperplastic polyps: no malignant potential. Most polyps are hyperplastic.
- Fundic polyps: no malignant potential.
- Adenomatous polyps: have malignant potential, developing adenocarcinoma
Note that all gastric polyps are rare, especially compared to the common colonic polyps
What are the 3 significant groups of malignant gastric neoplasms?
- Adenocarcinoma: can be intestinal (history of intestinal metaplasia, better prognosis) or diffuse (tumor cells arranged in sheets, arises de novo without previous gastritis, bad prognosis). By far the most common type.
- MALT lymphoma
- Carcinoid tumors
(almost never see squamous cell carcinoma of stomach)
What is EGC? What are the most common sites of metastases from gastric adenocarcinoma?
EGC: Early Gastric Tumor, confined to mucosa or submucosa - regardless of its metastaized to lymph node
Metastases sites:
- Lymph Nodes first, typically perigastric. May be left supraventricular lymph node (Virchov node)
- Liver: portal vein drainage usually spreads metastases to liver
- Peritoneal surface: may form massive peritoneal infiltration (“pertioneal carcinosis”)
- Ovaries: bilateral ovarian metastases are called Krukenberg tumors
5 risk factors for intestinal type of gastric adenocarcinoma
- Intestinal metaplasia due to H. pylori
- Nitrosamines
- Smoked foods
- Chronic atrophic autoimmune gastritis / pernicious anemia
- Familial adenomatous polyposis (FAP) mutation of APC genes
What is GIST?
seems also like a department favorite that is not talked about much in the books but was in the lecture
GI Stromal Tumor: tumor of Cajal pacemaker cells. Benign/malignant terminology is not used, but rather the size and the count of mitotic figures are used to determine the aggressiveness.
Need c-KIT histological diagnosis. c-KIT is receptor with tyrosine kinase activity, and in GIST the TK is permanently dimerized and active.
Difference in morphology between intestinal and diffuse gastric adenocarcinoma?
Intestinal: bulky, glandular, grow along broad cohesive front to form mass or ulcerated tumor. Neoplastic cells have mucin vacuoles, abundant mucin.
Diffuse: infiltrative growth pattern, large mucin vacuoles that push nucleus to periphery (signet ring cells). Gastric walls is stiffened with diffuse rugal flattening - “leather bottle” appearance (“linitis plastica”)
What are 4 possible complications of gastric carcinoid tumors?
- Endocrine cell hyperplasia
- Chronic atrophic gastritis
- Zollinger-Ellison Syndrome / Gastrinoma (excessive gastrin secretion -> hyperacidity of stomach and rest of GI tract). Peptic ulcers, diarrhea, and abdominal pain can result.
Effects can depend on the hormone produced, e.g. some carcinoid tumors can produce vasoactive substances.
