Flashcards
dec 14
Flashcards do conjunto (82)
- 1ORAL LICHEN PLANUSEtiology unknown, thought to be immune-mediated
Considered a chronic T-cell mediated inflammatory tissue reaction that attacks the basal cell layer - 2Clinical forms of oral lichen planusWHITE = RETICULAR pattern
RED = ATROPHIC/ULCER pattern
YELLOW = HEALING ULCER pattern
Often EROSIVE is used to describe OLP
with a RED and/or YELLOW component - 3Reticular (WHITE) lichen planusWickham’s striae (spider web like)
Likely asymptomatic - 4Erosive (RED YELLOW) lichen planuEpithelial atrophy, ulcerations, healing
ulcerations
May be painful
ex-Desquamative gingivitis - 5txTopical steroids
Systemic steroids
Immunosuppressants
immunomodulators - 6APHTHOUS ULCERATION (CANKER SORE)No single triggering agent is responsible,
may represent a T-cell mediated reaction
(TNF-α)
Occurs on nonkeratinized mucosa, heal without scarring in 7 to 14 days - 7presentsTHINK: Small, red halo ulcer that heals quickly then returns
are painful oral lesions that appear
as localized, shallow, round to oval ulcers with a grayish or yellow base - 8txMild corticosteroid gel or cream,
- 9Syndromes associated with aphthous ulcersMay be an initial manifestation of Crohn’s disease or other GI diseases
- 10HSV-1 ULCERATIONVesicular lesions with erythematous bases,
intraoral lesions rupture easily
HSV-1 mediated
Recurrent herpes occurs on
keratinized tissue, but primary herpes occurs everywhere intraorally - 11dxTzanck smear or biopsy reveal
multinucleated cells with viral features - 12Herpes simplex virusTHINK: Primary: Fever and painful vesicles and blisters
Secondary: painful vesicles that pop, people often sense them coming
Most patients (>85 percent) develop prodromal symptoms (e.g., pain, burning, tingling) about 24 hours before the appearance of painful lesions - 13ORAL CANDIDIASISMost common in immunocompromised (neonates, steroids, diabetes, AIDs) and patients with xerostomia
Candida albicans can be part of normal
microflora
White plaques can be
scraped off, can be recurrent if patient is
immunocompromised - 14dxKOH prep can help
diagnose cases - 15Clinical featuresOne of the most common fungal
infections in humans
Often occurs in immunocompromised
and/or debilitated patients - 16Pseudomembranous candidiasis or thrush“Cottage cheese” plaques that can be
scraped off (unlike leukoplakias)
When plaques are removed the mucosa may appear erythematous
Commonly occurs on buccal mucosa,
dorsal tongue, and palate
Patients can experience a burning
sensation or foul taste - 17someones say burning mouth thinkcandidiasis
- 18txNystatin
Mycelex - 19oral cell squamous carcinomamost common cancer in mouth
- 20dysplasiaChanges in cell morphology and architecture in just one part of the epithelium
- 21carcinoma in situChanges in cell morphology and architecture throughtout the whole epithelium
- 22squamous cell carcinomafrank invasion in basement membrane
- 23What does dysplasia mean(Dys-) abnormal (-plasia) growth
Cells appear abnormal
Architecture is abnormal
Describes cells that are not neoplastic or
malignant - 24Most Oral dysplasia never progress to carcinoma.
- 25InvasionTumor has breached the basement membrane
Malignant neoplasm of oral
epithelium. thats when we have basal cell cacinoma - 26Oral potentially malignant disorders (OPMDs)Clinical presentations that
carry a risk of cancer
development in the oral
cavity
Leukoplakia
Erythroplakia - 27most common site of oral cancerLip
sunlight - 28INTRAORAL: SQUAMOUS CELL CARCINOMAAggressive, with a propensity for local
invasion and early lymph node
metastasis
Smoking is the most important cause - 29locations•Tongue, FOM, and gingiva account for more than ½ of cases
- 30LeukoplakiaClinical term to describe a white plaque of
questionable risk that cannot be scraped off - 31ErythroplakiaClinical term to describe a red plaque of
questionable risk that cannot be scraped off - 32OROPHARYNX: SQUAMOUS CELL CARCINOMA, HPV-POSITIVE (OPSCC-HPV)•High-risk HPV, with type 16
>90% of all cases (18 less)
Often presents at an
advanced clinical stage
location-Base of tongue, tonsils, adenoids - 33OPSCC-HPV+50-56 Y
Sexual behavior
Reticulated epithelium
of crypts
Non-keratinizing
p16 +
82% 3 year survival rate - 34OPSCC-HPV60-70 Y
Smoking and alcohol
Surface epithelium
of oropharynx
Conventional SCC
p16 -
57% 3 year survival rate - 35Clinical uncertaintyDocument case: clinical description and photo
Lesions that persist for more than 2 weeks
need to be biopsied or evaluated by a
specialist - 36ORAL HAIRY LEUKOPLAKIA•EBV-related lesion seen in immunocompromised
patients
Most common EBV-relate
lesion in patients with AIDS - 37ORAL MUCOSAL MELANOMAMuch more aggressive than
cutaneous counterpart,
lesions at least stage III
70-80% of cases occur on
the hard palate or maxilla - 38SJÖGREN’S SYNDROMEChronic autoimmune
disease
Histologically characterized by lymphocytic infiltration of exocrine glands and organs
Associated with dry eyes (lacrimal glands) and dry mouth (salivary glands) - 39present•80% to 90% of cases are
seen in women
Patients generally present with salivary gland enlargement (parotid is most
commonly involved) - 40txsymptomatic relief
Dryness: artificial tears, artificial saliva
For patients with extraglandular
manifestations, immunosuppressive
medications are commonly used - 41SIALADENOSIS (HYPERTROPHY)Can be caused by eating disorders (bulimia), kwashiorkor, alcoholism and
metabolic disease - 42presentbilateral parotid enlargement
- 43dx and tx•Clinical observation, imaging or biopsy may be necessary for diagnosis
•Treat underlying disorder - 44SIALOLITHIASIS (SALIVARY STONES)•Forms when saliva rich in calcium
is stagnant
Most common in submandibular
gland and duct (tortuous path of
duct)
Can result in secondary infection or a
dysfunctional gland - 45dx and tx•Biopsy is indicated for larger
stones
Conservative therapy: hydration,
sucking on candy, moist heat,
massaging gland or milking duct
•Tx: analgesics, antipyretics - 46MUMPS•Caused by mumps virus
(paramyxovirus)
assocaited with Parotitis, orchitis, and
aseptic meningitis
May cause sterility (especially after puberty) - 47txanalgesics, antipyretics
- 48presentbilateral parotid enlrage
sudden fever - 49PLEOMORPHIC ADENOMAMost common salivary
gland neoplasm
Histologically characterized by chondromyxoid stroma admixed with plasmacytoid myoepithelial cells and
interspersed ducts - 50genesApproximately 70% of cases show PLAG1;
HMGA2 gene fusion - 51present•Most common in
3rd-6th decades of life, average age
of 45 years
•Need to identify epithelial and myoepithelial/stromal components
Small subset of PA’s can
become malignant - 52prognosisPAs have a
good prognosis if they
are completely removed
Tumors with a mucinous
stroma are more likely to recur - 53MUCOEPIDERMOID CARCINOMA•Most common salivary gland
malignancy (1/3)
50% appear on the palate
Tumor composed of mucous,
epidermoid, and intermediate
cells - 54genesSubset (70%) display MECT1/MAML2 translocation, t(11;19)
•Based on various histologic
features: cystic component, borders, nuclear atypia, perineural invasion - 55txPalatal lesions that are small (less than 2 cm) and do no involve bone can be managed by local excision with at least 1-cm clear lateral margins: block excision of underlying bone is done if there is bone destruction
HG MEC: surgery and adjuvant postoperative radiotherapy - 56WARTHIN TUMOR•AKA papillary cystadenoma
lymphomatosum
Almost exclusively arises in
parotid gland and periparotid LNs
Highly associated with older
males with a smoking history - 57present histo•Cystic and papillary proliferation of bilayered epithelium with a
lymphoid stroma - 58GASTROINTESTINAL MOTILITYGastrointestinal motility: smooth muscle contraction and relaxation within GIT
Regulates movement of luminal contents - predominantly antegrade movement via coordination of peristaltic and non-peristaltic flow.
Modulated by neural and humoral mechanisms. - 59Oropharyngeal DysphagiaDysfunctions in swallowing before food enters esophagus
Difficulty moving food or fluid bolus from the front of the mouth to the posterior oropharynx into the esophagus. - 60commonly seen inMost commonly caused by stroke, neurological disorders
Often seen in neuromuscular diseases like Parkinson’s disease, multiple sclerosis and myasthenia gravis.
Also common in end-stage dementia
In elderly, loss of UES elasticity or compliance, jaw strength, salivary production, dentition - 61Esophageal DysphagiaFood stuck in esophagus
Caused by disordered peristaltic motility of the esophagus
Most commonly caused by achalasia or scleroderma - 62Swallowing - Esophageal PhaseFood from esophagus to stomach (8-10 sec, may be 5-8 sec)
- 63AchalasiaDisorder of the lower esophageal sphincter (LES) to relax with swallow
Loss of peristalsis movement through the esophagus - 64cause***Functional loss of myenteric plexus in distal esophagus and LES
Imbalance of excitatory and inhibitory control of LES - 65GastroparesisA chronic condition of intermittent nausea and vomiting, early satiety, bloating and upper abdominal discomfort
due to gastric emptying slowed
immediate vomiting after meal - 66Pathophysiology of GastroparesisAlterations of myenteric neurons, loss of interstitial cells of Cajal
Reduced gastric retention and small bowel/colonic transit time - 67Decreased EmptyingFoods (fat>protein>CHO)
High osmolarity
Drugs-anticholinergics
GI Hormones-secretin, CCK, glucagon
Diseases/surgery-pseudo-obstruction, diabetic neuropathy, autonomic neuropathy
Stress, fear, depression
larger food particles (~> 7mm) - 68Increased EmptyingFoods (volume, liquids, low pH)
Drugs - cholinergics
GI hormones - gastrin, motilin
Diseases/surgery - irritable colon, pyloroplasty, partial gastrectomy
Gastric distension
Smaller food particles (2-3 mm) - 69motilin,
- 70grenlin.
- 71Peptic Ulcer Disease: Zollinger-Ellison SyndromePatient presents to your clinic :
Chief Complain: “I have Diarrhea and it looks Oily” - 72presentsIndigestion
Loss of appetite
Sporadic Abdominal pain--> relieved by eating and taking antacids
Diarrhea - 73how to dx Zollinger-Ellison syndrome, or gastrinoma1) elevated serum gastrin level
2) elevated basal level of gastric H+ secretion. - 74How does a healthy person respond to the pentagastrin stimulation test?.
- 75In the pentagastrin stimulation testa gastrin analogue is infused while gastric H+ secretion is monitored. (Gastric contents are sampled through a nasogastric tube.)
- 76In healthy persons the gastric analogueacts just like endogenous gastrin: it stimulates H+ secretion by gastric parietal cells (usually 3x higher than basal secretory rates).
- 77In our pt., the gastrin analougedid nothing. He had such high circulating levels of gastrin from the tumor that H+ secretion was already maximally stimulated. Pentagastrin could not further stimulate H+ secretion.
- 78In the secretin stimulation testpt’s serum gastrin level increased from the basal level of 800 pg/ml (already very elevated!) to 1100 pg/m!.
- 79In healthy persons, the secretin stimulation testcauses no change, or a decrease, in the serum gastrin level.
- 80In ZE, secretin directlystimulates gastrin secretion by gastrinoma cells, but not by antral G cells.
Therefore, when a person with Zollinger-Ellison syndrome is challenged with the secretin stimulation test, the serum gastrin level increases further. - 81The primary bile acids (cholic acid and chenodeoxycholic acid) are synthesized fromcholesterol in the liver.
The rate-limiting enzyme in this biosynthetic pathway is cholesterol 7 a-hydroxylase, which is feedback-inhibited by cholic acid. - 82The bile salt pool was depleted followingileal resection.
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- FlashCards sobre dec 14, criado por Shylla T em 13-12-2020.
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