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x Pathoma > 10. Gastrointestinal Pathology > Flashcards

10. Gastrointestinal Pathology Flashcards

1
Q

Cleft lip and palate: what is the reason behind the deformity?

A

failure of facial prominences to fuse (there are 5: one from the top, 2 from sides, 2 from bottom)

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2
Q

what is more common: cleft lip + cleft palate, or isolated cleft lip or palate?

A

the two usually occur together

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3
Q

what is an aphthous ulcer?

A

painful, superficial ulceration of the oral mucosa. inside the mouth.

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4
Q

what is the cause of an aphthous ulcer?

A

arises due to stress

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5
Q

Aphthous ulcer: how does it resolve?

A

resolves spontaneously. may recur

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6
Q

appearance of an aphthous ulcer?

A

grayish base (granulation tissue) surrounded by erythema

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7
Q

what is Behcet syndrome?

A

triad: recurrent aphthous ulcers, genical ulcers, uveitis

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8
Q

Behcet syndrome: cause?

A

immune complex vasculitis involving small vessels

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9
Q

Behcet syndrome: etiology?

A

unknown, can be seen after viral infection

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10
Q

Describe oral herpes (appearance)

A

vesicles involving oral mucosa that rupture, -> shallow, painful red ulcers

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11
Q

oral herpes: etiology?

A

usually HSV-1

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12
Q

oral herpes: first presentation? dormancy?

A

primary infection in childhood. lesions heal, virus remains dormant in ganglia of the trigeminal.

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13
Q

oral herpes: recurrences?

A

stress, sunlight cause reactivation of the HSV-1 virus, –> vesicles on the lips “cold sore”

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14
Q

what is squamous cell carcinoma?

A

malignant neoplasm of squamous cells lining the oral mucosa

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15
Q

Oral squamous cell carcinoma: risk factors? (2)

A

alcohol, tobacco use

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16
Q

oral squamous cell carcinoma: most common location?

A

floor of the mouth

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17
Q

squamous cell carcinoma: precursor lesions?

A

leukoplakia and erythroplakia

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18
Q

what is leukoplakia?

A

white plaque that cannot be scraped away; often represents squamous cell dysplasia

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19
Q

what is oral candidiasis? when is it seen?

A

white deposit on tongue, easily scraped away. seen in immunocompromised states. may be confused with leukoplakia (which cannot be scraped away)

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20
Q

what is hairy leukoplakia? when is it seen?

A

white rough patch on the lateral tongue. seen in immunocompromised pts (HIV). results from EBV-induced squamous cell hyperplasia. may be confused with leukoplakia

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21
Q

hairy leukoplakia: is it malignant?

A

no. hyperplasia but not dysplasia

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22
Q

what is erythroplakia?

A

red plaque, represents vascularized leukoplakia. suggests squamous cell dysplasia

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23
Q

erythroplakia v leukoplakia: which is more suggestive of squamous cell carcinoma?

A

erythroplakia due to angiogenesis

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24
Q

salivary glands; what type of gland? secrete what?

A

exocrine gland, secretes saliva

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25
Q

what are the 3 major salivary glands?

A

parotid, submandibular, sublingual

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26
Q

what are the minor salivary glands?

A

hundreds of microscopic glands distributed throughout oral mucosa

27
Q

Mumps: presentation?

A

infection with mumps virus, bilateral inflamed parotid glands.

28
Q

Mumps: what may also be present, in addition to parotid inflammation? (3 other areas of inflammation)

A

orchitis, pancreatitis, aseptic meningitis

29
Q

Mumps: what enzyme may be elevated?

A

serum amylase due to salivary gland or pancreatic involvement

30
Q

Mumps: major concern is for what? in what population?

A

sterility due to orchitis. population: teenagers, because pts under 10 don’t get orchitis with mumps

31
Q

what is sialadenitis?

A

inflammation of the salivary gland. usually unilateral

32
Q

what is the most common cause of sialadenitis?

A

sialolithiasis (obstructing stone) leading to S aureus infection.

33
Q

what is a pleomorphic adenoma?

A

benign tumor composed of multiple tissue types (stromal and epithelial)

34
Q

what is the most common tumor of the salivary gland?

A

pleomorphic adenoma

35
Q

pleomorphic adenoma: typical presentation?

A

mobile, painless, circumscribed mass at the angle of the jaw (parotid gland)

36
Q

why does pleomorphic adenoma have a high rate of recurrence?

A

has irregular margins; surgical resection may be incomplete

37
Q

pleomorphic adenoma: transforms into what? what are signs?

A

rarely transforms into carcinoma, characterized by facial nerve damage due to invasion

38
Q

what is a Warthin tumor?

A

benign cystic tumor with lymphocytes and germinal centers

39
Q

a Warthin tumor resembles what? why?

A

resembles a lymph node, because LN tissue is closely associated with the parotid. something about embryological dev…

40
Q

what is the second most common tumor of the salivary gland?

A

Warthin tumor

41
Q

Warthin tumor almost always arises where?

A

parotid

42
Q

mucoepidermoid carcinoma: what is it?

A

malignant tumor, made of mucinous and squamous (epiderm) cells

Most common malignant tumor of salivary gland (Most common tumor overall is pleomorphic adenoma which is benign)

43
Q

what is the most common malignant tumor of the salivary gland?

A

mucoepidermoid carcinoma

44
Q

mucoepidermoid carcinoma: usual presentation?

A

arises in parotid; commonly involves the facial nerve

45
Q

What is gastroschisis? What does it lead do?

A

Congenital malformation of the anterior abdominal wall (the 4 parts of the abdominal wall that need to join together didn’t). Leads to exposure of the abdominal contents outside the body.

46
Q

What is an omphalocele?

A

Persistent herniation of bowel into the umbilical cord.

47
Q

an omphalocele occurs due to what?

A

failure of herniated intestines to return to the body cavity during development. remember that the guts normally undergo a 90’ rotation during this process

48
Q

Omphalocele: what does it look like?

A

bowel contents external to the body, covered by a bubble-looking thing which is the peritoneum and the amnion of the unbilical cord.

49
Q

what is the difference in appearance of an omphalocele and gastroschisis?

A

whether you see the abd contents, or whether they are covered by tissue. gastroschisis: not covered, no wall over bowel. omphalocele: covered by peritoneum, part of umbilicus

50
Q

what is pyloric stenosis? when does it present?

A

congenital hypertrophy of pyloric sphincter muscle. presents in neonates: they will be normal for about 2 weeks, then this develops and presents.

51
Q

pyloric stenosis: how does it present?

A

babies cannot get the food past their hypertrophied pyloris, so they projectile vomit, they have visible peristalsis (in attempt to move food through) and you can feel the hypertrophy in the abdomen (olive-like mass)

52
Q

pyloric stenosis: the projectile vomit will be bilious or not? why?

A

NON bilious: the gastric contents have not passed through the pyloris, have not made contact with the bile yet

53
Q

pyloric stenosis: treatment?

A

myotomy: cutting away of some of the hypertrophied pyloric muscle

54
Q

acute gastritis: definition? cause?

A

acidic damage to the stomach mucosa. caused by imbalance: too much acid produced, too little protection/mucosal defenses

55
Q

what are the normal defenses that protect the stomach mucosa from acidic damage?

A

-mucin layer produced by foveolar cells -bicarb secretion by surface epithelium -normal blood supply

56
Q

how does the presence of a normal blood supply protect the stomach mucosa from acidic damage?

A

provides nutrients, picks up leaked acid (if acid leaks through and accesses the cells, the blood flow takes it away)

57
Q

risk factors for acute gastritis? (6)

A

-severe burn/Curling ulcer -NSAIDs -heavy EtOH consumption -chemotherap -increased intracranial pressure (Cushing ulcer) -Shock

58
Q

why is a severe burn a risk factor for acute gastritis?

A

causes hypovolemia, which leads to decreased blood supply

59
Q

why is NSAID use a risk factor for acute gastritis?

A

NSAIDs decrease prostaglandin levels (inhibit PG synthesis). Prostaglandins protect stomach mucosa (decrease acid production, stimulate bicarb production, stim mucus production, and increase blood flow)

60
Q

why is heavy EtOH consumption a risk factor for acute gastritis?

A

direct toxin to the cells

61
Q

why is chemotherapy a risk factor for acute gastritis?

A

kills off the cells that are turning over most quickly; can’t regenerate those cells quickly enough, leads to decreased mucus production

62
Q

why is increased intracranial pressure a risk factor for acute gastritis?

A

(cushing ulcer) increased stim of vagus nerve leads to increased acid production (vagus stim causes release of Ach, which binds to parietal cell receptors, which then incr acid production)

63
Q

why is shock a risk factor for acute gastritis?

A

due to decreased blood volume/decr perfusion of organs. multiple (stress) ulcers may be seen in ICU patients.

64
Q

acid damage results in what 3 things?

A

-superficial inflammation of the stomach lining -erosion (loss of superficial epithelium) -ulcers (loss of mucosal layer)

x Pathoma (19 decks)

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