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Systems Path 2 Test 1 > Chapter 14 > Flashcards

Chapter 14 Flashcards

1
Q

May appear after broad spectrum anitbiotics

A

Oral Candidiasis

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2
Q

Pseudomembranous candidiasis

A

thrush

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3
Q

risk of oral candidiasis

A

lowered immunity, diabetics

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4
Q

oral lesion—reactive mass to chronic irritation—fibrosis

A

fibroma MC along bite line

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5
Q

benign vascular mass [red/purple] on gingiva, fast growth

A

Pyogenic Granuloma—-bad name

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6
Q

who gets pyogenic granuloma

A

pregnant women, children—-pregnancy tumor

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7
Q

why do women get pyogenic granuloma

A

hormonal factors, irritation

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8
Q

reactive fibromas and pyogenic granulomas are what?

A

oral proliferative lesions

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9
Q

raised white patch inside oral cavity, cannot be scraped off

A

leukoplakia

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10
Q

what causes leukoplakia?

A

cellular irregularity, cigs, alochol, irritants

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11
Q

leukoplakia is an ex of dysfunctional cells how?

A

epithelial hyperplasia and Keratosis

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12
Q

Risk of leukoplakia

A

inflammation: cigs, alchohol, candidiasis..males 40-70

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13
Q

Diagnosis of leukoplakia

A

biopsy to rule out CA. 25% pre-cancerous»squamous cell carcinoma

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14
Q

Erythroplakia is important why?

A

Over 50% transition into oral CA

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15
Q

Hairy Leukoplakia is linked with what?

A

EBV virus, and immunosuppression

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16
Q

Verrucous Leukoplakia would be what

A

Oral HPV, hyperkeratosis, warty appearance

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17
Q

what does verrucous mean

A

wart, warty. yum

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18
Q

Oral CA develops from

A

Dysplasia, TP53 mutations

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19
Q

95 % of all cases of oral CA are this type

A

squamous cell carcinoma, multple primary tumors common

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20
Q

symptoms of oral CA

A

oropharyngeal pain/dysfunctiong

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21
Q

Prognosis of oral CA

A

less than 50% long term, early detection!

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22
Q

Risks of oral CA

A

alcohol, cigs, >30 years old, HPV-16

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23
Q

Lesions: raised plaque, firm–need biopsy

A

squamous cell carcinoma

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24
Q

irregular borders, maybe leukoplakia-like, whitish gray or erythematous—red types of changes

A

squamous cell carcinoma

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25
Q

locations of squamous cell carcinoma

A
  1. ventral tongue 2. floor of mouth 3. lower lip 4. soft palate 5. gingiva
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26
Q

better prognosis of squamous cell carcinoma–usually develops at back of mouth

A

following HPV infxn =]

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27
Q

salivary gland diseases affect

A
  1. parotid mc 2. sublingual 3. submandibular 4. minor
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28
Q

xerostomia is what

A

dry mouth—decrease saliva

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29
Q

who gets xerostomia–

A

old ppl, ADRs [adverse drug rxn], irradition, Sjogren

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30
Q

what is sjogren, for good measure

A

autoimmune, exocrine destruction

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31
Q

IgA and enzymes would be present in what

A

salivary gland pathologies

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32
Q

tongue fissuring, ulcerations, increased risk of candida

A

xerostomia

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33
Q

femal, less that 20 years old , painful sore in mouth

A

aphthous ulcer

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34
Q

risks of aphthous ulcer —what brings them on, actually

A

smoke, stress, trauma, fever, certain foods

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35
Q

Tx of a canker sore

A

b12, nsaids, corticosteroids

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36
Q

young children, 80% aysmptomatic, 10 to 20% acute herpetic gingivostomatitis

A

the initial HSV infxn

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37
Q

generally, what/where is hsv 1 and hsv 2

A

orofacial and genital, but location does not indicate type

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38
Q

ithching, burning, tingling, small vesicles 1-3 mm…HA, sore throat, malaise, fever

A

HSV

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39
Q

what provokes HSV

A

UV, fever, cold, trauma, URTI, pregnancy

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40
Q

cure for HSV

A

no cure, antivirals slow replication though

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41
Q

Why is HSV studied here, can it be bad?

A

It can spread to the brain, which is life-threatening

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42
Q

HSV-1, acute CNS inflammation/swelling

A

Herpesviral encephalitis

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43
Q

What are the risks for oral candidiasis?

A

decreased immune, broad-spectrum antibiotics, diabetics—something about milk and infants….ask jesse

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44
Q

DDx along oral candidiasis

A

leukoplakia, oral CA

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45
Q

pain when swallowing is referred to as

A

odynophagia

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46
Q

mc cause of esophagitis, 25-40% of adults

A

reflux esophagitis

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47
Q

idiopoathic, LES dys, inc gastric volume, obesity, hiatal hernia, pregnancy, smoke, booze

A

reflux esophagitis

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48
Q

esophageal inflamm secondary to injury of mucosa

A

esophagitis

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49
Q

MC outpatient GI complaint

A

GERD—type of esopagitis

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50
Q

over 40, dysphagia, heartburn, “sour brash”

A

esophagitis

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51
Q

treatment if GERD

A

antacids, PPIs (omeprazole)—poroton pump inhibitor

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52
Q

esophagitis due to chemical would be acute, self-limited due to

A

smoke, booze, pills, hot, acid/base, irradiation, chemo

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53
Q

secodnary to ulcer, immunosuppressed–could be fungal

A

infectious esophagitis due to candidiasis, HSV CMV

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54
Q

MC laceration of esopohageal lining

A

Mallory Weiss tear

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55
Q

what causes a mallor-weiss tear

A

forceful vomiting, acute illness/intoxication. INadequate LES relax leads to longitudibal esophageal tears. leaceration to gastroesophageal jxn

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56
Q

TX to mallory-weiss tear. what was the Dx

A

balloon tamponade..endoscopy

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57
Q

widening of the diaphragm, stomach protrudes into thorax

A

hiatal hernia

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58
Q

causes of hiatal hernia

A

congenital, aqcuired, idiopathic

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59
Q

MC type of hiatal hernia—bell shaped dilation

A

Axial, 95%

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60
Q

Non-axial hernia, tell me about it

A

more likely to cause problem, like strangulation. asymmetrical

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61
Q

hiatal hernia occurs in who

A

20& of adults 70% over 70

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62
Q

90% of hiatal hernias are asymptomatic, no question here, bro

A

okie dokie

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63
Q

a complication of having GERD, metaplasia of distal esophagus

A

Barrett Esophagus

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64
Q

Preneoplastic lesion. Stratified sdquamous into columnar epithelia, contain goblet cells

A

Barrett Esophagus—stomach cells into esophagus

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65
Q

10% of symptomatic GERD will become

A

Barrett esophagus

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66
Q

Risks for Barrett Esophagus

A

males 4x, caucasians 30-100x, obese, 40-60, family Hx

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67
Q

endoscopy of barrett esophagusd

A

red velvety mucosa, bands “tongues” extend supoeriorly

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68
Q

super bad complications of barrett esophagus

A

esophageal adenocarcinoma, ulcerations, strictures.

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69
Q

Tx of Barrett

A

STOP irritants: smoke, irritating foods, eating late

Meds, omeprazole, laser ablation,

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70
Q

benign esophageal tunor is technically what

A

leiomyoma–benign, smooth muscle tumor

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71
Q

the naughty esophageal tumor

A

adenocarcinoma or squamous cell carcinoma9/10 worldwide

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72
Q

50% of US esophageal cancers, risks

A

adenocarcinoma, Barrett, GERD, living in US lol

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73
Q

9 out of 10 esophageal cancers, worldwide

A

squamous cell carcinoma

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74
Q

cancer with features that develop late, with early lymphatic invasion, with is very bad

A

adenocarcinoma, poor prognosis of 25% for 5 years

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75
Q

featues of adenocarcinoma of esophagus

A

odynophagia, vomiting, cachexia, fatigue, weakness

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76
Q

cancer more common through irriation, greater than 45, more in african americans, rural, underdeveloped
achalasia–lower esophagus fails to relax

A

squamous cell carcinoma. very poor prognosis less than 10%

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77
Q

the stomach is a common cause of morbidity

A

but, benign gastritis can turn into agressive gastric CA

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78
Q

features of gastritis

A

epigastric pain, nausea, vomiting, could be specific, pinpoint—mucosal ulceration–hemorrhage.

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79
Q

vomiting hematemesis is what

melena is what

A

blood contact with stomach—coffee ground appearance

black, tarry feces

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80
Q

MC infxn of gastritis

A

h. pylori

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81
Q

risks of gaastritis

A

alcohol, nsaids, ibuprofen, naproxen—aleve, aspirin. AGE

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82
Q

how to NSAIDs cause gastritis

A

decrease bicarbonate, i guess

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83
Q

acute gastritis—acute erosive hemorrhagic gastritis

A

aucte onset, usually a trauma to the mucosa, most likely from the risks, like nsaids. pathogenesis tends to be multifactorial—

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84
Q

epigastric pain (gnawing, burning) nauseam vomit, anorexia, hematamesis–maybe

A

acute gastritis, dependent association with NSAIDs

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85
Q

tx of acute gastritis

A

PPIs, H2 receptor antagonists…decrease gastric acidity

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86
Q

multiple, small, shallow ulcers in the stomach or duodenum…what causes this

A

Acute Peptic Ulceration—-following severe physiological stress. or huge NSAIDs: drop bicarb/prostaglandins

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87
Q

examples of what traumas can cause Acute peptic ulcerations

A

shock, sepsis, trauma, burns—–ichemia ofthe area

could also be intracranial disease—(vagal nerve hypothesis)

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88
Q

nausea, upper abdominal “discomfort”—no hematemesis, or rare

A

chronic gastritis

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89
Q

what can be associated with chronic gastritis

A

Helicobacter pylori infxn., peptic ulcers, combined with other stressors

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90
Q

Risks and more about H pylori

A

poor childhood sanitation, MC asymptomatic, 70-90%of chronic gastritis ppl have h pylori

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91
Q

effects of Hy. pylori

A

increase acid prod., epithelia metaplaisa—risk for gastric CA

92
Q

Autoimmune gastritis–

A

MC elderly, antibodies against parietal cell, pernicous anemia

93
Q

Sites of Peptic Ulcer diesase

A

Duodeum 4x, gastric antrum—solitary, punched out lesion

94
Q

5 to 10 % with H pylori within the stomach will develop

A

peptic ulcer disease

95
Q

what is peptic ulcer disease

A

chronic, recurrent gastritis

96
Q

pain of peptic ulcer diease

A

gnawing burning, MC at night and 1-3 hrs postprandial
relieved by alkaline stuff
Hemorrhage would be medical emergency

97
Q

Tx of PUD

A

antibiotics, antacids, PPIs H2 antagonists

98
Q

pain relief immeidately postprandial

pain returns a couple of hours later–might get worse

A

duodenal ulcer

99
Q

pain of gastric ulcer

A

worse on an empty stomach or postprandial

BOTH are worse at night

100
Q

narrowing of pyloric sphincter, MC Dx shortly after birth

projectile vomit looks like milk, hyperperistalsis

A

pyloric stenosis 1/400 births. tuner syndrome increased(also aortic coarctation)
Tx. pyloromyotomy

101
Q

general inflammation and enlargement of glands(salivary)from infxn, traum or autoimmune

A

sialadenitis

102
Q

MC (viral) of sialadenitis and what does it cause in adults….pediatrics?

A

Mumps from paramyxovirus of the parotids

103
Q

how does mumps effect pediatrics….adults?

A

self limiting of parotid, pancreatitis and orchitis in adults in addition to parotids

104
Q

What, besides mumps, can cause sialadenitis, presents how?

A

S. aureus. dehydration and obstruction

105
Q

a salivary gland pathology where the glands are blacked or ruptured

A

mucocele, or mucous cyst, ranula

106
Q

where will mucocele production edema

A

lower lip in children & elderly

107
Q

salivary gland neoplasms, are rare, what is effected most often?

A

parotid glands 65-80% and 15-30% are malignant

108
Q

less common location of salivary neoplasms happen where and how malignant is it

A

submandibular gland -10%. 40% are malignant

sublingual & minor salivary glands (10-25%) and 50-90% malignant

109
Q

pleomorphic adenoma

A

benign, painless, slow growing but MOBILEneoplasm of the parotid gland. 60% of parotid gland tumors

110
Q

how can pleomorphic adenomas cause naughty trouble

A

may recur following excision, 2-10% transition into CA
Carcinoma ex pleomorphic adenoma
invasive, less mobile 50% 5 year

111
Q

details of pleomorphic adenomas—made of what and one more special thing

A

cartilage & bone

encapsulated

112
Q

Regurgitaion, Dx. just after birth

A

atresia of esophagus, tracheal fistula, stenosis(fibrosis)

Mechcanical esophageal lesion/obstruction

113
Q

achalasia, what is it and what type of obstruction is it?

A

failure of esophagus to relax, it is a functional obstruction

114
Q

what is aperistalsis?

A

uncoordinated peristalsis, it is a functional obstruction

115
Q

what is ectopia?

A 
ectopic gastric mucosa (inlet patch), upper 1/3 of esophagus
and asymptomatic (MC) irritation that is a risk of CA
116
Q

irritaion of upper esophagus that is MC asyptomatic, but can lead to cancer

A

ectopi, ectopic gastric mucosa

117
Q

triad of achalasia

A
  1. Incomplete LES relaxation
  2. Increased LES tone
  3. Esophageal aperistalsis
118
Q

symnptoms of achalasia

A

dysphagia, regurgitation, chest pain(heartburn), weight loss

119
Q

signs of achalasia

A

proiximal esophageal dilation

120
Q

Tx. of achalasia

A

botulism toxin, pneumatic dilatation

121
Q

primary achalasia is due to what

A

loss of inhibitory innervation to LES—idiopathic

122
Q

what is secondary achalasia secondary to?

A

Chagas disease, irradiation, diabetes, polio

Inflamm near Auerbachs plexus—pathognomonic

123
Q

pyloric stenosis

A

really? go to bed.

124
Q

MC dx shortly after birth, projectile milk like looking vomit

A

pyloric stenosis

125
Q

reactive of neoplastic mass projecting from mucosa—of stomach

A

gastric polyp—common in 5% endoscopies

—-associated with chronic gastritis

126
Q

MC form of gastric polyps

A

inflamm & hyperplastic polyp 75%. no way to turn into cancer

127
Q

2 other types of gastric polyps

A

fundic gland polyp 15% PPI

Gastric adenomas 10%

128
Q

30% of what transition into adenocarcinomas of the stomach

A

gastric adenoma, which is 10% of gastric polyps
will have dysplasia
—biopsy is only way to tell type

129
Q

> 90% of all gastric cancers

A

gastric adenocarcinomas

130
Q

5% and 3% of gastric cancers, respectively

A

lymphomas, carcinoids…

131
Q

where and what are risks for stomach cancer

A

country of Japan 20x.
Risks, chronic inflam: H. pylori, EBV 10%
—dysplastic adenomas

132
Q

symptoms: gastritic, altered bowels, nausea/anorexia

Weight loss, hemorrhage, anemia

A

gastric cancer—MC develop late, Dx. late :(

5 yr survival: 90% is early, but most late–20% MC

133
Q

disorders of small and large intestines simply involve what

A

malabsorption or diarrhea

134
Q

pain, distention, constipation, vomit

A

intestinal obstructions—MC small intestine

80% of all mechanical obstructions

135
Q

abdonimal wall defect–intestinal protrusion (inguinal/umbilical), edema, infarct?

A

herniation—mechanical obstruction

136
Q

inflam, fibrosis, adeherent intestinal segments

A

Adhesions–mechanical obstruction

137
Q

intussusception

A

telescoping of the proximal bowel into the distal segment

138
Q

congenital outpounching located on the small intestine

A

meckel diverticulitum
2 inches
2% of pop. 2% symptomatic, males have 2x risk

139
Q

congenital aganglionic megacolon

A

Hirschsprung Disease

140
Q

lacks neruologic ganglia in rectum and sigmoid colon

result of defective neural crest cell migration…1 in 5000

A

hirschsprung disease

141
Q

Dx. failure to pass meconium–
obstructs proximal bowel
sever dilation of proximal bowel

A

hirschsprung disease

142
Q

MC in males, but more sever in femals, Tx surgical excision of area without ganglia

A

hirshcsprung

143
Q

prob with arteries—superior mesenteric, inf mesenteric, celiac….

A

ischemic colitis, Ischemic Bowel Disease

a drop in BP or occlusion—-old ppl

144
Q

if bad enough, could result in mucosal infarction

A

occlusion of arteries—ischemic colitis

145
Q

causes o thrombosis for ischemic bowel

A

atherosclerosis, vasculitis, hypercoagulability

inflam, stati—cirrhosis

146
Q

a myocardial infarction, angioplasty, and endarterectomy causes what in regards to ischemic bowel

A

aterial, embolism

147
Q

non-occlusive ischemia is due what

A

drop in BP, heart failure, hemorrhage, shock, dehydration

148
Q

weight loss and muscle wasting, abbdominal distension

A

malabsoroption

149
Q

borborygmus, flatulence

A

malabsorpsotion do more and look at tslide syou missed

150
Q

non-infectious malabsorption

immune-mediated, reaction to gliandin—not glutenin, the 2 breakdown components of gluten

A

celiac disease
gluten-sensitive enteropathy
celiac sprue

151
Q

what has gluten

A

wheat, barley, rye.

152
Q

what kind of hypersensitivity is gluten disease

A

Type IV

153
Q

B & T cells damage S.I.—villous atrophy in the duodenum and jejunum
Crypt hyperplasia

A

celiac—many cases are familial!!! (HLA-DQ2 or DQ8)

154
Q

how is celiac disease formally diagnosed

A

IgA/IgG antibody / biopsy

people usually just kinda figured it out thru diet

155
Q

1% of US and Europe,
Caucasians
MC Dx age 30-60
Rarely, pediatric: 6-24 months

A

Celiac Disease

156
Q

possible iron deficiency anemia: fatigue, pallor
usually bloating, diarrhea
risk of intestinal adenocarcinoma!!!

A

celiac

157
Q

1 in 10 ppl with celiac may have immune probs other places…most notably

A

on the skin
Dermatitis Herpetiformis :)
arms, elbows, legs, buttocks, itchy—neutrophils

158
Q

tropical sprue

Cycles of: mucosal injury, malnutrition, inflammation

A

environmental enteropathy

159
Q

MC affects children, age 2-3years
living in or recentyl visted tropical areas
150 mil worldwide

A

environmental enteropathy

160
Q

seems to be autoimmune: villus flatting—like celiac

Infectious: responds to antibodies

A

environmental enteropathy

161
Q

decrease of lactase at SI brush border

cant digest lactose

A

lactase deficiency

162
Q

bloating, cramps, gas, diarrhea, MC 30 mins postprandial

A

lactose intolerance

163
Q

Acquired (MC): lactose intolerance

congenital:

A

young adulthood

auto. recessive, rare, life-threatening

164
Q

Dx of lactose intolerance?

A

breath hydrogen test

165
Q

12,000 children die each day of this disease of the small intestine
500 infants each year in US

A

infectious enterocolitis

166
Q

Microbial infxn: abdominal pain, urgency/incontinence, perianal discomfort, hemorrage

A

Infectious enterocolitis

167
Q

Agents of infectious enterocolitis can include

A

Bacteria, Virus, Protozoa

168
Q

Gram (-), comma shaped bacteria that will cause enterocolitis MC in India/Africa
1-5 day incubation

A

Vibrio cholerae

169
Q

Noninvasive: minimal tissue damage

So why does it cause bad times?

A

Secretes cholera toxin (remember it is gram -)

170
Q

what does cholera toxin do?

A

Opens CFTR—-chloride ion secretion

171
Q

Vomiting and watery diarrhea, cramping early from electrolyte imbalances….hypotension bc fluid loss
1 L of H20 per hour

A

cholera

172
Q

Tx of cholera

A

fluids, electrolytes, antibiotics, zinc

no Tx: 50-70% death

173
Q

Traveler’s Diarrhea

A

enterotoxigenic E. coli is MC :)))

174
Q

Defined by 3 or more unformed loose stools within 24 hours

A

travelers diarrhea

175
Q

MC bacterial enteric pathogen in the U.S.

contaminated chicken etc

A

Campylobacter enterocolitis

176
Q

Campylobacter enterocolitis can kind of kick start a couple of things

A

well, dysentery and fever, but reactive arthritis—HLA-B27 or Guillian Barre

177
Q

Last for less than 1 month, no Tx. needed

C. jejuni, Shigella, E. coli, Salmonella

A

Acute self-limited colitis

178
Q

Pseudomembranous Colitis

A

Clostridium difficile overgrowth, colon—-enterotoxins

fever, watery diarrhea, pain

179
Q

risks for pseudomembranous

Tx?

A

hospitalization, old age, down immunity

vancomycin or metronidazole

180
Q

MC gastroenteritis—-1/2 of all

children. ..
adults. …

A

viral!
Rotavirus
Norovirus

181
Q

MC parasitic infxn

A

Giardia lamblia-resists cold and chlorine
“Beaver Fever”
Fecal comtaminated water

182
Q

Giardia lamblia is non-invasive, so it does what?

A

alters, S.I. enzymes

183
Q

blind ended outpouching of the colon

A

sigmoid diverticulitis

95% of the time it will be sigmoid colon

184
Q

complications of diverticulitis

A

infxn, abscess, maybe hemorrhage

185
Q

risks of diverticulitis

A

age, refined foods, constipation—high intraabdominal pressure. 50% over age 60. 20% symptomatic

186
Q

presentation of diverticulitis

A

cramping, left lower abdominal pain, tenesmus (sensation of inadequate BM), diarrhea

187
Q

diverticulitis is progressive, they become larger and more numerous aaand Tx.???????????????????

A

They need to change their diet

188
Q

Super general term—–altered bowel habits
bloating, diarrhea OR constipation—speeding up or slowing down
chronic and relapsing abdominal pain

A

IBS

189
Q

MC peeps for IBS

A

20-40 MC

females, with psychological stress

190
Q

what defines IBS….is what it isn’t—-

A

No cellular abnormalities (gross, histologic)

Commins, 5-10% of US adults

191
Q

Tx. of IBS

A

fiberrr, lower carbs, stress management

192
Q

Abnormal loca immune response of da tummy
Idiopathic/hypersensitivity rxn
Crohn’s or ulcerative colitis

A

Inflammatory Bowel Disease

193
Q

who gets IBD

A

females, adolescence, Caucasians, hygiene hypothesis?

194
Q

MC in ileum, but can go eintre GI tract

transmural—throughtout the wall of GI–

A

Crohn disease (regional enteritis)

195
Q

rectum, distal colon

mucosal and maybe submucosal

A

ulcerative colitis

196
Q

hypothesis for crohn disease

A

t cell autoimmune rxn

no known cure

197
Q

presentation of crohn disease

A

melena 50%, mild diarrhea, fever, abdonal pain
“skip lesions”, granulomas, ulcerations, strictures
skin rxn, arthritis, AS ankylosing spondylitis, eye irritation, fatigue

198
Q

ok, Crohn is 1 in 500, what is Tx?

Risk for what

A

probiotics, immunosupressive meds,

GI adenocarcinoma

199
Q

Tx of Crohn?

A

probiotics, immunosuppressive meds

200
Q

having crohn is risk for

A

G.I. adenocarcinoma

8-10 years, after Dx.

201
Q

area of narrowing in the G.I. tract is called what

—transmural in crohns

A

stricture
“skip lesions” are common with Crohn’s
‘cobble sttone appearance

202
Q

what condition has a cobble stone appearance?

A

Crohn’!

203
Q

again, what is the MC location for Crohn’s

A

terminal ileum, ileocecal area

204
Q

superficial mucosa ulcerations are in what condition

MC begin in rectum—will have ‘pseudopolyps’

A

ulcerative colitis

Crohns lesions are “transmural”

205
Q

what should you be associated with ulcerative colitis?

A

toxic megacolon, polyarthritis, sacroiliitis, AS, eye irritation

206
Q

what gets this bad stuff (ulcerative colitis)

A

20-25 years old, 1 in 5,000.
smoking is inhibitory–opposite of crohn’s
increasing incidence!

207
Q

onset of ulcerative colitis

A

tenesmus–feeling of still have to pass poops
fever, abdominal pain, lower ab cramping
Relapsing episodes: “attacks”
stool: grossly bloody & mucoid “stringy”

208
Q

Dx of ulcerative colitis

A

coloscopy and biopsy

209
Q

dysplasia of UC increases what huu huh huh?

A

risk for adeno carcinoma

210
Q 
Crohns---IBD
malabsorptive
fissures, strictures, granulomas
entire GI tract, fibrosis,
skip lesions
A 
UC---IBD
not malabsorptive
pseudopolyps, non granulomatous
rectume/distal colon, little to no fibrosis
diffuse ulcerations
211
Q

what is a polyp

A

a mass, protrduiong into lumen

epithelial/mucosal proliferation

212
Q

inflammatory polyps follow inflammation so

what is a hamartoma?

A

mature cell types, minimal risk

213
Q

a polyp that resembles dysplasia

A

hyperplastic, well-differentiated, pilled-up epithelia, multiple
MC Dx. in elderly: 50- 60 years

214
Q

what is the bad polyp

Def is dysplastic

A

Adenomatous: neoplastic mass

“pre-malignant”—-adenocarcinomas

215
Q

adenomas of the GI tract aaaarrree

A

benign mass-but considered malignant until proven otherwise–sessile or pedunculated
can be a risk for adenocarcinoma is dysplasia happens
occult bleeding—-anemia

216
Q

what is familial adenomatous polyposis

A

a bunch of polyps MC 500-2500 whoa

217
Q

rare, autosomal dominatnt, aggressive situation of numerous adenomas, teenaged onset
almost 100% chance for colon CA by age 30

A

familial adenomatous polyposis

218
Q

how to find FAP

A

occult blood in stool, probably anemic

Fx Hx

219
Q

5% of US develops colorectal CA wow

A

40% of cases are lethal…so 1/10 CA deaths

220
Q

types of colorectal CA

A

adenocarcinomas

carcinoid tumors

221
Q

MC calignancy of the GI tract
130,00 new cases each year
55,000 deaths

A

colorectal adenocarcinoma
80% of Dx are age 50-70
risks: males, IBD, developed nations
US diet, 30x the risk

222
Q

inccreased retention time because of low fiber diet alters the microbiota

A

increases risk for bad stuff

223
Q

Insidious onset!

usre diarrhea and constipation

A

occult blood in stool, iron-deficiency—must rule out CA in elderly

224
Q

small intestine tumors

vague symptoms

A

mc in duodenum
1% of all gi malignancies
50% adenocarcinomas 50% carcinoid

225
Q

MC acute abdominal condition

7% of all population

A

acute appendicitis

226
Q

onset is

early: periumbilical/epigastric discomfort
late: RLQ tenderness—-deep/constant pain
- —progresses into sharp pain

A

appendicitis

227
Q

obstruction is common cause 50-80%

ischemia—inflammation

A

appendicitis

Systems Path 2 Test 1 (3 decks)

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