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GIGU 2 Exam 1 > Small Intestine And Colon - Dr. Dobson > Flashcards

Small Intestine And Colon - Dr. Dobson Flashcards

1
Q

most common site of GI neoplasia in Western populations

A

colon

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2
Q

when does the intestines rapidly grow and what happens

A

week 4 and 5

= causing the abd cavity to be overfull and intestines herniate out the umbilical cord

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3
Q

week 4

A

NCC enter foregut

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4
Q

week 7

A

NCC reach the hindgut

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5
Q

week 9

A

cloaca becomes patent and villus formation begins

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6
Q

week 11

A

mature SM layers along GI tract

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7
Q

procedure for the capsule endoscopy

A
  1. fasting prior to swallowing capsule
  2. Capsule goes through GI
  3. wireless recorder around waist receives signals from capsule by sensors on pt body
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8
Q

capsule advantages

A

no sedation

3D coloc images

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9
Q

80% of mechanical obstructions in GI are from what 4 things

A
  1. Hernia
  2. Adhesions
  3. Vovlulus
  4. Intussusception
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10
Q

common SX of SIO

A

constipation, ABD distention and Pain, Vomiting

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11
Q

Functional Bowel obstruction

A 
paralysis of ileus due to peristalsis disturbance from NO mechanical obstruction 
= usually from postoperative ileus
= hypokalemia 
= hypothyroidism
= anti-cholinergics
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12
Q

hernias can cause what

A

trapped vein causing blood to pool and get stuck leading to infarction

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13
Q

what can cause adhesions

A

surgery
trauma
intraabdominal infection
endrometriosis

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14
Q

most common cause of obstruction World wide and in US and in children under 2yo

A

World : Hernias
US : adhesion
children under 2yo : intussusception

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15
Q

vovulus happens most frequently where

A

Sigmoid colon**

cecum/ SI / stomach, rarely TC

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16
Q

patient with obstruction what do you do first

A

restore electrolyte imbalance

then do endoscopic decompression

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17
Q

who is in risk of intussusception

A

viral infection, rotavirus vaccination , tumor in GI, 1% Cystic Fibrosis patients

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18
Q

angiodysplasia

A

small fragile, swollen and easily rupturing small mucosal and submucosal vessels, usually in colon and right side of colon (AC) or cecum
= after 6th decade in life

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19
Q

SMA supplies what

A

illeum, AC, 2/3 TC

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20
Q

IMA supplies

A

1/3 TC, DC, Sigmoid Colon, Rectum

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21
Q

Celiac supplies

A

left stomach, liver, spleen

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22
Q

what vessels are big arteries that would cause ischemia in a large area of the instestines

A
  1. Ileocolic A
  2. Right Colic A
  3. Middle Colic
  4. Marginal A ** esp**
  5. Left Colic
  6. Signmoid A
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23
Q

Mesenteric Venous thrombosis happens how

A
  1. Hypercoagulable state
  2. Tumors
  3. Trauma
  4. Cirrhosis
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24
Q

Vascular Obstruction caused by

A
  1. severe atherosclerosis
  2. AAA
  3. Cardiac mural thrombi
  4. Vasculitis
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25
Q

chronic hypoperfusion causes by

A
  1. cardiac failure
  2. shock
  3. dehydration
  4. Drugs (vasocontrictors)
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26
Q

2 stages of ischemia

A

phase 1 : vascualr compromise
phase 2 : reperfusion injury from restoring Blood supply = leakage of gut bacteria into circulation, free radicals, N infiltration, inflammation

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27
Q

acute ischemia SX and who

A

usually over 70yo slightly more in F

- LLQ pain, need to poop, bloody D

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28
Q

Surgery should be done when in acute ischemia

A

if evidence of infarction = low bowel sounds, guarding, rebound tenderness

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29
Q

chronic ischemia SX

A
  1. ABD pain after 30min of eating, worsens over hour
  2. pain goes away after 1-3 hours
  3. if not treated can become severe acute ischemia
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30
Q

transmural artery occlusion mortality rate

A

10% first 30 days

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31
Q

which artery if occluded will cause worst outcome

A

SMA

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32
Q

angiodysplasia is how common in elderly

A

20% of intestinal bleeding cases in elderly

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33
Q

Abetalipoproteinemia

A

inability to absorb fat

D, malabsorption

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34
Q

Microvillous inclusion disease

A

abnormal microvilli inclusions giving D and malabsorption

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35
Q

environmental enteropathy

A

chronic fecal oral contamination giving inflammation and D and malabsorption

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36
Q

autoimmune enteropathy

A

autoimmune in children causing a lot of D they need to be on IV fluids

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37
Q

hallmark of malabsorption

A

steatorrhea = excessive fecal fat, bulky, grease, yellow, claycolored

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38
Q

3 most common reasons for malabsorption in US and one not as common only

A
  1. Pancreatic insufficiency
  2. Celiac Disease
  3. Crohn’s Disease
  • Graft vs Host hematopoietic stem cell transplantation
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39
Q

dysentery

A

painful, bloody, small volume D

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40
Q

Secretory D

A

isotonic stool, during fasting times
= low area to absorb, from bacteria or medications
= continual water pulled out into GI

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41
Q

Osmotic D

A

= lactase deficiency, excessive osmotic forces exerted by unabsorbed luminal solutes
= more concentrated D fluid

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42
Q

Malabsoptive D

A

X nutrient absorption = steatorrhea

fasting helps

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43
Q

Exudative D

A

D from inflammation disease

= purulent, bloody D continuing during fasting

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44
Q

Cystic Fibrosis and GI

A
  1. pancreatic abnormalities (85%-90% patients)
    = mucus clogs the pancreatic exocrine ducts
    = X fat absorption with no pancreatic excretion
    = vitamine def, squamout metaplasia of pancreatic duct lining
  2. mucous plugs in SI = SIO = meconium ileus
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45
Q

foods that cause celiac disease to flare up

A

wheat, rye, barley

autoimmune to own Lymphocytes with the gluten food products

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46
Q

what can put someone at risk of celiac disease

A

infection, tissue damage

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47
Q

how is gluten recognized and activating the immune system in CD

A

Gliadin (monomer of gluten) activates

  1. Innate IS : CD8+ (by IL15)
  2. Adaptive IS : CD4+ and Bcells
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48
Q

HLA involved in CD

A

DQ2 and DQ8 on the DC that show the gliadin to T cells

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49
Q

how to DX CD

A
  1. Villous atrophy
  2. tTG antibody serologic test (IgA antibody to tTG) **
  3. Gliadin AB are not very good to dx
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50
Q

SX of CD in adults

A

higher in F (30yo - 60yo)

  • chronic D
  • bloating
  • chronic fatigue
  • malabsorption
  • dermatitis herpetiformis
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51
Q

SX of CD in children

A

F= M (6mo = 24mo)

  • irritability
  • abd distention
  • chronic D, abd pain, N /V
  • weight loss
  • arthritis *, joint pain, ulcers, stomatits(inflamed mouth), anemia, delayed puberty
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52
Q

Dermatitis herpetiformis

A

pruritic, small vesicles, microabscess, subepidermal blister, IgA granular deposits
= IgA anti-gluten AB react with BM proteins (tTG)

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53
Q

Enviornmental Enteric Dysfunciton ( Enviromental Enteropathy, tropical enteropathy, tropical sprue)

  1. where
  2. how
  3. what happens
A
  1. subsaharan africa, Zambia, (northern australia)
  2. poor hygiene and sanitation
  3. malabsorption, D, lower growth
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54
Q

Autoimmune eneropathy

  1. what is it
  2. who
  3. what happens
  4. gene
A
  1. X- linked disorder
  2. children
  3. severe persistant D and autoimmune disease
  4. FOXP3 gene loss in the IPEX kind
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55
Q

Autoimmune eneropathy

  1. MOA
  2. Histology
  3. TX
A
  1. autoABs to enterocytes and goblet cells (sometimes parietal and islet cells)
  2. N in the intestinal mucosa (NOT seen in celiac D)**
  3. immunosuppressive drugs = cyclosporine, hematopoietic stem cell transplantation
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56
Q

IPEX is what

A

familial type of Autoimmune eneropathy

= immune dysregulation, polyendocrinopathy, enteropathy, X-linked

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57
Q

Lactase Deficiency

  1. other name
  2. MOA
A
  1. Disaccharidase

2. Lactose cant –> Glucose and Galactose = osmotic D

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58
Q

Congenital Lactase Deficiency

what and SX

A

mutation in lactase enzyme
AR
= explosive D, abd distention when milk ingestion

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59
Q

Acquired lactose deficiency

what is it and who and risks

A

downregulation of lactase enzyme gene expression (esp native americans, AA, Chinease)
= viral infections, bacterial infections, can resolve over time

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60
Q

Microvillous Inclusion Disease

  1. MOA
  2. gene
  3. histology
A

rare AR
= Vesicular transport limited from X brush boarder assemble
= MYO5B (encoding motor protein)
= accumulation of abnormal apical vesicles of microvilli and membrane components

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61
Q

Microvillous Inclusion Disease

  1. who
  2. DX
  3. TX
A
  1. European, Middle eastern, Navajo Native Americans
  2. immunostaning for brush boarder protein villin (CD10 immunohistochemistry)**
  3. parenteral nutrition and SI transplantation
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62
Q

Abetalipoproteinemia

  1. what MOA
  2. who
  3. SX
A
  1. AR, X assemble TAG right lipoproteins
  2. infants
  3. steatorrhea, failure to thrive, D
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63
Q

Abetalipoproteinemia

  1. Histology
  2. effects this disease has
A
  1. plasma has no lipoproteins with apolipoprotein B, defect in plasma membranes, Acanthocytes in blood smear
  2. vitamine deficiency
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64
Q

Abetalipoproteinemia gene and how it is supposed to work

A

MTG gene mutations
= transferes TAGs into the apolipoprotien B in the ER,
= matation causes TAGs to accumulate in ICF

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65
Q

Infectious enterocolitis broad SX and deaths per day in world

A

D, ABD pain, urgency, perianal discomfort, incontinence, hemorrhage
= 2000 deaths / day
= 10% deaths by age 5yo

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66
Q

fecal leukocyte count
few
moderate
many

A

few : < or = 2 oil immersion microscopic field
Moderate : 3 OIF - 9 OIF
Many : 10 or more OIF

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67
Q

Many fecal leukocytes means

A

invasive pathogen like shigella or salmonella

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68
Q

few fecal leukocytes means

A

IF high erythrocytes = amebiasis

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69
Q

PCR for Infectious enterocolitis

A

test for tcdC (toxin genes)

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70
Q

selective serology for Infectious enterocolitis

A

Giardia Ag

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71
Q

Vibrio cholerae

  1. bacteria type
  2. where
  3. MOA
A
  1. comma-shaped, gram -
  2. Ganges Valley India, Bangladesh
  3. over activated CFTR = pumping Cl- out and watery D
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72
Q

Campylobacter Enterocolitis

  1. other name
  2. from what
A
  1. C. jejuni = travelers D

2. food poisoning chicken, unpasteurizes milk, contaminated water

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73
Q

Campylobacter Enterocolitis

  1. SX
  2. can cause what 3 things**
A
  1. Bloody or Watery D, bloody only if invasive bacteria strain going throught tight junctions
  2. Reactive Arthritits : IF HLA-B27**, Guillain-Barre, Erythema nodosum
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74
Q

Campylobacter Enterocolitis and enteric fever

A

the bacteria proliferates in the lamina propria and causes nonspecific fever, abd pain

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75
Q

Guillain- Barre syndrome

SX and TX

A
  1. acute inflammatory demyelination of neurons in hands and feet usually traveling up the leg
  2. low or absent DTR
  3. Resp muscle weakness need to be on ventilator (when traveling up that far)
    TX : plasma exchange + IV Ig
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76
Q

erythema nodosum

A

inflammation in fatty layer of skin, off and on inflammed and reddish painful lumps legs front, then become bruise like and flatten out

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77
Q

Shigellosis

  1. bacteria type
  2. close related to what
  3. most common cause of what in the world
A
  1. gram -, unencapsulated, nonmotile, facultative anaerobes
  2. E. coli
  3. Bloody D
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78
Q

Shigellosis

  1. who in US
  2. deaths in world
A
  1. daycare children, migrant workers, traveling to low resource countries, nursing homes
  2. 75% death rate in children younger then 5yo
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79
Q

Shigellosis

  1. attacks where in the GI
  2. histology
  3. can look like and be confused with
A
  1. left colon, ileum
  2. M in dome epithelium over Peyer patche, hemorrhaging + ulcerated mucosa, pseudomembranes
  3. M cells and aphthous ulcers similar to what is seen in Crohns Disease
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80
Q

Shigellosis

  1. time line of infection
  2. children vs adults
  3. can mimic what disease
  4. DX
A
  1. incubation 1 week, 7-10day D, fever, abd pain (enteric fever) = initially watery and 50% becomes bloody 1 for up to month long
  2. more severe only shorter duration in children
  3. waxing and waning D = looks like new onset ulcerative colitis in adults
  4. stool culture
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81
Q

Shigellosis contraindication for TX and indicated TX

A

DONT give anit-diarrheal medication, prolongs infectiong and delay clearence
- give antibiotics

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82
Q

Shigellosis 3 complications

A
  1. Reactive arthritis
  2. Hemolytic uremic syndrome
  3. Toxic megacolon
83
Q

Salmonella

  1. who
  2. when
  3. infection is how easy
  4. DX
A
  1. children and older adults
  2. summer and fall
  3. very few bacteria to infect person (esp pt with acid suppression or atrophic gastritis)
  4. Stool cultures
84
Q

Salmonella causes what 2 things

A
  1. Typhoid fever, paratyphoid fever

2. Gasteroenteritis, food poisoning

85
Q

Typhoid fever
1. causes what
2, from what bacteria
3. who

A
  1. enteric fever
  2. Salmonella enterica
  3. children and adolescents however any range in non-endemic countries
86
Q

Salmonella Typhi and para typhi difference

A

typhi : in endemic countries

paratyphi : travelers (most are vaccinated against typhi)

87
Q

Salmonella Typhi and para typhi where can you most likely get this and how

A

India, Mexico, Philippines, Pakistan, El Salvador, Haiti

= food or contaminated water human to huma

88
Q

Salmonella Typhi and para typhi can be associated with what condition

A

Gallstones, chronic carrier of Typhoid fever, they colonize there

89
Q

Salmonella Typhi and para typhi

  1. SX
  2. can mimin sx of what abd pain
  3. Histology
A
  1. Bloody D, erythematous maculopapular rash (Rose spots), abd pain, anorexia, bloating, short asymp phase for bacterimia and fever and flu like sx
  2. appendicitis
  3. peyer pathches in terminal ileum enlarged plateau elevations, LN enlarged, N + M, oval ulcers in ileum
90
Q

Disseminated Salmonella Typhi causes what

A
  • soft enlarged spleen
  • parenchymal necrosis, M replace hepatocytes = typhoid nodules
  • encephalopathy, meningitis, seizures, endocarditis, myocarditis, pneumonia, cholecystitis
91
Q

Yersinia 3 species

A
  1. enterocolitica
  2. pseudotuberculosis
  3. pestis
92
Q

who is in more risk of sepsis and death from Yersinia

A

people with high non-heme Fe = chronic anemia, hemochromatosis
= Fe enhances virulence and dissemination

93
Q

Yersinia infects what part of GI and histology can be confused with what disease

A

Ileum, appendix, right colon

= crohns disease confusion in histology

94
Q

Yersinia histology

A

lymph tissue and peyer patch hyperplasia (it proliferates in LN)
hemorrhagic and ulcerative mucosa over lymph tissue

95
Q

Yersinia post infection complications

A
  1. reactive arthritis
  2. urethritis
  3. conjunctivitis
  4. myocartitis
  5. erythethma nodosum
  6. Kidney disease
96
Q

E. Coli are what type of bacteria

A

gram- bacilli, usually in healthy GI

97
Q

ETEC

A

Enterotoxigenic E. Coli

= travelers D, Campylobacter

98
Q

EPEC

A

Enteropathogenic E. Coli

= endemic D (world wide)

99
Q

EHEC

A

Enterohemorrhagic E. Coli

= E. Coli O157 : H7 and non-OH157 : H7

100
Q

EIEC

A

Enteroinvasive E. Coli
= bacteria similar to Shigella
= shiga-like toxin

101
Q

EAEC

A

Enteroaggregative E. Coli

= “stacked brick” morphology when bound to epithelial cells

102
Q

Pseudomembranous colitis is what and how does it happen

A

anti-biotic associated colitis or D, disrupts colon microbiota = C. Difficile overgrowth

103
Q

Pseudomembranous colitis can happen also in what patients with high risk to this

A

old age, hospitilized, immunosuppressed

104
Q

Pseudomembranous colitis histology

A

inflammatory cells and debri leyer, ischemia and necrotizing infections in GI(volcano like eruptions of N form colon crypts)

105
Q

Pseudomembranous colitis SX DX

A

fever, leukocytosis, abd pain, cramps, Watery D, hypoalbuminemia from protein loss
DX : histopathology showing C. Diff**

106
Q

Pseudomembranous colitis TX

A

metronidazole and vancomycin (resistant strains are growing)

107
Q

Pseudomembranous colitis complication that can happen

A

toxic megacolon

108
Q

Whipple Disease

  1. who
  2. SX triad
A
  1. caucasian men, very rare, farmers and soil and animal workers
  2. D, weight loss, arthralgia **
109
Q

Whipple Disease first described as

A

intestinal lipodystrophy

110
Q

Whipple Disease extraintestinal sx that can last months to years

A
  1. arthritis
  2. fever
  3. LAD
  4. neuro/cardiac/ pulmonary problems
111
Q

Whipple Disease hallmark in histology

A

dense accumulation in foamy M in SI laminal propria

112
Q

M in Whipple Disease

A

= have periodic acid and are Schiff PAS +, diastase resistant
= - acid-fast test

113
Q

mycobacterium stain what

A

+ Schiff PAS

+ acid fast

114
Q

what is the most common form of gasteroenteritis world wide and how is it spread

A

NOROVIRUS
fecal oral TR mostly
(easy spread in schools, hospitals, nursing homes, CRUISE SHIPS)

115
Q

norovirus is serious in

A

immunocompromised

116
Q

Rotovirus is what type of virus and who does it infect

A

encapsulated Double-RNA, high D death cause in world

= children 2mo-24mo (AB in breast milk protects baby first 6mos)

117
Q

Rotovirus TR where

SX and causes what

A

hosp, daycare, easy spread = outbreaks

= GI cant absorb so OSMOTIC DIARRHEA, from incomplete nutrient absorption

118
Q

Ascaris Lumbricoides

A

ingestion of embroyonated egg (from feces)
= hathced go into circulation from GI
= goes into lungs + coughed up to GI
= mature in SI

119
Q

Strongyloides Stercoralis

A

fecal transmission from skin contact usually walking barefoot (rhabditiform larvae becomes filariform larvae and can penetrate skin)
= goes to SI and then they lay eggs and those later migrate to other organs

120
Q

Intestinal hookworm

A

filariform larvae from rhabditiform larvae penetrates skin
= into BVs that go to lungs and then exit circulation in lungs
= coughed up and go to SI
= can become dormant in tissues

121
Q

Enterobius Vermicularis

A 
perianal fold eggs ingested by mouth
= goes to SI
= become adults in cecum
= GRAVID FEMALE goest to perianal region at night to lay eggs 
*childhood disease
122
Q

Schistomsoma spp.

A

from urine of feces and release miracidia that enter snails
= release to water from snails
= penetrate skin (walking in creek or barefoot)
= go to circulation into portal blood –> LIVER to mature
= then go to bowel/rectum/bladder veins to lay eggs

123
Q

Taeina

A

in feces that infect cattle and pigs through the vegetation they eat
= go to circulation and then muscles
= humans eat raw or undercooked meat and go to SI

124
Q

Diphyllobothriid Tapeworm

A

in feces to water to crustaceans to small fish to bigger fish to humans that eat them or other animals eating them to SI

125
Q

Amebias

A

feces (trophozoites and cycts) to ingested by humans to SI, brain, lungs, liver

126
Q

Cryptosporidium spp.

A

feces to water and food (swimming pools), to ingested to SI

major host in Cattle C. Parvum

127
Q

cholora is what type of D

A

secretory D

128
Q

colon 3 major functions

A
  1. absorb 5L fluids every day
  2. secrete mucins (protections and immune)
  3. microbiota digestion
129
Q

IBD most common people and places

A

caucasians, female, 3-5X more in jews, North America, Europe, Australia

130
Q

what happens in IBD

A

the innate M secrete too much TNF-a which makes too many CD4 helper cells over the number of Treg cells available, which recruits more lymphocytes
- these cytokines stimulate JAK2 and STAT3 which activated innate cells talking to adaptive cells

131
Q

therapies for IBD do what

A
  1. inhibit the inflammatory cytokines (IL23, TNF, IL12, IL6)
  2. epithelial GF
  3. block JAK STAT
132
Q

IL23 does what

A

activates CD4 Th17 cells and is enhanced with TNF superfamily 15

133
Q

crohns disease is associated with what receptors and cytokines

A 
IL23
JAKSTAT
CCR6
TNFS15
p40
134
Q

Ulcerative colitis is associated with what receptors and cytokines

A

IL23
JAKSTAT
p40

135
Q 
Crohns vs UC
CROHNS 
1. where
2. lesions 
3. stricture y/n
4. wall looks like
5. inflammation
6. pseudopolys y/n
7. ulcers look like 
8. Lymph y/n
A
  1. ileum + colon
  2. skip lesions**
  3. yes
  4. thick
  5. transmural
  6. moderate amounts
  7. deep knife-like ulcers
  8. yes
136
Q 
Crohns vs UC
UC 
1. where
2. lesions 
3. stricture y/n
4. wall looks like
5. inflammation
6. pseudopolys y/n
7. ulcers look like 
8. Lymph y/n
A
  1. Colon
  2. diffuse lesions
  3. no
  4. normal wall
  5. mucosal inflammation only
  6. yes many pseudopolyps
  7. superficial and broad
  8. some lymph
137
Q 
Crohns vs UC
CROHNS 
1. Fibrosis
2. Serositis
3. Granulomas
4. Fistula or sinuses 
5. perianal fistula 
6. malabsorption 
7. malignant potential 
8. recurr after surgery
9. toxic megacolon
A
  1. yes
  2. yes
  3. yes
  4. yes
  5. yes
  6. yes
  7. ONLY if in colon
  8. yes
  9. NO
138
Q 
Crohns vs UC
UC 
1. Fibrosis
2. Serositis
3. Granulomas
4. Fistula or sinuses 
5. perianal fistula 
6. malabsorption 
7. malignant potential 
8. recurr after surgery
9. toxic megacolon
A
  1. no
  2. no
  3. no
  4. no
  5. no
  6. no
  7. YES
  8. no
  9. YES
139
Q

what is having hypertrophy in CD

A

muscularis propria

and the mesenteric fat around it = creeping fat which starts to cover over the intestines

140
Q

early ulcer in CD and what it becomes later

A

aphthous ulcer , which many lesions form after and elongate together in serpentine way along bowl, deep narrow ulcers
= causes cobblestone appearance

141
Q

cell that can undergo metaplasia in CD

A

paneth cells

142
Q

UC replicates in ulcers how

A

individually does not exent on eachother = isolate islands
still form close to each other so abrupt line between effected colon and normal colon
= ALSO crypt abscesses form

143
Q

CD initial ER SX

A

RLQ pain, Bloody D, fever

144
Q

UC initial ER SX

A

can be as severe to cause medical emergency, and surgery

145
Q

IBD SX not associated with GI

A
  1. sclerosis cholangitis
  2. stomatitis + ulcers
  3. steatosis
  4. Gallstones
  5. peripheral arthritis and spondylosis
  6. kidney stones
  7. erythema nodosum
146
Q

CD serologic testing shows

A

Saccharomyces cervisiae ABs

147
Q

UC CD serologic testing shows

A

Perinuclear Anti-N cytoplasmic ABs

148
Q

if you cant tell apart CD and UC

A

indeterminate Colitis

10% patients

149
Q

what contributes to malignancy in IBD besides severity and duration

A

N responce

150
Q

Diverticulosis and inflammation can lead to

A

abscess or fistula, perforation = Medical EM

151
Q

Diversion colitis

A

colitis in diverted segments, redness friability and mucosal lymph follicles

152
Q

Microscopic colitis 2 types

A

Collagenous colitis

Lymphocytic colitis

153
Q

Collagenous colitis

A

Watery D, no WL, middle aged

154
Q

Lymphocytic colitis

A

Watery D, no WL, celiac disease and autoimmune disease

155
Q

Graft vs host sx

A

watery D that can becoem bloody D, due to destruction of many crypts

156
Q

Diverticulitis is what and found where

A

outpouching of muscularis propria forming polys on external side of bowel,
= japan, asia and africa (right side), western countries (left)

157
Q

Diverticulosis SX

A

asymptomatic, intermittent crampingm lower abd discomfort, constipation, distention, incontinence

158
Q

polys early stage and polyps with stalk are called what

A

early stage : small elevations of mucosa (sessile)

with stalk : pedunculated

159
Q

Hyperplastic polyps
where
what

A

left colon

low epithelial turnover delayed shedding = piling up of goblet cells and absorptive cells

160
Q

Inflammatory polyps can be seen in

A

solitary rectal ulcer syndrome

161
Q

solitary rectal ulcer syndrome TRIAD

A

rectal bleeding
mucus discharge
anterior rectal wall location

162
Q

solitary rectal ulcer syndrome the inflammatory poly can cause what

A

rectal prolapse

163
Q

hamartomatous polyps happen how and associated with

A

sporadically by TSG or OG mutation

increased risk of cancer

164
Q

juvenile polyps
who and where
SX and risks from this

A

sporadic (retention) or syndromic polyp
= under 5yo (severe)
= rectum (more severe if in SI or stomach)
= rectal bleeding , intussusception, obstruction, polyp prolapse
= early colon cancer

165
Q

Peutz Jaghers Syndrome

who what

A

AD at 11yo

Many Hamartomatous polyps and mucocutaneous hyperpigmentation (lips, nostrils, buccal mucosa, palms, genitals)

166
Q

Peutz Jaghers Syndrome polyps most common place

A

SI, colon, stomach (lower frquency in bladdr and lungs)
= INTUSSUSCEPTION happens, fatal
= STK11 mutation** (serine threonine kinase tumor suppressor)

167
Q

Histologic examination Peutz Jaghers Syndrome

A

CT, SM, Lamina propria, gland network HAMARATOMA so unorganized

168
Q

Adenomatous polys

A

intraepithelial neoplasms all sizes
more in males
precursor to adenocarcinoma (in most common colon cancer)

169
Q

adenomatous polys how can you measure risk of malignancy

A

the size of the polyp

170
Q

hallmark histology of colorectal adenomas

A
  1. nuclear hyperchromasia
  2. elongations
  3. stratification
171
Q

Sessile serrated polyposis cancer syndrome

A

rare disorder patient has mnay serrated polyps in colon abd increases risk of familial colon cancer
= MSI and BRAF mutation
= sawtooth appearance in bottom of crypt where poly is attached (wide)

172
Q

Familial adenomatous polyposis
mutation
where
what type of polyp

A

= APC mutation (APC / WNT pathway)
= AD
= any colon location
= tubular + villous typical adenocarcinoma

173
Q

Hereditary non-polyposis colorectal cancer
mutation
where
what type of polyp

A

= MSH2 and MLH1 mutation (X DNA mismatch repair)
= AD
= RIGHT side colon
=sessile serrated adenoma, mucinous adenocarcinoma

174
Q

Sporatic Colon cancer (70%-80%)
mutation
where
what type of polyp

A

= APC mutation (APC / WNT pathway, causing X TGF-B and activating KRAS) *
= not congenital
= Left side colon
= tubular, villous, typical adenocarcinoma

175
Q

Familial adenomatous polyposis
how old when sx
sx other then GI

A

teenagers (10yo-15yo)

- congenital hypertrophy of retinal pigment epithelium (seen at birth = screening)

176
Q

Familial adenomatous polyposis risks and percentage

A

100% untreated get adenocarcinoma usually by 30yo

- can also have polyps in stomach and ampulla of Vater

177
Q

most common type of adenocarcinoma

A

sporadic (familial and hereditary only 20%)

178
Q

adenocarcinoma most common in what continent
peak age
diet that can lead to this

A

North America
60yo-70yo
low fiber, high fat, refined carbs

179
Q

medication that can prevent adenocarcinoma

A

NSAIDS , COX2 inhibitors

there are a lot of COX2 in adenomas and cancers

180
Q

APC / WNT and MSI involvement in mutations causing adenocarcinoma happens exaclty how dna level

A

methylation silencing

181
Q

Sporadic Colon Cancer (10% - 15%)
mutation
where
what type of polyp

A

= MSH2 and MLH1 mutation (X DNA mismatch repair, causing microsatalite instability)
= not congenital
= LEFT side colon
= sessile serrated adenoma, mucinous adenocarcinoma

182
Q

APC is what

A

controls cell growth and differentiation TSG

in WNT signal pathway, and both APC genes have to be mutated for adenocarcinoma to happen

183
Q

microsatalite instability (MSI)

A

X DNA mismatch repair = accumulation of mutations in microsatallite repeats

184
Q

Lynch syndrome
what is it
age
where

A

Hereditary non-polyposis colorectal cancer (HNPCC)
= younger ages
= ascending colon

185
Q

polyps on right side special thing

A

grow on one side as polypoid exophytic masses, rare to cause obstruction

186
Q

polyps on distal or left colon special thing

A

annular lesions making napkin ring constriction and luminal narrowing
can cause obstruction

187
Q

right side polyp adenocarcinoma SX

A

fatigue and weakness from Chronic IDA

188
Q

left side polyp adenocarcinoma SX

A

occult bleeding, bowel changes, cramping, LLQ pain

189
Q

pectinate dentate line

A

transition from predecrodeum from transition zone (anal pecten) to anus anoderm

190
Q

above the transition zone

A

is teh anal canal with columnar epithelium = sensitive to cutting

191
Q

Tumors of anal canal above pectinate line

A

adenocarcinomas

192
Q

cancers in anal canal belwo pectinate line

A

SCC (or BCC or melanoma)

193
Q

anal canal cancers or rectal cancer infiltriating to anal canal spreads to what

A

superficial inguinal LNs

194
Q

anal canal and low rectal cancers infiltrate the anorectal ring can cause what and that is a contraindication for what

A

incontinence

dont do chemo-radiation or low anterior resection to preserve the sphincter

195
Q

hemorrhoids happen how and sx and where

A

persistent elevated venous P
(pain, rectal bleeding bright red)
EXTERNAL : below pectinate line, sensitive skin, painful
INTERAL : above PL on anal mucosa and painless (can be ligated or injected with sclerosant with no anesthesia)

196
Q

3rd degree perineal tear

A

torn anal sphincter and perineal muscles

197
Q

4th degree perneal tear

A

torn sphincter and rectum and perineal muscles

198
Q

true diverticulum of the cecum

199
Q

acute appendicitis
who
SX

A

adolescents and young adults, slightly more in males

= periumbilical pain localizing to RLQ (Mcburney), N/V/low fever/mild elevation in WBCs

200
Q

obstruction of appendix happens due to

A

Enterobius vermicularis

201
Q

Carcinoid

A

neuroendocrine tumor = most common conventional adenomas and carcinomas tumor of appendix

202
Q

Mucinous neoplasms

A

benign and malignant tumor or appendix

203
Q

Pseudomyxoma peritonei

what is it

A

syndrome of progressive intraperitoneal accumulation of mucinous ascites = mucin producing neoplsm

204
Q

Pseudomyxoma peritonei caused mostly from

A

mucinous tumor of appendix

GIGU 2 Exam 1 (12 decks)

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