Small Intestine And Colon - Dr. Dobson Flashcards

(204 cards)

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
chronic hypoperfusion causes by
1. cardiac failure 2. shock 3. dehydration 4. Drugs (vasocontrictors)
26
2 stages of ischemia
phase 1 : vascualr compromise phase 2 : reperfusion injury from restoring Blood supply = leakage of gut bacteria into circulation, free radicals, N infiltration, inflammation
27
acute ischemia SX and who
usually over 70yo slightly more in F | - LLQ pain, need to poop, bloody D
28
Surgery should be done when in acute ischemia
if evidence of infarction = low bowel sounds, guarding, rebound tenderness
29
chronic ischemia SX
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
30
transmural artery occlusion mortality rate
10% first 30 days
31
which artery if occluded will cause worst outcome
SMA
32
angiodysplasia is how common in elderly
20% of intestinal bleeding cases in elderly
33
Abetalipoproteinemia
inability to absorb fat | D, malabsorption
34
Microvillous inclusion disease
abnormal microvilli inclusions giving D and malabsorption
35
environmental enteropathy
chronic fecal oral contamination giving inflammation and D and malabsorption
36
autoimmune enteropathy
autoimmune in children causing a lot of D they need to be on IV fluids
37
hallmark of malabsorption
steatorrhea = excessive fecal fat, bulky, grease, yellow, claycolored
38
3 most common reasons for malabsorption in US and one not as common only
1. Pancreatic insufficiency 2. Celiac Disease 3. Crohn's Disease - Graft vs Host hematopoietic stem cell transplantation
39
dysentery
painful, bloody, small volume D
40
Secretory D
isotonic stool, during fasting times = low area to absorb, from bacteria or medications = continual water pulled out into GI
41
Osmotic D
= lactase deficiency, excessive osmotic forces exerted by unabsorbed luminal solutes = more concentrated D fluid
42
Malabsoptive D
X nutrient absorption = steatorrhea | fasting helps
43
Exudative D
D from inflammation disease | = purulent, bloody D continuing during fasting
44
Cystic Fibrosis and GI
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
45
foods that cause celiac disease to flare up
wheat, rye, barley | autoimmune to own Lymphocytes with the gluten food products
46
what can put someone at risk of celiac disease
infection, tissue damage
47
how is gluten recognized and activating the immune system in CD
Gliadin (monomer of gluten) activates 1. Innate IS : CD8+ (by IL15) 2. Adaptive IS : CD4+ and Bcells
48
HLA involved in CD
DQ2 and DQ8 on the DC that show the gliadin to T cells
49
how to DX CD
1. Villous atrophy 2. tTG antibody serologic test (IgA antibody to tTG) **** 3. Gliadin AB are not very good to dx
50
SX of CD in adults
higher in F (30yo - 60yo) - chronic D - bloating - chronic fatigue - malabsorption - dermatitis herpetiformis
51
SX of CD in children
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
52
Dermatitis herpetiformis
pruritic, small vesicles, microabscess, subepidermal blister, IgA granular deposits = IgA anti-gluten AB react with BM proteins (tTG)
53
Enviornmental Enteric Dysfunciton ( Enviromental Enteropathy, tropical enteropathy, tropical sprue) 1. where 2. how 3. what happens
1. subsaharan africa, Zambia, (northern australia) 2. poor hygiene and sanitation 3. malabsorption, D, lower growth
54
Autoimmune eneropathy 1. what is it 2. who 3. what happens 4. gene
1. X- linked disorder 2. children 3. severe persistant D and autoimmune disease 4. FOXP3 gene loss in the IPEX kind
55
Autoimmune eneropathy 1. MOA 2. Histology 3. TX
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
56
IPEX is what
familial type of Autoimmune eneropathy | = immune dysregulation, polyendocrinopathy, enteropathy, X-linked
57
Lactase Deficiency 1. other name 2. MOA
1. Disaccharidase | 2. Lactose cant --> Glucose and Galactose = osmotic D
58
Congenital Lactase Deficiency | what and SX
mutation in lactase enzyme AR = explosive D, abd distention when milk ingestion
59
Acquired lactose deficiency | what is it and who and risks
downregulation of lactase enzyme gene expression (esp native americans, AA, Chinease) = viral infections, bacterial infections, can resolve over time
60
Microvillous Inclusion Disease 1. MOA 2. gene 3. histology
rare AR = Vesicular transport limited from X brush boarder assemble = MYO5B (encoding motor protein) = accumulation of abnormal apical vesicles of microvilli and membrane components
61
Microvillous Inclusion Disease 1. who 2. DX 3. TX
1. European, Middle eastern, Navajo Native Americans 2. immunostaning for brush boarder protein villin (CD10 immunohistochemistry)**** 3. parenteral nutrition and SI transplantation
62
Abetalipoproteinemia 1. what MOA 2. who 3. SX
1. AR, X assemble TAG right lipoproteins 2. infants 3. steatorrhea, failure to thrive, D
63
Abetalipoproteinemia 1. Histology 2. effects this disease has
1. plasma has no lipoproteins with apolipoprotein B, defect in plasma membranes, Acanthocytes in blood smear 2. vitamine deficiency
64
Abetalipoproteinemia gene and how it is supposed to work
MTG gene mutations = transferes TAGs into the apolipoprotien B in the ER, = matation causes TAGs to accumulate in ICF
65
Infectious enterocolitis broad SX and deaths per day in world
D, ABD pain, urgency, perianal discomfort, incontinence, hemorrhage = 2000 deaths / day = 10% deaths by age 5yo
66
fecal leukocyte count few moderate many
few : < or = 2 oil immersion microscopic field Moderate : 3 OIF - 9 OIF Many : 10 or more OIF
67
Many fecal leukocytes means
invasive pathogen like shigella or salmonella
68
few fecal leukocytes means
IF high erythrocytes = amebiasis
69
PCR for Infectious enterocolitis
test for tcdC (toxin genes)
70
selective serology for Infectious enterocolitis
Giardia Ag
71
Vibrio cholerae 1. bacteria type 2. where 3. MOA
1. comma-shaped, gram - 2. Ganges Valley India, Bangladesh 3. over activated CFTR = pumping Cl- out and watery D
72
Campylobacter Enterocolitis 1. other name 2. from what
1. C. jejuni = travelers D | 2. food poisoning chicken, unpasteurizes milk, contaminated water
73
Campylobacter Enterocolitis 1. SX 2. can cause what 3 things**
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
74
Campylobacter Enterocolitis and enteric fever
the bacteria proliferates in the lamina propria and causes nonspecific fever, abd pain
75
Guillain- Barre syndrome | SX and TX
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
76
erythema nodosum
inflammation in fatty layer of skin, off and on inflammed and reddish painful lumps legs front, then become bruise like and flatten out
77
Shigellosis 1. bacteria type 2. close related to what 3. most common cause of what in the world
1. gram -, unencapsulated, nonmotile, facultative anaerobes 2. E. coli 3. Bloody D
78
Shigellosis 1. who in US 2. deaths in world
1. daycare children, migrant workers, traveling to low resource countries, nursing homes 2. 75% death rate in children younger then 5yo
79
Shigellosis 1. attacks where in the GI 2. histology 3. can look like and be confused with
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
80
Shigellosis 1. time line of infection 2. children vs adults 3. can mimic what disease 4. DX
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
81
Shigellosis contraindication for TX and indicated TX
DONT give anit-diarrheal medication, prolongs infectiong and delay clearence - give antibiotics
82
Shigellosis 3 complications
1. Reactive arthritis 2. Hemolytic uremic syndrome 3. Toxic megacolon
83
Salmonella 1. who 2. when 3. infection is how easy 4. DX
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
Salmonella causes what 2 things
1. Typhoid fever, paratyphoid fever | 2. Gasteroenteritis, food poisoning
85
Typhoid fever 1. causes what 2, from what bacteria 3. who
1. enteric fever 2. Salmonella enterica 3. children and adolescents however any range in non-endemic countries
86
Salmonella Typhi and para typhi difference
typhi : in endemic countries | paratyphi : travelers (most are vaccinated against typhi)
87
Salmonella Typhi and para typhi where can you most likely get this and how
India, Mexico, Philippines, Pakistan, El Salvador, Haiti | = food or contaminated water human to huma
88
Salmonella Typhi and para typhi can be associated with what condition
Gallstones, chronic carrier of Typhoid fever, they colonize there
89
Salmonella Typhi and para typhi 1. SX 2. can mimin sx of what abd pain 3. Histology
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
Disseminated Salmonella Typhi causes what
- soft enlarged spleen - parenchymal necrosis, M replace hepatocytes = typhoid nodules - encephalopathy, meningitis, seizures, endocarditis, myocarditis, pneumonia, cholecystitis
91
Yersinia 3 species
1. enterocolitica 2. pseudotuberculosis 3. pestis
92
who is in more risk of sepsis and death from Yersinia
people with high non-heme Fe = chronic anemia, hemochromatosis = Fe enhances virulence and dissemination
93
Yersinia infects what part of GI and histology can be confused with what disease
Ileum, appendix, right colon | = crohns disease confusion in histology
94
Yersinia histology
lymph tissue and peyer patch hyperplasia (it proliferates in LN) hemorrhagic and ulcerative mucosa over lymph tissue
95
Yersinia post infection complications
1. reactive arthritis 2. urethritis 3. conjunctivitis 4. myocartitis 5. erythethma nodosum 6. Kidney disease
96
E. Coli are what type of bacteria
gram- bacilli, usually in healthy GI
97
ETEC
Enterotoxigenic E. Coli | = travelers D, Campylobacter
98
EPEC
Enteropathogenic E. Coli | = endemic D (world wide)
99
EHEC
Enterohemorrhagic E. Coli | = E. Coli O157 : H7 and non-OH157 : H7
100
EIEC
Enteroinvasive E. Coli = bacteria similar to Shigella = shiga-like toxin
101
EAEC
Enteroaggregative E. Coli | = "stacked brick" morphology when bound to epithelial cells
102
Pseudomembranous colitis is what and how does it happen
anti-biotic associated colitis or D, disrupts colon microbiota = C. Difficile overgrowth
103
Pseudomembranous colitis can happen also in what patients with high risk to this
old age, hospitilized, immunosuppressed
104
Pseudomembranous colitis histology
inflammatory cells and debri leyer, ischemia and necrotizing infections in GI(volcano like eruptions of N form colon crypts)
105
Pseudomembranous colitis SX DX
fever, leukocytosis, abd pain, cramps, Watery D, hypoalbuminemia from protein loss DX : histopathology showing C. Diff****
106
Pseudomembranous colitis TX
metronidazole and vancomycin (resistant strains are growing)
107
Pseudomembranous colitis complication that can happen
toxic megacolon
108
Whipple Disease 1. who 2. SX triad
1. caucasian men, very rare, farmers and soil and animal workers 2. D, weight loss, arthralgia ****
109
Whipple Disease first described as
intestinal lipodystrophy
110
Whipple Disease extraintestinal sx that can last months to years
1. arthritis 2. fever 3. LAD 4. neuro/cardiac/ pulmonary problems
111
Whipple Disease hallmark in histology
dense accumulation in foamy M in SI laminal propria
112
M in Whipple Disease
= have periodic acid and are Schiff PAS +, diastase resistant = - acid-fast test
113
mycobacterium stain what
+ Schiff PAS | + acid fast
114
what is the most common form of gasteroenteritis world wide and how is it spread
NOROVIRUS fecal oral TR mostly (easy spread in schools, hospitals, nursing homes, CRUISE SHIPS)
115
norovirus is serious in
immunocompromised
116
Rotovirus is what type of virus and who does it infect
encapsulated Double-RNA, high D death cause in world | = children 2mo-24mo (AB in breast milk protects baby first 6mos)
117
Rotovirus TR where | SX and causes what
hosp, daycare, easy spread = outbreaks | = GI cant absorb so OSMOTIC DIARRHEA, from incomplete nutrient absorption
118
Ascaris Lumbricoides
ingestion of embroyonated egg (from feces) = hathced go into circulation from GI = goes into lungs + coughed up to GI = mature in SI
119
Strongyloides Stercoralis
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
Intestinal hookworm
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
Enterobius Vermicularis
``` 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
Schistomsoma spp.
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
Taeina
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
Diphyllobothriid Tapeworm
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
Amebias
feces (trophozoites and cycts) to ingested by humans to SI, brain, lungs, liver
126
Cryptosporidium spp.
feces to water and food (swimming pools), to ingested to SI | major host in Cattle C. Parvum
127
cholora is what type of D
secretory D
128
colon 3 major functions
1. absorb 5L fluids every day 2. secrete mucins (protections and immune) 3. microbiota digestion
129
IBD most common people and places
caucasians, female, 3-5X more in jews, North America, Europe, Australia
130
what happens in IBD
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
therapies for IBD do what
1. inhibit the inflammatory cytokines (IL23, TNF, IL12, IL6) 2. epithelial GF 3. block JAK STAT
132
IL23 does what
activates CD4 Th17 cells and is enhanced with TNF superfamily 15
133
crohns disease is associated with what receptors and cytokines
``` IL23 JAKSTAT CCR6 TNFS15 p40 ```
134
Ulcerative colitis is associated with what receptors and cytokines
IL23 JAKSTAT p40
135
``` 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 ```
1. ileum + colon 2. skip lesions**** 3. yes 4. thick 5. transmural 6. moderate amounts 7. deep knife-like ulcers 8. yes
136
``` 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 ```
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
``` 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 ```
1. yes 2. yes 3. yes 4. yes 5. yes 6. yes 7. ONLY if in colon 8. yes 9. NO
138
``` 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 ```
1. no 2. no 3. no 4. no 5. no 6. no 7. YES 8. no 9. YES
139
what is having hypertrophy in CD
muscularis propria | and the mesenteric fat around it = creeping fat which starts to cover over the intestines
140
early ulcer in CD and what it becomes later
aphthous ulcer , which many lesions form after and elongate together in serpentine way along bowl, deep narrow ulcers = causes cobblestone appearance
141
cell that can undergo metaplasia in CD
paneth cells
142
UC replicates in ulcers how
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
CD initial ER SX
RLQ pain, Bloody D, fever
144
UC initial ER SX
can be as severe to cause medical emergency, and surgery
145
IBD SX not associated with GI
1. sclerosis cholangitis 2. stomatitis + ulcers 3. steatosis 4. Gallstones 5. peripheral arthritis and spondylosis 6. kidney stones 7. erythema nodosum
146
CD serologic testing shows
Saccharomyces cervisiae ABs
147
UC CD serologic testing shows
Perinuclear Anti-N cytoplasmic ABs
148
if you cant tell apart CD and UC
indeterminate Colitis | 10% patients
149
what contributes to malignancy in IBD besides severity and duration
N responce
150
Diverticulosis and inflammation can lead to
abscess or fistula, perforation = Medical EM
151
Diversion colitis
colitis in diverted segments, redness friability and mucosal lymph follicles
152
Microscopic colitis 2 types
Collagenous colitis | Lymphocytic colitis
153
Collagenous colitis
Watery D, no WL, middle aged
154
Lymphocytic colitis
Watery D, no WL, celiac disease and autoimmune disease
155
Graft vs host sx
watery D that can becoem bloody D, due to destruction of many crypts
156
Diverticulitis is what and found where
outpouching of muscularis propria forming polys on external side of bowel, = japan, asia and africa (right side), western countries (left)
157
Diverticulosis SX
asymptomatic, intermittent crampingm lower abd discomfort, constipation, distention, incontinence
158
polys early stage and polyps with stalk are called what
early stage : small elevations of mucosa (sessile) | with stalk : pedunculated
159
Hyperplastic polyps where what
left colon | low epithelial turnover delayed shedding = piling up of goblet cells and absorptive cells
160
Inflammatory polyps can be seen in
solitary rectal ulcer syndrome
161
solitary rectal ulcer syndrome TRIAD
rectal bleeding mucus discharge anterior rectal wall location
162
solitary rectal ulcer syndrome the inflammatory poly can cause what
rectal prolapse
163
hamartomatous polyps happen how and associated with
sporadically by TSG or OG mutation | increased risk of cancer
164
juvenile polyps who and where SX and risks from this
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
Peutz Jaghers Syndrome | who what
AD at 11yo | Many Hamartomatous polyps and mucocutaneous hyperpigmentation (lips, nostrils, buccal mucosa, palms, genitals)
166
Peutz Jaghers Syndrome polyps most common place
SI, colon, stomach (lower frquency in bladdr and lungs) = INTUSSUSCEPTION happens, fatal = STK11 mutation**** (serine threonine kinase tumor suppressor)
167
Histologic examination Peutz Jaghers Syndrome
CT, SM, Lamina propria, gland network HAMARATOMA so unorganized
168
Adenomatous polys
intraepithelial neoplasms all sizes more in males precursor to adenocarcinoma (in most common colon cancer)
169
adenomatous polys how can you measure risk of malignancy
the size of the polyp
170
hallmark histology of colorectal adenomas
1. nuclear hyperchromasia 2. elongations 3. stratification
171
Sessile serrated polyposis cancer syndrome
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
Familial adenomatous polyposis mutation where what type of polyp
= APC mutation (APC / WNT pathway) = AD = any colon location = tubular + villous typical adenocarcinoma
173
Hereditary non-polyposis colorectal cancer mutation where what type of polyp
= MSH2 and MLH1 mutation (X DNA mismatch repair) = AD = RIGHT side colon =sessile serrated adenoma, mucinous adenocarcinoma
174
Sporatic Colon cancer (70%-80%) mutation where what type of polyp
= APC mutation (APC / WNT pathway, causing X TGF-B and activating KRAS) * = not congenital = Left side colon = tubular, villous, typical adenocarcinoma
175
Familial adenomatous polyposis how old when sx sx other then GI
teenagers (10yo-15yo) | - congenital hypertrophy of retinal pigment epithelium (seen at birth = screening)
176
Familial adenomatous polyposis risks and percentage
100% untreated get adenocarcinoma usually by 30yo | - can also have polyps in stomach and ampulla of Vater
177
most common type of adenocarcinoma
sporadic (familial and hereditary only 20%)
178
adenocarcinoma most common in what continent peak age diet that can lead to this
North America 60yo-70yo low fiber, high fat, refined carbs
179
medication that can prevent adenocarcinoma
NSAIDS , COX2 inhibitors | there are a lot of COX2 in adenomas and cancers
180
APC / WNT and MSI involvement in mutations causing adenocarcinoma happens exaclty how dna level
methylation silencing
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Sporadic Colon Cancer (10% - 15%) mutation where what type of polyp
= MSH2 and MLH1 mutation (X DNA mismatch repair, causing microsatalite instability) = not congenital = LEFT side colon = sessile serrated adenoma, mucinous adenocarcinoma
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APC is what
controls cell growth and differentiation TSG | in WNT signal pathway, and both APC genes have to be mutated for adenocarcinoma to happen
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microsatalite instability (MSI)
X DNA mismatch repair = accumulation of mutations in microsatallite repeats
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Lynch syndrome what is it age where
Hereditary non-polyposis colorectal cancer (HNPCC) = younger ages = ascending colon
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polyps on right side special thing
grow on one side as polypoid exophytic masses, rare to cause obstruction
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polyps on distal or left colon special thing
annular lesions making napkin ring constriction and luminal narrowing can cause obstruction
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right side polyp adenocarcinoma SX
fatigue and weakness from Chronic IDA
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left side polyp adenocarcinoma SX
occult bleeding, bowel changes, cramping, LLQ pain
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pectinate dentate line
transition from predecrodeum from transition zone (anal pecten) to anus anoderm
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above the transition zone
is teh anal canal with columnar epithelium = sensitive to cutting
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Tumors of anal canal above pectinate line
adenocarcinomas
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cancers in anal canal belwo pectinate line
SCC (or BCC or melanoma)
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anal canal cancers or rectal cancer infiltriating to anal canal spreads to what
superficial inguinal LNs
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anal canal and low rectal cancers infiltrate the anorectal ring can cause what and that is a contraindication for what
incontinence | dont do chemo-radiation or low anterior resection to preserve the sphincter
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hemorrhoids happen how and sx and where
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)
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3rd degree perineal tear
torn anal sphincter and perineal muscles
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4th degree perneal tear
torn sphincter and rectum and perineal muscles
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true diverticulum of the cecum
appendix
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acute appendicitis who SX
adolescents and young adults, slightly more in males | = periumbilical pain localizing to RLQ (Mcburney), N/V/low fever/mild elevation in WBCs
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obstruction of appendix happens due to
Enterobius vermicularis
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Carcinoid
neuroendocrine tumor = most common conventional adenomas and carcinomas tumor of appendix
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Mucinous neoplasms
benign and malignant tumor or appendix
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Pseudomyxoma peritonei | what is it
syndrome of progressive intraperitoneal accumulation of mucinous ascites = mucin producing neoplsm
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Pseudomyxoma peritonei caused mostly from
mucinous tumor of appendix