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Physiology (Digestive 1) Flashcards

1
Q

Split of GI tract

A
  1. Tubular system (Esophogus + Stomach + Small Intestine + Large Intestine/colon + rectum)
    • Tube that food goes through
  2. Non-tubular (Liver + pancreus + Gallblader)
    • Puts things into the tube
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2
Q

Layers of the Tubular GI System

A

In canal of GI tract:
Top - Lumen - Food is here

Mucosa
- Varies organ to origan

Submucosa - Loose connective tissue + Blood vessles)

Muscularis Propia - squeezes the Gi organs (does parastalsis to move food down)

Subserosa - Loose connective tissue

Serosa - Mesothelium
- Missing in some organs
- Interfaces with peritenial cavity

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3
Q

What layer in GI tract variers

A

Mucosa = Varies organ to origan (rest of the layers is the same throughout GI tract organs)

Because the mucosa does different jobs depedning on where in the process
- Mucosa = closer to the lumen that has the food = it is the varaible part

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4
Q

GI tumorgensis

A

GI tumorgenesis is similar throughout the GI tract

Start:
1. Normal Epithelium
2. +/- chronic inflamation (often occurs but not always)
- Provessing factor that eads to neoplasia
3. +/- metaplasia - some organs takes on histology of different organs (doesn’t occur in all)
4. Low Grade dysplasia (unversal)
5. High Grade Dysplasia
6. Cancer

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5
Q

Low and high grade Dysplasia

A

BOTH are universal in process

Cells are still in the basmemt membrane = not cancer yet

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6
Q

Esophogus Function

A

Convey food to stomach

NO digestion or Absorption

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7
Q

Esophgous Distictive Histology

A
  1. Non-keritimizing squamous mucosa in epithelium (different from skin)
  2. Submucosal glands (lubricate the esophogus)
  3. Muscularis propia contains skelatal muscle in upper esophogus
    • Creates volentray conrtol needed in upper region (smooth would be involentary)
  4. Adventitia (NOT serosa)
    • Because retroperitenal = no serosa
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8
Q

Layers of the esophogus

A

Squamas epithelium = startified
Dark line at top = where cells proliferate

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9
Q

Infection in esophgus

A

Esophagitis

Causes:
1. Medications
2. Trauma
3. Allergy
4. Radiation (ex. after cancer)
5. Inefctions
6. Reflux

Infections - have characteristic viral cytopathic effect (Seen on H/E)

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10
Q

CMV Esophogitus

A

CMV - makes cells big (CMV infected cells) (SEE large pruple circes)
- Get inclusion in cells (Cytoplasmic inclusions)
- Infects endothelial cells (where vessles are NOT on the surface)

IHC - Brown = CMV protein in nulcues (confirms presence of viral proetin)

CMV inclusions = more common in immunosupressive pateints

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11
Q

Viruses in the Esophogus

A
  1. CMV
  2. HSV
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12
Q

HSV Esophigutis

A

Vicera of epithelium (epithelium is inflamed)

HSV = herpes

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13
Q

herpes Inefction

A

Seen by 3 M’s
1. Modling - nuclei are shmooshed together
2. Multinucleation in one cell
3. Mergination - viral patches take over nucleus (push nucleic acid to the side)

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14
Q

Esophegeal tumergenesis

A

Steps:
1. Metaplasia (no neoplasia)
2. Dysplasia (non-invasive neoplasia)
3. Adenocacinoma (invasive neoplasm)

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15
Q

Example Metplasia in Esophogus

A

Barrets Esophogus

Get squamas epithelial –> intestinal epithelium
- See goblet cells white circles) = defined barretes

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16
Q

Normal Esophogus vs. Barret’s Mucosa

A

Normal Esophogus - Layers of squamous = normal

Barrets - Esophogus looks like intestinal epitheliam

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17
Q

Normal Intestine vs. Barret’s Mucosa

A

Images look similar (because get intestial epitheliam in esophgus during barrets)
- normal esophgus + aberrtes = both have goblet cells

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18
Q

High Grade dysplasia arising in Baerrt’s mucosa

A

When have metaplasia = have risk to gte low grade and then high grade dysplasia
- Cynslodigya displastic barrets = high risk –> can try and fix by removing a perice of the esophogus

Image - Karge nuclei + disorganized nuceli + stalked nuclei

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19
Q

Invasive Carcinoma with associated desmoplasia in Esophogus

A

Image = Esophogeal Adenocarcima

Desmoplasia = fibrotic stroma –> know cancer has invaded

If resection = know where cancer is by having a small biopsy but you might not know where the cancer is = rely on desmplasia to know that it is canver and not just high grade dysplasia

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20
Q

Risk factors for barets esophogus

A
  1. Chronic GERD (Acid goes to esophgus_
    • Risk factor for lower barret’s esophogus –> causes adenocarcinomas to be in lower esophgus more often
  2. ADvancing Age (>50 YO)
  3. Male
  4. Tobacco Use
  5. Central Obesity ( waist >40 inches)
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21
Q

Barret’s esophogus Stats

A

10% of patients with Barret mucosa have or will develope adenocarcima
- Includes Prevent adenoCA present at intial endoscopy (have barrets and cnacer at first biopsy) AND incident adonoCA develops subquentially

Overall incidence of progression to adenocarcima in Barrets pateints is 0.1-0.3%/year in first 5 years but 9% at 20 years

adenoCA = Adenocarcinoma = poor prognosis

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22
Q

Esophegeal Adenocarcinoma (tumor image)

A

Adenocarcima and barreys = often at the distal esophogus because often caused by GERD

Barret Mucosa = shows where to biopsy

Image - Pink on right side = stomach + see mass (cancer)

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23
Q

Treatment of Esophegeal Adenocarcinoma

A

There is a movment to treat endoscopically

Taking out the whole esophgus is a bigger procedure BUT if can do endoscopically it is beneficial

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24
Q

Esophogeal Adenocarcima (Histology)

A
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25
Q

Functions of the stomach

A

Overall: mixes and churns food with gastric juices to form chyme
- Begins chemical breakdown of proteins
- released digested food into the duodenum (in SI) as chyme
- Absorbes some fat soluble substances (Ex. alcholol + aspirin)
- Secretes Intrinic factor required to absorb B12 in the SI
- HAs antimicrobial functions
- Stimulates protein digesting enzymes

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26
Q

Layers of the stomach

A

Lumen = where food is

Muscularis propia - 2 layers of stomach muscle

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27
Q

Gross Anatomy of the stomach

A

Stomach = has multiple regions with difefrent roles

Middle area = body (fundus)
- makes pepsie + acid + intrisic factor
- Has cheif cells and parietal chells

Antrum
- Tells the body to make acid (regulatory function)
- Has Gastrin-producing endocrine cells (G-cells)

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28
Q

Mucosa of gastric fundus/body

A

Has:
1. Pits - Lined with mucosa producing cells
2. Glands - Has pareital cells and Cheif cells

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29
Q

Gastric fundic glands

A

See pareital cells (make Acid) + see Cheif cells (make pepsin)

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30
Q

Key cell in Stomach

A

Parietal cell

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31
Q

Parietal Cell

A

Filled with Secretory vesicles

H-K-ATPase Acid secreting pum (“proton pump”
- Basis for proton pump inhibitors to control acid secretion (used for Acid reflux) –> makes stomack condition less acidc = less damage to esophogus
- Activated by Ca+ and cAMP

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32
Q

Mucosa of antrum

A

Have:
1. Pits
2. Galnds - Have endocriine cells that make gastrin = stimulates acid secretion

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33
Q

Key Players of Acid Secretion

A
  1. Acetylcholine
  2. Gastrin
  3. Histamine
  4. Somatostatin

Overall - many cells secrete many thing (verycomplex)

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34
Q

Forms of Gastritis

A
  1. Acute
  2. Chronic includes common and uncommon forms)
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35
Q

Acute Gastritis1

A
  1. Acute hemorrahigc gastritis
  2. Acute infectous gastritis (can be bacterial with H.Pylori or Viral)
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36
Q

Chronic Gastritus

A

Common Forms:
1. Chemical gastritis - chemical injury to stomach (caused by NSAIDs + bile reflux)
2. Helicobacter Pyloru gastritus - become chronic
3. Autoimmune gastritus

Uncommon forms - many things (not listed)

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37
Q

Helicobacteria Pylori

A

Curved organisms with flagellae iver gastric epithelium

Helicobacteria Pylori = casues gastritus

Image - see inflamed stroma = look for Helicobacteria Pylori before calling it HP gastritus

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38
Q

Stains for detcting H.Pylori

A
  1. Giemsa
    • Inset = coccoid forms
      2 Immunosatins - shows HP is there
    • Arrows = Coccoid forms
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39
Q

Consequences of H.Pylori infection

A

Symptoms:
1. Many people are asymptomatic
2. Dyspepsia (abdominal pain)
3. get Peptic ulcers of the duodenum and antrum
4. get atrophy and intesinal metaplasia of nucosa
5. Increased risk for intestinal adenocarcinoma
6. MALT lymphoma

Have inflmation = risk for adenocarcinoma = get lymphoma of inflamed GI tract

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40
Q

What is H.Pylori associated with

A

H.Pylori is assoicated with metaplastic atrophic gastritues

Image - red is intesinal metaplasia

Before they had to comepleted a resection of Distal Antrum because Ulcer won’t stop bleeding = need to take out
- Now we know it is caused by HP = an treat the HP = don’ need to take out (prevent surgery for ulcers)

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41
Q

H. Pylori asscoiated with metaplastic atrophic gastritus (hystology)

A

Similar to metaplasia in Esophogus

See goblet cells = tell you intestinal metaplasia
- have risk for dysplaia and carcinoma

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42
Q

Gastric tumorgensis

A
  1. Metaplasia (no neoplasia)
  2. Dysplasia (non-invasive neoplasia)
  3. Adenocarcinamo (invasive neoplasia)
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43
Q

Risk factors of Gastric Adenocarcinoma

A
  1. Male >60
  2. H.Pylori infection - get chronic infection –> get metaplasia –> get carcinoma
    • Atrophic gut
  3. Intesinal matplasia* - Atrophic gut
  4. Chronic atrophic gastrtus* - Atrophic gut
  5. Pernicous anemia*
  6. Familail adenomatous poly posis*
  7. Prior partial gastrectoy
  8. Nitrate containing foods in diet
  9. Cigarette smoking
  • Endoscopic screening recomended
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44
Q

Gastric adenocarcinoma (intestinal typ)

A

Looks intestinal because arose from intestinal metaplasia
- See more distict glads
- Has intestinal morphology

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45
Q

Hereditary gastric Adenocarcinoma

A

Leads to a different Adenocarcinoma

Autosomal Dominent
Gastric cancers develope in youth

Mutated CDH1 gene (E-cadherin) - a tumor supressor gene in epithelial cells (germline mutation)
- get screening and profelactc gasterotimy

Second hit intiates neoplasia

Accounts for up to 40% of family gastic cancer

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46
Q

Gastric adenocarcinma (Diffuse type)

A

Has a bad prgnosis

Has small cells = easy to miss

Image = diffused AC
- Se siglet cells (circle with mucues inside and nucelus surounding)

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47
Q

Small bowl Function

A

Function - Absorbe nurteints
- Stomach breaks up food –> then Small intestine absorbs
- SI maximizes surface area so it can absorb more

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48
Q

Small bowl Histology

A

ALL abount increasing SA

  1. Glandular mucosa with villous architectire to maximize absorbption
    • Villous = fllaments of mucosa stick up
  2. Submucosal glands in the duodenum (burner’s glands) to neurtolize the gastric acid sectretion
    • Burner’s glands = stops gastric acid secretion
  3. pancreitic juice (digestive enzymes) and bild (emulsifier) enter at duodenal Ampulla of Vater to aid digestion
    • Bile = from gall blader
49
Q

Small Intestine (overall)

A

Small intestine is divided into:
1. Deodenum (25 cm/9in) - Adjust pH tonicity (has burners glands)
2. Jujunum (280 cm/9 ft) - Digestion and absorption
3. Ileum (350 cm/11.4ft - longest) - Bile salt absportion (has lymphoid aggerates)

50
Q

Layers of small bowl

A

Musocsa - has fingers sticking up lined by epihelium to increase Surface Area

51
Q

Small bowl Mucosal

A

Have:
1. Crypts
2. Villi

Normal Villia: Crypt ration = 4:1
- Shorter Villi = indictaed certain diseases

Villi = stick up into absorbic epithelium

52
Q

Villous Epithelium

A

PAS stain - stains goblet cells + mucin + shows brush boarder
- Brush boader = microvilli stick up

53
Q

Microvilli

A

Brush boader = microvilli
- Flagellar stick up = increase surface area

54
Q

Functional Unit of the Small Bowel

A

Understand stem cell dynamics

Crypt base = cylcing stem cells
TA compartmet = transitioning epithlium
Top = differentated –> then goes to shed into the lumen

Vils - digestion + absorption
Crypt - secretion

55
Q

Small intestion job

A

Overall: Absorption of sugar + protein + fat

Sugar/protein/fat = must be broken down enzymatically into fuctional units before it can be absorbed

Specific transprters in enterocytes mediate absorbption
- Have different trasnprters for different surgars + different for amino acids
- Transporters have a lot of restiction in specificty ; we know many of the transporters

56
Q

GI tract balance sheet

A

GI tract is very effecicient - Absorbs 98% of things we take in

57
Q

Malabsorption

A

Impaired uptake of any substances by the small intestine

If the smallnintestine has inflation = affects ability to absorb nutrients

Disease:
1. Celiac

58
Q

Malabsorption syndrome symptomes

A
  1. Diapria
  2. Steotorah (fatty stool)
  3. Weight Loss
  4. Deficney states (protein/vitamen dfiecieney)
59
Q

Celiac Disease

A

aka Gluten sensitive enteropathy + celiac sprue + non-topical Spure

Overal - inability to tolrate gliadin (alchol soluble fraction of gluten)
- Gluten = in wheat + rye + barley
- chroic autoimmune intestinal disorder

When gluten is ingestid into patients with celiac an immunologically meidated inflamatory response occurs which famages the mucosa of the intestine
- Histologocal chnages - get small bowl atrophy (microvilai are flat) which leads to maldigetion and malabsoprtion

60
Q

Pathophysiology of celiac disease

A

Pathohysiology = multidisiplinary disorder
- Need autoantibody

Comination of allergy to glute + innate/adpative immune + genetics

Overall - celiac us an imune disorder that is triggered by the envirnment (gluten) in genetically suceptible individuals

61
Q

Celiac (histology)

A

Have:
1. Villous blunting
2. Increased lymphocytes in epithelium (inflamtory disease)
3. Increased plasma cells and lymphocytes in lamina propria (inflamtory disease)

Image -
see flat at the tope

When stop eating gluten = intestne goes back to normal morphology (histology is reversible)

62
Q

Neoplasia in small intestine

A

Primar cancers are reare ; metastases are more common

If have adenocarcima in small intestine = often thing it is a metasteses
- If have tumor in dadenus = think it is from primary pandcreotic tumor

63
Q

Layers of the colon

A

Mucosa = unique part

64
Q

Coleractal Mucosa structure

A

Have crypts that go down (looks like test tubes in a rack)
- Regular achitecture in helathy = crypts
- If ahve infamatpry disease = interupts structure

65
Q

Coleractal Mucosa (histology)

A

See crypt is going down

66
Q

Function of Colon

A

Fluid absorption (function of mucosa?)

Lubricates stool to move down GI
- have more goblet cells + fewer absorptive cells

67
Q

Infamatory Bowl disease (overall)

A

Overall - Chronic inmatory condition of the GI tract
- ofte presnets in patents in teens-twenties ; have second peak from 50-70

Etiology is unknown but they think gentically predisposed hosts have an itestinal mucosal immune reaction to an envirnmental factor iwth the gut microbiota playing a central role

Potential predisposing fcators - Infections + Antibiotics _ NSAID use

68
Q

Pathogensis of IBD

A

Multifactoral - includes genetics + enviremnts triggers + mibrobial antigens/adjuvents + effector immune respose

Don’t know the exact cause of IBD or how to prevent it

69
Q

IBD histopathology

A
  1. Muscoal has acute imnatory infiltrate
    • Abudendent nuertpphils in epithelium –> causes accute cornus –> crypt (just if in epithelium)
      - Cyrptisis and crypt abcesses
  2. Basal Plasmacytosis - plasma cell on bottom of cypt (shows it is IBD)
  3. Crypt distortion (not organzied) - shows it is IBD
  4. Goblet cell depletion
  5. Paneth cels metaplasia

many things can cause nuetrophils to come + cyrptisis = also need chronic injury to get crypt distoration + plasma cells

70
Q

Types of IBD

A
  1. Ulcerative colits - mucosal ulceration in colon (onl mucosa is inflame)
  2. Chrons disease - Tranmural inflamation (Illetis + illeocolitis + colitus)
    • Inflmaation in entire wall of GI tract
  3. Other Colites - Other things cause inflamation in colon
    • Ex - microsopic colitis + diversion colitus + diverticular colitus + pouchitis)
71
Q

Ulcerative colitus vs. Chron’s diseae

A

Ulerative cholitis:
1. Diffuse mucoasl inflimation limited to colon
2. Afefcts colon (affects rectum and things more proximal)
3. May involove all or part of the rest of colon

Chrons:
1. Patchy transmural inflammation
2. May affect any part of GI

72
Q

IBD + carcinoma

A

IBD can set up inflamation –> leads to cracinoma = pateints have survelnce to check for inflamtion and Dysplasia

73
Q

Large Intesinve neoplasia

A

Colorectal carcinoma = colon cancer
- rectum = most distal part of colon
- Most comon cancer of GI tract
- hird highest incidence and cayse f cancer deaths

74
Q

Colon tumorgensis

A

Colon tumorgensis = prototyouc example of precnacer-cancer sequence (see genetics of multistep tumorgenesis)

Different types of precancer represent different genetic pathways of tumorgensis

Image - Colon Adenocarcinoma

75
Q

Colonic Adenocarcinoma

A

See Polyp (Precancer) + Mass (Cancer)

Colonoscopy = good –> finds precancer and removes the precancer at the same time

76
Q

Types of Polyps in colon

A

2 types = have different genetic paths

  1. Tubular Adenoma - Multistep CRC carcinogensis model
  2. Sessile serated Adenoma - Microsatolite instability pathway
77
Q

Tubular Adenoma

A

Neoplastic ; pre-malignent
- Most common neoplasmic polyp

Have low grade dysplasia

Histology:
1. Have high nucelus:cytoplasm ration (bigger nuclei)
2. Nucear elongation
3. Nucleo psuedostartification (bunch up on each other)
4. Nucleat changes extend to surface

78
Q

Multistep Colorectal carcinmoma Carcinogensis

A

Multistep Colorectal carcinmoma Carcinogensis = tumor progression model
- Have step wise progression ofr precancer neoplasia dirven by different mutation in ecah step

First hit = APC at 5q21(germline or somatic in neoplastic cell)
- Have loss of function of both alleles

79
Q

Sesile serrated adenoma

A

2nd path for colon cancer to take

Histology:
Cytosolic pertuesion = different
Crypt = dialted at the bases (“boots”/”flash”)

80
Q

Microsatilite instaility pathway

A

Cancer arises through mutations in genes that contro; DNA repair = get more fusion mutaions = hits other cancer genes

Start - Mutation in gene regulating growth and apoptosis = get cancer (MLH1, MSH2 gene etc.)

81
Q

Familial Adenomatous polyposis

A

Have germline mutation in APC (in 1 allele)

Fits Knudson’s two hit hypothesis for tumor supressor genes

Affect pateints ahve one inherited mutated allele ; 2nd hit occurs in the neoplasm

82
Q

Familial Adenomatous polyposis (images)

A

Have MANY polyps
- SO many adenomas = one is likley to get mutations it needs to get cancer
- Have heterozygosity in polyps

Treatment - usually take out colon

83
Q

Lynch Syndrome

A

Non-herditary polyposis syndrome (affects microsalitile pathway)

Autosomoal dominant inheritance pattern (only need one allele)

Germline mutaions in mismatch repair genes (MLH1, MSH2, MSH6, PMS2)

Inherite one defcetive allele ; second hit happens in neoplasm

Have Accelerated carcinogensis because mutation rae is higher (X1000 increased mutation rate) –> more likley to get mutation in genes that cause tumorgensis

Other cancers - endometriu + stomach + overy + uterus + brain + small bowl + hepatobiliary tract + opancreus + skin

84
Q

Alfred Warthin

A

His seamstress said she will die from colon cancer bevause eveyrone in her family did

First family decsrived with Lynch syndorme

85
Q

Lifetime risk of colorection CA

A

If have APC Colon cancer = test for MSI to see if can do immunotherapy

sporatic (under 10%) - 10% MSI ; 80% APC
- cancer with MSI = uniqley suceptive to immunotherapy (Use PDI)
- More sporatic via APC

Lynch - 100% MSI (risk is 50% in end)
- All MSI changes

FAP - 100% APC (All get cancer)

86
Q

Function of Pancreus

A

Makes degestive enzymes –> Puts enzymes into the duedenum

87
Q

Pancerus

A

See Head - leads into the deuadenum

Pancreus = retroperiteneal = under paretenium = not a lot of nerves = less symptoms = diagnosed late

88
Q

Anatomy of Pancreus/Blood vessels

A

See head + dumps into the duadenum

Superior mesonteric aretry/vein
- Located next to the pancreus
- Reason for pancreus is hard because the pancreus is next to big vessel

89
Q

Pancreus Histology

A

Acini - makes digetive enzymes –> puts enzymes into digetive ducts –> enzymes go to the duedenum

Islets - Have Langerhans cells

90
Q

What is normal pancreus composed of

A

Normal pancreus is composd mostly of Acinar Cells

Bid part of cpryt because makes enzymes???(Slide 97)

91
Q

Islats of langerhands

A

Make insulin and glucagon –> sceretes to blood through duct

92
Q

Pancreus function

A

Acinar cells - scerete pancreotic enzymes into pancreotic duct (Exocine - out)

Islets of langerhands - Secretes hormones into blood vessles (enodcrine - in)
- Secrete insulin + glucagon = controls blood surgar level

93
Q

Types of Pancreatitus

A
  1. Acute (short + self inflcited)
    • Glands will usualy return to nomal if underlying cause of inflmation is resolved
  2. Chronic
    • Irreversible destruction of pancreitic parenchyma

Acute = emergency vs. chronic is not an emergencey

94
Q

Causes of Acute Pancreatitus

A

Most common:
1. Alchol (65% in US
2. Biliray tract disease (Gallstones cause obstrcution)

Also have some less common causes (obscurtion of pacreitic duct systems due to tumors + drugs + trama + infections + genetic

95
Q

Genetic causes of Acute Pancreatitus

A
  1. Mutation in Cationic trypsinogen (PRSS1)
    • Recurrent attacs of pancreatitis since childhood
      - Most common is R122H mutation
    • Prevents protylitic inactivation of Trypsin (digestive enzyme) = can’t stop making trypsin = autodigest pancreus
  2. Mutation in protease inhibitor SPINK1
    • Normally prevents trypsin-catalyzed premature activation of zymogens
    • Mutation causes excess trypsin acivity
  3. Mutation in cystsic firbosis transmembrane regulator (CFTR)
96
Q

Chronic Pancretitis

A

Overall: Irreversible destruction of pancreotic paranchyma
- Leads to exocine insufincey (no Acinar cells)
- Leads to Endocrine insufincey (late)

Most common cause = Alchol abuse

Recurrent acute pancreatitis can result in chronic pancreatitus (caused by pancreus divisum + hereditary pancretitus + anatomical abnormalities)

NOT life threatening emergencey BUT 50% mortaility rate by 20 years

97
Q

Histology of chronic pancreatitis

A

Key features:
1. Paranchymal fibrosis
2. Loss of Acini (replaced with firbrosis)
3. Variably dialted ducts
4. “Englarged” islaets (look enlarged because eveyrthing else is gone)
5. Chronic inflamation

98
Q

Complications of chronic Pancreatitus

A
  1. Plural effusions
  2. Pain from perineral fibrosis
  3. pancreotic calcification
  4. Acites
  5. Stones in Pancreotic duct
  6. Diabetes
  7. Pancreotic cyst
  8. Fast malabsorption (sterorrehea + decreased vitamen K) - not making enzyme needed to absorb fat
99
Q

PDAC

A

Has glandular morphology

Symptoms:
1. Painless onstructive juancice (if the tumor is at the head of the pancreus blocking gallblader)
2. Back pain
3. Weightloss/Cachexia
4. Trouseau sign migratory thromboplhebits (blood clots that move around body)
5. New onset of diabetes

ALL are late symotoms (only 10-15% are resectable tumore)

100
Q

Profiling tumore

A

Tumor profile after surgery - done on tissue in surgery but the pancreus isonly 10% of pateints = need to keep in min wgere that is from and how that affects disease spectrim (think if it is represnetaive of the spectrum of disease)

101
Q

PDAC pathologic features

A
  1. Grossly firm + white + poorly defined mass
  2. Microscopically they form glands and scerete mucin
    • Called ductal (Ductal different? - slide 109)
  3. Intense desmoplastic repsonse (fibrotic)
  4. Poorly vascrularied
102
Q

PDAC image

A

White = mass ; Yellow = pancreus

103
Q

PDAC histology #1

A

See intense desmoplastic response (fibrosis)
- took tissue and did multiple anylsysis BUT majority of the tumor is fibrosis not cancer = need to pay attention to the cells that are there (Example - for DNA sequenceing might not afefct but for proteomics or expression it does affect = need to pay attention

See lighter circle - glands = cancer

104
Q

PDAC histology #2

A

See Perinueral invasion (invaded nerves)
- Invades locally

105
Q

PDAC histology #3

A

See invasion into veins
- Metastisis = invades in vessels = cancer spreads

106
Q

PDAC metastisis

A

Metastisis = common in PDACbecause the cacer invades into the veins
- Liver = most common location of metastisis (because portal vein)
- Pateints with metastisis to the lungs = better prognosis than metastis to the liver

107
Q

PDAC metastisis to liver

A

image - cross scetion of liver from pateint with metastic pancreitic cancer

In image - red is nomal ; rest is liver metastis

108
Q

PDAC Epidemeology

A

Risk factors:
1. Age - PDAc is a disease of elderly (80% beteen 60-80 YO)
2. Blacks > whites
3. Ashkenazi jews > gentiles
4. Smoking - cuase s20% of Pancreoic cancer (doubles risk)
5. Family histpry - 10% of pateints have family history
6. Diet - High in meats + low in fruits and vegtibles
7. Obesity
8. Diabetes - risk factor + symptom of disease (hard to seperate between the two)
9. Chronic pancreatitus - risk factor + symptom of disease
10. non-O ABO blood group

BRACA increases risk
- most germline mutations = not known

109
Q

What is Pamcretotic cancer

A

Pancreotic cancer is fundementally a genetic disease

Somatic mutation in somatic neoplastic cells = get cancer

110
Q

Genetic an Epigenetic events in Pancreotic cancer

A
  1. Mutaions (intergenic mutations) - point mutations
  2. Large deletion
  3. Aplifications - CNVs
  4. Genetic instability/chrmothripisis - chromsome shatters and then is put back together weird
  5. Mitocndrial mutations
  6. DNA methylations
111
Q

How do we get mutations that cause pancreotic cancer?

A
  1. Inherit mutated allele (BRACA2)
  2. Do something to damage DNA (ex. smoking)
  3. By change - 6 Billion BP in every cell –> can get error in cell divsion
    • Bad luck that the mutation is bad
112
Q

Types of pancreitic leisons

A
  1. PanIN - Small lesions (don’t see on imaging)
    • Get dysplasia –> high grade dyspalsia
    • Low rise for pray?
  2. IPMN- Large cystic (do see on imaging)
113
Q

Genetic progression towards invasive pancreatic cancer

A

Telemere shortening (earliest chnage) –> P16 –> p53/SMAD4/BRAZ2
- at p53 = get high grade transition to carcinoma

114
Q

Complex clonal evolution of precancers

A

NOT always linear

Precancer = poly cloncal
- Have mant clones in precacer –> one clone expands –> eventually get mutations that leads to progression

115
Q

Multifocal precancers cancer

A

Precancers are multifoacal

Image - 3D live image
- See different precusers in different colores
- have >10 precacers in one tissue
- Everyone has many precancers
- Not uncomon to have many precancers but abnormal to have pregressions (progression)of precancer to cancer)

116
Q

Role of inflamation

A

In some organs precancers are proceeded by inflamation and metaplasia

Inflamation roles in chronic infection is not as definedbut think inflamation is needed for neoplasm to happen

117
Q
A
118
Q
A
119
Q
A

Human Body (31 decks)

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