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GI - Tumors and Cancers (lower GI) (*Colorectal Cancer (dropped image…
GI - Tumors and Cancers (lower GI)
*Colorectal Cancer
Notes
older male with iron deficient anemia
-->
"GI cancer until proven otherwise"
--> because iron deficient anemia is extremely rare in men, otherwise
Adenoma --> Carcinoma Sequence
--> most colorectal cancers start from adenomatous polyps becoming malignant (ex: FAD)
Hereditary Non-Polyposis Colon Cancer
(HNPCC) = *LYNCH SYNDROME
Risk Factors/Mechanism
genetic mutation of MISMATCH REPAIR repair genes
MSH2 gene
MLH1 gene
*Polyp formation
almost always begins with APC gene mutation
Histology of Polyps
circles = tubular glands
--> for secreting things
villi = long stalks
--> for absorbing things
Serrated Polyps
premalignant
from CPG hypermethylation
*Adenomatous Polyp
an mass or growth that rises above mucosa
size most important for malignancy
polyps most common in the colon
*FAP = Familial adenomatous polyposis
opposite to LYNCH syndrome
--> think atleast black
families
getting
LYNCHED
aren't as bad as family
FAP
Risk Factors/Mechanism
genetic mutation of APC gene
MJ: "APC..."
"EASY AS FAP"
Signs and Symptoms
>100 tiny polyps in colon mainly
little to no bleeding
Prognosis/Evolution
100% will inevitably lead to colon cancer if untreated
FAP histology
hundreds of tiny polyps
Stages of Adenoma-to-carcinoma change in colorectal cancer
-
step 1 = APC
gene mutation (tumor supressor)
--> unregulated cell growth and adhesion
--> grow OUT first
--> this is out of control in FAP
--> reason why in FAP there are so many tiny and small polyps
-
step 2 = KRAS(MAPK) DCC p53
gene mutations (proto-oncogene)
--> KRAS(MAPK) = signalling for proliferation
--> DCC =
"DONT CKILL CKILL me"
= gene mutation avoids apoptosis
--> DCC = deleted in Colon cancer
Villous vs Tubular Polyps
VILLOUS are VILLANIS .. they have K+ rish MUCIN
--> mucin causes secretory diarrhea
--> is K+ rich and the water brings Na= with it
--> you get hyponatremia and hypokalemia
--> even when you stop eating or drinking
Tubular polyps are more benign
*Villous Polyps
VILLOUS are VILLANIS .. they have K+ rish MUCIN
--> mucin causes secretory diarrhea
--> is K+ rich and the water brings Na= with it
--> you get hyponatremia and hypokalemia
--> even when you stop eating or drinking
have very long finger like projected vili
Clinical Cases
1 more item...
*Small Intestine Tumours / Cancer
Sm. in. makes up 75% of GIT
Sm. In.
ONLY 3-5% of GIT tumours
most are
CARCINOID tumors
*Carcinoid Syndrome / Tumors
see notes in Oncology
best prognosis out of all lung cancers
CARCINOID
is in the name
CD illeum / bile salt liver connection
--> carcinoid from illeum to liver mets
Tx = octreotide (somatostatin analog)
--> for symptoms ONLY
requires surgical resection
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
Carcinoid Tumors
can be either typical = benign (most = 90%) or atypical = malignant
Carcinoid Syndrome
includes flushing and diarrhea, and less frequently, heart failure, emesis and bronchoconstriction
note that the patient in the clinical case has no signs of flushing, emesis or diarrhea
--> are these from GI carcinoids?
--> he presented with hematemesis, and Hx of pneumonia from bronchoconstriction
Notes
:
Carcinoid tumors are a more rare type of tumor
they can present anywhere in the body, but are most commonly in the lungs or GI tract (usually stomach or intestines)
they develop from uncontrolled growth of neuroendocrine cells so they have many secretions
--> mostly secrete serotonin 5 -ht
--> excess serotonin 5 -ht leads to
carcinoid syndrome
note that most carcinoid tumors are typical = meaning they are slow growing and do not invade other tissues or metastasize
Clinical Case:
CARCINOID
syndrome +
Rule of 1/3s
C
=
cutaneous
flushing
A
=
asthmatic
wheezing (fibrosis in lungs)
R
=
Right sided HF
and Valves
C
=
Cramping
+ Diarrhea
I
=
Illeum
/ intestines / proximal colon
--> distal illeum (#1 most common malignancy in illeum)
--> Chron's / Carcinoid hepato cycle similarity
--> think of Chrons in illeum / bile salt GB syndrome
--> Carcinoid starts in the illeum (like CD) / mets to the liver --> then carcinoid syndrome starts
N
=
Neuroendocrine
(Histamine, Serotonin, VIP)
--> VIP = vasoactive Peptide
O
=
Octreotide
(somatostatin analog) = treatment
I
=
INDOLEACETIC acid IN
the urine
5 -HIAA
-->
"2 Tyrant DOPES TRY to TRYP Raphe the TURKEY SERVER while he gives 5 HIAA fives to each table"
D
=
Deposits
of Fibrous tissue
--> plaque-like ddeposits of fibrous tissue is pathognomonic for Carcinoid Syndrome
Serotonin = think of the turkey server RAPHE (5 HIAA 5s) and the Tyrant DOPES:
"2 Tyrant DOPES TRY to TRYP Raphe the TURKEY SERVER while he gives 5 HIAA 5s to each table"
5 HIAA 5s
= 5 HIAA = 5 - hydroxyindoleacetic acid
--> breakdown product of Serotonin
--> serotonin metabolized in the liver into 5 HIAA normally so would be in the liver
--> in Carcinoid Syndrome, mets to liver gives 5-HIAA in the urine insteads
Carcinoid Tx = octreotide (somatostatin analog)
--> for symptoms ONLY
requires surgical resection
ILLEUM Carcinoid vs mets to Liver
Illeum only = NO symptoms since first pass metabolism of VASOACTIVE substances like 5ht
--> still high 5HIAA though
--> note that 5-HIAA is not an active metabolite though
Liver METS / bronchial carcinoid = YES symptoms and high 5ht
*Clinical Signs for GI Cancer / tumors
rectal bleed = #1
--> especially
FOB
= occult rectal bleeding
*Rectal Bleeding
Differentials:
Ulcerative Colitis
tumour/large polyp
cancer
(Soft) Excluded Differentials:
IBS
Chron's Disease (bleeding less common)
Bleeding types
OCCULT blood = Non-visible blood
VISIBLE blood
brighter red
at or distal to the cecum
"coffee ground" or black
at or proximal to the cecum
Colon Cancer Mutations and risks for CRC
APC = adenomatous polyposis coli
--> cause of FAP, but start of all adeno polyps
--> with added protoncogenes (KRAS/MAPK, p53) leads to cancer
MLH1 = Lynch syndrome
--> nonpolypous cancer - vs FAP
