In the colon, absorption is the major function. In health, the ascending and transverse regions of colon function as reservoirs (avg. transit time 15 h) and the descending colon acts as a conduit (avg. transit time 3 h)

Fluid absorption
A lot of absorption happens in the intestine but the colon can compensate when there is not enough absorption of water.
Sodium is first absorbed and its electrogenic so it produces a charge. This goes from the lumen in to the body and then is pumped out again.
Glucose creates an osmotic gradient which will draw water with it.

Defecation

Secretory diarrhea
Disorder in which there is both active intestinal secretion of fluid and electrolytes and decreased absorption. Therefore, there is a low stool osmotic gap. 

Inflammatory diarrhea
Occurs because of damage to the intestinal mucosal cell so that there is a loss of fluid and blood. Causes defective absorption of fluid and electrolytes. 

Abnormal motility
Normally seen in IBS or colonic cancer. Abnormal motility in the upper gut which causes frequent stool passage.
If there is too rapid transit, there may be maldigestion which can play a role in osmotic pressures. Too slow motility (from neural problems) this may lead to bacterial overgrowth which can also lead to diarrhea.
In IBS, there may be disturbed responses to stimuli which causes motor issues leading to diarrhea as well.
You can also have neurological diseases and drugs (morphine causes complete stopping of movement, anti-depressants can cause diarrhea, etc.). 

Steatorrhea
Fatty acids have an osmotic effect. If you have them in the lumen, they will draw water to them. 

Factitious diarrhea
Deliberately causing diarrhea. Mainly seen in self administration  of drugs like laxatives and diuretics. Can also be from deliberately diluting stool sent for analysis. 
Often seen in women with psychiatric disorders. 

EPO is produced in the kidney (small amount also by hepatocytes) 
- EPO binds to erythroid precursors and induces them to proliferate and mature 
- With adequate iron (and other substrates), EPO can cause rapid increase in RBC numbers

ANEMIA CAN RESULT FROM: 

Detailed history 

We get iron from our diet. Non-heme is derived from non-meat; it is less well absorbed than heme-iron which is derived from meat. 
In celiac disease where we have flattened cilia, we won't have absorption of iron --> manifestations of anemia. We also need the stomach cells to be working properly to have vitamin B12 substrate. 

Iron will then be absorbed. Several proteins facilitate this absorption and this mainly happens in the duodenum. It will then be stored as ferritin. The storage of iron can be regulated for more or less absorption by Hepcidin.

Iron deficiency
Step 1: don't have enough iron but your body will start to release ferritin 
Step 2: your stores are depleted and your serum iron will start to fall and hemoglobin synthesis will also start to fall. 
last stage: iron deficiency anemia when you don't have enough hemoglobin anymore to make new red blood cells

Aplastic anemia: when there is a lack of pluripotent stem cells in the bone marrow --> fewer RBCs being made. 

Differentiation to megaloblastic type:

Hemolytic anemia
Caused by destruction of RBCs. 

Hemolysis does not always lead to hemolytic anemia because there can be compensation. 

Extravascular: in most hemolytic conditions where the cells are removed from circulation by macrophages. Deliberate RBC destruction
Intravascular: destruction occurs within the circulation which leads to release of hemoglobin in the circulation. Can be caused by mechanical damage.

Clinical features
Fever, abdominal pain, dehydration, diarrhea. Usually lasts for one week. If it is more than 1 week, further investigations are necessary to rule out parasites and toxins. 

Systemic effects

Investigations
Necessary if the diarrhea has lasted more than 5-7 days