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Motility
The sympathetic nerve supply modulates motor functions and reaches the SI and colon alongside their arterial vessels.
Intestine

During fasting period → migrating motor complex (MMC) to clear nondigestible residue from the small intestine

After food ingestion → the SI produces irregular, mixing contractions of relatively low amplitude

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

Tonic contraction of the puborectalis muscle is important to maintain continence

During defecation, sacral parasympathetic nerves relax this muscle, facilitating the straightening of the rectoanal angle.

Internal sphincter: involuntary control.

External sphincter: voluntary control. Striated muscle.

Distention of the rectum results in transient relaxation of the internal anal sphincter via intrinsic and reflex sympathetic innervation

→ increase in intraabdominal pressure → increased pressure in the rectum → voluntary relaxation of the external anal sphincte

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Diarrhea is abnormal stool movements >250 g/day.
Loosely defined as the passage of abnormally liquid or unformed stools at an increased frequency.
Various different causes.

Infective
Inflammatory
Steatorrhea: passage of pale stools that float.

Organic cause: nocturnal bowel frequency and urgency

Functional cause: frequent small volume stools.

Overflow diarrhea: Where severe constipation causes a blockage in the bowel. The bowel begins to leak out watery stools around the blockage from higher up in the bowel. Often occurring in nursing home patients.

Pseudodiarrhea: frequent passage of very small stools; usually a problem of tenesmus. May be seen in IBS. Do not adhere to the actual definition of diarrhea (usually <250g/day)

Fecal incontinence: involuntary discharge of rectal contents.

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Osmotic diarrhea
When there is substance in the lumen that is hypertonic, it draws water into the bowel.

3 causes:
- ingested non-absorable substance
- generalized malabsorption, specific absorptive defect.
- specific absorptive defect

Osmotic gap- a measurement of the difference in solute types between serum and feces

Seen often in patients with EDs who take laxatives.

A solute itself has a strong attraction of water.

You always need to eat something to have osmotic diarrhea.

Often has pH <5

Ex. sweeteners which are sugar-free but osmotically active.

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.

The intestinal cells may be directly influenced to actively secrete.

Can be during fasting (as opposed to osmotic diarrhea)

Often has pH >6

Common causes

Enterotoxins (e.g. cholera, E.coli, c difficile)

Hormones

BIle salts in the colon

Fatty acids

Some laxatives

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.

Common causes

Infective conditions

Inflammatory conditions (U.C. or Crohn’s)

Blood and leukocytes present in stools. Often pain or fever from infection and other manifestations of inflammation.

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.

Main association is pancreatitis.

Often associated with weight loss

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.

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Erythropoiesis
EPO is the primary regulatory hormone in RBC production. EPO is needed to stop erythroid progenitor cells from undergoing apoptosis.
- EPO production is linked to tissue oxygenation (when oxygen is scarce, a transcription factor that is normally degraded will remain present and will upregulate the EPO gene)
Impared O2 to the kidney can be due to

reduced number of RBCs (anemia)

impared O2 loading of hemoglobin (hypoxemia)

lack of blood flow to the kidney (renal artery stenosis).

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:

lack of EPO production

lack of functioning erythroid marrow

lack of substrates (like iron) for RBC production

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Iron transport and regulation in the intestinal enterocyte

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Iron transport and regulation in the intestinal enterocyte

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A condition in which the hemoglobin level is below a certain threshold for specific age and sex.

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Classifications of anemia by mean cell/corpuscular volume

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Classifications of anemia by mean cell/corpuscular volume

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Can be classified on the cell volume or by the cause (below).

Microcytic anaemia with low MCV

Normocytic anaemia with normal MCV

Macrocytic anaemia with high MCV

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Classifications of anemia by pathophysiology

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Classifications of anemia by pathophysiology

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Decreased production/ Hypoproliferation

Account for at least 75% of anemias

Increased destruction
Accelerated loss

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Acute
- Due to blood loss or severe hemolysis.
- more here i'll find ita lter

Chronic
- the body will no longer compensate so there will be blood shunting (paleness)
- Murmur

Iron deficiency: brittle nails, spoon-shaped nails, atrophy of papillae of the tongue, angular stomatitis, brittle hair and syndrome of dysphagia/glossitis

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Peripheral blood smear

RBC indices, WBC count, platelet count, and morphology of RBC.

Bone marrow

Compare to findings in peripheral blood examination. Assess cellularity of marrow.

Detailed history

Family history

Drug intake

Alcohol use

EThnic background

Ask patient about menstruation patterns

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Iron deficiency anemia

Diet & absorption of iron

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 stores

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

Anemia of chronic disease

Anemia of chronic disease: the release of cytokines like IL-1 and TNF-alpha. Looks a lot like iron deficiency anemia but one difference is that there is increased serum ferritin with still low serum iron and low transferrin. The storage is OK, there is just poor release due to inflammation. Not related to RBC production.

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

Sideroblastic anemia

An immune or acquired disorder where there is an accumuatlion of iron in the mitochondria of the erythroblasts. Leads to different morphology due to iron accumulation (check this).

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Pathogenesis and effects of pernicious anemia

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Pathogenesis and effects of pernicious anemia

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An immune disorder where there is loss of parietal cells in the gastric mucosa --> damage in GI tract --> vitamin B12 malabsorption.

Understand this figure.

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RBC has a normal volume. Can be due to blood loss or some endocrine disorders.

Investigations:
Reticulocyte count
 High?  haemolytic/blood loss  body tries to compensate and produce more reticulocytes to replenish the blood that is lost
 Low?  Bone marrow disorder  bone marrow is unable to produce adequate amounts of red blood cells

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Megaloblastic
Definition: Immature RBCs especially nuclei. The vitamin B12 deficiency blocks DNA synthesis which has to do with the biochemical processes. Defiiency of folate produces an enzyme needed which slows biochemical processes.

Causes:
Hematological findings: Can see large immature RBCs with DNA disturbances.

W/o megaloblastic changes
Common causes

Pathological causes (alcohol excess or liver disease, hyperthyroidism, drugs)

Physiological (prengnacy/newborn)

Differentiation to megaloblastic type:

You don't see big cells with DNA disturbances; the nuclei look smaller.

Vitamin B12 and folate will be normal.

Hemolytic anemia
Caused by destruction of RBCs.

Autoimmune causes

Inherited causes

Hemoglobin abnormalities

Sickle syndromes

Metabolic disorders

Acquired hemolytic anemia, drug induced.

Mechanical damage (e.g. from damaged heart valves)

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.

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Definition
Diarrhea of sudden onset. Very common. Often short-lived.

Inflammatory: fever and bloody diarrhea associated with --
Non-inflammatory: watery diarrhea without blood. People can feel bloated, nausea.

Etiology
Traveler's diarrhea is very common form of acute diarrhea.
90% is infectious usually due to fecal-oral routes or contaminated water/food, because the intestinal microbiota doens't do it's job properly.

5 risk groups

Travelers

Consumers of certain foods (consumption of food at a picnic, banquet or restaurant may suggest infection of Salmonella, campylobacter, or Shigella, or E.coli)

Immunodeficient persons

E.g. AIDs, IgA deficiency, …

Daycare attendees

Institutionalized persons

Other causes

Medications (i.e. antibiotics, cardiac antidysrhythmics, antihypertensives, NSAIDs, antidepressants, chemotherapeutic agents, bronchodilators, antacids, laxatives)

Occlusive/non-occlusive ischemic colitis

Colonic diverticulitis

Ingestion of insecticides, mushrooms, arsenic, toxins in seafood

Anaphylaxis

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

Systemic infection

Pericarditis

Arthritis

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

Stools should be sent to laboratory for culture and examination for ova, cysts, and parasites and for C. difficile toxin assay

Sigmoidoscopy and rectal biopsy should be performed if labs don't yield diagnosis

Treatment

Oral and fluid electrolyte replacement

Antidiarrheal drugs

Antibiotics (depending on the cause)

Severe episodes → special oral rehydration solutions of salt and glucose to replace

Treatment is very specific to the cause of diarrhea and location in which you get it (e.g. don't give antidiarrheal drug if the diarrhea is suspected to be due to infection! Diarrhea is a mechanism of protection sometimes, better to just wait it out).

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Definition: diarrhea lasting >4 weeks. Most causes are noninfectious.

Etiology

Many (see definition of Diarrhea types)

Medications or surgery

Functional diarrhea with certain intolerances to foods (lactase deficiency)

Blood present can be IBD or malignancy

Diagnosis

Colonoscopy or biopsy to rule out malignancies in the case of blood presence.

Pain with bowel movement --> suspected IBD

Suspected IBD/functional diarrhea without help of dietary exclusion you can use serum casting (hematology, chemistry, immune profile,...)

Imaging studies

See figure below

Treatment

See table below

Depends on specific etiology and may be curative or  suppressive

If you have other systemic manifestations (i.e. lack of nutrients) this needs to be taken into account

Opioids or antidiarrheal agents in certain patients

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Algorithm for management of Chronic diarrhea

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Algorithm for management of Chronic diarrhea

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Blood smear appearance of different types of anemias

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Blood smear appearance of different types of anemias

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Severe anemia causes a systolic murmur. This is due to the heart trying to compensate, causing a murmur.