Anatomy and Physiology Essentials

Liver

“The liver is the largest gland in the body” (Marieb, 2000). It is located in the right upper
quadrant of the abdomen and protected by the rib cage (except its lower part). Because
of its size, the liver almost occupies the upper part of the abdomen and almost
completely covers the stomach (see image below). The liver is suspended from the
diaphragm and abdominal wall by the falsiform ligament. This ligament also serves as a
landmark representing the two major divisions of the liver between right and left part. In
turn, these parts “divide into superior and inferior portions of the posterior, anterior,
medial, and lateral segments” (Black and Hawks, 2005).

20% of the cardiac output goes to the liver. 1/3 of the blood being supplied to the liver
passes through the hepatic artery and 2/3 com from the portal vein. The hepatic artery
carries oxygen rich blood while the portal vein carries unoxygenated but nutrient-rich
blood from the digestive organs. “The superior and inferior mesenteric veins and the
splenic vein which receive blood from the pancreas, spleen, stomach, intestines, and
gallbladder, join to form the portal vein” (Black and Hawks, 2005). In this vein are
nutrients and/or toxins (like drugs and alcohol) and unoxygenated blood. They will be
brought to the liver for processing or detoxification and so we see here that the liver is a
key organ involved in proper glucose, fat, and protein concentrations in the blood. This
is the reason why we are safeguarded from the severe adverse effects of certain drugs
because in a way the liver “works hard” to lessen their potency. So, when a person
ingests so much harmful chemicals (like over intake of acetaminophen or alcohol) the
organ most likely to be affected first is the liver.

In detail, the terminal branches of the hepatic artery and the portal vein “join to form
common capillary beds, which constitute the sinusoids of the liver” (Smeltzer, et al,
2008). The liver cells or the hepatocytes are constantly supplied with oxygen and
nutrient rich blood. Hepatocytes in a lobule 1 are arranged around a venule (sinusoids
empty into this venule that occupies the center of a lobule, hence central veins). One
side of the hepatocytes face the sinusoids and the other side face the bile canaliculi. As
blood from the hepatic artery and portal vein converges and supplies the hepatocytes,
substances are exchanged. Consequently, these hepatocytes produce bile, secret them
in the bile canaliculi that connects to the bile ductules to the gallbladder. Kupffer’s cells
are located around the sinusoids. They engulf certain substances or particles (e.g.
bacteria) that enter through the portal system. Finally, as sinusoids empty into the
central veins, these veins join to form the hepatic vein which itself empties into the
inferior vena cava.
1
Lobule is the functional unit of a liver (see below).

The liver regulates glucose and its concentration in the blood. After meal, glucose is
taken up from the portal venous blood by the liver and is converted into glycogen.
Hepatocytes store glucose and release it into the bloodstream, through the process of
glycogenolysis, if needed. However, in times of need when glycogenolysis is not
enough gluconeogenesis or the “creation” of glucose by the liver by the use of amino
acids and protein breakdown occurs. Fat metabolism also occurs in the liver when
glucose metabolism is not enough.

The hepatocytes form bile. It is composed mainly of water and electrolytes. It is then
collected in the gallbladder and is emptied into the intestine when needed for digestion.
The functions of bile are excretory, as in the excretion of bilirubin 2 and it helps in the
emulsification and digestion of fats.

The process of gluconeogenesis has a by-product which is ammonia. Also, some

bacteria in the intestines produce ammonia. This substance is a toxin but the liver
converts it into urea that can be excreted in the urine.

Protein metabolism is also an important role of the liver: albumin, alpha- and beta-
globulins, blood clotting factors, transport proteins and plasma lipoproteins (Smeltzer, et
al, 2008). Therefore, liver damage results in the decreased synthesis of these proteins.
Vitamin K is also required by the liver for the synthesis of prothrombin and some clotting
factors. Certain vitamins and minerals are also stored in large amounts in the liver. The
liver metabolizes drugs.
2
In the small intestine, bilirubin is converted into urobilinogen and partially excreted in
the feces. However, much of it is reabsorbed into the liver and secreted into the bile
again.

Spleen
The spleen is a highly vascular organ located at the left side of the upper left abdominal
cavity. The spleen’s blood supply is being taken care of by the splenic artery. Although it
is the largest lymphoid organ, the spleen does not filter lymph instead; it filters and
cleanses blood of bacteria, viruses, and other debris. An important role of the spleen is
the recycling of iron from destroyed worn-out/old red blood cells and returning some of it
in the liver. Platelet storage and blood reservoir important during times of hemorrhage
are another important functions of the spleen. In the fetus, the spleen is an important
hematopoietic site or a blood cell-forming site but in an adult spleen, only lymphocytes
are created. “The spleen is also a major site of humoral immune responses to blood
borne antigens” (Black and Hawks, 2005).

Hepatic Portal Circulation

The aorta carries oxygenated blood from the heart to the abdominal aorta and to the
important arteries like the hepatic artery which gives blood to the liver; splenic artery
that supplies the spleen; superior mesenteric artery that supplies the small intestine and
inferior mesenteric artery that gives blood to the large intestine. The inferior mesenteric
vein drains the terminal part of the colon and carries the unoxygenated blood to the
splenic vein which itself drains the pancreas, left side of the stomach and spleen itself.
The superior mesenteric vein and the splenic vein join to form the hepatic portal vein.
The left gastric vein which drains the right part of the stomach goes directly to the
hepatic portal vein. (see below illustration)
Narrative Pathophysiology

Schistosomiasis (Bilhariasis or snail fever) is a very important tropical disease in the

Philippines. Its victims consist mostly of farmers and their families in rural areas.
However, other families who have more contact with fresh waters or rivers (due to
nature of work or location) contaminated with the snail oncomelania quadrasi, a known
host specifically of schistosoma japonicum, are also affected. Socioeconomic status is
an important predisposing factor. Educational level also contributes to the transmission
of the disease because of families or individuals who do not know the transmission
process frequently defecate in nearby rivers and wade in the same area. Religion also
plays a part as one of the predisposing factor in the disease process. “In some Moslem
countries the religious requirement of ablution- that is, washing the anal and urethral
orifices after urination or defecation, an act intended to achieve greater cleanliness- is
an important factor in transmission” (Roberts and Janovy, 2005). In the Philippines as of
2007, schistosomiasis is most common in Bicol, Samar and Leyte, and Davao (Public
Health Nursing, 2007).

Contact with the water infected with the snail oncomelania quadrasi or with schistosoma
japonicum eggs is the primary reason of transmission.

Embryonated eggs (ova) of adult schistosomes are expelled together with the feces of
an infected person in fresh water, those eggs then hatch due to the lower osmolarity of
the fresh water. Though the nature of hatching is poorly understood, current information
suggests that miracidium inside the egg increases in its ciliary activity then, due to the
osmosis, a vent opens in the side of the egg and the miracidium is released. In the
process, some eggs do not hatch and others hatch prematurely.

As the miracidia are released in the water, they immediately swim ceaselessly thereby
increasing the chances of encountering an important host. There are different hosts
depending upon the type of schistosoma. Particularly for Schistosoma Japonicum, the
snail Oncomelania quadrasi is the typical host. Upon contact of a miracidium into the
snail host, it penetrates into the snail. Immediately after penetration, it sheds its
epithelium and then develops into a mother sporocyst which continues to produce
daughter sporocysts, asexually, that will migrate into other parts of the snail’s body.
Production continues from 6-7 weeks. The daughter sporocysts will transform into the
infective stage called cercaria. These cercarias are then released by the snail into the
water where they sink toward the bottom and can remain in this state for 1-3 days. They
can potentially enter the skin of a man and other warm blooded animals like dogs, cows,
carabaos, that wade in the water.

Finally, upon contact with a human skin, cercarias attach and creep to find a suitable
place to enter specifically hair. They are particularly attracted to the natural amino acid
of the skin which is arginine. They also react positively to it. During this process, the
cercaria then produces its own arginine from one of its glands. Because of this, more
and more cercarias are attracted to that particular human skin and are prompted to
come closer to attach themselves. Upon contact with the human skin, it takes only 10-
20 seconds for a cercaria to completely disappear from the surface. From this moment
on, these cercarias are called schistosomules (little schistosomes). Within 24 hours,
these schistosomules are carried from the peripheral circulation into the lymphatics and
into the heart where they are pumped to the different parts of the body. However, those
schistosomules that are pumped into the mesenteric arteries, intestinal capillary bed,
and the liver are the ones who survive, grow, mature and develop, and reproduce.

From the heart, there are two different major paths that these schistosomules follow and
therefore, two different processes of development and maturation. First to be tackled is
the direction from the heart to either the hepatic or splenic artery. From the splenic
artery, schistosomules will travel into the spleen where some can be stranded and
contribute to the inflammation of the organ due to it being challenged. Also, these
schistosomules can lead to the post sinusoidal obstruction later on. From the hepatic
artery, they will go the liver and lodge into the sinusoids where they grow and mature
thereby being called schistosomes. After this, they will either travel to the intestinal
veins to undergo sexual reproduction or they continue to live in the liver where they
destroy liver cells (hepatocytes). If some schistosomes will travel to the liver,
inflammation ensues which contribute to the formation of hepatic abscess and
increased collagen formation. Hepatic abscess progresses to necrosis which also
aggravates the destruction of hepatocytes. Necrosis also results to the lowered albumin
formation by the liver and contributes to the fibrotic regeneration of hepatocyes. The
effect of lowered albumin formation is lowered osmotic pressure which contributes to
the fluid shifting or third spacing. Also, because of the increased collagen formation,
fibrotic regeneration primarily follows which is responsible to the formation of scar
tissues which will eventually compress the portal veins. Fluid shifting will eventually
result to arterial under filling which will be tackled next. Meanwhile, because the scar
tissue formation earlier contributes to the portal veins and its branches being
compressed, post-sinusoidal obstruction or intrahepatic obstruction occurs. Inability to
sufficiently drain blood into the central veins will result to the backing up of blood to the
liver and the spleen and the splanchnic (meaning visceral, e.g. GI tract, liver, spleen
and pancreas) arteries will then dilate to compensate for the steadily increasing
pressure. Because of the phenomenon, an increasing loss of blood from the general
circulation happens so the circulatory arterial blood volume will decrease. This will
activate certain hormonal processes in the body namely: rennin-angiotensin system,
sympathetic nervous system, and the anti-diuretic hormone response.
Earlier, it was discussed how the liver will undergo necrosis, another effect of this is the
decreased ability of the liver to metabolize hormones especially aldosterone. An
increasing aldosterone levels will prompt the kidney tubules to reabsorb sodium and
water. This phenomena combined with the previous fluid shifting contributes to the
hypervolemia and continued general circulatory arterial underfilling at the same time.
The under filling will prompt the body systems mentioned earlier to continue retention of
sodium and water. Finally, this continuing retention of fluids combined with
hypervolemia steadily increases the portal pressure. Two common consequences of
portal hypertension are ascites and varices and the actual patient hitherto have
experienced both based on his medical history. Another consequence that the patient
experienced was the increasing pressure on the splenic circulation which contributed to
the splenomegally. In addition, the previous inflammation of the spleen also contributes
in it. The ascites was treated with furosemide and the varices with a surgical
intervention by the previous physician in the previous hospital. Splenomegally was
treated with splenectomy.

Now, let’s go back to first station of the schistosomules before being pumped to the
body. The second destination of the schistosomules from the heart is to the aorta and
eventually to the superior and inferior mesenteric arteries. From these arteries, they will
travel to the intestinal capillary beds then to the intestinal veins where they mature and
meet with other schistosomules coming from the liver. It is here where the sexual
reproduction between male and female schistosomes occur. Subsequent mating
produces offspring by the females. Embryonated eggs (ova) produced by the females
are burrowed into the intestinal veins which then break into the intestines. After entering
the intestines they are expelled with the feces by the help of the peristaltic movements
of the large intestines outside the person. If that person defecated in the fresh water or
a nearby river, then the life cycle of the schistosomes continues and the spread of the
disease becomes inevitable.
Schematic Diagram

Predisposing Factors Precipitating Factors

-Socioeconomic status
-Educational attainment
-Geographical location
Actual contact with infected water
-Nature of work
-Religion (due to some ritualistic
washing in water among some
Moslem tribes)

Embryonated eggs (Ova) from feces

reaches fresh waters
Osmotically induced
opening of the vent of
the egg Miracidium emerges
Deficient knowledge on
disease transmission

Infects snail

Asexual reproduction
Health teaching
Production of offspring sporocysts

Cercaria transformation

Released into water

Direct contact with human skin

+ reaction with Attachment and

arginine in skin penetration

Own production Within 24

of arginine hours
Schistosomules
Other cercaria enter peripheral
attracted circulation

To be continued…
 Driven to the
heart

Superior and inferior

Aorta
mesenteric arteries

Hepatic Splenic
artery artery
Intestinal capillary bed

travels
Liver Spleen
travels Intestinal veins
Lodges in the Grow and
sinusoids Sexual
mature
reproduction

Destruction of Egg (ova) production

liver cells melena

Break into intestines

Inflammation

Expelled with feces

Hepatic ↑collagen formation
abscess
S/A
labs

Fibrotic regeneration of
hepatocytes
Necrosis
Inflammation
Clotting
Scar tissue
↓albumin factors
formation
formation affected

Portal vein and branches

↓osmotic PTT: 18.9 sec. compressed
pressure
Post
sinusoidal/Intrahepatic
Risk for bleeding obstruction

Inability to sufficiently drain

Fluid shifting
blood to central veins

To be continued…
 Blood backs up to
liver and spleen

Inability to
Splanchnic arterial
metabolize
vasodilation
hormones esp.
aldosterone
↓general arterial circulation

Increased Na
Renin-angiotensin,
and H2O operation
sympathetic nervous
retention by
system, ADH activated
kidneys
Risk for bleeding
due to rupturing
Hypervolemia

Endoscopy results

Continued arterial
underfilling

Increased portal Varices

pressure
Ascites

Increased pressure in
Distended abdomen
splenic circulation
furosemide

urination
Risk for bleeding
due to rupturing Splenomegaly
Distended abdomen

Risk for infection splenectomy

Palpable mass
Health teaching Wear masks

UTZ
pain
handwashing Vaccination/Multivitamins