Hepatobiliary stuff
When a person has liver failure, several s/s are often present. These include
jaundice of the skin, icterus, fatigue, dark colored urine that resembles Iced
Tea (“tea-colored urine”), and clay-colored stools. They will have elevated
LFTs (Liver Function Tests – this is lab work that includes ALT and AST). Since
the liver is where most protein and clotting factors are made, they will have
low protein levels and be more prone to bleeding. Additionally, the liver is
what converts ammonia into urea, so they could have elevated ammonia
levels (on blood work).
STUDY TIP – all of the above I got directly from slide 35.
Remember – we need protein (mainly albumin, made in the liver) to maintain
oncotic pressure. So with this altered Protein synthesis and metabolism,
these patients lose oncotic pressure which is manifested as edema and, in
particular, ascites. Ascites can be so severe that the fluid compresses
upward against the diaphragm and they can feel SOB. Lots of treatment
options including replacing albumin through a transfusion, a paracentesis
where the doc actually drains the fluid out of the peritoneal space with a
needle and collection bottle (google it) – (keeping in mind that unless the
underlying liver disease isn’t “fixed”, the fluid will come back), and last ditch
efforts is surgery in the form of creating a shunt inside the body that drains
the fluid back into the vena cava to be excreted by the kidneys. You’ll learn
about that in Med-Surg.
So why does a person’s liver fail? Lots of reasons. Cirrhosis (alcoholic and
non-alcoholic), fatty livre disease, some medications (large amounts of
Tylenol (acetaminophen) for long periods of time can cause liver failure),
certain viruses (think Hepatitis). Some people get autoimmune hepatitis – it’s
treated pretty much like every other inflammatory AI disease.
Start with the Hepatitises (I don’t think that’s a word, but it sounds like it
should be). Hep A, B, and C are spelled out in the slides – also go into the
text and be able to distinguish between them – how are they spread? Is there
a cure? All pretty much have the same s/s. Pay particular attention to Hep B –
that’s what you all are vaccinated against and likely what you will be
exposed to in your career. Read up on active infection, how it’s treated, and
what it means to be a carrier. Hep C infection carries a higher risk for
developing cancer.
Cirrhosis is end stage liver disease. As hepatic tissue dies, it is replaced with
fibrous tissue that doesn’t function. Look at the different etiologies. Read
about hemochromatosis – you likely will see this in your career. Go back to
the ammonia part – if the liver can’t metabolize it, and ammonia build up in
the blood, it can cause weird neurological things like altered mental status
and something called “asterixis” which is a flapping tremor. Google a video
of that. This is hepatic encephalopathy.
Portal hypertension results from increased capillary pressure and decreased
albumin. There is porto-systemic shunting (backwards pressure) that leads to
symptoms/manifestations such as esophageal varices. These varices are
under a good bit of pressure (and filled with blood) so if they rupture – you
got a massive GI bleed on your hands. And the patient’s risk of dying just
went up greatly. Treatment consists of stopping the bleeding, usually by
tamponading it with a special kind of a catheter inserted into the esophagus
then a balloon gets inflated. This is pretty much a last resort option (and of
course requires a doctor’s order) – but I’ve used my fair share. Google
Sengstaken-Blakemore tube. This could also be used for bleeding ulcers until
other intervention (such as EGD where the doc can go in and stop the
bleeding with a laser or sometimes medication directly injected into the
bleed) can take place. So keep in mind – if a patient has esophageal varices –
you don’t want to be dropping an NG tube into them – that tube could
rupture a variceal.
Gallbladder disease – cholecystitis is an inflammation of the GB.
Cholelithiasis means there are gallstones in the gallbladder. So these things
aren’t a major problem and often don’t produce symptoms, but if a stone
moves out of the GB and gets lodged in the cystic duct or common bile duct,
now that obstruction is going to cause problems. Gallstones are very
prevalent in adults. These stones are usually made out of cholesterol
(remember the liver manufactures cholesterol). Go back to A&P and review
the structure and connections of the liver, gallbladder, pancreas, and
duodenum. It’s also on page 1183 of your text. Now, acute cholecystitis is
usually the result of gallstone disease (90% of the time). People c/o
abdominal pain, RUQ tenderness, and have leukocytosis. These are the
HALLMARKS of GB disease. They also may have vague s/s such as low grade
fever, N/V, and anorexia. If the CBD is obstructed, they will show signs of
liver failure such as jaundice and others. The onset is usually pretty sharp
and may wax and wane. With chronic cholecystitis, sx may be vague but
people c/o pain and belching if they eat high fat foods. GB disease is
diagnosed through CT or ultrasound, clinical symptoms, and labs. There are
more sophisticated methods out there. Treatment usually involves removing
the GB (cholecystectomy).
Acute pancreatitis HURTS. I mean A LOT. There are mild forms and severe
life-threatening forms. The cardinal manifestation is abdominal pain, usually
in the peri-umbilical region or epigastric region. The pain can radiate to the
back, chest, or flank areas. Lab work shows elevated levels of amylase and
lipase. Diagnosis is also confirmed with a CT. Treatment depends on how
severe it is, some can go home and wait it out but some require
hospitalization. Treatment measures are aimed at giving pain relief,
maintaining hydration, and in some cases – making the pt NPO. There are
new studies on this, though. But for purposes of NCLEX hospital – they’re
gonna be NPO. The pain from this comes from the inflammation but also from
the fact that the enzymes made in the pancreas meant to break down food
are stuck in the pancreas – so essentially it is autodigesting. Who gets
pancreatitis? It’s from GB disease/gallstones or alcohol or (less commonly) a
side effect of some medications. Chronic, untreated pancreatitis can be
deadly and can lead to hemorrhagic pancreatitis.
Compare and contrast GB disease to pancreatitis.
Abdominal pain is the #1 reason for people coming to the ER – and as you
can see, the causes of that pain can be MANY. Getting a good history on the
patient is essential, then correlating s/s and manifestations.
Only thing I will write about pancreatic cancer is that it is deadly. 5 year
survival rate after diagnosis is less than 10%. Unfortunately, there is an
increasing incidence of it in the US, and it is projected to be the 2 nd leading
cause of death due to cancer by the year 2030. There are two paragraphs in
your text (pg 1189) describing clinical manifestations – rather than me type
them, go read up on them.
STUDY TIP:
Reading major points in your text is a great way to help commit this stuff to
memory. Your text also may explain things differently than your professor, so
that is also helpful. ALL my notes here are from your text and the slides from
class. I threw in some other stuff for a little flair. Main thing when studying –
you need to know the etiology, risk factors, manifestations (s/s) and
assessment findings, and what an RN needs to TEACH a patient about their
diseases. The text is more detailed in many areas than you need. If it isn’t
taught in class and isn’t on the slides – then you don’t need to read about it
in the text.
