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GNUR 293 Patho FInal
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- Anatomy Condensed Final Exam Review - GNUR 155
GNUR 293 Patho FInal
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GNUR 293 Patho FInalThe blood supply is delivered to the liver by way of - ANS-dual arterial sources (25%
arterial flow from the aorta & 75% hepatic artery)
The liver has a dual blood supply, delivering a blood supply (25%) from arterial inflow
from the aorta via the celiac trunk and hepatic artery (75%) and from the portal vein via
the capillary bed of the alimentary canal and pancreas.
Esophageal varices are a complication of liver disease and are a result of -
ANS-elevated portal pressure/portal HT
Esophageal varices result mainly from impaired blood flow through the liver. Increased
pressure in the portal system leads to portal hypertension and congestion of the
esophageal vessels resulting in varices.
Biliary obstruction could result in - ANS-Jaundice
& more specifically increased level of conjugated bilirubin
What term is used to describe the process of converting bilirubin from its freely
lipid-soluble form to the form that is tightly bound to the plasma protein albumin? -
ANS-Conjugation
Damaged or destroyed red blood cells are lysed and the oxygen-carrying hemoglobin
molecule is recycled. Separation of heme from globin yields biliverdin, which is
converted to bilirubin and released into plasma and transported to the liver. Free
unconjugated bilirubin is lipid-soluble and crosses easily into the brain of the neonate.
Conjugation by the liver tightly binds bilirubin to the plasma protein albumin.
What condition occurs when a form of bilirubin diffuses into the brain and causes a type
of encephalopathy? - ANS-in babies: kernicterus
Kernicterus refers to brain injury as a result of hyperbilirubinemia. The immature
blood-brain barrier allows free unconjugated bilirubin to enter the brain, which causes
encephalopathy through unknown mechanisms
The development of hepatocellular carcinoma is - ANS-Usually associated with chronic
viral hepatitis
,Hepatocellular carcinoma is often the result of years of injury from chronic alcohol
abuse, chronic viral hepatitis, or injury and is therefore more often seen in older
individuals.
Portal hypertension occurs as a result of - ANS--Obstruction of blood flow in the liver's
venous sinusoids
-Impaired drainage into the central veins
-A buildup of venous pressure
characterizes the nature and capabilities of the liver - ANS--Blood detoxification is a
function of the liver.
-The liver plays a role in the digestion of fats (bile)
-The liver is vulnerable to illness, but has considerable repair abilities
Which manifestation is typical of hepatocellular failure? - ANS--hypoalbuminemia
-glucose imbalance
-osteomalacia
Appropriate early treatment for infants with jaundice-related encephalopathy may
include which of the following? - ANS--Phenobarbital to increase the levels of UDPGT
-Phenobarbital to increase the levels of UDPGT
-Exchange transfusions
Universal vaccination against hepatitis of child is recommended for which Hep classes?
- ANS-Hep A & B
What is ascites related to? - ANS-portal hypertnsion & hypoalbuminemia
What role does the liver play in nutrient metabolism, bile synthesis, storage of vitamins
and minerals, urea synthesis, clotting factor synthesis, and detoxification? - ANS-(notice
the wide array of roles)
The liver functions as a digestive organ (bile salt secretion for fat digestion; processing
and storage of fats, carbohydrates, and proteins absorbed by the intestines; processing
and storage of vitamins and minerals); as an endocrine organ (metabolism of
glucocorticoids, mineralocorticoids, and sex hormones; regulation of carbohydrate, fat
and protein metabolism), a hematologic organ (temporary storage of blood, removal of
bilirubin from bloodstream, hematopoiesis, synthesis of blood clotting factors), and an
,excretory organ (excretion of bile pigment and cholesterol via bile, urea synthesis,
detoxification of drugs and other foreign substances).
Manifestations of liver disease due to hepatocelleular failure - ANS-Jaundice,
decreased clotting factors, hypoalbuminemia, decreased vitamins D and K, and
feminization (gynocomastia & female hair distributionb) are attributed to hepatocellular
failure.
Manifestations of liver disease due to portal HT - ANS-Portal hypertension may result in
GI congestion with the development of esophageal or gastric varices, hemorrhoids,
splenomegaly, and ascites.
hat clinical and laboratory findings would lead to a diagnosis of liver cirrhosis? -
ANS-Clinical and laboratory findings that would lead to a diagnosis of liver cirrhosis
include palpation of an enlarged, nodular liver, jaundice, gastric varices, hemorrhoids,
splenomegaly, ascites, decreased clotting factors, hypoalbuminemia, decreased
vitamins D and K, and elevated AST/ALT (more than 40 units)
s/s of alcoholic cirrhosis - ANS--weakness
-fatigue
-muscle wasting
-anorexia
-ascites *
-abnormal blood glucose levels
-elevated serum lipids
-feminization
-palmar erythema *
spider telangiectasia *
^ all are primarily due to hepato cellular failure
s/s of portal hypertension - ANS-varices (enlarged veins including hemorrhoids and
gastroesophageal)
splenomegaly (enlarged spleen)
Everything enlarged. Why? Pressure pushing out on veins + arteries.
Why is a patient with alcoholic cirrhosis at risk for GI bleeding? - ANS-The liver is
needed in synthesis of clotting factors; with heptacellular filkure, severe
hypoprothrombinemia can develop
, Upper GI bleeding may result from varices, portal HT, or gastroduodenal ulcer (all of
which are manifestations of cirrhosis)
What could be the cause of progressive mental deterioration in cirrhosis patients? How
is managed? - ANS--probable cause is portal-systemic encephalopathy resulting from
the failure of the liver to detoxify noxious agents due to hepatocellular dysfunction
-*ammonia* is the most readily identified toxin and its rising serum level correlates with
the decline in cerebral fx
-managed by reducing PRO intake (to reduce the production of metabolic wastes),
lactulose can be taking to enhance ammonia excretion in stool, antibiotics to reduce
normal flora involved in PRO breakdown and ammonia production
Hepatitis & Antigen Antibodies - ANS-IgE: detection of Hep A, acute (allergy reaction)
IgM: Hep A is Active (virus is mean and active)
IgG: Hep A is gone (gone/immune)
HBsAg (Hep B is infectious)
anti-HBV (recovered/immune to Hep B)
Hepatitis A - ANS-Type: ssRNA
Viral Family: Hepatovirus related to picomavirus
Route: fecal-oral (contaminated food/water)
Incubation: 2-4 weeks
Acute
Dx: IgM
Hepatitis B - ANS-Type: partially dsDNA
Viral Family: Hepadnavirus
Route: Parenteral, sexual contact, prenatal
Incubation: 1-4 months
10% chronic
Dx: HBsAg/HBcAg
*sexually transmitted*
Hepatitis C - ANS-Type: ssRNA
Viral Family: Flaviridae
Route: parenteral; intranasal, cocaine use @ risk factor
Incubation: 7-8 weeks
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