Metabolism

Suzanne Costello RN, MSN

 Metabolism
Review
 What is Metabolism???????
 What are the messengers involved in
metabolism?
 How are they controlled/regulated?
Hypothalamic-Pituitary
Axis (HPA)

 If hormone levels are too

↑ or ↓, the hypothalamus
signals the pituitary.
 Pituitary then ↑ or ↓
other hormones as
needed.
 Maintains homeostasis

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What are the Major Endocrine
Organs? What do they do?

 Hypothalamus
 Pituitary Gland – Anterior and Posterior
 Thyroid Glands
 Parathyroid Glands
 Adrenal glands
 Pancreas
 Pineal Gland
 Thymus
 Ovaries/Testes
Organs with Secondary
Endocrine Functions

 Bones
 Kidneys
 Stomach
 Small intestine
 Liver
 Skin
 Heart
 Adipose tissue
Concepts Related to
Metabolism
 Acid-base balance
 Perfusion
 Safety
 Addiction
 Tissue Integrity
 Stress and Coping
Exemplar 12.C
Liver Disease
pp. 844 - 854
 What are the functions of the liver?
 Metabolizes drugs
 Metabolism of proteins and
carbohydrates
 Produces plasma proteins
 Excretion of toxins
 Stores glycogen for energy
 Stores Minerals and fat soluble vitamins
 Produces bile
 Converts ammonia to urea for
elimination by the kidneys
Portal Circulatory
System
 Hepatic artery
 Portal vein
 Carries blood from stomach,
intestines, spleen and pancreas
 Carries absorbed products of digestion
to liver
 Branches come in contact with each
lobule
 Hepatic Vein runs from top of liver to
rejoin the Vena Cava
  End stage of Chronic Liver Disease
 Progressive, prolonged and irreversible
Cirrhosis:  Functional liver tissue destroyed and replaced by fibrous scar
tissue
Pathophysiology
 Nodules develop disrupting blood flow and blocking bile ducts
 Portal hypertension results from blockage
Cirrhosis:
Etiology
 Infection with Hepatitis B
or C
 Alcoholic cirrhosis
 Biliary Cirrhosis
 Post-hepatic Cirrhosis
 Severe long term right
sided failure
Risk
Factors
 High risk behaviors
 Socioeconomic
 Stress
 Addictive disorders – Alcohol
 Race of origin
 Non-Hispanic Blacks
 Mexicans
 Native Americans
 Cirrhosis
• End result of alcoholic liver disease
Alcoholic (or • Development directly related to alcohol consumption

Laennac) • Alcohol causes metabolic changes in the liver

• Regenerative nodules form, liver shrinks, nodular appearance

• Bile flow is obstructed within the liver or in the biliary system

Biliary • Retained bile damages and destroys liver cells
• Leads to inflammation, fibrosis and formation of regenerative nodules

Post- • Advanced progressive liver disease resulting from chronic Hepatitis B or C or

from an unknown cause

Hepatic • Leading cause is chronic viral hepatitis

• Liver is shrunken and nodular fibrosis and loss of liver cells
 Primary Effects of
Cirrhosis (Liver Dysfunction)
 Disrupted liver cell function
 Impaired bilirubin conversion and excretion
 Disrupted blood flow through liver
 Increased pressure in the portal venous system
 Portal hypertension
 Impaired Protein metabolism
 Disrupted glucose metabolism and storage
Impaired steroid hormone metabolism
 Stages of
Cirrhosis
Compensated Uncompensated

 Liver is beginning to scar  Most liver functions start to

 Still able to perform essential
functions
 Beginning to see changes in
labs
 May start to see signs and
symptoms.
fail
 Irreversible at this stage
 Will progress despite
treatment and change and
behavior
 Symptoms obvious
 Leads to liver failure and death
Clinical Manifestations
of Cirrhosis

 Early Manifestations:
 Loss of appetite
 Feeling weak or tired
 Anorexia
 Diarrhea/constipation
 Nausea
 Fever
 Unexpected weight loss
 Enlarged tender liver
 Dull, aching pain in the right upper
abdominal pain
 Complications
 Portal Hypertension
 Splenomegaly
 Ascites
 Esophageal Varices
 Portal Systemic Encephalopathy
 Hepatorenal Syndrome
 Spontaneous Bacterial Peritonitis
Portal
Hypertension
 Increased pressure in the portal vein
 Routes blood to the lower pressure veins
(Collateral vessels)
 Affected veins are located in esophagus,
rectum and abdomen
 Veins are fragile
 Portal hypertension increases hydrostatic
pressure in the capillaries, which leads to
fluid being pushed out.
 Ascites formation
Splenomegaly

 Portal hypertension
shunts blood to splenic
vein
 Spleen enlarges
 Increases destruction of
destruction for RBC’s,
WBC’s an platelets.
Which results in?

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Ascites
 Accumulation of plasma rich fluid in
the abdomen
 Causes: Portal hypertension
 Decreased proteins
(hypoalbuminemia),
hyperaldosteronism
 Fluid goes from intravascular
compartment to the extravascular
compartment – which is caused by
increased hydrostatic pressure and
decreased colloidal osmotic pressure
Esophageal
Varices
 Enlarged , thin-walled veins
that form in the esophagus
 Collateral vessels form when
blood is shunted from the
portal system as a result of
portal hypertension
 What is the patient at risk
for?
Portal Systemic Encephalopathy
(Hepatic Encephalopathy)

 Results for cerebral edema and the

accumulation of neurotoxins
 Ammonia (byproduct of protein
metabolism) contributes to hepatic
encephalopathy.
 Ammonia levels: 15-45mcg/dL
 Greater than 68 – critical
 Cerebral edema → Increased ICP →
cerebral hypoxia → death
Hepatorenal
Syndrome

 Renal failure with azotemia,

sodium retention, oliguria,
hypotension
 Develops in patients with
advanced cirrhosis
 Poor perfusion to and from
the kidneys
Spontaneous Bacterial
Peritonitis

 Abdominal discomfort
 Fever
 Increasing ascites
 Worsening
encephalopathy
 Decline in condition
Collaboration

 Care is holistic
 Include family in care
 Counseling, job coaching,
behavioral therapy and
nutritionist may be beneficial
in working with client and
family
Diagnostic
Tests
 Liver function tests
 CBC with Platelets
 Coagulation Studies
 Electrolytes
 Bilirubin – direct and indirect
 Serum albumin
 Serum ammonia
 Serum glucose and cholesterol
 Abdominal Ultrasound
 Esophagoscopy
 Liver biopsy
Pharmacologic
Therapy
 Diuretics
 Reduce fluid retention and ascites
 Spironolactone (Aldactone)
 Beta-blockers
 Nadolol (Corgard), isosorbide mononitrate
(Ismo, Imdur, Monoket)
 Lowers hepatic venous pressure
 Prevents rebleeding if esophageal varices
 Ferrous sulfate, folic acid
 Treat anemia
 Vitamin K
 Helps to reduce the risk of bleeding
 Pharmacologic Therapy
(Continued)
 Antacids  Lactulose
 Prescribed as indicted  Reduces the nitrogen load and lowers the
serum ammonia
 May be used in the treatment of H. pylori
 Reduces the manifestations of hepatic
 Oxazepam (Serax) encephalopathy
 May be used to treat acute agitation  Watch electrolytes closely
 Neomycin  Use with caution in diabetics
 Reduces the number of ammonia-  May need to increase insulin
forming bacteria in the bowel
Nutritional
Therapy
 Sodium intake restrict to less than 2 g/day
 Fluids restricted to reduce ascites and
generalized edema
 Unless ammonia levels are high, adequate diet is
allowed
 Protein should not be restricted
 High-calorie, moderate fat intake.
 Vitamin and mineral supplements as needed.
Liver
Transplant
 Indicated for some patients with
irreversible, progressive cirrhosis
 Decline in functional status
 Increase bilirubin levels
 Falling albumin levels
 Increasing problems with
complications
 Contraindications
 Malignancy
 Active alcohol or drug abuse
 Poor surgical risk
 Lifespan
Considerations
 Biliary Atresia  Cirrhosis
 Extrahepatic bile duct ducts fail to  Occurs in children due to hepatitis or
develop or are closed blockages
 Fatal if not treated  Can occur at any age

 Surgery only treatment – most need  Medical management

transplant  Liver transplantation is the only
 Leading cause for pediatric liver treatment for end-stage liver disease.
transplantation
 Death occurs if not treated by 2 years of
age.
 Goal of
Treatment/Care

 Reduce further liver damage

 Use holistic approach
 Teach client to make healthier lifestyle choices
 Minimizing symptoms of disease
Noticing/
Assessment

 Health History
 What do you need to know?
 What would be a concern?
 Physical Assessment
 Baseline needed
 What specific things would you
need to focus on?
 Palpate
 Measure
 Observe

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 Interpreting/
Problems

Fluid Volume: Ineffective

Confusion
Excess Protection

Impaired Skin
Nutrition
Integrity
Responding/
Interventions
 What interventions should be
used for each identified problem?
 Fluid Volume
 Mental Status
 Bleeding
 Skin Integrity
 Balanced nutrition
 Manage
Complications
Balance Fluid Volume Minimize Bleeding
 Paracentesis  Minimize bleeding – bleeding
 Relieves respiratory distress caused by
esophageal varices
ascites  Upper endoscopy to evaluate and treat
 Daily weight – low sodium diet  Large nasogastric tube
 Fluid restriction  Gastric lavage with normal saline
 Measure morning abdominal girth  Varices may be banded, sclerosed
 May be removed in small or large  Balloon tamponade (See next slide)
amounts.
 Somatostatin or Octreotide
Sengstaken-Blakemore
Esophageal-Gastric Balloon
Tamponade
 Use is bleeding is uncontrollable
 Gastric and esophageal balloons are
inflated
 Tension is applied to apply pressure
 Endotrachael tube before nasogastric
tube
 Watch for airway occlusion of balloon
rides up
 Short term measure
Transjugular
Intrahepatic
Portosystemic Shunt
 Relieve portal hypertension and
its complications of esophageal
varices and ascites
 Channel is created which allows
blood to flow from the portal vein
into the hepatic vein bypassing
the cirrhotic liver
 Relieves pressure in varices
 Allows better control of fluid
retention
Evaluation

 What should the evaluation of the patient with

cirrhosis include?
 Monitoring lab data: Which ones?
 Assess vital signs and level of consciousness
 Absence of bruising and bleeding
 Improved appetite
 Adequate urinary and bowel elimination
 Decreasing ascites
 Decreased pain