Transcript Endocrine and Hepatic Disorders - Faculty Sites

Diana Blum MSN
Metropolitan Community College
Nursing 2150
Endrocrine glands
 Pituitary gland
 Adrenal gland
 Thyroid gland
 Islets cells of the pancreas
 Parathyroid glands
 Gonads
Hormones and Target tissue
 Hormones-Natural chemicals that exert their effects of
a specific tissue
 Target tissue-usually located at a distance from the
endocrine gland with no direct connection between
the endocrine gland and the target tissue.
 Endocrine glands are “ductless glands”
Neuroendorcrine Regulation
 The primary function of the endocrine glands is to
regulation of overall body function.
 The body must maintain a homoeostatis to respond to
environmental changes.
 Temperature regulation
 Serum sodium levels
 As hormones travel through the body, they can
only recognize their target tissue. Each receptor
site type is specific to only one hormone
 Only the correct hormone can connect to the
correct receptor
 Once the hormone binds to the site the target
tissue will change the tissues activity
 Disorders of the endorcrine system are related to
either excess or deficiency of a specific hormone or to a
defect at its receptor site.
 Onset
 Slow or insidious
 Abrupt or life threatening
 Hormone secretion is dependant on the need of
the body for the final action of that hormone
 When the body moves away from homeostatis a
specific change or action is required or a response
is needed to correct the change
 Supply and demand
 Parathyroid
 Parathyoid hormone
 Adrenal Cortex
 Glucocorticoid
 Mineralacorticoids
 Testes
 testosterone
 Ovary
 Estrogen
 Progesterone
 Pancreas
 Insulin
 Glucagon
 somatostatin
Glands
 Small area of nerve and glandular tissue located
beneath thalamus on each side of third ventricle of
the brain
 Shares a small closed circulatory system with
anterior pituitary
 Known as hypothalamic-hypophysial portal system
 Hormones can travel directly to anterior pituitary
Hypothalamus
corticotropin-releasing hormone
Thyrotropin releasing hormone
Gonadotropin releasing hormone
Growth hormone releasing hormone
Growth inhibiting hormone
Prolactin inhibiting hormone
Melanocyte inhibiting hormone
 Located at base of brain in a valley of the
sphenoid bone called sella turcica
 PEA SIZED
 The hypothalamus and pituitary work together.
The hormones of posterior pituitary are
produced in hypothalamus and are sent through
portal system
 The hormones are stored in nerve endings of
posterior pituitary and are released into
blood when needed
The pituitary gland is
responsible for many hormones
and subsequent target tissues
and actions
 Anterior pituitary
 Thyroid stimulating hormone
 Adrenocorticotropic hormone
 Luteinizing hormone
 Follicile stimulating hormone
 Growth hormone
 Melanocyte stimulating hormone
 Posterior pituitary
 Vasopressin
 Oxytocin
 Triiosothyronine (T3)
 Thyroxine (T4)
 Calcitonin
Patho
 Adenohypophysis-controls growth, metabolic
activity and sexual development.
GH, PROLACTIN, TSH, AdrenoCorticoTropin
(ACTH), FSH, LH,
MSH
Disorders arise when the anterior pituitary does not
work effectively or when the hypothalamus is not
work effectively.
(Primary pituitary dysfunction vs. secondary
pituitary dysfunction)
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Hypopituitarism
Hyperpituitarism
 Deficiency in one or more hormones
 In rare cases, panhypopituitarism is present
(Decreased hormone production from the anterior
pituitary)
 Deficiencies in ACTH and TSH are most life
threatening as they correspond to vital hormones
from adrenal gland and thyroid gland. The other
hormones from the gonads LH and FSH interfere
with sexual reproduction
 GH
 Decreased bone density
 Fractures
 Decreased muscle strength
 Gonadotropins-
women
 Amenorrhea
 Anovulation
 Low estrogen
levels
 Breast atrophy
 Decreased libido
 Gonadotropins-male
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Decreased facial hair
Reduced muscle mass
Impotence
Decreased body hair
Loss of bone density
 Thyroid stimulating hormone (TSH)
 Weight gain
 Intolerance to cold
 Menstrual abnormalities
 Slow cognition
 lethargy
 Andrenocorticotropin-ACTH
 Decreased serum cortisol levels
 Pale sallow skin
 Headache
 Hypoglycemia
 hyponatremia
 Stimulation test
 Usually involve injecting agents that are known to
stimulate secretion of specific pituitary hormones
 Skull x ray
 CT scan
 MRI
 Replacement of deficient hormone
 Androgens


Women will be given combination of
estrogen and progesterone
Gonadatropin releasing hormone and human
gonadatropin are used to stimulate
ovulation
 Oversecretion usually caused by
pituitary tumor or hyperplasia
 Rare
 Can cause gigantism or acromegaly
 Gigantism-onset of GH hypersecretion occurs before
puberty
Agromegaly
 Andre the GIANT stood 7 feet tall and died at 46. He did
not treat his disease. Excessive secretion of GH occurs after
puberty
Clinical manifestations
 Facial feature abnormalities
 Proganthism
 Changes to vision
 Organmegaly
 Hypertension
 Dysphagia
 Deepened voice
Diagnostics
 Laboratory blood draw to determine which hormone is
excessively secreting.
 CT scan
 MRI
 Suppression test
Non surgical management
 Drug therapy
 Dopamine agonist
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
Parlodel
Dostinex
 Both of these drugs stimulate the production of dopamine and
inhibit the release of GH and PRL
 Somatostatin analogues
 Octreotide-inhibits GH release
 Somavert-growth hormone blocker
 Radiation therapy
 Takes a long time to be effective
 Not immediate is acute situations
 Side effects

Optic nerve damage
 Surgery through nose into sphenoid sinus cavity
 Monitor neurologic status
 Monitor fluid balance (transient diabetes insipidus)
 Instruct client not to sneeze, cough, blow nose
 Encourage deep breathing exercises
 Monitor pad for nasal drainage (test for glucose)
 Instruct patient to use dental floss and oral
rinse. Brushing teeth is not permitted for at least
10 days post op
Surgical Management of
Hyperpituitarism
 Preop
 Education, education education
Operative
Use of a microscope
makes incision in upper lip
graft taken from thigh to prevent leak in CSF
 Postoperative- Vital signs and:
 Monitor neurologic status
 Monitor fluid balance (transient diabetes insipidus)
 Instruct client not to sneeze, cough, blow nose.
 Encourage deep breathing exercises
 Monitor pad for nasal drip
 Instruct patient to use dental floss and oral rinse.
Brushing teeth is not permitted.ita
Disorders of the Posterior
Pituitary
 Diabetes insipidus
 Syndrome of Inappropriate Antidiuretic hormone
Three types of DI
 Nephrogenic-inherited
 Primary-defect in the hypothalamus or pituitary gland
 Drug related-Lithium
Key features
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Hypotension
Decreased pulse pressure
Tachycardia
Increased Hbg,hct and BUN
Increased UOP
Poor skin turgor
Irritablilty
Decreased coginition
Hyperthermia
Lethargy leading to coma
Excessive thirst
Decreased urine specific gravity
Nursing interventions
 Primary management is with medications.
 Lypressin
 DDAVP
 Pitressin
 Diabinese
SIADH
 ECF expands
 Decreased sodium levels
 supplement diet with sodium and potassium at
home
 Diuretics may be used to decrease volume
 Fluid restriction
 Fluid volume excess related to compromised
regulatory mechanism and intravenous overload.
 Altered thought process related to cerebral
edema
SIADH
Case study77 year old female is taken to the
ER for a fall at home.
Assesment reveals
Awake, alert and oriented
Complains of pain to right hip.
She has a history of hypertension
and asthma.
EKG shows NSR
CBC
wbc 9.4
rbc 3.9
hgb 12.1
hct 39.0
 BMP
 Glucose 92
 BUN 18
 Cr 1.1
 NA 130
 K 4.2
 CO2 37
 Cl 97
 Pulse ox 94% on RA
 VS 98.6, 84, 18, 156/93
On admission to ICU
 Na 116
 K 3.5
 Cl 86
 BUN 9
 Cr .8
 Glucose 126
 Hgb 9.1
 Hct 27
 Serum Osmolality 243
 Urine Osmolality 541
 Ms. Mills still remains confused but her respiratory status has
improved.
 Twenty four hours later her lab shows
Na 132
K 3.2
Cl 98
Serum osmolality 275
 Urine osmolality 400
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 At this time her IV solution is changed to D5 NS at 50 ml/hr. She is
weaned off the oxygen and is alert awake and oriented.
 Vitals show 99.2 100 20 130/78
 Discuss two other sodium disorders that must be
differientaited from SIADH?
 Why are elderly more prone?
 What are factors that contributed to the development
of SIADH in Ms. Mills
 Consists of four small glands located on the back
of thyroid gland
 Chief cell of this gland production and secretion
of PTH
 Regulates calcium and phosphorus metabolism
by acting on bone, kidneys and intestinal
tract
 Serum calcium is major controlling factor of
PTH (Parathyoid hormone)
 Hyperparathyroidism – increased secretion of
parathyroid hormone (PTH)
 PTH – helps regulate calcium & phosphate
levels by
 Stimulating bone resorption of calcium
 Renal tubular reabsorption of calcium
 Activation of increased serum calcium levels
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Weakness
Loss of appetite
Constipation
Increased need for sleep
Emotional disorders
Shortened attention span
Loss of calcium from bones (osteoporosis)
Fractures
Kidney stones
Neuromuscular abnormalities (muscle
weakness)
 PTH – increased
 Serum calcium –
exceeds 10 mg/dl
 Serum phosphorus
below 3 mg/dl
 Urine calcium, serum
chloride, uric acid,
creatinine, amylase, &
alkaline phosphatase increased
 GOAL – relieve S/S & prevent complications caused
by excess PTH
 SURGICAL THERAPY – parathyroidectomy
criteria:
 Calcium levels > 12 mg/dl
 Hypercalciuria
 Markedly reduced bone mineral
density
 Overt symptoms (neuromuscular)
 Under age 50
 Major postoperative complications
(parathroidectomy or thyroidectomy)
 Hemorrhage
 Fluid & electrolyte disturbances
 Tetany
 Tetany – neuromuscular excitability
associated with sudden decrease in serum
calcium levels
 Unpleasant tingling of hands & mouth
 If severe, laryngospasms (laryngeal stridor)
develop – give IV Calcium gluconate
Autotransplantation of normal
parathyroid
tissue in
forearm or neck
allows PTH
secretion to
continue with
normal calcium
levels
 Conservative management approach
 Annual exam testing for:
 Serum PTH, calcium, phosphorus, & alkaline
phosphatase levels
 Renal function
 X-rays (assess for metabolic bone disease)
 Measure urinary calcium excretion
 Continue ambulation & avoid immobility
 High fluid & moderate calcium intake
 Alendronate
(Fosamax)
 Estrogen or
progestin therapy
 Oral phosphate
 Diuretics
 Calcimimetic
agents (R-586)
 Hypoparathyroidism – inadequate
circulating PTH
 Uncommon
 Hypocalcemia
 Genetic defect
 Cause – accidental removal of
parathyroids or damage to vascular
supply of glands during neck surgery
(thyroidectomy, radical neck)
HYPOPARATHYROIDISM
Role of PTH
 Stimulate bone resorption of
calcium and increase calcium in
blood when calcium levels fall
 Sudden decrease in calcium causes tetany
 Tingling of fingers & lips
 Increased muscle tension – paresthesias & stiffness
 Painful tonic spasms, dysphagia, constricted feeling
in throat, & laryngospasms
 Chvostek’s sign & Trousseau’s sign – positive
 Patient anxious & apprehensive
 Serum calcium & PTH levels – decreased
 Serum phosphate levels - increased
 Chvostek’s sign –
contraction of facial
muscles in response to
light tap over facial
nerve in front of ear
 Trousseau’s sign –
carpal spasm induced
by inflating a blood
pressure cuff above
systolic pressure for a
few minutes
 Emergency treatment of tetany:
 IV Calcium gluconate – infuse slowly in 10 to 20
ml of NS over 10 minutes
 Hypotension, cardiac arrhythmias, or cardiac
arrest
 Venous irritation & extravasation
 Rebreathing – to alleviate acute neuromuscular
symptoms
 Oral calcium
supplements
 High-calcium meal
plan, including foods
such as dark green
vegetables, soybeans,
& tofu
 Lifelong treatment &
follow-up care
Function of the glands
 Thyroid gland
 Found in the anterior neck below the cricoid cartilage.
 Rich in blood supply
 Produce hormones t3 and t4
 Function of the thyroid gland
 Fetal development
 Control metabolic rate of all cells
 Regulate fat, carbohydrate, and protein production
 Increase red blood cell production
 Produces calcitonin-lowers calcium and phosphorus
levels by reducing bone breaksdown.
Function of the glands
 Adrenal glands
 They are vascular and tent shaped organs on top of the
kidneys
 Outer portion-cortex
 Inner portion-medulla
 Each area works independently
 Adrenal cortex is 90% of the adrenal gland
 Mineralocorticoids are produced in the cortex
 Adrenal steroids and corticosteriods are
produced in the cortex
 Sympathetic nerve ganglion that has secretory
cells
 Releases catacholamines (epinephrine and
norepinephrine)
 Not essential for life, however plays a role in
stress response
Disorders of the Adrenal Gland
Acute adrenal insufficiency or Addisonian insufficiency
 Life threatening
 Cortisol and aldosterone needs are greater than the
supply
 Related to stress, trauma, severe infection
Causes of Primary Adrenal
insufficiency
 Autoimmune disease
 Tuberculosis
 Fungal lesions
 AIDS
 Hemorrhage (Adrenal)
 Adrenalectomy
 Radiation
Causes of Secondary Adrenal
insufficiency
 Pituitary hormones
 Hypophysectomy
 High dose pituitary radiation
 Brain radiation
 Endogenous (Cushing disease)
 Adrenal hyperplasia
 Adenoma
 Carcinomas
 Exogenous (Cushing Syndrome)
 Asthma
 Autoimmune disorders
 Organ transplants
 Cancer chemo
 Allergic responses
 Fibrosis
Management of Adrenal insufficiency
 Hormone replacement
 Hyperkalemia management
 Hypoglycemia management
Diagnostic and labs for AC
 Complete Metabolic panel
 UA
 CT, MRI, skull x ray
 ACTH stimulation test (rapid and long)
Long term management
 Hydrocortisone
 Corrects glucocorticoid deficiency
Florinef maintains electrolyte balance
Adrenal gland hyperfunction
 The adrenal gland may oversecrete one or more of the
adrenal hormones
 AKA Cushing’s syndrome, Cushing disease or
hyperaldosteronism (excessive mineralocorticoid
production)
 Spectrum of clinical abnormalities caused by
excess corticosteroids, especially glucocorticoids
 Most common cause – iatrogenic administration
of corticosteroids (prednisone)
 ACTH-secreting pituitary tumor
 Patients with Cushing’s disease (hypercortisolism)
exhibit
 Problems with nitrogen, carbohydrate and mineral
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metabolism.
Slow turnover is of plasma fatty acids
“Buffalo hump”
High levels of corticosteroids decrease immunity by
destroying lymphocytes.
Increased androgen production causes hirutism
Clinical Manifestations
 Moon face
 Buffalo hump
 Weight gain
 Hypertension
 Muscle atrophy
 Paper like skin
 Hyperpigmentation
 Increased risk for infection
 Elevated blood sugars
 Mineralocorticoid excess –
hypertension (fluid retention)
 Androgen excess – pronounced acne,
virilization in women & feminization
in men
 Menstrual disorders & hirsutism in
women and gynecomastia & impotence
in men seen in adrenal cancer
Of particular importance on H&P:
1. Centripedal (truncal) obesity
2. “moon” facies
3. Purplish red striae on abdomen,
breast, or buttocks
4. Hirsutism in women
5. Menstrual disorders in women
6. Hypertension
7. Unexplained hypokalemia
Diagnostics and labs
 Patient will have
 Inc. BS
 Dec. lymph count
 Inc. sodium
 Dec. calcium
 Dec. potassium
 How does this compare to Addison’s disease?
 UA
 CT, MRI
 Overnight dexamethasone testing
 3 day low dose testing.
 8 day high dose testing
 Goal – normalize hormone secretion
 Adrenalectomy – indicated for Cushing
syndrome caused by adrenal tumors or
hyperplasia
 Drug therapy – goal is to inhibit adrenal
function
 Milotane (Lysodren) – suppresses cortisol production,
alters peripheral metabolism of cortisol, & decreases
plasma & urine corticosteroid levels; “medical
adrenalectomy”
 Side effects – anorexia, N/V, GI bleeding,
depression, vertigo, skin rashes, & diplopia
Management of Cushing’s
 Drug therapy
 Lysodren
 Elipten
 Radiation therapy

Treats pituitary adenomas

Surgery
 Removal of tumor or pituitary itself
 Corticosteroid excess causes pronounced
changes in physical appearance
 Weight gain
 Hyperglycemia – due to glucose intolerance
(cortisol-induced insulin resistance) & increased
gluconeogenesis by liver
 Protein wasting
 Control HTN &
hyperglycemia
 Correct hypokalemia
 Administer
hydrocortisone
 Teach about:
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NG tube
Foley catheter
IV therapy
CVP monitoring
Leg sequential
compression devices
 Increased risk of hemorrhage
 Marked fluctuations in metabolic processes
– due to manipulation of glandular tissue
during surgery, releasing large amounts of
hormones into circulation
 Unstable BP, fluid balance, & electrolyte
levels
 Critical period for circulatory instability –
24 to 48 hours after surgery
 High doses of corticosteroids
(hydrocortisone or Solu-Cortef) given IV
during & after surgery
 Morning urine
cortisol levels –
measured to
evaluate
effectiveness of
therapy
 If corticosteroid
dosage tapered too
rapidly – acute
adrenal insufficiency
 Bed rest after
surgery until BP
stabilizes
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1.
2.
3.
Primary cause – Addison’s disease
Secondary cause – lack of pituitary ACTH
secretion
Addison’s disease – all three classes of adrenal
corticosteroids reduced:
Glucocorticoids
Mineralocorticoids
Androgens
 Most common
cause of
Addison’s
disease –
autoimmune
response
 Most common in
white females,
aged 30 to 60
 Slow, insidious onset
 Progressive weakness & fatigue
 Weight loss & anorexia
 Skin hyperpigmentation – on sun-exposed
areas, at pressure points, over joints, & in
creases (due to increased secretion of B-
lipotropin, which contains melanocytestimulating hormone [MSH] or ACTH)
 Hypotension, hyponatremia, & hyperkalemia
 N/V & diarrhea
 Addisonian Crisis – life-threatening
emergency caused by insufficient
adrenocortical hormones or sudden sharp
decrease in these hormones
 Triggered by stress (infection, surgery, trauma,
hemorrhage, or psychologic distress
 Sudden withdrawal of corticosteroid therapy
 After adrenal surgery
 Sudden pituitary gland destruction
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Hypotension (postural)
Tachycardia
Dehydration
Hyponatremia
Hyperkalemia
Hypoglycemia
Fever
Weakness
Confusion
Shock
N/V
Diarrhea
 Vital signs
 Assess signs of fluid volume deficit &
electrolyte imbalance
 Daily weights
 Corticosteroid administration
 Protect from infection
 Need for lifelong steroid replacement
therapy
 Adjust steroid dose depending on level of
stress (fever, influenza, extraction of
teeth, & rigorous physical activity)
 Expected effects:
1. Antiinflammatory action – decrease
number of circulating lymphocytes,
monocytes, & eosinophils
2. Immunosuppression – decrease production
of antibodies
3. Maintenance of normal BP – potentiate
vasoconstrictor effects of
norepinephrine
4. Carbohydrate & protein metabolism –
glucose intolerance & insulin resistance
 Aldosterone-chief mineralocortoid
Maintains extracellular fluid volme
 Promotes sodium and water
reabsorption and potassium
excretion
 Aldosterone secretion is controlled
by renin angiotensin system, ACTH,
and potassium

 Cortisol is secreted from the adrenal
cortex
 Cortisol affects
Carbohydrate, protein, and fat
metabolism
 Emotional stability
 Immune function

 Androgens – contribute to growth & development in
both genders and to sexual activity in adult women
 Corticosteroid – refers to any one of these
three types of hormones produced by
adrenal cortex
Hyperaldosteronism (Conn’s)
 Increased secretion of aldosterone which results in
mineralcorticoid excess
 Most often caused by adrenal adenoma (primary
hyperaldosteronism)
 Elevated levels of angiotensin II are seen in
secondary hyperaldosteronism
Clinical manifestations
 Hypokalemia and elevated BP
 Headache
 Fatigue
 Nocturia
 Polydipsia
 Polyuria
 paresthesias
Diagnostic and labs
 UA specific gravity
 BMP
 CT
 MRI
Management of hyperaldosteronism
 Surgery for early stage
 Drug therapy
 Medication to increase K+
Pheochromocytoma
 Catecholamine producing tumor that arises in
chromaffin cells.
 Occurs in a single lesion on adrenal gland
 Releases epinephrine and norepinephrine
 Cause is unknown occur more in women then men.
 Could be inherited
Clinical Manifestations
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Intermittent episodes hypertension (classic)
Headache
Sweating
Palpitations
Impeding doom
 Drugs may induce hypertensive crisis
Diagnostic and Lab
 24 hour UA to test for VMA (vanillylmandelic acid) a
production of catecholamine metabolism)
 Ct
 MRI
Management
 Surgery- one or both of the adrenal glands are
removed.
 Monitor BP and treat if hypertensive crisis
 Hydrate
Function of the glands
 Gonads
 Male and female reproductive endocrine glands.
 Male gonads are the testes
 Female gonads are the ovaries
 These glands are present at birth but do not begin to
function until puberty
Function of the glands
 Pancreas
 Lies behind the stomach and has endocrine and
exocrine function.
 The islets of langerhans perform the endocrine
functions. The Islets have three cell types.
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Alpha-secrete glucagcon
Beta-secrete insulin
Delta- secrete somatostatin
Function of the glandspancreas
 The exocrine function involves the secretion of
digestive enyzmes through ducts that empty into the
doudenum.
 The main endorcrine function is to regulate blood
sugar.
Pancreas
 Glucagon is the hormone the increase blood
sugars
 The liver is the main target tissue for glucagon and
it causes glycogenolysis-conversion of glycogen to
glucose.
 Gluconeogensis-conversion of amino acids to
glucose. This enhances the transport of amino
acids to the muscle.
Pancreas
 Insulin
 Anabolic hormone, promotes the movement and storage
of carbohydrates, protein and fat.
 Insulin lowers the blood glucose levels by enhancing
glucose movement across the cell membrane.
Hepatic Disorders
Hepatic Disorders
 Most common liver function tests are
 ALT
 GGT
 AST
 Globulins
 Ammonia
 Cholesterol
Jaundice
 Bilirubin concentration in the blood is abnormally
elevated, all the tissues become yellow, green in color.
 Becomes clinically evident with serum bilirubin levels
above 2.3mg/dl
Types of Jaundice
 Hemolytic jaundice- increased destruction of the red
blood cells.
 Found in pts with hemolytic transfusion reactions,
Hepatocellular jaundice- inability of damaged liver cells to
clear normal amounts of bilirubin from the blood.
Usually caused by hepatitis disease, yellow disease or
Mononucleosis.
 Patients with Hepatocellular jaundice may be mildly ill
or severely ill.
 Patient presents with lack of appetite, nausea, fatigue,
weakness, and weight loss.
 Obstructive jaundice- extrahepatic obstruction
caused by an occlusion to the bile duct from a gall
stone, tumor, or inflammatory process.
 Hereditary hyperbilirubinemia- increased serum
bilirubin levels resulting from inherited disorders.
(Gilbert’s syndrome, Dubin-Johnson and Rotor’s
syndrome).
Portal Hypertension
 Obstructed blood flow through the damaged liver
results in increased pressure throughout the portal
venous system.
 Associated with hepatic cirrohosis
Ascites
 The pathophysiology of ascites is not clear. As a
result of liver damage, large amounts of albumin
rich fluid accumulate in the peritoneal cavity.
 Clinical symptoms
 Increased abdominal girth
 Rapid weight gain
 Shortness of breath
 Adominal striae
 Distended veins over the abdominal wall.
Treatment for Ascites
 Dietary modifications
 Diuretics
 Bed rest
 Paracentesis
http://www.youtube.com/watch?v=GNxVlxPOXSQ
 Transjugular intrahepatic protosystemic shunt
 Paracentesis – needle
puncture of abdominal
cavity to remove
ascitic fluid
 Reserved for patient
with impaired
respiratory status or
abdominal pain caused
by severe ascites
 Temporary measure –
fluid tends to
reaccumulate
 Peritoneovenous shunt
provides continuous
reinfusion of ascitic
fluid into venous system
Esophageal varies
 Dilated vein that are found in the submucosa of the
lover esophagus or extend into to the stomach.
 Clinical manifestations
 Bleeding



Hemataemesis
Melena
Signs and symptoms of hypovolemic shock
Diagnostics and Medical Management
• Upper endoscopy
• Portal Hypertension measurements
• Laboratory tests
• Medical management
•
Manage bleeding
Medical Management
 Balloon tamponade
 Sclerotherapy
 Pharmacological intervention
 Vasopressin with nitroglycerin
 Inderal
 Corgard
Medical management
 Esophageal banding therapy-the varies are banded by
using a modified endoscope loaded with elastic rubber
band that is slipped over the varies.
 Transjugular intrahepatic portosystemic shunting-
TIPS
 Esophageal Varices
 Goal – avoid bleeding & hemorrhage
 Avoid ingesting alcohol, aspirin, &
irritating foods
 Prophylatic treatment – nonselective Bblockers (propranolol or Inderal)
 Drug therapy – octreotide
(Sandostatin), vasopressin (VP),
nitroglycerin (NTG)
 Endoscopic therapies – sclerotherapy,
ligation of varices, & shunt therapy
 Supportive measures
 Fresh frozen
plasma & PRBCs
 Vitamin K
(aquaMEPHYTON)
 Histamine (H2)receptor blockers
(cimetidine or
Tagamet)
 Lactulose &
neomycin
Hepatic Encephalopathy
 A life threatening complications of liver disease
occuring with profound liver failure and results in
high levels of ammonia circulating in the blood.
 Clinical manifestations
 Minor mental changes ( early phases)
 Motor dysfunction
 Alterations in mood and sleep
 Asterixis( flapping tremor to hands)
 Hepatic Encephalopathy – neuropsychiatric
manifestation of liver damage
 Causes ammonia to enter systemic circulation
without liver detoxification
 Disorder of protein metabolism & excretion
 Major source of ammonia – bacterial & enzymatic
deamination of amino acids in intestines
 Normally, ammonia resulting from this deamination
process goes to liver via portal circulation & is
converted to urea which is then excreted by kidneys
 Fetor hepaticus
– musty, sweet
odor of patient’s
breath
 Due to
accumulation of
digestive byproducts that
liver unable to
degrade
Diagnositic and Medical Management
 EEG to determine level of brain waves
 Patient are usually referred for aliver transplant
after their first episode of encephalopathy.
 Medical management
 Lactulose-reduce the amount of ammomina in body.
 Rest – reduce metabolic demands of liver &
allow for recovery of liver cells
 Ascites – sodium restriction





2 g/day
Severe ascites – 250 to 500 mg/day
Control of F&E balance
Salt poor albumin
Diuretic therapy


Aldosterone antagonist (spironolactone or
Aldactone)
Loop diuretic (furosemide or Lasix)
 Goal – reduce ammonia formation by protein
restriction & reduction of ammonia
formation in intestines
 Measures to reduce ammonia formation in
intestines:
 Lactulose – traps ammonia in gut & laxative effect
of drug expels ammonia from colon
 Antibiotics – neomycin sulfate (poorly absorbed from
GI tract) given orally or rectally to reduce bacterial
flora of colon
 Prevent constipation
 Prevent causes – control GI hemorrhage & remove
blood from GI tract
 High in calories
(3000 kcal/day),
high carbohydrate,
moderate to low fat
levels
 Patient with
hepatic
encephalopathy –
very-low protein to
no-protein diet
 Ascites & edema –
low-sodium diet
 Imbalanced nutrition: less than
body requirements RT anorexia,
N/V, & impaired use & storage of
nutrients
 Impaired skin integrity RT edema,
ascites, & pruitus
 Ineffective breathing pattern RT
pressure on diaphragm & reduced
lung volume secondary to ascites
 Chronic progressive disease of liver
characterized by extensive
degeneration & destruction of liver
parenchymal cells
 Insidious & prolonged course
 9th leading cause of death in U.S.
 Excessive alcohol ingestion – single
most common cause of cirrhosis
 Four types of cirrhosis:
 Alcoholic – fat in liver cells
 Postnecrotic – complication of viral, toxic,
or autoimmune hepatitis
 Biliary – associated with chronic biliary
obstruction & infection
 Cardiac – results from long-standing,
severe right-sided heart failure
 Cell necrosis – destroyed liver cells
replaced by scar tissue
 Protein malnutrition
– common problem in
alcoholics
 Malnutrition &
alcohol – especially
damaging to
hepatocytes
 Alcohol alone has
direct hepatotoxic
effect & is known to
produce necrosis of
cells & fatty
infiltration
 EARLY MANIFESTATIONS
 GI disturbances – anorexia,
dyspepsia, flatulence, N/V,
diarrhea or constipation,
 Abdominal pain – dull, heavy
feeling in right upper quadrant
 Fever, lassitude, slight weight
loss
 Enlargement of liver & spleen
 LATER MANIFESTATIONS
 Jaundice – result of decreased ability to conjugate
& excrete bilirubin (hepatocellular jaundice)

Obstructive jaundice – pruritis
 Skin lesions – spider angiomas (small, dilated blood
vessels with bright red center point & spiderlike
branches that occur on nose, cheeks, upper trunk,
neck, & shoulders); palmar erthema (red area that
blanches with pressure located on palms of hands)
 Hematologic problems – thrombocyopenia,
leukopenia, & anemia caused by splenomegaly

Bleeding tendencies – epistaxis, purpura, petechiae, easy
bruising, gingival bleeding
 Endocrine disturbances
– S/S RT metabolism &
inactivation of
adrenocortical
hormones, estrogen &
testosterone
 Men – gynecomastia &
impotence
 Young women –
amenorrhea
 Older women – vaginal
bleeding
 Peripheral neuropathy
due to dietary
deficiency of thiamine,
folic acid, & vitamin B12
Hepatitis
 Numerous amounts of hepatitis
 Hep A
 Hep B
 Hep C
 Hep D
 Hep E
 Hep G
 Liver
 Inflammation
 Cytotoxic cytokines & natural killer cells that
cause lysis of infected hepatocytes
 Hepatic cell necrosis
 Proliferation & enlargement of Kuppfer cells
 Systemic Effects
 Rash, angioedema, arthritis, fever, & malaise
 Glomerulonephritis & vasculitis secondary to
immune complex activation
 Preicteric Phase – precedes jaundice &
lasts 1 to 21 days
 Period of maximal infectivity for HAV
 GI – anorexia, N/V, abdominal (right upper




quadrant) discomfort, constipation, or diarrhea
Decreased sense of smell
Weight loss
Malaise, headache, low-grade fever, arthralgias,
& skin rashes
Hepatomegaly, lymphadenopathy, & splenomegaly
 Icteric Phase – characterized by jaundice
(when bilirubin diffuses into tissues) &
lasts 2 to 4 weeks




Urine may darken
Pruitus
GI symptoms remain
Liver enlarged & tender
 Posticteric Phase – jaundice disappearing &
lasts weeks to months with average of 2 to
4 months
 Major complaint – malaise & easy fatigability
 Hepatomegaly remains but splenomegaly subsides
 Relapses may occur
Epidemiology
Hepatitis A
Hepatitis B
Hepatitis C
Hepatitis D
Hepatitis E
Cause
Virus (HAV)
Virus (HBV)
Virus
Virus
Virus
(HCV)
(HDV)
(HEV)
Mode of
Transmissio
n
Fecal Oral Route
Parenterally
Blood
Parenterally
Fecal Oral Route
Incubation
15-50 days
28-160 days
15-160 days
21-140 days
15-65 days
S/S
Flu like
symptoms
Rash
Rash
Rash joint pain
Flu like
symptoms,
severe in
pregnant
woment
 Fulminant hepatic
failure
 Chronic hepatitis
 Cirrhosis of liver
 Hepatocellular
cancer
 Liver biopsy –
percutaneous
procedure using CT
or ultrasound guided
needle inserted into
liver for hepatic
tissue
 After procedure –
keep patient lying on
right side for minimum
of 2 hours to splint
puncture site (prevent
bleeding)
Medical management of Hepatitis
 Bed rest during acute stages
 Patient teaching
 Prevention
 Nutrition & rest
 Adequate nutrition priority
 Increase intake of fluids (juices) to
deal with anorexia
 Avoid alcohol (during acute phase – not permanent)
 Drug Therapy:
 Chronic HBV
 Decrease rate of disease progression – a-
interferon
 Decrease rate of drug-resistance
 Chronic hepatitis C
 Reduce viral load
 Decrease disease
progression
 Promote
seroconversion
 Treatment – ainterferon &
Ribavirin
 HIV & HCV
 Hepatitis A
 Hepatitis A vaccine & immune globulin (IG)
 Vaccine – preexposure prophylaxis
 IG – before & after exposure; (6 to 8 weeks)
passive immunity
 Hepatitis B
 Routine vaccination schedule
 Postexposure prophylaxis – vaccine &
hepatitis B immune globulin (HBIG) used
 Hepatitis C
 No products to
prevent HCV
 CDC does not
recommend ainterferon for
postexposure
prophylaxis
 Unknown if
antivirals have
positive effect
 Rest & nutrition
 Prevent
transmission
 Regular follow-up
 Avoid alcohol
 Education re: ainterferon
Liver transplant
 Known as a solid organ liver transplant (OLTX).
 Used as last resort to treat end stage liver disease
 Immunosuppression is required for lifetime
 Prograf, Imuran, OKT3, cyclosporine
Post operative OLTX
 Straight to ICU with hemodynamic monitoring.
 Complications
 Bleeding
 Rejection
 Infection
Few hospitals in United States are sites for OLTX,
UNMC, UCLA, Univ of Pittsburgh, Duke are noted as
the best in the nation.