Exam 4 - Study Material (liver) Flashcards
What are the functions of the liver?
- Storage of nutrients
- Breakdown of erythrocytes
- Bile formation & secretion
- Synthesis of plasma proteins; cholesterol
- Immunity – Kupffer cells
- Conversion of ammonia into urea
- Inactivation - various substances (ammonia, toxins, steroids, other hormones)
What are some changes to the liver with aging?
- Decrease in size, weight
- Decreased portal blood flow
- Decreased metabolism of some medications
- Increased prevalence of gallstones
- Atypical presentation of biliary tract disorders
- Liver function test values remain unchanged
How is hepatitis A transmitted and what are the manifestations of hepatitis A?
How would you diagnose a patient with hepatitis A?
-
Gold standard: clinical picture & Serum IgM anti-HAV
- + at onset
- Peaks during acute/early convalescence
- Positive - 4-6 months
- Serum IgG anti-HAV:
- Early convalescence
- Detectable for decades
What are the risk factors for hepatitis B?
What are the manifestations of heptitis B? (viral)
- 70% are subclinical – asymptomatic
- Flu like symptoms
*
How would you diagnose a patient with heptitis B?
-
HBsAg – Hallmark serologic marker of HBV:
- 1-10 weeks after acute exposure
- Detectable up to 6 months
-
Anti-HBs (hepatitis B surface antibody):
- Appears – life-time immunity
- If “window period” (no HBsAg or Anti-HBs) – may be diagnosed by detecting IgM antibodies against HB core antigens
What are some risk factors for heptitis C?
- **Most common blood-borne infection **
- Most asymptomatic; not detected
- Incubation period 60-160 days
- IV drug users; blood transfusions
- HIV infection
- High-risk sexual behavior
- Hemodialysis
- Occupational exposure
- Perinatal transmission
What are the manifestations of a heptitis C infection?
elevated liver function tests, perhaps jaundice
How would you diagnose a patient with hepitis C?
- Anti-HCV antibodies
- Acute:
- If HCV-RNA with detectable replicating virus – needs Rx
- If HCV-RNA not detectable & no replications – no Rx
- Immunosuppressed; hemodialysis
- HCV RNA test even if anti-HCV negative
What are some characteristics of Hepatitis D?
What drugs can cause drug/toxin induced hepatitis?
- Acetominophen
- Some - Anesthetic agents; antidepressants; antibiotics, anti-metabolities
What are the acute and later symptoms of drug/toxin induced hepatitis?
- Acute: abrupt; chills, fever, rash, pruritis, anorexia, nausea, fatigue, anorexia, abdominal discomfort, headache
- Later: jaundice, dark urine, hepatomegely
What are the acute clinical manifestations of hepatitis?
- Hepatomegaly; splenomegaly
- Lymphadenopathy
- Jaundice
- Dark urine; light/clay-colored stools (because of lack of bile)
- Pruritus (itching –> scratching)
How would you treat drug/toxin induced hepatitis?
Rx: stop drug! S&S may slowly diminish; may need liver transplant.
Describe the convalescent phase associated with hepatitis A
- Major complaints: malaise, fatigue, hepatomegaly
- Almost all cases of HVA resolve
- Acute illness – 2-3 weeks
- Lab recovery -9 weeks
- Complications – rare:
- Fulminant hepatic failure
- Chronic hepatitis
- Cirrhosis of the liver
- Hepatocellular carcinoma
How would you manage patients with hepatitis A?
- Bed rest & nutritious diet – then progressive ambulation
- Small frequent feedings
- Low-fat option, high protein; adequate fluids
- For those with more severe hepatitis infections – enteral feedings may need to be considered
- No alcohol for at least 6 months following recovery
- Serial liver function studies monitors recovery
- Medications – avoid those that affect liver function
What medications will be given to a patient with hepatitis B?
- Not all respond to current therapeutic regimens
- A-interferon
- Antiviral agents
- Lamivudine (Epivir)
- Adefovir ( Hepsera)
How would you prevent hepatitis A transmission?
- Good hygiene, hand washing & sanitation
- Vaccination for travel to foreign countries with high incidence
- Hepatitis A vaccine
- Immune globulin (IG) if contact
How would you prevent transmission of hepatitis B?
- Standard precautions/infection control measures
- Screening of blood products
- Immunization:
- Series – 3 injections – 0,1 & 6 months
- Hepatitis B immune globulin (HBIG)
How would you prevent hepatitis C?
- No vaccine available
- Screening - blood products
- Prevention - needle sticks
- Reduce infection spread
- Avoid high risk behaviors
- Use barrier precautions when in contact with blood or body fluids
What would you teach a patient with hepatitis A,B, or C?
- Hepatitis A & B
- Education – re infection
- Vaccinations available
- Hygiene practices
- Hepatitis C
- Education – re infection
- Infection control measures
- Modification of high risk behaviors
- Treatment protocols
What is cirrhosis?
Chronic disorder; normal hepatocytes replaced with diffuse hepatic fibrosis (Scarring of the liver)
What can cause cirrhosis?
- Chronic alcohol consumption
- Hepatitis – C & B
- Primary biliary
- Non-alcoholic fatty liver
- Environmental factors; exposure to chemicals
- Predisposition regardless of alcohol intake or diet
- Alpha 1-antitryptsen deficiency (it maintains surfactant)
- Repeated episodes of heart failure (congestion and backing up of blood)
- Autoimmune
- Cause may not be known
What are the clinical manifestations of cirrhosis?
- Asymptomatic for long periods
- Systemic – fever, weakness, fever, weight loss
- GI disturbances
- Abdominal pain
- Amenorrhea
- Erectile dysfunction; gynecomastia
- Portal hypertension →hepatomegaly; splenomegaly → developing ascites
- Infection; spontaneous bacterial peritonitis
- Vitamin deficiencies
- Jaundice
- Hematologic
- Skin lesions
- Encephalopathy - subclinical
- Anemia
- Malnutrition
- Hematologic
- Neurologic changes
- Hepatic encephalopathy
- Day-night reversal; asterixis; tremor
- Delirium, drowsiness, coma
- Asterixis
- Fetor hepaticus – must smell from all of the urea
What would be used to diagnose a patient with cirrhosis?
- CBC; serum electrolytes
- Serum albumin
- Liver function tests
- Prothrombin times
- Stool for occult blood
- Esophagogastroduodenoscopy (EGD)
- Liver biopsy
- Liver scan
- Liver ultrasound
- Angiography
How would you manage a patient with cirrhosis?
- Rest – depends upon stage & S&S
- Nutrition
- Skin care
- Reduce risks for injury
- Monitor for bleeding
- B complex, folate acid; ferrous sulfate
- Vitamins – especially K
- Avoid: alcohol, aspirin, NSAIDs, acetaminophen
- For ascites – Na+ restricted to 400-800 mg/day
-
If poor response to Na+ restriction
- Spironolactone (Aldoctone) spares K+ & Furosemide (Lasix) wastes K+
- May restrict protein initially
- Re-introduce protein; daily 1.2 gm/kg/day
- Small frequent meals - high carbohydrate, low Na+ & protein; bedtime snack
- Medications: lactulose (helps get rid of ammonia and fluid); oral antibiotics
- Discontinue sedatives, analgesics, tranquilizers
- Monitor for complications & infections.
What are some complications with cirrhosis?
- Upper GI bleed
- Infections
- Hypokalemia
- Azotemia
- Drug side effects
- Too high protein ingestion
- Constipation
What are some characteristics of variceal hemorrhage?
- 1/3 of persons with varicies
- 1st bleeding episode – mortality of 30-50%
- Manifestations:
- Hematemesis
- Melena
- Hypovolemic shock
- Avoid alcohol, aspirin, irritating foods
- Report chronic coughing & URIs for Rx
- Rx - endocsopic sclerotherapy or banding
How would you manage a patient with variceal hemorrhage?
- Needs intensive care setting
- Hemodynamic support
- Balloon tamponade
- NG tube & gastric decompression
- 02, IV fluids, electrolytes, volume expanders
- Blood; blood products
- Medications:
- Somatostatin (Octretide) – preferred, causes vasoconstriction of the splenic vessels
- Vasopressin
- Monitor:
- Hemodynamic function
- Patient condition; associated symptoms
- Treatments including tube care & GI suction
- Oral care; I & O
- Implement measures to reduce anxiety & agitation
- Quiet calm environment; reassurance
- Education & support – family & pt.
What are the clinical manifestations of a Hepatocellular Carcinoma?
- May be asymptomatic
- Abdominal pain
- Anorexia, weight loss
- Weakness/malaise
- Anemia
- Jaundice
- Enlarged; irregular liver
- Cirrhosis symptoms
- Hepatomegaly
- Abdominal bruits
- Ascites
- Splenomegaly
- Weight loss; muscle wasting
- Fever
- Chronic liver disease signs
What are some riskfactors for cholelithiasis?
-
High:
- Multiparous women > age 40
- Obesity
- Native Americans
- **Others: **
- Estrogen therapy
- Diabetes mellitus
- Cirrhosis, hemolysis
- Infections of biliary tract
- Rapid weight loss; frequent weight changes
What are the manifestations of a choleliathiasis (gall stones)? – uncomplicated
- Most asymptomatic
- If symptomatic:
- Pain following fatty meal – ½ hr. – 6 hrs.
- N/V; diaphoresis
- Not exacerbated by movement; squatting, bowel movements or passage of flatus
- Several attacks before seeking medical attention
- May have refered pain in the shoulder
What are they atypical syptoms of cholelithiasis?
- Chest pain
- Nonspecific abdominal pain
- Belching, fullness after meals; early satiety
- Abdominal distention/bloating
- Epigastric or retrosternal burning
- N/V without biliary colic
What are the manifestations of a complicated cholelithiasis
What causes cholecystitis?
Causes:
- With obstruction; without obstruction (acalculous cholecystitis)
- Bacterial –> ecoili
- Neoplasms
- Anesthesia
- Opioids
- Inflammation
- Extensive fibrotic tissue
-
-
What are the manifestations of choleystitis?
- Fatty food ingestion 1 hr. + before initial pain onset
- Nausea/vomiting; diaphoresis
- Fever, tachycardia
- RUQ abdominal tenderness
- Possible + Murphy’s sign
- Guarding; rebound
- Jaundice (25%)
- May resolve in 7-10 days without treatment
- Possible complications
What are some diagnostic tests done for choloecystitis?
- CBC; WBC with differential
- Liver function tests; total bilirubin
- Serum amylase – they want to rule out any pancreatitis
How would you manage a patient with cholelithiasis?
Diet - ↓ fat, ↑protein, ↑carbohyrates
Medical dissolution therapy
- Ursodeoxycholic acid (UDCA)
- Ursodiol (actigall)
- Chenodeoxycholic acid (CDCA or Chenix)
Other dissolving options:
- Methyl tertiary terbutyl ether (MTBE)
- Oral drugs - bile salts
Nonsurgical removal:
- Endoscopic sphincterotomy ( ERCP)
- Intracorporal – mechanical shock waves Extracorporal shock wave lithotripsy (ESWl)
Surgical removal:
What are some nursing interventios for patients with biliary disorders?
- Assess and manage pain
- Oral care – especially if N/V
- Interventions for pruritis
- Personal hygiene as needed
- Intake & output
- Monitor for hemorrhage
- Assess; monitor for infection
- Assess – signs of obstruction
What are some nursing interventions for post-op care with biliary disorders?
- Low Fowler’s position
- NG tube to suction; IV fluids; I & O
- NPO; then soft, low-fat, high carbohydrate diet
- Maintain skin integrity; assess & promote biliary drainage if T-tube in place.
- Analgesics for pain; assess pain relief
- Encourage coughing & deep breathing
- Progressive ambulation
- Monitor & evaluate potential complications
What causes acute pancreatits?
Major causes:
- Gallstone - ~45%
- Chronic alcohol abuse - ~30%
- Hyper-triglycerides – 3rd most common cause 1000mg/dl +
Other causes:
- Endoscopic retrograde cholangiopancreatography (ERCP)
- Trauma
- Postoperative
- Drugs
Sphincter of Oddi dysfunction
How is a patient diagnosed with acute pancreatitis?
Diagnostic criteria - ≥ 2 of the following:
- Typical abdominal pain
- Amylase/lipase > 3x UL
- Confirmatory findings on US/CT imaging
What are the clinical manifestations of acute pancreatitis?
- Onset - abrupt
- Pain
- Systemic: Fever, tachycardia, hypotension, pallor, diaphoresis, N&V, weakness
- Abdomen – tender, most often no guarding, rigidity or rebound; distention, no bowel sounds
- Anxious
- Looks acutely ill; may sit with trunk flexed & knees flexed
- N/V; diaphoresis; fever
- Hypotension; shock
- Abdominal wall discoloration – Gray Turner’s; Cullen’s sign
- Diminished or absent bowel sounds
- Dyspnea; hypoxia
- Jaundice
- Renal failure
- Confusion &/or agitation
What are some laboratory diagnostic tests for acute pancreatitis?
- CBC with differential;
- Electrolytes
- Ca++
- Lipids, BUN, Sr. Creatinine, LFTS
- Prothrombin; other coagulation tests
- Serum amylase (20-110 U/L)
- Serum lipase (0-160 U/L)
- Blood glucose
- Arterial Pa02 – hypoxemia
How would you manage a patient with acute pancreatitis?
- Fluid replacement; electrolytes – use calloids
- Frequent hemodynamic monitoring
- Analgesia with parenteral opioids
- Maintain/monitor urine output >0.5cc/kg/h
- Bedrest, NPO, frequent oral care; skin care
- I & O
- Position – for comfort & respiratory effort
- Manage & stabilize metabolic complications
- Monitor for possible complications
What kind of nutrition plan will a patient with acute pancreatitis be on?
- NPO – initially; begin PO intake when no pain, no N/V, + bowel sounds, pt. hungry
- Bland - small, frequent feedings – ↑ protein; ↑ carbohydrate, ↓fat – solid preferred if at all possible.
- Supplemental fat soluble vitamins; nutritional drinks
- Nasograstric feedings if unable to take PO
- No caffeine or alcohol
What are some medications used for acute pancreatitis?
- Analgesia – morphine, dilaudid
- Antibiotics – only with infections
- Others medications tried – H2 blockers, glucagon, antacids, have not proven to be effective
- PPIs may still prescribed to prevent stress ulcers
- Most recently, NSAIDs via the rectal route has been proven to be most beneficial following ERCP
What are the 2 types of chronic pancreatitis?
- Chronic obstructive pancreatitis
- Chronic calcifying pancreatitis/alcohol induced
What are the clinical manifestations of chronic pancreatitis?
- Two primary symptoms – abdominal pain & pancreatic insufficiency
- Abdominal pain
- Pancreatic insufficiency
- Malabsorption
- Pancreatic diabetes
How would you manage a patient with chronic pancreatitis?
- Prevent further attacks
- No alcohol!
- Pain relief
- Diet – bland, ↓ fat, ↑ carbohydrate; protein
- Endocrine insufficiency may result from islet cell destruction which leads to diabetes
- Periodic blood glucose assessments; insulin may be required
- Exocrine insufficiency typically manifests as weight loss and steatorrhea
- If steatorrhea present, a trypsinogen level < 10 is diagnostic for chronic pancreatitis
- Manage with low-fat diet and pancreatic enzyme supplements (Pancrease, Creon) with meals & with a PPI
What are the manifestations of a pseudocyst?
- Most asymptomatic
- Abdominal pain, duodenal or biliary obstruction
- Vascular occlusion or fistula formation
- Spontaneous infection with abscess formation
How would you manage a patient with a psuedocyst?
- If small – follow up one year until cyst becomes about 12 cms
- Drainage & stenting if indicated
What are some disorders of the anterior pituitary gland?
- Disorders
- Tumors are the most common cause of primary anterior pituitary disorders
- Usually benign
- Produce symptoms of hypersecretion of 1 or more hormones
- # 1 prolactin
- # 2 Growth hormone
- Growing mass can produce neuro symptoms from increased ICP
What are some disorders asssociated with the posterior pituitary gland?
- SIADH
- Diabetes insipidus
What are some clinical findings associated with pituitary tumors?
- Headache
- hemianopia
- loss of visual acuity
- blindness due to pressure exerted on the dura and optic chiasm
- Disorder of target organ (ie, cushing’s syndrome)
What is hypopituitarism?
- Is a partial or complete loss of the anterior lobe’s function.
- Affects the function of endocrine glands that are stimulated by anterior pituitary hormones.
- Can be deficit of one hormone or all
- Deficient in LH & FSH
What causes hypopituitarism (anterior pituitary)?
Primary:
- pituitary tumors
- inadequate blood supply to the pituitary
- infections or inflammatory diseases
- sarcoidosis or amyloidosis
- irradiation
- surgical removal of pituituary tissue
- Sheehan syndrome
- autoimmune disease
Secondary:
- tumors of the hypothalamus surgical damage to pituitary
- inflammatory diseases
- head injuries
What are the manifestations of a patient with hypopituitarism?
Manifests two ways:
- Hyposecretion of the target organ
- S/S of a growing pituitary tumor
•Headaches
•Visual changes (either peripheral or central vision)
- Anosmia
- Seizures
What is hyperpituitarism (anterior) and what causes it?
- An oversecretion generally of prolactin or growth hormone.
- Most commonly caused by a benign tumor such as adenoma
- In adults - begins between ages 30-50 which is after the end plates of the bones have closed.
- Bones become deformed rather than enlongated.
What is prolactin hypersecetion?
- Prolactin Hypersecretion - most common endocrine abnormality caused by hypothalamus- pituitary disorders.
- Most common cause are pituitary adenomas
- Prolactin - necessary for lactation.
- Causes: physiological, pathological, pharmacological
What are the signs and symptoms of prolactin hypersecretion?
- galactorrhea
- amenorrhea
- decreased libido
- erectile dysfunction
What is the treament for hyperpituitarism?
- Surgery - outcomes based on size of tumor & basal prolactin level.
- Medical tx
- Bromocriptine or Cabergoline- dopamine agonist that stimulates dopamine receptors and affects both the hypothalamus and pituitary levels. Works by inhibiting PRL secretion by tumor.
What is acromegaly?
- Occurs in pituitary gland produces excess growth hormone in the adult.
- Occurs after the epiphyseal plates have closed.
- First noticed in hands and feet (excessive growth of soft tissue)
- Gigantism in children
What are the signs and symptoms of acromegaly?
- Swelling of feet and hands
- Facial features coarse as bones grow
- increased perspiration
- protruding jaw
- voice deepens
- enlarged lips, nose, & tongue
- thickened ribs (barrel chest)
- joint pain
- Degenerative arthritis
- enlarged heart
- enlargement of other organs
- Peripheral neuropathies
- Proximal muscle weakness
- Snoring/ sleep apnea – because of the growth of the tounge
- fatigue & weakness
- headaches
- loss of vision
- irregular menstrual cycles
- breast milk production in women
- impotence in men
What are the long term effects of acromegaly?
- Joint pain - leads to crippling degenerative arthritis
- Heart enlarged and impaired - leads to failure
- Tissue compresses on nerves - pain, loss of visual fields
- Headaches
How would you treat acromegaly?
- Surgery to remove the tumor - hypophysectomy (1st line)
- Radiation
- Drug therapy- octreotide (Sandostatin) – reduces GH levels
- Given SC 3Xs weekly
- Diet - may dev. DM or carbohydrate intolerance
- CHF - salt restriction
What is SIADH and what does it result in?
- Occurs despite normal or low plasma osmolarity
- Results in fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine with normal renal function
What are the manifestations of SIADH?
- Decreased Na+ and Cl- levels
- Muscle cramping, pain, weakness, risk for seizures
- Na+ (< 120 mEq severe vomiting, abdominal cramps, muscle twitching seizures)
- Stimulation of thirst, DOE, fatigue
- Decreased urine output and weight gain
- Decreased plasma osmolality – can lead to cerebral edema –> increased ICP
- Diagnostic – sodium level, urine and serum osmolality, urine specific gravity (> 1.005)
What are the nursing interventions for patients iwth SIADH?
- Frequent vital signs, LOC
- Daily weights, assess heart & lungs
-
Assess S/S hyponatremia,
- Seizure precautions
- Position HOB flat or < 10degree elevation
- Frequent oral hygiene - because they are going to feel thirsty
- Maintain fluid restriction (800-1000ml per day), strict I & O
- If sodium is < 120, they will give a hypertonic fluid
What is diabetes insipidus and what causes it?
- DI is a syndrome of altered water balance in which ADH is deficient or there is a renal resistance to its effects.
-
Caused primarily by inadequate secretion of ADH.
- Neurogenic or central DI
- Nephrogenic or renal DI
What causes central DI?
linfections of meninges, head injury, surgery of the Hypothalamus- pituitary, amyloidosis, TB
What causes Nephrogenic DI?
Physiologic:
- familia, sarcoma, multiple myeloma, SCD, CF, electrolye disturbances such as hypercalcemia or hypokalemia
Drugs:
- aminoglycosides, foscarnet, lithium, amphotericin B, cisplatinum, demeclocycline (helps treat SIADH), rifampin
What are the signs and symptoms of DI?
What are some lab findings for DI?
Serum chemistry
- Increased serum osmolality > 295 mOsm/kg
- Increased serum sodium > 148 mEq/L
Urinalysis
- Decreased urine osmolality 50-100 mOsm/kg
- Decreased urine sodium > 20 mEq/L
- Specific gravity 1.005
- Urine volume - > 6 liters per day
How would you manage a patient with DI?
- Correct underlying cause
- Medications
- Desmopressin (DDAVP) intranasally.
- Aqueous vasopressin (Pitressin) SC or IM
- short acting agent (4-6 hours)
- Aqueous vasopressin (Pitressin) SC or IM
- Diabinese, tegretol can be tried
- Nephrogenic DI – low-sodium diet, thiazide diuretics, indomethacin
Describe fluid therapy for DI patients?
- Hypotonic saline such as 1/4 or 1/2 strength saline.
- Titrated to hourly uop.
- Titration may be 500 ml uop for 1 hour is replaced by 500 ml of IV fluid bolus the next hour.
What 3 hormones does the thyroid secrete?
- Thyroxine (T4) - regulate cell metabolism & energy production, influence growth & development, & affect cell differentiation in the fetus.
- Triiodothronine (T3)
- Calcitonin - increases calcium deposits in bones, decrease serum calcium levels.
What is hyperthyroidism and what causes it?
- An increased production and secretion of thyroid hormone from thyroid gland.
-
Causes:
- Grave’s disease (most common, 60-90%)
- Plummer’s disease (toxic multinodular goiter)
- Thyroiditis
What is grave’s disease
- Most common cause of hyperthyroidism
- Autoimmune disorder
- Affects women more than men
-
Characterized by:
- diffuse goiter
- hyperthyroidism
- infiltrative ophthalmopathy
- infiltrative dermaopathy
What is plummer’s disease?
- Presents with multiple nodules and a milder form of hyperthyroidism
- More common in persons over 40 yrs.
- Not autoimmune
What is thyroiditis and what causes it?
- inflammation of the thyroid gland.
- Can lead to release of excess amounts of thyroid hormones
*
What are some characteristics of hyperthyroidism?
- Increased metabolic rate, heat production, O2, peripheral vasodilation
- Altered CHO, protein, & fat metabolism
- Increased body temp., Intolerance to heat, Warm & moist skin, increased appetite, metabolic fatigue, weight loss, muscle weakness
-
Blood glucose elev, decreased triglycerides, and cholesterol, hepatic dysfunction, increased # of stools
- They will develop hyperglycemia
- Diarrhea
- Altered CV functioning - hypermetabolic and adrenergic state
- Increased myocardial oxygen consumption, shortened systolic interval, increased cardiac output
- Tachycardia, palpitations, increased blood pressure, dyspnea, angina, atrial fib, CHF
- Nervousness, restlessness, decreased attention span, insomnia, emotional lability
What are the clinical manifestations of hyperhyyroidism?
- Feeling nervous, irritable, & excitable
- Increase appetite with progressive weight loss
- Heat intolerance with frequent perspiration
- Exophthalmos (bulging eyes) from decreased venous drainage
- Enlarged thyroid or goiter
- Dyspnea
- Insomnia
- Amenorrhea
- Tachycardia (90-160 beats/min)
- Increase in systolic BP
What are the symptoms of thyrotoxicosis?
- nervousness, hyperexcitable, irritable, apprehensive
- Palpitations
- Heat intolerant - perspire freely
- skin flushed continuously
- fine tremor of hands
- startled facial expression (exophthalmos)
How can you diagnose a patient with hyperthyroidism?
- Decreased TSH levels (becuase the thyroid is producing too much)
- Elevated free T4 levels
- Radio active iodine to differentiate Graves disease from other forms of thyroiditis
How do you treat patients with hyperthyroidism?
-
Anti-thyroid drugs - Propulthiouracil (PTU) or methimazole.
- Usually will control problem within a few weeks.
- Radioactive iodine - most widely recommended permanent treatment of hyperthyroidism.
- Acts relatively quickly
- If they take this they will be on life long synthroid (DON’T TAKE VITAMINS WITH THIS DRUG)
- Surgical removal
- Symptom management - beta blockers
What are some nursing diagnoses associated with hyperthyroidism?
- Altered nutrition RT exaggerated metabolic rate, excessive appetite, & increased GI activity
- Avoid giving anything that can cause diarrhea
- Avoid caffiene
- Ineffective coping RT irritability, hyperexcitability
- Altered body temperature
- Disturbance in self-esteem RT to changes in appearance, excessive appetite, & weight loss
What is hypothyroidism and what causes it?
- A decrease in the secretion of thryoid hormone.
- May be caused by an interference with thyroid hormone production or a reduction in thyroid mass.
What is hashimoto’s thyroiditis?
- An autoimmune process where the thyroid enlarges and becomes inefficient in converting iodine into thyroid hormone and compensates by enlarging.
- TSH levels will be high
- T4 levels low
- Thyroid antibodies in 95% of patients
What are the signs and symptoms of hypothyroidism?
- Fatigue
- Weight gain
- Anorexia
- Intolerance to cold
- Constipation
- Dry skin & brittle nails
- Swollen eyelids
- Coarse, dry hair
- Decreased libido
- Memory loss
- Irritability
- Abnormal menstrual cycles
What are some nursing diagnoses associated with hypothyroidism?
- Activity intolerance RT fatigue & depressed cognitive process
- Altered body temperature
- Constipation RT depressed GI function
- Altered thought process RT depressed metabolism & altered CV and respiratory status
How would you diagnose hypothyroidism and how would you treat it?
- §Primary – Increased TSH level
- lDecreased free T4 level
- lIncreased cholesterol, LDL, triglycerides
- l
- §Levothyroxine (synthroid) = DOC
- lOlder patients – need to know their cardiac status
What is hyperparathyroidism and what causes it?
What are the signs and symptoms of hyperparathyroidism?
- muscle weakness
- Loss of appetite
- Fatigue
- Constipation
- Emotional disorders
- Shortened attention span
- Osteoporosis, fractures, kidney stones
How would you diagnose hyperparathyroidism?
- Bone x-rays
- Lab tests to measure calcium & parathyroid hormone levels
How would you treat hyperparathyroidism?
- 1st priority - control elevated calcium levels –> give bisphosphonates
- Removal of gland
- Low calcium diet
What is hypoparathyroidism?
- Characterized by too little parathyroid hormone production
- Leads to decreased levels of calcium (hypocalcemia) & increased levels of phosphorus (hyperphosphatemia)
- Very rare condition
- usually caused because of loss of active tissue following thyroid or parathyroid surgery.
What are the signs and symptoms associated with hypoparathyroidism?
Clinical signs 2nd to hypocalcemia
- neuromuscular excitability, irritability, & muscle cramping (tingling in hands, fingers, & around mouth; severe - tetany)
Other symptoms
- Nausea, vomiting, diarrhea, & abdominal cramping
- Acute - can cause tetany (tonic spasms in the upper and lower extremities accompanied by pain)
What is chovstek’s sign?
- Elicited by tapping the patient’s face lightly over the facial nerve.
- Facial muscle twitching indicates a positive finding.
- Indicates hypocalcemia & occurs with hypomagnesia
What is trousseau’s sign?
- Elicited by grasping the patient’s wrist or inflating the blood pressure cuff on the upper arm to constrict the circulation for a few minutes.
- Palmar flexion is a positive finding.
- Indicative of hypocalcemia & hypomagnesia
What are the treatments for hypoparathyroidism?
Treatment
- Replacement of Calcium & vitamin D
- Calcium supplementation of 1.5-3 g/day
- Vitamin D – preferred preparations (Calcatrol)
- Diet – high in Ca++
- lTofu, dark green vegetables, soybeans
- Acute tetany - calcium gluconate IVP
Describe the care for a hypophysectomy
- Transsphenoidal approach used
- avoids disturbing the cranium
- incision is performed in upper gum line
- Pre-operative care
- sinuses are cleansed and antibiotic spray applied
- Cortisol given to tolerate stress
- After gland removed - muscle graft from anterior thigh used to pack dura and prevent leakage of CSF.
- Nasal packing inserted after incision closed
- Mustache dressing applied
Describe post op care for hypothysectomy
Neurological assessment
- Assess for s/s of target gland deficiences
- •Diabetes insipidus (DI), Addison’s disease, hypothyroidism
- Avoid coughing, sneezing, or blowing nose - CSF leak
- •encourage deep breath instead
- Strict I & O
- Oral hygiene
- NO toothbrush for 2 weeks
- •provide oral rinses and dental floss
- Assess for meningitis (HA, Inc. temp, nuchal rigidity)
- After packing removed- observe for rhinorrhea
- Monitor nasal drip for glucose (> 30 mg/dL)
- Avoid bending at the waist
- Prevent constipation
- Elevate HOB (at least 30 degrees at all times)
- Teach patient he may have anosmia for 3-4 months
- Lifelong replacement of cortisol (if total) or vasopressin for DI.
How would you care a patient having a thyroidectomy pre op?
What are some nursing interventions post op for a patient with a thyroidectomy regarding ineffective breathing patterns?
- Assess respiratory status
- Observe for bleeding
- Record amount/type of wound drainage
- Monitor proper functioning of drains
- Monitor patient’s neck for enlarging mass
- Assess cough, swallowing, and aspiration
- Maintain tracheostomy tray readily available
What is acute thyrotoxicosis and what causes it?
It is severe manifestations of hyperthyroidism, with symptoms of:
- elevated temperature
- increased tachycardia
- onset of dysrhythmias
- worsening tremors
- worsening mental status
- Abdominal pain
- (Delirium)
Causes:
- Grave’s disease
- nonadherence to prescribed therapy
What is the primary focus with acute thyrotoxicosis?
The Primary focus is fever (ie, 105 F) & cardiovascular changes:
Maintain cardiac output:
- Monitor CV status q 1hr
- Report changes such as tachycardia, dysrhythmias, s/s of CHF linitially see atrial fibrillation
- Decrease cardiac workload by decreasing physical & emotional stressors.
Maintain normothermia:
- Monitor temperature q 1 hr.
- use external cooling devices.
- Maintain room temp in cool range.
- DO NOT give salicylates (aspirin). Only Tylenol.
What are some nursing interventions for acute thyrotoxicosis?
- Administer oral propylthiouracil (PTU) as ordered.
- Administer iodine preps as ordered - maybe IV or PO.
- Administer dexamethasone as ordered.
- Administer propranolol as ordered.
- Other supportive therapy: O2, cardiac glycosides, etc.
What is a myxedema coma, and what are some problems that develop because of it?
It is a severe form of hypothyroidism that leads to:
- Develop respiratory problems (usually cause of death)
- function impaired by large tongue and sleep apnea
- respiratory effort decreased by hypoxic & hypercapneic ventiatory drives and respiratory mm weakness.
- Develop cardiac problems
- cardiac output low because of bradycardia & low stroke volume; may develop CHF
- Treatment: supportive
- Administer L-thyroxine (thyroid hormone) IV
What hormones does the adrenal cortex secrete?
- glucocorticoids (cortisol)
- mineralcorticoids (aldosterone)
- sex steroid hormones
What hormones does the adrenal medulla secrete?
- NE
Epinephrine
What is addison’s disease and what causes it?
It is a disorder characterized by decreased:
- mineralocorticoids
- glucocorticoids
- androgen secretion
Autoimmune process responsible for 80% of all cases - results in atrophy of gland.
- 90% of adrenal cortex destroyed before see manifestations
- Most significant deficiencies are cortisol & aldosterone
What are some characteristics of addison’s disease?
- Clinically rare disease
- Seen in persons 30-50 years old
- More common in women
What are the manifestations of addison’s disease?
Hyperkalemia - K+ levels of more than 7 meq/L
- aldosterone deficiency affects the ability of the distal tubules of the nephrons to conserve Na+, therefore Na+ is lost, and K+ is retained.
- Leads to arrhythmias and possibly cardiac arrest.
Hypotension, decreased cardiac output, tachycardia, decreased heart size:
- Na+ & water excreted - leads to- dehydration - which leads to - hypotension
- Decreased heart size - microcardia diminished workload of heart. Can lead to circulatory collapse, shock and death.
Decrease in glucocorticoids:
- Metabolic disturbances - glucocorticoids have an “anti-insulin” effect.
- Gluconeogenesis - decreases with resultant hypoglycemia & liver glycogen deficiency.
- Client grows weak, exhausted, and suffers from anorexia, wt. Loss, and N/V
- Decreased resistance to stress
Increased ACTH leads to Increased MSH:
- stimulates the epidermal melanocytes - which- increases skin pigmentation and mucus membranes
- Have a tanned or bronze appearance
- Mood changes - delusional thinking, difficulty with stress, lethargic, apathetic, depressed, forgetful, emotionally labile
What are some nursing interventions for hypoaldosteronism?
- Vital signs frequently- monitor for
- hypotension, tachycardia, tachypnea
- Fluid volume deficit
- watch uop and report < 30cc/hr
- fluid replacement
How would you treat hypoaldosteronism?
cortisol replacement- life long replacement
- Fludrocortisone (Florinef) - mineralocorticoid
- promotes inc. reabsorption of Na+ and loss of K+, H2O, H+ from distal renal tubules
What would you teach a patient with hypoaldosteronism regarding their medications?
- Take daily glucocorticoid in divided doses (2/3 on awakening in AM & 1/3 late afternoon)
- take medication with snack or meal
- increase dose as directed for increased physical stress
- never skip a dose; if sick notify MD
- always wear Medic-Alert bracelet
- learn how to administer emergency IM injections of hydrocortiosone
What is Adrenocortical hyperfunction (Cushing syndrome & Cushing disease)?
- Cushing syndrome occurs from chronic over exposure to excess cortisol. ↓ feedback inhibition by cortisol on CRH & ACTH
secretion - Cushing disease occurs from over production of pituitary ACTH by a pituitary adenoma.
- Can also be caused by hyperaldosteronism
What are the effects of prolonged increases in Cortisol levels?
- ↓ feedback inhibition by cortisol on CRH & ACTH release which leads to low levels of ACTH which leads to adrenal cortex atrophy which leads to ↓ cortisol secriton
- Loss of diurnal variation in cortisol secretion
What are the clinical manifestations of Cushing syndrome/disease?
- Bone effects
- Weight gain
- Glucose intolerance
- Protein wasting
Describe the bone effects of cushing’s disease/syndrome
- ↑ bone resorption
- ↓ bone formation & ↓ Ca++ absorption (intestine)
- ↑ renal Ca++ excretion (hypercalciuria → kidney stones)
All of these factors contribute to osteoporosis
Describe the effects of cushing’s disease/syndrome on weight
Weight gain – fat deposition & transient Na+ & H2O
retention (from mineralcorticoid effects of high cortisol)
Facial (moon face)
Cervical (buffalo hump)
Truncal (central obesity)
Describe the glucose intolerance associated with cushing’s disease/syndrome
- Cortisol-induced insulin resistance
- ↑ gluconeogenesis & glycogen storage by liver
Describe the protein wasting associated with cushing’s disease/syndrome
Catabolic effects of high cortisol on peripheral tissues leads to muscle wasting
What are the complications associated with cushings disease/syndrome?
- ↑ cortisol → ↑ vascular sensitivity to catecholamines → vasoconstriction/↑ BP
- Metabolic syndrome (central obesity, hypertension, glucose intolerance, dyslipidemias)
- Infections from immune system suppression
- Altered mental status (irritability, depression, psychiatric disorders) from cortisol effects on hippocampal neurons
- Hyperglycemia, glycosuria, hypokalemia, metabolic alkalosis
Who is at risk for cushings disease / syndrome?
- Take glucocorticoids more often than once every other day
- Have been taking glucocorticoids for longer than 3 weeks.
- Use long acting meds. such as dexamethasone
- Take parenteral preps of steroids
- take doses above what is needed
- Take doses after 4 pm
How would you manage patients with cushing’s syndrome?
- Fluid restriction Intake & output
- Medications that interfere with ACTH production may be used for palliation.
- If cause is a pituitary adenoma
- use surgery (hypophysectomy) or radiation
- If adrenal adenoma or carcinoma
- adrenalectomy
What are some nursing interventions for patient’s with cushing syndrome?
- Decrease controllable stressors
- Monitor physiological coping ability
- Monitor VS q 2-4 h especially for HTN and Inc. HR
- Monitor blood sugars
Control fluid volume excess
- Restrict fluids as prescribed; distribute fluids over 24 h.; use ice chips to prevent thirst.
- Provide low sodium diet
- Provide K+ supplement as required.
- Monitor daily weight, I & O, daily labs (Na+, K+, pH).
Prevent falls & infection
- Temperature q 4h
- assess mouth, lungs, skin, GU tract for s/s infection
- Limit staff & visitors with s/s of URI
- preventive measures - TCDB, oral hygiene q 2h, etc
What causes Hyperaldosteronism?
- Adrenal tumor, excessive cortex stimulation (angiotensin II, ACTH, ↑ K+), mineralcorticoid excess, adrenal hyperplasia
- Primary (adrenal cortex)
- Secondary (extra-adrenal, e.g., ↑ renin release/activation of angiotensin II, diuretic use)
- continuous excessive secretion of aldosterone leads to higher levels of angiotensin II
- mechanical obstruction of renal vessels (renal stenosis)
- renin-secreting tumors
What are the manifestations of hyperaldosteronism?
- HTN, hypokalemia, Hypernatermia
- ↑ Na+,
- hypervolemia
- metabolic syndrome (HTN, obesity, dyslipidemia, hyperglycemia),
- metabolic alkalosis,
- ↑ urinary K+,
- No edema – Na+ excretion rate “reset”
What are the clinical signs and symptoms of hyperaldosteronism?
- headache
- fatigue
- muscle weakness
- nocturia
- loss of stamina
- Paresthesias may occur if K+ depletion
- Dysrhythmias
- Metabolic alkalosis (tetany)
How would you manage patient’s with hyperaldosteronism?
- surgery
- adrenalectomy which may be unilateral or bilateral
- Must get K+ in normal range
- –give K+ sparing agent (spironolactone)
- –drug is aldosterone antagonist to promote fluid balance
- Low sodium diet
- glucocorticoids replacement with surgery
What is pheochromocytoma?
Is a catecholamine-producing tumor that arises in chromaffin cells.
- Most common are unilateral & on right side.
- Must benign; 10% malignant.
- Accounts for 0.1% of HTN
- Women, 40-60
What effect does the tumor have with a patient with pheochromocytoma?
Tumor synthesizes epinephrine & norepinephrine. Excessive catecholamines stimulate alpha & beta receptors and can have a wide range of adverse effects.
- Tachycardia
- Peripheral vasodilation
- Bronchodilation
- Increased myocardial contractility
- Glycogenolysis
- Free fatty acid secretion
What are the clinical manifestations of pheochromocytoma and how would you diagnosis it?
Presents with:
- severe headaches
- palpitations
- profuse diaphoresis
- flushing
- apprehension or feeling of impending doom
- Pain in the chest N/V
Diagnosis: 24 hr urine collection of metanephrines -a byproduct of catecholamine metabolism – 95% pts. +
How would you manage patients with pheochromocytoma?
§Management
lSurgery is the treatment of choice. Postoperative care is like patient who undergoes an adrenalectomy.
•Short-acting alpha-adrenergic blocking drug used to control HTN during surgery
lPreoperative
- Goals: adequate tissue perfusion, nutritional needs, comfort
- Hypertension is the hallmark - take regular BP lying & sitting
–avoid smoking, caffeine, do not change position quickly-effect BP
–Alpha-adrenergic blocking drugs used to bring HTN under control before surgery
