Exam 2: 7-10 Flashcards
What are the clinical manifestations of fluid volume deficit
o Thirst
o Dry Mucous Membranes
o Weight loss
o Flattened neck veins
o Diminished skin turgor
o Prolonged cap refill (more than 3 seconds)
o Decreased urine output
o Increased heart rate
o Decreased blood pressure
o Altered LOC
Hypovolemia is known as what?
o Decreased vascular volume, i.e – fluid volume deficit
What is a common cause of Hypovolemia
o Excessive body fluid loss (ie. Hemorrhage, excessive sweating, etc)
o Reduction of fluid intake (ie. Dehydration)
o Excessive excretion
o Loss of fluid to third space (results in decrease extracellular fluid volume)
With decreased intravascular volume, what two things might be interrupted
o Blood circulation
o Transportation of oxygen and nutrients to tissues
What are some of the physiologic responses to counter the manifestations of hypovolemia?
o Decreased blood flow to kidneys triggers RAAS: increases sodium and water reabsorption w/ aldosterone release
o Decreased BP stimulates sympathetic nervous system to increase HR, constrict arteries, and increase contractility of heart
What are some nursing managements associated with fluid volume deficit
o Measure all fluids that enter / leave body (I/O)
o Check electrolyte, CBC, and urine-specific gravity
o Assess for hypotension and weak pulses
o Assess respiratory system and tissue perfusion
o Check orientation, vision, hearing, reflexes, muscle strength
o Perform daily weights
What lab testing can be done to help provide insight into fluid volume status and guide treatment strategies
o Hemoglobin - increase w/ hypovolemic
o Hematocrit - increase w/ hypovolemic
o BUN - elevated w/ hypovolemic
o Creatinine - elevated w/ hypovolemic
o Urine-specific gravity - elevated w/ dehydration
o Blood glucose
o Electrolyte panel
o Plasma proteins
What are the clinical manifestations of fluid volume excess (Hypervolemia)
o JVD
o Bounding pulses
o Edema
o Increased weight
o Increased blood pressure
What are some causes of Hypervolemia
o Heart Failure
o Cirrhosis of liver
o Kidney failure
o Excessive fluid replacement
What are some treatments for Hypervolemia
o Loop diuretics
o Limiting water intake
Sodium loss typically occurs how?
**o Vomiting and diarrhea **
o GI suctioning
o Inadequate salt intake (not common)
o Diuretics
What are the normal ranges for sodium?
135 - 145
What does Na+ help maintain
o Blood pressure,
o blood volume
o pH balance
Altered ____ function can lead to N&V, lethargy, confusion, seizures, and coma with hyponatremia
o Neuronal
Excessive intake of _ and loss of body _ are the primary causes of hypernatremia
Sodium
Water
What are some clinical manifestations of hyponatremia?
FROM FLUID SHIFTING OUT OF ECF AND INTO CELLS = SWELLING
* Headache
* Irritiability
* Difficulty concentrating
* Vomiting, confusion, seizure -> severe
* Tachycardia, thready pulse
* Postural hypotension
* Dry membranes
What is the function of sodium in the body
conduct nerve impulses,
maintain the proper balance of water and minerals
What electrolyte is the primary determinant of blood osmolality?
Sodium
What is the nursing management associated w/ Hyponatremia
o 24 I/O record
o Check Specific urine gravity, will be less than 1.010
o Assess for bounding pulses and bulging neck veins
o Assess for putting edema w/ fluid excess
o Monitor daily weights
o Assess for BP and respiratory changes
Where is potassium mostly found?
o In muscles –> total body K+ determined in large by body size & muscle mass
What is primary function of potassium?
Major factor in resting membrane potential of nerve and muscle cells
Imbalances affect neuromuscular and cardiac function
What are some possible causes of Hypokalemia
o Excessive fluid loss / electrolyte loss
o Severe vomiting or diarrhea
o Diet low in K+
o DKA
How does Aldosterone affect K+?
o Adds Na+, which means and loses K
High aldosterone means low k+
What are the normal ranges for Potassium?
3.5 - 5
What are some clinical manifestations of hypokalemia
HYPERPOLARIZATION AND IMPAIRED MUSCLE CONTRACTION
- Skeletal muscle weakness, parestheisias
- Severe: paralysis
- Shallow breathing, arrest -> weakened muscles
- Decreased GI motility -> constipation, paralytic ileus)
- Weak, irregular pulse
- Hyperglycemia
What function does calcium have in the body?
o Blood clotting
o Generation of action potentials
o Muscle contraction
What is the normal range of calcium?
8.5 - 10
What are some common clinical manifestations of Hypercalcemia?
Decreased neuromuscular excitiability caused by increased threshold
- Lethargy, weakness, fatigue
- Decreased memory
- Depressed DTR
- Increased BP
- Confusion
- Anorexia, N&V
- Bone pain, fx
- Polyuria, dehydration
What are some causes of Hypercalcemia
- Excessive bone breakdown
- Thyroid disorders
- Excessive intake of calcium
Magnesium has functions similar to what other electrolytes
- Ca+
What are some clinical manifestations of hypomagnesia
Confusion
Muscle cramps, tremors
Hyperactive DTR
Chvostek’s sign
Trousseau’s sign
Dysrythmias
SIMILAR TO Ca+
What are some common causes of hypomagensia
o Inadequate intake of Mg due to malnutrition
o Malabsorption syndromes
o Severe burns
o Alcoholism
o Diuretic use
Hypomagnesia occurs in associated with what two other electrolyte imbalances
o Hypokalemia
o Hypocalcemia
What is the normal range for magnesium?
1.5 - 2.5
Pharm options for fluid excess
Diuretic ->
o Loop diuretic
o Thiazide diuretics
o Potassium-sparing diuretics
What medication increases urine production and causes decreased sodium reabsorption (resulting in water loss)
o Diuretics
What type of diuretic am i:
Reduces the reabsorption of sodium in the ascending loop of henle
o Loop diuretic
What type of diuretic am I:
Prevents NaCl reabsorption in the **distal convoluted tubule **
o Thiazide
What type of diuretic am i:
Reduces sodium reabsorption in the **distal tubule and collecting duce **
o Potassium-sparing
What are some clinical manifestations of dehydration
o Decreased LOC
o Prolonged cap refill
o Dry mucous membranes
o Decreased / absent tears
o VS changes
o Depressed fontanel, sunken eyes
o Decreased or absent urine output
What electrolyte is affected by hypoparathyroidism
Calcium
Parathyroid glands are responsible for regulation of what
o Blood calcium
‘Think “PC” – Parathyroid Calcium
If parathyroid hormone low, what does this mean blood calcium levels will be
o Low (less than 8.5)
How does the negative feedback loop work w/ the parathyroid?
o When parathyroid (and calcium) is low, PTH will be stimulated to increase Ca
o Calcium levels will rise until reaches appropriate levels -> PTH production stops
“PTH” -> puts the calcium high
What are the clinical manifestations of hypoparathyroidism?
o Trousseau’s sign – blood pressure cuff
o Chvostek’s sign - smile
o Diarrhea
o Circumoral tingling
THOSE OF LOW CALCIUM
What are the causes of hypoparathyrodism
o Hypomagnesium (Mg + Ca are bff’s)
o Autoimmune -> body attacks parathyroid
o Thyroidectomy -> complete removal of thyroid
o Radiation – can damage parathyroids
“HATR”
What is the purpose of the sodium-potassium pump
o To transport K+ into cells and transport Na+ out -> Requires ATP energy
o Done to provide energy for cell and help remove acid from body
____ are substances that donate hydrogen ions
Acids
__ are substances that accept hydrogen ions
Bases
What is the clinical measurement of the acid to base ratio called?
pH
What are the three types of buffer systems?
o Plasma
o Respiratory
o Renal
Of the three buffer systems, which is the quickest to react
o Plasma -> reacts in seconds to hydrogen ion level
Which buffer system reacts in minutes to excrete C02
Respiratory
Of the three buffer system, which takes the longest to respond?
o Renal -> **reacts in hours to days **to produce, absorb, and excrete acids/bases/ions
What is the purpose of the buffer systems?
o Mix acids and bases to resist pH change
What is the normal range for pH?
o 7.35 – 7.45
What is the normal range for PaCO2?
o 35 – 45
What is the normal range of HC03?
22 - 28
What ABG is associated w/ respiratory?
PaCO2
** NOT LOOKED AT W/ METABOLIC **
What ABG is associated w/ metabolic?
HCO3
** NOT LOOK AT W/ RESPIRATORY **
In Metabolic acidosis, what do the ABGs look like
o pH less than 7.35
o HCO03 less than 22
What are contributing mechanisms of Metabolic Acidosis?
o Increased production of nonvolatile acids (fasting, ketoacidosis, lactic acidosis)
o Decreased secretion of acids by kidneys -> leads to renal failure
o Increased loss of bicarbonate (HC03) – caused by diarrhea and GI suction
o Increase in chloride
What are some of the clinical manifestations associated with Metabolic Acidosis
o Anorexia
o N&V
o Weakness, Lethargy
o Confusion
o Coma
o Vasodilation
o Decreased h/r
o Flushed skin
What are some contributing mechanisms of Metabolic Alkalosis?
o Decreased H+ ions
o Increased HCO3 ions
o Loss of Cl- ions
What do ABGs look like in Metabolic Alkalosis?
o pH above 7.45
o HCO3 above 28
What is the difference between benign and malignant tumors?
o Benign: non-cancerous, remain localized, *closely resemble tissue origin *
o Malignant: cancerous, invasive, proliferate rapidly, potential to spread, *do not resemble tissue origin *
What are carcinogens?
o Agents that interfere w/ molecular pathway and cause tumors to form in the body
What are the two types of carcinogens?
o Direct: cause modifications in DNA and cell function
o Indirect: induce immunosuppression or chronic inflammation
What are some substances that can cause or promote cellular mutations?
o Radiation: gamma rays, x-rays, UV rays
o Hormones
o Chemicals – asbestos, insecticides, etc.
o Tobacco
o Microbes – viral infections: HPV, hepatitis -> leads to neoplasia and can alter genes or proteins
Carcinogens: Hormones
o Can be cancer tx
o Removing organs or tissues that secrete specific hormones can directly kill tumor cells
o Tamoxifen – estrogen modulator, blocks action of estrogen & inhibits tumor growth (used in breast cancer)
What is the initiation-promotion-progression theory?
o Steps involved in the development of neoplasms
Step 1 in the initiation-promotion-progression theory is what?
o Initiation: exposure event of cells to a carcinogenic agent, causes a mutation of a cell
Step 2 in initiation-promotion-progression theory is what?
o Promotion: promoter agent activates oncogene -> Mutated cells expand, grow, and reproduce
Step 3 in initiation-promotion-progression theory is what?
Progression: independent growth occurs, considered cancerous at this step
What are some general manifestations of cancer?
o Lymphadenopathy: enlarged lymph nodes throughout the body
o Unexplained Fever- results from the release of pyrogens from cancer cells
o Anorexia & taste receptor changes - present within the inflammatory response caused by the presence of circulating chemical mediators
o Cachexia- a result of feelings of fullness when eating coupled with release of chemical mediators
o PAINLESS palpable mass
o Loss of tissue function (depending on location)
What are the three goals of cancer treatment?
o Eradicate the neoplasm
o Control the growth and spread
o Reduce symptoms w/ curing the cancer
What are the risk factors for colon cancer?
o Age: over 50 years of age
o Family history
o Smoking
o Alcohol use
o Bowel disease
o Obesity, inactivity
o High-fat diet
What are some common clinical manifestations of colon cancer?
o Change in bowel habits
o Occult or frank blood in stool (cancer in ascending colon)
o Abdominal pain
o Visible blood in stool (cancer in descending colon)
o Bowel obstruction (w/ descending and rectum cancer)
o Anemia – may be first clue
What are some clinical manifestations associated with lung cancer?
o Persistent cough
o Hemoptysis (bloody sputum)
o Chest pain
o SOB
What are the common causes of lung cancer?
o Result of environmental exposures to particular toxins (i.e, smoke) combined w/ genetic susceptibility
What are the stages of lung cancer?
o Stage 1: cancer located only in lungs, not spread to lymph nodes
o Stage 2: cancer in lungs and nearby lymph nodes
o Stage 3: cancer in lungs, lymph nodes, and middle of chest
o Stage 4: cancer in both lungs, fluid around the lungs, and/or other organs
Treatment for lung cancer depends on what?
Cancer type
o Small cell: chemotherapy
o Non-small cell: surgery if possible, radiation for local control
What are the diagnostic tests associated with colon cancer?
o CBC
o Liver function tests (common place for spreading)
o Serum carcinoembryonic antigen (SCA) -> protein, will be high with cancer
o Colonoscopy
o Sigmoidoscopy
o Bx of suspicious lesions
How often should patients get colonoscopies?
o Every 10 years beginning at age 50
What is the treatment with colon cancer?
o Surgical resection with localized tumors
o Drug combination of chemotherapy, biological agents, and radiation for unresectable, locally advanced, or metastatic disease
Brain cancer is commonly a result of what?
o Metastatic spread from another site
What are the clinical manifestations of brain cancer?
o Depend on size and location of tumor
o Neurologic deficits from tumor eroding functional neurons -> vision changes,
numbness, weakness, or paralysis
o Cognitive, behavioral, personality changes: irritability, forgetfulness, depression
o Pressure increases: headaches (later sign), vomiting
o Seizures from irritation and disorderly discharge of neurons
What are the common diagnostic tests for brain cancer?
o Complete neurologic examination -> testing cranial nerves, reflexes, sensory function, motor function
o Direct visualization: radiographs, CT, MRI, cerebral angiography
What are the diagnostic tests for acute leukemia?
o Patient history and physical exam
o CBC – will show blasts (immature wbc) greater than 20%
o Microscopic examination of blood
Acute lymphocytotic leukemia (ALL) is most commonly seen in who?
Children
Acute myeloid leukemia (AML) is most commonly seen in who?
Adults
What are some clinical manifestations of acute leukemia?
Sudden onset:
o Immaturity of WBC and other cells originating in bone marrow
o Growing of leukemic cells in bone marrow
o Infiltration of leukemic cells in the CNS, lymph nodes, liver and spleen
What is the difference between Hodgkin’s and Non-Hodgkin’s Lymphoma?
Hodgkin’s has “Reed-Sternberg” cells, when they are not present it is classified as Non-Hodgkin’s
What are some clinical manifestations of Hodgkin’s Lymphoma?
**o Presentation of non-tender enlarged lymph node or group of nodes in neck **
o Low grade fever
o Fatigue
o Weight loss
o Pruritus
o Drenching night sweats
o *Mass @ mediastinum that is greater than 1/3 of chest diameter *
o Possible: enlarged spleen and liver
What are some diagnostic tests associated with Hodgkin’s Lymphoma?
o Patient hx, physical exam, lab studies
o Thoracic and abdominal studies
o **MOST SIGNIFICANT FEATURE: presence of Reed-Sternberg cells **
How is Hodgkin’s Lymphoma staged?
With Ann Arbor classification
o Stage 1: **single lymph node area **single extranodal site (ie. Spleen, pharyngeal lymphatic ring)
o Stage 2: **2 or more lymph node areas **on the **same side **of diaphragm
o Stage 3: lymph nodes on both side of diaphragm
o Stage 4: disseminated or **multiple involvement of the extranodal organs **
What are some clinical manifestations of Non-Hodgkin’s lymphoma?
o Painless and slowly progressive enlargement of lymph nodes (same as HL)
o Systemic: fever, night sweats, weight loss, increased risk for infection,
o *Paraneoplastic syndromes (group of disorders trigged by abnormal immune response -> peripheral neuropathy, MG *
What are the diagnostic tests associated w/ Non-Hodgkin’s Lymphoma?
**o Lymph node biopsy **
o Chest and abdominal CT scan -> visualize tumor and location
o CSF fluid can be positive for metastasis with aggressive NHL
What am i:
Liver disease characterized by interference of local blood flow and hepatocyte damage
Cirrhosis
What is the most common complication of cirrhosis?
o Ascites – accumulation of fluid in the peritoneal cavity
What are some clinical manifestations of cirrhosis?
o Moderate to severe abdominal discomfort
o Increase abdominal girth
o Increased weight
o Severe sodium retention
o Renal failure (oliguria and increase creatinine)
What is the diagnostic criteria for cirrhosis?
o Liver, renal, and cardiac function – determines systemic damage
o Physical exam and changes in body weight – to diagnose ascites
o Measurement of abdominal girth circumference
Why does cirrhosis result in ascites?
o Blood flow is slowed thru liver -> increases pressure in vein that brings blood to liver from intestines and spleen (portal vein)
o Increased pressure causes fluid to accumulate in legs and abdomen
What are some treatments for cirrhosis?
o Diuretics to promote fluid loss, balance Na
o Paracentesis: removal of ascitic fluid via cannula
What is Hydrocephalus?
o Fluid buildup in the ventricles deep within the brain
What causes Hydrocephalus?
o an imbalance between the amount of fluid produced and the rate of fluid reabsorption
o accumulation of CSF leads to ventricular enlargement and increased ICP.
How is hydrocephalus classified when CSF flow is obstructed?
o Noncommunicating
How is hydrocephalus classified when CSF absorption is impaired?
o Communicating
What are some causes of hydrocephalus?
o Intraventricular hemorrhage
o Neural tube defect (i.e, spina bifida)
o Meningitis
o TBI
o CSF flow obstruction
o Impaired CSF absorption
What are some clinical manifestations of hydrocephalus in infants?
o Enlarged head w/ bulging fontanels
o Scalp vein distention
o Difficulty feeding
**o High, shrill cry **
What are some clinical manifestations of hydrocephalus in older children / adults?
o Impaired motor and cognitive function
o Incontinence
o Death can result due to increased ICP
What are some diagnostic criteria for hydrocephalus?
o Head circumference measurement
o **Transillumination: shining light against head to see accumulation of fluid in tissue **
o Imaging studies: Ultrasound, CT, MRI, skull radiograph to see separation of skull bones
What is a pressure injury and how does it differ from an ischemic neuronal injury?
o Pressure injury occurs from increased CSF volume -> i.e, tumor, inflammation
o Ischemic injury is from inadequate perfusion to neurologic tissue, resulting in impaired oxygenation (i.e, stroke)
What type of injuries lead to coup/countercoup?
o Head trauma from a blunt force injury (when head strikes a hard surface from front and bounces back -> damage to both sides
Clinical manifestations of C1-C2 injuries
o Loss of involuntary function -> sweating, BP regulation, body temp regulation
o Requires respiratory support
o Above C4 may require respiratory support- ventilator
Clinical manifestations of C7-T1 injuries
o can straighten arms, may not have fine motor control
o Paraplegia usually results from injuries at the thoracic level
o Trunk and lower body control are lost at T1 (returns @ T9)
What clinical manifestations are present at T9-T12 injuries?
o return of sitting balance and abdominal muscle control
Quadriplegia occurs with injuries within what range of the spine?
paralysis of all four limbs;
o C1-C7/T1
Paraplegia occurs with injuries within what range of the spine?
paralysis of the legs and lower body
o injuries from the thoracic level -> T1-T12
When there is damage to the lumbar and sacral segments of the spine, what clinical manifestations can be present?
o loss of control of lower extremities -> bowel, bladder, sexual function may be affected
What is the cause of renal tubulopathy w/ maternal hydramnios?
o Excessive amniotic fluid because of increased fetal urine output -> Can complicate fetal life in first 28 days of life:
- increased urine output
- hypercalciuria (calcium in urine) leads to electrolyte imbalance
What are clinical manifestations of renal tubulopathy w/ maternal hydramnios?
o Fever
o Vomiting
o Diarrhea
o Metabolic alkalosis - associated with contracted extracellular fluid because of sodium chloride loss
What is the pathophysiology of cerebral palsy?
o Exact cause is not known, but central control of movement is altered
- Cerebral anoxia (interruption of o2 to brain), hemorrhage, or other neurologic insults
What is cerebral palsy?
o Group of disorders that result from damage to upper motor neurons (responsible for carrying out electrical impulses -> initiate and modulate movement)
o Stems from event that occurs in prenatal, perinatal, or post-natal period
o Symptoms appear during first few years of life
What are some clinical manifestations of cerebral palsy?
Delay in reaching milestones:
o Reaching for toy: 3-4 months
o Sitting: 6-7 months
o Walking: 10 to 14 months
o Development of seizures
o Impairments in motor dysfunction during physical activity (i.e, running)
o Trouble w/ fine motor skills, coordination w/ balance and walking
How is cerebral palsy classified?
o Based on type of motor dysfunction or by anatomy affected
What are some of the motor dysfunction classifications of cerebral palsy?
Spastic: inability of muscles to relax
o Hemiplegia: one arm and one leg on same side of body is involved
o Diplegia: both legs involved
o Quadriplegia: involving all 4 extremities, trunk, and neck muscles
o Athetoid / Dyskinetic: inability to control muscle movement
o Ataxic: inability to control balance or coordination
What are some diagnostic criteria for cerebral palsy?
o Apgar score of less than 7 at 5 minutes after birth (measures h/r, respiratory effort, color, reflexes, muscle tone)
o Metabolic acidosis – determined from analysis of umbilical cord
o Evidence of cerebral hypoxic-ischemic injury via MRI
o Organ system failure (renal, liver, cardiac, GI) due to hypoxic-ischemic encephalopathy (alteration of brain function)
What are some treatments for Cerebral Palsy?
o No cure
o Botox can be used to help loosen muscle
o Anti-seizure meds
o PT, OT, Braces
What are some clinical manifestations of Parkinson’s Disease?
TRAP!
o Tremors
o Rigidity (cog-well)
o Akinesia / Bradykinesia -> slowed / lack of movement
o Postural instability
What are some pharmacologic options for Parkinson’s disease?
o Levodopa-Carbidopa
o Entacapone + Levodopa-Carbidopa
o Amantadine alone or in combo w/ anticholinergic
o Dopamine agonists
Pharmacologic options for Parkinson’s disease: Levodopa-Carbidopa
Levodopa replaces dopamine, Carbidopa delays conversion of Levodopa until crosses BBB
Prolonged use = lose effectiveness. Higher doses needed, has more S/E
Pharmacologic options for Parkinson’s disease: Entacapone + Levodopa-Carbidopa
extends duration of action of Levodopa
Pharmacologic options for Parkinson’s disease: Amantadine alone or in combo w/ anticholinergic
can help reduce PD symptoms and decrease dyskinesia from Levodopa use
- should be reserved for younger due to anticholinergic effects (dry mouth, blurred vision, urinary retention)
Dopamine agonists
bromocriptine, pramipexole, rotigotine, ropinorole
activate DA receptors
What is the pathophysiology of MS?
Recurrent bouts of CNS inflammation results in damage to both the myelin sheath and axons -> slows nerve conduction impulses down the axon
What are some clinical manifestations of MS?
Specific nerves are affected at different times, contributing to variations seen in the course, s/s of disease
- Unilateral vision loss, cognitive loss, bladder dysfunction, gait and balance alterations, spasticity, paresthesia, slurred speech, fatigue, pain
- Presentation of signs/symptoms can depend on which pattern pt has
A MS exacerbation can be defined as what?
Demyelinating event of at 24 hrs with **NO fever or infection **
What are the 4 patterns of MS?
1.CIS: initial presentation of symptoms
- Relapse-remitting: periods of acute neurologic symptoms alternating w/ periods of symptom relief / return of neurologic function
- Primary progressive: slow, chronic deterioration of neurologic function -> not associated w/ exacerbations or remissions
- Secondary progressive: initial presentation of R/R (has exacerbations and remissions) followed by a pattern of slow, chronic deterioration as seen in PP
What are some diagnostic criteria of MS?
o Presence of s/s consistent with disease
o Complete medical history assessment and thorough neuro exam
o MRI to detect scarring or plaques in CNS
o CNS response to peripheral sensory stimuli **(evoked potentials test) **-> can indicate abnormal nervous system function
o Lumbar puncture – evaluate CSF for presence of IgG
