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Med Surg III - 2320 > Exam II > Flashcards

Exam II Flashcards

1
Q

A(n) _____ injury is caused by an external force contacting the head, suddenly placing the head in motion

A

Acceleration

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2
Q

A(n) _____ injury occurs when the moving head is suddenly stopped or hits a stationary object

A

Deceleration

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3
Q

A _____ brain injury is confined to a specific area of the brain and causes localized damage.

A

Focal

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4
Q

_____ injuries are characterized by damage throughout many areas of the brain.

A

Diffuse

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5
Q

Which type of brain injury is detected with CT scan or MRI?

A

Focal brain injury

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6
Q

Which type of brain injury may not initially be detectable by CT scan?

A

Diffuse

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7
Q

What type of skull fracture is associated with open dramatic brain injury?

A
  • linear
  • depressed
  • open
  • comminuted
  • basilar
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8
Q

With this type of fracture a simple, clean break in which the impacted area of the bone bends inward and the area around it bends outward.

A

Linear

This is the most common type of skull fracture

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9
Q

With this type of skull fracture in the bone is pressed inward into the brain tissue to at least the thickness of the skull

A

Depressed fracture

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10
Q

This type of skull fracture involves fragmented bone with depression into brain tissue

A

Comminuted

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11
Q

With this type of skull fracture the scalp and dura are lacerated, creating a direct opening to the brain tissue

A

Open fracture

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12
Q

This type of skull fracture occurs at the base of the skull, usually extending into the anterior, middle, or posterior fossa, and can result in cerebrospinal fluid leakage from the nose or ears

A

Basilar

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13
Q

A central nervous system infection can occur when this problem presents as a result of a skull fracture

A

Cerebrospinal fluid leakage

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14
Q

This type of skull fracture presents an increased risk for hemorrhage caused by damage to the internal carotid artery. It can also cause damage to cranial nerves I, II, VII, and VIII

A

Basilar

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15
Q

Contusion is a bruising of the brain tissue and is most commonly found at the site of impact which is called ?

A

Coup

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16
Q

A contusion is a bruising of the brain tissue and is most on only caused at the site of impact, called the _____ while the site opposite impact is called _____?

A
  • Coup
  • Contrecoup

Most common at the base of the frontal and temporal lobes

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17
Q

This type of injury is usually related to high-speed acceleration/deceleration, is typically seen in motor vehicle crashes. It causes shearing of marginal fibers and stretching of blood vessels in many areas of the brain

A

Diffuse Axonal Injury (DAI)

Can cause bleeding and biochemical cascade of toxic substances into the brain after the initial injury

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18
Q

What are the most prominent manifestations of DAI?

A
  • Cognitive impairment
  • Disorganization
  • impaired memory
  • inattentiveness
  • coma
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19
Q

How is the severity of TBI determined?

A
  • Glasgow Coma Scale
  • CT
  • MRI
  • presentation of symptoms
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20
Q

Mild traumatic brain injury is also called _____

A

Concussion

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21
Q

What are the characteristics of mild traumatic brain injury/concussion?

A
  • a blow to the head, transient confusion or feeling dazed/disoriented and one of the following:
  • loss of consciousness for up to 30 minutes
  • loss of memory for events immediately before or after accident
  • focal neurologic deficits
  • No evidence of brain damage on CT or MRI
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22
Q

What are the characteristics of moderate traumatic brain injury?

A
  • loss of consciousness for 30 minutes to six hours
  • GCS 9 to 12
  • amnesia that may last up to 24 hours

Often hospitalization to monitor for edema, bleeding, or in adequate perfusion is necessary

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23
Q

What are the characteristics of severe traumatic brain injury?

A
  • loss of consciousness for greater than six hours
  • GCS 3 to 8
  • focal and diffuse damage to the brain, cerbrovascular vessels/ventricals

Requires critical care monitoring of hemodynamics, neurological status, and intracranial pressure. There is a high risk for secondary brain injury from cerebral edema, hemorrhage, reduce perfusion, and biomolecular cascade

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24
Q

What is the normal level for intracranial pressure ?

A

10-15 mm Hg

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25
Q

How does the nurse manage cerebral edema?

A
  • Provide oxygen
  • Keep systolic BP within therapeutic range
  • Balance fluid intake and output
  • Balance fluid and electrolytes
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26
Q

This type of edema has abnormal permeability of cerebra vessels and plasma leaks out into the extracellular space and collects in white matter.

A

Vasogenic Edema

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27
Q

This type of edema occurs as a result of a hypoxic event. The brain no longer receives oxygen and starts to use anaerobic metabolism. This can also lead to vasogenic edema

A

Cytotoxic Edema

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28
Q

This type of edema creates fluid accumulation between the cells and is associated with increased BP or ICP

A

Interstitial Edema

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29
Q

What are the three major types of hemorrhage(Hematoma) that present after TBI?

A
  • Epidural
  • Subdural
  • Intracerebral
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30
Q

This type of hematoma results from arterial bleeding into the space between the dura and the inner skull and is often caused by a fracture of the temporal bone.

A

Epidural hematoma

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31
Q

This type of hematoma results from venous bleeding into the space beneath the skull and dura but above the arachnoid and most often is caused by tearing of the bridging veins or laceration of brain tissue.

A

Subdural Hematoma

This hematoma bleeds more slowly than an epidural hematoma

Either acute, subacute or chronic

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32
Q

This type of subdural hematoma presents within 48 hours of impact

A

Acute Subdural Hematoma

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33
Q

Type type of subdural hematoma presents within 48 hours to 2 weeks of impact

A

Subacute Subdural Hematoma

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34
Q

This type of subdural hematoma presents from 2 weeks to several months after injury

A

Chronic Subdural Hematoma

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35
Q

This type of hemorrhage is the accumulation of blood within the brain tissue caused by tearing of small arteries and veins in the subcortical white matter

A

Intracerebral hemorrhage

Can produce ICP and edema

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36
Q

This is an abnormal increase in CSF.

A

Hydrocephalus

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37
Q

What are the two types of brain herniation?

A

Uncal and Central

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38
Q

This type of brain herniation is caused by the shift of one or both of the temporal lobes and is life threatening

A

Uncal herniation

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39
Q

This type of brain herniation is caused by a downward shift of the brainstem and the diencephalon from a surpatentorial lesion

A

Central herniation

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40
Q

What are the signs and symptoms of Uncal herniation?

A
  • Ptosis (drooping eye lids)
  • Dilated and non-reactive pupils
  • Rapid and deteriorating LOC
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41
Q

What are the signs and symptoms of Central herniation?

A
  • Cheyne-Stokes respirations
  • Pinpoint and non-reactive pupils
  • Hemodynamic instability
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42
Q

What is Cushing’s Triad?

A

Classic but late sign of ICP:

  • Manifested by severe HTN
  • Widened pulse pressure (increased difference between diastolic and systolic)
  • Bradycardia

Typically indicates imminent death

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43
Q

What type of patient history should be collected with TBI?

A
  • When, where, how injury occurred
  • Loss of consciousness, how long?
  • Change in LOC since injury?
  • Any seizure activity?
  • Which is dominant hand?
  • Any eye disease or injuries?
  • Allergies?
  • Drug or alcohol use?
  • Violence in the home?
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44
Q

What are the clinical manifestations of TBI?

A
  • increased ICP
  • Hypotension
  • Hypoxemia
  • Hypercarbia

Subtle changes in BP, LOC and pupillary response to light can help determine neurologic deterioration

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45
Q

What are the priority nursing interventions in the ED with TBI patient?

A
  • Assess ABCs (airway, breathing circulation)
  • Spine precautions
  • Assess sensory perception
  • Glascow coma scale assessment
  • Vitals (Cushing’s Triad)
  • Pupil response
  • Motor responses (decerebrate, decorticate, flaccid)
  • CSF leak
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46
Q

What are spinal precautions?

A
  • Bedrest
  • No neck flexion with pillow or neck roll
  • No thoracic or lumbar flexion with HOB elevation
  • Manual control of cervical spine when collar is off
  • Log roll for positioning
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47
Q

Which two manifestations suggest hypovolemic shock with TBI patients?

A
  • Hypotension
  • Tachycardia
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48
Q

What are the late signs of ICP?

A
  • Nausea/Vomiting
  • Severe headache
  • Seizures
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49
Q

What is the abnormal body posturing that involves the arms and legs being held straight out, the toes pointed downward, and the head and neck being arched backward?

A

Decerebrate posture

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50
Q

What is the abnormal body posturing in which a person is stiff with bend arms, clenched fists, and legs held out straight. The arms are bent toward the body and the wrists and fingers are bent and held to the chest?

A

Decorticate posture

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51
Q

Bruising behind the ear or lower jaw is called _____?

A

Battle sign or Mastoid Ecchymosis

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52
Q

This type of fever presents with an absence of sweating and no diurnal (night and day variation). The fever is high and lasts several days to weeks and responds better to cooling measures than antipyretics.

A

Central fever

Caused by hypothalamic damage

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53
Q

What is therapeutic hypothermia and why is it used?

A

Rapidly cooling the patient’s core temperature between 89.6 and 93.2 for 24-48 hours after injury

This reduces brain metabolism and prevents the cascade of molecular and biochemical events that contribute to secondary brain injury in moderate to severe TBI

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54
Q

What are the four prerequisites of brain death?

A
  • Coma
  • Normal/Near normal core body temp
  • Normal systolic BP (>=100 mm hg)
  • At least one neurologic exam
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55
Q

What are the pharmacological interventions for TBI?

A
  • Mannitol (Osmitrol): osmotic diuretic for cerebral edema; most effective as bolus; Use filter
  • Furosemide (Lasix): loop diuretic, reduces rebound from Mannitol and also enhances Mannitol by reducing edema, blood volume and sodium uptake
  • Propofol (Diprivan): sedative - manage agitation
  • Morphine/Fentanyl: Opioids - agitation from pain; naloxone for reversal; Fentanyl has fewer effects on BP
  • Phenytoin (Dilantin): Antiepileptic - prevent seizures

** Dethamethasone (decadron) & Methylprednisolone: glucocorticoids - No benefit!

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56
Q

Which drugs are used to induce barbiturate coma?

A

pentobarbital (Nembutal, Novapentobarb): mechanical vent required complications include: decreased GI motility, Cardiac dysrhythmias from hypokalemia, hypotension, fluctuation in body temperature

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57
Q

What are the surgical interventions for TBI?

A
  • ICP management devices: keyhole craniotomy - inserted through a burr hole
  • Decompressive craniotomy: removal of a section of the skull
  • Craniotomy: skull opening immediately followed by closing
  • Evacuation of epidural or subdural hematoma

side lying restrictions and protective care

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58
Q

What is the discharge teaching for TBI?

A
  • assess family dynamics/coping strategies
  • Assess for patient care needs (24 hr care?)
  • Discuss memory and personality changes
  • Discuss support groups and respite care
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59
Q

_____ is a progressive, permanent change in cognition

A

Dementia

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60
Q

_____ is reversible change in cognition with treatment

A

Delerium

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61
Q

What are the risk factors for cognitive impairment?

A
  • advanced age
  • behaviors (substance abuse, poor decisions)
  • environmental exposure (lead, toxins)
  • congenital/genetic (FAS, Downs)
  • health related
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62
Q

Which diagnostic test is done to detect infarcts (vascular dementia)?

A

MRI PET

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63
Q

What is the function of the liver?

A

Clears toxins from the body

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64
Q

What is cirrhosis?

A

extensive, irreversible scarring of the liver

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65
Q

What are the most common causes of cirrhosis?

A
  • chronic alcoholism (Laennec’s)
  • chronic viral hepatitis (post necrotic cirrhosis)
  • nonalcoholic steatohepatitis (NASH); fatty liver
  • bile duct disease (biliary cirrhosis)
  • genetic diseases (biliary cirrhosis)
66
Q

With this type of cirrhosis the liver is scarred but can still perform essential functions without causing major symptoms

A

Compensated cirrhosis

67
Q

With this type of cirrhosis the liver function is impaired with obvious manifestations of liver failure

A

decompensated

68
Q

What are the complications of cirrhosis?

A
  • portal hypertension (increased pressure in portal vein)
  • ascites (3rd spacing)
  • esophageal varices (thin veins in esophagus)
  • coagulation defects
  • jaundice (bilirubin build up)
  • portal systemic encephalopathy (PSE) (build up of ammonia)
  • splenomegaly (enlarged spleen)
  • destroys platelets, risk for thrombocytopenia
69
Q

In this stage of PSE the patient is unresponsive, has a positive Babinski reflex, and significant ammonia build up, muscle rigidity, seizures

A

Stage 4 (non-reversible)

70
Q

In this stage of SPE the patient is disoriented to time/place/person and has asterixis (hand flapping)

A

Stage 2 (reversible)

71
Q

In this stage of SPE the patient is confused; is stuporous but arousable; has muscle twitching; hyperreflexia; and asterixis (hand flapping)

A

Stage 3 (non reversible)

72
Q

In this stage of SPE the patient has personality changes; behavioral changes (belligerent, agitated); unable to concentrate; emotional labile (euphoria, depression); fatigued; slurred/slow speech; disturbed sleep patterns

A

Stage 1 (reversible)

73
Q

What are the risks for cirrhosis and liver failure?

A
  • Hepatitis C (2nd leading cause)
  • Hepatitis B & D (combined)
  • Nonalcoholic Fatty Liver disease
  • Alcohol abuse
74
Q

How much alcohol does it take to cause cirrhosis?

A

Women: 2-3 drinks per day over minimum 10 years Men: 6 drinks per day over minimum 10 years

75
Q

What are we assessing for to determine liver disease?

A
  • Petechiae (red dots present on face/chest)
  • Ecchymosis (bruising from impaired clotting)
  • Spider angiomas (nose, cheeks, upper thorax, shoulders)
  • Ascites/Abdominal girth (daily weight/measurement)
  • Jaundice (yellowing of skin, bilirubin build up) - Fector hepaticus (fruity breath)
  • Palmar erythema (warm, bright red palms of hands)
  • Dry skin
  • Rashes
  • Vitamin deficiency (fat soluble - A, D, E, K)
76
Q

What are the expected lab results for cirrhosis/liver disease?

A

Increased: ALT, AST, LDH, Alkaline phosphatase, bilirubin, ammonia

Prolonged: Pr/INR

Decreased: Protein, albumin, platelets, RBC, WBC

77
Q

What are the diagnostic tests for cirrhosis/liver disease?

A
  • xray
  • MRI
  • ultrasound
  • biopsies
  • EGD (exploratory scope)
78
Q

What type of diet is given to a patient with ascites?

A

Low sodium

Requires Thiamine, Folate & Multivitamin supplements given via IV (Liver cannot store vitamins)

79
Q

What type of diet is given to a patient with cirrhosis?

A
  • High carb
  • High protein
  • Moderate fat
80
Q

What are the treatments for managing hemorrhage?

A
  • Inderal: Beta blocker to control BP, for prevention
  • Vassopressin & Octreotide acetate: vasoconstrics
  • Banding of esophageal varices
  • Sengstaken-Blakemore tube
  • Transjugular intrahepatic portal systemic shunt (TIPS)
81
Q

What are the complications when using a Sengstaken-Blakemore tube?

A
  • Aspiration
  • Asphyxia
  • Perforation
82
Q

What is the purpose for giving Neomycin, Flagyl or Vanco to a patient with liver disease?

A
  • They are intestinal antisceptics
  • They diminish protein breakdown
  • They decrease rate of ammonia production
83
Q

Why is vasopressin given to patients with liver disease?

A
  • Vasoconstrictor

Helps control hemmhorage

84
Q

Why is octreotide acetate given to patients with liver disease?

A

Suppresses secretions

85
Q

Why is aldactone given to patients with liver disease?

A

Diuretic used for ascites; helps maintain sodium and potassium balance

86
Q

Why is thiamine given to patients with liver disease?

A
  • Helps with sodium replacement with ascites
  • Helps with alcohol withdrawal
87
Q

Why is lactulose given to patients with liver disease?

A
  • It is a syrup given orally that helps reduce ammonia in the body.
  • Often used with hepatic encephalopathy
  • Monitor for hypokalemia and dehydration
88
Q

What are the two types of temporary pacers?

A
  • Transcutaneous: Outside the body with externally applied electrodes
  • Transvenous: Electrodes/Leads are threaded through the subclavian or femoral vein into the right atrium
89
Q

What is the function of temporary pacers?

A

Stimulate ventricular depolarization (contraction)

90
Q

What does a P wave on an EKG strip represent?

A

Atrial depolarization (contraction)

91
Q

What does a QRS complex represent on an EKG strip?

A

Ventricular depolarization

92
Q

What does a T wave represent on an EKG strip?

A

Full ventricular repolarization

93
Q

What are the important assessments to make on an EKG strip?

A
  • Determine heart rate: normal/abnormal
  • Determine rhythm: regular/irregular
  • Analyze P waves: Present?
  • Measure QRS: Consistent?
  • Analyze T wave: Present?
94
Q

What are the causes of Atrial irritability?

A
  • Stress
  • Fatigue
  • Anxiety
  • Inflammation
  • Infection
  • Caffeine, nicotine, alcohol
  • Drugs such as epinephrine, amphetamines, Digitalis, anesthetics
  • Electrolyte imbalance
95
Q

What are the signs and symptoms of atrial irritability, which causes premature atrial complexes?

A

Palpitations (not always present)

96
Q

What are the interventions for premature atrial complexes?

A

none, treat palpitations, or if they are frequent and lead to other dysrhythmias antidysrhythmics may be used

97
Q

What are the signs and symptoms of sustained ventricular response (Supraventricular Tachycardia 100-280 bpm)?

A
  • palpitations
  • chest pain
  • weakness
  • fatigue
  • SOB
  • nervousness
  • anxiety
  • hypotension
  • syncope
98
Q

What is the preferred treatment for supraventricular tachycardia?

A
  • Cardioversion: emergency situations (with mild sedative)
  • Adenosene: emergency situations if cardioversion unsuccessful (IV push 1-3 seconds)
  • Radiofrequency catheter ablation: recurrent episodes
99
Q

Patients with atrial fibrillation are at risk for…

A
  • Clots
  • Stroke
  • Decreased perfusion (can decrease as much as 20-30%)

Common with HTN, DM, HF, CAD

100
Q

What is the pharmacological treatment for atrial fibrillation?

A
  • Antidysrhythmics: Amiodarone, Multaq (rapid administration, followed by saline bolus)
  • Carotid sinus massage (few seconds, not common)
  • Cardioversion (mild sedative)
  • Radiofrequency catheter ablation: recurrent episodes
  • Bi-ventricular pacing
101
Q

Hypokalemia or Hypomagnesaemia can cause this type of dysrhythmia?

A

Premature Ventricular Contractions

102
Q

What is the criteria for placing a patient with PVCs on beta blockers?

A

5000 PVCs in 24 hour period

103
Q

A build up of nitrogen waste in the body is called ___?

A

Azotemia

104
Q

This condition manifests with n/v, muscle cramps, edema, dyspnea, paresthesia and metallic taste in the mouth

A

Uremia azotemia with manifestations

105
Q

What is normal GFR?

A

greater than 90mL/hr

106
Q

What are the risk factors for kidney disease?

A
  • infection
  • inflammation
  • pregnancy
  • dehydration
  • hypotension
  • hypertension
107
Q

What are the best ways to slow the progression of CKD?

A

careful management of diabetes, HTN, and heart failure

ACE inhibitors slow the progression of CKD in patients with HTN

108
Q

With this stage of kidney disease a person is at risk and has normal kidney function and GFR. Screenings take place and education to manage care for risk factors takes place

A

Stage 1: At risk

109
Q

With this stage of kidney disease GFR is reduced to less than 15mL/min, fluid and electrolyte/acid base balance required and excess amounts of urea and creatinine build up in the blood. Renal replacement therapy or kidney transplant required

A

Stage 5: End stage kidney disease

110
Q

With this stage of kidney disease GFR is reduced to 30-59 mL/min, azotemia is present and focus is placed on managing underlying conditions such as diabetes and blood pressure

A

Stage 3: Moderate CKD

111
Q

With this stage of kidney disease GFR is reduced to 60-89 mL/min, slight elevation of metabolic wastes appear in blood but BUN, creatinine, uric acid and phosphorus are not well defined. Urine output is increased and dilute often causing dehydration.

A

Stage 2: Mild CKD

112
Q

With this stage of kidney disease GFR is reduced to 15-29 mL/min, excessive amounts of BUN and creatinine build up in the blood, kidney’s cannot maintain homeostasis, severe fluid and electrolyte/acid base impairment, education is done to prepare patient for renal replacement therapy

A

Stag 4: Severe CKD

113
Q

What are the changes to urine output and osmolality as kidney disease progresses?

A
  • Urine output deceases
  • Osmolarity becomes fixed
114
Q

Creatinine comes from ____ in skeletal tissue. Excretion depends on muscle mass, physical activity and diet.

A

protein

115
Q

What are the electrolyte changes (sodium, potassium, acid base, calcium, phosphorus) that take place with CKD?

A
  • Sodium:

early stages-hyponatremia (lost in urine),

late stages-hypernatremia (decreased urine output)

  • Potassium:

late stages-hyperkalemia (decreased urine output)

  • Acid-base imbalance: later stages-metabolic acidosis, kussmaul breathing
  • Calcium/Phosphorus:

early stage- Calcium decreased, Phosphorus increased,

later stages-parathyroid compensates by creating more calcium and both calcium and phosphorus are increased

116
Q

Which vitamin is needed to enhance intestinal absorption of calcium?

A

Vitamin D - calcium binds to vitamin D

117
Q

What are the cardiac changes that take place with CKD?

A
  • HTN: secondary to sodium retention
  • Hyperlipidemia: fat retention
  • HF: workload of heart increased
  • Pericarditis: pericardial sac becomes inflamed by uremic toxins or infection
  • Anemia: later stages - Clotting/Platelet impairment: increased bleeding
118
Q

What are the GI changes that take place with CKD?

A
  • Halitosis (bad breath): excess ammonia due to uremia
  • Stomatitis (mouth inflammation): excess ammonia due to uremia
  • Anorexia/Nausea & Vomiting - Peptic ulcer disease
119
Q

What are the neurological manifestations of CKD?

A
  • Confusion
  • Lethargy
  • Weakness/pain in lower extremities
  • Seizures
120
Q

What are the cardiovascular manifestations of CKD?

A
  • HTN
  • Cardiomyopathy
  • Pericarditis
121
Q

What are the respiratory manifestations of CKD?

A
  • Tachyapnea
  • Uremic halitosis
  • SOB
  • Crackles
  • Kussmaul breathing
122
Q

What are the hematologic manifestations of CKD?

A
  • anemia
  • bruising
  • bleeding
123
Q

What are the GI manifestations of CKD?

A
  • anorexia
  • nausea/vomiting
  • metallic taste in mouth
  • stomatosis
124
Q

What are the muscular skeletal manifestations of CKD?

A
  • Muscle cramping
  • prone to fractures
125
Q

What are the urinary manifestations of CKD?

A
  • Polyuria (early stages)
  • Dilution (early stages)
  • Oliguria (late stages)
  • Concentration (late stages)
126
Q

What are the integumentary manifestations of CKD?

A
  • Yellow/Gray pallor
  • Pruritus (itching)
  • Ecchymosis (bruising)
  • Purpura (purple patches)
127
Q

What are the psychosocial assessments for CKD?

A
  • coping
  • understanding of disease
  • advanced directives
128
Q

What are the lab assessments for CKD?

A

Early stages:

  • Increased protein, glucose, RBC, WBC - Fixed/decreased urine osmolality - Dilute urine

Late stages: - Increased osmolality - Urine output decreased and concentrated - Protein should be controlled

129
Q

Patients should not gain/lose more than ___ lbs between dialysis sessions

A

2 lbs

130
Q

What is the nursing care priority with regard to monitoring pulmonary edema and patients taking diuretics?

A

Watch for ototoxicity

131
Q

What is the priority nursing care for decreased cardiac output?

A
  • Control BP!
  • Patient has decreased stroke volume and increased output.
  • ACE inhibitors and CCBs help with GFR
132
Q

What are the dietary restrictions for a patient with CKD?

A
  • reduced protein (protein main cause of uremia)
  • supplement iron and calcium (r/t anemia and increased phosphorous which decreases calcium)
  • sodium restriction (edema)
  • Potassium restriction (prevent dysrhythmias)
  • Phosphorous restriction (avoid hypocalcemia)
133
Q

What is the antidote for heparin?

A

Protamine Sulfate

134
Q

How long is heparin active in the body after dialysis?

A

4-6 hours

135
Q

What is the most effective type of cardiac drug for slowing the progression of CKD in patients with HTN?

A

ACE Inhibitors

136
Q

What is the most effective type of cardiac drug for improving GFR and blood flow to the kidneys?

A

CCBs-Amiodarone

137
Q

What dietary changes take place when a patient is on dialysis?

A

Protein is increased.

Protein is lost thru dialysis and is measured by Albumin levels (decreased indicate protein deficiency)

138
Q

Which over the counter medication should be avoided by patients with CKD?

A

Antacids containing magnesium These patients cannot excrete magnesium

139
Q

Which manifestations of CKD are used to determine candidates for hemodialysis?

A
  • Fluid overload not responsive to diuretics
  • Symptomatic hyperkalemia
  • Uremic manifestations present (n/v, decreased cognition, pruritus, decreased attention span)
140
Q

What nursing assessments are important for a patient with a arteriovenous fistula?

A
  • Palpate for thrills/Auscultate for bruits
  • Check distal pulses
141
Q

What are the complications with arteriovenous fistulas?

A
  • Thrombus
  • Infection
  • Ischemia
  • Heart failure
142
Q

What are essential post-dialysis assessments?

A
  • Weight
  • Vitals
  • Hypotension (bolus of normal saline)
  • Headache
  • Nausea/vomiting
  • Malaise/dizziness
  • Muscle cramps
  • Bleeding
143
Q

What are the complications of peritoneal dialysis?

A
  • peritonitis
  • infections
  • poor dialysate flow
  • leakage
144
Q

What is the criteria for kidney donation?

A
  • no HTN
  • no kidney disease
  • no systematic disease or infection
  • matching blood type
145
Q

What is the preop care for a patient undergoing kidney transplant?

A
  • dialysis within 24 hours of surgery
  • blood transfusion from donor before surgery
146
Q

What is the postop care for a patient undergoing kidney transplant?

A
  • evaluate labs to determine kidney function
  • assess for signs of infection/rejection
  • assess urine output hourly within first 48 hours (pink/bloody after surgery)
  • vitals (especially BP)
  • Watch for chest pain, edema, crackles
  • monitor weight
147
Q

What are the complications of kidney transplantation?

A
  • Rejection
  • Thrombosis
  • Renal artery stenosis
148
Q

What is the most important patient education for kidney transplant patients?

A

Stick to drug regimen Critical to avoiding rejection!!

149
Q

What are the risk factors for v-fib?

A
  • MI
  • Hypokalemia
  • Hypomagnesemia
  • Hemmorage
  • Drug therapy
  • SVT
  • shock
150
Q

What are the risk factors for PSE

A
  • high protein diet
  • hypovolemia
  • hypokalemia
  • constipation
  • gi bleed
  • drug use
151
Q

What are the risk factors for ventricular tachycardia 140-180 bpm?

A
  • ishemic heart disease
  • MI
  • cardiomyopathy
  • hypokalemia
  • hypomagnasemia
  • valvular heart disease
  • heart failure
  • drug toxicity
  • hypertension
152
Q

What are the pharmacological treatments for ventricular tachacardia?

A
  • mexiletine
  • sotalol

Monitor HR, BP; watch for tremors, dizziness, blurred vision, ataxia, confusion

153
Q

What is the treatment recommended for stable ventricular tachycardia?

A

Cardioversion

may require ablation for persistent episodes

Unstable is treated same as v-fib

154
Q

How long can a person survive while in v-fib?

A

3-5 minutes

155
Q

What are the mainfestations of v-fib?

A
  • patient becomes faint
  • immediate loss of consciousness
  • pulseless
  • apneic
  • seizures may occur
156
Q

What are the priority interventions for v-fib?

A

defibrilate immediately

if not available, use CPR

157
Q

Why is nitroglycerin used in treatment of kidney disease?

A

To reduce pulmonary pressure/edema

158
Q

What heart conditions are treated with Amiodarone (CCB, antidysrhythmic)?

A
  • A-fib
  • V-tach

Monitor BP, QT, HR, Rhythm, hypotension, use sunscreen)

159
Q

Why is Atproine used for heart disease?

A

Bradycardia

Can increase ICP

160
Q

Why is Adenosine (antidysrhythmic) used for heart disease?

A

Supraventricular Tachycardia

Administered via IV push quickly (1-3 seconds)

Immediately followed by asystole

Monitor HR and Rhythm

161
Q

Why is Mexiletine (antidysrhythmic) used for heart disease?

A
  • V-tach
  • PVCs
  • V-fib

Monitor HR & BP

watch for tremors, dizziness, blurred vision, ataxia, confusion

Med Surg III - 2320 (3 decks)

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