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4th Semester Nursing > MedSurg2 - Exam 1 > Flashcards

MedSurg2 - Exam 1 Flashcards

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1
Q

What is PEP?

A

Post-Exposure prophylaxis

Two ART drugs for 4 weeks. Start asap after exposure.

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2
Q

What cells does HIV affect and how does it work?

A

Virus starts as RNA
Enters CD4 cell (via gp120 receptors)
Reverse transcriptase —> splices into DNA
-all daughter cells infected
-programs cell to make more virus copies
Snips DNA into little pieces (budding)
Reduces lifespan of CD4 cell from 100d to 2d.

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3
Q

What does protease do in the HIV infection process?

A

It’s the enzyme responsible for budding - snipping the HIV-infected DNA into little pieces.

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4
Q

What is “Viremia”?

A

A high viral load

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5
Q

What are s/s during a Primary/Acute infection? When will this occur.

A

Starts at 2-4 weeks (if it starts at all)
Flu-like symptoms: HA, sore throat, malaise, Fever, NVD, rash

Might also have weight loss, thrush, swollen lymph nodes

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6
Q

What is seroconversion?

A

Within a few weeks, the body produces antibodies to HIV

  • lowers viral load
  • patient becomes asymptomatic
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7
Q

What is Chronic Asymptomatic Infection (HIV). Early Stage CD4 count vs Intermediate stage CD4 count?

A

Happens after seroconversion
T-cells and B-cells function normally
Viral load stays low. Will last for years. During intermediate stage (as it worsens), nonspecific sx (persistent fever, night sweats, severe fatigue, chronic diarrhea, recurring HAs, thrush and other opportunistic infections)

Early CD4 count: above 500
Intermediate CD4 count: 200-500

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8
Q

What are some opportunistic infections that occur in intermediate chronic HIV infection?

A 
Thrush/candidiasis
Vaginal candida
Shingles
Oral or genital herpes
Oral hairy leukoplakia
Kaposi Sarcoma - (technically, by the time this shows up, it’s closer to AIDS)
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9
Q

How to differentiate Thrush from Oral Hairy Leukoplakia?

A

Thrush: Can scrape off. Raw/painful underneath.

Oral Hairy Leukoplakia: Doesn’t hurt. On sides of tongue. Can change taste.

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10
Q

Primary goals for someone with a chronic HIV infection?

A

Med compliance
Prevent exposure
Help the immune system
NO live vaccines

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11
Q

What’s a normal CD4 count?

A

800-1200

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12
Q

Treatment for Thrush?

A

Nystatin mouthwash
Magic mouthwash (lidocaine)
Salt water or baking soda rinse (taste out of mouth)

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13
Q

What is Kaposi Sarcoma

A

Tumors of the vasculature
Occur all over body
No treatment

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14
Q

When is one diagnosed with AIDS?

A

HIV (+) and one of the following:
CD4 count below 200
1 opportunistic cancer present (Kaposi Sarcoma)
Wasting syndrome (10% sudden drop in body weight)
Specific opportunistic infection (ie, thrush in esophagus, lungs)

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15
Q

Main sx of AIDS

A 
Meningitis/encephalitis
Retinitis
TB/PCP/lung tumors
Hepatitis/Gastroenteritis
A/N/V
Changes in lab work (CBC, H&H, Platelets, WBC)
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16
Q

What is the “window period” (HIV testing)

A

Time between infection and development of antibodies

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17
Q

What are the three different HIV test types and what do they look for?

A

Nucleic Acid Test (looks for the virus itself)

Antigen/Antibody Test (tests for antibodies AND the p24 antigen)

Antibody Test (requires for seroconversion to have occurred)

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18
Q

What is the clinical testing policy for HIV?

A 
Antigen/Antibody test (takes 20-60m)
—>If negative, pt is HIV negative
—> If positive, RE-TEST
—> If still positive, test for antibodies. (If positive, HIV+)
—> If negative, take Nucleic Acid Test
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19
Q

What is the initial viral load in HIV+ patients?

A

LOTS: 1 million+ copies

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20
Q

What is considered a low viral load (HIV)?

A

40-500

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21
Q

What happen to WBCs & neutrophils in HIV?

A

WBCs drop below 4K (normal 4-11k)

Neutrophils drop below 1700 (normal 2500-8000)

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22
Q

What are the different MOAs for ART/HAART drugs?

A 
Entry inhibitors
Non-nucs (block RNA from going into DNA)
Nucs (Prevent 1-stranded DNA from becoming 2-stranded)
Integrase inhibitors (prevent DNA integration into the nucleus)
Protease inhibitors (prevent protease from snipping/budding)
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23
Q

Why use multiple ART therapies?

A

Lower doses
Less side effects
Less chance of mutation

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24
Q

Who should start ART therapy?

A

ALL HIV-infected individuals, regardless of CD4 count

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25
Q

How many ART meds should someone take for best efficacy? What’s the challenge in this?

A

3-4 meds.

Cost! Strict adherence to scheduling.

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26
Q

What are the vaccine restrictions for HIV patients?

A

No live vaccines (except MMR)

No contact with anyone who has had a live vaccine for 2-3 weeks

(No varicella, shingles, rotavirus)

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27
Q

Does HIV cross the placenta? How to protect fetus from HIV exposure?

A

No - it doesn’t cross the placenta

Avoid invasive procedures: amniocentesis, ROM, episiotomies.

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28
Q

What do you want to worry about with a pt with HIV whose membranes have ruptured? How can you prevent this?

A

Each hour the membranes have ruptured, the HIV transmission risk increases.

C-section before labor or ROM decrease the risk of transmission.

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29
Q

Diastolic vs Systolic HF

A

Diastolic: heart can’t fill effectively (not enough space OR can’t relax)
Systolic: Heart can’t eject effectively (problem with the pump)

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30
Q

Why might contractility be diminished?

A

Primary damage (MI, myocarditis)

Ventricular remolding d/t 2ndary cause (ie, HTN)

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31
Q

What is the ultimate effect of Heart Failure

A

Decreased cardiac output =

Inability to perfuse tissues and meet basic metabolic needs

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32
Q

Key characteristics of heart failure

A 
Activity intolerance (not enough O2 to cells - dyspnea, fatigue)
Maybe fluid overload (edema, pulm congestion)

Decreased QOL and life expectancy

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33
Q

Risk factors for HF

A 
Atherosclerosis (leads to hypertrophy)
Ischemic heart disease (dead tissue means poor ejection)
Hypertension
Advanced age
Diabetes (blood vessel damage)
Dysrhythmias (can cause or be caused by)
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34
Q

Symptoms of LHF

A 
Lung congestion (frothy sputum, dyspnea) and 
decreased systemic perfusion
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35
Q

Symptoms of RHF

A

Edema

Hepatosplenomegaly

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36
Q

Normal EF
Symptoms w/activity EF
Symptoms all the time EF

A

Normal: 50-70
Sx w/activity: 40-49% EF
Sx all the time: less than 40% EF

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37
Q

What test do you need to measure EF?

A

ECG

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38
Q

Why might Systolic dysfunction occur?

A

Overstretched heart
MI
Valve problems
Chronic hypoxia

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39
Q

What’s the EF look like in a pt with systolic dysfunction?

A

Low: less than 50

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40
Q

What does an EF look like in a pt with Diastolic dysfunction?

A

Normal: 50-70 (though the amt might be less)

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41
Q

Most common cause of diastolic dysfunction? What happens?

A

LVH d/t HTN: thickened stiff walls, ventricles can’t relax and fill during diastole.

High filling pressures and backup of pulmonary and venous system.

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42
Q

What are the s/sx of left sided heart failure? Why?

A

Lungs: Crackles, SOB, incr RR, accessory muscle use, maybe decreased SpO2, Paroxysmal Nocturnal Dyspnea, blood-tinged sputum (backup into the pulmonary system, increased pressures at lungs push fluid and sometimes RBCs into the lungs)

Orthopnea: occurs b/c fluid is returning to the heart more easily when pt lies down - increases preload. (Intervention: sit pt upright)

Elevated PCWP: pulmonary capillary wedge pressure.

Perfusion: incr HR, decreased cap refill, cool, pale skin, weak pulses, fatigue

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43
Q

S/Sx of Right-sided HF - why?

A 
Edema 
JVD
Ascites
Weight gain
Anorexia, GI distress
Hepatosplenomegaly, Cirrhosis
Fatigue (d/t the heart working harder)
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44
Q

How does the body compensate for the decreased cardiac output of heart failure?

A 
SNS activation (epi, norepi)
Neurohormonal response (RAAS activation)
Ventricular remodeling (dilation, hypertrophy)
Biomarkers (BNP with overstretch of heart)
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45
Q

What’s the effect of SNS activation in HF?

A

Increased HR, contractility and vasoconstriction of systemic peripheral circulation

INCREASES O2 demand, preload and afterload. Will initially increase CO, but will hurt the heart in the long run.

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46
Q

What drugs are given to decrease SNS activation in HF?

A

Beta-blockers

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47
Q

What happens as a result of the neurohormonal response to HF? How do we treat it?

A

RAAS activation (retains fluid, vasoconstriction)

ACE Inhibitors are the #1 choice for decreasing the RAAS response: highest up in the chain, preventing fluid retention and vasoconstriction.

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48
Q

Why isn’t ventricular remodeling helpful for the heart?

A

Dilation makes it less effective, increasing pressure inside the heart and stretching it more - CO goes down.

Hypertrophy gives it less space to fill, increases O2 demand of the heart and increases coronary circulation. This all increases the risk for dysrhythmias as well as decreasing CO.

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49
Q

What is BNP and how does it help the practitioner?

A

BNP is released when the heart is overstretched: will provide mild diuresis and vasodilation to compensate.

It’s helpful in diagnostics: if pt has dyspnea, BNP helps you determine if the problem is pulmonary or cardiac in origin. (HF = higher BNP)

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50
Q

What Is Acute Decompensated Heart Failure and what will it present like?

A

Body can’t compensate for poor heart output and/or the meds aren’t working.

First symptoms: Increased RR, Decreased PaO2, Restlessness.

Later: severe dyspnea, crackles, hemoptisis, cold clammy skin, tachycardia, anxiety, (cyanosis, late).

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51
Q

Clinical Profiles for ADHF: what are they (4) and which is the worst?

A

Relate to perfusion: warm/cold …. and lungs: wet/dry

Warm/Dry (best)
-this patient has no s/sx

Warm/Wet
-this patient’s perfusion is fine, but has dyspnea, orthopnea, edema, or PAWP increase.

Cold/Dry
-this patient has no lung trouble, but has poor cardiac output: hypotension, edema, cold extremities

Cold/Wet (this is the worst)
**PT at risk for CARDIOGENIC SHOCK**
PAWP is increased, decreased perfusion
Change in mental status, decreased O2, decreased UO, shock
(Management has failed)
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52
Q

When are you most likely to see Angina?

A

Can occur in HF, but will especially occur w/decompensation (ADHF) because of decreased O2/hypoxia.

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53
Q

What is a pleural effusion? What condition have we studied that it’s likely to occur with and how will it be treated?

A

When the lungs no longer adhere to the pleural cavity

  • fluid builds up, decreasing effectiveness of lung
  • Decreased (or noisy, maybe) lung sounds
  • Increased RR, HR and decreased SpO2
  • May have pressure or pain
  • Increased WOB

If large, drained with chest tube.

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54
Q

What do you want to assess for in a chest tube?

A

What’s draining
How much
Infection risk
Is it leaking

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55
Q

What’s the arterial BP that happens in the cath lab? What would you want to check if your patient has just come back from the cath lab or CICU?

A

They will place a probe in an artery, displaying HR/BP more accurately.
You’ll check the site of the arterial BP AND downstream of it: risk of bleeding is high.
(If it’s bleeding, 5m of pressure - moving around during transfer can open up wound).

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56
Q

What’s the Central Venous Pressure and how does it differ from the arterial blood pressure?

A

CVP is inserted into the right atrium and intended to give you a PRELOAD estimate.

arterial BP is just a more accurate way of measuring BP.

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57
Q

What are the risks for a patient who comes back to the floor after a Pulmonary Wedge Pressure has been done?

A

Infection
Bleeding
Clots
Dysrhythmias

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58
Q

What are the goals of treatment for HF?

A 
DECREASE CARDIAC WORKLOAD: 
Decrease intravascular volume
Decrease preload
Decrease afterload
Control HR and rhythm

(Eventually you’ll improve contractility, but Cardiac workload has to be managed first).

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59
Q

What are the two primary drugs used to treat heart failure?

A

ACE inhibitors and Beta Blockers

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60
Q

Why would calcium channel blockers be used in heart failure?

A

Decreased calcium in cell means that heart contractions are slightly delayed. This gives the heart a little more time to fill and is used in diastolic heart failure.

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61
Q

Why would diuretics be used in HF?

A

To decrease volume

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62
Q

What are the positive inotropes and why are they used in HF?

A

They are used (carefully) to increase contractility

“beta agonists”: Dobutamine, Digoxin

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63
Q

Why would you use morphine in HF?

A

Vasodilates systemic and pulmonary vessels

Manages both pain and anxiety

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64
Q

What positioning could you use for a pt in ADHF? Why?

A

Place at edge of bed with feet dangling

Allows lungs to expand
Blood moves to dependent spaces (feet), decreasing demand on heart

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65
Q

O2 for ADHF? How and why?

A

If severe, use a NRB mask
BiPap might help, too (positive pressure to keep lungs open)

If the heart has a decrease in O2, it can further decrease CO.
Pulm edema will also further decrease O2

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66
Q

What weight gains should a pt report (w/HF)

A

2 lb in one day, 4 lb in one week.

Same time, same clothes, weigh every day

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67
Q

What are the sodium restrictions for HF?

A

2-2.5g/day.

68
Q

What are the four phases of cardiac rehab? Benefit?

A
  1. In hospital
  2. Exercise training while on telemetry (and healthy eating)
  3. Exercise training (non-telemetry) supervised
  4. Indefinite… nothing new introduced

Benefit: 25% reduction in mortality

69
Q

What is a primary side effect of Furosemide?

A

Hypokalemia

70
Q

What are the rules for digoxin

A

Check pulse before giving. Hold if below 60.

71
Q

What should we know about potassium and digoxin?

A

Low potassium can lead to Digoxin toxicity!! (It increases the action of digoxin).

S/s: anorexia, Nausea, Vomiting and Yellow Vision

72
Q

Is Respiratory failure a disease or a symptom?

A

A symptom of another disease - not a disease itself.

73
Q

What is hypoxemic respiratory failure? How do you identify it?

A

A failure of oxygenation (either acute or chronic).

PaO2 won’t increase above 60 even when on a Simple Mask or Venturi mask.

74
Q

What is hypercapnic respiratory failure (generally)? What are the numbers we identify it with?

A

Cannot blow off CO2. ABG shows respiratory acidosis (pH less than 7.35 and CO greater than 45).

75
Q

What are V/Q mismatches associated with? What’s the difference between a High and Low V/Q mismatch?

A

V/Q mismatches are associated with Hypoxemic Respiratory Failure. (Something is messing with the exchange of gas from air to blood).

High VQ mismatch (more than 1) means that Ventilation is ok, but perfusion is down.

Low VQ mismatch (less than 1) means that Ventilation is obstructed somehow but perfusion is ok.

76
Q

What is a shunt?

A

V/Q = 0! Nothing is happening at the alveolar-capillary border.
Usually what’s happening in ARDS.

77
Q

An alveoli is completely full of fluid. What is this an example of? What kind of failure would it lead to?

A

This is an example of a shunt.

It would lead to hypoxemic respiratory failure.

78
Q

What is a diffusion limitation?

A

Anything (thickened membrane, damage, fluids) that is reducing gas diffusion at alveoli-capillary border. (V/Q could be normal).

79
Q

How could V/Q be normal but a person is still dealing with hypoxemic respiratory failure?

A

If both air flow and blood flow were decreased. Or, if air flow was usually normal (upon rest) but once exercising, diffusion took longer and the blood rushed past.

80
Q

If pain is restricting chest wall movement, would this be high or low VQ mismatch?

A

This would be low: Ventilation is down because lungs can’t expand - limited air is reaching the alveoli.

(Also, the pain is increasing muscle tension/stress and increasing oxygen consumption as a result - exacerbating the situation).

81
Q

Would a pulmonary embolism lead to a high or low VQ mismatch?

A

HighVQ mismatch. Ventilation is fine (plenty of air at the alveoli), but the embolus is cutting off blood flow to a portion of the lung.

82
Q

What are some causes of hypercapnic respiratory failure? What at what SpO2 is someone at risk?

A

Risk zone can start somewhere in the 88-92% range
Causes:
Abnormalities with the airways (air trapping leading to chronic overstretching and loss of elasticity)
CNS issues (medications, increased ICP)
Chest wall abnormalities (scoliosis, broken ribs, etc)
Neuromuscular conditions that lead to weakness/paralysis of respiratory muscles (spinal cord injury, muscular dystrophy)

83
Q

What does respiratory failure look like, s/s-wise?

A

**First sign: mental changes! Irritation, restlessness, confusion, drowsiness.

High HR, High or low RR, heightened BP

Orthopnea, Tripod Position, Accessory muscle usage, pursed lip ratio

Change in I:E ratio (inspiration:expiration)

84
Q

What if your patient in seeming respiratory failure goes from fast RR to slow RR?

A

Danger! Call rapid response!

85
Q

What is ARDS? What are the s/sx?

A

Sudden, severe, progressive resp failure: the alveolar capillary membrane gets damaged and FILLS with FLUID

Severe dyspnea
Hypoxemia
O2 supplementation doesn’t help

(Decrease in surfactant means decreased lung compliance
Diffuse pulmonary infiltrates EVERYWHERE in lungs - “white lung”)
Shunting may occur, leading to ventilator use.

86
Q

What are the causes of ARDS?

A

Typically, it’s sepsis.

Anything else that damages the alveolar capillary membrane:

  • trauma
  • lung infection
  • aspiration
  • prolonged pulmonary bypass
  • shock
  • fat emboli
87
Q

When does ARDS occur (timing)?

A

Anywhere from 1-7 days after the initial injury/assault, but typically within 24-48h.

88
Q

What type of acidosis would ARDS create?

A

It can create BOTH metabolic acidosis (because hypoxia leads to anaerobic respiration) AND respiratory acidosis.

This makes it super hard to recover from.

89
Q

What are some reasonable goals for ARDS patients?

A

Normal ABG
Baseline breath sounds
No dyspnea
Effective cough (can clear secretions)

90
Q

What things should you be thinking about when treating someone with ARDS?

A

Nutrition! They need sufficient Kcal - might need enteral/parenteral feedings
(Know that an increased RR means an increased aspiration risk)

Monitor I/Os, Daily weight

91
Q

What interventions would you use for a pt in ARDS?

A

O2 therapy (do they need bipap?)
Mobilize secretions (priority if blocked by gunk!!)
Coughing: Huff method or augmented coughing
Hydration and Guaifensien
Chest physiotherapy (move in direction of drainage, position for drainage)
Airway suctioning
PRONE positioning

92
Q

What are the rules for airway suctioning?

A 
Only use suction when withdrawing the catheter. 
100-120mm Hg. 
Sterile Gloves
10-15s at a time
20-30s between attempts.
93
Q

What sort of meds are used for a patient in ARDS (or resp failure)

A

Bronchodilators (albuterol)
Corticosteroids (PO: Prednisone, IV: methyprednisone, inhaled: budosenide, pulmicort).
IV diuretic: furosemide (if the origin of the problem is in the vasculature, like HTN)
IV antibiotics (if infection or even prophylaxis)
Benzodiazepines (Midazolam for intubation, Lorazepam if anxiety is exacerbating the condition)
Opioids (morphine) help with pain, vasodilation, anxiety.

94
Q

What’s the pathophys and s/s of a PE?

A

Occluded blood flow in the lungs changes the flow of blood in the heart (increased resistance back to the R side and decreased outflow from the L side). It’s also working harder to try to get the blood through (increasing O2 demand).

JVD
Hypotension, increased HR and decreased perfusion.
Chest pain (d/t poor coronary circulation).
Air hunger/Dyspnea
Hemoptisis
Anxiety/doom

(If mild, might just be cough, crackles and a fever!)
(If massive, could be s/s of shock + edema).

95
Q

Order of interventions for a PE?

A 
#1 Positioning! Semi-Fowlers
#2: O2
#3: Vital Signs
#4: Contact the doctor
#5: Anticoagulants
#6 - maybe - fibrinolytics (TPA/Alteplase). Lots of contraindications b/c they will unclot everything else.
96
Q

What’s the most used Diagnostic test for PEs?
What’s the best for an iodine allergy?
What’s the most accurate?
What’s the least accurate?

A

Most used: Spiral CT
For Iodine allergy: V/Q scan
Most accurate: Pulmonary angiography (uses contrast media)
Least Accurate: D-dimer blood test (looks for fibrinogen from clot)

97
Q

When would you intubate a pt?

A

ARDS/Resp Failure and anytime a pt cannot maintain ventilation on their own:

  • Apnea or Bradypnea secondary to resp failure
  • Upper airway obstruction
  • Severe Hypoxia
  • Ineffective airway clearance
  • Neuromuscular disease (paralyzed)
  • Coma
98
Q

What’s the procedure for intubation?

A
  • 100% O2 preoxygenation
  • Sedation (Versed) as needed
  • Monitor ECG, O2, Breath sounds
  • Have BVM and suction at bedside
  • DR can only attempt it for 30s at a time: must BVM w/ 100% O2 for 3-5m before trying again.
99
Q

What are the nursing responsibilities specific to intubation?

A
  • Stabilize the ETT tube with tape
  • Check the ET cuffs for leaks (auscultaste with stethoscope over throat; check pressure gauge daily)
  • Confirm tube position (BILATERAL breath sounds AND chest rise)
    • tube should be at teeth, CO2 should be checked, and Chest X-ray to confirm.
100
Q

When do you suction a ventilated patient? What’s the procedure?

A

Only suction if indicated (never routine)
There would be a decrease in O2 sats or ABGS…
or visible secretions in the ET tube…
or suspected aspiration of GI contents…
or a decrease in RR rate

Before suctioning, 100% O2 for 30-60s
No more than 15s each time
Afterwards, 100% O2 for 60s

101
Q

What’s PEEP for?

A

Positive End Expiratory Pressure:

  • maintains a low level of pressure during EXHALATION
  • prevents a decrease in functional residual capacity
  • props open alveoli
  • requires less work to reinflate
  • reduces V/Q mismatch
  • Allows lower O2 levels
102
Q

Best ways to prevent VAP (ventilator associated pneumonia)?

A

Head of bed up 30-50 degrees (allows drainage down esophagus)

Oral Hygiene
Managing gastric secretions
Sedation vacations
DVT prophylaxis (not sure why?)

103
Q

Of the following four substances, which do healthy kidneys typically retain and which do they typically excrete? (Na+, K+, H+, HCO3-)

A

Retain: Na+ and HCO3

Excrete: H+ and K+

104
Q

What are s/s of hyponatremia?

A

Mental changes, HA
N/V
Tiredness
Muscle spasms and seizures

105
Q

What are signs and symptoms of Hyperkalemia

A 
Arrythmias
Numbness and tingling
Trouble breathing
Chest pain
Tiredness/weakness
Nausea/Vomiting
106
Q

What are the s/s of acidosis?

A 
Fast breathing
Confusion
Vomiting / Nausea
Lethargy
Fruity breath (ketoacidosis)
Maybe even jaundice
107
Q

What will loop diuretics do to potassium levels?

A

Decrease them.

108
Q

What is the normal GFR?

A

Over 90 ml/m.

109
Q

What is Azotemia?

A

An increase in nitrogenous waste product levels (serum creatinine and BUN/urea)

110
Q

What is Uremia?

A

The clinical manifestations of azotemia:

  • fatigue, trouble concentrating/thinking
  • cramping, seizures, tremors
  • NV
111
Q

What is the normal range for serum creatinine?

A

0.6-1.3

112
Q

What is the normal range for BUN?

A

6-20mg/dL

113
Q

What is the normal range for Creatinine Clearance

A

59-137 ml/min

Happens over 24h, urine must be kept cold

114
Q

Diagnostic criteria for CKD?

A

GFR of less than 60ml/m for more than 3 months.

115
Q

What type of AKI (prerenal, intrarenal or postrenal) is decreased perfusion to the kidneys?

A

Prerenal

116
Q

What type of AKI (prerenal, intrarenal or postrenal) is glomerulonephritis?

A

Intrarenal

117
Q

What type of AKI (prerenal, intrarenal or postrenal) are kidney stones??

A

Postrenal (they occur in the collecting duct - after the glomerulus)

118
Q

What type of AKI (prerenal, intrarenal or postrenal) is a bladder infection?

A

Postrenal

119
Q

What is meant by the oliguric phase? Does it happen with AKI or CKD or both?

A

Oliguric phase happens with AKI. Starts at the initial insult/injury and lasts 1-3 weeks.

  • UO less than 400ml/day (approx 16.67ml/hr)
  • will often see fluid volume excess and edema

Might see Azotemia, Kussmal’s respirations, and electrolyte imbalances

120
Q

What electrolyte imbalances are you likely to see in the oliguric phase of AKI?

A

Decrease in Na (kidneys can’t retain)
Decrease in Ca (kidneys not activating D)
Increase in K (kidneys can’t excrete)
Increase in Mg (kidneys can’t excrete)
Increase in Phosphate (kidneys can’t excrete)

121
Q

What’s the SG likely to look like in the oliguric phase of AKI? (What’s the normal range?)

A

Normal is approx 1.002-1.030

If the AKI is intrarenal, it might be exactly 1.010 (the SG of blood)

If the AKI is prerenal (reduced blood flow), the SG will be high (over 1.25) because the kidneys would be still able to concentrate urine

If the AKI is postrenal, the SG likely won’t change

122
Q

What is the Diuretic phase and does it happen with AKI or CKD or both? What are the risks?

A

It happens in AKI only.

Kidneys start to be able to filter waste again, and there’s a ton of waste in the filtrate. Kidneys have difficulty concentrating the filtrate, so there’s osmotic diuresis of LOTS of fluid: 1-3L/day … even up to 5!

Risks: HYPOVOLEMIA, HYPOTENSION, HYPONATREMIA, HYPOKALEMIA

Can cause AKI all over again.

123
Q

What is the Recovery phase in AKI?

A

Starts when the GFR increases
BUN and Serum Creatinine will plateau and start to decrease

Can take up to 12 months for kidneys to recover.

Must be careful in this time frame, especially with hydration, medications, and when to seek help.

124
Q

What is a retrograde pyelogram and what would you want to know about your patient before giving it?

A

Iodine is injected into the ureter and it travels to the kidneys so that it can be picked up on imaging.

Would want to ask about allergies.

125
Q

What is a renal scan and what is the benefit (in contrast to a retrograde pyelogram)

A

A small amt of radioactive material gets injected into veins and is able to be seen in the kidneys, ureters and bladders.

Does not have iodine, so less allergies.

126
Q

Is contrast safe for kidney patients?

A

Only if they’re going to dialysis immediately afterwards.

127
Q

How to determine amount of fluid your pt can have?

A

Take today’s PO intake of fluids and add it to 600. This is the amount allowed for TOMORROW.

128
Q

Your patient has hyperkalemia. How could you treat it?

A

Insulin (with D50 or D10 to prevent hypoglycemia)
-this allows for K to be taken into the cells

  • Sodium Bicarbonate (increases action of the Na/K pump - more K into the cells… but it also contains sodium… so depends on Na levels/fluid).
  • Kayexalate (sodium polystyrene sulfonate) to bind K and excrete it (must assess for bowel sounds: diarrhea might prevent it from working. If bowels aren’t moving, you’d want to hold it).
  • Dialysis
129
Q

What do you want to remember to do before giving EPO?

A

Take blood pressure: could create clots and lead to a stroke, or could make BP even higher.

130
Q

What are the two primary causes of CKD?

A 
#1 Diabetes
#2 HTN
131
Q

Why does metabolic acidosis happen with CKD?

A
  • kidneys can’t reabsorb HCO3

- can’t excrete ammonia or H+

132
Q

What are two reasons that hyperkalemia happens in CKD?

A
  • kidney can’t excrete K+

- kidney can’t excrete H+, which, when increased in the bloodstream, pushes K+ out of the cell into the blood.

133
Q

Why are there cardiovascular problems with CKD?

A

Kidneys can’t flush out cytokines…. more are activated

-they do inflammatory damage to blood vessels, system-wide

134
Q

Why does immune function decrease with CKD?

A

Increased waste products in the system damage the T-cells - can’t fight infections as well

135
Q

Why would insulin resistance be related to CKD?

A

Kidneys can’t excrete insulin as well, meaning there’s more in the bloodstream. That means cells develop more insulin resistance and higher doses are needed.

136
Q

What do triglyceride levels have to do with CKD?

A

The increase in insulin levels stimulates triglyceride production in the liver. Increases atherosclerosis, HTN, CAD, PAD.

137
Q

Why are there musculoskeletal issues in CKD? (2 reasons)

A

Phosphate can’t be eliminated as well - calcifies in vessels and soft tissues when it meets with calcium.

Also, when kidneys can’t activate Vitamin D (needed for Ca absorption), body breaks down bones to increase calcium supply. Leads to bone fragility.

138
Q

What’s the name for activated Vitamin D?

A

Calcitriol

139
Q

What are two phosphate binders we learned about?

What should we know about them?

A 
Calcium acetate (Phoslo)
Aluminum hydroxide (Amphojel)

They can cause constipation because the binding happens in the GI tract.

140
Q

What are foods high in phosphate?

A

Dairy, legumes, Almonds/seeds, wheat germ/bran

141
Q

What stages of CKD would you want thiazide diuretics during? Why?

A

Stages 1-3. They decrease blood pressure and they have a longer duration of action.

Also, the body doesn’t build up resistance to them the same way it does to loop diuretics.

142
Q

What stages of CKD would you want loop diuretics?

A

Stages 3- ESRD. They work super fast, and they waste more K+.

143
Q

What sort of nutritional therapy can you implement in someone with CKD?

A 
Restrict Na
Restrict K 
Restrict Mg
Restrict Phosphate
Not too many fluids (weigh themselves daily)
144
Q

What are dietary sources of magnesium that can be avoided?

A

Dairy leafy greens, almonds, tofu

145
Q

What are dietary sources of potassium that can be avoided?

A

avocados, bananas, potatoes/tomatoes, OJ, dried fruits/nuts.

146
Q

What are s/s of hypermagnesemia?

A

Decreased deep tendon reflexes
Facial parasthesias
Weakness (extreme)

147
Q

What are the indications for dialysis?

A 
GFR of less than 15ml/m
Hyperkalemia
Metabolic acidosis
Neuro impairment
If fluid volume excess is compromising heart and/or lungs
148
Q

How long after the implantation of the Dacron cuff (for PD) can you begin dialysis therapy?

A

1-2 weeks.

149
Q

What are the two different types of PD?

A

Continuous ambulatory PD (manual exchange)

Automated PD (machine controls it at night)

150
Q

S/sx of peritonitis from PD?

A

Cloudy outflow with increased WBC count

Maybe abd pain, NVD, hyperactive bowel tones

151
Q

Why would pulmonary difficulties occur with PD?

A

Increased pressure on the diaphragm - especially at night when lying down.

152
Q

Why would protein loss occur with PD?

A

Because the peritoneal membrane is permeable to protein.

153
Q

Which preserves renal function better… PD or HD?

A

PD

154
Q

What do you want to assess Before HD? What about after?

A

Before:
Assess thrill and bruit of fistula.
Assess fluid status (BP, weight, lung/heart sounds, edema)
Assess electrolytes and blood glucose.

After:
See the pt IMMEDIATELY. (If s/s of hypovolemia - confusion, super low BP - then call the dr).
Assess for fluid status (BP, lungs, mental status, HA)
Assess access site for bleeding
Give daily meds
See if new labs have come back (electrolytes, bun, serum creatinine)

155
Q

How do fluid restrictions differ between HD and PD?

A

HD: 600-1000ml/day + UO.
PD: not restricted.

156
Q

How do protein restrictions differ with PD vs HD?

A

HD: limited to 1/2g/kg/day
PD: much less limitation (membrane permeable to proteins

157
Q

How do potassium restrictions vary from HD to PD?

A

HD: 2-4g/day
PD: no restrictions (hemodynamically stable state)

158
Q

How do sodium restrictions vary from HD to PD?

A

HD: 2-3g/day
PD: more sodium is ok

159
Q

Goals with a loop diuretic (CKD)

A

Increase sodium excretion
Increase K+ excretion
Decrease edema (lungs/body)
Decrease BP

160
Q

Goals with thiazide diuretic?

A

Decrease BP

Decrease risk of kidney stones

161
Q

Goals with a potassium sparing diuretic?

A

Decrease Na
Decrease BP

(By blocking aldosterone)

162
Q

Goals with an ACE inhibitor?

A

Decreases BP (#1 choice for this)

163
Q

Goals with a beta blocker (CKD)

A

Block SNS activation (decrease BP and HR)

164
Q

Goals with Statins (CKD)

A

Prevent liver from making cholesterol (remember increase in insulin means more triglycerides)
Prevents heart attacks, strokes, and poor circulation in feet

165
Q

Paroxysmal Nocturnal Dyspnea is associated with what-sided heart failure? Why?

A

Left-sided heart failure

Because of the sudden fluid shift and increase in preload

4th Semester Nursing (8 decks)

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