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final exam Flashcards

1
Q

Fluid volume 1kg=

A

1 Liter

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2
Q

anuria

A

<50 mL/24hrs of urine output
(<1-2 mL/hr)

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3
Q

earliest clinical manifestation of AKI

A

oliguria

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4
Q

oliguria

A

less than 0.5mL/hr (400mL in 24hrs)

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5
Q

Pathophysiology of AKI

A

reduced blow flow to the kidneys (shunting)
hypovolemia
hypotension
reduced cardiac output & HF
Obstruction of kidney or lower urinary tract
bilateral blood flow obstruction

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6
Q

RIFLE

A

Severity Level
Risk- decreased U/O for 6hrs; Cr 1.5
Injury- decreased U/O for 12hrs; Cr 2x baseline
Failure- anuria >12 hours; Cr 3x baseline

Outcomes levels of loss
Includes utilization of some type of renal replacement therapy
Loss (> 4 weeks)
Persistent AKI
End-stage kidney disease
>3 months of AKI

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7
Q

Prerenal failure

A

reduced blood flow to the kidney

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8
Q

Intrarenal/Intrinsic Failure

A

damage the glomeruli, interstitial tissue, or tubules

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9
Q

Postrenal failure

A

obstruction of urine flow

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10
Q

Prerenal Failure causes

A

*hypoperfusion
*FVD- GI Loss/ Hemorrhage/ renal loss (diuresis)
*Impaired Cardiac Efficiency- Cardiogenic shock (pump failure)/ dysrhythmias/ HF/ MI
*Vasodilation- anaphylaxis, sepsis (distributive shock)/antihypertensive medications

Early AKI (levels R & I) can be reversed.

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11
Q

prerenal clinical characteristics

A

decreased urine output
increased BUN/creatinine
increased urine osmolality
increased serum K+ and mag
FVD- H&H high/low. trend MAP

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12
Q

Intrarenal Failure causes

A

*Parenchymal Damage
*Prolonged Renal ischemia (2 hypoxia)- hemoglobinuria (blood trans reaction)/ rhabdo/ blocked blood flow
*Nephrotoxic Agents- aminoglycosides, NSAIDS, contrast dye/poisons/ chemo
*Infectious Processes- acute pyelonephritis/glomerulonephritis
*Disease Process- acute tubular necrosis

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13
Q

Intrarenal Clinical Characteristics

A

increased BUN/Creatinine
increased K+ & mag
often decreased urine output
increased weight
FVE

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14
Q

Postrenal Failure causes

A

-ureter, bladder, or urethral cancer, cervical cancer
-Kidney, ureter, or bladder stones
-BPH or cancer
-bladder atrophy
-calculi
-blood clots

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15
Q

What happens in Postrenal Failure

A

-obstruction distal to kidney
-pressure rises in the kidney tubules and causes decreased GFR

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16
Q

Postrenal Clinical Characteristics

A

increased BUN/ creatinine
decreased or sudden anuria

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17
Q

Postrenal clinical treatmeants

A

early intervention
relieve obstruction- surgery, cystoscopy, catheter, flush

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18
Q

uremia s/s

A

pruritis, muscle cramps, change in mental status, n/f, fatigue, anorexia, wt loss, seizures, decreased LOC, and/or MI

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19
Q

hyperkalemia s/s

A

n/v. chest pain, muscle weakness, numbness, tingling, GI pain, short QTI, peaked T wave, QRS prolongation, short PRI

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20
Q

Phases of Intrarenal AKI

A

Initiation Phase:
Begins with the initial insult and ends when oliguria develops
Oliguric Phase:
Increase in substances that SHOULD be excreted by kidneys (potassium, creatinine, urea (BUN), magnesium
Uremia s/s and hyperkalemia s/s develop
10-14 days
400 ml in 24 hours (0.5ml/kg/hr) or less
Diuretic Phase:
Gradual increase in urine output, stabilized lab values, achieve normal or elevated urine output levels
Still an altered kidney function, abnormal GFR
Recovery phase:
Can take 3-12 months to achieve this state
GFR is 1%-3% less than what it should be
Normal lab value ranges

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21
Q

Metabolic acidosis s/s

A

change in mental status, tachycardia., n/v, h/a, anorexia, fatigue -compensatory: tachypnea

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22
Q

AKI assessment

A
  • Determine AKI Cause
    Address Fluid Volume Status
    FVE or FVD
    FVD: Prerenal
    FVE: Intra/Post Renal
  • All AKI Types
    Rising BUN and Creatinine
    Increased serum potassium, and phosphorous, and magnesium
    Decreased serum calcium
  • Electrolyte management:
    Hyperkalemia - Perform EKG, Cardiac Monitor
    Administer sodium polystyrene (Kayexalate)
    Hypocalcemia and hyperphosphatemia
    Phosphorus binders: sevelamer (Renagel), lanthanum carbonate (Fosrenol)
    May require temporary HD
    May require calcium replacements
    Address Acid/Base Imbalances
    Metabolic Acidosis s/s
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23
Q

AKI Diagnostic findings

A

EKG
Renal ultrasound
Renal CT or MRI
X-ray (KUB)
Cystoscopy

Labs:
BUN
Cr
BNP
ABG
BMP (electrolytes)
U/A
Urine electrolytes

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24
Q

AKI medical management

A
  • Medical Management: restore normal chemical and fluid balance
  • Fluid management
    Prerenal- administer IV fluids
    Intra/Post Renal- fluid restriction, diuretics
  • Treat metabolic acidosis
  • Blood pressure management
    Prerenal- increase
    Intra/Post- avoid hypertension
  • Metabolic Acidosis
    ABGs, Sodium Bicarbonate administration
    Decreased serum CO2 levels and decreased pH.
  • Renal Replacement
    Dialysis
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25
Q

AKI prevention

A

AKI early identification
Prevent dehydration
Avoid hypotension
Limit exposure to nephrotoxins
Adequate fluid administration:Avoid over diuresis, maintain MAP, caution with nephrotoxic agents & IV contrast
Preserve renal function
Prevent complications
Balance FVE and FVD

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26
Q

Nutrition Therapy in AKI

A

High carbohydrate diet (limit fat intake d/t ketone production)
So carbs are used for energy, then protein can be used for tissue and muscle needs
Protein- very individualized
Limited to needed only, then increased when in diuretic phase

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27
Q

Nursing Management of AKI

A
  • All Types
    Monitor urine output and total I/O
    Weigh daily
    Cardiac monitoring
    ABG interpretation
  • Prerenal
    Administer IVF, blood products
  • Intrarenal
    Restrict fluids, renal diet
    Limit nephrotoxins (NSAIDs, chemo, contrast, aminoglycosides, etc.)
  • Postrenal
    Perform bladder scans, administer urine flow medications (tamsulosin, finasteride)
28
Q

Rhabdomyolysis

A
  • Toxic syndrome caused by the release of myoglobin from skeletal muscle
    Causes AKI
    Can cause intra-renal injury or ATN
  • Traumatic
    Crush injuries, burns, electrocution, falls with long down time
  • Non-traumatic
    Illicit drugs, heat stroke, medications (i.e. statins), malignant hyperthermia
29
Q

Rhabdomyolysis clinical characteristics

A
  • Muscle cramps, weakness and dark (tea-colored) urine
  • Increased serum creatine kinase
    Indicative of muscle injury or disease
  • Increased myoglobin
  • Increased BUN/Creatinine, potassium
  • AKI
30
Q

Rhabdomyolysis treatment & nursing management

A

-IVF, dialysis
-Monitor lactate Levels, CK, BUN/Creat, potassium
-Cardiac monitor, frequent VS, I/O

31
Q

Acute Tubular Necrosis causes

A
  • Ischemia:Pre-renal causes (shock)
  • Nephrotoxins:
    Antibiotics
    Heavy metals
    Poisons
    Anesthetics
    Radiopaque Contrast Dye
    Heme pigments:
    Myoglobin Rhabdomyolysis: Released from muscle tissue caused by damage
    Hemoglobin Intravascular hemolysis:blood transfusion reactions
32
Q

Acute Tubular Necrosis (ATN) characteristics

A
  • ATN is an AKI caused by damage to the kidney tubules
    -Damaged cells of epithelial tubules, kidney structures are damaged/ destroyed
    Tubules=tiny ducts that filter blood
    Epithelial cells take 7-21 days to regenerate
  • Most Common intrinsic AKI
  • ATN impairs release of ADH
  • U/A- Muddy brown casts present
33
Q

ATN Acute Tubular Necrosis treatment and Nursing management

A

Same as intrarenal failure
-Support, IVF, avoid nephrotoxins, treat complications

34
Q

Contrast Induced AKI

A

Contrast (IV, PO, PR) is used in a wide variety of diagnostic imaging.
Contains Iodine or gadolinium (gad) Molecular structure (3 ring) for tissue differentiation
Agents higher than blood osmolality (275-299 mOsm/kg) are hyperosmolar and can cause shifts of both solutes and water in a variety of organs – especially the KIDNEYS

35
Q

Renal Replacement Therapy

A

Needed when the pathologic changes of stage 4 and 5 CKD are life threatening or pose continuing discomfort to the patient

When conservative therapies such as diet, drugs, and fluid restrictions are no longer effective alone

Transplantation may be discussed at anytime

HD/CRRT or PD

36
Q

Hemodialysis (HD)

A

Most common renal replacement therapy used with ESKD & renal failure

Dialysis removes excess fluids and waste products and restores chemical and electrolyte balance

Passes patient blood through an artificial semipermeable membrane to perform the filtering and excretion functions of the kidney

37
Q

HD Vascular Access: Permanent

A

AV Fistula: An internal anastomosis of an artery to a vein– located in Forearm– needs to mature for 2-4 months or longer
AV Graft: Synthetic vessel tubing tunneled beneath the skin, connecting and artery and a vein– Located in forearm, upper arm, inner thigh– needs to mature for 1-2 weeks

38
Q

HD Vascular Access: Temp

A
  • HD Catheter: Dual or Triple Lumen- Inserted in Subclavian, internal jugular, or femoral vein: can be used immediately after insertion- need chest x-ray to confirm placement
  • Subcutaneous Device: An internal device with two metallic access ports and two catheters inserted into large central veins: Located in Subclavian– Can be used immediately after insertion
39
Q

HD Vascular Access nursing concerns

A

Limb alert
assessments: Bruit (swish heard)
Thrill (vibration felt)

40
Q

HD Nursing Care

A
  • Medications can be dialyzed out with HD and should not be administered just before or during HD
  • Vasoactive drugs can cause hypotension during HD (nitroglycerin, nitroprusside, etc.)
  • Coordinate meds with physician & HD RN
  • Post HD:
  • Monitor for s/s of side effects from treatment
  • Most common problems include:
    Hypotension
    h/a
    N/V
    Malaise
    Dizziness
    Muscle cramps
41
Q

Complications of HD

A
  • Dialysis Disequilibrium Syndrome (fluid volume shifts)
    -Cerebral edema and increased ICP
    -Neurological symptoms (h/a, n/v, restlessness, decreased LOC, seizures, coma, or death)
    -Hypotension (circulatory collapse)
42
Q

Peritoneal Dialysis information

A

Allows exchange of wastes, fluids, and electrolytes to occur in the peritoneal cavity

Slower than HD

Less hazardous

CKD patients can select HD or PD

PD is great for patients who are difficult to obtain vascular access on, can’t tolerate anticoagulation, who are unstable, and those with a chronic infection

Not a treatment for AKI

43
Q

Peritoneal Dialysis process

A

Sterile dialysate (1-2L) is introduced into the peritoneal cavity via an abdominal catheter and waste ducts are cleared by diffusion and osmosis

44
Q

Contraindications to Peritoneal Dialysis (PD)

A

peritoneal adhesions
extensive intra-abdominal surgery

45
Q

Complications of PD (peritoneal dialysis)

A

Peritonitis (inflammation of peritoneum)- most common
60-80% of long-term pts
Cloudy dialysate drainage, diffuse abdominal pain, and rebound tenderness
Tx: antibiotics, heparin, maybe removal of catheter

46
Q

Stomach & small intestine are ___

A

acidic

47
Q

Large intestine is ___

A

alkalotic

48
Q

What makes up the small intestine?

A

Duodenum, jejunum, ileum

49
Q

what makes up the large intestine

A

cecum, ascending colon, transverse colon, sigmoid

50
Q

Reabsorbs water, passages of wastes, neutralizes contents

A

Large Intestine

51
Q

an acute abdominal pain (non-traumatic), if not treated, is ____

A

life threatening

52
Q

Causes for acute abdominal pain

A

bowel obstruction (large or small)
appendicitis
diverticulitis

53
Q

Complications of acute abdominal pain

A

peritonitis
sepsis and septic shock

54
Q

Primary peritonitis

A

spontaneous bacterial peritonitis (ie PD catheter)

55
Q

Secondary peritonitis

A

perforated organs that leak contents (ie diverticulitis, trauma, infection. ingestion of sharp object)

56
Q

tertiary peritonitis

A

immunocompromised infection (chemo/aids/hiv)

57
Q

Peritonitis complications

A

Immediate hypermotility followed by paralytic ileus (consider bowel sounds)
* Peristalsis slows or stops in response to the inflammation
* Toxins and wastes enter the Abdominal cavity and can enter the blood stream
* Causing Sepsis and SEPTIC SHOCK
* Fluid backs up in the small intestine causing dilation and can leak into the abdominal cavity
* Air and Fluid collect in the Bowel

58
Q

peritonitis causes

A

Bacteria or chemicals entering the abdominal cavity causing widespread inflammation
* Fluid shifts from intestinal ECF to abdominal cavity, causing hypovolemia -HYPOVOLEMIC
SHOCK (consider risks r/t FVD)
* Bowel or appendix perforation, peritoneal dialysis contamination, leaked pancreatic enzymes

59
Q

Peritonitis clinical manifestations

A

Pain
* Mimics disorder causing the problem
* Begins as diffuse abdominal pain that transitions to constant, localized and increasing intensity
* Rebound tenderness and extremely distended abdomen
* Very Rigid, board like abdomen
* Anorexia, nausea and vomiting
* Increased abdominal pressure causing vena cava flattening, gut ischemia, ARF/anuria, worsening acidosis, difficulty ventilating
* Normal 0-5mmHg
* Diminished peristalsis with eventual Ileus
* Decreased or absent bowel sounds and absence of flatus and feces
* Tachycardia
* Hypotension (decreased CO)
* Fever
* Sepsis, hypovolemia, shock

60
Q

Peritonitis assessment and dx

A

Radiology: Abdominal Xray and CT Scan showing free air, bowel dilation and distension, bowel inflammation or edema/fluid in
the abdomen, abscesses
* Labs: Increased WBCs, disturbances in potassium, sodium and chloride

61
Q

Peritonitis Medical Management

A
  • NPO
  • Isotonic IVF-many LITERS
  • Pain management
  • Opioids
  • Electrolyte replacement
  • r/t AKI from decreased CO
  • Antibiotics
  • E.Coli, Klebsiella, Pseudomonas, Streptococcus
  • Broad spectrum until causative agent determined
  • Semi- Fowlers position
  • NG/OG tube to decompress the abdomen
  • Surgery: REPAIR CAUSE
  • Laparotomy
  • Pre/intra/post-op care needed
  • Drains and wound care
62
Q

Appendicitis pathophysiology

A

Inflamed and edematous appendix
* Occlusion caused by stool, foreign body or infectious material
* Causes ischemia and bacterial impedance
* Gangrene
* Perforation
* Appendix ruptures and contents can center peritoneum
* Occurs with 6 to 24 hours of appendicitis
* Most common complication: peritonitis

63
Q

appendicitis clinical manifestations

A

Constant pain that progresses to RLQ pain (McBurney’s Point)
* Rebound tenderness
* Rovsing’s Sign- push on LLQ & pain occurs in RLQ
* n/v
* Anorexia
* Fever

64
Q

Appendicitis assessment and dx

A

increased WBC, increased C-Reactive Protein (released from liver in response to
inflammation)
* Ultrasound showing enlarged appendix, CT scan
* Surgical Intervention (exploratory)
* Drainage of abscess
* Removal of appendix (appendectomy)

65
Q

TPN- Total Parenteral Nutrition

A

Intensive and complete nutrition supplement
* Hypertonic Solution with dextrose, minerals,
electrolytes, protein
* Given via a central line
* Monitor I/O, monitor blood glucose

66
Q
A

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