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NURS 2514 > 3 - Urinary Elimination + Chronic Kidney Disease > Flashcards

3 - Urinary Elimination + Chronic Kidney Disease Flashcards

1
Q

What is uremia? What causes uremia?

A

Uremia is a complex group of signs + symptoms resulting from the buildup of waste products + excess fluid associated w kidney failure.

Uremia can be caused by retained fluids, abnormal electrolytes, buildup of waste products and hormones, increased BMR, increased blood lipiproteins, acidosis, anemia, etc.

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2
Q

What is oliguria?

A

Diminished urine volume of less than 400 mL in 24 hrs

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3
Q

What is anuria?

A

Absence of urine production

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4
Q

What is pleural effusion?

A

Collection of fluid in the pleural space

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5
Q

What is thrombocytopenia?

A

Drop in platelet count below 150 x 10^9 mmoL / L

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6
Q

What is azotemia?

A

When nitrogen waste products that are normally excreted by the kidneys accumulate in the blood - such as blood urea nitrogen + creatinine

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7
Q

What is encephalopathy?

A

General term describing a disease affecting the function or structure of your brain

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8
Q

What is ecchymosis?

A

Bruising

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9
Q

What is stomatitis?

A

Inflammation of the mouth + lips

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10
Q

What is hyperparathyroidism?

A

Condition involving increased secretion of parathyroid hormone

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11
Q

What is paresthesia?

A

Burning / prickling / tingling / numbing sensation usually felt in the hands, arms, legs and feet

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12
Q

What is proteinuria?

A

Protein in the urine

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13
Q

What is uremic frost?

A

Manifestation of severe azotemia

Tiny, yellowish-white urea crystals are deposited on the skin which results in a frosted appearance as sweat evaporates.

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14
Q

What is renal osteodystrophy?

A

A disorder of the bones associated with chronic kidney disease that includes a number of skeletal disorders including:

  • osteitis fibrosa
  • osteomalacia
  • adynamic bone disorder
  • mixed osteodystrophy
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15
Q

What is acute tubular necrosis (ATN)?

A

Intrarenal kidney injury - necrosis of the renal rubular cells as a result of chronic ischemia, nephrotoxins, or sepsis.

The most common cause of acute kidney injury.

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16
Q

What is asterixis?

A

Manifestation of hepatic encephalopathy

Flapping tremors (“liver flap”) commonly affecting the arms and hands - looks like a birdie “flapping its wings”

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17
Q

What is dialysis? What is it used for?

A

Dialysis is the mvmt of fluid and molecules across a semipermeable membrane from one compartment to another - used to correct fluid + electrolyte imbalances and to remove waste products in renal failure. Also used to treat drug overdoses.

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18
Q

Do all patients with chronic kidney disease receive dialysis treatments?

A

No. CKD pts only receive dialysis when their symptoms, fluid volume status, or both, can no longer be maintained w/o it.

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19
Q

What are the 2 types of dialysis?

A

Hemodialysis and peritoneal dialysis

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20
Q

What is hemodialysis?

A

Hemodialysis is a type of dialysis that uses a machine to remove waste products and excess fluid from the body by pumping the blood through an artificial semipermeable membrane (called a dialyser)

Blood moves to dialyser outside the body –> back to body

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21
Q

What is an arteriovenous fistula (AVF)?

A

Preferred hemodialysis access - created by the surgical connection of a vein + artery [usually] in the forearm

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22
Q

What is peritoneal dialysis?

A

Occurs inside the body - uses the peritoneum (a natural semi-permeable membrane)

Dialysis fluid is infused into the peritoneal cavity - excess fluid + waste products pass across the membrane into the fluid which is then drained + discarded.

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23
Q

What is pericarditis?

A

Inflammation of the pericardial sac

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24
Q

How often does a pt on hemodialysis receive treatment?

A

treatment occurs 3x a week - 4hrs per session

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25
Q

How often does a patient on peritoneal dialysis recieve treatment?

A

Treatment takes 20-30 mins

  • CAPD: 4 exchanges per day
  • APD: attach to machine before bed, machine does exchanges for 7-10 hrs
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26
Q

What are the advantages of peritoneal dialysis?

A
  • fewer dietary restrictions than hemodialysis
  • home dialysis possible
  • less CV stress
  • less complicated than hemodialysis
  • portable system w CAPD
  • preferable for diabetic patient
  • relatively short training time
  • usable in pt w vascular access problems
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27
Q

What are the disadvantages of peritoneal dialysis?

A
  • contraindicated in pts w multiple abdominal surgeries, traume, unrepaired hernia
  • catheter can migrate
  • protein loss into dialysate
  • risk for aggravated dyslipidemia
  • risk for bacterial or chemical peritonitis
  • risk for exit-site and tunnel infections
  • risk for hyperglycemia
  • risk for self-image problems w catheter placement
  • surgery required for catheter placement
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28
Q

What are the advantages of hemodialysis?

A
  • effective potassium removal
  • home dialysis
  • less protein loss than w peritoneal dialysis
  • lowering of serum triglycerides
  • rapid fluid removal
  • rapid removal of urea + creatinine
  • temporary access can be placed at bedside
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29
Q

What are the disadvantages of hemodialysis?

A
  • added blood loss contributes to anemia
  • dietary + fluid restrictions
  • expensive equip necessary
  • heparinization may be necessary
  • hypotension during dialysisd
  • longer training time for home hemodialysis
  • self-image problems w permanent access
  • specially trained personnel necessary if in-centre option chosen
  • surgery for permanent access placement
  • vascular access problems
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30
Q

Define elimination

A

the excretion fo waste products primarily through the urinary system (pee) and the GI system (poo)

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31
Q

What are the 5 major roles of the kidneys?

A

1) filter metabolic wastes from the blood + excrete them from the body in the urine
2) regulate blood volume + blood pressure
3) produce erythropoietin in response to low blood O2 levels
4) regulate the amt of electrolytes in the blood + ECF by altering the urine conc and composition
5) regulat body’s pH by controlling the amt of H+ secreted and HCO3-

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32
Q

What is urea?

A

Metabolic waste - non-toxic byproduct that comes from the detoxification of ammonia

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33
Q

What is uric acid?

A

Metabolic waste - byproduct of the catabolism of DNA/RNA

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34
Q

What is creatinine?

A

By-product from the breakdown of creatinine phosphate

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35
Q

What can we test for in the blood to get an estimate of how well our kidneys are filtering?

A

urea + creatinine

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36
Q

How do the kidneys regulate blood volume + blood pressure?

A

By altering the volume of urine produced

Release the enzyme renin when they feel like they are not getting enough blood –> activates angiotensin II which promotes vasoconstriction + aldosterone secretion

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37
Q

What is the role of aldosterone in controlling urine volume?

A

Aldosterone tells the kidney to retain sodium + water - therefore producing a smaller urine output

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38
Q

Describe the position of the kidneys in the body

A

Retroperiotoneal position - partially protected by the lower ribs

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39
Q

Where do the kidneys receive blood from? Where do they return it to?

A
  • the kidneys receive blood from the renal arteries

- return their “cleansed” blood to the inferior vena cava through the renal veins

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40
Q

What covers the kidneys?

A

Each kidney is covered by a fibrous capsule + layer of adipose tissue.

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41
Q

Are there any pain receptors within the kidney? When is pain felt in the kidneys?

A

There are no pain receptors within the kidney - pain is only present when there is impingement on the renal capsule or ureter.

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42
Q

What is the medulla? What is its role?

A

The medulla is the inner part of the kidney - alters the composition of the filtrate + forms urine

Within the medulla are triangular shaped “medullary pyramids” - which is where urine is made

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43
Q

After urine is made in the medullary pyramids, how does it exit the body?

A
  • collects in the renal calyces
  • coalesces in the renal pelvis
  • travels down the ureter
  • urinary bladder
  • exits the body thru the urethra during contraction
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44
Q

What is the purpose of regulating the amt of blood that flows to the kidneys?

A

The purpose is to MAINTAIN FILTRATION - NOT to satisfy the metabolic needs of the tissue

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45
Q

How much blood do the kidneys receive per minute at rest?

A

The kidney’s receive 25% of the body’s cardiac output (1.3 L / min)

46
Q

What is the BP in the glomerular capillaries?

A

~ 55 mmHg

47
Q

What is glomerular blood pressure?

A

The driving force to create filtration

48
Q

How do we calculate glomerular blood pressure (BPg)?

A

BPg = BFg x Rg

BFg = blood flow thru the afferent arteriole

Rg = resistance to flow in the efferent arteriole

49
Q

How does afferent arteriolar dilation affect the BFg?

A

BFg increases w afferent arteriolar dilation

BFg decreases w/ constriction

50
Q

How does efferent arteriolar constriction affect the Rg?

A

Rg increases w constriction

Rg decreases w dilation

51
Q

What is the relationship between BPg and filtration?

A

When BPg increases, filtration increases

When BPg decreases, filtration decreases

52
Q

Where is the BP highest in the kidneys?

Where is the BP lowest in the kidneys?

A

BP is highest in the renal artery (~100 mmHg)

BP is lowest in the renal vein (0 mmHg)

53
Q

Order the following from highest to lowest BP.

  • afferent arteriole
  • efferent arteriole
  • glomerular capillary
  • renal artery
  • renal vein
  • intrarenal vein
  • peritubular capillary
A
  • renal artery
  • afferent arteriole
  • glomerular capillary
  • efferent arteriole
  • peritubular capillary
  • intrarenal vein
  • renal vein
54
Q

Describe the structure of the glomerular capillaries in terms of the cells they are comprised of and what they are covered + surrounded by.

A

Glomerular capillaries are comprised of endothelial cells which are covered by podocytes (epithelial cells). The glomerular capillaries are surrounded by the Bowman’s capsule

55
Q

Why are the endothelial cells that make up the glomerular capillaries fenestrated?

A

The endothelial cells have fenestrations (holes / pores) to aid in the filtration of the blood + increase their permeability

56
Q

What is the function of the macula densa cells of the distal tubule?

A

The macula densa cells sense changes in the concentration of the filtrate + dilate or constrict the arterioles as needed

57
Q

What is the function of the juxtaglomerular cells of the juxtaglomerular apparatus?

A

The juxtaglomerular cells secrete renin into the blood in response to a low BP or SNS stimulation.

58
Q

What is the glomerulus most commonly injured by?

A

The glomerulus is most commonly injured by immune complexes (antibody-antigen)

59
Q

Describe the difference between nephritic + nephrotic syndrome

A
  • if immune complexes are w/in the endothelial layer + therefore accessible to phagocytes (WBCs) - this is characteristic of nephritic syndrome; also blood in the urine
  • if immune complexes are w/in the epithelial cells (on the other side of the basement membrane) + not accessible to phagocytes (no WBCs) - characteristic of nephrotic syndrome; also no blood in the urine
60
Q

What is the GFR (glomerular filtration rate)?

What is the average GFR?

A

The glomerular filtration rate is the amt of blood plasma filtered through the capillaries in 1 minute.

Average GFR = 125 mL / min

61
Q

Identify the 3 factors that play a role in the regulation of the GFR

A

1) altering BPg (glomerular blood pressure)
2) increasing afferent dilation + efferent constriction (therefore increasing GFR)
3) decreasing flow + decreasing resistance (decreases GFR)

62
Q

Identify the 3 common manifestations of renal disease

A

1) elevated blood urea nitrogen (BUN)
2) elevated serum creatinine
3) failure to maintain Na+, K+, water, and acid base balance

63
Q

Identify the 4 common complications of renal disorders

A

1) HTN
2) symptoms of HF
3) peripheral edema
4) death

64
Q

What is the peritoneum?

A

The peritoneum is the layer of CT surrounding the GI tract

65
Q

Why is the medulla susceptible to ischemic damage?

A

B/c it is very metabolically active + there is a low oxygen tension

66
Q

What is prerenal disease? Provide some examples of prenal diseases.

A

Prerenal diseases are diseases that result from inadequate blood flow to the nephron. Examples include:

  • hypovolemia
  • hypotension
  • drug-induced reduction in perfusion
  • septic shock
  • stenosis of renal arteries
67
Q

What is intrarenal disease? Provide some examples of intrarenal diseases.

A

Results from intrinsic damage to the nephron. Examples include:

  • acute tubular nexrosis
  • glomerulonephritis
  • nephrotic syndrome
  • vasculitis
  • maligant hypertension
  • diabetic nephropathy
  • pyelonephritis
68
Q

What is postrenal disease? Provide some examples of postrenal diseases.

A

Postrenal disease results from urinary tract obstruction. Examples include:

  • ureter obstruction
  • prostate disease
  • malignancy
  • calculi
69
Q

What are the 4 main ways in which we can manage renal failure?
What if anemia is present?
What if inflammation is present?

A

1) attempting to treat the cause
2) conservative dietary manipulation
3) dialysis
4) renal transplant

if anemia is present - erythropoietin is used to stimulate bone marrow production of red blood cells

if inflammation is present - anti-inflammatory drugs and / or corticosteroids are often used

70
Q

Describe the difference between acute kidney injury and chronic kidney disease in terms of their onset

A

aki: sudden
ckd: gradual, often over many years

71
Q

Describe the difference between acute kidney injury and chronic kidney disease in terms of their most common cause

A

aki: acute tubular necrosis
ckd: diabetic nephropathy

72
Q

Describe the difference between acute kidney injury and chronic kidney disease in terms of their diagnostic criteria

A

aki: acute reduction in urine output and / or elevation in serum creatinine

ckd: GFR < 60 mL / min / 1.73 m2 for > 3 mo
and / or kidney damage > 3 mo

73
Q

Describe the difference between acute kidney injury and chronic kidney disease in terms of their reversibility

A

aki: potentially reversible
ckd: progressibe + irreversible

74
Q

Describe the difference between acute kidney injury and chronic kidney disease in terms of their mortality rate

A

aki: high mortality rate (~ 60%)
ckd: 19-24%

75
Q

Describe the difference between acute kidney injury and chronic kidney disease in terms of their primary cause of death

A

aki: infection
ckd: CVD

76
Q

Identify the 2 psychological manifestations of chronic kidney disease

A

anxiety + depression

77
Q

Identify the 4 neurological manifestations of chronic kidney disease

A
  • fatigue
  • headache
  • sleep disturbances
  • encephalopathy
78
Q

Identify the 5 cardiovascular manifestations of chronic kidney disease

A
  • hypertension
  • heart failure
  • coronary artery disease
  • pericarditis
  • peripheral artery disease
79
Q

Identify the sole ocular manifestation of chronic kidney disease

A

hypertensive retinopathy

80
Q

Identify the 5 gastrointestinal manifestations of chronic kidney disease

A
  • anorexia
  • nausea
  • vomiting
  • GI bleeding
  • gastritis
81
Q

Identify the 3 pulmonary manifestations of chronic kidney disease

A
  • pulmonary edema
  • uremic pleuritis
  • pneumonia
82
Q

Identify the 4 endocrine / reproductive manifestations of chronic kidney disease

A
  • hyperparathyroidism
  • thyroid abnormalities
  • amenorrhea
  • erectile dysfunction
83
Q

Identify the 3 integumentary manifestations of chronic kidney disease

A
  • pruritis
  • ecchymosis
  • dry, scaly skin
84
Q

Identify the 2 metabolic manifestations of chronic kidney disease

A
  • carbohydrate intolerance

- hyperlipidemia

85
Q

Identify the 2 manifestations of peripheral neuropathy as a result of chronic kidney disease

A
  • paresthesias

- restless leg syndrome

86
Q

Identify the 3 hematological manifestations of chronic kidney disease

A
  • anemia
  • bleeding
  • infection
87
Q

Identify the 3 musculoskeletal manifestations of chronic kidney disease

A
  • vascular and soft tissue calcifications
  • osteomalacia
  • osteitis fibrosa
88
Q

Describe the etiology of chronic kidney disease

A

CKD results from the gradual irreversible destruction of nephrons and loss of renal function. It results in an increased workload on the remaining nephrons, increased glomerular filtratrion presure (GFP), and hyperfiltration.

Hyperfiltration predisposes to fibrosis and scarring (glomerulosclerosis) and increases the rate of nephron destruction.

89
Q

Identify the 3 pathological stages of CKD

A
  1. reduced renal reserve
  2. renal insufficiency
  3. end-stage renal failure
90
Q

Describe the reduced renal reserve stage of CKD

A
  • up to 50% of nephrons can be lost w/o producing signs + symptoms
  • if the cause is not detected, damage will continue
91
Q

Describe the renal insufficiency stage of CKD

A
  • occurs when more than 20% of nephrons remain

- decreased GFR, reabs + secretion capacity - results in moderate azotemia such as elevated BUN

92
Q

Describe the end-stage renal failure of CKD

A
  • occurs when less than 20% of nephrons remain
  • GFR + tubular function are greatly reduced which result in:
    - oligura / anuria
    - marked azotemia
    - failure to concentrate urine
93
Q

Describe fluid, Na, and K imbalances as manifestations of CKD

A

sodium + volume overload are common in uremia

excess ingestion of sodium contributes to circulatory congestion, hypertension, ascites, edema, and weight gain

excess water can cause hyponatremia

also, a diminished reserve to conserve sodium and water during the time of loss (vomiting, diarrhea)

can lead to circulatory shock

hyperkalemia can become serious problem if GFR falls below 5 mL/min.

hemolysis, acidosis, and infection increase the risk of hyperkalemia

94
Q

Describe metabolic acidosis as a manifestation of CKD

A

occurs only moderately when GFR is greater than 20 mL/min – can be compensated by increased respirations

will become decompensated if GFR falls below 20 mL/min or if exposed to other acid loads (lactic acidosis, infection, pneumonia)

95
Q

Describe the bone + mineral manifestations of CKD

A
  • decreased activation of vit D results in decreased absorption of calcium from the gut and a fall in serum calcium levels

stimulates PTH secretion + bone breakdown to raise serum calcium

chronic acidosis contributes to bone breakdown

calcifications occur due to increased amts of calcium phosphate

96
Q

Describe the cardiovascular + pulmonary manifestations of CKD

A
  • symptoms of circulatory congestion, hypertension, and pulm. edema occur b/c of sodium + volume overload and hyperreninemia
  • irritation by uremic toxins can cause pericarditis
  • atherosclerosis is accelerated resulting in MI, stroke, and PVDF
97
Q

Describe the hematological manifestations of CKD

A
  • decreased prod of erythropoietin causes anemia
  • not corrected by dialysis - requires erythropoietin treatment
  • abnormal hemostasis + white cell function are also common in uremia, resulting in bleeding + immunosuppression
98
Q

Describe the neurological manifestation of CKD

A
  • sleep disorders
  • poor concentration
  • loss of memory
  • seizures
  • hiccups
  • twitching
  • coma
  • sensory peripheral neuropathy
99
Q

Describe the GI + skin manifestations of CKD

A
  • anorexia
  • N + V
  • bad breath (uremic fetor) when saliva enzymes breakdown urea into ammonium
  • skin changes - uremic frost + colour
100
Q

What is acute kidney injury (AKI)? What does it present as?

A

AKI represents a group of disorders that cause rapid deterioration in renal function resulting in azotemia.

AKI presents as rapidly rising BUN / creatinine and a diminished urine volume.

101
Q

What is one of the most common causes of AKI?

A

Sepsis

102
Q

Why are pts with pre-existing hypoperfusion at risk of developing AKI when they ingest NSAIDs or ACE inhibitors?

A

pts w pre-existing renal hypoperfusion (ex – HF, diabetes, renal stenosis) may develop AKI by ingesting NSAIDs or ACE inhibitors, as prostaglandins dilate the afferent arteriole and angiotensin II to constrict the efferent arteriole

103
Q

Describe the acute tubular necrosis as a manifestation of AKI

A
  • AKI will result in necrotic death of the tubule epithelial cells (acute tubular necrosis)
  • manifestations of AKI are a result of tubule obstruction by necrotic tissue. This increases the intratubular pressure and offsets the filtration pressure - results in a dramatic reduction of the GFR.
  • acute tubular necrosis results in a loss of tubular function and failure to concentrate urine
104
Q

Describe the initial signs / symptoms of AKI

A
  • elevated BUN + creatinine (AZOTEMIA) due to decreased GFR
  • oliguria caused by decreased GFR and / or tubule obstruction
  • hyperkalemia if the GFR is greatly reduced and there is significant acidosis
  • fatigue + malaise likely due to water intoxication (hyponatremia), hyperkalemia, acidosis, and elevated metabolic wastes
105
Q

Describe the later symptoms of AKI

A
  • if acute tubular necrosis occurs, there will be a low ratio of BUN:creatinine
  • dyspnea, orthopnea, rales + third heart sounds due to fluid overload
  • altered mental status when metabolic wastes accumulate in the blood
  • proteinuria, hematuria, and pyuria on urinalysis
106
Q

Identify 5 possible indications for dialysis

A

Acidemia (metabolic acidosis)

Electrolyte imbalances w EKG changes (hyperkalemia)

Intoxication from medication or infection r/t uremia

Overload of fluid (not responsive to diuretics)

Uremia complications such as pericarditis, encephalopathy, GI bleeding

107
Q

What are the potential complications of peritoneal dialysis?

A
  • adominal / back pain
  • outflow problems
  • hernias
  • protein loss
  • pulm complocations
  • infection
    • redness, tenderness, drainage at exit site
    • peritonitis
108
Q

what are the potential complications of hemodialysis?

A
  • hypotension
  • muscle cramps
  • loss of blood
  • sepsis
  • disequilibrium syndrome
109
Q

What should you assess if your pt is going for a HD treatment (pre + post dialysis?)

A

pre-dialysis

  • be aware of WHY your client is having dialysis
  • ensure their vitals are stable
  • review meds (some may be held)

post-dialysis

  • monitor LOC + mental status
  • monitor vital signs
  • auscultate heart + lung sounds
110
Q

Identify some nursing considerations you should make for a pt w/ an arteriovenous fistula

A
  • fistula must be protected from trauma + compression
  • monitor access site for signs of infection
  • no BP checks, venipuncture or IV on this arm
  • palpate for thrill + listen for bruit (turbulent blood flow)

NURS 2514 (10 decks)

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