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NURS 2003 > Week 9 > Flashcards

Week 9 Flashcards

1
Q

What is the most common bacterial infection in women?

A

UTIs

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2
Q

What is asymptomatic bacteriuria?

A

Bacteria that colonizes in the bladder but does not cause any problems.

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3
Q

What are some risk factors for renal calculi?

A
  • Family/ personal history
  • dehydration,
  • people who live in warmer climates.
  • diets high in protein, salt, and sugar.
  • Obesity
  • Digestive disease/ surgery
  • hyperparathyroidism, frequent UTIs
  • Vitamin C supplements, calcium antiacids etc.
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4
Q

What lab number indicates a clinically significant UTI?

A

10^5

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5
Q

What is the most common bacteria that causes a UTI?

A

E.Coli

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6
Q

What factors contribute to urinary calculi formation?

A

Metabolic, dietary, genetic, climatic, lifestyle, occupational influences.

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7
Q

The lower the pH the ____ soluble ____ acid and cystine are.

A

less; uric.

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8
Q

The _____ the pH the ____ soluble calcium and phosphate are.

A

higher; less.

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9
Q

What is a calculus?

A

Abnormal stone formation in the body tissues by an accumulation of mineral salts. stone in the urinary tract.

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10
Q

What are the 5 major categories of stones?

A
  1. Calcium Phosphate
  2. Calcium oxalate
  3. Uric Acid
  4. Cystine
  5. Struvite
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11
Q

What is the most common type of stone?

A

Calcium, 35-40% incidence rate. More frequent in men. Small.

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12
Q

What are some CM of urinary calculi?

A

Stones cause CM when the obstruct urinary flow. Common site is UPJ (where the ureter crosses the iliac vessels) and UVJ.

  • Flank Pain
  • hematuria
  • renal colic
  • nausea, vomiting
  • UTI
  • chills
  • fever
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13
Q

What are some diagnostic studies used to diagnose renal calculi?

A

Urinalysis, urine culture, IVP, retrograde pyelogram, ultrasound, cytoscopy. BUN and creatinine may be taken to assess renal function.

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14
Q

What are some ways to treat UTC?

A

Surgery (if stones are too large for spontaneous passage, stones associated with bacteria, stones causing impaired renal function, stones cause persistent pain, nausea or ileus, patient with one kidney).
Nutritional therapy may also be used.

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15
Q

Describe nutritional therapy used to manage UTC.

A

Limit oxalate. Avoid dehydration.

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16
Q

What is acute kidney injury?

A

An abrupt decline in kidney function, causing a rise in serum creatinine or a reduction in urine output or both.

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17
Q

What is the RIFLE criteria?

A

A classification system that is used to determine the 5 stages of AKI/CKD.
Risk: increased creatinine x 1.5
Injury: Increased creatinine x2.
Failure: Increased creatinine x3.
Loss: Persistent AKI = complete loss of renal function in less than 4 weeks.
E: End-Stage Renal Disease.

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18
Q

What are prerenal causes of AKI?

A
  • Reduction in systematic circulation causing a decrease in renal blood flow, leading to decreased glomerular perfusion.
  • Hypovolemia
  • Decreased CO
  • Decreased peripheral vascular resistance
  • ACE inhibitors
  • Angiostensin receptor blockers
  • Large amounts of dopamine
  • Large amounts of Epinephrine
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19
Q

What does a decrease in circulating blood volume do?

A

It causes autoregulatory mechanisms that increase angiostensin 2, aldosterone, norepinephrine, and antidiuretic. Prerenal AKI causes salt and water retention
and decreased urine output.

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20
Q

What happens when prerenal failure is prolonged?

A

It can cause intrarenal damage, resulting in acute tubular necrosis.

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21
Q

What are intrarenal causes?

A

Conditions caused by direct damage to the kidneys, resulting in impaired nephron function. Nephrotoxins, hemoglobin (released by hemolyzed RBCs), and myoglobin from necrotic muscle cells contribute to intrarenal causes.

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22
Q

What do nephrotoxins do to cause renal damage?

A

Cause obstruction of intrarenal structures by crystallization, or by damaging the epithelial cells of the tubules.

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23
Q

How does hemoglobin and myoglobin damage the nephrons?

A

Hemoglobin and myoglobin block the nephrons causing renal vasoconstriction.

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24
Q

What is acute tubular necrosis (ATN)?

A

Most common intrarenal cause of AKI. Result of renal ischemia, nephrotoxins, or sepsis.

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25
Q

What does renal ischemia do to the basement membrane and tubular epithelium?

A

It causes destruction of the basement membrane, and patchy destruction of the epithelial cells.

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26
Q

When is ATN reversible?

A

If the basement membrane is not destroyed and the tubular epithelium regenerates.

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27
Q

What are the clinical manifestations of ATN in the initiation phase?

A

Increase in serum creatinine and BUN, decrease in UO.

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28
Q

What are the CM of ATN in the maintenance phase?

A

Changes in UO, fluid and electrolyte abnormalities, and uremia. Oliguria is the most common manifestation.

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29
Q

Why does fluid volume excess happen in AKI?

A

UO decreases, fluid retention occurs. Edema and hypertension may occur.

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30
Q

Why does metabolic acidosis occur in AKI?

A

In AKI, kidneys can’t synthesize ammonia, leading to an excess in H+ ions. Serum bicarbonate levels decrease because it is being used up to balance out the positive ions.

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31
Q

Why does a sodium balance occur?

A

Damaged tubules cannot conserve sodium. Excessive sodium intake can cause volume expansion, hypertension, and HF. Hyponatremia or water excess can cause cerebral edema.

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32
Q

Why does hyperkalemia occur?

A

The kidneys are unable to excrete potassium due to their inability to regulate potassium.

33
Q

Why do hematological disorders occur?

A

Anemia- decreased erythropoietin production.

Uremia- decreases platelet adhesiveness.

34
Q

Why does a Ca and phosphate imbalance happen?

A

Decrease in activated vit D, causes a decrease in Ca absorption. This causes an increase in parathyroid hormone, leading to bone demineralization. This causes an increase in phosphate, which is worsened by damaged kidneys.

35
Q

Why does waste accumulate in the blood?

A

When kidney’s are damaged, they don’t do their job, hence why waste builds up in the blood.

36
Q

Why do neurological symptoms occur?

A

A build up of urea can cause fatigue, difficulty concentrating, seizures, stupor, and coma. Urea can cross the blood brain barrier.

37
Q

What is the recovery phase of AKI?

A

BUN and creatinine levels return to normal, as well as the GFR. Patients may experience a diuretic phase, where there kidneys figure out how to excrete water again, this may cause electrolyte abnormalities until the kidneys figure out how to concentrate urine.

38
Q

What are the diagnostic studies used to diagnose AKI?

A

Urinalysis (look for casts, cells, protein), renal ultrasound (info about anatomy and function), CT (ID lesions).

39
Q

What are some treatments of AKI?

A

Treat percipitating cause, fluid restriction, nutritional therapy (K+, Na, PO4 restrictions) Ca supplements, enteral nutrition, RRT.

40
Q

What is chronic kidney disease (CKD)?

A

Progressive, irreversible loss of kidney function. Characterized by a GFR of less than 60mL for more than 3 months.

41
Q

What characterizes end-stage renal disease?

A

GFR less than 15 mL. Requires RRT.

42
Q

What is the leading cause of CKD?

A

Diabetes.

43
Q

What are the clinical manifestations of CKD?

A

Uremia, waste product accumulation, altered carb metabolism, elevated triglycerides, electrolyte imbalances, anemia, infection.

44
Q

What is uremia?

A

Increased urea in the blood. Characterized by elevated serum creatinine and BUN, electrolyte imbalances, acidosis, anemia, fluid volume excess, nausea, loss of appetite, fatigue, decreased cognition, pruritis, neuropathy.

45
Q

why does serum creatinine increase?

A

The kidney’s are unable to excrete ammonia, so the creatinine increases.

46
Q

Why does altered carb metabolism occur?

A

Caused by impaired glucose from cellular insensitivity tp insulin. Kidney’s excrete insulin, so insulin levels may appear normal with renal failure.

47
Q

Why are the triglycerides elevated?

A

Hyperinsulemia stimulates hepatic production of triglycerides. CKD also decreases lipoprotein lipase.

48
Q

Why are magnesium levels altered?

A

Mg is excreted by kidneys, sometimes used as a phosphate binding agent. Hypermagnesemia typically not a problem.

49
Q

Why does anemia occur?

A

Normocytic, normochromic anemia is a result of decreased production of erythropoietin, which causes a decrease in RBC production. Elevated PTH also inhibits erythropoiesis.

50
Q

Why do bleeding tendencies occur?

A

Dysfunction in platelet aggregation occur because of uremia.

51
Q

Why does infection occur in patients with CKD?

A

Caused by changes in leukocyte function, and altered immune system. Cellular and humoral responses are suppressed. Malnutrition, hyperglycemia, and external trauma cause increased infection as well.

52
Q

What are the cardiovascular effects of CKD?

A

Hypertension- result of increased CO, worsened by Na retention. Causes retinopathy, encephalopathy, nephropathy.
HF- occurs from left ventricular hypertrophy, leads to pulmonary edema.
Cardiac Dysrythmias- result of hyperkalemia, hypocalcemia, decreased coronary artery perfusion.

53
Q

What are the respiratory effects of CKD?

A

Dyspnea- fluid overload, pulmonary edema, uremic pleuritis, pleural effusion.

54
Q

What are the GI effects of CKD?

A

Inflammation of GI mucosa as a result of excess uremia.

Diabetic gastroparesis, GI bleeding, constipation, malnutrition.

55
Q

What are the neurological effects of CKD?

A

High levels of uremic toxins cause axonal damage. CNS depression causes lethargy, apathy, difficulty concentrating, fatigue, irritability, altered mental ability, neuropathy.

56
Q

What is chronic kidney disease-mineral and bone disorder?

A

Clinical syndrome that is a result of electrolyte imbalances. Kidney function declines, leading to an increase in phosphorous in the blood system. Lack of activated Vit D causes a decrease in Ca. This leads to an increase in PTH, which causes bone demineralization.

57
Q

What causes overstimulated parathyroid glands?

A

Hyperphosphatemia, decreased vit D and hypocalcemia.

58
Q

What is renal osteodystrophy?

A

Skeletal disorder causing osteitis fibrosa (increased number of osteoclasts and osteoblasts, high bone turnover), osteomalacia (low bone turnover, abnormal mineralized bone) and dynamic bone disorder (low bone turnover with normal mineralization) and mixed osteodystrophy (high bone turnover, abnormal mineralization)

59
Q

what are the extracellular complications of CKD-MBD?

A

Soft tissue calcification. Excess phosphate and calcium. bind causing formation of insoluble deposits in vascular walls and soft tissue.

60
Q

What happens to the integumentary system?

A

Pruritis (itching) develops as a result of dry skin, calcium, and sensory neuropathy.

61
Q

What happens to the reproductive system as a result of CKD?

A

Infertility and decreased libido may occur. Decreased levels of estrogen, progesterone, and LTH cause menstrual changes. Men experience loss of testicular consistency decreased testosterone levels, and low sperm counts.

62
Q

What diagnostic studies are used to diagnose CKD?

A

BUN, serum creatinine, eGFR, CT scan, history, renal biopsy, renal scan, renal ultrasound, serum electrolytes, serum hemoglobin, urinalysis, urine culture.

63
Q

What are some collaborative therapies for CKD?

A

Adjust drug doses, antihypertensive therapy, Ca supplementation, correction of EFV or deficit. Erythropoietin therapy, nutritional therapy, RRT.

64
Q

What are some nutritional therapy strategies for CKD?

A

Protein restriction, Na and Fluid restriction, K+ restrictions, phosphate restriction.

65
Q

What is dialysis?

A

Movement of fluid and molecules across a semipermeable membrane from one compartment to another. Used to correct fluid and electrolyte imbalances, remove waste products in renal failure.

66
Q

What is peritoneal dialysis?

A

Method of removing waste products and excess fluid volume using the peritoneum as a filter. Dialysis fluid is infused through the peritoneal cavity, it is filtered then the waste is drained and discarded.

67
Q

What is hemodialysis?

A

Waste products and excess fluid are removed from the blood using a machine and pump outside the body.

68
Q

What are the 3 phases of PD?

A

Inflow, dwell and drain. Collectively called an exchange. Dialysis prescription is tailored to patients needs.

69
Q

What is automated peritoneal dialysis?

A

Done while pt sleeps, device called cycler used to perform dialysis exchanges. Patient is disconnected in the morning and leaves fluid in abdomen during the day.

70
Q

What is continuous ambulatory peritoneal dialysis?

A

Done during the day, consists of 4 exchanges, carried out manually.

71
Q

What are the contradictions of PD?

A
  1. Abdo surgical procedures may cause severe pathological conditions.
  2. Hernias
  3. Excessive obesity.
  4. Vertebral disease
  5. COPD.
72
Q

what are some complications of PD?

A

Exit site infection, peritonitis, abdo pain, outflow pains, hernias, lower back problems, bleeding, pulmonary complications, protein loss, carb and lipid abnromalities.

73
Q

What is arteriovenous fistulas

A

The prefered HD access, created surgically by connecting a vein to an artery.

74
Q

What is an arteriovenous graft?

A

HD access site created with a synthetic graft attached to an artery and a vein.

75
Q

What are central venous catheters?

A

When access is desperatly needed, a CVC may be placed temporarily to give access for dialysis.

76
Q

What are the complications of HD?

A

Hypotension, muscle cramps, loss of blood, hepatitis, sepsis, disequilibrium syndrome.

77
Q

What is continuous renal replacement therapy?

A

Alternative or adjunct method for treating CKD/AKI. Remove uremic toxins and fluids while adjusting acid-base status and electrolytes slowly and continuously.

78
Q

What is kidney transplantation?

A

Kidney is transplanted from one person to another. The donor can be either alive or dead. May cause some ethical issues. Typically survival is pretty good. Not used as much due to availability of organs.

NURS 2003 (12 decks)

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