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Med Surg > Kidney/Urinary > Flashcards

Kidney/Urinary Flashcards

1
Q

Phenazopyridine used for

A

UTI pain

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2
Q

Lower UTI (areas)

A

○ Cystitis (bladder)
○ Prostatitis (prostate)
○ Urethritis (urethra)

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3
Q

Upper UTI/Pyelonephritis (types)

A

○ Acute and chronic

○ Renal abscess and perianal abscess

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4
Q

S&S of a lower UTI

A 
Burning sensation during urination
Urinary frequency
Urgency (>Q3h)
Nocturia
Pelvic pain/back pain
Hematuria
Incontinence & delirium in older adults
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5
Q

S/S of upper UTI

A 
Chills
Fever
Leukocytosis
Bacteriuria
Pyuria
Low back pain
Flank pain
Nausea and vomiting
Headache
Malaise
Painful urination
Physical examination reveals pain and tenderness in the area of the costovertebral angle
**In addition, symptoms of lower urinary tract involvement, such as urgency and frequency, are common.
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6
Q

UTIs in older men

A

● The antibacterial activity of prostatic secretions that protect men from bacterial colonization of the urethra and bladder decreases with aging.
● The use of catheterization or cystoscopy in evaluation or treatment for prostatic hyperplasia or carcinoma, strictures of the urethra, and neuropathic bladder
● Confusion, dementia, or bowel or bladder incontinence.
● Most common cause of recurrent UTIs in older males is chronic bacterial prostatitis. Resection of the prostate gland may help reduce its incidence

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7
Q

UTIs in older women

A

● Women often have incomplete emptying of the bladder and urinary stasis.
● Due to the absence of estrogen, postmenopausal women are susceptible to colonization and increased adherence of bacteria to the vagina and urethra.
→ Oral or topical estrogen can be used to decrease incidence

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8
Q

What are renal calculi?

A

Formation of stones when concentration of calcium oxalate, calcium phosphate and uric acid increase.
Vary in size

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9
Q

Risk factors of renal calculi

A

Infection
urinary stasis
Immobility (slows kidney drainage)

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10
Q

Causes of renal calculi

A 
Hyperparathyroidism
Renal tubular acidosis
Cancers (e.g., leukemia, multiple myeloma)
Dehydration
Granulomatous diseases (e.g., sarcoidosis, tuberculosis), which may cause increased vitamin D production by the granulomatous tissue
Excessive intake of vitamin D
Excessive intake of milk and alkali
Myeloproliferative diseases such
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11
Q

Clinical manifestations of renal calculi

A

Depends on the location and presence of obstruction, infection or edema.

Obstruction = pressure
Infection = fever/chills
Edema = pain
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12
Q

Assessment and diagnosis of renal calculi

A

Dietary/medication history

Non contract CTBlood chemistry

24-hour urine test to measure calcium, uric acid, creatinine, sodium, pH, and total volume

Chemical analysis of stone

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13
Q

treatment for renal calculi

A

Goal is to eradicate the stone, determine the stone type, prevent nephron destruction, control infection and relieve obstruction

opioids, antispasmodics, NSAIDS, hot baths,, ureteroscopy, ECP shock water lithotripsy, percutaneous nephrolithotomy,

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14
Q

education of renal calculi

A 
● Signs and symptoms to report
● Follow-up care
● Urine pH monitoring
● Measures to prevent recurrent stones
● Importance of fluid intake
● Dietary education
Medication education as needed
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15
Q

Stomas should be

A

pink and moist

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16
Q

calcium stones

A

In the past, it has been recommended to restrict calcium in their diet. However, evidence has questioned this practice, except for patients with type II absorptive hypercalciuria (half of all patients with calcium stones), in whom stones are clearly the result of excess dietary calcium. Liberal fluid intake is encouraged. Medications such as ammonium chloride may be used, and if increased parathormone production (resulting in increased serum calcium levels in blood and urine) is a factor in the formation of stones, therapy with thiazide diuretics may be beneficial in reducing the calcium loss in the urine and lowering the elevated parathormone levels. Limit animal based protein and sodium intake. In calcium oxalate stone - limit foods high in oxalate.

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17
Q

Uric acid stones

A

the patient is placed on a low-purine diet to reduce the excretion of uric acid in the urine. Foods high in purine (shellfish, anchovies, asparagus, mushrooms, and organ meats) are avoided, and other proteins may be limited. Allopurinol (Zyloprim) may be prescribed to reduce serum uric acid levels and urinary uric acid excretion.

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18
Q

Ileal conduit

A

In the immediate postoperative period, urine volumes are monitored hourly. A urine output below 0.5 mL/kg/hr may indicate dehydration or an obstruction in the ileal conduit, with possible backflow or leakage from the ureteroileal anastomosis. A catheter may be inserted through the urinary conduit to monitor the patient for possible stasis or residual urine from a constricted stoma. The stoma is inspected frequently for color and viability. The patient and family are educated about how to apply and change the appliance so that they are comfortable carrying out the procedure and can do so proficiently. An average collecting appliance lasts 3 to 7 days before leakage occurs.

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19
Q

where is ADH manufactured?

A

hypothalamus

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20
Q

where is ADH stored?

A

posterior pituitary

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21
Q

functions of ADH

A

maintaining the osmotic pressure of the cells by controlling the retention or excretion of water by the kidneys and by regulating blood volume.

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22
Q

action of ADH

A

constricts blood vessels and reduces the excretion of urine by stimulating water resorption back into the bloodstream therefore increasing blood pressure

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23
Q

What is the function of RASS?

A

manages blood pressure by increasing low blood pressure and blood volume

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24
Q

What kind of cells release renin?

A

JG cells

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25
Q

what does renin do?

A

activates ANGIOTENSINOGEN in the liver and turns it into ANGIOTENSIN I

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26
Q

Where is ACE and what does it do?

A

in lungs and kidneys converts ANGIOTENSIN I to ANGIOTENSIN II

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27
Q

What happens when the adrenal cortex is stimulated to release aldosterone

A

INCREASES sodium/water reabsorption, DECREASING urine output and conserving fluid to maintain blood pressure.
Stimulates pituitary gland to release ADH (antidiuretic hormone)

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28
Q

what does ADH do?

A

Keeps in H20 and sodium to increase volume of blood

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29
Q

bladder capacity

A

300-500mL

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30
Q

overstretching of the bladder can lead to?

A

neurogenic bladder

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31
Q

urine specific gravity (lab value):

A

1.010-1.025

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32
Q

Urine pH (lab value):

A

4.5-8

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33
Q

anion gap (lab value):

A

8-12

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34
Q

Creatinine (lab value):

A

0.7-1.4

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35
Q

BUN (lab value):

A

10-20

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36
Q

Sodium (lab value):

A

135-145

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37
Q

potassium (lab value):

A

3.5-5

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38
Q

chloride (lab value):

A

98-106

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39
Q

bicarb (lab value):

A

24-31

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40
Q

pH (lab value):

A

7.35-7.45

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41
Q

CO2 (lab value):

A

35-45

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42
Q

glucose (lab value):

A

70-110

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43
Q

GRF (lab value):

A

125-200mL/min

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44
Q

BUN to creatinine ratio:

A

12-20 (15 optimal)

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45
Q

low BUN to creatinine ration means:

A

acute tubular necrosis, low protein intake, starvation, severe liver disease

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46
Q

High Bun to creatinine ratio means:

A

Pre renal disease, high protein intake, after GI bleed

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47
Q

high BUN to creatinine ration WITH raised creatine means:

A

post renal obstruction, pre renal uremia with renal disease

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48
Q

Why do we do 24 hour urine collections?

A

primary test of renal clearance used to evaluate how well the kidney performs this important excretory function.

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49
Q

How to do a 24 hour urine collection

A

● The client is initially instructed to void and discard the urine.

● The collection bottle is marked with the time the client voided.

● Thereafter, all the urine is collected for the entire 24 hours.

● The last urine is voided at the same time the test originally began.

● KEEP PEE ON ICE DURING COLLECTION

Midway through the collection, the serum creatinine level is measured.

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50
Q

Which drugs are nephrotoxic?

A 
Vancomycin
Amphotericin B
Metformin
NSAID'S
Contrast agents!!
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51
Q

Major causes of chronic kidney disease:

A 
○ Diabetes mellitus
○ Hypertension
○ Chronic glomerulonephritis
○ Pyelonephritis or other infections
○ Hereditary lesions
○ Vascular disorders
○ Medications or toxic agents
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52
Q

Required labs to diagnose CKD

A

GFR and Creatinine clearance

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53
Q

Persistent kidney injury

A

complete loss of kidney function >4 weeks

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54
Q

Acute kidney Injury RISK (GFR criteria):

A

GFR decrease >25%, creatinine increased 1.5x baseline and .5mL/kg/6 hours

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55
Q

Acute Kidney injury (GFR criteria):

A

creatinine increased 2x baseline, GFR decrease >50%, 0.5mL/kg/hr for 12 hours

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56
Q

Acute Kidney Failure:

A

increased creatinine 3x from baseline, GFR decreased >75%, <0.3mL/kg/hr for 24 hours OR anuria for 12 hours

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57
Q

End Stage Kidney Disease

A

ESKD >3 months

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58
Q

Kidneys and metformin:

A

increased risk for acute kidney injury and lactic acidosis with the use of iodinated contrast material for diagnostic studies; this drug should be stopped 48 hours prior to and for 48 hours after the use of contrast agent or until kidney function is evaluated and normal.

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59
Q

kidney disorder diet:

A

Low sodium
Low protein
High carbs
Increased water intake

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60
Q

describe glomerulonephritis?

A

Antigen-antibody complexes form in the blood and become trapped in the glomerular capillaries (the filtering portion of the kidney), inducing an inflammatory response.

61
Q

What is Glomerulonephritis

A

Inflammation of the glomerular capillaries

62
Q

Pathophysiology of glomerulonephritis:

A

Streptococcus infection puts patient at HIGH RISK

May be due to repeated episodes of acute nephritic syndrome, hypertensive nephrosclerosis, hyperlipidemia, chronic tubulointerstitial injury, or hemodynamically mediated glomerular sclerosis.

Kidneys are reduced to as little as ⅕ their normal size
Scar tissue distorts cortex
Rough and irregular surface of kidney
Scarring of glomeruli and tubules
Branches of renal arteries thicken
63
Q

clinical manifestations of glomerulonephritis:

A

May have no symptoms with severe disease and might be discovered with hypertension or elevated BUN/creatinine levels

Peripheral neuropathy with diminished deep tendon reflexes, neurosensory changes and pericarditis can occur late in the disease

64
Q

most patients with glomerulonephritis report:

A 
Loss of weight
Loss of strength
Increasing irritability
Nocturia
Headaches
Dizziness
GI disturbances
65
Q

Assessments/Diagnostics of glomerulonephritis:

A

Urinalysis to check specific gravity, protein and check for urinary casts
GFR
Chest x-ray (cardiac enlargement/pulmonary edema)
ECG (electrolyte abnormalities may show peaked T waves)
CT/MRI to show size of cortex

66
Q

Treatment of glomerulonephritis

A

Management of symptoms

Reduce BP with sodium/water restrictions and antihypertensives
Diuretics
Monitor daily weights
Dialysis
Plasmapheresis
67
Q

Polycystic Kidney Disease pathophysiology:

A

Characterized by the growth of numerous fluid-filled cysts in the kidneys, which destroy the nephrons.

**Can also cause cysts in the liver and problems in other areas, such as blood vessels in the

68
Q

Polycystic kidney disease as a genetic disease:

A

Autosomal dominant (most common)
Symptoms usually develop between 30-40 years of age
** half of patients develop CKD stage 5 and require renal replacement therapy

Autosomal recessive
rare inherited form
Symptoms begin in the earliest months of life or in utero.

69
Q

clinical manifestations of polycystic kidney disease:

A

Loss of renal function as cysts grow -

Hematuria
Polyuria (excessive urine production)
Hypertension
Development of renal calculi
Associated UTIs
Proteinuria
Abdominal fullness
Flank pain
70
Q

Assessments/diagnostics of polycystic kidney disease:

A

Family history
Palpation of abdomen (enlarged kidneys)
Ultrasound of kidneys

71
Q

treatments of polycystic kidney disease:

A

No cure

Supportive measures

Blood pressure control
Pain control
Antibiotics
Renal replacement therapy
Kidney donation
72
Q

pathophysiology of nephrotic syndrome:

A

Characterized by increased glomerular permeability and is manifested by massive proteinuria

73
Q

compilations of nephrotic syndrome:

A

Infection (due to a deficient immune response)
Thromboembolism (especially of the renal vein)
Pulmonary embolism
AKI (due to hypovolemia)
Accelerated atherosclerosis (due to hyperlipidemia).

74
Q

clinical manifestations of nephrotic syndrome:

A 
PENTAD
Edema
soft/pitting
Periorbital
Dependant areas
Proteinuria
Dyslipidemia
Lipiduria
Hypoalbuminemia
Increased risk of infection (loss of immunoglobulin/antibodies)
Ascites
Irritability
Headache
Malaise
75
Q

assessment/diagnostics of nephrotic syndrome:

A

Proteinuria >3.5g/day
Hallmark sign

Increased WBC in urine

Needle biopsy to confirm diagnosis

76
Q

treatment of nephrotic syndrome:

A

Treatment of underlying disease

Diuretics
ACE inhibitors
Lipid lowering agents

77
Q

dialysis techniques:

A

Hemodialysis
CRRT
Peritoneal dialysis

78
Q

Hemodialysis

A

prevents death but does not cure kidney disease and does not compensate for the loss of endocrine or metabolic activities of the kidneys

79
Q

when is hemodialysis used?

A

for patients who are acutely ill and require short-term dialysis for days to weeks until kidney function resumes and for patients with advanced CKD and ESKD who require long-term or permanent renal replacement therapy

80
Q

objective of hemodialysis

A

to extract toxic nitrogenous substances from the blood and to remove excess fluid.

81
Q

how often do patients get dialysis?

A

Most patients will undergo dialysis anywhere from 3-5x per week, but it is decided by their nephrologist and their current needs

82
Q

where do patients get hemodialysis?

A

can be performed at home or at a dialysis center.

83
Q

how does hemodialysis work?

A

blood, laden with toxins and nitrogenous wastes, is diverted from the patient to a machine via the use of a blood pump to the dialyzer, where toxins are filtered from the blood and the blood is returned to the patient.

84
Q

using a dialysis catheter for temporary vascular access for hemodialysis:

A

Immediate access to the patient’s circulation for acute hemodialysis is achieved by inserting a double-lumen, non-cuffed, large-bore catheter into the subclavian, internal jugular, or femoral vein by the physician

85
Q

using an arteriovenous fistula for permanent vascular access for hemodialysis

A
  • (AVF) that is created surgically (usually in the forearm) by joining (anastomosing) an artery to a vein, either side to side or end to side. Needles are inserted into the vessel to obtain blood flow adequate to pass through the dialyzer.
86
Q

using a arteriovenous graft for permanent vascular access for hemodialysis

A
  • Can be created by subcutaneously interposing a biologic, semibiologic, or synthetic graft material between an artery and vein.
  • Used in patients with compromised vascular systems whose vessels may not be suitable for an AVF
87
Q

Precautions of fistulas and/or grafts:

A

Protect the fistula/graft arm (LIMB RESTRICTION)
No blood pressures
No blood draws
No PIV
Make sure to ask about the fistula/graft in report
Assess the patency of the fistula at the beginning of the shift
Bruit (swoosh sound)
Thrill (vibration to touch)
Signs of infection
Call provider with concerns ASAP
Hold Cardiovascular medications prior to dialysis - gets filtered out.

88
Q

Peritoneal dialysis is the treatment of choice for patients with

A

Patients with kidney disease who are unable or unwilling to undergo hemodialysis or kidney transplantation.

  • Patients who are susceptible to the rapid fluid, electrolyte, and metabolic changes that occur during hemodialysis experience fewer of these problems with the slower rate of PD.
  • Patients at risk for systemic effects from heparin
89
Q

complications of peritoneal dialysis:

A

Peritonitis

  • Common and serious
  • First sign is cloudy dialysate fluid
  • Treated with antibiotics (10-14 days) and large amounts of protein into peritoneum

Leakage

  • Usually stops if dialysis is withheld for several days and is allows it to heal

Bleeding

  • Usually seen in menstruating women
  • Common in first few exchanges after a new catheter insertion
90
Q

What is peritoneal dialysis and how does it work?

A

Peritoneal membrane that covers the abdominal organs and lines the abdominal wall serves as the semipermeable membrane. A sterile dextrose dialysate fluid is introduced into the peritoneal cavity through an abdominal catheter at established intervals.
Once the sterile solution is in the peritoneal cavity, uremic toxins such as urea and creatinine begin to be cleared from the blood. Diffusion and osmosis occur as waste products move from an area of higher concentration (the bloodstream) to an area of lesser concentration (the dialysate fluid) through a semipermeable membrane (the peritoneum).

91
Q

Primary causes of respiratory acidosis:

A

Basically anything that prevents a person from expelling CO2 or impairs gas exchange

  • Respiratory depression/HYPOventilation
  • Obstruction (COPD/Asthma)
  • Pneumonia
92
Q

Primary causes of metabolic acidosis:

A

direct loss of bicarbonate, as in diarrhea, lower intestinal fistulas, ureterostomies, and the use of diuretics; early renal insufficiency; excessive administration of chloride; and the administration of parenteral nutrition without bicarbonate or bicarbonate-producing solutes

93
Q

primary causes of respiratory alkalosis:

A

hyperventilation, excessive “blowing off” of CO2

94
Q

primary causes of metabolic alkalosis:

A

Excessive alkali ingestion from antacids containing bicarbonate or from the use of sodium bicarbonate during cardiopulmonary resuscitation can also cause metabolic, vomiting, NG suctioning

95
Q

Blood gas normal values:

A

pH 7.35-7.45
PO2 80-100
CO2 35-45
HCO3- 22-28

96
Q

if the CO2 is out of range, it is

A

respiratory

97
Q

if the HCO3 is out of range, it is

A

metabolic

98
Q

ISOTONIC SOLUTION: 0.9% NaCl (Normal Saline)

A

Mainly used for fluid resuscitation. Used in HYPOnatremia *can cause acidosis in large quantities

99
Q

ISOTONIC SOLUTION: Dextrose 5% in water (D5W)

A

AKA sugar water → used in HYPERnatremia

100
Q

ISOTONIC SOLUTION: D5 ½ NS

A

Good maintenance fluid, often used in surgery. Can be used in HYPERnatremia. (Can also be classified as hypotonic)

101
Q

ISOTONIC SOLUTION: Lactated Ringers

A

used during surgery and resuscitation as pH doesn’t change.

102
Q

HYPOTONIC SOLUTION: 0.45% Sodium Chloride (0.45% NaCl) (NaCl 1/2 NS)

A

used in HYPERnatremia

103
Q

HYPERTONIC SOLUTION: 3% sodium chloride (3% NaCl)

A

used in HYPOnatremia

104
Q

What is an isotonic solution?

A

status quo, no change to fluid balance

105
Q

What is a hypotonic solution?

A

few solutes in solution, water from solution drawn into the cells

106
Q

What is a hypertonic solution?

A

lots of solutes in solution, drawing water out of the cells (think about why sea water dehydrates you, it’s because it’s a hypertonic solution)

107
Q

Major symptoms of Hyponatremia:

A

depressed and depleted, tachycardia, weak pulses, seizure and coma

108
Q

major symptoms of hypernatremia:

A

edema, bloating, thirst, DRY TONGUE, N/V, increase muscle tone

109
Q

Major signs of hypokalemia:

A

paralyzed intestines, hypoactive bowel sounds, constipation, abdominal distention, ST depression

110
Q

treatment protocol for hyperkalemia

A

Insulin, but be careful of hypoglycemia (can use dextrose concurrently)
Kayexalate
Dialysis

111
Q

major signs of hyperkalemia

A

hypotension, bradycardia, tight muscles, hyperactive bowel sounds, diarrhea

112
Q

Hyperkalemia ECG:

A

tall tented T waves, prolonged PR interval and QRS duration, absent P waves, ST depression

113
Q

hypokalemia ECG:

A

flattened T waves, prominent U waves, ST depression, prolonged PR interval

114
Q

pyuria:

A

white blood cells in urine

115
Q

dysuria:

A

painful urination

116
Q

diuresis:

A

increased urine volume

117
Q

nocturia:

A

excessive urination at night

118
Q

anuria:

A

decreased urine output of less than 50 mL in 24 hours

119
Q

oliguria

A

urine output less than 0.5 mL/kg/hr

120
Q

Pre-renal:

A

disrupted blood flow to the kidney

121
Q

Intra-renal:

A

damage to the renal tissue

122
Q

post-renal:

A

disrupted urine flow

123
Q

chronic kidney diseases are?

A

irreversible and progress to renal failure

124
Q

the most common kind of acute kidney injury is:

A

hypovolemia

125
Q

most post-renal AKIs are caused by:

A

back flow and buildup of urine into the kidneys

126
Q

common causes of CKD in older adults:

A

hypertension and diabetes mellitus

127
Q

how much function do the kidneys have in Stage 1 kidney disease?

A

90% or >

128
Q

how much function do the kidneys have in stage 5 kidney disease?

A

<15%

129
Q

you cannot live without dialysis after your kidneys are at what % of functionality?

A

15%

130
Q

most prominent manifestation of CKD?

A

Hyperkalemia

131
Q

What is the leading cause of kidney failure in the US?

A

polycystic kidney disease

132
Q

renal cancer is seen in more ____?

A

more ____?

men

133
Q

occupation exposure to petroleum, asbestos, and heavy metals are associated with:

A

renal cancer

134
Q

Can you go home with a hemodialysis catheter?

A

no

135
Q

What is the intracellular space?

A

fluid in the cells, makes up 2/3 of body fluid

primarily in skeletal muscle mass

136
Q

what is extracellular space?

A

fluid outside of the cells

137
Q

what are the three ECF spaces?

A

intravascular space- blood vessels (6L)
interstitial space- space between the cells (11-12L)
transcellular space- smallest compartment

138
Q

what is oncotic pressure associated with?

A

proteins

139
Q

What is third spacing?

A

large amounts of fluid shifting from intravascular to interstitial spaces with trauma, inflammation and sepsis

140
Q

what amount of water do we gain and lose a day for balance?

A

2500mL

141
Q

what is hydrostatic pressure?

A

pressure exerted by blood pressure on the walls of a blood pressure

142
Q

what is osmotic pressure?

A

pressure exerted by the plasma protein

143
Q

what is the most reliable indicator of urine concentration?

A

urine osmolality

144
Q

what is the purpose of acid-base balance?

A

to determine how much hydrogen is in the vascular system

145
Q

What happens when our pH is imbalanced?

A

the medulla tells the lungs to adjust the RR rate to blow off or retain CO2

146
Q

In acidosis, the RR:

A

increases (to improve by blowing off CO2)

147
Q

in alkalosis, the RR:

A

decreases (to improve by retaining CO2)

148
Q

What is the anion gap?

A

refers to the difference between the sum of all measured positively charged electrolytes (cations) and the sum of all negatively charged electrolytes (anions) in blood

Med Surg (5 decks)

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