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NUR 326 > urinary > Flashcards

urinary Flashcards

1
Q

Name where in the urologic tract a patient can experience an obstruction and the causes

A

Renal pelvis- stomach of the kidney; Cause: renal calculi
Ureter- takes urine from kidney to bladder; Cause: renal calculi, pregnancy, tumors
Bladder or pelvis; Cause: bladder cancer, neurogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures.

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2
Q

Describe the potential complications of urinary stasis and back-up pressure.

A

o Urinary stasis complications: infection, recurrent UTIs
o Back-up pressure complications: hydroureter, hydronephrosis, postrenal acute kidney injury.

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3
Q

Differentiate between hydronephrosis and hydroureter

A

Hydroureter: enlarged d/T backup of urine and increased pressure
Hydronephrosis: kidney is holding urine

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4
Q

Discuss why the manifestations of acute urologic obstruction can vary from person to person

A

Depends on the site, cause, and speed of onset

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5
Q

renal calculi: definition, size, shape

A

Definition: clumps of crystals in the urinary tract
Size: small (grain of sand) or large (golf ball)
Shape: smooth or jagged
Most common cause of renal obstruction.

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6
Q

Risk factors for nephrolithiasis

A

Sex: men, age: 20-30s, race: white, family hx, congenital defects, weather, obesity

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7
Q

specific risk factors for the 3 major types of kidney stones.

A

Calcium oxalate or calcium phosphate (70-80%)-IDIOPATHIC, Family hx, ↑ calcemia, ↑ oxaluria.
Struvite (15%)- UTI
Uric acid (7%) gout

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8
Q

most preventable cause of Calcium oxalate stones is _ and _ _.

A

dehydration & low UOP

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9
Q

Diet high in _, _ _ &, _ can cause these stones as well.

A

Na, oxalate intake & protein

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10
Q

patho for nephrolithiasis.

A

Urine is a solution of solvent (water) & solutes (particles).
Problem: super-saturation with a solute therefore crystals begin forming in the NEPHRON.
Crystal formation is enhanced by: PH changes: UTI, Excessive concentration of insoluble salts in the urine d/t dehydration, bone disease, gout, renal disease, Urinary stasis: immobility/sedentary lifestyle.

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11
Q

CM for nephrolithiasis.

A

Pain of Acute Renal Colic:
– location – “flank”
– radiation – “lower abd and groin”
– spasms – “colicky” last 20-60 minutes
– intermittent – “ureter spasms”
– sharp - “calculi scrape the ureter wall”
Accompanying symptoms:
– N/V
– Dysuria
– Chills, Fever →ONLY if infection is present
– Hematuria
– Foul smelling urine
– Diaphoresis

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12
Q

where do crystals begin forming

A

in the nephrons

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13
Q

pharmacotherapy of nephrolithiasis, including acute pain management and preventive management.

A

Acute pain: morphine or NSAIDS, IV fluids
Preventative meds:
Calcium= thiazide diuretics
Struvite= antibiotics
Urate= allopurinol

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14
Q

PYELONEPHRITIS (other names for this) & definition

A

UPPER UTI, KIDNEY INFECTION.
inflammation of kidneys

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15
Q

Risk factors for PYELONEPHRITIS

A

pregnancy, recurrent lower UTIs, abx resistant strain.

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16
Q

Protective factors for UTIs (Pulled from NUR 325.)

A

PH=acidic, presence of urea, men=prostatic secretions, women=urethral gland secretions, urine flow id unidirectional, immune system

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17
Q

etiology for pyelonephritis

A

ascending infection (starts at bottom & goes up the tract) or bloodstream infection (Ex. E. coli)

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18
Q

patho for pyelonephritis

A

Kidneys become inflamed & filled with infectious exudate.
Inflammatory response from untreated or recurrent UTIs can lead to kidney tissue DAMAGE.
Abscesses & necrosis can develop impairing renal function.

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19
Q

CM for pyelonephritis

A

Sudden onset: fever, chills, CVA tenderness
Lower UTI symptoms: dysuria, frequency, urgency
Hematuria
N/V, anorexia

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20
Q

Define urosepsis and describe the typical patient population who experiences it.

A

potentially life-threatening condition that occurs when a UTI spreads to the kidneys and causes sepsis, the body’s response to infection.
It’s a severe systemic response and has high mortality rates.
Ex. ELDERLY

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21
Q

Describe the different types of antibiotic therapy that can be used for UTI, and the factors that influence the treatment regimen.

A

Meds: Trimethoprim/sulfamethoxazole, Ciprofloxacin, nitrofurantoin
Community acquired = short course abx
Recurrent= 7-14 days, may need IV abx
Get UA, culture & sensitivity to determine severity of organism.

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22
Q

Trimethoprim/sulfamethoxazole (Bactim)

A

Class: Sulfonamides
MOA: don’t destroy bacteria but inhibit their growth= bacteriostatic by preventing the synthesis of folic acid needed for DNA synthesis
Indication: uncomplicated UTIs, respiratory infections, salmonella, shigellosis
SE: photosensivity
NC: ‘Sulfa allergies’

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23
Q

Ciprofloxacin (Cipro)

A

Class: Fluoroquinolones
MOA: destroy bacteria by altering their DNA. Interfere with the bacterial enzymes DNA gyrase and topoisomerase
Indications: UTIs, some STIs, upper and lower respiratory tract infections, gonorrhea, and other infections. anthrax: infection with Bacillus anthracis
SE: arthropathy (joint disease), often irreversible. Prolonged post-antibiotic effects: concentrated in the neutrophils.
NC: PO, IV, Topical. Minimal penetration of the BBB/CSF. Avoid in patients <18 & >60.

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24
Q

List the top 2 causes of end stage kidney disease (list the other causes as well)

A

Top 2 causes: DM-50%, HTN-30%, glomerulonephritis-10%, Other-10%

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25
Q

major risk factors for CKD

A

Family history, Increasing age (>60), Male, Black/African American, HTN, DM, smoking, Overweight and obesity

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26
Q

2 major signs of worsening CKD

A

Increased angiotensin 2 & proteinuria

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27
Q

CV s/s of CKD

A

HTN, HF, CAD, PAD, pericarditis

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28
Q

GI s/s of CKD

A

anorexia, N/V, GI bleeding, gastritis

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29
Q

neuro s/s of CKD

A

fatigue, headache, sleep disturbances, encephalopathy

30
Q

pulmonary s/s of CKD

A

Pulmonary edema

31
Q

integumentary s/s of CKD

A

pruritis, ecchymosis, dry, scaly skin.

32
Q

Describe how the loss of normal kidney function results in the clinical manifestations.

A
  1. No longer maintains F & E homeostasis: Edema, hyperkalemia, hyperphosphatemia, hypermagnesemia, metabolic acidosis
  2. No longer rids the body of wastes via urine: Anorexia, malnutrition, itching, CNS changes
    3.Decreased production of erythropoietin: Anemia
    4.Decreased activation of Vitamin D: Renal osteodystrophy
33
Q

Discuss the two different ways drugs are used in chronic kidney disease

A

Slow the rate of progression of CKD
Treat the complications of CKD

34
Q

Describe why ACE and ARBs are still used in patients with CKD, even when the drug book says we are supposed to use “caution” in patients with renal insufficiency.

A

For Blood pressure control.
Reduce BP to less than 140/90.
Other BP meds as needed to maintain SBP (110-130) 140

35
Q

List the drugs commonly used to treat these complications of CKD:

A

volume overload- loop diuretics, use w/ low salt diet
hyperkalemia- multiple (ex. = diuretic), Addressed with hemodialysis in ESRD
metabolic acidosis- SODIUM BICARBONATE (an alkaline agent)
hyperphosphatemia- CALCIUM CARBONATE (a phosphate binder)
renal osteodystrophy-CALCITRIOL (activated vitamin D)
anemia- erythropoietin (black box warnings)

36
Q

sodium bicarbonate

A

indications: To treat metabolic acidosis
Goals: Slow progression of CKD, Prevent bone loss, Improve nutritional status
Given PO
Initiate when HCO3 is less than 15 mEq/mL (Goal HCO3 18-20)
SE: bloating

37
Q

calcium carbonate

A

MOA: Binds to phosphate [phos binder]
Indication: treat hyperphosphatemia
Goals: Keep normal phosphate levels, decrease mortality
SE: hypercalcemia
NC:monitor calcium levels, Take with meals

38
Q

calcitriol

A

MOA: activated form of vitamin D; stimulate intestinal absorption of calcium/phosphate and bone mineralization
Adverse effects: Hypercalcemia, hyperphosphatemia
Indication: treat renal osteodystrophy

39
Q

Describe the clinical manifestations of calcium toxicity that the nurse should be aware of when administering calcium carbonate and calcitriol

A

HYPERCALCEMIA= Excess calcium acts as a sedative= reduced excitability of muscles & nerves.
Confusion, psychosis, seizures, comas
Nausea, upset stomach

40
Q

Explain acute kidney injury

A

Usually, the result of ischemic injury r/t loss of volume -> decreased perfusion (Toxins or sepsis are also common causes)
Kidney function can be mildly affected to severe.

41
Q

Define the types of AKI and the conditions that can cause them

A

Pre-renal: volume loss related, ex. Dehydration.
Intrarenal: acute tubular necrosis [chemical, kidney cell death], ex. Chemical/toxin, kidney disease, meds, vascular disease- HTN, DM.
Post-renal: not as common, obstruction causing cell death

42
Q

Manifestations of AKI

A

oOliguria (< 400 ml/24 hr)
oBegins 1 day after hypotensive event & lasts 1-3 weeks
oFluid volume excess- d/t kidney not filtering out
oMetabolic acidosis
oHyponatremia
oHyperkalemia
oWaste product accumulation- azotemia or uremia.
oNeurologic disorders

43
Q

Explain the treatment goals and how physiologic alterations from AKI are managed

A

address the cause

44
Q

Hematuria

A

blood in urine

45
Q

Azotemia

A

buildup of waste products

46
Q

oliguria

A

low UOP

47
Q

proteinuria

A

protein in urine

48
Q

Define and discuss the important characteristics of glomerulonephritis, including where the damage occurs.

A

Definition: a variety of conditions that cause inflammation of glomeruli.
Can be focal or diffuse
Focal= specific area of glomerulus.
Diffuse= can affect both kidneys & all areas of glomerulus.
Primarily an immune process
where the damage occurs Glomerulus: delicate network of arterioles within the bowman’s capsule. Tubules: massive consumer of oxygen.

49
Q

Discuss the layers of the glomerulus

A

1- endothelial
2-basement membrane- where a lot of the issues occur
3-podocytes (special epithelial cells)- cells produce the start of urine

50
Q

Describe the 2 main etiologies of glomerulonephritis, including what these 2 etiologies have in common

A

Two types of injury: 1. Antibodies attach to antigens of the glomerular basement membrane (“anti-GBM antibodies”) - 5% (Type II). 2. Antibodies react with circulating antigens and are deposited as immune complexes in the GBM – 90% (Type III)
BOTH forms have this in common: Accumulation of antigens, antibodies, and complement. Complement activation results in tissue injury.

51
Q

Discuss the HARP clinical manifestations of glomerulonephritis.

A

Abrupt sudden onset of acute glomerulonephritis
Hematuria
Azotemia
Retentions: Sodium & water retention, Oliguria- low OUP, Leads to HTN & edema
Proteinuria

52
Q

Describe the triggers of glomerulonephritis.

A

Post-Infectious: Poststreptococcal infection, Nonstreptococcal infection (Bacterial, viral, parasitic).
Primary Disease: Berger disease
Multisystem Disease: Goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis.

53
Q

pathogenesis of acute glomerulonephritis

A

Trigger (infection)
Immune complexes form (direct attack or complexes circulating & depositing into basement membrane)
Complement activated (start inflammatory process)
Release of mediators (causes further inflammation)
Tissue Injury!
Hematuria, Proteinuria, Decreased GFR

54
Q

chronic glomerulonephritis.

A

Long term inflammation of the glomerulus ->scar tissue
Manifestations: like presentation of acute glomerulonephritis
Prognosis: Slow progressive destruction ->ESRD

55
Q

define nephrotic syndrome

A

The glomerulus is too permeable to plasma proteins, Elimination of >3 grams of protein per day.

56
Q

etiology of nephrotic syndrome

A

Glomerulonephritis, Diabetes mellitus

57
Q

patho of nephrotic syndrome

A

Increased glomerular permeability →Proteinuria→Hypo-albuminemia

58
Q

CM of nephrotic syndrome

A

Edema, Hypertension.
Liver Problems: HLD, Hypercoagulation, Loss of antithrombin III and plasminogen

59
Q

Define & list manifestations of Glomerulopathy: Diabetes & Hypertension Complications

A

oDiabetic Nephropathy: Major complication, Gross thickening of the GBM; Ultimately leading to ESRD
oHypertensive Glomerular Disease: Decreased renal perfusion ->sclerotic glomerular changes
CM: Hematuria, Oliguria, Fluid retention, Increased BUN/Cr ratio, Proteinuria, Low albumin [hypoproteinemia]

60
Q

KIDNEY CANCER: risk factors, prognosis, manifestations, and chemotherapy treatment of renal cell carcinoma.

A

RF: SMOKING, obesity, age, male, genetics
Prognosis: depends on metastasis
Manifestations: Early: none
Late: CVA tenderness, hematuria, possible palpable abdominal mass.
Metastasis usually occurs in bone = bone pain or lungs = dyspnea, coughing.
Chemo tx: usually resistant to chemo if metastasized, surgery to remove kidney if not metastasized.

61
Q

BLADDER CANCER: risk factors, manifestations, and chemotherapy treatment

A

RF: SMOKING, male, occupation with exposure to toxins, low fluid intake
Manifestations: Early: hematuria
Later: frequency, urgency, dysuria
Chemo: depends on stage
Stage 1= intravesical chemo
Advanced stages= systemic chemo

62
Q

intravesical therapy for bladder cancer

A

Drug Name: BCG vaccine
MOA: simulates inflammatory response in the bladder, goal is for immune system to recognize cancerous cells and attack
SE: bladder irritation, systemic infection
Patient instructions: 1: empty bladder. 2: instill BCG vaccine into the bladder (dwell time 2 hours). 3: change positions q15 minutes
Safety: disinfect urine for 6hrs post treatment; watch for infection.

63
Q

Describe the functions of the kidney, including the endocrine functions

A

Maintain F&E homeostasis
Rid the body of water-soluble wastes via urine
3 endocrine functions: Produces erythropoietin- stimulates RBC production, Activates vitamin D, Produces renin, which helps regulate BP

64
Q

Explain why humans can live with only 1 kidney

A

Each kidney contains >1 million nephrons
Nephron is the functional unit of the kidneys.
We can function with 10-25% of nephrons

65
Q

Describe the 3 major tissues of the kidney

A

Renal pelvis: Large collecting area for urine that drains from the nephrons
Medulla: Contains 8-12 pyramids that consist of: Collecting tubules, Collecting ducts, Loops of Henle & capillaries
Renal cortex: Contains all glomeruli and 85% of nephron tubules

66
Q

A nephron must:

A

Filter water-soluble substances from the blood
Reabsorb filtered nutrients, water, and electrolytes
Secrete wastes and excesses.

Each nephron has a glomerulus and a tubule

67
Q

glomerulus

A

Filters fluid from the blood into tubules
Prevents passage of RBC’s and proteins
Surrounded by a Bowman’s capsule
The overall glomerular filtration rate is about 125 mL/min

68
Q

ureters

A

Two Ureters
Narrow tubes, 10-12 inches long
Drain urine from renal pelvis to bladder

69
Q

bladder

A

Reservoir for urine
Normal output is 1500 mL/day

70
Q

urethra

A

Small muscular tube from bladder neck to meatus
Female = 1-2 inches; Male = 8-10 inches long.

NUR 326 (15 decks)

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