Renal Conditions Flashcards

1
Q

etiology of pyelo

A

ascending infection or bloodstream infection

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2
Q

risk factors for pyelo

A

–pregnancy
–recurrent lower UTIs
–antibiotic resistant strain

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3
Q

what is pyelonephritis?

A

inflammation of the kidneys

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4
Q

what organism often causes pyelo?

A

e. coli

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5
Q

what can pyelo cause?

A

CKD or sepsis

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6
Q

patho of pyelo

A

inflammatory response –> kidney tissue damage

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7
Q

what can develop from pyelo?

A

abscesses and necrosis

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8
Q

symptoms of pyelo

A

–sudden onset of: fever, chills, CVA tenderness
–lower UTI symptoms
–hematuria may occur
–N/V
–anorexia

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9
Q

treatment of pyelo

A

antibiotics: trimethoprim/sulfamethoxazole (Bactrim), ciprofloxacin/nitrofurantoin (Macrobid)

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9
Q

who can’t Bactrim be prescribed to?

A

pregnant women

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10
Q

complications of pyelo

A

urosepsis

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11
Q

specifics of urosepsis

A

–more likely in elderly
–severe systemic response
–high mortality rates

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12
Q

treatment of severe pyelo

A

–IV antibiotics
–urinalysis
–urine culture

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13
Q

urinary obstruction locations

A

–renal pelvis
–ureter
–bladder or pelvis

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14
Q

what causes obstruction in the renal pelvis?

A

renal calculi

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15
Q

what causes obstruction in ureters?

A

–renal calculi
–pregnancy
–tumor

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16
Q

what causes obstruction in the bladder and urethra?

A

–bladder cancer
–neurogenic bladder
–prostatic hyperplasia
–prostate cancer
–urethral strictures

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17
Q

complications of obstruction

A

–stasis of urine flow
–backup pressure

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18
Q

where does backup pressure affect?

A

–hydroureter
–hydronephrosis
–postrenal acute kidney injury

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19
Q

potential complication of stasis of urine flow

A

infection when urine can’t flow freely

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20
Q

manifestations of acute obstruction

A

–depends on the: site, cause, speed of onset

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21
Q

which manifestation of acute obstruction primarily determines severity of pain?

A

speed of onset

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22
Q

nephrolithiasis

A

–renal calculi (kidney stones)
–clumps of crystals in urinary tract
–small as grain of sand to large as a golf ball
–may be smooth or jagged
–most common causes of renal obstruction

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23
Q

patho of nephrolithiasis

A

–urine is a solution of solvent and solutes
–problem = super-saturation with a solute
–crystals begin forming in the nephron

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24
Q

what is urinary crystal formation enhanced by?

A

–pH changes (UTI)
–excessive concentration of insoluble salts in the urine (dehydration, bone disease, gout, renal disease)
–urinary stasis (immobility/sedentary lifestyle)

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25
Q

risk factors for nephrolithiasis

A

–men
–20s-30s
–white
–family history
–congenital defect
–hot weather (dehydration)
–obesity

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26
Q

most common type of kidney stone

A

calcium oxalate or calcium phosphate

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27
Q

risk factors for calcium oxalate/calcium phosphate

A

–family history
–idiopathic
–increased calcemia
–increased oxaluria

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28
Q

risk factors for struvite (staghorn) stones

A

UTIs

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29
Q

risk factors for uric acid stones

A

gout

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30
Q

types of kidney stones

A

–calcium oxalate/calcium phosphate
–struvite
–uric acid

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31
Q

causes of calcium oxalate stones

A

–dehydration
–low urine output
–high sodium intake
–high oxalate intake
–high protein intake

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32
Q

symptoms of renal colic

A

–flank pain
–radiation to lower abdomen and groin
–colicky spasms (lasting 20-60 minutes)
–intermittent spasms
–sharp pain from ureter scraping ureter wall

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33
Q

accompanying symptoms of nephrolithiasis

A

–N/V
–dysuria
–chills, fever (only if infection)
–hematuria
–foul smelling urine
–diaphoresis

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34
Q

pharm for nephrolithiasis (acute pain)

A

–morphine or NSAIDs
–IV fluids

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35
Q

preventative pharm for nephrolithiasis

A

–calcium = thiazide diuretics
–struvite = antibiotics
–urate = allopurinol

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36
Q

most common type of kidney cancer

A

renal cell carcinoma

37
Q

risk factors for kidney cancer

A

–smoking
–obesity
–age
–male
–genetics

38
Q

prognosis of kidney cancer

A

depends on metastasis

39
Q

early manifestations of renal cell carcinoma

A

none

40
Q

late manifestations of renal cell carcinoma

A

–CVA tenderness
–hematuria (cola colored)
–possible palpable abdominal mass

41
Q

metastasis of renal cell carcinoma

A

usually occurs to bone or lung (bone pain and dyspnea)

42
Q

treatment of renal cell carcinoma

A

–usually resistant to chemo
–remove kidney

43
Q

bladder cancer specifics

A

–most common cancer in men
–urothelial carcinoma

44
Q

risk factors for bladder cancer

A

–smoking
–male
–occupations with exposure to toxins (rubber/paint)
–low fluid intake

45
Q

early onset symptoms of bladder cancer

A

hematuria

46
Q

late onset symptoms of bladder cancer

A

–frequency
–urgency
–dysuria

47
Q

treatment of bladder cancer

A

–chemo depending on stage
–stage 1=intravesical chemo
–advanced stages=systemic chemo

48
Q

frequency of BCG vaccine

A

weekly for 6-12 weeks

49
Q

use for BCG vaccine

A

intravesical therapy for bladder cancer

50
Q

MOA of BCG vaccine

A

–stimulates inflammatory response in the bladder
–goal = immune system to recognize cancerous cells and attack

51
Q

adverse effects of BCG vaccine

A

–bladder irritation
–systemic infection

52
Q

patient instructions for BCG vaccines

A

–empty bladder
–instill BCG vaccine into the bladder
–change position q 15 minutes

53
Q

post-treatment instructions for BCG vaccines

A

–disinfect urine for 6 hours post treatment
–watch for infection

54
Q

how is urine disinfected?

A

by bleaching

55
Q

who shouldn’t receive the BCG vaccine?

A

immunocompromised and HIV/AIDS patients because it’s a live vaccine

56
Q

glomerulonephritis

A

a variety of conditions that cause inflammation of glomeruli

57
Q

specifics of glomerulonephritis

A

–can be focal or diffuse
–3rd leading cause of kidney failure in the US
–primarily an immune process

58
Q

glomerulus

A

delicate network of arterioles within the Bowman’s capsule

59
Q

significance of the glomerulus

A

all blood in the body travels through these

60
Q

tubules

A

massive consumer of oxygen

61
Q

afferent arteriole

A

takes blood in

62
Q

efferent arteriole

A

takes blood away

63
Q

CO and kidneys

A

uses about 20% of CO

64
Q

blood pumps into the afferent arteriole and out of the efferent arteriole through…..?

A

a pressure gradient

65
Q

3 layers of glomerular capillary

A
  1. endothelium
  2. basement membrane
  3. podocytes
66
Q

podocytes

A

–special epithelial cells
–produce start of urine

67
Q

where does the reaction in glomerulonephritis occur?

A

basement membrane

68
Q

type II reactions

A

reactions occur on the cell surface and result in direct cell death or malfunction

69
Q

type III reactions

A

immune complexes are deposited into tissues and the resulting inflammation destroys the tissue

70
Q

type II glomerular injury

A

antibodies attach to antigens of the glomerular basement membrane (5%)

71
Q

type III glomerular injury

A

antibodies react with circulating antigens and are deposited as immune complexes in the GBM (90%)

72
Q

what do both forms of glomerulonephritis have in common?

A

–accumulation of antigens, antibodies, and complement
–complement activation results in tissue injury

73
Q

symptoms of acute glomerulonephritis

A

–abrupt sudden onset
–Hematuria
–Azotemia
–Retention: sodium and water (oliguria), HTN, edema
–Proteinuria

74
Q

what does HARP mean?

A

Hematuria
Azotemia
Retention: oliguria, HTN, edema
Proteinuria

75
Q

triggers of acute glomerulonephritis

A

–post-infectious (poststreptococcal usually)
–primary disease (Berger disease)
–multisystem disease (Goodpasteur syndrome, systemic lupus erythmatosus, vasculitis)

76
Q

Berger disease

A

buildup of IgA = inflammation in glomerulus

77
Q

why does acute glomerulonephritis occur post-strep infection?

A

antibodies that think GBM is foreign and attacks

78
Q

pathogenesis of acute glomerulonephritis

A

trigger –> immune complexes form –> complement activated –> release of mediators –> tissue injury –> hematuria/proteinuria/decreased GFR

79
Q

chronic glomerulonephritis

A

–long term inflammation of the glomerulus = scar tissue
–symptoms like acute

80
Q

prognosis of chronic glomerulonephritis

A

slow progressive disorder = ESRD

81
Q

nephrotic syndrome

A

–glomerulus is too permeable to plasma proteins
–elimination of >3 grams of protein per day

82
Q

What diseases lead to nephrotic syndrome?

A

–glomerulonephritis
–diabetes mellitus

83
Q

pathogenesis of nephrotic syndrome

A

increased glomerular permeability –> proteinuria –> hypoalbuminemia (third space)

84
Q

symptoms of nephrotic syndrome

A

–edema
–HTN
–liver problems (HLD, hypercoag, loss of antithrombin III and plasminogen)

85
Q

function of plasminogen

A

helps break down clots

86
Q

what happens with liver problems in nephrotic syndrome?

A

spilling proteins and losing fluid

87
Q

diabetic nephropathy

A

–major complication
–gross thickening of the GBM
–ultimately leading to ESRD

88
Q

hypertensive glomerular disease

A

decreased renal perfusion –> sclerotic glomerular changes (increased pressure on blood vessels)

89
Q

symptoms of glomerulopathy

A

–hematuria
–oliguria
–fluid retention
–increased BUN/Cr ratio
–proteinuria
–low albumin (hypoproteinemia)