Exam 2 Renal Conditions Flashcards

1
Q

Pyelonephritis

A

Inflammation of the kidneys

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2
Q

Pyelonephritis Etiology

A

Ascending infection or bloodstream infection

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3
Q

Pyelonephritis risk factors

A

pregnancy, recurrent lower UTIs, antibiotic resistant strain

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4
Q

Pyelonephritis response

A

Inflammatory == kidney tissue is damaged

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5
Q

Pyelonephritis extra

___ and ___ can

A

abscesses and necrosis can develop impairing renal function

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6
Q

Pyelonephritis clinical manifestations – sudden onset

A

Fever, chills, CVA tenderness (back)

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7
Q

Pyelonephritis other manifestations - 5

A

Lower UTI symptoms (dysuria), frequency and urge, hematuria, N/V, anorexia

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8
Q

Pyelonephritis Treatment - 3

A

Antibiotics - trimethoprim/sulfamethoxazole, ciprofloxacin, nitrofurantoin

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9
Q

Pyelonephritis complications

A

urosepsis

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

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10
Q

Urinary obstruction locations - 4

A

renal pelvis, ureter, bladder, or pelvis,

blockages in any point of the system prevent the flow of the liquid, causing the system to back up

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11
Q

Reval pelivs obstruction cause

A

renal calculi

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12
Q

ureter obstruction causes

A

renal calculi, pregnancy, tumors

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13
Q

bladder and urethra obstruction causes - 6

A

bladder cancer
neurogenic bladder
prostratic hyperplasia
prostrate cancer
urethral structures
pregnancy
(not usually kidney stones)

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14
Q

complications of obstruction - 3

A

stasis of urine flow (infection)
potential complications – back up pressure

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15
Q

back up pressure - 3

A

hydroureter
hydronephrosis
postrenal acute kidney injury (kidneys not working due to blockage)

ex. enlarged prostate

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16
Q

manifestations of acute obstruction depend on - 3

A

site, cause, speed of onset

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17
Q

which factor primarily determines the severity of pain?

A

speed of onset

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18
Q

nephrolithiasis

A

renal calculi or kidney stones

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19
Q

def of nephrolithiasis

A

clumps of crystals in the urinary tract
most common cause of renal obstruction

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20
Q

nephrolithiasis size and shape

A

small as grain of salt to large as golf ball
may be smooth or jagged

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21
Q

nephrolithiasis pathogenesis

A

urine is a solution of solvent and solutes. Problem is super saturated with solute so crystals begin forming in NEPHRON.

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22
Q

Crystal formation is enhanced by

A

PH changes (UTI)
Excessive concentration of salts - dehydration, bone disease, gout, renal disease
Urinary stasis - immobility, dedentary

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23
Q

nephrolithiasis risk factors - 7

A

sex - men
age - 20s to 30s
white
family history
congenital defect of kidney, urine system
weather - dehydration
obesity

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24
Q

Types of kidney stones: calcium oxidate/calcium phosphate

A

most common
family history
idiopathic
increase calcium, increase oxaluria

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25
Q

struvite

A

15%
urinary tract infection

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26
Q

uric acid

A

gout

27
Q

nephrolithiasis clinical manifestations - pain
location, radiation, spasms, sharp

A

location - flank
radiation - lower abd and groin
spasms - colicky and last 20-60 min
sharp - calculi scrape and ureter wall

28
Q

nephrolithiasis clinical manifestations symptoms - 6

A

n/v
dysuria
chills fever ONLY if infection
hematuria
foul smelling urine
diaphoresis

29
Q

nephrolithiasis pharmacology

A

morphine or nsaids (nothing long term)
iv fluids

30
Q

nephrolithiasis preventative meds

A

calcium - thiazide diuretics
struvite - antibiotics
urate - allopurinol

31
Q

urology cancers - kidneys

A

rare
renal cell carcinoma - 85%
prognosis depends on metastasis (not usually diagnosed until after metastisized)

32
Q

risk factors kidney cancer 5

A

smoking
obesity
age
male
genetics

33
Q

renal cell carcinoma clinical manifestations - early 1 and late 3

Metastasis
Usually

A

early: none
late: CVA tenderness, hematuria, possible palpable abdominal mass

metastisis usually to bone or lung - dyspnic
usually resistant to chemo – surgery

34
Q

urological cancer - bladder

A

fourth most common for men
urothelial carcinoma - lining of bladder

35
Q

risk factors bladder cancer 4

A

smoking
male
occupations with exposure to toxins
low fluid intake

36
Q

bladder cancer clinical manifestations

Early 1
Late 3

A

early - hematuria (pink/reddish)
late - frequency, urgency, disuria

37
Q

bladder cancer treatment

A

chemotherapy depends on stage
stage 1 = intravesical chemo
advanced stages - systemic chemo

38
Q

BCG vaccine

A

given for intravesical therapy
given weekly for 6-12 weeks

39
Q

BCG vaccine moa

A

stimulates inflammatory response in bladder - goal is for immune system to recognize cancerous cells and attack

40
Q

BCG vaccine adverse effects

A

bladder irritation, systemic infection – watch if immune compromised

41
Q

BCG vaccine patient instructions - 3

A
  1. empty bladder
  2. instill BCG vaccine into the bladder - dwell time 2H
  3. Change position q 15 mintues to allow med to touch all areas

Disinfect urine for 6 hours post treatment - watch for infection (Bleach urine)

42
Q

Glomerulonephritis def

Can be
Third
Primarily

A

a variety of conditions that cause the inflammation of glomeruli
- can be local or diffuse
-third leading cause of kidney failure
-Primarily an IMMUNE process

43
Q

Glomerulonephritis where

Delicate

A

glomerulus
delicate network of arterioles within the bowman’s capsule

44
Q

tubules

A

massive consumer of oxygen

45
Q

glomerular disorders

Alterations

A

alterations in glomerular capillary

46
Q

capillary membranes of glomerulus have three layers

A

endothelium
basal membrane - where most issues occur
podocytes

47
Q

type 2 reactions

A

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

48
Q

type 3 reactions

A

immune complexes are disposed into tissues and resulting inflammation destroys tissue

49
Q

etiology of Glomerulonephritis (2)

A
  1. antibodies attach to antigens of the glomerular basement membrane (anti GBM antibodies) = TYPE 2
  2. Antibodies react with circulating antigens and are deposited as immune complexes in the GBM - 90% - TYPE 3
50
Q

both forms have this in common

Accumulation
Complement

A

accumulation of antigens, antibodies and complexes

complement activation results in tissue injury

51
Q

Acute glomerulonephritis
Abrupt

A

abrupt onset of Glomerulonephritis

52
Q

characteristics of acute Glomerulonephritis 4

A

HARP
Hematuria
Azotemia - buildup of waste
Retention - sodium and water - oliguria (leads to HTN and edema)
Proteinuria - proteins in urine

53
Q

Acute Glomerulonephritis triggers - 3

Post infectious
Primary disease
Multisystem disease

A

post infectious - strep or nonstrep
primary disease - Berger disease (IgA causes inflammation)
multisystem disease - goodpasture syndrome, systemic lupis, vasulitis

54
Q

Acute Glomerulonephritis pathogenesis

A

Trigger > immune complex forms > complement activated > release of mediators > tissue injury > Hematuria proteinuria Decreased GFR

55
Q

Chronic Glomerulonephritis
Long
Manifestations
Prognosis

A

–Long term inflammation of the glomerulus - scar tissue
–manifestations same as acute
–prognosis: slow progressive destruction to ESRD.

56
Q

Nephrotic syndrome

A

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

57
Q

nephrotic syndrome etiology

A

glomerulonephritis
DM

58
Q

Nephrotic syndrome pathogenesis 3
Increased
Proteinuria
Hypo_

A

Increased glomerular permeability – not functional
Proteinuria - decreases albumin – third spacing
Hypo-albuminemia

59
Q

Nephrotic syndrome clinical manifestations

A

edema
hypertension
liver problems : hyperlipidemia, hypercoagulation, loss of antithrombin 3 and plasminogen

60
Q

Glomerulopathy: Diabetic nephropathy

A

major complication
gross thickening of GBM– decrease urine, increase buildup
ultimately leading to ESRD

61
Q

Glomerulopathy: hypertensive glomerular disease

A

scarring
decreased renal perfusion - sclerotic glomerular changes

62
Q

glomerulopathy manifestations

A

hematuria
proteinuria
oliguria
low albumin
fluid retention
increased BUN/Cr ratio

63
Q

Hydroureter

A

Dilation of proximal ureter

64
Q

Hydronephrosis

A

Dilation of renal pelvis and calicies