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NURSING PATHO > TEST 3 > Flashcards

TEST 3 Flashcards

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1
Q

rate at which a substance is excreted in the urine

A

renal clearance measures

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2
Q

glomerular filtration rate is measures

A

the volume of plasma that is filtered each minute

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3
Q

what tells you when a patient is in renal failure

A

GFR- glomerular filration rate

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4
Q

GFR normal kidneys

A

anything 60 or above

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5
Q

GFR kidney disease

A

15-60

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6
Q

GFR kidney failure

A

15 or less

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7
Q

what does blood urea nitrogen BUN tell you

A

dehydration- the higher the number the more dehydrated the patient is

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8
Q

what does this serum creatinine tell you

A

how the kidney is functioning/filtering

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9
Q

wastes product from muscles

A

creatinine

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10
Q

comes from protein breakdown

A

urea

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11
Q

ratio of bun to creatinine

A

10:1

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12
Q

why should protein not be in the urine

A

protein is a big substance so for it to be filtered that means there is something wrong with the filtration rate

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13
Q

proteinuria

A

protein in the urine

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14
Q

osmolarity and specific gravity

A

tells you about particles whether the solutes in the urine are concentrated or not ; anything greater than 1.10

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15
Q

higher the specific gravity in a urine test

A

more dehydrated ; higher the number the more solutes than water

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16
Q

antidiuretic hormone

A

doesn’t let you diurease ; not pee; against the release of water

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17
Q

normal pH of urine

A

4.5-8

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18
Q

complete absence of development of one or both kidneys (unilateral RA or bilateral RA respectively

A

renal agenesis

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19
Q

renal agenesis is a change in what gene

A

Pax2 gene- mutation

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20
Q

renal agenesis is an autosomal

A

dominant

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21
Q

most life threatening component of potter syndrome is

A

pulmonary hypoplasia; lungs not forming

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22
Q

The kidneys are small in size and have less than the normal number of calyces and nephrons

A

renal hypoplasia

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23
Q

Common cause for pediatric renal failure and adult onset disease

A

renal hypoplasia

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24
Q

enlargement of the kidney. urine collects in the infected kidney so it forms fluid like sacs

A

multicystic dysplastic kidney disorder

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25
Q

first thing they see in a child with multi cystic dysplastic kidney disorder is a

A

palpable abdomen

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26
Q

if you know they have a wilms tumor you never want to what

A

palpate

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27
Q

children who survive MDKD are at more risk for

A

hypertension and wilms tumor

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28
Q

Most common of all inherited kidney disease

A

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

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29
Q

ADPKD manifestations

A

progress is slow and chronic kidney disease is uncommon before 40; hypertension (RAAS), hematuria, kidney stones; flank pain

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30
Q

characterized by cystic dilation of the cortical and medullary collecting tubules

A

autosomal recessive polycystic kidney disease

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31
Q

what causes the autosomal recessive polycystic kidney disease

A

mutation in the PKHD1 gene

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32
Q

manifestations of autosomal recessive polycystic kidney disease

A

excessive urine, hypertension, enlarged spleen w low rbc and high wbc/platelets, breathing problems

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33
Q

fluid-filled sacs (cysts) develop deep within the kidneys, leading to chronic kidney disease with kidney failure.

A

medullary cystic kidney disease / nephronophthisis

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34
Q

who does medullary cystic kidney disease affect

A

children

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35
Q

Excessive thirst and abnormal urine starts in which ?

A

nephronophthisis

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36
Q

what happens with adolescence with medullary cystic kidney disease

A

turns into autosomal dominant tubulointerstitial kidney disease

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37
Q

What is the main concern with Simple and Acquired Renal Cyst

A

differentiate them from malignancies

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38
Q

an inflammatory response in the glomeruli of the kidney

A

Acute Nephritic Syndrome

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39
Q

what is the most causative organism for acute nephritic syndrome

A

Group-A beta-hemolytic streptococci

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40
Q

what does the glomerulus do

A

filters waste product from the blood

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41
Q

how do you diagnose a person with acute nephritic syndrome

A

serum test, urinalysis

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42
Q

manifestations of acute nephritic syndrome

A

sudden onset of hematuria, coke urine, oliguria, diminished GFR

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43
Q

less than 400 ml in a 24 hour period

A

oliguria

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44
Q

how much urine per hour

A

30 ml per hour

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45
Q

What is the best treatment option for an individual with acute nephritic syndrome?

A

antibiotics

Provide supportive care

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46
Q

mishaping of the monocytes and macrophages

A

Rapidly Progressive Glomerulonephritis

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47
Q

manifestations for Rapidly Progressive Glomerulonephritis

A

progress rapidly 3 mo, weak immune system

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48
Q

Why would plasmapheresis be beneficial for the Rapidly Progressive Glomerulonephritis patient?

A

a process that filters the blood and removes harmful antibodies; immunosuppressed so dont have anything to fight off

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49
Q

What organs does Goodpasture syndrome affect?

A

basement membrane; lungs and kidneys

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50
Q

1 risk factors for good pasture

A

smoking

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51
Q

an increase in the glomerular permeability causing albumins (plasma proteins) to be excreted in the urine.

A

nephrotic syndrome

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52
Q

damages clusters of small blood vessels; lose filtration, waste, and excess water

A

nephrotic syndrome

53
Q

manifestations of nephrotic syndrome

A

massive proteinuria, dyspnea, lipiduria, Hypoalbuminemia, Pleural effusion, Hyperlipidemia

54
Q

hallmark sign of nephrotic syndrome

A

generalized edema happens due to decrease in plasma proteins

55
Q

edema in nephrotic syndrome usually begins where

A

lower extremities. as it worsens it becomes more generalized

56
Q

why would you give diuretic for nephrotic syndrome

A

removes excess fluid

57
Q

diuretic that would help in lope of henle

A

lasix

58
Q

treatment of nephrotic syndrome

A

diuretic, statin, pril, beta-blocker slide56

59
Q

difference between nephritic and nephrotic

A

nephrotic you are losing large amounts of protein

60
Q

frothy urine means what

A

spilling proteins

61
Q

All persons with systemic lupus Erythematous Glomerulonephritis should undergo routine urinalysis to monitor for

A

hematurina and proteinuria

62
Q

first signs of systemic lupus erythematous glomerulonephritis is

A

in the urine test

63
Q

Renal disease affecting the tubules, interstitium, and pelvis of the kidney

A

acute pyelonephritis

64
Q

two types of pyelonephritis

A

acute-bacterial

chronic-couldve been bacterial followed by viral

65
Q

ascending infection

A

pyelonephritis

66
Q

causative organism of acute pyelonephritis

A

e. coli

67
Q

main clinical manifestation of acute pyelonephritis

A

malaise, moderate to high fever, nausea/vomitting, Painful palpation over the on the infected side (CVA), pyuria

68
Q

how to stop pyelonephritis

A

teach girls to wipe back to front

69
Q

Painful palpation over the on the infected side

A

costovertebral angle

70
Q

positive CVA (painful) what does it indicate

A

pyelonephritis

71
Q

The common factors in acute uncomplicated pyelonephritis included

A

healthy young women; no structural problems, lack of structural and urinary tract obstructions, lack of predisposing medical conditions

72
Q

acute complicated pyelonephritis

A

children or adults with structural defects

73
Q

most common cause of upper urinary tract obstruction

A

kidney stones ; urinary calculi

74
Q
  • acute, intermittent, excruciating
    • stones 1 to 5 mm
    • causes stretch of collecting system or ureter
    • skin cool and clammy
A

renal colic pain- kidney stones

75
Q
  • dull, deep, aches in back
    • stones produce distention of renal calyces or renal pelvis
    • intensity of pain varies from mild to severe
    • pain exaggerated by drinking large amounts of water
A

renal noncolicky pain-kidney stones

76
Q

1 causative factor of a kidney stone

A

calcium oxalate

77
Q

lithotripsy

A

crushing of the kidney stones by shock sound waves

78
Q

4 types of kidney stones

A

magnesium ammonium phosphate
uric acid
cystine stones
calcium

79
Q

The rapid loss of kidney function from renal cell damage

A

acute kidney injury

80
Q

acute kidney injury can be

A

reversible but has high mortality rate

81
Q

prerenal acute kidney injury

A

Hypovolemia
Decreased cardiac output
Decreased peripheral vascular resistance
Decreased renovascular blood flow

82
Q

intrarenal

A

Nephrotoxic injury
Interstitial nephritis
all diseases that are discussed

83
Q

postrenal

A 
BPH-benign prostatic hypertrophy
Bladder Cancer
Prostate Cancer
Calculi
Neuromuscular disorders
Spinal cord disease
Strictures
Trauma
slide 87
84
Q

outflow problem

A

postrenal

85
Q

use NSAIDS with caution why

A

aleve. ibuprofen are metabolized in the kidney.

86
Q

which ones can be resolved

A

pre and postrenal ; internal is a longer recovery

87
Q

Patients with AKI progress through phases

A

oliguric, diuretic, and recovery

88
Q

AKI labs

A

proteinura and hematuria, cbc (4-12), serum increases creatinine , BUN

89
Q

urine in the blood

A

uremia

90
Q

signs of uremia

A

epistaxis, frost, red eye

91
Q

classification staging for acute kidney injury

A 
RIFLE; Risk
injury
failure
loss
ESKD
92
Q

peaked T wave means

A

hyperkalemia

93
Q

U wave means

A

hypocalcemia

94
Q

AKI you should monitor which electrolyte

A

K+

95
Q

treating hyperkalemia

A

Dietary restriction- limit intake to 40 mEq day of potassium rich foods and drink

96
Q

give insulin to hyperkalemia why

A

potassium follows glucose back into rbc

97
Q

hyperkalemia can cause

A

muscle cramps, EKG changes, oliguria, drowsiness, abdominal cramping

98
Q

more susceptible to aki

A

elders;dehydrated, hypotensive, heart problems

99
Q

nephrotoxic medications

A 
Aminoglycosides- MYSIN
Amphotericin B
NSAIDs
ACE inhibitors
ARBs
IV contrast dye
100
Q

nephrotoxic medications

A 
Aminoglycosides- MYCIN
Amphotericin B
NSAIDs
ACE inhibitors
ARBs
IV contrast dye
101
Q

two major side effects of aminoglycosides

A

ototoxicity and nephrotoxicity - IRREVERSIBLE

102
Q

vancomyin side effect

A

infusing it too fast and they turn red

103
Q

foods high in potassium

A 
avocado
banana
potatoes
spinach 
beans
citrus juices
fish
104
Q

foods high in phosphorus

A 
meat
fast food
cheese
seeds
milk
canned foods
cola
105
Q

serious syndrome due to a direct or indirect muscle injury. It results from the death of muscle fibers and release of their contents into the bloodstream.

A

rhabdomyolysis

106
Q

a hormone secreted by the kidneys that increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues.

A

Erythropoietin

107
Q

which genes are infected in autosomal dominant polycystic kidney disease

A

PKD1 and PKD2

108
Q

Excessive thirst and urination start in childhood or adolescence for and in adolescence or adulthood for autosomal dominant tubulointerstitial kidney disease.

A

Nephronophthisis

109
Q

gene problem for Nephronophthisis

A

NPHP

110
Q

why would plasmapheresis be a treatment for rapid progressive glomerulonephritis

A

gets rid of toxins and antigens; macrophages become misshaped so this gets rid of them

111
Q

treatments for rapid progressive glomerulonephritis

A

plasma
transplant
dialysis

112
Q

treatments for nephrotic syndrome

A

Diuretic- remove excess fluid (edema)
”-statin”- treat hyperlipidemia
Ace-Inhibitor “-pril”- lower BP & restrict adrenal cortex from secreting aldosterone
Low sodium diet
Beta-Blocker- lower BP (decrease filtration rate)

113
Q

blood is filtered through the

A

glomerulus of the kidney

114
Q

treatment for lupus

A

oral corticosteriods
ace I
immunosuppressives

115
Q

someone with SLE should get what test first

A

urine analysis

116
Q

gene problems in medially cystic kd

A

MCKD1 and 2

117
Q

3 main symptoms for nephron and medullary cystic kidney

A

polyuria, polydipsia, enuresis (bed wetting); treat with desmopressin

118
Q

hallmark sign for pyelonephritis

A

significant malaise

119
Q

is acute tubular necrosis reversible

A

yes if caught early enough

120
Q

LES is suppose to relax and when it doesn’t its called

A

achalasia

121
Q

hallmark sign for gerd

A

barrett cells

122
Q

food relieves pain in

A

duodenal ulcers

123
Q

food does not relieve pain in

A

gastric ulcers

124
Q

ulcerative colitis eventually turns into

A

cancer

125
Q

Carbohydrate metabolism glycogenesis, glycogenolysis

Protein metabolism-synthesis of nonessential amino acids, clotting factors, urea formation

Fat metabolism-synthesis of lipoproteins, synthesis of fatty acids, breakdown of cholesterol

Detoxification drugs/harmful substances

A

liver

126
Q

what phase does distaste of smoking in hep happen

A

prodomal; first stage

127
Q

treatment for fulminant hep

A

supportive care and liver transplant

128
Q

triad for acute cholecystitis

A

constant pain in URQ
tenderness in URQ
inflammatory response

129
Q

Rhabdomyolysis- triad

A

darkened ua(coke colored urine), myalgia (muscle aches), weakness

NURSING PATHO (16 decks)

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