Exam 3 stuff Flashcards

1
Q

how quickly does AKI happen?

A

hours to days

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2
Q

what happens when kidneys lose fxn?

A

inability to maintain F&E and A+B balance

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3
Q

what are the three causes of AKI

A

prerenal
intrarenal
postrenal

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4
Q

examples of prerenal injury

A

shock, hypo, anything that blocks blood flow to the kidneys

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5
Q

examples of intrarenal injury

A

glomerulonephritis, lupus, drugs that damage the kidneys, toxins, ischemia

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6
Q

examples of postrenal injury

A

bladder cancer, kidney stones, prostate cancer/BPH

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7
Q

how do kidneys compensate when its pre + post injury? (3)

A

activating RAAS
constricting kidney blood vessels to raise the BP in kidneys
releasing ADH: less pee, more volume.

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8
Q

what does kidney compensation for AKI lead to (that also causes issues?)

A

oliguria
azotemia

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9
Q

assessment findings for AKI

A

oliguria (less than 400 mL/24 hrs)
FVO
crackles
increased O2 demand/RR/dyspnea
edema
N/V: r/t azotemia
confusion

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10
Q

dx for AKI

A

serum Cr, BUN
abnormal e- (esp K)
urine Na levels
Metabolic acidosis
Urine SG (dilute or conc.)
US
CT scans- no IV contrast though!!
MRI
X ray/KUB

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11
Q

interventions for AKI

A

INTERVENE EARLY!
maintain MAP
monitor Is & Os
fluid replacement or restriction
meds… diuretics
Venous monitoring
nutrition
RRT

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12
Q

what sort of nutrition is appropriate for someone with AKI

A

get a dietician on board!
40 g/day of protein (more if on dialysis)
K restrictions…
Fluid restrictions

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13
Q

how many stages are there of CKD?

A

5 stages! based on GFR fxn

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14
Q

what does stage 1 on CKD look like?

A

normal kidney fxn/GFR but increased risk for damage

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15
Q

what does stage 2 of CKD look like?

A

mild disease/decrease in fxn. decrease in GFR 60-80%

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16
Q

what does stage 3 of CKD look like?

A

moderate disease/azotemia present.
restriction fluids
GFR 30-59%

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17
Q

what does stage 4 of CKD look like?

A

severe disease
can’t maintain F&E, A&B
dialysis maybe
GFR 15-29

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18
Q

what does stage 5 of CKD look like?

A

GFR <15
dialysis def.
death or transplant

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19
Q

what does CKD do to the CV system?

A

HTN, malfxn of RAAS, HLD, HF, Pericarditis, cardiomyopathies

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20
Q

what does CKD do hematologically?

A

causes anemia r/t reduced EPO. can also cause reduced platelets

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21
Q

CKD and GI

A

stomatitis, colitis, anorexia, N/V, hiccups, PUD

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22
Q

CKD assessment findings r/t azotemia

A

anorexia, N/V, fatigue

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23
Q

what is the metallic taste during CKD r/t?

A

build up of uremic acid! can also have uremic halitosis

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24
Q

skin changes r/t CKD

A

pruritis, bronzed color, uremic frost, bruises

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25
Q

What are other assessment findings of CKD?

A

urinary changes, wt loss, drowsiness, confusion, neuropathies, FVO, dysrhythmias, HTN, s/s of anemia

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26
Q

goals (wt wise) for CKD

A

pts will not:
gain or lose 2 lbs overnight, 5 lbs in a week or 3 bw dialysis

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27
Q

what kind of meds for CKD

A

Diuretics!

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28
Q

when should we not use diuretics?

A

after dialysis has started

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29
Q

what are other meds for CKD?

A

anti-HTN, CCB, ACE inhibitors, BB

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30
Q

what can CCB do for CKD?

A

improve GFR and blood flow to kidneys

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31
Q

what do ACE inhibitors do for CKD

A

slow the progression of CKD

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32
Q

what are two other things r/t to CV and CKD that patients should do?

A

daily wts! and measure BP daily!

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33
Q

nutrition requirements for CKD

A

altered protein intake
fluid restrictions
K restrictions
Na restrictions
Phosphorus restrictions

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34
Q

what does altering protein intake do for CKD

A

uremia is the build up of protein waste. reducing protein intake can preserve kidney fxn! monitor albumin

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35
Q

when should a CKD pt increase protein intake?

A

after dialysis has started!

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36
Q

what are the forms of RRT? (3)

A

peritoneal dialysis
hemodialysis
CRRT

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37
Q

what are the different types of RR access?

A

AV fistula, AV graft, VasCath, PermCath, ABD cath

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38
Q

characteristics of an AV fistula

A

surgical connection of artery and vein!
increases venous blood flow
requires harvesting and maturation– 6 months!
vessel walls have to thicken before it can be accessed

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39
Q

characteristics of an AV graft

A

utilizes synthetic material
used as an alternative to a fistula

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40
Q

what are some care points for a fistula?

A

NO BP!! hang a sign over bed. feel for thrill and listen for a bruit Q4. assess distal pulses, s/s of infection.

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41
Q

what is the most common fistula complication?

A

thrombosis!
tPa can be used

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42
Q

what are other complications of a fistula?

A

strictures, infection, and ischemia

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43
Q

how is vascular access used?

A

SHORT TERM

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44
Q

what are the two types of vascular access points for RRT?

A

VasCath and PermCath

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45
Q

what are some complications of vascular access?

A

INFECTION! misplacement and dislodgement
only use femoral site if absolutely necessary
do not use for ANYTHING OTHER THAN DIALYSIS
bleeding

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46
Q

what is peritoneal dialysis?

A

utilizes the peritoneal cavity for the exchange of fluids, waste and e-.

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47
Q

how do they do peritoneal dialysis?

A

they infuse fluid into the peritoneal cavity and let it do its thang

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48
Q

what are some complications of PD?

A

infection
peritonitis
discomfort
bowel perforation

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49
Q

what do RBCs do?

A

deliver O2

50
Q

what do platelets do?

A

form platelet plugs! important for clotting

51
Q

what do WBCs do?

A

provide protection through immunity and inflammation

52
Q

normal level for RBCs

A

4-6 million

53
Q

normal level WBC

A

4,500-11,000

54
Q

normal level platelets

A

150K-450K

55
Q

what is the patho of leukemia?

A

excessive overgrowth of immature leukocytes!
which means…. that we have an abundance of WBCs that can’t fxn–> reduced immunity!

56
Q

three types of leukemia

A

lymphocytic
myelocytic
biphenotypic

57
Q

characteristics of acute leukemia

A

sudden onset
rapidly growing
severe symptoms

58
Q

characteristics of chronic leukemia

A

slow onset, many persist for months to years
slow growing
usually milder symptoms
may not require immediate tx

59
Q

what are some risk factors for leukemia?

A

radiation, viral infection, exposure to chemicals and drugs, genetic factors, immunity factors

60
Q

CV assessment findings with leukemia

A

tachy (r/t anemia)
hypo (r/t anemia)
slow cap refill (r/t anemia)
murmurs (r/t thickness of the blood)
bruits (r/t thickness of the blood)

61
Q

respiratory assessment findings with leukemia

A

tachypnea
infiltrates
respiratory infection: cough, dyspnea, abnormal breath sounds

62
Q

integumentary assessment findings with leukemia

A

pallor
cool
petechiae
skin infections
poor healing wounds
bleeding gums

63
Q

GI/GU assessment findings with leukemia

A

wt loss, N, GI bleeds, hematuria, liver enlargement and spleen enlargement

64
Q

CNS assessment findings with leukemia

A

HA, seizures, fever, fatigue, behavior changes, somnolence

65
Q

MS assessment findings with leuk

A

bone pain, joint swelling and pain, muscle weakness

66
Q

what will be low H&H wise with leuk?

A

H&H, platelets

67
Q

what can WBCs levels be with leuk?

A

they can be low, normal or high!
patients with high immature WBC count @ dx have poorer prog

68
Q

how do we dx leukemia?

A

bone marrow aspiration and biopsy
chromosome analysis
imaging
xray

69
Q

interventions for leuk

A

INFECTION PREVENTION!!!!
drug therapy

70
Q

for leuk patients, what should we watch for with temp?

A

a 1 degree increase is cause for concern!

71
Q

what is another super important piece of infection prevention for leuk patients?

A

maintain skin integrity!!

72
Q

what are the 3 phases of acute leuk tx?

A

induction
consolidation
maintenance

73
Q

what is the induction phase?

A

combination chemo (7 + 3)
prolonged hospitalization
infection related deaths are common during this time

74
Q

what is the consolidation phase?

A

another round of chemo
occurs early in remission

75
Q

what is the maintenance

A

months to years after induction and consolidation

76
Q

what is the first line drug for chronic leuk?

A

Gleevac (imatinib mesylate)
induces remission in early stages of CML

77
Q

what are some other chronic leuk drugs?

A

MABs, Targeted therapy, allogenic hematopoietic stem cell transplant

78
Q

complications of leuk

A

INFECTION
poor clotting

79
Q

what is Nadir?

A

period of greatest bone marrow suppression

80
Q

what is multiple myeloma?

A

WBC cancer of mature B-lymphocytes

81
Q

what happens when cancer cells excrete excess antibodies?

A

increase protein levels, “clog up” blood vessels to kidneys and other organs

82
Q

what doe myeloma cells do?

A

produce excess cytokines
excess cytokines increase cancer cell growth and bone destruction

83
Q

what else can excessive myeloma cells lead to?

A

reduction in the production of platelets, RBCs and WBCs leading to pancytopenia

84
Q

what are some assessment findings of MM?

A

elevated protein levels
elevated paraprotein levels
fatigue
bone pain
bruising
anemia
fractures
bacterial infections
kidney problems

85
Q

what are some prognosis factors for MM?

A

age, performance status, serum Cr, serum albumin, serum Ca, H&H levels

86
Q

how do we dx MM?

A

x-ray, high levels of IgG and plasma proteins
Bence jones protein in pee
bone marrow biopsy

87
Q

what do we look for on an x-ray for MM?

A

bone thinning and bone loss… swiss cheese appearance

88
Q

what are Bence Jones proteins?

A

protein composed of incomplete antibodies

89
Q

what are some interventions for MM?

A

pain mgmt!
tx options vary based on disease progression
Stem cell transplant

90
Q

what are the standard drug tx options for MM?

A

proteasome inhibitors
immunomodulating drugs
possible steroids

91
Q

intervention complications for mm?

A

myelosuppression!
toxicities
thromboembolic event…
neuropathy
N/V

92
Q

what is lymphoma?

A

cancer of the lymphoid cells and tissue

93
Q

what happens with lymphoma?

A

uncontrolled growth of T cells and B cells

94
Q

what are the two major forms of lymphoma? and what distinguishes them?

A

Hodgkin’s: reed sternberg cells
NHL: no reed sternberg cells

95
Q

what are some characteristics of hodgkin’s

A

reed sternberg
predictable progression

96
Q

what are some possible causes of hodgkin’s?

A

epstein barr virus
HIV
human T cell leukemia/lymphoma virus
exposure to chemicals

97
Q

characteristics of NHL

A

no reed sternberg
unpredictable progression!

98
Q

what are some risk factors of NHL?

A

immune system issues (transplants, HIV), chronic infections, exposure to harmful dust, pesticides and insecticides

99
Q

what is a major assessment finding for any lymphoma?

A

large, painless lymph nodes

100
Q

how do we dx lymphoma?

A

biopsy!

101
Q

what is another important step of dx with lymphoma?

A

staging! must be accurate and is a very detailed process

102
Q

what other findings are important dx factors for lymph?

A

history, LABS, bone marrow aspiration, and imaging.

103
Q

what is a little different about dx with NHL?

A

look at lactate dehydrogenase levels, beta 2-microglobulin levels, also look at CSF

104
Q

interventions with hodgkin’s

A

responds well to aggressive therapy!
radiation + chemo

105
Q

interventions with NHL

A

tx varies based on subtype of tumor.
chemo
MABs
radiation
CAR T cells
targeted therapies

106
Q

what are some intervention complications of hodgkin’s

A

CV disease, secondary malignancies, restrictive lung disease, endocrine dysfunction, hypothyroidism, infertility

107
Q

what are intervention complications of NHL?

A

cytokine storm!!
MAB reactions

108
Q

what is a cytokine storm?

A

comes from CAR T-cell therapy–> enhances patients own immune system to kill cancer cells. this charges up the immune system and releases a lot of inflammatory cytokines

109
Q

what are symptoms of a cytokine storm?

A

flu like
fever, fatigue, body aches, hypotension, edema, decreased UOP

110
Q

what is thrombocytopenia?

A

decrease in platelets

111
Q

what are some causes of thrombocytopenia?

A

increased destruction via spleen
decreased production of platelets
inherited
acquired
drug induced

112
Q

what is autoimmune thrombocytopenia purpura?

A

an autoimmune disease that involves the formation of antiplatelet antibody

113
Q

what is thrombotic thrombocytopenia purpura?

A

also an autoimmune disorder but one that causes abnormal platelet clumping leading to too few platelets in circulation

114
Q

what does TTP lead to/

A

inappropriate clotting –> ischemic events and no platelets left for when clotting is needed

115
Q

what are the first signs of thrombocytopenia seen?

A

skin and mucous membranes!

116
Q

in addition to excessive bleeding with thrombo, what else do we see that causes issues

A

microclots which block the capillaries of organs and tissues leading to ischemia

117
Q

what are interventions for thrombo?

A

blood transfusion, platelet transfusion, minimize injury risk

118
Q

what are drugs for thrombo?

A

drugs that suppress immune fxn like steroids

119
Q

what drugs do we use for ATP?

A

low dose chemo
IV IgG
IV anti-rho (helps prevent destruction of antibody coated platelets)

120
Q

what about drugs for TTP? + 1 intervention that is not a drug :)

A

platelet inhibitors
also not a drug but tx: plasma exchange

121
Q

what are surgical interventions for ATP?

A

splenectomy! only for pts who do not respond to drug therapy
give vax beforehand!!