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Critical Care 2 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

first line of defense cells in the immune system

A

Neutrophils
basophils
eosinophils
natural killer cells
dendritic cells
monocytes
macrophages

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2
Q

special proteins that are included in first line of defense

A

Complement proteins
Cytokines
anti microbial

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3
Q

foreign (to our body) proteins on pathogens are called

A

antigens

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4
Q

dendritic cells internalize the pathogens by

A

phagocytosis

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5
Q

which cell internalizes the pathogen by phagocytosis then displays the antigens on its surface

A

Dendritic cell

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6
Q

After the dendritic cells display antigens on its surface where are the dendritic cells carried

A

lymph nodes on spleen

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7
Q

After the dendritic cells display antigens on its surface, they are carried to the lymph nodes on the spleen where more specialized cells are made which are a part of the second line of defense

A

lymphocytes

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8
Q

what are the 2 main types of lymphocytes

A

B cells and T cells

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9
Q

B cells produce what

A

antibodies - proteins specifically directed at antigens on pathogens

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10
Q

Antibodies that are produced by B cells go where? what happens

A

they bind to the pathogens and then the macrophages clean these complexes up by phagocytosis

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11
Q

2 kinds of T cells

A

Helper cells
Cytotoxic cells

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12
Q

Helper T cells interact with ___ cells to get them to produce more ___

A

B cells
Antibodies

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13
Q

what does cytotoxic T cells do

A

they find the cells that pathogens are hiding in and kill these cells

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14
Q

what cells are made once an infection is cleared

A

Memory B cells
Memory T cells

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15
Q

JIA is arthritis of how many joints for at least ___ weeks in a child of what age?

A

1 or more joints for at least 6 weeks in a child younger than 16 yrs old

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16
Q

JIA in 4 or fewer joints

A

oligoarticular JIA

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17
Q

JIA in 5 or more joints

A

Polyarticular JIA

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18
Q

high spiking fevers of at least 2 weeks plus arthritis

A

what is systemic onset JIA

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19
Q

JIA with positive ANA increases risk of

A

iritis and uveitis

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20
Q

symptoms of systemic JIA

A

fatigue
anemia
fever
salmon-colored macular rash
hepatosplenomegaly
lymphadenopathy

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21
Q

ESR and CRP is typically normal in what type of JIA

A

Oligo

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22
Q

how often are optho eye screenings done in Systemic JIA vs Oligo or Poly JIA

A

Systemic JIA - every 12 mos
Oligo or poly JIA - every 6 mos
Oligo or Poly JIA if <7 yrs and Positive ANA - every 3-4 mos

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23
Q

Psoriatic arthritis symptoms

A

Arthritis in small and large joints
psoriatic rash
Dactylitis
Nail pitting

if no rash
-family h/o psoriasis in first degree relative

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24
Q

in psoriatic arthritis there is a risk of uveitis which requires

A

slit lamp exam every 6 months

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25
Q

psoriatic arthritis may have what positive markers

A

ANA
HLA B27

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26
Q

Enthesitis-related arthritis usually occurs in what age group

A

> 8 yrs

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27
Q

symptoms of Enthesitis-related arthritis

A

pain, stiffness and loss of mobility of the lower back
can present with arthritis in lower extremity joints

Positive HLA-B27

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28
Q

malar rash
photosensitivity (rash in reaction to sunlight)
oral ulcers
arthritis
serositis

A

Systemic Lupus erythematosus

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29
Q

Labs for SLE

A

CBC - potential cytopenias

CMP - Liver and renal function

ANA - positive ANA

Anti-dsDNA - at time of dx and to monitor activity

C3 and C4 low or undetectable levels during disease activity

Anti-Smith antibody - highly specific for SLE

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30
Q

what labs are used to monitor disease acitvity. SlE

A

Anti-dsDNA
C3 and C4

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31
Q

transplacental passage of maternal SSA or SSB antibodies

A

Neonatal lupus erythematosus

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32
Q

symptoms of Neonatal lupus erythematosus

A

fetal bradycardia
Congenital heart block in 30% (30-50% willl need pacemaker)

Rash will resolve 6 months later but heart block stays

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33
Q

Meds used in SLE

A

Hydroxychloroquine

Corticosteroids

Cyclophosphamide

other immunosuppressive
agents

NSAIDS

Calcium
Vit D

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34
Q

inflammation of sacroiliac joints (SI) and the axial skeleton

A

Ankylosing spondylitis (AS) and spondyloarthropathy

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35
Q

Low back pain characteristics for
Ankylosing spondylitis (AS) and spondyloarthropathy

A

worse in morning and improves with exercise

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36
Q

labs in Ankylosing spondylitis (AS) and spondyloarthropathy

A

High ESR and CRP
Positive HLA B27

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37
Q

Bamboo sign

A

This is Bridging syndesmophytes

characteristic of
Ankylosing spondylitis (AS) and spondyloarthropathy

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38
Q

recurrent parotitis

A

think sjogren syndrome

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39
Q

management of sjogren syndrome

A

artificial tears
pilocarpine tablets
antimalarial for skin rash and arthritis

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40
Q

sjogren syndrome has a risk of

A

lymphoma

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41
Q

Blood transfusions started in what years and why

A

maternal hemorrhage
1600s

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42
Q

A type lab tells you what

A

ABO and RH

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43
Q

Forward and reverse typing
what does this mean?

A

testing the antigens on the Red cell and they are testing what AB are in the plasma

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44
Q

Surface markers on blood typing is the presence or absence of what?

A

2 antigens (A and B) on RBC

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45
Q

Isohemaglutinins on blood typing is the presence or absence of what?

A

antibodies in the serum directed against missing A and B

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46
Q

Antibodies develop by what age so what does this mean if you are doing a type and screen in a baby <4 months

A

12 months of age

only need one type and screen test bc they only create one AB. immune system is still underdeveloped

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47
Q

The screen part of a type and screen is also known as

what does it do?

A

Indirect antiglobulin test or an “indirect coombs”

detects AB in the serum

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48
Q

Agglutination in the screen part of the type in screen is a ____ test

A

positive - must do further testing to evaluate for presence of AB and then identify the AB

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49
Q

how does the screen part of the type and screen work? (aka indirect antiglobulin test or indirect coombs)

A

you have antibodies in serum
They use a reagent
They are looking to see if the reagent causes the RBCs to clump
If It is positive then a Direct Antiglobulin Test (DAT) AKA Coombs is done

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50
Q

Direct Antiglobulin Test (DAT) is also known as

A

Coombs

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51
Q

Coombs is also known as

A

Direct Antiglobulin Test (DAT)

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52
Q

Patients can develop antibodies from

A

Pregnancy
Transfusion
Transplantation

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53
Q

Repeat type and screen every 72 hours is because

A

They need to re-screen the patient. This is to see if because they have been exposed to transfusion, have they now developed antibody

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54
Q

what is Allo vs Auto Antibody source

A

Allo - AB formed in response to
pregnancy
Transfusion
Transplantation
These antibodies are targeted against a antigen that is not present on the patients RBC

Auto
AB formed in response to patients own RBC

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55
Q

what type of Antibody source?
AB formed in response to
pregnancy
Transfusion
Transplantation
These antibodies are targeted against a antigen that is not present on the patients RBC

A

Allo

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56
Q

what type of antibody source?
AB formed in response to patients own RBC

A

Auto

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57
Q

How does AB formed after transfusion work

A

A pt is transfused. donor RBC can have antigens. You form antibodies against these antigens. Next time your transfused, you can develop hemolysis.

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58
Q

If the pt has developed antibodies against antigens from previous blood products we give them what

A

antigen negative blood product
(specifically Kell neg but can be other antigens)

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59
Q

Antigen vs Antibody
Where are these found

A

Antigen is on the RBC
Antibody are in the plasma

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60
Q

what is done to prevent bacterial contamination during blood product collection

A

the first 30 ml is separated into an alloquat that would contain the skin plug from puncture to help prevent bacterial contamination also for donor infectious disease contamination

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61
Q

Product is received to blood bank after testing usually by day

A

day 3

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62
Q

blood donors tested for Covid, why?

A

so they can use their plasma in very sick covid pt in hopes that they get their antibodies to help fight the infection

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63
Q

All blood products are filtered through ____ _____ filters

A

white cell - larger than red cells so these filters capture large amount of white cells (Leukoreduction)

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64
Q

term for
white cell - larger than red cells so these filters capture large amount of white cells

A

Leukoreduced

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65
Q

Leukoreduction helps to prevent

A

transfusion associated graft vs host disease

febrile non-hemolytic transfusion reactions (FNHTR)

transmission of disease - viruses live in white cells. The more you can decrease number of white cells, the more you decrease the risk such as CMV

HLA Alloimmunization -

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66
Q

when would leukoreduction not occur

A

in autologous (banking for self)

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67
Q

types of crossmatching

A

Serologic (Tube testing)- recipient plasma an donor RBC is spun to see if there is clumping = ABO incompatibility

Electronic - 2 confirmed ABO/Rh at TCH + no antibody history + negative current antibody screen

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68
Q

when is Serologic crossmatching used (tube testing)

A

if recipient is AB positive, otherwise electronic crossmatching is used

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69
Q

why is irradiation used
what circumstances?

A

Leukoreduction does not get rid of all white cells. Irradiation is used so remaining white cells cant replicate (leads to transfusion associated graft vs host disease - extremely rare but fatal)

Immunodeficient - don’t have the immune system to keep donor white cells at bay

-Transplant (pre and post bone marrow, solid organ)

-Immunocompromised (Malignancy, iatrogenic or acquired)

-Immunodeficiency (suspected/confirmed primary cellular or combined)

-Age consideration (Fetus, infant <3 months old)

-Other (Granulocytes, HLA matched platelets, directed donation from blood relatives)

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70
Q

_____% of donor population is CMV negative

A

10%

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71
Q

2 examples guest speaker gave for when they would use CMV negative blood product because it is so rare

A

SCID (severe combined immunodeficiency)

DiGeorge

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72
Q

why is the risk for CMV negative and CMV safe blood product nearly the same

A

due to the window period for CMV. You could have been exposed recent but not testing positive for it yet.

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73
Q

what is volume reduction for blood product

A

for platelets
plasma removed.
in fluid overload concerns and anaphylaxis

impacts quality of platelet product significantly

Adds 2 hrs to processing

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74
Q

Blood product washing

A

RBC and platelets

done for IgA deficiency and severe anaphylaxis

impacts quality of platelet product significantly

Adds 2 hrs to processing

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75
Q

word for partial unit of blood product

A

aliquot

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76
Q

1 apheresis unit for platelets is approx ___ mL

A

250

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77
Q

1 unit per “bag” of RBC is approx ____ -___ mL

A

250-400mL

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78
Q

1 unit increases hgb approx

A

1-2 g/dL

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79
Q

____ is the preservative now used in RBCs which means what

A

Adsol -
42 day storage
<50mL plasma
HCT 55-60%
less citrate

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80
Q

Platelets have a ___ day shelf life

A

5

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81
Q

Platelets increase count by

A

30k-60k

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82
Q

Jumbo unit of plasma is equal to how many regular

A

4-5

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83
Q

It takes about ____ minutes to thaw FFP

A

45

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84
Q

Plasma contains all of the _____ cascade

A

coagulation

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85
Q

Cryo contains factors

A

VIII
XIII
Fibrinogen

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86
Q

good fibrinogen level is >

A

200

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87
Q

most important in clotting

A

Fibrinogen - spiderweb for RBCs to attach to in order to clot

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88
Q

Concentrated amount of fibrinogen is found in what product

A

Cryo

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89
Q

most transfusion reactions occur in the first

A

15 min

however can start 4 hours later

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90
Q

what temp increase do you need to see to suspect a transfusion reaction and stop the transfusion

A

1 degree C or 2 degree F from pre-transfusion

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91
Q

differentials on temp increase for transfusion reactions

A

Acute hemolytic Transfusion Reaction (AHTR)

Bacterial contamination - maybe they are sick with another bacteria and just happen to spike

underlying condition

Febrile non-hemolytic transfusion Reaction (FNHTR)

Post transfusion purpura and transfusion associated graft versus host disease - rare but fatal

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92
Q

clinical presentation of Acute hemolytic Transfusion Reaction (AHTR)

A

-fever and chills (most common)
-Pain (back or infusion site)
-hypotension/shock
-hemoglobinuria
-impending doom

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93
Q

Work up for Acute hemolytic Transfusion Reaction (AHTR)

A

Positive DAT
Hemoglobinemia/uria
Elevated indirect and direct bilirubin
DIC findings (clot clot clot, bleed, bleed, bleed) -> plasma exchange these pt
RBC abnormalities

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94
Q

management for Acute hemolytic Transfusion Reaction (AHTR)

A

Stop the transfusion
hydration and diuresis
Plasma exchange?
Transfusion medicine
Prevention!

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95
Q

Febrile non-hemolytic transfusion Reaction (FNHTR) symptoms

A

This is a diagnosis of exclusion!
Fever (temp increase of about 2 degree F)

chills, shakes, rarely rigors

Mild dyspnea or tachypnea

usually within 4 hours of transfusion and resolves within 2 hours

Benign …uncomfortable but no long lasting deficits

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96
Q

Febrile non-hemolytic transfusion Reaction (FNHTR) usually occurs within ____ hours of transfusion and usually resolves within ___ hours

A

4
2

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97
Q

Febrile non-hemolytic transfusion Reaction (FNHTR) is from the ___ cells from a ____ release

A

White cells
cytokine release

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98
Q

Resp distress from transfusion reaction occurs ___ - ____ hours after transfusion

A

6-12

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99
Q

S/S of resp distress in transfusion reaction

A

Tachypnea
decreased oxygen saturation

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100
Q

What can cause respiratory distress in transfusion reactions

A

Anaphylaxis

TRALI (immune response)

TACO (volume intolerance)

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101
Q

TRALI is a _____ response

A

immune

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102
Q

TACO is a _____ intolerance

A

volume

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103
Q

difference in chest Xray in TRALI vs TACO

A

identical

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104
Q

What do you need order in resp distress after Transfusion reaction

A

BNP
Chest x ray

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105
Q

tell me about TACO

A

increased hydrostatic pressure (Pmv) from too fast of rate, too much volume or pt has congestive heart issues, renal issues or started the transfusion fluid overload.

causes leak of protein poor edema

diuresis and they usually do great

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106
Q

Tell me about TRALI

A

immunologic issue

Neutrophils live in lungs to keep them healthy. Occasionally a donor will form neutrophil antibody and when recipient has matching neutrophil antigen. Immune response -> capillary leak syndrome

This causes protein rich edema fluid to leak inside alvoli

they may respond to diuresis but will continue to be sick for the next 24-72 hours

Treat with resp support: may need to be intubated

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107
Q

TRALI vs ARDS

A

TRALI gets better in 2-3 days. ARDS takes much longer

108
Q

TRALI type I vs type II

A

in type one the pt had no resp symptoms at all. In type II, they had some resp symptoms before the transfusion and now much worse

109
Q

Allergic reaction to transfusion
stepwise approach to premedication

A

Stepwise approach

Premedicate
1. Benadryl (H1)
2. Benadryl (H1) + Hydrocortisone
3. Benadryl (H1) + Pepcid (H2) + Hydrocortisone and Zyrtec qhs

110
Q

General transfusion threshold is Hgb of ___

A

7

111
Q

Transfusion ___-___mL/kg

A

10-15mL /kg and only 1 unit at a time

112
Q

Our platelet threshold is

A

20,000 but they are working on adjusting down to 10,000 in non-bleeding patients

113
Q

TCH is moving to a massive transfusion protocol Plasma:RBC ratio

A

1:1

114
Q

remember, anemia is a ___ diagnosis

A

secondary….its a symptom

115
Q

s/s for anemia

A

pallor
DOE dyspnea on exertion)
SOB
Fatigue
Bounding pulses
pallor
Tachycardia

Severe
dizziness
palpitations
chest pain
CHF symptoms
hypotension
lethargy
confusion
arrhythmia
CHF signs

116
Q

anemia definition

A

reduced RBC measures (Hgb, HCT, RBC count) - normal depends on age, race, gender

117
Q

reasons for anemia

A

Bleeding

diet related (are they strict vegan and not getting any B12)

Family history of bleeding disorders?

Bone marrow suppression

Meds - NSAIDs, ASA, Bactrim or other antimicrobials

118
Q

cells responsible for transportation of O2/CO2 around the body

A

RBCs

119
Q

iron containing protein with the RBC that carries O2

A

hemoglobin

120
Q

the percentage of total blood volume occupied by RBCs

A

Hematocrit

121
Q

the average volume of a single RBC

A

Mean Corpuscular Volume (MCV)

122
Q

a measurement of the variability of red cell side

A

Red Cell distribution width (RDW)

123
Q

Higher Red cell distribution width (RDW) indicates

A

Greater variation in size

124
Q

small cells that assist with clotting

A

platelets

125
Q

blood cells that make up the immune system

A

WBC

126
Q

Onc labs

A

CBC with diff
Chem
Tumor Lysis labs (LDH, uric acid, phos level)
Blood cultures
DIC panel
Consider CRP, ESR
Infectious workup as indicated (UA, UC, resp panel, viral titers, Quantiferon if concerned for TB)

127
Q

Tumor lysis labs

A

LDH
uric acid
phos level

128
Q

most common and second most common childhood cancer

A

ALL
AML

129
Q

AML and ALL are caused by ____ mutations

A

sporadic not hereditary
other siblings and future children are not at higher risk and do not need to be tested

130
Q

Very elevated WBC, what level and what are you concerned for

A

> 191
high risk for
tumor lysis syndrome
vaso-occlusive crisis

131
Q

T cell ALL and Lymphoma can have a ___ on x ray

A

Mediastinal mass on chest x ray

132
Q

electrolyte disturbances associated with tumor lysis syndrome

A

Hyperkalemia
Hyperphosphatemia
hypocalcemia
hyperuricemia

133
Q

destruction may be due to a spontaneous or treatment related causes, resulting in electrolyte and metabolic imbalances
(oncology)

A

tumor lysis syndrome

134
Q

onc emergency associated with cytotoxic chemotherapy, including corticosteroids

A

Tumor lysis syndrome

135
Q

what organs are highest concern in tumor lysis syndrome

A

Kidneys: uric acid deposits in the kidney and causes injury

Liver: Uric acid deposits and can cause liver injury

Heart: elevated K+ can cause arrhythmia with v fib or v tach

136
Q

what medication is used to help keep uric acid from accumulating in tumor lysis syndrome

A

Allopurinol

137
Q

Gold standard for diagnosis for leukemia

A

Bone marrow biopsy

138
Q

time line for bone marrow biopsy in new onc diagnosis

A

within 72 hours

139
Q

To diagnose leukemia you need > ___% blasts in bone marrow

A

20%

140
Q

in flow cytometry
Lower CD numbers (CD4, CD8) are typically ____ cells

A

T cells

141
Q

in flow cytometry
Higher CD numbers (CD19, CD20) are typically ____ cells

A

B cells

142
Q

ALL induction treatment

A

Day 1: Lumbar puncture to look for CNS involvement

Intrathecal cytarabine: Day 1

Vincristine: Day 1, 8, 15, 22

Dexamethasone: Days 1-28

Pegasparagase: Day 4

Intrathecal Methotrexate: Day 8 and 29

Bone marrow biopsy is done again on day 29 to look for Minimal Residual Disease (MRD)

143
Q

After ALL induction there is a bone marrow biopsy to look for Minimal Residual Disease (MRD) -what is the hope?

A

Hope is the blast cells are <0.01% (down from >20% on initial bone marrow biopsy)

If > 0.01%, they are classified under high risk and will need more intensive chemotherapy moving forward

144
Q

Tumor lysis syndrome treatment

A

Stabilize cardiac membrane if evidence of heart involvement - Calcium Gluconate, lasix, Kayexalate, Insulin, albuterol

Elevated uric acid: Allopurinol (TID) or Rasburicase (once daily)

Hyperphosphatemia: AlternaGel (binds to phosphorous) q 4 hours

145
Q

Onc patients who present with fever:
What antibiotic choices for both
If immunocompromised and
not immunocompromised

A

not immunocompromised
Ceftriaxone - empiric

Immunocompromised
Vanc and Cefepime for empiric

146
Q

fever threshold for oncology pt

A

100.4

147
Q

Rasburicase helps lower uric acid by helping with ____

A

excretion of uric acid by turning uric acid into Allantoin

148
Q

Immature blasts are sticky and can cause similar issues seen in patients with sickle cell such as
-priapism, stroke, kidney inury

A

Vaso-occlusive issues

149
Q

what intervention can worsen or induce vaso occlusive crisis in a Leukemia pt

A

RBC transfusion

150
Q

criteria that makes you high risk in leukemia

A

Initial WBC at presentation >50k
Age <1 or >10 yrs
Testicular involvement (usually unilateral, large and firm)
CNS involvement

Also high risk if
-unfavorable genetics (such as Philadelphia chromosome
-Not under remission at end of induction (day 29)

151
Q

most common cause of anemia

A

blood loss

152
Q

Nutrient deficiencies leading to anemia

A

Iron
B12
Folate
leads to decreased effective RBC production

153
Q

Bone marrow disorders that lead to decreased effective RBC production causing anemia

A

SAA (severe aplastic anemia)
pure RBC aplasia
Marrow infiltration

154
Q

name 3 things that cause bone marrow suppression leading to decreased effective RBC production causing anemia

A

Drugs
chemotherapy
irradiation

155
Q

what can cause decreased bone marrow stimulation leading to decreased effective RBC production causing anemia

A

Decreased EPO
decreased T4
Decreased androgens

156
Q

Name 3 things that can lead to anemia of chronic disease leading to decreased effective RBC production causing anemia

A

Infection
inflammation
malignancy

157
Q

What 3 things can cause ineffective erythropoiesis leading to decreased effective RBC production causing anemia

A

Alpha/beta thalassemia
Sideroblastic anemias
MDS (myelodysplastic syndromes)

158
Q

what can cause intravascular hemolysis that causes increased RBC destruction/hemolysis which leads to anemia

A

Microangiopathic processes (TTP, HUS, aortic stenosis)

ABO incompatibility

infection

PNH (Paroxysmal nocturnal hemoglobinuria)

Venom

CU poisoning in wilson disease

159
Q

Where does extravascular hemolysis occur that causes increased RBC destruction/hemolysis which leads to anemia

A

liver
spleen

160
Q

what causes intrinsic hemolysis that causes increased RBC destruction/hemolysis which leads to anemia

A

enzyme deficiencies
hemoglobinopathies
membrane defects

161
Q

What causes extrinsic hemolysis that that causes increased RBC destruction/hemolysis which leads to anemia

A

AIHA (autoimmune hemolytic anemia)
IVIG infusions
liver disease
infections
toxins

162
Q

Low MCV
Normal MCV
High MCV
in anemia classification

A

Microcytic
Normocytic
Macrocytic

163
Q

MCV in Microcytic anemia

A

<80

164
Q

MCV in Normocytic anemia

A

80-96

165
Q

MCV in Macrocytic anemia

A

> 100

166
Q

Anemia differential?
MCV <80
Low Fe
High TIBC
Low ferritin

A

Iron deficiency anemia -> need to determine cause

167
Q

Anemia differential?
MCV <80
Low Fe
Normal or low TIBC
Normal or high ferritin

A

Anemia of chronic disease:
infection
inflammation
malignancy

168
Q

Anemia differential?
MCV <80
Normal to high Fe
Any TIBC
Normal to high ferritin

Iron overload present
Siderocytes on peripheral smear
Sideroblasts on bone marrow

A

Sideroblastic anemia: need to determine cause

169
Q

Anemia differential?
MCV <80
Normal to high Fe
Any TIBC
Normal to high ferritin

Teardrop red cells
Target cells
Splenomegaly
Positive family history

A

Alpha or Beta thalassemia: Perform hemoglobin electrophoresis

170
Q

anemia differential? with MCV 80-96
no blood loss
increased LDH
Increased indirect bilirubin
decreased haptoglobin

A

presence of hemolysis - determine why

171
Q

anemia differential? with MCV 80-96
low reticulocyte response

A

bone marrow suppression…determine why?

172
Q

anemia differential? with MCV 80-96
no blood loss
elevated creatinine

A

renal insufficiency

173
Q

anemia differential?
MCV >100
dysplastic features present
Cytopenias present

A

Myelodysplastic disorder

174
Q

anemia differential?
MCV >100
low B12
elevated methylmalonate
elevated homocysteine

A

B12 deficiency: determine cause

175
Q

anemia differential?
MCV >100
low folate
normal methylmalonate
elevated homocysteine

A

folate deficiency:
determine cause

176
Q

anemia differential?
MCV >100

A

increased reticulocytes
liver disease
hypothyroidism
drugs

177
Q

lab test?
uses venous blood to measure iron molecules that are bound to transferrin

A

serum iron

178
Q

lab test?
the sum of all iron binding sites on transferrin
-serves as an indirect measurement of transferrin

A

Total Iron Binding Capacity (TIBC)

179
Q

TIBC serves as an indirect measurement of

A

trasferrin

180
Q

Lab test?
extent to which sites on transferrin are filled by iron ions

A

Transferrin Saturation % Sat

181
Q

Lab test?
an intracellular protein that stores iron; correlates with total iron body stores. An acute phase reactant

A

Ferritin

182
Q

most common cause of blood loss in men and women

A

men: GI bleeding
women:Menstrual bleeding

183
Q

during Menstruation women lose average of about ___mg of iron /day

A

1 mg of iron/day

184
Q

causes of iron deficiency

A

blood loss
diet low in iron
malabsorption of iron

185
Q

name 3 problems that can cause malabsorption of iron

A

Celiac disease
H. pylori
autoimmune gastritis

186
Q

Treatment for iron deficiency

A

stabilize pt
stop blood loss
Replace with supplements PO/IV

-Ferrous salts: Ferrous sulfate( drug of choice), fumarate, gluconate, ect

187
Q

what ferrous salt is drug of choice for iron replacement

A

Ferrous sulfate

188
Q

When is iron best absorbed

A

before meals but best tolerated after meals

189
Q

Ferrous sulfate is best absorbed when taken with

A

OJ or ascorbic acid

Take 2 hrs before or 4 hours after antacids

Don’t take with calcium

190
Q

Don’t take ferrous sulfate with

A

calcium

191
Q

Take ferrous sulfate either ___ hrs before or __ hrs after antacids

A

2 before
4 after

192
Q

Side effects of ferrous sulfate

A

metallic taste
n/v
flatulence
constipation
diarrhea
epigastric pain
black/green stools

193
Q

Length of therapy for ferrous sulfate in iron def treatment

A

3 months to build up hgb/hct, another >=3 months to build up stores. Chronic therapy for chronic bleeding

194
Q

Acute iron poisoning causes

A

GI necrosis
CNS depression
Shock

195
Q

Emergency treatment for iron tox

A

Deferoxamine chelation

196
Q

any type of chronic disease >1-2 months duration can cause ___ due to inflammatory, infectious, malignancy

A

anemia

197
Q

low serum iron
low or normal transferrin/TIBC
high or low % saturation
High or normal ferritin

A

Anemia of chronic disease

198
Q

Low serum iron
high transferrin/TIBC
low % sat
Low ferritin

A

Iron deficiency anemia

199
Q

appetite for substances not fit for food

A

Pica

200
Q

Pica for ice

A

Pagophagia - can be seen in iron deficiency state

201
Q

symptoms for microcytic anemia

A

Pica
glossal pain
dry mouth
tongue papillary atrophy
Atrophic glossitis
Koilonychias (spoon nails)

202
Q

Diagnosis for Sideroblastic anemia

A

ringed sideroblasts on prussian blue reaction of BMA

increased serum iron
increased ferritin

203
Q

Common causes for Sideroblastic anemia

A

Drug induced
lead poisoning
chronic alcoholism

204
Q

Treatment for sideroblastic anemia

A

Treat cause
Remove offending agent

205
Q

Most common causes of macrocytic anemia

A

B12 and folate deficiency

206
Q

Macrocytic anemia is a _____ _____ disorder

A

DNA replication disorder - cells are arrested at an immature stage and do not divide correctly leading to larger cells

207
Q

classes of drugs that can cause macrocytic anemia

A

antiviral drugs
chemotherapeutic agents
long term use of antacids

208
Q

what foods are B12 (cobalamin) in

A

Meat
milk
cheese
eggs

209
Q

causes of B12/cobalamin deficiency

A

poor absorption

strict vegans

Alcoholism

Poor absorption (gastric bypass surgery, Crohn’s, Celiac)

Long term use of antacid

pancreatic insufficiency

Pernicious anemia (MCC): :lack of intrinsic factor in the gut to absorb B12

210
Q

other name for B12

A

Cobalamin

211
Q

B9/Folate deficiency causes

A

Poor intake

alcoholism

poor absorption

Medications (phenytoin, trimethoprim, sulfa drugs, pyrimethamine, methotrexate, OCPs (oral contraceptives)

212
Q

Meds that cause B9/folate deficiency

A

phenytoin
trimethoprim
sulfa drugs, pyrimethamine, methotrexate
OCPs (oral contraceptives

213
Q

B9 is

A

folate

214
Q

foods with folate

A

vegetables (esp dark green leafy vegetables - spinach, asparagus, Brussel sprouts)
Fruits and fruit juices
nuts
beans
peas
dairy products
poultry
meat (liver)
Eggs
Seafood
Grains

215
Q

dietary def that is a reversible cause of dementia

A

B12

216
Q

which deficiency can cause neuro symptoms?
B12 or Folate

most common symptom?

A

B12

most common is sock and glove parasthesias

217
Q

folic acid therapy

A

1mg PO daily for 1-4 months is sufficient

Parenteral form can be given for malabsorption

no established side effects

218
Q

B12 therapy

A

Generally
1mg IM daily x 1 week
1 mg weekly x 1 month
1 mg q month

Can also do daily 1-2 mg PO daily however erratic absorption

Inexpensive, no known side effects

Treat reversible causes to prevent life long supplementation

219
Q

Neurological side effects are usually reversible if treated within ____ months of onset

A

6

220
Q

labs to order in Normocytic anemia

A

peripheral smear
LDH
indirect bilirubin
haptoglobin
retic
Creatinine

221
Q

If you have low Hgb and low Hct with normal RDW and MCV

A

may be acute blood loss because body has had no time to compensate with increased production or fluid balance

222
Q

hormone made in cortex of kidney to tell bone marrow to produce more blood

A

Erythropoietin (EPO

223
Q

synthetic EPO

A

Epoetin or Darbepoetin

224
Q

Black box warning for EPO

A

increased clotting risk (MI, CVA, DVT)

pure red cell aplasia

225
Q

-immature RBCs
- a quantitative measure of bone marrow production for new RBCs, should rise in response to anemia

A

Reticulocytes

226
Q

cells in Erythropoiesis

A

Proerythroblasts
Basophilic erythroblasts
Polychromatophilic erythroblasts
Orthochromatophilic erythroblasts
Reticulocytes
Erythrocytes

227
Q

low ferritin is pathopneumonic for

A

iron deficiency anemia

228
Q

Alcohol has a direct toxic effect on the ____ _____ (when talking about anemia)

A

bone marrow

229
Q

Ethanol inhibits folate absorption in the

A

jejunum

230
Q

for lupus, having a sibling with lupus increases your risk for developing by

A

8-20 fold higher risk

231
Q

what genotypes have higher risk for SLE

A

Caucasians at higher risk with genotype by 2-3x
HLA-DR2 and HLA-DR3

African Americans
HLA-DR2 and DR7

232
Q

gender higher risk for SLE

A

Equal in <5yo but increases 4-5x in females <16

233
Q

what syndrome has increased risk for SLE

A

Males with Klinefelter syndrome have relative deficiency of androgens and increased frequency of SLE

234
Q

drugs that cause medication induced lupus syndrome

A

Drugs
Most commonly Antiepileptic drugs (shipp)
SHIPP, where
S- Sulfonamide
H -Hydralazine
I -Isoniazid
P -Procainamide and Phenytoin.

235
Q

factors (not genetic) that can induce lupus

A

Crystalline silica
cigarette smoking,
exogenous estrogens,
UV radiation,
viral infections and
industrial chemicals (industrial solvents, and pesticides)

Crystalline silica is a common mineral found in the earth’s crust. Materials like sand, stone, concrete, and mortar contain crystalline silica.

236
Q

When you see a limp, think

A

this may be a rheum issue

237
Q

proximal muscle weakness
Heliotropic rash
Gottron’s papules

A

Dermatomyositis

238
Q

Dermatomyositis revealed what elevated labs

A

CPK
Aldolase
LDH
AST, ALT

239
Q

In Dermatomyositis
What will you see on MRI and muscle biopsy

A

MRI: diffuse muscle inflammation
Muscle biopsy: inflammation, atrophy

240
Q

Purpura (and petechiae)
Joint complaints - soft tissue swelling (+/- arthritis)
ABd pain -> obstruction (intussusception)
Renal involvement -> hematuria, proteinuria, and HTN

A

Henoch-Schonlein Purpura (HSP)

241
Q

Scleroderma has what other organs involved

A

heart
GI tract
lung involvement

242
Q

types of scleroderma

A

Morphea
Linear scleroderma
coup de sabre

systemic sclerosis - tight shiny skin with distal tapering

243
Q

KD symptoms

A

Conjunctivitis (limbic sparing)
Rash
Adenopathy (cervical)
Strawberry tongue
Hands and feet
Burn (fever for 5 days)

244
Q

Diagnostic criteria for KD

A

fever for >= 5 days and 4/5 crash and burn

Bilat, nonpurulent limbic sparing conjunctivitis

Rash: polymorphic - trunk, extremities, groin

Adenopathy:
-cervical
-Unilateral
-Node >=1.5 cm

Strawberry tongue
-prominent papillae
-erythema of oral mucosa and lips

Hands and feet changes
-swelling
-erythema
-periungual desquamation 2 weeks after fever onset

245
Q

incomplete KD criteria

A

Children with >= 5 days fever and 2 or 3 compatible clinical criteria or
infants with fever for >= 7 days without other explanation

Then
CRP >3 and or ESR >= 40
plus 3 or more lab findings
1. anemia
2. platelet count of >=450,000 after the 7th day of fever
3) albumin <3 g/dL
4) elevated ALT
5) WBC of >=15,000
6) Urine >= WBC
or positive echocardiogram

Then treat

other path
CRP <3.0 and ESR <40
Then
serial clinical and lab re-evaluation if fevers persist
echocardiogram if typical peeling develops

246
Q

diff types of rash seen in KD

A

Maculopapular
Morbiliform
Targetoid
Scarlatiniform
Never vesicular

247
Q

what kind of rash is this

A

maculopapular

248
Q

describe rash

A

Morbiliform

249
Q

describe rash

A

Targetoid

250
Q

describe rash

A

Scarlatiniform

251
Q

describe rash

A

vesicular

252
Q

lab findings in KD

A

Anemia
leukocytosis
thrombocytosis,
elevated CRP
elevated ESR
Hypoalbuminemia
elevated ALT
sterile pyuria
pleocytosis

253
Q

Mainstays of KD treatment

A

IVIG
ASA moderate high dose for the first 48-72 hours and after fever subsided. Low dose for 4-6 weeks or until aneurysms resolve

If develop fever after IVIG 72 hours then it is refractory
2nd dose IVIG

IVIG 2 gm/kg and high-dose ASA 80-100 mg/kg/day every 6 hours
ASA dose is decreased to 3-5 mg/kg/day after the pt is afebrile for 48-72 hours. It’s then continued for 6-8 weeks for antiPLT affect. However, if coronary artery abnormalities are present, then ASA therapy is indefinite and based on risk level.

254
Q

“pulseless disease” primarily affects the aorta and its branches→ can result in stenosis and occlusion

A

Takayasu Arteritis (TA)

255
Q

Takayasu Arteritis (TA) gender and age

A

Frequently seen in females 15-30 years

256
Q

HTN followed by loss of pulses and (+) bruits
Malaise, fever, abd pain, elevations in acute inflammatory markers, wt loss, visual abnormalities, HA, dyarthrias, arthralgias, and seizure
Other PE findings= extremity systolic BP variance (10 mmHg), subclavian artery/abd aorta bruit, decreased or absent brachial artery pulse, or normochromic/normocytic anemia

A

Takayasu Arteritis (TA)

257
Q

Takayasu Arteritis (TA) s/s

A

HTN followed by loss of pulses and (+) bruits
Malaise, fever, abd pain, elevations in acute inflammatory markers, wt loss, visual abnormalities, HA, dyarthrias, arthralgias, and seizure
Other PE findings= extremity systolic BP variance (10 mmHg), subclavian artery/abd aorta bruit, decreased or absent brachial artery pulse, or normochromic/normocytic anemia

258
Q

dx Takayasu Arteritis (TA)

A

US, MRI, MRA, CT angio, biopsy of affected vessel
MRA may provide greater clarification of vessel changes but will not detect calcification, which can help determine chronicity of inflammation

259
Q

tx Takayasu Arteritis (TA)

A

corticosteroids to decrease progression, immunosuppression prevents restenosis and improves control, and endovascular intervention can increase 5 year survival to 80-95%. Typical cytotoxic medications include cytoxan, tocilizumab, MTX, and anti-TNF agents

260
Q

KD is predominantly in what age

A

5 yrs and younger
Very rare in children older than 12 or younger than 3 months

261
Q

Phases in KD

A

ACUTE PHASE 10-14 days
1. fever and classic presentation (CRASH and BURN) plus acute myocarditis
● SUBACUTE PHASE 2-8 weeks
1. Resolution of acute symptoms
2. Coronary aneurysms develop
● CONVALESCENT PHASE
1. Last many months
2. Clinical symptoms and lab findings resolve
3. Coronary aneurysms develop, persist, resolve

262
Q

In IgA deficiency has a high association with what type of reaction

A

anaphylaxis

263
Q

lupus with a type ___ hypersensitivity reaction

A

III

264
Q

Anaphylaxis is a type ___ hypersensitivity reaction

A

1

265
Q

most common anaphylaxis triggers

A

food (e.g., eggs, shellfish, nuts), medications (e.g., antibiotics, nonsteroidal anti-inflammatories), and stinging.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1339). Wolters Kluwer Health. Kindle Edition.

Critical Care 2 (14 decks)

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