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Critical Care 2 > Exam 2, deck 3 > Flashcards

Exam 2, deck 3 Flashcards

1
Q

most common age groups for VTE

A

neonates and teenagers

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2
Q

most common precipitating factor in VTE

A

Central venous access device (CVAD)

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3
Q

Anticoagulation in symptomatic and asymptomatic deep vein thrombosis or pulmonary embolism

A
  1. The American Society of Hematology (ASH) guideline panel recommends using anticoagulationin pediatric patients with symptomatic deep vein thrombosis (DVT) or pulmonary embolism (PE) (
  2. The ASH guideline panel suggests either using anticoagulation or no anticoagulation in pediatric patients with asymptomatic DVT or PE
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4
Q

Thrombolysis, thrombectomy, and inferior vena cava filters in VTE

A
  1. against using thrombolysis followed by anticoagulation; rather, anticoagulation alone should be used in pediatric patients with DVT, submassive PE

2.The ASH guideline panel suggests using thrombolysis followed by anticoagulation, rather than anticoagulation alone, in pediatric patients with PE with hemodynamic compromise

3.suggests against using thrombectomy followed by anticoagulation; rather, anticoagulation alone should be used in pediatric patients with symptomatic DVT or PE

  1. suggests against using inferior vena cava (IVC) filter; rather anticoagulation alone should be used in pediatric patients with symptomatic DVT or PE
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5
Q

Antithrombin replacement therapy in VTE

A
  1. The ASH guideline panel suggests against using antithrombin (AT)-replacement therapy in addition to standard anticoagulation; rather, standard anticoagulation alone should be used in pediatric patients with DVT/cerebral sino venous thrombosis (CSVT)/PE
  2. ASH guideline panel suggests using AT replacement therapy in addition to standard anticoagulation rather than standard anticoagulation alone in pediatric patients with DVT/CSVT/PE who have failed to respond clinically to standard anticoagulation treatment and in whom subsequent measurement of AT concentrations reveals low AT levels based on age-appropriate reference ranges
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6
Q

CVAD-related thrombosis

A
  1. suggests no removal, rather than removal, of a functioning CVAD in pediatric patients with symptomatic CVAD-related thrombosis who continue to require venous access

2, removal, rather than no removal, of a nonfunctioning or unneeded CVAD in pediatric patients with symptomatic CVAD-related thrombosis

  1. suggests delayed removal of a CVAD until after initiation of anticoagulation (days), rather than immediate removal in pediatric patients with symptomatic central venous line–related thrombosis who no longer require venous access or in whom the CVAD is nonfunctioning
  2. ASH guideline panel suggests either removal or no removal of a functioning CVAD in pediatric patients who have symptomatic CVAD-related thrombosis with worsening signs or symptoms, despite anticoagulation and who continue to require venous access
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7
Q

Use of Low-molecular-weight heparin vs vitamin K antagonists in DTE

A

The ASH guideline panel suggests using either low-molecular-weight heparin or vitamin K antagonists in pediatric patients with symptomatic DVT or PE (conditional recommendation based on very low certainty in the evidence of effects

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8
Q

what happens in DIC

A

hemostasis is out of control
leading to coagulation all over the place
leads to organ ischemia
This uses up platelets and clotting factors

Other parts of body start to bleed even with slight damage of walls.
They have too much and too little clotting

Fibrin degradation products in circulation interferes with clot formation making hemostasis even more difficult

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9
Q

DIC is also called

A

consumption coagulopathy

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10
Q

Lab findings in DIC

A

decreased platelets
decreased fibrinogen
prolonged PT/PTT
elevated D Dimer (fibrin degradation product)

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11
Q

Treatment DIC

A

support organs with
-Ventilator
-Hemodynamic
-Transfusions
all if needed

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12
Q

fever/neutropenia def by megan harvey

A

A single temp of 38.3C (101) or

2 episodes of 38 (100.4) and above within a 24 hr period

or

Temp of 39C (100.4) persistent for one hour taken axillary orally or by tympanic probe

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13
Q

ANC formula by meg harvey

A

WBC x (%segs +%bands)

ANC <1500 neutropenia
ANC <1000 moderate neutropenia
ANC <500 severe neutropenia
ANC <100-200 profound neutropenia

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14
Q

When is ANC typically at lowest

A

7-14 days from start of round of chemo

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15
Q

common infection culprits in febrile neutropenia

A

Gram + Bacteria - coag neg staph. Staph aureus, strepto viridans and midas
Gram - Bacteria, enterobacter, pseudomonas
Anaerobic Bacteria - Clostr dificille, propionbacterum acnes
Fungus
Viruses- hsv varicella zoster, ebv, cmv, ect
others - pjp

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16
Q

what studies do you avoid in febrile neutropenia

A

lumbar puncture
tap shunt or reservoir

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17
Q

Abx in febrile neutropenia

A

Monotherapy
-Cefepime 50mg/kg IV q 8
-Meropenem 20-40 mg/kg IV q8
-Zosyn 80-100 mg/kg IV q8

Dual therapy
-Ceftazidime 33-50mg/kg IV q 8 and
Tobramycin 7.5 mg/kg/day IV q8 or 7-9mg/kg IV Q24
(monitor trough levels weekly with aminoglycoside administration due to nephron and ototoxicity)

Anaerobes
-Clindamycin 40mg/kg IV q6 (aspiration pneumonia)
-Flagyl 7.5mg/kg IV q6
-give flagyl if concern for abd infection, typhlitis, perianal or mucosal skin breakdown

Add Vanc if
-AmL receiving high dose Cytarabine (Ara-C) with risk of S.viridans due to interruption of mucosal integrity and risk of sepsis
-hypotensive or have signs of shock
-Mucositis
-Prior h/o alpha hemolytic strep bacteremia
-Concern for catheter site infection or skin breakdown
-Colonized with resistant organisms only sensitive to vancomycin
-Cardiac vegitations

(At risk for tox, monitor trough levels with goal of 10-15 for bacteremia, 15-20 for meningitis)
(at risk for impaired renal function, monitor renal function, electrolytes and fluid balance daily)

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18
Q

Vanc trough level goal for bacteremia and meningitis

A

10-15 for bacteremia
15-20 for meningitis

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19
Q

when should you cover for fungal in fever neutropenia

A

fever persists for >1 week

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20
Q

When you have a fever neutropenia pt who you are going to cover for fungal, what to order first

A

fungal blood culture
serum galactomannan

consider ENT consult for eval of sinuses with flexible scope
CT of sinuses, chest and/or abdomen to evaluate for fungal nodes

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21
Q

antifungal agents in fever neutropenia

A

Echinocandins - covers most candida and at least fungistatic to Aspergillus. Empiric fungal agents of choice.
-Micafungin
-Caspofungin
-Anidulafungin

Triazoles - Fungicidal to Aspergillus. If clinically worsening
-Fluconazole
-Voriconazole
-Posaconazole

Amphotericin B
-Significant toxicity potential (nephrotoxic)
-Lipid formulation (Ambisome) has less side effects, but is more expensive

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22
Q

HSV and VZV require treatment with

A

IV acyclovir
Valacyclovir
Famciclovir

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23
Q

If hemoc has VZV how does effect treatment

A

cessation of chemotherapy administration

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24
Q

labs to monitor when give Acyclovir

A

nephrotoxic - monitor renal function and fluid intake closely

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25
Q

CMV in hemonc pt, treat with

A

Ganciclovir
if persistent infection or resistant - transition to Foscarnet or Cidofovir

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26
Q

Hemonc with influenza requires treatment with

A

Oseltamivir
Most effective if given within 48 hrs of symptom onset
Can be given prophylaxis if exposed to virus

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27
Q

Considered an atypical fungus, causes severe pneumonitis in immunocompromised patients

A

Pneumocystis Jiroveci

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28
Q

Pneumocystis Jiroveci diagnosis

A

confirmed by testing induced sputum, lower resp culture
Bronchoalveolar lavage sample
percutaneous needle or open lung biopsy

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29
Q

Pneumocystis Jiroveci prophylaxis in fever neutropenia

A

Bactrim
Pentamidine
consider addition of corticosteroid

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30
Q

in fever neutropenia, continue appropriate antimicrobials until pt

A

remained afebrile for at least 24 hours, negative blood cultures from admission for 48 hours, has neg blood cultures providing clearance of infection and with rising ANC demonstrating appropriate bone marrow recovery

Bone marrow recovery - ANC of >200 and rising on 2 consecutive CBCs

Resolution of neutropenia is ANC >500

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31
Q

type A blood has what AB in Plasma and what antigens on RBCs

A

AB in plasma: Anti-B
Antigens: A antigen

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32
Q

type B blood has what AB in Plasma and what antigens on RBCs

A

AB in plasma: Anti-A
Antigens: B antigen

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33
Q

type AB blood has what AB in Plasma and what antigens on RBCs

A

AB in plasma: None
Antigens in RBC: A and B

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34
Q

type O blood has what AB in Plasma and what antigens on RBCs

A

AB in plasma: Anti-A and Anti-B
Antigens on RBC: none

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35
Q

life threatening disease of bone marrow failure resulting in peripheral pancytopenia and bone marrow aplasia

A

Aplastic anemia

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36
Q

causes of aplastic anemia

A

congenital in 20%

Acquired - exposure to drugs, chemicals, ionizing radiation or viruses

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37
Q

s/s of aplastic anemia

A

History: mucosal/gingival bleeding, headaches, fatigue, easy bruising, rash, fever, mucosal ulcerations, or recurrent viral infections. *

Symptoms: pallor, tachycardia, petechial rash, purpura, ecchymoses, or jaundice.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 785-786). Wolters Kluwer Health. Kindle Edition.

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38
Q

what do labs show in aplastic anemia

A

*Decrease in hemoglobin, white blood cell (WBC) count, and platelet count.
*Reduction in or absence of the absolute number of reticulocytes.
* Peripheral blood smear; no abnormal cells.
*Reduction or absence of hematopoietic elements from bone marrow aspirate.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 786). Wolters Kluwer Health. Kindle Edition.

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39
Q

mgmt of aplastic anemia

A
  • Transfusions of RBCs and platelets.
  • Antibiotic therapy.
  • Bone marrow transplantation (BMT).
    *Immunosuppressive therapy if unable to receive a BMT.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 786). Wolters Kluwer Health. Kindle Edition.

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40
Q

A rare congenital hypoplastic anemia resulting in constitutional bone marrow failure.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 786). Wolters Kluwer Health. Kindle Edition.

A

Diamond-Blackfan Anemia

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41
Q

Mutation for Diamond-Blackfan on chromosome

A

19 which encodes for a ribosomal protein known as RPS19

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42
Q

s/s Diamond Blackfan anemia

A

*Symptoms: pallor, fatigue, irritability, syncope, and dyspnea during feeding.
*Physical examination: irregular heartbeat, hypotonia, short stature, and evidence of failure to thrive.
*Associated with physical defects including craniofacial, hands, upper limbs, cardiac, or genitourinary.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 787). Wolters Kluwer Health. Kindle Edition.

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43
Q

Diamond Blackfan Anemia is associated with what type of physical defects

A

craniofacial, hands, upper limbs, cardiac, or genitourinary.

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44
Q

what do labs look like in Diamond Blackfan Anemia

A

*Profound macrocytic anemia; WBCs and platelet count generally normal.
* Reticulocytopenia.
* Increased percentage of hemoglobin F for age.
* Elevated erythrocyte adenosine deaminase activity. *Decreased or absent erythroid precursors in bone marrow aspirate.
* Genetic screening; Diamond–Blackfan anemia—mutation in RPS19.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 787). Wolters Kluwer Health. Kindle Edition.

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45
Q

management in Diamond Blackfan Anemia

A

*Corticosteroids, frequent blood transfusion, BMT in some cases.
* Hematology, BMT, and endocrinology team involvement.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 787). Wolters Kluwer Health. Kindle Edition.

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46
Q

An enzyme that is crucial in aerobic glycolysis

A

Glucose-6-phosphate Dehydrogenase Deficiency (G6PD)

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47
Q

Children who have G6PD-deficient RBCs are susceptible to

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 805). Wolters Kluwer Health. Kindle Edition.

A

oxidative damage and hemolysis during certain conditions of stress, exposure to certain medications, foods, or chemicals. Occurs most often in males.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 805). Wolters Kluwer Health. Kindle Edition.

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48
Q

G6PD deficiency is most common in what gender

A

males

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49
Q

which variant?
G6PD activity is less than 10% of normal, resulting in severe neonatal jaundice or congenital nonspherocytic hemolytic anemia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 805). Wolters Kluwer Health. Kindle Edition.

A

Variant 1

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50
Q

G6PD activity is typically less than 30% of the normal range, resulting in an asymptomatic steady state. Individuals who carry this mutation are at risk for neonatal jaundice, acute hemolytic anemia, and favism.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 805). Wolters Kluwer Health. Kindle Edition.

A

variant 2

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51
Q

which variant?
G6PD Enzyme activity is greater than 85% of the normal reference range, resulting in no clinical manifestations. Considered the “wild type” disease.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 805). Wolters Kluwer Health. Kindle Edition.

A

Variant 3

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52
Q

G6PD is a ___ linked inherited disease that affects primarily ___

A

X-linked inherited disease that affects primarily men.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 805). Wolters Kluwer Health. Kindle Edition.

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53
Q

G6PD is an enzyme required for the production of the reduced form of ____________ which __

A

Nicotinamide adenine dinucleotide Phosphate (NADPH) which is critical in preventing oxidative damage

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54
Q

In G6PD deficiency acute exacerbations may occur with ingestion of ____ and what else

A

fava beans (Favism)
infection
Oxidative drugs ( antimalarials, sulfa containing drugs, ASA, quinolones)

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55
Q

s/s G6PD deficiency

A

Symptoms: fever, nausea, abdominal pain, diarrhea, and occasionally vomiting within 24 to 48 hours after oxidative challenge. *Findings: Dark brown or black discoloration of the urine is present within 6 to 24 hours after exposure (result of hemolysis); jaundice, pallor, tachycardia, hypovolemic shock, and hepatosplenomegaly may develop.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 806). Wolters Kluwer Health. Kindle Edition.

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56
Q

lab findings for G6PD deficiency

A

severe anemia with marked variation in size of RBCs resulting in increase in RBC distribution width

WBC may be elevated
Hemoglobinuria may be present

*Large polychromatic cells with spherocytic morphology as well as markedly irregular-shaped cells known as poikilocytes on peripheral blood smear. *Increased reticulocyte count; may reach levels as high as 30%. *Heinz body stain: As the RBCs circulate through the spleen, Heinz bodies are removed, resulting in classic “bite cells.” Heinz bodies are identified with methyl violet staining and are denatured hemoglobin and a manifestation of the oxidative injury to the hemoglobin.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 806). Wolters Kluwer Health. Kindle Edition.

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57
Q

Mgmt G6PD def

A

*Blood transfusion is indicated if the child is hemodynamically unstable or the hemoglobin level declines to <7g/dL.
*If the hemoglobin is <9 g/dL with evidence of persistent brisk hemolysis with hemoglobinuria, blood transfusion may be indicated.
*Dialysis may be indicated for acute kidney failure.
*Neonatal jaundice related to G6PD deficiency is managed with observation for mild cases, phototherapy, and hydration for more significant cases, and exchange transfusion may be beneficial for severe cases.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 806-807). Wolters Kluwer Health. Kindle Edition.

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58
Q

An acute, systematic, immune complex mediated, small-vessel vasculitis, which is self-limiting and resolves within about 4 weeks, considered the most common vasculitis of childhood.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 801). Wolters Kluwer Health. Kindle Edition.

A

Henoch-Schonlein Purpura

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59
Q

most common vasculitis of childhood

A

Henoch-Schonlein Purpura

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60
Q

Peak age presentation in Henoch-Schonlein Purpura

A

2-8

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61
Q

what months is it more common to see Henoch-Schonlein Purpura

A

fall, winter and spring

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62
Q

most serious complication of Henoch-Schonlein Purpura

A

Renal impairment

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63
Q

Henoch-Schonlein Purpura is usually precipitated by

A

an URI, medication or environmental trigger

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64
Q

what infectious agents associated with Henoch-Schonlein Purpura

A

Group A strep

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65
Q

what happens in Henoch-Schonlein Purpura

A

IgA complexes are deposited in the small vessels of the renal glomeruli, skin and GI tract causing petechiae, purpura, GI bleeding and Glomerulonephritis

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66
Q

s/S Henoch-Schonlein Purpura

A

*Recent upper respiratory tract infection and prodrome of fever and fatigue.
* Commonly presents with tetrad of symptoms:

*Rash: nonpruritic, erythematous papules or wheals that progress to petechiae, and nonblanching, palpable, purpuric lesions >10 mm diameter; found in dependent areas of body that are subject to pressure and extensor surfaces of the extremities. Trunk is usually spared, and lesions fade over 10 to 12 days.

  • Polyarthralgias: pain, swelling, decreased range of motion; Lower extremity joints most frequently involved.
  • “Bowel angina” - diffuse, colicky abdominal pain with melena and vomiting; approximately 70% of patients.
  • Renal symptoms with hematuria, proteinuria, and hypertension; approximately 20–60 % of patients weeks to months after initial presentation
  • Mild renal impairment may progress to nephrotic syndrome and ARF.
  • Renal biopsy consistent with focal and proliferative glomerulonephritis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 801-802). Wolters Kluwer Health. Kindle Edition.

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67
Q

lab findings in Henoch-Schonlein Purpura

A

*Based on clinical features and presenting symptoms; renal function should be evaluated at baseline. * Platelets normal or elevated. * BUN and creatinine may be elevated. * Normal coagulation studies. *Immune antibody panel—Presence of IgA antibodies in the blood, skin, or glomeruli may help to confirm diagnosis. * Urinalysis for evaluation of blood and protein.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 802). Wolters Kluwer Health. Kindle Edition.

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68
Q

management of Henoch-Schonlein Purpura

A

*Rest and activity limitations, with symptomatic management of systemic complications, NSAIDS.
*Oral prednisone; indicated for patients with kidney involvement.
*Henoch-Schönlein purpura resulting in severe kidney disease may require plasma exchange, high-dose IV immunoglobulin (IVIG), or immunosuppressant agents.
* Long-term management of hypertension may be required.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 802-803). Wolters Kluwer Health. Kindle Edition.

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69
Q

a disease of the microcirculation, is characterized by hemolytic anemia, thrombocytopenia, and acute renal failure (ARF).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 791). Wolters Kluwer Health. Kindle Edition.

A

Hemolytic Uremic Syndrome (HUS)

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70
Q

Hemolytic Uremic Syndrome (HUS) occurs most frequently in what age

A

children <4 years

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71
Q

Most common cause of acute renal failure

A

Hemolytic Uremic Syndrome (HUS)

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72
Q

what causes Hemolytic Uremic Syndrome (HUS)

A

*Contamination of water, meat, fruits, and vegetables with infectious bacteria; peak incidence during summer.

*E. coli 0157:H7 is the most common etiology of postdiarrheal (D+) HUS.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 791). Wolters Kluwer Health. Kindle Edition.

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73
Q

types of HUS

A

*D+ HUS—Postdiarrheal or typical HUS; occurs in previously healthy children who have had recent gastroenteritis. Mortality rate is 3% to 5%; associated with renal failure in 50% to 70% of patients affected. Bacterial verotoxins, absorbed through intestinal mucosa, are produced by E. coli O157:H7 infection (Shiga toxin; most common cause), Shigella dysenteriae, Citrobacter freundii, and other subtypes of E. coli (also Shiga toxin).

*D−HUS—Atypical or sporadic HUS is less common and more severe than D+HUS with an approximately 25% mortality rate. It is associated with end-stage renal disease in approximately 50% of cases. More common in adulthood, atypical D−HUS infection may have a familial link and may also begin in the neonatal period; occurs year round with no gastrointestinal (GI) prodrome. Causative factors include Inherited factor H deficiency (10%–20%); inhibits complement activation, Membrane cofactor protein mutations, Streptococcus pneumoniae infection, medications including Cyclosporine and Tacrolimus.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 791-792). Wolters Kluwer Health. Kindle Edition.

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74
Q

what does ESR and CRP look like in Oligo, poly and systemic JIA

A

They can be normal in Oligo
Poly may be mildly elevated
systemic will be more elevated

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75
Q

racoon eyes, abd discomfort, no trauma…what should you be thinking

A

neuroblastoma

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76
Q

butterfly or malar rash, think

A

Systemic lupus erythematosus

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77
Q

s/s Systemic lupus erythematosus

A

Photosensitivity - rash in reaction to sunlight
oral ulcers - usually painless
Nonerosive arthritis
Serositis (pleuritis)
Renal disorder (persistent proteinuria)
Seizures
Anemia, leukopenia, lymphopenia

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78
Q

main worry after BMT

A

Graft vs host disease

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79
Q

if suspecting Lupus (SLE), but ANA comes back negative. How likely is it to still be Lupus

A

Very unlikely positive in 99%

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80
Q

Anti-dsDnA is used at time of diagnosis and beyond for Lupus (SLE), why?

A

to monitor disease activity

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81
Q

C3 and C4 in Lupus (SLE)

A

low or undetectable during a flair

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82
Q

Anti Smith antibody is highly specific fof

A

Lupus (SLE) positive in 50% . not used to monitor disease activity

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83
Q

SSA or SSb Ab in Neonatal lupus erythematosus causes destruction to what

A

conductive system of the heart. Typically leads to congenital heart block. 30-50% of these babies will need a pacemaker

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84
Q

what is the mother given during pregnancy in suspected neonatal Lupus erythematosus

A

Dexamethasone for Fetal bradycardia to prevent further destruction of conductive system of heart

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85
Q

After birth in neonatal lupus erythematosus, what is the prognosis

A

most will need a pacemaker
they may have rash or other lupus symptoms
usually all symptoms resolve except heart block approx 6 months later

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86
Q

Video source: lupus (SLE) medication management

A

Hydroxychloroquine
corticosteroids
Cyclophosphamide (Cytoxan)
Other immunosuppressive agents
NSAIDS
Calcium (due to corticosteroids)
vitamin D (due to corticosteroids)

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87
Q

inflammation of sacroiliac joints (SI) and the axial skeleton

A

Ankylosing Spondylitis (AS) and Spondyloarthropathy

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88
Q

Ankylosing Spondylitis (AS) and Spondyloarthropathy s/s

A

Low back pain that is worse in the morning and improves with exercise

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89
Q

expected lab findings in Ankylosing Spondylitis (AS) and Spondyloarthropathy

A

High ESR and CRP
Positive HLA B27 (helps support dx but not required)

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90
Q

Radiology findings for Ankylosing Spondylitis (AS) and Spondyloarthropathy

A

Sacroiliitis with sclerosis

Bamboo sign: Bridging syndesmophytes

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91
Q

Bamboo sign on x ray

A

Ankylosing Spondylitis (AS) and Spondyloarthropathy

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92
Q

clinical presentation of sjogren syndrome

A

recurrent parotitis
keratoconjunctivitis sicca (more common in adults)

Keratoconjunctivitis sicca is chronic, bilateral desiccation of the conjunctiva and cornea caused by too little tear production or accelerated tear evaporation. Typical symptoms include intermittent itching; burning; blurring, a gritty, pulling, or foreign body sensation; and photosensitivity.

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93
Q

Labs to pay attention to in Sjogren syndrome

A

Anti-Ro (SS-A) or Anti-La (SS-B)

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94
Q

management of sjogren syndrome

A

Artificial tears
Pilocarpine tablets
Antimalarial for skin rash and arthritis

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95
Q

sjogren syndrome is associated with r/o

A

lymphoma

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96
Q

infections associated with reactive arthritis

A

GI infections
-shigella
-salmonella
-yersinia
-Campylobacter
-C.Diff
GU infections
-UTIS, ect

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97
Q

reactive arthritis is developed _____-___ weeks after infection

A

2-4

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98
Q

reactive arthritis is usually in how many joints

A

more than one but can be only one

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99
Q

typical triad s/s of reactive arthritis

A

Noninfectious urethritis
Arthritis
Conjunctivitis

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100
Q

expected labs in reactive arthritis

A

elevated ESR and CRP
HLA-B27 positive in 65-96% (helps support case but doesnt rule in or rule out)

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101
Q

treatment for reactive arthritis

A

supportive care

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102
Q

JDM s/s

A

muscle pain and weakness

Skin rash
-photosensitivity
-Gottron papules
-Heliotrope rash

Calcinosis cutis

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103
Q

labs to look for in JDM

A

Elevated CK level

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104
Q

Treatment in JDM

A

Prednisone
Sun voidance
Hydroxychloroquine

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105
Q

s/s systemic scleroderma

A

pruritic skin
Raynaud’s phenomenon
difficulty swallowing
shortness of breath
Joint pain and limitation of movement
weakness

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106
Q

lab to look for in systemic scleroderma

A

Positive SCL 70 (topoisomerase) in 2/3 of pt

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107
Q

pruritic skin
Raynaud’s phenomenon
difficulty swallowing
shortness of breath
Joint pain and limitation of movement
weakness

A

systemic scleroderma

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108
Q

muscle pain and weakness

Skin rash
-photosensitivity
-Gottron papules
-Heliotrope rash

Calcinosis cutis

A

JDM

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109
Q

recurrent parotitis
keratoconjunctivitis sicca (more common in adults)

A

Sjogren syndrome

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110
Q

target sign on US
what can it be seen in?
(they have a rash)

A

intussusception - can be seen in HSP

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111
Q

s/s in localized scleroderma

A

Streak involve the face En coup de Sabre
seizure
Uveitis

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112
Q

Treatment in localized scleroderma

A

mainly supportive
physical therapy if joints resolve

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113
Q

Streak involve the face En coup de Sabre
seizure
Uveitis

A

localized scleroderma

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114
Q

Prognosis in localized scleroderma

A

resolve spontaneously within 3-4 years

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115
Q

Behcet’s disease diagnostic criteria

A

recurrent oral ulcers 3 times over 1 year
+ at least 2 of the following

-Recurrent genital ulceration
-eye inflammation
-Characteristic skin lesions
-positive pathergy test

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116
Q

Treatment for Behcet’s disease (video)

A

Azathioprine
or
Infliximab

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117
Q

test to confirm Behcet’s disease

A

Pathergy test
- Pathergy test, in which your doctor inserts a sterile needle into your skin and examines the area one to two days later. If the test is positive, a small red bump forms under your skin where the needle was inserted. This indicates your immune system is overreacting to a minor injury

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118
Q

most common vasculitis in children

A

Henoch-Schonlein purpura (HSP)

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119
Q

s/s in Henoch-Schonlein purpura (HSP)

A

purpura
arthritis
GI
-abd pain
-GI bleeding

Nephritis
subcutaneous edema
scrotal edema

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120
Q

purpura
arthritis
GI
-abd pain
-GI bleeding

Nephritis
subcutaneous edema
scrotal edema

A

Henoch-Schonlein purpura (HSP)

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121
Q

diagnosis for Henoch-Schonlein purpura (HSP)

A

clinical diagnosis
Platelet count may be normal or elevated (if low, suggests different diagnosis)
occult blood may positive
ESR can be elevated
Screen for blood or protein in urine

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122
Q

In Henoch-Schonlein purpura (HSP) what do you monitor and for how long

A

Monitor for at least 6 months even if initial was normal

proteinuria
BP for HTN

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123
Q

treatment for Henoch-Schonlein purpura (HSP)

A

Supportive (hydration , NSAIDS)

Corticosteroid (controversial) however consider in:
-persistent nephrotic syndrome
-severe abd pain
-severe scrotal edema
-neurologic system involvement

Immunosuppressive in complicated cases

d/c causative drug

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124
Q

diagnostic criteria for Kawasaki disease (video)

A

Fever lasts longer than 5 days plus

4/5 of following main clinical features
-changes in peripheral extremities (redness, edema of hands and feet, followed by desquamation)
-polymorphous rash
-oropharyngeal changes
-bilat, nonexudative, painless bulbar conjunctival injection (redness in both eyes without discharge)
-acute non-purulent cervical lymphadenopathy with lymph node diameter greater than 1.5cm, usually unilateral

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125
Q

common associated symptoms of KD

A

Hydrops of gallbladder
d/v
abd pain
irritability
vomiting alone
cough or rhinorrhea
decreased intake
weakness
joint pain

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126
Q

echo protocols in KD (video)

A

at time of dx
repeat in 2nd week
again 1 month after all labs have normalized
1 year if at 8 week no coronary involvement

Refer to pediatric cardiologist at anytime if echo is abnormal

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127
Q

labs suggestive of KD

A

no specific lab test to dx

CRP >= 3 or ESR >=40
WBC >= 15000
Normocytic, normochromic anemia
Pyuria: >= 10 wbc (clean catch instead of cath is better, can miss the pyuria if collected by cath)
Serum ALT >50
Serum albumin <= 3.0 g/DI

After 7 days of illness, platelet cell count >= 450,000

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128
Q

tx for KD (video)

A

IVIG (withing first 10 days of illness)
-2g/kg infusion over 12-14 hrs
-watch for anaphylaxis and aseptic meningitis
-relieves acute inflammation to decrease risk of C. aneurysm

Oral ASA
-80 -10mg/kg/day until fever resolves
-decrease to 3-5mg/kg/day if fever resolved and stop if no cardiac involvement after 6-8 weeks

IVIG and ASA have a synergistic effect and gives antiplatelet activity

you can also give corticosteroids

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129
Q

s/s growing pain

A

diagnosis of exclusion
believed to be a type of stress injury

bilat extremity pain
intermittent pain
pain occurs during evening
can wake from sleep
resolves by morning
does not limit during the day
occurs after days of significant activity

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130
Q

diagnosis of exclusion
believed to be a type of stress injury

bilat extremity pain
intermittent pain
pain occurs during evening
can wake from sleep
resolves by morning
does not limit during the day
occurs after days of significant activity

A

growing pain

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131
Q

treatment for growing pain

A

reassurance
Ice
heat
massage
NSAID

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132
Q

s/s reflex sympathetic dystrophy

A

chronic pain syndrome
pain affect one or more limb
often result of trauma or surgery
limb becomes swollen, red, mottled, warm, cold, sweaty (sympathetic reflex)
-pain is usually out of proportion of touch (hyperalgesia)

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133
Q

diagnosis of reflex sympathetic dystrophy

A

clinical dx

Affected area may show demineralization on x ray

less uptake on bone scan

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134
Q

treatment in reflex sympathetic dystrophy

A

aggressive physical therapy
Gabapentin or
Amitriptyline

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135
Q

s/s Familial Mediterranean Fever (MEFV)

A

periodic fever

severe abd pain

Pleuritis

Pericarditis

scrotal swelling

Erysipelas-like rash may appear around ankle

arthritis, arthralgia, myalgia

key points: periodic fever + pain +/- family history

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136
Q

Familial Mediterranean Fever (MEFV) is autosomal

A

recessive

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137
Q

Complications of Familial Mediterranean Fever (MEFV)

A

Amyloidosis leads to proteinuria and renal failure

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138
Q

dx of Familial Mediterranean Fever (MEFV)

A

clinical dx

can be supported by genetic testing but not excluded by it

ESR, CRP, WBC usually elevated during attack

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139
Q

Treatment for Familial Mediterranean Fever (MEFV)

A

Colchicine

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140
Q

PFAPA stands for

A

Periodic fever
Aphthous Stomatitis
Pharyngitis
Cervical Adenitis

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141
Q

Age for PFAPA

A

6 mos - 7 years

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142
Q

Periodic fevers in PFAPA usually last how many days

A

5-7 days

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143
Q

In PFAPA, fever cycles usually stops by what age

A

Teenage years

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144
Q

Treatment for PFAPA (video)

A

NSAID
single dose of steroids
tonsillectomy

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145
Q

Periodicity for PFAPA is usually how long

A

less than 4 weeks

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146
Q

painful muscle
weakness
facial rash
elevated ck

A

dermatomyositis

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147
Q

painful, swollen knee joints,
limited rom for 8 weeks
all other exams and labs are normal
ESR and CRP normal

A

Oligoarticular JIA

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148
Q

rash worse on sun exposure
joint pain
chest pain
fatigue
anemia

A

SLE

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149
Q

4 year old boy
bilat leg pain at night
no pain in the morning
physical exam is normal
very active

A

growing pain

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150
Q

recurrent pain oral ulcers for the last 2 years
deterioration of vision
skin rash

A

Behcet’s disease

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151
Q

Recurrent fever
abd pain
scrotal swelling
rash on both ankles
elevated ESR
in between attacks ESR is normal
Negative MEFV

A

FMF

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152
Q

encompasses a complex group of disorders comprising several clinical entities with the common feature of arthritis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1347). Wolters Kluwer Health. Kindle Edition.

A

Juvenile Idiopathic Arthritis

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153
Q

*JIA is a ________disorder, and the subtypes have varying clinical and laboratory features that may reflect distinct immunopathogenic processes.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1347). Wolters Kluwer Health. Kindle Edition.

A

heterogeneous

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154
Q

labs in JIA (lippincott)

A

antinuclear antibody (ANA), rheumatoid factor, and anti–cyclic citrullinated peptide; a positive ANA test does not confirm a diagnosis of JIA but may be prognostic for uveitis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1349). Wolters Kluwer Health. Kindle Edition.

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155
Q

what category of drugs are used in JIA

A

Anti-inflammatory drugs: corticosteroids—oral and intra-articular injections.
* Immunomodulatory therapy with disease-modifying antirheumatic drugs.
* Tumor necrosis factor α inhibitors.
* Interleukin (IL) inhibitors.
* T-cell- and B-cell-targeted therapy.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1349). Wolters Kluwer Health. Kindle Edition.

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156
Q

A small- to medium-vessel vasculitis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1350). Wolters Kluwer Health. Kindle Edition.

A

KD

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157
Q

Joint pain only

A

arthralgia

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158
Q

When you call something Arthritis you should be using objective findings such as

A

Joint effusion
Warmth
reduced range of motion
+/- pain
usually not erythema

(dr muscal talk)

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159
Q

inflammation of tendon

A

tendonitis

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160
Q

inflammation of the part of the tendon that connects into the bone

A

Enthesitis

161
Q

gel phenomena

A

if they are in one position for a long time, stiff

162
Q

Arthritis stiffness pattern

A

worse with rest, better with activity

163
Q

% of kids with JIA have a pos ANA

A

only 50%

164
Q

acutely swollen joint, particularly if painful with limited motion should be presumed to

A

be infected and evaluated urgently

165
Q

arthrocentesis
WBC >100,000
% PMNs >75

A

Septic

Polymorphonuclear leukocytes (PMNs) are a type of white blood cell (WBC) that include neutrophils, eosinophils, basophils, and mast cells. PMNs are a subtype of leukocytes, which protect the body against infectious organisms. PMNs are also known as granulocytes

166
Q

Arthrocentesis
WBC <75,000
% PMNs <50

A

Inflammatory

Polymorphonuclear leukocytes (PMNs) are a type of white blood cell (WBC) that include neutrophils, eosinophils, basophils, and mast cells. PMNs are a subtype of leukocytes, which protect the body against infectious organisms. PMNs are also known as granulocytes

167
Q

Arthrocentesis
WBC <2000
% PMNs <25

A

Non-inflammatory

Polymorphonuclear leukocytes (PMNs) are a type of white blood cell (WBC) that include neutrophils, eosinophils, basophils, and mast cells. PMNs are a subtype of leukocytes, which protect the body against infectious organisms. PMNs are also known as granulocytes

168
Q

Arthrocentesis
WBC <200
% PMNs <25

A

normal

Polymorphonuclear leukocytes (PMNs) are a type of white blood cell (WBC) that include neutrophils, eosinophils, basophils, and mast cells. PMNs are a subtype of leukocytes, which protect the body against infectious organisms. PMNs are also known as granulocytes

169
Q

recent strep infection about 2-3 weeks prior
Positive ASO titer
+ Anti-DNAse B
asymmetric arthritis
Migratory arthralgias
doesn’t affect axial skeleton
Prompt response to NSAIDS/ASA
Short duration of arthritis
Pericarditis rare

A

Acute Rheumatic fever

170
Q

Acute Rheumatic fever
s/s and labs

A

recent strep infection about 2-3 weeks prior
Positive ASO titer
+ Anti-DNAse B
asymmetric arthritis
Migratory arthralgias
doesn’t affect axial skeleton
Prompt response to NSAIDS/ASA
Short duration of arthritis
Pericarditis rare

171
Q

can be symmetrical arthritis (not required)
not migratory
Can affect axial skeleton
slow response to NSAIDS/ASA
Prolonged duration
Can have pericarditis
30% + ASO titers
- Anti-DNAse B (no)

A

JIA

172
Q

antecedent streptococcal infection about 2 weeks prior so + ASO titer

Arthritis symmetry
Not migratory
can affect axial skeleton
slow response to NSAIDS/ASA
prolonged duration
Pericarditis rare
+ Anti-DNAse B

A

Poststreptococcal arthritis (PSRA)

173
Q

In Poststreptococcal arthritis (PSRA) how long do you need antibiotic prophylaxis

A

1 year

174
Q

Other than KD what rheum disease is ASA used routinely to prevent carditis

A

Acute rheumatic fever

175
Q

Meds mentioned in muscal lecture for Acute rheumatic fever

A

ASA 60-100mg/kg div qid
PCN prophylaxis (carditis?)
-PCN VK 250mg po BID
-Bicillin 1.2 million units q 4 weeks (>27kg)

176
Q

Polyarticular JIA with ANA + will need Optho screening how often?
evaluate for?

A

3-4 months
Anterior uveitis

177
Q

anterior uveitis involves what parts of eye

A

cornea and lens

178
Q

In Spondyloarthritis or Enthesitis-related arthritis what lab marker is specific but not sensitive

A

HLA-B27

179
Q

In Spondylarthritis or Enthesitis-related arthritis what lab marker is specific but not sensitive

A

HLA-B27

180
Q

exam finding that suggests Enthesitis

A

Press on Achilles tendon, if positive they will jump off table in pain

other joints to check:
shoulders
SI joints
chest wall
hip joints where femur connects to hip

181
Q

Is RF useful in diagnosing kids with JIA

A

useless

182
Q

Meds in JIA (muscal lecture)

A

Daily chronic administration of NSAIDS

Corticosteroids - bridge therapy

Disease modifying or immunomodulating agents
-Methotrexate, tumor necrosis factor blockers
-Enbrel
-Humira
-Remicaide

183
Q

rheum drug with side effect of retinopathy

A

hydroxychloroquine

184
Q

which type of arthritis is associated with symptomatic uveitis

A

Enthesitis Related arthritis (ERA)
In poly and oligo its typically asymptomatic

185
Q

IgA deficiency is highly associated with what type of allergy

A

anaphylaxis

186
Q

what happens in the second exposure in anaphylaxis

A

mast cell activation occurs rapidly because the antigen-specific IgE has already bound to the mast cells via IgE receptors, making the cascade of inflammatory reactions rapid.

*Activation of mast cells and basophils triggers a rapid release of various inflammatory and newly formed mediators, including histamine, tryptase, leukotrienes, prostaglandins, platelet-activating factor, and various cytokines.

*Mediators affect various target organs, including the heart, lungs, vasculature, gastrointestinal tract, and skin.

*Heart rate, myocardial contractility, coronary blood flow, and electrical conduction through the sinoatrial and atrioventricular nodes are affected by the release of histamine and platelet-activating factor, causing decreased cardiac output and possible myocardial ischemia.

*Bronchospasm and increased mucus production in the lungs can occur as a result of mediator release.

*Vasodilation and increased vascular permeability lead to hypotension, distributive shock, and eventually impaired oxygen delivery.

*Increased vascular permeability of the airways and intestinal tract causes laryngeal edema and gastrointestinal upset.

*Mucocutaneous symptoms of flushing, angioedema, urticaria, and pruritus occur as a result of histamine release.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 1340-1341). Wolters Kluwer Health. Kindle Edition.

187
Q

clinical presentation of Anaphylaxis

A
  • Rapid onset: minutes to hours. *Hives, itching, abdominal pain, emesis, stridor, wheezing, shortness of breath, laryngeal edema, hypotension, and shock.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1341). Wolters Kluwer Health. Kindle Edition.

188
Q

what labs are elevated in anaphylaxis

A

plasma histamine levels, serum total tryptase levels, and serum IgE levels, if measured during or following an anaphylactic episode, are all elevated.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1341). Wolters Kluwer Health. Kindle Edition.

189
Q

Mild Anaphylaxis where you gave only one dose epi, how long to monitor after

A

4-6 hours of obs after epi

190
Q

Moderate Anaphylaxis - slower to resolve and/or have asthma, how long do you obs after epi

A

6-8 hours

191
Q

severe anaphylaxis - hypotension, upper/lower airway compromise, multiple doses of epi, how long do you obs after epi

A

24 hours

192
Q

if pt has history of anaphylaxis, what other meds do you need to avoid

A

B blockers
Ace-Inhibitor
monoamine oxidase inhibitors
Tricyclic antidepressants

193
Q

Patients taking ____________ may be resistant to EPI and can lead to unopposed a- adrenergic vasoconstrictor effects wiring blood pressure and perfusion

A

B-adrenergic blockers

If on B blockers first line of choice is still two doses of epi but if not responding may consider glucagon -> reverses refractory hypotension and bronchospasm by increasing cAMP levels through non- B- receptor mechanisms and can be used as adjunctive therapy for B- blocked patients not responding to EPI.

194
Q

The bezold- Jarisch reflex

A

initial tachycardia followed by bradycardia
(anaphylaxis notes)

195
Q

In anaphylaxis blood tryptase levels peak at _____ hrs and return to baseline by ____ hrs after onset of symptoms. Compare to baseline checked at —- hours after onset of symptoms

A

1-2
5-6
24

196
Q

in anaphylaxis, Histamine lab is less clinically useful due to

A

short half life

197
Q

In anaphylaxis, what is the urine test?

A

Histamine metabolite N-methylhistamine
-24 hour urine collections may be elevated
-Urine prostaglandin levels may also be elevated

198
Q

allergy skin testing measures what

A

Skin testing or measurement of allergen specific IgE levels in the blood → can confirm allergy to clinically suspected triggers

199
Q

treatment of anyphylaxis

A

Assess ABCs and mentation… monitor continuously until reaction improves
Place in recumbent position
Severe →35% of intravascular fluid may shift to extravascular space within 10 minutes → sudden death d/t “empty ventricle syndrome”
GIVE EPI
A- adrenergic
Vasoconstriction, increased peripheral vascular resistance, decrease mucosal edema
B- adrenergic
Increased inotropy/ chronotropy, bronchodilation, decreased mediator release
Immediate treatment is vital → delays have been associated with poor outcomes and death
ONE SHOULD NOT WAIT FOR THE DEVELOPMENT OF POTENTIALLY LIFE THREATENING SYMPTOMS (RESPIRATORY OR CARDIAC) BEFORE EPI IS ADMINISTERED.
Give epi → onset of milder symptoms such as pruritus, urticaria, and angioedema alone.
No absolute contraindication to the use of epi
All other treatment → depends on response to initial epi administration

Route of administration
IM
Young children → ½ inch needle
Obsese children ¾ inch needle
Lateral thigh → vastus lateralis muscle

1mg/mL (1:1,000) dose of 0.01mg/kg (0.01mL/kg) →max dose 0.3mg but may dose up to 0.5mg in large pt or severe non responsiveness
First dose asap → repeated every 5 minutes

IV dosing
0.1mg/ml (1:10,000)
0.1ml/kg to max of 3-5mL

If paradoxical bradycardia occurs → atropine can be used → only after failing to respond to epi

Refractory hypotension
IV EPI 0.05-3mcg/kg/min titrated to lowest effective dose
Consider IV dopamine if not effective
Other options → IV vasopressin or methylene blue

Dosing of AIE devices
0.15mg <20kg technically this is for <15kg but no dosing exists from 15-30kg?
0.3mg >20 kg technically >30kg
New dosing of 0.1mg for children 7.5mg-15kg

200
Q

second line treatment in Anaphylaxis

A

After epi, fluids, assurance of adequate airway, breathing and circulation

H1 antihistamines → benadrly 1-2mg/kg body weight to max of 50
Only oral for mild cases 40-60% less bioavailability for PO benadryl although dosing is the same, may also give cetirizine

Glucocorticoid steroids
100% oral bioavailability

IV only for no PO intake possible

Oral dosing
1-2 mg/kg/dose max 60mg/dose

Can be given IM but no benefits over IV but complications IM
Atrophy at injection site
Increase risk of acute avascular necrosis of the hip joint if given in the thigh
Little evidence in tx of anaphylaxis
Inhaled SABA
Albuterol may be added after EPI for relief of wheezing especially with patient with pre existing asthma

H2 antihistamines (ranitidine)
Protect against stress and steroid induced gastritis
Data regarding efficacy is lacking

201
Q

what meds/drugs sensitize the myocardium to effects of epi, increasing cardiac toxicity

A

cocaine and amphetamines

202
Q

what does epi do in anaphylaxis

A

decreases laryngeal edema
treat hypotension and shock
cause bronchodilation
increase cardiac output by increasing heart rate and myocardial contraction

203
Q

how often can you repeat epi in anaphylaxis

A

every 5-15 min

204
Q

in anaphylaxis, how much NS is often required to treat hypotension

A

30-40ml/kg

205
Q

medication used for mis-c to block cytokine

A

Anakinra -IL-1 blocker

206
Q

Providers should consider mastocytosis or clonal mast cell disorder as an underlying diagnosis for idiopathic anaphylaxis.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1343). Wolters Kluwer Health. Kindle Edition.

A
207
Q

IgG present in blood gives us what clues into MIS-C

A

post infectious
this appears in blood 4-6 weeks after

208
Q

MIS-C criteria

A

< 21 yrs
present with fever
lab evidence of inflammation
requires hospitalization
>=2 organ systems
no other plausible diagnosis
+ or recent Sars-Cov 2 infection or Positive PCR within 4 weeks of symptoms

209
Q

*A group of genetic disorders that affect components of innate and adaptive immune systems and ultimately lead to susceptibility to infection.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1343). Wolters Kluwer Health. Kindle Edition.

A

immunodeficiencies

210
Q

s/s MIS-C

A

GI
mucocutaneous
neurological to include headache
others
resp sx
sore throat
myalgias
swollen hands/feed
lymphadenopathy

211
Q

Other dx to consider in mis c picture

A

Typhus
-kids generally look well except with high fever
-Doxy 48-72 hours they will start to defervesce
-Antibody testing -neg early in disease
-Typhus doesnt have a troponin leak like typhus
-Typhus will not need ICU admission

212
Q

labs to check in MIS C

A

SARS -Cov-2 RNA PCR
SARS-Cov-2 antibodies
CBC
Chem 10
Ferritin
Troponin
Albumin
Fibrinogen
BNP
LDH
D-Dimer
Procalcitonin
UA
ALT
AST
CRP

flu/rsv
Murine typhus
Urine, throat, wound cultures

213
Q

abnormal lab findings in Misc

A

lymphopenia
neutrophilia
mild anemia
thrombocytopenia

CRP, ESR, Ddimer, fibrinogen, Ferritin Procal (PCT), IL-6
all inflammatory markers elevated

If fibrinogen is low, you may have a bleeding problem soon (think DIC picture)

Mild disease: increased AST/ALT, LDH, low albumin, elevated triglycerides

214
Q

treatment for MISC

A

Path 1
If they have a complete kd (cKD-like) or incomplete kd (iKD-like) like picture

then

IVIG + steroids
plus
anakinra for shock or cardiac dysfunction

Path 2
does not meet iKD criteria but coronary dilated or other cardiac sign of KD (ie) valvulitis)
then
same as c/ikD like (path 1)

Path 3
If hypovolemic, cardiogenic
and/or distributive shock or
cardiac dysfunction

then
start steroids + anakinra ASAP

Box in corner
Cardiac indications for IVIG
(do not delay hyperinflammatory treatment)
troponin >1
or any two:
1. EF < 50%
2. Troponin >=0.1
3. Classic ECG changes (abnormal ST segments and/or low voltage QRS and/or AV conduction delay and/or ventricular arrhythmia

215
Q

what cells are responsible for coronary dilation in hyperinflammatory states

A

Neutrophils (IVIG helps to get rid of these to prevent coronary dilation)

216
Q

Primary warning signs of primary immunodeficiency

A

> =4 new ear infections within 1 year

Recurrent, deep skin or organ abscesses

> = 2 sinus infections within 1 year

persistent thrush in mouth or fungal infection on skin

> = 2 mos on antibiotics with little effect

Need for IV antibiotics to clear infections

> =2 deep seated infections including septicemia

> = 2 pneumonias within 1 year

Failure of an infant to gain weight or grow normally

A family history of primary immunodeficiency

217
Q

3 guiding principles of ICU medicine

A

DO2 = CO x CaO2 (amount of oxygen dissolved in blood carrying capacity)

MAP=CO x SVR

Never ignore tachycardia

218
Q

what monitoring/information do I need to look at in ICU to determine shock

A

physical exam:
are their peripheral extremities really cold
-is there a significant core to toe temp gradient

-Arterial line - is your lactate going up
acid/base status - base excesss?

CVL - mixed/central venous saturation, CVP

NIRS

219
Q

why is your pt in shock?

A

cardiac output issue?
-ECHO
-Physical exam

Oxygen demand issue (VO2)?

Vasoplegia?
Whats my BP?
Do I have a SVR issue as well?

220
Q

What am I going to do when pt is in shock

A

Is my function impaired?
Increase contractility
-Vasoactives
1) epinephrine
2) milrinone
3) dobutamine

Decrease afterload
1) Nipride/Cardene if BP can tolerate
2) Milrinone (If BP can tolerate) - to take full effect takes 4 hours
3) Positive pressure ventilation

If my oxygen demand (VO2) is excessive, reduce it!
-NIPPV (positive pressure ventilation
-Intubate
-Whiff of sedation
1) ativan
2) precedex - be careful bc it also has beta blockade. watch HR. Can effect cardiac output

221
Q

The real clinical conundrum in MIS-C is the patient is _____ and has ____ _______
what do you need to do?

A

Hypotensive
depressed function

Increase cardiac output as much as possible
1) increase contractility (i.e. epinephrine)
2) Optimize fluid status - be careful not to fluid overload. 2.5-5ml/kg
3) Positive Pressure Ventilation - CPAP

BP/SVR support?
-Norepinephrine
or Vasopressin (not a inotrope. Just effects SVR….nothing to help heart squeeze)
Be careful with both

VA ECMO when all else fails

222
Q

syndromes associated with primary immunodeficiency

A

22q11 deletion (DiGeorge syndrome)

Ataxia telangiectasia

223
Q

sinopulmonary infections with encapsulated organisms

A

Humoral Immunodeficiency

224
Q

failure to thrive, respiratory tract or gastrointestinal infections, candidal skin infections, Pneumocystis jiroveci pneumonia.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1345). Wolters Kluwer Health. Kindle Edition.

A

Combined SCIDs

225
Q

(CGD): infection with catalase-positive organisms (Escherichia coli, Pseudomonas, Klebsiella, Serratia, Salmonella, Candida, and Aspergillus).

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1345). Wolters Kluwer Health. Kindle Edition.

A

Phagocytic (CGD) Immunodeficiency

226
Q
  • Early complement defects: sepsis.
  • Late complement defects: Neisseria infections.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 1345). Wolters Kluwer Health. Kindle Edition.

A

Complement Immunodeficiency

227
Q

what AB is the primary player in allergic rx

A

IgE

228
Q

acute urticaria
anaphylaxis
oral allergy syndrome

is mediated by what AB?

A

IgE

229
Q

Food protein induced enterocolitis syndrome is mediated by what AB

A

Non-IgE mediated

230
Q

Atopic dermatitis
Eosinophilic Gastroenteritis
is mediated by what AB

A

Mixed IgE and non-IgE mediated

231
Q

allergic contact dermatitis
is mediated by what AB

A

Cell mediated

232
Q

Lactose intolerance is mediated by

A

Metabolic issue

233
Q

Caffeine intolerance is mediated by

A

pharmacologic issue

234
Q

Scromboid fish toxin is mediated by

A

Toxic issue

235
Q

Sulfites intolerance is mediated by

A

idiopathic

236
Q

An adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food

A

food allergy

237
Q

presence of IgE antibodies to a food, often in absence of clinical symptoms

A

Sensitivity

238
Q

s/s IgE mediated allergic reactions

A

oropharynx:
oral pruritis
lip swelling
tongue swelling
throat tightening

GI:
Crampy abd pain
nausea
vomiting
diarrhea

Cutaneous
Urticaria
angioedema

Resp
SOB
Stridor
Cough
Wheezing

Cardiovascular
-Feeling of faintness
-Syncope
-Chest pain
-dysrhythmia
-Hypotension

Conjunctival erythema
Tearing
Aura of impending doom
Seizures

239
Q

any food can induce anaphylaxis but the majority of the most severe reactions are triggered by

A

peanut
tree nuts
seafood

240
Q

Pollen-food Syndrome (oral allergy syndrome)

A

rapid onset oral pruritis and mild angioedema caused by raw fruits and vegetables

Pollen allergens are the primary sensitizers and homologous proteins in plant-derived foods elicit symptoms

30-70% of people with allergic rhinitis have oral allergy syndrome.

Cross reactivity
Birch -> Apple and carrot family

Ragweed -> Melons, Banana

Grass -> Melon, Tomato, Potato, Orange and Swiss chard

Mugwort-> Carrot family, cabbage family, onion family, pepper

241
Q

Pollen-food Syndrome (oral allergy syndrome)

Cross-reactivity foods associated with Birch allergy

A

Apple and carrot family

242
Q

Pollen-food Syndrome (oral allergy syndrome)

Cross-reactivity foods associated with Ragweed

A

Melons
Banana

243
Q

Pollen-food Syndrome (oral allergy syndrome)

Cross-reactivity foods associated with Grass

A

Melon
Tomato
Potato
orange
swiss chard

244
Q

Pollen-food Syndrome (oral allergy syndrome)

Cross-reactivity foods associated with Mugwort

A

Carrot family
cabbage family
onion family
pepper

245
Q

Labs for Immunodeficiency

A

CBC :
anemia
thrombocytopenia
lymphopenia
neutropenia

Quantitative immunoglobulins (IgG, IgA, IgM, IgE)

suggests immunoglobulin def:
Total protein - low
albumin - normal

Antibody titers to vaccines

Complement activity
-CH50
-C3
-C4

Nitroblue tetrazolium dye test: evaluate for CGD

246
Q

Primary vs secondary immunodeficiency

A

Primary - genetic, rare
Acquired - more common, caused by something (HIV, malnutrition, malignancy, DM, splenectomy, ect)

247
Q

treatment for cellular immunodeficiency

A

Bone marrow transplant depending on severity

248
Q

tx for Combined AB and cellular immunodeficiency

A

Strict isolation
BMT
IVIG
Pneumocystis prophylaxis (Bactrim)

249
Q

Tx for Phagocytic immunodeficiency

A

treat infection
Bactrim prophylaxis
Recombinant Gamma interferon

250
Q

Tx for complement immunodeficiency

A

prevent infection with vaccines

prompt treatment of infection

251
Q

How long do you have to remove a food from diet to see if linked to atopic dermatitis

A

7-14 days. Then reintroduce food. If you have an exacerbation, this pinpoints that food

35% of children with moderate-severe atopic dermatitis have food allergies as a trigger

252
Q

Prevalence of food allergy is higher in those with

A

atopic dermatitis
pollen allergies
latex allergy

253
Q

most common food allergen in children (chart of kids vs adult)

A

cows milk
egg
crustacean

adult - crustacian

254
Q

80% of cow milk, soy, egg, wheat allergy remit by

A

teenage years

255
Q

allergies to what are typically life long

A

peanuts
tree nuts
seeds
fish
shellfish

256
Q

If your allergic to a legume (peanut), you may have a cross-reactivity risk to/ risk of

A

other legumes 5%
-peas
-lentils
-beans

257
Q

If your allergic to a tree nut (walnuts), you may have a cross-reactivity risk to/ risk of

A

other tree nuts -37%
-brazil
-cashew
-Hazelnut

258
Q

If your allergic to a fish (salmon), you may have a cross-reactivity risk to/ risk of

A

other fish -50%
-swordfish
-sole

259
Q

If your allergic to shellfish (shrimp), you may have a cross-reactivity risk to/ risk of

A

other shellfish -75%
-crab
-lobster

260
Q

If your allergic to a grain (wheat), you may have a cross-reactivity risk to/ risk of

A

other grains - 20%
-barley
-rye

261
Q

If your allergic to cows milk, you may have a cross-reactivity risk to/ risk of

A

Beef - 10%
goats milk - 92%
Mare’s milk - 4%

262
Q

If your allergic to peach, you may have a cross-reactivity risk to/ risk of

A

Other Rosaceae - 55%
apple
plum
pear
cherry

263
Q

If your allergic to melon (cantaloupe), you may have a cross-reactivity risk to/ risk of

A

other fruits - 92%
watermelon
banana
avocado

264
Q

If your allergic to latex, you may have a cross-reactivity risk to/ risk of

A

35%
kiwi
banana
avocado

265
Q

If your allergic to kiwi, avocado, banana, you may have a cross-reactivity risk to/ risk of

A

Latex- 11%

266
Q

larger skin tests/higher IgE response means

A

higher likelihood of allergy not more severe allergy

267
Q

what type of immunodeficiency is r/t
gram negative MOs, viruses, protozoa, fungi, mycobacteria

A

Cellular immunodeficiency

268
Q

What type of immunodeficiency is related to gram positive encapsulated MOs and mycoplasma species

A

Humoral immunodeficiency

269
Q

What type of immunodeficiency is r/t staph and gram neg (Klebsiella, serratia)

A

Innate immunodeficiency

270
Q

What type of immunodeficiency is r/t recurrent Neisseria

A

complement immunodeficiency

271
Q

general precautions for immunodeficiency

A

leukoreduced, viral free blood transfusions

Post exposure prophylaxis for varicella

no live vaccines

education of schools/coaches ect regarding infection concerns

272
Q

Prophylaxis in humoral immunodef

A

ABX

273
Q

Prophylaxis in cellular and phagocytic immunodef

A

Abx
antifungal

274
Q

Prophylaxis in complement immunodef

A

pneumococcal and meningococcal vaccines

275
Q

stem cell transplant (HSCT) is only treatment option for

A

SCID
ADA (adenosine deaminase deficiency)
CGD (chronic granulomatous disease)

276
Q

what immunodef can get live vaccines

A

complement

277
Q

If antibody deficiency is present, then treatment with immunoglobulin therapy is required for how long

A

life - will need ongoing monitoring of IgG levels to ensure they’re adequately replaced

278
Q

examples include HIV, DM, malignancies, splenectomy, immunosuppressive medications, malnutrition, trauma

A

secondary immunodeficiencies

279
Q

is a retrovirus, whose infection occurs when the virus enters the body and binds to receptors on host T cells, fuses with the cell membrane, and then enters

A

HIV

280
Q

Seroconversion to HIV antibody positive occurs

A

between 10-14 days to 3-4 weeks

281
Q

HIV is lifelong because it infects what cells

A

long living memory T cells (CD4)

282
Q

the end result of destruction of HIV Is

A

HIV is lifelong because it infects the long-living memory T cells (CD4)
· The end result of destruction is the failure of T cell production and eventual immune suppression of both the cellular and humoral parts of the immune system

283
Q

How is HIV acquired

A

sex
contaminated blood exposure
perinatal transmission

284
Q

acute viral syndrome of HIV s/s

A

fever
fatigue
headache
myalgia
arthralgia
pharyngitis
lymphadenopathy
oral/genital ulcers
nausea
diarrhea
rash
aseptic meningitis
weight loss
oral candidiasis
peripheral neuropathy

o Aphthous ulcers, oral candidiasis, CMV retinitis
o New nodes in patients on antiretroviral therapy may indicate that the disease has progressed, and that treatment failure has occurred
o A new single large node is suspicious for lymphoma
· Skin findings
o HIV dermatitis: erythematous, papular, found in 25% of kids with HIV
o Thrombocytopenia: bruising, bleeding on skin/mucous membranes
o Shingles: vesicles along dermatomes
o Candida dermatitis: unresponsive to other therapies
· Pulmonary: lung disease, LIP, OIs
· Abdominal: hepatomegaly, splenomegaly

285
Q

acute viral syndrome for HIV generally occurs within

A

days, up to 10 weeks of initial infection

286
Q

Opportunistic infections associated with HIV

A

Pneumocystis jurovecii, bacteremia, lymphocytis interstitial pneumonitis (LIP)
o Kaposi sarcoma, toxoplasmosis, cryptococcosis, CMV

287
Q

In HIV what may be the first sign of infection during the asymptomatic phase

A

lymphadenopathy

288
Q

CD4 count in HIV is used for

A

reliable indicator for current risk of opportunistic infections

serial counts trending is most helpful

289
Q

surrogate marker of viral replication rate (rate of progression to AIDS and death is related to this)

A

viral load

290
Q

In HIV, brain CT you would be looking for

A

white matter degeneration

291
Q

In HIV, Abd us may show

A

calcifications in liver, spleen or kidneys

292
Q

Prevention of Mycobacterium avium complex (MAC) in HIV

A

Azithromycin or
clarithromycin

293
Q

Prevention of PJP in HIV

A

Cotrimoxazole

294
Q

vaccines and HIV

A

if symptomatic - no live vaccines

all should receive MMR-V separately (M, M, R, V) because they are all live

should receive annual killed flu vaccine

295
Q

Is HIV a reason to exclude kids from sports

A

no but consideration should be given for high impact sports like boxing

296
Q

anaphylaxis s/s for infants

A

Symptoms often cannot be communicated
Can be confused for normal behavior → drooling, crying, postprandial drowsiness , emesis/ reflux from colic, respiratory distress can be confused for croup, asthma, bronchiolitis or unresponsiveness from seizures/ sepsis.
Anaphylaxis can occur the first time a child eats a food so difficult to know the cause

297
Q

humoral is r/t

A

b cells

298
Q

cellular is r/t

A

T cells (T lymphocytes)

299
Q

Combined immunodeficiency is r/t what cells

A

B and T cells

300
Q

The major hallmark of any primary immunodeficiency is

A

susceptibility to infection

301
Q

immunodeficiency that is usually asymptomatic and does not generally carry increased risk of infection

A

IgA deficiency

302
Q

infection history usually seen in Humoral Immunodef

A

sinopulmonary
otitis media
GI
cellulitis
meningitis
osteomyelitis

haemophilus
pneumococci
streptococci
Giardia lamblia
cryptosporidium
enterovirus

also GI problems to include malabsorption

303
Q

infection history usually seen in Cellular immunodef

A

pulmonary
GI
Skin

candida
PJP
CMV, EBV, RSV, Parainfluenza, adenovirus
mycobacterium

also see FTT
oral candiddiasis
skin rashes
dermatitis
postvaccination diseases from live viral vaccines

304
Q

infection history usually seen in phagocytic disorders

A

severe skin and visceral infections by common pathogens

staph aurus
pseudomonas species
serratia
klebsiella
candida
nocardia
aspergillus

also see
granuloma formulation include granulomatous enteritis
poor wound healing
abscesses
oral cavity infections
anorectal infections

305
Q

infection history usually seen in complement disorders immunodef

A

meningitis septicemia
Neisseria infections:
meningococcal, pneumococcal

also Rheumatoid disorders lupus like syndrome, angioedema

306
Q

HIV testing can occur in ages

A

> 18 mos
moms abs before

307
Q

SCID is more commonly seen in what population

A

Navajo

308
Q

Agammaglobulinemia

subtype
age of onset
lab findings
associated findings

A

Humoral
>6 mos
absent IgG, IgA and IgM
absent AB responses
Absent B cells

Absence of tonsils and lymph nodes

309
Q

common variable immune deficiency
subtype
age of onset
lab findings
associated findings

A

Humoral
any age, peaks in second decade

low IgG
+/- IgA and IgM
Absent ab responses to vaccines
Normal to high numbers of B cells
+/- autoimmune cytopenias

autoimmunity
lymphoproliferative and granulomatous diseases
lymph nodes present to increased

hepatomegaly
splenomegaly

310
Q

Hyper IgM
subtype
age of onset
lab findings
associated findings

A

Humoral
>6 mos
Very low IgG adn IgA
Increased IgM
B cells normal to increased

Neutropenia
Autoimmunity

311
Q

Specific ab deficiency with normal IgG level and normal B cells
subtype
age of onset
lab findings
associated findings

A

Humoral
any age

Normal IgG
inability to produce AB to vaccines present

autoimmunity
lymph nodes normal to elevated
hepatomegaly
splenomegaly
increased association in syndromes

312
Q

Transient Hypogammaglobulinemia of infancy
subtype
age of onset
lab findings
associated findings

A

Humoral
> 6 mos to 4-5 years

Low IgG and IgA
specific Ab to vaccines present
Normal lymphoid tissue

313
Q

SCID

subtype
age of onset
lab findings
associated findings

A

Cellular

< 6 mos

decreased T cells
Increased or decreased B cells
decreased NK cells or normal
Low IgG, IgA, IgM

Absent lymphoid tissue
absent thymic shadow on x ray

314
Q

Wiskott-Aldrich syndrome

subtype
age of onset
lab findings
associated findings

A

Cellular
birth to 1 yr
low T cells
B cells normal
low IgM +/- increased IgA and IgE
decreased polysaccharide

low small platelets
lymphopenia
eczema
lymphoma
autoimmunity

315
Q

Humoral
>6 mos
absent IgG, IgA and IgM
absent AB responses
Absent B cells

Absence of tonsils and lymph nodes

A

Agammaglobulinemia

316
Q

Humoral
>6 mos
Very low IgG adn IgA
Increased IgM
B cells normal to increased

Neutropenia
Autoimmunity

A

Hyper IgM

317
Q

Humoral
any age

Normal IgG
inability to produce AB to vaccines present

autoimmunity
lymph nodes normal to elevated
hepatomegaly
splenomegaly
increased association in syndromes

A

Specific ab deficiency with normal IgG level and normal B cells

318
Q

Humoral
> 6 mos to 4-5 years

Low IgG and IgA
specific Ab to vaccines present
Normal lymphoid tissue

A

Transient Hypogammaglobulinemia of infancy

319
Q

Cellular

< 6 mos

decreased T cells
Increased or decreased B cells
decreased NK cells or normal
Low IgG, IgA, IgM

Absent lymphoid tissue
absent thymic shadow on x ray

A

SCID

320
Q

Cellular
birth to 1 yr
low T cells
B cells normal
low IgM +/- increased IgA and IgE
decreased polysaccharide

low small platelets
lymphopenia
eczema
lymphoma
autoimmunity

A

Wiskott-Aldrich syndrome

321
Q

Ataxia telangiectasia

subtype
age of onset
lab findings
associated findings

A

Cellular

<3 years
low IgA, IgE and IgG
Variable AB def
Increased alpha fetoprotein
Chromosomal instability

ataxia
telangiectasia
radiation sensitivity
increased frequency of malignancy

322
Q

DiGeorge
subtype
age of onset
lab findings
associated findings

A

Cellular
birth to any age

T cell low or normal
B cell normal
Immunoglobulins normal or low
low calcium
low PTH

heart defects
abnormal facies
autoimmunity

323
Q

IRAK4 deficiency

subtype
age of onset
lab findings
associated findings

A

Innate

infancy
lymphocytes and monocytes
toll and IL-1 receptor
signaling IRAK 4 pathway abnormal

324
Q

Cellular

<3 years
low IgA, IgE and IgG
Variable AB def
Increased alpha fetoprotein
Chromosomal instability

ataxia
radiation sensitivity
increased frequency of malignancy

A

Ataxia telangiectasia

325
Q

Cellular
birth to any age

T cell low or normal
B cell normal
Immunoglobulins normal or low
low calcium
low PTH

heart defects
abnormal facies
autoimmunity

A

DiGeorge

326
Q

Innate

infancy
lymphocytes and monocytes
toll and IL-1 receptor
signaling IRAK 4 pathway abnormal

A

IRAK4 deficiency

327
Q

Nemo
subtype
age of onset
lab findings
associated findings

A

innate
any age
lymphopenia
low igG
high IgM

conical teeth
colitis
ectodermal dysplasia
sparse hair
opportunistic infections

328
Q

innate
any age
lymphopenia
low igG
high IgM

conical teeth
colitis
ectodermal dysplasia
sparse hair
opportunistic infections

A

Nemo

329
Q

Hyper IgE (job syndrome)

subtype
age of onset
lab findings
associated findings

A

Other

any age
Normal T and B cells
increased IgE
staph aureus infections

thickened skin
pneumatoceles
eczema
nail candidiasis
broad nasal tip
delayed shedding of primary teeth
hypermobility of joints

330
Q

Other

any age
Normal T and B cells
increased IgE
staph aureus infections

thickened skin
pneumatoceles
eczema
nail candidiasis
broad nasal tip
delayed shedding of primary teeth
hypermobility of joints

A

Hyper IgE (Job syndrome)

331
Q

Chronic mucocutaneous candidiasis
subtype
age of onset
lab findings
associated findings

A

other

any age

T and B cell numbers normal
Impaired DTH to candida antigens
normal AB

skin and nail changes
autoimmunity

332
Q

other

any age

T and B cell numbers normal
Impaired DTH to candida antigens
normal AB

skin and nail changes
autoimmunity

A

chronic mucocutaneous candidiasis

333
Q

Chronic granulomatous disease
subtype
age of onset
lab findings
associated findings

A

other

> 6 months of age

Abnormal killing; faulty oxidative burst via NBT or flowcytometry testing
Granuloma on x ray

GI abnormalities
Abscesses

334
Q

Complement deficiencies

subtype
age of onset
lab findings
associated findings

A

other

Any age
Absent CH50
+/- absent alternate pathway
Absent specific complement
absent specific component

Autoimmunity
angioedema

335
Q

> 6 months of age

Abnormal killing; faulty oxidative burst via NBT or flowcytometry testing
Granuloma on x ray

GI abnormalities
Abscesses

A

Chronic granulomatous disease

336
Q

Any age
Absent CH50
+/- absent alternate pathway
Absent specific complement
absent specific component

Autoimmunity
angioedema

A

Complement deficiencies

337
Q

Treatment options in Humoral primary immunodeficiency

A

Abx
IVIG
Immunosuppressive medication and biologics

338
Q

Treatment options in Cellular primary immunodeficiency

A

HSCT (stem cell transplant)
Gene therapy
Immunoglobulin
ABX prophylaxis
Antifungal prophylaxis
Immunosuppressive medication and biologics

339
Q

Treatment options in Phagocytic primary immunodeficiency

A

Abx prophylaxis
antifungal prophylaxis
Gamma interferon
HSCT (stem cell tranplant)
Gene therapy

340
Q

Treatment options in Complement primary immunodeficiency

A

Abx prophylaxis
pneumococcal and meningococcal vaccines

341
Q

A disease of either a quantitative deficiency or qualitative defect of the von Willebrand protein.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 820). Wolters Kluwer Health. Kindle Edition.

A

Von Willebrand Disease

342
Q

*Patients who are deficient or have a defect of VWF are at risk for

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 821). Wolters Kluwer Health. Kindle Edition.

A

prolonged bleeding particularly from the mucous membranes

343
Q

why could repeated lab testing be needed to dx Von Willebrand disease

A

Von Willebrand protein levels may fluctuate

344
Q

what med stimulates release of VWF and Factor VIII

A

Desmopressin Acetate (DDAVP)

345
Q

*Used in managing recurrent bleeding in VWD, but do not stop active bleeding; slow the breakdown of clots to preventing rebleeding.

examples?

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 821). Wolters Kluwer Health. Kindle Edition.

A

Antifibronolytic agents

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 821-822). Wolters Kluwer Health. Kindle Edition.

346
Q

Meds used in VWB disease

A

Desmopressin Acetate (DDAVP) -> stimulates release of VWF and Factor VIII
* Management of prolonged or refractory bleeding and prior to minor elective procedures.

Antifibronolytic agents

  • Aminocaproic acid (Amicar); contraindicated with hematuria.
  • Tranexamic acid (Lysteda): FDA-approved for menorrhagia.

VWF concentrates are derived from human blood donation

347
Q

_______ has been demonstrated to have an impact on VWF levels, so knowledge of hormonal contraception or pregnancy is important when evaluating adolescents.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 822). Wolters Kluwer Health. Kindle Edition.

A

Estrogen

348
Q

is extracted from whole blood and contains coagulation, fibrolytic, and complement systems that assist in the restoration of coagulation disorders such as DIC.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 823). Wolters Kluwer Health. Kindle Edition.

A

FFP

349
Q

are responsible for hemostasis with resulting thrombus formation.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 823). Wolters Kluwer Health. Kindle Edition.

A

platelets

350
Q

obtained by centrifuging plasma and removing the precipitate. It is not used as commonly as FFP, but can be used to replace low fibrinogen levels and when certain factors are not available for treatment of coagulation disorders.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 823). Wolters Kluwer Health. Kindle Edition.

A

Cryoprecipitate

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 823). Wolters Kluwer Health. Kindle Edition.

351
Q

PRBC tranfused at ___ to ___ml/kg per transfusion

A

10-20ml/kg

352
Q

Platelets are transfused at __ unit per ever ___kg

A

1 unit/10kg

353
Q

FFP is transfused at

A

10-15ml/kg/transfusion

354
Q

Cryoprecipitate is transfused at
expect rise of?

A

1 unit per every 10kg

expect rise of 60-100mg/dl

355
Q

calculating prbc transfusion dose formula

A

Volume of PREC required (ml) = desired HCT - initial HCT x Total body volume. Divided by HCT

total body volume (infant - 100ml/kg
child-80ml/kg
adult - 65ml/kg)

356
Q

____ is possible when children drink large volumes of milk

A

anemia

357
Q

Stored PRBCs lack _____ content so children who receive any type of multiple transfusion requires what?

A

calcium
additional calcium

358
Q

PRBC s stored > 5 days are associated with

A

higher potassium concentration

359
Q

Based on illness severity, infants < ___ months will not require cross matching

A

4 months

360
Q

estimating circulating blood volume is based on an average calculation of

A

80ml/kg

adults are 70mk/kg

361
Q

Massive transfusion complications include

A

thrombocytopenia, hypocalcemia, coagulation factor depletion, hyperkalemia, and increased levels of lactic acid, leading to acid–base disorders, hypothermia, and altered or decreased oxygen delivery to tissues.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 824). Wolters Kluwer Health. Kindle Edition.

362
Q

each unit of RBC contains _____ iron

A

200-250mg

363
Q

Accumulation of iron leads to the formation of nontransferrin-bound iron, which is associated with

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 825). Wolters Kluwer Health. Kindle Edition.

A

progressive organ damage, primarily liver and heart disease.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 825). Wolters Kluwer Health. Kindle Edition.

364
Q

*In children, iron accumulation in the anterior pituitary gland will produce

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 825). Wolters Kluwer Health. Kindle Edition.

A

systemic endocrine disturbances, including delayed sexual maturation and growth failure.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 825). Wolters Kluwer Health. Kindle Edition.

365
Q

Congestive heart failure can be present in children as young as ___ years of age as a result of iron overload.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 825). Wolters Kluwer Health. Kindle Edition.

A

15

366
Q

chelation agents for iron tox

A

Iron chelation therapy is often required. * Chelation therapies are utilized to treat iron overload by binding metal ions that are then excreted through feces. * Deferoxamine, IV chelation agent. * Deferasirox, oral chelation agent is administered once daily.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 825-826). Wolters Kluwer Health. Kindle Edition.

367
Q

Administer blood products (RBC and platelets) through a _______ system to reduce the risk of febrile reactions, platelet alloimmunization, and CMV transmission.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (pp. 828-829). Wolters Kluwer Health. Kindle Edition.

A

a leukofiltration system

368
Q

Irradiate blood products to prevent

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 829). Wolters Kluwer Health. Kindle Edition.

A

Graft vs Host Disease

369
Q

Use leukoreduction for blood products (except granulocytes) to decrease

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 829). Wolters Kluwer Health. Kindle Edition.

A

decrease the risk of sensitization, the risk of CMV, and decrease the number of febrile nonhemolytic transfusion reactions. Administer CMV—negative blood.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 829). Wolters Kluwer Health. Kindle Edition.

370
Q

Washed products reduce the risk of

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 829). Wolters Kluwer Health. Kindle Edition.

A

inflammatory markers

371
Q

Administer single donor platelets to reduce the exposure to

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 829). Wolters Kluwer Health. Kindle Edition.

A

multiple donors, platelet alloimmunization and septic reactions

372
Q

For chronically transfused patients, administer units < __ days old.

Kline, Andrea M.; Haut, Catherine. Lippincott Certification Review: Pediatric Acute Care Nurse Practitioner (p. 829). Wolters Kluwer Health. Kindle Edition.

A

21

373
Q

methotrexate is used in what rheum disorders

A

JIA
JDMS
SS (Sjogrens syndrome)
SLE

374
Q

SE methotrexate

A

n/v
hepatotoxicity
Bone marrow suppression

375
Q

What category of drug is Methotrexate

A

DMARD

376
Q

Sulfasalazine is used in what rheum

A

JIA (ERA subtype)

377
Q

Category of drug is Sulfasalazine

A

DMARD

378
Q

Contraindications and SE of Sulfasalazine

A

Sulfa allergy
GI tox
monitor WBC count

379
Q

Hydroxychloroquine is used in what rheum

category of drug

A

DMARD
SLE

380
Q

SE of Hydroxychloroquine

A

Retinal hyperpigmentation
can cause retinal damage with vision loss

381
Q

Thalidomide
what rheum used in
cat of drug
SE

A

SJIA
DMARD

can cause peripheral neuropathy
teratogenic

382
Q

Mycophenolate mofetil (cellcept)
what rheum is used in
cat
se

A

Lupus nephritis class III/IV/V
JDMS
MCTD (mixed connective tissue disease)

Diarrhea
pancytopenia
decreases effectiveness of oral contraceptives

383
Q
  1. A previously healthy 12-year-old female developed hives, shortness of breath, and dizziness during her fourth-
    period class following lunch. For lunch the girl ate a peanut butter and grape jelly sandwich, an apple,
    a chocolate chip cookie, and a container of milk. Which of the following food items is most likely to have
    caused this reaction?
    A. Apple.
    B. Chocolate.
    C. Cow Milk.
    D. Grape Jelly.
    E. Peanut Butter.
A

E. Peanut Butter

384
Q

what allergies is a contraindication to propofol

A

soy and egg

385
Q

which of the following are the most common food allergens for children living in the USA

A

peanuts
tree nut
egg
milk
soy
flatfish
wheat

another source shellfish

386
Q

T/F
Specific IgE testing for food allergens is appropriate when clinical history supports a possible food allergy

A

True

387
Q

or the girl in the previous question, the school nurse administered a dose of epinephrine. Shortly afterwards
the girl felt well. Twenty minutes later, she began to experience similar symptoms. Which of the following
actions is most appropriate to initiate now?
A. Diphenhydramine.
B. Epinephrine.
C. Glucocorticosteroid
D. Placement into the recumbent position.
E. Ranitidine.

A

B. Epinephrine

388
Q

A 6-year-old male presented in late spring with large (3 cm by 3 cm) circular vesicular lesions with pinpoint
centers distributed in a linear fashion on both lower arms. This was the fourth incident of similar symptoms. He
has had no systemic symptoms. Which of the following is the most appropriate treatment for this child’s
lesions?
A. Diphenhydramine.
B. Epinephrine.
C. Leukotriene modifier.
D. Mid-potency topical steroid.
E. Ranititdine.

A

D. Mid-potency topical steroid.

389
Q

Over a 24-hour period a 10-year-old girl developed swelling of her face, including lips and eyelids plus both
hands. She had no itching or visible rash. She had a history of two previous similar episodes. She was otherwise
well except for a recent tooth extraction in concert with placement of dental braces. Which of the following is
the most appropriate next step in management for this child?
A. C3 and C4 testing.
B. Diphenhydramine.
C. Epinephrine.
D. Third-generation cephalosporin.
E. Penicillin skin testing.

A

C. Epinephrine.

390
Q

A 9-year-old boy developed nausea, abdominal cramping, vomiting, and diarrhea three hours after eating
supper. He had eaten fish sticks, potato salad, and milk. He had no rash, swelling or other cutaneous findings.
Which of the following treatments was most appropriate for this boy?
A. Epinephrine.
B. Diphenhydramine.
C. Fluids.
D. Glucocorticosteriods.
E. Oxygen.

A

B. Diphenhydramine.

391
Q

stinging insects associated with anaphylaxis

A

honey bee
wasp
hornet
yellow jacket
fire ant

392
Q

latex allergy examples

A

balloons
gloves
medical equiptment

393
Q

things in vaccinations causing anaphylaxis

A

Gelatin
egg
yeast
neomycin

394
Q

what food allergies are usually outgrown during first decade of life and which are usually lifelong

A

grown out
milk
egg
soy
wheat

lifelong
peanut
tree nut
fish
shellfish

395
Q

2 most frequent culprit for med related anaphylaxis

A

B lactam abx and NSAIDS

also chemo drugs (Cisplatinum and carboplatinum and biologic agents and monoclonal ab such as omalizumab)

396
Q

Latex allergy is caused by sensitization to
any of the antigens from the

A

Hevea brasiliensis tree

397
Q

dosing from lecture for epi

A

10kg-24.9kg -> 0.15mg
25kg and above 0.3mg

398
Q

Benadryl dosing

A

1.25mg/kg

399
Q

if pt has severe eczema, egg allergy or both, when is the soonest you can introduce peanut

A

4-6 mos

Critical Care 2 (14 decks)

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