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med/surg 2 > perfusion (pediatrics) > Flashcards

perfusion (pediatrics) Flashcards

Jan 16th

1
Q

3 main concepts associated with perfusion

A

-pain
-gas exchange
-patient education

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2
Q

what is sickle cell anemia

A

-an inherited red blood cell where hemoglobin is replaced by abnormal sickle/crescent-shaped cells

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3
Q

what can sickle cell anemia lead to

A

-obstruction(thrombosis forms easily)
-vascular inflammation (increases b/p & can lead to heart failure)
-increased RBC destruction (destroyed in 10-12 days, can lead to fatigue and jaundice)

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4
Q

what groups are sickle cell anemia usually seen

A

middle-eastern, african, meditarranian, aborignal people

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5
Q

what age group is sickle cell anemia usually undetected in

A

1 year of age and under d/t no s&s d/t increased amt of fetal hemoglobin which inc normal hemoglobin

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6
Q

screening at birth for sickle cell anemia

A

high performance liquid chromatography (HPLC)
hemoglobin analysis (eg. hb electrophoresis)

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7
Q

clincial manifestations of sickle cell anemia

A

-enlarged bones d/t bone marrow expanding to compensate(childhood)
-tachycardia, murmurs, enlarged heart, increased blood viscosity, heart failure, pulmonary hypertension
-hemolysis, thrombosis
-anemia, jaundice, pain

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8
Q

3 types of sickle cell crisis

A

-sickle crisis (vaso-occlusive crisis)
-aplastic
-sequestration

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9
Q

what happens in sickle crisis (vaso-occlusive crisis)

A

caused by thrombosis
-pain is major complaint
-can lead to organ damage (no perfusion)
-avascular necrosis (higher likelyhood in hips and shoulders but can happen anywhere)

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10
Q

what happens in aplastic sickle cell crisis

A

-usually secondary to parvovirus/respiratory virus
-bone marrow stops producing RBCs
-hemoglobin lvls drop rapidly which causes the aplastic crisis
-organ damage
-important to prevent infection in SCA

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11
Q

what happens in sequestration sickle cell crisis

A

-most life threatening
-sickle cells pool in 1 organ=decreases circulatory BV which lead to circulatory collapse & shock
-usually occurs in the spleen in kids, leads to decreased filtration of bacteria & creation of antibodies (leads to autosplenectomy, usually by age 10 d/y repeated sequestration)
-prone to infection

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12
Q

main organ affected in sickle cell crisis in kids

A

spleen
then lungs & CNS
-heart is last

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13
Q

main organs affected in sickle cell crisis in adults

A

lungs, liver
heart is last
(usually do not have a spleen by adulthood)

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14
Q

complications of sickle cell anemia

A

-acute chest syndrome (presents as pneumonia)
-pulmonary HTN/heart failure
-CVA
-autosplenectomy
-infection(pneumonia, osteomyelitis)
-reproductive problems(priapism, menses pain, impotence)
-renal failure
-chronic leg ulcers, dec wound healing
-blindness (d/t thrombi), retinal detachment
-avascular necrosis/bone marrow enlargement

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15
Q

diagnostic testing for sickle cell anemia

A

hemoglobin electrophoresis (idenitifies normal vs abnormal RBCs, can also identify carriers)
-newborn screenings

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16
Q

pharmacologic therapies for sickle cell anemia

A

-#1 hydroxyurea (taken for life, dec production of sickle cells, intense side effects & congenital defects)
-oral penicillin prophylaxis (2m-5y of age)
-ABX for any s&s of infection
-NSAIDS, Tylenol, aspirin, opioids(thombi pain)
-folic acid(inc RBCs)
-vaccines
-hematopoietic stem cell transplant(HSCT) not used often, needs a compatible donor

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17
Q

nonpharmacologic management for sickle cell anemia

A

-hydration(keep blood viscose, dec chances of thrombi)
-monitor for infection
-oxygen to prev/dec sickling
-exchange transfusions
-packed RBCs transfusions
-heat application(NEVER COLD)
-splenectomy

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18
Q

3 factors for hemostasis

A

1.constriction of the blood vessel
2.formation of platelet plug
3.activation of coagulation cascade

19
Q

3 types of hemophilia

A

Hemophilia A (classic hemophilia)
Hemophilia B
Von Willebrand disease (vWD)

20
Q

which types of hemophilia lead to deep tissue bleeds in joint/muscle

A

hemophilia A & B

21
Q

which types of hemophilia lead to bleeds in mucus membranes & skin surfaces

A

Von Willebrand Disease

22
Q

what is deficient in hemophilia A

A

Factor VIII

23
Q

what is deficient in hemophilia B

A

Factor IX

24
Q

what is deficient in Von Willebrand disease

A

Von willebrand factor and factor VIII deficiency

25
Q

classification of severe hemophilia A

A

-spontaneous bleeding WITHOUT trauma
<1% factor VIII
-most common (60-70%)

26
Q

classification of moderate hemophilia A

A

-bleeding with mild trauma
-1-5% factor VIII
-usually detected between 1-2yrs of age d/t inc # of injuries

27
Q

classification of mild hemophilia A

A

-bleeding with severe trauma or surgery
->5-40% factor VIII
-usually detected late

28
Q

what is the normal amount of factor VIII

A

50-150% factor

29
Q

what is needed for a diagnosis of hemophilia

A

-hx of bleeding episodes
-fhx of hemophilia
-lab tests: blood clotting fucntion, PTT(elevated), factor VIII assays
-PT and platelets will be normal
-DNA testing to determine carrier detection

30
Q

clinical manifestations of hemophilia

A

-prolonged bleeding anywhere from or in the body
-hemorrhage from any trauma (mild or severe)
-excessive bruising
-subcutaneous & IM bleeding(avoid IM injects)
-spontaneous hematuria
-hematomas
-hemarthrosis
-SQ bleeds on neck, mouth, thorax, spinal cord, GI, intracranial

31
Q

what is hemarthorsis?

A

bleeding into a joint cavity
-commonly in knees, elbows, ankles
-leads to bony changes & crippling deformities

32
Q

s&s of hemarthorsis

A

stiffness
tingling
aching
limitations in joint movement
-pain, swelling, redness, warmth, loss of movement

33
Q

management of moderate to severe hemophilia

A

-IV replacement of missing clotting factor
-prophylaxis therapy->periodic regular replacement (3x a week d/t clottig factor is filtered out in 12-24h, given prior to surgeries/procedures)
-on demand therapy after a bleed

34
Q

management of mild hemophilia

A

-desmopressing (DDADP); only increases factor VIII by 30%. given nasal,SQ,IV

35
Q

medications given for hemophilia

A

corticosteroids: hematuria or acute joint tissue bleed
-tranexamic acid & aminocaproic acid:holds clot in place once formed->blocks plasmin factor
-analgesics; dec pain

36
Q

can you give NSAIDs for hemophilia?

A

NO
it intereferes with platelet aggregation

37
Q

supportive management for hemophilia

A

exercise & physio
-rest, Ice, compress, elevate
-reduction of bleeding risks
-medic alert ID
-family support(educate & genetic counseling)
-good dental practices(dec bleeding and # of procedures needed)

38
Q

what is immune thrombocytopenic purpura (ITP)

A

-autoimmune disorder that destroys platelets
-acute or chronic
-common in women and kids ages 1-4
manifested by easy bruising, bleeding from mucus membranes, internal hemorrhage(hematuria, hematemesis, melena, menorrhagia)

39
Q

manifestations of ITP

A

-platelet count less than 150 x 10^9/L
-if <10 x 10^9/L = spontaneous bleeding (life threatening)
-rash
-pooling of blood under skin surface

40
Q

supportive management of ITP

A

-observation if no bleeding
-activity restriction if platelets <50
-no NSAIDs or aspirin
-no platelet tranfusions d/t autoimmune reaction

41
Q

medication management for ITP

A

-corticosteroids: given 2-4w to dec immune system (stunts growth in kids)
-IV immune globulin (IVIG); makes spleen not destroy platelets->works in 24-48h w/ chronic & no active bleed
-anti-D antibody; only for RH+ pt, dec destruction of platelets in spleen

42
Q

surgical procedures for ITP

A

splenectomy as a last resort

43
Q
A

med/surg 2 (17 decks)

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