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Heme/Lymph Exam 1 (Erik Hammond) COPY > Singh's Case Studies > Flashcards

Singh's Case Studies Flashcards

1
Q

66 y/o m with fatigue and fever, with hx of Myelodysplastic syndrome

A

fever, tachycardia, petechiae, conjunctival pallor

elevated WBC, decreased Hgb, decreased PLT

Peripheral blood 25% blasts with large nuclei and visible nucleoli

Leukocytosis with ANC of 186 (neutropenic)

Dx: Acute Myeloid Leukemia with infection

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2
Q

Treatment for pt with AML and infection?

A

Bone marrow shows 55% blasts, start on chemotherapy with antibiotics for presumptive infection, transfusion support as needed

recheck blast count after two weeks

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3
Q

Pt with AML and infection, has recurrent fever after abx treatment. What do you do?

A

he’s severely neutropenic from chemo, do a culture from central line. Make sure to check for fungal infection if gram stain is negative

treat bacteria/fungus and treat neutropenia with GM-CSF

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4
Q

What are the three phases of Chemo treatment?

A

Induction: initial chemo to induce a remission

Consolidation: intensify chemo to make sure no cancer cells are left in body

Maintenance: longer term therapy to maintain remission

Consider stem cell transplant for some cancers

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5
Q

What is the prognosis for our pt with AML?

A

age >60 and pre-existing MDS are concerning and there is a high rate of relapse

needs close monitoring

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6
Q

Next pt, 38y/o fm with complaints of weakness, bruising, menorrhagia

A

tachycardia, purpura, conjunctival pallor,

leukopenia, low Hgb, severe thrombocytopenia

prolonged PTT/PT

low fibrinogen

D-dimer elevated

Dx: DIC

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7
Q

How did we determine our 38y/o f pt has DIC?

A

Low PLT

Increased PT/PTT

decreased fibrinogen

fibrin clots forming/degrading leads to increased D-Dimer

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8
Q

What is underlying condition is causing the 38y/o f pt’s DIC?

A

WBC isn’t high, but circulating blasts show Auer rods

She is positive for t(15;17) which confirms Acute Promyelocytic Leukemia

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9
Q

How can Acute Promyelocytic Leukemia be treated?

A

PLT transfusion and factor replacement

Chemotherapy:

ATO: arsenic trioxide

ATRA: all trans retinoic acid

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10
Q

68yo female with fatigue, weight loss, abdominal fullness

A

exam shows splenomegaly

low Hgb, low reticulocytes, normocytic RBCs

Leukocytosis of 87,400 with mature neutrophils, eosinophils and basophils

normal PLT

low LAP

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11
Q

In the 68yo female with splenomegaly and severe leukocytosis, what does the bone marrow biopsy show? What does the blood smear show?

What translocation do you see?

What diagnosis does this lead to?

A

hypercellular bone marrow with mature granulocytes

macrophages with blue green cytoplasm (Pseudo-Gaucher cells)

t(9;22) (BCR-ABL TK)

Chromic Myelogenous Leukemia

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12
Q

How do we treat our pt with CML?

A

Imatinib

It is a TK inhibitor

Can monitor amount of BCR-ABL with cytogenics, FISH, or PCR to look at the molecular response to treatment

also follow the hematologic response to treatment as well

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13
Q

Why is it important to monitor CML closely?

A

It can progress to a more aggressive state

Two phases include:

Accelerated Phase: circulating blasts 10-19% with thrombocytopenia and basophilia

Blast Phase/crisis: blasts >20%

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14
Q

What about LAD makes you suspicious?

A

Subclavian/Supraclavicular nodes

fixed/hard nodes

size greater than 4cm

(tender is often benign)

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15
Q

What are three ways that you can test LN when you find LAD?

A

Fine needle aspiration

Needle Biopsy

Excision Biopsy

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16
Q

What is a fine needle aspiration?

A

it is a liquid sample that can show metastatic cells or be used for flow cytometry to assess the clonal nature of the cells

It is only used for NHL

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17
Q

What is a needle biopsy used for?

A

it examines a solid core of tissue and can pull out metastatic cells or be used for flow cytometry

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18
Q

What is an excisional biopsy used for?

A

Best way to diagnose lymphoma and the ONLY way to diagnose HL via Reed-Sternberg cells

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19
Q

14y/o f pt with abdominal pain in RLQ. CT shows mass adjacent to appendix. Pt started on Abx for presumptive appendicitis. Repeat CT 2 days later shows increased mass size. Pathology shows Burkitt Lymphoma. What would further pathology reports show?

Is there any metastasis?

What is the treatment?

A

MYC translocation of t(8;14)

WORST lymphoma translocation

intracranial mass and bone marrow involvement (CNS and BM involvment more likely with Burkitt’s than other NHL)

chemo with intrathecal admin.

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20
Q

In our pt with Burkitt’s Lymphoma, urine output decreases after chemotherapy initiation. What does her labwork show and why is this happening?

How do you treat?

A

Increase in plasma K, serum creat. and BUN

this is indicative of Tumor Lysis Syndrome

Treat with aggressive hydration

(the tumor burden and high response to chemo increases risk for TLS)

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21
Q

22 y/o male with fatigue, chest pain after ETOH consumption, night sweats and fever, pruritis, weight loss, no LAD or splenomegaly. Because of these B symptoms you do what type of test?

What does the pathology show?

What does this inidicate?

How do you treat it?

A

Excision biopsy of chest mass seen on imaging

Path shows Reed-Sternberg cells

Indicates a HL

Treat with chemo and mayne some radiation

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22
Q

When it comes to HL, what are three common ways of presentation?

A

LAD

B-symptoms (can be in NHL)

Mass on chest x-ray

(may be limited to mediastinal mass that produces minimal or no local mass effect sx)

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23
Q

Pt is an older male with conjunctival pallor, petechiae, and axillary/cervical LAD.

What do labs show?

What is the diagnosis?

A

slightly elevated WBC, low Hgb, decreased PLT

Blood smear shows 90% small lymphocytes

Flow cytometry shows monoclonal B cells

Dx: CLL/SLL

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24
Q

In our pt with CLL/SLL, his wife mentions that he was diangosed with CLL many years ago and told to return for monitoring, but he did not do so. REcords show that 6yrs ago, he had CLL present without anemia or thrombocytopenia. Now that he has new cytoppenias, what does this mean for the progression?

A

There is now bone marrow involvement indicating acceleration of the dz.

This can become Richter’s Transformation

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25
Q

13 y/o f with hx of menorrhagia, easy bruising, scrapes take a long time to stop bleeding, occasionally nose bleeds 1-2x per month. Dad with similar hx.

What do labs show?

What is the diagnosis?

How to treat?

Bonus genetics?

A

low hgb, normal PLT

PTT prolonged, PT normal

vWF ag: decreased

vWf: decreased

Factor VIII: normal

Dx: vWF Disease Type I

Tx: Desmopressin to help release vWF

Bonus genetics: 1, 2a and 2b are AD

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26
Q

6 y/o m with oral bleeding after dental procedure, hx of of easy bruising from minor trauma and bleeding into joints

Labs show?

Diagnosis?

Genetics?

Treatment?

A

normal PT, prolonged PTT

Factor XIII: only 3% normal activity

Factor IX: 98% normal activity

geneitc test for Hemophilia A: positive

X-linked recessive

Recombinant Factor XIII

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27
Q

What can an abnormal aPTT alone indicate?

A

if bleeding: VIII, IX, XI defects

no bleeding: XII, prekalikrein, kininogen, lupus, anticoagulants

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28
Q

What does an abnormal PT alone indicate?

A

VII defect

29
Q

What does an abnormal PT and aPTT together indicate?

A

anticoagulant therapy, DIC, liver disease, K deficiency, massive transfusion

rarely factor X, V, II defects

30
Q

32y/o female with recurrent vaginal bleeding 6wks post partum with epistaxis and fatigue. Family history of autoimmune disease.

Exam shows:

Labs show:

What should we further test?

How do we treat?

A

ecchymosis, pallor, hypotension and tachycardia, vaginal bleeding

anemia with normal PT and prolonged PTT that was not corrected with mixing study (therefore it isn’t a factor issue)

Test for antibodies. Negative Lupus/heparin, positive factor VIII inhibitor

fluids, factor VIII and factor VIIA bypass and immunosupression

31
Q

What happens if a mixing study of PT/PTT corrects?

If it doesn’t correct?

A

this means that there is a factor deficiency

means there is an inhibitor antibody present in the blood

32
Q

Acquired bleeding disorders can be of two varities:

Primary hemostatic disorders

Secondary hemostatic disorders

A

Primary:

drug induced platelet destruciton

aplastic anemia

ITP

mechanical PLT destruction (hypersplenism)

Secondary:

autoimmune inhibitors (VIII and V)

antiphospholipid antibodies

drug induced factor inhibition (heparin. warfarin)

consumption of factors

33
Q

What is acquired hemophilia A

A

Factor VIII inhibitor

seen in odler adults or post-partum

can be associated with other autoimmune diseases

may be seen in malginancy

Can occur in congenital hemophilia A as well

34
Q

What makes you suspect a DVT/PE?

A

Wells, Geneva criteria

  • hx of previous PE/DVT
  • cancer pt
  • immobilization?
  • hemoptysis
  • tachycardia
  • over 65
35
Q

How do you diagnose a thromboebolism?

What is a benefit of the D dimer?

A

D dimer

US or CT angiogram or VQ scan

high negative predictive value: if negative, no thromboembolitic event

36
Q

36 y/o female with abomdinal pain and vomiting. hx of SAB 12 years ago and on OCP now. Mother died of stroke at age 45.

Exam:

Dx:

What is the underlying cause for this diagnosis?

A

occult blood in stool and ileus on CT scan

WBC elevated with left shift

Bowel infaction due to mesenteric vein thrombosis?

Protein C def.

37
Q

Why did we diagnose our ileus pt with protein C deficiency?

How to treat?

A

current mesenteric vein thrombosis with hx of miscarriage and family history of you stroke

being on OCP can increase risk for clot

stop OCP, start on anticoagulation

38
Q

White thrombus is characterized how?

A

arterial

PLT rich

areas of shear stress

ATHEROSCLEROSIS

coronary/cerebral arteriers

39
Q

Red thrombus is characterized how?

A

venous

red cell rich

STASIS

lower extremities

40
Q

In the pt with protein C def., how did her mother’s stroke occur?

A

likely started as a DVT that ended up as a paradoxical embolism passing through a patent foramen ovale and getting into arterial circulation, going to brain and causing damage

found inf 55-60% of patients who have strokes under age 55

41
Q

68 y/o male with 3 months of fatigue and dyspnea on exertion, brittle nails, weight loss, pica (drinking paint)

Exam?

Labs?

Peripheral smear?

Diagnosis?

A

pale, conjunctival pallor, stomatitis, stable vitals, onychoscizia.

anemia with low MCV (microcytic) and increased RDW

ferritin: low
transferrin: high

transferring % sat: low

smear shows anisocytosis (increased RDW)

dx: iron deficient anemia

42
Q

Why is RDW helpful in anemia?

A

RDW is the earliest and most sensitive index that will change in iron deficient anemia

43
Q

What are some lab indications that iron is low?

What are some indications that the body is waiting for iron (ie. compensating) ?

A

low serum iron

low to normal serum ferrtin

low transferrin/TIBC saturation (stores/capacity)

increased TIBC, increased TFR

44
Q

In the elderly man with IDA can we just treat and send home?

A

No!

Look at occult blood in stool for GI bleed

Guess what, positive. Do scope and figure out what the underlying issue is.

45
Q

35 yo m with coffe grounds emesis x3 and 3 month hx of epigastric pain relieved by OTC antacids. hx of smoker and regular NSAID use. Begins to have chest pain.

Exam:

Labs:

EKG:

A

distended nontender abd, hypotenive and tachycardic

RRR with SEJ

cool extremities and weak pulse

Hgb low, normal reticulocytes, AB neg blood type

EKG: STEMI

46
Q

In our hypovolemic pt who just had a heart attack, we give a rapid transfusion of 1L NS and two units of blood. Repeat H/H shows?

What does surgery show?

A

Hgb increased by 1. Should increase by 1 for every one unit given. Thus he’s actively bleeding, so we need to figure out where from

Large ulcer that is nearly perforated; treated and bleeding controlled

47
Q

Blood group O

Blood that it can receive?

Plasma that it can receive?

A

Blood: Group O

Plasma: O, A, B, AB

48
Q

Group A blood

Can receive?

Plasma it can receive?

A

blood: A and O

PLasma: A and AB

49
Q

Group B blood

can receive which blood?

can receive which plasma?

A

blood: B and O

Plasma: B and AB

50
Q

Group AB blood

Can receive which blood?

can receive which plasma?

A

blood: O, A, B, AB
plasma: AB

51
Q

4 yo AA m with right leg pain after increasing elevation flying from nebraska to denver. Dyspnea on exertion. Fhx of some type of anemia.

Exam:

Labs:

Rad:

Smear:

Dx:

A

febrile, tachy, O2 sat at 91%,

Labs: Hgb low, MCV normal, fullness of LUQ

Femoral head fracture (pathologic)

smear shows cell sickling and elevated HgbS

Sickle Cell Anemia

52
Q

What are the genetics of Sickle cell Anemia?

A

AR causing predominance of HgS caused by glutamate to valine mutation

high in AA populations

53
Q

What are some effects of SCA?

A

Stroke

Acute chest syndrome (vasoocclusion in lungs leading to lower oxygenation)

renal issues with hematuria, even in SC trait

acute bone necrosis

autosplenectomy

54
Q

What are some treatments for SCA?

A

oxygen, breathing exercises,NSAIDs and narcotics, avoid high altitudes and strenuous acivity

keep HbS low with Hydroxurea

consider stem cell transplant

55
Q

25 yo f with hx of fatigue, weakness, dizziness, petechiae, pallor and gingival bleeding. She was recently treated with Bactrim for a UTI.

Labs show:

What do these labs indicate?

What is the diagnosis?

A

decreased WBC, decreased Hgb, decreased PLT

reticulocyte low

MCV high

RDW normal

either chemo/antivirals, ETOH or aplastic anemia

Aplastic anemia due to recent bactrim use

56
Q

Treatment for aplastic anemia

A

trasfusion, growth factor support

possible stem cell transplant

57
Q

Should you always try to palpate someone’s spleen?

A

probably not, unless you have a high index of suspicion for spleen related pathology

58
Q

What are large spleens typically indicative of?

A

hematologic malingnancy (useful in staging)

liver disease with portal hypertension

large spleen itself may be worsening a disease process (causing cytopenias)

59
Q

Hypersplenia is a type of splenomegaly with what features?

A

blood cells are being removed from body by the spleen

typically contributes to disease process

60
Q

What three diseases can cause the spleen to capture or break cells?

A

sickle cell anemia

heridtary spherocytosis

ITP

61
Q

SCA and the spleen

A

splenic sequestration of red cells can cause crisis

splenectomy can reduce need for transfusions

too many crises and you can get an autosplenectomy

62
Q

HS and the spleen

A

splenic sequestration and lysis can worsen anemia

splenectomy improves anemia

63
Q

ITP and the spleen

A

cases refractory to pharmaceutical therapy or cases with life threatening thrombocytopenia may benefit from splenectomy

Ab coated PLT in spleen are destroyed via RES

64
Q

If you see a giant spleen on pathology, what is a likely underlying cause?

If you see nodules in the spleen, what is most likely?

A

Hairy cell leukemia, CLL/SS

HL, follicular lymphoma

65
Q

While trauma is the most comon cause of splenic rupture, what are other causes?

A

splenomegaly from mono, CLL, hairy cell leukemia, surgical trauma

66
Q

How to diagnose splenic rupture

A

think about it (make sure to check for it)

LUQ pain

Kehr’s sign (diaphragmatic irritation when lying down, radiates to shoulder)

67
Q

What is overwhelming post-splenectomy infection

(when the surgeon says, “OPSI”)

A

bacteria that are resistant to opsonization are dealth with by the RES of the spleen

no spleen, no RES

starts with vague illness and progresses to fulminant sepsis in 2-3 days

highest risk 3yrs after splenectomy

make sure to vaccinate

68
Q

after splenectomy, what vaccines do you need?

A

Strep pneumoniae

n. menigiditis

H. influenzae B

69
Q

What on blood smear is seen after splenectomy/hyposplenia?

A

Howell-Jolly bodies (little dot in RBC)

Heme/Lymph Exam 1 (Erik Hammond) COPY (22 decks)

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