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PANCE Review > Hematology > Flashcards

Hematology Flashcards

1
Q

anemia - morphologic approach

A

microcytic (MCV<80)

  • iron deficiency
  • thalassemia, sickle cell

normocytic (MCV 80-100)

  • anemia of chronic dz
  • anemia of chronic renal failure
  • multifactorial (micro and macro balance out)
  • sickle cell

macrocytic (MCV>100)

  • Folic acid and Vit. B12 deficiency
  • alcoholics, liver dz
  • myelodysplastic syndrome
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2
Q

anemia and reticulocyte counts

A

reticulocytes are erythrocytes newly released from marrow (1-2 days)

  • still have small amount of RNA in them
  • can use to determine if anemia is decreased production (low retic count) vs. increased destruction (high retic count) since marrow is trying to pump out RBC to compensate
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3
Q

causes of anemia from:

  • decreased production
  • increased destruction
A

dec. production:
- lack of nutrients (iron, it B12, folate)
- bone marrow suppression (aplastic anemia,chemo)
- low trophic factors (CKD - low expo, low thyroid, testosterone)
- anemia of chronic dz (low sensitivity to expo)

inc destruction:

  • blood loss (chronic)
  • hemolytic: either inherited (sickle cell, thalassemia) to acquired (autoimmune, drug induced)
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4
Q

iron tests

A

serum iron

transferrin: binds iron in circulation
- TIBC
- % saturation = serum iron/TIBC
- Ferritin: iron stores

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5
Q

iron deficiency anemia: causes, s/sx, labs, tx

A

Causes:

  • increased requirements: bleeding (GI, menses), growth periods (pregnancy, lactation)
  • inadequate supply: intestinal malabsorption, gastric bypass surgery, Ca+ inhibits absoprtion

S/sx:

  • microcytic anemia
  • koilonychia (spoon nails)
  • glottitis/esophageal webs (Plummer-Vinson syndrome)
  • restless legs
  • Pica
  • hair loss

Labs:

  • low serum iron
  • low ferritin
  • TIBC is high (trying to bind iron) but % saturation low
  • reticulocytes high

Tx:

  • oral iron therapy (ferrous sulfate 325 BID)
  • recheck ferritin 6-8wks
  • vit C helps
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6
Q

hemoglobinopathies - 2 types

A

sickle cell disease

  • heterozygous (trait)
  • homozygous (SC anemia)

thalassemias

  • alpha: 4 subtypes
  • beta has 2 subtypes
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7
Q

normal adult hemoglobin - results of electrophoresis

A

HgB A: 95-98%
HgB A2: 1.5-3.5%
Hgb F (fetal): 0.5-1%

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8
Q

sickle cell hemoglobinopathy

A

Due to presence of abnormal HgB S, on deoxygenation, cells sickle and cause damage to vessels and trapping of dense sickle cells

  • splenic infarction with hypoxia (altitude)
  • hematuria common

Dx:
- presence of HgB S on electrophoresis

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9
Q

sickle cell trait (heterozygous)

A

usually asymptomatic

only develop crises at high altitudes (hypoxia triggers), or high stress situations (illness)

over time, can develop micro infarcts resulting in kidney damage and cardiac damage

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10
Q

sickle cell anemia (homozygous): definition, clinical findings

A

chronic hemolysis and pain crises

  • anemia
  • rectioculocytosis (high b/c trying to compensate for destruction)
  • hyperbilirubinemia

Clinical:

  • cardiac sxs from chronic overload (CHF) and micro infarcts/fibrosis
  • infections (strep pneuma and H. Flu) that spleen socially takes care of
  • gallstones
  • renal failure
  • painful crisis in hands and feet (from micro thrombi)
  • osteomyelitis (salmonelli typhi)
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11
Q

sickle cell pain crisis: cause, tx

A

can last days to weeks

cause:

  • dehydration
  • infection
  • stress

caution (these require transfusion):

  • acute chest syndrome
  • splenic necrosis

manage:

  • hydration +/- bicarb
  • oxygen
  • pain meds
  • folate to support hemolysis
  • tx infection
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12
Q

Beta-thalassmia

A

labs:

  • dec. or absent HbGA, increased HbGF and A2
  • Mediterranean descent

b-thal minor (trait)

  • homozygous
  • chronic anemia (not symptomatic)
  • dx: HgB electrophoresis: HbA w/ raised HbF and HbA2
  • tx: usually no tx needed

b-thal major (Colley anemia)

  • homozygous
  • severe anemia
  • sx: liver and spleen enlargement, stunted growth, bony deformities (chipmunk facies), hepatosplenomegaly, jaundice, cirrhosis, and thrombophilia.
  • dx: HgB electrophoresis: no beta chains synthesized; only HbF and HbA2
  • tx: bone marrow transplant; supportive care
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13
Q

alpha thalassemia syndromes

A

HgB chain affected: alpha globin chain pathology

Two alpha chain deletion:

  • common in Asians (alpha-th-1) or blacks (alpha-th-2)
  • typically mild.

Presence of one alpha chain: Hemoglobin H disease
- patients manifest a variant of chronic hemolytic anemia.

Absence of all four alpha chains = hydrops
- results in stillbirth

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14
Q

anemia of chronic disease (anemia of inflammation) - basics, causes, dx, tx

A

induced by inflammatory cytokines and hepcidin

  • results in normocytic anemia
  • reduction in RBC production in bone marrow

causes: MANY

Dx:

  • low serum iron
  • HIGH ferritin
  • TIBC is low and % saturation low
  • reticulocytes low

Tx:
- erythropoietin (EPO)

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15
Q

hemolytic anemia

A

caused by premature breakdown of RBCs

  1. hereditary spherocytosis (RBC membrane defects): see spherocytes that get chopped up by spleen; tx: remove spleen
  2. autoimmune processes (+ COOMBs)
    - tx with prednisone
  3. G6PD deficiency: usually drugs or FAVA BEANS stimulate hemoysis; see bite cells and Heinz bodies
  4. Drugs: antimalarials, analgesics (acetyl salicylic acid), chemo

Labs:

  • high reticulocyte count
  • inc. serum LDH
  • high indirect jaundice
  • positive COOMBS (if autoimmune)
  • reduced serum heptoglobin
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16
Q

aplastic anemia

A

PANCYTOPENIA

  • recurrent infections (low WBCs)
  • mucosal hemorrhage (low platelets)
  • fatigue, dyspnea (low RBCs)

marrow is profoundly hypocellular with dec. in all elements
- low reticulocyte count

cause: chemo, drugs, radiation, infection, unknown

Tx:

  • hematopoietic cell (stem cell) transplantation
  • immunosupressive regimes
  • supportive management (IVIG)
17
Q

vitamin B-12 deficiency (versus folate deficiency)

A

related to macrocytic anemia as well as neurologic symptoms
- serum B12 may be low or normal (which makes it tough for dx)

cause:
- pernicious anemia: autoimmune cause of B12 deficiency (antibodies to intrinsic factor)

sxs:
- depression, dementia, ataxia, slow reflexes, etc.

Dx:

  • methylmalonic acid high in B12 deficiency
  • homocysteine high in both B12 and folate deficiency

Tx:
- give B12 (cobalamin) SQ or PO

18
Q

folic acid deficiency

A

cause:
- nutritional deficiency (gastric bypass, alcoholic)

sxs:
- depression, dementia, ataxia, slow reflexes, etc.

dx:

  • serum folic acid level
  • monitor progress with homocysteine

tx:
- Folic acid 1 mg daily

NOTE: higher demands in pregnancy

19
Q

thrombocytopenia - most common cause

A 
splenic sequestration (in enlarged spleen)
 - can be ETOH induced
20
Q

idiopathic thrombocytopenia purpura (ITP)

A

idiopathic with autoimmune features

  • kids: follows viral illness; self-limited
  • adults: idiopathic, autoimmune

s/sx:

  • petechial hemorrhage
  • mucosal bleeding
  • thrombocytopenia (<20,000)

Dx: diagnosis of exclusion
- confirm not lab error (clumping of platelets)

Tx:
1st line: steroids
2nd: splenectomy

21
Q

thrombotic thrombocytopenia purpura (TTP)

A

rare disease; often triggered by systemic inflammatory process (HIV, malignancy, meds)

sxs: FAT-RN
F: fever
A: hemolytic anemia (schistocytes, helmet cells)
T: thrombocytopenia
R: renal impairment
N: neurologic: sz, AMS

Tx:

  • large-volume plasmapheresis (get rid of broken cells)
  • immunosuppressive agents
22
Q

platelet defect vs. clotting factor deficiency

A

platelet defect

  • bleed in skin, mucous membranes, GI tracts
  • bleeding after minor cuts; small ecchymosis
  • petechiae
  • mild bleeding after surgery

clotting factor deficiency

  • bleed in soft tissues (joints, muscles)
  • large, palpable ecchymosis
  • no petechiae
  • muscle hematoma common
  • delayed, severe bleeding after surgery
23
Q

coagulation tests

A

PT (prothrombin time)/INR: measures extrinsic pathway
- up in vit K deficiency, Coumadin, liver dz, DIC

PTT (partial thromboplastin time): measures intrinsic pathway
- up in vit K deficiency, Heparin, liver dz, DIC, hemophilia, vWD

D-dimer: specific to plasmin degradation of fibrin (picks up presence of clots)
- positive in DIC, PE, DVT

24
Q

coagulation pathway

A

Intrinsic Pathway: factors released into blood from platelets (ten, 10, 2, 1); endothelial cells are damaged, negatively charged surface, activates TEN, 10, II, I
o Twelve – factor XII (activated by negative surface)
o Eleven – Factor Xi
o Nine – Factor IX
o 10 – Factor X – common pathway
o 2 – Factor II (prothrombin)
o 1 – Factor I (fibrinogen)
o Note: factor XIII: makes fibrin bonds even stronger – adds net or mesh of fibrin

Extrinsic pathway: factors released by damaged tissue (tissue factor – comes from outside blood)
o Tissue factor activates Factor VII
o Factor VII activates Factors X and V
• Common pathway

Note: intrinsic and extrinsic pathways meet at Factor X and form common pathway:
• Prothrombin → thrombin (enzyme = prothrombinase)
• Fibrinogen → fibrin (enzyme = thrombin)
• Fibrin strands bind to all platelets and strong clot is formed

25
Q

von Willebrand disease (VWD) - definition, tx

A

most common bleeding disorder

  • heavy menses, mucosal or prolonged bless, post surgery bleeds
  • vWF is either defective or deficient

Labs (mostly normal)

  • PTT and bleeding time slightly elevated
  • vWF levels may be low
  • platelet aggregation test abnormal

tx:

  • DDAVP (desmopressin / synthetic vasopressin/ADH): inc. plasma WWF levels by stimulating secretion by endothelium
  • platelet or factor VIII transfusion
26
Q

hemophilias (bleed too much) - 2 types

A

clotting factor disorders - severe bleeds into joints / post-op (vs. low platelets)

sex-linked recessive
- genes on X chromosome

hemophilia A:
- deficient or defective factor VIII

hemophilia B (aka Christmas Tree dz)
 - deficient or defective factor IX
27
Q

thrombophilia / hyper coagulation disorders

A

factor V Leiden mutation
- resistent to protein C = unopposed coagulation pathway

Anti-Thrombin III deficiency: unchecked coagulation

Protein C&S deficiency: more rapid thrombin formation

Prothrombin gene mutation: inc. prothrombin levels

28
Q

Disseminated Intravascular Coagulation (DIC) - definition, population, causes, s/sx, tx

A

systemic d/o that causes both clot formation (thrombosis) and bleeding (hemorrhage)
- endothelial damage creates many clots, use up clotting factors and then bleed

population: hospital admits

causes:

  • tissue damage on large scale: burns, trauma, sepsis, vasculitis
  • procoagulant in blood: cancer, placental abruption
  • severe allergic reaction

s/sx:

  • bleeding, petechiae
  • renal: oliguria, ARF
  • dyspnea
  • thromboembolism: DVT, PE, CVA
  • seizures, coma

Labs: PT/INR, PTT, fibrinogen, TT all affected

tx:
- fix underlying cause and support (replace blood, clotting factors, etc.)

29
Q

trousseau syndrome

A

slower DIC that occurs in malignancy

30
Q

acute lymphocytic leukemia (ALL)

- T Cell or B Cell

A

General info:

  • peak incidence: 3-5
  • Philadelphia chromosome is adults (higher risk; uncommon)
  • risks: radiation, prior chemo, solvents, Downs
  • sx: BM failure, infections, bleeding, LAD, WBC abnormality (high or low)
31
Q

acute myeloid leukemia (AML)

A

General info:

  • peak incidence: age 60
  • > 30% blasts in peripheral blood
  • Auer Rods formed by aggregation of myeloid granules (in smear)
32
Q

chronic lymphocytic leukemia

A

General info:

  • most common form of leukemia in adults in western world
  • medial age: 62 yrs
  • therapy only initiated if sxs warrent
33
Q

chronic myelogenous leukemia (CML)

A

chromosome 22 translocation mutation - Philadelphia chromosome

  • raised WBC count
  • lifelong treatment but can make life-expectancy years
34
Q

multiple myeloma

A

accumulation of plasma cells in bone marrow or visceral/soft tissue

s/sx: CRAB
C: calcium-elevated from osteolytic bone destruction
R: renal-insufficieny from damage of protein deposition’
A: anemia: BM suppression
B: bone: lytic lesions (PUNCHED OUT LEASIONS)

  • found after eval for anemia, back pain, renal insufficiency, and large protein/albumin
  • rouleaux: stacking of RBCs
  • Dx: hallmark of MM is the finding of a monoclonal spike on serum protein electrophoresis

tx: incurable
- stem cell transplant
- immunosuppression

35
Q

non-hodgkins lymphoma - risks, s/sx,

A

6th most common cancer

  • many types
  • 85% of lymphomas
risks:
 - male, older
 - chronic immunosuppression
 - chromic autoimmune dz
chronic infections

s/sx:

  • weight loss
  • painless nodes
  • night sweats
  • fevers
  • pruritus
  • chest or abd pain
36
Q

Hodgkins lymphoma

A

General

  • bimodal: 15-30, >55 y/o, FH (HLA link)
  • very curable

s/sx:

  • weight loss
  • painless nodes
  • night sweats
  • fevers
  • pruritus
  • mediastinal mass
  • PAIN after ETOH consumption

d/dx:

  • biopsy with Reed Sternberg cells (multinucleate)
  • inc. LDH

PANCE Review (16 decks)

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