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Quarter 2 > Clin Med Final > Flashcards

Clin Med Final Flashcards

1
Q

Anemia in Women

A

<12

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2
Q

Anemia in Men

A

<14

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3
Q

Immature –> mature RBCs

A

3 days spent in bone marrow, 1 day in peripheral blood

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4
Q

“Old RBCs” removed by:

A

Spleen

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5
Q

Reticulocyte count

“retic count”

A

Indication of bone marrow production of RBC

Normal: 0.5-2%

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6
Q

Lots of blue on Peripheral Smear

A

means Lots of New!

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7
Q

Red Cell Distribution Width (RDW)

A

Measure of the variation in RBC size

Normal: 11-15%

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8
Q

Anisocytosis on a Peripheral smear

A

Variation in size of RBC

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9
Q

Reticulocyte count

A

indication of RBC production in bone marrow

0.5-2% is normal

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10
Q

Iron Deficiency Anemia

A

common in women of childbearing age, children, decreased income

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11
Q

Most common causes of Iron Deficiency Anemia

A

Blood loss*(adults), decreased iron intake, decreased iron absorption (Celiac, H.pylori, Bariatric surgery)

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12
Q

Sx of Iron Deficiency Anemia

A

Atrophic glossitis, angular chelitis, koilonychia
Pica-craving ice
Dysphagia- esoph webs/Plummer-vinson syndrome
Restless leg syndrome

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13
Q

Labs for Iron Deficiency Anemia

A

Everything is low except:
TIBC and RDW elevated!
TIBC bc there is more binding capacity-seats available for iron
RDW bc varying size “Anisocytosis”

will also see “poikilocytosis” varying shape

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14
Q

Tx for Iron Deficiency Anemia

Classic/traditional

A

Replace iron stores: Oral Ferrous Sulfate 325 mg (daily-TID)
Take on an empty stomach! need acidic conditions

Body should inc hemoglobin ~2-4 g/dL every 3 weeks until returned to baseline

continue 3-6 mo after anemia has corrected to replenish stores

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15
Q

Tx for Iron Deficiency Anemia

Select patients

A

Parenteral- if not absorbing or post bariatric surgery

Blood transfusions- not recommended for iron replacement

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16
Q

Thalassemia (alpha and beta)

A

Inherited, reduction in the synthesis of Globin chains (alpha or beta)

Africa, Asia, Mediterranean region

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17
Q

Result of Thalassemia

A

Ineffective erythropoiesis (incomplete production) and Hemolysis (destruction of RBC)

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18
Q

Thalassemia results

A

variable degrees of Anemia and Extramedullary hematopoiesis (outside of bone marrow)

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19
Q

Thalassemia effects

A

bone changes, impaired growth, IRON OVERLOAD

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20
Q

Alpha thalassemia

A

deletion of 1 or more of the 4 alpha-globin chains

1: silent carrier
2: alpha-thal-minor, mild microcytic anemia
3: hemoglobin H disease, moderate microcytic anemia
4: hydrops fetalis; usually fatal in utero

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21
Q

Beta thalassemia

A

Minor: dysfx of 1 beta globin chain, asympto, mild micro

Intermediate: less severe phenotype than major, not dependent on transfusion, chronic hemolytic anemia

Major: dyfx of BOTH beta chains, DEPENDS on transfusions, Severe Hemolytic Anemia, if untreated: 85% of children will die by 5YO

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22
Q

Thalassemia labs

A

MCV (size) is strikingly LOW- very very small cells

Normal/elevated RBC

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23
Q

Lab to check for Thalassemia

A

Hemoglobin Electrophoresis- detects the type of hemoglobin

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24
Q

Thalassemia tx

A

AVOID IRON SUPPLEMENTATION

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25
Q

Thalassemia tx

A

Chronic hemolysis- Folic acid supplementation

Severe thalassemia- Regular transfusion, Iron chelation therapy, Splenectomy

Severe BETA thalassemia major- Stem cell transplant

Genetic counseling

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26
Q

Sideroblastic Anemia

A

Hereditary or acquired

Abnormal RBC iron metabolism –> Diminished heme synthesis –> Iron accumulation

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27
Q

Hallmark of Sideroblastic Anemia

A

“Ring Sideroblasts” seen on Bone Marrow Aspirate

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28
Q

Sideroblastic Anemia- findings on Peripheral Smear

A

Siderocytes w/ “Pappenheimer bodies”

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29
Q

Sideroblastic Anemia

A

Acquired is more common in adults
Often a variant of MDS (Myelodysplastic Syndrome)
Other causes: chronic alcoholism, meds, copper deficiency)

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30
Q

Sideroblastic Anemia Labs:

A

RDW often elevated (many diff sizes)
Reticulocyte count: normal/low
Systemic Iron Overload!!

may be hard to distinguish from Hereditary Hemochromatosis
May –> irreversible organ damage

*Remember: Ring sideroblasts on Bone Marrow Aspirate are Hallmark finding!

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31
Q

Tx of Sideroblastic Anemia

A

Pyridoxine (Vit B6)
Refer to Hematology, tx underlying cause, discontinue offending drugs, remove toxic agents, Transfusion/ manage iron overload

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32
Q

Anemia of Chronic Disease

A

second most common cause of anemia worldwide (after Iron Def Anemia)

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33
Q

Anemia of Chronic Disease cause:

A

decreased RBC production by bone marrow, component d/t RBC lifespan shortened

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34
Q

Factors that contribute to Anemia of Chronic Disease

A

Hepcidin induced alteration in iron metabolism –> trapping of iron in macrophages and degreased gut iron absorption

Inability to increase Erythropoiesis in response to Anemia

Decrease of EPO- Erythrpoietin production

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35
Q

Anemia of Chronic Disease Labs and Tx

A

Mild anemia: Hb of 10-11
Normocytic! normal size
Serum Fe (Iron) and TIBC are both LOW in the setting of inflammation

Tx: Erythropoietin EPO replacement

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36
Q

Macrocytic Anemias (2)

A

B12 deficiency

Folate deficiency

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37
Q

Hemolytic Anemias (4)

A

Hereditary Spherocytosis
G6PD Deficiency
Sickle Cell Anemia
Autoimmune Hemolytic Anemia

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38
Q

Megaloblastic

A

meaning inability to synthesize DNA

B12 and Folate deficiency

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39
Q

1st step when diagnosing Macrocytic anemia (large)

A

Are reticulocytes increased?

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40
Q

Megaloblastic Anemia

A

Defective DNA synthesis –> Disordered RBC maturation and accumulation of cytoplasmic RNA –> reduced cell division –> larger RBCs

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41
Q

Drug induced Anemias

A

Meds that interfere with Purine or Pyrimidine metabolism

Hydroxyurea, chemo, and antiretrovirals (HIV drugs) are most common

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42
Q

Average daily need for Folic Acid

A

200-400

Increases to 400-800 for pregnant women, breastfeeding, or trying to conceive

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43
Q

Folate and Folic acid may be used interchangeably

A

Folate: dietary vitamin B9

Folic acid: synthesized with vit B9, added to processed foods

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44
Q

2-4 months deprivation of folic acid can result in MACROcytic anemia

A

same blood and bone marrow findings as B12 deficiency.

make sure to differentiate!!

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45
Q

Folate

A

absorbed in JEJUNUM

required for important steps in DNA synthesis

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46
Q

Cause of Folic Acid deficiency

A

Alcoholism, hemodialysis pts, elderly, end of pregnancy, Anticonvulsant meds-MTX, malabsorption (Rare), Hemolytic anemia

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47
Q

B12 deficiency UNIQUE sx

A

NEURO ABNORMALITIES

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48
Q

Folic Acid deficiency

A

there are NO neuro abnormalities

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49
Q

Folic Acid def labs

A

Low serum folate
Homocysteine elevated
Serum Methylmaolinc acid (MMA) is normal*

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50
Q

Peripheral smear of BOTH Folate def and B12 def:

A

Macro-ovalcytes and Hypersegmented neutrophils

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51
Q

Tx for Folic Acid def

A

Tx underlying cause

Replace Folic Acid!- 1 mg PO daily (more for malabsorption pts), better absorbed w food

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52
Q

Vit B12 def

A

B12 Cobalamin is only available from DIET
meat, eggs, milk
CAUTION with Vegans

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53
Q

Most common cause of B12 def

A

INABILITY TO ABSORB rather than not eating enough.

Ppl are eating enough but cannot absorb it properly

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54
Q

Daily vit B12 requirements

A

1-2 micrograms

Def typically develops over years- body has a large store of B12

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55
Q

B12 process of absorption

A

B12 binds to Intrinsic Factor (IF- which is secreted by gastric parietal cells) in stomach

B12 is released from the Cobalamin-IF complex where it is absorbed in the ILEUM

B12 is stored in liver

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56
Q

Cause of B12 deficiency

A

Pernicious Anemia (most common), decreased intake, meds (metformin, H2 antagonists, PPIs), Malabsorption (elderly), Any other condition which inhibits absorption (chronic gastritis, gastric surgery, ileal disease or surgery, bacteria overgrowth, pancreatic insufficiency)

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57
Q

Pernicious Anemia (auto-immune)

A

Immune mediated destruction/loss of Gastric Parietal Cells leading to impaired intrinsic factor secretion

Accompanied by decreased gastric secretion- loss of acidity

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58
Q

Sx of B12 def

A

Glossitis, stomatitis, GI sx

NEURO SX!!!!!: vibratory and position sense, Ataxia, Paresthesias- stocking glove, confusion/dementia

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59
Q

Neuro sx of B12 are caused because:

A

B12 def–> defective myelin synthesis in the CNS

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60
Q

B12 def labs:

A

Macrocytic (large)
Occasional: leukopenia, thrombocytopenia (low)
Anisocytosis & poikilocytosis

Serum Methylmalonic Acid MMA: Elevated
Homocysteine levels: Elevated

BOTH ARE ELEVATED

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61
Q

Tx of B12

A

Parenteral B12- daily IM/SQ injections of 1000 micrograms for 1 week

Then, weekly injections for 1 mo

Then, monthly injections for life

*Monitor potassium with tx

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62
Q

Hemolytic Anemias (7)

A 
G6PD deficiency
Hereditary spherocytosis
Sickle cell anemia
Autoimmune hemolytic anemia
Fragmentation syndromes
Incompatible blood transfusion
Paroxysmal nocturnal hemoglobinuria
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63
Q

Normal RBC lifespan

A

120 days

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64
Q

RBC survival b/w this amount can be compensated for by increased marrow production

A

20-100 days

anything under 20 days cannot be compensated for!

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65
Q

Clinical features of Hemolytic Anemia

A

Typical anemia sx + jaundice, gallstones (black, bilirubin stones), dark urine

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66
Q

Hemolytic Anemia lab findings

A

Low RBC
Reticulocyte count: increased
Polychromasia: BIG AND BLUE
Peripheral smear: immature and nucleated RBCs, Schstocytes (fragmented RBC)

Unconjugated bilirubin is increased

Serum Lactate Dehydrogeanase LDH is increased

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67
Q

Intravascular hemolysis lab

A

Decreased Serum Haptoglobin

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68
Q

Useful test in distinguishing b/w all diff types of Hemolytic Anemia

A

Direct antiglobulin test (DAT) aka Coombs test

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69
Q

Reticulocytosis is hallmark of

A

HEMOLYTIC ANEMIA
Lows of blue means lots of new

body is responding to the destruction of RBC by making a bunch of new

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70
Q

Extravascular hemolysis

A

destruction of RBC in the reticuloendothelial system: spleen, liver, lymphnodes, bone marrow

can be d/t: enzyme deficiencies, other hemoglobinopathies, membrane defects, liver disease, hypersplenism, infections, etc)

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71
Q

G6PD def

A

enzyme essential for ensuring normal lifespan of RBC- protect against oxidative stress

If not present, oxidative stress leads to Episodic Hemolytic Anemia

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72
Q

What causes oxidative stress?

A

Sulfa & Antimalarial drugs
Infections
Fava beans

severe def may cause chronic hemolysis

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73
Q

Clinical signs of G6PD def

A

usually asymptomatic during times of oxidative stress

African American and Mediterannean- usually males

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74
Q

G6PD def

A

African American and Mediterannean

X linked recessive
mostly males affected

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75
Q

G6PD deficiency sx DURING the hemolytic attack

A

Back or abdominal pain, normal anemia sx, Splenomegaly, jaundice

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76
Q

G6PD labs

A

during hemolytic episodes: Reticulocytes and Serum indirected bilirubin: elevated

Smear: Bite cells and HEINZ bodies (denatured hgb)

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77
Q

GDPD tx

A

attacks are usually self limited as RBC are naturally replaced

Avoid oxidative drugs, and probably fava beans too

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78
Q

Hereditary SPHEROcytosis

A

Autosomal dominant w/ Mild Hemolytic Anemia

intrinsic defect in the RBC membrane/cytoskeleton

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79
Q

Hereditary Spherocytosis

A

defect of membrane/cytoskeleton leads to

Normal size (MCV) BUT smaller surface area- they are dense and globular (like sphere) and lack central pallor

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80
Q

Problems with Hereditary Spherocytosis

A

since they are dense and spherical shaped, can’t deform as they pass thru vessels, get trapped in Splenic sinusoids –> phagocytosed by splenic macrophages (increased cell fragility)

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81
Q

Hereditary Spherocytosis

A

Autosominal dominant
Relation with spleen

If pt has spleen: RBC lifespan is shortened bc they get trapped here and phagocytosed early!

If pt has had Splenectomy!: normal RBC lifespan

82
Q

Hereditary Spherocytosis sx

A

often asympto, adapt well
Maybe jaundice, scleral icterus, pigmented black gallstones, Splenomegaly

Chronic hemolysis creates need for increased folate. If pts do not increase folate –> megaloblastic anemia

83
Q

Hereditary Spherocytosis labs:

A

Osmotic Fragility Test!!!
RBC will have increased hemolysis on exposure to hypotonic fluid d/t membrane defect

Hyperchromic microcytosis (little dense round RBC)

Coombs negative

84
Q

Tx of Hereditary Spherocytosis

A

Splenectomy- treatment of choice for severe disease

However, caution increased risk of infection of encapsulated organisms (i.e. pneumococcus) if pt has no spleen

  • get approp vaccines
  • delay splenectomy until adulthood
  • folate supplementation in meantime
85
Q

Sickle cell

A

Autosomal Recessive

RBC become sickle shaped when deoxygenated

disorder of hgb structure

resistance to malaria

86
Q

Sx of Sickle cell

A

typically start at 4-6 months

first, swelling of digits (dactylitis)

delayed growth and development

87
Q

Other sx of sickle cell

A

Functional asplenia

Aplastic crisis associated with Parvovirus B19 infections (erythema infectiosum/fifth disease “slapped cheek)

88
Q

Sx of sickle cell onsety by

A

Hypoxic conditions:

dehydation, altitude, intense exercise

89
Q

Chronic hemolysis feature of sickle cell

A

BUT can have an Aplastic crisis- a sudden decrease in Hgb, can be life threatening!

90
Q

Vaso-occlusive ischemic tissue injury

a component of Sickle Cell disease

A 
Pain crisis (most common)
Acute chest syndrome (new radiodensity on CXR + fever, requires aggressive tx)

Two most common above. Others include: osteonecrosis of femoral and humeral head, CVA, MI, splenic infarcts, skin ulcers, renal infarcts

91
Q

Sickle cell labs

A

Normocytic Normochromic
Reticulocyte count: elevated
Hgb electrophoresis: reveals Hb S!!!!! this is helpful in sickle cell diagnosis as well as thalassemia diagnosis

92
Q

Peripheral smear of Sickle Cell disease

A

sickled, nucleated, target cells, thrombocytosis and

HOWEL-JOLLY BODIES*

93
Q

Tx for Sickle Cell

unfortunately lifespan is still 40-50YO despite tx

A

Analgesics, fluids, oxygen during pain crisis
Hydroxyurea (chemo) to decrease incidence of painful crisis- suppresses bone marrow function of all cell lines

+avoid precip factors, RBC transfusion if needed, vaccinate against encapsulated organisms, Folate supp, bone marrow transplant

94
Q

Autoimmune Hemolytic Anemia (AIHA)

A

Antibodies adhere to surface of RBC and induce hemolysis

RBC with antigen-antibody complex are phagocytized by macrophages and spherocytes are formed –> become smaller and destroyed in the spleen

95
Q

AIHA

A

Primary (no underlying disorder) vs Secondary (identifiable underlying disorder)

96
Q

Clinical sx of AIHA

A

depend on type of antibody produced
IgM: “cold”
IgG: “warm” more common with chronic

at risk for blood Clots!

97
Q

Causes/associations of AIHA

A

Lupus, RA, Chronic lymphatic leukemia, Mycoplasma infection, Epstein Barr virus, HIV, Immunodef- prior organ or stem cell transplant, Prior blood transfusion, Drugs

98
Q

AIHA sx

A

typical others + lymphadenopathy (workup for underlying CA), Hemoglobinuria-dark urine, Acrocyanosis-dark purple to gray fingertips, nose in exposure to COLD

99
Q

Peripheral Smear of AIHA

A

Polychromasia (abn high level of new RBC), spherocytosis, nucleated RBC

100
Q

Coombs test (DAT) in AIHA

A

Positive

101
Q

Tx of AIHA

A

Warm: Corticosteroids first line, then Rituxumab, Splenectomy, Immunosuppressants, IVIG

Cold: avoid cold exposure, Rituxumab, Plasmapharesis

102
Q

Intravascular Hemolysis

A

Destruction of RBC WITHIN the bloodstream

103
Q

Fragmentation syndrome- Mechanical heart valve

A

Schistocyte on smear

Small vessels or mechanical heart valve problem cut up RBC in circulation

104
Q

Hemolytic Transfusion Rxn

A

Most antibodies to RBC are directed against the ABO/Rh blood grouping antigens

Blood transfusion rxns
Hemolytic disease of newborn (HDN) (erythroblastosis fetalis- this is why we give moms Rho Gam)

105
Q

Combs test can detect antibodies of the patient coating the transfused red cells

A

useful to avoid Hemolytic blood transfusion reaction

106
Q

Hemolytic Transfusion Redaction

A

during or within 4 hours of transfusion

delayed rxn can occur up to 4 weeks later!

Sx: fever, hemoglobinuria, severe HYPOTENSION, severe flank pain, pain @ infusion site, chest tightness, DIC oozing from site, N/V/D

If see these signs, stop right away: decreased BP, increased RR, hemoglobinuria, CP, low back pain, fever, tachy, chills

107
Q

Paroxysmal Nocturnal Hemoglobinuria

A

Rare acquired stem cell mutation

Mediated RBC lysis
Dark colored urine @ night
Venous thrombosis of large vesseles
Pancytopenia (low count of all types of Blood Cells- RBC, WBC, and platelets)

108
Q

How to diagnose Paroxysmal Nocturnal Hemoglobinuria

A

Flow cytometry, Osmotic fragility test, Coombs negative

109
Q

Tx of Paroxysmal Nocturnal Hemoglobinuria

A

Monoclonal antibody against complement C5
Steroids
Stem cell transplant

110
Q

In general, tx of Hemolysis often includes

A

Corticosteroids
Consider Splenectomy
Folic Acid Supp

111
Q

Aplastic Anemia

A

Acquired abn of hematopoietic stem cells

50% cases are idiopathic
20% d/t drug/chemicals
10% assoc w/viral illness (EBV, CMV, Hep)

112
Q

Aplastic Anemia

A

PANCYTOPENIA (low everything) is hallmark

bone marrow has absence of precursors for these cells

“Slide looks empty”

113
Q

Tx for Aplastic Anemia

A

BONE MARROW TRANSPLANT is preferred tx*

Heme referral, Transfusion as needed, immunosuppressant agents if bone marrow isnt option

114
Q

Innate

A

Natural Immunity

1st line of defense, rapid, no memory

115
Q

Complement system

A

group of 30+ plasma proteins that activate cascade like manner in response to an antigen

116
Q

Cascade of events in complement pathway

A
  1. Activation thru classical pathway
  2. Formation of C3 convertase
  3. Opsonization & Phagocytosis
  4. Inflammation
  5. Membrane attack complex (MAC) formation & lysis
117
Q

Classical pathway of Complement system

A

triggered by antibodies binding to an antigen

118
Q

C3 convertase

A

cleaves C3 which is the most abundant complement protein

119
Q

Opsonization

A

the coating of a pathogen by an antibody. This “tags” the pathogen ready for phagocytosisq

120
Q

MAC- Membrane attack complex

A

A group of complement proteins that form to cause lysis of the microbe

combine on the surface of the antigen- causing the cell wall to disintegrate and cell ruptures and dies

121
Q

Steps of Inflammation

A
  1. tissue damage
  2. chemical signals alert endothelial cells
  3. neutrophils become sticky and stop rolling along capillary
  4. mast cells release histamine
  5. histamine –> vasodilation between the endothelial cells (where the neutrophils will later squeeze out)
  6. fluid and leukocytes enter affected tissue
  7. neutrophils squeeze through the endothelium (called Extravasation)
  8. neutrophils attracted to the damaged site where they ingest/destroy bacteria
122
Q

WBC –> Granulocytes and Agranulocytes

A

Granulocytes “phils”

Agranulocytes “cytes”

123
Q

Neutrophils

A

First responders
Bacteria
Increase in Band Neutrophils
Leukocytosis with “left shift” indicative of acute BACTERIAL INFECTION

Lifespan: 6 hr-few days

124
Q

Neutrophilia

A

too many WBC

usually acute bacterial infection

125
Q

Neutropenia

A

not enough WBC

often Viral infections

126
Q

Basophils

A

Allergic response
Release granules that contain Histamine & Heparin.
Histamine: increases blood flow to area
Heparin: reduces clotting

Lifespan: hours-days

127
Q

Eosinophils

A

Target larger parasites (Worms)
Modulate allergic inflammatory response

Numerous in the mucous membranes of Respiratory, digestive, and lower urinary tracts

Lifespan: 8-12 days

128
Q

Mast Cells

A

just like basophils, release Histamine and Heparin
Present in barrier tissues like the mucosa

Imp role in ALLERGY & ANAPHYLAXIS

129
Q

Monocytes

A

largest WBC
found in blood & SPLEEN

Lifetime: hours-days

130
Q

Lymphocytes

A

B cells, T cells, and Natural killer cells

Lifetime: weeks for most, years for memory cells

131
Q

Spleen

A

largest lymphoid organ
Removes old RBC, stores RBC, and recycles iron

Makes antibodies

132
Q

Asplenia

A

Will see increase in circulating WBC and platelets

Diminished response to some vaccines

Increased vulnerability to Encapsulated bacteria:

  • Strep PNA
  • H. Influenzae
  • N. Meningitis

Do not give someone without a spleen an encapsulated bacteria immunization because they cant activate the antibodies that are usually made by spleen and cant use complement system bc this requires antibodies binding to antigen but they cant get thru hard shell

133
Q

MALT

A

Mucosal adenoid lymph tissue

can also be Nasal, Bronchal, or Gut

specialize in antigens passing through the mucosal epithelium

134
Q

Adaptive Immunity

A

second line of defense, very specific, has memory

135
Q

Humoral (B cell) immunity

A

use Antibodies

Defend against Extracellular pathogens

136
Q

Cell mediated (T cell) Immunity

A

Direct cell to cell contact

Defend against Intracellular pathogens

137
Q

B cell activation

A

1 step: happens when the antigen binds to the mature, naive B cell receptor

138
Q

B cells proliferate and make clones which become:

A

Plasma cell or

Memory B cell

139
Q

Types of antibodies: Ig__

A 
M
G
A
E
D
"My grandma always eats dessert"
140
Q

IgM

A

First responder
Indicates an Acute/Recent infection!

5-10 day half life

141
Q

IgM and IgG

A

activate the Complement system

Remember: complement system is activated by antibodies binding to antigens to “tag” them (these are examples of antibodies that can do this)

142
Q

IgG

A

second responder

Good at opsonization
Levels of M falls as this type, G, rises
MOST ABUNDANT type
21 day half life (one of the longer ones)

143
Q

Ideal results for titer drawings

A

No IgM activity but IgG activity is present with high avidity (means that igG is remembering the infection, but there is no igM because this is not an acute recent infection)

144
Q

igA

A

Mucosal membranes, eliminates pathogens through mucosa

145
Q

igE

A

activate B cells

146
Q

igG

A

can cross placenta!!!

147
Q

igM

A

cannot cross placenta - if you see this in fetus, this means the fetus itself has a recent/acute infection

148
Q

igA

A

mucosal membrane

can cross in breast milk (example of passive immunity)

149
Q

T cell activation

A

2 steps

1: TCR binds to MHC-antigen complex on the Antigen presenting cell (APC for short)
2: T cell receptor CD28 binds to the B7 on the Antigen presenting cell (APC)

150
Q

What receptors are located on the T cell?

A

TCR

CD28

151
Q

What receptors are located on the Antigen Presenting Cell?

A

MHC complex

B7

152
Q

What binds with TCR?

A

MHC

153
Q

What binds with CD28?

A

B7

154
Q

4 types of T cells

A

Helper & Cytoxic (bind to MHC)
Suppressor
Memory

155
Q

Antigen Presenting Cells (APCs) have MHCs on their surfaces

MHC= Major Histocompatibility Complex

A

MHC I: on surface of ALL nucleated cells

MHC II: on surface of B cells, dendritic cells, & macrophages

156
Q

MHC I (all nucleated)

1 to 8

A

present to Cytotoxic T cells

CD8+

157
Q

MHC II (on the 3 types)

2 to 4

A

present to Helper T cells

CD4+

158
Q

Leukemia

A

CA of Bone Marrow and Lymphatic system

159
Q

Types of Leukemia

A

Acute myeloid, Chronic myeloid, Acute lymphoblastic, Chronic lymphocytic

160
Q

Labs assoc with Acute myeloid leukemia

A

Auer Rods on peripheral smear

Elevated Uric acid and Lactic acid dehydrogenase LDH

161
Q

Other labs assoc with Acute myeloid leukemia

A

Elevated blasts (myeloid) >or equal to 20%

But, reduced platelets, neutropenia, and RBC

162
Q

Auer Rods

A

Acute myeloid leukemia

clumps of azurophilic granule material, form elongated needles in leukemic blasts

163
Q

Diagnostic test for AML

A

Bone marrow aspirate and Biopsy

Blasts form >/20% cellularity

164
Q

Most common acute leukemia in adults

A

AML- Acute myeloid leukemia

165
Q

Median age for Acute myeloid leukemia AML

A

65

M>F

166
Q

Diagnosis and Labs for AML

A

Blast cells >/20%

Increased Ca, K, Uric acid, and LDK

Auer Rods

167
Q

Risk of MDS progressing to

A

AML

168
Q

Peak time for MDS to onset after chemo/radiation treatment

A

4-6 years post tx

169
Q

Increased incidence of MDS

A

Older age, M>F, smoking, benzene (plastic, pesticides, gas, fumes), chemo/radiation

170
Q

MDS

A

Inneffective blood cell production- low counts of everything

Chronic cytopenias (anemia, neutropenia, thrombocytopenia)

171
Q

Only hope for cure for MDS

A

Allogenic Bone Marrow transplant

172
Q

Goal of tx for MDS

A

Minimize cytopenia, quality of life, delay onset of Leukemia

173
Q

Both types of myeloid CA are mid age

A

Acute myeloid leuk (AML) : 65

Chronic myeloid leuk (CML): 50

174
Q

The Lymph CAs are either young children or older adult average age

A

Acute: 2-5 YO
Chronic: 70 YO

175
Q

Reed steenburg cells

multi-nucleated popcorn cells

A 
Hodkin Lymphoma (15-30YO)
B sx
176
Q

CA with high assoc to Epstein Barr Virus

A

Hodkin Lymphoma

177
Q

Non Hodkin Lymphoma

A

66YO
hx, hair dye, pesticide
B sx

178
Q

Multiple Myeloma

A

66 YO
African American
CA of PLASMA cells
causes osteolytic lesions

179
Q

Labs for Multiple Myeloma

A

Paraproteins
M spike
Bence Jones proteins
Anemia

180
Q

Complications assoc with Multiple Myeloma

A

Hyperviscosity synd
Visual disturbance
Neuro sx- coma, vertigo, serizures

181
Q

Labs with Multiple Myeloma

A 
CRAB
C: calcium >10.5
R: renal insuff
A: anemia
B: bone lesions
182
Q

Hereditary Spherocytosis

A

Autosomal Dominant

Osmotic fragility test

183
Q

G6PD def

A 
X recessive
(X recess, no recess for these ppl bc we don't want them to undergo oxidative stress when playing soccer)

X recess. X linked recessive

184
Q

Hereditary Spherocytois

A

Splenectomy treatment of choice

185
Q

Sickle cell

A

Autosomal recessive

186
Q

There are two types of Autosomal disorders we talk about relating to blood

A

Hereditary spherocytosis: Autosomal DOMINANT

Sickle cell: autosomal recessive

187
Q

initial sx of Sickle Cell at 4-6 months

A

swelling of digits: dactylitis

188
Q

Sickle cell

A

Aplastic crisis associated with Parvovirus B19 infections

189
Q

Howell Jolly bodies

A

Sickle cell!!

even though people with this condition are not very Jolly

190
Q

Tx for sickle cell

A

Hydroxyurea (chemo) can decrease incidence of painful crisis by suppressing bone marrow function of all cell lines

191
Q

Hydroxyurea

A

tx for Sickle Cell

192
Q

Autoimmune Hemolytic Anemia (AIHA)

A

Autoantibodies attach to RBC membrane and damage it

RBC then destroyed in spleen

Warm or Cold

193
Q

IgM

A

cold

194
Q

IgG

A

warm

195
Q

Coombs test in Hereditary Spherocytosis

A

negative

196
Q

Coombs test in AIHA Autoimmune Hemolytic Anemia

A

Positive

197
Q

Tx for Warm AIHA

A

Corticosteroids

198
Q

Tx for Cold AIHA

A

Avoid cold exposure

199
Q

Shistocyte

A

RBC with bite eaten out of it

Mechanical

200
Q

Coombs test

A

detects antibodies of patient coating the transfused cells

important before blood transfusion

Quarter 2 (16 decks)

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