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Clinical Medicine > Heme > Flashcards

Heme Flashcards

1
Q

what are the causes of bone marrow failure?

A
  1. Nutritional deficiency: Vitamin B12, Folate, Iron
  2. Marrow toxins (myelosuppressive): Drugs (many), chemotherapy, radiation, ethanol
  3. Infections: HIV, HBV, HCV, EBV, CMV, Parvovirus B19- common childhood infection
  4. Marrow replacement: Infections (fungal, TB), sarcoid, leukemia, lymphoma, myeloma, metastatic carcinoma
  5. Autoimmune diseases
  6. Primary bone marrow diseases: Fanconi anemia, paroxysmal nocturnal hemoglobinuria, many others
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2
Q

3 requirements for hematopoiesis

A
  1. Healthy Bone Marrow
  2. Hormones/ Cytokines (stimulus—foot on gas pedal)
    -Erythropoietin- hormone from the kidney that stimulates marrow to produce RBCs, anemia from chronic renal failure is due to lack of Erythropoietin
    − Thrombopoietin- hormone from the liver that stimulates marrow to produce RBCs
    -Growth Factors- hormone that stimulates marrow to produce WBCs (gray cell)
  3. Nutritional Factors- ( gas tank)
    Iron (RBCs), Folate, Vitamin B12 (RBC, WBC, and platelets)
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3
Q

only cell without nucleus

A

rbc

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4
Q

cell whose nucleus divides a bunch then cytoplasm splits

A

megakaryocytes to platelets

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5
Q

which blood cell develops within its own lineage?

A

lymphocytes

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6
Q

which part of bone marrow is lined with endothelial cells and fibroblasts support the development of blood cells (not blood making tissue)

A

stroma

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7
Q

primary hematopoietic organ in fetus

A

liver

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8
Q

which organs can make blood if bone marrow diseased?

A

liver and spleen

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9
Q

what’s primary hematopoietic organ at birth?

A

bone marrow

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10
Q

what 2 things compromise blood?

A

formed elements (RBC,WBC, platelets) and plasma

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11
Q

whats in plasma?

A
  1. Water: main component
  2. Dissolved ions: Na+, K+, Cl-, H+, Mg++, Ca++
  3. Proteins (about 3 dozen): Carrier Proteins (Albumin (Uhaul van of drug system), Lipoproteins, Transferrin, Many others), Immunoproteins (IgG, IgA, IgM, IgD, IgE, Complement proteins), Coagulation proteins
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12
Q

which blood cell is only one that returns to BM?

A

lymphocytes

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13
Q

mechanisms of cytopenias

A
  1. Decreased Production (6 categories from below—sick bone marrow)
  2. Increased destruction/consumption
  3. Sequestration/spleen
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14
Q

what produces epo? can you measure epo with creatinine or kidney function tests?

A

kidney; no you can’t measure it that way because epo production via kidney is a completely separate function form how well it can clear stuff

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15
Q

what’s the test that can differentiate between destruction or production problem of RBCs, first test for evaluating anemia?

A

reticulocyte count

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16
Q

is a rx necessary for blood products?

A

yes

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17
Q

indications for fresh frozen plasma

A

• Indication: coagulation deficiencies
− Liver failure
− Disseminated intravascular coagulopathy (DIC)- all coagulation factors are consumed?
− Vitamin K deficiency- Vitamin K-dependent factors (II, VII, IX, X) (remember Warfarin inhibits this)
− Warfarin toxicity
− Massive blood loss

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18
Q

indications for platelets transfusin

A

• Indications: Thrombocytopenia (

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19
Q

how many platelets are in one unit from one donor? how many of those are usually pooled together for the patient?

A

10-15K; pool 6-8 people’s together to give them 60k

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20
Q

indications for pRBCs

A

− Hemodynamically unstable: P>100/min, RR>30/min, hypotensive, decrease O2 sats, dizziness, weakness, angina, and altered mental status
− Leukemic processes, hemolytic anemia, other anemias, surgical or traumatic blood loss can decrease RBCs
• Criteria: usually Hgb of

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21
Q

indications for albumin

A

• Indication: equalize the intra and extravascular osmotic pressure
− Situations of hypovolemia and hypoproteinemia
− Burn injury

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22
Q

percent Rh+ in population

A

70%

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23
Q

if someone is Rh- and you give them Rh+ blood what will happen?

A

they will not react much at first but will mount an immune response and develop anti-D ab and will attack Rh+ blood next time

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24
Q

what is the difference between type and screen and type and crossmatch?

A

type and crossmatch includes combining donor and recipients blood cells to look for agglutination

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25
Q

who is a universal donor (for RBCs)? for plasma?

A

o negative (no antigens for pt to attack); for plasma: AB (no antibodies to attack patients own blood)

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26
Q

clinical presentation of hemolytic transfusion reaction and tx?

A

patients blood attacks transfused blood
Clinical presentations: DIC, Acute Renal Failure, Acute Tubular Necrosis, Shock
− Triad of Fever, Flank pain and red/brown urine
tx: Medical Emergency- STOP TRANSFUSION immediately, Maintain airway, start Saline at 100-200ml/hr. Notify the blood bank immediately
− Obtain blood and urine samples.
− Vasopressors (Dopamine) indicated for hypotensive patients.

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27
Q

febrilel nonhemolytic transfusion rxns: what is it? clinical presentation, tx

A

interleukins and TNF alpha in RBCs that attack patients cells
Fever, Chills, Rigors, Mild Dyspnea
tx: tylenol or benadryl

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28
Q

delayed hemolytic transfusion rxn: defintion, clinical presetnation, tx

A

atpical ab in recipients blood that occurs 2-10 days later, mild presentation of Slight fever, falling hematocrit, mild increase of unconjugated bilirubin and spherocytes in blood smears
no tx necessary

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29
Q

can you get an anaphylactic transfusion rxn from blood?tx

A

yes: same presentation as other anaphylaxis: shock, hypotension, angioedema, respiratory distress
tx: stop transfusion, give epic

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30
Q

uritcarial transfusion rxn:

A

blood products given cause histamine release of hives or urticaria, not necessary to stop transfusion, can give bendadryl

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31
Q

post transfusion purpura; tx? can they get a platelet transfusion in the future?

A

sensitized to antigen on platlets; severe thrombocytopenia lasting days to weeks, usu 5-10 days after transfusion.
tx with corticosteroids (blunt immune response) can get platelets later but they should be washed first

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32
Q

what kind of rxn? sudden onset of respiratory distress during or after transfusion − Fever, tachypnea, tachycardia, and hypotension can occur. how do you tx?

A

immune response in pulmonary vasculature

• Treatment: Supportive. Mechanical Ventilation is required in 72% of the patients in one study.

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33
Q

blood product complications

A 
fluid overload
rxn to preservatives in it
coag defects d/t to massive transfusion and dilution
chelation of Ca2+
hyperkalemia
hypothermia (blood stored in cold)
iron overload
air embolism
citrate toxicity (anticoagulant)
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34
Q

which pregnancy would be most problematic for an Rh- mother without med intervention?

A

second one, In the first pregnancy, a mother’s Rh- blood will not attack Rh+ babies blood because she hasn’t developed antibodies against it yet
However, during delivery or any trauma, the babies blood can mix with hers and the mother can develop the anti-D antibodies
During her second pregnancy her anti-D Ab could cross the placenta and attack the babies blood

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35
Q

what med is given to prevent Rh- negative mother from attacking Rh+ baby?

A

rhogam: attaches to fetus’s Rh+ antigen, preventing the mother’s immune response

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36
Q

indications for rhogam

A

• all Rh- women: 1 dose @ 26-28 weeks gestation (early in 3rd trimester).
• Spontaneous/Induced Abortion >12 weeks gestation. (before that baby has not formed Ab yet)
• Ectopic pregnancy.
• Multifetal reduction.
• Invasive procedures: e.g. Amniocentesis.
• Threatened abortion.
• Fetal death in 2nd or 3rd trimester.
• Blunt trauma to the abdomen.
• Antepartum hemorrhage in 2nd or 3rd trimester.
-and after delivery

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37
Q

what is the largest lymphoid organ?

A

spleen

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38
Q

when should you biopsy the spleen?

A

NEVER. not done anymore b/c it can pop. just take it out if concerned.

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39
Q

why would you take out a spleen?

A
  • Immune cytopenias
  • Hematologic malignancy
  • RBC membrane/enzyme disorders
  • Thalassemia
  • TTP
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40
Q

someone has elevated WBCs and platelets, what should you consider?

A

that their spleen is taken out

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41
Q

how do you prevent post splenectomy sepsis?

A

vaccinate! h. flu, n. meningitidis, s. pneumo

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42
Q

why don’t we give splenic kids prophylactic abx ?

A

resistance

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43
Q

how do you manage infections in asplenic people?

A

they need an rx of abx to take, even if its seems viral, and take it then proceed to nearest healthcare facility

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44
Q

− To find, ingest, and kill invading microorganisms
− Bactericidal activity is mediated by production of hydrogen peroxide, superoxide, hydroxyl radicals, hypochlorous acid, nitric oxide

A

neutrophils

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45
Q

causes of increased and decreased neuttrophils

A
  • **Increase Neutrophils: bacterial infection, physiologic stress, corticosteroids
  • **Decrease Neutrophils: viral infection, drugs/toxins, some bacterial infections (Brucella)
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46
Q

• Secrete cytokines that induce fever and inflammation

Increase occurs with chronic infections (TB), lymphomas, and granulomatous diseases (sarcoid)

A

monocytes

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47
Q

what WBC is increased?
− Chronic inflammatory skin disorders (like bad eczema)
− Invasive parasitic diseases (checked when immigrants arrive)
− Hypersensitivity states (allergies, vasculitis)
− Certain malignancies (Hodgkin’s disease

A

eosinophilia

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48
Q

what causes basophilia?

A

occurs in allergic disorders and myeloproliferative diseases (CML, Polycythemia vera)
• After leaving the circulation, basophils differentiate into tissue mast cells

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49
Q

how do basophils become mast cells that release histamines?

A

Membranes contain high affinity IgE receptors, Ig antibodies to environmental antigens that cause allergies
• **Binding of antigen / IgE complex to basophil membrane causes degranulation and release of substances (e.g. histamine) with powerful vasoactive and inflammatory properties

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50
Q

• Increased in most viral infections

A

lymphocytes

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51
Q

causes of leukocytosis: reactive

A
  • Bacterial (neutrophils)/Viral/ Parasitic (eosinophilia) infection
  • Inflammation (eosinophils)
  • Allergy (eosinophils)
  • Physiologic stress
  • Drug induced
  • Asplenia
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52
Q

causes of leukcytosis: malignant:

A
  • Hematologic

* Non hematologic

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53
Q

practical # of WBCs (low and high) to call hematology

A

50000

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54
Q

causes of leukopenia: decreased production and destruction

A 
a)  Decreased production
•	B12 / Folate deficiency
•	Marrow aplasia / dysplasia
•	Marrow replacement (tumor, infection)
•	Marrow damage (drugs, toxins, radiation)
•	Autoimmune
b)  Increased destruction / consumption
•	Hypersplenism
•	Autoimmune
•	Overwhelming infection / sepsis
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55
Q

factors required for blood cell synthesis?

A

healthy bone marrow, “gas” nutrients like iron, b12, folic acid, gas pedal, foot on gas pedal=epo

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56
Q

best place to tell if someone is pale/anemic

A

palpebral conjunctiva

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57
Q

sx of anemia

A
  • Fatigue; ↓ stamina with exercise
  • Dyspnea
  • Tachycardia
  • Dizziness; lightheadedness
  • Fainting
  • Headache
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58
Q

important PMH questions for anemia

A
  • Hx of anemia?
  • Previous treatment and response
  • Transfusion history
  • Menstrual history, abnormal bleeding
  • Pregnancy (frequency)
  • Bariatric surgery
  • Medications:
  • NSAIDS
  • Anticoagulants
  • Myelosuppressive drugs
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59
Q

fm qxs in anemia

A
  • Ethnic background
  • Sickle Cell Anemia
  • Thalassemia
  • Presence of anemia in first degree relative
  • Age of diagnosis
  • Severity
  • Jaundice
  • Cholecystectomy
  • Splenectomy
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60
Q

soc hx qxs in anemia

A
  • Dietary Habits
  • Iron, B-12, folic acid
  • Vegetarian eating patterns
  • Alcohol Consumption
  • Folic acid- decreases absorption; interferes with conversion to active form and release
  • B-12- decreases absorption
  • G.I. bleeding
  • Immune suppression
  • Liver disease (independent of vit def)
  • Impaired biosynthetic processes

• Blood Donations

61
Q

anemia PE

A

• Pallor (skin, oral mucosa, conjunctiva, nail beds, palms); ecchymosis, petechiae
• Jaundice, hepatosplenomegaly (hemolytic anemia)
• Tachypnea, tachycardia; systolic flow murmur
• Edema
• Lymphadenopathy
➢ Stool occult blood

62
Q

normal hgb ranges for males and females

A

Adult male = 14.4-16.1 g/dL Adult female = 12.2-14.7 g/dL

63
Q

classification of anemia

A

10-12 g/dL

64
Q

anemia and high reticulocyte count=?

A

RBCs being destroyed

65
Q

low absolute reticulocyte count means?

A

decreased BM production

66
Q

normal absolute reticulocyte count

A

20000-75,000/microliter

67
Q

anemia + small red blood cells=?

A

iron deficiency anemia, thalassemia, lead poisoning

68
Q

anemia + big red blood cells?

A
  • ***B-12/folic acid deficiency
  • Pernicious Anemia
  • Liver disease
  • Hypothyroid
  • Drugs (e.g.TMP/SMX, Metformin, Hydrea)
  • Myelodysplastic syndrome
69
Q

lab test to help you determine size of RBCs (besides smear); what’s low, what’s high?

A

mean corpuscular volume MCV; low 100 think B12 or folate deficiency

70
Q

causes of normocytic anemia

A 
think anemia of chronic disease: •	
ACD/AI (most)
•	Renal Failure	
•	Early iron deficiency (acute bleeding or intermittent blood loss)	
•	CLL, CML, Aplastic Anemia
71
Q

anisocytosis

A

large variations in size of RBCs on RBC distribution width

72
Q

hypochromic vs. normochromic

A

hypochromic=low hemoglobin concentration in RBCs=pale centers

73
Q

total iron binding capacity should increase when?

A

total serum iron is low

74
Q

tx of anemia d/t to acute blood loss

A

volume expansion, transfusion

75
Q

tx of anemia d/t chronic blood loss

A

depends on seveirty, transfusions, oral/parenteral iron supplement

76
Q

lab workup for someone who is iron deficient?

A

Diagnosis

• ↓ Hgb (

77
Q

what’s a common cause of anemia worldwide?

A

parasites

78
Q

Pica

A

craving of non food items that is a sx of iron deficiency

79
Q

ddx of anemia

A
  • Anemia of Chronic Disease/ Anemia of Inflammation
  • Thalassemia
  • Sideroblastic Anemia
  • Myelodysplastic syndrome
  • Lead toxicity
80
Q

anemia: low TIBC, normal ferritin, normocytic, normochromic

A

anemia of chronic disease

81
Q

causes of B12 deficiency anemia

A

low dietary intake (rare), malabsorption, pernicious anemia

82
Q

neuro sx of B12 deficiency

A
  • Peripheral neuropathy
  • Parasthesias
  • ↓ vibratory and proprioception
  • Ataxia
  • Weakness, inability to walk
  • Dementia
  • Psychological disturbances
  • Sub-acute combined systemic degeneration (irreversible)
83
Q 
•	↓  Hgb and HCT
•	↑ MCV (usually > 100)
•	Low reticulocyte count
•	Pancytopenia (severe)
what kind of anemia?
A

usu B12 deficiency or folate deficiency, check serum B12 or antibodies for pernicious anemia

84
Q

causes of folic acid deficiency anemia

A

• Poor Dietary Intake (top 5 nutrient deficiencies → fortification):
Risks → elderly, diets lacking green, leafy vegetables, anorexia, and cancer

• Increased/Impaired Utilization
Risks → Premature infants, ETOH, hemolytic anemia, dialysis, ICU patients
Pregnancy and Lactation (additional 400 ug)
Anti-folate Drugs

• Impaired Absorption → gastric resection, ileal disease, alcohol abuse (also utilization and storage)

85
Q

if 3 blood cells lines are off you need a ____

A

bone marrow bx

86
Q

triad of hemolytic anemia

A
  • Normocytic or microcytic anemia
  • ↑ reticulocyte count
  • Hyperbilirubinemia (indirect)
87
Q

first 2 tests for hemolytic anemia

A

CBC with diff, reticulocyte count

88
Q

identifying and treating hereditary spherocytosis:

A

Child with:
Anemia
Jaundice
Splenomegaly

Labs:
Low hgb
High retic
MCV (N or slightly L)

MCH and MCHC usually elevated and combined with high RDW suggests diagnosis (sensitivity of 63% and specificity of 100%)

tx: Control anemia (transfusions)–if affecting growth
Folic acid for chronic red cell production?
Splenectomy may be required to control
Cholecystectomy if gallstones form

89
Q

indications for splenectomy

A

1 to treat a disease in which blood cells are destroyed in the spleen

90
Q

hemolytic anemia: pyruvate kinase deficiency

presentation, pathophys, dx, tx

A

missing glycolytic enzyme, cell has no energy, rigid=hemolyzed

presentation: decreased hgb, neonatal jaundice, increased retakes, abnormal cells on smear, enzyme test +

dx: enzyme test
tx: folic acid b/ high cell turnover, avoid transfusions and iron

91
Q 
structural hemolytic anemia: G6PD deficiency
pathophys
presentation
dx
tx
A

pathophys: x-linked, missing G6PD, can’t respond to oxidative stress, spleen removes them

presentation: CBC normal between episodes of stress, stress=drugs, fava beans, infection;
sx: malaise, weakness, abdominal or back pain, increased bilirubin, jaundice, dark urine/ hemoglobinuria

dx: normochromic, normocytic, during attack decreased hgb, increased relics, G6PD screening
tx: avoid offending agent, +/- transfusions in acute episodes

92
Q

microcytic anemia, increased reticulocyte counts, imbalance of alpha and beta chain global production, mutations in 1-4 of alpha genes

A

alpha thalaseemia

93
Q

beta-thalassemia major presentation

A

in first or 2nd year when hgb F production stops, severe anemia requiring regular transfusion, facial abnormalities

94
Q

labs in alpha and beta thalassemia

A 
Mild to severe anemia
decreased Hgb and HCT
decreased MCV (microcytic)
decreased MCH (hypo chromic)
increased reticulocytes
Hgb Electrophoresis 
Genetic mapping
95
Q

anemia with high reticulocytes and vaso occlusive episodes

A

sickle cell anemia

96
Q

tx of sickle cell

A

hydroxyurea: increases Hgb F, transfusions, folic acid, iron chelation if transfused, tx infections promptly

97
Q

pt walks in with low hgb, increased relics, no inherited deficiencies, what tests to do?

A

ask yourself: how low is hgb? past hgb levels for comparison? otherwise healthy? check LDH, bilirubin, and coombs

98
Q

patient with anemia, jaundice, splenomegaly, +/- syncope or HF
Positive Direct Coombs
Low hgb, high retic, high LDH, high indirect bili

A

warm antibody AIHA: igG attaches to RBCs at 37, stop offending drug give corticosteroids ASAP

99
Q 
patient with anemia, Acrocyanosis in fingers, feet, nose, and earlobes due to intra-arteriolar agglutination
Mild anemia
Jaundice, splenomegaly
RBCs clumping on smear
Fever
More common in elderly
A

cold antibody AIHA

100
Q

secondary causes of warm antibody AIHA

A 
Connective tissues disorders (SLE, RA)
Lymphoma, CLL
Carcinoma
Drugs-penicillin type, quinine, quinidine (etc.)
Post-viral (children)
101
Q

secondary causes of cold antibody AIHA

A 
Lymphoprolipherative disorders (NHL, CLL)
Infections (infectious mono, micoplasmal pneumonia, EBV, CMV)
102
Q

what are causes of + indirect coombs?

A

Hemolytic disease of the newborn
Hemolytic transfusion reactions
Allogenic BMT, liver, renal, and heart transplant

103
Q

what is a cause of coombs destruction of anemia?

A

mechanical shearing of RBCs

104
Q

name of a structural anemia that is a miler form of hereditary spherocytosis

A

hereditary elliptocytosis

105
Q

drugs that aggravate G6PD deficiency

A

antimalarials, nitrofurantoin, NSAIDS, quinidine, quinine, sulfonamides, aspirin

106
Q

normal fetal hgb type; adult type

A

fetal: alpha2 gamm2; adult: alpha2beta2

107
Q

test to look at hemoglobin type

A

hemoglobin electrophoresis

108
Q

four steps of blood clotting

A

primary hemostasis (platelets), secondary hemostasis (coagulation cascade) hemostasis stops, fibrinolysis (clot dissolves)

109
Q

most common inherited bleeding disorder, males and females affected

A

von Willebrand dz

110
Q

signs of a primary hemostatic defect

A

prolonged initial bleeding, petechiae, mucosal bleeding, bruising

111
Q

signs of a secondary hemostatic defec

A

hemarthrosis, ecchymosis, soft tissue bleeding

112
Q

labs and sx in von willebrand

labs: what will their iNR, aPTT, platelets look like? what other lab tests can you do to dx this disease?

A 
sx: primary problem: Epistaxis, dental bleeding, bruising, menorrhagia (initial bleeding after challenges)
labs:
•	Normal INR
•	Normal or mildly prolonged aPTT (if Factor VIII low)
•	Normal platelet count
•	Abnormal PFA-100 (PFCT)
•	↓von Willebrand antigen
•	Low factor VIII
•	Low ristocetin cofactor activity
113
Q

tx of von willebrand

A

avoid aspirin, DDAVP (desmopressin in inhaled form that releases VWF), amicar and lysteda (slows down clot dissolving), plasma derived factor VIII concentration)

114
Q

what are these clinical features indicative of? joint bleeds, esp around knee, soft tissue bleeds,
• Normal INR
• Markedly prolonged PTT
• Normal platelet count and function

A

hemophilia

115
Q

almost all people with DVT or thombophilia have triggers + ____?

A

genetic predisposition

116
Q

elevated levels of d-dimer may also be seen in?

A

• Elevated levels may indicate clot, also be seen with: cancer, infection, trauma, surgery, pregnancy, inflammation

117
Q

what are the two inherited mechanisms of thrombophilia? what factors are involved in each?

A
  1. Failure to control thrombin generation- Factor V Leiden, Prothrombin Gene Mutation, Protein C deficiency, Protein S deficiency
  2. Imparied neutralization of thrombin- Antithrombin-III deficiency
118
Q

Are mutations of Protein C, S, and Antithrombin more common? or are mutations of Factor V Leiden and prothrombin?

A

Factor V Leidin and prothrombin are more common

119
Q

when to screen for hereditary thrombophilias

A

• Young age at diagnosis of first clot (

120
Q

what are some acquired conditions that can cause thrombophilia?

A 
Conditions
•	  Antiphospholipid antibodies
•	  Malignancy
•	  Inflammatory Bowel Disease
•	  Nephrotic syndrome
•	  Myeloproliferative Disorders	 
•	 PNH
•	  CHF
•	  Sepsis / DIC
•	  HIT
121
Q

acquired triggers that can cause thrombophilia

A

Immobilization
• Surgery
• Trauma
• Pregnancy / Postpartum- increases thrombosis risk
• Estrogens (OCPs, HRT)- 3-4 fold increased risk
• Older Age

122
Q

how should you manage asymptomatic carriers of thombophilia?

A

prophhlax at times of risk, avoid OCPs, hormone replacement therapy, pay attention to FH

123
Q

who should get indefinite anticoagulation therapy?

A
  • Unprovoked event
  • Recurrent event
  • Life-threatening event
  • Factor V Leiden homozygote
  • Combined thrombophilias
  • Persistent antiphospholipid antibodies
124
Q

how are platelets produced?

A

megakaryocytes: endomitosis, nuceli keeps dividing and cytoplasm doubles in size then eventually gets too big and stuffs off “platelets” (part of the cytoplasm), each produces 2000-3000 platelets

125
Q

what important parts of platelet structure are there in the membrane and the inside?

A
  1. Membrane
    • Phospholipids- provide a surface for coagulation cascade
    • Glycoproteins
    − GP Ia/IIa: collagen receptor - platelet adhesion when collagen exposed
    − GP Ib/IX/V: vonWillebrand factor receptor - platelet adhesion
    − GP IIb/IIIa: fibrinogen receptor - platelet aggregation
  2. Granules
    • Dense granules: contain ADP, Ca++, and serotonin which contribute to platelet aggregation and coagulant activity
    • Alpha granules: contain a variety of proteins which contribute to platelet adhesion, aggregation, and coagulant activity (e.g. factor V, vonWillebrand factor, fibrinogen, platelet factor 4)
126
Q

mechanisms of thombocytopenia

A

decreased production, increased destruction, sequestration (hypersplenism)

127
Q

characteristics of drug induced thrombocytopenia

A

myelosuppression or immunologic, rapid onset, stop offending drug!

128
Q

clinical features of HIT? how to tx it?

A

• Low platelets, extreme bruising, microarterial thrombi from antibody attacking heparin/platelet com
STOP all heparin, consult heme
it is a clinical dx because labs to confirm can take too long

129
Q

ITP:
definition
clinical features

A

immune thrombocytopenic purpura
autoantibodies bind to platelets and accelerate splenic clearance

clinical features: 
symptoms for months
•	Petechiae in dependent regions
•	Ecchymoses
•	Menorrhagia, epistaxis, gingival bleeding- mucosal bleeding
•	Otherwise healthy
•	No lymphadenopathy or splenomegaly
labs: really low #, large platelets, nml coag times, increased megakaryocytes in marrow
130
Q

ddx of ITP

A

drug induced, HUS (hemolytic uremic syndrome), Aplastic anemia/leukemia (usu >1 sx), inherited platelet production abnormalities, sepsis, DIC, splenomegaly, ALPS, immune def.

131
Q

DIC
defintion
clinical features
tx

A

disseminated intravascular coagulation
excessive activation of coagulation systems usu after infection or in malignancy
clinical features:
• Microvascular thrombi cause widespread tissue ischemia, multiple organ dysfunction, and death
• Bleeding due to consumption of platelets and plasma clotting factors
• Thrombocytopenia
• Prolonged coagulation times (PT/INR, PTT)
• Low fibrinogen
• Schistocytes on blood smear- RBCs ripped apart in circulation
tx: tx underlying cause, consider heparin, transfuse platelets

132
Q

TTP definition, clinical features, tx

A 
definitio: endothelial injury, vonWillebrand factor cleaving protease, and systemic platelet aggregation
classic pentad of clinical features:
1.	Thrombocytopenia
2.	Microangiopathic hemolytic anemia
3.	Neurologic symptoms- ↓blood flow to brain
4.	Renal dysfunction
5.	Fever
tx: plasma exchange
133
Q 
would these conditions be an indication for allo or auto HSCT?
• Lymphomas
• Multiple myeloma (not curative!)
• APL (acute promyelocytic leukemia)
• Germ cell tumors
• Ovarian cancer
• Neuroblastoma
• Autoimmune disorders
• Amyloidosis
A

auto

134
Q

indications for allo transplant

A
  • AML, ALL
  • CML, CLL if failed tx
  • MDS
  • MPD
  • Relapsed multiple myeloma or lymphoma post auto xplant
  • Aplastic, fanconi, sickle cell, blackfan-Diamond anemias (uncommon)
  • Peds: errors in metabolism, epidermolysis bullosa, congenital immune deficiencies
135
Q

which is highest way of transmitting gHIV?

A

vertical (mother to child)

136
Q

what component does HIV need to get into a cell?

A

a cd4 receptor

137
Q

HIV life cycle

A

enters blood, attaches to CD4 cell, reverse transcriptase to DNA, integration in hosts DNA, replication, vision assembly, budding

138
Q

by what day of infection is hIV replicating?

A

day 4-11

139
Q

do retroviruses carry genetic info as DNA or RNA?

A

RNA then reverse transcript it to DNA and use host’s machinery

140
Q

Ryan White Care Act

A

(anyone can receive coverage for tx for HIV/AIDS)

141
Q

can you eradicate HIV?

A

NO

142
Q

how does hIV progress to AIDS?

A

. CD4+ T-cell count below 200 cells/μL

  1. CD4+ T-cell percentage of total lymphocytes of less than 15%
  2. Or one of the defining illnesses.
143
Q

ELISA test is + for HIV, what is next step?

A

western blot confirmatory test

144
Q

how long does it take following infection for hIV test to be positive?

A

22-27 days

145
Q

who should get tested for hIV?

A
  • Anyone requesting it, regardless of risk
  • Anyone with high risk behavior: MSM, IVDU, 1+ partners, exchanged sex for $ or drugs
  • Certain medical conditions: AIDS defining illness, oral candidiasis, generalized unexplained LAD, STIs, TB, pregnancy, pneumonias, recurrent vulvar candidiasis, herpes zoster, key is recurrent
  • Anyone who has been sexually assaulted
  • Anyone with occupational exposure
146
Q

who should get screened for HIV?

A

routine for everyone 13-64

repeat for those at high risk

147
Q

most common sx of HIV

A
  • Fever (96%)
  • LAD (74%)
  • Pharyngitis (70%)
  • Rash (70%)
148
Q

when are the most sx of HIV present?

A

in 1-4 weeks post exposure, after that they can get in a latent period and have less symtpoms

149
Q

DDX of acute HIV

A
  • Influenza
  • EBV mononucleosis/ Primary CMV infx
  • Severe (streptococcal) pharyngitis
  • Secondary syphilis • Toxoplasmosis
  • Drug reaction
  • Viral hepatitis
  • Primary HSV infection • Rubella
  • Brucellosis
  • Malaria
  • West Nile Virus

Clinical Medicine (19 decks)

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