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PAM Semester 2 > Clinical Medicine Exam 5 Heme/Onc > Flashcards

Clinical Medicine Exam 5 Heme/Onc Flashcards

1
Q

Blood Percentages

Plasma

A

55% of whole blood

Water 92%
Other solutes
electrolytes, nutrients, respiratory gases, waste

Proteins 7% (by weight)

Albumin 58%
Globulins 37%
Fibrinogen 4%
Regulatory proteins <1%

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2
Q

Blood Percentages

Erythrocytes

A

RBC

44% of whole blood

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3
Q

Blood Percentages

Buffy coat

A

<1% of whole blood

Platelets 150-400,000

Leukocytes 4.5-11,000

Neutrophils 50-70%
Basophils 0.5-1%
Eosinophils 1-4%
Lymphocytes 20-40%
Monocytes 2-8%
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4
Q

Blood volume

A

Approx. 5 liters
2 liters cellular/solid
3 liters plasma/liquid

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5
Q

How long do blood cells survive?

A 
Platelets = 7-10 days
RBC's = 120 days
WBC = vary by type
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6
Q

Formed elements of the blood

A

Erythrocytes

Buffy coat

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7
Q

Primary site of blood cell creation after birth

A

Bone marrow

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8
Q

Granulocytes

A

Neutrophil (bacteria)
Eosinophil (parasites)
Basophil (inflammatory)

Polynuclear, granules in cytoplasm

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9
Q

Agranulocytes

A

Natural killer cells

Lymphocytes ( 3types)
B cells
T helper cells
T suppressor cells

Monocytic cells (become macrophages)

Mononuclear, no granules

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10
Q

What is stem cell for blood cells

A

Hematopoietic stem cell

becomes two types of progenitor cells

Common myeloid progenitor cells
Common lymphoid progenitor cells

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11
Q

What do Common myeloid progenitor cells become

A 
RBCs
platelets
macrophages
neutrophils
eosinophils
basophils
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12
Q

What do Common lymphoid progenitor cells become

A 
Plasma B cells
Memory B cells
T suppressor cells
T helper cells
Cytotoxic T cells
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13
Q

Interleukin 4 is specific for

A

Basophils

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14
Q

Interleukin 5 is specific for

A

Eosinophils

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15
Q

Where is erythropoietin made

A

Peritubular interstitial cells of the kidney

Then goes to red bone marrow and stimulates accelerated red blood cell production.

This increases O2 transport

Takes 3-7 days

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16
Q

Red blood cell production cycle

A 
Erythropoietin
Normoblast (uncommitted stem cell)
Reticulocyte (nucleus ejected)
RBC
Diapedesis
Capillary
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17
Q

EPO Drugs

A 
Exogenous EPO
creates more red blood cells
increases O2 transport
increases hematocrit thickening blood
make the blood more difficult to pump
creates stress on heart, arrest, etc.
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18
Q

RBC structure

A

Anucleated
O2 binds reversibly to heme
CO2 bonds reversibly to globin
CO binds almost irreversibly

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19
Q

Hemoglobin

A

4 O2 molecules per molecule
when O2 is bound it is oxyhemoglobin
When CO2 is bound it is carbaminohemoglobin

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20
Q

Hemoglobinopathies

A

Sickle Cell
Thalassemias

Mutations can occur resulting in abnormal hemoglobin that lead to hemoglobinopathies

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21
Q

RBC Break down

A

Liver and spleen
Red pulp of spleen (erythrocyte graveyard)

hemoglobin broke into heme and globin

Heme broken down into iron and bilirubin.
(Iron reused, bilirubin excreted)

Globin hydrolyzed into free amino acids

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22
Q

Nutrients needed for RBC produciton

A

B12
Iron
Amino acids
Folic acid

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23
Q

Free iron

A

Free iron is toxic

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24
Q

Eosinophils

A

Eosinophils are inflammatory cells that defend against parasitic infections.

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25
Q

Basophils

A

Basophils release histamine, causing the inflammation of allergic and antigen reactions.

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26
Q

Monocytes

A

Monocytes migrate from the blood stream and become macrophages.

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27
Q

Lymphocytes

A

Lymphocytes contain three cell types that participate in the immune system.

B cell
T Helper cell
T Suppressor cells

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28
Q

Cytokines in Blood cell Production

A

Cytokines differentiate what type of blood cell forms

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29
Q

RBC of abnormal / varying sizes

A

Anisocytosis

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30
Q

Large RBC

A

Macrocytes

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31
Q

Small RBC

A

Microcytes

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32
Q

Irregular shape RBC

A

Poikilocytosis

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33
Q

RBC’s With Burrs (crenated)

A

Echinocytes

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34
Q

RBC fragments

A

Schistocytes

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35
Q

RBC with less color

A

Hypochromic cells

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36
Q

Where do platelets come from

A

megakaryocytes

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37
Q

Steps in coagulation

A

Trauma - Vascular Spasm
Formation of temporary plug (platelet plug)
Blood coagulation (Clot - Fibrin mesh)
repair & fibrinolysis

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38
Q

Extrinsic clotting factors

A
  • The extrinsic pathway starts with the exposure of blood clotting factors to the tissue factor, TF, in the extravascular tissue.

This pathway is induced by injuries to blood vessels.

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39
Q

Intrinsic clotting factors

A

The intrinsic pathway, which involves only factors within blood vessels, is thought to serve as a positive feedback loop, amplifying coagulation.

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40
Q

Fibrin formation

A

Fibrinogen is converted into fibrin though the use of thrombin

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41
Q

Three phases of coagulation cascade

A

Phase 1
Prothrombin activator

Phase 2
Prothrombin 3 and prothrombin activator become thrombin

Phase 3
Fibrinogen and thrombin become fibrin

Fibrin then also joins with thrombin to create a cross linked fibrin mesh

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42
Q

What happens to clots

A

Clots begin retracting within 30 minutes

Platelet growth factor stimulates fibroblasts and smooth muscle cells to multiply and repair damage.

Fibrinolysis terminates the clot
plasminogen helps dissolve fibrin helping break up clot

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43
Q

Blood clot dissolution cascade

A

Prekallikrein and factor X11 combine to form
Kallikrein

Kallikrein and plasminogen combine to form plasmin

Plasmin and fibrin polymer combine to degrade clots

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44
Q

Who did hematology begin with

A

Ancient Greece or ancient Egypt

Antoine Van Leeuwenhoek

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45
Q

Where do we find immature cells

A

Bone marrow biopsy

Bone marrow also contains fat cells
More fat as you get older

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46
Q

Where do we typically do a bone marrow biopsy

A

PSIS
Posterior superior Iliac Spine

Typically IO

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47
Q

Bone marrow calculation

A

100 minus age
example

a 30 year old is 100-30 = 70
they are expected to have 70% cells and 30% fat

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48
Q

Most useful tool in hematology

A

CBC

also most common lab in all of medicine

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49
Q

CBC components

A

RBC (Male - 4.3 -5.9, Female - 3.5-5.5 million)
WBC (4,500 -11,000) (also can be with Diff)
Hgb (Male - 13.5 - 17.5, female - 12.0 - 16.0)
Hct (Male - 41-53%, Female - 36-46%)
Plts (150,000 - 400,00)

Different values in pediatrics

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50
Q

RBC values

A

RBC
Male - 4.3 -5.9,
Female - 3.5-5.5 million

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51
Q

WBC values

A

WBC

4,500 -11,000) (also can be with Diff

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52
Q

Hgb Values

A

Hgb
Male - 13.5 - 17.5,
female - 12.0 - 16.0

decease during pregnancy

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53
Q

Hct Values

A

Hct
Male - 41-53%
Female - 36-46%

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54
Q

Platelet Values

A

Plts
(150,000 - 400,00)

decease during pregnancy

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55
Q

CBC short hand

A

Hgb
WBC Plt
Hct

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56
Q

What does hypervolemia do to CBC

A

All values will typically decrease due to excess water and more dilute blood.

When CBC is down, check patients volume status
(blood may be dilute)

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57
Q

What does Hypovolemia do to CBC

A

All values will typically increase due to decrease in water volume making the blood less dilute.

When CBC is up, check patients volume status
(blood may be very concentrated)

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58
Q

Low blood count name

A

-Cytopenias

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59
Q

High blood count name

A

-Cytoses or -philias

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60
Q

3 possibilities of cytopenia’s

A

Not producing enough blood cells

destroying blood cells

Losing blood cells

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61
Q

WBC with Diff

A 
Monocyte
Eosinophil
basophil
lymphocytes
neutrophils

Neutrophils are most dominant and have greatest number (not in peds under 5, lymphocytes)

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62
Q

Neutrophils= bands+ segmented; AKA?

A

Neutrophils= bands+ segmented; also called polymorphonuclear neutrophils (PMNs,) polymorphonuclear leukocytes (PMLs), or granulocytes

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63
Q

Leukopenia causes (decreased WBC)

A

Medications (including chemotherapy and some antibiotics)

Viral infections

Leukemias, lymphomas, myelodysplastic syndrome

Aplastic anemia

Radiation exposure

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64
Q

Leukocytosis- Elevated WBC

A

Neutrophils: infection, inflammation, steroid effect, CML
“left shift” ≥ 10% neutrophil bands

Eosinophils: hypersensitivity reaction, parasitic infections, lymphomas (Hodgkin’s), myeloid leukemias

Basophils: hypersensitivity reaction, CML

Monocytes: viral infections (ie EBV, CMV), bacterial infections

Blasts: acute leukemias, myelofibrosis (Never normal)

Lymphocytes: EBV infection, Bordetella pertussis, CLL
“Atypical” lymphocytes: infection, inflammatory response, lymphomas

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65
Q

Hemachromatosis

A

Iron overload

Risk factors
Hemoglobinopathies
RBC malignancies,
sideroblastic anemias,
multiple transfusions

Liver is most affected by Iron overload
lethargy

Labs
serum ferritin level significantly elevated, transferrin saturation elevated, and liver enzymes elevated

Tx- iron chelation

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66
Q

Hereditary Hemochromotosis

A

Inherited form of iron overload

Due to mutation in HFE gene on chromosome 6; predominant in those of Northern European descent
Usually asymptomatic until age 40-60 years

Men > women
Same signs/symptoms, lab findings, & imaging findings as acquired form

Bronze tan looking skin

Treatment: phlebotomy (blood letting)

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67
Q

Thrombosis

A

The obstruction of blood flow due to formation of clot (thrombus)

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68
Q

Difference between arterial and venous blood clots

A 
Arterial = (abnormal state of vessel wall, platelets)
High flow areas
white thrombus
Coronary arteries (MI)
Carotid arteries
Cerebral arteries (stroke)
Venous = (defect in proteins, hypercoagulability)
Low flow areas
Red thrombus
usually occlusive
DVT
PE
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69
Q

HIT

A

Heparin induced thrombocytopenia

Both arterial and venous clots

5-14 days after exposure

can be heparin or LMWH (lovenox)

can be a very small amount

Reduce the number of platelets while activating them

4 T's
Thrombocytopenia
Timing relative to heparin exposure
Thrombosis
Other

Can be confirmed by ELISA

Stop Heparin, no more heparin for life

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70
Q

Anti phospholipid syndrome

A

Both arterial and venous clots

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71
Q

Arterial clots

A 
Arterial = (abnormal state of vessel wall, platelets)
High flow areas
white thrombus
Coronary arteries (MI)
Carotid arteries
Cerebral arteries (stroke)
tx = antiplatelet therapies
Aspirin
Plavix (clopidogrel)
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72
Q

Venous clots

A 
Venous = (defect in proteins, hypercoagulability)
Low flow areas
Red thrombus
usually occlusive
DVT
PE

Tx =TPA

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73
Q

Virchow’s triad

A

Venous clots risk factors

Stasis of blood flow (usually immobility, long flights)
Endothelial injury (injury to vessel wall,{surgery, accident})
Hypercoagulability (Most are acquired, some hereditary)
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74
Q

Hypercoagulable states

A 
Pregnancy, postpartum
Antiphospholipid syndrome
Surgery
Estrogen use
Cancer
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75
Q

Malignancy and Hypercoagulable states

A

20% of people with DVT have a malignancy

Trousseaus syndrome associated with multiple cancers
Causes multiple clots all over body

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76
Q

Surgery and Hypercoagulable states

A

Surgery and up to a month after can cause Hypercoagulable states

due to increase in cytokines and coagulation factors

can increase platelet count and reactivity

the longer and more invasive the surgery the more risk for venous blood clots

can be over 50% risk in some orthopedic surgeries (Hip, knee replacement,) and cardiothoracic surgeries

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77
Q

Pregnancy or exogenous estrogen and Hypercoagulable states

A

Exogenous estrogen can be birth control

Risk increases between 4 and 50 times that of non pregnant women.

Symptoms can be delayed due to symptoms mirroring those of pregnancy

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78
Q

Antiphospholipid syndrome and Hypercoagulable states

A

Autoimmune, can be associated with other autoimmune disorders such as Sjogren’s, SLE

Both arterial and venous thrombus

Can cause pregnancy complications such as fetal loss, preeclampsia, placental insufficiency

If multiple fetal losses, work up APLA, could be due clots

Also associated with thrombocytopenia (25%)

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79
Q

Thrombocytosis

A

High platelet count

over 450,000
fairly common (especially in surgery)

Risk of thromboses doesn’t increase until over 1 million

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80
Q

Venous thromboembolism

A

DVT

PE

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81
Q

DVT

A

Usually in lower extremity
Prone to venous stasis

Upper extremity DVT is usually associated with Medical device like a port or PICC line, pacemaker

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82
Q

DVT symptoms

A

Unilateral calf pain, cramping, swelling
Constant, progressive, redness

Unilateral unequal edema

positive Homans sign

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83
Q

DVT symptoms

A

Unilateral calf pain, cramping, swelling
Constant, progressive, redness

(can be similar to venous insufficient, cellulitis, etc.)

Unilateral unequal edema

positive Homans sign

Elevate D Dimer (>80%)

Definitive is Ultrasound with venous doppler

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84
Q

What is definitive for DVT

A

Ultrasound with venous doppler

If blood clot is present, vein wont compress

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85
Q

Diagnosis of PE

A

Almost always the result of DVT

Symptoms: dyspnea, pleuritic chest pain, cough, hemoptysis

Tachycardia is most common sign in PE

ekg changes S1Q3T3 sign
S waves in lead I, Q waves and inverted T in lead III

D Dimer (95%)

Chest x ray Usually normal. rarely can show Westermark’s sign or Hampton’s Hump

DX: CT angiogram with IV contrast
If cant get contrast use VQ Scan

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86
Q

EKG changes in PE

A

S1Q3T3 sign

S waves in lead I
Q waves in lead III
Inverted T wave in lead III

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87
Q

3 classifications of PE

A

Massive (high mortality) causes hypotension

Sub Massive (not in main pulmonary, low mortality rates, may be asymptomatic

Low risk

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88
Q

Criteria for PE workup

A

Wells (most common)
PERC (used in ED)
Gestalt
Geneva

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89
Q

Treatment for VTE/PE

A

Anticoagulation is mainstay of therapy

3 months for distal (smaller vein) DVT

3-6 months for PE, multi-vessel, or proximal DVT (larger vein)

Antiplatelet therapy (aspirin, clopidogrel)
Thrombolytics/fibrinolytics (tPA)
Clotting cascade blockers/ Anticoagulants

Anti-coags are used to prevent the progression and embolization of the clot not to break it down.

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90
Q

Anti coagulation meds for VTE/PE

A

Indirect Thrombin inhibitors (heparin, enoxaparin{lovenox}, fondaparinux{Arixtra})
Direct Thrombin Inhibitors (dabigatran{pradaxa})
Direct Factor Xa Inhibitors/DOACs (rivaroxaban{xarelto}, apixaban{eliguis})
Vitamin K antagonists (warfarin)

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91
Q

Anticoagulation for treatment of VTE

A

Varies by extent of VTE, patient’s co-morbidities/other medications, & availability of reversal agents

  1. Oral anticoagulant monotherapy with rivaroxaban (Xarelto®) or apixaban (Eliquis®). No parenteral anticoagulant used. [small or asymptomatic/outpatient]
  2. Start parenteral* anticoagulant then “bridge” to warfarin (Coumadin®){ED, need IV]
  3. Start parenteral anticoagulant x 5 days then switch on 6th day to oral anticoagulant such as dabigatran (Pradaxa®)
  4. Start parenteral anticoagulant and continue. No oral anticoagulant used. (most symptomatic patients)
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92
Q

Why does warfarin require a bridge

A

Decreases likelihood of skin necrosis

Takes a few days to 5-10 to take effect

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93
Q

INR goal in VTE/PE

A

between 2-3

INR is based on goals

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94
Q

Heparin monitoring

A

PTT
60-80

Anti 10a levels are more preferred way

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95
Q

Absolute contraindications to anticoagulation

A 
Active bleeding
Major trauma
Recent or planned high risk surgery
Severe bleeding diathesis (as with liver failure)
Intracranial hemorrhage
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96
Q

IVC Filters

A

If anticoagulation is contraindicated in patient with VTE, consider an Inferior Vena Cava filter

Prevents emboli to lungs (PE)

Temporary

Little fingers catch DVTS so they cant reach lungs
Can cause vascular injury which can promote DVT

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97
Q

Treatment of Severe VTE

A

Rarely done

Fibrinolysis (ie IV tissue plasminogen activator) TPA

Pharmaco-mechanical thrombolysis (catheter-directed)

Surgical embolectomy (no longer done)

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98
Q

Superficial Venous Thrombosis/ Thrombophlebitis

A

Presents with erythema, tenderness, and palpable “cord”

Does not require systemic treatment, self-limited

Warm compresses may alleviate discomfort

Most common cause is IV insertion

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99
Q

What are inherited hypercoagulability also called

A

Thrombophilia

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100
Q

inherited hypercoagulability

A

may require life long anti coagulation therapy
usually under 40
family history

pregnancy issues

Leiden factor V (most common) (special gene test)
Protein C & S Deficiencies
Antithrombin III Deficiency (rare)(heparin resistant)

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101
Q

Are arterial or venous thromboses the major cause of morbidity and mortality

A

Both arterial and venous thromboses are a major cause of morbidity and mortality

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102
Q

Multiple VTE with no clear hypercoagulable state

A

Multiple VTE with no clear hypercoagulable state should trigger a workup for inherited thrombophilias

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103
Q

Anti coagulant drug of choice for renal issues

A

Warfarin

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104
Q

How long are red blood cells in circulation?

2 days
7-10 days
30 days
120 days

A

120 days

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105
Q

What is the treatment of choice for hereditary hemochromatosis?

Iron chelation therapy
Warfarin
Phlebotomy
Aspirin

A

Phlebotomy

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106
Q

Which one is characteristic of a venous thrombosis

Occlusive
Platelet rich
Occur in coronary and cerebral vessels
Dependent on state of vessel wall

A

Occlusive

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107
Q

Virchow’s triad include hypercoagulability, endothelial injury and___________?

Thrombophilia
Coagulopathy
Venous Stasis
Cardiomyopathy

A

Venous stasis

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108
Q

What are 3 things in Virchow’s triad

A

Venous stasis
Hypercoagulopathy
Endothelial injury

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109
Q

Which lab test for a fibrin split product and is highly sensitive for the presence of PE or DVT?

Fibrinogen
PTT
D Dimer
PT/INR

A

D-Dimer

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110
Q

What causes a false positive on D dimer

A

Pregnancy

age over 70

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111
Q

Which of the following is an absolute contraindication to anticoagulation therapy?

Platelet count of less than 50,000
INR> 1.5
Active bleeding ulcer
Frail / elderly patient

A

Active bleeding Ulcer

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112
Q

Hemostasis Steps

A

Platelet plug (antiplatelet therapy inhibits)
Adhesion, aggregation, activation, stabilization
Ex. Plavix, aspirin

Fibrin clot (anticoagulants inhibit)
Coagulation cascade
Ex. Heparin, Warfarin

Fibrinolysis (antifibrinolytics inhibit)
Fibrin clot degradation
Ex. TXA

Tissue repair

First 3 steps take 5 minutes (avg)

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113
Q

How long do the first 3 steps of hemostasis take?

A

5 minutes

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114
Q

Differnece between primary and secondary bleeding disorder

A

Primary is platelet problem
Platelets are less than 50,000

Secondary is a clotting disorder
(clotting factor)

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115
Q

Signs of primary bleeding disorder

A

Primary is platelet problem
Platelets are less than 50,000

Petechiae
Purpura
ecchymoses
Hematomas
Oral bleeding (gums)
Epistaxis
Hematuria
GI bleed
Menorrhagia (7days total or 3 days heavy flow)
116
Q

Signs of secondary bleeding disorder

A

Secondary is a clotting disorder
(clotting factor)

Hemarthrosis
Intramuscular hematomas (psoas muscle)
Intracranial hemorrhage
Severe GI Bleed
Deep Hemorrhages
117
Q

Are petechiae blanchable?

A

non blanchable

118
Q

What is purpura?

A

the patch version petechiae

Non blanchable

119
Q

Labs to draw in bleeding or unusual bleeding

A

CBC
tells you platelets and whether they are anemic

Coags
PTT (intrinsic pathway)
PT (extrinsic pathway)
INR (PT and INR are almost always reported together

Secondary tests
Thrombin time (clotting time)
Fibrinogen
LFT
Blood Smear
Platelet function test (bleed time)
Von Willebrand
Mixing studies

(can also test for each individual clotting factor)

120
Q

Thrombocytopenia

A

Platelet disorder
Platelets are too low

platelets under 140,00 (140,00-450,00)
Clinically significant if under 100,000

Under 50,000 (at risk for severe post traumatic bleed)
Can be very small trauma such as bump on head

Under 10,000 (risk for spontaneous bleed)
Gets transfusion

121
Q

3 reasons platelets might be low

A

Platelets are being lost
Platelets are being destroyed
Platelets are not being made

122
Q

HHIT SHOCK

A

HIT
HUS
ITP
TTP

Splenomegaly
Hereditary
Other
Chemo
Kasabach Merritt syndrome

Other includes=
Bone marrow, SLE, alcoholism, Malignancy, DIC sepsis, Viral, meds

123
Q

Thrombocytopenia due to Systemic Disorders

A

Sepsis/ infections: HIV, EBV, HepC, CMV, rubella, mumps, varicella, malaria, dengue fever, Rickettsiosis , H. pylori

Pregnancy & post-partum

Malignancy

Alcoholism

Systemic Lupus Erythematosus

Vitamin B12, iron, or folate deficiency

124
Q

Immune/Idiopathic Thrombocytopenic Purpura (ITP)

A

Autoimmune disorder with IgG antibodies against platelets (macrophages destroy platelets)

Affects both children and adults
(Kids usually self limiting, adults usually chronic)

Has same Signs/symptoms of thrombocytopenia
Appear healthy and well otherwise (feel fine)

Laboratory exams: Platelet count <50k, no anemia or leukopenia, enlarged platelets on peripheral smear, normal coagulation studies.

Normal RBC, WBC (only platelets affected)

Platelet-associated IgG antibody assay available
Testing not very specific

Diagnosis of exclusion

125
Q

ITP Treatment

A

If platelets are below 30,000 give treatment

Glucocorticoids are first line (prednisone 1mg/kg 1wk)

IVIG, Anti-Rho GAM, transfusion if bleeding

Usually respond within 3-5 days

second line is (typically for adults/chronic)
thrombopoietin receptor agonists, rituximab, immunosuppressive therapy, splenectomy for relapses

126
Q

Thrombotic Thrombocytopenic Purpura/ Hemolytic Uremic Syndrome (TTP/HUS)

A

Microangiopathy due to antibodies to ADAMTS13,

pregnancy, malignancy, HIV, drugs (quinine), infection

In kids usually shigella or E.coli infection

Pentad of features: 1. Thrombocytopenia, 2. Hemolytic anemia, 3. Fever, 4. Renal insufficiency, 5. Neurological deficits (headache, somnolence, delirium, seizures, paresis, or coma)

TTP and HUS are different

Medical emergency due to ischemic multi-organ failure

127
Q

Thrombotic Thrombocytopenic Purpura/ Hemolytic Uremic Syndrome (TTP/HUS)

Features

A

Pentad of features:

  1. Thrombocytopenia, (less than 20,000)
  2. Hemolytic anemia,
  3. Fever,
  4. Renal insufficiency,
  5. Neurological deficits (headache, somnolence, delirium, seizures, paresis, or coma)
128
Q

Difference between

Thrombotic Thrombocytopenic Purpura
and
Hemolytic Uremic Syndrome (TTP/HUS)

A

ADAMTS13 assay indicates TTP

129
Q

Thrombotic Thrombocytopenic Purpura/ Hemolytic Uremic Syndrome (TTP/HUS)

Treatments

A

Treatments: emergent plasma exchange if TTP >HUS, eculizumab if HUS>TTP, RBC transfusions, hemodialysis, IVIG, corticosteroids, rituximab, cyclophosphamide, splenectomy

130
Q

4 T’s of HIT

A 
4 T's
Thrombocytopenia
Timing relative to heparin exposure
Thrombosis
Other

Can be clotting and bleeding at same time

Inadequate antibodies PF4 (Platelet factor 4)

131
Q

Hemolysis, Elevated Liver enzymes, and Low Platelet (HELLP) Syndrome

A

Pregnant disorder
Peri-partum disorder (3rd trimester) on eclampsia spectrum

Present with High BP and proteinuria

Low platelet
High Liver enzymes
Hemolysis (RBC fragments on smear)

Risk of hepatic hemorrhage (RUQ Pain)
Placental abruption

TX: prompt delivery, RBC’s, platelets, Mag sulfate, antihypertensives

132
Q

What is platelet clumping considered

A

Pseudo Thrombotic Thrombocytopenic Purpura (TTP)

133
Q

First step for any thrombocytopenia

A

Examine peripheral blood smear

134
Q

Persistent thrombocytopenia, no clear etiology, over 60 years old

A

Bone marrow biopsy for cancer rule out

135
Q

Qualitative Platelet Disorders

A

normal number of platelets but they aren’t functioning properly

Von Willebrand’s Disease 
Drug induced
Uremic platelet dysfunction due to renal failure 
Liver failure
Cardiac bypass
Inherited
136
Q

Von Willebrand’s disease

A 
1% of population
Mild to severe
Inherited
History of bleeding
Acquired form (rare)
Special test just for it (RIPA)

Prolonged PTT, normal PT, normal platelet count

TX:
Desmopressin
Aminocaproic acid
TXA

137
Q

PFA 100

A

Tests platelet function and aggregation

138
Q

Pro clotting meds

A

Desmopressin
Aminocaproic acid
TXA

139
Q

Drugs that decrease platelet function

A

NSAIDs, aspirin, & clopidogrel (Plavix®)

NSAIDs and aspirin inhibit COX-1

Also avoid in preoperative period & if already on anticoagulants or SSRIs

Selective Cox 2 (Celebrex) doesn’t inhibit platelet function

Hold for 7-10 days prior to surgery

140
Q

Coagulopathy

A

Pro bleeding

141
Q

Labs to always get on bleeding patient

A

CBC

Coags

142
Q

Abnormal Coag studies

A

PT prolonged, PTT normal: Factor VII

PT normal, PTT prolonged: Factors VIII, IX, XI, XII

Both PT & PTT prolonged: Factors V, X

143
Q

Hemoaphilia

A 
X linked, more prominent in males
Type A (factor 8) deficiency
Type B (factor 9) is also called Christmas disease

Severe bleeding -
Spontaneous hemarthrosis, muscle hematomas, GI bleeds, circumcisions

Labs: Prolonged PTT with normal PT; Factor 8 or 9 assay is diagnostic.

***Mixing study required to rule out clotting factor inhibitors.

TX: factor infusions, TXA, avoid trauma/contact sports

144
Q

Vitamin K deficiency

A

Dark green leafy veggies

Most often due to malnutrition or fat malabsorption (ie Celiac’s) (not just low vegetables)

superficial bleeding & easy bruisability to severe bleeds

PT/INR is prolonged, PTT also prolonged if severe

Treat underlying cause, give vitamin K

Also associated with anaphylaxis, must be given under supervision

145
Q

Liver Failure Associated Coagulopathy

A

Liver makes thrombopoietin, prothrombin, fibrinogen
Thrombopoietin makes platelets, if you have liver failure this can cause increased bleeding.(significant liver failure)

factor V deficiency indicates liver failure over vitamin K deficiency

Tx: Administer fresh frozen plasma if bleeding

FFP has all the coag factors in it

146
Q

Disseminated Intravascular Coagulopathy (DIC)

A

Worst Coag Disease
80% mortality rate
Medical emergency

Labs: , low fibrinogen, Prolonged PT and PTT, platelet count <100k elevated D-dimer, elevated fibrin split products

**Very few things give low fibrinogen (DIC)**

platelet transfusion if bleeding predominates,

tissue plasminogen activator (TPA) if clots predominate

Causes:
Septic shock
Obstetrical complications
Cancer

147
Q

1:1 mixing study

A

take impaired clotting blood,
mix it with good blood
and see if the coagulation improves

If it improves person was deficient in clotting factor

148
Q

Clotting factor inhibitors

A

anti-factor-8

high incidence with hemophilia (rare otherwise)

1:1 mixing study

149
Q

Bleeding disorders occur as a result of?

A

Platelet
or
Coagulation factor

deficiencies

150
Q

Bleeding due to primary hemostasis/platelet disorder is usually more

A

superficial or less severe than secondary hemostasis/coagulation factor disorders

151
Q

A platelet count under 100 is?

A

clinically significant

and warrants work up

152
Q

Thrombocytopenia most commonly occurs due to?

A

Medications or
secondary illness

but can occur due to ITP, TTP/HUS, HIT, DIC, HELLP

153
Q

If platelet count and coag studies are normal and patient is still bleeding?

A

Need to rule out
qualitative platelet disorder
(Von Willebrand disease)

154
Q

Coagulopathies include?

A 
Hemophilia
Liver failure
Vitamin K deficiency
DIC
HELLP
155
Q

Anemia defenition

A

Low
Hgb (amount of hemoglobin)
Hct (volume/percent of RBC in blood)
RBC count (number of red blood cells)

Can be called anemic based on CBC values

156
Q

3 causes of anemia

A

being destroyed
not being produced
being lost

157
Q

Causes of anemia where RBC are being destroyed

A

Hemolysis:

Autoimmune
G6PD
PNH (Paroxysmal nocturnal hemoglobinuria)
TTP/HUS
Infections
Thalassemia
Sickle cell
Hypersplenism
158
Q

Causes of anemia where RBC are being lost

A

Acute
Chronic

Hypersplenism / splenic sequestration

159
Q

Causes of anemia where RBC are not being produced

A 
Hypoproliferative( produced in too few numbers)
     -Iron deficiency
     -Folic acid deficiency
     -Vitamin B12 deficiency 
     -Renal failure
     -Anemia of chronic disease
     -Hypothyroidism/-gonadism
     -Bone marrow suppression or failure (malignancy, 
      medications, aplastic anemia)

Ineffective or unstable erythropoiesis (ineffective)

  - Sickle cell anemia    
  - Thalassemias
 - Sideroblastic
 - Methoglobinemia
160
Q

3 main classes of anemia

A

Microcytic
Normocytic
Macrocytic (megaloblastic or non megaloblastic)

161
Q

Megaloblastic anemia vs non megaloblastic anemia

A

Megaloblastic
Abnormal nuclear maturation of RBC

Non-megaloblastic
Lots of immature RBC (reticulocytes)

162
Q

Microcytic anemia causes

A

TICS

Thalassemia
Iron deficiency
Chronic disease
Sideroblastic anemia

163
Q

Macrocytic megaloblastic anemia causes

A

Folate deficiency

Vitamin b12 deficiency

164
Q

Macrocytic non-megaloblastic anemia causes

A

Liver disease
alcoholism
Reticulocytosis
Drugs

165
Q

What are reticulocytes

A

Immature red blood cells

Larger than normal red blood cells

Can order a reticulocyte count or RPI

(represents bone marrow response to anemia, most often in hemolysis or bleeding)

166
Q

RBC indices (on CBC)

A 
MCV = Mean corpuscular volume
MCHC = Mean corpuscular hemoglobin concentration
MCH = Mean corpuscular Hemoglobin
RDW = RBC distribution width
167
Q

MCV

A

Mean corpuscular volume

(on CBC)

Average red blood cell size

<80 is microcytic
80-100 is normal
>100 is macrocytic

168
Q

MCHC

A

Mean corpuscular hemoglobin concentration

Average RBC concentration of hemoglobin

(on CBC)

<32 = hypochromic (undersaturated)
32-37 normal
>37 = Hyperchromic (oversaturated)

169
Q

MCH

A

Mean corpuscular hemoglobin

Average hemoglobin per red blood cell

(on CBC)

Volume not taken into account, MCHC is better measurement

170
Q

RDW

A

RBC distribution width

Measures variation in red blood cell size

(on CBC)

anistocytosis = variation in size of RBC
Poikilocytosis = variation in shape (only on smear)
171
Q

What is basophilic stippling associated with

A

Lead Poisoning

172
Q

What does lead poisoning show on a blood smear

A

Basophilic stippling

173
Q

Labs to consider for anemia

A

CBC

Others to consider

Iron study
Folate levels
B12 Levels
Full hemolysis workup
Occult stool
174
Q

Anemia approach to diagnosis

A

are they really anemic? Lab error, hypervolemic

Is it acute or chronic?
Symptomatic or asymptomatic?
(Acute is usually symptomatic, chronic not always)

Are they hemodynamically unstable?
Blood loss?

Age, sex, pregnant, menses?

Meds, infections, family history, substance use, Gi, diet

175
Q

Affects of anemia

A

Fatigue (especially if hgb <10)

Pallor (oral mucosa and conjunctiva)

Dyspnea

Systolic murmur (reverses when anemia is corrected)

176
Q

Hypoproliferative anemias

A

Iron, b12 folate deficiency

5 reasons for vitamin/mineral deficiency

inadequate intake
malabsorption
increased utilization or loss
drug inhibition
genetic defect
177
Q

Most common anemia world wide

A

Iron deficient anemia

178
Q

Iron deficient anemia

A 
almost always due to bleeding
rarely nutrition (3rd world)

Premenopausal women
pregnant women
adolescents

In adult men and post menopausal women
look for bleeding

PICA, spoon nails, dysphasia, Cheilosis

Crohns, celiacs

Typically microcytic (iron tell RBC to stop shrinking)

elevated transferrin
low iron and transferritin, ferritin

TX: cause, replace iron PO then IV

slight risk of anaphylaxis in IV iron

179
Q

Which of the following is sign of a secondary hemostasis disorder?

Petechia
Hemarthrosis
Epistaxis
Ecchymosis

A

Hemarthrosis

180
Q

What is a secondary hemostasis disorder

A

A clotting factor problem not a platelet problem

Platelet bleeding is usually more superficial

and clotting factor problem is usually a deeper bleeding

181
Q

Thrombocytopenia becomes clinically significant when the platelet count is less than?

A

100,000
Begin workup

Normal is 140 - 450

182
Q

Which of the following conditions is associated with E.coli 0157:h7 infection? especially in children?

ITP
Hemophilia
TTP
HUS

A

HUS

183
Q

Which of the following is a cause of thrombocytopenia mediated by antibodies to PF4 and associated with increased risk of thrombosis?

TTP
DIC
HELLP
HIT

A

HIT

Heparin induced thrombocytopenia

Antibodies to platelet factor 4 (PF4)

(All of these cause thrombocytopenia)

184
Q

In the US iron deficiency is most often due to which of the following

Inadequate intake
malabsorption
increased utilization or loss
drug effects
genetic defects
A

Increased utilization or loss

Bleeding is most common in US

185
Q

Megaloblastic anemia

B12 deficiency

A

Megaloblastic (macrocytic)
Abnormal nuclear maturation of RBC

B12 deficiency - B12 ingested, binds to intrinsic factor in stomach and is absorbed in the ileum, then transported into circulation by trans coalamin.

b12 essential for myelination of nervous system

B12 only found in foods of animal origin

usually due to absorption issue (celiacs, crohns)
Also post gastric/bariatric surgery. vegans. H. pylori

Smooth beefy red tongue

Peripheral neuropathy (common),
balance, GI, AMS, weight loss, anorexia

Labs: low b12 level, macrocytic, high RDW,

Give B12 injections (due to absorption issues)
Can give PO if not absorption
resolves in 2 months, if chronic, lifelong tx.

186
Q

Pernicious anemia

A

Sub class of b12 deficiency (megaloblastic anemia)

Low production of intrinsic factor which helps absorb b12

gastric bypass patients,
gastric atrophy in older people

Diagnosed by schilling test
(measures ability to absorb b12)

Tx: same as b12 deficiency

increased risk of gastric cancers

187
Q

Megaloblastic anemia

Folic acid deficiency

A

Very often occur together with b12 deficiency

folic acid is absorbed in the jejunum
requires b12 to enter the cells

leafy greens, liver, fruits, nuts

risk: malnourished (alcoholics)
geriatric, cancer patients

Meds that inhibit folic acid = bactrim, phenytoin, methotrexate (give with supplement)

Pregnancy, dialysis

Labs:Labs: low folate level, macrocytic, high RDW,

give folate

188
Q

Sideroblastic anemia

A

Microcytic

due to ineffective erythropoiesis

has all components for RBC but iron is not correctly incorporated into the red blood cell

Creates ringed sideroblasts (iron around RBC)

B6 deficiency, lead poisoning, myelodysplastic syndrome, copper deficiency, alcohol(usually macro), drugs, hereditary(very rare)

may cause hemochromatosis

treat cause

189
Q

Anemia of chronic kidney disease

A

kidney failure
cause low production of EPO

Normocytic, Low epo levels

Give EPO until anemia corrects

190
Q

Where are erythropoietin and thrombopoietin made?

A

erythropoietin is made in kidneys
Signal to bone marrow to make RBC’s

thrombopoietin is made in liver

191
Q

Anemia of chronic disease
or
Anemia of chronic inflammation

A

Caused by increase in proinflammatory cytokines which decrease erythropiesis

TTULAC
Thyroid, TB, UTI, Liver, Auto immune, cancers

Normocytic or microcytic

**Ferritin is elevated with inflammation***
Ferritin is elevated in response to inflammation just like CRP or ESR

Treat cause (no specific tx) (could eventually need transfusion)
can benefit from EPO injections

Usually macrocytic if alcohol is involved

192
Q

Aplastic anemia

A

Aplastic pancytopenia

Bone marrow failure resulting form damage to hematopoietic stem cells

Bone marrow failure
Not making any cells

Dx: bone marrow biopsy

65% are idiopathic

Autoimmune, chemo, toxin, drug, virus, radiation poison

Drugs, bone marrow transfusion

193
Q

Hemolytic anemias

A

bone marrow is making RBC’s but they are destroyed

jaundice, splenomegaly

Splenic sequestration
enlarged spleen due to too many RBC’s and fragments

Splenic resection, splenectomy

Labs: High MCV, RDW, Low hgb, high reticulocytes, high bilirubin, low haptoglobin, high LDH,
Fragments on smear

hemoglobinuria

Direct coombs test / antiglobulin test
if positive
autoimmune, drug, transfusion, infection or cancer
if negative
g6pd, PNH, TTP/HUS or DIC

First clues are physical exam and macrocytic anemia
then order other labs

194
Q

2 classes of hemolytic anemia

A

intrinsic
Many types
Vigorous exercise, self correcting

extrinsic
many types
Parvo virus(slapped cheek) (self limiting)
195
Q

AIHA

A

Auto immune hemolytic anemia

Caused by IgG or IgM antibodies attacking RBC’s

50% idiopathic
Autoimmune, malignancies, drugs
10% also have ITP (called Evans syndrome)
(antibodies against platelets) (poor prognosis)

Labs: hemolysis, +direct coombs test

Tx: SPIR
Splenectomy, rituximab, IVIG, prednisone

196
Q

G6PD deficiency

A

inherited, X linked, Black males
can affect anybody

decreased ability of RBC’s to deal with oxidative stress
Fava beans, dapsone, Bactrim, Macrobid, primaquine, infections

Labs: Heinz bodies, fragments, hemolysis
G6PD enzyme assay

Asymptomatic whole life until they get one of these oxidative drugs that causes a stressor.

Tx: no specific treatment, avoid oxidative drugs

197
Q

PNH

A

Paroxysmal Nocturnal hemoglobinuria
(not common) (inherited)

RBC’s have abnormal sensitivity to complement especially at night when the body is more acidic.

mostly in children,
hemoglobinuria worse in morning, improves throughout the day.

Dx: Flow cytometric assay which will be positive for CD55 and CD59

Tx: ecluzimab

198
Q

Anemia due to blood loss

A

external or internal

Labs: low hgb/hct
Chronic=iron deficiency (microcytic)
Acute = Elevated reticulocytes (macrocytic)
(stage depends on CBC whether it is acute or chronic)

Severe acute bleed can have delay in hgb/hct
(will still have signs of hypovolemia)

199
Q

What could a GI bleed show on labs

A

Aside from CBC

BUN could be high with a normal creatinine

200
Q

Hemoglobinopathies

A

Disorder of globin synthesis or stability
leads to anemia

Common in malaria regions
i.e. thalassemia and sickle cell

Dx: hemoglobin electrophoresis (test)

201
Q

Hemoglobin anatomy

A

Hemoglobin in a normal adult

Heme+4 globin units
(2 alpha chains, 2 beta chains)

Heme = iron + 4 protoporphyrins

99% Hgb A
1% Hgb B
almost no Hgb F
Hgb S is abnormal (s is for sickle)

202
Q

Thalassemia

A

Inherited
(not producing enough alpha or beta chains)

results in in effect

Microcytic anemia
Normal RBC count, hemoglobin is just not effective

Dx: hemoglobin electrophoresis (test)
Globin gene test (most effective)

Shows target cells on smear

Very severe will have extramedullary hematopoiesis

203
Q

Thalassemia Beta Major

A

Mediterranean, mid east, SE asia

Major = no beta chain hgb

Jaundice, pallor, failure to thrive

life long transfusion dependence & marrow transplant

204
Q

Thalassemia Beta Intermedi

A

dx: ages 2-4
may be transfusion dependent
can require splenectomy
varies in severity

205
Q

Thalassemia Beta Minor

A

Asymptomatic
carrier

may have very mild microcytosis or anemia

206
Q

Thalassemia Alpha Major

A

Mediterranean, mid east, SE asia but also African

Major:
Not making alpha chains (only “hgb barts”)
Hydrops fetalis (death in utero)

207
Q

Thalassemia Alpha intermedia

A

loss of three of four alpha chains

Also called HgH disease.

Usually not transfusion dependent, but will be anemic with Hgb 9-11 g/dL.

May have signs of chronic hemolysis and/or extramedullary hematopoiesis in spleen or liver.

208
Q

Thalassemia Alpha minor

A

loss of two of four alpha chains.
Non-specific signs/symptoms of anemia.
Common with African ancestry.

209
Q

Thalassemia Alpha minima

A

Loss of 2 of 4 alpha chains
Asian descent
not anemic but hypochromic

210
Q

Chipmunk facies

A

Beta thalassemia major
or
undiagnosed Alpha thalassemia intermediate

211
Q

When you see microcytic anemia

A

get iron studies

Thalassemia = normal
Iron deficiency = all low, high TIBC
Chronic disease = low everything, high ferritin
Sideroblastic = normal

212
Q

Sickle cell

A

causes cells to sickle
poor oxygen capacity
very painful (hours to weeks)
organ ischemia and infarct

if more than 3 crises Q year = poor prognosis

Priapism, infarcts, organ failure, leg ulcers PVD

acute chest syndrome (fever, cough, hypxoemia, tachy)

behavioral

Labs: HbgS, normocytic/normochromic
granulocytosis

Avoid high altitude, cold, manual labor

Tx: hydroxyurea
IV hydration
Pain meds
Transfusion
Splenectomy + vaccines
could need bone marrow transplant (can be curative)
213
Q

Methmoglobinemia

A

Acquired
can be iatrogenic

abnormal form of hgb

Causes:
Nitrites, drugs, anesthesiology

Can be lethal

Tx: IV methylene Blue

214
Q

5 types of hematological malignancies

A 
Leukemias
Lymphomas
Multiple myeloma
Myeloproliferative disorders
Myelodysplastic syndromes

All are diagnosed by bone marrow biopsy or lymph node biopsy (gold standard)

215
Q

Leukemia (acute)

A

Increase of blasts (precursor cells)

Very high WBC
Diff shows blasts

Causes anemia due to too many WBC’s in bone marrow

Bruising, bleeding, bone pain, infections

AML or ALL

Over 20% blasts is diagnostic of acute leukemia

216
Q

Leukemia (acute)

AML

A

> 20% myeloblasts (normally less than 5)
Also on bone marrow biopsy

Auer rods = AML

Down syndrome, radiation, drugs, chemo, smoking

7+3 Chemo +/- marrow

Intermediate to high risk

palliative = hydroxyurea

Dx: molecular recited, genetic features

217
Q

Leukemia (acute)

ALL

A

> 20% lymphoblasts (normally less than 5)
Also on bone marrow biopsy

Most common malignancy in children (3-5) 30% of all

High incidence of CNS involvement

Chemo, Marrow, CAR T cell therapy

Standard practice to do LP due to CNS involvement

218
Q

Omaya resevoir

A

Port to CSF for ALL

219
Q

Chronic Leukemia

A

Not all requires treatment

CML Chronic myelogenous leukemia
CLL Chronic lymphocytic leukemia

220
Q

CML Chronic myelogenous leukemia

A

Malignancy of mature granulocytes

Really high WBC

usually dx 55-65

can be asymptomatic, fatigue, fever, splenomegaly

Caused by translocation of chromosome 9 & 22
Philadelphia Chromosome (BCR-ABL gene)
Bone marrow biopsy to confirm

Blasts will not be over 20%

TKI Gleevec

221
Q

CLL Chronic Lymphocytic Leukemia

A

Lymphoid cells
Age of onset 70
WBC over 20,000

can be asymptomatic, fatigue, splenomegaly

Dx: peripheral Blood flow cytometry
Bone marrow biopsy
Lymph biopsy

Smudge cells on smear

Prone to ITP, Hemolytic anemia

Might be genetic (only blood cancer)

Tx: BTK, rituximab, chemo

222
Q

Lymphomas

A

Cancer of Mature B lymphocytes

Usually B cells
Rare = T or NK cells

Hodgkins and non hodgkins
S/S = lymphadenopathy, hepatosplenomegaly

B symptoms = Fevers, drenching night sweats, unintentional weight loss >10% in 6 months

Check lymph nodes
May have lymphocytosis, + LDH, hypercalcemia
Associated EBV, HIV
Pet scan
Biopsy required to confirm

B cell cancer, big lymph/liver/spleen, pet scan
drenching night sweats*

223
Q

Lymph nodes with lymphoma

A 
non tender / painless
Fixed
Firm / hard
>2cm
>2 weeks
unilateral
unusual locations
224
Q

Hodgkins lymphoma

A

B cell lymphoma
Reed sternberg cells in biopsy

age 20-30 or over 60
more in males

Painless lymphadenopathy above the waist
Painful with alcohol

Tx: ABVD +/- radiation

Considered pretty curable

225
Q

Non-hodgkins lymphoma

A

10 times more common than hodgkins
all other lymphomas

R CHOP, marrow, CAR T cell

Diffuse large B cell is most common type
MALT (H.pylori)
Others

226
Q

Multiple myeloma

A

Cancer of plasma cells (most mature B cells)

CRAB
Hypercalcemia, - Renal, Anemia, Bone lesions

lytic bone lesions

Age around 67

M spike is special test in serum or urine

High protein on smear
Rouleaux formation (stacking of RBC's)

RVD, Marrow, radiation, kyphoplasty

30% of periosteum must be gone for lytic lesions

227
Q

Waldenstroms Macroglobulinemia

A

Malignancy of lymphoplasmacytic cells that secret IgM

Low blood counts (cytopenias) +protein, abnormal coag tests

Usually kinda sick

S/S= lots splenomegaly, reynauds, weak, weight loss, fever, purpura

**Hyperviscosity syndrome*

Tx: early observation
Late = chemo, marrow

228
Q

Amyloidosis

A

Not a cancer

Protein misfolding disorder

Affects the organs

****big tongue, raccoon eyes
Amyloid protein deposits, Congo red stains

Can be fatal

TX similar to Multiple myeloma

229
Q

Myelodysplastcic syndrome

A

Pre cancerous syndrome

Can evolve into AML

Over 60

idopathic

gradually worsening cytopenia
<20% blasts

Sideroblastic

Ringed sideroblasts on smear

observation, hypomethylating, immunomodulators

Mild = observation
more severe = chemo +/- marrow

230
Q

Myeloproliferative Disorder/neoplasms

A

overproduction of myeloid cells (RBC, platelets, granulocytes)

**Mutation of JAK-2**

Can evolve into AML

**Massive splenomegaly**

female predominant

231
Q

Polycythemia Vera

A

Hgb over 15

Rule out other causes of high hgb (smoking, epo use, dehydration, RCC, altitude, COPD etc)

**Serum EPO will be low****

Headaches, tinnitus, blurred vision, fatigue, hypertension, erythema
**pruritis with warm shower*******

Risk of death from thrombosis

Tx: Phlebotomy, hydroxyurea, ruxolitinib

232
Q

Essential thrombocythemia

A 
Too many platelets
>1 million
Rule out other high platelet causes
usually asymptomatic
bone marrow biopsy required for DX

Tx: Observation, ASA, hydroxyurea, ruxolitinib

233
Q

Primary myelofibrosis

A

People are sick
poor prognosis

Too many stem cells
fibrosis of bone marrow

Teardrop RBC’c*
Unintentional weight loss
**massive splenomegaly**

Male dominant
over 60

Bone marrow biopsy, shows fibrosis

Treatment: ruxolitinib, prednisone+thalolidomide, INF-α, +/- allogeneic bone marrow transplant

234
Q

Myelodysplastic syndromes
VS
Myeloproliferative neoplasms

A

Myelodysplastic syndromes are disorders of underproduction

Myeloproliferative neoplasms are disorders of overproduction

235
Q

Misc. hematological malignancy info

A

Hematological malignancies and related disorders may present with cytoses or cytopenias on complete blood count

A peripheral blood smear may reveal abnormalities characteristic of a blood cancer

Lymphomas present with “B symptoms”, hepatosplenomegaly, and large, firm, fixed, & nontender lymphadenopathy

Acute leukemias present with sudden, significant symptoms and cytopenias with blasts >20%

Multiple myeloma presents with CRAB criteria and M-spike

Chronic leukemias, MDS, and MPNs are often found incidentally on routine CBC

When suspicion is high, tissue biopsy (typically bone marrow or lymph node) is needed to rule in/out a hematological malignancy

236
Q

Oncological emergencies

A 
Hyperleukocytosis/leukostasis
Hyperviscosity syndrome
Tumor lysis syndrome
Neutropenic fever/Sepsis
Superior vena cava syndrome
237
Q

Neutropenic fever / sepsis

A

Neutrophils <1000 (severe is <500) on diff

Single temp over 101 or sustained (1hr) over 100.4

people receiving chemo

only symptom

Labs: cultures, urine, chest xray, lactic acid, procalcitonin if hypotensive

+gram cocci (ports), - gram rods, fungus, tb

Emergency, immediate broad spectrum AB, admit

only 30% of the time you find the cause

238
Q

Hyperleukocytosis/leukostasis

Blast crisis

A

patients with acute leukemia
AML,ALL

WBC>50 mostly blasts

hypervisosity syndrome

Emergent hospital admittance for plasmapheresis

239
Q

Tumor lysis syndrome

A

Massive tumor cell lysis releasing all teh toxins into the blood
Large amounts of phosphorus, potassium, and nucleic acids

people with lots of cancer
usually iatrogenic after cancer treatment

High uric acid, phosphorus, = AKI
High potassium = arrhythmia or arrest
Low calcium = seizures tetany

allopurinol or IV hydration prophylaxis

admit, telemetry, correct electrolytes, iv hydration, possible dialysis

patients feel sick

240
Q

Hyperviscosity Syndrome

A

Waldenstroms macroglobinemia

Headache, blurred vision, altered mentation, stroke, paresis

Labs: serum viscosity

Emergent hospital admittance for plasmapheresis

241
Q

SVC Syndrome

A

Superior vena cava syndrome

Compression of blood flow in SVC by tumor

lung cancer

Face neck swelling, chest pain, dyspnea,
Swollen from the neck up

Chest xray, superior vena cava gram is gold standard

Tx: reduce tumor

242
Q

Types of blood products

A 
Whole blood
Packed RBC's
Platelets
FFP
Cryoprecipitate
243
Q

Apheresis

A

When blood is donated only one component is taken out and the rest is given back to the donor
(i.e. plasma)

244
Q

Most common blood type

A

O positive (40%)

245
Q

Least common blood type

A

AB neg (0.5%)

246
Q

universal donor (blood)

A

O neg

247
Q

Universal recipient (blood)

A

AB pos

248
Q

RH factor

A

antigen D

80% are positive

Sensitization (alloimmunization) may occur from transfusions or pregnancy

Rh negative mother is exposed to Rh positive antigens and develops antibodies. So, subsequent pregnancies at risk for erythroblastosis fetalis at time of delivery.

Rh immunoglobulin, ie Rhogam®, is given to Rh neg mothers with Rh pos fetus

249
Q

Transfusion decision criteria

A

Labs, clinical S/S, disease or goals

Not just lab values

250
Q

Main goal of RBC transfusion

A

Establish adequate O2 carrying capacity

251
Q

Main goal of Platelet transfusion

A

Stop or prevent bleeding

252
Q

Hemoglobin rock bottom

A

Hemoglobin<7
Should never go below this
give blood

253
Q

Platelet rock bottom

A

Platelets should never be allowed to go less than 10

give platelets

254
Q

What to give FFP or cryo for

A

need coagulation factors

DIC
HELLP
Etc.

255
Q

Options for pre-transfusion testing of patient:

A

Type and hold = wish list (unlikely will need)

Type and screen = layaway (might need in near future)
good for 72 hours

Type and cross = already bought clothes (patient definitely going to need blood)(only for this patient)

Trauma blood = immediate transfusion, doesn’t matter

Mostly for RBC’s

256
Q

How much will 1 unit of of RBC’s raise Hgb?

A

1g/dl

lasts up to 42 days

257
Q

How much will 1 unit of of platelets (pack) raise Hgb?

A

5000 - 10,000 (over 15mins)

1 pack of platelets = 4-6 units of platelets

258
Q

Washed RBC’s

A

reduce anaphylaxis

decreases WBC’s

259
Q

FFP

A

Fresh frozen plasma

lasts 1-7 years

coagulation factors

given for bleeding

once thawed use within 24 hours

increases coags by about 5%

Must be ABO compatible

260
Q

Cryo

A

Cryoprecipitate

Concentrated fibrinogen

Very good for DIC

261
Q

Transfusion reactions

A

most are immunological

immediate = <24 hours
or delayed >24hours

Typically to RBC’s, Platelets, or whole blood

Around 5% there is some kind of reaction

most occur within15 mins

most are not life threatening

**Stop transfusion****

262
Q

Hemolytic transfusion reaction

A

Human error

Person given wrong blood type

Life threatening

Jaundice, headache, palpitations, respiratory distress, fever, shock

Labs: Hgb will be even lower due to RBC’s destroying each other
+direct coombs, fragments on smear

Tx: stop transfusion, IV resuscitation, steroids, pressors

263
Q

Febrile nonhemolytic reaction

A

Most common type of transfusion reaction

Fever over 38 or +1 over baseline

Fever/chills without hemolysis, organ failure or shock

more transfusions, more risk (due to antibody buildup)

Tylenol

264
Q

Allergic reaction (transfusion)

A

Most are mild: urticaria, pruritis, flushing

Due to antibodies

stop transfusion, Benadryl

Anaphylaxis is very rare
Benadryl, steroids, epi

Mast cell mediated

265
Q

TRALI

A

Transfusion related acute lung injury

Due to antibodies

Patient will be sick
Dyspnea, SOB Fever, hypotension

Chest xray = bilateral pulmonary edema

Stop transfusion, supportive care (O2, diuretics)

Match platelets in future (HLA)

266
Q

Premedication for transfusion reaction

A

It is done but is not evidence based

267
Q

Delayed hemolytic reaction

A

Occurs 2-14 days after transfusion

unexplained fall of Hct/Hgb

S/S of hemolysis

+direct coombs,

usually no treatment required

268
Q

Alloimmunization

A

Sensitization to RBC antigen with first transfusion, then reaction with second transfusion

Primary immunization occurs days or weeks post transfusion or pregnancy (mother develops antibodies to fetal RBC antigens) and asymptomatic

With subsequent transfusions, patient may have fever/chills

RBC or platelet antibody screen will be positive

no treatment, find appropriate donor

269
Q

Graft versus host disease

A

due to left over things in RBC’s
T cells from donor attack bone marrow

very rare, possibly fatal

Rash, diarrhea, +liver enzymes

270
Q

Non immunological delayed transfusion reaction

TACO

A

Transfusion Related Circulatory Overload

Pulm edema within 6 hours

Dyspnea, peripheral edema,
Elevated systolic BP**

271
Q

Difference between TACO and TRALI

A

TRALI is immune mediated and TACO is not

With TACO, no fever and elevated BP

With TRALI Fever and low BP

Usually occurs in people that are already volume overloaded, anasarca, peripheral edema

Treat for volume overload
diuretics

Labs BNP will be elevated

272
Q

Non immunological delayed transfusion reaction

Transmission of infectious disease

A

All blood products tested for Hep B/C, HIV, Syphilis, & other pathogens

Bacterial contamination in blood processing may occur

Patient will present with signs/symptoms of sepsis hours after transfusion: fever, hypotension
(like septic shock)

Clinically similar to hemolytic reaction, but no signs of hemolysis

Culture patient and blood product

Lactic acid may be elevated

Requires broad spectrum antibiotics

May require vasopressors

273
Q

Non immunological delayed transfusion reaction

Hypothermia

A

Highest risk with refrigerated or room temperature blood products given at rapid rates

If high infusion rates are planned, a warming device is recommended

Patient may have chills, but hypothermic (temperature ≤35°C) instead of febrile upon temperature check

warm patient

274
Q

Non immunological delayed transfusion reaction

Metabolic Disturbances/Electrolyte Toxicity

A

Higher risk with multiple transfusions in a short period
Hyperkalemia: K+ leaks out of RBCs; concerning if renal insufficient

Acidosis: due to sodium citrate (anticoagulant in blood products). For patients with liver disease, not metabolized quickly enough and lactate produced.

Hypocalcemia: also due to sodium citrate, as it binds to calcium

Iron overload/hemochromatosis: about 200mg of Fe per unit pf pRBCs, accumulates and deposits in organs (liver, heart, endocrine).

May require iron chelation medication.

275
Q

What is cancer

A

diseases that have unrestrained cellular growth

Hallmarks of cancer cells:

Resisting apoptosis/cell death
Sustaining proliferative signaling
Evading growth suppressors (immune system)
Activating invasion and metastasis
Enabling replicative immortality
inducing angiogenesis
276
Q

Carcinogenesis

A

Multi step process
tissue and cellular changes

mutation of tumor suppressor genes or oncogenes

277
Q

Cancer general risk factors

A 
Older age
Sex (M>F)
race
Inherited
Toxins
Radiation
Pathogens (EBV, Hep b, H. pylori, HPV, etc)
278
Q

Gold standard of cancer Dx:

A 
Tissue sample (always need a biopsy)
Pap
FNA
marrow
lymph
279
Q

Cancer staging

A

Many different staging types

most common is TNM

280
Q

Number 1 cause of death in cancer patients

A

Infection

281
Q

Why are cancer patients at high risk for infection?

A

Malnutrition
immune deficiencies
breakdown of epithelial barriers
Bacteremia

282
Q

Cachexia

A

Weight loss
muscle loss
wasting syndrome

Requires intervention if over 10%

283
Q

Paraneoplastic syndrome

A

Tumor is able to produce hormones

i.e. ADH, ACTH, PTH, EPO, etc.

284
Q

Oncology branches

A

Medical oncology
(meds, chemo, antibodies, marrow)(given in cycles)

Immunotherapy

Surgical oncology
Radiation oncology

285
Q

Goals of cancer therapy

A

Palliative vs curative

Determine how frail or robust is this patient, how much therapy can they get

286
Q

Bone marrow transplant

A

Hematopoietic stem cell transplants

Basically give the patient a whole new immune system

most often for hematological malignancies

can be many complications GVHD, infections

Collect new marrow, chemo to remove old immune system, infuse new marrow

287
Q

Remission

A

Complete = disappearance of all measurable disease

partial = >50% reduction in disease

progressive disease is growth of >25% in new disease

Cure - >5 years without detectable disease

PAM Semester 2 (22 decks)

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