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NUNP531 Applied Pathophysiology > MIDTERM Week 2: Hematology > Flashcards

MIDTERM Week 2: Hematology Flashcards

1
Q

What % of blood is plasma?

A

55%

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2
Q

What is plasma composed of?

A

91% water, 7% proteins and 2% other solutes (like ions, nutrients, waste products, gases, lytes)

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3
Q

What are plasma proteins? (types) Which is most common in the blood?

A

albumin (60% of plasma proteins)
Globulin
Fibrinogen
Prothrombin

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4
Q

Functions of plasma proteins? (4 broad categories)

A

Clotting, defense (such as antibodies), transport, regulation

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5
Q

What is serum?

A

plasma that has been allowed to clot in la to remove fibrinogen & clotting factors

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6
Q

Life span of RBC

A

80-120 days

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7
Q

Normal range of RBCs

A

4.2-6.1 x 10^12/L

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8
Q

Life span of WBCs

A

High varied (unknown, some up to years)

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9
Q

Normal WBC count?

A

5-10 x 10^9/L

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10
Q

Lifespan of platelets?

A

8-11 days

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11
Q

Normal platelets blood levels?

A

150-400 x 10^9/L

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12
Q

Where does hematopoeisis happen?

A

In the bone marrow

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13
Q

What are the two types of stem cells?

A

mesenchymal stem cells (MSCs) aka stromal cells that differentiate into osteoblasts, adipocytes and chondrocytes & hematopoietic stem cells (HSCs)

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14
Q

What do hematopoietic stem cells become? (2 types of progenitor cells)

A

Myeloid & lymphoid progenitor cells

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15
Q

What do lymphoid progenitor cells differentiate into?

A

T cells, B cells, NK cells

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16
Q

What is a mature B cell called?

A

Plasma cell
= a fully differentiated B cell that produces a single type of antibody.

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17
Q

What do you call the large cell that breaks into platelets?

A

Megakaryocyte

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18
Q

What types of cells come from the myeloid progenitor cell?

A

Megakaryocytes, eosinophils, basophils, erythrocytes, monocytes & neutrophils
(just remember: all blood cells except NK, B & T cells)

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19
Q

What is the last immature form of an RBC called?

A

Reticulocyte

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20
Q

What % of RBCs should be reticulocytes?

A

• Reticulocyte count should be 1% of body’s RBCs (useful clinic index of erythropoietin activity

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21
Q

General outline of where WBCs come from/steps of differentiation

A

Most arise from HSCs in bone barrow
- differentiate to common lymphoid progenitors and common myeloid progenitors
- lymphoid progenitors –> lymphocytes released into bloodstream to go to lymphoid organs for further maturation
- Myeloid progenitor cells further differentiate into progenitors for erythrocytes, megakaryocytes, and mast cells and granulocyte/monocyte progenitors
- Monocytes mature into macrophages 1-2 days after release

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22
Q

General outline of how platelets develop from a megakaryocyte?

A

Megakaryocyte progenitor undergoes endomitosis (DNA replication but no anaphase and cytokinesis) –> huge nucleus with polyploidy develops & cell develops surface branches that progressively fragment into platelets
• Single megakaryocyte can produce thousands of platelets
• 2/3 enter circulation & 1/3 remain in splenic pool

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23
Q

Which WBCs are granulocytes?

A

The “PHILS”
Neutrophils, basophils, eosinophils

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24
Q

What types of WBCs are agranulocytes?

A

Monocytes, macrophages & lymphocytes

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25
Q

T/F all granulocytes are phagocytes?

A

True!
• Have many membrane-granules in cytoplasm that contain enzymes capable of killing microorganisms & catabolizing debris ingested during phagocytosis; also contain powerful biochemical mediators with inflammatory and immune fx’s

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26
Q

What hormone induces platelet production?

A

o Regulated by Thrombopoietin (TPO), hormone growth factor – produced by liver & induces platelet production in bone marrow

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27
Q

What is considered “primary hemostasis”?

A

Formation of a platelet plug at the site of injury

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28
Q

What is secondary hemostasis?

A

Formation of a fibrin clot

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29
Q

At what factor do the intrinsic and extrinsic clotting pathways converge?

A

X!

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30
Q

What are the extrinsic and intrinsic pathways named in this way?

A

Extrinsic is activated by factors in the tissue (extrinsic or outside the blood). Intrinsic is activated by factors already in the blood.

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31
Q

Where do DOACs act?

A

At factor X
(these re Direct Oral Anticoagulants…such as apixaban and rivaroxaban)

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32
Q
A
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33
Q

What is considered thrombocytopenia?

A

Platelets <150

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34
Q

Manifestations/S&S of thrombocytopenia?
When do we expect to see spontaneous bleeding?

A

• Concern for hemorrhage with small trauma if <50
• Spontaneous bleeding w/t trauma (10-15)  skin manifestations (petechiae, ecchymoses, purpura) or frank bleeding from mucous membranes
• Severe spontaneous bleeds if <10 (fatal if GI or resp tract, CNS)
• Heavy/long periods
• Headaches
• Hematuria
• Malaise, fatigue, general weakness

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35
Q

What is hemophilia?

A

an inherited bleeding disorder in which the individual is deficient in factor VIII (hemophilia A) or factor IX (hemophilia B) or factor XI (hemophilia C)

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36
Q

What role does vitamin K play in coagulation? What causes a deficiency?

A
  • needed for the production and regulation of procoagulant factors (VII, IX, X); and the anticoagulant factors within the liver (proteins C and S).

Vitamin K can either come from food sources (leafy green vegetables) or be naturally produced in the intestinal tract. The causes of Vitamin K deficiency in adults include poor nutrition, bulimia, destruction of normal gut flora by taking antibiotics, and conditions that affect fat malabsorption e.g. cystic fibrosis and warfarin therapy (warfarin inhibits activation of Vitamin K).

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37
Q

Where are most clotting factors made?

A

Liver

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38
Q

What med is most commonly responsible for thrombocytopenia? What is happening here?

A

Heparin
• HIT is an immune- mediated, adverse drug reaction caused by IgG antibodies against the heparin–platelet factor 4 complex
• The release of additional platelet factor 4 from activated platelets and activation of thrombin lead to increased platelet consumption and a decrease in platelet counts

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39
Q

How long after initiating heparin does HIT occur?

A

beginning 5 to 10 days after administration of heparin.

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40
Q

How severe is the change in platelet drop in HIT? Is bleeding common? What other contrary side effect may occur?

A

50% reduction
Bleeding uncommon
• 30% also at risk of thrombosis: venous or arterial, because a prothrombotic state is caused by antibody binding to platelets, inducing activation, aggregation, and consumption

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41
Q

WHat is idiopathic thrombocytopenia? What do we call it now? Is it acute or chronic?

A

Immune Thrombocytopenic Purpura (ITP)
Now recognized as immune process
Caused by autoantibodies against platelet antigens
Can be acute or chronic

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42
Q

QUESTIONS FROM HERE ARE FROM LECTURE:
What kind of units (conventional or SI) do we use in Canada?

A

SI

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43
Q

Which component of CBC will indicate BACTERIAL infection?

A

Neutrophils (may see a rise in all of the WBCs but most commonly see high neutrophils)

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44
Q

Main is the indicator of VIRAL infection on CBC?

A

Lymphocytes

45
Q

What does a high EOSINOPHIL count potentially mean? (3 categories)

A

Allergy, drug reactions, parasites
“rashes, wheezes and weird diseases” (may see elevated in ASTHMA attack)

46
Q

What does MCV stand for?

A

Mean corpuscular volume

47
Q

What does MCV tell us?

A

Macro, micro or normocytic

48
Q

What is a normal MCV?

A

80-100

49
Q

By definition, if a patient has an anemia, what value will be low?

A

Hemoglobin

50
Q

What are some common causes of microcytic anemia?

A

Iron deficiency (can be due to inadequate source or loss due to slow or quick bleed)

51
Q

What vitamin deficiencies lead to macrocytic anemia?

A

B12 & folate

52
Q

What kind of anemia does chronic alcohol consumption lead to and why?

A

Macrocytic
Have chronic inflammation of GI tract –> can’t absorb B12/folate

53
Q

Which drugs commonly cause macrocytic anemia?

A

Methotrexate, a lot of chemo drugs

54
Q

What is thalassemia?

A

Genetic condition. Microcytic cells & tons of them…may see normal Hb.

55
Q

What is “ethnic neutropenia”. Less racist term for this?

A

Duffy Null Neutropenia
Low neutrophil count
Not pathological
See in certain groups such as those of african decent

56
Q

Agranulocytosis - what is this and is it worrisome?

A

Severe deficiency of granulocytes (a = none)
Potentially myelodysplastic syndrome or other serious issue with bone marrow.
Also caused by old antipsychotics

57
Q

What is leukocytosis?
What medications cause this?

A

Elevated WBC
Steroids, ventolin, lithium & other medications

58
Q

What common medications cause thrombocytopenia?
What will you see in terms of symptoms & platelet count?

A

Heparin
Is immune mediated response that uses up platelets to make clots
See symptoms of clots but low platelet count

59
Q

Your patient was discharged yesterday from acute care hospital after tx for pneumonia. His platelet count was 8000 before discharge (baseline 200), Do you need to be worried?

A

No as concerning because is common to see highly fluctuating platelet count in acutely ill people. As long as they are not symptomatic, would not warrant great concern.

60
Q

You have a patient with cirrhosis, PLT baseline 50. No signs and symptoms of bleeding. Do you need to send them to hospital for urgent platelet transfusion?

A

Likely not. This may just be chronic level. Tolerate pretty low levels of platelets…as long as pt as asymptomatic.

61
Q

Is it normal to see large amount of immature leukocytes (blast cell) circulating in a patient?

A

No….could indicate severe infection (our body “dumps” these cells as ‘hail Mary’ to fight infection…called “bandemia”) but this would typically only result in lower levels

High levels (20, 30, 100) probably acute leukemia & needs emergency eval

62
Q

What is “left shift”

A

Way of describing immature cells being found

63
Q

In IDA, what will you see happening with RDW and and MCV?

A

Will see growing RDW as cells become different sizes due to lack of iron
Dec MCV = microcytic

64
Q

Is it necessary to prescribe oral iron multiple times per day?

A

No, finding similar absorption to do daily or every other day.

65
Q

Why might someone develop hives from eating chicken soup when has a pre-existing viral infection

A

Since the immune system is active. some sensitivities will become more pronounced, you have more eosinophils. Type 1 immune reaction.

66
Q

What is pernicious anemia? What illness is it associated with? What type of anemia is it? What types of cells do you see?

A

Caused by absence of intrinsic factor –> inability to absorb vitamin B12 from the small intestine

Associated with end stage of type A autoimmune gastritis

considered to be a type of megaloblastic anemia, which is characterized by the production of large, atypical, immature red blood cells by the bone marrow

67
Q

Is ferritin SPECIFIC or SENSITIVE test?

A

It is both
Very specific when LOW (there are very few things other than iron deficiency that cause low ferritin)

Sensitive to many things when HIGH - is considered acute phase reactant so can be indicative of infection, autoimmune diseases, etc…

68
Q

WHy do we have murmur with profound anemias?

A

Functional murmur. When you have anemia (less hemoglobin), the capacity of blood to carry oxygen to different parts of your body is decreased. The body senses that there is less oxygen and to compensate, it makes the heart pump more (hyperdynamic circulation)

69
Q

Where is B12 absorbed?

A

In the terminal ileum
Therefore those with ileostomy at particular risk of B12 deficiency

70
Q

What cells make intrinsic factor?

A

Parietal cells in the stomach

71
Q

S&S of Pernicious Anemia

A

weakness, fatigue, paresthesias of feet and
fingers, difficulty walking, loss of appetite, abdominal pain, weight loss, and a sore tongue that is smooth
and beefy red.
The skin may become “lemon yellow” (sallow), caused by a combination of pallor and
jaundice

72
Q

Why do you see neurological effects in pernicious anemia? Is this reversible?

A

Neurological manifestations result from nerve demyelination that may produce neuronal death.
The
posterior and lateral columns of the spinal cord also may be affected, causing a loss of position and
vibration sense, ataxia, and spasticity.
These complications pose a serious threat because they are not
reversible, even with appropriate treatment.

73
Q

What happens in sickle cell? What triggers sickling?

A
  • Immune condition
  • Make blood cells with different surface tension - when become deoxygenated, cell sickles (folds), become normal shape when oxygenated

Sickling also can be
triggered by acidosis (decreases Hb affinity for O2) and low flow vessels (Hb has lots of time to dump O2 and then is stuck deoxygenated)

Sickled cells tend to occlude vessels –> possible infarct just about anywhere

From lecture: anywhere where blood constriction occurs (such as applying tourniquet or entering cold water) can result in sickling…

74
Q

Why does sickle cell cause anemia?

A

Premature destruction of RBCs as cells become damaged from repeated sickling

75
Q

BACK TO NOTES (Not from lecture anymore)

A

xx

76
Q

Differentiate acute and chronic immune thrombytopenia
(Not sure if we would need to know this but i’m putting it here)

A

• Acute
o Frequently observed in children and typically lasts 1 to 2 months with a CR, can progress to chronic
o usually secondary to infections (particularly viral) or other conditions that lead to large amounts of antigen in the blood, such as medication allergies or systemic lupus erythematosus.
o Usually resolves once offending agent removed (virus, med) – often without sig clinical consequences

• Chronic
o Most common in women 20-40 yrs
o Progressively gets worse
o can occur from a variety of predisposing conditions or exposures (secondary) or have no known risk factors (primary)
o Often remission and exacerbations

77
Q

What are hemophilia A & B? What is this a deficiency of? What do you see recurring in these conditions?

A

Hemophilia A
• due to factor VIII deficiency
• most common hereditary disease
Hemophilia B
• due to Factor IX deficiency
• Clinical presentations of A and B are the same

Both hemophilias cause spontaneous and recurrent bleeding in the joints and soft tissues, progressively causing further damage to the skeletal muscles

Hemophilia A and hemophilia B are inherited as X-linked recessive traits, thus affecting mainly males and homozygous females. About 30% of all cases are caused by new mutations and not family history. All races are equally affected.

78
Q

Von Willebrand disease (vWD) - what does this result from? Common manifestations?

A

• caused by a deficiency or dysfunction of von Willebrand factor (vWF), a clotting protein

• autosomal dominant disorder
• The most common signs of the disease are nosebleeds and hematomas. Other signs include excessive menstrual bleeding, gums bleeding and prolonged bleeding from minor wounds.

79
Q

Venous thrombi
1) What is typically the cause?
2) Mainly composed of?

A

o Typically from combo of factors from Virchow’s triad
o Composition: mainly fibrin

80
Q

What type of meds do we usually use to treat venous thrombi vs arterial thrombi?

A

Venous: mainly anticoags (heparin, warfarin) – because composed of fibrin

Arterial: mainly antiplatelets (ASA, clopidogrel)

81
Q

What usually causes arterial clots?

A

Rupture of atherosclerotic plaques

82
Q

Where do arterial thrombi typically form?

A

Left heart chambers and arteries

83
Q

What is an arterial thrombi mostly composed of?

A

Platelets (so treat with antiplatelets!)

84
Q

What are the 3 components of Virchow’s Triad?

A

Endothelial damage
Hypercoagulability
Stasis

85
Q

What are some acquired causes of hypercoagulability?

A

Cancer
Chemo meds
OCR/HRT
Pregnancy
Obesity
HIT

86
Q

What do the suffixes -cytic and -chromic mean?

A

o Terms that end with -cytic refer to cell size; terms with -chromic refer to hemoglobin content

87
Q

What is anisocytosis?

A

Cells of different sizes

88
Q

What is poikilocytosis?

A

cells of different shapes

89
Q

What anemia might present with inc RBC count?

A

thalassemia

90
Q

What anemias are microcytic?

A

iron deficiency, thalassemia, or anemia of chronic disease

91
Q

If concerned of hemolytic types of anemia (such as sick cell), what lab value might you see elevated?

A

Haptoglobin - a protein present in blood serum which binds to and removes free hemoglobin from the bloodstream.

92
Q

What behaviors commonly cause macrocytic anemia?

A

Often due to medications or alcohol use.

93
Q

Where is iron stored? (2 organs)

A

Liver & spleen

94
Q

What is THE most common macrocytic anemia?

A

Pernicious

95
Q

How does B12 deficiency cause large cells? anemia?

A

Ineffective DNA synthesis –> cell growth without division

defective erythrocytes die prematurely (eryptosis), causing anemia

96
Q

Less obvious S&S of anemia (I feel like we all know the general weakness, fatigue, etc)

A

Claudication (muscle)
jaundice if due to hemolysis
Fatty changes in liver (can also occur in heart & kidney)
Early greying of hair, impaired healing & loss of skin elasticity
Abdo pain, N/V if GI hypoxic
o If d/t B12 deficiency, myelin degeneration occurs  parasthesias, gait disturbances, extreme weakness, reflex abn & spasticity

dec in blood viscosity –> hyperdynamic cardiovascular state (faster, more turbulent) –> inc stroke vol & heart rate –> can lead to cardiac dilation & heart valve insufficiency if not treated

97
Q

WHat is anemia of chronic disease?

A
  • Is mild & 2nd most common type of iron deficiency anemia
  • Due to ongoing inflammation caused by chronic diseases

Hemophagocytosis by macrophages cause shortened RBC survival (Braunstein, 2020)

Erythropoiesis is impaired due to decrease in both erythropoietin (EPO) and marrow responsiveness to EPO (Braunstein, 2020)

Iron metabolism is altered due to an increase in hepcidin, which inhibits iron absorption and recycling (Braunstein, 2020)

A reduction of number of RBCs causes a reduction in the consistency and volume of blood

98
Q

What is the main phagocyte in early inflammation?

A

Neutrophil

99
Q

which WBC comprises only 2-4% of leukocyte count and has Large, coarse granules

A

Eosinophils

100
Q

Basophils are associated with what? (when do you see them elevated)

A

o Associated with allergic reactions and mechanical irritation

101
Q

What % of WBCs are typically lymphocytes? What is their main function?

A

o 20-25% of WBC count
o Primary cells of the immune response
o Transiently circulate in blood and eventually reside in lymphoid tissue as mature T & B cells or plasma cells
o Humoral and cell-mediated immunity

102
Q

Monocytes & macrophages - how many nuclei? Fx?

A

o Large mononuclear phagocytes
o Participate in immune & inflm processes & ingest defective host cells
o Monocytes = immature macrophages

103
Q

Natural Killer cells provide defense against ___ &_____

A

Tumors & viruses

104
Q

WHat are the primary lymphatic organs?

A

Thymus & bone marrow

105
Q

Is megaloblastic anemia normo or hyperchromic?

A

Normo because have normal amount of hemoglobin

106
Q

Causes of acquired neutropenia?

A

Broad Causes of Acquired Neutropenia:

Decreased Marrow Production ex: radiation, chemo, leukemia, aplastic anemia

Increased Destruction ex: Splenomegaly, hemodialysis, autoimmune disease

Prolonged Infection ex: Gram-negative (Typhoid), viral (Flu, Hep B, measles, mumps, rubella, severe infections, protozoal infections (malaria)

Starvation & anorexia also on list

107
Q

Differentiate where T and B cells mature? Where do they originate

A

B cells: Maturation occurs in bone marrow; goes to spleen & lymph nodes and becomes plasma cell (antibody secreting B cell)

T cells: mature in thymus

Both originate in the bone marrow

108
Q

Function of B cells vs T cells?

A

B cells create antibodies

T cells differentiate into 2 types: Helper T cells (CD4) support other immune cells
Cytotoxic T cells (CD8) kill infected/cancerous cells

109
Q

What are Reed Sternberg cells? What illness do you see them in?

A

HODGKIN’S LYMPHOMA
 RS cells are malignant lymphocytes; large, binucleate. Release cytokines

NUNP531 Applied Pathophysiology (24 decks)

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