Lecture 9 - potential quiz questions

type of anemia that occurs when red blood cells are destroyed faster than the bone marrow can replace them.

one cell becomes another cell by activating/deactivtating genes

Kidney

Connective tissue

plasma

Erythrocytes, buffy coats, and plasma

RBCs

Mostly water, proteins (albumin), electrolytes, and dissolved gases

platelets and leukocytes

yolk sac

Liver

ALL Bones

Yellow and red marrow

the central cavity of your bones.

low concentration of hemoglobin. Can't carry enough oxygen

diffused cancer of WBC. Starts in the bone marrow

Cancer of lymphoid tissues, especially lymph nodes (starts here)

4 heme groups and 4 globins

Iron and protoporphyrin IX

Bilirubin

Chromosome 11: beta
Chromosome 16: alpha

In the macrophages of the spleen

alpha 2, beta 2

alpha 2, delta 2

alpha 2, gamma 2

Red blood cells lyse

Complete blood count

MCV
MCH
MCHC

RBC x 3 = HGB
HGB x3 = HCT

Pallor eye sockets, pallor tongue, pale nail-beds, pale palms

1. Decreased hematopoiesis
2. Abnormal hematopoiesis
3. Increased loss or destruction of RBCs

Aplastic anemia
and myelophthistic anemia

sickle cell disease - abnormal cell structure
Thalassemias and hemoglobinopathies

Parovirus-19

HSC

Less HSC, more adipocytes

anemia characterized by the presence of immature erythrocytes in the peripheral blood due to infiltration of the bone marrow by abnormal tissue (like melanoma cells; skin cancer cells that travel to bone marrow)

All 3 cells are falling in numbers

Deficiency of vitamin B12 and folic acid

Meat

Can't absorb vitamin b12

Single base mutations

Deletions !

Minor: one deletion
Major: both deleted
(beta)

3

4

bleeding
intrasplenic sequestration
immune hemolysis (warm and cold anitbodies)
infections (malaria)

decrease of iron in the body to produce healthy cells

a group of 11 proteins produced by the liver in response to infection. positive (concentration goes up; hepsidin) and negative (concentration goes down; albumin)

acute phase reactant. peptide hormone produced in the liver that plays a crucial role in iron homeostasis. Inhibits iron release.

Parietal Cells

1. Immune mediated HA
2. Non-immune mediated HA

a group of disorders passed down through families (inherited) in which there is abnormal production or structure of the hemoglobin molecule

Sickle Cell Disease

Yes, because sickle cell disease (SCD) causes early lysis of the RBCs.

red blood cells become crescent- or “sickle”-shaped due to a genetic mutation in hemoglobin (protein).

YES

There is a problem inside of the red blood cells

There is a problem outside of the red blood cells

1. Structural abnormalities
2. Sickle Cell Anemia
3. Thalassemia
4. Hereditary Spherocytosis

1. Antibodies
2. Infectious agents
3. Mechanical factors
4. Autoimmune hemolytic anemia
5. Hemolytic disease of newborn (HDN)
6. Transfusion reactions
7. Malaria
8. Prosthesis
9. DIC

One own's immune system mistakenly attacks and destroys red blood cells

warm and cold

IgG

IgM

Extravascular

Intravascular

outside of blood vessels, primarily the spleen and liver

Within blood vessels

High IgG titer with at least 2 Fc domains

5

As the blood travels to the center of the body

No, because IgM falls off the RBCs as the temperature in the body rises

Antibodies that can activate the complement at higher temperatures

a genetic disease that affects the structure of blood cells (RBCs). aka spherocytes

intracorpuscular defect aka problem inside of the red blood cell

Symptom

Cell membrane ankyrin or spectrin (alpha or beta chain).

Vertical proteins

Horizontal proteins

Spleen

Spherocytes get trapped in the spleen and the macrophages in the spleen degrade the RBCs

Surface area (NOT volume)

Spherocytes

Splenectomy - remove the spleen

normal proteins or complexes of proteins recognized by the immune system as foreign, leading to an autoimmune response.

antigens that are present on the surface of red blood cells (RBCs) and are recognized as foreign by the immune system of another individual.
(Ex: Rh- mother and Rh+ fetus, incompatibility in blood transfusion)

newly formed antigens on the surface of tumor cells that are recognized as foreign by the immune system.

Mismatched blood transfusion
Hemolytic Disease of Newborn (HDN)
Autoimmune hemolytic anemias

DAT - direct antiglobulin teset

IgG - can cross the placenta

rare type of blood cancer characterized by the OVERPRODUCTION of red blood cells (erythrocytosis), white blood cells (leukocytosis), and platelets (thrombocytosis)

Primary and Secondary PV

RBCs

High (> 45-50%)

It works harder/exerts more force bc blood gets thicker

1. CBC - Red blood cell count (erythrocytosis)
2. Erythropoietin (if its high or low)

You check the erythropoietin levels

Kidney is properly functioning

Primary

Secondary

Hypoxia (heart disease, lung disease, high altitude)
or
Excess erythropoietin production (kidney diseases, tumors - renal, hepatic, androgens)

JAK2 mutation (this gene is always on)

Leukopenia
Leukocytosis
Leukemia
Lymphoma

a decrease in the number of white blood cells (leukocytes) in the blood

an elevated white blood cell (leukocyte) count in the blood

a type of blood cancer due to an ACQUIRED MUTATION that affects the blood and bone marrow. Uncontrolled proliferation of WBC precursors in bone marrow.

Bone marrow

a type of blood cancer that affects the lymphatic system, which is part of the body's immune system.

Lymphatic tissue, primarily lymph nodes

Myeloid family
Lymphoid family

Neutrophils, monocytes, basophils, eosinophils, mast cells

T-cells, B-cells, and NK cells

Acquired (overall)

Myeloid leukemia

Lymphoid leukemia

acute vs chronic

Very quickly or sudden progression of the disease

Very slow progression of the disease

Acute myeloid leukemia
Acute lymphoid leukmeia
Chronic myeloid leukemia
Chronic lymphoid leukemia

Non-hodgkin's lymphoma (85%)
Hodgkin's lymphoma (15%)

HODGKIN'S LYMPHOMA

Bone marrow biopsy & aspiration
Lymph node biopsy

Type of cell found in lymph node biopsy, suggestive of hodgkin's lymphoma

Googly eyes

cancer of plasma cells that produce an abnormal antibody.
Disease of older people (>65 yrs)

abnormal plasma cells, known as myeloma cells, grow uncontrollably in the bone marrow, crowding out healthy blood cells and impairing their function.

Calcium phosphate

Hypercalcemia and hyperphosphatemia

Loss of water from the body, always thirsty, bleeding, easily wounded.

Bone destruction (osteolysis)

Chemotherapy - systemic treatment

Anemia, recurrent infections, and uncontrollable bleeding

Viruses (HTLV-1 and EBV)

Change the genetic makeup of the cells they infect and make them cancerous.

Translocations

t(8,14)

t(9,22)

A piece of chromosome 8 fuses to a piece of chromosome 14.

c-MYC gene

Immunoglobulin production

EBV

BCR-ABL gene

tyrosine kinase is produced and it keeps making white blood cells.

Follicular and diffused

a type of non-Hodgkin lymphoma (NHL) that occurs when white blood cells clump together to form lumps in lymph glands or organs

a fast-growing, aggressive type of non-Hodgkin lymphoma (NHL) that affects B-lymphocytes,

Set the tone of cell division

Acute lymphoblastic leukemia (ALL)
Acute myelogenous leukemia (AML)
Chronic myelogenous leukemia (CML)
Chronic lymphocytic leukemia (CLL)

Any age group

Lymph nodes, spleen, thymus, or bone marrow, but may also involve other organs (aka "extranodal spread of lymphoma"

Germinal center, mantle zone

where it started

Painful for non-cancerous, NOT painful for cancerous

4

single lymph node or group of nodes above the diaphragm

Both sides of the chest are affect and above diaphram

On both sides of the diaphragm; may include spleen or localized extranodal disease

Widespread in the tissues

Malignant disease of plasma cells which proliferate in bone marrow and destroy surrounding bone (bone factures)

Patients older than 65

Punched-out holes ("lytic lesions"
Hypercalcemia - high calcium = super thirsty
Renal Failure
Anemia
Leukopenia

your body's normal reaction to an injury that causes bleeding. (how we stop bleeding)

Vascular
Platelet
Coagulation

Steps needed to take in order to convert fibrinogen (soluble) to fibrin (non-soluble)

Intrinsic
Extrinsic

by external trauma that causes blood to escape from the vascular system.

by damage inside the blood vessel.

Common pathway

Tissue thromboplastin (Factor III) > Factor VII with calcium > common pathway

Factor XII > Factor XIIa > Factor XI > Factor IX > common pathway

Platelets, Ca2+, and Factor V help convert PROTHROMBIN TO THROMBIN

It helps convert Fibrinogen to Fibrin

Helps with clotting, stops blood.

PTT (partial thromboplastin time)
PT (prothrombin time) & INR (international normalized ratio) test

Intrinsic pathway

Extrinsic pathway

blue top with sodium citrate

Removes the calcium so the blood does NOT clot.

Plasma

Within seconds

a blood test that measures how long it takes for blood to clot.

The problem is in the EXTRINSIC PATHWAY

The problem is in the INTRINSIC PATHWAY

intrinsic, extrinsic and Common pathway

coagulation tests that help determine the cause of a prolonged clotting time by distinguishing between a factor deficiency or an inhibitor.

Mixing Half of plasma sample and half of normal patient

Factor deficiency

Inhibitor

aplastic anemia
leukemia
drugs
infectious agents

systemic lupus erthematosus
various forms of hemolytic anemia
drug-induced hemotologic disorders
idiopathic thrombocytopenia purpura (ITP)

blood disorder characterized by low platelet count.

In ITP, there is an excess of blood clotting formed with the help of vW factor due to autoantibodies that inhibit ADAMTS13

ADAMTS13 is primarily synthesized in the liver, and its main function is to cleave von Willebrand factor (VWF) anchored on the endothelial surface, preventing excessive platelet adhesion and reducing the risk of thrombosis.

8-10 days

spleen

Splenomegaly/ hypersplenism

disseminated intravascular coagulation

serious disorder in which the proteins that control blood clotting become overactive. Systemic activation of platelets

tiny

ischemic strokes

small tiny clots are forms which cause ischemic strokes and depletes all coagulation factors, so patients is bleeding internally.

TPA, tissue plasminogin activator, which breaks down clots

this anticoagulant will kill the patient. Person does not clot bc there is no coagulation factors, so person will clot and bleed internally more. Platelet will decline because platelets are being consumed.

a rare, inherited blood disorder that causes weak platelets due to deficiency or defect in alpha IIb/IIIa platelet integrin. FIBRIN CAN'T BIND TO PLATELETS

Creatinine and Urea

suggests that your kidneys may not be working properly. If urea nitrogen levels are higher than normal, it can affect platelets ability to bind to fibrin.

infection, tumors, shock

degrades fibrin polymers and destroys clotting factors; which causes abnoraml bleeding

factor VIII (8)

Factor IX (9)

True, mostly in males

Yes, mostly in males (x-linked recessive because males have one X chromosome and one y chromosome)