Hematologic system

Components of the blood

• plasma

• Rbc

• WBC

• Platelets

Plasma

• caries antibodies and nutrients to tissues

• Carries waste away

• Consists mainly of proteins

What proteins do we find in the plasma

• albumin

• Globulin

• Fibrinogen

Coagulation factors

Will be found in the plasma which will be part of the coagulation cascade

Erythrocytes (RBC) shape and why

• donut shape

• Have no nucleus

• The can deform to fit in narrow capillaries

Erythrocytes RBC life span

80 to 120 days

Cannot divide

Erthropoiesis

Formation of new red blood cells

1. If the kidneys that filter the blood realize there is low oxygen

2. The kidney will secrete Erythropoietin

3. which is the signal for proliferation and maturation in the bone marrow

4. The stem cells will cause the proliferation of the stem cells leading it to maturation

5. Once matured the cell will extrude the nucleus

6. The nucleus will combine with the reticulocytes

7. Then you have red blood cells

Don’t need to know

Reticulcocytes

Are the precursors for the red blood cell

Chronic kindny failure

Usually bare going to be suffering from anemia

Low red blood cell, htc, hemoglobin,

Leukocytes WBC

Help fight infections

WBC count

5,000 to 10,000

Higher than 10,000

Means infection or inflammation

Leukocytes divided into 2

• granulocytes

• Agranulocytes

Granulocytes

Neutrophils

Basophils

Eosinophils

Agranulocytes

Macrophages

Lymphocytes ( B cells,T cells, and natural killers)

Leukocytes distribution

Never let monkeys eat bananas

Neutrophils - most

Lymphocytes

Monocytes

Eosinophils

Basophils- least

Thrombocytes (platelets) concentration

• 150k to 450k

Thrombocytes (platelets) Is

Essential to normal blood clotting.innate the coagulation cascade.

Blood dyscrasis - problems in the blood

• trauma

• Chronic disease

• Surgery

• Malnutrition

• Drugs

• Toxins

• Radiation

• Genetics and congenital Defects

• Sepsis

She said just read for summary 👀

Hemoglobin men

14-16.5

Hemoglobin women

12- 15

Hematocrit men

40% to 50%

Hematocrit Women

37% to 47%

Mean corpuscular volume - normocytic

Size of RBC

80 to 100 Fl/red cell

Macroscytic anemia

Bigger than 100

Microcytic anemia

Smaller than 80

Mean corpuscular hemoglobin concentrations

How much hemoglobin is in red bleed cell

Low; pale in color

Anemia

Low hemoglobin, low hematocrit , low red blood cells

Anemias overall

Is less than 12 hemoglobin

Nutritional anemia

• iron deficiency anemia

• Vitamin B12 anemia

• Folic acid Anemia

Hemolytic anemia

Red blood cells that break down

• sickle cell anemia

• Thalassemia

Aplastic anemia

Bone marrow depression

• low RBC, Low WBC, Low Platelets

Can be caused by chemotherapy

Microcytic

Less than 80

• iron deficiency

• Thalassemia

• Anemia of chronic disease

Iron deficiency anemia caused

Caused by blood loss. Because we can’t recycle RBC but we can reuse iron from those other RBC, but if we don’t have enough RBC we will lose iron

Iron deficiency examples

• trauma

• Loss blood in the GI normally unknown

• Women if the have heavy menstrual

• Loss blood through urine

• Inadequate diet

• Pregnancy

Symptoms of anemia start showing when

Hemoglobin is 7-8

General anemia symptoms

• fatigue

• Weak

• Shortness of breath causing them to have tachycardia

• Pallor skin

• Brittle nails

• Glossititus (inflammation of tongue

• Decrease mental alertness

• Pica (eating dirt and other random things)

• Pagophagia (eat ice constantly)

Anemia lab findings for iron deficiency

Low ferritin

Microcytic RBC

Hypochromic: low MCHC ,pale blood cells

Increase Total iron binding capacity

Increase Total iron binding capacity for iron deficiency

total Iron finding capacity has a inverse relationship with iron. So if you have a lot of iron, you will have low iron finding capacity, but if you have low iron, you have an increase of total iron finding capacity.

Iron deficiency Anemia treatment

Fe iron supplement

Vitamin C improves reabsorption of iron

Improve diet

What will prohibit iron from being absorbed?

Milk

Thalassemia

Genetic defect that result in a or b chain hemoglobin

A thalassemia genetic defect

• Asian population

A thalassemia has 4 genes that are involved of the synthesis of the alpha-chain

4 genes that are involved of the synthesis of the a-chain

Asymptomatic = a-chain

1 defective gene

Fatal= a -chain

All 4 alpha genes are defective

Control of synthesizing of the B chain for B-thalassemia are

2 genes

Asymptomatic - B thalassemia minor

1 defective gene

B thalassemia major or cooley’s anemia

2 defective genes

Will need blood transfusions

B thalassemia effects

Mediterranean

• Italy and Greece peoples

Hemoglobin molecule

Is found in red blood cell, it helps us move iron around (so iron can help move oxygen around the body)

1. We have 2 A chains and 2 B chains, but they are mutated

Thalassemia blood cells

Are smaller and pale

Macrocytic

Over 100

• vitamin B12 deficiency

• Folate deficiency

Pernicious anemia

1. Vitamin B 12 found in animal products need to attach to intrinsic factor but can’t because we have low amount

Pernicious anemia Causes

• autoimmune disorder that destroy parietal cells (make intrinsic factors)

• Gastrectomy removal (also takes parietal cell that make intrinsic factors that absorb vitamin b12)

Vitamin B12 deficiency manifestations

Gastrointestinal

• glossitis

• Anorexia

• Diarrhea

Neurological

• numbness and parenthesis in extremities

• Weakness

• Ataxia

Vitamin12 last stage vs beginning stage

If you’re in the last stage, you can’t reverse it. If you were in the beginning stage and have numbness and all of the symptoms of the neurological, you can reverse it.

Vitamin B 12 deficiency diagnosis

Low Hbg and HTC

Over 100

Schilling test - they give a person marked vitamin b12 and then check there urine for 24 hrs. If in the urine absorption was done and if not then it would come out in the poop. So

So now they know that the are missing intrinsic factor and can treat the person

When you can have vitamin b12 deficiency

You can have vitamin B 12 deficiency and not pernicious anemia. There’s anemia is only when you’re lacking of intritic factor.

Vitamin B12 pernicious anemia

• give vitamin B12 shots there whole life every week and later 1 time a month

Folic acid deficiency anemia causes

• Larger than 100

• Poor nutrition

• ETOH alcoholism

Folic acid manifestation

• pallor

• Fatigue

• Palpitations

• GI symptoms

• No neurological symptoms

Folic acid deficiency treatment

• supplements

• Increase dietary intake, fruits, nuts, and vegetables

Sickle cell anemia

Defective hemoglobin molecule instead have HBG S

The issue with these S shaped hemoglobins is that they’re going to have a difficult time going through tiny capillaries and will end up plugging the cite

This leads to ischemia and pain because since it’s plugged, no oxygen can go through

Factors/ triggers that exhibit sickling all lead to decrease O2

• Hypoxia

• cold - Extreme temperatures

• Stress

• Physical exertion

• Dehydration*

• Illness

• Excessive exercise

• Infection

• Elevated blood viscosity

• High altitudes cause low oxygen

People with sickle cells it’s important to keep them

Hydrated

Sickle cell occlusion

1. In b hemoglobin we have a mutation

2. The hemoglobins when the oxygenated will begin sickling

3. There’s a point that it will be irreversibly sickled

4. Causing vessel occlusion leading to ischemia and infraction

Sickle cell manifestations

• pain

• Hemmat hematuria

• Lethargy

• Irritability

• Pale lips, tongue, palms, and nail beds

• Stroke

• Splenomegaly - gets swollen

• babies will be OK until they’re six months old

Sickle cell diagnosis

• genetic testing

• Hemoglobin electrophoresis

• Increase erythrocytes sedimentation rate mean inflammation

• High iron

• Low RBC survival

• Reticulocytosis high number

Treatment for sickle

• hydration

• Avoid low oxygen

• Give oxygen

• Pain management

Sickle cell anemia type

Autosomal recessive disorder

But in homozygous both are effect 80-90%

With heterozygous normally, they are not affected they’re just carriers, but with sickle cells 40% of them will be altered

Normocytic

• anemia of chronic disease

• Aplastic anemia

• Chronic renal failure

• Post hemorrhagic

Thrombocytopenia plaletes normal

150k - 450k

If we have abnormal amount of platelets

You will have bleeding

Thrombocytopenia levels

Less than 150,000

Causes of of decrease plaletes - thrombocytopenia

1. Immune thrombocytopenia purpura

2. Thrombotic thrombocytopenic purpura

3. Secondary thrombocytopenia

Immune thrombocytopenia purpura

Autoimmune disorder

Thrombotic thrombocytopenic purpura

ADAMTS 13

Secondary thrombocytopenia

Due to medication such as heparin example HIT

HIT (heparin induced thrombocytopenia)

Person is receiving Heparin and they began making antibodies against heparin

1. The are making antibodies against the plaletes

2. Those plaletes get removed by the spleen

3. Causing low platelets in blood causing thrombocytopenia

HIT (heparin induced thrombocytopenia)

It’s called this when more than 50% reduction of plaletes

HIT (heparin induced thrombocytopenia) Treatment

Stop heparin

HIT manifestation

• start bleeding

• epistaxis (nose bleed)

• Menorrhage (leading to excess menstral cycle)

• Hematuria

• GI bleeding blood in fecces

• Petechia or purpura

• Tachycardia

• Shortness of breath

• Change in mental status

• Death

Thrombocytopenia diagnosis

CBC- plaletes count

Coag studies - PT/PTT

Platelet antibodies studies

Coagulation studies

PT/PTT check because if higher than normal

It tells them if coagulation is take too long due to low platelets count

If they make thrumbus quickly they will have low PT/PTT

Thrombocytopenia treatment

• steroids

• Platelet transfusions

• Splenectomy

• Educate on risk of bleeding

• Thrombocytopenic precautions

Hemostasis

1. Vessel spasm- vascular construction

2. Formation of platelet plug aggregation

3. Formation of insolvable, fibrin clot - blood clotting coagulation cascades

4. Once healed clot dissolution

Coagulation casacade

1. Intrinsic and extrinsic pathway make fiber 10 xa and ca++

2. Fiber 10 makes prothrombin

3. Prothrombin makes Thrombin

4. Thrombin makes the transformation from fibrinogen to fibrin

What stops fibrin when it’s done

Anti thrombin 3 will inhibit thrombin and factor 10 when you don’t need anymore fibrin

Anti thrombin works

With heparin to stops factor 10 and fibrin

Other anticoagulant

Coumadin stop 2,6,4,5 need blood test constantly, taken by mouth

10 factor medication

Rivoroxaban

Coagulation casacade medications

Heparin

What dissolves fibrin in last stage

plasminogen gets activated by TPA and makes plasmin that dissolves Thrombus

Anti coagulation

Is to prevent thrombus

Anti plaletes medication

Avoid new aggregation of plaletes

Formation plug

1. We have vessel that broken down cause you got a cut

2. Outside that vessel is going to be exposed to the plaletes

3. Meaning collagen will be exposed

4. Von willeband factor will be attached to collagen

5. Next to it will have factor 8 and a platelet

Platelet plug release

ADP and TXA2 To attract more plaletes

2 medications that will effect ADP and thromboxane

Aspirin- inhibit thromboxane

Clopidogrel = plavix inhibit ADP

these are anti platelets

Regulation of blood coagulation factors

Protein C and protein S the work the same way as anti thrombin

work as anticoagulant - protein c

Accelerates the action of protein c- protein s