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Advanced Pathophysiology: Blood Cells and Anemia Overview, Exams of Pathophysiology

A.T. Still University of Health Sciences (ATSU)Pathophysiology

An overview of blood composition, blood cells, and anemias. It covers hematocrit, types of blood cells (erythrocytes, leukocytes, platelets), and their functions. It also discusses alterations in leukocytes, platelet pathology, and blood proteins like albumin and globulins. The document delves into the classification, symptoms, and causes of various types of anemias, including iron deficiency anemia, thalassemia, and aplastic anemia. It also touches on the diagnostic approaches for different anemias, such as microcytic, normocytic, and macrocytic anemias, and their respective lab values. Useful for medical students and healthcare professionals seeking a concise review of hematology and anemia.

Typology: Exams

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Advanced Pathophysiology Exam #2

Overview of the Blood -

•Blood☑️

•5000ml

•Plasma

•3000ml

Hematocrit defined -

- % of RBCs☑️

[higher value = higher viscosity = thicker blood)

- Example: Polycythemia may have Hct of 60-70%

Types of Blood Cells

- Erythrocytes [RBCs) -

- Transport O2☑️

- Small disc shape

- Lifespan = 120 days

- Carry Hgb [ferrous oxide, also an acid/base buffer)

- Made in the bone marrow - Iliac crest for sample in leukemia

[after age 20 in the vertebrae, sternum, ribs, iliac)

- Hgb Levels: 14-16g/dL in males / 12-14g/dl females

Cytic vs Chromic -

Cytic = Size of RBCs☑️

Chromic = Amount of Hgb

MCV and MCHC -

MCV: Mean corpuscular volume - [average size rbc]☑️

MCHC: normal Mean corpuscular Hgb concentration - [average amount of hemoglobin in the RBCs

compared to the average size of the RBCs. The amount of hemoglobin that was there

Morphology Size or Erythrocyte Volume Cytic Values -

- Normocytic: Normal RBC size☑️

[MCV = 83-99)

- Microcytic: Small RBC size

[MCV = 50-82)

- Macrocytic: Large RBC size

[MCV is > 100)

Chromic Values

[Hgb content) -

- Normochromic: Normal amount of Hgb [MCHC -Average amount of hemoglobin in the ☑️

RBCs compared to the average size of the RBCs.

[MCHC = 32-36)

- Hypochromic: Low amount of Hgb

1

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Advanced Pathophysiology Exam

Overview of the Blood - ☑️ •Blood •5000ml •Plasma •3000ml Hematocrit defined - ☑️ - % of RBCs [higher value = higher viscosity = thicker blood)

Example: Polycythemia may have Hct of 60-70% Types of Blood Cells
Erythrocytes [RBCs) - ☑️ - Transport O
Small disc shape
Lifespan = 120 days
Carry Hgb [ferrous oxide, also an acid/base buffer)
Made in the bone marrow - Iliac crest for sample in leukemia [after age 20 in the vertebrae, sternum, ribs, iliac)
Hgb Levels: 14-16g/dL in males / 12-14g/dl females Cytic vs Chromic - ☑️ Cytic = Size of RBCs Chromic = Amount of Hgb MCV and MCHC - ☑️ MCV: Mean corpuscular volume - [average size rbc] MCHC: normal Mean corpuscular Hgb concentration - [average amount of hemoglobin in the RBCs compared to the average size of the RBCs. The amount of hemoglobin that was there Morphology Size or Erythrocyte Volume Cytic Values - ☑️ - Normocytic: Normal RBC size [MCV = 83-99)
Microcytic: Small RBC size [MCV = 50-82)
Macrocytic: Large RBC size [MCV is > 100) Chromic Values [Hgb content) - ☑️ - Normochromic: Normal amount of Hgb [MCHC -Average amount of hemoglobin in the RBCs compared to the average size of the RBCs. [MCHC = 32-36)
Hypochromic: Low amount of Hgb

[MCHC is < 32)

Hyperchromic: Increased amount of Hgb [MCHC is > 36) Leukocytes [WBCs) - ☑️ - Defend the body against foreign proteins
Made in the bone marrow
9,000/mm^
CBC w/ Diff shows: Leukocytes broken down into: Neutrophils, Basophils, PMNs [polymorphonulcear), Bands Bands - {Infective process - ☑️ -Immature Leukocytes
Indicate an infective process
Increase in bands = 12 to 20 or more = shift to the left indicating a bacterial infection
If bands are not increased it is a shift to the right and a viral infection Alterations of Leukocytes Quantitative:

Bone marrow dysfunction
Premature destruction of cells a. May originate in lymphoid organs secondary to infectious process - ☑️ Leukocytosis equals increase WBC's Leukopenia Equals decreased wbc's Types of Leukocytes:

Granular - ☑️ - Categorized according to the presence or absence of granules in the cell cytoplasm
Granular Leukocytes:
PMNs - Polymorphonuclear leukocytes[2 or more lobes to the granular site)
Neutrophils
Eosinophils - Allergic reaction or parasites
Basophils Types of Leukocytes:
Non-granular - ☑️ Non-granular Leukocytes :
Lymphocytes
Monocytes
platelets or thrombocytes WBC Morphology/Fx [Shape and function] - ☑️ - Total WBC count increases with infection
As % of 1 increases, the %s of the others will decrease [shift in %) = Shift to the left or shift to the right

Blood Proteins

Albumin - ☑️ - Normal range is 3-
Sponge Responsible for blood osmotic pressure aka oncotic [pulling) force - Albumin and its presence in the bloodstream and with it , hydrostatic pressure and oncotic pressure functions and blood returns to the vascular tree.
Assists with wound healing Problems with low albumin levels - ☑️ - Low albumin = low oncotic pressure = leakage of fluids into the interstitial space = ascites and edema of dependent extremities
Albumin Usually <2 is incompatible with life although Reavis has seen people come back low albumin levels - ☑️ - Decreased albumin is usually from decreased liver fx
Reavis says that giving albumin IV does nothing because it doesn't stay in the vessels, it leaks out. Reavis surgeon story about Albumin - ☑️ - Liver CA pt had 19L of paracentesis fluid removed
MD filtered it and put it back into the pt IV which caused a spike in albumin resulting in a spike in oncotic pressure resulting in a crisis and increased CVP Blood Proteins
Globulins - ☑️ - Alpha
Beta
Gamma [Part of the inflammatory / immune process)
May be used to transport molecules Anemias - ☑️ - Not a disease
Reduced number of RBCs or quality/quantity Hgb
O2 carrying capacity of Hgb is reduced S/S of Anemias - ☑️ - Hypoxia
Night cramps
Angina
Fatigue
Weakness S/S of Anemias continued - ☑️ - Dyspnea with pallor
Tachycardia, palpitations, systolic murmur, hypertrophy, HF
Increased Epogen = bone pain and sternal tenderness
Increased 2, 3, DPG = reduction in Hgb affinity for O

What is the #1 Diff Dx for pt's c/o fatigue? - ☑️ ANEMIA Anemia Patho - ☑️ - Defined as a Hgb less than 10

Pernicious Anemia: = Lack of B12 and/or intrinsic factor)
Hypoxia [rate of RBC production is increased by erythropoietin in response to this
Bone Marrow suppression due to CA, drugs, radiation, chemo)
Disorders of hemostasis
Disorders of Leukocytes 5 Classifications of Anemias by etiology - ☑️ - Altered Hgb synthesis
Altered DNA from deficient nutrients
Stem Cell dysfunction
Bone marrow infiltration
RBC Destruction Class of Anemia:
Altered Hgb Synthesis - ☑️ - IDA (Iron deficiency anemia)
Thalassemia
Anemia of chronic disease Class of Anemia:
Altered DNA from deficient nutrients - ☑️ - Pernicious anemia [B12) Class of Anemia:
Stem Cell dysfunction - ☑️ - Aplastic anemia [cells not made at all)
Myeloproliferative leukemia Class of Anemia:
Bone marrow infiltration - ☑️ - CA
Lymphoma Class of Anemia:
RBC / Erythrocyte Destruction - ☑️ - Blood loss
Hemolysis INTRAcorpuscular [cell itself)
- Hgb S [sickle cell)
- G6PD [Oxidation-Glucose-6-phosphate dehydrogenase deficiency)
EXTRAcorpuscular [outside the cell)

☑️ - Iron deficiency anemia

Anemia of chronic disease
Labs to help differentiate: -a. Transferrin
b. Serum Fe
c. Ferritin
d. TIBC Pathology when the pt is Normocytic and Normochromic - Cell size normal / MCHC is normal - ☑️ MCV 82-92, MCHC 32-
Hemorrhage - acute blood loss
Hemolysis
Chronic diseases [ draw TIBC [total iron binding capacity] low and ferritin rises = anemia of chronic disease that is early on Anemia [aplastic and early iron deficiency] - ☑️ - EARLY iron deficiency [transferrin rises [when iron stores in body are low] and ferritin falls[blood cell contains iron] =Iron deficiency anemia
Aplastic Anemia - Cancer hypoplastic cell invading the bone marrow where red blood cells are made Macrocytic Values - ☑️ - Big RBCs MCV > 100 MCHC > 36 3 Types of Macrocytic Anemias
B12 deficiency
Folic acid deficiency
Antimetabolites - ☑️ - Low B12: normal folate
Must be used with Intrinsic factor which is missing from the stomach
Low B12 and normal Folate
Tx: B12 injections
Folic acid deficiencies:
Low folate
Causes neural tube deficits
Tx: Oral folic acid Macrocytic Anemias - Antimetabolites - ☑️ - Antimetabolites:
Pernicious [destruction of parietal cells /Gastric mucosa = no production of intrinsic factor which absorbs B12)
Tx: B Reavis pt story about B12 - ☑️ - Has a pt that comes in for B12 shots because it gives them more energy
Insurance does not pay for this bc the pt lacks a dx of pernicious anemia

Etiology of B12 Deficiency - ☑️ - Inadequate intake

Decreased absorption
Inadequate utilization
Usually occurs in the 5th or 6th decade of life Forms of B12 deficiency - ☑️ - Pernicious
Autoimmune disease producing autoantibodies to gastric parietal cells and their secretory produce [IF) - necessary for B12 absorption
Crohn's disease
Whipple's disease
Sprue [Increased cases)
Post Gastrectomy (B/c the parietal cells have been removed) -Drugs / Chemotherapy RDA [Recomm. Daily Allowance) of B12 - ☑️ - 2 micrograms/day [avg person gets 3-9/day)
Alcoholics are usually low in B12 because according to Reavis they only buy alcohol and not food so they have low dietary intake S/S of B12 deficiency - ☑️ 1.* Smooth/beefy red tongue + atrophy on top [atrophic glossitis) - not tongue rugae

- Fatigue
- Malabsorption/diarrhea from megaloblastosis of epithelial cells of small intestine 4.- Paresthesia/numbness from peripheral neuropathy / lesions in posterior-lateral columns spinal cord/cerebrum) S/S of B12 deficiency continued - ☑️ 5. Loss of vibratory and position sense

a. Loss of Sensory ataxia
b. Positive Romberg - balance test with eyes closed
c. Weakness
d. Spasticity

Cerebral manifestations: -a. Personality changes and memory loss -b. Psychosis Folate Deficiency - ☑️ - Etiology: Dietary deficits

S/S: Similar to B12 but WITHOUT NEURO SYMPTOMS
- So fatigue
Tx: PO Folic Acid
Dietary counseling with foods high in folic acid Foods high in Folic Acid -

Increased intestinal iron absorption
Deposited ino the liver, pancreas, heart, joints, pituitary gland and endocrine glands
This causes progressive tissue damage and functional impairment Hereditary Hemachromatosis (HH) Patho continued Not on lecture - ☑️ - Normally crypt cells have HFE protein that facilitates transferrin receptor dependent iron uptake
Disorder in crypt cells of the duodenum
HFE protein malfunctions cause relative iron deficiency = an increase in DMT- [Divalent metal iron transporter 1) -Equals increase in intestinal absorption S/S of Hereditary Hemachromatosis [HH) - ☑️ - Fatigue
Abdominal pain
Arthralgia
Weight loss
Change in skin color [marked)
- Decreased libido
Palpitations
Menstrual changes
Impotence [of both sexes according to Reavis)
Cirrhosis
Diabetes Diagnosis of Hereditary Hemachromatosis (HH)
Labs - ☑️ -CBC with deifferential
Elevated Transferrin saturation
Elevated ferritin levels
- Fasting in the AM when levels are the highest
Liver Bx [quantitative hepatic iron) Treatment of Hereditary Hemachromatosis (HH) - ☑️ - Early Dx and Tx prevent long-term complications
Goal is to remove excess iron periodically through:

Repeated phlebotomy - donate blood *Most efficient and least expensive Treatment of Hereditary Hemachromatosis (HH) cont - ☑️ **a. Donate blood [1-2 pints weekly) 1 Pint = 473mL until the levels decrease.
- Can take 2-3 years
b. Maintenance is blood donation every 3-4 months
- Monitor transferrin sat & ferritin levels annually

Hereditary Hemachromatosis (HH)

Dietary Changes - ☑️ - Avoid large amounts of red meat [high in iron)
Restrict iron supps or multivits high in iron
No vit C supplements [< or = to 500mg/day)
In absence of cirrhosis, alcohol intake in moderation
No raw shellfish
Black tea and grains help bind iron [this plays a minor role) Prognosis of Hereditary Hemachromatosis (HH)
Liver / spleen decrease in size - ☑️ - LFTs return to normal, but cirrhosis is irreversible
Check for hepatocellular carcinoma
Skin pigmentation decreases
Cardiac dysfunction improves
Diabetes may NOT improve, but disease progression may SLOW
Arthralgia, impotence, menstrual problems may NOT improve Increased Epogen = - ☑️ - Increased bone pain
Sternal tenderness Causes of Leukocytosis - increased WBC's - ☑️ - Infectious organisms
Exercise
Emotional changes
Temp changes
Anesthesia, surgery
Pregnancy
Drugs
Hormones
Toxins Alterations of Leukocytes - can be quantitative - ☑️ Quantitative

Bone marrow dysfunction 2.Premature destruction of cells a. May originate in lymphoid organs secondary to infectious process Leukocytosis is a defense mechanism... - ☑️ - Absolute Leukocyte count that is HIGHER than normal

Allergic disorders
Atopic dermatitis
Eczema
Pemphigus
Scleroderma
Parasitic infestation 1st thing to think about when you have a pt with watery diarrhea and Eosinophilia? - ☑️ - Gastroenteritis from a parasitic infection Basophilia - ☑️ - Too many Basophils
Response to inflammation/hypersensitivity
Contain histamines
Caused by:
Myeloproliferative disorders like
CML
Meyloid metaplasia = basophilia Basopenia [HASO] - ☑️ - Too few basophils
Caused by:
Hyperthyroidism
Acute infection
Long-term steroid therapy
Ovulation and pregnancy Lymphocytes and Infectious Mononucleosis [Mono) - ☑️ - Acute
Self-limiting
Neoplastic lymphoproliferative syndrome
Infection of B lymphocytes
From the EBV
Etiology: viral transmission, oral/fecal Lymphocytes and Infectious Mononucleosis - ☑️ - Incubation period is 30-60 days
Diagnosed with blood tests
Monospot may be false positive)
Heterophilic antibody test is the MOST ACCURATE way to dx Mononucleosis - HAT test Leukemia - ☑️ - Clonal malignant disorder of blood / blood forming organs

Accumulation of dysfunctional cells
Loss of cell division regulation causing uncontrolled proliferation of leukocytes which:
- causes overcrowding of bone marrow
- and decreased production and function of normal hematopoietic cell 4 Types of Leukemias - ☑️ - (ALL): Acute Lymphocytic
(AML): Acute Myelogenous
(CLL): Chronic Lymphocytic
(CML): Chronic Myelogenous Classes of Leukemias - ☑️ 1. Acute or chronic comes as Undifferentiated or immature [blast) cells

*Myeloid or Lymphoid Leukemia arise from:

80% are from B cells
15% - 20% are from T cells Acute Leukemias - ☑️ - Usually seen in the neonate period
Onset is abrupt
Survival is short Most common genetic error resulting in Leukemia - ☑️ - Reciprocal translocation between chromosomes 9 and 22 (Philadelphia chromosome) Chronic Leukemias - ☑️ - Have mature cells, but they don't function normally
Onset is gradual
Survival is longer ALL is most commonly seen in... - ☑️ Kids Clinical Manifestations of ALL - acute lymphocytic leukemia - ☑️ Anemia Bleeding DIC Infection Weight loss Bone pain -Elevated uric acid [by product of protein catabolism, urate concentration secondary to dehydration caused by anorixa or fever and drug TX]
TX: Chemotherapy, supportive TX, allopurinol for gout, bone marrow transplants CML [Chronic Myelogenous Leukemia) - ☑️ - Clonal, neoplastic expansion of multipotent myeloid stem cell [myeloproliferative disease) -NEB cells

Patho of Lymphoma - ☑️ - Expression of cytokines and hematopoietic growth factors by malignant cells

Complex autocrine and paracrine loop
Stimulate both malignant and nonmalignant stromal cells
Proliferative and secrete other growth factors S/S of Hodgkin's Lymphoma - ☑️ - Enlarged, painless mass, most often in the neck, but may be mediastinal [Growth of the mass is from cytokines and growth factors secreted by malignant cells)
Lymphadenopathy from local symptoms associated with pressure/obstruction S/S of Hodgkin's Lymphoma cont - ☑️ - Intermittent fever
Weight loss
Infection
Night Sweats
Splenomegaly-
Pruritis - itching Lab Findings of Lymphoma - ☑️ - Thrombocytosis
Leukocytosis
Eosinophilia
Elevated erythrocyte sedimentation rate (ESR)
Elevated alkaline phosphatase Diagnostic Indicator of Hodgkin's - ☑️ *** Reed-Sternberg cells with biopsy Non-Hodgkin's Lymphoma - ☑️ - Diverse group of disorders with malignant lymphoid system NOT microscopically like lymphoma
Etiology: UNK Findings of Non-Hodgkin's Lymphoma - ☑️ *Molecular rearrangements of oncogenes and immunoglobulin genes

Chromosomal mutations transform or lose critical oncogenes and tumor-suppressor genes environmental agents
Inherited genetic abnormalities NHL [Non-Hodgkin's Lymphoma) Evaluation and Management - ☑️ 1. Staging
Biopsy of nodes and bone marrow
Treatment Depends on stage, symptoms, age, co-morbidities A. Radiation, chemotherapy, bone marrow or stem cell transplant, monoclonal antibodies

Differences between Hodgkin's and Non-Hodgkin's (Page 1028, Table 29-7)

Spread - ☑️ - Hodgkin's:
Orderly spread by continguity
Non-Hodgkin's:
- Non-continguous spread - not orderly spread Differences between Hodgkin's and Non-Hodgkin's (Page 1028, Table 29-7)
B Symptoms [fever, Weight loss, Night sweats) - ☑️ - Hodgkin's:
- Common - to have B Symptoms [fever, Weight loss, Night sweats)
Non-Hodgkin's:
- Uncommon Differences between Hodgkin's and Non-Hodgkin's (Page 1028, Table 29-7)
Extranodal Involvement - ☑️ - Hodgkin's:
- Rare Extranodal Involvement
Non-Hodgkin's:
- Common Extranodal Involvement Differences between Hodgkin's and Non-Hodgkin's (Page 1028, Table 29-7)
Extent of disease - ☑️ - Hodgkin's:
- Often LOCALIZED disease
Non-Hodgkin's:
- Rarely localized, normally WIDESPREAD disease Differences between Hodgkin's and Non-Hodgkin's (Page 1028, Table 29-7)
Nodal Involvement - ☑️ - Hodgkin's:
- Localized to single axial group of nodes
- Mesenteric nodes and Waldeyer ring RARELY involved
Non-Hodgkin's:
- Multiple peripheral nodes
- Mesenteric nodes and Waldeyer ring COMMONLY involved Reavis story about pt with abd. mass r/t lymphoma - ☑️ - Pt c/o abd. mass, exploratory surgery was done, when pt opened up, their entire mesenteric nodes were one giant lymphoma. No resection was done, pt was closed up and send to oncologist.

S/S of Thrombocythemia - ☑️ - Hyperplasia of megakaryocytes

Splenomegaly
Periodic hemorrhages or thrombosis or both Alterations of Platelets/Coagulation - ☑️ 1. Purpura [start with this)
Diffuse hemorrhage into the skin -2. Thromboembolic disease [Coagulation proceeds needlessly)
1. Thrombocytopenia: Platelet count < 100,000/mm [symptomatic until count is < 10K)
2. Psuedothrombocytopenia is from a lab error [repeated lab test] S/S of ITP [Immune Thrombocytopenic Purpura) - ☑️ - Purpura
Weight Loss
HA
Fever Causes of Thrombocytopenia - ☑️ 1. Congenital [TAR syndrome, Wiskott-Aldrich or other gene etiologies)

Acquired [more common) a. Decreased platelet production [2ndary to viral infection, drugs, chemo, nutritional deficits, chronic renal failure, bone marrow hypoplasia, radiation, or bone marrow infiltration by CA] Causes of Thrombocytopenia cont - ☑️ 3. Acquired Increased platelet consumption a. Heparin induced) [HIT) b. ITP [Immune Thrombocytopenic Purpura) c. TTP [Thrombotic Thrombocytopenic Purpura) Heparin Induced Thrombocytopenia (HIT)
Common cause of drug induced thrombocytopenia a. 4% incidence, but lower with low-molecular wt hep - ☑️ 2. Immune mediated IgG antibodies against the heparin-platelet factor 4 complex = platelet activation throught platelet FcyIIa receptors Which Increases factor 4 and activated thrombin = increased platelet consumption = 5 - 10 days after initiation

Heparin Induced Thrombocytopenia [HIT)

S/S
Dx
Treatment - ☑️ - S/S:
50% decrease in platelet count
30% also at risk for DVT
Bleeding is UNCOMMON even with low platelet counts
Dx: Platelet counts, HIT antibodies
Treatment: Withdraw heparin - bleeding cascade will return to normal Immune Thrombocytopenia Purpura [ITP) - ☑️ - Formerly "Idiopathic"
IgG adheres to the platelet and initiates destruction
Other antibody-producing tissues produce autoantibodies
Chronic form common in adults, more often females
Acute form more common in children Reavis note on Heparin Induced Thrombocytopenia [HIT) - ☑️ Heparin given pre-op to prevent blood clots and another dose post-op. Pt will develop HIT 5-10 days later at home Reavis clinical story about ITP [Immune Thrombocytopenia Purpura - ☑️ 27 y/o migrant female with "rash"
Pt ststed she had virus 3 weeks prior
Had large purpura on her legs, arms and torso
Also c/o HA and fever, weight loss [Most likely residual from virus)
Platelet count was 50
Sent to the ER
Bone marrow bx to confirm dx of ITP
Treated with steroids Treatment of ITP [Immune Thrombocytopenia Purpura - ☑️ - Palliative not curative
Steroids to stop sequestering [in the spleen) and destruction
IgG
Anti-RhD
Immunosuppressive agents as last resort
For chronic relapsing: inactivation or removal of site of platelet destruction [the spleen) so a splenectomy Thrombotic thrombocytopenic purpura (TTP) - ☑️ 1. Platelets aggregate and cause occlusion

Chronic relapsing a. Rarely seen in children

Advanced Pathophysiology: Blood Cells and Anemia Overview, Exams of Pathophysiology

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