Patho test 4 smaller
Terms in this set (147)
Primary divisions of development of blood cells
Pluripotent stem cell > Common myeloid stem cell > E/Mega/Baso Erythroid Progenitor cell > Procrythroblasts > RBC
A hormone produced and released by the kidney that stimulates the production of red blood cells by the bone marrow.
hormone from liver stimulates platelet formation
a. Reduction in the total number of erythrocytes
b. Reduction in the quantity of hemoglobin
c. Altered structure or function of hemoglobin
General etiology of anemia
1. impaired erythrocyte production
2. Increased rate of erythrocyte destruction
3. Hemorrhage, acute or chronic
any combination of these
General pathophysiology of anemia
1. Decreased O2 carrying capacity of blood
2. Tissue hypoxia
3. Decreased blood viscosity
4. Hypoxic dilation of arterioles, capillaries and venules
Morphological classifications of Anemia: general types
1. Macrocytic - Normochromatic
2. Microcytic - Hypochromatic
3. Normocytic - Normochromatic
Morphological classifications of Anemia: Macrocytic - Normochromatic
Large RBC size and normal cellular Hb concentration
Morphological classifications of Anemia: Microcytic - Hypochromatic
Small abnormally shaped RBC's with lower thannormal Hb concentration.
Morphological classifications of Anemia: Normocytic - Normochromatic
Normal RBC shape and Normal Hb concentration
Macrocytic - Normochromatic: 2 types
Folate deficiency Anemia
Pernicious anemia etiology
Malabsorption of Vit B12 = defective DNA precurse synthesis
Pernicious anemia cause
Defective secretion of Intrinsic Factor (IF) by Parietal cells Required for the absorption of Vitamin B12
Pernicious anemia cause: congenital
Defective mechanism for synthesis, or secretion.
Pernicious anemia cause: acquired
Autoimmune, with genetic predisposition
90% have parietal cell antibodies
Autoimmune may be secondary to anabnormal response to Helicobactor Pylori infection.
Pernicious anemia cause: chronic atrophic gastritis
Alcohol ingestion, Hot tea,Smoking. Helicobactor Pylori
Pernicious anemia pathophysiology
1.Nerve Demyelination lateral and posterior tracts of spinalcord
2.Parethesia of fingers and toes, due to 1.
4. Spasticity and reflex abnormalities
These symptoms are not reversible even with proper treatment.
Pernicious anemia clinical manifestation: initial
1.Pernicious anemia develop slowly over 20 to 30 years. Mean age 60 years old.
2.Frequent infections, decreased WBCfunction
4.Cardiac and Kidney problems
Pernicious anemia clinical manifestation: hypoxia
1.Weakness and fatigue
2. Parethesia of feet and fingers.
3.Nerve demyelination of lateral and posterior tracts of spinal cord, leading to...
5.Red"Beefy" sore tongue
When can pernicious anemia lead to death
Death in 2-3 years of left untreated.
Pernicious anemia tx
IM injections of Vit B12 weekly until corrected then once/month
Pernicious Anemia cannot be cured, thus B Maintenance
Folate deficiency Anemia
Folate acts as a coenzyme for the synthesis of Purines and Thymine.
Hence, deficiency leads to an abnormal DNA synthesis .
Completely essential in diet, adults; 50-200 ug/day, pregnantor lactating mothers need more.
Folate deficiency Anemia etiology
Lack of folate in the diet,
e.g. lacking in vegetables
10% of Americans are deficient in folate stores.
(Also leads to Spina-bifida and Neural tube defects in new-born)
Folate deficiency Anemia pathophysiology
Classical symptoms of anemia, due to hypoxia.
No demyelination or the neurological manifestations seen as inpernicious anemia, unless other vitamins are also lacking.
Folate deficiency Anemia clinical manifestation
Fatigue, weakness, Pallor, with pale mucous membranes.
Cachectic symptoms due to hypoxia and poor diet.
Ulcerations of buccal area and tongue (Red beefy tongue)
Dysphagia, (difficulty swallowing)
Flatulence and watery diarrhea.
Cheilosis, Scales and fissures of the lips
Folate deficiency Anemia tx
1 mg of folate daily for 1 - 2 weeks then a decent diet afterwards.
Anemia in nursing homes
More than half of the residences in nursing homes are anemic. 1/3 of those are caused by Vit B12 deficiency, Folate deficiency, or Iron deficiency.
Microcytic - Hypochromatic types
Iron deficiency anemia
Iron deficiency Anemia
Most common type of anemia in the world
1/5 of world population
Especially in Women in child bearing age.
Fe deficiency in ++Children -> irreversible cognitive impairment.
Iron deficiency Anemia etiology: impoverished nations
A.Decrease intake of iron, iron poor diet,
B.Excessive Blood Loss(Hook worm infestation)
Iron deficiency Anemia etiology: developed nations
B. Chronic blood loss
e.g. 1. excessive menstrual bleeding
2.Gastric bleeding due to Acetylsalicylic acid (aspirin)Non-steroid anti-inflammatory NSAIDSUlcers
4. Cancer with Chronic bleeding and/orChemotherapy
C. 2 year olds, need more iron due to rapid growth
Iron deficiency Anemia etiology: in USA
A.9% of children 1-2 y are Iron Deficient
B.3% are anemic
C.13.9% of females have hypoferremia peaking during reproductive years decreasing after menopause.
E.4-6% of females are anemic
How much blood loss is enough to cause anemia
Iron deficiency Anemia pathophysiology: iron supply
B. Recycled from destroyed RBC
C. Both bound to transferrin in plasma
Iron deficiency Anemia pathophysiology: iron storage
A. Spleen, liver, bone marrow
B. Bound to ferritin or Hemosiderin for storage
Iron deficiency Anemia Stage I
Bodies iron stores are depleted, erythropoesis isnormal
Iron deficiency Anemia Stage II
Iron deficient erythropoiesis begins to decrease
Iron deficiency Anemia Stage III
Small, Hb-deficient cells replace enough normal cells to cause symptoms of anemia
Adaptive response for pathogen exposure.
Lactoferrin & Fever Help deny pathogens iron to survive
Hypoferremia clinical manifestations
Symptoms are gradual and most don't seek medical attentionsuntil Hb = 7-9 g/dl
Hypoferremia clinical manifestations: classical
pallor of mucous membranes,
dry lesions in buccal area with difficulty swallowing.
Cardiovascular compensation symptoms
Hypoferremia clinical manifestations: unique
`Brittle, ridged, concave nails
Hypoferremia clinical manifestations: neurological changes
Most likely caused by Hypoxia
2.Mental confusion and memory loss
3.Headache, numbness, tingling
Chronic iron deficiency in children causes...
irreversible cognitive deficiency
Iron deficiency Anemia evaluation
Iron stores are measured,
1.Directly, Bone marrow biopsy
2.Plasma ferritin and transferrin
Iron deficiency Anemia tx
1.Rule out sources of blood loss
2.150-200 mg/day Fe++ Therapy, 2/3 corrected in 1 month, continued for 6 -12 months
Sideroblastic Anemia etiology
ineffective Fe uptake++ leading to dysfunctional Hb synthesis.
RBC shows irons granules in a perinuclear ring.
Not used for Hb synthesis
Heredity is rare and is a recessive X-linked disease.
Sideroblastic Anemia pathophysiology: congenital
recessive X-linked disease. Female carries show Dimorphism in RBC's
Sideroblastic Anemia pathophysiology: acquired
a.Altered Mitochondrial metabolism causes ineffective Fe uptake —> dysfunctional Hb++synthesis
b.Ferric iron accumulates in erythroblasts
Sideroblastic Anemia pathophysiology: secondary anemia
B.Drug induced. Ethanol, + others
D.Lead or Zinc poisoning
Sideroblastic Anemia clinical manifestation: classical
weakness and fatigue, Cardiovascular and respiratory compensation.
Hb = 4-10 mg/dl
Sideroblastic Anemia clinical manifestation: unique
Signs of Fe overload.
Sideroblastic Anemia evaluation
Definitive diagnosis requires: Bone marrow biopsy
40% of patients with Sideroblastic Anemia develop AML
Sideroblastic Anemia tx
Removal of drugs that might cause the anemia.
Pyridoxine therapy 200-300
Chelation therapy for iron overload.
Prolonged administration of Erythropoietin.
Inversion of an exon in the alpha or beta hemoglobin chains.
Normocytic - Normochromatic types
Post Hemorrhagic Anemia:
Autoimmune Hemolytic Anemia:
Often associated with Panocytopenia, loss of stem cells (Chemotherapy)
Aplastic Anemia etiology
1.Idiopathic 75% No known cause, occurs after the age of 50. Thought to be a defective Telomerase RNA causing shortened telomeres. Premature stem cell death.
2.Secondary to Chemotherapy agents, Radiation, Zinc, Arsenic.
3.Viruses identified as causing Aplastic anemia,HIV, Hepatitis non A, non B, non C & Epstein Barr
4.Tc cell mediated destruction of hemopoietic stem cells.
Aplastic Anemia pathophysiology
Hypoplastic or aplastic bone marrow (little or no stem cells for erythrocytes) Bone marrow replaced with fat
Panocytopenia:All stem cells are reduced or absent.
Multipotent stem cells are unable to proliferate
Aplastic Anemia clinical manifestations: classical
Pallor, Weakness, Dyspnea, Cardiovascular compensation.
Aplastic Anemia clinical manifestations: unique
1.Frequent mild infections due to decrease granulocytes. (Share a common stem cell.)
2.Petechiae, due to lack of megakaryocytes
Aplastic Anemia evaluation
Bone marrow biopsy
Aplastic Anemia old tx
a.Removal possible cause of disease
c.Prevent or treat infections
d.Give more erythropoietin
Aplastic Anemia old tx prognosis
25%die within 4 months
75% die within 5 years
Aplastic Anemia new tx
Bone marrow Transplant from matched sibling
(This produces a 75 - 80% survival rate)
Allo-rejection remains the primary limitation to success
Post Hemorrhagic Anemia etiology
Loss of blood from hemorrhaging
Blood loss levels in healthy young adults
30% total bld loss & tolerate it.
40% = Symptomatic at rest
50%= Severe shock with Lacticacidosis.
How much blood loss can an older adult with heart disease tolerate
How much blood loss can a pediatric pt tolerate
Post Hemorrhagic Anemia Pathophysiology
1.Initially, Hypovolemia, = decreased BP, increased HR. Hct. Normal at first until fluid shifts from intracellular to extracellular.
2.Drastic secretion of Erythropoietin from Juxtaglomerular cells
3.Synthesis and release ofimmature RBC, with nuclei Reticulocytes.
4.External bleeding, loss of Fe++, slows RBC replacement,leading to iron deficient anemia
Post Hemorrhagic Anemia clinical manifestation
Classical signs, and low Bp if bleeding is moderate to severe.
Post Hemorrhagic Anemia tx
1.Volume replacement first. Saline, Colloids, or plasma
2.Whole blood transfusion for large volume losses.
3.Normal Hct will take 4-6 weeks, Hb will take up to 6-8 weeks.
4.Fe++ supplementation if iron depletion has occurred through external bleeding. (Fe++is conserved if bleeding is internal)
Premature or acceleration of RBC destruction
Bone marrow is capable of increasing RBC production...
8x the normal rate with max erythorpoietin secretion
Anemia from hemolysis
occurs when the destruction rate exceeds the production rate. Otherwise the hemolytic disease is asymptomatic.
Hemolytic Anemia etiology: acquired
1.Infection with hemolytic toxins, e.g. venoms
3.liver or kidney disease,
a. Hapten mediated
b. auto-antibody reaction drug induced
c. immune complex reaction
6.Infections, e.g. Cholera, Typhoid, Malaria
7.Mechanical Hemolysis, Artificial Valves, Dialysis
Hemolytic Anemia etiology: hereditary
1.Defective fragile RBC membrane.
2.Defective Hemoglobin, Sickle cell anemia
Hemolysis generally occurs in ...
lymphoid tissue, Liver and Spleen
1.Mediated by macrophages. or by IgG antibodies
Hemolytic Anemia clinical manifestations
A.Jaundiced due to extreme heme destruction.
B.Bones become malformed due to expansion of hemopoiesis.
C.Renal Damage due to clogging the glomeruli with RBC debris. -> also increases secretion of Erythropoietin.
Hemolytic Anemia tx
Splenectomy if it is the major site of hemolysis, (enlarged Spleen)
Treat or remove the underlying cause
Autoimmune Hemolytic Anemia:
Autoimmune Hemolytic Anemia: warm autoimmune
A.IgG bind optimally to RBC's at normal body temperature, (Type III)
B.Do not activate compliment,
C. Destruction is extravacular, (SpleenOpsonization of Macrophages)
Autoimmune Hemolytic Anemia: cold agglutinin
A.IgM antibody, at colder temperatures,
B.Usually occurs in fingers, toes, extremities.
C.Activation of compliment occurs,some hemolysis occurs depending on length of exposure.
D.Bluish discoloration, resolved when warmed.
E.Can lead to gangrene if exposure is prolonged.
Autoimmune Hemolytic Anemia: cold hemolysis
A.Cold initiates acute severe hemolysis.
B.Usually preceded by an upper respiratory infection
C.Causes hemoglobinuria, Jaundice, hepatomegaly and splenomegaly.
D.Urine may be reddish brown.
Chronic Inflammation anemia
Second most common
Chronic Inflammation anemia etioplogy
AIDS, Chronic bowel infections, malignancies,
1.Decreases RBC life span.
2.Failure of mechanisms of erythropoiesis
3.Disturbances of the iron cycle.
Chronic Inflammation anemia etiology: toxins
from bacteria coating the RBC's Hapten style —> autoimmunity
Chronic Inflammation anemia etiology: cytokines
suppression of bone marrow function.
Chronic Inflammation anemia etiology: impaired iron stores
A.Lactoferrin Secreted by neutrophils
B.Binds to Fe++ 260 times stronger than transferrin
C.Sequesters Fe++ so it is unavailable for Hb synthesis Meant to prevent bacterial uptake of Fe
Chronic Inflammation anemia pathophys
Same as other Anemias,
High total body Fe, but not available.
Chronic Inflammation anemia manifestations
Less severe than most other anemia
May appear as with symptoms of Fe anemia
Low serum Iron, with Normal Ferritin levels
Hemoconcentration due to Severe dehydration
Polycythemia: relative: etiology
Decreased HO intake
Diarrhea or Vomiting
Polycythemia: relative: tx
Polycythemia: Absolute: primary
abnormality in Marrow Stem cells
Polycythemia: Absolute: secondary
Secondary to another disease or environment
Neoplastic non malignant disorder
abnormal proliferation of RBC's
Non response to normal negative feedback mechanisms.
Increased activity of the erythropoietin receptor independent of erythropoietin.
Erythropoietin levels are normal or low normal
Polycythemia Vera Stage I
1-2 year Pre-diagnostic period, symptomatic
Polycythemia Vera Stage II
Polycythemia Vera Stage III
Spent Phase, Anemia occurs
Polycythemia Vera Stage IV
Acute AML 10% in 15 years, 50% in 20 Years
Polycythemia Vera without tx
50% die within 18 months
Polycythemia Vera pathophys
1.Blood becomes thick and viscous, increased afterload,can lead to CHF with Angina.
2.Hypercoagulative state leads to Thrombus formation
3.Infarction of distal tissue to thrombus
Treatment of Polycythemia Vera:
Phlebotomy, (Blood letting) 100-500 ml
Regular aspirin to prevent thrombus formation.
Overstimulation byChronic hypoxia
increased Secretion of erythropoietin
C.Tumor secretion of Erythropoietin
D. Smokers, Chronic CO poisoning
E. Chronic High Altitude exposure
Secondary Polycythemia pathophys
1.Increased viscosity and blood pressure
2.Increased risk of thrombosis
3.Splenomegaly or Hepatomegaly
Secondary Polycythemia tx
Phlebotomy and prevention of thrombosis with aspirin.
Leads to Type II Diabetes
1. Central Obesity
2. Elevated Blood Pressure
3. High normal Fasting blood Glucose
4. High Serum triglycerides/Low HDLs
pattern of breathing characterized by a gradual increase of depth and sometimes rate to a maximum level, followed by a decrease, resulting in apnea
difficulty breathing; subjective "air hunger"
ventilation of the lungs that does not fulfill the body's gas exchange needs (generally <12 breaths/min)
Deep, rapid breathing; usually body compensation during DKA
the condition of taking abnormally fast breaths
How does obstructive pulmonary disease breathing differ from that of restrictive pulmonary disease?
obstructive: low RR, deep breaths/high tidal volume (usually prolonged expiration). Think of COPD-ers!
restrictive: rapid RR, low tidal volume (think of binding a belt around your chest) ex. pneumothorax, obesity, broken ribs, emphysema etc.
What events interfere with O2 and CO2 perfusion across alveolar membranes? Why?
CO2 crosses the space between alveoli and the capillaries 20x easier than O2. Therefore, anything that will expand this space (like pneumonia) will cause an increase in PaCO2
What is FRC?
After a normal breath is expelled, it is the remaining air that can be pushed out. FRC is diminished with obstructive lung diseases.
How does FRC affect PaO2, PaCO2, and pH?
If FRC is diminished (like in obstructive lung diseases), PaO2 tends to go down (you use up the O2), PaCO2 goes up (cannot be breathed out) and pH goes down d/t retained CO2
Which diseases change FRC and how?
obstructive and restrictive lung diseases both decrease FRC. Obstructive lung diseases diminish the ability to breathe out. FRC and IRV are both decreased in restrictive lung diseases because the lungs/ribcage are too stiff to allow deep breathing in or out
If ventilation is high, but perfusion is low, how would PaCO2, PaO2 and pH be affected?
ventilation is sufficient, but PaCO2 would increase/PO2 would decrease because the inhaled O2 is not getting to bloodstream. Therefore, pH would also decrease.
If ventilation is low, but perfusion is sufficient/high, what will happen to PaCO2, PaO2 and pH?
PaCO2 will still buildup, PaO2 will be low, and pH will be low. Any kind of V/Q mismatch will lead to this
Why does right/left shunting happen and which diseases cause this?
When there is extra resistance in lungs, breathing will only fill the left lung (right lung has 3 lobes and more built-in resistance). Because of this, bloodflow to right lung will diminish and shunt to left lung. Occurs in pneumonia, atelectasis, and completely obstructed airways
What happens to the V/Q to cause R-->L shunting? How does this affect PaO2, PaCO2, and pH?
low V/Q; low PaO2 and pH, high PaCO2
How does acute bronchitis affect FRC? V/Q ratio? Shunting?
FRC is diminished d/t early closing of airways during expiration.
O2 diffusion abnormalities
fibrosis caused by inflammation
decrease surface area (emphysema)
most common cause of hypoxemia
a lot of air in alveoli without much blood
most common cause of pulmonary embolus
called alveolar dead space
little air in alveoli with lots of blood
Right ---> left
blood passes through lungs without picking up O2
completely obstructed airways
Acute respiratory failure
inadequate gas exchange
adult respiratory distress syndrome
acute lung inflammation and diffuse alveolar and capillary injury
Sepsis and multiple trauma (most common)
inhalation of toxic gases
inflammation d/t mechanical injury
increase capillary permeability leads out plasma proteins
loss of surfactant production
wedge pressure will be normal
massive inflammatory response
damage to the capillary endo cells and increase cap permeability
platelet aggregation, serotonin, thromboxane A2
Endotoxins released during sepsis
macrophages and neutrophils release TNF, cytokines, and IL1
What type of anemia can be used to one's advantage in a poor country?
an extrinsic factor in clotting
Disorders of coagulation etiology
defects or deficiencies in one or more clotting factors
Inherited coagulation disorders
usually involves a defect in one factor
Acquired coagulation disorders
Vit K deficiency
usually involves a deficiency in more than one or all of the clotting factors
Factor VII is the first to decline, followed by II and X
Liver cell damage is reflected in declines in factor V
Blood flow velocity alterations
too fast - turbulant flow
too slow - cellular components settle out of flow. Allows platelets to come in contact with vessel wall
Vit K deficiency
Involved in synthesis and regulation of clotting factors: II, VII, IX, and X
anticoagulant factor proteins C and S
caused by prolonged wide spectrum antibiotics
low plasma Ca will slow clotting time proportional to the magnitude of the deficit
damaged endothelial cells stop secreting thrombin inhibiting factors
massive activation of clotting factors leads to depletion of clotting factors and plasminogen
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