W4M1Hematology Flashcards
(194 cards)
1
Q
Hematology
A
The study of blood and its components
2
Q
Blood is mostly
A
water 92%, 8% solutes
3
Q
Functions of blood
A
1) delivery of substances needed for cell metabolism
2) Removal of the waste productions
3) Defense against antigens & injury
4) maintenance of Acid/Base balance
4
Q
Plasma comprises
A
About 55% of blood volume the rest being RBC
5
Q
What does plasma include:
A
water, electrolytes, proteins, gases, carbs, lipids, vitamins, & waste products
Proteins: albumin or globulin
6
Q
Most proteins are metabolized in the __ except for __
A
Liver except for Immunoglobulins
7
Q
Immunoglobulins are manufactured by
A
Beta-Cells
8
Q
Albumin is
A
a class of globulin protein that makes up 60% of plasma proteins. It’s iononized & carries a - charge and can bind to moleucles like H2O, cations, fatty acids, hormones, & pharmeceuticals
9
Q
Main function of albumin
A
maintenance of osmotic pressure in the vascular system
10
Q
Globulin
A
Heterogenous class of hydropdrophilic, hydrophobic, large & small
11
Q
Alpha globulins
A
Protease inhibitors
12
Q
Alpha 1 antitrypsin
A
Breaks down elastase in the lung
13
Q
Alpha 2 Haptoglobin
A
Haptoglobin binds to free Hb, prevents kidney damage, recycles free hemoglobin iron
14
Q
Protein C-Alpha 2 globulin
A
Plays a role in blood clotting
15
Q
Beta Globulins
A
proteins involved in iron & sex hormone transport
16
Q
Gamma Globulins
A
Serve an immune function
17
Q
Alpha 1 Antitrypsin Deficiency
A
The Alpha 1 antitrypsin is a protease inhibitor- inhibits (neutrophil) elastase which breaks down elastin fibers in the lungs.
Elastase good! It recycles worn out elastin.
In this deficiency, the elastase starts to break down normal elastin. < elasticity in the lungs and causes COPD and emphysema
18
Q
Fibrinogen
A
Soluble liver derived plasma protein. Can be converted by thrombin to a fibrous net like protein called fibrin
Fine balance btn clotting and anticoagulantion in the body
19
Q
How do deficiencies in fibrogen occur?
A
Result of disease or medication like a clinical syndrome (severe trauma or sepsis)
NOT GENETIC
20
Q
What happens in fibrinogen deficiency?
A
Other proteins in blood cells such as platelets and thrombin try to fill in the gap but this becomes overwhelming and bleeding ensues
21
Q
Disseminated Intravascular Coagulopathy
A
Blood clots form throughout the body’s small blood vessels. Can reduce or block flow through the blood vessels.
Increased clotting uses up platelets. When your body needs platelets there are none
22
Q
Symptoms of Disseminated Intravascular Coagulopathy
A
Manifested by Petechiae or purpura, severed anemia or death
23
Q
Facts about RBC
A
You know these
24
Q
Where are RBCs destroyed
A
The spleen by macrophages
25
Erythropoiesis
Birth of RBCs
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What can Hb bind to?
CO2, CO, Nitric Oxide
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Types of Hb
```
Hemoglobin A
Hemoglobin A2
Fetal Hb
Hemoglobin S- sickle cell
Hemoglobin C- leads to hemolytic anemia (bc abnormal blood cells are broken down)
```
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Platelets have granules that contain
Pro-inflammatory mediators & different growth factors: ADP, 5-HT, lysosomes, platelet-derived growth factors A2 & others
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What do platelets do?
He most asks
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Anemia’s
< in RBC volume
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Cytic means:
Cell size
Macrocidc=large
Microcidic=small
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Chromic means:
Cel Hb content
Hyperchromic= lots
Hypochromic= little bit
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What do you look for in CBC
Hb (12-16 F) (13.5-17.5 M)
Hematocrit-% of RBC in the blood as a ratio per solute ( a % 36-46 F, 41-53 M)
During menstruation Hm lowered with stress or dehydration
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Macrocytic Anemia
“Large cell”
| An insufficient quantity of Hb and the RBCs are larger than their normal volume so there are less of them
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Magaloblastic macrocytic Anemia
Inhibition of DNA synthesis during RBC production, the cell cycle doesn’t continue to division-> continuous cell growth without division = macrocytosis
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What are the causes of Megaloblastic Macrocytic Anemia?
B12 Deficiency (Lack of intrinsic factor)
Folic Acid
Malabsorption
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B12 insufficiency is due to
Inadequate absorption
Gastritis,
Alcohol abuse
Roux-en-Y Gastric Bypass
The special cells in the stomach (parietal cells) are missing or insufficient
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Macrocytic Anemia symptoms
Weakness fatigue from not having enough oxygen in your blood
Patients experience paraesthesias (burning and prickling sensations ) hands & feet
Big beefy tongue. Codocytes
Colitis
Cracked lips
Stomatitis (red inflammation of the mucus membranes of the mouth)
Diarrhea not uncommon as well
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How do you treat Macrocytic Anemia
Stop whatever causes the symptoms
Stop the alcoholism
Supplements with vitamins
Reduce caffeine intake for gastritis
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Microlyric Anemia
Abnormally small RBCs
| Usually hypochromic: the quality of the Hb is very low giving the cells a pale complexion
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Why does microlytic anemia occur?
Disorder of iron metabolism:most common
Disorder of heme synthesis
Disorder of globin synthesis
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Iron deficient anemia causes
Ongoing blood loss
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Iron deficiency anemia 3 stages
1) Fe stores are depleted bc Fe / RBCs not recycled
2) there’s a < in Fe and Production
3) these Hb deficient RBCs start to replace normal RBCs
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Signs and symptoms of iron deficiency anemia
Fatigue, pallor, SOB, kilonychia (spooning of nails), stomatitis, glossitis “reddening of tongue”
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How can we diagnose iron deficiency anemia?
CBC
Mean Corpuscle Volume: low in iron deficiency anemia bc RBCs are smaller
Mean Corpuscular Hb: they have less Hb content- Poikilocytosis variation in RBC shape
Anisocytosis: RBC are of unequal size and maturity
Iron serum: a low serum, low ferritin (protein that carries free Fe)
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Treatment for Iron Deficiency Anemia
If there’s a bleeding source stop the bleeding. If it’s intrinsic factors, start transporting factors,
Replace iron through IV supplementation
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Normalcitic Anemia
All normal, there just aren’t enough of them
Normal in older adults
Causes < in bone marrow production of RBCs and an > of destruction as seen with hemolytic anemia
Pregnancy produces a delusional effect by > plasma volume and B2 and B6 deficiencies
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Normalcitic Anemia
Aplastic
Hemolytic
Posthemorrhagic
Chronic Inflammation
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Aplastic Anemia
- when the marrow does not produce RBCs
- often idiopathic
- symptoms include fatigue, pallor, easy bruising
- some meds like anticonvulsants cause inhibition of the enzyme folate which is important for DNA Synthesis
- excessive exposure to ionizing radiation
- viruses can cause aplastic anemia. The Parvovirus 19
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Parvovirus 19
Causes Fifth’s disease identified by low grade fever, a rash, arthritis, and aplastic anemia.
-P antigen binds parvovirus, allows parvovirus entry into the cell once and its cytotoxic
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Hemolytic Anemia
Abnormal breakdown of normal red blood cells
Intrinsic & General challenges: thalassemia, sickle cell anemia,Spherocytosis
Extrinsic Challenges: autoimmune disorders- lupus, rheumatoid arthritis, inflammatory states
Paroxysmal nocturnal Hb
Penicillin: can induce RBC to an early death
Lead: toxic to RBC
Footstrike Runners Disease: constant running causes early breakdown of RBCs
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Polycythemia Vera
Disorder of the bone marrow in which the bone marrow produces too many RBCs
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Pathophysiology of RBCs
Erythropoiesis: RBC generation stimulates when O2 levels are low
Kidneys release Erythropoietin, which binds to JACK/AK in bone marrow stimulating RBC produciotn
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Pathophysiology of Polycythemia Vera
A mutation of stem cells cause uncontrolled RBC production. Also > WBC & platelet pxn due to > GF for hematopoietic stem cells
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Signs & Symptoms of Polycythemia Vera
Steady Red complexion from RBC in capillary beds. Puritis (itchy skin), headache, fatigue, splenomegaly(> size bc too many RBC)
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Polycythemia Vera patients at risk for
Thrombosis (DVT), myocardial infarction, or stroke
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Polycythemia vera patient's CBC:
> Hb & hematocrit, RBC
BUT LOW EPO
This is due to negative feedback
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Myelofibrosis
Late complication of polycythemia vera. Myelofibrosis can cause scaring of the bone marrow & more severe anemia
Hepatosplenomegaly
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Treatment for Polycythemia Vera
Simple phlebotomy to target H&H, give aspirin, use chemotherapy or hydroxyurea which < the availability of nucleotides for DNA replication
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Hemochromatosis:
Disorder of iron overload. It can be genetic bc of mutations of iron transport proteins. CAN ALSO BE AQUIRED
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Hemochromatosis, ways to aquire
chronic hemolysis, iron overdose, with large blood transfusions
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Hemochromatosis
Autosomal recessive disorder. Chromosome 6 has HFE gene that regulated the iron gene & its transport. Itcan > iron absorption and can > the deposition of iron into tissues leaving the tissues overwhelmed as the iron gets tucked away into tissue beds
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Signs and symptoms
Not usually recognized until 30-50 years. Cirrhosis, DM< arthritis, cardiomyopathy and a tanning/discoloration of the skin (ROS grab Fe and cells die in tissues)
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How to diagnose Hemochromatosis
Measure the serum ferritin and analysis of the hFG gene itself
MRI can see the deposits, esp. in liver
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How to treat Hemochromatosis
Phlebotomy and Chelator which are chemicals that bind to metal and make them more eater soluble
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Porphyria
affliction of the enzyme that participates in the production of porphyrins
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Porphyrins are
Organic rings that bind to other molecules such as oxygen which forms Hb & Mg2+ which can form chlorophyll & Cobalt which , when combined with vitamin B12, is a separate enzyme all together
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When porphyrins are bound to oxygen
they're called Heme
| Hb is actually: Protoporphyrin 9
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What happens with Porphyria?
It's an OVERPRODUCTION of porphyrins which are cytotoxic
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Acute porphyria...
First affects the CNS and GI tracts and can cause mental status changes like confusion, psychosis, weak muscles, nausea, vomiting, photosensitivity, blisters in sun. dark colored urine
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How to diagnose porphyria
measuring the precursor such as porphobulinogen.
| A measure of urinary PPG is the first step in diagnosing this disorder
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Treatment of porphyria
Treat abdominal pain, many need glucose infusion
| Give hematin, which inspires negative feedback to < porphyrin
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Thrombocytopenia
```
Platelets <150,000 mm^3
> risk for hemorrhage
Pathophysiology
Congenital
Acquired
```
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Thrombocytic Thrombocytopenia
There's an > risk for clotting disorders the signs include petechiae and purpura
hemorrhage, stroke, headache, MI
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Pathophysiology for Thrombocytopenia
acquired mononucleosis HIV, immune disorders, cancers, meds (heparin induced thrombocytopenia)
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Idiopathic Thrombocytopenia
an autoimmune or antibody that might be active against one or more of the glycoproteins that reside on the platelets including Glycoprotein 1A or 2A or glycoprotein 2B3A
The immunoglobulin will bind to that glycoprotein and it will be lost to the immune system
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Disorders that can > the consumption of platelets
Heparin induced thrombocytopenia, Thrombotic Thrombocytopenic anemia,
Idiopathic thrombocytopenia,
& Disseminated Intravascular Coagulopathy
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Pathology of Thrombotic Thrombocytopenic Anemia
Loss of platelets + an > in thrombosis or an > in platelet aggregation related to plasma metalloprotease (metal based enzyme that cleaves Adam T13), which cleaves the large precursor Von Williebrand Factor
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What happens when Von Willebrand Factor remains uncleaved?
they attract a large # of platelets when they aggregate they can eventually break off and occlude other vessels. The body's platelet count < bc al platelets are in one clump
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Strict definition of Heparin Induced Thrombocytopenia
when you administer enough heparin that the platelet count < by 50%
Involves an immunoglobulin against Heparin platelet Factor 4 (binds to & consumes it)
Heparin is also used for central venous catheters and peripherally inserted. Don't install with someone who has a history
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Petechiae vs Purpura
Purpura are larger patches similar to petechiae
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Leukemia in general
```
several types of blood cancers, classified by the predominant cell type effected as the speed at which the disease occurs
Uncontrolled proliferation of leukocytes
Bone Marrow Overcrowding
< Fxn of hemapoietic cells
< Fxn of hematopoietic cells production
```
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Acute Lymphocyitc Leukemia definition
A disorder of abnormal lymphoblastic production. (lymphoblast eventually become lymphocytes). Our T, B & NK cells of the immune system ALL causes damage by overcrowding the bone marrow thereby < the prxn of other cells & by infiltrating other organs such as the CNS
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Acute Lymphocytic Leukemia Pathophysiology
Some signal promotes uncontrollable cell proliferation
| Fusion genes. Radiation exposure. Benzene. HTLV-1: a retrovirus that inserts the genes into the host
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Fusion Genes
Previously separated genes become linked together by translocation, deletions, or inversion. Fusion genes are often oncogenes that block apoptosis
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Symptoms of Acute Lymphocytic Leukemia
Fatigue, anemia, weakness, recurrent unexplained infection, fever, bone pain, swelling of lymph nodes, splenomegaly, & petechiae
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How to diagnose Acute Lymphocytic Leukemia
Close history & physical exam, CBC (elevated WBCs), blood smear (will show fewer lymphoblasts or progenitor cells
Bone marrow biopsy Philadelphia chromosome (evidence of translocation btn chromosomes 9 & 22)
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Lympphoblasts are
are early progenitors of the mature lymphocyte which will either become a T cell, B cell or Natural Killer Cell
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HCLV1
First IDed human retrovirus. Has helped us learn about HIV and ALL. Inserts Bronco genes, increases T Helper Cell proliferation by > cytokine proliferation.
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Chronic Lymphocytic Leukemia define
B-cells accumulate in bone marrow and crowd out healthy cells
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Symptoms of CLL
May be asymptomatic. Fatigue or lymphadenopathy. WBC count > with large # lymphocytes present. All B-cells are clones and exactly the same.
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Pathophysiology of CLL
From secondary to deletions in chromosomes 7, 13, 14, & 17.
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Diagnosis of CLL
Cytometry, bc all B-cells will look the same (are clones) we use cytometry to distinguish that
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Treatment of CLL
Mostly supportive. chemo is an option. Splenectomy is (immature B-cells migrate there).
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Acute Myeloid Leukemia
Disorder of the myeloid cell line. Overproduction of basophils, eosinophils, and neutrophils
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Symptoms of Acute Myeloid Leukemia
fatigue, bruising, SOB
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Acute Myeloid Leukemia diagnosis
Elevated WBC count especially at the myeloid cell line but also anemia and thrombocytopenia
Bone marrow biopsy will show early progenitor cells of the myeloid (flow cytology)
It is an acute leukemia so it can proliferate quickly
Fusion genes have been implicated.
Alkylating agents (used in Chemo meds) may put people at higher risk
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Chronic Myeloid Leukemia is...
“Philli” Philadelphia chromosome. It is the translocation of 2 parts of chromosome 9 and chromosome 22. This creates a continuously active protein that controls the cell cycle & inhibits cell repair.
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Diagnose Chronic Myeloid Leukemia
CBC will show elevated WBCs especially neutrophils, basopihls, & eosinophils. Bone marrow biopsy is definitive as is cyto microscopal techniques for detecting Philidelphia chromosome
Treatment is chemo
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How to look for Philadelphia Chromosome
Fluorescent in-situ hybridization
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Hodgkins Lymphoma definition
Spreads from one lymph node to the next.
REED-STERNBERG CELLS PRESENT- are mature B cells that have become malignant, are unusually large, and carry more than one nucleus.
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Hodgkins Lymphoma symptoms
Night sweats, splenomegaly, fatigue, anemia, swelling of lymph nodes
The Pathophysiology is widely unknown. Connected to Agent Orange, Epstein-Barr virus & HIV
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Non-Hodgkins Lymphoma
Cancer affect T and B cells, overproduction
| NO!!! R-S cells
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Non-Hodgkins Lymphoma Risk Factors
PCBS (Polychlorinated Biphenyls)
Viruses: Epstein-Barr, Kaposi's sarcoma (after HIV)
HTLV-1
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Non-Hodgkin's lymphoma symptoms
same as the others, risk for lupus
Chemo and radiation
Slow progressing disease may live normal life
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Anaplastic
Loss of cellular differentiation
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carcinoma
the cancer's origin was epithelial
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Adenocarcinoma
origin of the cancer was from glandular tissue or ductal
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Sarcoma
tumor that occurs in bones or soft tissues
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Carcinoma in situ
it is a pre-invasive cancer but still a cancer. It is easily cured by surgical manipulation
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Metastatic
the cancer is going to distillate to other parts of the body and requires systemic treatments
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Neovascularization
the ability of the tumor to put out substances that increase vascularization of the tumor to > blood supply
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Oncogen
The ability of the body to regulate normal cell growth and proliferation. A mutation in an oncogen occurs in tumor suppressor Gene. Many cancers have the ability to turn off this tumor suppressor Gene. Turning off the regulatory Gene causing the cancer to be able to grow in size
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What causes the most cancer internationally
tobacco then obesity then alcohol then infection/STD, then radiation, then Nutrition
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radiation/UV light causes increased risk of
lymphomas and leukemias
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does pollution have a separate role from tobacco smoking in causing cancers?
Yes
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BRCA 1 gene
cervical/ BREAST
uterine
pancreatic
COLON cancer
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BRCA 2 gene
```
pancreatic
stomach
gallbladder
bile duct
melanoma
```
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Hallmarks of cancer 1)
| Tumor Initiation
The process that produces the initial cancer cells
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Hallmarks of cancer 2)Tumor Promotion
The process by which the population of cancer cells expands and I diversifies its phenotypes
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Hallmarks of cancer 3)
| Tumor Progression
leading to the spread of the tumor to an adjacent or distal sight of metastisis
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Hallmarks of cancer 4) Point Mutation
alterations in a nucleotide
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Hallmarks of cancer 5)
| Colonal Proliferation
the selection and reproduction of only one type of cell
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Hallmarks of cancer 6)
| Gene Amplification
is the result of a repeated a region of a chromosome so instead of two normal copies of a chromosome chromosome there are tens or even thousands of copies
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Hallmarks of cancer 7)
| DNA Methylation
The gene itself does not change but something is added to it this includes DNA methylation and non-coding RNA
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Hallmarks of cancer 8)
| Non-Coding RNA
miRNA, siRNA
127
Hallmarks of cancer 9)
| Chromosomal Translocation
Causes much larger changes in chromosome structures. It happens when one piece of a chromosome is translocated or transferred to another chromosome
128
Hallmarks of Cancer 10)
| Colonal Expansion
Colonal Expansion of lymphocytes is a hallmark of vertebrate adaptive immunity. A small number of precursor cells that recognize a specific antigen proliferate into expanded clones, differentiate and acquire various effector and memory phenotypes, which promote effective immune responses.
129
Epidermal Growth Factor
Epidermal Growth Factor and its receptors in mammalian CNS. Epidermal growth factor (EGF) is a common mitogenic factor that stimulates the proliferation of different types of cells, especially fibroblasts and epithelial cells.
130
Tumor Suppressor Gene
are normal genes that slow down cell division, repair DNA mistakes, or tell cells when to die (a process known as apoptosis or programmed cell death). When tumor suppressor genes don't work properly, cells can grow out of control, which can lead to cancer.
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Angiogenesis Factor
is defined as the growth of new blood vessels. This process is essential for healing, growth, development, and maintenance. The body controls angiogenesis by balancing stimulatory and inhibitory factors. Disease occurs when this delicate balance is disturbed.
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Tumor Associated Macrophage
TAMs affect most aspects of tumor cell biology and drive pathological phenomena including tumor cell proliferation, tumor angiogenesis, invasion and metastasis, immunosuppression, and drug resistance.
133
symptoms of cancer
pain, fatigue, cachexia (wasting syndrome), anemia, leukopenia, thrombocytopenia, paraneoplastic syndrome
134
paraneoplastic syndrome
is a set of symptoms that occur with cancer, due to substances a tumor secretes or due to the body's response to a tumor
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SIADH
Syndrome of Inappropriate Antidiuretic Hormone secretion, body retains too much water. causes a very dilute PLASMA. Very concentrated urine. Can cause mental status changes
136
Paraneoplastic syndromes
SIADH,
Small cell carcinomas of the lungs
Intracranial neoplasms
Hypoglycemas, Myestenia, Cushing Syndrome (ACTH like tumors), Hypercalemia
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Why is anemia associated with cancer
Anemia associated malignancy due to chronic bleeding (colon), chemo, and malnutrition
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Excisional Biopsy
The complete removal of the cancer
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Incisional biopsy
removing part of the cancer for diagnosis
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Core Needle Biopsy
particularly in Prostate liver or lung cancer allows us to get enough tissue To really understand the origin and pleomorphic nature of the cancer
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Fine Needle Aspiration
Obtains cells for cytology but does not retain tissue structure
142
Exfoliative cytology from the cervix from the sputum, urine, colon/ endoscapy
Allows us to get cells that are shed but no true tissue
143
Stages of cancer
1) cancer at its origin
2) Locally invasive
3) Cancer has spread to regional structure like lymph nodes
4) Cancer has spread to distant sites. Nonoperateble
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The World Health Organization also has a T N M system
T being tumor spread, N indicating Nodal involvement, and M indicating distant metastasis
145
Tumor Markers
are biologically reproduced from the tumor and help us understand the activity of the disease but in general do not make good screening tools. CA125 Often seen in ovarian cancer But has a 15% false positive rate. Which makes it a poor screening test
146
What makes a good screen test
effective, safe, well tolerated (not invasive) nad very few false positives and false negatives
147
What makes a good screening test:
* Effective
* Safe
* Well tolerated
* Least Invasive
* Low rates of false positive and false negative
* Valid and Reliable – Sensitive and Specific
* Cost per life save
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Treatment
Stage 1 surgery
Radiation to kill cancer cells (esp. stage 1 & 2)
Chemo
Immunotherapy- boost own immune systems to destroy cancer cells
Targeted Therapy: looks at oncogenes
Target Chemotherapy: cancer can be diverse
149
Skin homeostasis is visible though___ and controlled __
Skin changes can be see through temperature. controlled by
| Hypothalamus
150
Liver is modulated by___ controlled by ___
variable factor: glucose, controlled/regulated by insulin
151
Kidney variable factor vs controlled by
Variable factors: WAter, urea, electrolytes
Controlled by: Water (ADH), Urea & lytes via urine formation
152
Lungs variable factor controlled by
Carbon dioxide and oxygen
| Regulated by respiratory center in the brain
153
cellular injury states
Reversible (cells recover)
| Irreversible (cells die)
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Phases of disease
| pathogenesis, exposure to injury
```
Latent or incubation period
Prodromal period
Acute phase
Remission/exacerbation
Convalescence
Recovery
```
155
Atrophy
< cell size
156
Hypertrophy
> cell size, huge muscles
157
Hyperplasia
> # of cells,
158
Metaplasia
Replacement of one cell type with another
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Dysplasia
Derranged cell growth
160
Cardiac atrophy
atrophy of cardiac muscle lead to numerous cardiac problems related including decreased cardiac output and cardiac failure
161
Benign Prostatic Hypertrophy
Hypertrophy and hyperplasia of smooth muscles. increase in size causing obstruction
162
Left ventricular hypertrophy
> cell size, causes much larger QRS, > energy expenditure required
163
Hyperplasia
> number of cells in a tissue or organ
In response to injury
Compensatory
Hormonal (endocrine disease)
164
Pathologic Hyperplasia
May be pre-cancerous change
165
Metaplasia
replacement of one cell with another type.
| Chronic injury or irriation
166
Dysplasia
Deranged cell growth
| persistent severe injury or irritation
167
Cushings syndrome
metaplasia?
168
Cell Dysplasia
```
Abnormal size shape or arrangement
Anisocytosis
Poikilocytosis
Hyperchromatism
Presence of mitotic figures (an unusual # of cells which are currently dividing)
```
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Anisocytosis
cells of unequal size
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Poikilocytosis
abnormally shaped cells
171
Hyperchromatism
Excessive pigmentation
172
Barrett;s Esophagus
Metaplastic cells
173
Dysplasia cells are indicative of
cancer. It's abnormal
174
Normal cell responses to stress
atrophy, hypertrophy, hyperplasia, metaplasia
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Cell injury is caused by
in inability ot maintain homeostasis
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S-t depression in EKG
Cardiac ischemia due to hypoxia
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Cyanosis
a VERY late sign of hypoxia
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What's the most common cause of cellular injury
hypoxic due to ischemia
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anoxia
absence of oxygen supply to an organ or tissue
180
reperfusion injury
The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than (or along with) restoration of normal function
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Hypoxic-ischemic- encephalopathy
a shortage of the O2 in the blood-> shortage of blood flow to the brain-> brain damage
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Hydropic degeneration
s a condition in which excessive amounts of water accumulate in dysfunctional cells
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Xenobiotic
narcotics. foreign chemical found in your system that's not expected to be present (any drugs but emphasis on the bad)
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Contusion
bruise
185
Cellualr acuumulations (infiltrations) can be manifestations of cellular injury
even normal things
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Vitiligo
cells lose pigmentation
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BRiusing causes freed RBC ...
phagocytosis of RBC by macrophages cause hemosiderin and iron free pigments
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hemosiderin
causes the color of bruising
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when cells are broken down
calcium gets released and aggravates cell damage
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Necrosis
Summary of cellular changes after local cell death and the process of cellular autodigestion (autolysis)
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Gangrenous necrosis
death of tissue from severe hypoxic injury
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Coagulative necrosis
necrosis occurs primarily in the kidneys, heart, and adrenal glands and is caused by protein degradation
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Liquefactive necrosis
ischemic injury to the neurons and glial cells
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fat necrosis
occurs in the breast, pancreas, and other abdominal structures and is caused by the cellular dissolution of enzymes called lipases
