Umkc Dental Pathology1 2012 Exam 1 Lec. Intro, Spectrum Of Human Dz, Cell Injury&adapt

Front 1

What is Health?

Back 1

- A STATE of complete PHYSICAL, MENTAL, and SOCIAL wellbeing, and not merely the absence of disease or infirmity.
-A PROCESS of CONTINUOUS ADJUSTMENT to the CHANGING (enviroment) DEMANDS of living and of the CHANGING MEANINGS we give to life

Front 2

What is Disease?

Back 2

- An ABNORMAL CONDITION that may IMPAIR bodily FX, cause Discomfort, Social Problems, Death.

Front 3

What may diseases include?

Back 3

1. Injuries
2. Disabilities
3. Disorders
4. Syndromes
5. Infections
6. Alterations of Behavior
7. Atypical Varioons of Structures and Fx
8. Neoplasms
Dz= abnormal fx or impairment

Front 4

Pathology = is a _______ Discipline between ____ _____ and ____ ____.
(pathology is visual)

Back 4

Pathology = is a _BRIDGING_ Discipline between _BASIC SCIENCE_ and _CLINICAL PRACTICE_.

Front 5

General vs. Systemic Pathology:
1. General Pathology-
-ex:

Back 5

- the Basic Rxn of Cells & Tissues to the Abnormal Stimuli that Underlie All Diseases.
=ALL organ systems
-Ex: Adaptation, Cell Injury & Death, Inflamation & Repair, Immunity, Genetic Disease, Neoplasia, Hemodynamics

Front 6

General vs. Systemic Pathology:
2. Systemic Pathology-
ex:

Back 6

-The specific responses of ORGANS and Tissues to stimuli:
ex: Cardiovascular system, GI system, Endocrine system, genitoruinary system, Hematopoietic system, Hepatobilary system, CT, CNS

Front 7

Path: Academic Discipline vs. Medical Specialty:
1. Anatomic Pathology (med)-
-4 ex:

Back 7

Anatomic Path- Diagnosis of disease based on the examination of TISSUES & CELLS
ex: 1. Surgical path, 2. Cytopathology, 3. Autopsy path, 4. Forensic path

Front 8

Path: Academic Discipline vs. Medical Specialty:
2. Clinical Pathology (lab med)-
-6ex:

Back 8

Clinical Path- Diagnosis of disease based on the analysis of BODY FLUIDS.
ex: 1.Clinical chem, 2.Hematopathology, 3.Blood banking & transfusion medicine, 4. Medical Microbiology, 5. Medical cytogenetics, 6. Immunology

Front 9

What is a lesion?

Back 9

Lesion- any clinical or molecular abnormality.
- Anything abnormal clincally or moleculuarlly
=>LESIONS CAN BE VISIBLE OR INVISIBLE

Front 10

Examples of VISISBLE Lesions-
6 (but more than that)

Back 10

1. Traumatic ulcer
2. Leukoplakia
3. Carious Lesions-(some xerostomia related caries)
5.Melonoma-Palatal Mucosa
6. Basal Cell Carcinoma

Front 11

Visible Lesions:
1. Traumatic ulcer- is? Cancerous?
2. Leukoplakia- is?
3. Melonanoma- Palatal Mucosa- cancerous/ malaginant or beningned?
location importance?

Back 11

1. Traumatic ulcer -discountity in the epithelium- Not cancer- just traumatic tumor
2. Leukoplakia- whice lesion calus like, can't be wiped away
3.Melonoma- Palatal mucosa= Lesion on palatal mucosa- not beigned, MOST COMMMON SITE FOR MELONAMOA= PALATE

Front 12

Visible Lesions may range from the ____ to the ______
ex?

Back 12

Visible Lesions may range from the _INSIGNIFICANT_ to the _GROTESQUE_
ex-Basal Cell Carcinoma- Advanced= has potential to evade locally
- Exepahlotrigeminal Angiomotosis- Sturge Weber syndrome= ANGIOMA

Front 13

Why may a lesion be invisible? (location)
Example?

Back 13

-Bc it is located deep within the body.
ex: lung cancer lesion in xray- metastic to gingiva
(Squamos cell carcinoma or bronchial carcinoma - metastic to gingiva before found)
-Breast cancer- metatsitc lesion of mandible bone.

Front 14

Why else may a lesion be invisible?
3 examples:

Back 14

BC it is a MOLECULAR LESION
ex: 1. PKU (phenylketonuria)
2. Schizophrenia
3. Diabetes Melitus

Front 15

Lesion invisible bc it's a molecular lesion:
1. PKU-invisible BIOCHEMICAL Lesion
-Inherited by:
-Caused by:
-Problem w/phenylalanine:
-Solution:
-Diagnosis:

Back 15

-Inherited by: Autosmal Recessive Disorder of Phenylalanine megabolism=> DEVELOPMETNAL dz.
-Caused by: MUTATION in the Enzyme that conversts Phenylalanine to Tyrosine (PHENLYALANINE HYDROXYLASE)
-Problem w/phenylalanine: It's TOXIC to DEVELOPING Brain & causes Profound, Irrreversible Mental Retardation (COGNITIVE DISORDER)
-Solution: resticted die
Diagnosis: - GUTHERIE TEST baby

Front 16

what is the most common form of skin cancer?

Back 16

Basal Cell Carcinoma

Front 17

Taxonomy-

Back 17

Science of Classification

Front 18

Nosology-

Back 18

Deals w/ Classification of Dz.

Front 19

Naming a dz ideally should?

Back 19

Give a clue to the CAUSE or ORGAN SYSTEM involved

Front 20

Disease Names Change overtime/Not static: What is the name NOW?
1.Moniliasis-
2. Geographic Tongue-
3. Odontogenic Keratocyst-
4. Calcifying Odontogenic Cyst-

Back 20

1.Moniliasis- CANDIDIASIS
2. Geographic Tongue- ERYTHEMA MIGRANS
3. Odontogenic Keratocyst- KERATOCYSTIC ODONTOGENIC TUMOR
4. Calcifying Odontogenic Cyst- CALCIFYING CYSTIC ODONTOGENIC TUMOR

Front 21

Some Diseases have multiple names ex- what are they called NOW?
1.Periapical Cementosseus Dysplasia-
2. Paget Disease of Bone-

Back 21

1.Periapical Cementosseus Dysplasia- CEMENTOMA
2. Paget Disease of Bone-OSTEITIS DEFORMANS

Front 22

Some disease may be id by eponyms (person name):
1. lou Gehrig Disease-
2. Christmas Disease-
3.Lesch-Nyhan Syndrome-
4. Garlin Syndrome-
5. Garlin Cyst-
6. Pindborg Tumor-

Back 22

1. lou Gehrig Disease-AMYOTROPHIC LATERAL SCLEROSIS
2. Christmas Disease- CLOTTING FACTOR 9 DEFICENCY
3.Lesch-Nyhan Syndrome- HYPOXANTHINE-GUANINE PHOSPHORIBOSYLTRANSERASE (HGPRT) DEFICIENCY
4. Garlin Syndrome- BASAL CELL NEVUS SYNDROME
5. Garlin Cyst- CALCIFYING ODONTOGENIC CYST
6. Pindborg Tumor- CALCIFYING EPITHELIAL ODONTOGENIC TUMOR

Front 23

Diseases vary in their PREVALENCE:
Rare Disease= Ds w/ prevelance? = _____ disease
From rarre to common:

Back 23

LOW
= ORPHAN's Disease
Rare--> common:
Ewing Sarcoma--> Garlin syndrome, Multiple Endocrine Neoplasia 2, sickle cell anemia, treacher collins, CF, Marfans.

Front 24

What are the 4 Key aspects of a Disease Process?

Back 24

1. Etiology
2. Pathogensis
3. Morphological Changes
4. Clinical significance

Front 25

4 Key Aspects of Dz Process:
1. Etiology-
ex: Mucoviscidosis (Cystic Fibrosis)

Back 25

- CAUSE of a Disease process
ex: CAUSE of CF= Mutation in CFTR (CF Transmembrane Conductance Regulator) Gene- Varying degress of gene
= Systemic Dz- effects lungs & pancreas)

Front 26

4 Key Aspects of Dz Process:
2. Pathogenesis-
ex: Mucoviscidosis (Cystic Fibrosis)

Back 26

-MECHANISM of Disease development
ex: MECHANISM of CF=Accumulation of Bacteria & degeneration of DNA & immune cells
=>Chloride channel fx- Absent or defected & Airways plugged with CF's thick, viscous mucus secretions.
*1.Defective PROTEIN product
2.Defective Chloride CHANNEL
3.Viscous SECREATIONS
4.Ineffective CLEARANCE
5.Plugging & INFECTIONS
6. Tissue DAMAGE

Front 27

4 Key Aspects of Dz Process:
3. Morphological Changes-
ex: Mucoviscidosis (Cystic Fibrosis)

Back 27

-STRUCTURAL Changes induced in cells & organs
Ex- Struct/fx- Airways, liver, pancreas, si, skin (sweat glands)

Front 28

4 Key Aspects of Dz Process:
4.Clincial Significance-
HOW CF DIAGNOSED??

Back 28

- FUNCTIONAL consequences of the Morph changes
DIAGNOSED: Sweat Cholride Test

Front 29

What are the 6 Categories of Disease?

Back 29

1. Developmental
2. Infectious
3. Neoplastic
4. Metabolic
5. Immune Mediated-
6. Reactive-

Front 30

Catergories of Dz-6:
1. Developmental-
-3 ex

Back 30

1. Developmental- Genetic, environmental Infleuenced
ex: 1. Cherbuism- Autosomal Dominant- chubby cheecks, radioluceny trhogught jaw- expansion of jaw
2.Gardner Syndrome- A.Domninant- A familial intestinal polyposis syndrome (oolyposis of colon- pink lesion- malignant trasformation-remove to reduce colon cancer)
3. amelogensis Imperfecta- chalky looking enamel- easily fractures (misdiagnosis0 sever Flurosis)

Front 31

Catergories of Dz-6:
2. Infectious-
Ex-3

Back 31

2. Infectious- Bacteria, Viruses, Fungi
Ex: 1. 1' Herpetic Gingivostomatitis- (80% of pop infected w/ herpes)- subclinical- fever, multiple ulcers--> VIRAL Dz
2. Acute Pseudomembraneous Candidiasis- Yeast infection= Thrush- wipes off
3. Histoplasmosis- 1' lung infection, (ms, valves, fever???) -misdiagnosised: infection/neoplasm

Front 32

Catergories of Dz-6:
3. Metabolic-
Ex-2

Back 32

3. Metabolic- Endocrine
Ex:
1. Acromegaly- Growth hormone- secreting pituitary Adenoma-(condyle response- proliferation to class3 due to response to GH.. Pathogensis)
2. Hypothyrodism- short stature, generalized delayed dental erruption= young dental age

Front 33

Catergories of Dz-6:
4.Neoplastic-
ex-5

Back 33

4.Neoplastic-benign, malignant
ex: 1. Squamous Cell Carcinoma-stony hard
2.Metastic Brochogenic Carcinoma to gingiva- oral-lung cancer metastic to gingiva
3.Acute Leukemia- -biopsy- generalized enlargement to lungs
4. Hemangioma- benign vascular -bloodvessles- enlargement (ex tongue)
5. Neurofibromomatosis- lesions on skin- non painful, oral mucoasa.= ADinherited.

Front 34

Catergories of Dz-6:
5. Immune- Mediated
ex-4

Back 34

5. Immune-mediated- Allergy, hypersensititvitym autoimmunity
Ex: 1. Recurrent Apthous (ulceration) Stomatitis- Minor Aphtha- WBC T-lymph- below mucosa & attack mucosa - no scar
2. Mucous Membrane Pemphigoid- Desquamative Gingivitis- epithelium sluff off- # of dz can cause this
3.Autoimmunine Thrombacytopenic Pupura- AB to platlets sequestered to spleen=> Level of Platelets DECREASE - bleeding into skin (redish-purplen dots on skin) = Decrease level of platlets leads to this dz.
4. Allergic Conctact stomatitis- Buccal mucosa irritation- immune mediatead mucositious- to cinamon in gum- allergy or nickle allergy

Front 35

Catergories of Dz-6:
6. Reactive-
3ex-

Back 35

6. Reactive- TRAUMATIC, physical, chemical, factitial (pt. caused), iatrogenic (unknown caused) injuries.
=> Body Rxn to irritant.
ex: 1. Pyogenic Granuloma-proliferation of blood vessels- (ex calculous bridge holding tooth in)
2. Gingival Hyperplasia (generalized)- Diabetes Melluties
3. Trigeminal Neuroaliga- Episodic triger zone = vigourous tooth brushing.
4- ish ( dental hypoplasia- rxn to radioation in childhood- or DEVELOPMETNAL**)

Front 36

Stages in the Cellular Response to Stress and Injury- 6 ish

Back 36

1. Normal Cells (homeostasis)--> injury or stress to cells-->
2. Adaptation ( Hypertrophy, hyperplasia, atrophy, metaplasia) -->
Morphologic Alterations (steps 3&4)
3. cell Injury -->
4. Reversibile cell Injury-->
5.Irreversible Cell Injury-->
6. Cell Death ( apoptosis or necrosis)

Front 37

What is hypertrophy?

Back 37

-Increase Size of an organ due to the Increased SIZE of its cells, w/out an increase in cell 3 (hyperplasia)

Front 38

Where is pure hypertrophy occur?

Back 38

Only in skeletal and Cardiac Muscle

Front 39

Increased size of salivary glands- Parotid and submandibular Increases in alcholics causing SIALADENOSIS0 also in bulimics- what is this due to?

Back 39

hypertrophy

Front 40

what is Hyperplasia
2- forms

Back 40

-Increase Size of tissue or organ due to INCREASED # of Cells.
2 forms- (mostly smooth m.)
1. Physiologic
2.Pathologic

Front 41

Some Hyperplasia's are physiologic-3

Back 41

1. Erythroid Bone Marrow hyperplasia at high altitudes- bone marrow repicate to store more O2.
2. Cyclic Enlargement of Endometrium & Breast during Menstrual Cycle ( back to normal after)
3. Regrowth of Liver Parenchyma after surgical excision is Compensatory

Front 42

Some hyperplasias are pathologic-1

Back 42

1. Epithelial hyperplasia caused by HPV- on lip cauflower looking - squamos carcinoma

Front 43

Hyperplasia may be combined with Hypertrophy- 2

Back 43

1. Enlargement of uterus of pregnancy, myometrial smooth muscle cells increased
2. Benign Prostatic Enlargement

Front 44

Hyperplasia's:
1. Fibrous Hyperplasia-
2. Inflammatory papillary Hyperplasia-

Back 44

Both due to ill fitting dentures
1. Fibrous Hyperplasia- fibroma-tissue
2. Inflammatory papillary Hyperplasia- palate

Front 45

Hyperplasias:
3. Osseous Hyperplasia-
4. Sub-pontic Osseous Hyperplasia-

Back 45

3. Osseous Hyperplasia- HARD TISSUE - bony hard- above teeth in gums=Exostosis= bone proliferation
4. Sub-pontic Osseous Hyperplasia- Reactive lesion- w/ dentures= bone proliferation- reactive to contents in anatomical location

Front 46

Hyperplasias:
5. Hyperplastic Dental Follcle-
6. Condylar Hyperplasia-

Back 46

5. Hyperplastic Dental Follcle-Enlarged radiolucency follicle.
6. Condylar Hyperplasia-Idiopatic Unilateral growth of mandibular condyle ( clinically- facial assymetry= open bite)

Front 47

Hyperplasias:
7. GINGIVAL HYPERPLASIA
-9 (5 dz)

Back 47

1.Inflammatory Hyperplasia-Due to poor hygiene and diabetes
2. Drug-Induced Enlargement- Ca+ Channel Blocker, Cyclosporine, dilantin
3. Leukemic infiltrates
4. Amyloid Infiltration
5. Klippel-Trenaunay Webber syndrome
6. Juvenile hyaline fibromatosis
7. Cowden Syndrome
8. Wegener Granulomatosis
9. others- ooo

Front 48

Hyperplasias:
8. Gynecomastia-

Back 48

Hyperplasia of male breast
- hormone secreating tumor that causes this

Front 49

What is Atrophy and what are the 2 types?

Back 49

Atrophy- Reduction of Size of Cells, Tissues or Organs
2 types: Pathologic & Physiologic atrophy

Front 50

Pathologic Atrophy-2

Back 50

Pathologic Atrophy-
1.atrophy of SKELETAL MUSCLE following DENERVATION- loss of innervation to skeletal m.
2.Atrophy of the BRAIN due to Ischemia

Front 51

Physiologica Atrophy- 2

Back 51

1. Atrophy of the uterus after pregnancy- back to normal
2. Involution of the thymus in early adult life

Front 52

Pathologic Atrophy may result from: 6 things-

Back 52

1. Disuse- don't use lose- cast
2. Denervation- nerve supply compromised
3. Lack of Trophic hormones
4. Ischemia- Reduction in Blood Supply
5. Malnutrition
6. Idiopathic- Romber syndrome- hemofactial atrophy)

Front 53

Atrophy of Brain in Atherosclerotic dz or alzheimer dz- what happens?

Back 53

Gyri- narrower
Sulcus- wider

Front 54

What is metaplasia?

Back 54

The replacement of 1 Mature Cell Type by another 1, so it can netter cope in its present environment
- usually a "tougher" cell type

Front 55

What is the metaplasia that occurs in smokers?

Back 55

Replacement of Bronchial STRATIFIED COLUMNAR epithelium by SQUAMOUS Epithelium = SQUAMOUS METAPLASIA- protects for litmited amt of time

Front 56

What is the Intestinal Medipalsia of the esophagus called and waht is it caused by?

Back 56

Barrett's esophagus- Caused by chronic irritation by gastric juices in GASTROESOPHOGEAL REFLUX.

Front 57

IS metaplasia reversible?

Back 57

YES reversibly and tissuye reverts back to its normal state after irriatnt has been removed
HOWEVER, if irritant persists, metaplasia may progress to dysplasia and the to NEOPLASIA!

Front 58

Necortizing Sialometaplasia

Back 58

- Palate only= reactive condition
- salivary gland tissue=> squamos tissue

Front 59

How Cells adapt to NON-LETHAL INJURY-
Adaptive-4
vs.
Non-adaptive- 2

Back 59

Adaptive- hyperplasia, hypertrophy, atrophy, metaplasia
NON-ADAPTIVE:
1. Aplasia
2. Hypoplasia

Front 60

Agenesis?

Back 60

- Complete absence of an organ (organ was never there)
(aplasia -used sometimes but not same meaning)

Front 61

Aplasia?

Back 61

Absence of an organ w/ retention of the organ rudiment.
(Agensis- -used sometimes but not same meaning)

Front 62

Reacher Collins Syndrome

Back 62

Mandibulo-Facial Dysplasia
- Agenesis of exterior portion of ear

Front 63

Agensis vs aplasia in a radio graph of teeth- missing vs smaller than normal??

Back 63

Agensis= congenitally missing
Aplasia- teeth present but smaller than normal

Front 64

Hypoplasia?

Back 64

Incomplete development of an organ
-Organ never reaches its normal size

Front 65

Dysplasia?

Back 65

= Abnormal Formation.
bad growth, pre malignant lesion...

Front 66

Epithelial dysplasia-

Back 66

Can appear red, white, or both, abnormal maturation of epithelial cells
-precancerous biopsy used

Front 67

Ectodermal Dysplasia-

Back 67

Not precancerous
-Ecto derm- skin, hair, sweat glands

Front 68

Fibro-osseous dysplasia

Back 68

commonly seen in jaw bone radiolucent radiograph

Front 69

Fibrous Dysplasia

Back 69

Enjlarged jaw- tumor in jaw, causes expansion of the mandible

Front 70

Reversible Changes (cells?)

Back 70

1. Cellular swelling (hydropic, casuclar, change)
2. Fatty Change- LIVER-> alcholoics go back unless too far

Front 71

Irreversible changes (cells)

Back 71

- now get cell death- which occurs in 1 of 2 ways:
1. necrosis
2. apoptosis
(mechanism difference between the 2)

Front 72

Necrosis-

Back 72

Enxymatic digestion & leakage of cellular contents
- messy, cells break down, inflame cells,

Front 73

Apoptosis-

Back 73

Phagocytosis of apoptotic cells & fragments. -death of cell 1 at a time--> clean- macrophages there handy to clean things up.

Front 74

What are the 3 nuclear changes that signal cell death in NECROSIS?

Back 74

1. Pyknosis
2. Karyorrhexis
3. Karyolysis

Front 75

Nuckear changes that signal cell death in Necrosis:
1. Pyknosis-

Back 75

-small, dark, & shrunken nucleus..
(dark nucleus=hyperchromatic)

Front 76

Nuckear changes that signal cell death in Necrosis:
2. Karyorrhexis-

Back 76

-nuclear fragmentation.
(-nuckeus in small pieces)

Front 77

Nuckear changes that signal cell death in Necrosis:
3. Karyolysis

Back 77

- dissolution of the nucleus.
(Can't really see anything)

Front 78

What tells you Whether cells have DIED or not? (in Necrosis?)

Back 78

The NUCLEI
(-Pyknosis, karyorrhexis, karolysis)

Front 79

What tells you HOW the cells have Died?? (in Necrosis?)
-4General tissue patterns of necrosis

Back 79

the CYTOPLASM
- 1. Coagulative necrosis
2. Liquefactive necorsis
3. Casseous necorsis
4. Fat necrosis

Front 80

-4 General tissue patterns of necrosis (Cytoplasm-How cells have died)
1. Coagulative necrosis-

Back 80

- Typically seen in HYPOXIC Injury (myocardial infarct)
(-Most often seen in heart, but can see in kidneys)
-->Have Basic Shape but No Internal detail

Front 81

-4 General tissue patterns of necrosis (Cytoplasm-How cells have died)
2. Liquefactive necrosis-

Back 81

Typically seen in bacterial infections!
-(Brain- cerebral infarcts, and Abcess formations- pus)

Front 82

-4 General tissue patterns of necrosis (Cytoplasm-How cells have died)
3. Caseous necrosis

Back 82

Necrotic tissue is converted into a Cheesy Mass (Tuberculosis)
-(Can't tell granulomatous inflamation??????? idk?)

Front 83

-4 General tissue patterns of necrosis (Cytoplasm-How cells have died)
4. Fat necrosis-

Back 83

Characteristically seen in ACUTE Pancreatitis

Front 84

Apoptosis-

Back 84

Programmed Cell Death through Activation of an INTERNAL SUICIDE PROGRAM
( very clean, engineered celll sucided, neat & clean)

Front 85

What is Capsases?
What does Capases fx/do?

Back 85

Capases- Enzyme responsible for Apoptosis of selected unwanted cells,
Capases fx:-Selectively Eliminates unwanted cells w/minimal disturbance to the surrounding cells.

Front 86

In Apoptosis- after capases selectively eliminates the unwanted cell- what happens to the cell and its parts (PM, etc)?

Back 86

The PM- remains intact but its structure is Altered so that it becomes a Target for Phagocytosis
-The dead cell is Rapidly Cleared before its contents have leaked out &therefore does NOT elicit an INFLAMMATION reaction. (inflamation is what cuases messy necorsis)

Front 87

Apoptosis: Physiologic vs. Pathologic
1. Physiologic- 4 examples of when

Back 87

1. Programmed destruction of cells during embryogenesis
2. Hormone-dependent Involution of Tissues in the Adult
3.Deletion of potentially harmful Self-reactive lymphocytes
4. Cell Death induced by cytotoxic T-cells (Virally-infected or neoplastic cells)

Front 88

Apoptosis: Physiologic vs. Pathologic
2. Pathologic-4 examples of when apoptosis is pathological

Back 88

1. If DNA repair mechanism can't cope w/damage, the cells kills itself by apoptosis. ( if dna can't repair)
2. Cell death in certain viral infections (hepatitis)
3.Pathologic atrophy in organs after obstruction. (ex salivary glad tissue -atrophy &individual cells death-apop)
4. Cell Death in Tumors*

Front 89

What are the 2 typpes of Pigments?

Back 89

1. Exogenous Pigments
A.Carbon- anthracosis (air polutant)
B.Tatooing -skin & mucosal tattoos. (amalagam embedded in tissue)
2.Endogenous Pigments
A.Lipofucscin
B. Melanin-formed in mylanocytes
c. Hemosiderin-hemoglobin derived
d. Bilirubin

Front 90

2 Pigment types
1. Exogenous Pigments
- 2 ex

Back 90

1. Carbon- anthracosis (air polutation.
2. Tatooing -skin & mucosal tattoos. (amalagam embedded in tissue)

Front 91

2 Pigment types
2.Endogenous Pigments
-4 ex

Back 91

1. Lipofucscin- yellow brown- aging pigments- wear & teat, move free.??
2. Melanin-formed in mylanocytes- dark
3. Hemosiderin-hemoglobin derived =>By product of RBC contains iron
4. Bilirubin-By product of RBC but does NOT contain Iron

Front 92

What is a Pathologic Calcification?
What are the 2 types of Pathologic Calcification?

Back 92

Pathologic Calcification- the Abnormal Deposition of Calcium Salts in Tissue
2 types:
1. Dystorphic calcifications
2. Metastatic calcifications

Front 93

2 types of Pathologic Calcification:
1. Dystrophic Calcification-

Back 93

- Occurs in NONViable tissues or Dying tissues in the presence of Normal Serum Calcium levels

Front 94

2 types of Pathologic Calcification:
2. Metastatic Calcification-

Back 94

Occurs in VIABLE tissues & is associated with Hypercalcemia
(serum calcium is elvated)