Pathophysiology Cell & Tissue Function

Front 1

4 Types of Tissue

Back 1

I. Muscle Tissue
II. Nerve Tissue
III. Epithelial Tissue
IV. Connective Tissue

Front 2

Muscle Tissue

Back 2

A. Contract for Movement & Support

B. Skeletal muscle

----1. voluntary (works when you want it to)

C. Cardiac Muscle

----1. Only found in the heart

----2. Involuntary (works all the time)

D. Smooth Muscle

----1. involuntary (works all the time)

Front 3

Nerve Tissue

Back 3

A. Gives signals to muscles, informs us of environmental conditions (hot, cold, humid)

B. ex. Brain, Spinal Cord, Nerves

Front 4

Epithelial Tissue

Back 4

A. Lines our organs

B. ex. Stomach lining, skin

Front 5

Connective Tissue

Back 5

A. Connects, supports, and protects other tissues

1. ligaments, tendons, cartilage, bone, blood, fibers (organ walls)

Front 6

Endoplasmic Reticulum

Back 6

System of paired membranes and flat vesicles that connect various parts of the inner cell.

Front 7

Golgi Apparatus

Back 7

Modifies substances produced in the ER and packages them into secretory vesicles.

Front 8

Anaerobic Metabolism

Back 8

Converts pyruvate into lactic acid.

Occurs in the absence of oxygen.

*Build-up of too much lactic acid can lead to acidosis.

Front 9

Aerobic Metabolism

Back 9

Metabolizes pyruvate via Kreb's cycle (citric acid cycle) to make ATP.

Requires Oxygen

Front 10

Diffusion

Back 10

The process of becoming widely spread, as in the spontaneous movement of molecules or other particles in solution from an area of higher concentration to an area of lower concentration, resulting in an even distribution in the particles in the fluid.

Front 11

Facilitated Diffusion

Back 11

a process by which substances are transported across cell membranes by means of protein carrier molecules; also called facilitated transport

Front 12

Active Transport

Back 12

the movement of ions or molecules across a cellular membrane from a lower to a higher concentration, requiring the consumption of energy.

Front 13

****The cellular response to stress is.....?****

Back 13

Cellular Adaptation through:

1. Atrophy
2. Hypertrophy
3. Hyperplasia
4. Metaplasia
5. Dysplasia

Front 14

Atrophy

Back 14

A wasting or diminution of size, often accompanied by a decrease in function of a cell, tissue, or organ.

e.g. Nursing home, not moving

Front 15

Hypertrophy

Back 15

The enlargement or overgrowth of an organ that is due to an increase in the size.

e.g. Muscle growth from lifting weights

This is good for building muscle, but not when it happens to the heart muscle (due to hypertension).

Front 16

Hyperplasia

Back 16

An abnormal multiplication or increase in the number of normal cells of a body part.

e.g. Breastfeeding and pregnancy or cirrhotic liver.

Front 17

Metaplasia

Back 17

Change in type of adult cells in a tissue to a form that is not normal in that tissue.

Replacement of one mature cell by another to compensate for some type of damage like the lung cells of smokers.

Front 18

Dysplasia

Back 18

The alteration in size, shape, and organization of adult cell types.

Precursor to cancer (pelvic exam - pap-smear)

Front 19

Neoplasm

Back 19

altered cell differentiation & growth

Front 20

Benign neoplasm

Back 20

tumor of well-differentiated cells, resemble cells of tissues-do not metastasize/invade other tissues, grow slowly

Front 21

Malignant neoplasm

Back 21

grow rapidly, invade tissue, metastasize, lack well defined capsule/margins

Can secrete hormones/induce inflammatory response/activate enzymes

Mimic other cells by secreting hormones, etc, evade apoptosis (cell death)

Front 22

Cell Injury & Death Caused By...

Back 22

1. Physical Agents

2. Radiation Injury - UV light, ionizing radiation

3. Chemical Injury - lead, pesticide, ect.

4. Biological Injury - Viruses, Gram negative bacteria create endotoxins that are very dangerous to the host even after antibiotic kills the bacteria.

5. Nutritional Imbalances - not eating enough, eating too much.

Front 23

Mechanism of cell injury by free radicals

Back 23

1. O2 reacts with molecules, leads to imbalance in electron stability of molecule, forming free radical.

2. Free radical tries to “steal” electrons from surrounding molecules to become stable.

3. Chain reaction of free radicals damage surrounding protein, lipid, and carbohydrate cell membranes, enzymes, and DNA

Front 24

Oxidative Stress

Back 24

body can’t eliminate effect of free radicals

Front 25

Antioxidants

Back 25

“scavenge” free radicals (vitamins, enzymes)

Front 26

Environmental contributors of free radicals

Back 26

pollution

radiation

cigarette smoke

herbicides

Front 27

How Antioxidants May Prevent Against Free Radical Damage

Back 27

Antioxidants neutralize free radicals by donating one of their own electrons, ending the electron-"stealing" reaction.

The antioxidant nutrients themselves don't become free radicals by donating an electron because they are stable in either form. They act as scavengers, helping to prevent cell and tissue damage that could lead to cellular damage and disease.

Front 28

Vitamins that act as antioxidants

Back 28

Vitamin E

Vitamin C

Front 29

Vitamin E

Back 29

The most abundant fat-soluble antioxidant in the body.

One of the most efficient chain-breaking antioxidants available. Primary defender against oxidation. Primary defender against lipid peroxidation (creation of unstable molecules containing more oxygen than is usual).

Front 30

Vitamin C

Back 30

The most abundant water-soluble antioxidant in the body. Acts primarily in cellular fluid. Of particular note in combating free-radical formation caused by pollution and cigarette smoke. Also helps return vitamin E to its active form.

Front 31

Peroxidation

Back 31

creation of unstable molecules containing more oxygen than is usual

Front 32

*** What is the MOST common cause of cellular injury? ***

Back 32

Hypoxia

Front 33

Hypoxia

Back 33

Deprives O2 to cell
----Interrupts metabolism
----Interrupts generation of ATP
----Injury to cell depends on cell’s/tissue’s need for O2

Front 34

Mechanism of hypoxia

Back 34

1. Cell switches to anaerobic metabolism, using glycogen stores for energy>lactic acid byproduct

2. Failure of ATP>Failure of Na/K pump

3. Leakage of cell contents/Cell Death

Front 35

Hypo-oxygenation in relation to free radicals

Back 35

Metabolites from hypo-oxygenation can cause free radicals.

Front 36

Compartment Syndrome

Back 36

Abdomen distends due to massive amounts of liquid in intestines and vessels cannot perfuse the area of tissue; so you must relieve pressure.

After reperfusion, free radicals are released.

Front 37

***Apoptosis***

Back 37

Programmed cell death, eliminates aged/injured cells

Controls tissue regeneration

Front 38

***Normal physiologic process of apoptosis***

Back 38

Destruction of cells during embryonic process (webbed fingers and toes become regular).

Destruction of endometrial cells during menses.

Breast tissue regression after breast feeding.

Front 39

***Pathologic process from lack of apoptosis***

Back 39

***Carcinogenesis***

***ALS/Alzheimer’s/Parkinson's***

Front 40

Cell Death

Back 40

1. Necrosis

2. Gangrene

Front 41

Necrosis

Back 41

Cell death in an organ/tissue that is still alive.

----Enzymatic digestion of cell components

----Initiation of inflammatory response

Front 42

3 Types of necrosis

Back 42

1. Liquefaction Necrosis
2. Coagulation Necrosis
3. Caseous Necrosis

Front 43

Caseous Necrosis

Back 43

A type of tissue death in which all cellular outline is lost and tissue appears crumbly and cheeselike, usually seen in tuberculosis.

Also called caseous degeneration .

Front 44

Coagulation Necrosis

Back 44

Acidosis develops and denatures the enzymatic and structural proteins of the cell.

Necrosis in which the affected cells or tissue are converted into a dry, dull, fairly homogeneous eosinophilic mass as a result of the coagulation of protein.

This type of necrosis is characteristic of hypoxic tissue and is seen in infarcted areas.

Front 45

Liquefaction Necrosis

Back 45

Usually caused by focal bacterial infections, because they can attract polymorphonuclear leukocytes. The enzymes in the polys are released to fight the bacteria, but also dissolve the tissues nearby, causing an accumulation of pus, effectively liquefying the tissue (hence, the term liquefactive).

Front 46

Infarction

Back 46

Tissue death which occurs when an artery supplying an organ or part of the body becomes occluded and no other source of blood supply exists.

Front 47

Gangrene

Back 47

Considerable mass of tissue undergoing necrosis
1. Dry
2. Moist
3. Gas

Front 48

Dry Gangrene

Back 48

Results from interference with arterial blood supply to a part without interference with venous return and is a form of coagulation necrosis. The irritation caused by dead tissue produces a line of demarcation.

Usually confined to extremities.

Can turn to wet gangrene if bacteria is introduced.

Peripheral vascular disease - from smoking, clean, not infected, dead tissue.

Front 49

Moist (Wet) Gangrene

Back 49

Area is cold, swollen, and pulseless.

Skin moist, black, and under tension. Blebs form on the surface, liquefaction occurs, and a foul odor is caused.

No line of demarcation between normal and diseased tissue.

Spread of tissue damage is rapid.

Front 50

Gas Gangrene

Back 50

results from infection of devitalized tissues by one of several Clostridium bacteria.

Bubbles of hydrogen sulfide gas form in the muscles from the the bacteria's metabolism

Front 51

Autosome

Back 51

All chromosomes except for the sex chromosomes.

Front 52

Locus

Back 52

position of gene on chromosome

Front 53

Allele

Back 53

alternate forms of gene on same locus

Front 54

Autosomal Dominant Inheritance

Back 54

* Male/female offspring affected equally

* One of the parents is usually affected

* If one of the parents is heterozygous affected, the children have a 50% chance of being affected

* If both parents are heterozygous affected, the children have a 75 % chance of being affected

Front 55

Autosomal Recessive Inheritance

Back 55

* Male/female offspring affected equally

* If both parents are unaffected but are carriers for the trait, each offspring has a 1/4 chance of being affected

* If both parents are affected, all of their children will be affected

* If one parent is affected and the other is not a carrier, all of their offspring will be unaffected but will be carriers

* If one parent is affected and the other is a carrier, each of the offspring will have a 1/2 chance of being affected

Front 56

Sex-linked Inheritance

Back 56

* Caused by genes located on sex chromosomes

* Also called X-linked

* Female has XX, male has XY

Front 57

X-linked Dominant Inheritance

Back 57

* If have abnormal trait will have 1 affected parent

* If a father has X-linked dominant disorder, all daughters and none of the sons will be affected

* If a mother has an X-linked dominant disorder, there is a 50% chance that her children will be affected

* May be lethal in males, family hx of miscarriage and predominance of female offspring

Front 58

*** X-linked Recessive Inheritance ***

Back 58

* Primarily affected people are males with unaffected parents

* All daughters of an affected male will be carriers

* Sons of affected males are unaffected and can’t transmit the disease

* The unaffected males of a female carrier don’t transmit the disease

Front 59

*** Common x-linked recessive disorders***

Back 59

1. glucose-6-phosphate dehydrogenase deficiency.

2. Hemophelia A

3. X-linked agammaglobulinemia

Front 60

Single-Gene

Back 60

Autosomal Dominant
Autosomal Recessive
X-Linked Dominant
X-Linked Recessive

Front 61

Multifactorial

Back 61

More than one gene contributes to a trait

Front 62

***Marfan Syndrome***

Back 62

Autosomal Dominant Disorder

Connective tissue disorder with abnormalities in the skeletal, ocular, and cardiovascular systems.

Affects men/women equally, 1 in 20,000 people

Diagnosis based on physical characteristics and family history

Dysfunction of the gene that codes for fibrillin I which codes for microfibrils found in the extracellular matrix (responsible for making of elastice fibers necessary in heart valves, vasculars, and tendons.

Front 63

**** Marfan Syndrome Clinical Manifestaions ****

Back 63

1. Connective tissue disease

2. Retinal detachment, myopia

3. Skeletal: Joint hypermobility (circus contortionist), spinal deformities, “pigeon” chest, long thin body, pectus excavatum, arachnodactyly

4. Heart: Mitral valve prolapse

5. Vascular: Aortic valve disease, weakness of aorta leading to dissection

Front 64

**** Cystic Fibrosis ****

Back 64

Autosomal Recessive Disorder

Major cause of severe chronic respiratory disease.

Respiratory infections due to dried out airways.
Mucus clogs lungs leading to chronic respiratory infections.

Pancreatic duct obstruction.
Mucus obstructs the ducts of the pancreas, preventing digestive enzymes from reaching the intestines.

Can cause fatty, oily stools, and possible diabetes

Chloride Transport decrease

Mutation in Gene CFTR (Cystic Fibrosis Transmembrane Regulator)on chromosome 7

Front 65

**** Testing and treatment for Cystic Fibrosis ****

Back 65

Test: Sweat test show elevated sodium chloride

Treatment: Preventative therapy and lung transplant

Front 66

*** Phenylketonuria (PKU) ***

Back 66

Autosomal Recessive Disorder

Defect in amino acid metabolism.

Inability of the body to convert the essential amino acid phenylalanine to tyrosine (a precursor to melanin).

Accumulation of this AA is toxic and causes neurological disorders, mental retardation.

Light color hair & skin

Front 67

*** Treatment of Phenylketonuria ***

Back 67

Treat: Diet restriction of phenylalanine

Babies are tested at birth. Phenylalanine must be eliminated from the diet by day 7 from birth to prevent disease.

Front 68

Tay-Sachs Disease

Back 68

Autosomal Recessive Disorder

Accumulation of glycolipids in the brain neurons & retina due to failure of lysosome (enzyme) function.

Progressive destruction of neurons in brain, spinal cord, autonomic nervous system leading to mental retardation and motor problems

Blindness, seizures, death occurs by 2 to 5 years

Predominately in Eastern Jews (Ashenazi) population, 1 : 30.

No treatment but genetic screening available

Diagnosed in babies between 6-10 months.

Front 69

2 Types of Chromosomal Disorders

Back 69

1. Alterations in the structure of one or more chromosomes with rearrangement/deletion of chromosome part
-----Radiation/chemical exposure
-----Viral infections


2. Abnormal number of chromosomes
-----Failure of chromosomes to separate during oogenesis/spermatogenesis

Front 70

*****Down's Syndrome****

Back 70

Trisomy 21 - Chromosome 21 has 3 copies instead of 2


Most common chromosomal disorder

Risk increases with maternal age-increased risk for exposure to environmental factors.
1/25 in moms above 45

Front 71

*** Clinical Manifestations of Down's Syndrome ***

Back 71

* Protruding tongue
* Flat nasal bridge
* Small ears
* Single palmar (simian) crease

** Mental retardation
** Heart problems

Advice for pregnant mom:

less than 35, triple screen - check for alphafetoprotein.

greater than 35, amniocentesis, chorionic villi sampling.

Front 72

Turner’s Syndrome

Back 72

Partial or total inactivation of X chromosome

Have 45 chromosomes - 22 pairs of autosomes and 1 sex chromosome - usually the X

Present in 1 in 2,500 live births

Often results in spontaneous abortions

Diagnosed through genetic testing

Front 73

Clinical Manifestations of Turner's Syndrome

Back 73

Depend on degree of inactivation/deletion of X

Short stature (but proportionate, unlike Down's Syndrome) and webbing of neck

Lack of secondary sex characteristics

Absent ovaries, amenorrhea

COA and bicuspid aorta

Normal intelligence, but may have difficulty driving, nonverbal problem solving, math

Front 74

Teratogenic Agents

Back 74

* Agent that produces abnormalities during embryonic or fetal development

* Birth defects due to: Radiation, chemicals/drugs, infectious agents

Front 75

Teratogenic effect dependent on...

Back 75

Timing and dose of exposure

Maternal health and nutrition

Paternal reproductive health

Front 76

***Infectious Agents-TORCH***

Back 76

T-Toxoplasmosis (protozoan in cat feces, undercooked meat)

O-Others (Varicella, listeriosis, leptospirosis, EBV)

R-Rubellas

C-Cytomegalovirus (opportunistic infection)

H-Herpes

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Can cause microcephaly, hydrocephalus, eye/hearing problems