Patho exam 1

Etiology

cause of a particular disease

Idiopathic Disease

Condition where cause in unknown

Atrophy

Major Characteristic:

cell decreases in size, leads to water away of tissue cells; apoptosis can get triggered

.

Occurs in response to:

inactivity, denervation, prolonged immobility or in Alzheimer’s disease.

Hypertrophy

Major Characteristic:

Individual cells increase in size, more tissue mass.

Occurs in response to:

Increase in workload or excessive hormonal stimulation 

Hyperplasia

Major Characteristic:

increase number of cells not size

Occurs in response to:

due to metabolic demands

Metaplasia

Major Characteristic:

one type of mature cell type replaces other; reversible

Occurs in response to:

Chronic inflammatory’s irritation

Dysplasia

Major Characteristic:

Cell mature abdominally within a tissue; precancerous changes. 

Occurs in response to:

Chronic irritation

Anaplasia

Major Characteristics:

cell becomes undifferentiated and immature. 

associated with malignancy. 

Occurs in response to:

associated with malignancy

Intracellular accumulation of calcium

Major Characteristic:

Build Up of salts within stressed cells, within the cytoplasm

Occurs in response to:

Stress

Intracellular accumulations of fat

Major Characteristic:

Build up for lipids with stressed cells; can be permanent or toxic or harmless. 

Occurs in response to:

stressed hormonal substance like lipids produced acid.

What are free radicals?

Free radical is when cellular tissue damage caused by excess unstable molecules (oxidative stress)

ex: age older cells

What biochemical changes can occur to a cell under free radical attack?

• attack lipid in the cell membrane 

• increasing permeability

• protein oxidation, DNA damage, mitochondria dysfunctions disruptions of signaling pathways. 

• can lead cell death, mutation, or turn malignant

What biochemical changes occur to cells in response to hypoxia and/or ischemia?

Acidosis, cell proteins to denature and coagulate; death by lack of oxygen.

all necrotic tissue is hypoxic

Hypoxia

have reduced oxygen (oxidative phosphorylation)

Ischemia

improper blood flow to tissues more rapid & severe damage. 

What are the major antioxidants mechanisms in the body?

• enzymatic antioxidant

• non-enzymatic antioxidants

• metal-binding proteins

• repair/removal system

How do thermal or acid/base injuries affect cells biochemically?

Acidosis develops, cell proteins are denatured and coagulates.

Mechanisms of Apoptosis

programmed cell death. cell kill themselves when not associated to disease process prevention.

1. cellular shrinkage and bed forms

2. chromatin degradation

3. mitochondrial breakdown and capsize activation

4. DNA breakdown

5. fragmentation

6. eat me signal and phagocytosis

Liquiefaction

cell dies; but lysosomal enzyme aren’t destroyed, instead released & liquidity the tissue

Coagulative

acidosis occur, cell denature + coagulate → form gray mass

Fat

breakdown of fatty tissues into fatty acidsq

caseous

inflammation with yellow chessy appearance

Infarction

area of cell death caused by lack of oxygen

Gangrene

considerable area of necrotic tissue that is present

Dry Gangrene

turns brown/black, no bacterial invasion

Wet Gangrene

cold, swollen, pulseless and skin is moist and black bacterial infection almost always present, foul odor

Gas Gangrene

invaded by anaerobic, spore forming bacteria, produces bi-product of hydrogen sulfide gas. 

How can excessive intracellular calcium be toxic to cell?

because activates nuclear enzymes, which leads to DNA breakdown→ triggering apoptosis

Apoptosis

Major Characteristics: Controlled self-digestion chromatin (DNA + Protein) in the nucleus is degrading

Occurrence: not dissociated w/ a disease process programmed cell death.

Effect on neighboring cells: Not trigger an inflammatory cascade, phagocytic cells like macrophages.

Effects on wound healing: Don’t interfere / cell replacement or tissue regeneration.

What are Major players involved: Enzymes, ATP, chromatin, Mitochondria, capsizes, nuclear enzyme, phophatigylserine, phagocytic cells.

Necrosis

Major Characteristics: Unregulated process liquefaction necrosis, coagulative fat, caseous, necrosis, infarction, gangrene.

Occurrence: associated w/ disease process, injured beyond repair. 

Effect on neighboring cells: Release intercellular content, triggers an inflammatory cascade, inflammation surrounding tissue. 

Effects on wound healing: interfere w/ cell regeneration, scar tissue, bad healing.

What are Major players involved: Lysosomal enzyme, cell protein, fatty acid, fat-like substances, bacterial invasion, anaerobic spore-forming bacteria, toxins. 

Compare and contrast electrical signals with chemical signals.

Electrical:

Speed: faster

Medium: Ion flow

Range: Short to Medium

Signal: Brief

Transmission: Within Cells (Neurons/Muscles)

Chemical:

Speed: slower

Medium: molecular diffusion or circulation

Range: Short or very long

Signal: can persist

Transmission: between cells/tissues

What kind of signals pass through gap junctions? 

electrical & chemical metabolic signals

Where do you find gap junctions?

In nervous system → between neurons→ form electrical synapses;

neurons, cardiac muscles, smooth muscles, epithelial cells/tissue, developing embryos

Leakage Channels

always open

Ligand-Gated Ion Channels

open w/ binding of a specific neurotransmitter (ligands)

Voltage-Gated Ion Channels

open and close in response to membrane potential changes

Why do some cells respond to a chemical signal while other cells ignore it? 

needs right receptor; intercellular pathways

Electrical Potential

membrane potential; the voltage difference between the inside and outside of a cell due to ion distributions

Depolarization:

first phase of action potential; process of the membrane potential moving closer to zero or beginning to positive → due to Na+2 entering the cells.

Repolarization: 

the membrane returns to its resting membrane potientals

Hyperpolarization

the inside of the membrane becomes more negative than the resting potential

Threshold

The critical level of depolarization (-55 to -50 mV)

Action Potential 

• long distance signals; magnitude is constants, and is maintained throughout the length of axon

• local current flow or statutory conduction

• only results in depolarization

how long does action potential last:

short lived

how long does graded potential last:

they are long distance signals their magnitude is constant and maintains throughout the length of axon

does action potential vary in intensity?

their magnitude varies directly w/ the strength of stimulus

does graded potential vary in intensity?

Their magnitude is constant (all or none)

does the action potential travel long distances without losing their intensity?

They decrease in intensity w/ distance

does graded potential travel in long distances without losing their intensity?

the long distance signals and their magnitude is maintained throughout axon length

Does action potential result in both depolarizations and hyper polarization?

results in depolarizations or hyperpolarization

Does graded potential result in both depolarizations and hyper polarization?

only depolarization

Why does graded potentials lose strength as they move through the cytoplasm?

The lose strength because the provides resistance to ion flow. 

Do action potentials lose strength as they are conducted through the axon?  Why or why not?

No, action potential are long distance signals, its all or none. They are maintained throughout the entire length of the axon. 

Absolute Refractory Period

• timing: prevents the neuron from generating an action potential

• neuron response: prevents neuron from generating AP

• Ion channel states: Na+ opens; K+ closed

• Purpose/effect: Ensures that each AP is separated and enforces one way transmissions of nerve impulses.

Relative Refractory Period

• timing: interval following the absolute refractory period 

• neuron response: neuron can generate AP, only if stimulus is strong enough. Threshold increases.

• Ion channel states: Na+ closeed; K+ open

• Purpose/effect: strong stimulus to increasing frequency of AP events.

Where can receptor proteins be found in target cells?

• Enter-cellularly

  • cell surface, ligand-gated ion channels, G-protein receptors

• Intracellularly

  • steroid/nuclear receptors bind to nonpolar ligands. 

Lipophobic (hydrophilic) signal molecule

• polar receptor location

• extracellular, ligand gated ion channels & G protein coupled receptor

• faster onset and short-medium duration.

• directly opening chemically gated ion channels

• activates secondary messenger pathway

Lipophilic signal molecules

• nonpolar only

• intracellular receptor locations

• slower onset and longest duration 

• activates receptors 

• inductions of protein synthesis

How does extracellular calcium enter the cell? 

enters during the synaptic transmission. Also on postsynaptic membrane, neurotransmitters binds to the ligand-gated ion channels, open to let in Na+, Ca+2 into cell. 

Where and how is intracellular calcium stored?

Stored within endoplasmic reticulum

Sudden increate of Ca2+ acting as secondary messanger;

What effects can a calcium spark initiate?

• activates kinase enzymes

• activates gene and induction of protein synthesis

• phosphorylation of channels proteins

• Sudden increate of Ca2+ acting as secondary messenger; open and close ion channels

Slow dividing cells

take days to years to complete their cell cycle (ex. neurons, skeletal muscle cells, cardiac muscle cells)

Rapid dividing cells

undergo mitosis in rapid rate and complete cell cycle in hours (ex. hair, mucosal cells, epithelial cells)

Cell Cycle Phases

• Go phase

• G1 phase

• S phase

• G2 phase 

• M phase

Go Phase

cell is not actively dividing or replicating its DNA

G1 Phase

Pre-synthesis; period of protein biosynthesis

S Phase

cell synthesis or replicates DNA

G2 Phase

Post synthesis; pre-mitosis phase after DNA synthesis completed, before cell division

M Phase

Mitotic Phase; mitosis / cell division occurs

Most vulnerable part of cell cycle:

S phase; increases mitosis rates, failure of checkpoints, defective tumor supressor

tumor supressor gene

mutation in p53 protein fails to stop cycle & trigger apoptosis, allowing damaged cells to divide and pass on.

what mechanism are in place to prevent replication of a cell with mutated DNA?

The cell cycle has checkpoints to prevent mutations and boundaries to prevent backtracking.

Side effects of non-specific mechanism for cell cycle regulation?

Hair cells → hair lose

Mucosal cells → grow faster resulting in damage such as mouth sores & digestive issues. 

Epithelial cells → skin related side effects

Bone marrow cells → suppression leading to anemia, low platelets, immunosuppression (Low WBC)

Cell Differentiation

process which by dividing cell become more specialized

specialized cells

closely resembling the origin tissue, specific function

undifferentiated cells

immature cells, lost resemblance and specialization

Development of tumors

loss of differentiated cells, anaplasia, dysplasia

More differentiated

more aggressive tumor cells.

Tumor grading

Stage I (similar to OG) → Stage IV (too differentiated, size, shape is malignant)

Changes in poorly differentiated cells

Cellular pleomorphism → Shape and size of cells

Nuclear pleomorphism → Shape and size of nuclei

Nuclear Hyperchromatic

Proto-oncogene

type of regulator gene that controls mitosis

Oncogene

as genes that, along w/ proto-oncogene, controls metosis

Neoplasm

New growth, neoplasm is abnormal, uncontrolled tissue growth, causing lumps of tissue/ tumors. composed of immature cells. 

Contact Inhibition

normal controls of cell division, cancer cells do not respond to contact inhibiton

Cyclin

allows cells cycle to progress from G1→ S phase

cyclin dependent kinases

part of mechanism that allows the cell to advance through the G1 checkpoint. tumor suppressor proteins p16, p21 mentioned as CDK indicators.

CDK inhibitors

prevent progression of cell cycle, until DNA damage is repaired p16, p21

Myc

cell proliferation mediators, described as transcription factos

Retinoblastoma protein

inhibits by retinoblastoma protein (Rb) tumor suppressor protein, brakes on cell division at G1 checkpoint, by binding and inhibiting actions of transcription factors, like myc or E2F once phosphorylated, releasing these transcription factors, allowing cell cycle to proceed

Benign tumors

• margins are well defined, and tumor maybe encapsulated

• cell grow locally in a non-aggressive manner; do not invade

• effects of surround tissue: expansion creates pressure or pain

• systemic effects: are rare unless sig. portion of organ affected/ tumor secretes hormones uncontrollably. 

• doesn’t metastasize

• good prognosis

• treatment is usually surgical excision. 

Malignant tumor

• differentiated completely that it shows no resemblance to original tissue

• margins are poorly defined

• invades and destroys surrounding tissue. cancer cells are are secrete enzymes. that breakdown g proteins, spreading 

• surrounding tissue effected by compressing nearby blood vessels leading to neurosis & inflammation leading organ dysfunction

• systematic effects: weight loss, fever, loss of appetite, anemia, unusual bleeding and paraneoplasmic syndromes.

• likely to metastasize, new growth at different sites

• poor prognosis

• treatment: chemotherapy, radiation, surgery

Paraneoplastic syndrome

additional complications that occur as a result of substances related from tumor cells 

effects → neurologic, blood clots, hormonal effects