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UWS Path I test 1

What does Bursa do?

Cushions areas of joints that are subject to friction during movement.

What is the primary function of the tonsils and adenoids?

To protect the entry into the respiratory system.

What is the function of bone marrow?

Produces blood cells.

What is the primary function of lymphocytes?

Play important role in immune reactions.

What is the primary functin of the adnexa of the eye?

Accessory structures that provide extrnal protection and allow the eyes to move.

What is the function of the middle ear?

It transmits sound waves to the inner ear.

What are the functions of sebaceous glands?

Secrete sebum to lubircate the skin and discourage the growth of bacteria on the skin.

What is the function of hair?

It aids in controlling the loss of body heat.

What is the primary function of the adrenal glands?

Regulate electrolyte levels, influence metabolism, respond to stress.

What is the function of pancreatic Islets?

Control blood levels and glucose metabolism.

What is the function of the Pineal gland?

Influences the sleep-wakefulness cycle.

What is the function of the pituitary gland?

Secretes hormones that control the activity of the other endocrine glands.

What is the function of the thyroid gland?

Stimulate metabolism, growth, and activity of the nervous system.

What is hypertrophy?

Enlargment due to increase in size not number of cells.

Hypertrophy is often combined with what?

Hyperplasia (abnormal multiplication of cells).

Hypotrophy is what and it is AKA?

A wasting of tissues, organs, or entire body. Aka atrophy.

What causes endometrial hyperplasia?


What is metaplasia?

The reversible replacement of one differentiated cell type with another mature differentiated cell type.

What is anaplasia?

A change in the structure of cells and a change in their orientation to each other.

What is aplasia?

The defective development or congenital absence of an organ or tissue.

What is dysplasia?

Abnormal tissue growth with loss of cell orientation, shape, and size

Dysplasia is always what?


When is cell injury reversible and when is it irreversible?

Reversible- when the abnotmal stress/stimuli persists for a short period of time. Irreversible- when the stress/stimuli persists or is severe.

What will swelling be like for reversible damage?

It will be generalized.

What is a bleb?

A bubble or blister.

What type of cells will have bleb's ones with reversible or irreversible damage?


What type of cells will have damage to the plasma membrane ones with reversible or irreversible damage?


What type of cells will have swelling of the ER ones with reversible or irreversible damage?

Both but irreversible damge has contiunued swelling of ER.

Cells with both reversible and irreversible damage have swollen mitochondria, but what is the difference in cells with irreversible damage?

They have vacuolization which is a Ca 2+ influx.

What happens to the nucleus in cells with reversible or irreversible damage?

Reversible- chromatin clumps. Irreversible- Nuclear condensation, fragmentation and dissolution.

What is the pH like for cells with reversible or irreversible damage?

Reversible has low intracelluar pH. Irreversible- continued low intracellular pH.

What type of cells have calcification ones with reversible or irreversible damage?


What happens to reversible damaged cells when looking at them with light microscope?

They have fatty changes (steatosis).

What is the difference between necrosis and apoptosis?

Necrosis- common after ischemia and chemical injury CELL SWELLING. Apoptosis- is programmed cell death and CELL SHRINKAGE.

What happens to the plasma membrane during necrosis and apoptosis?

Necrosis- it is disrupted. Apoptosis- Intact/altered.

What happens with the cells contents with necrosis and apoptosis?

Necrosis- enzymatically digested. Apoptosis- intact.

What type of adjacent inflammation is present with necrosis and apoptosis?

Necrosis- frequent adjacent inflammation. Apoptosis- no adjacent inflammation.

What causes necrosis and apoptosis?

Necrosis- invariably pathologic. Apoptosis- Often physiological.

Cells get injured due to what 2 types of deprivation?

1. Hypoxia- inadequate oxygenation. 2. Ischemia- loss of blood supply.

Give an example of a genetic derangement that causes cell injury?

Sickle cell anemia.

Mitochondrial damage that causes cell injury is due to what?

Increased Ca2+, oxidative stress, activated phospholiapase A2.

Aerobic respiration gives us how much ATP?

36 atp

What do we get from anareboic respiration?

2 ATP, and lactic acid.

Where will Vitamin E be doing free radical protection?

In the membranes.

Glutothione is stored mostly where to do what?

Stored in the retina to protect against all redox reactions.

Why is homogenated milk bad for us?

Xanthine oxidase is better absorbed in body.

What is the role of P-450?

Detox. It is enzymes that increase the solubility of compounds and help excrete them.

What is the down side of P-450?

While detoxing it can make some reactive oxygen intermediates which can injure cells.

Where are the P-450 enzymes found at?

In the Smooth ER of hepatocytes.

Free radical injury is induced through what?

membrane lipid peroxidation, protein modification, DNA breakage.

How are free radicals degraded?

Through enzymes, spontaneous decay, and antioxidants.

Reperfusion after anoxia (an abnormally low amount of oxygen in the body tissues) induces what?

Free radical production.

What is thrombolytic therapy?

Use of drugs to break up clotts.

What commonly happens after thrombolytic therapy?

Reperfusion after anoxia and often causes injury through free radical production.

Name 3 types of oxygen radicals?

1. Hydrogen peroxide. 2. Superoxide. 3. Hydroxyl radical.

The P-450 detoxes what?


What will lysosomal catabolism do with a subcellular response to injury?

heterophagy and autophagy.

What are 2 types of toxic cell injury?

1. Direct toxin. 2. Indirect toxin.

Give an example of a direct toxin?

Heavey metals like mercury.

How will heavy metals like mercury be toxic to cells?

It disrupts the S-S bonds.

Give an example of an Indirect toxin?

CCl4 it is metabolized in the liver to CCl3 and this is more toxic.

What leaks from damaged mitochondria?


What happens to the mitochondria with subcellular injury?

Increased number with cellular hypertrophy and decreased number with cellular atrophy. Also mitochondria may assume extreme large and abnormal shapes.

What is damaged subcellularly that will interfere with organelle and molecular transport, cell architecture, cell-to cell signals, cellular mobility and phagocytosis?

Cytoskeletal abnormalities.

What are chaperones?

Heat shock protiens (HSP).

What will HSP (heat shock proteins) respond to?

They respond to a variety of chemical/physical stimuli.

What are the 3 roles of HSP?

1. Protein folding. 2. Disaggregation of protein-protein complexes (unclumping). 3. Protein transport to cell organells.

What happens to albumin C with increased temperatures?

It denatures.

Where will proteins mostly break down at?

At sistein where the s-s bridges are.

Coagulative necrosis happens with necrosis to what areas?

Heart, liver, and kidney.

Coagulative necrosis is a result of what?

Protein denaturation.

What will coagulative necrosis look like?

Preservation of basic cell outline for several days.

Liquefactive necrosis happens where?


Liquefactive necrosis is characteristic of what 2 things?

1. Bacterial infection. 2. CNS stroke.

Liquefactive necrosis is a result of what?

Enzymatic digestion.

Gangrenous necrosis is associated with what area?

Limbs and GI tract.

Gangrenous necrosis is usually a limb with loss of blood and what?

Coagulation necrosis.

What is wet gangrene?

Coagulation necrosis with liquifactive action of bacterial infection and attracted leukocytes.

Caseous necrosis occurs where?

It is seen in tuberculosis infections.

What is the appearance of caseous necrosis?

Cheesy white appearance.

What is the tissue architecture like with caseous necrosis?

It is obliterated.

Fat necrosis occurs where?

In the pancreas

What will fat necrosis look like?

Chalky area.

Is fat necrosis a typical necrosis pattern?


What will fat necrosis look like under microscope?

Foci of shadowy outlines of fat cells with basophilic calcium deposits surrounded by inflammatory reaction.

Coag. necrosis is stimulated by what?

Hypoxia and toxins.

Histologicaly what will coag. necrosis look like?

cellular swelling, organelle disruption.

What happens to DNA with coag. necrosis?

Random diffuse from tissue damage and membrane injury.

What is the tissue reaction of coag. Necrosis?


What is the stimulus for apoptosis?

Mainly physiologic but can be pathologic.

What will cells undergoing apoptosis look like histologically?

Cellular shrinkage, chromatin condensation, apoptotic bodies.

What happens to DNA with apoptosis?

It breaks down by internucleosomal (between the nucleosome.)

What is the tissue reaction like during apoptosis?

No inflammation phagocytosis of ABs

Give an example of a pathologic pathway that could lead to apoptosis?

Injurious stimuli like radiation or hypoxia.

What will Apoptosis look like when in agarose gel culture cells?

It will look like a ladder pattern of DNA fragment.

What will necrosis or coag. Necrosis look like when in agarose gel culture cells?

It will look like diffuse smearing of DNA.

What is the receptor and the ligand that will signal apoptosis?

Ligand- FAS. Receptor- TNF

When a cell undergoes apoptosis what will leak out of the mitochondria?

Cytochrome C

When apoptotic cells breakdown they break down into what?

Apoptotic bodies.

What happens to apoptotic bodies and how?

They are phagocytosed and they have ligands on them for phagocytic receptors.

What wil execution caspases do?

Once a cell is told to undergo apoptosis from: injury, withdrawal from growth factors, ligand FAS and receptor TNF, or cytotoxic T cells then the execution caspases start the degradation of cytoskeleton and nuclear proteins.

The FAS ligand brings what together in close proximity?

Several FAS death domains.

With several FAS death domains in proximity what happens?

Autocatalysis of caspase and this leads to apoptosis.

Where is the brain of a cell?

The membrane.

What are 2 catagories of intracellular accumulations?

1. Exogenous material. 2. Endogenous metabolites.

What is hemosiderin?

An endogenous metabolite that is an accumulation of iron from RBC.

What is anthracosis?

Accumulation of a pigment that blackens the lings and the involved lymph nodes.

Give 2 examples of endogenous metabolites without using hemosiderin?

1. Lipids. 2. Pigment from tattoos.

What is steatosis?

Abnormal accumulation of triglycerides in parenchynmal cells also it is a fatty change.

Where will steatosis usually happen at?

The liver, but can happen in the heart, muscles, and kidneys.

Steatosis can be caused by what?

Alcohol abuse, toxins, protein malnutrition, Diaetes M., Obesity, and anorexia.

What will alcohol dehydrogenase do with alcohols?

It converts them into aldehydes or ketones.

What will alcohol dehydrogenase do with methanol and ethylene glycol?

Methanol- converts it to formaldehyde. Ethylene glycol- converts it to oxalic acid.

Under a microscope what will intracellular accumulations of Cholesterol and cholesterol esters look like?

Foamy appearance.

What is an intracellular accumulation of cholesterol and cholesterol esters in arteries called?


What are xanthomas?

Intracellular accumulations of cholesterol in the skin and tendon masses.

What are reabsorption droplets?

Intracellular accumulations of protein in proximal renal tubles.

What are russell bodies?

excess secretory protein synthesis which leads to intracellular accumulations of protein that leads to a distended ER with large eosinophilic inculsions.

What is amyloidosis?

Aggregation of abnormal proteins.

What are some neuro diagnosis of Intracellular accumulations of protein?

Alzheimer's, Huntington's, parkinsons's, Maybe Diabetes M. Type II.

What will help protect agains intracellular accumulations of proteins?


What is the pattern of hyaline cartilage intracellular accumulation?

There is no specific pattern of accumulation due to the variety of alteration.

What will hyaline cartilage accumulations look like in a microscope?

Homogenous GLASSY pink appearance.

What are some examples of intracelluar hyaline accumulations?

reabsorption droplets, russel bodies, Mallory alcoholic hyalin.

Where will intracellular accumulations of glycogen be found at?

In clear vacoules within the cytoplasm.

What causes intracellular accumulations of glycogen?

Glucose metabolism disorders like Diabetes M., and Genetic disorders that lead to glycogen storage disease.

Glycogen accumulations have Numbers like GSD type I-V and these are associated with an enzyme deficiency and a type of disease for the next five questions give the enzyme deficiency and type of disease for the numbers given.


GSD Type I?

Glucose-6-phosphatase, Von gierke's disease.

GSD Type II?

acid maltase, Pompe's disease.


Glycogen debrancher, cori's disease or Forbe's disease

GSD Type IV?

Glycogen branching enzyme, Andersen disease.

GSD Type V?

Muscle glycogen phosphorylase, McArdle disease.

What is Lipofuscin?

An endogenous intracellular accumulation of a brown pigment.

What is melanin?

A black pigment.

Hemosiderin is what?

A accumulation of Iron from RBC and it is considered an endogenous intracellular accumulation of a golden-brown pigment.

What does dystrophic mean?

Bad growth or abnormal growth.

What is dystrophic calcification?

Abnormal growth of calcium.

Dystrophic calcification deposition occurs where?

Only locally in dying tissue.

Dystrophic calcifications happens under what serum levels of calcium?

Under normal serum calcium levels.

What calcium metabolsim pathology is present with dystrophic calcification?


Dystrophic calcification effects arteries and hearts how?

Arteries- atherosclerosis, heart- damaged heart valves.

What will pull Ca2+ out of body?


Besides pulling Ca2+ out of the body what else will EDTA pull out of the body?

Heavy metals.

Metastatic calcifcation deposits calcium where?

IN otherwise normal tissues.

What is blood serum like during metastatic calcification?

The Calcium levels in serum are high it is also high in tissues.

Metastatic calcification is usually due to what?

Secondary hypercalcemia.

What is the most common cause of hypercalcemia?


What are the 4 pricipal causes of metastatic calcification?

1. Increased PTH from a primary tumor on the parathyroid glands. 2. Bone destruction. 3. Vitamin D related. 4. Renal failure leading to increased phosphate retention leading to secondary hyperparathyroidism.

Metastatic calcification principally affects what?

Interstitial tissue of the vasculature, kidneys, lungs, gastric mucosa.

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