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Pathopharmacology > Unit 2 Pathphysiology - Chapter 2 Altered Cellular and Tissue Biology > Flashcards

Unit 2 Pathphysiology - Chapter 2 Altered Cellular and Tissue Biology Flashcards

1
Q

Dysplasia

Cellular Adaptation

A

atypical hyperplasia

abnormal change - size, shape, and organization of mature tissues cells; may not progress to cancer, if they do not involve entire epithelium may be reversible

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2
Q

Metaplasia

Cellular Adaptation

A

reversible replacement of one mature cell type by another, sometimes less differentiated, cell type; asssociated w/ tissue damage, repair, and regeneration; can develop from reprogramming stem cells (epithelial or connective tissue/bone marrow stem cells) d/t cytokines and growth factors in cell environment

e.g. smoker => lungs replaced with stratified squamous epithelial cells (no mucus or cilila)

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3
Q

Causes of cellular injury?

Cellular Injury

A

Hypoxia (most common?), free radicals, toxic chemicals, infections, injury, immune response, genetic factors, lack of nutrients, trauma

ultimately cell stress

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4
Q

What is necrosis, apoptosis, autophagy, accumulation, and pathologic calcification?

Cellular Injury

A
  1. necrosis - severe cell swelling and breakdown of organelles
  2. apoptosis - cellular self-destruction (programmed)
  3. autophagy - recycling factory; degrades organelles
  4. accumulation - water, pigments, lipids, glycogen, protein
  5. pathologic calcifcation - accmulation of calcium
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5
Q

Biochemical themes for cell death

Cellular Injury

A

A. ATP depletion (swelling; loss of cell integrity)
B. Lowered levels of oxygen + increased levels of oxygen-derived free radicals (destroy cell membranes and structures)
C. Increased intracellular Ca++ & loss of calcium steady state (d/t ischemia and chemicals)
D. Defects in membrane permeability (early loss of membrane d/t all forms of cell injury)

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6
Q

Sequence of events l/t cell death

Cellulary injury

A
  1. Decreased ATP production
  2. failed active transport mechanisms
  3. cellular swelling
  4. ribosomes detach from ER
  5. mitochondrial swelling (calcium accumulation)
  6. vacuolation
  7. leaked digestive content from lysosomes
  8. autodigestion
  9. lysis of plasma membrane
  10. death!
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7
Q

One particular sx that hypoxia can cause?

cellular injury

A

Inflammation (inflammed lesions can eventually become hypoxic)

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8
Q

First thing after hypoxic injury?

cellular injury

A

Ischemia

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9
Q

Reperfusion injury

cellular injury

A

Restoration of o2 after ischemic injury can result futher injury d/t the oxygen intermediates or radicals

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10
Q

Inherent reactive oxygen species (ROS)

cellular injury

A

Aerobic metabolism; important in cell function + communication, signaling pathways; regulates protein expression, posttranslational modifications, alteration of protein stability => protein stability, dictating protein fx, alter location or interactions

This includes redox-dependent regulation as well; proliferation and differentiation, immune fx, stem cell renewal, autoimmunity

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11
Q

What can cardiac ischemia and reperfusion injury cause cellwise?

cellular injury

A
  • ROS
  • pH alterations
  • Osmotic changes
  • gap junciton changes
  • Inflammatory signaling
  • Calcium overload of mitochondria
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12
Q

Mitochondrial permeability transition pore (MPTP)

cellular injury

A

D/t rapid pH restoration in cell b/c of the reperfusion, causes large pore to appear on mitochondria leaking many ATP+ and solutes l/t apoptosis.

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13
Q

What happens in low, moderate, or high levels of ROS?

cellular injury

A
  • Low (normal immune system)
  • Moderate (stem-cell differentiation and renewal via signal pathways)
  • High (hyperactive signal pathways => inflammation, cancer, cell death)
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14
Q

Free radical

cellular injury

A

a molecular species of independent existence that contains a single unparied electron in outer orbit

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15
Q

Oxidative stress

cellular injury

A

disturbance in balance between the production of and antioxidant defenses important in membrane damage process induced by free radicals; this process can active signaling pathways b/c ROS controls enzymes + transcription factors

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16
Q

Oxidative stress is an important mechanism in which general conditions? (4)

cellular injury

A
  • cell injury
  • cancer
  • degenerative diseases (alzheimer’s)
  • aging
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17
Q

What processes create free radicals?

cellular injury

A
  • redox reactions in metabolic processes (transferring of electrons)
  • absorb extreme energy sources (UV, radiation)
  • enzyme metabolism of exogenous (external) chemicals, drugs, and pesticides
  • processing of transition metals (e.g Iron, copper)
  • nitric oxide “NO” (chemical mediator, can act as independent radical)
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18
Q

Effects of free radicals? (3)

cellular injury

A
  • liquid peroxidation (destruction of unsat. fatty acids)
  • alter proteins + protein loss + misfolding
  • DNA mutations
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19
Q

How are ROS created and deactivated?

cellular injury

A
  • mitochondria or enzymes in cytoplasm (xanthine oxidase or cytochrome p-450)
  • inactivated by enzyme superoxide dismutase (SOD or O) or spontaneously
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20
Q

Hydrogen peroxide (H2O2)

cellular injury

A

cellular signaling molecule (free radical); created from SOD enzyme

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21
Q

Hydroxyl radicals

cellular injury

A

hydrolysis of water d/t ion radiation or interact w/ metals (mainly Fe and Cu) l/t macromolecule modification and toxicity

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22
Q

Nitric Oxide

cellular injury

A

important mediator and act as a free radical; in neuronal cells (neurotransmission), endothelial cells (vessel relaxation), neutrophils/macrophages (vessel relaxation + pathogen suppression)

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23
Q

Antioxidant and list of them?

cellular injury

A

blocks synthesis + inactivates free radicals; vitamin E, vitamin C, cysteine, gluathione, albumin, ceruloplasmin, transferrin

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24
Q

Enzymes important for terminating free radicals?

cellular injury

A

Superoxide dismutase (converts superoxide to h2o2)

catalase (in peroxisomes) decomposes h2o2

glutathione peroxidase (decompases h2o2 and OH-)

Hydrogen peroxide and hydroxide

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25
Q

What is the greatest source of ROS?

cellular injury

A

mitochondria

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26
Q

Aside from energy (ATP) production, what else is mitochondria responsible for?

cellular injury

A
  • intracellular ca++ regulation
  • ROS production/scavenging
  • regulate apoptotic cell death
  • activate caspace proteases (control inflammation and cell death)
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27
Q

Does mitochondria contain own DNA? Does it have an new emerging role?

cellular injury

A
  • Yes, mtDNA (mitochondrial DNA) and it encodes various enzymes involved in oxidative phosphorylation (delivery of electrons via NADH + FADH2, electron transport + proton pumping, form water by splitting o2, ATP Synthesis) for CNS, skeletal muscle, cardiac muscle, liver, and kidneys.
  • role of mediating environmental changes and genomic responses
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28
Q

Excessive hydrogen peroxide and OH radicals can cause what?

cellular injury

A

Damage lipids, proteins, and mtDNA => cell death

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29
Q

Specific conditions implicated when Mitochondrial oxidative stress occurs?

cellular injury

A

Alzheimer’s, parkinson’s, prion disease (infectious brain disease), amyotrophic lateral sclerosis (ALS or loss of muscle control), aging

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30
Q

List the toxicity pathways or cellular stress response pathways

cellular injury

A
  • hypoxia
  • ER stress
  • mental stress
  • inflammation
  • osmotic stress
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31
Q

Effects of chaparral and ma huang on liver?

cellular injury

A

Dietary supplements that are hepatotoxins

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32
Q

Liver responsible for conversion of toxins to intermediates that can adversely affect body?

cellular injury

A

true

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33
Q

Phytochemicals

cellular injury

A

Being investigated for benefits amongst select fruts + plants: chamomile (sleepiness, anxiety, GI - flower), silymarin, carrot, ginger root, milk thistle seed, rosemary, tumeric

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34
Q

Large envirnomental health risk?

cellular injury

A

air pollution

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35
Q

Risks of air polluation

cellular injury

A

stroke, heart disease, lung disease, respiratory disease, including asthma

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36
Q

Heavy metals common in toxicity?

cellular injury

A

lead, mercury, arsenic, cadmium

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37
Q

What is the recommended medical tx for children w/ high blood lead levels?

cellular injury

A

chelation therapy when greater than or equal to 45 mcg per deciliter

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38
Q

Iron (Pb) exposures affects what most in body?

cellular injury

A

alteration of cellular ion status (cations, transport mechanisms, metal enzyme cofactors)

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39
Q

Minamata Disease

cellular injury

A

Causes deafness, blindness, intellectual disability, cerebral palsy (disorder of muscle, tone, and posture), and CNS defects in children exposed in utero; leaked methylmercury from industry into water

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40
Q

How are iron (Pb) and mercury similar?

cellular injury

A

Iron and mercury both bind to sulfhydral groups (delineating or describe general role and structure of proteins and enzymes) in some proteins l/t CNS and kidney damage.

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41
Q

What can slow down absorption of alcohol? And recommended drinking amount for men + women?

cellular injury

A

Milk and fatty foods

two drinks per day for men; one drink per day for women (12 oz beer, 4 oz wine, 1.5 oz 80 proof spirit, 1 oz 100 proof spirit)

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42
Q

What is alcohol converted into?

cellular injury

A

acetylaldehyde

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43
Q

Most common chemical asphyxiant? Other gases?

cellular injury

A
  • Carbon monoxide
  • Others: cyanide (genetic trait for smell - most population lack), hydrogen sulfide (sewer gas)
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44
Q

dry-lung drowning

cellular injury

A

in 15% drowning little or no water enters lungs b/c vagal nerve-mediated laryngospasms.

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45
Q

conditions for potential of disease producing microorganism (3)

cellular injury

A
  1. invade and destroy cells
  2. produce toxins
  3. produce damaging hypersentivity rxns
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46
Q

What one of the main systems is responsible for membrane alterations during immunologic injury?

cellular injury

A

complement

opsonization (enhancing phagocytosis of antigens); chemotaxis (attracting macrophages and neutrophils); cell lysis (rupturing membranes of foreign cells); and clumping (antigen-bearing agents).

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47
Q

Antibodies can cause immunologic damage in what conditions? (Membrane wise)

cellular injury

A

Interfere w/ membrane by occupying receptors in diabetes mellitus and myasthenia gravis (autoimmune cause weakness in skeletal or voluntary muscles)

Autoantibodies in diabetes 1 against insulin or islet cells

Myasthenia gravis (MG) is a disease of the postsynaptic neuromuscular junction (NMJ) where nicotinic acetylcholine (ACh) receptors (AChRs) are targeted by autoantibodies. Causing muscle weakness and fatigue (autoimmune)

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48
Q

Genetic d/o can injure cells by altering following: (4)

cellular injury

A

Plasma membrane’s structure, shape, receptors, or transport mechanisms

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49
Q

Vitamin A purpose

cellular injury

A

metabolism of visual pigments

50
Q

vitamin K purpose

cellular injury

A

prothrombin synthesis

Prothrombin is a protein made by the liver. Prothrombin helps blood to clot. The “prothrombin time” (PT) is one way of measuring how long it takes blood to form a clot, and it is measured in seconds

51
Q

vitamins E and C purpose

cellular injury

A

antioxidation rxn’s

52
Q

pyroxidine (vitamin b6) purpose

cellular injury

A

affects amino acid transfer rxn’s

53
Q

flavin (FAD/FMN)
nicotinamide (NAD)
Purpose of them?

cellular injury

A

help transfer electrons in various reactions

54
Q

vitamin d purpose

cellular injury

A

calcium and phosphate metabolism

55
Q

Primary accidental hypothermia

cellular injury

A

previously health person exposed to the changes that occur w/ cold; can commonly happen in warmer regions; neonates and eldery great risk groups; homeless or even climbers

56
Q

secondary hypothermia

cellular injury

A

occurs d/t systemic d/o; e.g - hypothyrodism, hypoglycemia, adrenal insuffciency, metabolic alterations w/ uremia (high waste products in blood d/t kidney filter failure), neurolgic injury, extensive burns, acute MI, skin diseases, hepatic failure

57
Q

risks of cold water diving?

cellular injury

A

submersion into cold water inducing high incidence of cardiac dysrhythmias

58
Q

cold-shock response and diving response?

cellular injury

A
  1. triggers tachycadria from sympathetic nervous system
  2. while the diving response promotes a parasypathetically mediated bradycardia
  3. both happening l/t automatic conflict > dysrhythmias
59
Q

Frostbite

cellular injury

A

Continued exposure to cold; vasodilation => swellling l/t affected nerves // thrombosis as well

When the body is exposed to very low temperatures, it tries to prevent heat loss by redirecting the blood away from the extremities such as fingers and toes.

If exposure is prolonged, ice will start to form inside and around skin cells. The ice crystals block the movement of blood through the fine mesh of capillaries, which means the tissue is deprived of oxygen and nutrients. The longer the tissue remains frozen, the greater the amount of damage.

60
Q

Heat cramp

A

result of exercise d/t sweat; tx - salt replacement

61
Q

heat exhaustion

cellular injury

A

most common; loss of salt + h2o; hypotension secondary to hypovolemia

62
Q

heat stroke

cellular injury

A

high environmental temp and humidity; core temp of 106 f (41 c) is life threatening; vasodilation and decreased blood volume

63
Q

Malignant hyperthermia

cellular injury

A

elevated temp, increased muscle metabolism, muscle rigidity/spasm, rhabdo, acidosis, CV alterations, tachycardia and tachypnea, respiratory and metabolic acidosis, brown urine, hyperkalemia, elevated CK and myoglobulin, DIC, patchy, discolored skin (mottled) - lack of blood flow!, sweating

inheritied d/o of skeletal muscle sarcoplasmic reticulum in response to inhalation anesthetics (halothane, isoflurane, sevoflurane, desflurane or succinylcholine. MH is a genetic disorder passed down through families) or succinylcholine (depolarizing muscle relaxant - anectine and suxamethonium)

Inherited rxn to certain drugs used during surgery

dantrolene (Dantrium, Revonto, Ryanodex) is used to treat the reaction by stopping the release of calcium into muscles.

64
Q

Sudden infant death syndrome (SIDS) - recommendations to prevent

cellular injury

A

position supine, use firm sleep surface, breast feed, room-sharing w/o bed-sharing, routine immunizations, use of a pacifier

avoid soft bedding, overheating, exposure to smoke

65
Q

Decompression sickness

cellular injury

A

Decompression sickness occurs when rapid pressure reduction (eg, during ascent from a dive, exit from a caisson or hyperbaric chamber, or ascent to altitude) causes gas previously dissolved in blood or tissues to form bubbles in blood vessels. Symptoms typically include pain, neurologic symptoms, or both.

slowly reintroduce gas bubbles to blood if not then ischemia d/t gas emobli causing cellular hypoxia

66
Q

blast injury

cellular injury

A

sudden increase or decrease in atmospheric pressure transmitted via air or water onto human body

67
Q

3 types of high altitude illnesses

cellular injury

A

high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE), acute mountatin sickness (AMS)

68
Q

High altitude cerebral edema vs High altitude pulmonary edema

cellular injury

A

cerebral edema version - hypoxia induced cerebral vasodilation and increased in blood flow, which leak too; pulmonary edema version - hypoxic pulmonary hypertensive response (vasoconstrict l/t leakage from blood vessels to lungs to air sacs)

69
Q

Cellular swelling

cellular injury

A

shift of extracellular water into cells; in hypoxia, reduced ATP and ATPase levels permit sodium to enter cell (usually transported out), where as K+ diffuse out, this increased na+ l/t increased osmotic pressure, whichc draws more water

70
Q

Vacuolation

cellular injury

A

Cisternae of ER distend, rupture, and coalesce (form one mass) => form large vacuoles that isolate water from cytoplasm

71
Q

Progressive vacuolation resulting in cytoplasm swelling is called ____ ?

cellular injury

A

vacuolar degeneration

72
Q

Mucopolysaccharidoses (MPSs)

cellular injury

A

carbohydrate excess d/o

73
Q

Mucolipidoses (MLs)

cellular injury

A

carbohydrates and lipids excess accmulation

74
Q

MPSs and MLs are classified as ……..?

Mucopolysaccharidoses (MPS) and mucolipidosis (ML)

celluar injury

A

lysosomal storage disease; they involve increased storage of carbohydrates or lipids or both

glycosaminoglycans, present in mucus or fluid around joints (muco-) — polysaccharidoses

75
Q

Carbohydrate, lipids, or both accmulation concern which conditions?

cellular injury

A

Tay-sachs (absence of enezyme beta-hexosaminidase A that breakdown fatty acid => accmulate gangliosides affecting brain and spinal cord) // flaw in hexa gene when passed on
Muscular: muscle weakness, problems with coordination, rhythmic muscle contractions, or stiff muscles
Whole body: feeling faint or wasting away
Also common: difficulty speaking, difficulty swallowing, hearing loss, seizures, or vision loss

fabry disease (enzyme alpha-glactosidase-A cannot breakdown fatty materials or lipids)
Episodes of pain in the hands or feet.

Gaucher diease (cannot breakdown lipids d/t lacking enzyme glucocerebrosidase b/c GBA recessive gene - affect bone marrow, liver, spleen // affect jewish population)
Enlarged spleen.
Enlarged liver.
Eye movement disorders.
Yellow spots in the eyes.
Not having enough healthy red blood cells (anemia)
Extreme tiredness (fatigue)
Bruising.
Lung problems

**Niemann-Pick disease ** (lack ASMD, unable to metabolize fat, collect in macrophages)
Acid sphingomyelinase deficiency (ASMD) is a rare progressive genetic disorder that results from a deficiency of the enzyme acid sphingomyelinase, which is required to break down (metabolize) a fatty substance (lipid) called sphingomyelin. Symptoms may include:

enlarged liver and spleen (hepatosplenomegaly)
difficulty coordinating movement (ataxia)
abnormal eye movements (vertical supranuclear gaze palsy)
poor muscle tone (hypotonia)
severe liver disease.
frequent respiratory infections.
difficulty with speech.
difficulty with swallowing and feeding.

Pompe disease (buildup of glycogen in the body’s cells) — progressive weakness to heart and skeletal muscle

Classic type:

Weak muscles
Poor muscle tone
Enlarged liver
Failure to gain weight and grow at the expected rate (failure to thrive)
Trouble breathing
Feeding problems
Infections in the respiratory system
Problems with hearing

Non-classic type:

Motor skills delayed (such as rolling over and sitting)
Muscles get steadily weaker
Abnormally large heart
Breathing problems

mucopolysaccharidoses (corneal clouding, joint stiffness, intellectual disability)

76
Q

steatosis

cellular injury

A

intracellular lipid accmulation in liver

77
Q

Two ways protein accmulation can harm body?

cellular injury

A
  1. Metabolites from protein digestion can affect other organelles when released from lysomsomes
  2. Excessive proteins push against organelles
78
Q

What is present in multiple myeloma in terms of proteins?

celluar injury

A

russell bodies d/t excess proteins in B lymphocytes

Any small intracellular body found within another (accmulute in ER inside cytoplasm) – Russell bodies

Cancer of WBC

79
Q

What color does lipofuscin (aging pigment) give to cells undergoing atrophic changes?

cellular injury

A

yellow-brown

80
Q

Most common exogenous pigment

cellular injury

A

carbon or coal dust

81
Q

What condition causes the rare bronze or hyperpigmentation appearance?

cellular injury

A

Addison’s disease (melanogenesis)

Does not produce steroid hormones: cortisol; aldosterone => hypoglycemia, hypotension, wt loss, GI disturbance (n/v, abdominal pain), weakness, hair changes

Adrenal crisis:
profound fatigue, dehydration, low bp, serum NA down, serum K+ (d/t renal failure) elevated

82
Q

Albinism

cellular injury

A

inherited d/o; decrease in melanin production

83
Q

Iron enters blood from what 3 major sources?

cellular injury

A
  1. tissue stores
  2. intestinal mucosa
  3. macrophages digesting RBC
84
Q

How does hemoprotein accmulation occur?

cellular injury

A

excessive iron stored

85
Q

How does brusing appearance change in regards to hemosiderin (greater levels of iron)?

cellular injury

A

initial bruise/hemorrhage starts red-blue then lysis of RBC causing hemosiderin to build up (yellow-brown pigment) causing that yellow-brown appearance

86
Q

Condition for repeated transfuion or prolonged iron administration?

cellular injury

A

hemosiderosis

87
Q

an excess of billirubin, bile derived from hemoglobin, can cause what?

cellular injury

A

jaundice or icterus (bilirubin level exceed 1.5 -2 mg/dl rather than 0.4 - 1) // yellowing of skin

88
Q

Hyperbilirubinemia

cellular injury

A

build up of bilirubin in blood; d/t hemolytic jaundice, liver diesase, or gallstones/pancreatic tumors

89
Q

Since unconjugated billirubin can damage membrane and proteins, what can provide some protection?

cellular injury

A

Albumin can bind to them

90
Q

Dystrophic calcifcation

cellular injury

A

occurs in dead tissues of necrosis

91
Q

Metastatic calcification

cellular injury

A

occur in undamaged tissues d/t hypercalcemia // hyperparathyroidism (osteoclast and calcium reabsorption via kidney and phosphate excreted, hyperthyroidism (thyroid causes more bone resorption and excretion), addison disease (volume depletion and renal not excreting Ca++), toxic lvl vitamin D (intestinal and renal absorption)

92
Q

How is urate produced?

cellular injury

A

end product of purine (animal products from liver, intestine, muscles [exoogenous] and endothelium; dead cells from DNA/RNA [endogenous] — adenine and guanine) catabolism; missing enzyme urate oxidase then urate must be removed via bowel and urine

93
Q

Tophus

cellular injury

A

firm nodular subq deposits of urate crystals surrounded by fibrosis

Uric acid is a normal body waste product. It forms when chemicals called purines break down. Purines are a natural substance found in the body. They are also found in many foods, such as liver, shellfish, and alcohol. They can also be formed in the body when DNA is broken down.

When purines are broken down to uric acid in the blood, the body gets rid of it when you urinate or have a bowel movement. But if your body makes too much uric acid, or if your kidneys aren’t working well, uric acid can build up in the blood. Uric acid levels can also increase when you eat too many high-purine foods or take medicines like diuretics, aspirin, and niacin. Then crystals of uric acid can form and collect in the joints. This causes painful inflammation. This condition is called gout. It can also lead to kidney stones.
Niacin – vit b3 (made and used by body to turn food into energy)

94
Q

Lactate dehydrogenase (LDH)

cellular injury

A

released from RBC, liver, kidney, skeletal muscle

Tissue damage

95
Q

Creatine kinase (CK)

cellular injury

A

release from skeletal muscle, brain, heart

Increased amounts of CK are released into the blood when there is muscle damage such as a heart attack, skeletal muscle injuries, certain muscle disorders, or strenuous exercise. A CK level may also rise when excessive alcohol, cocaine, and certain medications are taken, such as a statin for elevated cholesterol.

When CK adds phosphates to creatine, it turns the creatine into the high-energy molecule, phosphocreatine, which your body uses to generate energy (muscles)

96
Q

aspartate aminotransferase (AST)

cellular injury

A

release from heart, liver, skeletal muscle, kidney, pancreas

Metabolize amino acids aspartate w/ glutamate important

Aspartate non essential + glutamate (NT)

97
Q

alanine aminotransferase (ALT)

cellular injury

A

liver, kidney, heart

98
Q

alkaline phosphatase (ALP)

cellular injury

A

liver, bone

ALP is an enzyme found in the liver and bone and is important for breaking down proteins. Higher-than-normal levels of ALP may indicate liver damage or disease, such as a blocked bile duct, or certain bone diseases.

99
Q

amylase

cellular injury

A

pancreas

An amylase is an enzyme that catalyses the hydrolysis of starch into sugars. Amylase is present in the saliva of humans and some other mammals, where it begins the chemical process of digestion.

100
Q

aldolase

cellular injury

A

skeletal muscle, heart

enzyme helps the body break down sugars to produce energy.

101
Q

troponins

cellular injury

A

heart

102
Q

Necroptosis

cellular death

A

necrosis driven by regulated or programmed molecular pathways

103
Q

difference between necrosis and apoptosis?

cellular death

A
  • necrosis: swelling; disrupted membrane; leak out; inflammation; pathologic
  • apoptosis: reduced size; fragmented nucleosomes; intact membrane; no inflammation; physiologic; apoptotic bodies remove cellular content
104
Q

gas gangrene

cellular death

A

cause gas bubbles to form in muscle cells via enzymes and toxins - clostridium; lyse RBC can be fatal

105
Q

ER stress

cellular death

A

excessive accmulation of misfolded proteins => apoptotic cell death // linked to CNS degenerative disease

106
Q

Liquefactive necrosis

cellular death

A

ishcemic injury to neurons and glial cells in the brain => cyst + pus

107
Q

coagulative necrosis

cellular death

A

kidneys, heart, adrenal glands - hypoxia caused by severe ischemia or chemical injury (mercuric chloride) => opaque state (protein albumin => gelatinous state)

108
Q

caseous necrosis

cellular death

A

TB pulmonary infection (combination of coagulative and liquefactive necrosis) => clumped cheese

109
Q

Fat necrosis

cellular death

A

breasts, pancreas, abdominal structures =? creates soap b/c free fatty acids from breakdown bind with ca++, mg, na+ (saponification)

110
Q

caspace

cellular death

A

aspartic acid-specific proteases; amplify suicide cascade; cleave other key proteins => killing cell quickly and neatly

111
Q

mitochondrial pathway

cellular death

A

intrinsic pathway

112
Q

death receptor pathway

cellular death

A

extrinsic pathway

The extrinsic pathway involves the binding of ligands to cell surface ‘death receptors’ (DR) which in turn initiates the caspase cascade.

113
Q

gangrenous necrosis caused by

cellular death

A

caused by hypoxia and subequent bactieral invasion

114
Q

Autophagy

cellular death

A

important in homeostasis; lysosomes breakdown cyatoplasmic parts and organelles and then salvage key metabolite

115
Q

senescense

aging

A

the process of aging; permanent proliferative arrest

116
Q

inflammaging

aging

A

increased levels of body cytokines and proinflammatory markers; changes with aged immune system

117
Q

Frality

aging

A

common clinical syndrome in OA

118
Q

Somatic death

Somatic Death

A

death of entire organism

119
Q

Manifestations of somatic death

Somatic Death

A

cessation of resp/circ, low temp, dilation of pupils, loss elasticity, loss transparency in skin, rigor mortis (muslce stiffening), discoloration (livor mortis)

120
Q

Putrefaction is obvious after how long (rotting)?

somatic death

A

24-48 hours after death

121
Q

sarcopenia

somatic death

A

loss of muscle mass

Pathopharmacology (99 decks)

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