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Adv Patho > Mod 1: cell injury > Flashcards

Mod 1: cell injury Flashcards

1
Q

Cell injury: hypoxia
Causes
Clinical manifestation

A

Cause: decreased O2 or blood,rbc,hgb dysfunction

Sickle cell, hemorrhage, iron deficiency, asphyxiation

Ischemia triggers inflammation

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2
Q

Cell injury: Hypoxia patho

Cell swelling caused by
Ca causes-

Protein synthesis affected by

A

vO2=vmitochondrial function = v ATP production and ^anaerobic metabolism (eventually stops)

vATP=impair and fail K and Na pumps = ^Na+Ca in cell=water swells into cell

Ribosomes detach from ER + malfunction= no protein synthesis

Intracellular Ca= cytoskeleton, membrane, DNA,chromatin damage, vAtp, inflammation

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3
Q 
Cell injury markers:
CK
LDH
AST/ALT
Trop
A

CK-found in muscle cells
LDH- muscle, liver, lungs, heart, rbc, brain
AST/ALT-liver
Trop-heart

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4
Q

Cell injury: ischemic reperfusion

Free radicals created by

Apoptosis caused by

effects

A

o2 restored= xanthine dehydrogenase -> xanthine oxidate -> metabolizes purine catabolites (hypoxanthine +xanthine)

Purine catabolites accumulated bc of vATP = large amt of free radicals (superoxide, H2O2) when metabolized=membrane damage + mitochondrial Ca overload

Ph alterations, osmotic changes, inflammation, mitochondrial Ca overload==open mitochondrial permeability transition pore= ATP escapes=apoptosis

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5
Q

Free radical injury:

causes death by

A

Stealing electrons= cell injury/death
Can overwhelm mitochondria+ exhaust antioxidants=oxidative stress=injury, aging, disease

Cause lipid peroxidation

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6
Q

Reactive oxygen species cause what kind of injury

A

Cause endothelial injury= inflammation, hypertrophy, proliferation, apoptosis, fibrosis, angiogenesis vascular remodeling~atherosclerosis

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7
Q

Ethanol injury
deficiencies
dysfunction of _, effects

A

vFolic acid, magnesium, B6, thiamine, Phosphorus
Brain+peripheral nerve dysfunction~wernikes enceph, neuropathy, korsakaff phychosis
Head/neck CA d/t acetalhyde
Alters cell signaling, neuro inflammation, ox stress, brain development

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8
Q 
Apoptosis (Normal programmed death)
triggered by (3)
A

Severe cell injury
misfolded proteins (d/t mutation/free rad damage) accumulate on ER=ER stress
Infections (viral)
Obstruction in organ ducts

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9
Q

Autophagy
2 types
triggered by
provides

A

Autodigestion of cell
Catabolic-degradation of cell components
Anabolic-preserves metabolites=metabolic +nutrition homeostasis
Triggered when cells lack nutrition
Provides ATP for survival during metabolic stress, eventually leads to death

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10
Q 
aging 
effects (4)
senescence
activation of 
increase of
morbidity risk ^ d/t:
A

Telomere erosion,ER stress, DNA damage, epigenetic stress

Senescence=loss of tissue repair abilities, release proinflammatory molecules
Activation of clotting cascade=hypercoag
Increase of cytokines=inflammation
Rise in IL-6, Timor necrosis factor alpha, c reactive protein=morbidity risk

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11
Q

Body changes w aging

rise in:
skin changes:
structural changes:

A

Crp , IL6 rise seen in high visceral tissue/fatty diey

Less collagen=wrinkly and dry

Increased free radical damage
Structural changes in bones, fascia, tendons, ligaments, joints

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12
Q

More body changes w age

A

Thymus atrophy, less ova/sperm, decreased response to hormones, vGastric emptying, atrophy, sarcopenia, shorter, thinning limbs, ^fat 70/50, insulin resistance,
Cv disease risk

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13
Q

Altered cell metabolism: Ethanol

rise in :
NAD/NADH ratio rise caused by
effects (4)

A

Ethanol metabolizes
to acetalhyde in cytoplasm
In mitochondria-Acetalhyde->acetate by ADH
Oxidized niacin -> NADH during ethanol-acetate conversion=^^^NAD/NADH ratio in liver=
Pyruvate->lactic acid=Lactic acidosis
Oxaloacetate->malate=prevents gluconeogenesis=fasting hypoglycemia
Glyceraldehyde3phosphate->glycerol3phosphate-combines with fatty acids= triglycerides in liver =hepatosteatosis
decreases citric acid cycle production of NADH=acetylcoa used for ketogenesis+lipogenesis =ketoacidosis + hepatoseatosis

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14
Q 
Ketogenesis
Triggers
Role of acetylcoA
Effect on oxaloacetate
Hepatocytes role
Mitochondria
A

Starvation/DM (no energy) =^B.oxidation cycle=^amt of acetylcoa-used in citric acid cycle, combines w oxaloacetate to =citrate
Oxaloacetate used in gluconeogenesis
when oxaloacetate depleted=^acetylcoa->ketone bodies (acetoacetate, acetone, B-Hydroxybutyrate)

forms ketones in mitochondria of hepatocytes

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15
Q

Atrophy

Body cause

Cellular cause (2)

A

Decrease in cell and eventually organ size

Body cause: decreased-workload,pressure, blood supply/nutrition, hormonal stimulation

Cellular cause: increased catabolism-less organelles, imbalance between protein synthesis and degradation
Includes autophagy (self eating)
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16
Q

Hypertrophic

Body cause

Cellular cause

A

Caused by increased workload

Cell:
hormonal stimulation, ^protein in ER/membrane/myofilaments/myochondrium NOT cell fluid

17
Q

Hyperplasia
Cause

Example

A

Results from growth factors stimulating cells to divide

Resection/damage of liver= regeneration
Hormonal: mammary glands/uterus while pregnant
Endometrial CA dt GH

18
Q

Metaplasia

Cause

Example

A

Pre-CA, reversible
Chronic irritation/injury/stress signal stem cells-new cellular pathway (bc cytokines/GFs)=new cell better able to handle stressor/injury

Columnar->squamous in smokers, most common
Squamous->columnar in gerd (CA may arise) (Barrets esophagus)

19
Q

Dysplasia
Cause
Example

A

From severe persistent injury

Spreads to basement membrane in epithelial cells-preinvasive neoplasm

Pre-ca “carcinoma in situ”/not truly adaptive

Cervical dysplasia

20
Q

Oxidative stress=what diseases (4)+death how

affects pregnancy how

A 
heart disease(sclerosis), alzheimers, parkinsinons, amyotropic lateral sclerosis, arrythmias~death
preeclampsia, intrauterine growth retardation, miscarriage
21
Q

lipid peroxidation effects (damage 4, v1,^1)

A

damage Chromatin, mitochondria, DNA, proteins that maintain ion pumps + cellular transport, + vProtein synthesis, increased cell membrane permeability

22
Q

Antioxidants

A

C,E, cysteine, glutathione, albumin, ceruloplasmin, transferrin

23
Q

Free radicals created by

ROS deactivated by

A

cell metabolism, radiation/uv light, chemicals/drugs/pesticide metab, metal transition, nitric oxide(chem mediator/free rad)
deactivated by superoxide dismutase

24
Q

ROS play role in (5)

A

CV (ischemic/HF) disease, htn, hld, dm, sleep apnea

25
Q 
Ethanol cellular injury
metabolism effects (5)
A

ethanol->acetalhyde by alcohol dehydrogenase
======NAD->NADH
===
Pyruvate->Lactic acid =lactic acidosis
Oxaloacetate (used in gluconeogenesis)->malate= fasting hypoglycemia
Glyceraldehyde3phospate->glycerol3phosphate= combines w fatty acids=triglycerides=hepatosteatosis
Decreases citric acid cycle production of nadh=acetyl-CoA for ketogenesis and lipogenesis =hepatosteatosis+ketoacidosis

26
Q

Ethanol effects on the developing brain (FAS)

A 
neuroinflammation (vCell signaling)
=ox stress
vThiamine
alters autophagy
prevents brain from developing/malformation
27
Q

Necrosis

A 
rapid loss of membrane
organelle swelling
mitochondrial dysfunction
=local cell death+autolysis (autodigestion)
infarct=area of necrosis
28
Q

Autophagy key component in

A

cellular proliferation, development, remodeling
aging, CA
Neurodegen./CV disease
antigen presentation, inflammation, infection,
metabolic disease
cell death

29
Q

Cellular aging =5

A

telomere erosion, dna damage, epigenetic stress, ROS accumulation, endoplasmic reticular stress

30
Q

Starvation

A

glucose levels maintained by hepatic glycogenolysis and release of fatty acids,
hepatic gluconeogenesis occurs from lactate +alanine
3+days-adipose stores used for brain until gone, protein degradation=organ failure/death

Adv Patho (70 decks)

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