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quiz 1 Flashcards

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1
Q

3 causes to cell injury

A
  • deficiency
  • intoxication
  • trauma
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2
Q

primary deficiency

A

-lack of specific nutrient

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3
Q

Pellagra

A
  • B3 deficiency
  • inflammation of skin
  • cosals necklace
  • facial lesions
  • dementia
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4
Q

BeriBeri

A

B1 deficiency

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5
Q

secondary deficiency

A

nutrient in diet, lack of absorbtion

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6
Q

pernicious anemia

A
  • lack of RBCs
  • stomach not secreting intrinsic factor
  • autoimmune
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7
Q

exogenous toxins

A
  • infection(food contamination)
  • chemical(interfere with biochemical factors)
  • overdose of meds
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8
Q

Endogenous toxins

A
  • genetic (lack of enzyme production)

- activation of alternative pathways(phyenylketonuria, ionizing radiation, accumulation of normal body byproducts)

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9
Q

alkaptonuria

A
  • lack of alkapton oxidase

- urine turns black when exposed to air

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10
Q

ochronosis

A

alkapton overflows to tissue, specifically IVD, attraction of Ca salts causing calcification, blue ears

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11
Q

phenylketonuria

A

lack of phenylalanine hydroxylase

-brain damage at 15 cannot walk/speak

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12
Q

hyperuricemia

A

-gout
-increased uric acid in blood
2 causes:
-decreased kidney fx
-increased purine in diet

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13
Q

gouty arthritis

A

uric acid crystal build up in joints, extreme pain, cells puncture by sharp crystals, crystals release inflammation producing enzyme, usually 1st metatarsal

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14
Q

soft tissue gout

A

uric acid crystal penetrate the bursae of mainly olecranon and cartilage of proximal forearm and ears, tissue bulging

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15
Q

gouty kidney

A
  • asymptomatic
  • silent killer
  • deposits of uric acid crystals in kidney, complications 15 years later
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16
Q

Trauma- 5 ways

A
  • Direct Contact
  • Hypothermia
  • Hyperthermia
  • mechanical pressure
  • microorganisms
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17
Q

Frostbite

A

crystallization of cytoplasmic fluid, causing expansion and destruction of cells and tissues, skin turns black

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18
Q

Hyperthermia

A

fire, ionizing radiation high dose, electrical current

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19
Q

aneurysm

A

pouching of an aterial wall due to underdevelopment aterial layer, can rupture

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20
Q

Malaria

A

plasmodium malaria carried mosquito

  • enter RBCs begin maturation
  • result is mass destruction of RBCs=hemolytic anemia
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21
Q

Types of Cell Change

A
  • Functional
  • Structural Reversible
  • Structural Irreversible
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22
Q

Consequence of cell injury

A

-morphological and functional damage, either causing the other

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23
Q

Types of Functional Reversible

A
  • Cell and Tissue Accumulation
  • adaptive responses to cell change
  • inadequate neuro stimulus
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24
Q

Cell and Tissue Accumulation

A
  • hydropic change
  • fatty change
  • residual bodies
  • hyaline change (intracellular and intercellular)
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25
Hydropic change
- cell unable to produce ATP(mitochondrial damage) - NA/K pump unable to function and Na accumulates in cell increasing osmotic pressure - cell swells with water - vaculues try to separate into pieces - cell becomes cloudy
26
portal vein hypertension
-obstruction of liver vascular due to cell accumulation
27
Fatty Change
aka steatosis - accumulation of triacylglycerides in parenchymal cells - take up room in the cell inhibiting function - liver, kidney, heart
28
causes of fatty change
- protein malnutrition - intoxication(alcohol) - anoxia - obesity - diabetes mellitus
29
Residual bodies
scar/fragment of cell damage - lysosomes attempt to break down as much of the damaged cell as possible but residual bodies remain - liver, kidney, nervous
30
Lipofuscin
most common residual body, parts of sub-cellular membranes which are indigestible, pigment of aging
31
Hyaline Changes
-accumulation of pink glass like protein, resembling hyaline cartilage
32
Intracellular hyaline changes
- reabsorbtion droplets - mallory alcoholic - russel bodies - dutcher bodies
33
Reabsorbtion droplets
- within renal proximal tubules | - abnormal protein loss in the urine that tubules attempt to reabsorb
34
Nephritic syndrome
minimal change disease - protein is deposited within the cells of the distal convoluted tubule - once excess protein excretion stops the cells will release the deposited protein
35
Mallory Alcoholic hyaline (mallory bodies)
- found in liver- hepatocytes | - result from overconsumption of alcohol, is reversible with change in drinking habits
36
Russell bodies
- intracytoplasmic accumulation of proteins in plasma cells | - multiple myeloma-malignant condition, uncontrolled proliferation and disorder function of plasma cells in bone marrow
37
Dutcher bodies
-intranuclear accumulation of proteins -identified monoclonal tumors -
38
waldenstrom macroglobulinemia aka lymphoplasmacytic lymphoma
- characterized by hyperviscosity of the blood, due to overproduction of IgM antibodies - hyperviscosity syndrome
39
Intercellular change
- extracellular accumulation - structural irreversible - hyaline ateriosclerosis - amyloidosis
40
Hyaline ateriosclerosis
- type of intercellular hyaline change - hardening of arterioles due to hyaline (protein) accumulation - causes arterioles to become brittle and/or obstructive
41
Lacunar infarction
- hyaline ateriosclerosis in brain | - thalamus, putamen, globus pallidus
42
parenchymal (intracerebral) hemorrhagic stroke
rupture of hardened
43
Types of Functional Reversible cell change
- Cell and Tissue Accumulation - adaptive responses to cell change - inadequate neuro stimulus
44
parenchymal (intracerebral) hemorrhagic stroke
- type of hyaline ateriosclerosis - rupture of hardened arterioles, - causes hypertension
45
Amyloidosis
- type of structural irreversible - extracellular accumulation - generic term for variety of protein materials abnormally deposited in tissue - mainly autoimmune - deposits found between cells of brain, liver, kidney, skin - idiopathic - kidney most vulerable, extreme proteinuremia
46
Functional Reversible/ Adaptive Responses to cell change
- alternative metabolism - altered size - inadequate neurological stimulus - inadequate hormone stimulus
47
Alternative metabolism
- type of functional reversible - cells use alternative pathways in order to obtain ATP - otherwise the body will breakdown fat, then protein for energy
48
oxphos- ?ATP | Anaerobic glycolysis- ?ATP
- 32 ATP | - 2
49
Hypertrophy
- organ/cell enlargement due to increased demand - not increase # of cells - functional reversible
50
Hypertension
- heart muscle hypertrophy - increases demand - functional reversible
51
atrophy
cell/organ shrinkage due to decreased demand | -functional reversible
52
osteoporosis
- disuse atrophy - combination of disuse and hormone imbalance (decreased androgens) - major locations ribs, vert body, femur neck, wrist) - adaptive (functional reversible)
53
pressure atrophy
- cell/tissue compressed or nerve supply compressed - ex. kidney stones - adaptive (functional reversible)
54
poliomyelitis
- inadequate neuro stim - viral/contagious - decreased motor function - atrophy of skeletal muscles bc lack of stimulus from CNS - prevention with vaccination only - functional reversible
55
hoshimotos
- inadequate hormone stimulus, functional reversible - autoimmune, ultra-antibodies attach to TSH and thyroid not stimulated - thyroid atrophies - discovered 1913
56
graves disease
- functional reversible - antibodies that act like TSH causing overstim - hyperplasia of thyroid - exopthalamos- eye bulging
57
Structural Reversible
-cell is damaged but nucleus is intact, cell survives | -
58
examples of structural reversible
- loss of ribosomes - damage/swellling to mitochondria - blebs - myelin figures
59
bleb
- pouching of cell membrane, bulge of cytoplasm | - 1-2 reversible, 3+ irreversible
60
myelin figure
-dissection of cell membrane | 1-2 reversible, 3+ irreversible
61
structural irreversible
-destruction of nucleus, cell death
62
karyolysis
melting/dissoluition of nucleus
63
pyknosis
condensing/skrinkage of nucleus
64
karyorrhexis
-fragmented/segmented nucleus
65
necrosis
- death of cells or tissues thru injury or disease, localized - condition of cell death - necrotic tissue normally digested by cell lysosome enzymes, expelled upon cell injury
66
Coagulative necrosis
- implies preservation of basic outline of coagulated cells for a span of some days - most common type - size, shape, strength preserved - denaturation of cytoplasmic proteins - breakdown of organelles - cell swelling
67
myocardial infarction
- ex of coagulative necrosis - occurs due to lack oxy/blood supply to heart - cells maintain strength to prevent rupture of the heart against normal BP
68
infarct
zone of necrosis due to deficiency of O2/blood supply to the heart - result of infarction - loss of muscle fiber detail
69
white infarct
- white - develops in tissue with only one blood supply - heart, spleen
70
red infarct
- develops in tissue with at least a dual blood supply | - lung, liver, intestine
71
Liquefaction necrosis
- complete digestion of dead cells, resulting in transformation of these tissues into a liquid viscous mass - can occur often in CNS
72
ischemic stroke(infarction)
- liquefaction necrosis - brain tissue under goes liquefaction - 6 months for brain to remove necrotic tissue - cavitation (holes) results which fill with CSF and white tissue

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