Disorders of Cell and Tissue Metabolism

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144 Terms

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Cellular homeostasis
cell maintains its morphofunctional integrity
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How is cell injury developed?
If the adaptive capability is exceeded or if the external stress is inherently harmful or excessive
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if the stress is severe, persistent, or rapid in onset, it results in ___________ ____ ________ and necrosis or apoptosis of cells
irreversible injury
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physiologic vs pathologic adaptation
responses of cells to normal stimulation vs to stress
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Labile tissue - made by + ex
cells which retained the ability to proliferate in post-natal life and have a high rate of turnover, hematopoietic cells
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Stable tissues + ex
good regenerative ability but low rate of turnover, bone
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Permanent/differentiated tissues - made by + ex
cells which have lost the ability to proliferate being divided only during fetal life, muscle + neurons
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Hyperplasia
enlargement of an organ or tissue due to the increase of cells
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During hyperplasia in ________ tissues, the structure of the tissue is not affected
labile
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Two types of hyperplasia
compensatory and hormonal
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mechanical factors, chronic hypoxia, hormones overproduction, chronic inflammations, tissue repair, genetic factors are all causes of ___________
hyperplasia
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Consequences of hyperplasia
malignant transformation (reversible)
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Hypertrophy
increase in the size and weight of an organ or tissue due to increase of cells in volume, without division
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Hypertrophy is caused either by
increased functional demand or by growth factor or hormonal stimulation
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2 types of pathologic hypertrophy
adaptive (after workout) and compensatory
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The mechanisms driving cardiac hypertrophy involve at least two types of signals:
mechanical triggers and soluble mediators (for cell growth)
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Consequences of hypertrophy
metabolic disorders, sclerosis
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Atrophy
decreasing of tissue or organ size by the loss of cell substance
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Cellular atrophy results from a combination of decreased _________ _________ and increased __________ ___________
protein synthesis, protein degeneration
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Generalized atrophy is associated with
cachexia, malnutrition, senile atrophy
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Local atrophy is associated with
decreasing in size, vessels with winding direction
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mechanical factors, loss of innervation, malnutrition, hormonal insufficiency, aging are causes of ____--
atrophy
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What organs undergo involution/physiological atrophy
thymus + genital organs
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Hypoplasia
failure of organ or whole body development, of morphogenesis, decreasing in size
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Aplasia
lack of development/morphogenesis of an organ
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Agenesis
lack of an organ and its primitive embryological structures
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Metaplasia
transformation of a mature tissue into another mature tissue
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In which type of cell adaptation does a cell type sensitive to a particular stress is replaced by another cell type better able to withstand the adverse environment?
metaplasia
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The influences that induce metaplastic change in an epithelium, if persistent, may predispose to
malignant transformation
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Types of metaplasia
squamous (smokers) + columnar (intestinal)
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dystrophy
Metabolic disorders with morphological changes
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Which disorders are reversible? Dysmetabolism, dystrophy, necrosis
dysmetabolism and partially dystrophy
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Hypoxia, physical, infectious + chemical agents, immunological rxns, cell aging, metabolism errors and nutritional imbalances are causes of what?
cell injury
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Reversible cell lesions
- Cellular swelling
- Na + /K+ pump
- Steatosis (Fatty change)
- Disorders of ER
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Irreversible lesions - apoptosis and necrosis - what happens?
mitochondria + cell membrane fxn loss, cell fragmentation, nucleus necrosis, death
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hydroelectrolitic balance disorder
cell hyperhydration due to its inability to regulate the ionic and fluid balance across the plasma membrane
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where do hydroelectrolitic balance disorders occur
kidney, liver, myocardium
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Parenchymatous (granular) changes of hydroelectrolitic balance disorder
swollen mitochondria, reversible or leads to other metabolic disorders or necrosis
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Hydropic or vacuolar degeneration of hydroelectrolitic balance disorder
swollen cytoplasm, reversible process or cell necrosis
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Fatty change
accumulation of triglycerides in the cytoplasm of those cells which do not contain them in physiological conditions
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Fatty change - unaffected vs affected metabolism
unaffected - fatty infiltration, lipid accumulation caused by hyperlipemia
affected - = fatty change caused by hypoxia/anoxia + toxins infections
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Morphology of fatty change
enlarged organ, yellow, soft, friable, greasy when cut
clear vacuoles in cytoplasms
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localization of fatty change in liver
@ lobule periphery - hyperlipemia
in center - hypoxia
diffuse - toxins
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localization of fatty change
liver
heart (diffuse)
kidney (tubular epithelial cells)
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___________ is a simple protein (scleroprotein)
keratin
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orthokeratosis
Thickening of stratum corneum without retained nuclei (hyperkeratosis w/o parakeratosis)
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Hyperkeratosis
thickening of the stratum corneum
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causes of hyperkeratosis
congenital + mech factors, sun, viruses
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Parakeratosis
increased epidermal turnover
lack of stratum granulosum and lucidum + retention of small nuclei in the stratum corneum
pinkish red plaques with fine, silver scales
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Dyskeratosis
abnormal keratinization occurring prematurely in the inferior epidermal layers
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leukoplasia
mucosal keratinisation, abnormal location of keratinization process
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cholesteatoma
abnormal location of keratinization process in tympanic cavity
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__________ is a T cell-mediated inflammatory disease
psoriasis
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Verrucae are proliferative lesions of _______________ that are caused by ________
squamous epithelial cells
HPV
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intracell accumulation of proteins causes
nephrotic syndrome, Russel bodies - plasma cells, alcoholic hyaline
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bronze diabetes is caused by intracell accumulation of
hemosiderin
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lipoidosis is an intracell accumulation of phospholipids and causes
Gaucher, Tay-Sachs disease
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glicogenosis (intracell accumulation of glycogen) causes
diabetes, Gierke disease, inflammations (in granulocytes)
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Intracellular hyaline deposits occurs where?
1. droplets in renal tubes
2. Mallory bodies, alcoholic hialin (liver)
3. Russel bodies (plasmocytes)
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intracell accumulation of cholesterol causes
Cholesterolosis (gallbladder), Xantelasma, Aortic atherosclerotic plaques
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Hb pigments w/o iron
bilirubin, porfirin
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Hb pigments w/ iron
hemosiderin, hemomelanin (malaria pigment), acid hematin
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Non-hemoglobin pigments
melanin, lipofuscin (aging pigment), lipochrom, lutein
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exogenous pigments
Pneumoconioses (dust accumulation in lungs), dietary + skin pigmentations
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________ is the end product of heme degradation
bilirubin
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Localized accumulation of bilirubin occurs within
echymosis (Hb - Biliverdin - Bilirubin)
tissues with necrosis
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If unconjugated bilirubin levels rise, this unbound fraction may diffuse into ________ and produce toxic injury
tissues
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Pathways of bilirubin metabolism
Hb - Biliverdin - Bilirubin-Albumin complex - thru liver - urobilirubin
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Jaundice and icterus
yellow-orange coloration of the skin and whites of the eyes caused by high levels of bilirubin in the blood (hyperbilirubinemia)
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Mechanic (obstructive or post-hepatic) jaundice - cause
obstruction of the bile ducts
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Mechanic (obstructive or post-hepatic) jaundice - consequences
conjugated Bi
billiary acids (cholemia)
pale faeces (acholia)
steatorrhea (fat in stools)
lack of Ubg in urine
cholangitis
billiary hepatitis/cirrhosis
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Hepatocellular (intrahepatic) jaundice - cause
lesions of hepatocytes
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Hepatocellular (intrahepatic) jaundice - consequences
high levels of alcalin phosphatase + cholesterol
decolored faeces (hypocholia)
Bi- and Ubg-uria in urine
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Hemolytic (pre-hepatic) jaundice - cause
increased hemolysis
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Hemolytic (pre-hepatic) jaundice - consequences
hypercolored faeces (hypercholia)
in urine: Bi- and Ubg-uria
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Morphology of severe jaundice
icterus viridis (green) icterus melas (black)
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morpho of jaundice in liver
plugs of Bi in hepatocytes
bilirubin cylinders (bile ducts)
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morpho of jaundice in kidney
biliary infarction
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morpho of jaundice in brain
nuclear jaundice (only in newborns)
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Gilbert-Meulengracht syndrome
Congenital disorders of Bilirubin metabolism, reduction of glucuronil-transferase activity fluctuating jaundice, tiredness
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Crigler-Najjar syndrome
Congenital disorders of Bilirubin metabolism, lack of glucuronil-transferase, death within first year of life
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Dubin-Johnson syndrome
Congenital disorders of Bilirubin metabolism, decreasing excretion of bilirubin, fluctuating jaundice, Bi and pigments within hepatocytes, conjugated Bi, hepatomegaly
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Rotor syndrome
Congenital disorder of Bilirubin metabolism, fluctuating jaundice, benign outcome
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lipofuscin
- yellow-brown insoluble pigment in lysosomes, 'aging' pigment
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lipofuscin accumulates in
hepatocytes
myocardium
neural cells
seminal vesicles
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decreased melanin consequences
albinism, vitiligo, leucoderma
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Hyperpigmentation (melanin accumulation) consequences
chloasma (pregnancy), Addison disease, Peutz-Jeghers syndrome acanthosis nigricans, xeroderma pigmentosum
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Pneumoconioses vs Anthrachosis
Pneumoconioses - dust, occupational lung diseases
Anthrachosis - carbon, coal worker's pneumoconiosis
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types of melanic tumours
nevi, benign and malignant lentigo, malignant melanoma
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Silicosis
disease due to silica or glass dust in the lungs; occurs in mining occupations
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Asbestosis
Mg silicate, causes fibrosis and risk for mesothelioma
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Congenital metabolic diseases are due to
protein synthesis with defective function
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Phenylketonuria (PKU)
Inherited defect of enzymes in the phenylalanine/tyrosine pathway, hyperphenylalaninemia-with impaired brain development (benign is asymptomatic)
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Alpha-1-antitrypsin
plasma glycoprotein synthesized by hepatocytes which has an important role in inhibition of proteases, elastase, cathepsin G and proteinase 3 (neutrophils @ inflammation)
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lack of alpha-1-antitrypsin - consequences
pulmonary emphysema - loss of alveolar wall elasticity, cause
cholestasis - liver cirrhosis
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cystic fibrosis - cause
- dysfunction of chloride ion channels in cell membranes
- mutations in the gene CF
- abnormal water and electrolyte transport across cell membranes
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cystic fibrosis - symptoms
mucus with abnormally high viscosity in glands lumen, cystic dilatation of glands
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cystic fibrosis - localization
pancreas, bronchia, gut, testis
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Gierke disease
Glycogen storage disease, in liver + kidney
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Pompe's disease
Glycogen storage disease, in heart, liver and muscles