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0

Increase in SIZE of cells?

Hypertrophy

1

What are the 2 causes of Hypertrophy?

1. Increase functional demand *
2. Increase hormonal stimulation

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What is the mechanism of hypertrophy?

Increase production of cellular proteins

3

Give 2 examples of Physiologic Hypertrophy.

1. Pregnant uterus (due to estrogen)
2. Athlete's heart (increase stroke volume but decrease heart rate)

4

Give 3 examples of Pathologic Hypertrophy.

1. Left ventricular hypertrophy (Hypertensive patients)
2. Post Myocardial Infarct heart
3. Sarcoplasmic Endoplasmic Reticulum in barbiturate users and alcoholics (increase detoxification)

5

What is the stimulus for the physiologic hypertrophy of the uterus during pregnancy?

Estrogen

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Increase NUMBER in cells?

Hyperplasia

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What are the 2 cause of Hyperplasia?

1. Increase functional demand.
2. Increase hormonal stimulation

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Physiologic Hyperplasia is divided into 2?

1. Hormonal hyperplasia (increase functional capacity of a tissue when needed)

2. Compensatory hyperplasia (increases tissue mass after damage or partial resection)

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What are the 2 main mechanisms of Hyperplasia?

1. Growth factor driven proliferation of mature cells.

2. Increase new cells from stem cells.

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Give 2 examples of physiologic hyperplasia.

1. Pubertal breast changes (hormonal)
2. Liver regeneration (compensatory)

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Give 3 examples of pathologic hyperplasia?

1. Endometrial hyperplasia
2. Benign Prostatic hyperplasia
3. Angiogenital warts

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Decrease in the cell SIZE and NUMBERS.

Atrophy

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Give 7 causes of Atrophy.

1. Decreased workload (atrophy of disuse)
2. Denervation (loss of innervation)
3. Diminished blood supply (ischemia)
4. Loss of endocrine stimulation
5. Aging (senile atrophy)
6. Malnutrition (cachexia - muscle wasting)
7. Pressure

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What is the stimulus for hypertrophy in the heart?

Chronic hemodynamic overload (from hypertension or faulty valves)

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What are the triggers for hypertrophy?

1. Mechanical triggers (stretch receptors)
2. Trophic triggers (polypeptide growth factors-IGF-1) and Vasoactive agents (angiotensin II and a-adrenergic agonists)

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Give 3 mechanisms of atrophy.

1. Decrease protein synthesis
2. Increase protein degradation (Ubiquitin-proteasome pathway)
3. Autophagy

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Give an example of a physiologic atrophy.

Embryonic atrophy (notochord, Thyroglossal duct)

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Give 4 examples of pathologic atrophy.

1. Post fracture atrophy
2. Brain atrophy in CVD
3. Senile atrophy
4. Cachexia (muscle wasting)

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It is define as the replacement of one differentiated cell type with another cell type.

Metaplasia

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What is the main cause of metaplasia?

Chronic irritation

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What are the 3 types of metaplasia with 1-2 examplea each?

1. Columnar to squamous (smokers, vit. A deficiency)
2. Squamous to columnar (barrett's esophagus, cervical cancer)
3. Connective tissue (myositis ossificans)

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What is the mechanism of Metaplasia?

Reprogramming of stem cells

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What are the causes of cell injury?

1. Chemical agents and drugs
2. Oxygen deprivation
3. Physical agents
4. Infectious agents
5. Immunologic reactions
6. Nutritional imbalances
7. Genetic derangements

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A condition whereby deficiency of oxygen, which causes cell injury by reducing aerobic oxidative respiration.

Hypoxia

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Loss of blood supply from impeded arterial blood flow or reduced venous drainage in a tissue.

Ischemia

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What is the most common epithelial metaplasia?

Columnar to squamous (smokers, vitamin A deficency)

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What are the 2 processes that produces ATP?

1. Oxidative phosphorylation (major pathway)
2. Glycolytic pathway (from body fluids or hydrolysis of glycogen)

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Type of injury where there is reduced oxidative phosphorylation with resultant depletion of energy stores, cellular swelling and organelle alterations.

Reversible cell injury

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What is the first manifestation of reversible cell injury?

Cellular swelling (hydropic changes)

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Which transport mechanism in cell is automatically activated once cellular swelling occurs?

Na/K/ATPase (-4mV)

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Morphologic characteristics of necrosis

1. Increase EOSINOPHILS
2. Necrotic cell have more glassy homogenous appearance
3. Cytoplasm becomes vacuolated and appears moth-eaten appearance

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Dead cells are replaced by large, whorled phospholipid masses and the phospholipid precipitates are pagocytosed by other cells or degraded into fatty acids.

Myelin figures

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What is the result of calcification of such fatty acid residues in necrosis?

Calcium soap formation

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What are the 3 patterns of nuclear changes in necrosis?

1. Karyolysis (basophilia of chromatin may fade)
2. Pyknosis (nuclear shrinkage and increased basophilia)
3. Karyorrhexis (pyknotic nucleus undergoes fragmentation)

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Type of necrosis where general tissue architecture is preserved for a few days.

Coagulative necrosis (characteristic of hypoxic death of cells in all tissues EXCEPT the BRAIN)

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What do you call the localized area of coagulative necrosis?

Infarct (myocardial infarct as best example)

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Type of necrosis where there is complete digestion of dead cells which resulted to transformation of tissue into a liquid viscous mass (pus).

Liquefactive necrosis

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Give 3 examples of liquefactive necrosis.

1. Brain ischemia
2. Abscess formation
3. Pleural effusion

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A coagulative necrosis involving multiple tissue planes usually applied to the limb.

Gangrenous necrosis (dry gangrene)

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When bacterial infection is superimposed, coagulative necrosis is modified by the liquefactive action of bacteria and attracted leukocytes.

Wer gangrene type of gangrenous necrosis

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A distinctive form of coagulative necrosis where architecture is not preserved and formed a cheesy white gross appearance of the area of necrosis.

Caseous necrosis

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Collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border.

Granuloma formation / Granulomatous reaction

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Give me 5 diseases which causes caseous necrosis.

1. Pulmonary tuberculosis
2. Syphilis
3. Histoplasmosis
4. Coccidiodiomycosis
5. Cryptococcosis

44

What type of granuloma does sarcoidosis produced?

Non-caseating granuloma

45

Type of necrosis where there is focal areas of destruction, typically occuring as a result of release of activated pancreatic lipases into the substance of panceas and peritoneal cavity.

Fat necrosis (enzymatic type)

46

The grossly visible chalky white areas produced when released fatty acids combine with calcium in fat necrosis:

Fat saponification

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A type of necrosis where sudden trauma causes fat cells to rupture:

Traumatic fat necrosis (eg. Breast trauma)

48

What electrolyte abnormality occurs in acute pancreatitis as a result of saponification?

Hypocalcemia (saponification consumes calcium)

49

This refers to the state of reduced oxygen availability which may be caused by reduced amounts or saturation of hemoglobin?

Hypoxia

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This refers to the reduced blood flow, usually a consequence of mechanical obstruction in te arterial system:

Ischemia

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The most common clinical expression of cell injury by oxygen deprivation:

Ischemic injury

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A type of necrosis when complexes of antigens and antibodies are deposited in the walls of arteries? (Immune complexes + fibrin that leaks out : bright pink ans amorphous appearance)

Fibrinoid necrosis

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A pathways of cell death that is induced by a tightly regulated intracellular program which cells destined to die. Programmed cell death:

Apoptosis

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What are the 4 main morphologic features of apoptosis?

1. Cell shrinkage
2. Chromatin condensation
3. Formation of cytoplasmic blebs and apoptotic bodies
4. Phagocytosis of apoptotic cells or cell bodies, usually by macrophages

55

Comparison of necrosis and apoptosis according to cell type:

Necrosis - enlarged (swelling)

Apoptosis - reduced (shrinkage)

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Comparison of necrosis and apoptosis according to the nucleus:

Necrosis - pyknosis, karyolysis, karyorhexis

Apoptosis - fragmentation into nucleosome- size fragments

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Comparison of necrosis and apoptosis according to cell membrane:

Necrosis - disrupted

Apoptosis - intact; altered structure, esp orientation of lipids

58

Comparison of necrosis and apoptosis according to cellular contents:

Necrosis - enzymatic digestion; may leak out of cell

Apoptosis - intact; may be released in apoptoti bodies

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Comparison of necrosis and apoptosis according to adjacent inflammation:

Necrosis - frequent

Appptosis - none

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Comparison of necrosis and apoptosis according to role:

Necrosis- invariably pathologic

Apoptosis - often physiologic but may be pathologic after DNA damage

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Which membrane-bound organelles undergo apoptosis after they have completed their function? (Suicide bags of cells)

Lysosomes

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Most characteristic feature of apoptosis:

Chromatin condensation

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What are the biochemical changes in apoptosis?

1. Activation of caspases
2. Dna ans protein breakdown
3. Membrane alterations and recognition by phagocytes

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What is the marker for cells undergoing apoptosis?

Activation of caspases

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What are the 2 main apoptotic proteins?

1. Bax
2. Bak

66

What are the 2 main anti-apoptotic proteins?

1. Bcl-2
2. Bcl-x

67

It is the process of lysosomal digestion of materials ingeated from the extracellular environment:

Heterophagy

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Refers to lysosomal digestion of the cell's own components/contentss and a survival mechanism in times of nutrient deprivation:

Autophagy
Note: intracellular organelles and portions of cytosol are first sequestered from the cytoplasm in an AUTOPHAGIC VACUOLE. The vacuole fuses with lysosomes or golgi elements forming AUTOPHAGOLYSOSOME.

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What are components of the intracellular accumulations?

1. Lipids
2. Proteins
3. Glycogen
4. Pigments
5. Hyaline change

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The abnormal accumulations of triglycerides within parenchymal cells:

Steatosis (fatty change)

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Stain used to check for steatosis (fatty change)

Sudan IV or Oil Red-O

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What are the causes of steatosis?

1. Toxins
2. Protein malnutrition
3. Diabetes mellitus
4. Obesity
5. Anoxia

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Morphology of fatty change:

Clear vacuole within parenchymal cells

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In industrialized nations, the most common cause of significant fatty change in the liver:

Alcohol abuse

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Morphology of fatty change in the liver:

Liposomes close to the ER progressing to fatty change

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Morphology of fatty change in the heart:

Maybe uniform or with alternating bands of yellow and red (tigered effect)

77

What are the most common causes of fatty liver?

1. Alcoholism
2. Non-alcoholic fatty liver (diabetes and obesity)

78

Clusters of foamy cells are found in the subepithelial connective tissue of the skin and in tendons, producing tumorous mass known as:

Xanthomas

79

Refers to the focal accumulations of cholesterol-laden macrophages in the lamina propria of the gallbladder:

Cholesterolosis (strawberry gallbladder)

80

In this lysosomal storage disease, an enzyme involved in cholesterol trafficking is mutated, and hence cholesterol accumulates in multiple organs:

Niemann-Pick disease, type C

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Eg of disease: Intracellular accumulations of protein where there is reabsorption droplets in proximal convoluted tubules:

Nephrotic syndrome

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Eg of disease: Intracellular accumulations of protein where there is excess of normally secreted proteins:

Multiple myeloma (russel bodies)

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In multiple myeloma, the ER becomes hugely distended, producing large, homogenous eosinophilic inclusions called:

Russel bodies

84

Eg of disease: Intracellular accumulations of protein where there is defective transport and secretion, mutations in the protein significantly slow folding, resulting in build up of partially folded intermediates, which aggregated in the ER of the liver and are not secreted:

Alpha 1 - anti-trypsin deficiency

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Eg of disease: Intracellular accumulations of protein where there is accumulation of cytoskeletal proteins:

Alzheimer disease
(Neurofibrillaru tangles), Hiramo bodies

86

Eg of disease: Intracellular accumulations of protein where there is aggregation of abnormal proteins:

Amyloidosis

87

Refers to alteration within the cells or in the extracellular space, which gives a homogenous, glassy, pink appearance on H and E stain:

Hyaline change

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Give an example of hyaline change:

Hyaline arteriosclerosis in long standing hypertension and DM

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Glycogen storage disease type I:
Deficient enzyme and cardinal clinical feature:

Von Gierke
(Glucose-6-phosphatase deficiency)

Severe hypoglycemia, hepatomegy

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Glycogen storage disease type II:
Deficient enzyme and cardinal clinical feature:

Pompe
(Alpha-1,4-glucosidase)
Cardiomegaly, muscle weakness, death by 2 years

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Glycogen storage disease type III:
Deficient enzyme and cardinal clinical feature:

Cori
(Glycogen debranching)
Mild hypoglycemia, liver enlargement

92

Glycogen storage disease type IV:
Deficient enzyme and cardinal clinical feature:

Andersen (amylopectinosis)
(Branching enzyme)
Infantile hypotonia, cirrhosis, death by 2 years

93

Glycogen storage disease type V:
Deficient enzyme and cardinal clinical feature:

McArdle
(Muscle glycogen phosphorylase)
Muscle cramps and weakness on exercise

94

Glycogen storage disease type VI:
Deficient enzyme and cardinal clinical feature:

Hers disease
(Hepatic glycogen phosphorylase)
Hypoglycemia, cirrhosis

95

Glycogen storage disease type VII:
Deficient enzyme and cardinal clinical feature:

(Muscle phosphofructokinase)
Muscle cramps

96

Glycogen storage disease type VIII:
Deficient enzyme and cardinal clinical feature:

(Hepatic phosphorylase kinase)
No neuromuscular symptoms, hypoglycemia

97

The most common exogenous pigment:

Carbon/coal dust

98

Accumulations of carbon or coal dust blacken the tissues of the lungs. This condition is called:

Anthracosis

99

In coal miners, the aggregates of carbon dust may induce a fibroblastic reaction or even emphysema causing a serioua lung disease called:

Coal worker's pneumoconiosis

100

An insoluble pigment, aka as lipochrome and wear and tear or aging pigment. This is seen in the heart and liver of aging patients or patients with severe malnutrition and cancer cachexia:

Lipofuscin

101

Lipofuscin accumulates in the colon following prolonged use of Anthraquinone-containing laxatives. What is the clinical condition called?

Melanosis coli (benign condition)

102

It as an endogenous, non-hemoglobin-derived brown black pigment formed when the enzyme tyrosinase catalyzes the oxidation of tyrosine to dihydroxyphenyalanine in melanocytes:

Melanin

103

What is the black pigment that occurs in patients with alkaptonuria, a rare metabolic disease?

Homogentisic acid

104

What do you call the pigmentation where the homogentisic acid is deposited in the skin, connective tissue and cartilage?

Ochronosis

105

Hemoglobin derived, golden yellow to brown, granular or crystalline pigment in which form iron is stored in cells. It is the major storage forms of iron:

Hemosiderin (visualized using PRUSSIAN BLUE)
Note: iron is converted to blue black Ferric Ferrocyanide

106

Progressive accumulation of the iron in hemosiderin causes pigmentation of the following organs:

Hemosiderosis
1. Liver
2. Pancreas
3. Heart
4. Endocrine organs

107

Hereditary extreme accumulation of iron associated with liver, heart and pancreatic damage resulting to liver fibrosis, heart failure and diabetes mellitus:

Hemochromatosis

108

What is the most frequent cause of acquired hemochromatosis?

Repeated blood transfusions

109

What is the treatment for hemochromatosis?

1. Phlebotomy
2. Chelation (Deferoxamine, Deferasinox)

110

What are the 2 types of pathologic calcifications?

1. Dystrophic calcification
2. Metastatic calcification

111

Type of calcification emcountered in areas of necrosis:

Dystrophic calcification
- formation of crystalline calcium phosphate
- heterotrophic bone may be formed

112

In dystrophic calcification, the progressive acquisition of outer layers may create lamellated configurations called:

Psammoma bodies

113

Diseases/cancers that may have Psamomma bodies:

1. Papillary thyroid cancer
2. Serous cystadenocarcinoma of ovaries
3. Meningioma
4. Mesothelioma

114

Type of calcification that occur in normal tissues due to hypercalcemia:

Metastatic calcification

115

What are the 4 principal causes of hypercalcemia?

1. Increase secretion of PTH (parathyroid tumors)
2. Destruction of bone tissues (multiple myeloma, leukemia)
3. Vitamin D related disorders
4. Renal failure (retention of phosphate leading to hyperparathyroidism)

116

Which lung cancer causes paraneoplastic hypercalcemia?

Squamous cell carcinoma

117

Which type of lung cancer causes paraneoplastic SIADH and Cushing syndrome?

Small cell lung carcinoma

118

It is the result of a progressive decline in the proliferative capacity and life span of cella and the effects of continuous exposure to exogenous influences that result in the progressive accumulation of cellular and molecular damage:

Cellular aging

119

A state where after a fixed number of cell division, all cells become arrested in a terminally nondividing state:

Cellular senescence

120

These are short repeated sequences of DNA (TTAGGG) present at the linear ends of chromosomes and protecting chromosomal termini from fusion and degradation.

Telomeres

121

With each cell division, there is incomplete replication of chromosome ends which ultimately results in cell cycle arrest:

Telomere shortening