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General Pathology > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

What is pathology?

A

A study of disease (suffering)

It deals with conditions, illness, disorders, sickness and syndromes

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2
Q

What is etiology?

A

The origin of a disease (Why)

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3
Q

Etiology studies the risks of disease origins be they _____ or ______

A

inherited; environmental

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4
Q

What is pathogenesis?

A

They are the steps in development of a disease (how)

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5
Q

Etiologic factors affect what specifically?

A

Cellular change

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6
Q

What are the type of morphological changes that etiology studies?

A

Gross or microscopic.

Biochemical, structural, and functional changes

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7
Q

Homeostasis requires these adaptations to stress

A

Physiologic (breast development during pregnancy) and pathologic (Streptococcal pharyngitis)

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8
Q

Cells adapt to stress in order to do what?

A

Attempt to preserve viability and function

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9
Q

What type of cellular adaptations can occur due to stress?

A

Hypertrophy, hyperplasia, atrophy, and metaplasia

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10
Q

There are moments in which the ability to adapt may be exceeded. These moments are when there are

A

Reversible and irreversible cell injury (cell death)

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11
Q

What is the definition of phenotype (as they appear in the notes)?

A

Observable characteristics or traits such as appearance and function (behavior)

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12
Q

What is THE adaptation of the cardiac myocyte in order to work against Hypertension, Coronary artery disease, congenital abnormality and/or valvular stenosis?

A

Hypertrophy

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13
Q

When we talk about cellular adaptations and we refer to hypertrophy, what actually happens?

A

Increase in size of cells and or organs (no new cells)

The cells would be incapable of replication

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14
Q

This increase in size or hypertrophy results from

A

Overloading or Growth factors

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15
Q

What is lymphadenopathy?

A

Problems with lymph nodes which are usually accompanied by the swelling of lymph nodes

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16
Q

Growth factor that cause hypertrophy could either be _____ or ____

A

Physiologic (Lifting weights)

Pathologic (hypertension -> Cardiac hypertrophy)

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17
Q

Where does rheumatic fever comes from?

A

It might come from unmanaged streptococcal infections

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18
Q

When we refer to hyperplasia as a celullar adaptation, what happens in the body?

A

Increase in the actual number of cells which must be able to replicate.

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19
Q

What are the physiological examples of hyperplasia?

A

Development of female breasts

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20
Q

What are the pathologic examples of hyperplasia?

A

Human papilloma virus (warts/verrucas) ((Genital: Condylomata acuminata))

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21
Q

Hyperplasia may also be accompanied by hypertrophy in the _____ _____

A

Pregnant uterus

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22
Q

Hyperplasia actually responds to control mechanisms (Decreases in growth factors) unlike what kind of growth?

A

Neoplasia

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23
Q

What is metaplasia?

A

Reversible replacement of 1 mature cell type by another (change from 1 cell type to another more resilient cell type)

Adaptation to prolonged stressors (smoking, GERD)

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24
Q

What is atrophy, when related to cell adaptations?

A

Reduction in cell size may be due to a decrease in protein synthesis and an increase in protein breakdown which usually leads to a decrease in function but does not mean that the cell is dead

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25
Q

What are the causes of atrophy?

A

Disuse (immobilization), ischemia (decrease of blood and or nutrients), Denervation, Endocrine disruption, and aging (senility)

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26
Q

There are two types of irreversible cell injury. What are they and are they physiologic and/or pathologic?

A

Apoptosis which is physiologic

Necrosis which is pro inflammatory and pathologic

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27
Q

What is stenosis?

A

A narrowing of a valve or canal

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28
Q

When the heart can no longer deal with the “stress” caused by factors such as HTN, CAD or valvular stenosis. What usually happens?

A

There is swelling and steatosis which could typically lead to cell death in which case could cause a Myocardial infarction or “heart attack”

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29
Q

What is the risk for metaplasia?

A

Malignant transformations

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30
Q

During cell injury, what happens to the cell?

A

Stressors exceed adaptive ability or directly induce abnormality in the cell

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31
Q

What causes cell injury?

A

Trauma (physical, thermal, irradiation) Ischemia, hypoxia, poison/toxin, infection, immune reactions, nutritional imbalance, aging

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32
Q

Celullar injury is always irreversible (true or false)

A

No there are types of reversible cell injuries

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33
Q

Reversible (transient or mild ) cell injury usually causes

A

Cellular swelling, fatty accumulation (steaosis)

No damage to membranes or nucleus

Healing occurs if stressor is removed

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34
Q

Irreversible (Prolonged or severe) cell injury can be caused by

A

Mitochondrial dysfunction or disturbed membranes

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35
Q

Irreversible injury always leads to what two types of cell death?

A

Necrosis and/or apoptosis

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36
Q

The causes of necrosis are always ______

A

pathological (ie Trauma, toxins, ischemia)

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37
Q

Is necrosis pro inflammatory?

A

Yes

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38
Q

The only cause for apoptosis is physiological

T or F

A

False, it could also be due to pathological reasons. It is also non inflammatory

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39
Q

Regarding atrophy of the brain, what could ahterosclerosis do?

A

Widen sulci and narrow gyri

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40
Q

Other than malignant transformation, what is the risk of Metaplasia?

A

Loss or altered function of the old cell

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41
Q

The process of apoptosis begins with the _____of chromatin. Later on the membrane _____ and thus the cell fragments and the ____ ____ comes loose.

In the end, The _____ ____ is “eaten” by phagocytes

A

Condensation; blebs; apoptotic body; apoptotic body

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42
Q

In necrosis, the first sign of this process would be the _____ of the ER and mitochondria. If the injury progresses, the ___ ___, organelles and nucleus start to break down and thus leading to leakage of their contents.

This causes ______ in the body

A

swelling; plasma membrane; inflammation

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43
Q

What does Karyolysis entail?

A

Nuclear fading or dissolution of the nucleus; Chromatin dissolution due to the action of DNAases and RNAases

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44
Q

What does pyknosis entail?

A

Shrinkage of the nucleus; DNA condenses into shrunken basophilic mass

45
Q

What does Karyorrhexis entail?

A

Nuclear fragmentation; Pyknotic nuclei membrane ruptures and undergoes fragmentation

46
Q

What is tissue necrosis?

A

Death of living tissue

47
Q

What does death of living tissue entail?

A

Loss of membrane integrity, leakage of contents

48
Q

What are the morphologic patterns of Tissue necrosis?

A

Coagulative, Liquefactive, caseous, fat and fibrinoid

49
Q

What is coagulative necrosis?

A

Vascular occlusion which leads to ischemia which leads to death.

Infarction could be such an example (myocardial infarction)

CNS ischemia is an exemption to this rule

50
Q

What happens to the tissue in coagulative necrosis?

A

Tissue structure is preserved, and firm.

The proteolytic enzymes are denatured

51
Q

What is gangrene?

A

coagulative necrosis in an extremity

52
Q

What could cause gangrene?

A

Peripheral vascular disease such as Diabetes and atherosclerosis

53
Q

What are the types of gangrene?

A

Dry, wet and Gas Gangrene

54
Q

What is liquefactive necrosis?

A

A type of necrosis in which dead cells are completely digested. The tissue becomes a liquid viscous mass

55
Q

What could cause liquefactive necrosis?

A

Most common cause would be Bacterial infections (yellow pus, abscess)

Fungal infections

Lack of oxygen in the CNS might cause it as well

56
Q

What is caseous necrosis?

A

A type of necrosis which has a “cheese like” appearance with a friable and yellowish white coloration.

Tuberculosis

Enclosed within a distinctive border

57
Q

What is a granuloma?

A

A byproduct a casseous necrosis. It is a walled off accumulation of macrophages

58
Q

What causes casseous necrosis?

A

Tuberculosis infections

Mycobacterium tuberculosis

59
Q

What is fat necrosis?

A

Local fat destruction

60
Q

What could cause fat necrosis?

A

Acute pancreatitis which could leak pancreatic enzymes and saponification of fat will occur

Trauma to the breast

61
Q

What is the gross morphology of Fat necrosis?

A

Chalky white particles

62
Q

what is fibrinoid necrosis?

A

A type of tissue necrosis that requires light microscopy to see.

It is due to autoimmune reactions (type 3 hypersensitivity) this produces an immune complex into which a fibrin is added. This complex attaches to arterial walls and weakens them which could lead to aneurysms

63
Q

What could cause fibrinoid necrosis?

A

Polyarteritis nodosa, systemic lupus erythematosus, malignant hypertension, and transplant rejections

64
Q

What is apoptosis?

A

Programmed or regulated cell death

65
Q

Which cells typically go through apoptosis?

A

Unneeded or irreparable cells

66
Q

There are two ways apoptosis happens it could be ____ or ____

A

Physiologic or pathologic

67
Q

Examples of physiological apoptosis would be

A

Embryonies, endometrium sloughing off, and breast tissue

68
Q

Pathological cause for apoptosis would be:

A

Dna damaged cells, misfolded proteins, and viral infections this kind of apoptosis may accompany atrophy (duct obstruction)

69
Q

What causes celullar fragmentation?

A

Activation of caspases

70
Q

The mitochondrial intrinsic pathway is stimulated by

A

Decrease in growth factor, DNA damage, and misfolded proteins

71
Q

What enzyme plays a key roles in Mitochondrial pathway in apoptosis?

A

Caspase 9

72
Q

What happens to the mitochondrial membrane during apoptosis via the mitochondrial pathway?

A

increases permeability

73
Q

The death receptor pathway of apoptosis begins with these molecules binding with other surface molecules…

A

Tumor Suppressing

74
Q

How does death receptor apoptosis work?

A

eliminating self reacting lymphocytes or virus infected cells

75
Q

What enzyme plays a key role in death receptor apoptosis?

A

Caspase 8

76
Q

What is autophagy?

A

“self eating”; Lysosomal digestion of celullar components

77
Q

Cells usually utilize autophagy as a _____ mechanism due to lack of nutrients

A

Survival

78
Q

The survival mechanism of autophagy creates _________ ______

A

Autophagic Vacuoles and organelles are sequestered and digested

79
Q

What happens to the cell when continued nutrient deprivation happens?

A

Autophagy will stop then apoptosis will ensue

80
Q

How do we rid ourselves of misfolded proteins?

A

Autophagy

81
Q

An example of misfolded proteins causing neurological problems would be _____ ______ in alzeheimers disesa

A

Beta amyloids

82
Q

What are the 6 types of celullar injury?

A

Depletion of ATP, Mitochondrial Damage, Influx or calcium and oxidative stress, defects in membrane permeability, and DNA/protein damage

83
Q

What could lead to Depletion of ATP?

A

Hypoxia, nutritional deficiency, mitochondiral damage or toxins

There would be a decrese in Oxidative phosphorylation

84
Q

What could lead to mitochondrial damage?

A

Hypoxia, toxins, and irradiation

85
Q

What are some of the effects of mitochondrial damage?

A

Loss of membrane potential leading to necrosis

Production of ROS leading to apoptosis

86
Q

What causes influxes of calcium in the cell?

A

Ischemia and toxins

87
Q

What could cause Oxidative stress?

A

Accumulation of ROS

88
Q

What could cause accumulation of ROS?

A

Ischemia - reperfusion, toxic chemicals, irradiation, celullar aging, inflammation

89
Q

What could cause defects in membrane permeability?

A

Ischemia, toxins, physical trauma, complement activation

these could lead to a decrease in phospholipid production thus causing a breakdown of cytoskeletal filaments leading to membrane damage

90
Q

What could cause Dna and protein damage?

A

severe oxidative stress,

irradiation, abnormal protein folding

91
Q

What typically occurs when DNA and Protein damage occurs in the cell?

A

apoptosis

92
Q

What is Ischemia or hypoxic injury as related to cells?

A

Its a type of acute celullar caused by decrease in blood supply. This impacts both types of metabolism in the cell leading to mitochondrial damage and a build up of Waste products

93
Q

How would ischemia/hypoxia be reversible?

A

With restoration of Oxygen

94
Q

What might happen with persistent ischemia?

A

Irreversible injury (it could lead to necrosis or minimal apoptosis)

95
Q

What is an ischemia reperfusion injury?

A

Temporary ischemia and its eventual restoration of flow that leads to injury

96
Q

What is an example of ischemia reperfusion injury?

A

Myocardial infarction and stroke

97
Q

What is a direct chemical injury to the cell?

A

Cells that absorb, use, excrete or store a toxin which leads to membrane damage and is therefore directly cytotoxic

98
Q

What is an indirect chemical injury to cells?

A

It is a conversion of chemicals and result in reactive metabolites

99
Q

What causes intracellular accumulations?

A

Celullar injury and aging

100
Q

Usually accumulations happen in which parts of the cells?

A

Cytoplasm, organelles, and nucleus

101
Q

What could cause intracelulllar accumulations?

A

Abnormal metabolism, defective protein folding, defective or absent enzymes, and ingestion of indigestible materials

102
Q

What is Steaosis?

A

abnormal accumulation of lipids in a cell. When this is within tissue is known as parenchyma (liver, heart, skeletal muscle, kidney)

103
Q

The most common fatty acid in steatosis are

A

Triglycerides

104
Q

What are the causes of steatosis?

A

Toxins, malnutrition, diabetes, obesity, anoxia

Alcoholism and Type 2 diabetes can also cause this

105
Q

What is pathologic calcification?

A

abnormal accumulation of Ca++ salts

106
Q

What are the type of pathologic calcifications?

A

Dystrophic and metastatic calcification

107
Q

What is Dystrophic calcification?

A

is encountered in areas of necrosis of any type. It is virtually inevitable in the atheromas of advanced atherosclerosis, associated with intimal injury in the aorta and large arteries and characterized by
accumulation of lipids . Although dystrophic calcification may be an incidental finding indicating insignificant past cell injury, it may also be a cause of organ dysfunction.

108
Q

What is celullar aging?

A

the result of a progressive decline in the life span and functional capacity of cells.

General Pathology (10 decks)

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