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Unit 1 Flashcards

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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
What are the causes of atrophy?
Disuse (immobilization), ischemia (decrease of blood and or nutrients), Denervation, Endocrine disruption, and aging (senility)
26
There are two types of irreversible cell injury. What are they and are they physiologic and/or pathologic?
Apoptosis which is physiologic Necrosis which is pro inflammatory and pathologic
27
What is stenosis?
A narrowing of a valve or canal
28
When the heart can no longer deal with the "stress" caused by factors such as HTN, CAD or valvular stenosis. What usually happens?
There is swelling and steatosis which could typically lead to cell death in which case could cause a Myocardial infarction or "heart attack"
29
What is the risk for metaplasia?
Malignant transformations
30
During cell injury, what happens to the cell?
Stressors exceed adaptive ability or directly induce abnormality in the cell
31
What causes cell injury?
Trauma (physical, thermal, irradiation) Ischemia, hypoxia, poison/toxin, infection, immune reactions, nutritional imbalance, aging
32
Celullar injury is always irreversible (true or false)
No there are types of reversible cell injuries
33
Reversible (transient or mild ) cell injury usually causes
Cellular swelling, fatty accumulation (steaosis) No damage to membranes or nucleus Healing occurs if stressor is removed
34
Irreversible (Prolonged or severe) cell injury can be caused by
Mitochondrial dysfunction or disturbed membranes
35
Irreversible injury always leads to what two types of cell death?
Necrosis and/or apoptosis
36
The causes of necrosis are always ______
pathological (ie Trauma, toxins, ischemia)
37
Is necrosis pro inflammatory?
Yes
38
The only cause for apoptosis is physiological T or F
False, it could also be due to pathological reasons. It is also non inflammatory
39
Regarding atrophy of the brain, what could ahterosclerosis do?
Widen sulci and narrow gyri
40
Other than malignant transformation, what is the risk of Metaplasia?
Loss or altered function of the old cell
41
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
Condensation; blebs; apoptotic body; apoptotic body
42
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
swelling; plasma membrane; inflammation
43
What does Karyolysis entail?
Nuclear fading or dissolution of the nucleus; Chromatin dissolution due to the action of DNAases and RNAases
44
What does pyknosis entail?
Shrinkage of the nucleus; DNA condenses into shrunken basophilic mass
45
What does Karyorrhexis entail?
Nuclear fragmentation; Pyknotic nuclei membrane ruptures and undergoes fragmentation
46
What is tissue necrosis?
Death of living tissue
47
What does death of living tissue entail?
Loss of membrane integrity, leakage of contents
48
What are the morphologic patterns of Tissue necrosis?
Coagulative, Liquefactive, caseous, fat and fibrinoid
49
What is coagulative necrosis?
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
What happens to the tissue in coagulative necrosis?
Tissue structure is preserved, and firm. The proteolytic enzymes are denatured
51
What is gangrene?
coagulative necrosis in an extremity
52
What could cause gangrene?
Peripheral vascular disease such as Diabetes and atherosclerosis
53
What are the types of gangrene?
Dry, wet and Gas Gangrene
54
What is liquefactive necrosis?
A type of necrosis in which dead cells are completely digested. The tissue becomes a liquid viscous mass
55
What could cause liquefactive necrosis?
Most common cause would be Bacterial infections (yellow pus, abscess) Fungal infections Lack of oxygen in the CNS might cause it as well
56
What is caseous necrosis?
A type of necrosis which has a "cheese like" appearance with a friable and yellowish white coloration. Tuberculosis Enclosed within a distinctive border
57
What is a granuloma?
A byproduct a casseous necrosis. It is a walled off accumulation of macrophages
58
What causes casseous necrosis?
Tuberculosis infections Mycobacterium tuberculosis
59
What is fat necrosis?
Local fat destruction
60
What could cause fat necrosis?
Acute pancreatitis which could leak pancreatic enzymes and saponification of fat will occur Trauma to the breast
61
What is the gross morphology of Fat necrosis?
Chalky white particles
62
what is fibrinoid necrosis?
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
What could cause fibrinoid necrosis?
Polyarteritis nodosa, systemic lupus erythematosus, malignant hypertension, and transplant rejections
64
What is apoptosis?
Programmed or regulated cell death
65
Which cells typically go through apoptosis?
Unneeded or irreparable cells
66
There are two ways apoptosis happens it could be ____ or ____
Physiologic or pathologic
67
Examples of physiological apoptosis would be
Embryonies, endometrium sloughing off, and breast tissue
68
Pathological cause for apoptosis would be:
Dna damaged cells, misfolded proteins, and viral infections this kind of apoptosis may accompany atrophy (duct obstruction)
69
What causes celullar fragmentation?
Activation of caspases
70
The mitochondrial intrinsic pathway is stimulated by
Decrease in growth factor, DNA damage, and misfolded proteins
71
What enzyme plays a key roles in Mitochondrial pathway in apoptosis?
Caspase 9
72
What happens to the mitochondrial membrane during apoptosis via the mitochondrial pathway?
increases permeability
73
The death receptor pathway of apoptosis begins with these molecules binding with other surface molecules...
Tumor Suppressing
74
How does death receptor apoptosis work?
eliminating self reacting lymphocytes or virus infected cells
75
What enzyme plays a key role in death receptor apoptosis?
Caspase 8
76
What is autophagy?
"self eating"; Lysosomal digestion of celullar components
77
Cells usually utilize autophagy as a _____ mechanism due to lack of nutrients
Survival
78
The survival mechanism of autophagy creates _________ ______
Autophagic Vacuoles and organelles are sequestered and digested
79
What happens to the cell when continued nutrient deprivation happens?
Autophagy will stop then apoptosis will ensue
80
How do we rid ourselves of misfolded proteins?
Autophagy
81
An example of misfolded proteins causing neurological problems would be _____ ______ in alzeheimers disesa
Beta amyloids
82
What are the 6 types of celullar injury?
Depletion of ATP, Mitochondrial Damage, Influx or calcium and oxidative stress, defects in membrane permeability, and DNA/protein damage
83
What could lead to Depletion of ATP?
Hypoxia, nutritional deficiency, mitochondiral damage or toxins There would be a decrese in Oxidative phosphorylation
84
What could lead to mitochondrial damage?
Hypoxia, toxins, and irradiation
85
What are some of the effects of mitochondrial damage?
Loss of membrane potential leading to necrosis Production of ROS leading to apoptosis
86
What causes influxes of calcium in the cell?
Ischemia and toxins
87
What could cause Oxidative stress?
Accumulation of ROS
88
What could cause accumulation of ROS?
Ischemia - reperfusion, toxic chemicals, irradiation, celullar aging, inflammation
89
What could cause defects in membrane permeability?
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
What could cause Dna and protein damage?
severe oxidative stress, | irradiation, abnormal protein folding
91
What typically occurs when DNA and Protein damage occurs in the cell?
apoptosis
92
What is Ischemia or hypoxic injury as related to cells?
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
How would ischemia/hypoxia be reversible?
With restoration of Oxygen
94
What might happen with persistent ischemia?
Irreversible injury (it could lead to necrosis or minimal apoptosis)
95
What is an ischemia reperfusion injury?
Temporary ischemia and its eventual restoration of flow that leads to injury
96
What is an example of ischemia reperfusion injury?
Myocardial infarction and stroke
97
What is a direct chemical injury to the cell?
Cells that absorb, use, excrete or store a toxin which leads to membrane damage and is therefore directly cytotoxic
98
What is an indirect chemical injury to cells?
It is a conversion of chemicals and result in reactive metabolites
99
What causes intracellular accumulations?
Celullar injury and aging
100
Usually accumulations happen in which parts of the cells?
Cytoplasm, organelles, and nucleus
101
What could cause intracelulllar accumulations?
Abnormal metabolism, defective protein folding, defective or absent enzymes, and ingestion of indigestible materials
102
What is Steaosis?
abnormal accumulation of lipids in a cell. When this is within tissue is known as parenchyma (liver, heart, skeletal muscle, kidney)
103
The most common fatty acid in steatosis are
Triglycerides
104
What are the causes of steatosis?
Toxins, malnutrition, diabetes, obesity, anoxia Alcoholism and Type 2 diabetes can also cause this
105
What is pathologic calcification?
abnormal accumulation of Ca++ salts
106
What are the type of pathologic calcifications?
Dystrophic and metastatic calcification
107
What is Dystrophic calcification?
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
What is celullar aging?
the result of a progressive decline in the life span and functional capacity of cells.

General Pathology (10 decks)

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