Ch 2- Cell Responses and Adaptations (Dobson Lect) Flashcards by Deleted Deleted

Define:

Disease

“Any deviation from or interruption of the normal structure or function of a part, an organ, or system of the body as manifested by characteristic symptoms and sign ; the etiology, pathology, and prognosis may be known or unknown”

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Define:

Disorder

“A derangment or abnormality of function; a morbid physical or mental state/condition”

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Define:

Neoplasm

“Any new and abnormal growth; specifically a new growth of tissue in which the growth is uncontrolled and progressive”

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Define:

Syndrome

“A set of symptoms that occur together; a symptom complex; the sum of signs of any morbid state”

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What is an adaptation?

Adaptations are reversible functional and structural responses to changes in physiologic states and some pathologic stimuli

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What are 4 examples of adaptation that were discussed in lecture?

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

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Is cell injury reversible?

UP TO A CERTAIN POINT IT IS

If the stimulus persists or is severe enough, the cell will suffer from irreversible injury

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Define:

Hypertrophy

Increase cell and organ size

*Hyper-trophy = you always want a BIG trophy*

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Define:

Hyperplasia

Increased cell numbers

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Define:

Atrophy

Decreased cell and organ size

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Define:

Metaplasia

Change in phenotype of differentiated cells

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What does the difference in heart size reveal?

What was the mechanism of this?

Hypertrophy

Increased production of cellular proteins

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This comparitive image demonstrates what type of hyperplasia?

Physiologic hypertrophy of the uterus

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A hallmark of cardiac metabolism before birth is?

The predominance of carbohydrate use for energy

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After birth, cardiac metabolism switches energy source to the utilization of?

Oxidation of fatty acids

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Why is it important to know the differences in fetal vs adult cardiac metabolism energy sources?

(*reminder: fetal uses carbohydrates, adult uses fatty acid oxidation)

It’s important because in several pathophysiologic conditions [ex: hypoxia, ischemia, hypertrophy, atrophy, diabetes, and hypothyroidism] the postnatal heart returns to “fetal” gene program

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What is this image an example of?

(Left : Normal kidney)

(Right: (Physiologic compensatory hyperplasia)

***This is physiologic because it was due to loss of sister kidney. This kidney developed more renal cells to compensate.

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What is one of the most concerning outcomes from repetitive hyperplasic events?

Transformation to malignancy

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Where are the most common sites for developing cancerous malignancy?

Sites where hyperplasia are common!!!

Examples Include:

Breast

Endometrium

Prostate

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What is this image revealing?

Hyperplasia can become cancerous if checkpoints go unregulated

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What is this a picture of?

A patient with ALS that shows atrophy of the thenar eminence

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What are the common reasons for atrophy? (6)

Decreased workload
Loss of innervation
Diminished blood supply
Inadequate nutrition
Loss of endocrine stimulation
Pressure

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What is the mechanism of atrophy?

Atrophy results from:

Decreased protein synthesis (due to reduced metabolic activity) and increased protein degradation in cells (proteosomes and/or autophagy)

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What is the mechanism of metaplasia?

Result of a reprogramming of stem cells in normal tissues, or of undifferentiated mesenchymal cells present in connective tissue

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The influences that predispose to metaplasia, if persistent, can intiate \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Malignant transformation

Which tissues do NOT have stem cells in them? What does that mean in terms of metaplasia?

Heart & Brain Cannot undergo metaplasia!!! \*Likely a test question\* cough cough

What is this histologic slide revealing?

Bronchus Metaplasia!!! Notice the difference in cell types that are directly adjacent to each other

What are the **microscopic features** of _reversible cell injury?_

Cell swelling Fatty change

_Features of Necrosis and Apoptosis_ Feature: **Cell size** What happens with necrosis vs. apoptosis?

Necrosis: Enlarged (swelling) Apoptosis: Reduced (shrinkage)

_Features of Necrosis and Apoptosis_ Feature: **Nucleus** What happens with necrosis vs. apoptosis?

Necrosis: Pyknosis --\> Karyorrhexis --\> Karyolysis Apoptosis: Fragmentation into nucleosome-size fragments

_Features of Necrosis and Apoptosis_ Feature: **Plasma membrane** What happens with necrosis vs. apoptosis?

Necrosis: Disrupted Apoptosis: Intact; altered structure

_Features of Necrosis and Apoptosis_ Feature: **Cellular contents** What happens with necrosis vs. apoptosis?

Necrosis: Enzymatic digestion; may leak out of cell Apoptosis: Intact; may be released in apoptotic bodies

_Features of Necrosis and Apoptosis_ Feature: **Adjacent Inflammation** What happens with necrosis vs. apoptosis?

Necrosis: Frequent Apoptosis: NONE!!!

_Features of Necrosis and Apoptosis_ Feature: **Physiologic or pathologic role** What happens with necrosis vs. apoptosis?

Necrosis: Invariably _pathologic_ Apoptosis: Often _physiologic_, means of eliminating unwanted cells, may be pathologic after some forms of cell injury, especially DNA damage

# Define: Karyolysis

Nuclear fading

# Define: Pyknosis

Nuclear shrinkage

# Define: Karyorrhexis

Nuclear fragmentation

Go read morphology box pages 42-44 of robbins

now

What are these blue lines indicating?

Patterns of necrosis Pie shaped/wedge shaped (right: liquifactive necrosis of the brain)

What type of necrosis is this?

Caseous necrosis (Cheese like)

**Caseous necrosis** is associated with what infection?

TB (mycobacterium tuberculosis)

**Caseous necrosis** is described as?

Yellow-white and "cheese like"

Caseous necrosis is described as: "...the necrotic area appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border; this appearance is characteristic of a focus of inflammation known as a \_\_\_\_\_\_\_\_\_\_\_\_\_"

Granuloma

What are the principal biochemical mechanisms and sites of damage in cell injury?

Mitochondrial damage Entry of Ca2+ Membrane damage Protein misfolding, DNA damage

Reduction in ATP levels is a fundamental cause of \_\_\_\_\_\_\_\_\_\_\_\_\_\_

Necrotic cell death

Increased production or decreased scavenging of ROS may lead to an excess of these **free radicals,** a condition called \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Oxidative stress

Oxidative stress has been implicated in the following:

- Cancer - Cell injury - Aging - Alzheimers disease

ROS are produced in large amounts by \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Activated leukocytes

Why are ROS generated by neutrophils and macrophages?

Produced during **inflammatory reactions** aimed at destroying microbes and cleaning up dead cells and other unwanted substances

Where are the most important sites of membrane damage during cell injury?

Mitochondrial membrane Plasma membrane Lysosomal membranes

The release of _____________ into the bloodstream occurs by different sources, including primary tumor, tumor cells that circulate in peripheral blood, metastatic deposits present at distant sites, and normal cell types.

cfDNA (cell free DNA)

What are the arrows pointing at?

Apoptotic bodies

What are the two major mechanisms of **apoptosis?** Which of the two is most common?

Mitochondrial (intrinsic) pathway \*\*\*more common\*\*\* Death receptor (extrinsic) pathway

The process of apoptosis may be divided into two phases. What are they?

Initiation phase Execution phase

Caspases are associated with?

APOPTOSIS

What are the major players in the mechanism of **apoptosis?**

BCL2 family Cytochrome C Caspases Apoptosome

What is the MAJOR **anti-apoptotic** protein?

BCL2

What are the MAJOR **pro-apoptotic** proteins?

BAX and BAK

Describe the **death receptor (extrinsic)** apoptotic pathway

This pathway is initiated by engagement of plasma membrane death receptors on a variety of cells with the ligand for **Fas**. **FasL** is expressed on **T cells** that recognize self antigens and on some **cytotoxic T lymphocytes**.

The death receptor (extrinsic) apoptotic pathway can be inhibited by a protein called?

FLIP

What are specific examples of diseases caused by **misfolding of protein?**

Cystic Fibrosis Familial hypercholesterolemia Tay-Sachs disease Alpha-1 antitrypsin deficiency Creutzfeldt-Jacob disease Alzheimer disease

What is the purpose of **autophagy?**

Autophagy functions as a **survival mechanism** under various stress conditions, by maintaining the integrity of cells by _recycling essential metabolites_ and clearing cellular debris.