Chapter 1. Cell Adaption & Injury – Medical School Pathology Summary, Notes, Practice Test Questions and Answers – Moosmosis
In this easy-to-understand lesson, we summarize important notes from Pathoma’s Chapter 1. Cell Adaption and Injury. This lesson also includes main summary, note points, practice exam/test questions, and answers for fellow medical school students learning pathology. Happy learning!
Pathoma: Chapter 1. Cell Adaption & Injury – Medical School Pathology Summary and Notes
Hyperplasia vs Hypertrophy
Hypertrophy = involves gene activation, protein synthesis, and production of organelles
Hypertrophy = SIZE CHANGE
Hyperplasia = Number of cells CHANGE
Example of Hypertrophy = Cardiac hypertrophy
Example of Hyperplasia = Benign prostate hyperplasia (BPH)
What is an example of where hyperplasia CANNOT progress to cancer?
Answer: BPH or benign prostate hyperplasia (note: it has benign in it! so cannot become cancer)
Benign hyperplasia (Ex: BPH) vs Pathologic Hyperplasia
Pathologic Hyperplasia Examples: 1) Endometrial hyperplasia –> that can progress to dysplasia and cancer
What’s the mechanism by which cellular components are degraded?
Answer: Autophagy
Decrease in cell size occurs via: 1) ubiquitin proteosome degradation of cytoskeleton or 2) autophagy of cellular components
What type of epithelium is present in Barrett’s esophagus?
Answer: Columnar mucinous non-ciliated epithelium (A healthy esophagus is supposed to have squamous epithelium –> but barret’s = columnar epithelium)
What is Metaplasia?
Metaplasia = reprogramming of stem cells, REVERSIBLE with removal of the stressor
Example of metaplasia = GERD (because it is reversible once treated)
Is metaplasia reversible?
Answer: yes!
What is the mechanism of action of metaplasia?
Answer: Reprogramming of stem cells
Example of Metaplasia not predisposing to cancer? –> Apocrine metaplasia (Associated with fibrocystic changes of breast)
Can Metaplasia progress to dysplasia and cancer?
Answer: yes, metaplasia can progress to dysplasia and cancer. Examples include Barrett esophagus. EXCEPT apocrine metaplasia.
Corneal metaplasia = from lack of vitamin A
What is dysplasia?
Dysplasia = reversible with alleviation of inciting stress
If stress persists, dysplasia progresses to carcinoma
Carcinoma = Cancer = Irreversible
What is hypoplasia?
Hypoplasia = decrease of number of cells (lack of cells in an organ or tissue)–> Streak ovary in Turner syndrome
Hypoxia = low oxygen delivery to issue
Ischemia = decreased blood flow through an organ
In Budd-Chiari syndrome, there is a thrombosis of <<<HEPATIC VEIN>>>>
What is the most common cause of Budd-Chiari syndrome?
Answer: Polycythemia vera
Hypoxemia vs Methemoglobinemia
Hypoxemia = Low partial pressure of O2 in blood
The earliest sign of carbon monoxide poisoning is…
Answer: Headache; other classic findings == cherry red appearance of skin , can lead to coma and death
Oxygen can only bind hemoglobin if the iron is in the Fec7::2+ state
Methemoglobinemia = Iron in heme is oxidized to Fe3+ –> which cannot bind O2
PaO2 normal // SaO2 decreased
Why are newborns particularly vulnerable to methemoglobinemia?
Answer: Low methemoglobin reductase activity
Chocolate-colored blood suggests:
Answer::Methemoglobinemia}}
Treatment for methemoglobinemia = IV methylene blue
MOA of IV Methylene blue = helps reduce Fe3+ back to –> Fe2+
What happens to the GI absorptive surface are in the setting of ischemia?
Answer: Decreases
Initial phase of injury is reversible
-Hallmark = cellular swelling
-Leads to loss of microvilli, membrane blebbing, and swelling of RER
The decrease in protein synthesis which occurs during reversible cellular injury is due to:
Answer: RER swelling ⇒ Ribosome detachment}
The hallmark of irreversible cellular injury is:
Answer: Membrane damage}}
Where is the electron transport chain located?
Answer: Inner mitochondrial membrane}}
In the setting of irreversible cellular injury, proteolytic enzymes are released from the:
Answer: :Lysosomes}}
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