chapter 1 pathoma Flashcards
What happens when stress on an organ increases?
An increase in organ size occurs through hypertrophy (increase in cell size) and/or hyperplasia (increase in cell number).
What processes are involved in hypertrophy?
Hypertrophy involves gene activation, protein synthesis, and production of organelles.
How does hyperplasia occur?
Hyperplasia involves the production of new cells from stem cells.
Do hyperplasia and hypertrophy occur together?
Yes, they generally occur together (e.g., the uterus during pregnancy).
What is the limitation of permanent tissues like cardiac muscle, skeletal muscle, and nerve in terms of hyperplasia and hypertrophy?
Permanent tissues cannot make new cells and undergo hypertrophy only, not hyperplasia.
What is an example of hypertrophy without hyperplasia?
Cardiac myocytes undergo hypertrophy, not hyperplasia, in response to systemic hypertension.
What can pathologic hyperplasia lead to?
Pathologic hyperplasia (e.g., endometrial hyperplasia) can progress to dysplasia and eventually cancer.
What is the notable exception to hyperplasia increasing cancer risk?
Benign prostatic hyperplasia (BPH) does not increase the risk for prostate cancer.
What causes atrophy?
Atrophy is caused by a decrease in stress, such as decreased hormonal stimulation, disuse, or decreased nutrients/blood supply.
How does atrophy occur?
Atrophy occurs via a decrease in both cell size and number.
How does the decrease in cell number occur during atrophy?
Decrease in cell number occurs via apoptosis.
What mechanisms are involved in the decrease in cell size during atrophy?
The decrease in cell size occurs via ubiquitin-proteosome degradation of the cytoskeleton and autophagy of cellular components
How does ubiquitin-proteosome degradation work?
In ubiquitin-proteosome degradation, intermediate filaments of the cytoskeleton are tagged with ubiquitin and destroyed by proteosomes
How does autophagy contribute to atrophy?
Autophagy involves the generation of autophagic vacuoles that fuse with lysosomes, where hydrolytic enzymes break down cellular components
What is metaplasia?
Metaplasia is the change in cell type due to a change in stress on an organ.
What is a classic example of metaplasia?
Barrett’s esophagus is a classic example of metaplasia.
What type of epithelium normally lines the esophagus?
The esophagus is normally lined by nonkeratinizing squamous epithelium, which is suited to handle the friction of a food bolus.
What happens to the esophageal lining in response to acid reflux?
Acid reflux causes metaplasia to nonciliated, mucin-producing columnar cells, which are better able to handle the stress of acid.
Is metaplasia reversible?
Yes, metaplasia is reversible with the removal of the driving stressor
Can Barrett’s esophagus be reversed?
Yes, treatment of gastroesophageal reflux may reverse Barrett’s esophagus.
What can persistent metaplasia lead to?
Persistent metaplasia can progress to dysplasia and eventually result in cancer.
What is a potential consequence of Barrett’s esophagus?
Barrett’s esophagus may progress to adenocarcinoma of the esophagus.
What is a notable exception to metaplasia leading to cancer?
Apocrine metaplasia of the breast carries no increased risk for cancer.
How can vitamin A deficiency lead to metaplasia?
Vitamin A is necessary for differentiation of specialized epithelial surfaces. In its deficiency, the thin squamous lining of the conjunctiva undergoes metaplasia into stratified keratinizing squamous epithelium, known as keratomalacia.
What is a classic example of metaplasia in mesenchymal (connective) tissue?
A classic example is myositis ossificans, where connective tissue in muscle changes to bone during healing after trauma.
What is dysplasia?
Dysplasia refers to disordered cellular growth, often related to precancerous cells.
What is an example of dysplasia that can lead to cancer?
Cervical intraepithelial neoplasia (CIN) represents dysplasia and is a precursor to cervical cancer.
What causes dysplasia to arise?
Dysplasia often arises from longstanding pathologic hyperplasia (e.g., endometrial hyperplasia) or metaplasia (e.g., Barrett’s esophagus).
What is aplasia and give an example ?
Aplasia is the failure of cell production during embryogenesis (e.g., unilateral renal agenesis).
What is hypoplasia and give an example?
Hypoplasia is a decrease in cell production during embryogenesis, resulting in a relatively small organ (e.g., streak ovary in Turner syndrome).
Which type of cells are more susceptible to ischemic injury?
Neurons are highly susceptible to ischemic injury, whereas skeletal muscle is relatively more resistant.
How does the rate of ischemia affect cellular injury?
Slowly developing ischemia (e.g., renal artery atherosclerosis) results in atrophy, while acute ischemia (e.g., renal artery embolus) results in injury.
How does hypoxia affect cellular function?
Oxygen is the final electron acceptor in the electron transport chain of oxidative phosphorylation. Decreased oxygen impairs oxidative phosphorylation, resulting in decreased ATP production, which leads to cellular injury.
what is ischemia and what are the causes of ischemia ?
Ischemia is decreased blood flow through an organ. It can arise from decreased arterial perfusion (e.g., atherosclerosis), decreased venous drainage (e.g., Budd-Chiari syndrome), or shock (generalized hypotension resulting in poor tissue perfusion).
What is hypoxemia?
Hypoxemia is a low partial pressure of oxygen in the blood (Pao2 < 60 mm Hg, Sao2 < 90%).
What are the causes of hypoxemia?
Causes include:
High altitude (decreased barometric pressure)
Hypoventilation (increased PAco2 results in decreased PAo2)
Diffusion defect (e.g., interstitial pulmonary fibrosis)
V/Q mismatch (e.g., right-to-left shunt, atelectasis)
What is the effect of hypoventilation on oxygen levels?
Hypoventilation increases PAco2, leading to decreased PAo2 and, consequently, hypoxemia.
How does diffusion defect lead to hypoxemia?
A diffusion defect (e.g., interstitial pulmonary fibrosis) thickens the diffusion barrier, making it harder for oxygen to enter the blood.
What is V/Q mismatch and how does it cause hypoxemia?
V/Q mismatch occurs when blood bypasses oxygenated lung (circulation problem, e.g., right-to-left shunt) or when oxygenated air cannot reach the blood (ventilation problem, e.g., atelectasis).
How does anemia affect oxygen levels?
In anemia, Pao2 and Sao2 remain normal, but there is a decrease in RBC mass, which limits the blood’s ability to carry oxygen.
What happens in carbon monoxide poisoning regarding oxygen?
In carbon monoxide poisoning, Hb binds to carbon monoxide more readily than oxygen, reducing the oxygen-carrying capacity of the blood.
What is the effect of carbon monoxide (CO) on hemoglobin?
CO binds hemoglobin more avidly than oxygen, leading to normal Pao2 but decreased Sao2.
What is a classic finding of carbon monoxide poisoning?
A cherry-red appearance of the skin is a classic finding.
What is methemoglobinemia and what are the associatd oxygen levels?
Methemoglobinemia occurs when iron in heme is oxidized to Fe3+, which cannot bind oxygen, leading to normal Pao2 but decreased Sao2.
What are common causes of methemoglobinemia?
It is seen with oxidant stress, such as sulfa and nitrate drugs, or in newborns.
What is a classic finding of methemoglobinemia?
Cyanosis with chocolate-colored blood is a classic finding.
What is the treatment for methemoglobinemia?
The treatment is intravenous methylene blue, which helps reduce Fe3+ back to the Fe2+ state.
How does hypoxia lead to cellular injury?
Hypoxia impairs oxidative phosphorylation, resulting in decreased ATP production, which disrupts cellular functions.
What cellular functions are disrupted by low ATP?
Low ATP disrupts the Na+-K+ pump (causing sodium and water buildup), the Ca2+ pump (leading to Ca2+ buildup), and aerobic glycolysis (causing a switch to anaerobic glycolysis and lactic acid buildup).
What is the hallmark of reversible cellular injury?
The hallmark of reversible injury is cellular swelling.
What changes occur in the cell during reversible injury?
Cytosol swelling leads to loss of microvilli and membrane blebbing, while swelling of the rough endoplasmic reticulum (RER) results in dissociation of ribosomes and decreased protein synthesis.
What is the hallmark of irreversible cellular injury?
The hallmark of irreversible injury is membrane damage.
What are the effects of plasma membrane damage in irreversible injury?
Plasma membrane damage causes cytosolic enzymes to leak into the serum (e.g., cardiac troponin) and additional calcium to enter the cell.
What happens when the mitochondrial membrane is damaged during irreversible injury?
Mitochondrial membrane damage leads to loss of the electron transport chain and cytochrome c leaking into the cytosol, which activates apoptosis.
What occurs when lysosomal membrane damage happens in irreversible injury?
Lysosomal membrane damage causes hydrolytic enzymes to leak into the cytosol, where they are activated by high intracellular calcium.
