Respan Dataset Explorer

Primary pyrogens according to their origin are divided into:

Question 83Answer

1.
Tumor necrosis factor-α


2.
Non-infectious (proteins, fats, less often nucleic acids or nucleoproteins)


3.
Interleukin-6


4.
Infectious (lipopolysaccharides, endotoxins, lipoteichoic acid, and exotoxins acting as superantigens)


5.
Interleukin-1

Primary pyrogens can be categorized based on their origin into two main groups: **infectious** and **non-infectious** pyrogens. Based on the options provided, the correct classifications are:

1. **Infectious (lipopolysaccharides, endotoxins, lipoteichoic acid, and exotoxins acting as superantigens)**  
   - This option represents pyrogens derived from pathogens, which stimulate fever.

2. **Non-infectious (proteins, fats, less often nucleic acids or nucleoproteins)**  
   - This option represents pyrogens that originate from non-pathogenic sources, which can also induce fever.

### Specific Pyrogens
- **Tumor necrosis factor-α (TNF-α)**: This is a cytokine that acts as a primary pyrogen and contributes to fever, but it is not categorized based on its origin like infectious and non-infectious pyrogens.
  
- **Interleukin-1 (IL-1)**: This is another cytokine that acts as a pyrogen, also contributing to the fever response.

- **Interleukin-6 (IL-6)**: Similar to TNF-α and IL-1, this cytokine can also induce fever.

### Summary of Key Answers
- **Infectious pyrogens**: **Option 4.**
- **Non-infectious pyrogens**: **Option 2.**
- **Cytokines that act as pyrogens**: Options 1 (TNF-α), 3 (IL-6), and 5 (IL-1) are examples of pyrogens but are not classified based on their origin like options 2 and 4.

Thus, the correct classifications of primary pyrogens by their origin are **Option 2** and **Option 4**. The other options refer to specific pyrogenic substances (cytokines) but do not describe their origin.

What is a typical pathological process, which develops as a result of insufficient  supply of the body with oxygen or disorders of its use by the tissues; it leads to the decreased synthesis of ATP and accumulation of lactic acid in the tissues.

The pathological process you are describing is **hypoxia**. 

### Explanation:
- **Hypoxia** refers to a state in which there is insufficient oxygen supply to tissues, leading to inadequate aerobic metabolism.
- As a result, the cells rely more on anaerobic metabolism, which leads to decreased synthesis of ATP (adenosine triphosphate) and the accumulation of lactic acid in the tissues, causing metabolic acidosis. 
- This can occur due to various reasons, such as respiratory disorders, cardiovascular issues, anemia, or environmental factors like high altitude.

In summary, hypoxia leads to energy deficits in cells and the accumulation of metabolic byproducts, particularly lactic acid, due to a shift from aerobic to anaerobic metabolism.

What is a decrease in cell size with a decrease in its function

A decrease in cell size along with a decrease in its function is referred to as **atrophy**. 

### Explanation:
- **Atrophy** is a cellular process characterized by a reduction in the size of cells, which results in a decrease in the overall size of the tissue or organ. This process can happen due to various factors:
  - Reduced workload or disuse (e.g., muscle atrophy from lack of exercise)
  - Insufficient blood supply (ischemia)
  - Nutritional deficiencies
  - Aging (senile atrophy)
  - Hormonal changes or deprivation (e.g., loss of estrogen after menopause can lead to atrophy of certain tissues)
  
- As cells undergo atrophy, not only do they shrink in size, but their functional capacity also diminishes, leading to decreased tissue or organ function. 

Thus, atrophy is an important pathological condition that reflects a decline in cell health and performance due to various stressors.

Patient F., 22 years, suffers from severe difficulties in respiration. The blood test revealed:

рН of arterial blood = 7,24
раСО2 = 54 mm Hg
НСО3– = 25 mmol/L
ВЕ = -1 mmol/L

Determine the type of acid-base state disorder in the patient:

Question 86Answer

1.
non-respiratory (metabolic) mechanism


2.
non-respiratory (exogenous) mechanism


3.
respiratory mechanism


4.
subcompensated acidosis


5.
decompensated acidosis

To analyze the acid-base state of the patient with the given blood gas values:

- **pH** = 7.24 (Acidemia; normal range is 7.35-7.45)
- **pCO2** = 54 mm Hg (Elevated; normal is 35-45 mm Hg)
- **HCO3⁻** = 25 mmol/L (Normal; normal range is 22-26 mmol/L)
- **BE (Base Excess)** = -1 mmol/L (Near normal; this indicates that there's not a significant metabolic contribution to the acidosis)

### Interpretation:

1. **Acidemia** (pH < 7.35) indicates an acid-base disturbance.
2. The elevated **pCO2** suggests a respiratory cause for the acidosis since it reflects impaired carbon dioxide removal (which can result from respiratory failure).
3. The **HCO3⁻** level is within normal limits, which indicates that metabolic compensation has not occurred significantly. 
4. The Base Excess being near normal (-1) reinforces this.

### Conclusion:

Given the high pCO2 and low pH, combined with normal HCO3⁻ and BE, this indicates a **respiratory acidosis**.

The options for classification include:

1. **Non-respiratory (metabolic) mechanism**: Incorrect, as the primary issue is respiratory.
2. **Non-respiratory (exogenous) mechanism**: Incorrect.
3. **Respiratory mechanism**: While this is true, it does not specify whether compensated or decompensated.
4. **Subcompensated acidosis**: This implies some compensation but not sufficient to normalize pH, which is not the case here considering the significant elevation of pCO2.
5. **Decompensated acidosis**: More appropriate term since there is a clear respiratory acidosis, as evidenced by significant acidemia and elevated pCO2 without adequate compensatory increase in HCO3⁻.

Given these points, the best answer is:

**5. Decompensated acidosis**.

Choose the examples of extracellular manifestations of cell adaptation to injury.

Question 87Answer

1.
Regeneration


2.
General hypoxia activates the work of the respiratory, circulatory, blood and tissue metabolism


3.
Activation of the function of intact liver or kidney cells when damage to the cells of a part of the organ


4.
Narrowing of arterioles with a decrease in heart function


5.
Hypertrophy

The examples of extracellular manifestations of cell adaptation to injury from the options provided are:

2. **General hypoxia activates the work of the respiratory, circulatory, blood and tissue metabolism**  
3. **Activation of the function of intact liver or kidney cells when damage to the cells of a part of the organ**  
4. **Narrowing of arterioles with a decrease in heart function**  

### Explanation:

- **General hypoxia activates the work of the respiratory, circulatory, blood and tissue metabolism**: This represents an adaptive response on an extracellular level as it engages the body's systems to cope with reduced oxygen availability.

- **Activation of the function of intact liver or kidney cells when damage to the cells of a part of the organ**: This is an extrinsic adaptation where the remaining healthy cells of the organ compensate for the loss of function due to injury.

- **Narrowing of arterioles with a decrease in heart function**: This is a physiological response to maintain blood pressure and perfusion despite decreased cardiac output, representing a systemic extracellular adaptation to the cardiac injury.

### The other options, which are more cellular than extracellular adaptations:

1. **Regeneration**: This involves cellular processes rather than extracellular adaptations and refers specifically to the healing and replacement of lost cells.

5. **Hypertrophy**: While it involves cells increasing in size, it is primarily a cellular adaptation and does not represent an extracellular adaptation in itself.

Thus, the correct examples of extracellular manifestations of cell adaptation to injury are **2, 3, and 4**.

Choose the endogenous forms of hypoxia.

Question 88Answer

1.
Respiratory hypoxia


2.
Normobaric hyperoxic hypoxia


3.
Tissue hypoxia


4.
Circulatory hypoxia


5.
Hyperbaric hyperoxic hypoxia

The endogenous forms of hypoxia from the provided options are:

1. **Respiratory hypoxia**  
3. **Tissue hypoxia**  
4. **Circulatory hypoxia**  

### Explanation:

1. **Respiratory hypoxia**: This occurs due to inadequate oxygen intake or exchange at the level of the lungs, which can stem from conditions like chronic obstructive pulmonary disease (COPD), pneumonia, or other respiratory disorders.

3. **Tissue hypoxia**: This is the condition where tissues do not receive enough oxygen, irrespective of the overall oxygen levels in the blood, and can be caused by local factors affecting the delivery or utilization of oxygen at the cellular level.

4. **Circulatory hypoxia**: This results from inadequate blood flow to tissues, which may occur due to heart failure, shock, or vascular obstructions, leading to reduced oxygen delivery.

### The non-endogenous forms of hypoxia in the provided options:

2. **Normobaric hyperoxic hypoxia**: This refers to a condition where there is an excess of oxygen at normal atmospheric pressure, which does not fit within the category of endogenous hypoxia.

5. **Hyperbaric hyperoxic hypoxia**: This is a state where there is excess oxygen at elevated atmospheric pressure, and similar to normobaric hyperoxic hypoxia, it does not represent endogenous hypoxia.

Thus, the endogenous forms of hypoxia are **1 (Respiratory hypoxia)**, **3 (Tissue hypoxia)**, and **4 (Circulatory hypoxia)**.

Match the chemoattractants with their groups by origin.

Toxins of microbes

Answer 1 Question 89
Endogenous
C3a component of a compliment system

Answer 2 Question 89
Endogenous
Peptides of bacterial origin

Answer 3 Question 89
Exogenous
Kinins

Answer 4 Question 89
Exogenous

Here’s the correct matching of the chemoattractants with their groups by origin:

1. **Toxins of microbes**  
   **Answer 3:** Exogenous

2. **C3a component of a complement system**  
   **Answer 1:** Endogenous

3. **Peptides of bacterial origin**  
   **Answer 3:** Exogenous

4. **Kinins**  
   **Answer 1:** Endogenous

### Correct Summary of Matching:
- **Toxins of microbes** → **Exogenous**
- **C3a component of a complement system** → **Endogenous**
- **Peptides of bacterial origin** → **Exogenous**
- **Kinins** → **Endogenous**

In summary, exogenous chemoattractants originate from outside the body (e.g., microbial toxins and bacterial peptides), while endogenous ones are produced within the body (e.g., C3a and kinins).

Patient L., 71 years, suffers from diabetes. He was admitted to hospital in coma. The blood test revealed:

рН of arterial blood = 7,05
раСО2 = 21 mm Hg
НСО3– = 8 mmol/L
ВЕ = -17 mmol/L
Ketone bodies in blood plasma = 9 mmol/L

Determine the type of acid-base state disorder in the patient:

Question 90Answer

1.
decompensated acidosis


2.
non-respiratory (excretory) mechanism


3.
non-respiratory (metabolic) mechanism


4.
respiratory mechanism


5.
subcompensated acidosis

To analyze the acid-base status of Patient L, we assess the provided blood gas values:

- **pH** = 7.05 (Acidemia; normal range is 7.35-7.45)
- **pCO2** = 21 mm Hg (Low; normal range is 35-45 mm Hg)
- **HCO3⁻** = 8 mmol/L (Low; normal range is approximately 22-26 mmol/L)
- **BE (Base Excess)** = -17 mmol/L (Significantly negative, indicating a large deficit of bicarbonate)
- **Ketone bodies in blood plasma** = 9 mmol/L (Indicating ketoacidosis, often seen in uncontrolled diabetes)

### Interpretation:

1. **Acidemia** (pH < 7.35): This indicates the presence of acidosis.
2. **Low HCO3⁻**: Indicates a primary metabolic acidosis due to a deficit in bicarbonate.
3. **Low pCO2**: The low pCO2 suggests that the body is attempting to compensate for the acidosis via hyperventilation (the respiratory system is trying to blow off CO2 to raise the pH).

### Conclusion:

Given that the patient has a very low pH (7.05) and low bicarbonate (8 mmol/L), combined with the presence of ketone bodies indicating a metabolic cause (likely diabetic ketoacidosis), we categorize this situation as primarily metabolic acidosis. 

### Classification Options:
1. **Decompensated acidosis**: This might be assumed because the pH is significantly low (indicating acidosis), and the compensation by the respiratory system (low pCO2) might not be sufficient.
2. **Non-respiratory (excretory) mechanism**: This does not precisely describe the primary defect here.
3. **Non-respiratory (metabolic) mechanism**: This is true as the underlying cause is metabolic acidosis due to a lack of bicarbonate and accumulation of ketone bodies.
4. **Respiratory mechanism**: This is incorrect; the primary issue is metabolic, not respiratory.
5. **Subcompensated acidosis**: This suggests some compensation, but the level of acidosis (pH = 7.05) is severe and typically indicates a clinical state beyond subcompensation.

### Best Choice:
The most accurate answer considering the situation would be:

**3. Non-respiratory (metabolic) mechanism**

This accurately captures the underlying cause of the acidosis (ketoacidosis) and indicates a metabolic origin. However, given the severity of the acidosis, one could also argue for **1. Decompensated acidosis** based on clinical context, as it reflects the overall state of acid-base balance. Given the parameters, if forced to select one primarily related to the mechanisms, **3** is the preferable choice.

Choose the manifestations of isoosmolar hypohydratation.

Question 91Answer

1.
Impairments  of the central, organ-tissue and microhemocirculation


2.
Development of heart failure, especially with prolonged hypervolemia


3.
An increase in blood volume


4.
Hypoxia


5.
A decrease of total blood volume

In an isoosmolar hypohydratation (often termed isotonic dehydration), the body loses water and electrolytes in approximately equal proportions. The manifestations of isoosmolar hypohydratation include:

1. **Impairments of the central, organ-tissue and microhemocirculation**: This can occur as decreased intravascular volume impacts circulation and perfusion.

4. **Hypoxia**: Reduced blood volume can lead to insufficient oxygen delivery to tissues.

5. **A decrease of total blood volume**: Isoosmolar hypohydratation leads to a loss of total body fluid without a change in osmolality, resulting in decreased blood volume.

### The other options and their relevance:
2. **Development of heart failure, especially with prolonged hypervolemia**: This is not directly related to isoosmolar hypohydratation as prolonged hypervolemia (increased blood volume) is not a characteristic of this condition.

3. **An increase in blood volume**: This contradicts the nature of hypohydration; there would be a decrease in blood volume instead.

### Correct Answers:
The manifestations of isoosmolar hypohydratation are **1 (Impairments of the central, organ-tissue and microhemocirculation)**, **4 (Hypoxia)**, and **5 (A decrease of total blood volume)**.

Choose the subsequence of white blood cells emigration to the inflammation focus.

1

Answer 1 Question 92
Monocytes
2

Answer 2 Question 92
Neutrophils
3

Answer 3 Question 92
Lymphocytes

The correct subsequence of white blood cell emigration to the site of inflammation generally follows this order:

1. **Neutrophils**  
   **Answer 2:** Neutrophils are usually the first responders to the site of inflammation. They migrate quickly to the site to respond to bacterial infection or injury.

2. **Monocytes**  
   **Answer 1:** After neutrophils, monocytes migrate to the inflammation focus. They can differentiate into macrophages at the site and play a crucial role in phagocytosis and further inflammatory responses.

3. **Lymphocytes**  
   **Answer 3:** Lymphocytes usually arrive later in the inflammatory process, particularly in chronic inflammation or in response to specific pathogens.

### Correct Sequence:
1. **Neutrophils** (first)
2. **Monocytes** (second)
3. **Lymphocytes** (third)

In summary, the correct order of white blood cell emigration to the inflammation focus is:
- **Neutrophils → Monocytes → Lymphocytes**.