Flashcards

Atrophy

Cells shrink when not used; e.g., muscles shrink if not exercised; mostly permanent cells such as heart and muscle cells.

Hypertrophy

Cells grow bigger when working harder; e.g., muscle growth from exercise; mostly permanent cells such as heart and muscle cells.

Hyperplasia

Cells increase in number when needed; e.g., liver cells regenerate or increase breast growth during pregnancy; mostly occurs in labile cells, sometimes stable.

Metaplasia

Cells change type when exposed to irritation; e.g., lung cells change due to smoking.

Dysplasia

Cells grow abnormally, which can be a warning sign for cancer.

Necrosis

Uncontrolled cell death occurring when cells are severely damaged; e.g., during a heart attack.

Apoptosis

Controlled/organized cell death that removes unneeded or damaged cells without causing inflammation. (cells shrink/break into smaller pieces to be disposed of by body)

Acute inflammation

Immediate and non-specific immune response causing redness, swelling, heat, pain, and loss of function.

Chronic inflammation

Lasts longer than 2 weeks, resulting in tissue damage or scarring.

Exudate

Fluid leaking out of blood vessels during inflammation, comes in forms like serous, fibrinous, purulent, and hemorrhagic.

Systemic inflammation

Occurs when inflammation affects the entire body, causing fever, chills, muscle pain, and an increased heart rate.

NSAIDs

Non-steroidal anti-inflammatory drugs that inhibit COX-1 and COX-2 enzymes, reducing pain and inflammation.

Glucocorticoids

Steroid hormones synthesized in the adrenal gland that reduce inflammation and suppress immune responses.

Wound healing stages

Inflammatory phase (haemostasis, acute inflammation), proliferative phase (granular tissue formation), and remodelling/maturation phase.

What are cell types - based on replication abilities

• Labile cells - constantly replicating (e.g. skin cells).

• Stable cells - replicate when needed (e.g. liver cells).

• Permanent cells - cannot replicate (e.g. neurons, heart cells)

Primary intention healing

Occurs in clean, narrow wounds with minimal scarring.

Secondary intention healing

Occurs in wider, severe wounds, increasing infection risk and resulting in more noticeable scarring.

Factors influencing wound healing

Age, nutritional status, anemia, circulatory issues, chronic diseases, infection, and long-term medication use can affect wound healing.

What can cause cell injury (HATING)

H - Hypoxia or Ischemia

A - Aging

T - Trauma or Toxins

I - Infection or Immunological problems

N - Nutrition Deficiencies

G - Genetic abnormalities

Necrosis

Uncontrolled cell death that occurs when cells are severely damaged by injury, infection, or lack of blood supply, leading to inflammation and tissue breakdown.

Liquefactive necrosis

A type of necrosis where the affected tissue becomes transformed into a liquid viscous mass (pus).

Coagulative necrosis

A type of necrosis where affected tissue firms up and becomes pale due to protein denaturation, often seen in cases of ischemia.

List the 4 types of exudate

1. Serous exudate

2. Fibrinous exudate

3. Purulent exudate

4. Haemorrhagic exudate

Define serous exudate

A watery exudate consisting mainly of water with small amounts of protein and white blood cells (commonly found in burns and allergic reactions)

Define fibrinous exudate

A thick and sticky exudate with a high cell and fibrin content. Due to its viscosity and stickiness, it may inhibit healing and cause scarring or layers adhering to each other (adhesions).

Define purulent exudate

 A thick, yellow/green fluid (pus) that contains more leukocytes, cell debris, and micro-organisms (typically found in bacterial infections).

Define haemorrhagic exudate

Fluid containing many RBC and indicates greater tissue and local blood vessel damage

What tests are used to confirm systemic inflammation

• C-Reactive Protein (CRP) test measures the level of a specific protein in the blood that rises when inflammation is present.

• The Erythrocyte Sedimentation Rate (ESR) test checks how quickly red blood cells settle in a sample of blood, with faster rates indicating higher levels of inflammation.

• An elevated White Blood Cell (WBC) count, particularly an increase in neutrophils, signals infection or inflammation in the body.

Basic enzyme pathway of NSAIDs

Following a tissue injury phospholipase A2 converts phospholipids into arachidonic acid, arachidonic is then converted into COX-1 and COX-2. NSAIDs will selectively inhibit COX enzymes to reduce the production of prostaglandins, thromboxane and prostacyclin which are mediators of pain and inflammation.

MOA of selective COX-1 inhibitors (with example medication)

Selective COX-1 inhibitors block the COX-1 enzyme (and COX-2, but mostly COX-1), inhibiting conversion of arachidonic acid into prostaglandin A2. This results in reduced production of thromboxane A2 and prostacyclin, which plays a key role in platelet aggregation.

E.g. aspirin.

MOA of non-selective COX inhibitors (with example medications)

Non-selective COX inhibitors block both COX-1 and COX-2 enzymes, inhibiting conversion of arachidonic acid into prostaglandin A2 as well as preventing proinflammatory prostaglandins. This leads to a decrease in the production of prostaglandins and thromboxane. This results in reduced pain, inflammation, and fever.

E.g. ibuprofen and naproxen.

MOA of selective COX-2 inhibitors (with example medication)

Selective COX-2 inhibitors specifically target the COX-2 enzyme, reducing the conversion of arachidonic acid into proinflammatory prostaglandins while sparing COX-1. This leads to decreased pain and inflammation with a lower risk of gastrointestinal side effects.

E.g. celecoxib.

What is the function of the COX-1 enzyme

1. COX-1 play a crucial role in the production of prostaglandins which is responsible for maintaining the protective mucosal lining of the stomach (prevents damage from stomach acid).

2. COX-1 is involved in the formation of thromboxane A2, which promotes blood clotting by stimulating platelet aggregation.

3. COX-1 helps maintain renal blood flow, particularly in conditions of low blood volume, ensuring proper kidney function.

4. COX-1 is involved in the formation of prostacyclin which acts as a vasodilator

   **COX-1 is ALWAYS active in the tissue (unlike COX-2 which is induced during inflammation)

What is the function of the COX-2 enzyme

COX-2 is induced in response to stimuli such as inflammation or infection (unlike COX-1 which is always active)

1. COX-2 is responsible for the conversion of arachidonic acid into proinflammatory prostaglandins

   one of these prostaglandins being prostacyclin which is responsible for vasodilation at the injury site = increase vascular permeability to allow immune cells to reach affected tissue.

   causes → redness, heat, swelling, pain

Gram-positive bacteria

have a simple cell wall

stains purple due to retaining the violet stain

Gram-negative bacteria

have a complex cell wall

stains pink due to the wash removing the violet stain and taking up the pink stain

List the chain of infection in order

1. infectious agent

2. reservoir

3. portal of exit

4. mode of transmission

5. portal of entry

6. susceptible host

Exotoxins

• a toxin produced inside pathogenic bacteria

• it is released into surroundings following lysis

• is unstable / denatured above 60 degrees

• highly toxic to humans

Endotoxins

• toxins that are ONLY found in the cell wall of gram- bacteria

• are very heat tolerant

• released into surroundings when the bacteria die (causing break of cell wall)

• very toxic to humans at high concentrations

Systemic Inflammation

inflammation that effects the whole body not just localised area. Causes of systemic inflammation can be autoimmune diseases, infections or chronic conditions.

symptoms → fever, chills, myalgia, tachypnoea, increased HR and BP

What are the metabolic actions of glucocorticoids (6)

metabolic actions

• decrease cellular uptake of blood glucose

• stimulates glucogenesis in the liver

• stimulates lipolysis

• increase protein catabolism

• decrease osteoblast activity

• increase osteoclast activity

What are the anti-inflammatory actions of glucocorticoids (1)

anti-inflammatory actions

• inhibits phospholipase A and COX enzymes, therefore preventing the synthesis of key inflammatory chemical mediators

What are the immunosuppressive actions of glucocorticoids (1)

immunosuppressive actions

• inhibits the action and proliferation of immune cells (e.g. lymphocytes, macrophages), therefore reduces the production of antibodies

Antigen

a toxin or other foreign substance which induces an immune response in the body, especially the production of antibodies.

MOA of glucocorticoids

Glucocorticoids (e.g., administered as cortisone, prednisone, dexamethasone) are naturally produced in the adrenal gland and help reduce inflammation by

• Inhibiting cytokine production (suppressing immune signals that cause inflammation)

• Inhibiting COX-2 and phospholipase, reducing prostaglandins and leukotrienes, which leads to decreased vasodilation, vascular permeability, and bronchoconstriction.

what are the 3 stages of wound healing

1. inflammation phase

2. proliferation phase

3. remodelling / maturation phase

what occurs in the inflammatory phase of wound healing

1. haemostasis → blood clot forms to seal wound and stop bleeding

2. acute inflammation → blood vessels dilate, allowing WBC to clean up dead tissue and microorganisms

what happens in the proliferation phase of wound healing

1. granular tissue formation → fibroblasts secrete growth factors with promote the growth of new blood vessels and epithelial cells to close the wound

   → fibroblasts also lay down collagen and extracellular matrix to support new tissue growth

what happens in the remodelling / maturation phase of wound healing

(starts 3 weeks after initial injury)

1. granular tissue becomes scar tissue which is avascular (having no blood supply)

2. scar tissue turns into scar over time and eventually returning to original state

bactericidal

kills the bacteria

bacteriostatic

aid the body’s immune system to kill the bacteria

MOA of antibiotic → inhibiting protein synthesis (with examples)

protein is needed for growth and repair, some antibiotics inhibit the ribosomes (site that creates protein) which results in bacteria being unable to replicate

• e.g. aminoglycosides, tetracyclines, macrolides

MOA of antibiotic → inhibiting cell wall synthesis (with examples)

cell walls need to be synthesised for bacteria to divide and replicate, otherwise water enters cell via osmosis causing bacterial cell to burst and lyse

• e.g. cephalosporins, penicillin, glycopeptides

MOA of antibiotic → inhibiting DNA / RNA synthesis (with examples)

DNA synthesis occurs in the nucleus, antibiotics can block the transcription of DNA which will prevent microbial growth

• e.g. fluoroquinolones

MOA of antibiotic → inhibiting folate synthesis (with examples)

all cells need folic acid to produce ATP (human cells obtain folic acid from diet), whereas bacteria make their own. Therefore, if the antibiotic agent interferes with folic acid synthesis in bacteria, it cannot produce the proteins needed for growth.

• e.g. sulphonamides

how does bacteria resist antibiotics (3)

1. Efflux pumps - some bacteria have pumps that actively remove the antibiotic from their cells, so the drug never reaches a high enough level to work

2. Enzyme production - certain bacteria make enzymes that destroy or deactivate the antibiotic

3. Target modification - bacteria may change their internal structures so the antibiotic cant bind and do its job

what is the 5 step of viral infection in human host

1. Attachment phase - Attaches to host cell using protein spikes

2. Penetration and uncoating phase - virus fused with host cell dissolving its capsid which introduces genetic material into the cell

3. Replication phase - DNA viruses replicate easily, while RNA viruses must reverse-transcribe into DNA before replication.

4. Host cell machinery - Virus synthesises the proteins and other components required to construct new viruses (using host cell's resources)

5. Release - new viruses are released from the host cell, often leading to cell destruction of host cells in the process

what are the 4 groups of mycosis

1. Systemic mycosis - these infections can affect internal organs and are often life-threatening

2. Subcutaneous mycosis - Usually occur in tropical areas and affect the skin and underlying tissues, often through wounds (e.g. Skin, fascia and bone)

3. Cutaneous mycosis - Involves epidermis, hair & nails i.e., athletes' foot (tinea).

4. Superficial mycosis - Involves the outer epidermis (skin) and hair.

MOA of ‘azoles’ antimycotics

disrupt fungal cell membrane synthesis by blocking ergosterol production (therefore, membrane becomes weak and vulnerable to immune attack)

• e.g. ‘triazoles’ and ‘imidazole’

Protozoa (+ treatment)

• protozoa is a single-celled parasites, which can cause infections such as malaria, amebiasis and giardiasis

• symptoms → fever, GI issues, organ specific symptoms

treatment

1. Metronidazole - used for amebiasis and giardiasis, disrupts DNA in parasites

2. Chloroquine - traditionally for malaria, limited use due to resistance

3. Atovaquone-Proguanil - disrupts energy pathways in parasites

Helminths (+ treatment)

• parasites that are worms

• e.g. roundworms, hookworms, tapeworms

• symptoms → GI distress, anaemia, weight loss

treatment

1. Mebendazole - inhibits glucose uptake in worms

2. Albendazole - broad spectrum, use with cause, especially in pregnancy

3. Ivermectin - causes paralysis in parasites

what are the 5 stages of infection

1. Incubation - microorganism enters the body, finds a suitable environment, and begins reproducing (no symptoms visible yet)

2. Prodromal - early non-specific symptoms such as fatigue, headache, fever, loss of appetite appear as the immune system is activated

3. Acute period of illness - illness reaches its peak with severe symptoms, if unresolved can lead to sepsis or death (duration depends on pathogen virulence and hosts immune response)

4. Period of decline - pathogen count decreases and symptoms begin to improve (host is still vulnerable to secondary infections or chronic conditions)

5. Period of convalescence - recovery phase where host returns to normal