causes of disease #1 Flashcards

1
Q

How Bacteria Cause Disease.

A

Causes disease by releasing harmful toxins that stop cells from working.

Examples of bacterial toxins:

Neurotoxins: Affect the nervous system (e.g., tetanus - lockjaw).

Respiratory toxins: Affect respiratory epithelial cells (e.g., whooping cough).

Diarrheal toxins: Affect digestive epithelial cells (e.g., shiga toxin).

Most bacteria cause localized disease.

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2
Q

how Viruses Cause Disease

A

Cause disease in two ways:

Take over host cells, use their organelles to replicate, then burst the cell to spread infection.

Insert their DNA into host DNA, leading to mutations that can cause cancer or other illnesses.

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3
Q

Physiological Immune and Inflammatory Response to Infection

A

Chemical release: Histamine and other chemicals signal an immune response.

Vasodilation: Blood vessels widen to bring immune cells and clotting factors.

Increased capillary permeability: Fluid and immune cells move into infected tissue.

White blood cell migration: Macrophages and neutrophils move to the infection site.

Phagocytosis: White blood cells engulf and destroy pathogens.

Tissue repair: Inflammation subsides, and tissue regenerates or undergoes fibrosis.

Regeneration: Original tissue regrows.

Fibrosis: Collagen replaces tissue, making it less flexible.

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4
Q

Types of Pathological Immune Reactions

A

Type 1 Hypersensitivity (Overreaction):

IgE antibodies cause allergic reactions by making WBCs release histamine.

Symptoms: Stuffy nose, watery eyes, hives.

Severe reaction: Anaphylaxis.

Type 2 Hypersensitivity (Self-Attack):

Autoimmune diseases where the immune system attacks the body’s own cells.

Can be triggered by viral infections altering DNA.

Can cause destruction of organs or overstimulation of tissues.

Type 3 Hypersensitivity (Immune Blockage):

Antibody-antigen complexes get stuck in capillaries, triggering inflammation.

Example: Glomerulonephritis.

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5
Q

Medications for Hypersensitivity Reactions

A

Antihistamine (e.g., cetirizine): Blocks histamine receptors, preventing inflammation.

Adverse effects: Drowsiness, sedation.

Epinephrine (for anaphylaxis): Causes bronchodilation and vasoconstriction.

Adverse effects: Tachycardia, hypertension, tremors.

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6
Q

Acute vs. Chronic Inflammation

A

Acute Inflammation:

Short-term, protective response.

Heals tissue and fights infection.

Chronic Inflammation:

Long-term inflammation leading to tissue damage.

Example: Osteoarthritis.

Causes remodeling with collagen, reducing function (especially harmful in heart and muscles).

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7
Q

Medications for Inflammation

A

Corticosteroids (e.g., prednisone): Reduces inflammation and inhibits WBC migration.

Adverse effects: High blood sugar, increased infection risk, hypertension, osteoporosis, fat redistribution, psychotic effects, withdrawal effects if not tapered.

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8
Q

Ischemia & Hypoxia

A

Ischemia: Decreased blood flow, usually from blocked arteries.

Hypoxia: Lack of oxygen in tissues, leading to less ATP and acid buildup.

Acidosis: Too much acid buildup in the body.

Necrosis: Death of tissue cells due to prolonged hypoxia.

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9
Q

Types of Acidosis

A
  1. Lactic Acidosis (from hypoxia):

Occurs when oxygen is low and cells switch to anaerobic respiration.

Leads to lactic acid buildup and blood pH drop.

  1. Ketoacidosis (from lack of glucose):

Occurs when the body breaks down fats for energy, producing acidic ketones.

Common in diabetic ketoacidosis.

Symptoms: Dehydration, nausea, vomiting, confusion, coma.

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10
Q

acute inflammation

A

cause- infection, injury or tissue damage

duration - short term

process - white blood cells clean up damage, inflammation subsides, and healing begins.

symptoms- redness, warmth, swelling, pain

outcomes - healing or resolution

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11
Q

Chronic inflammation

A

cause - repeated injury, long-term exposure to irritants

duration - long term

Process - ongoing immune response cause continues tissues damage, leading to fibrosis (scaring)

main cells involved - macrophages, lymphocytes

symptoms- persistent pain, tissue destruction, scarring

outcome- tissue hardening, organ dysfunction

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