Pathophysiology Prelims (BSMT-2B)

A set of vocabulary-style flashcards covering key concepts, terms, and conditions from the Pathophysiology prelim notes.

Etiology

Underlying causes and modifying factors responsible for initiation and progression of disease.

Pathogenesis

Mechanisms of development and progression of disease, including cellular and molecular changes.

Signs

Objective manifestations observed by others.

Symptoms

Subjective experiences reported by the patient.

Hypoxia

Oxygen deficiency; can result from ischemia, anemia, pulmonary disease, or CO poisoning.

Ischemia

Reduced blood flow causing insufficient oxygen delivery to tissues.

Arteriosclerosis

Thickening/narrowing of arterial walls leading to reduced blood flow.

Carbon monoxide poisoning

CO binds hemoglobin with high affinity, reducing oxygen transport.

Toxins

Air pollutants, drugs, alcohol, and other substances that can injure cells.

Innocuous substances

Normally harmless substances (e.g., glucose, salt, water, oxygen) that can be harmful in excess.

Infectious agents

Pathogens (viruses, bacteria, fungi, protozoans) that injure cells.

Immunologic reactions

Autoimmune, allergic, or chronic immune responses causing tissue damage.

Genetic abnormalities

Mutations or defects leading to disease (e.g., sickle cell anemia, Down syndrome).

Nutritional imbalances

Protein-calorie deficiency or excess; malnutrition and obesity-related diseases.

Kwashiorkor

Protein deficiency with edema despite adequate calories.

Marasmus

Severe deficiency of both protein and calories with wasting.

Physical agents

Trauma, extremes of temperature, radiation, or pressure changes causing cell injury.

Aging

Cellular senescence and reduced ability to handle stress, leading to injury over time.

Adaptation

Cell’s reversible changes to prolonged stress to protect tissue.

Atrophy

Decrease in size or number of cells due to reduced workload or nutrients.

Hypertrophy

Increase in cell size due to increased workload or hormones.

Hyperplasia

Increase in cell number from sustained stimulation or irritation.

Metaplasia

Change from one mature cell type to another; usually reversible.

Barrett’s esophagus

Glandular metaplasia of the lower esophagus due to chronic GERD, increasing cancer risk.

Cervical metaplasia

Normal transformation of cervical epithelium; persistent HPV exposure can lead to dysplasia.

Dysplasia

Abnormal maturation of cells; premalignant and potentially reversible.

Necrosis

Death of groups of cells due to injury; often triggers inflammation.

Coagulation necrosis

Denaturation with preserved tissue architecture; common in MI.

Liquefactive necrosis

Tissue becomes liquid; typical of bacterial infection.

Caseous necrosis

Cheesy-looking necrosis in granulomatous inflammation (e.g., TB).

Fat necrosis

Enzymatic death of fat tissue (e.g., in breast/pancreas).

Fibrinoid necrosis

Fibrin deposition in vessel walls; seen in immuneV mediated diseases.

Apoptosis

Programmed cell death; controlled, non-inflammatory, via caspases.

Inflammation

Protective response to injury; acute or chronic with cardinal signs.

Cardinal signs of inflammation

Redness, heat, swelling, pain, and loss of function.

Acute inflammation

Early, short-lived response with vascular and cellular changes; neutrophil-dominated.

Chronic inflammation

Prolonged inflammation with tissue destruction and repair; lymphocytes predominate.

Granulation tissue

New vascularized tissue in repair: vessels, fibroblasts, collagen.

Tissue repair

Process to restore normal structure; depends on viability of original cells.

Labile cells

Cells that continuously divide to replace lost cells (e.g., stem cells).

Stable cells

Cells that replicate only when stimulated (e.g., fibroblasts).

Permanent cells

Cells that do not regenerate (e.g., cardiac muscle); scar replaces lost tissue.

PDGF

Platelet-derived growth factor; promotes tissue repair and cell proliferation.

TGF-β

Transforming growth factor-beta; modulates repair and fibrosis.

VEGF

Vascular endothelial growth factor; promotes blood vessel formation.

Innate (non-specific) immune system

Immediate, non-specific defense present at birth; reduces workload on adaptive system.

First line of defense

Surface barriers (skin, mucous membranes) and chemical barriers (lysozyme).

Lysozyme

Enzyme in saliva/tears that breaks down bacterial cell walls.

Second line of defense

Internal defenses: phagocytes, fever, NK cells, antimicrobial proteins, inflammation.

Phagocytes

Cells that engulf and destroy pathogens (e.g., neutrophils, macrophages).

Neutrophils

Main acute inflammatory cells; phagocytose and release toxic substances.

Macrophages

Large phagocytes; present antigens and orchestrate inflammation.

Natural killer (NK) cells

Lymphocytes that kill virus-infected or cancer cells; induce apoptosis.

Antimicrobial proteins

Proteins such as interferons and complement that attack pathogens.

Humoral immunity

Antibody-mediated immunity via B cells and antibodies.

B cells

Lymphocytes that produce antibodies against soluble antigens.

Antibodies (Immunoglobulins)

Proteins that neutralize pathogens and mark them for destruction.

Cellular immunity

T cells and other cells that respond to intracellular pathogens.

T cells

Lymphocytes that mediate cellular immunity and can induce apoptosis.

Cytokines

Signaling molecules that regulate immune responses and inflammation.

Pathogen

Microorganism capable of causing disease.

Virulence

Degree of pathogenicity of a microorganism.

Opportunistic pathogens

Microbes that cause disease when host defenses are weak.

Normal flora

Commensal bacteria normally associated with the host.

Infection

Breach of a body surface by a microorganism; not always disease.

Dermatophytosis

Fungal infection of skin, hair, and nails by dermatophytes.

Tinea capitis

Scalp ringworm; often shows green fluorescence with Wood’s lamp for Microsporum.

Onychomycosis

Toenail or fingernail fungal infection.

Candidiasis

Overgrowth of Candida; mucocutaneous infections (cutaneous or oral).

Scabies

Infestation by Sarcoptes scabiei; burrows in stratum corneum with intense itch.

Pediculosis

Infestation by lice (e.g., head lice, Pediculus humanus capitis).

Viral warts

HPV-induced skin lesions; types 6/11 genital/cutaneous; 16/18 cervical.

Herpes simplex

HSV infection; type 1 oral/facial; type 2 genital; phases include prodrome, vesicle, ulcer, crust.

Varicella-zoster virus

Varicella (chickenpox); latency in dorsal root ganglia; can reactivate as shingles.

Impetigo

Superficial bacterial skin infection (Staph aureus or Strep pyogenes); contagious.

Furunculosis and folliculitis

Staphylococcus aureus causing folliculitis (pustule) and boils.

Cellulitis

Bacterial infection of dermis/subcutaneous tissue (Staph/GAS).

Necrotizing fasciitis

Rapidly spreading toxin-mediated necrosis; emergency debridement.

GAS gangrene

Clostridium perfringens infection with gas gangrene in poorly perfused tissue.

Leprosy

Mycobacterial infection (M. leprae) affecting skin and nerves.

Jaundice

Yellow discoloration of skin/sclera due to elevated bilirubin.

Bilirubin

Heme breakdown product; becomes conjugated in liver and excreted.

Urobilinogen

Bilirubin metabolite formed in gut and excreted in urine; part of bilirubin circulation.

Pre-hepatic jaundice

Jaundice due to hemolysis before bilirubin reaches the liver.

Hepatic jaundice

Liver pathology (e.g., hepatitis) causing jaundice.

Post-hepatic (obstructive) jaundice

Obstruction of bile drainage (e.g., gallstones) causing jaundice.

Psoriasis

Multifactorial skin disease with T-cell mediated inflammation and silvery scales.

Auspitz sign

Bleeding when scales are scraped off in psoriasis.

Urticaria (hives)

Type I hypersensitivity with itchy welts; histamine-mediated.

Osteoporosis

Low bone mineral density ≥2.5 SD below the mean.

Osteopenia

Bone density 1.0–2.5 SD below the mean.

Osteoarthritis

Degenerative joint disease with cartilage loss and osteophyte formation.

Heberden’s nodes

DIP joint bony enlargements seen in osteoarthritis.

Bouchard’s nodes

PIP joint bony enlargements seen in osteoarthritis.

Rheumatoid arthritis

Seropositive autoimmune arthritis with RF/anti-CCP; joint destruction.

Septic arthritis

Joint infection (gonococcal or Staphylococcus); acute emergency.

Osteomyelitis

Bone infection, commonly Staphylococcus aureus or Gram-negatives.

Fracture

Break in a bone.

Compound fracture

Open fracture with skin break; higher infection risk.

Dislocation

Displacement of joint surfaces, loss of normal articulation.