The document provides a comprehensive overview of cellular structures, functions, and various biological processes involving cell injury, inflammation, and immune responses. It discusses cellular components such as the nucleus, mitochondria, and ribosomes, as well as processes like apoptosis, necrosis, and the immune response, including types of hypersensitivity reactions. Additionally, it covers various diseases, infections, and their mechanisms, alongside descriptions of healing processes and immune system functions.

2. The smallest
structural and
functional unit
of an organism

3.  Cell Membrane
 Semi-permeable membrane surrounding the cytoplasm of a cell
 Regulates what comes in and out of the cell
 Nucleus
 Control center of the cell
 Holds genetic material
 Nucleolus
 Site of ribosome production
 Nuclear Membrane
 Double membrane enclosing a cell nucleus
 Nuclear Chromatin
 DNA molecule

4.  Cytoskeleton
 Framework skeleton of the cell
 Very organized
 Composed of 3 types of fibers
 Microfilaments, smallest component
 Provide stiffness, structure, and shape to the membrane by forming cortical cytoskeleton
 Intermediate Filaments, middle component
 Allows the cell to be stretched or bent without breaking
 Has a net to hold genetic materials in the nucleus of the cell
 Microtubules, biggest component
 Transports cellular materials
 Divides chromosomes during cell division

5. Cytoskeleton

6.  Mitochondria
 Powerhouse of the cell
 Converts nutrients into energy
 Golgi Apparatus
 Modifies, sorts, and packages proteins for
secretion
 Transports lipids around the cell
 Creates lysosomes
 Centriole/Centromere
 Organize microtubules and provide
structure for the cell
 Pull chromatids apart during cell division
 Ribosomes
 Found in the cytoplasm and rough ER
 Make proteins
 Endoplasmic Reticulum
 The highway of the cell
 Rough Endoplasmic Reticulum
 Site of protein production
 Transports proteins to the golgi apparatus
 Smooth Endoplasmic Reticulum
 Production of large molecules, such as fats
 Transports molecules to the golgi apparatus

8. Occluding Junctions
 Tight junctions
 Impermeable to large molecules
Adhering Junctions
 Permeable to tracer particles
Desmosomes
 Tiny adhesion plates between adjacent epithelial cells
Gap Junctions
 Pits or holes
 Permeable to small tracer particles

9. Cell Adhesion Molecules
 Mediate cell-cell interaction and cell-extracellular matrix interaction
Cytokines
 Soluble proteins secreted in response to various stimuli
 Main role: activation of immune cells
Membrane Receptors
 Can be located on the outer cell membrane, inside the cell, or can be
transmembrane

10. Enzyme-linked receptors
 Control cell growth
Ion Channels
 Exchange of ions like sodium, potassium, and calcium
G-Protein Receptors
 Trans-membranous receptors
 Activate phosphorylating enzymes for metabolic and synthetic
functions of the cell

11. G1 phase, pre-mitotic gap
 Messenger RNAs for the proteins and the proteins themselves are
synthesized
 These molecules are required for DNA synthesis
S phase
 Replication of nuclear DNA
G2 phase, pre-mitotic gap
 Short phase in which the correctness of the DNA synthesized is
assessed
M phase
 Process of mitosis
 Forms two daughter cells

13.  Prophase
 Chromosome divides into 2 chromatids held by centromere.
 Nuclear membrane disintegrates
 Metaphase
 Microtubules are arranged between the 2 daughter centrioles to form a spindle.
 Chromosomes line up at the spindle.
 Anaphase
 Centromeres divide and each set of separated chromosomes move to the
opposite sides of the spindle.
 Cell membrane begins to divide.
 Telophase
 Nuclear membrane forms around each set of chromosomes
 Nucleus is reconstituted
 Cytoplasm of 2 daughter cells completely separates.
 G0 phase
 Daughter cells may remain in the cycle to undergo division further or enter rest
stage

15. Atrophy – decrease in the size of cells
Hypertrophy – increase in the size of cells
Hyperplasia – increase in the number of cells
Metaplasia – mature cell type is replaced by a different
mature cell type
Dysplasia – cells within a tissue vary in shape and size
Anaplasia – undifferentiated cells have variable nuclear and
cell structures
Neoplasm – tumor cells

16.  Ischemia
 Oxygen deficit due to respiratory or circulatory problems
 Hypoxia
 Reduced oxygen in tissues
 Oxygen Deficit
 Results in decreased energy production, loss of Na pump, and
increased intracellular Na
 Temperature
 Results in inactivation of enzymes, damage to organelles, protein
coagulation, or disruption of cell membrane
 Abnormal Metabolites
 Caused by genetic disorders or altered metabolism

17.  Apoptosis
 Programmed cell death controlled by genetics
 Necrosis
 Death of most or all of cells in an organ or tissue due to disease, injury, or
blood supply failure
 Liquefaction
 Dead cells liquefy due to the release of enzymes and form a lesion with pus
and fluid remains of necrotic tissue
 Coagulation
 Blood changing to a solid or semi-solid state as a result of proteins being
altered or de-natured
 Caseous
 Form of coagulation necrosis producing a thick, yellowish, cheesy discharge

19. Chemical Agents
 Exogenous – from the environment
 Endogenous – from inside the body
Physical Agents
 Hypothermia – increased blood viscosity, hypovolemic shock, and decreased
blood pressure
 Hyperthermia – general vasodilation and decrease in circulating blood volume
 Radiation – primarily affects actively dividing cells
Biological Agents
 Insects/Animals – direct injection of toxin
 Food Poisoning

20. Type, duration, and severity of infectious agent
Type, status, and adaptability of target cell
Underlying intracellular phenomenon
Morphologic consequences of reversible cell injury

21. Reversible Cell Injury
If the ischemia or hypoxia is of short duration, the effects may be
reversible if circulation is rapidly restored.
4 notable morphologies
Hydropic Change – accumulation of water within the cell
Fatty Change – accumulation of fat within the cell
Hyaline Change – accumulation of eosinophils within the cell
Mucoid Change – accumulation of mucus within the cell

22. Irreversible Cell Injury
 Persistence of ischemia or hypoxia results in irreversible
damage of cell structure and function, leading to cell death
Subsequent Inflammatory Reaction
 Ischemia reperfusion is followed by an inflammatory reaction
 Incoming activated neutrophils use oxygen quickly to release
oxygen free radicals

23. Chemical Injury
 Direct cytotoxic effects
 Conversion to reactive toxic metabolites
Physical Injury
 Mechanical force leading to state of shock
 Result of atmospheric pressure changes or radiation

24. First Line Defense
 Physical Barriers
 Fluids
Second Line Defense
 Phagocytosis
 Inflammation
Third Line Defense
 Antibodies
 Cell-Mediated Immunity

25. Physical Barriers
Unbroken skin, mucous
membranes, nasal hair, or body
clots
Fluids
Enzymatic fluids
Chemical fluids – saliva, tears,
sweat, or gastric secretions

26. Phagocytosis
Neutrophils and macrophages engulf cells, debris, and
foreign matter
Inflammation
Automatic response of the body to cell injury

27. Vascular Response
Vasodilation
Increased capillary
permeability

28. Cellular Response
Migration of cells to injury
site
Cells destroy the ineffective
organism, remove damaged
cells, and release
inflammation mediators

29. Dolor – pain
Calor – heat
Rubor – redness
Tumor – swelling

30. Mild Fever
Malaise
Fatigue
Headache

31. Drugs may decrease capillary
permeability, reduce the number of
leukocytes, and reduce the number
of mast cells

32. Stage 1
 Skin is still intact
 Ulcer is red or pink, like a sunburn
Stage 2
 Partial thickness skin loss involving epidermis
 Ulcer is a blister, scrape, or abrasion
Stage 3
 Full thickness skin loss involving dermis
Stage 4
 Full thickness skin loss that includes muscle or bone

34. Healing – the attempt of the body to restore normal
structure and function following injury
Resolution – tissue or organ is totally restored to normal
structure and function
Regeneration – replacement of damaged parenchymal cells by
the same type of cells; require cell division

35. Primary Intention
Healing of a clean wound without tissue loss
Secondary Intention
Wounds are created by major trauma
Significant loss in tissue or damage
Wound can granulate, surgeon may pack wound or use
drainage system

37. Tertiary Intention
Delayed primary closure or secondary suture
Wound is initially cleaned, debrided, and observed, typically
4 to 5 days before closure
Wound is purposely left open

38. Transudate – clear and watery
Exudate – creamy, yellow, thick, proteins, WBC
Purulent – yellow, thick, leukocytes, necrotic debris
Serosanguineous – clear, tinge of red, thin and water,
contains serum and blood
Sanguineous – bloody, bright red = fresh, dark red = older
Infected Pus – hues of green/yellow/blue, thick, pathogens

39. Serous
 Watery, mostly fluids
 Some proteins and white blood cells
Fibrinous
 Thick and sticky
 High fibrin content
Purulent
 Thick, yellow-green
 Leukocytes, cell debris, microorganisms
Abscess
 Pocket of purulent exudate or pus found in a solid tissue

40. Arterial Insufficiency
Thrombosis in acute cases
Arteriosclerosis in chronic cases
Gangrene – dry vs. wet vs. black
Claudication – pain with walking
Venous Insufficiency
Incompetent valves
Inefficient calf pump
Distended capillary beds

42. Humoral Immunity
Antibodies are produced to protect the body
Cell-Mediated Immunity
Lymphocytes are programmed to attack non-self cells

43. Antibody
Protect the body
Stored in blood
Antigens
Proteins on cell surface
Complement System
Antigen-antibody complex activated during immune
reaction
Cell damage when activated

44. Macrophages
Present throughout the body
Derived from monocytes
Initiate immune response
Engulf foreign materials
Process foreign antigens
Display foreign antigens to lymphocytes
Secrete monokines and interleukins

45. Lymphocytes
T lymphocytes
 Cytotoxic T cells – destroy cells that bind to the antigen and release
enzymes
 Helper T cells – facilitate the immune response by activating and
regulating
 Memory T cells – remember antigens
B lymphocytes
 Made in the bone marrow
 Located in spleen and lymphoid tissue
 Produce antibodies

47. NK Cells
Kill tumor or virus infected cells without having prior
exposure

48. IgG – most common. Activates complement and crosses the
placenta. Participates in both primary and secondary immunity.
IgM – can activate the complement. Involved in blood typing.
Natural antibodies.
IgA – not found in blood. Found in tears, saliva, and
colostrums.
IgE – associated with allergic reactions
IgD – function is relatively unknown

49. Type 1: Allergic reaction.
 Exposed to allergens causes development of IgE’s.
 Activates mast cells and causes inflammation.
Type 2: Cytotoxic hypersensitivity.
 Antigen on the cell membrane reacts with circulating IgG’s.
 Activates the complement and destroys cells with the antigen.
Type 3: Immune Complex Hypersensitivity
 Antigen and antibody combine to form immune complexes that cause
inflammation and tissue destruction
Type 4: Cell Mediated Hypersensitivity
 Delayed response by T-lymphocytes
 No antibodies are present

50. Affects the central windpipe
Airway disorders
Interventions: avoid triggers, use medications properly,
and monitor peak flow rate
Asthma

52. Multiple Sclerosis
Autoimmune de-myelination of the nerves in
the brain and central nervous system
 Clinically Isolated Syndrome – only suffer
one attack
 MS classification – multiple attacks at least
1 month apart, with damage to at least 2
separate CNS areas
Diagnostic Tests: MRI, visual evoked
potential, and CSF analysis
Interventions: modify disease course, treat
attacks, and manage symptoms

53. Myasthenia Gravis
Antibodies destroy acetylcholine receptors at
neuromuscular junctions
Guillian-Barre Syndrome
De-myelination of peripheral nerves
Reversible – on its own.

54. Fibromyalgia
 Generalized musculoskeletal pain for at least 3 months
 Diagnosis – multiple tender points affect all quadrants; pain felt
in at least 11 of the 18 tender points
Rheumatoid Arthritis
 Autoimmune destruction of joints, affecting multiple joints in a
symmetrical pattern
 Inflammation can affect organs
Scleroderma
 Affects micro-vessels of the skin and organs
 Causes hypoxia in all tissues

55. Sjogren’s Syndrome
 Loss of fluids for tears or saliva
Hashimoto’s Disease
 Autoimmune thyroid disease
 Causes hypothyroidism
Grave’s Disease
 Underlying reason for Hyperthyroidism

56. Inflammatory Bowel Disease – group of disorders with
inflammation of the intestines
Crohn’s Disease
 Ulcers are found throughout the intestines, except for the
rectum
Ulcerative Colitis
 Ulcers are found in the lower intestines and may begin in the
rectum

57. Type 1 Diabetes
 Autoimmune destruction of pancreas cells due to the lack of
insulin
Meningitis
 Viral is the most common
 Bacterial is more severe than viral
HIV

58. Active Viral Infection
Virus attacks the host cell and injects genetic material
Virus uses the host cell to produce viral proteins and nucleic
acid
New viruses are made in the cytoplasm or reduced by lysis and
bud from the host cell
Latent Viral Infection
Virus enters in a similar fashion as an active infection
Virus replicates slowly or has a delayed replication
Viral proteins are inserted into the cell membrane of the host cell
to cause an immune response

59. Portal of Entry: mucosal membrane, usually nasopharynx
Transmission: close contact with person who has viral
meningitis may infect you with the virus, but the chances of you
developing meningitis are low
Strong local immune system
By the time the virus disseminates, a sufficient immune
response has been mounted in the periphery to eliminate
the pathogen

60. Meningitis-B has a protein on the outside of the cell that
tells the immune system it’s a human cell
 The immune system never attacks the virus
Some types of Meningitis are swallowed by macrophages
 Virus is not broken down
 Cause the macrophages to commit suicide, or “apoptosis”
Many people have bacteria living inside their nasal cavity
 Bacteria is harmless
 Problem arises when the virus enters the bloodstream
Most cases resolve on their own

61. Direct Contact – actual physical contact between source and
susceptible person
Indirect Contact – organisms from infected reservoir are
transmitted to susceptible host via inanimate object
Droplet – transmission via droplets expelled from respiratory
secretions by coughing, sneezing, or talking
Aerosol – airborne; particles containing microorganisms remain
suspended in air for long periods of time
Vector – animals capable of transmitting disease
Fecal-Oral – ingestion of contaminated food and water to infect
the digestive system

62. Incubation Period
 Period between exposure to a pathogen and when signs/symptoms are first
apparent
Prodromal Period
 Period between the end of the incubation period and the point at which the
characteristic symptoms of the illness appear
Acute Period
 Phase of rapid multiplication of the pathogen with exponential growth and peak
in its’ population
 Symptoms are pronounced – specific to the organ affected as well as in general
because the immune system response is strongest
Convalescence Period
 Host recovers gradually and returns o baseline
 Pathogen load declines but may not be completely eliminated
 Host may continue to be a source of infection

63. If an infection is fatal,
these steps will not
occur.

64. Nosocomial Infection – infections that occur in the
healthcare setting
Acute Infection – fully developed infectious disease with
peak clinical signs
Chronic Infection – micro-organism continues to replicate in
the body and causes milder symptoms
Subclinical Infection – microbe can reproduce in the body
but does not present clinical signs
Septicemia – bacteria reproduces and circulates in the
bloodstream