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midterm Flashcards

1
Q

inside the cells release residual content

A

autophagosomes

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2
Q

different (outside) pinocytosis fused with primary lysosomes

A

heterophagosomes

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3
Q

study of “cause” of a disease

A

Etiology

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4
Q

deals with “how a disease develops”

A

Pathogenesis

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5
Q

cell Adaptions

A 
Prolonged exposure of cells to negative or exaggerated normal conditions causes
various adaptations to:
– Cell, tissues, organs
■ Atrophy
■ Hypertrophy
■ Hyperplasia
■ Metaplasia
■ Intracellular accumulations
■ Aging
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6
Q

Intracellular Accumulations

Three types of intracellular accumations

A
  1. Anthracosis (coal/carbon particles)
  2. Hemosiderosis
  3. Lipid accumulation
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7
Q

early stages of black lung disease
– Exogenous material accumulation
– Seen in lungs of coal miners and cigarette smokers

A

Anthracosis (coal/carbon particles)

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8
Q

Accumulation of blood-derived brown pigment
– Derived from hemolyzed red blood cells
– Eg. Hereditary hemochromatosis – genetic disorder of liver (overabsorption of iron
from food)

A

Hemosiderosis

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9
Q

Decrease in size of a cell, tissue, organ or entire body
– Can be a reduced size of a cell, reduced number of cells or both
– Aging and damaged organelles are eaten by autophagosomes and digested
■ Undigested residues form lipid-rich brown pigment called lipofuscin
■ Undigested proteins are taken up by ubiquitin (scavenger protein) and marked for
destruction

A

atropy

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10
Q

hypertrohy

A

Hypertrophy – increase size of tissue or organs due to enlargement of individual cells
– “trophe” = food overfed
– Hypertrophy in cardiac muscles of the heart (as in hypertension) and skeletal muscle (as in bodybuilders)

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11
Q

increase in size of tissue or organs due to an increased number of cells
– Chronic stimulation – callus (corn) – overgrowth of stratum corneum
– Hormones – uterus (endometrial hyperplasia due to action of estrogen)
– Hyperplasic polyps of intestines; Benign prostatic hyperplasia in elderly men

A

Hyperplasia

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12
Q

– Change of one cell type into another
– Eg. Smokers – columnar cells of the bronchial mucosa stratified squamous
epithelium
■ Reversible change
■ If stimulus remains the metaplasia may progress to dysplasia

A

Metaplasia

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13
Q

– Disorderly arrangement of cells and nuclear change

– Can progress to neoplasia (Cancer)

A

■ Dysplasia

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14
Q

– Fatty livers (steatosis) due to chronic alcohol abuse or diabetes mellitus

A

Lipid Accumulation

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15
Q

Cell Death

■ Two Reasons Why Cells Die:

A 
1. Irreversible cell injury
– Necrosis: localized death of cells or tissues in a living organism
■ Coagulative
■ Liquefactive
■ Caseous
■ Enzymatic fat Necrosis
2. Apoptosis (“dropping out”)
– Programmed cell death (single cells)
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16
Q

– Most common
– Cause: anoxia
■ Rapid inactivation of hydrolytic enzymes prevents lysis
– Outcome: cell membrane is preserved, organelles and nucleus coagulate
– Solid internal organs: heart, liver, kidneys

A

Coagulative Necrosis

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17
Q

– Cause: cell is completely digested by hydrolytic enzymes – Eg. brain infarct
– Outcome: Dissolution of tissues soft and liquify
– Brain, skin, joints

A

■ Liquefactive Necrosis

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18
Q

– Cause: Tuberculosis (TB) patients center part of tuberculous granuloma
becomes necrotic and cells fall apart
■ Cheesy
■ Also found with fungal infections (histoplasmosis)
– Lungs

A

Caseous Necrosis (special form of coagulative necrosis)

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19
Q

– Caused by lipolytic enzymes and limited to fat tissues usually around the pancreas
– Cause: rupture of pancreas (acute pancreatitis)
■ Enzymes release into adjacent fat tissue degrade fat into glycerol and free fatty acids
■ Forms calcium soaps

A

■ Enzymatic Fat Necrosis (special form of liquefactive necrosis)

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20
Q

condensation of chromatin

A

Pyknosis

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21
Q

fragmentation of nucleus  ‘nuclear dust’

A

Karyorrhexis

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22
Q

dissolution of nuclear structure as a result of enzymatic digestion

A

Karyolysis

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23
Q 
■ Active form of PROGRAMMED cell
death by ‘suicide genes’
■ Affects single cells
– Cell divides into apoptotic bodies
taken up by macrophages
A 
apoptosis
■ Physiologic Apoptosis –
– Eg. Fetal development
■ Pathologic Apoptosis –
– Eg. Liver cells infected with
hepatitis
Note: Lack of apoptosis can be seen in disease – Eg. Chronic Lymphocytic Leukemia
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24
Q

What are oxygen radicals, and how do they damage cells?

A

Toxic oxygen radicals are formed in small amounts in cells, but they are rapidly catabolized.
Reversible cell injury:
- hydrogen peroxide (H2O2)
- hydroxyl radicals (OH)

cause direct DNA, protein, and membrane damage.

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25
Q

How do toxins, microbes, and chemical mediators of inflammation kill cells?

A

Toxins kill cells through direct and indirect effects on cell structure and function.
Microbes kill cells by mediating direct cell lysis (some viruses) by activating host immune effector cells (viruses and bacteria), and through the release of cytotoxic chemicals.
Mediators of inflammation and immunity can also kill cells through activation of programmed cell death (apoptosis) and through the assembly of membrane channels (membrane attack complex).

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26
Q

cause -exogenous injury
mechanism-multiple,organs
cells affected- multiple organs
outcome-cell membrane ruptures, tissues death and bacterial infections

A

necrosis

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27
Q 
cause-exogenous or edogenous 
mechanism-active programmed process
cells affected-single
cell changes-round up, fracmented cell membrane in tact
outcome-phagocytosis by macrophages
A

apoptosis

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28
Q

Organism establishes parasitic relationship
with host
· Invasion + multiplication of organism =
immune response
· Damage to host:
– Microorganism’s toxins, replication, or indirectly
by competing for nutrient
– By our own immune system

A

infection

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29
Q

results when a person eats food
containing toxins that cause illness. Toxins are produced by
harmful microorganisms, the result of a chemical
contamination, or are naturally part of a plant or seafood.
Some bacteria cause an intoxication. Viruses and parasites do
not cause foodborne intoxication.
– Bacteria: Clostridium botulinum, Staphylococcus aureus, Clostridium
perfringens, and Bacillus cereus.

A

intoxication

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30
Q

are substances that
typically cause fever
Bacteria
Cytokines

A

(‘pyrogenic’):

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31
Q

Local infection spreading into the lymphatic
system
– Lymphangitis
– Moves towards local lymph node

A

red streak

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32
Q

Definition: adverse conditions that cause a cellular response that remains within the
range of homeostasis
– Injury stops cell returns to it’s original steady state
Caused by brief hypoxia (deficiency of oxygen), brief anoxia (total lack of oxygen) or
low concentration of toxins

A

Reversible cell injury
Cell’s response to exposure to low doses of
toxins, brief hypoxia or anoxia
– Cellular swelling (hydropic changes – swelling of
cytoplasm and cytoplasmic organelles)
■ A. Normal microvilli
■ B. Swollen microvilli
■ C. Invagination of the cell membrane leading to
formation of membrane-bound vacuoles
■ D. Swollen mitochondria and dilated RER
■ E. Loss of intercellular contact
– Changes in cell membrane permeability
■ Na+/K+ ATPase pump
– Cell returns to original steady state with cessation of injury

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33
Q

Due to cells exposed to heavy doses of toxins,
anoxia or severe or prolonged hypoxia
– Will eventually lead to cell death

A

Irreversible cell injury
1.Caused by heavy doses of toxins, anoxia and prolonged hypoxia
2.Causes loss of cell integrity and rupture of the cell membrane
3.Dead cells release their contents (especially cytoplasmic enzymes)
into extracellular fluid (blood)
– measured through laboratory blood tests – something is really wrong!

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34
Q

Causes of antibiotic resistance

A

 Antibiotic Overuse – creation of ‘superbugs’ – antibiotic-resistant organisms
 Methicillin-resistant Staphylococcus aureus (MRSA)
 Multi-drug resistant Mycobacterium tuberculosis
 Vancomycin-resistant Enterococci
 Multi-drug resistant Pseudomonas aeruginosa
 Fluoroquinolone-resistant Clostridium difficile
Antibiotic Resistance – Other Factors
 Increased travel/exposure – with globalization
 TB on the rise; 2nd leading cause of death due to infectious disease worldwide  Susceptible sub-populations:
 Kids in daycare
 Aging
 Hospital populations
 3 rd world poverty – stress, poor nutrition, close quarters (easy spread), lack of medical care
-use in agriculture

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35
Q

Signs and symptoms – know what they are

Signs and Symptoms of Infectious Diseases

A 
 Many and varied
  Can be systemic (fever) or local (pus) 
 Depends on: 
– Etiologic agent
 – type and virulence 
– System affected 
– Health of the individual
Common Systemic Signs & Symptoms
  Fever  Chills  Sweat  Malaise  Nausea  Vomiting  Change in leukocyte type and/or number  Enlarged lymph nodes  Possible cognitive changes in the elderly
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36
Q

many types and variety of causes of rash

A

FYI Common Rashes with Infections
 Maculopapular eruptions: – Measles, Rubella, Fifth Disease, Roseola
 Nodular lesions: – Streptococcus, Pseudomonas
 Diffuse erythema: – Scarlet Fever, Toxic Shock Syndrome
 Vesiculobullous eruptions: – Varicella, Herpes zoster
 Petechial purpuric eruptions: – Epstein Barr Virus

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37
Q

-Can be associated with many infectious diseases, not just sepsis
 Easily palpated – Cervical – Inguinal – Axillary  Other reasons for inflamed lymph nodes: – Cancer – Rheumatoid Arthritis – Medications

A

− Lymphangitis

38
Q

local infection spreading into the lymphatic system – Lymphangitis – Moves towards local lymph node

A

red streak

39
Q

−- Secondary to an infection
 Usually from: – Hemolytic Streptococcus and/or Staphylococcus
 Lymph nodes most often affected: – Submandibular – Cervical – Inguinal – Axillary

A

sepsis

40
Q

why no fever with aging?

A 
– Impaired thermoregulatory system 
– Masking effects of drugs 
 1 st symptoms of infection in elderly may be: 
– Confusion 
– Memory loss 
– Delirium
41
Q 
An organism that elicits a pathologic response in the
host
· Depends on:
· Site of invasion
· Number of pathogens, and virulence
· How well they disseminate in host
· IMMUNE STATUS OF THE HOST
A

pathogen- chain of transmission

42
Q

An environment in which an organism can live and multiply
 Animal, plant, soil, food, organic substance
 Humans
 Human and animal reservoirs can be symptomatic or asymptomatic

A

A reservoir

43
Q

pathogens that don’t cause
disease in people with intact immune systems, but can
cause devastating disease in hospitalized or
immunocompromised people

A

Opportunistic pathogens:

44
Q

– refers to the potency of the pathogen
in producing sever disease and is measured in
case fatality rate

A

Virulence

45
Q

Originating or taking place in a hospital, acquired
in a hospital, especially in reference to an
infection.
– A.k.a. Hospital acquired infections (HAI)
– Most common are UTIs (from catheters or
urologic procedures), blood infections
(from IV catheters or surgical wounds), and GI
infections

A

Nosocomial infections

46
Q

where the organism leaves the reservoir
 Corresponds to entry point on next host
 Examples:
– Respiratory droplets, blood, vaginal secretions,
semen, tears
– Urine, feces
– Open lesions, pus

A

portal of exit

47
Q

Mode/Mechanism of Transmission
HOW THE ORGANISM GETS FROM INFECTED HOST TO NEW HOST:
· Contact – directly or indirectly.
– Direct = physical contact Indirect= via an inanimate intermediate object, called a fomite.
– Ex. Intercourse - HIV vs. touching a handrail – enteric pathogens
· Airborne – disease-causing organisms float on air currents in
the room. Often propelled from respiratory tract through
coughing/sneezing.
– Ex. TB, Chickenpox

A

· Droplet – different then airborne because they do not remain
suspended in air but fall within 3ft of course. Produced by
coughing/sneezing.
– Ex. Influenza
· Vehicle – occurs when infectious organisms are transmitted
through a common source to many potential susceptible hosts.
– Ex. Salmonella in contaminated food
· Vector –involves insects and/or animals that act as
intermediaries between 2 or more hosts
– Ex. Lyme disease via Black-legged or Deer Ticks

48
Q 
Where the pathogen invades/enters:
 Ingestion
 Inhalation
 Bites
 Contact with mucous membranes
 Percutaneous
 Transplacental
A

portal of entry

49
Q 
FACTORS:
 Age, sex, ethnicity
 Health & nutrition
 Hormonal balance
 Co-morbidities
 Living conditions
 Personal behaviours (drug use, hygiene, diet,
sexual practices)
A

Host Susceptibility

50
Q

smallest, RNA or DNA covered with proteins – Antibiotics don’t help – Antiviral meds only moderately effective · Entirely dependent on host · Some anti-viral meds are specific – Acyclovir - ’s DNA replication

A

virus

51
Q

Very small self-replicating bacteria with no cell wall, dependant on host for nutrition ·

A

Mycoplasmas

Eg. M.hominis; M.pneumoniae

52
Q

Single celled organisms with cell wall;
independent
· Replicate by growing and dividing in half – they can do this in any tissue ·
Classified by shape (spherical-cocci, rod-shaped - bacilli, spiral-shaped - spirochetes), staining (Gram positive/negative), motility, spores, O2 /nonO

A

bacteria
aerobic and anaerobic
example-normal gut flora-anaerobic
– Staphlococcus aureus is aerobic (lungs, skin)

53
Q

Small obligate intracellular parasites – non-motile gram negative bacteria
· Primarily animal pathogens that produce disease in humans
· Transmitted via insect bites (tick, flea, louse, mite) · Require host for replication · i.e. Q Fever (Coxiella); “Trench Fever” carried by lice (Rochalimaea)

A

Rickettsiae

54
Q

Smaller than bacteria but larger than viruses
– Obligate intracellular - Dependent on host for replication
– Always contain both RNA and DNA (unlike viruses) – Susceptible to antibiotics – curative - Most common STD - Leading cause of P.I.D. - Leading cause of preventable blindness in neonates

A

Chlamydiae

55
Q

-large, multicellular organisms that are generally visible to the naked eye in their adult stages. · can be either free-living or parasitic in nature. · In their adult form, helminths cannot multiply in humans.

A

Helminths (worms)
There are three main groups of helminths:
– Flatworms (platyhelminths) – these include the trematodes (flukes) and cestodes (tapeworms).
– Thorny-headed worms (acanthocephalins)
– Roundworms (nematodes)
– the adult forms of these worms can reside in the gastrointestinal tract, blood, lymphatic system or subcutaneous tissues.

56
Q

Unicellular organism that produce hyphae (filamentous outgrowths) · Contain nuclei (eukaryotic) · Cell walls · Yeasts or molds · Reproduce by budding off · Eg. Candida albicans

A

Fungi (yeast/mold)

57
Q

Single cells or groups of cells · Motile, free living in moist environments · Cell membrane, no cell wall · Divide similar to bacteria · Eg. Giardia

A

protozoa

58
Q

Inflammation of a lymph vessel

A

− Lymphangitis -

59
Q

Inflammation of one or more lymph nodes

A

− Lymphadenitis -

60
Q

Increased lymph fluid in the tissues

A

− Lymphedema -

61
Q
  • Enlargement of the lymph nodes
A

− Lymphadenopathy

62
Q

Four cardinal signs of inflammation (Celsus 30 BC-38 AD) must know!

A

Heat (calor)

Redness (rubor)

Swelling (tumor)

Pain (dolor)

Loss of function (function laesa - added later in 1900

63
Q

Five classical signs of inflammation

A 
(Acronym – SHARP or PRISH) 
Swelling 
Heat 
Altered Function/Immobility 
Redness 
Pain
64
Q

-the act or process of forming a margin specifically : the adhesion of white blood cells to the walls of damaged blood vessels.

A

1 Margination

65
Q

-A condition occurring during inflammation in which leukocytes adhere to the linings of capillaries.

A

2 Pavementing
Attach to endothelium = pavementing

Protrusions from cytoplasm stick to endothelial cells (especially postcapillary venules)

66
Q

movement of a motile cell or organism, or part of one, in a direction corresponding to a gradient of increasing or decreasing concentration of a particular substance.

A

4 Chemotaxis

67
Q

-a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.

A

5 Exudate

68
Q

is extravascular fluid with low protein content and a low specific gravity (< 1.012). It has low nucleated cell counts (less than 500 to 1000 /microliter) and the primary cell types are mononuclear cells: macrophages, lymphocytes and mesothelial cells.

A

6 Transudate-

69
Q

invasion of site with necrosis and pus acute inflammation

A

7 Suppurative-

70
Q

-a blood protein produced in response to and counteracting a specific antigen. Antibodies combine chemically with substances which the body recognizes as alien, such as bacteria, viruses, and foreign substances in the blood.

A

16 antibodies

71
Q

– several proteins that are activated in a cascade acting on one another Numbered 1-9 (C1, C5..)
All pathways converge to form the Membrane Attack Complex (MAC) (key to destruction of foreign agent)
Bores holes into membranes of microbes or body’s owncells
Fill with fluid → cell death

A

Complement System
3 pathways that activate the complement cascade
1. Classical pathway – activated by antigen-antibody complexes.
2. Alternative pathway – activated by bacterial endotoxins, fungi, snake venom
3. Lectin pathway – activated by binding of lectin to bacteria

72
Q

Derived from phospholipids of cell membranes
Form leukotrienes and prostaglandins
Polyunsaturated fatty-acid found in brain, muscle and liver

A

Arachidonic Acid Derivatives

73
Q

increase vascular permeability and promote chemotaxis
Formed through the LOX pathway (lipoxygenase pathway)
Bronchospasm – contract smooth muscles in bronchi

Anaphylactic shock

A

Leukotrienes –

74
Q

Stimulate vasodilation, increase vascular permeability

Formed through the COX pathway (cyclooxygenase pathway)

Pain and fever

A

Prostaglandins

75
Q 
Site of wound 
Mechanical factors 
Size of wound 
Presence or absence of infection 
Circulation issues 
Nutritional and metabolic factors 
Age
A

Wound Healing

Depends on:

76
Q

Deficient scar formation – poor formation of granulation tissue

Inadequate collagen production can lead to wound dehiscence

A

Complications of Wound Healing

Excess scar formation

Keloid scar – hypertrophic scars

Can lead to disfigurement and loss of function

77
Q

Immune Response
Innate Immunity (born with)
Nonspecific, protective
No memory

A

Acquired Immunity
Specific
Has memory

78
Q

Immunity acquired by introduction of an antigen into the host
environmental exposure
Vaccination

A

Active Immunity

79
Q

Immunity acquired when antibodies produced by one person are transferred to another
trans placental transfer, breast milk, antibody inoculation

A

passive immunity

80
Q

Major anti-bacterial and anti-viral antibody
most abundant type in blood
Only antibody to cross placenta
Responsible for the protection of the newborn for the first 6 months of life

A

IgG

81
Q

primary or initial immune response
Largest antibody
stays in blood vessels

A

IgM

82
Q 
Defends external body surface 
Found on mucous membranes 
Found in secretions 
Saliva 
Breast milk 
Urine 
Seminal fluid 
Tears 
Nasal fluid
A

IgA

83
Q

Controls lymphocyte activation or suppression

Found exclusively on B-cells

A

IgD

84
Q

Primary factor in eliminating parasitic infections
Functions during allergic reactions
Activates mast cells to release histamine
Associated with anaphylaxis, hives, allergen induced asthma

A

IgE

85
Q

ediated by Antibodies (Ab) present in body fluids or secretions
Humoral = body fluids
Blood, Lymph, Interstitial Fluid
Aka. Antibody-Mediated Immunity

B Lymphocytes
Formed in bone marrow
Mature in bone marrow
Differentiate into Memory B-cells or plasma cells
Plasma cells secrete Immunoglobulins (Antibodies) to mount an immune response
Bind Antigen to display it for destruction
Memory B-cells
‘remember’ Antigen after first exposure

A

Acquired Immunity - Humoral
1. Humoral - B Lymphocytes (B-cells)

Protects against extracellular microbes and their toxins (eg. bacteria

86
Q

All viruses and some bacteria hide inside cells where antibodies cannot reach them
T-lymphocytes can recognize these hidden organisms and destroy the cells
Also implicated in transplant rejection, hypersensitivity reactions, and some autoimmune diseases

Interaction with antigen→ activates T-lymphocyte to produce specialized Tcells (or sensitized T-cells): 
Helper T-cells (75% of all T-cells) 
Cytotoxic T-cells 
Suppressor T-cells 
Memory cells
A
  1. Cell Mediated – T Lymphocytes (T-cells)

Defense against intracellular microbes (eg. viruses)

87
Q

Lines of Defense

A

1st line of defense- skin, mucosal, hair, pH barriers

INNATE

2nd line of defense – inflammation

INNATE

3rd line of defense - immune system cells

ACQUIRED

88
Q

Move through the blood vessel wall to inflamed tissue

Phagocytosis → swelling and pain

A

Emmegration (aka transmigration) (leukocyte rolling across endothelium)

89
Q

Properties of smooth muscle cells and fibroblasts

Contract like muscle cells and secrete cell matrix substances like fibroblasts

Holds edges of damaged tissue together

A

Myofibroblasts

90
Q

Precursors of blood vessels

Proliferate from small blood vessels at the edges of damaged tissue

Appear 2-3 days after injury. By day 6 new blood vessels are formed

Provide a route for scavenger cells to remove tissue debris and scabs

Allow oxygen and nutrients to flow to injured site

A

Angioblasts (angio = vessels)

91
Q

Produce extracellular matrix

Fibronectin – provides the glue to hold cells together in wound healing

Collagen – from fibrils in interstitial spaces

A

fibroblasts

gen path (5 decks)

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