exam 1 Flashcards
1
Q
what characterizes hydropic swelling
A
condition of reversible cell injury characterized by a large, pale cytoplasm and a normally located nucleus
first manifestation of almost all forms of cellular injury
caused by different insults
2
Q
what causes hydropic swelling
A
interference with the normal function of Na/K pump and other ion pumps in the plasma membrane
3
Q
what is associated with hydropic swelling
A
ultrastructural changes: cellular swelling and swelling of organelles (mitochondria and ER), formation blebs in the membrane, clumping of nuclear chromatin
4
Q
atrophy
A
decrease in the size and function of the cell, usually recognized as diminution in the size and function of an organ
5
Q
hypertrophy
A
increase in the SIZE of the cell accompanied by an increase in the size of the organ and an augmented functional capacity; can be physiologic or pathologic
6
Q
conditions that may lead to hypertrophy
A
hormonal stimulation
increased functional demand
7
Q
hyperplasia
A
increase in the NUMBER of cells in an organ or tissue, resulting in increased volume/size of the organ and an augmented functional capacity; can be physiologic or pathologic
8
Q
condition that may lead to cell hypertrophy
A
hormonal stimulation (hormonal hyperplasia) increased functional demand (compensatory hyperplasia) persistent cell injury
9
Q
metaplasia
A
conversion of one differentiated cell type to another; often involves epithelial tissue
10
Q
sequences of metaplasia
A
- columnar/glandular epithelium –> squamous epithelium (metaplasia of tracheal/bronchial epithelium caused by smoking)
- squamous epithelium –> glandular epithelium; barret metaplasia of the esophagus as result of chronic presence of refluxed gastric acid
11
Q
dysplasia
A
alteration in the size, shape and organization of the cellular components of a tissue; affects the epithelium; considered a preneoplastic leasion
12
Q
dysplasia may involve…
A
variations in the size and shape of cells;
disorderly arrangement of the cells within the epithelium; enlargement, irregularity and some level of hyperchromatism of the nuclei
13
Q
neoplasia (anaplasia)
A
malignant alteration of the cells of a tissue
14
Q
features of anaplasia
A
loss of polarity; loss of specialized functions; pleomorphism; altered nuclear/cytoplasmic ratio; hyperchromatism; enlarged/multiple nucleoli; abnormal mitotic figures; tumor giant cells
15
Q
injurious agent –> entry of calcium causes…
A
increased mitochondrial permeability
activation of multiple cellular enzymes
16
Q
injurious agent –> lysosomal membrane damage
A
enzymatic digestion of cellular components
17
Q
what can injurious agent cause
A
decrease in ATP mitochondrial damage entry of Ca increased ROS membrane damage protein misfolding, DNA damage
18
Q
depletion of ATP causes
A
defective functioning of the sodium pump
increase in anaerobic glycolysis
detachment of ribosomes
19
Q
features of defective Na pump
A
cellular and organelle swelling; loss of microvilli; formation of blebs
20
Q
increase in anaerobic glycolysis causes
A
clumping of the nuclear chromatin
21
Q
detachment of ribosomes causes
A
decrease in protein synthesis
deposition of lipids
22
Q
ROS react with
A
fatty acids –> oxidation–> generation of lipid peroxides –> disruption of plasma membrane/organelles
proteins–> oxidation –> loss of enzymatic activity, abnormal folding
DNA–> oxidation –> mutations, breaks
23
Q
defects in membrane permeability causes
A
defects in O2 availability –> decreased levels of ATP, production of reactive oxygen species
increased levels of cytosolic Ca2+
24
Q
what characterizes necrosis
A
denaturation of proteins; digestion of the cell by degradative enzymes (autolysis); fragmentation and phagocytosis of the cellular debris by leukocytes; dead cells may ultimately be replaced by large, whorled phospholipid masses called myelin figures
25
coagulative necrosis
slow digestion of the cell by degradative enzymes; the basic outline of the dying cells is preserved for some time (days) until cellular debris are removed by phagocytosis by leukocytes
26
liquefactive necrosis
rapid death and dissolution of the ells affected: cells are rapidly degraded by the proteolytic enzymes of its own lysosomes (autolysis) or the ones from the accumulated white cells (heterolysis); result is often an access of cyst; mainly characteristic of focal bacterial infections nd the hypoxic death of the cells within the CNS
27
fat necrosis results from
pancreatitis or trauma
28
caseous necrosis
lesion of TB
29
fibrinoid necrosis
usually affects injured bloods vessels; characterized by the accumulation of plasma proteins in the walls of the vessels
30
initial nucleus events in apoptosis
DNA fragmentation into fragments of specific sizes --> chromatin condensation --> nuclear fragmentation: formation of nuclear bodies
31
apoptotic bodies
composed of cytoplasm and organelles with or without nuclear bodies
32
final events of apoptosis
phagocytosis of apoptotic bodies by adjacent healthy cells or by macrophages; degradation of the apoptotic bodies in the lysosomes; no or minimal inflammation
33
mechanisms of apoptosis
extrinsic - mediation by membrane receptors: death receptors
intrinsic - mediated by cell damage and intracellular sensors: p53 and proteins of the Bax, Bak family
34
entosis
a nonapoptotic mechanism of cell death in which the dying cell is first internalized into another cell
35
when does entosis occur
as a result of epithelial cell detachment from eh extracellular matrix
36
how does cell internalization occur in entosis
through cell invasion not through phagocytosis
37
how does cell death occur in entosis
through lysosome-mediated degradation
38
roles of entosis
development, cancer prevention, metabolic stress
39
theories of cellular aging
1) aging as accumulated somatic damage
| 2) aging as a genetic program
40
acute inflammation
short duration, mostly characterized by vascular changes that lead to edema of the surrounding tissue and infiltration by neutrophils (also called polymorphonuclear leukocytes) or "polls"
41
chronic inflammation
longer duration, characterized by lymphocytes and macrophages (monocytes), tissue destruction by these cells and an attempt at tissue repair via proliferation of blood vessels (angiogenesis) and connective tissue
42
systemic signs of inflammation
fever
increased white cell count (leukocytes)
enlargement of lymph nodes
43
serous exudate
composed mainly of plasma fluids and proteins with few white blood cells
44
purulent exudate (suppuration)
contains tissue debris and many white blood cells in addition to plasma fluids and proteins
45
steps of microscopic events in inflammatory response
1) injury
2) constriction the microcirculation
3) dilation of small blood vessels
4) increase in permeability of small blood vessels
5) exudate leaves small blood vessels
46
histamine
present in mast cells; it is released; it causes severe blood vessel dilation and airway constriction and that's why you can get anaphylaxis
47
serotonins and bradkinins
products of cells that mediate inflammation in particular causes sensation to pain and discomfort
48
leukotriene, prostaglandins
platelet-activating factors, help in clotting
49
events of acute inflammation
1) margination
2) adhesion or pavementing
3) chemotaxis and emigration
4) phagocytosis and intracellular degradation
5) extracellular release of leukocyte products (causes tissue damage)
50
outcomes of acute inflammation
1. resolution
2. scarring
3. abscess formation
4. progression to chronic inflammation
51
chronic inflammation is characterized by
1. infiltration with mononuclear "chronic inflammatory" cells which include macrophages, T lymphocytes, and plasma cells
2. tissue destruction largely due to the inflammatory cells themselves
3. repair involving new vessel proliferation (angiogenesis) and scarring (fibrosis)
52
settings of chronic inflammation
1. persistent infections
2. prolonged exposure to toxic agents
3. autoimmune disease
53
chronic inflammatory cells
1. tissue macrophages
2. t lymphocytes
3. plasma cells
4. eosinophils
54
tissue macrophages
originate as monocytes in the blood; they will migrate out to the site of injury 24-48 horus after the onset of acute inflammation, where they are then called tissue macrophages
55
t lymphocytes
stimulate macrophage activity by producing their own cytokines
56
plasma cells
B lymphocytes that make antibodies
57
eosinophils
associated with allergic reactions and parasites
58
systemic manifestations of chronic inflammation
fever
| leukocytosis
59
fever
endogenous pyrogens (IL-1, TNF-alpha)
60
leukocytosis
an increase in the numbers of circulating leukocytes due to release of IL-1, TNF-alpha
61
increased erythrocyte sedimentation rate (ESR)
reflects high plasma levels of acute phage proteins
| acute phase response = fever, leukocytosis, decreased appetite, altered sleep patterns, acute phase proteins
62
types of chronic inflammation
1. non-specific inflammation
| 2. granulomatous inflammation
63
non-specific inflammation
mononuclear cell infiltrate with a proliferation of fibroblasts and new blood vessels; chronic inflammation can be the initial response in viral infections, parasitic infections, autoimmune disease and malignancy
64
granulomatous inflammation
```
characterized by granulomas (collections of activated macrophages called epitheloid cells surrounded by a rim of lymphocytes, +/- giant cells; IFN-gamma and IL-4 released by T lymphocytes modifies macrophages, sometimes resulting their fusion to form multinucleate giant cells. granulomatous inflammation occurs in response to:
bacterial infection
fungal infection
inorganic metals or dusts
foreign body reactions
diseases of unknown cause
```
65
orofacial granulomatosis
non-specific inflammation affecting the orofacial tissues: a diagnosis of exclusion
unknown etiology
66
chelitis granulomatosa (of Miescher)
non-tender, persistent labial swelling
67
Melkersson-Rosenthal syndrome
labial swelling, fissured tongue and facial palsy
68
VEGF
vascular endothelial growth factor --> proangiogenic
69
FGF
fibroblast growth factor - stimulates fibroblasts to lay down collagen; helps promote scarring
70
CD4+ cells
recognize antigens (class II major histocompatibility antigens) on antigen-presenting cells (APCs)
71
helper type 1 (Th1)
secrete various pro inflammatory cytokines (interferon gamma, interleukins (IL-2, IL-12) activate additional macrophages; associated with cell-mediated response (cytotoxicity) against intracellular pathogens (viruses), organ transplantation
72
helper type 2 (Th2)
secrete interleukins (Il-4, IL-5, IL-10); associated with B-cell activation with antibody release against extracellular pathogens (bacteria), allergic responses
73
CD 8+ cells
exert suppressor and cytotoxic functions; recognizes antigens on many cell surfaces (major histocompatibility complex class I molecules); kill target cells that express these specific antigens (prevents spread of infection to healthy cells); inhibit activation phase of immune responses
74
cytokines
groups of proteins secreted primarily by T lymphocytes in response to antigen exposures: (IL), interferons, chemokine, tumor necrosis factor
75
functions of cytokines
cell-cell chemical messengers; amplify the immune response; promote inflammation, fever, pain in response to infection
76
APCs
derived from hematopoietic stem cells: monocytes, macrophages, dendritic cells, B cells
77
function of APCs
engulf antigens and present them to T cells
78
monocytes and macrophages express...
MHC II molecules, Fc Ig receptors other receptors on their cell surfaces
79
dendritic cells
specialized APCs; found in B-cell rich lymphoid follicles, thymus, many peripheral sites (GI tract, lung, aGU tract, skin); present antigen to T-cells
80
dendritic cells express...
MHC I and II molecules
81
HLA
human leukocyte antigen = MHC
82
gene loci for MHC
short arm of chromosome 6
83
class I MHC
take to the surface of APCs engulfed antigens and then present CD8+ T cells during graft rejection (tissue transplantation) and killing of virally-infected cells
84
class II MHC
(immunity-associated) are taken to the surface of APCs and B-cells engulfed antigens and then present to CD4+ T cells
85
b lymphocyte activation requires
cross-linking of B-cell receptors presented with antigens by accessory cells (APCs); cognate T-cell/B-cell help (cooperation when T-cells and B-cells recognize the same antigen); leads to B-cell proliferation; occurs in lymphoid germinal centers; cytokines IL-5, IL-6
86
type I hypersensitivity
immediate-type or anaphylaxis (antibody mediated)
87
type II hypersensitivity
cytotoxic type (antibody mediated)
88
type III hypersensitivity
immune complex disease (antibody mediated)
89
type Iv hypersensitivity
cell-mediated or delayed type
90
atopy
chronic local allergy such as allergic rhinitis (hay fever), allergic asthma, dust mite allergy, drug allergy, food allergy, eczema
91
anaphylaxis
severe systemic reaction, can lead to death
92
anaphylaxis rate
2% of patients (1/50)
93
anaphylaxis death rate
63-99 deaths/year (0.3%)
94
uticaria
hives
95
pruritis
itching
96
angioedema
swelling of face, around eyes, lips, tongue, uvula and hands
97
therapies for allergies
- avoidance of allergen
- corticosteroids keep the plasma cell from synthesizing IgE and inhibit T cells
- monoclonal drugs that inactivate IgE
- cromlyn acts on the surface of mast cell, no degranulation
- antihistamins, aspirin, epinephrine, theophylline counteract the effects of cytokines on targets
98
mechanisms of type II sensitivity
1) IgG or IgM antibodies are produced against various antigens (antigen-antibody coupling) and bind on cell surfaces (fixed cellular reaction), activates complement, which recruits PMNs to site, leading to cell lysis (cytotoxcitiy)
2) IgG or IgM antibodies bind to specific target cell receptor (does not lead to cell death) but changes cellular function
3) IgG or IgM antigbodies bind to a part of the intrinsic structural connective tissue component, complement activation recruits PMNs to site, leading to tissue damage to basement membranes through membrane attack complexes
99
cytotoxic IgG, IgM
transfusion reactions involves IgM antibodies with complement to lyse RBCs
hemolytic anemia (pernicious)
rhesus disease (hemolytic disease of the newborn) - involves maternal IgG antibody exposure to fetus with different blood type; subsequent pregnancy -maternal antibodies destroy fetal RBCs; some autoimmune disorders (Goodpasture syndrome)
100
noncytotoxic antibodies against cell surface receptors
Graves disease, myasthenia gravis
101
Goodpasture syndrome
antibodies are directed against type IV collagen (structural protein found within the basement membranes of the lungs and kidneys), activate complement, which recruits PMNs and causes tissue injury (glomerulonephritis, pulmonary hemorrhage)
102
autoimmune disorders in context of noncytotoxic reacitons
antibodies bind to specific cell surface receptors, but do not lyse cells; changes target cell function
103
examples of type III hypersensitivity
systemic lupus erythematosus, rhematoid arthritis, vasculitis, other variants of glomerulonephritis
104
type III hypersensitivity - immune complex mediated
IgG, IgM and occasionally IgA antibodies target exogenous or endogenous circulating antigens, forming an immune complex that become implanted into tissue basement membranes; immune complexes activating phagocytosis, which damage tissues
105
type IV hypersensitivity
T-cell mediated; DELAYED ANTIGENIC REACTION (24-48 hrs); primarily involves lymphocytes and monocytes; DOES NOT INVOLVE ANTIBODIES
106
examples of type IV hypersensitivity
contact dermatitis, granulomatous diseases, insulin-dependent diabetes, chronic thyroiditis, sjogre syndrome, primarily biliary cirrhosis, viral destruction, transplant rejection, possible tumor cell damage
107
type IV hypersensitivity mechanism
foreign proteins or chemical ligands interact with accessory cells (macrophages, dendrites cells) that express class II major histocompatibility molecules; accessory cells secrete IL-12 which activates T cells (CD4); activated T cells secrete interferon and interleukin (IL-2) activating more macrophages and trigger profilic T-cell production; activated CD4 cells (TH1) produce cytokines, which recruit and activate lymphocytes, monocytes, fibroblasts and other inflammatory cells-leading to tissue damage
108
autograft
individual receives own tissue for grafting to another site
109
isograft
graft tissue obtained from an identical twin
110
allograft
graft tissue received from a genetically different host but of the same species
111
xenograft
graft tissue received from a different species
112
autoimmune hemolytic anemia
red blood cells affected
anemia, fatigue, weakness, splenomegaly; anemia can be sever and even fatal
113
goodpasture's syndrome
lungs and kidneys affected
shortness of breath, coughing up blood, fatigue, swelling and itching. prognosis is good if treatment begins before sever lung or kidney damage occurs
114
graves' disease
thyroid gland affected
hyperthyroidism
115
pemphigus
skin affected
large blisters form on the skin; the disorder can be life-threatening
116
type 1 diabetes
beta cells of the pancreas are affected; symptoms include excessive thirst, urination, and appetite as well as various long-term complications; lifelong treatment with insulin
117
rheumatoid arthritis
joints or other tissues, such as lung, nerve, skin and heart tissue are affected
symptoms may include fever, fatigue, joint pain and stiffness, deformed joints, shortness of breath, loss of sensation, weakness, rashes, chest pain, and swellings under the skin; the prognosis varies
118
scelorderma
excessive collagen disposition in skin and internal organs such as lung, GI tract, heart and kidneys
thickened skin, edema, ischemia of fingers, pain
119
multiple sclerosis
brain and spinal cord
the covering of affected nerve cells is damage and therefore cell cannot conduct nerve signals normally. symptoms may include weakness, abnormal sensations, vertigo, problems with vision, muscle spasms and incontinence
120
systemic lupus (erythematosus)
joints, kidneys, skin, lungs, heart, brain and blood cells
symptoms of anemia and those of kidney, lung, or heart disorders may occur; a rash may develop; the prognosis varies widely, but most people can lead an active life despite occasional flare-ups of the disorder
121
vasculitis
blood vessels
symptoms may include rashes, abdominal pain, loss of vision and symptoms of nerve damage or kidney failure; the prognosis depends on the extent of tissue damage
122
diagnosis for presence of inflammation
ESR (often increased because proteins that are produced in response to inflammation interfere with the ability of red blood cells (erythrocytes) to remain suspended in blood.
presence of specific antibodies (antinuclear antibodies - present in systemic lupus; rheumatoid factor - present in rheumatoid arthritis)
123
primary/congenital immunodeficiency disease causes
antibody ID impaired production
T-cell ID
combined ID reduced Abs T-cell defect
124
antibody ID diseases
bruton x-linked
agammaglobulinemia
selective IgA deficiency
common variable ID
125
T cell ID diseases
DiGeorge syndrome
| chronic mucocutaneous candidaiasis
126
combined ID reduced Abs T cell defects
adenosine deaminase deficiency
| weskit-aldrich syndrom
127
probability of HIV infection
function of both the number of infective HIV virions in the body and the number of cells available at the site that have appropriate receptors
128
normal CD4 values
500-1200 cells/microliter
129
clinical AIDS
a decrease in total CD4 count below 500 cells/microliter
130
indication of high probability for development of AIDS-related opportunistic infections/neoplasms
CD4 count below 200
131
kaposi's sarcoma
a cancer of the blood vessels, which is characterized by purplish lesions on the skin
132
possible reason for AIDS-related malignancies
decreased activity of NK cells which target tumor cells
133
Pneumocystis carinii pneumonia (PCP)
a life-threatening opportunistic infection; which virtually always affects lungs, but other organs can be involved, including the lymph nodes, spleen, liver and bone marrow; symptoms include fever, a day cough, chest tightness and difficulty breathing
134
herpes simplex virus
can cause oral herpes or genital herpes which are relatively common infections but can be much more frequency and sever in HIV-infected individuals
135
mycobacterium avium complex (MAC)
bacterial infection; can cause recurring fever, painful intestines, weight loss, and anemia. almost half of those with late-stage HIV disease are infected with the MAC bacteria
136
Cytomegalovirus (CMV)
CMV is a herpes-type virus that can cause eye disease and blindness. Usually causes disease when the CD4+ count is very low.
137
TB
In HIV infection, active TB often occurs early, and is sometimes the first sign that the person has HIV. Symptoms include cough, fever, night sweats, weight loss, and fatigue.
138
Oral/oropharyngeal candidiasis
the most common HIV-related opportunistic infection and can occur even in those with a fairly high CD4+ count; Oral candidiasis are associated with increased risk for the subsequent development of opportunistic infections and the onset of oral candidiasis is used in classifying the patient as having AIDS as defined by the CDC.
