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GPAT > exam 1 > Flashcards

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

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2
Q

what causes hydropic swelling

A

interference with the normal function of Na/K pump and other ion pumps in the plasma membrane

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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

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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

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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

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6
Q

conditions that may lead to hypertrophy

A

hormonal stimulation

increased functional demand

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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

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8
Q

condition that may lead to cell hypertrophy

A 
hormonal stimulation (hormonal hyperplasia)
increased functional demand (compensatory hyperplasia)
persistent cell injury
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9
Q

metaplasia

A

conversion of one differentiated cell type to another; often involves epithelial tissue

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10
Q

sequences of metaplasia

A
  1. columnar/glandular epithelium –> squamous epithelium (metaplasia of tracheal/bronchial epithelium caused by smoking)
  2. squamous epithelium –> glandular epithelium; barret metaplasia of the esophagus as result of chronic presence of refluxed gastric acid
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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

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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

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13
Q

neoplasia (anaplasia)

A

malignant alteration of the cells of a tissue

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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

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15
Q

injurious agent –> entry of calcium causes…

A

increased mitochondrial permeability

activation of multiple cellular enzymes

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16
Q

injurious agent –> lysosomal membrane damage

A

enzymatic digestion of cellular components

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17
Q

what can injurious agent cause

A 
decrease in ATP
mitochondrial damage
entry of Ca
increased ROS
membrane damage
protein misfolding, DNA damage
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18
Q

depletion of ATP causes

A

defective functioning of the sodium pump
increase in anaerobic glycolysis
detachment of ribosomes

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19
Q

features of defective Na pump

A

cellular and organelle swelling; loss of microvilli; formation of blebs

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20
Q

increase in anaerobic glycolysis causes

A

clumping of the nuclear chromatin

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21
Q

detachment of ribosomes causes

A

decrease in protein synthesis

deposition of lipids

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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

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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+

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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

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25
Q

coagulative necrosis

A

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

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26
Q

liquefactive necrosis

A

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

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27
Q

fat necrosis results from

A

pancreatitis or trauma

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28
Q

caseous necrosis

A

lesion of TB

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29
Q

fibrinoid necrosis

A

usually affects injured bloods vessels; characterized by the accumulation of plasma proteins in the walls of the vessels

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30
Q

initial nucleus events in apoptosis

A

DNA fragmentation into fragments of specific sizes –> chromatin condensation –> nuclear fragmentation: formation of nuclear bodies

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31
Q

apoptotic bodies

A

composed of cytoplasm and organelles with or without nuclear bodies

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32
Q

final events of apoptosis

A

phagocytosis of apoptotic bodies by adjacent healthy cells or by macrophages; degradation of the apoptotic bodies in the lysosomes; no or minimal inflammation

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33
Q

mechanisms of apoptosis

A

extrinsic - mediation by membrane receptors: death receptors

intrinsic - mediated by cell damage and intracellular sensors: p53 and proteins of the Bax, Bak family

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34
Q

entosis

A

a nonapoptotic mechanism of cell death in which the dying cell is first internalized into another cell

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35
Q

when does entosis occur

A

as a result of epithelial cell detachment from eh extracellular matrix

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36
Q

how does cell internalization occur in entosis

A

through cell invasion not through phagocytosis

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37
Q

how does cell death occur in entosis

A

through lysosome-mediated degradation

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38
Q

roles of entosis

A

development, cancer prevention, metabolic stress

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39
Q

theories of cellular aging

A

1) aging as accumulated somatic damage

2) aging as a genetic program

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40
Q

acute inflammation

A

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”

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41
Q

chronic inflammation

A

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

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42
Q

systemic signs of inflammation

A

fever
increased white cell count (leukocytes)
enlargement of lymph nodes

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43
Q

serous exudate

A

composed mainly of plasma fluids and proteins with few white blood cells

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44
Q

purulent exudate (suppuration)

A

contains tissue debris and many white blood cells in addition to plasma fluids and proteins

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45
Q

steps of microscopic events in inflammatory response

A

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

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46
Q

histamine

A

present in mast cells; it is released; it causes severe blood vessel dilation and airway constriction and that’s why you can get anaphylaxis

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47
Q

serotonins and bradkinins

A

products of cells that mediate inflammation in particular causes sensation to pain and discomfort

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48
Q

leukotriene, prostaglandins

A

platelet-activating factors, help in clotting

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49
Q

events of acute inflammation

A

1) margination
2) adhesion or pavementing
3) chemotaxis and emigration
4) phagocytosis and intracellular degradation
5) extracellular release of leukocyte products (causes tissue damage)

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50
Q

outcomes of acute inflammation

A
  1. resolution
  2. scarring
  3. abscess formation
  4. progression to chronic inflammation
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51
Q

chronic inflammation is characterized by

A
  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)
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52
Q

settings of chronic inflammation

A
  1. persistent infections
  2. prolonged exposure to toxic agents
  3. autoimmune disease
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53
Q

chronic inflammatory cells

A
  1. tissue macrophages
  2. t lymphocytes
  3. plasma cells
  4. eosinophils
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54
Q

tissue macrophages

A

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

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55
Q

t lymphocytes

A

stimulate macrophage activity by producing their own cytokines

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56
Q

plasma cells

A

B lymphocytes that make antibodies

57
Q

eosinophils

A

associated with allergic reactions and parasites

58
Q

systemic manifestations of chronic inflammation

A

fever

leukocytosis

59
Q

fever

A

endogenous pyrogens (IL-1, TNF-alpha)

60
Q

leukocytosis

A

an increase in the numbers of circulating leukocytes due to release of IL-1, TNF-alpha

61
Q

increased erythrocyte sedimentation rate (ESR)

A

reflects high plasma levels of acute phage proteins

acute phase response = fever, leukocytosis, decreased appetite, altered sleep patterns, acute phase proteins

62
Q

types of chronic inflammation

A
  1. non-specific inflammation

2. granulomatous inflammation

63
Q

non-specific inflammation

A

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
Q

granulomatous inflammation

A 
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
Q

orofacial granulomatosis

A

non-specific inflammation affecting the orofacial tissues: a diagnosis of exclusion

unknown etiology

66
Q

chelitis granulomatosa (of Miescher)

A

non-tender, persistent labial swelling

67
Q

Melkersson-Rosenthal syndrome

A

labial swelling, fissured tongue and facial palsy

68
Q

VEGF

A

vascular endothelial growth factor –> proangiogenic

69
Q

FGF

A

fibroblast growth factor - stimulates fibroblasts to lay down collagen; helps promote scarring

70
Q

CD4+ cells

A

recognize antigens (class II major histocompatibility antigens) on antigen-presenting cells (APCs)

71
Q

helper type 1 (Th1)

A

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
Q

helper type 2 (Th2)

A

secrete interleukins (Il-4, IL-5, IL-10); associated with B-cell activation with antibody release against extracellular pathogens (bacteria), allergic responses

73
Q

CD 8+ cells

A

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
Q

cytokines

A

groups of proteins secreted primarily by T lymphocytes in response to antigen exposures: (IL), interferons, chemokine, tumor necrosis factor

75
Q

functions of cytokines

A

cell-cell chemical messengers; amplify the immune response; promote inflammation, fever, pain in response to infection

76
Q

APCs

A

derived from hematopoietic stem cells: monocytes, macrophages, dendritic cells, B cells

77
Q

function of APCs

A

engulf antigens and present them to T cells

78
Q

monocytes and macrophages express…

A

MHC II molecules, Fc Ig receptors other receptors on their cell surfaces

79
Q

dendritic cells

A

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
Q

dendritic cells express…

A

MHC I and II molecules

81
Q

HLA

A

human leukocyte antigen = MHC

82
Q

gene loci for MHC

A

short arm of chromosome 6

83
Q

class I MHC

A

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
Q

class II MHC

A

(immunity-associated) are taken to the surface of APCs and B-cells engulfed antigens and then present to CD4+ T cells

85
Q

b lymphocyte activation requires

A

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
Q

type I hypersensitivity

A

immediate-type or anaphylaxis (antibody mediated)

87
Q

type II hypersensitivity

A

cytotoxic type (antibody mediated)

88
Q

type III hypersensitivity

A

immune complex disease (antibody mediated)

89
Q

type Iv hypersensitivity

A

cell-mediated or delayed type

90
Q

atopy

A

chronic local allergy such as allergic rhinitis (hay fever), allergic asthma, dust mite allergy, drug allergy, food allergy, eczema

91
Q

anaphylaxis

A

severe systemic reaction, can lead to death

92
Q

anaphylaxis rate

A

2% of patients (1/50)

93
Q

anaphylaxis death rate

A

63-99 deaths/year (0.3%)

94
Q

uticaria

A

hives

95
Q

pruritis

A

itching

96
Q

angioedema

A

swelling of face, around eyes, lips, tongue, uvula and hands

97
Q

therapies for allergies

A
  • 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
Q

mechanisms of type II sensitivity

A

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
Q

cytotoxic IgG, IgM

A

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
Q

noncytotoxic antibodies against cell surface receptors

A

Graves disease, myasthenia gravis

101
Q

Goodpasture syndrome

A

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
Q

autoimmune disorders in context of noncytotoxic reacitons

A

antibodies bind to specific cell surface receptors, but do not lyse cells; changes target cell function

103
Q

examples of type III hypersensitivity

A

systemic lupus erythematosus, rhematoid arthritis, vasculitis, other variants of glomerulonephritis

104
Q

type III hypersensitivity - immune complex mediated

A

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
Q

type IV hypersensitivity

A

T-cell mediated; DELAYED ANTIGENIC REACTION (24-48 hrs); primarily involves lymphocytes and monocytes; DOES NOT INVOLVE ANTIBODIES

106
Q

examples of type IV hypersensitivity

A

contact dermatitis, granulomatous diseases, insulin-dependent diabetes, chronic thyroiditis, sjogre syndrome, primarily biliary cirrhosis, viral destruction, transplant rejection, possible tumor cell damage

107
Q

type IV hypersensitivity mechanism

A

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
Q

autograft

A

individual receives own tissue for grafting to another site

109
Q

isograft

A

graft tissue obtained from an identical twin

110
Q

allograft

A

graft tissue received from a genetically different host but of the same species

111
Q

xenograft

A

graft tissue received from a different species

112
Q

autoimmune hemolytic anemia

A

red blood cells affected

anemia, fatigue, weakness, splenomegaly; anemia can be sever and even fatal

113
Q

goodpasture’s syndrome

A

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
Q

graves’ disease

A

thyroid gland affected

hyperthyroidism

115
Q

pemphigus

A

skin affected

large blisters form on the skin; the disorder can be life-threatening

116
Q

type 1 diabetes

A

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
Q

rheumatoid arthritis

A

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
Q

scelorderma

A

excessive collagen disposition in skin and internal organs such as lung, GI tract, heart and kidneys

thickened skin, edema, ischemia of fingers, pain

119
Q

multiple sclerosis

A

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
Q

systemic lupus (erythematosus)

A

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
Q

vasculitis

A

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
Q

diagnosis for presence of inflammation

A

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
Q

primary/congenital immunodeficiency disease causes

A

antibody ID impaired production

T-cell ID

combined ID reduced Abs T-cell defect

124
Q

antibody ID diseases

A

bruton x-linked
agammaglobulinemia
selective IgA deficiency
common variable ID

125
Q

T cell ID diseases

A

DiGeorge syndrome

chronic mucocutaneous candidaiasis

126
Q

combined ID reduced Abs T cell defects

A

adenosine deaminase deficiency

weskit-aldrich syndrom

127
Q

probability of HIV infection

A

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
Q

normal CD4 values

A

500-1200 cells/microliter

129
Q

clinical AIDS

A

a decrease in total CD4 count below 500 cells/microliter

130
Q

indication of high probability for development of AIDS-related opportunistic infections/neoplasms

A

CD4 count below 200

131
Q

kaposi’s sarcoma

A

a cancer of the blood vessels, which is characterized by purplish lesions on the skin

132
Q

possible reason for AIDS-related malignancies

A

decreased activity of NK cells which target tumor cells

133
Q

Pneumocystis cariniipneumonia (PCP)

A

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
Q

herpes simplex virus

A

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
Q

mycobacterium avium complex (MAC)

A

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
Q

Cytomegalovirus (CMV)

A

CMV is a herpes-type virus that can cause eye disease and blindness. Usually causes disease when the CD4+ count is very low.

137
Q

TB

A

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
Q

Oral/oropharyngeal candidiasis

A

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.

GPAT (3 decks)

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