Exam 1: Important Words Flashcards
1
Q
Etiology
A
Cause of a disease
infectious disease: etiology is infectious organism
2
Q
Pathogenesis
A
Biochemical and molecular mechanisms of disease development
3
Q
Morphology
A
Appearance of cells/tissue/organs
4
Q
Clinical features (manifestations)
A
Functional consequences of morphological changes
5
Q
Hypoxia
A
Not enough oxygen
6
Q
Modes of Cell Death
Necrosis
Signalling
Unregulated (pathological)
A
Cell breaks down/explodes and contents are released
Spread/damage neighboring cells
7
Q
Modes of Cell Death
Apoptosis
Multiple
Regulated (physiological)
A
Cell disassembles and packages contents for phagocytosis
Avoids damage of surrounding cells
8
Q
Modes of Cell Death
Necroptosis
A
Regulated necrosis
9
Q
Modes of Cell Death
Anoikis
A
Detachment-induced cell death
10
Q
Modes of Cell Death
Ferroptosis
A
Iron based cell death
11
Q
Necrosis
Necrotic Tissue
A
Loss of nuclei
Breakdown of membranes
Cells have ruptured
12
Q
Necrosis
Coagulative
A
Loss of cell architecture but not tissue architecture
13
Q
Necrosis
Liquefactive
A
Digestion of cells results in viscous mass
Cells gone but more liquid
14
Q
Necrosis
Caseous
A
Fragmented cells and granular debris surrounded by inflammation
Cells are gone but more solid; Cheese like
15
Q
Necrosis
Fibrinoid
A
Immune complexes and fibrin in walls of blood vessels
Fbrin from blood gets into blood vessel wall and attaches to immune complexes
16
Q
Apoptotic Signaling
Extrinsic
A
Death receptors on the plasma membrane are activated and transduce a signal through intracellular signalling pathways to activate caspases
Signal initiated from outside cell
17
Q
Apoptotic Signalling
Intrinsic
A
Mitochondrial signals induce release of pro-apoptotic proteins that activate caspases
Signal initiated from inside cell
18
Q
Apoptotic Signalling
Caspases
A
Specific proteases that disassemble the cell for packaging into apoptotic bodies
Biochemical markers of apoptosis
Inflammatory
Cysteine Aspartases
19
Q
Caspases
Initiators
A
Autocatalytic
20
Q
Caspases
Executioners
A
Cleavage
21
Q
Bcl-2 Protein Family
A
B cell lymphoma 2
22
Q
Stress and Death
p53-induced cell death
A
Critical in DNA damage repair
Activates negative regulators of cell cycle progression
Induces apoptosis promoting genes
23
Q
Stress and Death
ER stress/UPR
A
Halts protein translation and upregulates chaperone expression to fold proteins properly or activate cell death
24
Q
Stress and Death
PIDDosome
A
Formed in response to p53 signaling caused by DNA damage to repair or destroy damaged cells
25
# Stress and Death
ER stress
Accumulation of misfolded proteins
26
# Stress and Death
Unfolded Protein Response (UPR)
Stress response that promotes degradation of extra proteins and increased chaperone production to improve folding
27
# Immune Response: Inflammation
Clinically
redness, swelling, pain
28
# Immune Response: Inflammation
Histologically
Edema, WBC
29
Edema
## Footnote
Mediated by mast cells (immediate) and eosinophils (later response)
30
# Immune Response: Inflammation
Pyogenic
Pur production
31
# Immune Response: Inflammation
Granuloma
macrophages surrounded by T cells
| Mass of immune cells
32
# Immune Response: Inflammation
Tumor Necrosis Factor (TNF)
Important mediator (cytokine)
33
# Immune Response: Inflammation
Acute Inflammation
Dilation of small blood vessels
Increased microvasculature permeability
Migration and activiation of immune cells
34
# Immune Response: Inflammation
Chronic Inflammation
Infiltration by macrophages, lymphocytes, plasma cells
Increased tissue destruction
Attempts at healing
35
# Meningitis
Meninges
Cover for CNS/protectant
1. Dura mater
2. Arachnoid/subarachnoid
3. Pia mater
36
# Meningitis
Immunoglobulin A (IgA)
Produced by plasma cells associated with mucosa
First line of defense
Not inflammatory
Primarily acts thru exclusion
37
# Meningitis
Ciliostasis
Prevents movement of bacteria out of bronchial tubes
38
# Meningitis
Adhesie Pili
Projections from bacteria that can bind non-ciliated mucosal cells
| Can cross epithelium once bound
39
# Meningitis
Exotoxins
High antigenic (antitoxin neutralizes)
Highly Toxic (fatal in micorgram quantities)
Ususally do not insuce fever
Usually bind to specific receptors
| Excreted by cell
40
# Meningitis
Endotoxins
Weakly immunogenic
Toxic at 10-100s micrograms
Induce fever
No specific receptions
| Part of cell wall
41
# Trichinosis
Enteric Phase
Occurs in GI Tract
Strong immune response to larvae
Increased intestinal mobility
42
# Trichinosis
Muscle phase
Larva exit blood vessels and enter skeletal muscle - infects muscle fibers
43
# Integumentary Disorders
Growths
Cyst
Malformation
Benign/malignant neoplasm
44
# Integumentary Disorders
Dermatitis
Non-neoplastic
| Rash
45
Psoriasis
Inflammatory skin disease
Scaling skin condition
46
# Psoriasis: Angiogenesis
VEGF
Released from keratinocytes
Stimulate epidermal hyperplasia vascular growth, leukocyte infiltration
47
# Psoriasis: Verucae
Verrucae
Squamoproliferative
Generally self limiting
48
Pemphigus
Autoimmune formation of blisters
49
Foliaceus
Subcorneal lesion
50
Vulgaris
suprabasal lesion
50
Bullous Pemphigoid
Subepidermal, nonacantholytic lesion
51
Mendelian Disorders
Monogenic Disorders
Generally rare (usually incompatible with life)
Single gene defect causes disorder
High penetrance
52
Chromosomal Abnormalities
Uncommon
Extra chromosomal material (or lacking)
53
Complex Multigenic DIsorders
Far more common
Complex interaction of geentic defect with environmental factors
| Predisposition
54
Autosomal
Located on chromosomes 1-22 rather than X or Y (sex linked)
54
Penetrance
Whether or not the variant genotype can be inferred on the basis of defined phenotypic criteria
| Can you infer genotype from phenotype
## Footnote
Can you identify disorder based on appearance or clinical observation
54
Autosomal Recessive
Recessive need both copies to express
54
Nondisjunction
Failure of two homologus chromosomes (or two sister chromatids) to separate at metaphase of meiosis I (or meiosis II/mitosis)
54
Autosomal Dominant
Only need one copy of gene to express characteristic
If you have the gene you will express it
54
Sex-Linked
characteristics (or traits) that are influenced by genes carried on the sex chromosomes
| Males will express because they only have one X
55
Phenylalanine Hydroxylase
Catalyzes conversion of Phe to Tyr
Mutated in PKU
55
Neurofibromin I (NF1)
GTPase (GAP) that is responsible for inactivating Ras
mutated in Neurofibromatosis I
56
Hypopigmentation
Paler than normal due to lack of tyrosine
57
Hemolytic Anemia
Lack of RBCs because they are being lysed
58
Vaso-occlusive Crisis
Blockage of blood vessels results in hypoxic injury and infarcts
59
Opsonization
Binding of antibodies and complement molecules to allow recognition of bacteria by phagocytes
60
Familial Mental Retardation 1
Mutated gene in Fragile X Syndrome
61
DNA Methylation
Represses DNA expression by reducing availability for transcription
62
Fragile X
Cytogenetic abnormaility is constriction of long arm of X Chromosome
63
FMRP
| FMR protein
cytoplasmic protein highly expressed in the brain and testes
Binds RNA
Regulates protein synthesis at synapses
64
Meiotic Non-disjunction
Improper seperation of chromosomes during meosis and/or mitosis
65
Partial trisomy
Increase in part of a chromosome
66
Thymis hypoplasia
Thymus is too small
67
Parathyroid hypoplasia
Parathyroid gland is too small
68
Type 1 Diabetes
Reduced insulin production due to autoimmune destruction of pancreatic beta cells
69
Type 2 Diabetes
Insulin resistance
| Insulin is created but body doesnt respond to it
70
Amyloid
Deposit that stains with iodine (starch)
71
Serum amyloid P (SAP)
Binds to motifs common to all amyloid proteins
Ca2+ dependent
May protect amyloid from proteolysis or phagocytosis
72
Tumors
Abrnomal masses
Growth is unlike surrounding tissues
Failure of cell death
73
Parenchyma
Functional portion of an organ
In tumors, cancer cells themselves
## Footnote
Determines tumor behavior
74
Stroma
Supportive protion of an organ
In tumors, CT, blood vessels, and lymphatic infiltrates that surround it
## Footnote
Affects parenchymal behavior
75
-plasia
growth
76
Dysplasia
Unregulated or irregular growth
| Bad growth
## Footnote
Disordered
77
Metaplasia
Replacement of one cell type with another
| Transcending Growth
78
Anaplasia
Dedifferentiation
| Back or re growth - Lack of differentiation
## Footnote
Most likely to grow from stem cells present in the tissue
79
Neoplasia
New growth
80
Differentiation
Stem cell changes to form another (usually more specialized) cell type
81
Cachexia
Progressive loss of both fat and lean tissue
82
Paraneoplastic Syndromes
Cancer patient has symptoms unrelated to exisiting tumor
83
Benign
Gross and microscopic appearance similar to surrounding normal tissue
usually localized
84
Malignant
Incade and destroy adjacent structure
85
Metastasize
Travel to distant sites (away from organ of origin)
86
Invasiveness
Invades neighboring tissue within the same organ
87
Mixed Tumor
Divergent differentiation of neoplastic clone
88
Teratoma
Derived from totipotent cells
Mixture of adult tissue types
89
Leiomyoma
Benign Smooth Muscle tumor
90
Chondroma
Benign Cartilage tumor
91
Fibroma
Benign Fibrous tumor
92
Adenoma
Benign tumor of the glands
93
Papilloma
Benign fingerlike projections
94
Cystadenoma
Benign large cystic mass
95
Polyp
Macroscopic projection out of the epithelial free surface into a lumen
| Can be benign or malignant
96
Sarcomas
Mesencymal origin malignant tumor
97
Carcinoma
Epithelial origin malignant tumor
98
Undifferentiated tumor
Malignant tumor of unknown origin
99
Grading
Determined by cytology
Assumes behavior and differentiation are related
100
Clinical Staging
Physical exam, imaging, lab tests
101
Pathological Staging
biopsies; includes clinical information
| Clinical + biopsy
102
Restaging
After recurrence; usually just use original staging
103
Staging
Determined by surgery or imaging
Based on
* Location of primary tumor
* tumor size
* lymph node spread (local vs. regional)
* Distant metastases
104
TNM System
Numbers are assigned to each characteristic based on a scale for individual cancers
T = tumor size
N = lymph node mestastases
M = other metastases
105
Hyperplasia
Excessive cell growth
106
Hypoplasia
Not enough/reduced cell growth
107
Atrophy
Excessive cell death
108
Oncogene
Result in proliferation and cell growth
inhibit cell death
109
Tumor Suppressor
Inhibit cell growth
Initiate cell death
110
Growth factors
Integral membrane proteins cleaved by proteases
Can have juxtacrine effects
111
Juxtacrine effects
Activate neighboring cells
112
Ras
Membrane bound G protein immediately downstream of receptors
activated growth factors and cytokines to promote cell growth and prevent apoptosis
## Footnote
Activated form has GTP bound
113
Src
Non-receptor tyrosine kinase
Regulates cytoskeleton, cell migration, adhesion and invasion
114
Myc
Intracellular sensor and transducer of extracellular stimuli
Binds to E-box DNA recognition sequences
115
S phase
DNA synthesis
Incomplete replication detected
116
M phase
Mitosis
Improper spindle detected
117
G1 and G2 phases
Growth phases
Damaged DNA detected
118
G0
No cell division
119
Cyclins
Activate Cdks
Synthesized and degraded at specific points in the cell cycle
120
Cdks
activated by Cyclins
Kinases that regulate cell cycle progression by activating/inactiviating crucial proteins
121
Cyclin D1
Activates Cdk4 and Cdk6
Mediates G1 to S phase transition
| Activate/inactivate transcription factors to drive stages of cell cycle
122
123
NF2 (Merlin)
Inhbits RTKs and integrins at membrane
Inhibits E3 ubiquitin ligase in nucleus
124
p53
Activated by genotoxic stress (dsDNA breaks)
Inhibits cell cycle progression to allow repair
PIDDosome
125
Rb protein
Regulates differentiation of cells by interacting with transcripton factors
Inhits cell cycle progression
| Discovered in children w/ retinoblastoma
126
BRCA 1/2
Mediators of DSB repair and replication fork collapse
## Footnote
Associated with inherited breast cancer susceptibility
127
BRCA 1
Acts in both checkpoint activation and DNA repair
128
BRCA 2
Acts in homologous recombination
129
Von Hippel Lindau protein (VHL)
Ubiquitin ligase that targets HIFIα for destruction
130
HIFIα
Under hypoxic conditions, activates alternative metabolic pathways
Induces VEGF
Counteracts Myc activity
131
The Warburg Effect
Excessive glycolysis in the presence of oxygen
132
Angiogenesis
Development of new vasculature
133
Primary Immunodeficiency Syndromes
Genetic
134
Secondary Immunodeficiency Syndromes
Effect of other disease like cancer, infection, or malnutrition
135
Hypersensitivity
Stimulated by antigens
Imbalance between effectors and limitors
136
Exogenous
Environmental
Nonpathogenic
137
Endogenous
Self
138
Immediate (Type 1) hypersensitivity
Productin of IgE antibody
| Allergies
139
Antibody-mediated (Type II) Hypersensitivity
Production of IgG, IgM
140
Immune complex-mediated (type III) hypersensitivity
Deposition of antigen-antibody complexes
| Systemic Lupus Erythematosus
141
Cell-mediated (Type IV) Hypersensitivity
Activated T Lymphocytes
| Multiple Sclerosis
T1D
142
IgE
Produced by plasma cells in mucosal membranes in response to allergies
Activation of tyrosine kinase
143
Histamine
Released in response to IgE
Binds G protein couples receptors (H1-3) on endotherlial cells, nerve cells, and smooth muscle cells
144
Transforming Growth Factor (TGF-)β
Generally considered immunosuppressive
Activates myofibroblasts to produce ECM
Inhibits ECM degradation
145
IL-13
Activates TGF-β
146
Platelet-derived growth factor (PDGF)
Regulates proliferation and differentiation of stromal cell during embryogenesis
May either promote differentiation of adult stem cells and/or stimulate existing stromal cells
147
Allopurinol
inhibits xanthine oxidase, resulting in an accumulation of hypoxanthine and xanthine, compunds more soluble than uric acid
| Used to treat Gout
