Test 1 1/3 Flashcards
(154 cards)
1
Q
Etiology vs. pathogenesis
A
E: why a disease occurs
P: how a disease occurs
2
Q
Three outcomes of cell injury
A
Reversible
Cell adaptation
Cell death
3
Q
Causes of cell injury
A
No O2 Infectious agents Injury Chemicals Immune response Genetic abnormalities Nutritional imbalance
4
Q
4 cell targets
A
Cell membrane
Mitochondria
Cell proteins
DNA
5
Q
T/F clinical signs and symptoms appear at the same time as molecular/biochemical changes
A
FALSE - several steps removed
6
Q
Mechanisms of cell injury (5)
A
ATP depletion ROS Ca2+/membrane permeability Mitochondrial damage DNA/protein damage
7
Q
Hypoxia/ischemia increases what
A
Ca, Na, H20, K Lactic acid (anaerobic glycolysis)
8
Q
ROSs cause damage in what 3 ways
A
Lipid peroxidation
Protein fragmentation
SS breaks in DNA
9
Q
How does the body control ROS
A
Enzymes
Antioxidants
Serum proteins
10
Q
After cell injury, 4 cell adaptations
A
Size
Number
Functional mods
Intracellular accumulations
11
Q
4 types of necrosis and example of each
A
Coagulative (Aspirin burn, most common)
Liquefactive (abcess)
Caseous (tuberculosis)
Enzymatic (fat necrosis)
12
Q
4 structures/processes that maintain cell viability
A
Plasma membrane
Mitochondria
Macromolecular synthesis
Nucleus
13
Q
Apoptosis is involved in what 3 normal cell processes
A
Normal cell turnover
Embryogenesis
Immune function
14
Q
Excessive apoptosis is involved in what diseases (5)
A
Aids Ischemia Neurogenerative diseases Myelodysplasia Toxin induced liver injury
15
Q
What diseases can inhibit apoptosis
A
Cancer
Autoimmune diseases
Viral diseases
16
Q
5 steps in apoptosis
A
Chromatin condensation Progressive cell shrinkage Plasma membrane blebbing Apoptotic bodies Phagocytosis
17
Q
Differences b/t necrosis and apoptosis
A
Stimuli: N(pathologic), A(physiologic, pathologic)
N(multiple cells, swell, lysis)
A(single cell, shrinks, chromatin, apoptotic bodies)
Response: N(inflammation), A(no inflammation)
18
Q
Chronic stress/injury cause cells to _
A
Undergo adaptive changes
19
Q
T/F similar responses at the cell level can produce different morphological changes in different organs
A
TRUE
20
Q
Metaplasia:
A
Alteration in cell differentiation with concurrent alteration of tissue/organ function
21
Q
Increased cytoplasmic Ca causes what
A
Activate degradative enzymes
22
Q
biochemical alterations occur _ to morphological changes
A
Before
23
Q
Vasodilation is mediated by what 3 things
A
NO
PG’s
Histamine
24
Q
Two types of fluid in inflammation and differences b/t them
A
Transudate: low protein, low specific gravity
Exudate: high protein, high spec. Gravity, can be fibrinous/purulent/sanguineous
25
Non-inflammatory transudate vs. inflammatory
NI - endothelium intact
| I - early endothelial cell contraction
26
Endothelial cell contraction vs retraction
Con - forms intercellular gaps, mediated by histamine/bradykinin, occurs rapidly and lasts 30 min
Ret - restructuring of cytoskeletal proteins, 4 to 6 hours to develop and lasts 24 hours
27
What do activated endothelial cells do
Make PGI and NO (vasodilation)
Contract
Retract
Increased expression of cell adhesion molecules
Synthesis and release of inflammatory mediators
28
What are 5 things that leukocytes do
```
Margination
Rolling (selectins)
Adhesion (integrins)
Emigration/transmigration
Chemotaxis
```
29
4 steps in phagocytosis
Attachment
Engulfment
Degranulation
O2 burst
30
PMNs are also called
Neutrophils
31
_ cells are first responders
| _ cells are second responders and more chronic
Neutrophils
| Monocytes/macrophages
32
Monocytes/macrophages live for _ in tissues
Months
33
Difference b/t cellulitis/abscess/ulcer
C: warm swollen tissue, infiltration by PMN
A: collection of PMNs or pus
U: erosion of an epithelial surface exposing connective tissue
34
Acute vs chronic inflammation
Chronic has immune response, years, systemic, maybe not reversible, macrophages instead of neutrophils
35
Two types of chronic inflammation
Non-specific
| Granulomatous
36
Inflammatory mediators (3)
Histamine
Prostaglandins/leukotrienes
Thromboxane
37
Labile vs. stable vs. permanent
L: continuously dividing
S: some replication
P: non-proliferative
38
First intention vs. second intention
First is a deep thin cut, little scarring if no infection
Second is wide and shallow, more scarring, less function
39
5 ways growth factors can affect wound healing
```
Epithelial proliferation
Monocyte chemotaxis
Fibroblast proliferation
Angiogenesis
Collagen synthesis
```
40
Besides growth factors, what else can affect wound healing
```
Infection
Steroids
Nutrition
Mechanical factors
Poor tissue perfusion
```
41
What is edema
Increased fluid in interstitial tissues
42
Hyperemia:
Congestion:
H: increased tissue blood volume due to increased flow (active)
C: increased blood volume due to impaired venous return (passive) blockage or backup
43
Internal bleeding from large to small
Hematoma
Ecchymosis
Purpura
Petechia
44
_ are like sandbags, the initial hemostatic plug
Platelets
45
3 parts to hemostasis
Endothelium
Platelets
Coagulation cascade
46
_ holds together platelets
Fibrinogen
47
Platelets do what 3 things, and what do they secrete to do them
Adhesion: vWf
Secretion: ADP, Ca2+
Aggregation: ADP, TXA, Thrombin
48
The extrinsic/intrinsic pathway are parts of the _. The extrinsic pathway deals with _ and the intrinsic pathway deals with _. The final products are _ and _
Coagulation cascade
Tissue factor
Factor XII
Thrombin and fibrin
49
_ and _ counter-regulate hemostasis
Fibrinolysis
| Thrombomodulin
50
Virchow's triad (pathogenicity of thrombosis)
Endothelial injury
Alterations in blood flow
Hypercoagulability
51
Hypercoagulability can be caused by either _ or _ such as:
Inherited conditions (factor V Leiden)
Acquired conditions (prolonged bed rest, extensive tissue injury)
52
T/F thrombosis looks the same in all locations
FALSE
arterial - white
Venous - red
53
DIC:
| Caused by:
Disseminated intravascular coagulation - over activation of coagulation cascade
```
Caused by infection (G- bac)
Pregnancy complications
Neoplasm
Shock
Massive injury
```
54
Red vs. white infarction
Red- hemorrhagic, venous occlusion
White - pale, arterial occlusion in solid organ
55
4 things that influence infarct development
Nature of vascular supply
Rate of occlusion
Vulnerability to hypoxia
O2 Carrying capacity
56
Three types of shock
Cardiogenic - low blood pumping
Hypovolemic - have enough blood
Septic - bacteria
57
Septic shock mechanism
PAMPS bind to toll like receptors
58
3 stages of shock
Nonprogressive - compensatory mechanisms maintain perfusion
Progressive - inadequate perfusion, DIC, anaerobic metabolism, lactic acidosis
Irreversible - tissue injury unrecoverable, organ failure, death
59
Parenchyma vs. stroma
Parenchyma is functional tissue of organ
Stroma is supporting connective tissue and blood vessels
60
Adenoma vs papilloma
A: benign glandular epithelial tumor
P: benign surface epithelial tumor with finger like projections
61
Hamartoma
Choristoma
Teratoma
H: proliferation of tissue normally at that site
C: collection of tissue NOT normally at that site
T: derived from more than one germ layer
62
Oma vs sarcoma vs. carcinoma
Oma is benign, sarcoma is a mesenchymal malignancy, carcinoma is epithelial malignancy
63
T/F there are benign lymphomas and melanomas
FALSE
64
Differentiation of neoplastic cells
How well the parenchyma cells resemble their normal tissue of origin
65
Poorly differentiated cells
Anaplastic
66
T/F dysplasia is cancer
False, disorderly but not neoplastic
67
Most, but not all, benign tumors have a _
Fibrous capsule
68
T/F malignancies have a capsule
False
69
How do malignancies grow
Infiltrate, invade, and destroy
70
Hallmark of malignancy
Metastasis
71
3 metastasis pathways and what is usually affected
Seeding in body cavities (pleura/peritoneum)
Lymphatic spread (lymph nodes)
Hematogenous spread (liver/lungs)
72
US cancer deaths/yr
600,000
73
Proportion of cancer risk attributable to environment
66%
74
3 categories of genetic predisposition to cancer
Inherited cancer syndrome
Familial cancer
Defective DNA repair
75
Inherited cancer syndrome vs. familial cancer
ICS: due to single gene mutation and show autosomal dominant transmission
F: close relatives, early age onset, multiple/bilateral tumors
76
_ % of all human cancers have an identifiable heritable basis
5-10%
77
_ is the basis for all carcinogenesis
Nonlethal genetic damage
78
Carcinogenesis usually affects which 3 types of regulatory genes
Protooncogenes
Cancer suppressor genes
Apoptosis genes.
79
Diff b/t protooncogenes and oncogenes
Oncoprotein production is unregulated
80
2 ways oncogenes are activated
Structural mutation resulting in abnormal product
Altered regulation of gene expression, resulting in increased production of a normal growth promoting protein
81
Glioblastoma is associated with which growth factor
Platelet derived growth factor (PDGF)
82
How do growth factor regulators contribute to growth signal self sufficiency
Overexpression of receptors makes cancer cells hyperresponsive to normal GF levels
83
30% of all human tumors contain mutated _ oncogene
RAS
84
Difference b/t mutated RAS and normal RAS
It's normally inactivated quickly, mutant stays active stimulating constant cell proliferation
85
What is the nuclear transcription factor most often affected in neoplasm
MYC gene
86
Burkitt's lymphoma is an example of a disorder marked by _
MYC dysregulation
87
CDK, what does it do
Cyclin dependent kinase
| Bind to cyclin and if disregulated, favors cell proliferation
88
Knudson's two hit hypothesis
Two mutations in the genome of a cell are required to induce retinoblastoma
(One of the hits can be genetic)
89
Most common target for genetic alteration in human tumors
TP53 (tumor suppressor gene)
90
how does TP53 work
Product acts in nucleus to inhibit cell cycle progression
When DNA is damaged, it accumulates and inhibits cell proliferation, allowing time for DNA repair
If repair mechanisms fail, it activates apoptosis genes
91
Prototypic anti-apoptosis gene, how does it work
BCL2
Protects cells from apoptosis, allowing them to survive for extended periods
Results in steady accumulation of cells
92
Two phases of invasion and metastasis
Invasion of extracellular matrix
Vascular dissemination and adhesion/homing of tumor cells
93
What happens in the invasion of ECM
Tumor cells detach from each other and attach to ECM components (collagen, glycoproteins, proteoglycans). Then they degrade matrix components and migrate
94
Cancer requires alterations of _ and two or more _
Several oncogenes
Cancer suppressor genes
95
Why do tumors become more aggressive over time
Acquisition of multiple mutations during tumor growth making multiple subclones with different characteristics that are selected for survival
96
3 karyotypic changes in tumors and examples
Balanced translocation - CML chromosome 22 and 9
Deletion - retinoblastoma Rb, colon and oral cancer
Gene amplifications - neuroblastoma and breast cancer
97
3 classes of carcinogenic agents
Chemicals
Radiant energy
Oncogenic viruses
98
Difference b/t procarcinogen and ultimate carcinogen
Pro has to be metabolically converted, ultimates are ready now
99
Examples of RNA oncogenic viruses
DNA?
RNA - human T cell leukemia virus type I
DNA - HPV, EBV, Burkitt lymphoma, Hep B, HHV8
100
How does cancer survive antigens and Cytotoxic T cells, NK cells and macrophages
(5 ways)
Cancer survives most in immunocompromised people
Antigen negative variants
Less HLA antigens
Lack of T cell costimulation
Immunosuppression
101
Grading vs. staging of cancer
Grading is estimating the aggressiveness of cancer
Staging describes cancer extent (size of primary lesion, lymph node involvement, metastatic spread)
102
Two cancers with a specific antigen
Prostate
| Carcinoembryonic
103
Principle mechanisms of vascular disease
Narrowing or obstruction of lumina
Weakening of vascular walls
104
Monckeberg's sclerosis
Calcifications in muscular walls, no encroachment on lumen, clinically insignificant
105
Two types of arteriolosclerosis
Hyaline: hypertension and diabetes mellitus
Hyperplastic: malignant hypertension
106
Atherosclerosis occurs when _ form and protrude into lumen
Atheromas
107
Rick with atherosclerosis has all risk factors. He is/has: (7 things)
```
75 yr old
Male
High LDL cholesterol
Cigarette smoker
With:
Diabetes
Hypertension
Family history of atherosclerosis
```
108
Atherosclerosis response to injury hypothesis
Endothelial injury
Accumulation of lipoproteins (in vessel wall)
Monocyte adhesion - foam cells
109
How does smooth muscle recruitment happen in the atherosclerosis response to injury hypothesis
Activated platelets release factors to recruit smooth muscle
110
What can happen to atherosclerotic plaques?
```
Calcification
Ulceration
Fissure formation
Thrombosis
Embolization
Hemorrhage into plaque
Medial weakening
```
111
5 complications of atherosclerosis
```
Ischemic heart disease
Cerebral infarct
Gangrene
Renal artery stenosis
Aortic aneurysm
```
112
Other than the hypertension risk factors, 2 things that can cause hypertension
Reduced renal sodium excretion (increased plasma volume, increased cardiac outupt)
Increased peripheral vascular resistance
113
Blood pressure = _ x _
Cardiac output x peripheral resistance
114
Complications from hypertension
```
Concentric left ventricular hypertrophy
Atherosclerosis
Retinal injury
Nephrosclerosis
Dissecting hematoma of the aorta
```
115
Compensated vs. decompensated hypertensive heart disease
C: left ventricular concentric hypertrophy provides normal cardiac output
D: hypertrophy can’t save you, less stretchy, LV dilation and gradual onset of congestive heart failure
116
Concentric hypertrophy:
Thickening of left ventricular wall at the expense of L ventricle chamber, no increase on outside cardiac dimensions
117
Accelerated malignant hypertension
Rapid onset
Very high BP
Cerebral edema, papilledema, encephalopathy, renal failure, cerebral hemorrhage
118
6 mechanisms of heart disease
```
Failure of pump
Flow obstruction
Shunted flow
Leaky flow
Conduction disorders
Rupture of heart/major vessel
```
119
Congestive heart failure
Don’t pump enough blood to supply metabolic requirements of organs
120
When the heart can’t keep up with organ blood needs, neurohumoral systems can be activated. This means:
Norepinephrine released, up heart rate and contractility
Activation of renin-angiotensin system with water/salt retention (increased circulatory volume)
121
Frank-starling mechanism of compensating for CHF
Increased end diastolic filling volume stretches cardiac muscle, and at first they contract stronger but eventually will give out
122
Myocardial hypertrophy is a compensatory mechanism for what
CHF
123
5 causes of left side heart failure
```
Ischemic heart disease
Hypertension
Myocarditis
Cardiomyopathy
Valvular disease
```
124
Causes of right side heart failure
Left side heart failure
Pulm hypertension
Valve disease
Septal defects
125
Right ventricle failure
Congestion of liver
| Edema
126
Causes of congenital heart disease
Rubella, maternal diabetes
| Chromosomal abnormalities
127
Noncyanotic vs cyanotic CHD
NC: atrial septal defect, shunting b/t atria. Ventricular septal defect. Patent ductus arteriosus.
C: tetralogy of fallot: 1 ventricular septal defect, 2. Narrowing of right ventricular outflow, 3. Overriding of the aorta over VSD, 4. Right ventricular hypertrophy
Transposition of the great arteries (r into aorta, L into pulm vein)
128
What is an Ischemic heart disease
A disorder where myocardial blood supply and myocardial oxygen demand are imbalanced
129
What can contribute to IHD
```
Coronary artery atherosclerosis
Coronary artery thrombosis
High myocardial oxygen demand
Decreased blood volume
Decreased oxygenation
Decreased oxygen carrying capacity
```
130
4 clinical types of ischemic heart disease
Angina pectorals
Myocardial infacrction
Chronic IHD with CHF
Sudden cardiac death
131
Angina pectorals
Intermittent chest pain caused by transient reversible myocardial ischemia
132
Stable vs. unstable angina
Stable hurts with exertion
Unstable hurts with no exertion, longer lasting (more serious)
133
Acute myocardial infarction
Necrosis due to ischemia
134
MI complications
```
Arrhythmia
CHF/shock
Mural thrombus
Mitral valve regurgitation
Myocardial rupture
Infarct expansion to involve R ventricle
Chronic ischemic heart disease
```
135
Primary vs. secondary cardiomyopathies
P: disease confined to heart muscle
S: myocardium is involved as part of a systemic disorder
136
Functional patterns of cardiomyophathies, what are they
Dilated - dilation of all 4 chambers
Hypertrophic - stiff, thick ventricles prevent filling
Restrictive - wall of ventricles becomes stiff due to systemic conditions
137
Myocarditis can be due to what 4 things
Pyogenic bacteria
Viruses
Parasites
Hypersensitivity to drugs
138
Mitral valve stenosis is a result of _
Rheumatic fever
139
Features of acute rheumatic fever
Arthritis
Carditis
Erythema marginatum
Subcutaneous nodules
140
Aschoff bodies
Granulomatous inflammation, mononuclear cells and fibroblasts
141
What leads to mitral valve stenosis
Recurrent bouts of acute rheumatic fever
142
Mitral valve regurgitation
Valve fails to close completely, allowing backflow. Caused by IHD and endocarditis.
Mitral valve prolapse = leaflets balloon into the left atrium during systole
143
Marfan syndrome
Floppy mitral valve
144
Aortic valve stenosis occurs in whom
Chronic rheumatic valvular disease
Advanced age
Bicuspid aortic valve congenital malformation
145
Infective endocarditis
Cause:
Predisposing factors:
Pathogenetic factors:
Bacterial/fungus/unusual infection in heart valve
Abnormal heart valves, prosthetic valves, IV drug use, intracardiac shunts, diabetes, immunosuppression
Endocardial or endothelial injury due to abnormalities in blood flow
Fibrin thrombi
Organisms in blood
146
Complications from IE (5)
```
Rupture of chordate tendineae
Spread of infection into myocardium or aorta
Thromboembolism with infarction
Septic thrombi with metastatic abscesses
Valvular dysfunction and CHF
```
147
Takayasu arteritis
Giant cell arteritis, large vessel, granulomatous, Female, <40 years, weak arm pulses
148
Kawasaki syndrome
Medium vessel, antiendothelial cell antibodies triggered by VIRAL INFECTION, mucocutaneous lymph node syndrome, infants and young children
149
Wegener’s granulomatosis
Small vessel, necrotizing granulomas, neutrophil related endothelial damage mediated by PR3-ANCA, sinusitis, pneumonitis, renal failure, glomerulonephritis
150
Immune mediated pathogenesis to vasculitis
Antineutrophilic cytoplasmic antibodies
Anti-endothelial cell antibodies
Cell-mediated immune mechanisms
151
ANCAs are associated with
Polyangiitis
| Wegener granulomatosis
152
Polyarteritis nodosa
Acute relapsing chronic, fever, weight loss, hematuria, renal failure, hypertension, abdominal pain, Melina
153
Buerger disease
```
Thromboangiitis obliterans
Endothelial injury from substance in cigarette smoke
<35 yrs
Gangrene, ischemic ulcers
Vasculitis with thrombosis
```
154
Dissecting aortic hematoma
What is it, complications, predisposing conditions
```
Aneurysm
Tear b/t mid and outer third of media
Rupture - hemorrhage
Branch obstruction
Hypertension and connective tissue disorders (marfan)
```
