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Gen Path > Test 1 1/3 > Flashcards

Test 1 1/3 Flashcards

1
Q

Etiology vs. pathogenesis

A

E: why a disease occurs
P: how a disease occurs

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2
Q

Three outcomes of cell injury

A

Reversible
Cell adaptation
Cell death

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3
Q

Causes of cell injury

A 
No O2
Infectious agents
Injury
Chemicals
Immune response
Genetic abnormalities
Nutritional imbalance
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4
Q

4 cell targets

A

Cell membrane
Mitochondria
Cell proteins
DNA

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5
Q

T/F clinical signs and symptoms appear at the same time as molecular/biochemical changes

A

FALSE - several steps removed

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6
Q

Mechanisms of cell injury (5)

A 
ATP depletion
ROS
Ca2+/membrane permeability
Mitochondrial damage
DNA/protein damage
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7
Q

Hypoxia/ischemia increases what

A 
Ca, Na, H20, K
Lactic acid (anaerobic glycolysis)
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8
Q

ROSs cause damage in what 3 ways

A

Lipid peroxidation
Protein fragmentation
SS breaks in DNA

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9
Q

How does the body control ROS

A

Enzymes
Antioxidants
Serum proteins

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10
Q

After cell injury, 4 cell adaptations

A

Size
Number
Functional mods
Intracellular accumulations

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11
Q

4 types of necrosis and example of each

A

Coagulative (Aspirin burn, most common)
Liquefactive (abcess)
Caseous (tuberculosis)
Enzymatic (fat necrosis)

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12
Q

4 structures/processes that maintain cell viability

A

Plasma membrane
Mitochondria
Macromolecular synthesis
Nucleus

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13
Q

Apoptosis is involved in what 3 normal cell processes

A

Normal cell turnover
Embryogenesis
Immune function

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14
Q

Excessive apoptosis is involved in what diseases (5)

A 
Aids
Ischemia
Neurogenerative diseases
Myelodysplasia
Toxin induced liver injury
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15
Q

What diseases can inhibit apoptosis

A

Cancer
Autoimmune diseases
Viral diseases

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16
Q

5 steps in apoptosis

A 
Chromatin condensation
Progressive cell shrinkage
Plasma membrane blebbing
Apoptotic bodies
Phagocytosis
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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)

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18
Q

Chronic stress/injury cause cells to _

A

Undergo adaptive changes

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19
Q

T/F similar responses at the cell level can produce different morphological changes in different organs

A

TRUE

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20
Q

Metaplasia:

A

Alteration in cell differentiation with concurrent alteration of tissue/organ function

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21
Q

Increased cytoplasmic Ca causes what

A

Activate degradative enzymes

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22
Q

biochemical alterations occur _ to morphological changes

A

Before

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23
Q

Vasodilation is mediated by what 3 things

A

NO
PG’s
Histamine

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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

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25
Q

Non-inflammatory transudate vs. inflammatory

A

NI - endothelium intact

I - early endothelial cell contraction

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26
Q

Endothelial cell contraction vs retraction

A

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

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27
Q

What do activated endothelial cells do

A

Make PGI and NO (vasodilation)
Contract
Retract
Increased expression of cell adhesion molecules
Synthesis and release of inflammatory mediators

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28
Q

What are 5 things that leukocytes do

A 
Margination
Rolling (selectins)
Adhesion (integrins)
Emigration/transmigration
Chemotaxis
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29
Q

4 steps in phagocytosis

A

Attachment
Engulfment
Degranulation
O2 burst

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30
Q

PMNs are also called

A

Neutrophils

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31
Q

_ cells are first responders

_ cells are second responders and more chronic

A

Neutrophils

Monocytes/macrophages

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32
Q

Monocytes/macrophages live for _ in tissues

A

Months

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33
Q

Difference b/t cellulitis/abscess/ulcer

A

C: warm swollen tissue, infiltration by PMN
A: collection of PMNs or pus
U: erosion of an epithelial surface exposing connective tissue

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34
Q

Acute vs chronic inflammation

A

Chronic has immune response, years, systemic, maybe not reversible, macrophages instead of neutrophils

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35
Q

Two types of chronic inflammation

A

Non-specific

Granulomatous

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36
Q

Inflammatory mediators (3)

A

Histamine
Prostaglandins/leukotrienes
Thromboxane

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37
Q

Labile vs. stable vs. permanent

A

L: continuously dividing
S: some replication
P: non-proliferative

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38
Q

First intention vs. second intention

A

First is a deep thin cut, little scarring if no infection

Second is wide and shallow, more scarring, less function

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39
Q

5 ways growth factors can affect wound healing

A 
Epithelial proliferation
Monocyte chemotaxis
Fibroblast proliferation
Angiogenesis
Collagen synthesis
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40
Q

Besides growth factors, what else can affect wound healing

A 
Infection
Steroids
Nutrition
Mechanical factors
Poor tissue perfusion
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41
Q

What is edema

A

Increased fluid in interstitial tissues

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42
Q

Hyperemia:
Congestion:

A

H: increased tissue blood volume due to increased flow (active)

C: increased blood volume due to impaired venous return (passive) blockage or backup

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43
Q

Internal bleeding from large to small

A

Hematoma
Ecchymosis
Purpura
Petechia

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44
Q

_ are like sandbags, the initial hemostatic plug

A

Platelets

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45
Q

3 parts to hemostasis

A

Endothelium
Platelets
Coagulation cascade

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46
Q

_ holds together platelets

A

Fibrinogen

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47
Q

Platelets do what 3 things, and what do they secrete to do them

A

Adhesion: vWf
Secretion: ADP, Ca2+
Aggregation: ADP, TXA, Thrombin

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48
Q

The extrinsic/intrinsic pathway are parts of the _. The extrinsic pathway deals with _ and the intrinsic pathway deals with _. The final products are _ and _

A

Coagulation cascade
Tissue factor
Factor XII
Thrombin and fibrin

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49
Q

_ and _ counter-regulate hemostasis

A

Fibrinolysis

Thrombomodulin

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50
Q

Virchow’s triad (pathogenicity of thrombosis)

A

Endothelial injury
Alterations in blood flow
Hypercoagulability

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51
Q

Hypercoagulability can be caused by either _ or _ such as:

A

Inherited conditions (factor V Leiden)

Acquired conditions (prolonged bed rest, extensive tissue injury)

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52
Q

T/F thrombosis looks the same in all locations

A

FALSE
arterial - white
Venous - red

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53
Q

DIC:

Caused by:

A

Disseminated intravascular coagulation - over activation of coagulation cascade

Caused by infection (G- bac)
Pregnancy complications
Neoplasm
Shock
Massive injury
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54
Q

Red vs. white infarction

A

Red- hemorrhagic, venous occlusion

White - pale, arterial occlusion in solid organ

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55
Q

4 things that influence infarct development

A

Nature of vascular supply
Rate of occlusion
Vulnerability to hypoxia
O2 Carrying capacity

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56
Q

Three types of shock

A

Cardiogenic - low blood pumping
Hypovolemic - have enough blood
Septic - bacteria

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57
Q

Septic shock mechanism

A

PAMPS bind to toll like receptors

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58
Q

3 stages of shock

A

Nonprogressive - compensatory mechanisms maintain perfusion
Progressive - inadequate perfusion, DIC, anaerobic metabolism, lactic acidosis
Irreversible - tissue injury unrecoverable, organ failure, death

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59
Q

Parenchyma vs. stroma

A

Parenchyma is functional tissue of organ

Stroma is supporting connective tissue and blood vessels

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60
Q

Adenoma vs papilloma

A

A: benign glandular epithelial tumor

P: benign surface epithelial tumor with finger like projections

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61
Q

Hamartoma

Choristoma

Teratoma

A

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

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62
Q

Oma vs sarcoma vs. carcinoma

A

Oma is benign, sarcoma is a mesenchymal malignancy, carcinoma is epithelial malignancy

63
Q

T/F there are benign lymphomas and melanomas

64
Q

Differentiation of neoplastic cells

A

How well the parenchyma cells resemble their normal tissue of origin

65
Q

Poorly differentiated cells

A

Anaplastic

66
Q

T/F dysplasia is cancer

A

False, disorderly but not neoplastic

67
Q

Most, but not all, benign tumors have a _

A

Fibrous capsule

68
Q

T/F malignancies have a capsule

69
Q

How do malignancies grow

A

Infiltrate, invade, and destroy

70
Q

Hallmark of malignancy

A

Metastasis

71
Q

3 metastasis pathways and what is usually affected

A

Seeding in body cavities (pleura/peritoneum)

Lymphatic spread (lymph nodes)

Hematogenous spread (liver/lungs)

72
Q

US cancer deaths/yr

73
Q

Proportion of cancer risk attributable to environment

74
Q

3 categories of genetic predisposition to cancer

A

Inherited cancer syndrome
Familial cancer
Defective DNA repair

75
Q

Inherited cancer syndrome vs. familial cancer

A

ICS: due to single gene mutation and show autosomal dominant transmission

F: close relatives, early age onset, multiple/bilateral tumors

76
Q

_ % of all human cancers have an identifiable heritable basis

77
Q

_ is the basis for all carcinogenesis

A

Nonlethal genetic damage

78
Q

Carcinogenesis usually affects which 3 types of regulatory genes

A

Protooncogenes
Cancer suppressor genes
Apoptosis genes.

79
Q

Diff b/t protooncogenes and oncogenes

A

Oncoprotein production is unregulated

80
Q

2 ways oncogenes are activated

A

Structural mutation resulting in abnormal product

Altered regulation of gene expression, resulting in increased production of a normal growth promoting protein

81
Q

Glioblastoma is associated with which growth factor

A

Platelet derived growth factor (PDGF)

82
Q

How do growth factor regulators contribute to growth signal self sufficiency

A

Overexpression of receptors makes cancer cells hyperresponsive to normal GF levels

83
Q

30% of all human tumors contain mutated _ oncogene

84
Q

Difference b/t mutated RAS and normal RAS

A

It’s normally inactivated quickly, mutant stays active stimulating constant cell proliferation

85
Q

What is the nuclear transcription factor most often affected in neoplasm

86
Q

Burkitt’s lymphoma is an example of a disorder marked by _

A

MYC dysregulation

87
Q

CDK, what does it do

A

Cyclin dependent kinase

Bind to cyclin and if disregulated, favors cell proliferation

88
Q

Knudson’s two hit hypothesis

A

Two mutations in the genome of a cell are required to induce retinoblastoma
(One of the hits can be genetic)

89
Q

Most common target for genetic alteration in human tumors

A

TP53 (tumor suppressor gene)

90
Q

how does TP53 work

A

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
Q

Prototypic anti-apoptosis gene, how does it work

A

BCL2

Protects cells from apoptosis, allowing them to survive for extended periods

Results in steady accumulation of cells

92
Q

Two phases of invasion and metastasis

A

Invasion of extracellular matrix

Vascular dissemination and adhesion/homing of tumor cells

93
Q

What happens in the invasion of ECM

A

Tumor cells detach from each other and attach to ECM components (collagen, glycoproteins, proteoglycans). Then they degrade matrix components and migrate

94
Q

Cancer requires alterations of _ and two or more _

A

Several oncogenes

Cancer suppressor genes

95
Q

Why do tumors become more aggressive over time

A

Acquisition of multiple mutations during tumor growth making multiple subclones with different characteristics that are selected for survival

96
Q

3 karyotypic changes in tumors and examples

A

Balanced translocation - CML chromosome 22 and 9

Deletion - retinoblastoma Rb, colon and oral cancer

Gene amplifications - neuroblastoma and breast cancer

97
Q

3 classes of carcinogenic agents

A

Chemicals
Radiant energy
Oncogenic viruses

98
Q

Difference b/t procarcinogen and ultimate carcinogen

A

Pro has to be metabolically converted, ultimates are ready now

99
Q

Examples of RNA oncogenic viruses

DNA?

A

RNA - human T cell leukemia virus type I

DNA - HPV, EBV, Burkitt lymphoma, Hep B, HHV8

100
Q

How does cancer survive antigens and Cytotoxic T cells, NK cells and macrophages

(5 ways)

A

Cancer survives most in immunocompromised people

Antigen negative variants

Less HLA antigens

Lack of T cell costimulation

Immunosuppression

101
Q

Grading vs. staging of cancer

A

Grading is estimating the aggressiveness of cancer

Staging describes cancer extent (size of primary lesion, lymph node involvement, metastatic spread)

102
Q

Two cancers with a specific antigen

A

Prostate

Carcinoembryonic

103
Q

Principle mechanisms of vascular disease

A

Narrowing or obstruction of lumina

Weakening of vascular walls

104
Q

Monckeberg’s sclerosis

A

Calcifications in muscular walls, no encroachment on lumen, clinically insignificant

105
Q

Two types of arteriolosclerosis

A

Hyaline: hypertension and diabetes mellitus

Hyperplastic: malignant hypertension

106
Q

Atherosclerosis occurs when _ form and protrude into lumen

107
Q

Rick with atherosclerosis has all risk factors. He is/has: (7 things)

A 
75 yr old
Male
High LDL cholesterol
Cigarette smoker
With:
Diabetes
Hypertension
Family history of atherosclerosis
108
Q

Atherosclerosis response to injury hypothesis

A

Endothelial injury
Accumulation of lipoproteins (in vessel wall)
Monocyte adhesion - foam cells

109
Q

How does smooth muscle recruitment happen in the atherosclerosis response to injury hypothesis

A

Activated platelets release factors to recruit smooth muscle

110
Q

What can happen to atherosclerotic plaques?

A 
Calcification
Ulceration
Fissure formation
Thrombosis
Embolization
Hemorrhage into plaque
Medial weakening
111
Q

5 complications of atherosclerosis

A 
Ischemic heart disease
Cerebral infarct
Gangrene
Renal artery stenosis
Aortic aneurysm
112
Q

Other than the hypertension risk factors, 2 things that can cause hypertension

A

Reduced renal sodium excretion (increased plasma volume, increased cardiac outupt)

Increased peripheral vascular resistance

113
Q

Blood pressure = _ x _

A

Cardiac output x peripheral resistance

114
Q

Complications from hypertension

A 
Concentric left ventricular hypertrophy
Atherosclerosis
Retinal injury
Nephrosclerosis
Dissecting hematoma of the aorta
115
Q

Compensated vs. decompensated hypertensive heart disease

A

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
Q

Concentric hypertrophy:

A

Thickening of left ventricular wall at the expense of L ventricle chamber, no increase on outside cardiac dimensions

117
Q

Accelerated malignant hypertension

A

Rapid onset
Very high BP
Cerebral edema, papilledema, encephalopathy, renal failure, cerebral hemorrhage

118
Q

6 mechanisms of heart disease

A 
Failure of pump
Flow obstruction
Shunted flow
Leaky flow
Conduction disorders
Rupture of heart/major vessel
119
Q

Congestive heart failure

A

Don’t pump enough blood to supply metabolic requirements of organs

120
Q

When the heart can’t keep up with organ blood needs, neurohumoral systems can be activated. This means:

A

Norepinephrine released, up heart rate and contractility

Activation of renin-angiotensin system with water/salt retention (increased circulatory volume)

121
Q

Frank-starling mechanism of compensating for CHF

A

Increased end diastolic filling volume stretches cardiac muscle, and at first they contract stronger but eventually will give out

122
Q

Myocardial hypertrophy is a compensatory mechanism for what

123
Q

5 causes of left side heart failure

A 
Ischemic heart disease
Hypertension
Myocarditis
Cardiomyopathy
Valvular disease
124
Q

Causes of right side heart failure

A

Left side heart failure
Pulm hypertension
Valve disease
Septal defects

125
Q

Right ventricle failure

A

Congestion of liver

Edema

126
Q

Causes of congenital heart disease

A

Rubella, maternal diabetes

Chromosomal abnormalities

127
Q

Noncyanotic vs cyanotic CHD

A

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
Q

What is an Ischemic heart disease

A

A disorder where myocardial blood supply and myocardial oxygen demand are imbalanced

129
Q

What can contribute to IHD

A 
Coronary artery atherosclerosis
Coronary artery thrombosis
High myocardial oxygen demand
Decreased blood volume
Decreased oxygenation
Decreased oxygen carrying capacity
130
Q

4 clinical types of ischemic heart disease

A

Angina pectorals
Myocardial infacrction
Chronic IHD with CHF
Sudden cardiac death

131
Q

Angina pectorals

A

Intermittent chest pain caused by transient reversible myocardial ischemia

132
Q

Stable vs. unstable angina

A

Stable hurts with exertion

Unstable hurts with no exertion, longer lasting (more serious)

133
Q

Acute myocardial infarction

A

Necrosis due to ischemia

134
Q

MI complications

A 
Arrhythmia
CHF/shock
Mural thrombus
Mitral valve regurgitation
Myocardial rupture
Infarct expansion to involve R ventricle
Chronic ischemic heart disease
135
Q

Primary vs. secondary cardiomyopathies

A

P: disease confined to heart muscle

S: myocardium is involved as part of a systemic disorder

136
Q

Functional patterns of cardiomyophathies, what are they

A

Dilated - dilation of all 4 chambers
Hypertrophic - stiff, thick ventricles prevent filling
Restrictive - wall of ventricles becomes stiff due to systemic conditions

137
Q

Myocarditis can be due to what 4 things

A

Pyogenic bacteria
Viruses
Parasites
Hypersensitivity to drugs

138
Q

Mitral valve stenosis is a result of _

A

Rheumatic fever

139
Q

Features of acute rheumatic fever

A

Arthritis
Carditis
Erythema marginatum
Subcutaneous nodules

140
Q

Aschoff bodies

A

Granulomatous inflammation, mononuclear cells and fibroblasts

141
Q

What leads to mitral valve stenosis

A

Recurrent bouts of acute rheumatic fever

142
Q

Mitral valve regurgitation

A

Valve fails to close completely, allowing backflow. Caused by IHD and endocarditis.

Mitral valve prolapse = leaflets balloon into the left atrium during systole

143
Q

Marfan syndrome

A

Floppy mitral valve

144
Q

Aortic valve stenosis occurs in whom

A

Chronic rheumatic valvular disease
Advanced age
Bicuspid aortic valve congenital malformation

145
Q

Infective endocarditis
Cause:
Predisposing factors:
Pathogenetic factors:

A

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
Q

Complications from IE (5)

A 
Rupture of chordate tendineae
Spread of infection into myocardium or aorta
Thromboembolism with infarction
Septic thrombi with metastatic abscesses
Valvular dysfunction and CHF
147
Q

Takayasu arteritis

A

Giant cell arteritis, large vessel, granulomatous, Female, <40 years, weak arm pulses

148
Q

Kawasaki syndrome

A

Medium vessel, antiendothelial cell antibodies triggered by VIRAL INFECTION, mucocutaneous lymph node syndrome, infants and young children

149
Q

Wegener’s granulomatosis

A

Small vessel, necrotizing granulomas, neutrophil related endothelial damage mediated by PR3-ANCA, sinusitis, pneumonitis, renal failure, glomerulonephritis

150
Q

Immune mediated pathogenesis to vasculitis

A

Antineutrophilic cytoplasmic antibodies
Anti-endothelial cell antibodies
Cell-mediated immune mechanisms

151
Q

ANCAs are associated with

A

Polyangiitis

Wegener granulomatosis

152
Q

Polyarteritis nodosa

A

Acute relapsing chronic, fever, weight loss, hematuria, renal failure, hypertension, abdominal pain, Melina

153
Q

Buerger disease

A 
Thromboangiitis obliterans
Endothelial injury from substance in cigarette smoke
<35 yrs
Gangrene, ischemic ulcers
Vasculitis with thrombosis
154
Q

Dissecting aortic hematoma

What is it, complications, predisposing conditions

A 
Aneurysm
Tear b/t mid and outer third of media
Rupture - hemorrhage
Branch obstruction
Hypertension and connective tissue disorders (marfan)

Gen Path (3 decks)

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