Pathology Flashcards
(199 cards)
1
Q
What is the mechanism by wc the lesions are produced?
A
Pathogenesis
‘HOW’ of dse
2
Q
What is the increase in cell SIZE that occurs in tissues incapable of cell division?
A
Hypertrophy
3
Q
What can be the stimulus for hypertrophy?
A
Increase in fxnal demand
Increase in hormonal stimulation
4
Q
Mechanism for hypertrophy
A
Increase cellular protein production
5
Q
Hypertrophy examples in physiologic & pathologic
A
Physiologic: Gravid uterus, muscle of body builders
Pathologic: LVH
6
Q
What is the increase in NUMBER of cells that occurs in tissues capable of cell division?
A
Hyperplasia
7
Q
Stimulus of Hyperplasia
A
Hormonal or compensatory mechanism
8
Q
Mechanism of Hyperplasia
A
- Growth factor driven proliferation of mature cells
- Increase output of new cells from tissue stem
9
Q
Examples of physiologic and pathologic hyperplasia
A
Physiologic: pubertal breast changes, liver regeneration
Pathologic: endometrial hyperplasia
10
Q
What is the decrease in cells SIZE and NUMBER?
A
Atrophy
11
Q
Stimulus of Atrophy
A
- Decrease workload, denervation
- Ischemia
- Malnutrition
- Loss of endocrine stimulation
- Pressure
12
Q
Mechanism of Atrophy
A
- Decrease protein synthesis
- Increase protein degradation
- Autophagy
13
Q
Examples of physiologic and pathologic atrophy
A
Physiologic: embryonal atrophy (notochord & thyroglossal duct)
Pathologic: senile atrophy of brain
14
Q
What is a differentiated cell type replaced by another cell type?
A
Metaplasia
15
Q
Stimulus and mechanism of metaplasia
A
Stress that leads to reprogramming of stem cells
16
Q
Examples of metaplasia
A
- Columnar to squamous: Vit A deficiency
- Squamous to columnar: Barrett’s esophagus
17
Q
What happens during atrophy or loss of brain substance?
A
Narrow gyrus and widen sulci
18
Q
What is defined as the effect of a variety of stresses d/t etiologic agents a cell encounters, wc result in changes in its internal and external environment?
A
Cell injury
19
Q
What causes cell injury?
A
1) O2 deprivation (hypoxia) and Ischemia
2) Physical agents
3) Chemicals and drugs
4) Infectious/Microbial agents
5) Immunologic
6) Genetic derangements (mutate)
7) Nutritional derangements/imbalances
20
Q
What are morphologic alterations in reversible cell injury?
A
Cell swelling (eosinophilic) Fatty change
21
Q
Ultrastructure changes
A
- Plasma mem alterations (bleb, blunt, loss microvilli)
- Mitochondrial changes (swell, amorphous densities)
- Dilation of ER (form myelin figures)
- Nuclear alterations (disaggregation of granular & fibrillar)
22
Q
What are the two processes underlying changes in necrosis?
A
Denaturation of proteins
Enzymatic digestion
23
Q
Necrotic cells are more eosinophilic (pink) than
A
viable cells
24
Q
What appears “glassy” homogenous, vacuolated cell membranes, fragmented?
A
Necrotic cell - it is mainly as a result of the loss of glycogen
25
What are dead cells that may be replaced by large, whorled phospholipid masses?
Myelin figures (seen in reversible injury)
26
What nuclear change is a small dense nucleus?
Pyknosis
27
What nuclear change is a faint dissolved nucleus?
Karyolysis
28
What nuclear change is a fragmented nucleus?
Karyorrhexis
29
What is the most common tissue pattern of necrosis?
Coagulative necrosis
30
Protein denaturation with preservation of cell & tissue framework
Coagulative necrosis
31
A. wedge-shaped kidney infarct (yellow)
B. loss of nuclei and an inflammatory infiltrate
"tombstone" appearance
Coagulative necrosis
32
Digestion of dead cells, resulting in the transformation of the tissue into a liquid viscous mass (pus)
Liquefactive necrosis
33
Localized bacterial infection (abscesses) and in the brian
Liquefactive necrosis
34
Autolysis or heterolysis predominates over protein denaturation
Liquefactive necrosis
35
What isn't a pattern of cell death but a term commonly used in clinical practice?
Gangrenous necrosis
36
What type of gangrene is predominantly coagulative?
Dry gangrene
37
What type of gangrene is more liquefactive (w abscess)?
Wet gangrene
38
Tuberculous lesions
| Soft, friable, cheese-like
Caseous necrosis
39
Microscopic: amorphous eosinophilic material w cell debris (fragments of nucleus and inflammatory cells)
Like homogeneous pink substance
Caseous necrosis
40
In fat necrosis, how does release of FA (wc attract Ca salts)then complex w Ca soaps (saponification) happen?
Lipase activation
41
What can be seen in pancreatitis?
Fat necrosis
42
Gross: white chalky areas (fat saponification)
Microscopic: vague cell outlines, Ca deposition
Fat necrosis
43
Necrosis: Immune rxns involving BV
Fibrinoid necrosis
44
Brain
Liquefactive
45
Heart, kidneys
Coagulative
46
Limb
Gangrenous
47
TB
Caseous
48
Vasculitis
Fibrinoid
49
What is the fundamental cause of necrotic cell death?
ATP depletion
50
What is the consequence of ischemic & toxic injury?
ATP depletion
51
In ATP depletion, what will reduced Na pump activity (dt hypoxia) then increase influx of Na, H2O and Ca cause?
Cell swelling
52
What happens when there is hypoxia?
Increase glycolysis then glycogen depletes, lactic acid increases and there'll be intracellular acidosis
53
What is the consequence of increased cytosolic Ca, ROS and O2 deprivation?
Mitochondrial damage
54
Abn oxidative phosphorylation then formation of ROS leads to necrosis
Mitochondrial damage
55
What happens when Ischemia/toxins --> Ca influx + release of Ca from mitochondria and ER?
- activates phospholipases --> degrades mem phospholipids (wc inc mem perm that leads to cell swelling or leakage of caspases)
- activates proteases --> brks down mem and cytoske CHONs
- activates ATPases --> ATP depletion
- activates endonucleases --> chromatin fragmentation
56
What are important mediators of cell injury?
Ca ions
57
What is the most common type of injury?
Ischemic and hypoxic injury
58
What happens when there's mechanical obstruction in the arteries?
Ischemia then reduce venous drainage, compromised delivery of substrates for glycolysis
59
What are the mechanisms of ischemic cell injury?
Sequence of events:
1Decreased O2 tension
2Loss of oxidative phosphorylation
3Decreasee prodxn of ATP
4Failure of Na pump --> loss of K --> influx of Na and water --> cell swell
5Ca influx
6Progressive glycogen loss, decreased CHON synthesis
60
What is the death of cells after bld flow resumes and is also associated w neutrophilic infiltration?
Ischemia-reperfusion injury
61
What are the mechanisms of ischemia-reperfusion injury?
- inc generation of O2-derived free radicals
- resulting inflammation and recruitment of PMNs
- activation of complement
62
What is the difference between direct and indirect chemical injury?
Direct - bind to critical molecular component
| Indirect - conversion to reactive toxic metabolites
63
Anti-apoptotic
BCL2
BCL-XL
MCL1
64
Pro-apoptotic
BAX
| BAK
65
Sensors
BAD, BIM, BID, Puma, and Noxa
66
What is the activation of death receptors on the cell membrane (TNFR1 and Fas) called?
Extrinsic (Death Receptor) Pathway
| - caspases 8 & 10
67
Initiator caspases --> executioner caspases --> nuclear fragmentation; endonuclease activation; brkdwn of cytoskeleton
Execution Phase
68
What are examples of apoptosis?
```
Growth factor deprivation
DNA damage
Protein misfolding
TNF family receptors
Cytotoxic T lymphocytes
```
69
What does necroptosis resemble?
Necrosis morphologically
| Apoptosis mechanistically
70
What is the cause of necroptosis?
TNF and viral proteins
71
Necroptosis is caspase-independent and it activates
RIP1 and RIP3 (Receptor Interacting Proteins) complexes --> increases ROS and decreases mitochondrial ATP prodxn --> necrosis
72
What is the most common lipid?
TAGs
Other lipids: CHOL, CHOL esters, phospholipids
73
What occurs when a normal constituent (tags) accumulates, leading to increase in intracellular lipids?
Steatosis - most common in liver
74
True or False. Is steatosis reversible?
True. Though it may lead to cirrhosis if in excess.
75
What is the reabsorption droplets in proximal renal tubules?
Nephrotic syndrome
76
What is the excess of normally-secreted proteins?
Plasma cells actively producing Igs (Russell Bodies)
| Seen in MM
77
What is the defective intracellular transport and secretion?
a1-antitrypsin deficiency
78
What is the accumulation of cytoskeletal proteins?
Alzheimer's dse (neurofibrillary tangles)
79
What is the aggregation of abn proteins?
Amyloidosis
80
Intracellular hyaline
a1-antitrypsin deficiency
81
Extracellular hyaline
Hyaline arteriosclerosis in HPN and DM
82
Examples of exogenous pigments
Carbon or coal dust (anthracosis)
| Tattooing
83
Examples of endogenous pigments
Lipofuscin
Melanin
Homogentisic acid
Hemosiderin
84
Sign of lipid peroxidation
| Lipids + phospholipids in complex w protein
Lipofuscin
85
Alkaptonuria (ochronosis)
Homogentisic acid
86
What is dystrophic tissue type?
Necrotic
87
What is the metastatic tissue type?
Viable
88
Where is serum Ca increased? Dystrophic or Metastatic?
Metastatic
| Causes: excess PTH, bone resorption, vit D dis, renal failure
89
Clinical importance of Dystrophic
Psamomma bodies- sand-like lamellated concretions
P Papillary thyroid CA
S Serous cystadenoCA of ovaries
M Meningioma
M Mesothelioma
90
Clinical importance of Metastatic
Lung involvement
| Nephrocalcinosis
91
What are the mechanisms that counteract aging?
Decreased IGF-1 signaling
| Increased sirtuins
92
What are proteins that fxn in response to food deprivation and DNA damage and are found in red wine?
Sirtuins - promote longevity eyyy tara laklak jk minimal
93
What is due to vascular dilatation and congestion?
Rubor
94
What is dt vascular dilatation?
Calor
95
What is dt mediator release?
Dolor
96
What is due to increased vascular permeability?
Tumor
97
What is dt pain, edema, tissue injury?
Functio laesa
98
What elicits inflammation regardless of the cause of cell death, wc may include ischemia (reduced bld flow, cause of MI), trauma, and physical and chemical injury?
Tissue necrosis
99
What elicits inflam by themselves or bcs they cause traumatic tissue injury or carry microbes? Necrotic cells also trigger
Foreign bodies
100
What are the 5 steps in inflammatory rxn?
```
1 Recognition of the infectious agents
2 Recruitment of leukocytes
3 Removal of the agent
4 Regulation (ctrl) of the response
5 Resolution (repair)
```
101
In sensors of cell damage, what happens when molecules that are recognized, result from injury s/a UA, ATP, reduced K, DNA
They activate inflammasome (multiprotein cytosolic complex) --> IL-1 prodxn --> leukocyte recruitment --> inflammation
102
For the Fc tails of antibodies and complement proteins
Leukocyte receptors
103
What recognize microbes coated (opsonized) w Ab and complement?
Leukocyte receptors
104
Complement
MBL
Collectins
Circulating proteins
105
What recognizes microbial sugars and promotes ingestion of microbes and the activation of complement system?
MBL
106
What can bind to and combat microbes?
Collectins
107
Increase blood flow
Dilation of small vessels
108
What happens when there's increase microvascular permeability?
Plasma proteins and leukocytes leave the circulation
109
What is an extravascular fluid has a high protein conc and contains cellular debris?
Exudate
110
What implies increase in the permeability of small BV triggered by tissue injury and an ongoing inflammatory rxn?
Exudate
111
What is a fluid w low protein content, little or no cellular material, and low SG?
Transudate
112
What is an ultrafiltrate of plasma that is produced as a result of osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability?
Transudate
113
What is an accumulation of leukocytes along the endothelium?
Stasis
- activation of endothelial cells and expression of increased levels of adhesion molecules --> adhere to endothelium--> migrate to interstitial
1 arterioles
2 capillary beds
114
Heat and redness
Erythema
115
Slowly moving red cells; seen as vascular congestion and localized redness of involved tissue
Stasis
116
What is the hallmark of acute inflammation?
Increased vascular permeability
117
What happens when there is endothelial injury?
Endothelial cell necrosis and detachment --> immediate and sustained endothelial peakage
118
What occurs rapidly after injury and is reversible and transient (15-30mins)?
Endothelial cell contraction or "immediate transient response"
119
Vessel lumen to tissue interstitium
Margination, rolling, adhesion to the endothelium, transmigration across endothelium, migration in interstitial tissues
120
Necrosis response
1° neutrophils during first 6 to 24 hrs
| Then replaced by monocytes after 24-48 hrs
121
Rolling in Endothelial cell vs Leukocytes
Endothelial cell: E and P selectins
Leukocytes: Sialyl Lewis
122
Firm adhesion in Endothelial cell vs Leukocytes
Endothelial cell: ICAM and VCAM
Leukocytes: Integrins
123
Transmigration (diapedesis) in Endothelial cell vs Leukocytes
Both PECAM 1
124
Migration (Chemotaxis) in Endothelial cell vs Leukocytes
Endothelial cell: Bacterial products (C5a, IL-8, LT b4, Kallikrein)
Leukocytes: Leukocyte surface G protein-coupled receptors
125
What are synthesized from arg, molecular O2 and NADPH?
Nitric oxide
126
What can kill microbes by increasing mem perm?
Leukocyte granules
127
What contains MPO, bactericidal factors (lysozymes), acid hydrolases and neutral proteases?
Azurophilic (1°) granules
128
What contains lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator and histaminase?
Specific (2°) granules
129
What inflam mediators are either preformed and released by granules exocytosis or synthesized de novo following a stimulus?
Cell-derived mediators
130
What inflam med are typically synthesized in the liver and circulate as inactive precursors wc are activated by proteolysis?
Plasma-derived mediators
131
Its release is triggered by physical injury, immune-mediated (allergies), anaphylatoxins (C3a and C5a), cytokines (IL-1 and IL-8), and neuropeptidases (substance P)
Histamine (dilator) - inc perm of venules
132
Sources: plts and neuroendocrine cells
Serotonin (constrictor)
133
Primary fxn is as a neurotransmitter in the GI tract
Serotonin (constrictor)
134
What eicosanoid can cause vasodilation?
PG PGI2 (prostacyclin), PGE1, PGE2, PGD2
135
What eicosanoid can cause vasoconstriction?
Thromboxane A2, leukotrienes C4, D4, E4
136
What eicosanoids can inc vascular permeability?
Leukotrienes, C4, D4, E4
137
What eicosanoids can undergo chemotaxis, leukocyte adhesion?
Leukotrienes B4, HETE
138
Act primarily as chemoattractants and activators
Chemokines
139
Ig-Ag complex
| Activated by MBL w bacterial surface proteins
C1
140
What are the anaphylatoxins?
C3a, C5a, and C4a
141
What promotes histamine release --> vasodilation and inc vasc perm?
Anaphylatoxins
142
Chemoattractant to neutrophils, monocytes, eo and baso
| Activates lecithin-type oxidized receptors in PMNs and monocytes --> inflamm mediators
C5a
143
Plt-Activating Factor in various concs
High: ikaw jk vaso- and bronchoconstriction
Low: histamine-like effects
144
Products of coagulation
Protease-activated receptors
145
Distinctive form of chronic inflammation
Granulomatous inflammation
146
What is composed of neoplastic cells?
| - based on classification of tumors and their behavior
Parenchyma
147
What is composed of CT, BV, and variable numbers of cells of adaptive and innate IS?
Reactive stroma
148
Soft and fleshy tumor that has scant CT
| Desmoplasia
Reactive stroma
149
What are tumors forming gross or microscopic finger like projections?
Papilloma
150
What is a tumor projecting macroscopically above mucose?
Polyp
151
Derived from neoplastic clone of a single germ layer that differentiates into more than one cell type
- mixed saliv gland tumors cont epi cells
- myxoid stroma that may contain islands of cartilage or bone
Mixed tumors
152
Various parenchymal cell types representative of more than one germ cell layer
- arise from totipotential cells capable of forming endodermal, ecto, and mesenchymal tissues
- can be benign or malignant
Typicla: testis, ovary, rare in midline embryonic rsts
Teratomas
153
Ectopic rests of nontranformed tissues
- pancreatic cells under the small bowel mucosa
Choristoma
154
Masses of disorganized tissue indigenous to a particular site
- many are clonal w char acquired chromosomal abn
Hamartoma
| - lung hamartomas exhibit cartilage, bronchi, and BV
155
What is the hallmark of malignancy?
| "To form backward"
Anaplasia
156
Variation in size and shape
Cells within the same tumor arent uniform, but range from small cells w an undifferentiated appearance, to tumor giant cells
Pleomorphism
157
Malignancy: large, irreg, hyperchromatic nuclei w coarsely clumped chromatin sometimes w large nucleoli
Inc N:C ratio 1:1 vs normal of 1:4 or 1:6
Abn nuclear morphology
158
Nuclear pleomorphism, hyperchromatic, nuclei, and tumor giant cells
Rhabdomyo sarcoma
159
What is always found in association w tissue damage, repair, and regeneration?
Metaplasia
| - stratified sq epi replacing respi epi in bronchioles of smokers
160
What is the disordered growth char by a constellation of changes that includes a loss in the uniformity of the individual cells and loss in archi orientation? Mild to severe
Dysplasia
| - can occur adjacent to frank malignancy
161
When dysplastic changes are marked and involves the full thickness of epi but lesion doesn't penetrate the basement mem, it is considered a preinvasive neoplasm and is referred to as
Carcinoma in situ
162
Exudates
| High protein content
Inflammatory
163
Transudates
| Low protein content
Non-inflammatory
164
How does heart failure lead to edema?
Either
- Increase capillary hydrostatic pressure
- Reduced bld flow --> RAAS activation --> retention of Na and H2O (renal failure) --> increase BV --> EDEMA
165
How does malnutrition, decrease hepatic synthesis, and nephrotic syndrome lead to edema?
Decrease plasma albumin then decreased plasma osmotic pressure
166
What appears in tissues w loose CT matrix s/a the eyelids (periorbital edema)?
Edema from renal dysfxn
167
What is the appearance of sulci and gyri in brain edema?
Narrowed sulci and distended gyri
168
What is the active process in wc arteriolar dilation leads to increased bld flow?
Hyperemia
169
Affected tissues turn red (erythema) dt engorgement of vessels w oxygenated bld
Hyperemia
170
What os the passive process resulting from reduced outflow of bld from a tissue?
Congestion
171
What os the passive process resulting from reduced outflow of bld from a tissue?
Congestion
172
Dusky reddish-blue (cyanosis) dt red cell stasis and accumulation of deoxygenated Hb
Congested tissues
173
Engorged alveolar capillaries w alveolar septal edema and focal intra-alveolar hemorrhage
Acute pulmonary congestion
174
Septa are thickened and fibrotic
| Capillary rupture may cause focal hemorrhage; and subsequent brkdwn results in Hemosiderin-laden macrophages
Chronic pulmonary congestion
175
Distended central vein and sinusoids
Ischemic necrosis of centrilobular hepatocytes w periportal steatosis
Acute hepatic congestion
176
Hemorrhagic centrilobular hepatocytes accentuated against uncongested tan liver (nutmeg)
Hemosiderin-laden macro; variable degrees of hepatocyte dropout and necrosis
Chronic passive hepatic congestion
177
Difference of turbulence and stasis in abn bld flow
Turbulence: arterial and cardiac thrombi
Stasis: venous thrombi
178
What are laminations composed of pale plt and fibrin deposits alternating w darker red cell-rich layer?
Lines of Zahn
- signifies thrombus has formed in flowing bld
- distinguish antemortem clots from nonlaminated clots in postmortem
179
Thrombi occuring in the heart chambers or in aortic lumen
Mural thrombi
180
Usually begins at sites of turbulence or endothelial injury
Arterial thrombi
- frequently occlusive
- friable meshwork of plt, fibrin, rbc, and degenerating leukocytes
181
What are the most common sites of arterial thrombi?
Coronary arteries
Cerebral arteries
Femoral arteries
182
What usually begins at sites of stasis?
Venous thrombosis
- almost invariably occlusive
- firm, attached to vessel wall and cont lines of Zahn
183
What is the most common site of venous thrombosis?
Calf vein
| - resp of DVT
184
What are the 4 fates of thrombus?
1 Propagation
2 Embolization
3 Dissolution
4 Organization and Recanalization
185
Where does superficial venous thrombi occur in the setting of varicosities?
Saphenous veins
186
Sx of venous thrombosis
Local congestion
Swelling
Pain and tenderness
Rarely embolize
187
DVT involves one of the large leg veins - at or above the knee
Popliteal
Iliac
Femoral veins
188
Sx of DVT
Local pain and edema dt venous obstruction
189
What can give rise to pulmonary infarction?
DVT
190
Originate from DVT and are most common form of thromboembolic disease
Pulmonary embolism
191
Ischemic necrosis of femoral heads, tibia, and humerus
Caisson dse
192
What is the 5th most common cause of maternal mortality worldwide?
Amniotic fluid embolism
193
Areas of ischemic necrosis c/b occlusion of either the arterial supply (most common) or venous drainage (less frequent)
Infarction
194
What is the most common cause of infarction?
Arterial thrombosis or arterial embolism
195
Its etiology includes:
- local vasospasm, hemorrhage into atheromatous plaque, or extrinsic vessel compression (tumor)
- torsion of a vessel, traumatic vascular rupture, or vascular compromise by edema or by entrapment in a hernia sac
Infarction
196
Morphology: wedge, w occluded vessel at apex and periphery of organ at base
Histo: ischemic coagulative necrosis
Replaced by scar tissue
Infarction
197
Venous occlusion
Loose tissue
Dual circ (eg lung and smol int)
Hemorrhagic (red) infarction
198
What occurs in solid organs w end-arterial circulation (heart, spleen, kidneys)?
Pale (white) infarction
199
What occurs in solid organs w end-arterial circulation (heart, spleen, kidneys)?
Pale (white) infarction
