Path Final Additional cards Flashcards
1
Q
What is hypertrophy?
A
1) General increase in the bulk, not due to tumor formation2) increase in size of cells not #
2
Q
What happens to tissue once it stretches or stress is put on a tissue?
A
It will adapt to the stress
3
Q
What is atrophy or hypotrophy?
A
wasting of tissue from death and reabsorption of cells, diminished cellular proliferation, decreased cellular volume, pressure, ischemia or malnutrition that leads to lessened function or hormonal changes
4
Q
What causes atrophy in the brain?
A
Aging and reduced blood supply
5
Q
How does a brain that has undergone atrophy appear grossly?
A
The brain has narrowed gyri and widened sulci
6
Q
What causes atrophy of the thyroid gland?
A
Longstanding autoimmune disease
7
Q
What is hyperplasia?
A
increase in # cells excluding tumor formation
8
Q
What causes endometrial hyperplasia?
A
Estrogen.
9
Q
What causes calluses on the heels of feet?
A
Stresses due to constant wear on feet (ie: tight shoes)
10
Q
What is BPH?
A
Benigh Prostatic hyperplasia
11
Q
What is hypoplasia?
A
incomplete development of tissue (ie: neural fold defects)
12
Q
What is metaplasia?
A
reversible replacement of one differentiated cell type with another differentiated cell type (ie: barrett’s esophagus where cells have migrated from the stomach to the esophagus due to constant stress)
13
Q
What is anaplasia?
A
A change in the structure of cells and a change in their orientation to each other.
14
Q
What is aplasia?
A
The defective development, or congenital absence of an organ or tissue
15
Q
What is dysplasia?
A
Abnormal tissue growth with loss of cell orientation, shape, and size
16
Q
What is dysplasia?
A
Abnormal tissue growth with loss of cell orientation, shape, and size
17
Q
Dysplasia is always what?
A
Pre-cancerous
18
Q
What type of cell injury is found with lysosome swelling and rupture?
A
Irreversible as necrosis will occur
19
Q
What cell injury occurs when fat calcification begins?
A
Irreversible
20
Q
What happens to reversible damaged cells when looking at them with light microscope?
A
They have fatty changes (steatosis).
21
Q
Is nuclear clumping the same as nuclear condensation?
A
NO!
22
Q
What is the difference between necrosis and apoptosis?
A
Necrosis- common after ischemia and chemical injury CELL SWELLING. Apoptosis- is programmed cell death and CELL SHRINKAGE.
23
Q
Does necrosis or apoptosis has neighbor or adjacent cell inflammation?
A
Usually necrosis
24
Q
What happens to the plasma membrane during necrosis?
A
It is disrupted
25
What happens to the plasma membrane during apoptosis?
Intact/altered.
26
What happens with the cells contents with necrosis ?
enzymatically digested
27
What happens with the cells contents with apoptosis?
intact and packaged to be phagocytosed
28
What causes necrosis?
Inavriably pathologic
29
What causes apoptosis?
Often physiological
30
What does serum CK-MB check for?
Cardiac tissue ischemia
31
What does serum CK-BB check for?
Brain Tissue ischemia
32
What does serum CK-MM check for?
Generic muscle ischemia
33
What does cytochrome c do once it is outside of the mitochondrial membrane?
It induces secondary apoptotic effects
34
What are the sources of internal calcium?
1) mitochondrial damage2) cell injury (external calcium enters cell)3) ER damage
35
Where will Vitamin E be doing free radical protection?
In the membranes.
36
Glutothione is stored mostly where and to do what?
Stored in the retina to protect against all redox reactions.
37
What is the role of P-450?
Detox. It is enzymes that increase the solubility of compounds and help excrete them.
38
What is the down side of P-450?
While detoxing it can make some reactive oxygen intermediates which can injure cells.
39
Where are the P-450 enzymes found?
In the Smooth ER of hepatocytes.
40
What process is NADPH oxidase found in?
Pentose Shunt
41
Is iron required in the human body?
yes but excess can cause oxidative changes
42
Is copper required in the human body?
Yes but only in trace amounts
43
Free radical injury is induced through what?
membrane lipid peroxidation, protein modification, DNA breakage.
44
How are free radicals degraded?
Through enzymes, spontaneous decay, and antioxidants.
45
Why is homogenated milk bad for us?
Xanthine oxidase is better absorbed in body and causes more free radicals in circulation
46
Reperfusion after anoxia (an abnormally low amount of oxygen in the body tissues) induces what?
Free radical production.
47
What are some free radicals found in the body?
Super oxide, peroxide, hydroxide and nitrous oxide
48
What are some antioxidants that neutralize the free radicals in the body that are found in the cytosol?
Superoxide dismutaseGlutathionePeroxidaseFerritinCeruloplasminQuercitin
49
What is the function of ferritin?
Moves iron around the body
50
What is the function of ceruloplasmin
Transports copper around the body
51
Where is quercitin found?
in orange peel (white part)
52
What can initiate injury via free radicals?
Radiation exposure, metabolism of drugs (phase I), redox reaction, nitric oxide, transition metals, leukocyte oxidative burst
53
How do free radicals cause cell injury?
Through membrane lipid peroxidation, protein modification and DNA breakage
54
What are the different types of necrosis?
1) Coagulative2) Liquefactive3) Caseous4) Fat5) Fibrinoid6) Gangrenous
55
Coagulative necrosis happens with necrosis to what areas?
Heart, liver, and kidney.
56
Coagulative necrosis is a result of what?
Protein denaturation.
57
What will coagulative necrosis look like?
Preservation of basic cell outline for several days.
58
Liquefactive necrosis happens where?
Brain
59
Liquefactive necrosis is characteristic of what 2 things?
1. Bacterial infection. 2. CNS stroke.
60
Liquefactive necrosis is a result of what?
Enzymatic digestion.
61
Gangrenous necrosis is associated with what area?
Limbs and GI tract.
62
Gangrenous necrosis usually results in what?
limb with loss of blood and Coagulation necrosis.
63
What is wet gangrene?
Coagulation necrosis with liquifactive action of bacterial infection and attracted leukocytes.
64
Caseous necrosis occurs due to what?
It is seen in tuberculosis infections.
65
What is the appearance of caseous necrosis?
Cheesy white appearance.
66
Caseous necrosis is a distinct form of which type of necrosis?
Coagulative necrosis
67
What is makes caseous necrosis a special form of coagulative necrosis?
Tissue architecture is obliterated unlike coagulative necrosis
68
How does Caseous necrosis look microscopically?
1) amorphus granular debris of fragmented coagulated cell2) amorphus granular debris enclosed within distinctive inflammatory border (granulmatous reaction)
69
Can scarring from caseous necrosis be seen via x-ray? And how long does scarring last?
Yes it can be seen in x-ray and the scarring remains with the patient for life
70
Fat necrosis occurs where?
In the pancreas
71
Is fat necrosis a typical necrosis pattern?
No
72
What will fat necrosis look like under microscope?
Foci of shadowy outlines of fat cells with basophilic calcium deposits surrounded by inflammatory reaction.
73
What will fat necrosis look like grossly?
Chalky area due to fat saponification
74
Is fat necrosis focal or widespread?
Focal area of fat destruction usually due to lipase release
75
What does P-450 do? What is an unfortunate result?
P-450 neutralizes toxins but creates free radicals
76
What is the stimulus for coagulative necrosis?
Hypoxia, toxins
77
What is the stimulus for apoptosis?
Physiologic and pathologic
78
What is the histology of the coagulative necrosis?
Cellular swellingcoagulative necrosisorganelle disruption
79
What is the histology for apoptosis?
Cellular shrinkageChromatin condensationApoptotic bodies
80
What is the DNA Breakdown in coagulative necrosis?
Random, diffuse
81
What is the DNA Breakdown in apoptosis?
Internucleosomal
82
What are the mechanisms of coagulative necrosis?
ATP depletionMembrane injuryFree radical damage
83
What are the mechanisms of apoptosis?
Gene activationEndonucleasesProteases
84
What is the tissue reaction of coagulative necrosis?
Inflammation
85
What is the tissue reaction of apoptosis?
No inflammationPhagocytosis of ABs
86
During what instances does apoptosis occur?
1) Embryogenesis2) hormone induction (menstruation)3) immune cell-mediated death4) injurious stimuli (ie: radiation, hypoxia)5) regulation of cell population and tumor suppression6) atrophy (ie: endometrial lining during menopause)
87
Which type of cell death is more controlled?
Apoptosis
88
Which type of cell death involves more cells?
Necrosis
89
What are the two types of pathologic calcification?
Dystrophic calcificationMetastatic calcification
90
Where does Dystrophic calcification occur?
Deposition occurring locally in dying tissue
91
What happens to the serum calcium level of the dystrophic calcification?
Nothing, it is normal serum calcium level
92
Is there any calcium metabolism pathology associated with dystrophic calcification?
No, no calcium metabolism pathology
93
What are some examples of dystrophic calcification?
Atherosclerosis of arteries, damaged heart valves
94
Where does metastatic calcification occur?
Deposition in otherwise normal tissue
95
What happens to the serum calcium level of the metabolic calcification?
Systemic elevation calcium levels in the blood and all tissues
96
What usually causes metastatic calcification?
Usually due to secondary hypercalcemia
97
What happens to calcium levels in injured cells with dystrophic calcification?
The calcium levels will increase due to release from ER and mitochondria
98
What happens to mitochondrial initiation with dystrophic calcification?
The mitochondrial permeability transition increases and therefore calcium diffuses through into the cell.
99
What is arachidonic acid?
Arachidonic acid is derived from phospholipids through the action of phospholipases
100
How is arachidonic acid metabolized?
1) Lipoxygenase pathway2) Cyclooxygenase pathway
101
What are the 5 arachidonic acid derivatives?
1) Leukotrienes2) Lipoxins3) Thromboxane4) Prostacyclin5) Prostaglandins
102
What is the function of leukotrienes?
Chemoxtaxis, vascular permeability and bronchospasm
103
What is the function of lipoxins?
vasodilatation, inhibition of neutrophil chemotaxis, and monocyte adhesion
104
What is the function of thromboxane?
Platelet aggregation, thrombosis
105
What is the function of Prostacyclin?
Opposes the effects of thromboxane
106
What is the function of Prostaglandins?
Smooth muscle contraction
107
Is Omega 3 fatty acids (fish oil) a good substrate for conversion?
No it is a poor substrate
108
Are animal fats good for conversion to substrate?
Yes, animal fat is a good substrate
109
Generally, what lymphokines are released with macrophage activation and lead to inflammation?
Interleukin-1 and Tumor Necrosis factor
110
What are the acute-phase reactions activated by interleukin-1 and tumor necrosis factor?
1) Fever2) increased sleep need3) decreased appetite4) Increased acute-phase proteins5) hemodynamic effects (shock)6) Neutrophilia (attract neutrophils)
111
What are the endothelial effects activated by interleukin-1 and tumor necrosis factor?
1) increased leukocyte adherence2) Increased prostacyclin synthesis3) Increased procoagulant activity4) decreased anticoagulant activity5) Increased Interleukin and platelet derived growth factor
112
What are the fibroblast effects activated by interleukin-1 and tumor necrosis factor?
1) increased proliferation2) increased collagen synthesis3) increased collagenase4) increased protease5) increased prostaglandin synthesis
113
What are the leukocyte effects activated by interleukin-1 and tumor necrosis factor?
Increased cytokine secretion (interleukin 6 and 8)
114
What does long term tumor necrotic factor production lead to?
Cachexia (wasting away syndrome)
115
What leads to the pathogenesis of fever?
TNF and IL-1 that changes the set point of internal temperature in the hypothalamus
116
What are two types of edema?
Exudate and Transudate
117
What is exudate made of?
It is rich in protein and blood cells and are typical of inflammation
118
What is transudate made of?
- Contains less protein and fewer cells
| - an ultra-filtrate of plasma fluid
119
What is a typical cause of transudate?
Typical of hydrostatic or osmotic pressure pathology
120
What is the specific gravity of transudate?
Specific gravity is usually less than 1.012 and a protein content of less than 2gm/100mL
121
What are some factors towards the pathogenesis of Edema?
1) increase in hydrostatic pressure2) Increase in wall permeability3) Decrease oncotic pressure (decrease albumin concentration)4) Lymphatic obstruction
122
Is transudate hypocellular or cellular?
Hypocellular
123
Is transudate protein rich or poor?
Protein poor
124
What is the specific gravity of transudate?
Specific gravity <1.012
125
What is transudate due to?
Increased hydrostatic pressureDecreased Oncotic pressureNa+ retention
126
Is exudate hypocellular or cellular?
Cellular
127
Is exudate protein rich or poor?
Protein rich
128
What is the specific gravity of exudate?
Specific gravity >1.020
129
What is exudate due to?
Lymphatic obstruction or Inflammation
130
What are the 4 mechanisms of MMP regulation?
1. regulation of synthesis by growth factors or cytokines. 2. Inhibition of synthsis by corticosteroids or TGF-beta. 3. secreted in inactive form. 4. Blockage of the enzymes by specific tissue inhibitors of metalloproteinase.
131
The inflammation phase of wound healing lasts how long?
3 days.
132
The granulation tissue phase of the healing process takes place when?
0.3 days until 10 days.
133
The wound contraction phase of the healing process takes place when?
3 days to 30 days.
134
What will clean up an injured site after the healing process?
Macrophages.
135
What type of scaring occurs with primary intention healing?
Minimal scarring
136
What type of scaring occurs with secondary intention healing?
Broader scar result of granulation
137
What type of scaring occurs with tertiary intention healing?
Wound is purposely left open
138
What type of injury is primary intention healing?
Little tissue loss.
139
Most surgical wounds heal by which intention?
Primary intention healing. (wound edges are directly next to each other)
140
How is a primary intention wound is closed?
By sutures, staples or adhesive.
141
What is allowed to happen to the wound with secondary intention healing?
It is allowed to granulate.
142
Why can the healing process be slower with secondary intention healing?
Due to the presence of drainage from infection and surgeons may pack the wound with gauze or use a drainage system.
143
How long will a tertiary intention scar be left open?
4-5 days.(where the wound is initially cleaned, debrided and observed before closure)
144
What is Keloid?
Excess collagen deposition in the skin forming a raised scar.
145
What is inflammation?
The reaction of the blood vessels, leading to the accumulation of fluid and leukocytes in the extravascular tissues
146
What is the function of inflammation?
A protective response- eliminate microbes and toxins- eliminate necrotic cells and tissues- prepare for tissue repair
147
What do neutrophils do?
First responder (acute inflammation) bacterial or fungal infection
148
What forms pus?
Increased activity and death of neutrophils
149
What general percentage of WBC's do neutrophils make up?
60%
150
What do lymphocytes do?
Chronic inflammation- T cell and B cell response/activation
151
What general percentage of WBC's do lymphocytes make up?
30%
152
What do monocytes do?
Long lived Phagocyte that present pathogen parts to T cells
153
What are monocytes when they are in tissue?
Macrophages
154
What general percentage of WBC's do monocytes make up?
5-6%
155
What do eosinophils do?
Parasite and Allergic response
156
What general percentage of WBC's do eosinophils make up?
2-3%
157
What do basophils do?
Allergic and antigen response and releasing the chemical histamine
158
What are basophils when they are in tissue?
Mast Cells
159
What general percentage of WBC's do basophils make up?
<1%
160
What is the order from largest to smallest of the WBC's?
NeutrophilsLymphocytesMonocytesEosinophilsBasophils(Never Let Monkeys Eat Bananas)
161
Where do T lymphocytes mature?
Thymus
162
Where do B lymphocytes mature?
Bone maroow
163
Are thrombocytes WBCs?
No they are platelets
164
What is the function of thrombocytes?
To plug up holes
165
What is the life span of an RBC?
120 days
166
What is the life span of WBC?
days to years
167
What is the life span of a platelet?
8 days
168
What are the two types of inflammation?
Acute and Chronic
169
What is the duration and onset speed of acute inflammation?
Rapid onset and short duration (min/hours/days)
170
Is there edema with acute inflammation?
Yes
171
What type of leukocyte is predominantly present with acute inflammation?
Predominantly neutrophils, but also eosinophils and antibody mediated
172
What is the duration and onset speed of chronic inflammation?
Slower onsetLong duration (wks, months, years)
173
What are some characteristic appearances of chronic inflammation?
Presence of new blood vessels, fibrosis, and tissue necrosis
174
What type of leukocyte is predominantly present with chronic inflammation?
Predominantly macrophages and lymphocytes
175
What are the key signs and symptoms of acute inflammation?
1) Redness2) Heat3) Swelling4) Pain5) Loss of function
176
What is the Latin term for redness?
Rubor
177
What is the Latin term for heat?
Calor
178
What is the Latin term for swelling?
Tumor
179
What is the Latin term for Pain?
Dolor
180
What is the Latin term for Loss of function?
Functio laesa
181
What vascular changes occur with inflammation?
1) Vascular dilation and increased blood flow (causing erythema and warmth)2) Extravasation and deposition of plasma fluid and proteins (edema)3) Leukocyte emigration and accumulation in the site of injury
182
What is the net flow of fluid of microvasculature in normal circulation?
Small flow out of the precapillary arteriole but returned in the precapillary venuole
183
What happens to the net flow of the microvasculature with acute inflammation?
Arteriole pressure is increased and the mean capillary pressure is increased due to arteriolar dilation. The venous pressure increases and the osmotic colloidal pressure is reduced due to protein leakage across the venule which results in an excess of extravasated tissue
184
What is oncotic pressure?
Pressure bringing in fluid into vasculature from tissue due to albumin concentration
185
What causes oncotic pressure?
Albumin concentration
186
What controls arteriole pressure?
Sphincters of muscles that clamp off blood flow
187
What collects the small flow out of the capillary bed?
Lymphatic system
188
What is hyperemia?
Increased blood flow
189
What occurs with the precapillary sphincter during normal circumstances?
The precapillary sphincters are closed
190
What occurs with the precapillary sphincter during acute inflammation?
The precapillary sphincters are open
191
During normal flow how are the RBC's and platelets and neutrophils distributed?
Scattered
192
Where in a circulatory vessel is the flow the fastest?
The middle because of laminar flow
193
What is the term for the stacking of RBCs as they move towards laminar flow?
Rouleaux of RBC
194
What does marginalization of neutrophils refer to?
When the neutrophils are pushed aside and moving towards the endothelium
195
What is the rouleaux relation to erythrocyte sedimentation rate?
It elevates the ESR
196
What are the steps of leukocyte extravasation?
1) Margination2) Pavementing3) Extravascular migration
197
What is the main leukocyte of margination?
Neutrophils
198
What are the parts of the pavementing stage of leukocyte extravasation?
1) rolling2) tight binding3) diapedesis/migration
199
What are some parts of tight binding of the pavementing stage of leukocyte extravasation?
1) integrin activation2) stable adhesion
200
What occurs in extravascular migration?
Chemokines and cytokines direct the leukocyte to go to specific area
201
What are the 3 steps of phagocytosis of a particle?
1) recognition and attachment- microbes bind to phagocyte receptors2) engulfment- phagocyte membrane zips up around microbe3) killing and degradation- fusion of phagosome with lysosome- killing of microbes by lysosomal enzymes in phagolysosome
202
What 2 groups are the mediators of inflammation divided into?
1) plasma derived2) cell derived
203
Do mediators of inflammation act only on a single cell?
No, they are multifunctional and act on many cells and tissues
204
Are mediators of inflammation biochemically the same or diverse?
Biochemically diverse including biogenic amines, peptides and arachidonic acid derivatives
205
What is a histamine?
Biogenic amine that is from a cell derived source (stored in cell)
206
Where histamines released from?
Platelets and mast cells
207
What is the function of histamine?
Stimulates retraction of endothelial cells of the venules and leads to gaps therefore increased permeability
208
Is the action of histamine short or long and why?
The action of histamine is short because it is inactivated by histaminase
209
What vitamin stabilizes mast cells?
Vitamin C, during an acute response
210
What is bradykinin?
Plasma protein in the liver that is derived from kininogen through the enzymatic action of kallikrein?
211
what is Kallikrein do and what is it activated by?
Kallikrein acts on the clotting and fibrinolytic systems of the blood and activated by Hageman factor
212
What does bradykinin induce?
Pain
213
What is the relationship between bradykinin and histamine?
They both have a similar action
214
What were the mast cells called before they exited the blood vessel?
Basophils
215
What does neoplasia mean?
New Growth
216
What does tumor mean?
Swelling, formation of masses
217
What does cancer mean?
Tissue invasion appearance like crawling crab
218
What does oncology mean?
Study of Swelling
219
What does carcinoma in situ mean?
Means "in its place" but is a tumor that has not penetrated the basement membrane
220
Are all tumors a neoplasia?
Yes
221
Is a neoplasia always a tumor?
No, sometimes there's no distinct mass as in leukemia or malignant disease of bone marrow
222
What are the 3 types of reversible plasias?
1) Hyperplasia2) Metaplsia3) Dysplasia
223
What are the 3 types of irreversible plasias?
1) anaplasia2) neoplasia3) desmoplasia
224
What is anaplasia?
Irreversible Abnormal cells lacking differentiation; like primitive cells equated with undifferentiated malignant neoplasms
225
What is desmoplasia?
Irreversible Fibrous tissue formation in response to neoplasm
226
What are the two classifications of tumors?
BenignMalignant
227
How are tumors classified?
Histologically
228
How do the growths of benign and malignant tumors differ?
Benign tumors are slow and expansive and malignant tumors are fast and invasive
229
Are both benign and malignant tumors metastatic?
No, Benign tumors are not metastatic
230
How do the external surface features of benign and malignant tumors differ?
Benign = smoothMalignant = irregular
231
Do both benign and malignant tumors have capsules?
No, only benign tumors have capsules
232
Are both benign and malignant tumors capable of necrosis?
No, only malignant tumors are capable of necrosis
233
Are both benign and malignant tumors capable of hemorrhage?
No, only malignant tumors are capable of hemorrhage
234
How does the architechture of benign and malignant tumors differ?
Benign = resembles normal tissue of originMalignant = Does not resemble normal tissue of origin
235
How does the cells of benign and malignant tumors differ?
Benign = well differentiatedMalignant = Poorly differentiated
236
How do the nuclei of benign and malignant tumors differ?
Benign = normal size and shape; uniformMalignant = pleomorphic (variable in shape)
237
How does the mitosis of benign and malignant tumors differ?
Benign = few in mitosisMalignant = many and irregular
238
What is a regular nuclear to cytoplasmic ratio?
1:06
239
What does a nuclear to cytoplasmic ratio of 1:2 or 1:3 signify?
It means they are neoplastic
240
What does metastasis mean?
Change in position
241
What are the main pathways of metastasis?
1) lymphatics2) blood (hematogenous spread)3) Seeding surface of body cavities (transcoelomic spread)
242
What are some other pathways of metastasis?
Intraepithelial
243
What are the steps of hematogenous metastatic cascade?
1) primary tumor2) metastatic clone evolves3) proliferation of the clone and invasion of vessel4) transport by circulation5) emobilization6) invasion7) new tumor formation at the site of metastasis
244
What is transcoelomic spreading?
Direct seeding of a cavity by neoplastic cells within that cavity therefore there is no plane of resistance to spreading
245
What is intraepithelial spread?
1) Tumor cells infiltrate between the cells of normal epithelium without invading the underlying stroma
246
What is the best example of intraepithelial spread?
Paget's disease of the nipple where cells of ductal carcinoma in situ grow into nipple skin and resemble eczema
247
What is tumor-induced angiogenesis?
The biologic role of tumors to overcome limitation of nutrient and oxygen delivery
248
What do mesenchymal tumors with the -oma ending mean?
It stands for a mesenchymal benign tumor
249
What do mesenchymal tumors with the -sarcoma ending mean?
It means that it is a mesenchymal malignant tumor
250
What do epithelial tumors with the adenoma ending mean?
It is a benign epithelial tumor
251
What do epithelial tumors with the carcinoma ending mean?
It is a malignant epithelial tumor
252
What are the three exceptions to the "oma" being benign rule? Why?
LymphomaMultiple myelomaGliomaBecause they only exist via blood cells, lymph system and glial cells
253
What is common between squamous cell carcinoma and adenocarcinoma?
They both are surrounded by non-neoplastic stroma
254
What are some tumors of blood cells and lymphocytes?
LeukemiaLymphomaMultiple Myeloma
255
What are some tumors of neural cells?
GanglioneuromaNeuroblastoma
256
What are some tumors of glial and nueral suporting cells?
Glioma and meningioma
257
What are some germ cell tumors?
Teratoma, embryonal carcinoma and seminom/dysgerminoma
258
What are blastomas?
Blastomas are malignant tumors composed of embryonic cells originating from embryonic primordia
259
What is a teratoma?
Teratomas are derived from germ cells and contain tissues that are formed from all three germ layers: etoderm, mesoderm and endoderm
260
What are eponymic tumors?
These tumors carry the name of physicians who have described them first
261
What does Hodgkin's disease affect?
lymph nodes
262
What does Ewing's sarcoma affect?
Bones
263
What does Kaposi's sarcoma affect?
Skin
264
What is tumor staging based on?
Clinical assessment during gross examination, surgery, x-ray examinations
265
What is the grading of tumors based on?
Based on histologic examination
266
What does the TNM system of staging take account for?
T = size of tumorN = presence of lymph node metastasesM = Distant metastases
267
What is the grading scale of the TNM system?
0-4 in each category TNM
268
What grading of M signifies metastases?
a 1 represents metastasis
269
What do the roman numeral stages of tumor range from?
0 to IV
270
What is a stage 0 tumor?
A carcinoma that is in situ
271
What is a stage I cancer?
Cancer that is localized to one part of the body
272
What is a stage II cancer?
A locally advanced (same as stage III but specific criteria differ according to diagnosis)
273
In Hodgkin's disease what is the difference between stage II and stage III?
Stage II: lymph nodes on only one side of the diaphragmStage III: lymph nodes above and below the diaphragm
274
What is a stage IV cancer?
Canvers that have metastasized or spread to other organs or throughout the body
275
what is the Ann Arbor staging for? and what stages are there?
For lymphomas ranging from stage I - IV
276
What is a stage I in the Ann arbor staging?
Cancer is located in a single region, usually one lymph node and the surrounding area. Stage I often will not have outward symptoms
277
What is a stage II in the Ann arbor staging?
Cancer is located in two separate regions, an affected lymph node or organ within the lymphatic system and a second affected area, and that both affected areas a confined to one side of the diaphragm (ie: both are above the diaphragm or both are below the diaphragm)
278
What is a stage III in the Ann arbor staging?
Cancer has spread to both sides of the diaphragm, including one organ or area near the lymph nodes or the spleen
279
What is a stage IV in the Ann arbor staging?
Diffuse or disseminated involvement of one or more extralymphatic organs, including any involvement of the liver, bone marrow, or nodular involvement of the lungs
280
What does the tumor grades range from?
Grade I - III
281
What is tumor grading based on?
Histologic examination
282
What is a grade I tumor?
well differentiated
283
What is a grade II tumor?
Moderately well differentiated
284
What is a grade III tumor?
undifferentiated
285
Overall, which has more predictive value, grading or staging of tumors?
Staging
286
Is the difference between normal and malignant cells qualitative or quantitative?
Quantitative
287
Are cancer cells more or less adapted to survive unfavorable conditions and are they more or less differentiated than normal cells?
Cancer cells are less differentiated and more adapted to survive under unfavorable conditions as they require less oxygen to survive
288
In which gender has deaths from lung cancer plateaued? and which is continuing to rise?
Males = plateauFemales = rise
289
Is cancer the leading cause of death in the US?
No it is number 2, heart disease is 1st
290
Define Incidence
The number of new cases that have been registered over a specific time in a defined population
291
Define prevalence
The number of all cases, new and old, within a defined population at a defined time
292
Define Mortality
The number of deaths attributed to cancer during a specified period in a defined population
293
Define morbidity
number suffering from a disease that has been registered over a specific time in a defined population
294
What is the most important risk factor and most common initial symptom for lung cancer?
Smoking -> Cough
295
What is the most important risk factor and most common initial symptom for breast cancer?
Family history of cancer -> lump
296
What is the most important risk factor and most common initial symptom for colon cancer?
Family history of colonic polyps -> blood in stool
297
What is the most important risk factor and most common initial symptom for cervix cancer?
Promiscuity (early intercourse or multiple partners) -> vaginal bleeding (spotting)
298
What is the most important risk factor and most common initial symptom for uterus cancer?
Hormonal: imbalance and treatment -> vaginal bleeding
299
What is the most important risk factor and most common initial symptom for skin cancer?
Sun exposure -> sun lesion
300
What is the most important risk factor and most common initial symptom for prostate cancer?
Old age -> dysuria
301
What cancer has the highest incidence in men?
Prostate
302
What cancer is the second highest incidence in men and women?
Lung & bronchus
303
What cancer is the third highest incidence in men and women?
Colon & rectum
304
What cancer has the highest incidence in women?
Breast
305
What cancer has the highest mortality in men and women?
Lung & bronchus
306
What cancer has the third highest mortality in men and women?
Colon & rectum
307
What cancer has the second highest mortality in men?
Prostate
308
What cancer has the second highest mortality in women?
Breast
309
Where does metastatic cancers usually travel to?
LiverLungBrainBone
310
What does metastatic cancer usually indicate?
A poor pronosis
311
How does the insertion part of viral carcinogens?
Slow transforming oncogenic RNA viruses, insert into the genome and activate a latent cellular oncogene, which is then capable of transforming the normal cell into a malignant cell
312
What are the different types of human carcinogenic viruses?
DNA viruses and RNA viruses
313
What are some examples of human carcinogenic DNA viruses?
- Human Papilloma virus- Epstein-Barr virus- Hepatitis B and C virus- Kaposi's sarcoma-associated herpesvirus
314
What are the types of HPV that can cause cervical, penile/anal carcinoma?
16 and 18
315
What can epstein-barr virus cause?
Burkitt's lymphoma (B cell neoplasia)Nasopharyngeal carcinoma
316
What can Hepatitis B and C virus cause?
Liver cancer
317
What can Kaposi's sarcoma-associated herpesvirus cause?
Kaposi's sarcoma, a type of skin cancer
318
What is a type of RNA virus and what can it cause?
Human T-cell leukemia/lymphoma virus and it can cause adult T cell leukemia (HIV group)
319
What are human oncogenes?
Homologous to viral oncogenes and thus called cellular oncogenes
320
What do human oncogenes represent?
Represent activated normal genes (proto-oncogenes)
321
How does an oncogene function?
An oncogene has gained function and becomes a cancer-inducing agent
322
How many damaged allele does it require to activate an oncogene?
Only 1 damaged allele
323
What are different ways of transformation of proto-oncogenes into oncogenes?
1) point mutation2) gene amplification3) chromosomal rearrangement4) insertion of viral oncogene
324
What do tumor suppressor genes do?
Protect the cells against activated or newly acuired oncogenes
325
What happens to a tumor suppressor gene that has lost function?
It is no longer a cancer-inhibiting agent
326
How many tumor suppressor gene alleles out of the two need to be lost in order for expression of disease?
Both alleles
327
What are different types of Hereditary cancer?
1) Neurofibromatosis type 12) familial adenomatous polyposis coli3) Wilms' tumor4) Skin tumors in xeroderma pigmentosum5) chromosomal fragility syndromes (Bloom's syndrome, Fanconi's syndrome)
328
What are some cells that pose an immune response to tumors?
1) Natural Killer Cell2) Macrophage3) Neutrophil4) B lymphocyte5) Cytotoxic T lymphocyte
329
What is the immunotherapy of Cancer?
1) some tumors involute spontaneously under the influence of immune factors2) BcG (attenuated tuberculosis bacillus of calmette and Guerin) is used for treatment of bladder cancer3) Tumor vaccines are used for treatment of melanoma and renal cell carcinoma
330
Should tumor markers be used as a primary tool for cancer diagnosis?
No
331
What should tumor markers be used for?
Confirming a diagnosis, to monitor for tumor recurrence and to monitor response to therapy
332
What is the Tg tumor marker detect?
Thyroglobulin. Thyroid cancers
333
What is active hyperemia?
Dilatation of arterioles leading to blushing, exercise, inflammation
334
What is passive hyperemia?
Venous back pressure; often associated with hydrostatic edema, cyanosis- heart failure - pulmonary edema and heart failure cells
335
What does a chronic passive congestion of lungs lead to?
Leads to edema and RBC extravasation into alveoli
336
What is a chronic passive congestion of lungs accompanied by?
Accompanied by anoxia & often results in pulmonary fibrosis
337
In a chronic passive congestion of the lungs, what does an alveolar macrophage do?
Alveolar macrophages take up RBC & degrade hemoglobin = hemosiderin accumulation
338
Cardiac hemorrhage is often what? And what is it caused by?
- often fatal
| - MI, Gun Shot Wound, stabbing wound
339
What is an aortic hemorrhage caused by?
- MVA (organs kee moving at a high speed and rips off part of aorta via ligamentum arteriosum - weakness due to copper deficiency -> aneurysm
340
What will an arterial hemorrhage look like? What causes it?
- penetrating wound, fractured bones
| - presents as a bright red, pulsating/squirting
341
What will cause a capillary hemorrage? What does it do to venous pressure?
- Trauma, weakness due to vitamin C (scurvy) -increase in venous pressure
342
With the venous, how does it present as a hemorrhage?
Dark/bluish color, oozing
343
In a hemorrage what are some signs and symptoms?
- Intracerebral hemorrhage
- Hematemesis or hemoptysis
- Cardiac hemorrhage
- Venous hemorrhage
- Aortic hemorrhage
- Capillary hemorrhage
- hematochezia or melena (from anus)
- Hematuria
344
What are some clinically important forms of hemorrhage?
- skin/surface hemorrhage
- large accumulation of blood in body cavities/space
- hemoptysis
- epistaxis
345
What are some different types of skin/surface hemorrhage?
- petechia
- purpura
- ecchymosis
346
What is a petechia?
<1 mm and speckles of blood vessels
347
What is purpura?
Between 1 mm- 1cm and larger blotches
348
What is ecchymosis?
Large/blotchy bruises
349
What are some large accumulation of blood in body cavities/spaces?
Hemothorax, hemopericardium, hemoperitoneum, or hemarthrosis
350
What is a hemoptysis?
Respiratory tract/expectoration of blood
351
What is a epistaxis?
Nose bleed
352
What is hematemesis?
Vomiting blood
353
What is hematochezia
anorectal bleeding
354
what is melena
passage of black blood in stool
355
what is hematuria
blood in urine
356
What is metrorrhagia?
bleeding not related to normal monthly menses
357
what is menorrhagia?
Profound menstrual bleeding
358
What happens in a massive hemorrhage?
Blood loss, hypovolemic shock, exsanguination, death
359
If <500 ml of blood is lost what happens?
homeostatic compensation but it is reversible
360
If 1000-1500 ml of blood is lost what happens?
Circulatory shock
361
If >1500 ml of blood is lost what happens?
Lethal
362
What are some of the types of hemorrhage?
- Massive hemmorhage
- Hematoma
- Intracerebral hemorrhage
- Chronic hemorrhage
363
What can an intracerebral hemorrhage lead to?
Stroke, death
364
What can a chronic hemorrhage lead to?
Slow blood loss, iron deficiency anemia (70 ml for normal menstruation)
365
Which hemorrhage has a better outcome, Subdural or epidural hemorrhage?
A subdural hemorrhage because the lower pressure veins bleed more slowly than arteries
366
What Is the different types of pathogenesis causes of Edema?
1) Inflammatory2) Hydrostatic3) Oncotic4) Obstructive5) Hypervolemic
367
Why does inflammatory lead to the pathogenesis of edema?
Increases permeability & hyperemia
368
How does hydrostatic lead to the pathogenesis of edema?
Increased arterial pressure (hypertension)Increased venous back pressure (heart failure)
369
How does the oncotic pressure lead to the pathogenesis of edema?
Hypoalbuminemia due to:-loss/proteinuria- decreased protein synthesis
370
How does the obstruction lead to the pathogenesis of edema?
- Most often b tumor or chronic inflammation- Filaria (worm) -> elephantiasis
371
How does hypovolemia lead to the pathogenesis of edema?
Usually d/t sodium and water retention:- kidney function, renin, angiotensinogen, & aldosterone- Kidney disease -> increased renin release -> angiotensinogen -> increased aldosterone -> increased Na retention -> increased water retention
372
What are some clinical forms of edema?
1)Cerebral edema2) Pulmonary edema (d/t left-sided heart failure, post-surgery)3) Pitting edema of the lower extremities4) Periorbital (facial) edema5) Hydrothroax6) Hydropericardium7) Hydroperitoneum (ascites)8) Anasarca (Extremegeneralized edema)
373
What is TORCH(ES) syndrome?
a medical acronym for a set of perinatal infections (i.e. infections that are passed from a pregnant woman to her fetus).
374
When should we test for TORCH(ES) syndrome?
Early in pregnancy.
375
What will the T in Torches syndrome stand for and how do we get it?
Toxoplasma we get it from cat shit so stay away from Julie.
376
What will the O in TORCHES syndrome stand for?
Others that are less common like Epstein-Barr virus, Varicella virus, Listeria monocytogenes, leptospira.
377
What will the R in TORCHES syndrome stand for?
Rubella.
378
What will the C in TORCHES syndrome stand for?
Cytomegalovirus (CMV).
379
What will the H in TORCHES syndrome stand for?
Herpesvirus.
380
What will the (ES) in TORCH(ES) syndrome stand for?
Syphylis.
381
What does rubella cause?
1) Small (microcephaly)/strucuraly abnormal brain2) Heart defects.
382
What will Toxoplasma cause?
1) Microcalcification of basal ganglia and dilation of lateral ventricles (hydrocephalus)2) CNS defects.
383
What will cytomegalovirus (CMV) cause?
The same as Toxoplasma.
384
What will herpesvirus affect?
1) CNS defects2) Skin lesions.
385
What are 2 types of chromosomal anomalies?
Structural and numerical anomalies
386
What is Aneuploidy?
Loss or gain of chromosomes.
387
What are 2 types of aneuploidy?
Hyperdiploidy- 46+1 or 46+2. Hypodiploidy- 46-1 or 46-2.
388
What is monosomy?
Missing one chromosome
389
What is Trisomy?
Gaining an extra chromosome (3 of one chromosome)
390
What is the most common risk factor for Down syndrome?
Paternal age increases risk of having a baby born with down syndrome
391
What disorder is associated with Down syndrome?
Trisomy 21 (D= drinking age 21)
392
What disorder is associated with Edward's syndrome?
Trisomy 18 (E = election age 18)
393
What disorder is associated with Patau's syndrome?
Trisomy 13 (P = puberty age 13)
394
Of the 3 disorders Down, Edward's and Patau's, which one is most common?
Down Syndrome
395
What happens to a baby's hands with down syndrome?
Simian crease.
396
Down syndrome or trisomy 21 leads to what mental issues?
Most commonly leads to mental retardation
397
How will down syndrome affect the head?
Flat facial profile and epicanthic folds
398
How will down syndrome affect the heart?
Congenital heart defects like septum primum due to endocardial cushion defects.
399
How will down syndrome affect the limbs and feet?
HypotoniaA gap between first 2 toes.
400
What is the life expectancy with edwards sydnrome aka trisomy 18?
less than 1 year.
401
What will edwards syndrome cause?
Severe mental retardation.
402
How will edwards syndrome affect the head?
1) Prominent occiput2) micrognathia (small jaw)3) low set ears.
403
How will Down syndrome affect the umbilicus and intestines?
Causes umbilical hernia and intestinal stenosis
404
What is the incidence of down syndrome?
1 in 700 births
405
How will edwards syndrome affect the heart?
Congenital heart defects will be present.
406
How will edwards syndrome affect the hands and feet?
Hands- Clenched hands Feet- Rocker-bottom feet.
407
What is the life expectancy with down syndrome?
45-50 years old
408
What is the incidence of Edward's syndrome?
1 in every 8000 births
409
What some limb changes with Edward's symptoms
Limited hip abductionRocker bottom feet
410
What is the incidence of Edward's syndrome?
1 in 8000
411
What are some neurological issues with patau symptoms?
Microcephaly and mental retardation
412
What are some head changes with patau symptoms?
Cleft lip and palateMicrophthalmia
413
What are some limb issues with patau symptoms?
1) Polydactylyl2) Focker -bottom feel
414
What is the incidence of Patau syndrome?
1 in 15000
415
What is the life expectancy of Down syndrome?
45-50
416
What is the life expectancy of Edwards syndrome?
<1 year
417
What is the life expectancy of Patau syndrome?
<1 year
418
In which disorder(s), (Downs, Edwards, Patau) does mental retardation occur?
Yes, severe in Edwards and Patauand the most common cause is Down Syndrome
419
What are some other disease risks for Down Syndrome?
ALL, Alzheimer's >age 35
420
What are two disorders that are caused by abnormalities of sex chromosomes?
1) Turner syndrome2) Klinefelter syndrome
421
Who can get turner's syndrome and who can get Klinefelter's syndrome?
They are abnormalities of sex chromosomes so only females can get Turners and Only males can get Klinefelter's syndrome.
422
Pathogenesis of sex chromosome abnormalities are due to what?
Nondisjunction.
423
What is nondisjunction?
Failure of paired chromosome to separate.
424
How common is Turners syndrome?
1 in every 3,000 female births.
425
What are the symptoms of Turners syndrome? (It's super long, sorry)
1) Short stature2) heart- shaped face3) low posterior hairline4) webbing of neck5) heart disease and coarctation of aorta6) broad chest and widely spaced nipples7) pigmented nevi (moles)8) cubitus valgus(elbows turned in)9) streak ovaries, hypoplastic uterus, amenorrhea10) peripheral lymphedema at birth.
426
Are Turner's considered male or female?
Female presentation
427
What symptoms will Klinefelter's syndrome present with?
1) Tall long arms and legs2) lack of beard body hair and pubic hair3) gynecomastia4) female like hips5) testicular atrophy.
428
Is Klinefelter syndrome considered male or female?
Male presentation (based on penis presentation)
429
What type of disorder is spherocytosis?
A congenital RBC membrane disorder. IT is an autosomal dominant disease.
430
What are 3 possible symptoms of spherocytosis?
anemia, jaundice, splenomegaly.
431
How is spherocytosis diagnosed?
requires demonstration of increased RBC osmotic fragility and negative direct antiglobulin test.
432
How often will spherocytosis patients less than 45 years old need a splenectomy?
Rarely.
433
With spherocytosis what causes RBC abnormalities?
Alterations in membrane proteins.
434
What alternations in membrane proteins of RBC happens with spherocytosis?
Surface area is decreased disproportionately to the intracellular content.
435
What will decreased surface area of a RBC membrane cause?
Flexibility needed for the cell to traverse the spleen's microcirulation.
436
With western treatments how will spherocytosis be cured?
Splenectomy.
437
Presence of spherocytes in the peripheral blood smear suggest what?
1. Hereditary spherocytosis (HS). 2. Autoimmune hemolytic anemia (AIHA).
438
When there are spherocytes in the peripheral blood smear how can you distinguish between hereditary spherocytosis or autoimmune hemolytic anemia?
Coomb's test.
439
What will a negative and positive Coomb's test mean?
Negative- Hereditary spherocytosis. Positive- Autoimmune hemolytic anemia.
440
Huntington's disease is what type of disorder?
An autosomal dominant characterized by chorea and progressive cognitive deterioration.
441
How will Huntington's disease be diagnosed?
Genetic testing.
442
What is treatment of Huntington's disease like?
Supportative.
443
What type of relatives of patients with Huntington's disease should be tested?
first-degree relatives.
444
Will Huntington's disease effect males or females more?
Both equal.
445
What parts of the CNS will Huntington's disease effect?
Caudate nucleus atrophies, medium spiny neurons in the corpus striatum degenerate, and levels of neurotransmitters gamma aminobutyric acid and substance P decrease.
446
What genes are effected with Huntington's disease?
Gene on chromosome 4.
447
The gene on chromosome 4 (Huntington's disease) will lead to what?
Abnormal repetition of DNA sequence CAG that codes for amino acid Glutamine.
448
The gene product of abnormal CAG codes that make glutamine leads to what?
a large protein called huntingtin and it has large stretches of polyglitamine residue.
449
How will the huntingtin protein lead to huntington's disease?
Unknown.
450
The more CAG repetitions means what?
The earlier the disease begins and the more severe the effects.
451
What will huntington's disease be like from generation to generation?
over time it leads to more severe phenotype and more CAG codes that make more polyglitamine residues.
452
How do Symptoms of Huntington's disease develop?
Insidiously (inconspicuous or seemingly harmless way ).
453
When do Signs and symptoms of Huntington's disease develop?
start between 35-50, but can develop before adulthood.
454
What are the signs and symptoms of Huntington's disease?
Dementia or psychiatric disturbances, abnormal movements including tongue protrusion.
455
Death usually occurs how long after the first signs and symptoms of Huntington's disease appear?
13-15 years.
456
What will the cause of death usually be with Huntington's disease?
Coronary heart disease or pneumonia
457
What is the secondary or aquired immunodeficiency?
AIDS aquired immunodeficiency syndrome.
458
What will cause severe combined immunodeficiency, and what type of immunodeficiency is it?
It is primary and caused by a defect of lymphoid stem cells pre-B, Pre-T cells.
459
What is the most common type of primary immunodeficiency diseases?
Isolated deficiency of IgA.
460
What % of people have Isolated deficiency of IgA?
1 out of every 700 people
461
What is isolated deficiency of IgA like in the population?
Often asymptomatic.
462
What type of immunodeficiency disease is DiGeorge's syndrome and what causes it?
It is a primary one caused by T-cell deficiency related to aplasia of thymus associated with aplasia of parathyroid glands.
463
What type of virus is HIV aka Human immunodeficiency virus?
RNA retrovirus.
464
AIDS infects what?
T helper Cells (CD4+).
465
Where is AIDS stored at?
Macrophages and related phagocytic cells.
466
What are the clinical presentations of HIV/AIDS?
acute illness, asymptomatic infection, persistent generalized lymphadenopathy.
467
What are 5 pahtologic findings in AIDS?
1. Lymphadenopathy. 2. Kaposis sarcoma. 3. Nephrophaty. 4. Weakness. 5. oral thresh.
468
What type of infections happen with AIDS?
Opportunistic.
469
What 3 places are prone to opportunisitic infections?
1. Lungs. 2. GI tract. 3. CNS.
470
What are the 3 tumors that develop with AIDS?
1. Lymphoma of lymph nodes or GI tract. 2. Lymphoma of the CNS. 3. Kaposis sarcoma.
471
All antibodies are composed of what?
Light and heavy chains.
472
Which chains of antibodies are changeable and which chain is the same?
Light- same. Heavy are specific for each Ig.
473
What is another name for light and heavy chains?
Light-Fc. Heavy-Fab.
474
What is the largest Ig?
IgM.
475
What is the function of the IgM?
To neutralize microorganisms.
476
The IgM has how many complement binding sites?
five.
477
What is the first Ig to appear?
IgM.
