General Pathology Flashcards
1
Q
What are the 4 aspects of a disease process?
A
- Etiology - cause
- Pathogenesis - mechanism
- Morphology - appearance
- Functional consequences
2
Q
What are the possible outcomes of cellular stress?
A
- Cell adaptation
- Temporary abnormality with recovery
- Permanent structural damage
- DNA damage/mutation
- Cell death
3
Q
What are the 6 major causes (etiologies) of cellular injury?
A
- Physical - trauma
- Chemical - drugs, ETOH
- Metabolic - hypoxia, vitamin def, glycemia
- Immunologic - allergy/autoimmunity
- Genetic - chromosomnal abnormality
- Infection - bacteria, virus, parasite
4
Q
What types of cells are the most susceptible to injury?
A
Metabolically active cells
5
Q
What changes can be seen under the light microscope during reversible cell injury?
A
- Cellular swelling/hydropic change and vacuolization
2. Fatty changes
6
Q
What is vacuolization?
A
Small, clear vacuoles within the cytoplasm; these
represent distended and pinched-off segments of the endoplasmic reticulum
7
Q
Injured cells stain more intensely with: H or E
A
E – more pronounced and pink with greater injury
8
Q
The 4 major systems of the cell particularly vulnerable to cell injury:
A
- Membranes– cell, ER, lysosomes
- Energy production
- Proteins/enzymes (structural+regulatory)
- DNA-nucleus
9
Q
What is the commonly agreed upon point of no return in cellular injury?
A
Mitochondrial damage
10
Q
Often the target of toxic substances, which are not directly toxic, but suffer metabolic activation by target cell, i.e. CCl4
A
SER
11
Q
When an injurious agent affects the lysosomes, cell degeneration is said to occur. This can produce:
A
- Autophagy
- Hereditary absence of enzyme in lysosomes
- Failure degradation phag’ed material
- Liberation and activation of lysosomal enzymes (residual body)
12
Q
This event plays a central and common role in most pathological contidtions
A
Lack of oxygen!
13
Q
What are the 4 main mechanisms (not etiologies) of cellular injury?
A
- Hypoxia
- Free radicals
- Chemical injury
- Viral injury
14
Q
Reversible cell changes are known to occur when the duration of ischemia is short and in the following sequence:
A
- Impaired mitochondria (aerobic respir)
- Dec ATP
- Anaerobic glycolysis
- Glycogen depletion
- Intracellular acidosis with chromatin clumping
15
Q
Why does cell swelling occur?
A
Failure of Na/K ATPase pump to keep Na outside
+ accumulation lactate, inorganic phosphate
16
Q
What happens in reversible cell damage?
A
Cell swelling, detached ribosomes, blebs, myelin figures (dissociated lipoproteins), mitochondrial swelling
17
Q
Irreversible injury is characterized by:
A
- Severe vacuolization of mitochondria
- Damage to plasma membrane
- Swelling lysosomes
- Massive Ca++ influx
18
Q
What are the biochemical pathways involved in irreversible cell injury?
A
- Loss of phospholipids (dec. synthesis + breakdown)
- Cytoskeletal alterations (proteases, damaged connections)
- Free radicals
- Lipid breakdown products – free FA’s with detergent character
19
Q
Once re-oxygenation occurs in a cell so structurally damaged, what happens?
A
Influx of Ca++ into the cell and mitochondria, phospholipases, proteases, endonucleases, inflammatory mediators
20
Q
How does the body protect against free radicals?
A
Antioxidants, catalase, glutathione peroxidase, SOD)
21
Q
Why are free radicals so dangerous?
A
Lipid peroxidation, nucleic acid mutations, cross-linking of proteins for degradation
22
Q
Which is the major organ of lipid metabolism?
A
Liver
23
Q
Describe the fatty change of the liver in CCl4 poisoning.
A
CCl4–>CCl3 in the SER. Lipid peroxidation and cellular swelling; Accumulation of lipid in the ER, inability of the cells to synthesize lipoprotein necessary for triglycerides to leave the hepatic cell
24
Q
How do viruses affect cells?
A
Cell death (lysis), cell skeleton (respiratory cilia), fusion of cells, host immunological response
25
Under routine microscopy, the most recognizable cellular changes include:
Swelling and fatty chagne
26
Physiological apoptosis includes:
Embryogenesis, hormone-dependent involution, cell deletion, deletion of auto-reactive T cells, tumor growth control
27
What are the 5 major cell adaptations?
Hypertrophy, hyperplasia, atrophy, metaplasia, dysplasia
28
T/F Apoptotic cells are seen singly or in small clusters. Bright eosinophilic cytoplasm and condensed, irregular nuclei
T
29
Accumulation of this agent is associated with cellular aging or senescence.
Lipofuscin
30
Inflammation is a dynamic process that starts with.... and ends with...
Injury; healing/repair
31
T/F In order for inflammation to occur, the injury must be non-lethal
T
32
Differentiate between exudation and transudation
Exudate: has protein
33
Differentiate between acute and chronic inflammation.
Chronic: lymphocytes
Acute: PMN's
34
The most important feature of inflammation is the accumulation of: __________________________.
Leukocytes in the affected tissue
35
What is rouleaux?
RBC's become sticky and hence force the WBC's towards the periphery; aids in margination
36
Who are the most important chemotactic factors?
Bacterial products, complement fractions, arachidonic acid metabolites, cytokines/chemokines
37
During phagocytic engulfment, who is the second messenger?
Ca++
38
The 3 major steps of phagocytosis
1. Recognition/Attachment
2. Engulfment
3. Killing
39
What are the 5 key characteristics (clinical manifestations) of acute inflammation?
Redness, swelling, pain, heat, loss of function
40
The 4 major features of acute inflammation:
1. Vascular events
2. Cellular events
3. Phagocytosis
4. Mediators of inflammation
41
The major vascular events in acute inflammation
1. Vasoconstriction
2. Vasodilation
3. Increased vascular permeability
4. Increased blood viscosity
42
Explain the several mechanisms behind increased vascular permeability.
1. Histamine -- small venules
2. Cytokines -- cytoskel rearrangement
* *3. Endothelial injury (immediate sustained)**
4. WBC-dependent
5. Vascular endothelial growth factor
43
Describe the cellular events of acute inflammation.
1. Margination- sludging RBC/WBC towards periphery
2. Rolling- selectins
3. Adhesion- ICAM/VAM
4. Transmigration- PECAM
5. Chemotaxis- C5a, cytokines, chemokines
44
What are the 3 major steps of phagocytosis?
1. Recognition (opsonization)
2. Engulfment
3. Killing (ROS)
45
When leukocytes arrive at the site of cell injury, they will...
1. Engulf, degrade, complex bacteria and debris
2. Lysosomal enzymes
3. Chemical mediators
4. Toxic radicals
46
What is rouleaux?
Peripheral orientation of WBC's because of sludging of RBC's; WBC's pushed towards periphery
47
LFA-1 is also called
CD11a/CD18
48
MAC-1 is also called
CD11b/CD18
49
Who are the first leukocytes to arrive at the site of cell injury?
PMN's
50
Liquefactive necrosis
Hydrolysis -- BRAIN & BACTERIAL INFECTIONS
51
Coagulative necrosis
Classic -- happens everywhere except the brain
52
Caseous necrosis
TB/Lung
53
Fat necrosis
Occurs when lipases are freed; free fa's released and combine with calcium to form soaps
54
What are the 5 major types of necrosis?
1. Coagulative
2. Fat
3. Liquefactive
4. Caseous
5. Gangrenous
55
Among histamine and serotonin, which is only present in platelets (vs. mast cells/basophils)?
Serotonin
56
Who are the major cell-derived vascular permeability mediators in inflammation?
1. AA metabolites
2. PAF
3. Amines (histamine, serotonin)
4. Endothelins
57
Who are the major plasma derived chemical mediators of inflammation?
1. Coagulation/kinin system
| 2. Complement
58
Who is the most important plasma protein system of inflammation?
Complement
59
Granulomatous chronic inflammation is characteristic of which infections/diseases?
1. Infections: TB, syphillis, cat-scratch, fungi, protozoa
2. Persistent foreign body
3. Rheumatic fever
4. RA
5. Sarcoidosis
60
Trace the normal flow of lymphatic fluid
Lymph node --> general circulation --> RES
61
What are 5 major defects of leukocyte function?
1. Number circulating cells
2. Adherence
3. Migration/Chemotaxis
4. Phagocytosis
5. Microbicidal activity
62
What are the 4 major morphological patterns of acute/chronic inflammation?
1. Serous
2. Fibrinous
3. Suppurative/purulent
4. Sanguinous
63
Differentiate between granulomatous and non-specific chronic inflammation
Non-specific: mononuclear cells, C/T, fibroblasts
| Gran: R-E, macrophages, giant cells, rim of lymphocytes
64
Differentiate between granulomatous and non-specific chronic inflammation
Non-specific: mononuclear cells, C/T, fibroblasts
| Gran: R-E, macrophages, giant cells, rim of lymphocytes
65
Define abscess
Localized collection of pus (trypsin overwhelms and destroys damaged tissue)
66
Define paronychia
Side/Base of fingernail
67
Define Felon
Anterior portion of distal phalynx (secondary to penetrative wound)
68
Define empyema
Collection of pus in pleural cavity
69
Define pseudomembranous inflammation
Toxin/Fibrin/necrotic epithelial cells, WBC's on mucosal surfaces
70
Define sinus
Abnormal communication between solid organ/tissue and skin
71
The 4 organs with the best regenerative capacity
Liver, lung, kidney, spleen
72
What is the best way to accomplish cell growth in regeneration/repair?
Recruit cells from G0 into the cell cycle
1. Growth/stimulation factors
2. Loss of growth inhibitor
3. Cell-cell; cell-matrix interactions
73
What is the best way to accomplish cell growth in regeneration/repair?
Recruit cells from G0 into the cell cycle
1. Growth/stimulation factors
2. Loss of growth inhibitor
3. Cell-cell; cell-matrix interactions
74
The most important cell-cell/cell-matrix interaction in healing involves
Fibronectins (HMW adhesive glycoproteins) which bind to EC components and cell surfaces
75
Who produces fibronectin?
Fibroblasts, endothelial cells, monocytes
76
4 Major functions of fibronectin
1. Migration of new epithelial cells
2. Chemotactic for monocytes, fibroblasts
3. Stimulate endothelial cell migration
4. Release fibroblast growth factor from monocytes
77
4 Major functions of fibronectin
1. Migration of new epithelial cells
2. Chemotactic for monocytes, fibroblasts
3. Stimulate endothelial cell migration
4. Release fibroblast growth factor from monocytes
78
What does granulation tissue consist of histologically?
Meshwork of capillaries, fibroblasts, inflammatory cells, ECM
79
What does granulation tissue consist of histologically?
Meshwork of capillaries, fibroblasts, inflammatory cells, ECM
80
What is the objective of crust formation?
1. Stops bleeding
| 2. Barrier to infection
81
What are the 4 major factors influencing the rate of healing?
1. Age
2. Size of wound
3. Secondary infection
4. Diet (Vitamin C, D, protein)
82
What is amyloid? How does it appear under the light microscope? Congo red? Polarized light?
Abnormal ECF proteinaceous deposit
| H/E seen as glassy pink; Congo-red: red; Polarized light (apple green)
83
Amyloid: alpha-helix or beta-pleated?
Beta-pleated
84
The non-fibrillary component of amyloid is...
The P component, strong affinity for fibrils, made of serum-alpha-1-glycoprotein
* Similar in structure to CRP
85
What are the 2 major types of amyloid and what is the difference between them?
AL: Ig- light lambda chains (B cell malignancy)
AA: derived from serum AA (associated with chronic inflamm)
86
Which amyloid is associated with chronic disease?
SAA/AA
87
Describe the relationship between genetic disorders, age-related disorders, renal dialysis and amyloid.
Genetic - transthyretin in Fam. Amyloid Polyneuropathy
Age: B2 amyloid -- Alzheimers
Dialysis -- B2 microglobulin
88
What are the macroscopic descriptors for a liver/organ with amyloid?
Pale, waxy, firm
89
What is the general trend for an organ affected by amyloidosis?
Hypertrophy --> Atrophy
90
Heart amyloid: AL or AA
AL
91
The first organ usually affected by amyloidosis (my favorite!)
kidney
92
Lipofucsin is often the result of...
Free radical breakdown of intracellular membranes
93
Lipofuccsin usually accumulates in aging...
liver, cardiac, brain
94
Hemosiderin is best visualized using this stain
Prussian blue
95
Pts with hemochromatosis develop...
Heart failure, DM, cirrhosis
96
Pts with what pigment disorder are at an increased risk of HCC?
Hemochromatosis
97
Wilson's disease
Cu storage disorder (overload -- brain/liver)
98
Cause of dystrophic calcification...
Cell injury
99
Metastatic calcification is caused by...
hypercalcemia
100
Deposition of calcium in metastatic calcification occurs in these tissues...
Alveolar walls lungs, gastric mucosa, renal tubules, blood vessels
101
Risk factors for gout
Genetics, 20-30 years HU, ETOH, obesity, thiazides
102
Differentiate between primary and secondary gout
1: HGPRT/unknown enzyme (90%)
2: nuc. Acid turnover, CKD, errors metabolism
103
Differentiate between acute and chronic gout under the microscope
Acute: PMN's, macrophages with urate crystals
Chronic: tophi, macroscopically on joints and destruction of cartilage
104
What are the 4 phases of tumor growth?
1. Transformation (Differentiation)
2. Growth of transformed cell (Rate of growth)
3. Local invasion
4. Distant mets
105
Differentiate between staging and grading of a tumor.
```
Staging = spread = T/S--size, N--nodes, M---mets
Grading = grading of differentiation
```
106
What are the 3 major routes of metastasis?
1. Seeding via body cavity
2. Lymphatics
3. Blood -- most common liver and lung
107
Angiogenic growth factors share a common use of this secondary messenger system.
Tyrosine kinase
108
What are the 3 major phases of metastasis?
1. Invasion of ECM
2. Movement through I/S tissue
3. Vascular dissemination and homing of tumor cells
109
CEA measurement is mainly used as a tumor marker to monitor
colorectal carcinoma
110
Give several examples of how cancer cells can invade the ECM.
Decreased cadherins, collagenase, captepsin, MMP's
111
How do tumor cells travel in the vascular system?
1. Single cell
| 2. Multiple cell emboli with platelets and WBC's
112
Give several examples of tumor Ag.
Oncogene/ RAS, BCR-ABL
PSA
HPV/EBV
CEA (colon)
113
What are the 4 major mechanisms of anti-tumor defense?
Cd8, natty killer, TNG/free rads of macrophages, complement
114
Carcinoid
Neuroendocrine tumor
115
At what number doubling does a tumor become clinically detectable? How many more until lethal?
30 & 10
116
Give examples of some angiogenic growth factors of tumors.
1. FGF, VEGF, PDGF (platelet derived), Hypoxia-inducbile factor
117
How are cells normally lost in tumors?
Apoptosis, ischemia, host defense
118
T/F Tumors with high growth factors are susceptible to chemotherapy
True
119
What is Ki67?
Microscopically measure cell growth
120
What is anaplasia?
Invasive neoplasm with lack of differentiation
121
What are microscopic features of anaplastic malignant cells?
Variable size/shape -- cell + nuclei, increased nuc:cyto ratio, hyperchromatic nucleu, increased/abnormal mitosis
122
Define choristoma
Collection of normal cells in an abnormal location
123
Define hamartoma
a focal growth that resembles a neoplasm but results from faulty development in an organ
124
Pediatric tumors generally get this suffix.
--- blastoma
125
What is the etiology of cancer cachexia?
Decreased food intake, decreased storage/synthesis of fat, TNF
126
Is cancer cachexia a result the nutritional demand of the tumor?
No
127
What is a paraneoplastic syndrome?
Paraneoplastic syndromes are rare disorders that are triggered by an altered immune system response to a neoplasm. They are defined as clinical syndromes involving nonmetastatic systemic effects that accompany malignant disease.
128
Why are paraneoplastic syndromes important?
May be earliest manifestation of occult cancer; significant problems, mimic metastatic disease, lead to wrong diagnosis
129
How does one make a definitive clinical diagnosis of cancer?
Under the microscope!
130
What technique is used to analyze DNA ploidy and to characterize leukemias and lymphomas?
Flow cytometry
131
What is immunocytochemistry?
Look at nuclear and cytoplasmic proteins
| * Coat the cell with antibody and see if any antigen is present (i.e. PSA)
132
CEA
Gastric, Pancreatic, Colonic, Breast
133
AFP
HCC
134
Biochemical tumor markers: screening/follow-up or diagnosis
Screening/F-U
135
What is molecular diagnostic method of cancer?
PCR, hereditary disposition, gene presence/absence/mutation
136
EBV infection is associated with which virus?
EBV
137
What are 4 common cancers of children?
Osteosarcoma, Neuroblastoma, Wilms, Retino (WON-R)
138
Which 3 cancers show familial clustering?
Breast, Ovarian, Colon
139
Name the genes associated with these AD disorders: Familial polyposis, Li Fraumenii, Multiple Endocrine Neoplasia
APC, p53, MEN1/RET
140
Several disorders of defective DNA repair exist. Name 4 (3 AR, 1 AD) and the cancer associated with each.
AR: XP (sq. cell ca), Ataxia teleng (Lymphoma, ALL), Fanconi anemia (AML)
AD: HNPCC -- MLH/MSH
141
Give 3 examples of oncogenic DNA viruses
1. HPV - cervical cancer
2. EBV - nasopharyngeal + Burkitt's lymphoma
3. HBV - HCC
142
What is a classical example of an RNA oncogenic virus?
HTLV-1
143
What are several features of RNA oncogenic viruses?
Acute, slow transforming
144
What is a classical example of a bacterial infection associated with cancer?
H. pylori -- B cell lymphoma of MALT
145
How do DNA viruses cause cancer?
Proteins that bind with specific host proteins -- products of tumor suppressor genes -- involved in regulation of cell proliferation
146
What is the mechanism of chemical carcinogenesis?
Initiator: causes mutation
Promoter: causes clonal expansion
147
What is the mechanism of UV radiation carcinogenesis?
Pyrimidine dimers/DNA damage; overwhelemed nucleotide excision repair (sq. cell, basal cell, melanoma)
148
What is the mechanism of ionizing radiation carcinogenesis?
DNA damage, alters proteins, injures membranes, free radicals
149
What is the key event of molecular carcinogenesis?
NON-LETHAL genetic alteration
150
Carcinogenesis affects 4 major classes of genes. What are they?
Oncogenes, TS genes, apoptosis regulating genes, mutator (caretaker/DNA repair) genes
151
Discuss the three mutations to proto-oncogenes and give examples of each.
1. Point mutation - RAS (colon cancer)
2. Translocation - (9,22) & (8,14)
3. Amplification - N-MYC (neuroblastoma); Her2 (BRCA)
152
What is the most common mutation in all cancers?
RAS
153
What signal transduction cascade is used in translocated oncogenes?
Tyrosine kinase
154
What are the 5 major types of oncoproteins?
Growth factors, growth factor receptors, signal transduction, nuclear regulatory factors, CDK's
155
Give 7 examples of TS genes and examples
1. P53 - LiFraumenii
2. Rb
3. NF1 - neurofibromatosis
4. BRCA1/2
5. APC - APC
6. DCC - colon cancer deletion
7. WT-1 - Wilm's tumor
156
Who needs 2 hits: TS or oncogenes?
TS
157
A mutation in BCL-2 is...
Associated with CLL & other B-cell lymphomas
158
Give an example of a DNA repair gene mutation
MSH2, HNPCC
159
Telomeres
Shorten with age; cancer cells have telomerase, which maintain their ability to replicate 4eva
160
KRAS
Oncogene for colon/panc cancer
161
Rb associated with 2 childhood tumors
Rb, osteosarcoma
162
BLC-2 mutation
B cell lymphomas
163
BCR-ABL mutation
t(9,22) - CML
164
Describe the relationship between KRAS, EGFR, ALK in non-small cell lung cancer.
KRAS--EGFR--ALK
| only therapies for EGFR, ALK -- TKI's
165
_____ are major genetic factors in chemotherapy drug response
SNP's
166
What is Trouseau's syndrome?
Unexplained thrombophlebitis, recurrent; look for underlying abdominal malignancy, i.e. pancreatic cancer (release of pro-coagulants)
167
What is Virchow's triad?
1. Endothelial injury
2. Loss of laminar flow (turbulent, stasis)
3. Hypercoagulable state
168
What are several etiologies of hypercoagulability?
Hereditary: Factor 5 Leiden, Antithrombin 3, Protein C, S
Acquired: contraceptives, terminal cancer, severe trauma, depressed cardiac function
169
Describe the abnormal blood flow associated with thrombus formation
Stasis: allows aggregation of platelets, prevents anti-coag factors, aneurysm
Turbulence: ath plaques, structural damage
170
Differentiate between the morphology of an arterial vs. venous embolus
Arterial: (PALE) heart, aorta, aneurysm, occulsive (coronary, carotid, femoral, mesenteric)
Venous: takes shape of vessel (RED); deep veins of leg
171
How does a DVT present?
50%: ankle, foot pain, tenderness
| 50%: asymptomatic
172
An arterial thrombus: (acute, slow, heart)
Actute: infarct
Slow: atrophy, fibrosis
Heart: systematic emboli
173
The most clinically significant emboli are from the _____ to the _____ & _______.
Heart, lower extremities/brain
174
Describe the 3 possible outcomes of invasion by a microorganism.
1. No infection
2. Infection (multiplication without damage)
3. Disease (multiplication and damage)
175
Differentiate between infection and disease
Disease requires damage
176
Microorganisms travel in tissue planes of: _________ _____________
least resistance
177
Differentiate between bacteremia and septicemia
Bacteremia: temporary, bacteria in the blood (brushing teeth)
Septicemia: bacteria multiply in the blood; fever/chills, distant foci of spread
178
Differentiate between direct and indirect damage by a microorganism
Direct: tissue destruction, vascular damage, ischemic injury
Inidirect: toxins, enzymes, host response
179
Describe the typical host response to the following:
1. bacteria
2. virus
3. TB/leprosy
4. fungus
5. parasites
6. Schistosoma
7. Clostridium perfringens
8. Diptheria/clostridium diff
1. bacteria - acute inflammation with PMN's
2. virus - lymphocytes, macrophages (intracellular)
3. TB/leprosy - caseuous necrosis with Langhan foreign body
4. fungus - mixed acute + chronic
5. parasites - eosinophila
6. Schistosoma - fibrosis
7. Clostridium perfringens - necorsis (gas gangrene)
8. Diptheria/clostridium diff - pseudomembrane
180
What is a Langhan foreign body?
Granuloma of TB (vs. foreign body granuloma)
181
Schistosoma causes
Schistosoma - fibrosis
182
What are the 6 methods to diagnose an infectious disease?
1. Clinical features -- classical history, physical
2. Epidemiology -- geographical area
3. Isolate the organism -- pus, blood, tissue, fluids
4. Antibody titers -- >4-fold increase in titers
5. Biopsy of tissue -- stains, PCR, immunohistochemistry
6. Therapeutic response -- malaria, TB
183
Describe the bacterial origin of meningitis of the following age-groups: neonate, infant, adolescent, 20-60 years old
Neonate (2-months): S. agalaciae, E. coli, L. monocytogenes
Infant: N.m, S. pneumonia, H. influenzae
Adolescent: N.m
20-60 years old: N.m, S. pneumonia, L. monocyotgenes, gram negative bacilli
184
What cause of bacterial meningitis has largely been eradicated because of a vaccination?
H. influenzae
185
What is the classic finding at autopsy of a patient with meningococcal septicemia?
Bilateral adrenal hemorrhages
186
Neisseria gonorrhea dissemination
Can disseminate (blood) tenosynovitis, arthritis, hemorrhage, skin lesions, endocarditis
187
Male/Female/Fetal manifestation gonorrhea
Male: urethritis, epididymitis, uretheral d/c
Female: cervicitis, salpingitis (PID/ fallopian scarring, infertility)
Neonate: purulent conjunctivitis (erythromycin +/- silver nitrate)
188
Salmonella typhi (Typhoid/Enteric fever) uses 1 particular immune cell...
Ileal wall/PP's blood liver/spleen (nodules) gallbladder ileum (ulcers -- perforate)
**MACROPHAGES**
189
Clinical manifestations of typhoid. Carriers are treated with...
Step-ladder fever, diarrhea, leukopenia, anemia; depressed heart/bone marrow
Carriers-- cholecystectomy
190
Offending agents of gram negative septicemia
E. coli, H. influenza, Pseudomonas aeraginosa, Klebsiella, protus, serratia
191
Staphylococcus aureus clinical manifestation
Inflamm: folliculitis, furuncle, carbuncle, impetigo, paronychia, cellultitis, osteomyelitis ++ endocarditis (IVDU), pneumonia+empyema (secondary to viral infection)
Toxin: rash, vomiting, diarrhea, scalded skin syndrome (toxic necrosis epidermis)
192
Streptococci (Group A beta-hemolytic) pyogenes clinical manifestation
Trunk, limbs, oral pallor, strawberry tongue
| Elderly: cellulitis, tonsillitis, cervical LA, pharyngitis
193
Streptococcal (pneumonococcal) pneumonia
* Lobar pneumonia
* Healthy young adults, cold, strain, exhaustion
* Cough, fever, chest pain, bloody sputum
* Spreads through pores of Kohn to involve entire lobe; does not damage bronchioles or alveolar walls
* 1. Congestion (fibrin, RBC, PMNS)
* 2. Red: decreased RBC, increased PMN's -- lung loses spongy consistency (looks like liver)
* 3. Gray: decreased fibrin, increased macrophages
* 4. Resolution: cough it up
* Complications: abscess, fibrosis (which can lead to) empyema
194
Bronchopneumonia
* Patchy involvement of lung
* Destruction of bronchioles, alveoli
* Coalesce to involve entire lobe
* Children, elderly, bed ridden (extremes of age)
* Abscess + empyema)
195
Bronchopneumonia offending agents
• Offending agents: Klebsiella, E. coli, pseudomonas, group A staph
196
Rheumatic fever
* Post streptococcal (Group A beta-hemolytic)
* 2-3 week lag
* ACCNE (arthritis, carditis, chorea, subQ skin nodules, erythema) + fever
* Ab generated by M protein of bacteria cross-react with glycoprotein of the heart
* Deposition on tissues/inflammation at site of deposition
* Rheumatic mitral stenosis
* Hallmark: Aschoff bodies in heart -- cardiac histiocytes, central necrosis, collection of lymphocytes and macrophages
197
Post streptococcal GN
* Initial sore throat/skin infection
* 1-4 week lag in kids (Group A beta-hemolytic)
* IgG + complement deposition in BM of glomerulus
* Oliguria, hematuria, elevated BUN, Cr, decreased GFR (nephritic)
* Resolves spontaneously
198
Cryptococcus neoformans (torulosis)
**Minimal inflammatory infiltrate ** lung lesions -- CNS/meningitis
198
Cryptococcus neoformans (torulosis)
**Minimal inflammatory infiltrate ** lung lesions -- CNS/meningitis
199
Candida albicans (Moniliasis)
Superficial: oral-thrush, vaginal, GIT
Deep: pseudohyphae with budding
Disseminated: Secondary to IV glucose admin
199
Candida albicans (Moniliasis)
Superficial: oral-thrush, vaginal, GIT
Deep: pseudohyphae with budding
Disseminated: Secondary to IV glucose admin
200
Fungal infections
* Air, soil
* Few infect humans
* Most are opportunistic (AIDS, DM, heme malignancies, treatment with BS abx)
* **Tendancy to invade blood vessels: hemorrhage, thrombosis, infarction -- EXCEPT Cryptococcus -- does not cause inflammation
* Mixed purulent, granulomatous
* PAS: pink; Silver stain: black, Micinargen: red--capsule
200
Fungal infection characteristics
* Air, soil
* Few infect humans
* Most are opportunistic (AIDS, DM, heme malignancies, treatment with BS abx)
* **Tendancy to invade blood vessels: hemorrhage, thrombosis, infarction -- EXCEPT Cryptococcus -- does not cause inflammation
* Mixed purulent, granulomatous
* PAS: pink; Silver stain: black, Micinargen: red--capsule
201
Rickettsia (3 bugs)
```
R. prowazeki (endemic typhus)
Rocky mountain spotty fever
Q fever (Cloxiella)
***Vasculitis, thrombosis, hemorrhage, vascular necrosis
*Extravasation RBC
```
201
Rickettsia (3 bugs)
```
R. prowazeki (endemic typhus)
Rocky mountain spotty fever
Q fever (Cloxiella)
***Vasculitis, thrombosis, hemorrhage, vascular necrosis
*Extravasation RBC
```
202
Viral infection characteristics
* Cytopathic damage cell death (acute damage)
* Perinuclear swelling (HPV/cervix-- degenerative changes)
* Nuclear inclusions: chicken pox, HSV (+giant cells), CMV
* Cytoplasmic inclusions: Rabies (dog bite, neck spasm, dysphagia, hydrophobia, Negri body)
* Multinucleated giant cells: herpes, measles (Walden-Finkerty), HIV
* Cell proliferation: warts, HPV (cervical neoplasia)
