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Term 4 > General Pathology > Flashcards

General Pathology Flashcards

1
Q

What are the 4 aspects of a disease process?

A
  1. Etiology - cause
  2. Pathogenesis - mechanism
  3. Morphology - appearance
  4. Functional consequences
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2
Q

What are the possible outcomes of cellular stress?

A
  1. Cell adaptation
  2. Temporary abnormality with recovery
  3. Permanent structural damage
  4. DNA damage/mutation
  5. Cell death
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3
Q

What are the 6 major causes (etiologies) of cellular injury?

A
  1. Physical - trauma
  2. Chemical - drugs, ETOH
  3. Metabolic - hypoxia, vitamin def, glycemia
  4. Immunologic - allergy/autoimmunity
  5. Genetic - chromosomnal abnormality
  6. Infection - bacteria, virus, parasite
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4
Q

What types of cells are the most susceptible to injury?

A

Metabolically active cells

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5
Q

What changes can be seen under the light microscope during reversible cell injury?

A
  1. Cellular swelling/hydropic change and vacuolization

2. Fatty changes

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6
Q

What is vacuolization?

A

Small, clear vacuoles within the cytoplasm; these

represent distended and pinched-off segments of the endoplasmic reticulum

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7
Q

Injured cells stain more intensely with: H or E

A

E – more pronounced and pink with greater injury

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8
Q

The 4 major systems of the cell particularly vulnerable to cell injury:

A
  1. Membranes– cell, ER, lysosomes
  2. Energy production
  3. Proteins/enzymes (structural+regulatory)
  4. DNA-nucleus
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9
Q

What is the commonly agreed upon point of no return in cellular injury?

A

Mitochondrial damage

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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

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11
Q

When an injurious agent affects the lysosomes, cell degeneration is said to occur. This can produce:

A
  1. Autophagy
  2. Hereditary absence of enzyme in lysosomes
  3. Failure degradation phag’ed material
  4. Liberation and activation of lysosomal enzymes (residual body)
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12
Q

This event plays a central and common role in most pathological contidtions

A

Lack of oxygen!

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13
Q

What are the 4 main mechanisms (not etiologies) of cellular injury?

A
  1. Hypoxia
  2. Free radicals
  3. Chemical injury
  4. Viral injury
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14
Q

Reversible cell changes are known to occur when the duration of ischemia is short and in the following sequence:

A
  1. Impaired mitochondria (aerobic respir)
  2. Dec ATP
  3. Anaerobic glycolysis
  4. Glycogen depletion
  5. Intracellular acidosis with chromatin clumping
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15
Q

Why does cell swelling occur?

A

Failure of Na/K ATPase pump to keep Na outside

+ accumulation lactate, inorganic phosphate

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16
Q

What happens in reversible cell damage?

A

Cell swelling, detached ribosomes, blebs, myelin figures (dissociated lipoproteins), mitochondrial swelling

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17
Q

Irreversible injury is characterized by:

A
  • Severe vacuolization of mitochondria
  • Damage to plasma membrane
  • Swelling lysosomes
  • Massive Ca++ influx
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18
Q

What are the biochemical pathways involved in irreversible cell injury?

A
  1. Loss of phospholipids (dec. synthesis + breakdown)
  2. Cytoskeletal alterations (proteases, damaged connections)
  3. Free radicals
  4. Lipid breakdown products – free FA’s with detergent character
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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

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20
Q

How does the body protect against free radicals?

A

Antioxidants, catalase, glutathione peroxidase, SOD)

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21
Q

Why are free radicals so dangerous?

A

Lipid peroxidation, nucleic acid mutations, cross-linking of proteins for degradation

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22
Q

Which is the major organ of lipid metabolism?

A

Liver

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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

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24
Q

How do viruses affect cells?

A

Cell death (lysis), cell skeleton (respiratory cilia), fusion of cells, host immunological response

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25
Q

Under routine microscopy, the most recognizable cellular changes include:

A

Swelling and fatty chagne

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26
Q

Physiological apoptosis includes:

A

Embryogenesis, hormone-dependent involution, cell deletion, deletion of auto-reactive T cells, tumor growth control

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27
Q

What are the 5 major cell adaptations?

A

Hypertrophy, hyperplasia, atrophy, metaplasia, dysplasia

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28
Q

T/F Apoptotic cells are seen singly or in small clusters. Bright eosinophilic cytoplasm and condensed, irregular nuclei

A

T

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29
Q

Accumulation of this agent is associated with cellular aging or senescence.

A

Lipofuscin

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30
Q

Inflammation is a dynamic process that starts with…. and ends with…

A

Injury; healing/repair

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31
Q

T/F In order for inflammation to occur, the injury must be non-lethal

A

T

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32
Q

Differentiate between exudation and transudation

A

Exudate: has protein

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33
Q

Differentiate between acute and chronic inflammation.

A

Chronic: lymphocytes
Acute: PMN’s

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34
Q

The most important feature of inflammation is the accumulation of: __________________________.

A

Leukocytes in the affected tissue

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35
Q

What is rouleaux?

A

RBC’s become sticky and hence force the WBC’s towards the periphery; aids in margination

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36
Q

Who are the most important chemotactic factors?

A

Bacterial products, complement fractions, arachidonic acid metabolites, cytokines/chemokines

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37
Q

During phagocytic engulfment, who is the second messenger?

A

Ca++

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38
Q

The 3 major steps of phagocytosis

A
  1. Recognition/Attachment
  2. Engulfment
  3. Killing
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39
Q

What are the 5 key characteristics (clinical manifestations) of acute inflammation?

A

Redness, swelling, pain, heat, loss of function

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40
Q

The 4 major features of acute inflammation:

A
  1. Vascular events
  2. Cellular events
  3. Phagocytosis
  4. Mediators of inflammation
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41
Q

The major vascular events in acute inflammation

A
  1. Vasoconstriction
  2. Vasodilation
  3. Increased vascular permeability
  4. Increased blood viscosity
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42
Q

Explain the several mechanisms behind increased vascular permeability.

A
  1. Histamine – small venules
  2. Cytokines – cytoskel rearrangement
    * *3. Endothelial injury (immediate sustained)**
  3. WBC-dependent
  4. Vascular endothelial growth factor
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43
Q

Describe the cellular events of acute inflammation.

A
  1. Margination- sludging RBC/WBC towards periphery
  2. Rolling- selectins
  3. Adhesion- ICAM/VAM
  4. Transmigration- PECAM
  5. Chemotaxis- C5a, cytokines, chemokines
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44
Q

What are the 3 major steps of phagocytosis?

A
  1. Recognition (opsonization)
  2. Engulfment
  3. Killing (ROS)
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45
Q

When leukocytes arrive at the site of cell injury, they will…

A
  1. Engulf, degrade, complex bacteria and debris
  2. Lysosomal enzymes
  3. Chemical mediators
  4. Toxic radicals
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46
Q

What is rouleaux?

A

Peripheral orientation of WBC’s because of sludging of RBC’s; WBC’s pushed towards periphery

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47
Q

LFA-1 is also called

A

CD11a/CD18

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48
Q

MAC-1 is also called

A

CD11b/CD18

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49
Q

Who are the first leukocytes to arrive at the site of cell injury?

A

PMN’s

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50
Q

Liquefactive necrosis

A

Hydrolysis – BRAIN & BACTERIAL INFECTIONS

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51
Q

Coagulative necrosis

A

Classic – happens everywhere except the brain

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52
Q

Caseous necrosis

A

TB/Lung

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53
Q

Fat necrosis

A

Occurs when lipases are freed; free fa’s released and combine with calcium to form soaps

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54
Q

What are the 5 major types of necrosis?

A
  1. Coagulative
  2. Fat
  3. Liquefactive
  4. Caseous
  5. Gangrenous
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55
Q

Among histamine and serotonin, which is only present in platelets (vs. mast cells/basophils)?

A

Serotonin

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56
Q

Who are the major cell-derived vascular permeability mediators in inflammation?

A
  1. AA metabolites
  2. PAF
  3. Amines (histamine, serotonin)
  4. Endothelins
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57
Q

Who are the major plasma derived chemical mediators of inflammation?

A
  1. Coagulation/kinin system

2. Complement

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58
Q

Who is the most important plasma protein system of inflammation?

A

Complement

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59
Q

Granulomatous chronic inflammation is characteristic of which infections/diseases?

A
  1. Infections: TB, syphillis, cat-scratch, fungi, protozoa
  2. Persistent foreign body
  3. Rheumatic fever
  4. RA
  5. Sarcoidosis
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60
Q

Trace the normal flow of lymphatic fluid

A

Lymph node –> general circulation –> RES

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61
Q

What are 5 major defects of leukocyte function?

A
  1. Number circulating cells
  2. Adherence
  3. Migration/Chemotaxis
  4. Phagocytosis
  5. Microbicidal activity
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62
Q

What are the 4 major morphological patterns of acute/chronic inflammation?

A
  1. Serous
  2. Fibrinous
  3. Suppurative/purulent
  4. Sanguinous
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63
Q

Differentiate between granulomatous and non-specific chronic inflammation

A

Non-specific: mononuclear cells, C/T, fibroblasts

Gran: R-E, macrophages, giant cells, rim of lymphocytes

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64
Q

Differentiate between granulomatous and non-specific chronic inflammation

A

Non-specific: mononuclear cells, C/T, fibroblasts

Gran: R-E, macrophages, giant cells, rim of lymphocytes

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65
Q

Define abscess

A

Localized collection of pus (trypsin overwhelms and destroys damaged tissue)

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66
Q

Define paronychia

A

Side/Base of fingernail

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67
Q

Define Felon

A

Anterior portion of distal phalynx (secondary to penetrative wound)

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68
Q

Define empyema

A

Collection of pus in pleural cavity

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69
Q

Define pseudomembranous inflammation

A

Toxin/Fibrin/necrotic epithelial cells, WBC’s on mucosal surfaces

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70
Q

Define sinus

A

Abnormal communication between solid organ/tissue and skin

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71
Q

The 4 organs with the best regenerative capacity

A

Liver, lung, kidney, spleen

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72
Q

What is the best way to accomplish cell growth in regeneration/repair?

A

Recruit cells from G0 into the cell cycle

  1. Growth/stimulation factors
  2. Loss of growth inhibitor
  3. Cell-cell; cell-matrix interactions
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73
Q

What is the best way to accomplish cell growth in regeneration/repair?

A

Recruit cells from G0 into the cell cycle

  1. Growth/stimulation factors
  2. Loss of growth inhibitor
  3. Cell-cell; cell-matrix interactions
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74
Q

The most important cell-cell/cell-matrix interaction in healing involves

A

Fibronectins (HMW adhesive glycoproteins) which bind to EC components and cell surfaces

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75
Q

Who produces fibronectin?

A

Fibroblasts, endothelial cells, monocytes

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76
Q

4 Major functions of fibronectin

A
  1. Migration of new epithelial cells
  2. Chemotactic for monocytes, fibroblasts
  3. Stimulate endothelial cell migration
  4. Release fibroblast growth factor from monocytes
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77
Q

4 Major functions of fibronectin

A
  1. Migration of new epithelial cells
  2. Chemotactic for monocytes, fibroblasts
  3. Stimulate endothelial cell migration
  4. Release fibroblast growth factor from monocytes
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78
Q

What does granulation tissue consist of histologically?

A

Meshwork of capillaries, fibroblasts, inflammatory cells, ECM

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79
Q

What does granulation tissue consist of histologically?

A

Meshwork of capillaries, fibroblasts, inflammatory cells, ECM

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80
Q

What is the objective of crust formation?

A
  1. Stops bleeding

2. Barrier to infection

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81
Q

What are the 4 major factors influencing the rate of healing?

A
  1. Age
  2. Size of wound
  3. Secondary infection
  4. Diet (Vitamin C, D, protein)
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82
Q

What is amyloid? How does it appear under the light microscope? Congo red? Polarized light?

A

Abnormal ECF proteinaceous deposit

H/E seen as glassy pink; Congo-red: red; Polarized light (apple green)

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83
Q

Amyloid: alpha-helix or beta-pleated?

A

Beta-pleated

84
Q

The non-fibrillary component of amyloid is…

A

The P component, strong affinity for fibrils, made of serum-alpha-1-glycoprotein
* Similar in structure to CRP

85
Q

What are the 2 major types of amyloid and what is the difference between them?

A

AL: Ig- light lambda chains (B cell malignancy)
AA: derived from serum AA (associated with chronic inflamm)

86
Q

Which amyloid is associated with chronic disease?

A

SAA/AA

87
Q

Describe the relationship between genetic disorders, age-related disorders, renal dialysis and amyloid.

A

Genetic - transthyretin in Fam. Amyloid Polyneuropathy
Age: B2 amyloid – Alzheimers
Dialysis – B2 microglobulin

88
Q

What are the macroscopic descriptors for a liver/organ with amyloid?

A

Pale, waxy, firm

89
Q

What is the general trend for an organ affected by amyloidosis?

A

Hypertrophy –> Atrophy

90
Q

Heart amyloid: AL or AA

A

AL

91
Q

The first organ usually affected by amyloidosis (my favorite!)

A

kidney

92
Q

Lipofucsin is often the result of…

A

Free radical breakdown of intracellular membranes

93
Q

Lipofuccsin usually accumulates in aging…

A

liver, cardiac, brain

94
Q

Hemosiderin is best visualized using this stain

A

Prussian blue

95
Q

Pts with hemochromatosis develop…

A

Heart failure, DM, cirrhosis

96
Q

Pts with what pigment disorder are at an increased risk of HCC?

A

Hemochromatosis

97
Q

Wilson’s disease

A

Cu storage disorder (overload – brain/liver)

98
Q

Cause of dystrophic calcification…

A

Cell injury

99
Q

Metastatic calcification is caused by…

A

hypercalcemia

100
Q

Deposition of calcium in metastatic calcification occurs in these tissues…

A

Alveolar walls lungs, gastric mucosa, renal tubules, blood vessels

101
Q

Risk factors for gout

A

Genetics, 20-30 years HU, ETOH, obesity, thiazides

102
Q

Differentiate between primary and secondary gout

A

1: HGPRT/unknown enzyme (90%)
2: nuc. Acid turnover, CKD, errors metabolism

103
Q

Differentiate between acute and chronic gout under the microscope

A

Acute: PMN’s, macrophages with urate crystals
Chronic: tophi, macroscopically on joints and destruction of cartilage

104
Q

What are the 4 phases of tumor growth?

A
  1. Transformation (Differentiation)
  2. Growth of transformed cell (Rate of growth)
  3. Local invasion
  4. Distant mets
105
Q

Differentiate between staging and grading of a tumor.

A 
Staging = spread = T/S--size, N--nodes, M---mets
Grading = grading of differentiation
106
Q

What are the 3 major routes of metastasis?

A
  1. Seeding via body cavity
  2. Lymphatics
  3. Blood – most common liver and lung
107
Q

Angiogenic growth factors share a common use of this secondary messenger system.

A

Tyrosine kinase

108
Q

What are the 3 major phases of metastasis?

A
  1. Invasion of ECM
  2. Movement through I/S tissue
  3. Vascular dissemination and homing of tumor cells
109
Q

CEA measurement is mainly used as a tumor marker to monitor

A

colorectal carcinoma

110
Q

Give several examples of how cancer cells can invade the ECM.

A

Decreased cadherins, collagenase, captepsin, MMP’s

111
Q

How do tumor cells travel in the vascular system?

A
  1. Single cell

2. Multiple cell emboli with platelets and WBC’s

112
Q

Give several examples of tumor Ag.

A

Oncogene/ RAS, BCR-ABL
PSA
HPV/EBV
CEA (colon)

113
Q

What are the 4 major mechanisms of anti-tumor defense?

A

Cd8, natty killer, TNG/free rads of macrophages, complement

114
Q

Carcinoid

A

Neuroendocrine tumor

115
Q

At what number doubling does a tumor become clinically detectable? How many more until lethal?

A

30 & 10

116
Q

Give examples of some angiogenic growth factors of tumors.

A
  1. FGF, VEGF, PDGF (platelet derived), Hypoxia-inducbile factor
117
Q

How are cells normally lost in tumors?

A

Apoptosis, ischemia, host defense

118
Q

T/F Tumors with high growth factors are susceptible to chemotherapy

A

True

119
Q

What is Ki67?

A

Microscopically measure cell growth

120
Q

What is anaplasia?

A

Invasive neoplasm with lack of differentiation

121
Q

What are microscopic features of anaplastic malignant cells?

A

Variable size/shape – cell + nuclei, increased nuc:cyto ratio, hyperchromatic nucleu, increased/abnormal mitosis

122
Q

Define choristoma

A

Collection of normal cells in an abnormal location

123
Q

Define hamartoma

A

a focal growth that resembles a neoplasm but results from faulty development in an organ

124
Q

Pediatric tumors generally get this suffix.

A

— blastoma

125
Q

What is the etiology of cancer cachexia?

A

Decreased food intake, decreased storage/synthesis of fat, TNF

126
Q

Is cancer cachexia a result the nutritional demand of the tumor?

A

No

127
Q

What is a paraneoplastic syndrome?

A

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
Q

Why are paraneoplastic syndromes important?

A

May be earliest manifestation of occult cancer; significant problems, mimic metastatic disease, lead to wrong diagnosis

129
Q

How does one make a definitive clinical diagnosis of cancer?

A

Under the microscope!

130
Q

What technique is used to analyze DNA ploidy and to characterize leukemias and lymphomas?

A

Flow cytometry

131
Q

What is immunocytochemistry?

A

Look at nuclear and cytoplasmic proteins

* Coat the cell with antibody and see if any antigen is present (i.e. PSA)

132
Q

CEA

A

Gastric, Pancreatic, Colonic, Breast

133
Q

AFP

A

HCC

134
Q

Biochemical tumor markers: screening/follow-up or diagnosis

A

Screening/F-U

135
Q

What is molecular diagnostic method of cancer?

A

PCR, hereditary disposition, gene presence/absence/mutation

136
Q

EBV infection is associated with which virus?

A

EBV

137
Q

What are 4 common cancers of children?

A

Osteosarcoma, Neuroblastoma, Wilms, Retino (WON-R)

138
Q

Which 3 cancers show familial clustering?

A

Breast, Ovarian, Colon

139
Q

Name the genes associated with these AD disorders: Familial polyposis, Li Fraumenii, Multiple Endocrine Neoplasia

A

APC, p53, MEN1/RET

140
Q

Several disorders of defective DNA repair exist. Name 4 (3 AR, 1 AD) and the cancer associated with each.

A

AR: XP (sq. cell ca), Ataxia teleng (Lymphoma, ALL), Fanconi anemia (AML)
AD: HNPCC – MLH/MSH

141
Q

Give 3 examples of oncogenic DNA viruses

A
  1. HPV - cervical cancer
  2. EBV - nasopharyngeal + Burkitt’s lymphoma
  3. HBV - HCC
142
Q

What is a classical example of an RNA oncogenic virus?

A

HTLV-1

143
Q

What are several features of RNA oncogenic viruses?

A

Acute, slow transforming

144
Q

What is a classical example of a bacterial infection associated with cancer?

A

H. pylori – B cell lymphoma of MALT

145
Q

How do DNA viruses cause cancer?

A

Proteins that bind with specific host proteins – products of tumor suppressor genes – involved in regulation of cell proliferation

146
Q

What is the mechanism of chemical carcinogenesis?

A

Initiator: causes mutation
Promoter: causes clonal expansion

147
Q

What is the mechanism of UV radiation carcinogenesis?

A

Pyrimidine dimers/DNA damage; overwhelemed nucleotide excision repair (sq. cell, basal cell, melanoma)

148
Q

What is the mechanism of ionizing radiation carcinogenesis?

A

DNA damage, alters proteins, injures membranes, free radicals

149
Q

What is the key event of molecular carcinogenesis?

A

NON-LETHAL genetic alteration

150
Q

Carcinogenesis affects 4 major classes of genes. What are they?

A

Oncogenes, TS genes, apoptosis regulating genes, mutator (caretaker/DNA repair) genes

151
Q

Discuss the three mutations to proto-oncogenes and give examples of each.

A
  1. Point mutation - RAS (colon cancer)
  2. Translocation - (9,22) & (8,14)
  3. Amplification - N-MYC (neuroblastoma); Her2 (BRCA)
152
Q

What is the most common mutation in all cancers?

A

RAS

153
Q

What signal transduction cascade is used in translocated oncogenes?

A

Tyrosine kinase

154
Q

What are the 5 major types of oncoproteins?

A

Growth factors, growth factor receptors, signal transduction, nuclear regulatory factors, CDK’s

155
Q

Give 7 examples of TS genes and examples

A
  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
Q

Who needs 2 hits: TS or oncogenes?

A

TS

157
Q

A mutation in BCL-2 is…

A

Associated with CLL & other B-cell lymphomas

158
Q

Give an example of a DNA repair gene mutation

A

MSH2, HNPCC

159
Q

Telomeres

A

Shorten with age; cancer cells have telomerase, which maintain their ability to replicate 4eva

160
Q

KRAS

A

Oncogene for colon/panc cancer

161
Q

Rb associated with 2 childhood tumors

A

Rb, osteosarcoma

162
Q

BLC-2 mutation

A

B cell lymphomas

163
Q

BCR-ABL mutation

A

t(9,22) - CML

164
Q

Describe the relationship between KRAS, EGFR, ALK in non-small cell lung cancer.

A

KRAS–EGFR–ALK

only therapies for EGFR, ALK – TKI’s

165
Q

_____ are major genetic factors in chemotherapy drug response

A

SNP’s

166
Q

What is Trouseau’s syndrome?

A

Unexplained thrombophlebitis, recurrent; look for underlying abdominal malignancy, i.e. pancreatic cancer (release of pro-coagulants)

167
Q

What is Virchow’s triad?

A
  1. Endothelial injury
  2. Loss of laminar flow (turbulent, stasis)
  3. Hypercoagulable state
168
Q

What are several etiologies of hypercoagulability?

A

Hereditary: Factor 5 Leiden, Antithrombin 3, Protein C, S
Acquired: contraceptives, terminal cancer, severe trauma, depressed cardiac function

169
Q

Describe the abnormal blood flow associated with thrombus formation

A

Stasis: allows aggregation of platelets, prevents anti-coag factors, aneurysm
Turbulence: ath plaques, structural damage

170
Q

Differentiate between the morphology of an arterial vs. venous embolus

A

Arterial: (PALE) heart, aorta, aneurysm, occulsive (coronary, carotid, femoral, mesenteric)
Venous: takes shape of vessel (RED); deep veins of leg

171
Q

How does a DVT present?

A

50%: ankle, foot pain, tenderness

50%: asymptomatic

172
Q

An arterial thrombus: (acute, slow, heart)

A

Actute: infarct
Slow: atrophy, fibrosis
Heart: systematic emboli

173
Q

The most clinically significant emboli are from the _____ to the _____ & _______.

A

Heart, lower extremities/brain

174
Q

Describe the 3 possible outcomes of invasion by a microorganism.

A
  1. No infection
  2. Infection (multiplication without damage)
  3. Disease (multiplication and damage)
175
Q

Differentiate between infection and disease

A

Disease requires damage

176
Q

Microorganisms travel in tissue planes of: _________ _____________

A

least resistance

177
Q

Differentiate between bacteremia and septicemia

A

Bacteremia: temporary, bacteria in the blood (brushing teeth)
Septicemia: bacteria multiply in the blood; fever/chills, distant foci of spread

178
Q

Differentiate between direct and indirect damage by a microorganism

A

Direct: tissue destruction, vascular damage, ischemic injury
Inidirect: toxins, enzymes, host response

179
Q

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
A
  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
Q

What is a Langhan foreign body?

A

Granuloma of TB (vs. foreign body granuloma)

181
Q

Schistosoma causes

A

Schistosoma - fibrosis

182
Q

What are the 6 methods to diagnose an infectious disease?

A
  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
Q

Describe the bacterial origin of meningitis of the following age-groups: neonate, infant, adolescent, 20-60 years old

A

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
Q

What cause of bacterial meningitis has largely been eradicated because of a vaccination?

A

H. influenzae

185
Q

What is the classic finding at autopsy of a patient with meningococcal septicemia?

A

Bilateral adrenal hemorrhages

186
Q

Neisseria gonorrhea dissemination

A

Can disseminate (blood)  tenosynovitis, arthritis, hemorrhage, skin lesions, endocarditis

187
Q

Male/Female/Fetal manifestation gonorrhea

A

Male: urethritis, epididymitis, uretheral d/c
Female: cervicitis, salpingitis (PID/ fallopian scarring, infertility)
Neonate: purulent conjunctivitis (erythromycin +/- silver nitrate)

188
Q

Salmonella typhi (Typhoid/Enteric fever) uses 1 particular immune cell…

A

Ileal wall/PP’s  blood  liver/spleen (nodules)  gallbladder  ileum (ulcers – perforate)
MACROPHAGES

189
Q

Clinical manifestations of typhoid. Carriers are treated with…

A

Step-ladder fever, diarrhea, leukopenia, anemia; depressed heart/bone marrow
Carriers– cholecystectomy

190
Q

Offending agents of gram negative septicemia

A

E. coli, H. influenza, Pseudomonas aeraginosa, Klebsiella, protus, serratia

191
Q

Staphylococcus aureus clinical manifestation

A

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
Q

Streptococci (Group A beta-hemolytic) pyogenes clinical manifestation

A

Trunk, limbs, oral pallor, strawberry tongue

Elderly: cellulitis, tonsillitis, cervical LA, pharyngitis

193
Q

Streptococcal (pneumonococcal) pneumonia

A
  • 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)
    1. Red: decreased RBC, increased PMN’s – lung loses spongy consistency (looks like liver)
    1. Gray: decreased fibrin, increased macrophages
    1. Resolution: cough it up
  • Complications: abscess, fibrosis (which can lead to) empyema
194
Q

Bronchopneumonia

A
  • Patchy involvement of lung
  • Destruction of bronchioles, alveoli
  • Coalesce to involve entire lobe
  • Children, elderly, bed ridden (extremes of age)
  • Abscess + empyema)
195
Q

Bronchopneumonia offending agents

A

• Offending agents: Klebsiella, E. coli, pseudomonas, group A staph

196
Q

Rheumatic fever

A
  • 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
Q

Post streptococcal GN

A
  • 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
Q

Cryptococcus neoformans (torulosis)

A

**Minimal inflammatory infiltrate ** lung lesions – CNS/meningitis

198
Q

Cryptococcus neoformans (torulosis)

A

**Minimal inflammatory infiltrate ** lung lesions – CNS/meningitis

199
Q

Candida albicans (Moniliasis)

A

Superficial: oral-thrush, vaginal, GIT
Deep: pseudohyphae with budding
Disseminated: Secondary to IV glucose admin

199
Q

Candida albicans (Moniliasis)

A

Superficial: oral-thrush, vaginal, GIT
Deep: pseudohyphae with budding
Disseminated: Secondary to IV glucose admin

200
Q

Fungal infections

A
  • 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
Q

Fungal infection characteristics

A
  • 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
Q

Rickettsia (3 bugs)

A 
R. prowazeki (endemic typhus)
Rocky mountain spotty fever
Q fever (Cloxiella)
***Vasculitis, thrombosis, hemorrhage, vascular necrosis
*Extravasation RBC
201
Q

Rickettsia (3 bugs)

A 
R. prowazeki (endemic typhus)
Rocky mountain spotty fever
Q fever (Cloxiella)
***Vasculitis, thrombosis, hemorrhage, vascular necrosis
*Extravasation RBC
202
Q

Viral infection characteristics

A
  • 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)

Term 4 (3 decks)

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