Pathology Flashcards

1
Q

Apoptosis

A
  • Noninflammatory cell death. Nuclear fragmentatoin and blebs forming
  • Lupus may occur because of self reaction to apoptoti blebs
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2
Q

Intrinsic Pathway

A
  • Loss of a growth factor or cellular injury leads to death of cell
  • Increase in bax and decrease in BCL-2 leads to an increase in cyt c leakage from mitochondria leading to activation of caspaces
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3
Q

Extrinsic Pathway

A

FAS-L from T cells interacts with FAS on cell activating BAD and caspaces
-Also can be from perforin and granzyme that cause activation of caspaces

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4
Q

Ca

A

Increase in intracellular Ca causes activation of caspaces and cellular death

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5
Q

Necrosis

A

-Inflammatory process from irreversible cell damage

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6
Q

Gangrene

A

-Ischemic death. If not infected is considered dry, and if is infected, is considered wet

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7
Q

Fibrinoid Necrosis

A

-Occurs in vasulitis and in RA

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8
Q

Soponification

A

-Lipase digestion post infarct leads to Ca binding within dead tissue and decrease in plasma calcium

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9
Q

Irreversible Cell Injury

A
  • Plasma Membran Ruptire
  • Influx of Ca
  • Lysosomal or mitochondrial Rupture
  • Nuclear fragmentation
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10
Q

Brain areas vulnerable to ischemic injury

A

-Pyramidal cells of hipocampus and purkinje cells of cerebellum

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11
Q

Kidney

A
  • Straight portion of the proximal tubule (medulla)
  • Thick ascending limb of the loop of henle (medulla)
  • Both have limited blood supply and increased metabolic demand
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12
Q

Shock

A
  • Cardiogenic/hypovolemic: Increased TPR, decreased CO, cool clammy patient
  • Septic: Vasodialtion leads to warm, red patient with decreased TPR and normal CO
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13
Q

Acute Inflammation

A

-Neutrophil, eosinophils, complement, Ab

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14
Q

Chronic

A

-Monocytes and lymphocytes predominate

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15
Q

Leukocyte extravasation

A
  • Margination becuse of dilation and turbulent flow
  • Rolling: P selectin from WP and E selectin, release due to IL-1 and IL-6 interact with sialyl lewis acid X on leukocytes
  • Tight adhesion: ICAMs on endothelium and Integrins on leukocytes
  • Tranmigration: Pecam, homotypic
  • Chemotactic by: Bacterial products (LPS), IL-8, C5a, LTB4, Kalikrein
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16
Q

Free Radical Damage

A
  • Lipid Peroxidation, protein damage, DNA damage
  • Radiation, drugs, etc
  • Eliminated by SOD, Catalase, Peroxidase, glutathione, ACE
17
Q

Free Radical Diseases

A
  • Retinopathy of prematurity, bronchopulmonary dysplasia
  • Carbon tetrachloride, acetomenaphin cause liver damage
  • Hemochromatosis causes liver cirrhosis
  • Reperfusion injury
18
Q

Wound Healing

A
  • Initially Neutrophil, platelets, macrophages cause inflammation
  • 3 days macrophages clear debris and granulation tissue with type 3 collagen begins to form
  • 7 days granulation tissue replaced with type I collagen
  • Wound healing delayed with Zn, Cu, Vit C deficencies
  • Keloid is overexuberant produciton of granulation tissue (type 3 collagen)
  • Hypertrophic scar is overprodcution of type 1 collagen
19
Q

Granulomas

A

-Casseating: Mycobacteria and fungal, bartonella
-Also seen in:
RA (Rheumatoid Nodules), fibrinous necrosis also seen in joints
-Churgg Straus and Wegners
-Rheumatic Fever
-Chrons
-Trepnoma (Gummas)
-Sarcoidosis
-Foreign Body
-Listeria
-Schistosomiasis

20
Q

Fe Poisoning

A

Common among children

  • Acutely leads to GI ulceration and bleeding due to free radical damage mediated by peroxiadtion of membran lipids by Fe
  • Chronically causes acidosis with anion gap
21
Q

Amyloidosis

A
  • Beta pleated sheets with apple green birefringence
  • AL (Primary) multiple myeloma and can present systemically (Heart, bruising, renal, neuro)
  • AA: SAA secondary to chronic inflammatory conditions (RA) has a systemic presentation
  • Tissue Tranthyretin: slower onset and most commonly seen in heart and nerves. Mutation can lead to hereditery form, but more commonly is due to senile, or old age
  • Alzheimers: APP
22
Q

Neoplastic Progression

A
  • Dysplasia leads to anaplasia and carcinoma in situ which is not through BM
  • Loss of E Cadherin allows for spread
  • Gain of collagenases and integins allow for spread to blood
  • Proper “Soil” allows spread to other organs
23
Q

Cachexia

A

Weight loss and fatigue with chronic illness

-TNF alpha, IL-6 and IFN y mediated

24
Q

Tuberous Sclerosis

A
  • AD mutation in TSG, incomplete penetrance
  • Most common symptoms are siezures, hypopigmentation (ash leaf spots)
  • Presence of harmatomas, most commonly giant cell astrocytoma in the brain (98%), also angiomyolipoma of the kidney and cardiac rhabdomyoma
25
Q

P16

A

Melanoma

26
Q

DCP4

A

Pancreatic carconima

27
Q

DCC

A

Colon Cancer

28
Q

AFP

A

Germ cell tumors and HCC

29
Q

CA-125

A

Ovarian Cancer

30
Q

Bombesin

A

Nonsepecific visceral malignancy

-similar to acanthosis nigricans

31
Q

EBV Cancers

A
  • Hodgkins and Burkitts lymphoma
  • Nasopahryngeal
  • CNS lymphomas in AIDS patients
32
Q

Cigarette

A

Laryngeal, Lung
Bladder, Kidney
Pancrease

33
Q

Arsenic

A

-SCC of skin and angioarcoma

34
Q

PTHrP

A

Most classic is squamous cell lung

-also breast, renal

35
Q

Vitamin D3 (1,25)

A

Sarcoidosis

-Lymphomas, mostly Hodgkins type, but can also be non hodgkin type

36
Q

EPO

A

VHL associated: Renal Cell, Pheo, Hemangioblastoma

-also HCC

37
Q

Psamomma

A
  • Papillary thyroid, breast, ovary, etc

- Mesothelial sturcutrues (Mesothelioma, meningioma)