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Last Minute Step 1 Facts > Chapter 1, 2, and 3 Stuff > Flashcards

Chapter 1, 2, and 3 Stuff Flashcards

1
Q

Metaplasia is reversible

Under persistent stress, metaplasia can progress to dysplasia and eventually to cancer
The one exception is…

A

apocrine metaplasia

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2
Q

Dysplasia often arises from a longstanding pathological…

A

hyperplasia or metaplasia

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3
Q

Is dysplasia reversible or irreversible?

A

Dysplasia is also reversible; however, carcinoma is not

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4
Q

What is the hallmark of irreversible cell damage?

A

Irreversible cell damage hallmark → cell membrane damage

Does it to the plasma membrane, the mitochondrial membrane (and thus the leakage of cytochrome c into cytosol), and the lysosomal membrane

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5
Q

The morphologic hallmark of cell death is…

A

The morphologic hallmark of cell death is loss of the nucleus
This occurs via condensation (pyknosis), fragmentation (karyorrhexis), and dissolution (karyolysis)

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6
Q

Red infarction arises if blood renters…

A

…a loosely organized tissue

Pulmonary or testicular infarction

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7
Q

Pancreatitis can exhibit what two types of necrosis?

A

Pancreatitis → can result from 2 things
Digestion of the pancreas ITSELF = liquefactive necrosis
Digestion of the fat surrounding the pancreas = fat necrosis

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8
Q

In dystrophic calcification, the damaged tissue…

A

…acts as a nidus for calcification in the setting of normal serum calcium

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9
Q

In metastatic calcification, high …

A

…serum or phosphate levels lead to calcium deposition in normal tissues

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10
Q

What is fibrinoid calcification?

A

Fibrinoid calcification: necrotic damage of blood vessel wall → leaking of proteins (fibrin) into the blood vessel wall → get bright pink staining; associated with malignant HTN
Especially associated with preeclampsia
Fibrinoid necrosis of the placenta occurs

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11
Q

What are the three basic principles of amyloidosis?

A

BASIC PRINCIPLES
A. Amyloid is a misfolded protein that deposits in the extracellular space, thereby
damaging tissues.

B. Multiple proteins can deposit as amyloid. Shared features include􏰠􏰣 beta-pleated sheet configuration; congo red staining and apple-green birefringence when viewed microscopically
under polarized light

􏰜􏰣C. Deposition can be systemic or localized.

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12
Q

What are the 2 types of systemic amyloidosis?

A

primary and secondary

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13
Q

Primary systemic amyloidosis is associated with what?

A

Associated with plasma cell dyscrasias (e.g., multiple myeloma)

Primary amyloidosis is systemic deposition of AL amyloid, which is derived from immunoglobulin light chain.

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14
Q

What gets deposited in secondary amyloidosis?

A

Secondary amyloidosis is systemic deposition of AA amyloid , which is derived from serum amyloid-associated protein (SAA).

􏰠􏰣SAA is an acute phase reactant that is increased in chronic inflammatory states,
malignancy, and Familial Mediterranean fever (FMF).

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15
Q

What is familial Mediterranean fever?

A

FMF is due to a dysfunction of neutrophils (autosomal recessive) and occurs in
persons of Mediterranean origin.

Presents with episodes of fever and acute serosal inflammation (can mimic appendicitis, arthritis, or myocardial infarction)

High SAA during attacks deposits as AA amyloid in tissues.

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16
Q

What are the major types of localized amyloidosis?

A
  1. Senile cardiac amyloidosis
  2. Familial amyloid cardiomyopathy
  3. Non-insulin-dependent diabetes mellitus
  4. Alzheimer disease
  5. Dialysis-associated amyloidosis
  6. Medullary carcinoma of the thyroid
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17
Q

Senile cardiac amyloidosis

vs. Familial amyloid cardiomyopathy

A

Senile cardiac amyloidosis:
Non-mutated serum transthyretin deposits in the heart.

Usually asymptomatic; present in 25% of individuals > 80 years of age

Familial amyloid cardiomyopathy:
􏰠Mutated serum transthyretin deposits in the heart leading to restrictive cardiomyopathy.

  1. 5% of African Americans carry the mutated gene.
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18
Q

What are mast cells activated by?

A

Mast cells are activated by tissue trauma, C3a and C5a, or by cross-linking of IgE

What explodes out of the mast cell?
Immediate response = histamine (does vasodilation and VP)
Late response = production of arachidonic acid metabolites (LTs in particular)

19
Q

what is hageman factor?

A

Hageman factor
Inactive proinflammatory protein produced by liver
Activated upon exposure to subendothelial or tissue collagen

20
Q

how does fever occur?

A

Pyrogens from bacteria stimulate macrophages to release IL-1 and TNF → these stimulate cyclooxygenase activity in the perivascular cells of the hypothalamus → this produces PGE2 → goes and increases the temperature set point

21
Q

LAD is a defect in what specific part of the integrin?

A

autosomal defect of integrins specifically the CD18 subunit

22
Q

CD25 polymorphisms are associated with…

A

MS and TIDM

23
Q

~Type IV rxn

~Can be a primary DO or associated with RA
RF is present in these patients EVEN when they don’t have RA

What does this refer to?

A

Sjogrens!

24
Q

What are pregnant women with anti-SSA (the antibody associated with sjogrens) at risk for?

A

Pregnant women with anti-SSA are at risk for delivering babies with neonatal LUPUS and congenital HB

Some pregnant SLE patients have anti-SSA and B….so make sure to screen

25
Q

What is diffuse scleroderma?

A

Diffuse type exhibits skin and early visceral involvement.
􏰞􏰣 Almost any organ can be involved; esophagus is commonly affected, resulting in disordered motility (dysphagia for solids and liquids).
2. Characterized by ANA and anti-DNA topoisomerase I (Scl-70) antibody

26
Q

What is diffuse scleroderma?

A

Diffuse type exhibits skin and early visceral involvement.
􏰞􏰣 Almost any organ can be involved; esophagus is commonly affected, resulting in disordered motility (dysphagia for solids and liquids).

Characterized by ANA and anti-DNA topoisomerase I (Scl-70) antibody

27
Q

What is localized scleroderma?

A

Localized type exhibits local skin and late visceral involvement.

􏰞􏰣Prototype is CREST syndrome: Calcinosis/anti-Centromere antibodies, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias of the skin.

28
Q

What are the important growth factors for wound healing?

A

Important Factors:
TGF-alpha: epithelial and fibroblast growth factor

TGF-beta: important fibroblast growth factor; also inhibits inflammation

PDGF: growth factor for endothelium, smooth muscle, and fibroblast

FGF: important for angiogenesis; also mediates skeletal development

VEGF: angiogenesis

Vitamin C, copper, and zinc are all important for wound healing

29
Q

what are the cancers associated with alcohol?

A

Squamous cell carcinoma of oropharynx and upper esophagus, pancreatic carcinoma, and hepatocellular carcinoma

30
Q

what are the cancers associated with smoking?

A

Carcinoma of oropharynx, esophagus, lung, kidney, and bladder

31
Q

vinyl chloride vs. aflatoxins?

A

vinyl chloride = angiosarcoma

aflatoxins = hepatocellular carcinoma

32
Q

what are the cancers associated with arsenic?

A

Squamous cell carcinoma of skin, lung cancer, and angiosarcoma of liver

33
Q

what are the cancers associated with EBV?

A

Nasopharyngeal carcinoma, Burkitt lymphoma, and CNS lymphoma in AIDS

34
Q

oncogene PDGFB is associated with

A

astrocytomas

35
Q

oncogene CCNDl (cylin Dl) is associated with

A

Mantle cell lymphoma

36
Q

oncogene CDK4 is associated with

A

melanoma

37
Q

vimentin stains for what

A

mesenchyme

38
Q

desmin stains for what

A

muscle

39
Q

GFAP vs neurofilament

A

neuroglia (GFAP) and neurons (neurofilament)

40
Q

thyroglobulin stains for

A

thyroid follicular cells

41
Q

s-100 stains for

A

melanoma

42
Q

chromogranin stains for

A

neuroendocrine cells

43
Q

what does anaplastic mean

A

Anaplastic: a complete lack of differentiation of cells in a malignant neoplasm

44
Q

what is the warburg effect?

A

Warbug effect: shift of glucose metabolism away from mito ox phos to straight up glycolysis

Last Minute Step 1 Facts (16 decks)

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