Pathology Flashcards Preview

Step 1 High Yield > Pathology > Flashcards

Flashcards in Pathology Deck (25)
Loading flashcards...
1
Q

In the intrinsic pathway, what are the functions of the following…
BAX:
Bcl-2:
Apaf-1:

A

BAX: Pro-apoptotic proteins
Bcl-2: prevents cytochrome C release by binding to and inhibiting Apaf-1
Apaf-1: Normally induces the activation of caspases (unless t(14:18))

2
Q

What is the function of the Fas-FasL interaction?

A

After Fas crosslinks with FasL, multiple Fas molecules coalesce, forming a binding site for a death domain - containing an adapter protein FADD which activates caspases
- Also necessary in thymic medullary negative selection

3
Q

In coagulative necrosis ________ is first, followed by enzymatic degradation
In liquefactive necrosis enzymatic degradation is first due to release of _________ enzymes

A

In coagulative necrosis protein denaturation is first, followed by enzymatic degradation
In liquefactive necrosis enzymatic degradation is first due to release of lysozomal enzymes

4
Q

What is chromatolysis?

What are the 3 characterizations:

A

Changes following axonal injury which reflect increased protein synthesis in effort to repair the damaged axon
Characterized by:
Round cellular swelling
Displacement of nucleus to the periphery
Dispersion of nissl substance throughout the cytoplasm

5
Q

Dystrophic calcification is found in patients with ________ calcium levels
Metastatic calcification is found in patients with ________ calcium levels

A

Normal

Increased

6
Q

Extravasation occurs at __________ _________

A

Postcapillary venules

7
Q

What is responsible for tight binding during extravasation?
Vasculature:
Leukoctes:

A

Vasculature: ICAM-1 and VCAM-1
Leukoctes: CD11/18 integrins (LFA-1) and VLA-4 integrin

8
Q

What is responsible for diapedesis during extravasation?
Vasculature:
Leukoctes:

A

Vasculature: PECAM-1
Leukoctes: PECAM-1

9
Q

How does carbon tetrachloride lead to fatty liver change?

A

CCl4 produces free radicals which induce cellular injury through membrane damage (lipid peroxidation, protein modification) thus causing cellular swelling (destruction of Na/K+ pump and Ca2+ pump leads to sodium, calcium and water buildup in the cell) which leads to RER swelling to the point where ribosomes detach and thus are unable to create apolipoproteins (which remove fat from the liver) thus leading to fatty liver

10
Q

____ from macrophages induce and maintain granuloma formation

A

TNF-α

11
Q

Amyloidosis is the abnormal aggregation of proteins into __-_______ structures

A

β-pleated

12
Q

Dialysis related amyloidosis is due to fibrils composed of…

A

β-2 microglobulin

13
Q

What is desmoplasia?

A

Fibrous tissue formation in response to neoplasm (linitis plastica in diffuse stomach cancer)

14
Q

What is cachexia?

What mediates it?

A

Cachexia: Weight loss, muscle atrophy, fatigue

Mediated by TNF-α, IFN-gamma, and IL-6

15
Q

What gene product is disrupted in a ras mutation and what is it’s normal function?

A

GTPase

Normally allows RAS-GTP to become RAS-GDP which shuts off replication

16
Q

NF1 gene product:

NF2 gene product:

A

NF1 gene product: RAS-GTPase activating protein (neurofibromin)
NF2 gene product: Merlin protein (schwannomin)

17
Q

VHL gene product?

A

inhibits hypoxia inducible factor 1a

18
Q

S-100 is the tumor marker for…(more than 1)

A

Neural crest origin tumors

Melanomas, neural tumors, schwannomas, Langerhans cell histiocytosis

19
Q

When are psammoma bodies seen?

A

Papillary carcinoma of thyroid
Serous papillary cystadenocarcinoma of the ovary
Meningioma
Malignant mesothelioma

20
Q

Cancer incidence: (top 3)

Cancer mortality: (top 3)

A

Incidence: Prostate/Breast > Lung > Colon/rectum
Mortality: Lung > Prostate/Breast > Colon/rectum

21
Q

What cancers can release PTHrP?

A

Squamous cell lung carcinoma
Renal cell carcinoma
Breast cancer

22
Q

Describe the following parts of apoptosis…
Karyorrhexis:
Pyknosis:
DNA laddering:

A

Karyorrhexis: Nuclear fragmentation
Pyknosis: Nuclear shrinkage
DNA laddering: A sensitive indicator of apoptosis; during karyorrhexis, endonucleases cleave at internucleosomal regions, yielding 180-bp fragments

23
Q

Name the protein defect in the following hyperlipoproteinemias…
Familial chylomicronemia syndrome (Type I):
Hypercholesterolemia (Type II):
Dysbetalipoproteinemia (III):
Hypertriglyceridemia (IV):

A

Familial chylomicronemia syndrome (Type I): LPL and ApoC-II
Hypercholesterolemia (Type II): LDLr and ApoB-100
Dysbetalipoproteinemia (III): ApoE
Hypertriglyceridemia (IV): ApoA-V

24
Q

Name the major manifestation of the following hyperproteinemias…
Familial chylomicronemia syndrome (Type I):
Hypercholesterolemia (Type II):
Dysbetalipoproteinemia (III):
Hypertriglyceridemia (IV):

A

Familial chylomicronemia syndrome (Type I): Acute pancreatitis
Hypercholesterolemia (Type II): Premature coronary artery disease
Dysbetalipoproteinemia (III): Premature coronary artery disease
Hypertriglyceridemia (IV): Increased pancreatitis risk

25
Q

What happens with loss of the VHL tumor suppressor gene in renal cell carcinoma?

A

Increased IGF-1 (promotes growth) and increased HIF transcription factor (increases VEGF and PDGF)