Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

Apoptosis findings

A
  • Cell shrinkage
  • Chromatin condensation
  • Membrane blebbing
  • Formation of apoptotic bodies (which are then phagocytosed)
  • Eosinophilic cytoplasm
  • Basophilic nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sensitive indicator of apoptosis

A

DNA laddering (fragments in multiples of 180 bp)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Occurs when a regulating factor is withdrawn from a proliferating cell population

A

Intrinsic (mitochondrial) apoptotic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

BAK

A

Pro-apoptotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What makes bcl-2 anti-apoptotic

A

Bcl-2 prevent cytochrome c release by binding to and inhibiting APAF-1. APAF-1 normally binds to cytochrome c and induces activation of caspase 9, inhibiting caspase cascade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Extrinsic (death receptor) apoptotic pathway

A

2 pathways:

  • Ligand receptor interactions (FasL binding to Fas [CD95] or TNF-α binding to TNF)
  • Immune cell (cytotoxic T-cell release of perforin and granzyme B)

Fas-FasL interaction is necessary in thymic medullary negative selection. Mutations in Fas ↑ numbers of circulating self reacting lymphocytes due to failure of clonal deletion.

Defective Fas-FasL interactions cause AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Autoimmune lymphoproliferative syndrome caused by

A

Defective Fas-FasL interactions (form of extrinsic apoptotic pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Compare coagulative and liquefactive necrosis

A

Coagulative → proteins denature then enzymatic degradation

Liquefactive → enzymatic degradation first then proteins denature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Compare wet and dry gangrenous necrosis

A

Dry → ischemia; coagulative necrosis

Wet → superinfection; liquefactive superimposed on coagulative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ischemia of kidney

A
  • Straight segment of proximal tubule (medulla)

- Thick ascending limb (medulla)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cellular injury reversible with O2

A
  • Cellular/ mitochondrial swelling (↓ ATP → ↓ activity of Na+/K+ pumps)
  • Nuclear chromatin clumping
  • Membrane blebbing
  • ↓ glycogen
  • Fatty change
  • Ribosomal/ polysomal detachment (↓ protein synthesis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Irreversible cellular injury

A
  • Mitochondrial permeability/ vacuolization; phospholipid-containing amorphous densities within mitochondria (swelling alone is reversible)
  • Nuclear pyknosis (condensation), karyorrhexia (fragmentation), karyolysis (fading)
  • Plasma membrane damage (degradation of membrane phospholipid)
  • Lysosomal rupture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Contains multiple blood supplies

A
  • Liver
  • Lung
  • Intestine
  • Testes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Solid organs with single (end-arterial) blood supply

A
  • Heart
  • Kidney
  • Spleen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Functio laesa

A
  • Loss on function

- Characterization of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chronic inflammation

A
  • Mononuclear (monocyte/macrophage, lymphocytes, plasma cells) and fibroblast mediated
  • Characterized by persistent destruction and repair
  • Associated with blood vessel proliferation, fibrosis
  • Granuloma: nodular collections of epithelioid macrophages and giant cells
  • Outcomes include scarring and amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Chromatolysis

A

Reaction of neuronal cell body to axonal injury. Changes reflect ↑ protein synthesis in effort to repair damaged axon. Characterized by:

  • Round cellular swelling
  • Displacement of the nucleus to the periphery
  • Dispersion of Nissl substance through cytoplasm

Concurrent with Wallerian degeneration → degeneration of axon distal to site of injury; macrophages remove debris and myelin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Dystrophic calcification

A
  • Ca2+ deposition in abnormal tissues secondary to injury or necrosis
  • Seen in TB (lungs and pericardium), liquefactive necrosis of chronic abscesses, fat necrosis, infarcts, thrombi, schistosomiasis, Monckeberg arteriolosclerosis, congenital CMV + toxoplasmosis, psammoma bodies
  • Normocalcemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Metastatic calcification

A
  • Widespread (ie diffuse, metastatic) deposition of Ca2+ in normal tissue secondary to hypercalcemia or high calcium-phosphate product levels
  • Ca2+ deposits predominantly in interstitial tissues of kidney, lung, and gastric mucosa (these tissues lose acid quickly; ↑ pH favors deposition)
  • NOT normocalcemic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Step 1 Extravasation: Margination and rolling

A
  • Defective in leukocyte adhesion deficiency type 2 (↓ Sialyl-Lewis-x)

Vascular/stroma: Leukocyte

  • E-selectin: Sialyl-Lewis-x
  • P-selectin: Sialyl-Lewis-x
  • GlyCAM-1, CD34: L-selectin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Step 2 Extravasation: Tight-binding

A
  • Defective in leukocyte adhesion deficiency type 1 (↓ CD18 integrin subunit)

Vascular/stroma: Leukocyte

  • ICAM-1 (CD54): CD11/18 integrins (LFA-1, Mac-1)
  • VCAM-1 (CD106): VLA-4 integrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Step 3 Extravasation: Diapedesis

A
  • WBC travels between endothelial cells and exits blood vessel

Vascular/stroma: Leukocyte
- PECAM-1 (CD31): PECAM-1 (CD31)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Step 4 Extravasation: Migration

A

Chemotactic products released in response to bacteria:

  • C5a
  • IL-8
  • LTB4
  • Kallikrein
  • Platelet-activating factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Inhalation injury and sequelae

A
  • Pulmonary complication associated with smoke and fire

- Caused by heat, particulates (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Tensile strength after scar formation

A

70-80% of tensile strength regained at 3 months, little additional tensile strength will be regained afterward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Compare collagen organization of hypertrophic and keloid scars

A

Hypertrophic → parallel organization

Keloid → disorganized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

PDGF

A
  • Secreted by activated platelets and macrophages
  • Induces vascular remodeling and smooth muscle migration
  • Stimulates fibroblast growth for collagen synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

FGF

A

Stimulates angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

EGF

A

Stimulates cell growth via tyrosine kinases (eg EGFR, ErbB1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

TGF-β

A
  • Angiogenesis
  • Fibrosis
  • Cell cycle arrest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Metalloproteinases

A

Tissue remodeling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

VEGF

A

Stimulates angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Inflammatory stage of wound healing

A
  • Up to 3 days after wound
  • Effector cells → platelets, neutrophils, macrophages
  • Clot formation
  • ↑ vessel permeability and neutrophil migration into tissue
  • Macrophages clear debris 2 days later
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Proliferative stage of wound healing

A
  • Day 3 - weeks after wound
  • Effector cells → fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages
  • Deposition of granulation tissue and type III collagen
  • Angiogenesis
  • Epithelial cell proliferation
  • Dissolution of clot
  • Wound contraction (mediated by myofibroblasts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Remodeling stage of wound healing

A
  • 1 week - 6+ months after wound
  • Effector cells → fibroblasts
  • Type III collagen replaced by type I collagen
  • ↑ tensile strength of tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Bacterial infections that cause granuloma formation

A
  • Mycoplasma
  • Bartonella henselae
  • Listeria monocytogenes
  • Treponema pallidum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Parasitic infections that cause granuloma formation

A

Schistosomiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Fungal infections that cause granuloma formation

A

Endemic mycoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Granuloma formation

A
  • TH1 cells secrete IFN-gamma, activating macrophages

- TNF-alpha from macrophages induces and maintains granuloma formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Compare causes of exudate and transudate accumulation

A

Exudate → lymphatic obstruction (chylous), inflammation/infection, malignancy

Transudate → ↑ hydrostatic pressure (eg HF, Na+ retention), ↓ oncotic pressure (eg cirrhosis, nephrotic syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does ESR work

A

Products of inflammation (eg fibrinogen) coat RBCs and cause aggregation. The denser RBCs aggregate and fall at a faster rate within a pipetic tube. Often co-tested with CRP levles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

↑ ESR

A
  • Most anemias
  • Infections
  • Inflammation (eg giant cell arteritis, polymyalgia rheumatica)
  • Cancer (eg metastases, multiple myeloma)
  • Renal disease (end-stage or nephrotic syndrome)
  • Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

↓ ESR

A
  • Sickle cell anemia (altered shape)
  • Polycythemia (↑ RBCs “dilute” aggregation factors)
  • HF
  • Microcytosis
  • Hypofibrinogenemia
44
Q

AL (primary) amyloidosis

A
  • Due to deposition of proteins from Ig Light chains
  • Can occur as a plasma cell disorder or associated with multiple myeloma
  • Often affects multiple organ systems, including renal (nephrotic syndrome), cardiac (restrictive cardiomyopathy, arrhythmia), hematologic (easy bruising, splenomegaly), GI (hepatomegaly) and neurologic (neuropathy)
45
Q

AA (secondary) amyloidosis

A
  • Seen with chronic inflammatory conditions such as rheumatoid arthritis, IBD, spondyloarthropathy, familial Mediterranean fever, protracted infection
  • Fibrils composed of serum Amyloid A
  • Often multisystem like AL amyloidosis
46
Q

Dialysis-related amyloidosis

A
  • Fibrils composed of β2-microglobulin in patients with ESRD and/or on long-term dialysis
  • MAY PRESENT AS CARPAL TUNNEL SYNDROME
47
Q

Heritable amyloidosis

A

Heterogeneous group of disorders, including familial amyloid polyneuropathies due to transthyretin gene mutation

48
Q

Age-related (senile) amyloidosis

A
  • Due to deposition of normal (wild-type) transthyretin (TTR) predominantly in cardiac ventricles
  • Slower progression of cardiac dysfunction relative to AL amyloidosis
49
Q

Organ specific amyoidosis

A
  • Amyoid deposition localized to a single organ
  • Most important form is amyloidosis in Alzhemier disease due to deposition of beta-amyloid protein cleaved from APP
  • TIIDM → islet amyloid polypeptide (IAPP) → amylin in pancreatic islets
  • Normal aging → atrial amyloidosis → atrial natriuretic peptide
50
Q

Lipofuscin

A
  • A yellow-brown “wear and tear” pigment associated with normal aging
  • Formed by oxidation and polymerization of autophagocytosed organellar membranes
  • Autopsy of elderly person will reveal deposits in heart, colon, liver, kidney, eye and other organs
51
Q

Compare grade and stage

A

Grade → degree of cellular differentiation and mitotic activity on histology

Stage → degree of localization/spread based on site and size of primary lesion, spread to regional lymph nodes, presence of metastases; TNM, where M is often most important

52
Q

Compare hamartoma and choristoma

A

Hamartoma → disorganized overgrowth of tissues in their native location)

Choristoma → normal tissue in a foreign location

53
Q

Paraneoplastic hypercalcemia

A

PTHrP → squamous cell carcinomas of lung, head and neck; renal, bladder, breast and ovarian carcinomas

↑ 1,25-(OH)2 vitamin D3 (calcitriol) → lymphoma

54
Q

Paraneoplastic polycythemia

A

↑ EPO → renal cell carcinoma, hepatocellular carcinoma, hemangioblastoma, pheochromocytoma, leiomyoma

55
Q

Paraneoplastic pure red cell aplasia

A

Anemia with LOW reticulocytes → thymoma

56
Q

Good syndrome

A

Paraneoplastic hypogammaglobulinemia → thymoma

57
Q

Trosseau syndrome

A

Migratory superficial thrombophlebitis → adenocarcinomas, especially pancreatic

58
Q

Paraneoplastic nonbacterial thrombotic (marantic) endocarditis

A

Deposition of sterile platelet thrombi on heart valves → adenocarcinomas, especially pancreatic

59
Q

Anti-NMDA receptor encephalitits

A

Psychiatric disturbance, memory deficits, seizures, dyskinesias, autonomic instability, language dysfunction → ovarian teratoma

60
Q

Opsoclonus-myoclonus ataxia syndrome

A

“Dancing eyes, dancing feet” → neuroblastoma (children), small cell lung cancer (adults)

61
Q

Paraneoplastic cerebellar degeneration

A

Antibodies against Hu, Yo, Tr antigens in Purkinje cells → Small cell lung cancer, gynecologic and breast cancers, and Hodgkin lymphoma

62
Q

Paraneoplasic encephalitis

A

Antibodies against Hu antigens in neurons → small cell lung cancer

63
Q

ALK

A
  • Oncogene
  • Receptor tyrosine kinase
  • Lung adenocarcinoma
64
Q

BCR-ABL

A
  • Oncogene
  • Tyrosine kinase
  • CML, ALL
65
Q

BCL-2

A
  • Oncogene
  • Anti-apoptotic molecule
  • Follicular and diffuse large B cell lymphoma
66
Q

BRAF

A
  • Oncogene
  • Serine/threonine kinase
  • Melanoma, non-Hodgkin lymphoma
67
Q

c-KIT

A
  • Oncogene
  • Cytokine receptor
  • Gastrointestinal stromal tumor (GIST)
68
Q

c-MYC

A
  • Oncogene
  • Transcription factor
  • Burkitt lymphoma
69
Q

HER2/neu (c-erbB2)

A
  • Oncogene
  • Tyrosine kinase
  • Breast and gastric carcinomas
70
Q

JAK2

A
  • Oncogene
  • Tyrosine kinase
  • Chronic myeloproliferative disorders
71
Q

KRAS

A
  • Oncogene
  • GTPase
  • Colon cancer, lung cancer, pancreatic cancer
72
Q

MYCL1

A
  • Oncogene
  • Transcription factor
  • Lung tumor
73
Q

MYCN

A
  • Oncogene
  • Transcription factor
  • Neuroblastoma
74
Q

RET

A
  • Oncogene
  • Tyrosine kinase
  • MEN 2A and 2B, medullary thyroid cancer
75
Q

APC

A
  • Tumor suppressor gene

- Colorectal cancer (associated with FAP)

76
Q

BRCA1/BRCA2

A
  • Tumor suppressor gene
  • Breast and ovarian cancer
  • DNA repair protein
77
Q

CDKN2A

A
  • Tumor suppressor gene
  • Melanoma, pancreatic cancer
  • p16, blocks G1 → S phase
78
Q

DCC

A
  • Tumor suppressor gene
  • Colon cancer
  • DCC → deleted in colon cancer
79
Q

DPC4/SMAD4

A
  • Tumor suppressor gene
  • Pancreatic cancer
  • DPC → deleted in pancreatic cancer
80
Q

MEN1

A
  • Tumor suppressor gene
  • MEN1
  • Menin
81
Q

NF1

A
  • Tumor suppressor gene
  • NF1
  • Ras GTPase activating protein (neurofibromin)
82
Q

NF2

A
  • Tumor suppressor gene
  • NF2
  • Merlin (schwannomin) protein
83
Q

PTEN

A
  • Tumor suppressor gene

- Breast cancer, prostate cancer, endometrial cancer

84
Q

Rb

A
  • Tumor suppressor gene

- Retinoblastoma, osteosarcoma

85
Q

TP53

A
  • Tumor suppressor gene
  • Most human cancers, Li-Fraumeni syndrome
  • p53, activates p21, blocks G1 → S phase
86
Q

TSC1

A
  • Tumor suppressor gene
  • Tuberous sclerosis
  • Hamartin protein
87
Q

TSC2

A
  • Tumor suppressor gene
  • Tuberous sclerosis
  • Tuberin protein
88
Q

VHL

A
  • Tumor suppressor gene
  • von Hippel-Lindau disease, renal cell carcinoma
  • Inhibits hypoxia inducible factor 1a
89
Q

WT1/WT2

A
  • Tumor suppressor gene

- Wilms tumor (nephroblastoma)

90
Q

2nd leading cause of lung cancer after cigarette smoke

A

Radon

91
Q

Alkaline phosphatase

A
  • Metastases to bone or liver
  • Paget disease of bone
  • Seminoma (placental ALP)
92
Q

AFP

A
  • Hepatocellular caricnoma
  • Hepatoblastoma
  • Yolk sac (endodermal sinus) tumor
  • Mixed germ cell tumor

Normally made by fetus. Transiently elevated in pregnancy. High levels associated with neural tube and abdominal wall defects, low levels associated with Down syndrome.

93
Q

hCG

A
  • Hydatiform mole
  • Choriocarcinoma
  • Testicular cancer
  • Mixed germ cell tumor

Produced by synciotrophoblasts of the plascenta

94
Q

CA 15-3/ CA 27-29

A

Breast cancer

95
Q

CA 19-9

A

Pancreatic adenocarcinoma

96
Q

CA 125

A

Ovarian cancer

97
Q

Calcitonin

A

Medullary thyroid carcinoma

98
Q

CEA

A

CarcinoEmbryonic Antigen

Very nonspecific but produced by around 70% of colorectal and pancreatic cancers. Also produced by gastric, breast and medullary thyroid carcinomas.

99
Q

PSA

A
  • Prostate specific antigen
  • Prostate cancer

Can also be elevated in BPH and prostatitis. Questionable risk/benefit for screening.

100
Q

P-glycoprotein

A
  • Multidrug resistance protein 1 (MDR1)
  • Classically seen in adrenal cell carcinoma but also expressed by other cancer cells (eg colon, liver)
  • Used to pump out toxins, including chemotherapeutic agents (one mechanism of ↓ responsiveness or resistance to chemotherapy over time)
101
Q

Cachexia

A

Weight loss, muscle atrophy, and fatigue that occur in chronic disease (eg cancer, AIDS, heart failure, COPD)

Mediated by TNF, INF-gamma, IL-1, IL-6

102
Q

Sarcomas generally spread

A

Hematogenously

103
Q

Carcinomas generally spread

A

Lymphatically

104
Q

Carcinomas that spread hematogenously

A
  • Renal cell carcinoma
  • Choriocarcinoma
  • Hepatocellular carcinoma
  • Follicular thyroid carcinoma
105
Q

Site of metastases → brain

A

Lung > breast > prostate > melanoma > GI

106
Q

Site of metastases → liver

A

Colon&raquo_space; stomach > pancreas

107
Q

Site of metastases → bone

A

Prostate, breast > lung, thyroid, kidney

Breast → mixed
Lung → mixed
Thyroid → lytic
Kidney → lytic
Prostate → blastic

Predilection for axial skeleton

Step 1 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions