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M2 > Pathbio 1 > Flashcards

Pathbio 1 Flashcards

0
Q

Neurofibromin

A

GTPase Activating Protein important for inactivation of RAS

  • downregulation of proliferation
  • enhances RAS intrinsic GTPase activity
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1
Q

What is RAS?

A

Signal transducing protein activated by growth factor.

  • GTP binding protein (G protein)
  • GF-R -> (GDP -> GTP) -> on
  • -activation of MAP kinase pathway -> transcription and proliferation
  • has intrinsic GTPase activity, but enhanced by GAP -> off
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2
Q

What is MYC and how is it controlled?

A

MYC - transcription activated by Growth Factor
Binds MAX protein - forms heterodimer
MYC-MAX binds DNA -> upregulation of pro-cell division genes
Downregulated by MAX homodimers and MAD-MAX heterodimers

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3
Q

p53

A

at DNA checkpoints during cell cycle, if DNA damage is detected, p53 is induced

p53 -> increased p21 -> CDK inhibitor expression -> arrest of cell cycle and DNA repair

  • -Success: p53 induced transcription of p53 degrading protein
  • -Fail: p53 induced transcription of pro-aptotic protein (BAX) and repression of pro-proliferative proteins
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4
Q

What is the most common change seen in Metaplasia?

A

Columnar -> Squamous epithelial cell types

ex: pseudostratified, ciliated, columnar epithelium of respiratory tract -> stratified squamous in smokers

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5
Q

What type of metaplasia is seen in GERD patients?

A

stratified squamous of lower esophagus -> gastric / intestinal type glandular epithelium (columnar) - mucus production to protect against acid erosion

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6
Q

What happens in lysosomal storage disorders?

A

Enzymatic dysfunction (inherited deficiency or acquired inhibition) -> accumulation of lysosomal contents and potential cellular injury

Neutrophils and macrophages accumulate debris - can’t break down

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7
Q

In what process of cellular change is the ubiquitin pathway important?

A

Atrophy

ubiquitin pathway destroys cellular components by lysosome and proteasome activity

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8
Q

How does metaplasia occur?

A

product of chronic trauma or irritation
Cytokine, GF and ECM signals -> transcriptional changes in STEM CELLS or reserve cells -> differentiation toward new cell type.

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9
Q

Myositis ossificans

A

Metaplasia of skeletal muscle -> bone following trauma

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10
Q

Kartagener syndrome

A

primary ciliary dyskinesia accompanied by situs inversus, chronic sinusitis, bronchiectasis

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11
Q

Etiologic factors in fatty change of the liver

A

Starvation - increase fatty acid uptake from adipose
Kwashiorkor and CCl4 toxicity - decreased apoprotein synth-> lipoprotein export
ETOH abuse, diabetes, obesity, hypoxia - alter TG synth / removal

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12
Q

What stain is used for visualizing fat?

A

Oil Red O

stains fat inclusions red vs. clear seen in H&E staining

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13
Q

4 examples of cellular cholesterol accumulation

A
  1. atherosclerosis - arterial plaque
  2. xanthoma - hyperlipidemia
  3. sites of necrosis w/ 2ndary inflammation
  4. cholesterolosis - sub-epithelial plaque of gallbladder
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14
Q

Cholesterol cleft

A

extracellular crystallization of cholesterol esters

Seen microscopically as clear crystalline clefts (ex. atherosclerotic plaque)

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15
Q

Russel body

A

protein inclusion in plasma cell - excessive immunoglobin production

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16
Q

3 examples of intracellular protein accumulation

A
  1. proteinuria: increased protein reabsorption by proximal tubule cells - globular inclusions
  2. Immunoglobin accumulation - Russell bodies in plasma cells
  3. a1 antitrypsin mutation - misfolding of protein, no cellular export, accumulation in hepatocytic ER
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17
Q

What is PAS staining used for?

A

Carbohydrate staining

Glycogen inclusions appear magenta (vs. clear in H&E stain)

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18
Q

What cell type produces bilirubin?

A

Macrophages

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19
Q

biliverdin

A

open chain form of porphyrin ring

formed in macrophage

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20
Q

What is conjugated bilirubin and where is it found?

A

Bilirubin conjugated to glucuronides by glucuronidyl transferase
Produced in hepatocytes
found in biliary system

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21
Q

What processes can be responsible for elevated serum conjugated bilirubin?

A

Hemolytic anemia - increase bilirubin production
Hepatocyte dysfunction - decrease conjugation
-genetic - inborn error of metabolism (glucuronyl transferase deficiency) - jaundiced baby
-acquired (virus or ETOH)

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22
Q

What are causes of increased serum conjugated bilirubin?

A

Hepatocyte dysfunction - decreased bilirubin secretion
-genetic
-acquired
Cholestasis - intra or extrahepatic biliary obstruction

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23
Q

What is a good lab test for cholestasis?

A

Alkaline phosphatase - increased levels indicative

- induced by bile stasis
- hepatic origin confirmed by increased GGT (gamma glutamyl transpeptidase) level

test for elevated conjugated bilirubin is less sensitive

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24
Q

How is cholestasis appreciated microscopically?

A

Dilated greenish bile canaliculi and bile ducts in liver sections
w/ obstruction - biliary back-up, bilirubin pigment visible
also seen in hepatocytes.

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25
Q

What stain is used to differentiate hemosiderin inclussions?

A

Prussian Blue

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26
Q

3 etiologies of hypoxia

A
  1. decreased oxygenation of blood
  2. decreased oxygen carrying capacity of blood
  3. ischemia
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27
Q

5 etiologic factors of cell injury and death

A
  1. ATP depletion
  2. increased cytosolic Ca++
  3. free radical generation
  4. mitochondrial injury
  5. cellular and subcellular membrane injury
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28
Q

Deleterious reactions assoc. w/ ATP depletion

A
  • decreased activity of Na/K ATPase -> increased intracellular H2O
  • increased anaerobic glycolysis -> lactic acidosis
  • decreased function of Ca++ pump -> enzymatic activation
  • ER dysfunction -> decreased and abnormal protein synthesis
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29
Q

What is the normal ratio of cytosolic to extracellular Calcium?

A

1:15,000

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30
Q

What kind of necrosis is associated with acute pancreatitis?

A

Fatty necrosis

Inappropriate release of pancreatic lipases

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31
Q

4 serum markers of necrosis

A
  1. troponins (esp myocardial necrosis, e.g. MI)
  2. transaminases (ALT / AST)
    • ALT: liver specific AST: also found in heart, kidney, skeletal muscle
  3. lactate dehydrogenase - LD is non-specific
  4. amylase and lipase - pancreas
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32
Q

Serum Troponins

  • indicate what?
  • pathologic mechanism?
A

Sensitive and specific early marker of myocardial necrosis (via ischemia)

Significant membrane damage -> increased permeability -> increased serum troponin

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33
Q

ALT / AST

-markers for what?

A

Transaminases
ALT: specific marker of hepatic necrosis
AST: assoc. w/ hepatic necrosis, but less specific. Also expressed in heart, kidney, sk. muscle

*level of elevation not indicative or predictive of extent of damage or prognosis

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34
Q

LD / LDH

A

Lactate dehydrogenase

  • non-specific serum marker for necrosis
  • LD1: heart, erythrocytes
  • LD2: WBC
  • LD3: Lung
  • LD4: Kidney, pancrease, placenta
  • LD5: sk. muscle and liver
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35
Q

Amylase and Lipase

-markers of what?

A

Pancreatic enzymes
Damage related to obstruction of pancreatic duct (gallstone)
Acinar cell injury
**Lipase more sensitive and specific for acute pancreatitis

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36
Q

4 apoptotic pathways

A

Extrinsic: FAS - FASL -> activation of FADD (fas assoc. death domain) -> capsase activation

Intrinsic: decreased growth /survival factor -> increased pro-apoptotic gene expression (BAX) and decreased anti-apop gene expression (BCL-2) -> capsase

P53: DNA damage detected -> p53 -> cell cycle arrest and DNA repair. If fail -> increased BAX, decreased BCL-2 -> capsase

Perforin/Granzyme: Cytotoxic Tcell recognition of foreign Ag + MHC-I -> perforin release, then granzyme -> capsase activity

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37
Q

Telomerase

A

Enzyme that regenerates telomeres after incomplete duplication during cell division

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38
Q

Dystrophic calcification

A

takes place w/ normal serum Ca levels and metabolism
Cell damage -> increased permeability -> calcium influx -> addition of PO4 -> calcium phosphate crystals that can deposit in cells and tissues

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39
Q

Psammoma bodies

A

Product of Dystrophic Calcification

  • circular concretions w/ concentric layering
  • papillary carcinomas
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40
Q

What stain is used to differentiate amyloid from other extracellular aggregations?

A

Congo red
under light microscopy appears red-orange
under polarized light microscopy appears green-yellow biofringence

41
Q

What is amyloid?

A

extracellular accumulation of protein. May be normal or abnormal protein.
Usually normal, but misfolded. Must be produced in great enough quantity to overcome degradation.

42
Q

What are the major types of amyloid?

A

AL: Amyloid light chain: light chain of Ig (usually lambda)
AA: Amyloid associated: hepatic acute phase protein - serum amyloid-associated protein
AB: B-amyloid - brain only. Fragment of Amyloid Precursor Protein (APP)
a-secretase: soluble fragments
B-secretase: AB fragments -> amyloid plaque

43
Q

2 types (and subtypes) of localized amyloidosis

A
  1. Cerebral Amyloidosis: AB amyloid (alzheimer’s and cerebral amyloid angiopathy)
  2. Endocrine Amyloidosis: AE amyloid
    a) medullary thyroid carcinoma (from calcitonin w/ C cell malignancy)
    b) T2DM - amyloid or islet associated polypeptide
    c) isolated atrial amyloidosis - from ANF
44
Q

2 examples of hereditary amyloidosis

A
  1. Familial Mediteranean Fever (AA)
    • Autosomal recessive - disorder of pyrin - recurrent fever and inflammation, overproduction of IL1
  2. Familial Amyloidotic Neuropathies (ATTR)
    • Autosomal dominant disorder of transthyretin - peripheral and autonomic nerves
45
Q

What is the most common location of amyloid deposits and what are the symptoms?

A

Kidney

Proteinuria and eventual renal failiure

46
Q

What is primary amyloidosis?

A

Accumulation of light chain amyloid (AL) - systemic

Plasma cell dyscrasia: Multiple myeloma or Bcell lymphoma

47
Q

What is secondary amyloidosis?

A

Reactive amyloidosis - result of chronic inflammation (RA, IBD, TB). Long standing hepatic production of SAA -> eventual misfolding. Accumulation of AA

48
Q

What is hemodialysis associated amyloidosis?

A

Accumulation of AB2M

B2 retained in serum. Especially effects joints and tendon sheaths (carpal tunnel)

49
Q

What occurs in amyloidosis of the liver?

A

Amyloid accumulates in the space of Disse -> pressure atrophy of hepatocytes.

Generally no decline in liver function.

50
Q

What occurs in amyloidosis of the spleen?

A

Amyloid predominates in either white (sago spleen) pulp or red pulp (lardaceous spleen)

Results in increased number of platelets in peripheral blood since the amyloid filled organ can’t filter and sequester platelets.

51
Q

What happens in amyloidosis of the heart - what is the effect of different locations of deposit?

A

Subendocardial deposits: conduction disturbances and arrhythmias.

Myocardial deposits: pressure atrophy of cardiomyocytes -> restrictive cardiomyopathy -> CHF

52
Q

What type of amyloid is most typically associated with arthropathy or carpal tunnel?

A

AB2M

seen in hemodialysis patients

53
Q

In an inflammatory response what vessels become leaky?

A

Venules due to cell contraction and transcytosis and leukocyte mediated injury
Arterioles due to damage (burns, toxins)

54
Q

4 receptor types involved in leukocyte activation

A

TLR: binds microbial products (LPS)
G protein-coupled receptors: bind peptides, chemokines, C5a, AA metabolites
Cytokine receptor: binds cytokines (IFNgamma)
Opsonin receptor: binds IgG, C3b, etc.

55
Q

What is EGF and what does it do?

A

Epithelial Growth Factor - induces proliferation of epithelial cells and fibroblasts

56
Q

What is HGF and what does it do?

A

Hepatocyte Growth Factor - replication and motility of most epithelial cells

57
Q

What is VEGF and what does it do?

A

Vascular Endothelial Growth Factor - CRITICAL for angiogenesis

58
Q

What is PDGF and what does it do?

A

Platelet Derived Growth Factor - induces migration and replication of fibroblasts, smooth muscle cells and monocytes

59
Q

What is FGF and what does it do?

A

Fibrobalst Growth Factor - promotes angiogenesis and influx of cells needed for tissue regeneration and healing

60
Q

What is TGF-B and what does it do?

A

Transforming Growth Factor B - strong stimulus for fibrosis. Promotes motility and proliferation of fibroblasts and production of ECM components.
***inhibits inflammation: inhibits WBC and epithelial cell reproduction

61
Q

what is the signalling pathway for most healing associated Growth Factors?

A

GF -> Intrinsic Tyrosine Kinase Receptor

Receptor dimerization -> TK activity ->-> RAS and MAP Kinase

62
Q

What is compensatory hyperplasia? How is it initiated?

A

Restoration of functional mass (not anatomy) after injury
ex: partial liver removal

Cytokines (IL-6, TNF) and Growth Factors secreted by NON-PARENCHYMAL cells -> parenchymal proliferation

63
Q

What stain is useful to visualize collagen?

A

Trichrome - blue staining

64
Q

Myeloperoxidase

A

Neutrophil enzyme - in azurophilic granules
H2O2 + Cl- -> 2HOCl (hypochlorous acid)

Heme cofactor

65
Q

5 roles of macrophages in wound healing

A

Debridement: phagocytosis and collagenase
Antimicrobial: Nitric acid (HNO3), Reactive Oxygen Species
Chemotaxis (prolif. of fibroblasts and keratinocytes): PDGF, TGF-B, TNF, IL-1, KGF-7
Angiogenesis: VEGF, PDGF, FGF-2
Deposition / Remodelling of ECM: TGF-B, PDGF, TNF, OPN, IL-1, Collagenase, MMP

66
Q

What cell type is responsible for wound contraction? In what type of wound healing is this observed?

A

Myofibroblasts

Second Intention Wound Healing

67
Q

What is wound dehiscence?

A

Rupture of a wound along a surgical suture

Due to: malnutrition, circulatory status, infection, mechanical stress

68
Q

4 types of excessive scarring

A
  1. “proud flesh” excessive granulation tissue
  2. hypertrophic scar: excessive collagen deposition -> raised scar
  3. keloid: extreme deposition of aberrant collagen bands -> extensive scarring
  4. contracture: extensive wound contraction -> deformity
69
Q

4 major neutrophil chemotactic factors

A

C5a, TNF, leukotrienes, bacterial products

70
Q

What is the precursor to bradykinin and what does it do?

A

High Molecular Weight Kininogen

w/ Kallikrein increases activation of Hageman factor (factor XII)

71
Q

What is a “waived” test?

A

easily performed tests available at Physician’s office
-Pregnancy, Rapid strep, rapid flu, mono spot

Clinical laboratory improvement act (CLIA 88) - regulates lab testing

72
Q

What effect on lab results will physical activity have?

A

Transient: elevations in CK, AST, LD

Long lasting: elevation in some lipoproteins

73
Q

How long should a patient fast before lab testing?

A

About 12 hours for basal levels

74
Q

What lab parameters will chronic alcohol consumption effect?

A

Elevate hepatic GGT (gamma glutamyl transferase) and MCV (mean corpuscular volume)

Change in AST/ALT to 2:1

75
Q

Sensitivity =?

A

Sensitivity = True (+) / (True (+) + False (-))
sensitivity: capture all disease positive + some false positives.

Probability that test detects disease when disease is present
SnOUT

76
Q

Specificity = ?

A

Specificity = True (-) / (True (-) + False (+))
Probability that test indicates non-disease when disease is absent

SpIN

77
Q

Positive Predictive Value

A

Likelihood that a positive test identifies a person positive for disease

= True (+) / True (+) + False (+)

78
Q

Primary vs. secondary malnutrition

A

Primary: malnutrition due to inadequate intake
Secondary: other cause (Absorption, use/storage, increase loss, increase need)

79
Q

Symptoms of Vit A deficiency

A

Night blindness
squamous metaplasia and keratinization of corneal epithelium
xeropthalmia, keratomalacia, Bitot’s spots (clouding)
Immune deficiency
Follicular hyperkeratosis (skin)

80
Q

What is anascara?

A

Severe, widespread edema

81
Q

What is ascites?

A

Edema fluid w/in the peritoneal cavity

82
Q

In what disorder is periorbital edema sometimes seen?

A

Renal failure (nephrotic syndrome)

83
Q

When is hepatic periportal congestion seen?

A

Fatty liver change

84
Q

What is hemorrhagic diathesis?

A

Predisposition to bleed

85
Q

What causes petechiae?

A

1: Platelet problem: too few or abnormal (qualitative or quantitative)
2: Increased intravascular pressure (mechanical)

86
Q

4 ways in which uninjured endothelium is antithrombolitic

A
  1. barrier
  2. antiplatelet: Prostacyclin, NO, ADPase
  3. anticoagulant: Heparin like molecules, thrombomodulin, TFPI
  4. fibrinolytic: t-PA
87
Q

What is Trousseau Syndrome?

A

form of secondary hypercoagulability - migratory thrombophlebitis
Caused by malignancy - procoagulant factors produced by the tumor.

88
Q

What is heparin induced thrombocytopenia?

A

Life threatening complication of heparin therapy.
Occurs 5-10 days post exposure
Autoantibodies to heparin / PF4 complex -> platelet activation, amplification of coagulation pathway and hypercoagulability

Increased risk of large vessel thrombosis
Decreased platelet count (consumption and clearance)

89
Q

What is antiphospholipid antibody syndrome?

A

Secondary hypercoagulability
Mechanism not well understood
Ab to phospholipids and/or plasma proteins assoc. w/ phospholipids
Elevated aPTT and hypercoagulability - paradox
Primary: denovo (drug reaction) Secondary: autoimmune disease (lupus, etc)
recurrent thromboemboli, pregnancy complications, thrombocytopenia

90
Q

2 subtypes of thrombi

A

Mural - adherent to walls of large chambers: LV, aortic aneurism
Vegetation - attach to heart valves - infective and non-infective

91
Q

Findings associated with Disseminated Intervascular Coagulation

A

Prolonged PT and PTT
Decreased platelet count (thrombocytopenia)
Increased fibrin degradation products (D-dimer)

92
Q

What is a paradoxical embolus?

A

A systemic embolus originating in the venous circulation or right side of the heart that passes through a septal defect to enter systemic ciruclation.

93
Q

How do fat embolisms originate? What are the symptoms?

A

Long bone fractures, or rarely burns and extensive soft tissue injury

Fat embolism syndrome: vascular occlusion and endothelial injury:
-dyspnea, thrombocytopenia -> petechia, anemia

94
Q

What is caisson disease?

A

Chronic decompression sickness

-> multiple foci of ischemic necrosis (femoral heads, tibia, humeri)

95
Q

In what setting is bone marrow emboli most often seen?

A

CPR w/ rib fracture

96
Q

Define shock

A

Systemic hypoperfusion -> widespread hypoxia

97
Q

Differentiate cause, mechanism and means of death.

A

Cause: specific disease or injury that initiates process leading to death (natural or unnatural)
Mechanism: physiologic derangement that is incompatible with life
Means: one word summary about circumstances surrounding death: natural, unnatural, accident, suicide

98
Q

What percent arterial stenosis is critical?

A

70% stenosis

99
Q

WWWhat cell types are present in a fibrous plaque?

A

Sm. muscle, macrophage, T lymphocytes

M2 (19 decks)

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