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Step 1 2019 First Aid Flashcards > Patho - FA 206 - 219 > Flashcards

Patho - FA 206 - 219 Flashcards

1
Q

Barrett esophagus is an ex. of what type of cellular injury? What is it?

A

metaplasia - replacement of one cell type with another. Barrett - respiratory ciliated columnar epith with stratified squamous epith

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2
Q

Barrett esophagus can lead to what type of neoplasia?

A

Esophageal adenocarcinoma

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3
Q

Dysplastic changes ex?

A

loss of uniformity of cell size and shape (pleomorphism); loss of tissue orientation; nuclear changes (eg, inc nuclear:cytoplasmic ratio and clumped chromatin).

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4
Q

Reversible cell injury

A

Dec ATP –> mitoch swelling ƒ Ribosomal/polysomal detachment ƒ Plasma membrane changes (eg, blebbing) ƒ Nuclear changes (eg, chromatin clumping) rapid loss of fxn

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5
Q

Irreversible cell injury

A

ƒ Breakdown of plasma membrane ƒ Mitochondrial damage/dysfunction ƒ Rupture of lysosomes ƒ Nuclear degradation

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6
Q

Process of Nuclear Degradation

A

= pyknosis (nuclear condensation) –> karyorrhexis (nuclear fragmentation caused by endonuclease-mediated cleavage) –> karyolysis (nuclear dissolution)

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7
Q

How is the cell membrane affected in apoptosis vs necrosis?

A

In apoptosis, Cell membrane typically remains intact without significant inflammation (unlike necrosis).

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8
Q

Signs of apoptosis cellularly? (histologically)

A

Characterized by deeply eosinophilic cytoplasm and basophilic nucleus, pyknosis, and karyorrhexis.

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9
Q

Indicator of apoptosis?

A

DNA laddering (fragments in multiples of 180 bp

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10
Q

Name 2 pro and 2 anti apoptotic proteins in the Bcl 2 family

A

Pro - BAX BAK Anti - Bcl-2 Bcl-XL

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11
Q

How do BAX/BAK inititate apoptosis?

A

BAX and BAK form pores in the mitochondrial membrane –> release of cytochrome C from inner mitochondrial membrane into the cytoplasm –> activation of caspases.

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12
Q

How does Bcl-2 (-) apoptosis?

A

Bcl-2 keeps the mitochondrial membrane impermeable, thereby preventing cytochrome C release.

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13
Q

Disease assoc with Bcl-2? What genetic defect?

A

follicular lymphoma; t(14,18)

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14
Q

List the 2 pathways of extrinsic death via ligand?

A

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

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15
Q

Which pathway of cell death is used in the thymus to filter out non-functional lymphocytes?

A

Fas-FasL interaction is necessary in thymic medullary negative selection.

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16
Q

Disease caused by defect Fas/Fas-L interactions?

A

autoimmune lymphoproliferative syndrome

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17
Q

Ischemia/infarcts cause coagulative necrosis everywhere except? what type of necrosis there?

A

in the brain, where u have liquefactive necrosis

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18
Q

How does liquefactive necrosis occur?

A

Neutrophils release lysosomal enzymes that digest the tissue

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19
Q

Histo signs of liquefactive necrosis?

A

Early: cellular debris and macrophages Late: cystic spaces and cavitation (brain)

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20
Q

Define granuloma

A

Focus of epithelioid cells (activated macrophages with abundant pink cytoplasm) surrounded by lymphocytes and multinucleated giant cells (formed by fusion of several activated macrophages).

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21
Q

Which infections lead to caseous necrosis?

A

TB, systemic fungi (eg, Histoplasma capsulatum), Nocardia

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22
Q

two types of fat necrosis?

A

Enzymatic: acute pancreatitis (saponification of peripancreatic fat) Nonenzymatic: traumatic (eg, injury to breast tissue)

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23
Q

Why does fat necrosis have a chalk like appearence?

A

free fatty acids from fat breakdown will bind calcium (saponification)

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24
Q

What type of hypersensitivity reaction leads to fibrinoid necrosis?

A

HS-III

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25
Q

Another cause of fibrinoid necrosis?

A

Plasma protein leakage from damaged vessel

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26
Q

Differences between wet and dry gangrene?

A

Dry - ischemic, coagulative necrosis Wet - superinfection, liquefactive superimposed on coagulative

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27
Q

Region most vulnerable to infarct - brain?

A

ACA/MCA/PCA boundary areas

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28
Q

Region most vulnerable to infarct - heart?

A

Subendocardium

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29
Q

Region most vulnerable to infarct - kidney?

A

Straight segment of proximal tubule (medulla) Thick ascending limb (medulla)

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30
Q

Region most vulnerable to infarct - liver?

A

Area around central vein (zone III)

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31
Q

Region most vulnerable to infarct - colon?

A

Splenic flexure, rectum

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32
Q

Neurons most vulnerable to hypoxemia/ischemia?

A

Purkinje cells of the cerebellum and pyramidal cells of the hippocampus and neocortex (zones 3, 5, 6).

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33
Q

red infarcts are seen where?

A
  1. Occurs in venous occlusion and tissues with multiple blood supplies (eg, liver, lung A, intestine, testes) 2. w/ reperfusion (eg, after angioplasty). Red = reperfusion
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34
Q

3 enzymes that fight free radicals?

A

catalase, superoxide dismutase, glutathione peroxidase

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35
Q

3 vitamins that fight free radicals (antioxidants)?

A

Vitamins A,C,E

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36
Q

3 examples of oxygen toxicity leading to free radical injury?

A

retinopathy of prematurity (abnormal vascularization), bronchopulmonary dysplasia, reperfusion injury after thrombolytic therapy

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37
Q

2 drugs that lead to free radical injury?

A

acetaminophen OD, carbon tetrachloride

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38
Q

Mech of carbon tetrachloride injury?

A

converted by cytochrome P-450 into CCl3 free radical–> fatty liver & centrilobular necrosis

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39
Q

Where is carbon tetrachloride used (bonus)?

A

Dry cleaning, refrigerants, lava lamps, used to be used in fire extinguishers

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40
Q

How do calcium deposits look on H&E?

A

deeply basophilic

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41
Q

Where does metastatic calcification occur? why?

A

In interstitial tissues of kidney, lung, and gastric mucosa (these tissues lose acid quickly; Inc pH favors Ca2+ deposition)

42
Q

2 causes of metatstatic calcification and examples?

A

hypercalcemia: (eg, 1° hyperparathyroidism, sarcoidosis, hypervitaminosis D)

high calcium-phosphate product levels: (eg, chronic kidney disease with 2° hyperparathyroidism, long-term dialysis, calciphylaxis, multiple myeloma)

43
Q

primary amyloidosis seen in what diseases? what protein accumulates?

A

plasma cell disorders; AL

44
Q

fibril protein in 2ndary amyloidosis?

A

serum amyloid A

45
Q

Diseases with 2* amyloidosis?

A

Chronic inflammatory conditions, (eg, rheumatoid arthritis, IBD, familial Mediterranean fever, protracted infection)

Secondary = Serum amyloid A = Super long inflammation

46
Q

B2 microglobulin seen in?

A

Dialysis related amyloidosis

47
Q

B-amyloid protein seen in?

A

Alzheimers

48
Q

Amyloid precursor protein seen in (bonus)?

A

Diffuse axonal injury (BAPP)

49
Q

Type of fibril protein seen in DB?

A

Islet amyloid polypeptide (IAPP)

50
Q

fibril protein in medullary thyroid cancer?

A

calcitonin

51
Q

wild type tranthyretin seen in which disease/part of body?

A

senile (age related) amyloidosis; cardiac ventricles

52
Q

ventricular endomyocardium deposition of mutated transthyretin leads to what?

A

restrictive cardiomyopathy,arrythmia

53
Q

mediators of rubor and calor?

A

histamine, prostaglandins, bradykinin, NO

54
Q

mediators of endothelial contraction that leads to swelling?

A

LTC4, LTD4, LTE4, histamine, serotonin

55
Q

mediators of pain

A

bradykinin, PGE2, histamine

56
Q

Process of fever production

A

Pyrogens (eg, LPS) induce macrophages to release IL-1 and TNF –> Inc COX activity in perivascular cells of hypothalamus –> inc PGE2 –> inc temperature set point.

57
Q

inducement of plasma APP

A

IL6 ( 6 years old is A cute Phase)

58
Q

Positively upregulated APPs

A

Ferritin, Fibrinogen, Serum amyloid A, Hepcidin, C-reactive protein

59
Q

Negatively downregulated APPs

A

Albumin, Transferrin

60
Q

Function of CRP?

A

Opsonin, fixes complement and facilitates phagocytosis

61
Q

What happens to transferrin during Acute phase?

A

internalized by macrophages to sequester iron

62
Q

Function of Hepcidin

A

dec iron absorption (by degrading ferroportin) and dec iron release (from macrophages) –> anemia of chronic disease

63
Q

How do RBCs normally stay separated?

A

RBCs normally remain separated via ⊝ charges

64
Q

What leads to RBC aggregation? Which lab test reflects this?

A

Inflammatory products coat the RBCs, which will dec the neg charge, leading to aggregation –> Inc ESR

65
Q

Inc ESR?

A
  • Most anemias
  • Infections
  • Inflammation (eg, giant cell [temporal] arteritis, polymyalgia rheumatica)
  • Cancer (eg, metastases, multiple myeloma)
  • Renal disease (end-stage or nephrotic syndrome)
  • Pregnancy
66
Q

dec ESR?

A

Sickle cell anemia (altered shape) Polycythemia (inc RBCs “dilute” aggregation factors) HF Microcytosis Hypofibrinogenemia

67
Q

Why is exudate cloudy?

A

b/c it’s cellular

68
Q

When do macrophages appear in the inflammatory process?

A

2-3 days after onset

69
Q

The inflammasome leads to the activation of which interleukin?

70
Q

Mediator of inflammation resolution and healing

A

IL10 and TGF-B

71
Q

IL seen in persistent acute inflammation

A

IL8

Persist-eight inflammation

72
Q

What is an abscess?

A

acute inflammation walled off by fibrosis

73
Q

Which cells are activated in chronic inflammation (diff from acute)

A

(antigen presentation by macrophages and other APCs –> activation of CD4+ Th cells

74
Q

E selectin and P selectin are involved in which part of leukocyte extravasation?

A

Margination and rolling

75
Q

E selectin is upregulated by?

A

IL 1 and TNF

76
Q

P selectin released from ?

A

Weibel Palade bodies

77
Q

In which disease is margination and rolling defective?

A

leukocyte adhesion deficiency type 2 (dec Sialyl LewisX)

78
Q

What binds to L selectin on a leukocyte?

A

GlyCAM-1, CD34 on endothelium/stroma binds to L selectin on a leukocyte

79
Q

Adhesion between endothelium and leukocyte defective in which disease? What is the defect?

A

Tight binding (adhesion)— defective in leukocyte adhesion deficiency type 1 ( dec CD18 integrin subunit)

80
Q

Chemotactic factors (IMP)

A

Chemotactic factors:

  1. C5a,
  2. IL-8,
  3. LTB4,
  4. kallikrein,
  5. PAF (platelet-activating factor )
  6. bonus from Q bank - also fibrinotides from clotting cascade, and formylmethionyl peptides from bacteria
81
Q

Chronic inflammation is the result of the interaction of which cells?

A

macrophages and T cells

82
Q

What do T cells release to activate macrophages?

A

ƒ Th1 cells secrete IFN-γ –> macrophage classical activation (proinflammatory) ƒ Th2 cells secrete IL-4 and IL-13 –> macrophage alternative activation (repair and antiinflammatory)

83
Q

chronc HCV / H.pylori infection lead to which neoplasias?

A

Chronic HCV - hepatocellular carcinoma H Pylori - chronic gastritis –> gastric adenocarcinoma

84
Q

Mediator that (+) angiogenesis

A

FGF, TGF B, VEGF

85
Q

Function of PDGF?

A

Secreted by activated platelets and macrophages

  • Induces vascular remodeling and smooth muscle cell migration
  • Stimulates fibroblast growth for collagen synthesis
86
Q

mediator of tissue remodeling

A

metalloproteinases

87
Q

EGF works thru which enzymes?

A

tyrosine kinases

88
Q

cells seen up to 3 days after a wound?

A

platelets, neutrophils, macrophages

89
Q

cells seen post day 3 of a wound?

A

Fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages

90
Q

What type of collagen seen in wound healing?

A

Collagen type III (re-three-cular) in the second phase of wound healing (day 3- weeks), replaced by collagen type I

91
Q

What delays 2nd phase of wound healing

A

vitamin C and Cu def

C’s for Second phase

92
Q

What delays 3rd phase of wound healing? Why is it needed?

A

Zinc def (req for collagenase function to replace Collagen III to I)

Z is last letter, for last phase of wound healing

93
Q

Diff b/w caseating and non caseating granulomas? Where are they seen?

A

Caseating: associated with central necrosis. Seen with infectious etiologies (eg, TB, fungal). Noncaseating A: no central necrosis. Seen with autoimmune diseases (eg, sarcoidosis, Crohn disease

94
Q

Mechanism of granuloma formation?

A

APCs present antigens to CD4+ Th cells and secrete IL-12
–> CD4+ Th cells differentiate into Th1 cells
Th1 secretes IFN-γ –> macrophage activation
Macrophages inc cytokine secretion (eg, TNF) –> formation of epithelioid macrophages and giant cells.

95
Q

Why should you always check for latent TB before giving anti TNF therapy?

A

Anti-TNF therapy can cause sequestering granulomas to break down –> disseminated disease.

96
Q

What in blood rises with granulomatous diseases?

A

Associated with hypercalcemia due to INC 1α-hydroxylase-mediated vitamin D activation in macrophages

97
Q

Infectious causes of granulomatous disease?

A

ƒ Bacterial:

  • Mycobacteria (tuberculosis, leprosy),
  • Bartonella henselae (cat scratch disease; stellate necrotizing granulomas),
  • Listeria monocytogenes (granulomatosis infantiseptica),
  • Treponema pallidum (3° syphilis)

ƒ Fungal: endemic mycoses (eg, histoplasmosis)
ƒ Parasitic: schistosomiasis

98
Q

Non infectious causes of granulomatous disease?

A

ƒ Immune medated:

  • Sarcoidosis,
  • Crohn disease,
  • 1° biliary cholangitis,
  • subacute (de Quervain/granulomatous) thyroiditis

ƒ Vasculitis:

  • granulomatosis with polyangiitis (Wegener),
  • eosinophilic granulomatosis with polyangiitis (Churg-Strauss),
  • giant cell (temporal) arteritis,
  • Takayasu arteritis

ƒ Foreign material: berylliosis, talcosis, hypersensitivity pneumonitis

ƒ Chronic granulomatous disease

99
Q

type of collagen in hypertrophic scar

100
Q

type of collagen in keloid scar

A

type I and III

101
Q

Scar formation assoc with inc in what?

A

excess TGF-B

Step 1 2019 First Aid Flashcards (63 decks)

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