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

Patho - FA 206 - 219 Flashcards

(101 cards)

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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
Another cause of fibrinoid necrosis?
Plasma protein leakage from damaged vessel
26
Differences between wet and dry gangrene?
Dry - ischemic, coagulative necrosis Wet - superinfection, liquefactive superimposed on coagulative
27
Region most vulnerable to infarct - brain?
ACA/MCA/PCA boundary areas
28
Region most vulnerable to infarct - heart?
Subendocardium
29
Region most vulnerable to infarct - kidney?
Straight segment of proximal tubule (medulla) Thick ascending limb (medulla)
30
Region most vulnerable to infarct - liver?
Area around central vein (zone III)
31
Region most vulnerable to infarct - colon?
Splenic flexure, rectum
32
Neurons most vulnerable to hypoxemia/ischemia?
Purkinje cells of the cerebellum and pyramidal cells of the hippocampus and neocortex (zones 3, 5, 6).
33
red infarcts are seen where?
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
34
3 enzymes that fight free radicals?
catalase, superoxide dismutase, glutathione peroxidase
35
3 vitamins that fight free radicals (antioxidants)?
Vitamins A,C,E
36
3 examples of oxygen toxicity leading to free radical injury?
retinopathy of prematurity (abnormal vascularization), bronchopulmonary dysplasia, reperfusion injury after thrombolytic therapy
37
2 drugs that lead to free radical injury?
acetaminophen OD, carbon tetrachloride
38
Mech of carbon tetrachloride injury?
converted by cytochrome P-450 into CCl3 free radical--\> fatty liver & centrilobular necrosis
39
Where is carbon tetrachloride used (bonus)?
Dry cleaning, refrigerants, lava lamps, used to be used in fire extinguishers
40
How do calcium deposits look on H&E?
deeply basophilic
41
Where does metastatic calcification occur? why?
In interstitial tissues of kidney, lung, and gastric mucosa (these tissues lose acid quickly; Inc pH favors Ca2+ deposition)
42
2 causes of metatstatic calcification and examples?
**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
primary amyloidosis seen in what diseases? what protein accumulates?
plasma cell disorders; AL
44
fibril protein in 2ndary amyloidosis?
serum amyloid A
45
Diseases with 2\* amyloidosis?
Chronic inflammatory conditions, (eg, rheumatoid arthritis, IBD, familial Mediterranean fever, protracted infection) **S**econdary = **S**erum amyloid A = **S**uper long inflammation
46
B2 microglobulin seen in?
Dialysis related amyloidosis
47
B-amyloid protein seen in?
Alzheimers
48
Amyloid precursor protein seen in (bonus)?
Diffuse axonal injury (BAPP)
49
Type of fibril protein seen in DB?
Islet amyloid polypeptide (IAPP)
50
fibril protein in medullary thyroid cancer?
calcitonin
51
wild type tranthyretin seen in which disease/part of body?
senile (age related) amyloidosis; cardiac ventricles
52
ventricular endomyocardium deposition of mutated transthyretin leads to what?
restrictive cardiomyopathy,arrythmia
53
mediators of rubor and calor?
histamine, prostaglandins, bradykinin, NO
54
mediators of endothelial contraction that leads to swelling?
LTC4, LTD4, LTE4, histamine, serotonin
55
mediators of pain
bradykinin, PGE2, histamine
56
Process of fever production
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
inducement of plasma APP
IL6 ( 6 years old is A cute Phase)
58
Positively upregulated APPs
Ferritin, Fibrinogen, Serum amyloid A, Hepcidin, C-reactive protein
59
Negatively downregulated APPs
Albumin, Transferrin
60
Function of CRP?
Opsonin, fixes complement and facilitates phagocytosis
61
What happens to transferrin during Acute phase?
internalized by macrophages to sequester iron
62
Function of Hepcidin
dec iron absorption (by degrading ferroportin) and dec iron release (from macrophages) --\> anemia of chronic disease
63
How do RBCs normally stay separated?
RBCs normally remain separated via ⊝ charges
64
What leads to RBC aggregation? Which lab test reflects this?
Inflammatory products coat the RBCs, which will dec the neg charge, leading to aggregation --\> Inc ESR
65
Inc ESR?
* 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
dec ESR?
Sickle cell anemia (altered shape) Polycythemia (inc RBCs “dilute” aggregation factors) HF Microcytosis Hypofibrinogenemia
67
Why is exudate cloudy?
b/c it's cellular
68
When do macrophages appear in the inflammatory process?
2-3 days after onset
69
The inflammasome leads to the activation of which interleukin?
IL-1
70
Mediator of inflammation resolution and healing
IL10 and TGF-B
71
IL seen in persistent acute inflammation
IL8 Persist-eight inflammation
72
What is an abscess?
acute inflammation walled off by fibrosis
73
Which cells are _activated in_ chronic inflammation (diff from acute)
(antigen presentation by macrophages and other APCs --\> activation of CD4+ Th cells
74
E selectin and P selectin are involved in which part of leukocyte extravasation?
Margination and rolling
75
E selectin is upregulated by?
IL 1 and TNF
76
P selectin released from ?
Weibel Palade bodies
77
In which disease is margination and rolling defective?
leukocyte adhesion deficiency type 2 (dec Sialyl LewisX)
78
What binds to L selectin on a leukocyte?
GlyCAM-1, CD34 on endothelium/stroma binds to L selectin on a leukocyte
79
Adhesion between endothelium and leukocyte defective in which disease? What is the defect?
Tight binding (adhesion)— defective in leukocyte adhesion deficiency type 1 ( dec CD18 integrin subunit)
80
Chemotactic factors (IMP)
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
Chronic inflammation is the result of the interaction of which cells?
macrophages and T cells
82
What do T cells release to activate macrophages?
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
chronc HCV / H.pylori infection lead to which neoplasias?
Chronic HCV - hepatocellular carcinoma H Pylori - chronic gastritis --\> gastric adenocarcinoma
84
Mediator that (+) angiogenesis
FGF, TGF B, VEGF
85
Function of PDGF?
Secreted by activated platelets and macrophages * Induces vascular remodeling and smooth muscle cell migration * Stimulates fibroblast growth for collagen synthesis
86
mediator of tissue remodeling
metalloproteinases
87
EGF works thru which enzymes?
tyrosine kinases
88
cells seen up to 3 days after a wound?
platelets, neutrophils, macrophages
89
cells seen post day 3 of a wound?
Fibroblasts, myofibroblasts, endothelial cells, keratinocytes, macrophages
90
What type of collagen seen in wound healing?
Collagen type III (re-three-cular) in the second phase of wound healing (day 3- weeks), replaced by collagen type I
91
What delays 2nd phase of wound healing
vitamin C and Cu def C's for Second phase
92
What delays 3rd phase of wound healing? Why is it needed?
Zinc def (req for collagenase function to replace Collagen III to I) Z is last letter, for last phase of wound healing
93
Diff b/w caseating and non caseating granulomas? Where are they seen?
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
Mechanism of granuloma formation?
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
Why should you always check for latent TB before giving anti TNF therapy?
Anti-TNF therapy can cause sequestering granulomas to break down --\> disseminated disease.
96
What in blood rises with granulomatous diseases?
Associated with **hypercalcemia** due to **INC 1α-hydroxylase-mediated vitamin D activation** in macrophages
97
Infectious causes of granulomatous disease?
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
Non infectious causes of granulomatous disease?
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
type of collagen in hypertrophic scar
Type III
100
type of collagen in keloid scar
type I and III
101
Scar formation assoc with inc in what?
excess TGF-B

Step 1 2019 First Aid Flashcards (63 decks)

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