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MOD > MOD Exam 1, Chp 1-4 > Flashcards

MOD Exam 1, Chp 1-4 Flashcards

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1
Q

[FA] A pt undergoes thrombolysis for acute limb ischemia. What type of free radical injury is of greatest concern? What specific radical is formed?
What 4 things happen in this?

A

Reperfusion injury (eg, from superoxide formation)

Increase Ca
Increae ROS
incresae neutrophils
increase Complement

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2
Q

[FA] What causes the yellow-brown color of the macrophages seen on autopsy of an elderly woman?

A

autophagocytosis (this is lipofuscin)

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3
Q

[FA] Name some tissues where lipofuscin is commonly found on autopsy.

A

All tissues, but especially the heart, colon, liver, kidneys, and eyes

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4
Q

[FA] What is atrophy and what causes it? What’s the mechanism?

A

(caused by disuse, denervation, hypoperfusion, loss of hormones, poor nutrition)
autophagy and ubiquitin-proteasome pathway

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5
Q

[FA] Bx of a blood vessel in a 60 yo woman w/headaches and vision loss shows immunoreactive components. Type of hypersensitivity reaction?

A

Type III hypersensitivity reaction. This is fibrinoid necrosis. Seen in hypertensive emergency, polyarteritis nodosa, preeclampsia

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6
Q

[FA] 36 yo pt w/hypercalcemia presents w/hypervitaminosis D. Where does one tend to see the deposits, and what is the mechanism of deposition?

A

Deposits usually occur in interstitial tissues of kidney, lungs, and gastric mucosa (tissues losing acid ↑ pH, favoring Ca2+ deposition)

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7
Q

[FA] Free radicals damage cells by which 3 main mechanisms?

A

Membrane lipid peroxidation, protein modification, and DNA breakage

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8
Q

[FA} Free radical damage by carbon tetrachloride causes what pathologic change in the human body?

A

Fatty change in the liver (CCl4 is converted into CCl3 free radical by cytochrome P-450, leading to ↓ apolipoprotein synthesis)

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9
Q

[FA] Coagulative necrosis occurs after ischemia/infarction except in stroke. What is the key difference as compared w/liquefactive necrosis

A

Coagulative necrosis, enzymatic degradation due to injury blocks proteolysis;
liquefactive, enzymes released from neutrophils digest tissue

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10
Q

What is the mechanism for chromatin clumping? Is this reversible?

A

Mitochondria damage –>
Decrease ATPase –> anaerobic oxphos – lactic acid –> acidic pH –> hcromatin clumping

Yes reversible

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11
Q

What does the mitochondrial permeability transition pore let in?

A

H+ leaks, no gradient for oxphos

  • formation of ROS
  • Cytochorme C release
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12
Q

In cellular damage where does the excess Calcium come from?

A

Smooth ER first, then influx across membrane with the MPTP

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13
Q

What are myelin figures?

A

Evidence of membrane damage, seen on histo.

Large phospholipid coagulations

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14
Q

DNA methylation results in what?

A

Transcription silencing

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15
Q

What does major basic protein do?

A

It is contained in granules of eosinophils and is highly toxic to parasites

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16
Q

What cells contains FcERI receptors? What does this bind to?

A

Mast cells, binds to Fc portion of IgE

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17
Q

What does chromatin do?

A

linkers for nucleosome

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18
Q

In order to track DMII and HTN, what DNA variations can you look for?

A

SNPs in neutral positions, causes a linkage disequilibrium

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19
Q

Fxn of peroxisomes?

A

Fatty acid metabolism

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20
Q

Fxn of phosphatidyliniositol?

A
  • Phosphorylated so IC proteins can bind. Hydrolyzed to generate intracellular signal;
    Glycophosphatidylinisisotl
  • allows extracellular proteins to bind
  • Associated with Caveolae mediated endocytosis as well
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21
Q

What does phosphatidylserine have to do with clotting?

A
  • Cofactor with a negative charge
  • pulls Ca and Na into the cell,
  • serving as a nucleation site
  • platelets to change shape
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22
Q

How do proteins get into the membrane?

A

They must be attached to a lipid on the cytosolic side

Such as prenyl - cholesterol; or a fatty acid.

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23
Q

What is potocytosis?
Pinocytosis?
Receptor-mediated?

Which allows large macromolecule ssuch as LDL to enter?

A

Potocytosis: Caveolae associated. cAMP

Pinocytosis:

  • Clathrin
  • LDL large guys

Receptor-Mediated:
Fuse with acidic lysosome

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24
Q

What causes familial hypercholesterolemia?

A

LDL receptor defects

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25
What type of cytoskeletal filament is vimentin? What is it's fxn?
Mesenchymal cells | intermediate filament
26
Where are clathrins? Cadherins? Catenin? Claudin? Connexins?
Clathrins - Pinocytosis Cadherins - desmosomes catenin & claudin - types of occluding jxn fibers Connexins: Gap jxns
27
how does a cell attach to the ECM? how does a cell attach to another cell? Spot desmosomes use what protein?
hemidesmosome, integrins and focal adhesion complexes. E-cadherins (belt desmosome) & spot Spot desmosomes: s desmogleins/desmocollins
28
How are ubiquitins put on proteins?
E1,E2,E3 ligases
29
How are lysosomes tagged for degradation?
LC3 and M6P
30
What is the fxn of SHH in cell surface triggers?
Proteolysis cascade
31
What is the Receptor Tyrosine Kinase cascade? What can bind to RTK?
Growth factor binds --> activate RAS --> PI3K --> Akt --> mTOR and RAF --> MAPK --> Activates MYC protein --> Cell Cycle Progression Can bind: insulin, PDGF and EGF (platelet derived GF and epidermal GF)
32
What growth factor is associated with ERBB2 and breast cancer? Where is the source and what is the fxn?
Epidermal Growth Factor EGF. Source: macrophages, keratinocytes, salivary glands Fxn: Produce keratinocytes and fibroblasts, form granulation tissue.
33
What growth factors aid in wound healing (make collagen)?
EGF - epidermal PDGF - platelet derived FGF - fibroblasts TGFb
34
What growth factors aid in hepatocyte regeneration? | What is the source of these guys?
TGFalpha HGF Source: TGFalpha: macrophages, keratinocytes, HGF: Fibroblasts, liver stroma
35
There is a growth factor that is induced by hypoxia, relased by mesenchymal cells, and causes angiogenesis. What are the 3 fxns of these factors and what are they?
Vascular Endothelial GF General fxn: proliferation of endothelial and incresd vascular permeability - Ab against VEGF used for renal and colon cancers - Anti-VEGF treats we macular degeneration as well (blood leaks into macula) - Increase VEGFR causes preeclampsia
36
PDGF have a few types. which ones are always active? | What is it's fxn?
AA, AB, BB active CC, DD need activated PDGF recruits smooth muscle cells
37
MET is a receptor that is overexpressed in many tumors. WHat specific growth factor does it increase?
HGF (scatter factor)
38
What do smads have to do with anything?
TGFb activates these when they bind to serine and threonine I and II. increases transcription
39
What is basement membrane made out of? | interstitial matrix ECM?
BM: overlying epithelium and underlying mesenchhymal cells, and IV collagen Intersitital matrix: fibroblasts
40
What is lysyl oxidase?
Dependent on Vitamin C to make collagen. Ascorbic acid deficient pts will have a hard time with wound healing and bleeds easy. Ehler Danlos Syndrome & osteogenesis imperfecta (2 yo with fractures)
41
What are the nonfibrillar collagens and their fxns?
VIII: anchor fibrils to BM IV - planar basement membranes IX - FACITS in cartilage
42
What is elastin composed of?
Fibrillin
43
What is the purpose of water hydrated gels?
Proteoglycans Resist compressive forces in the joints Hyaluronan attach to proteoglycans. These are both negative and pull cation and water
44
What are the adhesive glycoproteins and their fxns?
Fibronectin: - Provides scaffolding in wound healing Laminin: connect ECm to IV collagen Integrins: Firm adhesion from epithelium to leukocytes
45
What Cyclins and CDK phosphorylate retinoblastoma? What removes the G2-M block? What activates S phase?
D/CDK4 D/CDK6 E/CDK2 B/CKD1 S phase: - A CDK2, A CDK1
46
Which stem cell is embryogenic?
PLURIPOTENT from inner cell mas (think: pulp from blastocyst) Adults is Multipotent and all is totipotent
47
Myositis ossificans is an example of what tissue adaptation?
formation of bone within muscle after trauma = metaplasia
48
Growth of uterus during pregnancy is caused by what cellular adaptation?
hypertrophy
49
Which cellular adaptation has a strong association with hormones? Give examples of physiologic?
hyperplasia - Female breast during puberty - Liver regeneration - Bone marrow, EPO = 8x increase in RBC progenitors
50
What is the mechanism of hypertrophy? What transcription factors are used and what signaling pathway? What can we do to prevent hypertrophy? Which isoform is stronger? What protein is upregulated in associatino with hypertrophy?
Transcription factors: GATA NFAT, MEF2 Signaling Pathway: PI3K/AKT (physiologic) GPCR for pathologic - inhibit transcription factors - isoform b is stronger ANF --> expressed in heart in fetal heart
51
What pathway is used in atrophy?
Ubiquitin-proteasome pathway and autophagy Results in lipofuscin granules
52
What are lipofuscin granules and when would you see htem? What is hemosiderin?
When a cell is atrophy-ing. mainly when lipid peroxidation is happening bc it's a product of ROS/autophagy Hemosiderin - lots of RBC destruction bc it's iron
53
Vitamin A deficiency can cause what?
Metaplasia bc it alters gene transcription
54
A histological slide is given. You see cells that are very pink, myelin figures, calcification, with no nucleus. What is happening to the cells?
Necrosis
55
How can you increase the success of a stem cell transplant?
Reprogram somatic cells to become pluripotent with MYC and SOC2 genes and by using Cas9 and CrISPER to alter DNA sequences myc has to do with oncogene
56
You see a brain slide that is very pink, had myelin figures and calcification. There are cystic spaces and cavitation. What stage of necrosis and what type of necrosis are we?
Liquefactive and late stage
57
Macrophages walling off a bacteria usually involves what bacteria and what type of necrosis?
Caseous and TB/fungi Called a granuloma
58
Preeclampsia is involved with which necrosis? What is the mechanism? What other conditions are associated?
Fibrinoid. Type III hypersensitivity bc forms immune complexes with fibrin HTN emergency and immune rxns in vessels
59
What 2 necrosis is associated with the pancreas?
Peripancreatic fat- fat. Pancreatic parenchyma - liquefactive necrosis
60
How is . OH generated? How is O2- generated? How is ONOO generated?
H2O is hydrolyzed by radiation or the Fenton rxn - O2- via NADPH oxidase from leukocytes - Iron/copper O2- and NO interact via NO synthase
61
How can you get rid of O2-? h2O2? OH. ? ONOO? Where does OCL- fit in? What antioxidants can delay decay?
O2- = SOD -> H2O2 +O2 H2O2 = glutathione peroxidase --> H2O OH. = glutathione peroxidase --> H2O ONOO= peroxiredoxins p450 CCl4 --> .CCl3 (decrease apolipoproteins)
62
How does a cell protect against hypoxia?
hypoxia inducible factor 1 --> promotes new blood vessel formation via VEGF
63
What are the 4 ways that ischemia reperfusino injury happens?
Oxidativeve stress (ROS) IC Calcium overload is way bad Inflammation = neutrophils = damage Complement system
64
Toxic chemical injury is bad for what organs? and what toxins do we think of?
Mercury binds to sulfhydryl groups. Bleach Cyanide Worse for absorbing guys like GI and Kidney
65
What are 4 involutions that are physiological apoptosis? | What are 3 other physiological situations
Involution - Prostate after castration - Follicular atresia - Endometrium - Regression of Lactation Other: - Embryogenesis - T cell self reactive - Retired cells
66
What can damage DNA? You can get pathological atrophy of the pancreas, kidney and parotid via what method?
hypoxia, radiation, chemo Duct obstruction
67
What are the sensors in the cell that define when to apoptosis? What are smac and diablo? What can activate BAX/BAK? Which caspace is activated in intrinsic? Extrinsic? Executioners? Pyrpoptosis?
BH3, BIM BId BAM smac/diablo neutralize inhibitors of apoptosis So causes apoptosis p53 and BH3 Intrinsic: 9 Extrinsic 8 Caspace 3 + 6 Caspace 1
68
What is FADD? what is the caspase associated?
bunch of Fas combined | Caspace 8
69
What is hte job of p53?
Arrests cell in G1 until DNA damage is fixed, then if no fix, then apop
70
What protein, when deficient, causes hepatocyte apoptosis and emphysema? What is this associated with in abnormal intracellular acuumulation? What is it's major fxn?
alpha antitrypsin Can't fold, package or secrete very well. ANtiprotease that inhibits neutrophil elastase
71
What is the pathway of necroptosis? When is necroptosis physiological? Pathological?
TNF --->RIP1/RIP3 makes necrosome --> increase permeability of lysosomes Damage to mitochondria Growth plates Path: - Steatohepatitis - Acute pancreatitis - Parkinsons - Microbes that deactivate caspaces
72
What are the 3 types of Lysosome autophagy? What are 4 diseases that autophagy plays a role in?
``` chaperone mediated (bring stuff to lysysome) microatuophagy (inward invagination) macroautophagy (autophagolysosome) ``` Cancer Neurodegenerative Infectious diseases Irritable Bowel Syndrome
73
An increase in cholesterol within the IC can cause?
Atherosclerosis Xanthoma Cholestolosis Niemann pick disease Type C
74
What is a russell body?
Big eosinophilic inclusions of the ER as it tries to pump out Igs
75
Accumulation of cytoskeletal proteins happens in pts with what 2 conditions?
- alcoholic: hyaline - there is keratin in the eosinophilic cytoplasm - alzheimers: too many neurofilaments huntingotn and parkinson too for protein accumulation
76
When would you see giant cells? | What inflammation thing medaites this?
- Granulomatous inflammation (caseous and non caseous) - foreign bodies IFN gam!!
77
What is Werner's syndrome? | Bloom syndrome?
DNA helicase sucks, so can't repair DNA mutated genes encode proteins in repairing DnA double strand breaks
78
CDKN2A activates what? fxn?
acivates p16 and INK4a - protects from uncontrolled proliferation and leads to sensence
79
What does a sirtuin do? Wat does IGF do?
increases longevity. NAD dependant protein deacetylase IGF is released in response to GH and activates AKT mTOR pathway to promote replication. You want to reduce this. Calorie restriction reduces it.
80
WHat triggers an ainfalmmasome?
uric acid, ATP, decreased K, DNA outside nucleus. | Sensors of Cell damage
81
What receptors allow for diapedesis of leukocytes?
CD31 onleukocytes | PECAM on endothelium
82
How does the leukocyte move? (filopodia and all that)
Whent hey bind to cams it intiaties GPCR --> increase Ca --> Rac/Rho --> ACtin at front can move, myosin at back of cell
83
What medication can you give to decrease inflammatio? | What physiological substances are released that decrease inflalmmation by inhibiting leukocyte recruitment?
TNF antagonist Integrin antagonist Lipoxins
84
What are COX 1 and 2 stimulated by? Why is it importnat that there are 2 receptors?
Phospholipase 2, IL1, TNF (+ LPS, an exogenous bacterial pyrogen) Cox1- constitutively expressed in GI and kidney COX2 - inflammatory stimuli COX-2 can thereby get inflammation withoutharming kidneys and GI tract,
85
What are chemotactic for fibroblasts?
PDGF, GFG, TGFb
86
How do NSAIDs work?
Inhibit Cox. = no prostaglandin synthesis
87
Main fxns of TNF?
- Expression of endothelial adhesion molecules, - decreased CO, - insulin resistance, - leukocyte productin, - cachexia
88
What is the mechanism of hereditary angioedema? Paroxysmal nocturnal hemoglobinuria? describe the 2 pathways
C1 inhibitor inhibits classic pathway Deficient GPI regulators decay accelerating factor binds to GPI --> - DAF inhibits C3 convertase - CD59 inhibits MAC
89
Where do you find serous inflammation? | Fibrinous?
Serous = peritoneum, pleura, pericardium. Exudate. Fibrinous = menignes, pericardiu
90
How do ulcers form?
Make a hole in surface tissue due to shedding of inflamed necrotic tissue
91
Name the acute phase proteins and their fxn
``` FFSHC Ferritin - X Fibrinogen - makes platelet plug Serum Amyloid - leads to amyloidosis Hepcidin - Decreases iron absoprtion (= more ROS) C-reactive - opsonin ```
92
What is the triad of shock? and what causes shock?
Triad: - Procoagulation - hypotensive - hyperglycemia bc insulin resistance too much IL1, TNF
93
What is the matrix metalloproteinases?
- remodel the deposited ECM - Degrades basmenet membrane - inhibited by TIMPs? and TGFb
94
What can inhibit TGFb?
glucocorticoids
95
Myofibroblast contraction happens in what healing intention?
Second
96
A pt wants to play baseball after an appendectomys urgery. When is it safe?
@ 3 months it's 70-80% healed
97
Stellate cells are equivalent to what cell?
myofibroblasts
98
Alpha granules release what? Dense granules release what?
Have P selectin - fibrinogen, factor V, vWF, PDGF, TGFb ADP, Ca, Serotonin, Epi
99
Where are PARs located?
- inflammatory cells | - platelets
100
A pt presents with Bernard- Soulier Syndrome, MOA? Pt presetns with Glanzmann thrombasthenia, MOA?
GP1b deficient GpIIb/GpIIIa deficient
101
Severe bleeding disorders result from what factors defects?
V, VII, VIII, IX, X 5, 7, 8, 9, 10
102
Fxns of thrombin?
``` I finbrinogen --> 1a fibrin V--> Va VIII XI XIII (stabilizes fibin clot) ``` binds PARs = platelet activation and pro inflammation anticoagulation
103
what is the biggest anticlot factor? how is it made? what degrades it?
plasminogen --> tPA --> PLASMIN a2plasmin
104
What is the fxn of Protein C? What activates it?
inactivate 5 and 8 | thrombomodulin
105
What is thrombomodulin?
Activates thrombin & PRotein C
106
20 yo pt presents with DVT. Wha tmutation do they likely have?
Factor V Leiden | Arg --> Glu on 506. V resistant to degradation by protein C
107
What is PF4?
If you give heparin, antibodies will be made to it that bind to similar receptors located on endothelium and platelets to activate them, using up all the platelets. PF4 is areceptor similar to heparin that appears on platelets and endothelium
108
What is antiphospholipid syndrome?
antibodies against b2glycoprotein, cardiolipin and coagulants. = recurrent thrombosis Syphilis testing can falso positive bc anticardiolipin are similar.
109
What does a phlebothrombosis look like if it's superficial? where are these usually located
pain and swelling, increased risk of varicose ulcers. | Usually in great saphenous
110
A pt presents with low platelet count, increase PT/PTT, and increased D Dimer. Dx and MOA? What causes this dx?
``` DIC Increased microthrombi take up the platelets and also shear them. The body is in a state of systemic pro thrombic activation, but there aren't enough platelets. Cause: - STOP Making New Thrombi S: Sepsis, T -Trauma (rattlesnakebite) O: Obstetric P: Pancreatitis M: Malignancy (adenocarcinoma, promyelocytic leukemia) N: Nephrotic syndrome T: Transufsion ```
111
An emboli in the lungs most likely was a thrombus where? Emboli in the systemic was a likely thrombus where? a fat and marrow emboli was most likely from where? Air emobli? amniotic fluid emboli?
DVT Cardiac mural thrombi Skeletal fracture iatrogenic! or decompression sickness obstetric troubles
112
Pt presents with diffuse petechial rash, neurological sxs and SOB. Hx of broken bone 2 days ago. Dx?
Fat and marrow emboli. Fat got into vascular sinusoids. | petechial rash is related to rapid thrombocytopenia.
113
What are the bends? the chokes? Caisson disease?
bends - bubbles in joints chokes - pulmonary edema/collapsed lung (atelactasis) Caisson: necrosiss of femoral heads, tibia, humerus.
114
A G2P3 presents with severe dyspnea, cyanosis, and shock. Neuro impairment and pulmonary edema
Yes amniotic fluid emboli
115
What is the shock flow chart? start from teh bottom
- Tissue ischemia, - -> DIC from PAI and TF/Factor XII - vasodilation and increased permeability - - >IL6, IL8, NO, PAF ROS - systemic effects such as heart coniditions and fever - immunosuppression - -> IL10 and apop from TNF, IL1
116
in the compensatory (non progressive phase) what's going on? | Progressive/noncompensatory?
Low BP --> Incresae HR Lactic acid and low urine production
117
What is the effect of shock on the adrenal glands? kidneys? lungs?
Adrenals: cortical cell lipid depletion Kidneys: acute tubular necrosis lungs: diffuse alveolar damage
118
EGF and FGF use what signaling cascade? | what about epidermal cels to the nucleus?
MAP Kinsae RAS proteins
119
What growth factors are significant in angiogenesis?
FGF and VEGF
120
Fxns of TGF-b?
- SYNTHESIS and DEPOSITION OF CT proteins - increased fibroblast migration and proliferation - increased synthesis of collagen and fibronectin - decrsaed degradatino of ECM by MMPs - Fibrosis - Antiinflammatory
121
What's a guy big in vasodilation and inhibiting platelet aggregation?
PGI2
122
Small specific neutrophil granules release what? Larger azurophils release what?
Small: lysozymes, collagenase genlatinase Larger azurophil: MpO, bactericidal facotrs, acid hydrolases
123
What is the mitochondrial pore made out of? | What drug targets it?
Cyclophilin D Cyclosporine
124
To activate the MHC class 1, what must you have?
Proteasomes
125
Hageman deficiency?
XII asymptomatic
126
How does Wnt and frizzled work?
Frzzld activated by Wnt. Fxn: regulates beta catenin levels beta catenin activates disheveled protein which inhibits ubiquitination of beta catenin
127
A thrombus in a vessel wall gets digested from the inside out, but then fills back in with bacteria. This is called?
Mycotic aneurysm
128
What cell-cell or cell-matrix interaction or process is involved in leukocyte extravasation
Tight jxnsget messed up occludin Transcytosis
129
There is a tumor in the nucleus of a cell, what intermediate filament is used as a marker? In the fibroblasts and endotheluim of the vasculature? Muscle cells? brain?
Lamin A, B, C Vimentin (mesenchymal cells in the fibroblasts and endothelium) Desmin glial fibrillary acidic protein
130
What is the characteristic sign of atrophy
autophagy and decreased protein synthesis
131
OKay give me the low down on MMPs TIMPs and ADAMs
MMP deposit ECM into a wound. They are inhibited by TIMPs, which are produced by mesenchymal cells ADAMs: enzymes on a PM that cleave GF: TNF TGFb EGF
132
In hypertrophy, the most common stimulus for skeletal muscle is? Cardiac muscle? Physiologic hypertrophy is signalged via what? Path?
Skeletal: workload Cardiac: Hemodynamic Physio: PI3 - AKT Pathological: hormones/GFs
133
What is the mechanism of: hypertrophy? Hyperplasia? Metaplasia? Necroptosis
Hypertrophy, Phys = AKT/PI3 hyperplasia = hormones (estrogen in endometrial tissue) and Growth factors Metaplasia: - reprogramming of stem cells Necroptosis: TNF, Rip1, RIP3
134
What suppresses appetite when you have cancer?
TNF
135
What inhibits mTOR to increase lifespan?
Rapamycin, promotes autophagy
136
Red streaks around a wound indicate what may be happening?
Lyphangitis!!!
137
What 3 things can prevent clot propogation?
NO, PGI2, ADP phosphatase tPA (afte formation. fibrinolysis)
138
A liver is nutmeg in color and laden with hemosiderin macrophages. What 2 things can you assume about the liver? what causes hemosiderosis?
Chronic passive congestion and hemorrhagic necrosis Hemosiderosis: excess dietary iron hemolytic anemia repeated blood transfusion
139
pt has mild bleeding disorders with a PTT time that is high.
Factor XI deficiency | Thrombin acn activate V, VIII, and XI so don't NEED XI to activate.
140
Pt presents with high PTT, but is asymptomatic.
Factor XII. (hageman) This guy is the initiation of the cascade in vivo
141
pt presents with increased bleeding from nose, vaginally. They have petechiae and purpura. If the pt also gets hemarthrosis what would be the dx?
Von Willebrand Disease Coagulation factor defects
142
What is trousseau's syndrome
Upregulated gene expression in malignant cells
143
What can Growth factors do to cells?
- Promote cells to go into cell cycle - Remove blocks on progression - Prevent apoptosis - Enhance synthesis of proteins
144
What are these caused by? Coagulative necro? Liquefactive? Caseous? Fat Fibrinoid
Ischeamia or infarction that denatures enzymes Liquefactive: Bacterial abscess, brain, neutrophils taht release lysosomal enzymes that digest tissue. Caseous: TB and fungi; macrophages Fat: Lipase released = saponification Fibrinoid: Immune rxns, preecmapplsia, HTN emergency. Immune complexes with fibrin = Type III HSN
145
When do you get overactive apop?
Neurodegenerative
146
Pyroptosis mechanism?
bacteria --> inflammasome -- IL1 --> IL 1 --> Fever and luekocyte
147
What is MYC?
transcription factors that regulate the expression of genes that are needed for growth are MYC
148
Where does metastiatic calcification reside? Why?
in the kidney, lung and gastric mucosa, because H+ is lost quickest here, and increase pH favors Ca+ deposition

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