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

MOD Exam 1, Chp 1-4 Flashcards

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
Q

What type of cytoskeletal filament is vimentin? What is it’s fxn?

A

Mesenchymal cells

intermediate filament

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26
Q

Where are clathrins? Cadherins? Catenin? Claudin? Connexins?

A

Clathrins - Pinocytosis
Cadherins - desmosomes
catenin & claudin - types of occluding jxn fibers

Connexins: Gap jxns

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27
Q

how does a cell attach to the ECM?
how does a cell attach to another cell?
Spot desmosomes use what protein?

A

hemidesmosome, integrins and focal adhesion complexes.

E-cadherins (belt desmosome) & spot

Spot desmosomes: s desmogleins/desmocollins

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28
Q

How are ubiquitins put on proteins?

A

E1,E2,E3 ligases

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29
Q

How are lysosomes tagged for degradation?

A

LC3 and M6P

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30
Q

What is the fxn of SHH in cell surface triggers?

A

Proteolysis cascade

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31
Q

What is the Receptor Tyrosine Kinase cascade?

What can bind to RTK?

A

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)

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32
Q

What growth factor is associated with ERBB2 and breast cancer?
Where is the source and what is the fxn?

A

Epidermal Growth Factor EGF.

Source: macrophages, keratinocytes, salivary glands

Fxn: Produce keratinocytes and fibroblasts, form granulation tissue.

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33
Q

What growth factors aid in wound healing (make collagen)?

A

EGF - epidermal
PDGF - platelet derived
FGF - fibroblasts
TGFb

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34
Q

What growth factors aid in hepatocyte regeneration?

What is the source of these guys?

A

TGFalpha
HGF

Source:
TGFalpha: macrophages, keratinocytes,
HGF: Fibroblasts, liver stroma

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35
Q

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?

A

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
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36
Q

PDGF have a few types. which ones are always active?

What is it’s fxn?

A

AA, AB, BB active
CC, DD need activated

PDGF recruits smooth muscle cells

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37
Q

MET is a receptor that is overexpressed in many tumors. WHat specific growth factor does it increase?

A

HGF (scatter factor)

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38
Q

What do smads have to do with anything?

A

TGFb activates these when they bind to serine and threonine I and II. increases transcription

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39
Q

What is basement membrane made out of?

interstitial matrix ECM?

A

BM: overlying epithelium and underlying mesenchhymal cells, and IV collagen

Intersitital matrix: fibroblasts

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40
Q

What is lysyl oxidase?

A

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)

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41
Q

What are the nonfibrillar collagens and their fxns?

A

VIII: anchor fibrils to BM
IV - planar basement membranes
IX - FACITS in cartilage

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42
Q

What is elastin composed of?

A

Fibrillin

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43
Q

What is the purpose of water hydrated gels?

A

Proteoglycans Resist compressive forces in the joints
Hyaluronan attach to proteoglycans.
These are both negative and pull cation and water

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44
Q

What are the adhesive glycoproteins and their fxns?

A

Fibronectin:
- Provides scaffolding in wound healing
Laminin: connect ECm to IV collagen
Integrins: Firm adhesion from epithelium to leukocytes

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45
Q

What Cyclins and CDK phosphorylate retinoblastoma?

What removes the G2-M block?

What activates S phase?

A

D/CDK4
D/CDK6
E/CDK2

B/CKD1

S phase:
- A CDK2, A CDK1

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46
Q

Which stem cell is embryogenic?

A

PLURIPOTENT from inner cell mas (think: pulp from blastocyst)

Adults is Multipotent
and all is totipotent

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47
Q

Myositis ossificans is an example of what tissue adaptation?

A

formation of bone within muscle after trauma = metaplasia

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48
Q

Growth of uterus during pregnancy is caused by what cellular adaptation?

A

hypertrophy

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49
Q

Which cellular adaptation has a strong association with hormones? Give examples of physiologic?

A

hyperplasia

  • Female breast during puberty
  • Liver regeneration
  • Bone marrow, EPO = 8x increase in RBC progenitors
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50
Q

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?

A

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

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51
Q

What pathway is used in atrophy?

A

Ubiquitin-proteasome pathway
and autophagy
Results in lipofuscin granules

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52
Q

What are lipofuscin granules and when would you see htem?

What is hemosiderin?

A

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

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53
Q

Vitamin A deficiency can cause what?

A

Metaplasia bc it alters gene transcription

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54
Q

A histological slide is given. You see cells that are very pink, myelin figures, calcification, with no nucleus. What is happening to the cells?

A

Necrosis

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55
Q

How can you increase the success of a stem cell transplant?

A

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

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56
Q

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?

A

Liquefactive and late stage

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57
Q

Macrophages walling off a bacteria usually involves what bacteria and what type of necrosis?

A

Caseous and TB/fungi

Called a granuloma

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58
Q

Preeclampsia is involved with which necrosis? What is the mechanism?
What other conditions are associated?

A

Fibrinoid.
Type III hypersensitivity bc forms immune complexes with fibrin
HTN emergency and immune rxns in vessels

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59
Q

What 2 necrosis is associated with the pancreas?

A

Peripancreatic fat- fat.

Pancreatic parenchyma - liquefactive necrosis

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60
Q

How is . OH generated?

How is O2- generated?

How is ONOO generated?

A

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
Q

How can you get rid of O2-? h2O2? OH. ? ONOO?

Where does OCL- fit in?

What antioxidants can delay decay?

A

O2- = SOD -> H2O2 +O2

H2O2 = glutathione peroxidase –> H2O

OH. = glutathione peroxidase –> H2O

ONOO= peroxiredoxins

p450 CCl4 –> .CCl3 (decrease apolipoproteins)

62
Q

How does a cell protect against hypoxia?

A

hypoxia inducible factor 1 –> promotes new blood vessel formation via VEGF

63
Q

What are the 4 ways that ischemia reperfusino injury happens?

A

Oxidativeve stress (ROS)
IC Calcium overload is way bad
Inflammation = neutrophils = damage
Complement system

64
Q

Toxic chemical injury is bad for what organs? and what toxins do we think of?

A

Mercury binds to sulfhydryl groups.
Bleach
Cyanide

Worse for absorbing guys like GI and Kidney

65
Q

What are 4 involutions that are physiological apoptosis?

What are 3 other physiological situations

A

Involution

  • Prostate after castration
  • Follicular atresia
  • Endometrium
  • Regression of Lactation

Other:

  • Embryogenesis
  • T cell self reactive
  • Retired cells
66
Q

What can damage DNA?

You can get pathological atrophy of the pancreas, kidney and parotid via what method?

A

hypoxia, radiation, chemo

Duct obstruction

67
Q

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?

A

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
Q

What is FADD?

what is the caspase associated?

A

bunch of Fas combined

Caspace 8

69
Q

What is hte job of p53?

A

Arrests cell in G1 until DNA damage is fixed, then if no fix, then apop

70
Q

What protein, when deficient, causes hepatocyte apoptosis and emphysema?
What is this associated with in abnormal intracellular acuumulation? What is it’s major fxn?

A

alpha antitrypsin

Can’t fold, package or secrete very well.

ANtiprotease that inhibits neutrophil elastase

71
Q

What is the pathway of necroptosis?

When is necroptosis physiological?

Pathological?

A

TNF —>RIP1/RIP3 makes necrosome –> increase permeability of lysosomes
Damage to mitochondria

Growth plates

Path:

  • Steatohepatitis
  • Acute pancreatitis
  • Parkinsons
  • Microbes that deactivate caspaces
72
Q

What are the 3 types of Lysosome autophagy?

What are 4 diseases that autophagy plays a role in?

A 
chaperone mediated (bring stuff to lysysome)
microatuophagy (inward invagination)
macroautophagy (autophagolysosome)

Cancer
Neurodegenerative
Infectious diseases
Irritable Bowel Syndrome

73
Q

An increase in cholesterol within the IC can cause?

A

Atherosclerosis
Xanthoma
Cholestolosis
Niemann pick disease Type C

74
Q

What is a russell body?

A

Big eosinophilic inclusions of the ER as it tries to pump out Igs

75
Q

Accumulation of cytoskeletal proteins happens in pts with what 2 conditions?

A
  • alcoholic: hyaline - there is keratin in the eosinophilic cytoplasm
  • alzheimers: too many neurofilaments
    huntingotn and parkinson too for protein accumulation
76
Q

When would you see giant cells?

What inflammation thing medaites this?

A
  • Granulomatous inflammation (caseous and non caseous)
  • foreign bodies

IFN gam!!

77
Q

What is Werner’s syndrome?

Bloom syndrome?

A

DNA helicase sucks, so can’t repair DNA

mutated genes encode proteins in repairing DnA double strand breaks

78
Q

CDKN2A activates what? fxn?

A

acivates p16 and INK4a - protects from uncontrolled proliferation and leads to sensence

79
Q

What does a sirtuin do?

Wat does IGF do?

A

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
Q

WHat triggers an ainfalmmasome?

A

uric acid, ATP, decreased K, DNA outside nucleus.

Sensors of Cell damage

81
Q

What receptors allow for diapedesis of leukocytes?

A

CD31 onleukocytes

PECAM on endothelium

82
Q

How does the leukocyte move? (filopodia and all that)

A

Whent hey bind to cams it intiaties GPCR –> increase Ca –> Rac/Rho –> ACtin at front can move, myosin at back of cell

83
Q

What medication can you give to decrease inflammatio?

What physiological substances are released that decrease inflalmmation by inhibiting leukocyte recruitment?

A

TNF antagonist
Integrin antagonist

Lipoxins

84
Q

What are COX 1 and 2 stimulated by? Why is it importnat that there are 2 receptors?

A

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
Q

What are chemotactic for fibroblasts?

A

PDGF, GFG, TGFb

86
Q

How do NSAIDs work?

A

Inhibit Cox. = no prostaglandin synthesis

87
Q

Main fxns of TNF?

A
  • Expression of endothelial adhesion molecules,
  • decreased CO,
  • insulin resistance,
  • leukocyte productin,
  • cachexia
88
Q

What is the mechanism of hereditary angioedema?

Paroxysmal nocturnal hemoglobinuria?

describe the 2 pathways

A

C1 inhibitor inhibits classic pathway

Deficient GPI regulators

decay accelerating factor binds to GPI –>

  • DAF inhibits C3 convertase
  • CD59 inhibits MAC
89
Q

Where do you find serous inflammation?

Fibrinous?

A

Serous = peritoneum, pleura, pericardium. Exudate.

Fibrinous = menignes, pericardiu

90
Q

How do ulcers form?

A

Make a hole in surface tissue due to shedding of inflamed necrotic tissue

91
Q

Name the acute phase proteins and their fxn

A 
FFSHC
Ferritin - X
Fibrinogen - makes platelet plug
Serum Amyloid - leads to amyloidosis
Hepcidin - Decreases iron absoprtion (= more ROS)
C-reactive - opsonin
92
Q

What is the triad of shock? and what causes shock?

A

Triad:

  • Procoagulation
  • hypotensive
  • hyperglycemia bc insulin resistance

too much IL1, TNF

93
Q

What is the matrix metalloproteinases?

A
  • remodel the deposited ECM
  • Degrades basmenet membrane
  • inhibited by TIMPs? and TGFb
94
Q

What can inhibit TGFb?

A

glucocorticoids

95
Q

Myofibroblast contraction happens in what healing intention?

96
Q

A pt wants to play baseball after an appendectomys urgery. When is it safe?

A

@ 3 months it’s 70-80% healed

97
Q

Stellate cells are equivalent to what cell?

A

myofibroblasts

98
Q

Alpha granules release what?

Dense granules release what?

A

Have P selectin

  • fibrinogen, factor V, vWF, PDGF, TGFb

ADP, Ca, Serotonin, Epi

99
Q

Where are PARs located?

A
  • inflammatory cells

- platelets

100
Q

A pt presents with Bernard- Soulier Syndrome, MOA?

Pt presetns with Glanzmann thrombasthenia, MOA?

A

GP1b deficient

GpIIb/GpIIIa deficient

101
Q

Severe bleeding disorders result from what factors defects?

A

V, VII, VIII, IX, X

5, 7, 8, 9, 10

102
Q

Fxns of thrombin?

A 
I finbrinogen --> 1a fibrin
V--> Va
VIII
XI
XIII (stabilizes fibin clot)

binds PARs = platelet activation and pro inflammation
anticoagulation

103
Q

what is the biggest anticlot factor? how is it made? what degrades it?

A

plasminogen –> tPA –> PLASMIN

a2plasmin

104
Q

What is the fxn of Protein C? What activates it?

A

inactivate 5 and 8

thrombomodulin

105
Q

What is thrombomodulin?

A

Activates thrombin & PRotein C

106
Q

20 yo pt presents with DVT. Wha tmutation do they likely have?

A

Factor V Leiden

Arg –> Glu on 506. V resistant to degradation by protein C

107
Q

What is PF4?

A

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
Q

What is antiphospholipid syndrome?

A

antibodies against b2glycoprotein, cardiolipin and coagulants. = recurrent thrombosis

Syphilis testing can falso positive bc anticardiolipin are similar.

109
Q

What does a phlebothrombosis look like if it’s superficial? where are these usually located

A

pain and swelling, increased risk of varicose ulcers.

Usually in great saphenous

110
Q

A pt presents with low platelet count, increase PT/PTT, and increased D Dimer. Dx and MOA? What causes this dx?

A 
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
Q

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?

A

DVT
Cardiac mural thrombi

Skeletal fracture

iatrogenic! or decompression sickness

obstetric troubles

112
Q

Pt presents with diffuse petechial rash, neurological sxs and SOB. Hx of broken bone 2 days ago. Dx?

A

Fat and marrow emboli. Fat got into vascular sinusoids.

petechial rash is related to rapid thrombocytopenia.

113
Q

What are the bends? the chokes? Caisson disease?

A

bends - bubbles in joints
chokes - pulmonary edema/collapsed lung (atelactasis)
Caisson: necrosiss of femoral heads, tibia, humerus.

114
Q

A G2P3 presents with severe dyspnea, cyanosis, and shock. Neuro impairment and pulmonary edema

A

Yes amniotic fluid emboli

115
Q

What is the shock flow chart? start from teh bottom

A
  • 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
Q

in the compensatory (non progressive phase) what’s going on?

Progressive/noncompensatory?

A

Low BP –> Incresae HR

Lactic acid and low urine production

117
Q

What is the effect of shock on the adrenal glands? kidneys? lungs?

A

Adrenals: cortical cell lipid depletion
Kidneys: acute tubular necrosis
lungs: diffuse alveolar damage

118
Q

EGF and FGF use what signaling cascade?

what about epidermal cels to the nucleus?

A

MAP Kinsae

RAS proteins

119
Q

What growth factors are significant in angiogenesis?

A

FGF and VEGF

120
Q

Fxns of TGF-b?

A
  • 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
Q

What’s a guy big in vasodilation and inhibiting platelet aggregation?

122
Q

Small specific neutrophil granules release what?

Larger azurophils release what?

A

Small: lysozymes, collagenase genlatinase

Larger azurophil:
MpO, bactericidal facotrs, acid hydrolases

123
Q

What is the mitochondrial pore made out of?

What drug targets it?

A

Cyclophilin D

Cyclosporine

124
Q

To activate the MHC class 1, what must you have?

A

Proteasomes

125
Q

Hageman deficiency?

A

XII asymptomatic

126
Q

How does Wnt and frizzled work?

A

Frzzld activated by Wnt.
Fxn: regulates beta catenin levels
beta catenin activates disheveled protein which inhibits ubiquitination of beta catenin

127
Q

A thrombus in a vessel wall gets digested from the inside out, but then fills back in with bacteria. This is called?

A

Mycotic aneurysm

128
Q

What cell-cell or cell-matrix interaction or process is involved in leukocyte extravasation

A

Tight jxnsget messed up

occludin

Transcytosis

129
Q

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?

A

Lamin A, B, C

Vimentin (mesenchymal cells in the fibroblasts and endothelium)

Desmin

glial fibrillary acidic protein

130
Q

What is the characteristic sign of atrophy

A

autophagy and decreased protein synthesis

131
Q

OKay give me the low down on MMPs TIMPs and ADAMs

A

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
Q

In hypertrophy, the most common stimulus for skeletal muscle is?

Cardiac muscle?

Physiologic hypertrophy is signalged via what?
Path?

A

Skeletal: workload

Cardiac: Hemodynamic

Physio: PI3 - AKT
Pathological: hormones/GFs

133
Q

What is the mechanism of:

hypertrophy?
Hyperplasia?
Metaplasia?

Necroptosis

A

Hypertrophy, Phys = AKT/PI3

hyperplasia = hormones (estrogen in endometrial tissue) and Growth factors

Metaplasia:
- reprogramming of stem cells

Necroptosis: TNF, Rip1, RIP3

134
Q

What suppresses appetite when you have cancer?

135
Q

What inhibits mTOR to increase lifespan?

A

Rapamycin, promotes autophagy

136
Q

Red streaks around a wound indicate what may be happening?

A

Lyphangitis!!!

137
Q

What 3 things can prevent clot propogation?

A

NO, PGI2, ADP phosphatase

tPA (afte formation. fibrinolysis)

138
Q

A liver is nutmeg in color and laden with hemosiderin macrophages. What 2 things can you assume about the liver?

what causes hemosiderosis?

A

Chronic passive congestion and hemorrhagic necrosis

Hemosiderosis:
excess dietary iron
hemolytic anemia
repeated blood transfusion

139
Q

pt has mild bleeding disorders with a PTT time that is high.

A

Factor XI deficiency

Thrombin acn activate V, VIII, and XI so don’t NEED XI to activate.

140
Q

Pt presents with high PTT, but is asymptomatic.

A

Factor XII.
(hageman)
This guy is the initiation of the cascade in vivo

141
Q

pt presents with increased bleeding from nose, vaginally. They have petechiae and purpura. If the pt also gets hemarthrosis what would be the dx?

A

Von Willebrand Disease

Coagulation factor defects

142
Q

What is trousseau’s syndrome

A

Upregulated gene expression in malignant cells

143
Q

What can Growth factors do to cells?

A
  • Promote cells to go into cell cycle
  • Remove blocks on progression
  • Prevent apoptosis
  • Enhance synthesis of proteins
144
Q

What are these caused by?
Coagulative necro?

Liquefactive?

Caseous?

Fat

Fibrinoid

A

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
Q

When do you get overactive apop?

A

Neurodegenerative

146
Q

Pyroptosis mechanism?

A

bacteria –> inflammasome – IL1 –> IL 1 –> Fever and luekocyte

147
Q

What is MYC?

A

transcription factors that regulate the expression of genes that are needed for growth are MYC

148
Q

Where does metastiatic calcification reside?

Why?

A

in the kidney, lung and gastric mucosa,

because H+ is lost quickest here, and increase pH favors Ca+ deposition

MOD (3 decks)

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