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Pass Program > Chapter 12 Cellular Physiology > Flashcards

Chapter 12 Cellular Physiology Flashcards

1
Q

What is it called when nucleus shrinks and forms blebs?

A

pyknosis

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2
Q

What is it called when nucleus breaks into chunks?

A

Karyorrhexis

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3
Q

What is it called when the nucleus dissolves?

A

karyolysis

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4
Q

What is the marker for cell death?

A

phosphatidylserine

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5
Q

Who notices who is programmed for cell death?

A

Cyclin D (BigD!)

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6
Q

Who recognizes the label , attaches to it, and destroys the cell?

A

caspases

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7
Q

What is the gene in control of apoptosis?

A

p53

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8
Q

What labels proteins for destruction?

A

ubiquitin

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9
Q

If you see some part that should have apoptosed (i.e. webs between fingers, etc) what failed to happen?

A

apoptosis

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10
Q

In which event, apoptosis or necrosis, the cell membrane dissolves first, then the nucleus?

A

apoptosis

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11
Q

Which event, apoptosis or necrosis, involves inflammation?

A

necrosis

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12
Q

most common cause of necrosis

A

ischemia

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13
Q

9 types of necrosis

A
  1. ischemic
  2. purulent
  3. liquefactive
  4. granulomatous
  5. caseous
  6. fibrinoid
  7. fat
  8. gangrenous
  9. hemorragic
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14
Q

MC location of liquefactive necrosis

A

brain

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15
Q

What cause granulomatous necrosis?

A

virus, fungus, etc.. (T cells and macrophages)

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16
Q

caseous

A

TB!

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17
Q

Fibrinoid MCC in child

A

HSP

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18
Q

fibrinoid necrosis MCC in adult

A

HTN, diabetes

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19
Q

MCC of uremia in children

A

HUS

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20
Q

MCC of uremia in adults

A

HTN, diabetes

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21
Q

What are the signs of vasculitis?

A

schistocytes, bleeding from skin and mucosa; increased bleeding time

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22
Q

MC location of fat necrosis

A

pancreas (from chronic pancreatitis: damaged pancreatic cells release lipase that split TRI, forming free fatty acids that combine with Ca) and breast (after trauma)

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23
Q

MC cause of pancreatitis in children

A

trauma 2)coxsackie and mumps

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24
Q

MC cause of pancreatitis in adults

A
  1. gallstones 2. alcohol
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25
Q

What is the difference between dry gangrene and wet gangrene?

A

Dry gangrene from vasculitis because loss of blood supply; wet gangrene involves a superimposed infection

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26
Q

Which bacteria is responsible for gas gangrene?

A

clostridium perfringens

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27
Q

What bacteria is responsible for necrotizing fascitis?

A

MRSA

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28
Q

Where can hemorrhagic necrosis be seen?

A

any organ with dual blood supply: liver, brain, GI tract

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29
Q

treatment for abscess of lung

A

great surgically (drain) and IV antibiotics

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30
Q

Medication to relieve the symptoms of Peripheral Arterial Disease (PAD)

A

Cilostazol: prevents PLT aggression; dilate vessel

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31
Q

Main cause of monosomy or trisomy

A

nondisjunction

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32
Q

In which phase of cell division does nondisjunction occur?

A

anaphase (chromosomes do not properly separate or disjoin)

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33
Q

percentage of risk of any disease in the public

A

1-3%

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34
Q

chance of getting a disease with one risk factor (approximately)

A

10%

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35
Q

Chance of getting a disease with 2 risk factors?

A

(about 20% or more)

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36
Q

In which disease did the child inherit only one sex chromosome and manifests with webbed neck, cystic hygroma, gonadal streaks, widely-spaced nipples and coarctation of aorta?

A

Turner’s

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37
Q

In coarctation of the aorta, if the right upper limb has a strong pulse, but the left upper limb doesn’t, where is the coarctation?

A

proximal to L. subclavian artery

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38
Q

in coarctation of the aorta, if the upper limbs have strong pulses, but the lower limbs do not, where is the coarctation?

A

distal to left subclavian artery

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39
Q

If the child is pink proximal to nipples, but cyanotic distal to nipples, what kind of coarctation?

A

Coarctation proximal to left subclavian with a patent PDA which draws deoxygenated blood from pulmonary artery down into descending aorta (so lower limbs are cyanotic).

40
Q

MCC of ASD in Down’s syndrome?

A

lack of septum secundum because no endocardial cushion

41
Q

Which trisimony the child is born with rocker bottom feet, triphalangeal thumb, overlapping fingers, microencephaly, micrognathia

A

Edwards (trisimony 18)

42
Q

Which trisimony the child is born with polydactyly, holoprosencephaly, GU problems, and possible omphacele

A

Patau (trisimony 13)

43
Q

What are two possible later complications of Down’s syndrome?

A

ALL and Alzheimer’s

44
Q

What is it called when neural crest cells failed to migrate to distal colon?

A

Hirschprung’s disease

45
Q

Why early onset of Alzheimer’s in Down’s syndrome?

A

APP gene is on chromosome 21, unable to be cleaved to betalipoprotein E4

46
Q

MOA Donepezil

A

inhibits breakdown of Ach via inhibition of acetylcholinesterase

47
Q

MOA Memantine/Galantamine

A

blocks glutamate’s inhibitory effect on the NMDA pathway

48
Q

Which checkpoint is there in the cell cycle from G1 to S?

A

Rb checks DNA, p53 induce apoptosis if abnormality found

49
Q

Where else in the cell cycle does p53 initiate apoptosis if damage to DNA is detected?

A

G2 to M checkpoint

50
Q

Why are patients predisposed to gout with any chemotherapy?

A

Destroying cells will cause purines to break down which will get converted to uric acid.

51
Q

If you want to attack rapidly dividing nucleus, which vitamin should you take away?

A

folate, that’s why we have so many chemo that attack folate (i.e. Methotrexate)

52
Q

Which drug should be given with methotrexate to prevent anemia?

A

leukovorin (folinic acid)

53
Q

In which phase do we often use antimetabolites?

A

S phase (to inhibit DNA synthesis)

54
Q

MOA of purine analogs (azathioprine, 6 mercaptopurine (6-MP); 6 thioguanine

A

inhibit de novo purine synthesis (put will make uric acid up, so give allopurinol)

55
Q

What are the labs in tumor lysis syndrome?

A

K up, LDH up, uric acid up; Ca down, phosphate up; stone formation

56
Q

MOA of Cladribine

A

inhibit enzymes involved in DNA metabolism, including DNA polymerase and ribonucleotide reductase

57
Q

5 fluorouracil and cytarabine (ara-C) are examples of which class of chemotherapies

A

pyrimidine analogs

58
Q

MOA of 5 FU

A

inhibits thymidylate synthase

59
Q

MOA of ara-C

A

inhibits DNA polymerase

60
Q

What is the difference between uracil and thymidine?

A

a methyl group

61
Q

What is the methyl carrier

A

THF

62
Q

Cyclophosphamide, Busulfan, Nitrosureas (Carmustine, Lomustine), Chlorambucil are all examples of which class of chemotherapies?

A

alkylating agents

63
Q

We often use alkylating agents for which kinds of cancers?

A

slow growing, chronic such as MM and CLL

64
Q

MOA cyclophosphamide

A

fat soluble, goes to liver, liver makes it water soluble by making free radicals, free radicals kill cancer, water soluble goes out kidneys, so it is harmful to kidney and bladder

65
Q

MOA of cisplatin, carboplatin

A

kill cellls through cross-linking like alkylating agents

66
Q

When is cisplatin used?

A

GU cancers (testicular, ovarian, bladder)

67
Q

What is dacarbazine and procarbazine used for?

A

Hodgkin’s lymphoma

68
Q

Doxirubicin, bleomycin, dactinomycine are all which class of chemotherapies?

A

anti-tumor antibiotics

69
Q

What is doxirubicin used for?

A

leukemia, lymphoma

70
Q

What is doxirubicin’s MOA?

A

inserts itself between DNA bases (intercalation); generates free radicals causing DNA breaks

71
Q

What is Bleomycin used for?

A

Hodgkin’s, testicular cancer, squamous cell cancer

72
Q

What is dactinomycin used for?

A

Wilm’s tumor (along with vincristine)

73
Q

What class of drugs are vinblastine, vincristine, and paclitaxel?

A

microtubule inhibitors

74
Q

What are vinblastine and vincristine used for?

A

leukemias, lymphomas

75
Q

In which phase of the cell cycle does Paclitaxel work?

A

M phase; stuck in M phase

76
Q

MOA of topoisomerase inhibitors

A

inhibit topoisomerase II (increase breakdown of DNA)

77
Q

Which cancers are topoisomerase inhibitors used for?

A

testicular cancer, small cell lung cancer (etoposide); lymphoma (teniposide)

78
Q

What are the markers for natural killer cells?

A

CD16, CD56

79
Q

MOA of hydroxyurea

A

inhibits ribonucleotide reductase; used in CML and Sickle cell

80
Q

MOA Bevacizumab

A

VEGF inhibitor; used in colon, lung, renal cell cancer

81
Q

MOA of imatinib

A

tyrosine kinase inhibitor of BCR-ABL use in CML

82
Q

MOA rituximab

A

antibody against CD20 receptor of B cells; used for CLL, IBD, Hodgkin’s

83
Q

MOA of tamoxifen and raloxifene

A

SERM (Selective Estrogen receptor modulators) antagonist at breast and agonist at bone

84
Q

MOA Transtuzumab

A

antibody against HER2, for HER2+ breast cancer

85
Q

What SE do all “mabs” cause?

A

allergies, and cardiac fibrosis (eosinophils irritate myocardium)

86
Q

What is dystrophic calcification?

A

calcification on lysosome destroys cell and release acid hydrolase which destroy RNA/DNA
(first N/K pump stops first, cell swells and Na/Ca pumps stop and Ca cannot get out and accumulates on lysosomes)

87
Q

Which organelle breaks down fatty acids through beta oxidation?

A

peroxisomes

88
Q

What guides protein into the rough ER?

A

pre-sequence (all get cleaved off)

89
Q

What guides protein to Golgi apparatus? What is the “chaperone” ?

A

pro-sequence; HSP-90 (grab prosequence and sends to concave side of Golgi) ;

90
Q

Which pro-sequence does not get degraded?

A

C peptide of insulin

91
Q

What will Golgi add to proteins?

A

mannose 6 phosphate

92
Q

Where is it sent after Golgi?

A

lysosome

93
Q

What is the chaperone of a protein to the mitochondria?

A

HSP-70

94
Q

problem of digoxin

A

blocks Na channels; sodium and Ca cannot get out; increases contractility but might cause Ca to build up on lysosomes, cause cell death

95
Q

How long does it take for irreversible cell death in most tissues? in the brain?

A

6 hours; in brain 20 minutes

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