Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards DIT > DIT Foundations Mnemonics and Associations > Flashcards

DIT Foundations Mnemonics and Associations Flashcards

1
Q

Week 4 of embryo devo?

A

4 chambered heart and 4 limb buds (easy to remember)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Week 8 of embry devo?

A

Fetal movement (8 rhymes with gait)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Week 10 of embryo devo?

A

TEN is when you see PENis. visible genitalia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does FGF do?

A

Lengthening of limbs by stimulating mesoderm. FGF is Full Growth Fimbs (limbs, but it starts with F)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does Hox do?

A

Segmental devo of embryo, problems canc ause synpolydactyly or limbs in wrong place.

retinoid acid can screw it up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does sonic hedgehog gene do?

A

pattern along anterior posterior axis, problems can cause holoprosencephaly (one eye, also see holoprosencephaly in fetal alcohol syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Most common cause of neural tube defects (RFF)

A

Folic acid deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Most common cause of congenital malformations in US (RFF)

A

Alcohol use in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most common cause of congenital intellectual disabilities in US (RFF)

A

FAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are Nissl bodies?

A

RER in neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Smooth ER does what?

A

Detox and steroid synth (liver and adrenal cortex have lots of them)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

COP1 vs COP2?

A

COPI is retrograde (Golgi to RER), COPII is anterograde (ER to Golgi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What amino acid can be modified in golgi by N-oligosaccharides?

O-oligosarcharides can be added to what in the golgi?

A

N-oligosaccharides on asparagine (have N in the R group)

O-oligosacharides on serene and threonine (have OH on amino acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is added to lysosomal enzymes in golgie?

A

Mannose 6 phosphate. Problem is I-cell disease. Cis golgi issue.

HIGH LEVELS lysosomal enzymes in plasma

Coarse facial features restricted joint movement

corneal clouding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What three things do peroxisomes do?

A
  1. Beta oxidation of very long chain fatty acids and branched chain fatty acids
  2. Synthesis of plasmalogens (phospholipids found in MYELIN)
  3. Oxidases and catalases for metabolizing ethanol and other toxic stuff
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nuclear lamin mutations can cause what 2 diseases?

A

Progeria (kids look like old people)

Muscular dystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What type of tissue is associated with vimentin?

A

Intermediate filament staining:

Connective tissue, SARCOMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What type of tissue is associated with desmin?

A

Intermediate filament staining:

desMin in Muscle

Rhabdomyosarcoma and leiomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What type of tissue is associated with cytokeratin?

A

Intermediate filament staining:

Epithelial cells. Carcinoma is tumor of epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of tissue is associated with GFAP?

A

Intermediate filament staining:

Glial fibrillary acid proteins. GLIAL cells

Glioblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What type of tissue is associated with neurofilament?

A

Intermediate filament staining:

Neurons

Neuroblastoma, primitive neuroctodermal tumor

22
Q

Drugs on microtubules?

A

Microtubules Get Constructed Very Poorly

Mebendazole: Benzimidazoles: anti-worms (because they are bendy, like mebendazole, albendazole, thiabendazole)

Griseofulvan: antifungal (ringworm and nail fungus)

Colchicine: anti-inflamm for gout, b/c phagocytes can’t move to where they need to go

Vincristine/vinblastine prevent polymerization

Paclitaxel: Stabilizes them, (taxing to stay polymerized)

23
Q

What is kartegeners syndrome?

A

Immotile cilia b/c dynein arm defect.

Infertility
bronchiectasis
chronic sinusitis
situs inverses

24
Q

What protein is important for receptor mediated endocytosis?

A

Clathrin. It binds to adaptin in the plasma membrane (adapt in is bound to extracellular proteins). It is clathrin that causes the involution of the membrane.

25
Q

Corticosteroids target in arachidonic acid pathway

A

Phospholipase A2 (no arachidonic acid cleaved off from phophatidyl choline)

26
Q

Zileuton target?

A

Lipoxygenase (no lukotrienes are made, so no bronchoconstriction and decreased neutrophil chemotaxis)

27
Q

What does montelukast/zafirlukast target?

A

Lukotriene receptors: less bronchoconstriction and less neutrophil chemotaxis

28
Q

Bcl-2 does what?

A

anti-apoptotic (4 letters in anti and Bcl-2)

29
Q

Bax does what?

A

proapoptotic that puts channels in mitochondrial membrane. RELEASES cytochrome C to activate caspases

30
Q

What activates caspaces?

A

Cytochrome C from mitochondria after bax opens them

31
Q

What are two receptors for extrinsic pathway of apoptosis?

A

Fas-Receptor and TNF receptor. They then activate caspaces for cell death

32
Q

What do CD8 T cells release?

A

Perforin and granzyme B. Perforin puts holes in membrane then granzyme B activates the caspaces directly.

33
Q

What is CD95?

A

Fas receptor (it is a death receptor for Fas Ligand)

34
Q

What are the three inflammatory mediators?

A

IL-1, IL-6, TNF-alpha

35
Q

Three markers for vasodilation in inflammation?

A

Histamine, serotonin, bradykinin

36
Q

What two cofactors are required for fibrosis and remodeling after inflammation?

A

Vitamin C in fibroblasts laying down collagen,

tissue remodling done by metalloproteinases, ZINC

37
Q

What are the 4 chemotatic products released in response to bacteria drink migration stage of extravasation of leukocytes?

A

C5a
IL-8
LTB4
Kallikrein

38
Q

What is going on in leukocyte adhesion deficiency syndrome?

How does it present?

A

Abnormal integrin molecules

Delayed separation of umbilicus in newborns and recurrent bacterial infections

39
Q

What is transudate? what is it from?

What is exudate? what it from?

A

Watery. From high hydrostatic pressure or low oncotic pressure.

EXudate has EXtra stuff in it (proteins and inflammatory cells). From lymphatic obstruction or inflammation.

40
Q

What is a granuloma? And what signal is causing it?

A

Collection of macrophages. They make TNF-alpha which makes a granuloma.

BEFORE USING ANTIGRANULOMA, do a TB test.

41
Q

What are the granuloma diseases we should know?

A 
Tb
Fungal
Sarcoidosis
Wegeners granulomatosis
Berylliosis (berylium mine)
Cat scratch fever (barte]onella)
Listeria
Leprosy (those mycobacterium)
Syphilis
Crohn's (in gut)
Chronic granulomatous disase (NADPH oxidase deficiency)
Foreign bodies
42
Q

Receptors in each stage of leukocyte extravagation:

A
  1. Rolling: E-selectin (endothelium), P and L selectin for platelet and leukocyte respectively
  2. Tight binding: ICAM-1 on endothelium and Integrin LFA (of nuetrophil)
  3. Diapedesis: PECAM (diaPEdesis) on neutrophil and endothelium
  4. Migration. None
43
Q

4 types of collagen

A

Strong, slippery, bloody, BM

Type 1: bONE (strong). Skin, bone, detnin, scar tissue

Type 2: carTWOlage (slippery)

Type 3: Bloody. Blood vessels, skin, uterus, fetal tissue, skin and granulation tissue (Ehlers-Danlos (ThreE-D)

Type 4: basement membrane (goodpasture)

44
Q

What does vitamin C do for wound healing?

A

Hydroxylation of lysine and proline residues of preprocollagen

45
Q

Is osteogenesis imperfecta autosomal dominant? What is the problem?

A

OI type 1 is autosomal dominant. (That painting video for right brain bonus emphasized it)

Not enough Type 1 collagen. Problem with the triple helix formation.

Presents with fractures
Dental abnormalities
Blue sclera

OI type II is autosomal recessive and you die in utero

46
Q

Ehlers danlos is a problem with what?

A

Trick question: TWO TYPES

Classical type: type V (and some type I) collagen and stretchy skin and mobile joints: elastic man in circus

Vascular type: III (ThreE D). Ruptures and of organs and vasculrature

47
Q

Whats wrong in alport syndrome? RFF

A

Type IV issue

Can’t see, can’t pee, can’t hear high C (we learned about it in CRRAB)

Kidney disease
Hearing problems
Cataracts (blindness)

48
Q

What is wrong in Marfans? RFF

A

Fibrillin issue (defect in sheath around elastin).

Dissection, lens dislocation, flexible joints, Loose mitral valve, tall, pectorus excavatum

49
Q

What is going on in young person with emphysema? What are they at risk for?

A

Alpha 1 antitrypsin deficiency. Elastase not broken down. Also can be stuck in liver and destroy liver.

50
Q

Does muscle hypertrophy or hyperplasia?

A

Hypertrophy. Duh. They are in G0

51
Q

What is going on in Barrets esophagus? What is the concern?

A

GERD irritates bottom esophagus

METAPLASIA: From squamous to columnar (to protect from acids of stomach)

Risk of ADENOCARCINOMA (secreting tumor)

52
Q

What is a lipofuscin granule?

A

Reidual body within in cell tahtis yellow-brown and from free radical induced lipid oxidation (from atrophy and aging)

Boards DIT (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions