Cell Biology Biochemistry Usmle

Front 1

Rough Endoplasmic Reticulum (RER) functions differently from Smooth Endoplasmic Reticulum (SER) how?

Back 1

RER: makes secretory (exported) proteins and adds N-linked oligosaccharide to proteins
SER: site of steroid synthesis (so lots in adrenal cortex) and detoxification of drugs/poisons (lots in liver hepatocytes).

Front 2

Nissl bodies are what and are found where?

Back 2

A neuronal RER found in the dendrites

Front 3

The Golgi is the packaging center the cell and delivers to what three areas?

Back 3

Plasma membrane, lysosomes, and secretory vesicles.

Front 4

Which amino acids are modified by the Golgi?
How are they modified?

Back 4

Asparagine: modifies the N-oligosaccharide

Serine and threonine: addition of O-oligosaccharides

Front 5

Proteins that need to go to lysosomes have what carbohydrate added to them by the Golgi?
A failure of the addition of thus sugar results in what disease?

Back 5

Mannose-6-phosphate
Failure of addition leads to the lysosomal storage disorder known as I-cell disease.

Front 6

What happens in I-cell disease?

Back 6

Products can't be targeted to lysosomes due to lack of the addition of M6P, and thus are secreted out of the cell.
Result: coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes. Often fatal in childhood.

Front 7

Vesicular trafficking protein: COP I
Function?

Back 7

retrograde direction, Golgi--> (back to) ER

Front 8

Vesicular trafficking protein: COP II
Function?

Back 8

anterograde direction, RER--> cisGolgi

Front 9

Vesicular trafficking protein: Clathrin
Function?

Back 9

TransGolgi --> lysosomes, plasma membrane --> endosomes

Front 10

Microtubules are incorporated into what kind of cellular structures?

Back 10

Flagella, cilia (bronchioles, sinuses, sperm, fallopian tubes), mitotic spindles.
Also involved in: axoplasmic transport in neurons!

Front 11

The molecular motor protein Dynein transports cell cargo in which direction?

Back 11

retrograde (+ --> -)

Front 12

The molecular motor protein Kinesin transports cell cargo in which direction?

Back 12

anterograde (- --> +)

Front 13

Cilia is in what kind of arrangement?

Back 13

9+2 microtubule arrangement (allows for bending)

Front 14

If your cilia doesn't work (the dynein does't work), what condition do you have?

Back 14

Kartagener's Syndrome aka Primary Ciliary Dyskinesia: infertiliy, bronchiectasis, recurrent sinusitis, and a/w situs inversus.

Front 15

Phagocytes rely on what cellular structure to get to where they need to?
A defect in this structure's polymerization leads to?

Back 15

Microtubles.
Chediak-Higashi Syndrome: decreased phagocytosis resulting in recurrent pyogenic infections, partial albinism, and peripheral neuropathy.

Front 16

The membrane lipid, Phosphatidylinositol, is converted to Arachidonic Acid by what enzyme?
What drugs can inhibit this enzyme?

Back 16

Phospholipase A2.
Inhibited by Corticosteroids

Front 17

Arachidonic acid can be converted to Hydroperoxides by what enzyme?
What drug inhibits this enzyme?

Back 17

Hydroperoxides. Zileuton inhibits, so no Leukotrienes.
(ZiLEUton-LEUkotriene)

Front 18

Leukotriene B4 does what?

Back 18

Neutrophil chemotaxis

Front 19

LTC4, LTD4, and LTE4 are leukotrienes that cause what?
What drugs inhibit them and what are they used to treat?

Back 19

Bronchoconstriction.
Zafirlukast and Montelukast (aka Singulair), used to treat asthma and allergies.

Front 20

Arachidonic acid can be converted to endoperoxides (Prostacyclin, Prostaglandins, and Thomboxane) by which enzyme (s)?
What drug inhibits these enzymes?

Back 20

Cyclooxygenase (COX-1, COX-2)
Inhibited by NSAIDS, acetominophen, COX-2 inhibitors, and aspirin.

Front 21

Prostacyclin (i.e. PGI2; platelet gathering inhibitor) has what actions?

Back 21

Decrease platelet aggregation, causing vasodilation.
Decrease uterine tone.

Front 22

Prostaglandins (i.e. PGE2) has what actions?

Back 22

Decrease Vascular tone, and Bronchiole tone
Increase Pain, Uterine Tone, Temperature, Gastric mucus production.

Front 23

Thromboxane (ie.e TXA2) causes what?

Back 23

Increase Platelet aggregation and Vasoconstriction.

Front 24

Which endocrine hormones use the cAMP pathway?

Back 24

"FLAT CHAMP"
FSH, LH, ACTH, TSH
CRH, hCG, ADH (V2 receptor), MSH, PTH
others: calcitonin, GHRH, glucagon
Alot of these are from the anterior pituitary i.e. FLAT

Front 25

Which endocrine hormones use the cGMP pathway?

Back 25

ANP, NO (EDRF)
Think vasodilators

Front 26

Which endocrine hormones use the IP3 pathway?

Back 26

"GOAT"
GnRH, Oxytocin, ADH (V1 receptor), TRH
iP3-PP (posterior pituitary)

Front 27

Which hormones utilize your Cystolic steroid receptor?

Back 27

"VET CAP"
Vitamin D, Estrogen, Testosterone, Cortisol, Aldosterone, Progesterone

Front 28

Which hormones utilize your Nuclear steroid receptor?

Back 28

T3 and T4

Front 29

Which hormones use the Intrinsic Tyrosine Kinase?

Back 29

Insulin, IGF-1, FGF, PDGF
Think growth factors

Front 30

Which hormones use the Receptor-Associated Tyrosine Kinase?

Back 30

GH, prolactin

Front 31

What is the most abundant protein in the human body?

Back 31

Collagen

Front 32

Type I Collagen is in which tissues?

Back 32

The strong collagen
Bone, Skin, Tendon, dentin, fascia, cornea, late wound repair

Type ONE: bONE

Front 33

Type II Collagen is in which tissues?

Back 33

The slippery collagen
Cartilage (including hyaline), vitreous body, nucleus pulposus.

Type TWO: CarTWOlage

Front 34

Type III Collagen is in which tissues?

Back 34

The bloody collagen
Reticulin: skin, blood vessels, uterus, fetal tissue, granulation tissue (all of this is highly vascularized)

Front 35

Type IV Collagen is in which tissues?

Back 35

Basement membrane or basal lamina

Type IV: Under the Floor

Front 36

mnemonic for: Collagen I, II, III, IV

Back 36

the Strong, Slippery, Bloody BM

Front 37

Ehlers-Danlos Syndrome is due to the faulty synthesis of what?
What are the s/s?

Back 37

Collagen (Type III: bloody collagen)
Hyperextensible skin, tendency to eaisly bleed, hypermobile joints.
A/w joint dislocation, berry aneurysms, organ rupture

Front 38

Osteogenesis Imperfecta ("brittle bone disease") is what kind of disorder (acquired or genetic)? What type of collagen is abnormal?
What are the S/S?

Back 38

Genetic bone disorder.
Abnormal Type I (strong/bone collagen).
S/S: Multiple fractures with minimal trauma, Blue Sclerae, abnormal middle bones leading to Hearing Loss, and Dental imperfections (no dentin).

Front 39

Alport's Syndrom is due to what abnormal collagen type?
What is it characterized by?

Back 39

Abnormal collagen type IV, makes up the BM (genetic defect).
Nephritis and deafness, may be a/w ocular disturbance. "Can't see, can't pee, can't hear."

Front 40

Elastin is rich in which amino acids?
It is broken down by which enzyme? More importantly, what inhibits this degrader?

Back 40

Proline and Glycine
Degraded by Elastase, which is inhibited by alpha1-antitrypsin

Front 41

An alpha1-Antitrypsin deficiency results in what? Why?

Back 41

Emphysema, because the deficiency allows uninhibited elastase activity.

Front 42

Which acute phase reactants are involved with inflammation?

Back 42

IL-1, IL-6, TNF-alpha

Front 43

What drugs act on microtubules?

Back 43

-bendazoles and -taxols
Griseofulvin
Vincristine/Vinblastina
Colchicine