U-World (advanced editing) Flashcards
(103 cards)
PECAM-1 is a molecule that allows for what step of neutrophil migration?
Transmigration (getting the neutrophil across the endothelial cell).
*remember the steps are: (1) marination, (2) rolling, (3) adhesion, (4) transmigration and chemotaxis, (5) phagocytosis

Explain the mechanism as to how pancreatic beta cells release insulin into the bloodstream in response to elevated glucose levels.
- Glucose comes into the pancreatic beta cells via the GLUT 2 transporter
- Glucose is broken down into ATP by glycolysis
- The increased ATP level within the cell causes closure of the K+ channel
- Since the K+ channel is closed, K+ cannot get out—> inc K+ within the cell, so it gets de polarized (anytime there’s inc positive charge into a cell that’s depolarization)
- The depolarization stimulates Calcium influx into the cell
- The calcium allows for insulin vesicles to get exocytosed and insulin + c-peptide are released out of the cell into the bloodstream

Where is the most common ectopic thyroid tissue site?
the tongue (lingual thyroid)
*The thyroid gland starts as the thyroid diverticulum in the pharynx and descends into the neck. Failure for the thyroid to fully migrate on down to the neck can interfere with swallowing, etc.

Think about the synthesis of the catecholamine epinephrine (epi). What amino acid is it synthesized from? What is the enzyme that converts NE—> epi? What hormone promotes this conversion?
Epi is made from Tyrosine. NE—> epi by PNMT (phenylethanolamine-N-methyltransferase) and cortisol stimulates this conversion.

Hydrophobic amino acid residues like Ala, Val, Leu, I’ll, Phe, Trp, Met, Pro, and Gly serve what function for proteins?
Anchor proteins to the phospholipid membrane

Besides letting glucose into cells to regulate blood sugar, what does insulin do?
Cell growth and DNA synthesis and promotes synthesis of glycogen, lipids, and proteins.
(*It specifically promotes glycogen synthesis by activating protein phosphatase.)

What glucose transporters are represented by the circles? Triangles?

circles (more insulin binding—> more expression of these receptors): GLUT 4 (the insulin-dependent channel- needs insulin to get expressed and allow glucose into the skeletal/ fat cells)
triangles (more insulin binding—> no change in expression of these receptors): GLUT 1, 2, 3, 5 (insulin-independent channels on other cells)

Turner syndrome presents with what findings in the: neck, nipples, height, aorta (2 things), kidneys, and ovaries?
neck is wide
nipples are spread far apart
short stature
coarctation of the aorta and bicuspid aortic valve
horshoe Kidney
streak ovaries (don’t get a period)

Patient presents with lips that look like this. He also had his thyroid removed after a mass was discovered. What is the most likely diagnosis and what gene is most likely mutated causing this?

MEN 2b
(multiple endocrine neoplasia: mucosal neuroma, thyroid medullary carcinoma, and pheochromocytoma)
*mucosal neuroma means these lesions on the lips and mouth
What biochemical change (also mention the specific amino acid residues) will occur on insulin receptors leading to insulin resistance?
Phosphorylation of serine and threonine residues on insulin receptors (by serine kinase)—> insulin resistance (insulin binds to receptor–> but less glucose is able to come into the cell)
(*this type of phosphorylation can be induced by TNF-alpha, catecholamines, glucocorticoids, and glucagon).

Patient has high free thyroid hormone, low TSH. Shins look like this. What is the disease? Explain the finding on the shins.

Graves’ disease (most common cause of hyperthyroidism).
In Graves you have an antibody that stimulates TSH receptors on the thyroid—> causes the thyroid gland to produce too much TH= hyperthyroidism. But since you also have TSH receptors on your shins and on optic muscles, the disease affects these places. Stimulation of receptors in shins and eyes—> increased production of GAGs—> non-pitting edema in shins and thickened ocular muscles that push the eyeballs out.
What causes gigantism?
Excess growth hormone (GH)—> excess liver production of IGF-1 acting on growth plates of bones.

What effect does estrogen have on bones? What does this mean for post-menopausal women?
Estrogen decreases osteoclast activity, so there’s less breaking down of bone.
Post-menopause: decreased estrogen—> more osteoclast activity (don’t have the protective estrogen to keep osteoclasts in check)—> increased risk for osteoporosis and fractures of the bones

Name which enzymatic step in this vitamin D activation pathway the following things will have an affect on.
- Getting some sunlight
- Increasing vitamin D in your diet
- Increase in PTH
- Increase in Calcium

- Sunlight: Step A (7-dehydrocholesterol—> cholecalciferol)
- Diet: Step B (cholecalciferol—> 25-hydroxyvitamin D3)
- PTH: Step C (25 vitamin D—> 1,25 vitamin D)
- Calcium: INHIBITS step C (if you have inc Calcium, you don’t want to activate vitamin D into 1,25 to inc Calcium more)

You give a hypOthyroid patient T3 for treatment. What will happen to the patient’s T4 levels and rT3 levels after treatment (increase, decrease, or stay the same)?
Since T4–> T3 (active) and you now have increased T3, T4 levels will GO DOWN (negative feedback). Since T4 is used to make rT3 and there’s less of it available, rT3 levels will also GO DOWN.

What is this describing?

Klinefelter syndrome
Label the parts of the breast.

(Sinuses- collecting reservoirs for milk during lactation)

A 14 year old girl just had menarche (started her periods) 1 year ago. She complains of irregular periods (doesn’t have them every month), and when she has them she bleeds heavily for 7-10 days. She also has spotting when she’s not on her period. What is most likely the issue?
girls just starting their periods and women getting ready to end their periods often have irregular cycles. What’s going on is an ANOVULATORY CYCLE. Estrogen builds up, thickening the endometrium, but PG does not come into play to shed the lining when pregnancy does not occur. So bleeding does not happen until the endometrium becomes so thick that some cells will shed at once—> heavy bleeding.

An episiotomy is performed on a women to expediate childbirth. An incision is made at the posterior vaginal opening. What pelvic floor muscle was cut into?
The perineal body

What is postpartum ovarian vein thrombosis? Where could the clot go from the right ovarian vein (more common)? How about from the left ovarian vein?
Increased coagulation from pregnancy + endothelial damage from delivery—> ovarian vein thrombosis. This would present as fever and flank pain (no specimens detected if UTI is suspected).
Right ovarian vein—> IVC
left ovarian vein—> left renal vein

What causes a septate uterus?

The septum doesn’t completely go away/ resorb/ involute.
What causes a bicornuate uterus?

Mullerian ducts don’t completely fuse.
What causes a didelphys uterus?

Mullerian ducts don’t fuse at all.
What branch off the common iliac artery goes down to the leg as the femoral artery? What branch off the common iliac artery branches into smaller arteries to feed a bunch of pelvic structures?
external iliac—> goes down leg as femoral artery
internal iliac—> branches to feed pelvic structures





















































































