Uworld new

Question 1

Isonazid MOA

Answer 1

Isoniazid inhibits pyridoxine phosphokinase (this normally converts pyridoxine to its active form pyrixodal 5’ phosphate

it also inhibits intracellualr catalaze peroxidase

Question 2

How does Isonazid cause anemia

Answer 2

The enzyme pyrixodal 5’ phosphate that is inhbited by isonazid is a cofactor for ALA synthase (sigma aminolevulinitic acid synthase), which is the RATE LIMITING STEP in heme synthesis. So if you inhibit it you get a microcytic, hypochrmic anemia

Question 3

What type of anemia does Isonazid cause

Answer 3

Microcytic Hypochormic anemia with RINGED SIDEROBLASTS (Iron is transported to developing erythrocytes that can’t form heme-> granules accumulate around nucleus-> sideroblast)

Question 4

What does pyrixodine deficiency cause, what drug can cause?

Answer 4

Dermatitis, stomatitis, neuropathy, confusion—INH can cause so give pyridoxine

Question 5

Symptoms of temporal arteritis

Answer 5

headache (potentially scalp tenderness with hair combing), maybe some thickening of the vessel (it is giant cell artertiis after all), jaw claudication, chewing pain; complication is occlusion of opthalmic artery-> blindness. Also polymyalgia rheumatic often (pain and stiffness of proximal muscles, esp in morning)
can get fever, fatigue weight loss

Question 6

What mediates acute decompensated heart failure?

Answer 6

Increased sympatheitc nervous system activity (also RAAS and ADH secretion). Basically trying ot get more blood out so you increase heart rate and contractility (so MORE Left vent diastolic pressure), vasoconstrict, and increased extracell volume. This cuases like half of the freaking symptoms though

Question 7

Calculate maintenance dose

Answer 7

MD= Cpss * CL/Bioavail fraction
(fraction is 1 if IV)
make sure to adjust for time interval

Question 8

An infant has PKU like symptoms, are given treatment, and still are acting like they have PKU and elevated prolactin; the fuck is going on?

Answer 8

They have a dihydropterine reductase deficiency. This enzyme supplies the BH4 reduction to BH2. This is used in both the PKU->Tyrosine AND the Tyrosine->DOPA sequence. So even if you give extra tyrosine they’ll still be fucked up. The elevated prolactin is because this pathway isn’t working so they aren’t making dopamine to inhibit prolactin. I guess this could happen if tyrosine hydroxylase (which catalyzes the second rxn) was fucked up too. Not sure.

Either way, normally PKU is phenylaline hydroxlase

Question 9

An infant has billious emesis, abdominal distension, air fluid levels/small bowel dilation and a green inspissated mass in the distal ileum; what is this, what will kill this person?

Answer 9

This is likely a meconium ileus; which happen in kids with CF. So if this cat were to die, it would probably be pneumonia.

Question 10

Symptoms of trauma to left frontal lobe vs trauma to right frontall lobe

Answer 10

Left: (handles more exec function and personality) so get apathy and depression
Right: disinhibited behavior

Question 11

What do you use to calculate GFR? RPF? (clearance of)

Answer 11

Inulin (GFR), PAH (RPF)

Question 12

Give someone epi, then give them either phentolamine or phenoxybenzamine and measure vascular tone); how will the graphs differ?

Answer 12

Phentolamine is a REVERSIBLE competitive inhibitor; so it shifts the graph right.
Phenoxybenzaine is an IRRVERSIBLE NONCOMPETITIVE so it’ll shift the graph down
(these are both alhpa blockers)

Question 13

What are neurophysins used for; if you didn’t have them what woiuld happen?

Answer 13

Carrier proteins for oxytocin and ADH (so if you dont have get diabetes insipidus)

Question 14

What are complications of obsturctive slseep apnea?

Answer 14

Pulmonary hypertension and right heart failure (also will definitely get systemic hypertension, biggest correlate)

Question 15

Tx for mycoplasma pneumoniae

Answer 15

Either a Macrolide or a tetracycline

Question 16

What structures should DBS target ofr parkinsons

Answer 16

Thalamus or GPi

Question 17

What might present as a flame shaped hemorrhage or a dot on fundoscopy

Answer 17

Severe hypertension in retinal precapillary arterioles->endothelial disruption-> plasma leakage and fibrous necrosis; get patchy loss of vision like a shadow passed over it

Question 18

What is absorbed more in CF

Answer 18

Sodium

Question 19

What urea cycle disorder might present with hyperammonemia and elevated urinary orotic acid (and frmo the hyperammoneia vomiting, tachypnea, confusion and coma)

Answer 19

Ornithine Transcarbamylase deficiency

Question 20

What is the main mechanism of action of a systemic progestin vs a locally acting

Answer 20

Systemic (eg the pill and progestin implants/injections): Suppresses GnRH and pituitary gonadotropin secretion, inhibiting ovulation

Local: Progestin only/Levo IUD (Mirena): thicken cervical mucus, impair sperm penetration

Copper IUD creates cytotoxic inflammatory response in uterus

Question 21

What beta blocker might you start in an MI (in someone with COPD)? Why?

Answer 21

Metoprolol; can do Esmolol for COPD situations (its really short I think, but both are nonselective). Reduce HR, CO, myocardial oxygen demand

Question 22

Describe: Dissociative amnesia, Dissociative identiy disorder, Depersonalization/derealizatino disorder

Answer 22

Dissociative amnesia: The fugue state. Can’t recall important infromation due to a truamtic event (walter white)

Dissociative identify: trauma/abuse-> multiple personalities

Depersonalization: Get feelings of detachment from or being an observer of one self, derealization, but recognize reality

Question 23

What is Hartnup disease?

Answer 23

Presents like niacin deficiecny (so pellegra skin erruptions, cerebral ataxia), with excessive neutral amino acids in the urine, it is impaired transport of neutral amino acids in the small intestine and the PCT. Can tx by giving niacin

Question 24

What type of muscle fiber is myoglobin rich, oxygen poor?

Answer 24

Slow twitch (type I), use mostly aerobic respriation (have high mitochondria)

Question 25

What substance goes through the glycolytic pathway and is metabolized hte fastest

Answer 25

Fructose (and fructose 1 phosphate); they skip the rate limiting step of phosphofructokinase (PFK-1) and can dive right in

Question 26

Have a sequence of purified nucleic acids with short sequences of repeated deoxythmidine residues fixed to latex beads; what will bind really easily to it?

Answer 26

Mature mRNA; in this case, the poly A tail (its a bunch of Ts, so complimentary binding)

Question 27

What does the PAS reaciton (periodic acid schiff) stain?

Answer 27

Oxidizes carbon-carbon bonds and gives a magenta color. Does so for glycogen, glycolipids, polysach of fungal cell wall, mucosubstances surrected by epithelia and basement membranes

Question 28

What is Milrinone?

Answer 28

a selective phosphodiesterase enzyme 3 inhibitor; causes systemic arterial and venous dilation by increasing cAMP in vascular tissues. Also, it increases cAMP in cardiac myocytes, promotoing calcium influx and causing myocardial contractility (positive ionotropy)

Question 29

What might present with sudden, painless and permenant monocular blindness with a pale retina and a cherry red macula?

Answer 29

central retinal occlusion secondary to athero and thromboembolism

Question 30

What is biotin needed as a cofactor for? Unique situation it could happen in?

Answer 30

Carboxylase reactions, there are really only three (btw this is vit B7)
Pyruvate carboxylase (pyruvate->oxaloacetate) for gluconeogenesis
Acetyl-CoA Carboxylase (acetyl-coa->malolyl-CoA) Fatty acid synthesis
Propinoyl-CoA Carboxdylase (Propinoyl-Coa->methamonyl-CoA)—fatty acid oxidation

Can happen with poor diet, or a congenital disorder—-but the big one is due to excess raw egg white consumption (get high levels of biotin binding avidin in egg whites)

Symptoms: nonspecific like mental status changes, myalgias, anorexia, chronic dermatologic changes (macular dermatitis), and even metabolic acidosis (more pyruvate to lactic acid conversion goin on)

Question 31

What is beta endorphin derived from?

Answer 31

POMC. So it shares an origin with ACTH and MSH. just think of the link between stress and opioid system.

Question 32

What do you need niacin for in the TCA cycle?

Answer 32

Basically need it for dehydrogenase and reductase reactions (also cell signaling and repair). More specifically you need NAD and NADP (and it is a precursor for that, NAD for TCA cycle, NADP for glycolysis and beta oxidation slash HMP shunt).

so cofactor for: isocitrate dehydrogenase, alpha ketoglutarate dehydrogenase, maltate dehydrogenase (NOT succinate dehydrogenase; it uses FAD)

dont forget pellagra has PHOTOsensitive dermatitis (and other features like diarrhea, dementia)

Question 33

How does insulin promote glycogen synthesis

Answer 33

via tyrosine kinase/PI3; activates protein phosphatase.