Official Step 1 High Yield Concepts Thread

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Transposony

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Let's discuss our doubts/offer clarifications about mechanisms/concepts for Step 1

ASK ANY QUESTIONS here.

To kick start the thread here is something I didn't know:

1. Penicillin-binding proteins (PBPs) are actually enzymes (transpeptidases & carboxypeptidases) which cross-link peptidoglycan. Penicillins binds to these enzymes and inactivating them thereby preventing cross-linkiing of peptidoglycan.

2. Periplasmic space (Gram -ve) contain proteins which functions in cellular processes (transport, degradation, and motility). One of the enzyme is β-lactamase which degrades penicillins before they get into the cell cytoplasm.
It is also the place where toxins harmful to bacteria e.g. antibiotics are processed, before being pumped out of cells by efflux transporters (mechanism of resistance).

There are three excellent threads which you may find useful:

List of Stereotypes

Complicated Concepts Thread

USMLE images
 
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why do muscarinic antagonists cause flushing of skin? This is probably a really dumb question but I just can't wrap my head around it
Inhibition of muscarinic receptors --> inhibits muscarinic sweat gland receptors --> no sweating --> dysfunctional body temperature regulation (i.e. increased body temperature) --> dilated peripheral blood vessels (as a compensatory mechanism to decrease temperature) --> skin flushing
 
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why do muscarinic antagonists cause flushing of skin? This is probably a really dumb question but I just can't wrap my head around it
Muscarinic antagonists blocks sweating. So, the only way body can lose heat is by cutaneous vasodilation.
 
@Phloston 273 (1 point different than my "goal" score)
2) Name three drugs with MOA same as clopidogrel - prasugrel, ticagrelor, ticlopidine
7) What kind of metaplasia is seen in Barrett esophagus? Frame your answer as NKSS is converted to non-ciliated columnar with goblets. And be as specific as possible.
3) Of those three drugs in #2, which one causes neutropenia? ticlopidine



Any D2 antagonist.
@Phloston
1) MOA of clopidogrel - ADP receptor blocker on platelets
6) Name three risk factors for SCC of esophagus - Smoking, achalasia, Plummer-Vinson syndrome
11) Which aortic arch derivative gives rise to a structure closest to that which is most often ruptured in epidural hematoma? - 1st arch, Maxillary artery-->middle meningeal

OTC antidote?
@Phloston
4) What drug used to treat an enveloped, linear DNA virus causes neutropenia? Ganciclovir
5) The organism treated by the drug in #4 causes what classic infection in immunocompromised patients? CMV retinitis
9) MOA of dipyridamole --> increases cAMP in platelets by inhibiting it's degradation by PDE3--> Less ADP--> Less platelet aggregation.
It is also an adenosine uptake inhibitor--> increased extracellular concentration of adenosine --> Vasodilation.

As per original post:

1) MOA of clopidogrel
2) Name three drugs with MOA same as clopidogrel
3) Of those three drugs in #2, which one causes neutropenia?
4) What drug used to treat an enveloped, linear DNA virus causes neutropenia?
5) The organism treated by the drug in #5 causes what classic infection in immunocompromised patients?
6) Name three risk factors for SCC of esophagus
7) What kind of metaplasia is seen in Barrett esophagus? Frame your answer as ___ is converted to ___. And be as specific as possible.
8) Of the following, which one(s) is/are reversible: hyperplasia, hypertrophy, metaplasia, dysplasia, neoplasia, desmoplasia
9) MOA of dipyridamole
10) What are the male/female manifestations of the urethral folds, genital tubercle, urethral sinus, labioscrotal swelling?
11) Which aortic arch derivative gives rise to a structure closest to that which is most often ruptured in epidural hematoma?

------------------

1) ADP P2Y12 receptor antagonist (per USMLE rules, we can't disclose actual test questions, but a heads up that that P2Y12 bit is on the real deal, as ******ed as that is)
2) Prasugrel (greater efficacy but more hemorrhagic strokes age 75+; like clopidogrel, associated with increased risk of TTP), ticlopidine, ticagrelor
3) Ticlopidine causes neutropenia. That's why it's not recommended unless someone needs prasugrel/clopidogrel (e.g., post-stenting) but can't tolerate them or has a contraindication.
4) Viral family is herpesviridae. In contrast, HepB is DNA, enveloped and circular (this seemingly minor distinction is actually HY and tested on Step 1). So potential viruses are HHV1-8 --> HSV1/2, VZV, EBV, CMV, HHV-6/7, KSHV. Ganciclovir, used for CMV, is associated with neutropenia. On the Step 1, look out for mouth ulcers, sore throat or simply reduced WBCs on lab report data after Tx for infection.
5) CMV retinitis. If CD4 ultra-low --> CMV colitis and esophagitis. UWorld assesses CMV colitis btw. Linear ulcers or "owl eyes."
6) Smoking, EtOH most common, followed by any of the following: achalasia, strictures (prior chemical/heat trauma), webs (e.g., Plummer Vinson), immunosuppression. A lot of things cause SCC. Achalasia is the strange one because you'd think lower 1/3 of esophagus = adenocarcinoma, but achalasia actually causes SCC.
7) Non-keratinized stratified squamous --> Intestinal columnar (columnar with goblet cells)
8) Hyperplasia, hypertrophy, metaplasia and dsyplasia are all reversible. The big one is dysplasia. Most people don't realize that's reversible.
9) Phosphodiesterase inhibitor that prevents breakdown of both cAMP and cGMP. The former decreases platelet aggregation; the latter increases arteriolar vasodilation, inducing reflex tachycardia (used for cardio stress testing in those who can't exercise). There are other mechanisms behind dipyridamole, but these are the ones to know.
10) Genital tubercle: glans penis vs glans clitoris AND corpos cavernosum/spongiosum vs vestibular bulbs; HY point is this is the answer for epispadias.
Urogenital sinus: bulbourethral (Cowper) glands vs greater vestibular (Bartholin) glands AND prostate gland vs urethral/periurethral (Skene) glands
Urogenital folds: ventral shaft of penis and penile urethra vs labia minora; HY point is this is the answer for hypospadias.
Labioscrotal swelling: scrotum vs labia majora
11) Epidural hematoma is from rupture of middle meningeal artery, a branch of the maxillary artery. Maxillary artery is first aortic arch. Aortic arches are stupid, but the USMLE likes them.
 
P2Y12 going in my FA right now @Phloston!

Can someone remind me of the significance of Aldo increasing H+ATPase activity in the alpha-intercalated cells?

PS @Phloston please don't delete your posts in this thread.. they're gold.
 
which organism can lead to meningitis in patient who take corticosteroid ?
which organism can lead to meningitis in compromised patient ?
 
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mechanism of contraction alkalosis in CF?
There are different mechanisms contributing to the contraction alkalosis in different CF patients. Dysfunctional CFTR >> excessive Cl and Na lost in the final sweat >> ECF contraction >> decreased filtered load of HCO3 (hence alkalosis) + Cl depletion results in increased reabsorption of HCO3 + Aldosterone secretion >> K wasting >> transcelluar shift of H to fix the hypokalemia and enhanced proton secretion

which organism can lead to meningitis in patient who take corticosteroid ?
which organism can lead to meningitis in compromised patient ?
For compromised - cryptococcus neoformans, for steroid induced fungal meningitis seems to be quite common as well

What reaction forms coporphobilinogen (i.e. how is it increased in AIP)?
AIP -- defective porhobilinogen deaminase >> accumulation of porhobilinogen which spontaneously polymerizes in the urine to form coporphobilinogen
 
Which PAMP does CD (cluster of differentiation)14 bind to?
What cell does mainly express CD 14?
Another cell marker of that cell?
Which toll-like receptor binds to the same PAMP as CD 14?
 
For compromised - cryptococcus neoformans, for steroid induced fungal meningitis seems to be quite common as well
MMRS mention that listeria monocytogenes is the second most common cause of meningitis after pneumococcus in patient > 50 y , and it is the most common cause of meningitis in patients with lymphoma, on corticosteroid, or receiving organ transplantation .
 
what is your diagnosis based on these symptoms :
1- hearing loss , pain in bone , with blue sclera -->
2- 6 years old boy has hearing loss and hematuria -->
3- stiff neck , fever, hearing loss, seizures, and hydrocephalus -->
4- nystagmus,vomiting, ptosis, gait dystaxia, and hearing loss -->
5- dyspnea, pneumothorax, polycystic kidney, and epilepsy -->
6- ptosis , miosis , dyspnea, cough , and pain in shoulder -->
7- 25 y woman has fever, pain in right upper quadrant,bacteremia -->
 
Not positive about most of these but I'll give it a shot

what is your diagnosis based on these symptoms :
1- hearing loss , pain in bone , with blue sclera -->
OI
2- 6 years old boy has hearing loss and hematuria --> Alport Syndrome
3- stiff neck , fever, hearing loss, seizures, and hydrocephalus --> Schwannoma
4- nystagmus,vomiting, ptosis, gait dystaxia, and hearing loss -->
Lateral pontine syndrome?
5- dyspnea, pneumothorax, polycystic kidney, and epilepsy --> Marfan w/ADPKD 😀
6- ptosis , miosis , dyspnea, cough , and pain in shoulder --> Pancoast Tumor
7- 25 y woman has fever, pain in right upper quadrant,bacteremia --> Ascending cholangitis
 
Ground glass liver on histo?
Lymphocytic infiltrate in portal venous system with steatosis?
Meningitis at the base of the brain?
 
Ground glass liver on histo?
Lymphocytic infiltrate in portal venous system with steatosis?
Meningitis at the base of the brain?

I´ll give it a try:
Ground glass liver on histo? - HBV hepatitis?
Lymphocytic infiltrate in portal venous system with steatosis? - not sure
Meningitis at the base of the brain? - TB
 
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What medication would you use to treat active TB in an HIV+ patient?
Is this a trick question?
Rifampin will rev up the P450 and, therefore, mess with the HAART but without it the recurrence rate is very high.
So, not much of a choice there.
 
how does papilledema occur in hypertensive emergency?
Hypertension >> increased CBF >> increased ICP >> disruption of axoplasmic flow within the optic nerve >> leakage of water and protein into the extracellular space around optic disc >> optic disc edema
 
Can you guys help clarify the varus/valgus stress tests for me?

In the MCL test (abnormal passive abduction) you are exerting a medially directed (laterally originating) force, which (if MCL is injured) will result a valgus deformity (i.e. knee moves medially and distal tib/fib move laterally). So the force originates laterally, but pushes medially.. which is considered a valgus force.

In the LCL test (abnormal passive adduction) you are exerting a laterally directed (medially originating) force, which will result in a varus deformity (i.e. knee moves laterally, distal tib/fib moves medially). So the force originates medially, but pushes laterally.. which is a varus force.

So basically varus "deformity" and varus "force" are in opposite directions (same for valgus force/deformity)?
 
FA says albinism can be caused by failure of neural crest migration during development. If that's the cause, then wouldn't melanocyte count be low/absent in those areas.. and hence go against the paradigm that melanocyte number is normal in albinism?
 
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