NBME 17 discussion

[fatwalletuab]

Can you guys correct me on this
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8.old woman with DVT. Platelet dropped significantly after a week of tx. Drug of action?
a. activate tissue plasminogen -----action of tPA
b. Interferes with carboxylation of coag factors ----action of warfarin
c. irreversibly inactivate COX -----Aspirin
d. Potentiates the action of antithrombin iii (correct answer, action of Heparin, and this is Heparin induced Thrombocytopenia HIT)
e. selectively inhibits factor Xa (Heparin does thrombin factor 2 and factor Xa)
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14.ER doctor successfully delivered a baby, womanis now having severe bleeding. Pelvic exam shows an ope cervix and heavy vaginal bleeding. Ligation of a branch of which of the following arteries is most appropriate?
a. external iliac (gives femoral and inferior epigastric artery)
b. internal iliac ( Correct answer I think, bcz Uterine artery is a branch of internal iliac artery)
c. internal pudendal (supplies the external structure, but also a branch of internal iliac)
d. median sacral (supply coccyx)
e. Obturator (gives blood supply to the leg obturator muscles)
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16. A patient cries ad says it's a bad news, isn't it?! when a doc is about to tell him the progression of carcinoma to the terminal phase. Most appropriate response?
a. How have you been since the last time I saw you?
b. lets talk about hte positive aspect first
c. look on the bright side of things
d. tell me how you are feeling
e. there are other people who have it alot worse than you
f. Yes it is
g. you've had several years better off than many others with this disease.

I was debating on A or D. I picked D and it's wrong....is that bcz it didn't end with a question mark? wth
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32. A guy with chrons disease. You give antibiotics and prednisone, he got better in 3 weeks, in addition to resolving the infection, the most likely MOA of this pharmacotherapy is which of the following?
a. antibody binding
b. complement activity
c. mast cell degranulation
e. neutrophil function
f. T-lymphocyte function

I marked e. but it's wrong....so I'm guessing T-lymphocyte fumction F? as to decrease T and B cell couns. However, neutrophil count is increased.
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10. 45 year old lady diagnosed with invasive ductal cell CA breast . she was started on tamoxifen and serum analysis showed decreased conc. of enoxifen the active metabolite of prodrug tamoxifen. Genetic analysis showed homozygous presence of CYP450 2D6*4 alleles. WHich of following best represents the likelihood that this patient sister has same alleles?
1.0% 2. 25% 3. 50% 4. 75% 5 100%
Can anyone solve for this one??? thanks!
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49. Old man with 2 year history of decrased force of his urinary stream and increase frequency. BUN is 55 and Creatinine is 5. Ultrasound of Urinary tract shows bilateral hydronephrosis and dilated ureters. What is the mechanism of this patient's renal failure?
a. Decreased hydrostatic pressure in the glomerular capillary
b. decreased renal plasma flow
c. Increased hydrostatic pressure in Bowman space
d. Precipitation of protein in the renal tubules
e. Precipitation of uric acid in the renal tubules
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4. A 27 yo woman with fever, malaise, abdominal pain, vaginal discharge for 4 days. Pregnancy test is negative, Leukocyte count is up. Bilateral lower quadrant tenderness with rebound and guarding. Pelvic exam shows cervical bilateral adnexal tenderness. Most likely diagnosis?
a. appendicitis
b. bacterial vaginosis
c. Chancroid
d. Diverticulitis
e. Gonorrhea
f. Herpies genitalis
g. Trichomonias

Gonorrhea...I picked chancroid on the exam...because I thought chancroid can have those bubonic thing bilaterally....i guess the answer is gonorrhea?!
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6. A study is designed to evaluate the efficacy of coenzyme Q10 in improving cardiac output in pts with CHF. 60 pts with CHF are recruited for the study. Each subject is assigned by coin toss to one of two groups (standard care or standard care plus coenzyme). Which of the following best describe this study design?
a. case-control
b. case-series
c. Crossover
d. Cross-sectional
e. Historical cohort
f. Randomized clinical-trials

I'm guessing F. is the correct answer bcz by giving q10, you're giving a treatment (intervention) to the study. And the coin toss gives the randomness.

a. Case-control: have 2 groups, one health as the control and one diseased. Trying to evaluate the risk factor. So the example will be: 60 pt with CHF drink more and smoke more. Healthy individuals smoke and drink less. Risk factors are smoking and drinking alcohols.
d. Cross-sectional: snap shot, trying to find out in a population who have CHF. You know the prevalence but not incidence.
e. I don't think it is either retrospective or prospective
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A guy completed amoxillin develop watery-brown stools in the past 24 hours. Clostridium difficile toxin is positive. Pathological finding is most likely to be present?
a. Bacterial Overgrwoth of the colonic surface
b.Flask-shaped ulcers in the colon
c. Giardia trophozoites linning the duodenal mucosa
d. Necrotizing granulomatous inflammation
e. PEsudomembranes of fibrin and inflammatory debris

They want us to pick e. But I have seen many qbank and wiki sources say a). Can someone tell me why not AAAAAAAAAAAAAAA??
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A 1 week old girl screening sho a possible defectin fatty acid oxidation, physical exam shows no abnormality. Which of the following is the most appropriate next step in diagnosis?
a. arterial blood gas analysis
b. measurement of serum acylcarnitine conc.
c. measurement of serum amino acid conc.
d. measurement of serum electrolyte conc.
e. measurement of serum lactic acid conc.
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34. 40 yo woman has a mole on her back that has increased in size during the past 4 mo. PE shows Raise irregular lesion with variegated black-tan pigmentation and ill-defined margins. Examination of tissue from the tissue shows pleomorphic, hyperchromatic cells within clear islands that tend to coalesce and are present at all levels of the epidermis, with extension into the paipillar dermis. What is it?
a. basal cell carcinoma
b. blue nevus
c. cafe au lait spot
d. intradermal nevus
e. lentigo simplex
f. melanoma
g. seborrheic keratosis

I think it is f melanoma

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7. A 42 year farmer has a 7mm red scaly plaque on helical rim of left ear . A photomicrograph of tissue obtained on biopsy of plaque is shown. whats the diagnosis ( Picture was shown)
a. Actinic keratosis b. Basal cell CA c. Keratocanthoma d. Malignant melanoma e. Merkel cell CA

I think it's a. actinic keratosis

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[Adjet]

a 68 yo woman w/ recent onset DM2 & poorly controlled HTN despite HTZ tx. BP 150/96. Serum glucose 130. + Proteinuria. What other med should added?
A. Amlodipine
B. Clonidine
C. Hydralazine
D. Lisinopril (correct)
E. Triamterene

Is this one of those "which med has been shown to decrease mortality" questions, or can someone please explain this to me? Thanks!

Yes: pg 292 in FA 2016 "ACE inhibitors or angiotensin II receptor blockers, β-blockers (except in acute decompensated HF), and spironolactone ↓ mortality. Thiazide or loop diuretics are used mainly for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms and mortality in select patients."

Edit: My bad thought it was HF. For DM2 w/ HTN, ACE inhibitors kill two birds with one stone because they are also renal protective

 

[Peanut01]

42yo F with 1-mo Hx of abdominal pain, after eating fatty meals. BMI 31. PE shows jaundice and tenderness of RUQ. Increase of which liver function?

Can anyone explain why cholesterol synthesis is the answer ?

 

[tjon29]

My guess would be E here. AST:ALT ratio is greater than 1.5 would tend to indicate alcoholic hepatitis --> mallory hyaline. First Aid says this is with "sustained, long-term consumption" so I don't know if 12 beers a day for a week and a half will fit the bill or not but that's my guess.

this was my question... can 10 days really give you alcoholic hepatitis?
i chose alpha1-antitrypsin because i figured maybe that predisposed him to an early onset alcoholic hepatitis?

 

[Transposony]

42yo F with 1-mo Hx of abdominal pain, after eating fatty meals. BMI 31. PE shows jaundice and tenderness of RUQ. Increase of which liver function?

Can anyone explain why cholesterol synthesis is the answer ?

Fat fertile female of forty with s/s/o of Gallstones. Then you have to think about the pathogenesis of cholesterol gallstones.

 

[Transposony]

this was my question... can 10 days really give you alcoholic hepatitis?
i chose alpha1-antitrypsin because i figured maybe that predisposed him to an early onset alcoholic hepatitis?

Tender liver points to hepatitis, jaundice points to cholestatis due to swollen hepatocytes and AST/ALT ratio points to alcohol ----> acute alcoholic hepatitis.

 

[Transposony]

Again a quick Q.

A 6 year old boy who recently emigrated from Russia is brought to the physician by his parents b/c of unstable gait and incoordination for 2 weeks. He has had frequent pale, bulk stools for 4 years and two episodes of bacterial pneumonia and chronic cough since the age of 1 year. He is below 3rd %ile for height and weight. Increased rhonchi are heard over both lungs. Neuro exam shows ataxia, absence of DTR, loss of propioception. Stool analysis shows increased fat concentration. Which of the following vitamin is deficient?

A) Biotin
B) Niacin
C) Vitamin C
D) Vitamin D
E) Vitamin E

Is the answer Vitamin E?

Cystic fibrosis---> Fat malabsorption and fat soluble vitamins with neurological symptoms --> Vit E

 

[Inventor of Post-Its]

6 yo girl brought by her mother bcuz of 4 day hx of round shiny bumps in areas where she has eczema. Mother remembers similar bumps on a playmate 3 wks ago at a pool party. No other sx. Firm, smooth, umbilicated papules 2 to 4 mm in diameter. Which group?
Adeno
Flavi
Herpes
Paramyxo
Pox

Smooth umbilicated papules are classic molluscum.

45 yo m poorl controlled dm type 2, 1 m hx of low grade fever. Hemodialysis for esrd. Tem 37, hr 72, bp 144/92. Has a subclavian catheter. Lungs are clear no murmur. Two of the blood cx gram pos, nonhemolytic, catalase negative cocci in pairs and chains.
Causal organism?
E faecalis
Listeria
Aureus
S epidermidis
S pneumoniae

Cocci: not listeria
Pairs and chains: not either staph
Nonhemolytic: not strep pneumo

Thanks in advance.

Saw this one hadn't been answered and this thread has been a huge help for me so figured I'd add to it.

 

[wickey4083]

and what you suspected was right it surface kappa ( i forgot the exact number but the ratio of kappa and lamda its like 1/2 or 1/3 forgot which one it favors, i think lamdbda (ill redo that part on pathoma he explains it very well) so when you see one of either so out of proportion its its a clonal expansion.
the other thing that makes me think that reasoning is right ( other than me getting it right on the nbme) was that you can get absolute cd3 t cells number or cd20 Bcells
any or cd4:cd8 ratio screwed up in any other scenario like infection (HIV CD4:CD8), dgeorge would have absolute B cell count. Hope what i said makes sense and it wasn't all wrong lol first time post something.

thanks [/QUOTE]
that's how kappa and lambda work
Anti-kappa and anti-lambda detect surface light chain immunoglobulins on normal and neoplastic B-cells in human lymphoid tissue. In normal lymphoid tissue the kappa and lambda cell ratio is approximately 2:1, but values in excess of that ratio indicate monoclonality caused by either a lymphoproliferative disorder or neoplasia such as lymphoma.

 

[Rahas]

According to pathoma, kappa:lambda is normally 3:1.

Monoclonality changes the ratio either to 6:1 or reverses it to 1:3.

 

[wickey4083]

the man who went to africa and comes back with fever, headache, abdominal discomfort, but got all "appropriate vaccinations" before trip...
a- babesiosis - wrong
b- leishmaniasis
c-malaria - was this as simple as malaria? did i take "vaccination" to mean prophylactic therapy when really it didnt'... or did he get another strain of malaria? thanks for input!
d-toxoplasaosis
e- trypanosomiasis
Not sure why. Nothing else fit.

i think it is bc malaria is in the africa, but babes is in the northeastern US

 

[Rahas]

since when does malaria have a vaccine (although I think Bill Gates has made one now, but the efficacy is poor around <50%)

 

[wickey4083]

a 68 yo woman w/ recent onset DM2 & poorly controlled HTN despite HTZ tx. BP 150/96. Serum glucose 130. + Proteinuria. What other med should added?
A. Amlodipine
B. Clonidine
C. Hydralazine
D. Lisinopril (correct)
E. Triamterene

Is this one of those "which med has been shown to decrease mortality" questions, or can someone please explain this to me? Thanks!

bc acei is the best choice for HTN with diabetes, bc it can improve the GFR

 

[wickey4083]

42yo F with 1-mo Hx of abdominal pain, after eating fatty meals. BMI 31. PE shows jaundice and tenderness of RUQ. Increase of which liver function?

Can anyone explain why cholesterol synthesis is the answer ?

bc it makes the chol stone, i think that's why the chol syn increase

 

[wickey4083]

just saw a reason why ascites patients need to use spironolactone:
Diuretics that block aldosterone receptors in the distal convoluted tubule are preferred because of the presence of hyperaldosteronism in patients with cirrhosis. Loop diuretics may be used in combination, but are ineffective when used alone. The initial starting dose of spironolactone is 100 mg once daily and can be titrated up to a maximum of 400 mg once a day. Absorption of spironolactone is improved if administered with food. The diuretic effect can be seen within 48 hours, but the peak onset of action is 2 weeks, due to impaired metabolism in cirrhotic persons and a half-life of up to 5 days.[17] Therefore, the dose should be adjusted only once a week. Side effects include hyperkalemia and painful gynecomastia. Amiloride can be used instead of spironolactone, starting at 5 mg per day. The latter is sometimes preferred because of its shorter half-life and quicker onset of action. However, it is much more expensive than spironolactone and has also been shown to be less effective in a randomized, controlled trial.

 

[SJSTEN]

Guys I'm sorry, can someone please give me advice?
June 02 NBME 16 - 236 (540)
June 05 UWorld SIM1 - 256 (630) <-- Now, if only that meant anything
June 08 NBME 18 - 232 (510)
June 11 NBME 17 - 223 (480)
So. Confidence is pretty destroyed. Have gone systematically downhill over the course of just under two weeks. I don't even know how someone does that...
Was really hoping to get my score up into the high 230s or 240
I'm scheduled to take STEP1 next Monday. Not able to delay it more than 2-3 days, tops.
What do I do?

 

[Notetoself1609]

All of the answers are in bold. These are 100% verified because I got them correct on my exam.

What makes it not an adrenal carcinoma decreasing Aldo production? Also, why is the serum Na low? Is it from dilution? ACTH secretion from a tumor would result in increased aldo = increased Na, so I'm confused as to how you can distinguish.

 

[AlteredScale]

What makes it not an adrenal carcinoma decreasing Aldo production? Also, why is the serum Na low? Is it from dilution? ACTH secretion from a tumor would result in increased aldo = increased Na, so I'm confused as to how you can distinguish.

There were other details that weren't mentioned in the quote you had besides the lab values. The patient also had hx of weight loss. That in itself should point you towards considering malignancy in your differential. Small cell carcinoma of the lung have the ability of producing ACTH OR ADH. So you're right in that if it was producing ACTH that it would show increased Na. But it would also present with hyper pigmentation as well as other sx of hyperaldosteronism and hypercortisolism.

This patient had a urine osmolality that was very high as well as a serum Na that was low meaning something was affecting the renal function to negate diuresis which most likely in this case was ADH.

 

[tndlkar]

bc acei is the best choice for HTN with diabetes, bc it can improve the GFR

I believe that ACE inhibitors actually decrease GFR initially (ATII constricts efferent arteriole -> inhibition leads to efferent dilation -> lower FF and GFR). It is used to prevent diabetic nephropathy because it decreases microalbuminuria, glomerular damage from overfiltration and pathological remodeling of the podocyte slit diaphragms preventing future worsening of albuminuria (this last one isn't tested on step; kind of like how B-blockers prevent pathologic remodeling of heart post-MI).

 

[2015istheYear]

Sounds like hypocalcemia to me.

Answer choices?



Macrophages. Langerhans are cutaneous dendritic cells.

Tuberculous lesions = granulomas. Granulomas = CD4/Macrophages.

So I get where you got this from, but it's not correct. See below:


Langhans giant cells (LGC) are large cells found in ALL granulomatous conditions (Step referecnes them most in sarcoidosis & TB). NOT TO BE CONFUSED with Langerhans giant cells, which as you said are DCs.

LGC are formed by fusion of epithelioid cells (Macs):

AIDS pt w/TB w/ no activated Th cells cannot produce LGCs bc they require Th cells & monocytes to come into close contact causing interaction of CD40-CD40L and this causes IFNg secretion by Tcells which causes upreg & secretion of fusion-related molecules (DC-STAMP - dendritic cell-specific transmembrane protein) by the monocytes, which results in LGC formation. A healthy person would have Langhans giant cell formation in their granulomas but the AIDS pt just has regular Macrophages in theirs.

 

[2015istheYear]

This one was weird. I picked 25% and got it right.

They didn't give any info for the parents so I just figured there are 4 possibilities for the sisters genotype, AA, Aa, aA, and aa. Both parents must have at least one recessive allele and AR disorders are most often rare so I figured both parents were heterozygous.

#1 CYP450 mutations are pretty much always associated with being autosomal recessive disorders.
So if you look at the Punnet square, the parents MUST be heterozygotes to produce a homozygote in an AR Dz:

 

[Peach Newport]

Bump

Question:
They have two groups of people with fibromyalgia. They give one group lidocaine injections into the triggerpoints and one group saline injections into the triggerpoints. Both groups report similar pain relief. Why is this?

I was stuck between the answer choices “placebo effect” and “uncontrolled confounding.” I chose uncontrolled confounding because you’re still sticking a needle into trigger points and injecting a substance that takes up space. There is evidence, after all, that acupuncture relieves pain. It seems like the definition of a potential confounder - maybe the pain relieving effect was mostly due to the needle and/or the mass effect of fluid injection, and not necessarily the effect of the lidocaine.

But of course the answer was placebo effect

Why am I wrong

 

[Murrish]

Have tried to find an explanation but cant seem to find one about the MLF question. I got it right but was a 50/50

The picture was of PONS. I know the ipsilateral MLF is damaged relative to the affected eye. My understanding is that MLF goes from PONS CN6 to contralateral CN3 in Midbrain. So isn't that mentioned MLF going to be on contralateral side(relative to eye damaged) in Pons and end on ipsilateral side in midbrain?
The only way answer C makes sense if the crossing of MLF happens before entering Midbrain. Am I missing something?
Thx in advance I am so confused rn.

 

[GodBlessMeToBecomeMD]

Did anyone think this was easier than previous NBMEs? I did much better on this than previous ones.

yes, definitely, i did only NBME 16 and couple UWORLD Self Assesments, this one- the easiest)

 

[GodBlessMeToBecomeMD]

hi. I was just thinking, if the disease has to be coded in allele #1, it can explain all of the sick cases. BUT if its AD, as you said, 1.2(alleles 1,3 inherited) has to be affected as well, but he's healthy..., it means, the mode of inheritance has to be X-linked recessive, that's why 1.2 is healthy(she is Xx or 3.1) and the right answer is 2.3, because both this alleles don't pass the disease,

 

[Ethylsuxonmine]

Ahhh I went down 11 points on NBME 17 from 16. I went from high 230s, to high 220s. I blanked on so many potentially easy things. Anyways here are most of them. Any help would be appreciated as I take the exam in less than a week
Guy lifting weights suddenly experiences painful swelling right inguinal area. Picture of resected part of small intestine. Dx?

1. adhesions
2. emboli
3. intussusception (this i think)
4. strangulation
5. volvulus

55 y/o man with sepsis gets confused and anxious. Treated with vanco/ceftriaxone. Temp 104, BP 84/50. Warm flushed skin. Give what solution?

1. dextrose in water only w/ saline
2. dextrose in water only
3. 0.45% saline
4. 0.9% saline (pretty sure answer is just regular saline)
5. 3% saline (not this)

Woman on triiodothyroxine for her hypothyroidism develops tremors and fatigue. She doubles her dose because of the fatigue. What do we expect on thyroid function test?
I said “decrease TSH, Increase free thyroxine, increase free T3”. I assume I was wrong about the free thyroxine? Does free thyroxine decrease because of something to do with thyroid binding globulin?

Man w/ generalized tonic clonic seizures. He has pins and needles in mouth, hands, feet. Involuntary contractions of muscles. Hyperflexia. Abnormality of what serum ion?

1. bicarb
2. calcium
3. chloride (i picked)
4. potassium
5. sodium

I am drawing a complete blank on this and can't find it in first aid. I know I did this in UW.

woman w/ metastatic breast cancer has gradual onset decreased muscle contractions in left hand and left leg. Strength, DTR, sensation, proprioception normal. Where is metastatic tumor found on the left side?

1. cerebellum
2. cerebrum
3. cervical spinal cord (I think its this. I missed the "left side" at the end of the question)
4. lumbar spinal cord
5. thoracic spinal cord

Underweight baby born w/ petechia rash, microcephaly, and hepatosplenomegaly. Serology of mom shows CMG IgG (+) and CMV IgM (-). Infant serology CMV IgG (+)/IgM (+). Explanation?

1. active transfer maternal Ab
2. congenital CMV infection (I think its this but why on earth is infant IgM (+) for CMV. IgM cant cross placenta)
3. False negative maternal serology
4. False positive infant serology (I picked this thinking the IgM + was a mistake. How can a neonate produce IgM on its own?!)
5. Passive transfer IgM and IgG to infant

Craniopharyngioma derived from? Is the answer “diverticulum of root of embryonic oral cavity?” Another easy question ahh

Woman who’s 18 weeks pregnant gets hyperthroidism. What lab value confirms hyperthyroidism?

1. free T4
2. Radioactive iodiine uptake
3. serum total T3

^I read this wrong and thought it was autoimmune so picked antibody answer

Broken mandible. What additional structure injured?

1. inferior alveolar nerve
2. levator labii superioris
3. maxillary artery
4. parotid gland (picked this thinking jaw went backwards and damaged it)
5. tongue (im guessing tongue?)

14 y/0 boy brought in by mom for bilateral headaches aching in his temples. Hes not been himself lately. He is clumsy, has broad based ataxic gait. Slow to answering questions. Whats he abusing?

1. cocaine
2. ethanol (my choice. I realize now theres no way a 14 y/o would get B1 deficiency)
3. inhaled glue (is this the answer?)
4. methamphetamine
5. PCP

Inhaled glue/gasoline --> TOLUENE TOXICITY
- AMS (confusion, forgetfulness)
- Rhabdomyolysis (broad-based gait)
- Temporal lobe epilepsy (bilateral temporal HA)
- Type 1 RTA (hyperchloremic, hypokalemic, normal anion-gap)

previously healthy 35 y/o has one year history of depression, impulsiveness, and difficult. Grimaces intermittently and has rigid jerking purposeless movements. What historical factor relevant to diagnosis?

1. dietary insufficiency
2. exposure environmental toxins (thought it was lead poisoning. Nope)
3. family hx
4. pet w/ unexplained illness
5. tick bite
6. travel

55 y/o woman 6 week history of low energy, irritability, and crying spells. She has difficulty sleeping. Taking lorazepam for GAD for 15 years. Had postmenopausal sx for 1 year treated with estrogen therapy. Constricted affect. She feels testy and speech is slowed. Cause?

1. estrogen toxicity
2. GAD
3. lorazepam toxicity
4. MDD
5. menopause

3 y/o with sickle cell has fever and increased foot pain for 3 weeks. Hematocrit stable. Increased leukocytes with prominence of neutrophils.

Osteomyeltiis or avascular necrosis? Another easy question ahh. I think its osteomyelitis.

20 weeks gestational pregnancy. Increased fundal height. Increases amniotic fluid. Cause?

1. cleft lip
2. encephalocele (i picked. wrong)
3. renal agenesis
4. tracheoesophageal atresia (i think this is the answer)

constipated old man. Distended abdomen. What nerve not working?

1. interior rectal
2. pelvic splanchnic
3. perineal (my choice. wrong)
4. sacral sympathetic

 

[Patchface]

1. The stomach is where the left lung should be, compressing the esophagus. The tube is in the stomach, but the stomach is in the left chest, compressing the mediastinum to the right.

2. Cocaine+widened mediastinum+diminished pulses in the left upper extremities=dissection.
3. Sulfasalazine is used to treat colonic Crohns as well as UC. As far as I remember the other ulcer treating drugs were for peptic ulcers (bismuth or whatever isn't going to do anything in the colon for example)
4. Old people don't always get fevers when septic. Sepsis is high output cardiac failure- fluids won't be as helpful bc of the capillary leak- all the fluid is getting out of the vasculature and not exerting a pressure.
5. I thought this was a stupid question. So her parents are either both homozygotes, both heterozygotes, or one heterozygote, one homozygote for the 3d64 allele. I think you have to assume that the allele is uncommon or else tamoxifen wouldn't be as useful. So fitting with this reasonable assumption, say her parents are both heterozygotes and this gets you to the correct answer. Somebody please correct me if there is some better logic for this!

I'm still confused here. The calculation would be simple if it were just asking about a random sister. But the sister in the problem already has the same kind of breast cancer, so it's asking for a probability given that she has the same problem. Since it needs both alleles, then it should be 100% probability that she has the same alleles. No?

6. First off LDL receptor deficiencies are much more common. Second (not 100% confident) B100 is involved with LDL and VLDL, but the stem states it is a specific increase in LDL. So the answer is A. Most LDL is actually taken up by the liver (I think around 70%) for storage. Most cholesterol meds (including statins) MOA is ultimately aimed at increasing LDL receptor density in the liver.