INCORRECT Flashcards

1
Q

92 year old woman comes with progressive dementia and large purpuric lesions. The patient seems well cared for, and the family states that SHE HAS HAD THESE LESIONS ON AND OFF FOR YEARS NOW AND OCCUR IN THE ABSENCE OF ANY TRAUMA. What can be the explanation for the purpuric lesions?

A) Abuse by a family member
B) Atrophy of dermal collagen.

A

A) Abuse by a family member—> you did this, it could be the answer. They haven’t provided with anything against it but the patient seems to be well cared for.

B) Atrophy of dermal collagen- CORRECT.
This is called actinic purpura–> The cause is aging skin has reduced collagen fibrils leading to INCREASED skin fragility)
Aging skin means less collagen fibrils synthesis when the cross-linking function is STILL normal.

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2
Q

A 46 year old man comes with left atrial dilatation, the left ventricle is normal. This 46-y old man has orthopnea, dyspnea and a midsystolic murmur best heard at the cardiac apex. What is the most likely cause of these findings?

A) Mitral Stenosis
B) Mitral Regurgitation

A

This is an example of how they used our knee-jerk response.

A) Mitral Stenosis–> seems correct, and the knee-jerk response when we see Left atrial dilatation. But the murmur is systolic and MS has diastolic rumbling murmur!
B) Mitral Regurgitation- CORRECT.
(MR–>Systolic/Holosystolic murmur best heard at cardiac apex, radiates to axilla)

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3
Q

Aspirin’s:
pKa (6.0/10.0)
protein binding in plasma (20%/98%)
Volume of distribution ( 1/10)

A

pKa-6.0
protein binding in plasma-20%
Volume of distribution-1

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4
Q

Treatment of psoriasis should be done with which of the following?

A) Cyclophosphamide
B) Methotrexate
C) Tretinoin cream
D) Tetracycline

A

METHOTREXATE

(Other options for psoriasis that are not included in the options are cyclosporine, adalimumab/infliximumab (soluble TNF-α), Ixekizumab/ secukinumab ( used for psoriatic arthritis treatment as well, it’s IL-17A), Ustekinumab (IL-12/IL-23 Psoriasis, psoriatic arthritis)

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5
Q

You just gotta learn some things as it is:
PCWP=
LVEDP=

A

PCWP is a measure of Left Atrial Pressue i.e. LAP and its range is 4-12 mm Hg.

LVEDP= 10

(In Mitral Stenosis, PCWP is greater than LVEDP)

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6
Q

For cardiogenic shock, remember 3 things

A

Cold, clammy extremities with increased PCWP, and obviously because heart is not working so CO is decreased.

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7
Q

For cardiogenic shock, how will the following values change:

  1. Capillary Hydrostatic Pressure ( ↑, ↓)
  2. Interstitial Hydrostatic Pressure ( ↑, ↓)
  3. Interstitial Oncotic Pressure ( ↑, ↓)
A
  1. Capillary Hydrostatic Pressure ↑- Because as heart is unable to pump, the fluid accumulates in capillaries.
  2. Interstitial Hydrostatic Pressure ↑- This accumulation in capillaries causes water to be pushed into the interstitium, and hence the hydrostatic pressure in interstitium is increased as well.
  3. Interstitial Oncotic Pressure ↓- As interstitium dilutes because of all the plasma coming in, the oncotic pressure decreases.
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8
Q

A boy has a palpable mass in the ventral midline of the neck just inferior to hyoid bone. What is the mass called and what is it embryological origin?

A

It is a thyroglossal duct cyst.
The answer for its embryological origin was–> endoderm of foramen cecum but basically thyroglossal duct cyst’s remnant is foramen cecum of tongue!!

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9
Q

13 year old girl is on immunosuppressants after renal transplant. Examination of LN tissue biopsy shows a monomorphous population of B lymphocytes. Which of the following pathogen is the cause of this findings?

A) CMV
B) EBV

A

A) CMV
B) EBV- CORRECT. (Because is says MONOMORPHOUS POPULATION OF B-lymphocytes)–> lymphoproliferative disease in transplant patients.

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10
Q

BLUNDER BLUNDER BLUNDER.
For hereditary spherocytosis, genetic testing would like to show which one out of the following?

A) Heterozygous Mutation in the ankyrin gene.
B) Homozygous Mutation in the ankyrin gene.

A

Heterozygous Mutation in the ankyrin gene—> BECAUSE THIS IS AN AUTOSOMMAL DOMINANT DISEASE AND YOU DIDN’T KNOWWWW.

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11
Q

An 18 year old woman gets a colectomy done because of FAP. What are the chances of her offspring will develop colorectal adenocarcinoma?

A

50%—-> Autosommal dominant disease

FAP—> 100% chance of getting colorectal carcinoma, and it is an AD disease to there’s a 50% chance of her offspring having FAP.

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12
Q

The patient asks the physician for a sufficient quantity of medication to allow her to commit suicide. The physician refuses to do so and informs the patient that he will do everything he can to manage her pain. The physician’s decision in this situation most consistent with which principal?

A

Non-maleficence.

And you did beneficence–??? YOU CRAZY WOMAN

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13
Q

What does insulin stimulate? And also tell enzymes.

A

It stimulates:
1. Glycogenesis–> Make glycogen!! via Glycogen synthase, protein phosphatase.
2. Fatty Acid Synthesis—> Acetyl CoA carboxylase (asked in NBME 20)
3. Cholesterol Synthesis—> HMG-CoA reductaste
(This is why, insulin resistance is associated with Hypertriglyceridemia/ Type 4 hyperchlosterolemia—-> insulin ziaada hoti hai inn logon mein tou Triglycerides bhee ziaada bantay hein, the pathogenesis can also be called Hepatic overproduction of VLDL.)
4. Production of Glucose-6-phosphate–> insulin stimulates Glucokinase in liver to convert Glucose into G-6-P.
5. MORE Glycolysis, and LESS Gluconeogenesis—–> because in Fed state—-> ↑ Insulin—> this causes to become lazyyyy, and so ↓cAMP—>↓ protein Kinase A—> ↓ FBPase-2—-> ↑ PFK—> More glycolysis.
(Khaanay kay baad we says P-FUCKK, so that’s increased and the rest is decreased)

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14
Q

Which hormones cause insulin resistance?

A

> Sirolymus/Rapamycin—-> causes insulin resistance–> S/E inlude Diabetes.
Growth Hormone–> Acromegaly has diabetes.
Cortisol–> Cushing Syndrome.

(Insulin resistance ki waja sey inn dono conditions mein hyperglycemia hota hai, and too reduce insulin in these people we give somatostatin/octeotride.

> Human Placental Lactogen causes insulin resistance and if the insulin produced by the mother is not enough to overcome it then the mother gets GESTATIONAL DIABETES—-> asked in uworld)

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15
Q

Receptors and insulin release?

A

Insulin itself is a GF. The receptor it works on is a receptor tyrosine kinase with intracellular domain–> can cause transition of cell from G1 to S.
Alpha 2—-> decrease insulin release.
(Alpha is dominating, so yeah)
M3, Beta-2—-> INCREASE insulin release.
(Beta blockers avoided in diabetics!!!)

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16
Q

Insulin and ions?

A

Insulin causes hypokalemia and hypernatremia.
Hypokalemia—> Pushes K into cells (Hence, in DKA we also give K with Insulin), and also stimulates Na+/K+ ATPase pump which takes in 2K, and gives out 3Na.

Hypernatremia—> causes Na-retention.

17
Q

Insulin Resistance associated with?

A

Acromegaly
Cushing syndrome
Non alcoholic fatty liver disease—-> associated with insulin resistance—–> ALT>AST
(Remember ALT for lipidsss extraa)
Acanthosis nigracans.
PCOS–> There’s increased insulin because to release extra FH:LSH, there’s increased ACTH–> that causes increased cortisol—> increased cortisol causes Increased insulin release.

18
Q

Neonatal ARDS and Insulin?

A

Insulin promotes Neonatal Acute respiratory syndrome.

In these kids, there’s increased insulin because the mother was diabetic and the fetus was exposed to hyperglycemia.

19
Q

There’s DECREASED insulin in which tumor? What is the treatment of that tumor?

A

Somatostatinoma has DECREASED Insulin, and decreased cholecystokinin.
(Decreased insulin causes it to manifest as diabetes, decreased cholecystokinin causes it to manifest as steatorrhea)

The peculiar thing is, we give somatostatin in somatostatinoma for treatment!

20
Q

The cause of increased insulin in oral glucose intake, but not when glucose is give IV?

A

Oral glucose causes an INCREASE in Insulin because of the hormone GIP released by K-cells of Duodenum and Jejenum.
( Dj-k is a GIP)

21
Q

Insulinoma stains positive for?

A
It is a neuroendrocrine tumour just like the following:
Pheochromocytome
Small Cell Lung Cancer
Carcinoid
Gastrinoma
Medullary Thyroid carcinoma.

All of the above share a common property of Chromogranin amine precursor uptake decarboxylase (APUD)—> (eg, chromogranin A, neuron-specific
enolase [NSE], synaptophysin, serotonin, histamine, calcitonin).
Treatment: surgical resection,
somatostatin analogs.

22
Q

Not in NBME, but methotrexate is high-yield.

Mechanism of Action of Methotrexate, and conditions in which it used as a treatment?

A

It is a dihydrofolate reductase inhibitor so it DECREASES [dTMP] in cells!–> Affects the DNA synthesis/ S-phase!

Used in the treatment of:
leukemias(ALL), 
lymphomas,
choriocarcinoma, 
sarcomas.
Non-neoplastic: ectopic
pregnancy, Hydatiform mole, medical abortion (with misoprostol), rheumatoid arthritis, psoriasis (you didn't know this), IBD, vasculitis.
23
Q

S/E of methotrexate

A

> Causes neural tube defects as a teratogen.
Causes pulmonary fibrosis/Restrictive lung disease.
Bonemarrow myelosupression—-> can be reversed by giving LEUCOVORIN/FOLINIC ACID.
(In uworld it was asked, what should be given with methotrexate?, what treats methotrexate overdose?)
It is a weak acid just like aspirin, so methotrexate overdose can also be treated with alkanization of urine.
Causes megaloblastic anemia due to FOLATE/ Vitamin B9 deficiency which will show labs of ↑ homocysteine, normal methylmalonic acid. No neurologic symptoms (vs B12 deficiency)–> Learn by you can come late at home. so folate deficiency means increased homocysteine.

24
Q

An 18 year old woman, comes to the physician because she has never had menstruation. Physical examination shows a 10com invagination where the vagina would normally be present. No uterus is palpable on rectal examination. Labs show INCREASED FSH, Normal testosterone in the range of females, and normal estradiol.
Which of the following structure is normal in the patient?

A) Testis
B) Ovaries

A

Ovaries.
This is mullerian agenesis. Normal ovaries but absent uterus. Because ovaries are working, females with fully developed 2° sexual characteristics (hair).

You did testis—> because you were thinking this is androgen insenstivity syndrome. In which, a normal appearing woman is basically of the genotype 46 XY. uterus and fallopian tubes absent due to persistence of anti-Müllerian hormone from testes. BUT TESTIS ARE FOUND IN LABIA MAJORA, AND INCREASED TESTOSTERONE AND ESTRADIOL. NO AXILLARY/PUBIC HAIR!!–> because bhaee, receptors hee insenstive hein!

25
Q

Newborn male shows decreased levels of Blood T3 and T4. However, has a normal TSH and free T4. What is this?

A

TBG Deficiency.

Normal, free. okay?

26
Q

What do you know about 3 conditions of hypothyroidism:
Primary Hypothyroidism
Pseudohypoparathyroidism type 1A
Pseudopseudohypoparathyroidism

A

Primary Hypothyroidism–> LOW PTH–> so hypocalcemia, hyperphosphatemia.
Pseudohypoparathyroidism type 1A–> AD, GNAS mutation—> resistance to PTH. So HIGH PTH–> hypocalcemia, hyperphosphatemia.
Pseudopseudohypoparathyroidism–> paternal mutation—> Sab normal hota hai labs mein, normal maternal allele maintaining renal responsiveness to PTH

27
Q

Empty sella syndrome is associated with idiopathic ____________.

A

Idiopathic intracranial Hypertension.

28
Q

MEN2A and 2B common?

A

2 things common:
>Medullary Thyroid carcinoma
>Pheochromocytoma
(Pheo pheo 2)

29
Q

Which MEN syndrome has neuromas?

A

MEN 2B–> Bee bee nuisance!!

30
Q

Mechanism of action of non-insulin injectables:

A
  1. Pram-lintide—> Amylin analog–> DECREASE glucagon release.
  2. Exanatide, Liraglutide (GLP-1 analogs—-> exactly same as Amylin, but these also INCREASE glucose-dependant insulin release. S/E includes pancreatitis.
31
Q

What test should be done before prescribing metformin?

A

Serum Creatinine.
Causes lactic acidosis—> (use with caution in
renal insufficiency)

32
Q

Mechanism of action of Metformin?|

High yield

A
  1. Stimulate AMPK (not written in FA, copied from uworld)
    2.inhibit mitochondrial gluconeogenesis by inhibiting mGPD.
    ↓ hepatic glucose production & ↑ peripheral glucose uptake
33
Q

What occurs physiologically in aging?
A) Increase cardiac muscle mass
B) Increase in systolic blood pressure.
C) Increase in compliance of arteries.

A

Increase in systolic blood pressure

34
Q

What will a person, with Hb 18.5 and normal peripheral blood smear likely have?

A) Hypersplenism
B) COPD
C) Myelodysplastic syndrome

A

COPD—> COPD causes REACTIVE polycythemia–> obstructive lung disease causes a reduced Sao2, so increased EPO causes increased Hb.

Hypersplenism–> overreactive spleen eats up so many cells—> pancytopenia–> occurs in Hep C, alcoholic and non-alcoholic liver disease.

Myelodysplastic syndrome—>defects in cell maturation of nonlymphoid lineages, peripheral blood smear will show eye-mask shaped nuclei in neutrophils, or basophilling stipping (sideroblastic anemia occurs in myelodysplastic syndrome)

35
Q

A woman with flu-like illness, and then heart issues (exercise tolerance, SOB) is infected by which of the following?

A) Adenovirus
B) Herpesvirus
C) Picornavirus.

A

PICORNAVIRUS (Basically, she got coxsackie virus.)

picornavirus include: (PERCH)--->non-enveloped single stranded positive linear!
Polio
Echo
Rhino
Coxsackie
Hav
36
Q

A woman with cough comes to you, and you prescribe her amoxicillin, the symptoms don’t get better. Her cold agglutinin test is positive. The medicine didn’t work on her because?

A

penicillin ineffective since Mycoplasma has no cell wall.

The exact answer was: Lack of peptidoglycan.

37
Q

31 year old man, has large yellow soft mass deeply infilterating the gluteus? What is it called?
A) Lipoma
B) Liposarcoma

A

Liposarcoma.

38
Q

Girl comes to you with:

  • CBFA1 mutation
  • retained deciduous teeth
  • Can places shoulders anteriorely together
  • X ray shows open sutures and wormian bones.
  • Low ALP activity.

Which cells are dysfunction?

A

All they wanted you to know, was the OSTEOBLASTS FUNCTION is reflected by ALP levels.