INCORRECT Flashcards
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) 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.
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
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)
Aspirin’s:
pKa (6.0/10.0)
protein binding in plasma (20%/98%)
Volume of distribution ( 1/10)
pKa-6.0
protein binding in plasma-20%
Volume of distribution-1
Treatment of psoriasis should be done with which of the following?
A) Cyclophosphamide
B) Methotrexate
C) Tretinoin cream
D) Tetracycline
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)
You just gotta learn some things as it is:
PCWP=
LVEDP=
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)
For cardiogenic shock, remember 3 things
Cold, clammy extremities with increased PCWP, and obviously because heart is not working so CO is decreased.
For cardiogenic shock, how will the following values change:
- Capillary Hydrostatic Pressure ( ↑, ↓)
- Interstitial Hydrostatic Pressure ( ↑, ↓)
- Interstitial Oncotic Pressure ( ↑, ↓)
- Capillary Hydrostatic Pressure ↑- Because as heart is unable to pump, the fluid accumulates in capillaries.
- 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.
- Interstitial Oncotic Pressure ↓- As interstitium dilutes because of all the plasma coming in, the oncotic pressure decreases.
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?
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!!
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) CMV
B) EBV- CORRECT. (Because is says MONOMORPHOUS POPULATION OF B-lymphocytes)–> lymphoproliferative disease in transplant patients.
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.
Heterozygous Mutation in the ankyrin gene—> BECAUSE THIS IS AN AUTOSOMMAL DOMINANT DISEASE AND YOU DIDN’T KNOWWWW.
An 18 year old woman gets a colectomy done because of FAP. What are the chances of her offspring will develop colorectal adenocarcinoma?
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.
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?
Non-maleficence.
And you did beneficence–??? YOU CRAZY WOMAN
What does insulin stimulate? And also tell enzymes.
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)
Which hormones cause insulin resistance?
> 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)
Receptors and insulin release?
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!!!)