High-yield youtube guy videos

Question 1

Aortic Co-arctation
Infant–> Preductal (Bicuspid aortic valve in Turner’s–> Aortic Coarctation, William’s syndrome–> Overly friendly, elfine faces, Chromosome 7 mutation–> Aortic coarctation is preductal/ Also called supravalvular aortic stenosis)

Adults—> Postductal co-arctation of aorta. (Fibrosis of ductus arteriosus making the aortic lumen small)

How will aortic coarctation manifest as?

Answer 1

1. In kids, there will be exercise intolerance of some sort, limb pain after some playing, rib notches because of formation of collateral circulation.
   Harsh systolic murmur as LSB.
   In neonates, GIVE PGE1 analog(alprostadil) —> that will decrease vascular tone—> Keeps ductus arteriosus OPEN.
2. In adult, or acquired coarctation of aorta.
   HTN in upper limbs, DECREASED BP in lower limbs. This leads to intermittent claudication (person complains of pain after some walking because of lack of blood supply to the legs).
   Bounding pulses in upper extremities as well as carotids, decreased femoral pulses.
   Left Ventricular Hypertrophy—-> Left Axis deviation/ Tall R waves in V5,6 on ECG.

Question 2

Urine darkens upon exposure?

Answer 2

Alkaptonuria.

Homogentisic acid oxidase is deficient.

Question 3

Empiric treatments for meningitis in neonates, adults (20-50), elderly (more than 50 years of age)?

Answer 3

Empiric treatment means starting the treatment before the test results come out:
–>Neonates : Ampicillin (for listeria), Cefotaxime (better than ceftriaxone, hence this is used in neonates, Vancomycin( for GBS)
Remember, vancomycin has activity against Strep and Staph.
Remember, E.COLI is a common cause of meningitis in neonates and this can be tested!

Adults: (Due to strep pneumo, Neisseria)—> Ceftriaxone (for Neisseria), Vancomycin, Dexamethasone (Dexa is shown to have activity against Strep Pneumo only—> Once, the test results come out and say that it is not strep pneumo–> we STOP dexa)

Elderly: Ampicillin (Listeria), Ceftriaxone (for Neisseria), vancomycin (staph and strep), Dexamethasone.

Rule of thumb is:
>Add ampicillin for Listeria in neonates and elderly. In case, they are allergic to ampicillin—> give Bacteram, TMP-SMX.
> Vancomycin is added for Strep pneumo in adults, elderly but in neonates it is added for GBS.
> Neisseria doesn’t cause meningitis and neonates!! and it causes meningitis in adults and elderly—> Hence, we add ceftriaxone only in adults and elderly,
> Dexa is added for Strep pneumo and that only occurs in adults, elderly.

Question 4

Which drug will you give for prophylaxis of Neisseria meningitides in a woman who is pregnant?

Answer 4

In a normal person, we give Rifampin for prophylaxis of Neisseria Meningitides.
(MOA—> Inhibits DNA-dependant RNA polymerase)

In a pregnant, woman we cannot give rifampin for prophylaxis so we will give CEFTRIAXONE.
(MOA–> Binding to PBP)

Question 5

Lumbar Puncture findings key points?

Answer 5

So remember:
1. For VIRAL meningitis, no organisms will be visualized under the microscope–> Hence, called ASEPTIC MENINGITIS.
2. If LP shows a leukocyte count greater than 1000, it is BACTERIAL MENINGITIS.
3. If LP shows, leukocytes less than 1000–> The cause is VIRAL OR FUNGAL. For fungal, the protein is greater than 200. In Viral, protein is less than 200.
(Virus is so small, so protein bhee 200 sey kam hoga)
4. If Glucose levels are in single digit, that is less than 10—-> TB,
5. Sometimes, they give LP findings for a question related to GBS–> In GBS, the only abnormal finding on LP is INCREASED PROTEIN. (Normal LP proteins should be less than 45)

Question 6

Xanthochromia on LP?

Answer 6

Scenario can tell a person with ADPKD–> Berry Aneurysms—> Berry aneurysms cause SAH—> If nothing seen on CT scan( Ideally, SAH is visible on CT in the first 24 hours only)—> LP done and it shows XANTHOCHROMIA.

Blood is seen on LP—> IN meningitis caused by HSV-2.
(HS1—> causes ENCEPHALITIS—> B/L temporal lobe hmg/necrosis—> PERSONALITY CHANGES.)

Question 7

Cryptococcus neoformans causing meningitis characteristics?

Answer 7

• Narrow-based budding. (Sometimes the only clue they give is this, and we can’t figure it out because we only know that blastomycosis has broad-based budding.)
• Urease positive. (Sometimes this is the only hint they give in this stem.)
• India Ink stain (THICK unstained/clear capsule, mucicarmine staining.
• AGRRESSIVE TREATMENT (Amphotericin B and Flucytosine acutely and then shifted to FLUCONAZOLE—> MOA can be asked?
  Amphotericin B—> Binds to ergosterol (asked) and makes pores/holes n cell membranes. Causes HYPOKALEMIA AND HYPOMAGNESIMIA so supplementation with K and Mg is necessary. (asked)
  Flucytosine–> In the body, cytosine deaminase converts it to 5-FU.

MOA of fluconazole—> Azoles inhibit ergosterol synthesis by inhibiting the CYP-450 enzyme ( 14–α–demethylase) that makes ergosterol from lanosterol.

Question 8

Which antifungal drug affects production of lanosterol?

Answer 8

Terbinafine—> It inhibits Squalene epoxidase, which converts squalene into squalene epoxide.

Question 9

Which systemic fungal pathogen has a doubly refractile wall?

Answer 9

Blastomycosis dermatitis—-> famous for BROAD-BASED BUDDING.

Question 10

CN10 vs CN12?

Answer 10

CN10 and CN12 both in Medulla.
But CN10 is in Lateral Medulla–> As, 10 cannot be divided into 12 into an even number!–> so Blood supply is PICA/vertebral artery.
And CN12—> is in Medial Medulla–> ASA.

CN10 palsy—> Loss of Gag reflex, uvula deviated AWAY from the lesion

CN12 palsy—> Tongue deviates TOWARDS the lesion.
(TOVELVE–> Towards)

Question 11

CN1 fact?

Answer 11

Only nerve that doesn’t have thalamic relay.

Question 12

Dysphagia, hoarseness seen in which artery stroke?

Answer 12

PICA/vertebral.

Question 13

Intractable vomiting?

Answer 13

Area postrema in MEDULLA.

Mejhoola–> Uncrontrollable vomiting

Question 14

Cause of vertical gaze palsy in a pinealoma?

Answer 14

Pineoloma is just above the dorsal midbrain. It compresses the SUPERIOR COLLICULUS which is reponsible for vertical gaze.

Question 15

Cushing’s triad?

Answer 15

So respiratory centre in the brainstem is damaged and there is decreased respiration—-> this causes RETENTION OF CO2—> increased CO2 in blood causes vasodilation in the brain—->vasodilation means more blood in the vessels which means Increased ICP—> CPP is MAP-ICP, CPP is cerebral perfusion pressure—> So in increased ICP we need to maintain CPP, and to do this we increase MAP—> This leads to systolic HTN—> To compensate increased SBP, the HR decreases.

Reduced respiration, Systolic HTN, Decreased HR.

Question 16

CN3 palsy due in tumour compression vs in diabetes?

Answer 16

CN III neuropathy can occur due to nerve compression and causes include transtentorial (uncal) herniation, neoplasms, and aneurysms of the posterior cerebral and posterior communicating artery (asked, asked, asked)—> CN3 neuropathy due to compression presents with loss of accommodation and dilated pupil because the P-ANS fibers making a net around the nerve are damaged first and don’t supply to sphincter pupillae anymore.

In CN3 palsy due to nerve ischemia, such as that in Diabetes—> Pupil is normal.

Question 17

Chiari malformation and Dandy walker malformations–> Manifestation and association?

Answer 17

Chiari I—> Cerebellar tonsil herniates–> Will present in an ADULT with cerebellar ataxia.
Can rarely present with horner’s syndrome too.
Associated with Syringomyelia( spinothalamic tracts affected–> cape like pain and temp defecit), Ehlor-Danlos and Marfan Syndrome.

Chiari II—> Cerebellar vermis and tonsillar herniation through foramen magnum–> impinges on the brainstem much deeper–> will manifest in a CHILD–> Hydrocephalus and that causing sunset eyes due to raised ICP, lateral rectus palsy.
Associated with spina bifida with myelomeningocele.

Dandy-Walker Syndrome—> Hypoplasia/Absence of cerebellar vermis.

Question 18

What is physiological splitting?

Answer 18

Physiological splitting occurs during inspiration, because during inspiration intrathoracic pressure is less/negative—> Causes more blood to be entered in the heart—-> More blood is supposed to go into the pulmonary artery and hence–> P2 comes later than A2!

In expiration, there’s no splitting because intrathoracic pressure is HIGH–> Heart contracts early—> No time for more blood to be collected in the heart.

Question 19

What are the specific auscultation finding in ASD?

Answer 19

Wide fixed splitting of S2.
Wide because—> ASD is a L-R shunt. As there’s more blood in the RA of an ASD patient as compared to the volume of blood in a normal person—> A lot of blood is pumped into PA–> this causes pulmonic component of S2 to come later than A2 in both inspiration and expiration.

Fixed—> pressures equalize in between RA and LA, whether it is expiration or inspiration.

Systolic murmur seen in 2nd left IC.
(Pulmonic area is TWOLIC)

Question 20

Eisenmeger syndrome happens in which shunt and is what shunt itself?

Answer 20

Larro Eisa tension mein, werna RL jaao gey.
Happens in Left-to-Right shunt.
then Pulmonary HTN occurs.
Then when the shunt reverses into Right-to-left—> so eisenmenger occurs as/or itself is a R-L shunt.

Question 21

What is the most common ALL?

Answer 21

B-ALL is the most common type.
Remember, CALLAY BALL for ALL kids–> (t12:21)–> imagine a ball rotating like these numbers are.
Most commonly occurs in kids aged 2-5 years of age, but in Down’s syndrome kids it occurs in children MORE THAN 5 YEARS of age.

CALLA- CD10+—-> An important prognostic factor for this ALL.

T-ALL manifest as–> Mediastinal mass–> SVC syndrome.

Question 22

Leukemia related to gums?

Answer 22

Acute Monocytic leukemia.

Question 23

APML?

Answer 23

AML——-> Itraati hui AML down’s waaay bachon kay saath nahyin khael rahi kiyun kay barri hai unsey 15,17 saal.
AML is common in 60 years of age, but in Down’s Syndrome kids it is associated with kids less than 5 years of age.
ATRA–> All trans retinoic acid used for treatment.
Translocation is—> T(15,17)

Question 24

CML?

Answer 24

Camel is able to go to bakkar at 9:22 pm, with 30 people.
CML—-> translocation is (9:22)
Median Age is: 30-60 years of age.
BCR-ABL fusion protein mutation.
Basophilia–> How Randy Neill told this?–> Treat with imatinib.

Question 25

CLL?

Answer 25

smudge cells seen!
Common manifestations are:
Increased WBC, enlarged LN–> if only these 2 symptoms are there—> NO TREATMENT.
Splenomegaly, low platelets, Anemia—> Treat with Fludarabine, Rituximab (CD20 inhibitor)

Question 26

If, Rituximab is mentioned. Which disease should come to your mind?

Answer 26

Make sure you confirm that the question is not about PML–> It is a disease which occurs due to destruction of oligodendrocytes–> When JC virus is reactivated in people taking Natalizumab (α4-integrin inhibitor), Rituximab (CD20).
(JC Virus is also called POLYOMAVIRUS–> It was the circular ear of that boy in the cap diagram. Hence, it is a DNA nonenveloped circular and DS.

Question 27

Streptomycin uses?

Answer 27

Used as an empiric treatment for infective endocarditis, sepsis (works amazing against gram negative AEROBES because it needs oxygen to enter the bacterial nucleus and bind to its 30S ribosome, works synergistically with Beta-lactams such as in wards they say use amp-gentamycin)

Direct therapy for pseudomonas, nocardia (is a gram positive aerobe though)

Question 28

Ecthyma gangrenosum is caused due to which virulence factors of pseudomonas aeruginosa?

Answer 28

-Exotoxin A ( INACTIVATES ELONGATION FACTOR 2 LIKE DIPHTHERIA—-> protein synthesis inhibition),
-elastase (degrades elastin - important for blood vessel destruction),
-phospholipase C (degrades cellular membranes),
and pyocyanin (generates reactive oxygen species).

Ecthyma gangrenosum occurs when there’s PERI-VASCULAR bacterial invasion, and destruction of blood vessels causing ulcers and necrosis of skin due to insufficient blood flow.

Question 29

Which aminoglycoside should be used for drug-resistant gram negative aerobes?

Answer 29

Amikacin, Streptomycin (stronger aminoglycosides)

Question 30

The story of important VIRAL bugs that cause interstitial/atypical pneumonia?

Answer 30

So, atypical pneumonia means B/L multifocal opacities and it follows a more indolent course.
Start from RSV–> common cause of pneumonia in infants more than 4 weeks old but less than 1.5 years, premature infants are at a much greater risk hence palvizumab can be given as a caution.—> Belongs from PARAMYXOVIRUS family, other important viruses in the same family are:
Measles
Mumps
Parainfluenza—> Just like influenza because has hemagglutinin and neuraminidase. But in a different family.

Paramyxoviruses and Orthymyxovirus/Influenza virus are same Negative Single Stranded RNA, but Paramyxo is non-segmented and Orthomyxo is segmented.

Influenza virus–> Called orthomyxovirus so many times. Simple flu, the flu shots we get are against this.

Now, come to Adenovirus—->
Causes sore throat, and watery diarrhea.
After diarrhea it can cause intussusception in kids. (The question might say that the kid had an infection with Double stranded Linear DNA virus, and what can be a possible complication?—> Intussusception, and also causes MYOCARDITIS)

Question 31

Friedreich's ataxia
ALS
NF1
NF2
Tuberous Sclerosis

Answer 31

Friedreich’s ataxia—> Autosommal Recessive, iron binding protein is defective and hence, IMPAIRED MITOCHONDRIAL FUNCTIONING. GAA trinucleotide repeats on Chromosome 9 (same as Tuberous Sclerosis)
Ataxic gait—> because of spinocerebellar tracts.
Diabetes.
Hypertrophic Cardiomyopathy.
Pes Cavus (like charcot marie tooth disease—> it is Autosommal Dominant, stokes-ladder gait, foot drop because of degenerated Peroneal Nerve.

ALS–> Myotrophic—> UMN and LMN are both affected. Riluzole is used to treat—-> can be asked/ high-yield. MOA of Riluzole is decreasing excitatory glutamate.

NF1–> Chromosome 17–> Cafe au lait spots, neurofibromas, OPTIC NERVE GLIOMA (can show a CT scan)

NF2–> Chromosome 22–> Merlin gene defective–> B/L vestibular schwannomas at cerebello-pontine angle. Can show a picture.

Tuberous Sclerosis (Chromosome 9)—>
A lot of dermatological manifestations but the most unique ones are:
>Ash-leaf macular patches (DD with tinea versicolor–> cause of hypopigmentation is that degradation of lipids results in acids that cause inhibition of tyrosinase which is important for melanin production)
> Shagreen patches (Thickened/leathery skin patches)

High-yield—-> INFANTILE SPASMS–> either they’ll describe this as spastic posture of a child, or say that there is hypsarrthmia on EEG—> T/m is high-yield because it is so unique—> Give ACTH.

Question 32

Sturge-Weber Syndrome

VHL

Answer 32

Sturge-Weber—–> Port wine stain (V1, V2 distribution) and associated with leptomeningeal angioma that causes seizures and intellectual disability.
High-yield is—–>
CT shows tram-track calcification
MRI with Gadolinium shows atrophy of brain because ussi side per calcifications hein.

VHL---> Pheochromocytoma (episodic headaches, HTN remember!!)
Clear RCC (HIGH-YIELD), Hemangioblastoma.

(VHL and NF1,2—> are Autosomal Dominant, loss of tumour suppressor gene!