damn, i was way off. i put green leafy vegetables thinking the increased folate content can cause bacterial overgrowth. pretty sure i had a uworld question that said something like that.
Restriction enzymes cut at palindromic sequences... i knew this would bite me in the ass someday.+ We are testing two pieces of DNA- one with a mutation, one without.+ We need to use a restriction enzyme to cut exactly where the mutation is in order to see which piece of DNA has the sequence of interest (the restriction enzyme site). I chose 5' ACCG, which would cut the mutated strand and not the wild type. Why is this wrong? because when you write the complementary strand you get TGGC, which is not a mirror image of ACCG. + Correct answer 5' CCGG, the complementary strand: GGCC. This is a palindromic sequence (1), would cut the mutated strand of DNA and not the wild type (2), which when using gel electrophoresis the mutated strand would show 2 bands small bands, while the non mutated strand would show one large band (3)
decreased compliance of the vessels means you need to put more pressure in them to get flow. the stiffness/decreased compliance occurs with age- leading to an isolated increase in Systolic pressure.
The disease is MELAS. Mitochondrial encoded tRNA leucine 1 is the mutation. Apparently associated with high tone deafness. It is apparent its mitochondrial with maternal transmission, though unfortunately the etiology is utter memorization / process of elimination. Maybe next time the stragy will focus more on mitochondiral diseases and see that this choice is the only mitochondiral answer choice.
Rokitansky Kuser Hauser syndrome.
Hormones are normal as well as gonads.
INTERNAL GENITALIA are malformed (mainly uterus/tubes). Uterus can also be unicornate or there can be didelphysis or whatever that word is. though you don't need to know that long name by heart it helps with speed. Understand: Hormone profile is normal. If this patient had testes, the testosterone and estrogen would likely be opposite.
MEN 1 - P P P . Parathyroid, pancreas(gastrin in this case), pituitary lesion. not key to answering this question.
pt comes with symptoms of hypercalcemia, moans, groans, thrones (peeing), psych overtones.
Look at pth and calcium. we see high ca and high pth. We know that high calcium would lower pth...this means the high caclium was due to the high pth (i.e. parathyroid adenoma)
Question is actually asking: what are the effects of PTH? a, c, opposite of PTH
D and E i believed aren't related to PTH
B-Sounds something like the pathogenesis of pseudohyperparathyoidism
F- we definitely know that PTH increases Ca , so by increasing osteoclast maturation/activity you liberate calcium into the blood. this is the best answer.
hate this whole scramble thing: In one line: 2 * q * 80%.
This is for diseased individuals (two q alleles).I = 1/1600 = q^2 The frequency of q = 1/40
Now carriers is 2 p q. P is close to one assuming HW eqm (p+q=1). There's an additional step in this question due to the two different mutations.
so 2(q) = 1/20. 80% of these carriers are deletions so multiply 1/20 * 0.8 = 1/25
costochondritis is inflammation of the joints of the rib cage.(An inflammation of the cartilage that connects a rib to the breastbone). pain is reproducible with palpation, worse with movement and can be sharp in character. most importantly cardio / pulmonary findings will be negative.
costochondritis is inflammation of the joints of the rib cage.(An inflammation of the cartilage that connects a rib to the breastbone). pain is reproducible with palpation, worse with movement and can be sharp in character. most importantly cardio / pulmonary findings will be negative.
hardest part for me was differentiating absence of schwann cells vs abnormal myeling sheaths. Schwann cells come from neural crest cells so we would expect to see other neural crest migration issues in my opinion. CMT disease has motor and sensory issues because PMP-22 peripheral myelinating protein is mutated. leads to abnormal myelination of the peripheral nerves. foot drop from sensory degradation, muscle atrophy from motoneuron involvement (also peripherally myelinated)
another way to remember this is NERD. NSAIDs-exacerbated respiratory disease (NERD), when blocking COX there is shunting of the Arachadonic acid breakdown into the LOX (lipooxegenase pathway) which can cause build up of leukotrienes and cause an asthma-like condition.
Genetics- The following is a helpful way to do all the allele frequency questions / carrier frequency questions.
AR : I = q^2 (the cases are ONLY shown in homozygotes). The carriers are 2pq
X linked : Boys : I = q . Boys carrying ONE allele are affected individuals. GIRL CARRIERS (heterozygous females) : I = 2PQ. This gets us to the answer. On the other hand AFFECTED GIRLS (incidence in girls) would be I= q^2 - extremely small (choice e)
Experiment is asking which would increase pulmonary lymph flow, which I interpreted as which of these increases blood flow/intravascular volume. Endothelin, phenylephrine, low o2 concentrations all cause vasoconstriction. Co2 unlike in other organs (i.e. brain, muscle) does not cause vasodilation in the lungs so i left this one to the side. IV saline will for sure increase intravascular volume and blood flow so I leaned more toward this. The other explanation made a good point about the albumin solution in that it may cause reabsorption due to a high oncotic pressure (i.e. with albumin)
its an external hemorrhoid, pic is of an anus with a hematoma round the 7 o'clock position. there is pain and bleeding with wiping which points me toward an external hemorrhoid. with the other answer choices being infectious causes the only two left were venous htn and lymphatic obstruction. because increased straining and increased pressure on the inferior and middle rectal veins went with venous htn. (not to be confused with superior rectal vein which is linked to portal htn and internal/ painless hemorrhoids)
Is the correct answer Radon? If so, make sure you associate radon exposure to basements. Radon is in the soil and ya gotta dig up some soil to have a basement.
p53 is an important tumor suppressor gene, particularly in its ability to cause a cell to undergo apoptosis in the event of damage. p53 protein activity also holds the cell at the G1/S regulation point (B), limiting DNA synthesis.
I think this is actually just a complication of a Meckel's Diverticulum - Acute Meckel's Diverticulitis - which would be consistent with his presentation of acute abdomen + tarry black stools + CT/gross findings. It can be described as a mimic of appendicitis (as seen here).
I think if they wanted us to think this was Crohn's + Meckel they would have given us a more classical Crohn's presentation (skip lesions, insidious onset, non bloody stool)
Blood at the meatus is the red flag (see what I did there?) for urethral injury, which should be evaluated for with a retrograde urethrogram. The membranous the most commonly injured by fracture. In contrast, the spongy urethra is most likely to be injured during traumatic catheter insertion or in a straddle injury.
Why not superoxide dismutase? Its the step right in between NADPH (chronic granulomatous disease) and MPO
what about the increase in pulmonary vascular resistance ? doesnt PCWP fall in hemorraghic shock
The left-sided system is much higher pressure than the right side, hence the aortic valve closing is usually louder than the pulmonic valve. A P2 louder than A2 means that the pulmonary arterial pressure is significantly elevated.
from @melchior
From the UW ID 666 explanation, although type II pneumocytes normally differentiate into type I pneumocytes after proliferation, they do not differentiate in idiopathic pulmonary fibrosis due to altered cell signals and altered basement membrane, which is why type II pneumocytes are increased.
explanation by @benwhite_dotcom is incorrect
Narcotic use for acutely painful conditions is both reasonable and important. Short-term use (immediately post-surgical) does not lead to long-term dependence (or so people have thoughtโฆ). And yes, drugs addicts should also receive narcotics to control pain.
From Goljan:
Platelet problem = epistaxis, echymoses, petechia, bleeding from superficial scratches
Coagulation problem = late re-bleed, Menorrhagia, GI bleeds, hemarthroses
He presents with an anticholinergic toxidrome: hot as a hare, dry as a bone, mad as a hatter (FA2020 p241, the anticholinergic toxidrome is the same as an atropine overdose and jimsonweed actually contains atropine).
The antidote for antichlinergics is phyostigmine, an acetylcholinesterase inhibitor that acts as an indirect cholinergic agonist. (FA2020 p240)
The concept being tested is "what does PTH do that leads to hypercalcemia" https://i.ibb.co/sKPdVj3/image.png
In addition to PTH = osteoclast activity = increased calcium, this person could also be exhibiting symptoms of MEN1.
I believe this stem may be inferring MEN 1 syndrome - possible gastrinoma (peptic ulcer disease dx), parathyroid adenoma, and pituitary adenoma (causing SIADH). But, you don't need to even know this to get this right - just asking the effect of high PTH on the system - causes increased osteoclast activity as well as maturation.
Sildenafil is a PDE5 inhibitor that runs the risk of causing hypotension in patients on nitrates due to the synergy of the mechanisms of action. [FA2020 p246]
Nitrates, like nitroglycerin, work by increasing NO production which in turn acts to increase cGMP in smooth muscle causing vasodilation. PDE5 inhibitors act by decreasing the breakdown of cGMP in smooth muscle, enhancing the action of NO to cause vasodilation. Thus, when combined there can be systemic vasodilation that leads to dangerous hypotension.
He presents with an anticholinergic toxidrome: hot as a hare, dry as a bone, mad as a hatter (FA2020 p241, the anticholinergic toxidrome is the same as an atropine overdose and jimsonweed actually contains atropine).
The antidote for antichlinergics is phyostigmine, an acetylcholinesterase inhibitor that acts as an indirect cholinergic agonist. (FA2020 p240)
Just wondering if someone could explain the difference between collagen and elastin for this one? I thought either or could be used for tensile strength. Anyone have clarification, don't know why collagen is the best answer!
Child has albinism. Defective melanin synthesis due to deficiency of enzyme tyrosine hydroxylase. FA 2020, page 476
Natural transformation is when bacteria take up naked bacterial chromosomal DNA in their environment (usually from cell lysis). A cell "lysate" is what remains of bacterial genes when the bacteria is dead (can be extracted from bacteria, as shown here). The SHiN bugs all can undergo transformation. You know it is transformation even without knowing which bugs can do so because it doesn't take up the DNA when DNase is added (it kills any free environmental DNA in the lysate)
This is mesenteric artery stenosis causing postpranidal intestinal ischemia/angina. I definitely did not know this answering the question and I personally got to the answer by attempting to logically think through the symptoms:
If anyone has a better explanation please offer it.
Fatty Acid degradation
-Occurs in mitochondria or peroxisomes
First step - uptake of the fatty acids by the cell and addition of CoA to them
Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)
Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )
An Acyl CoA dehydrogenase catalyzes the initial step
.
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation
The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )
Fatty Acid degradation
-Occurs in mitochondria or peroxisomes
First step - uptake of the fatty acids by the cell and addition of CoA to them
Second step - Uptake of the Fatty Acyl CoA molecule into the mitochondria by the Carnitine Shuttle *( which involves removal and then addition of the CoA molecule again to the fatty acid once inside the mitochondria)
Once in the mitochondria the fatty acid may undergo , Beta-oxidation ( a process in which a fatty acid is oxidized/cleaved at the Beta carbon to generate Acetyl CoA in several cycles )
An Acyl CoA dehydrogenase catalyzes the initial step
.
Look out for Hypoketotic Hypoglycemia in defects of fatty acid degradation
The 2 main subtypes to be aware of are -a problem with the carnitine shuttle ( systemic carnitine deficiency) - or with an Acyl CoA dehydrogenase ( eg MCAD deficiency )
hardest part for me was differentiating absence of schwann cells vs abnormal myeling sheaths. Schwann cells come from neural crest cells so we would expect to see other neural crest migration issues in my opinion. CMT disease has motor and sensory issues because PMP-22 peripheral myelinating protein is mutated. leads to abnormal myelination of the peripheral nerves. foot drop from sensory degradation, muscle atrophy from motoneuron involvement (also peripherally myelinated)
Genetics- The following is a helpful way to do all the allele frequency questions / carrier frequency questions.
AR : I = q^2 (the cases are ONLY shown in homozygotes). The carriers are 2pq
X linked : Boys : I = q . Boys carrying ONE allele are affected individuals. GIRL CARRIERS (heterozygous females) : I = 2PQ. This gets us to the answer. On the other hand AFFECTED GIRLS (incidence in girls) would be I= q^2 - extremely small (choice e)
Dudes and dudettes, let me tell you how high yield Pathoma Ch. 1-3 are. Dr. Sattar is the freaking man.
Anyway, this is reversible cell injury because of swelling. If the Na/K ATPase is not working, Na is not leaving. Na follows water, so water is getting stuck in the cell, leading to swelling.
Most important is recognizing that it's reversible cell injury - everything else (except PFK lol) is talking about cell death
Dr. Jason Ryan from BB emphasized that just because something is statistically significant, does not automatically mean it is clinically significant!
In agreement with the other post: (see FA2020 p331)
You would want to check FREE T4 because pregnancy increases Thyroid binding globulin. It is possible she might have increased overall T4, but NOT have hyperthyroidism because the free T4 is normal (i.e. her increases amount of thyroid binding globulin has bound more T4, and since our bodies respond to the concentration of free T4 only, the hypothalamus should ensure that the free T4 is kept constant; this would appear as increased overall T4)
Another way of thinking of this:
If we increase bound T4 and keep free T4 the same, we would still increase overall T4. Thus to know if she truly has hyperthyroidism we must look at free T4 concentration.
Patient with Primary Hypothyroidism (problem with the gland itself ) treated with T3
So what happens when we give our Patient T3.
- firstly , we inhibit secretion of TSH from the pituitary gland . ( TSH decreases ).
This means less stimulation of the Thyroid and less hormone production . The Throid hormone it primarily makes and releases is T4 , ( and so T4 decreases ) . Naturally you would also expect a decrease in T3 but patient is taking exogenous T3( and so T3 increases )
Differential Diagnosis of Newborn/Neonatal Vomiting
-Benign gastroesophageal reflux ( i.e immature lower esophageal sphincter )
regurgitation of food shortly after feeding .
No further symptoms , healthy children with normal development
-Hypertrophic pyloric stenosis
Regurgitation - projectile nonbilious vomiting
electrolyte imbalances ( alkalosis and hypokalemia ) * physical examination may reveal an olive mass on palpation of epigastrium
*typically starts from between 2nd and 7th week of age
-Midgut volvulus /Malrotation /Duodenal atresia * bilious vomiting * abdominal distention * Imaging may reveal signs like the double bubble sign ( duodenal atresia ) etc
Note: The list is not exhaustive as there are many more causes associated with newborn vomiiting
i was so confused by this question. is this because the rest are human antigens, so why would we have antibodies against them? but HPV is antibody toward E6 is foreign...?
Hep C - RNA virus (not enveloped) (picorna family + ssRNA).
Viruses are intracellular- so their products are displayed on MHCI molecules (using tap1/tap2 to shuttle the viral proteins broken down by proteosome) and are shipped to the cell surface of infected cells. Since this is MHC I we know CD8+ t cells (cytotoxic T lymphocytes) are responsible for attacking the infected cells.