to snoo-finity ... and beyond!
to snoo-finity ... and beyond!
NRTI's are associated with possible side effects of anemia, granulocytopenia, and myelosuppression.
The baby does not get any maternal IgM, IgA or IgE as they do not cross the placenta, so if IgM is found it may suggest the baby has encountered an infection in utero.
IgG is passed down to the baby as a means of passive immunity until the baby can form their own antibodies of different types. So if you see anything other than IgG (e.g. IgM) you know it must be d/t an infection.
Methanol is toxic by two mechanisms:
First, methanol can be fatal due to its CNS depressant properties in the same manner as ethanol poisoning.
Second, in a process of toxication, it is metabolized to formic acid via formaldehyde in a process initiated by the enzyme alcohol dehydrogenase in the liver. Methanol is converted to formaldehyde via alcohol dehydrogenase (ADH) and formaldehyde is converted to formic acid (formate) via aldehyde dehydrogenase (ALDH).
Formate is toxic because it inhibits mitochondrial cytochrome c oxidase, causing hypoxia at the cellular level, and metabolic acidosis, among a variety of other metabolic disturbances.
Foreign body inflammatory facial skin disorder characterized by firm, hyper-pigmented papules and pustules that are painful and pruritic. Located on cheeks, jawline, and neck.
Commonly occurs as a result of shaving (“razor bumps”), primarily affects African-American males.
Images: shorturl.at/fpwY1
This is an interesting one. I like to remember it this way: in people with narcolepsy, all the “right kinds” of sleep are happening at all the “wrong times” of day. During the day, when a power nap would typically throw you immediately into REM, this kid is only entering Stage 1 or 2 (lightest sleep = slightest noises jar him back to reality). At night, when he should peacefully drift into Stage 1, 2, and so on, he instead completely zonks out. Classic narcolepsy.
From UpToDate: “Narcolepsy can be conceptualized as a disorder of sleep-wake control in which elements of sleep intrude into wakefulness and elements of wakefulness intrude into sleep.”
Narcolepsy has one of the following 3 chraracter - 1. Cataplexy 2. dec orexin in csf 3. REM latency <15 min
its ass with (not dx criteria( Hypnagogin/pompic hallcination. Sleep paralysis
Acyclovir, famciclovir, valacyclovir are guanosine analogs. They undergo conversion to acyclovir monophosphate via virus encoded thymidine-kinase. Ultimately, they inhibit viral DNA polymerase by chain termination.
Mutated viral thymidine kinase can cause resistance.
Fronto-temporal dementia characterized by personality change is usually Picks
Frontotemporal dementia (formerly known as Pick disease): Early changes in personality and behavior (behavioral variant), or aphasia (primary progressive aphasia). May have associated movement disorders (eg, parkinsonism).
While this presents very similiarly to Hungtington's, you can differentiate it because in this stem it says "atrophy of the frontal lobes bilaterally" whereas Huntington's has atrophy of caudate and putamen with ex vacuo ventriculomegaly.
Little finger = ulnar nerve.
C8-T1 are the roots of the ulnar nerve, which is a branch of the medial cord. The ulnar nerve is not found in the carpal tunnel (the medial nerve is).
Ulnar n. damage can lead to loss of wrist flexion and adduction, flexion of medial fingers, abduction and adduction of fingers (interossei), actions of medial 2 lumbrical muscles. Loss of sensation over medial 1 1/2 fingers, including hypothenar eminence.
As described in the question stem, this mutation occurs within an intron (a gene segment which is transcribed [DNA->RNA] but not translated). RNA splicing enzyme(s) grab RNA and “loop it”; an intron is cut out and the exons on either side of the intron are adjoined, like this:
exon1—intron—exon2 => exon1—exon2
Typically, this splicing occurs at the very edges of the intron (what I denoted with the “—” character). But in our case, a mutation within the intron is causing RNA splicing enzyme to recognize a new site: the splicer cuts within the intron (instead of at the very edge, as it should). So, we get something that looks like this:
exon1—intr—exon2
That’s a totally different mRNA molecule, and it's going to make our β-globin protein look (and behave) awfully strange.
headshot
This was the picture that I liked the most for this question. If you imagine that the injury is at the level of the left subclavian vein (LSV) and thoracic duct (TD) crossing each other, maybe it will help you realize that the left breast & left upper extremity bypass the injury. The right lung is drained by the right lymphatic duct, not the TD (see one of the links bellow). And the heart is where eventually all the drainage is going to end up to be pumped again (TD -> LSV -> SVC -> heart).
No abnormalities, only some vomiting, looks well w/ no failure to thrive. Most likely immature LES.
It’s a common disease that impacts babies and children. GERD stands for gastro esophageal reflux disease. Dr. Viraine Weerasooriya, a pediatric gastroenterologist on the medical staff of Golisano Children’s Hospital of Southwest Florida, says infants are prone to having reflux until their gut matures at about 12 to 18 months. But GERD is more than just reflux. “What this implies is individuals who have problems with gastro contents that move up to the esophagus or into the mouth.
Of all the options, psoas major is the only one that is really associated with the lumbar vertebrae.
Q. Lumborum involves the transverse process of L1 but Psoas Major originates from L1-L5
Uworld specifically says that Psoas abscess means the patient will prefer flexion to avoid stretching the muscle. That's why Psoas did not make sense to me since the patient preferred extension, which would be stretching out the muscle.
On the other hand it's right on the vertebra and it's associated with TB.
Definition of adjustment disorder:
Emotional symptoms (eg, anxiety, depression) that occur within 3 months of an identifiable psychosocial stressor (eg, divorce, illness) lasting < 6 months once the stressor has ended.
If symptoms persist > 6 months after stressor ends, it is GAD.
While I can get on board with Adjustment Disorder, I don't see how this answer is any better than Somatic Symptom Disorder. From FA:
Variety of bodily complaints lasting months to years associated with excessive, persistent thoughts and anxiety about symptoms. May co-appear with illness.
SSD belongs in a group of disorders characterized by physical symptoms causing significant distress and impairment.
The pons has nerves 5-8, so the trigeminal would be affected here
Principle Sensory Nucleus of the Trigeminal is located in the Pons, as is the Motor Trigeminal Nucleus of the pons. This presentation is probably dealing more with the Principle Sensory Nucleus.
I do understand that the principal nucleus of the trigeminal nerve is located at the pons. But since this patient is having trigeminal neuralgia wouldn't you be disrupting the pathway involved in pain and temperature, which in this case would be the spinal nucleus (located in the medulla)?
Besides, I found this at an article
A recent hypothesis attributes the pain of trigeminal neuralgia to a central mechanism involving the pars oralis of the spinal trigeminal nucleus.[5]
MS is a demyelinating disease. That's why I didn't pick cortex or thalamus; they are grey matter. I picked medulla because I the spinotrigeminal nerves traverse the medulla. I guess we are just supposed to assume the demyelination is happening in the pons? I don't know.
Nowhere have I been able to find why the hell this is a thing.
As an edit: 108,001 people reported to have side effects when taking Hydrochlorothiazide. Among them, 25 people (0.02%) have Breast discharge
" Other classes of medications that cause hyperprolactinemia include antidepressants, antihypertensive agents, and drugs that increase bowel motility. Hyperprolactinemia caused by medications is commonly symptomatic, causing galactorrhea, menstrual disturbance, and impotence. It is Important to ensure that hyperprolactinemia in an Individual patient is due to medication and not to a structural lesion in the hypothalamic/pituitary area; this can be accomplished by (1) stopping the medication temporarily to determine whether prolactin levels return to normal, (2) switching to a medication that does not cause hyperprolactinemia "
https://www.ncbi.nlm.nih.gov/pubmed/16092584
"Non-dose-dependent side effects — Although low-dose therapy seems to minimize the metabolic complications induced by a thiazide or thiazide-like diuretic, it may not necessarily eliminate other side effects. As an example, as many as 25 percent of men treated with 25 mg/day of chlorthalidone develop a decline in sexual function [34]. Sleep disturbances can also occur, particularly if the patient is on a low-sodium diet [34]. How these problems occur is not known."
Possible explanation:
If the pt is taking a thiazide (which is K depleting), it might have also been given with a K sparing drug such as spirinolactone.
Spirinolactone has endocrinologic effects such as gynecomastia and galactorrhea.
Goljan had a lecture that mentioned that "If a patient has galactorrhea, review every drug they're taking since many drugs cause galactorrhea."
The only thing of possible relevance in this Q-stem is that she takes a medication, therefore the answer of "drug effect" is the most likely reason for her galactorrhea.
Thiazides can cause acute interstitial nephritis, a form of renal failure. Without the renal excretion of prolactin, it can build up in the serum and result in galactorrhea.
Thiazide=> hypercalcemia=> Oxytoxin (Gq coupled protein-> incr Ca2+)=> nipple discharge
The tubes are catheters put in for urine to flow into a bag. So urine output is going to increase. The patient is also hyperkalemic. Aldosterone responds to hyperkalemia by increasing K+ excretion.
Hyperkalemia will stimulate aldosterone secretion even if renin is suppressed due to his hypertension. Although Na+ will be reabsorbed, this will be transient (should resolve once the potassium levels normalized) and since his urine output will most likely return to normal, his blood pressure should also normalize.
This patient has small cell carcinoma. This type of cancer is associated with paraneoplastic syndromes such as: Cushing Syndrome, SIADH, or antibodies against Ca2+ channels (Lambert-Eaton) or neurons. Amplification of myc oncogenes is also common.
SIADH (Syndrome of inappropriate antidiuretic hormone secretion) is characterized by:
Body responds to water retention with aldosterone and ANP and BNP. That is what causes the increased urinary Na+ secretion which leads to normalization of extracellular fluid volume and the euvolemic hyponatremia.
This is an example of Shingles. Herpes simplex and herpes zoster viruses cause abnormal cell division in epidermal cells, and this creates multinucleated giant cells.
A Tzank smear showing multinucleated giant cells is characteristic of Varicella Zoster Virus infections. (HSV will have similar findings).
Why is it that the answer isn't also glossopharyngeal since you test CN IX by saying "Ah" also? Please help! Thanks!!
Mycobacterium avium complex infections are a common opportunistic infection in patients with advanced AIDS (CD4 count <50).
CD4+ cells activate B-cells which form follicles and cause enlargement of lymph nodes. Therefore, in an AIDS patient, to enlarge the lymph nodes, the CD4+ dysfunction must be resolved.
This a CYP 450 inhibitor (SICKFACES.COM); its the O.
Add on to the other comment: SICKFACES.COM (when I Am drinking Grapefruit juice) is the mnemonic for remembering the CYP450 Inhibitors:
M etronidazole
A miodarone
Itraconazole requires the acidic environment of the stomach to be absorbed. Omeprazole inhibits the H+/K+ pump of the stomach, thereby decreasing the acidity of the stomach. So when the patient takes Omeprazole and Itraconazole together, Itraconazole won't be absorbed into the body. That's why it has no effect.
It's recommended to take medications at least 2 hours prior to taking an antacid.
So you know that 65% of the data will fall within 1SD of the mean. So if you subtract 100-65 you will get 35. Which means that about 16% will fall above and 16% will fall below 1 SD. They are asking for how many will fall above 1 SD. I'm sure there is a better way of doing this, but thats how I got it lol.
When you have a traveler who has intermittent abdominal symptoms and diarrhea, and who has traveled to the likes of northern Africa and such, Schistosomiasis needs to be on your radar. At least, that’s how I’ve incorporated this nugget into my mental space.
It also looked exactly like schistosome on the slide--it had the little spine. Entamoeba would have had a bunch of RBCs inside.
Lysine is used in elastin and collagen cross linking; it is cross linked by lysyl oxidase to make collagen fibers
Analysis of the elastin in the question showed a decreased number of desmosine cross-links. Desmosine is made up of four lysine residues. Therefore abnormal elastin is likely missing lysine necessary for the formation of these desmosine cross-links. Wikipedia article on Desmosine.
Capitate and lunate are in the center of the palm. Capitate is not an option, so lunate is the answer.
Dislocation of lunate may cause acute carpal tunnel syndrome.
A 37-year-old nurse is accidentally stuck with a needle used ...
Inhibits reverse transcriptase