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Welcome to motherhen’s page.
Contributor score: 41


Comments ...

 +1  (nbme18#10)

Kartagener syndrome, an autosomal recessive ciliary disorder. Presents with triad of chronic sinusitis, bronchiectasis and situs inversus.

Since the brother is known to be phenotypically normal, he can either be AA, Aa or Aa. Thus, there is a 2/3 chance is a carrier.

stefanmil  Can you explain how is this Kartagener? It didn't come to my mind at all :/ thanks +
kcd0321  I thought it was Cystic fibrosis: chronic cough with "thick" green sputum, cramps in the abdomen (malabsorption issues because of pancreatic insufficiency maybe), and then the frequent respiratory infections. Its also AR so the same principle of AA, Aa, or Aa, so he has a 2/3 chance of being a carrier. +1

 +0  (nbme18#45)

Are these gottron's papules from dermatomyositis? Pareaneoplastic syndrome from adenocarcinoma, esp ovarian?

j44n  it is not. The pt has a history of being immunocompromised. Also, gottron's are over the hands and dermatomysitis can present with a rash over the eyelid as well! There is also no history muscle weakness at the proximal muscles (shoudler/ hip area) and no mention of an elevated creatine kinase! - hope this helps :) +1

 +2  (nbme18#20)

Leukocyte adhesion deficiency, a defect in integrin LFA1. Neutrophils are unable to adhere and migrate to infection sites, instead accumulating in blood. This explains the absence of neutrophils at infection sites and elevated neutrophils in blood.

Side note: Physeo is a great free resource with sketchy-like images to help remember immunodeficiencies and more. Not at all sponsored, just stumbled upon it during dedicated and shocked it isn't more widely known about. https://physeo.com/immunology/


 +3  (nbme18#18)

Celiac disease, an autoimmune intolerance to gliadin leading to enterocyte damage and subsequent malabsorption


 +1  (nbme18#17)

Parathyroid tumor releasing PTH, increasing Ca and ALP. This is seen in MEN1 tumors: parathyroid, pituitary and pancreas.

Note, parathyroid tumors can also be seen in MEN2A.


 +2  (nbme18#16)

Alcohol-based products disrupt the lipid membrane envelope


 +2  (nbme18#46)

Barium swallow shows failure of LES relaxation, causing distal stenosis of the LES ("bird's beak" sign) proximal dilation indicative or achalasia- or in this case "pseudoachalasia" secondary to Chagas (FA2020 p370). This is caused by the loss of inhibitory neurons in the myenteric (Auerbach) plexus.

lokotriene  FA2020 p376* +

 +4  (nbme18#40)

This is describing Hyper IgM syndrome; without CD40 ligand, T cells are unable to provide the secondary signal to activate B cell class switching. This prevents IgM from switching into IgD, G, E and A, and thus an accumulation of IgM - hence the name "hyper IgM" - and deficiency in the rest (causing infections like S.pyogenes early in life, PCP, cryptosporidium and CMV).

Note in this question the cause of Giardia infection from lack of IgA (lack of mucosa/GI protection) must be distinguished from Selective IgA Deficiency. Lack of CD40L ligand defines it as Hyper IgM syndrome.

Answer choices:

  • Complement activation= IgM and IgG

  • Cross placenta= IgG

  • Attach eosinophil Fc receptor= IgE

  • Attach mast cells= IgE

  • Easy secretion across mucosa= IgA

jer040512  To further add: IgG opsonizes +1

 -2  (nbme18#31)

Sudden onset of severe infectious symptoms suggests Toxic-Shock Syndrome Toxin of Staph Aureus. This is most commonly seen in tampons left in for long periods of time or nasal packing of nosebleeds. A positive nares culture of TSST producing S. Aureus would support this diagnosis.


 +0  (nbme16#4)

Enlarged RV and decreased systolic function is indicative of dilated cardiac myopathy. As the ventricle diameter increases past a certain point, there is less force to contract causing myopathy


 +2  (nbme16#48)

In other words, what is the active product of the thyroid gland that is needed for normal development? Only thyroxine, iodine and thyroglobulin are in the thyroid gland. Of these, thyroxine is the active hormone produced that would affect development.

cheesetouch  *refuting thyroglobulin * Wikipedia: Thyroglobulin (Tg) acts as a substrate for the synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3), as well as the storage of the inactive forms of thyroid hormone and iodine within the follicular lumen of a thyroid follicle +

 +0  (nbme16#30)

Phenoxybenzamine is an irreversible non-competitive antagonist on alpha receptors that prevents catecholamine (hypertensive) crisis. It is used preoperatively for pheochromocytomas.





Subcomments ...

submitted by hungrybox(1026),

I really didn’t understand this question even after reading all the answers here so I emailed Dr. Klabunde (the expert)!

Here’s what he said:

This is a case of acute heart failure following an acute ischemic event (ST elevation in anterior leads). SVR increases because of neurohumoral activation, which helps to maintain BP. PCWP increases because acute HF causes blood to back up into the pulmonary circulation. Increased pulmonary blood volume causes all the pulmonary pressures to increase. PVR DECREASES because the pulmonary vasculature has a very high compliance, and therefore passively distends in response to increase volume. This passive dissension decreases the PVR.

motherhen  I thought in cardiogenic shock, PWCP can be increased or decreased depending on if the blood is backing up in the lungs (LHF) or body (RHF). Can someone clarify how we know which is happening here? +1  
motherhen  *PCWP +  
jsanmiguel415  They say it's an "anterior STEMI" which to me meant V3, V4 aka LAD, which supplies the left ventricle so increased PCWP. If PCWP was decreased it would mean right ventricle is disrupted which is more RCA and would be II, II, AVF or an inferior leads +2  


submitted by hungrybox(1026),

I really didn’t understand this question even after reading all the answers here so I emailed Dr. Klabunde (the expert)!

Here’s what he said:

This is a case of acute heart failure following an acute ischemic event (ST elevation in anterior leads). SVR increases because of neurohumoral activation, which helps to maintain BP. PCWP increases because acute HF causes blood to back up into the pulmonary circulation. Increased pulmonary blood volume causes all the pulmonary pressures to increase. PVR DECREASES because the pulmonary vasculature has a very high compliance, and therefore passively distends in response to increase volume. This passive dissension decreases the PVR.

motherhen  I thought in cardiogenic shock, PWCP can be increased or decreased depending on if the blood is backing up in the lungs (LHF) or body (RHF). Can someone clarify how we know which is happening here? +1  
motherhen  *PCWP +  
jsanmiguel415  They say it's an "anterior STEMI" which to me meant V3, V4 aka LAD, which supplies the left ventricle so increased PCWP. If PCWP was decreased it would mean right ventricle is disrupted which is more RCA and would be II, II, AVF or an inferior leads +2  


submitted by beeip(124),
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anC neoany xenalip hatw er'yeht netggti at eerh? oHw anc ntbolheahce be ddtaenici dna dtr?noacnidaecit

sniperx3  I think it's because Bethanechol acts on M3 receptors which can treat her urinary problems but it might exacerbate her asthma symptoms since there are M3 receptors on the lungs. +37  
suckitnbme  I definitely had to read this question multiple times to understand it. +2  
brotherimodu  I read it like 6 times and gave up +1  
motherhen  I definitely had to read this question multiple times to still not understand it +1  


submitted by sajaqua1(531),
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sunshinesweetheart  p 269 FA 2019 +  
motherhen  [P]rimary= [P]revention [S]econdary= [S]creening [T]ertiary= [T]herapy +3  
rockodude  almost picked alcohol because that may lead to fetal alcohol syndrome, relevant to women of childbearing age, but regular exercise made more sense. complete abstinence of alcohol is a little extreme for a general recommendation +  
jurrutia  Abstinence from alcohol is a form of primary prevention, because alcohol causes many bad outcomes. However, exercise is more important. +  


submitted by vshummy(161),
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oS hte best i dcuol ndif aws in Frsti Aid 1209 pg 643 duern catDibie Ksaiti.sdoeoc ehT cimygrhelpyea adn ayhklmereaip ueasc na ictmoos riiessud so hte ineret body gets teeedpld fo sfulid. enHce ywh atpr of hte atmtneret ofr KDA si IV d.siufl Yuo thmgi evne rley no atth ciepe of iifonrnomat nloea ot wraesn tish u,tnisoqe atth ADK is ttereda hwti IV ludis.f

fulminant_life  I just dont understand how that is the cause of his altered state of consciousness. Why wouldnt altered affinity of oxygen from HbA1c be correct? A1C has a higher affinity for oxygen so wouldnt that be a better reason for him being unconscious? +6  
toupvote  HbA1c is more of a chronic process. It is a snapshot of three months. Also, people can have elevated A1c without much impact on their mental status. Other organs are affected sooner and to a greater degree than the brain. DKA is an acute issue. +6  
snafull  Can somebody please explain why 'Inability of neurons to perform glycolysis' is wrong? +3  
johnson  Probably because they're sustained on ketones. +3  
doodimoodi  @snafull glucose is very high in the blood, why would neurons not be able to use it? +2  
soph  @snafull maybe u are confusing bc DK tissues are unable to use the high glucose as it is unable to enter cells but I dont think thats the case in the neurons? +1  
drmomo  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909073/ states its primarily due to acidosis along wth hyperosmolarity. so most relevant answer here would be dehydration +1  
drmohandes  I thought the high amount of glucose in the blood (osmotic pressure), sucks out the water from the cells. But you also pee out all that glucose and water goes with it. That's why you have to drink and pee a lot.. +7  
titanesxvi  Neurons are not dependent on insulin, so they are not affected by utilization of glucose (only GLUT4 receptors in the muscle and adipose tissue are insulin dependent) +25  
drpatinoire  @titanesxvi You really enlightened me! +  
mutteringly  I don't make the connection of what titanesxvi said to the question - can someone explain? +  
motherhen  @mutteringly it explains why the answer choice "inability of neurons to perform glycolysis" is wrong +1  


submitted by azibird(177),

Endothelin (ET)-1, a potent vasoconstrictor peptide from vascular endothelial cells, is also synthesized and secreted by cardiomyocytes and induces hypertrophy of cardiomyocytes through activating phospholipase C, protein kinase C, extracellular signal-regulated kinase (ERK) 1 and ERK2, and upregulation of c-Fos and c-Jun.

https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000112596.06954.00?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

motherhen  is this super out of left field or am I supposed to know this +10  
ab721  @motherhen I don't know if this is correct, but I personally tried to reason this one out. If hypertrophy is occurring, more sarcomeres are added which means more beta-myosin. Hypertrophy also means the cell is doing more work, so a transcription factor is likely to be upregulated. From there, the only option with both of those increased had endothelin increased as well, though unclear why that's necessarily increased. +5  
motherhen  genius +1  
yerpderp  Loud S2 made me think of pulmonary hypertension which would have an incr endothelin +1  
geekymle  that loud s2 was from systemic hypertension. +  
utap2001  systemic hypertension -> induce LV hypertrophy -> induce pulmonary hypertension -> endothelin increase, plus loud S2 and S4 gallop +  


submitted by azibird(177),

Endothelin (ET)-1, a potent vasoconstrictor peptide from vascular endothelial cells, is also synthesized and secreted by cardiomyocytes and induces hypertrophy of cardiomyocytes through activating phospholipase C, protein kinase C, extracellular signal-regulated kinase (ERK) 1 and ERK2, and upregulation of c-Fos and c-Jun.

https://www.ahajournals.org/doi/full/10.1161/01.CIR.0000112596.06954.00?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

motherhen  is this super out of left field or am I supposed to know this +10  
ab721  @motherhen I don't know if this is correct, but I personally tried to reason this one out. If hypertrophy is occurring, more sarcomeres are added which means more beta-myosin. Hypertrophy also means the cell is doing more work, so a transcription factor is likely to be upregulated. From there, the only option with both of those increased had endothelin increased as well, though unclear why that's necessarily increased. +5  
motherhen  genius +1  
yerpderp  Loud S2 made me think of pulmonary hypertension which would have an incr endothelin +1  
geekymle  that loud s2 was from systemic hypertension. +  
utap2001  systemic hypertension -> induce LV hypertrophy -> induce pulmonary hypertension -> endothelin increase, plus loud S2 and S4 gallop +  


submitted by suckitnbme(176),

X-ray shows a fracture of the surgical neck of the humerus. This where the axillary nerve and the posterior circumflex humeral artery travels.

motherhen  Additionally, axillary nerve supplies sensory innervation for lateral aspect of shoulder. Radial does lateral elbow and musculocutaneous does lateral forearm. +  


submitted by sinforslide(50),
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Teh iepntat laedwk fbeoroat on het hebca adn hda i,iosrcsrh whchi meksa mih unlblrveea for .V iflcnsvuui m.aetecarbi .V uniuvcfisl rameectiba hsa a yerv orop ooris.gpsn

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sinforslide  Also see UWORLD ID: 15255 +4  
suckitnbme  Vibrio species are mostly non-lactose fermenters except Vibrio vulnificus +6  
motherhen  I thought V.vulnificus could only cause food poisoning from eating shellfish; turns out contact with wound infections causes it too (hence why walking barefoot on the beach is a risk factor) +2  
ootscoot  I think they threw this one in here for all the Sketchy loyalists. Gotta keep us on our feet. +  


submitted by banana(13),

If you got all tangled up on this question like me:

anatomic dead space= conducting airways

Alveolar dead space= alveoli that are ventilated but not perfused (wiki)

physiologic dead space=anatomic dead space+ alveolar dead space

Po2: just no

motherhen  When I get mixed up on dead space vs shunt, I anchor myself on the meaning of anatomic dead space: the parts of the airway that don't have associated blood vessels for gas exchange (nose, trachea, bronchi). From there I work backwards to what shunt means: blood vessels that don't have enough air. +1  


submitted by bingcentipede(243),

IV normal saline will increase hydrostatic pressure in the vasculature. This isotonic solution is freely filtered across the capillaries, which is collected by lymphatics and can be picked up in this experiment.

motherhen  Why does albumin solution not have this effect? +3  
notyasupreme  I think it's because albumin in saline is hypertonic, which would cause the opposite effect of what the experiment was going for. Fluid would go across the capillaries into the vasculature, rather than vice versa. +2  


submitted by bingcentipede(243),

This is hereditary spherocytosis. The image stinks, but the cells are not super pale in the middle and they're round. Her dad also had a splenectomy (HS is autosomal dominant), which is the definitive treatment for HS.

Pt is also normocytic (90.2 um^3), so a lot of the other answer choices can be eliminated based off this.

In the end, screw this picture because it's not clear and you can't zoom in.

motherhen  Sad picture... I definitely thought this was B-thalessemia since the image looked like different size and shaped RBCs (anisopoikilocytosis). But if I squint my eyes real hard and turn sideways I guess I can also see those spheres +3  
furqanka  beta thal, iron def and inadequate epo would have low reticulocyte count. impaired oxidative enzyme aka g6pd deficiency affects mostly males and would have bite cells +1  


submitted by lfcdave182(31),

FA 2020, pg 108

Interferon Gamma: Activates macrophages to induce granuloma formation