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Welcome to motherhen’s page.
Contributor score: 4

Comments ...

 +0  (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.

 +0  (nbme18#45)

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

 +0  (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.

 +0  (nbme18#18)

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

 +0  (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.

 +0  (nbme18#16)

Alcohol-based products disrupt the lipid membrane envelope

 +0  (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.

 +0  (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

 +0  (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

 +1  (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.

 +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 azibird(92),

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.

motherhen  is this super out of left field or am I supposed to know this +  
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. +  

submitted by suckitnbme(129),

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(41),
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sinforslide  Also see UWORLD ID: 15255 +3  
suckitnbme  Vibrio species are mostly non-lactose fermenters except Vibrio vulnificus +3  
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) +  

submitted by banana(10),

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. +  

submitted by bingcentipede(129),

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? +2  
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. +1  

submitted by bingcentipede(129),

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 +1  
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 +  

submitted by lfcdave182(24),

FA 2020, pg 108

Interferon Gamma: Activates macrophages to induce granuloma formation