to snoo-finity ... and beyond!
Welcome to kateinwonderland's page.
Contributor score: 4
Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb?
How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis??
normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis
At the end of the fourth week, the yolk sac presents the appearance of a small pear-shaped opening (traditionally called the umbilical vesicle), into the digestive tube by a long narrow tube, the vitelline duct. (Wiki)
sorry my bad this was the wrong question i responded to but i still got this one (ED one) and the gynecomastia one wrong
i think it's liver for this one because they say it has regenerative potential and because even though the small intestine has regenerative potential, it can apparently fibrose? i have no idea, i put small bowel
@bigbootycorgi : I put small intestine too. From what I've searched after, it says that liver fibrosis reversible -> no evidence of fibrous scarring
Just to add to that, a cirrhotic liver is a small shrunken liver so you wont be able to find hepatomegaly anyways. The other signs are the stigmata of Liver disease
Could the pneumothorax also cause less ventilation due to decreased lung surface, retaining more CO2 causing respiratory acidosis? That's how I got to the answer at least.
I think pneumothorax would increase RR because you're probably hypoxic. Also I'm sure when you have a lung collapse on you you'd be scared and that would trigger your sympathetic so your RR will go up either way.
there is no bilateral lung opacities as you would see in ARDS
-V:sup. rectal v -> inf. mesenteric v. -> splenic v. -> portal v
-internal iliac LN
-V:inf. rectal v -> internal pudendal v->internal iliac v->common iliac v->IVC
-superficial inguinal LN
(FA 2018 p360)
Venous drainage above pectinate, most to the portal vein, some to internal iliac v via middle rectal vein. I think the real solid key here is that the clinical vignette suggests hepatic cirrhosis.
Classification of Vascular Lesions
Vascular malformations (flat lesions)
-Salmon patch (also known as nevus simplex or nevus telangiectaticus)
-Port-wine stain (also known as nevus flammeus)
Hemangiomas (raised lesions)
-Superficial hemangioma (also known as capillary nevus hemangioma)
-Deep hemangioma (also known as cavernous hemangioma)
It’s just canker sores, they come and go. I think in herpes the gingivostomatitis really only happens when you first get infected. After that you just get recurrent cold sores.
Herpes zoster is not the same as herpes simplex virus.
you would see dermatome rash in zoster
cf) Just in case someone wanted to know the causative organism of aphthous ulcers
:The precise cause of canker sores remains unclear, though researchers suspect that a combination of factors contributes to outbreaks, even in the same person.
Unlike cold sores, canker sores are not associated with herpes virus infections.
Herpes Zoster doesnt cause gingivostomatitis. Herpengina can cause vesicular lesion in mouth but happens to children in summer season by entero virus
I'm wondering if this could be a mild case of Behcet syndrome without genital involvement
It sure can be Behcet or Pemphigus if the q provides us with more info. Canker sores just come and go for years with unclear mechanism. Also herpes zoster is shingles by VZV, not HSV1.
Is there a situation where you would pick fibromuscular dysplasia over atherosclerosis if given both options? Thanks for your help!
Atherosclerosis affects PROXIMAL 1/3 of renal artery
Fibromuscular dysplasia affects DISTAL 2/3 of renal artery
Why is there ↓ size in both kidneys? This threw me off
@gonyyong : Maybe because narrowed renal a. d/t atherosclerosis led to renal hypoperfusion and decrease in size?
Fibromuscular dysplasia occurs in young females according to Sattar Pg 67, 2018.
Normally you will see Fibromuscular dysplasia in a young female 18-35 with high or resistant hypertension. She is older has a history type II DM predispose you to vascular disease and normal to moderate elevation in BP