I figured they were trying to get at the life expectancy of an RBC, but wouldn’t supplemental O2 technically replace the CO bound to RBCs? FA even mentions that CO binds competitively to RBCs, and isn’t that the whole point of giving hyperbaric/100% O2?

DKA (acidosis) > Potassium shifts out of the cell > hyperkakemia

FA 2019, pg 578

Easiest way to think of this is that this is Gatorade. Sure everyone thinks that sports drinks have glucose for the energy (which is also true) but they also contain sugar because the Na/Glucose co-transporter in the small intestine helps drive electrolyte intake. Without glucose, you don’t pull in sodium nearly as efficiently in the gut and the first makers of the Gatorade formula at UF found that once they gave glucose and electrolytes instead of just water to the football team during practice, they didn’t get as dehydrated and their electrolyte balance was a lot more stable.

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

I found this when trying to understand why increased NO caused headaches: Nitrates/nitrites are a very common headache and migraine food triggers (WebMD) and raise nitric oxide levels. High levels of nitric oxide are associated with migraine (Study). Headaches and migraines are also very common in medications that boost nitric oxide, such a viagra (study), but it is unclear why this happens. The original hypothesis was that nitric oxide increases blood vessel size and triggers a migraine, but the viagra study and others disproved this. Newer studies on nitric oxide shows that it increases the peptide (CGRP) that is considered responsible for triggering migraines (Study) after increases in inflammation. Because nitric oxide is associated neurogenic inflammation diseases, it's likely that headaches and migraines from nitric oxide are a warning sign of this inflammation (Study).

The research is basically stating that nitrates raise nitric oxide levels and high nitric oxide levels increase inflammation and headaches and migraines. However, the exact reason why this happens is unknown.

https://www.quora.com/Why-do-nitrates-cause-headaches

In my opinion this is kinda rude as an intial action. if the person continues to go back to the topic, I would say having a chaperone would help.... idk why Interrupting the patient with a more neurtal topic isnt the answer

Aren't M1 receptors found in the brain and are responsible for motion sickness?

What is the neoplastic chondrocytes filling lacunes?

Contraction atelectasis occurs when local or generalized fibrotic changes in the lung leads to collapsed alveoli. It can an occur after radiation therapy, necrotizing pneumonia, or granulomatous disease

Read pathoma...... chapter 1 p 5 on "cell death" Liquefactive necrosis occurs in brain infarct ( proteolytic enzymes from microglial cells liquify the brain) & Abscess (proteolytic enzymes from neutrophils liquify tissue [in this case pulmonary parenchyma]) & pancreatitis (same thing)

Mild jaundice with increased unconjugated in an older fellow is decreased UDP-glucuronyltransferase activity. Particularly in context of stress (appendectomy)

Neuropathic Pain after stroke is central Post stroke pain Syndrome

caused by contralateral thalamic lesions

Pg. 504 FA19

"Excitatory amino acids" refers to glutamate, while "Biogenic" apparently refers to tyrosine, the precursor AA to dopamine and norepi.

• CholecystokinIn is secreted from the I cells of the duodenum and jejunum.
• Gastrin is released from the G cells of the antrum of the stomach.
• IF is secreted by the stomach and absorbed in the terminal ileum with B12.
• Pepsin is secreted from the chief cells of the stomach and plays a role in protein digestion.
• Secretion of VIP increases intestinal water and electrolyte secretion by acting on the parasympathetic ganglia

i got this question right but why couldnt it be ginko biloba?

1. Hemostasis (blood clotting): Within the first few minutes of injury,
   1. platelets in the blood begin to stick to the injured site.
   2. This activates the platelets, causing a few things to happen.
   3. They change into an amorphous shape, more suitable for clotting, and they release chemical signals to promote clotting.
   4. This results in the activation of fibrin, which forms a mesh and acts as "glue" to bind platelets to each other.
   5. This makes a clot that serves to plug the break in the blood vessel, slowing/preventing further bleeding.[5][6]
      
      
2. Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris.
   1. This happens through the process of phagocytosis, where white blood cells "eat" debris by engulfing it. 
   2. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase.
      
      
3. Proliferation (growth of new tissue): In this phase, angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction occur.
   1. In angiogenesis, vascular endothelial cells form new blood vessels.
   2. In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix (ECM) by excreting collagen and fibronectin.
   3. Concurrently, re-epithelialization of the epidermis occurs, in which epithelial cells proliferate and 'crawl' atop the wound bed, providing cover for the new tissue.
   4. In wound contraction, myofibroblasts decrease the size of the wound by gripping the wound edges and contracting using a mechanism that resembles that in smooth muscle cells.
   5. When the cells' roles are close to complete, unneeded cells undergo apoptosis.

4. Maturation (remodeling): During maturation and remodeling,

   1. collagen is realigned along tension lines, and cells that are no longer needed are removed by programmed cell death, or apoptosis.
      
      
5. Approximate times of the different phases of wound healing,[10] with faded intervals marking substantial variation, depending mainly on wound size and healing conditions, but image does not include major impairments that cause chronic wounds.

FA 2018 p. 609. Suspect urethral injury if blood is seen at the urethral meatus. Mechanism of posterior urethral injury = pelvic fracture, which we see in this patient. Urethral catheterization is relatively contraindicated.

Morphine is a mu opioid agonist - one adverse effect of opioids is mast cell degranulation that is IgE-independent. Release of histamine is akin to an anaphylactic reaction --> pruritis, etc.

Also another key is it says normal appearing girl one of the things about the AIS is that they do get secondary sexual characteristics...turner girls don't look normal they'd be short and stubby no boobs fat neck etc

As per FA 1) fatty infiltration 2) cellular ballooning 3) eventual necrosis

This boy has achondroplasia, which is caused by an autosomal dominant mutation in Fibroblast Growth Factor Receptor 3. FGF signaling is needed for proper cartilage function, and without it, the long bones of the body will not grow because the growth plate (made of chondrocytes) does not function. However, bones that undergo membranous ossification, like the bones of the head, will grow normally. This results in the patient having short extremities with a normal size trunk and large head relative to the limbs.