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[iocur]

Neuroregeneration - Peripheral Nervous System

Unlike the CNS, the PNS is capable of regeneration and does plenty of it.

After an injury to the axon, peripheral neurons activate a variety of signalling pathways which turn on pro-growth genes 

This growth is also governed by chemotactic factors secreted from Schwann cells. 

Phagocytes, Schwann cells, and macrophages migrate to the lesion site in order to clear away debris such as damaged tissue (inhibitory to regeneration). 

When a nerve axon is severed, the end still attached to the cell body is the proximal segment, while the other end is the distal segment. 

Proximal end swells and experiences some degeneration, but then begins to sprout axons which regrow as long as the cell body is intact, and they have made contact with the Schwann cells in the endoneurial tube. 

The distal segment experiences Wallerian degeneration - axons and myelin degenerate, but the endoneurium remains.

Schwann cells grow in ordered columns along the endoneurial tube, creating a band of Büngner cells that protects and preserves the endoneurial channel.

Macrophages and Schwann cells release neurotrophic factors that enhance re-growth.

The remaining endoneurial tube directs axon growth back to the correct targets.

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Blood Typing - ABO

A blood type (also called a blood group) is a classification of blood, based on the presence and absence of antibodies and inherited antigenic substances on the surface of red blood cells (RBCs). 

inherited from both parents. 

A total of 36 human blood group systems exist - ABO and the Rh determine someone’s blood type (A, B, AB and O, with +, − or null denoting RhD status) 

Typing is essential for suitability in blood transfusion

Antibodies in an individual’s plasma are directed against blood group antigens that their own RBCs lack

(this is confusing, it’ll take a while before you can look at blood typing stuff without having to think)

The ABO blood group system involves two antigens and two antibodies found in human blood. 

antigen A and antigen B - on the RBCs

antibody A and antibody B - in the serum

All humans can be classified into 4 groups:

Antigen A with antibody B

Antigen B with antibody A

Antigen AB has no antibodies

Antigen nil (group O) with antibody A and B.

Agglutination (clotting) reaction occurs between similar antigen and antibody. This is a seriously dangerous reaction (essentially all your blood turns to jelly) - if a patient with A  antibody in their serum is given blood with A antigen on the surface, they could die.

Group O = universal donor –> has no antigens on the RBCs, can be given to anyone and no agglutination will occur because nothing to react with the antibodies in serum

Group AB = universal acceptor –> no antibodies in serum, so nothing to react with any antigens on RBCs that are introduced.

[iocur]

also, our order of draw in our textbooks is different than most others (and shortened) so rather than the BLRGLDLGY, it’s more like YLRGGLG

and i cant make mnemonics

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I absolutely love lectures, it’s just that the lab time is exhausting, in 3 weeks we need to do 15 successful evac venipunctures, 5 butterfly draws, and 5 hematocrits + glucose tests

also i have to study for the HESI and get that set up because i’m going to try to get into the nursing program

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i don't want to look at any more pee for a while

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Just some good ol’ images about abnormal ST elevation. 

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Parathyroid

Parathyroid glands are four small glands of the endocrine system which regulate calcium and phosphate. They are located in the neck behind the thyroid.

Parathyroids are NOT related to the thyroid (just neighbours). however they share a similar blood supply, venous drainage, and lymphatic drainage.

You can easily live with one (or even ½) parathyroid gland.

Function

Parathyroid glands control calcium and phosphate levels by producing Parathyroid Hormone (PTH). 

Calcium:

PTH increases blood calcium levels by directly stimulating osteoblasts and thereby indirectly stimulating osteoclasts (through RANK/RANKL mechanism) to break down bone and release calcium.

 PTH increases gastrointestinal calcium absorption by activating vitamin D, and promotes calcium conservation (reabsorption) by the kidneys.

Phosphate:

PTH is the major regulator of serum phosphate concentrations via actions on the kidney. 

Inhibites of proximal tubular reabsorption of phosphorus. 

Activates vitamin D - absorption (intestinal) of Phosphate is increased.

Hypoparathyroidism

Decreased function of the parathyroid glands with underproduction of parathyroid hormone. 

Lead to low levels of calcium in the blood, often causing cramping and twitching of muscles or tetany (involuntary muscle contraction), and other symptoms. 

Can be inherited, but it is also encountered after thyroid or parathyroid gland surgery, and it can be caused by immune system-related damage 

The treatment of hypoparathyroidism is limited as there is no exact form of the hormone that can be administered as replacement. 

Tumours can form on the parathyroid glands, but they are usually benign adenomas.

[iocur]

Phlebotomy Acronyms

So here are some acronyms you might see on a regular basis.

1. CBC = Complete blood count

2. HCT= Hematocrit

3. HGB= Hemoglobin

4. CMP= Comprehensive metabolic panel

5. BMP= Basic metabolic panel

6. BNP= B - Type Natriuretic peptide

7. GTT= Glucose tolerance test

8. PTT= Partial thromboplastin time

9. PT= Prothrombin time

10. PSA = Prostate specific antigen

11. RPR = Rapid plasma regain ( Screening test for syphilis)

12. K = Potassium

13. ESR = Erythrocyte sedimentation rate

14. Stat = immediately

[iocur]

medical dramas are always just

Patient In The CT Machine, When Will They Seize

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Good news for religious medical students and care providers! I wonder if the sterile hijabs can be fashioned in other styles as well.

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there are so many massage therapy forms and techniques it's fascinating

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i have so many injections to do this week

i know my issues with them though, i think i’m just too gentle and overly cautious, which is just kind of how i am

not pulling the skin taut enough during intradermals for fear of being too rough

not pulling out fast enough with IM or SQ

really doesn’t look professional and is also wasting me a lot of time

i know that it’s good to be cautious but a lot of the time i do it to where its a detriment.

anyways, i have 1 more ID, i think 4 more deltoids, 3 more SQs, 1 more vastus laterales, and then 5 glutes because i was sick the day that we got checked off. that one i’m nervous about because of the sciatic nerve.

and THEN we have 5 Z-tracks to do. our final is at the end of the week and injections are very tiring for me because of hyper empathy which is cool and great.

i’m sure i can do it, and luckily after this it’s medical law and ethics which i expect to be a fairly easy class. i think i have an easier time with law jargon than most people, and we’ve been taught it periodically throughout our program.

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the line between NOS and NEC seems very minute and it’s a bit frustrating

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Autosomal Dominant Disorders

USMLE Quick Review:

Autosomal dominant is one of many ways that a trait or disorder can be passed down through families.

In an autosomal dominant disease, if you get the abnormal gene from only one parent, you can get the disease. Often, one of the parents may also have the disease.

•Achondroplasia: –Defect with Fibroblast growth factor receptor 3 (FGR3) – constitutively active (gain of function). –Short limbs relative to the trunk, prominent forehead, low nasal root, redundant skin folds on arms and legs.

•Familial Hypercholesterolemia: –Defect with LDL receptor (commonly). –Impaired uptake of LDL, elevated levels of LDL cholesterol, cardiovascular disease and stroke. Symptoms more severe in homozygous individuals.

•Huntington Disease (Also Huntington Chorea): –Defect with Huntingtin (HD) – CAG repeat expansion within exon 1. –The disorder is characterized by progressive motor, cognitive and psychiatric abnormalities. Chorea – nonrepetitive involuntary jerks – is observed in 90% of patients.

•Marfan Syndrome: –Defect with Fibrillin-1 gene (FBN1) that encodes a microfibril-forming connective tissue protein. –Abnormalities of the skeleton (disproportionate tall stature, scoliosis), heart (mitral valve prolapse, aortic dilatation, dissection of the ascending aorta), pulmonary system, skin (excessive elasticity), and joints (hypermobility). A frequent cause of death is congestive heart failure.

•Myotonic Dystrophy: –Defect with a protein kinase gene (DMPK) – CTG repeat expansion in 3’ untranslated region of the gene. –Muscle weakness, cardiac arrhythmias, cataracts and testicular atrophy in males. Children born with congenital form have a characteristic open triangle-shaped mouth.

•Neurofibromatosis I: –Microdeletion at 17q11.2 involving the NF1 gene. –The disorder is characterized by numerous benign tumors (neurofibromas) of the peripheral nervous system, but a minority of patients also show an increased incidence of malignancy (neurofibrosarcoma, astrocytoma, Schwann cell cancers and childhood CML – chronic myelogenous leukemia).

•Osteogenesis Imperfecta: –Defect with either of the genes encoding the α1 or α2 chains of type I collagen. – Null mutations produce a milder form of the disease. Missense mutations that act in a dominant negative manner are often perinatal lethal. The disorders are associated with deformed, under-mineralized bones that are subject to frequent fracture. 

•Polycystic Kidney Disease: –Mutations in either polycystin-1 (PKD1) or polycystin-2 (PKD2) gene. –Heterozygous individuals are predisposed to polycystic kidney disease because they are likely to lose the second good copy of the gene during their lifetime. Multiple renal cysts, blood in urine, end-stage renal disease and kidney failure.

[iocur]

so apparently our school offers an online program for a BSHCA, so that’s another one to add to the pile of ‘careers I am considering for later in my life’.

credits can transfer from my MAA program, we are provided decent-sized scholarships due to being previous students, and overall it should only take 15 months. the capstone project sounds extremely interesting, and we would still have access to the school’s tutoring services and online library... and I know that I could make more with that than as a medical assistant, but then I would more likely than not be missing out on clinical duties.

I would take classes such as marketing and accounting, which I am worried about due to dyscalculia, but the rest of it sounds appealing.

I can lock in the tuition within the next two months if I like, so I’m just debating it right now.

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teachers in public school: "if you even THINK about making your short answer questions NOT a complete sentence and you start it with 'because' or anything similar you will FAIL this assignment. if you think this is hard wait until you get into college"

college professors: "yeah whatever lmao we dont care as long as you get the point across"