Acquired Nevomelanocytic Nevi (aka moles)

nevomelanocytic-nevi

Nevi (or moles) are very, very common. They are generally well-circumscribed dark spots (or “papules” to use the dermatological terminology) that can appear at any time in someone’s life.

Histologically they are composed of groups of melanocytic nevus cells and can be found in the epidermis, dermis or both.

The problem with nevi is that they are pigmented and people tend to get worried about pigmented things on the skin (for good reason as melanoma can be a pretty scary disease).

Common acquired nevi are grouped into three categories (I’ll leave out congenital and dysplastic nevi for now)

  1. Junctional: the nevus cells are completely in the epidermis, just above the dermal-epidermal junction. Clinically they are <1 cm, flat or minimally elevated and dark in colour.
  2. Compound: the nevus cells are in both the epidermis and the papillary dermis (top layer of the dermis), and cross the basement membrane. Clinically they are raised, and a medium-brown colour.
  3. Dermal: the nevus cells are completely in the dermis. Clinically they are raised and almost always pigment less as the cells lose their capacity for melanization when in the dermis. They usually have telangectasia and may or may not have hair. They don’t tend to appear until the 2nd or 3rd decades of life.

Pierre-Robin Sequence

pierre-robin-sequence

Pierre-Robin Sequence is not a syndrome, it’s a sequence. While it is a collection of features, one happens because of the one that came before.

The features are:

  • Retrognathia/micrognathia (posterior mandible or very small mandible)
  • Glossoptosis (downwards/posterior displacement of the tongue due to the small mandible
  • Airway obstruction (because the tongue is in the way)

Pierre-Robin Sequence is associated with cleft palate (50% of children with the sequence have cleft palate). There are two proposed theories:

  1. The first is that the tongue simply gets in the way of the palate from fusing
  2. The second is that the tongue prevents the newly fused palate from staying fused (this is currently the more popular theory)

PRS, though not a syndrome itself, is associated with multiple syndromes including Stickler Syndrome, velocardiofacial syndrome, fetal alcohol syndrome and Treacher Collins Syndrome.

PHACE Syndrome (hemangiomas)

PHACE_syndromeThere are no shortage of congenital syndromes that are acronyms arranged into some sort of vaguely pronounceable word. There will be lots of doodles about these, but we’ll start off with a more uncommon one – PHACE Syndrome.

PHACE Syndrome is a collection of findings that go along with large infantile hemangiomas. They’re the more worrisome (but less obviously disfiguring) things you need to look for when you see a baby with a large hemangioma on the face or multiple hemangiomas.

  • Posterior fossa brain malformations
  • Hemangiomas
  • Arterial anomalies
  • Cardiac anomalies and coarctation of the aorta
  • Eye abnormalities
  • Sternal cleft

The most common symptom of PHACE is cerebrovascular abnormalities, followed by cardiac anomalies (coarctation, aortic arch anomalies, VSDs). If you suspect PHACE, do clinical exam of the skin and eyes and MRI of the head, neck and chest.

Other cool facts

  • PHACE occurs in full-term normal birth weight infants (other hemangiomas tend to occur in preterm infants)
  • Quite common, more girls than boys (8:1)
  • Don’t confuse it with Strurge-Weber (port wine stain, associated with the facial dermatomes)
    • Port wine stains don’t proliferate and then regress like an infantile hemangioma

Brachial Plexus Part 1 – anatomical relations

brachial_plexus

The brachial plexus is the bane of many med students’ existence during any sort of neuro block. So many nerves, so many connections, so many seemingly arbitrary names of different sections. It’s just a woven mess of misery. (especially when they start getting into the “where is the lesion” questions)

Thus I’ve decided to have a couple posts about the brachial plexus, hopefully demystifying it to some extent. This first doodle is about the brachial plexus and its anatomical relationship to some of the structures that show why anatomists who named the parts weren’t as crazy as they seem.

Important structures to remember because they explain why parts are named the way they are:

  1. Vertebrae
  2. Anterior and posterior scalene muscles
  3. Subclavian artery
  4. The arm (in its anatomical position)

Vertebrae: There are 7 cervical vertebrae and 12 thoracic vertebrae. To make things confusing the cervical spinal nerves exit ABOVE their named vertebrae (except for C8) while the thoracic, lumbar and sacral exit BELOW. This messes up the whole numbering system because there are SEVEN cervical vertebrae but there are EIGHT cervical spinal nerve roots. The brachial plexus generally includes the nerve roots C5-T1*
* I say generally because there’s are anatomical variations such as a “prefixed” plexus that goes from C4-C8 and a “postfixed” plexus that goes from C6-T2

Scalene Muscles: The brachial plexus is nestled between the scalenes in the neck. At this point the plexus is oriented up and down and therefore the trunks are superior (closest to your noggin), middle, and inferior.

Subclavian Artery/Anatomical Position: The artery is in front of the plexus at the level of the trunks and then the plexus starts to wrap around it (or at least seems to because we don’t keep our arms straight out to our sides in “anatomical position” at all times). The cords are named for their relationship to the artery. One is lateral (again, if the arm was held out to the side), one is posterior and one is medial (think closest to armpit).

 

Subdivisions of the Brachial Plexus

The parts are: Roots/Trunks/Divisions/Cords/Branches or, as I remember them being a classy east coast Canadian: Real/Truckers/Drink/Cold/Beer

Then you might think, “But how do I remember which of the terminal branches comes off where?” For that I think of the two “M” branches being on the M: Musculocutaneous, Median and (M)Ulnar and that the whole thing together can just be said as “MARMU” Pick the mnemonics you want, the brachial plexus is rife with them. I personally just like the sound of the word marmu.

Types of sutures (and when to use them)

sutures

There are many types of sutures and they differ by size, material and needle. I made this handy chart to help remember how long each type of material lasts in the body and what it’s commonly used for:

50% Strength Gone Reactivity Use
Ethibond
(coated polyethylene)
indef n/an/a + Tendon
Mersilene
(uncoated polyethylene)
indef n/a + Tendon
Nylon 20%/y n/a + Skin
Silk 1 year >2y ++++ Vessel ligation, drains
Prolene
(polypropylene)
indef n/a Skin
Steel indef n/a Tendon, sternum
Fast Gut 6d 20d ++++ Skin
Plain Gut 7d 70d ++++ Skin
Chromic Gut 28d 90d ++++ Oral mucosa
Monocryl
(Poliglecaprone 25)
7d 110d +++ Skin, subcuticular
PDS
(Polydioxanone)
21d 100d ++ Internal organs, fascia
Vicryl
(Polyglactin 910)
21d 90d ++ Skin, soft tissue

Key:
* Monofilament
* Braided

The “Safe Position” for the Hand

safe-position

People can be whiners sometimes. Their hand will be in a cast for some break and you’ll take it off and they will say, “my hand is stiiiiifffff

It’s not just them, the mechanics of their hand is working against them and if the cast wasn’t positioned properly, it can make matters much worse as far as stiffness is concerned. This is why when a hand or wrist is being casted or splinted, care is taken to put it in the position that will minimize stiffness.

The “safe position” is also known as the intrinsic plus position as it favours the weaker motions of MCP flexion and IP extension that are difficult to recover.

Wrist: The weight of your hand, gravity and resting muscle tension all work together to pull the wrist into flexion. When the wrist is flexed, there is more tension on the extrinsic extensor muscles and they pull the MCP joints into extension. The extrinsic flexors are stronger than the extensors and pull the IP joints into flexion. Taking the tension off the extensors limits their pull across the MCP joints.

The position of flexed wrist, extended MCP joints and flexed IP joints is known as intrinsic minus.

Metacarpal Phalangeal (MCP) Joint: These joints are a little funny due to the collateral ligaments on either side. These ligaments pass slightly above the axis of rotation of the joint, this means that when the joint is flexed, they’re at their longest and when the joint is extended, they’re at their shortest. This is due to the famed “CAM EFFECT.” Though often quoted, you have to wonder, what is a cam*? This website explains it well.

* This does not apply to all those people who remember basic mechanical principles or were trained in something more hands-on than neuroscience

Interphalangeal (IP) Joints: The ligaments around the IP joints are at maximum stretch when they are fully extended (aka 0 degrees)

Severity (Classification) of Burns

burn_depth

Burns are typically classified by their depth into (or through) the skin.

  1. 1st degree: just in the epidermis
    • Pink, hot, no blisters
    • Like a typical sunburn
  2. 2nd degree: into dermis, painful, wet
    • Superficial: unruptured blisters, hair & glands spared, erythematous (red) but blanch with pressure
    • Deep: ruptured blisters, hair often gone, can convert to a 3rd
  3. 3rd degree: through the dermis aka full thickness
    • Lack vascularization, dry, leathery, no sensation

Zones of a Burn

A burn isn’t a homogenous spot on the skin; more heat means more damage (who knew!)

  • 40 – 44 C: enzymes malfunction, protein denature
  • >44 C: damage occurs faster than the cell can handle
  • Damage keeps going after the heat source is removed
  1. Zone of Coagulation: The cells are dead and their proteins have denatured. Denatured proteins coagulate – think fried eggs. This is what forms the eschar of the burn.
  2. Zone of Stasis: The cells aren’t quite dead but the blood supply isn’t the best. If the circulation gets worse (usually due to vessel constriction and thrombosis) the cells in this area will die too. This is why it can take a couple days for a burn to “declare” itself.
  3. Zone of Hyperemia: “Hyperemia” means an increase in blood flow, in this case because of vasodilation. The cells in this area are alive and generally recover.

The image above shows a superficial 2nd degree burn. 

The Standard Drink

standard_drink

A “standard drink” is a measure of pure ethanol consumed. One standard drink represents 10 grams of pure ethanol.

This means that based on the alcohol percentage of certain drinks, the “standard” size changes. The important thing to be aware of is to think of it as a Standard Drink because the size that equals 10 g of ethanol isn’t necessarily the standard size that is served. This is why it’s a good habit when asking “how many glasses of _______ do you drink” to ask about the size of the glass.

This design was actually originally made for an event, but I’m reposting it here because it’s useful and I like it and I haven’t had a chance to draw anything new recently.

Maculopapular Childhood Rashes

rashes

BUY THIS AS A STUDY CARD

A kid without a rash just isn’t a kid.

Chicken Pox

  • Incubation: 10-21d, infective until crusted over
  • Rash: vesicles on macules (dewdrops on rosepetals),
  • Very pruritic!
  • Other symptoms: 1-3d prodrome of fever and respiratory symptoms
  • Treatment: supportive, acyclovir for severe disease, VZIG for post-exposure prophylaxis
  • Complications: 1st or 2nd trimester = congenital varicella syndrome

Roseola

  • Incubation: 5-15d
  • Rash: pink macules and maculopapules, starts on neck.
  • Non-pruritic!
  • Other symptoms: HIGH FEVER, cough, respiratory symptoms, erythematous pharynx, tonsils & TMs
  • Treatment: supportive
  • Complications: febrile seizures
  • * Generally affects kids <5 years old

Measles

  • Incubation: 10-14d, dx with measles IgM
  • Rash: maculopapular, starts on face.
  • Non-pruritic!
  • Other symptoms: the 3 Cs
    • 1) Cough 2) Coryza (runny nose) 3) Conjunctivitis
    • Koplik spots in mouth 1-2d before rash
  • Treatment: supportive, prophylactic Ig
  • Complications: secondary bacterial infection, encephalitis (1:1000), subacute sclerosing panencephalitis (1:100000)

Rubella aka German Measles

  • Incubation: 14-21d, infective 5d before rash and 7d after
  • Rash: pink maculopapular, starts on face.
  • Pruritic!
  • Other symptoms: non-specific
  • Treatment: supportive
  • Complications: congenital rubella syndrome (very bad*), first four months of pregnancy highest risk (this is why we check rubella immunity status in prenatal screening)

* Congenital Rubella Syndrome
“Blueberry muffin baby” (purpura). Cataracts/congenital glaucoma, congenital heart disease, hepatosplenomegaly, jaundice, microcephaly, developmental delay

Fifth Disease aka Erythema Infectiosum

  • Incubation: 4-14d, infective prior to onset of rash
  • Rash: slapped cheeks (raised uniform maculopapular lesions on cheeks), may appear on extensor surfaces
  • Usually not pruritic
  • Other symptoms: flu-like illness ~3d prior to rash
  • Treatment: supportive, blood transfusions if aplastic crisis
  • Complications: arthritis (10%), vasculitis
    • Aplastic crisis: reticulocytopenia, not bad in normal people, very bad anemia if you already have chronic hemolytic anemia
    • During pregnancy: fetal hydrops/fetal loss

* This is a good one to actually know the virus name! PARVOVIRUS B19

Other rash descriptors to think about

  • Sandpaper rash: scarlet fever (Group A Strep), they also have strawberry tongue, fever and sore throat
  • Pink macules with central clearing: erythema marginatum (one of the major Jones criteria for rheumatic fever)
  • Palpable purpura: Henoch-Schonlein Purpura
  • Non-blanching petechiae: BAD (meningococcal disease), could be other things too, but need to rule out meningitis

The 6 Hs of Pulseless Electrical Activity (PEA)

6-Hs

When you find someone without a pulse but then hook up the monitor and there is a rhythm, your first thought it probably “CRAP!” But as you start CPR, you need to be thinking about what caused it because not much will help the person except correcting the underlying problem.

So like most of medicine, there is a handy mnemonic for remembering the main causes: The 6 Hs and 5Ts

The 6 Hs

  1. Hypoglycemia
  2. H+ (acidosis)
  3. Hyperkalemia/Hypokalemia (potassium disturbances only get counted once)
  4. Hypovolemia
  5. Hypoxia
  6. Hypothermia

The 5 Ts

  1. Trauma
  2. Tension pneumothorax
  3. Tamponade
  4. Toxins
  5. Thrombosis

(I’ll make a T doodle at a later date)

The other handy mnemonic for the Hs I learned from this video (so I take no credit for it)Diabetic crashing with a wide QRS

  • Diabetic = Hypoglycemia or H+ acidosis
  • Crashing = bad vitals
    • Low BP +/- tachycardia (hypovolemia)
    • Low O2 (hypoxia)
    • Low temperature (hypothermia)
  • Wide QRS = hyperkalemia
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