Inservice Exam

Front 1

Sudden, painless loss of vision, with flashes and floaters

Back 1

Retinal detachment

Treatment: Tilt head back to allow spontaneous reattachment. Optho consult for reattachment

Front 2

Age related macula degeneration types and treatment.

Back 2

Dry type, releases drusen which occludes vision. No proven treatment. Antioxidant vitamins A, C and E may help.
Wet type, new blood vessels occlude vision. Treatment w laser photocoagulation

Front 3

blurry vision is only complaint

Back 3

central retinal vein occlusion. Different from central artery occlusion on fundoscopy. In CVO, blood can get into retina, but can't get out, so you get increased pressure and extravasation (hemorrhage and edema) as opposed to the pale retinal of CAO. No spec therapy, Don't heperinize bc can increase bleading and cause blindnes

Front 4

Back 4

Central artery occlusion.

treatment like stroke.
1. antithrombolytics: aspirin and heparin
2. eyeball massage/pressure

Front 5

Glaucoma pathophys and treatment

Back 5

aqueous humor is made in the ciliary body, travels from posterior to anterior chamber and exits canal of schlem. When iris dilates, scrunches up like rolling up a shirt and blocks exit. Treatment is based on 1) stopping production of AqH w prostoglandin inhibitors, 2) constricting the pupil with beta blockers and pilocarpine, 3) placing a hole to facilitate drainage.

Front 6

What is the diagnoses

Back 6

Abnormal cup to disc ratio from glaucoma. Normal ratio is cup is no more than 30% of ratio. As aqueous humor builds up, ratio increases, can lead to blindness. Must stop production of aqueous humor. Use acetozolamyde, latonoprost, betablockers, pilocarpine, and mannitol.

Front 7

diagnoses

Back 7

Cataracts. Opacification of lens
Caused by trauma, aging, and sunlight.
Treatment is surgically replace the lens

Front 8

Diagnoses

Back 8

Sub conjunctival hemorrhage
Note: sclera is the white of the eye, conjunctiva is the clear layer that extends over the sclera attaching to the cornea (clear layer over pupil and iris) at the limbis. Therefore the blood stops at the limbis. Not sight threatening. Caused by low platelets and trauma. Reabsorbs spontaneously

Front 9

Diagnoses

Back 9

Keratitis, opposite concept of subconjuntival hemorrhage...effects the keratin of the cornea. Site threatening. Often caused by herpes. On visual exam you see nothing b/c cornea is so clear you can't perceive the damage. Pt will have pain, sight threatening, but nothing visible. Use flouracene which binds to the cornea that is denuded (loss of layers) so the damage lights up (same with visualizing cornea abrasion). If damage is from trauma, will grow back in a day. Pitfall. Uveitis is defined as inflammation of the uveal tract of which the anatomy includes the iris, ciliary body, and choroid. The iris regulates the amount of light that enters the eye, the ciliary body produces aqueous humor and supports the lens, and the choroid provides oxygen and nourishment for the retina. When the inflammation is limited to the iris it is termed iritis. If the ciliary body is also involved, then it is called iridocyclitis. Treated with steroids. But if you give steroids to keratitis, you make them blind

Front 10

Back 10

Front 11

Back 11

Front 12

Back 12

Front 13

Back 13

1) A Dennie–Morgan fold, also known as a Dennie–Morgan line or an infraorbital fold, is a fold or line in the skin below the lower eyelid caused by edema in atopic dermatitis. The presence of Dennie–Morgan folds is used as a diagnostic marker for allergy.
2) Ichthyosis vulgaris: very dry skin, fish like scales.
3) Pityriasis alba is a common skin condition mostly occurring in children and usually seen as dry, fine-scaled, pale patches on the face. It is self-limiting and usually only requires use of moisturizer creams.

Front 14

Back 14

1) hyper linear palms
2) Keratosis pilaris is a common, autosomal dominant, genetic follicular condition that is manifested by the appearance of pink tiny papules (rough, slightly red, bumps on the skin). It most often appears on the back and outer sides of the arm (though the forearm can also be affected), and can also occur on the thighs, hands, and tops of legs, sides, buttocks. Feels like goosebumps to pts

Front 15

Back 15

Hand dermatitis: can be atopic, contact, psoriasis

Front 16

Treatment for atopic derm: maintenance

Back 16

Front 17

treatment for atopic derm: therapy

Back 17

Front 18

Dx for Dizziness

Back 18

1) vertigo
2) syncope: arrhythmia, aortic stenosis, orthostatics
3) seizure (electrical)
4) Disequilibrium--elderly+DM+peripheral neurop+night= no sensory input from eyes, "floating"=falls

Front 19

vertigo syndrome

Back 19

nystagmus
vertigo
postural instability
N/V

Front 20

Vertigo types

Back 20

How long does it last?
seconds: BPV
min-hrs: TIA, miniere's (will have hearing loss), migraine variant, recent surgery/trauma (fistula)
DAYS: labyrintitis vs inferior cerebellar stroke. (Labyrintitis will be in the young w no stroke risk and physical exam of peripheral symptoms; inferior cerebellar stroke will be in the older, will have stroke risks, on PE will have central findings.

Front 21

PE for vertigo

Back 21

Look for nystagmus, do complete neuro exam (focal findings?), qualifiying symptoms.
Nystagmus: peripheral vertigo will be horizontal, fatiguable when gazed is fixed, worse towards fast phase; Central will verticle or rotational
Neuro exam: central causes will have focal findings, can't walk. Peripheral will have a romberg where they fall away from fast phase, they can walk but perhaps with difficulty

Front 22

Vertigo treatment

Back 22

labaryntitis can treat with antivert
Central causes, need MRI and admit to ICU

Front 23

GI bleed Approach

Back 23

A-Bring advanced airway and resus equip to bedside, prepare for intubation
B-oxygenate. Low Hb, therefore raise saturation to 100%
C-Hypotensive, give 2L NS/lactated ringer, then blood as needed. If they are on aspirin, think of replacing platelets. Less than 20-50? FFP, 10-15ml/kg. Think about giving desmopressin (DDAVP).
IOUT:
NG tube, folly and follow urine out put, EKG, CXR (looking for free air, correct placement of minnesota tube if used
troponin, PT/PTT, type screen/cross, cbc, bmp/cmp?, lactate?

Front 24

variceal GI bleed treatment

Back 24

octreotide 50micrograms bolus+50micrograms/hr
Abx (ceftriaxone, or cefotaxime, or PO cipro 500-700 x 7 dys)
Protonix 80mg bolus+8mg/hr
Once stable, beta blocker or nitrates
Endoscopy (even if octreotide controls bleeding, always do endoscopy

Front 25

GI Bleed Dx

Back 25

usually upper GI: usually variceal.

Front 26

priapism types

Back 26

low vs high flow
High flow: from things like trauma. Blood is fast in and fast out. No pain. Treat w angiography w interventional radio
Low flow: disease of cavernosa. Caused by vasoactive drugs injections (prostaglandins), sickle cell, and drugs like heparin, steroids in body builders. Treat with ice and exercise, terbutaline 5-10mg PO x 2 q 20min (SC .25-.5mg), phenylephrine PO. If doesn't work inject 1) phenylephrine 200mics, put turnecat at base of penis so it doesn't become systemic and then monitor BP, can give second and third doses. 2) or use epinephrine or norepi injections. 3) or methlene blue (but will turn penis blue a few days) 4) or use sildinofil.
Variant of intermittent priapism in sickle cell. use baclofan, dig, or phenylephrine injections.

Front 27

Dialisis: common complications

Back 27

fluid overloaded and edema before dialisis, fluid depleted after. Fever from bacteria in extracorporal flow.
Increase K before, decreased K after, both can cause arrythmias.
Na, Mg, Ca, dialized drugs can all lead to seizures

Front 28

Dialisis: rules for emergency dialysis.

Back 28

1) refractory increased potassium
2) refractory acidosis
3) acute pulmonary edema
4) coagulopathy (uremia can lead to decrease platelet function)
5) ATN
6) uremic encephelapothy and uremic carditis.

Front 29

dialysis

Back 29

most that die in ED is from sepsis
be careful w RSI, sux bumps K by 1
albuterol decreases K by 1
Dig more toxic with low K

Front 30

esophogeal rupture risk factors

Back 30

scoped recently (can present up to 2 wks after)
ETOH w N/V

Front 31

Esophogeal rupture symptoms

Back 31

fever
chest pain
SOB
subcutaneous emphysema
tachy
(can present looking like PE)
meclers triad: chest pain, vomiting, subcutaneous emphysema

Front 32

esophageal perforation: workup

Back 32

Xray: shows pleural effusion, pneumomediastinum
Esophogram (if xray normal) replace barium w/ water soluble contrast (doesn't rule out if normal)
CT chest (if normal esophogram), doesn't give location of porforation

Front 33

esophogeal perforation treatment

Back 33

Abx
thoraxic surgery consult

Front 34

esophageal perforation risk factors

Back 34

HIV+candida
increase pressure from lifting/#2/vomit
tubed
scoped

Front 35

Hematemesis approach

Back 35

Two populations
1) actively bleeding
Give erythromicin 3mg/kg IV 30 min before scope
2) Reported bleed
NG tube (doesn't rule out

Front 36

Hematemesis epi

Back 36

most common causes are variceal, followed by PUD

Front 37

Hematemesis treatement

Back 37

80% stop bleeding w/out treatment
of those who rebleed, most do so in first 72 hrs
decreasing acidity lowers chances of rebleed (raise stomach pH above 6)
protonix 80mg bolus + 8mg/hr infusion
octreotide will help non variceal bleeds as well
add abx early in variceal bleeds
pressure on variceal veins causes rebleed,

Front 38

Hematemesis workup

Back 38

check level of increase heart rate and decreased BP
check liver failure symptoms (variceal)
NG tube
check H/H
endoscopy