Family Medicine Deck 1 Flashcards

1
Q

New Mammogram Guidelines from the American Cancer Society

A

Start at 45 unless risk factors exist
Annually 45-54
Every 2 years 55 + until life expectancy is less than 10yrs
Clinical Breast Exams are NOT recommended

The radiologists still recommend annually after 40 (for obvious reasons) and the U.S. Preventive Services Task Force still recommends every other year after 50. Congress trumped the task force recommendation though with a ‘ you still have to cover annual mammograms from 40+

Dr. Leohr recommends annually after 50 and is doing away with routine breast exams and breast exam education though women will continue to be encouraged to “know their own lumps and bumps”. He explains the differing opinions to his patients

Barb and Dr. Howsen continue to do breast exams annually and recommend mammogram with explanations like Dr. Loehr

Dr. Ryan doesn’t routinely do breast exams and recommends mammogram annually after 50 with explanations like Dr. Loehr

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2
Q

Natural and effective cough syrup

A

Buckwheat Honey

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3
Q

PMDD (Premenstrual Dysphoric Disorder) High impact low dose medication protocol

A

Prozac 10-20mg (Deb says 10, Jamie says 20) days 18-28

Sarafem is the product approved + marketed for PMDD
and it comes in 10, 15 and 20mg doses

Why fluoxatine as opposed to a different SSRI? Fluoxatine has a LONG half life and leaves the blood slowly. There is less chance of SSRI with drawl. You can go from taking it daily to every other day to every three then weekly and so on. Some people with mild depression do take it weekly or every three days. Whereas if you miss a day of Paxil or Effexor there WILL be withdrawal sxs.

SSRI withdrawal sxs: NVD, headache, sweating, tremor, insomnia or somnolence, fuzzy brain, psychosis even.

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4
Q

1st line antibiotic for anything skin

A

Keflex (Cephalexin)

Drawback - QID dosing

staphlococcus, group A beta-hemolytic streptococcusHaemophilus influenzae, Klebsiella spp, Moraxella catarrhalis, Proteus mirabilis,

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5
Q

Tekturna/ Aliskiren Hemifumarate

A

HTN Med with FEW unintended side effects. Hyper-K+
Is an unwanted side effect of inhibiting RAAS anywhere
since Sodium is not conserved (this is what lowers BP) it
isn’t exchanged for K+. Thus K+ remains in the serum
and Na+ is flushed in the filtrate.

-Direct RENIN Inhibitor, stops RAAS at the 1st step
by binding renin’s active site and preventing
Angiotensinogen, thus preventing activation of
Angiotensinogen to Angiotensin II
-Since Angiotensinogin and Renin ONLY BIND each
other, stoping RAAS at Renin does not much about
in other systems whereas Inhibiting Angiotensin II with
an ACE has impact anywhere Angiotensin II impacts
(such as the lung and that blocked bradykinin cough)

RISKS: Don’t use a Renin Blocker WITH and ACE/ARB
and DONT use it in DMII or Renal Impairment.

Do use it with a HCTZ (Tekturna HCT) if mono therapy isn’t enough.

Tekturna is 3rd gen and an even more bioavailable 4th gen is expected to gain FDA approval soon

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6
Q

Reiter’s Syndrome

A

AutoImmune Triad:

1) Inflammation of Lg Joints
2) Inflammation of Eye (Conjunctivitis/Uveitis)
3) Nongonoccocal Inflammation of Urethra (in men) or Cervix
4) Hands and feet: Enthesitis (at Achilles insertion or at Plantar Fascia)

A syndrome of reactive arthritis wherein the immune system gets excited by an infection somewhere and goes a little crazy. Key will be pain/burning on urination in men that is not caused by infection (UA will be Negative) but a CBC may be positive for infection elsewhere (usually lower GI or Urogenital infection. Common bugs that trigger are: Salmonella, Shigella and Chlamydia. Gonorrhea has its own arthritis…)

DX: mainly clinical, look for the triad, swab and test before treating. HLA-B27 is a genetic marker that is + in 75% of Reiters patients. CRP and ESR should be + but RF should be negative as should lupus marker ANA.

Rx the initial infection first - if you don’t know where it is, go broad with your antibiotic.

Rx the overactive immune system next if neutralizing the infection doesn’t work. Steroids, Methotrexate, Sulfasalazine… If there is uveitis, refer for eye exam asap.

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7
Q

Pitting Edema

A

Press for 5 seconds, if pit remains, you have it.

Legs + Ankles in Ambulatory Patients

Sacral area in bedridden patients.

+1 to +4 are the casual references. +1 leaves a good thumb-print. +4 you might leave a 2-3 inch deep indent, very severe.

Note how far up the leg the pitting extends (measure it)

Measure circumference. Pick a distance in centimeters that you’ll remember like 20cm. Measure down from the knee joint and always measure calves at that point so you’ll know exactly where you’re measuring on all your patients and can compare from one visit to another.

Rx is essentially Diuretics. Loops if its really bad. Of course, this is a huge flag for CHF so consider that. This is a good place for a LOOP but watch your

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8
Q

Loops block

A

Na/K/Cl Transporter in the thick ascending loop of Henley.

They FLUSH everything: Na+, K+, Mg+, Water… so be on the lookout for electrolyte derangements on the HYPO side.

By flushing all that water, they lower blood volume and decrease swelling and BP so watch for Orthostatic HypOtension

Reducing blood water content is a risk for concentrating Uric Acid and can precipitate a BOUT of GOUT. Not a good choice for a gouty person.

If renal function is poor, Loops won’t work so well and higher doses may be needed or addition of a HCTZ can be considered.

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9
Q

Hypo Natremia sxs, Causes, dx, rx:

A
Sxs:  Nausea/Vomit (early)
         Altered Mental Status
         Muscle Weakness
         Twitchy, Seizure
          Coma (always check electrolytes asap in coma)

Cause: Na+ loss via failure to concentrate urine or Meds
or a massive increase in blood volume via edema.
-SIAH
-DM
-

DX: Normal Serum Sodium is 135-145. Its severe if below
125 mEq/L

Rx: NS IV

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10
Q

Coma Cocktail for:

A

Any Coma of Unknown Origen:

D: dextrose, 
O: OXYGEN
N: naloxone and flumazenil for benzos
T:  thiamine for Alcoholic Encepalopathy/Wernike
     Korsakoff's Psychosis
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11
Q

UTI

A

1st line Macrobid (Nitrofurantoin)
- 100mg BID X 7 Days
- Turns Urine Brown
- Acute Pulmonary Sensitivity Possible (very rare)
STOP med
CXR will show infiltrates like pulm edema
-Hepatoxicity poss with long term rx

-Really only kills E Coli these days so infection from a
different bug (GC/Chlam, Pseudom) will get worse…
-Not in pregnancy AFTER WEEK 38 as it may
cause hemolysis in the newborn whose system
is separating from will not have the ability to break it
Mom’s at that point but won’t yet be able to
metabolize glutathione.

2nd Line: Bactrim DS BID X 10 days

3rd line; Cipro
-500 mg BID X 3-5 days (Mild Only) otherwise 7-14 days

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12
Q

Phimosis, Paraphimosis

A
Phimosis= Foreskin closed at tip
Paraphimosis= Foreskin stuck behind glans 911!!

Steroid Cream to help foreskin loosen after age 9 and slide more easily but stopping may allow recurrence

Circumcision is the final fix if manual stretching during normal childhood exploration does not result in an easily sliding foreskin.

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13
Q

HypOmagnesemia

A

Sxs: WEAKNESS, muscle cramps, Torsades, VTach ,Tetany

Cause: Diuretics are the most common cause as Mg is
reabsorbed in the loop of henley, which is
the target for most diuretics in one spot or
another.
Alchoholism + Thiamine Deficiency
Inpatients often suffer electrolyte
derangement.
- Digitalis can cause it
-HypERmagnesemia almost always
caused by meds, usually diuretic.

Dx: 1.5 - 2.5 mg/dL is normal

Rx: Oral replacement for mild
IV Magnesium Sulfate for Torsades and Ecclampsia

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14
Q

Kernig and Brudzinski

A

MENINGITIS CLINICAL TESTS

Kernig: Lie flat, knees bent, GENTLY lift head toward
chest. Pain in neck/back is +.

Brudzinski: Lie flat, knees bent, passively lift lower leg and extend until straight as in sciatica stretch. Pain in neck, back is +, pain in hamstrings is NOT

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15
Q

Wellbutrin’s marketing name as a smoking cessation product:

A

Zyban

Recall Wellbutrin/Bupropion is a NorEpi Dopamine Reuptake Inhibitor.

The other one is Chantix- a different animal altogether being a “Partial Cholinergic Nicotinic Agonist”

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16
Q

Bronchiolitis: Sxs, Cause, Dx,

A

j

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17
Q

Buspar MOA

HOW do we use Buspar?

A

5HT3 Partial Agonist

Take care in using with other Serotonergics.

You can use Buspar as a mono therapy for Anxiety. It takes a while to work and dose adjustment should be approached slowing to ensure it has TIME to work. Works nicely with Melatonin (taper melatonin, not a forever drug). Unlike Benzos, its not addictive and there isn’t a difficult withdrawal syndrome.

You COULD use it with low dose xanax for rescue.

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18
Q

FODMAPS Diet

A

n

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19
Q

Holmes-Adie Syndrome

A

k

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20
Q

INR Ranges

Afib
Mech Valve

Antibiotics not with Warfarin

INR Formula while on Antibiotics

A

Afib 2-3

Mech Valve 2.5-3.5

All abx will cause a change
Avoid Macrolides, Bactrim, Metronidazole, TB Antibiotics
Avoid
Cephalos are OK
Pen VK or Pen G are fine
Monitor Dicloxacillin and Nafcillin for incr. INR
Tetracyclines require monitoring for incr INR

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21
Q

Warfarin + Heparin Antidotes

A

Vit K and Protamine

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22
Q

If Acute Otitis Media presents with prurient Conjunctivitis what should you prescribe in an under 5?

A

Augmentin

You will skip the Amoxacillin step and proceed right to Augmentin even in an under 5.

80-90mg/Kg/day under 6 BID X 7-10 days

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23
Q

Desmopressin for clotting? DDVAP

A

Usually we see it for nocturnal enuresis in kids or for
SIADH or even for plummeting Bps in the ED but…..

A "side effect" of Desmopressin therapy is clotting factor 
up-regulation.  DDVAP increases serum:
Von Willibrand factor
Factor 8 and
TPA
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24
Q

Von Willibrand management?

A

DDVAP
Progestin
Hormonal Birth Control for females

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25
Q

Mono…

A
Sore throat
Fever
Prurient Tonsils
Swollen posterior Nodes
Swollen Submandibulars
Tender Spleen
Malaise

Monospot won’t work until 10 days in to sxs
Strep will be Negative, rapid and culture

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26
Q

Pertussis/Whooping Cough

A

After 21 days of coughing, no longer infectious

  • Before 21 days, quarantine the child
  • Treat family and contacts with Zithromax
  • Refer to Health Department
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27
Q

A1C values in pregnancy. Is there a special scale that accounts for the increased blood volume and thereby the increased total Hb?

A

k

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28
Q

Thyroglossal Cyst

A

k

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29
Q

Normal TSH

A

Adult 21 to 54 yrs 0.4 - 4.2

Adult over 55 yrs 0.5 - 8.9

30
Q

Wegener’s Vasculitis

Granulomatosis with Polyangitis

A

Inflammation of the sm/med size blood vessels:

Classic Triad is:
1) Upper Airway damage: Eye/Nose/Pharynx/Trachea
2) Lower Airway damage: Asthma/Fibrosis, Granlomas
3) Kidney Damage: Progressive Glomerulonephritis
with
ANCAS (Anti-neutrophil Cytoplasmic Antibodies) on biopsy

  • Lung + Kidney Damage can be fatal
  • It’s an autoimmune thing, managed by Rheumato.
  • Saddle Nose, septum gets attached
    • Uveitis
    • Scleritis
    • Tracheal Stenosis
  • Asthma, Difficulty breathing, Granulomas in Lung not TB

-Glomerulonephritis, glomerulus gets attacked
-Kidney Biopsy shows ANCA (anti-neutrophil
cytoplasmic antibodies)

RX is Immune Suppressant

  • Rituximab: CD20 Mab
  • Methotrexate
  • Corticos
31
Q

Centor Scale for…

A

Strep Throat

If you google it, you may find an actual calculator @ MDcalc.com

Point system for whether to rapid strep or treat w/o rapid or not at all:

Age 3-14      +1 point
        14-44    0 points
        45+      -1 points
Fev 100.4+   +1 point
Cough          0 points
No Cough    +1 point
Cerv Aden   +1
Tons. Exud   +1 points

3 Points: Rapid Strep
5 Points: Empirically Treat, no test, Penicillin or Amox

32
Q

Gemfibrozil

A

l

33
Q

Eaton-Lambert Syndrome

A

Autoimmune, Antibodies to Voltage gated Ca++ channels

Presents like Myasthenia Gravis(MG) with muscle weakness

 - proximal arms and legs, close to trunk
 - Not usually eye ptosis, differs from MG on that

“Lambert’s Sign” Strength improves with repeated testing
-doing the hand grip or leg strength testing in series
improves results. Not so in MG

34
Q

Rhinorrhea vs coryza

A

Rhinorrhia is a runny nose, not necessarily stuffy
often the cause of post nasal drip, just too much
mucus being produced due to cold/flu/allergy etc

Coryza is inflammation of the nasal membranes.
This is the stuffy nose, it can be runny but
doesn’t have to be. It often makes one feel off
balance.

Rhinitis is inflammation of the entire nose and it’s
usually runny too.

You can be so unlucky as to have all three together - commonly seen in the COMMON COLD

35
Q

The COUGHS… Causes and Treatments…

 Lingering with fits:

 Barky, worse at night:

 Wet, Productive:

 Dry Cough:
A

Lingering with fits: Pertussis/Whooping cough. Starts w/a
cold, stuffy nose, low fever. Cold sxs resolve in 5 or
so days but cough worsens into fits that interfere with
breathing. There may be an actual
INSPIRATORY WHOOP, a high pitched effort to inspire
during a coughing fit. There may be coughing unto
emesis. Or there may be neither.
Rx: It will self resolve so long as breathing is not
overly impeded but Macrolides are the RX
Contageous during Catarryl stage, isolate for
3 weeks from onset of cold sxs and treat the
family and daycare contacts, alert Health Dept
Vaccine in weak in Pertussis so exposure is a
Risk for all, vaccinated and unvaccinated alike

BARKY, Worse at night: CROUP …Multiple Pathoghens
include RSV, Parainfluenza, Adenovirus, HIB
Moraxella, Strep Pyog + Pneumo, even Dyptheria
and Staph cause it, more commonly virus but not
always.
The BARK is from swollen larynx + trachea d/t
being overrun with WBCs
So… VACCINATE…. Use Cold shower mist (NOT
HOT!!!)
If Inspiritory STRIDOR is present and/or
RETRACTIONS/TRIPODING, RACEMIC EPI and
steroids are needed, this is SEVERE CROUP, a 911.

Wet/Productive: Gunky stuff like the common
cold (Adenovirus) or the catch all URI. Bronchitis
is productive as is Pneumonia. Bronchitis isn’t usually
feverish and gunk clears somewhat on coughing.
Pneumonia is feverish, often very high
Rx COLD: Rest, Fluids
Rx BRONCHITIS: Viral, Rest, Fluids NO ABX
Rx PNEUMONIA: CXR then usually MACROLIDE
Could be Viral ( RSV, Para Influenza)
usually in winter only though. If there is fever,
Chest Pain and chills, most likely bacterial.
-Comm Acq is usually Strep Pneumo and you can
still treat this with Pennicillin. I would
choose Augmentin myself. Can use Doxy or
a Macrolide, Clarithromycin not Azithro.

Dry Cough:  IRRITATION
     Allergies
     Pollution
     GERD
     TB
     Cancer
36
Q

Cough Last Average of 18 days… Citation

A

Ann Fam Med. 2013 Jan-Feb;11(1):5-13. doi: 10.1370/afm.1430.
How long does a cough last? Comparing patients’ expectations with data from a systematic review of the literature.
Ebell MH1, Lundgren J, Youngpairoj S.

37
Q

Review of the GABA Receptor

A

GABA activation of its receptor CALMS the NERVES/CNS

2 kinds of GABA receptor: Gaba-A + Gaba-B

GABA-A are FAST Ligand gated Cl- Ion Channels. Activation opens the channel allowing negative Cl- ions to flood the neuron. This lowers the resting potential of the membrane making it impossible to reach threshold and thereby impossible tofire an action potential. The neuron is quite effectively “Calmed”

 - GABA (gamma amino butyric acid) is THE ligand and as the only other thing that binds directly where GABA binds is     
 - Mucimol, the active agent in psyilocybin mushrooms which are hallucinogens.

GABA-B is a G-Protein Coupled Receptor, meaning it is a massive, folded protein in the membrane of the neuron which senses rather than binds it’s ligand GABA, then changes shape which kicks off intracellular activities that depolarize the neuron far more than does opening the Cl- ion channel via GABA-A. This prevents the neuron from firing an action potential for much longer than does activaton of GABA-A.

GABA AGONISTS
-GABA activates both the A and B
-Baclofen- Central muscle relaxant, rx for spasticity
Activates Gaba B receptor but not A

PAMs (positive allosteric Modulators) do not activate
A or B but, when GABA is bound to A
PAMs enhance its action, opening the Cl-
ion channels wider and keeping them
open longer. They don’t have any effect
though when GABA is not bound to A.
PAMs bind the GABA receptor at a site
protein receptor that changes shape
(allostearic) and kicks off some intra-
cellular change that modifies the
GABA A receptor.

GABAPENTINOIDS are derivatives of GABA. They don’t bind GABA A or GABA B but they BLOCK the voltage-
gated Ca++ channels on the same cells that bear GABA A and GABA B receptors, namely excitable cells/neurons. If Ca++ cannot flood the cell, the intracellular charge cannot rise to threshold and an action potential cannot be kicked off.

So… GABA (gamma amino butyric acid) is the endogenous neurotransmitter that ‘calms’ neurons by binding its receptor and opening Cl- channels to hyper-polarize the neuron, making it so negative it can’t possibly be brought to threshold. If it can’t get to threshold, the voltage gated Ca++ channels can’t open and no action potential can be propagated (i.e. the cell can’t be excited, i.e. no seizure, no spasm, no anxiety….) . If we want to manipulate the effect of GABA with meds we have several choices: we can give BACLOFEN, which actually binds were GABA itself binds, albeit more weakly than GABA. We can give a PAM, to bind it’s allostearic protein and enhance the effect of GABA at GABA-A or…. we can give GABAPENTIN or PREGABALIN (Lyrica) which acts entirely independently of GABA by blocking the voltage gated Ca++ channels and keeping the intracellular voltage below threshold in that way. GABA itself has nothing to do with Ca++ channels but in the end, blocking Ca++ influx achieves the same effect as increasing Cl- influx.

38
Q

Headache, Neck Stiffness, Fever, Altered Mental Status

Think….

A

Meningitis. Rule this out before proceeding with Ddx

Workup: Lumbar Puncture w/opening pressure, cell count
CSF chemistry and Culture
*Be sure to check FIRST for PAPILLOEDEMA
as it’s presence makes LP high risk for
BRAIN HERNIATION which presents as
decreased GCS, decerebrate +/or decorticate
posture

              CT before LP if Papilloedema or any 
               Neurologic defects are noted, esp SEIZURE
                But start antibiotics ASAP

                If there is pneumonia on CXR or clinically
                Think step pneumo for the meningitis bug

                 Get blood cultures, nasopharyngeal swab
                  and cultures of any skin lesions before
                  LP and before starting antibiotics

RX:  Treat SHOCK with IV fluids and O2
       AGGRESSIVELY control SEIZURE 
               -Lorazapam 0.1mg/Kg IV with either
               - Phenytoin 15mg/Kg IV or for children
               -Phenobarbitol 5-10mg/Kg IV
        -Empiric ABX should be broad and if pt is Acute,
        add Dexamethasone simultaneous to IV ABX.  
                 -neonate:  Ampicillin + Cefotaxime
                 -1mo to 50yrs:  Vanco + Ceftriaxone or 
                  Cefotaxime  Vanco get through BBB during
                   infection because it's more porous.
                 -Over 50 yrs:  Vanco + Ampicillin + Ceftriaxone
                 -Ceftriaxone handles strep pneumo better
                   than Cefotaxime d/t resistance

If you suspect actual Neisseria Meningititus Cephtriaxone is the drug of choice so you should be ok starting the Vanco-Cephtriaxone IV.

Add Doxy to the empiric mix if it’s tick season or you think it’
might be syphillis.

Vaccinate contacts and Rx with Cipro for Neisseria

  - Cipro 500mg single dose for adults
  - Rifampin 4 doses in 2 days for adults and children alike
  - Children only, 1 IM Ceftriaxone by body weight
39
Q

Why use Digoxin in Heart failure

A

It both enhances ventricular contractility and reduces AFIB
by enhancing vagal tone and actually slowing the SA firing.

Beta Blockers are preferred for rate control in general in AFIB but if there is AFIB and Heart Failure, Dig might be just the thing

40
Q

Testing for HIV

A

ELISA for screening

WESTERN BLOT for confirmation , though this will not tell
HIV1 from HIV2 so the newer HIV1/HIV2 p24 antigen test with RNA evaluation is gold std over the western blot but not as available. The newer test is more sensitive , earlier

41
Q

CSF: Bacterial infection findings vs viral

A

Bacterial CSF or FUNGAL:

  • Cloudy CSF
  • High opening pressure (over 25mmHg, norm = 10-20mm)
  • Low Sugar
  • Increased Protein (over 50)
  • WBCs over 100/microliter

Viral:

  • Clear CSF
  • Normal opening pressure of 10-20mmHg
  • Elevated WBC over 1000, lymphocyte shift
  • Sugar usually normal
  • Protein elevated as in bacterial (over 50)
42
Q

Nursemaid’s Elbow

-Presentation, Dx and Rx

A

Anxious child guarding one arm (can be bilateral though…)
Parents describe child suddenly refusing to use arm
-Pulling arms through coats
-Swinging child between 2 parents or pulling wrist/hand
-Affected arm is usually slightly flexed + pronated
with weight of the arm supported by non affected hand

Radial Head Subluxation is the technical name. The radial
head is lashed to the ulna by the annual ligament, like a thick fibrous rubber band. When the wrist is pulled and twisted just so… it slips out of the annual ligament, down just a bit. The ligament gets caught then between the slipped radial head and the distal humerus at the elbow joint. If the radial head is also dislocated, there may be a lump visible because the head will have completely slipped it’s annular ring and been pulled up by the brachioradialis muscle. This is more difficult to fix.

Get an X-Ray if there is Hx or indication of a fall/fracture otherwise….

Rx is MANUAL REDUCTION of the subluxation/dislocation.
-Supination during elbow Flexion while applying
pressure over the radial head is the fix. A click means
you did it. Have the child reach for a popsicle to prove
its fixed.
- Fully extend the arm in supination while supporting
the elbow with other hand. While applying pressure
to the radial head at the elbow, Flex the arm in
supination. Try 2-3X then get an X ray if it won’t
pop.

43
Q

Buckle Fracture/ Torus Fracture of the distal radius

A

Usually children as result of a FOOSH. Its an incomplete
compression fracture which differs from the greenstick
in that it is not and likely will not displace, whereas
greenstick may displace. Usually at the distal radial metaphysis at the wrist.

There will be severe pain and guarding and Hx of a fall so
XRAY that forearm!!!

Xray will not show a definitive fracture but perhaps a
slight bulging will be seen near the growth plate but not through it.

Rx is splinting or casting if splinting is not tolerated. Volar wrist splint “cock-up” encircles the thumb and supports the wrist while leaving the fingers free to move. Also sold under the name Futuro.

44
Q

Basal vs Squamous Cell Carcinomas

A

Both are Non-Melanomas

Basal: Think NOSE, head, neck, shoulders…
-Pearly white or pink Dome with TELANGIECTASIAS
- Doesn’t metastasize
-Could be blue, black or brown but always domed
- Often umbilicated or w/central atrophy + a raised ring
This type is called Superficial as contrasted with
domed and sometimes looks like psoriasis or even
tinea - but it has telangiectasis and tinea doesn’t
-Telangiectasias are the key

Squamous: Arises from Actinic Keratoses
- Scaly red plaque usually with central ulceration
often described as a lesion that won’t heal. Actinic
Keratoses are usually brown, when they morph to
Sq. Cell they turn red/pink.
-NO TELANGIECTASIAS ON SQUAMOUS CELL
it gets it’s nutrients by invading the dermis
-Metastasizes in 5% of pts
-Keratocanthoma looks like a horny scab on a red
papule. It’s not cancerous but must be tested
-Punch biopsy it and if +, get it all off.

Rx is essentially the same: cut it out, freeze or burn it off
If that doesn’t work, Mohl shaving is gold std but
usually reserved for larger plaques.

45
Q

Clinical Presentation of Insulin Resistance

A

-Obesity, esp Truncal
-BMI over 25 (esp over 30 which is obese)
-Hirsuitism in females
-Acanthosis Nigrans
-Cystic Acne in females
-Frontal Baldness in females
-Menstrual Irregularity or Infertility in females
-Hyperglycemia sxs like fruity breath, dyspnea
altered mental status, extreme thirst
-Xanthelasma at the eyes
-Foot ulcerations in setting of truncal obesity

46
Q

Ant/Post Drawer and Lachman Tests for …

A

ANT. CRUCIATE INTEGRITY

Anterior Drawer: Tests integrity of ANT. Cruciate Ligament

  • Pt supine, Knee bent
  • Sit on foot
  • Pull tibia anteriorly. If it moves, ACL is compromised

Posterior Drawer: Same position, press backwards.
-Take care, if they’re both torn, the tibia will wiggle on the
femur.

Lachman: ACL integrity , Superior to Ant. Drawer test

  • Pt supine
  • Grasp femur and tibia
  • Push femur DOWN and tibia UP
  • Wiggle room suggests ACL tear
47
Q

McMurry Test for …

A

McMURRY for MENISCAL TEAR

-Pt supine
-Raise lower leg, flexing knee at +/- 90 degrees
-YOUR hand across the flexed knee joint while applying valgus force to the knee (inward) and simultaneously
Rotating the lower leg essentially in a circle, hitting both
internal and external rotation.

48
Q

TSH Range

A

k

49
Q

Hypothyroid

A

Fatigue, Constipation

50
Q

Metanx

A

k

51
Q

BPPV,
DX
Rx?

A

Dx: Dix Halpike
Rx: Eppley

Describe

52
Q

posterior cervical nodes drain

A

m

53
Q

Mg Deficiency and Heart Disease

A

-Mg concentrated in Left Ventricle
-Mg ++ controls Ca++ EXIT from myocytes. If Ca++ doesn’t
exit on time, the LV hyper contracts, stays contracted
longer and gets tired (heart failure and hypertrophy)

  • Mg++ is lost when we supplement Ca++
  • Need 700 mg of Mg and 700mg of Ca / day

-Best test is RBC Mg test, serum Mg not very helpful
Most labs offer the RBC Mg test

-Figs, Prunes, Avocados, dried dates are all rich sources,
of Mg++ Epsom bath soaks and Mg spray are nice as its
best to take Mg in slowly. Divided oral doses or transdermal.

54
Q

How does cacao help prevent CVD? What veggie can decrease HTN in males if consumed regularly?

A

Cacao flavanoids activate nitric oxide synthase in humans, which in turn liberates NO2 which in turn dilates smooth muscle. Catechins are also known to have protective pleotrophic effects, up regulating protective genes. Go for 1000 mg of epicatechin (a cocoa flavanol) per day and retest HTN after 4 days. Note, cacao and milk chocolate are not equal and “dutched” cocoa is no good….
http://www.medscape.com/viewarticle/855226?nlid=92659_764&src=wnl_edit_medp_imed&uac=229172HX&spon=18&impID=914729&faf=1#vp_2

+Catechin (the most powerful flavanoid isomer) and Epicatechin can be purchased straight up these days. As are all flavanoids, its a benzene ring-based compound. Highest in It is also found in white tea (highest conc. of the teas) then green + black tea respectively, red wine and prune juice in high concentrations.

BEETS lower HTN, unfortunately better in males than females. A beet a day… and an avocado and a little bitter cocoa with no sugar.

55
Q

elevated amylase

A

Something’s up in the pancreas, possibly acute pancratitis.

Alcoholic (males over 35: 4-5 ETOH/day X 20 yrs is the risk category)? ETOH sets off the inflammatory cascade in ascinar cells. Acute is resolvable. Stop Drinking. Chronic is not resolvable.

Acinar cells produce the pancreatic digestive enzymes, including amylase and lipase. When they rupture, they release them into the blood stream and into the abdominal cavity where they digest all manner of things they ought not.

GALLSTONES:
Stone blocking the Ampulla of Vader - common bile duct meets pancreatic duct) or in the common pancreatic duct or even further on at the Sphincter of Odi (Fat, Female, Forty…)? Small gallstones are the culprits here as large ones get stuck inside the gallbladder but little ones can get down into the ducts. Can lead to chronic pancreatitis.

 Dx:  RUQ, Epigastric Pain?  Murphy may or may not be
         (+).  Sonogram will tell you if there are stones inside
         the gallbladder or if there is gallbladder wall 
         thickening but it isn't great for the Hepatic,       
         Common Bile and/or Pancreatic Ducts.  For those   

         you NEED
         a HIDA scan to find blockages.  So... Physical Exam, 
         then sono and, regardless of whether sono is + or -
         order the HIDA.  It will catch what sono missed and
         even if sono was +, it will flesh out exactly where
         stones are lodged.

 Rx:  get those gallstones out at first sign, BEFORE bits
        break off and the pancreas gets involved.  Likely this
        means Cholecystectomy but perhaps ERCP can get 
        and get them out if they're tiny.  Still, the gallbladder
        will keep making them if it already is making them 
        unless massive lifestyle changes are made that 
        include balancing hormones, decreasing 
        cholesterol intake, promoting bile salt secretion in
        the liver (obviously, cirrhosis undermines this so
        d/c the ETOH and other toxins...).  

        You can also try to dissolve cholesterol stones AND
        pigment stones alike by increasing BILE SALTs, as 
        they are usually the missing ingredient in bile:  

UROSIDOL (Actigall) and CHENODIOL (Chenix) are BILE ACIDS that get recycled via the colon and the enterohepatic circulation back to the liver and made into new bile salts by addition of taurine and glycine. Taurine and glycine have to be added to bile salts before they’re incorporated into bile because otherwise, they’d be too acidic and would ulcerate the duodenum on contact. If the liver is diseased though, they won’t work or if the colon can’t reabsorb them (constipation) they won’t get back to the liver… They’re best for dissolving tiny stones, it can take years, Meanwhile, acute and or chronic pancreatitis remain risks.

         If the gallbladder is removed, or patients are up
         for lifestyle changes, Dr David Williams
         recommends supplementing bile salts as the 
         compromised gallbladder doesn't have enough
         of them and is therefore making stones of its
         excess cholesterol and/or the removed gallbladder 
         is no longer concentrating bile salt at all and
         so fewer salts  are getting to the intestine. He
         recommends CHOLACOL by standard process, 2
         tabs w/meals.  Sauerkraut or its juice 1-2x a week for 
         breakfast, beets and artichokes.  

Surprisingly, acute pancreatitis is 3X more common in African Americans than whites.

56
Q

How do gallstones form?

A

Bile is made up of Cholesterol, Bile pigments (bilirubin) and Bile salts. The ratio is critical so, if there aren’t enough
bile salts, for instance, then there is excess cholesterol and it gets made into cholesterol stones. If there is too much bilirubin coming from the liver (as in cirrhosis or Hepatitis or other liver disease that raises Billir) then there will be left over bilirubin and “Pigment” stones will result.

Bile salts are made in the liver from TAURINE ( AA in fish + meat) and GLYCINE ( AA synth by the liver or found in gelatins). Glycine is synthesized from SERINE, AA also found in protein rich foods, meats eggs, dairy, soy, asparagus. A diseased liver may not make glycine from serene though…

CONSTIPATION reduces the liver’s ability to make bile salts because the bacterial flora in the colon remove taurine and glycine (now waste products) from the bile salts that get down there and this makes the remaining bile acids reabsorb-able. The bile acids are recycled back to the liver via the ENTEROHEPATIC circulation and remade into Bile salts there by being conjugated with new TAURINE and GLYCINES.

Bile acids have to be conjugated before they get released into the pancreatic duct and into the duodenum as they would otherwise be too acidic . Note the SECRETIN is released in response to CHYME pH and causes the Pancreas to secrete BiCarb FIRST thing upon chyme entering the duodenum and Bile gets secreted somewhat later after CCK signals the Gallbladder to contract and the liver to make more bile. The liver needs to keep making bile throughout the meal as it takes a lot of it to emulsify the fats into micelles, that’s why the enterohepatic system in the terminal ilium and colon recycles bile acid back to the liver throughout the meal. If this didn’t occur, the bile stored may not be sufficient to the task of emulsifying the fat in even a single meal. Plus some bile gets stuck in feces and is excreted.

Bile acids taken orally don’t seem to harm the duodenal mucosa, perhaps because the pancreas is able to adjust the pH since they’re coming in from the stomach instead of being secreted into the pancreas as they would be if the liver just wasn’t conjugating acids to salts?

To improve Bile Salt Production Dietetically:
Add Taurine, Serine and Glycine rich foods to the diet. Stop drinking ETOH, Increase fiber and water to ensure constipation isn’t mucking up the bile acid recycling system and add actual bile acids or salts to the diet if necessary. Personally, if I was trying to treat gallstones without surgery or ERCP, I would go right for the prescription bile acids: UROSIDOL + CHENODIOL, unless Hepatitis/Cirrhosis/constipation would prevent them working, then I’d go straight to ingesting bile salts themselves per Dr. David Williams OTC Cholacol.

SXS of excessive bile salt supplementation will be diarrhea as salts the colon cannot reabsorb are laxative.

57
Q

Cholescintigraphy, other name?

A

HIDA scan

Radioactive contrast collects in the gallbladder (DO REMEMBER TO ORDER THE SCAN with CONTRAST!!!) and then the gallbladder is induced to contract by injection of Cholecystokinin (CCK) and photos show where the radioactive bile gets stuck.

58
Q

Low Bile Acid and Weight Gain???

A

This article is mostly about how impaired gut flora decreases bile acid creation from bile salts in the colon and how the decreased bile acid recycling leads to hypercholesterolemia and adiposity in the host (aka the patient).

It might be extrapolated from there that absence of a gallbladder will most likely result in fewer bile salts getting to the colon to be recycled and thus we might conclude that gallbladder removal is itself an independent risk for obesity and that bile acids or bile salts ought to be added back into the diet directly as the original system by which they are concentrated has been removed.

Biological Sciences - Microbiology:
Susan A. Joyce, John MacSharry, Patrick G. Casey, Michael Kinsella, Eileen F. Murphy, Fergus Shanahan, Colin Hill, and Cormac G. M. Gahan
Regulation of host weight gain and lipid metabolism by bacterial bile acid modification in the gut
PNAS 2014 111 (20) 7421-7426; published ahead of print May 5, 2014, doi:10.1073/pnas.1323599111

59
Q

Post Cholecystectomy Syndrome

A

NVD, bloating and RUQ pain after eating following gallbladder removal.

Common, up to 40% of pts experience it.

Could be that the stone formation problem wasn’t the gallbladder, it was just most obvious there as the stones can get so big during bile concentration and storage. Microstones can still get generated in the liver when bile composition is out of whack and thus those stones just roll on down the hepatic ducts to the pancreas wreaking havoc as they go…

This is a case for balancing the bile composition!! Most likely the bile acids are either not getting reabsorbed in the gut leading to a decrease in bile salt production in the liver (which leads to cholesterol stones falling out of bile as there is too much cholesterol and not enough bile salt skewing the bile ratio). OR… the liver is just not producing bile salts (hepatitis, cirrhosis, alcoholism on board damaging the liver???) OR… perhaps steroid hormones are out of whack. Too much estrogen? Too many fat cells releasing estrogen? Serum estrogen somehow causes hyperlipidemia.

You may need to ERCP those new little stones out of the ducts or pancreas while balancing the bile composition.

Balance bile composition by:

1) Decreasing dietary Cholesterol. By diet control or with cholesterol absorption blocking drugs like Ezetimbe. Main side effect of Ezetimbe is steatorrhea and diarrhea/bloating. There is risk of severe allergic rxn.

2) Increase bile salts by
a) supplementing bile ACIDS. UROSIDOL (Actigall) and CHENODIOL (Chenix). These will not only act directly on fats in the small intestine but they appear to have pleiotrophic protective effects on the small intestine muscosa AND they appear to decrease the pH of the small intestine making it uninviting to bacteria, which ought not be there in the first place.
b) supplementing bile SALTS. Salts can act directly in the small intestine to improve lipid metabolism and can have the same pleiotrophic effects as endogenous bile salts. However, they won’t be able to be recycled if the liver and colon aren’t healthy and you’ll just have to keep taking them until the liver and colon heal. Even if the liver is healthy and able to conjugate recycled acids to salts, you need a functioning colon to utilize bile salts as the salts themselves don’t go back to the liver, the colon biome needs to de-conjugate them and sent them back to the liver as bile acids.

3) Heal the Liver or Colon or both, whichever organ malfunction is mucking up bile salt getting to the small intestine and then getting recycled back to the liver.
a) Treat Constipation
-Increase water intake
-Modify diet to increase veggie + fruit intake
-Stool Softeners to get things moving
-Stop narcotics, switch to something else or use
the percoset that is coated in Naloxone

 b) Treat liver disease
       - Test for Hep C
      -Stop ETOH and drugs
      -Treat Hep A and B, Vaccinate to prevent them
      -Try a liver cleanse diet, what is there to lose at 
        this point?  Perhaps it will work!
60
Q

RUQ pain starts hours after eating, knowing all you do about how bile works, how will you proceed?

A

Exam: Screen for liver damage underlying Gallbladder sxs

 -Try to determine pain onset in relation to eating

 -Give Murphy a try, it might work but will likely be 
        Negative unless the gallbladder is actively
        inflamed.
 -Do a thorough ETOH screen.  AND do a thorough
        Hep B/C screen.  If the liver is compromised, fixing 
        the gallbladder may not solve the problem.
 -Ask about Constipation.  That interferes with bile acid
        recycling.  
 -Portal Hypertension will also interfere with bile acid
         recycling and cause liver damage.  Beer belly???
         Caput Medusa?  Esophageal bleeding or 
         varicosities??
  -IS YOUR PATIENT JAUNDICED?????? Don't forget to 
          check the palms.  Redness on the THENAR +
          HYPOTHENAR EMINANCES (emini??) is 
          indicative of liver damage.  This may be ITCHY
          and the palms might just look blotchy.
   -Dark colored Urine?
   -Hepatomegaly?
  -Smoking status, counsel cessation.  There is a 
    connection between smoking and gallstone 
    pancreatitis.
  -Screen for high Ca++ as it is associated with 
    Acute Pancreatitis without stones
    Supplements?  Too many TUMS?  Vit D w/o K2?

TESTS: Look for liver/pancreas damage as well as stones…

1) CMP: LFTs, Bilirubin, Pancreatic enzymes and Lipids
Amylase is the marker
Triglycerides around 1000 also a marker
2) Hep A,B,C test
3) CBC w/diff: infection, also serum [Ca++]
3) Sono the Gallbladder
4) Order the HIDA scan WITH contrast when ordering the
Sono (if insurance will allow….) You’re going to need it
regardless of what the sono tells you. SKIP the sono
and go right TO the HIDA if you can.

Rx: This depends on how advanced the damage is. If it’s just cholecystitis, diet and bile acids might work along with addressing constipation (esp if drugs are causing constipation). If we’re at Cholangitis or Pancreatitis, we need to move faster:
1) ERCP if small stones in the ducts are responsible.
2) Consider trying to dissolve the stones with Bile Acids if
you can’t get at them with ERCP. Rectify cholesterol
excesses with Ezetimbe if tolerated, this may
normalize bile composition. Look for sources of
excessive Estrogen.
2) Cholecystectomy if pt cannot stand to try to dissolve
the stones. But supplement bile acids orally thereafter
and counsel pt that not having a gallbladder DOES have
impact, often obesity, but also often NVD and bloating
in Post Cholcystectomy Syndrome. They need to
take the bile acids orally after removal.
3) RX liver disease
4) HyperTRIglyceridemia will resolve with fasting and bowel rest unless it is genetic… Try Fenofibrate or Gemfibrozil (Lopid)

61
Q

Prometrium

A

Prescription Oral Progesterone

100 or 200mg capsules

Have to prescribe extra as 1st pass takes a bite out of it.

62
Q

BEST test for hormone levels?

A

24 Hr Urine test

  • Inconvenient unless on a foley
  • Expensive
  • Still the best test, heck, get a perfect GFR this way while you’re at it.
63
Q

Typical ESTRIOL dose?

A

1.25mg transdermally BID

64
Q

Estrogen and Progesterone act on bone how?

A

Estrogen (even estriol) suppresses RANK signaling which prevents osteoclast activation.

Progesterone is involved in activating osteoblasts.

65
Q

Re-stenosis?

A

Post Stent stenosis inside the stent of over 50% occlusion

The achilles heel of angioplasty and stenting.

Drug Eluding Stents re-stenose +/- 20%, bare metal 40-50%

When stent is placed, lumen is immediately increased and blood flow returns( this is called Acute Gain). Over time though, there is an immune reaction to the stent and smooth muscle builds up beneath it, squeezing it closed ( This is called Late Loss). The hope is that there is a Net Gain between the original diameter of the sclerosed (un-stented) lumen and the diameter after the late loss. If there is a function Net Gain in lumen diameter after the late loss, then the stenting was successful.

Blood Clots in the presence of Metals. Stents are metal.
1st 30 Days Post Stent are critical. Without Dual Antiplatelet Therapy (Plavix and Aspirin), thrombus formation at or close to the stent is common. Angina results, possibly MI. Blood clot risk at the stent decreases once the metal has been “endothelioid” i.e., covered over by endothelium. This is, of course, the beginning of restenosis, but it keeps the clot risk down so we’ll take it…

bonified ReStenosis takes longer, 3-12+ months.

Prevention of Thromboiss (0-3 mo post stent) and (Restenosis 3-12+ mo post stent) includes:

1) Plavix for a year after stenting and using plavix eluting stentis
2) Because INFLAMMATION is part of the immune response to the foreign body stent, you will likely see both plavix and 81 mg +/- Aspirin being used post stent’

66
Q

Red Man Syndrome

A

Vancomyin INFUSION rxn wherein FLUSHING of the Head + Neck begin 4-10 min after infusion starts. This is due to mast cell degranulation and is NOT anaphylaxis. IV Benedryl can relieve the symptoms but it’s best to avoid causing them by infusing Vanco SLOWLY, no more than 10mg/minute, preferably over 60 minutes.

Vanco kills Gram (+) bacteria and is reserved for for Rx
of Beta Lactam resistant bacteria or for cases where
there is Penicillin Allergy:
-MRSA (IV) and
-C. Diff (orally)

67
Q

Tessalon Perles/ Benzonatate

A

Non-Narcotic Prescription Anti-tussive

It is a Centrally Acting Antitussive called Benzonatate

100 mg capsules up to 3X a day

68
Q

Benzos for cough suppression?

A

Clonazapam is the most potent anti-tussive of the benzos. Even though clonazapam and diazepam have similar muscle relaxing capacities, clonazapam is 6x more effective as antitussive than is diazepam.

Even so, Out Patient - probably better to go the Benonatate route for cough suppression and prescribe Tessalon Perles 100mg up to TID as Klonapin has so many other issues. Keep it in mind though, especially IV, for Palliative care.

69
Q

Acute Bronchitis, sxs, causes, rx

A

Cough, Runny Nose, Congestion, sore throat, burning/pain on coughing from adam’s apple down to sternum (burn stays central, in the bronchi,does not radiate out into the lungs…. that’s pneumonia and/or pleurisy…)

NOT fever, wheezing (fever + wheeze = Pneumo)
NOT usually body aches (fever and aches = Flu)

ACUTE BRONCHITIS IS 90% VIRAL, Adenovirus or Coronavirus or Influenza. DON’T USE ANTIBIOTICS UNLESS YOU SUSPECT

Consider PERTUSSIS Risk (cough over 10 days, cough in fits unto emesis, incompletely vaccinated, daycare…) If you suspect Pertussis, take a naso-pharyngeal swab, alert the Health Dept and prescribe Azithromycin and quarantine for 21 days. Give Azithromycin Rx to family members if swab comes back (+). Azithromycin reduces transmission ONLY, it does not treat pertussis or reduce symptoms…

Consider CHLAMYDIA Pneumo- give macrolide or doxy

Consider MYCOPLASMA Pneumo - give macrolide or doxy

the ANTIBIOTICS WON’T HELP conversation:
Once you’ve established that there is no fever over 100.4 and no history of low grade fever (Mycoplasma + Chlamydia) and that there were intact or are still cold symptoms like runny nose, hoarse voice, sore throat that is not Strep (you might test, but w/o fever, why?), and once you’ve cleared Pertussis as a concern (no whoop, no coughing to emesis), embark on the following conversation.

This is Acute Bronchitis and it will resolve on its own within 3 weeks. The bad news is that there is no medication that will hasten resolution other than good self care. Even symptom relief is questionable (though the Tessalon Perles and Afrin may help sleep at night) as your COUGH is IMPORTANT as it CLEARS the virus-laden mucus from your BRONCHI… The good news is that you will not benefit from use of antibiotics and let me tell you why that’s good news…. Antibiotics have significant side effect risks, many of which are not apparent for weeks to months after treatment and are usually centered around GI disturbances. They kill off your good bacteria in the GI and GU tracts and you’re left defenseless. This may be worth it if you’ve taken them to treat a bacterial infection like pneumonia, but if you’ve taken them to treat a viral infection for which they are 100% ineffective.

70
Q

No dextromethorophan under two, why?

A

Over medication leads to sedation and risks death

AND it doesn’t work in bronchitis cough suppression in kids under six anyway.

Try Honey in over Ones - probably fine in under ones but we’re still dealing with the botulism risk expectations from a hundred years ago.