Download BonusDoc OMS II Exam 1 Spring 2015

Contains More OMM than usual (OMM and case extras are at the end of the document)
Case 1: TIA: Time to vacuum the carotids [carotid endarterectomy]
61 y/o M w/ a cc of numbness in the LLE/LUE
Brief episodes of numbness on left both upper and lower extremities *2 days ago, resolved on its own
Past episode *2 months ago
PMH: Stable angina (Coronary artery disease), HTN
Meds: Atenolol, HCTZ, ASA, Nitro PO (1/150 grain ~ 0.4mg)
Skin: Scaly, oily flaking rash over bridge of nose/scalp = seborrheic dermatitis (scaly greasy rash)
Head: Fundoscopy showed copper wiring (= widened/enhanced arteriolar light reflex); A/V nicking, cotton
wool spots (hemorrhage)
Neck: Bruit (sound of turbulent blood flood) over Rt carotid artery
Chest: SOB w/ Angina; S4 gallop
Extremities: No edema (seen in heart failure), claudication (seen in peripheral vascular disease)
Neuro exam: nl, no hx stroke
● No pronator drift (pt unable to hold arms out fully extended, indicative of an upper motor
neuron lesion)
● No extinction to double, simultaneous stimuli (pt will neglect stimuli contralateral to a lesion,
particularly when the right PTO is involved but could be in other places.)
● Cerebellar tests: finger to nose, rapid finger tapping, heel-shin, Romberg
○ Dysdiadokinesia is usually tested by a rapid alternating movement of the handslooks at cerebellar function
● No Babinski reflex (UMN lesion, only normal in infants)
OMM: Decreased CRI; B/l cervical musculature tight, r>l; C3-6 FSrRr; Rt occipitomastoid suture
compressed
****The fish diagram was a bonus twice last year, and second semester knowing normal values was
necessary to get 3 of the bonus points. They may give a list of values [example: 100, 4.0, 15, 140, 25, 1.0, 90]
and say these are representative of normal labs. Where do they belong? Points may be assigned depending on
number correctly placed.
Lipid profile
Calculation of LDL: LDL = TC - HDL - (TG/5.0)
CXR: Ectasia (distension) of
the aorta (caused by HTN) [similar to aortic aneurysms]
CT WITHOUT CONTRAST (Fresh blood shows up bright, so does contrast, giving contrast to someone
who has signs/symptoms of stroke would obscure blood).
MRI of head (to rule out an infarct)
EKG: to rule out A-fib, or other arrhythmias
ECHO: mild LV systolic dysfx, ejection fraction 45% (nl >55%); no valve abnormality, thickened left
ventricle (accounts for auscultated S4); no clots on walls (important source of emboli)
Carotid ultrasound/doppler: showed "headlight" sign in the plaque-> density (usually calcifications)
attenuating the signal
Stenosis: Rt internal carotid artery, calcified >80% stenosis
Carotid arteriogram, MRA (magnetic resonance angiography); DSA (digital subtraction angiography)>confirmed the stenosis
Tx w/ carotid endarterectomy; better diet
Facial: Seborrheic dermatitis was treated w/ 1% hydrocortisone and the scalp seborrheic dermatitis was tx'd
w/ Ketoconazole
Case 2- Wilson’s Disease.
20 y/o white F with liver dz, and behavioral problems with a cc of hematemesis
ROS
Fatigue, abdominal pain, epistaxis/gum bleeding
Med Hx:
● 4 years ago: was inaccurately diagnosed w/ acute viral hepatitis (elevated AST)
●
●
●
●
●
●
3.5 years ago: increased prothrombin time, thrombocytopenia and splenomegaly. Liver biopsy ->
subacute hepatitis and early cirrhosis. Put on predisone 60mg that was tapered over 6 months and
then started on 20 mg. Also put on azathioprine
3 years ago: repeat liver biopsy -> chronic active hepatitis and cirrhosis
2 years ago bleeding gums and frequent epistaxis, alleviated w/ discontinuation of azathioprine
1 year ago: generalized edema and ascites, attributed to prednisone so stopped. put on spironolactone
and HCTZ
Menarche at 12, secondary amenorrhea at 15 (symptoms of Wilson’s, but remember that pregnancy
is most common cause of secondary amenorrhea) [B-hcg was negative]
Behavioral problems-dx of oppositional defiant d/o; graduated high school late
Surg Hx: liver biopsy, had prednisone and azathioprine after surgery
Meds: Spironolactone 25 mg TID, 500 mg/day HCTZ, OTC Acne meds (Neutrogena); Denies supplement
NKDA, denies food, envt allergies
Wilson's is inherited in an autosomal recessive fashion, the ATP7B gene on chromosome 13 (could
come up on USMLE, but not likely COMLEX)
Soc Hx:
● Denies drug use
● Not currently sexually active-did not always use protection, (+the risk of Hep B/C)
● Problems with employment clumsy and having shitty handwriting
PE
Skin:
●
●
●
●
Stria on buttocks and abdomen
petechiae LE [clotting is all messed up]
spider angiomata on arms and chest. (the liver normally metabolize estrogen; the hyperestrogenic
state is responsible for this and gynecomastia in alcoholics)
face +open and closed comedones
HEENT: The irises have an unusual color pattern- golden brown pigmented corneal rings are??
Kayser 1Flescher rings!!!**
Result of deposition of copper in the descemet membrane (where the cornea meets the sclera); detectable by
slit lamp
1
**Apparently not pathognomonic, and clinically that might be true, but if you EVER see a board question
w/ K-F rings = Wilson's.
Extremities: 2+ edema (protein is low, she is third spacing her fluids)
Abdomen:
● liver 10cm overall, 4cm below RCM and firm
● shifting dullness and fluid wave;
● Spleen 5-6 cm below MCL
● presacral edema 2+
Neuro:
●
●
●
●
●
●
●
●
●
●
●
●
Affect normal (affect = weather)
Mood irritable. (mood= season)
Speech slowed and dysarthric.
Strength, CN, DTR, and Sensory exam nl.
Intention tremor of the hands, called a "wing beating tremor" in Wilson's-if you see
Parkinsonian sx in a young person, Wilson's should be on your list of differentials
Shuffling gait-see above
Deficient rapid alternating movement of the hands.
Romberg, Babinski negative.
Intelligence normal assessed w/ calculation/questions
Asterixis absent. Asterixis = “Hand flapping” (can indicate hyperammonemia, severe liver dysfx)
Reitan trail/Trail Making Tests # connection tests: 32 seconds for part A, 64 seconds for part B:
NORMAL
○ Pt is instructed to connect a set of 25 dots/targets both fast and accurately; can dx
Alzheimer's, frontal lobe lesions and dementia etc
○ In part A,the targets all number (should take ~90 seconds or less; average is 29 seconds); in
part B letters and numbers are alternated (should take 3 minutes or less; average is 75
seconds)
Not mentioned, but a buzzword for Wilson's: Risus Sardonicus, or wry smile
Hella TART in the OA, AA, and T5-9 on the Rt.
CBC
●
●
●
normocytic (as determined by MCV) hypochromic (as determined by MCHC) anemia (could be
dilutional)
leukopenic
thrombocytopenic
Coag: PT/INR (extrinsic pathway!) elevated; aPTT nl [PeT and PiTT, to help remember intrinsic or
extrinsic pathway labs]
LFTS:
● Uric Acid low (liver is responsible for breaking down amino acids)
● Ammonia nl
● Alk Phos elevated at 163 (Bilirubin normal)
●
●
●
●
ALT/AST high
Phosphorous low at 1.8
Protein/Albumin low [Explains her edema]
Globulin WNL, but shows diffuse hyperglobulinemia (assoc w/ liver dysfx; liver clears
immunoglobulins)
Endoscopy [Cuz she is bleeding from somewhere]
● Grade II varices in the esophagus (often, left gastric vein w/ esophageal veins) w/o active bleeding
○ Grade 1 – Small, straight esophageal varices
○
○
●
Grade 2 – Enlarged, tortuous esophageal varices occupying less than one third of the lumen
Grade 3 – Large, coil-shaped esophageal varices occupying more than one third of the lumen
"alligator skin/snake skin" in the stomach and esophagus due to portal htn-> congestive
gastropathy
Hepatitis serology -neg; (see extras for interpretation charts)
Antibodies: All of the below were neg
ANA (not specific for much of anything)
Antimitochondrial (primary biliary cirrhosis)
Anti-smooth muscle (Autoimmune hepatitis)
Money tests:
Serum ceruloplasmin (copper-carrying protein in the blood) low-> WILSON's
Serum copper low (not a great test, according to Robbins)
Urine copper high
****Summary what you NEED to Dx Wilson’s: Serum copper (high), urine copper (high),
ceruloplasmin (low) ***
Ferritin (does she have hemochromatosis or anemia of chronic dz??) [Ferritin can be elevated or normal in
anemia of chronic disease, since it is a marker of inflammation, as well as a marker of iron stores]-> nl
A1 antitrypsin (deficiency causes emphysema and cirrhosis at a young age<40)-> nl
Rx: Penicillamine (chelates copper+other metals) and Pyridoxine (Vit B6)
● Penicillamine causes pyridoxine and is also hematotoxic, as our pt found out later when her WBC
count and platelets tanked
● We replaced her penicillamine w/ trientine to reduce the toxic effects
● Didn't use this, but zinc is another potential treatment
Wedged hepatic venous pressure measurement returned to normal, her ascites went down; we even fixed her
acne!Everybody lived happily ever after except for her homeless sister
Case 3- Ruptured Berry aneurysm and vasospasm. The Berry Aneurysm Strikes Back
55 y/o M w/ a CC of LOC, N/V, HA
● 3 weeks ago: HA - gradual onset, mild (5/10 pain), frontal/above eyes, assoc w/ tinnitus
●
●
○ Constant w/o throbbing
3 days ago: Suddenly got a lot worse (8/10 pain), went to the ED
○ Afebrile, all lab tests nl, so sent home w/ some Claritin (loratadine, second generation H1
blocker) and Acetaminophen
Today: when he was TAKING A SHIT (straining) his headache suddenly exploded (this and
orgasm are two known triggers for rupture) and he passed the &^&% out
Med Hx
● Borderline htn-> Risk factor
Soc Hx
● 40 year pack Hx smoking-Risk factor
PE:
T: 98.9 BP 175/105 (intracranial bleeds can spike your pressure). P 70 R 18 Pulse Ox 98%
HEENT: Photophobia (sign of meningeal irritation)
Neck: Pain w/ Nuchal Rigidity (sign of meningeal irritation)
Neuro
● Oriented x 3 and Drowsy. (Obtunded = less than full alertness and would be appropriate to use in
this case)
● CNs II-XII intact, Strength, sensation, reflexes nl
● Finger to nose/ Rapid alternating hand movements (Cerebellum!) nl
● No pronator drift or Babinski sign (UMN)-> know these terms
● No Brudzinski sign
Msk:
●
●
●
C spine: Decreased ROM, especially w/ rotation
T-spine: Paraspinal spasm b/l
Cranial Rhythm= bowling ball
CT SCAN (without contrast!):
Blood in the suprasellar cistern, mild ventriculomegaly w/ dilation of temporal horns (not uncommon in
bleeds)
With elevated intracranial pressure there is a substantial risk of causing herniation and thus death if you do an
LP. However, if the CT had been inconclusive, an LP is the next step. We'd see RBCs in the CSF, or
xanthochromia.
W/ a Dx of SUBARACHNOID HEMORRHAGE, we threw some drugs at the pt
● Labetalol (lower the blood pressure, however with elevated Intracranial pressure, ICP, mean arterial
Press must remain on high side in order to profuse the brain.
● Morphine
● Promethazine (H1 blocker, anti-emetic, Brand name = Phenergan)
● Nimodipine (CCB, used in cases of SAH to reduce the risk of vasospasm)
○ Dihydropyridine (another Ca channel blocker, prophylaxis vasospasm)
● Famotidine
○
○ H2 blocker, Brand name = Pepcid
○ Stress ulcer prophylaxis
Fun fact, didn't happen here but a Cushing ulcer in the stomach is a result of increased
intracranial pressure. This is not to be confused with a Curling ulcer, which is caused by
trauma, burn ("Cushion the brain"; "Curling iron burn")
Consult to neurosurg, who ordered a 4-vessel Cerebral Angiogram and the pt was assessed as Hunt-Hess
Grade II
Hunt and Hess grading system —index of surgical risk. The initial clinical grade correlates with the
severity of hemorrhage. Know at least the name of the grading system of for SAH.
●Grade 1: Asymptomatic or mild headache and slight nuchal rigidity
●Grade 2: Moderate to severe headache, stiff neck, no neurologic deficit except cranial nerve palsy
●Grade 3: Drowsy or confused, mild focal neurologic deficit [WTF wasn’t he drowsy]
●Grade 4: Stupor, moderate or severe hemiparesis
●Grade 5: Deep coma, decerebrate posturing
●The grade is advanced one level for the presence of serious systemic disease (hypertension, diabetes, severe
arteriosclerosis, chronic pulmonary disease) or vasospasm on angiography
Decerebrate posturing:
Shit got real:
●
●
●
6 hrs later, the pt had significant mental status changes, and now had a left pronator drift despite CT showing
no new hemorrhage
○ Repeat angiogram showed a berry aneurysm of the anterior communicating artery w/
vasospasm (most common location!) -> we had to cancel the surgery due to vasospasm
Complications
○ Fever, Diarrhea
○ Hypercarbia (excess CO2) (respiratory depression, which incidentally could cause a metabolic
acidosis)
○ Pneumonia (bibasilar pulmonary infiltrates and a left shift-> baby neutrophils! BANDS)
■ Sputum showed Gram +, COAGULASE+ Staph (would be in clusters)
■ Coagulase test distinguishes S Aureus from other staph (Epidermidis, S Saprophyticus);
it's a CLI test!
More meds to throw at the pt
○ Zosyn (Piperacillin/Tazobactam) – kills gram negatives AND MRSA. [It is crap-tacularly
expensive]
○ Dobutamine (B1 ag)
○
○
Labetalol (Beta and Alpha antagonist)
Metronidazole for the C Diff [ Metroniadzole = Flagyl. Used for BV and C. Diff]
Procedures:
●
●
●
Swan-Ganz catheter w/ the goal of keeping Cardiac index (Cardiac Output/Surface Area of the
Body) >4.0
○ Just a side note: "Wedge pressure" is indicative of left atrial pressure
Pushed Hella IV fluids and discontinued labetalol to allow the systolic BP to increase to 180 mmHgTriple H therapy for SA Hemorrhage: Hypertension, Hemodilution, Hypervolemia
Eventually, craniotomy w/ Aneurysm clipping
Case 4- Glioblastoma "Butterfly" almost makes it sound pretty
61 /o M w/ a sudden onset of straight twerking in the RUE and face
●
Third instance of seizure symptoms in the last 2 weeks, each resolving on its own in a few minutes;
nothing prior to two weeks ago. All occurred at rest w/o prodrome. Pt is right handed
PE:
BP 160/95, P 68/Regular, R 12, T 97
*Wasn't brought up, but a potential reason for this HTN is that the brain attempts to keep cerebral perfusion
pressure up by increasing MAP in the face of increased intracranial pressure-> CPP= MAP-ICP
HEENT: Fundoscopy revealed A/V nicking. Visual acuity was normal
Neuro:
● Weakness in the LOWER face-indicative of a contralateral upper motor lesion of CN VII
● Motor-4+ strength in the RUE and RLE with dragging of the right leg w/ circumduction
(hemiplegic gait)
● Slight decrease in proprioception on the rt
● Deficits in coordination.
● DTRs 3+ on the right
● Babinski + on the rt
● Inability to read
● Temperature and other sensations normal
● Finger-to shin preserved (cerebellum is ok)
● Extinction to double stimulus (parietal lobe damage is implied in neglect syndromes)
● Visual fields grossly intact
● Wernicke (expressive) aphasia-damage to the inferior temporal gyrus
● Anomic aphasia (cannot recall words or names for things); our pt could give the correct answer if
options were given "Is this a hamster, your mother or a flying giraffe?"
●
●
●
●
Gerstmann's syndrome-implies damage to the dominant PTO/inferior parietal lobe
Finger agnosia (doesn't know which piggy went to market)
Acalculia (Inability to do math)
Left-Right confusion
Dys/Agraphia (Inability to write)
Cranial findings:
Left Lateral strain pattern; aka "parallelogram head"
● a pathological strain named for the position of the greater wing of the sphenoid
● Occiput will be more lateral on the contralateral (right in this case) side
● the corresponding hand will be pronated
● Two parallel vertical axes; one through the sphenoid and one in the foramen magnum
● Rx w/ HVLA to ALL THE SUTURES
○ Just kidding, intracranial mass means OMM is totes contraindicated
Non-contrast brain CT (get it w/o contrast to avoid missing a hemorrhage!)- decreased density in the left
temporo-parietal region w/ low-density demarcation (suggesting edema); hyperintense areas=hemorrhage. [This is usually
followed by a contrast CT and then MRI]
MRI: increased intensity in the L hemisphere on T1 (gray matter is gray, white matter is white, best for
viewing normal anatomy) in the temporo-parietal region; mass effect suggested by displacement of septum
and lateral ventricle
EEG showed a slowed rhythm in the L cerebral hemisphere w/ intermittent spikes
● Epileptiform discharges at 1.5 Hz
● Larger spike amplitude on the L
● Muscle twitch was noted during an episode-> seizures were happening
Rx: hella steroids for hella days; Dilantin (phenytoin) for the seizures
CT diagnosed with a Grade 4 Astrocytoma
Glioblastoma Multiforme, most common brain tumor in adults It is the most common primary
malignant brain tumor in adults, it is also the most deadly.
Mets are the most common malignant brain tumors in adults, and there are plenty of benign
tumors that are harmful due to mass effect.
All your histo buzzwords:
● Pleomorphic cells w/ mitoses (characteristic of malignancy)
● PSEUDOPALISADING NECROSIS
● Vascular proliferation
● Not mentioned in the case, but these are "butterfly tumors"-they cross the midline
These tumors have an awful prognosis, and after a round of radiation our pt passed. Glioblastoma median
survival rate is less than 15 months
Case 5-Parkinson’s disease The moral of the story is don't get old
60 y/o F w/ a CC of "difficulty using the right arm"
●
●
●
●
●
Clumsiness and shakiness (pill rolling?!?) *2 months in the right hand, getting progressively worse.
Note: Parkinson's sx usually begin unilaterally
Tremor does NOT change with alcohol
○ Early Parkinson's and Essential tremor can present clinically in very similar ways. Pts will
often self-medicate w/ alcohol to relieve the tremor.
Saliva on her pillow (drooling is likely due to decreased swallowing, rather than over production)
Is "slower" and "acting depressed" per the kids-hypomimia=masked facies
Other terms to lead you back to parkinson’s: Flat affect, Cog wheel rigidity, Pill-rolling tremor,
festinating gait.
Fam Hx: Mom had a "slight shake of her head" in old age-doesn't really tell us much; there are familial
Parkinson's syndromes, many cases are sporadic
PE
HEENT: Face symmetrical w/ little expression
Extremities: Rt shoulder has a tender spot over AC joint; moves w/ some discomfort. All other extremities
have full ROM
Neuro:
● A&O*3 (dementia comes on later in Parkinson's dz, one way of distinguishing it from dementia w/
Lewy bodies = Parkinson’s + dementia and often visual hallucinations.)
● CN II-XII intact
○ Just a note: according to neuro the sense of smell can be one of the first things to go in
Parkinsons; keep dat coffee and orange peels around! (CN I testing)
● Decreased rapid coordination in the RUE/RLE brought out by finger tapping and pronationsupination (bradykinesia)
● Gait testing: Right arms swings less and she takes short steps-> shuffling gait
● Initiation of gait is slow and unsteady, but does not lose her balance (retropulsion; we would
expect this in Parkinson's, but it's early on in her dz course)
● Resting tremor, disappears w/ action
● Neg Babinski, Neg Kernig, Muscle strength normal
Osteopathic Cranial findings: Elongation vertically; prolonged extension phase
Lab Tests:
CBC showed an MCV that was sliiiiightly out of range (96)-> a facilitator did point out THREE
TIMES that MCV is measured in femtoliters, which is 10^-15 L. The abnormal value itself didn't
mean anything,
Ca (hypOcalcemia causes tetany-think about DiGeorge syndrome!) - normal
Clinical dx of Parkinson's was made; pt was started on pramipexole (dopamine agonist, D3>D2 selective)
with an increasing dose. To improve tremor, we added Trihexyphenidyl. (Tremor is the only sx of
Parkinson's that anti-muscarinics like Trihexyphenidyl would improve for Parkinson's pts)
After a few years she stopped responding as well, so we added Levodopa (dopamine itself can't cross the
BBB!) with Carbidopa (Dopa decarboxylase inhibitor, prevents conversion in the periphery to lessen
peripheral effects of dopamine like vomiting)
This regimen worked for a few years, at which time she began to have depression and memory loss;
pallidotomy was discussed.
If we were to take a look at her brain, recall that we'd have a loss of pigmented neurons in the substantia nigra
in the midbrain, and potentially Lewy bodies (intracytoplasmic, eosinophilic inclusions)
Case 6- Alzheimer’s Almost forgot to write up this case, uh oh...
62 y/o M w/ "trouble at work", worsening *1 year
● Forgetting client's names and appointments, misplacing his keys
● Less interested in hobbies-seems depressed (according to his wife-> he denies any problems himself;
hella anosognosia=unawareness of a deficit)
Soc Hx: 30 pack year-hx (puts him at +risk for multi-infarct dementia, which is the second leading cause of
dementia after Alzheimer dz)
PE: Normotensive
Neuro (Most of components of the Folstein Mini Mental Status Exam)
● A&O*2 ->Was one day off on the date (better than most medical students)
● Digit span (specifically tests attention)-> normal Performed serial 7s well
● Showed semantic dysnomia-> called the receiver part of the telephone a handle and a watch band
a belt
○ Naming difficulties are often the first/earliest signs of an aphasia; our pt otherwise had no sx
of aphasia
● Repeated 3 objects immediately (attention) but could not recall them after 3 minutes
● Drew/copied simple designs well, but incorrectly slanted one of the internal lines the wrong way
when copying a cube-> sign of early cortical dysfunction
● No apraxia. Apraxia = deficit in planning or putting together an intended movement. An Apraxic
pt would perfectly capable of doing a task spontaneously, but cannot do the same task if asked to
follow a command.
● Depressed mood, w/ normal affect, No evidence delusions/hallucinations
● Normal motor/sensory, Gait nl, No tremor
Osteopathic: Apparently we didn't get a cranial exam, but we sure looked at his L-spine
Neuropsych Testing- was explicitly told this wasn't going to be a bonus, but we administered:
● Geriatric depression Scale, Wechsler Adult Intelligence scale, Wechsler Memory Scale, Trail Making
Part B, Verbal fluency
All of the above were low-normal [All of the tests including the MMSE are most useful to follow a patient’s
course]
Labs:
ALL NORMAL:
● Vit B12 (subacute combined degeneration of the spinal cord) [B12 deficiency is a possible
cause of dementia]
● Thiamine (Wernicke-Korsakoff syndrome, mostly happens in alcoholics-> would result in ataxia,
optic problems, and memory deficits and confabulation)
● VDRL (is it tertiary syphilis ? )
Brain CT: Showed "mild atrophy" w/ mild symmetrical dilatation of the ventricles and prominent
sulci-> hydrocephalus ex vacuo; no true excess of CSF, a result of cortical atrophy
CSF: Normal (ruling out chronic meningitis, and also R/O Neuro Syphilis)
>Just a note: India ink=Cryptococcus, out of date clinically but still a decent buzzword. [Let’s put it this way,
India ink is probably a term that Comlex will still use. But still know latex agglutination tests.] (If you have a
choice between India ink and Latex agglutination. pick the latex according to FA)
Dx'd w/ Alzheimer dz (basically by exclusion)
The drugs:
● Donepezil (AchE inhibitor) [Dementia responses to increasing acetylcholine in the brain]
● Vit E (antioxidants)
● Sertraline (SSRI)
● Memantine (NMDA Antagonist)
Continued to decline; all joking aside this is an ugly shitty dz to watch a family member go through....
Know Apo E e4 allele as a genetic/familiar risk factor. Also mutations in APP and presenilin. Highly
heritable.
Case 7-Crohn's-Rx w/ milking of the terminal ileum (Please don’t CONTAINDICATED!!)
22 y/o white M w/ a cc of abdominal pain, low blood count, rectal bleeding and diarrhea
● GI issues *6 years. Diarrhea -> formed, not runny, non-bloody
● Rectal bleeding daily, Stool + for occult blood
● Microcytic, hypochromic anemia on repeated CBC
● Early satiety-> wt loss
Denies:
● Eye problems, Back/Joint problems, Rashes
●
Extraintestinal manifestations of Crohn's dz: Migratory polyarthritis, Erythema nodosum, ankylosing
spondylitis, pyoderma gangrenosum, aphthous ulcers, uveitis, kidney stones
Past Meds:
● Cimetidine (H2 blocker) [Inhibits p450s , can cause gynocomastia, and rarely but very serious can
cause agranulocytosis/neutropenia/thrombocytopenia, so we generally don’t use this drug anymore!
Other better H2 blockers include Zantac = Ranitidine or Pepcid = Famotidine]
● Sulfasalazine (salicylate+sulfa derivative used in RA and IBD-that's from the pharm one-liners, you're
welcome)-> discontinued because of nausea
Current Meds
● Ferrous sulfate
● Hydrocortisone enema (ahhhhhh, holy shit)
Soc Hx
● Does not smoke = smoking is a risk for Crohn's disease but is actually protective against
Ulcerative Colitis.
● Not currently sexually active (MSM at + risk for squamous cell CA of the anal canal; HPV)
Fam Hx noncontributory- combined with normal sigmoidoscopies, rules out familial colon CA syndromes
like FAP or Lynch syndrome
PE
Abdomen: Soft w/o organomegaly. RLQ had tubular fullness w/ moderate tenderness (Ileocecal area is the
most commonly involved in Crohn's)
Rectal: No masses, fissures or hemorrhoids. Normal prostate. Stool hemoccult +.
CBC: Microcytic, Hypochromic anemia; slightly elevated platelets w/ normal WBC
Blood chem: Slightly hypochloremic-> diarrhea
Iron - > Iron deficiency
● Ferritin (storage form of iron): low
○ Important from distinguishing iron-deficiency from anemia of chronic dz
● TIBC: Within range
● Transferrin saturation (trafficking protein in iron): Low
Could be due to bleeding; another possibility is he is not absorbing it due to involvement of the duodenum.
Ruling out a chronic infx (like a parasite!)
● Normal WBC (eosinophils?)
● Stool culture (without special orders, would detect Yersinia Enterocolitica, Campylobacter
Jejuni, Salmonella and Shigella)
● O&P=Ova and Parasites=negative
UGI w/ SBFT (small-bowel follow through X ray)
● Strictures of irregular appearing bowel in the duodenum and jejunum, terminal ileum [string sign]
●
Prominent small bowel lubes w/ folds; edema and stricture in terminal ileum
Abdominal CT:
Distal ileum w/ thickened walls of a long segment, showing a "target like" appearance
● Nonspecific-> IBD, Radiation, Infx, Ischemia, Vasculitis, 5-FU
● Diffuse thickening, thickened sigmoid-> showing skip lesions and entero-colonic fistulas
Colonoscopy and Endoscopy:
Colonoscope was passed w/o difficulty to the cecum (ulcerative colitis would run continuously from the
rectum)
● Ileal orifice stenotic and inflamed
○
While ulcerative colitis can involve the distal ileum (it's called backwash ileitis if you took Ch 17 in path), for boards think
limitation to colon. [Crohn’s on the other hand can be anywhere in GI tract]
● Granulomatous inflammation w/ multinucleated giant cells
● Transmural inflammation
● Cobblestone mucosa
Upper GI endoscopy-> small aphthous ulcers in duodenum
Rx'd:
●
●
●
●
Prednisone
Mesalamine (5-ASA)
Fe-Dextran
Asked to consider Inflixamib (anti-TNF antibody)
OMM and EXTRAS:
Sympathetic levels, nerve name and an osteopathic tx sigmoid colon. How would parasympathetic tone
be affected in diarrhea?
OMM-if you really don't want to read this: just don't frackin do HVLA, lymphatic techniques are
soooo contraindicated in malignancy/fragility and know the sympathetic levels. Also, pedal pump
for DVT prophylaxis.
Know sympathetic levels, names of ganglions and what part of the GI system they supply.
*Overall goal of OMM = consider the patient’s body as a unit; support structure and functional components;
support and enhance the homeostatic mechanisms involved.
- Normalize structure to improve function at area of concern, as well as parasympathetic and sympathetic
innervation to the area(s) involved.
- Lymphatics to facilitate normal flow to remove waste products from the area and improve delivery of
oxygen, nutrients, and medication (if applicable). - Be aware of contraindications!
- Also consider compensatory patterns, fascial restriction in other areas of the body, daily activities, reflex
mechanisms, and/or other reasons the patient is not improving as expected from OMM (and other medical
care). - In addition to reconsidering other medical diagnoses, etc.
CASE 1 Extras – TIA
Potential techniques for this patient: Recommend waiting until after healed from surgery (endarterectomy)
prior to treating.
 Parasympathetic – Vagus nerve (OA, AA, C2)
 Posterior cervical myofascial ***AVOID ANY MANIPULATION OVER AREAS WITH
POTENTIAL CLOT (anterior cervical area/carotid arteries in this patient.)
 Cervical counterstrain
 Suboccipital release
 OA decompression
 Sympathetic - Thoracic (T1-4) and cervical sympathetic chain ganglia
 Rib raising
 Muscle Energy, Still techniques, FPR, Myofascial, HVLA (NOT in cervical area)
 Cervical sympathetic ganglia (HEENT, heart)
 Cranial techniques
 CV4 hold
 Occipitocondylar decompression
 Thoracic inlet - BLT
***Contraindicated techniques for this patient:
 Avoid cervical HVLA
 Avoid direct treatment over atherosclerotic vessels
 *Note: Would only complete cranial techniques if proficient and no other contraindications
CASE 2 – Wilson Disease
Potential techniques for this patient:
 Parasympathetic – Vagus nerve (OA, AA, C2)
 Myofascial, Muscle Energy, HVLA, Still techniques, FPR
 Cervical counterstrain
 Chapman’s points - liver, heart, spleen, etc.
 Suboccipital release
 OA decompression


Sympathetic – T1-T9 (T1-4 HEENT; T1-6 heart; T5-9 liver/spleen/upper GI), celiac ganglia,
and cervical sympathetic chain ganglia
 Rib raising
 Abdominal collateral sympathetic ganglia – Celiac
 Muscle Energy, Still techniques, FPR, Myofascial
 Cervical sympathetic ganglia (HEENT, heart)
Lymphatics
 Thoracic inlet 1st
***Thoracolumbar HVLA contraindicated in this patient with hepatosplenomegaly!!!


Posterior and anterior cervical area
Cranial venous sinus drainage
 Order: TCOS: Transverse Sinus, Confluence of Sinuses, Occipital Sinus,
Superior Sagittal Sinus -> then metopic suture?
Abdominal diaphragm – indirect (be cautious of hepatosplenomegaly)

Cranial
 Vault hold
 Occipitocondylar decompression (CN XII)
 CV4 hold (CRI)
 Trigeminal stimulation (CN V1-3)
 Venous sinus drainage as above
Case 3: subarachnoid hemorrhage d/t cerebral aneurysm
 Patient required further evaluation and medical management prior to considering Osteopathic
evaluation and treatment
 Can always evaluate and treat Chapman’s points
* *** VERY IMPORTANT TO FOLLOW STRICT ISOLATION PRECAUTIONS FOR THIS PATIENT
WITH NOSOCOMIAL INFECTIONS
 PNEUMONIA
Parasympathetic
 Vagus nerve – OA, AA, C2
 As patient awakens from ventilator - do full cervical eval – can do oculocervical technique (muscle
energy, by using eyes rather than turning neck)
Sympathetic
 Rib raising
Lymphatics
 Thoracic inlet (1st)
 Doming the diaphragm – abdominal diaphragm



IMPORTANT: Require more training on ventilators (type/settings) to complete this technique on a
ventilated patient and require supervision
Splenic pump – to improve immune response to infection
Pedal pump (gentle, especially when patient intubated)-> DVT Prevention
Other – for these techniques – also see important message regarding ventilation training as above
 C3-5 (phrenic nerve)
 Ribs as needed
 Sternum - BLT
DIARRHEA
Parasympathetic BONUS
 Vagus nerve – OA, AA, C2
 Pelvic splanchnic nerves (S2-4) - Sacral rocking
Sympathetic
 Rib raising
 Paraspinal inhibition at upper lumbar (T5- L2)
 May also use MFR, ME, HVLA (limited by hospital bed)
 Relative contraindication to treat the collateral ganglia (Celiac, superior mesenteric, and
inferior mesenteric)
Lymphatics
 Thoracic inlet (1st)
 Doming the diaphragm – abdominal diaphragm
 Splenic pump – to improve immune response to infection
 Pelvic diaphragm - Ischial tuberosity spread (can be done supine with hips flexed)
 Pedal pump (gentle, especially when patient intubated)
HTN
Parasympathetic
 Vagus nerve– OA, AA, C2
Sympathetic
 Rib raising (T1-5 cardiac; T10-11 renals [not necessarily for this patient])
 Inferior mesenteric ganglion – renal/adrenal (not necessarily for this patient)
Lymphatics – thoracic inlet, doming the diaphragm, etc. as necessary
 Patient can be supine or seated for all treatments above
Case 4 – Dominant hemisphere brain tumor with seizures
*The case does not mention that this patient would likely have been placed on hospice care after determining
that the glioma would not be resected [The real world unfortunately because death is an uncomfortable
conversation, hospice is spoken about very late in most disease courses.
* In general cranial techniques would be contraindicated for this patient
unless benefit(s) outweigh the risk(s) when patient is in hospice care (after discussion with mentally
competent patient with patient consent and documentation of this)
Otherwise treatment may consist of:
Parasympathetic
 OA release
 Cervical treatment – likely MFR, counterstrain, ME
Sympathetic
 Rib raising
 ***Pedal pump – very important since patient likely bedbound and to DECREASE RISK
OF DVTs
Other treatment(s) based on patient’s symptoms, somatic dysfunction, and lack of contraindications.
* HTN
 ***this patient would be monitored for HTN since he had elevated BP on initial PE
 Recheck BP at initial visit, continue to monitor
 If patient does have HTN treat with medications as needed and OMM (as below)
 *Also be aware that corticosteroids will increase his BP, among other potential side effects.
Parasympathetic
 Vagus nerve– OA, AA, C2
Sympathetic
 Rib raising (T1-5 cardiac; T10-11 renals [not necessarily for this patient])
 Inferior mesenteric ganglion – renal/adrenal (not necessarily for this patient)
Osteopathic Cranial findings:
OCF:
●
●
●
●
●
●
●
Exhalation = Extension
Midline bones extend
Paired structures internally rotate
↑ A-P diameter
↑ Vertical diameter
↓ Transverse diameter
Sacrum nutatation : SBS extension will cause sacral base to move anterior. Nutation (sacral flexion)
Nutation = Sacral base NODS forward
Flexion = External Rotation
Midline bones flex: sphenoid, occiput, ethmoid, vomer
Sacrum counternutation : Flexion at SBS will cause the dura to be pulled cephalad, moving the sacral base posterior
through the superior transverse axis of the sacrum. Counternutation of sacrum (sacral extension)
↓ A-P diameter
↓ Vertical diameter
↑ Transverse diameter
Paired structures externally rotate
OCF: Physiologic Strains
Flexion / Extension
Torsion: Twisting
● Twisting of the SBS at AP axis
● Named for the gr. Wing of sphenoid that is higher
Sidebending & Rotation
● Rotation about AP axis AND sidebending around 2 vertical axises
● Named for side of convexity (SBRR or SBRL)
Pathological = trauma
Lateral Strain
● Lateral deviation of basosphenoid on occiput. (Parallelogram head)
● Two vertical axes
● Named for direction of basosphenoid (RLS or LLS)
Vertical strain
● Vertical deviation of basosphenoid
● Two transverse axes
● Named for direction of basosphenoid (Superior or Inferior)
Compression-bowling ball head
● Fusion of SBS, limited ROM
Cases 5 and 6: Parkinson+Alzheimer Dz
Normalize Autonomic nervous system – in general and/or specific to complaints
Parasympathetic
 Vagus - OA, AA, C2
 S2-4 (pelvic splanchnic nerves) – Sacrum, innominates
Sympathetic
 sympathetic chain ganglion

Thoracics





Rib raising
MFR, BLT, ME, HVLA, Still, FPR
Lumbar (down to L2)
Cervical chain ganglia
Collateral ganglia (Celiac, superior mesenteric, inferior mesenteric)
Case 7: Crohn’s Disease:
 May affect anywhere from mouth to anus; therefore, treat all areas as noted below and others as
necessary.
 Loose stool component – pelvic splanchnic stimulation
 Treatments may include: MFR, ME, HVLA, Still techniques, FPR, BLT, counterstrain, rib raising,
sacral rocking, etc.
Based on physician and patient preference and lack of contraindications.
Parasympathetic – assess and normalize if need be
 ** Vagus nerve - Upper/middle GI
 ** Pelvic Splanchnic nerves (S2-4) – lower GI
Sympathetic – assess and normalize if need be
 ** T1-L2
 ** *Collateral ganglia (Celiac, Superior mesenteric, Inferior mesenteric) CONTRAINDICATED WITH ACTIVE CROHN’S FLAIR
Lymphatics (in order)
1. Thoracic inlet
2. *Abdominal diaphragm – relative contraindication with active Crohn’s flair (though may
use indirect technique)
3. *Abdominal mesenteric lift – CONTRAINDICATED WITH ACTIVE CROHN’S
FLAIR
4. Pelvic diaphragm
5. Pedal pump
Other
 ** Specific joints if patient has arthritis component
 Will often respond well to Still (medium velocity techniques)
 Note - Also avoid colonic milking technique for these patients. Strictures may occur due to
inflammation, which may narrow the bowel lumen and actually cause constipation! Another
reason it is important to get a history and do a complete physical, as discussed in this PBL case
to make sure there are no contraindications you may otherwise miss.
Case 2 extras:
Hepatitis Serology:
(Same, just presented differently)
Case 4 extras:
Doubt you will get a photo on the bonus, but good for PBL exam and reference for boards:
Some more useful things to have handy for exam/boards:
Cushing ulcer is caused by stimulation of vagal nuclei due to the increased intracranial pressure which leads to
increased secretion of gastric acid
Cushing's triad
Cushing's triad (not to be confused with the Cushing reflex) is a sign of increased intracranial pressure. It is the triad
of:
1. Hypertension (progressively increasing systolic blood pressure)
2. Bradycardia
3. Widening pulse pressure (an increase in the difference between systolic and diastolic pressure over time)
Cushing's triad suggests a cerebral hemorrhage in the setting of trauma or an space occupying lesion (e.g. brain tumor)
that is growing and a possible impending fatal herniation of the brain.
EXTRAS case 7: Know this, love it, be it.
Fun mnemonic for GI absorption: "Dude Is Just Feeling Ill, Bro"
● Duodenum-Iron
● Jejunum-Folate (and most nutriants)
● Ileum-B12