Bonus Document Fall 2014 Exam 2 OMSII
Case 1- Return of the Kidney - nephrotic syndrome
73 y/o M with a cc of 6 weeks swelling in the extremities
No recent flu-like illness, numbness, tingling, rashes, paresthesias, palpitations/heart problems,
hematuria, changes in bowel habits
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25-lb gain over 6 weeks (edema), IV Furosemide (Lasix) helped things; oral didn't. Urinated off
20lbs over 5 days!!
Med Hx - kidney stones, enlarged prostate – BPH
BPH:
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Dribbling since prostate surgery
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Prostate job: “TURP” 6 years ago [Transurethral Resection Prostate]
 TURP only addresses urethral encroachment
PSA: within range 4 [Prostatic Specific Antigen]
 Note: Crappy test, clinically has fallen out of favor
Vitals: BP 130/80; O2 Sat 93% on room air
HEENT showed no periorbital edema (common presentation in nephritic syndromes)
Abdomen: nontender, nl, no shifting dullness (ascites -> cirrhosis could account for his
hypoalbinunemia)
Extremities: pitting edema 2+ do the knees
Rectal: Prostatic enlargement (Grade II enlargement), Hemoccult negative
Musculoskeletal: Somatic dysfx T11-L1; paraspinal hypertonia
Tests:
● H&H low-> likely dilutional effect
● Total Cholesterol: 400 high (This is an effect of the nephrotic syndrome, the liver kicks up its
production of lipoproteins.) compensation for protein loss
● CH50 (complement, total)-> Low (Compliment is inappropriately activated in a lot of these
immune-mediated disorders, including membraneous nephropathy)
● CH50 (complement total): 49 LOW (70-160) [CH50 tests for compliment function of
the classical pathway]
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Low albumin, proteins, high LDH
Uric Acid: elevated; Calcium reduced 8.0 LOW (8.6-10.4) (pseudohypocalcemia) (both side
effects of furosemide)
PSA was nl
ANA: negative [Anti-Nuclear Antibodies, test non-specific for autoimmune disease]
LFT
Total protein: 6.0 LOW (6.1-7.7)
Albumin: 1.6 LOW (3.8-5.1)
LDH: 297 HIGH (71-207)
UA
Specific gravity: 1.008
Protein: 3+ HIGH
Microscopic: occasional granular casts, oval fat bodies
24 hour urine protein: 5.5g(>3.5= you've got that nephrotic syndrome)
Serum Protein Electrophoresis: reduced Albumin (he's peeing it out) and elevated Alpha2 (marker
of acute or chronic inflammation)
Peak 1 Albumin: 1.6 LOW
Peak 3 Alpha 2: 0.9 HIGH (secondary to acute or chronic inflammation)
(probably not gonna be a thing, but just in case):
● Decreased albumin: nephrotic syndromes, acute inflammation (amino acids being used by
the liver to make acute-phase reactants)
● Increased alpha 1: Acute, chronic inflammation,; cancer
● Decreased alpha 1: A1-antitrypsin
● Decreased alpha 2: Hemolysis
● Increased beta globulins: problem in breaking down fats (familial hypercholesterolemia),
estrogen
● Decreased beta globulins: Low LDL, malnutritions
● Increased gamma globulin (G,A,M in that order): multiple myeloma if monoclonal
and other cancers, acute/chronic inflammation if polyclonal, autoimmune, liver dz
PA and lateral films showed hilar adenopathy and poor inspiration. but no edema/obstruction.
Renal Echogram was normal. Each kidney was 12.6 cm (nl)
Repeat CBC showed BUN elevated at 26 and Creatinine 1.4
>Editorial comment: this is an interesting BUN/Creatinine ratio that would be more typically in
the range of a pre or postrenal azotemia
Renal Biopsy (the money test here) showed mild mesangial changes in the glomeruli w/ thick
basement membranes. Interstitium was normal.
Immunofluorescence showed
+IgG and C3-> granular, diffuse basement membranes -> PRIMARY MEMBRANEOUS
GLOMERULONEPHRITIS
Mild mesangial changes in the glomeruli with thick basement membranes
IgG: +++ HIGH—Fine granular diffuse glomerular basement membranes
C3: +++ HIGH—Fine granular diffuse basement membranes [Fibrogen, light chains]
What the heck might these other tests mean? (Not exhaustive by any means, just examples)
● IgM-might clue you into fsgs, mixed cryoglobinemia
● IgA-IgA nephropathy (Berger's dz- most common nephritic syndrome in the world)
● C1Q-MPG1
● Fibrinogen – Crescentic glomerulonephritis (eg Goodpastures, Wegener's)
● Light Chains: Multiple myeloma (dat bence-jones protein)
Tx'd with 5 mg thiazide (metolazone) and 40 mg po furosemide, lisinopril
Immune suppression treatment (prednisone and cyclophosphamide) discussed but pt wasn't into it.
Same thing with lipid lowering drugs, can’t really afford his pills [what a fantastic world]
Metolazone – thiazide like diuretic Acts on distal convoluted tubule. Inhibits the sodium chloride
symporter.
Furosemide – Loop diuretic. Acts on Thick ascending limb Inhibits NKCC2. Can cause hypomagnesium
and Hypokalemia.
Pt was instructed to avoid NSAIDs-> inappropriate constriction of the afferent arteriole because you're
interfering with prostaglandins
Osteopathic treatment
Decrease muscle hypertonia with direct inhibition to the T10-L2 region and gentle articulations in
rotation and side bending to the levels T10-L2
Thoracolumbar region
Muscle energy was utilized for somatic dysfunction at level T10-L2
*why give metolazone and furosemide? The use of Metolazone and Furosemide together even at low doses
metolazone significantly potentiates the diuretic effects of furosemide and therefore simplifies the
treatment of fluid retention. Sometimes furosemide dose has to be lowered after metolazone is started, to
avoid an excessive negative fluid balance.
Protein in urine:
Multistix
Criterion
Neg
Neg
Trace
15 mg/dL
1+ (30 mg/dL)
30 mg/dL
2+ (100 mg/dL)
100 mg/dL
3+ (300 mg/dL)
≥500 mg/dL
4+ (>2000 mg/dL)
≥500 mg/dL
Albumin
Alpha 1
Alpha 2
Beta
1.6 LOW
0.2 Normal
0.9 High
0.6 Normal
43.7%
5.5%
24.3%
16.3%
Gamma
0.4 Normal
10.2%
IgM, IgA, CLQ
HDL
Hemoglobin
Globulin (iron and other
carrying)
antibodies
UptoDate:
Serum protein electrophoresis (SPEP) — Serum protein electrophoresis (SPEP) is an inexpensive
and easy to perform screening procedure to detect an M-protein. SPEP is usually done by the agarose gel
method (agarose gel electrophoresis). The resulting M-protein, if found, can be quantitated using a
densitometer tracing of the gel (figure 2A-B). Thus the SPEP serves two purposes: detect presence or
absence of an M-protein in the serum, and, in conjunction with the total protein concentration, enable
measurement of the concentration (“size”) of the M-protein.
Capillary zone electrophoresis is an alternative and slightly more sensitive method of performing SPEP. It
measures protein on-line via light absorbance techniques; protein stains are not necessary and no point of
application is seen [11,12]. The electrophoretograms are similar to those produced with high resolution
agarose gel SPEP.
In the electrophoretic methodologies (agarose or capillary zone), proteins are classified by their final
position after electrophoresis is complete into five general regions:albumin, alpha-1, alpha-2, beta, and
gamma (figure 2A). These regions, which also use a Greek lettering system, do not refer to the
immunoglobulin class to which an M-protein may belong, and refer only to mobility through the support
medium. The various immunoglobulin classes (IgG, IgA, IgM, IgD, and IgE) are usually located in the
gamma region of the SPEP, but they may also be found in the beta-gamma and beta regions, and may
occasionally extend into the alpha-2 globulin area
***Creatinine clearance calculations***
Calculation information: This formula is applicable only if the serum creatinine is stable.
Est. Creatinine Clearance = [[140 - age(yr)]*weight(kg)]/[72*serum Cr(mg/dL)]
(multiply by 0.85 for women). http://www.mcw.edu/calculators/creatinine.htm
The use of Metolazone (thiazide) and Furosemide together even at low doses metolazone significantly
potentiates the diuretic effects of furosemide and therefore simplifies the treatment of
fluid retention. Sometimes furosemide dose has to be lowered after metolazone is started, to avoid an
excessive negative fluid balance. There are cases that clearly demonstrate the importance of daily checks
on the patient's body weight after starting combined therapy with furosemide and metolazone.
http://www.ncbi.nlm.nih.gov/pubmed/7280609
Case 2 – Fried his kidneys, by bottoming out his pressure - ATN
75 y/o m with a past med hx of hypertension presents w/ hypotension, respiratory illness, possible drug
rxn
>Two weeks before visit, pt had a dry cough, fever (103-104), URI
>Cephalexin was tried and didn't help, abx and htn meds were discontinued
>Pt woke up with SOB/fever->unrelieved by positional changes
>Denies chest pain/tightness/edema
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Hospital records showed: Severe HTN (210/110), P 140, T 104, RR 28 and shallow +WBCs.
Elevated CO2
Elevated BUN and Low BUN/Creatinine Ratio
CPK elevated at 469 but CK MM (specific for muscle) CK MB/Troponin (Heart) CK BB (Brain) all
normal
 muscle is getting broken down , he's not having a heart attack
Chest X-Ray was taken which showed Pulmonary edema
Later showed consolidation in the superior segment of the right lower lobe suggestive of lobar
pneumonia
ECG showed sinus tach, LVH, nonspecific ST/T wave changes
Pt given acetaminophen and furosemide and IV Nitroglycerin (NTG), at which point BP
completely bottomed out fell precipitously to 50/palp [So low that diastolic cannot be
heard only palpated].
Given two liters of intravenous normal saline.
Endotracheally intubated
General: End tidal CO2 readings of 35-40mm Hg after intubation
Mildly agitated and bucking the ventilator [pts breathing is out of sync with the ventilator]
Dopamine given to get his BP back up: Low dose dopamine was started as a continuous infusion
with return of his systolic blood pressure to 100-110 systolic.
Dopamine activates different receptors at different doses.
○ Low dose dopamine--renal perfusion: dopamine receptors in kidney
○ Medium dose: beta receptors
○ High dose: alpha receptors
Monitor I/Os, pulses, temp
Physical exam: the abnormals
● Rhonchi and rales
● Signs of consolidation-be familiar with tests like egophany, whispered pectoriloquy, etc
● Fundoscopy showed AV-nicking and copper wiring (is this ever going to be an extra credit
question??); pigment crescent variation which looked totally freaky but is a normal variant
Hematology:
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Hgb, platelets, Hct low
WBC Elevated (leukocytosis)
Neutrophilic Lymphocytopenia
BUN and BUN/Creatinine ratio abnl
ABG showed a mild alkalosis, possibly attributable to hyperventilation
pH: 7.48 HIGH [metabolic acidosis]
Sputum culture showed gram+ diplococci w/ PMNs-> Strep Pneumo (empiric treatment w/
ceftriaxone w/azithromycin; later switched to Penicillin G when sensitivities came back)
Received vigorous fluid resuscitation and his dopamine was continued (2ug/k/min) with no detriment to
his BP. Weaned off the ventilator over 12 hours. After extubation, his blood pressure was 107/73 his heart
was 103, resp was 25 maintained on 4L of O2. Urine output averaged 20cc.hr. Bolus injection of
furosemide 80mg did not increase flow of urine.
Urine output remained shitty despite furosemide and all the rib raising/MFR he coulda asked for.
Modified thoracic pump was initiated after the patient was removed from ventilator.
Chapman’s points were treated q6h.
(TART was found in T10-12; L1 with palpable tenderness at 11/1 o clock.)
Gentle OMM initiated in the form of rib raising in the thoracic and lumbar area and myofascial release
techniques.
UAs were normal at first, but on day 3 of the hospital stay he got 1-5 WBC/hpf "high powered field"; 10-15
RBCs, and Renal Tubular Epithelial Cells (means the problem is intrinsic to the kidney, if we got
casts they might look granular or "muddy brown")
● The presence of “muddy brown casts” of epithelial cells are pathognomonic for ATN. The
necrotic tubular cells combine with blood and become brown casts seen in the urine.
Urine chemistry showed elevated Urine Osmolality at 1400 and Increased FEna at 5%.
(Note: A low BUN/Creatinine ratio ie <10 and an increased FeNA are two ways to distinguish a prerenal
azotemia from ATN)
Kidney biopsy was Nl->putative diagnosis of Acute Tubular Necrosis because of his hypotensive episode
● Other diagnostic possibility was TTP (classic pentad of fever, CNS signs, microangiopathic
hemolytic anemia, thrombocytopenia and renal failure), but pt was showing no evidence of
hemolysis (no increased urine urobilinogen, the blood values were normalizing, etc)
Developed acute tubular necrosis (ATN) secondary to his hypotensive episode. The hematologists
thought that thrombocytopenia and purpura-hemolytic uremic syndrome (TTP-HUS) was a possibility
that plasma exchange was indicated. They believe that he had anemia secondary to sepsis or
renal failure.
Sent home on diuretics, potassium supplement and a very strict regimen of thoracic pumping
From Up To Date (?):
Low Dose dopamine:
increases kidney profusion
Increases urine output
Increases Renal Blood flow
Medium dose dopamine may:
increase Renal blood flow
Increase Cardiac output
Increase Heart Rate
Increase Cardiac Contractility
High dose dopamine:
Increase Blood Pressure
Stimulate Vasoconstriction
Case 3 - Get the “ENDOCRINE PANEL” [Not a real test]- Pituitary-dependent Cushing's
syndrome [Cushing Disease]
21 y/o F with a "hormonal situation"
● moon face/buffalo hump/striae
● Supraclavicular and dorsal fat pads increase
● hirsuitism (facial hair/male distributions)
● Developmental delay
● Hx of a tumor (astrocytoma) in the hypothalamic/pituitary area
● Periods "less regular than before"
● Cold intolerance
● Acne (well…depends on which part of the case you read.)
● Growth failure (cortisol is not nice to bones)
Denies
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HTN/edema
weight changes
changes in urine/stool
Diabeetus
Physical Exam:
Skin: showed plethora, a redness in the face due to increased blood flow. In cases of excess cortisol, this
is because the epidermis is thinned so the blood vessels are relatively closer to the surface.
Abdomen: Central/truncal obesity...and apparently no striae. Nope. She has striae. Promise.
Extremities: No muscle atrophy-> you might expect this in cases of excess cortisol
TEST:
CBC
● Neutrophilic leukocytopenia - glucocorticoids reduce adhesion/margination, so the bone
marrow keeps producing them
Lipid profile
● Elevated TG's, otherwise unremarkable. In full-blown Cushing's, we'd expect disturbances. We
attributed this to her working at McDonald's, because 'Murica.
"Endocrine" Panel:
Prolactin: normal
Serum B-hCG: NEGATIVE
TSH: normal
● Elevated serum cortisol = 19.9 (range 2-10)
● (they mentioned it being measured at 4pm because cortisol is secreted in a diurnal pattern, with
levels highest in the AM and falling from there)
○ The next reading of her cortisol at 8am was actually normal
● Elevated DHEA-S
○ This is an androgen specific to the adrenal cortex
Dexamethasone suppression test
Dexamethasone is synthetic (super potent) cortisol. In a normal pt, administration of a low dose around
midnight will lead to low levels of cortisol in the AM. Failure to suppress a low dose does not distinguish
the etiology of the dz. High dose dexamethasone tests are used for that-> high dose dexamethasone will
suppress pituitary sources of ACTH (Cushing's disease); ectopic sources of ACTH like a small cell lung
cancer or adrenal adenomas will not be suppressed on high-dose dexamethasone.
Dexa 0.5mg q. 6h administered for two days
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Low dose dexamethasone showed nl serum cortisol levels but increased cortisol in the urine;
ACTH levels were nl
● A two-day dexamethasone test was administered (.5 mg/q6h for 2 days), which showed nl urine
cortisol
Ruling out ectopic and adrenal sources of cortisol/ACTH: We didn't get imaging w/ contrast because the
pt was a wimp, but the adrenals looked nl. Chest CT was clear.
Pituitary MRI: T1 weighted (grey matter is gray, white matter is white, fat is white and water is dark)
showed an enlarged fourth ventricle that was irregular. That and a partially empty sella were attributed to
her past surgery. Pituitary gland was compressed into the floor of the sella. Sella is filled with CSF.
[Empty sella syndrome, can be caused by radiation]
[T1 MRI is best modality for brain anatomy, MRI contrast doesn’t have a large effect on T1 ]
More physics than you need to EVER know, but it is kind of cool: MRI measures hydrogen resonances. A measured frequency pulses through the
body and aligns the spinning resonances of the hydrogen ions (think water) in the body. T1 images are obtained by the ions that return to their
equilibrium rate the fastest. T2 waits a little longer and gets the image from the ions that return to their equilibrium at a slower rate. Adding
contrast causes the areas with (non-blood brain barrier protected) blood flow to enhance by further slowing those hydrogen ions’ return to
equilibrium
In the two months it took us to do all of this crap, the Pt has florid (obvious) Cushing's syndrome and a
peptic ulcer.
Note: Corticosteroids inhibit the production/action of prostaglandins, which are protective in the
stomach mucosa. Hence a pt on steroids or w/ Cushings would be more prone to these
Ddx: Pituitary-dependent Cushing's syndrome (later confirmed by immunohistochemistry that she
had a microadenoma (2mm) that was secreting ACTH)
● Microadenomas are <10 mm
● Cushings disease when cortisol hypersecretion is due to pituitary excessive secretion of ACTH.
We did not catheterize her inferior petrosal sinus (what we might do to see which side is secreting
ACTH ectopically); it was obvs better to just cut the pituitary out (transphenoidal hypophysectomy;
recall the sella is in the sphenoid bone)
Tx'd before the surgery: ketoconazole (used for antifungal and ACTH suppression, inhibits p450
enzymes) and famotidine (H2 blocker for gerd) until her surgery.
After she was de-pituitarized, we tx'd: prednisone (synthetic cortisol), Levothyroxine (Synthroid), and
DDVAP (Desmopressin; synthetic ADH for volume regulation. Also stimulates release of von
Willebrand factor from endothelial cells by acting on the V2 receptor.)
Addison’s disease: Failure of adrenal corticies to produce adrenocortical hormones. It is most
frequently caused by primary atrophy of adrenal cortex by autoimmunity against the cortex cells.
Mineralocorticoid deficiency: lack of aldosterone – causes less sodium reabsorption, water is lost in
urine, hyponatremia, hyperkalemia, mild acidosis, blood volume drops
Glucocorticoid deficiency: cannot maintain significant quantities of blood glucose between meals
because there is lack of control of gluconeogenesis
Melanin Pigmentation: dark melanin pigmentation of the mucous membranes and skin. This is
caused by excess ACTH secretion trying to compensate for lack of adrenalcorticoids.
Addisonian Crisis: output of glucocorticoids does not increase during stress. A person is likely to have
an acute need for excessive amounts of glucocorticoids. Stress dosing with meds.
Case 4-Did you take that diabetes run in path yet? We really want you to take that. – Diabetic
complications neuropathy, micro/marcovascular disease, nephropathy
29 y/o suuuuuuper compliant diabetic (type I) M with a sudden loss of vision in the L eye *2 days;
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ROS/PE:
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Loss of sensation in LE – typical stocking part of the "glove and stocking" pattern
Unsteady gait – from peripheral neuropathy
Retinopathy – had a vitreous hemorrhage in the right (tx'd w/ panretinal photo-coagulation)
○ "OD"-vision in right eye; "OS"-vision in left eye; "OU" vision in both eyes
Family Hx DM type 1 (for boards, know HLA DR3/4)
Meds-Glargine (long acting/basal)+Lispro (short acting/at meals); doesn't follow an 1800 calorie
ADA diet
No polydipsia/urea
HTN 230/130 (Macrovascular complications/MI is the most common cause of death in
diabetics); Pulse 120 - regular, w/ hyperdynamic precordium (you can see the heart beating out
of his chest, Kali-Ma style)-> attributed to his LVH
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Malignant HTN systolic greater than or equal to 180, Diastolic greater than or
equal to 120.
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Hypertensive urgency Diastolic greater than or equal to 120
S4 -"Tennessee"; atria filling against a noncompliant ventricle ("atrial kick")
○ Pt did not have an S3 "Kentucky", which can be a nl sound in a young person, which
happens during diastolic filling in patients >40 S3 = heart failure
From Wikipedia:
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The fourth heart sound or S4 is a rare extra heart sound that occurs immediately before the normal two "lub-dub"
heart sounds (S1 and S2). It occurs just after atrial contraction and immediately before the systolic S1 and is caused by the
atria contracting forcefully in an effort to overcome an abnormally stiff or hypertrophic ventricle.
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The third heart sound or S3 is a rare extra heart sound that occurs soon after the normal two "lub-dub" heart sounds
(S1 and S2). The S3 is associated with heart failure. It occurs at the beginning of diastole, approximately 0.12 to 0.18
seconds after S2.[1] This produces a rhythm classically compared to the cadence of the word "Kentucky" with the final
syllable ("-ky") representing S3. One may also use the phrase "SLOSH’-ing-in" to help with the cadence (SLOSH S1, -ing
S2, -in S3), as well as the pathology of the S3 sound.,[2] or any other number of local variants.
S3 may be normal in people under 40 years of age and some trained athletes but should disappear before middle age. Reemergence of this sound late in life is abnormal[3] and may indicate serious problems like heart failure. The sound of S3 is
lower in pitch than the normal sounds, usually faint, and best heard with the bell of the stethoscope.
1+ Edema B/L but hair in the pretibial regions [hair on top toes - checks arterial sufficiency in
distal circulation (Lack of hair would worry you for circulation/microvascular problems)]
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Neurological: Decreased vision bilaterally. Motor strength 4+. Decreased pinprick up to the
mid-calf bilaterally. Slightly decreased proprioception of the large toes bilaterally.
Vibration sense was absent at the ankles. [Diabetic peripheral neuropathy]
MSK: TART palpated in upper cervical area and in the thoraco lumbar junction. Small tender
areas just above the umbilicus (at 11:00 and 1:00) and posteriorly B/L adjacent to the spinous
process L1. [Chapman’s points kidneys]
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Fundoscopy showed retinal hemorrhage in the R eye and tractional retinal detachment in the L
eye, "rippley" effect. [Folding on fundascopic exam may clue you in to detached retina]
Cloudy vitreous B/L. There were vitreous hemorrhages bilaterally
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Normochromic, normocytic anemia, low RBC [Kidney disease -> low EPO]
Elevated WBC, platelets
Neutrophilic lymphocytopenia
CBC:
Blood Chem:
● Na down, K+ elevated
○ Clinical: administer K+ when administering glucose to a pt in DKA, because insulin
drives K+ into cells and the pts will become hypokalemic when you treat him
● Elevated BUN/Creatinine
● Criteria for diagnosis of DM
○ Random glucose >200 with symptoms
○ fasting glucose >126
○ Oral glucose tolerance test >200 @ 2 hours
● HbA1c -> 12 (Normal 4-5.9, good DM control <7)
○ Indicator of blood glucose control over the last 120 days
Tx'd w/ Nitroprusside for the BP dysfx, IV line for +BP
Oh and the eye stuff:
Vitreous hemorrhage and hypertensive emergency
Ophthalmologist recommended surgery [To be performed 48 hours post maintained BP]
B/L severe proliferative retinopathy with dense vitreous hemorrhage. In left eye probably
retinal detachment superiorly
Underwent vitrectomy membranectomy, laser photocoagulation.
Renal US showed
● Increased renal parenchymal echogenicity b/l; nonspecific (no hydronephrosis-> diabetics get
UTIs easily due to urinary retention)
Kidney stuff:
● Granular casts, hyaline casts
○ Granular=intrarenal dysfx
○ Hyaline casts=protein, nonspecific indicator
● Oval fat bodies, Lipid casts-> Nephrotic syndrome
Proteinuria, Hematuria, Glucose 3+ [~1000 mg/dl plasma concentration estimate]
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○ No ketones
HTN tx'd with nifedipine (Calcium channel blocker), clonidine (Alpha 2 agonist), furosemide (loop)
Enalapril was begun, got super hyperkalemic (> 6.0), so it was stopped
You generally put diabetics on ACE inhibitors to dilate the efferent arteriole, reducing GFR and
the high filtration pressures diabetics tend to have
ECG: peaked T waves (sign of hyperkalemia); L atrial/ventricular enlargement
(U waves/flattened T waves a sign of hypokalemia) [Past bonus!]
Sodium Polystyrene sulfonate was used to tx hyperkalemia
Required a kidney/pancreas transplant, went on prednisone, cyclosporine, azathioprine (all for
immunosuppression)
● Pancreatic duct emptied into urinary bladder-you can use this for a UA for pancreatic f(x)
[Monitors rejection]
● Patients go into surgery diabetic and can leave the OR no longer diabetic
Case 5 -You got diabetes! Everybody gots diabetes! – Preeclampsia
20 y/o Type I diabetic (13 year history) F; 34 weeks pregnant seeking prenatal care.
● Swollen ankles* 1 month
Pitting Edema
1+
Barely detectable impression when finger is presssed into skin.
2+
Slight indentation.
15 seconds to rebound
3+
Deeper indentation.
30 seconds to rebound.
4+
> 30 seconds to rebound.
http://web.missouri.edu/~proste/tool/cv/pitting_edema.htm
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+frequency of migraines [Could indicate HTN]
Occasional heartburn
30 lb wt gain (25-35 nl for full term)
Burning/itching w/ pee (denies +frequency)
○ +white/clumpy discharge-Candida (pseudohyphae) - Cottage cheesy
○ Recurrent yeast infections are a complication of DM
Significant hx of HPV (types 6,11 typical for warts; 16/18 are the cervical CA ones) [Know these!]
Denies n/v/changes in bowel movements/SOB/changes in stream (color/odor)
2 previous miscarriages-> this makes her a G3P0020
○ Gravida Para Notation: G=#pregnancies, P= "Florida Power And Light" (Full
Term, Preterm, Abortions, Living Children)
○ Uncontrolled DM is a course of miscarriage in early pregnancy
2100 ADA diet
Glucose 100-200; "sometimes 250-300"
Hospitalizations:
Recent tooth infx, "diabetes got out of control"
Meds
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PE:
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Lispro [Humalog] 22 units w/ meals; NPH [aka Humulin] (long-acting insulin-insulin of choice
in pregos)
○ Has had to increase dose throughout pregnancy
Mylanta:
 Aluminium hydroxide – 200mg
 Magnesium hydroxide – 200mg
 Simethicone – 20mg
+BP (140/85) ->Criteria for preeclampsia (>140/90; w/ proteinuria OR low platelets); you might
also see hyperreflexia/clonus
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Of note: New ACOG guidelines (Nov 2013) have recently changed criteria, grading and
treatment for hypertension in pregnancy. Not in your text books or boards but keep in mind
when on rotations.
Baby fetal heart tones 130 (110-160 nl)
Vagina :
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Previous misscariages (decidual tissues/products of conception) D & C s (Dilation and
Curettage)
condyloma acuminata - tx'd with podophillin* (a resin). (Editorial: this drug is out of
date, contraindicated in diabetics and pregnant ladies) condylomata acuminate
o Podophyllin – arrests (or used to) epithelial growth by binding directly to
micortubules.
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Prior yeast infx had been treated w/ Nystatin/Monostat for her and her dude.
○ Also showed an ectropion-basically when the endocervical columnar epithelium
protrudes into the os and becomes all stratified and squamous. (Caused by
pregnancy, estrogen or cervical lacerations by delivery among other things)
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Cheilitis = a sign of nutritional deficiencies (loads of vitamin deficiencies have this sign),
contact irritation, infx, or Candida
Gingivitis – bleeding gums are common in pregnancy
Mouth:
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Tests:
Pap normal and Thayer Martin (media for gonorrhea) negative
Blood type A+ (so we don't have to worry about Rh compatibility, or hemolytic dz of the newborn.
For boards, that's a type II hypersensitivity rxn! Only matters if mother is RH negative and
father is RH positive. If it was an issue, we'd administer RHOGAM.
● Rubella titer 1:24 (ie nl) (ToRCHHS infections: Toxo, Rubella, CMV, Herpes, HIV,
Syphilis. Rubella and CMV are two causes of "blueberry baby")
● Blood sugar showed proteinuria and shitty diet control
Blood Chem
● Hypokalemic,Ca, Mg -> dilutional (hypervolemic state in pregnancy)
● Low creatinine -> increased GFR (nl in pregnancy)
○ +Renal blood flow (by 80%!!)
● Fasting glucose 115
● K+ 3.7 LOW (Normal for pregnancy)
● Creatinine: 0.5 LOW (Normal for pregnancy)
● Fasting glucose: 115 HIGH
● Mg: 1.2 LOW (Normal for pregnancy)[Changes relate to blood sugar levels and preeclampsia
among other things]
CBC
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WBC: 13.5 HIGH (Normal for pregnancy)
Platelets: 250 NORMAL [if abnormal consider Preeclampsia or HEELP]
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Protein: 2+ HIGH
Glucose: 1+ HIGH
WBCs: 5 HIGH
Leukocyte esterase: positive
Nitrite: positive
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+WBC, leukocyte esterase, nitrite, bacteria-> She's got a UTI
proteinuria, glucosuria -> DM
UA
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Pt was admitted and swabbed for Group B Strep - (normally ordered at ~36 weeks, but we were
thinking about inducing her) and UTI tx'd (later determined to be E Coli) with ampicillin
HbA1c was 12.7 (eek Goal should be < 7.0 or better yet <6.5 ) [Tells history of blood glucose control
for 120 days – the life span of RBCs, unless there is a hemolytic condtion]
Renal tests - proteinuria WNL, but reducing creatinine clearance -> fetus squishes renal arteries,
reducing GFR very late in pregnancy
Fetal non stress test (put baby on the heart monitor, chill out for 20 minutes)= 5 accelerations (>2
recommended, so that's good)
Growth @ 35 weeks measured biparietal diameter=nl (concern w/ babies to DM mothers, can be
huge)
Amniocentesis showed Lethicin/Sphingomyelin ratio 2.1; Phosphatidylglycerol low
(determinants of fetal lung development) [Seems likely Bonus]
Fetal head was Ballottable - baby's head is down and pressing on the head allows for motion out of
the pelvis.
Cervix was unripe
Pt returned at 36 weeks, was induced (via oxytocin) and eventually delivered a macrosomic (growthpromoting effects of insulin) baby. (Had to do a C section eventually)
● If you were to peek at their islets of langerhans, you'd see diffuse hyperplasia because the
baby's pancreas works overtime to deal w/ mom's hyperglycemia; hence hypoglycemia in the
infant after delivery)
● Infant became hypoglycemic 2 hours after birth
● Treated with IV dextrose for 48 hours
APGAR (appearance, pulse, reflex, activity, respirations) was decent-7 and 9.
Case 6 – Resisting Censored Dead Baby Joke - Ectopic Pregnancy
26 y/o G3P011** F w/ a CC of abdominal pain and heavy (non-clotting, bright red, no tissue) bleeding.
FDLNMP 7 weeks ago "might be pregnant"
** (....teeeeechnically G2P011 since we hadn't done the BhcG yet....)
Gravida 3 [2, we did not have a confirmed pregnancy at this time] Para 1011 TPAL: Term Preterm
Abortion Live birth
Had a miscarriage one year ago—four months [S/P SAB @ 16wks – 1yr ago]
Bleeding has soaked through two pads
Denies n/v/fevers, chills, night sweats, SOB, chest pain, dysuria, constipation, diarrhea
 Recently tx’d w/ Bactrim for UTI [Trimethoprim Sulfamethoxazole = Bactrim]
 Bactrim is contraindicated in pregnancy.
Musculoskeletal:
TART in the upper cervical and lower thoracic areas: OA F RRSL
Abdomen:
Mid-lower abdominal/suprapubic tenderness w/ involuntary abdominal guarding. Nl bowel sounds, soft
and distended. [Should have performed tests for appendicitis]
Pelvic exam:
Bright red blood at the introitus/perineum. Speculum exam-pink mucosal membrane w/ blood
clots/blood-> cervix was bleeding. Cervix closed. No cervical motion tenderness->"chandelier sign"
(suggests PID or ectopic pregnancy); Uterus consistent w/ gestational age of 6 weeks. Right adnexal
tenderness.
[Last year a bonus was Cervical Motion Tenderness = ______ and not an insignificant number of
folks put down neck pathologies]
CBC/Blood chem nl
● If she were super pregnant, we might expect Hct to be low because of her hypervolemic state.
Estrogen and +Aldosterone would play a role here
B-hcg +
● Serum hCG: 14,000 [Peaks around 90,000 around 8-11 weeks gestation]
● Things to consider w/+ hcG-> Normal pregnancy, ectopic pregnancy, hydatidiform mole (w/
hella elevated b-hcG); can be a tumor marker for Germ cell tumors: (seminomas, dysgerminoma)
or choriocarcinomas
○ B-hcG test is specific for the B subunit (because it shares its alpha subunit w/ TSH, FSH,
and LH)
● B-hcG rises ~day 8, peaks ~weeks 10-12, falls down but not undetectable by weeks 16-20
US:
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Eccentric shaped gestational sac without evidence of a fetal pole. 'Pseudo sac' in the uterus
(caused by the prego hormones' effect on uterine lining).
Complex heterogeneous mass that looks consistent with a 7 week+ fetus. Fetal tissues were in the
right adnexa w/o surrounding myometrial tissue->ectopic (most common location-> ampulla
of the uterine tube)
Intervention:
 Tiopental and gentanyl; succinylcholine was used for muscle relaxation and endotracheal
intubation was performed.
 Nitrous oxide, oxygen, isoflurane.
 laprascopic removal of the tissues; adhesions were noted [PID can lead to Ectopic pregnancy].
 Right fallopian tube was noted to be dilated and an unruptured apullary ectopic pregnancy was noted
 20-25 cc of dark old blood noted in the rectouterine pouch aka Pouch of Douglas [most dependent
portion of female pelvis, where fluid pools when sitting or standing]
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Dilute vasopressin was injected within the mesosalpinx and ectopic pregnancy was removed.
Rt ovary stuck to right pelvic side wall. Rt fallopian tube somewhat blunted. Left fallopian tube stuck
to abdominal wall. Adhesions were released.
B-hCG followed to zero [persistent elevation in retained products of conception]
Because the patient was Rh+, RHOGAM (Rho D immune globulin) was not a consideration here
General US considerations:
Normal nongravid uterus would show an 'endometrial stripe' (darkness of the endometrium on US, tells
us how thick the endometrium is)
Physiological changes during pregnancy
Hormonal: levels of progesterone and estrogen rise continuously, increased B-hCG—maintains
progesterone secretion, increased prolactin levels
Physical: weight gain (25-35lbs)
Breast size: increases (1-2 cup sizes)
Cardiovascular: plasma and blood volume increase 40-50% to accommodate for the fetus—increase in
plasma volume due to increased aldosterone; increase in heart rate, stroke volume and cardiac output;
vasodilation due to excess progesterone
Hematology: increased blood volume but not increased RBC so Hct low because of dilution
factor
Edema in feet
Renal: GFR increases by 50%--as a result: decreased creatinine, and BUN and glucosuria may be seen
GI: nausea and vomiting due to excess B-hCG
MSK: lumbar lordosis
Case 7-We get it, sex kills you. Squamous cell carcinoma of the cervix- Stage III
33 y/o F w/ a CC of infertility *4 years
 Periods irregular
 Menarche at age 12
 FDLNMP 10 days ago
 sometimes 2-3 months between periods
 Could indicate anovulation
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No Miscarriages or abortions
 G0 P0
Denies hx STDs but had untreated "pelvic pain" in high school. Early age of first intercourse
(14yo). Multiple past sexual partners (~5)
 Could be PID
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Denies pain/bleeding w/ intercourse
 Pain with intercourse is called dyspareunia
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Denies galactorrhea
 (gallactorrhea + amenorrhea = possible prolactinoma).
No hirsutism or weight gain
 (Signs endocrine dysfunction)
Denies family hx of infertility, mom had ovarian CA
Adequate attempts at fertilization
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Have intercourse 2-3 times a week, use variety of positions

Infertility can be diagnosed following one year of trying
Husband has not been tested (denies hx hernia repair, mumps, trauma or chilling in hot tubs)
 [Infertility is male based 40-50%]
Last pap exam 3 years ago
 Has never had an abnormal pap
PE:
Abnormal findings:
 Right adnexal tenderness
 Inflammation at squamocolumnar junction
 Transition zone between endocervix and exocervix
 Where sample during PAPs because that's where cells are most susceptible to HPV
 Retroverted uterus (normal uterus=anteverted, anteflexed).
No condyloma acuminata (warts, usually HPV 6 and 11) noted. [Condyloma lata are a sign of
secondary syphilis]
Tests:
 "STI Panel":
 HIV (Elisa as a screening/Western to confirm)
 Chlamydia (NAAT-nucleic acid amplification test)
 RPR (Syphilis)
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 Gonococcal culture
Ovulatory Biphasic basal body temp: progesterone is responsible for the ++ in body temp during
ovulation (effect on hypothalamus) [Temperature following ovulation increases 0.5 degress]
Post-coital testing-looking for hostile cervical mucous or anti-sperm antibodies
Semen analysis: all within range
 >10 motile sperm were present 6 hours post-intercourse
Pap smear:
Pap smear showed dysplastic cells w/ smaller, pyknotic, irregular nuclei-> ddx of LSIL
(Squamous intraepithelial lesion)
Pyknosis = irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or
apoptois.
Karyorrhexis = fragmentation of the nucleus
(Cervical Intraepithelial Neoplasia I-> 1/3 of the thickness of the epithelium, caused by HPV; CINII=2/3
and CIN III=to the basement membrane) Grading of paps.
Pt referred colposcopy, which would have explored this further, patient failed to follow up despite 3
letters delivered via certified mail. [Covers our asses for liability] \
She returned two years later w/ fatigue, intermenstrual bleeding, fullness in the pelvis and postcoital bleeding. (70% women will clear CIN I or keep it), CBC shows Microcytic Anemia
[MCV <80]
Pelvic exam showed a blood stained introitus with a cauliflower lesion replacing cervix.
Lesion/Cervix was 6cm in diameter and fixed to the anterior pubic ramus [That is about the size of a
clementine].
Cervical biopsy: full thickness of epithelium has been replaced by immature undifferentiated cells with
enlarged mildly hyperchromatic cells proliferating in a disorderly fashion.
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Area of induration (induration = sclerosis or hardness) extended from anterior vaginal wall-> lower
1/3 vagina. Tumor extended into the left parametria, but not to the side wall. Tumor was stage III
because of involvement of the distal vagina
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Somatic Dysfunction:
 Cervix is innervated from S2-4
 Uterus is innervated from T10-L1
 Her Pelvic diaphragm is tight and restricted in motion.
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Punch biopsy of the cervix
 showed small cell carcinoma of the cervix.
CBC/UA was significant for mild microcytic anemia and RBC in the urine, likely due to the bleeding.
She had evidence of Left hydronephrosis (mass effect blocking the ureter)
Pt underwent external radiation treatment
○ Sx diarrhea, responding to diphenoxylate (opioid agonist antidiarrheal)
○ Anal discomfort, responded to hydrocortisone
Radiation treatment didn't work
○ Tandem and interstitial Syed template implant, 45 hours of radiation tx w/ Cesium
The cancer then metastasized to the abdomen and the pt passed away
○ One option she could have had if the cancer hadn't spread as much could have been a pelvic
exenteration-removal of the tumor, bladder, and rectum
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Staging of Cervical Cancer:
OMT considerations from the first 3 cases:
Case 1: Nephrotic syndrome, renal pathology
* Lymphatics – always treat thoracic inlet 1st, then abdominal diaphragm, then pelvic diaphragm
* Gentle effleurage “wringing” of extremities, working from distal to proximal areas in movements, also
pedal pump
* *Note – If you have any concerns for malignancy, these techniques are contraindicated! In our case, the
patient likely has BPH with normal PSA; however, avoid these techniques if he would require further
evaluation for to confirm whether malignancy is present. Also, the patient had long tobacco use history
and hilar adenopathy, which should have been further evaluated for potential malignancy.
o In patient without these concerns and if no malignancy concerns can do these techniques.
* Normalize sympathetic and parasympathetic to the kidneys and urinary bladder
* Chapman’s points – kidneys
Case 2: ATN – general treatment options for abnormalities in the case
* Pneumonia, pulm edema –
o Treat thoracic inlet first
o Vagus nerve - normalize parasympathetics
o Thoracic spine treatments - normalize sympathetics
o Rib raising
o Sternal MFR
o Rib dysfunctions
o Lymphatic techniques
*Be sure to use modified, gentle techniques if patient intubated
* Renal pathology – normalize sympathetics/parasympathetics
* Post-intubated patient
o Treat OA/AA, remainder of cervical (ie. C3-5 for phrenic nerve/diaphragm), hyoid, anterior cervical
fascia
* There are often dysfunctions here post intubation
o Rib raising, rib dysfunctions, and abdominal diaphragm
Case 3: Cushing’s syndrome, micro-pituitary adenoma
* Beware: avoid lymphatics in patient with suspected malignancy (in beginning of case we were not sure if
pituitary, adrenal, lung, or other ectopic ACTH producing tumor)
o Can use these techniques once cleared by Neurosurgery following removal of her pituitary adenoma
* Beware: avoid HVLA in this patient due to increased risk of osteoporosis with Cushing’s syndrome, also
skin thinning with easy bruising
* Beware: avoid aggressive MFR techniques due to skin thinning with increased bruising
* Overall: diagnose and treat the patient first, then do OMT as necessary when symptoms improving, as
near the end of the case. Otherwise, very gentle techniques as necessary, while keeping the above
contraindications in mind.
Actual bonuses were:
 What would a microscopic analysis of urine with very high cholesterol and no other abnormalities (no
proteinuria, etc) look like? [Maybe something to do with urea?]
 EKG finding in hyperkalemia = Peaked t waves
 What is an noninvasive test to acutely assess fetal well-being in high risk pregnancy? – [Nonstress
test? http://www.webmd.com/baby/checking-fetus-in-high-risk-pregnancy ]
 What does a retinal detachment look like on fundoscopy -

Triad of preeclampsia = maternal hypertension, proteinuria, and edema