I.

Blunt Abdominal Trauma (BAT)

a. Hemodynamically Stable: Order a CT scan - If on CT Scan:
i. Bowel/pancreas injury – Laparotomy
ii. Significant hemoperitoneum extravasation – Laparotomy
iii. Solid organ injury w/out hemoperitoneum - Observation
b. Hemodynamically Unstable: Perform either a FAST or DPL
i. Results of FAST
1. No hemoperitoneum - Consider a DPL or another diagnosis
2. Hemoperitoneum – Laparotomy
ii. Results of DPL
1. No hemoperitoneum - Consider another diagnosis for the
hemorrhagic shock... DO NOT DO A FAST
2. Hemoperitoneum - Do laparotomy
II. Any gunshot wound  Exploratory laparotomy
III. Any stab wound
a. Hemodynamically Stable  perform a FAST
b. Hemodynamically Unstable  peritoneal irritation, equivocal FAST
or evisceration  Exploratory Laparotomy
IV. BAT:
a. If there are any s/s of peritoneal irritation (tenderness, rebound
tenderness and guarding)  Exploratory Laparotomy
b. In Both Hemodynamically Stable and Unstable  Perform a FAST
i. FAST  if NEGATIVE –
1. Stable – CT w/contrast
2. Unstable – DPL
ii. FAST  if POSITIVE +
1. Exploratory Laparotomy

V. Blunt Abdominal Trauma (BAT)

 a. Hemodynamically Stable: Order a CT scan - If on CT Scan:
i. Bowel/pancreas injury – Laparotomy
ii. Significant hemoperitoneum extravasation – Laparotomy
iii. Solid organ injury w/out hemoperitoneum - Observation
b. Hemodynamically Unstable: Perform either a FAST or DPL
i. Results of FAST
1. No hemoperitoneum - Consider a DPL or another diagnosis
2. Hemoperitoneum – Laparotomy
ii. Results of DPL
1. No hemoperitoneum - Consider another diagnosis for the
hemorrhagic shock... DO NOT DO A FAST
2. Hemoperitoneum - Do laparotomy
VI. Any gunshot wound  Exploratory laparotomy
VII. Any stab wound
a. Hemodynamically Stable  perform a FAST
b. Hemodynamically Unstable  peritoneal irritation, equivocal FAST
or evisceration  Exploratory Laparotomy
VIII. BAT:
a. If there are any s/s of peritoneal irritation (tenderness, rebound
tenderness and guarding)  Exploratory Laparotomy
b. In Both Hemodynamically Stable and Unstable  Perform a FAST
i. FAST  if NEGATIVE –
1. Stable – CT w/contrast
2. Unstable – DPL
ii. FAST  if POSITIVE +
1. Exploratory Laparotomy

EEG Patterns
1. 3 Hz spike and slow wave - Absence seizures
2. Focal spikes at the temporal lobe - temporal lobe epilepsy, temporally-
located intermittent rhythmic delta activity (TIRDA)
 3. Hypsarrythmia - Infantile spasm and west syndrome
4. Lateralized periodic discharges (LPDs; previously referred to as periodic
lateralized epileptiform discharges or PLEDS) - Status epilepticus. large
cerebral injury, such as stroke, encephalitis, or rapidly growing cerebral
malignancies.
5. Midline spikes: - tonic clonic seizures
6. Triphasic waves - Hypoxic ischemic encephalopathy
7. Polyspike and wave discharges - Myoclonic epilepsy.

1. Maltose = Glucose Alpha 1-4 Glucose

2. Lactose = Galactose Beta 1-4 Glucose
3. Sucrose = Glucose Alpha 1-2 Fructose
Just start working at the part that says 'ECF volume' (understanding
the rest is bonus). You will see that hyponatremia can be seen with
decreased, normal, or increased volume states. Your job is to not
only know the differential for each of these states but to understand
what is going on with aldosterone and ADH at each point.

Hypervolemic hyponatremia is caused by increased aldosterone

AND increased ADH. These cases are characterized by decreased
"effective circulating volume" (e.g. CHF) that results in unregulated
RAAS activity -> aldosterone -> increased sodium
retention/hypervolemia. The body starts increasing ADH secretion
as well to try to increase plasma volume which causes the
hyponatremia (remember i said there is crossover? turns out the
body also tries to use ADH to increase volume status at the
expense of maintining normal osmolality ).

Euvolemic hyponatremia is due to increased ADH (e.g. SIADH) and

~normal aldosterone. I don't recall what the exact mechanisms of
hypothyroid and hypocortisolism are but you should remember
these are part of the differential.

Hypovolemic hyponatremia is due to decreased sodium with

relatively less decrease in free water. These can either be high aldo
or low aldo states depending on the cause.
Urine Na+ can be used to distinguish be renal (high urine Na+)
from extrarenal (low urine Na+) sodium loss
I actually think 'vomiting' in this chart is incorrectly placed under the
high urine Na category; it is actually a low urine Na+ state.
Not sure if that answers what you were asking

his was the best explanation I found, with ANP playing a role in the
resulting euvolemic hyponatremia (= natriuresis):

The continued presence of ADH as in SIADH with water intake

causes retention of ingested water. While a large fraction of this
water is intracellular, the extracellular fraction causes volume
expansion. Volume receptors are activated and peptides (eg, atrial
natriuretic peptide from heart ) are secreted, which causes
natriuresis with some degree of accompanying naturesis and
diuresis. As a general rule ANP tends to antagonize the effect of
ADH and AT-II. Thus, these patients are euvolemic or are slightly
volume-expanded.

The plasma sodium concentration is the primary osmotic

determinant of ADH release. However, in persons with SIADH, a
non-physiologic secretion of ADH results in enhanced water
reabsorption, leading to dilutional hyponatremia. Sodium excretion
is intact, and the amount of sodium excreted in the urine varies with
diet. Ingestion of water is an essential prerequisite to the
development of dilutional hyponatremia; regardless of cause
(pituitary ,pulmonary)...... hyponatremia does not occur if water is
restricted.

Kaplan

fo osteoblasts -Spinal Cord Compression

Autoimmune hepatitis - Lymphocytic portal inflammation
Euthyroid Sick Syndrome - low T4 and T3, normal TSH
Nocardia - Acid Fast
Hyperalcemia with mental status changes - IV Normal Saline +
Furosemide
Cerebral Amyloid Angiopathy - lobar hemorrhage

• Diverticultitis - MC causes colovesical (enterovesical, vesicoenteric)

fistula - can also be caused by adenocarcinoma of the sigmoid colon
pneumaturia is pathognomonic - CT Scan of the abdomen and pelvis with
contrast —> NPO + IV antibiotics
• 8 year old skateboard +LOC —> CT Scan shows hypodense lesion in
the pons & hyperdense focus within the basilar artery -> NEXT -
Angiography of the neck vessels (dissection of one or both of the cerebral
arteries)
• Paget Disease - Osteitis deformans, increased bone turnover,
deafness, nerve compression symptoms, “or simply an elevated ALP”
Normal Calcium and Phosphorus - Tx Bisphosphonates
• Lyme Disease**** erythema migrans rash with a central clearing,
(early localized disease) followed an early disseminated disease (stiff
neck, photophobia, and slurred speech, makes it a CNS problem)
Oral therapy is good for rash, the joints, serology to confirm
Children - Amoxicillin
CNS - IV Ceftriaxone
Joint problems - PO Doxycycline
• Elderly women - new onset ascites - Peironeal carcinomatosis —>
Exudative: consequence of neoplasia, infection or inflammatory states.
Transudatee MC associated with liver cirrhosis, CHF, Budd-Chiari, and
hepatic metastasis
• Torades de Pointes -
Unstable - Unsynchtonized cardioversion
Stable - IV Mg sulfate is DOC
Refractory to medical treatment - temporary pacemaker
• aff
The patient is placed on aspirin, nitrates, a beta blocker, and a Staten,
however, angina like symptoms are reported two months later.
Maximum medical therapy has been achieved with a goal heart rate of 55
to 60 bpm. If this not met the next step is to increase the dose of
metoprolol. ******* coronary angiography is only done with stable
angina when a patient is still having symptoms with optimal medical
management. Heart rate goal is a important part of medical
management. Thus he should undergo coronary angiography. The
coronary angiogram maps out the diseased vessels and dictate future
management such as angioplasty or standing. If the angiogram shows left
main coronary artery disease or 2 to 3 vessel disease he would be a
candidate for CABG.

Eptifibatide and percutaneous transluminal coronary angioplasty and

tirofiban (glycoprotein 2b3a inhibitors) are NOT used in stable angina.

The indications for prescribing an ACE inhibitor in a patient with

stable angina Are:
• DM
• Hypertension
• Low ejection fraction (<50%)
• Presence of proteinuria

Acute Pericarditis > A j20-year-old male college student complaining of

chest pain for eight days Pain is sub sternal and mildly worse with activity
although he has been 30 the last week. There is some radiation of the
pain to the neck and back. A deep breath worsens the pain as does
recumbency. The pain is improved by sitting. upright and leaning
forward. Cardiac auscultation reveals a scratchy sound heard best at
they left lower sternal border. The most likely to confirm the diagnosis
is the = Electrocardiogram ***** friction rub is diagnostic of
pericarditis. $$$ but it needs to be distinguished from a pleural rub
(Which will not have 3 components or be in sync with the cardiac cycle)
EKG is most useful for diagnosing pericarditis. Diffuse concave ST
elevation
1. Allergic Rhinitis: Intranasal steroids – pale blue nasal muscosa

- Caused by exposure to airborne allergen

- Activation of B cell and Cytotoxic RT cell
IgE causes release of inflammatory mediators

CF: Rhinnorhea, sneezing, conjunctival erythema, tearing, Pruritus

2. Chronic Alcoholism SAST>ALT

3. Porcelain GB (significant intramural calcification, thickened
calcified wall, , no periholecystic fluid ) Prophylactic
cholecystectomy
4. Transcutaneous pacing (acute)  then transvenous
5. NTD Myelmenigeocele  assoc with Dandy Walker Type 2 
hydrocephalus
6. Salmonella Typhi  Galllbladder Carcinoma
7. Cholinesterase Inhibitors for Alzheimers
a. Tacrine
b. Donepepzil
c. Rivastigmine
d. Galantamine
8. Septic Shock – high CO, low TPR
9. Strep Pharyngitis – IM Benzathine Penicilli

Constrictive Pericarditis Cardiac Tamponade

KUSSMAUL SIGN: - JVD w. Pulsus Paradoxus (decrease in
inspiration SBP by more than 10mmHg
with INSPIRATION)
Type 4 RTA – Hyporeninemic hypoaldosteronism
Liver abscess complicating biliary tract disease is described as a pyogenic
abscess (to contrast it with amebic abscess), and it requires drainage. The
p[percutaneous route is favored. The difference between amebic and
pyogenic abscess may be radiographically indistinguishable. Clinical suspicion
based on age and epidemiologic risk factors is therefore more impt. Those
who have pyogenic liver abscesses are more likely to have a greater degree of
jaundice, bacteremia/sepsis, and history of gallbladder disease or surgery.
Amebic abscess should be suspected in young male patient who have recently
revealed to endemic areas or who are immigrants of endemic areas. Amebic
abscess, when suspected, does not require immediate percutaneous drainage.
It should be treated with metronidazole. And serologic testing performed (for
E. Histolytica). If the patient does not improve in a few days, percutaneous
drainage may be required.