INTERNAL MEDICINE NOTES

Physical exam
- Cardiac: Remember BALLS for S3 and S4: Bell-apex-light pressure-left side
- Pulmonary
- Bronchial breath sounds sound like you are breathing through a paper towel tube and
have expiratory phase > inspiratory phase. Normal in the central lungs, abnormal over
the periphery - suggest consolidation (loud or normal volume, bronchial breath sounds)
- Vesicular breath sounds - have inspiratory phase >> expiratory phase.
- Inspiratory wheeze - think upper airway pathology

CXR notes
- Framework
- Image quality - roneophrotictation, inspiration (5-7 anterior ribs above diaphragm),
penetration
- Penetration
- On PA, the thoracic spine disc spaces should be barely visible through the heart but no
bony details of the heart.
- On lateral, the spine should darken as you move caudally due to more air in the lung in
the lower lobes and less chest wall - top of the spine should be brighter
- Under penetrated → everything is bright. Over penetrated → everything is dark
- Orientation
- PA
- Assess for rotation by looking at the clavicular heads and seeing if they are
equidistant from the spinous process of the thoracic vertebral bodies.
- Rotation to the left can increase heart size, while rotation to the right can
decrease heart size. Makes sense if you think about the position of the
heart in the chest
- Assess for the adequacy of inspiration - anterior ends of 5-7 ribs should be
visible above the diaphragm in the mid-clavicular line. Less → incomplete breath
in, more than 7 → lung hyperexpansion (if hyperexpansion, the costophrenic
angle can be blunted and give the false impression of pleural effusion)
- If lung inspiration is inadequate, lungs will look denser - might look like
consolidation
- Silhouette sign
- Right upper lobe is against the ascending aorta, right middle lobe is
against the right atrium, right lower lobe is against the right
hemidiaphragm
- Left upper lobe is against the aortic arch, lingula is against the left
ventricle, left lower lobe is against the left hemidiaphragm and the
descending aorta
- Only bone can obliterate bone!
- Kerley B lines = thickened edematous interlobular septa. Caused by pulmonary
edema, lymphangitis carcinomatosa, malignant lymphoma, atypical pneumonia,
interstitial pulmonary fibrosis, sarcoidosis, pneumoconiosis
- Lateral xray:
- film is against the left chest → right sided structures (ribs) get magnified and
appear larger
 - Left hemidiaphragm is higher than the right (usually).
- Left hemidiaphragm disappears anteriorly but right hemidiaphragm does not. Can
only see part of the left hemidiaphragm because of the silhouette sign - heart sits
on top of it. Right hemidiaphragm will also continue posteriorly past the smaller
left ribs and end at the larger and more posterior right ribs
-
- Heart
- PA: Right border is right atrium (should almost be straight up and down), left border is left
ventricle. Lateral: posterior border is left atrium, anterior border is right ventricle.
- Enlargement
- Normal heart size is < 50% of the chest diameter on PA film and 25-30%
cranial/caudal length of the sternum - assuming adequate inspiration
- Left atrial enlargement: double density of the right heart border, prominent left
atrial appendage, angle of the carina is increased > 90 degrees because it lies
just above the left atrium
- Lung pathology
- Atelectasis: Increased linear density, the apex tends to be at the hilum. Can be
associated with lost volume → other structures will move in, e.g., elevated
hemidiaphragm, elevated horizontal fissure
- Cardiac pulmonary edema: cephalization of the pulmonary vessels, kerley B lines
(thickened, edematous interlobular septa), peribronchial cuffing, bat wing pattern,
increased cardiac size
- Pneumonia
- With lobar pneumonia, look for silhouette sign to dermine the lobe affected
- Contrast atectasis - pneumonia has normal or increased volume (not loss), not
centered at the hilum
- Pleural effusion - blunting of costophrenic angles and the pleural fluid will form a
meniscus with the chest wall
- Pneumothorax: Most easily seen at the apices on PA image
- Pulmonary embolism - most often the CXR is normal!
- Interstitial pulmonary fibrosis - ground glass opacification, volume loss, linear opacities
- Hilar adenopathy: Inflammation (sarcoidosis, silicosis), cancer (lymphoma, metastasis,
bronchogenic carcinoma), infection (TB, histo, mono) - can be confused with enlarged
pulmonary vessels. The vessels appear to have smooth contours while adenopathy is
lumpy-bumpy
- TB: any time you suspect TB, also think of histo and blasto, though they are far less
common
- Masses in general: size, shape, location, extent & distribution, circumscription (sharp edges?),
density, homogeneity
- Tubes and lines
- NG tube - should be below the level of the diaphragm and at least 10 cm beyond the
gastro-esophageal junction. The tip should lie on the left - if it is midline, then it’s in the
duodenum - that’s a naso-enteric tube
- Endotracheal tube - should be 5 cm from the carina, with head neither flexed nor
extended. Minimal safe distance is 2 cm. With head flexion, the tube can move down 2
cm. With head extension, the tube can move up 2 cm.
- Central venous catheter tip - enters through the subclavian or jugular veins, travel to the
junction left subclavian vein and superior vena cava
Health Maintenance

Men and Women

1) Varicella: adults > 60 yrs

Women
1.) Mammogram
a.) Women 40-50 yrs: every 1-2 years
b.) Women > 50: every year
2.) Cervical cancer
a.) First one at 21 yrs or w/in 3 years of sexual activity, then second one is one year later.
b.) If first two are negative → every three years until age 35
c.) Every 5 years until 65
3.) STDs - screen women for chlamydia and gonorrhea, everyone for HIV
4.) Osteoporosis
a.) DEXA scans for women starting at age 65

Men
1) AAA - > 65 yrs if ever smoked. Do w/ ultrasound
 OUTLINE OF STEP UP TO MEDICINE

Chapter 1: Cardiovascular System

Diagnosis of CAD
1. ECG
2. Stress tests: If positive → cardiac cath
a. Stress ECG - 75% sensitive if patients can get HR to 85% of max. Watch for ST
depression, HR, or ventricular arrhythmias
b. Stress echo - more sensitive than stress ECG. Can be used to dx CAD in the presence of
preexisting ECG abnormalities.
c. Enhance stress tests with IV radioisotopes (thallium 201) - helps to determine fixed vs.
reversible ischemia. But more expensive, radiation, and not helpful w/ LBBB
d. Pharmacologic stress tests - adenosine and dyridamole are vasodilators, also
dobutamine
3. Holter monitors for silent ischemia (portable ECG), syncope, dizziness
4. Cardiac catheterization with coronary angiograpy = gold standard for CAD
a. Cath: info on hemodynamics, intracardiac pressure, CO, O2 saturation.
i. Do if + stress test, angina that’s a diagnostic dilemma or occurs after MI or
despite medical therapy, severe symptoms, evaluate valvular disease, determine
need for surgery
b. Coronary angiography: can do PCI with stent or balloon at the same time!

Stable angina
● Treatment options in general:
○ Reduce risk factors
○ Meds:
■ Aspirin and beta blockers (atenolol, metoprolol with B1 > B2) have mortality
benefits.
■ Nitrates for angina.
■ Can add calcium channel blockers if beta blockers or nitrates aren’t enough, but
no mortality benefit.
■ If CHF → add ACE inhibitor or diurectics
○ Revascularization: improves symptoms, does not reduce risk of MI! Can do PCI
(angioplasty) or CABG.
● Treatment options for CAD by disease severity:
○ Mild disease: Normal EF, mild angina, single vessel. Aspirin, BB, nitrates. Consider
CCBs.
○ Moderate disease: Normal EF, moderate angina, two vessels. If symptoms w/ meds,
consider PCI or CABG
○ Severe disease: Decreased EF, severe angina, three vessels/left main/LAD. PCI or
CABG. Generally CABG is the standard for really bad disease, but PCI may be just as
good.

Unstable angina: treat like MI but no fibrinolysis

 ● Meds improve most patients within 1-2 days. Choice of whether to do more aggressive mgmt
early is controversial. If respond to meds, then do a stress ECG to assess need for
cath/revascularization. If no response to meds within 48 hours, go straight to cath/revasc.
● Acute meds:
○ Aspirin + clopidogrel for 9-12 months
○ Glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban)
○ Beta blockers,
○ Heparin - goal is PTT 2-2.5 x normal, but LMWH is better and don’t need to follow PTT
○ Nitrates
○ Oxygen if hypoxemic
○ Morphine
○ Replace electrolytes - especially K+ and Mg2+
● Chronic meds: aspirin (or other antiplatelet agents), beta blockers, nitrates, reduce risk factors by
treating HTN, DM, hyperlipidemia - if LDL is high, use a statin

Variant angina:
● Episodes at rest, often at night, associated with ventricular arrhythmias - can be fatal. Hallmark is
transient ST elevation during chest pain - test with ergonovine
● Treat with vasodilators (CCBs, nitrates) & risk factor modification

Myocardial infarction
● Asymptomatic in up to ⅓ patients: especially if post op, elderly, diabetic, female
● Cardiac enzymes:
○ Troponins: Rise in 3-5 hours, peak in 1-2 days, decline in 5-14 days. Troponin I can be
falsely high in renal failure; troponin T is better
○ CK-MB: Rises in 4-8 hours, peaks in 1 day, normalizes by 2-3 days.
● Treatment:
○ Medications: (MONAH is an ACE Babe)
■ Aspirin, beta blockers, and ACE inhibitors reduce mortality and should be part of
long term maintenance therapy
■ Statins reduce risk of further coronary events and should be part of maintenance
therapy
■ Oxygen, nitrates, morphine, and heparin (LMWH is better) - but no mortality
benefits
○ Revascularization w/ thrombolysis, PCI, or CABG
■ PCI is better than thrombolysis when done early and by skilled person, but it’s
only available at skilled centers.
● If get a stent - add clopidogrel to aspirin - at least 30 days for metal stent,
1 year for drug-eluding stents
■ Thrombolysis up to 24 hours after onset of pain, best w/in 6 hours - alteplase is
best.
● CI’d if recent trauma or CPR, hx of stroke, recent surgery, dissecting
aortic aneurysm, active bleeding or bleeding problems.
■ Do emergency CABG only if the person is unstable
○ Cardiac rehab reduces symptoms and prolongs survival!
● Acute complications:
○ CHF is most common cause of death. If mild, treat with ACEi or diuretic. If severe, may
need invasive hemodynamic monitoring
 ○ Arrhythmias - pretty much any of them can happen. What follows is just a selection.
■ PVCs - just observe. But they can lower SV and coronary artery filling time - may
predict Vfib or VT
■ Afib
■ Ventricular tachycardia - electrical cardioversion if unstable. If stable, IV
amiodarone
■ Sinus bradycardia - common in the early stages of acute MI, may be protective
by reducing oxygen demand. If severe or symptomatic, can use atropine
■ AV block - have to treat second degree type II and 3rd degree blocks. With
anterior MI, have to use a pacemaker. With inferior, can try IV atropine at first.
● Long term complications
○ High risk of stroke w/in five years - especially if low EF and older age

CHF
● Treatment for systolic dysfunction: Standard is loop diuretic, ACE inhibitor, and BB. May also add
digoxin, hydralazine/nitrate, and spironolactone depending on severity
○ ACE inhibitors have a mortality benefit in all levels of CHF! Can use ARB if ACEi not
tolerated
○ BB decrease mortality in post MI CHF - evidence for metoprolol, bisoprolol, and
carvedilol. Slows tissue remodeling, decreases oxygen consumption. Also antiarrhythmic.
Give to stable patients with Class 1,2,3 CHF.
○ Spironolactone has a mortality benefit in class 3-4 CHF
○ Hydralazine + nitrate lowers mortality
○ CCBs have no role in treatment of CHF! However safe to use amlodopine and felodipine
if CCBs are needed for another indication
● Treatment for diastolic dysfunction: few options, treat symptoms with BB, diuretics.
○ AVOID spironolactone and digoxin
● General guidelines
○ Class I to II: loop diuretic + ACE inhibitor
○ Class II to III: Add BB
○ Class III to IV: Add digoxin instead of BB, add spironolactone
● Acute CHF - differential includes PE, asthma, PNA
○ oxygen, diuretics, IV nitroglycerin if no hypotension - reduces afterload, maybe
dobutamine - digoxin takes several weeks to work! No role in acute setting.

Pericarditis
- ST elevation in all leads except AVR

Arrhythmias
● PACS - no significance in normal heart (50% of people have them), but can be a precursor of
ischemia in a diseased heart. Can cause palpitations or PSVTs - if symptomatic, BBs
● PVCs - Can occur w/ or w/out disease - but associated with increased mortality! If symptomatic,
treat with BBs. But use of antiarrhythmics to suppress PVCs after MI assoc’ed with increased risk
of death

Cardioversion vs. Defibrillation vs. Transcutaneous pacing:

 ● Cardioversion shock is in synchrony with the QRS - have to be careful to avoid shocking during
the T wave, can cause VFib. Indicated for AFib, AFlutter, SVT, VT with a pulse
● Defibrillation: shock is not coordinated with the QRS complex - converts dysrhythmia to sinus
rhythm. Use for VFib or VT without a pulse
● Transcutaneous pacing is used for asystole - defibrillation usually won’t work

Ventricular tachycardia
● Sustained VT
○ Stable patient with mild symptoms and systolic BP > 90 - use pharmacologic therapy
(amiodarone is best, also IV procainamide or IV sotalol)
○ Unstable patient - immediate cardioversion if a pulse, defibrillation if no pulse. Follow with
IV amiodarone
○ Place an ICD, unless EF is normal
● Nonsustained VT (< 30 seconds)
○ Don’t treat if no underlying heart disease and asymptomatic - no increased risk of death
○ Otherwise order an electrophysiologic study - if it shows inducible, sustained VT, then
place an ICD. Drugs are second line - amiodarone is the best.

Ventricular Fibrillation
● Defibrillation and CPR! Give up to 3 shocks, reassess rhythm in between
● Add epineprhine and then shock - will increase myocardial and cerebral blood flow and decrease
defibrillation threshhold
● Try IV amiodarone followed by shock - lidocaine, Mg, and procainide are alternatives
● If successfully restablish sinus rhythm, then keep on IV amiodarone. Implantable defibrillator is
best long term therapy.

Warfarin is metabolized by the P450 system -

● this system is inhibited by acetaminophen, NSAIDs, antibiotics and antifungals, amiodarone,
cimetidine, cranberry juice, ginko biloba, Vit E, omeprazole, thyroid hormone, and SSRIs
● Induced by carbamazepine, ginsing, green veggies, oral contraceptives, phenobarbital, rifampin,
St John’s wort

End Stage Renal Disease limits anticoagulation choices! Enoxaparin, fondaparinux (injection factor 10a
inhibitor) and rivaroxaban (oral factor 10a inhibitor) aren’t options, because low GFR increases anti-10a
activity levels and bleeding risk. Gotta use unfractionated heparin.

Myocarditis
- Often viral - coxsackie, adenovirus, HSV6, enterovirus. Causes dilated cardiomyopathy with
diffuse hypokinesia → low EF. Diagnose with echo

Abdominal aortic aneurysm

Screen men 65-75 who have ever smoked 100 cigarettes in their life. Follow yearly if < 4 cm and every 6
months if > 4 cm. Surgery if > 5 cm.
 -
Hypertrophy
- Eccentric: in response to volume overload/increased preload (exercise, pregnancy) - add
cardiomyocytes in sequence. Get bigger chamber, but wall thickness is about the same
- Concentric: add cardiac myocytes in parallel in response to afterload increase - get thicker wall,
chamber size might decrease
- Dilated cardiomyopathy

Infective endocarditis
- Vascular sx: emboli cause focal neuro deficits or renal/splenic infarcts, pulmonary infarcts,
mycotic aneurysm, conjunctival hemorrhages, Janeway lesions (not painful)
- Immunologic phenomena: osler’s nodes, roth spots, glomerulonephritis, arthritis or positive RF
- FROM JANE: Fever, Roth spots, Osler nodes, Murmur. Janeway lesions, anemia, nail
hemorrhage, emboli
- Bugs
- Dental procedures or manipulation of the respiratory tract: Strep viridans (includes
mutans, sanguinis), Eikenella (culture negative)
- Colon cancer or IBD ulcers: Strep bovis
- Hospital aquired UTI: Enterococcus
- Staph aureus and epidermidis: Most common causes of healthcare associated infective
endocarditis. Prosthetic devices, catheters
- IV drug users: staph aureus - can have septic emboli that go to the lung and cause
pneumonia

Digoxin toxicity - cholinergic sx including nausea, vomiting, diarrhea, blurry yellow vision (think Van
Gogh). On EKG - can increase PR interval, decrease QT, cause ST scooping, T wave inversion,
arrhythmia, and AV block.
● Factors predisposing to toxicity: renal failure (decreased excretion), hypokalemia, verapamil,
amiodarone, quinidine (decrease digoxin clearance, displace digoxin from tissue binding sites)
● Antidotes: anti dig Fab fragments, slowly normalize K+, Mg2+, cardiac pacer

Cholesterol emboli
- Suspect after vascular procedures in a patient with risk factors for atherosclerosis and a
constellation of acute/subacute renal failure, typical skin findings (blue toes, livedo reticularis,
ulcers, gangrene), eosinophilia, GI symtoms (ischemia, pancreatitis), stroke, hollenhurst plaques
on ocular exam, etc.
Chapter 2: Pulmonary System

Lung cancer paraneoplastic syndromes

● Small cell: SIADH, ACTH, Lambert Eaton Syndrome
● Squamous cell: PTH-rp

Sarcoidosis:
● Can have lots of extrapulmonary manifestations - anterior uveitis, splenomegaly, hepatomegaly,
arthritis (esp ankles), central diabetes insipidus, erythema nodosum (inflammation of fat cells,
especially on the shins - looks like large red bruises)

Warfarin goals: 6-12 months after PE and Afib - aim for 2-3. With prosthetic heart valves, go higher - 2.5
to 3.5. Over 4 presents a high risk of bleeding

Pulmonary embolism
- S1Q3T3 pattern indicates right heart strain - present in 10% of PEs. Have S wave in lead I, Q
wave and inverted T in lead III

Pneumonia.
- First step is risk assessment: like CURB-65 algorithm. Give one point for confusion, uremia (BUN
> 20), tachypnea (RR > 30), Blood pressure < 90/60, and age > 65.
- < 2 points → outpatient. If CAP, give doxy or macrolide if otherwise healthy. If
unhealthy, give floroquinolone (levofloxacin or moxifloxacin) or beta lactam + macrolide
- If 2-3 points → inpatient. If CAP, treat like an unhealthy outpatient
- If 4 or more poitns → inpatient ICU for either IV beta lactam + macrolide or beta lactam +
floroquinolone.
- Pneuomcystis jiroveci is an important cause of atypical pneumonia in immune compromised
adults.
- Fever, dyspnea, nonproductive cough, diffuse interstitial infiltrate. Basically suspect if an
IC’ed person has hypoxia and dyspnea. Dx by inducing sputum production with
hypertonic saline (best) or by bronchoalveolar lavage (good for evaluation of malignancy
and opportunistic infection)
- Legionella pneumonia - intracellular gram negative rod. Spread by water (e.g., cruise ships).
Suspect if patient has pneumonia with high fever, GI symptoms, and confusion, hyponatremia.
Sputum gram stain will show neutrophils, but no bugs. Have to use charcoal agar or urinary
antigen testing. Treat the same as other atypicals.
- Anaerobes: foul smelling sputum. Use clindamycin.
- Uncomplicated CAP:
- Treat for 5-7 days after fever resolves

Pleural effusion:
1. First step is to determine whether the PE is exudate or transudate - do a thoracentesis. The
exception is if the effusion is clearly from CHF, then just give diuretics.
 a. If any of the following are true, then it’s exudate: pleural protein/serum protein > 0.5,
pleural LDH/serum LDH > 0.6, pleural LDH > ⅔ the normal upper limit for serum
LDH.
i. Shortcut: pleural protein > 3, LDH > 100, cholesterol > 45
b. Exudates are caused by increased capillary permeability, while transudates are from
decreased oncotic pressure or elevated hydrostatic pressure
c. Cirrhosis can cause right sided pleural effusion due to increased permeability of the right
hemidiaphragm. Known as hepatic hydrothorax.
2. If exudate, then determine if it’s complicated, uncomplicated, or empyema
a. Empyema is purulent and has bacteria on gram stain
b. Look for glucose < 60, pH < 7.2 → suggests bacterial infeection (complicated effusion),
rheumatoid pleurisy, drug induced lupus, tuberculosis, or malignancy. pH < 7.2 means
that the fluid almost certainly has to be drained!
i. When the empyema is localized, complex, and has a thick rim, surgery is the
only answer. Chest tube won’t do the trick.
c. PE can cause exudate or transudate, but will not affect the pH and glucose

Empyema:
Most often occurs from untreated pneumonia due to bacterial seeding of a pleural effusion. Initially the
bugs are the same as in the pneumonia, but then a mixed aerobe/anaerboe picture develops - this is one
reason why empyema is often unresponsive to abx

ARDS:
- Oxygenate by increasing PEEP - up to 15 safe.

Drug induced lupus: hydralazine, procainamide, isoniazid. Can cause a picture suggestive of complicated
pleural effusion

COPD exacerbation: Give antibiotics if 2 of 3 of the following - increased dyspnea, cough, and sputum
(volume or color change), moderate to severe exacerbation, or need for mechanical ventialation.
Azithromycin, floroquinolones, or penicllins/beta lactamases

Digital clubbing - not caused by COPD! Consider lung cancer, bronchiectasis (also seen in cystic fibrosis)

Acute bronchitis
- Usually no fever - just sore throat, cough, maybe sputum - even bloody. Often viral, so abx aren’t
indicated.

Hypertrophic osteoarthropathy = digital clubbing + sudden onset arthropathy - usually affecting the wrists
and hands.
- Hypertrophic pulmonary osteoarthropathy = subset of the condition caused by underlying lung
disease - cancer, TB, bronchiectasis, or emphysema

Mediastinal masses
- Anterior: thymoma, retrosternal thyroid, teratoma. Can cause chest heaviness, discomfort,
Horner’s syndrome, hoarseness, and facial and upper extremity edema
- Middle: Bronchogenic cysts, tracheal tumors, pericardial cysts, lymph node enlargement, and
aortic aneurysm of the arch
 - Posterior: neurogenic tumors including meningocele, enteric cysts, diaphragmatic hernias,
esophageal tumors, and aortic aneurysms
- Lymphoma - can be anywhere

Hypoxemia
- Caused by reduced inspired oxygen, hypoventilation, diffusion limitation, shunt, and V/Q
mismatch
- Calculate the A-a gradient: Normal is < 15, over 30 is abnormal. Alveolar oxygen is 150-
PaCO2/0.8. Then subtract arterial oxygen to get the gradient
- Elevated A-a gradient
- V/Q mismatch: pulmonary embolism, atelectasis, pleural effusion, pulmonary edema
Chapter 3: GI System

Esophagitis
Drug induced - tetracyclines (acid), aspirin/NSAIDs, alendronate, KCl (causes local hyperosmolality),
quinidine, iron

Dysphagia
- Solids and liquids at onset → motility disorder.
- If oropharyngeal (cough, nasal regurgitation, choking) → do a videofluoroscopic modified
barium swallow.
- If esophageal → do a barium swallow first, then confirm the dx with esophageal
manometry
- Solids only, or solids then liquids → mechanical obstruction. Do endoscopy, unless hx of risk
factors for perforation (prior radiation, complex strictures, prior surgeries, caustic injuries) - then
do a barium swallow first and then endoscopy

Dyspepsia
- If risk factors for gastric or esophageal cancer → EGD. This includes age> 55, weight loss,
bleeding, anemia, dysphagia, early satiety
- If NSAID use → give PPI
- If have risk factors for H pylori (high prevalence area, possible exposure at home) → do breath
test or stool test for H pylori. Then give abx and PPI if positive. If no improvement → endoscopy

Malabsorption
- Can do d-xylose testing to assess the absorptive function of the proximal small intestine - d-
xylose is a monosaccharide that doesn’t need to undergo any digestive process before
absorption. It is absorbed in the small bowel and then excreted in the urine. IIf the small bowel
muscosa is disrupted (e.g. Celiac disease), then the sugar won’t be absorbed and urinary levels
will be lower than expected. Can have false positives from delayed gastric emptying or bacterial
overgrowth (they ferment the sugar) and from renal dysfunction, urinary retention, or ascites.
- Celiac disease: Malabsorption, villous atrophy, can have iron deficiency anemia and joint pains.
Anti-endomysial and anti-tissue transglutaminase antibodies are highly predictive, but can
be negative if there is a selective deficiency of IgA, which is common for Celiac patients. If
antibody tests are negative, but suspicion for Celiac is high, then measure total IgA levels to
assess for IgA deficiency

Lactose intolerance: diagnose with hydrogen breath test, hydrogen will increase after ingestion of
lactose due to bacterial metabolism. The diarrhea will be acidic due to fermentation products and will
have a high osmotic gap = 290 - 2(stool sodium + stool potassium). The osmotic gap is > 50
mOsm/kg in all forms of osmotic diarrhea.

Diarrhea

Factitious diarrhea (laxative abuse)

- Causs very frequent watery stools, including at night. Colon shows melanosis coli - dark brown
discoloration (pigment) with lymph follicles shining through as pale patches
HIV: can cause mono like syndrome of lymphadenopathy (can be nontender!), arthralgias, nightsweats,
weight loss, and diarrhea,

Carcinoid syndrome: Flushing, diarrhea, bronchospasm. Tumor is usually in the lung or the small intestine

VIPoma: Vasoactive intestingal peptide binds to intestinal epithelial cells to increase fluid and electrolyte
secretion into the intestinal lumen. The tumor is often in the pancreatic tail. Have watery secretory
diarrhea (pancreatic cholera) with low stool osmolal gap (< 50), can be tea colored and odorless. Also
facial flushing, lethargy, nasuea, vomiting, abdominal pain and weight loss. Can also have muscle cramps
and weakness due to hypokalemia

C Diff:
- Unexplained leukocytosis in hospitalized patients should raise suspicion for C Diff, even without
diarrhea!
- Dx: Stool toxin testing. If negative but high clinical suspicion, do colonoscopy or sigmoidoscopy
with biopsy to look for psuedomembranes
- If mild-moderate (WBC < 15k), give oral metronidazole. If severe, give oral vanco unless ileus -
then add IV metronidazole or switch to rectal vanco. If really severe, do surgery.
Other infectious diarrheas
- Clostridium perfringens: Toxin mediated foodborn illness → nonbloody diarrhea and abdominal
pain
- Rotavirus: Outbreaks among kids, sometimes adults too. Nonbloody diarrhea and vomiting
- Staph aureus: food poisoning - staph happens stat - onset is a few hours after eating, vomiting,
nonbloody diarrhea, pain
- CMV: Pneumonia with diffuse patchy infiltrates (dx with bronchoalveolar lavage), upper
and lower GI ulcers (can cause diarrhea and pain), bone marrow suppression, arthralgias,
myalgias, and esophagitis

PUD
- Duodenal ulcers - pain relief with eating. 90% are caused by H pylori - treat with PPI and abx
- Gastric ulcers at risk of cancer. Adenocarcinoma of the stomach is often found at a late stage -
must first do CT scan and then other staging procedurs to decide whether to do surgical resection
(limited diseae) or chemo/palliative care (advanced disease)

Gastrinoma (Z-E syndrome)

- Suspect in patients with multiple ulcers and thickened gastric folds on endoscopy. Diagnose with
serum fasting gastrin level > 1000 pg/mL. Level < 110 rules it out. In the intermediate zone, follow
up with a secretin test - secretin will inhibit normal gastric G cells, but it stimulates gastrinoma
cells.

Glucagonoma
- Rare neuroendocrine tumor - causes diabetes (but easy to control), diarrhea, anemia, weight
loss, and necrotic migratory erythema

SBO
 - Nausea and vomiting is more common with SBO than with colonic obtruction, where the ileo-
cecal valve is competent
- Can usually manage initially with conservative measures (bowel rest, NG decompression, pain
control, fluids, correction of metabolic derrangements. If patient doesn’t respond, can do small
bowel follow through IF the patient is clinically stable. But if not, go to surgery
- Fever, tachycardia, leukocytosis, and metabolic acidosis indicate increased risk of strangulation -
refer them for urgent surgery!

IBD:
- UC is assoc’ed wth primary sclerosing cholangitis - watch for cholestatic pattern on LFTs,
hypergammaglobulinemia, increased serum IgM, and/or atypical p-ANCA (so does churg strauss
and microscopic polyangitis)
- UC has risk of toxic megacolon - even very eary in the disease or in patients with no previous
diagnosis.
- Watch out for fever, HR > 120, neutrophilic leukocytosis, anemia, and signs of volume
depletion, hypotension, electrolyte imbalance, or altered sensorium. Get an abdominal
xray!!
- Avoid sigmoidoscopy and colonoscopy - risk of perforation

IBS
Rome crtiteria: recurrent abdominal pain/discomfort for more than 3 days/month for the last three months
and at least two of three: improvement with bowel movement, change in stool frequency, change in stool
form. Usually also report stool urgency and feeling of incomplete evacuation after BM.

Smal Intestine Bacterial Overgrowth

- Often due to anatomic or dysmotility disorders.
- Abdominal bloating, flatulence, diarrhea. May have weight loss and nutritional deficiency in
severe cases. Gold standard for dx is endoscopy with jejunal aspirate showing > 10^5 organisms.

Colon cancer
- CRC is the most common cause of large bowel obstruction in adults
- Right side diameter > left side → right side bleeds, left side obstructs
- Monitoring for recurrence: 90% are within 3 years. Do annual CT of abdomen & pelvis and CXR
for up to 5 years; colonoscopy at 1 year and then every 3 years, CEA every 3-6 months
- Polyps: risk factors for cancer transformation include sessile, villous, > 2.5 cm in size.
Hyperplastic polyps are non-neoplastic

Diverticulosis
- Dx with barium enema, which is contraindicated in diverticulitis because of the risk of perforation
(same for colonoscopy). Do CT with oral and IV contrast instead.

Diverticulitis:
- Do CT for diagnosis - xray won’t provide much info beyond perforation or not.

Ischemic colitis:
- Hypotension → decreased blood flow to watershed areas. Little or no pain, bleeding is self-limited
after restoration of circulation
Acute mesenteric ischemia
- Throw a clot → complete occlusion of an artery. Severe pain with otherwise normal exam.

Cirrhosis:
- Most common causes are Hep B and C, alcohol, NAFLD, hemochromatosis (suspect if family hx
of cirrhosis, hx of diabetes, bronze skin, high transferrin saturation, calcium pyrophosphate
dihydrate deposition → chondrocalcinosis = psuedogout)
- Less common: Auto immune, PBC (more common in women, itching and fatigue precede
cirrhosis), PSC (90% also have IBD), alpha 1 antitrypsin (coexisting lung involvement), cardiac
cirrhosis from right heart failure, medications (methotrexate, isoniazid), Wilson’s disease (also
called hepatolenticular degeneration due to deposition of copper in the basal ganglia)
- PBC: treat with ursodeoxycholic acid, methotrexate is second line. Glucocorticoids don’t
help. Liver transplant is the only definitive cure.
- NAFLD: peripheral insulin resistance → increased peripheral lipolysis, TG synthesis, and
hepatic uptake of fatty acids. This causes intrahepatic fatty acid oxidation, which
increases oxidative stress and proinflammatory cytokines.

Ascites:
- To determine whether ascites is due to portal HTN, do the SAAG:
- measure the serum ascites albumin gradient (difference between serum albumin and
ascites albumin). If > 1.1, portal HTN is likely. If < 1.1, portal HTN is unlikely (more likely
to be transudative than exudative, such as from pancreatic ascites).
- Treat ascites first with salt and water restrictin (2L/day). Then spironolactone, then add
furosemide if necessary. Aggressive diuresis (> 1 L/day) isn’t good because risk of hepatorenal
syndrome. Can tap 2-4L of ascites fluid per day, with or without albumin.
- Diuretics can also precipitate hepatic encephalopathy by causing hypokalemia, which
increases renal ammonia production
- Metabolic alkalosis converts ammonium (can’t cross BBB) to ammonia, which can cross
the BB barrier
- SBP: WBC > 500, neutrophils > 250. Culture is often negative. Most common bugs are klebsiella,
e coli, and strep pneumo.
- Ceftriaxone is good for SBP

Varices
- Suspected variceal hemorrhage: Give IV octreotide, antibiotics (ceftriaxone) and volume
resuscitate. Keep Hgb > 9
- For small, nonbleeding varices - prophy with propranolol or nadalol. Can do variceal ligation for
patients who can’t do beta blockers

Hepatorenal syndrome:
- liver failure → portal HTN → increased NO in splanchic circulation → systemic vasodilation and
underperfusion of the kidneys. Won’t respond to volume administration. Liver transplant is the
only cure.
- Dx supported by very low urine sodium (< 10) and elevated Cr. No blood or protein in urine →
intrinsic renal disease is less likely.

Whipple’s disease
 - Macrophages loaded with tropheryma whippelii - partially destroyed bugs are present in
macrophage lysosomes (PAS positive). Small bowel lamina propria is the most common site of
involvement.
- Macrophages compress lacteals → can’t transfer chylomicrons → fat malabsorption and
steattorhea.
- Other common sites includes joint synovium (arthritis), cardiac valves, lymph nodes, and CNS
(dementia, other neuro findings). Can also have cough.

Hepatitis
- Alcoholic: AST and ALT almost always < 500, with AST twice
- Drug induced:
- Cholestasis: chlorpromazine, nitrofurantoin, erythromycin, anabolic steroids
- Fatty liver: tetracycline, valproate, anti-retrovirals
- Hepatitis: halothane, phenytoin, isoniazid, alpha-methyldopa
- Toxic or fulminant liver faiilure: carbon tetrachloride, acetaminophen
- Granulomatous: allopurinol, phenylbutazone
- OCPs: can cause abnormal LFTs without evidence of necrosis or fatty change
- Autoimmune: antismooth muscle antibodies
- NASH: biggest risk factors are DM, hyperTG, and obesity. Also TPN and steroids, amiodarone,
diltiazem, tamoxifen, and HAART increase the risk.
- Hepatitis B
- Screening for active infection: Test for Hepatitis B surface antigen and anti-HBc IgM.
The window occurs when surface antigen has been cleared but anti-surface antibodies
are not present yet - so if you just tested for surface antigen and antibodies, you’d miss
the infection. But IgM to core is present during the window, so test for that.
- Four phases:
- immune tolerance (lots of virus replication, little inflammation because immune
response is low)
- Immune clearance: Hb surface antigen is positive. Hbe antigen is initially
positive, then gets cleared. Variable ALT elevation due to immune distruction.
Can have increased HBV DNA and IgM anti-core
- Inactive carrier: Hbe antigen negative, Hbe antibody positive. Hb surface antigen
still positive. DNA is low or undetectable. Need 3 normal ALT levals AND 2-3
normal HBV viral tests over 1 year to confirm inactive carrier state
- Reactivation = Hbe antigen negative chronic hepatitis - HBV DNA elevated,
elevated ALT. HBe antigen still negative.
- Treatment:
- Entecavir and tenofovir (nucleotide reverse transcriptase inhibitor also used for
HIV) are the preferred therapies because of low drug resistance and can use
them in decompensated cirrhosis.
- Can also use lamivudine (NRTI) in HIV patients or interferon in young,
compensated patients
- If fulminant hepatic failure, then emergent liver transplant is the only option!
Defined as the onset of hepatic encephalopathy within 8 weeks of acute liver
failure (agitation, confusion, asterixis)
- HCW exposure: If unvaccinated, give Hep B vaccine and immune globulin. If vaccinated,
usually don’t need prophylaxis, but may need a booster vaccine.
- Associated with polyarteritis nodosa - necrotizing vasculitis in small and medium
vessels likely due to deposition of circulating antigen/antibody complexes
 - Hepatitis C
- Can be asymptomatic or present w/ nonspecific symptoms like arthralgias, myalgias.
Transaminase levels usually wax and wane. Can be associated with porphyria cutanea
tarda (fragile skin, photosensitivity, rash with vesicles and erosions on the back of the
hands), essential mixed cryoglobulinemia (due to immune complexes that deposit in
small to medium vessels and may be assoc’ed with low complement levels, palpable
purpura, arthralgias, and renal complications (usually membranoproliferative
glomerulonephritis).
- Okay to breastfeed with HCV, no need for C section. Vertical transmission rate is low (2-
5%). Get vaccinated for A and B even during pregnancy

Acute liver failure

- Defined as acute onset of severe liver injury with encephalopathy and impaired synthetic function
in a patient without cirrhosis or underlying liver disease
- PT is the most important prognostic indicator! If PT rises, be concerned - even if AST and ALT
drop. Declining transaminases can indicate a decrease in functional liver tissue

Liver parasites
- Amoebiasis - entameoba histolytica causes the formation of anchovy paste abscesses. Watch for
bloody diarrhea, then formation of cyst/abscess - will be uniform with a thin wall. Treat with
metronidazole. Transmission is fecal oral. Increased risk with gay men and travel to Mexico.
- Echinococcus - dog tape worm. Causes characteristic calcified “eggshell” cysts in the liver, risk of
anaphylaxis if they rupture. Life cycle requires sheep.

Liver cancer
- angiosarcoma - older men who have been exposed to toxins like vinyl chloride, inorganic arsenic,
and thorium dioxide
- Hepatic adenoma - benign epithelial tumors that are usually in the right lobe. Most often in young
and middle aged women with a history of OCP use. Risk of rupture and bleeding, 40% risk if
symptomatic (dull pain). Resect if symptomatic, otherwise d/c OCPs and monitor with imaging
and AFP - risk of malignant transformation.
- Focal nodular hyperplasia: common non malignant tumor of hyperplastic hepatic cells that grow in
response to hyperperfusion by anomalous arteries in the center of the mass.

Gallstones
- Asymptomatic gallstones - no treatment! Only 20% will develop symptoms.
- Treat symptomatic gallstones with laparoscopic cholecystectomy. However if the patient isn’t a
good surgical candidate, can try to disolve the stones with ursodeoxycholic acid. But it is
expensive and associated with high risk of relapse when stopped.
- Most gallstones are cholesterol based. Pigment gallstones are made of calcium bilirubinate. Can
also have mixed stones. Only pure pigment stones can be seen on xray - cholesterol stones and
mixed stones are radiolucent.
- Pregnancy and OCP use are gallbladder risk factors because estrogen increases cholesteroal
secretion, while progesterone decreases bile acid secretion and slows gallbladder emptying.

Emphysematous cholecystitis:
 - Common form of acute cholecystitis due to infection of the GB with gas forming bacteria
(especially clostridium). See air-fluid levels in the gallbladder and curvilinear gas shadowing in the
GB

Cholangitis:
- Charcot’s triad: fever, RUQ, jaundice.
- Treat with abx first - 80% get better. If don’t improve, treat with ERCP.

Acute pancreatitis
- Most often caused by alcohol, gallstones, or meds (anti-seizure meds, diuretics, and antibiotics)
- Requires 2 of 3: acute epigastric pain radiating to the back, amylase & lipase > 3x normal, or
imaging (focal or diffuse pancreatic enlargement). Only need imaging if the other two are unclear.
- Lipase is more useful than amylase - rises in 4-8 hours instead of 6-12 and lasts 8-14 days
instead of 3-5.

Chronic Pancreatitis
- Most often caused by chronic alcohol abuse.
- After 90% loss of function, get fat and protein malabsorption (steatorrhea). Often have epigastric
pain 15-30 mins after eating that is initially intermittent and then becomes persistent
- Amylase and lipase can be normal! Get an abdominal CT - calcifications are diagnostic. IF
nothing seen, then do ERCP or MR cholangiopancreatography

Pancreatic cancer
- Presents with anorexia, epigastric pain, jaundice, and weight loss. Tumors in the head of the
pancreas cause steatorrhea. The pain is subacute (days to weeks).
- Dx: If jaundice → ultrasound. If note diagnostic, do CT scan. If no jaundice → CT with contrast.
ERCP is a good tool, but invasive - reserve for patients with nondiagnostic ultrasound and CT.

Iron deficiency anemia

Do FOBT. Follow w/ colonoscopy, even if FOBT is negative. Then upper endoscopy (do 1st if lots of
NSAIDs or PUD). Then capsule endoscopy.
Chapter 4: Endocrine

Pituitary adenoma
Low levels of hormones. Might see slightly elevated prolactin level due to impairement of dopamine
inhibition - if prolactin level is really high, suspect prolactinoma

Hyperprolactinemia
- Order TSH and pregnancy test because hypothyroid and pregnancy can cause this condition.
- Recall that dopamine inhibits prolactin release! Dopamine antagonist drugs (metoclopromide,
antipsychotics) can cause hyperprolactinemia
- Prolactinoma
- Can treat with bromocriptine or cabergoline, dopamine agonists. Surgery if symptoms
progress, but high rate of recurrence after surgery!

Acromegaly:
- Coarse facial features, arthralgias, uncontrolled HTN, increased ring/hat size, skin tags, carpal
tunnel syndrome
- Dx with elevated IGF-1 (somatomedin C) or with oral glucose suppression test (GH should
suppress with glucose). Spot GH testing is NOT helpful because levels fluctuate amongst people.
Can also do MRI of the pituitary.
- Tx with surgery, with radiation after if IGF-1 remains elevated. Can also give octreotide or other
somatostatin analog to suppress GH

Central diabetes insipidus

Desmopressin is primary therapy. Can also use chlorpropamide (a sulfonylurea!!) that increases ADH
secretion and enchances the effect of ADH

SIADH
- Causes hyponatremia and volume expansion - but no edema because sodium is excreted due to
ANP. Will have inhibition of RAAS system, too.
- Acute hyponatremia can cause brain swelling!
- Treatment -
- Asymptomatic: Correct underlying cause, water restrict, can use normal saline and loop
diuretic, lithium and demeclocycline inhibit ADH in the kidney
- Symptomatic: Restrict water, give isotonic saline - hypertonic only in severe cases
- Raise serum sodium only by 0.5 mEq/L per hour

Hypothyroid
- Estrogen will increase TBG concentration by decreasing clearance of the protein. Testosterone
and anabolic steroids will decrease TBG concentration by increasing the clearance. These
relationships can affect levothyroxine needs!
- Can cause hyperlipidemia - both cholesterol and TGs. Can also cause anemia (normocytic and
normochromic), hyponatremia from decreased free water clearance, and asymptomatic AST and
ALT elevation
Hyperparathyroidism
- 80% caused by adenomas, then hyperplasia. Only 1% cancer.
- Chloride/phosphorus ratio > 33 (33 to 1 rule) is diagnostic of hyperPTH - chloride is high because
of renal bicarb wasting from PTH
- Secondary hyperparathyroid
- Can be caused by CKD through multiple mechanisms - hyperphosphatemia,
hypocalcemia, low 1,25 dihydroxy vitamin D. PTH levels are usually much higher in
secondary than primary.
- CKD - chronic phosphate retention stimulates PTH production. But phosphate also
interferes with renal activation of Vitamin D and it also binds circulating calcium to lower
calcium levels

Diabetes
- Goal BP is 130/80 → give ACE or ARB if higher
- Goal LDL is 100
- Daily baby aspirin
- Diabetic patients 40-75 should receive a statin regardless of baseline lipid levels! Give high dose
statin if 1 year risk of cardiac events is > 7.5%, otherwise cuse a moderate intensity statin
- Type 2: If severe hyperglycemia (> 240), use insulin.
- Morning hyperglycemia - can be caused by either the Dawn effect (high GH overnight →
hyperglycemia) or the Somogyi effect (hypoglycemia overnight → reactive hyperglycemia).
Check insulin levels at 3am - if high, then Dawn → increase overnight insulin. If low, then
Somogyi → decrease overnight insulin.

Diabetes oral meds

- thiazolidinediones (-glitazone) - can cause weight gain and heart failure
- GLP-1 agonists (exenatide, liraglutide) - can cause weight loss, low risk of hypoglycemia,
associated with acute pancreatitis
- DPP-4 inhibibtors (sitagliptin) - increase endogenous incretins, low risk of hypoglycemia, can use
in CKD,
Vitamin D deficiency
- Most patients have bone pain and muscle weakness, along with high PTH → low phosphate and
low-normal Calcium. Have decreased bone density and psuedofractures.
- Contrast osteoporosis - normal PTH, Ca, and PO4, no pain.

Hypocalcemia
- Metabolic alkalosis increases the % of calcium bound to albumin, reducing free ionized (active)
calcium - this can cause symptoms of hypocalcemia (crampy pain, paresthesias, carpo-pedal
spasms)

Hypercalcemia
- Causes
- Most often primary hyperparathyroidism.
- Can also be familial hypocalciuric hypercalcemia - both can have elevated calcium with
elevated PTH. Caused by abnormal calcium-sensing receptors on parathyroid cells and
renal tubules - just don’t respond! High calcium won’t suppress PTH production. Dx with
low urine calcium.
 - Hypercalcemia of cancer - low PTH and moderate to severe hypercalcemia
- Hypercalcemia of immobilization - treat with fluids and bisphosphonates
- Diagnosis
- 24 hour urinary calcium can help to distinguish primary hyperPTH (high urine calcium)
from familial hypocalciuric hypercalcemia (low urine calcium) - do this before
parathyroidectomy because that procedure won’t address the familial issue.
- Treatment
- If moderate or severe, give normal saline and calcitonin. Can do hemodialysis if the
patient has renal insufficiency or heart failure
- Steroids for chronic suppresion of hypercalcemia in granulomatous diseases

Addrenal insufficiency
- Weight loss, fatigue, muscle weakness, orthostatic hypotension, headache
- Screen with early morning cortisol (NOT 24 hour free cortisol - that is used for Cushing’s
screening) -will be low. Also do ACTH levels and do cosyntropin stimulation test (give synthetic
ACTH, see if adrenal gland responds). If serum cortisol increases with ACTH, the patient doesn’t
have primary adrenal insufficiency.
- Primary adrenal insufficiency - will have low aldosterone
- Can be caused by TB (calcification of the glands), fungal infections, CMV, auto immune
attack, hemorrhagic infarction - meningicoccemia.
- Antifungals (ketoconazole) that prevent ergosterol production can actually cause adrenal
insuffiency by inhibiting adrenal steroid synthesis
- Secondary adrenal insufficiency (e.g., after suddenly stopping exogenous steroids) - will have
normal aldosterone! RAA system is intact
- Risk after > 3 weeks of steroids. Normal HPA axis functioning takes 6-12 to recover

Cushing syndrome:
- Increased ACTH dependent hormones → hypertension (Vasoconstriction), insuline resistance
(hyperglycemia), and mineralocorticoid activity (hypokalemia)

Factitious thyrotoxicosis
- Low TSH and low RAIU, but high free T4 and free T3 (or only high free T3 if taking that directly)
→ measure serum thyroglobulin. Will be high in thyroiditis, iodide exposure, and extraglandular
production. Low if taking exogenous hormones.

Thyroid nodule
- First do clinical evaluation, TSH, and ultrasound. If suspcion for cancer, then FNA. If no cancer
risk factors or suspicious US findings, then TSH is the guide - if normal or elevated, then the
nodule is cold - do FNA. If TSH is low, then the nodule may be hot or not - do iodine scan to see
if the nodule is hot or cold. If nodule is hot, treat for hyperthyroid, if cold, do FNA.
- Suspicious US findings - hypoechoic, microcalcifications, internal vascularity

Sick euthyroid
Acute, severe illness can cause abnormal thyroid tests! Most often normal TSH and free T4, but low free
T3 due to decreased conversion of T4 to T3. This could be due to decreased caloric intake and increased
cytokines

Hyperthyroid and hypothyroid can both cause HTN!

 - Hyperthyroid actually decreases systemic vascular resistance, but it increases ionotropic and
chronotropic effects by increasing expression and sensitivity of beta1 receptors.
- Hypothyroid can cause HTN by increasing systemic vascular resistance (cold extremities, cold
sensitivity!)

Hyperthyroid
- PTU can cause vasculitis!
- Struma ovarii - ovarium teratoma that makes thyroid hormones
- Radioactive iodine is the best treatment for Grave’s, but don’t do it if the patient is pregnant or
has very severe opthalmopathy

Hashimoto’s thyroiditis
Increased risk of thyroid lymphoma!

Subacute thyroiditis
- lymphocytic - painless
- granuloamatous/de quervain’s - painful

DKA
- Treat with NS, regular insulin, and correction of the electrolyte imbalances along with the
underlying cause. Give HCO3- only in extenuating circumstances - pH < 7.1, bicarb < 5, severe
hyperkalemia. Otherwise can be dangerous - can cause cerebral swelling, decrease oxygenation
by shifting the o2 dissociation curve to the left, and lead to hypokalemia and alkalosis
- Monitor response to treatment by watching arterial pH or serum anion gap - monitoring ketones
directly is less reliable because as treatment is started, beta hydroxybutyrate is converted to
acetoacetate, which is the substrate detected by the nitroprusside reaction that is usually used to
detect ketones. Consequently, serum ketones correct later than arterial blood pH or anion gap.

Nonketotic hyperglycemia
- Start with normal saline and insulin, then give 5% dextrose when blood glucose reaches 250 -
this prevents the development of cerebral edema

SIADH
- Treat with demeclocycline, which blocks ADH mediated insertion of aquaporins in the collecting
tubules. Can combine with hydrochlorothiazide for an additive effect.
- Tolvaptan is a V2 vasopressin antagonist that will cause selective water loss in the kidney without
affecting sodium or potassium. Expensive.

Central diabetes insipidus

Treat with desmopressin

Nephrogenic diabetes insipidus

Treat with sodium restriction and thiazide diuretics! These deplete the body of sodium → increase
reabsorption of Na and water in the proximal tubules.

MEN2A and 2B
Patients with the RET proto-oncogene should undergo total thyroidectomy in childhood because the risk
of invasive medullary thyroid cancer is nearly 100%!!
Pheochromocytoma
Treat the hypertensive crisis with an alpha blocker FIRST, then a beta blocker. Doing a beta blocker will
result in unopposed stimulation of vascular alpha receptors by circulating catecholamines, which can
result in a rapid increase in BP!

Testicular tumors
- Leydig tumors: can make testosterone, along with estrogen thanks to conversion by aromatase.
Most common type of testicular sex cord stromal tumor, occurs in all ages including kids
- Choriocarcinoma - increased beta HCG
- Teratoma
- Seminoma - usually normal tumor markers
- Yolk sac (endodermal sinus tumor) - increase serum AFP
Chapter 7: Renal

Renal tubular acidosis

Metabolic acidosis is rarely seen in CKD until there is advanced disease (GFR < 20) -
- Type 1: Low tubular ammonium production because of failure to excrete enough H+ into the
urine in distal tubule (Type 1 → A for ammonium). Get kidney stones (calcium phosphate)
- Type 2: Defective tubular bicarb reabsorption - can be a component of Fanconi syndrome or
caused by carbonic anhydrase inhibitors (Type 2 → B for bicarb)
- Type 4: Impaired function of the collecting tubule → retention of H+ and K+. Often seen with
poorly controlled DM - damages the juxtaglomerular apparatus, causing hyporeninemic
hypoaldosteronism.
- Note that the kidney exchanges chloride for bicarb → so if urine chloride is high, more bicarb has
been reabsorbed and H+ excretion is increased

Fanconi Syndrome: Impaired reabsorption in the PCT - lose nearly all AAs, glucose, bicarb and
phosphate. Can cause metabolic acidosis. Caused by hereditary defects (Wilson’s disease), ischemia,
toxins, drugs

Bartter Syndrome: Autosomal recessive. Reabsorptive defect in the thick ascending loop of Henle - the
Na/K/2Cl cotransporter is broken → hypokalemia and metabolic alkalosis with hypercalcemia

Gitelman Syndrome: Autosomal recessive. Defective reabsorption of NaCl in the DCT - less severe than
Bartter Syndrome. Causes hypokalemia with metabolic alkalosis, but no hypercalciuria (basically like a
thiazide diuretic)

Liddle Syndrome: Autosomal dominant! Increased sodium reabsorption in the distal and collecting
tubules (increased activity of the epithelial sodium channel) - kind of acts like primary
hyperaldosteronism! Causes hypertension, hypokalemia, metabolic alkalosis, and decreased aldosterone
→ treat with amiloride

Primary aldosteronism
- Serum aldosterone-renin ratio > 20. Contrast secondary aldosteronism (e.g., due to renal
artery stenosis): ratio is < 10!
- Do an adrenal suppression test - salt loading to see if aldosterone level drops. If not, do CT. If a
discrete mass is found, do adrenal vein sampling to differentiate between hyperplasia and
adenoma.
- Treatment
- Unilateral adenoma or unilateral hyperplasia → surgery
- Bilateral hyperplasia → meds

Aldosterone saves sodium and pushes potassium out

Renal artery stenosis: causes secondary hyperaldosteronism (hypokalemia, metabolic alkalosis,

hypertension)

Acute oliguria
1. Causes
 a. Postoperative urinary retention:
i. Common complication of surgery and anesthesia. Bladder distention from
general anesthesia or from epidural anesthesia → inefficient detrusor muscle
activity → acute urinary retention.
ii. Risk increases with age, high fluid intake, and concurrent use of other meds
(anticholinergics, opiates). Abdominal discomfort is a sign!
2. Workup of post operative oliguria
a. Start with bladder scan to assess volume. If distended → Foley catheter. If not distended,
consider prerenal or renal causes

Spinal cord compression: Lower extremity weakness, bowel/bladder INCONTINENCE (not retention!),
brisk LE deep tendon reflexes, and decreased rectal tone

Urinary retention
- Normal post void residual is less than 50 mL

Contrast nephropathy: Contrast causes vasoconstriction and tubular injury.

- Prevent with IV fluids, acetylcysteine can help - vasodilatory and antioxidant properties. Can also
use non-ionic contrast for patients with renal insufficiency (Cr > 1.5) or diabetes
- If person has a true contrast allergy (hives, flushing, angioedema, etc), then prednisone can help.

Crystal-induced kidney injury

- Caused by acyclovir, sulfonamides, methotrexate, ethylene glycol, protease inhibitors
- Prevent with adequate hydration!

Analgesic nephropathy
- The most common form of drug-induced renal failure. Papillary necrosis and chronic
tubulointerstitial nephritis are the most common pathologies

Acute interstitial nephritis

- Presents with rash, eosinophilia, eosinophiluria, pyuria 7-10 days after drug exposure!
- Beta lactams, PPIs

Acute tubular nephrosis

- Causes acute renal failure, not insidious progression of renal failure. Most commonly seen in
ischemic or nephrotoxic acute renal failure. Have muddy brown casts.

Hematuria
- Locating the source
- From glomeruli (basement membrane disorder, glomerulonephritis): blood and protein,
RBC casts/dysmorphic RBCs, more often microscopic than gross
- From elsewhere in the kidney (stones, cancer, polycystic kidney disease, infections,
papillary necrosis, infarction): blood but no protein, normal appearing RBCs
- Renal cause will not have clots!
- Timing of blood can indicate location!
- Blood at the beginning of urination → lesion in the ureter
- Terminal hematuria → prostate or bladder
- Entire urinary cycle → ureter or kidneys
 - Causes
- Benign recurrent hematuria: thin basement membrane nephropathy - benign familial
condition that presents with isolated microscopic hematuria. No worsening kidney
function or gross hematuria.
- Cystoscopy indicated for gross hematuria or for microscopic hematuria with risk factors for
bladder cancer - cigarette smoking, environmental exposures (painters, metal workers), chronic
cystitis, iatrogenic causes (cyclophosphamide, pelvic radiation)
- Suspect myoglobinuria when urinalysis is positive for blood but then microscopic exam shows few
RBCs! Standard urinalysis can’t distinguish between myoglobin and hemoglobin. Myoglobinuria is
usually caused by rhabdomyolysis

Glomerulonephritis: Hypertension, gross hematuria and red cell casts, mild proteinuria, acute kidney
injury
- IgA nephropathy:
- 5 days after URI or pharyngeal infection.
- Causes recurrent gross hematuria, see mesangial IgA deposits on kidney biopsy. Usually
benign, but can cause RPGN or nephrotic syndrome with worse prognosis
- Henoch Schonlein purpura is a systemic form affecting the glomeruli, skin, joints, and
intestines.
- Post streptococcal glomerulonephritis:
- 10-20 days after skin or throat infection.
- Low C3 complement levels, elevated anti-streptolysin O or anti-DNAse B. See
subepithelial humps of C3 complement
- More common in kids but can happen in adults. Kids have better prognosis - can cause
CKD in adults.

Nephrotic syndrome
1. Types
a. FSGS: African american, hispanic, obesity, HIV, heroin
b. Membranous: adenocarcinoma and solid tumors (not lymphoma!), NSAIDs, Hep B, lupus.
i. This is the nephrotic syndrome most likely to cause renal vein thrombosis
c. Membranoproliferative: Hep B & C.
i. See dense intramembranous deposits that stain for C3 - also called dense
deposit disease. Caused by IgG antibodies against the C3 convertase of the
alternative complement pathway (also called C3 nephritic factor). These
antibodies reacting with the C3 convertase cause persistent complement
activation and kidney damage.
d. Minimal change: Kids, NSAIDs, lymphoma
2. Associated with the following complications
a. Renal vein thrombosis,
b. Protein malnutrition,
c. Iron-resistant microcytic hypochromic anemia (loss of transferrin),
d. Vitamin D deficiency due to increased loss of cholecalciferol binding protein
e. Decreased thyroxin due to loss of thyroxine binding globulin
f. Increased risk of infection
g. Increased risk of atherosclerosis and MI from hyperlipidemia

Diabetes:
 - Causes increased ECM, basement membrane thickening, mesangial expansion, fibrosis
- First sign of disease is glomerular hyperfiltration - it injures the glomerulus. ACE inhibitors
protect the kidney by reducing intraglomerular hypertension
- Next sign of disease is thickening of the basement membrane - this is the first problem that can
be quantitated.

Hypertension: Causes arteriosclerosis of afferent and efferent arterioles and glomeruli

Amyloidosis: Consider in patients with enlarged kidneys and chronic inflammatory states - will cause
proteinuria.
- Can present with asymptomatic proteinuria or nephrotic syndrome
- Cardiomegaly with heart failure
- Sensory and motor peripheral neuropathy
- Visible organ enlargement - like macroglossia
- Bleeding diathesis
- Waxy, thickening, easy bruising of skin
- Dx with abdominal fat pad aspiration, treat and prevent with colchicine

Polycystic kidney disease

- Flank pain, hematuria, palpable kidneys. No significant proteinuria or edema.

Acute pyelonephritis
- Treat with oral levofloxacin

Papillary necrosis
- NSAID: nsaids, sickle cell, analgesic abuse, infection, and diabetes mellitus

Palpable purpura
- Cryoglobulimenia: palpable purpura, glomerulonephritis, joint pains, enlarged spleen + liver,
peripheral neuropathy, and low complement. Usually associated with Hepatitis C.
- Henoch-Schonlein purpura: childhood disease. Palpable purpura on the butt, abdominal pain,
joint aches, proteinuria and hematuria with RBC casts. Normal serum complement!
- Microscopic polyangiitis - fever, malaise, abdominal pain, hematuria, purpura. ANCA positive.
Normal complement.

Renal cysts
- Simple cyst: wall is smooth, not septated, content is homogenous, no contrast enhancement,
usually asymptomatic, no need to follow
- Malignant cystic mass: thick irregular wall, loculated, septae, heterogenous content, contrast
enhancement, can cause pain/hematuria/HTN, requires follow up imaging and urologic evaluation
for cancer
ESRD
- Normocytic, normochromic anemia from deficiency of erythropoeitin. Give Epo is Hb < 10. Most
common side effects are worsening of hypertension (subq is better than IV), headache, and
flulike symptoms.

Dialysis
 - Most common cause of death is cardiovascular disease - 50% of all deaths. Also most common
cause in transplant patients.
- Uremia:
- Platelet dysfunction - will have normal PT and PTT, but increased bleeding time.
Treatment is DDAVP (increases the release of von Willebrand factor = factor 8)

Kidney stones
- Types of stones
- Calcium oxalate are the most common! (75-90%) Enveloped shaped
- Calcium phosphate - primary hyperparathyroidism and RTA
- Cystinuria: Impaired amino acid absorbtion (several modes of inheritance). Cysteine is
poorly soluble in water → forms hexagonal stones. The urinary cyanide nitroprusside
test can detect elevated cystine levels.
- Treatment of stones
- First stone - just say to increase fluids > 2L per day. No metabolic work up necessary.
- Repeated stones - 24 hour urine collection to look for metabolic disorders
- Decrease dietary protein and oxalate - high protein diet is associated with an
increased risk of calcium stones
- Decrease sodium intake - calcium gets reabsorbed with sodium. Also give
thiazide diuretics
- Increase fluid intake
- Increase dietary calcium - this seems paradoxical, but lowering dietary calcium
makes the problem worse! Low dietary calcium means that more oxalate is
absorbed in the gut, which is then excreted into urine and forms calcium oxalate
stones. However excess calcium supplementatin (not from food) can cause
stones.
- Avoid mega doses of vitamin C - leaads to increased formation of oxalate stones,
especially in patients with renal failure
- Uric acid stones:
- Form in acidic urine → treatment is to alkalize the urine! Use oral potassium
citrate. Can also add allopurinol if there are recurrent symptoms despite initial
measures, esp if hyperuricosuria or hyperuricemia happens

Prostate disease

Prostatitis - names tell you the findings!

- Noninflammatory chronic prostatitis: Afebrile, irritative voiding symptoms, normal urinalysis and
physical exam, prostatic secretions will have normal number of WBCs and negative for bacteria
- Chronic bacterial prostatitis: Afebrile, irritative voiding symptoms with normal urinalysis. But now
prostatic secretions show elevated leukocytes and are positive for bacteria
- Inflammatory chronic prostatitis: Afebrile, irritable voiding symptoms. Prostatic secretions have
WBCs but no bacteria
- Acute bacterial prostatitis: Fever, irritative voiding symptoms, urinalysis shows bacteria and
WBCs. Avoid catheterization during acute prostatitis because of urethral inflammation - if urinary
retention, do suprapubic catheterization.

Benign prostatic hypertrophy

 - All patients with BPH on DRE should have urinalysis to assess for infection and hematuria
(bladder cancer and kidney stones). Patients with life expectancy > 10 years should have a PSA
test

Priapism
- Recall trazodone and prazosin (alpha blocker for HTN) can cause it!
Ambulatory Medicine

Blood pressure cuff - bladder length should be at least 80% of arm circumference and width should be at
least 40% of arm circumference (ratio of 2:1)

Cardiovascular screening
- Diabetes screening in all patients with sustained BP > 135/80, and for everyone over 45 or who
have additional risk factors. Can do fasting glucose, 2 hour glucose tolerance test, or HgA1c
Cancer screening
- Lung cancer: adults 55-80 with more than 30 pack year history of smoking who currently smoke
or who have quit in the past 15 years
- PAP - every 3 years 21-29, then 30-65 have a pap every 3 years or a Pap and HPV testing every
5 years

Vaccines
- Pneumovax (13) for everyone > 65, followed by the 23 valent vaccine 6-12 months later.
- If < 65with high risk underlying conditions (CSF leaks, sickle cell, cochlear implants,
asplenia, IC, chronic renal failure) → 13 then 23
- If < 65 and chronic smokers or chronic medical conditions like lung disease, heart
disease, diabetes, and chronic liver disease → just do 23
Chapter 6: Connective Tissue and Joint Disease

ESR: Elevated in infection, cancer, rheum diseases, tissue necrosis, pregnancy

CRP: inflammation and infection. Much more sensitive and specific for infection than ESR - if CRP > 15,
bacterial infection is likely present

Rheumatoid Arthritis
- Joint stiffness > 1 hour in the morning, joint swelling, symptoms > 6 weeks. Symmetric joint
distribution, no DIPs
- Rheumatoid nodules - elbows, sacrum, occiput
- Pleural fluid has very low glucose!
- Pulmonary fibrosis
- Cervical spine instability - can be fatal! Can have subluxation of cervical vertebrae
- High risk of osteoporosis!
- Usual onset is 20-40 years
- Can be mimicked by parvovirus, but that won’t have joint swelling or prolonged morning stiffness
(maybe only 15 mins)
- Tests
- RF in 70%
- Anti-cyclic citrullinated peptide antibodies usually positive
- HLA DR4
- Treatment
- Methotrexate is first line, also leflunomide, hydroxychloroquine, sulfasalazine, anti-TNF
drugs
- Felty syndrome: RA with neutropenia and splenomegaly. Can have non healing leg ulcers,
recurrent infections

Lupus
- Tests
- Anti-ANA: Sensitive, used for screening - follow with anti-dsDNA and anti-Smith
- Anti-dsDNA and anti-smith: specific, use for ruling in
- Assoc’ed with HLA DR2 and DR3
- In new onset lupus nephritis, must get a renal biopsy! The different types of renal disease have
different treatments. Biopsy is also important for staging and to create a baseline
- Lupus arthritis can present like RA, but no joint deformity!
- Parvo can mimic lupus arthritis, but lupus arthritis is usually chronic rather than acute.
Also has other findings like malar or discoid rash, hematologic abnormalities, fever,
malaise, weight loss, etc.
- Prognosis
- Can cause pancytopenia due to AI peripheral destruction of all 3 cell lines
- Renal disease is a big killer - treat with cyclophosphamide. Infection is also a killer.
- In general, treat with hydroxychloroquine
- Drug induced:
- No renal or CNS involvement! Usually no malar rash, ulcers, or alopecia
- Hydralazine, procainamide, isoniazid, chlorpromazine (dopamine antagonist used for
dementia), methyldopa, quinidine
- Still ANA positive!
Antiphospholipid syndrome
- Associated with lupus and other collagen vascular diseases (scleroderma).
- Prolonged PT or PTT is not corrected w/ addition of normal plasma

Sjogren’s
- HLA DR3
- Look for occult lymphoma! Increased risk of NHL - most common cause of death
- Schirmer test: filter paper in eye
- Treatment: Pilocarpine (cholinergic agent) or cevimeline, NSAIDs, steroids for arthralgias,
arthritis

Scleroderma:
- Cytokines stimulate fibroblasts → overproduce (normal) collagen
- ANA positive, anti-topoisomerase-1 positive
- First sign is usually raynaud’s, then cutaneous fibrosis (sclerodactyly), GI involvement
(esophagus, delayed gastric emptying, c/d, abdominal distention), interstitial fibrosis/pulmonary
HTN, cardiac involvement
- Biggest cause of death is lung disease!
- Diffuse vs. Limited (CREST is a variety of limited).
- Diffuse has widespread skin and visceral involvement, fast onset, poor prognosis - ANA
and antitopoisomerase I antibody, but no anti-centromere antibody
- Limited involves distal extremities and face, delayed onset, anti-centromere antibody
- CREST: calcinosis of the digits, raynaud’s, esophageal dismotility, sclerodactyly,
telangectasias

Mixed connective tissue disease

- Features of lupus, RA, systemic sclerosis, and polymyositis

Raynaud’s:
- Primary: symmetric, usually women 15-30 yrs
- Secondary: asymmetric: usually male > 40 - associated with tissue ischemia (necrosis,
numbness, ulcers) and systemic disease (AI or vascular)

Dermatomyositis
- Heliotrope sign (eye rash) and gottron’s papules (pathognomic) - rash on the joints.
- CPK elevated > 10x normal, anti-Jo-1 and anti-Mi-2
- 15% get cancer

Polymyositis
- Muscles of mastication and facial expression are classically spared, but may have dysphagia

Viral arthritis
- Inflammatory, symmetric arthritis that resolves within 2 months - parvovirus, hepatitis, HIV,
mumps, rubella
- Can have positive RF factor and weakly positive ANA

Gout
 - Caused by over production of uric acid (prophylaxis with allopurinol) or decreased excretion (treat
with probenecid or sulfinpyrazone - but these drugs are contraindicated if patient has a history of
renal stones)
- Negaitvely birefringent crystals = YUPA - yellow when parallel to the plane of light (e.g.,
North-South = up and down, will have yellow lines like I’s, and blue dashes horizontally)
- Stop drinking alcohol! Alcohol is metabolized to lactate, which competes with urate for renal
excretion → causes build up of uric acid
- Risk factors: CKD (can’t excrete), polycythemia vera, lesch nyhan syndrome

Pseudogout:
- Can see with hyperPTH because of excess calcium (get deposition of calcium pyrophosphate
dihydrate)
- Psuedogout is positively birefringent, smaller crystals (more like tic tacs than needles)

Joint aspiration
- WBC 0-200 = normal, 200-2000 = osteoarthritis, 2000-50,000 = inflammatory, 50k+ = septic joint

Inclusion body myositis

- Proximal and distal weakness
- Loss of DTRs

Seronegative spondyloarthropathies

Ankylosing spondylitis
- Often goes with IBD and psoriasis, also anterior uveitis.
- Limited motion in lumbar spine, bilateral sacroilitis, ethesitis (inflammation at tendon insertions
into bone)
- Diagnose w/ xray - NOT HLAB27! Only 5% of HLA B27 have it, though 95% of AS have
HLAB27
- Complications: restrictive lung disease, cauda equina syndrome, spine fracture, osteoporosis
- Treat with NSAIDs (indomethacin), anti-TNF meds (etanercept, infliximab)

Reactive arthritis
- Enteric or GU infection→ urethritis, conjunctivitis, asymmetric oligoarthritis - also entesitis
and mucocutaneous lesions/ulcers
- Usually HLA B27 positive
- Reiter’s syndrome is an example - can’t see, can’t pee, can’t climb a tree. Campylobacter jejuni,
yersinia enterocolitica, salmonella, shigella
- Treat with NSAIDs, sulfasalazine, and immune suppressants like azathioprine
- Can be tough to distinguish from gonococcal septic arthritis, but reactive arthritis pts will be
afebrile and have other features like ethesitis and low back pain

Psoriatic arthritis
- Skin disease for months to years first
- Assymetric and polyarticular, pencil in cup deformity
- NSAIDs, maybe RA drugs if really bad

Vasculitis
 - Large: takayasu, temporal
- Temporal - 40% also have polymyalgia rheumatica. Follow with serial chest xrays
because risk of aortic aneurysm
- Medium: PAN, kawasaki, wegener, churg strauss, microscopic polyangiitis
- Wegener: sinus, pulmonary disease, glomerulonephritis. Poor prognosis (< 1 year
survival)
- PAN: No lung involvement! Neutrophils invade all layers → fibrinoid necrosis
- Treat with steroids, then cyclophosphamide
- Small: HS purpura, hypersensitivity vasculitis, Behcet’s
- Behcet’s:
- oral and genital ulcers, arthritis, eye problems (anterior uveitis), CNS involvement
- intracranial HTN, meningoencephalitis, can progress to dementia! Fever, weight
loss, erythema nodosum.
- Most common in Turkish, Asian, and middle eastern
- Hypersensitivity: often a drug rxn (penicillins, sulfa). Very good prognosis
- Buerger: Small and medium

Drugs
- Hydroxychloroquine
- Malaria prophy, lupus, RA
- Methotrexate:
- First line for RA; if it doesn’t work, add sulfasalazine or hydroxychloroquine. If that doesn’t
work, add TNF alpha inhibitors.
- Risk of hepatotoxicity, cytopenias, stomatitis
- Don’t use methotrexate in Hep B, Hep C, TB, or pregnancy
- Leflunomide
- Pyrimidine synthesis inhibitor
- Risk of hepatotoxicity, cytopenias
- Hydroxychloroquine:
- Use for lupus, RA.
- TNF and IL-1 suppressor, like sulfasalazine
- Risk of retinopathy - have to do yearly eye exams
- Sulfasalazine
- TNF and IL-1 suppressor
- Can cause hepatotoxicity, stomatitis, hemolytic anemia
- TNF inhibitors: adalimumab, certolizumab, etanercept, infliximab, golimumab
- Risk of infection, demyelination, CHF, malignancy!
- Inflammatory bowel disease, ankylosing spondylitis, rheumatoid arthrits
- Cyclophosphamide
- Use in Lupus if CNS or renal findings
- Risk of hemorrhagic cystitis and bladder cancer

Steroids
- Chronic steroid use can cause avascular necrosis of the femoral head! Progressive pain
with no restriction on ROM and normal xray early on. Diagnose with MRI
- Use for: Sarcoidosis

Baker’s cyst
 - Tender mass in popliteal fossa develops from excess fluid production by inflamed synovium - RA,
osteoarthritis, cartilage tears.
- Can burst and release contents into the calf, looks like DVT

DeQuervain’s tenosynovitis:
Classically affects new mothers who hold their babies with the thumb outstretched (abducted/extended).
The abductor pollicus longus and extensor pollicis brevis are affected - passive stretch of the tendons
elicits pain
Chapter 8: Electrolytes

Hypocalcemia
- Tetany, increased DTRs, muscle cramps, convulsions
- Severe hypoMg can mimic because it decreases PTH secretion and decreases peripheral
response to PTH!
- Causes: multiple blood transfusions - citrate binds ionized calcium!
- Low albumin can cause spurious hypocalcemia since much of calcium is albumin bound

Hypomagnesemia
- Can cause refractory hypokalemia!
- Can cause hypocalcemia! Causes decreased PTH release and PTH resistance. Hypothyroidism
induced by hypomagnesemia isn’t associated with high phosphorus levels, unlike other causes of
hypoPTH.

Hypokalemia
- Muscle weakness and cramps
- Can happen in Cushing’s disease - cortisol will bind to aldosterone receptors and cause
potassium wasting!!
- Hypomagnesemia can cause refractory low potassium levels - Mg is necessary for potassium
uptake and maintanence of intracellular potassium!

Hyperkalemia
- Sx: tall peaked T waves, shortening of the QT interval, PR prolongation and widening of the QRS,
weakness, metabolic acidosis. Can cause bradycardia with sine wave pattern on EKG.
- Causes
- Most often acute or chronic kidney disease and medications or disorders that impair the
renin-angiotensin axis (e.g., adrenal failure - no aldosterone)
- Drugs: nonselective beta blockers, ACE inhibitors, ARBs, K+ sparing diuretics,
cardiac glycosides (digoxin), NSAIDs (impair local prostaglandin synthesis →
reduced renin and aldosterone secretion)
- Shift of potassium out of cells (uncontrolled hyperglycemia, metabolic acidosis)
- Increased tissue catabolism (tumor lysis, trauma, guillain barre, rhabdomyolisis, burn and
crush injuries)
- Management:
- Get an EKG!
- Avoid succinylcholine - a depolarizing neuromuscular junction blocker that is often
used during rapid sequence intubations - can cause significant potassium release and life
threatening arrhythmias.
- Rapid treatments for patients with EKG changes, moderate to severe hyperkalemia, and acute
onset (rhabdomyolysis)
- Calcium infusion as calcium glucaronate, calcium chloride for patients with EKG
changes (stablizes cardiac membranes, reduces myocardial excitability - transient effect,
does not actually correct hyperkalemia
- Shift potassium intracellularly with insulin with glucose, beta 2 agonists, sodium
bicarb. Does not affect total body potassium. Insulin + glucose is faster than beta 2
agonists!
 - Removal of potassium from the body (slow) is indicated in the setting of CKD
- Loop diuretics with normal saline if no EKG changes
- Cation exchange resins (sodium polystyrene sulfonate) - work in the GI tract to trade
sodium for potassium, thereby eliminating potassium through stool
- Hemodialysis - ESRD, very severe hyperkalemia
- Meds that cause hyperkalemia
- Anything that interferes with renin-angiotensin-aldosterone pathway: ACE inhibitors,
ARBs, K+ sparing diuretics, cardiac glycosides (digoxin - inhibits the Na/K ATPase),
NSAIDs (impaire local prostaglandin synthesis → reduce renin and aldosterone
secretion), cyclosporine (blocks aldosterone), heparain (blocks aldosterone production)
- Shifts of potassium outside of cells: Beta blockers
- Cellular destruction: Succinylcholine: Causes extracellular leakage of potassium through
acetylcholine receptors
- Blockage of the sodium channel in the renal epithelium: Amiloride, spironolactone,
trimethoprim

Hyponatremia
- Either hypovolemic, euvolemic, or hypervolemic - can assess with physical exam and with urine
sodium (> 20 suggests not hypovolemic)
- Hypovolemic: volume depletion (blood loss), adrenal insufficiency (no aldosterone), GI
losses, renal losses (diuretics). RAA and ADH are activated - increased ADH without
sodium repleneshment will cause hyponatremia! Watch for this in someone with a poor
diet
- Euvolemic: SIADH from drugs or malignancy, primary polydipsia, secondary adrenal
insufficiency, hypothyroid
- Hypervolemic volume expanded with edema: CHF (don’t want to hold onto sodium
when volume overloaded!), cirrhosis, CKD or nephrotic syndrome
- Hypervolemic - volume expanded without edema: SIADH
- Treatment for SIADH:
- Mild: Water restriction, loop diuretic
- Moderate: Hypertonic saline. Using normal saline will just worsen the
situation - the patient will lose all of the sodium in urine but hold onto free
water.
- Severe: Hypertonic saline and ADH antagonist (conivaptan)
- Correct symptomatic hyponatremia with 3% or hypertonic saline at no more than 0.5
mEq/L/hr. Correcting it too fast can cause osmotic demyelination or central pontine myelinolysis
- Can estimate change in serum sodium = (infused Na + infused K - serum sodium)/ (total body
water +1)
- TBW = weight in kg x % of body weight that is water - varies by age and gender (young
men = 0.6, young women and old men = 0.5, old women = 0.45)

Hypernatremia:
- Hypovolemic:
- Severe: Start with normal saline - will be hypotonic relative to plasma. Once volume
status is corrected, can switch to half normal saline (0.45%) in order to better replace the
free water deficit
- Less severe: D5/half normal saline
- Hypervolemic and euvolemic
 - Can give oral free water if the patient can tolerate it.

Tumor lysis syndrome:

- Potassium and phosphate levels are increased because they are intracellular ions that get
released
- Get hypocalcemia because phosphate binds calcium
- Get elevated levels of uric acid from degradation of cellular proteins

Acid-base disorders
1. Is the patient acidemic or alkalemic - look at the blood pH
a. Henderson Hasselbalch: pH = pK + log (conjugate base/acid). For CO2 and bicarb, pH =
6.1 + log (HCO3/(0.03xCO2))
2. Is the primary disturbance metabolic or respiratory?
3. If metabolic acidosis:
a. Is there an increased anion gap?
b. Is the respiratory compensation appropriate? Winter’s formula - PCO2 = 1.5 x HCO3 + 8
+/- 2. This formula is used on for metabolic acidosis!
c. If there is an anion gap, is there a concomitant metabolic problem?
i. Use the anion gap to estimate what the HCO3 would be if no anion gap were
present: Adjusted HCO3 = actual HCO3 plus the anion gap
4. If metabolic alkalosis, is respiratory compensation appropriate? Use PCO2 = 0.9 x bicarb + 8 +/-
2
5. If a respiratory problem is present, is it acute or chronic
a. For each 10 mm Hg change of PCO2, the pH changes by 0.08 for acute resiratory
response and 0.03 for chronic respiratory response
b. For acute respiratory acidosis, HCO3 goes up by 1 for each 10 mm Hg change in PCO2
c. For acute respiratory alkalosis, HCO3 drops by 2 for each 10 mm Hg change in PCO2
-
Metabolic acidosis
- Acute kidney injury will have rise in Cr and hyperkalemia
-
Metabolic alkalosis
- Saline responsive (low urine chloride): GI losses (vomit or diarrhea), urinary losses, decreased
oral intake - initiates the metabolic alkalosis, and then it’s maintained by the RAA system
(increase sodium absorption, dump H+ and K+)
- Low urine chloride is due to hypovolemia and hypochloremia
- Saline resistant (high urine chloride): Primary hyperaldosteronism, cushing’s syndrome, severe
hypokalemia - end up with increased intravascular volume → kidneys dump sodium (as much as
they can, anyway) and chloride

Mixed disorders
- Aspirin toxicity - suspect if fever, tinnitus, and tachypnea. Causes metabolic acidosis due to
salicylic acid and respiratory alkalosis due to increased respiratory drive → pH can be near
normal!
Chapter 9: Hematologic

Microcytic Anemias

Microcytic anemia:
● Thalassemias: Can have teardrop cells and target cells
○ Alpha thalassemia: Will have normal Hgb electrophoresis!!
○ Beta thalassemia: Will have increased levels of HgbA2 (A2, delta2)
■ Beta thalassemia minor/trait: Will have increased levels of hemoglobin A2 (2
alpha chains and 2 delta chains). Have hypochoromic microcytic anemia with
some target cells, fewer than with HgbC. Usually no problems.
■ Beta thalassemia major (B0B0): Presents at 6 months with progressive anemia
to the point of heart failure, hepatosplenomegaly, and weakness. Need blood
transfusions every month to avoid death. Will have some target cells, but fewer
than HgbC
● Lead poisoning:
○ Acute: abdominal pain, constipation. Then chronic: fatigue, irritability, insomnia,
hypertension, neuropathy, nephropathy, neuropsych disturbances, myalgias
● Malabsorption → B6 deficiency:
○ Celiac disease: Watch out for dermatitis herpatiformis and an associate with Type 1 DM.
Can screen with IgA anti-tissue transglutaminase antibody (very sensitive). Upper GI
endoscopy with small bowel biopsy confirms the diagnosis

Normocytic anemia
● Sickle cell
○ Valine for glutamic acid at the 6th position on the beta chain
● Hemoglobin C:
○ Autosomal recessive mutation in B chain of Hgb (glutamate → lysine).
○ In heterozygous state, no anemia, but will have target cells and Hgb C crystals
(hexagonal and eosinophilic).
○ Homozygous state causes moderately severe hemolytic anemia, reticulocytosis, and
splenomegaly with lots of target cells.

Hemolytic anemias

Signs
- Blood smear
- Shistocytes → intravascular hemolysis
- Spherocytes or helmet cells → extravascular hemolysis
- Heinz bodies (denatured hemoglobin) → G6PD deficiency. Need a special stain to see
it! Seems to usually be on the periphery, attached to the RBC membrane. Will get bitten
out by the spleen → bite cells
- Howell Jolly bodies: little pieces of RBC nucleus, can see without special stain (contrast
Heinz bodies). See them when spleen is nonfunctional. Also seen in myelodysplastic
syndromes.
 - Haptoglobin will be low! Haptoglobin binds free hemoglobin so that it can be cleared by the
RES, so low haptoglobin means that it has been busy binding free hemoglobin and hemolysis has
occurred

G6PD deficiency:
- G6Pd catalyzes the reduction of NADP to NADPH, which is necessary to make glutathione which
protects RBCs from oxidative injury - it is the only source of NADPH in RBCs
- In the absence of G6PD and the presence of oxidizing agents (bacterial toxins, sulfa drugs,
antimalarials, nitrofurantoin), Hgb → methemoglobin → denatured globin, and sulfhemoglobin.
These molecules form insoluble masses (Heinz bodies) that attach to RBC membranes, decrease
pliability, and promote hemolysis in the reticuloendothelial system
- See Heinz bodies (with special stains) and bite cells

Sickle cell trait

- Renal complications: hematuria (from renal papillary ischemia or necrosis), renal medullary
carcinoma, UTIs. May be unable to concentrate urine and have distal renal tubular acidosis (can’t
excrete H+)

Hereditary spherocytosis
- Autosomal dominant defect in spectrin → loss of RBC membrane surface area. Get destroyed by
the spleen.
- Diagnose with osmotic fragility test (use hypotonic saline)
- Treat with splenectomy - follow with penicllin prophy for 3-5 years or until adulthood. Risk of
sepsis is increased > 30 years out!

Autoimmune hemolysis
(1) Warm autoimmune hemolytic anemia
(a) IgG induced and hemolysis is primarily extravascular (IgG bound RBCs Go to the spleen,
where it’s warm)
(b) Can be idiopathic or caused by cancer (lymphoma, leukemia - especially chronic
lymphocytic leukemia), collagen vascular diseases (lupus), and drugs like alpha methyl
dopa
(c) Direct coomb’s test: RBCs coated with IgG
(d) Treatment: steroids, splenectomy, immunosuppression, RBC transfusions, folic acid
supplements
(2) Cold autoimmune hemolytic anemia
(a) IgM binds RBCs at cold temps → complement activation and intravascular hemolysis
(b) Idiopathic (old people) or caused by infection (mycoplasma pneumonia, infectious mono)
(c) RBCs coated with complement alone or positive cold agglutinin titer
(d) Steroids not helpful!

Paroxysmal Nocturnal Hemoglobinuria

- Deficiency of anchor proteins that link complement inactivating proteins to RBC membranes
(CD55, CD59)
- Can get venous thrombosis! Can evolve into aplastic anemia, myelofibrosis, and acute leukemia!
- Can cause anemia or pancytopenia
- Diagnosis
- Ham’s test: Put RBCs in acid serum → NPH cells will lyse, normal cells don’t
 - Sugar water test: NPH cells lyse
- Flow cytometry for the anchor proteins (best)

Acute intermittent porphyria

- 5 P’s: port wine colored urine, psychological disturbances, polyneuropathy, painful abdomen,
precipitated by drugs, alcohol, starvation
- Can look like PNH, but won’t have thrombosis.

Porphyria cutanea tarda

- Most common porphyria. Tea colored urine, blisters in the sun

Platelet disorders
Platelet functioning
- VWF binds exposed subendothelial collagen and then platelets bind VWF using the GP1b
receptor (deficient in bernard soulier syndrome).
- Adhesion induces shape change in platelets and degranulation with release of multiple mediators
- ADP from dense granules promotes platelet activation and aggregation - induces
exposure of GPIIB/IIIa receptors, which bind to fibrinogen (problem in Glanzmann
thrombocytopenia).
- Clopidogrel blocks the ADP receptor to decrease platelet activation and
aggregation
- TXA2 is made by COX and promotes aggregation.

Thrombin time - measures fibrinogen concentration

Vitamin K deficiency - Manifests like warfarin. PT is prolonged but PTT and other studies are normal

Anticoagulants
- Factor 10a inhibitors: The direct inhibitors are rivaroxaban (oral) and apixaban (oral), indirect is
fondaparinux
- Direct thrombin inhibitors: argotroban, bivalirudin, and dabigatran (oral)
- If INR is < 2, don’t increase warfarin without first starting heparin because of the risk of transient
hypercoagulable state.
- Treat warfarin indued skin necrosis with Protein C and stopping warfarin
- Thrombolytics are for hemodynamically unstable patients, immediate limb ischemia, etc
- IVC filter - when anticoagulation is contraindicated or the patient has failed anticoagulation
(recurrent or extended clot while FULLY anticoagulated) - doesn’t count if INR is below target

Thrombocytopenia:
- Due to decreased production, increased destruction, or sequestration (e.g., hypersplenism in
portal HTN!).
- Increased bleeding time, normal PT and PTT
- Cutaneous and mucosal bleeding (including GI, can be life threatening) - not bleeding into tissues
and joints

Heparin induced thrombocytopenia

- Most often with unfractionated heparin, less likely with low molecular weight heparin but can still
happen!
 - Suspect if platelets drop by 50%.
- Can cause clots → DVT, PE!
- Type 1: Give heparin, it directly causes platelet aggregation, platelets drop but generally stay
above 100k. Happens within 48 hours.
- No treatment needed, can continue heparin
- Type 2: Heparin induces ab-mediated injury to platelets - antibodies against heparin-platelet
factor 4 complexes cause platelet activation, thrombocytopenia, and pro-thrombotic state (venous
and arterial). Happens 3-12 days after starting drug, but can happen < 1 day if heparin has been
given before. Discontinue heparin immediately!
- Treatment: stop heparin, give lepirudin (thrombin inhibitor) or another agent
(rivaroxaban, etc) if anticoagulation is needed. Don’t give warfarin until platelet count is
normal (> 150k)

Immune/Idiopathic Thrombocytopenic Purpura

- IgG against platelets.
- Two kinds - childhood form often follows viral illness, self-limited. Chronic form more common in
adults (esp women 20-40), spontaneous remission is rare.
- Treat with steroids and IVIG if platelets < 30k in adults. In kids, can observe unless bleeding. Do
not give platelets unless life threatening - they will likely just get consumed.
- Can also be caused by viruses! Test for HIV and HCV

Thrombotic Thrombocytopenic Purpura

- Rare disorder where platelets are consumed, formed microthrombi that occlude small vessels in
pretty much any organ → hemolytic anemia, renal symptoms, neuro symptoms. Cause is
unknown!
- Presents with hemolytic anemia, thrombocytopenia, fever, acute renal failure (mild), and
fluctuating, transient neuro signs
- Deficiency of or autoantibody against von willebrand factor cleaving protease (ADAMTS-13) →
accumulation of long multimers and platelet aggregation.
- Triggers: HIV
- Life threatening emergency! Treat with large volume plasmapheresis, corticosteroids,
splenectomy. AVOID PLATELET TRANSFUSIONS

Thrombocytosis
- Reactive: Iron deficiency, splenectomy, inflammation, cancer
- Primary: myeloproliferative disorders, essential thrombocytosis, chronic myeloid leukemia

Bernard-Soulier Syndrome
- Autosomal recessive - disorder of platelet adhesion to subendothelium deficiency in glycoprotein
GP1b-!x.
- Have low platelets that are large in size. (Big bullshitter)

Glanzmann’s Thrombasthenia
- Autosomal recessive - disorder of platelet aggregation due to deficiency in platelet glycoprotein
GPIIb-IIa
- Platelet count is actually normal!

Von Willebrand Factor

 - Autosomal dominant!
- VWF protects factor 8 from destruction. Give factor 8 to all VWD patients (any kind) after trauma
or during surgery. Always give it to type 3.
- VWF
- Made in Weibel Palade bodies of endothelial cells and alpha granules of platelets.
-
- Type 1: decreased levels of VWF
- Type 2: qualitative abnormalities of VWF
- Type 3: No VWF
- Prolonged bleeding time, PTT may also be prolonged but can be normal
- Avoid aspirin and NSAIDs - will decrease COX activity even further! Also avoid IM injections
because of bleeding risk

Hemophilia A
- Intracranial bleeding is a big risk!
- Prolonged PTT, low factor 8, normal VWF
- Treatment
- pain - codeine + acetaminophen. Avoid aspirin and NSAIDs - can worsen platelet
dysfunction
- Replace Factor 8
- DDAVP can increase factor 8 levels (because increases VWF)

Hemophilia B: Less common than Hemophilia A

- Deficiency in Factor 9. Treat by replacement. No DDAVP

Antiphospholiipid Syndrome
- Prothrombotic antibodies will cause a spuriously prolonged PTT in vitro - but in fact, it is
procoagulant!

Vascular disorders

Osler-Weber-Rendu syndrome
AD. Diffuse telangiectasias, recurrent epistaxis, and widespread AV malformations - when in the lungs,
can cause chronic hypoxemia and reactive polycythemia from shunting

Blood doping

Can see high hematocrit with steroids, epo, and autologous blood transfusions. Only steroids will cause
testicular atrophy and gynecomastia

Transfusions

Transfusion reactions
- Seconds to minutes: Anaphylaxis - immediate wheezing, etc. Caused by recipient anti-IgA
antibodies when recipient is IgA deficient (risk in celiac disease!)
- Prevent by using IgA deficient plasma and washed RBC products
- Minutes to an hour: ABO incompatibility - immediate hemolysis reaction
- 1 hour to several hours
 - Febrile nonhemolytic transfusion reaction: Small amounts of plasma and leukocyte
debris in red cell concentrate → release cytokines that cause fevers, chills, and malaise,
without hemolysis
- Transfusion-related acute lung injury - respiratory distress within 6 hours of
transfusion. Noncardiogenic pulmonary edema with interstitial infiltrates. Caused by
donor anti-leukocyte antibodies.
- Primary hypotension reaction: Transient hypotension in patients taking ACE inhibitors because
of bradykinin in the donated blood that can’t be degraded. Happens w/in 6 hours

Neoplasms

Monoclonal Gammopathy of Undetermined Significance (MGUS)

- 10% of patients > 75 years old
- Diagnosis: IgG < 3.0 grams, less than 10% plasma cells in bone marrow, bence jones proteinuria
< 1 g/day, and NO end organ damage
- Get a skeletal xray survey to look for lytic lesions - THEY WILL NOT SHOW UP ON BONE
SCAN!

Multiple myeloma
- An elderly patient with bone pain, renal failure, and hypercalcemia has MM until proven
otherwise!
- 50% of patients with MM will develop renal insufficiency - obstruction of the tubules by
paraproteins (Bence Jones proteins). Also hypercalcemia, hyperuricemia, amyloid deposition,
and pyelonephritis
- Diagnosis: At least 10% abnormal plasma cells in bone marrow PLUS M protein (monoclonal
protein, usually IgG) in serum or urine, or lytic bone changes (cancer cells release osteoclast
activating factor). Might see stacked RBCs on smear (Rouleaux formation)
- Treatment: Preferred is autologous hematopoietic cell transplant (especially in younger people).
Do chemo with alkylating agents otherwise.

Waldenstrom’s macroglobulinemia
- Malignant plasmacytoid lymphocytes make IgM - it’s large and causes hyperviscosity of the
blood.
- Diagnose: IgM > 5, Bence Jones proteinuria sometimes, no bone lesions
- Fatigue, weight loss, neuro symptoms, lymphadenopathy, splenomegaly, anemia, abnormal
bleeding, and hyperviscosity - can cause blindness!
- No cue. Do chemo and plasmapheresis for hyperviscosity

Hodgkin lymphoma
- Bimodal onset: 15-30 and > 50
- Different types
- Lymphocyte predominance: few RS cells with lots of B cells
- Nodular sclerosis: most often in women, most common (70%)
- Mixed cellularity: RS cells with pleomorphic background
- Lymphocyte depletion: lack of reactive cells, worst prognosis

Non-Hodgkin Lymphoma
 - 2x as common as Hodgkin and tends to present with more advanced disease. B cells (85%) or T
cells.
- Treat with CHOP regimen (cytoxan, adriamycin, vincristine)
- Indolent:
- Small lymphocytic lymphoma (related to CLL),
- Follicular lymphoma (most common): painless peripheral lymphadenopathy, mean age of
onset is 55 years, can transform into diffuse large B cell lymphoma, associated with
t(14,18) translocation
- Intermediate
- Diffuse large cell - usually B cell. Presents as large extranodal mass, locally invasive
- High grade - aggressive with rapid dissemination, but may respond to chemo
- Lymphoblastic lymphoma. A T cell lymphoma - can progress to T-ALL. More common
in kids.
- Burkitt’s lymphoma: B cell lymphoma, more common in kids. T(8,14) translocation
- African: facial bone and jaw, linked with EBV
- American: abdominal organs
- Miscellaneous
- Mycosis fungoides: T cell lymphoma of the skin, presents with eczematoid skin lesions
→ generalized erythroderma
- Sezary syndrome: Skin and blood stream
- HIV: Usually Burkitt’s or diffuse large B cell. Poor prognosis.

Lymphoma in general
- Ann Arbor staging: Stage 1 = 1 node, 2 = 2 nodes on same side of diaphragm, 3 = both sides of
diaphragm, 4 = dissemination of disease outside of lymph system
- Hodgkin staging extra details:
- A = no symptoms
- B = fever, weight loss, night sweats (worse prognosis)

Meyloid cell development:

Common myeloid progenitor → myeloblast, erythroblast, megakaryoblast
Myeoloblast:
→ Promyelocyte → myelocyte → metamyelocyte → mature cell
→ Monoblast → promonocyte → monocyte
Acute leukemia: has more myeloblasts and promyelocytes
Chronic leukemia: more immature myelocytes and metamyelocytes

Acute Leukemias
- Fever is rare! Suggests infection! Contrast chronic leukemia - more fever.
- ALL has a better prognosis than AML
- WBC count varies from 1k to 100k
- AML:
- One important variety is acute promyelocytic leukemia. Has the t(15:17) translocation.
Treat with all-trans retinoic acid
- Promyelocytes and myeloblasts
- M3 subtype has auer rods
- ALL
Chronic Leukemias
- Cells are mature but defective
- CML
- Associated with philadelphia chromosome t(9,22) -- better prognosis when present. Treat
with tyrosine kinase inhibitors (imatinib, dasatinib, nilotinib)
- BLOOD SMEAR IS INDISTINGUISHABLE FROM LEUKEMOID REACTION → Must get
leukocyte alkaline phosphotase level - will usually be low in CML but can be elevated
or normal in leukemoid reaction. If still not clear, then test for t(9;22).
- Has more immature myelocytes and metamyelocytes
- CLL
- A B CELL DISEASE! See smudge cells
- Most common leukemia after age 50. Related to small lymphocytic lymphoma.
- Hairy cell leukemia
- A type of B CELL derived chronic leukemia. Fine, hair like projections on the
cells. Positive for tartrate resistant acid phosphatase stain (TRAP) and the
CD11c marker. More benign than most leukemias, but bone marrow can become
fibrotic.
- Treat with cladribine, a purine analog
- Prognosis: gets worse with lymphocytosis → adenopathy → splenomegaly → anemia →
thrombocytopenia

Myeloproliferative disorders

Polycythemia vera: Malignant RBC production.

- Hyperviscosity → thrombotic problems (DVT, CVA, MI, portal vein thrombosis)
- Bleeding
- Itching - especially after showers!
- Treat with repeat phlebotomy!

Myelodysplastic syndromes
- Ineffective hematopoiesis - apoptosis of myeloid precursors. Causes pancytopenia even with
hypercellular bone marrow.
- CBC might show Howell-Jolly bodies.

Essential thrombocythemia
- Platelet count > 600k, but have to exclude reactive thrombocytosis (infection, inflammation,
bleeding) and other myeloproliferative disorders
- Most often causes thrombosis, but can also cause bleeding due to defective platelet function
- The platelets are hypogranular and abnormally shaped. Bone marrow has increased
megakaryocytes
- Treat with antiplatelet agents and low dose aspirin. Sometimes hydroxyurea.

Paraneoplastic syndromes
- Adenocarcinoma: Clubbing, hypertrophic osteoarthropathy
- Squamous cell carcinoma: Central, necrosis & cavitation, PTH-rp → hypercalcemia
- Small cell carcinoma: ACTH → cushing’s, SIADH, LEMS
- Large cell carcinoma: Gynecomastia, galactorrhea (large cell causes large breasts)
 - Trousseau’s syndrome: Migratory superficial thrombophlebitis - especially in weird places like
the arms or chest. Associated with pancreatic cancer, lung cancer, stomach/colon cancer, and
acute leukemias. Can cause chest pain. Get a CT scan!

Other cancer clues

- Most head and neck cancer is squamous cell carcinoma - watch out for firm lymph nodes
- Firm, solitary lymph nodes - concerning for lymph node metastasis

Solitary lung nodule

- Defined as a nodule < 3 cm, surrounded by lung tissue, no adenopathy
- High malignancy potential → excise
- Intermediate→ additional imaging (PET) and biopsy
- Low malignancy risk → serial CT scans
- Note: solitary lung nodules are not typical of TB!

Breast cancer
- Mammogram not helpful before age 35 because breast tissue is too dense
- BRCA1 - breast and ovarian cancer, BRCA2 - breast cancer in men (most often invasive ductal
carcinoma - men have few lobules)
- Premalignant in situ lesions - no invasion of the basement membrane
- Ductal carcinoma in situ: may have a mass. Risk of developing invasive ductal
carcinoma → remove.
- Paget’s disease of the breast: DCIS that extends up the ducts to reach the skin
of the nipple. Suspect if rash on nipple doesn’t get better with OTC creams. Often
associated with underlying adenocarcinoma
- Lobular carcinoma in situ: rarely have a mass, no calcifications. Dyscohesive cells
lacking e-cadherin.
- Increased risk of breast cancer in either breast, but risk is not reduced by
removing the lesion! May do observation, selective estrogen receptor modulators
(tamoxifen), and prophylactic bilateral mastectomy.
- Ductal carcinoma
- Presents as a mass
- Four kinds
- Tubular carcinoma - good prognosis
- Mucinous carcinoma - relatively good prognosis
- Medullary carcinoma - large, high grade cells growing in sheets with lymphocytes
and plasma cells. BRCA1 association. Relatively good prognosis
- Inflammatory carcinoma - cancer in the dermal lymphatics. Inflamed, swollen
breast, can be mistaken for acute mastitis. Poor prognosis.
- Lobular carcinoma
- Invasive, grows in single file pattern, lack of e-cadherin, may have signet ring cells
- Treatment
- Presence of ER and PR indicates response to antiestrogenic agents (tamoxifen). Both
are in the nucleus (steroid receptors)
- HER2/neu is an oncogene that codes for a growth factor receptor on the cell surface -
target with herceptin (trastuzumab), an antibody against the receptor. Also indicates
good response to anthracycline chemo.
- Triple negative carcinoma has the worst prognosis.
Bone cancer
- Giant cell tumor:
- Benign and locally aggressive tumor that usually presents with pain, swelling, and
decreased range of motion.
- Osteolytic with “soap bubble” appearance. Hits the epiphyseal region of long bones -
often the distal femur and proximal tibia around the knee
- Osteoid osteoma
- Sclerotic, cortical lesion with a central lucency. Causes pain that is worse at night, not
related to activity, and is quickly relieved by NSAIDs

Hereditary Nonpolyposis Colorectal Cancer (Lynch Syndrome)

- Amsterdam criteria: At least 3 relevatives with colorectal cancer, including 1 first degree. Involves
at least 2 generations, at least one case before age 50, and FAP has been excluded
- Two kinds
- Lynch syndrome I = hereditary site specific colon cancer
- Lynch II: Cancer family syndrome - associated with high risk of endometrial cancer, 43%
of women in affected families.
Cancer Pain
- High dose NSAIDs won’t work. Start with short acting morphine and transition to long acting when
pain is controlled
- Fentanyl patches take 8-12 hours to take effect

Chemotherapy Side Effects

Febrile neutropenia
- Neutropenia = ANC < 1500. If < 1000 → higher risk for bacterial infection.
- Febrile neutropenia = Fever with neutropenia. Seen in chemo. Might mean early stages of
infection.
- Chemo can disrupt skin/mucosal barriers of mouth and GI tract → bugs can enter the
bloodstream. Biggest risk is psuedomonas.
- Get blood cultures and then give empiric treatment with psuedomonas coverage
(piperacillin-tazobactam, cefepime, meropenem)

Graft vs. Host Disease

- Maculopapular rash mostly on the face, hands, and feet. Diarrhea positive for blood. Abnormal
LFTs and jaundice.
- Donor t cells recognize host major and minor antigens
Chapter 10: Infectious Disease

TB
- Primary TB presents w/ lower lobe infiltrates, reactivation presents with apical nodules or cavitary
lesions

Influenza
- Prominent constitutional symptoms - high fevers, myalgias, headache, cough, coryza (inflamed
mucous membranes). Throat exam usually unremarkable. Acute onset. Less emphasis on runny
nose, sneezing, etc.
- Give antivirals (oseltamivir, zanamivir) to anyone who presents within the the first 48 hours. After
that, only treat patients who aren’t improving or who are at high risk for complications (old,
pregnant, native American, obese, chronic medical conditions)

Strep throat
- Centor criteria: Tonsillar exudates and hypertrophy, pharyngeal erythema, tender anterior
cervical adenopathy, fever, no cough,

Pneumonia
- Legionella → Legionaire’s disease: Gram negative rod. Pneumonia, GI symptoms (diarrhea),
elevated LFTs, hyponatremia. Treat with quinolone or macrolide. Catch it from water - no human-
to-human transmission!

Infectious arthritis
- Parvovirus - acute, symmetric arthritis of the hands, knees, ankle joints. 15 mins of morning
stiffness. Also fever, fatigue, diarrhea.
- Hep C and mixed cryoglobulinemia - palpable purpura, lymphadenoapthy, nephropathy,
neuropathy

Osteomyelitis
- Staph aureus is the most common cause in kids and adults
- Puncture wound through a shoe → psuedomonas aeruginosa. Treat with quinolones (-floxacins,
good for gram negative rods of GI and GU tracts)

Leprosy
- Numb, hypopigmented patch of skin! Get a skin biopsy - see acid-fast bacilli (mycobacterium
leprae)
- Leprosy is a chronic granulomatous disease that affects peripheral nerves and skin, caused by
mycobacterium leprae. Presents early as a numb hypopigmented plaque, then later peripheral
nerve damage causes muscle atrophy with crippling deformities of the hands.

Fungus
- Blasto: skin manifestation are well circumscribed warty nodules and plaques that progress to
microabscesses. Also affects the prostate
- Histo: acute pneumonia with fever, cough, malaise - usually not serious unless IC’ed. Hilar
adenopathy
 - Coccidiomycosis - Southwest, central & south America. Nonspcific - fever, fatigue, dry cough,
weight loss, pleuritic chest pain. Can have skin findings like erythema multiforme and erythema
nodosum, also joint aches
- Mucormycosis: surgery and IV amphotericin

Meningitis
- Treatment
- H flu or neisseria: ceftriaxone
- S pneumo: Give dexamethasone in addition to abx
- Listeria: ampicillin
- Gram negative rods (psuedomonas): Cefepime or ceftazidime
- Empiric treatment:
- IC’ed patient: cover for S pneumo, neisseria, listeria, and gram negative rods including
psuedomonas. Use vanco + ampicillin + cefepime or ceftazidime. Need to include
ampicillin for listeria coverage.
- Alll adults: Give dexamethasone - effective for preventing strep pneumo complications
-
-
Zoonosis
- Ancylostoma braziliense = cutaneous larva migrans:
- Helminth infection caused by larva of the dog/cat hookworm.
- Classically causes severely itchy, elevated, serpiginous reddish brown lesions on the skin
that elongate at a rate of several mm per day as the larvae migrate.
- Present in warm areas, get it from sand contaminated with cat or dog poop
- Bartonella henselae
- Cat scratch disease characterized by self-limited lymphadenopathy. Treat with
azithromycin because the lymphadenopathy and systemic symptoms can be debilitating
- Human or dog bite: Amoxicillin-clavulanic acid

Malaria
- P falciparum is often resistant to chloroquine - prophylax with mefloquine, atovoquine, or
doxycycline
- Babesia is transmitted by the Ixodes tick! Happens in the northeast. Causes hemolysis. Clinically
significant illness occurs in people over 40, patients without a spleen, and IC’ed people. Can have
fever, drenching sweats, malaise, jaundice, dark urine, etc.

RASHES

Rash on palms and soles

- Rocky Mountain Spotted Fever: rash STARTS on the wrists and ankles and then spreads. Toxic
appearance, high fever, conjunctivitis, diffuse myalgias
- Secondary syphillis: Rash starts on the trunk and then spreads. Difuse lymphadenopathy
- Viral exanthem from enteroviruses (especially coxsackie A): Rashes on the palms and soles but
no diffuse lymphadenopathy

Rashes sparing the palms and soles

 - Rubella: fever, occipital and/or posterior cervical lympadenopathy folowed by a rash that spreads
rapidy in a cranial-caudal pattern and spare the palms and soles. Can have arthritis that lasts up
to a month - especially women
- Measles: Rash develops cranial-caudal, similar to rubella. But rash spreads more slowly and
have high fever (> 104) and no arthritis.

Toxic shock
Rash - not localized and not painful.

Necrotizing fascitis: Staph aureus, strep pyogenes, c perfringens

Cellulitis
- Erysipelas: a specific type of cellulitis - inflammation of the superficial dermis → swelling, sharp
demarcation, erythematous, raised borders. Often on the face. Most often caused by Group A
strep

STDS

Syphillis
- Jarisch-Herxheimer reaction - when primary or secondary syphillis is treated with penicillin, the
spirochetes die fast and cause the release of antigen-antibody complexes in the blood that can
look like an acute flare up of syphillis
- Secondary syphillis - rash starts on the trunk and then goes to the palms and soles. Will have
generalized lymphadenopathy, maybe sore throat.
- Use penicillin. If allergic, can use doxycycline - unless pregnant. If pregnant, do penicillin
desensitization.

HIV
- Presents with fever, arthralgias, sore throat, LAD, mucocutaneous lesions, diarrhea, weight loss
- Treat with 2 nucleoside reverse transcriptase inhibitors and one NNRTI or one protease inhibitor
- Protease inhibitors: All end in NAVIR
- NRTIs: Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didanosine, stavudine
- NNRTIs: Nevirapine, efavirenz, delavirdine (NED never ef’d Dela)
- Prophylaxis:
- Primary (before first infection)
- Bactrim - pneumocystis jiroveci (CD4 < 200) and toxoplasma (CD4 < 100) - but
sulfadiazine and pyrimethamine are used to treat toxo infections
- Itraconazole - histo (CD4 < 150, Ohio and Mississippi river valleys)
- Azithromycin or clarithromycin - for mycoplasma avium complex (CD4 < 50)
- Ganciclovir: prophy of CMV with CD4 < 50 and serum IgG is positive, or when
biopsy for CMV is positive (pneumonia, abdominal pain, esophagitis, diarrhea)
- Secondary (after infection)
- Acyclovir - severe or frequent HSV recurrences, regardless of CD4
- Fluconazole - prophy against cryptococcus neoformans, coccidiodes in patients
who have had the disease in the past. Also for frequent candida infections
- Isoniazid - +PPD (>5 cm) or recent contact with TB
-
 - Side effects of treatment meds:
- Protease inhibitors: hyperglycemia, GI intolerance, lipodystrophy
- Indinavir (protease inhibitor): crystal induced nephropathy and hematuria -
monitor with urinalysis and serum creatinine
- NRTI’s - lactic acidosis, bone marrow suppression, peripheral neuropathy
- Didanosine (NRTI) - pancreatitis
- Abacavir (NRTI) - hypersensitivity
- Zidovudine - anemia
- NNRTI’s - Stevens Johnson, hepatotoxicity
- Nevirapine (NNRTI) - liver failure
- Health care worker exposure:
- Get HIV testing to establish a baseline and repeat testing at 6 weeks, 3 months, and 6
months. Treat with 3 drug regimen in the mean time.

HIV esophagitis
- Usually candida - but will have oral thrush and mild-moderate pain. Severe pain suggests viral
causes - do endoscopy.
- For mild symptoms with oral thrush, treat empirically for candida with fluconazole. For severe
symptoms or no trhush, do endoscopy for viral causes.
- White plaques → candida. Treat with fluconazole
- Large linear ulcers → CMV. Treat with gancicylovir
- Vesicles & round ulcers → HSV. Give acyclovir
- Apthous ulcers → systemic therapy

Opportunistic infections
- Pneumonia:
- Nocardia: weakly acid fast, brancing, filamentous rod. Can disseminate to brain and skin!
Treat with bactrim.
- Histoplastmosis:
- Central US.
- In immune compromised hosts, the pneumonia is diffuse or cavitary. Also have
RES involvement causing hepatosplenomegaly, adenopathy, and
pancytopenia (because histo hides in macrophages). Can also have oral
ulcers.
- Healthy pts can have no treatment or do oral itraconazole, IC’ed patients need
amphotericin B and then can switch to oral itraconazole
- Diagnose in IC’ed with urine or serum antigen testing
- Pneumocystis pneumonia (PCP): dyspnea, non-productive cough, normal white count,
severe hypoxia, bilateral interstitial infiltrates. CD4 < 200. Treat with bactrim or dapsone.
- Mycobacterium avium complex: low grade fever, cough, weight loss. Treat with
azithromycin or clarithromycin + ethambutol
- Aspergillosis: Affected patients usually have CD4 < 50. Fever, cough, dyspnea.
- Meningitis/Neuro
- Cryptococcus neoformans: develops over 2 weeks - subacute! Causes high ICP. Treat
with amphotericin B with flucytosine. Maintenance with fluconazole
- JC virus - progresssive multifocal leukoencephalopathy
- Skin
 - Bartonella can cause bacillary angiomatosis - cutaneous and visceral (liver) angioma-like
blood vessel growths that regress with abx and are prone to hemorrhage
- Eyes
- CMV retinitis when CD4 < 50

UTI
- If urine is alkali/basic: Proteus! Secreates urease, which hydrolyzes urea to ammonia and CO2.
Ammonia then combines with hydrogen to make ammonium, decreasing the free hydrogen
concentration and promoting the production of struvite stones, which become a permanent
source of bacteria! Eradication of the infectious staghorn calculi is very difficult - can’t do with abx.
Stone and fragments have to be removed!
- Uncomplicated cystitis: Initrofurantoin, bactrim, fosfomycin (one dose!)
- Complicated cystitis: If diabetic, CKD, pregnant, immune compromised, obstruction, hospital
acqired, etc. Do urine culture before therapy! Generally use flouroquinolones.

Pyelonephritis
- Treat high risk people (catheters, IC’ed, diabetes, etc) with IV abx and then transition to oral after
2-3 days
- Flouroquinolones as inpatient or outpatient, also ceftriaxone

Actinomyces
- Abscesses at the head and neck with characteristic granular yellow pus (“sulfur granules”)
- Anaerobic filamentous gram positive bacteria, not acid fast
- Treat with penicillin G

Lyme disease
- Not in southern United States!
- Erythema migrans rash is pathognomonic for Lyme disease - if see it, just treat. No testing. 80%
have it.
- Give doxycylcine prophy if tick was attached > 36 hours. Recall that it is contraindicated in kids
< 8 and pregnant women. In kids, can do amoxicillin, azithromycin, or cefuroxime
- Treat neuro and cardiac manifestations with ceftriaxone

Ehrlichiosis
- Southeastern and south central US
- Flu like illness (high fever, HA, myalgias), confusion, leukopenia and thrombocytopenia,
elevated LFTs, Rash is uncommon!! Think of this if someone is bitten by a tick but doesn’t
have erythema migrans.
- Treat empirically with doxycycline while waiting for labs.
- Diagnosis - see intracytoplasmic morulae in monocytes

Typhoid fever
- Fever first week, then salmon colored rash in second week, then hepatosplenomegaly with
abdominal complications in the third week.

Parasites
- Taenia solium (pork tapeworm): Humans are the definitive hosts! If human eats cysts in pig meat,
the worm is happy - adult tapeworm lives in the jejunum and secretes eggs into feces. Then an
 animal eats the feces and the bug encysts in the animal tissue, starting the cycle again. But if
human consumes eggs (from human feces) - then can get cystercosis! Multiple small fluid filled
cysts in the brain parenchyma
- Trichinellosis: Eat undercooked meat (usually pork) that has encysted larvae - they excyst in the
acidic conditions of the stomach, become adults, and release larvae that migrate and encyst in
striated muscle.
- Intestinal stage: either no symptoms or abdominal pain, diarrhea, vomiting, etc
- Muscle stage 4 weeks later: myositis, fever, splinter hemorrhages in the nails,
periorbital edema, eosinophilia, maybe elevated creatinine kinase and leukocytosis
Chapter 11: Skin and Hypersensitivity

Acne
- Obstructive or inflammatory
- Start with benzoyl peroxide → topical retin A → topical antibiotic → systemic antibiotic → oral
retin A

Rosacea
- Like acne, but onset 30-50 and no comedones
- Thickened skin on the nose = rhinophyma
- Avoid temp extremes, hot drinks, alcohol
- Treat with topical metronidazole, oral antiobiotics for maintenance. Can do accutane if that fails.

Seborrheic dermatitis
- Can be dandruff or located elsewhere. Treat with ketoconazole, corticosteroids

Pityriasis rosea
- Herald patch, followed by christmas tree rash. Itchy. May take several weeks to go away, just
give antihistamines for the itch. No real treatment. Not contagious. Maybe related to HSV 7.

Erythema nodosum
- Painful, red subq nodules, usually on the anterior tibia. May have low grade fever, malaise, joint
pain
- Caused by
- Infection: strep, syphilis, TB, fungus
- AI: inflammatory bowel disease, behcet’s, sarcoidosis
- Medications: COP, sulfa, amiodarone, abx
- Pregnancy
- Idiopathic
- Treat with NSAIDs and work up to find the cause

Erythema multiform → SJ syndrome → TENs

- HSV can cause EM, but doesn’t cause more severe disease

Genital warts: HPV 6 and 11 (16 and 18 cause cancer)

Scabies
- Severely itchy! Often worse at night. Linear marks with a darker dot at the end, representing the
female mite.
- Common areas are fingers, interdigital, and wrists. Usually spares the head + neck
- Treat with permethrin cream: paralyzes the parasites. Just do one overnight treatment, must
apply all over body and treat close contacts, too. No longer contagious after 1 treatment but
itchiness may take awhile to resolve

Tineas
- Treat capitis and unguium (onychomycosis) with oral griseofulvin
- Treat corporis (ringworm), pedis, and cruris (jock itch) with topical antifungals
Psoriasis
- Auspitz sign
- Caused by overproliferation of skin → immature skin has abnormal keratinization
- Treat with topical steroids, topical Vit D derivatives, or systemic therapy in severe cases:
methotrexate, cyclosporine, infliximab. Can also do UV light.

Vitiligo
- Autoimmune disease. Treat with topical steroids, photochemotherapy

Drug allergies
- Usually happen within 1 month of starting the drug - rarely within 1 week

Dermatitis herpetaformis
- Treat with gluten free diet and dapsone

Porphyria cutanea tarda

- Deficiency of uroporphyriin decarboxylase, an enzyme in heme synthesis. Confirmed by elevated
urinary porphyrin.
- Painless blisters, increased skin fragility on the dorsal surfaces of the hands, facial hypertrichosis,
and hyperpigmentation.
- Associated with hepatitis C. Can be triggered by substances like ethanol and estrogens -
discontinue them!
- Can treat with phlebotomy, hydroxychloroquine, or alpha interferon

Acanthosis Nigricans
- Benign is assoc’ed with insulin resistance, but can be malignant = associated with cancer

Icthyosis:
- Normal skin at birth, with gradual progression to dry, scaly skin. Can be hereditary or acquired

Skin cancer
- Basal is most common, squamous is 2nd most common.
- Squamous is more dangerous than basal cell because it metastasizes frequently
- Melanoma: First do excisional biopsy, then once confirmed, take bigger margins. Don’t start with
big margins! Can disrupt cutaneous lymph flow and prevent ID of sentinel nodes

Frostbite
- Rapidly rewarm with warm water!

Eye problems
- Chalazion: Granulomatous condition, where painful swelling → nodular rubbery lesion.Persistent
chalazion may be due to sebaceous carcinoma. If recurrent, do histopath evaluation.
- Hordeolum - stye = acute infection of a gland, often with staph. Do warm compresses.

Random lesions
- Dermatofibroma: Almost like a keloid - nontender, discrete, firm, hyperpigmented lesions that
are usually < 1 cm
Cherry angioma (senile hemangioma) in adults, strawberry hemangioma in kids
 -
Eyes

Optic neuritis
- rapid impairment of vision in one eye (rarely both) and pain on eye movement. Marked changes
in color sensation, afferent pupillary defect and field loss, usually central scotoma
- More common in MS

Contact lens keratitis

- Usually psuedomonas or serratia (think bathroom bugs). A medical emergency!

Acute angle closure glaucoma

- Red, painful eye and blurred vision. Pupil is fixed and mid-dilated. Often HA and nausea
- Usually occurs after pupil dilation, which can happen in darkened movie theaters, during
stress, or with drugs
- Atropine is contraindicated - can dilate the pupil and worsen the glaucoma
- Pilocarpine: opens canals of Schlemm - a cholinomimetic agent

Anterior urveitis = irisitis

- Iris is a mess! Pupil is constricted. Also red conjunctiva. But cornea is usually spared
- Pain, miosis, photophobia. Can have visual loss

Episcleritis
- Inflammation of the episcleral tissue between the conjunctiva and sclera
- Localized, patchy redness - usually mild pain and discharge. Can occur with RA and other
autoimmune disorders, but usually idiopathic. Generally self-limited. No affect on vision or
cornea

Endophthalmitis
- Infection of the globe itself (bacterial or fungal), especially the vitreous - due to disruption of the
external surface of the eye (trauma, surgery, etc)
- Pain, decreased visual acuity, swollen eyelids and conjunctiva, purulenthaziness of globe
contents and may have hypopyon (pus in anterior chamber)
- Treat with intravitreal abx or vitrectomy
- Can happen up to six weeks after surgery

Subconjunctival hemorrhage
- Trauma or valsalva. Red on the sclera

Viral conjunctivitis
- usually preceded by URI

Dacrocystitis
- Infection of the lacrimal sac - red medial canthus, press on it and pus comes out (lovely). Usually
staph aureus or beta hemolytic strep.

Glaucoma
- Open angle glaucoma
 - More common in African Americans. Especially common w/ family history and diabetes.
- Gradual loss of peripheral vision, cupping of the optic disc
- Tx: Eye drops like timolol

Diabetic retinopathy
- Usually asymptomatic until very late in the disease - then poor night vision, curtain falling with
vitreous bleed, or floaters due to resolution of bleed
- Background or simple retinopathy
- Dilation of veins, microaneurysms, retinal hemorrhages, edema, hard exudates
- Pre-proliferative:
- Cotton wool spots
- Proliferative or malignant
- Neovascularization

Macular degeneration
- Loss of fine visual acuity - straight grid lines appear curved. Causes central scotoma
- Most common cause of blindness in industriaal world - age and smoking are risk factors
- Dry/Atrophic
- Drusen and patchy depigmentation in the macular region - basically ulceration of the
macula
- Slow loss of vision in one or both eyes
- Wet/Exudative
- New blood vessels that leak and scar the retina
- Acute distortion in vision, with wavy lines or loss of central vision, usually one eye

Cataract
- Progressive thickening of the lens, blurred vision, problems with nighttime driving, glare

Papilledema
- Can have an enlarged blind spot

Amaurosis fugax
- Transient vision loss like a curtain falling down - most often caused by retinal emboli from the
ipsilteral carotid. May see areas of white retina (edema) following the arterioles.
- See chery red spots and diffuse retinal whitening
- Must evaluate the carotids and treat atherosclerosis to reduce risk of stroke
- Treat with ocular massage (dislodge clot) and high flow oxygen

Detached retina
- Flashes, floaters, curtain falling - usually starting from periphery

Central vein thrombosis

Painless, sudden or subacute vision loss. Can progress to painful ischemia
- see dilated veins with scattered and diffse hemorrhages (blood and thunder), disc swelling,
cotton wool spots

Hypertensive retinopathy
 - Usually no acute vision loss. Initial focal spasms of arterioles → progressive sclerosis and
narrowing
- See ateriovenous nicking, copper or silver wiring, exudates, or hemorrhages

Vitreous hemorrhage
- Trauma, retinal tear, vitreous detachment. Often diabetic retinopathy. Can cause floaters

Allergic conjunctivitis
- Treat with mast cell stabilizing agents: olopatadine and azelastine

HSV keratitis
- Pain, photophobia, decreased vision, dendiritic ulcers on the cornea, maybe also corneal
vessicles

Herpes zoster ophthalmicus

- Shingles with eye involvement

HiV
- CMV retinitis: Most common cause of serious eye problems. Painless. Fluffy or granular retinal
lesions near retinal vessels and associated hemorrhages. Usually no conjunctivitis or keratitis
- HSV retinitis and VSV retinitis: Rapidly progressing bilateral necrotizing retinitis (acute renal
necrosis) - keratitis and conjunctivitis with eye pain, followed by fast vision loss. Widespread pale
peripheral lesions and central necrosis of the retina.
Ears

Rinne test for conductive hearing loss

- Hold vibrating tuning fork against the mastoid bone until pt can no longer hear it - then move it
just ouside the ear - patient should be able to hear air for twice as long as bone. If not, conductive
hearing loss.

Weber test
- Place tuning fork at the middle of the head - normal is hearing equally in both hears.
- Conductive hearing loss: Hear it louder in the ear with a problem, because that ear can’t hear
ambient room noise!
- Sensineural loss: It is quieter in the affected ear, because that ear can’t sense the vibration

Rinne - hold on mastoid, then Weber - hold in the Midline

outside ear

Normal Air conduction > bone Sounds the same on both sides
conduction on both sides

Conductive loss Bone conduction > air Sounds louder on the problem
conduction in the affected ear side, because that side doesn’t
hear ambient noise

Sensineural loss air conduction > bone Unaffected ear sounds louder
conduction on both sides
(normal)

Mixed loss bone conduction > air Unaffected ear sounds louder
conduction in the affected ear,
other ear is normal

Conductive hearing loss

- cerumen impaction, middle ear fluid or infection, otosclerosis, bony tumors
- Otosclerosis is common in 20-30s

Presbycusis
- High frequency hearing loss that occurs w/ age - can’t hear over lots of background noise.

Otoosclerosis
- Chronic conductive hearing loss, bony overgrowth of the stapes. Middle age. Low frequency
loss

Meds and hearing

- Aspirin - tinitus
- Loop diuretics, aminoglycosides - sensineural hearing loss

Meniere’s disease
 - Distention of the endolymph compartment of the inner ear → vertigo episodes that last about 20
minutes to 1 day, with low frequency sensineural hearing loss and tinnitus
- Treatment: low salt diet, avoid alcohol, caffeine, nicotine. If that doesn’t work, consider diuretics,
antihistamines, anticholinergics

Malignant otitis externa

- Severe infection seen in elderly diabetic patients - often caused by psuedomonas. Inner ear pain
and discharge that doesn’t respond to topical abx - treat with antipsuedomonals (cipro)
- Note rhizopus doesn’t cause this- just causes sinusitis that can extend into the orbit and brain
Miscellaneous

Adult Still’s Disease - high fevers, rash, arthritis

Erectile dysfunction
When treating patients who are taking both an alpha blocker (e.g., doxazosin for BPH) and sildenafil
(PDE inhibitor), give them within a 4 hour window to lower the risk of hypotension

Immune supressants:
- Calcineurin inhibitors: Block production of IL-2
- Tacrolimus: nephrotoxicity, hyperkalemia, hypertension, tremor
- Cyclosporine: same as tacrolimus, plus hirsutism and gum hypertrophy
- Purine analogs
- Azathioprine (converted to 6-mercapto-purine): Dose related diarrhea, leukopenia,
hepatotoxicity
- Mycophenolate: Reversible inhibitor of inosine monophosphate dehydrogenase, rate limiting
enzyme for de novo purine synthesis. SE is bone marrow suppression

Acute back pain

- Herniated disc: Can cause spinal nerve impingement → unilateral radicular pain in a dermatomal
distribution, positive straight leg test. Sitting and leaning forward make the pain worse!
- In mechanical back pain (herniated disc), do early mobilization, NSAIDs, muscle
relaxants. PT and bed rest don’t help.
- Compression fracture: acute intense pain, local spinal tenderness, obvious predisposing factors
(postmenopausal, osteoporosis, steroids)
- Cauda equina syndrome: Caused by large midline disk herniation. Saddle anesthesia, bladder
atony with overflow incontinence, bilateral sciatica, saddle anesthesia, and loss of anal sphincter
tone.
- Back pain from cancer is worse when lying down due to distention of the epidural venous plexus,
while back pain from degenerative joint disease is better when lying down
- Workup
- Cord compression signs/symptoms → MRI
- Red flags or sciatica → xray and ESR
- Red flags: age > 50, nighttime pain, constitutional sx, hx of caner, trauma, IV
drug use, infeection risk, > 1 month without improvement
- If abnormal, then get MRI
- No red flags, cord compression, or sciatica → conservative therapy for 4-6 weeks

Knee Pain
- Patellofemoral syndrome:
- subacute to chronic pain worse when climbing up or down stairs or with squatting
- Caused by overuse (most common), misalignment, trauma
- Dx: Patellofemoral compression test: extend knee while pressing on patella, also worse
with squat - no imaging necessary
- Tx: stretch and strengthen the thigh muscles
- Patellar tendonitis
 - Athletes - this is jumper’s knee. Episodic knee pain with pain and tenderness at the lower
patella
- Osgood Schlatter syndrome = pain at the tibial tubercle
- ONLY IN KIDS - GROWTH SPURTS. Pain at the tibial tubercle caused by
chronic/repetitive strain at the insertion of the patellar tendon on the tibial tubercle

Cervical spondylosis
- 10% of people over 50 years. Chronic neck pain and limited lateral movement due to
osteoarthritiis and secondary muscle spasm. Can cause sensory deficits due to osteophyte
induced radiculopathy

POISONINGS

Cyanide
- House fires! Also carbon monoxide
- Binds to Fe3+ → can’t become Fe2+ and bind oxygen. Methemoglobin also binds oxygen more
tightly at the Fe2+ sites. Then cyanide packs another whammy by inhibiting cytochrome oxidase -
can’t make ATP via oxidative phosphorylation. Cells switch to anaerobic metabolism → more
lactic acid
- Antidote treatment is hydroxocobalamin or sodium thiosulfate - durectly bind cyanide molecules
- If no antidote available, give nitrites to induce methemoglobinemia - cyanide binds Fe3+ so
methomoglobinemia provides an alternative binding site

Methemoglobinemia
- Oxidation of Fe2+ to Fe3+ - Fe3+ is itself unable to bind oxygen, but it increases the affinity of
Fe2+ for oxygen, which causes left shift in the oxygen curve (left shift is like the LUNGS - bind
oxygen more avidly there)
- Happens with exposure to oxidizing agents - dapsone, nitrates, topical or local anesthetics
Biostatistics

Types of studies
- Observational studies
- Case control: retrospectively associate outcomes with risk factors. Start by selecting
cases with certain outcomes (e.g., drug resistant TB) and controls without that outcome
(drug sensitive TB). Then look for associated risk factors
- Retrospective cohort: Look for risk factors first, then look at outcomes