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 its in the duodenum - thats 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

1.)
a.)
b.)
2.)
a.)
b.)
c.)
3.)
4.)
a.)

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

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 thats 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 arent 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 dont 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 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 its 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.
CId 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 assoced 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 wont 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)
Dont 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 Johns wort
End Stage Renal Disease limits anticoagulation choices! Enoxaparin, fondaparinux (injection factor 10a inhibitor) and
rivaroxaban (oral factor 10a inhibitor) arent 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: oslers 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 ICed 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 its exudate: pleural protein/serum protein > 0.5, pleural LDH/serum LDH > 0.6,
pleural LDH > 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 its 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 wont 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 arent 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, Horners 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 doesnt 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 wont 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 doesnt 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 assoced 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 nonneoplastic
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 wont 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), Wilsons disease (also called hepatolenticular degeneration due to deposition of copper in
the basal ganglia)
PBC: treat with ursodeoxycholic acid, methotrexate is second line. Glucocorticoids dont 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) isnt 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 (cant 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 cant do beta
blockers

Hepatorenal syndrome:
liver failure portal HTN increased NO in splanchic circulation systemic vasodilation and
underperfusion of the kidneys. Wont 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.
Whipples 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 cant 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, youd 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 dont 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 assoced 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 isnt 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 airfluid levels in the gallbladder and curvilinear gas shadowing in the GB
Cholangitis:
Charcots triad: fever, RUQ, jaundice.
Treat with abx first - 80% get better. If dont 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 dont respond! High calcium wont
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 wont 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 Cushings 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 doesnt 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 Graves, but dont do it if the patient is pregnant or has very severe
opthalmopathy
Hashimotos thyroiditis
Increased risk of thyroid lymphoma!

Subacute thyroiditis
lymphocytic - painless
granuloamatous/de quervains - painful

DKA
Treat with NS, regular insulin, and correction of the electrolyte imbalances along with the underlying cause. Give HCO3only 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 (Wilsons 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 cant 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.
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
i.

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 wont 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
Assoced 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

Sjogrens
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 raynauds, 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, raynauds, esophageal dismotility, sclerodactyly, telangectasias

Mixed connective tissue disease

Features of lupus, RA, systemic sclerosis, and polymyositis

Raynauds:
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 gottrons 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 Is, 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 (cant 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
Reiters syndrome is an example - cant see, cant pee, cant 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, Behcets
Behcets:
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 doesnt work, add sulfasalazine or hydroxychloroquine. If that doesnt work, add TNF alpha inhibitors.
Risk of hepatotoxicity, cytopenias, stomatitis
Dont 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

Bakers 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
DeQuervains 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 isnt associated with high phosphorus levels, unlike other causes of hypoPTH.

Hypokalemia
Muscle weakness and cramps
Can happen in Cushings 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 (dont 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

1.
a.
2.
3.
a.
b.
c.
i.
4.
5.
a.
b.
c.
-

Acid-base disorders
Is the patient acidemic or alkalemic - look at the blood pH
Henderson Hasselbalch: pH = pK + log (conjugate base/acid). For CO2 and bicarb, pH = 6.1 + log (HCO3/(0.03xCO2))
Is the primary disturbance metabolic or respiratory?
If metabolic acidosis:
Is there an increased anion gap?
Is the respiratory compensation appropriate? Winters formula - PCO2 = 1.5 x HCO3 + 8 +/- 2. This formula is used on
for metabolic acidosis!
If there is an anion gap, is there a concomitant metabolic problem?
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
If metabolic alkalosis, is respiratory compensation appropriate? Use PCO2 = 0.9 x bicarb + 8 +/- 2
If a respiratory problem is present, is it acute or chronic
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
For acute respiratory acidosis, HCO3 goes up by 1 for each 10 mm Hg change in PCO2
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 its 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, cushings 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 (cant 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!

(c)
(d)
(2)
(a)
(b)
(c)
(d)

Autoimmune hemolysis
Warm autoimmune hemolytic anemia
IgG induced and hemolysis is primarily extravascular (IgG bound RBCs Go to the spleen, where its warm)
Can be idiopathic or caused by cancer (lymphoma, leukemia - especially chronic lymphocytic leukemia), collagen vascular
diseases (lupus), and drugs like alpha methyl dopa
Direct coombs test: RBCs coated with IgG
Treatment: steroids, splenectomy, immunosuppression, RBC transfusions, folic acid supplements
Cold autoimmune hemolytic anemia
IgM binds RBCs at cold temps complement activation and intravascular hemolysis
Idiopathic (old people) or caused by infection (mycoplasma pneumonia, infectious mono)
RBCs coated with complement alone or positive cold agglutinin titer
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
Hams test: Put RBCs in acid serum NPH cells will lyse, normal cells dont
Sugar water test: NPH cells lyse
Flow cytometry for the anchor proteins (best)

(1)
(a)
(b)

Acute intermittent porphyria

5 Ps: port wine colored urine, psychological disturbances, polyneuropathy, painful abdomen, precipitated by drugs,
alcohol, starvation
Can look like PNH, but wont 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, dont 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) - doesnt 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. Dont 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 2040), 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)

Glanzmanns 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 cant 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.

Waldenstroms macroglobulinemia
Malignant plasmacytoid lymphocytes make IgM - its 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.
Burkitts 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 Burkitts 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 cushings, SIADH, LEMS
Large cell carcinoma: Gynecomastia, galactorrhea (large cell causes large breasts)
Trousseaus 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.
Pagets disease of the breast: DCIS that extends up the ducts to reach the skin of the nipple. Suspect if rash on nipple
doesnt 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 wont 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 arent 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 Legionaires 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 ICed. 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:
ICed 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 ICed 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 cranialcaudal 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 efd 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
NRTIs - lactic acidosis, bone marrow suppression, peripheral neuropathy
Didanosine (NRTI) - pancreatitis
Abacavir (NRTI) - hypersensitivity
Zidovudine - anemia
NNRTIs - 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, ICed patients need amphotericin B and then can switch to oral
itraconazole
Diagnose in ICed 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 - cant 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, ICed, 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 doesnt 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, behcets, 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 doesnt 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 assoced 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. Dont 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 cant hear ambient room noise!
Sensineural loss: It is quieter in the affected ear, because that ear cant sense the vibration
Rinne - hold on mastoid, then
outside ear

Weber - hold in the Midline

Normal

Air conduction > bone

conduction on both sides

Sounds the same on both sides

Conductive loss

Bone conduction > air

conduction in the affected ear

Sounds louder on the problem

side, because that side doesnt
hear ambient noise

Sensineural loss

air conduction > bone

conduction on both sides
(normal)

Unaffected ear sounds louder

Mixed loss

bone conduction > air

conduction in the affected ear,
other ear is normal

Unaffected ear sounds louder

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 - cant 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

Menieres 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 doesnt 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
doesnt respond to topical abx - treat with antipsuedomonals (cipro)
Note rhizopus doesnt cause this- just causes sinusitis that can extend into the orbit and brain
Miscellaneous

Adult Stills 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 dont 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 jumpers 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+ cant become Fe2+ and bind oxygen. Methemoglobin also binds oxygen more tightly at
the Fe2+ sites. Then cyanide packs another whammy by inhibiting cytochrome oxidase - cant 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