1.

Gout
a. Starts w/asymptomatic hyperuricemia & progresses to monoarticular arthritis
b. Great toe is MC 1
st
joint affected
c. Podagra: severe swelling & pain in great toe due to deposition of monosodium urate
crystals
d. Uric acid crystals form in renal tubules & collecting system nephrolithiasis
e. In chronic disease, urate crystals can deposit in soft tissues tophi
f. Tophi can ulcerate & drain chalky material
g. Diuretics have hyperuricemic effect due to hypovolemia-assoc. enhancement of uric
acid reabsorption in proximal tubule
2. AD PKD
a. Sx (most are asx): hematuria, flank pain (due to nephrolithiasis, infection, cyst rupture,
hemorrhage)
b. Signs: HTN, palpable mass, proteinuria, CKD
c. Extrarenal features: cerebral aneurysms, hepatic & pancreatic cysts, cardiac valve
disorderes (MVP, AI), colonic diverticulosis, ventral & inguinal hernias
d. Dx: US will show multiple renal cysts (alt is CT, MRI)
3. Hepatorenal syndrome
a. Dangerous complication of end-stage liver disease; in 10% pts w/cirrhosis
b. Characterized by decreased glomerular filtration in ABSENCE of shock, proteinuria or
other clear cause of renal dysfn AND failure to respond to 1.5 L normal saline bolus
c. Due to renal vasoconstriction in response to decreased total renal BF & vasodilatory
substance synthesis
d. Essentially renal failure that does not respond to volume resuscitation
e. Type 1: rapidly progressive, most die w/in 10 wks w/out tx
f. Type 2: slowly progressive, survival rate of 3-6 mos
g. MCC of death are infection & hemorrhage
h. No medication proven beneficial & mortality for these pts on dialysis is high
i. Liver transplant is the ONLY tx w/benefit
4. HBV
a. Tx
i. Who do you treat
1. Acute liver failure
2. Clinical complications of cirrhosis
3. Advanced cirrhosis w/high serum HBV DNA
4. Pts w/out cirrhosis but w/+ HBeAg, HBV DNA > 20,000 & serum ALT >
2x upper limit of normal
5. Prevent HBV reactivation during chemo or immunosuppression
ii. Available tx
1. IFN: for younger pts w/compensated liver disease, short-term
2. Lamivudine: not as much due to higher drug res; may have role in HIV
pts
3. Entecavir: in decompensated cirrhosis, less drug res than lamivudine
4. Tenofovir: most potent w/limited drug res, preferred drug where
approved
5. Lower Back Pain
a. Musculoskeletal
i. Mechanical (muscle strain, spasm, degenerative arthritis): improves w/rest,
worsens w/exercise, not worse at night during sleep, see improvement over 2-4
wks w/symptomatic tx
1. Normal neuro exam
2. Negative SLR
3. Possible paraspinal tenderness
ii. Herniated nucleus pulposus/disk disease
1. Radiculopathy (usually L4-5)
2. Possible + SLR
3. Possible neuro deficits
iii. Spinal stenosis
1. Pseudo-claudication
2. Better w/spine flexion
3. Worse w/extension
4. Older age
iv. Compression fracture
1. Older age
2. MC in F
3. Trauma/fall (may be minor)
b. Inflammatory
i. Ankylosing spondylitis, reactive arthritis, psoriatic arthritis, IBD
1. Better w/activity or exercise
2. No improvement w/rest
3. Gradual onset
4. HLA-B27 present
ii. Ankylosing spondylitis
1. Age < 40, gradual onset of lower back pain
2. Improves w/exercise, assoc. w/hip or buttock pain
3. Also can see anterior uveitis & enthesitis (inflamm of tendon insertion
site at bone)
4. Involves apophyseal (facet) joints of axial skeleton
5. If suspected, measure inflamm markers (ESR, CRP), HLA-B27 typing &
imaging of spine (dont do imaging in pts w/uncomplicated LBP)
c. Malignancy
i. Metastatic CA to bone
1. Hx of malignancy
2. Age > 50 yo
3. Worse at night
4. Unintentional weight loss
5. Cauda equina syndrome: weakness, urine retention/incontinence,
saddle anesthesia)
d. Infectious
i. Osteomyelitis, discitis, abscess
1. Recent infection
2. IVDA
3. Diabetes
4. Fever, exquisite point tenderness
6. Drug-induced HSR type 1
a. In some pts, can form drug-specific IgE on exposure to drug occupies receptors on
mast cells & basophils
b. If drug is encountered again, these cells can activate sx
c. Rapid onset & sx can be mild (urticaria, pruritus, flushing) to severe (laryngeal
angioedema, anaphylaxis)
d. MC: B-lactams, neuromuscular blockers, quinolones, platinum-containing chemo agents,
foreign proteins (i.e. chimeric Abs)
e. Mild manifestations of drug allergy tx w/anti-histamines & discontinuation of med
7. Herpes zoster ophthalmicus
a. Infection due to VZV
b. Mostly in elderly or immunocompromised
c. Remains latent in trigeminal ganglion
d. When immunosuppressed, virus travels via ophthalmic branch to forehead & eye
e. Sx manifest then: fever, malaise, burning, itching in periorbital region
f. See vesicular rash in distribution of cutaneous branch of 1
st
divison of CN V
g. See conjunctivitis & dendriform corneal ulcers
h. Tx w/in 72 hrs after eruption w/high-dose acyclovir reduces complications
8. Herpes simplex keratitis
a. Presents w/pain, photophobia, decreased vision
b. See dendritic ulcer, some minute clear vesicles in corneal epithelium
c. Dont see typical vesicular rash of herpes zoster or systemic sx
9. Dacryocystitis
a. Infection of lacrimal sac due to obstruction of nasolacrimal duct
b. Pain, swelling, tenderness, redness in tear sac area
c. Can see mucous or pus
10. Bacterial keratitis
a. In contact lens wearers, after corneal trauma
b. Cornea is hazy w/central ulcer & adjacent stromal abscess
c. Can see hypopyon
11. Multiple system atrophy (Shy-Drager syndrome)
a. Degenerative disease characterized by
i. Parkinsonism
ii. Autonomic dysfn: postural hypotension, abnormal sweating, disturbance of
bowel or bladder control, abnormal salivation or lacrimation, impotence,
gastroparesis, etc.
iii. Widespread neuro signs: cerebellar, pyramidal or LMN
b. Consider when pt w/Parkinsonism + autonomic sx
c. Anti-Parkinsonism drugs are ineffective; tx via intravascular volume expansion
w/fludrocortisone, salt supplementation, a-adrenergic agonists, constrictive garments to
lower body
12. Chronic venous insufficiency
a. Presentation: bilateral lower extremity pitting edema, varicose veins, venous ulcer
b. Can cause peripheral edema
c. Normal JV suggests normal CVP so RHF & LHF will be less likely causes
d. These are fnal or anatomic abnormalities that lead to venous reflux or dilated lower-
extremity vv
e. Present w/leg discomfort, pain or swelling that worsens w/prolonged standing &
improves after walking or limb elevation
f. Leg exam may show abnormal venous dilation (telangiectasia, varicose veins), pitting
edema, skin discoloration, dermatitis/eczema, lipodermatosclerosis or skin ulcers
g. Initial tx is leg elevation, exercise, compression stockings
h. Dont respond to initial conservative tx venous duplex US to ID venous reflux or
insufficiency
i. Persistent sx & documented reflux endovenous ablation
13. RA
a. MC in F; age of onset 30-50 yo
b. Morning stiffness > 1 hr, symmetric joint swelling (MCP, PIP, wrists, knees)
c. Can also have systemic sx (fatigue, fever, anemia) b/c it is autoimmune
d. At increased risk of developing osteopenia & osteoporosis due to combined effects of
disease process, glucocorticoid therapy, F sex & decreased ability to perform WEIGHT-
BEARING exercises that prevent osteoporosis
14. Vasovagal syncope vs seizure
a. Circumstances
i. Seizure: sleep loss, emotions, alcohol w/drawal, flashing light
ii. Syncope: upright position, emotions, heat, crowded place
b. Clinical clues
i. Seizure: aura (i.e. olfactory hallucinations), can occur w/sleeping or sitting
positions, head movements, tongue biting, rapid & strong pulses
ii. Syncope: sx of presyncope (i.e. lightheadedness), unlikely to occur w/sleeping or
sitting position (except in cardiac arrhythmia), rarely several clonic jerks can
occur w/prolonged cerebral hypoperfusion, pallor & diaphoresis, weak & slow
pulses
c. Sequelae
i. Seizure: delayed return to baseline, sleepy & confused afterward (postictal
state)
ii. Syncope: immediate spontaneous return
15. Subconjunctival hemorrhage
a. Benign
b. Can be due to simple trauma from rubbing eye vigorously, violent coughing spells,
hypertensive episodes or coagulopathy
c. Usually due to minor bruising & does not require any workup
d. Usually disappears in 24-48 hrs
e. Best tx is simple observation
f. Sometimes pt can have HBP; if so, lowering BP might be helpful
16. Glucagonoma
a. Clinical presentation
i. Necrolytic migratory erythema: erythematous papules/plaques on face,
perineum, extremities; lesions enlarge & coalesce over next 7-14 days w/central
clearing & blistering, crusting & scaling at borders
ii. DM: mild hyperglycemia easily controlled w/oral agents & diet; does not require
insulin
iii. GI: diarrhea, anorexia, abd pain, occasional constipation
iv. Other: weight loss, neuropsych (ataxia, dementia, proximal mm weakness),
assoc. w/venous thrombosis
b. Dx
i. Hyperglycemia w/elevated glucagon > 500 pg/ml
ii. Normocytic normochromic anemia due to ACD or glucagon directly affecting
erythropoiesis
iii. Abd imaging (CT or MRI) to localize tumor and/or mets
17. Perivalvular abscess
a. In 30-40% pts w/infective endocarditis
b. Development of new conduction abnormality in pt w/infective endocarditis should raise
suspicion for development of perivalvular abscess w/extension into adjacent cardiac
conduction tissues
c. Aortic valve involvement & IVDA are predictors of periannular extension of infection
18. Stroke
a. When pt presents w/new-onset neuro deficits, occipital headache, PMH of vascular
disease, HTN & a-fib, think about stroke
b. Non-contrast head CT must be done
i. Ischemic strokes candidates for thrombolytic therapy
ii. Intracranial hemorrhage need neurosurg, would suffer from thrombolytics
c. If pt is on warfarin, has hx of HTN & presents w/focal occipital headaches, likely
hemorrhagic stroke
d. Hemorrhagic strokes show up right away on non-contrast head CT as white hyperdense
regions w/in brain parenchyma (ischemic strokes dont show up until > 24 hrs after
event)
e. Fibrinolytic therapy improves neuro outcomes in pts w/ischemic strokes when given
w/in 3-4.5 hrs of sx onset
i. BEFORE giving tPA (alteplase), get non-contrast head CT to make sure not
hemorrhagic stroke & screen for other C/I to therapy
19. PE
a. Presents w/sudden-onset pleuritic chest pain, cough, dyspnea & hemoptysis
b. Dehydration can be a RF
c. Also see low-grade fever & mild leukocytosis
d. Chest CT showing wedge-shaped infarction is pathognomonic; this will occur distal to
completely occluded pulmonary artery
e. Pulmonary infarcts can also be seen on CXR as Hamptons hump
f. Pulmonary artery filling defects seen on contrast-enhanced CT
g. Common cause of both transudative & exudative pleural effusions
20. Infective endocarditis
a. Vascular phenomena
i. Systemic arterial emboli (focal neuro deficits, renal or splenic infarcts)
ii. Septic pulmonary infarcts
iii. Mycotic aneurysm
iv. Conjunctival hemorrhages
v. Janeway lesions: macular erythematous nontender lesions on palms & soles
b. Immunologic phenomena
i. Oslers nodes: painful, violaceous nodules seen on fingertips & toes
ii. Roth spots: edematous & hemorrhagic lesions of retina
iii. Glomerulonephritis
iv. Arthritis or + rheumatoid factor
21. Trigeminal neuralgia
a. Pain in distribution of branches of CN V
b. Dx is clinical & based on characteristic pain (severe, intense, burning or electric shock-
like)
c. Sx occurs in paroxysms that lasts seconds to minutes many times a day
d. Trigger factors vary, cause is unknown
e. DOC is carbamazepine
22. HEV
a. RNA virus that cause illness similar to that of HAV
b. Hepatic bx: focal necrosis, ballooned hepatocytes, acidophilic hepatocytic degeneration
c. Transmission is through fecally contaminated water in endemic areas w/rare person-
person
d. Usually in India, Asia, Africa, Central America; highly unusual in US
e. MC in people 15-40 yo
f. Incubation period of 15-60 days w/abrupt onset of sx
g. Sx: jaundice, malaise, anorexia, nausea, vomiting, abd pain, fever, hepatomegaly
h. Labs: elevated serum bilirubin, ALT, AST
i. Dx is confirmed w/detection of HEV RNA by PCR in serum or feces or by detection of
IgM Abs to HEV
j. Infection is self-limited, no chronic carrier state
k. No progression to chronic hepatitis, cirrhosis or HCC
l. Fulminant hepatitis can occur, esp in pregnant women (esp 3
rd
trimester)
m. Can be vertically transmitted w/significant perinatal M & M
n. Not much known about IG use in HEV prevention so not recommended; travelers to
endemic areas should be advised to minimize exposure to water of unknown purity
23. Amebic liver abscess
a. Protozoal disease due to Entamoeba histolytica
b. Primary infection is in colon bloody diarrhea
c. Ameba may be transported to liver by portal circulation liver abscess
d. Generally single & in R lobe
e. Abscess on superior surface of liver can cause pleuritic-like pain & radiation to shoulder
f. Dx can be made by stool exam for trophozoites, serology & liver imaging
g. Aspirate from abscess is sterile
h. Tx w/metronidazole
i. Hx of travel to endemic area followed by dysentery & RUQ pain w/single cyst in R lobe
of liver = amebic liver abscess
24. Cholesterol embolization
a. When portions of atherosclerotic plaque break off & travel distally into circulation
b. Can occur spontaneously but most are preceded by angiography where plaque is
disrupted by catheter or guidewire
c. Skin manifestations in feet are common (blue toe syndrome)
d. Can also see livedo reticularis (reddish to cyanotic discoloration of skin)
e. Acute renal failure is present secondary to emboli traveling in renal aa
f. GI sx: abd pain, nausea, can develop pancreatitis
g. See increased eosinophils in blood and/or urine, decreased complement levels
25. Condylomata acuminata (anogenital warts)
a. Due to HPV
b. Verrucous, papilliform; skin-colored or pink
c. Unlike condyloma lata: flat or velvety
d. No systemic sx
e. 3 tx options
i. Chemical or physical agents: trichloroacetic acid, 5-FU epinephrine gel,
podophyllin
ii. Immune therapy: imiquimod, IFN-a
iii. Surgery: cryosurgery, excisional procedures, laser tx
f. Choice of tx depends on # & extent of lesions
i. Podophyllin is topical anti-mitotic agent that leads to cell death; teratogenic &
so C/I in pregnancy; other adverse effects are local irritation & ulceration
26. Hazard ratios
a. Ratio of an event rate occurring in tx arm vs non-tx arm
b. Ratio < 1 = tx arm had lower event rate
c. Ratio > 1 = tx arm had higher event rate
27. Types of bias
a. Lead time bias
i. When 2 interventions are compared to dx disease & 1 intervention dx disease
earlier than the other w/out effect on outcome
ii. Makes it appear as if the intervention prolonged survival when it just dx disease
sooner
b. Measurement bias
i. From poor data collection w/inaccurate results
c. Observer bias
i. When observer is influenced by prior knowledge or details of the study that can
affect results
ii. Avoid by using blinded studies
d. Recall bias
i. When study participant is affected by prior knowledge to answer question
ii. More common in case-control studies than in randomized clinical trials
e. Susceptibility bias
i. Type of selection bias
ii. Tx regimen is selected for pt based on severity of their condition w/out taking
into account other possible confounding variables
28. SAAG (serum ascites-albumin gradient)
a. Peritoneal fluid can accumulate due to many causes: portal HTN (increased hydrostatic
pressure w/in livers capillary beds), trauma, infection, pancreatitis, malignancy
b. To distinguish among the causes, must differentiate transudative from exudative fluid
accumulations using SAAG
c. Subtract ascites [albumin] from serum [albumin]
d. Difference of 1.1 g/dl or greater transudative process consistent w/portal HTN
29. Causes of metabolic alkalosis
a. Hyperemesis gravidarum significant volume depletion primary met alk
w/respiratory compensation
30. Management of hypercalcemia
a. Asymptomatic or mild (Ca < 12)
i. No immediate tx
ii. Avoid thiazides & Li, volume depletion and prolonged bed rest
b. Moderate (Ca 12-14)
i. No immediate tx required unless symptomatic
ii. Tx is similar to that for severe hypercalcemia
c. Severe (Ca > 14) or symptomatic
i. Short-term/immediate tx: normal saline hydration + calcitonin, avoid loop
diuretics unless volume overload (HF) is present
ii. Long-term tx: bisphosphonate (zoledronic acid)
31. Clinical features of Wallenberg syndrome
a. Lateral medullary infarct due to occlusion of PICA or vertebral artery
b. Vestibulocerebellar sx
i. Vertigo, falling to side of lesion
ii. Difficulty sitting upright w/out support
iii. Diplopia & nystagmus (horizontal & vertical)
iv. Ipsilateral limb ataxia
c. Sensory sx
i. Abnormal facial sensation or pain (early sx)
ii. Loss of pain & temp in ipsilateral face/contralateral trunk, limbs
d. Ipsilateral bulbar muscle weakness
i. Dysphagia & aspiration
ii. Dysarthria, dysphonia, hoarseness (ipsilateral vocal cord paralysis)
e. Autonomic dysfn
i. Ipsilateral Horners syndrome (ptosis, miosis, anhidrosis)
ii. Intractable hiccups
iii. Lack of automatic respiration (esp during sleep)
32. Side effects of thiazide diuretics
a. Hyperglycemia
b. Hyperlipidemia (LDL, TG)
c. Hyperuricemia
d. Hypercalcemia
e. Hyponatremia & hypokalemia
33. Granulomatosis w/polyangiitis (Wegeners disease)
a. Systemic vasculitis of small and medium-sized arteries
b. Mostly among whites aged 30-50 yo
c. Upper airway sx bloody/purulent nasal discharge, oral ulcers, sinusitis
d. Lower airway sx dyspnea, cough, hemoptysis
e. Renal disease renal insufficiency, microscopic hematuria, RBC casts (RPGN)
f. Systemic sx fever, weight loss, fatigue
g. CXR nodular densities, alveolar/pleural opacities
h. All pts who are suspected should be tested for c-ANCA
i. Definitive dx from bx of site of active disease (preferably nasopharyngeal)
j. Tx high-dose corticosteroids, cytotoxic agents
34. TCA overdose
a. CNS depression, hypotension, seizures
b. Anticholinergic effects dilated pupils, hyperthermia, intestinal ileus
c. Decreases myocardial conduction velocity QRS prolongation, risk of ventricular
arrhythmia
d. Major cause of mortality is secondary to hypotension make sure you do ABCs
e. Give Na bicarb if hypotension, QRS prolongation or ventricular arrhythmia is present
i. Improves systolic BP, narrows QRS complex, decreases incidence of ventricular
arrhythmia
35. Effect of excess O2 on COPD
a. Increased dead space ventilation