What is the pain of lumbar disc herniation caused by?

How does pain classically present?

What might you see on PE?

Caused by herniation of nucleus pulposis through annulus fibrosis, and subsequent impingement on nn roots -> LE radiculopathy

Classically presents with lower back pain/stiffness and radiculopathy (the ladder 2/2 compression of nn root by extruded disk)

PE - neurological deficits present, positive straight leg raise test

What is the pain of degenerative disk disease caused by?

How does it present?

Caused by wearing away of intervertebral disk -> bone on bone

Presents as chronic lower back pain. Morning stiffness <30 mins, pain is worsened with exertion and relieved with rest.

  -Pt may have LE radiculpathy as well 2/2 osteophyte causing compression of nn roots

What is lumbar spinal stenosis caused by?

How does the pain classically present?

Causes are multiple:

  -Can be acuired 2/2 degenerative changes

  -Can be congenital (achondroplasia)

Pain is worsened with activity and relieved with rest (like OA), pain is also relieved with spinal flexation (b/c flexation increases size of spinal canal).

-UA

-Chem panel

-Fasting glucose (if pt is DM, check for microalbuminuria)

-Lipid panel

-ECG

A pregnancy test!!!

Thiazides, ACE-Is and ARBs, and Ca²⁺ channel blockers are contraindicated in pregnancy

Beta-blockers and hydralazine are safe

What is the first-line anti-HTN drug for African-American pts and why?

What comorbidities preclude use of that drug?

What drug can you give instead?

Thiazide diuretics are best initial choice b/c "salt-sensitive" HTN is more common in AA

If they have DM or HL you shouldn't use thiazides b/c they worsen glucose tolerance and HL. Use ACE-Is instead

Recall HyperGLUC: glycemia, lipidemia, uricemia, calcemia

A 62 y/o male with Hx of HTN, DM, and Asthma is brought in b/c of sever substernal cp radiating to shoulder. Exam shows an anxious, pale, diaphoretic individual whose vitals are: BP 160/96, HR 130, RR 30. He undergoes cardiac catheterization and stent placement, and is subsequently placed on aspirin, carvedilol, captopril, and simvastatin. Hours later begins complaining of SOB. Exam shows bilateral wheezing. EKG shows old infarct, and CKMB trends down from when was admitted.

Dx?

Dx - Asthma exacerbation

  -Precipitated by beta-2 blockade by the non-selective beta-blocker given to the pt (carvedilol)

1) Decrease HR and CO

2) Decrease Renin release

What's the first-line anti-HTN agent for pts w/ DM, or CHF, or MI, or chronic kidney disease?

Qid 2159

What is the goal BP in pts with HTN?

What if they have DM or renal insufficiency as well?

Qid 3903

<140/90

If DM or renal insufficiency, then 130/80 is the minimum goal b/c there groups of pts are especially sensitive to high BP. This is the recommendation by JNC-7 report.

A 40 y/o male comes in for his first health maintenance exam with you. He has no past medical Hx and has no complaints. Vitals are BP 162/98, HR 92. Repeat BP is the same. His BMI is 29.

NSIM?

Perscribe a thiazide diuretic

  -This pt's BP is in the severe range, and so initiating pharmacotherapy is appropriate instead of waiting 1-2 months to confirm the Dx

SU pg 411 (Quick Hit)

Diabetes

SU pg 411 (Quick Hit)

-TSH (hypothyroidism)

-LFTs (chronic liver disease)

-BUN and creatinie, urine proteins (nephrotic syndrome)

-Glucose levels (DM)

What is the first-line lipid lowering drug for:

1) Lowering LDL

2) Raising HDL

3) Lowering TG

1) Lowering LDL - Statins

  -HMG CoA Reductase inhibition -> decreased cholesterol synthesis -> increased LDL-R synthesis -> increased LDL clearance

2) Raising HDL - Niacin

3) Lowering TG - Niacin

Note: Niacin is 2nd line drug for lowering LDL

Increases TG levels (b/c liver increases synthesis of VLDL in response to decreased LDL)

Cholesterol gallstones (Fibrates also do this)

Niacin - worsens hyperglycemia

Niacin also causes hyperuricemia

Recall: Thiazides also cause hyperglycemia, lipidemia, uricemia, calcemia (hyperGLUC)

The CAPRICORN trial showed that the beta-blocker carvedilol reduces risk of death in pts with post-MI Left-ventricular dysfunction

How does a tension headache present?

Tx?

-steady, aching pain that encircles the head (tight band-like pain around head)

-most intense around neck or back of head

-neck muscle tightness/tenderness (posterior cervical, temporal, frontal)

Tx: NSAIDs, acetaminophen, or aspirin

How do Cluster Headaches present?

Tx?

PPx?

-Excruciating periorbital pain (behind the eye), almost always unilateral

-Pain is deep, burning, searing, or stabbing

-A/W ipsilateral lacrimation, facial flushing, nasal stuffiness

  -Pathophysiology is related to hyperactive parasympathetic NS on cavernous sinus

-Usually begins a few hrs after pt goes to bed, and awakens them from sleep

Tx: O2 inhalation is treatment of choice, sumatriptan is also beneficial; combination of the two is very effective

PPx: Verapamil is DOC

Bowel sounds

  -obstruction will have hyperactive BS

  -ileus will have hypoactive BS

What does the herald patch of pityriasis rosea typically resemble?

Tx?

It typically resembles ring worm

Tx: just antihistamines for pruritis, otherwise no Tx is necessary as it remits w/in 6-8 weeks

What is patellofemoral syndrome characterized by? Can pt bear weight?

What physical exam test can help Dx it?

Tx?

Definition: diffuse knee pain, worsened with walking, running, going up/down stairs, and squating/sitting for long periods of time. Pt can bear weight

  -It's most frequenlty encountered problem in sports medicine clinics!

Pts will have a positive patellar grind test, where examiner elicits pain when pressure is exerted on patella into trochlear grove on an extended kneee.

Tx: encourage strengthening of the quadriceps and hip rotators; otherwise conservative management

What are the Ottowa ankle rules for determining if a pt requires an ankle X-ray following an ankle sprain?

What are the Ottowa knee rules?

Ankle:

X-ray should be obtained if:

  -pt is unable to walk 4 steps immediately after injury

  -tenderness over distal 6 cm of tib/fib, including malleoli

  -midfoot or navicular tenderness

  -tenderness over proximal 5th metatarsal

Knee:

-55 y/o or older

-isloated patellar tenderness

-tenderness of head of fibula

-inability to flex knee at 90 degrees

-inability to bear wight for four steps immediately after injury (regardless of limping)

A 25 y/o female twisted her leg while playing basketball. She says she felt a "pop," and immediate signficiant swelling. She is able to bear weight but says she feels "unstable." Exam shows tense effusion in her L-knee and is unable to extend it fully.

Dx?

Dx - ACL tear

  -this is the classic presentation

EKG

  -should be done even if diagnostic yield is low

  -it's risk free and can help r/o most concerning cardiac causes of syncope

-pts older than 50

-positive FHx of colon cancer

-moderate-severe BRBPR

Otherwise, you can just get an anoscopy to look for hemorroids, anal fissure, polyps, proctitis, rectal ulcers

Define the following terms:

-allodynia

-parasthesia

-hyperesthesia

-allodynia - severe pain from an innocuous stimulus

-parasthesia - sensation of "pins and needles"

-hyperesthesia - increased sensitivity

A 62 y/o woman comes to you b/c of dyspnea. She as a Hx of COPD, HTN, and DM. She also smokes and drinks heavily. Her evaluation also reveals that she is in heart failure. Which of the following interventions will lead to a functional improvement in this patient??

A) Optimizing COPD Tx

B) Smoking cessation

C) Optimizing HTN Tx

D) Abstinance from alcohol

E) Optimizing DM Tx

(Pretest Family Medicine, #406)

D) Abstinance from alcohol

  -All of these interventions should be done but only abstaining from EtOH has been show to improve function significantly. Those with alcoholic cardiomyopathy actually see improvement of LV function with abstinance.

  -Optimizing DM and HTN Tx will minimize the negative effects these conditions have on the heart, but will not improve damate already done

  -Cigarette smoking should be discontinued, but generally does not lead to functional improvement

Peripheral vertigo - latency time to vertigo and/or nystagmus when performing DHPM is 3-10 secs, symptoms are severe, direction of nystagmus is fixed, and repeating DHPM lessens Sx

Central vertigo - no latency of onset of Sx; Sx are mild in intensity, and direction of nystagmus changes, and repeating DHPM does not lessen Sx

Which two statins are the most potent at lowering LDL?

Which two have highest rates of myopathy?

Which two have the lowest rates of myopathy?

-Most potent at lowering LDL: rosuvastatin and atorvastatin (RAke down LDL)

-Most myotoxic: simvastatin and lovastatin (SLow muscles down)

-Least myotoxic: pravastatin and fluvastatin (PH/Faster muscles)

What is a major drawback to the ELISA test as a screen for HIV?

How can this be avoided?

-It may give a false-negative result if pt is in the "window period of acute HIV infection."

-This can be avoided by using newer 4th generation screening tests which combine ELISA with HIV p24 antigen test

Every 6 months

  -because the incidence of cervical dysplasia in HIV positive women is ~40%!

Dialysis

  -b/c it's the most dialyzable toxin

What percent of overweight/obese pts lose and maintain 20 lbs by conventional dietary techniques alone?

40lbs?

20 lbs - 20%

40 lbs - 5%

-Roux-en-Y gastric bypass can result in loss of up to what percent of pt's initial weight?

-What is the operative mortality?

-This surgery is limited to pts of what BMI?

Pretest FM, #475

-Loss of up to 50% of pt's initial weight

-Mortality is 0-1% in first 30 days

-Limited to pts with BMI >40, or >35 if there are obesity-related comorbidities present

What are some recommended activities for the prevention of osteoporosis?

Which of the following is best for Dx of osteoporosis screening in women?

a) History and Physical

b) Serum calcium levels

c) Serum calcitonin levels

d) Imaging

d) Imaging, specifically DEXA scan

  -H&P is not sufficiently sensitive to screen for osteoporosis

What treatment for osteoporosis has an analgesic effect with regard to bone pain?

Pretest FM, #482

Calcitonin

  -it is often perscribed for pts who have suffered an acute osteoprotic fracture

What kind of history might a person give you that leads more towards a musculoligamentous strain as a cause of back pain?

Is there usually radiation to LE?

-Pt may recall episode of bending/twisting or of the back "giving way" when lifting a heavy object leading to immediate pain

-UW says there's usually no radiation to LE

In general, when you are presented with a pt how has an overwhelming opportunistic infection and you are concerned for possible HIV infection is the NSIM to:

A) treat the overwhelming infection

B) Test for and treat HIV

A) treat the overwhelming infection

  -No time should be wasted in treating an opportunistic infection if the infection is extensive

  -Delaying treatment for HIV testing and HAART therapy can be dangerous!

  -Also remember that staring an AIDs pt on HAART therapy will not raise their CD4 count fast enough to save them from a serious opportunistic infection, therefore you need to treat the overwhelming infection first!!!

Define Stage I and Stage II HTN.

What is the pharmacologic Tx for each (assuming lifestyle modification failed)?

Stage I: systolic 140-159, diastolic 90-99

  -Tx: Hydrocholothiazide, as long as pt is not DM, CAD, CHF, or CKD (if they are -> ACE-I)

Stage II: systolic >/= 160, diastolic >/= 100

  -Tx: Hydrocholothiazide + ACE-I (or ARB or CCB or beta-blocker)

Note: SU pg 411 suggests that pts with new BP reading in the moderate-severe HTN range be started on pharmacotherapy right away instead of waiting 1-2 months to confirm Dx

How much more prevalent is HTN in blacks than whites?

How about the complication rates of HTN (stroke, renal failure, heart disease)?

-HTN is twice as common in blacks than whites

-Blacks have higher complication rates too

-No, individual susceptibility to the effects of high salt intake on BP varies significantly from person to person

-However, when you take the population as a whole low salt diet does reduce BP

estrogen in OCPs can result in increased synthesis of angiotensinogen in liver

1) CAD

2) LVH

3) Stroke

4) Renal failure

To obtain an accurate BP reading, a pt:

-needs to have their arm in what position?

-needs to sit quietly for how long before measuring BP?

-should use a BP cuff where the bladder encircles what percentage of their arm?

-arm at level of heart

-sit quietly for at least 5 mins before-hand

-wear a cuff where the bladder encircles at least 80% of arm

Also, make sure they didn't drink any caffinated beverages or smoke before-hand

How much can the following decrease systolic BP?

-weight reduction

-DASH diet

-decreased sodium intake

-exercise 30 min Qday

-decrease EtOH use to <2 drinks/day

-weight reduction: 5-20 mmHg (per 10 lbs)

-DASH diet: 8-14 mmHg

-decreased sodium intake: 2-8 mmHg

-exercise 30 min Qday: 4-9 mmHg

-decrease EtOH use to <2 drinks/day: 2-4 mmHg

Very little effect, however it does significantly reduce risk of CV disease

  -recall, weight reduction has greatest effect on BP, in fact you can expect a 5-20 mmHg change per 10 lb WL

Thyroid function testing b/c HL occurs with increased frequency in hypothyroid pts.

  -mechanism: decreased LDL-R, so there's decreased LDL clearance

Endocrine:

-hypothyroidism

-DM

-Cushing's

Renal:

-Nephrotic

-Uremia

Name 5 classes of medications that can result in dyslipidemia.

What component of lipid panel

-HIV protease inhibitors - elevate serum lipids

-glucocorticoids - elevate serum lipids

-estrogen - TG levels may further increase in pts w/ hyperTG

-thiazide diuretics - increases LDL, total chol., TG (VLDL)

-beta-blockers - increases TGs (VLDL), and lower HDL

TG: increases

HDL: increases

Total Cholesterol: no effect

--

By assocation, LDL decreases (LDL = Total cholesterol - HDL - TG/5)

Intake of soluble or insoluble fiber lowers cholesterol?

Intake of solube or insoluble fibers lowers risk for colon cancer and GYN cancer?

-Soluble fiber intake lowers cholesterol

-Solube and insoluble fiber intake lowers risk for colon cancer (due to excretion of lipocolic acid) and GYN cancers (due to excretion of excess estrogen)

Accoring to Pretest FM #425, high fiber diet also improves glycemic control.

How do you calculate LDL?

Do you need to fast to get an LDL?

LDL = total cholesterol - HDL - TG/5

Yes, you need to fast to get an LDL b/c you need an accurate TG to calculate LDL, and TG are the main component of chilomicrons (diet derived).

 1) Exercise - most effective, raises HDL by up to 15 points

2) Weight loss - raises HDL by 5-10 points

3) Smoking cessation - raises HDL by 5-10 points

Note: Eating oat bran and decreasing life stress can lower LDL, but does not raise HDL

HDL

  -however, a high HDL doesn't garruntee immunity from CAD

Note: C-reactive protein levels predict risk for MI and stroke even better than LDL levels do. Levels above 3.0 indicate high risk for MI oar stroke

Pretest FM, #439

TG level!

  -b/c chilomicrons (made from the food you ate) are mostly composed of TGs, while less than 3% is composed of cholesterol

  -this is why you don't need to fast to get an HDL and total cholesterol level, but you do need to fast to get a TG and LDL (you need TG level to calculate LDL)

Is estrogen replacement therapy efficacious with regards to cardiovascular outcomes in post-menopausal women with established CAD?

What about in women w/o established CAD?

According to the HERS trial, estrogen replacment has not shown to be efficacious in preventing CV outcomes in post-menopausal women with CAD.

The study did not address the issue in women w/o CAD.

When do we start screening for HL and how often?

What do we test when we screen for HL?

-USPSTF recommends you begin screening healthy adults for HL at 35 for men and 45 for women.

-If pt smokes, has DM, HTN, FHx CAD or HL, begin screening at 20

       -Screen Q 5 years

-For healthy adults, screen by measuring non-fasting total cholesterol and HDL

    -If Total <200 and HDL >35, repeat screening in 5 years

    -If Total >240 or between 200-240 w/ multiple RFs for CAD, get complete fasting lipid panel (incl. TGs and calculated LDL)

     -Calculating LDL level is not necessary for just routine screening

-For adults with CAD, get complete fasting lipid panel

Lowering which of the following reduces serum cholesterol (Total cholesterol and LDL) more?

-saturated fat

-cholesterol

Saturated fat

  -foods rich in omega-3-FA (fish) are particularly beneficial

How does exercise effect:

-HDL

-BP

-DM

-HDL increases

-BP decreases

-weight loss a/w exercise results in increased insulin receptor synthesis -> decreased insulin resistance

At what TG level should pts be treated pharmacologically?

What is first line Tx?

Pts with TG > 500 mg/dL should be treated with medications

  -Niacin is first-line drug for hyperTG

  -Gemfibrozil is also excellent at decreasing TG

-lowers LDL by causing increased LDL-R synthesis

-increases TG

  -BABR don't inhibit the synthesis of VLDL nor the conversion of VLDL -> LDL, so as LDL runs low more VLDL is converted to LDL, and liver compensates for this low VLDL by increasing VLDL synthesis

54 y/o male p/w headache for 3 days. Pt says it's an aching pain encircling his head that is worse as the day progresses. He says he recently got a new job and has been very stressed. He denis aura, n/v, or photophobia. Exam shows tenderness to posterior cervical, temoral, and frontal mm.

Dx?

Tx?

Dx: Tension HA

Tx: NSAIDs, acetaminophen, and ASA are standard Tx for mild/moderate HA

Fill in the mneumonic "VOMIT" for secondary causes of headache.

Vascular: SAH, sub/epi-dural hematoma, intraparenchymal hemorrhage, temoral arteritis

Other causes: malignant HTN, pseudotumor cerebri, postlumbar puncture, pheochromocytoma

Medication/drug related: nitrates, EtOH withdrawal, chronic analgesia use/abuse

Infection: meningitis, encephalitis, cerebral abscess, sinitis, herpes zoster, fever

Tumor

What is the "menstrual migrane" thought to be due to?

What's the treatment?

-It's thought to be linked to estrogen withdrawal

-Treatment is similar to that of nonmenstural migraines (sumatriptan, ergotamines) except that estrogen supplementation is sometimes added

What is the abortive therapy of choice for a mild migraine? Severe?

What are the drugs of choice for prophylaxis?

-Mild: NSAIDs or acetaminophen

-Moderate-Severe: sumatriptan>ergotamine (b/c sumatriptan is more selective of 5HT receptor than ergotamines)

-Prophy: TCAs and propranolol

  -2nd line agents for prophy: verapamil, valproate, and methylsergide

CXR to r/o pneumothorax

  -remember pneumothorax is emergent and takes presidence over simple identification of the cause of the cough

What is the treatment of choice for Whooping cough?

What can you do to limit risk of spread to close contacts of pts w/ Whooping cough?

-Tx: a macrolyde antibiotic (azithromycin, erythromycin, clarithromycin) regardless of vaccination status

-You can limit spread by perscribing 14 day course of erythromycin (regardless of their vaccination status)to household contacts

What's the treatment for postnasal drip?

What if sinusitis is also present?

What if allergic rhinitis is present?

Postnasal drip: first generation anti-histamine/decongestant

Sinusitis: consider AbX

Allergic rhinitis: consider nonsedating long-acting oral antihistamine (loratadine)

Label the following URI features as either viral, bacterial, or both:

-rhinorrhea

-myalgias

-yellow sputum

-cough

-headache

-fever

-rhinorrhea - viral

-myalgias - viral

-yellow sputum -bacterial

-cough - both

-headache - viral

-fever - both

A 17 y/o male p/w with difficutly breathing through his left nostril. He says this has been constantly progressive for months. He also admits to frequent nose bleeds. Exam shows visible nasal mass.

Dx?

Tx?

Dx: Angiofibroma

Tx: surgical removal

32 y/o male p/w with worsening cough for 8 days. He says cough is productive of whitish sputum, and he also endorses subjective fever. No wheezing or crackles are heared on lung exam, and CXR is normal.

Dx?

Tx?

Dx: acute bronchitis

Tx: close observation and supportive care

  -most causes are viral and don't require AbX

  -Note: if supporive treatment, cough suppressants, anti-histamines, and bronchodilators fail, suspect airway hyperresponsiveness (Tx: PO or inhaled steroids)

What might you suspect when an infant predominantly breathes through their mouth, and develops cyanosis when feeding but is relieved by crying?

How do you confirm Dx?

Choanal Atresia

Confirm Dx by CT scan w/ intranasal contrast

What is the MCC of common cold?

What are other common causes?

What is the most common route of infection?

-MCC is rhinovirus - there are >100 serotypes and there's no cross immunity amont serotypes

-Other viruses include corona virus, parainfluenza virus, adenovirus, coxackievirus, RSV

-MC route of infection is hand-to-hand transmission

-Viral URI (absolute MCC)

-Allergic rhinitis (2nd MCC)

-anatomic obstruction

-smoking

-environmental pollutants

-immunodeficiency

-GERD

Name 2 things that help differentiate Meniere's disease from Acoustic Neuroma.

How are the two similar in presentation?

-Meniere's is characterized by discrete attacks of Sx, whereas Acoustic Neuroma is characterized by constant slow progression of Sx

-Acoustic neuroma can also be a/w facial weakness not seen in Mineire's disease

-Both p/w tinnitus, hearing loss, and vertigo

What are the 3 MCC of acute bacterial sinusitis?

What are the causes of chronic sinusitis?

How is the Dx of sinusitis made?

acute: Strep pneumo, H flu, and anaerobes

chronic: same as above + Staph aureus, gram (-) rods

Dx of sinusitis is made clinically

1) onset of purulent rhinorrhea/nasal discharge

2) tooth pain

3) biphasic Sx

  -worsening Sx after initial improvement

  -signifies bacterial infection on top of a viral URI

4) persistent Sx for >/= 10 days w/o improvement

5) fever >/= 102F

In the management of acute sinusitis, what are:

-2 things the pt can do to aide in drainage?

-AbX of choice?

What how do AbX management of chronic sinusitis differ from acute?

-both saline nasal spray and decongestants (psuedoephedrine or oxymetazoline) aide in drainage

-Amoxicillin-clavulanate is drug of choice (according to Qid 3285)

For Chronic sinusitis, treat with broad-spectrum penicillinase-resistant AbX

What is the first priority in a pt with epiglottitis?

Airway management!

  -epiglottitis is a pediatric emergency, so perform endotracheal intubation

  -signs of impending airway obstruction include restlessness, anxiety, impaired inspiration, and muffled "hot potato" voice

What position might kids with epiglottitis put their head in?

What is the classic thing you see on X-ray?

-Pts may hyper-extend their neck to maximize airway diameter

-Neck X-ray may how "thumb sign" (swollen epiglottis) and obliteration of the vallecula (depression at back of tongue, just in front of epiglottis)

A 2 y/o girl is broght in by her mother b/c of fever of 101 and cough for 2 days. She says her daughter has a dry "barking" cough, and makes a high pitched noise when breathing in.

Dx?

Organism?

Tx?

Dx: croup (tracheolaryngobronchitis)

Organism: RSV

Tx: corticosteroids or nebulized epinephrine

  -if these fail, then you can consider intubation if pt's condition does not improve

A 2 y/o girl is brough to your clinic with worsening fever and respiratory distress. She initially to your clinic 5 days ago w/ temp of 100.9, barking cough, and stridor for which she was treated with nebulized epinephrine. Her temp today is 104, and she is in significant respiratory distress--in fact, she now has stridor with inspiration and expiration.

Dx?

Tx?

Dx: Secondary Bacterial Tracheitis (a complication of croup)

Tx: Endotracheal intubation + AbX

What is the most common cause of sore throat?

What 2 symptoms point more towards a viral cause of sore throat?

Viral infection

  -These include: Adenovirus, parainfluenza, rhinovirus, Epstein-Barr virus, herpes simplex

Cough and runny nose point more towards a viral etiology

What is Centor Criteria for working up Strep Throat?

What do you do if you have:

0-1 points?

2-3 points?

4-5 points?

-Fever

-Tonsular exudates

-Tender anterior cervical LAN

-Absence of cough

-Age <15 (if >44, subtract a point)

0-1: No Cx or AbX

2-3: Throat Cx + AbX if Cx is positive

4-5: Empirical AbX

Is Centor Criteria better at ruling in or ruling out Strep Throat?

Is the Rapid Strep antigen test specific or sensitive for Strep throat?

-It is good at ruling out strep throat b/c it has an 80% NPV if 4/5 points are negative

  -Recall: Centor criteria are fever, absence of cough, tender anterior cervical LAN, tonsular exudates, age < 15

Rapid Strep antigen test is specific (95-99%) but not sensitive (70%). This means you can be more certain about a positive test (low false positive). Because of the higher false negative, a negative result can be followed up with a throat culture.

What type of lymphadenopathy do you typically see in:

-Strep throat?

-EBV Mono?

-CMV Mono?

Strep throat: anterior cervical LAN

EBV Mono: posterior cervical LAN

CMV Mono: no cervical LAN

-WL

-persistent vomiting

-dysphagia

-odynophagia

-GI blood loss

-FHx of GI cancer

-pts >55 with new onset dyspepsia

1) avoid EtOH and caffeine

2) stop smoking

3) raise the head of the bed when sleeping

4) avoid eating before sleeping

1) decreased esophageal motility to clear refluxed fluid (such as in CREST syndrome)

2) gastric outlet obstruction

3) hiatal hernia (common finding in pts w/ GERD)

4) dietary factors (EtOH, tobacco, chocolate, high-fat foods, coffee)

What diagnostic test(s) are necessary for typical, uncomplicated GERD?

None!

  -Endoscopy with biopsy is indicated if GERD is atypical, cancer or a complication of GERD is suspected, or persistent GERD (despite Tx)

It's indicated when suspicion for GERD is high but EGD is normal

  -this is b/c 24-hr pH monitoring has the best sensitivity and specificy for GERD of any test (it's the Gold Standard)

A 42 y/o female with Hx of GERD comes to you for check up. She was Dx'd with GERD 15 years ago and is on a PPI. She has no complaints, and in fact says for the past few months her hearburn has improved so much she hasn't been taking her PPIs. She does complain of slight difficulty swallowing but she is not too worried about it.

Dx?

NSIM?

Dx: peptic stricture (or could be esophageal cancer)

  -recall, stricutres can block reflux and lead to improvement of hearburn

NSIM: endoscopy w/ biopsy (to r/o esophageal adenocarcinoma)

Suspect aspiration of gastric contents

  -the macrophages are phagocytosing fat from the gastric contents

1) behavioral modification (avoid fatty foods, coffee, EtOH, orange juice, chocolate, etc) and antacid

2) add H₂ blocker (can be used instead of or with antacid)

3) switch to PPI

4) add promotility agent like meteclopramide (DA blocker)

5) combination H₂ blocker and PPI

6) anti-reflux surgery (fundoplication) if:

  -failure of phases 1-5

  -respiratory problems 2/2 aspiration

  -severe esophageal injury (ulcer, hemorrhage, stricture, Barrett's)

Viruses (rotavirus, Norwalk, etc)

entertotoxic E. coli

food poisoning (Staph, B. cerreus, C. perfringins)

What 4 complications of diarrhea are indications for laboratory testing?

What lab test do you get?

1) bloody stool

2) systemic Sx, including fever

3) dehydration

4) abdominal pain, n/v

If any of these are present, get a fecal smear for leukocytes

  -if positive: get stool Cx and consider C. diff toxin assay

  -if negative: symptomatic treatment (unless they have bloody diarrhea)

In what patients with dirrhea are AbX definitely recommended?

What AbX is typically given?

-high fever, bloody stool, or severe diarrhea

-stool culture positive

-C. diff toxin assay positive - give metronidazol

Typically we give quinolones (except for C. diff pts)

27 y/o male comes to your clinic for HA, n/v. He said both the symptoms started 2 days ago and have progressively worsened. He also notes watery (non-bloody) diarrhea as well as myalgias. Pt denies recent travel or sick contacts or recent AbX use. He is in a monogamous relationship and uses condoms regularly. Vitals are T: 100.7, BP 120/78, HR 90, RR 18.

Dx?

Tx?

Dx: Viral gastroenteritis

Tx: Symptomatic Tx

What is the MCC of acute bacterial diarrhea?

What is the treatment?

Campylobacter jejuni

Tx: erythromycin

hypercalcemia

hypokalemia

uremia

• Initial management - dietary fiber, bulk forming laxatives (psyllium, methylcellulose, together with adequate fluids)
• For patients who do not tolerate bulk forming laxatives or respond poorly to fiber, use osmotic laxative if tolerated

Recommendation from UpToDate

-Define IBS.

-What is the prevalence in the general population?

-What are 3 commonly associated findings?

-Sx are exacerbated by what?

-IBS is an idiopathic disorder a/w an intrinsic bowel motility dysfunction

-Affects 10-15% of all adults

-Commonly a/w depression, anxiety, and somatization (psychiatric Sx often precede bowel Sx)

-Sx are exacerbated by stress and irritants in intestinal lumen

What is your first priority in a pt who p/w caustic substance ingestion?

Besides the above, what is the NSIM?

-First priority is to maintain a patent airway

-Upper GI endoscopy w/in first 24 hrs to assess extent of injury and dictate management

Note: nasogastric lavage and oral antidotes are not recommended in caustic substance ingestion since they mae increase extent of injury

How does gastric lavage work?

What is it used for?

Process of placing a tube into stomach, irrigating it w/ warm water or saline, and suctioning it along w/ stomach contents

-It's done for pts who've ingested poisons or overdosed on drugs (e.g. EtOH)

  -it is not used for caustic substance ingestion or if pt has unprotected airway or is at risk for GI hemorrhage

What are the following types of vomitus a sign of?

-bilious

-feculent

-undigested food

-projectile

-coffee ground

-bilious: obstruction is distal to ampulla of Vater

-feculent: distal intestinal obstruction, bacterial overgrowth, gastrocolic fistula

-undigested food: esophageal problem (achalasia, stricture, diverticulum)

-projectile: increased intracranial pressure or pyloric stensois

-GI bleeding

-coffee ground

-Dehydration, metabolic alkalosis, hypokalemia

-Dental caries

-Aspiration pneumonitis

-Mallory-Weiss tears, Boerhaave's syndrome

1. Pregnancy

2. Obesity

3. Prolonged sitting or standing

  -esp. common in truck drivers and pilots

4. Anal intercourse

Perform anoscopy or proctoscopy

  -if no etiology is found, colonoscopy or sigmoidoscopy is considered

Is rubber band ligation is a treatment for internal or external hemorrhoids?

Hemorrhoid excision is done for which?

-Band ligation is done for internal hemorrhoids

  -rubber bands applied to hemorrhoidal bundle leads to necrosis and sloughing of lesion

-Hemorrhoidectomy is done for thrombosed external hemorrhoids

What is an anal fissure?

What part of the anus does it most commonly present in?

-Anal fissure is a slit-like tear of anal canal

-MC in posterior or anterior anal verge

-Tenderness and contraction of paraspinal mm

-Straight leg raise test and neuro exam are typically normal

Classically what are the aggrivating and relieving factors (aside from pharmacologic Tx) for:

-lumbar disc herniation

-lumbar spinal stensois

-disc herniation

  -aggrivated by lumbar flexation and sitting (think of being hunched over at a desk), and with activity

  -relieved by rest

-spinal stensosis

  -aggrivated by lumbar extension (standing, walking downhill)

  -relieved by lumbar flexation (resting, sitting, walking uphill), hence the term neurogenic claudication

What is the NSIM for pts with lumbar disc hernation?

-If neurologic deficits (motor, sensory, incontinence) - MRI

-If no neurologic deficits - early mobilization and NSAIDs

  -radiculopathy does NOT count as neurologic deficit, so this includes pt with radiculopathy (including sciatica)

#1 breast

#2 lung

#3 prostate

Neoplasms classically don't involve the disk space

  -recall from Goljan's lectures that, neoplasms typically don't invade cartilagenous structures

  -infections classically do involve the disk space

Epidural abscess

  -in fact, the classic triad is fever, spinal pain, neurologic deficits (b/c it can compromise blood supply to spinal cord and/or compress spinal cord)

  -in verebral osteomyelitis, fever is present in only 50% of pts, and blood Cx is only (+) in 75%

If any of the following are present, you must get a cervical radiograph:

-neck pain/tenderness

-loss of full range of motion

-unable to ambulate after event

-age >65

-numbness/tingling in UE

-high speed MVA

What is the MCC of low pack pain in pts younger than 26 y/o?

What's it caused by?

Spondylolithesis

  -it's a developmental disorder characterized by forward slip of vertebrae (usually L5 over S1)

  -recall, common causes of back pain in adults that are uncommon in kids include disc herniation and lumbosacral strain

What is the straight leg raise test test?

Does it have a higher sensitivity or specificity?

What does it mean when pt has back pain at lower elevations of the leg (earlier during the test)?

It's used to detect nerve root compression

  -it is a sensitive test for the above

  -the earlier the onset of pain (i.e. lower elevation) the more specific the result and the greater the severity of disk herniation

  -also, contralateral leg pain produced by test is more specific for disk herniation

In general, imaging is not required for all pts with back pain.

What red-flag signs should be present for you to get imaging?

How long should a pt w/o those red-flag signs be treated symptomatically before you get imaging?

Red-flag signs:

  -age >50

  -Hx of cancer

  -WL

  -Night-time pain

  -neurologic signs

  -lack of exacerbation w/ mov't

If no red-flag signs, pt should be treated symptomatically first for 3-4 weeks before considering imaging

-Pts with neurologic signs (motor or sensory deficits, cauda equina)

-Pts who have failed a course of conservative Tx (rest, PT, and NSAIDs) for at least 3 months

How do you perform a McMurray test?

What is it used to evaluate?

-With the knee in a flexed position, examiner places a varus stress + external rotation to test for lateral meniscal tear then valgus stress + internal rotation to test for medial meniscal tear

-A positive test is when examiner elicits pain or feels/hears a popping sensation

How do pts with a meniscal tear of the knee present?

What is the most common mechanism of injury?

When is surgery indicated?

-Pts p/w lateral or medial knee: effusion, pain/tenderness, knee popping, catching, locking, or "giving out"

-MC mechanism of injury is twisting of knee when foot is planted

-Surgery is indicated injury is a/w persistent effusions, disabling Sx, large/complex tears

  -Note: surgery is more effective when pt does not have contomittant arthritic changes

How do pts with Osgood Schlatter Disease (Traction Apophysitis) present?

What might you see on physical exam?

-Pts p/w pain worsening w/ running, jumping, kneeling, and improves with rest (as opposed to patellofemoral syndrome where pts commonly p/w pain at rest too)

-Exam may show edema and tenderness over tibial tubricle

-Patellar Tendonitis p/w point tenderness at inferior pole of patella

-Traction Apophysitis p/w point tenderness at Tibial Tubricle

  -a firm mass can sometimes also be felt 2/2 hypertrophic bone formation

What is Osgood Schlatter caused by?

What's the treatment?

-OS (aka Traction Apophysitis) is seen in adolescents and is caused by rapid growth of the quadricepts putting increased traction on apophysis of tibial tuberosity (where patellar tendon inserts)

-Tx: activity restriction, stretching exercises, and NSAIDs

-What two vitamins can a baby become deficient in when you switch them from cow's mile to goat's milk?

-When is it recommended that cow's milk be added to a baby's diet?

-Folate and pyridoxine (B6)

-Cow's milk should be added no earlier than 1 year of age b/c it's low in iron and can cause occult intestinal blood loss

What is osteochondritis dissecans?

How does it present?

An area of necrotic bone and degenerative changes in the overlying cartilage. The bone/cartilage piece may separate from the underlying bone and become a loose body in the joint

-P/w bone or joint pain, catching, and popping

  -do not confuse with meniscal tear (which also p/w catching/popping sensation)

What are the 3 most common conditions the a Baker's cyst is seen in?

How might it present if it ruptures?

1) RA (MC)

2) OA

3) Meniscal tear

If it tears, the fluid may extend into the calf and mimic thrombophlebitis or acute DVT

In general when are the following indicated for the work up of knee pain?

-X-ray

-MRI

X-ray - if degenerative disease is suspected or if there is a Hx of trauma or acute injury

MRI - if ligamentous instability is apparent or a meniscal tear is suspected

  -remember, MRI is great at evaluating soft tissue

What are the 3 ligaments of the lateral ankle?

Of the 3, which one is the MCly injured when you sprain your ankle?

1) Anterior talofibular ligament (MCly injured)

2) Calcaneofibular ligment

3) Posterior talofibular ligment

1) Rest, ice, compression, elevation (RICE) first in the acute period

2) Controlled pain-free range of motion exercises w/ gradual return to weight bearing

3) PT after acute phase of swelling subsides

What is transient synovitis of the hip thought to be due to?

How do pt's present?

What position does the pt typically situate the leg?

-Thought to be due to mild trauma or viral URI

-Pts are usually kids 3-10 years old and p/w hip pain, decreased range of motion, +/- fever, and hip will be in flexed, slightly abducted, and externally rotated position (think of a kid sitting indian style)

How does the pain of supraspinatus (rotator cuff) tendonitis typically present?

When is MRI indicated?

-Insidious onset of poorly localized pain over shoulder. Pain occurs subacromially when pt is asked to abducted affected arm

-Pain decreases when injected with lidocaine

-MRI is indicated when pt has weakness of abduction to r/o rotator cuff tear

-Initial treatment is forearm splinting (counterforce brace)--do not spling or wrap elbow itself

-If this doesn't help, then consider PT for strengthening/stretching extensors of forearm

How does De Quervain's tenosynovitis present?

What's it due to?

What physical exam finding may be present?

Tx?

-P/w pain at radial aspect of wrist (especially when pinch gripping), may radiate to elbow or thumb

-Due to inflammation of abductor pollicis longus and extensor pollicus brevis tendons

-Finkelstein Test may be positive: pain produced when pt clenches thumb w/ fist and unlar deviates wrist

-Tx: Thumb spica splint and NSAIDs

What 4 main conditions can be a/w Carpel Tunnel Syndrome?

What's the pathophys behind the cause of CTS in each?

When is the pain classically worst?

-CTS can be a/w:

  -hypothyroidism - build up of GAGs

  -DM, pregnancy - build up of fluid

  -ERSD on dialysis - build up of amyloid

  -RA - (build up of) inflammation

-Pain is classically worse at night

  -sometimes pt may have pain/numbness along entire arm (as far as shoulder!!!)

Tinel sign - tap over median nerve at wrist crease -> causes parasthesias in median nn distribution

Phalen's test - wrist flexation for 1 minute -> paresthesias in median nn distrubution

-Note: a negative Tinel and/or Phalen does not r/o CTS

1) WBC count > 12,000

2) Temp >39C (102F)

3) ESR > 40

4) Refusal to bear weight

-If 3/4 criteria met, further workup is indicated to r/o septic arthritis

-Hip X-ray should be done to r/o Legg-Clave

What test definitively diagnoses CTS?

When is it indicated?

Electromyography and nerve conduction velocity

Indicated if Dx is not clear from clinical findings or if pt develops weakness or persistent Sx

What's the treatment for carpal tunnel syndrome?

When is surgery indicated?

1) Wrist splint (volar carpal splint) worn at night

  -purpose is to prevent wrist flexation during sleep (which compresses nerve)

2) NSIADs

3) Local corticosteroid injection if both 1 and 2 fail

4) Surgicy is indicated if pt has persisetent Sx despite trying steps 1-3, or if Sx are limiting pt's activities or quality of life

What's the typical WBC count in a joint aspirate from:

-normal joint

-Non-inflammatory arthritis (OA, trauma)

-Inflammatory athritis (RA, gout, pseudogout, Reiter's)

-Septic arthritis

-normal: <200

-non-inflammatory: 200-2000

-inflammatory: 2000-50,000

-septic: >50,000

What are the diagnostic criteria for pre-eclampisa?

Severe Pre-ecclampsia?

Onset of ANY of the following at or beyond 20 wga:

-systolic BP >/= 140

-diastolic BP >/= 90

-proteinuria >/= 0.3 grams in 24 hrs

Severe:

-systolic BP >/= 160

-diastolic BP >/= 110

-proteinuria >/= 5 grams in 24 hrs

What's the imaging of choice when you suspect osteoarthritis?

What might you see?

-Plain radiograph of effected joint

-May see:

  -joint space narrowing (due to loss of cartilage)

  -osteophytes (aka bone spur)

  -subchondral sclerosis--most severe at points of maximal pressure

  -subchondral cysts--occur as result of increased transmission of intra-articular pressure to the subchondral bone

With osteoarthritis of the hip, where is the pain typically located?

Where does it sometimes radiate?

What is the most effective lifestyle modifcation in the management of OA?

What specific activity can you recommend?

-Weight loss is most effective measure in slowing down progression of OA

-Swimming is an ideal exercise b/c it involves minimal involvement of weight-bearing joints

The is the maximum recommended number of corticosteroid injections per year for treatment of osteoarthritis?

What is the concern with frequent corticosteroid injections?

-More than 3-4 per injections per year is not recommended

  -pts can expect up to 3 months of relief

-Frequent steroid injections can cause hastening of osteoarthritic process (recall that corticosteroids inhibit collagen synthesis)

Define Type I and Type II osteoporosis.

Who are they more common in?

What fractures do you see more commonly in each?

Type I: excess loss of trabecular bone. Seen in post-menopausal women; vertebral compression fractures and Colles fractures

Type II: equal loss of both cortical and trabecular bone. Most often seen in men and women >70; femoral neck fractures, pelvic fractures, proximal humerus fractures

It showed that, regarding the treatment of osteoporosis, calcitonin:

   -has no effect at the hip

   -decreases risk of vertebral fractures by 40%

   -slightly increases bone density in lumbar area

1) Daily calcium

2) Daily Vit D

3) Weight bearing exercise

4) Smoking cessation

Advanced age

  -hence the term, age related macular degendation

  -other RFs include: female, caucasian, smoking, HTN, and FHx

What are the two categories of Macular Degeneration, and what are they due to?

What might you see on ophthalmoscope?

Nonexudative ("dry"): atrophy and degeneration of central retina. Exam may show yellow-white deposits called drusen form under the pigment epithelium

Exudative ("wet"): leakage of serous fluid into retina followed by neovascularization (link this with DM retinopathy in your mind!) -> sudden visual loss

1) Diabetic retinopathy (MCC in adults <65)

2) Age Related Macular Degeneration (MCC in adults >65)

3) Cataracts

4) Glaucoma

What is a possible treatment for exudative age related macular degeneration?

-Laser photocoagulation

-Ranibizumab (and several other related drugs), given as intraocular injection, has been shown to be effective in reducing the rate of visual loss due to "wet" ARMD

  -SUS2 page 442 mentions that certain vitamins containging antioxidants are thought to be beneficial

What typically precipitates acute closed angle glaucoma?

What might pt complain of?

Dilation of the iris in pts with pre-existing anatomically narrow anterior chamber. Can occur with:

  -dim lighting

  -anti-cholinergic meds

  -sympathomimetic meds

Pt might complain of rapid onset severe pain and vision loss, seeing halos around lights, n/v, and HA

1) Topical medications - typically beta-blocker first, alpha-antagonist, carbonic anhydrase inhibitor, and/or prostaglandin analogue (singly or in combination)

2) Laser or surgical treatment for refractory cases

IV mannitol (according to UWorld)

  -also, refer to ophthomologist immediately

What is the most important RF for the development of cataracts?

What might pt complain of and what interesting phenomenon might they experience?

-Age!

  -half of people over 75 have cataracts

  -other RFs include: smoking, glucocorticoid use, prolonged UV exposure, trauma, DM, Wilson's, Downs

-Pt may complain of glare and difficulty driving at night

  -Pt may also give history of increasing near-sightedness and no longer requiring reading glasses--phenomenon known as second sight

What is "second sight," and what condition is it seen in?

What's it due to?

1) Eye pain that doesn't respond to therapy

2) Flashers, floaters, or decrease in visual acuity

3) Corneal opacification

4) Hx of recent eye suervery

5) Hx of penetrating or blunt trauma

6) Hx of chemical exposure (esp alkali)

7) Orbital cellulitis

Define:

-Blepharitis

-Hordeolum

-Chalazion

-Blepharitis: chronic inflammation of the eyelid

-Hordeolum: asbcess of upper or lower eye lid

  -Both blepharitis and hordeolum are caused by Staph aureus and respond to warm compresses

-Chalazion: chronic granulomatous inflammation of meibomian gland (a sebaceous gland at rim of eye lid)

How does blepharitis look on exam?

Tx?

Eyelid margins are red and swollen with crusting that sticks to lashes

  -recall, blepharitis is chronic inflammation of eyelid, usually due to S. aureus

Tx: lid scrubs and warm compresses

  -give topical AbX for severe cases

How might you differentiate episcleritis from scleritis based on clinical presentation?

Tx for each?

Episcleritis (self limiting inflam of vessels beneath conjunctiva) p/w redness, irritation, dull ache, and watery discharge

  Tx: none required; NSAIDs for sympt relief

Scleritis (inflam of sclera a/w systemic disease) p/w redness and significant eye pain (severe, deep pain). It can lead to visual impairment and this thus an ophtho emergency

  Tx: prompt ophthalmologic referal; topical and systemic corticosteroids

In newborns, when does GC conjunctivits occur and how is it treated?

When does CT conjunctivitis occur and how is it treated?

-GC: occurs between days 2-5, causes a highly purulent conjunctivitis

  -Tx: Ceftriaxone drops

-CT: occurs between days 5-14, causes discharge that my be scant, mucoid, or frankly purulent

  -Tx: Systemic erythromycin (to decrease risk of chlamydia pneumonia--which occurs 3-14 weeks after birth)

What is the most frequent viral cause of conjunctivitis?

What is the most frequent bacterial cause of conjunctivitis?

What type of discharge do you see in each?

Viral: Adenovirus; watery discharge (which is also seen in allergic conjuntivits)

SU pg 445, Pretest FM #313

Bacterial: S. pneumoniae; purulent discharge

  -can also be caused by Gram negatives

What might you see on the cornea of a pt with Trachoma conjunctivitis?

Tx?

-If pt is in the active phase of Trachoma, you may see follicular conjunctivitis and pannus (neovascularization) formation on the cornea

  -Note: concurrent infections occur in nasopharynx leading to nasal discharge

-Tx: systemic tetracyclin or azithromycin immediately

Which chlamydial serotyes cause Trachoma and which cause Inclusion conjunctivits?

Which is worse?

Trachoma: serotypes A-C

  -this is worst one, as it can lead to corneal scarring and blindness!!!

  -in fact, its the MCC of blindness worldwide

Inclusion conjunctivitis: serotypes D-K (think of the fat soluble vitamins)

  -Sx similar to viral conj, no corneal scarring or blindness

  -transmitted through genital-eye contact

-Allergic conjunctivits: eye itching, hyperemia, tearing, conjunctival and/or eyelid edema, sometimes photophobia

-Atopic keratoconjunctivitis: eye itching, tearing, thick mucus discharge, blurred vision, and photophobia

   -this is a severe form of occular allergy

Ocular pain (vision loss is also very concerning)

  -the presence of either of these suggest something more serious

What is the treatment for:

-viral conjunctivitis?

-acute and hyperacute bacterial conjunctivitis?

-chlamydia conjunctivitis?

-allergic conjunctivitis?

-viral: cold compress, hand washing

-acute bacterial: broad spectrum AbX (cipro, erythromycin)

-hyperacute bacterial (gonococcal): 1 dose of IM ceftriaxone + topical therapy

-chamydia: systemic tetracyclin or erythromycin for 2 weeks; also, treat sexual partner

-allergic: remove allergen, cold compress, topical antihistamines

What is the NSIM in a pt with suspected Amaurosis Fugax?

How do pts present?

-NSIM: Duplex U/S of the neck to identify plaques

-P/w sudden, transient, monocular loss of vision sometimes described as a "curtian coming down" over their eye (also seen in pts with retinal detatchment)

Occular massage to hopefully dislodge embolus

  -hyperbaric oxygen therapy has also been tried

Depends on severity:

-Mild to moderate (<20 apneic episodes on polysomnography w/ mild Sx):

    -weight loss

    -avoid EtOH and sedatives

    -avoid supine position during sleep

-Severe (>20 apneic episodes w/ arterial O₂ desaturation)

    -Nasal CPAP - prefered b/c it's noninvasive and has proven efficacy

    -Uvulopalatopharyngoplasty - removal of redundant tissue in oropharynx to allow more air flow (as confirmed by MRI)

    -Tracheostomy is last resort

Define narcolepsy.

Name 5 key features of narcolepsy.

-Narcolepsy is an inherited disorder of REM sleep regulation (i.e. REM sleep involuntarily occurs at random and inappropriate times)

-Key features:

   -excessive sleepiness during the day

   -involuntary "sleep attacks" at any time lasting several mins

   -cataplexy - loss of mm tone occuring w/ intense emotional stimulus (e.g. laughter, anger)

   -sleep paralysis

   -hypnogogic hallucinations - vivid hallucinations (visual/auditory)--"dreams" while awake

What is the most common cause of syncope?

What percent of cases of syncope does account for?

What is a main clue to Dx of this type of syncope?

-vasovagal (aka "situational", "neurocordiogenic", "vasodepressor" or "simple faints") is MCC

-It acounts for up to 50% of cases of syncope

-main clue to Dx is presyncopal symptoms (pallor, diaphoresis, lightheadedness, nausea, dimming vision, roaring in ears)

1) EtOH

2) sedatives (prolonged use can cause tolerance and withdrawal rebound insomnia)

3) caffeine

4) beta-blockers

5) stimulants (amphetamines)

6) decongestants

7) some SSRIs

8) nicotine

What is the drug of choice for transient sleep onset problems?

What about for sleep maintenance?

Sleep onset problems: zolpidem (Ambien) or ezopiclone (Lunesta)

Sleep maintenance problems: zaleplon (Sonata)

   -this is b/c the halflife is shorter and can be taken in the middle of evening to sleep

What is exostoses and what can it cause?

Who is it seen in?

-Exostoesis are bony outgrowths of external auditory canal related to repetitive exposure to cold water

-Can cause conductive hearing loss

-Seen in scuba divers and swimmers

What is otosclerosis?

Who is it seen in?

-Otosclerosis is bony fusion of stapes to oval window due to abnormal remodelling of otic capsule in relation to possible autoimmune process

-Results in conductive hearing loss

-Seen in middle aged individuals

What is presbycusis?

Who is it seen in?

-Presbycusis - gradual, symmetric hearing loss due to degeneration of sensory cells and nn fibers at base of cochlea

-Results in sensorineural hearing loss, esp high frequency sounds

-Mostly seen in elderly pts--in fact, it's MCC of diminished hearing in elderly

A 40 y/o male comes to you saying he's noticed diminished hearing that has slowly progressed over the past year. His history is noteable for working at a DJ at a nightclub for 18 years.

What's the pathophysiology of his hearing loss?

Pt has noise-induced hearing loss

  -caused by damage to hair cells in organ of Corti

  -occurs w/ chronic exposure to sound levels > 85 dB

-Amingoglycosides

-Furosemide and ethacrinic acid

-Cisplatin

-Quinidine is ototoxic

-Aspirin is ototoxic

Aside from the Weber and Rinne tests, what kinds of sound might pts with the following lose:

-conductive hearing loss?

-sensorineural hearing loss?

-Conductive: decreased perception of sound (esp. low frequency), but can hear loud noises well

-Sensorineural: difficulty hearing loud noises, decipheing words (poor speech discrimination), loss of high frequency sound (doorbell, phone, female voice), and tinnitus is often present

What's the treatment for a pt with cerumen impaction as cause of diminished hearing?

What's the MCC of dysphagia/odynophagia in HIV patients?

Tx?

Candida esophagitis

  -Tx: 1-2 week course of fluconazol

  -If Sx persist, then get an endoscopy w/ biopsy to investigate other possible etiologies

  -Next MCC is CMV esophagitis -> Gancyclovir

CMV: Large, shallow, superficial ulcerations

HSV: Multiple, small, and well circumscribed lesions that have a "volcano-like" (small and depp) appearance

In pts with venous thromboembolus how long should heparin be continued when bridging to warfarin?

How long should they be on warfarin?

-Start Heparin + warfarin, then d/c heparin at 5-6 once pt is therapeutic with warfarin

-Pt should be on warfarin for at least 6 months if it's their first thromboembolus. If it's their second, then lifetime anticoagulation is indicated

What ist the MCC of incontinence in elderly and nursing home patients?

What about in women <70 y/o?

Elderly and nursing home patients - urge incontinence

Women <70 y/o - stress incontinence

How do you define the 4 NYHA Classes of Heart Failure?

What is the management of each?

Class I: Cardiac disease w/o Sx, and no limitation in ordinary activity--ACE-Is are first-line, start loop diuretic if volume overloaded

Class II: Mild Sx (sob, angina) and slight limitation during ordinary activity--add beta-blocker

Class III: Marked limitation in activity 2/2 Sx, even during less than normal activity but comfortable at rest--add beta-blocker (same as Class II)

Class IV: Severe limitation. Experiences Sx even while at rest. Mostly bedbound--add spironolactone

Do the following cause urgency, dribbling, or both:

-alpha blockers

-beta blockers

-anticholinergics

-alpha blockers diminish sphincter tone -> dribbling but not urgency

-beta blockers inhibit bladder relaxation -> urgency and dribbling

-anticholinergics cause urinary retention -> urgency, frequency, and dribbling

What GU abnormality can alcohol, sedatives, and hyponotics all cause?

What are the random "Is" that alcohol can cause?

Urinary incontinence

Alcohol can cause: insomnia, impotence, and incontinence

-anticholinergic medications (oxybutynin)

-TCAs (imipramine)

-bladder retraining (behavioral therapy)

  -helps regain contorl of voiding reflex that's been lost (goal is to increase the amount of time btwn voiding, "timed toileting")

anticholinergics

alpha agonists

epidural/spinal anesthetics

-intermittent self-catheterization is best b/c it:

     1. allows for documenting of post-void resid.

     2. provides symptomatic relief

-cholinergic agents (bethanacol)

-alpha-blockers (terazocin, doxazocin)

A urinalysis to exclude infection and hematuria

  -Urine Cx only if dysuria and positive UA

22 y/o female Hx of depression managed with citalopram comes in b/c of cough. Infection is ruled out, and she is perscribed a cough suppressant. She returns 2 days later with HR of 140, sweating, mydriasis, intermittent tremor or twitching, and hyperreflexia. 

Dx?

Why did this occur?

Seratonin syndrome

  -this probably occured because of the drug-drug interaction between SSRIs and dextromethorphan

  -Note: this drug-drug interaction can result in neuroleptic malignant syndrome as well!

A 47 y/o male with Hx of HTN and CAD p/w bleeding gums. He says that he noticed it 2 days ago while brushing his teeth, and it keeps recurring. His medication include enalipril, metoprolol, and aspirin. Pt was recently placed on sertraline for premature ejaculation. Vitals, CBC, and BMP are wnl.

What is the most likely Dx?

Depression!

  -especially suspect if pt denies weakness

  -NSIM in ANY pt who p/w fagitue is to r/o depression
  -up to 2/3 of cases of chronic fatigue is due to depression, anxiety, or both

1. CBC (anemia)

2. TSH (hypo/hyperthyroidism)

3. Fasting glucose (DM)

4. BMP (electrolyte abn., esp. hypo/hyper-kalemia, hypercalcemia)

5. UA, BUN/Cr

6. LFTs

What is the diagnostic criteria for chronic fatigue syndrome?

How do you treat chronic fatigue syndrome?

Dx criteria:

  -profound fatigue > 6 months not 2/2 medical or psychiatric disorder

  -not due to exertion nor alleivated with rest 

  -significantly affecting quality of life

  -any 4 of:

    -short term memory loss or loss of conc.

    -mm or jj pain (1 point each)

    -sore throat

    -tender LN

    -unrefreshing sleep

    -HA

Any RF that contributes to atherosclerosis

  -HTN

  -Smoking

  -HL

  -DM

1) Cognative behavioral therapy, including exercise, social, and psychological behavior modifications

2) Antidepressants

3) NSAIDs for relief of HA and arthralgias

Define each of the following:

-physiologic fatigue

-physical fatigue

-psychological fatigue

-physiologic: generally 2/2 overwork, lack of sleep, or a defined physical stress, such as pregnancy

-physical: 2/2 infections, endocrine imbalance, anemia, CV disease, and cancer

      -although it makes sense that physical fatigue would be a/w external sources, and physiologic with internal sources, you're just going to have to flip the 2 in your mind...

-psychological: a/w depression, stress, anxiety, or adjustment rxn

How do you define and manage the following:

-Anginal Equivalent?

-Atypical Angina?

-Anginal equivalent are symptoms of dyspnea, diaphoresis, extreme fatigue occuring in a pt at high risk of cardiac disease

-Atypical angina is pain similar in quality/characteristic to angina, or occuring with exertion but not both

 Management of both are identical for that of angina: EKG and troponins

1. Libido - desire/interest in sex

     -this phase requires androgens and intact sensory system

2. Arousal (excitement) - involves psychological component of getting an erection

3. Vascular inflow - requires patent vasculature, adequate BP, and functional vasomotor system supplying corpus cavernosum

      -by far MCC of an inability to attain erection

-free testosterone (get this first)

-prolactin - supresses GnRH

-FSH and LH

-TSH - hypothyroid pts may have elevated TRH, which directly stimulates prolactin release

22 y/o male with no PMHx comes to you saying he has been having trouble attaining an erection. This is particularly concerning to him as he is getting married soon. Pt denies having penile tumescence. He denies any head or GU trauma and takes no medications. Vitals are wnl.

Dx?

Psychogenic cause of ED

  -Hx of abscent penile tumescence is key clue

  -results in dysfunctional arousal phase of attaining an erection. This is separate from libido!

Genetic - Downs syndrome

Non-genetic - Fetal alcohol syndrome

  -These children have midfacial abn (short palpebral fissures, epicanthal folds, long filtrum, thin upper lip), cardiac defects (ASD, VSD), multiple joint abn

Yes

  -especially in sons of parents with alcoholism

Diet! Pt should receive a diet that is:

  -high in calories

  -high in carbohydrates

  -has multivitamins

6-24 hrs: Sx of refelx hyperactivity, including anxiety, insomina, tremors, diaphoresis

48 hrs: hallucinations and withdrawal seizures

48-96 hrs: delerium tremens (HTN, agitation, tachycardia, hallucinations, fever)

What complications can alcoholism have with respect to the following organ systems:

-GI

-Cardiac

-CNS

-GI: gastritis, PUD, esophagitis, Mallory-Weiss tears, liver disease (fatty liver, hepatitis, cirrhosis, portal HTN, pancreatitis

-Cardiac: dilated cardiomyopathy (reversible!), essential HTN (if >3 drinks/day)

-CNS: Wernicke's (Confusion, Ataxia, Nystagmus), Korsakoff's psychosis (amnesia, confabulation)

What complications can alcoholism have with respect to the following organ systems:

-Pulmonary

-Nutrition

-Sexual

-Psychiatric

-Pulmonary: pneumonia, aspiration (Klebsiella)

-Nutrition: deficiencys of many vitamins/minerals, especially folate (blocks abs), thiamine, magnesium (recall, hypoMg is commonly a/w hypoCa and hypoK, see SU pg 307)

-Sexual: decreased libido -> impotence

-Psychiatric: depresion, anxiety, insomnia (EtOH allows pp to fall asleep but interferes w/ ability stay asleep)

Depends on Age:

< 30 y/o - ultrasound

    -simple cyst -> FNA

    -complex cyst or mass -> image guided Bx

>30 y/o - ultrasound and mammogram

    -suspicion for malignancy -> core Bx

1) Esophagus (squamous cell carcinoma)

2) Oral (squamous cell carcinoma)

3) Liver

4) Lung

What is the single best treatment for alcoholism?

What pharmacologic drug has been shown to improve abstinence rates?

-Single best treatment: alcoholics anonymous

-Drug with best abstinence rate: naltrexone

   -it reduces the craving for alcohol

   -has been proven to decrease frequency of replapse. Data on disulfiram is inconclusive

How does Naltrexone work with respect to:

-Opiate abuse?

-EtOH abuse?

-Opiate abuse: saturates opiate receptor sites  and leaves them unavailable for opiate attachement

-EtOH abuse: reduces the reinforcing effect of EtOH, thus not allowing pt to become drunk

   -recall, natrexone reduces the craving for EtOH

1) lung

2) oral cavity 

3) pharynx/larynx

4) esophagus

5) bladder

6) cervix

7) pancreas

8) renal

Infection with H. pylori

  -it results in 60% of gastric and 90% of duodenal ulcers

  -NSAID over use is the 2nd most important RF

Why should nicotine patches not be used at night during sleep?

Should pts continue smoking when on the patch?

-Because it can cause headaches

   -Also, recall that nicotine can cause insomnia!

-Pt should not continue smoking when on the patch

Bupropion (zyban) is contraindicated in pts with...

Name a drug other than bupropione that is used for smoking cessation.

Varencline

  -partial agonsist of nicotinic Ach-R

  -somewhat more effective than Bupropione in short term and long term smoking cessation

  -SE: nausea, insomnia, abnormal dreams

According to the USPSTF, when should you start screening for HTN?

Start at 18 y/o

  -recommendation is to recheck every 2 years, but this has not been firmly established

According to the American Diabetes Association, when is it recommended to screen for DM?

What 3 tests are used to screen?

CHECK WITH AARON

-Screen patients over 45 y/o with multiple RFs for DM (obesity, HTN, FHx)

-Pts should be screened by:

  1) HbA1c > 6.5%

  2) Fasting glucose > 125

  3) Random glucose > 200 w/ hyperglycemia Sx

USPSTF recommends screening ALL adults with sustained BP >135/80 for DM.

SU recommends screening healthy adults >45 every 3 years. For at risk adults, screen earlier.

-TG and LDL do require fasting

  -TG are the main component of chilomicrons (diet derived), and LDL is calculated using TG

-HDL and Total cholesterol do not require fasting

Repeat in 3 years

  -if normal, interval is extended to Q 5 years

At age 10

  -if positive, consider colectomy

  -if negative or if pt refuses colectomy, perform colonoscopy Q 1-2 years

At what age should a pt with FHx hereditary nonpolyposis colorectal cancer (HNPCC) be screened?

How often should they have colonoscopy if pt is positive for HNPCC?

-Screen pts at age 21

  -if positive, perform colonoscopy Q 2 years until age 40, and then every year thereafter

With regard to breast cancer screening, when and how of often should women get the following:

-self examination of breast?

-physical examination of breast?

-mammogram?

-self exam: start at 20, Q 1 year

-physical exam: start at 20, Q 3 years until age 40, and yearly thereafter

-mammogram: start at 50, Q 2 years until age 75 (after 75, women no longer require mammogram)

When should women start having Pap smears?

How often should they get them?

-Start at age 21, regardless of onset of sexual activity

  -Q 2 years

  -If pt is 30 or older and had 3 consecutive negative Pap smears, increase to Q 3 years

  -If pt is 35 pt can have concomittant HPV testing, and if negative -> Q 5 years

Every 6 months regardless of previous results

  -this is b/c the incidence of cervical dysplasia in HIV positive women is 40%

Screen the following pts:

-All sexually active women age 24 and younger

-Women over 24 at high risk (multiple sex partners, new sex partner)

What the recommendation by the USPSTF regarding depression screening?

Dementia screening?

-All adults should be screened for depression (and provided appropriate Tx and f/u)

-USPSTF does not recommend for or against screening for dementia

-The USPSTF does not recomend routine screening of general population for glaucoma

-For high risk patients (positive FHx), refer to an eye care provider for evaluation

  -Remember to refer all DM pts to an ophthomologist for annual fundoscopic exams

Informally test hearing on a periodic basis in elderly patients

-Younger patients do not need to be screened unless they're at increased risk (occupational expsoure [>85 dB])

What the recommendation by the USPSTF regarding osteoporosis screening?

What is used for screening?

-All women > 65 should be screened

-Women >60 with RFs for ostoeporosis (smoking, EtOH use, steroid use, lack of weight bearing exercise, low Ca²⁺ or Vit D intake) should be screened

-Screen with a DEXA scan

-Hep B

-Rotavirus

-TDaP

-H. flu B

-Pneumococcal

-Inactivated polio

What the recommendation by the USPSTF regarding administering the influenza vaccine?

The following pts are highly rec'd to get it:

-All adults > 50 y/o should be vaccinated

-Adults < 50 y/o w/ chronic medical problems (CHF, DM, lung disease, ESRD)

-Health care workers

-Pregnant women in 2nd-3rd trimester

The following pts should receive it:

-All adults > 65 y/o

-Adults < 65 y/o with chronic medical cond'ns (CHF, DM, lung disease, ESRD), and functional asplenia (HbSS)

-a second dose 5 years after the first is required for immunocompromised or asplenic pts

When is the primary series of TDaP given?

How often should pts receive a booster?

-Primary series (3) given at 1 mo, 2 mo, 6-12 mo

-Td booster Q 10 years

-TDaP vaccine should replace 1 Td booster in pts between 19-65 b/c of increased reports of pertussis in U.S (CDC Guidelines)

What is the MCC of hepatocellular carcinoma in the U.S.?

What is the MCC of cirrhosis in th U.S.?

HCC: Chronic Hep B

Cirrhosis: Alcoholism

What two hematologic findings is seen in pts with the measles?

How can you treat it?

-Leukopenia

-Thrombocytopenia

   -Treat with VitA supplementation

Who does the CDC recommend get the shingles vaccine (zostavax)?

Anyone 60 years of age and older

  -regardless of whether they've had the chickenpox or shingles

  -this is b/c it prevents against future recurrence

-Healthy adults and kids should receive active immunization with varicella vaccine w/in first 3-5 days of exposure to virus

    -Beyond 5 days, efficacy decreases

-Immunocompromized pts and pregnant women exposed to virus should be passively immunized (with VZIG) w/in 72 hrs

Can a person develop shingles when they receive the vaccine?

Should a person receiving the shingles vaccine avoid pregnant women?

-Yes they can develop shingles, but it's rare (1%)

-Pts receiving the vaccine do not need to avoid pregnant women as long as the woman is immunocompetent

Which of the following are contraindications to vaccination?

-mild illness (common cold, low grade fever, mild diarrhea)

-recovery phase of illness

-recent exposure to communicable disease

-breastfeeding

-current AbX therapy

-Hx of nonspecific rxn to PCN

What's the MC organism and treatment for:

-Otitis Media

-Otitis Externa

-Otitis media

   -Organisms: S. pneumoniae, non-typable H. influenzae (Hib vaccine doesn't cover this), M. catarallis

   -Tx: Amoxicillin x 10 days; if this fails, try Amoxicillin-clavulanate

-Otitis externa

  -Organism: P. aerigenosa

  -Tx: PO ciprofloxicin

What are the top 3 causes of typical community acquired pneumonia?

What are the top 3 causes of atypical community acquired pneumonia?

Typical - S. pneumoniae, H. influenzae, anaerobic gram (-) rods (e.g. Klebsiella)

Atypical - Mycoplasma, Chlamydia pneumoniae/psittaci, Legionella

What is the MC organsim causing cellulitis?

What is the MC organism causing necrotizing fascitis?

Cellulitis - S. pyogenes and S. aureus

Nec Fasc - depends on the type

  Type I (head/neck/groin): anaerobic speces (clostridium, bacteroides, peptostreptococcus) + facultative anaerobic strep (other than GAS) + enterobacteracea

  Type II - S. pyogenes (or other beta-hemolytic strep) + S. aureus

How do the following work in treating acne:

-topical retinoids?

-benzoyl peroxide?

-topical antibiotics?

-topical retioinds cause peeling of the skin, which prevents clogging of the pores

   -Best Initial Tx of comedonal acne

-benzoyl peroxide and topical AbX (erythromycin or clindamycin) destroy acne causing bacteria (P. acnes)

Define cutis marmorata.

Who is it seen in?

-A lace-like patter of erethyma in response to cold or stress (looks similar to livido reticularis)

-Can persist in diseases like Downs and Edwards

Where else can mongolian spots be seen other than the buttocks (4)?

What is it caused by?

-shoulders

-arms and wrists

-legs and ankles

-abdomen

-Caused by entrapement of melanocytes in the dermis during their migration from the neural crest to the epidermis

What is rosacea thought to be due to?

What is the rhinophyma of rosacea due to?

-Rosacea is though to result from hair follicle mites. Other mechanisms according to UpToDate include abn in innate immunity, inflam rxn to cutaneous microorganisms, UV damage, and vascular dysf

-Rhinophyma is caused by solid appearing edema 2/2 sebaceous gland hyperplasia and lymph edema

What are commonly known triggers for rosacea?

What is the treatment for rosacea?

-Triggers include: hot drinks, hot weather, rapid change in body temp, emotion, EtOH

-Tx: topical metronidazole 2 times/day for several months, and PO tetracycline for maintenance

What are common locations for seborrheic dermatitis to occur?

Tx?

-scalp (dandruff), hairline, behind ears, external ear canal, folds of skin around nose, eyebrows, armpits, under breasts, groin area

-Tx:

  1) Dandruff shampoo is usually adequate

  2) Topical corticosteroids for severe cases

For irritant contact dermatitis and allergic contact dermatitis, fill in the following:

-common causes?

-does it require prior sensitization?

-is it immunologic?

-irritant: caused by chemical or physical insult to skin (detergents, acids/alkalis, freq hand washing), it does not require prior sensitization, and is not immunologic

-allergic: caused by exposure to allergen (poison ivy/oak/sumac, iodine, nickel, rubber, neomycin, topical anesthetics, cosmetics), it does require prior sensitization, and is immunologic (Type IV hypersensitivity)

1) Avoid contact allergen/irritant!!!

2) Apply cool tap water compresses

3) Apply topical corticosteroids

4) For severe cases, use systemic corticosteroids

What skin lesion appears as a pruritic, papulosquamous eruption of "herald patches" resembling ring worm, classically described as being in a Christmass tree appearance?

What is it thought to be caused by?

Tx?

-Pityriasis Rosea

-Thought to be caused by Herpes type 7

-Tx: none is necessary, antihistamines for pruritis

1) Strepotoccus infections

2) sarcoidosis (granulomatous!)

3) IBD (Crohns is granulomatous!)

4) fungal infection (granulomatous!)

5) pregnancy

6) meds (OCPs, sulfas, amioderone)

7) syphilis

8) TB (granulomatous!)

What 5 medication are a/w erethyma multeforme?

What 2 infections are a/w erethyma multiforme?

Can you prophylax against EM?

-sulfas (MC), PCN, phenytoin, allopurinol, barbiturates

-HSV and mycoplasma

-For recurrent and debilitating HSV associated EM, acyclovir may be given prophylactically for prolonged periods

-SJS is aka Erethyma multeforme major

-SJS involves up to 10% of body surface are

-TEN involves > 30% of body surface area

  -Involvement between 10-30% body SA is called TEN/SJS overlap

Note: unlike SJS and TEN, in erethyma multeforme (minor) mucous involvement is rare

Is there an association with cancer in pts with:

-Bullous Pemphigoid?

-Pemphigus vulgaris?

-Pemphigoid - no

-Pemphigus - yes, a rare form of pemphigus is paraneoplastic pemphigus (PNP) and is sometimes seen with lymphomas

What is the most common STD?

Treatment?

-Anogenital warts (conduloma acuminatum) caused by HPV 6, 8, or 11

-Topical podophyllin

When do you begin screening pts with inflammatory bowel disease for colorectal cancer?

How often do you screen them?

-Begin screening colonoscopies 8 years after diagnosis of IBD is made

-Screen Q 1-2 years

What's the MC organism is responsible for and treatment of infectious arthritis in the following pts:

-healthy adults?

-immunocompromised pts?

-sex workers?

-healthy adults: S. aureus, oxicillin or vancomycin (if MRSA suspected)

-immunocompromised: gram (-), broad spectrum AbX (3rd cephalosporin or aminoglycoside) or 4th gen ceph if pseudomonas suspected

-sex worker: gonococcus, ceftriaxone

Giving a patient with shingles acylclovir can provide what 3 things as far as therapy?

How soon after lesion appears should be therapy begin?

1) reduces pain

2) decreases length of illness

3) reduces risk of postherpetic neuralgia

-Therapy should begin no later than 72 hours after lesion appears

  -Therapy can be started if >72 hrs if: immunocompromised, >/= 50 y/o, eye inv.

Seborrheic dermtitis

Tinea versicolor

What's the pathogenesis behind the rash of scabes?

How do you Dx?

How do you Tx?

-Pathogenesis: mites tunnel though epidermis, lay eggs, and deposit feces leading to a type IV hypersensitivity rxn against mites, eggs, and feces -> pruritis

-Dx: examining scrappings of the burrows under a microscope to look for ova and mites

-Tx: Permethrin is firstline, causes paralysis of parasite

    -should be applied heat to toe

    -close contacts of pt should be treated too (even if asymptomatic)

What's the MC causative organism of and Tx for:

-Tinea corporis?

-Tinea capitus?

-Tinea cruris?