Biostats
Hazards Ratio: Measure of how much effect something actually had. Value of 1.00 means there is no difference between the two groups. A ratio < 1 indicates a protective effect, and > 1 indicates a detrimental effect. If the confidence interval of the hazard ratio includes 1.00 (null value), then the effect wasn’t statistically significant. If the interval doesn’t include the value, the difference was significant.
Cardiology
Community Health Centers
LDL levels: keep < 100 in pt w/ known CHD risk equivalent (CAD, MI, PVD, or inpatient DM). If pt has none of these problems, can keep below < 160 if 0-1 RF, < 130 if >=2 RF. Consider drug therapy only ay 30 above the threshold, unless > 2 RF.
Initial DOC for newly diagnosed HTN is thiazide diuretic. Common side effect is photosensitivity, leading to a rash in sun exposed areas. Rx by stopping med, or avoid sun exposure. Thus, this is a common side efx of meds in newly diagnosed HTN.
Best RF to modify to reduce risk of CAD is LDL. HTN is also good but not as good as LDL. Other stuff helps too (exercise, stop smoke, control DM), but they don’t lower risk as much as LDL and HTN. Secondary HTN: Consider it in a young patient w/ high blood pressure. 90% of secondary HTN is d/t unidentified cause. Otherwise, the MCC is renovascular HTN. Look for abd or flank bruit in pt with renovascular HTN. Other causes: peho (headaches, tachy), Cushing’s disease (edema), advanced renal disease (edema).
Retinal abnormalities is a long term effect of HTN, not seen early in disease.
DM is the single most important predictor of adverse CV outcomes. Such a good predictor that DM is considered a CHD equivalent. In women, the prediction is evn more important.
For people with DM, keep BP < 130/85, versus 140/90 in a healthy person.
AAA: Cutoff for surgery is > 5 cm diameter. If smaller, do periodic imaging. Rapid growth can also need surgery. Big time RF is smoking. Other RF don’t have as much impact as smoking cessation does.
Office
Amlodipine side efx: fluid retention and urticarial rash.
ACEI side efx: angioedema, urticaria. Rash is usually psoriatic, not photosensitivity in nature. Note that ARB might also cause angioedema if a pt has bad experience w. ACEI.
Paroxysmal a fib: present w/ EPISODIC palpitation possibly associated w/ symptoms. Same CVA risk as normal afib, so need warfarin. Either rate or rhythm control is effective if asymptomatic. If there are marked or persistent symptoms (palpitation, dizzy, dyspnea) rhythm control is better. Amiodarone is the preferred drug for rhythm control if pt also has some other structural heart disease (cardiomyopathy, CHF, CAD). Flecainide can work ONLY if pt has NO structural heart disease. It can lead to fatal arrhythmias if you give it to pt w/ structural heart disease.
Ibutilide: use for acute termination of a-fib.
Fibrinogen: associated w/ increased CV risk. > 3.43 is a double risk. > 2.7 is high. Drug therapy to decrease fibrinogen hasn’t been shown to be preventative. However, stopping further increase helps. Within statins, lovastatin and atorvastatin increase levels, while prava and simva don’t increase. Thus,
if someone is at a high level for fibrinogen, must think about which statin to use if pt also has high LDL.
Nonsusstained ventricular tachy: >=3 consecutive ventricular beat w/ rate > 120, and the episode lasts < 30 sec. If you see this, pt most likely has structural heart diease. Ex. Prior MI scarring, ventricular hypertrophy, mitral valve prolapse (midsystolic click). If you pick up this rhythm on EKG, next step is to get echo and stress test to r/o ischemia.
CHF: ACEI are the main therapy. Improve survival and delay progression of disease. Indicated even if pt is asymptomatic. Only contraindications are poor tolerance to drug, or renal failure or hyperkalemia. CHF: standard therapy is diuretic, ACEI, bb, digoxin, or spironolactone. ACEI is the best, and won’t exacerbate confusion in a pt. digoxin could worsen confusion.
If ACEI isn’t well tolerated (angioedema), then hydralazine and isosorbide dinitrate is a common combination. Side efx might include drug induced lupus. Manifest as flu like symptoms (fever, malaise, myalgia, facial rash). LAD, splenomegaly can also happen. Antihistone antibody is marker of drug induced lupus. Rx is to stop drug. Hydralazine is safe in pregnancy (as are dopa, labetalol) CHF as a cause of hypoNa. The decreased CO and SBP decreases perfusion P at carotid baroreceptor, so body stimulates ADH and rennin angiotensin despite volume overload. This causes even more fluid retention, leading to hypoNa. Must correct levels gradually, not acutely. Best Rx is water restriction.
CHF: syndrome which results from impaired ventricular emptying (systolid) or relaxation (diastolic). Symptoms: fatigue, weakness (d/t reduced CO), edema (d/t fluid retention). Exertion exacerbates all symptoms. Its’s a syndrome, so it’s a clinical diagnosis based on H and P. PND, orthopnea, raised JVP, rales, S3, CXr findings (increased vascular congestion or silhouette) are major criteria. Dx is 2 major or 1 major + 2 minor. Minor criteria: bilateral LE edema, hepatomegaly, dyspnea on exertion, nocturnal cough).
Digoxin toxicityL N/V, anorexia, confusion, visual disturb, cardiac abnormalities. Drugs that can cause toxicity: verapamil, quinidine, amiodarone, spironolactone.
Hypercholesteremia + hypertriglyceridemia (>200): DOC is a statin. . If statin isn’t good alon,e add gemfibrozil or niacin.
Lone a fib: a-fib which occurs w/o any other signs of clinical heart disease (r/o CAD, TH, PE, HTN, DM, CHF). Warfarin is not necessary, just aspirin is good enough.
Unstable angina: no matter what, need a coronary angio ASAP to look at blockage and see it’s severity. If angio reveals pt to be high risk, consider percutaneous coronary intervention (PCI) or CABG. Remember that DM will increase rate of progression a lot.
Evaluating heart ischemia in pt w/ prior CABG, poor heart function, or if there already exist baseline EKG changes: use adenosine or dipyramidole to induce ischemia and watch the technetium-99. (sestamibi). Stress echo should only be done if adenosine cant be used for some reason. Remember that arthritis can also impair exercise.
Adenosine can induce bronchospasm, so if pt has COPD or asthma, adenosine is contraindicated. Use dobutamine instead.
Orthostatic HypotensionL dx with fall or 20 SBP or 10 DBP. Can happen after standing up or even eating. Drop in BP must happen within 2-5 min of standing.
2 MCC ortho hytpo: autonomic dysfunction or intravascular volume depletion. Autonomic dysfunction (DM neuropathy). Drugs: antihyptrtensives, vasodilators, anti-angina drugs.
Ca channel blocker: peripheral edema is common side efx. The –dipines are common, but diltiazem can also cause it.
Exercise stress test is FSOM in pt w/ angina symptoms..
Weight loss is the best non-drug way to decrease BP. Benefit in overall CV risk is unclear but probably helps.
Other firstline drug for HTN besides ACEI is b-blocker.
Positive stress test: > 1 mm downsloping ST depression. NSOM is to do cardiac cath to see where the lesions are, and to possibly to balloon stenting.
Right sided endocarditis: commonly see R sided involvement or septic pulmonary emboli. Septic emboli manifests as scattered bilateral rales. Pulmonary infiltrates on both sides. IVDU is the likely cause. Otherwise, R sided disease is very uncommon.
Coumadin management: If INR > 3 but < 5, just hold drug for a few days to get level to therapeuritic. If INR > 5 but < 9, stop drug and give small dose of vit K (1-2 mg). If > 9 but < 20, higher dose of vit K. If > 20, consider FFP. If at anytime pt is bleeding, give FFP.
Drug interaction w/ warfarin: Amiodarone increases warfarin action. If need to have the two together, reduce warfarin by 25%.
MVP: MC valve abnormality in industrialized nations. Mid to late systolic click, most easily heard over LV.
Mitral regurg: holosystolic decrescendo murmur (can be 2ndary to MVP) heard in apex, radiates to axilla. Increases w/ grip, decrease w/ valsalva.
Systolic <> in LU sternal border: pulmonic stenosis.
Mitral stenosis: low pitched diastolic rumble heard over the apex best when pt is lying L lat decubitis. The narrowing of the valve leads to increased P in LA, which backflows into increased P in pulmonary vasculature and R side of heart. MCC is rheumatic fever. May present as hemoptysis. LA can enlarge, leading to elevation of L mainstem bronchus, and flattening of L heart border.
Mitral stenosis: opening snap with diastolic rumble. Best heard mid clavicular on L side between 5th and 6th ribs.
MC congenital heart malformation: VSD. If large enough, may be symptomatic. Murmus is pansystolic murmur at LL sternal border. Should get an echo. VSD is not congenitally cyanotic, only if its big enough.
Polypharmacy: Using too many diuretics, a-blocker, or nitrates can induce ortho hypo.
MCC perioperative mortality: cardiac death. Highest risks: unstable angina and critical aortic stenosis. Exercise angina and MI < 6 mo ago are also decently big RF, but less than the other two.
Amiodarone induced lung toxicity: MC presentation is as a chronic interstitial pneumonitis. Nonprod cough, fever, pleuritic CP, focal or diffuse interstitial opacity on CXR. Rx with d/c drug. If really bad, consider steroids.
Inpt facility
Metformin: higher chance of lactic acidosis (contraindicated) if renal insufficiency, hepatic dysfunction, or CHF. Thus, if pt goes to a procedure that needs contrast (ex. Cardiac cath), you must d/c metformin a bit before the procedure.
Acute MI: sinus bradycardia could happen after MI. FSOM is IV atropine. If that doesn’t work, then must intervene w/ thrombolysis or PTCA (angio). In the meantime, probably need to do transvenous cardiac pacing while setting up the thrombolysis . Remember that thrombolysis is contra in recent abd surgery (2 wks).
If need to intervene in CAD in a pt with DM, CABG is better than angio. DM has higher chance of restenosis, so angio or balloon + stent isn’t good enough.
Multifocal atrial tachy: > 3 P waves of different morpho;logies. Narrow QRS, variable PR segment. MCC is hypoxia and COPD. Thus, someone showing this arrhythmia must first analyze their O2 status, since correction may eliminate the arrhythmia. Other causes are hypoK and hypoMg. Rx is always reverse the cause. If the initial therapy doesn’t work, try bb or verapamil if bb is contra (COPD, asthma).
Acute heart failure: MCC are papillary m. rupture, infective endocarditis, chordae tendinae rupture, and chest wall trauma . A mitral regurg makes you think of ruptured chordae tendinae. Dx DDx for chrdae tendinae rupture: IE, ischemia, MV rupture.
Ehlers Danlos syndrome: mitral valve degeneration can happen, leading to chordae rupture. Pes planus and scoliosis are common findings. Joint hypoermobility, hyperextensibility. Marfans can also cause rupture.
Anticoagulation for mechanical valves: mechanical mitral and aortic valves need INR between 2.5-3.5. Torsades de pointes: look for an EKG showing a QT interval prolongation, followed by some sort of clear arrhythmia. Frequent variation in QRS morphology is more likely torsades. Rx for torsades with hemodynamic compromise is immediate defibrillation. Once pt is stable, then give MgSO4. Remember that the lab value for Mg is unreliable, so just give it regardless of levels. If Mg therapy fails, then do temporary transvenous pacemaker.
Synchronized cardioversion: for v-tach, a fib.
s/p MI, best to hold sexual activity for 6 weeks after the event. If there were complications because of the MI, need to further evaluate.
A-fib: First line for rate control is Ca channel blocker. Diltiazem is good. Propranolol is good alternative if diltiazem is contra (significant CHF, cardiac conduction system disease).
Cancer drugs w/ CV side efx: -rubicin and mitoxantrone. These are cardiotoxic, so should get baseline radionuclide ventriculography (RVG) can detect early toxicity. This can do noninvasive serial monitoring of cardiac function. Multiple gated blood pool (MUGA) is also good. Echo isn’t good enough because can’t do serial evals. Used more in kids getting chemo, to avoid radiation exposure. ED
If someone presents with cardiac symptoms, but all the first line tests come back negative, consider doing continuous EKLG monitor for 24 h to evaluate for arrhythmias.
Stress test with radioactive stuff: perfusion defect is a place where blood flow is not the same as elsewhere. Lateral wall of LV is supplied by L circumflex, so defect there is likely this vessel.
In a pt with acute MI, Ca channel blockers may actually be harmful. Think about this b/c often they might be on the drug to control HTN. In contrast, bb, ACEI, and statins can help prevent CAD.
2nd degree AV block: Rx with permanent cardiac pacemaker insertion. (aka transvenous pacemaker). This helps prevent progression to Type III block. Remmebr that 3rd degree block is a random, no relationship at all btw A and V beating on EKG.
Acute MI management: FSOM include O2, IV access and give aspirin and nitro. ACEI aren’t used acutely but reduces mortality if taken for the weeks after an MI. bb helps w/ decrease myocardial demand and controls HR. Can give after aspirin, nitro, and morphine.
Acute MI: If EKG shows ST segment elevation in 2 contiguous leads, then thrombolytics are indicated, and if pt presents within 12-24 h of symptoms. Must give NO before getting the EKG. Contra for thrombolytics are active bleed, any intracranial event (bleed, ischemia, neoplasm), SBP > 180, or trauma. Don’t confuse with ST segment depression, which is just ischemia.
Flash pulmonary edema: Presents w/ acute onset of SOB. No previous history necessary. Hypertensive crisis can cause it, so look for a very high BP. CXR looks like lots of edema, and there willl be diffuse crackles. FSOM in any flash pul edema is give O2 (O2 sat will be low), morphine, and IV furosemide (loop diuretics). If the cause is HTN crisis, the preferred drug to give is IV NO or nitroprusside.
Other causes of flash pul edema: mitral stenosis or acute aortic/mitral regurg. Thus, after someone has an episode of this, get an echo. Bb are CONTRAINDICATED in acute heart failure, can slow heart too much and lead to death.
Cardiogenic pulmonary edema: Initial Rx is similar: O2, morphine (reduces work of breathing), and a loop diuretic.
Cardiogenic shock complicated by hypotension: dopamine is a good choice.
Acute pericarditis: can be infarct associated, and happen after an MI (esp. transmural). The associated CP depends on position, and worsens w/ deep inspiration. EKG has diffuse ST elevation w/ PR depression. Rub is heard voer L sternal border (a scratchy sound), which gets louder as pt leans forward. Rx is NSAIDS (or anything for pain).
Dressler’s syndrome: happens in MI pt and after cardiac surgery. Usually develops weeks/months after MI not days. Presents w/ fever, leukocytosis, pleuritic chest pain, and pericardial rub. Thus, very similar to pericarditis, but look at the time course.
Q waves are indicative of old infarct (days old sometimes)
Aortic stenosis: Area of aortic valve < 1 cm2 is considered severe stenosis. Onset of symptoms has a big effect on prognosis, so prompt intervention is important in symptomatic aortic stenosis (syncope, angina, dyspnea). Rx w/ aortic valve replacement will reduce mortality. Balloon valvulotomy has only transient efficacy, and high procedural morbidity.
Carotid artery dissection: presents w/ unilateral headache + associated Horner’s syndrome (miosis, ptosis, and anhidrosis) on the affected side only. Thus, symptoms aren’t bilateral. Some causes are trauma, CT disease, smoking, seatbelts in MVA. Dx is MRA. If MRA fails, then catheter angio is definitive test. Rx is with anticoagulation w/ heparin or platelet agents. Pt with this dissection is at high risk of developing cerebral infarction.
MCC of CHF is ischemic heart disease. Thus, if you diagnose a new case of CHF, and are still trying to look for etiology, first r/o coronary lesions with a cardiac stress test. Other causes of CHF are HTN, and valve or renovascular disease. BNP is not useful in this case. BNP’s main purpose is to distinguish between cardiogenic pulmonary edema from primary pulmonary conditions.
Acute aortic dissection: Usually presents in older male with long history of HTN and atherosclerosis. In younger pt, think CT disease (Marfan, Ehler Danlos), inflammatory vasculitis, aortic valve problem, or cocaine. Presents w/ sudden onset of sharp tearing chest or back pain. If tear happens in ascending aorta, pt may develop acute aortic insufficiency, causing acute heart failure. Dissection could also extend into coronary vessels, leading to cardiac tamponade or hemothorax. PE shows difference in BP between 2 arms. CXR can show mediastinal widening. TEE is Dx of choice. FSOM is to give bb to lower SBP and LV contractility to < 100-120 mmHg and < 60 bpm. If bb is not enough to lower BP, give sodium nitroprusside. After this is achieved, go to surgery right away.
Syncope w/o any apparent cause is most likely neurocardiogenic. Prodrome of nausea, lightheadedness, pallor, and diaphoresis. Precipitating events include prolonged standing, exertion, venipunture, or painful stimulus.
Ventricular tachy vs. sus supraventricular tachy: supra has regular, narrow QRS complexes. Ventricular tachy has wide QRS complexes.
A flutter is in a sawtooth pattern.
WPW syndrome: delta wave is a upstroke of QRS that is slurred. It may present as SVT. If verapamil or bb are given to WPW pt, v fib may occur d/t increased accessory pathway conduction.
Pericardial effusion: can happen in response to pericarditis or any malignancy. If too much fluid gets out, and tamponade develops, presents as Beck’s triad: hypotension, muffled heart sounds, and elevated JVP. SOB is present. Dx is echo emergently and Rx is surgery. Equal diastolic P on all chambers on cardiac cath is aldo present. Pericardiocentesis is life saving.
Chest pain relieved by NO is probably cardiogenic. Get cardiac enzymes.
A-fib which is hemodynamically unstable: Must do synchronized cardioversion. (in sync w/ the R wave). If pt is stable, then you can convert to normal w/ drug (amiodarone, sotalol). These agents aren’t for long term rate control. Long term rate control is with diltiazem or metoprolol.
Asynchronized cardioversion is TOC for ventricular fibrillation
Acute arterial occlusion: MCC are recent MI and afib. Presents as sudden symptoms usually in LE (numbness, coldness, delayed capillary refill, pulse deficit in distal adrteries). Very important to immediate IV heparin followed by continuous heparin infusion.
Cocaine induced myocardial ischemia: Initial Rx is nitrates, benzos, or Ca channel blocker. If no improvement with these (d/t possibility of coronary artery thrombosis), then do immediate coronary angiography. A distinct feature of cocaine induced vasospasm is that it might lead to coronary artery thrombosis.
Acute coronary syndrome: STEMI on EKG requires urgent cardiac cath. Non-STEMI can be managed with serial cardiac enzymes, as can unstable angina without any EKG changes.
TCA overdose: hypotension, anticholingergic effects, CNS symptoms, cardiac arrhythmia. Can lead to QRS prolongation and reentrey arrhythmia (v-tach, vfib, torsades). Best agent for TCA induced cardiotoxicity is sodium bicarbonate. Lidocaine is the best anti-arrhythmic for TCA induced arrhythmias.
Syncope can be diagnosed by EKG + H/P in 70% of cases. FSOM in a new syncopal episode is EKG. Neurological testing (CT hea,d EEG) are usually not valuable unless something in the H and P clearly shows that it’s a neurological etiology.
Dermatology
Malignant melanoma: signs of malignancy include irregular borders, increasing in size, odd colors. They are generally more than 5 mm in diameter. Excisional biopsy is the FSOM to confirm diagnosis and stage the lesion. Eventually, if it is melanoma, you’ll want to do a complete excision, which is curative a lo the time.
Melanoma: Majority of melanomas are associated with excess sun exposure. It happens more often in fair skinned people, and usually develops in areas of the body that are intermittently exposed to intense sunlight. Should wear protective clothing when exposed to the sun. Sunscreen can reduce incidence of basal and squamous cell cancer, but no evidence it helps to prevent melanoma.
When hairs have split ends, it means that there is a toxic/chemical reaction causing the hair loss. Numerous drugs can cause hair loss (ex Li, thallium, chemo) but they do not affect the hair shaft or produce split ends.
Psoriasis: inflammatory skin disorder characterized by hyperproliferation and abnormal differentiation of the epidermis. There are sharply demarcared erythematous plaques involving the scalp, knees, extensor surface of elbows, neck, and back. Plaques are raised, with a thick silvery scale covering the surface. Psoriasis can also involve nails and joints, leading to psoriatic arthritis. Nail involvement presents as pitting over the nail plates. The arthritis can present with early morning stiffness which is relieved by physical activity. Some drugs can worsen psoriasis (b-blocker, Li, ACEI, NSAIDs, and anti-malarials). Dx is a clinical one. Histology shows epidermal hyperplasia or hyperproliferation with neutrophilic infiltration in the stratum corneum and thiined to absent layer of the epidermis.
Worsening of psoriasis by certain drugs: As a general rule, all drug induced skin rashes should be managed by d/c the drug.
Rx of psoriasis: depends on severity of disease. Mild localized skin disease is Rx with topical steroids (betamethasone)or emollients or coal tar products (anthralin or calcipotriene). For extensive/widespread disease, Rx include methotrexate, cyclosporine, UV radiation, or immunomodulators. Methotrexate is the initial DOC for pt with psoriasis and arthritis.
Tinea Versicolor: fungal infection of skin caused by Malassezia furfur. Presents with multiple small circular macula which vary in color (white, pink, brronw). Rash is more prominent in summertime. Generally the lesionsare the only symptom. Rx with terbinafine anti fungals. Alternatively, any of the azoles can also be used.
Onychomycosis: fungal infection of toenails or finger nails. MCC is Trichophyton rubrum. Nail dystrophies from other diseases can mimic this (psoriasis, lichen planus). You can confirm dx with KOH exam of the nail scrapings. The KOH exam will show dermatophytic hyphae and arthrospores. Terbinafine is the TOC. An alternative is itraconazole.
Rosacea: chronic acneiform condition characterized by vascular dilation in the central face. Presents in adults 30-60. There are exacerbations and remissions. Symptoms include facial erythema, telangiectasias, and papules/pustules. Looks a lot like acne, but no comedoens are present. Rx with topical metronidazole. Pt with rosacea often have ocular symptoms. Chalazion is a common one (it’s a cyst in the eyelid). Other eye complications include foreign body sensation, and conjunctivitis. Alopecia Areata: Discrete, smooth and circular areas of hair loss over the scalp with no scaling. Usually develops over a few weeks and has a recurring pattern. There is usually regrowth of hair in the involved areas over time. There is no associated scalin, scarring, or inflammation. Rx is with topical or intralesional steroids. Even after Rx, there is still a chance of recurrence, although it does speed up hair growth.
Tinea capitis: Can present with a patch of hair loss on the scalp. The lesion is well demarcated, scaling, and somewhat erythematous. Dx is usually with KOH exam of the hair stubs. Microsporum canis is a cause, which will have a bright green fluorescence when lesion isobserved under Wood’s UV lamp.
Keloid: benign fibrous growth that develops in scar tissue. These lesions can be painful and fdisfiguring. Rx with intralesional steroids. Look for hx of traum a(ex earring piercings)
Actinic Keratosis: Presents as slowly growing reddish brown skin lesion. It’s pre-malignant, with potential to become squamous cell cancer of the skin.
Tetracycline: often used for Rx of acne. Doxycycline is a phototoxic agent and make ppl more susceptible to sunburn. On a side note, doxy can also cause esophageal ulceration if you don’t drink it with enough liquid. Rx for sunburn includes replacement of lost fluids and relief for pain/pruritis with NSAIDs. Diphenhydramine can be used for the itching.
Isotretinoin (systemic retinoid): can cause hypertriglyceridemia in up to 25% of pt. Thus, there is a risk of acute pancreatitis. Look for the kid who is getting isotretionoin for acne Rx who develops pancreatitis. If a pt develops triglyceridemia > 800, should d/c the drug.
Topical Retinoid: teratogenic. Topical retinoids aren’t associated systemic side effects (hyperTG or hepatotoxic).
Herpes Zoster: d/t reactivation of latent VZV infectio earlier In life. Any kind of stress on the body (fracture, infection, surgery) can reactivate the latent infection. Presents with grouped vesicles in a specific dermatome, usually unilateral. Pain is another prominent feature. Rx with acyclovir. Localized zoster lesions are transmitted only via direct contact with the open lesions. Contact prevautions aren’t necessary in the community setting. In the hospital, however, should put the pt in contact isolation until all the lesions have crusted. As age increases, there is a higher chance that a recurrence will happen.
Postherpetic neuralgia (PHN): Defined as persistence of pain or other symptoms for > 1 month after resolution of skin lesions of herpes zoster. It’s described as a burning sensation in the involved dermatome. Agents proven to be effective for the pain include TCA, topical capsaicin cream, gabapentin, and long acting oxycodone.
Photoaging: arises from aging and UV light damage. Intrinsic aging tends to cause fine wrinkles on an otherwise smooth skin surface. If there is photodamage, it can result in coarse, deep wrinkles on a rough skin surface. Photoaged skin is often marked with actinic keratoses, telangiectasias, and brown spots. Cigarette smoke can have significant impact on skin (more wrinkles, especially at lateral corneres of eyes). Rx with tretinoin. It helps reduce fine wrinkles, mottled hyperpigmentation, and roughness of the face. It can also reduce actinic keratoses.
Erythrasma: infection of skin that occurs most often in intertriginous spaces and is d/t C. minutissimum. Use of wood lamp shows coral red fluorescence cause by Corynebacterium porphyries.
Pityriasis rosea: self limited condition, manifests first as a single primary plaque (herald patch). A generalized eruption develops 1-2 weeks later, with fine, scaling papules and plaques in a christmas tree distribution.
Poison Ivy dermatitis: presents with a pruritic dermatitis composed of papules and vescicles which are distributed in a linear fashion. Multiple lesions can be present in various areas around the bodhy, since touching other parts of body will transfer the poison ivy resin. More serious reactions can evolve into vescicles which can exude a serous fluid.
Tinea pedis: MC dermatophyte infection. Usually accompanied by involvement in another area (hands, necknails, or groin). Presents as a slowly progressive, pruritic, erythematous lesion, usually btw the toes and extending to the sole and side of the foot. There is a sharp border btw the involved and uninvolved skin. Self limting, but recurrent. Rx with antifungal cream.
Seborrheic Dermatitis (dandruff): Pink-red erythema and scaliness in the scalp, face, and sometimes upper trunk. Pruritis is usually mild. Rx with selenium shampoo. Sometimes it’s the first presenting sign of HIV infection.
Lichen Planus: generally presents in middle age. Involves skin, nails, mucous membranes of the mouth and external genitalia. Lesions are shiny, discrete, intensely pruritic, polygonal shaped violaceous plaques and papules that are present on the flexural surfaces of the extremities. Wristss are commonly involved. A characteristic whitish lacy pattern is often seen on the surfaces of the papules and plaques. Mucous membranes of the mouth and external genitalia can also be involved. Dx is clinical. Histology can show hyperkeratotic epidermis with irregular acanthosis and focal thickening in the granular layer of the epidermis. Lichen planus is seen in association with liver disease, especially advanced disease 2/2 hep C infection. Consider screening for it with H and P if you see lichen planus.
Acne Rx: Mild acne is Rx initially with topical retinoid. Moderate acne can be Rx with topical retinoid and benzoyl peroxide or topical antibiotic. More severe acne is treated with adding a topical antibiotic or systemic abx. Abx are used only in combination with the other stuff. Very severe cases can be rx with oral isotretinion is no response after 3-6 omnths with combo of abx, topical retinoid, and benzoyl peroxide.
Pressure Ulcer: Stage 1 has nonblanchable erythema of intact skin. Stage 2 has a partial thickness loss of the epidermis, dermis, or both. Stage 3 are deeper, causing a full thickness loss with damage which might involve underlying fascia. Stage 4 are very deep, and can possibly extend into the bone, muscle. Should cover wound with dressing/saline moistened gauze. Pt should be turned every 2 hours to prevent.
Sporotrichosis: funal infection d/t sporothrix schenckii. Usually seen in ppl who do outdoor activities. Starts as a popular lesion over the site of inoculation. Eventually, the lesion ulcerates and tehr eis non-=purulent drainage over the lesion. Dx is clinical, and with culture. Itraconazole for 3-6 months is Rx.
Tattoo: Laser removal of tattoos can be done, but they lead to scar marks and skin discoloration. Porphyria curanea tarda: d/t deficiency of oroporhyinogen decarboxylase. Painless blisters, and an icreased fragility of the skin are seen. There can also be facial hypertrichosis and hyperpifmentation. Dx is with elevated urinary uroporphyrins. Phlebotomy or hydroxychloroquine can provide relief. There is often an association with hep C, and if pt also has Hep C, can give interferon alpha.
Electrolytes
HyperCa: usually lack of specific findings on physical exam. Some possibilities include anxiety, depression, mild muscular weakness, constipation, and PUD.
hypoCa: Can occur during or immediately after surgery (esp if lots of transfusions were involved). hyperreflexia may be present, chvostek’s sign is present (facial m. contract with tapipnof the facial nerve).
Plasma osmolality: calculated as 2 x Na + glucose / 18 + BUN / 2.8. Normal is Around 280-290 Euvolemic Hypoosmolar hypoNa: Has various etiologies. HypoTH, adrenal insufficiency, SIADH are common ones. Treating the underlying condition will also correct the electrolyte imbalance.
hypoNa: if pt is symptomatic, or if the number is very severe (ex 110), then needs Na placement using hypertonic saline solution. Postop hypoNa is common, d/t SIADH 2/2 anesthesia. Rx severe hypoNa with infusion of 3% hypertonic saline, increasing Na by 3 in the first 3 hours, and 0.5-1 per hour for the next 12-18 hours. Frequent monitoring is necessary to prevent a rapid increase (can lead to central pontine myelinolysis). Don’t raise Na by more than 12 in the first 24 hours. The increase in serum Na level for a pt achieved by infusion of 1 L of 3% hypertonic saline can be calculated with the wollowing. (513 – Na)/(total body water + 1).
Remember small cell cancer causing SIADH.
Hyperosmolar Hyperglycemic state (HHS): complication of poorly controlled T2DM. Characterized by AMS, sugars > 800, bicarb > 15, Osm > 320, and presence of minimal ketones. Hyperglycemia can cause either hypoNa or hyperNa in uncontrolled DM. Hyperglycemia can cause increases in serum osmolality, which acuses osmotic water movement out of the cells, diluting the ECF and leading to dilutional hypoNa. TO correct this, have to calculate the corrected value of serum Na. Add 1.6 to the Na for each 100 of glucose over baseline (100). Thus, these pt are often much more hyperNa than their number would indicate. Rx with hydrating by half-normal saline solution.
hypoK: can cause a paralytic ileus. Rx with K replacement (for GI stuff) and to prevent any cardiac complications. Some causes include diuretic induced hypoK (esp if pt is on HTN, CHF therapy). Loop diuretics are a big cause. hypoK itself can actually precipitate hepatic encephalopathy
hyperK: Some warning signs are if K is > 7, if there are EKG changes (peaked T waves), and acuity. First thing to do in an emergent situation is to give IV Ca gluconate to stabilize membrane of cardiac conduction tissue and prevent arrhythmias.
Alcoholic ketoacidosis: presents with iketonuria and mildly elevated glucose. Can impair mental function. Glucose can be low, high, or normal. Rx with D5W and thiamine. Insulin is usually not needed.
hypoMg: can mimic some signs of hypoCa (hyperactive DTR,),muscle cramp. But is often associated with alcoholism, prolonged NG sunction, diarrhea, or diuretic use.
Hypophosphatemia: MCC is continuous glucose infusion in hospitalized pt. Pt are usually alcoholic or debilitated. Hypophosphatemia can impair ATP generation and muscle weakness can result. If the resp muscles get weak, is an indication to not wean from mechanical ventilation. Cardiac contractility is also decreased in hypophosphatemia, and can cause cardiomyopathy.
Zinc deficiency: common in ICU, d/t prevalence of RF (diarrhea, diuresis, malnutrition, CRF, burns). There can be increased susceptibility to infection and a skin rash.
Endocrine
Deep Vein Thrombosis: anticoagulation is indicated for all symptomatic DVT. This is to make sure it doesn’t spread to lungs. Rx with heparin for 5 days, and start warfarin start at the same time (4-5 dya overlap). Give heparin until INR becomes 2-3 for 2 days. For a first case of DVT, should rx with anticoagulation for at least 3 months.
Estrogen replacement increases risk of venous thromboembolism (VTE) by 2x. HRT should be d/c in pt with increased risk or a documented DVT. When dcing, make sure to taper the hormone. It’s not recommended to just increase anticoagulation or using heparin just so pt can continue to use HRT. HRT: Risk of VTE increases with HRT. Higher risk of DVT and PE, esp in women w/ known CAD. HRT has a beneficial effect on lipids (decrease LDL, increase HDL), but not good prevention for CAD (actually icreases events). HRT actually increases breast cancer risk. Only 2 clear indications for HRT are prevent osteoperosis and control of vasomotor symptoms.
HRT affects metabolism of thyroid hormones. The levothyroxine requirement increases. Remember than OCPs are also hormone therapies.
Warfarin can cause a transient hypercoagulable state, rarely leading to warfarin induced skin necrosis.
Erectile Dysfunction: NOT a normal art of aging. Common in DM pt, so look for early morning or nocturnal etrerction to see what cause is. If DM, won’t even have morning erection.
Pheochromocytoma: Episodic increase in BP (episodic headache/blurry vision)/palpitation). Dx initial w/ urine VMA and metanephrine. Remember that a-blockers can interfere w/ the urine test results. If you have biochemical confirmation of diagnosis, next step is to start pt on a-blockers. This is required preop to restore intravascular volume (along w / salt and fluid intake). MC drug is phenoxybenzamine (40-80 mg qd) for 10-14 days before going into surgery. Once on a-blockade, then can scan pt’s abd for the mass and go to surgery. Although a-blockers decreases mortality a lot of the pt, Still a chance of hypotension during surgery soon after removing the tumor. Rx this with NS bolus followed by infusion. If during surgery pt becomes acutely HYPERtensive, give phentolamine.
Long term use of glucocorticoid leading to chronic suppression of hypothalamic-pituitary-adrenal axis: can lea dto 2ndary or tertiary adrenal insufficiency. Happens by suppression of ACTH and cortisol, respectively. ACTH doesn’t control of aldosterone, so aldosterone are usually normal. Thus, hypotension usually isn’t a problem, but vascular collapse w/ stressful situations (ex infection) can happen d/t decreased cortisol (maintains vascular tone). Rx with fluid repletion and stress dose of corticosteroids. IV dexamethasone is preferred Rx. Can also do cosyntropin (ACTH) stimulation test afterwards.
HyperTH: diarrhea, amenorrhea, wt loss, weakness. Screen w/ TSH.
Medullary Thyroid Cancer: if after thyroidectomy, calcitonin is still elevated, then that means the disease was metastatic. NSOM is to get CT of neck/chest ot look for the cancer. If can’t see anything, abd CT or PET scan might help. Medullary thyroid cancer cells don’t uptake iodine, so total body iodine scan isn’t useful.
TH replacement for thyroid cancer in remission: give levothyroxine at a dose which suppresses TSH below the normal range (btw 0.1-0.3). If there was distant metastasis, lower the TSH to even less than 0.1. Side efx of suppressing thyroid this much include bone loss and a-fib. Levothyroxine should be taken on an empty stomach and separate from other meds because Levothyroxine absorption is impaired by many medicines. Ca and Iron are common causes.
Subclinical hypoTH: elevated TSH levels, with normal T4 levels. Rx only if there are antithyroid antibodies, abnormal lipids, symptoms of hypoTH, or menstrual dysfunction. Also, you usually treat pt w/ TSH > 10.Thus, FSOM if you find subclinnical hypoTH is to look for antibodies.
TSH secreting pituitary adenoma: presents w/ thyrotoxicosis. Palpable thyroid, warm extremities, mild tremor. High TSH as well as T3 and T4. A similar thyroid profile is seen in Thyroid hormone resistanece syndrome, which actually presents w/ hypoTH symptoms. Can differentiate the two with serum a-subunit levels (increased in pt w/ TSH adenoma).
Subacute thyroiditis: Presents w/ thyrotoxicosis (d/t release of stored hormones by inflammatory damage possible d/t viral infection). Thyroid gland is enlarged and tender. This thyroiditis has decreased radioactive iodine uptake. Because the hormones causing the thyrotoxicosis are preformed, drugs which inhibit synthesis of TH (PTU, methimazole) won’t work. Rx is with NSAIDS and beta blocker. Disease usually follows a course of thyrotoxic for a few weeks, then become hypothyroid for a few months.
Iodine uptake: increased diffuse uptake seen in toxic multinodular goiter. Increased patchy uptake seen in toxic adenoma.
Postpartum Thyroiditis: Often d/t autoimmunity, so anti-thyroid antibodies are elevated. Triphasic course. Strts as thyrotoxicosis a few weeks after delivery, with a low, radioactive iodine uptake. Then, there is a hypoTH phase lasting a few months. Lastly, there is usually recovery. In 80% of pt. Other pt might become permanently hypoTH.
Central HypoTH: Both TSH and T4 are low. Sometimes TSH might alos be slightly elevated (w/ non-active TSH). MRI should be done to look for mass lesion in sellar area. When you suspect central hypoTH, very important to r/o concomitant central adrenal insufficiency. You could precipitate adrenal crisis if you try to treat a pt who has both. Cosyntropin stimulation test is good to screen for adrenal insufficiency.
Subacute lymphocytic thyroiditis: aka painless thryroiditis. Can have hyperTH symptoms, which are usually transient. There is mild enlargement of gland, but it is painless. Mechanism of hyperTH is also d/t preformed hormone. Commonly seen in pt w/ amiodarone, interfereon-alpha, or interleukin-2 therapy. Usually, no Rx is needed d/t transient nature, but Rx with bb is indicated to control hyperTH phase.
Thyroid Lymphoma: malignancy that happens in pt w/ Hashimoto’s thyroiditis. Present w/ rapidly enlarging goiter w/ compressive symptoms. Gland is firm or hard, and retrosternal extension is common (raise arm will develop venous engorgement of neck veins?). Rx with radiation and chemo. Good response. Hashimotis has very high TSH with low T4. Antithyroid peroxidase antibodies present.
Grave’s Disease Rx: Methimazole is known to cause a scalp defect (aplasia cutis) during pregnancy. If a pt becomes pregnant and is on methimazole, switch them over to PTU. Obviously, radioactive iodine is contraindicated. If response to PTU doesn’t work during pregnancy, surgery is indicated. Treatment cannot wait until after pregnancy, since risk of thyroid storm is very high.
Acute management of tachycardia in a hyperTH pt: b-blocker.
Autoimmune polyglandular failure: pt with 1 autoimmune disorder are predisposed to get other ones. Thyroid, DM, adrenal, gonads, atrophic gastritis are possible. Ex. Pt with previous hx of well controlled DM, suddenly is getting hypoglycemic. Posibly d/t arrenal failure, causing low cortisol. Check the ACTH (cosyntropin) levels.
Polyglandular autoimmune failure type II: Schmidt’s syndrome. Includes addison’s type 1 DM, and thyroid disease.
Sarcoidosis: Generalized LAD is present. Weaknes, loss apetite, wt loss. Sarcoid granulomas make 1-a-hydroxylase, which coverts inactive vit D to active. PTH will be suppressed, with increased urinary Ca increased. CXR may show bilateral hilar adenopathy or multiple parenchymal nodules.Rx hyperCa caused by sarcoidosis with glucocorticoids and hydration. Response is good and fast, usually normal within days.
Metformin Rx in PCOS: if pt becomes pregnant, should d/c metformin. It is category B. However, it can also induce ovulation in some pt. Thus, you should continue the metformin (to help pt get pregnant) and d/c it as soon as you have a documented pregnancy. To control sugars during pregnancy, insulin is good.
Fasting blood glucose levels: > 126 (on 2 separate occasions) is for DM diagnosis. Between 100-126 means fasting lucose is impaired, and these pt are at increased risk of CAD just by having this. < 100 is normal.Late/Chronic complications of DM: nephropathy (microalbuminuria), retinopathy, neuropathy.
Random blood glucose > 200 is also concerning. Should do a second test to confirm.
Insulin: NPH or lente is intermediate acting. Ultralente or glargine is long acting. T1DM often requires combo of basal insulin in addition to boluses at mealtime. (using regular or lispri/aspart, which are ultrarapid acting)
DKA: Initial Rx is give IV NS with K and insulin infusion at 7 units /hr. Continue NS until blood suger gets to 250. Afterwards, change NS to D5 + ½ NS w/ K added. Dextrose is important because it decreases ketone levels. Also at this suger level, decrease insulin to 1-2 units/hour. When its time to stop the insulin infusion (blood suger < 100?), switch to subcutaneous insulin. Should give injection injection 30-60 min before planning to stop insulin infusion. Failure to do so leads to recurrence of DKA.
Management of DM during labor and C-section: Requirement of insulin increases during pregnancy, esp during 2nd trimester (d/t secretion of placental hormones which are diabetogenic). After birth, decrease in these hormones, causing the pt’s insulin requirement to drop drastically. For T1DM, should keep pt on usual dose of insulin night before, to prevent DKA. During procedure, start insulin drip and infuse D5W+1/2 NS with 40 mEq of KCl. IV insulin is nice because its effects don’t last more than 30 min (d/t short half life). Tight insulin control during the procedure has been shown to prevent complications in the ICU and post-CABG patients.
Diabetic Neuropathy: Initiall, diminished vib sensation and ankle reflexes. Later, weakness and decreased or lost reflexes elsewhere (esp knee). Formicatino (ant crawling on skin) can happen. Dx with nerve conduction studies (axonal pattern of nerve damage). Rx with with TCAs. Since TCA is contra in heart disease, alternative is gabapentin (studeies show it’s equally as effective as TCAs). Autonomic neuropathy: One symptom is delayed gastric emptying. This leads to a post meal hypoglycemia, since the insulin taken isn’t corresponding with the meal. Blood sugar will fluctuate wildly with a big range. Dx this with nuclear studies to study gastric emptying. Some Rx is metoclopramide or erythromycin. Usually change in eating pattern is needed.Ex. smaller, more frequent meals.If conservative rx doesn’t work, do a jejunostomy tube. Another option is to use cisapride (risk of torsades, so use only if absolutely necessary).
Diabetic retinopathy: Generally takes years to develop. Early on, however, if glycemic control isn’t achieved, thre may be swelling of the optic lens, which can also cause blurry vision. Controlling sugars can prevent or stop its progress. Good control of HTN can also help. Oral hypoglycemics don’t usually work, insulin is usually needed. If full blown diabetic retinopathy develops, blindness can happen, d/t vitreous bleeding and retinal detachment. Rx severe cases with laser photocoagulation. DM is MCC of blindness in USA.
Exercise in DM: Both T 1 and 2 can achieve glycemic control w lower dose of insulin if they exercise regularly. The dose taken before excercising should be decreased (remember that insulin takes 4-5 hours to start working). Some exception: if suger > 250, shouldn’t exercise because it can precipitate DKA. Pt with diabetic retinopathy should avoid weightlifting (increased eye pressure). Conversely, well controlled DM pt who starts excercising more might develop hypoglycemia episodes.Insulin pumps are useful for pt who exercise.
Blood sugar control affect on prognosis: Definitely decreases risk for development of microvascular complications (retinopathy, nephropathy, neuropathy). No proof that it will decrease risk of macrovascular stuff (ex. MI). Specifically for the neuropathy, the sugar control will decrease risk of occurance of peripheral neuropathy, but it cannot necessarily reverse damage which is already done. Metformin is especially useful for managing DM I obese pt.
Chronic pancreatitis islet damage leading to DM: To differentiate btw T2DM and islet destruction, measure c-peptide and insulin. T2DM has higher C-peptide and insulin vs. islet damage. Metformin is contra in alcoholics, so be wary of that (esp in chronic pancreatitis). Glitazones are contraindicated in CHF. Insulin can be used to manage sugar, but there is higher chance of hypoglycemic reaction in pt with islet destruction. (d/t poor glucagons response to hypoglycemia)
Risk of a parent with T1DM passing it on to their child: 3-6%<.
Nonfunctioning Pituitary Adenoma: presents w/ hypogonadism with suppressed LH and FSH levels, with increased a-subunits. May cause a prolactinoma because of compression of pituitary stalk, but is not a prolactinoma. Rx with transphenoidal surgery.
Conn’s Syndrome: Primary hyperaldosterone. Aldosterone increases Na and water absorb, and increases K excretion. Thus pt presents with polyuria, polydipsia, with hypertension and hypoK. Polyuria is d/t hypoK, since K normally helps concentrate urine. Dx with plasma aldosterone to plama rennin ratio. > 30 means too much aldosterone for the rennin. Renin is suppressed in Conn’s.
Parathyroid Diseases: PseudohypoPTH is d/t resistance of PTH on its target tissue. PTH will be high. Can be associated w/ other disease, like Albright hereditary osteodystrophy (short, round face, short 4 and 5th metacarpals).
Calcium Phosphorus PTH Vit D
PseudohypoPTH Low High High normal
hypoPTH Low High Low normal
Vit D Deficient Low Low High low
Primary HypoPTH: PTH is often high normal, but are inappropriately elevated considering how much hyperCa there is. This is b/c the inhibitory mechanism of Ca on PTH is impaired in these pt. This occurs in hyperPTH d/t adenoma or hyperplasia. Indications for parathyroidectomy include: bone mineral density score < -2.5, any complication of hyperPTH(kidney stone, bone disease), Ca > 1 above normal. Urine excretion of Ca > 400, pt younger than 50 yo, 30% decrease in creatinine clearance.
Prolactinoma: First line Rx is dopaminergic receptor agonist, regardless of how but the tumor is. Tumor size will decrease with this Rx, within days.
Post-partum bone mass loss: Most pt will lose some bone mass during first 4-6 months of postpartum, but usually regains the lost mass. Long term heparin might predispose to more bone loss. If oyu just d/c breast feeding, you can preserve or even improve bone density. This keeps Ca out of breast milk and in the bone.
Hypoglycemia + increased insulin level: insulinoma, exogenous insulin, and sulfonylura. C peptide at normal levels rules out exogenous use. If suspect sulfonylura, look at social Hx (taking the med?, health care worker with easy access?)
Glucagonoma: Has characteristic rash which is a necrolytic migratory erythema. Rash which will initially spread, then start to clear from center. Later, the rash will have borders which are elevated and crusty. Mets is common with these tumors (often to liver). Rx is surgery. Dx is confirm by measure glucagons levels.
MCC AMS in elderly: infection (UTI/pneumonia), medication, and metabolic abnormalities. Apathetic thyrotoxicosis is seen more in the elderly. Presents w/ apathy, depression, loss apetite, severe ewight loss. Dx with Thyroid function tests.
Amiodarone induced thyroid disease: hypothyroidism is the majority, but thyrotoxicosis could also happen. The thyrotoxicosis could be activation of Grave’s disease or by destructive thyroiditis. If it’s activation of Grave’s, should give methimazole or PTU. If it’s d/t destructive thyroiditis, Rx with steroids. Amiodarone can decrease the conversion of T4 to T3, leading to a apttern on TFT of elevated T4 with decreased T3.
Pituitary Incidentaloma: Just incidental pituitary tumors are common, usually innocuous. Usually these tumors remains small. If there are no clinical or lab evidence of pituitary dysfunction, can just follow with periodic MRI to make sure doesn’t get bigger. If you discover these, first do lab tests to check for hormone abnormalities. TSH, FSH/LH, free T4, IGF-1, Prolactin, dexamethasone suppression test. Subclinical thyrotoxicosis: Suppressed TSH levels with normal T4 and T3. MCC is using levothyroxine, nodular thyroid disease, Grave’s, and thyroiditis. If induced by levothyroxine, just reduce dose. If pt is asymptomatic, just recheck TSH after some time. If pt was symptomatic, consider methimazole after doing a radioactive iodine scan. Pt with multinodular goiter have 5-10%/year chance of getting symptoms, so should treat thes guys.
HypoTH, even if severe, is not a contraindication for an emergency surgery procedure. No increased mortality for hypoTH. Just higher postop risk of ileus and hypoNa.
Hyperglycemic Hyperosmolar Nonketotic state: happens in T2DM. Can be precipitated by infections and steroid use. These pt need very high doses of IV insulin d/t insulin resistance. Once blood sugar is controlled, dose of insulin needed drops a lot, and start pt on subcutaneous insulin. Afterwards, switch to regular insulin before meals, and NPH insulin as a basal level. For the periods between meals.
Incidental adrenal Masses: pretty common, just adrenal masses discovered incidentally while working up for another problem. Asymptomatic. Still, always get adrenal function tests when you see this. 24 h catecholamine, metanephrine, VMA, 17-ketosteroid, and dexamethasone suppression test. Surgery is indicated for: functional tumor, malignant tumor (has a characteristicheterogenous appearance on imaging), and all tumors > 4 cm. All other masses can be followed w/ serial abd imaging, and remove if indicated.
Nelson’s Syndrome: Clasically, presents as bitemporal hemianopsia (or other visual field defect), hyperpigmentation, and pituitary enlargement after a previous bilateral adrenalectomy for Cushing’s disease. Need to do MRI and plasma ACTH levels to Dx. If you see very high ACTH and pituitary microadenoma w/ on MRI, it’s diagnostic. The pituitary enlarges because of the loss of feedback by the adrenal steroids after the surgery. Should Rx with surgery or pituitary radiation. Probably more rare nowadays, since the preferred Rx for Cushing’s disease is now primary pituitary surgery rather than bilateral adrenalectomy.
High anion gap met acidosis: Normal anion gam is 12. MCC high AGMA is renal failure, ketoacidosis, lactic acidosis, or intoxication w/ aspirin, ethylene glycol, or methanol. Remember metformin can cause lactic acidosis, esp in elderly, or pt with heart, renal, or hepatic failure.
Toxic nodule: present w/ S/S of hyperTH, along w/ increased focal uptake in the thyroid.
MEN 1: 3 P’s. HyperPTH, pituitary tumor, and pancreatic tumor (gastrinoma). Zonger Ellision is commonly the gastrinoma, presenting w/ multiple ulcers. Should do a parathyroidectomy if pt is hyperCa. In addition, the ulcers improve a lot after the surgery
Osteoperosis: if suspected, do a bone mineral density scan (DEXA scan). T and Z scores reported. T score is compared t young healthy adults. Z score is compared to same age. T scores: normal is > 1.0. Osteopenic is between -1.0 and -2.5. < -2.5 is osteoperosis. Secondary causes of osteoperosis should also be part of workup (CBC, CMP, PTH, urinary Ca). Rx with bone specific drug treatment is recommended for all post menopause and score < -2, or < -1.5 but also have RF for fragility fractures (low bone density, hx of fracture, FH, smoking). Ca and vit D is recommended for everybody. Alendronate (decreases bone resorption) us the usual Rx.
Osteoperosis after gastric bypass: pt who have gastric bypass have malabsorption, and need higher intake of Ca and vit D to maintain homeostasis. Decreased absorption of vit D leads to low phosphorus, then a high PTH. There is increased urine phosphate loss. The high PTH maintains a normal serum Ca. Thus, should supplement diet with vit D and Ca, adjusting accordingly if needed to get to the right Ca and vit D levels.
Osteo refractory to bisphosphonates: usually, response is very good. Consider secondary causes of osteoperosis. Multiple myeloma is oen possibility. Suspect it if there is very rapid progression with multiple fractures. Other symptoms are wt loss, pallor, fatigue. Dx with serum protein electrophoresis. MEN 2: 2A is medullary thyroid cancer, pheo, and hyperPTH. 2B is the same medullray thyroid + pheo, but with GI neuroma as well as Marfanoid fatures. If you’re gonna do surgery on the medullary thyroid, remember to give a-blockers for 10-14 days before, since pt likely also has pheo. It’s MANDATORY to screen for pheo if you see the thyroid mass. If you try to do surgery without knowing the pt has pheo, VERY BAD.
If a pt has DM, other CV risk factors have to be lower than for normal ppl. Remember that DM is a CAD equivalent. Thus, Must keep LDL < 100, otherwise need a statin.
Immobilization leading to hyperCa: Usually see in pt with high bone turnover rate (adolescents and older pt with Paget’s disease). When immobilized, ther is increased bone resorption and decreased bone formation. Leads to high Ca, with low PTH. Vit D usually normal. Bisphosphonates (-dronate) are useful to prevent bone resorption.
Ca correction rule w/ albumin: For each 1 g of albumin below 4, must add 0.8 to the Ca.
Cushing’s disease: Presents w/ HTN, hyperglycemia, osteoperosis,mood swings, hypoK and met acidosis. increased urinary cortisol, non-suppressible cortisol even with high dose, and very low CATH. Indicative of an adrenal etiology. If the cause was central the ACTH would be normal or elevated. Thus, FSOM is to get CT scan of adrenals.
Management of thyroid nodule: First, get TSH. If normal, go FNA. If decreased, do a radionuclide scan to evaluate functional status. If there is a hot nodule, you can just observe since functional glands aren’t malignant.
Thyroid nodule which has normal TSH: If < 1 cm, just observe and follow w/ thyroid US annually. Do FNA if > 1 cm.
Papillary Thyroid Cancer: Rx is near total thyroidectomy. Thyroglobulin is used as a tumor marker after treatment, since it is only made by the thyroid. Prognosis for thyroid cancers usually very good (since they are generally slow growing). You can’t only od a subtotal thyroidectomy, since that way you’re unable to get accurate measurements of thyroglobulin.
Paget’s disease of bone: abnormal bone remodeling. Initially, there is excess osteoclastic bone resorption, and the replacement bone deposition starts. The bone becomes very irregular and gives a “mosaic” pattern, but basically, it’s poorly modeled and brittle. There is increased bone turnover (shown as increased alk phos: marker to follow the disease activity and response to Rx, and increased urinary telopeptide: marker of bone resorption). Nuclear bone scan also shows increased uptake. Classic present is increased hat size (don’t confuse with acromegaly). There is loss hearing loss d/t loss of bone density in cochlea. Can also present w/ stiffness nad impaired mobility in a joint. Disease is sometimes self-limited.
Rx of Paget’s: First, do serum alk phos to get idea of activity of disease. Optional is to do a full body bone scan to see which bones have been affected. Indication for Rx is bone pain, hyperCa, neuro symptom, heart failure, involvement of weight bearing bones. Asymptomatic don’t need Rx. Rx is with oral or IV bisphosphonates (-dronate). It’s more effective than calcitonin.
Celiac disease: could present w/ low vit D and iron deficiency anemia without any malabsorption symptoms. Dx with anti-endomysial and anti-tissue transglutaminase antibodies. Gold standard is small intestine biopsy.
Euthyroid Sicks syndrome: commonly see in hospitalized patients. On labs, see decreased T3 with normal T4 and TSH (low T3 syndrome). When pt recovers from the illness, the TSH will transiently go higher. No overt symptoms, maybe some fatigue. No need for levothyroxine, just repeat TFT in some weeks since should resolve spontaneously.
Management of chronic hypoPTH: Usually give high dose vit D and Ca. Try to keep Ca somewhere between 8.5 and 9. Sometimes these pt will have increased urinary Ca. If a pt has high urinary Ca and borderline low serum Ca, adding a thiazide diuretic will help to decrease urine Ca and increase serum Ca.
Indications for PTHdectomy in secondary or tertiary hyperPTH (ex in CRF) pt are: Ca > 10.5, severe hyperphosphatemia, PTH > 1000, intractable bone pain, intractable pruritis, soft tissue calcification. Iodine induced thyrotoxicosis: Could happen during coronary angiography. Presents w/ fatigue, shakiness, wt loss, palpitations. Usually self limiting once the iodine is d/c, but can persist for months. Usually refractory to antithyroid meds. B-blocker can be used for mild symptoms. If very severe, could try antithyroid meds.
Familial Hypocalciuric Hypercalcemia: same PTH/Ca/phosphorus profile as primary hyperPTH. High Ca, low phosphorus, and high PTH. Look for hypocalciuria. Typically, urine Ca is < 200. Can Rx with conservative therapy, including hydration, physical activity, and moderate Ca intake.
Exogenous thyroid: In pt who are hyperTH d/t exogenous source, their thyroglobulin will be undetectable. Thyroglobulin only comes from the thyroid gland, so exogenous TH would suppress the gland. A primary TH disease would still have thyroglobulin.
Glucocorticoid affect on normal HPA regulation: using > 3 weeks will likely start suppressing HPA axia., leading to tertiary adrenal insufficiency. Short term use (< 3 weeks) wont cause HPA distortion. They can be stopped rapidly without causing any hormonal issues.If trying to taper after long term use, one regimen is to switch to hydrocortisone, then gradually taper over a period of 1-2 months. Untreated acromegaly: 3x increase in mortality, d/t cardiovascular disease. HTN and LV dysfunction are common at time of diagnosis of acromegaly. Also various conduction defects and myocardial fibrosis. CV disease if early can actually be reversed after acromegaly is treated.
During stress, most pt have increase in insulin resistance. Thus, in a pt with DM, if they have a stress, can cause hyperglycemia. Injectible steroids usually are gone from circulation within 1 week, so might cause hyperglycemia in the meantime, but not after.
Squamous cell carcinoma of lung: can produce PTH-related proteins, leading to hyperCa. Tough to distinguish between malignancy and primary hyperPTH, but the Ca in malignancy is usually much much higher .
HyperCa: divide into PTH dependent and PTH independent. Can distinguish btw the two by measuring PTH. Thus FSOM in hyperCa is always PTH measurement.
ACEI has been shown to reduce insulin resistance. Metformin has also been shown to reduce risk of development of new onset T2DM. b-blocker and thiazides increase risk for development of DM afer prolonged use.
Sulfonylurea (chlropropamide, glyburide) OD: These can induce hypoglycemia which is severe and prolonged. D50 doesn’t work for these pt because the D50 just increases insulin secretion, causing further hypoglycemia. Octreotide is a somatostatin analogue which inhibits insulin secretion. Once you give this, the D50 can do its job.
Somatostatinoma: somatostatin is an inhibitory hormone for various hormones. Classic triad of gallstones, malabsorption, and diabetes. Cause DM by inhibiting insulin secretion. Dx is somatostatin > 160.
Hashimotos Thyroiditis: high titer of antimicrosomal (anti-TPO) antibodies. Primary hypoTH can cause various symptoms including: enlargement of tongue, ascities, increased BP, and increased cholesterol. The most common one is hyperlipidemia. Usually it’s isolated LDL elevation. Rx with levothyroxine will usually decrease cholesterol.
Graves Disease: main Rx is with radioiodine ablation. If there is already opthalmopathy, then need to also give steroids to prevent its worsening. If severe opthalmopathy is present, should defer radioactive ablation. Antithyroid meds are usually used mainly in elderly pt with htyrotoxicosis, to “cool off” the thyroid gland, since tadioactive iodine can temporarily worsen thyrotoxicosis, which elderly cant tolerate.
Thyroid storm: Main drugs used are PTU/methimazole, steroids, iodine, and b-blockers. Sometimes radioactive iodine ablation can precipitate this.
DM drugs: with renal failure, must not use metformin or gluburide. Insulin is indicated. Also look for metabolic acidosis as a reason to stop metformin.
hypoTH MUST be treated in pregnancy. Generally, the dose of levothyroxine goes up while pregnant. And check TSH more frequently, This is b/c TH is necessary for child to develop intellectually in utero.
ENT
Battery ingestion: can lead to mechanical damage, but more concerning is tissue damage d/t chemicals in battery (corrosive injury, liquefaction necrosis). Batteries lodged in the esophagus should be removed immediately with endoscopc visualization. Batteries that have made it into the stomach usually pass without complications.
Malignant otitis externa: Invasive infection of external auditory canal and bones forming the skull base. Infections starts as external otitis and progresses rapidly to involve adjacent bones at base of skull. Pt presents with otalgia and purulent drainage or discharge from the ear. Finding of granulation tissue at the floor of the bone-cartilage junction is pathognomonic. Some RF are DM, HIV, recent aural irrigation for removal of cerumen. MCC is pseudomonas aeruginosa. Thus, Rx should include ciprofloxacin, piperacillin, ticarcaillin, or ceftazidime.
Foreign body ingestion: If pt is asymptomatic and have a negative radiograph, there is no need for further Rx. In all other symptomatic pt or pt with hx of sharp object ingestion (bones, toothpicks, needles), an urgent endoscopy should be done to remove the foreign body and prevent esophageal perforation.
Meniere’s Disease: triad of periodic vertigo, unilateral hearing loss and tinnitus.
BPPV: acute vertigo attacks that are provoked by change in position. No accompanying hearing loss. MCC is canalithiasis (Ca rocks in the posterior semicircular canal). FSOM is the canalith repositioning procedure, which are maneuvers to get the rocks out of the posterior semicircular canal.
Snoring: Generally, 44% of aults have mild, habitual snoring that is unassociated with apnea and sleep interruption. OSA is present in 4% of middle aged men. OSA has severe airway resistance, with increased inspiratory effort and episode sof hypoventilation, O2 desasturation, and transient arousal from sleep. EtOH and sedative hyponotics predispose a pt to OSA, and increases severity of OSA. Pts who snore but have no other signs or symptoms of OSA should be advised to lose weight, stop smoking, and avoid alcohol near bedtime.
Recurrent Sinusitis: repeated bouts of acute sinusitis without leaving significant damage. In contrast, chronic sinusitis has more subtle and variable symptoms, associated with mucous tissue damage. Cigarette smoke and air pollution can damage cilia responsible for moving mucus through sinuses. Other causes can include chronic disorders that cause inflammation in airways (CF, Kartagener syndrome, Wegener’s granulomatosis).
Presbycusis (hearing loss associated with aging): Sensorineural hearing loss in the elderly. Progressive disease. Starts with high frequency range of hearing. Decreased ability to discriminate speech is more apparent in a noisy, distracting environment. One of the more frequent causes of social withdrawal and isolationin the elderly (must r/o dementia and depression)
Active nosebleed: can be 2/2 hot climate with low humidity or minor nasal trauma. Anterior nasal septal mucosa is the MC source of epistaxis in kids and young adults. Anterior bleding source is favored by findings of clear oropharynx while upright. Bleeding is first controlled by applying pressure with a cotton pledget impregnated with a vasoconstrictor, like phenylephrine, and a topical anesthetic like lidocaine. If these fail, nasal packing is the next step.
Acute mastoiditis: only happens as a complication of AOM. Whn the inflammatory response during AOM results in mucosla response of the mastoid air cells, and the response doesn’t clear, can lea dto mastoiditis. Pus can accumulate in the mastoid cavities. Sometimes, pus spreads further and can lead to dangerous complications like neck abscesses.
External otitis: arises 2/2 skin maceration and failure or skin cerumen barrier to provide protection. Assocaited with swimming, excess cleaning/itching of ear canal, and using of objects that occlude ear canal (headphones, hearing aid). MCC are Pseudomonas and staph aureus. Pain can be caused by tragal pressure or movement of the auricle. Rx starts with cleaning of the ear canal (healing is aided by cerumen clearing).
Glottic cancer: Stage T1 means its confined to vocal cords. T1a means its confined to one vocal cord. T2 means it extends to supraglottis or subglottis with impaired vocal cord mobility. Can present with a change I voice. Laser excision of the lesion or radiotherapy is the primary nonsurgical Rx of early stage glottic tumors.
Diphenhydramine: its sedating, so should be d/c before doing any activity that requires a high level of alertness.
Rhinitis: If after H and P, you still cant figure out a cause, the next step I snasal cytology. If you see neutrophils it means infectious cause. Eosinophils suggests that allergic rhinitis is the cause. Note that these things are not specific.
Scuba diving: MC associated condition is ear barotraumas. Use of nonsedating decongestants before diving reduces incidence of ear and sinus barotraumas by 75%. Pseudoephrine is a good choice.
