Approach to Thyroid Nodule - all patients with thyroid nodules require evaluation of serum TSH and ultrasound - any

nodule >5 mm with suspicious sonographic features (particularly microcalcifications) should undergo FNA - any nodule > cm should undergo FNA - when performing repeat FNA on initially non-diagnostic nodules! "#$-guided FNA should %e employed - nuclear scanning has minimal value in the investigation of the thyroid nodule Two Distinct Features of Primary Hypogonadism & The decrease in sperm count is affected to a greater e'tent than the decrease in serum testosterone level (& )i*ely to %e associated with gynecomastia Two Features of Secondary Hypogonadism & Associated with an equivalent decrease in sperm count and serum Testosterone (& )ess li*ely to %e associated with gynecomastia "pper to )ower ("+)) $egment ,atio is &&& - -ncr in achondroplasia! short lim% syndromes! hypothyroid! storage diseases& - .ec in /arfan0s! 1linefelter0s! 1allman0s syndromes! and testosterone def& 2olycystic 3varian $yndrome - 4A-,-AN 5 4irsutism! 4yperAndrogenism! -nfertility! -nsulin ,esistance! Acanthosis Nigricans Alcohol electrolyte a%normality 5 hypomagnesemia! hypophosphatemia! hypocalcemia! hypoglycemia! hypo*alemia meta%olic causes of constipation 6 dia%etes mellitus 6 hypothyroidism 6 hypercalcemia! hypo*alemia! uremia Vitamin 812 Deficiency Symptoms 6 /acrocytic anemia! pallor! $37! fatigue! chest pain! palpitations 6 8onfusion or change in mental status (if advanced) 6 .ecreased vi%ration sense 6 .istal num%ness and paresthesia 6 9ea*ness with "/N findings 6 .iarrhea! anore'ia .ifferential .iagnosis of Tetany - 6 4ypocalcemia 6 /eta%olic al*alosis (with hyperventilation) - 6 4ypo*alemia 6 4ypomagnesemia

Acquired Hypot yroidism! - most commonly 4ashimoto0s thyroiditis (autoimmune destruction of the thyroid) - signs and symptoms similar to hypothyroidism in adults! %ut also5 o delayed %one age! decline in growth velocity! short stature! goiter o se'ual pseudo precocity5 early se'ual development with short stature and delayed %one age o does not cause permanent developmental delay - treated with )-thyro'ine : flg#*g#d "rowt ormone deficiency - height ;<rd percentile decreased growth velocity - midline craniofacial anomalies episodes of hypoglycemia - delayed %one age! pu%erty Fro#en S oulder $Ad esi%e &apsulitis' -ncreased -ncidence of - .efinition 5 disorder characteri=ed %y progressi%e pain Adhesive 8apsulitis 6 2rolonged immo%ili=ation and stiffness of the shoulder usually resolving (most significant) spontaneously after > months 6 Female gender - /echanism 6 Age >@? yrs o primary adhesive capsulitis idiopathic! usually 6 .ia%etes mellitus (5') 6 8eiAical disc disease associated with dia(etes mellitus) may resolve 6 4yperthyroidism spontaneously in ?- > months 6 $tro*e 6 /o secondary adhesive capsulitis5 poorer outcomes 6 Trauma and surgery due to prolonged immo(ili#ation s oulder! and syndrome5 8,2$#,$. characteri=ed %y arm and shoulder pain! decreased motion and diffuse swelling following myocardial infarction! stro*e! shoulder trauma - 8linical Features
8onditions Associated with an

gradual onset (w*s to months) of diffuse s oulder pain with5 decreased acti%e and passi%e ,3/! pain worse at nig t and often prevents sleeping on affected side increased stiffness as pain su%sides5 continues for B- ( months after pain has disappeared - -NC 5 '-rays may %e normal! or may show deminerali=ation from disease - Treatment o active and passive ,3/ (physiotherapy) o N$A-.s and steroid inDections if limited %y pain o manipulation under anesthesia and early physiotherapy o arthroscopy for de%ridement#decompression o o o o 4ypocalcaemia is most commonly caused %y hypoparathyroidism! a deficiency or a%normal meta%olism of vitamin .! acute or chronic renal failure! or hypomagnesaemia& -n hypoparathyroidism! serum calcium is low! phosphate is high! and 2T4 is undetecta%leE renal function and concentrations of the (5hydro'y and !(5-dihydro'y meta%olites of vitamin . are usually normal& The features of pseudohypoparathyroidism are similar to those of hypoparathyroidism e'cept for 2T4! which is mar*edly increased& -n chronic renal failure! which is the most common cause of hypocalcaemia! phosphate is high and al*aline phosphatase! creatinine! and 2T4 are elevatedE (5-hydro'y vitamin .< is normal and !(5-dihydro'y vitamin .< is low& -n vitamin . deficiency osteomalacia! serum calcium and phosphate are low! al*aline phosphatase and 2T4 are elevated! renal function is normal! and (5-hydro'y vitamin .< is low& The most frequent artifactual cause of hypocalcaemia is hypoal%uminaemia! such as occurs in liver disease or the nephrotic syndrome& Ta%le F 4ypocalcaemic clinical features of neuromuscular irrita%ility -------------------------------------------------------------------------------2araesthesia! usually of fingers! toes! and circumoral regions Tetany! carpopedal spasm! muscle cramps 8hvoste*0s sign a Trousseau0s sign % $ei=ures of all types (i&e& focal or petit mal! grand mal or syncope) 2rolonged GT interval on H8I )aryngospasm 7ronchospasm -------------------------------------------------------------------------------a 8hvoste*0s sign is twitching of the circumoral muscles in response to gentle tapping of the facial nerve Dust anterior to the earE it may %e present in : per cent of normal individuals&

% Trousseau0s sign is carpal spasm elicited %y inflation of a %lood pressure cuff to (: mm4g a%ove the patient0s systolic %lood pressure for < min&

hypo*alemia (see Figure () - defin* normal -8 J 5:- B: J H8 J<!5-5K o serum L1MN ;<&5 mHq#)

o mild hypo*alaemia! with serum potassium in the range <&: to <&5 mmol#l! o serum potassium concentration less than (&5 mmol#l
- Approach to 4ypo*alemia o & emergency measures5 o(tain +&"E if potentially life threatening! %egin treatment immediately o (& rule out transcellular s ifts of 1M as cause of hypo*alemia o <& assess contri%ution of dietary 1M inta*e o @& (@-h 1M e'cretion or spot urine 1M and urine creatinine (calculate urine 1M#8r ratioE normal is appro'imately @)

o 5& TT," O transtu%ular potassium gradientO ("*#2*)#("3$/#23$/) o B& if renal 1M loss! chec* -P and acid!(ase status

o F& may also assess plasma renin and aldosterone levels! serum L.g2MN - 8#2 o 8A$ arrhythmias occur at varia%le levels of 1ME more li*ely if digo'in use! hypomagnesemia! or 8A. H8I changes are more predictive of clinical picture than serum L1MN

 " waves most important (low amplitude wave following a T wave) flattened or inverted T waves depressed $T segment prolongation of G-T interval Jpredispose to torsades de pointK o 1id Nephrogenic .- ma*e the collecting tu%ule resistant to A.4 O polyuria o 8N$ )ethargic irrita%ility paraesthesia 2pt encephalopathy attac*s o /$1 5 myalgia ! generali=ed wea*ness ! muscle cramps o I- 5 N and A and constipation - According to severity o Asymptomatic if mild o if severe5 with severe hypo*alemia5 2-, prolongation! wide G,$! arrhythmiasE increases ris* of digitalis to'icity Jtherefore digitalis is 8- in hypo1K muscle necrosis Jrha%domyolysisK! and rarely paralysis with eventual respiratory impairment - Treatment o treat underlying cause o if urine output and renal function are impaired! correct with e'treme caution o ris* of hyper*alemia with potassium replacement especially high in elderly! dia%etics! and patients with decreased renal function o %eware of e'cessive potassium repletion! especially if trans cellular shift caused hypo*alemia o if true 1M deficit! potassium repletion (decrease in serum L1MN of mHq is very roughly ::-(:: mHq of total %ody loss) oral sources- food! ta%lets (1-.urP)! 18l liquid solutions -A - usually 18l in saline solutions! avoid de'trose solutions (may e'acer%ate hypo*alemia via insulin release) ma'& @: mmoi+) via peripheral vein! B: mmoi+) via central vein! ma'& infusion (: mmol+h o 1M -sparing diuretics (triamterene! spironolactone! amiloride) can prevent renal 1M loss o restore /g(M if necessary %ec Jhypo1 cause hypo/gK hyper1 ,ha%domyolysis! Nausea! 2rotect heart5 HII5 2ea*ed#narrow

8alcium gluconate $hift 1M into cells5 -nsulin ,! Na48:<! sal%utamol hypo1 /eta%olic Nausea! 1-.urP! 1M serum al*alosis! insulin! vomiting! sparing L1MN diuretics! fatigue! diuretics! ;<&5 anore'ia! muscle -A solutions mHq#) sal%utamol! ry cramps Jli*e with (:-@: mHq 4yperAld tetanyK! 18- per liter constipation! over <-@ h

insulin deficiency! meta%olic acidosis

palpitations! muscle stiffness! arefle'ia

T wave! decreased 2 wave! prolonged 2, interval! widening of G,$! AA %loc*! A fi% HII5 " waves most important! flattened# inverted T waves! prolonged GT! depressed $T /ay need to restore /g(M

N3TH 5 Acidosis diminishes potassium upta*e %y cells (Ta%le ) and causes hyper*alaemia& The increase in the plasma potassium concentration is greater with meta%olic than respiratory acidosis! and occurs with hyperchloraemic %ut not with organic acid-induced forms Jfor eg lactateK of meta%olic acidosis& $timulation of insulin release %y organic acids appears to account for this divergent response! e'plaining the pathophysiology of distur%ed potassium homeostasis in dia%etic *etoacidosis& At presentation! when insulin is deficient! potassium is redistri%uted in a fashion compara%le with mineral acid-induced meta%olic acidosis and patients are hyper*alaemic& 4owever! the preceding *aliuresis (caused %y polyuria) has rendered the %ody enormously deficient in potassium! and the plasma potassium concentration falls rapidly as soon as insulin is provided! allowing potassium to return to the cells& -ndeed! dangerous hypo*alaemia can develop if adequate potassium is not given during treatment& Hyper/alemia - serum L1MN >5&: mHq#) - Approach to 4yper*alemia o & emergency measures5 o%tain H8I! if life threatening %egin treatment immediately o (& rule out factitious hyper*alemiaE repeat %lood test o <& hold e'ogenous 1M (23 and -A)! and any 1M retaining medications o @& assess potential causes of transcellular shift o 5& estimate IF, (calculate 8r8l using 8oc*croft-Iault) o B& if normal IF,! calculate TT1I O ("*#2*) #("osm#2osm)

 in setting of hyper*alemia! TT1I ;F Osuggests decreased effective aldosterone function in setting of hyper*alemia! TT1I > F O suggests normal aldosterone function

- sign and symptoms o usually asymptomatic %ut may develop symptoms o I- 5 nausea o 8A$ palpitations H8I changes and cardioto'icity (do not correlate well with serum L1MN) pea*ed and narrow T waves

 decreased amplitude and eventual loss of 2 waves prolonged 2, interval widening of G,$ and eventual merging with T wave (sine-wave pattern) AA %loc* ventricular fi%rillation! asystole o /$1 muscle wea*ness! muscle stiffness! ascending paralysis! o 8N$ 5 paresthesias! arefle0ia! o resp 5 hypoventilation o renal impaired renal ammonia!genesis and meta%olic acidosis - Treatment o acute therapy is warranted if H8I changes are present! or if patient is symptomatic o tailor therapy to severity of increase in L1MN and H8I changes L1MN ;B&5 and normal H8I treat underlying cause! stop 1M inta*e! increase the loss of 1M via urine and#or I- tract (see %elow) L1MN %etween B&5 and F&:! no H8I changes5 add insulin to a%ove regimen L1MN >F&: and#or H8I changes5 first priority is to protect the heart! add calcium gluconate to a%ove o & 2rotect the 4eart calcium gluconate -( amps ( : m) of :Q solution) -A antagoni=es cardiac to'icity of hyper*alemia! protects cardiac conduction system! no effect on serum L1MN onset within minutes! lasts <:-B: min o (& $hift 1M into 8ells regular insulin (-nsulin ,) :-(: units -A! with -( amp .5:9 (give .5:9 %efore insulin) onset of action 5-<: min! lasts -( h monitor capillary %lood glucose q h %ecause of ris* of hypoglycemia can repeat every @-B h Na48:< -< amps (given as < amps of F&5Q or >&@Q Na48:< in ) .59) onset of action 5-<: min! transient effect! drives 1M into cells in e'change for 4M more effective if patient has meta%olic acidosis

 R(-agonist (AentolinP) in ne%uli=ed form (dose O ( cc or : mg inhaled) or :&5 mg -A onset of action <:-?: min! stimulates NaM#1M AT2ase caution if patient has heart disease as tachycardia may result from this high dose of R agonist o <& Hnhance 1M ,emoval from 7ody via urine (preferred approach) furosemide (S@: mg -A)! may need -A N$ to avoid hypovolemia fludrocortisone (synthetic mineralocorticoid) if suspect aldosterone deficiency via gastrointestinal tract cation-e'change resins5 calcium resonium or sodium polystyrene sulfonate (1aye'alateP) (increasingly falling out of favor due to ris* of colonic necrosisE wor*s %y %inding NaM in e'change for 1M! and controversial how much 1M is actually removed - main %enefit may %e the diarrhea it causes) plus lactulose 23 to avoid constipation (must ensure that patient has a %owel movement after resin is administered ) 1aye'alateP enemas with tap water (and definitely not with sor%itol as rectal sor%itol can cause colonic necrosis) dialysis (renal failure! life threatening hyper*alemia unresponsive to therapy) hyper1 ,ha%domyolysis! insulin deficiency! meta%olic acidosis hypo1 serum L1MN ;<&5 mHq#) /eta%olic al*alosis! insulin! diuretics! anore'ia! sal%utamol! Nausea! palpitations! muscle stiffness! arefle'ia Nausea! vomiting! fatigue! muscle cramps 2rotect heart5 8alcium gluconate $hift 1M into cells5 -nsulin ,! Na48:<! sal%utamol 1-.urP! 1M sparing diuretics! -A solutions with (:-@: mHq 18per liter over <-@ h HII5 2ea*ed#narrow T wave! decreased 2 wave! prolonged 2, interval! widening of G,$! AA %loc*! A fi% HII5 " waves most important! flattened# inverted T waves! prolonged GT! depressed $T /ay need to restore /g(M

4ypern -nadequate 4(: atremia inta*e

Hyponatremia

(elderly#disa%led or
inappropriate excretion of H(: (diuretics! )i M .l) Hypo-osmolar ldilutional e.g. .H/, cirrhosis, ascites' and hyperosmolar *usually glucose' Hyper-89H and malignancy account for approx. :+7 of cases

Lethargy, weakness, irritability, and edema. Seizures and coma occur with severe elevations of Na levels !" #$% mmo&L' 0cute1 Neurologic symptoms (2 to cerebral edema, headache, decreased L34, depressed reflexes ;ultisystem including .&S, 4l *groans', renal<stones', rheumatological. ;S= *bones', psychiatric *moans' Laryngospam, hyperreflexia, parasthesia, tetany, .hvostek2s and 9rousseau2s sign

Salt restrict and give free water

No more then #( mmo&L in () h drop in Na *+.$ mmo&L,h' due to risk of cerebral edema, seizures, death

5ater restrict 0cute1 correct rapidly 67 Na.! #-( cc,kg,h .hronic1 !& NS furosemide !sotonic saline furosemide if hypervolemic >isphosphonates, dialysis, chelation l?390 or oral phosphate' 0cute lionized .a( A+.B m;' re@uires immediate treatment1 !& calcium gluconate #-( g in # +(+ min followed by slow infusion

Limit total rise to % mmo&L in () h *+.$ mmo&L,h maximum' as patients are at risk of central pontine myelinolysis

Hypercalcemi a

8atients with more severe or symptomatic hypercalcemia are usually dehydrated and re@uire saline hydration as initial therapy 8rolonged GT interval can arise leading to arrhythmia as can upper airway obstruction

Hypocalcemia

!atrogenic, low ;g( , liver dysfunction, #2 hypo-89H

hypo/ g serum magne sium ;:&F: mmol+ ) ( &F mg#d))

I- losses 6 starvation# mala%sorption 6 vomiting#diarrhea 6 alcoholism 6 acute pancreatitis 6 e'cess renal loss 6 (T hyperald due to cirrhosis and 84F 6 hyperglycemia 6 hypo*alemia 6 hypercalcemia 6 loop and thia=idetype diuretics 6 nephroto'ic medications 6 proton-pump inhi%itors

sei=ures! paresis! 8hvoste* and Trousseau signs! H8I changes (widened G,$! prolonged 2,! T-wave a%normalitie s)

6 treat underlying cause 6 /g(M -/#-AE cellular upta*e of /g(M is slow! therefore repletion requires sustained correction 6 discontinue diuretics in patients requiring diuretics! use a 1M -sparing diuretic to minimi=e magnesuria

How often s ould you follow up on a patient wit newly diagnosed ypot yroidism1
+V2D+3&+!-AS+D A3S4+5 $i' to > wee*s after the start of levothyro'ine therapy you should ree'amine patients and measure their serum thyroid-stimulating hormone (T$4) (strength of recommendation L$3,N5 &! common practice and e'pert opinion)& -f thyroid function is normal at that time! e'amine the patient and measure serum T$4 again in @ to B months %ecause clearance of levothyro'ine increases in the euthyroid (normal) state ($3,5 &! e'pert opinion)& 3nce the proper maintenance dose of levothyro'ine is achieved! evaluate the patient and o%tain a serum T$4 at least annually! or as clinically indicated ($3,5 &! e'pert opinion)& +%idence summary There is very little patient-oriented research to help answer this question& Airtually all of the literature is %ased on %ench research and e'pert opinion& 4ait at least 6 wee/s to follow up after starting t erapy $erial serum T$4 measurements are adequate to follow adults with newly diagnosed! uncomplicated primary hypothyroidism& 4owever! serum thyroid hormone levels normali=e %efore serum T$4& $erum thyroid hormone concentrations increase first! then the T$4 secretion falls %ecause of the negative feed%ac* action of levothyro'ine on the pituitary and hypothalamus& )evothyro'ine has a -wee* plasma half-lifeE a steady state is achieved a%out B wee*s (B half-lives) after the start of treatment or a change in dose& The T$4 level should! therefore! %e evaluated no earlier than B wee*s after initiating therapy or adDusting levothyro'ine dosage& !( The full effects of thyroid hormone replacement on the T$4 level may not %ecome apparent until > wee*s of therapy&< FAST T5A&, Patients older t an 67 years must (e monitored annually to a%oid o%erreplacement & ec/ TSH 8 to 6 mont s after initial follow!up -f the initial dose doesnUt require adDustment! reevaluate the patient and measure serum T$4 again in @ to B months %ecause levothyro'ine clearance can increase after the euthyroid state is esta%lished&@ -f a dosage change is needed! ma*e adDustments every B wee*s! %ased on serum T$4 values! until T$4 values return to the reference range& $uccessful treatment reverses all the signs and symptoms of hypothyroidism! although some neuropsychologic and %iochemical a%normalities! such as depressed mood and lipid a%normalities! may persist for several months& < .onitor sta(le patients annually) especially t e elderly

H'amine the patient and measure serum T$4 annually after identifying the proper maintenance dose! more often if an a%normal result or a change in the patientUs status occurs&( 8ertain situations such as pregnancy! initiation of new medications! or liver or *idney disease may require more frequent monitoring& Ienerally! once a sta%le maintenance dosage of levothyro'ine is achieved! the dosage will remain adequate until the patient has a significant weight change or reaches his or her seventh or eighth decade& Although monitoring less often than once a year can %e Dustified in younger adult patients whose weight is sta%le! patients older than B5 years must %e monitored annually to avoid overreplacement& 9ith age! thyroid %inding may decrease! and the serum al%umin level may decline& This can result in a (:Q reduction in the dose of levothyro'ine required&5!B 5ecommendations The American Association of 8linical Hndocrinologists (AA8H) recommends reassessment and repeat la% wor* at least B wee*s after any change in levothyro'ine %rand or dose& The AA8H practice guidelines suggest follow-up with appropriate interim history! physical e'am! and pertinent la% studies at B months! and then annually after the T$4 level has normali=ed&F ---------2nfections in patients wit dia(etes mellitus* A re%iew of pat ogenesis &93&:;S293S -nfectious diseases are more prevalent in individuals with ./& The main pathogenic mechanisms are5 hyperglycemic environment increasing the virulence of some pathogensE lower production of interleu*ins in response to infectionE reduced chemota'is and phagocytic activity! immo%ili=ation of polymorphonuclear leu*ocytesE glycosuria! gastrointestinal and urinary dysmotility& http5##www&nc%i&nlm&nih&gov#pmc#articles#2/8<<5@?<:#