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MANAGEMENT OF PATIENTS
https://t.me/medicina_free
WITH RENAL DISEASES
Samir Singh, Mark A. Oghalai
CHAPTER 19
1. What are the six main functions of the kidney?
1. Elimination of metabolic waste (foreign substances, drugs, urea, uric acid)
2. Maintenance of fluid balance
3. Maintenance of electrolyte balance
4. Maintenance of acid and base balance
5. Endocrine and metabolic functions (erythropoietin secretion and vitamin D conversion)
6. Regulation of blood pressure
2. What are the three basic processes that take place in the nephron (functional unit
of the kidney)?
Filtration, reabsorption, and secretion.
3. Which compound is used as a sensitive, indirect measurement of glomerular
filtration rate (GFR)?
Creatinine is a natural product of the body (breakdown product of creatinine phosphate found in
muscle). It is used because it is freely filtered by the glomeruli and minimally secreted by peritubular
capillaries. It can result in an overestimation of GFR by 10% to 20%, which is clinically acceptable.
4. What is renal failure?
Renal failure is defined as impairment in renal function, as measured by the GFR. It is classified as
either acute or chronic.
5. What is acute renal failure (ARF) or acute kidney injury (AKI)?
This syndrome is characterized by sudden decline in renal function, resulting in retention of nitrog-
enous waste with corresponding elevations of serum creatinine (relative increase of 50% or absolute
increase of 0.5 to 1.0 mg/dL) and blood urea nitrogen (BUN).
6. What is the RIFLE criteria?
It is one method of staging AKI.
Risk: 1.5-fold increase in serum creatinine or GFR decrease by 25% or urine output <0.5 mL/kg/hr for
6 hours
Injury: Twofold increase in serum creatinine or GFR decrease by 50% or urine output <0.5 mL/kg/hr
for 12 hours
Failure: Threefold increase in serum creatinine or GFR decrease by 75% or urine output <0.5 mL/kg/
hr for 24 hours or anuria for 12 hours
Loss: Complete loss of kidney function (requiring dialysis) for more than 4 weeks
End-stage renal disease: Complete loss of kidney function (requiring dialysis) for more than 3 months
7. What are the major classes of ARF/AKI?
• Prerenal. Renal blood flow decreases enough to lower the GFR, which leads to decreased clear-
ance of metabolites (BUN, creatinine, uremic toxins). This class is the most common type and is
associated with insufficient renal perfusion. Examples include hypovolemia, hypotension, impaired
cardiac function (CHF), cirrhosis and hepatorenal syndrome, decreased renal perfusion with concomitant NSAID, ACE inhibitor, and/or cyclosporine use, and sepsis. It is potentially reversible.
• Renal. Kidney tissue is damaged such that glomerular filtration and tubular function are signifi-
cantly impaired. The kidneys are unable to concentrate urine effectively. Glomerular diseases (acute
glomerulonephritis, Goodpasture’s syndrome, Wegener’s granulomatosis, poststreptococcal glomerulonephritis, lupus), acute tubular necrosis (ischemic AKI, nephrotoxic AKI), and acute interstitial
nephritis (allergic interstitial nephritis) fall under this classification.
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• Postrenal. Least common cause of AKI. Obstruction of any segment of the urinary tract causes
increased tubular pressure that leads to decreased GFR. Urine is produced but cannot be
excreted. Benign Prostate Hypertrophy is the most common cause of urethral obstruction.
Other possible causes include nephrolithiasis, neoplasm, retroperitoneal fibrosis and ureteral
obstruction.
8. What is FENa? How is it used to determine which type of ARF/AKI is present?
Fraction of excreted sodium (FENa) is the percentage of sodium filtered by the kidney that is excreted
in urine. It is calculated as follows:
[(Urine Na)/(Plasma Na)/(Urine creatinine)/(plasma creatinine)] × 100
FENa below 1% suggests prerenal etiology. FENa above 2% to 3% suggests ATN or other kidney
damage.
9. What are some of the urinalysis findings in ARF/AKI?
• Prerenal:benignsediment,fewhyalinecasts,absenceofproteinandblood
• Renal:
• ATN: muddy-brown casts, renal tubular cells/casts, granular casts, trace protein, absence
• Acute glomerulonephritis: dysmorphic RBCs, RBCs with casts, WBCs with casts, fatty casts,
• Acute interstitial nephritis: RBCs, WBCs, WBCs with casts, eosinophils, 1+ protein, 2+ blood
• Postrenal:benign,mayormaynotseeRBCs,WBCs,absenceofproteinandblood
10. How is ARF/AKI managed?
General measures include avoiding medications that decrease renal blood flow, adjusting medication
• Prerenal:Treattheunderlyingdisorder,givenormalsalinetomaintaineuvolemiaandrestoreblood
• Renal:Supportivetherapy.Removeoffendingagent/cause.Ifpatientisoliguric,atrialoffurosemide
• Postrenal:Abladdercathetermaydecompresstheurinarytract.
11. What is chronic renal failure (CRF) or chronic kidney disease (CKD)?
It is defined as either decreased kidney function (GFR <60 mL/min) or kidney damage (structural
12. What are the stages of CRF/CKD?
There are five stages that are defined by the estimated GFR. Therapy is guided by the stage of CRF/
13. What are some causes of CRF/CKD?
• Diabeticnephropathy(mostcommoncause,30%ofallcases)
• Hypertension(25%ofcases)
• Chronicglomerulonephritis(15%ofcases)
• Interstitialnephritis,polycystickidneydisease,obstructiveuropathy
• UntreatedARF/AKI
14. What are the clinical manifestations of CRF and end-stage renal disease (ESRD)?
The clinical manifestations of CRF and ESRD depend on the stage of the disease and include:
• Fluidandelectrolytedisturbances(hyperkalemiaduetodecreasedurinarysecretion,hypermagne-
• Peripheralneuropathy
of blood
4+ protein, 3+ blood
doses for level of renal function, correcting fluid imbalance, correcting electrolyte abnormalities, and
optimizing cardiac output.
pressure, stop antihypertensive medications, and give dialysis if symptomatic uremia, intractable
acidemia, hyperkalemia, or volume overload develops.
may help increase urine flow.
or functional) for at least 3 months regardless of cause. CRF/CKD is an irreversible, advanced, and
progressive renal insufficiency.
CKD.
Stage 1 (normal): GFR 90 mL/min
Stage 2: GFR 60 to 89 mL/min
Stage 3: GFR 30 to 59 mL/min
Stage 4: GFR 15 to 29 mL/min
Stage 5: GFR <15 mL/min
semia due to reduced urinary loss, hyerphosphatemia)
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• Hypertensionandpericarditis
• Anemiaandthrombocytopenia(duetouremia,plateletsdonotdegranulateinuremicenvironment)
• Uremiaanduremicosteodystrophy
• Nauseaandvomiting
• Tirednessandinsomnia
• Pruritusandhyperpigmentation
• Sexual/reproductivesystemdisturbances(decreasedtestosteroneinmen;amenorrhea,infertility,
and hyperprolactinemia in women)
15. How is CRF/CKD managed, and what are some complications?
Dietary restrictions (low protein, low salt, restricted potassium magnesium and phosphate intake),
ACE inhibitors (dilate efferent arteriole of glomerulus), control of BP, glycemic control, correction of
electrolyte and acid/base abnormalities, supplementation with oral calcium and vitamin D to prevent
secondary hyperparathyroidism, management of pulmonary edema (diuretics and dialysis).
Life-threatening complications of CRF/CKD include hyperkalemia, pulmonary edema (from
volume overload), and infection (pneumonia, urinary tract infection, sepsis).
16. What are the main treatment options for ESRD?
• Peritonealdialysis
• Hemodialysis
• Renaltransplant
17. What are the absolute indications for dialysis?
Absolute indications can be remembered by the mnemonic AEIOU:
A: Acidosis that is intractable and severe
E: Electrolyte disturbances that are persistent
I: Intoxications (methanol, eythylene glycol, lithium, aspirin, NSAIDs)
O: Overload (hypervolemia) unmanaged by other therapy
U: Uremia (severe)
18. What is secondary hyperparathyroidism?
As the kidneys lose their ability to convert vitamin D, intestinal absorption of calcium decreases, caus-
ing hyperparathyroidism.
19. What are the oral manifestations of renal disease?
Patients with renal disease or CRF often demonstrate orofacial signs and symptoms that are not
necessarily specific for ESRD but are related to the systemic manifestations of the disease. The most
common of these manifestations are:
• Enamelhypoplasiaandstainingofteeth
• Halitosisandmetallictaste
• Stomatitisandxerostomiasecondarytouidintakerestriction
• Gingivalbleeding,ecchymosis,petechiae,andpaleandinamedgingiva
• Osteolyticbonedefectsinthemandible,mandibularcondyles,andmaxilla;lossoflaminadura;and
decreased trabeculation of bone
• Skeletalfacialdeformitiessecondarytoalteredgrowth
• Accelerateddentalcalculusaccumulation
20. What are the lab findings in patients with CRF/CKD?
• ElevatedBUNandcreatinineresultingfromdecreasedglomerularltration
• Metabolicacidosissecondarytoimpairedtubularfunction,causinganaccumulationofammonia
• Multipleelectrolyteabnormalities,includinghyperkalemia,hypocalcemia,andhypermagnesemia
• Anemiafromdecreasedrenalproductionoferythropoietin
• Thrombocytopenia(duetouremia)
21. How does renal disease affect the pharmacodynamics of administered drugs?
The effects of drugs may be potentiated by increased volume of distribution, decreased protein bind-
ing, and decreased glomerular filtration and renal tubular secretion. Renal failure may modify drug
bioavailability, distribution, pharmacologic action, or elimination when the kidney excretes the drug or
its metabolites. For the ESRD patient, most drugs are administered in an initial loading dose to provide
therapeutic blood concentrations. Sustained effects are controlled by dosage adjustments and timeinterval alterations and are based on serum drug levels.
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22. How do nonsteroidal antiinflammatory drugs (NSAIDs) affect renal function?
NSAIDs inhibit prostaglandin synthesis and, therefore, decrease prostaglandin-associated intrinsic
renal vasodilatation. The net result is renal afferent arteriole constriction and eventual decrease in
renal perfusion pressure.
23. What classes of drugs should be avoided in patients with renal disease?
• Nephrotoxicdrugs,includingNSAIDs,aminoglycosides,andintravenous(IV)dyes
• Drugsthatareconvertedtotoxicmetabolites,includingmorphine,meperidine,andpropoxyphene
• Drugsthatcontainexcessiveelectrolytes,includingpenicillinGandmagnesiumcitrate
24. What analgesics should be avoided in patients with renal disease?
• Aspirin
• Acetaminophen
• NSAIDs
• Meperidine(accumulationofmeperidinecanresultinseizures)
• Morphine(dosedecreasedsecondarytoaccumulationofmorphine-6-glucuronide)
25. What antibiotics should be avoided in patients with renal disease?
• Cephalosporins
• Tetracycline
• Erythromycin
• Aminoglycosides
26. In severe renal dysfunction patients, are metabolic end products from local
anesthetics contraindicated?
No. Local anesthetics are metabolized in the liver and plasma and then excreted. Therefore anesthet-
ics can accumulate and not be a factor in patients with renal disease.
27. What effect might general anesthetics have on renal blood flow and GFR?
General anesthetics that can cause myocardial depression also can cause decreased renal blood flow
and a GFR that is proportional to the depth of anesthesia. Methoxyflurane is no longer in use because
of fluoride-induced nephrotoxicity. Halothane, enflurane, and isoflurane produce much lower fluoride
levels and are safer to use with regard to nephrotoxicity. Therefore, it is important to choose the type
of agent and the appropriate level of anesthesia in renal failure patients to minimize further injury and
likelihood of renal failure.
28. What is Compound A? Which volatile anesthetic produces it?
Compound A (trifluoroethyl vinyl ether) is produced from the breakdown of sevoflurane. It is nephro-
toxic with prolonged exposure and low fresh gas flows (<2 L/min). The package insert recommends
fresh gas flows >2 L/min.
29. Which metabolites from halogenated general anesthetics can lead to nephrotoxic
renal failure?
Inorganic fluoride from the metabolism of methoxyflurane. Sevoflurane also increases inorganic
fluoride, and its use is controversial in patients with renal disease.
30. Which halogenated general anesthetics do not significantly increase plasma inor-
ganic fluoride concentrations?
Isoflurane, halothane, and desflurane.
31. At what time before and after surgery should dialysis be performed?
One day before surgery and 1 to 2 days after surgery to correct potassium and fluid balance while
minimizing bleeding complications.
32. What lab tests should be performed for renal failure patients before surgery?
CRF patients should have bleeding time, prothrombin time (PT), partial thromboplastin time (PTT),
platelet count, complete blood cell count (CBC), and a basic metabolic panel (BMP). Bleeding time is
the most sensitive test for a bleeding tendency in CRF patients. If the bleeding time is elevated, the
patient should receive vigorous dialysis and, if necessary, deamino-d-argininevasopressin(DDAVP)
intravenously or nasally, at a dose of 0.3 μg/kg, 30 minutes before surgery. Hyperkalemia also can
be corrected with preoperative dialysis. If surgery is emergent and dialysis cannot be performed
preoperatively, hyperkalemia should be treated aggressively to decrease the arrhythmogenic effect
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ofhyperkalemia.ThiscanbedonebyIVinfusionofcalciumchloridetostabilizethemyocardium,
glucose to prevent hyoglycemia, and insulin to drive potassium intracellularly.
33. What is the cause of CRF-induced anemia?
Decreased erythropoietin production from the kidneys.
34. What is the treatment for CRF-induced anemia before surgery?
Anemia in CRF patients should be treated with administration of recombinant human erythropoietin
until the patient’s hematocrit is raised to at least 30% to 33%.
35. What is the difference between peritoneal dialysis and hemodialysis?
In peritoneal dialysis, a hypertonic solution is placed into the peritoneal cavity via an implanted cath-
eter or a temporary catheter, and removed a short time later. The peritoneum serves as the dialysis
membrane. During the removal process, dissolved solutes such as urea are drawn out. Peritoneal
dialysis does not require anticoagulation, the patient can learn to perform dialysis on his or her
own, and it is less expensive than hemodialysis. However, peritoneal dialysis requires more frequent
sessions than hemodialysis, is less effective, and has a higher incidence of complications such as
infection, hyperglycemia, hypertriglyceridemia, peritonitis, hypoglycemia, and protein loss. The most
common use for peritoneal dialysis is the treatment of patients with ARF/AKI.
Hemodialysis is the most commonly used method of dialysis for CRF/CKD/ESRD and is
performedat2-to3-dayintervals.Surgicalplacementofapermanentarteriovenous(AV)stula
forlarge-borecannulationisrequired;thepatient’sbloodislteredthroughadialysismachineand
returnedtothepatientviatheAVstula.Administeringheparinpreventsclotting.Hemodialysismay
also be performed through a central line dialysis catheter or a tunneled central line dialysis catheter.
Hemodialysis is considered to be more efficient than peritoneal dialysis and shortens the time of dialy-
sis.PatientsreceivinghemodialysisareatriskforcontractinghepatitisB,hepatitisC,andHIVbecause
of multiple blood exposures. They may be predisposed to developing hypotension due to rapid removal
of intravascular volume and hypo-osmolality due to solute removal. In addition, these patients are at
riskforinfectionoftheirAVshunts,whichpredisposesthemtosepticemboli,septicemia,infective
endarteritis, and infective endocarditis.
Alternativestotraditionalhemodialysisincludecontinuousarteriovenoushemodialysis(CAVHD)
andcontinuousvenovenoushemodialysis(CVVHD).Theseareoftenusedinhemodynamicallyunstable
patients with ARF/AKI. Lower flow rates of blood and dialysate enable dialysis to occur while minimizing rapid shifts in volume and osmolality.
36. What steps should be taken before surgical procedures in ESRD patients?
• Reviewlabvaluestodetectpossiblebleedingdiathesis(bleedingtime,plateletcount,PT,PTT)and
electrolyte abnormalities.
• Monitorbloodpressure.
• Avoidnephrotoxicdrugssuchasacyclovir,aspirin,NSAIDs,andhigh-doseacetaminophen.
• Decreasedosageofdrugsmetabolizedbythekidney.
• Aggressivelymanageorofacialinfections.
• Ensurethatpatientsreceivinghemodialysisdonotundergosurgeryforatleast4hoursafterhemo-
dialysis to avoid heparin-induced bleeding.
37. What pre-surgical adjustments need to be made in drug dosing or interval in
patients with CRF?
See Table 19-1.
38. What medical considerations should be given to patients receiving dialysis before
oral surgical procedures?
No adjustments are required for patients receiving peritoneal dialysis, but there are several concerns
for patients receiving hemodialysis. Surgically created bacteremia can cause infection of the
AVstula.Becausegraftendothelializationtakesupto3to6monthsafterplacement,standard
American Heart Association antibiotic prophylaxis is strongly recommended for the first 6 months
after fistula placement and may be beneficial for all graft patients undergoing oral surgery. The arm
thatcontainstheAVshuntshouldnotbeusedforbloodpressurerecordingbecausetheshuntcould
collapse.Likewise,IVadministrationofmedicationsshouldbeavoidedinthearmbecauseclot
formationcouldjeopardizetheshunt.ThequalityoftheAVthrillshouldbeassessedinitiallyandthen
periodically during surgery. During long surgeries, the use of a circulating heating pack over the arm
is advocated.
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Table 19-1. Pre-surgical Drug Adjustments Made in Chronic Renal Failure
Patients
DRUG PRE-SURGERY ADJUSTMENT
Aspirin Increase interval between doses and avoid drug
completely if glomerular filtration rate is low
Acetaminophen Increase interval between doses and avoid drug
completely in cases of severe failure
PenicillinV,cephalexin,tetracycline Increase interval between doses in severe failure
Ketoconazole Reduce dose
Lidocaine, codeine, erythromycin, clindamycin,
No adjustment necessary
metronidazole
Patients should be screened for bleeding tendencies because hemodialysis destroys platelets.
Surgery should be delayed for at least 4 hours after hemodialysis to prevent heparin-induced bleeding.
PatientsshouldbescreenedperiodicallyforhepatitisB,hepatitisC,andHIV.Universalprecautions
should be followed by the surgical team when treating any patient undergoing hemodialysis. The
positioning of the access site must be observed during surgery to avoid pressure on the site.
39. What physical finding is associated with a functioning AV fistula?
Palpable thrill due to high-velocity flow.
40. How are bleeding problems prevented and managed in patients with renal failure?
Bleeding encountered in patients with renal failure is best managed initially with local hemostatic
procedures, such as good surgical technique, primary wound closure, hemostatic agents and topical
thrombin,andelectrocautery.PreoperativeIV(0.3μg/kg) or intranasal (3.0 μg/kg)DDAVPtemporarily
corrects the increase in bleeding time in uremic patients for up to 4 hours. It also may be useful as
a therapeutic modality in acute postsurgical hemorrhage. Cryoprecipitate has a peak effect in 4 to
12 hours and duration of 24 to 36 hours but generally is reserved for acute bleeding that is not easily
managed. Conjugated estrogen, which has a duration of up to 30 days and peak effects in approximately 2 to 5 days, also may be used.
BiBliography
Agabegi SS, Agabegi ED, Ring AC: Step-up to medicine, ed 3, Baltimore, 2013, Lippincott Williams & Wilkins.
Bennett WM, Muther RS, Parker RA, et al.: Drug therapy in renal failure: dosing guidelines for adults. Part I: antimicrobial
agents, analgesics, Ann Intern Med 93:62–89, 1980.
Carl W, Wood RH: The dental patient with chronic renal failure, Quintessence Int 7:9–15, 1976.
Cooper DH, Krainik AJ, Lubner SJ, Reno HE, Micek ST: Washington manual of medical therapeutics, ed 32, St Louis, 2007,
Lippincott Williams & Wilkins.
Duke J: Renal function and anesthesia. In Duke J, editor: Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.
Little JW, Falace DA: Chronic renal failure and dialysis. In Little JW, Falace DA, editors: Dental management of the medi-
cally compromised patient, ed 6, St Louis, 2002, Mosby.
Oghalai MA: Renal patient. In Abubaker AO, Benson KJ, editors: Oral and maxillofacial surgery secrets, ed 2, Philadelphia,
2007, Mosby/Elsevier.
Silverstein KE, Adams MC, Fonseca RJ: Evaluation and management of the renal failure and dialysis patient, Oral Maxillofac
Surg Clin North Am 10:417–427, 1998.
Silverthorn DU: Human physiology: an integrated approach, ed 4, San Francisco, 2007, Benjamin Cummings.
Stoelting RK, Dierdorf SF: Renal disease. In Stoelting RK, Dierdorf SF, editors: Anesthesia and co-existing disease, ed 3,
London, 1993, Churchill Livingstone.
Stoelting RK, Miller RD: Renal disease. In Stoelting RK, Miller RD, editors: Basics of anesthesia, ed 3, Philadelphia, 1994,
Churchill Livingstone.
Swell SB: Dental care for patients with renal failure and renal transplants, J Am Dent Assoc 104:171–177, 1982.
Westbrook DS: Dental management in patients receiving hemodialysis and kidney transplants, J Am Dental Assoc
96:464–468, 1978.
ZiccardiVB, Saini J, Demas PN, et al.: Management of the oral and maxillofacial surgery patient with end-stage renal
disease, J Oral Maxillofac Surg 50:1207–1212, 1992.
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TO PATIENTS WITH ENDOCRINE
DISEASES AND THE PREGNANT
CHAPTER 20
PATIENTS
Sidney Eisig, Vincent Carrao
MANAGEMENT CONSIDERATIONS TO PATIENTS WITH
ENDOCRINE DISEASES
1. What is the embryologic migratory path of the thyroid gland?
The thyroid gland develops during the third week of gestation and courses down a path along the
thyroglossal duct originating from the floor of the primitive pharynx. This holds particular interest for
oral and maxillofacial surgeons due to the fact that it is possible to trap ectopic thyroid tissue at the
base of the tongue and/or generate thyroglossal duct cysts along its migratory path.
2. What is the role of iodine in thyroid function?
Iodine is crucial for thyroid function; iodine is bound to albumin in the blood and is readily and
efficiently taken up by the thyroid. The iodine is then used to synthesize thyroid hormone. Without
iodine availability there would be no production of thyroid hormone.
Dietary intake of iodine is therefore crucial for thyroid function and homeostasis. The most com-
mon cause of hypothyroidism is due to poor dietary intake of iodine.
3. What is Hashimoto’s thyroiditis?
Hashimoto’s thyroiditis is a form of hypothyroidism caused by an autoimmune process. The
autoimmune process produces atrophy of the thyroid follicles due to large infiltrates of lymphocytes
producing germinal centers.
The result is a decrease in thyroid hormone production, and therefore an increase in thyroid
stimulating hormone (TSH) expression from the anterior pituitary attempting to stimulate the
nonfunctional atrophic thyroid follicles.
4. What is the relationship between T3 and T4?
T4 is more abundant than T3. T4 is converted to T3 by the converting enzyme deiodinase (I, II, or III).
T4 and T3 are bound by various proteins in the blood. The unbound hormone in the blood regulates
the expression of TSH that stimulates the thyroid gland to secrete thyroid hormone. Although there
is less T3 production compared to T4, T3 has a much greater receptor affinity at the various tissue
receptors, and thus greater systemic effect.
5. What is thyrotoxicosis?
Thyrotoxicosis is a state of excess thyroid hormone; hyperthyroidism is defined as an increase in
thyroid function. They are often associated with one another but not always.
Graves disease is the most common form of thyrotoxicosis.
6. What are the signs and symptoms of thyrotoxicosis?
Some of the common signs of thyrotoxicosis are increased weight loss, nervousness, hyperactivity,
irritability, hyperreflexia, sinus tachycardia, osteopenia, and atrial fibrillation.
Some of the common symptoms include warm skin, sweating, heat intolerance, fine hair, alopecia, oligomenorrhea, amenorrhea, diarrhea, and eyelid retraction (proptotic appearance).
7. What lab thyroid function test and findings characterize sick euthyroid syndrome?
Sick euthyroid syndrome is a euthyroid condition common in the critically ill patient. It is due to exces-
sive conversion of thyroxine (T4) to reverse triiodothyronine (rT3) instead of its more potent isomer, T3,
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and possibly hypothalamic suppression of TSH. These patients are clinically euthyroid. Lab findings
include a normal to low TSH, low to normal T4, and low free T4 index. Direct free T4 by equilibrium
dialysis, however, is normal. Reverse T3 is high, and T3 is low.
8. What common postoperative complication is associated with subclinical
hypothyroidism?
Significant respiratory suppression with inability to wean from a respirator can be seen in patients
who have even mild untreated hypothyroidism that is otherwise asymptomatic. Thyroid function tests
alone may be needed to make this diagnosis. Preoperative TSH is the best screening test. This test
would be elevated even in mild hypothyroidism.
9. What is the most common cardiac arrhythmia present in the elderly with
hyperthyroidism?
Hyperthyroidism in the elderly may be of the clinical form or the apathetic form. In the latter, patients
rarely present with classic signs and symptoms, such as anxiety, sweating, weight loss, or palpitations. Rather, they may present with depressed mood or somnolence, cognitive impairment, or poor
appetite. A TSH that is suppressed is the most sensitive indicator of hyperthyroidism. Even patients
who are elderly and symptomatic are at a significantly increased risk for cardiac arrhythmia—most
commonly atrial fibrillation.
10. What is the function of the parathyroid hormone (PTH)?
The parathyroid gland is made up of four separate glands that are anatomically positioned behind the thy-
roid. The function of the parathyroid is to regulate serum calcium balance. The system for which calcium
balance is achieved results from PTH release related to calcium levels. PTH acts upon the bone, kidneys,
and gastrointestinal tract. In the example of calcium deficiency, PTH will be released to allow for increased
bone resorption, decreased renal excretion of calcium, and increased dietary absorption of calcium.
A common cause of hypercalcemia is hyperparathyroidism.
11. What is the significance of hypercalcemia?
Hypercalcemia can cause a short QT interval, arrhythmias, nausea, vomiting, fatigue, constipation, and
renal tubular defects.
Hypercalcemia is a significant finding on routine laboratory testing. It is most often caused by hyper-
parathyroidism, but it is important to rule out a malignancy associated with an increase in serum calcium.
12. What is calcitonin?
Calcitonin is a hormone mostly produced by the thyroid gland. It is somewhat of an antagonist to PTH due to
its prevention of osteoclastic activity. This activity plays little to no role in calcium homeostasis in humans.
13. What is the embryologic path of the pituitary gland?
The developmental path of migration of the pituitary gland is of particular importance to oral and max-
illofacial surgeons. The gland travels along the midline cell migration of the nasopharyngeal Rathke’s
pouch; therefore a craniofacial midline cleft or deformity may also result in pituitary dysplasia.
14. What hormones are produced by the anterior and posterior pituitary?
The anterior pituitary produces six major hormones: thyroid stimulating hormone (TSH), luteinizing
hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL), adrenocorticotropic hormone (ACTH),
and growth hormone (GH).
The posterior pituitary produces two major hormones: oxytocin and antidiuretic hormone (ADH).
15. What is a pituitary adenoma?
A pituitary adenoma is a benign tumor of the pituitary gland. It is the most common cause of hyperse-
cretion or hyposecretion of the pituitary gland. The selective hormone deficiency or excess depends on
the one of the six hormone-producing tissue responsible for the adenoma. It makes up approximately
15% of all intracranial tumors.
An MRI is the preferred imaging modality for identification of a pituitary tumor.
16. What is McCune-Albright syndrome?
McCune-Albright syndrome is a disorder associated with fibrous dysplasia, café au lait spots, preco-
cious puberty, and a variety of endocrine anomalies including acromegaly, ovarian dysfunction, and
adrenal adenomas. This syndrome is of particular concern to the oral and maxillofacial surgeon secondary to facial bone expansion. These patients may need osseous recontouring surgery or simple observation, always keeping in mind the possible need for further work-up from an endocrine perspective.
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17. What is acromegaly?
Acromegaly is a condition of excess growth hormone, often hypersecretion of a pituitary adenoma. It
is characterized by an increase in linear growth of both hard and soft tissues.
18. What are the clinical features of acromegaly?
The typical clinical features are hand and foot enlargement, frontal bossing, coarse facial features,
class three skeletal facial deformity, and malocclusion.
19. What is the difference between acromegaly and gigantism?
Both disease entities are caused by an excess of GH and are often due to hypersecretion for a pituitary
tumor. In gigantism, the excess circulating GH occurs before closure of the epiphyses, thus causing
great stature, in contrast to acromegaly, in which the presence of excess GH occurs after the growth
plates have closed.
20. What are the three kind of steroids produced by the adrenal cortex?
1. Glucocorticoids (e.g., cortisol)
2. Mineralocorticoid (e.g., aldosterone)
3. Androgen precursors (e.g., dehydroepiandrosterone [DHEA])
21. What is the regulatory control over adrenal cortex steroid production?
Glucocorticoid and androgen precursors are under the control of the hypothalamus pituitary adrenal
axis (HPA).
Mineral corticoids are regulated by the renal angiotensin adrenal system (RAA).
22. What is the function of aldosterone?
Aldosterone increases sodium retention and increases potassium excretion. It also regulates the
release of renin by increasing renal arterial perfusion pressure.
The release of renin from the juxtaglomerular cells of the kidney converts angiotensinogen to
angiotensin l in the liver. ACE converts angiotensin I to angiotensin II, thus activating aldosterone release.
23. What is Cushing’s syndrome?
Cushing’s syndrome is defined by excess production of cortisol, which is a glucocorticoid. The signs
and symptoms include abdominal obesity, diabetes, hypertension, hirsutism, and hypokalemia.
ACTH is secreted from the anterior pituitary following circadian rhythms, which can be altered by
exercise, acute illness, hypoglycemia, physical stress, and psychological stress.
The adrenal-hypothalamic-pituitary feedback loop is governed by the amount of circulating
glucocorticoid; therefore the higher the glucocorticoid, the less ACTH release, thus decreasing the
demand on the adrenal gland to produce more glucocorticoid.
The overproduction of glucocorticoid can be due to a tumor, a genetic translocation, or local
adrenal gland dysfunction.
24. Describe adrenal insufficiency.
The two types are primary and secondary adrenal insufficiency.
Primary adrenal insufficiency can have multiple etiologies resulting in loss of both glucocorticoids and mineral corticoid secretion.
Secondary adrenal insufficiency can also have different etiologies resulting in a decrease or loss
of glucocorticoid secretion only.
25. What is adrenal crisis?
Adrenal crisis is a life-threatening physiological state brought about by insufficient cortisol production
in the presence of an increase in physiologic demand. It is usually brought about in response to major
physical stress, such as major surgery, trauma, or sepsis.
26. What is the clinical presentation of adrenal crisis?
The acute presentation consists of severe circulatory collapse resulting in profound refractory hypo-
tension even in the face of vasopressors. The other possible symptoms can be delirium, confusion,
lethargy, and severe abdominal pain.
27. What is the syndrome of inappropriate antidiuretic hormone (SIADH)?
SIADH is essentially an increase in secretion of ADH due to increase in activity of the posterior pituitary
gland. The hypersecretion of the gland can be due to a variety of reasons resulting in hyponatremia
and increased water retention.
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28. What are the causes of SIADH?
The common causes include small cell lung carcinoma, tuberculosis, pneumonia, meningitis, and head
trauma. Other causes include pharmacologic agents such as clofibrate, cyclophosphamide, and the
oral hypoglycemic chlorpropamide. Less common causes include mechanical ventilation, narcotics,
and hypercarbia.
29. What is the clinical presentation for patients with SIADH?
A few of the most common presenting clinical signs are seizures, headache, nausea, vomiting, coma,
and delirium. The concomitant lab findings are hyponatremia, increase of urine concentration, and low
blood urea nitrogen.
30. How is SIADH diagnosed?
A clinical exam may reveal weakness, lethargy, seizure, confusion, and coma. Lab findings usually
show persistent hyponatremia, serum hyposmolarity > plasma, and an inappropriately concentrated
urine and abnormally high Na. Dehydration must be ruled out before diagnosis of SIADH can be made.
31. What is the treatment for SIADH?
Treatment for SIADH depends on the symptoms. Mild to moderate symptoms are treated with fluid
restriction (500 to 1000 mL/24 hr). Severe water intoxication (symptomatically severe hyponatremia)
requires hypertonic saline (3%, 200 mL) in addition to free water restriction. Water restriction is effective in most cases of chronic SIADH. Demeclocycline, which inhibits ADH action at the renal tubular
cell, can also be used.
32. Which hormone is also known as vasopressin, and where is it produced and
released?
Antidiuretic hormone (ADH). ADH is produced and released in the posterior pituitary.
33. What causes ADH release?
ADH is released in response to changes in the serum osmolality detected by the hypothalamus. Osmo-
lality that decreases to about 295 mOsm/kg initiates release.
34. What effect does an increased release of ADH have on urine concentration?
Because ADH affects the renal collecting tubule’s permeability, water will be reabsorbed, resulting in a
more concentrated urine.
35. Where are angiotensin I and II produced, and how does angiotensin II affect blood
pressure?
Angiotensin I and II are produced in the kidney. Angiotensin II actively increases vascular tone, stimu-
lates catecholamine release, and increases Na reabsorption (at the distal tubule). It also stimulates
release of aldosterone from the zona glomerulosa of the adrenal cortex.
36. What is azotemia?
Nitrogen retention resulting from factors other than primary renal disease.
37. What is a pheochromocytoma?
A pheochromocytoma is a tumor that produces catecholamines that have significant effects on blood
pressure. There are various blood assays and urine analyses that can be utilized to identify high levels
of circulating catecholamines. They vary in their sensitivities and can occasionally produce false positives. Preferred imaging for a pheochromocytoma is an MRI T2 weighted with gadolinium, although a
CT scan with contrast is also acceptable.
Treatment is surgical removal.
38. What is the rule of tens concerning a pheochromocytoma?
• 10%intraadrenal
• 10%extraadrenal
• 10%malignant
39. What are the common symptoms of a pheochromocytoma?
The classic triad of symptoms is palpitations, sweating, and headache.
Hypertension is the mainstay of the disease process; however other clinical findings may include
anxiety, arrhythmias, pulmonary edema, heart failure, and intracranial bleeding.
A few other processes can mimic these symptoms and clinical findings: the use of amphet-
amines or cocaine, essential hypertension, anxiety, and intracranial lesions.
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