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28. How does sorbitol accumulation lead to diabetic complications?
Cells of the tissues that do not require insulin for glucose transport (see question 22) become
hypertonic. In Schwann’s cells, the hypertonicity causes loss of feeling in extremities and a decrease
in sensation. In the lens of the eye, water accumulation leads to cataracts, macular edema, and
glaucoma. Damage to endothelial cells leads to thickening of basement membranes, resulting in
microangiopathies of the retina, arterioles of the kidneys, and small vessels of the skin.
29. What is the importance of nonenzymatic glycosylation of hemoglobin?
The degree of nonenzymatic glycosylation is dependent on the amount of plasma glucose levels.
Therefore high levels result in more glycosylation of hemoglobin. The normal hemoglobin A1c is 4%
to 6%. In diabetics, levels may reach 16% to 20%. Because the lifespan of a red blood cell is about
120 days and the glycosylation occurs continuously over that span, hemoglobin A1c concentrations
provide an index of the average blood glucose over the preceding 60 to 90 days.
30. How does glycosylation of platelets affect microvascular disease?
Glycosylation of platelets increases platelet adhesiveness. This allows platelets to produce excessive
thromboxane, which makes the platelets hypercoagulable. This hypercoagulable state predisposes a
diabetic to microvascular disease.
31. What are the criteria for the diagnosis of diabetes mellitus?
The diagnosis is made based on one or more of the following criteria (perform tests on two separate days):
• Signsandsymptomsplusarandomplasmaglucoseconcentration≥200 mg/dL
• Afastingplasmaglucose≥126 mg/dL on two occasions
• Oralglucosetolerancetestwitha2-hourpostprandialglucoseconcentration≥200 mg/dL and a
time 0 serum glucose level >126 mg/dL; hemoglobin A1c >6.5
32. What considerations should be taken in diabetic patients who require contrast
imaging?
Patients with diabetes are susceptible to developing radiocontrast-induced acute renal failure. If IV
contrast is necessary, give generous hydration before administering contrast agent. If the patient is
on metformin, hold it for 48 hours after contrast is given to prevent renal damage. Make sure renal
function has returned to baseline before resuming it.
33. What test is accepted by the American Diabetes Association for diagnosing
diabetes?
The fasting plasma glucose test is a diagnostic marker for diabetes. The patient fasts overnight for at
least 8 hours, and the test is performed the next morning. This test is performed only on non-pregnant
adults who are not taking any medications and do not have any other metabolic conditions that would
lead to abnormal results. A normal fasting plasma glucose is usually 65 to 110 mg/dL.
34. What is the oral glucose tolerance test, and how is it performed?
This test measures a person’s ability to handle a glucose load over a period of time. The patient fasts
overnight. In the morning, the fasting blood glucose is determined. The patient then ingests a 75-g
glucose load. In children and non-pregnant adults, the blood glucose is tested every 30 minutes for
2 hours. The test is considered normal if the fasting blood glucose is <110 mg/dL and the 2-hour
postprandial blood glucose is <140 mg/dL.
35. What are the different categories of hypoglycemia?
Categories of hypoglycemia can be broken down depending on the level of plasma glucose and
associated signs and symptoms (Table 21-1).
Table 21-1. Categories of Hypoglycemia
PLASMA GLUCOSE LEVEL SIGNS/SYMPTOMS
Mild 60-70 mg/dL Tachycardia, palpitations, pallor, shakiness, irritability
Moderate 50-60 mg/dL Impaired central nervous system function: confu-
Severe >40-50 mg/dL Loss of consciousness, difficulty awakening, seizures
sion, inability to concentrate, slurred speech,
blurred vision
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36. How do you treat mild to moderate hypoglycemia?
Initially, treat with 10 to 15 g of carbohydrates. Give the patient one-half cup of orange juice or a regu-
lar soft drink, three to five hard candies, one cup of milk, three glucose tablets, or two tbsp. of raisins.
Evaluate plasma glucose levels as soon as possible. If symptoms do not improve in 15 minutes, treat
with an additional 10 to 15 g of a carbohydrate source.
37. How do you treat severe hypoglycemia?
If a glucagon kit is available, the patient should be given a subcutaneous injection of glucagon.
The adult dose is 1 mg; children younger than age 5 years, 0.5 mg; and infants younger than 1 year,
0.25 mg. If no kit is available and the patient can swallow without risk of aspiration, 15 to 50 g of a
carbohydrate source can be given on the inside of the cheek. Sources include glucose gel, 1 to 4 tsp
of honey (except in infants), syrup, orjelly.Whenthepatientismorealert,followwithaliquidsuchas
orange juice.
38. What is the best route to administer agents to stimulate insulin release?
Oral glucose and amino acids have a greater stimulatory effect on insulin than intravenously
administered solutions because of stimulation of intestinal hormones by ingested substances. These
hormones include gastric inhibitory peptide, cholecystokinin (CCK), glucagon, and gastrin. All are
stimulators of insulin secretion.
39. What are the different insulin preparations?
See Table 21-2.
40. What are the effects of surgery on glucose control?
Surgery and general anesthesia cause a stress response with release of epinephrine, glucagon, cor-
tisol, growth hormone, interleukin-6, and tumor necrosis factor alpha. These neurohormonal changes
result in insulin resistance, decreased peripheral glucose utilization, impaired insulin secretion,
increased lipolysis, and protein catabolism. These effects can lead to hyperglycemia and ketosis in
some cases.
41. How do you manage a patient with diabetes that is controlled by diet only?
If plasma glucose levels exceed and remain above 250 mg/dL as a consequence of surgical stress or
infection, sliding-scale short-acting insulin therapy should be instituted.
42. How do you manage a surgical patient who controls diabetes with oral hypoglycemic agents?
Short-acting sulfonylureas and oral agents should be withheld on the operative day. Metformin and
long-acting sulfonylureas (Chlorpropamide) should be held 1 day before planned surgical procedures. Metformin is typically held 48 hours postoperatively. Renal function should be normal prior to
resuming treatment. Glucose values should be checked regularly postoperatively, and elevated levels
>180 mg/dL may be treated with short-acting sliding-scale insulin.
43. What is the management of a patient with insulin-controlled diabetes who is
undergoing major surgery?
Basal insulin is required at all times. Most diabetic patients who receive insulin use a combination of
intermediate-acting (NPH) and regular insulin. The formulation is 70% NPH and 30% regular insulin.
In these patients, total insulin dosage is usually given in the morning or divided between morning and
afternoon. Typically two-thirds of the NPH and regular insulin formulation is given in the morning and
one-third is given in the afternoon.
Table 21-2. Insulin Preparations
TYPE OF INSULIN ONSET PEAK DURATION
Short-acting Regular 0.5-1 hr 2-4 hr 5-7 hr
Intermediate-acting Isophane (NPH) 1-2 hr 6-14 hr 18-24 hr
Lente 1-2 hr 6-14 hr 18-24 hr
Long-acting Ultralente 6 hr 18-26 hr 36+ hr
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For short procedures (<2 hours):
If breakfast is delayed, patients may delay taking their usual short-acting insulin until after
surgery and before eating. Those who take long-acting insulin may continue basal insulin
For intermediate procedures (breakfast and lunch are delayed/missed):
• Omit any short-acting insulin on the morning of surgery.
• For patients who take two types of insulin (intermediate/long-acting and rapid/short-acting),
• For patients who take insulin (intermediate/long-acting and rapid/short-acting) two or more
• Start dextrose containing intravenous solution to provide 3.75 to 6.25 g glucose/hour to avoid
• For patients who develop hyperglycemia, supplemental short-acting insulin may be administered
• During surgery, plasma glucose, serum electrolytes, and arterial blood gases (ABGs) should be
• Once the patient has resumed oral intake, NPH insulin is started. The patient’s plasma glucose is
For long and complex procedures:
44. What is an example of an order for typical sliding-scale insulin?
See Table 21-3.
45. What are the classes of oral diabetic agents?
See Table 21-4.
without any change to the usual regimen.
only in the morning, give one-half to two-thirds of their usual total morning insulin dose
(both types).
times a day, give one-third to one-half of the total morning dose (both types of insulin).
metabolic changes of starvation.
subcutaneously.
monitored.
monitored, and the insulin dosage is adjusted with regular insulin as needed.
IV insulin is usually required. Blood glucose and electrolytes should be closely monitored (no less
than hourly). Generally, insulin infusions should be started early in the morning prior to surgery to allow time to achieve glycemic control. The most common infusion is the glucose
insulin potassium (GIK) infusion. It contains 10% dextrose, 10 mmol of potassium chloride,
and 15 units of short-acting insulin.
Table 21-3. Typical Sliding-Scale Insulin (Regular Insulin)
BLOOD GLUCOSE INSULIN DOSE
150-200 2 units
201-250 4 units
251-300 6 units
301-350 8 units
351-400 10 units
>400 Notify provider (10-14 units and adjust SSI)
Table 21-4. Classes of Oral Diabetic Agents
TYPE MECHANISM OF ACTION SITE OF ACTION
Biguanides Enhances insulin sensitivity Liver, GI tract
Decreases GI absorption
Decreases hepatic glucose production
Sulfonylureas Stimulates pancreas to produce more insulin Pancreas
Alpha-glucosidase
inhibitor
Thiazolidinediones Reduces insulin resistance Fat, muscle
Reduces glucose absorption from gut by reducing
enzymes required for carbohydrate breakdown
GI tract
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46. Which oral hypoglycemic is categorized as a biguanide?
Metformin (Glucophage) reduces hepatic glucose production, decreases GI glucose absorption, and
increases target cell insulin sensitivity.
47. What is the pharmacology of the sulfonylureas?
These type 2 diabetic agents acutely increase insulin secretion from the beta cells and potentiate
insulin action on several extrahepatic tissues. Long-term sulfonylureas increase peripheral utilization
of glucose, suppress hepatic gluconeogenesis, and possibly increase the sensitivity or number of
peripheral insulin receptors.
48. What drugs make up the sulfonylureas?
See Table 21-5.
49. What are the contraindications to the use of metformin in type 2 diabetes?
Metformin therapy is strictly contraindicated in alcoholics, patients with significant renal insuf-
ficiency or failure (serum creatinine >1.5 and >1.4 for women), and patients with liver disease.
These conditions considerably increase the risk of lactic acidosis, a fatal side effect. Patients who
are older than age 70 and those with low cardiac ejection fractions also are not candidates for
metformin therapy. Patients who are about to receive iodine contrast dye, such as before cardiac
catheterization, or who are to undergo major surgery should discontinue metformin 48 to 72 hours
before the procedure.
50. What is the pharmacology of the meglitinides?
These type 2 diabetic agents quickly stimulate insulin release by the beta cells of the pancreas to
reduce postprandial hyperglycemia. These drugs are taken before each of three meals.
51. What drugs make up the meglitinides?
See Table 21-6.
52. What is the pharmacology of the thiazolidinediones?
These type 2 diabetic drugs lower blood glucose by improving the target cell response to insulin in
muscle and fat. At the same time, they do not increase pancreatic secretion of insulin. The thiazolidinediones are taken once or twice a day with food. These drugs can be used by themselves or in
combination with sulfonylureas, metformin, or insulin. However, thiazolidinediones can have a rare
but serious effect on liver function requiring regular liver function tests. This could affect the length of
time that the amide local anesthetics are in circulation.
Table 21-5. Sulfonylureas
DRUG BRAND NAME DOSE DURATION
Tolbutamide Orinase 2 g 6-12 hr
Tolazamide Tolinase 250 mg 10-18 hr
Glipizide Glucotrol 10-15 mg 12 hr
Glyburide Micronase 5-10 mg 16 hr
Acetohexamide Dymelor 1 g 8-12 hr
Chlorpropamide Diabinese 250 mg 1-3 days
Table 21-6. Meglitinides
DRUG TRADE NAME DOSE ONSET OF ACTION DURATION
Repaglinide Prandin 0.5-2 mg bid 15-60 minutes 4-6 h
Mitiglinide Starlix 120 mg bid 1-30
bid, Twice a day.
minutes before meals
20 minutes 4 h
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53. What drugs make up the thiazolidinediones?
See Table 21-7.
54. What is the pharmacology of the alpha-glucosidase inhibitors?
These type 2 diabetic agents help the body to lower blood glucose levels by competitively inhibiting
pancreatic alpha-amylase and intestinal brush border alpha-glucoside, resulting in delayed breakdown of ingested complex carbohydrates, therefore slowing the absorption of glucose. These drugs
should be taken with the first bite of a meal. The alpha-glucosidase inhibitors can be used alone or in
combination with a sulfonylurea metformin or insulin.
55. What drugs make up the alpha-glucosidase inhibitors?
Acarbose (Precase) and miglitol (Glyset). These drugs have <2% absorption as active drug because
they work in the gastrointestinal tract. The metabolism is exclusively via the gastrointestinal tract.
56. What is the oral combination drug Avandamet?
Avandamet is a combination of biguanide and thiazolidinediones, such as metformin and Avandia. It is
used to treat type 2 diabetics who are not adequately controlled with metformin alone. The dosage is
determined by starting Avandia 4 mg/day and adding it to the current metformin dose. If the patient is
already taking Avandia, then add metformin so that the patient is getting l000 mg/day.
57. What is the oral combination drug Metaglip?
Metaglip is the combination of sulfonylurea and biguanide, such as glipizide (Glucotrol) and metformin.
This drug can be used as initial therapy for management of type 2 diabetes when hyperglycemia
cannot be controlled with diet and exercise, or as second-line treatment when neither drug by itself
controlshyperglycemia.Dosagesareexpressedasglipizide/metformincomponents.Whenused
as initial therapy, 1.25 mg/250 mg is taken daily or twice daily with meals. As second-line therapy,
2.5 mg/500 mg or 5 mg/500 mg is given twice daily with meals.
58. What is the oral combination drug Glucovance?
Glucovance is the combination of sulfonylurea and biguanide, such as glyburide and metformin. It can
be used for initial management of type 2 diabetes, or as second-line therapy when a sulfonylurea or
metformin alone cannot control hyperglycemia. In addition, Glucovance with a thiazolidinedione may
be required to achieve adequate control.
Glucovancedosagesareexpressedasglyburide/metformincomponents.Whenusedasinitial
therapy, 1.25 mg/250 mg is taken with a meal once daily. Patients with an HgA1c >9% or fasting
plasma glucose >200 mg/dL are started at 1.25 mg/250 mg twice daily. The maximum dose is not to
exceed 10 mg/2000 mg. For those patients previously treated with a sulfonylurea or metformin alone,
the initial dose is 2.5 mg/500 mg or 5 mg/500 mg twice a day.
59. What is pramlintide?
Its brand name is Symlin, and it is a synthetic form of the hormone amylin, which is produced in the
beta cells of the pancreas. It slows gastric emptying, suppresses glucagon, and regulates appetite. It
is an injectable drug that has been recently approved by the FDA. Pramlintide has been approved for
type 1 diabetics who are not achieving their A1c goal levels, and for type 2 diabetics using insulin and
unable to achieve their A1c goals. It has been shown to modestly improve HgA1c levels, as well as
promote modest weight loss without causing increased hypoglycemia.
60. What is exenatide?
Exenatide (Byetta) is a glucagon-like peptide-1 agonist that mimics incretin and promotes insulin
secretion, suppresses glucagon, and slows gastric emptying. It is an injectable drug approved
Table 21-7. Thiazolidinediones
DRUG TRADE NAME DOSE ONSET OF ACTION DURATION
Rosiglitazone Avandia 4-8 mg qd or bid Delayed 12 weeks
Pioglitazone Actos 14-45 mg qd Delayed Several weeks
Troglitazone Rezulin Not available Not available Not available
bid, Twice a day; qd, daily.
CHAPTER 21 MANAGEMENT OF THE DIABETIC PATIENT 227
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by the FDA for the treatment of type 2 diabetics who have not been able to achieve their target
HgA1c levels using metformin, a sulfonylurea, or a combination drug. As with pramlintide,
exenatide is injected with meals, and patients using it have experienced improved HgA1c levels
and modest weight loss.
61. How do insulin pumps work?
Insulin pumps deliver short-acting insulin 24 hours a day through a catheter placed subcutaneously.
Insulin doses are separated into basal rates, boluses, and doses to correct glucose levels.
62. What is a basal rate and a bolus?
A basal rate is a constant rate of insulin delivered over 24 hours, keeping blood glucose levels
in range between meals and overnight. The rate of insulin can be programmed to deliver different amounts of insulin at different times of the day and night. A bolus amount of insulin is
used to cover the carbohydrate in each meal or snack. There are buttons on the insulin pump
that will deliver the bolus if the meal is larger than planned, and a larger bolus of insulin can be
programmed to cover it.
63. What are the differences between type 1 and type 2 diabetes?
Type 1:
• Suddenonset
• Occursatanyage(typicallyyoung)
• Bodyhabitusisusuallythin
• Ketosisiscommon
• Autoantibodiesarepresentinmostcases
• Endogenousinsulinisloworabsent
Type 2:
• Gradualonset
• Occursmostlyinadults
• Patientsarefrequentlyobese
• Ketosisisrare
• Autoantibodiesareabsent
• Endogenousinsulincanbenormal,decreased,orincreased
64. What is the response of insulin and glucagon to dietary protein?
An increase in both hormones.
65. Which hormones are considered ketogenic? Why?
Epinephrine, glucocorticoids, glucagon, and growth hormone because they promote lipolysis.
66. What is the response by insulin to parasympathetic stimulation?
Insulin release will be increased.
67. How will epinephrine that is released from the adrenal medulla affect plasma
glucose?
Epinephrine decreases glycogen synthesis in the liver. In addition, its release is increased in response
to hypoglycemia.
68. Where is the major site of action for glucagon?
The breakdown of hepatic glycogen to glucose.
69. What hormones antagonize the action of insulin on blood sugar?
• Growthhormone
• Glucagon
• Cortisol
• Epinephrine
70. What are the most common types of infections in diabetics and why?
Diabetic patients have enhanced susceptibility to infections of the skin, tuberculosis, pneumonia,
and pyelonephritis. Together, these infections cause the death of about 5% of diabetics. In addition,
diabetics are very susceptible to fungal infections. The susceptibility to infections is a combination of impaired leukocyte function, inability to make antibodies against the bacteria, and vascular
insufficiency.
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BiBliography
Agabegi SS, Agabegi ED: Ring AC: step-up to medicine,ed3,Baltimore,2013,LippincottWilliams&Wilkins.
Cada DJ, Covington TR, Hebel SK, editors: Drug facts and comparisons,StLouis,1998,WoltersKluwer.
Cooper DH, Krainik AJ, Lubner SJ, Reno HE, Micek ST: Washington manual of medical therapeutics, ed 32, St Louis, 2007,
LippincottWilliams&Wilkins.
Gregory BA: Diabetes. In Abubaker AO, Benson KJ, editors: Oral and maxillofacial surgery secrets, ed 2, Philadelphia, 2007,
Mosby/Elsevier.
Khan NA,GhaliWA, Cagliero E: Perioperative management of blood glucose in adults with diabetes mellitus, UpToDate,
2014,WoltersKluwer.
Kumar V, Abbas A, Fausto N: Robbins & Cotran pathologic basis of disease, ed 7, Philadelphia, 2005, Saunders.
Roser M: Management of the medically compromised patient. In Kwon PH, Laskin DM, editors: Clinician’s manual of oral
and maxillofacial surgery, Carol Stream, IL, 1997, Quintessence.
Silverthorn DU: Human physiology: an integrated approach, ed 4, San Francisco, 2007, Benjamin Cummings.
Steil CF: Diabetes: an overview. In CVS pharmacy pharmaceutical care module—diabetes,Woonsocket,RI,1998,CVS
Pharmacy.
THEIMMUNOCOMPROMISED
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SURGICALPATIENT
Ludmils Antonos Jr., Osama Soliman, Noah Sandler,
A. Omar Abubaker
1. What are the major components of our immune system, and how do they
function?
The immune system is the body’s main way of fighting infections. Our immune system is composed of
both an innate and adaptive system. The innate components are congenital, and the adaptive immunity develops throughout one’s life. Adaptive immunity can be further divided into humoral and cellular
immunity. The innate immune system is composed of the skin (which acts as a barrier to prevent
invasion from foreign organisms), phagocytes, the complement system, and interferons. The humoral
portion of the adaptive system is composed of B-cells that produce antibodies (immunoglobulins) that
attach themselves to the surface of invading cells or organisms that help phagocytes detect them and
then engulf them. B-cells also help activate the complements system. Humoral immunity is a very
important component for attacking bacteria. The cellular portion of adaptive immunity is more useful
in the defense against viruses, parasites, and cancer cells. Cellular immunity is a T-cell-mediated
response. There are two types of T-cells: the helper T-lymphocytes and the killer T-cells. The helper
T-cells recognize and flag the invading organism to the killer T-cells, which in turn destroy the target
organism.
2. What are the main organs involved in providing immunity?
The major human immune system is composed of several organs including the skin, spleen, tonsils,
bone marrow, and lymph nodes.
3. What is the main problem with immunocompromised patients?
Immunocompromised patients usually suffer from one or more types of immunodeficiency disorders
that decrease the patient’s immune system’s ability to mount an adequate immune response to
various immunological assaults. This in turn makes patients more susceptible to develop viral and
bacterial infections as well as malignancies.
4. What are the types of immunodeficiency?
Immunodeficiency can be either primary or acquired (secondary). Primary immunodeficiency is usu-
ally caused by a defect in a specific aspect of the immune system, such as a specific immunoglobulin.
Acquired immunodeficiency can be secondary to disease or iatrogenic causes, such as the result of
chemotherapy, and may involve more than one aspect of the immune system.
5. Which types of immunodeficiency disorders are more common?
Acquired (secondary) immunodeficiency disorders are much more common than hereditary (primary)
ones.
6. What are the types of primary immunodeficiency disorders?
The WHO lists over 150 different primary immunodeficiency disorders. They are all categorized in one
of five categories: B-cell deficiencies, T-cell and combined T-cell and B-cell deficiencies, phagocyte
deficiencies, complement deficiencies, and periodic fevers.
See Box 22-1 for common specific disorders.
7. What are the common causes of acquired (secondary) immunosuppression and
immunodeficiency in hospitalized patients?
Acquired (secondary) immunodeficiency can be caused by any of several factors, including:
• Malnutrition:Mostcommoncauseworldwide
• Drugs:Especiallycytotoxicdrugs(chemotherapy)
• Iatrogeniccauses:Suchaspost-transplantdrugimmunosuppression
229
CHAPTER 22
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Box 22-1. Common Immunodeficiency Disorders
B-cell Deficiencies
• X-linkedagammaglobulinaemia(Bruton’sDisease),(XLA)
• Commonvariableimmunodeciency(CVID)
• SelectiveIgAdeciency
• IgGsubclassdeciency
• Immunodeciencywiththymoma(goodsyndrome)
• Transienthypoagammaglobulinaemiaofinfancy(THI)
• Hyper-IgMsyndrome.-ar(AutosomalRecessive)
T-cell and Combined T- and B-cell Deficiencies
• Severecombinedimmunodeciency(SCID,severalforms)
• Catch22syndrome(DiGeorgesyndrome,DGS)
• X-linkedlymphoproliferativesyndrome(Duncan’ssyndrome)
• Hyper-IgMsyndrome:xl(cd40liganddeciency)
• MHCclassIIdeciency(barelymphocytes)
• Ataxia-teleangiectasia(LouisBar’ssyndrome)
• Wiskott-Aldrich’ssyndrome
• IPEX
• Hyper-IgMsyndromes,autosomalrecessive(AR)-Forms
• Chronicmucocutaneouscandidiasis
Phagocyte Deficiencies
• Chronicgranulomatousdisease(CDG)
• Interferong/interleukin12,andreceptors,deciencies
• Familialhemophagocyticlymphohistiocytosis(FHI)
• Congenitalagranulocytousis(Kostmann’ssyndrome)
• Cyclicneutropenia
• Leukocyteadhesiondeciency(LAD)
• Chédiak-higashi’ssyndrome
• Griscelli’ssyndrome(GS)
• Hyper-IgEsyndrome(HIES)
Complement Deficiencies
• Properdindeciency
• Mannan-bindinglectindeciency(MBL)
• Hereditaryangioedema(HAE)
• Anddecienciesofallothercomplements
Periodic Fevers
• Traps(tumornecroticfactorreceptorassociatedperiodicsyndrome)
• FamilialMediterraneanfever(FMF)
• Hyper-IgDsyndrome(HIDS)
• PFAPAandothers
http://www.ipopi.org//index.php?mact=News,cntnt01,detail,0&cntnt01articleid=117&cntnt01returnid=38
• Viruses:HIV,CMV
• Lymphoreticularmalignancy
• Proteinloss:Duetonephroticsyndrome
• Advancedage
• Burns
• Organfailure,forexample,renaldiseaserequiringperitonealdialysis
• Diabetes
• Radiation
• Surgery
• Trauma
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8. What are the different classes of systemic immunity?
Systemic immunity can be classified into an antigen-specific or nonspecific immunity. Antigen-
specific can be either humoral or cell-mediated immunity. Parts of the nonspecific immunity system
are the phagocytes and complement cascade.
9. What is the effect of deficiency in cell-mediated immunity, and what are the
appropriate methods of testing for such deficiency?
Decienciesincell-mediatedimmunitypredisposethepatienttoinfectionfromgram-negativeorgan-
isms, mycobacteria, viruses, Pneumocystis jiroveci pneumonia (PJP) (formerly known as Pneumocystis
cariniipneumonia[PCP]—themostcommonopportunisticinfectioninpersonswithHIVinfection),
and Toxoplasma.Thebesttestforcell-mediatedimmunityisdelayed-typehypersensitivity(DTH)skin
testing, in which patients’ reactions to intradermal injections of Candida, tuberculin, Trichophyton, and
otherantigensareobserved.DirectmeasurementofT-cellfunctionbytheuseofmonoclonalantibodiesis,however,amorespecictest.TheratioofhelperT-cells(CD4)tosuppressorT-cells(CD8)
(normally1.8:2.2)isoftenusedasameasureofthisimmune-typefunction.
10. How is deficiency in humoral immunity manifested, and what are the appropriate
methods of testing for humoral immunity?
Deciencyinhumoralimmunitypredisposespatientstoinfectionfrompyogenicbacteria,hepatitis
viruses, Cytomegalovirus, parasites, and P. jiroveci.Measuringserumimmunoglobulinlevelstests
humoral immunity. Testing for the presence of antibodies to previous vaccination or infections can
also indicate the status of the patient’s humoral immunity. Other tests for humoral immunity, such as
circulating B-cell count and in vitro B-cell testing, can also be performed.
11. What infections are caused by deficiency in polymorphonuclear neutrophils
(PMNs)?
Decienciesofneutrophilicleukocytes(leukopenia)predisposepatientstoinfectionsfromstaphy-
lococci, Serratia, Escherichia coli, Pseudomonas, Proteus, Enterobacter, Salmonella, Candida, and
Aspergillus.Absoluteneutrophilcount(ANC)andmostfunctionsofpolymorphonuclearleukocytescan
be tested by obtaining a CBC with differential and an absolute neutrophil count test.
12. What is the effect of deficiency in complement, and how can complement functions be tested?
DeciencyincomplementpredisposespatientstoinfectionsfromNeisseria and viruses. The status of
complement cascade can be measured by the C’H50 (50% hemolyzing dose of complement) assay
andbyindividualassayorC3andC4levels.
13. What are the possible complications of immunosuppressive drugs in transplant
patients?
Although newer immunosuppressive medications have reduced the amount and severity of acute
transplant rejection, these new regimens are not without consequences. An increased risk of infection is seen in these patients secondary to decreased host resistance, with an increased risk for graft
rejection in patients with severe infection. Infection is also the leading cause of death in transplant
patients. Therefore, any transplant patients with active infections should be treated aggressively.
Another risk for transplant patients is the increased incidence of de novo cancer. There may be a
100-fold increased incidence of cancer in the transplant patient. The most prevalent neoplasms
are lymphoma and squamous cell carcinoma of the lips and skin. The incidence of tumors such as
non-Hodgkin’s lymphoma is approximately 2%, and this risk increases with the duration of immu-
nosuppressivetherapy.Mostoftheselesionsoccurintheheadandneck,gastrointestinaltract,and
transplanted allograft. These lesions are seen primarily with the use of cyclosporine and tacrolimus
andarebelievedtoberelatedtotheinhibitionofEpstein-Barrvirus(EBV)cytotoxicT-cells.Transplant
patients on immunosuppressive therapy, therefore, should be examined carefully for lip and skin
lesions, nonhealing ulcers, and lymphadenopathy, and questionable lesions should undergo biopsy.
14. What are the most common types of orofacial infection seen in immunocompromised patients?
T-cell deficiency is commonly found in post-transplant patients on immunosuppressive therapy, in
AIDSpatients,insomepatientswithcertainformsofcarcinoma,andinpatientsreceivingtreatment
forcancer.Viralandfungalinfectionsaremorecommoninthesepatients.Viralinfectionsaremost
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